Midgut Ischaemia

DEFINITION
Specifically referring to disruption of the blood flow through the superior mesenteric artery, which variably supplies the gut from proximal jejunum to colon.
Arterial, Non-occlusive or venous.
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INCIDENCE

Incidence

Uncommon but serious
Age
Elderly

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

Arterial
Atherosclerotic / atherothrombotic.
Embolic (most notably in AF or post-MI).
- commonly lodge in area of origin of middle colic.

Non-occlusive
In setting of systemic hypoperfusion, commonly ICU patients on inotropes
- no fixed stenosis or occlusion
Is varied and difficult to diagnose, especially in these patients.
- signs of shock or peritonitis may need exploration

Mesenteric Venous Thrombosis
Vascular congestion due to poor venous outflow, may be precipitated by intraabdominal inflammatory processues
- appendicitis, diverticulitis.
Hypercoaguable states in general

Chronic Mesenteric Ischaemia
Stenosis or occlusion of at least 2/3 main arterial trunks.
Symptoms often induced by eating
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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 invasion with sepsis and shock follow ongoing ischaemia.
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

Tissue highly vulnerable to reperfusion injury.

Prognosis
High mortality.
Extensive gangrene invariably fatal.

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MANIFESTATIONS
Symptoms

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.

Variable Features

Also distension (48.2%).
Presenting with vascular collapse (37.4%)
Diarrhoea (32.8%)
Bloody stools (late sign, 22.4%)
Bloody vomit (11.9%)

Late Features

Hypotension.
Sepsis and multi-organ failure.

Systemic


Prodromal phase

Rarely anaemia of occult blood loss.

Acute Ischaemia

Non-specific unwellness.

Signs


Observe

Abdo distension (~50%).
Bowel sounds may be absent.

Palpate

Vague tenderness (85.5%).
Usually a suspicious paucity of physical signs.

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.

Visceral Angiography

If normal, does not necessarily exclude bowel ischaemia.

Barium Study

May show bowel dysfunction, even in prodromal phase.

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MANAGEMENT

Therapeutic

ABCs - resuscitate.
IV antibiotics (broad spectrum); take cultures first.

Operative
Laparotomy if features of peritonism
- 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.
- autologous vein grafts preferred in this setting
Else urgent angiography (or as adjunct to a necessary laparotomy)
- can confirm diagnosis and administer thrombolytic therapy or vasodilation via angiocath.
Epidural may help relieve any contributing vasospasm.

Chronic
Options are endovascular therapy and open surgery
Fewer complications with endovascular therapy but higher long term failure rate (repeat interventions ok though).
--> PTA and stenting particularly useful for patients not suitable for surgery. 
Endovascular options are percutaneous angioplasty with or without stenting.
Open revascularization to aorta with side-biting clamp and dacron grafts or PTFE.
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