Postoperative Mesenteric Ischaemia

Postoperative mesenteric ischaemia is reduced intestinal blood flow after surgery, causing bowel ischaemia and necrosis. It is a surgical emergency with high mortality.

Epidemiology. It occurs in about 0.1% to 2% of abdominal aortic surgery, 0.1% to 0.4% after cardiac surgery (up to 1% in some series), and 0.5% to 1% after major abdominal surgery. Mortality ranges from 30% to 80%, and rises with delay.

Types. Non-occlusive mesenteric ischaemia (low flow and vasoconstriction, 20% to 30% of cases), arterial embolism or thrombosis, mesenteric venous thrombosis, and ischaemic colitis (after aortic surgery with inferior mesenteric artery ligation).

Risk factors. Cardiac surgery and cardiopulmonary bypass, aortic surgery, low cardiac output, hypotension, vasopressors (vasopressin, high dose noradrenaline), digoxin, atrial fibrillation, atherosclerosis, renal failure, hypovolaemia, hypercoagulability and age over 70 years.

Pathophysiology.

Splanchnic vasoconstriction in low flow states (non-occlusive) or vessel occlusion (embolism, thrombosis) reduces mucosal perfusion. Mucosal injury causes barrier failure, translocation of bacteria and sepsis. Reperfusion injury worsens necrosis.

Abdominal pain out of proportion to examination (early), distension, vomiting, bloody diarrhoea, fever, ileus, tachycardia, hypotension, peritonitis (late), rising lactate and metabolic acidosis. Signs may be hidden in sedated patients, in whom unexplained acidosis, rising vasopressor need, ileus or feed intolerance may be the only clues.

Red flags.

• Rising lactate over 2 mmol/L with abdominal signs.
• Unexplained metabolic acidosis.
• Peritonitis.
• Bloody stool.
• Rising vasopressor requirement.

CT angiography of the abdomen (arterial and portal venous phases) is the first investigation: shows vessel occlusion, bowel wall thickening or non-enhancement, pneumatosis and portal venous gas. Lactate (not sensitive or specific), blood gas, full blood count, amylase and C-reactive protein. Diagnostic laparoscopy or laparotomy for unstable patients. Colonoscopy for ischaemic colitis. Do not delay imaging for biochemical results.

Differential diagnosis.

• Bowel obstruction.
• Perforated viscus.
• Pancreatitis.
• Anastomotic leak.
• Clostridioides difficile colitis.
• Intra-abdominal sepsis.

Resuscitate: oxygen, crystalloid, correct hypovolaemia, and optimise cardiac output while minimising vasoconstrictors (reduce vasopressin and high dose noradrenaline).

• Heparin (unfractionated, for embolism, thrombosis and venous thrombosis once bleeding excluded): 80 units/kg IV bolus (maximum 5,000 units) then 18 units/kg/h; adjust to anti-Xa 0.3 to 0.7 units/mL or activated partial thromboplastin time ratio 1.5 to 2.5; maximum monitored by levels; monitor platelets (heparin induced thrombocytopenia), bleeding and renal function; reduce in renal impairment.
• Piperacillin-tazobactam: 4.5 g IV every 6 hours (broad spectrum cover for translocation) for 5 to 7 days, longer if abscess; maximum 18 g daily; monitor renal function and counts; reduce for creatinine clearance under 40 mL/min.
• Metronidazole 500 mg IV every 8 hours may be added if the antibiotic chosen lacks anaerobic cover; maximum 1.5 g daily; monitor for neuropathy and reduce in severe hepatic impairment.
• Papaverine 30 to 60 mg/h by intra-arterial infusion (specialist interventional use) for non-occlusive mesenteric ischaemia; continue 24 hours with repeat angiography; monitor blood pressure and heparin interaction.

Surgical management: urgent laparotomy with resection of non-viable bowel, revascularisation (embolectomy, bypass, stent) for arterial occlusion, and a planned second look operation at 24 to 48 hours. Endovascular revascularisation is an option for arterial occlusion in selected patients.

Venous thrombosis: anticoagulation for at least 3 to 6 months.

Monitoring. Lactate every 2 to 4 hours, haemodynamics, abdominal examination, urine output and drain output.

Referral and escalation. Vascular and general surgery urgently, interventional radiology and critical care. Early discussion with the family about prognosis.

Special groups. Older adults and patients on vasopressors are at highest risk.