Acute mesenteric ischaemia
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DR. N. WHEELER. ACUTE MESENTERIC ISCHAEMIA. BASIC ANATOMY. Celiac artery, SMA, and IMA supply foregut, midgut, and hindgut, respectively Celiac artery: Supplies lower esophagus, stomach, duodenum, liver, pancreas, and spleen SMA:

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Acute mesenteric ischaemia



Basic anatomy


  • Celiac artery, SMA, and IMA supply foregut, midgut, and hindgut, respectively

  • Celiac artery:

    • Supplies lower esophagus, stomach, duodenum, liver, pancreas, and spleen

  • SMA:

    • Communication between superior and inferior pancreaticoduodenal arteries is an important anastomosis that helps to maintain bowel perfusion in atherosclerotic disease of the mesenteric vessels

    • Supplies the ileum, cecum, ascending colon, the transverse colon and communicates with the IMA.

    • Right and middle colic arteries are an important supply of blood to the marginal artery of Drummond

  • Basic anatomy1


    • IMA:

      • Smallest mesenteric vessel

      • Supplies distal transverse, descending, sigmoid colon, rectum

      • Rectal branches offer anastomosis between visceral blood supply and the common supply

    • SMV drains the small intestine, cecum, ascending colon, transverse colon, stomach, pancreas and duodenum

    • IMV drains descending colon, sigmoid colon, rectum

    • IMV joins the splenic vein, which then joins the SMV to form the portal vein. The portal vein enters the liver



    • Insufficient blood perfusion of small bowel or colon may result from:

      • Embolic (50%) or Thrombotic arterial (25%) occlusion

      • Thrombotic venous occlusion (10%)

      • Non-occlusive processes (20%)

    • Injury severity is inversely proportional to mesenteric blood flow (number of vessels involved, systemic mean blood pressure, duration of ischemia, and collateral circulation)

    • SM vessels are more frequently involved than the IM vessels (larger diameter and better collaterals with inferior vessels)

    • Damage may range from reversible ischemia to transmural infarction with necrosis and perforation

    • Injury complicated by reactive vasospasm in SMA after initial occlusion and Arterial insufficiency causes tissue hypoxia, leading to bowel wall spasm initially(vomiting or diarrhea)

    • Mucosal sloughing may cause bleeding into the GIT



    • Minimal abdominal tenderness is present at this stage despite symptoms of intense visceral pain

    • If ischemia persists disruption of mucosal barrier occurs and bacteria, toxins, and vasoactive substances are released into the systemic circulation

    • This can cause septic shock, cardiac failure, or multi-organ failure before bowel necrosis actually occurs

    • With worsening hypoxic damage the bowel wall becomes edematous and cyanotic

    • Bowel necrosis occurs in 8-12 hours from onset of symptoms

    • Transmural necrosis leads to peritonism and indicates bad prognosis

    Acute mesenteric arterial embolism


    • Caused by embolism

    • Typical causes:

      • Mural thrombi - MI

      • Atrial thrombi - mitral stenosis and AF, vegetative endocarditis

      • Aortic thrombi - mycotic aneurysm, thrombi at sites of atheromatous plaques, sites of vascular aortic prosthetic grafts interposed between heart and SMA

    • Occlusion is sudden and no time to develop compensatory increase in collateral flow

    • Ischemia is more severe

    • SMA is most susceptible to emboli due to small angle and greater diameter, with IMA less commonly affected

    • CDC) Injury Center: special form of AMI due to systemic air embolism in high-energy blast injuries secondary to severe primary blast injury to the lung

    Acute mesenteric arterial thrombosis


    • Late complication of preexisting visceral atherosclerosis

    • Symptoms do not develop until 2 of 3 arteries are stenosed or completely blocked

    • Slow process of atherosclerotic stenosis before acute occlusion allows time for development of collateral circulation

    • Thrombus formation results in acute cessation of blood flow to GIT resulting initially in mucosal ischaemia and necrosis causing bloody stools

    • Bowel wall also becomes necrotic leading to bacterial overgrowth and bowel perforation, sepsis and death

    • Patients usually have history of atherosclerotis at other sites (eg, CAD, strokes, PVD) or other vascular disease (Aortic Aneurysms, dissections, trauma)

    • Drops in cardiac output after MI, CCF may cause AMI in pre-existing visceral atherosclerosis

    • Patients frequently present with history of chronic mesenteric ischemia and symptoms of intestinal angina before acute event

    Nonocclusive mesenteric ischemia


    • Precipitated by severe reduction in mesenteric perfusion secondary to arterial spasm or decreased cardiac output

    • Causes:

      • Cardiac failure

      • Shock

      • Use of potent vasopressors in critically ill patients

    • Bowel perfusion, like cerebral perfusion, is preserved in hypotension therefore NOMI represents a failure of autoregulation

    • Vasoactive drugs (eg, digitalis, cocaine, diuretics, and vasopressin) may also cause regional vasoconstriction

    • Gross pathologic arterial or venous occlusions are not observed

    Mesenteric venous thrombosis


    • Secondary MVT -!>80% result of processes that predispose patients to form clot in mesenteric circulation

    • Primary MVT occurs in the absence of any identifiable predisposing factor

    • Causes:

      • Malignancy

      • Blood disorders - Sickle cell disease, Protein C & S deficiency

      • Post surgery - after ligation of the splenic vein, portal vein or SMV

    • Mechanism for ischemia is a massive influx of fluid into the bowel wall and lumen, resulting in systemic hypovolemia and haemoconcentration

    • Subsequent bowel edema and decreased venous outflow impedes inflow of arterial blood and leads to bowel ischemia

    • Much younger population

    Mesenteric venous thrombosis1


    • Symptoms may be present longer

    • Infarction rarely observed with isolated SMV thrombosis, unless collateral flow in peripheral arcades or vasa recta is also affected

    • Fluid sequestration and bowel wall edema are more pronounced than in arterial occlusion

    • Colon rarely involved due to good callateral supply

    • Abu-Daff et al - 30-day mortality in these patients was strongly linked to colonic involvement in ischemia and to short-bowel syndrome.[26] Lack of anticoagulation also may have been a factor. The 5-year mortality, according to the investigators, was primarily related to short-bowel syndrome.



    • All-cause mortality 71% (59-93%)

    • Once bowel wall infarction has occurred the mortality is as high as 90%

    • Survivors have a high risk of rethrombosis and poor QOL due to short-gut syndrome

    • Predictors of mortality: older age, hepatic and renal impairment, metabolic acidosis, hypoxia, intramural pneumatosis, and sepsis

    • Mortality is highest for thrombotic AMI followed by NOMI, embolic AMI and venous thrombotic AMI

    • Early and aggressive diagnosis and treatment shown to reduce mortality if diagnosis made before onset of peritonitisis

    • Madrid study - described 21 patients with SMA embolus

      • Intestinal viability achieved in 100% of patients if symptoms <12 hours, 56% if <12-24 hours, and 18% if > 24 hour

    Acute mesenteric ischaemia

    Acute mesenteric ischaemia



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