Mesenteric ischaemia

This is a common enough event in the ICU that one might have expected something earlier - but, in all recorded history of the CICM exam (at least for which I have any previous papers) a serious discussion of ischaemic gut has only ever come up once, in Question 12 from the first paper of 2017. This SAQ asked for a detailed exploration of mesenteric ischaemia, specifically asking candidates to "outline the pathophysiology, diagnosis and treatment".

What does an intensivist need to know about this for their final exams? Not much, if Oh's Manual is anything to go by. Mesenteric ischaemia comes up once as a quarter-page discussion in Jamie Cooper's chapter on lactic acidosis (p/160 of the 7th edition), where much is made of how difficult it is to diagnose, and how one must have a high index of suspicion. Nothing in the way of concrete recommendations or instructions is offered, which is characteristic of the Manual (and defies the definition of a manual).

For good quality reading on this topic, the time-poor candidate is directed to either this 2014 review by Schofield et al or this NEJM article by Clair and Beach (2016). Each has helpful exam-ready headings like "Pathophysiology" and "Diagnosis". These articles were remixed into the summary which follows. Most of the discussion will be about acute mesenteric ischaemia as it is seen more commonly in critical care environments, but chronic mesenteric ischaemia is also a thing - more akin to claudication of the gut - which will receive some minimum of attention here. For more detail about this very different beast, the exam candidate with infinite time resources is directed to the excellent review by Pecoraro et al (2012)

Pathophysiology of mesenteric ischaemia

There are several major ways this thing can happen:

  • Acutely:
    • 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)
  • Chronically
    • Gradual onset of arterial insufficiency

Arterial embolism into mesenteric territory

  • This results in an acute occlusion of the vessels
  • The origin of the thrombus is typically the heart
  • AF is the main cause, but other possibilities exist (eg. LV apical thrombus, a large abdominal aortic aneurysm, or cholesterol emboli after angiography or IABP insertion)

Arterial atheroma rupture in the mesenteric arteries

  • Atherosclerosis of mesenteric vessels can result in plaque rupture and mesenteric ischaemia
  • 75% of these patients have pre-existing chronic mesenteric ischaemia; in 90% of cases the acute ischaemia is due to a progressive atheromatous narrowing at the origin of the mesenteric vessels.

Non-occlusive mesenteric ischaemia

  • The mesenteric circulation is a vascular bed with high vascular resistance
  • Any increase in SVR can lead to mesenteric hypoperfusion
  • Typically this is seen in patients requiring high-dose vasopressors

Venous mesenteric infarction

  • This is basically a DVT of the gut, with resulting oedema and diminished perfusion.
  • Risk factors include portal hypertension, hypercoagulability, thrombocytosis and any sort of local inflammation (eg. pancreatitis or diverticulitis).

Chronic mesenteric arterial insufficiency

  • Atherosclerosis of mesenteric vessels leads to chronically diminished flow though the mesenteric circulation
  • Generally speaking, this leads to the development of extensive collateral circulation
  • The collateral circulation allows a major visceral arterial occlusion to be clinically silent, and to go virtually unnoticed

Diagnosis of mesenteric ischaemia


  • 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


  • Classic “pain out of proportion to examination”
  • Epigastric bruit
  • Peritonism
  • Clinical features of shock


  • Features of organ system dysfunction, eg. rising creatinine
  • Raised lactate
  • Neutrophilia


  • Doppler ultrasound of the mesenteric vessels
  • CT with IV contrast, two-phase to detect venous thrombosis
  • Catheter angiography (also allows thrombolysis)

Management of mesenteric ischaemia in the ICU

Specific management

  • Aggressive:
    • Endovascular repair
    • Open repair with or without vascular bypass
    • Catheter-directed clot aspiration or  thrombolysis
    • Stenting of dissected segments
  • Conservative:
    • Heparin infusion (this is probably the only therapy required for venous mesenteric ischaemia)

Supportive management

  • Airway protection may be required (high risk of aspiration)
  • Mechnical 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


Acosta, Stefan, and Martin Björck. "Modern treatment of acute mesenteric ischaemia." British Journal of Surgery 101.1 (2014).

Schofield, Nick, et al. "Acute mesenteric ischaemia." Journal of the Intensive Care Society 15.3 (2014): 226-230.

Clair, Daniel G., and Jocelyn M. Beach. "Mesenteric ischemia." New England Journal of Medicine 374.10 (2016): 959-968. (pdf)

Pecoraro, Felice, et al. "Chronic mesenteric ischemia: critical review and guidelines for management." Annals of vascular surgery 27.1 (2013): 113-122.