Acute Mesenteric Ischemia 

Acute mesenteric ischemia (AMI) is a syndrome in which inadequate blood flow through the mesenteric circulation causes ischemia and eventual gangrene of the bowel wall. Broadly, AMI may be classified either as arterial or venous disease.

Arterial disease may be subdivided into nonocclusive mesenteric ischemia (NOMI; see the image below) and occlusive mesenteric arterial ischemia (OMAI). OMAI may be further subdivided into acute mesenteric arterial embolus (AMAE) and acute mesenteric arterial thrombosis (AMAT). Venous disease takes the form of mesenteric venous thrombosis (MVT). Thus, for practical purposes, AMI comprises 4 different primary clinical entities: NOMI, AMAE, AMAT, and MVT.

The 4 types of AMI have somewhat different predisposing factors, clinical pictures, and prognoses. A secondary clinical entity of mesenteric ischemia occurs because of mechanical obstruction, such as internal hernia with strangulation, volvulus, intussusception, tumor compression, and aortic dissection. Occasionally, blunt trauma may cause isolated dissection of the superior mesenteric artery (SMA) and lead to intestinal infarction.

Because the 4 types of AMI share many similarities and a final common pathway (ie, bowel infarction and death, if not properly treated), they are discussed together.

In 1930, Cokkinis remarked, “Occlusion of the mesenteric vessels is apt to be regarded as one of those conditions of which the diagnosis is impossible, the prognosis hopeless, and the treatment almost useless.”^[1] This quote indicates some of the extreme difficulties faced by physicians treating AMI. Symptoms are nonspecific initially, before evidence of peritonitis presents. Thus, diagnosis and treatment are often delayed until the disease is advanced.

Fortunately, since 1930, many advances have been made that allow earlier diagnosis and treatment. Whereas the prognosis remains grave for patients in whom the diagnosis is delayed until bowel infarction has already occurred, patients who receive the appropriate treatment in a timely manner are much more likely to recover.^[2]

Typically, the celiac artery (CA) supplies the foregut, hepatobiliary system, and spleen; the SMA supplies the midgut (ie, small intestine and proximal mid colon); and the inferior mesenteric artery (IMA) supplies the hindgut (ie, distal colon and rectum).^[3] However, multiple anatomic variants are observed. Venous drainage is through the superior mesenteric vein (SMV), which joins the splenic vein to form the portal vein.

AMI arises primarily from problems in the SMA circulation or its venous outflow. Collateral circulation from the CA and IMA may allow sufficient perfusion if flow in the SMA is reduced because of occlusion, a low-flow state (eg, NOMI), or venous occlusion.

The IMA seldom is the site of lodgment of an embolus. Because of its smaller lumen, only small emboli can enter this vessel. When lodgment occurs, the embolus lodges at the site where the IMA divides into the left colic, sigmoidal, and superior hemorrhoidal arteries. In such instances, collateral flow from the middle colic and middle hemorrhoidal arteries (through the vascular arcades of the IMA distal to the embolus) may sustain the perfusion of the left colon.

Insufficient perfusion of the small bowel and colon may result from arterial occlusion by embolus or thrombosis (AMAE or AMAT), thrombosis of the venous system (MVT), or nonocclusive processes such as vasospasm or low cardiac output (NOMI).

Embolic phenomena account for approximately 50% of all clinical cases, arterial thrombosis for about 25%, NOMI for roughly 20%, and MVT for less than 10%. Rarely, isolated spontaneous dissections of the SMA have been reported.^{[4, 5, 6, 7]} Hemorrhagic infarction leading to perforation is the common pathologic pathway whether the occlusion is arterial or venous.

Injury severity is inversely proportional to the mesenteric blood flow and is influenced by the number of vessels involved, systemic mean blood pressure, duration of ischemia, and collateral circulation. The superior mesenteric vessels are involved more frequently than the inferior mesenteric vessels, with blockage of the latter often being silent because of better collateral circulation.

Damage to the affected bowel portion may range from reversible ischemia to transmural infarction with necrosis and perforation. The injury is complicated by reactive vasospasm in the SMA region after the initial occlusion. Arterial insufficiency causes tissue hypoxia, leading to initial bowel wall spasm. This leads to gut emptying by vomiting or diarrhea. Mucosal sloughing may cause bleeding into the gastrointestinal (GI) tract.

At this stage, little abdominal tenderness is present, producing the classic intense visceral pain that is disproportionate to physical examination findings.

As the ischemia persists, the mucosal barrier becomes disrupted, and bacteria, toxins, and vasoactive substances are released into the systemic circulation. This can cause death from septic shock, cardiac failure, or multisystem organ failure before bowel necrosis actually occurs.

As hypoxic damage worsens, the bowel wall becomes edematous and cyanotic. Fluid is released into the peritoneal cavity; this explains the serosanguineous fluid sometimes recovered by diagnostic peritoneal lavage. Bowel necrosis can occur in 8-12 hours from the onset of symptoms. Transmural necrosis leads to peritoneal signs and heralds a much worse prognosis.

Embolic AMI (AMAE) is usually caused by an embolus of cardiac origin. Typical causes include mural thrombi after myocardial infarction, atrial thrombi associated with mitral stenosis and atrial fibrillation, vegetative endocarditis, mycotic aneurysm, and thrombi formed at the site of atheromatous plaques within the aorta or at the sites of vascular aortic prosthetic grafts interposed anywhere between the heart and the origin of the SMA.

The vascular occlusion is sudden, so the patients have not developed a compensatory increase in collateral flow. As a result, they experience worse ischemia than patients with thrombotic AMI. The SMA is the visceral vessel most susceptible to emboli because of its small take-off angle from the aorta and higher flow. Most often, emboli lodge about 6-8 cm beyond the arterial origin, at a narrowing near the emergence of the middle colic artery.

According to the US Centers for Disease Control and Prevention (CDC) Injury Center, a special form of mesenteric ischemia may result from systemic air embolism in those who sustain high-energy blast injuries. These patients sustain severe primary blast injury to the lung, a condition referred to as “blast lung.”

Thrombotic AMI (AMAT) is a late complication of preexisting visceral atherosclerosis. Symptoms do not develop until 2 of the 3 arteries (usually the celiac and superior mesenteric arteries) are stenosed or completely blocked. Progressive worsening of the atherosclerotic stenosis before the acute occlusion allows time for development of additional collateral circulation.

Most patients with thrombotic AMI have atherosclerotic disease at other sites, such as coronary artery disease, stroke, or peripheral arterial disease. A drop in cardiac output from myocardial infarction or congestive heart failure (CHF) may cause AMI in a patient with visceral atherosclerosis.

Thrombotic AMI may also be a complication of arterial aneurysm or other vascular pathologies, such as dissection, trauma, and thromboangiitis obliterans. In inflammatory vascular disease, smaller vessels are affected. Thrombosis tends to occur at the origin of the SMA, causing widespread infarction. These patients frequently present with a history of chronic mesenteric ischemia in the form of intestinal angina before the emergent event.

NOMI is precipitated by a severe reduction in mesenteric perfusion, with secondary arterial spasm from such causes as cardiac failure, septic shock, hypovolemia, or the use of potent vasopressors in patients in critical condition. Because bowel perfusion, similar to cerebral perfusion, is preserved in the setting of hypotension, NOMI represents a failure of autoregulation. Many vasoactive drugs (eg, digitalis, cocaine, diuretics, and vasopressin) may also cause regional vasoconstriction. Gross pathologic arterial or venous occlusions are not observed.

MVT often (ie, >80% of the time) is the result of some processes that make the patient more likely to form a clot in the mesenteric circulation (ie, secondary MVT). Primary MVT occurs in the absence of any identifiable predisposing factor. MVT may also occur after ligation of the splenic vein for a splenectomy or ligation of the portal vein or the superior mesenteric vein as part of damage control surgery for severe penetrating abdominal injuries. Other associated causes include pancreatitis, sickle cell disease, and hypercoagulability caused by malignancy.

MVT often affects a much younger population. Symptoms may be present longer than in the typical cases of AMI, sometimes exceeding 30 days. Infarction from MVT is rarely observed with isolated SMV thrombosis, unless collateral flow in the peripheral arcades or vasa recta is compromised as well. Fluid sequestration and bowel wall edema are more pronounced than in arterial occlusion. The colon is usually spared because of better collateral circulation. The chronic form of SMV thrombosis may manifest as esophageal variceal bleeding.

Causes of embolic AMI (AMAE) include the following:

• Cardiac emboli - Mural thrombus after myocardial infarction, auricular thrombus associated with mitral stenosis and atrial fibrillation, septic emboli from valvular endocarditis (less frequent)
• Emboli from fragments of proximal aortic thrombus due to a ruptured atheromatous plaque
• Atheromatous plaque dislodged by arterial catheterization

Causes of thrombotic AMI (AMAT) include the following:

• Atherosclerotic vascular disease (most common)
• Aortic aneurysm
• Aortic dissection
• Arteritis
• Decreased cardiac output from myocardial infarction or CHF (thrombotic AMI may cause acute decompensation)
• Dehydration from other causes

Causes of NOMI include the following:

• Hypotension from CHF, myocardial infarction, sepsis, aortic insufficiency, severe liver or renal disease, or recent major cardiac or abdominal surgery
• Vasopressive drugs
• Ergotamines
• Cocaine
• Digitalis (whether digitalis use causes NOMI or patients who develop NOMI are older and are more likely to have been prescribed digitalis is unclear)

Causes of MVT include the following (>80% of patients with MVT are found to have predisposing conditions):

• Hypercoagulability from protein C and S deficiency, antithrombin III deficiency, dysfibrinogenemia, abnormal plasminogen, polycythemia vera (most common), thrombocytosis, sickle cell disease, factor V Leiden mutation, pregnancy, and oral contraceptive use
• Tumor causing venous compression or hypercoagulability (paraneoplastic syndrome)
• Infection, usually intra-abdominal (eg, appendicitis, diverticulitis, or abscess)
• Venous congestion from cirrhosis (portal hypertension)
• Venous trauma from accidents or surgery, especially portocaval surgery
• Increased intra-abdominal pressure from pneumoperitoneum during laparoscopic surgery^[8]
• Pancreatitis
• Decompression sickness

United States statistics

The overall prevalence of AMI is 0.1% of all hospital admissions; this figure may be expected to rise as the population ages. The exact prevalence of MVT is unknown because many cases are presumed to be limited in symptomatology and to resolve spontaneously. In 1989, the incidence of diagnosed MVT was reported to be 2 cases per 100,000 admissions over 20 years at the Albert Einstein College of Medicine Montefiore Medical Center.

International statistics

Outside of the United States, reported rates of AMI are probably lower in countries with limited diagnostic capability or whose populations have a shorter life expectancy because AMI is primarily a disease of older individuals.

Age-related differences in incidence

AMI is frequently considered a disease of people older than 50 years. Younger people with atrial fibrillation or risk factors for MVT, such as oral contraceptive use or hypercoagulable states (eg, those caused by protein C or S deficiency), may present with AMI.

Sexual differences in incidence

No overall sex preference exists for AMI. Men might be at higher risk for occlusive arterial disease because they have a higher incidence of atherosclerosis. Conversely, women who are on oral contraceptives or are pregnant are at higher risk of MVT.

Racial differences in incidence

No racial predilections are known for AMI. However, people of races with a higher rate of conditions leading to atherosclerosis, such as black people, might be at higher risk.

The prognosis of AMI of any type is grave. Overall, the mortality rate in the last 15 years from all causes of AMI averages 71%, with a range of 59-93%. Once bowel wall infarction has occurred, the mortality rate is as high as 90%. Even with good treatment, up to 50-80% of patients die.

Survivors of extensive bowel resection face significant long-term morbidity because of the reduced intestinal mucosal surface available for absorption. However, with rapid treatment, the mortality rate can be reduced considerably, and patients may be spared bowel resection. In a report from Madrid of 21 patients with SMA embolus with little delay in initiating maximal treatment, intestinal viability was achieved in 100% of patients if the duration of symptoms was shorter than 12 hours, 56% if it was 12-24 hours, and only 18% if it was longer than 24 hours.

Early recognition and treatment of NOMI has been shown to reduce the mortality rate to 50-55%. Symptomatic MVT has a 30-day mortality rate of 13-15%.

A long-term follow-up study of 31 patients who had surgery and survived the acute episode, revealed 2- and 5-year survival rates of 70% and 50%. Deaths were mainly related to cardiovascular comorbidity and malignant disease. With appropriate anticoagulation, only 1 patient died after a recurrent attack of arterial mesenteric thrombosis.

Educate patients who survive to discharge about short-bowel syndrome. Educate surviving patients about the importance of taking warfarin or other discharge medications to prevent recurrence.

For patient education resources, see the Environmental Exposures and Injuries Center, as well as The Bends - Decompression Syndromes.