Perspective

Mesenteric ischemia results from lack of adequate blood flow to and oxygenation of the mesentery and intestines. The clinical course consists of rapid progression from bowel ischemia to infarction, sepsis, and usually death. The incidence of acute mesenteric ischemia is increasing because of an aging population and the prolonged survivability of patients with severe cardiovascular disease and other significant medical conditions.

Four types of mesenteric ischemia must be considered: acute mesenteric ischemia, nonobstructive mesenteric ischemia (NOMI), mesenteric vein thrombosis, and chronic mesenteric ischemia (or mesenteric angina). The most deadly of these is acute mesenteric ischemia, which results from sudden obstruction of blood flow to the intestines and has a mortality rate approaching 90%.

Epidemiology

Mesenteric ischemia accounts for 0.1% of all hospital admissions and 1% of emergency department (ED) visits for abdominal pain in geriatric patients. Cases of mesenteric vein thrombosis are more difficult to estimate accurately but have been reported at 2 per 100,000 admissions over a period of 20 years at one center.^1–3

The overall mortality associated with mesenteric ischemia is between 60% and 93% but rises precipitously once bowel wall infarction has occurred. Mortality remains greatest for acute mesenteric ischemia resulting from obstruction or embolic phenomena. Patients with an early manifestation of NOMI have mortality rates of 50% to 55%, whereas patients with mesenteric vein thrombosis have a 15% mortality at 30 days.^1–3 Those affected by chronic mesenteric ischemia have a more prolonged course, are relatively protected by dual blood supply, and present the physician with more numerous chances for intervention.

Pathophysiology

Any patient with advanced age, atherosclerosis, thromboembolic disease, atrial fibrillation, and processes leading to chronic low-flow states is at risk for the development of arterial mesenteric ischemia (Tables 34.1 and 34.2).^1,2,4,5 Mesenteric venous obstruction carries its own separate risk factors, which are similar to those for venous thrombosis anywhere in the body.

Table 34.2 Incidence of Ischemic Bowel Diseases

^* Percentage of all cases of acute mesenteric ischemia.

Acute mesenteric ischemia is a result of the precipitous onset of hypoperfusion caused by occlusive or nonocclusive obstruction of either arterial or venous blood flow. Acute hypoperfusion occurs in 65% of cases and carries a mortality rate exceeding 60%. Occlusive arterial obstruction is most commonly caused by embolic or thrombotic obstruction of the superior mesenteric artery (SMA). NOMI is often due to vasoconstriction of the splanchnic system. Occlusive venous obstruction occurs with thrombosis or segmental strangulation. Mesenteric venous thrombosis is the main cause of mesenteric ischemia in younger patients without cardiovascular disease.

Acute arterial embolism causes a dramatic cessation of blood flow, with rapid progression from ischemia to infarction. As the bowel wall necroses, contamination with intraluminal bacteria leads to peritonitis, sepsis, and toxin-mediated hypotension.

Nonocclusive infarction, which represents 25% of all cases of acute ischemia, is most often caused by splanchnic hypoperfusion and vasoconstriction. Risk factors for nonocclusive disease include advanced age, acute myocardial infarction (AMI), acute cardiac decompensation, and heart failure. Diuretics contribute to a decrease in splanchnic perfusion in patients with profound heart disease, whereas medications such as digoxin and alpha-blockers cause regional vasoconstriction and may add to a low-flow state. Cocaine can cause splanchnic vasoconstriction and should be suspected as a cause of mesenteric ischemia in younger patients.

Bowel perfusion is generally preserved during periods of hypotension; therefore, NOMI represents failure of the normal autoregulatory systems.^2,6,7 Patients with chronic renal failure may have bowel ischemia after hemodialysis, probably from hypoperfusion, which promotes preferential shunting of blood from the splanchnic circulation to preserve flow to the cardiac and cerebrovascular systems.

Although acute mesenteric vein thrombosis accounts for a small proportion of cases of ischemic bowel disease (5% to 10%), the ease of diagnosis with computed tomography (CT) has allowed identification of a greater number of patients with venous thrombosis. Symptoms are even less specific than those of arterial obstruction and are manifested over a longer period before bowel infarction occurs. Thrombus secondary to hypercoagulable states develops first in the smaller vessels and later progresses into the larger veins; clots associated with cirrhosis, neoplasm, or local injury (operative, trauma) start at the site of obstruction and evolve distally.⁴

Thrombotic arterial ischemia occurs late in the course of severe mesenteric atherosclerotic disease and involves the three major sources of intestinal blood supply: the celiac artery, the SMA, and the inferior mesenteric artery (IMA). Symptoms are typically manifested when two of the three vessels are significantly stenosed or completely obstructed.

A review of the anatomy of arterial blood flow to the intestines is helpful in understanding the pathophysiology of mesenteric ischemia.

The celiac artery arises anteriorly from the abdominal aorta at the level of the 12th thoracic vertebra. The celiac artery branches into the common hepatic, splenic, and left gastric arteries. These vessels supply their corresponding organs with significant redundancies, so ischemia in these areas is rare.

The SMA comes off the aorta 1 cm below the celiac artery and terminates as the ileocolic artery. This latter vessel supplies the majority of the blood delivered to the small intestine, as well as some flow to the pancreas, right colon, and transverse colon.

The IMA originates from the aorta 7 cm distal to the SMA. It provides blood to the distal transverse colon, descending colon, and rectum.

There is a significant array of collateral blood vessels and flow patterns. The small intestine is especially vulnerable to ischemia, however, because the terminal arterioles enter the intestinal wall without collateral pathways.⁴ Splanchnic blood flow requirements vary continuously but can account for up to 35% of cardiac output.

Venous drainage of the system occurs via the superior mesenteric vein, which empties into the portal vein.

Presenting Signs and Symptoms