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Bowel ischaemia

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Acute mesenteric ischaemia

Mesenteric vein thrombosis


Ischaemic bowel injury in the distribution of the superior mesenteric vessels. Ranges from reversible alterations in bowel function to transmural necrosis of the bowel wall


SMA embolus

- 40-50% of episodes of acute mesenteric ischaemia
- emboli usually originate from LA or LV mural thrombus
- approx 20% have synchronous emboli in other arteries

Non occlusive mesenteric ischaemia

- 20-30% of episodes
- probably results from splanchnic vasoconstriction initiated by vasoactive medication or a period of decreased cardiac output. Vasoconstriction may persist even after the precipitating cause has been eliminated or corrected
- predisposing factors: MI, CCF, aortic, hepatic and renal disease, major cardiac and intra-abdominal operations
- a more immediate precipitating cause (eg pulmonary oedema, arrhythmia, shock) is frequently present although the consequent mesenteric ischaemia may not become manifest for hrs-days

SMA thrombosis

- acute ischaemic episode often superimposed on chronic ischaemia so 20-50% of patients have a history of abdominal pain +/- malabsorption for weeks-months
- associated with cardiac, cerebral and peripheral vascular disease

Mesenteric vein thrombosis

- may present acutely, subacutely or as a chronic process
- < 5% of cases of acute mesenteric ischaemia
- click here for more details

Clinical features

- early identification requires high index of suspicion
- acute abdominal pain varying in severity, nature and location in 75-98%
- pain is usually out of proportion to physical findings in early stages
- rapid and forceful bowel evacuation
- unexplained abdominal distension or GI bleeding may be only features, especially in non-occlusive disease
- distension is a late feature and is often the first sign of impending bowel infarction
- stool +ve for occult blood in 75%. May precede all other features
- right-sided abdominal pain associated with the passage of maroon or bright red blood in stool, although characteristic of colonic ischaemia, also suggests the diagnosis of acute mesenteric ischaemia
- no abdominal findings early in course of intestinal ischaemia but as infarction develops there is increasing tenderness, rebound tenderness, and guarding
- nausea, vomiting, melaena, haematemesis, massive abdominal distension, back pain and shock are late features indicating compromise of bowel viability


  • WCC > 15 in 75%
  • metabolic acidosis in 50%
  • plain AXR normal in early stages. Late: formless loops of small bowel or small intestinal "thumbprinting". Less commonly "thumbprinting" of right colon
  • laparoscopy may be useful in patients whose clinical condition precludes angiography but examination is limited to the serosal surface making it unreliable for identifying mucosal necrosis early in its course
  • angiography: mainstay of diagnosis of and initial treatment of both occlusive and non-occlusive forms. (NB mesenteric vasoconstriction can occur in hypotensive patients and those with pancreatitis as well as in patients with non-occlusive mesenteric ischaemia)
  • duplex scanning: can identify portal and superior mesenteric vein thrombosis and, in some patients, SMA occlusion
  • CT has also been used to identify arterial and venous thromboses as well as ischaemic bowel, but only in the late stages of the disease


  • aggressive resuscitation
  • plain AXR to exclude other diagnoses and to look for infarcted bowel. NB normal AXR does not exclude diagnosis
  • angiography. Should be performed even if decision to operate has been made on clinical grounds in order to manage the patient properly at laparotomy. Moreover relief of mesenteric vasoconstriction is essential to treat emboli and thromboses as well as non-occlusive ischaemia
  • intra-arterial papaverine via angiographic catheter placed in SMA: 30-60 mg/h. Majority of papaverine is cleared during passage through the liver but there is a risk of systemic hypotension. Daily repeat angiogram to determine whether papaverine should be continued
  • laparotomy to restore blood flow and to resect non-viable bowel. If diagnosis of non-occlusive ischaemia is made, laparotomy should be performed if there is clinical suspicion of infarcted bowel
  • post-operative anti-coagulation: probably advisable 48 h post op in order to prevent late thrombosis following embolectomy or arterial reconstruction
  • broad spectrum antibiotics (associated with improved survival)


Approx 50% mortality even with vasodilator therapy

Mesenteric vein thrombosis

Infrequent but distinct form of gut ischaemia

Associated with:

Hypercoagulable states

- peripheral DVT
- neoplasms
- protein C & S deficiency
- antithrombin III deficiency
- oral contraceptive
- pregnancy
- polycythaemia vera
- thrombocytosis


- pancreatitis
- peritonitis
- inflammatory bowel disease
- pelvic or intra-abdominal abscess

Portal hypertension

- cirrhosis
- congestive splenomegaly
- following sclerotherapy of varices


- post-op
- following splenectomy
- blunt abdominal trauma


- decompression sickness


Thrombosis due to cirrhosis, or operative injury starts at site of injury and extends peripherally whereas thromboses caused by hypercoagulable states start in smaller veins and propagate into major trunks. When collateral circulation is inadequate and venous drainage from a segment of bowel is compromised there is increasing congestion of the affected bowel with oedema, cyanosis, and thickening with intramural haemorrhage. Ultimately similar changes affect the mesentery. Serosangineous peritoneal fluid accompanies early haemorrhagic infarction. Late in the process when transmural infarction occurs it may be impossible to distinguish venous from arterial occlusion

Clinical features

- varied and non-specific
- abdominal pain usual but location, duration, nature and severity vary widely
- nausea and vomiting
- GI bleeding (bloody diarrhoea and haematemesis) indicate bowel infarction
- abdo tenderness in almost all patients
- decreased bowel sounds, abdo distension in most patients
- clear signs of peritonitis in only 2/3 initially
- guarding and rebound develop as bowel infarction occurs
- pyrexia


- AXR. When abnormal almost always reflects presence of infarcted bowel
- angiography can establish definitive diagnosis before infarction occurs
- CT can establish diagnosis in over 90%
- ultrasound may be difficult because of overlying gas


In absence of evidence of bowel infarction a trial of anticoagulant or thrombolytic therapy may prove worthwhile but immediate laparotomy is indicated if signs of infarction develop. Infarcted bowel should be resected and anticoagulation started immediately post-op (recent studies show clear evidence of benefit from immediate anti-coagulation)


Mortality 20-50%

Further reading

Kaleya RN, Boley SJ. Acute mesenteric ischaemia. Crit Care Clin, 1995; 11(2):479-512

© Charles Gomersall December 1999


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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