Question 3

Discussion

Syllabus topic/section: 2.1.18 Perioperative Issues in Intensive Care; L2 Vascular surgery

Candidates who were familiar with endovascular repair, stent malpositioning and specific haemodynamic management for optimisation of GI blood flow gained more marks. Candidates who failed to demonstrate proficiency in detailing investigation findings by noting details of graft position and patency as well as indirect signs of ischaemic colitis such as wall thickening and intramural gas are advised to revise their approach to achieve detail required to the level of the transitional fellow.

Some candidates who did less well misread the question and discussed open AAA repair. Candidates are reminded that wise use of the perusal time will aid in avoiding simple yet costly mistakes in approach to these questions.

Interpretation

a) Mechanisms:

• Global hypoperfusion: 
  • ruptured AAA with haemorrhagic shock
  • low cardiac output (coronary arteries are in the same state as the aorta)
  • vasoconstrictor exposure
  • reperfusion injury after flow is restored
• Abdominal hypoperfusion:
  • abdominal compartment syndrome
  • pressure from retroperitoneal haematoma
  • bowel lumen pressure increase (eg. dilatation due to ileus)
• Regional vascular territory hypoperfusion: 
  • Stent coverage of mesenteric arteries
  • embolic occlusion (clot, cholesterol, air)
  • dissection of mesenteric arteries
  • Failure of collateral supply:
    • Watershed territories, especially the splenic flexure and rectosigmoid
    • Coexisting atheromatous disease
  • Stent malfunction: migration, malposition, limb kinking, oversized stent, stent thrombosis or endoleak-related high aneurysm sac pressure

b) Investigations and expected findings

• Blood gas and laboratory tests: 
  • lactate: expected to be raised
  • pH, SBE: metabolic acidosis
  • Rising biomarkers of end-organ dysfunction (eg. EUC,  LFTs)
• CT mesenteric angiogram: 
  • Stent mischief
    • Malposition, migfration, kinking, endoleak
  • Acute arterial ischaemia:
    • Bowel wall thinning (“paper thin”)
    • Diminished or absent mural enhancement on arterial phase
    • Obviously, a large occluded vessel
  • Acute venous ischaemia:
    • Mural thickening
    • Mural stratification (one should not usually be able to clearly see the layers of the bowel wall on CT)
    • Mesenteric stranding / oedema
  • Generally,
    • Bowel dilatation
    • Pneumatosis coli, where the bowel wall has gas in it
    • Portal venous gas (distinguishable from gas in the biliary tree because it is seen in the periphery of the liver, whereas biliary gas is more central and perihilar).
    • Pneumoperitoneum of perforation
• DSA (angiography):
  • vessel occlusion/dissection
  • endoleak
  • stent malposition
• Endoscopy 
  • early: generic colitis (inflamed bowel with areas of ulceration),
  • later: Grade II, and III, transmural ulceration progressing to grey and black as the bowel becomes gangrenous. 

c) Management:

• Reperfusion: reposition the stent, bypass/reimplant mesenteric arteries
• Optimise perfusion:
  • Cease enteral nutrition)
  • Aim for a higher MAP (~80) while avoiding vasopressors
  • Decompress the gut with NG
  • Control the abdominal compartment pressure:
    • paralysis
    • controlled fluid resuscitation
    • open the abdomen
• Supportive care
  • TPN, antibiotics (eg. piperacillin/tazobactam or a 3rd generation cephalosporin plus metronidazole)
• Remove ischaemic bowel
  • Gut at Grade II or III is likely to have transmural necrosis and probably needs to come out before it makes everything worse
  • Partial or total colectomy is often required
  • The laparotomy gives the option of evacuating any haematoma that has accumulated, or to revascularise any mesenteric vessels that require revascularisation
  • The abdomen can be left open to improve the perfusion of the residual bowel

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