Introduction
Mesenteric ischemia can be either acute or chronic. The acute variant is a life-threatening disease of sudden onset and has several distinctly different causes. Most patients who are diagnosed with acute visceral ischemia have progressed to the point of bowel necrosis. Early recognition of acute ischemia is essential to permit timely intervention prior to bowel necrosis, irreversible multisystem organ failure, and death. It occurs in the aging population in most developed countries with increasing frequency and is associated with many low flow states, some of which are induced in the hospital, and may occur in visceral arteries or veins.
Chronic visceral ischemia, on the other hand, is a manifestation of systemic atherosclerosis and is not immediately life threatening. The quality of life for patients with chronic ischemia can be significantly improved by surgical revascularization of one or more visceral arteries.
Acute Mesenteric Ischemia
Acute mesenteric ischemia is now encountered with increasing frequency. The consequences of unrecognized ischemia and infarction of the viscera are devastating; in many patients, multisystem organ failure and death are unavoidable. The causes of acute mesenteric ischemia are listed in Table 79-1 . The most frequent causes are embolization to the superior mesenteric artery (SMA) and thrombosis of the SMA, accounting for roughly 50% and 25% of cases, respectively. Arterial emboli, which occur most commonly in the SMA, usually lodge 3 to 10 cm distal to the vessel origin, particularly where the vessel begins to narrow at the origin of the middle colic artery. SMA thrombosis, on the other hand, generally occurs at its origin. Patients who present with thrombosis often have had chronic mesenteric ischemia, which predisposes them to sudden occlusion of an already stenotic vessel.
| Cause | Source | Approximate Incidence (%) |
|---|---|---|
| SMA embolus | Cardiac | 50 |
| SMA thrombosis | Underlying atherosclerosis | 25 |
| NOMI | Low flow states, medication | 20 |
| Mesenteric venous thrombosis | Hypercoagulable states | 5 |
Nonocclusive mesenteric ischemia (NOMI), which accounts for 25% of cases of intestinal ischemia, results from hypovolemia, cardiac failure, sepsis, digitalis therapy, and alpha-adrenergic drugs. The increasing use of vasopressors that diminish bowel blood flow is responsible. Not surprisingly, the need for and use of vasopressors of any kind, when linked with a variety of hypotensive states, sets any patient up for mesenteric arterial or venous occlusions. Digitalis may cause abnormal mesenteric vasospasm and is at least partially involved with the majority of cases of NOMI. Mortality rates from NOMI are as high as 70% because of the difficulty of early diagnosis. Patients undergoing hemodialysis who experience periods of hypotension during dialysis are at risk for NOMI. These patients classically present with an occluded dialysis shunt that is an indicator of the hypotensive episode. NOMI typically involves the watershed areas of the splenic flexure and left colon, except in rare instances of hypotension related to trauma, which more often produces right colon ischemia.
Acute mesenteric venous thrombosis is caused by hypercoagulable states and results in massive influxes of fluid into the bowel wall and lumen. Conditions associated with visceral venous thrombosis include any of the inherited hypercoagulable states ( Box 79-1 ), cirrhosis, inflammatory bowel disease, trauma, pancreatitis, and cancer. The mortality rate with mesenteric venous thrombosis is greater than 80%; those figures may change because venous thromboses are now often seen on abdominal CT scans in relatively well patients. Such patients must be watched carefully even in the absence of acidosis and leukocytosis.
Protein C and S deficiency
Antithrombin III deficiency
Dysfibrinogenemia
Abnormal plasminogen
Polycythemia vera
Factor V Leiden mutation
Thrombocytosis
Sickle cell disease
Other, more unusual causes of acute mesenteric ischemia include aortic dissection, cardiopulmonary bypass, and median arcuate ligament compression. Visceral artery occlusion will develop in some patients with aortic dissection and is an absolute indication for repair of the dissection. Mesenteric ischemia has been described in patients after cardiopulmonary bypass and appears to be a type of NOMI. Patients in whom NOMI develops after cardiopulmonary bypass often, but not always, are those subjected to intraaortic balloon pumps or vasopressor support for cardiac dysfunction. Median arcuate ligament compression of the SMA or celiac axis is another unusual cause of mesenteric ischemia that may require surgery to release the ligament and revascularize the involved vessels. Although familial variants of both arterial and venous occlusion exist, fortunately, they are rare.
Clinical Presentation
Patients with acute mesenteric ischemia have sudden onset of abdominal pain that is often “far out of proportion” to the findings on physical examination. Patients may have nausea, vomiting, and either frank or occult gastrointestinal bleeding. Obtaining a thorough patient history is crucial in the early differentiation of the various forms of mesenteric ischemia. Specific history taking should include cardiac arrhythmias, pain with weight loss, malignancy, and hematologic abnormalities. Presentation may follow an episode of hypotension or the recent institution of digitalis therapy (both suggestive of NOMI). Acidosis and profound leukocytosis are the most frequently recognized laboratory test results.
Acute ischemia has three phases of presentation:
- 1.
The initial phase is extremely painful and may consist of abdominal pain, vomiting, diarrhea, and gastrointestinal hemorrhage.
- 2.
The intermediate phase is more vague and nonspecific.
- 3.
The final phase signifies that bowel necrosis has occurred, and pain may temporarily disappear.
Evaluation
Patients with acute mesenteric ischemia may have substantial leukocytosis, fever, metabolic acidosis, and peritonitis, but these signs often occur late, when bowel necrosis has already occurred. Serum amylase and lactate levels are often elevated. Lactate may be the most useful laboratory test, because it is often elevated in the early stages of ischemia, when other tests are less informative. Elevated D-dimer levels may aid in diagnosis but are not specific to ischemia. Other diagnostic assays including D-lactate, intestinal fatty acid binding protein, and the isoenzyme of glutathione S-transferase have been reported, but none has reached routine clinical practice. Diagnostic peritoneal lavage has been used but may only demonstrate white blood cells when frank bowel necrosis or perforation is present. Diagnostic laparoscopy can confirm the diagnosis.
Plain radiographs are generally nonspecific but are useful to exclude other intra-abdominal processes. Radiographic signs that suggest visceral ischemia include bowel wall thickening, intestinal pneumatosis, and portal vein gas, with the last being a sign of advanced disease. Use of intraluminal contrast medium is contraindicated because it can interfere with later angiography.
Ultrasonography, which is used to demonstrate flow in the SMA or celiac axis, is frequently obscured by dilated, gas-filled bowel loops. A computed tomographic (CT) scan of the abdomen and pelvis can show bowel wall thickening, pneumatosis in the bowel wall, or portal vein gas, and it is currently the study of choice. In fact, the latest multidetector CT angiography has high sensitivity and specificity in diagnosing acute mesenteric ischemia ( Fig. 79-1, A and B ), but the gold standard in the diagnosis of acute mesenteric ischemia remains biplanar mesenteric arteriography. Both anteroposterior and lateral views of the visceral vessels are necessary to fully visualize all three visceral vessels. Angiography can usually differentiate emboli from thrombosis, and the vasospasm of NOMI is readily apparent in smaller, branching arterioles, which may not be as well characterized on CT angiography ( Fig. 79-2 ).
