Summary
Thyroid
6
Hyperthyroidism
8
Hypothyroidism
10
Thyroid Tumours
12
Parathyroids
13
Hyperparathyroidism
13
Hypoparathyroidism
13
Mammella
14
Benign Mammary Injuries
14
Breast Carcinoma
14
Lung
24
Hemoftoe
24
Volet Costal
24
Diaphragmatic Relaxation
24
Pleural Empyema
24
Pneumothorax Hypertension
24
Haemothorax
25
Lung Carcinoma
25
Abdomen
29
Abdominal Pain
29
Laparoscopy
40
Ernie
47
Inguinal Hernia
52
Crural Hernia
61
Umbilical Hernia
62
Dawn Line Hernia
64
Improper Erniations: Diastasis Of The Rectus Muscles
64
Diaphragmatic hernias
64
Bochdalek's Posterolateral Hernia:
65
Hernia Of The Morgagni-Larrey Foramen
66
Phrenic Centre Hernia
66
Agenesis Of A Haemidiaphragm
67
Boyd's Lumbar-Costal Hernia
67
Traumatic Diaphragmatic Hernias
67
Eventratio E Relaxatio
68
Hiatal hernia.................................................................................................................................................. 69
Laparocele......................................................................................................................................................73
Peritoneal Pathology.....................................................................................................................................75
Peritonitis....................................................................................................................................................... 75
Peripatetic...................................................................................................................................................... 81
Subphrenic abscess....................................................................................................................................... 82
Dysphagia...................................................................................................................................................... 84
Oesophagus....................................................................................................................................................85
Achalasia........................................................................................................................................................85
Diffuse Esophageal Spasm.......................................................................................................................... 88
Esophageal Diverticula................................................................................................................................ 88
Gerd................................................................................................................................................................ 89
Barrett's Esophagus.......................................................................................................................................95
Esophageal Carcinoma.................................................................................................................................97
Benign Tumours of the Oesophagus........................................................................................................ 101
Leiomyomas............................................................................................................................................101
Esophageal varices...................................................................................................................................... 101
Stomach........................................................................................................................................................103
Peptic Ulcer................................................................................................................................................. 103
Zollinger-Ellison Syndrome.................................................................................................................. 107
Piloric Stenosis............................................................................................................................................107
Gastric Carcinoma...................................................................................................................................... 108
Gist................................................................................................................................................................116
Small intestine.............................................................................................................................................117
Meckel's Diverticulum............................................................................................................................... 117
Large intestine.............................................................................................................................................122
Diverticular Colon Disease........................................................................................................................122
Acute Appendicitis..................................................................................................................................... 130
Appendicular mucocele..............................................................................................................................135
Appendicular Carcinoid............................................................................................................................. 135
Proctite......................................................................................................................................................... 136
Colon-Rectal Polyps...................................................................................................................................136
Colorectal Carcinoma.................................................................................................................................140
Pilonidal Cyst (Sinus) Or Sacrococcygeal Cyst......................................................................................148
Ano............................................................................................................................................................... 149
Anatomy Of The Anal Canal.................................................................................................................... 149
Condylomas of the anus.............................................................................................................................149
Perianal abscess...........................................................................................................................................150
Anal Fistula................................................................................................................................................. 152
Haemorrhoids.............................................................................................................................................. 155
Rectal Prolapse............................................................................................................................................159
Solitary Rectal Ulcer.................................................................................................................................. 161
Angiodysplasias.......................................................................................................................................... 161
Ragade..........................................................................................................................................................162
Carcinoma of the anus................................................................................................................................164
Chronic Inflammatory Intestinal Diseases...............................................................................................166
Crohn's disease............................................................................................................................................166
Perianal Crohn's Disease....................................................................................................................... 167
Ulcerative Rectocolitis............................................................................................................................... 178
Liver............................................................................................................................................................. 180
Liver Failure................................................................................................................................................180
Acute liver damage.....................................................................................................................................180
Portal Hypertension....................................................................................................................................181
Hepatic adenoma.........................................................................................................................................182
Focal Nodular Hyperplasia........................................................................................................................183
Liver abscess............................................................................................................................................... 183
Hydatid cyst.................................................................................................................................................185
Hemangioma................................................................................................................................................186
Liver Carcinoma......................................................................................................................................... 186
Resective liver surgery.......................................................................................................................... 188
Biliary Ways................................................................................................................................................190
Biliary calculosis.........................................................................................................................................190
Adenomyomatosis Cholecyst....................................................................................................................201
Carcinoma Of The Gallbladder.................................................................................................................201
Cholangiocarcinoma................................................................................................................................... 202
Pancreas....................................................................................................................................................... 204
Acute pancreatitis....................................................................................................................................... 204
Chronic pancreatitis....................................................................................................................................213
Pancreatic Carcinoma.................................................................................................................................214
Insulinoma................................................................................................................................................... 221
Ampulloma.................................................................................................................................................. 221
Spleen...........................................................................................................................................................222
Splenosi........................................................................................................................................................223
Splenomegaly.............................................................................................................................................. 223
Cysts.............................................................................................................................................................224
Echinococcus Cysts.................................................................................................................................... 224
Pseudocysts..................................................................................................................................................224
Acute And Chronic Phlogoses.................................................................................................................. 225
Acute Torsion And Mobile Spleen...........................................................................................................225
Splenic artery aneurysm.............................................................................................................................226
Splenic infarction........................................................................................................................................226
Benign Neoplasms......................................................................................................................................226
Malignant Neoplasms.................................................................................................................................227
Spleen Surgery............................................................................................................................................ 227
Surgical Jaundice........................................................................................................................................ 232
Intestinal Occlusions.................................................................................................................................. 235
Digestive Haemorrhages............................................................................................................................246
Rene..............................................................................................................................................................257
Nephrovascular Hypertension................................................................................................................... 257
Renal Vein Thrombosis............................................................................................................................. 257
Renal Failure............................................................................................................................................... 258
Dialysis.........................................................................................................................................................258
Haematuria...................................................................................................................................................259
Renal Carcinoma.........................................................................................................................................262
Oncocytoma.................................................................................................................................................267
Angiomyolipoma........................................................................................................................................ 268
Surrene......................................................................................................................................................... 269
Adrenal Neoformations..............................................................................................................................269
Pheochromocytoma.................................................................................................................................... 270
Traumatology.............................................................................................................................................. 277
Abdominal Trauma.....................................................................................................................................277
Liver Trauma...............................................................................................................................................281
Splenic trauma:........................................................................................................................................... 283
Transplants...................................................................................................................................................288
Liver Transplantation................................................................................................................................. 292
Kidney Transplantation..............................................................................................................................296
Heart Transplant......................................................................................................................................... 299
Pancreas Transplantation........................................................................................................................... 300
Gonads......................................................................................................................................................... 301
Testis............................................................................................................................................................ 301
Varicocele.................................................................................................................................................... 301
Hydrocele.....................................................................................................................................................304
Haematocele................................................................................................................................................ 306
Piocele..........................................................................................................................................................306
Scrotum Acute.............................................................................................................................................306
Testicle torsion............................................................................................................................................ 307
Testicular Carcinoma..................................................................................................................................308
Skin and Subcutaneous Pathologies......................................................................................................... 313
Sebaceous cysts...................................................................................................................................... 313
Lipomas................................................................................................................................................... 314
Lymph nodes...........................................................................................................................................315
Erisipela....................................................................................................................................................... 315
Vascular Pathology.....................................................................................................................................316
Mesenteric Ischaemia/Angina Abdominis...............................................................................................316
Aop............................................................................................................................................................... 316
Varices Of The Lower Limbs................................................................................................................... 320
THYROID
The thyroid gland lies on the tracheal shield and is located between the large sternocleidomastoid
muscles, under the layer of the ribbon muscles of the neck.
The thyroid gland is vascularised by:
- Two right and left superior thyroid arteries (supplying the right and left upper pole/lobe)
- Two right and left lower thyroid arteries (supplying the right and left lower pole/lobe)
- Neubauer's IMA artery (vascularising the isthmus).
So there are 5 arteries and they anastomose to each other in full channel, and therefore if the surgeon
does not have full control over all 5 arteries, he will have a bleeding surgical field. In fact, especially
in the past, the fear of haemorrhages during thyroid surgery was very high, and the thyroid was long
considered a bleeding organ. In the past, thyroid surgeries were not started unless at least two blood
bags were present in the operating theatre.
The thyroid gland is a gland located in the anterior part of the neck, which produces the hormones T3
and T4 and as it increases in volume it tends to push towards the respiratory tract, below, which is
characterised by rigid structures.
Fundamental to the production of thyroid hormones is the presence of an adequate supply of iodine in
the blood, and therefore dietary intake is important, which explains how in areas of endemic goitre,
this is due to a diet low in iodine or rich in vegetables such as broccoli or cabbage, which are foods
that inhibit the absorption of iodine in the intestines. Iodine is therefore essential for thyroid function.
The daily requirement of iodine is 150 mcg/day, which prevents goitre. A prolonged diet of < 50
mcg/day leads to hypothyroidism with multinodular goitre; whereas a diet of 1000 mcg/day of iodine
leads to hyperthyroidism with toxic nodular goitre.
When the iodine supply is reduced, the gland goes into metabolic stress and therefore undergoes
hypertrophy in order to maintain constant hormone levels in the blood. Hypertrophy means an increase
in volume that over the years may give rise to the symptoms described above. Thanks to the intake of
iodized sea salt, this pathology (goitre) has greatly diminished, in fact, the endemic iodine-deficient
areas have been reduced.
Goitre is a pathological condition characterised by hyperplasia and hypertrophy of the thyroid gland,
as a result of various pathological conditions that can affect it. It is a condition t h a t greatly affects
the population, which may be of surgical interest, but not always.
N.B. Goitre becomes surgical when it gives compression symptoms, when nodules are detected and
when the symptoms of hyperthyroidism, if the goitre is a toxic goitre, can no longer be managed with
medical therapy.
The thyroid gland is related to the trachea, oesophagus, recurrent laryngeal nerves, and blood vessels:
hence, a key concept in the surgical treatment of thyroid pathology: surgery is indicated in the
presence of symptoms attributable to a mass occupying space in a particular anatomical district,
because it is not very extensible.
The structures that may be affected by an increase in gland volume are:
1) The trachea: it is a rigid structure, if the gland engages in the upper respiratory tract where the
confined elements are rigid (clavicle and ribs), it causes a gradual and progressive crushing of
the trachea, with reduction of the respiratory space. The symptom that the patient will report is
dyspnoea, especially in the evening;
2) The oesophagus: it is affected if the mass grows more posteriorly. The symptom that the
patient will report is dysphagia.
3) Recurrent nerves: a compression of these structures is referred to as dysphonia.
4) Carotid and jugular vessels: primarily the jugular vein, which may be associated with
presentation of
taurine neck (these are rare paintings).
When it comes to thyroid surgery, some gaps must be bridged:
1) Recognising and preserving the recurrent laryngeal nerve: the recurrent laryngeal nerve should
not be loaded on webbing during surgery, because its excessive compression can lead to
transient injury. Today, the surgeon isolates it, does not load it, but follows it as it enters the
larynx up to the tubercle of Zuckerkandl, so that the disconnection of the nerve occurs without
trauma, respecting its point of emergence at the laryngeal level. This represents a fundamental
repere point, which guides us in separating the nerve from the gland itself.
The function of the laryngeal nerve is to abduct (move away) the vocal cords, and therefore a
bilateral lesion causes adduction and therefore asphyxia, which if not treated with intubation,
leads to death. Here, the surgeon waits for the anaesthetist to awaken the patient, approaches
and becomes aware of the laryngeal stridor, which can be an alarm bell of chord adduction. A
unilateral lesion may cause a bitonal, metallic voice, i n any case the voice may drop
transiently as a result of a small nerve lesion, but after a few days it gets over
2) Control of haemostasis: when disconnecting the thyroid gland from the recurrent nerve, it must
not involve the use of electrical means such as electrocautery, which causes burns, cauterises
the area and stops medium to small haemorrhages. This electrocautery action causes the socalled 'Joule effect', the dissipation of heat is responsible for injury to the recurrent laryngeal
nerve; this device should not be used in the area adjacent to the tubercle of Zuckerkandl, in
fact, mechanical ligatures are performed here for the small bleeding vessels.
3) Saving of the parathyroid glands: there are 4, sometimes 5 or 6.
The typical areas where they are found are posterior to the superior and inferior poles of the
right and left thyroid lobes. They are irrigated by the relevant thyroid arteries:
o The two upper parathyroids are fed by the posterior sphincter branch of the upper
thyroid (right and left);
o The two lower parathyroids are nourished by the posterior sphincter branch of the lower
thyroid (right and left);
The parathyroids are small endocrine glands responsible for calcium and phosphorous
metabolism. The good surgeon who performs a total thyroidectomy will have to measure
calcium post-operatively, because in the case of high ligation, at root level, of the upper and
lower thyroid pedicles, the posterior nutritive branch directed to the parathyroids is sacrificed,
and therefore even if left in situ, they would suffer ischaemia: PTH levels then plummet,
calcemia falls, leading to iatrogenic hypoparathyroidism, whereby the patient may experience a
tetanic crisis (beginning with tingling in the extremities of the limbs or lips, leading to tetanic
contractions of the muscles). The surgeon's task must be to respect the nourishing branches by
ligating the pedicles selectively, after they have been dislodged, thus ligating only the anterior
and middle branches (avoiding also ligating the posterior branch that carries nourishment to the
parathyroids). This is not always easy because sometimes the parathyroids may be hidden by
surrounding fat residues, or may be located within the thyroid gland itself.
Altered production of thyroid hormones leads to two pathological conditions:
- If too much is produced: hyperthyroidism
- If little is produced: hypothyroidism (and this is associated with a compensatory volumetric
increase of the gland)
HYPERTHYROIDISM
It occurs when the thyroid gland overworks, disengaging itself from the hypothalamus-pituitary-gland
feedback and is characterised by increased thyroid hormones in the blood and acceleration of all
metabolic reactions and effects:
- Cardiovascular
- Muscular
- Cerebral
- Renal and Ecc.
In these cases, drug therapy only succeeds in limiting the symptoms in certain cases. And since the
hyperfunction of the gland cannot be controlled by drug therapy, there are indications for surgery.
Characteristic symptoms are:
- Nervousness
- Hyper-reactivity
- Agitation
- Tachycardia
- Shaking hands
- Hot flashes
-
Continuous sweating
Weight loss
Muscle weakness
Tendency to diarrhoea
There are different forms of hyperthyroidism: causes include genetic and environmental factors
(smoking, stress, viral infections, drugs, excessive iodine intake).
1) Basedow's disease (diffuse toxic goiter): it is more frequent in the female sex, there is an
enlargement of the gland in toto and presence of ophthalmopathy (with protrusion of the
eyeballs), due to an autoimmune process affecting the retro-orbital tissues. Then there may also
be infiltrative dermopathy or pretibial myxedema
2) Plummer's adenoma (toxic nodular goiter): it is common in the elderly, asymmetrical, not
the whole gland in fact goes into hyperthyroidism, but only a nodule, with hyperfunctioning
follicular adenoma, which then leads to compression of the surrounding parenchyma, hence the
asymmetry. There are no ocular changes. It is found upon palpation, and the clinical
manifestations are those of hyperthyroidism, with increased serum thyroid hormones and
suppressed TSH;
3) Chronic or sub-acute thyroiditis: is of viral or autoimmune origin. The thyroid gland is
increased in volume and painful to palpation.
Medical therapy includes:
- Hormone therapy inhibiting the hypothalamic-pituitary-thyroid axis;
- Suppressive therapy: anti-thyroid drugs are used: methimazole and propyl-thiouracil. In the
case of a subsequent surgical approach, it should be stopped first, because it increases bleeding
(in fact, the nodule becomes hypervascularised during therapy. Then if we only have a
hyperfunctioning nodule, with the remaining portion of parenchyma suppressed, the diatribe is
still open as to whether to perform a thyroidectomy or a haemithyroidectomy, especially when
the nodule affects only one lobe, avoiding medico-legal disputes);
- Radiometabolic therapy with iodine131;
- Beta-blockers: to reduce cardiovascular symptoms;
For multinodular and diffuse goiter, the surgical therapy of choice is total thyroidectomy. A
basicervical incision is made between the medial margins of the two sternocleidomastoid muscles,
taken as repere points. The median raphe of the ribbon muscles, which may be attached to the thyroid
capsule, is opened, the superior and inferior vascular pedicles are dominated, then the middle thyroid
vein, which allows the gland to be pulled out completely. This is followed by recognition and isolation
of the recurrent nerve and control of haemostasis.
HYPOTHYROIDISM
It occurs when the gland produces little hormone, or when it is forced to hypertrophy in order to
produce a sufficient amount. It is associated with insufficient amounts of hormones and a slowdown in
metabolic functions.
Symptoms:
- Apathy
- Weight gain with significant water retention
- Constipation
- Bradycardia
- Depression
- Sensitivity to cold
- Fatigue
A particular picture is that of cretinism, which is linked to primitive congenital or endemic form
hypothyroidism (iodine deficiency), with serious consequences on neurodevelopment and skeletal
growth, resulting in dwarfism, mental retardation and some cases muscular rigidity and deafness.
The forms of hypothyroidism include:
-
Congenital primitive hypothyroidism: from iodine deficiency, thyroid dysgenesis,
dyshormogenesis
Acquired primary hypothyroidism: from Hashimoto's thyroiditis, thyroid surgery,
radiotherapy, medication;
Secondary and tertiary hypothyroidism: from hypothalamo-pituitary disorders.
1) Dietary iodine deficiency: rarer today, but until recently very common in inland Sicily.
2) Hashimoto's thyroiditis: a chronic condition more frequent in women, which is characterised
by a significant decrease in hormone production and the gland undergoes parenchymatisation,
becomes harder and more fibrous and dislodges with difficulty due to the tenacious adhesions
created with the surrounding structures. This is an autoimmune disease caused by antibodies
that cause progressive degeneration of the gland.
3) Postpartum thyroiditis: a transitory condition that occurs to some women after childbirth, and
then regresses over time
Medical therapy
Eutirox which reduces TSH levels and puts the gland at rest and reduces its trophism.
Thyroid disorders affect women more, probably due to hormonal imbalances that can arise in
pregnancy, menopause, and the influence of oestrogen on urinary sodium excretion.
Diagnosis
1) Examination of the neck: inspection and palpation. The thyroid gland is usually neither visible
nor palpable.
On inspection, the patient is asked to swallow, so the thyroid gland tends to rise. On inspection,
asymmetry or not and the presence of tumefactions can be detected. The vascular-nervous bundle is
assessed for possible jugular turgor (taurine neck)
On palpation: one must stand behind the patient with two hands, making the patient relax. The
presence of palpable thyroid gland swelling is already an expression of increased volume, although not
yet relevant as a clinical subjectivity. Palpation helps to assess volume, consistency and relationship
with neighbouring organs.
● The consistency is parenchymatous, so in the presence of hard ligamentous swelling,
hypomobile to the skin planes, neoplastic pathology is suspected.
● In the presence of a small swelling, but evident symptoms of a space-occupying mass, one
must think of a goitre descending further and further into the mediastinum; an increase in the
lower poles, also due to the effect of gravity, tends to reach the anterior mediastinum, will give
early signs and the clinic will make itself felt earlier, affecting the trachea and oesophagus.
● An increase in volume that goes posteriorly, towards the spinal column, can also be deceptive:
thus, it is a mass that is not very exophytic, but sinks laterally or posteriorly, wedging itself
into that anatomical tracheo-oesophageal space. Usually, dysphonia is instead related to a
goitre developing posteriorly.
● In contrast, a goitre that starts in the isthmic area gives a sign of itself anteriorly, whereas a
goitre that starts in either lobe may camouflage itself and make its way posteriorly. An isthmicstarting goitre, in which there is evident alteration of the profile of the neck anteriorly, may be
paucisymptomatic because the volumetric increase has an external outlet and does not
compress the oesophagus and trachea.
2) Hormone dosages
3) Anti-thyroid antibodies
4) Diagnostic imaging :
- ETG (echo)
- Thyroid scintigraphy
They allow us to distinguish altered morphological structures of the thyroid gland and distinguish
parenchymatous nodules from cystic nodules.
In the case of thyroid scintigraphy, the patient is given an iodine tracer that concentrates in the thyroid
gland, because it is the only organ in our body where iodine concentrates. This is also useful for
radiotherapy for thyroid cancer patients, in which toxic iodine 131 is used.
Prevention: proper diet with iodine-rich foods (fish, seafood..) and reduction of foods that prevent
absorption such as cabbage and broccoli. The use of iodized salt has led to a reduction in the
occurrence of endemic goitre, as a pinch o f salt already ensures the correct sodium intake.
TUMOURS OF THE THYROID
Women are affected 4 times more frequently than men and correlates with a 5-year survival after
diagnosis of 70%.
Risk factors include:
- Thyroid goiter
- Exposure to radiation (e.g. Chernobyl disaster)
- Familiarity
They are classified into:
- Benign: hyperfunctioning thyroid adenomas
- Malignant: adenocarcinomas:
o papilliferous and follicular adenocarcinomas
o Medullary adenocarcinomas (dangerous)
o anaplastic adenocarcinomas (incurable and inauspicious)
Surgical therapy is indicated for:
1) Failure of medical therapy
2) Bulky or even mimetic goitre posteriorly or towards the anterior mediastinum, giving spaceoccupying syndrome, compressing surrounding structures such as trachea, oesophagus and
recurrent nerves
3) Thyroid dysplasia or neoplasia (neoplastic transformation of goitre)
+Hemithyroidectomy - indications
The removal of a single thyroid lobe is
indicated in cases of microfollicular
(potentially malignant), toxic adenoma, the
fetal, embryonal adenomas and goitre with or
without nodules,
unilateral, when it causes compression of adjacent organs or represents an aesthetic defect. The
technique is similar to that of total thyroidectomy.
Thyroid surgery today is plannable and safe: ligation of the vascular pedicles has enabled surgeons to
operate very precisely on dry surgical fields, without haemorrhaging, and this allows effective
isolation of the recurrent nerves and the parathyroids, whose structure can be respected, except in
extreme cases, where there is a diagnosis of a tumour, which is why part of the nerves will be removed
if they are infiltrated by the tumour. The same applies to the parathyroids.
In reality, if the surgeon operates on the goitre for tumour pathology, the surgeon's aim is to be radical
and therefore any injury to recurrent nerves is justified. Oncological radicality presupposes that the
surgeon goes into the healthy area, sacrificing neighbouring structures as well. Ideally, at least one
recurrent nerve and one parathyroid should be preserved, but if this is not possible, there is no risk
from a medico-legal point of view.
Good neoplastic surgery is radical, unless there has been involvement of satellite, central
compartment, and laterocervical lymph nodes. In the latter cases radicality is not guaranteed by total
thyroidectomy and adjuvant therapy with radioactive iodine will be required to achieve disease
clearance.
The indications for adjuvant treatment are:
- Dimensions > 5 mm
- Lymph node positivity
PARATIROIDS
HYPERPARATHYROIDISM
We distinguish three types of hyperparathyroidism:
● Primitive, caused by an overproduction of PTH by the main cells. As a consequence, there is
substantial calcium absorption resulting in hypercalcaemia and hypophosphatemia due to
excessive phosphate excretion;
• In 80% of primary hyperparathyroidisms we find a single adenoma;
• Other less frequent causes may be a primary hyperplasia of the gland, which may be diffuse
or nodular (5-10%);
• Parathyroid carcinoma (<5%)
• MEN
• Paraneoplastic syndrome in the course of poorly differentiated neuroendocrine tumours
● Secondary (extrinsic), caused by target organ resistance to parathormone with increased
production to compensate for hypocalcaemia and hyperphosphatemia. It is caused by
pathologies such as chronic renal insufficiency, vitamin D deficiency or intestinal
malabsorption; this stimulus, prolonged over time, can induce hyperplasia of the main cells,
which regresses if the cause disappears, but which can progress and turn into tertiary
hyperparathyroidism
● Tertiary, PTH production disengages from control mechanisms, becoming autonomous.
HYPOPARATHYROIDISM
● It is defined as inadequate secretion of parathormone or ineffective secretion of hormone. The
consequence is inadequate calcium absorption resulting in hypocalcaemia and
hyperphosphatemia.
● In 10% of cases it is a post-surgical iatrogenic condition, but it can be autoimmune-based,
isolated or associated with other endocrinopathies, such as Addison's disease, then
hypoadrenalism as well as infiltrative processes such as metastases, amyloidosis, Wilson's
disease, haemochromatosis;
MAMMELLA
BREAST LESIONS BENIGN
Fibrocystic mastopathy. It should not be considered a disease, as it represents only a physiological
modification of the gland related to an exaggerated response to hormonal stimuli. It consists of the
formation of cysts of variable size and proliferative phenomena of the glandular component and
connective sclerosis.
It is frequent in women between the second and fourth decades and is characterised by
parenchymatous thickening with ill-defined margins associated with pain and tension. Nonproliferative lesions such as cysts or mild epithelial hyperplasia and proliferative lesions such as florid
epithelial hyperplasia and sclerosing adenosis are present. The latter two lesions represent a risk
condition for the development of carcinoma. Hyperplasia and adenosis may be responsible for
discharge from the nipple.
Fibroadenoma affects young women and may be multiple or bilateral. It presents as a nodule with
sharp or lumpy margins, parenchymatous in consistency, mobile on the underlying planes, non-painful
with typically slow growth. The risk of malignant transformation is nil. It is advisable to remove it,
however, because:
1. if large in size, may give aesthetic problems
2. may distort the evidence of a carcinoma
The benign phylloid tumour predominantly affects women between the second and fourth decade.
Compared to fibroadenoma it is also characterised by considerable stromal hypercellularity. The
diagnosis of benign, bordeline or malignant lesion is given by the number of mitoses per field. From a
palpatory point of view there is no difference from fibroadenoma. The diagnosis must be confirmed by
histology.
CARCINOMA OF THE BREAST
Clinical approach to suspected breast cancer
Breast cancer is the leading malignant tumour in women by incidence. In recent years, the mortality
rate has fallen due to the spread of screening and early diagnosis, and the education of the population.
The woman performs self-examination and can come to the doctor if she finds a lump. It is important
to educate patients about the pathology and the diagnostic-therapeutic procedure.
The correct clinical procedure always involves physical examination, ultrasound and mammography,
and possibly MRI. In the presence of an unconfirmed suspicion or a small lesion, a wait-and-see
attitude should not be adopted: diagnosis and treatment must be early to minimise complications and
mortality.
Family history: inquire about incidence in close relatives (mother, grandmother, sisters). Most cases
of breast cancer are sporadic, but many more are familial (20%) and a small proportion are hereditary
(5-10%, due to transmission of the mutated oncosuppressor BRCA-1/2).
Physiological and pharmacological history: mainly oestrogen exposure is assessed, which is to be
considered an FdR for breast cancer. It is therefore asked to:
● Menarche, late menopause, pregnancies, age at first pregnancy;
● Lactation (PRL inhibits LH and FSH);
● Hormonal and oestrogen-progestin therapies (e.g. oestrogen in menopause, treatment of
infertility).
Pathological history: the occurrence of the nodule is relevant.
● Painful and of recent and sudden onset is probably benign (e.g. inflamed cyst).
● Indolent present for weeks or months has a higher risk.
● Skin and nipple alteration, nipple discharge
∙
+ previous breast diseases
Objective breast examination
It consists of the inspection and palpation of five quadrants, in relation to the nipple: 1) Outer nipple;
2) Supero-internal; 3) Infero-internal; 4) Infero-external; 5) Central (nipple-areola). Additional terms
such as 'middle-internal quadrant', 'infero- central quadrant' are often used inappropriately to describe
lesions that straddle the quadrants proper.
It is important, during the examination, not to make the patient feel uncomfortable: do so in the
presence of a third person (also to avoid accusations of harassment) and in a well-lit and heated room,
while maintaining conversation (also to reassure the patient with a lump and to understand her cultural
level and knowledge about breast cancer).
Inspection
It evaluates the breast profile and symmetry, highlighting tumefactions and tegmental alterations such
as diffuse or sectorial erythema (suspected carcinoma) - nipple retraction - ulcerations (neoplastic
sign) - eczematous lesions - orange peel oedema (typical of carcinomatous mastitis) - venous ectasia.
It delimits superficial masses, and estimates their shape and volume. It should be conducted in a welllit environment, with the light grazing the skin to better appreciate any swelling and other alterations
in the surface profile.
The inspection should be conducted both with the pectorals at rest and contracted, and in various
positions. The standard position is standing or sitting, with the hands behind the nape of the neck;
some alternatives include the arms along the sides or the lying position, with the hands behind the
nape of the neck. Bending the trunk forward allows one to observe retraction if the neoplasm is
adherent to the muscular plane. Particularly important
is the inspection of the submammary groove because neoplasms in this area, especially if deep, can
escape mammography (for breast positioning).
Nipple and areola inspection
● Position: symmetry of the areolae - displacement of the nipple (up, down, laterally, medially) deviation, distortion or rotation of the nipple on its longitudinal axis.
● Conformation
o Inverted nipple (indented but reducible with titillation, sucking or squeezing): common
paraphysiological condition. It is benign in itself, but predisposes to infection (galactophoritis,
recurrent abscesses, periareolar fistula).
o Retracted nipple, irreducible, due to retraction of lymphatic vessels (? Duret's ridges?): is
secondary to inflammatory, neoplastic or scar processes (e.g. after a conservative
mastectomy, scarring may lead to nipple retraction, mimicking re-initiation of carcinoma).
o Destroyed nipple: this is typical of advanced breast cancer to the point where the original site
of the areola-nipple complex is no longer recognisable.
● Discolouration and inflammation of the areola-nipple complex: e.g. Paget's nipple disease is a
rare neoplasm of the mammary ducts, which expand to the mammary areola, manifesting as
itching, redness and scaling (eczema-like lesion).
● Presence of fistulas, which form from abscesses.
Nipple secretions: should be described in their mode (spontaneous or provoked), origin (mono- or
pluri-oreficial) and appearance (milky - purulent - serous, clear or opaque - haemorrhagic).
● Hemorrhagic secretion, unilateral and mono-orificial: may be a sign of intraductal papilloma
(benign, removable with galactophorectomy) or breast carcinoma.
● A brownish secretion from fibrocystic mastopathy, bilateral and pluri-oreficial, may mimic
haemorrhagic secretion but is not worrying. It may also take on other colours: green, grey, yellow,
milky.
● Serous secretion: this is usually due to ductal ectasia, rarely to carcinoma.
● Lactescent secretion: physiological after childbirth, far from pregnancy may lead one to suspect a
PRL-secreting pituitary tumour.
Palpation
It is always performed with the hand flat and fingers together, with the fingertips and not the tips,
with small slow movements, exploring all quadrants radially (also applies to the abdomen). A
lubricating gel can be used to reduce friction and better appreciate a possible lump. The patient lies on
the couch. When the breast is large, in the supine position it tends to move laterally on the hemithorax:
in this case, the patient is told to rotate her torso 30-40° to the opposite side,
to hold the gland anterior to the wall (for palpation and ultrasound). Positions: pz lying, s. and
medially rotated, with ipsilateral arm raised and lowered, and sitting.
On palpation, consistency and elasticity of the breast tissue can be appreciated, depending on the
trophism of the glandular and adipose tissue. In addition, a lump may be appreciated.
Local signs and symptoms of breast cancer:
● Change in size, contour or asymmetry of the two breasts on inspection.
● Nodule or palpable mass, usually painless, hard, adherent to the underlying parenchyma and
therefore not mobile; the nodule is jarring when cut due to calcification.
● Retraction of overlying skin, spontaneous or provoked (putting the lump between index finger and
thumb: dimpling).
● Single-orifice haematic or serum secretion (also present in intraductal papilloma).
● Skin changes (characteristic of advanced disease), such as orange peel skin (due to infiltration of
superficial lymphatics), erythema/eczema of the nipple (Paget's disease), nipple retraction (which
must be distinguished from introflection), change in colour or appearance of the areola.
Breast lump
Roughly spherical thickening, palpable or not. When the lesion is palpable, its shape - surface - size consistency - mobility - tenderness can be appreciated. Texture can be appreciated, for sufficiently
large nodules, by squeezing it between index finger and thumb. Phlogosis generates oedema and may
lead to overestimating the size of a nodule, also making it painful.
A mobile nodule, not adhering to deep planes, is probably benign (e.g. fibroadenoma, cyst).
A carcinoma is generally immobile (with exceptions, usually at the breast margins), and has an
irregular surface and margins. Other factors discriminating malignant formations are painfulness,
sudden appearance and progressive growth, and hard-moist consistency (typical of carcinoma, as
opposed to the tense-elastic consistency of fibroadenoma).
Axillary and supraclavicular lymph node locations should always be examined. Tumours in these
locations may have metastatic origin from breast carcinoma, especially if they are hard lymph nodes.
Magnetic resonance imaging
is indicated for the:
● Pre-surgical evaluation if mammography with multicentricity or multifocality,
● Search for occult carcinoma in patients with suspected lymph node metastases,
● In the post-mastectomy follow-up of women with genetic risk,
● The study of dense breasts of young patients,
● In the follow-up of neoadjuvant therapy (if mammography is not diriment) or conservative surgery
with radiotherapy, ultrasound doubt of recurrence on surgical scar.
It has high sensitivity and low specificity: 100% negative predictive value for infiltrating carcinoma.
Ultrasound
Indicated in symptomatic young patients (< 30; > 30 mammograms), but also in older patients as a
complementary examination to mammography and for the study of axillary lymph nodes. It highlights
nodules in the parenchyma, distinguishes them into solid and cystic, shows their morphology and
measures their size (e.g. TNM).
● Cyst (100% diagnostic accuracy): spherical anechogenic area with defined margins, with posterior
reinforcement
● Benign nodule (85-95%): definite shape with regular margins, homogenous echogenicity
● Carcinoma (T1 75%, T2 90-95%, T3 90-100%): irregular morphology and margins,
ultrasound inhomogeneity, acoustic absorption/posterior shadow cone (lateral acoustic striae, due
to the presence of calcifications), hyper-ecogenicity of the subcutaneous fat. Medullary carcinoma
and other differentiated forms may have features similar to those of benign nodules
(fibroadenoma). Eco-colour Doppler: 90% of carcinomas are hypervascularised (intra- and
perilesional), with anarchic vessel distribution and increased flow velocity.
Ultrasonography is the first investigation to be done in case of clinical features suggestive of
malignancy.
If the nodule is solid and not cystic, it is probably a carcinoma, and there is an indication for biopsy.
However, radiological examination (mammography) is performed to check for possible multifocality
(on the same quadrant) or multicentrality (on different quadrants) of the lesion.
Some carcinomas mimic benign nodules on both ultrasound and mammography (regular margins,
smooth surface, mobility, tense-elastic consistency).
Mammography
It is a low-dose Rx examination (<5 mGy, with the digital mammograph), important for screening and
early diagnosis in asymptomatic patients.
In the older woman, following the normal fibro-adipose regression of the gland, the prevalence of the
adipose and therefore radiolucent component favours the visibility of (radiopaque) nodules.
Therefore, the sensitivity of mammography is greater in older women than in younger ones. In
addition, the image is influenced by the water content, which in turn varies with hormonal stimuli: a
greater presence of water increases the density, and reduces the possibility of highlighting nodules by
contrast with radiolucent tissue. For this reason, mammography should not be performed in the days
before menstruation, which are the days of greatest water imbibition of the gland.
Mammography screening (secondary prevention) of the female population between the ages of 4570 years (> 40aa because the stroma-gland ratio increases, after the age of 70 the incidence decreases),
annually.
It reduces mortality (10-year survival N0 80%, N3 <30%), allows conservative surgical and less
aggressive medical therapies, reduces treatment costs.
One criticism of screening programmes concerns the diagnostic anticipation or lead time bias: by not
taking into account the asymptomatic period of the natural history of the disease, even without
treatment it appears that the screened population has better survival, but in reality one has only brought
forward the time of diagnosis: they do not live longer, it is the disease that is discovered earlier.
Mammography is carried out according to two projections: cranio-caudal (compression in the frontal
plane) and latero-medial (compression in the sagittal plane), providing three-dimensional
information: the cranio-caudal projection provides information on the horizontal plane, the mediolateral oblique projection on the vertical coordinates (e.g. whether the lump is in the upper or lower
quadrant) and on the axillary cavity.
It should also always be performed with a clinico-ecographic diagnosis of certainty, to exclude the
presence of further non-palpable lesions.
It is important that the operator is skilled in the correct positioning of the breast in the instrument.
Connective (radiopaque) and adipose tissue participate in the radiological image of the breast
(radiolucent). The epithelium is practically irrelevant to the realisation of the image.
Neoplastic nodules are radiopaque. Carcinomas present as circumscribed opacities with:
● Irregular margins (starry-looking opacity);
● Granular micro-calcifications or mould (comedo-carcinoma), often clustered; NB: calcifications
not suspected of malignancy are coarse, larger diameter, rounded and regular, often isolated and
not clustered.
● Parenchymal distortions and asymmetric areas of increased density (compared to the contralateral
breast).
BI-RADS (Breast Imaging-Reporting and Data System) classification of breast lesions
● BI-RADS 1: normal picture, negative examination
● BI-RADS 2: obvious but definitely benign lesions (e.g. inflammatory lymph node), ultrasound
follow-up
● BI-RADS 3: probably benign lesions, ultrasound follow-up and micro-biopsy
● BI-RADS 4: suspicious lesions (e.g. with irregular margins, or with internal granularity).
● BI-RADS 5: definitely malignant lesions. (+4), always biopsy.
Non-palpable nodules
Lesions may not be objectable on physical examination, depending on location, lump and breast size,
and fat density. On mammography, non-palpable lesions may be revealed as: nodules (26%) parenchymal distortions (7.5%) - microcalcifications (47%) -
nodules with microcalcifications (17%) - distortions with microcalcifications (2.5%). For lesions
evident on mammography but not palpable, histological typing (biopsy) is indicated. Non-palpable
lesions may also be seen on ultrasound and MRI.
Breast carcinomas: these are divided into carcinomas in situ (not extending beyond the basal
membrane of the epithelium) and infiltrating carcinomas, distinguishable on histological
examination.
Tomosynthesis
Mammography variant that produces 3D images with scans every mm. It increases sensitivity, with
radiation levels comparable to those of conventional digital mammography.
Other radiological investigations: pneumocystomammography - galactography.
Galactography or ductulography
It is indicated in cases of haematic or serum haematic nipple discharge. It is performed after injection
of water-soluble mdc through the nipple.
● Contraindications: purulent discharge, mammographically established neoplasm, mdc allergy.
● Aspects suggestive of malignant neoplasia (many similarities with benign ones: it is a specific
investigation that must be followed by other techniques): filling defects, duct obstruction,
irregularities in the duct wall, deep-seated lacunae.
Biopsy of breast lesions
● Fine needle aspiration biopsy (FNAB, needle aspiration): allows cytological but not histological
examination, so it does not distinguish infiltrating carcinomas from those in situ.
It gives many false negatives (high specificity but low sensitivity).
It can be performed on nipple secretions, apposition or abrasion material from erosive nipple
lesions, cystic fluid, needle aspiration from solid nodules, non-palpable breast lesions.
● Core biopsy (microbiopsy) with a 14G Tru-cut needle, with or without aspiration. Compared to
FNAB, it allows bio-morphological characterisation of the tumour.
Compared to surgical biopsy, it is cheaper and faster, removes less healthy tissue, can be
performed on an outpatient basis, and produces less pain and psycho-emotional stress.
Freehand, under ultrasound or stereotactic (mammoth) guidance.
● Wire-guided surgical biopsy
● R.O.L.: radioguided occult lesion localisation.
Biopsy guidance may be manual, stereotactic, ultrasound or radiotracer mediated. There is a risk of
missing the lesion: in case of negativity 'I have to be convinced: either I repeat the examination or I
remove the lesion anyway' (?).
Stereotactic method: the coordinates are calculated by computer, using two X-rays with the axis
rotated by 15°, and transmitted to the stereotactic table for biopsy. If there are signs of malignancy in
the biopsy specimen, exeresis of the entire lesion can be performed at the same time, with the same
stereotactic table, by inserting a wire instead of a needle (wire-guided exeresis). This procedure is less
invasive but more difficult than a traditional mastectomy. At the end, in Rx it is verified that the
excision was complete.
Microbiopsy Core Biopsy
Core biopsy is performed with a shearing needle, consisting of a cylindrical cannula and a
removable core, the movement of which wedges the extracted tissue frustule into a recess in the distal
portion. The procedure can be performed manually or with a BARD gun, which automatically shoots
the needle forward 22 mm: it can be used for breast, liver, pancreas, kidney, lung (risk of iatrogenic
pneumothorax), prostate (with a thinner needle), but not for thyroid.
Vacuum-assisted biopsy (VAB, biopsy with retroaspiration)
It uses a needle-cannula which allows multiple tissue shafts to be extracted with one needle (as
opposed to core biopsy with the shearing needle, which requires a new needle to be inserted for each
shaft taken). The shearing needle costs 7 euro, the needle-cannula 400: this technique is used when, in
the presence of lesions with irregular morphology, several samples may be needed to obtain a suitable
sample. The shafts are then radiographed to check for microcalcifications, which confirm that the
sample came from the lesion.
Within 1-2 weeks, you will have the result of the biopsy:
● Non-invasive tumour (10%): does not invade the basement membrane (mammary intraepithelial
neoplasia), therefore has no metastatic potential. Carcinoma:
o Ductal in situ: originates from the ductal cells and is confined within the ducts.
Characterised by mammographic micro-calcifications. There are comedo, papillary, solid and
cribriform variants.
It is preceded by a dysplastic lesion called atypical ductal hyperplasia.
o Lobular in situ: not detectable on mammography (often an occasional biopsy finding).
It is often multicentric and bilateral. It is preceded by atypical lobular hyperplasia.
● Invasive cancer (90%)
o Favourable: tubular, mucinous, papillary carcinoma.
o Less favourable: infiltrating ductal carcinoma (70-80%), infiltrating lobular carcinoma (510%), medullary.
o Unfavourable: inflammatory carcinoma or mastitis carcinomatosa (1%, clinical presentation
form); results in reddening of the breast and orange peel skin (at least one third of the skin),
without a recognisable palpable mass underneath.
Very poor prognosis (5-year survival of 20%).
Staging
It is performed by assessing tumour size, lymph node involvement and distant metastases.
● Stage I: very small tumour, <2 cm. Survival at 5 years 80-95%.
● Stage II: very small tumour with lymph node involvement or small tumour, 2-5 cm.
● Stage III: large with lymph node involvement.
● Stage IV: metastases (also to contralateral or supraclavicular lymph nodes). Survival at 5 years
10%.
From stage IIIA onwards (tumour > 5 cm or at least 4 lymph nodes involved), it is indicated to
complete the staging with examinations such as chest CT, CT/RM abdomen and pelvis, bone
scintigraphy or PET/CT.
In stages I-IIB (tumour <5 cm and up to 4 lymph nodes), they are only performed on clinical
indication.
Lymphatic drainage of the breast is provided by axillary (mainly), supraclavicular and internal
mammary lymph nodes (of the mediastinal chain, for medial tumours). Axillary lymph nodes are
usually involved in an orderly manner (1% lymph node jump), according to 3 levels:
● Lymph nodes lateral to the pectoralis minor muscle (inferior),
● Posterior to the pectoralis minor (central),
● Medial to the pectoralis minor (upper).
Rarely, metastasis to the contralateral axillary cord is possible due to retrosternal bypasses between the
two internal mammary lymphatic systems.
Metastatic sites: bone, lung and pleura, liver; encephalon (not frequent, only in some histotypes).
Prognosis
Most important prognostic factors, indicators of:
● Differentiation: histology, grading, hormone receptors.
● Invasiveness: lymph node status and number (the most important prognostic factor), vascular and
perineural invasion, angiogenesis.
● Aggressiveness: tumour size, p53 status.
● Proliferation: number of mitoses, fraction of cells in S phase.
Surgical treatment
Ductal carcinoma in situ: quadrantectomy and radiotherapy on residual breast (>50% reduction in
risk of recurrence); rarely (3.6%, large CDIS) lymph nodes in mastectomy specimens are positive.
Invasive malignant tumours:
● Radical mastectomy: exeresis of the entire breast, some chest wall muscles and dissection of
axillary lymph nodes level I, II and sometimes III.
● Modified radical mastectomy: only with lymph node dissection I and II.
Mastectomy is indicated in the case of risk factors for local recurrence, lymph node positivity (> 14 lymph nodes), advanced disease (T3 or T4).
Conservative surgery (quadrantectomy): it is equivalent both in terms of local control (risk of
recurrence) and overall survival, so today it is the standard. Followed by radiotherapy within 6 months
. Contraindications to conservative treatment: collagen disease in active phase, pregnancy, previous
RT on chest wall, large multicentric or multifocal tumour, large tumour with small breast (poor
aesthetic result), very large breast.
Dissection of axillary lymph nodes
It has sequelae (lymphoedema, paresthesias) so one tries to spare it whenever possible.
In the case of clinically negative lymph nodes (even with ultrasound), a sentinel lymph node biopsy is
proposed and a complete dissection is only performed if it is positive (with vital dye and radio-tracer).
The sentinel lymph node technique has a high accuracy (false negative 3%); it is contraindicated in the
case of clinically positive lymph nodes, pregnancy, previous axillary surgery, locally advanced disease
(from IIIB)
POLMON
EMOFTOE
Haemophotoe refers to the expulsion of phlegm with traces of blood. It is blood discharge that then
originates from the throat, lung or any other part of the respiratory tract. The colour of sputum ranges
from light to bright red.
VOLET COSTAL
Costal volet is represented by multiple fractures in ≥ 3 adjacent ribs that result in a segment of the
chest wall separating from the rest of the rib cage; it is an indicator of injury to the underlying lung.
DIAPHRAGMATIC RELAXATIO
Failure to develop all or part of a haemidiaphragm (➔ diaphragm), more rarely both. It is a
congenital pathology that cannot be distinguished from acquired forms of the paralytic type.
EMPYEMA PLEURAL
Pleural empyema is a collection of pus in the pleural space. It can occur as a complication of
pneumonia or a lung, liver or subdiaphragmatic abscess. Pleural empyema can also occur following a
thoracotomy (surgical opening of the chest) or penetrating trauma with secondary infection.
Sometimes, it is caused by neoplastic processes (lung cancer, breast cancer
, lymphoma or
any
tumour
metastatic to the pleura), pulmonary embolism,
tuberculosis or viral infections.
Empyema
pleural empyema can
provoke dyspnoea pain chest pain e
discomfort
during inspiration. Detection is by objective examination and chest X-ray; thoracentesis
and analysis of the pleural fluid are often necessary to establish the cause.
Treatment: drainage
PNEUMOTHORAX HYPERTENSIVE
Hypertensive pneumothorax develops when damage to the chest wall or lung is such that air can pass
into the pleural space but not out of it (a one-way valve). As a result, air accumulates and compresses
the lung, eventually displacing the mediastinum, compressing the contralateral lung, and increasing
intrathoracic pressure
enough to decrease venous return to the heart, causing shock. These effects can develop rapidly,
particularly in patients on positive pressure ventilation.
EMOTORACE
Haemothorax is the accumulation of blood in the pleural cavity. The cause of haemothorax is a
laceration of the lung, intercostal vessels, or an internal mammary artery. It may result from blunt or
penetrating trauma. Haemothorax is often accompanied by pneumothorax (haemopneumothorax).
The volume of haemorrhage varies from minimal to massive. Massive haemothorax is most often
defined as the rapid accumulation of blood ≥ 1000 mL.
Patients with large haemorrhagic volume are often dyspnoic and have diminished breath sounds and
dullness to percussion (often difficult to appreciate during the initial assessment of patients with
multiple lesions). Findings may be irrelevant in patients with smaller haemothoraxes. Shock is
common.
CARCINOMA LUNG
Epidemiology
More than 95% of malignant tumours are carcinomas, arising from the epithelial tissues that make up
the bronchi and lung parenchyma. Much rarer (0.5%) are sarcomas and lymphomas. Less than 5% of
lung neoplasms are benign (hamartomas) or low-grade malignancies (carcinoids).
The incidence in Italy is 99-108.5 new cases per 100,000 inhabitants per year. It should be noted that
there is a gradually decreasing trend in men (since the second half of the 1980s), while there is a
continuous increase in women: mortality increased by 150% between 1994 and 2014. Thus, there is an
increase in lung cancer in women.
Lung cancer is the leading cause of cancer death in men and second in women after breast cancer.
Globally, mortality is estimated to reach a rate of 18.4 %, but the gap in epidemiological terms
between the curve for breast cancer and lung cancer is decreasing, i.e. lung cancer is falling
significantly.
Risk factors
Cigarette smoking, heavy smokers (more than 40 cigarettes per day) have a 60 times higher risk of
developing the disease than non-smokers. There are environmental factors: asbestos, environmental
pollution as by-products of petrol combustion and many other fossil fuels.
Smoking among young people is certainly one of the leading causes even in the female sex.
Histological classification
1. Microcytoma or SCLC (small cell lung cancer) 20-25% of cases
2. Non-small cell lung cancer or NSCLC (non-small cell lung cancer) 75-80% of cases where we
have undifferentiated carcinoma; large cell carcinoma; squamous cell carcinoma;
adenocarcinoma.
Clinic
•
Dry, constipated cough resistant to therapy or modification of the usual morning cough in the
smoking patient. One should have no qualms about prescribing a chest X-ray to a patient who
after 7-10 days of a fever or a sudden onset of a constipated cough does not respond to therapy
with cough suppressants or trivial fluidisers prescribed as ex adjuvant therapy.
•
Fever
•
Mucopurulent secretion
•
Hemoftoe
Systemic symptoms are non-specific (weight loss, asthenia, anorexia). There are symptoms of
extrapulmonary intrathoracic extension:
-
Superior vena cava syndrome,
Bitonal voice due to recurrent nerve involvement
Paralysis of a haemidiaphragm due to phrenic nerve involvement
Pleural-pericardial effusion,
Dyspnoea if there is significant compression of the main bronchus or trachea,
Dysphagia as a compressive element towards the middle third of the oesophagus where
lymphadenopathy secondary to neoplastic pathology of the lung may be more present.
There are signs and symptoms of extrathoracic extension (lymphadenopathy, headache, metastasisrelated bone pain).
There are signs and symptoms of paraneoplastic syndromes such as ACTH and ADH production.
Instrumental examinations
Double projection X-ray of the chest, possibly a spiral CT scan of the total body should also be
done. In a hospital setting, a biopsy, whether CT or echo-guided, of a lung lesion should be done.
A CT PET scan as a last-level investigation to also see if there are any further elements that can light
up with the PET scan and give assessments of possible metastatic situations.
Staging
Diagnosis and staging is done with:
- Endoscopy with fibro bronchoscope,
- Mediastinoscopy and then video assisted.
If we have a small-cell lung tumour, we must speak of localised disease or diffuse disease.
In the case of non-small-cell cancer, we have to do a TNM: Tx evaluation of bronchial lavage or
sputum
T0 no tumour
Tis is a carcinoma in situ
T1 tumours< 3cm and divided into T1a, T1b, T1c
T2a 3-5 cm;
5-7 cm
T3 tumours >7 cm or any size but involving the wall
of the thorax or the pericardium or the phrenic nerve or with satellite nodules within the same
lobe
T4 are tumours either >7cm or any tumour that has invaded the mediastinum, heart, great
vessels, etc.
peribronchial or hilar ipsilateral and intrapulmonary lymph nodes mediastinal ipsilateral or
subcarenal lymph nodes
contralateral mediastinal and hilar lymph nodes
M1 a
M1 b
M1c
Therapy
Surgery is indicated mainly in non-small-cell tumours. Chemotherapy for small-cell tumours.
As part of the operability of a lung injury, we must consider:
- Anatomical operability, i.e. volume assessment and the possibility of resecting the
-
nodule or part of the lung so as to achieve a radical exeresis
Oncological operability i.e. the likelihood of surgery with respect to the stage of the neoplasm
Functional operability in which the surgeon is faced with an assessment of residual
respiratory function after radical exeresis.
Type of resections:
Lobectomy, thus the fundamental unit of the single lung
Pneumonectomy, must be done with adequate reasoning in relation to functional operability
because in the subject with severe pulmonary emphysema with initial respiratory insufficiency,
performing a pneumonectomy corresponds to determining irreversible respiratory insufficiency
Atypical resection (wedge resection) in patients with reduced functional reserve, a more
targeted resection is done with a lung-preserving attitude
Bronchial sleeve resection in patients with reduced functional reserve in
single bronchus can be resected by making a terminal anastomosis on the bronchus itself.
ADDOME
PAIN ABDOMINAL
Abdominal pain is a common symptom found in various morbid conditions, representing a defence
mechanism and an alarm signal. In addition, it is often associated with the assumption of a particular
position, called the antalgic position, in the hope of deadening or reducing the pain.
For example:
- Patients with acute pancreatitis (in which algic symptoms can escalate to 'pancreatic drama')
are characterised by abdominal flexion, which they maintain in an attempt to reduce pain
- Flexion of the hip on the abdomen, due to appendicitis or pyelitis
- Squatting position, parietal immobility in peritonitis
- Forward flexion in biliary colic
- Compression on the abdomen relieving colic pain (described in the literature). When there
is no antalgic attitude and the pain is colic-like, move towards renal colic.
Abdominal pain can be caused by:
1) Diabetic ketoacidosis, which gives metabolic changes in tissue
2) Direct irritation:
- From chemical
- By mediators secondary to ischaemia or inflammation (e.g. peritonitis)
3) Distension/tension of the capsules of parenchymatous organs (there are algic receptors at the
level of the kidney, spleen and liver capsules, e.g. stasis liver or hepatitis)
4) Distension/tension of a hollow viscera due to distension from content, under high pressure
(intestinal occlusion) or due to spastic contraction (algic receptors in the smooth muscle tunic).
5) Meso stretch (the meso is a structure that anchors the organ to the abdominal wall. In its
context are blood vessels, lymph vessels, loose connective tissue and nerves)
6) Traction on the mesentery, ligaments and peritoneum (the parietal peritoneum is much more
sensitive to algogenic stimuli than the visceral one)
7) Neoplastic ab extrinsic infiltration or compression of nerve structures
In the evaluation of the patient with abdominal algic symptoms, we proceed with:
a) Accurate anamnesis
b) Assessment of pain symptom characteristics
c) Assessment of accompanying symptoms
d) Evaluation of the type of ducting
e) Assessment of abdominal wall behaviour: whether it is contracted or if there is a globular
abdomen
f) Assessment of general impairment
The medical history allows us to orientate on the possible cause of abdominal pain, also allowing a
DD: (based on the location of the pain)
1) Age:
- >70 years:
.diverticulitis
.mechanical occlusion by faecaloma (at the level of the sigma and the rectal ampulla):
diagnosed w i t h EDAR, which at the same time can be therapeutic because it dilates the anal
sphincter and then releasing it, by reflex mechanism, triggers defecation, stimulating the rectal
ampulla; it can also fragment the faecaloma
.abdominal arteriopathies
- < 15:
. appendicitis
. Meckel's diverticulum
.intestinal invagination
2) Sex:
- Women: adnexitis (pain from aggravating inflammation) and/or ovarian cysts
- Men: torsion of the funiculus (acute scrotum)
3) Previous surgeries and/or pathologies: find out if there are previous GI tract diseases: ulcers,
IBD (Crohr's disease or UCR), or if the patient has family members with such problems.
In cases where surgical scars are present on inspection, an adherence syndrome is suspected: leading
to ab extrinsic compression by reabsorption of fluid collections that are present in the abdomen from
previous operations and that form bridles that compress the abdominal organs. There will never be an
acute syndrome, but through a careful anamnesis, the patient will report irregular alvus with subocclusive conditions alternating with diarrhoeal alvus. Disease recurrence may also be suspected.
The characteristics of the pain symptom are then assessed:
1) Typology:
- Acute or chronic
- Superficial (somatic, parietal or epicritic) or deep (visceral)
- Colico (intermittent) or continuous
2) Location or seat
3) Alleviated or worsened by?
4) Irradiation
5) Intensity and duration
Returning to the characteristics of pain:
1) Colic (or intermittent): characterised by phases of acuity and then quiescence. It may be
localised, as in biliary colic; or diffuse, as in intestinal obstruction, and the patient is unable to
locate it well. Thus an example of colic pain is that of intestinal obstruction, which the woman
compares to labour pains (whereas in the case of perforation of a
hollow bowel there will be stabbing pain). Mechanical bowel obstruction colic has a sinusoidal
or oscillatory pattern, with an acme and a defervescence. The acme is related to the peristaltic
waves upstream of the occlusion site that try to overcome the obstacle, so much so that in the
final phase of an intestinal occlusion of a mechanical type that has not been properly
diagnosed, there is the exhaustion of the waves of hyperperistalticism until reaching a picture
of paralytic ileus (which has nothing to do with the paralytic ileus that follows the perforation
of hollow viscera or peritonitis). Thus a picture of unresolved or delayed mechanical bowel
obstruction results in paralytic ileus.
2) Continuous (with violent onset): may be due to:
- Acute pancreatic
- Perforation: from a state of well-being, a piercing pain ensues. Perforation can occur following
gastroscopy, due to:
. intake of spicy foods
.arthropathy, leading to the intake of large quantities of NSAIDs
.gastric peptic ulcer
- Intestinal ischaemia: at anamnestic collection, the patient reports pain after eating meals. It
may be due to an atherosclerotic process of the splanchnic district.
- Ruptured aortic aneurysm: abdominal pain is accompanied by signs and symptoms of shock
(haemodynamic instability)
3) Continuous (with gradual increase):
- Appendicitis: the site of pain is in the right iliac fossa
- Diverticulitis: site is in the left iliac fossa
- Cholecystitis: right hypochondrium Often fever is present.
Then pain is distinguished into:
- Deep visceral
- Parietal, somatic, epicritic
Deep visceral pain
It is a dull, dark pain, which is interpreted, depending on the cause, as:
- Crampiform
- Current
- Tenebrating
- Lacerating
- By dagger blow
It is a pain that is usually poorly localised and is felt in the middle regions of the abdomen. It
originates from abdominal organs that go:
- Relaxation
- Spasm
- Ischemia
The stimulus then reaches the CNS via the fibres of the autonomic nervous system. It is often
accompanied by neurovegetative symptoms: nausea and vomiting, sweating and arterial hypotension.
For example
In the case of a gastric ulcer perforation, the patient reports a stabbing, stabbing pain (also in other
bowel perforations). In the case of dull pain, such as that typical of duodenal ulcers infiltrating the
pancreas.
Parietal, somatic or epicritic pain
The pain is described as well localised, asymmetrical, skin hyperesthesia (precisely in this case, during
the EO of the abdomen, one must first observe the patient without placing one's hands on the abdomen,
let alone on the area where the patient feels pain. The patient will expect his hands to be placed where
he feels the pain and will tend to contract, distorting the parietal resistance response, in case of acute
appendicitis, for example. Therefore, palpation should never be performed starting from the point
where the patient feels the pain, but on the other quadrants, distracting the patient a little. This pain is
caused by mechanical or phlogistic stimulation of the algoreceptors of the parietal peritoneum.
It is exacerbated by:
- Movements of the patient
- From coughing
- From breathing
The defensive contracture of the parietal musculature is constant.
Somatic pain is often more acute than visceral pain and can often be detected with semeiological
manoeuvres such as:
. Blumberg's sign: slight compression at the abdominal level (starting from areas that are not
spontaneously painful), which, in the presence of initial involvement of the peritoneum, as in an
appendicular inflammation, leads to contracture.
. Murphy's sign: two fingers below the anterior margin of the 10th rib. Usually assesses problems at
the hepatic-cholecystic level, the patient is asked to inhale, as with the lowering of the diaphragm, the
hepatic margin or, in the case of acute cholecystitis, the bottom of the gallbladder is appreciable,
which in hydropic conditions can reach the transverse umbilical line (like a Tunisian grenadier).
Referred pain (pain radiation)
It is a pain that is felt far from the site of the injury and is localised:
- Both muscle-cutaneous territory
- Both deep tissue
Usually, the affected structures have the same embryological derivation as the dermatomere of the
suffering viscera.
For example:
1) Appendicular pain:
The pain starts as periumbilical pain and then becomes epigastric. later, it is felt in the right iliac fossa
(unless the appendix has unusual localisations: pelvic, retrocecal, right hypochondrium, etc.).
2) Cholecysto-coledocytic lithiasic pain:
The pain begins as epigastric, evoking dyspeptic disturbances (vagal reflex reaction), which typically
occur after a high-fat or high-fibre meal, or after ingestion of artichokes (cholecystokinetic), with
stimulation of gallbladder contraction.
Then from the epigastrium, the pain migrates to the right hypochondrium, and then radiates
posteriorly, to the ipsilateral subscapularis, entering DD with a right basal pleuropneumonia. Fever is
more frequently associated with lithiasis of the choledochus than of the gallbladder. Murphy's
manoeuvre is performed, and if it is positive, depending on the intensity of the pain, it is rated from 1+
to 3+.
Consider the signs and symptoms associated with abdominal pain:
1) Fever (axillary and rectal T measurement)
2) Jaundice (usually surgical jaundice is from biliary tract stasis due to mechanical causes, with
pain in the right hypochondrium)
3) Nausea and vomiting (assess the characteristics of vomiting: gastric, biliary, faecal): For
example, typical biliary colic from gallbladder lithiasis is accompanied by associated
symptoms such as nausea, vomiting, feverishness. It usually occurs following a large dinner in
which fatty foods predominate. Often, patients discover as a result of biliary colic that they
have gallbladder lithiasis. Then, if one delves deeper into the anamnesis, one may already
notice a history of dyspeptic pain complaints preceding the onset of the first painful cholic
episode: bitter berry, "breaded" tongue, gravative pain in the epigastrium.
4) Diarrhoea or constipation
5) Alvo closed to faeces and gas (gas closure indicates an even more serious situation)
6) Anorexia and weight loss: it correlates with possible neoplasms, of the stomach or colon.
Sarcophobia is also often associated, suddenly the patient sees meat and starts to feel nauseous.
This is a prodromal symptom in gastric or colic neoplasia. Then in the colon the clinical
symptomatology changes depending on the site. The ascending colon and transverse colon are
volumetrically larger than the descending colon, sigma and rectum. Thus in acute, right colon
neoplasms almost always correlate with weight loss, small fever elevation and progressive
anaemia. With n e o p l a s m s o f the left colon, as the lumen of the colon is narrower, there
will first be sub-occlusive episodes that often resolve spontaneously, but are underestimated by
the patient and the attending physician because they resolve on their own. The patient will have
2-3 days of difficulty in evacuating, then suddenly unblock with repeated diarrhoeal discharges
and then the thing is forgotten, unless it suddenly recurs several months later. These are
'cauliflower' shaped neoplasms, which increase in size. As long as the faeces can pass laterally
over the neoplasm, the patient will not become occluded; but as they increase in size, we move
from a subocclusion to a true intestinal occlusion.
7) Dyspepsia
8) Haemorrhage: assess whether there is or is reported to be: haematemesis, melena,
haematochezia, proctorragia, haematuria, metrorrhagia
9) Claudicatio intermittens
10) Arrhythmogenic heart disease: may be an expression of coagulopathies, which may give rise to
intestinal arterial occlusive pictures, but generally occur in the brain or lungs.
DD OF ABDOMINAL PAIN
a)
-
Right hypochondrium:
Biliary pathology
Liver pathology
Subphrenic abscess: often resulting from cholecystectomy surgery
Right colic flexure (hepatic) neoplasm: if diagnosed late and is extensive, it is appreciable on
palpation (painful), and may also give intestinal subocclusion (usually peculiar in left colon
neoplasms).
- Right kidney disease: e.g. right renal colic, which many women compare to labour pains due to
the intensity of the pain, which may be associated with fever and vomiting. It is often
associated with specific urinary disorders (stranguria, dysuria, pollakiuria, etc.).
- Duodenal peptic ulcer: actually the pain, described as a stabbing, is in the left hypochondrium
or mesogastrium (simulates pancreatic girdle pain)
- Right basal pleuropneumonia: may simulate biliary colic from gallbladder lithiasis.
With ultrasound, DD can be done early on.
b) Right iliac fossa:
- Acute appendicitis
- Acute mesenteric lymphadenitis: almost always of tubercular origin, it is often found in
immigrants, due to the hygienic and unsanitary conditions in which they are found.
- Terminal illeitis: today it is referred to as Chron's disease with predominantly ileal localisation,
as lesions can be localised from the oesophagus to the rectum.
- Caecal neoplasms: they are rarely very voluminous
- Left colon occlusion: pain can be appreciated on the right, due to gas displacement on
palpation (Rosving manoeuvre)
- Meckel's diverticulitis
- Right gynaecological pathology
- Right renal-ureteral colic
c) Epimesogastrium:
- Gastroduodenal ulcer: it loses its characteristics when it becomes penetrating (even into the
pancreas), giving continuous pain, no longer related to eating. Today, the gastroduodenal ulcer
is no longer treated surgically; in fact, gastric surgery is reserved for cases of gastric neoplasia,
bariatric surgery, or haemorrhage, where endoscopic treatments have failed, using titanium
metal clips, ligatures, and adrenaline infiltration. Only perforated ulcers require surgery
because they cause generalised chemical peritonitis as stomach contents spill into the
peritoneum.
- Acute pancreatitis: gives Dieulafoy's so-called 'pancreatic drama' (delafua'). It manifests with
pain in both hypochondria, which leads the patient to assume antalgic positions such as praying
to Mohammed. Usually, the oedematous form prevails, caused by gallstones, which migrate
into the choledoch, reaching Vater's papilla. In the acute necrotic haemorrhagic form of
pancreatitis, surgery is to remove the areas of necrosis.
-
Intestinal infarction: with dark red blood discharge, possible in patients with a history of
embolism, AF, thrombosis
Choking of an intestinal loop: this is due to compression of the vascular pedicle: ischaemia.
Choking can occur in any type of abdominal hernia, typical of umbilical and inguinal hernias
Fissured aortic aneurysm: typical is melena, where the fissure of the aorta occurs in the
duodenum, thus generating epimesogastric pain
Acute Enterocolitis
Postero-inferior IMA: (these are called Monday infarctions, because on Sundays people used to
overeat). Very serious, often occurring in non-cardiac subjects, with epigastric pain
WITHOUT radiation to the left arm and neck. It may result in cardiac tamponade, and at
autopsy the cardiac chambers are found ruptured. The patient who arrives at the PS is
immediately given a troponin assay, kept under observation on site and re-evaluated after 6-8
h, the troponin is re-dosed and the ECG is repeated. Troponin can give false positives,
especially in subjects who have undergone abdominal surgery, where it reaches high values.
d) Left hypochondrium:
- Acute distension of the splenic capsule: following a two-stage rupture of the spleen. Following
the trauma, a subcapsular haematoma forms, which grows, until the capsule tears, resulting in
haemoperitoneum and haemorrhagic shock. A patient who has a visible perisplenic collection
on ETG after an accident is kept under observation for 24 hours, monitoring blood count, heart
rate and blood pressure, because capsule rupture is an unpredictable event. In patients who
have had a splenectomy, it is necessary to have vaccinations and an infectivological
consultation, as infections will be more frequent in these individuals.
- Splenic infarction
- Splenic abscess
- Rupturing splenic artery aneurysm: it often ruptures in the duodenum, resulting in haemorrhage
in the patient, melena, but negative gastroscopy.
- Acute distal pancreatitis: (in pancreatic neoplasms, the localisation is important, as at the head
level there is compression of the biliary tract, with painless sub-atheric or jaundiced pc; at the
body-tail level there is deceptive pain, simulating shoulder pain and leading to diagnostic
errors)
- Neoplasm of the left colic (splenic) flexure: predominantly stenosing, occluding or
suboccluding forms. Pain will be present when the faeces no longer have the capacity to pass
through the neoplasm, which has become so large over time that intestinal occlusion will
subsequently occur.
- Left kidney disease
- Left Basal Pleuropneumonia
e) Left iliac fossa
-
-
Left colon diverticulitis: in the case of microperforation, a stercoraceous peritonitis is created
that is initially saccate, as the meso of the sigma (mesosigma) circumscribes the area. All this
can be seen on CT. Initially we will do antibiotic therapy keeping the patient fasting,
leucocytes will be monitored, and colonoscopy will be performed after 3 days to avoid further
perforation of other diverticula. Several repeated attacks of acute diverticulitis lead to a
peridiverticular connective reaction, causing stenosis of the intestinal lumen. In this case, it will
be necessary to intervene in election with resection surgery, recanalising the pc in one go. In an
emergency, in a pc with stercoraceous peritonitis, surgical treatment involves intestinal
resection with temporary colostomy and recanalisation of the pc after 3 months. A
complication of diverticulitis is microperforation in the bladder, causing inveterate cystitis,
which can be detected on CT scan.
Neoplasm of the sigma
Infectious, ischaemic, ulcerative colitis
Sigma volvulus
Urological pathology
Left gynaecological pathology
f) Hypogastrium
-
-
Acute bladder retention: often of prostatic origin. A catheter is inserted or, if this is not
possible, a cystostomy with insertion of a temporary balloon catheter is performed to close the
breach. In a long-standing prostate patient there will be paradoxical ischuria: involuntary loss
of urine droplets
Cystitis: sometimes also haemorrhagic
Uterine pathology
- Pelviperitonitis EO of the abdomen:
INSPECTION
1) Shape of the abdomen:
- Globular abdomen: advanced stage of intestinal obstruction
- Flat, tense and contracted abdomen: sign of parietal peritoneal involvement
2) Presence of swellings:
- Umbilical seat
- Crural seat (mainly women)
- Inguinal seat
Swellings can be found that refer to herniary obstruction or choking, with district and colic pain,
due to blocked intestinal transit.
Clogged or non-reducible hernia is caused by hernia stricture after compression of the vascular
pedicle. It is a complication of hernias, which is
characterised as swellings that do not fit in the abdomen. A clogged hernia should never be
reduced. For example, in the case of an inguinal clogged hernia, the tumefaction is returned to the
abdomen through the external inguinal ring by means of the Taxis manoeuvre. In the case of a
clogged hernia, this manoeuvre is not practised, rather, an ice pack is placed on the swelling to
reduce the oedema, and if the hernia does not retract, then the patient must be operated on. The
colour of the intestinal loop is assessed: if it has a pinkish colour, the intestinal loop is retracted
into the abdomen, and plastic surgery of the inguinal canal is performed. If the intestinal loop is
purplish (ischaemic phase), anatomical patches soaked in warm saline are placed for 20 minutes
and waited for. If the intestinal loop returns to a rosy colour, the problem does not arise. If it
continues to be purple, then a segmental resection will be performed, followed by an anastomosis
of the two stumps. Hernial stricture, volvulus and intestinal invagination are the causes of
mechanical intestinal stricture occlusion due to involvement of the vascular pedicle.
3) Presence of surgical scars: it is important to look for them in order to detect previous surgery.
PALPATION
1) precise localisation of pain
2) search for masses: of neoplastic origin; ovarian cysts; abscesses (supra-mucosal or
appendicular platelet); abdominal aorta aneurysms
Certain pathological conditions are assessed by means of semeiological manoeuvres:
- Blumberg's sign: i.e. rebound pain, in which we compress the abdomen of the patient and it
allows itself to be compressed but when we then release it, the patient experiences a very
peritonitis
strong pain.
- Mc Burney's sign: for appendicitis
- Giordano's sign: renal colic
- Murphy's sign: cholecystitis
One should always look for the so-called 'parietal resistance', which can be appreciated by first
superficial and then deep palpation, indicative of an initial peritonitis, which if left untreated will
result in full-blown peritonitis.
In peritonism one has:
- Visceral-motor reflex hypertonus: involuntary, it mainly affects the muscles innervated by
the spinal nerves of the visceral pain afferent metameres, and is exacerbated on palpation, but
is not a pathognomonic sign of peritonitis
- Contracture (muscular defence) from somatic-motor pain reflex: expression of
circumscribed (when localised to a quadrant) or diffuse (ligneous abdomen, negative
prognostic sign) peritonitis.
The contracture is spontaneous, and progressively reaches the lumbar muscles and the diaphragm
(when bending the leg over the thigh, the pain will be accentuated).
PERCUSSION
1) Evaluation of free gas in abdomen: sign of perforation of hollow organ in abdomen. Gas tends
to collect towards the wall with the patient supine, and on percussion a periumbilical tympanic
sound will be heard
2) Free effusion (fluid) in the abdomen: it is appreciated on percussion because the fluid in the
abdomen, if it is abundant, can be appreciated along the hips, or it can be appreciated in
orthostatism or in cases of effusion confined to the small pelvis, with anal or vaginal palpation
the fluid in the hollow of the Douglas (in women for example for annexitis) can be appreciated,
causing pain (cry of the Douglas).
AUSCULATION
1) Peristalsis:
- Hyperperistalticism is typical in the intestinal loop upstream of the obstruction;
- Hypoperistaltism
- Peristaltic silence: in the advanced phase of an intestinal occlusion, affecting the loop upstream
of the occlusion, as a result of wall failure.
RECTAL EXPLORATION
In cases of abdominal pain it should ALWAYS be performed. It is performed in the Sims,
genupettural, gynaecological position. The index finger is lubricated, the fingertip is placed first and
then the whole finger is put in and once the internal anal sphincter is released, the rectal ampulla is
palpated and evaluated:
- Rectal ampoule masses
- Presence of foreign bodies
- Blood and/or mucus (alarm bells for pathologies that are almost always cancerous)
- Empty rectal ampoule (alvo closed to faeces)
- Presence of faecalomas
- Douglas pain
Laboratory examinations
1)
-
Dehydration and electrolyte imbalances
increased Hct and protidemia (haemoconcetration)
increased azotemia
evaluation of hourly diuresis via bladder catheter
rehydration of the patient with nasogastric tube
Correcting electrolyte imbalances (Na, K, Cl): e.g. in the case of a high intestinal occlusion
(stomach), the loss of chloride ions prevails, while as one goes down, the loss of potassium
ions increases, with consequences for intestinal motility.
2) Enzymatic alterations: CRP, ESR, in the case of acute pancreatitis: increased amylase and
lipase
3) Catabolic reaction:
- Increased blood glucose (due to peripheral insulin resistance)
- Hyperazotemia
- Reduced plasma albumin
4) EGA: e.g. in low intestinal occlusions acidosis prevails, in higher ones alkalosis.
- Respiratory alkalosis due to hyperventilation
- Metabolic acidosis due to hypovolemic or septic shock
- Hypoxaemia in ARDS
5) Leukocytosis: can be determined in the case of sepsis. There will be mobilisation of splenic
and medullary leucocyte reserves. A significant increase in leucocytes in the post-operative
period is a sign of the onset of sepsis, and if this is correlated with a T increase >38, for 3
consecutive post-operative days, a blood culture will be required, and possibly a change in
antibiotic therapy. Leukocytosis will be absent in anergic (immunocompromised) and elderly
subjects.
Instrumental examinations
1) Rx abdomen
2) Tc and ETG abdomen
In the case of direct X-ray of the abdomen:
- If there is a suspicion of perforation of a hollow viscera (stomach, duodenum, sigma), on direct
X-ray of the abdomen (also known as a blank abdomen), the right subdiaphragmatic air
crescent is presented, and on percussion the disappearance of the area of hepatic obtuseness,
and the patient can be taken directly to the operating theatre, without resorting to abdominal
CT.
- Generalised paralytic ileus: this occurs in non-circumscribed peritonitis. We will have an
anarchic radiological picture, different from the typical and orderly picture of mechanical
intestinal occlusions (intestinal loops with hypertrophic folds juxtaposed in semicircles and the
presence of hydroaerial levels).
- Disappearance of the mm iliopsoas profile
- Water level within an abscess
- Dilated sentinel loop upstream of the occlusion
In the abdominal ultrasound, one can observe:
Free spill in abdomen
- Identification of inflammatory processes affecting the viscera: e.g. thickening of the
appendicular wall
- Identification of saccate collections or abscesses
Therapy
Medical:
- Antibiotics
- Correction of hydro-electrolyte and acid-base imbalances
-
-
Therapy for hypovolemic shock: this occurs after the third compartment has been formed,
because the intestinal loop upstream of the occlusion is dilated with stagnation of liquids,
intestinal secretions, gas, which are subtracted from the general economy of the organism and
thus hypovolemic shock occurs
Nose-gastric probe: allows gastric secretion (contains cholecystokinin and secretin) to be
channelled externally, which in the case of acute pancreatitis (alcoholic or lithiasic) allows the
pancreas to be put to rest, preventing its secretion.
Surgical :
- ERCP: in case of gallstones
- Washing and drainage of the peritoneal cavity: e.g. stercoureous pancreatitis
Following surgery, a drain can be placed for safety until the second to third post-operative day.
In case of acute appendicitis or acute cholecystitis, the indication is to operate the patient within 6-8h.
LAPAROSCOPE
Laparoscopy is a minimally invasive technique that allows minimally invasive operations to be
performed through small skin incisions in order to induce a pneumoperitoneum, i.e. a 'virtual space'
working chamber, so that instruments can die.
Among the pioneers of laparoscopy is Mouret, who performed the first laparoscopic removal of the
gallbladder. In the past it was believed that to be a good laparoscopic surgeon you had to be a very
good open surgeon, but this is no longer the case, you can only be a good open surgeon if you are a
good laparoscopist.
Today, laparoscopy has become the gold standard in the treatment of various abdominal pathologies
and is indicated for:
1) Esophagus:
- Oesophageal achalasia
- Reflux disease
- Oesophagectomy for neoplasia (non-absolute indication)
- Removal of epiphrenic oesophageal diverticulum
2) Stomach:
- Gastroresection for neoplasia
- Bariatric surgery
3) Liver and biliary tract:
- Cholecyst stones
- Choledochal calculosis
- Cysts and liver abscesses
- Liver resections for benign and malignant neoplasms
4) Spleen:
- Splenectomy
-
Spleen-sparing surgery in patients in whom a subtotal splenectomy is performed, i.e. a
spleen token is left (in benign pathology), so that the patient has a resolution on the surgical
issue, without having a deficit on the immunological issue
5) Pancreas:
- Head and body resection for benign and malignant neoplasms (now reduced for limited
benefits)
- Pancreas tail resection (also in distal splenopancreasectomies)
6) Kidney:
- Total nephrectomy
- Polar resections
7) Surrene:
- Adrenalectomy
8) Prostate:
- Prostatectomy (robotic approach more appropriate)
9) Colon-rectum:
- Appendectomy
- Right hemicolectomy
- Left hemicolectomy
- Anterior rectum resection
- Rectopexes for prolapse
10) Abdominal wall :
- Inguinal hernia surgery
- Plastic for laparocele
- Diaphragmatic hernia repair
11) Gynaecological pathology:
- Total hysterectomy for benign disease
- Simple mono/bilateral ovariectomy
- Enucleoresection of ovarian cysts
- Treatment of endometriosis
- temporary or permanent tubal closure
- treatment of bladder and vaginal prolapse
Laparoscopic surgery is characterised by:
- indirect vision (through a monitor)
- monitor (which transmits images of the peritoneal cavity)
- camera
- optics
The magnified vision of the camera and optics, as opposed to the direct vision we have in traditional
surgery, has made it possible to be more precise and technically efficient. What is lacking is 'tactile
sensitivity', which is mediated through instruments and not by our hands, and therefore the distinction
of one texture from another is not fully allowed.
Then, whereas in traditional surgery, surgeons stood 360° around the operating table with direct
vision, brightness was provided by the operating lamps placed above the heads of the
surgeons, and the pc was in a supine position on the operating table. Today, the surgeons are no longer
arranged 360°, but in such a way as to ensure vision with the pc between surgeon and monitor, and the
scialitic lamp has been replaced by point lighting in the peritoneal cavity, ensuring excellent vision and
the pc is placed on the operating table in different positions.
The instruments for performing laparoscopic surgery are:
1) trocars
2) optical: which has a camera at the apex that transmits images to the monitor
3) fibre-optic cable
4) laparoscopic column, which includes:
- full H2-3D monitor
- light source
- CO2 insufflator
- washing and suction system
- video recording system
5) operating instruments, which are introduced into the peritoneal cavity via trocars, thus:
traumatic or atraumatic grasping forceps, scissors, clips applicators, hooks, wire feeders.
OPTICS
Today, optics of 5-10 mm are used. It has a camera at its apex, which provides vision at different
angles. It is connected to a camera via a fibre-optic cable, which transmits the brightness provided by a
light source.
The camera at the end of the optic is connected to a transducer that converts the signals into images,
which are then reproduced by the monitor.
LAPAROSCOPIC COLUMN
Under physiological conditions, the peritoneal cavity is a virtual cavity. It becomes real with the
insufflation of CO2, which expands the space between the parietal and visceral peritoneal sheets,
creating a chamber.
The gas that has been used is CO2, an ideal gas, because, in addition to creating the working chamber,
it is an inert gas, has high diffusibility, is soluble in blood and is then well buffered by the bicarbonate
buffer, Hb and plasma proteins, and so there will be a harmless disposal of CO2.
Insufflators are set to insufflate at a certain speed, at a certain amount, around a pressure of about 1014 mmHg in the peritoneal cavity.
In addition, the insufflator is equipped with a heating system for the insufflated CO2, so as not to
create different T gradients between inside and outside the peritoneal cavity.
The insufflation of CO2 into the peritoneal cavity takes place using two techniques:
1) Closed technique according to Verres: involves the introduction into the peritoneal cavity of
the Verres needle, equipped with a spring-loaded obturator system that is activated by covering
the needle tip, a
once all layers of the abdominal wall have been traversed, in order to avoid the iatrogenic
injuries that the tip could cause to organs in the peritoneal cavity.
The Verres needle is introduced into Palmer's point, located in the left hypochondrium, the
midpoint between the xiphoid process (more medially) and the left ribs (more laterally).
The needle is connected to a tube, which in turn is connected to the CO2 insufflator in the
peritoneal cavity.
Once the working chamber has been created, before introducing the trocar, a manoeuvre is
performed which consists of aspirating CO2 with a syringe, with a few cc of physiological
saline inside. If nothing is sucked in, then the working chamber has not been created;
2) Open technique according to Hasson: involves opening all layers of the abdominal wall to
introduce the Hasson blunt trocar, which ensures the insufflation of CO2 and the creation of
the working chamber. This technique is considered the safest because when the trocar is
introduced, there is no injury to the intraperitoneal organs. The Hasson trocar is introduced by
exploiting the umbilical scar, the skin layer is incised; at the level of the umbilical scar, the
serous, muscular and aponeurosis layers of the fascia cooperate and therefore it is easy to enter
the peritoneal cavity safely.
TROCARS
These are multi-use metal instruments, after sterilisation or in disposable plastic material.
They consist of a sleeve (the outer part) through which a spindle (the innermost part) is introduced.
When the trocar is introduced through the abdominal wall, the mandrel is extracted, as it is equipped
with a tip that allows it to pass through the wall; then the sleeve is introduced into the peritoneal
cavity, and through it the instruments are introduced to perform the surgery.
Trocars have:
- Variable size: 3-5 mm to 10-12 mm, depending on the instrumentation and optics used for
surgery.
- Valves that allow instruments to be introduced without losing the positive pressure in the
peritoneal cavity provided by CO2 insufflation.
- Tap, which allows the trocar to be connected to tubes that allow CO2 to be introduced into
or withdrawn from the peritoneal cavity.
Of fundamental importance is the anatomy of the abdominal wall: both in terms of musculoskeletal
composition and blood supply.
a) Musculoskeletal composition:
The antero-lateral abdominal wall is the set of soft parts (skin,) muscles, covered by the anterior fascia
and posterior fascia; and then the innermost layer the parietal leaflet of the peritoneum; all within a
rectangular bony frame, consisting of:
- Upper: lower thoracic margin
- Inferiorly: upper edge of the pelvic girdle
- Rear: from the transverse apophysis of the lumbar vertebrae
A system of rectus muscles, organised around the two vertical pillars to the right and left of the linea
alba, develops within this bony framework.
They are flanked by the broad muscles, which are organised in 3 layers: and from the surface to the
depth are respectively: the external oblique muscle, the internal oblique muscle, transverse abdominis
muscle.
b) Irritation of the abdominal wall: It is given by:
- Inferior epigastric artery
- Mammary artery
The two arteries join to form the main vascular axis of the abdominal wall, which is called the
MAMMARY-EPIGASTRIAL TRUNK.
The inferior epigastric artery originates from the external iliac, leads medially and upwards to the
rectus muscles and splits into a medial and a lateral branch.
Complications related to the introduction of trocars:
- They can occur after surgery, e.g. laparocele, a swelling that develops on a previous
surgical scar
- Local haemorrhages, due to vessel involvement, may occur during surgery or immediately
after trocars extraction
- They may involve viscera, such as liver or spleen
The view of the operating field is indirect, via the monitor, which must be in front of the surgeon with
the operating field in between.
Alignment between the operator, the optics, the surgical field and the monitor is of paramount
importance, and after alignment is ensured, trocars are introduced, which allow the optics to be
introduced, equipped with a camera that provides vision, capturing images that pass through a
transducer that transforms them into images through the monitor.
The arrangement of the trocars is important both in terms of the distance between them and in terms of
their position in relation to the surgical field, in order to determine an ideal angle between 45-90°.
Unlike traditional surgery, in which the patient is placed in a supine position, in the case of
laparoscopy, positions are assumed on the operating table that change both at the beginning and during
surgery, so that the organs can be moved.
The positions are:
- Trendelemburg: the patient has the head down and the legs upwards, so that the viscera,
due to gravity, move towards the head;
- Anti-Trendelemburg: the patient is positioned with the head upwards and the legs
downwards, so that the viscera, due to gravity, slide downwards and lead to the formation
of a larger space in the upper quadrants.
- Lithotomics
- On the side: the patient is positioned on the right or left side, depending on the anatomical
part to be reached. The patient is positioned on his/her side, useful for surgery on organs
lateral, such as the spleen (the splenic lodge), in the posterior left hypochondrium, or the
adrenals or kidneys.
The patient is positioned on the contralateral side, in relation to the organ to be acted on.
INSTRUMENTS
Once the trocars have been introduced, through the shirt, tools can be introduced. Among these we
have:
- Separate grippers for traumatic and atraumatic grippers
- Scissors
- Needle holder for intra-abdominal sutures
- Mechanical suturing machines for stitching the organs to be dissected and sewn up
- Electrifiable instruments, which conduct electrical energy and allow haemostasis and
dissection of organs in the peritoneal cavity.
Depending on the problem of the patient, it is important to take precautions:
- The pressures created in the peritoneal cavity, usually set by the operator, in patients with
cardiovascular disease are lower than the pressures created in healthy patients;
- The Trendelenburg position causes a reduction in GC, with a reduction in PVC. The
reduction in cardiac output can be up to 50%, baroreceptor stimulation systems are then
activated with reflex bradycardia, in terms of direct vagal response and systemic
vasodilation, which leads to arrhythmias, and also to an increase in PAO, peripheral
vascular resistance and pulmonary vascular resistance.
- in the case of impaired lung function, pneumoperitoneum increases intra-abdominal
pressure and consequently intra-thoracic pressure, which leads to a reduction in lung
volume and CFR (functional residual capacity). Possible CO2 retention, upward
displacement of the diaphragm, and reductions in respiratory excursions can lead to
hypercapnia, with respiratory acidosis, reduced lung compliance, increased airflow
resistance and reduced lung capacity.
Then it is also important to maintain thermal homeostasis, and to avoid hypothermia, which is
prevented by the CO2 heating system.
The anaesthetist performs a pre-operative assessment in which he evaluates:
1) Absolute contraindications:
- heart disease with an ejection fraction of less than 30 per cent
- Severe COPD
- Endocranial hypertension
- Haemodynamic instability (PAO and Hb are assessed)
- Severe caogulopathies (assessed by INR)
In the presence of such conditions, the intervention cannot be carried out.
2) Relative contraindications:
- Plurilaparotomies
- Older age (the elderly have comorbidities)
- Presence of large masses in the peritoneal cavity
- Obesity
- Pregnancy
Presence of conditions that, if known and treated correctly, allow surgery to be performed.
ADVANTAGES OF LAPAROSCOPY:
- Laparoscopy guarantees reduced intra-operative and post-operative bleeding, thanks to the
accurate haemostasis enabled by the 3-5 magnification of the images and the mechanical
action on the vessels given by the positive pressure from the insufflation of CO2 into the
peritoneal cavity;
- Greater, almost microscopic precision
- A reduction in morbidity and post-operative infections. Infections may occur intraperitoneally and at the site of the surgical lesion
- Channelling is excellent, resumption of regularity of alvo
- Nausea and vomiting do not occur after laparotomy
- Reduction of short- and medium-term wound complications, in terms of infection and
occurrence of laparocele
- Aesthetic results and micro-incisions
- Three-dimensional vision through the use of glasses and a 3D system
- Reduction of post-operative pain
- Early mobilisation
- Reduced hospitalisation and convalescence time
DISADVANTAGES OF LAPAROSCOPY:
- It is operator-dependent
- Lack of tact
- Longer operating times for some interventions
- Two-dimensional vision
- Higher costs in terms of technological equipment
ERNIE
A hernia is the leakage of a viscera or part of a viscera, lined with integument (since the herniating
viscera protrudes forward and is lined with the integument lining the body), through an area of
weakness in the wall, an orifice or a natural channel.
It differs from a laparocele, which is the leakage of a viscera or part of a viscera, lined with tegument,
through an area of wall weakness or an orifice, secondary to surgical injury.
Prolapse is different, which is the exit of a viscera through a natural opening of the body, without any
lining: e.g. in rectal prolapse, the rectum exits through the anal canal, which is a natural orifice, but is
not lined with tegument.
Procidence, on the other hand, is the leakage of a viscera, without any integumentary lining, through a
traumatic breach.
Evisceration is caused by a full-thickness breach of the abdominal cavity, which is followed by the
exit of the viscera.
Hernias are classified into:
1) Internal: displacement occurs within the body. Examples are:
- Diaphragmatic (to which hiatal hernia belongs)
- Iatrogenic: through a breach of the meso. For example, an operated patient who has had a
breach of the mesocolon created is not resutured and loops can slip through this breach;
- Retrocavity of epiplons. It consists of:
. anteriorly: posterior face of the stomach
.posteriorly: posterior wall of the abdomen
. left: spleen
. right: small omentum
It communicates with the abdominal cavity through the foramen of Winslow.
For example, in the case of circumscribed peritonitis, such as subphrenic abscess, which
can be on the right or left, usually on the right, but when on the left, the collection is found
in the retrocavity of the epiplon.
2) External: the movement of the viscera takes place outside the body.
- Abs
- Cerebral (encephalocele)
- Medullary (myelomeningocele)
- Lung (pneumocele)
External abdominal hernias are the most frequent and for them to form, the coexistence of:
- Presence of locus minoris resistentiae (predisposing factor)
-
Increased abdominal pressure (determining factor), which may be chronic or sudden.
For example, a person who lifts too much weight, especially with spread legs, such that
excessive pressure is exerted, so much so that it overcomes the resistance of the abdominal
wall, and thus results in the leakage of a viscera.
3) Congenital: we have a hernia sac present from birth, but there must be an anatomical
predisposition linked to the weakness of the muscular-aponeurotic planes and then the
triggering factor due to increased intra-abdominal pressure.
An example of a congenital hernia is the external oblique inguinal hernia (which can also be
acquired), which is due to the lack of obliteration of the peritoneal-vaginal duct in the male.
Usually during embryo-fetal development, a testicular outline is formed in the abdomen, covered
by peritoneum, and then this descends to the deep inguinal (or internal) orifice, rotates, and then
descends into the scrotum. This movement leads to the formation of a peduncle of peritoneum, the
vaginal peritoneal duct, which usually obliterates at birth, but if it remains pervious, leads to
external inguinal oblique hernia. In this case, the elements of the spermatic funiculus are found in
the centre of the hernia sac (in acquired external oblique inguinal hernias, however, they are found
outside the hernia sac).
4) Acquired: these are by far the most frequent and always require the coexistence of anatomical
predisposition, i.e. weakness of the muscular-aponeurotic planes, linked to various reasons; and
increased intra-abdominal pressure.
Ex:
- Dilation of normal routes or orifices
- Formation of traumatic pathological pathways or orifices
- Formation of pathological post-operative paths or orifices (laparoceles)
The pathophysiology of hernias is due to an imbalance between intra-abdominal pressure and wall
resistance. If the tissues are intact, nothing happens, in fact if muscle contraction occurs correctly, the
tension on the inguinal orifice is relieved.
In fact, partial or total leakage of the viscera therefore occurs in the case of coexistence between:
1) Predisposing factors:
- Anatomical alterations: congenital or acquired leading to wall weakness, with formation of
locus of minor resistentiae.
- Heredity: due to excessive connective tissue laxity
- Age: the older you are, the more frequent a hernia is
- Gender: inguinal hernias are found more in men, while crural hernias are more common in
women
2) Determining factors:
- all those conditions that lead to exertion and cause an increase in intra-abdominal pressure,
which is usually between 20-40 cmH20 and instead reaches 100-150 cmH20.
- Drive mechanism: especially acute
- Traction mechanism (rare)
- Direct or indirect traumatic mechanism (trauma)
The hernia has components consisting of:
a) Porta herniaria: orifice through which the herniated viscera exits
b) Route
c) Herniary bag
d) Content: the herniated viscera. Usually almost all abdominal viscera can herniate, but those
that herniate most frequently are the loops of the small intestine and the large omentum.
e) Accessory Enclosures
The hernia sac consists of:
- Collar (the tighter the collar, the greater the consequences may be)
- Body
Fon
do Also may be:
- Complete or incomplete
- Pluriloculated or multiple
- Inhabited or uninhabited or with saccular cyst (also in acquired hernias)
- Cylindrical, conical, pyriform, saddlebag-shaped or rosary-shaped.
In the case of inguinal hernias with a pluriloculated hernia sac, insistent rubbing by restraining leather
belts, for example, creates inflammatory and traumatic phenomena, which lead to the formation of
Cloquet's stigmata: i.e. fibrous thickenings that lead to a reduction in the size of the hernia sac and
favour the formation of girdles that lead to the hernia's narrowing.
In fact, a small hernia port or a small hernia sac favours hernia stricture, which explains why stricture
is so common in e.g. umbilical hernias, in which the hernia port is usually small.
In the case of large hernias, moreover, the sac is almost always multi-chambered, and each
concameration has its own herniated door, which is usually small, and this favours strangulation.
Complications
Hernias can lead to complications, which are represented by:
- Irreducibility
- Inflammation
- Clogging
- Choking
Irreducibility, inflammation and obstruction are prodromal events that promote stricture, which is the
most feared complication.
1) Irreducibility or incarceration: a hernia is irreducible when the viscera can no longer re-enter
the cavity from which it herniated. Sometimes, irreducibilities are partial, so the h e r n i a t e d
viscera can re-enter but not completely. Whereas it is reducible if the viscera
can be repositioned in the cavity from which it herniated; in this case it must be an
uncomplicated hernia, and then the contents can be repositioned in the cavity from which it
herniated, by means of the manual reduction manoeuvre, known as the Taxis manoeuvre. It
can be determined by:
- Inflammatory or traumatic intrasaccular adhesions
- Clogging (faeces cannot pass through the herniated viscera)
- Choking
2) Inflammation:
It often affects umbilical hernias. It can be:
- Traumatic
- Infectious (often from pyogenes) (especially if umbilical) More:
- Acute: rare, e.g. violent blunt trauma
- Chronic (from repeated microtrauma) And then, it can affect:
- Only the herniated organ (content): epiploitis, appendicitis, annexitis, enteritis.
- Involving sac and contents: herniated peritonitis. Clinically, we will have the classic
signs of inflammation:
- Temperature rise
- Leukocytosis
- Increased ESR and CRP
3) Clogging: accumulation of intestinal material in the herniated loop, which obstructs its transit
and prevents the viscera from being reducible. It is common in large hernias, especially when
the colon is herniated, where the formation of a true faecaloma can occur. It will occur more:
- Elderly people (less efficient peristalsis)
- Bulky hernias (slow and difficult intestinal transit)
- Irreducible hernias (perhaps due to the presence of adhesions)
Clogging involves watchful waiting in order to assess the general condition of the patient.
4) Choking: this is the most serious complication and requires urgent surgical treatment. It is the
abrupt and sudden constriction of the herniary contents, by a choking cingulum (herniary port),
which causes compression of the vascular pedicle of the herniary contents, and thus serious
consequences on the circulation of the organ (ischaemia)
It is common in cases of:
- Small, inelastic herniary door
- Adults and the elderly (especially women)
- Small hernias
- Large hernias (rare)
It causes intestinal transit to stop, with mechanical ileus.
From a pathophysiological point of view, one will have: choking girdle□ venous stasis□
impeded reflux□
stasis oedema (but arterial inflow remains) □ anoxia (then) □ haemorrhagic infarction
(haemorrhagic suffusions, in which the loop becomes reddened, full of petechiae)□
gangrene□ perforation.
Injuries are first reversible and then irreversible.
The etiopathogenesis sees the presence of strain associated with:
- Sudden increase in abdominal pressure
- Sudden increase in content
- Sudden passage of a viscera through a narrow orifice Anatomical conditions that
favour the
throttling:
- Presence of fibrous elements
- Bag dimensions
- Intra-saccular choking At the anamnesis it is important to ask:
- When the acute event (i.e. abdominal pain) occurred
- When the hernia has become irreducible
The time lapse between the onset of these symptoms and the arrival of the patient to the
doctor's attention is important for the choice of treatment: if more than 6-7 hours have elapsed,
it is advisable to open the patient because there is a risk that ischaemic suffering of the
herniated organ may have occurred.
Two particular types of throttling can be recognised:
- Richter's choke: where only a small part of the intestinal wall leaks out and only this small
part will suffer;
- Retrograde choking: the viscera comes out, but it is the presence of a return loop (Wshaped) that compresses the vessels of the herniated viscera and then sends this portion
inside the abdominal cavity into necrosis, rather than the portion that comes out.
In this case, after a certain number of hours, it is better to open the patient up and check if
there are any other loops affected by vascular distress than to make a simple groin incision.
The clinical symptomatology of hernias also depends very much on the organ being
strangled:
1) Sudden increase in the volume of the hernia, which becomes painful and irreducible and
does not change its volume under coughing fits
2) Acute abdomen:
- Abdominal pain
- Nausea and vomiting
- Alvo closed to faeces and gas
- Compromising the general state
3) Hyperacute form with stercaceous perforative peritonitis (if the viscera is intestine),
leading to death if no action is taken.
Strangulated hernias of the ileum and colon can lead to the formation of a pyo- steraceous
phlegmon, which tends to open towards the surface forming an entero-cutaneous fistula.
Other rare complications:
- Traumatic hernia rupture
- Herniaria tuberculosis
- Neoplasia herniaria (i.e. neoplasms of the viscera that are then herniated
HERNIA INGUINAL
Anatomy of the inguinal region
The anterior abdominal wall consists of:
- Rectus muscles of the abdomen
-
External oblique muscle
Internal oblique muscle (in humans it gives rise to the cremasterian muscle, which runs along
the inguinal canal and then covers the testicle)
Transverse muscle
The inguinal canal consists of 4 faces and 2 orifices. The 4 faces are:
-
-
Anterior: aponeurosis of the external oblique
Posterior: transversalis fascia lining the transverse muscle of the abdomen; it has three
reinforcing ligaments to give it greater strength. There are two vertical ligaments, the
interfoveolar ligament (Hesselbach's ligament) and the inguinal sickle (Henle's ligament), and
a horizontal reinforcing ligament, Thompson's ileopubic benderella, formed by the union of the
transversalis fascia, with a frontal arrangement, and the posterior margin of the inguinal
ligament.
Upper: lower margin of the internal oblique and transverse muscle
Inferior: upper face of the inguinal ligament of Poupart or Fallopian tube; from the anteroupper iliac spine to the pubic tubercle; in the middle part, some bundles go towards the ileopectine eminence (ileo-pectine benderella) forming the neuromuscular lacuna (lateral) and the
vascular lacuna (medial). In the terminal part it inserts on the pubic tubercle and emits the
lacunar ligament (del Gimbernat's),
The two orifices are:
- Superficial or external inguinal ring; bordered by fascicles from the lower portion of the
aponeurosis of the external oblique muscle; in particular, the lateral abutment inserts on the
pubic tubercle, the medial abutment reaches the pubic symphysis and the posterior abutment
reaches the contralateral pectine crest. The medial and lateral pillars form a long fissure that
is closed laterally by arcuate fibres called intercrural
- Deep or internal inguinal ring; located in the context of the transversalis fascia, and bounded
medially by the concave lateral margin of the interfoveolar ligament of Hesselbach and the
inferior epigastric vessels. Corresponds to the point where the parietal peritoneum and
transversalis fascia invaginate to accompany the descent of the testicle into the scrotum
The inguinal canal is crossed:
-
In humans: spermatic cord
In women: round ligament of the uterus
The spermatic funiculus contains:
- Deferent duct
- Deferential artery (branch of the umbilical artery)
- Deferential veins
- Internal spermatic artery (branch of the aorta)
- Funicular artery (branch of the external spermatic artery)
- Pampiniform plexus venous vessels
- Lymphatic vessels
- Nerves
Usually the contents of the hernia are the epiploon, small intestine or even the colon.
In topographical anatomy, the femoral triangle or Scarpa's triangle (from Antonio Scarpa) is a region
located in the upper, anterior and medial part of the thigh. It appears as a depression in the shape of a
triangular pyramid with the apex pointing downwards and the base at the top.
The femoral triangle is delimited
in the upper corner by the inguinal ligament, which runs from the anterosuperior iliac spine to
the pubic tuberosity.
in the lateral edge by the sartorius muscle, which runs from the anterosuperior iliac spine to
the medial surface of the tibia, medial to the tibial tuberosity.
in the medial corner by the long adductor muscle, which runs from the anterior aspect of the
upper pubic branch to the linea aspra of the femur.
The apex is directed inferiorly and corresponds to the overlap of the sartorius and adductor longus
muscles. It continues inferiorly with the canal of the femoral vessels. The base is formed by the lacuna
vasorum.
The lateral wall is characterised by the iliopsoas muscle. The medial wall is characterised by the
pectineus muscle. Between the pectineus and psoas muscles is the iliopectineal fossa, lined by the
iliopectineal fascia.
The anterior wall consists of the fascia lata, centrally presenting the fascia cribrosa for the passage of
numerous blood vessels (including the great saphenous vein) and lymphatics.
Scarpa's triangle is divided by the iliopectine banderelle into two parts or gaps:
1) Lacuna muscolorum (lateral): wider. It is occupied by the ileopsos muscle and the crural nerve;
2) Lacuna vasorum (medial or crural ring). Where the (more medial) vein and the (more lateral)
femoral artery are present. In addition, between the vein and the ligament of Gimbernat there is
a space called the lymphatic lacuna (or infundibulum) in which the Cloquet's lymph node,
which occupies the medial portion of the lacuna, is present.
In topographical anatomy, the crural, or inguinofemoral, region defines the portion of the Lacuna
Vasorum of the Femoral Triangle, or of Scarpa. It can also be referred to as the crural canal, which
houses the femoral vessels and the Cloquet's lymph node. It corresponds to what is referred to in
semeiotics as the thigh root.
The crural canal is bordered by:
-
Upper: inguinal ligament
Inferiorly: pectineus muscle and Cooper's ligament
Medially: Gimbernat's lacunar ligament
Laterally: femoral vein
Inguinal hernias
An inguinal hernia is a hernia that passes through the abdominal wall and runs partially or completely
through the inguinal canal. They make up 90 per cent of abdominal hernias and are rare in women.
Physiologically, the dynamic mechanisms that strengthen the abdominal wall during intra-abdominal
pressure increases are:
1) Keith's crotch sluice
2) Lytle's Sling
3) Contraction of the two pillars of the external oblique, with narrowing of the external inguinal
orifice
4) Creamery contraction.
These mechanisms create a counterpressure on the transversalis fascia, which reduces the effects of
intra-abdominal pressure.
Usually inguinal hernias form at the points of least resistance in the abdominal wall, i.e. the inguinal
dimples, which are divided into:
1) Internal: between the middle and lateral umbilical ligaments. This is where the internal oblique
hernia originates
(infrequent)
2) Media: between the lateral umbilical ligament and the inferior epigastric artery. Originates the
direct hernia.
3) Lateral: lateral to the inferior epigastric artery. External oblique hernias originate.
They stand out:
- Internal oblique hernias
- Direct hernias
- External oblique hernias
External oblique hernia
It may be:
- Congenital
-
Acquired
Such hernias can:
- Penetrating the internal or deep inguinal orifice
- Stopping inside the inguinal canal
- Emerging from the external inguinal orifice
- Make your way to the bottom of the scrotum or to the large lip.
Congenital
External oblique inguinal hernias are the only ones that can be congenital and this is due to the lack of
obliteration of the vaginal peritoneal duct in men and the duct of Nuck in women.
In men: while in congenital external oblique inguinal hernia the elements of the funiculus are located
inside the hernia sac, in the case of acquired external oblique inguinal hernias or in direct hernias (both
are very rare), the hernia sac is not intrafunicular but is placed lateral to the elements of the spermatic
funiculus. This is very important for the surgical act, often for various causes the ductus deferens can
be mistaken for a plica of the herniary sac and it is cut erroneously and therefore to avoid this it is
important to hold with one hand all the elements of the funiculus and try to recognise absolutely the
ductus deferens while cutting with the scissors; the ductus deferens will look like a large spaghetti,
harder than the surrounding tissues. This could pose a medical-legal problem, since re-anastomosis of
the vas deferens is not at all easy, it is microsurgery. Congenital external oblique inguinal hernia is due
to the lack of obliteration and thus persistence of the peritoneo-vaginal duct, which leads to the
existence of a hernia sac that will later be occupied by small intestine.
In the embryonic period, the testicle, covered by peritoneum, descends from the abdominal cavity to
the internal inguinal orifice, rotates and drags the peritoneum along, forming the vaginal peritoneal
duct, which then closes at birth.
It can be had:
1) Congenital hernia tip
2) Congenital interstitial hernia
3) Congenital funicular hernia
4) Testicular or inguinal-scrotal hernia
In women: is due to the abnormal persistence of Nuck's duct, through which the round ligament of the
uterus passes. It is distinguished:
1) Congenital hernia tip
2) Congenital interstitial hernia
3) Bubboncele
4) Congenital hernia of the large lip
Acquired (or indirect)
It also penetrates through the external inguinal dimple (i.e. the deep or internal inguinal ring), and
travels partly or wholly through the inguinal canal, until it reaches as far distally as the scrotum or
great labrum. Usually the peritoneo-vaginal duct and Nuck's duct are perfectly obliterated and the
hernia sac will be extra-funicular (in men). Much more frequent in the male sex.
Depending on the extent, a distinction is made:
- Hernia tip: the hernia sac barely faces the internal orifice
- Interstitial hernia: the sac remains in the inguinal canal
- Bubbonocele: the sac faces the external orifice
- Inguino-scrotal: the sac descends into the scrotum
- Hernia permagna: one or more loops screw the scrotum
Direct hernia (acquired)
It is rare, has no gender predilection, although it is more common in the elderly male, and is always a
weakness or stress hernia.
It is called direct, because the viscera emerges directly from the external inguinal orifice, without
passing through the inguinal canal, but by pushing anteriorly on the posterior wall of the inguinal
canal, consisting only of the fascia transversalis, which will not be reinforced by the ligament of Henle
and the ligament of Hesselbach.
The herniation point of the direct hernia is the so-called Hàsselbach's Triangle. It is bordered by the
rectus muscle, the epigastric vessels and the inguinal ligament and through this the direct hernia is
formed; it is the only area covered only by the transversalis fascia and therefore represents the weak
point of the posterior plane of the inguinal region.
It makes its way through the middle inguinal dimple, and usually has a wide collar (hence less risk of
choking), is usually small, hemispherical and does not descend into the scrotal sac or labia majora.
The position of the sac is important because when the patient is operated on, as soon as the inguinal
canal is opened, the funiculus is isolated, the elements are isolated, and it is immediately realised that
it is a direct inguinal hernia.
In this case, one does not even open the hernia sac, but directly sinks the herniated part and closes it,
reinforcing the posterior wall of the inguinal canal, then the fascia transversalis, doing a capitonnage,
i.e. a long continuous suture, and then a plastic surgery is done, as also in the external oblique hernia.
Internal oblique hernia (acquired)
It is a weakness hernia, which is very rare. It is called vesico-pubic. It is usually very small and often
does not or only slightly exceeds the external inguinal ring. It only has a close relationship with the
funiculus or the round ligament.
Two etiopathogenetic mechanisms are hypothesised:
- Externalisation of a fat pad of Retzius' peri-vesical space (external supravesical hernia)
- Introflexion of the peritoneum into the space of Retzius, with formation of a sac (internal
supravesical hernia)
Clinic
The pc presents:
- Acute, localised, muscle-type pain, which tends to go into remission within a few days.
- In the absence of complications, there will be modest complaints:
. dull pain, which increases with coughing or due to other increases in intra-abdominal P
.sense of weight or local discomfort
. digestive disorders
.slight alterations in bowel
. it often irradiates to the ipsilateral testis or supra-retropubic location.
Clinical symptoms also differ according to the presence or absence of complications.
The diagnosis is based on:
- Anamnesis and clinical symptoms
- EO: is performed first with the patient in orthostatic position and then in supine decubitus:
1) INSPECTION:
.can be negative, especially in small hernias in the resting pc, and these can perhaps be seen
better by making the pc cough.
. voluminous hernias have a cylindrical shape (such as external oblique) or a hemispherical
shape (such as direct and internal oblique)
Hernia does not heal with medical aid, the only treatment is surgery. And in the presence of young
subjects, for example, who report symptoms attributable to the presence of a hernia, but the hernia on
examination cannot be seen, the best attitude to adopt is to wait and see, establishing a more or less
close follow-up, depending on the case.
The examination of the hernia patient states that if the patient does not have any swelling, but reports
that when standing for a certain amount of time, even without exertion, he/she begins to have a sense
of weight or a very modest burning sensation/ching pain in the right or left iliac fossa or laterally.
Sometimes this pain also occurs when sitting for too long. This is
of rather vague symptomatology, it is always good to go and inspect the inguinal canal and see if there
are any small hernia tips. Still other times, the patient reports directly to the doctor that they have an
inguinal swelling.
Therefore, to examine a hernia, the patient must stand in front of us without underwear and we observe
whether there are any swellings (they may not even be present). And one has to understand whether
these are located above or below the inguinal ligament.
2) PALPATION: it is performed in orthostatism and also in clinostatism. The glove-finger
introflexion manoeuvre is performed, which allows the inguinal canal to be explored; it is
sometimes difficult to perform, especially when the scrotum is contracted due to the cold, in
those patients who have a highly developed cremasterian muscle, so it is always better to have
the patient lie down and lie supine. In the male patient, the "gloved finger" introflexion
manoeuvre of the scrotum must be performed: stand on the right side of the patient, use the
index finger of the right hand, hook the bottom of the scrotum and gently go up towards the
external inguinal orifice, and feel if it is small/large, penetrable/non-penetrable, and invite the
patient to cough. Then the patient is made to lie down and the whole operation is repeated,
which allows better detection of small hernias. If the hernia is visible in the scrotum, we will
already have made a diagnosis, but in any case we try to reduce it, while the patient is standing,
and then we do the introflexion manoeuvre. If we are not able to reduce i t , we put the patient
in supine decubitus, and try to reduce the hernia, and then do the glove-finger introflexion
manoeuvre of the scrotum. If, on the other hand, the scrotal hernia is an inguinal-scrotal hernia.
In the case of a hernia that is clogged and therefore not reducible, one never performs the Taxis
manoeuvre, in which a potentially ischaemic intestinal loop would re-enter. It is advisable to put an ice
pack in the swelling, and if it does not re-enter on its own, go to the PS. Then during surgery in the
case of a purple intestinal loop, laparotomic patches soaked in warm saline are placed for 20 minutes,
and we see if it slowly regains colour, and thus that there is revascularisation. In that case, then the
intestinal loop is reinserted into the abdomen, the peritoneum is closed and the inguinal canal is
plasticised by placing a prosthesis and obliterating the internal and external inguinal canal.
Inguinal hernia goes into DD or complicates in/with:
1) Funiculus cyst: this can be congenital or related to an inflammatory event. It has a rounded
shape and is found at the base of the scrotum.
2) Spermatocele: related to closure of the vas deferens for usually inflammatory reasons, with
accumulation of spermatozoa downstream of the obstruction (these are quite rare cases)
3) Acute lymphadenitis: may mimic choking
4) Testicular neoplasia: they present a hard, stone-like consistency in the scrotal sac;
5) Varicocele: the Curling sign is implemented, by having the patient lie down, push towards the
external inguinal orifice, if it is a hernia, leaving the pressure exerted it will reappear; if it is a
varicocele it will not reappear, unless you put the patient back upright. In the treatment, the
venous vessels of the pampiniform plexus are isolated and ligated at their highest point. It is
almost always present on the left, because the left spermatic vein
ends at a right angle on the renal vein, and so the connective valves fail more easily. The
spermatic vein on the right ends on the ipsilateral renal vein at an acute angle, and in the case
of a varicocele on the right, it is almost certainly due to a compression on the vessel caused by
another pathology. (also in the case of fibrosis of the pampiniform plexus).
6) Hydrocele: this is a clear ooze, which can be highlighted by transillumination, placing an LED
bulb on the skin, on the opposite side from observation, and the mass will appear more or less
red and dark. The hydrocele can be cleared by puncturing it, but it almost always reforms, so
the standard treatment is surgical. If a hydrocele is stung several times, infectious facts can set
in, which can lead to pachivaginalitis, i.e. the vaginal tonaca becomes hard as if it were a pig's
rind, as thick as parchment, making treatment difficult. The hydrocele is treated by draining it
and then doing an eversion and/or resection of the vaginal. (also in case of fibrosis of the
lymphatics). The tests to be done are:
o Thermography: to see if there are temperature variations between one testicle and the
other
o Ultrasound
o Spermiogram
7) Crural hernia
8) Testicular atresia (in the case of arterial vessel fibrosis)
Treatment:
Non-prosthetic techniques
Non-prosthetic techniques consist of opening the inguinal canal, isolating the sac and then
reconstructing the abdominal wall.
1) Mugnai Ferrari: the canal is obliterated, but the spermatic funiculus is passed under the
muscular-fascial plane
2) Bassini: the inguinal canal is reconstructed (bringing the conjoined tendon closer to the
inguinal ligament) and the spermatic cord is repositioned inside it
3) Postemski (used in Palermo): the inguinal canal is eliminated and the spermatic funiculus is
left above the muscle-fascial plane, but the complication can be hernia recurrence.
4) Shouldice: no longer used
Prosthetic techniques
Today, prostheses are used to reinforce the abdominal wall to help 'relieve' pressure. These prostheses
consist of polypropylene nets and a plug to occlude and repair the hernia port.
Complications after the use of prostheses are:
1) Sepsis
2) Haematoma
3) Urinary retention
4) Genital sequelae
An operation that is used for recurrences is Stoppà's, where the skin is incised, the anterior parietal
peritoneum is disconnected until it reaches the inguinal orifice, and then a patch or net is put in place
and left, because the weight of the viscera itself pushes the peritoneum closed.
Today's techniques are:
1) Lichtestein: hernioplasty with prolene mesh
2) Trabucco: in which the channel is opened and the bag is removed.
3) Transinguinal-preperitoneal
4) Laparoscopic-preperitoneal
Laparoscopic techniques
The laparoscopic techniques are certainly more modern and more widely used today, although there
are also disadvantages (as well as advantages) in their use, one of which is the fact that the
laparoscopic correction of hernias in principle requires general anaesthesia, whereas an operation
according to the procedures described above must be performed under local anaesthesia, unless there
are other particular and specific indications related to the patient's pathology.
1. IPOM: intraperitoneal onlay mesh involves the placement of endoperitoneal prostheses that
come into direct contact with the intestinal loops
2. TAPP: transabdominal peritoneal plasty involves placing the prosthesis outside the peritoneum
by cutting a flap of serosa to cover the prosthesis, i.e. in the context of the abdominal wall.
3. TEPP: totally extraperitoneally plasty consists of disconnecting the peritoneum from the
underlying structures by reducing the sac without access to the abdominal cavity. This is also
in the context of the abdominal wall, without access to the peritoneum.
These techniques have undoubted advantages, as well as a broader, more specific and more complete
view of the surgical field, they do not create adhesions, they do not cause post-operative pain, and
recovery is particularly fast.
Focus: TAPP
In addition to the advantages already illustrated, this (laparoscopic) technique allows us to correct
hernias, even bilateral ones, with a single operation and with only laparoscopic incisions, and the
exploration of the abdominal cavity in the case of concomitant pathologies is also possible.
The limitations are relegated first and foremost to the need for general anaesthesia and the possible
incidence of injury to intra-abdominal organs (a risk that is, however, reasonably low in view of the
fact that this is the eventuality to be taken into account for all laparoscopic surgeries, despite the fact
that the number of cases is very small).
TAPP involves the use of a prosthesis that is inserted through trocars into the peritoneal pocket
created; this prosthesis is not sutured but involves the use of glue, fibrin and non-resorbable or only
partially resorbable spirals. This predisposes to foreign body or inflammatory reactions and this can be
one of the limitations of this technique
Among the most serious complications are vascular lesions and haematomas due to the damage that
the prosthesis in chronic can create on the vessels of the abdominal wall, particularly on the spermatic
vessels, the vas deferens and the epigastric vessels. Other types of complications are rarer, falling
within the 0.6% range, and are infections, occlusions and visceral injuries.
HERNIA CRURAL
It exits through the crural/femoral ring? (or lacuna vasorum) in Scarpa's triangle and is the most
frequent hernia after the inguinal hernia. It is found at the level of the root of the thigh, below the
inguinal line. It is a n acquired hernia and is due to a wall weakness, much more frequent in women,
but rare in girls.
The most frequent type of crural hernia is that of the lymphatic lacuna or infundibulum: infundibular
or lympholacunar hernia.
Other, rarer types of crural hernia:
- Musculolacunate hernia
-
Vasolacunate hernia
Pectoral Hernia of Cloquet
Laugier's hernia
The hernial door of the infundibular hernia is delimited by:
- Anterior: inguinal ligament
- Rear: Cooper's ligament
- Medially: Gimbernat's ligament
- Laterally: femoral vein
The herniary sac, from the inside outwards, consists of:
1) Pre-peritoneal loose connective tissue (pre-peritoneal lipoma)
2) Fascia transversalis
3) Fascia cribrosa (anterior wall of the crural canal)
4) Subcutis
5) Cute
Clinical variants classify it into:
1) Hernia tip (just committed)
2) Interstitial (or incomplete) hernia penetrating the infundibulum
3) Complete hernia (crosses the cribriform fascia)
Clinical and EO
Pain will occur during standing or following exertion that increases intra-abdominal P. The pain
subsides in supine decubitus and in flexion of the thigh.
When a crural hernia is small, it is more difficult to diagnose than a small inguinal hernia because there
is more tension in the tissues and inguinal ligament.
On palpation and inspection a tumefaction is appreciated above and below the line of Malgaigne.
Lateral to the herniary collar, the pulsation of the femoral artery is appreciated; the herniary sac may
rise upwards, making it more difficult to distinguish from an inguinal hernia.
It can often be complicated with choking due to the smallness of the herniary port.
Close to the sac, laterally, there is constantly a lymph gland called Cloquet's lymph node, in fact the
main DD of the crural hernia is with lymphadenopathy
Treatment is surgical.
HERNIA UMBILICAL
It is the most frequent abdominal hernia after inguinal and crural. It is determined by the fact that the
umbilicus is a locus of least resistance.
Omphalocele, a paediatric condition, is a protrusion of a more or less large part of the intestine
through a median wall defect at the base of the umbilicus.
Gastroschisis is the protrusion of a part of the intestine through a wall defect usually to the right of the
umbilicus.
They are distinguished in:
1) Congenital form (in children): due to a delay in normal umbilical ring closure
2) Acquired form (in adults): from weakness.
Development of the umbilicus
During embryonic development the abdominal wall is open in front, then gradually closes and the
umbilical ring remains.
-
Early embryonic stages: the abdominal wall is largely open forwards, and the progressive
extension of the abdominal wall towards the midline gradually circumscribes the coelomic
cavity and results in the formation of the umbilical ring.
-
-
At the end of the third month: the umbilical ring is reduced to a small opening through which
they pass:
a) Rudiments of the vitelline duct and the allantoic duct
b) Vascular structures that establish the union between placenta and embryo (umbilical cord:
umbilical vein at the top and two umbilical arteries at the bottom)
At birth: obliteration of these vascular structures. The umbilical scar is very solid in the lower
part.
The upper half of the umbilicus is therefore a weak area. Through the umbilical ring pass:
- Onphalo-mesenteric or vitelline canal
- Onphalo-mesenteric vessels or calves
- Allantois
- Part of the abdominal viscera
In children: it is due to a delay in umbilical ring closure; it is typical of premature infants; it usually
has an omental content; it is usually never treated; it never constricts and tends to heal spontaneously.
Surgical treatment is only indicated if it persists beyond 6 years of age
In adults: it is a weakness hernia, it prefers obese and multiparous women, it usually has a narrow
collar which favours choking and it usually has omental content.
From the outside in, the umbilical hernia consists of:
- Cute
- Subcutis
- Fascia transversalis
- Pre-peritoneal fat
- Herniary sack (often multiloculated)
Umbilical hernia can be:
- Direct
- Indirect (open umbilical canal up and down)
- With pre-peritoneal diverticulum (umbilical canal open at the bottom and closed at the top)
Clinically we will have:
1) Non-pathognomonic digestive disorders
2) More or less considerable distension of the umbilical scar
3)
Overlying skin often in pain: cyanotic, thin, oedematous, sometimes ulcerated Can
frequently complicate: choking
The reduction in abdominal pressure that occurs in large laparoceles can lead to a decrease in
respiratory function. It can occur in large umbilical hernias or in rare
in cases where there are permagne inguinal hernias, that when the viscera come out of the inguinal
canal, and especially if the leakage is substantial, the respiratory mechanics will adapt to the new
condition, so if we retract the viscera and suture after the operation, the patient may go into respiratory
failure. A past technique consisted of performing a sort of pneumoperitoneum in order to re-accustom
the abdominal cavity in the pre-operative to having more content, so that in the post-operative the
respiratory mechanics would not suffer a defiance. Today, this technique is no longer used, but it is
advisable to use a containment band for a few days in the pre-operative period (especially in the supine
position), to give a sort of re-education to breathing that is as normal as possible.
HERNIA OF THE LINE ALBA
Another type of abdominal wall hernia is the epigastric hernia, located medially at the linea alba and
due to a defect in the linea alba through which fat escapes
pre-peritoneal.
Another hernia, although not so rare, is the hernia of Spigelium, which normally originates on the
lateral portion of the semilunar line of Spigelium, which is nothing more than the superior and lateromedial margin of the fascia transversalis.
IMPROPER HERNIATIONS: DIASTASIS OF THE MUSCLES RECTUS
A separate element is diastasis of the rectus muscles, which is not a true herniation, but is due to a
receding of the rectus muscles themselves, and an increase in the size of the linea alba, and is
characteristic of obese men and women who have lost weight.
HERNIAS DIAPHRAGMATIC
Diaphragmatic hernias can be congenital, acquired spontaneously, acquired traumatically and then by
eventratio and diaphragmatic relaxatio.
Congenital hernias are predominantly in males, they form because the diaphragm, in embryonic
development, closes at the end, separating the thoracic cavity from the abdominal cavity, but its fibres
are in the centripetal direction, so some bundles may leave gaps and the outcome is this hernia; among
these we have: the posterolateral of Bochdalek; the foramen of Morgagni-Larrey (these are quite
obvious and are formed because the positive abdominal pressure causes the hernia t o be in the caudocranial sense, through the diaphragm you can therefore see an opening); the hernia of the top of the
diaphragm, the hernia from agenesis of a hemidiaphragm, so you find the abdominal viscera or
organs in the thorax; Boyd's posterior costo-lumbar hernia, where t h e r e i s t h e most complex
insertion posteriorly, there is the final closure of the foramina and the bundling of the various bundles.
Spontaneous are those of the oesophageal hiatus, classic sliding or paraesophageal/rolling.
There are also traumatic ones, which are mostly found on the left, because the liver, which has its own
protective function towards the right hemidiaphragm, is missing there.
Then we have eventratio and relaxatio:
Eventratio: when a large part of the viscera through the diaphragm, predominantly always on the left
side, spontaneously move into the thoracic cavity due to a hypoplasia of the diaphragm; they may be
associated with pathologies, but are in any case rare.
Relaxation: Here the diaphragm has lost its muscle tone, consequently its restraining capacity is lost,
and the viscera, due to positive abdominal pressure, tend to rise into the thoracic cavity; this creates
predominantly respiratory problems, due to a reduced capacity for lung expansion.
Embryogenesis of the diaphragm:
The diaphragm develops from several embryonic sources. The muscle, the associated connective tissue
and the central tendon develop from three sources: from the transverse septum, the pleuroperitoneal
folds and the somites.
1. The transverse septum is the first structure present in the development of the diaphragm and
serves as the initial barrier between the thoracic and abdominal cavities.
2. The pleuroperitoneal folds (also known as the retrohepatic mesenchymal plate) are the second
major component of the development of the diaphragm. The pleuroperitoneal folds are two
transitory pyramid-shaped structures lying on either side of the oesophagus and protruding
from the body wall between the pleural and peritoneal cavities.
3. The somites, similar to the muscles of the trunk and limbs, are the source of muscle cells of the
diaphragm.
POSTEROLATERAL HERNIA OF BOCHDALEK:
It is the most frequent congenital hernia. It results from a defect in the development of the posterolateral portion of the diaphragmatic dome at the level of Bochdalek's foramen (transverse septum,
pleuro-pericardial folds). It almost always occurs on the left, due to the occlusion of this access on the
right by the hepatic dome. It lacks a herniary sac.
Symptoms: Almost always surgical urgency in the neonatal period with respiratory and circulatory
compromise requiring treatment within the first 48 hours of life. In less severe cases it may go
unnoticed for years until manifesting in adulthood with dyspnoea, occlusive or sub-occlusive crises, or
be a chance finding on chest X-ray.
Diagnosis:
Chest X-ray
-
Digestive Tube X-ray
-
DC Opaque Clisma
-
CT SCAN
-
Magnetic Resonance Imaging (MRI)
-
Doppler Ultrasound
Surgical treatment: Access may be by the abdominal or thoracic route. By the thoracotomy route, in
case of choking of a viscera or repeated sub-occlusive episodes.
HERNIATION OF THE FORAMEN DE MORGAGNI- LARREY
It occurs in 3 per cent of the population; it develops due to the persistence of an anterior, retrosternal
paramedian lacuna; lack of welding of the sternal and costal bundles of the diaphragm; it occurs on the
right side in 90 per cent of cases, due to the presence of the pericardial sac on the left side; as a rule, it
has a peritoneal sac; initially only the pre-peritoneal fat creeps in, then the peritoneum, then (in about
half of the cases) the large omentum and transverse colon. As a rule, the hernia, being anterior,
exceeds the liver.
Symptoms: Random occurrence in children or young people, or following investigations for persistent
epigastric and costal pain
Diagnosis:
Chest X-ray
-
DC Opaque Clisma
-
CT SCAN
-
MRI
-
Doppler Ultrasound
Surgical treatment: Laparotomic incision, opening of the abdomen and reduction of the herniated
viscera with eventual excision of the sac. This is not a complex operation (except in cases where
pieces of the diaphragm are missing) because it involves pulling down what is herniated in the
abdomen and then the breach is closed with non-absorbable stitches, because it is an area subjected to
greater traction, anchoring the diaphragm to the rectus abdominis muscles or even reinforcing it with a
flap of transverse or oblique muscle.
HERNIA OF THE PHRENIC CENTRE
They are hernias that are generally rare and small, and may be sac-like.
[NB: Why is it important to assess the presence or absence of the sac? The sack is important because it
separates the two cavities, in fact the power of the abdominal pressure is discharged onto the sack so it
is still circumscribed, if this was not present we would have lung collapse. In children, you have to
intervene early, otherwise you may see the collapse, probably of just one
lung (thanks to the mediastinal pleura which, by separating them, ensures the integrity of at least one
of the two).
Treatment: abdominal or thoracic surgery, reduction and suturing of the breach with possible
duplication of margins.
AGENESIS OF A HEMIDIAPHRAGM
They too are rare and characterised by displacement of a considerable part of the viscera in a
hemithorax. This is because there is a lack of the sac and a large part of the diaphragm: peritoneal
reflections are missing because there are no parietal leaflets lining the diaphragm above and below,
resulting in a single cavity.
Treatment: Surgery requiring double-entry. Use of prostheses to reconstruct the haemidiaphragm that
are reshaped as the child grows. There is a need to increase the capacity of the abdomen to
accommodate the viscera.
LUMBOCOSTAL HERNIA BY BOYD
It should be distinguished from Bochdalek's as it is posteriorly bounded by the quadratus lumborum. It
contains mostly retroperitoneal fat, sometimes the adrenal.
Treatment: surgery
DIAPHRAGMATIC HERNIAS TRAUMATIC
They are a consequence of diaphragmatic injuries:
From closed trauma (laceration of the diaphragm due to increased intra-abdominal and/or
endothoracic pressure)
From penetrating wound (laceration of the diaphragm by sharp or pointed bodies)
The laceration site is most frequently found on the left (80-95 %), because on the right the hemicuple
is protected by the liver.
Diaphragmatic breaches mostly depart from the phrenic centre or hiatus towards the costal arch; more
rarely, the tear is parallel to the chest wall; even rarer is the disconnection of the diaphragm from the
postero-lateral chest wall.
The contents of the hernia are represented:
Gastric fund (31.8%)
-
Colon (27.2%)
-
Spleen
-
Tenuous loops
-
Omento
-
Kidney and adrenal gland (in the case of posterior disconnection)
Symptoms: they are related to the size of the tear and especially to the volume of herniated content.
Bronchitis and relapsing pneumonia
-
Dyspnoea
-
Chest pain
-
Abdominal pain
-
Nausea and vomiting
-
Closure of the alvo
Diagnosis: obtuseness of the pulmonary plexic sound (this is because certain organs such as the colon,
stomach, etc., which have residual contents, if they have an occlusion on percussion will give an
obtuse sound; normally the lung should not); decrease in vesicular murmur; intestinal borborigrams in
the thorax (perceptible with the phonend and corresponding to the sounds of peristalsis; if you hear
borborigrams, there is almost always no intestinal occlusion).
Instrumental examinations:
Chest X-ray (diagnostic in 70%)
-
X-ray digestive tract
-
X-ray clisma opaque
-
Echotomography
-
CT thorax-abdomen
-
Magnetic resonance imaging
Treatment: treatment is surgical and must be timely: suturing of the breach after reduction of the
herniated viscera; treatment of concomitant injuries. Access routes:
Thoracic: here the diaphragm is better addressed, it allows rapid cable retention
pleural cavity and easy suturing of the diaphragmatic breach; exposed to increased
postoperative complications and does not allow the assessment of abdominal viscera injuries
Abdominal: better repositioning of herniated viscera and control over haemorrhages and
injuries of abdominal organs; suturing of the diaphragm is less easy
EVENTRATIO AND RELAXATIO
Permanent superelevation of a haemidiaphragm without interruption or modification of the muscle
insertions. Eventratio is mainly neonatal, there is a congenital hypoplasia of the diaphragm, traction at
birth on the cervico-brachial plexus. In adults it is called relaxatio and there is slatentisation of
congenital hypoplasia and phrenic nerve injury. Predominantly in males (70% of cases); left
haemidiaphragm 75% of cases.
Cardio-respiratory symptoms: coughing, dyspnoea on exertion, orthopnoea, recurrent pneumonia,
cardiac arrhythmias (from contact pacing), cyanosis (from dyspnoea).
Abdominal symptoms: dyspepsia, dysphagia, gastro-oesophageal reflux. Instrumental diagnostics:
Chest X-ray
-
Radioscopy of the chest
-
Rx gastro-duodenal transit
-
Thoracic-abdominal Tc
-
Bronchoscopy
-
Spirometry
-
Arterial haemogasanalysis
HERNIA IATAL
Herniation of a viscera (commonly part of the stomach) into the thoracic cavity, through the
oesophageal hiatus, in two ways. Acquired, spontaneous.
● Slipping hernia (sliding, type 1, 95%): the gastro-oesophageal junction slips up. It is a very
frequent condition, favoured by age and increased abdominal P (obesity, exercise, pregnancy,
coughing). Present in 50% of the population with GERD, 70% of the population >60-70 years old.
The oesophagogastric junction and the cardia translocate rostrally due to laxity of the oesophageal
brake membrane and widening of the mm duct of the hiatus (due to increased abdominal P).
Mucosal folds are identified above the diaphragmatic narrowing.
● Rolling hernia or para-oesophageal hernia: involves viscera other than the cardia such as gastric
fundus (generally to the left of the GE junction due to liver encumbrance to the right), with GE
junction retention in situ (type 2) or not (type 3), or colon (type 4, mixed or complex hernia,
+milza, duodenum). In contrast to those caused by slipping, the herniary sac formed by the
parietal diaphragmatic peritoneum will be present. Since this portion is attached to the mediastinal
parietal pleura, the peritoneum should not be dissected (risk of pneumothorax).
● Brachiesophagus: congenital anomaly with short oesophagus.
Clinical manifestations
● Sliding gives rise to gastro-intestinal symptoms, including gastro-oesophageal reflux syndrome.
● Para-oesophageal hernia leads to the consequences of the occupation of the mediastinal space. In
addition, in the distressed gastric mucosa a haematous gland is created, which can give chronic
anaemia (especially in the elderly, due to poor regeneration). In the simple case they are due to
transit obstruction and bleeding. Usually, associated with slippage, are the symptoms of gastrooesophageal reflux.
o Dysphagia (43%): the overturning of the stomach blocks the bolus at the oesophago-gastric
junction.
o Retrosternal heartburn (50 per cent): this is the reflux burn, present for the gliding
component.
o Chest pain (37%) due to stomach distension in the mediastinum (apnoea and
chest pain should alarm of imminent death ??).
o Blood in the faeces and anaemia (34%), due to strangulation and haemorrhage in the
herniated mucosa, but not melena. Hyperchromic macrocytic anaemia or hypochromic
microcytic anaemia.
o Regurgitation (31%)
o Abdominal bloating (31%), due to accumulation of gas in the stomach (transit is obstructed).
o Abdominal pain (27%), due to traction on the peritoneum.
o Cough (23%), due to mediastinal occupation (stimulates bronchi) or regurgitation (pharynx).
o Post-prandial feeling of fullness.
Ingestion of food can trigger or aggravate the discomfort, which can be relieved by sometimes difficult
belching due to the compression exerted by the herniated stomach on the distal oesophagus. Most
patients adapt to this situation by feeding themselves liquid or semi-solid foods. However, paraoesophageal hernia must be kept under control because of the risk of complications.
Para-oesophageal hiatal hernias most often evolve into mixed hernias because the stomach moves,
dragging the oesophago-gastric junction as well, and sliding symptoms (GERD) also appear. With
time, the anchoring systems loosen and the stomach tends to move almost completely into the thorax,
ultimately dragging the duodenum as well. On Rx, the stomach in the thorax will appear, very
evident. The typically elderly patient develops dyspnoea, anaemia and gastro-oesophageal reflux.
Barring acute complications, such as strangulation/strangulation of the viscera, even a hernia of this
magnitude is a condition compatible with life. The slow development of the volvulus allows the
stomach to adapt and makes necrotic phenomena rare. Ulcers up to perforation are also rare, but
possible. Haematemesis and melena (60%) are possible.
N.B. Normally, surgeries are not performed on patients beyond the sixth to seventh decade of life
because of adaptation phenomena (tissues wear out?).
● In mixed hernia, one has both. In addition, anaemia can be worsened by the use of antacid drugs
that, by increasing the gastric pH, hinder iron absorption.
Complications of para-oesophageal hernia (surgery required)
Gastric volvulus is a frequent complication: the fundus of the stomach rises and the entire stomach
turns over on its longitudinal axis. It also results in distortion of the ligamentous apparatus of the
gastric fundus, which can also pull the spleen towards the hiatus. Gastric volvulus pain is referred to
the precordium and mimics cardiac ischaemia.
Endoscopic signs of hiatal hernia are:
● Distance between lower dental arch and reduced cardias: normally 40-43 cm; it varies greatly
from person to person, and is not always related to height. However, it has its value if it is 36-37
cm.
● Distance between the Z line and the increased cardias: the Z line normally lies at or no more
than 2-3 cm above the level of the cardias; it is of value if it exceeds 6-7 cm.
● Stomach upsurge: once you enter the stomach, you can see the gastric folds rise up (sign of hiatal
hernia); it can be evoked by asking the patient to pontare.
● "Cardial 'scampanatura', which can be seen by inverting the tip of the instrument and from the
size of which one can tell if a hiatal hernia is present.
● Common cavity' image: visualisation of the oesophageal lumen in continuity with the gastric
lumen by pointing the endoscope upwards.
X-ray with baryta meal Slipping hernia
Two narrowings (double ring) are evident:
● superiorly, the superior oesophageal sphincter;
● inferiorly, the portion of the stomach constricted in the oesophageal hiatus.
The double narrowing is also evident on manometry (examination that measures the luminal pressure
in the oesophagus by inserting a catheter through the nose), which will show an inversion at the supraoesophageal cardia (?).
In paraesophageal hernia, the X-ray with baryta meal shows the convergence of the gastric folds.
Chest X-ray
Usually a hiatal hernia (from sliding and rolling) is also evident on a normal X-ray, where part of the
stomach is seen in the chest (gastric bubble, hydroaerial level?).
Treatment is surgical
● Total fundoplicatio according to Nissen (-Rossetti): it is proposed to create around the portion
of
●
●
●
●
●
●
abdominal oesophagus, mobilised around its entire circumference, a wrap with the gastric fundus.
The suture must be anchored to the anterior oesophageal wall and, at the highest part, to the
anterior margin of the diaphragmatic hiatus (to avoid transient slippage of the new valve
mechanism). The gastric fundus, the distension of which causes the transient relaxations, is
removed and used to create a sleeve around the distal 4 cm of the oesophagus, increasing the
opposition pressure. The operation is only performed on subjects with severe disease and sphincter
hypotonia: increasing the pressure on a still tonic LES (e.g. 40 mmHg) results in dysphagia.
o Complications: stenosing plastic - plastic breakdown - gastric fundus slippage with iatrogenic
hiatal hernia.
180° posterior fundoplication according to Toupet: the valve is fixed posteriorly to the pillars of
the diaphragm and laterally on the left and right margins of the oesophagus; it reduces the
postoperative dysphagia characteristic of Nissen's operation.
180° anterior fundoplication or Dor's surgery.
Posterior 270° fundoplication: the valve is fixed posteriorly to the pillars of the diaphragm;
laterally, the abutment between the oesophagus and the valve is made in two overlapping planes.
Belsey Mark IV surgery ''anatomical'' repair of the EI by the left thoracic route: no in use.
Allison's surgery ''anatomical'' repair of hiatal hernia via the thoracic route.
Stretching gastroplasty according to Collis: by abdominal route with mechanical suture.
Tubularisation of the stomach.
LAPAROCELE
A pathological condition characterised by the escape of a viscera through a muscular-aponeurotic
breach of the abdominal wall at a previous surgical incision (usually laparotomies and longitudinal
surgical wounds).
Primary laparocele has a variable incidence depending on the site, while that secondary to laparoplasty
has a higher incidence.
Risk factors:
1) General conditions:
- Obesity (fat infiltrates the muscle-fascial plane; promotes infections; increases abdominal P
due to mass effect; reduces respiratory compliance)
- Nutritional disorders (hyponutrition correlates with reduced muscle tone)
- Advanced age
- Dysmetabolic diseases (CRI, diabetes)
- Chronic respiratory failure (COPD patients)
- Neoplasms
- CNS diseases
- Liver cirrhosis
2) Local conditions:
- Post-operative course with vomiting, bladder globe, abdominal meteorism, prolonged
paralytic ileus (conditions that increase abdominal P)
- Incision site and type of incision (especially median region and vertical incisions)
- Wound infections (involvement of the muscle-fascial layer)
3) Factors related to surgical technique:
- Local traumatisms
- Section of motor nerve structures (with muscle paralysis)
- Technical Errors
- Presence of enterostomies (peristomal laparocele) They are classified according
to:
1) Location:
- Mid-abdominal
- Lateral abdominal
- Supra-umbilical
- Sub-umbilical
- Lumbar
- Perineal
2) Size:
- Small (< 5 cm)
- Medium (5-10 cm)
- Large (>10 cm)
- Parietal disaster
3) Reductibility:
- Reducible (spontaneously or by manual manoeuvre)
- Containable (once reduced it stays in place)
- Not containable
The characteristics of laparocele are:
- Volume of hernia often conspicuous
- Skin envelopes often thin and transparent
- Frequent viscero-saccular adhesions (irreducible hernia, risk of strangulation)
- More or less wide herniary door Clinic:
1) Breathing difficulties of varying degrees (especially in large laparoceles): in the inspiratory
phase, the lowering due to contraction of the diaphragmatic muscle is normally balanced by the
abdominal P caused by the abdominal wall counterpressure (which is insufficient in
laparoceles)
2) Abdominal volet: after surgical correction of large laparoceles, the repositioning of bowel
masses in an abdomen no longer accustomed to containing them leads to a sudden increase in
pressure values; this results in a stable rise of the diaphragm, which creates the conditions for a
serious dynamic imbalance in respiration.
Complications:
-
-
Chronic respiratory insufficiency: due to altered respiratory dynamics: pre- and postoperative spirometry is required. The surgical correction of a voluminous laparocele, and
especially of parietal disasters, can be complicated by acute respiratory insufficiency, due
to altered respiratory dynamics (stable rise of the diaphragm no longer used to counteract a
high abdominal P)
Venous insufficiency
-
Tendency to distension of the hollow viscera (especially the colon) and altered peristalsis
Tendency to hypotrophy of abdominal muscles
The preparation of the patient involves:
- Weight loss
- Metabolic readjustment (control of hyperglycaemia, dyslipidaemia)
- Study of respiratory function
- Respiratory physiotherapy
- Intestinal preparation
Surgical treatment: involves isolation of the hernia sac with reduction of the contents and repair of the
abdominal wall defect by placing one or more prostheses. The prosthesis may be:
-
Soprafascial
Retromuscular preperitoneal (polypropylene)
Intraperitoneal
PATHOLOGY PERITONEAL
PERITONITE
It is a pathological condition characterised by an inflammatory process affecting the peritoneal
membrane. Usually, it is caused by the spillage of organic fluids into the abdominal cavity and the
subsequent microbial proliferation (in fact, it is unlikely and only in the initial stages that the
inflammation is not related to microbial proliferation: we speak in this case of aseptic or chemical
peritonitis).
The peritoneum is a serous membrane consisting of two sheets: parietal and visceral, which line the
abdominal cavity and most of the viscera present there. The two leaflets delimit a virtual cavity that is
called the peritoneal cavity; the latter is closed in men, while in women it communicates with the
outside through the tubal orifices.
The parietal peritoneum has somatic sensitivity (with epicritic pain, and contracture of the overlying
muscle area). The visceral peritoneum has neurovegetative sensitivity (with ill-defined pain).
The peritoneum has several capabilities:
- Secreting: under physiological conditions, the serosa produces a modest amount of serous
fluid;
- By reabsorption: with an important role played by the blood and lymphatic microcirculation
(the peritoneal and sub-mesothelial lymphatic networks are joined to the pleural subpleural and
sub-mesothelial networks: pleura-peritoneum connection. Due to the suction phenomenon
exerted by the negative pressure of the pleural cavity on the positive pressure of the abdominal
cavity, infections of the peritoneal cavity tend to spread upwards to the pleural cavity and not
vice versa.
- Reactive: any inflammatory stimulus causes hyperemia with marked exudative phenomena.
- Plastic and reparative
- Fibrinolytic capacity: production and release of t-PA and consequent fibrinolytic activity. But,
under the action of ischaemia, infection, trauma (especially if abdominal), the peritoneum
reduces its fibrinolytic activity, which leads to the formation of adhesions.
Peritonitis is among the causes of non-traumatic acute abdomen, along with:
- Intestinal infarction
- Intestinal obstruction
- Digestive haemorrhages
-
Emobilia
Portal hypertension
Severe mechanical cholestasis
Caustic injuries
Regardless of the underlying cause (infectious, chemical, traumatic), inflammation of the peritoneum
results in:
- Defensive contracture of the abdominal muscles above
- Bowel paresis (paralytic ileus, due to inhibition of the related smooth muscle)
Peritonitis is classified according to:
1) Evolution:
- Acute
. primitive
.secondary
.diffused
.circumscribed
- Cronica
. non-specific
.specific: e.g. TB. This is referred to as tuberculous or chronic granulomatous peritonitis of
tuberculous origin. It is uncommon today, especially in industrialised countries. It is found
more in third world countries. We see, for example, several cases in immigrants, who are
immunocompromised, malnourished, living in poor hygienic conditions. Chronic
granulomatous microgranules are often found, especially in women at the adnexal level.
2) Extension:
- Localised or localised
- Diffuse or generalised
3) Aetiopathogenesis:
- Primitive
- Secondary (most frequent)
4) Nature :
a) Chemical peritonitis: can be caused by:
- Bile (coleperitoneum)
- Gastroenteric juice
- Pancreatic juice
- Urine (uroperitoneum)
- Mucus
- Blood (haemoperitoneum)
- Faeces (stercoraceous peritonitis): as in sigma perforations, in cases of acute diverticulitis
b) Septic peritonitis:
- Primitive (rare)
- Secondary a:
. focus of infection of an abdominal viscera (by contiguity)
. perforation of a viscera with bacterial content
.intestinal infarction
.outbreak of extra-intestinal infection
Primary peritonitis: this is an inflammation that is usually due to a bacterial invasion that cannot be
attributed to an infectious focus starting in an abdominal organ, nor to contamination from outside
from a penetrating wound (e.g. infectious metastases, during general infections). It is important to
remember that in the case of a patient with a penetrating wound, one must not specimen it at all, as
there is a risk of perforating the peritoneum and causing peritonitis. A CT scan is used.
Secondary peritonitis: the inflammation is due to a bacterial invasion or chemical insult of the
peritoneum due to:
1) Propagation from an abdominal inflammatory focus:
-
Acute appendicitis
Diverticulitis
Liver abscess
Acute salpingitis
Acute cholecystitis: gallbladder stones can lead to inflammation of the walls of the gallbladder
itself, thus giving rise to cholecystitis.
2) Non-traumatic perforation of a hollow viscera: inflammation of one of these organs can lead to
non-traumatic perforation and promote peritonitis:
- Ileal perforation
-
Perforated peptic ulcer
Perforation of colic neoplasm
Perforated diverticulitis
Perforation appendicitis/cholecystitis gangrenosum
3)
-
Ischaemia with gangrenous evolution of a hollow viscera:
Intestinal infarction
Herniary choking
Intestinal invagination: a colonoscopic method, which relies on air insufflation, can unclog
these invagination sites.
- Volvulus: it usually occurs in subjects who have a dolichocolon, i.e. a particularly long and
tortuous colon. It is the twisting of the viscera on its own axis and if the vascular pedicle is
involved, it is called strangulation, resulting in ischaemia. In the first instance, endoscopic
derotation is attempted, and if this is unsuccessful, one goes to the operating theatre.
These last 3 clinical manifestations are part of the mechanical type of intestinal obstruction, in which
we have compression of the vascular pedicle.
4)
-
Post-traumatic peritonitis :
Visceral contusion
Intestinal necrosis due to injury of the months
Burst injury of hollow viscera
Visceral injuries from penetrating wounds
-
Perforation of hollow viscera by foreign bodies
Traumatic haemoperitoneum: e.g. in a patient who has suffered a stabbing, which has
affected the liver and the full-thickness diaphragm, connecting the thoracic cavity with the
abdominal cavity.
5) Post-operative peritonitis:
Every time a patient is re-operated, whether short or long after the first operation, a picture of
adherence syndrome is expected. One approach that is recommended is the laparoscopic approach,
which is less invasive, especially in those patients who have already undergone a laparotomy
(which can lead to post-operative peritonitis). Ex:
- Anastomotic dehiscence
- Post-operative pancreatitis
- Intra-operative bacterial contamination
- Ischaemia of hollow viscera after vessel ligation
-
-
-
Pathophysiology
There will be an inflammatory process, with exudate:
Serous
Serum-fibrinous
Hemorrhagic
Purulent
It starts with a circumscribed inflammation of the peritoneum, which leads to:
Severe hydro-electrolyte loss in the intestinal extracellular lumen
Hyperemia and peritoneal vascular congestion
Seizure of liquids in the 'third space
- Reduced cardiac output and increased vascular resistance And then systemic repercussions, with
hypovolaemia and cold shock.
Or, inflammation confined to the peritoneum can lead to:
Peritoneal uptake of exotoxins, endotoxins, and bacteria
Activation of mediators of inflammation and complement
- Increased cardiac output and reduced vascular resistance And then systemic repercussions, with
sepsis and heat shock.
Diffuse acute peritonitis is almost always due to polymicrobial infection, and to define the severity of
the clinical picture, the type of micro-organism and the infecting microbial load must be defined.
-
Germs can reach the peritoneum:
From the outside: e.g. penetrating wound
From the abdominal viscera: by diffusion or perforation of viscera (most common)
By blood: infectious mestatases during generalised infections
Lymphatic route: from the pleural cavity to the peritoneum or from the retroperitoneum to the
peritoneum.
Diagnosis
The diagnostic procedure involves:
1) Anamnesis: the patient reports a painful symptomatology and an attempt is made to define the
characteristics of the pain:
- Localisation: when assessing a pain that is not diffuse but localised, the patient must be treated
by the surgeon, because if on the one hand we have the large omentum that tamponades and
stems the extravasation, since it is a process with septic evolution, we still have saccate
peritonitis, which has the possibility of abscess evolution, which can lead to septic shock, when
the infection becomes diffused from localised. The surgeon, by means of various non-invasive
methods, will have to modulate the drainage of the abscess: "undercover" with guided ETG-TC
aspirations; or in cases where the peritonitis tends to be diffuse, a laparoscopic or open surgical
procedure is performed.
- Mode of onset
- Duration
- Intensity
- Irradiation
- Assessing accompanying, systemic signs and symptoms
The purpose in assessing the characteristics of the pain is to be able to formulate a diagnostic
hypothesis on the pathology that caused the peritonitis. It is inadvisable to undertake pain-relieving
treatment, as this masks the symptoms and may lead to underestimation of the clinical picture, which
could progress to septic shock.
The patient presents with:
- Suffering face and appearance
- Pale complexion
- Hollow cheeks and eyes (Hippocratic facies)
- Tachycardic, tachypnoid, sweating, visible dehydration of skin and mucous membranes
- Disorientation and agitation
- Fever (a T < 36°C is an ominous prognostic sign)
- Nausea and vomiting (reflex)
- Closure of alvo to faeces and gas (in the case of paralytic ileus)
Then in the case of septic or hypovolemic shock we will see the presence of pale skin with bluish
mottling, a sign of hypoperfusion.
2) To the EO:
a) Inspection: the patient is often in forced decubitus, immobile, with hypomobility to breath
acts, as the normal respiratory act is interrupted or altered by the pain itself
b) Palpation: there is a defensive reaction (e.g. in the case of appendicitis, the doctor presses
his hand into the right iliac fossa and the response is a defensive reaction of the abdomen),
which consists of:
- Defensive muscular contracture of the rectus abdominis and broad abdominis muscles, at first
circumscribed, then diffuse and intense (plank abdomen, ligneous)
- Skin hyperesthesia: already on superficial palpation, there will be pain and a defensive reaction
of contracture
-
Frequent positive Blumberg's sign: i.e. rebound pain, in which we compress the abdomen of
the pc and it allows itself to be compressed but when we then release it, the pc experiences a
very strong pain.
c) Percussion:
Reduction or loss of the area of hepatic obtuseness, in forms with perforation, and tendency of the area
to gather upwards (radiological counterpart is the subdiaphragmatic air crescent), with tympanism.
d) Auscultation:
Presence/absence of borborigrams which are noises made by intestinal peristalsis. In the case of
paralytic ileus, there is auscultatory silence, known as 'sepulchral silence'.
e) Edar:
It does not usually cause pain. In the case of peritonitis, the pressure exerted on the Douglas' cavity in
women or in the recto-vesical cavity in men, where the exudate, the effusion, collects, causes a
tremendous vivid pain ('Douglas' cry').
Evaluate the presence of faeces in the rectal ampulla, for possible alterations in alvo (although the
presence of faeces does not mean alvo pervio, because the faeces may go back to before).
Ask if the alvo is pervious to faeces or gas.
Therefore, the clinic with a history and a thorough physical examination becomes essential.
3)
-
Laboratory tests are then requested:
Anaemia
Neutrophilic leukocytosis
Increased cytolysis indices (transaminases, LDH, CK-MB, creatine kinase)
Alterations in renal function
Alteration of the acid-base and hydro-electrolyte balance (pH, electrolytes, etc.)
4) Again, instrumental examinations (those most strictly necessary for the patient):
- Direct X-ray of the abdomen
- ETG abdomen
- CT abdomen with or without mdc (outperforming previous methods)
Abdominal ultrasound may be more decisive in parenchymatous organs and should be reserved for
young subjects and pregnant women. The difference between Rx or CT and ETG is that the former
involves the administration of radiation that is harmful (not without neoplastic complications) to the
patient, whereas ETG emits ultrasound that appears to be harmless to the human body.
Therapy
1) Medical:
- Antibiotic therapy (beware of antibiotic resistance)
- Correction of hydro-electrolyte alterations (sodium, potassium, chlorine values)
- Shock therapy
- Placement of the naso-gastric tube (SNG) In the peritonitic patient, the triad is placed:
a) Nose-gastric probe: serves to detach a section of intestine whose function is impaired, and
where there may be stagnation. In the case of haemorrhage, it makes it possible to monitor and
understand whether haemorrhage is present and what type of haemorrhage it is. For example,
in the case of peritonitis, depending on the content that this tube drains, whether it is faecaloid
or gastroenteric/biliary, one understands the peritonitis problem).
b) Bladder catheter: renal function can be monitored not only through creatinine and azotemia,
blood pressure, but also through diuresis, and thus urine volume.
c) Peripheral venous catheter: two are often placed, in two different locations, to allow the
withdrawal and administration of: antibiotics, hydration, nutritional therapy, anticoagulant
drugs and others.
2) Surgical
- Treatment of the pathology responsible for the peritonitis picture:
removal of infectious focus: suturing of visceral perforation; resection of perforated viscera;
external drainage of perforated viscera; external drainage of peritonitic focus;
- Thorough peritoneal toilet with washing and drainage.
After the bowel that caused peritonitis is removed, everything is washed with warm saline, dried, and
drained.
PERIVISCERITI
These are fibrous-adhesive (or productive sclero-lipomatous) peritonitis surrounding one or more
segments of the digestive tract and take the form of a membrane or bridle.
They can be:
- Congenital
- Secondary (in most cases): due to inflammatory processes of the underlying viscera or surgery.
Aetiopathogenesis:
1) Inflammatory (from inflammation):
- Acute: appendicitis, cholecystitis, salpingitis, etc.)
- Chronic: perigastritis or periduodenitis from peptic ulcer; perisigmoiditis from diverticulitis,
etc.).
2) Traumatic: accidental or surgical;
3) From ionising radiation (e.g. used for oncological purposes).
The most frequent locations of periviscences are:
- Duodenal bulb
- Blind
- Last ileal loop
- Attachments (in women)
- Great omentum, often involved
Clinically, the symptomatology is site-specific, often leading to intestinal occlusion, from adherence
syndrome.
Diagnosis:
- Anamnesis
- EO
- Radiographic examinations: ultrasound and Tc abdomen
- Exploratory laparotomy/laparoscopy
A particular form of chronic peritonitis is encapsulating fibroblastic or 'obstructive sclerosing'. It is
characterised by a whitish membrane enveloping the intestine, usually the small intestine being the one
most affected, which is encapsulated, as if in a shell, by a connective tissue membrane.
The aetiopathogenesis is not fully known and is probably due to postphlogistic, traumatic or infectious
causes.
The clinic is that of circumscribed peritonitis:
- Abdominal colic (from difficult transit)
- Dyspepsia
- Sub-occlusive phenomena Diagnosis is enabled by:
- EO: palpable abdominal mass often present
- Rx abdomen
- CT (gold standard)
SUB- PHRENIC ABSCESS
ACUTE CIRCUMSCRIBED PERITONITIS
There is an inflammatory process (serous, serofibrinous or purulent) that by spontaneous evolution or
because it is blocked by surrounding viscera and organs, is localised in a limited location. Of all of
them, the best known is diaphragmatic peritonitis
Diaphragmatic peritonitis and subphrenic abscess
The abscess forms between the diaphragm (top) and the transverse mesocolon and transverse colon (
bottom).
The aetiological agent in most cases is E. coli. In most cases it occurs as a post-operative consequence
of operations on the biliary tract, duodenum or stomach or as a complication of peritonitis.
Among the most common causes:
- Gastro-duodenal lesions: peptic ulcers and neoplasms
- Appendicitis (especially acute retrocecal appendicitis)
- Hepatobiliary lesions: acute cholecystitis; liver abscesses, suppurative liver cysts.
Pathogenetic mechanisms:
- Direct infection from contiguous organs (>60%)
- Propagation through the lymphatic route
- Metastatisation through the bloodstream
Clinic
1) General symptomatology:
- Abrupt onset: septic-type fever, chest pain, dyspnoea, hiccups; although it often has an
aggravating and subtle onset
- In advanced stages: septic patients (pallor, asthenia, severe organic wasting, small and frequent
pulse, marked neutrophilic leucocytosis)
2) Local symptomatology:
- Punctal pain at the base of the hemithorax
- Irradiation to the neck (if the abscess is under the diaphragmatic dome)
- Dyspnoea (almost always), with costal breathing (the diaphragm is immobilised as an antalgic
defence)
- Hiccups (from irritation of the phrenic and vagus nerves)
It can evolve into:
- Septic shock (progressively)
- Abscess rupture in free peritoneal cavity
- Fistulisation in a hollow viscera
- Pleural empyema, as an evolution of an already complication, namely: basal pleuritis.
EO
-
-
Inspection: motionless chest base
Palpation:
.point of greatest pain at the site where the collection tends to superficialise
.liver sometimes protruding from the costal arch (in the case of abundant collections)
Percussion:
. non-gaseous collections simulate pleurisy (basal obtuseness)
.gaseous collections simulate a basal pnx
Instrumental diagnosis
-
Radiological examination
ETG upper abdomen
TC
Eco- or Tc-guided exploratory puncture
Treatment includes surgical drainage or by means of percutaneous catheters placed under endoscopic
or CT guidance. Treatment of the primary site of infection is also essential.
DYSPHAGIA
Dysphagia is classified into:
● Oropharyngeal (cervical, high) or oesophageal (retro sternal, low);
● Organic or functional, depending on the cause, is added later to the definition. Organic means
that there is an organic process, morphological alteration that results in alteration of function, a
tumour at oesophageal level is an organic dysphagia. Or there is nothing organic but there is a
motor dysfunction e.g. of the lower sphincter that does not release, achalasia is e.g. functional
dysphagia;
● Partial or total, depending on liquid solids or gases we can have partial dysphagia if i t i s
only for solids, if it is only for liquids or total if it is for both solids and liquids.
● Continuous/increasing or intermittent. Continuous is always, it does not change in intensity.
Ingravescent occurs first for solids then also for liquids, it is then aggravated and is typical of
neoplastic stenosis. Often in functional diseases dysphagia is intermittent, sometimes there is
other times there is not.
● Painful (odinophagia), typical of acute tonsillitis, sore throat.
● Paradoxical. It was dysphagia occurring first for liquids then for solids; e.g. achalasia.
Aetiology of oropharyngeal dysphagia
-
CNS: Parkinson's, multiple sclerosis, ALS, tumours;
SNPs: poliomyelitis, peripheral neuropathies, myasthenia gravis;
Muscular: muscular dystrophy, primitive myositis, SLE;
Local lesions: inflammatory (pharyngitis, abscesses), tumours, extrinsic compressions, oropharyngeal surgical resections;
Motor disorders of the upper oesophageal sphincter: hypertonic UES (globe, spasm), hypotonic
UES (oesophago-pharyngeal regurgitation), cricopharyngeal achalasia, premature UES closure
(Zenker's diverticulum).
EXOFAGO
ACALASIA
It is a primitive dyskinesia of the oesophagus, a deficit of oesophageal motility, with reduced or
uncoordinated peristalsis and failure of sphincter release (post-deglutition). It is generally
idiopathic. 25- 60 years. Electively affects the smooth mm.
Aetiological hypotheses
● Loss of ganglionic neurons of the Auerbach myenteric plexus (both excitatory and inhibitory)
due to immunophlogosis (autoimmunity, HSV1 etc. - often auto-Ab+) - impairment of the
motor nucleus of the vagus
● Deficiency of myorelaxant mediators (e.g. NO, VIP, CCK).
● Infectious cause: Chagas disease: a rare form of infectious Brazilian achalasia, from
Trypanosoma Cruzi (a protozoan with tropism for the SNE, which destroys the Auerbach and
Meissner plexuses).
In the absence of the LES release reflex and efficient peristalsis, ingested material accumulates in the
oesophageal body until it reaches a pressure sufficient to force its opening. Over time, the
accumulation causes the wall to wear away and the oesophagus to dilate. In addition to dilatation, its
lengthening is also determined: ''S'' (sigmoid) or ''L'' (sock-like) oesophagus.
Degrees of expansion
●
1 (<4 cm)
●
2 (4-6 cm)
●
3 (>6 cm, even 10-12 cm).
Symptoms
Symptomatology in 3 stages according to Plummer: 1) simple dysphagia; 2) moderate stagnation; 3)
conspicuous stagnation.
● Paradoxical oesophageal dysphagia and regurgitation: the subject experiences a retrosternal
blockage which, once sufficient pressure is reached, disappears due to the opening of the LES.
Solids, which are heavier, can more easily force the LES open. Liquids, on the contrary, give
regurgitation more easily.
● Retrosternal constrictive pain: this is due to oesophageal spasms from uncoordinated and
inefficient peristalsis attempting to force progression through the LES. The pain is more intense in
the early stages of the disease, and decreases as the oesophagus becomes thinner and dilated.
● Pirosi
● Weight loss: the subject with painful dysphagia tends towards hypoalnutrition. These are thin
people who lose weight and are subjected to psychiatric treatment, antidepressants, because the
condition is so rare and is diagnosed late.
● Respiratory infections: chronic infected regurgitation can give bronchitis or pneumonia ab
ingestis or
lung abscesses.
Diagnosis
● (EGDS) Gastroscopy: used to exclude obstructive organic causes, e.g. oesophageal cancer.
It is observed:
- 'snap passage': in endoscopy, there will be a snap in the passage from the oesophagus to the
LES
- Oesophageal dilatation
- Retained food and/or candidiasis
● Videofluorography: in early stages shows segmental and uncoordinated peristalsis. In the late
stages the mdc (barium) accumulates in the distal (very dilated) oesophagus until the pressure
opens the sphincter, then it pours into the stomach. In SLE, the barium transits in a rat-tailed
(cigar-stitched, pig-tailed) fashion. It does not show peristalsis.
● Oesophageal manometry: demonstrates irregular peristalsis and sphincter hypertone.
o Conventional: measures endoluminal P changes within the hollow viscera, induced by wall
contraction and not directly the contractile activity of the walls themselves, using a perfusion
system and specific probes connected to external transducers and introduced nasally. This is no
longer done today;
o High-resolution system: seamless topographic representation of intra-oesophageal pressures,
obtained through the use of probes with multiple built-in transducers.
Usually manometry is done before, during and after surgery, to compare and demonstrate where
we start from and where we end up as a result.
It classifies three types of achalasia, based on the presence of peristalsis (P/p), sphincter release
(R/r) and wave amplitude greater than 50 mmHg (V/v).
o Classical achalasia (p-r-v): the oesophagus does not move, the tube registers little or no
activity, and everything goes down by gravity. There is also mega-oesophagus due to absence
of tone.
o Achalasia with release (p-R-v): sphincter release is usually shorter than normal, but still
sufficient to allow material to pass through.
o Achalasia with peristalsis (P-r-v): disordered, non-functional, often painful contractions that
do not spread caudally. Produces Rx image with pearl necklace oesophagus.
Treatment (+side 99-107)
● Myorelaxant drugs: e.g. calcium channel blockers and nitro-derivatives.
● Botulinum toxin in situ. Usually in elderly and defecated patients for whom neither endoscopic
nor surgical therapy can be guaranteed. The toxin is injected at the LES with a needle. Limited
effectiveness.
● Pneumatic endoscopic dilatation of the SLE: this is done in several sessions and often gives
recurrences. It promotes the stretching of the smooth muscle of the LES. Pcs must be dilated
periodically, but the more they are dilated, the more scarring can occur, giving stiffening and
fibrosis.
● Surgical sphincterotomy: last resort for patients resistant to other therapies, gives chronic reflux.
● Laparoscopic extramucosal (video)myotomy. Before surgery, it is important that the presence of
oesophageal candidiasis be excluded and therefore in the pre-operative, antibiotic therapy is
suggested; in fact, if the patient is operated on with candidiasis in place, the risk of perforation is
greatly increased. The extramucosal cardiomyotomy according to Heller consists of a
longitudinal resection of the oesophagus tonaca mm up to the mucosal tonaca, with extension of
the incision downwards for 2-3 cm, up to the small gastric curvature. This allows for the loss of
oesophageal pressure. The operation is completed by an anti-reflux plastic, by passing the stomach
fundus, freed from the short gastric vessels, posteriorly to the oesophagus (posterior plastic or
second Toupet, suturing the stomach fundus on the right margin of the myotomy) or anteriorly (
anterior plastic or second Dor, covering the oesophageal mucosa with the gastric fundus, which is
sutured on both sides of the myotomy). The latter is the preferred one, and is performed
laparoscopically, with full 3D technology, providing a three-dimensional view, such that the
operation becomes much more efficient and precise. Anterior plastic surgery according to Dor
involves opening the pars flaccida, and preserving the pars densa (the pars flaccida and densa of
the small omentum represent a point of recognition of the nerves of Latarjet: nerves that branch off
from the anterior and posterior vagus nerve, to the oesophagus, where it gives rise to the Latarjet
nerves, which are responsible for the motor activity of the biliary and gastric system), one does not
open the retro-oesophageal space posteriorly, but only retains the anterior face of the oesophagus.
One therefore opens this
lax tissue (pars flaccida) and we reach Bertelli's membrane (which separates the abdominal cavity
from the mediastinal cavity) and open its anterior portion and thus give us the possibility to enter
the thorax. We begin the myotomy, that is, an opening of the muscles between the thoracic and
abdominal tracts, which have a longitudinal orientation more superficially and a circular
orientation more deeply, and immediately below there is the oesophageal mucosa. Then
videofluorography confirms the success of the operation. Be careful not to cause iatrogenic lesions
in the mediastinum.
● Pre-Oral Endoscopic Myotomy (POEM During POEM the space of the submucosa is
approached, creating a new space called the 'third space' (third space endoscopy). Through this
third space theoretically all pathologies of the mm layer of the GI tract could be treated, such as
the endoscopic removal of tumours originating from the submucosa or the mm.
Ster = submucosal tunneling
resection
endoscopic resection Set=
submucosal endoscopic tumour
OESOPHAGEAL SPASM DIFFUSE
Symptomatic diffuse oesophageal spasm is part of a spectrum of motility disorders variously
characterised by non-propulsive contractions and hyperdynamic contractions, sometimes in
association with elevated lower oesophageal sphincter pressure. The symptoms are chest pain and
sometimes dysphagia.
The diagnosis is made with the barytised meal or manometry. Treatment is difficult but includes
nitrates, calcium channel blockers, botulinum toxin injection, surgical or endoscopic myotomy and
antireflux therapy.
DIVERTICULA OESOPHAGEAL
An oesophageal diverticulum is an eversion of the mucosa through the muscular layer of the
oesophagus. There are different types of oesophageal diverticula, each with a different origin:
● Zenker's diverticulum (pharyngeal) is a false diverticulum, posterior sacciform
extroversions of mucosa and submucosa through Killian's triangle (transverse bundles of
the cricopharyngeal muscle and oblique bundles of the thyropharyngeal muscle - part of
the lower constrictor of the pharynx), probably caused by an incoordination between
pharyngeal propulsion and cricopharyngeal release.
● Mid-oesophageal (traction) diverticula are caused by traction resulting from
inflammatory lesions of the mediastinum or, secondarily, from disorders of oesophageal
motility.
● Epiphrenic diverticula are located just above the diaphragm and are usually associated
with motility disorders (e.g. achalasia, diffuse oesophageal spasm).
It may be asymptomatic or cause dysphagia and regurgitation. Diagnosis is made with the baritone
meal; surgical repair is rarely necessary.
GERD
Gastro-oesophageal reflux is the upflow of gastric contents into the oesophagus due to insufficient
anti-reflux media (e.g. LES). It is referred to as a disease when exposure of the distal oesophageal
mucosa to gastric juice causes inflammatory or metaplasic symptoms or lesions that can be detected
on gastroscopy, and extra-oesophageal manifestations. It is a chronic disease. 15% of the Western
population suffers from it, 30-40% of individuals experiencing heartburn monthly.
GERD can be considered the result of insufficient anti-reflux media:
● Allison's ligament (right diaphragmatic pillar, which wraps around the oesophagus as it passes
through the hiatus);
● angle of His (acute angle between the oesophagus and the gastric fundus, still exacerbated by the
presence of air);
● Von Gubaroff valve (mucous plica acting as a valve) - Bertelli's membrane;
● positive abdominal pressure on the subdiaphragmatic oesophageal tract, lost with hiatal
hernia;
● Automatic oesophageal peristaltic clearance triggered by any reflux.
● Lower oesophageal sphincter (F) The LES is the sphincter that separates the oesophagus from
the stomach and constitutes its last 4 cm, where the oesophageal muscle fibres (circular and
longitudinal) intersect with the semilunar fibres from the angle of His. It is constitutively
contracted and opposes the reflux of gastric juice with a pressure of 20 mmHg: in the absence of
the LES, gastric contents would be sucked into the oesophagus by the pressure gradient with the
thorax. The sphincter straddles the hiatus (supra-diaphragmatic and sub-diaphragmatic portions)
and is enveloped by the right pillar of the diaphragm (sling or Allison's lace), which is essential
to its continence. With each respiratory act, the contraction of the diaphragm causes an increase
in abdominal P and a reduction in thoracic P, which favours reflux. The opening of the sphincter is
triggered by deglutition (at 2s) and is autonomous from peristalsis: the sphincter is already open
when the peristaltic wave triggered by the same deglutition arrives, which in fact has the effect of
closing it (post-delgutory contraction). A delay of this peristaltic wave can cause reflux through
the sphincter, which is open too long. There is also a reflex mechanism of transient or
inappropriate sphincter release, independent of deglutition but triggered by distension of the
proximal stomach to vent gas contained therein (eructation is a gaseous reflux). These relaxations
are more frequent in the postprandial period (at about half an hour and for about an hour and a
half), due to the increased filling and peristaltic activity, which increase wall pressure and tension.
They can be detected with:
● pH meter (pH drops with reflux);
● pressure gauge (pressure at the LES drops from 25 mmHg without the subject having
swallowed).
The opening of the sphincter is thus coupled with the reflux of:
● CO2 and other gases, collected in the bottom of the stomach;
● acid from the acid pocket (the proximal, lower pH zone, where acid tends to collect in the postprandial phase, due to the tendency to float - measured with the pH meter).
SLE incontinence: transient refluxes are physiological, but become pathological due to increased
frequency and acidity. In the advanced stages of the disease, SLE presents strongly
hypotonic (the physiological pressure of 20 mmHg is reduced to 5-10 mmHg). The sick person differs
from the healthy one in the frequency of transient acid reflux.
Risk factors of GERD
● Increased abdominal pressure: pregnancy (but also because progesterone favours the release of
the SLE) - obesity and overweight (47% in I.) - exertion.
● Smoking - alcohol - coffee - drugs - chocolate (contains xanthines, which release SLE).
● Carbonated drinks: CO2 promotes relaxations by distending the stomach and forcing the
sphincter.
● Hiatal hernia: the sphincter is located in the thorax, not subject to diaphragmatic constriction but
to negative thoracic pressure. Inhalation increases abdominal pressure and, instead of
constricting the LES, tends to dilate it, leading to reflux. Further herniation, with the LES, of the
cardia further facilitates reflux, creating a kind of permanent gas and acid pocket.
● Reduced oesophageal clearing, usually operated by non-deglutitory peristalsis and swallowing of
saliva (cleanses the lumen and neutralises the acid with the bicarbonate it contains) e.g. xerostomia
.
● Other gastric dysfunctions: hypersecretion - delayed emptying - duodenal reflux.
● Behavioural factors: e.g. eating fast (the number of transient relaxations increases in the hour
after the meal) - large or frequent meals (the stomach distends and transient relaxations increase) eating before bedtime (clinostatism promotes reflux, and in sleep swallowing is only 7 acts/h and
salivation is poor).
● Supine or right lateral decubitus: the correct position is left lateral, or with 20 cm underneath.
Symptoms of GERD
There is no correlation between clinical and anatomo-pathological picture: many subjects with
oesophageal lesions report no symptoms, paucisymptomatic subjects may have advanced disease and
subjects with very marked symptoms may have mild disease. Two symptoms are, however, typical.
● Heartburn: retro-sternal burning, radiating to the middle part of the chest, neck or shoulders; it is
completely absent in 5% of cases. It gives rise to a suspicion of GERD if felt twice a week.
● Acid regurgitation: oral emission of indigestible material or its perception in the oropharynx as
acidic liquid or food residue (as distinct from vomiting, which is explosive and preceded by
nausea and retching). It is usually postural, caused by forward flexion of the trunk, and is the most
specific symptom.
Retrosternal heartburn and perceived regurgitation, even once a week, are symptoms of pathology:
physiological refluxes exist but are not perceived (F). Based on these symptoms, 20-25% of
Americans - 17-20% of Europeans - 5% of Asians are affected by GERD.
Inconstant symptoms
● Frequent excretion: the gas is mainly swallowed air, together with CO2 produced by the reaction
between HCL and wall bicarbonates and a proportion produced by food (e.g. bread).
● Dysphagia (low): perception of incoordination of the swallowing act, due to reflux, oesophagitis,
spasm, a tumour. Transit of food or a sensation of food stopping may be perceived.
● Odinophagia: pain on swallowing, more rare
● Oesophageal spasm pain: responsible for 50% of cardiac-like precordialgia
(retrosternal or high epigastric, constrictive, oppressive or burdensome).
● Nausea, vomiting, dyspnoea: symptoms in common with gastritis.
Extra-oesophageal symptoms
● Arrhythmias: e.g. extrasystoles, paroxysmal atrial fibrillation (FAP). Probably due to stimulation
of the gastric fundus (hiatal hernia).
● Reflux asthma, for:
o Inhalation of refluent material;
o Direct stimulation of parasympathetic fibres that innervate both the distal oesophagus and the
bronchial tree itself (?).
● Pulmonary fibrosis - Obstructive apnoea
● Halitosis - sialorrhoea (salivary hypersecretion) - acid tooth erosions - sore mouth syndrome.
● Otolaryngological manifestations of laryngo-pharyngeal reflux: pharyngeal pyrosis - excess
mucus, throat clearing - chronic cough - voice alteration due to vocal cord involvement - globe
sensation (closed throat, due to SLE hypercontraction) - otitis and sinusitis.
Progression and complications of GERD
Increased frequency of transient releases and chyme acidity can lead to:
● NERD (non-erosive reflux disease): 2/3, symptoms but no abnormalities at endoscopy, half have
normal oesophageal pH.
● Oesophageal erosion and ulceration with oesophagitis as an acute response to the acid insult, 1/3
;
● Barret's metaplasia (chronic adaptive response);
● Oesophageal adenocarcinoma.
Diagnosis
● History: retrosternal heartburn and regurgitation. Dysphagia gives rise to suspicion of stenosis
or neoplasia.
● Drug therapy: if the answer is positive, the diagnosis is probably correct. Often, however, the
patient has already started taking medication before seeking medical advice.
Endoscopy: does not highlight GERD, but complications (erosion - Barret's metaplasia adenocarcinoma). It also allows biopsy and differential diagnosis. It is indicated for:
● patients with symptoms suggestive of malignancy (e.g. dysphagia - anaemia - weight loss);
● chronic patients who are also asymptomatic (e.g. because they have been taking antirefluxants for
years).
pH-metry: electrodes inserted nasally, left 5 cm above the LES for 24 hours, record refluxes
(including physiological refluxes) and give information on oesophageal clearance, based on the
duration of the acid peak after an episode. Number of refluxes, duration and pH are compared with
reference values. It is a specific and sensitive test and distinguishes possible (drug-resistant) bile
refluxes.
Manometry: measures the endoluminal pressure of the oesophagus, related to its motor activity
(contraction and release), introducing a nasal tube into the stomach (40 cm from the incisors
?) and extracting it 1 cm at a time. Under pathological conditions the LES opposition pressure (vn 2025 mmHg) may be less than 10 mmHg or even 0. The LES is said to be incompetent when it cannot
oppose abdominal pressure, which in turn may be increased by coughing, pregnancy, obesity, exercise.
Manometry may confirm sphincter hypotonia or a peristalsis deficit.
X-ray with barium meal: highlights any underlying morphological changes e.g. hiatal hernia. Tests
for observation of barium reflux also exist, but are little used.
● Videofluorography (cine-oesophagography): recording of barium swallowing. It verifies the
transit (patency peristalsis) and possibly reflux.
● Water siphon test: the examination is performed in a refluxogenic position (e.g. in left lat.
decubitus), and shows reflux of barium into the oesophagus. It may, however, show transient
physiological releases.
Therapy
GERD drugs are responsible for 7% of NHS spending. In the USA they cost 14bn
$/year, in Italy 1 bn, worldwide 26 bn. There is an abuse of prescription and self-medication. The
behavioural interventions would greatly lower social spending (and the earnings of the f. houses).
Antacids (e.g. Malox): basic salts (aluminium, magnesium, iodine) that neutralise HCl, variously
combined and dosed. The parent is NaHCO3, the most powerful and the one that gives the best
immediate relief. The bicarbonate, however, reacts to form H2O and CO2, which distends the stomach
and in the long run increases reflux (it is no longer used).
Antirefluxants (e.g. Gaviscon): these are alginates, extracted from seaweed, which form a floating
gel on the acid chyme in the stomach. Taken after meals (at 20-30 min), they mechanically obstruct
reflux, remaining in the stomach until emptying. They only work in orthostasis. They are usually
combined with antacids, and sometimes with simethicone (which thickens gas).
H2-antagonists (e.g. ranitidine): inhibitors of the histamine H2-receptor and thus of the exposure of
proton pumps on parietal cells, generally reducing HCl production by 1/3. Other stimuli of parietal
secretion: vagal acetylcholine - gastrin (G-cells).
Proton pump inhibitors (prazols): they are absorbed by the cell, pass through it and escape into the
secretory canaliculus, inhibiting H+/K+ ATPase pumps. They are the most powerful and most widely
used drugs. In simple oesophagitis they are used in cycles (e.g. of 3 months), resolving the
inflammation and any recurrence. In the case of metaplasia, therapy is instead prolonged for life.
● The inhibition is not total, so the digestive capacity is preserved. However, the pH elevation
interferes with the absorption of iron, calcium, vit. D and other molecules.
● In addition, the appearance of intragastric cystic polyps is associated with these drugs, but these
disappear with the discontinuation of treatment.
Prokinetics (e.g. Plasil): stimulate peristalsis and accelerate gastric emptying, reducing the time for
possible reflux.
Protocols
● Pz with reflux symptoms: PPI for 2-4 weeks at standard dose (20 mg omeprazole or 40 mg
isomeoprazole). If the symptoms resolve, endoscopy is not necessary and if they reappear, the
same therapy (on-demand) will be done.
● Pz with NERD: PPI for 2-4 weeks at standard dose and if successful therapy only as needed.
● Patients with endoscopic findings of oesophagitis:
o for GERD grade A-B you can try PPIs;
o for GERD grade C-D, PPIs are given for 4-8 weeks (and then continued) and the
possibility of surgery is assessed.
Patients with protracted remission who need intake as required: 1/3 of patients. Patients with
''seasonal'' relapses who need courses of anti-secretory therapy: ½ of patients. Patients who need
continuous anti-secretory therapy: ¼ of patients. Patients who do not respond to medical therapy and
need surgery: 1/10 of patients.
GE Joint Pathology Surgical Therapy Objectives
● Creation of a valve mechanism at the lower end of the oesophagus.
● Repositioning of the last 3 cm of the distal oesophagus in the abdomen and reconstitution of the
angle of His
● Diaphragmatic hiatus repair
Belsey's requirements for an ideal anti-reflux intervention
● Eliminating symptoms and complications of reflux
● Restoring a satisfactory quality of life without the need for further therapy
● Allowing belching to relieve gastric distension
● Allow vomiting when necessary
● Ensure permanent control of the EJR documented by oesophageal pH metry.
Main indications (very limited, extreme ratio 1-10% of cases):
● Ineffectiveness of medical treatment in controlling severe symptoms,
● Severe oesophagitis,
● Serious complications (ab ingestis pneumonia, paroxysmal tachycardia).
● Hiatal hernia
● Operating does not always resolve the symptoms (60% continue taking PPIs), 85-90% are satisfied.
Preoperative evaluation: EGDS - oesophageal manometry - oesophageal pHmetry 24hoesophagogram Rx.
Choice of access route: laparatomic 'open' - thoracic 'open' - laparoscopic - thoracoscopic.
Choice of anti-reflux method Procedures
● Total fundoplicatio according to Nissen (-Rossetti): it is proposed to create a wrap around the
portion of the abdominal oesophagus, mobilised to its full circumference, with the gastric fundus.
The suture must be anchored to the anterior oesophageal wall and, at the highest part, to the
anterior margin of the diaphragmatic hiatus (to avoid transient sliding of the new valve
mechanism). The gastric fundus, the distension of which causes the transient relaxations, is
removed and used to create a sleeve around the distal 4 cm of the oesophagus, increasing the
opposition pressure. The operation is only performed on subjects with severe disease and sphincter
hypotonia: increasing the pressure on a still tonic LES (e.g. 40 mmHg) results in dysphagia.
o Complications: stenosing plastic - plastic breakdown - gastric fundus slippage with iatrogenic
hiatal hernia.
● 180° posterior fundoplication according to Toupet: the valve is fixed posteriorly to the pillars of
the diaphragm and laterally on the left and right margins of the oesophagus; it reduces the
postoperative dysphagia characteristic of Nissen's operation.
● 180° anterior fundoplication or Dor's surgery.
● Posterior 270° fundoplication: the valve is fixed posteriorly to the pillars of the diaphragm;
laterally, the abutment between the oesophagus and the valve is made in two overlapping planes.
● Belsey Mark IV surgery ''anatomical'' repair of the EI by the left thoracic route: no in use.
● Allison's surgery ''anatomical'' repair of hiatal hernia via the thoracic route.
● Stretching gastroplasty according to Collis: by abdominal route with mechanical suture.
Tubularisation of the stomach.
OESOPHAGUS OF BARRETT
Indicates an acquired condition of intestinal metaplasia of the oesophageal mucosa (S: non-gastric),
cranial to the Z-line, as a functional adaptation to the chronic acid insult of GERD. An acquired
condition in which the stratified squamous epithelium of the distal oesophagus is replaced by
metaplastic columnar epithelium with malignant potential.
Metaplasia does not alter the basic symptomatology of GERD (indeed it may reduce pain), but
represents a pre-cancerous state for evolution to adenocarcinoma (duodenal-type reflux). In contrast,
gastric-type metaplasia (gastric juice) does not correlate with carcinogenesis.
Barrett's is frequent and increasing, with the incidence rising in recent years from 0.37 to
10.5/100k/year (relative risk in male x2). The prevalence is:
● 0.9-4.5% in the general population;
● 1-2% in subjects performing oesophago-gastro-duodenoscopy for any reason (asymptomatic);
● 6-12% of patients with GERD who undergo EGDS.
Endoscopy
It is indicated in subjects with severe or long-standing disease, even if controlled, and after the age of
50. It highlights metaplasia as a deep red area (muciparous columnar epithelium) in contrast to the
oesophageal pink area (stratified squamous epithelium). It also allows biopsies to assess the degree of
dysplasia. The endoscopic report must indicate the longitudinal and circumferential extent of the
lesions.
The Prague Classification
carcinogenic:
subdivides injuries according to length, which
correlates with risk
● ultra-short Barret's oesophagus, with longitudinal extension beyond the GE junction <1 cm
● Barret's oesophagus short, with extension 1-3 cm;
● Barret's oesophagus long segment, with extension >3 cm.
Oncological risk and treatment
The risk averages 0.5%/year, depending on the extent of the lesion and the degree of dysplasia, and is
effectively reduced by treatment with PPI (continuous, not in cycles).
● Low-grade dysplasia: therapy can induce remission. A check-up is therefore performed at 6
months. If dysplasia persists, therapy is continued chronically and a follow-up with endoscopic
and histological control every year is indicated. 5% risk at 5 years.
● High-grade dysplasia: therapy is with PPI at higher doses, and check-ups every 3 months. In
specialised centres, preventive mucosectomy is also possible. 20% risk at 5 years.
● In the absence of histological signs of dysplasia, a second confirmatory check-up at 12 months is
indicated, followed by a follow-up with periodic checks every three years.
It is useful to consider the maximum circumferential extent (C) and maximum length (M) of the
lesion. No study confirms with absolute certainty that antisecretory therapy or antireflux surgery can
bring about regression of Barrett's oesophagus or prevent adenocarcinoma. Oesophagectomy, despite
its high mortality, remains the best treatment for high-grade dysplasia in otherwise healthy patients.
Endoscopic radiofrequency ablation is a viable alternative.
Many researchers have found that EB is strongly associated with the duration of GERD symptoms.
Complete elimination of symptoms in patients with EB does not guarantee normalisation of intraoesophageal acid exposure. 50-60% of patients with EB show persistently pathological intraoesophageal pH despite the disappearance of symptoms with medical therapy. The role of intraoesophageal pH control in the long-term treatment of EB is unclear.
ESGE (European Society for Gastroenterology and Endoscopy) Guidelines 2019
1. The diagnosis of EB is made if the distal oesophagus is lined with columnar epithelium for a
minimum length of 1 cm (in the form of tongues or with circular extension) with evidence on
histological examination of specialised intestinal metaplasia.
2. Varying surveillance intervals based on the length of the EB
● For patients with an irregular Z-line or columnar oesophagus < 1 cm, routine biopsies or
endoscopic surveillance are not required.
● For EB > or = 1 cm and 3 cm, surveillance should be repeated every 5 years
● For EB >/= 3 cm and < 10 cm surveillance should be repeated every 3 years
● EB with extension =/> 10 cm endoscopic surveillance at centres experienced in this respect should
be recommended (Prof disagrees)
● In patients with limited life expectancy and advanced age, endoscopic surveillance should be
discontinued.
3. The diagnosis of any grade of dysplasia (including indefinite dysplasia) in EB requires
confirmation by an anatomic pathologist experienced in GI pathology. The need for a review by a
second anatomopathologist originates from the findings of various studies that have shown that the
majority of patients with a diagnosis of low-grade dysplasia are downstaged (non-dysplastic EB)
by pathologists experienced in GI pathology.
● Patients with visible EB lesions (either typed as dysplasia or early cancer) should be referred to
centres experienced in EB: all visible abnormalities, irrespective of the degree of dysplasia should
be removed with major endoscopic resection techniques to achieve optimal histological staging
(the risks of the procedure are reduced).
All patients with EB >/= 10 cm with a confirmed diagnosis of low-grade dysplasia, high-grade
dysplasia or as early cancer, should be referred to a centre specialised in the surveillance and treatment
of EB.
ESOPHAGEAL CARCINOMA
Oesophageal tumours are predominantly malignant, with benign lesions accounting for less than 1%
of all oesophageal neoplasms (e.g. adenoma, papilloma, leiomyoma (!), lipoma, fibroma, angioma).
The once rare carcinoma is now the 8th most frequent malignant tumour and the 5th most frequent in
terms of mortality. The incidence is 2-5 cases/100k/y, with x3 risk in M and peak around 65 years of
age. 7-8% of GI tumours, 1% of all malignant tumours. 5-year survival of 10-20%.
Carcinoma occurrence rate in oesophageal precancerosis:
● Caustic stenosis (2-5%) - Plummer-Vinson syndrome (sideropenic dysphagia, 10%) - Barrett's
oesophagus (8-10%) - Oesophageal achalasia (3-8%) - Zenker's diverticulum (0.3%) - Tylosis
(90%) - Leukoplakia (75%).
Two forms can be distinguished.
● Squamous cell carcinoma: correlates with smoking and alcohol and affects the upper/middle
portion. More frequent in the East, >M. FdR: nitrosamines and derivatives, diets deficient in
certain vitamins and trace elements, very hot drinks, fungal contaminants, caustic injury,
papillomavirus.
● Adenocarcinoma: correlates with GERD and affects the lower third of the oesophagus and the
GE junction. It can be considered a chronic complication of GERD, often preceded by intestinal
metaplasia (Barret). The incidence is increasing in the West: all individuals with GERD (20% of
Europeans) should be considered at risk. Macroscopy: most frequently fungoid, polypoid or
vegetating, rarely ulcerated or infiltrating.
Oesophagus vascularisation
The main branches of the arterial vasculature are from the inferior thyroid a., the bronchial a., the
diaphragmatic a., and the left spiral a..
The venous radius is very particular in the oesophagus and gives us an idea of the possible metastases
that are created in neoplastic pathology: the lower third drains into the portal vessel system, the upper
portion drains directly into the epicardiac vessels.
Clinic
● Progressive dysphagia: related to the volume of the lesion, first for solids and then for liquids,
first episodic and then constant. It indicates an occupation of 2/3 of the dm.
● Weight loss: depends partly on the tumour and partly on the tendency to hypoalphy secondary to
dysphagia.
● Anaemia, in cases of ulceration and chronic blood oozing.
● Pneumonia ab ingestis: can occur due to a defect in swallowing at an advanced stage.
● Odinophagia, regurgitation, chest pain, haemorrhages (haematemesis and melena), aortic
fistulas, respiratory symptoms (aspiration for stenosis, oesophago-tracheal fistulas), dysphonia
(recurrent nerve invasion), Bernard-Horner syndrome.
Natural history and tumour spread
● Very long initial cancer phase, up to 20 years.
● Oesophagitis □ dysplasia □ Ca in situ □ early cancer □ advanced cancer
● 4 types of tumour spread + continuity:
1. Transversal transmural or by contiguity (lack of serosa)
2. Intramural longitudinal (through the submucosal lymphatic network - skip metastasis)
3. Lymph node (cervical, mediastinal, abdominal lymph nodes, possible Virchow's lymph node)
Cervical oesophagus drains to deep cervical lymph nodes directly or via paratracheals;
thoracic drains to upper mediastinal; abdominal to left gastric lymph nodes. NB multiple
connections.
4. Distant or haematogenic (less frequent and later, liver, lung, kidney, bone, etc.).
Instrumental diagnosis
The first examination is endoscopy:
● morphological study of the lesion (e.g. vegetative, ulcerated mass, etc.)
● the ultrasound study (echo-endoscopy) of the wall (T) and mediastinal and epigastric lymph
nodes;
● biopsy of carcinoma and lymph nodes for histological study.
CT thorax-add: second-level examination, mainly for searching for metastases (lung, liver, etc.).
Radiology with barium: may show stenosis or ulcerative changes; if negative does not exclude the
diagnosis.
Ultrasound of the neck for the study of cervical lymph nodes + PET scan
Staging and therapy
High-grade dysplasia / Carcinoma in situ: associated with nodal involvement in 3% of cases. It is
treated with mucosectomy and eventual lymph node removal.
Infiltrating but resectable carcinoma: stages I-III, with nodal micrometastases in 90% of cases. In
the past, an extremely demolitive open operation (distal oesophagectomy with gastrectomy) was
performed, with a post-operative mortality of 3-10% and a high risk of recurrence. Today, they are
performed:
● neoadjuvant radiotherapy with radio-sensitising chemotherapy, which sometimes even leads
to complete regression;
● tumour and lymph node resection usually thoracoscopic and laparoscopic.
o In the case of negative resection margins, the prognosis is excellent, and only follow-up
follows.
o If there are signs of disease on the resected patient, adjuvant chemotherapy is administered.
Unresectable disease, due to metastasis or infiltration of the full-thickness wall. The prognosis is
bleak. A stent can be placed endoscopically to reduce dysphagia, and palliative chemotherapy is
given.
Oesophageal surgery
Demolition phase: oesophagectomy - posterior mediastinectomy, lymphadenectomy.
Oncological criteria oesophagectomy:
● Resect at least 6 cm of healthy oesophagus upstream of the macroscopic margin of the lesion
● Perform posterior cell-mediastinectomy and loco-regional lymph-adenectomy (always if curative
purpose)
Access routes if the tumour is: supracarenal (1 thoracic - 2 abdominal - 3 cervical), subcarenal
(1 - 2)
Right posterolateral thoracotomy (in all cases of neoplasms of the thoracic oesophagus) allows:
● Optimal exposure of mediastinal structures
● Facilitates oesophagectomy with cellulomediastinectomy and lymphadenectomy
Reconstructive phase: oesophagoplasty, which can be performed with a jejunal tract (according to
Merendino) or a colon tract (according to Belsey).
In the case of resectable tumours (30-40%) and patients in good general condition (fit for surgery),
treatment has curative intent.
T h e therapy of choice is surgical exeresis: oesophagectomy (demolition phase) with subsequent
oesophagoplasty (reconstructive phase). It is performed for tumours of the oesophagus:
● Cervical: total oesophagectomy, total pharyngolaryngectomy with definitive tracheostomy
and reconstitution of digestive continuity with pharyngo-gastric anastomosis. In particularly
advanced cases a thyroidectomy and parathyroidectomy may be associated
● Upper thoracic: 3-stage total oesophagectomy according to Nabeya (slides 203-205)
1. Right thoracotomy (mobilisation of the oesophagus and mediastinal lymphadenectomy),
2. Laparotomy (preparation of the reconstruction organ, usually the stomach),
3. Cervicotomy (realisation of digestive anastomosis).
● Mid and lower thoracic: Lewis-Tanner procedure.
Subtotal oesophagectomy with intrathoracic anastomosis, with a first phase of abdominal stomach
preparation and a second thoracic phase of oesophagectomy, lymphadenectomy and anastomosis
packing.
Surgery can also be for palliative purposes, to reduce dysphagia. The most widely used procedure
for the treatment of dysphagia in inoperable patients is the placement of endoprostheses, under
endoscopic control and after dilatation. Other palliative treatments are: dilatations, ND- laser-YAG
laser therapy, internal shunts (bypass).
Absolute indications for oesophageal stenting (endoprosthesis)
● Neoplasms: oesophageal - oesophago-gastric junction - medistine neoplasms
● Tracheo-oesophageal or oesophago-bronchial fistula
● Benign stenosis: caustic - peptic - iatrogenic (post-actinic, post-operative, post-sclerotherapy)
Endoscopic palliative treatment: endoscopic placement of endoprostheses
● Valid alternative to laser resection (they can also be used simultaneously)
● Longer-lasting palliative effect
● Directions:
o Neoplasms more than 5 cm in diameter, stenosing and circumferential of the thoracic
oesophagus
o Presence of 'malignant' fistulas
o All conditions in which dilation is ineffective or too difficult for the patient and the doctor
● Contraindications:
o Cervical and Cricopharyngeal Tumours
o Total obstruction of the lumen preventing the passage of a guide wire
o Non-circumferential tumour proliferation preventing proper anchorage of the prosthesis
o Excessively soft or necrotic lesions
o Profusely bleeding wounds
o Nearly horizontal orientation of the lumen
o Dilatation difficulties
● Complications:
o Perforation of the oesophagus already affected by the lesion the tumour is at the oesophagogastric junction
o Necrotized neoplastic prosthesis clogging
o Dislocation of the prosthesis that can migrate into the stomach
o Tumour growth above the prosthesis
BENIGN TUMOURS OF THE OESOPHAGUS
The benign tumours originating from the muscular layer are all myomas and lipomas; from the
submucosa they are of mesenchymal origin, i.e. fibromas and myxomas, and have a predominantly
endoluminal development; while those originating from the outer layer have a predominantly
exophytic or intramural development, i.e. towards the outer wall of the viscera and the surrounding
organs.
LEIOMIOMI
The characteristics of leiomyomas are:
▪ never reach a large size;
▪ have a capsular, ovoid structure;
▪ generally multilobulated, mammellate;
▪ they have an extramucosal development (they do not invade the mucosa), but deform both the
external and internal contours of the viscera.
In most cases they are asymptomatic, until they reach a size that leads to foreign body disease,
compression of the oesophagus, with usually dysphagic symptoms for solids, this when they reach
about the size of a walnut.
The diagnosis is instrumental, they are often occasional findings: one will see an extrinsic
compression, or an alteration of the mucous membrane profile by endoscopy performed for another
reason, and continuing with more in-depth investigations such as a CT scan it turns out that there is a
lesion of the muscular structure.
VARICES OESOPHAGEAL
Understanding the pathogenesis of oesophageal varices cannot be separated from a thorough
knowledge of the anatomy of the body's venous system. Simplifying the concepts as much as possible,
let us recall how the portal vein has the task of conveying blood from the spleen, pancreas and
intestine to the liver.
When the blood circulation of the liver is compromised and blood struggles to flow in and out of it flowing into the suprahepatic veins (whose job is to return it to the heart via the inferior vena cava) the pressure within the portal vein increases. This is referred to as portal hypertension.
If the outflow of blood along a vessel is obstructed or the amount of blood circulating in it increases
excessively, there are collateral routes that can bypass the obstruction. Thus, in the presence of portal
hypertension, vein bursting is prevented by the diversion of blood into other venous branches, which
ensure its return to the heart. To fulfil this function, the collateral circles somehow try to adapt to
accommodate the increased amount of blood pervading them.
In particular, at the level of the gastro-oesophageal junction, submucosal veins swell to become true
varicose dilations: oesophageal varices. A similar situation occurs in the haemorrhoidal district, with
the formation of anorectal varices, better known as haemorrhoids.
The most common causes of oesophageal varices:
● Cirrhosis (scarring of the liver)
● Scarring or obstructive intrahepatic congenital processes
● Thrombosis (presence of clots obstructing the portal vein, splenic vein or suprahepatic veins)
● Schistosomiasis (parasitic infection typical of tropical countries)
In Italy, over 90% of portal hypertension is due to liver cirrhosis
STOMACO
ULCER PEPTIC
A peptic ulcer is defined as a disruption of the integrity of the gastric or duodenal mucosa, leading to
local circumscribed excision that exceeds the muscolaris mucosae (as opposed to erosions, which only
superficially involve the mucosa and do not tend to become chronic), caused by the action of gastric
juice. Similar lesions can occur in a gastroresected patient in the oesophagus and anastomotic loop.
Peptic ulcer is a chronic condition that tends to scar and recur, but is reversible with treatment. It
affects 10% of the population over a lifetime.
Classification and aetiology
● Acute ulcer: usually has an ischaemic cause; unlike chronic ulcers, it can affect young people.
● Chronic ulcer: no more than 30-40% of patients have hypersecretion. Possible causes include:
o H. pylori infection;
o use of NSAIDs;
o gastrinoma (rare);
o IBD (rarely affecting stomach and duodenum)
In Palermo, most ulcers are from NSAIDs, and about 20% from H. pylori. Associated genetic factors
include blood group 0 and certain HLA haplotypes. The main risk factors for developing gastric or
duodenal ulcers are H. pylori and NSAIDs, but also chronic obstructive pulmonary disease, chronic
renal insufficiency, tobacco use and advanced age.
It is produced by the imbalance between:
● Harmful factors (pepsin, HCl), increased by stress - smoking - alcohol - food - caffeine;
● Protective factors (HCO3-, mucus), reduced by NSAIDs (by reduction of Pg-D and Pg-G) ATS or arteriopathies - H. pylori (damages gastric mucosa and HCO3- production, present in
most cases of peptic ulcer) Secreting epithelium and vessels that irrigate the epithelium.
Gastric ulcer (body, bottom)
It usually involves the cardia or small curvature, and may be associated with either hypersecretion
(normo-secretion) or hyposecretion (due to atrophic gastritis).
● It is less frequent than duodenal ulcer, and arises later (on average at 50-70 years of age);
● It has a prevalence of 2.5% (x2 in men).
● Defects in the defence capacity of the mucosa may be present.
● It manifests itself with epigastric pain.
● They are more likely to be silent than duodenal ones.
● May evolve to gastric carcinoma (2%): a biopsy is necessary to exclude this possibility.
Characteristics of neoplastic gastric ulcer: > 2 cm, irregular shape, irregular mucosal folds, rigid
and inelastic wall.
Duodenal ulcer (pyloric antrum, duodenal bulb)
● It is statistically more frequent (x5) and early (40-60 years on average), with a genetic influence
compared to gastric ulcer;
● It is always associated with acid hypersecretion (increased gastric acid and decreased
bicarbonate).
● 90% of duodenal ulcers occur in the first 3 cm of the duodenum.
● It is most closely related to colonisation by H. pylori, which is present in 95% of cases;
It occurs in 10% of the Western population, incidence is decreasing, probably due to the lower
prevalence of H. pylori.
● They are mostly small (< 1 cm) well-circumscribed ulcers, which may sometimes reach the muscle
tonaca. Only rarely are they malignant, no oncological risk.
● It manifests itself with bar pain;
● Deepening (penetrating ulcer) a duodenal ulcer on the postero-medial wall may involve the
pancreas or the gastro-duodenal artery (giving profuse haemorrhage).
Anatomically pyloric ulcers are pathophysiologically duodenal ulcers. Most of them are now due to
NSAIDs.
Presentation
It may be asymptomatic (in 10-40% of cases), especially for duodenal ulcers.
● Epigastric pain: arises after food intake (50% - early for UG, late for UD) or during the night
(30%), but may also be absent. In 20% of gastric ulcers, but not in duodenal ulcers, it has posterior
irradiation. When related to acid hypersecretion it is relieved by antacids (bicarbonate, Mg
hydroxides) and food. (G) It is often nocturnal, due to gastro-oesophageal and duodeno-gastric
reflux (bliare reflux damages the antral mucosa and promotes its metaplasia);
o Duodenal ulcer: epigastric pain 30 minutes to 3 hours after the meal, and is relieved by antacids
or another meal; (G) irradiated bar.
o Gastric ulcer usually occurs within 30 minutes after a meal.
● Epigastric stiffness is the most frequent (20%) physical sign of the presence of ulcers.
● Nausea - vomiting - dyspepsia - anorexia - weight loss - belching
● Siderpene anaemia (from blood dripping).
Diagnosis and therapy
Endoscopy localises the ulcer and allows biopsies (for H. pylori and tumour markers). The ulcerous
lesion has a fibrin base, and is surrounded by scarlet inflammation (with haemorrhagic staking) and
radial gastric folds. The measurement of acid secretion is always inaccurate and has no diagnostic
value.
Peptic ulcer is classified using the Forrest classification:
- FIa: active pulsating bleeding of a pervious vessel, especially if arterial (e.g. from the bottom
of an ulcer)
- FIb: active nappus bleeding (blood comes out continuously, like a veil)
- FIIa: no bleeding in progress, there is a visible vessel at the bottom of the ulcer, but not
bleeding.
- FIIb: a platelet clot is seen attached to the bottom of the ulcer
- FIIc: patch of haematin (black) at the bottom of the ulcer
- FIII: lesion without signs of recent bleeding or with the ulcer floor covered by fibrin.
Medical and behavioural therapy:
● To reduce symptoms, the patient will eat frequent, non-abundant meals and avoid smoking,
alcohol and coffee.
● Eradication of H. pylori if present - PPI for 2-3 months - discontinuation of gastrolesic drugs;
Other drugs that can be used
● Antacids (e.g. Malox) and antirefluxants (e.g. Gaviscon) - not with PPIs (they reduce absorption).
● Sucralfate: taken one hour before meals (1g) acts as a physical barrier against acid secretion.
● Misoprostol: a synthetic PG-E analogue, it counteracts the gastrolesiveness of NSAIDs.
Gastroresection with digunal anastomosis (Billroth II or Y-shaped)
When the ulcer persists despite therapy, a gastroresection is performed:
● Typical, where only the bottom is left;
● Exclusionary, selective ('for the sour part' ?);
● Step-by-step, even more selective.
After the resection, the remaining portion of the stomach will not be connected to the duodenum ('the
duodenal stump is not touched'), but a gastro-diagiunal anastomosis will be made.
● Billroth II: a jejunal
digiunal loop, regularly connected upstream to the duodenum, is anastomosed
laterally to the gastric stump (in an isoperistaltic or antiperistaltic direction).
● Y-anastomosis (gastroresection and gastro-dysjunction-stomy and isolated loop to Roux and
entero-entero-ostomy): a digiunal loop is resected and anastomosed directly to the gastric stump
(via antecolic or retrocolic route), and the stump in series with the duodenum is connected to the
wall laterally. Preferable technique to avoid alkaline reflux (chronically leads to neoplasia).
Complications: stump fistulisation - afferent loop syndrome (there is dilatation of the anastomosed
loop and a feeling of heaviness, sweating, abdominal pain, biliary vomiting) - post-anastomotic ulcer
(from persistence of acid tissue or alkaline reflux) - small stomach syndrome (eating small meals) efferent loop syndrome (stenosis of the gastro-enteric anastomosis)
Complications of peptic ulcer
They affect 25% of patients, with a higher risk for the elderly and those treated with NSAIDs. Up to
10% of patients with ulcers may present directly with complications.
Bleeding (15-20%): must be stopped endoscopically (with coagulator and haemostatic clips) or
surgically (with transfusion stitches). > in elderly patients and 30-day mortality of 5-10%.
The presentation depends on the scope.
● Low flow: gives microcytic anaemia and occult faecal blood is detected.
● At high flow rates: gives acute anaemia - melena or haematemesis - hypotension to the point of
shock.
Treatment
●
●
●
●
●
Transfusions to stabilise haemodynamics
Nose-gastric probe: sucks out blood and clots and allows washing with cold water and HCO3Pump inhibitors - antacids - somatostatin
Endoscopy: bipolar coagulator - haemostatic clips - adrenalin infiltration
Combined laparoscopic and endoscopic intervention: in 25% of cases the bleeding cannot be
stopped except by applying transfusion stitches around the ulcer (laparoscopy). The endoscope
indicates where to apply them, and verifies that the bleeding has stopped.
● Left gastric a. ligation or vagotomy (to reduce blood flow)
● Resection of the bleeding part, for unstoppable bleeding.
Treatment by type
In case of:
1) FIa-Ib and IIa: endoscopic haemostasis is performed (these are lesions with a risk of
persistent bleeding or re-bleeding), which is done by placing two clips one upstream and one
downstream of the vessel, to which is associated the injection of adrenaline, or also thermal or
mechanical therapy or sclerosing injection.
2) FIIb: Consideration should be given to either removing the clot or adopting the endoscopic
treatment best suited to the picture revealed. Perhaps remove the clot and then see what to do.
3) FIIc and III: Endoscopic haemostasis is not recommended, as the risk of re-bleeding is low.
Infiltration with adrenaline is also useless. Oral therapy with PPI, once a day, is opted for.
Penetration: this is a form of perforation in which an ulcer deepens into neighbouring organs such as
pancreas (for duodenal) - choledoch - liver (left hepatic lobe for liver disease) - colon. It is typical of
ulcers of the medial aspect of the second duodenal portion, where stitches cannot be given due to the
risk of occluding the choledoco. Furthermore, to surgically explore the posterior face of the
duodenum, it must be disconnected from the vena cava through the Kocher manoeuvre.
Perforation (2-10%): results in chemical and then septic peritonitis (in 12-24h), circumscribed (
covered perforation) or diffuse depending on the rapidity of onset (perforation of the posterior wall of
the stomach gives a subphrenic abscess in the back of the epiploon). This results in an acute abdomen
(globular and painful, with Blumberg's sign subdiaphragmatic tympanic airway) and paralytic ileus,
leading to septic shock. Mortality at 30 days of 20%.
● Diagnosis: globular and painful abdomen with diffuse colic tympanism - subphrenic air sickle
● Medical therapy: antibiotics - PPI - nasogastric tube
● Raffia (suturing of the lesion): in most cases, together with antacids, it is decisive. It is always
combined with pyloroplasty (transversal incision of the pylorus, then sutured longitudinally): it
prevents gastric dilatation and rupture of the raffia due to tensile stress ("Plug the hole with the
epiploon" - "It is done on the anterior stomach, in the duodenum it is complicated").
● Ulcer exeresis
Scarring stenosis (gastric occlusion, 1-2%): this is usually post-pyloric (due to a recurrent duodenal
ulcer) and leads to gastric ectasia (with the typical picture of occlusion). In general it gives vomiting,
nausea, meteorism, postprandial fullness, weight loss, dehydration, metabolic alkalosis. It is treated
with endoscopic or surgical dilatation, or in severe cases with distal gastroresection with enteroanastomosis. In particularly defecated subjects, anastomosis is performed without gastric resection.
Carcinogenesis: affects 2% of gastric ulcers within 3 years of diagnosis, but not duodenal ulcers.
The ulcer appears engorged and with raised, rigid and irregular borders.
ZOLLINGER SYNDROME- ELLISON
The strong predisposition to the development of multiple severe peptic ulcers secondary to
hypersecretion of gastric acid by excessive gastrin release from a gastrinoma defines ZollingerEllison syndrome. Gastrin-secreting G cells are part of the diffuse neuroendocrine system and derive
from the neural crest; in addition to the gastric antrum, they are found in abundance in the pancreas.
Normal gastrinemia is < 100 pg/ml fasting and 300-400 pg/ml after meals. Hypergastrinemia is typical
of the syndrome. Prior to measuring gastrinemia, it is necessary to discontinue any PPI therapy, which
may alter the results.
Symptoms: mimic a typical peptic ulcer or reflux oesophagitis; may include a
chronic diarrhoea from excessive acid, which irritates the intestinal mucosa and draws fluid back by
osmosis.
STENOSIS PYLORIC
Hypertrophic pyloric stenosis is the narrowing of the stomach opening due to the thickening
(hypertrophy) of the muscle between the stomach and intestine. The hypertrophied muscle creates a
partial blockage (obstruction) that interferes with the passage of gastric contents into the small
intestine.
Infants feed well but vomit violently (projective vomiting) immediately after eating, thus risking
dehydration and malnutrition.
The diagnosis is based on the results of abdominal ultrasound. Typically, the problem is corrected by
administering fluids through a vein (intravenously) and a minor surgical procedure.
GASTRIC CARCINOMA
Gastric carcinoma is the fifth most frequent neoplasm by mortality and the second most frequent in the
GI tract (1st colon). Age > 60-70 years, M:F 2:1. In 95% of cases it is an adenocarcinoma. In most
cases the symptoms are nuanced and non-specific: dyspepsia at the beginning, and in advanced stages
weight loss - anaemia - melena - pain - nausea - ascites - jaundice (advanced stages).
Risk factors
● Familiarity and heredity: e.g. E-cadherin mutation - Lynch syndrome (mutation of mismatch
repair genes MSH2 or MLH1, proncipally related to non-polyposis colic carcinoma).
● Diet: salt, smoked foods, other carcinogens
● Intestinal metaplasia of the gastric epithelium, proportional to the spread of metaplasia
● Gastroresection
● Peptic ulcer
● H. Pylori infection.
● Gastric abutment in gastro-resectees: 15 years after surgery, at the level of the intestinal
anastomosis. Endoscopic check-ups every 2 years.
● Pernicious anaemia: relative risk similar to that of atrophic gastritis of the fundus.
● Gastric polyps: follow-up at 2 years after removal.
● Menetrier's hypertrophic gastropathy.
● Anachlorhydria (or hypochlorhydria), is an element of particular concern, especially due to the
self-prescribed use and abuse by many of the so-called proton pump inhibitors, which if taken over
the long term can lead to a gastric hypochlorhydria picture and constitute an additional risk factor
for gastric cancer.
N.B.
Hyperplastic polyp: this is the most frequent benign gastric neoplasm (80%). It may be solitary or
multiple (50%), size generally <1 cm, antral localisation (60%). The risk of degeneration to carcinoma
is very low (1-3%). They arise from chronic mucosal inflammation, often associated with H. pylori
infection. Regenerative and inflammatory based (it is an adaptation phenomenon secondary to
inflammation): the number of glands is not increased but there is cell crowding.
Adenomatous polyp: is a benign gastric neoplasm (20%). It is often single, 0.5-3 cm in size, most
frequently localised at the antral level. It may present with epigastric pain and digestive haemorrhage
(melena, haematemesis, anaemia). Especially if villous, it may degenerate to carcinoma (30-40%). The
number of glands is numerically increased.
Protective factors: fruit and vegetable consumption. Environmental factors carry more weight than
genetic ones.
Primary prophylaxis: reduction of foods rich in nitrites and nitrates and smoked foods, reduction of
salt in the diet, eradication of H. Pylori, reduction of alcohol and tobacco.
Precancerous conditions: benign gastric diseases that carry an increased risk of developing
carcinoma; precancerous lesions are often present in their context. The most frequent are:
● Chronic atrophic gastritis: type A or fundic gastritis (associated with autoimmune gastritis and
pernicious anaemia) and type B or multifocal antral gastritis (associated with chronic H. Pylori
infection);
gastritis with predominantly antral localisation, associated with chloric-peptic over-secretion and
duodenal ulcer, carries a low risk of ADK. At 15-year follow-up, 10% of subjects with atrophic
gastritis develop ADK (risk 25 times higher than the general population). Endoscopic check-ups
every 2-3 years.
● Intestinal metaplasia: presence of specialised intestinal epithelium (muciparous calyciiform cells
and pseudovilli) in the gastric mucosa; appears in advanced stages of chronic atrophic gastritis.
Incomplete intestinal metaplasia is associated with 'intestinal-type' gastric ADK.
● Mild dysplasia: regresses in 60% of cases, but can also evolve to moderate and severe dysplasia
(and this to ADK)
● Benign gastric ulcer: it is unclear whether it is in fact already an ulcerated carcinoma (more of a
sign than a risk factor) or whether it will undergo malignant transformation. Follow-up at 3-6
months.
Macroscopic types of early gastric cancer
● Type I: protruding or polypoid.
● Type II: superficial (IIa elevated, IIb flat, IIc depressed).
● Type III: excavated.
Macroscopy
From an anatomopathological point of view, the macroscopic pictures that we can see on the surgical
piece endoscopically are:
● A vegetative form that proliferates within the intestinal lumen;
● Ulcerated (crater-like) form;
● Infiltrating form in which we predominantly see a plaque;
● Scirrhotic form is mainly reproduced in the context of the submucosa up to the picture of
plastic linitis, which is practically a complete hardening of the entire gastric wall and becomes
a sort of rigid, inelastic tube related to the neoplastic infiltration of the submucosal layers and
all states of the gastric pouch.
Bormann classification
● Polypoid form (type 1)
● Ulcerated polypoid form (type 2)
● Ulcer-infiltrating form (type 3)
● Diffuse infiltrating form (type 4).
Histological variants
● Adenocarcinoma that can be papillary, tubular, mucinous, ring-cell type with castellation. The
further we move away from what is the classic adenocarcinoma the greater the neoplastic
aggressiveness, the more the form is undifferentiated or evolves towards the undifferentiated,
deviates from what are the normal cells of the mucosa in which the neoplasm arises the greater
the aggressiveness of the neoplasm and consequently the worse the prognosis
● Adenosquamous carcinoma;
● Flat epithelial carcinoma;
● Undifferentiated carcinoma.
Histological classification of Lauren
● Cardial ADK: often based on Barret's oesophagus (reflux disease, obesity, etc.). Mutations
involved (beginning to be studied by next generation sequencing): p53, p16. Its incidence is
increasing in the western world.
● Intestinal-type gastric ADK: more frequent, older age, prevalent antral localisation, higher
incidence in high-risk areas. It is preceded by precancerosis. Evolution of a chronic gastritis;
glandular structures maintaining polarity and aggregation, evidently less aggressive
● Diffuse gastric ADK: less frequent, younger age, worse prognosis (tends to infiltrate
downwards). Not preceded by precancerosis. Difficult to detect at endoscopy because the mucosa
is retained. Loss of E-cadherin. Ring-shaped cells with a bezel. More aggressive.
● ADK mixed.
In countries with screening (East) for gastric cancer, it is common to be diagnosed at the 'early gastric
cancer' stage, i.e. ADK confined to mucosa and submucosa, with rare lymph node involvement and 5year survival of 90% after removal.
Symptomatology:
● Early GC: absent symptoms (25%) or mild dyspeptic complaints (without weight loss or
anaemia). Possible occurrence of precancerous conditions and lesions.
● Early stage (not initial), practically absent signs and non-specific symptoms: dyspepsia (80%;
epigastric dyspepsia, without remission-relapse alternation, often without temporal relation to
meals), asthenia, weight loss (60%), fever. The laboratory may show sideropenic anaemia or
elevation of tumour markers such as CEA and CA19.9.
● Late stage: epigastric pain and early satiety, dysphagia (especially if localised at cardial level),
nausea, food vomiting, melena (piceous, foul-smelling stools), haematemesis, weight loss.
Epigastric palpable mass in thin subjects. Troiser's lymph node (supraclavicular) presence of a
lymph node in a lymph node chain extending across the mediastinum to the left supraclavicular
fossa with the presence of pathological lymph nodes in the left supraclavicular fossa but these are
late signs and related to patients who are no longer operable.
● Very high tumour markers. Possible cholestasis due to biliary tract compression or presence of
liver metastases.
● Metastatic stage: jaundice or hepatomegaly from liver metastases, neoplastic ascites from
peritoneal carcinosis, worsening dyspnoea from lung metastases (more frequent in castellated ring
cell carcinoma and plastic lymphitis), ovarian mass (Krukenberg tumour), palpable supraclavicular
lymph nodes.
Instrumental diagnosis:
● EGDS: is the procedure of first choice (high diagnostic accuracy), allowing visualisation of the
mucosa and removal of suspected precancerous lesions. Useful techniques are endoscopic
magnification (magnification of the image to capture details, useful for screening) and
chromoendoscopy (with vital dyes especially in the case of flat lesions). The main complication is
haemorrhage, which is treated with injection of sclerosing agents or by placing endoclips.
Echoendoscopy plays a very important role in staging, allowing evaluation o f infiltration of the
gastric wall (T accuracy 80-90%) and possible involvement of adjacent lymph nodes (N accuracy
70-90%). It also has a very high accuracy in the case of submucosal lesions (GISTs, leiomyomas).
● CT scan with mdc and ultrasound: these are very important for staging.
● PET: it is more sensitive than CT for detecting distant metastases.
Staging:
● T1 mucosa or submucosa, T2 muscle, T3 serosa, T4 adjacent structures;
● N1: 1-6 lymph nodes, N2: 7-15; N3: >15 (it is the number of lymph nodes that is important and not
so much their proximity to the primary tumour; previously it was N1 perigastric < 3 cm from the
tumour, N2 perigastric > 3 cm, N3 para-aortic, retroperitoneal, etc).
● M1: positive peritoneal cytology.
Pathways of spread of gastric carcinoma:
● Continuity (up to 4 cm from the macroscopic margin),
● Contiguity (adjacent organs also > 4 cm from the macroscopic margin; transverse colon, omentum,
pancreas, regional lymph nodes)
● Lymphatic (distant lymph nodes: supraclavicular),
● Peritoneal dissemination (makes the prognosis much worse and is an absolute contraindication to
surgery, except of a palliative nature),
● Blood (liver, lungs, CNS, skeleton).
Positive prognostic factors: female sex, distal site, T1, intestinal histotype, G1, negative lymph
nodes, absence of vascular and lymphatic invasion, R0 margins.
Treatment:
● Early GC type 1 <2 cm and type 2a-b <1 cm: endoscopic mucosectomy.
● Early GC type 2c-3 or >2 cm or N+: subtotal gastrectomy with lymphadenectomy; subtotal
gastrectomy is indicated in tumours of the lower third of the stomach; it is a
gastrodigiunoanastomosis with anastomosis at the foot of the loop according to Braun with
the loop coming from the biliary tract or pancreas, with preserved duodenum, and anastomosed to
the stomach after which the jejunal loop descends since it always has its own continuum and at this
lower point there is a communication between the afferent loop to the stomach and the efferent
loop from the stomach to facilitate the passage of the bile-pancreatic juice instead of towards the
gastric lumen directly into the efferent loop where it meets with the food bolus from the gastric
cavity; or the Roux or Y-shaped loop (left-hand drawing) . These anastomoses are partial.
● non-early resectable GC (40-50%): gastrectomy surgery (distal or subtotal for antrum lesion,
enlarged subtotal for body lesion and total for proximal lesion, in the upper third) with proximal
and distal margins >6 cm and D2 type locoregional lymphadenectomy (at least 15 lymph nodes),
associated with splenectomy in case of neoplastic impairment of the spleen (or positive splenic
hilum lymph nodes or splenic artery) and with en bloc resection of the organs attached to the
neoplasm. Here too we have the same reconstructions as before, but instead of doing them with the
gastric stump, they are done with the oesophageal stump.
● Terminolateral oesophagodigiunoanastomosis with or without anastomosis at the foot of the
Braun loop
● Terminolateral (or termino-terminal) oesophagodigiunoanastomosis on excluded digiunal loop
according to Roux
● Criteria for non-resectability: distant metastases, invasion of the peritoneum, invasion of
major vascular structures.
N.B. Removal of lymph nodes
● D0: incomplete removal of first level stations
● D1: removal of N1 lymph nodes;
● D2: extends to the lymph node groups of the left gastric artery, common hepatic artery, celiac
trunk, splenic hilum and splenic artery;
● D3: also includes lymph nodes of the hepatoduodenal ligament, retropancreatic, mesenteric
artery
Some studies have shown that the difference in OS between D1 and D2 is not significant; perhaps the
ideal would be an enlarged D1 in order to examine a sufficient number of lymph nodes.
Palliative surgery
Performed mainly in advanced but mobile tumours, it can be a tumour-only exeresis without
oncological radicalisation in order to control either bleeding or occlusive phenomenon.
Inoperable: possible shunt (bypass with Billroth reconstruction 1 or 2 or Y-shaped Roux loop)
+ there is no point in following the lymphadenectomy because if you lose the radical intent, there is no
point in doing it.
Doubt of operability: exploratory laparoscopy. In case of no oncological radicality, chemotherapy
and radiotherapy is performed (does not greatly increase OS, further studies needed). In case of R0,
surveillance is performed for low-risk tumours and adjuvant therapy for those at high risk of
recurrence (pT3-4 or N+). Patients who are candidates for chemotherapy should still have a good PS
(0- 2). For the purpose of radiotherapy we remember that gastric ca. is not very radio-sensitive, it is
used only for palliative purposes and in some protocols as adjuvant especially when there is a problem
concerning the cardia.
Complications of surgery
Early complications of surgical treatment are:
● Bleeding,
● Stenosis of the anastomosis,
● Gastric atony,
● Dehiscence of the anastomosis.
While late complications are:
● Disease relapse,
● Metabolic deficiencies.
Post-gastrectomy functional syndromes or post-cibal syndromes
In 25% of the surgical procedures performed on the stomach, dysfunctions occur that we call postcibal syndromes. Some arise in a transitory form, others in a permanent form.
Dumping syndrome
Characterised by episodes of nausea, diarrhoea and tachycardia. They are early or late, after a meal
due to the passage of chyme into the small intestine too rapidly resulting in hypovolaemia from fluid
recall.
Thus, the immediate passage of the food bolus in the context of the digiunal loop in the absence of the
pyloric valve, which has been blown out due to the resective operation, results in an abrupt passage
and a hypovolemic condition due to osmotic phenomena, peaks of blood glucose with the body's
response with hyperincretion of insulin followed by hypoglycaemia.
A diet rich in protein and fat and low in carbohydrates, as well as bed rest after meals, significantly
reduce the speed of gastric emptying and thus the osmolarity of the gastric contents, which controls
symptoms. It is also advisable to eat small, frequent meals and avoid drinking, which accelerates the
transit from the stomach to the jejunum, to slow down the contents.
When this syndrome despite physical and behavioural precautions is not controlled, an inversion of the
digiunal segment is assessed.
Alkaline reflux gastritis
Characterised by biliary pain and vomiting that does not alleviate the pain in contrast to afferent loop
syndrome. Can be associated with gastric or oesophageal lesions with risk of malignant
transformation.
Some intestinal reconstructions facilitate the passage of strongly alkaline bile-pancreatic juice in the
context of the gastric mucosa, through the gastro-digiunal anastomosis, or in the context of the
oesophageal mucosa, through the oesophago-digiunal anastomosis. This condition can lead precisely
to alkaline reflux gastritis.
In these cases the use of metoclopramide, which stimulates gastric emptying and decreases reflux,
can help. To avoid this complication, it is advisable during surgery to operate according to the Roux
loop gastrojejunostomy technique.
Chronic diarrhoeal syndrome with protido-dispersion
Due to irritation of the intestinal mucosa by acid chyme with hormonal hypersecretion of the VIP with
a picture of chronic diarrhoea. However, these phenomena are limited in time and tend to recede. Only
in 1% of cases are they refractory to medication.
In this case, all foods that can increase peristalsis should be avoided such as liquids, lactose, fat. It is
also recommended to take anti-diarrhoeal medication.
afferent loop syndrome
It manifests itself with dyspepsia and pain immediately after meals associated with biliary
vomiting, which, however, soothes the pain.
It occurs mainly after reconstruction according to Braun and is caused by an incongruous passage of
food in the afferent loop. The food then instead of entering the efferent loop enters the afferent loop,
which dilates with pain and biliary vomiting. The pain goes into remission after the vomiting episodes.
Again, small, frequent meals and avoiding drinking are recommended. If the condition persists, a
second corrective intervention may be considered.
Efferent loop syndrome
Characterised by postprandial abdominal pain, nausea and vomiting due to delayed gastric
emptying due to atony of the viscera, as it may be denervated and lose muscle tone during surgery.
In this context, we must consider that the substantial picture is one worthy of peristaltic drug therapy.
Thus, in principle, a patient who has undergone partial or total gastric surgery should be advised to
follow a dietary regimen of no longer the canonical three meals a day but seven, in order to distribute
calories and avoid complications of this kind.
GASTRIC MALTS
These are MALT lymphomas, usually B-cell lymphomas, which in most cases arise following
chronic antigenic stimulation by H. pylori to the point of selection of an aberrant clone. API2 MALT
translocation t(11;18). Extra-nodal B-cell lymphoma of the marginal zone of mucosa-associated tissue.
To cure them, the infection must be eradicated.
GIST
Gastrointestinal stromal tumours (GISTs) are cancerous (malignant) tumours that develop from a
specific type of cells (mesenchymal cell precursors) in the wall of the oesophagus, stomach or
intestine. Most (60-70%) of these tumours develop in the stomach, 20-25% in the small intestine and a
small percentage develop in the oesophagus, colon and rectum. The average age at diagnosis is 50-60
years.
Most gastrointestinal stromal tumours are caused by a mutation in a gene, called C-KIT, that controls
cell growth.
Individuals undergoing radiotherapy of the abdomen for treatment of other tumours may subsequently
develop gastrointestinal stromal tumours. Usually, these tumours grow slowly but can grow more
rapidly and spread to other sites (metastasise).
Symptoms of stromal tumours of the gastrointestinal tract depend on the location of the tumour but
include abdominal pain, bleeding, indigestion and feeling full after eating a small meal. Nausea and
vomiting may occur if the tumour is large enough to block the digestive tract.
INTESTINE SMALL INTESTINE
DIVERTICULUM OF MECKEL
It is the most common congenital anomaly of the gastroenteric tract (1-2% prevalence). Remnant of
the onphalo-mesenteric duct that joins the primitive intestine to the yolk sac in foetal life (normally
closes by 7-8 weeks of gestation). Other possible outcomes of a failure to close this duct are: onphalomesenteric fistula, enterocyst, umbilical cord (i.e. a fibrous band between the small intestine and the
umbilicus).
● Located in the antimesenteric border of the ileum, at a variable distance up to approx. 120 cm
from the ileocecal valve.
● Length: 1 to 10 cm. Diameter: 1 to 4 cm.
● Formed by all three intestinal tonacas, internally in slightly less than half of the cases it is lined
with gastric-type mucosa and sometimes pancreatic tissue can also be found.
● Apex: free (>) - connected to the umbilicus - adherent to other structures (<).
In 90% of cases it is asymptomatic and is an occasional finding during laparotomy. In the remaining
cases it manifests itself with symptoms related to: haemorrhage (>50%) - phlogosis - intestinal
obstruction.
Complications
They may be due to
● Acid secretion of the ectopic gastric mucosa:
o Haemorrhage: melaena (adults) and haematochezia (children)o Diverticulitis - perforation: simulates acute appendicitis. Initially the pain is periumbilical, but
later it is localised where the diverticulum is located.
o Neoplastic transformation (0.5%).
● Mechanical in nature:
o Intestinal obstruction as a result of: Invagination of the diverticulum in the intestine (the
diverticulum in turn causes invagination of the ileum) or Volvulus of an intestinal loop around
the diverticulum when its apex is attached to the umbilicus or another structure + intestinal
evagination outside the umbilicus, twisting of the diverticulum;
o Herniation of the diverticulum: Littré hernia, more frequent on the right.
Meckel's diverticulum is the leading cause of rectal bleeding in children under 5 years of age, and
originates from peptic ulceration of the ileum adjacent to the diverticulum's ectopic gastric mucosa.
The onset is sudden, unaccompanied by pain. The blood emitted is first dark red (Florentine red,
tending to dark purple) and then bright red. Bleeding is conspicuous, sometimes preceded by modest
abdominal pain, and usually ceases spontaneously to recur later.
Differential diagnosis
Dd is difficult. The search for Meckel's diverticulum is a must in all cases of acute abdomen in
where at laparotomy the appendix is unharmed. Abdominal ultrasound - X-ray of the digestive tract
with mdc - CT scan: they almost never manage to show it.
In cases where it is covered by gastric mucosa, its presence can be detected by
scintigraphy with 99Tc (merckel scan).
Therapy
Removal of the diverticulum by resection of the ileal segment encompassing it, followed by a terminal
ileal-terminal anastomosis.
Neuroendocrine tumours
Neuroendrocrine tumours or NETs originate from aggregates of neuroendocrine cells in various
organs, most frequently the intestine, stomach, pancreas and lungs. They are relatively rare tumours
and account for approximately 0.5% of all malignant tumours. In Italy, a prevalence of about 4-5 cases
per year per 100,000 inhabitants is estimated. They are a heterogeneous series of neoplasms with
varied clinical behaviour and can affect all ages. They are often associated with hereditary syndromes
such as MEN1, von Hippel-Lindau S., neurofibromatosis 1 and tuberous sclerosis.
Headquarters
The most commonly affected site is the pancreas and gastrointestinal system, together accounting
for about 2/3 of all NETs. Another site that is fairly affected is the lung; while less frequent sites are
the adrenal and paraganglia, thyroid and parathyroids, adenohypophysis and Merkel cells of the skin.
They can be distinguished on the basis of clinical presentation into non-functional and functional
Non-functional
They account for about 80 per cent of all NETs, patients in most cases are asymptomatic, and the
diagnosis is usually made by chance during endoscopic and/or radiological examinations performed
for other reasons.
Symptomatology (non-specific) may sometimes occur later and this depends on the organ involved
because it is symptomatology from local compression or from distant metastatic disease. Thus, one
may encounter:
● Anaemia
● Bleeding
● Abdominal pain
● Vomiting
● Slimming
● Jaundice
Working
They are the remaining 20% of all NETs and the clinical picture is related to the excessive production
of certain hormones:
● Diarrhoea and skin redness - carcinoid syndrome
● Hypoglycaemia - insulinoma
● Heartburn and vomiting - gastrinoma
Focus: carcinoid syndrome
Carcinoid syndrome develops in some patients with carcinoid tumours, particularly those originating
from the ileum, and is characterised by skin flushing, abdominal cramps and diarrhoea. After several
years, right heart valvulopathy may develop.
The syndrome is due to vasoactive substances (including serotonin, bradykinin, histamine,
prostaglandins, polypeptide hormones) secreted by the tumour, which is typically a metastatic
intestinal carcinoid.
The diagnosis is made on the basis of the clinic and the demonstration of increased urinary excretion
of 5-hydroxyindolacetic acid. Tumour localisation may require scintigraphy or exploratory
laparotomy.
Symptoms are controlled with somatostatin analogues, octreotide, but surgical removal should be
carried out where possible; in the case of malignant tumours, chemotherapy may be used.
Laboratory diagnosis
Laboratory medicine is very useful in functioning tumours. It involves the search in plasma or urine
for peptides produced by the neoplasm and/or other disease-specific markers.
One goes in search of:
● Plasma insulin
● Plasma glucagon
● Plasma gastrin
● Urinary 5-hydroxyindolacetic acid (5-HIAA), a urinary catabolite of serotonin that can be
observed at very high levels in the urine of carcinoid syndrome patients;
● Neuron-specific enolase (NSE), sensitivity ranging from 40-70%.
● Chromogranin A, sensitivity ranging from 70-90% of cases; particularly sensitive in forms
already metastatic at clinical onset compared to localised primary forms with welldifferentiated grading and a low degree of malignancy; high plasma levels of chromogranin A
may lend itself well as an indicator of poor prognosis. The marker has features suitable for
monitoring the patient during treatment as well as during
follow-up, demonstrating a concordance between the change in plasma levels and the clinical
evolution of the disease.
Instrumental diagnostics
The gold standard examination is the CT scan with mdc, since NETs present specific features with
this type of instrumental investigation. They are highly vascularised tumours, in fact their visualisation
improves after administration of contrast medium during the arterial phase followed by wash-out
during the portal venous phase.
On MRI, neuroendocrine tumours are typically characterised by low s i g n a l i n t e n s i t y a t T1 and
high signal intensity at T2 (low sensitivity). Rather than making a tumour diagnosis, this diagnostic
method is useful in the topographical characterisation of lesions that had not previously been
diagnosed as neuroendocrine but are later found to be so on histological examination.
Echoendoscopy has a high sensitivity for the identification of pancreatic NETs and duodenal
gastrinomas, and has an additional advantage in that it allows fine-needle aspiration biopsies to be
taken.
Then there is somatostatin receptor-based imaging; the advantage of this method is that it involves
the whole body and is therefore useful for both detection and staging; moreover, receptor sensitivity is
also very important for therapeutic purposes with regard to the use of somatostatin analogues.
But the ideal method for studying and detecting such neoplasms is the PET-68Ga DOTATE and 68Ga DOTATOC (Gallium PET), which is very expensive and not easily available, in fact in Sicily it
is only available in Catania. With this PET you have a higher spatial resolution than with the
OCTREOScan.
From the point of view of evolution, NETs can be distinguished into:
● Localised form
● Metastatic form: the sites most affected by metastasis are the liver, bones and lungs.
Biological behaviour
Although function may influence prognosis, in fact insulinomas are generally indolent and benign
tumours, the biological behaviour of most functioning NETs is defined by the tumour's grade and
stage of disease, as with non-functioning tumours.
Grading: identification on histological examination, from surgical specimen or fine needle, of mitotic
index (IM) and Ki67 expression. Based on these values, NETs are distinguished from NEC
(neuroendocrine carcinoma). NETs are distinguished into G1, G2, G3 and are all well differentiated
in contrast to NECs which are poorly differentiated.
The 2019 WHO classification (Figure 1) has included a new lesion category, namely Mixed NonNeuroendocrine-Neuroendocrine Neoplasms (MiNEN), which contain all those rare cases in which
there is the simultaneous presence of adenocarcinoma with a small neuroendocrine component.
Therapy
Surgical therapy is the first choice in most localised forms and in selected cases of metastatic
tumours.
Other therapeutic approaches involve the alternative use of Somatostatin analogues, i.e. synthetic
hormones that can slow tumour growth and control symptoms in the case of functioning tumours.
There is the possibility of Radioreceptor therapy, which involves the administration of a
radiolabelled somatostatin-like drug intravenously, allowing selective irradiation of tumour cells.
Other possibilities are:
● Molecular target therapies: drugs that are administered per os and exploit the presence of
specific molecular targets;
● Chemotherapy: reserved for patients with advanced tumours;
● Loco-regional therapies: minimally invasive interventional radiology procedures, mainly
used for the treatment of difficult-to-remove or multiple liver metastases (ablation chemoembolisation)
INTESTINE LARGE INTESTINE
DIVERTICULAR DISEASE OF THE COLON
In the Western world, 70% of the population over 80 years of age has diverticulosis (average age of
presentation: 60 years). In Europe, it affects 5% of the population under 40 years of age. Of these, only
20-30% develop symptomatic disease and only 1-2% require hospitalisation.
● Diverticulum: from Latin 'divertere' (to take out)
● Diverticulosis: condition caused by the presence of numerous diverticula
● Diverticulitis: consists of inflammation and the resulting possible risk of perforation of a
diverticulum
● Diverticular disease: a condition that includes both symptomatic and asymptomatic diverticula
● Peri-diverticular disease: indicates the apparent thickening of the muscle tonaca that is considered
a precursor to the development of diverticula (sawtooth opaque schism).
● True diverticulum: herniation of the entire intestinal wall, often congenital, solitary and rare in
the colon.
● Pseudodiverticulum (almost never single, often symmetrical) or intramural diverticulum
Usually small (approx. 1 cm), it consists of protrusion of mucosa and submucosa through the
tonaca mm of the colon, and develops preferentially in the left colon and sigma, at points where
the vasa recta penetrate through the tonaca mm propria, disrupting the integrity of the wall mm.
They almost always form on the mesenteric side of the anti-mesenteric tapeworm. Narrow
relationship between the rectal artery and the neck of the sac (frequent haemorrhages). The wall of
the pseudodiverticula consists of mucosa, submucosa and serosa.
Pathophysiology and pathogenesis
● Increased colic wall weakness - Parietal weakness factors: e.g. shortening of the tenie connective tissue changes in the submucosa - connective tissue syndromes.
•
Shortening of the tapeworms □ Deformation (myocosis) that narrows the colic lumen □
Muscle contractions divide the lumen into isolated compartments
• Age: both elastin and collagen levels in the colic wall increase (they maintain the colon's
visco-elastic properties of resistance to parietal stretching). The accumulation of elastin
makes the tapeworms stiff and the circular mm becomes wrinkled by contracting against
the tapeworms. In the elderly, however, the elastin, although abundant, is defective and the
collagen of the submucosa instead retains its resistance. When the longitudinal mm and the
circular mm lose their resistance to stretching, the mucosa and submucosa tend to evert
through the mm layers, leading to the formation of diverticula
● Increased endoluminal pressure (especially in the sigma) In most cases, it is constipation or
irritable bowel syndrome that causes a chronic increase in pressure in the lumen from the
physiological 20-40 mmHg to 90 mmHg, accompanied by hypertrophy of the muscular layer.
● Low-residue diet: the absence of fibre reduces the ability of faeces to retain water, making
them hard and fragmented (reduces lumen and increases P per La Place
??). Recent studies actually seem to correlate diverticulitis with diets rich in fibre.
● Increased and uncoordinated motility: generates high-pressure loci between two
hyperperistaltic segments, favouring drive eversion. It can occur e.g. in irritable bowel
syndrome.
● Muscle hypertrophy of the wall: increased pressure generated.
Sigma (head office, 90%). Tract in which the radius/P ratio, according to Laplace's law, is less
favourable. Hypertrophy of the circular muscle layer, induced by reduced dietary fibre intake and
consequent constipation, leads to excessive muscular activity and segmentation of the colon,
formation of small closed chambers at high pressure (>90 mmHg; normally it is 20-40 mmHg) and,
finally, diverticulosis.
Classification of diverticular disease (CDD) 2014
● Grade 0: diverticulosis, of occasional occurrence.
● Grade 1: uncomplicated acute diverticulitis - uncomplicated symptomatic disease. Manifests
with intermittent pain, fever and/or haematochezia. Colonoscopy or an optic clisma is indicated
for dd with IBD and CCR; subdivided into 1a (without phlegmonous reaction), 1b (with
phlegmonous reaction)
● Grade 2: acute complicated diverticulitis - recurrence of grade 1 (?). CT scan or opaque schism
indicated. Subdivided into 2a (micro-abscesses <1cm), 2b (macro-abscesses), 2c (perforation)
● Grade 3: chronic diverticular disease.
● Grade 4: diverticular bleeding
Diverticular disease can become complicated due to diverticulitis can be divided into acute
diverticulitis and chronic diverticulitis that can be considered acute-recurrent or even smouldering.
Complicated diverticular disease
Higher incidence in patients who abuse anti-inflammatory drugs. Obese males have a higher risk of
developing a severe and aggressive form. It should be suspected if: elderly patient - pain and palpable
mass in the flank/left iliac fossa - fever - leukocytosis. NB immunocompromised patients tend to show
more nuanced symptoms with fewer signs of inflammation.
Complications of diverticulosis
Diverticulitis
Inflammation: the button-shaped diverticulum traps faecal material and gives rise to bacterial
growth with inflammation, fermentation and potential further complications. It can occur due to
stagnation o f faecal material within a diverticulum, possibly due to inflammatory processes of the
mucosa.
● Abdominal pain: in the absence of complications it is the main symptom of diverticulitis,
generally referred to the left iliac fossa or suprapubic region, it tends to be constant rather than
colicky and is of varying intensity depending on the extent of the inflammation (he says cramplike, exacerbated by eating, relieved by gas emission). In most cases it lasts a few days and then
disappears completely, until the eventual re-exacerbation of the disease. EO: pain in the left iliac
fossa and lower abdominal quadrants which may vary from a sense of discomfort on deep
palpation to obvious signs of peritonitis.
● Alterations in alvus (common): intermittent diarrhoea or alternating constipation-diarrhoea. In
the presence of stenosis, constipation becomes the predominant symptom, accompanied by
abdominal distension, in some cases a palpable abdominal mass.
● Nausea and vomiting (less frequent).
● Modest thermal elevation usually detectable. NB in case of peritonitis or abscess, high grade
hyperpyrexia occurs.
● Urinary disorders: dysuria and pollakiuria, which can be attributed to the compression exerted
by the inflamed colon on the bladder wall or to the direct involvement of the bladder wall by the
inflammatory process.
Consensus conference on acute diverticulitis
Simple acute diverticulitis is considered to be a simple infection that does not extend to the
peritoneum; dangerous air bubbles or little dangerous fluid without the abscess then within 5 cm of the
inflamed intestinal segment is already a complicated form and requires hospitalisation and antibiotic
therapy.
● 1b: abscess below 4 cm;
● 2a: abscess greater than 4 cm;
● 2b: air more than 5 cm away from the inflamed intestinal segment.
Abscess (most frequent)
It follows the spread of a diverticulitis with peridiverticulitis or the microperforation of a
diverticulum, under conditions that favour the localisation of the process: perforation of the mesentery,
presence of previous adhesions in the peritoneal cavity, tamponade by the omentum.
● Peri-sigmoid abscess: typical clinical picture of diverticulitis. Marked infectious syndrome (septictype fever). Mass in the left haemiadomen (1/3 of cases)
● Mesenteric or pelvic abscess: clinical picture of intestinal obstruction, fever, fluctuating abdominal
mass at the level of the Douglas excavation (50% of cases).
Clinic
● The pain is circumscribed, almost always in the lower quadrants, and on palpation it is often
possible to appreciate a mass in the left iliac fossa.
● Septic-type hyperpyrexia and leucocytosis are always present; nausea and vomiting sometimes
appear.
Diagnosis
● CT (!, 1st choice): with mdc in the rectum, intraluminal changes, transmural abnormalities and the
spread of the inflammatory and infectious process around the colon are detected
● Opaque schism (+, 2°): if there is any doubt of perforation, it should be performed with fat-soluble
mdc (not barium)
● Colonoscopy: should be avoided in acute phases.
Perforation (infrequent but very serious)
Free in the peritoneum or plugged by the omentum. It begins with acute pain, usually referred to the
lower quadrants, but with a tendency to spread rapidly to the whole abdomen. Marked distension of
the abdominal cavity (pneumoperitoneum) then appears, followed by parietal contracture. Possible
occlusion in a febrile context.
Direct X-ray of the abdomen: presence of free air in the peritoneum and, later, hydroaerial levels.
o Perforation with circumscribed peritonitis: a conservative approach is attempted for 24h with
percutaneous drainage inserted under CT guidance. If there is an improvement we continue
with percutaneous drainage, otherwise a recto-colic resection with recanalisation is performed
in one time.
o Perforation with diffuse peritonitis: emergency surgery is performed
Hinchey classification
● Hinchey I: perilous abscess confined to the mesocolon, thus wall or boundary with the
mesocolon; Ia: confined to the perilous inflammation or phlegmon; Ib: in the case of the
perilous abscess confined, thus within the wall the abscess formation itself is substantially
evident.
● Hinchey II: pelvic abscess, therefore slightly at a distance from the colon;
● Hinchey III: diffuse, purulent peritonitis, so with a perforation that then covered and an
infection of the peritoneum due to the perforation that then spread to the whole peritoneum,
so we find pus in the whole peritoneum, a picture that needs emergency surgery;
● Hinchey IV: diffuse stercoraceous peritonitis because the perforation did not cover and
continued to pour faeces into the peritoneum giving stercoraceous peritonitis. This picture
also requires surgery.
Fistulisation
It is the result of drainage of an abscess (or inflammatory process), of diverticular origin, in the:
Surrounding hollow organs, fistulas:
● Colo-vesical (50-60%): recurrent cystic episodes, pneumaturia and occasionally faecaluria,
preceded by the clinical picture of diverticulitis;
● Colo-vaginal (25%): vaginal discharge of faeces, blood, pus, mucus or gas.
● Colo - colic (rare).
Outwards through the abdominal wall: colo-cutaneous fistulas (rare).
Since the uterus acts as an anatomical barrier, fistulas are more frequent in men than in women.
Intestinal obstruction
It is important to distinguish the occlusive form due to peritonitis or pelvic abscess from the
inflammatory form. It results either from inflammatory stenosis of the affected segment or from
adherential phenomena that, starting from this, involve the adjacent intestinal loops (diverticular
pseudotumour, in chronic/a pousse forms: formation of a mass mimicking a neoplasm). Intraparietal
lesion with oedema and submucosal sclerosis with retraction of the mesocolon. Often difficult to
differentiate with neoplastic stenosis. In late stages fibrous stenosis.
Haemorrhage (5%)
It is easy to find and is related to the close relationship between the diverticulum and the perforating
branch of the colon marginal artery. Carcinoma and ulcerative rectocolitis (other lower causes). This
is the main cause of lower digestive haemorrhage: it is often chronic and minor, but should be
investigated to exclude other causes.
It is more frequent in males and elderly subjects and is especially more frequent in subjects who have
diverticula in the right colon, this probably due to a question of erosion of the diverticular wall and
collar in a colon that is evidently less thick because there is less muscle in the right colon and therefore
more easily can undergo erosion of the collar and thus a bleeding process.
It may occur due to compression ischaemia or mechanical erosion of the mucosa, and produce
haematochezia or occult faecal blood, anaemia. Red blood in the faeces (not associated with pain),
massive haemorrhage is quite rare.
Medical therapy is not very effective. It can only be endoscopic and if we have a relapse picture, left
hemicolectomy or at least sigmoidectomy is definitely the therapy of choice.
Diagnosis of disease
● Clinical + Laboratory: leukocytosis and increased acute phase indices
● Nuclear scintigraphy: very sensitive, detects bleeding of 0.1-0.5 ml/min Performed with two
different methods: 1)99 mTc colloidal sulphide; 2) GR labelled with99 mTc (!): performed to
confirm t h e presence of active haemorrhage prior to angiographic examination.
It is not used for pre-surgical study or in critical patients (□angiography).
● Mesenteric angiography: when colonoscopy is not possible and in bleeding amounts > 0.5 ml/min.
It allows visualisation of the bleeding site. Leakage of mdc into the intestinal lumen is a sign of
bleeding in progress.
● Rx abdomen: to exclude occlusion (loops distended with gas) and perforation (free gas in
abdomen, under the diaphragmatic sickle).
● Abdominal ultrasound: to look for retroperitoneal abscesses or fistulas (between intestinal or
entero-vesical loops).
● CT scan of abdomen: to reveal peridiverticulitis (inflammation of the peridiverticular fat and
oedema).
● Endoscopy: not to be performed urgently, due to the high risk of perforation of inflamed
diverticula; serves to exclude the presence of neoplastic stenosis.
● Colonoscopy: 1st choice (after acute bleeding), in doubtful cases should be supplemented with
EGDS. It allows three types of bleeding to be distinguished: intra-diverticular - peridiverticular - inter-diverticular mucous.
● Laparoscopy - exploratory laparotomy
DD: Appendicitis - Gynaecological diseases - Inflammatory bowel diseases - Ischaemic colitis Mesenteric ischaemia - Nephrolithiasis - Tumour perforation.
Therapy
In the presence of diverticula, which are usually asymptomatic, there is no therapeutic rationale.
Conversely, control over these diverticula must come through regular physical activity and thus
prevention of symptoms and evolution.
In uncomplicated diverticular disease, medical therapy has the function of reducing bacterial activity,
bacterial overgrowth, inflammation, fibre degradation and also reduces gas production. Medical
therapy involves the use of Rifaximin+Metronidazole - either one or the other or in combination - plus
bacterial flora and fibre supplements.
In the case of uncomplicated diverticulitis: antibiotics - spasmolytics - anti-inflammatories;
prebiotics and
probiotics.
The patient with complicated diverticulitis should be kept fasting, hydrated (also parenterally) and
treated with combinations of broad-spectrum, Gram-specific antibiotics.
After two or more diverticulitic episodes, the indication is given for surgery (resection and
anastomosis at once), to be performed in an election, during an interval of clinical silence.
If medical therapy fails and the inflammatory process develops into an abscess or a
peritonitis, from perforation, surgery becomes indispensable.
o Perforation with circumscribed peritonitis: a conservative approach is attempted for 24 hours.
If there is an improvement we continue with percutaneous drainage, otherwise a recto-colic
resection with recanalisation is performed in a time.
o Perforation with diffuse peritonitis: urgent surgery is performed.
Pz Hinchey I, therefore with a paracolic abscess or phlegmon: medical therapy and possibly surgical
therapy in election.
The procedure to remove the abscess is percutaneous, it can be CT guided or ECO guided, it can be
transrectal or transvaginal if the abscess is posterior, it can be transrectal or transvaginal
obviously rarely because in that case we have done nothing more than stimulate the formation of a
fistula between the sigma and the rectum in the first case and between the sigma and the vagina in the
second case, sometimes the endoscopic transluminal route can be an additional help. The relief and
drainage of the abscess necessitates a culture examination with antibiogram and after 24-48 hours I
must absolutely expect lysis of the fever, a significant improvement of the sepsis, otherwise I must go
for surgery as a matter of urgency.
N.B. The abscess should not be subjected to percutaneous drainage when there are particularly
important neighbouring structures, for example when it is close to large vessels such as the iliac vein,
the iliac artery, when the patient is in an inadequate general condition, perhaps because of a major
spinal deformity, or even when it is too small - under 3 cm - because there is obviously no point in
draining an abscess under 3 cm and it is unlikely to evolve, if the patient is adequately covered by
antibiotic therapy. So in that case, intravenous antibiotic therapy and serious CT checks to see how the
situation evolves
Pz Hinchey II
● In 75-80% of cases, percutaneous drainage is sufficient to control the sepsis (an abscess
larger than 5cm in diameter hardly responds to simple antibiotic therapy). This will be
followed by the so-called long-stage procedure, i.e. a one-stage resective procedure, when the
sepsis is controlled. The procedure consists of resection and anastomosis in one time, i.e.
resection of the pathological sigma and then the creation of an anastomosis between the
descending colon and the rectum, which are the intestinal segments respectively upstream and
downstream of the pathological sigma that has been removed.
● Conversely, in 20-25% of cases, if the percutaneous drainage fails to control the sepsis, we
move on to emergency surgery and in that case we can go ahead with a procedure that can
always be either a one-stage or a two-stage procedure, called a 'two-stage procedure', which
basically means that we can limit ourselves to doing the resection and pack the colostomy and
then, a few weeks later, we will reoperate the patient to reunite the descending colon with the
rectum.
Hinchey III and IV patients who are almost always candidates for the 'two-stage procedure', i.e. the
so-called Hartmann surgery, i.e. the resection of the sigma and the placement of a colostomy on the
descending colon.
Surgical procedures: (resection of rectum and left colon, 25-30 cm)
● 3-stage operation (colostomy and drainage; resection-anastomosis; colostomy closure),
● Two-stage operation (resection and double colostomy, or resection, terminal colostomy and
closure of the rectal stump i.e. Hartmann's operation, or resection-anastomosis and protective
colostomy; closure of the colostomy),
● One-time operation (resection-anastomosis, without colostomy).
APPENDICITIS ACUTE
A pathological condition characterised by inflammation of the appendix. It is the most frequent cause
of persistent abdominal pain in adolescents, but it is not uncommon in elderly subjects, who are also
the worst to treat, especially if it is a pc with diabetic neuropathy, with a misdiagnosed picture and the
doctor perhaps initially prescribing antibiotic treatment, here these appendicitis can become chronic
and perforate. Surgically treating a truly diseased appendicitis is not always easy, as it is often not in
its normal anatomical position.
In fact, the appendix can have different/ectopic localisations:
1) 65% of cases are retrocecal
2) 30% of cases are totally or partially pelvic: digito-ano-rectal exploration (EDAR) i s
recommended in cases where appendicitis is suspected in the pelvis (Douglas scream). On
history, in addition to abdominal pain, alvo closed with faeces but no gas for a few days is
reported. This site complicates the diagnosis, especially in women.
3) 5% of cases are extraperitoneal
In addition, cases of:
- Intestinal malrotation: pain will be felt in the left hypochondrium (DD with sigmoid
diverticulitis)
- Situs viscerum inversus: the appendix is in the left iliac fossa.
The latter two localisations, especially in the past, created problems when the approach was
laparotomic (today, however, laparoscopy is much easier).
Aetiopathogenesis
Inflammation of the appendix usually occurs as a result of obstructive factors:
1) In 60% appendicular lymphatic follicles;
2) In 35% faecal stasis or coprolites;
3) In 5% canalicular obstruction by :
- foreign bodies
- stenosis
- Tumours
In recent years, intestinal carcinoids are increasingly being associated with the appendix (even in
young people), which mimic appendicitis, but then on histological examination turn out to be
something else. In these cases we proceed with right haemicolectomy, and pre- and postchromogranin assays. Another tumour of the appendix is appendicular mucocele, which may evolve
into mucinous cystadenocarcinoma, one of the abdominal tumours with the worst prognosis.
Since the intraluminal contents of the appendix are highly septic, severe obstruction, in addition to
increased mucus production, leads to an infectious process, supported by resident bacteria, such as
E.coli, Klebsiella, Proteus, Pseudomonas, Streptococcus faecalis, Clostridium
Perfringens. The bacteria feed the inflammation involving the appendicular wall and the attached
vascular component.
This results in ischaemic suffering (resulting from the inflammation and compression of the wall),
which, if prolonged over time, leads to a necrotic-tissue condition, which evolves into gangrene and
then perforation (usually 24-36h after the initiation of the inflammatory process and thus inability of
the inflammatory process to cool down).
If, as a result of the perforation, involvement of the peritoneal cavity is triggered, which in most cases
is circumscribed, with a possible appendicular abscess (circumscribed peritonitis), but can also be
generalised (generalised stercular peritonitis), especially in cases of immunocompromised individuals
or if the perforation is early.
Circumscribed appendicular peritonitis is referred to as 'appendicular platron' because it is a hard
area that on percussion will give obtuseness, it is due to the epiploon and the epiploic appendages that
go to cover the initial perforative inflammatory phenomenon.
From an anatomopathological point of view, acute appendicitis follows steps:
1) Catarrhal appendicitis: oedematous and congested appendix with thickened meso;
inflammatory infiltrate, no peritoneal reaction, gives restitutio ad integrum
2) Phlegmonous appendicitis: purulent content and presence of inflammatory pseudomembranes;
presence of microabscesses, mucosal erosions, parietal venous thrombosis, and massive
inflammatory infiltrate. May result in peritonitis after perforation
3) Appendicitis gangrenosa: necrotic areas associated with fetid pus. This leads to diffuse
stercoraceous peritonitis.
In the diagnostic process:
Clinical examination
Anamnestic collection: note and investigate the subject's symptoms, who will have severe abdominal
pain.
Symptoms include:
a) Abdominal pain: in the vast majority of cases it is a visceral pain that originates in the
epigastric or periumbilical region and then later moves to the right iliac fossa. There may be
signs of peritoneal irritation, which is why it is important not to administer painkillers, which
may mask the evolution of the clinical picture (perhaps antispastics are used) for DD with renal
colic. In elderly or immunocompromised subjects, pain may begin along the lateral quadrants
of the abdomen, making diagnosis more difficult and delayed (often the picture immediately
becomes gangrenous). In the case of retrocecal localisation, the pain is localised to the right
lumbar region, with a symptomatology that may mimic urinary inflammation (to rule out this
hypothesis, the patient should be asked if he or she has had stranguria, pollakiuria, dysuria or
other symptoms in the previous days).
associated symptoms. If such symptoms were present, an EDAR could be performed, which
would simultaneously rule out uro-gynaecological pathology). It is possible for pain to radiate
along the medial aspect of the thigh. In the case of an appendix in the pelvic area, pain
generally occurs in the anterior wall of the abdomen in the retropubic area, possibly associated
with bladder or rectal tenesmus (EDAR confirms the possibility of a case of pelvic appendix);
b) Nausea and vomiting: in 95 per cent of cases, patients present with episodes of food vomiting,
which occur a few hours after the onset of symptoms.
c) Anorexia
d) Diarrhoea: rare
e) Constipation: persistent urge to evacuate, which is not satisfied by the alvine discharge.
f) Fever: may be lacking in the elderly and immunocompromised, as well as leucocytosis. Very
high in cases of peritonitis.
g) Alvo open to gases but not faeces
Objective examination
Objective signs in patients with acute appendicitis are:
- Precociously:
. hypomobility to breath acts
.maximum pain at Mc Burney's point (located in the first third of the line that ideally joins the
umbilicus to the right anterosuperior iliac spine) with no defensive reaction.
- Late:
. positivity of the Blumberg manoeuvre or rebound manoeuvre: light compression is applied
followed by decompression starting from apparently pain-free regions, looking for areas of
contracture accompanied by skin hyperesthesia; typically the manoeuvre i s always performed
near the Mc Burney point and its positivity is given by the pressure denoting circumscribed
inflammation of the peritoneal leaflet.
. Rosving manoeuvre, often inconstant. Initially, pressure is exerted in the left iliac fossa and
then upwards to compress the descending colon: if air is present, the gas progressing
backwards towards the right iliac fossa should cause pain and therefore the manoeuvre is
positive.
.manoeuvre of the psoas muscle: while lifting the right lower limb of the patient while keeping
the knee rigid, flexing the thigh on the pelvis, a slight compression is exerted on the right iliac
fossa and a reflex contraction of the psoas is induced, which in turn compresses the cecum and
appendix. The manoeuvre is positive if it elicits pain (bed of the gallbladder)
In the case of appendix in pelvic position with peritonitic process and effusion at the level of
the Douglas cavity, pain can be evoked by EDAR, especially at the right rectal wall (Douglas
cry)
Laboratory examinations
1) Leukocytosis: GB >10,000/mm3
2) Neutrophilia >78% of the leucocyte count
The rise in temperature, in the presence of alvus open to gas and not faeces, further confirms the need
for early intervention. It is possible that in the following hours the patient will report an improvement
in symptoms, with a decrease in fever and leucocytosis, from a laboratory point of view. If the patient
adds that for a couple of months he has tended to have diarrhoea for a couple of days a week, it is
important to temporarily postpone surgery and to schedule a colonoscopy for the following day,
because there is a suspicion of Chron's disease. If the colonoscopy is negative, the doubt of IBD is
removed.
X-ray examinations
1)
2)
3)
4)
No Direct abdominal X-ray in white or opaque clisma
Abdominal ultrasound evaluating:
Increased appendix volume
Thickening of the appendicular wall
Presence of saccate or abscess collections at the appendicular or periappendicular site
Presence of free effusion in abdomen
CT abdomen with mdc
Exploratory laparoscopy (in doubtful cases)
It goes into DD, with all those conditions leading t o acute secondary peritonitis, by propagation of the
inflammatory focus into the abdomen:
- Acute cholecystitis (if the appendix is ectopic)
-
-
Diverticulitis (in case of malrotation, and left appendix)
Liver abscess
Acute salpingitis (in women)
Acute mesenteric lymphadenitis (almost always associated with TB in patients coming from
areas with poor hygiene; poverty; hypo-nourishment)
- Right renal colic But also:
Right colon neoplasm
IBD (Chron's disease)
Alvarado Score
To facilitate diagnosis given the various cases of pain in the right iliac fossa, diagnostic scores have
been developed, such as Alvarado's, if it has
a very high positive predictive value for a score >7.
Therapy
1) Medical:
- Restoration of hydro-electrolyte balance (especially if the patient has vomited)
- Massive antibiotic therapy (initially intravenous bolus) and to be continued post-operatively
- Double peripheral venous access
- Nose-gastric probe
- Bladder catheter
2) Surgical: appendectomy, accompanied at the same time by drainage of any abscess collections
and cleansing of the abdominal cavity (usually warm physiological saline solution plus a
disinfectant and/or topical antibiotic is used to perform a toilet of the peritoneal cavity,
especially if perforated appendicitis has already been found). Keep the drain in place for 2-3
days.
In the laparotomic approach, there were three cuts made:
- Right pararectal
- Crusade
- Low
It provides:
a) Access to the abdominal cavity, using retractors
b) Dilatation of the aponeurosis of the external oblique muscle with the same tape retractors
c) Using blunt-tipped scissors, the bundles of the internal oblique muscle and transverse muscle
are opened
d) Using two Klemmer forceps, the peritoneum is found and the peritoneum itself is dissected
between the two forceps, and the abdominal cavity is entered.
e) Tie off the base of the appendix and dissect the appendicular artery after it has been tied off.
f) With the pliers, the meso is put under tension and gently detached from the appendix, so as to
isolate it
g) Tobacco bag packaging of the appendix
h) Appendix Section
i) Appendicular abutment sunk into the cecum
j) Closure of the peritoneum and previously dissected muscle planes
Today, laparoscopy is preferred: the appendix is detached from its meso, so as to make it mobile, by
means of an ultra scissor (siser) (ultrasonic scalpel that allows haemostasis and cutting). Once the
appendix has been mobilised, a loop is introduced at the base of the appendix, to isolate it from the
cecum (do not squeeze too tightly, as it could be perforated). Once it is tied (and isolated from the
intestine) it can be dissected using the ultra scissors. Once it has been dissected, it is placed inside the
endobag (a bag) so that it can be easily removed from the outside.
MUCOCELE APPENDICULAR
Mucocele of the appendix is understood to be a distention of the viscera by accumulation of mucus
within it; possible causes are: retention due to obstruction of emptying by faecalitis and congenital
abnormalities, epithelial hyperplasia, cystadenomas (63-84%) and cystadenocarcinomas (11-20%).
The distension of the lumen is progressively more pronounced in the four 'causative' subtypes
described, up to the possible rupture of the viscera with consequent dissemination of muco-secreting
epithelial cells in the peritoneal cavity, configuring the fearsome picture of pseudomyxoma peritonei.
The clinical presentation is varied. In 25% of cases appendicular mucocele is asymptomatic and the
diagnosis is made during investigations performed for other reasons. Otherwise it may present with a
picture mimicking acute appendicitis; in some cases it presents as a palpable mass. Finally it may
present with a complication, such as invagination occlusion, enteric haemorrhage, compression
hydronephrosis on the right ureter, pseudomyxoma peritonei.
CARCINOID APPENDICULAR
Appendicular carcinoid is a usually benign tumour, occasionally diagnosed in 36% of cases, with a
survival rate of over 95%.
When the tumour is less than a centimetre in size (70-90%) it should be treated with a simple
appendectomy. When larger, however, it shows a high metastatic trend and should therefore be treated
with a right haemicolectomy.
PROCTITE
Proctitis is the inflammation of the mucous membrane of the rectum (rectal mucosa). The
inflammation originates from numerous causes, from infection to radiation therapy.
Depending on the cause, proctitis may be painless or very painful. The diagnosis is made on the basis
of an objective examination of the inner surface of the rectum.
If proctitis is caused by an infection, it can be treated with antibiotics. Corticosteroids can be applied
to the affected areas or sometimes taken orally to treat proctitis caused by radiotherapy.
COLON POLYPS- RECTAL
Colorectal polyps
A polyp is a macroscopic protrusion of the mucosa, up to several cm in size (polyps of at least 5 mm
in diameter are considered significant). They can be:
● Single or multiple;
● Flat (raised, flat, not repressed or excavated areas, mixed raised with central depression and mixed
depressed with raised margins) or exophytic (pedunculate, semi-pedunculate or sessile; sessile
carries a greater risk of CCR).
● Congenital - inflammatory - neoplastic (adenomas or adenocarcinomas).
Neoplastic mucous polyps
Adenomas: are benign neoplastic mucous polyps formed by cell expansion not limited to a segment of
the glandular crypt. They have a malignant potential depending on size, number of lesions, degree of
dysplasia and the presence of the villous component.
Evolution to CCR is frequent and takes about 10-12 years (adenoma-carcinoma sequence).
● Tubular adenomas: more frequent.
● Tubulo-villous adenomas :
● Villous adenomas: more frequent in the rectum, they are larger than the others and present as
sessile cauliflower-like lesions.
● Serrated polyps: prevalent proximal to the splenic flexure and <1 cm.
Adenocarcinomas are the malignant evolution of adenomas, either in situ or infiltrating. An adenoma
with high grade dysplasia (cell atypia) should be considered a carcinoma in situ.
Most adenomas are asymptomatic. Adenomas >1 cm may give:
● Haemorrhage, with anaemia, rectorrhagia or occult faecal blood;
● Sudden changes in defecation;
● Rectal prolapse;
● Abdominal pain;
● Obstruction;
● Hypersecretory syndrome (for villous adenomas), with hypokalaemia and marked mucous
secretion.
Other injuries
● Non-neoplastic mucous polyps: e.g. inflammatory - hyperplastic (adenomatous-like, in the
elderly) - juvenile - hamartomatous polyps in Peutz-Jeghers syndrome. They have no malignant
potential.
● Non-polypoid neoplastic lesions: slightly elevated, depressed or flat.
● Submucosal lesions: lymphoid nodules - lipomas - carcinoids - fibromas - leiomyomas endometriosis.
Polyposis
● Familial adenomatous polyposis: these are multiple polyps that riddle the entire surface of the
colon but may also affect other parts of the gastrointestinal tract. They are tubular adenomas
but have a very high incidence of progression to adenocarcinoma of 100%. It is due to
mutations in the APC gene located in the short arm of chromosome 21; it accounts for 1% of
colorectal carcinomas.
● attenuated familial adenomatous polyposis, which has a somewhat later incidence and is
characterised by a smaller number of polyps that develop mainly in the ascending colon and
progresses to neoplastic disease to a slightly lesser extent;
● Gardner's syndrome: even rarer, it is merely a variant of familial polyposis in which classic
adenomas are associated with other lesions in other organs such as multiple osteomas,
epidermoid cysts, uterine fibroids, congenital hypertrophy of t h e retinal pigment epithelium,
and thyroid tumours;
● Turcot syndrome: this is also rare; it is the coexistence of FAP and hereditary non-polyposis
colorectal cancer (HNPCC) also called Lynch syndrome.
Endoscopic screening
Repeat at 5 years in the case of low-malignancy polyps and at 3 years if at greater risk. Endoscopy
also plays an important role in deciding whether surgery is necessary or not (for very large polyps,
surgery may be necessary in any case). In general, all adenomatous polyps have malignant potential
and should be removed.
The choice of the therapeutic act to be applied is made by assessing: diameter of the polyp (<1 cm
are rare foci of ADK), type of polyp (villous is more risky), infiltration of the submucosa (divided
into three layers; if only the superficial third is invaded, endoscopic treatment will also be fine).
Depending on the size and morphological characteristics of the polyp, it is possible to perform:
- Polypectomy with loop and diathermy
- Endoscopic mucosectomy
- Endoscopic submucosal dissection (ESD)
Endoscopic polypectomy
It is considered curative when histology reveals a non-invasive lesion or a well-differentiated invasive
lesion with a free resection margin of at least 2 mm.
Chromoendoscopy: makes use of vital dyes that are injected onto the lesion in order to demarcate it
and determine whether it is endoscopically resectable or not and to assess its vascularity. Modern
endoscopes are equipped with a special light and do not need this technique (virtual
chromoendoscopy).
● For the removal of pedunculated polyp, a loop is used. The polyp is strangled at the base, then
closed around it, a current is run through it and then it is resected and removed.
● For the removal of sessile polyps, physiological saline or hyaluronic acid can be injected
submucosa. If, following infiltration, the polyp rises, it is not infiltrated and can be extirpated
without risk of complications ('injection and cut'); if it does not rise, it can be marked with
particles so that it can be easily found in the event of a histological indication for surgery.
Endoscopic mucosectomy
This is another technique that uses an instrument, a kind of 'cup', that sucks inside the endoscope.
Saline solution is always injected, which lifts the sessile lesion without a stalk, which is then sucked
into this 'glass' (or cap) and then throttled and removed.
Endoscopic submucosal dissection
It is an endoscopic dissection not only of the mucosa but also of the submucosa. It has rather precise
indications in the procedure:
- Very flat sessile polyps with a wide implantation base
-
Excision of the lesion larger than 2 cm but without fragmentation, i.e. in one go
The technique is not yet up-to-date because they are very time-consuming techniques that require
dedicated instrumentation and whose execution time is quite long (more than two hours), so it is also a
major inconvenience for the patient.
Colonoscopy complications
Every procedure has a certain degree of complications: diagnostic colonoscopy has a fairly low
degree of complication, while operative colonoscopy, i.e. when a lesion is removed, has a somewhat
higher incidence of complications but which never exceed 3%, such as bleeding, which is the most
frequent complication. Another complication that is the bogeyman for all endoscopists is perforation.
The prevention of bleeding is done with different techniques:
- Positioning of clips
- Submucosal injection of adrenalin or glue
- Endoloop, for sessile polyps. These are ligatures, in which the base of the polyp is tied with a
ligature and only then is the ligature (the loop) removed inside the colon
Bleeding can be treated with:
- Thermocoagulation, with the diathermic loop through which an electric current passes
- Elastic binding
- Clips
- Endoloop
- Ansa choking the polyp
Endoscopy vs surgery
For small lesions that do not reach the muscular tonaca (and in some cases the submucosa) certainly
endoscopic therapy is the therapy of choice: i.e. small malignant polyps, intramucosal
adenocarcinomas or carcinoma in situ (i.e. early colorectal cancer) can be treated by endoscopy and
must be treated by endoscopy. Whereas larger diseases, above T2, with or without lymph node
metastases must be treated by the surgeon and then surgical resection of the intestine must be
performed.
-
-
Low-risk polyps, i.e. those with a resection margin of at least 2 mm from infiltration, without
lymphovascular infiltration and with a low grading, have a low risk of having to be operated on
by the surgeon and therefore a low risk of recurrence or distant lymph node metastasis.
High-risk polyps are those whose resection margin is less than 2 mm, which have
lymphovascular infiltration, resection margin infiltration is present, and have a higher grading,
i.e. the degree of differentiation is lower.
Indications for surgery
-
Polyp in the vicinity of another tumour: so when there are two lesions and one is frankly
neoplastic, then surgery must be done
Frankly neoplastic polyp in a subject with no particular contraindications to surgery
-
Too big polyps
Polyps in areas not easily accessible (blind areas)
Recurrent polyps
Small but frankly advanced cancers
When one does not have the appropriate instrumentation or experience, in such cases it is
certainly preferable not to put the patient at risk and to refer him to the surgeon.
COLORECTAL CARCINOMA
It is the second most fatal neoplasm in the world, after lung cancer.
;
;
% FAP - 3% HNPCC).
Risk factors
●
●
●
●
●
●
Familiarity or genetic syndrome (FAP, HNPCC) or history of Kcolon - dysplasia - polyps
Age >50 years (early onset <40 years is a sign of poor prognosis)
Obesity - sedentariness - smoking - alcohol - carcinogens - irradiation of the pelvic region
IBDs, and in particular CU (x5.6)
Immunodeficiency
Diet: low in fibre (which accelerates gastrointestinal transit by reducing contact time between
carcinogens and mucosa) and high in fat, especially animal fat and cholesterol (increased
synthesis and secretion of bile acids and increased cell proliferation). Red meat.
Ureterosigmoidostomy.
● Daily consumption of low doses of aspirin protective
Pathogenesis
Most CCRs develop from pre-existing adenomas, according to the adenoma-carcinoma sequence:
initiating mutations produce the adenoma (hyperproliferation, inhibition of apoptosis, increasing
degree of dysplasia), and with promotion they progress to carcinoma.
80% of CCRs develop from adenomatous polyps, 20% from serrated adenomas (?).
Genetically, three pathways can lead to sporadic CCR that have in common the activation of the Wnt
pathway.
● Chromosome instability pathway (CIN - 85%): APC → kRAS → DCC → p53, SMAD,
PIK3CA. In CU-related carcinomas there is an early mutation of p53, and only later of APC.
● Microsatellite instability pathway (MSI - 15%): MMR, hMLH1 → microsatellite mutations,
p53. Microsatellite instability is due to mutation or hypermethylation of mismatch repair (MMR)
genes, similar to what occurs in Lynch syndrome (morphologically similar).
● Promoter methylation pathway (CIMP): several oncosuppressors are silenced by promoter
methylation, and B-RAF mutations with reduced apoptosis are common. It is the most frequent
pathway in carcinomas evolved from serrated adenomas.
Focus: Lynch Syndrome
This is an autosomal dominant syndrome and is the most frequent form of hereditary large bowel
adenocarcinoma although it still accounts for 2% of all colorectal carcinomas. It is now characteristic
that this syndrome is caused by the mutation of genes of the mismatch repair (MMR) system family
and as a result of this solid tumours develop only in the colon-rectum (Lynch syndrome 1) or may be
associated with cancers of the endometrium, ovary and urinary tract (Lynch syndrome 2). In Lynch
syndrome, however, the tumour mainly affects the right colon and the occurrence of other tumours
may be simultaneous (synchronous tumours) or at a distance (metachronous tumours).
Macroscopy: vegetating (protrudes into the lumen), ulcerated (bowl-like morphology with irregular
margins), infiltrating (affects the full thickness of the wall) or stenosing (causes an obstruction to
intestinal transit). Each form is associated with a different clinic. Usually the macroscopic features also
correlate with the site of the lesion:
1) Right:
- Vegetant
- Ulcerated
2) Left:
- Stenosante
Histology: adenocarcinoma is the most frequent. The mucinous histotype has a worse prognosis and
responds worse to chemotherapy.
Symptoms
They depend on the site and stage of the neoplasm: in the right colon they are later and more systemic,
whereas a neoplasm in the sigma or rectum more easily gives rectal bleeding and/or tenesmus.
● Bleeding (78%): occult or manifest with rectal bleeding (58%, >in the sigma-rectum), anaemia
●
●
●
●
●
●
(57%, > in Cdx). Cd with amorroids - anal fissures - diverticulosis - IBD.
Chrompiform abdominal pain: frequent (52%) in late phase. Dd with IBD - IBS - diverticulitis.
Weight loss (39%): it is greater in Cdx/sx because the disease has a longer duration due to the
calibre of the lumen (the neoplasm grows and draws in nutrients)
Diarrhoea (22%): dd with IBS - diverticulitis - IBD; alterations of the alvus especially in the
sigma- rectum.
Nausea and vomiting (22%)
Tenesmus (10%)
Regardless of the site in 10% of cases it starts with intestinal occlusion, 5% perforation.
Symptomatology according to shape, macroscopic growth appearance and location:
● Right colon: the lumen is wide and the walls thin and extensible (passage of liquid faeces) and
vegetative forms are more frequent. Symptomatology is late: anaemia (from oozing), asthenia. In
advanced stages pain, palpable mass, weight loss.
● Left colon: collects slightly more formed faeces and often the morphology is sleeve-like. Basic
symptoms: change in alvus (intermittent, sometimes diarrhoeic and sometimes constipated),
appearance of appreciable blood; abdominal pain as distention affects the other hemicolon.
Presentation is generally earlier.
● Rectum: more obvious symptoms, although the presentation may be subtle in non-occlusive
ulcerated bowl-shaped forms. Rectal bleeding or haematochezia, sense of rectal heaviness,
emission of stools of reduced calibre (ribbon-like, pencil-shaped), alternating between diarrhoea
and constipation (because the stools find a mechanical obstacle and undergo bacterial degradation
and become fluidised; may also occur in chronic diverticulitis).
Complications
● Haemorrhage - mechanical occlusion - perforation (at the level of the sigma due to erosion of
the wall; at the level of the cecum due to increased upstream pressure in the case of tight stenosis
of the rectum).
● Invasion or compression of neighbouring structures (bladder, ureters, vagina)
● Metastases (local or distant) e.g. hepatic impairment: hepatomegaly, jaundice, ascites.
CCR diagnosis and staging
● Rectal exploration: allows the diagnosis of 30-40% of neoplasms, not only because of rectal
localisation (20%) but also because of the possibility of finding other abnormalities such as traces
of blood.
● Occult blood in faeces: it is effective in screening but there are many false positives and not
infrequently also false negatives.
● Colonoscopy: is part of population screening from the age of 50, with variable frequency
depending on clinical risk factors. Another option is virtual colonoscopy. Together with
endoscopic biopsy it allows TNM or Dukes staging.
● Optic Clism of the colon: it has been superseded by CT. It allowed characteristic images such as
'apple core' to be seen.
● CT scan: very important for diagnosis and staging
● Ultrasound abdomen: to look for liver metastases.
● Echendoscopy: to estimate the degree of wall invasion.
● MRI: very useful in evaluating the pelvic cavity and mesorectum (where lymphatic and blood
vessels pass; its involvement is associated with a worse prognosis) and the sphincter portion of the
rectum.
Diffusion modes:
● Local: continuity in a circumferential direction (occlusion, it is ''better for the patient'') or
longitudinal in the viscera (affects resection margins); contiguous or radial (dangerous fat);
exfoliative dissemination (if the visceral peritoneum is exceeded, with possible peritoneal
carcinosis).
● Distant: via the bloodstream through the portal (liver) or systemic (lung; especially in the case of
the lower rectum) circulation; via the lymphatic route: danger lymph nodes, intermediate, etc.
Lymphatic drainage of the colon, the lymphatics of:
● Cecum, CA and CT prox drain to the lymphatics attached to the superior mesenteric aa (middle
colic and ileocolic aa);
● CT, CD, sigma and rectum drain to the lymphatics located along the course of the lower mesenteric
aa (left colic and sigmoid aa).
Classification of Dukes
- A: limited to the mucosa
- B1: reaches the muscle tonaca; negative lymph nodes
- B2: infiltrates and exceeds muscle; negative lymph nodes
- C1: extends up to the muscle tonaca without overcoming it with positive lymph nodes
- C2: passes the muscle tonaca with positive lymph nodes
- D: Distant metastases
Therapy
Multi-media approach with surgery, chemotherapy, radiotherapy and endoscopy (e.g. in a patient with
a substenosing neoplasm, a metal stent can be inserted to pass the acute phase of the occlusion and
make the procedure easier).
Staging, therapy by stage and 5-year survival (S) after surgical excision
Stage I (Dukes A)
T1/2 N0 M0 Max
muscle tunic
Stage II (Dukes B)
T3/4 N0 M0 Peritoneum
Dangerous fabric
Stage III (Dukes C)
N1/3 M0
Lymph nodes
Resection
surgical
without chemo
S: 100%
Resection
and
adjuvant
chemotherapy if there are FdRs
of minimal residual disease and if
there is no high microsatellite
instability (do not benefit from
chemo)
S: 50-75%
Resection
with
chemoradiotherapy
S: 30-50%
Stage IV (Dukes D)
M1
Distant metastasis
Chemo o surgery
selected sites
S:5%
at
T1: infiltrates submucosa (contains lymphatics and may give metastasis) and muscularis propria.
T2: infiltrates the subserosa minimally.
T3: extensive subserosal infiltration.
T4a: visceral peritoneum; T4b: invasion of other organs or structures.
FdR of minimal residual disease: high grade, complications, lymphovascular or perineural invasion,
high ratio of positive/examined lymph nodes, resection of few lymph nodes, mucinous histotype, high
CEA, etc.
The rectum begins at the level of the body of S3, where the large intestine loses its mesentery.
● Intraperitoneal: transverse - cecum - sigma - 1/3 Sup rectum.
● Extraperitoneal: CA - CD - 2/3 Inf of rectum. Infiltrates kidney, spleen etc. has an even later
presentation.
Surgery
Wherever possible, this is the first approach. The possibility of radically resecting the neoplasm
depends on:
● Local extension: if infiltration of contiguous structures is present, surgical radicality is related to
the possibility of en bloc removal of everything involved in the neoplastic process. Peritoneal
carcinosis excludes any curative potential.
● Regional extension: spread to the lymphatic system conditions prognosis; extensive
lymphadenectomy is essential for correct staging and has curative value. Involvement of the
interaortocaval lymph nodes is considered an indication of generalised disease.
● Distant metastatisation: only a few confined liver or lung metastases are amenable to excision
with radical intent. In some cases synchronous liver metastases can be resected simultaneously
with the primary tumour, with R0 resection (haemicolectomy + right hepatectomy of the V, VI,
VII and VIII segments).
Oncological radicalisation, surgical demolition must include:
● Intestinal segment site of neoplasm with safe margins (5-7 cm in the colon; 2-3 cm in the rectum)
● Removal of the associated mesentery with district lymphatic drainage stations up to the origin
of the vascular pedicle (extensive lymphadenectomy). It is necessary to remove at least 12 lymph
nodes in the colon (14 in the mesorectum) for the operation to be valid (the more are removed the
more valid the operation).
● Ligation of the vascular pedicles at the emergence from the mesentery, to be performed before
manipulating the tumour (no touch isolation technique).
● For rectal tumours: removal of rectum, mesorectum and the vascular and lymphatic support up to
the origin of the inferior mesenteric artery. By respecting the nerves of the pudendal plexus (nervesparing technique), problems such as neurological bladder, retrograde ejaculation and erectile
dysfunction are avoided.
● For tumours < 5 cm from the anal margin, which are small, well-differentiated and without
lymphovascular and perineural infiltration, a distal margin of 1 cm may be considered acceptable.
Types of surgery:
● Right haemicolectomy: for tumours of cecum, CA, hepatic flexure and proximal CT. Resection of
the last ileal loop, cecum, ascending colon, hepatic flexure and ligation at the origin of the right
ileo-colic artery; mesentery with pertinent lymph nodes; then terminus-lateral or latero-lateral
anastomosis between ileum and colon in one operation
● Left haemicolectomy: tumours of distal CT, splenic flexure, CD and sigma (up to recto-sigmoid
junction; colo-rectal anastomosis). Ligation of the inferior mesenteric artery at the origin and the
inferior mesenteric vein at the subpancreatic level.
● Anterior rectal resection: for tumours of the sigmoid-rectal junction, upper and middle rectum;
low colorectal anastomosis. Same vein and artery ligatures as left haemicolectomy.
● Abdominal-perineal amputation according to Miles: for tumours of the lower rectum (less than
3 cm from the anal margin): removal of the distal CD, sigma, rectum and anus in its entirety (anal
canal, skin, sphincter apparatus, elevator muscles and cell-adipose tissue of the ischio-rectal and
pelvi-rectal fossae); definitive colostomy in the left iliac fossa.
● Trans-anal techniques (another option for rectal cancer): Low morbidity and mortality rates.
They are indicated only for low-risk T1 tumours (mobile, < 3-4 cm, well or moderately
differentiated, < 8 cm from the anal margin and without clinically detectable lymph node
involvement), with cure rates comparable to those of abdominal procedures.
The main limitation of these techniques is the inability to assess the status of loco-regional lymph
nodes.
R0 resections cannot be defined as: not en bloc, with infiltrated margins, with residual disease in
regional lymph nodes, with regional lymph nodes that cannot be assessed.
The choice of a colostomy or ileostomy depends on:
- How high is the neoplasm
- Condition of the intestine upstream of the neoplasm (i.e. how compromised it is, either because
it is upstream of a mechanical occlusion by stenosing neoplasm, or because it causes
overdistension; which in turn causes diastasis of the walls)
- From the general condition of the patient
- From age
- From comorbidity
There are colostomies and ileostomies:
a) Terminal, full-thickness (transitional or definitive): in which the colon or ileum tracts end
up, after resection, attached to the full-thickness wall: the final part of the resected, interrupted
tract is taken outside, through the full-thickness abdominal wall (the abdominal wall has
various thicknesses from the peritoneum down to the skin), with the packing of a colostomy or
ileostomy in which the intestinal contents come out through it;
b) Barrel or rod-mounted: this is nothing more than an outward diversion of a section of colon
or ileum without resecting the intestinal tract itself. This technique consists of opening the
intestine at a point on the anterior wall, taking it out and thus keeping the intestinal continuity
intact, so that the intestinal contents instead of continuing down through the intestinal loop,
flow outwards. Only a very small portion continues towards the residual part of the intestine.
Liver metastases: most are metachronous and liver failure is the main cause of death. They can be
divided into resectable (attempting R0), unresectable and potentially resectable with preoperative
chemotherapy (maximum 3-4 cycles), surgery if there is a response and then postoperative chemo.
Anti-VEGFs should be discontinued for about 30 days before and after surgery to avoid bleeding,
delayed healing, etc.
After non-curative surgery, adjuvant therapy is performed with:
● chemotherapeutic agents (5-fluoro uracil, folates, oxaliplatin, etc.);
● MAB, e.g. anti-EGFR;
●
radiotherapy.
Radiotherapy complications
Acute: diarrhoea, crampy abdominal pain, proctitis-tenesmus, dysuria.
Late (>6 months post-RT): diarrhoea, proctitis, obstructive tenuous symptoms, incontinence.
Screening and surveillance in colon cancer
There is a difference between screening and surveillance:
- Screening: is an organised programme of early diagnosis conducted on an entirely
asymptomatic population, and serves to direct a diagnosis towards an early-stage disease. It is a
low-cost investigation and must reach the entire target population at risk, and the earlier the
disease is identified at the earliest stage of its natural history, the more likely it is to be treated
effectively.
- Surveillance: is the monitoring of that population that has already been identified as patients at
risk of neoplastic disease or with neoplastic disease for example those neoplastic or preneoplastic diseases such as hereditary diseases.
In colon cancer, a certain type of screening with non-invasive investigations was initially hypothesised
but it turned out that there is a certain level of non-significance of some investigations because the best
investigation is obviously the colonoscopy.
Screening should also be done in those conditions of familiarity: in fact, patients who have colon
cancer have been told that their closest family members should also have a colonoscopy. In particular,
there are AIOM recommendations which are:
- Individuals who have only one first-degree relative with CCR and diagnosed after the age of
fifty, have a double/triple the risk of the general population and are therefore screened with
colonoscopy from the age of forty
- Individuals who have a first-degree relative with CCR before the age of 50 or two first-degree
relatives have an even higher risk and therefore screening is recommended from the age of 40
or at an age 10 years younger than the relative's age at diagnosis.
Screening is not necessarily colonoscopy, in fact there are various types of screening possible:
- Faecal occult blood detection
- Sigmoidoscopy
- Combination of occult blood in faeces and sigmoidoscopy
- Virtual colonoscopy or video capsule
- Double-contrast schism, an examination that is increasingly rarely done
In some cases, the faecal occult blood test (which is another screening modality) has been
hypothesised in the beginning and has some efficacy but the possibility of false negatives or false
positives is higher than for a colonoscopy.
Bowel preparation colonoscopy
- PEG-based (polyethylene glycol) solutions that can be administered at high volumes (3-4
litres) or even low volumes (2 litres)
- Sodium phosphate cathartics
- Magnesium laxatives
SELG-Esse 1000 is a macrogol containing salts where 'S' stands for simethicone which reduces the
amount of gas.
PILONIDAL CYST (SINUS) OR CYST SACROCOCCYGEAL
Frequent in young people who have particular hypertrichosis in the intergluteal fold within the
coccygeal raphe. This area is rich in saprophytic flora. This cyst is generally characterised by the
abnormal presence of hair bulbs.
The pilosebaceous apparatus assumes a deep stratification and is unable to have an outlet to the
outside and grows in depth. Over time, the ball of hair is incorporated into a granuloma that has a rigid
plane underneath (the coccyx). Moreover, being mechanically stressed by walking, trauma, hormonal
stimuli, secretions from the intergluteal groove, a purulent reaction can occur due to that abundant
saprophytic flora. The inflammation gives a striking painful symptomatology.
The congenital hypothesis linked to embryonic vestiges on which inflammatory factors are triggered
was more in vogue in the past. More frequent in men.
Clinic
Initially, it is scarce. However, it may become important due to suppuration of the cyst with formation
of fistulous trachytes.
Therapy
In emergencies, surgery with incision and drainage is used. Even here we do not have the certainty of
a cure, but precisely because it is treated urgently it can often recur because perhaps the cleaning is not
very good.
In the election, the non-inflamed cyst and any fistulous trachytes are removed. It must be a profuse
excision, reaching as far as the presacral fascia. Recurrence is less likely here.
At this point one can close with the OPEN technique (second intention) with a very long healing time
of about 6 months with a low recurrence rate (1.4%) compared to the CLOSED technique where
healing takes about 20 days but recurrences are more frequent (3.4%).
Cave: treat this cyst early because it may eventually involve the rectum.
ANO
ANATOMY OF THE CANAL ANAL
80% sporadic CCR 16% familial CCR 4% hereditary CCR (
Rule of 4: each individual segment of the anal canal, lower rectum, middle rectum and upper rectum
has a length of about 4 cm, which changes by plus or minus 2 cm (i.e. 4+2) depending on the
constitution of the subject.
Each individual segment has a length of 4 cm and the rule of 4 makes it possible to distinguish very
precision, with the introduction of an anoscope in a caudocranial direction from the anus to the rectosigmoid joint, the first 4 cm segment for the anal canal, the second 4 cm segment for the lower rectum,
then the middle rectum and finally the last 4 cm segment to the recto-sigmoid joint.
In addition to the anatomy of the lumen with Houston's valves, one must also consider the junction
elements between the stratified pavimentous epithelium of the anal canal and the cylindrical
epithelium of the colon mucosa, which come together at the dentate line.
Outside the dentate line, there is the intestinal mucosa and submucosa and then a muscular structure
that is considered the internal sphincter, which is nothing more than a thickening of the muscular
wall of the large intestine that, at this level, takes on the dignity of the anal sphincter, a sleeve made of
smooth muscular tissue. Outside of this is the external anal sphincter which is a thickening of the
elevator muscle of the anus, also called the 'pelvic diaphragm', which closes down the pelvis and
prevents herniation of the viscera below the perineal plane.
Between these two sleeves, there is the inter-sphincter space.
CONDYLOMAS OF THE ANUS
They are caused by infection with the papilloma virus (HPV, subtypes 16 and 18 above all), which is
an oncogenic virus; in fact, from condyloma, which is a benign lesion, one can progress to squamous
cell carcinoma. They are usually found in the perineal area.
From the pathophysiological point of view: the chronic inflammatory insult and the continuous
regenerative stimulus that HPV infection causes, initially leads to cell hyperplasia (of basal cells above
all), which then gradually, with the accumulation of mutations, can lead to the onset of carcinoma.
For such diseases, then the HPV vaccine becomes essential for prophylactic purposes.
They are classified into:
- Plans
- Acuminate (or 'cockscombs')
Condyloma of the anus in fact stands in DD with anal squamous cell carcinoma, which will be treated
with abdominal-perineal amputation according to Miles, a fairly demolitive operation.
Signs of possible transformation/malignancy :
- Large dimensions
- Possible bleeding
- Ulcerations
- Occurrence of relapses
- Growth in a short time
-
Therapy includes:
Cryotherapy
Imiquimod
- Podophyllotoxin
- Laser
- Surgery: excisional condyloma biopsy and histological examination to exclude neoplastic
diagnosis
ABSCESS PERIANAL
An abscess is a purulent collection in a newly formed cavity. If it were pre-formed we would call it an
empyema. This newly formed cavity is formed because our organism reacts against these bacteria that
locate themselves in a certain region of our body, usually a soft tissue or parenchyma. The tissue
inside an abscess is destroyed because in addition to the bacteria, there are the neutrophils that have the
function of destroying the bacteria (as well as the tissue): the result of this is that the tissue goes into
colliquation and thanks to the fibrotic reaction all around it, there is the formation of an abscess. The
abscess then has to be drained: it cannot stay inside the body as bacteria could take the blood route
causing sepsis. So the abscess has to be drained, and this drainage can be surgical or spontaneous
(fistula).
The peri-anal abscess forms from the anal glands of Hermann (which are located at the level of the
serrated line), which become inflamed, following the obstruction of one of the glandular ducts that
flow precisely at the level of this line into the crypts of Morgagni and then infection occurs. Then the
micro-abscess that then forms from the anal gland then flows into the inter-sphincteric space and this
is the primum movens for this pathology to spread everywhere.
A fistula, on the other hand, is a continuous solution, congenital or acquired, which does not tend
towards spontaneous healing and which connects a natural or pathological cavity with the outside or
two natural cavities with each other. The fistula then is a form of protection of our organism against
this bacterium, in fact it tends to eliminate all waste either within a cavity (e.g. the fistulas of Chron's
disease, with the formation of entero-enteric fistulas) or by taking the skin route (entero-cute).
The formation of an anal abscess represents the acute expression of the event, while the fistulous
passage (or fistula) represents its chronicisation.
Abscesses and peri-anal fistulas represent the expression of the same inflammatory phenomenon that
recognises as a common pathogenetic event: infection and obstruction of the anal glands [which can
be caused by:
- Microtrauma of the mucosa
- Anal intercourse
- Presence of diarrhoeal stools
- Emission of stools of increased consistency
- Foreign bodies
- Infections of fissures and haemorrhoids (rare)]
Classification
These are therefore pus-filled cavities in the intersphincteric space and are classified into:
1) Perianal/marginal abscess (60%): the purulent process descends from the gland towards the
subcutis and drains directly outside. It is easily recognised near the anal rima
2) Ischio-rectal abscess (25%): the inflammatory process extends towards the external sphincter
3) Intersphincteric/intramuscular abscess (5-10%): from the anal glands between the smooth
and striated sphincter
4) Pelvi-rectal or supra-elevatory abscess (5%): the infection spreads cranially, beyond the
e l e v a t o r muscles, between the peritoneal sac and the elevator muscle of the anus. Very
dangerous as it is separated from the viscera by the peritoneum alone
Clinic
Clinical symptoms are characterised by:
Signs of inflammation: of the perianal skin (perineal abscess) or the gluteal region (ischiorectal
abscess)
- Tumefaction (tumor)
- Intense pain (dolor); the painful symptomatology is exacerbated by sitting, movement and
defecation. In the case of a pelvi-rectal abscess: 'deep' rectal pain, radiating to the buttocks and
associated with dysuria.
- Rubor
General symptoms: fever with chills will occur (continuous or intermittent type, with afternoonevening peaks). In more advanced stages purulent material may drain spontaneously, sometimes with
streaking
bleeding, usually either from the anus or from the area of greatest abscess fluctuation. Bleeding usually
occurs in the presence of an associated fissure.
They will be important in the diagnosis:
- Inspection
- Neutrophilic leukocytosis.
- EDAR: often difficult to implement due to intense pain.
- Echography of the perineal and/or transrectal tissues can clarify all the features of the abscessal
swelling and its relationship with the sphincter system.
Abscess therapy consists of incision of the abscess and its drainage.
For small abscesses (< 2 cm), resolution is first attempted with broad-spectrum antibiotic therapy, such
as levofloxacin, for about 1 week, which may decrease the pain. In fact, the patient reports tremendous
pain, because until the fistula forms and there is only the abscess, this purulent collection creates
tension that presses on the walls (the skin). Usually, after administration of the antibiotic, the abscess
matures, there is spontaneous drainage to the outside and the patient will have relief; often the patient
reports having found in his or her pants some foul-smelling purulent fluid coming out of this swelling,
which is decreasing in volume.
FISTOLA ANAL
Small pathological and infected tunnels that connect the anus with the surrounding skin. To be defined
as such, anal fistulas must develop in a precise anatomical location, known as the 'pectinate or anorectal line', which separates the rectum from the anus, in which the exocrine anal glands, which
become inflamed, are located. It occurs more frequently in men than in women. In the vast majority of
cases they originate from perianal abscesses.
Causes
●
●
●
●
●
●
perianal abscess
Crohn's disease
radiotherapy proctitis
laceration of the anorectal mucosa (e.g. foreign bodies)
mycosis (in immunocompromised patients)
obstetrical damage in women (episiotomy to avoid laceration, although episoraffia is operator
dependent)
Classification according to structure
● Straight fistulas: they present a single communication canaliculus. They are generally the initial
presentations (if left untreated, they evolve branches that become much more difficult to treat as
generous tissue removal is not possible).
● Fistulas with branches: several connecting channels are observed.
● Horseshoe fistulas: they connect the anal sphincter to the skin surrounding it, passing the rectum
first. It is said of a fistula that opens at the opposite side from its origin.
Classification according to the location of the fistulous canaliculus:
● High'' fistulas: above the toothed line.
● Low'' fistulas: below.
Classification of Parks
● Superficial fistulas, i.e., submucosal fistulas with a course that does not involve the sphincter
plane of either the internal or external sphincter
● Inter-sphincteric fistula or type I, (70%): located between the internal anal sphincter and the
external anal sphincter. It crosses the internal sphincter (but not the external sphincter) at the
dentate line and runs in the inter-sphincteric space, opening at the margin of the anal orifice. They
may extend downwards to the perianal skin, upwards (blind) or open into the rectum. They are the
result of a perianal abscess.
● Transsphincteric fistula or type II, (20-25%): the intersphincteric space and the external anal
sphincter are crossed. The external striated sphincter muscle is then 'pierced'. Depending on the
height at which they pass through the muscle, they are distinguished into high, medium and low.
They are the result of an ischio-anal abscess.
● Supra-sphincteric fistula or type III (5%): they cross the internal sphincter, pass upwards (into
the inter-sphincteric space) around the external sphincter above the pubo-rectal mm, then head
downwards penetrating the elevator mm before heading towards the skin below. Usually due to
surgical errors. They are the result of an abscess above the mm elevator of the anus.
● Extra-sphincteric fistula or type IV(2%): originates above the sphincter complex and does not
involve the sphincters, but travels downwards through the m. elevator of the anus. It has a fistulous
route that starts above the internal anal sphincter and ends in the external skin orifice. It often
arises from an abscess that has formed inside the intestine, rectum, pelvic outlet. It is mostly seen
in patients with Crohn's disease.
Goodsall's law applies to the direction of the medium:
● If the external orifice is located in a quadrant anterior to the anal margin, the via has a rectilinear
direction
● If the external cutaneous orifice is located in a posterior quadrant, the fistulous passage to the
internal orifice follows a sinusoidal line.
Clinic
● Itching, swelling
● Irritation of the mucosa with granulomatous reaction around the external fistula orifice.
● Secretion/leakage of pus, faeces or mucus and blood: there is no longer any tightness of the
sphincter a
causes swelling and the patient finds these in his or her underpants□ a wet anus is created,
which predisposes to dermatitis and mycosis.
● Intense pain (especially during defecation)
●Fever and fever Diagnosis
The identification of the external orifice on inspection is simple (hyperemic and excoriated skin,
''small fleshy cap''), unfortunately t h e precise identification of the fistulous pathway is rather
complex. In cases of internal (blind) fistula, one recognises the discharge of pus from the anus. Once
the external fistula has been identified on the skin, the internal fistula is sought under anoscopy.
The path of the fistula is studied with:
- Inserting a mirror
- Transrectal ultrasound (trans-anal): ultrasound probe that allows a three-dimensional
scan of the anal canal, and a precise view of the fistula, its course, location of the primary
abscess, observation of the relationship with the sphincters and peri-rectal fat.
- MRI pelvic excavation.
- Fistulography: mdc is inserted into the fistulose pathway.
Surgical treatment
It is based on the following timing: identification of the fistula and the via - >incannulation of the via >treatment of the medium.
Surgical techniques:
● Fistulotomy (for rectilinear fistula): insert the speculum, incise the fistula and lay it flat, with
healing by second intention for inflammatory granulation. The surgeon opens the fistula by book.
It is the simplest operation, non-problematic conditions.
● Fistulectomy: excision of the tissue segment affected by the fistulous vessel and repair of the
breach by lowering the overlying mucosal flap. After introduction of the speculum.
● Passage of the seton: the speculum is inserted, a thread (seton because it was originally made of
silk) is inserted from the external skin orifice until it reaches the anal cavity (beyond the internal
orifice). The surgeon then joins the two ends of the thread by putting them under tension. Slowly
(even months) and gradually the seton dissects the space between the anal fistula and the anal
canal. In the meantime, the resulting inflammation is a stimulus for repair (creates progressive
fibrosis/healing). It is indicated in trans-sphincteric.
Innovative treatments, fistula closure with:
● Quartz silver: sclerosant injection; element that is deposited in the fistula and stimulates healing,
due to the presence of quartz, which has an irritating action and creates fibrosis
● Laser: as in varicose veins, you insert the probe inside the fistulous passage and slowly burn the
path to create a scar
● Use of mesenchymal stem cells from adipose tissue in gel form, allowing direct contact between
these cells and the wall.
HEMORROIDS
Anatomy
Continence depends on:
1)
Sphincter action:
-
-
Internal anal sphincter: smooth muscle, involuntary
External anal sphincter: striated muscle, voluntary
2) Extra-sphincteric action:
Recto-anal angle (angle between 60-105 degrees): determined by the pubo-rectal sling
(puborectal muscle)
Flutter valve mechanism: due to the action of intra-abdominal pressure on the intestinal
walls (squeezing them causes a reduction in the ability of the walls to descend into the anal
canal)
Flap valve mechanism: compression of the rectal wall on the anal canal creates occlusion
of the lumen and thus continence.
The haemorrhoid pads (upper, middle and lower) act as an elastic shock absorber, swelling
and deflating as the faeces pass through, and this determines the maintenance of continence
and protection of the sphincter apparatus during defecation. It consists of 3 mucous and
submucosal vascular plexuses, both arterial and venous, supported by elastic connective
and smooth muscle fibres (Parks' ligament).
Defecation: consists of the passage of faeces in the sigma-rectum: activation of the rectal-anal
inhibitory reflex □ release of the internal anal sphincter□ release of the external anal sphincter
(evacuation can be prevented by (voluntary) contraction of the same.
Definition
We speak of haemorrhoid disease (incorrectly called: haemorrhoids) when these anal pads are
pathological, i.e. when there is abnormal dilatation of the haemorrhoid plexuses: the pads become
swollen and inflamed, leading to haemorrhoid disease.
Aetiology
1) Primitive: the cause is unknown, but there are several hypotheses (risk factors):
- Prolonged standing (sport, work, etc.)
- Alteration of the perivascular connective, due to strong family component
- Venous meiopragia (for strong family component)
-
Bowel d i s o r d e r s : constipation□ mechanical pontic action; chronic diarrhoea□
action
faecal-related chemicals that can damage the connective and elastic fibres of anal cushions
- Sphincterial hypertone
2) Secondary: the cause is portal hypertension (there is an inversion of the circulation and through
the lower mesenteric then blood stagnation at the level of the haemorrhoid plexuses).
Secondary haemorrhoids are not operated on, as the underlying cause must first be addressed
(cirrhotic patient).
Depending on the plexus involved:
1) Internal: if above the gear line
2) External: if below the gear line
Initially, there is always involvement of the plexuses above the dentate line (internal haemorrhoids),
but then the increase in volume and prolapse of these plexuses leads to the development of external
haemorrhoids.
Pathophysiology
In the presence of risk factors: there is alteration of the supporting connective tissue □ prolapse of the
haemorrhoid plexuses □ torsion of the vessels □ oedema □ reduced oxygen supply □ acidosis □
thrombosis
□ ischaemia.
Clinic
The signs and symptoms of haemorrhoidal disease are:
1) Proctorrhagia (bleeding): self-limiting, intermittent, bright red and occurring at the end of
defecation. As a result of prolapse, the haemorrhoidal artery and vein form a binding that
obstructs the outflow of the haemorrhoidal blood, during evacuation the haemorrhoids swell
and bleeding occurs from the trauma with the faeces. If bleeding is present, anoscopy and
EDAR are sufficient in the young; in the elderly, a colonoscopy is recommended. If the latter is
negative, the patient can remain quiet for about five years.
2) Burning
3) Rectal tenesmus: feeling of insufficient evacuation, which triggers a vicious circle as the
patient sits on the toilet and tries to strain by contracting the abdominal muscles with
the increased pressure, but already having grade II and III haemorrhoids, these will be
stretched further downwards, worsening the situation.
4) Wet anus: is determined because continence is not complete
5) Perineal itching: due to the fact that the damp environment facilitates fungal infections.
6) Foreign body sensation: even when the anal cushion has been retracted, it gives the sensation
of a foreign body or faecal residue.
7) Mucorrhoea
8) Pain: this is not typical, it occurs in complicated haemorrhoids. Usually if there is pain, there is
no bleeding, because the pain is caused by congestion of the haemorrhoidal pad, and if it is
congested, it cannot bleed. When, on the other hand, the haemorrhoid pad bleeds, it is not
thrombosed and there is no pain.
When pain is present then one thinks of complicated haemorrhoids:
a) Choking: e.g. subject with prolapsed haemorrhoids who sits on them. The haemorrhoids
oedematise and cause intense pain for several days.
b) Thrombosis: rare in internal haemorrhoids, more frequent in external ones, as an evolution of
the choking and consequent obstruction of venous drainage caused by hypertension of the
internal anal sphincter. It is accompanied by intense and sudden pain. An incision with a local
anaesthetic is sufficient to free the thrombus and provide immediate relief; or medical
treatment with drugs that act on the sphincter's hypertone (nifdipine, botulinum toxin, etc.) is
used.
c) Anorectal prolapse: as the mucosa slides down and connective and muscle fibres break down,
the vessels tend to dilate and prolapse
d) Haemorrhages
Golingher classification
-
Grade I: only bleeding and the haemorrhoids remain inside the anal canal;
Grade II: haemorrhoids that prolapse in the anus as a result of defecatory effort, but are
able to re-enter spontaneously;
Grade III: haemorrhoids that prolapse in the anus as a result of defecatory effort, but are
able to re-enter following manual intervention;
Grade IV: haemorrhoids unable to re-enter
Usually grade IV is associated with complications, in fact, if the haemorrhoids do not recede, there
may be thrombosis.
Diagnosis
The diagnosis includes:
1) Anamnestic collection: these are pts who have bowel disorders (especially constipation) and/or
a family history. It is asked:
-
Dietary habits: fibre and fluid intake, alcohol consumption, smoking, coffee;
Remote pathology: previous operations, pregnancies, episiotomy, lacerations, relationship
between pregnancy and proctopathies;
- Taking drugs: anti-coagulants, contraceptives, NSAIDs
- Sexual habits: sexual practices with manipulation and anal trauma.
2) EDAR (digito-ano-rectal exploration): at inspection alone, unless it is a grade 1 haemorrhoid,
the haemorrhoids can be seen quite easily; in any case, it should always be performed, also to
rule out neoplastic causes: 75% of rectal tumours are located 6-7 cm from the anal orifice, so
one can reach them with the finger;
- It is performed with the patient in Sims position (left lateral decubitus with the lower limbs
flexed), but also in genupectoral or gynaecological position
- The patient must be made comfortable
- The index finger is inserted in a non-traumatic but gradual manner and the fingertip is used
to assess the anal canal at 360°.
3) Anoscopy
4) Rectosigmoscopy: in the young
5) Colonoscopy: is done in patients with a family history of CCR and intestinal polyposis. It
becomes mandatory over the age of 50.
Treatments
-
Conservative and pharmacological (I-II grade)
Parasurgical (I-II grade)
Surgical (III-IV grade)
1) Conservative and pharmacological
- Diet rich in fibre and waste to soften stools: vegetables, fruit (such as pears, kiwi)
- Supplements: they increase water retention in the colon and thus increase faecal mass.
- Washing with lukewarm water and antiseptics
- Use of anti-inflammatory ointments
- Laxatives
- Analgesics
- Corticosteroids
- Nitroglycerin
- Flavonides
2) Para-surgical: e.g. in those 80-year-old pts with haemorrhoids that bleed, but the pt cannot be
anaesthetised.
- Sclerotherapy: using a fenestrated anoscope, a sclerosing medium is introduced into the
perivascular area of the submucosa, which sclerotizes the tissue by stimulating granulation
and fibrosis with shrinkage of the abnormal haemorrhoid pads, which return to normal
- Infrared coagulation: heat has the same effect as elastic ligation in the long run
-
-
Elastic ligation: this consists of placing one or more rubber bands at the base of the
haemorrhoidal pads using a hollow clamp, so as to choke and cause necrosis of the mucosa.
A fibrous scar is formed that favours the solidification of the haemorrhoidal mucosa to the
anal wall. It is a very painful procedure
Cryotherapy: consists of the application of a cryostatic probe, also causing necrosis of the
pathological anal cushion.
Sclerotherapy and infrared coagulation are only used in grade I haemorrhoids, and at most in the early
stages of grade II. Elastic ligation and cryotherapy are good for grade II.
3) Surgical:
- Milligan-Morgan haemorrhoidectomy (grade III and IV): resection of main anal pads
with the external haemorrhoid plexus. It is the gold standard for grade IV haemorrhoids. It
removes the haemorrhoids down to the underlying muscle and leaves the wounds open.
Healing is long and painful. A trefoil is created whose petals are the wounds and between
which muco-cutaneous bridges must always remain open: in fact, if healing closes two
petals, anal stenosis occurs.
- Longo's technique (prolassectomy with Stapler, haemorrhoidectomy-degree III): the
Stapler mechanical circular suture machine, introduced transanally, dissects a ring of
mucosa above the dentate line and sutures its distal and proximal margins with metal
staples, thus repositioning the haemorrhoids in their natural location in the anal canal. The
suture is inside the anal canal, in areas with little innervation, so the post-operative pain is
very reduced. A tobacco bag suture is made: circular and is closed by pulling).
- Transanal haemorrhoidal deatherialisation + pessia (surgery without removal of tissue,
grade III): consists of Doppler-guided ligation of the submucosal endings of the
haemorrhoidal arteries (usually 6), resulting in volumetric reduction of the haemorrhoidal
pads.
RECTAL PROLAPSE
A pathological condition characterised by protrusion of the walls of the rectum through the anal
orifice. It is divided into:
1) Partial or incomplete or mucous: only prolapse of the rectal mucosa (may be reducible
spontaneously, manually and non-reducible)
2) Complete: prolapse of the entire wall of the rectum (i.e. of all its tunics)
From a pathophysiological point of view: rectal prolapse has a pathogenesis that is not very well
understood, but recognises predisposing and determining factors.
- Predisposing factors:
. insufficient support and suspension apparatus of the rectum
. acquired weakness of the perineum (e.g. after natural childbirth)
. sphincter weakness
- Determining factors: the main trigger is the development of excessive pressure within the
abdominal cavity:
. cough
.expulsive constipation
.work and/or sports efforts
Clinic
Clinical symptoms are characterised by:
1) Appearance of tissue protruding from the rectum
2) Difficulty in passing stools
3) Feeling of incomplete evacuation
4) Multiple emission of small quantities of faeces
5) Prolonged ponzamento (evacuation push), to the point where
manual evacuation manoeuvres must be performed
to
allow evacuation
6) Sense of anal and perineal weight that tends to increase with standing and after evacuation
7) Tenesmus: feeling of having to evacuate even with empty rectal ampoule
8) Bleeding during evacuation, loss of mucus, wet anus
9) Difficulty in retaining gas and faeces, in the form of actual incontinence or constipation
10) Association of other genito-urinary disorders: genital prolapses, bladder prolapses (cystocele)
with or without associated urinary incontinence.
Complications (rare)
-
Ulcerations
Choking: can be created in patients with anal hypertone so that the prolapse becomes
irreducible even manually
Spontaneous rupture of the prolapsed rectum
Diagnosis
-
Anamnesis: collection of information on the clinical history of the patient
EO:
. inspection: the patient is invited to sit on a comfortable chair with a hole. If the prolapse does
not appear, diagnosis is almost impossible: a perineal eversion and the donut-like appearance
of the anus during pouncing can be appreciated
. specific examinations: EDAR; rectoscopy; defecography; double-contrast opaque schism;
anal manometry.
Treatment
Although constipation and defecatory straining may contribute to the development of rectal prolapse,
simply correcting these problems is not sufficient to improve prolapse once it has already set in.
There are many ways to surgically correct rectal prolapse. The approaches used today are:
1) Abdominal approaches: (open surgery or laparoscopy): are based on the principle of suspension
(pessia) of the rectum invaginating.
2) Perineal approaches: which aim to eliminate prolapse by resection of the viscera;
The two approaches have different methods that will then be chosen by the surgeon according to the
characteristics of the patient and the type of rectal prolapse.
Abdominal approach: □ anterior resection of the rectum and rectopexy; most
procedure involves cutting (resection) of the prolapsed rectum tract, followed by fixation (rectopexy),
using sutures, of the remaining rectal cavity. Rectopexy is usually performed at the sacral or pre-sacral
level. The surgeon will mobilise the rectum from the pelvis, but will only operate anteriorly on the
rectum, staying away from the nerve fibres that innervate the intestines and genitals. The end result
will be the lifting of the rectum from the pelvis, restoring normal anatomy and function.
Perianal approach: perineal procedures are applied for older patients or when abdominal surgery
would be too risky. This approach results in fewer complications and less pain. It can also be
performed under local anaesthesia. Among the procedures used are Altemeier surgery and STARR.
The latter is performed through the anus without incisions and without external scarring. The
redundant rectal mucosa is removed with a mechanical suturator that cuts off the excess tissue. At the
end of the operation the patient will have a suture line on the anterior and posterior wall of the rectum.
SOLITARY ULCER OF RECTUM
Rectal solitary ulcer syndrome is a rare disease involving straining during defecation, with a sense of
incomplete evacuation and sometimes with the passage of blood and mucus from the rectum.
It is caused by localised ischaemic damage or prolapse of the distal rectal mucosa. Diagnosis is clinical
with confirmation by flexible sigmoidoscopy and biopsy. Treatment is, for mild cases, an adequate
bowel regimen, but if rectal prolapse is the cause, surgery is sometimes necessary.
ANGIODYSPLASIAS
The term angiodysplasia refers to a vascular malformation, which can affect: arteries, veins,
lymphatic vessels, capillaries. Malformations may also be arteriovenous or mixed. They can cause
rectal bleeding.
RAGADE
The fissure is a linear continuum (ulcer) of the anal canal at the level of the muco-cutaneous transition
zone, which does not tend to heal.
It locates (then classifies according to location):
- Posterior commissure 70-80%: less vascularised area (at 6 o'clock)
- Anterior commisura (at 12 o'clock): those related to natural childbirth, hence to trauma.
- Laterally (at 3 o'clock): linked to pathologies such as OCS, Chron's disease, HIV-related
diseases.
It is also divided into:
- Acute fissure: a live, flat-edged lesion; causes acute pain and bleeding (often after emission of
a very hard faecal cylinder). The lesion may progress to healing within a few days or to
chronicity.
- Chronic rhagades: the lesion has hardened, thick, sclerotic borders and is sometimes
accompanied by sentinel marisca, a masserelle of perianal skin.
The aetiology is not well known, but the most accredited hypothesis sees the involvement of
hypertension of the internal anal sphincter (probably related to psychic stress): emission of hard
stools leads to increased strain, and in the long run results in sphincter hypertonia and thus
compression of the vessels (especially for the lower rectal vessels that pass through the internal anal
sphincter) and thus
ischemia□ necrosis□ ulceration and progressive deepening with defecatory acts. Then with the
involvement of the sensitive fibres the characteristic intense pain on defecation arises.
The clinic is characterised by:
1) Intense pain: it is frequent, paroxysmal and burning (described as pinpoint pain); it appears
after defecation and may last for several hours. The patient will tend to avoid the act of
defecation, thus favouring the development of harder and harder stools and therefore more
trauma
□ pain □ pain will generate spasm, establishing a vicious circle. The pc will become
constipated.
2) Itching: in the initial phase
3) Haematochezia: small superficial bleeding of bright red blood, spurting, a few drops of blood
are reported; faecal cylinder painting.
4) Serous secretion
5) Dysuria (painful urination): only in men due to 12 o'clock lesions, which irritate the prostatic
nerve plexus.
Diagnosis
-
-
-
Anamnesis: the presence of pain with these characteristics is already indicative of pathology.
Inspection: we do not proceed with the EDAR especially if we notice a high sphincter tonicity,
as we will definitely have an uncooperative patient due to pain. Skin changes, anal swellings,
redness, abscesses near the anal orifice must also be assessed.
Appropriate stretching of the anal orifice to visualise the anal fissure. The index finger is
inserted and evaluated:
o Sphincter tone
o Other affections: presence of blood, faeces, formations
o Prostate in men: consistency, homogeneity
o Vaginal and uterine alterations in women
The pressure at the level of the anal sphincter is measured by manometry, which allows two
parameters to be derived:
o Anal pressure at rest
o Anal pressure and stress
Treatment
1) Conservative and pharmacological: (ACUTE)
- Diet: specific diets rich more or less in fibre according to the alteration of the alvus:
constipated (60-70%), normal or diarrhoeal
- Hygienic measures: washing with warm water to relieve pain
- Medication: is aimed at reducing internal sphincter hypertone. For those who do not have
hypertone, the aim is to improve vascularisation.
. in the acute phase: trinitin (topical), the most widely used, or botox (botulinum infiltrations at
high doses, may give inconsistency)
.in the chronic phase: sympatho-lithics or topical calcium channel blockers (ointments or
patches).
2) Parasurgical :(CHRONIC)
- Anal dilatations: cones of different sizes that aim to progressively relax the sphincter and
reduce tension.
- Balloon dilatations: under local or regional anaesthesia, a balloon is introduced, imparting
graduated pressures of up to 150-250 mmHg, in relation to sphincter pressure values.
- Anal Divulsion: under local or regional anaesthesia, several fingers are progressively
introduced up to the whole hand, which results in the rupture of several sphincter fibres, which
can lead to healing of the fissure, there is an increased risk of incontinence.
3) Surgical:
- Lateral sphincterotomy (most commonly used): the sphincter is interrupted at 3 and 9 o'clock.
The most distal part of the internal anal sphincter is dissected, with an oblique incision; the
most feared risk is incontinence (which, however, is more frequent in case of posterior
sphincterotomy)
-
Posterior sphincterotomy: the sphincter is interrupted at 6 o'clock. Excision of the fissure is
also planned and the loss of substance is then covered with an advancement flap (anoplasty)
and the risk of incontinence is very high
N.B. the incision (or section) must not be excessively generous, but it must be such a section that the
tone is not lost completely, but is reduced sufficiently to allow the margins of the ulcer to settle
spontaneously. Then, even if the ulcer heals, it is important to eliminate the cause of the ulcer, i.e. the
development of hard stools, and thus reduce defecation to a minimum. A proper diet, the intake of
plenty of water and the use of mild laxatives to reduce the consistency of stools, or alternatively,
agents that increase faecal mass in order to facilitate evacuation, should then be recommended.
Complications of sphincterotomy are:
- Transient incontinence (especially gas)
- Iatrogenic incontinence (in the case of injury to the external anal sphincter)
- Recurrence: especially when the sphincter is not dissected in its entirety (the section may in
fact be partial or total)
- Haematoma (if there has not been proper haemostasis with an electric scalpel)
CARCINOMA OF THE ANUS
It has a higher incidence between the ages of 50 and 60, usually in patients who may have had an anal
wart for about 20 years. It is a neoplasm that evolves slowly, with several years passing before the
lesion turns into a carcinoma.
Predisposing factors include:
1) Chronic anorectal pathologies: fistulas, fissures, haemorrhoids (these are constant stimuli t o
proliferation, to c h r o n i c inflammation: in fact chronic inflammation □ dysplasia □
carcinoma)
2) Previous venereal diseases: condylomas (HPV 16 and 18)
3)
Women: presence of condylomata in the cervix Several histotypes are
differentiated:
-
Spinocellular carcinoma: this is the most frequent and may originate from the anatomical anal
canal and perianal region.
Cloacogenic (or basal cell carcinoma): the second most frequent, it originates from the
transition zone
Muco-epidermal carcinoma: originates from the glands of the anal canal or the transition zone
(rare)
Adenocarcinoma: rare; often the extension to the anal canal of neoplasms of the rectal ampulla.
The clinic is characterised by:
-
Itching
Serum-mucosal leaks
Pain
Bleeding
Difficulties in evacuating and faecal incontinence (in more advanced forms)
Then, depending on the stage of the disease, general symptoms such as:
-
Tiredness
Inappetence
Febbricola
Weight loss
It is important to do DD with:
- Hemorrhoids
- Rectal prolapse
- Rectum-anus polyps
- Condylomata acuminata of the anus
Therapy
1) If the lesion has a circumference < 2/3: chemo-radiotherapy is opted for, which will be curative
in 75% of cases; otherwise an abdominal-perineal resection is opted for.
2) If the lesion has a circumference >2/3: abdominal resection is done; then if inguinal lymph
nodes are positive, ingunal lymphadenectomy is done; if the lymph nodes are negative, chemoradiotherapy is done
In abdomino-perianal amputation according to Miles, an access is created within the perineum and
the resection of the affected tract (ano-rectum) is performed. Nowadays, a less invasive technique is
used for these types of tumours: TME: total-mesorectal excision by trans-anal route, which can be
performed laparoscopically with special sutures to make the operation less invasive.
CHRONIC INFLAMMATORY DISEASES INTESTINES
CROHN'S DISEASE
Chronic inflammatory granulomatous disease with a sclerocytial evolution. Regarding its
epidemiology:
● It is more frequent in industrialised countries;
● There is a male : female ratio which is 1:1.
● People between 20 and 30 years of age are most frequently affected, sometimes with a second
peak of incidence in the 6th to 7th decade of life;
● The incidence is 2/100000 per year;
● The prevalence is 20-40/100000.
It is a phlogosis that affects the entire thickness of the intestinal wall and is therefore called
transmural, but is also distributed not continuously but in segments: skip lesions.
Anatomically, it typically affects the terminal ileum, in fact its first description was that of regional
ileitis, however it can also involve the entire gastrointestinal tract (i.e. from the oral cavity to the
anus).
From a clinical point of view, the symptoms and signs of CD are:
● Cramp-like abdominal pain, spread throughout the abdomen;
● Diarrhoea with repeated evacuations (10 or more). There is bacterial overgrowth and reduced
fluid absorption at the colic level;
● Sometimes steatorrhea.
● Malabsorption due to damage of the mucosa of the small intestine.
Extra-intestinal involvement: articular (arthritis and spondylitis) and ocular (conjunctivitis and
uveitis).
+The presence of hydroaery levels, which generally indicate intestinal obstruction, in a person with
Crohn's disease should never lead to an emergency operation because the ideal in this case is to have
an operation as an elective one. Those hydroaerial levels that we often see are an expression of a
transit obstruction of the intestine, but this is not necessarily due to a scarring fibrosis that may involve
the intestine, but it may be due to that oedema characteristic of the acute phases of the disease and
which then with medical therapy may go into defervescence resolving itself without the need for
surgery.
According to the guidelines, delayed surgery is preferred in an adult patient with Crohn's disease
presenting with acute small bowel obstruction, provided there is no ischaemia or peritonitis. One of
the options that may be considered is the endoscopic dilation balloon, which may be used depending
on local expertise, i.e. the receiving centre, or patient preference
Complications (see later)
The fistula is the site of fibrosclerotic evolution, which is why it becomes the most classic
complication. Fistulas are frequent in both chronic regional ileitis and CD of the colon. The sclerosclerotic process causes the loops of intestinal segments to adhere to each other; the extension of the
phlogosis creates adhesions that will set the stage for fistulisation. Fistulas can be:
●
●
●
●
Entero-enteric fistulas;
Entero-vesical fistulas;
Retroperitneal fistulas;
Enterocutaneous fistulas (less frequent).
Surgical therapy
When the disease is limited with a terminal ileus <40 cm laparoscopic resection may be an
alternative to infliximab therapy. Reference is made only to an area of the intestine that is 40 cm
before the ileocecal valve and not others, because when Crohn's disease extends to that area it will
certainly lead the patient to surgery sooner or later, so doing infliximab and blocking the disease today
will not reduce the risk of surgery so doing laparoscopic surgery in this case may be a viable
alternative to solve a problem that will perhaps present itself in an acute phase at a later stage.
PERIANAL DISEASE FROM CROHN'S DISEASE
Perianal fistulas from Chron's disease
This particular aspect of Crohn's disease relates to the perianal site and has a different incidence from
the normal involvement of the ileo-caecal region of Crohn's disease, is observed in an average of 2580% of patients. In 10-20% of cases, perianal disease occurs before the diagnosis of Crohn's disease is
made; it usually presents with the most frequent sign, the perianal fistula.
Perianal disease predominantly affects younger age groups, especially those under 35 years of age,
and, of course, is associated with Crohn's disease affecting colic or rectal forms.
The Crohn's disease phenotype with perianal disease has a more aggressive pattern than that with ileocaecal disease, especially if it is already present at initial diagnosis.
Pathogenesis
The formation of perianal disease involves two theories:
● Hypothesis of fistulas, most frequent pattern, starting with deep, penetrating ulcers
● Microbiological, genetic and immunological involvement that could explain the aggressive
and chronic behaviour of perianal lesions compared to other forms of Crohn's disease.
Classifications of perianal disease
Montreal Classification
There is a 2005 Montreal classification that uses the perianal pattern as a distinguishing element from
the previous classification of Crohn's disease (1998 Vienna Classification).
Subdivision according to clinical behaviour:
● B1
not
stenosing
non-penetrating
● B2 stenosing
● B3 penetrating
● P perianal
The two classifications also differ in terms of the age of diagnosis: in the Vienna classification it was
divided into under 40 years and over 40 years; subsequently, it was noted that patients with onset at
the age of under 16 years have more aggressive, rapid and important evolutions over their lifetime and
therefore 3 age groups were divided:
∙
∙
∙
There has been no change with regard to localisation:
● L1 terminal ileum
● L2 colon
● L3 ileo-colon
● L4 upper section
In the classification of fistulas, Parks' classification is valid (see section: anal fistulas).
Cardiff Classification (1978)
78 classification still valid for Crohn's disease which includes ulceration, fistula, abscess and stenosis;
it concerns the classification of Crohn's disease perianal disease and therefore
● Grade 0: for an absence of ulceration;
● Grade 1: for the presence of a superficial lesion that may be:
o rear and/or front
o side
o with big skin tags
● Grade 2: for much deeper ulcers:
o In the anal canal
o In the lower rectum
o Concerning extension to the perineum
American Gastroenterological Association (AGA) classification of 2003
When faced with a patient with perianal Crohn's disease or pathologies that make one suspect this
diagnosis, one must first carry out an objective examination of the perianal area and endoscopic
assessment that may lead to the evaluation of:
● Simple, so-called low fistulas, not associated with abscess, stenosis or proctitis and not
involving other organs (bladder or vagina); single external orifice;
● Complex fistulas, are considered high (high intersphincteric, transsphincteric, suprasphincteric
or extrasphincteric), are often associated with abscesses and may also involve the vagina with
important consequences for the woman's social status and may give rectal stenosis and
macroscopic proctitis; the external orifice may be multiple;
Perianal fistula clinic
Examples of involvement of the perineum when there is perianal disease include abscesses and
perianal fistulas.
They typically present themselves with:
● Anal, gravitative or urenic pain, the latter especially when the internal orifice of the fistula is
at the level of the anal canal in which there are nerve endings that are also stressed during the
presence of a fissure and constitute, especially during the defecatory phase, a major irritative
insult of the nerve endings of the perianal skin resulting in urenic pain that lasts for several
hours after defecation itself.
● Anal and/or perianal swelling
● Purulent secretion that may be at the anal or vaginal level, whereby it is important to assess
purulent secretions not only at the skin level but also within the lumen of t h e anal or vaginal
canal, because sometimes the abscess or fistulous passage that has formed does not drain at the
skin level but elsewhere in t h e anal or vaginal canal. Anal or vaginal exploration results in the
detection of pus in the context of the lumen of the viscera and consequently in the detection of
the abscess that has self-drained into the cavity.
● Rectal bleeding/proctorage
● Mucorrhoea, an emission of mucus during defecation
● Faecal incontinence, can occur because the inflammatory process involving the sphincter
plane, even crossing it at several points, can lead to transient or definitive deficits in sphincter
function and thus cause incontinence, which can be classified in different ways, as previously
explained.
● Alterations of the alvus in a constipated sense or more in a diarrhoeal sense. The term
diarrhoea indicates either an increase in the number of bowel movements or an increase in
faecal volume, the latter never being the cause of diarrhoea in perianal disease because there is
no evidence that Crohn's disease affects faecal volume, but instead causes an increase in the
number of discharges because, by creating a phlogistic process in the rectum, it can cause
tenesmus and thus also a reduced continence capacity of the rectum, hence the urgency to
expel faecal material from the rectum even when this is small.
Grading (?)
● Discharge, incontinence :
1. Absence of incontinence;
1. Mucous-like incontinence that the British call 'ceiling', related to the sensation of a wet
anus that occurs half an hour to an hour after normal post-defecation cleansing; it is a mild
mucous secretion.
2. Incontinence of the purulent type, the mucous portion is more abundant or even frankly
purulent
3. Substantial incontinence
4. True faecal incontinence
● Pain is related to activity restriction:
1. Pain not affecting activity
2. With a minimum of discomfort, so no great restriction on daily activities
3. Moderate discomfort, with some limitations such as sitting for long periods or the use of a
motorbike or bicycle for travel
4. More pronounced discomfort with greater limitations, such as the inability to sit for more
than the minimum time required, for example, for work activities
5. Severe pain, leading to severe limitations such as having to be bedridden without being
able to carry out any kind of daily activity.
● Restriction of sexual activity:
1. None
2. Slight entity
3. Moderate
4. Evidently marked
5. Impossible
● Type of perianal picture:
1. Absence of injuries
2. Ragade
3. <3 fistulas
4. >3 fistulas
5. Ulceration of the anal sphincter or fistulas with significant loss of skin substance in both
the anal and perianal canal
● Formation of abscesses, i.e. a thickening condition either of the fibrotic type, when there is a
regressing phlogistic picture, or of the soft-elastic or tense-elastic type, when the phlogistic
process is in a particularly active phase.
1. No abscess
2. Minimal abscess
3. Moderate
4. Substantial
5. Particularly voluminous abscesses
Objective examination
To begin the objective examination, it is important to have the patient assume the Sims position or
genupectoral. Inspection, palpation, digito-anorectal exploration and anoscopy.
Anoscopes can be of various sizes in terms of both calibre and length. Within 10 cm we speak of an
anoscope, the proctoscope will be 13 cm long and the rectoscope will be longer because it can also do
a recto-sigmoidoscopy (25 cm).
For the evaluation of perianal fistulas, the guidelines often say "Examination Under Anaesthesia". It is
frequent that anaesthesia is necessary to complete the examination of the patient; the inflammatory
process is sometimes so important and heated that the resulting pain picture does not allow an
adequate examination.
Instrumental examinations
In addition to the objective examination, an MRI of the pelvis and/or an echotomography is
essential.
In association with these main examinations, for Crohn's disease perianal disease, rectoscopy is
important to see the state of the rectal mucosa, anorectal manometry to assess the state of
functionality of the sphincters, to be able to assess the initial and final post-treatment moment in order
to have a finding of improvement of the incontinence picture.
A PNMTL is also performed, an electromyography related to the pudendal nerve, a mixed-type nerve
whose passage is on the ischiatic tuberosity, so that it can be compressed with the explorer finger that
is introduced into the rectum. There is a glove called St. Marks' glove which is equipped with two
electrodes, one on the tip of the index finger and the other at the base of the index finger, so that the
introduction of the explorer finger on the ischial tuberosity allows the entire course of the nerve which
is outside the anal canal and the lower rectum to be followed by means of the electrodes. The detection
of the impulse given via the upper and lower electrodes, thus the speed of conduction of the pudendal
nerve, gives an insight into the functioning of the pudendal nerve itself and, therefore, allows us to
assess the possibility of functioning of the nerve which, sometimes, when the inflammatory process is
particularly important, may even be compromised in its entirety.
Treatment of abscesses and fistulas
When you have a perianal abscess, the first thing that needs to be done is incision and drainage.
Superficial abscesses will only be treated with incision and drainage, deep ones, on the other hand,
must be treated with setone.
ECCO (European Crohn's Colitis Organisation) guidelines state that CT or echo-guided drainage of
well-accessible intra-abdominal abscesses is recommended as a first approach, although not on a
particularly high level of evidence (evidence level 4). Therefore, if this patient does not respond to the
established medical therapy, he should undergo drainage by image
guided. When there is successful guided drainage by imaging of an intra-abdominal abscess, medical
treatment without surgical therapy should be considered.
The same guidelines say that a surgical option may be recommended in the event that medical
treatment is unsuccessful in controlling sepsis.
The setone is the treatment of choice for deep abscesses and also for fistulas, because the moment an
abscess is incised and, thus, an abscess collection whose origin is from an internal orifice of the anal
canal is opened in the skin, that abscess is transformed into a fistula, which is the manoeuvre required
to allow the abscess to heal.
The seton is a wire with a gauge of approximately a couple of millimetres or a little less; the fistula is
specillated and then by introducing a blunt-headed ferrule into the fistulous context, by running it in
from the external orifice to the internal orifice, it will then be possible to pass the wire hooked to the
ferrule. This will keep both the internal and external orifices drained and thus allow the abscess to
drain continuously and steadily in the weeks following placement while keeping the internal and
external orifices and thus the abscess drainage pathways open.
Low (simple) or submucosal perianal fistulas require a fistulotomy, i.e. cutting along the
longitudinal axis of the fistula, to heal.
Instead, complex or high fistulas require the seton. This drainage wire called setone plays a crucial
role in sphincter preservation, because otherwise the so-called 'flattening of the fistula', i.e. the incision
along the longitudinal course, if the fistula were to include muscular structures, would also involve the
muscular incision itself and an inevitable definitive incontinence. In this context, the seton has the role
of sparing traumatic actions on the sphincter plane and subsequent healing.
Another treatment is fistulectomy (cone like technique), i.e., the execution of a circumferential
incision of the perianal skin on the external orifice on the surface of the fistula and then the ascent
towards the subcutaneous planes more and more cranial with a technique called 'cone like', because a
cone is described whose apex reaches the internal orifice of the fistula and the entire fistulous pathway
is treated and the endorectal advancement flap is removed in the same manner.
N.B. an early recurrence of perianal fistula should be immediately imagined as Crohn's disease, then
we may have confirmation or denial.
More severe pictures of perianal fistula may require faecal diversion with ileostomy
or colostomy, sometimes, proctectomy is also necessary.
In the most severe cases, in fact, in spite of the systems of therapy already listed, adequate control of
the perianal disease is not achieved and one is therefore forced, initially, to exclude faecal transit from
the rectum region or even to perform a proteomy, i.e. removal of the rectum.
Difference between colostomy and ileostomy. In the first case the colon is abutted to the abdominal
wall and being terminal, there is no continuity between the colon upstream and the colon downstream
of the colostomy which is closed. In the ileostomy (right), the ileum is abutted to the abdominal wall
and the rest of the colon is uninhabited with the only point of transit being the anal orifice, therefore,
the entire alimentary canal is exhausted with the ileum.
The choice of the ileum or colostomy is made in relation to the extent to which the colon is involved
by the disease; the colon is the seat not of the digestive process, but of the process of reabsorption of
liquids and electrolytes, so the more colon we are able to spare and conserve to the alimentary tract,
the less electrolyte imbalance the patient will have and especially the less liquid stools the patient will
emit within his colostomy bag.
Apart from faecal diversion and the need to rest the intestine downstream of the ostomy, i.e. the
sigmoid-rectal area in the case of colostomy and the entire large intestine in the case of ileostomy, it
may very often be necessary to undergo a proctectomy, a much more demolitive operation involving
the removal of the rectum and anus, which entails the placement of a, in this case, definitive ostomy.
Proctectomy is only to be considered in very serious cases w h e r e , despite all conservative
interventions, these have failed. The number of patients requiring this type of treatment is very low. In
the MICI outpatient clinic, an average of 1 or 2 patients may need proctectomy within a year.
Medical treatment
When a doctor finds himself having to work in an emergency room or in a so-called 'trench' post, he
must first use full-dose Ciprofloxacin (500 mg x2 per os) and full-dose Metronidazole (500 mg 3vv
per day).
In the context of perianal disease, there is some study of glues and plugs, i.e., the introduction of
adhesive substances into the fistulous passage.
An important role is played by biological drugs, which are now increasingly numerous and whose
progenitor is infliximab. It is now widely demonstrated, on a strong level of evidence and
recommendation grade B, that therapy with biologics is quite effective in the induction and
maintenance of clinical remission, the closure of entero-cutaneous perianal and recto- vaginal fistulas,
and the maintenance of their closure.
These are the 3 pivotal elements of the use of organics that one must understand:
● Induction and maintenance of clinical remission, which is essential because the moment the
seton and drainage of the perianal fistula is acted upon, allows the use of biologics, which
otherwise, in the presence of purulent material, cannot be used, is strongly contraindicated.
● Closure of enterocutaneous, perianal and rectovaginal fistulas, always preceded by their
drainage.
● Maintaining closure.
In past years, the use of the biological drug directly in the perianal fistula has been studied. Local
administration has comparable efficacy to systemic treatment for managing Crohn's disease patients
with perianal fistulas.
The problem is that while the efficacy of local treatment is comparable to systemic administration, the
latter provides greater protection against recurrences or return of disease throughout the entire
digestive tract, whereas if only the drug is used in the perianal area, with local inoculation, only that
lesion is treated, with the systemic method, on the other hand, there is also a very important preventive
treatment with infliximab and with biological drugs in general.
+ Perioperative management of medical therapy
The ECCO guideline section tells us that the patient's nutritional status must be taken into account
preoperatively in the patient requiring surgery for Crohn's disease. One must try to achieve
nutritional optimisation of the patient before surgery with enteral or parenteral nutrition - this is
recommended in patients with nutritional deficiencies.
The ECCO guidelines tell us that pre-operative steroid use is associated with an increased risk of
post-operative complications. Therefore, a gradual reduction of the steroid in the pre-operative
period must be carried out in order to reduce p o s t - o p e r a t i v e complications but with great care to
avoid an increase in disease-related complaints. So cortisone must be reduced, but at the same time it
must not be reduced recklessly because the disease may resume its course and a patient with active
disease may have to be operated on.
The use of anti-TNF preoperatively does not constitute an increased risk of post-operative
complications. Therefore the discontinuation of these medications at a time prior to surgery is not
mandatory, in particular it is mandatory for cortisone whereas it is not for anti-TNF.
Consideration must be given to performing a temporary ostomy (colostomy or ileostomy) when
steroids cannot be discontinued or significantly reduced before surgery so as to avoid any postoperative complications. In fact, since the steroid is a drug that reduces the protein synthesis
indispensable to the healing and consolidation processes of anastomoses, this induces the surgeon not
to do a resection with consequent anastomosis, but to do a resection, removing the intestinal tract that
is the site of the disease so as to solve the patient's symptomatic problems, packing a colostomy or
ileostomy depending on the intestinal tract resected and postponing recanalisation by a few months
when one is well away from the use of the steroid that the patient needed until a few days before the
operation.
Perianal disease: other clinical pictures
The marisca (which Anglo-Saxon authors refer to as skin tag) is a masserelle of skin that protrudes
from the surface of the anus or perianal region. It is essentially a non-painful, non-pathological
exuberance of skin in the anal region that forms as a result of traumatic outcomes
There are two types of skin tags or marisques:
● The typical Crohn's disease is large, oedematous, hard, cyanotic and painful.
● Other skin changes such as long fibroepithelial polyps, large flat skin growths known as
'elephant ear' growths
These manifestations do not need to be exported: they are an expression of perianal inflammatory
disease, but should not be subjected to surgery.
Haemorrhoid disease, can perfectly mimic Crohn's disease and vice versa, so when haemorrhoids
occur they may be an expression of Crohn's disease. Considering that haemorrhoidectomy is
contraindicated in individuals with Crohn's disease, if it is known that the patient has Crohn's disease,
a haemorrhoidectomy will not be performed, but it will be treated with medical treatment so that in
combination with the therapy system for Crohn's disease, a regression of the acute picture will occur.
One must be less than 'generous' in making an indication for haemorrhoidectomy because if it is
performed in a subject with Crohn's disease that is missed, the post-operative complications will be
much more conspicuous both in terms of their magnitude and in terms of numbers.
Wound healing may be difficult or may not occur at all, because the mucosa is the site of a chronic
inflammatory process in which there will be no easy remission of the wound. The same is true for
rectal stenosis, because when the haemorrhoidal process is significant, the fibrotic postphlogistic
evolution may lead to a picture of stenosis.
Ragade: in contrast to the typical fissure, it is painless. Whereas the typical fissure gives quite a lot of
pain.
When the fissure is an expression of Crohn's disease, it heals spontaneously in more than 80 per cent
of patients, because, as the disease evolves poussé, with a recrudescence phase, a plateau and then a
regression, the fissure will also follow the course of a spontaneous regression.
Surgery, again, should be avoided. It is easier to use vasodilator drugs such as nitroglycerin,
isosorbide dinitrate, diltiazem, botulinum toxin, which having a vasodilating, temporary muscle
relaxant effect can be used to promote the healing of the fissure and so when this effect regresses a few
weeks after local administration, it is possible to have a return to sphincter function comparable to that
which was present before the treatment.
Anal stenosis and rectal stenosis: these may be transitory or definitive, established forms in which
the stenosis is no longer dilatable and does not regress except with surgical therapy. They are usually
complications of ulceration of the anal canal and rectum, abscesses and perianal fistulas, where the
suppurative phlogistic process has evolved into a fibrotic process that leads to a loss of elasticity of the
connective tissues surrounding the anal canal or rectum and consequently a rigidity of the rectum
itself.
These anal and rectal stenosis are merely the counterpart of stenosis often found in the small intestine.
Symptoms related to stenosis are:
o Urgency: the patient, having a reduced capacity and volume of the rectum, will have a higher
frequency of evacuations due to the fact that the amount of faeces that can stagnate in the
rectum is less;
o Incontinence: if the phlogistic process that evolves into fibrosis has involved the sphincter
apparatus and, therefore, has gone into fibrosis, the elasticity and functionality of the muscle
will be lost;
o Tenesmus: because the inflammatory process is responsible for tenesmus when there is a
stimulation of the receptors and consequently the continuous need to go to the bathroom. There
is a stimulation of the receptors not related to the presence of faecal material in the context of
the anal canal, but related to the inflammatory process that exerts an irritating and nociceptive
action on the receptors;
o Frequency and difficulty of defecation: the former because there is less capacity of the
rectum, the latter because if the anal canal does not dilate sufficiently, there may be difficulty
in passing and often the faeces in this case have a ribbon-like appearance.
When they are multiple in number, they must be treated with stricturoplasty, i.e., a treatment to
widen the stenosis by dilating the intestinal lumen. This is done in the small intestine, anus and rectum
when these complications occur.
Recto-vaginal fistulas as a complication of perianal Chron's disease. Surgical treatment should only
be done if the inflammation is regressing, only in the absence of rectal and colon activity. Primary
closures, advancement flaps or faecal diversion can be done, which is very often necessary, at least
temporarily, to a l l o w healing of the sutures made between the rectum and vagina to a l l o w
separation of the two organs that have suddenly found themselves in a single fetal reservoir due to the
disease.
Carcinoma may be a condition that must be taken into account. Squamous cell carcinoma may be
present in individuals with inveterate Crohn's disease and adenocarcinoma may also be present.
RECTOCOLITIS ULCERATIVE
UCS is an ulcer-inflammatory disease confined to the colon. As far as epidemiology is concerned:
●
●
●
●
It is a ubiquitous disease but more present in developed countries;
There is a preference for the female sex and Jewish ethnicity;
There is a peak in incidence, young age between 20 and 25 years old
Incidence 4-12/100000 inhabitants;
The aetiological hypotheses are:
● Dietary factors: higher consumption of refined cereals and lower consumption of dietary fibre;
● Drugs such as oral contraceptives.
Smoking appears to act as a protective factor while an increased risk has been found in people who
stop smoking
Except in the most extensive and severe cases, it only affects the superficial layers of the wall, namely
the mucosa and submucosa. It extends continuously proximally from the rectum, which i s therefore
always affected. In fact, the most limited initial form of OCR is usually ulcerative proctitis.
The clinical manifestations are:
● Pain in the lower abdominal quadrants, cramping, relieved by defecation;
● Diarrhoea that unlike that in CD is a remitting and relapsing mucosanguinolent diarrhoea,
which testifies to its localised and more ulcerative nature;
● Peristalsis is altered and this can sometimes cause constiptic changes;
● Tenesmus and defecatory urgency.
Endoscopy
Hyperemic, bleeding and friable mucosa (signs of ulcerations) + small ulcers that tend to converge
and are the consequence of the destruction of the epithelial cell surface by the neutrophilic
inflammatory infiltrate. When there are ulcers, the mucosa tends to regenerate, creating the
inflammatory pseudopolyps, i.e. polypoid-like protrusions consisting of phlogistic infiltrate.
Differences with CD in which the destructive character of the inflammation and thus the thinning of
the wall prevails.
Complications
Since there is a widening of the lumen and a thinning of the wall, in the case of OCR we have other
types of classic complications, which are:
● Toxic megacolon: refers to dilation and relaxation of the wall, with disruption of the nerve
ganglia;
● Perforation: because diffuse ulceration of the mucosa, with this thinning of the wall, can lead
to intestinal perforation.
Focus: megacolon
Toxic megacolon is an abnormal gaseous distension of the colon, with acute onset, independent of
obstructive processes. Significant total or segmental dilatation of the colonic wall causes symptoms
such as bloating and abdominal pain, fever and shock.
Toxic megacolon is a complication of inflammatory bowel disease. Ulcerative colitis and Crohn's
disease are the most common causes of toxic megacolon in Italy and other industrialised countries,
while in developing regions and among debilitated patients toxic megacolon due to infectious
processes of the colon leading to pseudomembranous colitis prevail.
Unlike in a common colitis, in the presence of toxic megacolon the inflammatory process is not
limited to the superficial layers of the intestinal wall (mucosa), but goes deeper, also involving the
submucosal, muscular and serous tonaches. By affecting the nerve endings of the plexuses, the
inflammatory process can lead to muscular paralysis of the colon, with arrest of the progression of the
enteric contents and consequent distension. Due to the increased pressure, local venous and arterial
vessels are progressively occluded, facilitating necrotic and perforative processes. In addition, the
absorption of water and electrolytes through the intestinal mucosa is impaired.
Diagnostic confirmation is obtained by a plain X-ray of the abdomen, which in the presence of toxic
megacolon shows an abnormal increase in the diameter of the colon (at least 6 cm at the level of the
transverse colon), with possible signs of emphysema of the wall with mucosal dislodging. A CT scan
may follow. Biohumoral examinations show leukocytosis, haemoconcentration, increased ESR and
indices of inflammation, anaemia and electrolyte imbalances with a tendency to metabolic alkalosis
(increased blood pH).
Surgical treatment: decompression.
LEAF
FAILURE LIVER
Liver failure can be caused by many types of liver disease, including: viral hepatitis (more commonly
known as hepatitis B or C), cirrhosis and liver damage from alcohol or drugs such as paracetamol.
This condition occurs when an extensive part of the liver is compromised.
Liver failure may develop rapidly, within days or weeks (acute liver failure), or gradually, over several
months or years (chronic liver failure).
Liver dysfunction produces many effects:
● The liver is no longer able to adequately metabolise bilirubin (a waste product formed when
old red blood cells are destroyed) in order to eliminate it from the body. Bilirubin tends to
accumulate in the blood and is deposited in the skin. This causes jaundice.
● The liver can no longer synthesise sufficient proteins to promote coagulation. The result is a
tendency to bleeding and bruising (coagulopathy).
● The blood pressure in the veins that carry blood from the intestine to the liver is often
abnormally high (portal hypertension).
● Fluid may accumulate in the abdomen (ascites).
● Brain functions can deteriorate because the liver cannot remove toxic substances as it normally
does and these accumulate in the blood. This condition is called hepatic encephalopathy.
● New veins (called collateral vessels) can form that bypass the liver. Commonly, they form in
the oesophagus and stomach. Here, the veins dilate and twist. These veins, called varicose
veins of the oesophagus (oesophageal varices) or of the stomach (gastric varices), are fragile
and bleed easily.
● Up to half of all individuals with liver failure also have renal failure. Liver failure leading to
renal failure is called hepatorenal syndrome.
● There is a malfunctioning of the immune system that increases the risk of infection.
● Subjects may present metabolic abnormalities, such as low blood potassium levels (
hypokalaemia) or low blood sugar levels (hypoglycaemia).
LIVER DAMAGE ACUTE
Causes
Excessive intake of paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs), some medicines
(including antibiotics and anticonvulsants) and some phytotherapics (e.g. kava and ephedra),
hepatitis A, B, C, and E viruses, and other viruses (such as Epstein-Barr, cytomegalovirus and herpes
simplex), certain toxins (such as that of the fungus Amanita phalloides), autoimmune hepatitis,
vascular diseases (such as Budd-Chiari syndrome) and rare metabolic diseases (such as
hepatolenticular degeneration).
Clinical manifestations
Altered mental status (usually part of porto-systemic encephalopathy) and jaundice. Manifestations of
chronic liver disease such as ascites go against the acuity of the condition, but may be present in
subacute liver failure. Other symptoms may be non-specific (e.g. malaise, anorexia) or result from the
causative disorder. Fetor hepaticus (sweetish breath odour) and motor dysfunction are common.
Tachycardia, tachypnoea, and hypotension may occur with or without sepsis. Signs of cerebral oedema
may include dullness, coma, bradycardia, and hypertension. Patients with infection sometimes have
localised symptoms (e.g. cough, dysuria), but these may be absent. Despite the prolonged international
normalised ratio (INR), bleeding is rare unless patients are in disseminated intravascular coagulation.
This is because patients with acute liver failure have a rebalanced distribution of pro- and
anticoagulant factors and, if anything, these patients are more frequently hypercoagulable.
Acute liver failure should be suspected if patients without underlying chronic liver disease or cirrhosis
have an acute onset of jaundice and/or elevated transaminases accompanied by coagulopathy and
changes in mental status. Patients with known liver disease who decompensate acutely are not
considered to have acute liver failure, but rather acute-on-chronic liver failure, which has a different
pathophysiology from acute liver failure.
Laboratory tests to confirm the presence and severity of liver failure include liver enzymes, bilirubin
levels and prothrombin time. Acute liver failure is usually considered confirmed if the sensorium is
altered or the prothrombin time is prolonged (> 4 seconds) or if the international normalised ratio
(INR) > 1.5 in patients who have clinical and/or laboratory evidence of acute liver damage.
HYPERTENSION PORTAL
The portal vein, formed by the superior mesenteric vein and the mesenteric-lienal trunk formed by the
confluence of the inferior mesenteric vein and the splenic vein, drains blood from the abdominal
gastrointestinal tract, spleen and pancreas into the liver. In the blood channels lined by the
reticuloendothelium (sinusoids), blood from the terminal portal venules converges with blood from the
hepatic artery. The blood then flows away from the sinusoids into the suprahepatic veins, which in
turn drain into the inferior vena cava.
Normal portal pressure is 5-10 mmHg. Portal hypertension results mainly from increased resistance to
blood flow in the portal vein. A frequent cause of this resistance is the presence of cirrhotic liver
disease; less frequent causes include blockage of the splenic vein and portal vein (portal thrombosis)
and cases of impaired venous outflow from the liver (hepatic venous thrombosis or inferior cava
obstruction), arteriovenous fistula, idiopathic portal hypertension, primary biliary cholangitis,
sarcoidosis, congenital liver fibrosis, schistosomiasis.
In cirrhosis, tissue fibrosis and regenerating nodules increase resistance in the sinusoids and terminal
portal venules. However, other potentially reversible factors may contribute; these include the
contractility of the cells lining the sinusoids, the production of vasoactive substances (e.g., endothelin,
nitric oxide), the various systemic mediators of arteriolar resistance, and possibly also the swelling of
hepatocytes.
Subsequently, portal hypertension creates portal vein collaterals. They can slightly reduce portal vein
pressure but can cause complications. Submucosal, congested and serpiginous vessels (varices) in the
distal oesophagus and sometimes in the gastric fundus can rupture, causing sudden and catastrophic
gastrointestinal bleeding. Bleeding rarely occurs if the portal pressure gradient is >12 mmHg. Vascular
congestion of the gastric mucosa (portal pressure congestion gastropathy) can cause acute or chronic
bleeding independent of varices. The formation of visible collateral circles on the abdominal wall is
also common; veins radiating from the umbilicus (caput medusae) are rarer and indicate significant
flow in the umbilical and periumbilical veins. Collateral circles that form around the rectum can cause
rectal varices that may bleed.
Portal-systemic collateral circles divert blood from the liver. Thus, less blood reaches the liver when
portal flow increases (decreasing liver reserve). In addition, toxic substances from the gut are diverted
directly into the systemic circulation, contributing to porto-systemic encephalopathy. Venous
congestion within the visceral organs due to portal hypertension contributes to the formation of ascites
through altered Starling forces. Due to the increased pressure in the splenic vein, splenomegaly and
hypersplenism frequently occur. Thrombocytopenia, leucopenia and, less frequently, haemolytic
anaemia may develop.
ADENOMA LIVER
Benign neoplasm with a much lower incidence than hepatocarcinoma. It is more frequent in
women of childbearing age, and in 50% of cases it is related to taking oestrogen.
● Symptomatology: 50% asymptomatic or with vague pain, may begin with the sudden onset of
acute pain (indicative of the occurrence of an infarct or intratumoural haemorrhagic episode).
Subsequent tumour rupture may occur in the subglissonian site, with formation of subcapsular
haematoma, or in the peritoneal cavity, with formation of haemoperitoneum and severe
haemorrhagic shock.
● Macroscopy: spheroidal, smooth-surfaced capsular lesion, >5 cm in diameter, frequently in subcapsular location, yellow to brown soft consistency.
● Microscopically: characteristic is the total absence of portal spaces and bile ducts in its context.
May contain areas of biliary collection, intratumoural haemorrhage or infarct zones. Noninfiltrated blood vessels: dd well-differentiated cell adenocarcinomas.
● Ultrasound: hyperechogenic nodular lesion with well-defined margins sometimes containing one
or more anaecogenic central areas. Not capable on its own of dd with malignant lesions.
● CT: hypodense structure with intense enhancement following mdc administration.
● Symptomatic adenomas or those complicated by haemorrhage require resective surgical therapy,
while asymptomatic and small (<6 cm) adenomas, in the absence of complications, can be treated
conservatively, with periodic ultrasound checks. Estroprogestins should be discontinued.
NODULAR HYPERPLASIA FOCAL
It is a usually single nodular lesion with no malignant potential, arising in a normal liver. The colour is
dark red or brown and the average diameter is 2-3 cm.
Most of the patients are asymptomatic. Symptomatic patients (>5 cm) report: pain and a feeling of
weight in the right hypochondrium. Bleeding and intralesional infarction are infrequent.
Ultrasound: the lesion can be missed as the ecostructure is very similar to that of normal parenchyma.
CT and MRI: identify the lesion. Needle biopsy for diagnosis of certainty.
Surgery is only indicated in severely symptomatic patients due to the size of the lesion and in cases of
uncertain diagnosis.
ABSCESS LIVER
More frequent in patients aged >40 years. They may be single or multiple, a few mm to several cm.
They do not always arise as a primary lesion.
1) Cryptogenic (increasing): possible cause of infection of hepatic micro infarcts secondary t o
splanchnic thromboembolism.
2) By pyogenes, mechanisms of liver infection: suppurative cholangitis associated with biliary tract
obstruction induced by benign or malignant neoplasms, by:
- Direct diffusion from contiguous outbreaks
- Ascending route along the biliary tract - Haematogenous spread through the hepatic aa
- Diffusion with portal blood
- External contamination
Clinical:
- Septic-type fever (remitting or continuous)
- Shivering shivers
- Anorexia
- Pain in the right hypochondrium with irradiation to the ipsilateral shoulder
- Severe impairment of general condition (nausea and vomiting, weight loss, anorexia).
Therapy: surgical drainage and antibiotic therapy
3) Amebic abscess (secondary to intestinal infection)
Amebic dysentery outbreaks usually result from faecal contamination of drinking water. In 3-4% of
cases it complicates with an amoebic liver abscess: right lobe x10 vs. left.
Pathogenesis: ingestion of cysts □ release in the distal tenuous and colon of trophozoites □ portal
blood □ liver □ portal capillaries □ abscess
Parasites induce thrombotic obstruction of the finest portal branches resulting in necrosis of the
vascular wall and intrahepatic dissemination of trophozoites. The liver abscess proper originates from
the colliquation and confluence of small hepatic areas by lytic enzymes and the cytolytic action of the
parasite.
NB. only in the presence of a persistent or chronic intestinal infection with repeated passage of
trophozoites in the portal blood can the liver be reached and multiple miliary abscess areas formed.
Animal studies have shown that abscess formation occurs if there is persistent or chronic intestinal
infection and previous sensitisation to amoebic antigens.
Clinical: insidious onset - dramatic; lasting a few days or fading for months.
-
Right hypochondrium or epigastrium pain;
Weight loss;
Fever;
Compromising general conditions
GI symptomatology (15%)
Jaundice (infrequent, due to compression)
Laboratory: leukocytosis (75%) - anaemia and hypoalbuminemia (50%) - hyperbilirubunukaemia (
10%) - impaired liver function indexes (25%)
Diagnosis
It can also be placed without the finding of intestinal infection (cysts/trophozoites in the faeces present
in only 15% of cases).
Serological tests Ab anti entamoeba histolytica (positivity > 98%). Abscess contents fluid or
gelatinous abscess varying in colour from yellowish to pink to brown. Colliqued material within the
abscess is bacteriologically sterile: the search for entamoeba in the abscess pus is of little significance.
Aspiration of chocolate-coloured, bacterial-free necrotic material is sufficient to establish the
diagnosis.
Complications (often fatal)
Concentric expansion to the hepatic surface and rupture into the peritoneal cavity (acute abdomen and
shock, especially on the left side) or extension to neighbouring organs by contiguity. Pleuropulmonary
complications (the most important) resulting from trans-diaphragmatic rupture of the abscess within
the pleural cavity.
Haematogenous spread of the parasite may result in single or multiple brain abscesses (very high
mortality, with no distinctive signs and symptoms).
Therapy: metronidazole; open drainage; closed drainage.
CYST HYDATID
50-70% of Echinococcus granulosus cysts in humans are localised in the liver. In Italy, the disease is
endemic in Sardinia, Sicily, Campania and Apulia (regions whose inhabitants are pastoralists). The
primary host of the disease is the dog, while the intermediate host is ruminants (sheep, cows) and
occasionally humans.
The hydatid cyst is circumscribed by a wall with three concentric layers:
1) outer layer or pericystis,
2) intermediate layer or chitinous membrane,
3) inner or germinative layer.
Clinical picture (25% of patients are asymptomatic)
● Persistent pain and feeling of weight in right hypochondrium or lower portion of right
hemithorax.
● Others (rarer): anaphylactic shock (resulting from cyst rupture) and obstructive jaundice
(may be due to rupture of the cyst in the biliary tract).
Surgery
It is necessary for cysts in a subcapsular or very voluminous position, which are at increased risk of
complications, and in young patients in good general condition.
● Complete removal of the cyst, avoiding contamination of the peritoneum, and obliteration of the
residual cavity; the most commonly performed operation is pericystectomy, consisting of
enucleoresection of the cyst from the liver parenchyma, following the cleavage plane formed by
the cyst wall. Partial pericystectomy in cases where it is too large and would coincide with a
hepatectomy.
● Liver resection is rarely necessary
EMANGIOMA
A benign vascular liver formation is most frequently found, and is more frequent in women (6:1).
They are usually nodular lesions with a fibrous capsule, single or multiple, with a soft consistency and
an average diameter of 1-3 cm (may reach 10-20 cm).
● Most patients are asymptomatic. Angiomas >4 cm may induce the appearance of pain, a feeling
of weight and a palpable mass in the right hypochondrium. Atypical presentation: presence of
heart failure with recurrent lipotimia episodes.
● Complications: acute thrombosis, with entrapment of figured elements and risk of pulmonary
embolism (Kasabach-Merritt syndrome), and spontaneous (very rare) or post-traumatic
rupture in the peritoneal cavity.
● Echography: irregular hyperechogenic areas well demarcated from the surrounding parenchyma.
● CT: hypodense lesions with characteristic and persistent enhancement after mdc injection.
● Surgery reserved for symptomatic cases or those at risk of complications due to the large size of
the tumour.
HEPATIC CARCINOMA
It is the most frequent primary malignant tumour of the liver. It arises around the age of 50-60. In 90%
of cases it arises on chronic hepatopathy (alcohol, anabolic agents, haemochromatosis, smoking,
tobacco, arsenic, irradiation, a1 antitrypsin deficiency). HBV - HCV (pathogenesis): repeated cycles
of cell death and regeneration (+ HBV direct carcinogen). Aflatoxin B: mycotoxin produced by
Aspergillus Flavus, potent carcinogen, dose-dependent.
Clinical picture (symptoms and signs)
● The disease runs silent in the early stages, making early diagnosis difficult.
● The most frequent presentation is the sudden decompensation of a stable cirrhosis, with dull,
deep and worsening pain in the right hypochondrium and epigastrium, weight loss, fever, asthenia
and anorexia.
● Other less frequent symptoms depend on the tumour's peculiar location: jaundice (if it compresses
the main biliary tract) - severe abdominal pain (if it distends Glisson's capsule or ruptures in the
peritoneum) - respiratory symptoms (in the case of a large subdiaphragmatic mass).
● Signs: hepatomegaly (most frequent occurrence) - appreciable mass under the costal arch (a
times) - ascites and splenomegaly (in case of concomitant cirrhosis).
● Paraneoplastic
syndromes
(hypoglycaemia,
erythrocytosis,
hypercalcaemia,
hypercholesterolaemia, porphyria cutanea tarda, gynaecomastia, carcinoid s., hypertrophic
osteoarthropathy, polyneuropathies, PAH, hyperthyroidism).
● Metastasis by blood (50%): lung (95%) - adrenal - intestine - bone - spleen - heart - kidney. By
lymphatic route: hepatic hilum - peripancreatic lymph nodes. Early invasion of portal venous
structures giving rise to retrograde neoplastic thrombi responsible for diffuse intraparenchymal
metastases.
Diagnosis
● History and EO
● Macroscopy: single/ infiltrating mass with multicentric/multinodular shape (in cirrhotics, !dd
regenerating nodules). Its consistency is soft (explains the possibility of intraperitoneal rupture).
Areas of necrosis and haemorrhage may be present in large lesions.
Laboratory:
very high (80%, levels in relation to the size of
the neoplasm) vn Ca19.9 (dd colon and cholangiocarcinoma).
● Echography (1st level); Echo-guided biopsy in case of benign nodules/metastases;
● Angio-CT (hypervascular pattern with early venous washing), useful for accurately distinguishing
between vascular and biliary structures and between healthy and pathological tissue.
Child-Pugh score
It is a scoring system used to assess the severity of chronic liver disease, especially cirrhosis. It is
based on the evaluation of five clinical parameters, bilirubin tot, albuminemia, INR, ascites and
hepatic encephalopathy, each of which can be assigned a score between 1 and 3. Depending on the
score, three Child- Pugh classes can be identified: A, B and C.
Curative treatment
In selected patients with a single nodule <5 cm or 3 nodules <3 cm (stage A of the Barcelona
classification (BCLC - Barcelona Clinic Liver Cancer)).
● Surgical resection (20-30% at the time of diagnosis): single nodule and Child-Pugh A, normal
bilirubin and absence of portal hypertension (porto-caval gradient <10 mmHg). In the case of
cirrhotic livers, surgery must involve sparing as much of the parenchyma as possible: the
interventions of choice are atypical resections (with a resection margin from the tumour of at least
1-2 cm), peripheral resections and segmentectomies.
● Transplantation: single nodule but portal hypertension or elevated bilirubin, or 3 nodules with
Child-Pugh A-B.
● Percutaneous ablation (''interstitial therapy'') with alcohol, radiofrequency, cryotherapy or
microwave (interstitial hyperthermia techniques): in patients who are not candidates for transplant
due to their age or comorbidities.
Non-curative treatment
B-C stage BCLC patients, 3-year survival 10-50%: selective hepatic aa chemoembolisation with
microspheres or lipid emulsion substance or systemic chemotherapy with Sorafenib.
Symptomatic treatment (stage D BCLC): Survival < 3 months.
Treatment of liver metastases
Synchronous (present at the time of primary tumour diagnosis) or metachronous (appearing some
time after bowel surgery). The maximum number of removable metastases is believed to be 3.
Synchronous metastases: should only be resected if small and localised to the left lobe or organ
surface. If metastases are localised to posterior liver segments and are of a certain size, since they
require extensive hepatectomy, resection should be delayed by a few months to reduce the operative
risk.
Resective surgery liver
Incisions for liver resections: bilateral subcostal - subcost bil a mercedes - median sternotomy.
Major liver resections
Hepatectomy
main portal cleft
dxasports the liver parenchyma to the right of the
(60/70% of the liver parenchyma) including segments V - VI - VII - VIII. Exposure of the hepatic
hilum: cholecystectomy - preparation of the hilar elements. Isolation of the right hepatic duct,
ligation of the right hepatic aa, preparation and division of the right portal branch.
● Left hepatectomy removes the parenchyma on the left side of the main portal cleft (segments II,
III, IV).
● Enlarged right hepatectomy: the liver parenchyma located to the right of the falciform ligament
(segments V, VI, VII, VIII, IV) is resected. It is the most demolitive operation, removing 80/85%
of the liver parenchyma.
● Left lateral segmentectomy is the resection of the parenchyma on the left side of the falciform
ligament. From an anatomical point of view the term is improper because the true left lateral
segment is only II. More correct is the definition of left bisegmentectomy of segment II and III.
Atypical resections (segmental, wedge resection): performed without respecting the anatomical
scissural planes. They are usually resections of small peripheral superficial liver lesions, not in the
vicinity of large-calibre vascular and biliary structures.
Typical minor resections: they involve the resection of single or associated hepatic anatomical
sectors or segments and are therefore referred to as sectorectomies, segmentectomies,
bisegmentectomies.
Difficulties in liver resective surgery related to:
● Type of lesions (e.g. better metastases from large intestine K or neuroendocrine tumours);
● Number of lesions and size (the larger they are, the lower the oncological effectiveness es
metastasis);
● Localisations, easiest are: left resections (on the right the liver is larger and has a greater
connection with the inferior vena cava) - excisions of superficial and anterior masses.
● Morpho-functional conditions of the liver: e.g. cirrhotic liver (increased operative mortality).
VIEWS BILIARS
STONES BILIARY
Biliary lithiasic disease is divided into two chapters:
- Intrahepatic biliary lithiasis: in which there is stone formation within the hepatic canaliculi
up to the right and left hepatic ducts
- Extrahepatic biliary lithiasis: (most frequent): in which the presence of stones in the
gallbladder and main biliary pathway (VBP): common hepatic duct and gallbladder
Gallbladder lithiasis
The gallbladder is the storehouse of bile that is constantly produced throughout the day and its
production increases in the post-prandial periods. The bile is produced by the liver, then from the left
and right hepatic ducts it goes to the common hepatic duct and from there to the cystic duct and on to
the gallbladder.
Bile consists of:
Bile salts
- Bile pigments (bilirubin)
- Cholesterol
- Calcium salts
- Fatty acids
- Phospholipids
The gallbladder empties when food is ingested, thanks to the action of digestive hormones (e.g.
cholecostokinin and secretin) that stimulate its contraction.
Risk factors
They are represented by the 4Ps:
- Female
- Forty
- Fat
- Fertility
So we will have:
1) Female sex (also due to taking oestrogen: oestrogen reduces the secretion of bile salts and
increases the secretion of cholesterol)
2) Obesity (in fact, gallstones are made up of cholesterin, which results from cholesterol
metabolism)
3) High-fat diet
4) Age between 30-50 years
5) Fertile women
6) Conditions favouring biliary stasis
7) Diabetes
Pathophysiology
The formation of stones is due to 3 main mechanisms:
1) Lithogenic bile (biliary hypersecretion of cholesterol): due to obesity, high-fat diet, drugs,
increased hepatic uptake of cholesterol, or increased HMG-CoA reductase activity
2) Formation of cholesterin micro-aggregates
3) Cholecystic hypomotility: causes stasis of bile. For example in a gastric resection operation,
the vagus nerves run along the anterior aspect of the oesophagus and then run to the right and
left and are involved in gastric secretion and motility, but also in the motility of the gallbladder.
So in the case of gastric resection, there will be a drastic reduction in the motility of the
gallbladder, which becomes more atonic, and this clearly creates biliary stasis within the
gallbladder and this favours stone formation. In addition, in these pts, there will be a
restoration of intestinal continuity through the Billroth or a roux loop, which do not allow an
eventual exploration of the biliary tract endoscopically. And so if later on the gastro-resected
pc were to develop acute cholecystitis or choledochal lithiasis, one is forced to perform a much
more demanding intervention: choledochotomy, with reclamation of the biliary pathway, when
in fact everything is done via ERCP today.
These conditions lead to the formation of gallstones, which can be distinguished into:
a) Pure cholesterinics: yellow (90%)□ are the most common
b) Mixed cholesterins
c) Bilirubin: black, brown (e.g. patients with haemolytic anaemia or chronic hepatopathy)
However, before moving on to actual stone formation, one speaks of 'biliary sludge', i.e. biliary sludge,
consisting of:
- Calcium salts
- Cholesterol crystals
- Mucina
Clinic
The clinical symptoms of the patient are characterised by:
1) Asymptomatic: the stones form slowly, the gallbladder then becomes accustomed to the stones
and often the ultrasound diagnosis is accidental, like the lithiasis finding itself.
2) Gallbladder colic: gravative-urengeal, cholic pain, which starts in the epigastric area, then
moves to the right hypochondrium, until it radiates to the ipsilateral shoulder (it is pain due to
intense contractions of the gallbladder trying to push the stone towards the cystic duct); even in
the presence of biliary sludge - i.e. dense bile, pain like colic occurs
bile even in the absence of stones, because as this bile is dense and not very mobile, the
gallbladder struggles to get it out.
3) Nausea and vomiting: frequently accompany episodes of biliary pain
4) Dyspepsia: it is a general malaise, a sense of poor digestion (slow and laboured). In fact, a
person with biliary sludge (bile sands) or stones may never have had dyspepsia in his or her
life.
5) Bitter mouth feeling
In the case of:
- Lithiasis of the main biliary tract: colic, fever and jaundice (Charcot's triad)
- Intrahepatic biliary tract lithiasis: fever, jaundice, pain
In this case, jaundice will be the main sign, and it is linked to the presence of stones in the bile ducts,
which give obstruction, preventing the proper reflux of bile. This is referred to as obstructive jaundice.
Complications of gallbladder lithiasis
Gallbladder lithiasis can complicate in:
1) Acute cholecystitis: which will then have different degrees:
- Gallbladder hydrops: when a stone wedges at the level of the infundibulum, internal mucous
secretions accumulate and the gallbladder increases in volume until it becomes paradoxically
palpable
- Empyema of the gallbladder: in case of bacterial overinfection, there will be an accumulation
of purulent fluid inside the gallbladder. In fact, the stone obstructing the escape of bile into the
hydropic gallbladder is not watertight and therefore germs in the digestive system can enter the
gallbladder and give rise to bacterial overinfection
- Gallbladder phlegmon: determined as a progression of gallbladder empyema
- Necrosis/gangrene of the gallbladder, up to perforation
2) Obstructive jaundice:
- Migration of stones in the main biliary pathway (VBP)
- Mirizzi's syndrome type I and II: the stone gets stuck in the cystic duct or infundibulum, to
the point of creating adhesions and thus ab extrinsic compression of the VBP (common hepatic
duct or choledoch), obstructing it and causing obstructive jaundice.
3) Acute biliary pancreatitis
4) Gallbladder fistula: these are cholecyst-duodenal or cholecyst-colic fistulas, usually of long
duration, in the presence of large stones, the decubitus effect of which, in addition to wall
inflammation, create alterations in the parietal microcirculation, with the onset of ischaemic
phenomena, which promote necrosis and thus fistulisation. The stone erodes the wall of the
gallbladder, and the stone coming out of the gallbladder can reach as far as the ileocecal valve,
where it stops, leading to, mechanical intestinal occlusion, we speak of biliary ileus (DD from
the choleperitoneum).
N.B. Usually the asymptomatic patient with biliary sludge is recommended medical therapy with
'Deursil', i.e. ursodesoxycholic acid, which increases the amount of bile acids, decreasing the
concentration of cholesterol and making the bile more fluid. But in the case of both bile sludge and
stones, which do not correlate with obvious clinical symptoms, so asymptomatic and
paucisymptomatic patients are still advised to undergo cholecystectomy
Biliary sludge and microlithiasis, in fact, can lead to frightening complications, because, unlike a
large stone, which cannot pass out of the gallbladder, they can be discharged outside the gallbladder,
the persistence of which in the main biliary tract gives jaundice; or if bile stagnation affects the duct
of Wirsung, it can give acute pancreatitis.
Diagnosis
Diagnosis involves 3 main steps:
1) Abdominal EO: will be evaluated:
- Distended palpable gallbladder
- Cystic sore spot (interstitiation between the margin of the rectus abdominis and the costal arch
)
- Positive Murphy's sign: stop of inhalation on deep palpation of the gallbladder in the right
hypochondrium, as inhalation lowers the diaphragm, which brings the liver downwards and the
bottom of the gallbladder protrudes under the costal arch and on palpation the patient feels
pain); the pain is due to the contact between the irritated organ and the parietal peritoneum, as a
reflex reaction
2) Haematochemical examinations: these are usually normal in the asymptomatic or
paucisymptomatic patient. In the case of complications, there will be:
- Increased cholestasis indices: in case of stone migration from the gallbladder to the VBP (the
patient will have jaundice) - gamma-GT, alkaline phosphatase, total, direct and indirect
bilirubin
- Increased liver function indices: coagulation factors, albumin, pseudokinesterase, bilirubin,
increased transaminases (which are indices of cytolysis)
3) Instrumental examinations: the gold standard is abdominal ultrasound, which is able to see
gallstones: hyper-hecogenic formations with a posterior shadow cone and mobile with
decubitus. And especially in the elderly, the mobility of the stones excludes the presence of
endoluminal lesions, such as: neoplasms, leomyomas, adenomyomatosis; Biliary sludge, on
the other hand, on ultrasound examination we see it as a bile with low amplitude echoes and a
posterior focus, stratified by severity.
N.B. In the case of leiomyomas of the gallbladder, the patient is always treated by cholecystectomy,
but in the case of elderly patients with a protruding lesion in the lumen, it could be a gallbladder
cancer, and in this case, in addition to cholecystectomy, because of the continuity between liver and
gallbladder, 4-5 hepatic segments must also be resected (taking care not to puncture the gallbladder,
because there is a very high risk of peritoneal carcinosis).
Then the diagnosis can be ascertained by CT scan, which, however, does not have the same
sensitivity in assessing the presence of ETG calculi, however (since especially cholesterin
calculi are radiolucent), nor does it visualise any calculus that has become wedged in the
infudibulum
.
It can highlight indirect signs of complications such as acute cholecystitis or choledochal
lithiasis: pericolecystic effusion, dilation of the bile ducts
Then as a level II-III examination we have the cholangio-RMN, performed only in selected
cases, when for instance we have doubts of choledochal lithiasis or if a cholangiocarcinoma has
to be excluded.
The diagnostic criteria for acute cholecystitis are:
-
-
1) Local signs of inflammation:
Positive cystic point
Positive Murphy sign
Palpable mass/pain (due to distension or overdistension of the gallbladder)/tension in right
hypochondrium
2) Systemic signs of inflammation:
Fever
Leukocytosis
Elevated PCR and ESR
3) Instrumental investigations:
Ultrasound: allows us to see the inside of the organ, wall thickness, relationship with the liver
CT abdomen with mdc: allows us to study effusions, lymph nodes, perforations of the
gallbladder and to understand the severity of the affections.
Cholangio-RM: where ETG and CT do not provide useful data for diagnosis.
Then there are the difficult acute cholecystitis: there is no unambiguous definition, certainly their
definition is partly related to the experience of the operator. To identify them, a grading or scoring
system is needed. When we talk about difficult, we mean in relation to, for example, operating time or
post-operative complications. The definition takes into account:
1)
2)
3)
-
Age >60 years
Male gender
Clinical parameters:
Repeated and sub-occurring colic (in which the interval between one colic and the next is
shortened)
- Previous surgery
- Cirrhosis (there is a greater tendency for stones to form in cirrhotic patients)
- Diabetes
- Obesity
- Jaundice
4) Blood parameters:
- Hyperbilirubinemia
- Leukocytosis
- Increased pancreatic enzymes: amylase and lipase
5)
-
Increased liver enzymes and cholestasis
Hepatobiliary ETG:
Wall thickness > 4 mm (usually 1-2 mm)
Peri-colecyst fluid
Increased gallbladder volume
Cystic dilatation and VBP
VBP lithiasis
Considering these parameters, a score is determined, divided into four grades:
1) Grade 1: soft-walled gallbladder without adhesions, with a free, thin cystic pedicle that has no
adhesions, or if there are they can be detached easily and are generally located at the
infundibulum;
2) Grade 2: a mucocele has formed with the gallbladder excluded, because the presence of stones
means that it can no longer discharge, resulting in recurrent colic. The bile pigment part is
almost reabsorbed and the bile becomes white, almost transparent. The cystic pedicle is
covered with fat and there may be simple adhesions.
3) Grade 3 and 4: there is empyema or gangrene, or there may even be a tumour, and the cystic
pedicle is impossible to recognise and the adhesions are dense and fibrous. Especially in the
elderly with a significant degree of empyema, a subtotal cholecystectomy is performed: since
the artery and cystic duct cannot be identified and given the very high risk of damaging the
VBP, the cholecyst is removed at the infundibulum, leaving the portion of the infundibulum
bound, rather than causing damage to the biliary pathway, which would have far worse
consequences. In fact, an injury to the biliary tract increases the risk of death tenfold.
Treatment
The surgical treatment par excellence is cholecystectomy, which today is performed laparoscopically
in 90% of cases (first performed by Muoret, who later became its pioneer). Thanks to the introduction
of laparoscopy, except in selected cases, this modality represents the gold-standard and the
laparotomic approach has been abandoned, as it is too invasive, for the removal of a small organ.
The laparotomic approach is reserved for those 10% of patients who cannot undergo the laparoscopic
approach, perhaps presenting comorbidities due to possible complications, including those cases in
which a conversion is necessary during laparoscopy, which may be due to:
- Failure to recognise Calot's triangle
- VBP dilatation
- Mirizzi syndrome
- Iatrogenic injury of the VBP
The laparotomic approach included:
- As a matter of urgency, an incision along the linea alba ran from the xiphoid, through the
umbilicus, to below the umbilicus;
- In the election, a right subcostal incision.
Laparoscopy is performed through small incisions in the abdominal wall, which a l l o w small trocars
to be introduced, through which forceps of varying diameters are inserted to manipulate the structures
and perform the surgical act. A pneumoperitoneum is determined in the subject by insufflating air
through the main trocar: the abdominal wall is dilated, the diaphragm is raised.
Two techniques are envisaged:
1) French (most common)
2) Americana
The French technique involves the use of 3-4 trocars:
- First trocar: this is inserted through an incision in the umbilical scar, and allows the optical
camera to be introduced into the peritoneum, through which the gallbladder is extracted at the
end of the operation
- Second trocar: 5 mm placed in the right iliac fossa
- Third trocar: 10 mm left hypochondrium
- Fourth trocar: 5 mm at sub-xiphoid level.
The various trocars are placed in a horseshoe or radial pattern around the right hypochondrium, where
the gallbladder is located. The French technique gives the best exposure and visualisation of the
elements of the hepatic hilum. In addition, according to the French school, the surgeon positions
himself between the legs of the patient, with the monitor facing him, and the first assistant positions
himself to the right of the surgeon, then to the left side of the patient.
In the American/English school, the first operator stands to the left of the patient (who is supine, with
closed legs) and the assistant stands to the side of the surgeon.
The various stages of the intervention include:
1) We identify Calot's triangle, which is a closed space formed by connective tissue existing
between the liver, VBP and accessory VB, which allows us to remove the gallbladder properly
and safely, consisting of:
- Caudate lobe of the liver
- Cystic duct
- Common liver duct
2) Identification of the gallbladder hilum, which consists of a biliary part and a vascular part. The
biliary part is represented by the cystic duct, which connects the infundibulum of the
gallbladder with the VBP; cystic artery (on which the lymphatic pathway and the cystic vein
rest, which are two such small structures that they are not isolated), branch of the right hepatic
artery. These two structures are clipped upstream and downstream with titanium metal clips
and then the section between the metal clips of the cystic duct and cystic artery is made using
scissors
3) Enucleation of the gallbladder from the hepatic bed (4-5 segment): this results in a detachment
of the gallbladder, which is covered anteriorly and laterally by serosa
4) Control of haemostasis: the current cauterises the small venous and arterial structures and
gradually detaches the entire biliary sac from its connections with the liver.
5) Then the gallbladder is introduced into an endobag and extracted from the peritoneal cavity
through the umbilical scar.
Drainage is often not even necessary and if the patient is well the next day, he can even start eating.
Laparoscopy can lead to complications in the case of:
-
-
Obesity: not because of the thickness of the panniculus adiposus but because of the
pathologies to which obesity is correlated, namely diabetes and respiratory pathologies (which
are aggravated by the elevation of the diaphragm, following pneumoperitoneum)
Previous abdominal surgery: especially laparotomic abdominal surgeries encourage
inflammatory reactions that lead to scarring, with the formation of adhesions that can become
intertwined between the camera and the organ to be removed, which can lead to a perforation
of the intestinal loop (and then the adhesions must first be lysed).
It is certainly not a risk-free procedure, as the gallbladder is in close contact with the hepatic hilum
and therefore the possibility of complications is high. The cystic artery is a branch of the right hepatic
artery and if this artery is injured, the right liver suffers significant damage. The cystic duct converges
on the common hepatic duct, which then continues with the choledocochlea, and thus the bile duct
could be injured. One has to be careful not to puncture the gallbladder, as one could contaminate the
surgical field, since bile is not sterile and thus contamination, leading to abscesses, could occur postoperatively.
Timing of surgery
The best TIMING will also be crucial, so understand:
1) When is the best time to intervene on acute cholecystitis
2) Which surgery should be performed: laparotomy or laparoscopy.
3) What is the optimal treatment depending on the severity of the acute cholecystitis, preferring
surgery or conservative treatment (i.e. whether to operate the patient or try to cool him down)
It is type A evidence to perform the cholecystectomy as soon as possible, and then to implement early
treatment within 24-72h of the diagnosis/onset of symptoms. In this case, it preserves the patient from
the risk of:
- Softness
- Blood loss
- Complications
This reduces the duration of surgery and also the post-operative recovery time.
Open vs Laparoscopic
While it is assumed that laparoscopic treatment is to be preferred, there are complex pictures that do
not allow laparoscopic treatment but require opting for open treatment of necessity.
There are conditions in which we have patients with comorbidities such that neither laparoscopic nor
laparotomic treatment can be considered, and in these cases, interventional radiologists intervene with
percutaneous cholecystostomy, a palliative method: it consists of placing a drain at the level of the
bottom of the gallbladder percutaneously, in an ETG/TC-guided mode. It is a procedure to decompress
the gallbladder, so if you have an abscess, you drain it. However, at a certain point this drainage has to
be removed, and fortunately, it happens that the sclerosis and fibrosis that occur, cause the fundus to
"water down" and become scleroatrophic, or "parietalise" as if it were a kind of ostomy. It is indicated
for elderly, high-risk, cardiopathic patients, with a high anaesthetic risk, then conservative treatment is
opted for.
Surgery vs Conservative Treatment
Depending on the severity of the acute cholecystitis:
- Grade I or mild acute cholecystitis: PCs in good general clinical condition with only local
inflammatory phenomena and no distant organ dysfunction. These patients may benefit from
laparoscopic treatment (as soon as possible).
- Grade II-III or moderate/severe acute cholecystitis: there is distant organ dysfunction with a
MOF of the respiratory and cardiovascular system.
In cases of synchronous cholecysto-coledocytosis:
1) Sequential endoscopy-laparoscopy
2) Single-time VLS (videolaparoscopy)/open
The sequential endoscopy-laparoscopy involves first performing an ERCP, and then, if there are no
complications (such as acute pancreatitis), moving on to laparoscopic cholecystectomy. The main
indication is for patients with certain or very high-risk choledochal lithiasis.
First a clearance, a toilet, of the VBP is performed, then a cleansing consisting of stone removal either
through 'Dormia's basket' or through 'balloon'. First a sphincter sphincter papilla of Oddi at the
duodenal level is sphinctered (and bleeding or acute pancreatitis may occur) and mdc is injected
retrogradely, after a guide wire has been inserted, which allows the catheter to enter, then in fact the
wire is removed and the mdc is introduced. A period of time between the ERCP and laparoscopic
surgery of approximately 24-48h must pass.
Advantages:
- Less invasive procedure
- Success rate >90%.
- Excellent results
- Simpler logistics (resolves jaundice and obstruction that can lead to acute pancreatitis; also
deals with gallstones)
Finally, this method:
- It avoids the prolongation of surgery due to intraoperative cholangiography: in cases of doubt
about the bile duct, intraoperative cholangiography should always be performed, because it
allows a check-up. If you think that what you are looking at is the cystic duct but you are not
sure, you introduce a probe, insert the mdc and take the x-rays, opacify the biliary tree and
visualise it on the x-ray, so that you can confirm or not that the surgical strategy you are using
is appropriate.
- A minimally invasive approach is maintained
- It reduces the possibility of conversion and open exploration of the VBP if the laparoscopic
approach fails.
Disadvantages:
- Two strategic procedures
- Possibility of anatomical variants in the
- High costs
- Morbidity and mortality not low
This approach is the most recommended. The choice of this method depends on several elements:
1) Patient characteristics: procedure of choice in high-risk surgical patients
2) Clinical presentation (acute VBP obstruction associated with inflammatory phenomena)
3) Timing of diagnosis: this is the method of first choice in the case of documented calculosis preoperatively. If the diagnosis is post-operative, a reverse sequence is done for mis- diagnosis.
4) Local conditions: depend on:
-
From the number of calculations
Intrahepatic stone localisation
Previous resective gastric surgery
Presence of paravaterian diverticulum (at duodenal level, near Vater's papilla, making
endoscopy complicated)
- Mirizzi syndrome
5) Local expertise and training:
- Adequate number each year
- Appropriate instrumentation
The only VLS/open time
Advantages:
- Minimally invasive procedure
- Complete extraction of calculations
- Avoiding manipulation of the Vater papilla
- Studying the anatomy of VBP
Disadvantages:
- Increased surgical skills
- Anatomical variants
- Correct interpretation of intraoperative cholangiography
- Extended operating time
The choice of this method is due to:
- PC characteristics
- Clinical presentation (no in case of inflammation)
- Timing of diagnosis (recommended in case of intra-operative diagnosis of lithiasis of the VBP)
- Local conditions (location and number of stones, location and insertion of cystic duct, diameter
of VBP, previous abdominal surgery)
- Local expertise and training
The choice of the surgical technique to be adopted is based on the interpretation of the intraoperative
trans-cystic cholangiography:
1) Trans-cystical approach:
- Single calculation
- Calculations < 8 mm
- Papilla-impacted calculi in the absence of VBP dilatation
- Lateral implantation cystic duct
2) Principle choledochotomy:
- Multiple calculosis
- Calculations >8 mm
- Calculi 2-3 times the diameter of the cystic duct
- Calculosis proximal to cystic duct implantation
- Calculi impacted at the papilla, with dilatation of the VBP
- Posterior and/or lateral implantation cystic duct
Colangitis
Reynolds' pentad and Charcot's triad
Reynolds' pentad is a set of signs and symptoms that suggest a diagnosis of ascending obstructive
cholangitis, a severe infection of the biliary system. It is a combination of Charcot's triad (jaundice,
fever, abdominal pain), with shock and an altered mental state. Sometimes, the two additional signs
are listed simply as hypotension and mental confusion.
ADENOMYOMATOSIS GALLBLADDER
Adenomyomatosis is a condition of unknown cause characterised by hyperplasia of the tissues of the
gallbladder wall, resulting in eversion of the mucosa within the lumen. It may be diffuse (multiple
adenomas) or localised (single adenoma, usually on the fundus).
Both the tumour and pseudo-tumour forms are in most cases asymptomatic lesions of occasional
occurrence; the symptoms, when present, are quite similar to those of a biliary colic, attributable to
obstruction of the biliary outflow via the cystic duct.
CARCINOMA OF THE GALLBLADDER
Adenocarcinoma of the gallbladder is the most frequent extrahepatic biliary tract tumour. Age 70
years, women 3-4:1, in most cases in patients with a history of cholelithiasis, gallbladder with calcific
("porcelain-like") walls and polyps >1 cm.
Preoperative diagnosis is difficult, as it is often and for a long time paucisymptomatic. It may begin
with the acute symptoms of biliary colic or, milder, of chronic cholecystitis: continuous pain in the
right hypochondrium, weight loss, jaundice (onset with jaundice means unresectable mass in 95% of
cases), palpable mass (10%).
Diagnosis
● Abdominal ultrasound: on diagnostic suspicion, and in any case in the case of jaundice, it is the
first examination to be requested (it can detect liver swelling between the fourth and fifth segments
).
● Ecoendoscopy (2nd level), which also allows for an ultrasound-guided cyto-aspirate (EUS- FNAB
).
● Total body CT is indicated for preoperative staging.
● Laboratory: anaemia, cholestasis enzymes, tumour markers CEA and CA19.9.
TNM classification
● T1: infiltration of the lamina propria (T1a) and tunica muscularis (T1b).
● T2: infiltration of the tunica muscularis down to the subserosa, liver not infiltrated.
● T3: infiltration of the serosa, hepatic parenchyma or one of the pericolecystic organs
(omentum, pancreas, duodenum, stomach, extrahepatic biliary tract).
● T4: infiltration of the hepatic artery or portal vein or two hazard organs; inoperable.
● N1: positive local lymph nodes (at the hepatic hilum and along the hepatic artery).
● N2: distant positive lymph nodes (pericaval, superior mesenteric, celiac); from an oncological
point of view, they are considered distant metastases.
Treatment
Surgical resection where possible (25%)
● For T1 tumours, simple cholecystectomy is considered sufficient.
● For T2-T3 neoplasms, en bloc resection of the neoplasm with segments IV and V, in whole or
partial for at least 2 cm depth, and regional lymphadenectomy is performed. Intraoperative highdefinition ultrasonography is useful to identify liver metastases and lymph nodes along the
hepatoduodenal ligament: lymph nodes beyond the N1 station, positive on intraoperative
histological examination, contraindicate further surgery.
In disseminated disease (metastases, extensive hepatic and peritoneal invasion), palliative biliary
drainage or biliary-digestive bypass may be performed. 1-year mortality of unresectable 95%.
CHOLANGIOCARCINOMA
More frequent in men, the incidence is 1-8 /100k/year, at an average age of 65. In 95% of cases it
presents as adenocarcinoma, in nodular - papillary - diffuse forms.
FdR: chronic parasitic infections of the biliary tract - congenital anomalies with ectatic ducts - SPC (12%/y) - congenital liver fibrosis - ulcerative colitis - occupational (trichloroethylene) - drugs
- cholestasis. Diabetes and smoking x2.
Depending on the site of origin and the biliary tract involved, cholangiocarcinoma is divided into:
● Intrahepatic (5-10%), separates from the extrahepatic by the origin of the 2nd order bile ducts;
● Peri-hepatic (50-60%) or Klatskin tumour (part of the extrahepatics, divided from the ''distal'');
● Extra-hepatic (30-50%)
Bismuth-Corlette classification of peri-iliary cholangiocarcinoma:
● Type I: neoplasm of the common hepatic duct, distal (>1 cm) to the confluence of the right and
left branches.
● Type II: involves the confluence of the left and right main ducts.
● Type III: involves the confluence and extends to the primary branches of the dx (IIIa) or sx (
IIIb) branches.
● Type IV: confluence and both branches are largely invaded at the neoplasm, in continuity or with
multifocal appearance.
Presentation: clinical manifestations are late (negative prognosis).
● Obstructive obstructive jaundice (painless): direct hyperbilirubinaemia - choluria - acholic
stools itching
● Abdominal pain, upper quadrants, right hypochondrium (biliary colic and cholangitis rare)
● Fever - nausea and vomiting - weight loss - anorexia
● Alkaline phosphatase - g-GT - often hypertransaminasemia - sometimes hypoalbuminemia.
● Sometimes the distended gallbladder can be palpated (Courvoisier's sign).
The suspected diagnosis is made by ultrasound (dilated biliary tract in the absence of stones) and
confirmed by cholangio-RM and CT scan (which allow staging).
Treatment
The only potentially decisive treatment is surgical resection.
Resectable about 1/3, more easily than the lower third; vascular and lymphatic invasion indicate
unresectable. Surgery is more radical than for gallbladder cancer:
● Intrahepatics: the only option is liver resection (10-20% of patients are candidates);
● Peri-ilary type I: the affected biliary tract is resected and the biliary-digestive continuity is
reconstituted with a Roux-excluded digial loop;
● Type II: the involvement of the confluence forces a bidutto-dyjunostomy, extended to an
anastomosis with 3-4 ducts as one proceeds upwards in search of a histologically uninjured slice.
● Type III: involvement of secondary ductile branches obliges resection of the right (IIIa) or left
(IIIb) lobe.
+Palliative interventions: placement of
endoprosthesis, diversion of bile flow
excluding neoplasia.
to fasting
PANCREAS
Acute pancreatitis is a
of the pancreas, due to the leakage of activated pancreatic enzymes from the ductal system, with their
elevation in both serum and urine, leading to self-digestion and thus more or less widespread
destruction of the pancreatic gland itself. This inflammatory process can also involve neighbouring
structures and organs and only in advanced stages even distant organs (from the pancreatic lodge).
Aetiology
1) Alcohol abuse and biliary lithiasis (a stone migrated into the choledoch that impinges on
Vater's papilla, causing an increase in pressure, which is transmitted within the Wirsung,
resulting in a slowing down or stopping of the release of pancreatic enzymes, which are
released within the pancreas itself, causing the pancreatic cells to digest) account for 90% of
the causes.
2) Idiopathic (difficult to diagnose)
3) Post-ERCP (acute pancreatitis is one of the complications of ERCP, along with haemobilia,
choleperitoneum, and acute suppurative cholangitis from the use of iodine medium). It is an
iatrogenic cause related to lithiasic pathology, and is an endoscopic method used for the
removal of stones from the main biliary tract, as well as the placement of a stent in cases of
biliary tract neoplasia. A catheter is introduced into the biliary tract, through which mdc is
injected for visualisation. A positive pressure is created that pushes the mdc into the duct of
Wirsung, resulting in pancreatitis.
4) Post-operative: following major abdominal surgery
5) Congenital dyslipidaemias
6) Post-traumatic
7) From drugs
8) Hypercalcaemia
9) Bacterial, viral and parasitic infections
10) Vascular abnormalities
Focus: alcohol pancreatitis
It is the main cause in chronic pancreatitis, and the acute form arises as a complication of the chronic
one.
Pathophysiological mechanism: alcohol abuse:
- It sensitises the acinar cells to the action of cholecystokinin and secretin (hormone of the
gastrointestinal neuroendocrine system that is responsible for the production of bile and
contraction of the gallbladder)
-
-
Promotes the production of pancreatic enzymes (stimulated, even in the absence of food intake,
as alcohol is often taken on an empty stomach, with no correspondence between what is
introduced into the gastrointestinal tract and the release of enzymes)
It causes vagal stimulation, with spastic contracture of the sphincter of Oddi.
It sensitises the pancreatic parenchyma to the action of the virus such as Coxackie B3
It activates pancreatic stellate cells, increasing collagen production (a mechanism underlying
chronic pancreatitis)
This will result in: increased protein secretion, reduction of the pancreas' own defence systems,
membrane disruption
Focus: biliary pancreatitis
Drift:
-
Gallstones and cholesterolosis
Biliary sludge
Choledochal cysts and choledochocele
Sclerosing cholangitis
Cholangiocarcinoma and ampullary tumours
Peri-ampullary duodenal diverticula
Pancreas divisum with obstruction of the accessory duct
Pancreatic duct-biliary junction abnormalities.
The pathogenetic mechanism:
1) Direct obstruction: this is an often biliary stone that wedges at the level of the choledocochlea
and obstructs the papilla of Vater, which comes into close contact with the pancreatic duct of
Wirsung. Thus, an obstruction at this level leads to an increase in endobiliary pressure, pushing
bile into the Wirsung, with activation of the enzymatic cascade and destruction of the
pancreatic ducts and cells by the direct lytic action of the bile itself.
2) Passage of the biliary sludge: passage of the biliary sludge causes fatigue in the contraction of
the sphincter of Oddi. The oedematous papilla becomes an obstacle to biliary progression, thus
increasing the pressure of the biliary pathway and then refluxing into the Wirsung, with
damage to it.
Focus: post-ERCP pancreatitis
ERCP has diagnostic and interventional purposes. Complications include:
1) Bleeding:
- Sphincterotomy with diathermocoagulation (with incision of Vater's papilla, which is then
cauterised)
- Trauma of the inserted catheter
- Positive pressure mdc injection
2) Biliary tract infections
3) Duodenal perforations
4) Acute pancreatitis
To avoid such complications, in the uncertainty of lithiasic pathology, second-level diagnostics
involves the use of cholangio-RM, without mdc injection; whereas ERCP was the gold standard in the
past.
Pathophysiology
Regardless of the causes, the obstruction of the outflow of pancreatic enzymes dissolved in pancreatic
juice, which usually escape through Vater's papilla, stagnate at the pancreatic level, leading to
intraparenchymal activation of pancreatic enzymes, with self-digestion of the pancreas itself.
One will therefore have:
1) Obstacle to runoff;
2) Intra-parenchymal enzyme activation (trypsin, lipase, amylase, protease, phospholipase,
elastase, the kinin and prostaglandin system, etc.) and overcoming of defence systems (by
reducing PSTI glycoprotein alpha1 antitrypsin, which inhibits the action of proteolytic
enzymes)
3) Alterations of the membrane and thus self-digestion of the pancreas and also involvement of
the peripancreatic tissues
In addition, in the case of acute pancreatitis, this also results in:
- Damage to the microcirculation: there will be increased permeability of the capillaries in the
stroma, with endothelial damage, blood stasis, vasodilatation, so these enzymes are released
directly into the bloodstream.
- Activation of inflammatory mediators: the inflammatory insult leads to production of proinflammatory cytokines (TNFa, IL-6, IL-8), resulting in tissue damage.
Trypsin also activates the complement with activation of the kinin and prostaglandin system and this
results not only in local and peripheral vasodilation but also, as a consequence, in a spillover of these
activated pancreatic enzymes to the whole organism compromising not only intra-abdominal but also
systemic organs. (integrated systems theory)
From a morphological point of view, acute pancreatitis is divided into:
1) Oedematous phase: the process is self-limiting at an early stage. The inflammation is localised
to the pancreas in the acinar epithelial zone, up to the interstitial phase (85-90%). It tends to
heal in about 7-14 days
2) Necrotizing phase: the previous phases evolve towards vascular compromise, with ischaemia
and necrosis of the pancreas. It heals in a longer time because destroyed necrotic tissue has to
be replaced.
3) Necrotizing-haemorrhagic phase: this is usually observed post-mortem, because it almost
always correlates with the pc's exitus, the pc hardly ever recovers; it occurs if the
peripancreatic vessels are self-digested and destroyed; the small terminal vessels can be
destroyed and can cause haemorrhage. The resulting collections can become infected and we
speak of acute necrotising suppurative pancreatitis;
Clinic
Clinically, the patient with acute pancreatitis is characterised by:
1) Abdominal pain: this is the cardinal symptom, it is a very intense pain, so much so that one
speaks of 'pancreatic drama'. It typically arises at the epigastric site, and then radiates towards
the two upper abdominal quadrants, right and left, one speaks in fact of band/belt/bar pain. It is
a continuous, intense pain that is difficult to control with mundane analgesic therapy (morphine
is not given, because it could lead to further paralysis of the sphincter of Oddi)
2) Fever
3) Nausea and biliary vomiting (a nasogastric tube is inserted, which conveys vomit outside,
and by conveying gastric secretion outside, pancreatic stimulation is avoided).
4) Jaundice (in the case of biliary pancreatitis)
5) Gray-Turner's sign (bruising of the hips)
6) Cullen's sign (periumbilical ecchymosis)
7) Paralytic Ileo
8) Tetanus-like crises: there will be hypocalcaemia, because the calcium salts bind to the
liquefied peripancreatic fat and form the famous wax casts.
-
It goes in DD with:
Peptic ulcer
Colangitis
Cholecystitis
Visceral perforation
Mesenteric ischaemia
Hepatitis
Laboratory examinations
-
They are crucial in the diagnosis of acute pancreatitis.
Increased serum amylase and lipase (increased by 3 times the physiological value) and urinary amylase
Marked neutrophilic leucocytosis (justifying the intense release of inflammatory mediators)
Increased Hct (due to haemoconcentration)
Hypocalcaemia
- Increased indices of inflammation: CRP and ESR In case of cholestatic aetiology:
-
Increased cholestasis indices: gamma-GT, LDH, alkaline phosphatase, transaminase, bilirubin
-
In case of evolution in a necrotic-haemorrhagic sense:
Increased blood glucose
Increased azotemia and creatininemia, with impaired renal function
Increased transaminases
-
Acute forms of pancreatitis with characteristic pain but no increase in pancreatic enzymes:
Alcoholic pancreatitis
Hypertriglyceridemia pancreatitis
-
Laboratory elements in the assessment of severity that are used in clinical practice include:
C-reactive protein
The interleukin assay in laboratories that allow it
These parameters have a particularly high sensitivity and specificity both at the beginning, in the first
24 hours and in the following 48 hours.
Predictive criteria for severity
Ranson's criteria (see later)
● Age over 55,
● Elevated white blood cells,
● Blood glucose > 200 mg/dL,
● Particularly high LDH
● 10% decrease in haematocrit in the first 48 hours,
● Increase in azotemia in the first forty-eight hours,
● Decrease in calcemia always forty-eight hours,
● Hypoxaemia
● Alteration of acid-base balance
Three or more of these parameters give us an indication of severe disease with a sensitivity rate as
high as 90%.
Glasgow Criteria
They take into account not only what is present in Ranson's criteria (i.e. age, leucocytosis, blood
glucose, LDH and transaminase parameters) but also albumin, indices of renal function, calcemia and
blood pressure.
Instrumental examinations
1) ETG abdomen: does not tell us specifically whether it is pancreatitis or not, the pancreas being
a retroperitoneal organ. We will note well the oedema, hypoechogenic area surrounding the
head of the pancreas, for example, and then it also tells us the presence of anaecogenic
peripancreatic fluid collection, which indicates that the inflammation is going beyond the
expected limits. Especially when combined with clinical and laboratory tests, it is diriment
2) Rx abdomen: this allows us to see the so-called sentinel loop, i.e. an upstream dilatation of the
intestinal loop with water levels. This is the intestinal loop that is most directly and
immediately affected by the inflammatory process.
3) Tc with mdc: as well as showing us the oedema, it can highlight possible complications. There
will be the famous wax casts, at the level of the peri-pancreatic fat, in the retro-peritoneal
lodges. The CT scan is the only one that allows us to stadiagnate the pancreatitis, and thus
understand the level of severity it has reached.
Pancreatic damage on CT scan is assessed by the Balthazar classification:
a) Normal pancreas
b) Pancreatic oedema
c) Edema also affects the peri-pancreatic fat
d) Presence of liquid in a single location
e) Two or more poorly defined liquid collections, air in the parenchyma or peripancreatic.
4) Cholangio-RM: in cases of biliary aetiology. In fact, doing an ERCP to a patient who has or
has recently had pancreatitis is very imprudent, as it is itself the cause of acute pancreatitis. It
could perhaps be performed once the pancreatitis has cooled down, to perform a
sphincterotomy for stones or to put in a prosthesis to help the outflow of bile.
Then an ECG could be done in the advanced stages (necrotic-haemorrhagic form), because there is a
risk of cardiac depression, due to the release of the MDF (cardiac depressant factor) which makes the
heart contract less, causing arterial hypotension, so less blood will go into the circulation and this leads
to very serious consequences, such as the failure of the typical function of the intestinal barrier, and
thus a bacterial translocation occurs with bacterial flora that will be found at the level of the pancreatic
necrosis zones (infected necrosis) and can lead to septic shock.
Diagnosis
Diagnosis of acute pancreatitis requires the presence of at least 2 of 3 criteria:
1) Clinic
2) Laboratory and biohumoral
3) Instrumental
Classification criteria for the severity of pancreatitis have been developed over time, and the most
widely used is the Ranson staging: it is assessed on admission and after 48h (it is based on criteria
clinical-laboratory):
1) On admission:
-
Age >55 years in alcoholic forms and 70 in bile forms
GB
Blood glucose
LDH
GPT or ALT
If less than 3 indices are present, the prognosis is favourable and therefore the interstitial form is
thought to be self-healing.
2)
-
48 hours after admission:
Anaemia
Oliguria
hypocalcaemia
Hypoxaemia
Metabolic acidosis
Seizure of liquids
If more than 3 indices are present, a severe prognosis will be made.
Therapy
Acute oedematous pancreatitis usually resolves on its own:
- Fasting and hydration (500 cc saline solution)
- Administration of drugs that inhibit pancreatic secretion (especially in the past): octreotide,
gabesylate mesylate
- Analgesic therapy: with opioid derivatives. NSAIDs should not be used, mainly because of
gastrolesiveness
- Placement of SNG: only if the patient vomits, so as to divert the gastric secretion outside, so as
not to stimulate the already suffering pancreas, and then also to measure and then balance the
amount of fluid emitted
- Correction of hyperglycaemia
- Electrolyte recovery
- Nutritional intake, if acute pancreatitis is slow to resolve, through cannulation of a central vein.
It is indeed useful to take at least two peripheral venous accesses
- Antibiotic coverage: carbapenems, quinolonics, penicilins, cephalosporins are used. The ideal
would be an efficacy factor of 1, which means that the antibiotic is able to eliminate all the
bacteria found after translocation. Treatment should last 3 weeks, starting with a broadspectrum antibiotic, waiting for the results of the antibiogram and then using a more selective
therapy.
- Removal of pathogenic noxa
-
Clinical-laboratory-radiological monitoring.
Complications
Systemic: SIRS (systemic inflammatory response syndrome) and MODS (multi-organ dysfunction
syndrome). The release of pro-inflammatory cytokines and pancreatic enzymes through the
bloodstream lead to organ impairments such as:
- ARDS (up to shock lung)
- IRA (perform bladder catheterisation to assess diuresis)
- Hyperglycaemia
- Shock
- CID
- Hypocalcaemia
- Sensorimotor impairment (assessed by GCS)
Premises:
- Gastrointestinal bleeding
- Venous thrombosis and pseudo-aneurysm
- Pancreatic necrosis: which may be sterile or infected (as in most cases, by Gram- and
anaerobes). It is one or more diffuse or focal areas of non-viable pancreatic parenchyma and is
associated with necrosis of peripancreatic adipose tissue. The gold standard for the diagnosis of
pancreatic necrosis is CT scan with mdc, by which areas of hypodense parenchyma, with a
circumference > 3cm or comprising more than 30% of pancreatic tissue, can be seen.
Fundamental is the distinction between sterile necrosis and infected necrosis.
- Formation of pancreatic and peri-pancreatic collections, which are subdivided into: fluid
and corpusculate: deposited necrotic material. They appear early in most acute pancreatitis, and
are located in the pancreatic and peropancreatic sites. They are collections in which a wall of
fibrous tissue and granulation tissue is absent; they never have a wall of fibrous tissue, which
differentiates them from pseudocysts and abscesses (which are the evolution of fluid
collections); they occur in 30-50% of cases of severe acute pancreatitis; they can regress
spontaneously in most cases; they are the precursors of pseudocysts and abscesses;
- Pancreatic fistula: often a complication of drain placement surgery.
- Colic stenosis: a colic resection with temporary or permanent ostomy is elective.
Then by pancreatic necrosis, as late complications:
1) Pancreatic pseudocyst (outcome of sterile necrosis): a collection outside the pancreas,
containing pancreatic juice rich in enzymes, with a colour similar to 'cotto fiorentino', separated
by a fibrous granulation wall. It is almost always sterile, and the presence of bacteria is an
expression of contamination. Usually once a week through the placement of drainage, a
chemical examination of the fluid is performed, and amylase and lipase values are assessed. In
the past, they were attacked after at least 3-4 months, with careful follow-up with CT scans,
because the wall of the pseudocyst must increase in thickness in order to allow attachment to a
digiunal loop. Today they are treated with ETG or CT-guided drainage and antibiotics. (dd
with true cyst? In true cyst there is epithelial lining)
2) Pancreatic abscess (outcome of infected necrosis). They consist of solid or necrotic material.
It is a circumscribed purulent collection in the vicinity of the pancreas, containing or not a
modicum of glandular necrosis. It differs from infected necrosis in its clinical picture and the
extent of associated necrosis. There will be fever and increased white blood cell count.
Treatment of complications
1) CT-guided percutaneous drainage with fluid evaluation and fluid culture (for pancreatic and
peripancreatic fluid collections and pseudocysts):
- If the culture is negative, supportive antibiotic therapy is done and, if necessary, repeated after
5-6 days to monitor the progress of the collection.
- If the culture is positive and there is necrosis, the condition of the patient is assessed:
o if the patient is clinically stable, and one does not expect evolution towards more
serious complications (MOF) one continues antibiotic therapy and observes, postponing
endoscopic or surgical therapy if the approach fails.
o If the patient worsens or manifests itself as unstable ab initio, with a risk of evolution
towards SIRS or MOF, an endo-retroperitoneal washing/drainage of the necrotic
collections/areas/abscesses is carried out, with 3 right and 3 left communicating
drainage tubes, with antibiotics administered 24 hours a day; and if t h e r e is no
response (no clinical improvement), a surgical approach is carried out, which may be
endoscopic or open, to try to stem the evolution of the picture.
2) Endoscopic drainage:
- Transpapillary: if the pseudocyst communicates with the main pancreatic duct (Wirsung),
placing a stent.
- Transmural: a fistula is created between the pseudocyst and the gastric or duodenal lumen. This
approach is only used if it can be reached via the oesophago-stomach-duodenal route.
3) Surgical approach: necrosectomy is the removal of the necrotic parts from which the infection
arises and from which further necrosis starts.
- Laparoscopic necrosectomy
-
Open necrosectomy
Open necrosectomy is the most widely used and can be determined by means of:
a) Open packing: the abdomen is opened, the necrosis is removed, repeated washings of the
abdominal cavity are carried out, which remains open and is filled with gauze, and the patient
is medicated several times with clean gauze;
b) Sequential laparotomies: the abdomen is packed with gauze and closed with hinges, which
allow the abdomen to be opened and closed to ensure periodic gauze changes and washings;
c) Necrosectomy and closed-loop abdominal lavage: drains are placed in the pancreatic lodge to
make continuous irrigations. The fluid washes in and out and is then observed t o see if
improvement is occurring.
d) Close packing: a technique used when there is not much chance of surgery, hoping that it will
be self-limiting. The abdomen is closed and packed with resorbable gauze.
PANCREATITIS CHRONIC
Pathological condition characterised by chronic, fibrosing inflammation of the pancreas, with
permanent damage and organ dysfunction. This results in reduced pancreatic enzyme production,
malabsorption and steatorrhea. In addition, destruction of the islets of Langerhans, which are mainly
present in the body and tail, leads to reduced hormone production, resulting in diabetes mellitus.
It is ranked in:
1) Diffuse form: Involvement of the entire pancreatic gland, which appears enlarged (sausagelike appearance), hypodense, after MRI and CT administration of mdc.
2) Focal form: goes in dd with neoplastic diseases (adenocarcinoma).
The main causes are:
1) Alcohol abuse
2) Acute pancreatitis that becomes chronic
3) Genetic diseases: such as cystic fibrosis (a mucoviscidosis), in which pancreas and lungs are
the organs most involved
4) Pancreas divisum
5) Autoimmune
6) Drugs
Focus: Pancreas divisum
Pancreas divisum is characterised by the lack of fusion of the dorsal (Santorini) and ventral (Wirsung)
pancreatic ducts, as a result of which the pancreas is drained mainly by the dorsal duct that drains into
the papilla minor. Two main variants can be distinguished, 'complete' (more frequent) and 'incomplete'
depending on whether or not communication between the two ducts persists. ERCP is considered the
gold standard for diagnosis, although newer imaging techniques, such as cholangio-RM and echoendoscopy, due to their less invasive nature and lower risk of complications compared to ERCP, are
increasingly gaining ground in the definitive diagnosis of this condition.
Clinic
It is more nuanced than acute pancreatitis:
- Pain, often due to compression of pseudocysts
- Diabetes mellitus, destruction of Langerhans islet cells
- Malabsorption, with slow and uncomfortable digestion, despite the fact that the patients are fed
properly, they do not gain weight and continue to lose it.
-
Steatorrhea: oily and very smelly stools because they are full of undigested fats
Therapy
Therapy includes:
1) Abstention from alcohol
2) Steroids (in case of autoimmune genesis)
This is a substitution-type therapy, in which pancreatic enzymes introduced in the form of tablets to be
taken during meals are basically used.
Again, supportive therapy is aimed at:
- Pain control
- Nutritional contribution
Surgical therapy is rarely used and consists of pancreatic shunting (anastomosis between the pancreas
and intestine) and is palliative.
PANCREATIC CARCINOMA
The pancreas is a retroperitoneal organ, consisting of:
- Head
- Body
- Tail
- Hook process
The hooked process is in close relationship with important vascular structures such as the superior
mesenteric vein, which then becomes the portal vein (together with the inferior mesenteric vein and
the splenic vein) and the superior mesenteric artery, but also the celiac tripod (consisting of the
common hepatic artery, left gastric artery and splenic artery).
Given the close relationship with these vascular structures, not all pancreatic tumours are surgically
removable and completely resectable and this correlates with an inauspicious prognostic outcome for
the patient.
Risk factors include:
-
Cigarette smoking
Alcohol abuse
BMI >30
Poor exercise
Power supply
Genetics
-
Chronic pancreatitis
Diabetes
Familiarity for pancreatitis
Familiarity with pancreatic carcinoma
Macroscopy
From an anatomical-pathological point of view, pancreatic adenocarcinoma presents as a hard,
fibrosclerotic (due to the intense desmoplastic reaction) and poorly vascularised mass, to the extent
that areas of necrosis central to the neoplasm may be created.
Histology
1) Ductal adenocarcinoma (the most represented)
2) Cystic tumours: serous cystic neoplasms and mucinous cystic neoplasms
3) Pancreatic neuroendocrine tumours: which on histological examination usually have a
poorly differentiated appearance, with more than 20 mitoses per field and a ki67 >20%
(ki67 is an index o f proliferation). Precisely on the basis of ki67 they are distinguished
into NET low grade (low to medium grade) and NET high grade (high grade).
4) Intraductal papillary mucinous neoplasms (IPMN): these are pre-cancerous lesions, which
affect the main pancreatic duct or secondary ducts, and in an unspecified time, tend to
degenerate towards ductal adenocarcinoma.
Head office
Ductal adenocarcinoma, which is the most common, is localised in 70% of cases in the head of the
pancreas, 20% in the body and 10% in the tail.
Localisation at the level of the head allows such neoplasms to be diagnosed in a reasonable time, since
we will have the appearance of jaundice (due to compression of the biliary tract), abdominal pain and
dyspeptic disorders (due to infiltration of the duodenum). In contrast, tumours of the body and tail do
not give any sign and are therefore diagnosed late, when we will have distant metastases.
The clinic is characterised by:
- Abdominal or lumbar pain
- Weight loss
- Meteorism
- Nausea
- Vomiting
- Jaundice and acholic stools
Laboratory examinations
There is an increase in:
- Transaminases
- Bilirubin
- Alkaline phophastasis
- GT Range
- Marker CA19.9
It enters DD with all causes of obstructive jaundice, including neoplastic ones, such as Klutskin's
tumour, a duodenal tumour or Vater's papilla; intrahepatic causes such as cholangiocarcinoma, or
metastases; but benign causes should also be considered.
Instrumental examinations
The first level examination is ETG, but it will never give a diagnosis of certainty, in fact the pancreas
is a retroperitoneal organ, and the diagnosis is made less easy by the intense desmoplastic reaction;
certainly if we detect a hypoechogenic pancreatic mass associated with jaundice, the doubt of
pancreatic k must come.
Spiral CT or MRI with a targeted study will then be crucial. A CT scan of the pancreas also includes
CT angiography, to find out the relationship of the neoplasm with vascular structures.
The study of the pancreas includes:
- First baseline CT scan
- Second early and a late arterial (or parenchymatous) scan
- Third portal scan, which allows us to accurately assess the portal vein and other venous
structures, such as the superior mesenteric vein.
Again, echo-endoscopy becomes important in cases of doubtful CT or MRI. It allows us to better
assess the vascular relationships and also allows us to perform the biopsy, which should only be done
in cases of:
- Metastatic disease
- Doubtful Imaging
- Patients to be introduced to new treatment protocols (such as adjuvant therapy)
Thus, it allows us to visualise the main biliary tract and pancreatic duct in more detail and, if
necessary, a needle biopsy can also be performed.
PET plays a role for stadiative purposes, especially in patients starting adjuvant chemotherapy, so
follow-up becomes important.
Staging
Staging is done with CT scanning with mdc, which gives us the best information about the neoplasm
and its relationship with neighbouring structures. It is crucial because it tells us whether it is a
resectable, borderline or unresectable tumour. It also allows us to identify the presence of metastases
in the liver, or if there is, for example, infiltration of the mesenteric portal trunk. MRI is
superimposable. Cholangio-RM plays an important role in staging.
There are two different societies to define ductal adenocarcinoma:
-
NCCN Cancer Network that distinguishes tumours according to the TNM and is the one
referred to by all surgeons and oncologists in the western world;
Japanase Pancreas Society: differs mainly in the N factor.
T
● T1: < or = 2 cm (limited to the pancreas)
● T2: >2 cm (limited to the pancreas)
● T3 and T4: extend beyond the pancreatic capsule
o T3 does not involve the celiac trunk or the superior mesenteric artery;
o T4 are involved and therefore the tumour will not be resectable.
N
The NCCN classification divides pts into:
● N0: no metastasis to regional lymph nodes
● N1: presence of metastases to regional lymph nodes
The Japanese Pancreas Society classification distinguishes N1, N2, N3, based on the presence of
metastases in the lymph nodes of groups 1, 2, 3.
● Group 1: pancreatic lymph nodes of the anterior face and the retropancreatic;
● Group 2: regional lymph nodes of the coeliac tripod, hepatic artery proper, and proximal and
distal mesenteric artery
● Group 3: more distant lymph nodes, such as the right and left cardials.
The Japanese have always believed in a lymphadenectomy that is as extensive as possible, in order to
control all possible sites of metastasis and spread by the neoplasm (and this also applies to gastric
cancer). But studies and randomised trials have seen that extensive, distant lymphadenectomy does not
lead to increased survival, but results in a
increased comorbidities post-operatively, when non-locoregional lymphadenectomy is performed.
It usually tends to infiltrate neighbouring structures and organs: perivisceral fat, gallbladder,
duodenum, choledoch, Wirsung's duct and the retro-peritoneal vascular structures, also affecting the
locoregional lymph nodes, which become sleeves, and nerve structures (perineural infiltration),
which causes abdominal pain.
It is precisely its close relationship with these structures that makes it a tumour with a high capacity to
spread: perineural, lymphatic and haematic (in the latter case, it tends to give metastases to the liver;
but sometimes there can be skip metastases, which go beyond the liver filter, and arrive directly at the
lung.
According to the TNM classification, we will have staging I (A and B), II (A and B), III and IV, the
therapeutic approach and thus survival changes
● Stage I and II is surgically resectable, since the neoplasm is confined to the pancreas and there
is no lymph node involvement, so it can be radicalised, and then CT and RT are performed
(although less is used post-operatively nowadays), and a survival of about 24% at 5 years;
● Stage III, i.e. advanced disease, and significantly lower survival
● Stage IV in which 5-year survival is practically nil.
Thus, the surgical approach is planned for stages I-II, which correlates with a survival of ¼ of the
patients.
Resectability criteria
1) Resectable: those tumours that have no contact with vascular structures such as (coeliac trunk,
superior mesenteric artery, common hepatic artery + at venous level): either no contact or in
any case less than 180°, therefore with reserved vein
2) Borderline pts with involvement with the superior mesenteric vein < 180°, but presence of any
deformity or is liable to thrombosis; or contact < 180° for the celiac tripod and also the superior
mesenteric artery. Contact means that t h e r e i s a lack of adipose tissue to form a cleavage
plane that allows the surgeon to remove it completely; absence of contact is a sign of
infiltration; if there is infiltration, a vascular resection may be performed, which may be
venous or arterial. Pcs are operated on, but they will be R1, so they leave a small residue, even
microscopic, of resection, and they vary according to the location of the tumour:
-
If in the head: make contact with the common hepatic artery without dissecting the celiac axis
or at the hepatic bifurcation
- If in the tail body: contact with the coeliac tripod is assessed (tumours are shifted more to the
right)
3) Unresectable: the tumours are locally advanced, have involved loco-regional vascular
structures, such that removal is technically unfeasible, despite the absence of distant
metastases.
If the patient is metastatic, even if resectable, the various chemotherapy protocols, which are the same
worldwide, are implemented, depending on the status of the patient.
Tumours of the head of the pancreas: duodenocephalopancreasectomy
DCP surgery consists of removal of:
- Duodenum
- Pancreas head
- First digiunal loop
In the Whipple variant, the distal part of the pyloric antrum is resected; in the Traverso- Longmire
variant, the pylorus is preserved; plus 3 anastomoses:
1) Pancreato-dyjejunostomy: reconstitutes the continuity between the body-tail of the
pancreas with a digiunal loop.
2) Hepatico-diugnostomy (or biliary-digestive): reconstructing the continuity between the
main biliary pathway then the duodenum and a digiunal loop,
3) Gastro-dyjunostomy
DCP surgery involves: after the resectability of the neoplasm has been ascertained, assessing the
relationship with neighbouring vascular structures:
-
It binds the gastroduodenal artery that supplies the pancreas head and pylorus
Isolation and ligation of the main bile duct below the confluence (i.e. near the division of the
hepatic duct into right and left)
Section of the stomach and section of the pancreas
Ligature of the first digiunal loop
Then anastomosis between the digiunal loop and the remaining portion of the pancreas
(pancreatic-diagiunal anastomosis)
Bilodigestive anastomosis: anastomising the choledocoel to the intestinal loop
The same loop is then anastomosed to the stomach
Standard lymphadenectomy (no extensive, according to the Japanese current):
- Suprapiloric lymph nodes (5)
- Infrapyloric lymph nodes (6)
- Lymph nodes arranged along the hepatic artery (8A)
-
Lymph nodes near the choledoch and cystic duct (12B and 12C)
Postero-superior and postero-lower pancreatic head lymph nodes (13B and 13C)
Lymph nodes located along the superior mesenteric artery (14)
The mortality rate is very high, also due to a complication related to the operation, namely the
pancreatic fistula: since we anastomose pancreatic tissue with a soft consistency to an intestinal loop
that has a different consistency, pancreatic juice can leak from this anastomosis, damaging the stitches
applied by the surgeon or creating an abdominal accumulation, or even in the worst cases leading to
copious haemorrhages, which can lead to the patient' s exit in the most severe cases.
The patient with pancreatic fistula presents:
- Fever
- Abdominal pain
- Dyspnoea
- Signs of peritonism
The diagnosis is made by the amylase assay in the drainage fluid, which is three times higher than the
serum value. This can lead to postoperative sepsis.
The treatment of this complication can be:
- Conservative: fasting, parenteral nutrition, daily assessment of drainage output
- Pharmacological: using drugs such as somatostatin that reduce splanchnic flow and pancreatic
secretions
- Surgical: percutaneous drainage if an abscess is present or the possibility of re-intervention if
necessary.
Treatment of body-tail neoplasms: distal splenopancreasectomy
Unlike
neoplasmsthe head of the pancreas, those of the tail in which there is no vascular
involvement can be removed by laparoscopy. It involves:
- opening of the gastrocolic ligament
-
access to the organ
removal of the neoplasm
spleen removal (it is a lymph node station that may be affected by cancer cells)
Palliative treatments
In the case of palliative treatments we go endoscopically, e.g. introduction of stents, such as duodenal
stents to bypass the obstruction; today this is done through ERCP.
Not in all cases where there is jaundice is a stent placed, but the indications are in the case of:
- Colangitis
- Persistent fever
In fact, although it greatly improves liver function, because the liver of the patient with jaundice is in
pain, it causes duodenal reflux into the biliary tree, and this can lead to new cholangitis, an
inflammation of the biliary tract that then has to be anastomosed with an intestinal loop and can lead to
sepsis.
INSULINOMA
Insulinoma is a rare pancreatic beta-cell tumour that hypersecretes insulin. The main symptom is
fasting hypoglycaemia.
Diagnosis is made by a test that involves fasting for 48-72 h along with determination of glycaemia
and insulinemia, followed by endoscopic ultrasound. Treatment, when possible, is surgical. Drugs that
block insulin secretion (e.g. diazepoxide, octreotide, calcium antagonists, beta-blockers, phenytoin) are
used in patients who do not respond to surgery.
AMPULLOMA
The concept of ampulloma is a topographical surgical concept, as a neoplasm occurring at that level
may have a different genesis, and from a practical point of view a biopsy of the papilla may show a
neoplasm originating from the small intestine, pancreas or biliary tract.
40-70 years, exophytic or stenosing polypoid masses, early obstructive jaundice, cramp-like pain,
nausea, vomiting and weight loss, anaemia = occult blood in faeces.
+Enucleation
Pancreatic enucleation is usually a simple technique, but should be reserved for benign pancreatic
tumours that are not located in contact with the main pancreatic duct. Precise preoperative evaluation,
aimed at characterising the lesion and its relationship with the main pancreatic duct, as well as
intraoperative ultrasound, are therefore required.
Enucleation is an operation that allows a high cure rate and preservation of pancreatic function, at the
price, however, of significant immediate morbidity, represented essentially by pancreatic fistula.
MILZA
Anatomy
-
The vascularisation of the spleen is represented by:
Splenic artery, direct branch of the Celiac Tripod,
-
Polar arteries,
-
Segmental arteries, which are branches of the splenic artery,
-
Short vessels connect it with the stomach,
-
Retzius vessels, which connect it with the retro-peritoneum and the posterior abdominal wall.
The venous vasculature is equal to the arterial one.
-
The spleen is a haemopoietic organ and histologically consists of:
a red pulp,
-
a white pulp.
The spleen has well-established fixation elements that hold it in place and that in trauma can break,
leading to rupture of the spleen. The ligaments of the spleen are crucial for a surgeon and are:
Gastro-splenic ligament, which connects it to the fundus of the stomach;
Brachiocholic ligament (Sustentaculum lienis), which connects the apex of the spleen to the
left lower diaphragmatic dome;
Pancreatic-lienal ligament
Spleen abnormalities
There are also accessory spleens, which are not an uncommon finding (30-40%).
In most cases they are asymptomatic because they are small, no more than 3 cm in diameter,
and are often detected as round images on imaging at the level of the splenic hilum.
There are also ectopic spleens, which may be in other locations, which is why it will be
It is necessary to rule out neoplasms or other, making an appropriate differential diagnosis.
They are most frequently found at the level of the gastro-splenic ligament and in the body-tail
of the pancreas. From a clinical point of view, the importance of accessory spleens is
highlighted in the case of splenectomy, because in such a case the accessory spleen could be
problematic, since failure to detect it previously would result in the need to repeat t h e
operation to remove the accessory spleen, which could have taken
considerable size to vicariate the function of the removed spleen.
SPLENOSI
Splenosis is the presence of heterotopic nodules of splenic tissue in the splenectomy and is due to the
'insemination' of the spleen pulp following trauma or surgery, implanting itself in the abdominal
cavity.
The main problem is to exclude that it is not in fact a neoplasm, because from a symptomatological
and radiological point of view, it can be difficult to make a differential diagnosis with neoplastic
diseases.
More frequently they are distributed in the peri-splenic site following surgery or splenic trauma.
SPLENOMEGALIA
Splenomegaly occurs when the spleen has chronic hypertrophy, because acute hypertrophy is mostly
due to vascular problems.
Clinic
● Compression symptoms on surrounding organs
● Palpation;
● Percussion.
Diagnostic imaging
-
Ultrasound (colour Doppler study) detects an increased spleen volume;
-
CT scan with and without m. d. c., which allows for a good assessment even in acute phases;
-
MRI.
Invasive diagnostics
Biopsy: when there is a suspicion of splenosis or accessory spleen, the biopsy can be
considered as a second-level diagnostic approach, but exposes to bleeding;
Selective angiography: in the case of doubtful masses, it allows the assessment of the
characteristics
morphological radiology, but it can also be decisive, as it can be used if necessary to
embolise the lesion;
Scintigraphy
CISTI
-
The most frequent cysts from an infectious point of view are Echinococcus cysts, but there are
different types of cysts:
Vero (epithelium or endothelium): they have a capsule,
-
Epidermoidal (congenital): hemangiomas and cystic lymphangiomas.
They are completely asymptomatic because they are not neoplasms, but only give rise to compression
phenomena when they become very large or if complications arise in the event of rupture or
abscessualisation
The diagnosis may be accidental and fortuitous, as an occasional finding. In these cases, splenectomy
is decisive.
CYSTS FROM ECHINOCOCCUS
Echinococcus cysts account for 4% of abdominal hydatidosis, most of which develop in the liver.
They almost never become particularly large and are therefore almost always asymptomatic.
If the capsule of the hydatid cyst ruptures, there can of course be dissemination of the parasite
throughout the peritoneum, especially when the cyst is viable, such as when it has cystic walls.
When they do not reach a large size, enucleation of the cyst can be done; when they become large,
splenectomy is necessary without affecting the pericyst.
Almost always the cyst is sterile, so it must be removed when it is large, but almost always it is small
and can be left in, with albendazole being treated with medication.
PSEUDOCISTS
Pseudocysts are almost always post-traumatic.
-
Features:
-
70% of all cysts,
-
by colliquation of haematomas, infarcts and phlogosis.
-
Clinical and Therapy:
-
They are asymptomatic and should not be treated if they are small;
On the other hand, if they become infected or if there is a significant size, removal of the
pseudocyst can be done, but unfortunately more often a preventive splenectomy is done, because the
location of the pseudocyst can cause splenic bleeding, which is difficult to stop.
ACUTE INFLAMMATION AND CHRONIC
-
TB and Malaria: In Italy, Malaria is more unique than rare, but TB is rather frequent.
Therefore, if there are symptoms of compression, mass phenomenon or risk of rupture,
removal of the spleen is indicated.
-
Abscess: in the case of intrasplenic or perisplenic abscess formation, splenectomy may be
indicated if, for example, drainage of the perisplenic collection alone does not solve the
problem.
ACUTE TORSION AND MOBILE SPLEEN
Mobile spleen or acute torsion is a rare congenital anomaly due to excessive ligament laxity. It is much
more frequent in the female sex, because all ligaments tend to be more lax due to the oestrogen
hormone balance.
-
Types:
-
Ptosis;
-
Migration of the spleen to another abdominal quadrant due to the length of the ligaments;
-
Ectopia, i.e. the presence of an atypical district, such as on the right or in the left hemithorax,
given by an ascending spleen through diaphragmatic hernias within the thorax.
-
Clinical: asymptomatic, occasional findings (mainly Migration and Ectopia)
-
Diagnosis: this is done by ultrasound and CT scan.
-
Therapy: Splenectomy, which is not indicated in ptosis, but only in the case of secondary vascular
complications, where surgery becomes urgent.
SPLENIC ARTERY ANEURYSM
-
The clinic is almost always silent, unless there is a complication, such as an arterio-venous fistula,
fistula with other organs or rupture of the aneurysm. In the latter case, of course, the approach is
emergency from both a diagnostic and a therapeutic point of view.
-
The diagnosis is basically made with CT with M.D.C., with Angio-CT and with angiographies, which
can be therapeutic through the use of endovascular devices.
-
Therapy is rarely surgical nowadays, as the splenic artery aneurysm is treated with the placement of
endovascular prostheses/stents, but when this fails, then emergency splenectomy is indicated, which
can be extended to the tail of the pancreas due to its involvement by the aneurysm itself.
INFARCTION SPLENIC
-
Aetiology: Splenic infarctions are not so rare, especially following pancreatitis, following
neoplastic splenomegaly and endocarditis.
-
Clinical: it is extremely variable.
-
Diagnosis: always done by CT scan with m.o.c.
-
Therapy: the indication for splenectomy is only in severe forms with a major inflammatory
abscess development involving the entire organ.
NEOPLASMS BENIGN
-
Benign neoplasms of the spleen are rare, and even here splenectomy is only indicated for large
neoplastic diseases or in cases of suspected malignancy.
-
Types: these are basically haemangiomas and hamartomas that are identified as accessory
findings in the case of examinations performed for other reasons.
-
Therapy:
-
splenectomy is indicated in particularly large cases;
-
a partial or polar resection of the spleen is almost always performed.
NEOPLASMS MALIGNANT
-
Types:
-
Primary neoplasms: sarcomas, leukaemias and blood diseases,
-
Secondary neoplasms: in some cases the spleen may be the site of metastatic localisation from
K stomach, breast, lung and prostate.
-
Clinical: they are asymptomatic.
Therapy: splenectomy is indicated in the case of oligometastatic disease, i.e. with the presence
of only a single metastasis in the spleen and the absence of metastases elsewhere or of peritoneal
carcinosis, or of lesions leading to an increase in size, which are extremely rare in the case of tumours.
Thus, splenectomy for secondary neoplastic diseases is very rare, because elective and exclusive
localisation in the spleen is extremely rare, but it does exist.
SPLEEN SURGERY
Indications for splenectomy
Rupture of the spleen. in case of external trauma or iatrogenic trauma (can occur in
case of operations on the left colon for traction of the spleno-colic ligament, during operations
on the stomach or pancreas that cause tears in the splenic capsule), whose bleeding, if not
tamed with conservative manoeuvres, is an indication for splenectomy.
Hypersplenisms: Neutropenia, idiopathic pancytopenia, Banti's congestive splenomegaly,
Myelofibrosis, Chronic infectious states, Collagen disorders, Chronic inflammatory diseases,
Lipoidosis. Under these circumstances, the spleen assumes considerable size, resulting in either
compression of the other organs or spontaneous rupture of the spleen itself even after minimal
trauma, becoming an indication for splenectomy.
● Congestive Splenomegaly (Banti's Syndrome - secondary to portal hypertension), a rare
syndrome in which splenectomy is a very rare indication, since splenic artery ligation is
mostly done, as it has been seen that intraoperative and immediate perioperative mortality
in cases of splenectomy from Banti's Syndrome is high, due to vascular changes in the
spleen that frequently give rise to bleeding, surgical haemorrhage.
● Tesaurismosis, in which various substances can be accumulated in the splenic parenchyma
making splenectomy a decisive intervention.
Infections. Some pathogens (viruses, bacteria such as TCB and parasites) can inflame the
spleen, causing splenomegaly. If infections are very serious and treatments are
ineffective, the ultimate remedy is removal of the inflamed organ. Some examples of
pathogens, which cause splenomegaly (and could potentially require splenectomy), are the
malaria plasmodium and the syphilis bacterium.
Blood diseases. Some serious blood diseases, such as sickle-cell anaemia, the
thalassaemia, polycythaemia vera or idiopathic thrombocytopenic purpura, may require
splenectomy. The decision to remove the spleen, however, is only taken after all other possible
treatments have failed.
Focus: haematological diseases
● Spherocytosis, which is an autosomal dominant transmission disorder, affects red blood
cells, which take on a sphere-like morphological alteration, being trapped and
phagocytosed by spleen cells. This results in anaemia due to splenic sequestration of red
blood cells and splenomegaly. In such a case, splenectomy is considered therapeutic with
100% cure in the sense that the spherocytes are not trapped, having a life comparable to
that of red blood cells of normal morphology.
● Thalassaemia, especially frequent in Mediterranean countries. Erythrocytes are trapped in
the spleen and significant splenomegaly ensues.
● Sickle cell anaemia, in which there is an alteration of the beta chains of haemoglobin, with
splenic entrapment, splenomegaly and the need for splenectomy.
● Autoimmune haemolytic anaemias, characterised by anti-erythrocyte antibodies leading to
splenic red blood cell sequestration with splenomegaly.
Cysts or benign tumours The spleen can develop cysts or b e n i g n tumours, which can be
alter the normal anatomy. If these malformations are large or if their complete surgical removal
is impossible, splenectomy is the only viable remedy.
Mobile spleen and acute torsion of the pedicle.
Vascular alterations, which are not uncommon especially in patients with
pancreatic type (splenic artery aneurysms not amenable to endovascular therapy, arteriovenous
fistulas, infarction). In the course of acute pancreatitis, lesions of the splenic artery can also
develop, resulting not only in splenic artery digestion, but also, above all, in arteriovenous
fistulas, between the splenic artery and neighbouring organs
Tumours. Certain neoplasms, such as chronic lymphatic leukaemia, Hodgkin's lymphoma, the
non-Hodgkin's lymphoma or hairy cell leukaemia, can also affect the spleen, causing it to
enlarge (splenomegaly). As in the previous case, if all treatments for splenomegaly are
ineffective, splenectomy is required.
Special cases. On very rare occasions, the spleen may enlarge without a precise cause, or
better without a documentable cause through diagnostic tests. In such cases, setting up a
therapy is difficult, because the trigger is unknown. Therefore, the only
remedy,
for
avoid
the
complications of splenomegaly, is splenectomy.
Surgical technique
Today, access to the abdominal cavity is provided in an emergency in the case of major bleeding of the
spleen. Laparoscopy is no longer indicated, but access is always laparotomic at the midline.
The left hypochondrium is easily reached, where, before going on to remove the spleen, the initial
attempt is to tame the bleeding, which can be done either by compression against neighbouring organs
or even better by clamping the splenic artery at the level of the celiac tripod (after opening the epiplon
retrocavity), which stops the bleeding.
Conservative spleen surgery
Conservative treatment, understood as evaluation for a less invasive intervention or even nonintervention on the spleen lesions, must be done after complete evaluation of the risks and benefits of
all treatment options, such as complete surgery, splenectomy, partial surgery or non-surgery
(conservative treatment).
After assessing the risks and benefits, one may consider adopting a wait-and-see attitude, using
haemostatic substances, biological glues, to stop or reduce bleeding.
In the case of not particularly large, not full-thickness lesions of the spleen, a splenoraffia, a suture of
the spleen, or in some cases a partial splenectomy, can be used.
This can be done when there is an injury to the spleen that does not exceed the first or second degree,
i.e. subcapsular haematomas that affect less than 10 per cent of the surface or lacerations of the
capsular surface that are not actively bleeding and that injure the spleen by less than 1 cm or
haematomas that affect up to 50 per cent and do not increase in volume or lacerations of the capsule
that do not exceed 3 cm and do not involve deep vessels.
The use of electrocoagulators or thermocoagulators or lasers is only indicated in cases of really small
bleeding.
Spleen Raffia
In the case of always small lesions of grade I,II or III at the most, such as subcapsular lesions affecting
more than 50% but with haematoma with subcapsular ruptures with active bleeding, intra-parenchymal
lesions greater than 2 cm or tending to expansion, lacerations greater than 3 cm of the spleen involving
deep vessels, in these cases we can use a conservative technique with sutures, with U- or X-stitches, or
we can use inert tissue plates, which prevent the threads from further lacerating the parenchyma and
fix the stitch so that the stitch itself can approximate the margins of the suture.
Partial splenectomy
A kind of mesh encapsulating the spleen used to be used, nowadays it is no longer used because when
the lesion was such that this prosthesis was necessary, wrapping the whole spleen and compressing it,
the complications could be greater than those due to splenectomy.
Access is median in emergencies, while in elections a lateral access may be used, but this is rare and
depends on the surgeon.
Complications of splenectomy
Complications can develop that can affect 20 to 30%. These include:
- Left pleural effusion from irritation of the diaphragm,
-
Bronchopneumonic outbreaks,
-
Acute pancreatitis,
-
Pancreatic fistulas,
-
Subdiaphragmatic abscesses,
-
Devascularization stomach injuries,
-
Plateletosis due to the fact that platelets are no longer sequestered by the spleen, this occurs
between postoperative days 7 and 15 and can also cause peripheral thrombophlebitis.
Treatment of plateletosis is with aspirin, but it is self-limiting within a month in most cases.
-
Bacterial sepsis, because splenectomy leads to an alteration of the blood-crack structure and
parameters; due to the suppression of splenic immune function, therapy is broad-spectrum
antibiotics, with penicillin, amoxicillin and erythromycin, which can be maintained for life. +
in the case of splenectomy, certain types of vaccination are mandatory, such as influenza,
pneumococcal, meningococcal, and haemophilus influenzae type b, and in the case of
plateletosis, cardioaspirin, i.e. 100 mg aspirin, is indicated. The key ones are haemophilus
influenzae and meningococcus, which in some cases are also done during hospitalisation. The
other vaccinations, especially the flu vaccination, follow the same recommendations as for the
healthy population, and splenectomy is not a contraindication.
Non-surgical treatment
Conservative treatment can be implemented in cases of minor spleen trauma, while in haematological
diseases of surgical interest it is not contemplated.
Wait-and-see treatment can be performed in selected patients with minor spleen trauma, but also in
young patients in whom splenectomy could lead to serious consequences due to long life expectancy.
In any case, the criteria for avoiding surgical treatment of splenic trauma are: age < 60 years with
minor trauma, haemodynamic stability, absence of concomitant pathologies; this can be implemented,
however, after careful and continuous observation for at least 72 hours.
Patients are excluded who:
- have a major state of shock,
-
have a haemoperitoneum,
-
are on anticoagulant or anti-platelet therapy (e.g. there are patients on double anti-platelet
therapy such as heart patients)
-
w e r e evaluated as possible responders to non-surgical treatment, but that within 72h evolve
to a condition of major haemorrhagic shock with all the signs of haemorrhage; exploratory
laparotomy and evaluation of possible complete splenectomy or conservative treatment with
raffia or glue, depending on the size of the laceration, is mandatory in these cases.
In the case of spleen trauma, non-surgical treatment can be performed, combined with clinical,
instrumental observation with CT scans and laboratory observation with serial haemochromes and
constant monitoring of vital parameters to assess the possible evolution towards a picture of
haemorrhagic shock.
JAUNDICE SURGICAL
Jaundice is defined as a condition in which bilirubin levels exceed 3 mg/dl, and this condition may be
preceded, especially in neoplastic forms, by a condition called sub-atheros, when bilirubin exceeds
1.5 mg/100 ml.
Obstructive or surgical jaundice is due to an obstruction of bile outflow in the VBP (occlusions of
the accessory biliary tract do not give jaundice).
A condition of cholestasis results, which is due to the accumulation of bilirubin upstream of the
obstruction, such that hepatocytes no longer pour bile into the bile ducts, but into the bloodstream.
Surgical jaundice then divides into:
- Lithiasis: e.g. a gallstone that leaks and becomes wedged at the level of the VBP, in the
choledoch. But in cholecystomised patients, the stone may also be generated directly in the
VBP or in the intrahepatic biliary tract (rare).
- Non-lithiasis: neoplastic or inflammatory causes:
o
Cholangiocarcinoma (most frequently Klatskin tumour)□ at the confluence of the
hepatic ducts
o Tumour of the head of the pancreas: the last part of the choledoch is intrapancreatic, and
in the case of a neoplasm of the head of the pancreas, it is compressed, or even
infiltrated
o Liver tumours
o Tumour of the papilla of vater (ampulloma)
o Chronic pancreatitis
o
Scarring stenosis of the biliary tract (following surgery)□ iatrogenic
o Phlogistic stenosis of the VBP
o Mirizzi's syndrome: formation of large calculi in the infundibulum which, increasing in
volume, compresses the VBP ab estrinsically.
Clinic
1) Jaundice of the skin and mucous membranes (which will be acute-onset, is called rampant, in
the case of lithiasis, while in neoplasms or chronic phlogosis, there will be an aggravating
jaundice and is preceded by sub- jaundice)
2) Hypo-acolic stools (absence of bile pigment in stools)
3) Urinary hyperchromia (marsala-coloured complexion), dark colour, due to elimination of
conjugated bilirubin excreted with urine
4) Itching (due to accumulation of bilirubin and bile salts in the skin) with scratching lesions
Then there may be other accompanying signs and symptoms:
- Bleeding from altered coagulation (due to altered intestinal absorption of vit K)
- Bradycardia (for circulating bile salts)
- Nervous disorders (for circulating bile salts)
- Asthenia, headache, dizziness
Moreover, in the case of lithiasic aetiology, there could be:
-
Colic-like pain from the epigastrium to the right hypochondrium with irradiation to the right
shoulder after a large meal.
Dyspepsia
Fever (if there is acute cholecystitis or cholangitis)
In contrast, in the case of inflammatory or neoplastic aetiology: the pain is dull and deep and slowonset.
EO
The gallbladder is physiologically not palpable, it becomes palpable if it is hyperextended, as in the
case of: hydrops, empyema, neoplasia, obstruction downstream of the cystic duct by neoplasia.
There may be:
- Courvasier-Terrier sign: palpable, dilated gallbladder associated with cholestatic jaundice, due
to compression by neoplasm (e.g. pancreatic head, klatskin tumour), rather than lithiasis. In the
case of jaundice from choledochal stones, nothing is found.
- Positive cystic point: intersection of the costal arch and lateral margin of the right rectum of the
abdomen
- Positive Murphy sign
Laboratory examinations
-
Increase in direct bilirubin and also indirect bilirubin due to 'carry-over' effect
Increased cholestasis indices (gamma GT, alkaline phosphatase)
Indices of liver function: with reduced coagulation factors, albumin, pseudocholineesterase
and increased bilibrubin
Increased transaminases (cytolysis indices) AST and ALT
Increased pancreatic indices: amylase and lipase in acute biliary pancreatitis
Diagnostic imaging
1) Ultrasound: checks for dilatation of the bile ducts and the presence of stones in the gallbladder
and also in the bile ducts
2) Cholangio-RMN: it studies the biliary tree better and shows us exactly if there is an obstruction
3) Multilayer CT scan with mdc: especially in the case of neoplasia it allows staging of the
disease (e.g. head of pancreas)
4) Endoscopic cholangiography
5) Percutaneous transhepatic cholangiography: this is performed by the interventional radiologist
with ultrasound guidance in cases where ERCP cannot be performed. It allows bile to flow
outwards, by decompression of the hyperextended pathways.
6) ERCP: Endoscopic retrograde cholangio-pancreatography. A sphincterotomy of Oddi's
sphincter is performed, a guide wire is introduced into the biliary tract, a probe or catheter is
introduced and the guide wire is removed, and mdc is injected, and Dormia's basket is used, in
the removal of stones. It is usually performed for therapeutic purposes in the presence of
calculus in the VBP. It can give complications:
o Acute pancreatitis
o Haemorrhage
o Perforation
7) Nose-biliary probe: this is inserted endoscopically as in ERCP, upstream of the stone to drain
bile and reduce jaundice, pending removal of the stone. It is introduced through the nose and
passes through Vater's papilla and upstream of the obstruction.
OCCLUSIONS INTESTINAL
Intestinal obstruction is by definition a complete or incomplete stoppage of intestinal canalisation, i.e.
the progression of liquid, solid and gaseous intestinal material; material may be represented either by
digested material or even already by faeces undergoing reabsorption, i.e. in the final compaction phase
of the faecal bolus. It is possible to speak of a complete and persistent halt or interruption of the transit
of intestinal contents in a segment. A synonym for 'intestinal obstruction' is 'ileus' ('twisting'), a very
serious pathological condition.
Epidemiology
From an aetiological point of view, in about 70% of cases, mechanical occlusions are due to
adhesions. A small percentage is attributed to tumours (5-20%). Then there are hernias (2-10%). And
finally chronic inflammatory pathology, such as Crohn's disease (5-7%).
The aetiology affecting the jejunum and the colon is different.
In the former case, the causes are more attributable to non-neoplastic, post-inflammatory
pathologies such as adhesions;
In contrast, the causes of colic occlusion are mainly attributable to neoplasms (65%).
Clinically speaking, it is rare to be faced with a complete intestinal occlusion (acute intestinal
occlusion); incomplete intestinal occlusions, i.e. intestinal sub-occlusions, where solids are unable to
pass, as opposed to liquids and gases that are allowed to transit, are more common.
Intestinal obstruction, according to classification, can be:
Mechanical; one speaks of mechanical ileus when there is a physical obstacle to the transit
of intestinal contents.
Paralytic/dynamic; paralytic ileum occurs when, although there is no
a physical obstacle to the progression of the intestinal contents, there is a lack of peristalsis;
there is inefficient peristalsis and diffuse relaxation of the intestinal wall that does not allow the
food bolus to progress
Pseudo-occlusion (rare) one speaks of intestinal pseudo-occlusion when a
only tract of intestine is aperistaltic, not allowing transit of intestinal contents; due to a
myogenic or neurogenic lesion that may be chronic-recurrent in nature. It is compatible with
life only if incomplete.
+still, there may be an ileum called functional ileus, a consequence of chemical or pharmacological
intoxication (?).
Paralytic Ileo
Paralytic ileus is a condition characterised by a complete absence of intestinal peristaltic activity that
generates a clinical picture of occlusion even in the absence of a mechanical obstruction to transit.
It is not always intestinal paralysis proper: there is an atonic variety, there is a spastic variety, i.e. an
incoordinated hyperactivity of intestinal motility usually in the presence of heavy metal poisoning; the
variety associated with vascular occlusion concerns intestinal strangulation or infarction.
The inhibition of motility is due to the adrenergic system, as a consequence of reflex mechanism, in
response to:
- Painful stimulation of peritoneal receptors (stimulated in turn by pain states of various kinds)
- Peritoneal irritation or inflammation
Causes
- Intraperitoneal: diffuse or circumscribed peritonitis, haemoperitoneum, choleperitoneum,
uroperitoneum; trauma of the abdomen or penetrating wounds in the cavity; laparotomies,; it
can be said that this eventuality is one of the consequences of open surgery, in fact, thanks to
laparoscopic surgery we are witnessing a more rapid functional recovery of intestinal
contractile activity, so much so that the post-surgery ileus in patients who undergo
laparoscopic surgery, in a certain sense, lasts less than in patients who undergo traditional
open surgery; the dynamic ileus associated with surgery is also a result of the administration
of muscle relaxants;
- Vascular: intestinal ischaemia, mesenteric insufficiency or intestinal infarction;
- Retroperitoneal: pancreatitis, retroperitoneal blood spillage (aortic aneurysm rupture or pelvic
fracture), spinal cord injury or spinal trauma;
- Reflexes: renal or biliary colic, torsion of funiculus or ovarian cyst,
- Extra-abdominal: basal pneumonia or pleurisy, myocardial infarction, chest trauma or chest
wounds, cerebral stroke, neurosurgical interventions; diseases of the nervous system, in
particular head trauma can lead to reduced visceral motor nerve activity, as can meningitis,
spinal cord syndromes, lumbar sympathectomy
- Systemic causes: electrolyte imbalances (hypokalaemia, hypomagnesaemia), metabolic
imbalances (diabetes, uremia, alkalosis), drugs* (anticholinergics, narcotics), toxic-based
paralytic ileus (saturnism - chronic lead intoxication - an occupational disease of printers, given
the lead composition of the printing characters)
*Many elderly people take tranquillisers that may have a summation effect resulting in a delayed
peristalsis with pharmacological ileus and at the same time, this reabsorption gives rise to a
reabsorption phase of the faecal component (watery part) such that at the level of the sigma or rectal
ampulla, faecalomas may occur
From a pathophysiological point of view, we will have a loss of tone of the intestinal wall with a total
arrest of intestinal peristalsis.
Mechanical Ileo
It is therefore possible to classify mechanical occlusions etiologically, topographically and
pathogenetically.
Aetiological classification
According to the aetiological classification, a distinction can be made: Endoluminal intestinal
occlusions
parietal intestinal occlusions, for intrinsic lesions to the wall itself parietal intestinal occlusions,
for extrinsic lesions to the wall.
Intraluminal injuries:
Calculus (or biliary ileum);
Bezoari;
Foreign bodies;
Coprolites;
Faecalomas;
Parasites (roundworms);
Neoplasms -> a particular type of neoplasm causes intraluminal lesion, usually neoplasms do
not give intraluminal but intramural lesions.
Extrinsic or extramural lesions (from outside the viscera something causes compression of the wall):
Post-operative adhesions (adhesion bridges) Post-phlogistic adhesions;
External and internal hernias;
Volvoli;
Haematomas;
Abscesses;
Vascular causes.
Neoplasm -> not from the occluded portion of the intestine, but from another portion or
abdominal organ.
Intrinsic or intramural injuries (compression from the viscera wall itself):
Congenital (malrotation and duplication, atresias and stenosis), typical of paediatric patients;
one must assume these when, for example, one is dealing with a child who presents at the
outpatient clinic, whose mother reports that he has never emitted meconium: in this case one
can be almost certain that this is an atresic pathology. If, on the other hand, following the
emission of meconium no stool is no longer emitted, in those cases, the child most probably has
hypertrophic pyloric stenosis
Inflammatory (autoimmune and diverticula) -> lead to thickening of the wall and thus lack of
transit;
Post-operative stenosis; post-operative stenosis occurs upstream and downstream of the heads
accollated (anastomosis), following resection. The stenosis is therefore located exactly at the
point where there is more scarring, at the point where the two tracts of intestine have been
rejoined.
Actinic stenosis (post radiotherapy); Invaginations;
Endometriosis.
Neoplasia
Topographical classification
Topographical classification has clinical significance, as there is a symptomatic difference between an
ileal occlusion and a colic occlusion.
Ileal occlusion:
High Ileal -> the higher the affected portion, the more vomiting symptoms will be present.
Low Ileal -> later vomiting.
Colon occlusion: belongs to the distal occlusions and has a very different symptomatology than ileal
occlusions.
Pathogenetic classification
In relation to the pathogenetic mechanism that caused the occlusion:
Compression
Compression occurs because there is something from outside compressing the intestinal wall. The
intraluminal pressure cannot counteract the pressure from outside. This occurs because the intestinal
wall is not rigid.
From an aetiological point of view, compression recognises extramural injuries such as adhesions,
neoplasms, abscesses and h e r n i a s as causes. Hernia represents a special case: it forms
because, at the moment when the viscera goes into the h e r n i a sac, the hernia collar girdle
results in a choke, i.e. a compression-driven occlusion with clear signs of vascular distress.
Choking
In the case of hernias, there is not only abestrinsic compression of the intestinal wall, but at the same
time there is compression of the vessels of the meso that irrigate the occluded portion of the intestine (
stricture). There are conditions in which there is vascular distress, but it is not caused by the
compression, e.g. in volvulus. In choking, the blood supply in that particular loop is deficient, leading
to tissue necrosis.
Obstruction
Obstruction is due to the fact that there is a solid mass within the intestinal lumen that prevents the
intestinal contents from passing through. This mass, of course, must be the same size or larger than the
intestinal lumen.
Obstruction can be caused by foreign bodies (oesophagus, pylorus, anastomoses), bezoars and
parasites (pylorus, ileo-cecal valve, intestinal anastomoses), gallstones (duodenum, ileo-cecal valve),
faecalomas (rectal ampulla), meconium ileus.
Stenosis
Etiologically, stenosis is related to intramural lesions. It represents a narrowing that can cause an
impediment to the normal transit of intestinal contents.
Congenital;
Inflammatory;
Post-operative.
Neoplastic;
Initially, the transit in stenosis is preserved, because it is a gradual process, which progressively
compromises the lumen; in this case, the clinical condition will be subocclusion. Upstream of the
stenosis there is a gradual dilatation of the intestinal lumen, for 2 reasons:
It contains more faecal material;
At first, peristalsis upstream of the stenosis is overactive, almost spastic with
strong pain, because the intestine tries to overcome the obstacle and pass the intestinal contents
through the small orifice that remains; after this phase of progressive increase of the peristaltic
waves, dilatation occurs, i.e. peristalsis is less and less and the wall upstream of the stenosis is
increasingly stretched.
Angle
Occlusion is determined when the angle between the intestinal loops, in addition to being acute, is
fixed for
adhesion between two loops (loop-loop) or between loop and parietal peritoneum.
In the case where there is a bridle of adherence between a loop and the abdominal wall, this bridle
pulls the loop towards the wall (not the meso, because it remains attached to the posterior wall of the
abdomen and cannot be pulled) forming an acute angle and consequently creating the conditions for a
mechanical occlusion; or the adherence is formed between two intestinal loops bringing them closer
together and thus forming an acute angle and consequently an occlusion.
From an aetiological point of view, angulation is to be referred to extramural injuries, because it is
determined by something (adherential bridle) acting from outside.
Intestinal volvulus (sigma and cecum)
Volvulus is formed when the torsion of the sigma or cecum along their longitudinal axis on the
mesenteric pedicle occurs.
Because the sigma is very long
By torsion around an adherential bridle
For congenital defects of peritoneal packing (rare)
Strangulation
In the volvulus condition there is also impairment of the vascular supply, because when the intestinal
torsion occurs, not only the intestine turns, but also the meso and thus also the vessels contained in it.
In this case, it is not choking but strangulation.
Intussusception (mainly in children)
It is the invagination of a part of the intestine into the next loop. Penetration of the invaginating
segment occludes the lumen.
The intestine introfects like a 'glove finger' into the next loop, leading to occlusion. The disorder sets in
acutely in infants, often at the time of weaning; or subacutely in adults, at a polyp lesion that sucks
down the intestine above.
N.B. Choking, volvulus and intussusception are forms of mechanical ileus with primary vascular
distress; the other cases have no vascular distress.
N.B. Mechanical ileus, when simple, is a discontinuous ileus because it is linked to peristalsis: there
may be alternating more or less close attacks and then moments of apparent calm. At this point it is
important to look at the clinic, the natural history, how long it has been going on; when the bowel '
gives up' (the hyperperistalticism trying to overcome the obstacle is exhausted) it is clear that the
picture gradually worsens and one moves towards a picture of ileus that is no longer mechanical, even
if the eventual cause was mechanical, but inexorably one arrives, in the advanced history of the
disease, at an ileus typically of a dynamic type.
Pathophysiology
When there is something mechanical that leads to non-transit, it is due to the accumulation of liquids
and gas that there is an upstream post spastic peristalsis distension.
Occlusion after distension leads to a reduction in absorption and a reversal of the flow of faecal
material upstream of the occlusion (with fluid passing through the mucosa from the outside to the
inside).
The endoluminal sequestration of water, electrolytes and proteins will lead to the formation of
parietal oedema and transudation of the intestinal contents themselves into the peritoneal cavity.
In addition to internal sequestration, there is a further (external) fluid loss that occurs with the
compensatory mechanism of vomiting, leading to dehydration and hydro-electrolyte alterations (early
dehydration in high occlusions, with hypochloremia and hypokalemia and metabolic alkalosis; late
dehydration in low occlusions due to increased reabsorption and less significant hydro-electrolyte
alterations).
From a pathophysiological point of view, there will be an alteration of gases:
● Inhibition of gas reabsorption with increased thickening of the intestinal wall and increased
hydrostatic pressure in the venous district;
● Increased gas production due to increased bacterial flora (not normally present);
● Increased relaxation.
If there is an increase in intraluminal pressure due to the fact that there is an occlusion further
downstream, there is a circulatory alteration in the wall of the distended loop, resulting in venous
stasis and the opening of arteriovenous shunts: this will lead to a decrease in the perfusion of the
mucosa, which will then be in pain. If there is alteration of the mucosa - due to hypoxia of the lining
cells, destruction of the mucous barrier, increased capillary permeability - so-called bacterial
translocation may occur.
Local alterations. Upstream of the occlusions themselves there may be motor alterations of
hyperperistalticism with atony downstream. The anatomo-functional alterations of the wall differ
depending on whether the vascularisation is compromised or not (without s t r i c t u r e ; with
stricture: suffering, ischaemia, necrosis, perforation). Pre-occlusive distention leads to an impaired
absorption capacity.
General alterations concern hydro-electrolyte imbalances (with important distinction between
supravaterian and subvaterian occlusion, as the first will lead to metabolic alkalosis with hypokalemia
due to prevalent loss of sodium, the second metabolic acidosis and hyperpotassemia with prevalent
loss of sodium, due to loss of basic ions through stagnation of biliopancreatic and enteric juices) and
loss of plasma and blood in the intestinal lumen and peritoneum (the latter will occur in the presence
of neoplasia, inflammation).
Hypokalaemia leads to the establishment of a vicious circle because it reduces muscular contractility
as nerve conduction is reduced; from an objective point of view, one could also note the presence of
asthenia or sensory obnubilation and it also leads to electrocardiographic alterations from conduction
defects.
Hypochloremia occurs mainly in high occlusions with gastric vomiting, leading clinically to metabolic
alkalosis, hypocalcaemia and tetany.
Hyponatriemia results in additional water loss and clinically dry skin, dry tongue, hypotension,
oliguria and hyperazotemia.
Focus: colic occlusions
There are two types of colic occlusions that create two distinct mechanisms:
● Occlusion with a competent ileo-caecal valve creating the closed loop mechanism. If the valve
is competent it tends to close physiologically and prevent colic contents from flowing into the
ileum. However, this leads to a build-up of fluid quantities in the colon and to the cecum and
ascending colon becoming increasingly swollen/dilated, until this wall widens to such an extent
that it creates the conditions for the so-called diastatic rupture or perforation of the cecum
and ascending colon (muscle fibres give way and the wall is perforated).
● Occlusion with incompetent ileo-caecal valve creating the open loop mechanism. If the valve
is incompetent, there is a compensatory mechanism, i.e. there is no diastasic rupture of the
ascending colon and cecum, but the contents reflux into the ileum. This results in ileal
contamination, but perforation will not occur.
Mechanical ileum clinic
● Closure of the alvus to faeces and gas sometimes one may experience diarrhoeal faeces
emission despite being occluded because it is the result of the emptying of the part of the
intestine distal to the occlusion due to the existence of distal peristalsis; we speak of false
channelling (if the patient has had gas and not faeces emission we speak of sub-occlusion; the
alvus may be diarrhoeic, because only semi-liquid faeces manage to pass through the occluded
or sub-occluded segment; in these circumstances, days of constipation followed by an episode
of unformed faeces or even incontinence can be observed)
● Abdominal distension (at the point where the occlusion is located) and of the loops;
● Pain; it varies according to the site where the occlusion is present: in pyloric and duodenal sites
it will be intermittent and epigastric but not cramp-like; in the mid-distal portions of the small
intestine it will be cramp-like, with a crescendo and regression with a 5-minute interval
separating one colic from the next. In colonic occlusions the pain is less intense, duller and
deeper, sometimes diffuse, at the hypogastric site or in the left iliac fossa; when it becomes
very intense and persistent and is associated with a muscular defence reaction of the wall
abdominal (occurs when the occlusion is associated with inflammation), strangulation or
perforation must be suspected;
● Nausea and vomiting
o High occlusion (pylorus, duodenum, jejunum): vomiting is early, constant, continuous,
abundant and the vomited material is predominantly biliary.
o Low occlusion: vomiting is less frequent, later, darker in colour, malodorous and faecal.
In colic occlusions vomiting is usually absent, may present late, if there is a large
distension and only when there is an incompetent ileo-caecal valve.
Other symptoms:
● Tachycardia, dry skin, dry tongue, oliguria, hypotension, drowsiness, dullness of the
sensorium, asthenia, indications of dehydration and hypovolaemia due to significant fluid loss
(5 to 9 L), which spills either into the intestinal lumen or, in the case of perforation, also into
the peritoneal cavity. In addition to vomiting, hypovolaemia may be accentuated by aspiration
through a nasogastric tube due to post-operative paralytic ileus.
● Ascites
●
●
●
●
●
Visible peristalsis
Palpable hernias or swellings
Pain on palpation
Visible or occult blood in faeces
Fever in occluded patients occurs in case of ischaemia.
Dynamic ileum clinic
-
Nausea and Vomiting (from gastric stasis)
-
Relaxation and closure of the alvo (by stopping colic motility)
-
Pain (less intense and less localised than that from mechanical occlusion) in the dynamic
ileum, the patient tends to report a poorly defined pain of a gravitational type, there is the
presence of an abdomen that is now exhausted, globular
N.B. Absolutely avoid, therefore, in the case of suspected mechanical ileus, administering antispastics and/or painkillers to the patient, which resolve the painful symptoms but delay surgery,
inexorably worsening the patient's prognosis.
Objective examination
1. Inspection: see if the patient presents a distended abdomen, whether meteoric, diffuse or
sectorial distension, as the former is an indication that the pathology is in the advanced stages,
whereas if the distension is sectorial, one will be faced with the early stages of mechanical
ileus and tend to have the entire upstream portion of the obstruction
2.
3.
4.
5.
distended, while the downstream portion will even be empty. Thus, one will see a distended
abdomen in sectoral areas that may be the upper or lower quadrants depending on the level at
which the occlusion occurred.
Palpation is very important because it allows one to assess whether the abdomen is tense,
whether it is elastic, one could also have a tactile perception of peristalsis, especially in thin
subjects.
It must be remembered that a tympanic sound is always an expression of an accumulation of
air in the abdominal cavity.
Auscultation attention must be paid to abdominal silence because it is typically an expression
of dynamic ileus, but it can also be an expression of an ileus that was initially mechanical but
has evolved into a dynamic ileus. The presence of borborigrams is obviously an expression of
an early phase of mechanical ileus, as in the continuation of the natural history of the pathology
they may also be absent, especially if from an early phase of mechanical ileus one moves on to
a dynamic ileus. Everything in relation to the presence or absence of peristalsis, because if
peristalsis is intense, especially in an early phase, these borborigmas are an expression of the
force expressing the contraction upstream of the obstacle and the lapping of gaseous solid and
liquid elements.
Rectal exploration. The patient is placed in left lateral decubitus with the thighs flexed on the
pelvis, and the index finger is gently introduced into the rectal ampulla. By means of this
examination one may sometimes be able to feel the presence of a faecaloma at the apex of the
rectal ampulla, and in these cases a direct resolution of the case can be carried out, by
mechanically removing the faecaloma, with the introduction of a finger at first, and then, after
waiting for the relaxation of the internal sphincter, the second finger can be introduced,
perhaps inviting the patient to sit down as if he were going to take a dump.
Instrumental examinations
Direct Rx of the abdomen in white, which is based on natural contrast imaging: the same elements
contained within the bowel, i.e. the liquid mass, the gas and the solid part constitute the hydroaerial
levels. In mechanical ileus on Rx there is distention limited to the portion of the bowel upstream of the
obstruction, with the presence of hydroaerial levels, which are therefore district. In dynamic ileus there
is diffuse distention of the loops with hydroaerial levels in turn diffused over the entire colic and
intestinal frame. Typical hydroaerial levels are termed stepped or inverted U-shaped.
Opaque schism, a minus lesion (apple core sign) is visible, now almost completely abandoned as it
has been supplanted by CT.
CT scan, which is now the examination of choice as it provides more detailed images and thus gives
more information about the nature of the ileum.
Treatment
Surgery is more successful if patients come to the doctor's attention at an early stage of the disease's
natural history, because obviously t h e longer the natural history of the disease, the more subsequent
complications related to hydroelectrolyte imbalances occur, and the likelihood of an intestinal
perforation with subsequent peritonitis also increases.
In the case of volvulus, in early cases the surgeon can intervene by derotating the intestine and saving
the loop, but in some cases too much time is lost and the vascular compromise is irreversible, so that it
will no longer be possible to save the loop, since the part of the intestine affected by the volvulus will
have gone into necrosis, so it will be necessary to remove the entire infarcted part of the intestine or,
even worse, one could be faced with a picture of acute peritonitis due to the rupture/perforation of the
affected section of intestine, which further complicates the patient's prognosis.
Another very dangerous picture is hernial stricture and even in this case, if action is not taken quickly,
there is the risk of having to do not only a hernia reduction, but also a resection of an intestinal loop.
The surgical objective in the first instance is to resume vascularisation, firstly by removing the
choking girdle and then with 'resuscitative' manoeuvres that serve to vasodilate and improve the lack
of perfusion in this part of the intestine.
In the case of biliary ileus: usually the migration of the calculus is due to the formation of cholecystoduodenal fistulas. The resolution in this case is to remove the stone from the loop and then close the
fistula.
In the event of a high occlusion, giving abdominal discomfort, strong nausea and continuous biliarygastric vomiting, a decompression manoeuvre with a nasogastric tube could be attempted, resolving
the patient's discomfort, even if only partially; certainly, analysing the quality of the vomiting, the
necessary clinical-diagnostic reasoning must then be made as well as the right questions to the patient,
for example on the time of onset of the symptoms. Another intervention that can be implemented
immediately is the administration of saline solution to hydrate the patient.
HAEMORRHAGES DIGESTIVE
Digestive haemorrhage refers to all blood loss occurring at any level of the digestive tract or attached
glands.
They can be distinguished into:
1) Manifest: when the patient presents clear clinical manifestations: haematemesis, melena,
enterorrhagia, proctorragia, up to pictures of shock and/or acute anaemia.
2) Occult: one is faced with a patient with chronic anaemia of NND (undefined diagnosis), which
often correlates with neoplastic aetiology and is detected by faecal occult blood evaluation,
which has been used in recent years as screening in the field of oncology.
Digestive haemorrhages are classified in various ways:
a) Based on location:
- Upper digestive haemorrhages: from the oesophagus to the ligament of Treiz (oesophagus,
stomach, duodenum, liver and pancreas). Haemorrhages that are very difficult to control
and occur acutely are often located at this level.
- Lower digestive bleeding: from the ligament of Treiz to the rectum.
It is essential to identify the origin of the haemorrhage, in order to begin the correct diagnostic and
subsequently therapeutic process.
b) Based on clinical manifestations:
- High: blood regurgitation, haematemesis, melena, haemobilia
- Low: rectorrhagia, haematochezia
Enterorrhagia is a very generic definition that does not fit into either category, it indicates
haemorrhage of any origin.
c) Based on the amount of Hb lost, then the magnitude:
- Chronic-subclinical (these are haemorrhagic stillhydes, often occult, with progressive
anaemia. The patient is usually pale, tachycardic, asthenic with sideropenic anaemia).
- Mild to moderate (<1000 ml)
- Acute-severe (approx. 1000ml)
- Massive (>1500 ml, with haemodynamic instability, up to haemorrhagic shock)
Causes of high digestive bleeding
1) Esophagus:
- Rupture of oesophageal varices: taking a correct history for liver cirrhosis
- Mallory-Weiss syndrome: it is determined in chronic alcoholics and there is a longitudinal
tear in the mucosa of the gastro-oesophageal junction, caused by very intense vomiting and to
have the clinical manifestation, it must extend to the muscolaris mucosae, which is very rare.
In most cases, the arrest is spontaneous and one can intervene through
-
the use of SNG and washing with refrigerated solution, otherwise endoscopic electrocautery
can be used after the acute phase. It enters DD with Boehaave's syndrome (bioerev), which is
caused by increased pressure inside the oesophagus, following episodes of intense vomiting
accompanying eating disorders such as anorexia or bulimia, and more rarely by forced
coughing or other. It may result in pneumomedistine or mediastinitis and later fatal sepsis. If
the bleeding does not stop, surgery is performed.
Peptic oesophagitis
Oesophagitis other than peptic ulcers
Caustic injuries
Oesophageal diverticula
Foreign bodies
Endoscopic/iatrogenic lesions
Benign and malignant tumours
2) Stomach:
- Peptic ulcer: duodenal and then gastric
- Acute erosive haemorrhagic gastropathy: stress or drug-induced (we do not speak of
gastritis, because there is in fact no inflammation). When they occur in dialysed patients, we
speak of acute uremic gastropathy. In history there is immoderate use of NSAIDs or steroids.
These are bleeding erosions of the gastric mucosa, limited to the epithelium and not extending
beyond the muscolaris mucosae. They have the appearance of haemorrhagic suffusions or true
ulcers, often multiple with polycyclic contours. But also Curling's ulcers: these are stress
ulcers, with a reduced resistance of the mucosa to acid-peptic secretion, typical of large burns.
Underlying this is the opening of pre-capillary arteriovenous shunts and splanchnic
vasoconstriction, which reduce blood flow, resulting in ischaemic suffering of the epithelium.
- Hiatal hernia
- Anthro-gastric vascular ectasia small, diffuse dilated vessels distributed over the mucosa of
the gastric antrum that bleed spontaneously. We also speak of a 'watermelon stomach' when the
vascular ectasia is arranged on the folds and converges at the pylorus.
- Angiodysplasias: nowadays diagnosed to a greater extent thanks to the use of endoscopy.
- Dieulafoy's lesion: an aberrant artery in the thickness of the gastric submucosa that can be up
to 5 mm in diameter, about 10 times the diameter of normal mucosal capillaries. Pulsation of
the vessel leads to its rupture and thus bleeding
- Benign and malignant tumours
3)
-
Duodenum:
Duodenitis
Peptic ulcer
Aorto-duodenal fistula
4) Pancreas:
- Acute pancreatitis necrotic-haemorrhagic form
- Wirsung-ragia
5) Liver:
- Emobilia: may be spontaneous or traumatic
The most frequent causes of high digestive bleeding are:
a) Gastro-duodenal peptic ulcer
b) Acute erosive-haemorrhagic gastropathy
c) Oesophageal varices
d) Mallory-Weiss syndrome
e) Aorto-duodenal fistula
Causes of low digestive bleeding
1) Small intestine:
- Chron's disease : is a chronic inflammatory bowel disease with poussé evolution,
characterised by flare-ups, especially at the ileal level (terminal ileitis)
- Diverticula of the small intestine
- Meckel's diverticulum: complication due to the presence, in its context, of heterotopic or
ectopic islands of gastric mucosa: these undergo acute ulceration, with massive bleeding,
which poses diagnostic difficulties for endoscopy, as they mask the presence of faeces
(absence of piceo blood, melena), giving a brick-red colour. Meckel's diverticulum blood has a
'Florentine baked brick' colour, neither bright red nor black. Blood loss is observed on
angiography (the loss must be at least greater than 4ml/min) and is stopped by the placement of
a Gianturco coil (a therapeutic tool used to embolize aneurysms or blood vessels).
- Angiodysplasias
- Intestinal infarction
- Aorto-duodenal fistula
- Benign and malignant tumours
2)
-
Colon-rectum:
Severe enteritis (infectious, actinic, from chemotherapy)
IBD (inflammatory colitis: both Crohn's disease and UCR)
Solitary rectal ulcer
Diverticular disease
Ischaemic colitis / mesenteric infarction
Angiodysplasias
Iatrogenic injuries: surgical and endoscopic
Polyps
Malignant tumours
3)
-
Anal canal:
Proctiti
Anal fistulas
Haemorrhoids
Rhagades (give intense painful symptoms)
Anal trauma
Malignant tumours
The most frequent causes of low digestive bleeding are:
- Diverticular disease of the colon (which has other complications besides haemorrhage,
diverticulitis, perforation and fistulisation often in the bladder)
- Angiodysplasias (especially in the right colon)
- Benign (polyps) and malignant tumours of the colon
- Chronic inflammatory bowel diseases
Clinic
The clinical pictures that are associated with digestive haemorrhages are:
1) Blood regurgitation: the emission of blood from the mouth in the absence of vomiting. It
usually originates from the oesophagus.
2) Haematemesis: emission of blood from the mouth by the vomiting mechanism. It differs from
haemophthisis, in which the blood comes from the respiratory system, which was very
common in the past due to tuberculosis. Today, it is more related to pulmonary neoplasia,
when it has corroded the lung wall. It is usually of oesophageal or gastro- duodenal origin: e.g.
in a cirrhotic patient with oesophageal varices. The blood will be bright red undigested, and it
will be important to dd with partially digested fatty acid blood, i.e. caffeine vomit, which is
darker in colour, and is attributed to the slower emission of blood, and which in contact with
hydrochloric acid, changes its colour properties.
3) Melena: evacuation of blood or faeces mixed with blood, which are blackish, piceous;
furthermore, the faeces must be pultaceous (not completely formed) and particularly foulsmelling. It is usually of gastro-duodenal, digiuno-ileal origin. The transit time of the blood
material must be long enough to allow the transformation of haemoglobin into haemetin by the
digestive juices (digested blood). This usually involves haemorrhages above the ligament of
Treiz. He goes into DD with hyperpigmented stools (pseudomelena or false melena)
following the ingestion of certain foods or drugs (iron, charcoal, or bismuth, liquorice, beetroot,
blueberries), which give a blackish colour to the stools.
4) Haemobilia: presence of blood in the biliary tree. Haemobilia may be due to an iatrogenic
cause (e.g. complication of ERCP) or non-iatrogenic (trauma, parasitosis, lithiasis of the
gallbladder due to involvement of a small vessel, angiomas eroding an intrahepatic biliary
branch, erosions of the main biliary pathway due to passage of a stone, bleeding tumours
within a biliary branch); these types of haemorrhages are difficult to recognise and treat; they
have all the manifestations of upper digestive haemorrhages (melena or even rectorrhagia) but,
as the bleeding occurs within the biliary tract, which then
end in the duodenal papilla, you don't always when you go in with the gastroscope can see the
bleeding or, in the opposite case, if the bleeding is important, you don't see anything anyway.
Techniques such as embolisation or angiography, help a lot because they not only allow you to
arrive at a diagnosis easily, but also allow you to go and treat these situations
5) Enterorrhagia: blood emitted through the rectum. One does not have a certain idea about the
source of bleeding, one usually just locates it in the small intestine: between jejunum and
ileum.
6) Rectorrhagia or proctorragia: emission of bright red blood during defecation, after defecation
or independently of defecation. Bleeding that occurs independently of defecation is suggestive
of neoplasia, when it occurs after defecation, it is suggestive of haemorrhoidal disease.
7) Haematochezia: the presence of small amounts of blood in the faecal cylinder. It is usually
typical of polyps.
8) Drop-by-drop bleeding: this is associated with benign, but nevertheless very annoying
pathologies, such as fissures, caused by tearing of the anal fissure. This is the emission of
blood during defecation and especially at the end of defecation.
Diagnosis History
1) Identify the site of the haemorrhage: thus distinguishing between high and low (high:
haematemesis and melena; low: haematochezia and rectorrhagia)
2) Identify a plausible cause of bleeding. It is not certain that other causes of bleeding do not also
co-exist.
3) Assess the age of the patient:
- Infants/children (0-12 years): Meckel's diverticulum, intestinal duplication, intestinal
invagination (usually by 24 months of age, due to intestinal peristalsis dyskinesia)
- Young (12-30 years): Meckel's diverticulum, polyps, ulcerative colitis/Crohn's disease
- Adults (< 60 years): polyps, neoplasms, diverticular disease, angiodysplasia
- Adults (> 60 years): neoplasms, diverticular disease, polyps
4)
-
Research:
Alcohol abuse
Taking gastrolesive drugs
Treatment with anticoagulants
Gastrointestinal disorders: for the upper: history of ulcers, for the lower: abnormal bowel
movements, pain from haemorrhoid disease
Liver diseases: cirrhotic pc
Investigating previous bleeding
Objective examination
- Finding non-gastrointestinal bleeding (massive nosebleeds: very copious blood, expelled from
the mouth)
- Identifying any palpable masses
- Digito-ano-rectal exploration (EDAR: to identify anorectal pathology)
- Assessment of chronic liver disease/cirrhosis: spider nevi, jaundice, gynaecomastia, palmar
erythema, splenomegaly
- Then assess arterial pulse, blood pressure, oxygen saturation. In critical haemorrhage, the patient
will be hypotensive, pale and with a weak pulse.
Laboratory examinations
They assess haemodynamic stability:
1) CBC and platelets: evaluation of Hb to determine whether bleeding is acute or chronic. The
CBC is assessed serially, at 1-2-6h, depending on the severity of the haemorrhage.
2) Electrolytes: abundant potassium losses can lead to cardiac arrhythmias
3) Ammonemia: assesses liver function
4) Creatinine and azotemia: assesses renal function
Instrumental examinations
1) EGDS (oesophago-gastro-duodenoscopy): assesses high digestive bleeding, is 90-95% accurate
and has both diagnostic and therapeutic value. It represents the gold standard. From the
therapeutic point of view, it allows haemostatic treatment, by means of: electrocoagulation,
sclerosis of oesophageal varices, application of fibrin glue, plastic clips; it cannot be done in
the case of significant bleeding; it allows histological diagnosis;
2) Colonoscopy: assesses low digestive bleeding. In urgency it is to be avoided unless it is needed
for a volvulus derotation. It allows us to go from the anal rima to the first ileal loop. Impossible
to perform in cases of massive bleeding. Allows us to make a histological diagnosis, and to
place DD from bleeding from unperforated diverticulitis and from neoplastic pathologies.
3) Selective arteriography of the celiac tripod and superior mesenteric artery: this is performed
within the first hour that the patient comes to our observation; after this time, something else is
done. We selectively cannulate these vessels to identify the oozing of blood. At the therapeutic
level, action is taken with local injection of vasoconstrictors (vasopressin) or embolisation.
4) Scintigraphy with Technetium 99: not in emergencies but in elections, and is mainly used in
sine haemorrhages.
Approach to the patient with digestive haemorrhage
Take a blood sample for Hb, Hct, platelets, PT and aPTT (coagulation values are crucial, especially in
those with underlying coagulation disorders, which worsen bleeding)
The first thing to do is to assess the severity of the bleeding (based on the Hb value in g/dl and the
clinical picture of the patient). We distinguish:
1) Massive haemorrhage: these are patients who go into haemorrhagic shock, arterial hypotension
even in the supine position, with loss of 20-25% of circulating blood volume.
2) Moderate haemorrhage: patient with orthostatic arterial hypotension and loss of 15-20% of
circulating blood volume.
3) Mild haemorrhage: insignificant, in which there is a change in some vital parameters and loss
of 15% of circulating blood volume.
It is then assessed whether the blood loss occurs at :
- Low flow: where haemodynamic stability can be maintained.
- High flow rate: where maintaining haemodynamic stability is impossible.
Other indices to consider are:
- Age > 60 years
- Presence of concomitant diseases (lung, heart, liver, kidney);
- Presence of vital signs on admission (blood pressure < 100 mmHg; heart rate > 100 bpm)
- Colour of stools (indicating the extent of bleeding)
- Need for transfusions (> 3 units to achieve haemodynamic stability or to maintain stable Hb
over 24h).
When the patient has Hb values < 9g/dl, the patient should be approached with:
- Peripheral or large-calibre venous access in the neck vessels in the severe patient (by the
anaesthetist).
- Vesical catheterisation
- Dual-pathway SNG placement; the dual-pathway SNG is then used, so that a continuous
washing of the stomach with pre-chilled saline can be performed, in order to locally block
the bleeding; if blockage occurs, the blood that flows back onto the bag placed on the floor
becomes 'pink'; if, on the contrary, there is no local blockage, the blood that flows back is
bright red.
- Monitoring of HR, PAO and SO2
Haemodynamic support should be ensured depending on the severity of the bleeding (remembering
that until cross-testing has been done, and the blood group is known, always transfuse zero negative).
The ESGE 2019 guidelines say that after the initial assessment of the patient and his haemodynamic
status, stabilisation should be followed immediately, with restoration of intravascular volume.
We intervene first by compensating for blood loss with plasma expanders (crystalloids) until blood is
available and the infusion of high volumes of fluid (>1500 ml/day), and finally concentrated
haemopods (>4 units/day - in the case of blood loss with Hct <25% with ongoing bleeding or Hb
< 8g/dl), and meanwhile the blood count is continuously assessed. The aim is to restore an Hb between
7-9 g/dl.
Correction of coagulopathies by fresh frozen plasma and platelet concentrates. In the case of very low
platelets and a long time for platelet concentrates to arrive, it is better to perform up to 6-7 bags of
plasma.
Treatment of high digestive bleeding
In patients with acute upper digestive tract haemorrhage awaiting endoscopy, in addition to
rebalancing haemodynamic conditions with adequate fluid and, if necessary, blood infusions, a bolus
bolus of 80 mg PPI should be administered as an e.v. infusion, followed by continuous infusion (first
80 mg and then 8mg/h for 72 h after endoscopy), but PPI administration should not delay the
performance of endoscopy. The 2019 ESGE guidelines do not recommend aspirative SNG placement
or to perform a lavage.
Then in pts with ongoing severe or active high gastro-intestinal bleeding, 250 mg erythromycin i.v. is
administered 30 to 120 minutes before endoscopy in a single dose. Indeed, such administration of
erythromycin prior to endoscopy appears:
- Significantly improves vision
-
Reduces the need for a second endoscopy
Reduces the number of blood units to be transfused
Reduces length of hospital stay
Once haemodynamic balance is achieved, an upper tract endoscopy is performed:
1) Very early (>12 h)
a) In patients with high-risk clinical features, i.e. with haemodynamic instability that persists
despite attempts at volumetric rebalancing
b) Hematemesis
c) Presence of blood in the SNG
d) In cases where discontinuation of anticoagulant therapy is contraindicated
2) Early (< 24h)
3) Delayed (>24h)
Medical therapy consists of administering subcutaneous octreotide or somatostatin to reduce
splanchnic flow.
Oesophageal varices
Medical therapy:
- Parenteral administration of vasopressin
The gold standard diagnostic and therapeutic method is endoscopy:
- Adrenalin injection
- Sclerotherapy with polidocanol or sodium tetradecyl sulphate
- Mechanical therapy with ligation of bleeding varices (using haemoclips, i.e. metal clips to
reduce or avoid the bleeding event)
-
-
Tissue adhesives such as cyanoacrylate
Heat therapy with APC (argon plasma coagulation) or diathermocoagulation with monopolar
or bipolar
Radiological therapy: selective embolisation with Gianturco helix placement
Sengstaken-Blakemore probe: as a last resort, useful for tamponading oesophageal varices,
consisting of a balloon that inflates, and allows compression of the varices and prevents the
emission of blood to tamponade massive haemorrhages. It has momentary efficacy, because
after 72 hours they must be deflated and during their decompression they can often carry the
scabs that had formed on the wall to which they were tightly attached.
Surgical therapy: is performed for: failure of medical and/or endoscopic therapy, haemorrhagic
recurrence, after endoscopic therapy (after two endoscopic attempts), massive haemorrhages
that cannot be controlled
Peptic ulcer
After diagnostic and therapeutic gastroscopy, intravenous PPIs should be started. Peptic ulcer is
classified using the Forrest classification:
- FIa: active pulsating bleeding of a pervious vessel, especially if arterial (e.g.
from the bottom of the ulcer)
- FIb: active nappus bleeding (blood comes out continuously, like a veil)
- FIIa: no bleeding in progress, there is a visible vessel at the bottom of the ulcer, but not
bleeding.
- FIIb: a platelet clot is seen attached to the bottom of the ulcer
- FIIc: patch of haematin (black) at the bottom of the ulcer
- FIII: lesion without signs of recent bleeding or with the ulcer floor covered by fibrin.
In case of:
4) FIa-Ib and IIa: endoscopic haemostasis is performed (these are lesions with a risk of
persistent bleeding or rebleeding), which is done by placing two clips one upstream and one
downstream of the vessel, to which is associated the injection of adrenaline, or also thermal or
mechanical therapy or sclerosing injection.
5) FIIb: Consideration should be given to either removing the clot or adopting the endoscopic
treatment best suited to the picture revealed. Perhaps remove the clot and then see what to do.
6) FIIc and III: Endoscopic haemostasis is not recommended, as the risk of re-bleeding is low.
Infiltration with adrenaline is also useless. Oral therapy with PPI, once a day, is opted for.
Therefore, the therapy of first choice is endoscopy:
- Injection therapy with adrenaline diluted 1:10,000 or 1:20,000;
- Sclerotherapy with injection of adrenaline and polidocanol; or polidocanol only; or ethanol; or
sodium tetradecyl sulphate
-
Mechanical therapy with metal clips and elastic lagatures
Thermal therapy with thermal probes allowing monopolar or bipolar electrocoagulation
Yag laser therapy
The ESGE guidelines do not provide for routine endoscopy once haemostasis has been achieved.
● In case of bleeding, after initial success, endoscopy is recommended for a second haemostasis.
● If the second treatment fails, the patient is started on an alternative treatment, either surgical or
angiographic embolisation.
As a last resort following the failure of two endoscopic interventions, surgical therapy is considered,
and thus gastroresection. In those cases where it is necessary, the age of the patient is strongly
considered for the surgical approach.
- If the patient is elderly, 80 years of age, with co-morbidities such as CKD, chronic
bronchopathy, previous IMA, after two unsuccessful endoscopic attempts, the decision will be
made to do a vessel raffia, or in the case of a perforated peptic ulcer, an ulcer raffia will be
done.
- If the patient is young or an adult and has no comorbidities, a gastroresection via gastrodyjunostomy and an isolated Roux loop at the base of the gastro-dyjunostomy, plus an enteroentero-stomy of the loop to avoid alkaline reflux, is performed.
If it is not a peptic ulcer, but erosive oesophagitis, gastritis, duodenitis, high-dose PPIs are used.
Endoscopic haemostasis is not necessary.
Treatment of low digestive bleeding
Medical therapy consists of the administration of octeotride or somatostatin, which reduces splanchnic
flow.
Endoscopic therapy: it is not recommended, as in high digestive haemorrhages, in emergencies, unless
it serves to unwind a volvulus.
Diverticular disease
We proceed with colic resection at the level of the sigma (surgical therapy of choice) and then proceed
with immediate intestinal recanalisation, which is generally contraindicated in acute pictures where
inflammation is present (in fact, nowadays there is less of a tax on not recanalising the patient in the
acute phase, whereas previously it was dogmatic).
In the past, in the case of acute diverticulitis with peritonitis, whether circumscribed or generalised,
resections of the sigma in the tract with the perforated diverticula and a temporary colostomy were
imposed, which was removed after three months, and then recanalisation was performed.
Angiodysplasias
Open segmental resection is performed. In election by video-laroscopic route
Haemorrhages with unidentified site
Subtotal colectomy is performed: the endoscopist locates the site of the haemorrhage by performing an
intraoperative endoscopy. If the site is not found, subtotal/total colectomy is performed and a
protective ileostomy is performed.
RENE
URETERAL STITCHES
●
●
●
●
Upper: intersection of transverse umbilical line and outer margin of the rectus m.
Middle: intersection of the bis-iliac line and the raised vertical at the side of the pubis
Bazy's Soprapubic
Inferior: is detected by rectal and/or vaginal exploration by pressing on the ureter's outlet point
in the bladder.
HYPERTENSION NEPHROVASCULAR
Nephrovascular disease is one of the most frequent causes of curable hypertension but is responsible
for < 2% of all cases of hypertension. Stenosis or occlusion of a main renal artery, an accessory renal
artery or one of their branches can cause hypertension by stimulating the release of renin from the
iuxtaglomerular cells of the affected kidney. A reduction in arterial lumen of ≥ 70% is required and a
significant poststenotic gradient must also be present before the stenosis can contribute to elevated
blood pressure. Overall, approximately 80% of cases are caused by atherosclerosis and 20% by
fibromuscular dysplasia.
It is usually asymptomatic except in long-standing cases. Auscultation of a murmur in one or both
arteries is possible in <50% of patients. Diagnosis is made by objective examination and duplex
echodoppler, scintigraphy or MR angiography. Angiography is performed prior to definitive treatment,
either surgically or by angioplasty.
THROMBOSIS OF THE VEIN RENAL
Renal venous thrombosis is the thrombotic occlusion of one or both major renal veins leading to acute
kidney injury or chronic kidney disease. Frequent causes include nephrotic syndrome, primary
hypercoagulability defects, renal malignancies, extrinsic compression, trauma and, rarely,
inflammatory bowel disease.
Symptoms of renal failure may be present, and sometimes nausea, vomiting, flank pain, macroscopic
haematuria, reduced diuresis or systemic manifestations of venous thromboembolism.
CT, MR angiography or renal venography are used for diagnosis. With treatment, the prognosis is
generally good. Therapy involves anticoagulants, support of renal function, and treatment of the
underlying pathology. Some patients benefit from thrombectomy or nephrectomy.
INSUFFICIENCY RENAL
Kidney failure is the inability of the kidneys to adequately filter metabolic waste products from the
blood. Kidney failure is linked to several causes. Some lead to a rapid decline in kidney function (
acute kidney injury, also called acute renal failure). Others lead to a gradual decline in kidney function
(chronic kidney disease, also called chronic renal failure).
In addition to being unable to filter metabolic wastes from the blood (such as creatinine and urea
nitrogen), the kidneys have a reduced ability to control the amount and distribution of body fluids (
water balance) and the levels of electrolytes (sodium, potassium, calcium, phosphates) and acid in the
blood. If renal failure continues, blood pressure increases. The kidneys lose the ability to produce
sufficient quantities of a hormone (erythropoietin), which stimulates the formation of new red blood
cells, leading to a reduction in their number (anaemia). The kidneys also lose the ability to produce
sufficient calcitriol (the active form of vitamin D), which is vital for healthy bones. In children, kidney
failure affects bone development. In both children and adults, kidney failure can cause weakening and
disruption of bones.
Although decreased kidney function can affect people of all ages, both acute and chronic kidney
failure are more common in the elderly than in the young. Many of the disorders that cause kidney
failure can be cured by restoring kidney function. With the advent of dialysis and kidney
transplantation, kidney failure has become a manageable condition that is no longer fatal.
DIALYSIS
Dialysis is an artificial process of removing waste and excess fluid from the body, necessary when the
kidneys are not functioning properly. There are two types of dialysis:
● Haemodialysis: In haemodialysis, blood is removed from the body and pumped by a device
outside the body into a dialyzer (artificial kidney). The dialyser filters metabolic waste from
the blood and then reintroduces the purified blood back into the subject's body. Haemodialysis
requires repeated access to the blood stream. Although the doctor can create temporary access
by inserting a large intravenous catheter into a large vein, an artificial connection between an
artery and a vein (an arteriovenous fistula) is usually created surgically to simplify long-term
access. During this procedure, generally the radial artery of the forearm is joined to the
cephalic vein. The cephalic vein subsequently widens and its blood flow increases, making the
vein suitable for repeated sampling.
● Peritoneal dialysis: The peritoneum is a membrane that lines the abdominal cavity and covers
the organs it contains. In peritoneal dialysis, this membrane acts as a filter. This membrane has
a large surface area and a rich network of blood vessels. Substances can easily pass from the
blood into the abdominal (peritoneal) cavity through the peritoneum. A liquid (dialysate) is
infused into the abdominal cavity up to the space
peritoneal via a catheter. The dialysate must be left in the abdomen long enough for the waste
to slowly pass from the blood into it. Afterwards, the dialysate is drained, discarded and
replaced with fresh dialysate. The use of a soft silicone tube or a porous polyurethane catheter
allows the dialysate to drain safely and is not harmful. The catheter can be placed temporarily
next to the patient's bed or permanently, by surgery. A permanent catheter of a certain type
adheres to the skin over time and can be closed when not in use.
When evaluating the type of dialysis to be performed, several factors must be taken into account,
including lifestyle.
● Haemodialysis is recommended for persons who have suffered recent abdominal trauma or
undergone abdominal surgery or who have abdominal wall defects that would make peritoneal
dialysis difficult.
● Peritoneal dialysis is better tolerated than haemodialysis by individuals whose blood pressure
varies frequently, oscillating between periods of high or normal pressure and periods of low
pressure.
EMATURIA
Haematuria is the presence of blood in the urine, and it is an important sign: it should always be
investigated as to the cause and origin of the bleeding, because in 30-40% of cases it may have a
cancerous cause (always better to do one more test than less). Very often the patient underestimates
it, thinking that it is diet-related (in fact, asymptomatic cases (20%) are more likely to be cancerous,
while the presence of painful or irritative symptoms suggests cystitis).
● Microhaematuria: Invisible to the naked eye, it is defined by the presence of >3/5 haematomas
per microscopic field at 40X magnification. It is often a casual finding in routine examinations, but
should be investigated. Lower values (1-2 GR per field) may give an indication to repeat the
examination. 5% of healthy subjects have >1 GR per field.
● Macrohaematuria: 1 ml of blood in 1 L of urine is visible to the naked eye, as it changes the
colour of the urine, turning it red or brown ('old' blood or blood of kidney origin).
Origin and aetiology of haematuria
Medical causes: haematuria is a symptom of a general morbid condition.
Surgical causes: haematuria is due to an intrinsic cause in the urinary system.
Virtually any pathology of the urinary tract can produce haematuria. The origin may be: bladder
(40%) - prostate (24%) - kidney (15%) - ureter (7%) - urethra (5%). The age of onset may be
suggestive of the underlying cause (e.g. elderly neoplastic).
● Upper or lower urinary tract infection (37%): in women, the most frequent cause is
haemorrhagic cystitis, suggested by irritative/painful symptoms and history (e.g. onset after
coitus).
● Urinary tract tumours (22%): urothelial tumours (more frequent in elderly and smoking males)
and renal tumours (including Wilms' tumour in children). Symptom of onset in 85% of bladder
tumours and 40% of kidney tumours.
● Cervico-prostatic obstruction (13%): for prostatic hypertrophy or prostatic carcinoma.
● Calculosis (10%): prevalent cause in young adults, suggested by typical pain.
● Trauma (1%)
● Congenital malformations: to be suspected in the newborn.
● Glomerulonephritis: e.g. in a child with a history of pharyngitis (!). In paediatric age, haematuria
is more frequently of nephrological origin.
● Tubulopathies and nephritis
● Vascular pathology
● Fever and dehydration (especially in infants)
● Hypersensitivity to NSAIDs
● Benign recurrent idiopathic haematuria: rare, diagnosed when all tests are negative.
● Alport syndrome: paediatric nephropathy associated with deafness.
● Orthostatic haematuria or from physical stress: e.g. from running.
● Hypertension: 20% of poorly controlled hypertensives have microhaematuria.
The distribution of the aetiology is different in the two sexes:
● In men, the most frequent causes of haematuria are bladder carcinoma (30%), prostate
adenoma or benign prostatic hypertrophy (20%) and urinary stones (10%);
● In women, urinary calculosis (30%, almost always microhaematuria), bladder carcinoma
(20%), cystitis (15%) and cystocystocele (5%).
Differential diagnosis History
● Family history (hereditary nephropathies, uratic calculosis), personal physiological (age, sex,
work, menstrual cycle), remote and forthcoming pathological (duration of haematuria, frequency,
intensity, related symptoms).
● Risk factors for bladder cancer: mainly older age and smoking. In addition, occupational
exposure to aromatic amines (e.g. industrial workers, greenhouse w o r k e r s , workers in contact
with rubber, textiles and paints), family history, exposure to cyclophosphamide or pelvic
radiotherapy and, in developing countries, infestation with Schistosoma haeumatobium (bladder
bilharzia).
● Cystic symptomatology: e.g. stranguria and pollakiuria suggest cystitis.
● Haematuria with clots: may indicate either haemorrhagic cystitis or urothelial cancer.
● Renal colic: the patient probably has a kidney stone, or has passed it out with urine.
● Absence of symptoms: a silent clinic must lead one to suspect a carcinoma (e.g. bladder ca. in
situ).
● Feverish illnesses - hypertension - sporting activity
● Antiplatelet and anticoagulant drugs: anticoagulants do not cause bleeding per se (!), but can
activate bleeding of a previously silent nephro-urological lesion (e.g. K).
Laboratory examinations
Guyon's three-glass test: historical test, in disuse.
● Initial bleeding: urethral origin.
● Terminal bleeding: bladder origin
● Uniform bleeding in the three glasses: renal origin (but any bleeding, if abundant enough, can
produce uniform total bleeding).
Urine examination
● Leukocyturia with bacteria: indicates low (cystitis) or high (pyelonephritis) infection. On
chemical examination, leucocyte esterase and nitrite can be detected in the presence of ureaseproducing bacteria.
● Sterile leukocyturia: may be TB (Zihel Nihelsen) - necrotic carcinoma - calcinosis.
● Dysmorphic haematomas and proteinuria: probable glomerulopathy.
● Erythrocyte cylinders: pathognomonic of glomerulonephritis.
● Wax cylinders: suggestive of nephropathy.
Urinoculture or cytological examination of urine, depending on clinical suspicion.
Instrumental examinations
● Ultrasound of the urinary tract (1st level)
● abdominal CT scan with mdc (uro-CT - 2nd level): studies the entire urinary system, displays
any maps and allows the study of renal uptake (e.g. uptake masses may be tumours, non-capture
masses benign cysts) and the reconstruction of the lumen of the renal pelvis, ureter and urinary
bladder (but not the urethra).
● Cystoscopy (3rd level): is performed indicated on the basis of the CT findings, to study what has
been observed or in cases where the CT scan is negative (e.g. ca. in situ). If one already has the
diagnosis on the CT scan one does not perform it (in a diagnostic sense); e.g. if a clear bladder
carcinoma is observed on the CT scan there is no point in wasting time with cystoscopy, one does
surgery directly (cystoscopy resection).
Conditions to be distinguished from haematuria
Other types of urethral bleeding
● Haemospermia: the presence of blood in the semen is of much greater concern to the patient, but
is almost always benign (sign of prostatic inflammation or seminal vesicles).
● Urethrorrhage: emission of blood from the urethra independently of urination, due to trauma (e.g.
catheterisation, endoscopy) or infection. It can be confused with haematuria because urination
clearly results in the expulsion of blood accumulated in the urethra.
Pseudohaematuria: other causes of red or dark urine (haematuria must always be confirmed under
microscopy)
● Bilirubinuria: direct bilirubin, e.g. during haemolysis, produces marsala-coloured urine.
It is suspected for the association of jaundice (e.g. yellowish conjunctiva).
● Haemoglobinuria: in cases of intravascular haemolysis, e.g. in haemolytic crises in favism.
● Myoglobinuria: e.g. in a crash syndrome (crush muscle injury).
● Drugs: e.g. rifampicin makes the urine red/orange (drug history).
● Food: substances found in beets and blackberries can colour urine.
● Black urine: from methaemoglobinuria or aminoaciduria (due to presence of homogentistinic a.).
If the cause is not found, risk factors are considered and the patient is kept under observation for three
years, examined and a urine test and ultrasound performed every six months; if haematuria persists
after one year, the diagnostic procedure is repeated from the beginning. In 5-10% of patients, the cause
of haematuria remains unknown.
Pneumaturia
Air escapes from the urethral canal during urination, typically a consequence of bladder fistulas related
to locally advanced neoplastic disease, Crohn's disease, diverticular disease or, more rarely, urinary
tract infections associated with gas production.
RENAL CARCINOMA
Heidelberg Classification
Renal neoplasms are subdivided:
1)
2)
-
Benigni:
Papillary adenoma
Metaphrenic adenoma
Oncocytoma
Malignant:
Clear cell carcinomas
Papillary carcinoma
Chromophobe cell carcinoma
Carcinomas of the collector ducts
-
Unclassified
Renal carcinoma includes all carcinomas originating from the nephrons or collector ducts, which
account for 85% of the total. It constitutes 2-3% of malignant tumours in general, with peak incidence
at around 60 years of age. 4K/y. The incidence has increased in recent years, probably due to the
increase in imaging techniques (geographically more present in areas of higher development). It is
more frequent in males and in the West.
Risk factors
●
●
●
●
●
●
Smoke
Obesity
Hypertension
Familiarity
IRC.
Von Hippel-Lindau syndrome (5-8%): hereditary form linked to the transmission of a
mutated VHL gene (oncosuppressor localised on cr. 8q) with an incidence of 1/36k births. It
causes the onset of bilateral (clear cell) renal tumours in young patients (on average at 26
years of age - they cause 40% of deaths), associated with retinal angiomas - CNS
hemangioblastomas - pheochromocytomas - cysts. VHL: encodes for a protein that causes
HIF degradation in the presence of oxygen. VHL+ tumours (which also include most sporadic
renal tumours) are therefore characterised by marked angiogenesis, and are treated with
angiogenesis inhibitors.
While controversial FDRs are:
- Analgesics
- Diuretics
- Asbestos
- Ionising radiation
- Diet rich in fruit and vegetables, probably because foods rich in minerals can overload the
kidney (much debated).
It is characterised by slow but silent growth (it has enough room to grow without giving compression
symptoms), so it is metastatic in 25% of cases at diagnosis.
Histogene
sis
but renal papillary and clear cell
carcinoma (60%). (5-10%).
∙
∙
● Intercalar cells of the collecting duct originate chromophobe tumours (5-10%),
● Collector duct carcinoma main cells.
Pathological anatomy
It appears as a yellowish-white spherical mass without a capsule (it rather has a pseudocapsule that
isolates it from the surrounding parenchyma), inhomogeneous, with areas of haemorrhage and
necrosis. The growth, which may occur outwards or towards the hilum and pelvis, progressively
compresses the healthy renal parenchyma and results in its atrophy and fibrous replacement.
Mainz histological classification
● Clear cell ca. (80%): originates from the epithelium of the proximal tubules, and has a severe
prognosis (!). It most often localises at one pole of the kidney (upper or lower) and reaches a large
size. It is characterised by thysurismosis (lipids and glycogen), which dissolve during cell
processing and give the clear colour on microscopy (!). The cytoplasm remains distinct, and the
nuclei are central and round (target-like). Associated with VHL mutation, it is characterised by a
rich vascular network (supported by VEGF production) and thus diffuse microhaemorrhages. It
can be distinguished from clear cell ca. of other organs by the expression of the CD20 marker.
● Papillary Ca. (6-15%): originates from the epithelium of the proximal tubules and is often
multifocal/bilateral. Macroscopically it forms sessile polyps (also inside renal cysts), which are
never present in clear cell carcinomas, and papillae with connective-vascular axes rich in
histiocytes. The most typical mutations are MET and trisomies 7, 16 and 17. It expresses CK7.
● Chromophobe Ca. (2-5%): originates in the collecting ducts and has a good prognosis.
Macroscopically it is fleshy and dark due to the presence of secretory vesicles containing iron,
which can be observed under microscopy with Perls staining. The cell membranes are well
defined and the central nuclei with clear perinuclear halos.
● Carcinoma of the collecting ducts (Bellini's tumour - 1%): rare, it originates in the renal
papillae from the main cells of the epithelium of the distal collecting ducts and has the worst
prognosis of all histotypes (due to infiltrating and very rapid growth compared to classical renal
tumours). It is also most often symptomatic. Morphologically it is solid and yellowish due to
necrosis (due to rapid growth compared to angiogenesis). It infiltrates the tubules, contains mucin
and a conspicuous inflammatory infiltrate and is characterised by a major desmoplastic reaction.
The distal portion of the tumour, beyond the papillae, no longer has a renal epithelium but a
transitional one, hence some classify it among the urothelial ca. More differentiated forms may
have tubular organoid structures or pseudoglands.
Prognosis (from best to worst): chromophobe > papillary > clear cell > collecting ducts cell.
Clinical presentation
It is asymptomatic until advanced stages, and is often an incidental finding on ultrasound or CT
scan (50%, incidentaloma).
● Macrohaematuria (80%)- lumbar gravative pain (45%)- palpable mass (30%): classic triad of
advanced stages (!, 5-10%).
● Bilateral oedema of the lower limbs and varicocele: due to compression of the vena cava or
invasion of the vena cava (a sudden right varicocele not reduced by clinostatism is typical in this
case).
● Fever, weight loss
● Endocrine and non-endocrine paraneoplastic syndromes also occur in 30% of cases. Normally
the paraneoplastic symptoms disappear with nephrectomy; if this does not occur, the disease is
probably already metastatic.
o Anaemia/polyaemia: due to EPO deficiency (anaemia), or more rarely EPO production.
o Non-metastatic liver dysfunction (Stauffer's s.): possibly due to production of
hepatotoxins. Hepatomegaly should be sought and alkaline phosphatase measured.
o ACTH production (s. Cushing's) - PRL (gynaecomastia-galactorrhoea) - insulin
(hypoglycaemia) - gonadotropins (gynaecomastia, hirsutism, amenorrhoea, reduced libido)
o Hypercalcaemia - hypertension - amyloidosis - neuro-myopathy - vasculopathy - coagulopathy
- impaired glucose metabolism - nephropathy.
Remote dissemination
● Marked veno-tropism (the tumour itself propagates): renal vein - cava - right atrium.
● By haematogenous route (70-80%): lung, liver, bone, CNS, contralateral kidney, skin.
● Lymphatic route (20-25%), lymph nodes: hilar, pre/paracaval, interorthocaval (right),
retroaortic
(left).
When it invades the Gerota capsule, the tumour can then invade neighbouring organs.
On the right: the kidney relates to the liver, mainly through its upper pole, while the lower pole relates
to the ascending colon; medially at the hilar level, it relates to the duodenum (in fact, to isolate the
right renal hilum, the Kocher manoeuvre is required, which involves mobilising the duodenum and the
head of the pancreas to access the right kidney).
On the left: the vascular pedicle is much longer, because the space between the hilum and the vena
cava is greater, but the arterial pedicle is stockier, whereas the venous pedicle is longer (in contrast to
the right). It has relations with the body-tail of the pancreas the upper pole; the lower pole with the
transverse/descending colon; posteriorly with the diaphragm and the ileo-psoas.
Diagnosis and staging
● Ultrasound: first level (renal masses are often found in ultrasound scans performed for other
reasons e.g. gallstones).
● CT abdomen (with and without mdc): second-level examination, confirms the diagnosis (!).
● Abdominopelvic CT scan: for staging (bone scans are not routinely indicated).
● In selected cases, MRI or CT angiography is performed to search for neoplastic venous thrombi.
● Angiography: pre-operative evaluation in conservative surgery in the presence of malformations
or ectopias. It can be useful for diagnostic purposes and to get an idea of the anatomical
distribution
of the renal hilum. There are, in fact, anatomical variables, mainly affecting the arteries: double or
triple, arising from a single vessel, and thus making surgical management difficult.
TNM and Robson staging
● Stage 1: tumour confined to the kidney and <4cm (T1a) or >4cm <7cm (T1b). 5-year survival of
96% after surgery.
● Stage 2: tumour confined to the kidney but >7 cm (T2) or invades the capsule. S: 82%.
● Stage 3: infiltration of the renal vein (T3a) or subdiaphragmatic (T3b) or supradiaphragmatic
(T3b) vena cava - invasion of peri-renal adipose tissue (T3) - invasion of a single lymph node
(N1). S: 64%.
● Stage 4: infiltration beyond the Gerota capsule, including e.g. the homo-lateral adrenal (T4) invasion of more than one lymph node (lumbar aortic) (N2) - metastasis in distant organs (M1). S:
23%.
1 and 2: Tumour localised within the renal adipose capsule
3: Extra-capsular tumour confined to the Gerota's fascia (it is a natural barrier, fat pad).
Treatment
● Stage T1 (<7 cm): conservative surgery (partial nephrectomy) NSS (nephrone sparing surgery):
treatment of choice, only one pole (upper or lower) is resected. It is performed much more
frequently due to increased incidental diagnostic findings (abdominal diagnostics are much more
common than in the past). Indications of need: monorenal insufficiency pts
- bilateral or elective forms: dm < 4 cm (7cm) - single lesion
● Localised disease (>7 cm): classic surgery (radical nephrectomy), without adjuvant CT (!).
Radical nephrectomy is reserved for cases where the tumour is of considerable size or w h e r e i t
reaches deep into the excretory system or is in an ileal position. Perhaps in the future Sunitinib
(VEGFR and PDGFR inhibitor) + aorto-caval lymphadenectomy: only in patients with evidence
of N+ on instrumental examinations + adrenalectomy: only with clear adrenal involvement (T4)
Focus: nephrectomy
Nephrectomy can be done open, laparoscopically (the trocar enters from the flank not the umbilicus)
or even by robotic technique. Radical nephrectomy is contraindicated in the case of bilateral tumours
(e.g. s. VHL) or in single-kidney patients, because it would force a diagnosis.
Clean surgery must be performed, without any bleeding sources, which would make the surgical field
dirty, especially in laparoscopic surgery. Moreover, it ensures oncological radicality, in fact if the
surgeon succeeds in dominating the blood flow in the context of the neoplasm, he can avoid the
possible escape of cells that can then give distant metastases.
Considering the anatomical arrangement of the kidney: the first structure the surgeon encounters when
exploring the renal region is the renal vein, which is isolated and not ligated, then he looks for the
artery, which is in a site rich in fat, and then ligates the vein. In fact, if the vein were ligated first
(which is anterior at the level of the hilum, as opposed to the artery, which is posterior), the
parenchyma would become engorged with blood (congestion of the parenchyma), because the inflow
continues but there is no outflow. The second step is to dissect the vessels. The kidney thus remains in
the context of the peri-renal fat between the visceral peritoneum and fascia of the Gerota.
The amputation phase continues with the isolation of the adrenal capsule, which is amputated for
reasons of oncological radicality, when it is affected.
Removal of: kidney - adrenal - ureter up to the iliac vessels - perirenal fat and Gerota's fascia +
cavotomy
+The thrombus present in the vena cava can be removed, in fact one clamps the vena cava above and
below the renal vein, plus the contralateral renal vein outlet. The cava is incised, the thrombus is
removed, clamped, and everything is declamped.
● Unresectable disease: systemic anti-VEGFR therapy (sunitinib- pazonapib- cabozantiniblevantinib - atixinib) and immunotherapy with nivolumab (anti-PD1) and ipilimumab (antiCTLA4) + INF-a - IL-2 (activates LAK cells) - activated LAK cells. Anti-VEGF is preferred in
low-risk patients and immunotherapy in high-risk ones. The timing of starting medical therapy
depends on the clinical picture and performance status.
Radiotherapy and traditional CT give poor results and are in disuse.
Follow-up: abdominal ultrasound - CT scan of chest and abdomen.
ONCOCITHOMA
It originates from the epithelial cells of the distal tubules. It is benign, although 'notes' of malignancy
have been shown in some cases. In 94% of cases it is unilateral, the remaining 6% bilateral.
In most cases the finding is incidental, usually asymptomatic, and unlikely to give symptoms such as
haematuria, flank pain, palpable mass.
Macroscopically, it has a wagon wheel appearance. The diagnosis, which is often incidental, is made
by ETG.
Total nephrectomy is rarely used.
ANGIOMYOLIPOMA
It is a benign tumour, consisting of adipose tissue and abnormal vessels. It is unilateral in the vast
majority of cases and is usually associated with tuberous sclerosis.
It is usually asymptomatic, and only in 10% of cases may result in retroperitoneal haemorrhage.
The diagnosis is made on ultrasound, which is seen as a hyperechogenic lesion. On CT scan it is seen
as a hypodense lesion, while on arteriography it appears as a very vascularised mass.
Therapy includes:
- Follow-up if the diameter is less than 4 cm (asymptomatic)
- Conservative surgery
SURRENE
ADRENAL NEOFORMATIONS
The adrenal gland is an endocrine gland, which has a cortical and a medullary portion, and secretes
hormones. Altered secretory function leads to clinical syndromes, and therefore a multidisciplinary
approach is required, with endocrinologists, pathophysiologists, surgeons and nutritionists working
together.
Anatomy
The adrenal gland is found within the Albarran-Chatelin quadrilateral: a niche that includes the kidney
and adrenal gland, both right and left, and is bordered by:
- Front sheet: Gerota band
- Back sheet: Zuclerkandl's band
Between these two is adipose tissue. The adrenal gland is easily identified, as it is located next to the
inferior vena cava.
Right: Chatelin's quadrilateral:
- Medially: inferior vena cava
- Laterally and Posteriorly: psoas muscle
- Upper: diaphragm and right hepatic lobe
- Inferiorly: right renal vein and right renal artery (originating from the aorta)
Left: Chatelin's quadrilateral is less identifiable, in fact the anatomical findings are not well defined:
- Medially: aorta
-
Laterally and posteriorly: psoas muscle
Upper: diaphragm
Inferiorly: upper margin of the kidney
For vascular connections, these are few and their knowledge is crucial for a possible adrenalectomy
(on the right they are not always recognisable).
The arterial side:
- Superior adrenal artery (branch of the diaphragmatic aorta)
- Middle adrenal artery (from the aorta and bypasses the inferior vena cava)
- Inferior adrenal artery (from renal artery)
The venous side:
- Middle adrenal vein (flows into inferior vena cava)
- Superior adrenal vein (flows into the diaphragmatic vein and then into the inferior vena cava)
PHEOCHROMOCYTOMA
Benign neoplasm of the adrenal medullary, secreting catecholamines. Named after the chromaffin cells
of the adrenal medullary. It manifests itself with crises of systolic hypertension interspersed with
normal inter-critical periods. Its incidence in the hypertensive population is <0.1%.
In about 20% of cases, pheochromocytoma is associated with familial syndromes:
● MEN 2A: medullary thyroid carcinoma, pheochromocytoma, hyperparathyroidism.
● MEN 2B: medullary thyroid carcinoma, pheochromocytoma, mucous neurinomas, marfanoid
habitus, ganglioneuromatosis.
● von Recklinghausen disease (NF1): café au lait stains, pheochromocytoma, neurofibromatosis.
● von-Hippel-Lindau disease: retinal haemangioma, CNS haemangioblastoma, cysts and carcinoma
of the kidney, pheochromocytoma, pancreatic cysts, cystadenoma of the epididymis.
Paraganglioma: a neoplasm very similar to pheochromocytoma found in paraganglia.
Pathological anatomy
● Histology: extremely compressed and thinned cortical image (it has become almost a peripheral
portion) and expanded medullary with a very variegated, disordered and inhomogeneous
appearance. Pleomorphism and hyperchromasia are not necessarily indicative of malignancy
● Cytology: sustentacular cells, the 'zellballen', which are typical and quite recognisable large cells.
● Immunohistochemistry, done with chromogenic agent (di-amino-benzillin) which operates in
brown and indicates cells expressing chromogranin. Neuron-specific enolase Ag expressed in the
neuroectodermal lineage.
● Biochemical tests: Chromogranin A (blood marker, associated with other neuroendocrine
tumours, e.g.
carcinoids), vanillymandelic acid (catabolite of catecholamines, urine).
Cancer of the three 10%
● 10% metastasis/malignant (often lymphatic, also blood-borne□ liver, lung,
bone). It is the only criterion for malignancy (as with endocrine neo-endocrinology, the clinicaldiagnostic value of atypia is nil).
● 10% bilateral;
● 10% extra-adrenal.
Clinic
● Hypertension often associated with paroxysms, headache, sweating and palpitations.
● Adrenergic secretion: paroxysmal hypertensive crisis associated with anxiety, tremor, headache,
palpitations, cramp-like pain in the epigastrium, sweating, pallor and cyanosis of the face.
● Noradrenergic secretion: persistent PAH (more difficult differential diagnosis).
Laboratory diagnosis
Postulated by the detection of excessive or altered production of catecholamines and/or their
metabolites. The most commonly measured compounds are the catecholamines themselves
(norepinephrine and adrenaline), metanephrines (metanephrine and normetanephrine) and
vanillymandelic acid.
Surgical resection: resolving in most cases.
Preparation for surgery: In pre-operative pheochromocytomas that are secreted, therapy with
catecholamine antagonists is appropriate, the preparation takes 7 to 10 days, today more doxazosin is
used, which is an alpha1 selective; previously more phenoxybenzamide was used, which is an alpha1
and alpha2 blocker.
Indication of adrenalectomy for benign pathology
1)
2)
-
Secreting neoformations:
Cushing's syndrome (from cortisol-secreting adenoma)
Cushing's disease after failure of pituitary surgery therapy
Primitive hyperaldosteronism
Pheochromocytoma
Non-secreting neoformations: > 3.5 cm
Adenoma
Myelolipoma
Lipoma
Secreting neoformations
Cushing's Syndrome/Disease
They are characterised by hypercortisolism from different origins.
● Cushing's disease is hypersecretion of pituitary or ectopic ACTH, resulting in bilateral adrenal
hyperplasia;
● Cushing's syndrome there is the presence of secreting adrenal adenoma with suppression of
the hypothalamic-pituitary-adrenal axis.
● Iatrogenic form, due to the abuse of cortisone drugs.
The clinical picture is characterised by:
- Asthenia and muscle weakness
- Obesity of the face and neck (moon facies and buffalo hump)
- Central obesity with thin limbs due to muscle atrophy
- Hirsutism (in women)
-
Ruby streaks on abdomen, breasts and buttocks
Hyperglycaemia, up to frank diabetes
Osteoporosis
Behavioural alterations (assessing gaze)
Primitive hyperaldosteronism (Conn's disease)
It is due in most cases to an aldosterone-secreting corticoadrenal adenoma, usually single and
unilateral, but can sometimes occur bilaterally involving both adrenals. Dd with the secondary form
correlates with renin hypersecretion.
The clinical picture is characterised:
- Poorly controllable hypertension
- Asthenia and muscle weakness (from hypokalemia)
- Headache
- Paresthesias
- Muscle cramps
- Intermittent tetanic crises
Pheochromocytoma (see later)
Lesion of the adrenal medullary (90% of cases) or of extrasurrenal origin (extrasurrenal, pelvic,
mediastinal paraganglia). It is rare, and in 10% of cases it is bilateral and malignant (until proven
otherwise).
Symptoms are due to overproduction of adrenaline, noradrenaline, other vasoactive substances
(dopamine, VIP, endothelin, etc.). The clinical symptoms are characterised by:
- Paroxysmal hypertensive crises: due to the prevalence of adrenalin elevation, with systolic
peaks of even >300 mmHg, from a few minutes to a few hours, without apparent cause or
following stimuli of a different nature (urination, coughing, defecation).
- Permanent hypertension: prevalence of norepinephrine elevation. It does not differ from
essential hypertension, with which it can also initially be confused. However, common antihypertensive therapy is ineffective.
Non-secreting neoformations
Non-secreting neoformations are observed if they are >3.5 cm in size, and since they are nonsecreting, they are asymptomatic in most cases, and are often found occasionally, so they are
diagnosed during radiological examinations conducted for other reasons, hence the term
incidentalomas.
Their management includes:
- Hormone study, ruling out secreting
- X-ray study: assesses morphology, dimensions (dimensional criterion).
In fact, the surgical criterion becomes the size criterion, and a cut-off ranging from 3.5 -10 cm has
been developed for this. Whereas, no non-secreting lesion < 3.5 cm should be operated on. Above 10
cm, the approach is highly complex, and therefore the possibility of a laparoscopic and laparotomic
approach is analysed (in fact, as the size of the lesion increases, the technical difficulties increase).
Then, in addition to a dimensional criterion and the reference cut-off, there is also a discretionary
criterion to be considered, which depends on the surgeon: he must have the maturity to decide to
operate on masses above 10 cm, taking into account his capabilities.
Indications for adrenalectomy for malignant pathology:
1)
2)
-
Primary malignant tumours:
Corticosurrenal carcinoma (ACC)
Pheochromocytoma
Sarcomas
Solitary adrenal metastases:
Mammella
Lung
Rene
Melanoma
Guidelines:
1) According to the American Society for Gastrointestinal Endoscopy: laparoscopic treatment for
malignant lesions is always contraindicated for dimensions > 6 cm;
2) Per the European Society of Endocrine Surgeons: laparoscopic adrenlectomy can be considered
for ACC (stage I-II) for lesions up to 10 cm.
Adrenalectomy surgery for malignant pathology must take into account:
-
Cleavage plane (line, space, margin, given by the part removed and the anatomical part that is
to remain).
Excision of the mass en bloc, with an R0 resection, which involves removing not only the mass
but also the affected lymph nodes (lymphadenectomy). Thus, the absence of peritoneal
dissemination is guaranteed (an aspect in favour of laparoscopy, and to t h e disadvantage of
laparotomy, compared to the past, because the coarse manipulation given by the surgeon's
hands is lacking and is instead guaranteed by 5-10 mm instruments that tend not to
disseminate, because they have a greater grip).
Diagnosis
1) Clinical assessment of the pc (syndromic complexity of the pc): clinical manifestations are
different depending on the overproduced substance;
2) Hormonal/laboratory assessment (i.e. functional framing of the lesion):
3)
-
study of cortisol at 8 am and 6 pm;
ACTH study at 8 am and 6 pm;
free urinary cortisol in 24h;
plasma retinal activity in orthostatism;
assay of urinary metabolites of catecholamines.
Instrumental evaluation:
First step: Ultrasound
Second step: CT scan with and without mdc; it will provide fundamentally important
morphological information, whether the lesions are benign or malignant, whose presentation is
totally different. The dimensional criterion is taken into account, as well as the involvement of
neighbouring organs (either by continuity or contiguity) and the lymph node study.
Treatment
There has been a shift from open surgery (today reserved only for cases of large malignant lesions or
with involvement of neighbouring organs) to minimally invasive surgery, i.e. laparoscopy.
The laparoscopic approach was first pioneered by Gagner, who demonstrated reduced perioperative
morbidity and mortality, less post-operative pain, earlier resumption of feeding, shorter hospitalisation,
reduced occurrence of laparocele, and improved aesthetic outcome through this approach.
In traditional surgery, subcostal incision, from the xiphoid process to the iliac crest, or incision along
the linea alba: from the xiphoid to below the umbilicus (the linea alba is the preferred site for wide
laparotomic incisions made in major abdominal surgery)
Today, therefore, laparoscopic treatment becomes the gold standard for such pathology, and has
indications for both benign and malignant lesions, and f o r b o t h secreting and non-secreting
neoformations. As the size increases, so do the technical difficulties and thus the risks. However, up to
lesions of 10 cm, provided they are benign, laparoscopy could be used.
With laparoscopy, depending on the anatomical part to be treated, right or left adrenal, the position of
the patient on the operating table changes:
-
-
Right lateral transperitoneal approach: the patient is placed in left lateral decubitus with an
inclination of 70-80° to the operating table. The operating table is broken at the costal border at
an angle of 140°. Four trocars are inserted radially under the right costal arch: T1: optics, T2:
right hand operator, T3: left hand operator, T4: liver palpator;
Left lateral transperitoneal approach: the patient is placed in right lateral decubitus, with an
inclination of 70-80° to the operating table. The operating table is broken at the level of the
costal border at an angle of 140°. In this case the trocars are 3: T1: optics, T2: operator's right
hand, T3: operator's left hand. The surgeon then has a monitor in front of him so that he can see
what he is doing.
-
Retroperitoneoscopic posterior approach: the adrenal lodge is approached posteriorly through
the lumbar wall, without crossing the parietal peritoneum or the visceral peritoneum. The
patient is in the prone position with thighs flexed over the pelvis and legs flexed over the
thighs. A 1.5 cm incision is made under XII costa to create the working chamber. Advantages:
lower incidence of paralytic ileus in the post-operative period direct access to the adrenal
lodge; Disadvantages: reduced operating field
In the case of the right adrenal:
1) Posterior peritoneal leaflet opening
2) Lower coronary ligament opening of the right liver
3) Complete section of the right triangular suspensory ligament of the liver; this frees the adrenal
gland from its connections with the liver;
4) It descends down to the psoas muscle, which is located posteriorly in the Albarran- Chatelin
quadrilateral, until it identifies the middle adrenal vein, which flows directly from the adrenal
into the inferior vena cava;
5) The middle adrenal vein is isolated, it is closed between clips now made of polycarbonate
(previously of titanium);
6) The adrenal gland in its own adrenal lodge is cleared of connections to neighbouring organs:
psoas (post), inferior vena cava (med), right renal vein (inf), diaphragm (super), abdominal
wall muscles (lat)
7) It frees the adrenal gland
8) Fits inside a bag: endobag
9) The adrenal gland is pulled out of the umbilical scar.
In the case of the left adrenal gland:
1) Left colic flexure dislocation
2) Detachment of splenopancreatic block, move to the medial side; the spleen is seen and the
parietal peritoneum is interrupted from the visceral;
3) The tail of the pancreas is highlighted;
4) Diaphragm identification
5) Identification of the Albarran-Chatelin quadrilateral, but there are no clear margins as on the
right, there are fewer anatomical landmarks.
6) The mass to be removed is identified
7) You can see the superior adrenal vein flowing into the diaphragmatic
8) Liberation of the left triangular ligament
9) Identification of the oesophageal abutment
10) The superior adrenal vein is released with polycarbonate clips for a better seal.
11) Removal of the adrenal gland with the endobag (bag in which the adrenal gland is placed, to
prevent neoplastic dissemination)
12) Fibrin glue is placed to reposition the splenopancreatic block in its lodgement.
The disadvantages of laparoscopy are:
- Extensive mobilisation of neighbouring organs
- Possible injury to visceral organs (also in traditional surgery)
-
Technical difficulties due to previous open surgery: these give rise to physiological reparative
scar phenomena that lead to adhesions that can be understood and considered viscero-visceral
or viscero-parietal. Minimally invasive laparoscopy considerably reduces the formation of the
adhesion syndrome.
When approaching laparoscopic adrenalectomy is the possibility of using new technologies, namely:
- 3D: enabled by a particular optics, the quality of which depends on the quality of the lenses
inside, in which we have a standard system, i.e. cylindrical lenses, and two lens systems as if
they were two eyes, so that a three-dimensional image is reconstructed through a software
system on a screen that is viewed through specific 3D glasses, and the monitor will also be
particular. The distance between operator and screen will be between 2-2.5 m (optimal distance
for 3D viewing). Today we operate with the lights off, in order to achieve better brightness.
- Robotics
The advantages of 3D laparoscopy are several:
- Facilitates surgical training: ability to see in 3D and therefore better.
- Encourages fine and precise movements
- Allows visualisation of details
- In small cavities: such as the adrenal lodge, it allows better visualisation of structures and thus
a technical advantage.
A case-control study was performed, comparing 3D adrenalectomy with traditional 2D. It was seen
that although the time and complications of 3D are less than 2D, these data were not statistically
significant.
A meta-analysis on robotics shows reduced blood loss, and less hospitalisation than laparoscopic
adrenalectomy (but the latter is faster)
TRAUMATOLOGY
ABDOMINAL TRAUMA
Trauma is an external violent event that threatens the physical integrity of the subject, causing injury
and/or death.
It is ranked in:
- Major trauma: in the case of injuries capable of posing an immediate or potential risk to the
survival of the patient
- Polytrauma: in the case of injuries to two or more body districts (abdomen, chest, limbs), such
that vital functions are unstable and there is a potential immediate risk to survival.
Depending on the type of trauma:
- Road trauma
- Assault
- Precipitation
- Burn or electrocution
Based on the injury mechanism (i.e. the force that caused the event itself):
- Traction
- Compression: e.g. by seatbelt or airbag explosion, can lead to rib fractures; or burst rupture of a
hollow viscera, leading to intestinal perforation
- Deceleration and acceleration: lead to even fatal consequences, such as the avulsion of
parenchymatous organ stalks, such as the spleen or liver.
- Flexion or torsion
Traumas are divided into:
1) Closed or non-penetrating trauma: due to blow or kickback injury, when the patient has an
intact abdominal wall: e.g. road or work trauma
2) Open or penetrating trauma: where there is communication between the abdominal cavity and
the external environment, due to injuries from a white weapon or firearm.
Today, the approach to trauma has changed: from an aggressive attitude on the part of the medical
staff with early laparatomies, in an attempt to stabilise the patient or go straight to correcting any
lesions revealed by the pre-operative examinations; today there are protocols spread throughout the
world, we speak of NOM (non-operative management): which allows the patient to be well identified
and, based on his condition and clinical characteristics, to direct him towards the best therapeutic
pathway, with better survival.
ATLS (advanced trauma life support) protocol, the principles of which are the same as those of the
primary assessment of the patient:
-
Airways and column control
Breathing
Circulation
Disability
Exposure/enviromental
Therefore, respiratory and haemodynamic stabilisation is essential first, and after the patient has been
stabilised, a second assessment begins, in which a careful history and adequate EO will be taken.
The risk factors for intra-abdominal injuries:
1) Assess whether the patient is hypotensive and has a baseline deficit with haemogas with
bicarbonates < 21 mmol/L
2) Presence of macro-haematuria, evidenced by the placement of a bladder catheter
3) Note the presence of a haemothorax or pneumothorax; there is often an association between
thoracic and abdominal trauma.
4) Presence of haematomas and/or abrasive lesions of the abdominal wall, in closed abdominal
trauma, not having a penetrating wound, and secondary to a possible blow to the patient and
because the patient may have altered sensory perception, cannot provide us with information
on the site of pain
5) Presence of rib fractures
6) Signs of peritonitis
The EO can be distorted by alterations in sensory perception, e.g. due to head/spinal trauma, or the
presence of alcohol or drugs in traffic accidents, or bone injuries, which can lead to difficulties in
assessing the condition of the patient.
For diagnosis:
- Echo Fast: an ultrasound scan that is done in the patient who has had a trauma, and has the
great advantage of assessing the presence of fluid in at least four specific areas: hepato-renal,
splenic, pelvic, pericardial (cardiac tamponade must be excluded). It can be repeated even a
short time later, and thus will be useful in follow-up.
- Chest X-ray
- Rx pelvis
Essential in trauma management:
1) Treat the condition that puts the patient most at risk of death and intervene in it;
2) It is crucial to intervene in the Golden Hour: therefore interventions to stabilise and improve
the clinical condition should be implemented by the doctor in the first hour, in order to have
better results in terms of survival;
3) Medical interventions must not cause further damage (e.g. care when mobilising the spine)
4) Assess, intervene and re-evaluate: it is important that periodic re-evaluations of the patient are
carried out, to highlight any injuries or conditions that may have been missed at the first
evaluation, or re-evaluate pathological conditions that were considered secondary or less
important at the first evaluation.
5) It is not essential to make a diagnosis immediately: first, what poses the greatest risk to the life
of the patient must be treated.
Classification A, B, C
All of these evaluations allow us to categorise the pts into 3 types: A, B, C, based on:
- Vital parameters
- Estimated blood loss
- Need for additional crystalloids
- Need for transfusions
- Blood to be used
- Early presence of the surgeon
Then the therapeutic diagnostic procedure also depends closely on the haemodynamics of the patient:
1) STABLE PZ (A and B): with vital parameters and estimated blood loss not reaching 20-40%;
therefore, there will be vital parameters that return to normal or otherwise respond to
crystalloids. In type A the need for transfusion is low; in type B it is slightly higher. We
continue with a CT scan with mdc and this allows NOM, reducing unnecessary early
laparotomies and also the possibility of late ones.
2) UNSTABLE PZ ( C) : vital parameters, despite resuscitation manoeuvres, remain altered;
blood loss is >80% and therefore the need to perform haemotransfusions is timely, and very
often there is not even time to perform a haemogroup and cross tests, and therefore 0-negative
blood is used. In this case, there is a high suspicion of intra-abdominal haemorrhage and organ
rupture with haemodynamic instability, and therefore immediate surgery is performed, without
the need for a diagnosis of the nature of the lesion. The patient goes to the operating theatre
immediately and a laparotomy (gold standard) is performed.
Important is the role of CT with mdc, which has advantages:
- Identifies traumatic injuries to abdominal organs
- Assesses the severity of injuries
- Highlights any associated haemoperitoneum
In haemodynamically stable patients, a difference must be made in treatment:
- Surgical
- NOM (non-operational management), i.e. with re-evaluation of imaginig at 4-6h
There are exclusion criteria for conservative treatment:
- Evidence of injury to a hollow or diaphragmatic viscera
-
Unavailability of 24-hour interventional radiology and emergency surgery and the possibility
of transfusion medicine, as well as intensive monitoring of the patient.
In such cases, the patient cannot be treated conservatively.
NOM:
- The patient must be haemodynamically stable (A)
- There must be no lesions requiring surgical correction such as hollow viscera or possible
diaphragm lesions
- Not used in cases of penetrating injuries
- Close monitoring of the patient such as vital parameters, laboratory tests and radiological
follow-up and 24-hour availability of an interventional radiology and transfusion medicine
service and surgical treatment in case of failure (exploratory laparotomy)
- CT scan finding of active bleeding requires angiography with selective embolisation of the
arterial branches that are bleeding.
- If the patient becomes haemodynamically unstable, NOM is discontinued and surgery is
performed.
In the case of haemodynamically unstable patients, they are immediately taken to the operating theatre,
where everything is attempted, despite the high risks.
Damage Control Surgery
Laparotomy aimed at trying to stabilise the pc, sometimes by extreme procedures such as packing
organs such as the liver or spleen, which may be bleeding, without proceeding to major surgery. Thus,
the intent is a timely, rapid intervention aimed at haemodynamic stabilisation of the patient, without
intervening on the causes of the condition.
Three phases can be distinguished:
a) Phase 1: exploratory laparotomy. This is a rapid intervention aimed at a macroscopic
assessment of the 4 abdominal quadrants and any bleeding lesions and at stabilising the patient
by packing, i.e. placing gauze in the 4 quadrants of the abdomen so that the compression itself
can bring about a stop to the bleeding and rapid closure of the skin; then once haemodynamic
stability has been achieved, after the active bleeding has stopped, we move on to the second
phase. If packing also fails to control the bleeding, we move on to the Pringle manoeuvre, in
which the hepatic hilum (portal vein, common hepatic artery and common hepatic duct) is tied
off and the bleeding is stopped by blocking the blood supply.
b)
treat hypothermia, hypoperfusion, haemoglobin, and
coagulation, and control intra-abdominal pressure, which must be < 25 mmHg, to avoid
abdominal compartment syndrome.
c) Stage 3: Surgery must take place no later than 48-72h after stage 1, and consists of definitive
treatment of the lesions with depacking and exploration of the abdominal cavity, with control
of residual haemorrhages; debridment of devascularised sectors of parenchymatous organs and
possible packing of intestinal anastomoses that were not done before, and then proceeding to
the closure of the abdominal wall; ligations of vessels and temporary shunts may be done.
Complications:
- Haemorrhages
- Infections
EPATIC TRAUMAS
Liver injuries are divided into:
1) Open trauma: wounds from vulnerable bodies
2) Closed traumas:
- Parenchymal ruptures
- Compression
- Flexion
- Kickback (following sudden deceleration or acceleration during a fast movement: e.g. a
worker falling from a scaffold).
Liver injury scale (according to AAST)
-
-
Grade I: haematoma: subcapsular < 10% of organ surface; laceration: capsular lesion;
parenchymal lesion < 1 cm deep
Grade II: haematoma: subcapsular < 10-50% area; intraparenchymal < 10 cm in diameter;
laceration: parenchymal lesion 1-3 cm in depth; parenchymal lesion < 10 cm in length
Grade III: haematoma: subcapsular >50% area or expanding; subcapsular or parenchymal
ruptured; intraparenchymal >10cm or expanding; laceration: parenchymal lesion >3cm
deep
Grade IV: laceration: injury 25-75% of 1 lobe or involving 1-3 Couinaud segments;
vascular: vascular injury with bleeding involving the peritoneum
Grade V: laceration: lesion >75% of 1 lobe; vascular: venous lesion (retrohepatic vena
cava; suprahepatic veins)
Grade VI: vascular: hepatic disconnection
While subcapsular ruptures result in intrahepatic haematomas and haemobil damage; hepatocapsular
ruptures lead to immediate haemoperitoneum (there is no two-stage rupture as in the spleen).
Spontaneous haemoperitoneum, which characterises liver trauma, goes in DD with spontaneous
haemoperitoneum from:
- Ectopic pregnancy
- Ovarian cyst torsion
- Body rupture of the uterus
Traumatic haemobilia is rare and can also be found in cases of:
- Recent abdominal trauma
- Recurrent biliary colic
- Haematemesis and/or melena
- Transient obstructive jaundice
- Biliary calculosis
- Liver abscesses
- Hepatic artery aneurysm
- Iatrogenic (manoeuvres minimally invasive),
such as
retrograde cholangiopancreatography)
ERCP
(endoscopic
There may be cases of spontaneous haemobilia in cases of:
- Gallbladder lithiasis
- Paroxysitosis by schistosomiasis
Faced with a suspected penetrating or non-penetrating liver trauma, the haemodynamics of the patient
is always evaluated, if it is unstable it means that the lesion is stage IV, and the patient will go to the
operating theatre, while if the haemodynamics is stable, a CT scan with mdc is performed, an expert
radiologist classifies whether we are dealing with a minor or major lesion, moderate or major, and
based on the presence of free air, any evisceration or signs of peritonitis, impalement or thickening of
the intestine, we evaluate in addition to this, those factors that make exploratory laparotomy necessary,
or if in the absence of these signs, the patient has active bleeding.
According to the WSES, up to grade 2-3 lesions can be treated with NOM (non-operative
management), while subsequent grades require surgical treatment.
In contrast to splenic lesions, in liver lesions when haemorrhage is uncontrollable, abdominal packing
is used. The patient remains under anaesthesia with monitoring of vital parameters and laparotomy
pads soaked in warm saline are placed in the liver lodge, leaving the abdomen open. After several
hours, the patches are removed and the bleeding source usually closes. This manoeuvre is used when
there is no other alternative.
SPLENIC TRAUMA:
Splenic injuries are divided into:
1) Open trauma, for example:
- Firearm
- White weapon: in this case, a specillum should never be used to assess the entry wound of
the white weapon. In fact, when the speculum is inserted and the foreign body entered the
abdomen, with the intention of assessing how far the foreign body had penetrated into the
abdomen, it is possible to detect a visceral perforation, because perhaps the bursal cutter
had p e n e t r a t e d an intestinal loop. Therefore, specillation is not recommended.
- Iatrogenic: after gastroresection surgery or in case of spleen involvement in pancreatic tail
neoplasms (where splenectomy becomes necessary).
2) Closed traumas: direct or indirect (by recoil); there may be either a direct contusion
mechanism to the abdomen or left hemithorax; or a recoil, i.e. a sudden deceleration or
acceleration, during a fast movement (as may happen to a worker who falls from a scaffold,
landing on the ground). Basically, one has to consider that the spleen is a friable, mobile, richly
vascularised organ, located in the left hypochondrium, under the rigid rib cage, which on the
one hand protects it, but on the other hand makes it easily compressible against it and also
against other viscera.
3) Spontaneous rupture: when the spleen is meiopragic*, it is usually in patients who may have
a positive history of mononucleosis, malaria, TB, leukaemia (often leukaemic patients suffer a
splenic infarction). The presence of a meiopragic spleen may, for example, influence the choice
of type of delivery: natural childbirth poses a risk of ruptured spleen due to pushing, which
may cause lesions and therefore caesarean section is preferred.
*meiopragia: pathological condition of decreased resistance or functional capacity of a congenital or
secondary organ or system.
In most cases, splenic trauma occurs in traffic accidents, which rarely result in splenic trauma alone,
but are often also associated with liver, intestinal, pancreas, vessel, mesentery, diaphragm, kidney, etc.
trauma (i.e. polytrauma patient). The frequency of polytrauma is directly proportional to the severity
of the splenic injury and thus the need for splenectomy.
Comparing the trauma of the spleen with that of other abdominal organs, such as the liver and kidney,
we see that:
1) The spleen is a fragile organ, with a two-stage rupture mechanism, and may give
haemoperitoneum; one must also consider the possibility of a particularly mobile spleen, with
torsion on the vascular pedicle (which may lead to splenic infarcts) or the presence of a splenic
artery aneurysm (which may fistula into the digestive tract, and give atypical symptoms, with
melena).
2) The liver is an altogether resistant organ, with an immediate rupture mechanism, and can also
give haemoperitoneum. One must also consider the possibility of rupture of the
extrahepatic biliary tract, or rupture of the gallbladder, or disconnection of the biliary pathway,
all of which result in choleperitoneum.
3) The kidney is a resistent organ, with a rupture mechanism that self-tamps, and usually gives
haematoma.
The mechanism of spleen rupture occurs 'in two stages', which justifies the fact that the striking
symptomatology associated with spleen rupture, i.e. the haemorrhagic shock that results, does not
occur acutely, but usually after hours, days or even weeks.
In fact, after splenic trauma, a small subcapsular haematoma usually forms, which then grows and
tears the splenic capsule, resulting in massive haemorrhage, which can result in haemorrhagic shock.
For this reason, it is essential not to discharge a patient with abdominal trauma and possible splenic
trauma prematurely, but to keep him under observation, making sure that vital parameters remain
stable.
The diagnostic procedure involves:
1) Medical history:
- Often a person who has been in a car accident, is taken directly to the operating theatre, is
unconscious, and therefore the medical history is collected with the help of relatives or the
report of the 118 doctors who first rescued the patient, and in the medical file this help is
recorded.
- Essential is the description of the injury (e.g. car accident in a car without a seatbelt, airbag
deployment, etc.); Fall from a height, with disengagement from its ligaments, due to recoil.
- Investigate whether the patient has had any infections in the preceding days: e.g. malaria or
infectious mononucleosis; or whether he or she has lymphoproliferative processes, all
conditions that make the spleen increased in size, more fragile and therefore more
susceptible to trauma (hence meiopregic).
- Clinical findings are often blurred. The patient with a ruptured spleen should be managed
with a 'watchful waiting' attitude, with close clinical follow-up; there may be no or mild
pain in the left hypochondrium or lower quadrants (in the case of haemoperitoneum);
haematoma in the splenic lodge, with blood collection in the Douglas cavity; in the case of
complete rupture, there will be the picture of haemorrhagic shock, with: typical changes in
blood pressure and pulse, pallor, increased sweating, psychomotor agitation, air hunger.
2) EO abdomen: palpation and percussion of the abdomen do not reveal anything striking, except
for a certain 'pastiness' of the abdomen, due to the abdominal defence, which certainly cannot
be compared in intensity to the abdominal defence reaction, which we have in cases of acute
abdomen. There may be plexus obtuseness in the left quadrants, in fact that is where the blood
collects and begins to coagulate. Kehr's sign: in which the patient feels pain on pressure in the
left space between the muscle fibres of the sternocleidomastoid, due to irritation in the phrenic
nerve.
3) Instrumental examinations:
- TC
- ETG
- Puncture-wash (i.e. intraoperative diagnostic peritoneal lavage): when there was no Tc or
ETG, a needle was inserted (preferably not on the scar from a previous operation, because
there might be an intestinal loop at the site) and the fluid that flowed out was examined. It
was often pink or red due to the presence of blood, but in the case of a polytraumatised
patient, it could also contain pancreatic enzymes.
Rupture can manifest itself with haematomas of the spleen, which can be:
● Subcapsulars,
● Intra-splenic, within the parenchyma,
● Peripheral, on the surface of the spleen,
● Parailari.
William L Buntain's classification of splenic lesions
-
Grade I: subcapsular haematoma or capsular lesion without parenchymal damage.
Grade II: single or multiple lesion of the capsule with parenchymal damage, but without
damage to the hilum
Grade III: deep hilar damage, with vascular injury
Grade IV: fragmented spleen or hilar avulsion
The possibility of conservative treatment decreases as one progresses through the various grades.
Spleen Injury Scale:
-
-
Grade I: subcapsular haematoma < 10% area, laceration: capsular lesion but with
parenchymal lesion < 1 cm depth.
Grade II: subcapsular haematoma <10-50% area or intraparenchymal < 5cm in diameter;
laceration: parenchymal lesion 1-3 cm deep, not involving vessels
Grade III: haematoma: subcapsular >50% area or expanding; subcapsular or
intraparenchymal ruptured; intraparenchymal >5cm or expanding; laceration: parenchymal
lesion >3cm deep or involving vessels;
Grade IV: laceration: segmental or hilar vessels with devascularisation >25%.
Grade V: laceration: multifragmented spleen, vascular: hilar lesion with devascularisation.
From grade III onwards, one proceeds surgically.
Some authors, using the CT findings, have created a scale to which a score is given, which correlates
with the prognosis of the patient.
CT finding:
- Parenchyma:
o tear: 1
o breakage: 2
o poly-fragmented: 3
- Perisplenic fluid spillage: 1
- Free abdominal fluid spillage: 1
- Pelvic fluid effusion: 1
The severity of splenic as well as hepatic lesions can also be assessed by the degree of
haemoperitoneum:
- Minimum
-
Moderate
Impressive
Therapy
The therapeutic strategy in splenic trauma takes into account the importance of this organ from an
immunological point of view; unnecessary splenectomies must be avoided.
When the CT scan shows a minimal lesion of the splenic parenchyma, which does not deepen, the
patient is kept under observation, with:
- Double venous access
- Blood pressure and pulse monitoring
- Bladder catheterisation if necessary (if Hb and red blood cell values have fallen)
- Haemochrome every 6h
- Repeat the ETG to see if the perisplenic collection is stable in its quantity, or is
implemented.
If the haematoma is stable for 2-3 days and the haematochemical values are stable, the patient can be
discharged.
If too much blood is lost during observation and the GR and Hb values decrease, surgery should be
opted for and, pending typing, 0- blood can be started.
If the lesion is larger from the start, or there is an increase in haematoma, and the monitored
parameters are not stable, splenectomy (indicated when the proportion of parenchyma involved by the
trauma is high), usually in a laparoscopic approach, or splenoraxy (with parenchyma sparing) is opted
for: surgical suturing of the traumatic lesions.
vascular of the spleen, to stop the bleeding, while waiting for the appropriate surgical instruments to
be used after suction of the blood content in the abdomen.
Complications related to the surgery are:
- Acute pancreatitis
- Bleeding
- Subphrenic abscesses
In addition, the splenectomy patient presents:
- Increased risk of infections (immunodepression will occur)
- Platelet rebound
They may have sepsis from:
- Pneumococci
- Haemophilus influentiae
- Meningococci
It is therefore useful to seek infectious counselling and to recommend vaccinations.
TRANSPLANTS
Organ transplantation is the replacement of a diseased organ (no longer functioning, in organ failure)
with a healthy organ taken from a donor. Today, transplantation is the ideal therapy for chronic organ
failure.
Despite the fact that patients are put on the list, they often die without a transplant because of the
limited availability of organs. This mainly concerns the heart, because unlike the kidney, where the
patient can have dialysis, for the heart there are no equally effective replacement machines.
Nomenclature
- Grafting: no vascular anastomoses
- Transplantation: involves arterial and venous vascular anastomoses
- Explantation: surgical removal of an already transplanted organ
- Withdrawal: surgical removal of a donor organ
- Autotransplantation: the donor is the organ receptor
- Isotransplantation: between genetically identical individuals
- Allograft: between individuals of the same species, but genetically different
- Xenotransplantation: between individuals of different species. What stopped this practice
was xenozoonosis, the possibility of transmission of diseases from animals to humans.
- Orthotopic: organ transplanted at the site of the native organ: heart, lung, kidney
- Heterotopic: organ transplanted in a different location, e.g. the kidney
Donors fall into two categories:
1) Living donors: healthy donors who give up an organ, when it is bilateral: e.g. kidney, or
portion of an organ, such as liver or pancreas;
2) Cadaver donors, which is divided into:
-
Beating heart: brain dead
Non-beating heart: in eastern countries, this is the most commonly used solution, because
for religious reasons, organs from a subject with a beating heart are not used.
The multi-organ donor is a subject with absent brain activity, who has died of irreversible brain injury.
Law No. 578 of 93 associates death with the concept of electrical brain death, which identifies the
absence of life (until then, the concept of death was mainly linked to cardiac death).
These are usually individuals who have reached brain death due to:
- Blunt-force trauma to the brain
- Major cerebro-vascular accidents
- Post-anoxic brain damage
- Primary non-metastasising brain neoplasms.
The DD between coma and brain death is crucial: comatose individuals have a minimum of preserved
brain activity (in fact, they can wake up even years later).
In the case of brain death, the head is separated from the rest of the body. Thus, the subject has a
dichotomy between encephalic activity and the rest of the body. He continues to have a heartbeat, but
respiration is maintained mechanically; in fact, the breathing centres, which are located at the level of
the bulb, are damaged in these pts.
The cardiac electrical activity becomes uncoupled from higher controls and a rhythm known as
ideoventricular, which can be spontaneously interrupted, is realised, here anaesthetists try to support
cardiac activity through vasoactives and the perfusion of peripheral organs is maintained. Every braindead subject must be considered a possible donor. At the scene of the trauma, ventilation is
appropriate, because otherwise brain death leads to cardiac arrest.
Cardiac death can be ascertained by any qualified physician, who, upon noting the cessation of cardiac
death, completes the death certificate.
Brain death, on the other hand, must be established by a specific medico-legal commission, consisting
of an anaesthetist, neurologist and medico-legal expert, who assess from a clinical and instrumental
point of view whether brain activity is present for 6 hours (12 in children). In children, monitoring
must be done for 12 h, because the younger the brain, the more chance it has of recovery. Every halfhour, the evaluation of brain and spontaneous respiratory activity takes place and it is noted that there
is a lack of osteo-tendon reflexes and nociception. At the end of 6 hours, a death certificate is drawn
up, which will, however, date death back to 6 (12) hours earlier.
This subject will go:
- In the mortuary, to be buried
- In the operating theatre, for organ removal
In the allocation of organs, this is done through transparent laws, where the concept of compatibility
between recipient and donor prevails.
As far as the donor is concerned, despite compatibility, it should still be studied with an accurate
medical history and then assess the cancer risk of the patient.
Screening and instrumental examinations will be carried out, even on the cadaver itself, to see if there
are any suspicious alterations, because the risk of transmitting the neoplasm to the recipient is high,
considering that he or she is undergoing immunosuppression.
Viral pathologies and their possible transmission are taken care of.
Organ processing and preservation
In the case of ischaemia, there is reduced pump activity, which through ATP consumption normally
gives rise to intracellular hyperkalemia and extracellular hypernatremia, leading to a cancellation
of the action potential, and the activities of the pumps and that of ATP are lost, so we will have a
migration of Na+ into the cell and K+ out, and then there will be cellular oedema, then a cellular
swelling, leading to the bursting of the cell, with release of lysosomal enzymes, with organ
disintegration. This mechanism has allowed us to understand how to treat and preserve organs when
they cannot be properly perfused for transplantation.
Important is the perfusion of the harvested organs through a 4°C hyperkalemia solution.
N.B. 4°C is the cut-off below which one cannot go, because below this temperature water
solidification occurs, with cell crystallisation, and the water inside the cells solidifying, would lead to
an increase in volume and the cells lose their vitality. In addition, at 4°C there is also a slowing down
of the biological activities of the cells, and thus an attempt is made to compensate for the lack of O2.
Such perfusion determines:
- Cooling, reducing cellular activity
- Hyperkalemia, with membrane equilibrium and absence of swelling, as electrolyte passages
are inhibited
- Wash out of the donor's blood elements triggering less immunological intolerance
mechanisms in the recipient.
Organ removal - In situ perfusion
An incision line is made: it starts at the jugular and passes through the sternum (which is opened with
an electric saw and then spread with the Fennel retractor) to the pubis (this is called a jugulo-umbilical
-pubic incision). The abdominal cavity is divaricated with Balfour's retractor.
The possibility of harvesting organs with beating hearts allows all organs to retain their perfect
pathological anatomy.
When the heart shuts down, the organs most susceptible to ischaemic damage are e.g. the heart itself,
liver, pancreas, brain, adrenal gland, while e.g. the kidneys are resistant, but thanks to the beating
heart, perfusion can be performed with the organ still attached to the vascular hilum, through cannulas:
- An aortic perfusion cannula, introduced at the carrefour, which must not occlude the
emergence of the renal arteries;
- A cannula in the aortic arch
A hyperkalemic solution is inserted from both cannulas, which will lead to cardiac arrest in diastole.
Perfusion solutions are:
- Eurocollins: with glucose, always hyperkalemic
- U.W. solution (university of Wisconsin): contains more lactobionate (m-stabiliser).
It is the most widely used today
Now the organs are perfused by this hyperkalemic solution that cools them down and only then will
they be harvested, organ by organ.
First the liver is taken, then the pancreas, then the kidneys and possibly the intestines in the abdominal
cavity; while in the thoracic cavity first the heart and then the lungs (the heart is taken as soon as
possible in an emergency because it is excessively exposed to ischaemic damage). In fact, the heart
must be harvested and transplanted as quickly as possible to reduce the cold ischaemic time, i.e. the
time from perfusion with hyperkalemic solution to re-implantation.
-
A cannula in the vena cava (third cannula): to allow the outflow first of blood and then of
the perfusion solution, to avoid hypertension which can damage organs. It is also useful to
understand the time and quality of the perfusion, in fact, blood wash fluid indicates good
perfusion.
N.B. This third cannula is not always put in for reasons of speed or habit, so instead of putting it in, the
vena cava in the abdominal cavity is opened directly and the fluid is sucked out with aspirators.
+the organs are not touched prior to perfusion, leaving the microcirculation intact for in situ perfusion:
the surgeon has more time for harvesting, compared with beating-heart methods (it was a race against
time before: since the donor is haemodynamically unstable, if the cadaver goes into arrest, organs such
as the heart and liver are lost). After harvesting, perfusion is performed; less vasospasm of the
microcirculation; shorter operating times; containment of blood loss: in the past, there was the risk of
damaging some arteries before perfusion (which took place over the counter), leading to blood loss
which made the cadaver unstable from a haemodynamic point of view].
+Organs harvested from donors in cardio-respiratory arrest:
- Cornea
- Heart valves
- Vascular segments
- Bone segments
The kidney is harvested with the entire aorto-caval block and perirenal fat. Then with bench surgery
the fat structure is removed and as soon as the kidney is re-implanted in the right or left iliac fossa,
where the renal lodge is recreated, it is looked at if it starts to produce urine and the anastomosis
between the ureter and bladder of the patient is made.
Organ preservation
The organs are stored inside a basin, where granular ice is placed at 4°C, and here the organ undergoes
bench surgery, which prepares the organ for transplantation. Sterile gauze is used, which does not
allow contact between organ and ice.
An ex vivo perfusion is performed on a bench, and the bag containing the perfusion fluid is attached at
a height of about 1.5 m.
Ice Storage
With storage on ice, you have time to transport the organ to the centre where it is to be transplanted.
For example, if two kidneys are harvested, one is sent to the patient who we know is already in need,
the other is sent to the national circuit to study to whom it can be given.
Ice storage is the 3-bag technique: a first bag, which contains the organ wrapped in gauze and
perfusion solution at 4°C but no ice, is placed inside a second bag, which contains ice. Everything is
then placed in a third bag.
If the exchanges are intercontinental, as is the case with the heart and liver, which are life-saving
organs, a machine is used, where the transfusion fluid and an oxygenation circuit are located.
Then, together with the organ, other information about the organ should be sent, such as the possible
alterations found, and the amount of perfusion fluid used.
Mosaicism: the ability of an individual to have a double genetic profile: both maternal and paternal
chromosome lines are taken into account, which explains why a female kidney can be transplanted
into a male and vice versa. Thanks to mosaicism, it is possible to silence a genetic profile
and express the other and adapts to the recipient's sex. It provides for the simultaneous expression of
both genetic profiles, i.e. both male and female, and favours either one or the other when then
transplanting.
LIVER TRANSPLANTATION
It was first performed in the 1960s by Thomas Starzl (father of transplantation). The success of
liver transplantation was achieved slowly for various reasons (patients arriving extra-terminally in a
critical condition, difficulty of the technique...). Quite complex surgical technique but possibility of
return to a practically normal life.
-
It is life-saving
Orthopaedic: should be placed subdiaphragmatically, right hypochondrium
First hepatectomy of the native liver on the recipient, then transplantation of the donated liver.
Directions
The main motivation for transplantation is HCV-related cirrhosis more in Southern Europe, whereas in
Northern Europe and America transplantation is mainly for alcoholic cirrhosis.
-
End-stage hepatopathy
-
Diffuse liver neoplasms
Acute fulminant liver failure: from hepatotropic virus infection, from fungi and from drugs
(paracetamol)
Metabolic diseases: thesaurismosis
Congenital diseases: alpha1 anti-trypsin deficiency, primitive haemochromatosis, glycogenosis
(type 2 is Pompe's disease)
Severe liver trauma
Wilson's tumour
Historical transplantation indications for HCC
-Mazzaferro's 1996 criteria
Nodule <3-5 cm
o Number of nodules <3
o No vascular invasion
o No lymph node spread.
Today they are important:
o No. nodules
o > dimensions
o Grading! With any biopsy or instrumental examinations
o
-
Limitation of the resectability of liver neoplasms: the residual liver mass from the eventual resection
of the tumour may not be sufficient to guarantee perfect homeostasis in the patient. OLTx for HCC is
debated because immunosuppression may lead to recurrence of the neoplasm in the transplanted liver.
Therefore, the indication for transplantation for tumour reasons has been abandoned by many centres
for this reason.
HCV transplantation, also debated for: high rate o f infection recurrence, impossibility of
carry out prophylaxis, 95% of viremic pts before transplantation will also be viremic after □ in
In reality, only 5% of transplant recipients develop cirrhosis again, most develop only mild
hepatopathy.
Donors
-
Cadaver: two haemiplegates (right and left) can be obtained from the donated liver [split liver]:
one part is transplanted into a paediatric patient (segment II and III, left haemiplegate) and the
remaining part is transplanted into a woman or a microsomic, short man
o Ideal
o Marginal
N.B. Split liver is a liver transplant with division and donation to two different pts; the anastomotic
suturing of the vessels is done with detached stitches as this transplant is usually done in pts
paediatric so the detached stitch suture determines the possibility of vessel growth while the
continuous one does not.
-
Living: segments (2-3 above all) can be taken from the liver of an adult to be implanted in a
paediatric patient
Ideal donor
- Ischaemic time <12 h
- Weight: should not exceed that of the receiver by 20% (there must be a weight match between
the two)
- Age: there is no precise limit, even from pts up to 70 years of age with a good clinical
condition
- General clinical conditions
o Exclude trauma, organ disease (HBsAg+, Anti-HCV+)
-
Biochemical parameters □ ALT, AST, FA, bil
Marginal donor
Age >70
years
-
Resuscitative course
o Cardiac arrest
o Sepsis
o
-
Haemodynamic instability □ especially if he has received drugs that cause
vasoconstriction on the microcirculation (not good for the trophism of the organs
themselves that are candidates for donation)
Liver pathology
o Trauma
o Steatosis 40-60%.
o HCV+ (for HCV+ recipients)
So age is not an absolute contraindication to the use of the liver for transplantation. Donors > 50 years
old are + 22%.
Living donation
- Donation of a haemifegato to a paediatric (seg II-III) or adult recipient (right lobe mainly)
- A recipient already on the waiting list and with a medical urgency for a transplant
-
The donor must be 'guaranteed' □ therefore super-specialised centres with surgeons specialised
-
in this transplant surgical technique.
Psychological support
-
Risk awareness □ Mortality 0.3-0.5%
Pre-operative donor assessment
-
The surgeon must know the anatomy of the vascular and biliary systems. They perform:
o Angio-RM and Cholangio-RM
-
Assess liver volume to ensure perfect liver function of the remaining liver in the donor and
transplanted liver.
Cadaveric donor transplantation
-
-
-
-
Hepatectomy in the cadaveric donor
o After perfusion of the organ with cannulas placed at the iliac carrefour, section of the
superior cava, section of the v porta, hepatic a and inferior cava; then disarticulated by
the suspensory ligaments (sickle and triangular); then preserved using the three-bag
technique.
Hepatectomy of the recipient's diseased liver:
o Dissect hepatic artery, suprahepatic cava vein, subhepatic cava vein, portal vein to
remove the liver
o Clamping the portal vein, the subdiaphragmatic vena cava, the subhepatic vena cava:
haemodynamic changes (venous hypertension is established) so it is important to do an
extracorporeal circulation that collects the blood from the inferior vena cava and injects
it from the axillary vein (specialist talk)
o Following hepatectomy of the diseased liver on the recipient there is an 'anepatic' phase
in which the recipient will no longer have any liver function
Orthotopic transplantation
4 terminus-terminal anastomoses
o Donor suprahepatic cavity with that of the recipient
o Subhepatic quarry
o A. hepatica
o V. door
Choledoco anastomosis of the donor and the recipient.
Complications
Sometimes so severe that they require re-transplantation: a new liver is sought in a matter of hours
(national alert is triggered), otherwise the patient dies.
- Hepatobiliaries
o
Primary functional failure □ Excessive ischaemia, poor preservation, age
o
Small-for-size syndrome □ Volumetrically and functionally insufficient transplanted
liver
o Acute and chronic rejection □ Most frequent cause of organ dysfunction
o
Hepatitis HBV, HCV (recurrence), CMV, HSV
o Anastomosis dehiscences □ Careful post-operative control of the surgeon due to the
large number of anastomoses performed
-
Extra-hepatic □ mainly related to excessive immunosuppressive therapy (especially in
first days after the transplant) [transplant centres have individual rooms for the transplant
recipient's stay, with air purification systems and sterile equipment and devices].
o Infections □ Main cause of death especially in the first 2 months. Bacteria
nosocomial (klebsiella, pseudomonas) or mycetes
o Lymphoproliferative diseases
o Solid neoplasms
o Various: atelectasis (sometimes involving severe hypoxaemia), hypertensive crisis,
haemorrhagic strokes
Survival
-
-
From cadaver donor
o
Whole livers □ 62% at 5 years
o
Split livers □ 59% at 5 years
From a living donor □ 71% at 5 years
Unresolved issues
- Insufficient number of donors
- Many deaths on waiting lists
-
Maximum retention time 12-15 h □ is a semi-urgent surgery
-
The immunological tolerance target was not achieved □ next years' target
-
Post-transplant HCV reinfection
KIDNEY TRANSPLANT
We distinguish three phases:
Cadaver retrieval Over-the-counter surgery Transplantation
The receiver:
Increase in the number of patients on the waiting list: many elderly and diabetic patients or
patients with co-pathologies are now on the waiting list because the technique gives excellent
results.
The recipient patient must be studied in his or her own department before being put on the
waiting list. Preparing the patient with terminal CRI for transplantation
Clearance of any infectious focus (including caries), potential danger of sepsis.
Absolute contraindications to transplantation (valid for all transplants, not just kidney) Life expectancy
< 1 year
Recent malignant neoplasm
Untreated chronic infection
Uncontrollable psychiatric disorders: do not underestimate. Pts can enter deep
crisis, post-transplantation or they may even suspend post-transplantation immunosuppressive
therapy (e.g. young people!) which should be continued for life
Drug addiction
Ideal donor
Young subject
Absence of infectious or neoplastic diseases
Good haemodynamic stability and good function of the organs to be harvested Absence of
chronic disease (diabetes or hypertension)
Over-the-counter surgery
Carried out at the local transplant centre prior to implantation of the kidney by the specialist surgeon:
he must be specialised in bank surgery as the organ is bloodless and its colour different from normal
(there is an absence of the normal operating field, which usually helps the surgeon with colour vision).
It serves to clean the organ of adnexa:
∙
∙
(how many arteries, veins..) and ureters.
In polytraumatised patients, the kidney may be injured (marginal kidney): it can be stitched up during
over-the-counter surgery, allowing the use of these marginal kidneys.
Marginal 'suboptimal' kidney
-
Elderly people > 65 years,
Creatininemia > 1.5 mg/dl
Clearance < 90 ml/min
Diabetes
Hypertension
> multiple arteries
Glomerulosclerosis > 15%
Cold ischaemic duration > 36 h.
The outcome is not the same as a non-marginal organ transplant, but certainly in the absence of organs
to transplant, it is a viable option.
Technique
-
Kidney transplantation is heterotopic.
Native kidneys remain in situ, they are not removed.
The kidneys should be transplanted into the iliac fossa (the left kidney into the right iliac fossa
and the right kidney into the left iliac fossa) and the vessels should be anastomosed
-
The renal transplant artery anastomoses terminally-terminally with the hypogastric artery
The renal vein is anastomosed with the common iliac vein
-
After declamping the blood vessels with subsequent revascularisation of the organ, the ureters
are anastomosed in the dome
Revascularisation allows the transplanted kidney to change from a waxy colour to a brick-red colour.
If there are no map-like phenomena, it means that the microcirculation is well vasodilated, so there is
good oxygenation of the renal parenchyma.
Map staining phenomenon: occurs if the microcirculation is partly vasoconstricted, then warm
laparotomies are placed to vasodilate the constricted areas.
Immunosuppressive therapy
It serves to make the organ accepted, which is always recognised as non-self → rejection is possible
even in the presence of excellent compatibility (unless it is an isotransplant or from monochorionic
twins)
Drugs:
-
-
Steroids: in the past these were mainly used with side effects: moon facies, hirsutism,
Calcineurin inhibitors (fungal derivatives)
o cyclosporine, marked the success of transplants by being able to lower the dose of
steroids
o tacrolimus
Azathioprine
Mycophenolate mofetil..
Rejection
Acute
Hyperacute: missing today
Chronic: yet to be controlled. The transplant is not eternal, lasting about 10 years, because
the trapaint organ deteriorates in function. However, thanks to immunosuppressive drugs, it has
been reduced.
Monitoring
Eco-colour doppler
FNAB: tissue frustules to assess functionality and possible rejection.
Complications
Vascular: Thrombosis of renal arteries and veins.
urological.
Today's issues
Shortage of organs for transplantation, e.g. due to a reduction in the number of cranioles compared to
the past. The donor pool has therefore expanded by keeping marginal organs for transplantation in
'marginal' patients (i.e. patients in good clinical condition).
HEART TRANSPLANT
Antique transplant: the first in 1967 by Christian Barnard fooling his US master Cooley
Directions
- Criteria:
o Cardiac index < 2-2.5 L/min/m2
o FE of VS < 20-25%.
o Maximum systemic O2 consumption < 14 ml/kg/ min
- When no form of conservative surgery is feasible
- When quality of life is poor and expected survival is limited, despite optimal medical tp
- In 90% of cases in two conditions:
o Dilated cardiomyopathy
o Non-conservatively treatable ischaemic heart disease.
Transplantation, technique
-
-
Orthopaedic
Excision of the native heart: incision of the thoracic cage, isolation of the carotid afferent and
efferent vessels; immediate extracorporeal circulation via a roller pump (external mechanical
pump that artificially ensures perfusion of the entire body)
Immediate vein and artery anastomosis
Surgery must be very rapid: the transplanted heart must resume contractile activity (restored
with a defibrillator) and for this it must be in the best possible condition assured by the speed
of the technique
Results
-
Reduced mortality: at 30 days □ 8%
-
Survival
o At 1 year 85-90%.
o At 5 years 70-80%.
o At 10 years 50-60%.
-
Immediate complication: graft failure, i.e. haemodynamic inefficiency due to excessive
recipient lung R. It is a life-saving transplant.
Problems
- Shortage of organs: deaths on the waiting list.
PANCREAS TRANSPLANTATION
Pancreas transplants are performed in diabetics if their pancreas is unable to produce enough insulin.
More than 80% of diabetics who undergo a pancreas transplant after the operation have normal blood
sugar levels and no longer need insulin, but on the other hand must take immunosuppressants, with the
risk of infection and other side effects.
Since injectable insulin is a safe and reasonably effective treatment for diabetes, getting rid of the need
to take insulin is not considered a good enough reason to consider a pancreas transplant. Therefore,
this procedure is normally only performed in a diabetic subject if:
Renal insufficiency is also present.
It is impossible to keep blood glucose levels within an acceptable range, especially when the
subject cannot perceive an excessive drop in blood glucose.
Occasionally, when blood glucose levels remain low for too long, organs, including the brain, suffer
permanent damage.
GONADI
TEXTBOOK
VARICOCELE
Varicocele is a pathological varicose dilatation of the veins of the pampiniform testicular plexus,
related to an incontinence of the valves.
Varicocele develops (developmental disease) from puberty onwards, and from around 16 years of
age it causes chronic damage to the testicle resulting in hypofertility in 50% of cases. It affects 10%
of young adults, and is more frequent on the left (x8) because the left (internal) spermatic vein flows
into the renal vein at 90°, while the right makes an acute angle into the vena cava.
Anatomy
Pampiniform plexus: venous plexus contained in the spermatic cord, which drains blood from the
testicle. It consists of three groups of veins that anastomose freely:
● anterior spermatic veins (flowing into the internal spermatic vein and thus into the VCI);
● middle deferential veins (accompany the ductus deferens and flow into intrapelvic veins);
● posterior spermatic veins, which flow into the inferior epigastric and pudendal vv.
Left spermatic vein: it originates from the pampiniform plexus, runs in the spermatic funiculus at the
level of the inguinal canal and then runs dorsally and cranially in the retro-peritoneum until it connects
perpendicularly to the ipsilateral renal vein. Very often several internal spermatic veins are present,
anastomosed to each other. On the right the internal spermatic vein drains at an acute angle into the
vena cava.
In the presence of left internal spermatic vein reflux, gonadal venous discharge occurs in the:
● Deferential veins (internal iliac tributaries)
● Cremasteric veins (tributary to the external iliac)
● Anterior and posterior scrotal veins (saphenous and internal pudenda)
● Right internal spermatic vein via numerous anastomoses.
Very often the ectasia of these venous districts is therefore the effect and not the cause of varicocele. A
vicious circle is created as these systems are communicating.
Pathogenesis
● Same pathophysiology as for varicose veins of the lower limbs (there are no semilunar valves
breaking the blood column of the VCI): hydrostatic pressure at the level of the left spermatic
vein.
● Congenital absence of valves in the SPIsx vein (hypothesis)
● Nutrcraker (ab extrinsic compression) of the superior mesenteric artery on the left renal vein
(accounts for high flow varicocele in pre-pubescent, I)
● Nutracker of the right common iliac artery on the left (reflux occurs through the vas deferens, I)
● Puberty-induced arterial-venous discrepancy in the testicular district (justifies post-pubertal
varicocele, tends to increase over time due to progressive vv whitening and devascularization)
● Presence of anastomosis between the SPI and the cava and/or common iliac and/or capsular vv of
the kidney, and/or femoral vv
● Right (2%) or bilateral (3%) varicocele must make us think of a secondary varicocele e.g.
retroperitoneal tumour compression, renal tumours (e.g. Wilms') or hydronephrosis, thrombosis of
the renal vein. Another alarm factor in addition to the site is age of onset > 40 and sudden onset.
Varicocele and the reproductive system
Forty per cent of infertile males have varicoceles, and in about half of these cases the spermiogram
and fertility improve by resolving the varicocele (improvements occur mainly if the correction occurs
before the age of 14). Hypotheses on the origin of the damage:
●
●
●
●
●
●
●
●
Increased intrascrotal (and testicular) temperature caused by blood congestion
Increased hydrostatic P in the venular bed and reduced fluid reabsorption of the testis
Altered PO2
Reflux of (toxic) metabolites from the kidney and adrenal system (not confirmed)
Altered Leydig cell activity
Reduced testosterone biosynthesis secondary to reduced 17-30 lyase and 17-hydroxylase activity
Reduced concentration of total and free serum testosterone
High levels of 11b-hydroxyandrostenedione and 17°-OH-P
Diagnosis
● Symptoms: localised gravitative pain in the left side (especially if the patient stands a lot)
● EO: on inspection the scrotum appears more elongated; palpation is the most important
moment (should be performed with the pc standing in front of you, thumb and forefinger
gently, worm-bag s e n s a t i o n ).
● Seminological tests (qualitative-quantitative alteration of sperm): reduced concentration and
total sperm count (oligospermia: <15 M/ml); reduced motility (asthenospermia) and
teratospermia.
● Ultrasound (for number, location, diameter of intra scrotal veins): predictive of varicocele the
presence of diameter >3mm in clinostatism.
● Trans-femoral and trans-brachial spermatic venography (radiological diagnosis): is the
gold standard in the diagnosis of varicocele, visualising the anatomy and any collateral circles.
Indicated in recurrent or persistent varicoceles, complex and invasive investigation, high cost,
no first level.
Clinical classification (palpatory)
● Clinical grade I varicocele: appreciable only by scrotal doppler ultrasound, which shows venous
reflux. It may be subclinical, or be sought because the patient complains of gravitational pain
(sense of weight and scrotal tension).
● Clinical grade II varicocele: palpable by performing the Valsalva manoeuvre, which by
increasing pressure in the abdomen increases the blood volume in the incontinent veins.
● Clinical grade III varicocele: palpable in basal conditions (orthostatism). On palpation, ectasic
veins are appreciated as a 'bag of worms' or 'chicken intestine'.
● Clinical grade IV varicocele: evident on inspection because it deforms the scrotum. Often
accompanied by hypotrophy of the ipsilateral testicle.
Classification according to scrotal colour-echo-Doppler
● Varicocele of the first type: venous reflux can only be evoked with the Valsalva manoeuvre
(other manoeuvre: squeeze-release of the funiculus).
● Varicocele of the second type: phasic basal venous reflux with breathing.
● Varicocele of the third type: continuous basal venous reflux.
Indications for the correction of varicocele in paediatric age for the prevention of infertility
●
●
●
●
●
Testicular atrophy
Difference of at least 2 ml in volume of the affected testis compared to the contralateral one
Severe unilateral varicocele or bilateral varicocele
Gonadotropin-relasing hormone stimulation abnormal test
Symptoms: pain, feeling of heaviness, testicular swelling
WHO guidelines indicate that only advanced cases (grade III and IV) should be treated. In reality,
however, since the operation is minimally invasive and the disease can worsen, mild cases are often
operated on.
Therapy
The therapy consists of closing the plexus veins; the drainage of the testicle will then be carried out,
via anastomosis, by the cremasteric or epididymis-deferential veins.
● Sclero-embolisation (trans-femoral; trans-jugular; trans-brachial): a sclerotizing substance is
injected through the renal vein, reached with radioscopic guidance by puncturing the femoral vein.
The more voluminous the varicocele, the more likely a recurrence will be. Sclerosing agents (e.g.
Trombovar) that obliterate the vessels of the pampiniform plexus by chemical phlebitis.
Embolising agents (spirals, tampons). Detachable silicone balloons, inflated and released at the
spermatic veins.
● Tauber's microsurgery: approximately one cm incision at the base of the scrotum.
● Varicocele microsurgery according to Marmar: a single incision is made in the inguinal region
above the attachment of the shaft (M: in the scrotum), the duct and the vas deferens artery are
isolated and the veins are selectively ligated, respecting the lymphatics. It gives a lower probability
of recurrence.
● Goldstein's intervention
● Ivanissevich or Palomo operation: the spermatic vein is tied off as high as possible, without
incising the peritoneum, but by untying it. General or peri-medullary anaesthesia. No satellite
veins should be left if several spermatic veins are present.
● Video-laparoscopic intervention: the internal spermatic vein is identified (can be seen through
the peritoneum). Bell sign: the scrotum is stretched and the movement is also transmitted to the
intraperitoneal spermatic vein.
● Resection of ectasic veins: more invasive, it is performed in grade IV varicoceles through a
subinguinal scrotal incision of about 2 cm, and eliminates the risk of recurrence.
Very serious complications: the surgeon exchanges the spermatic vein with the ureter (if the ureter is
clamped, a peristaltic vermiform movement is triggered that does not occur in the vessel).
+Varicocele in women (gonadal veins): gravative pain in the lower abdomen (FIsx) radiating to the
large lip on the left side. The pain occurs especially after a woman stands for a long time.
HYDROCELE
It is a pathological condition characterised by the presence of a collection of citrine yellow fluid
(lymph) between the vaginal tonaca and the testis (between the two sheets of the vaginal tonaca:
propria - communis). The collection is typically trans-illuminable and manifests as indolent swelling.
Aetiopathogenesis
● Primitive or idiopathic
o Abnormal descent of the testicle or incomplete closure of the peritoneo-vaginal duct
(communicating or congenital hydrocele): the testicle descends as it grows (goes back),
exploration is done with the index finger (if it reaches the inguinal canal it means it is pervious.
A congenital hernia can form (initially of the large omentum)
o Rupture of small cysts of the epididymis (e.g. from minor running-related injuries)
o Disturbances of capillary hydrostatics and the balance between secretion and absorption of
serous fluid (e.g. in undernourished children typical of 3rd world countries).
● Secondary or symptomatic
o Acute or chronic orchiepidimitis
o Surgical operations on the external genitalia or spermatic funiculus (for the treatment of inguinal
hernias, there is increased pressure, since implants or plugs are used, this type of complication
due to the inflammatory state resulting from the permanence of a foreign body). Chronic postoperative pain syndrome due to nerve compression from post-operative fibrosis (hernia
spermatic funiculus surgery).
o Testicular neoplasia.
● In young children, it may be related to failure to close the peritoneal-vaginal duct (the scrotal
cavity is in communication with the peritoneal cavity and peritoneal fluid accumulates there due to
gravity). It tends to resolve spontaneously within 12 months, otherwise it can be drained.
Predisposing condition for congenital inguinal hernias.
● In adults, especially over the age of 40, it may be due to water retention in the lower limbs or be
the manifestation of an inflammation of the testicle (e.g. epididymitis) or a testicular tumour. It
may also be due to reopening of the peritoneo-vaginal duct, or be idiopathic. Mild cases do not
require treatment, while symptomatic ones are treated with drainage. (M) is non-communicating
and secondary to reduced testicular lymphatic drainage due to trauma, inflammation or iatrogenic
intervention (removal of lymphatics in varicocele surgery).
Clinic
It is almost always asymptomatic; if it reaches a considerable size, it causes local discomfort and
heaviness due to a weight-bearing effect.
EO
Hemiscrotum increased in volume compared to the contralateral generally 2-3 cm, apricot-orange and
on palpation a smooth-surfaced, uniform tense-elastic swelling is appreciated. Positive
transillumination. Ultrasound.
Treatment
Percutaneous drainage (drainage under ultrasound guidance or not: the prof also drained 300cc,
pouring betadine at the end of the procedure causes the walls to collaborate).
Non-communicating forms are operated on only when they are conspicuous in size or clinically
troublesome. Surgery in this case consists of drainage of the excess fluid and removal and eversion of
the vaginal tonaca (own excess) in order to prevent possible recurrences.
EMATOCELE
A haematocele is a haemorrhagic effusion in the vaginal tunica of the scrotum (between the two
serous bands), usually of traumatic origin. It presents as a painful swelling of varying size depending
on the extent of the effusion.
PIOCELE
Purulent collection within the vaginal tunic, due to infection by pyogenic bacteria.
The epididymis is free in the scrotum and therefore the mesothelial 'appendix' sheet of the peritoneum
has the role of protecting and reducing friction in the scrotal bursa (like the pleura for example).
ACUTE SCROT
The term acute scrotum refers to a non-specific clinical picture of suffering of the endoscrotal organs
(testicle, funiculus, vaginal tunic), characterised by:
● Acute-onset pain
● Tumefaction
● General signs of inflammation
It is one of the most frequent causes of medical litigation, as it may represent a surgical emergency (it
does not endanger the life of the patient but may seriously impair the function of the gonads)
Most frequent causes of acute scrotum:
● Testicle torsion
● Orchiepidimitis
Other causes of acute scrotum:
● Strangulated inguinal hernia
● Trauma (testicle fracture, haematocele, haematoma)
● Spermatocele and symptomatic varicocele
● Hemorrhage in testicular k
● Gangrene of the scrotum
● Acute scrotal swellings 2arie to intra-abdominal pathologies
Early differential diagnosis between the two most frequent causes of acute scrotum is essential; the
criteria may be:
● Age of the patient
● EO (characteristic for testicle torsion)
● Urine examination
● Imaging techniques → ECD (readily available in emergency situations, allows the evaluation
of flow signals at the level of the epididymis in addition to parietal thickness) and scintigraphy
(gold standard in the diagnosis of testicular torsion, but poorly available in emergencies).
N.B. Scrotal masses and k to the testis do not fall under dd for acute scrotum because they are NOT
painful.
TESTICLE TORSION
It consists of torsion of the spermatic funiculus, resulting in compression of the blood vessels that
nourish the testis. It is most frequent in young people (12-18, relatively frequent also in the neonatal
period where there is a great laxity of the gubernaculm testis), with an incidence of 1/4000/year in
subjects under 25 years of age. It is among the leading causes of acute scrotum and represents an
urgent surgical need.
In the early stages after torsion there may be only venous stasis, but the stagnation resulting from this
causes testicular oedema and increases the pressure to the point of compression of the arteries. In the
case of complete torsion, the testicle suffers ischaemia and goes into necrosis in 6-12 hours.
Clinic
It presents with acute testicular tumefaction, scrotal erythematous oedema (there must be no doubt
about it) and very intense testicular pain, which may radiate to the inguinal area (or ipsilateral
iliac fossa, lumbar region) and enter dd with renal colic (which radiates to the same area), but also
with orchiepidimitis. Neurovegetative symptoms such as nausea, vomiting (due to ischaemic necrosis)
are also present.
Differential diagnosis: acute bacterial orchiepididymitis
It differs in the following signs (see clinic on, inspection!, difficult palpation with the painful pc)
● ascended and horizontalised testicle ('if a testicle is at the bottom of the scrotum there is no
torsion');
● abolition of the cremasteric reflex;
● pain does not decrease by lifting the testicle (negative Phren's sign);
● reduction or absence of testicular blood flow on echocolordoppler (!).
On the other hand, all indications of urinary (e.g. leucocytes in the sediment) or prostate (e.g. sore,
warm and enlarged prostate) infections, in addition to the absence of these signs, point towards
epididymitis, since testicular infection is usually secondary.
Another possibility during acute scrotum is an acute severe varicocele due to thrombophlebitis.
Surgery
derotation - fixation to the scrotal walls with non-resorbable stitches - prophylactic fixation
contralateral testicle. In any case, whenever testicular torsion cannot be ruled out when in doubt, the
scrotal cavity is operated on and directly explored (testicle viability can be assessed).
The torsion must be resolved surgically within 6 hours (! - urgent), otherwise the testicle may atrophy
and must be removed (frequent cause of medico-legal litigation), orchiectomy and insertion of a
prosthesis.
TESTICULAR CARCINOMA
Testicular cancer accounts for 1% of male malignancies (and 5% of urological tumours), but it is by
far the most frequent malignancy in young adults aged 15-40 years (!). Overall, there are three peaks
of incidence: 2-4 yr (t. yolk sac) - 20-40 yr (germinal)
- >60 aa (lymphomas). However, it has an excellent prognosis, with a 5-year survival of 95%, due to
the
good curability.
Risk factors
● Cryptorchism (15%): the most important, and should always be sought in children. Orchidopexy
of the testicle performed before puberty reduces the risk of cancer: it is recommended between 6
and 12/18 months.
● Familiarity: family members of an affected person should be advised to perform self-examination
once a month.
● History of contralateral testicular cancer - testicular atrophy - Klinefelter syndrome
● Subfertility
● GCNIS (germ cell neoplasm in situ)
● Intersex disorders: presence of testicular tissue in apparently female subjects.
Testicular trauma does not increase the risk, but it is often the reason for examinations leading to the
discovery of a subclinical tumour mass (in AP puts it among the FdRs).
Normal histology of the testis
● Seminiferous tubules: tubular structures surrounded by a basement membrane and myoepithelial
cells
(they contract to move the secretion) and containing two cell types.
o
Germ cells (1st and 2nd order spermatocytes - spermatids - spermatozoa): these are found
scattered in the tubules, in relation to the Sertoli cells, forming the 'ornaments' of the tree.
o Sertoli cells: large cells, forming tight junctions (blood-testicular barrier) and enveloping the
germ cells with offshoots, forming a 'Christmas tree' structure.
● Stroma: formed by loose connective tissue and containing Leydig cells (large, tiled, eosinophilic,
with a vesicular nucleus), which secrete androgens.
Histogenesis of testicular tumours
The most frequent testicular tumours are actually secondary tumours: reticuloendothelial neoplasms
and
metastases from lymphomas, leukaemias, prostate, lung, kidney and skin cancer.
Primary tumours are divided into three groups, and may be pure or have several histological
patterns.
● Germ cell tumours (90%):
o Seminomas: most frequent around the age of 40; the pure or typical form produces neither α-FP
nor β- hCG and has marked lymphotropism.
o Non-seminomas (non-seminomatous germ cell tumours): embryonal carcinoma (20%);
teratoma and teratocarcinoma (produce neither α-FP nor β-hCG); endodermal breast or yolk
sac tumour (occurs in infancy; produces α-FP and not β-hCG); choriocarcinoma (1%, is the
most aggressive and produces β-hCG)
o Mixed forms including seminomatous and non-seminomatous cells.
● Sexual cord stromal tumours (5-10%): Leydig, Sertoli or
granulosa or gonadoblastoma.
● (!) Mixed germ-stromal tumours: e.g. gonadoblastoma. Increased AFP in the presence of
seminomatous histology supports the diagnosis of a mixed tumour.
● (+) Testicular lymphomas: these are the most frequent tumours in the elderly, over the age of 60
(!).
A more recent classification divides testicular tumours into two groups according to histogenesis:
● tumours arising from GCNIS (germ cell neoplasia in situ, which gives rise to most germ cell
tumours) (!);
● cancers not arising from GCNIS.
Paratesticular tumours: they affect the envelopes of the testis. They include: adenomatoid tumour cystadenoma of the epididymis - desmoplastic round cell tumour - neuroectodermal melanotic tumour
- mesothelioma
Clinic
It generally presents as a monolateral indolent hard-ligneous mass (but is bilateral at diagnosis in
2% of cases); more rarely there may be pain (20-30%, due to an increase in volume sometimes due to
intratumoural haemorrhage) and manifestations of dyscrinia such as gynaecomastia (7%) - abdominal
or supraclavicular adenopathy.
+Abdominal pain from retroperitoneal compression, lymph stasis in the lower limbs or appearance of
varicocele, secondary hydronephrosis (compression of the ureter), neurological compression syndrome
of the lumbar plexus, thoracopulmonary syndrome (haemoptysis, coughing, dyspnoea, chest pain),
fractures or bone pain, cervical lymphadenopathy.
Diagnosis
Once the mass is appreciated (bimanual palpation), a testicular ultrasound is performed to
characterise it (hypoechogenic, more or less inhomogeneous nodule) and to study the contralateral
testicle (and the inguinal region, high-frequency 14 MHz surface probes), ultrasound of the complete
abdomen.
The search for the following tumour markers is also indicated:
● alpha-fetoprotein: specific for non-seminomas, and very often positive in yolk sac tumours. If it
is positive in a patient with a histological diagnosis of seminoma, it means that it is a mixed tumour
with seminomatous and non-seminomatous cells.
● β-hCG: frequently increased in non-seminomas (especially in choriocarcinomas), but also in 30%
of seminomas.
● LDH: non-specific marker of cell damage, increases in 80% of advanced testicular tumours in
proportion to tumour volume.
Specific molecular markers
● n-Myc: seminoma - embryonal carcinoma
● c-Ki-Ras: immature seminoma
● c-erb B1: teratoma
A thoracic-addomino-pelvic CT scan is performed for staging purposes, looking for metastases in
the pre-.
/para-aortic, lung and liver. In case of suggestive symptoms or an advanced tumour, bone
scintigraphy and brain MRI can also be performed.
The following must be considered in the differential diagnosis: orchiepididymitis, inguinal hernia,
torsion of the funiculus, hydrocele, haematocele, cysts of the epididymis, malignant or benign
neoformations of the epididymis or spermatic funiculus.
TNM staging
It is special because it includes the S-parameter for circulating tumour markers.
Primary tumour
● Tis: Germ cell tumour in situ (GCNIS)
● T1: tumour limited to the testis; may invade the tunica albuginea but not the tunica vaginalis.
● T2:
o invasion of the vaginal tunic;
o tumour limited to testis and epididymis but with vascular/lymphatic invasion.
● T3: invasion of the spermatic funiculus.
● T4: invasion of the scrotum.
Regional lymph nodes (retroperitoneal, pre- and para-aortic)
●
1-4 lymph nodes.
●
5 or more lymph nodes (or lymph node mass >2 cm before biopsy).
●
lymph node mass >5 cm.
Distant metastasis
● M1a: metastasis to non-regional lymph nodes or to the lung.
● M1b: metastasis in other organs, including non-regional lymph nodes.
Circulating tumour markers
●
within the norm.
●
LDH <1.5* and hCG <5k and AFP <1000
●
LDH 1.5-10* or hCG 5-10k or AFP 1-10k
●
LDH >10* or hCG >10k or AFP >10k
*for the upper limit of the standard
Staging
● Stage I: tumour limited to the testis.
● Stage II: involvement of retroperitoneal lymph nodes.
● Stage III: involvement of supradiaphragmatic lymph nodes or other distant organs.
High lumbar aortic lymph nodes (retrocaval, caval and inter-caval aortic on the right, preaortic and
lateroaortic on the left)
IGCCCG (International Germ Cell Cancer Collaborative Group): a prognostic system applied to
metastatic germ cell tumours, taking into account histology and location of the primary tumour,
location of metastases and pre-chemotherapy levels of circulating markers.
Focus: regional lymph node stations affected by different urological tumours
● Bladder and prostate cancer: iliac (intrapelvic) lymph nodes
● Tumours of the penis and scrotum: inguinal lymph nodes.
● Tumour of the testis: para-aortic and para-caval lymph nodes. This is due to the embryological
origin of the testis, which forms in the abdomen near the kidney and then descends into the
scrotum 'carrying' its own vessels (e.g. the spermatic vein flows into the kidney).
● Renal tumours: para-aortic and para-caval lymph nodes at the level of the renal a. and v. origin.
The lymph node stations follow the course of arterial vessels: para-aortic → common iliac lymph
nodes
→ external iliac → femoral lymph nodes (can be explored in the groin, in Scarpa's triangle, at the
emergence of the femoral artery from the pelvis) → internal iliac lymph nodes (run with the
hypogastric or internal iliac artery on either side of the pelvis into the obturator hollow, and then
continue along the pudendal artery which behind the ischial tuberosity leads to the perineum and
genital organs).
Treatment
In all suspected cases we proceed with inguinal orchiectomy (!): neither testicular biopsy nor scrotal
access is indicated, due to the risk of dissemination (!!) + placement of testicular prosthesis
(testosterone supplementation may be necessary, and cryopreservation of sperm is possible).
Interventions:
● Intraoperative tumourectomy and histological analysis for small or suspected benign lesions
(organ sparing surgery);
● Orchifunicolectomy (removal of testicle and spermatic cord up to the inner inguinal ring) for
voluminous lesions or in the presence of metastatic disease at preoperative staging.
In the case of a testicular tumour, a high inguinal incision has to be made during orchidectomy, the
testicle has to be pulled out and the spermatic cord has to be closed at the inner inguinal ring ('because
in this way the lymphatics of the tumour are not connected to the inguinal lymph nodes, as is the case
when operating through a scrotal incision').
On the basis of the definitive histological analysis, completion of therapy may be carried out by
adjuvant chemotherapy or radiotherapy, or by retroperitoneal lymphadenectomy surgery (possibly
using a nerve sparing technique).
Marker dosing before surgery and 5-7 days afterwards is indicated.
Depending on the stage and risk, they may follow:
● simple surveillance;
● retroperitoneal lymphadenectomy;
● adjuvant chemotherapy with BEP protocol (bleomycin, etoposide, cisplatin);
● radiotherapy (only for seminomas).
Survival with treatment at 5 years is 95% (and 99% if diagnosed at stage 1). Follow-up after curative
therapy lasts 5 years and is performed by marker assay and thoracic Rx or thoraco-addomino-pelvic
CT.
SKIN AND SUBCUTANEOUS PATHOLOGIES
They can give rise to hyperacute phlogosis that can develop into abscesses, and they can also give rise
to aesthetic alterations.
1. Subcutaneous pathologies
-
Sebaceous cysts
Lipomas
Lymph nodes
Polonidal cyst
Haematomas
They are malformations of surgical attention
2. Skin disorders
They are generally benign, easy to diagnose but for the patient also annoying. These include:
-
Cutaneous papillomas, polypoids that become large enough to give silhouette changes
Seborrhoeic warts, on the extremities. Those on the soles of the feet are the most annoying,
a sense of 'pebble in the shoe' that can give alterations in walking.
More
Skin lesions that are malignant or doubtful must be treated in cooperation with the dermatologist.
CISTI SEBACEE
Tumours of varying size, especially in the scalp or in areas that are perhaps not very evident, can reach
a considerable size because they are not treated. More frequent in the scalp, face, chest wall.
True sebaceous cysts from obstruction of the excretory duct of the gland can result in hyperacute
inflammation with the need for emergency surgery to drain the abscess contents. It is therefore
important not to delay treatment.
To be distinguished from dermal inclusion cysts, typical in the area of previous traumas, which
involve a deconstruction of the gland especially in the outer portion, where the 'mouth' sprouts on the
skin surface and which serve to release the sebum that lubricates the skin. If it is damaged, there will
no longer be this communication with the outside and so it continues to produce, but not to be emitted
to the outside.
They assume relationships and adhesions with the overlying skin, which is important from a
therapeutic point of view.
Surgical indications
When the swellings exceed half a cm, they are palpable and therefore a simple surgical excision may
be recommended. It is done under local anaesthesia and the cyst including the cyst wall is completely
removed. The excision is done by also removing the lozenge of skin where the cyst is attached. The
swelling is removed intact. The cyst wall will be whitish and sebum is contained inside.
They are also removed when they become infected. Antibiotics are useful in the early stages. With
regard to antibiotics, if all the elements of inflammation have not yet developed, antibiotic therapy can
still be helpful in stopping the inflammatory process and preventing it from developing into an
abscess. If the surrounding cellulitis is already present then it is not so useful.
Often, however, the patient does not initiate treatment but rather causes trauma by squeezing.
However, when it becomes infected, the ideal is to incise and drain the cyst, but this does not give the
certainty of having removed the whole capsule and this can result in a recurrence over time.
It is more correct to speak of a new operation when the cyst has been drained, so it will be done when
the inflammatory process has resolved; a second operation is recommended to remove that lozenge of
skin to make sure that all residue has been removed.
When the cyst is incised, an almost caseous pus with a pungent odour comes out. It is washed out with
gauze, which with its rough surface helps to remove as much of the capsule as possible (without
having the certainty of complete elimination). However, if there is infection this enucleation does not
give certainty of complete excision of the cyst wall.
The ancients preferred closure by second intention of the surgical wound. It is a safe method but it
prolongs healing time and the dressings are poorly tolerated by the patient. Closing by first intention,
on the other hand, requires some certainty of having done a good cleaning to avoid residues giving
reinfection, so if the margins are doubtful it is better to leave it for second intention. But of course this
is almost pre-antibiotic era, but nowadays even wounds that are not so perfect are closed by first
intention thanks to antibiotics.
LIPOMS
They are very frequent benign tumours. They can alter aesthetics especially in exposed areas. In all
cases, however, they are benign and must be distinguished from subcutaneous liposarcomas, which
are, however, very rare. They are asymptomatic. They also grow rapidly. More frequent from 40 to 60
years of age. There are also angiolipomas and neurolipomas, which are, however, more painful.
Solitary lipomas more frequent in women, multiple ones in men. Multiple lipomatosis with autosomal
dominant transmission more frequent in men where there is multicentric development of lipomas.
They develop from the adipose layer between the superficial fascia and the underlying muscle fascia.
Intramuscular lesions are often painful. They have a soft consistency, mobile in the superficial and
deep planes, so a correct EO allows these lesions to be appreciated. It may be useful to continue with
an ultrasound to understand the relationship with the underlying muscles as well. Ultrasound is always
useful before incisions.
Surgical indications
When it gives spontaneous or provoked pain, due to aesthetic considerations or malignant
degeneration (fixed, hard ligamentous mass) Surgical technique: excision under local anaesthesia,
except for large size. Skin incision with a length of 1/3 the diameter of the lipoma. No vascular pedicle
in small lesions (may be present in larger lesions or angiolipomas). Intervention more difficult in
"racemose" lipomas with a very thin capsule and clustered appearance, where non-radiation leads to
recurrence; they are more frequent in the nape of the neck and upper back.
LINFONODS
The lymph node stations of the superficial planes are:
- Laterocervicals are studied for suspected lymphomas on indication of biopsy by the
haematologist
- Overclaves
for disease lymphoproliferative disease o
for metastases
from
thoracic/abdominal carcinoma
- Axillaries
- Inguinals
They are generally enlarged due to inflammatory processes [in the lower (inguinal) or upper (axillary)
extremities] or neoplastic lesions (breast cancer - axillary lymph nodes). A lymph node that is enlarged
and painful on palpation points towards an inflammatory process
-septic , if, on the other hand, they are elastic but not painful, they are the site of lymphoproliferative
processes. In the past, one could also think of tubercular caseosis.
Surgery
Cervical and axillary ones are more difficult to extract. Moreover, they are usually in close proximity
to vessels, so be careful with dissection and haemostasis. The vascular pedicle must always be ligated
beforehand.
HERISIPELA
Erysipelas is an acute skin infection, involving the deep dermis and partly the hypodermis, caused by
pyogenic bacteria; group A beta-haemolytic streptococcus is the main culprit, but staphylococcus
aureus or other less common germs are sometimes involved. Diagnosis is clinical. Treatment consists
of the administration of oral or EV antibiotics.
VASCULAR PATHOLOGY
MESENTERIC ISCHAEMIA/ANGINA ABDOMINIS
Abdominal angina (also known as angina abdominis) is a clinical syndrome characterised by severe
post-prandial abdominal pain. Similar to the better known angina pectoris, abdominal angina is also
due to an ischaemic picture, i.e. a progressive reduction in blood flow, which becomes insufficient to
meet the demands of certain organs. Unlike 'pectoris', which affects the heart, angina abdominis is
related to chronic intestinal ischaemia.
For the condition to manifest itself, stenosis (occlusion of at least 50% of the lumen) of at least two of
the three major mesenteric vessels is required.
The symptoms of abdominal angina are most evident after meals, as digestion increases the intestine's
demand for oxygen, and thus blood, at such times. The abdominal pain, cramp-like and localised under
the sternum (epigastric site, corresponding to the central part of the upper half of the abdomen), may
continue for several hours after the meal, and is accompanied by diarrhoea, flatulence and
malabsorption. The severity of the pain associated with angina abdominis is such that the subject is
forced to refrain from eating as much as possible; the patient loses weight and may develop cachexia.
If the condition is not adequately treated (by baypass or angioplasty), the occlusive phenomenon may
worsen, leading to thrombosis with mesenteric infarction; this results in irreversible necrosis of the
affected intestinal segment and peritonitis.
AOP
Peripheral arteriopathy obliterans is a medical condition in which there is a localised obstructive
lesion downstream of the renal arteries, with hypoperfusion of the lower limbs. The aetiology is in the
vast majority of cases atherosclerotic in nature. Acute or chronic ischaemia results.
Mortality is high (3 times that of an age-matched control population) and the incidence of acute cardio
-vascular events is high.
Risk factors: these are the classic ones of atherosclerosis:
●
●
●
●
●
Male gender;
Ethnicity.
Cigarette smoking (e.g. 60 cigarettes per day)
Diabetes;
Dyslipidaemia
● Arterial hypertension (which creates mechanical damage to the vessel endothelium that
normally keeps the thromboxane-prostacyclin haemostatic balance in balance, maintains
vasomotion, acts on coagulation problems; the endothelium can therefore be injured either by
inflammatory factors or by haemodynamic factors);
● Renal failure;
● Metabolic syndrome
● Ischaemic heart disease
● States of hypercoagulability
● Cerebrovascular accidents
Clinic
Clinically, AOCP is manifested by the 5Ps (Anglo-Saxon literature):
1.
2.
3.
4.
5.
Pain
Pallor (pallor)
Paresthesias (paresthesia)
Absence of peripheral pulses (pulselessness)
Paralysis
Leriche-Fontaine classification
According to the Leriche-Fontaine classification, AOCP is classified into four stages:
● 1st stage absence of premonitory symptoms/signs
● 2nd stage exertional pain (claudicatio intermittens):
o Stage 2A running range > 200 metres
o Stage 2B running range < 200 metres
● Stage 3 Pain at rest: localisation is distal, affecting the toes, the foot, also with irradiation to the
legs. It increases with clinostatism and with exposure to cold, while it decreases in orthostatism
and with exposure to heat.
● 4th stage trophic disorders: necrosis and gangrene
One could make a presumptive diagnosis based on the site of the pain:
Localisation of pain
ATS lesion localisation
calf
femoro-popliteal
hip-gluteus
aorto-iliacs
malleolus-foot
tibialis
leg
popliteal
thigh
iliac-femoral
EO
It is based on 3 semeiological times (inspection, palpation and auscultation, while percussion is not
useful).
The inspection is used to assess skin colour (pale, cyanotic), thinning of the hair, nail dystrophies,
oedema, various skin lesions, muscle trophism, symmetry/asymmetry between the two limbs and
finally any pulsating aneurysms, interdigital fissures (caused by mycosis);
Palpation is used to assess the temperature, for example the presence of any thermal step (remember
that it is assessed with the back of the hand) and also allows us to palpate the peripheral wrists (telling
us if there is normosfigmia, hyposfigmia or absence of the wrists). If on inspection we had seen a
pulsation we go to palpate that area, the sensation we get is that of a tremor. The wrists that we can
palpate at the level of the lower limbs are:
● Femoral pulse (at the level of Scarpa's triangle) there are 3 femorals:
o Common femoral (which is the palpable one),
o Deep femoral (running posteriorly),
o Superficial femoral (running in the medial aspect of the thigh).
Shallow and deep cannot be palpated;
● Popliteal pulse (at the level of the popliteal cord): this is assessed by flexing the leg in a
supine position or by having the patient lie prone and bend the leg a little (about 30°); it is a
very difficult artery to palpate;
● Posterior tibial artery pulse: in the medial malleolus .
● Pulse of the pedidian artery (on the back of the foot, this would be the end of the anterior
tibial artery)
Auscultation allows us to tell whether there is stenosis or not, from the possible presence of the
systolic murmur. The arteries that can be auscultated are: the iliac, but one cannot discriminate
whether it is the common or the external, while the internal cannot be auscultated; the common
femoral (as opposed to the superficial and the deep, which cannot be auscultated); the popliteal,
which can be auscultated with the smaller bell of the phonendum. The tibial and pedidian cannot be
auscultated.
On auscultation, the murmurs indicate the presence of turbulent flow and therefore stenosis. The
extent of the stenosis can be established auscultatorily: the murmur becomes more prominent and rude
as the stenosis becomes more severe. A murmur in a non-restricted artery can be caused by
hyperthyroidism (due to hyperkinesis).
Vascular objective examination of the lower limbs:
● Pale limb;
● Thermothermal cold;
● Painful both at rest and on palpation;
● Hypaesthesia (reduced sensitivity); sensitivity is assessed with a pencil point or brush passed
over the area while the subject's eyes are closed;
● Hyposfigmia of the femoral wrist;
● Absence of the popliteal, tibial and pedidio poles;
The most important compensation circle we have in our legs is the deep femoral artery.
DD DVT: in DVT the limb shows signs of congestion, whereas in this case the limb is pale and cold.
Signs and symptoms
AOP
TVP
Cute
Pale and cold at the thermotatto Red and thermally warm.
In severe cases cyanotic and
cold (phlegmasia cerulea
dolens)
Pain
At
rest,
with
nocturnal Worsens in orthostatic position,
exacerbations, it involves the improves with walking (as the
extremities and forces the
patient to hold
feet out of bed.
muscle pump) and with the
position
clinostatic
With movement, the pain
or placing the
worsens (the demand increases position
limb in unloading
metabolic
which not is
balanced
by
normal
blood perfusion)
Tumor
Absent
Present
Ancillary symptoms
Paresthesias and paralysis of
the limb
Feeling of heaviness
Ancillary signs
concerned
Ischaemic-based ulcers or
Gangrene
to the limb
Dyschromia from previous
DVT or
Peripheral wrists
Absent
superficial thrombophlebitis
Present
Skin adnexa alterations
Present
Absent
The instrumental examinations are:
● ABI index (ankle/arm): in this case it will be less than 1 (normal value 1);
● Arterial echo-colour doppler
● Angio-CT abdomen and lower limbs
Therapy
The strategy to improve the patient's symptoms is to make him walk as much as possible, exercising
him and trying to reduce the pain. The ideal would be treadmill training, but more simply, 'brisk
walking' can be done. First of all, one assesses how long it takes the patient to complete a certain
route, then one asks him to do it in an ever shorter time. The aim is to activate the collateral circles,
since the most important vasodilatory stimulus in our organism is precisely ischaemia, which causes
the release of various vasoactive substances.
● Antiplatelet
● Vasoactives (a-blockers, nitrates, calcium channel blockers)
● Painkillers
Surgical therapy
●
●
●
●
Angioplasty
By-pass
Amputation
Thromboendarterectomy (DVT)
VARICOSE VEINS OF THE LOWER LIMBS
Dilatation and tortuosity of superficial venous vessels with associated valve system insufficiency.
Varicose veins are characterised by elongation, dilatation and tortuosity of the affected (superficial)
venous vessel. It involves the 3 tonaches of the vessel: intima, media, adventitia.
Pathology with a high prevalence in the population, especially women. If advanced, it is a pathology
of surgical interest (various types of more or less invasive interventions). They have a frequency of
between 15-35%. They affect women more frequently, but in men the damage is more severe.
They can be:
● Congenital (very rare)
● Acquired
o Primitive (due to valve or wall defect, called essential)
o Secondary (due to thrombosis at the level of the saphenous-femoral ostium at the ileum
resulting in an absent or limited drainage of the great saphenous vein, so that all the
blood stagnating upstream is secondary to a thrombotic stop of the venous drainage).
In the thigh the manifestation is minimised by the panniculus adiposus compared to the leg (from the
knee down). On inspection, cocooning can be seen.
Lower limb venous circulation
Superficial venous system
● Great saphenous vein or internal vein: arises from the medial/internal malleolus of the leg to
the outlet at inguinal level (lacuna vasorum) on the femoral vein through the saphenous femoral
ostium.
● Small saphenous or external vein: arises from the external malleolus and flows into the
popliteal cavity
Deep venous system
● Tibial veins
● Popliteal veins
● Femoral veins
Semilunar valves: these have the role of lowering the blood column (they dampen P) and allow
unidirectional flow (circulation is anti-gravitational).
Femoral saphenous ostium: a semi-lumenal valve located at the inguinal level where the great
saphenous vein flows into the femoral vein. Its insufficiency results in regurgitation from the femoral
(and therefore vv iliac-caval) to the great saphenous vein. This is the primum movens for the
development of the pathology. It is accompanied by insufficiency of the other small semilunar valves.
Communicating veins: carry blood from the superficial to the deep circulation.
In the case of valvular insufficiency/incontinence, there is a reversal of flow and hyperreflux in the
superficial circulation, which is not accustomed to such P in the absence of containing muscles, so
varicose veins are observed. True reflux occurs. The valves have the role of fragmenting/splitting the
blood column. When there is no longer this columnar fragmentation the column of blood exerts a P of
gravity especially in the most declivous parts which in this case are at the level of the malleolus.
Predisposing factors (to be analysed at the history)
●
●
-40 yr, max. peak 50-60 yr)
(think correlation with oestrogen)
● Familiarity (next of kin must be analysed)
● Pregnancy (repeated), compression stasis: the volumetric increase of the uterus in the abdomen
goes
compressing the caval system□ difficulty in venous drainage reflected at lower limb level
● High heels: the heel raises the heel vs. the forefoot and causes Lejark's plantar pump/heart to be
lost (less return to the heart). In addition, the foot is in an equine position and the twins contraction
during walking is lost (mm contraction of the sura).
● Prolonged standing (standing still): the column of blood in the vessel strains the vessel. E.g.
occupational diseases: surgeons (there must be a predisposition).
● Obesity: plays an important role in slowing down venous return at central level
Typical symptomatology
● Gravitational pain: is given by the P that the blood column exerts. Greater in the most declivous
regions. Less in the morning (during the night the blood column is lowered), greater in the
evening, decreases with walking, but increases with prolonged standing (dd arterial: claudicatio
intermettens)
● Subcutaneous oedema: in the most declivous parts (ankles), presence of fovea in the malleolar
region, especially in the evening.
● Skin pigmentation: amber-coloured appearance because chronic venous insufficiency results in
hemosiderin deposition.
Complications
In the long run there is an arteriolar effect with stasis and tissue damage. (+ aesthetic)
● Eczema: the patient sometimes has itching due to stagnation of blood and lesions from lack of
trophism
● Necrosis and ulceration: these are difficult to resolve, usually at the malleolar areas
● Phlebo-thrombosis: occurs because in venous dilatations blood tends to stagnate and especially in
the summer period blood tends to thrombose. The formation of the thrombus triggers an
inflammatory reaction. If not treated properly, a blood clot can form, resulting in PEPT.
● Venous haemorrhage: can be significant (copious), the column of blood (not interrupted) is in
continuity with the cava. The doctor must make an abundant containment bandage. They
generally develop from minor damage: malleolar region and foreign body.
Semeiological evidence
● Trendelemburg test, assesses the continence of the saphenous-femoral ostium: the patient is
placed supine with the limb (rigid, thighs flexed on the pelvis and leg hyperextended) raised t o
allow emptying of the superficial circulation (cocoons are lost). A tourniquet is then applied to the
root of the thigh, the patient is then placed in an orthostatic position and, after removing the
tourniquet, we observe the presence of varices.
● Perthes test, assesses the continence of the communicating veins: the patient remains in an upright
position, we apply a tourniquet to the root of the limb, we then invite the patient to make flexionextension movements of the leg (thus activating the muscular pump): in the case of valve
continence we may notice the disappearance of the varices.
● Swartz test, evaluates the valvular continence of a specific varicose segment placed between two
fingers of the hand in light compression of the ostium, exerting repeated percussion on the
upstream vein with the index finger of the other hand.
Instrumental semiotics (usually history, EO is sufficient) pre-intervention
● Non-invasive, echo-colour-doppler: it investigates the direction of the flow that will be reversed.
I first analyse reflux at the level of the OSF (regurgitation), it allows us to assess its continence: it
can
be partially continent and there is incontinence during pontication manoeuvres (increased intraabdominal P and slowed venous return); if reflux is present in orthostatism it means that the loss of
continence is (almost) total. The doppler then goes to analyse the whole venous tree, the good
dopplerist goes to point out the most tortuous tracts and the insufficient perforating veins.
● Invasive: phlebography
Surgery
Medical therapy: elastic stockings
It is unlikely that there is a need for emergency surgery. More frequent is the scheduling of elective
surgery, however, the pathology should not be allowed to progress towards complications (drift). The
surgeon's enemy is the adhesions that form as a result of inflammation, e.g. thrombophlebitis
complicates the operation.
The interventions used are:
Stripping (removal of the affected vein) under general or spinal anaesthesia in patients with
cardiorespiratory pathologies; stripping should always be completed with sclerotherapy of the smaller
collaterals of the saphenous vein
Surgery involves an incision at the inguinal level with identification and isolation of the outlet of the
great saphenous vein in the femoral. Depending on the stage of the pathology, it can be performed:
● In the early stages a ligation of the great saphenous vein and its collaterals at the outlet to the
femoral vein (OSF), without stripping
● In cases of insufficiency, tortuosity the vein must be removed, long stripping: subcutaneous
removal, after ligation of the collateral veins, by means of a probe: this enters at the inguinal level
and exits at the malleolar level (medial malleolus). Malleolar time: the great saphenous vein is
isolated at the malleolar level and the probe is felt to arrive. Sometimes the probe does not proceed
smoothly through the great saphenous vein but can become wedged in the tortuosity, in these cases
it is preferable to make small surgical incisions (eyelets) to advance it.
In the days following the surgical event, the limb must be bandaged with elastic gauze, and
extravasation must be avoided. These are mainly a form of containment for the oedema that will form
post-surgery.
Sclerotherapy under local anaesthesia: closure by chemical effect: a tissue irritant is injected into the
vessel, which causes the walls to collaborate and prevents the formation of thrombi; a superficial
vessel phlebitis is created, allowing it to be destroyed; it is an immediate treatment and the vessel is
eliminated and the patient must be bandaged for at least 24 hours. Its field of application is limited to
those patients who do not want or cannot undergo traditional surgery, or to those cases where surgical
therapy h a s failed.
Operations where valves are implanted are also planned.
short stripping: incision either in the groin or ankle (approach from below preferred) □ isolation of
the junction between saphenous and femoral veins□ detachment of the 3 collaterals (epigastric,
circumflex and pudendal) (which can give recurrences)□ insertion from below or above of the probe□
proceeding inside the saphenous vein along its entire length and then put
an ogive (a kind of plug) on the extremity □ the saphenous vein is stripped (pulled out)□ the
saphenous canal is compressed to avoid haematoma (a possible complication that can give pain).