Question 13

College answer

Most candidates interpreted pathophysiology as causes, and so scored poorly on first section of the question. In general, there was a lack of specific knowledge, with many answers giving generic answers, and many answers were not at the required level of knowledge / expertise.

Discussion

Trainees are reminded that the following "model answer" is hugely overcooked, it is much longer than anything the trainees could be expected to write under exam conditions, and it is left here more as a comprehensive list of all the possible things they could write rather than as a model for what they should write. 

Pathophysiology: two classification systems, acute vs. chronic or occlusive vs. non-occlusive

• Acute mesenteric ischaemia:
  • Arterial embolism (40% of cases)
  • Arterial thrombosis from ruptured atheroma (20-35% of cases)
  • Arterial dissection (<5% of cases)
  • Non-occlusive mesenteric hypoperfusion (10-15% of cases)
  • Venous infarction (5-15% of cases)
• Chronic mesenteric ischaemia:
  • Gradual onset of arterial insufficiency
• Occlusive vs non-occlusive pathophysiology:
  • Occlusive: obstruction of the vessels, eg. by embolism
    • Venous mesenteric ischaemia is a subset of this: diminished perfusion due to venous occlusion and oedema 
  • Non-occlusive: mesenteric hypoperfusion due to reduced blood flow, eg. in severe shock

Assessment:

• History 
  • History of atherosclerosis
  • Hypercoagulable background
  • AF
  • Vasculitis
  • Recent abdominal surgery
  • Historical features associated with chornic mesenteri ischaemia, eg:
    • Postprandial pain ("mesenteric angina"), 30-60 minutes after eating
    • Weight loss
    • Diarrhoea or constipation
    • Early satiety
• Examination
  • Classic “pain out of proportion to examination”
  • Epigastric bruit
  • Peritonism
  • Clinical features of shock
• Biochemistry
  • Features of organ system dysfunction, eg. rising creatinine
  • Raised lactate
  • Neutrophilia
• Imaging
  • Doppler ultrasound of the mesenteric vessels
  • CT with IV contrast, two-phase to detect venous thrombosis
  • Catheter angiography (also allows thrombolysis)

Specific management:

• Occlusive mesenteric ischaemia:
  • Endovascular repair
  • Open repair with or without vascular bypass
  • Catheter-directed clot aspiration or  thrombolysis
  • Stenting of dissected segments
• Non-occlusive mesenteric ischaemia:
  • Management of the shock state which focuses on maximising splanchnic blood flow (eg. decreased doses of vasopressors, increased inodilators
  • Catheter-directed vasodilators may be an option (eg. papeverine)
  • Stenting could be an option if chronic SMA stenosis is making this condition worse
• Venous mesenteric ischaemia:
  • Anticoagulation
  • Endovascular clot retrieval
• In all cases
  • Bowel resection of the infarcted bowel may be the only option

Supportive management

• Airway protection may be required (high risk of aspiration)
• Mechanical ventilation (increased work of breathing due to acidosis)
• Circulatory support (vasodilated shock state)
• Analgesia and anaesthesia (opiates may actually be preferred, as they "rest the gut" by paralysing its motility)
• Neuromuscular junction blockers may help organ perfusion by their effect on abdominal compartment pressure
• Electrolyte correction (particularly correction of acdi-base balance)
• Fluid resuscitation (extensive third-space losses are to be expected)
• Abdominal compartment pressure - serial measurements 
• Parenteral nutrition (the patient should remain fasted)
• Antibiotics of a broad spectrum, eg. piperacillin/tazobactam or meropenem