Treatment of Acute Visceral Artery Occlusive Disease
Peter H. Lin
Ruth L. Bush
Alan B. Lumsden
Vascular occlusive disease of the mesenteric vessels is a relatively uncommon but potentially devastating condition. Mesenteric occlusive disease usually occurs in individuals with underlying systemic atherosclerosis. This disease process may evolve in a chronic fashion, as in the case of progressive luminal obliteration due to atherosclerosis. On the other hand, mesenteric ischemia can occur suddenly, as in the case of thromboembolism. Despite recent progress in peri-operative management and better understanding in pathophysiology, mesenteric ischemia is considered one of the most catastrophic vascular disorders, with mortality rates ranging from 50% to 75%. Delay in diagnosis and treatment are the main contributing factors in its high mortality. It is estimated that mesenteric ischemia accounts for 1 in every 1,000 hospital admissions in this country. The prevalence is rising due in part to the increased awareness of this disease, the advanced age of the population, and the significant comorbidity of these elderly patients. Early recognition and prompt treatment before the onset of irreversible intestinal ischemia are essential to improve the outcome.
Anatomy and Pathophysiology
Mesenteric arterial circulation is remarkable for its rich collateral network. Three main mesenteric arteries provide the arterial perfusion to the gastrointestinal system: the celiac artery (CA), the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). In general, CA provides arterial circulation to the foregut (distal esophagus to duodenum), hepatobiliary system, and spleen; the SMA supplies the midgut (jejunum to mid-colon); and the IMA supplies the hindgut (mid-colon to rectum). The CA and SMA arise from the ventral surface of the infradiaphragmatic suprarenal abdominal aorta, while the IMA originates from the left lateral portion of the infrarenal aorta. These anatomic origins in relation to the aorta are important when a mesenteric angiogram is performed to determine the luminal patency. In order to fully visualize the origins of the CA and SMA, it is necessary to perform both an anteroposterior and a lateral projection of the aorta, because most arterial occlusive lesions occur in the proximal segments of these mesenteric trunks.
Because of the abundant collateral flow between these mesenteric arteries, progressive diminution of flow in one or even two of the main mesenteric trunks is usually tolerated, provided that uninvolved mesenteric branches can enlarge over time to provide sufficient compensatory collateral flow. In contrast, acute occlusion of a main mesenteric trunk may result in profound ischemia due to lack of sufficient collateral flow. Collateral network between the CA and the SMA exist primarily through the superior and inferior pancreaticoduodenal arteries. The IMA may provide collateral arterial flow to the SMA through the marginal artery of Drummond, the Riolan arc, and other unnamed retroperitoneal collateral vessels termed meandering mesenteric arteries. Lastly, collateral vessels may provide important arterial flow to the IMA and the hindgut through the hypogastric arteries and the hemorrhoidal arterial network.
Regulation of mesenteric blood flow is largely modulated by both hormonal and neural stimuli, which characteristically regulate systemic blood flow. In addition, the mesenteric circulation responds to the gastrointestinal contents. Hormonal regulation is mediated by splanchnic vasodilators, such as nitric oxide, glucagon, and vasoactive intestinal peptide. Certain intrinsic vasoconstrictors, such as vasopressin, can diminish the mesenteric blood flow. On the other hand, neural regulation is provided by the extensive visceral autonomic innervation.
Clinical manifestation of mesenteric ischemia is predominantly postprandial abdominal pain, which signifies that the increased oxygen demand of digestion is not met by the gastrointestinal collateral circulation. The postprandial pain frequently occurs in the mid-abdomen, suggesting that the diversion of blood flow from the SMA to supply the stomach impairs perfusion to the small bowel. This leads to transient anaerobic metabolism and acidosis. Persistent or profound mesenteric ischemia will lead to mucosal compromise with release of intracellular contents and byproducts of anaerobic metabolism to the splanchnic and systemic circulation. Injured bowel mucosa allows unimpeded influx of toxic substances from the bowel lumen with systemic consequences. If full-thickness necrosis occurs in the bowel wall, intestinal perforation ensues, which will lead to peritonitis. Concomitant atherosclerotic disease in cardiac or systemic circulation frequently compounds the diagnostic and therapeutic complexity of mesenteric ischemia.
Types of Mesenteric Artery Occlusive Disease
There are four major types of visceral ischemia involving the mesenteric arteries, which include:
Acute embolic mesenteric ischemia
Acute thrombotic mesenteric ischemia
Chronic mesenteric ischemia
Nonocclusive mesenteric ischemia
Despite the variability of these syndromes, a common anatomic pathology is involved in these processes. The SMA is the most commonly involved vessel in acute mesenteric ischemia. Acute thrombotic mesenteric ischemia frequently occurs in patients with underlying mesenteric atherosclerosis, which usually involves the origin of the mesenteric arteries while sparing the collateral branches. The development of collateral vessels is more likely when the occlusive process is a gradual rather than a sudden ischemic event. In acute embolic mesenteric ischemia, the emboli typically originate from a cardiac source and frequently occur in patients with atrial fibrillation or following myocardial infarction (MI). Nonocclusive mesenteric ischemia is characterized by a low-flow state in otherwise normal mesenteric arteries. In contrast, chronic mesenteric ischemia is a functional consequence of a long-standing atherosclerotic process that typically involves at least two of the three main mesenteric vessels: the CA, SMA, and the IMA.
Several less common syndromes of visceral ischemia involving the mesenteric arteries can also cause serious debilitation. Chronic mesenteric ischemic symptoms can occur due to extrinsic compression of the celiac artery by the diaphragm, which is termed “the median arcuate ligament syndrome.” Acute visceral ischemia may occur following an aortic operation, due to ligation of the IMA in the absence of adequate collateral vessels. Furthermore, acute visceral ischemia may develop in aortic dissection that involves the mesenteric arteries. Finally, other unusual causes of ischemia include mesenteric arteritis, radiation arteritis, and cholesterol emboli.
Clinical Presentation
Abdominal pain out of proportion to physical findings is the classic presentation in patients with acute mesenteric ischemia and occurs frequently following an embolic or thrombotic ischemic event of the SMA. Clinical manifestations may include sudden onset of abdominal cramps in patients with underlying cardiac or atherosclerotic diseases. The abdominal pain is often associated with bloody diarrhea, as a result of mucosal sloughing secondary to ischemia. Fever, diarrhea, nausea, vomiting, and abdominal distention are some common but nonspecific manifestations. Diffuse abdominal tenderness, rebound, and rigidity are ominous signs and usually herald bowel infarction.
Symptoms of thrombotic mesenteric ischemia may initially be more insidious than those of embolic mesenteric ischemia. Approximately 70% of patients with chronic mesenteric ischemia have a history of abdominal angina. In these patients, the chronicity of mesenteric atherosclerosis is important, as it permits collateral vessel formation. The precipitating factor leading chronic mesenteric ischemia to become an acute thrombotic occlusion is often an unrelated illness that results in dehydration, such as diarrhea or vomiting. This may further confuse the actual diagnosis. If the diagnosis is not recognized promptly, symptoms may worsen, which can lead to progressive abdominal distention, oliguria, increasing fluid requirements, and severe metabolic acidosis.
Abdominal pain is only present in approximately 70% of patients with nonocclusive mesenteric ischemia. When present, the pain is usually severe but may vary in location, character, and intensity. In the absence of abdominal pain, progressive abdominal distention with acidosis may be an early sign of ischemia and impending bowel infarction. The diagnosis of nonocclusive mesenteric ischemia should be considered in elderly patients with sudden abdominal pain who have any of the following risk factors: congestive heart failure, acute MI with cardiogenic shock, hypovolemic or hemorrhagic shock, sepsis, pancreatitis, and administration of digitalis or vasoconstrictor agents such as epinephrine.
Diagnostic Studies
Various clinical possibilities should be considered in a patient with an acute onset of severe abdominal pain. Perforated gastroduodenal ulcer, intestinal obstruction, pancreatitis, cholecystitis, and nephrolithiasis occur more commonly than acute mesenteric ischemia. Laboratory evaluation is neither sensitive nor specific in distinguishing these various diagnoses. In the setting of mesenteric ischemia, complete blood count (CBC) may reveal hemoconcentration and leukocytosis. Metabolic acidosis develops as a result of anaerobic metabolism. Elevated serum amylase and lactate levels are nonspecific findings. Hyperkalemia and azotemia may occur in the late stages of mesenteric ischemia.
Plain abdominal radiographs may provide helpful information to exclude other causes of abdominal pain, such as intestinal obstruction, perforation, or volvulus, which may exhibit symptoms mimicking intestinal ischemia. Pneumoperitoneum, pneumatosis intestinalis, and gas in the portal vein may indicate infarcted bowel. In contrast, radiographic appearance of an adynamic ileus with a gasless abdomen is the most common finding in patients with acute mesenteric ischemia.
Upper endoscopy, colonoscopy, or barium radiography does not provide any useful information when evaluating acute mesenteric ischemia. Moreover, barium enema is contraindicated if the diagnosis of mesenteric ischemia is being considered. The intraluminal barium can obscure accurate visualization of mesenteric circulation during angiography. In addition, intraperitoneal leakage of barium can occur in the setting of intestinal perforation, which can lead to added therapeutic challenges during mesenteric revascularization.
The definitive diagnosis of mesenteric thrombosis is made by biplanar mesenteric arteriography, which should be performed promptly in any patient with suspected mesenteric occlusion. It typically shows occlusion or near-occlusion of the CA and SMA at or near their origins from the aorta. In most cases, the IMA has been previously occluded secondary to diffuse infrarenal aortic atherosclerosis. The differentiation of the four different types of mesenteric arterial occlusion may be suggested with biplanar mesenteric arteriogram. Mesenteric emboli typically lodge at the orifice of the middle colic artery, which creates a “miniscus sign” with an abrupt cutoff of a normal proximal SMA several centimeters from its origin on the aorta. Mesenteric thrombosis, in contrast, occurs at the most proximal SMA, which tapers off at 1 to 2 cm from its origin. In the case of chronic mesenteric occlusion, the appearance of collateral circulation is usually present. Nonocclusive mesenteric ischemia produces an arteriographic image of segmental mesenteric vasospasm with a relatively normal-appearing main SMA trunk.
Mesenteric arteriography can also play a therapeutic role. Once the diagnosis of nonocclusive mesenteric ischemia is made on the arteriogram, an infusion catheter
can be placed at the SMA orifice and vasodilating agents, such as papaverine, can be administered intra-arterially. The papaverine infusion may be continued postoperatively to treat persistent vasospasm, a common occurrence following mesenteric reperfusion. Transcatheter thrombolytic therapy has little role in the management of thrombotic mesenteric occlusion. Although thrombolytic agents may transiently recannulate the occluded vessels, the underlying occlusive lesions require definitive treatment. Furthermore, thrombolytic therapy typically requires a prolonged period of time to restore perfusion, and the intestinal viability may be difficult to assess.
can be placed at the SMA orifice and vasodilating agents, such as papaverine, can be administered intra-arterially. The papaverine infusion may be continued postoperatively to treat persistent vasospasm, a common occurrence following mesenteric reperfusion. Transcatheter thrombolytic therapy has little role in the management of thrombotic mesenteric occlusion. Although thrombolytic agents may transiently recannulate the occluded vessels, the underlying occlusive lesions require definitive treatment. Furthermore, thrombolytic therapy typically requires a prolonged period of time to restore perfusion, and the intestinal viability may be difficult to assess.
Treatment Strategies
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