Bowel Infarction

Bowel infarction is irreversible transmural intestinal necrosis caused by sustained ischaemia.

It represents the end stage of several processes, including acute mesenteric arterial occlusion, mesenteric venous thrombosis, strangulated obstruction, volvulus, internal hernia and severe nonocclusive mesenteric ischaemia.

Once infarction is established, restoring perfusion alone is insufficient. Necrotic bowel must be removed while every possible centimetre of viable intestine is preserved.

Pain may initially be severe with limited physical findings if infarction follows vascular occlusion. As transmural necrosis progresses, the abdomen becomes tender with guarding and eventually generalised peritonitis.

Late manifestations include ileus, abdominal distension, gastrointestinal bleeding, fever, hypotension, metabolic acidosis, oliguria and septic shock.

In strangulated obstruction, a transition from intermittent colic to persistent focal pain should raise concern for evolving infarction.

Peritonitis in mesenteric ischaemia strongly predicts irreversible bowel injury.

CT angiography or contrast enhanced CT according to suspected cause: establishes the vascular or mechanical process and assesses bowel viability. Reduced or absent bowel enhancement, pneumatosis, portal venous gas or perforation support advanced irreversible injury, although operative assessment ultimately determines viability.

Check blood gas, lactate, full blood count, renal function, electrolytes and coagulation. Crossmatch blood.

Hyperkalaemia and worsening metabolic acidosis may become pronounced after extensive necrosis or reperfusion.

Bowel infarction is an emergency.

Begin balanced crystalloid resuscitation, correct major electrolyte and acid base disturbances and start broad spectrum antibiotics because mucosal barrier failure and necrosis cause bacterial translocation.

A practical adult regimen is:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, adjusted for renal function.

If the mechanism is mesenteric vascular occlusion, administer full dose unfractionated heparin unless contraindicated and pursue revascularisation urgently.

Peritonitis, perforation or established necrotic bowel requires emergency exploration.

At surgery, first correct the reversible cause where feasible. Release strangulation, detorse volvulus or restore mesenteric arterial flow before deciding the final resection length.

Resect frankly necrotic bowel only. Marginal bowel may recover after restoration of blood flow, warming and physiological correction. Massive unnecessary resection can convert a survivable vascular catastrophe into permanent intestinal failure.

Primary anastomosis is appropriate only when bowel perfusion is clearly satisfactory and the patient is physiologically stable.

In severe shock, major contamination, bowel oedema or uncertain viability, use damage control principles. Leave stapled bowel ends in discontinuity if necessary, apply temporary abdominal closure and return for a second look operation in 24 to 48 hours.

Document residual small bowel length, presence of ileum, ileocaecal valve and remaining colon. These determine the subsequent risk and severity of short bowel syndrome.

When adequate source control has been achieved for associated intra abdominal infection, prolonged antibiotics are unnecessary. Current Surgical Infection Society guidance recommends no more than approximately 4 days after effective source control unless infection remains uncontrolled.