1
The peritoneum and Peritonitis
LEARNING OBJECTIVES
To recognize and understand:
• The clinical features of localised and generalised peritonitis
• The common causes and complications of peritonitis
• The principles of surgical management in patients with peritonitis
• The clinical presentations and treatment of abdominal/pelvic abscesses
PERITONEUM
The peritoneum is a single layer of flat mesothelial cells resting on a bed
of loose connective tissue, It is divided into 2 two parts:
1-The parietal peritoneum is the part that lines the entire abdominal
cavity, covering the inner surfaces of the abdominal wall and pelvis. It is
reinforced by the fascia transversalis, which lies external to it.
2-The visceral peritoneum covers all the intra-abdominal viscera and
mesenteries.
Innervation
1-The parietal peritoneum is sensitive and is innervated by both somatic
and visceral afferent nerves. The anterior parietal peritoneum is the most
sensitive and any local insult to the parietal peritoneum leads to
Protective voluntary muscle guarding and then reflex muscular spasm.
2-The visceral peritoneum receives innervation only from the autonomic
nervous system and is relatively insensitive.
Functions of the peritoneum
A-In health
■ Visceral lubrication
■ Fluid and particulate absorption
B-In disease
■ Pain perception (mainly parietal)
■ Inflammatory and immune responses
■ Fibrinolytic activity
SCOPE OF DISEASE
The peritoneum, mesentery and omentum may be the site of a variety of
conditions that reflect their relationship to other anatomical structures or
in some instances their primary functions
2
Causes of peritoneal inflammation
■Bacterial, gastrointestinal and non-gastrointestinal
■Chemical, e.g. bile, barium
■Allergic, e.g. starch peritonitis
■Traumatic, e.g. operative handling
■Ischaemia, e.g. strangulated bowel, vascular occlusion
■Miscellaneous, e.g. familial Mediterranean fever
Paths to peritoneal infection
■ Gastrointestinal perforation, e.g. perforated ulcer, appendix,diverticulum
■ Transmural translocation (no perforation), e.g. pancreatitis, ischaemic
bowel
■ Exogenous contamination, e.g. drains, open surgery, trauma
■ Female genital tract infection, e.g. pelvic inflammatory disease
■ Haematogenous spread (rare), e.g. septicaemia
Microorganisms in peritonitis
1-Gastrointestinal source
■Escherichia coli
■Streptococci
■Bacteroides
■Clostridium
■Klebsiella pneumoniae
3
2- Other sources
■Chlamydia trachomatis
■Neisseria gonorrhoeae
■Haemolytic streptococci
■Staphylococcus
■Streptococcus pneumoniae
■Mycobacterium tuberculosis
■Fungal infections
Gross changes
’
Inflamed areas become opaque and adhere together because of fibrin
deposition
1. Excess purulent exudate accumulates.
2. Paralytic ileus occurs at first as a reflex to minimize spread, and is then
accentuated by the toxic effect of pus. Finally mechanical intestinal
obstruction from fibrinous adhesions may complicate the picture.
Fate of peritonitis
The fate depends on the virulence of the organisms on one side and the
efficiency of treatment and the body resistance on the other:
1- Resolution. The peritoneum has great resistance to infection. If the
source of infection is controlled or removed, peritonitis resolves rapidly.
2- Localization (abscess formation). If complete resolution fails, pus
localizes to form an abscess which may be local or remote:
■ Localization may occur around the primary focus (e.g., in acute
appendicitis or cholecystitis) by adhesions of intestine and omentum
around the inflamed organ to form an abscess.
■ Localization may occur in one of the anatomical compartments of the
peritoneal cavity to form a remote abscess, e.g. a subphrenic, iliac or
pelvic abscess depending on the position.
3- Flaring up. This causes generalized peritonitis. The factors which
predispose to it include:
• High virulence of the organisms.
• Sudden perforation of a hollow viscus which does not allow the
defensive mechanisms to localize the source of infection.
• Persistent source of infection.
• Stimulation of peristalsis by eating, enemas or purgatives.
• Rough handling of a localized collection during surgery.
• Immunosuppression as in diabetes mellitus, AIDS, and in patients
receiving corticosteroids or chemotherapy.
• Generalized peritonitis is likely to occur in children because the greater
omentum, which has an important role in localizing inflammatory
processes, is small in size and note well developed.
ACUTE PERITONITIS
Types
• Primary
• Secondary
• Tertiary (Due to superadded infection peritonitis following treatment of
secondary/Primary)
4
PRIMARY PERITONITIS
• Primary ("spontaneous") peritonitis occurring in the absence of
gastrointestinal perforation is caused mainly by hematogenous spread but
occasionally by transluminal or direct bacterial invasion of the peritoneal
cavity.
• Impairment of the hepatic reticuloendothelial system and compromised
peripheral destruction of bacteria by neutrophils promotes bacteremia,
which readily infects ascitic fluid that has reduced bacterium-killing
capacity.
• Primary peritonitis is most closely associated with
1-Cirrhosis and advanced liver disease with a low ascitic fluid protein
concentration. Recurrence is common in cirrhosis and often proves fatal.
2-It is also seen in patients with the nephrotic syndrome
3-Systemic lupus erythematosus,
4-Splenectomy during childhood.
Clinical Findings
The clinical presentation simulates secondary bacterial peritonitis, with
1- Abrupt onset of fever
2- Abdominal pain, distention, and rebound tenderness.
3- One fourth of patients have minimal or no peritoneal symptoms.
5- Most have clinical and biochemical manifestations of advanced cirrhosis
or nephrosis.
Investigations
1- Leukocytosis, hypoalbuminemia, and a prolonged prothrombin time are
characteristic findings.
2- Examination of the ascitic fluid, which reveals a white blood cell count
greater than 500/L and more than 25% polymorphonuclear leukocytes.
3- A blood-ascitic fluid
5
• Albumin gradient greater than 1.1 g/dL
• Raised serum lactic acid level (> 33 mg/dL), or a reduced ascitic fluid
pH (< 7.31) supports the diagnosis.
4- Bacteria are seen on Gram-stained smears in only 25% of cases.
Culture of ascitic fluid inoculated immediately into blood culture media at
the bedside usually reveals a single enteric organism, most commonly E
coli, klebsiella, or streptococci, but Listeria monocytogenes has been
reported in immunocompromised hosts.
Treatment
1-Systemic antibiotics with third-generation cephalosporins (eg,
cefotaxime) or a beta-lactam-clavulanic acid
2- Correcting dehydration and electrolyte imbalance,
3- Early surgery is required unless spontaneous infection of pre-existing
ascites is strongly suspected, in which case a diagnostic peritoneal tap
is useful. Laparotomy or laparoscopy may be used.
Prognosis
The 50% average mortality rate is due to peritonitis in only about a third
of cases. Multiple organ failure as indicated by gastrointestinal bleeding,
hepatic encephalopathy, and renal failure are ominous signs.
ACUTE SECONDARY BACTERIAL PERITONITIS
Pathophysiology
Peritonitis is an inflammatory or suppurative response of the peritoneal
lining to direct irritation. Peritonitis can occur after perforating,
inflammatory, infectious, or ischemic injuries of the gastrointestinal or
genitourinary system. Common examples are listed in Table 1.
Table. Common Causes of Peritonitis
Severity Cause
Mortality Rate
Mild
< 10%
Appendicitis
Perforated gastroduodenal ulcers
Acute salpingitis
Moderate Diverticulitis (localized perforations) < 20%
Nonvascular small bowel perforation
Gangrenous cholecystitis
Multiple trauma
Severe
Large bowel perforations
Ischemic small bowel injuries
Acute necrotizing pancreatitis
Postoperative complications
20–80%
6
Secondary peritonitis
• Results from bacterial contamination originating from within viscera or
from external sources (e.g. penetrating injury). It most often follows
disruption of a hollow viscus.
• Extravasated bile and urine, although only mildly irritating when sterile,
are markedly toxic if infected and provoke a vigorous peritoneal reaction.
• Gastric juice from a perforated duodenal ulcer remains mostly sterile for
several hours, during which time it produces a chemical peritonitis with
large fluid losses; but if left untreated, it evolves within 6–12 hours into
bacterial peritonitis. Intraperitoneal fluid dilutes opsonic proteins and
impairs phagocytosis.
Clinical Findings
SYMPTOMS AND SIGNS
• The clinical manifestations of peritonitis reflect the severity and duration
of infection and the age and general health of the patient. Physical
findings can be divided into
(1) abdominal signs arising from the initial injury
(2) manifestations of systemic infection.
• Acute peritonitis frequently presents as an acute abdomen.
Local findings: include abdominal pain, tenderness, guarding or rigidity,
distention, free peritoneal air, and diminished bowel sounds—signs that
reflect parietal peritoneal irritation and resulting ileus.
Systemic findings: include fever, chills or rigors, tachycardia, sweating,
tachypnea, restlessness, dehydration, oliguria, disorientation, and,
ultimately, refractory shock. Shock is due to the combined effects of
hypovolemia and septicemia with multiple organ dysfunction.
Physical signs depend upon: Very young and very old patients as well
as in those who are
1-Chronically debilitated
2-Immunosuppressed, or receiving corticosteroids and in postoperative
patients.
3-Delayed recognition is a major cause of the high mortality rate of
peritonitis.
Summary box.6
Clinical features of peritonitis
• Abdominal pain, worse on movement, coughing and deep respiration
• Constitutional upset: anorexia, malaise, fever, lassitude
• GI upset: nausea ± vomiting
• Pyrexia (may be absent)
• Raised pulse rate
• Tenderness ± guarding/rigidity/rebound of abdominal wall
• Pain/tenderness on rectal/vaginal examination (pelvic peritonitis)
• Absent or reduced bowel sounds
• ‘Septic shock’ (systemic inflammatory response syndrome
(SIRS) and multiorgan dysfunction syndrome (MODS)) in later stages
7
Investigations in peritonitis
■ Blood studies should include a complete blood cell count, cross
matching, arterial blood gases, electrolytes, a blood clotting profile, and
liver and renal function tests.
■ Samples for culture of blood, urine, sputum, and peritoneal fluid should
be taken before antibiotics are started. A positive blood culture is usually
present in toxic patients.
■ Raised white cell count and C-reactive protein are usual
■ Serum amylase > 4× normal indicates acute pancreatitis
■ Abdominal radiographs are occasionally helpful
■ Erect chest radiographs may show free peritoneal gas (perforated
viscus)
■ Ultrasound/CT scanning often diagnostic
■ Peritoneal fluid aspiration (with or without ultrasound guidance) may be
helpful
Differential Diagnosis
1-Specific kinds of infective (eg, gonococcal, amebic, candidal) and non
infective peritonitis may be seen.
2-In the elderly, systemic diseases (eg, pneumonia, uremia) may produce
intestinal ileus so striking that it resembles bowel obstruction or
peritonitis.
Treatment
1-Fluid and electrolyte replacement
2-Operative control of sepsis
3-Systemic antibiotics are the mainstays of treatment of peritonitis.
PREOPERATIVE CARE
Treatment
• Intravenous fluids for resuscitation are essential. It improves the tissue
perfusion, corrects the hypotension and also improves the urine output.
Normal saline, Ringer’s lactate are usually used. Usual requirement is 2
ml/kg/hour.
• Nasogastric tube aspiration—to decompress bowel; to reduce toxic fluid;
to prevent aspiration.
• Total parenteral nutrition, CVP line to perfuse and to monitor.
• Blood transfusion.
• Catheterisation with maintenance of adequate urine output (30 ml/hour)
(0.5 ml/hour/kg).
• Antibiotics—Ampicillin, gentamicin, metronidazole, ceftazidime,
cefoperazone, cefotaxime, tazobactum, piperacillin, meropenem, linezolid,
etc.
• Use of dopamine, steroids, and management of shock.
• Often ICU and ventilator support is required during postoperative period.
• Monitoring the patient using PO2, PCO2, electrolytes, and pulse
oximeter.
OPERATIVE MANAGEMENT
1-Control of Sepsis
• The objectives of surgery for peritonitis are to remove all infected
material, correct the underlying cause, and prevent late complications.
8
Except in early, localized peritonitis, a midline incision offers the best
surgical exposure.
• Materials for aerobic and anaerobic cultures of fluid and infected tissue
are obtained immediately after the peritoneal cavity is entered. Occult
pockets of infection are located by thorough exploration, and
contaminated or necrotic material is removed.
• Routine radical debridement of all peritoneal and serosal surfaces does
not increase survival rates. The primary disease is then treated. This may
require resection (eg, ruptured appendix or gallbladder), repair (eg,
perforated ulcer), or drainage (eg, acute pancreatitis). Attempts to
reanastomose resected bowel in the presence of extensive sepsis or
intestinal ischemia often lead to leakage. Temporary stomas are safer
2-Peritoneal Lavage
In diffuse peritonitis, lavage with copious amounts (> 3 L) of warm
isotonic crystalloid solution removes gross particulate matter as well as
blood and fibrin clots and dilutes residual bacteria.
3-Peritoneal Drainage
Drainage of the free peritoneal cavity is ineffective and often undesirable.
Not only are drains quickly isolated from the rest of the peritoneal cavity,
but they still act as a channel for exogenous contamination.
Summary box
Management of peritonitis
General care of patient
• Correction of fluid and electrolyte imbalance
• Insertion of nasogastric drainage tube and urinary catheter
• Broad-spectrum antibiotic therapy
• Analgesia
• Vital system support
Operative treatment of cause when appropriate
• Remove or divert cause
• Peritoneal lavage ± drainage
POSTOPERATIVE CARE
■ Intensive care monitoring, often with ventilatory support, is mandatory
in unstable and frail patients. Achieving hemodynamic stability to perfuse
major organs is the immediate objective, and this may entail the use of
cardiac inotropic agents besides fluid and blood product supportive
measures.
■ Antibiotics are given for 10–14 days, depending on the severity of
peritonitis. A favorable clinical response is evidenced by well-sustained
perfusion with good urine output, reduction in fever and leukocytosis,
resolution of ileus, and a returning sense of well-being. The rate of
recovery varies with the duration and degree of peritonitis.
■ The early removal of all nonessential catheters (arterial, central venous,
urinary, and nasogastric) reduces the risk of secondary infected foci.
■ Drains should be removed or advanced once drainage diminishes and
becomes more serous in nature. Excessive or prolonged suction may
produce fistulas or bleeding even within a few days.
9
Complications
Systemic complications of peritonitis
■ Bacteraemic/endotoxic shock
■ Bronchopneumonia/respiratory failure
■ Renal failure
■ Bone marrow suppression
■ Multisystem failure
Abdominal complications of peritonitis
■ Adhesional small bowel obstruction
■ Paralytic ileus
■ Residual or recurrent abscess
■ Portal pyaemia/liver abscess
Prognosis
The overall mortality rate of generalized peritonitis is about 40% (Table1).
Factors contributing to a high mortality rate include
1-The type of primary disease and its duration
2-Associated multiple organ failure before treatment
3-The age and general health of the patient.
■ Mortality rates are consistently below 10% in patients with perforated
ulcers or appendicitis; in young patients
■ In those having less extensive bacterial contamination; and in those
diagnosed and operated upon early.
■ Patients with distal small bowel or colonic perforations or postoperative
sepsis tend to be older, to have concurrent medical illnesses and greater
bacterial contamination, and to have a greater propensity to renal and
respiratory failure; their mortality rates are about 50%. Markedly poor
Localized septic peritonitis ( Intraperitoneal abscess )
Surgical Anatomy
There are four intraperitoneal and three extraperitoneal spaces.
A-Intraperitoneal Spaces
1-Right anterior intraperitoneal space (Right subphrenic space):
Causes: Abscess here occurs due to cholecystitis, perforated duodenal
ulcer, postoperative, appendicitis
2-Left anterior intraperitoneal space (Left subphrenic space):
Causes for abscess here are surgeries of the stomach, tail of the
pancreas, spleen, colon (splenic flexure), diverticulitis.
3-Left posterior intraperitoneal space Most common cause here is
pseudocyst of pancreas. Rarely perforated gastric ulcer.
4-Right posterior intraperitoneal space (Right subhepatic space)
Causes: Appendicitis, cholecystitis, postoperative, perforated duodenal
ulcer, intestinal obstruction.
10
B-Extraperitoneal Spaces
1-Right extraperitoneal space is right perinephric space ( 5)
Causes: Abscess here are due to tuberculosis, trauma, haematoma
2-left extraperitoneal space is left perinephric space.(6)
Causes: Abscess here are due to tuberculosis, trauma, haematoma.
3-Midline extraperitoneal ( 7 )
Causes: Pus collects here commonly due to ruptured amoebic liver
abscess and pyogenic abscess of the liver.
Lcalized septic peritonitis ( Intraperitoneal abscess )
• An intraperitoneal abscess has better outcome than generalized
peritonitis. It indicates that the defensive mechanisms successfully
localized the source of infection. These protective mechanisms include the
omentum (abdominal policeman) and the matting of loops of bowel
around the source of infection.
11
• The common sites of intraperitoneal abscesses are the iliac fossae,
pelvis and the subdiaphragmatic space
Iliac abscess
Aetiology
On the right side it is due to
1. Acute appendicitis.
2. Perforated duodenal ulcer, the exudate trickling through the right
paracolic gutter
On the left side it may be due to
1. Perforated diverticulitis.
2. Perforation of carcinoma of the sigmoid colon.
On either side
1. Spread from the female genital organs.
2. Secondary to generalized peritonitis.
Clinical features
■ Symptoms. Pain, swelling, hectic fever, vomiting and constipation.
■ Signs. Tenderness and rigidity over the site of the abscess. The
overlying skin may show signs of inflammation.
Investigations
■ Blood picture reveals polymorphnuclear leucocytosis.
■ Ultrasound examination can determine the site of the abscess and the
volume of pus.
Treatment
The principles of treatment are
1.
Drainage of pus
2.
Controlling the cause
3.
The use of effective antibiotics
The abscess should be drained through an extraperitoneal muscle cuffing
incision. Nowadays, it is possible to do percutaneous drainage of the
abscess guided by ultrasound or CT scan. An inflamed appendix is not to
be removed in the acute setting. An interval appendicectomy after 6
months is much easier and safer.
Pelvic abscess
Definition: A pelvic abscess is a collection of pus in the recto-vesical
pouch or in the pouch of Douglas.
Causes
1. Acute appendicitis.
2. Localization of resolving diffuse peritonitis.
3. Pelvic inflammatory disease in females.
12
Clinical features
1.
Hectic fever and toxaemia.
2.
Deep pelvic pain.
3.
Diarrhoea and tenesmus are due to rectal irritation. Mucous
diarrhoea occurring in a patient with an inflammatory peritoneal lesion is
nearly pathognomonic of a pelvic abscess.
4.
Burning micturition and frequency are due to bladder irritation.
5.
Pelvic abscess may present suprapubically (mass, redness).
6.
By digital rectal examination there is fullness and yielding
tenderness in front of rectum.
7.
If neglected, it bursts through the rectum or the vagina.
Treatment
■ If the abscess is pointing in rectum, transrectal drainage is
recommended.
■ If it is pointing in vagina the abscess is to be drained through the
posterior fornix.
■ If it is pointing suprapubically, suprapubic extraperitoneal drainage is
considered as a possible route. In general, provided the abscess is shut
off from the general peritoneal cavity, rectal drainage of a pelvic abscess
is preferable than suprapubic drainage, which breaks down nature’s
barriers and exposes the general peritoneal cavity to the dangers of
spreading infection.
■ Ultrasound or CT guidance. A fine catheter is left in the abscess cavity
to continue the drainage.
13
A, CT scan demonstrates a right lower quadrant abscess (closed arrow) with an
appendicolith (open arrow). B,The same patient after placement of a percutaneous
abscess drainage catheter (closed arrow). The abscess has resolved. The
appendicolith (open arrow) is seen medial to the catheter.
Subphrenic abscess Anatomy of subphrenic spaces
■ The subphrenic region is considered as that portion of the abdominal
cavity which extends from the diaphragm above to the transverse colon
and mesocolon below.
■ The region is divided by the liver into suprahepatic and infrahepatic
compartments. The falciform ligament divides the suprahepatic
compartments into right and left portions. The subphrenic spaces,
therefore, include the following:
1. Right suprahepatic space. This is the space that lies between the right
leaf of the diaphragm and the superior and anterior surfaces of the right
lobe of the liver. Medially there is the falciform ligament.
2. Right infrahepatic space. (Hepatorenal Pouch of Morison). Above and in
front there are the liver and gallbladder while below and behind there are
the upper pole of the right kidney, lower part of the right suprarenal gland
and the second portion of the duodenum
3- Right extraperitoneal space. The space lies between the bare area of
the liver and the diaphragm.
4. Left suprahepatic space. The space is bound by the diaphragm, the left
lobe of the liver, stomach and spleen.
5. Left anterior infrahepatic space. The boundaries of this space are the
liver above and in front, and the stomach and lesser omentum below and
behind.
6. Left posterior infrahepatic space. This is the lesser sac.
7. Left extraperitoneal space. This is the space around the upper pole of
the left kidney and left suprarenal gland.
14
Aetiology
1. Residual pus collection following generalized peritonitis.
2. Inflamed or perforated viscera, e.g., appendix, gall bladder or peptic
ulcer.
3. Lymphatic spread from chest infection.
4. Post-operative collection of infected bile after biliary surgery.
Clinical features
A subphrenic abscess should be suspected whenever a hectic fever
develops or persists after the treatment of any inflammatory lesion within
the abdomen as stated, “pus somewhere, pus no where else, pus under
the diaphragm”.
(A)
General
1.
Slight or absent pain but there is epigastric discomfort and pain
referred to the shoulder (phrenic nerve irritation).
2.
Hectic fever.
3.
Tachycardia.
4.
Severe toxaemia with anorexia, vomiting, sweating, wasting with
rapid deterioration of the general condition.
5.
Persistent hiccough.
(B)
Local Inspection
■
Impaired chest movement on the affected side.
■
Rarely bulging of the lower ribs or upper abdomen.
Palpation
■ Tenderness may be present over the lower ribs and intercostal spaces,
or below the costal margin.
■ There may be swelling and rigidity of the upper abdomen.
■ Downward displacement of liver with upward displacement of the apex
of the heart.
15
Auscultation
Impaired air entry and crepitations over the lung base of the affected side
may be detected.
Investigations
1. White blood cell count shows leucocytosis and shift to the left.
2. Plain chest X-ray and screen:
a. Thickened, elevated and fixed diaphragm (tented diaphragm).
b. Obliteration of costophrenic space by a minimal pleural effusion may be
seen.
c. Gas under the diaphragm or air fluid level is sometimes seen when the
cause is a perforated viscus, or when there is infection with gas forming
organisms.
3. Ultrasound and CT scanning have proved very useful. They can localize
the exact anatomical site and size of the abscess.
Figure CT scan of abdomen showing subphrenic abscess.
Treatment
If conservative treatment fails, the abscess should be drained.
■ A subphrenic. abscess can be aspirated under ultrasound or CT
guidance. A fine catheter is left in the abscess cavity to continue the
drainage.
■ Thick pus and a multilocular abscess are indications to abandon this
technique in favour of open drainage by:
1. The posterior extrapleural extraperitoneal approach (when located
posteriorly).
a. The 12th rib is excised subperiosteally and a transverse incision is done
in its bed in line with the first lumbar transverse process through the
lowest fibres of the diaphragm.
b. A finger is inserted and worked until the abscess bursts (above the
kidney between the diaphragm and liver). Fibrous septa are broken to
open all locale.
c. A drain is inserted.
2. The anterior extraperitoneal approach (when located anteriorly).
a. Small subcostal incision.
b. All layers are divided but not including the peritoneum.
c. A finger is inserted and worked until the abscess bursts, and a drain is
left in place.
16
Figure: A, Computed tomography (CT) scan demonstrates a left
subphrenic abscess post splenectomy (arrow). B, A catheter (arrow) is
placed within the abscess. C, CT scan several days later demonstrates the
catheter in the subphrenic space (arrow), with no residual abscess. The
catheter was subsequently removed.
Tuberculous peritonitis
Aetiology
The disease is always secondary to a tuberculous focus elsewhere that
reaches the peritoneum through:
■ Direct spread, e.g., tuberculous lymphadenitis, enteritis and salpingitis
(the commonest cause).
■ Blood spread, e.g., pulmonary tuberculosis.
■ Lymphatic spread e.g., from pleura or bowel.
Pathology
Five types are encountered
1. The acute miliary type
a. The peritoneum is studded with tubercles.
b. The exudate is straw coloured.
c. It resembles acute peritonitis and the diagnosis is frequently made
during operation.
2. Caseous type (purulent form)
a. It affects young females as a complication of tuberculous salpingitis.
b. The peritoneum is studded with tubercles and is thickened.
17
c. Multiple collections of caseous material are present among the
adherent bowel and omentum. Cold abscess may form and it may point to
produce sinuses or fistulae.
3. Ascitic type (the commonest type)
a. The peritoneum is studded with tubercles.
b. There is a copious amount of straw coloured fluid.
C. The greater omentum is thickened, fibrosed and frequently rolled up
forming a sausage shaped mass above the umbilicus.
4. Encysted type (localized form of the ascitic type)
a.
The fluid is encysted by fibrous adhesions and coils of bowel.
b.
It produces an intra-abdominal cyst which may be mistaken for
ovarian and mesenteric cysts.
5.
Adhesive type (fibrous or plastic form): This type is
characterized by extensive peritoneal adhesions which may lead to
intestinal obstruction.
Clinical features
1.
The disease usually affects children and young adults of both sexes.
2.
There are recurrent attacks of abdominal pain, vomiting and
distension.
3.
Tuberculous toxaemia with night fever, night sweats, anorexia and
wasting is present.
4.
The abdomen is felt doughy with multiple palpable swellings which
may be lymph nodes, omentum and tuberculomas. Ascites is a common
finding.
5.
Tenderness and guarding may be present.
6.
A sausage shaped mass above the umbilicus may be felt (rolled
omentum).
7.
Per-vaginal examination may reveal a tubo-ovarian mass.
Summary
Tuberculous peritonitis
■ Acute (may be clinically indistinguishable from acute bacterial
peritonitis) and chronic forms
■ Abdominal pain, sweats, malaise and weight loss are frequent
■ Ascites common, may be loculated
■ Caseating peritoneal nodules are common – distinguish from metastatic
carcinoma and fat necrosis of pancreatitis
■ Intestinal obstruction may respond to antituberculous treatment without
surgery
Investigations
1. Blood picture may reveal anaemia and lymphocytosis. ESR is raised.
2. Tuberculin test is highly positive.
3. Plain chest X-ray.
4. Abdominal ultrasound may reveal loculated or free ascites or multiple
swellings due to caseous collections of pus among adherent loops of
intestine.
5. Abdominal tapping is performed in the ascitic type. The aspirated fluid
is clear and straw coloured with a specific gravity above 1020. It is very
18
rich in lymphocytes. It is difficult to demonstrate TB bacilli by direct films.
To demonstrate them animal inoculation or culture is necessary.
6. Laparoscopy allows direct visualization of the characteristic tubercles
and biopsy. A solid proof of the diagnosis is obtained, which is an
essential prerequisite for the administration of anti-tuberculous drugs.
7. Exploration. In many cases a diagnosis is reached after exploration and
biopsy of suspicious lesions.
Treatment
■ Treatment is essentially medical. At least two antituberculous drugs,
e.g. (isonicotinic acid hydrazide and rimactane) are prescribed for at least
one year.
■ Operation is indicated in a few cases, e.g., intestinal obstruction.
(A )
(B)
Figure (a) Chest computed
tomography from a 55-year-old man
showing miliary tuberculosis; (b and c)
representative computed tomography
images from the same patient
showing gross ascites, nodular
stranding in the omentum and
mesentery as well as nodular
enhancement of the peritoneum –
tuberculous peritonitis
(C)
19
Bile peritonitis
Causes of bile peritonitis
1-Perforated cholecystitis
2-Postcholecystectomy
■ Cystic duct stump leakage
■ Leakage from an accessory duct in the gall bladder bed
■ Bile duct injury
■ T-tube drain dislodgement (or tract rupture on removal)
3-Following other operations/procedures
■ Leaking duodenal stump postgastrectomy
■ Leaking biliary–enteric anastomosis
■ Leakage around percutaneous placed biliary drains
4-Following liver trauma
Treatment
■ Laparotomy (or laparoscopy) should be undertaken with evacuation of
the bile and peritoneal lavage. The source of bile leakage should be
identified and treated accordingly. Infected bile is more lethal than sterile
bile. A ‘blown’ duodenal stump should be drained as it is too edematous to
repair, but sometimes it can be covered by a omentum patch. The patient
is often jaundiced from absorption of peritoneal bile, but the surgeon
must ensure that the abdomen is not closed until any obstruction to a
major bile duct has been either excluded or relieved.
■ Bile leaks after cholecystectomy or liver trauma may be dealt with by
percutaneous (ultrasound guided) drainage and endoscopic biliary
stenting to reduce bile duct pressure. The drain is removed when dry and
the stent at 4–6 weeks.