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Diagnosis during laparotomy, tubercles on the peritoneum and
omentum which will undergo caseation
Differential diagnosis: peritoneal carcinomatosis
Treatment: peritoneal lavage, fluid and tissue for analysis
B. Chronic tuberculous peritonitis is rare:
c/f: 90% of patients with abdominal pain, 60% are with fever and
loss of weight, ascites 60%, night sweating 37%. Abdominal mass
is found in 25-30% of patients.
Origin of the infection:
1. Tuberculous mesenteric LN
2. Tuberculosis of the ileocaecal region
3. Tuberculous pyosalpinx
4. Blood borne infection: pulmonary TB (miliary)
C. Varieties of tuberculous peritonitis:
1- Ascitic form
2- Encysted form
3- Fibrous form
4- Purulent form
9. Peritoneal bands and adhesions:
· Congenital bands and membranes: anatomical anomalies in
newborn children causing usually intestinal obstruction.
· Peritoneal adhesions: abnormal deposit of fibrous tissue after
peritoneal injury (operation or peritonitis) the commonest cause
of intestinal obstruction and secondary female infertility
· Talc granuloma: (mg silicate) cause adhesions and tube granuloma
k bitartrate is suitable
· Starch peritonitis: in sensitive patient. It causes painful ascites
of limited duration
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Adhesions lower abdomen. Adhesions upper abdomen.
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Acute Mesenteric Ischemia
Rarely an episode of mesenteric vascular occlusion may be followed
by survival of the gut and gradual stricture formation. A variety of causes
converges to produce segmental gangrene of the small bowel, with or
without involvement of the adjacent caecum and proximal colon. Large
vessel occlusion by either embolus or thrombus is the commonest in
elderly adults.
Acute mesenteric ischemia is interruption of intestinal blood flow by
embolism, thrombosis, or a low flow state. It leads to mediator release,
inflammation, and ultimately infarction. Abdominal pain is out of
proportion to physical findings. Early diagnosis is difficult, but
angiography and exploratory laparotomy have the most sensitivity;
other imaging modalities often become positive only late in the disease.
Treatment is by embolectomy, revascularization of viable segments, or
resection; sometimes vasodilator therapy is successful. Mortality is high.
Pathophysiology
The intestinal mucosa has a high metabolic rate and, accordingly, a high
blood flow requirement (normally receiving 20 to 25% of cardiac
output), making it very sensitive to the effects of decreased perfusion.
Ischemia disrupts the mucosal barrier, allowing release of bacteria, toxins,
and vasoactive mediators, which in turn leads to myocardial depression,
systemic inflammatory response syndrome, multisystem organ failure,
and death. Mediator release may occur even before complete infarction.
Necrosis can occur as soon as 10 to 12 h after the onset of symptoms.
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Etiology
Three major vessels serve the abdominal contents: the celiac trunk, the
superior mesenteric artery (SMA), and the inferior mesenteric artery
(IMA).
The celiac trunk supplies the esophagus, stomach, proximal duodenum,
liver, gallbladder, pancreas, and spleen. The SMA supplies the distal
duodenum, jejunum, ileum, and colon to the splenic flexure. The IMA
supplies the descending colon and sigmoid colon and the rectum.
Collateral vessels are abundant in the stomach, duodenum, and rectum;
these areas rarely develop ischemia. The splenic flexure is a watershed
between the SMA and IMA and is at particular risk of ischemia.
Mesenteric blood flow may be disrupted on either the venous or arterial
sides. In general, patients > 50 are at greatest risk and have the types
of occlusions and risk factors shown in the Table below. However,
many patients have no identifiable risk factors.
Mesenteric ischemia of small bowel.
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Causes of acute mesenteric ischemia
Occlusion type Risk factors
Arterial embolus
(> 50%)
Coronary artery disease, heart failure, valvular
heart disease, atrial fibrillation, history of arterial
emboli
Arterial
Generalized atherosclerosis
thrombosis (10%)
Venous
thrombosis
(5–15%)
Hypercoagulable state, inflammatory conditions
(e.g. pancreatitis, diverticulitis), trauma, heart
failure, renal failure, portal hypertension,
decompression sickness
Nonocclusive
ischemia (25%)
Low flow states (e.g. heart failure, shock,
cardiopulmonary bypass) and splanchnic
vasoconstriction (e.g., vasopressors, cocaine)
Symptoms and Signs:
The early hallmark of mesenteric ischemia is severe pain but minimal
physical findings. The abdomen remains soft, with little or no
tenderness. Mild tachycardia may be present. Later, as necrosis develops,
signs of peritonitis appear, with marked abdominal tenderness, guarding,
rigidity, and no bowel sounds. The stool may be heme-positive
(increasingly likely as ischemia progresses). The usual signs of shock
develop and are frequently followed by death. Sudden onset of pain
suggests but is not diagnostic of an arterial embolism, whereas a more
gradual onset is typical of venous thrombosis. Patients with a history of
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postprandial abdominal discomfort (which suggests intestinal angina)
may have arterial thrombosis.
When acute infarction occurs the pain at onset may be colicky but
soon becomes continuous and intense. Shock from depleted blood
volume is early in onset and is accompanied by metabolic acidosis.
Clinical examination reveals first local and later generalized tenderness
or rigidity. Bowel sounds are absent.
Diagnosis
Clinical diagnosis is more important than diagnostic tests. The major
differential diagnostic problem is acute pancreatitis. Serum amylase
concentrations are likely to be somewhat raised in mesenteric vascular
occlusion. Mesenteric angiography if diagnosis unclear.
Early diagnosis is particularly important because mortality increases
significantly once intestinal infarction has occurred.
Mesenteric ischemia must be considered in any patient > 50 with
known risk factors or predisposing conditions who develops sudden,
severe abdominal pain.
Patients with clear peritoneal signs should proceed directly to the
operating room for both diagnosis and treatment. For others, selective
mesenteric angiography is the diagnostic procedure of choice. Other
imaging studies and serum markers can demonstrate abnormalities but
lack sensitivity and specificity early in the course of the disease when
diagnosis is most critical. The radiological findings are usually minimal.
Plain abdominal x-rays are useful mainly in ruling out other causes of
pain (eg, perforated viscus), although portal venous gas or pneumatosis
intestinalis may be seen late in the disease. These findings also appear
on CT, which may also directly visualize vascular occlusion-more
accurately on the venous side.
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Gangrene of small bowel.
Doppler ultrasonography can sometimes identify arterial occlusion,
but sensitivity is low.
MRI is very accurate in proximal vascular occlusion, less so in distal
vascular occlusion.
Serum markers (e.g. creatine phosphokinase, lactate) rise with
necrosis but are nonspecific findings that are seen later.Intestinal fatty
acid binding protein in the urine may prove valuable in the future as
an early marker.
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CTA shows filling defect in SMA (arrowhead) and patent superior
mesenteric vein.
Prognosis
If diagnosis and treatment take place before infarction occurs, mortality
is low; after intestinal infarction, mortality approaches 70 to 90%. For
this reason, clinical diagnosis of mesenteric ischemia should supersede
diagnostic tests, which may delay treatment.
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Treatment
1. Surgical treatment: embolectomy, revascularization, or resection.
2. Angiographic: vasodilators or thrombolysis.
3. Long-term anticoagulation or antiplatelet therapy.
If diagnosis is made during exploratory laparotomy, options are surgical
embolectomy, revascularization, and resection. A “second look”
laparotomy may be needed to reassess the viability of questionable areas
of bowel. If diagnosis is made by angiography, infusion of the vasodilator
papaverine through the angiography catheter may improve survival in
both occlusive and nonocclusive ischemia. A 60-mg bolus is given
over 2 min, followed by an infusion of 30 to 60 mg/h. Papaverine is
useful even when surgical intervention is planned and is sometimes given
during and after surgical intervention as well. In addition, for arterial
occlusion, thrombolysis or surgical embolectomy may be done. The
development of peritoneal signs at any time during the evaluation
suggests the need for immediate surgery.
Mesenteric venous thrombosis without signs of peritonitis can be
treated with papaverine followed by anticoagulation with heparin and
then warfarin. Patients with arterial embolism or venous thrombosis
require long-term anticoagulation with warfarin. Patients with
nonocclusive ischemia may be treated with antiplatelet therapy.
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