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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