Midgut Ischaemia / Infarction
DEFINITION
Specifically referring to distruption of the blood flow through the
superior mesenteric artery, which variably supplies the gut from
proximal jejunum to colon.
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INCIDENCE
Incidence
Important though uncommon.
Age
Elderly
Gender
Geographical distribution
Risk factors
Predisposing conditions
Cardiac Arrhythmia.
Vessel disease, especially past-MI.
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AETIOLOGY
Pathogenesis
Anything which disrupts the flow through the superior mesenteric vessel.
Sieve
Atherosclerotic / atherothrombotic.
Embolic (most notably in AF or post-MI).
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BIOLOGICAL BEHAVIOUR
Natural history
Depends upon cause.
May be sudden due to acute blockage (eg an embolus) or gradual
occlusion (eg athersclerotic).
- compensatory flow is possible in gradual occlusions.
Gradual occlusions may have a prodromal phase lasting weeks or months,
so called 'angina of the bowel'.
Acute illness lasts many hours, days or even weeks before onset
of infarction, peritonitis and finally vascular collapse.
Pathophysiology
Once ischaemia sets in, huge fluid loss into the bowel occurs.
Vasoactive substances released further diminish perfusion.
Enzyme-rich mucosa releases many free-radicals.
Mucosal disruption (necrosis) and bacterial translocation / invasion
with sepsis and
shock follow ongoing ischaemia.
- ischaemia promotes anaerobe growth including clostridial species.
Diagnosis is delayed to this stage in up to 85%.
Pathology
Appears haemorrhagic due to
blood reflow into the damaged area.
Early: congested, dusky, foral
eccymotic discolouration.
- lumen may contain blood or sanguineous mucous.
Usually sharply demarcated where blood supply good and bad.
Late: within 1-4 days outright
gangrene and perforation is present.
Complications
Perforation
- though with any significant length (>30cm), pt will succumb to
consequences of dead bowel before perforation occurs.
Tissue highly vulnerable to reperfusion injury.
Prognosis
High mortality.
Extensive gangrene invariably fatal.
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MANIFESTATIONS
Symptoms
Beware - difficult to diagnose.
Local
Prodromal
Vague pain post-prandially, with resulting anorexia.
Altered bowel habit, weight loss (malabsorption), vomiting (less
common).
Many such pts have been diagnostic neurotic by GPs, due to lack of
clinical findings to explain pain.
Acute
Pain (100%), - most important.
- severe, central, vague, and often out of proportion to any objective
signs.
Can be quite sudden if acute cause, eg an embolus.
Often present 12-48 hrs (and up to 2 weeks) before admission.
Abdo tenderness (85.5%) and vomiting (81%).
Warning Triad
Constant sudden onset abdo pain, early vomiting and odd absence of abdo
signs.
Have they got cardiac disease??
Variable Features
Also distension (48.2%).
Presenting with vascular collapse (37.4%)
Diarrhoea (30%-50%)
Bloody stools (late sign, 22.4%)
- 80% FOB +ve
Bloody vomit (11.9%)
Late Features
Hypotension (may be unresponsive to fluids)
Sepsis and multi-organ failure.
Systemic
Prodromal phase
Rarely anaemia of occult blood loss.
Acute Ischaemia
Non-specific unwellness.
Signs
Koelmeyer's Quintet
Vague hx, vague pain, vague abdo exam, vague x-ray, elevated WCC.
Observe
Abdo distension (~50%).
Bowel sounds may be absent.
Palpate
Vague tenderness (85.5%).
Usually a suspicious paucity of physical signs.
- remember peritoneal irritation is limited.
Auscultate
Bowel sounds may be absent
Underlying Cause
Eg cardiac arrhythmias, previous MIs, risk factors for vessel
disease.
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INVESTIGATIONS
Immediate laparotomy if suspected.
Haematology
Marked leucocytosis often found early.
Blood gases are helpful - metabolic acidosis suggests a sick patient.
Biochemistry
Serum phosphate may be increased.
Imaging
AXR
Usually vague.
Early nothing, later ileus, air in portal vein and liver.
May show thickened wall, but rarely will show air in bowel wall.
Visceral Angiography
May show evidence of occlusion, but cannot exclude small areas of
infarction.
Barium Study
May show bowel dysfunction, even in prodromal phase.
Laparotomy
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MANAGEMENT
Therapeutic
ABCs - resuscitate.
IV antibiotics (broad spectrum); take cultures first.
Operative
Laparatomy.
Either restore flow, resect dead bowel, or sigh and close up -
depending on how advanced disease is.
Restoring flow usually involves bypassing block, or performing an
embolectomy.
Can administer thrombolytic therapy or vasodilation via angiocath.
Epidural may help relieve any contributing vasospasm.
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