Core Clinical Problem: Abdominal Mass
Underpinning Sciences
Basic Medical Sciences
Structure or function of internal abdominal organs including their
surface markings
Clinical Sciences
Pathophysiology of index conditions or their underlying cause
Behavioural Sciences
Population Health Sciences
Preventative measures for reducing incidence of bowel cancer and
diverticular disease
Role of alcohol in chronic liver disease (hepatomegaly) and portal
hypertension (splenomegaly)
Index Conditions
Common or less
common but dangerous
Hepatomegaly (see problem 67)
Splenomegaly (see problem 5)
Englarged kidney's (e.g. polycystic disease)
Bowel masses (malignant, inflammatory, faecal)
Enlarged bladder
Aortic aneurism
Uterine/ovarian masses (e.g. pregnancy, fibroids, cysts, malignant)
Abdominal wall hernias
Lymph nodes
Infective causes
Uncommon but
illustrative
Structure of internal abdominal organs
Contents of the abdominal cavity that can cause masses Stomach
 Bladder
 Pancreas
 Lymph nodes
 Small bowel
 Female reproductive tract
(ovary, fallopian tube, uterus
 Large bowel- including
and cervix)
appendix
 Gallbladder
 Liver
 Aorta- and other vessels
 Spleen
 Kidneys
 Adrenal glands
Abdominal mass or distension
An abdominal mass is sometimes discovered by the patient, but more commonly by a
medical examination. An older patient with a definite palpable mass is likely to have a
malignant tumour, but benign cysts, inflammatory masses, aneurysms or atypical
hernias may be responsible. Occasionally masses have a ‘medical’ cause, e.g.
hepatosplenomegaly of chronic lymphocytic leukaemia. Commonly, one of the ‘five
Fs’- foetus, flatus, fluid, fat or faeces- may masquerade as a ‘surgical’ mass or
distension. An abdominal mass may be discovered without any related clinical
features; usually, however, the patient has GI symptoms, anaemia or jaundice in
addition.
Clinical assessment of an abdominal mass:
History: provides clues to specific organ involvement and important features to
include are- how long has it been there; how did the patient come to notice it; is it
always present or does it sometimes disappear (e.g. a hernia may reduce); is it getting
bigger or smaller? A history of intra-abdominal malignancy years before should be
regarded with grave suspicion: the disease may have recurred or a related new
primary developed. This is especially common in large bowel cancer but uncommon
after 7 years.
Examination: general examination should be to seek systemic signs of disease (e.g.
cachexia, anaemia and jaundice) or signs of malignant dissemination (e.g.
supraclavicular lymphadenopathy in suspected gastric cancer). Abdominal and pelvic
examination must be thorough and, if appropriate, proctoscopy and sigmoidoscopy
should be performed.
Examination of an abdominal mass: the location of the mass, its relations to other
structures, its mobility and its physical characteristics, such as size, shape, consistency
and pulsatility give valuable information about the organ of origin and likely
pathology. Hernias, e.g. incisional, umbilical and sometimes interstitial (Spigelian)
hernias, may present as localised swellings but they usually shrink or reduce
completely when the patient is supine or under anaesthesia. Unless the diagnosis of a
hernia is considered, it may be overlooked. An incarcerated hernia is more
appropriately considered a true ‘mass’.
Examination of masses in specific regions of the abdomen
Mass in the RUQ- usually hepatobiliary in origin. If so, it will be continuous with the
main bulk of the liver both to palpation and percussion. When the liver is diffusely
enlarged, the inferior margin is regular and well defined and the consistency is usually
normal. When infiltrated with primary or secondary cancer, the palpable liver may be
hard and irregular or the liver may appear diffusely enlarged. Carcinoma of the
gallbladder is indistinguishable from hepatic cancer on palpation. Rarely, a Reidel’s
lobe- a congenitally enlarged part of the right lobe- is mistaken for a pathological.
Less commonly, a right hypochondrial mass is a diseased gall bladder. When a liver
mass is suspected, other signs of liver disease should be sought. A mass continuous
with the liver above and with a typical pear-shaped rounded outline is likely to be a
mucocoele of the gall bladder. A more diffuse tender mass may be an empyema of the
gall bladder.
Epigastric mass- a mass in the epigastrium is usually due to a cancer of the stomach
or transverse colon or sometimes omental secondaries from ovarian carcinoma.
Cancer involving the left lobe of the liver may also present in this way. These masses
are usually hard and irregular and are mobile or fixed according to the degree of
invasion. Occasionally an epigastric mass is an isolated enlargement of the left lobe of
the liver or massive para-aortic lymph nodes due to lymphoma or testicular
secondaries. A pulsatile epigastric mass is likely to be an abdominal aortic aneurysm.
Mass in the LUQ- a cancer of the stomach or splenic flexure of the colon may
present as a mass in the left hypochondrium. Tumour masses can usually be
distinguished clinically from an enlarged spleen as the latter often has a discrete
‘edge’ and lies more posteriorly.
Mass in the loin or flank- most likely to be of renal origin and felt best on bimanual
palpation. Very rarely a hernia occurs in the lumber region.
Mass in the left iliac fossa- masses in the left iliac fossa usually arise from the
sigmoid colon. A hard faecal mass may be mistaken for a cancer but it can often be
indented like putty. A solid sigmoid mass is usually due to a tumour or a complex
diverticular inflammatory mass. Ovarian masses and sometimes eccentric bladder
lesions may be palpable in either iliac fossa. These lesions, however, arise from out of
the pelvis and can often be pushed up on to the abdominal examining hand by digitial
pressure in the rectum or vagina (bimanual palpation-most effectively performed
under GA). Hernias in the groin are common and may be chronically irreducible
(incarcerated). Occasionally, are interstitial (Spigelian) hernia develops above the
groin in either iliac fossa. This presents a somewhat confusing picture on examination
by virtue of its site and because the peritoneal sac herniates between layers of the
abdominal wall.
Suprapubic mass- usually arise from pelvic organs such as the bladder or uterus and
its adnexae. A palpable bladder is most commonly due to chronic urinary retention
and the patient should be catheterised and then examined again. A distended bladder
is dull to percussion and disappears on catheterisation. Bladder enlargement is usually
symmetrical and may extend above the umbilicus. The margins may be difficult to
define accurately because of the bladder’s soft consistency. Only massive bladder
tumours are palpable and would be accompanied by urinary tract symptoms and urine
abnormalities. Sometimes large bladder stones are palpable abdominally. A uterus
may be palpable abdominally when enlarged by pregnancy or fibroids. Ovarian
tumours, particularly cysts, may become enormous and extend well up into the
abdomen; again, bimanual examination helps to distinguish the origin.
Mass in the right iliac fossa- the right iliac fossa is a common site for an
asymptomatic mass. It may be due to unresolved inflammation of the appendix which
becomes surrounded by a mass of omentum and small bowel, giving rise to an
‘appendix mass’. There is usually a recent history of right iliac fossa pain and fever. A
carcinoma of the caecum may become very large without causing symptoms of
obstruction because the caecum is large and distensible, and the faecal stream at this
point is quite liquid. Thus, a caecal carcinoma often presents as an asymptomatic right
iliac fossa mass; iron deficiency anaemia is often evident by this stage. Crohn’s
disease of the terminal ileum often presents with a tender mass, usually with typical
symptoms of pain and diarrhoea.
Central abdominal mass- may originate in the large and small bowel, as a result of
malignant infiltration of the greater omentum or from retroperitoneal structures such
as lymph nodes, pancreas, connective tissue or the aorta. Retroperitoneal masses are
often only palpable if they are large. One of the most common central abdominal
masses is an aneurysm of the abdominal aorta. Aneurysms usually arise just above the
aortic birfurcation (at the umbilical level) which explains their central location in the
upper part of the abdomen. The characteristic feature of an aneurysm is its expansile
pulsation; other solid masses may transmit pulsation from large vessels nearby, but
these masses are not expansile. Several different types of hernia may present near the
centre of the abdomen. Most common is an incisional hernia which protrudes through
part or the whole of an abdominal wall incision. This may occur at any time after the
operation, from days to years later. It usually results from poor closure technique or
post-operative infection. Para-umbilical or umbilical hernias, common in the obese,
occur centrally and diagnosis is usually straightforward. Divarication of the recti
(rectus abdominal muscles, not a true hernia) involves the recti being splayed apart,
often as a result of pregnancy or obesity, leaving the central anterior abdominal wall
devoid of muscular support. This condition is easily recognisable because of its
typical ‘keel’ shape and its symptomless nature; treatment is rarely necessary.
Divarication and midline hernias can best be demonstrated when the abdominal
muscles are contracted, e.g. the supine patient raises both heels from the bed.
Rectal mass and findings on pelvic examination- An abdominal or pelvic mass may
be palpable solely on rectal (or vaginal) examination. The mass may be a rectal cancer
or a cancer in the loop of the sigmoid colon lying in the pelvic cavity; the latter is
unlikely to be visible on sigmoidoscopy. Sometimes, secondary deposits from an
impalpable tumour in the upper abdomen may seed the pelvic cavity. This may
produce a hard anterior lump or even a solid mass filling the pelvic cavity. The latter
condition is known as a frozen pelvis. Frozen pelvis can also occur with
endometriosis or local spread of a carcinoma of cervix or, rarely, prostate.
Interpretation of finding of ascites
Ascites is defined as a chronic accumulation of fluid within the abdominal cavity and
had many causes, some malignant and some non-malignant. Ascites can usually be
recognised clinically only when the volume exceeds 2 litres, but even then it is easily
overlooked. Dullness to percussion in the flanks and suprapubic region with central
resonance is suspicious of ascites and should be tested with shifting dullness.
Malignant ascites- in ovarian or colonic cancer, the peritoneum is sometimes seeded
with tumour deposits which secrete a protein-rich fluid containing malignant cells.
This malignant ascites may reach a volume of several litres. The peritoneum may be
peppered with thousands of minute seedlings without a palpable mass or there may be
several large masses hidden by the ascetic fluid. Such widespread peritoneal
involvement may cause abdominal distension which is often difficult to recognise on
abdominal examination. It should be suspected if a patient with a past history of GI or
ovarian carcinoma has other symptoms suggestive of malignancy such as anorexia or
marked weight loss.
Lymphatic obstruction- A rare cause of ascites is massive obstruction of abdominal
lymphatic drainage. This is usually caused by malignant involvement of para-aortic
lymph nodes with lymphoma or metastatic testicular malignancy. Chylous ascites, in
which the ascitic fluid is milky-white, is rare and is due to proximal lymphatic
obstruction and the presence of chylomicrons in the fluid originating from mesenteric
lymphatics.
Tuberculosis- abdominal tuberculosis is an uncommon cause in developed countries
but is common in the developing world. TB can occasionally present as ascites; this
form is characterised by multiple tiny peritoneal tubercles, clinically indistinguishable
from tumour secondaries. If discovered at operation, biopsies must be taken because
the condition is usually curable, unlike its malignant counterpart.
Non-surgical- Ascites is commonly caused by gross congestive cardiac failure,
constrictive pericarditis, severe hypoalbuminaemia or portal venous obstruction, the
last occurring in cirrhosis and occasionally with liver metastases.
Diffuse abdominal distension
In diffuse distension without a palpable abdominal mass, sinister causes need to be
excluded. Gas within the bowel is a common cause for long-standing and often
intermittent abdominal pain and distension. It usually occurs in healthy young adults,
particularly women, in association with irritable bowel syndrome or air swallowing
during hyperventilation. Chronic gaseous abdominal distension may also be found in
elderly patients with partial volvulus of the sigmoid colon. Clinical assessment will
usually diagnose these problems and avoid necessary investigation. Gross faecal
loading may also be responsible for abdominal distension. This is often seen in
children with abdominal pain and sometimes in young adults with IBS. Asymptomatic
chronic constipation is common in the elderly, and a faecal mass palpable through a
thin abdominal wall can give the impression of a sinister mass.
Approach to investigation of an abdominal mass or distension
Laboratory tests: Blood, urine and stool investigations will be performed as
suggested by the history and examination, e.g. full blood count, function tests,
dipstick urinalysis and faecal occult bloods.
Radiology: a chest X-ray should be performed if malignancy is suspected. Ultrasound
or CT scanning is useful for demonstrating the size and origin of a mass and one or
other is often the first choice if pathology is suspected in the liver, biliary tree,
pancreas, aorta or pelvic organs, or to confirm ascites. For pelvic masses, transvaginal
or transrectal ultrasound is usually the investigation of first choice. CT scanning is the
most valuable in defining masses in the retroperitoneal area, e.g. pancreas, aorta or
kindeys, but may be the investigation of choice for suspected large bowel cancer in
frail patients. Ultrasound or CT scanning can be used to guide needle biopsy or
aspiration cytology precisely. Contrast studies, e.g. barium meal, barium enema or IV
urography, may be indicated by the clinical findings.
Endoscopy: flexible endoscopic techniques such as gastroscopy or colonoscopy
enable direct examination and biopsy of many GI lesions. Gastro-duodenoscopy is
indicated if symptoms are suggestive of oesophago-gastroduodenal pathology,
flexible sigmoidoscopy or colonoscopy if the findings suggest large bowel pathology,
and ERCP may be used to outline the biliary and pancreatic duct systmens if
appropriate.
Other methods of tissue diagnosis: A tissue diagnosis should be obtained even if
disseminated malignancy seems obvious. It can influence paaliative and supportive
treatment and, occasionally, an apparently hopeless case proves on histology to be
treatable or even curable. Examples are TB, lymphoma or a germ cell tumour such as
teratoma. Techniques of obtaining tissue for histology include needle or excision
biopsy of enlarged cervical lymph nodes, and percutaneous biopsy of liver or an intraabdominal mass (which may be guided by ultrasound or CT). Paracentesis abdominis
(i.e. needle aspiration of ascitic fluid) is a safe and simple way of obtaining a
specimen for cytology and microbiology. Finally, when less invasive methods have
failed to provide the necessary information, direct biopsy of tumour at diagnostic
laparoscopy or open operation usually provides the definitive diagnosis.
Pathophysiology of index cases
HepatomegalyCauses of hepatomegaly: Apparent hepatomegaly= low-lying diaphragm, Reidel’s
lobe (this is a normal anatomical variant of liver tissue from the right liver lobe).
Cirrhosis (only early in the disease).
Inflammation= hepatitis, schistosomiasis, abscesses (pyogenic or amoebic).
Cysts= hydatid, polycystic
Metabolic= fatty liver, amyloid, glycogen storage disorder
Haematological= leukaemias, lymphoma, myeloproliferative disorders, thalassaemia
Tumours= primary or secondary carcinoma
Venous congestion= heart failure (right), hepatic vein occlusion
Biliary obstruction- particularly extrahepatic.
SplenomegalyCauses of splenomegaly: Infection- a) acute, e.g. septic shock, infective endocarditis,
typhoid, infectious mononucleosis.
b) chronic, e.g. tuberculosis and brucellois
c) parasitic, e.g. malaria, kala-azar and
schistosomiasis.
: Inflammation- rheumatoid arthritis, sarcoidosis, SLE
: Haematological- haemolytic anaemia, haemoglobinopathies and the leukaemias,
lymphomas and myeloproliferative disorders.
: Portal hypertension- liver damage
: Miscellaneous- storage diseases, amyloid, primary and secondary neoplasias,
tropical splenomegaly.
Massive Splenomegaly- is seen in myelofibrosis, chronic myeloid leukaemia, chronic
malaria, kala-azar or rarely, Gaucher’s disease.
Enlarged kidneys (e.g. polycystic disease)Causes of enlarged kidneys:
Cystic disease: Solitary or multiple renal cysts are common, especially with
advancing age: 50% of those aged 50 years or more have one or more such cysts.
Such cysts are often asymptomatic and are found on excretion urography or
ultrasound performed for another reason. Occasionally there cause pain or haematuria.
Cystic degeneration (the formation of multiple cysts which enlarge with time) occurs
regularly in the kidneys of patients with ESRF.
Autosomal dominant polycystic kidney disease: ADPKD is an inherited disorder
usually presenting in adult life. Characterised by the development of multiple renal
cysts variably associated with extrarenal (mainly hepatic and cardiovascular)
abnormalities. In about 85% of cases the gene responsible (PKD1) has been located
on chromosome 16. A second gene, PKD2, which has been mapped on chromosome 4
account for the vast majority of cases. These abnormalities are distinct from the
autosomal recessive form of polycystic disease (due to mutations in the PKHD1 gene
on chromosome 6p21.1-p12), which is often lethal in early life. The protein
corresponding to the PKD1 gene, polycystin 1, appears to be an integral membrane
glycoprotein involved in cell-to-cell and/or cell-to-matrix interaction and functions as
a mechanosensor. The protein corresponding to the PKD2 gene appears to function as
a calcium ion channel, regulating calcium influx and/or release from intracellular
stores. Polycystin-1 acts as the regulator of PKD2 channel activity by its colocalisation in cilia of collecting tubular cells. Disruption of the polycystin pathway
results in reduced cytoplasmic calcium, which in principle cells of the collecting duct
causes increase in cAMP via stimulation of calcium-inhibitable adenyl cyclase and
inhibition of cAMP phosphodiesterases. Present as acute loin pain and/or haematuria
owing to haemorrhage into a cyst, cyst infection or stone formation, loin discomfort
owing to increasing kidney size, complications of hypertension, complications of
associated liver cysts, symptoms of renal failure.
Renal vein thrombosis- this is usually of insidious onset, occurring in the nephrotic
syndrome, with a renal cell carcinoma, and in conditions associated with an increased
risk of venous thrombosis (e.g. antithrombin deficiency or the presence of
anticardiolipin antibodies) Anti coagulation is indicated.
Hydronephrosis- this occurs due to obstruction of the urinary tract at any point. The
thing causing the obstruction may be intraluminal, intramural or extramural, the
frequency is the same in men as women. Obstruction with continuing urine formation
results in:
 Progressive rise in intraluminal pressure
 Dilatation proximal to the site of obstruction
 Compression and thinning of the renal parenchyma, eventually reducing it to a
thin rim and resulting in a decrease in the size of the kidney.
Acute obstruction is followed by transient renal arterial vasodilatation succeeded by
vasoconstriction, probably mediated mainly by angiotensin II and thromboxane A2.
Ischaemic interstitial damage mediated by free oxygen radicals and inflammatory
cytokines compounds the damage induced by compression of the renal substance.
Tumour in the kidneys (renal cell carcinoma, nephroblastoma in children) malignant
tumours comprise 1-2% of all malignant tumours and the male to female ratio is 2:1 Renal cell carcinoma- arise from the proximal tubular epithelium. They are
most common renal tumour in adults. They rarely present before the age of 40
years, average presentation being 55yrs. In von-Hippel-Lindau disease, an
autosomal dominant disorder, bilateral renal cell carcinomas are common and
haemangioblastomas, phaeochromocytomas and renal cysts are also found.
Renal cell carcinomas are highly vascular. May present with haematuria, loin
pain and a mass in the flank. Malaise, anorexia, weight loss (30%) may occur
and 5% of patients have polycythaemia, 30% have hypertension, pyrexia is
present in about 20% if patients and 25% present with mets. Prognosis
depends on the degree of differentiation of the tumour and whether or not mets
are present. 5-year survival ranges from 60-70% in tumours confined to the
renal parenchyma, 15-35% with lymph node involvement, and only
approximately 5% in those who have distant mets.
 Nephroblastoma- mainly seen in the under 4s. It most commonly presents as
an asymptomatic abdominal mass, haematuria, hypertension or abdominal
pain. Diagnosis is established by excretion urography followed by
arteriography. It needs treatment with a combination of nephrectomy,
radiotherapy and chemotherapy has much improved survival rate, even in
children with mets. Survival is 90% in early disease or 70% in advanced
disease.
Bowel masses (malignant, inflammatory, faecal)This could be anywhere from the stomach downwards. Most commonly the mass may
be a bowel tumour (most likely a CRC) but there are many other bowel causes, e.g.
distension due to obstruction, intussusception, pyloric stenosis, volvulus, faecal
impaction. Even omphalocoele could be described as a bowel mass.
Enlarged bladderIn a male it is usually caused by urinary retention. Urinary retention is less common in
females and a gynaecological cause is more common. If there is a catheter in situ it is
important to check it is not kinked or blocked, and an attempt should be made to flush
the catheter to clear any blockage.
Aortic aneurismFor the abdominal aorta, an antero-posterior (AP) diameter of 3cm is generally
accepted as being an aneurysm. Aneurysms of the abdominal aorta and the iliac,
femoral and popliteal arteries have often been labelled as complications of
atherosclerosis but it is more likely that the primary disorder is degeneration of the
elastin and collagen of the arterial wall. Aneurysms are relatively uncommon; they are
found mainly in males over 70 years of age and even less commonly in women in
whom they present an average of 10 years later. At least a quarter of these patients
have more than one aneurysm. Degenerative aneurysms are usually fusiform in shape,
slowly expanding in diameter. As the aneurysm becomes larger, the vessel wall thins,
expansion accelerates and the risk of rupture increases. The majority of abdominal
aortic aneurysms involve only the infrarenal aorta; some extend distally to involve
one or both common iliac arteries. A few extend proximally to become thoracoabdominal aneurysms. Presentation: aorto-iliac aneurysms are often found
incidentally. The patient may notice a pulsatile abdominal mass or a pulsatile mass
may be discovered on abdominal examination. An aneurysm may also be noticed
incidentally on radiological investigation for some other disorder- as calcification on a
plain abdominal X-ray, as an obvious aneurysm on CT or, most commonly, on
ultrasound scanning for urinary symptoms. Nearly half of the cases that reach
surgeons present because of symptoms of leakage or rupture into the retroperitoneal
tissues. This mode of presentation carries a very high mortality. Pain is the most
common symptom of a leaking aneurysm. The patient often gives a history of
transient or more persistent cardiovascular collapse (fainting, hpotension). The
clinical picture ranges from an ‘actue abdomen’ to abdominal or back pain of up to a
week’s duration and the diagnosis is usually confined by finding a pulsatile abdominal
mass. Intraperitoneal rupture and often extraperitoneal rupture are rapidly fatal and
are frequently an unrecognised cause of sudden death in the elderly.
Indications for surgery= leaking or ruptured aneurysms (this is a surgical emergency),
symptomatic aneurysms, expanding aneurysms (> 0.5cm/year) and size (if > 5.5cm).
Uterine/ovarian masses (e.g. pregnancy, fibroids, cysts, malignant)Endometrial cancer: rapidly increasing incidence due to increased obesity
worldwide. Lifetime risk is 2% in the general population, with a median age at
presentation of 60 years. It is all to do with unopposed oestrogen activity causes of
this are: 1) Obesity- due to aromatisation of androgens to oestrogens; 2) Tamoxifenthis has oestrogenic effects of the uterus as opposed to the anti-oestrogenic effect it
has on breast tissue; 3) PCOS- where the increase andogrens produced are converted
to oestrogens in the adipose tissue; 4) exogenous oestrogen- e.g. in the form of HRT
or alternative medicines. Protective factors include high parity, pregnancy, oral
contraceptives and smoking. Women with HNPCC gene mutation have a 40-60%
lifetime risk of developing endometrial cancer. The most common symptom is
abnormal uterine bleeding (intermenstrual or heavy prolonged bleeding in the
premenopausal women and post-menopausal bleeding). Diagnosis is by endometrial
biopsy (Hysteroscopy and pipelle biopsy).
Adenocarcinoma is the type in >80% and is the most curable. Others are uterine
papillary serous carcinoma and clear cell carcinoma which often present with
extensive intra-abdominal disease and these carry poor survival. The grade of tumour
is based on tumour architecture and reflects the amount of solid tumour. Spread of the
tumour is by lymphatic, haematologic, direct extension and transtubal. 75% of
patients diagnosed with stage I disease. Treatment is surgical with adjuvant
chemotherapy and radiotherapy in stage III-IV disease. Survival is 85% for stage I but
less than 5% for stage IV. May also have uterine sarcoma (5%) of cases.
Ovarian cancer: This is epithelial ovarian cancer (85-90%), malignant germ cell
tumours (5-7%), malignant sex-cord stromal tumours (5-7%). Mortality from this is
higher than all other gynae cancers combined.
Epithelial ovarian cancer- mean age at diagnosis 60 years old. Risk includes low
parity, family history of breast or ovarian cancer and living in industrialised western
countries. Protective factors include mulitparity, breast-feeding and chronic
anovulation, oral contraceptive use decreases the incidence of ovarian cancer by up to
50%. Hereditary factors are present in 5-10% of cases (associated with BRCA 1 and
2). There are no reliable screening tests. High risk women (BRCA 1) may be offered
prophylactic BSO reduces their risk of ovarian and breast cancer. Presentation is by
symptoms such as bloating, increased abdominal size, and urinary symptoms. Early
satiety, recent bowel changes or “indigestion” are common complaints of advanced
disease. Weight loss is unusual. Early ovarian cancer may be detected on pelvic exam
as an adnexal mass. Transvaginal sonography is the most sensitive method to evaluate
an adnexal mass. CT abdomen-pelvic and chest X-ray are helpful for treatment
planning. Staging is surgical and complicated: Stage 1 is confined to the ovary, Stage
2 is direct extension to the pelvis/pelvic organs, Stage 3 distant extension to the
peritoneum, liver, bowel. Stage 4 is spread above the diaphragm. 75% present with
advanced disease. Treatment is by TAH, BSO and cytoreductive surgery to remove all
visible disease. Adjuvant therapy is used in disease above stage II and platinum-based
chemo is the best. Response to therapy can be measure by monitoring CA125. 80% of
advanced tumours will relapse.
Malignant germ cell tumours: younger age at diagnosis (20 years). Can be
dysgerminomas, yolk-sac or immature teratomas- these need surgery and
chemotherapy.
Malignant sex-cord stromal tumours: can be either granulosa cell tumour and sertolileydig cell tumours. Treatment is surgical.
Fibroids: benign proliferation of smooth muscle and connective tissue. Fibroids may
increase in size during oestrogen therapy and decrease in size following the
menopause. These may be subserosal, intramural, submucous. These may be
asymptomatic or with abnormal uterine bleeding, pelvic pressure or pain. On
examination there may be an enlarged irregular uterus on bimanual examination. Most
patients need no treatment and can simply be monitored, treatment should be started if
there is concern the mass is a sarcoma, if the uterus is causing significant
hydronephrosis or if women are suffering with recurrent miscarriage. Management is
with GnRH agonists to shrink the fibroids, uterine artery embolization to decrease
flow, or hysterectomy.
Benign ovarian cystic masses: These can be functional cysts, dermoid cysts (bening
teratomas), serous cystadenoma, mucinous cystadenomas or ovarian endometriomas
(“chocolate cysts”).
Abdominal wall herniasInguinal, Femoral, Epigastric, Umbilical, Paraumbilical, Spigelian, incisional and
divarication of the recti.
Lymph nodes- These may be enlarged in cases of lymphoma or in metastatic spread
of a tumour, commonly a tumour in the lower abdomen/pelvis. They may also be
enlarged (not sufficient to feel) in mesenteric adenitis.
Infective causes- TB may be a cause of a mass in the abdomen. Hepatitis A is another
cause of an abdominal mass, with an acute enlargement of the liver.
Pancreas- another cause of an abdominal mass is that of a pancreatitic tumour and
this may be painful or painless, and may lead to jaundice.
Preventative measures for reducing incidence of bowel cancer and diverticular
disease
Diet is an important factor in the development of CRC, and is more common in
developed countries, with lowest rates in Asia and Africa. It is thought that the
Western diet of low-fibre and high-fat diet may be in some way be responsible.
Studies of migrants from areas of low incidence to those of high incidence have
shown that they rapidly achieve the cancer incidence of their new homeland. Daily
intake of red or processed meat has been shown in large European EPIC study to
increase the risk by 30%; conversely twice weekly intake of fish reduces it by 30%. It
is likely that excess dietary fats also act as carcinogens. Excess beer appears to
increase the risk of CRC, whereas wine does not. Any type of alcohol in excess
appears to hasten malignant change in adenomas. The typical low-fibre Western diet
result results in much slower whole-gut transit time and it may be that carcinogens in
the stool thereby maintain contact with the bowl mucosa for longer. Low fibre diets
are usually low in fruit and raw vegetables and consequently low I antioxidants,
which are thought to have a protective role.
Epidemiological studies have shown a reduction in colorectal cancer in people taking
low dose aspirin daily (75mg) as prophylaxis against CVD. Recent evidence also
suggests that type 2 diabetic patients have a 50% increase in risk, particularly if
control of glycated haemoglobin is poor. There is some evidence that long-term usage
of insulin increases colorectal cancer risk but the risk is small when compared with
the absolute benefit of good glycaemic control.
Ulcerative colitis, a chronic inflammatory condition of the large bowel, carries an
independent risk of bowel neoplasia. After 10 years of active disease, the cancer risk
rises by 1% each year.
Managing all these things will help reduce the risk of CRC in patients.
Diverticular disease causes substantial morbidity in the older population, particularly
in the West, and is a very common cause for hospital admission and operation. In
developed countries, localised outpouchings or diverticula are present in the bowel
wall in at least 1/3 of people over the age of 60. There is strong evidence that this can
be caused or aggravated by a chronic lack of dietary fibre but there may also be a
genetic element. Females are affected more than males (though this obviously can not
be altered).
Fibre is important for bowel health!
Role of alcohol in chronic liver disease (hepatomegaly) and portal hypertension
(splenomegaly)
Large amounts of alcohol are needed to be drunk in order to actually cause liver
disease. The amount of alcohol that produces damage varies and not everyone that
drinks heavily will suffer from physical damage. Only 20% of people who drink
heavily develop cirrhosis of the liver. The effect of alcohol on different organs in the
body is not the same; in some patients the liver is affected, in others the brain or
muscle.
In general the effects of a given intake of alcohol seem to be worse in women:
160g ethanol per day (20 single drinks) carries a high risk
80g ethanol per day (10 single drinks) carries a medium risk
40g ethanol per day (5 single drinks) carries little risk
1 unit is 8g of alcohol.
Ethanol is metabolised in the liver by 2 pathways, resulting in an increase in the
NADH/NAD ratio. The altered redox potential results in increased hepatic fatty acid
synthesis with decreased fatty acid oxidation, both events leading to hepatic
accumulation of fatty acid that is then esterified to glycerides. The changes in
oxidation-reduction also impair carbohydrate and protein metabolism and are the
cause of the centrilobular necrosis of the hepatic acinus typical of alcohol damage.
Acetaldehyde is formed by the oxidation of ethanol and its effect on hepatic proteins
may well be a factor in producing liver cell damage. The exact mechanism of alcohol
hepatitis and cirrhosis is unknown, but since only 10-20% of people who drink
heavily will suffer from cirrhosis, a genetic predisposition is suggested.
Immunological mechanisms have also been proposed.
Alcohol can produce a wide spectrum of liver disease from fatty change to hepatitis
and cirrhosis:
 Fatty Change- the metabolism of alcohol invariably produces fat in the liver,
mainly in zone 3. This is minimal with small amounts of alcohol, but with
larger amounts the cells become swollen with fat (steatosis) giving, eventually,
a Swiss cheese effect on haematoxylin and eosin stain. Steatosis can also be
seen in obesity, diabetes, starvation and occasionally chronic illness. There is
no liver cell damage, the fat disappears on stopping alcohol. In some cases
collagen is laid down around the central hepatic vein (perivenular fibrosis) and
this can sometimes progress to cirrhosis without a preceding hepatitis. Alcohol
directly affects stellate cells, transforming them into collagen-producing
myofibroblast cells. Cirrhosis might then develop if there is an imbalance
between degradation and production of collagen.
 Alcoholic hepatitis- in addition to fatty change there is infiltration by
polymorphonuclear leucocytes and hepatocyte necrosis mainly in zone 3.
Dense cytoplasmic inclusions called Mallory bodies are sometimes seen in
hepatocytes and giant mitochondria are also a feature. Mallory bodies are
suggestive of, but not specific for, alcohol damage as they can be found in
other liver disease, such as Wilson’s and PBC. If alcohol consumption
continues, alcoholic hepatitis may progress to cirrhosis.
 Alcoholic cirrhosis- this is classically of the micronodular type, but a mixed
pattern may also be seen accompanying fatty change, and evidence of preexisting alcoholic hepatitis may be present.
Clinical features: Fatty liver- there are often no symptoms are signs. Vague abdominal
symptoms of nausea, vomiting and diarrhoea are due to the more general effects of
alcohol on the gastrointestinal tract. Hepatomegaly, sometimes huge, can occur
together with other features of chronic liver disease.
Alcoholic hepatitis- the patient may be well, with few symptoms, the hepatitis only
being apparent on the liver biopsy in addition to fatty change. Mild to moderate
symptoms of ill-health, occasionally with mild jaundice, may occur. Signs include all
the features of chronic liver disease. Liver biochemistry is deranged and the diagnosis
is made on liver histology. In the severe case, usually superimposed on patients with
alcoholic cirrhosis, the patient is ill, with jaundice and ascites. Abdominal pain is
frequently present, with a high fever associated with the liver necrosis. On
examination there is deep jaundice, hepatomegaly, sometimes splenomegaly, and
ascites with ankle oedema. The signs of chronic liver disease are also present.
Alcoholic cirrhosis- this represents the final stage of liver disease from alcohol.
Nevertheless, patients can be very well with few symptoms. On examination, there
are usually signs of chronic liver disease. The diagnosis is confirmed with liver
biopsy. Usually the patient presents with one of the complications of cirrhosis. In
many cases there are features of alcohol dependency as well as involvement of other
systems, such as polyneuropathy.
Complications of cirrhosis:
 Portal hypertension and gastrointestinal haemorrhage
 Ascites
 Portosystemic encephalopathy
 Renal failure
 Hepatocellular carcinoma
 Bacteraemias, infections
 Malnutrition
Portal hypertension: the portal vein is formed by the union of the superior mesenteric
and splenic veins. The pressure within it is normally 5-8mmHg with only a small
gradient across the liver to the hepatic vein in which blood is returned to the heart via
the inferior vena cava. Portal hypertension can be classified according to the site of
obstruction:
- Prehepatic- due to blockage of the portal vein before the liver
- Intrahepatic- due to distortion of the liver architecture, which can be
presinusoidal (e.g. in schistosomiasis) or postsinusoidal (e.g. in cirrhosis)
- Posthepatic- due to venous blockage outside the liver (rare).
As portal pressure increases above 10-12mmHg, the compliant venous system dilates
and collaterals occur within the systemic venous system. The main sites of the
collaterals are at the gastro-oesophageal junction, the rectum, the left renal vein, the
diaphragm, the retroperitoneum and the anterior abdominal wall via the umbilical
vein.
The collaterals at the gastro-oesophageal junction (varices) are superficial in position
and tend to rupture. Portosystemic anastomoses at other sites seldom give rise to
syptoms. Rectal varices are found frequently (30%) if carefully looked for and can be
differentiated from haemorrhoids, which are at the lower end of the anal canal.
Portal vascular resistance is increased in chronic liver disease. During liver injury,
stellate cells are activated and transform into myofibroblasts. In these cells there is de
novo expression of the specific smooth muscle protein α-actin. Under the influence of
mediators, such as endothelin, nitric oxide or prostaglandins, the contraction of these
activated cells contributes to abnormal blood flow patterns and increased resistance to
blood flow. In addition the balance of fibrinogenic and fibrinolytic factors is shifted
toward fibrinogensis. This increased resistance leads to portal hypertension and
opening of portosystemic anastomoses in both precirrhotic and cirrhotic livers.
Patients with cirrhosis have hyperdynamic circulation. This is thought to be due to the
release of mediators, such as nitric oxide and glucagon, which leads to peripheral and
splanchnic vasodilatation. This effect is followed by plasma volume expansion due to
sodium retention and this has a significant effect in maintaining portal hypertension.
Hypersplenism: this can result from splenomegaly due to any cause. It is commonly
seen with splenomegaly due to haematological disorder, portal hypertension,
rheumatoid arthritis (Felty’s syndrome) and lymphoma. Hypersplenism produces:
Pancytopenia, haemolysis due to sequestration and destruction of red cells in the
spleen, increased plasma volume. Treatment is often dependent on the underlying
cause, but splenectomy is sometimes required for severe anaemia or
thrombocytopenia.