Mesenteric Ischemia
Takki Momin
John Ricotta
Mesenteric ischemia is a rare, life-threatening condition characterized by compromise of the splanchnic circulation resulting in bowel ischemia. Recognition of this disorder has been increasing, and it is estimated to occur in 1 of every 1,000 hospital admissions [1]. It is often encountered in association with other critical illnesses and has a wide spectrum of clinical presentation, making the diagnosis difficult to establish. In mild cases, asymptomatic reversible mucosal ischemia may ensue, whereas frank bowel necrosis and perforation may follow prolonged malperfusion. The classic finding of pain out of proportion to physical examination is often present, but some patients may have only vague abdominal complaints [2]. Frank bowel necrosis with peritonitis portends a poor prognosis with a mortality rate that can reach 90% [3]. Associated cellular injury often induces a systemic inflammatory response that triggers a cascade of events leading to multiorgan failure and death, even after successful intestinal resection. Effective treatment of this disease requires prompt diagnosis, rapid restoration of circulation, surgical resection of nonviable bowel, and supportive care [4].
Anatomy of the Mesenteric Circulation
The small bowel and colon are principally supplied by the celiac artery (CA), superior mesenteric artery (SMA), and inferior mesenteric artery (IMA). These arteries communicate through an extensive network of collateral blood vessels that can preserve arterial perfusion to the splanchnic organs when one or more of the main arteries occludes or becomes stenotic due to atherosclerotic disease. The gastroduodenal artery and pancreaticoduodenal arcades provide an important source of collateral flow between the CA and SMA. The SMA and IMA communicate through several collateral vessels including the marginal artery of Drummond and the meandering artery also known as the arc of Riolan. The hypogastric artery can provide collateral flow to the IMA through the hemorrhoidal and sacral arteries in the pelvis [5,6] (Fig. 151.1).
Etiology
Mesenteric ischemia can occur acutely, resulting in rapid development of bowel ischemia, or chronically, producing postprandial pain, fear of eating, and weight loss. Acute ischemia may result from acute arterial occlusion due to thrombosis or embolism, acute occlusion of intestinal venous outflow, or ischemia from impaired flow without fixed obstruction in the setting of sepsis and shock. Chronic ischemia is usually the result of progressive atherosclerotic narrowing of multiple mesenteric arteries.
Acute Mesenteric Insufficiency
Arterial insufficiency accounts for approximately 95% of cases of acute mesenteric insufficiency (AMI) and may be embolic (50%), thrombotic (25%), or nonocclusive (20%). The remaining 5% of cases of AMI are due to mesenteric venous thrombosis [7]. The most common source of arterial emboli is the heart. Patients will typically have a history of atrial fibrillation, myocardial infarction, left ventricular aneurysm, or a prosthetic heart valve [8]. The SMA is the most frequent site of embolization because of the preferential flow pattern established at the origin of the artery where it takes an oblique angle [9]. More than half of the emboli will lodge at or near the branch point of the middle colic artery, a point of anatomic narrowing in the SMA. When this occurs, flow through the proximal jejunal branches continues, producing a distinct pattern of bowel ischemia with preservation of proximal jejunum [10].
 Figure 151.1. Schematic of splanchnic circulation. Rutherford Vascular Surgery. Abdominal and Iliac Aneurysms, 1431–1436, Copyright Elsevier (2005). |
Acute thrombosis is usually superimposed on chronic coexisting atherosclerotic occlusive disease. The thrombus develops within the proximal SMA or CA in close proximity to the origin of the vessel where it is affected by atherosclerotic disease. In patients with asymptomatic, compensated mesenteric occlusive disease, acute ischemia develops from abrupt thrombosis of a diseased but patent artery (usually the SMA) as a consequence of plaque disruption or flow disturbance beyond a high-grade orificial stenosis [11].
In nonocclusive mesenteric ischemia, the reduction in blood flow usually occurs from low cardiac output or splanchnic vasoconstriction. This is often seen in the intensive care setting, associated with a number of underlying medical conditions such as congestive heart failure, cardiogenic shock, renal disease, hypovolemia, and sepsis [10,12,13]. In addition, vasoactive agents like digitalis and α-adrenergic agonists can induce mesenteric ischemia by splanchnic arteriolar vasoconstriction [13]. Intestinal hypoperfusion can also result from the release of inflammatory mediators associated with severe systemic illness such as pancreatitis, sepsis, trauma, and burns [14,15]. Abdominal compartment syndrome should also be considered as a potential cause of mesenteric ischemia. Excessive intra-abdominal pressure, measured as a bladder pressure more than 25 mm Hg, leads to direct compression of the inferior vena cava and portal vein as well as decreased flow in the inferior vena cava and superior vena cava [16].
Acute mesenteric ischemia may also result from extrinsic mechanical compression of either the arterial or the venous supply to the bowel when local blood supply becomes compromised by a strangulated hernia or intussusception [17]. Sacrifice of a major visceral branch or surgical interruption of the collateral circulatory pathways in the setting of prior visceral artery occlusion may, on rare occasions, result in acute mesenteric ischemia [18]. A well recognized example is ischemia to the sigmoid colon following ligation of the inferior mesenteric artery during aortic resection, or left colectomy, in a patient who has an asymptomatic SMA occlusion and relies on the IMA for visceral perfusion. Aortic dissection may occasionally cause mesenteric ischemia by creating a static or dynamic obstruction at the origin of one or more of the visceral vessels [19]. In this circumstance, perfusion to the mesenteric arteries may be established by either a fenestration procedure or surgical revascularization [19,20].
Mesenteric venous thrombosis (MVT) is an infrequent cause of bowel ischemia. Over 80% of patients diagnosed with MVT are associated with an underlying identifiable coagulation disorder that predisposes them to venous thrombosis. These include both inherited hypercoagulable disorders such as protein C or S deficiency, antithrombin III deficiency, factor V Leiden mutation, and methylenetetrahydrofolate reductase mutations and acquired hypercoagulable states such as malignancy, oral contraceptive use, polycythemia vera, thrombocytosis, trauma, or critical illness [21,22,23]. The presentation of patients with MVT varies depending on the extent and location of thrombus. Patients typically present with anorexia and nonspecific, vague abdominal pain that may be acute, but is more commonly insidious. Peritonitis is rarely seen and restricted to patients with frank bowel necrosis. The triad of thrombus within the SMV, thickened small bowel wall, and free fluid in the peritoneal cavity as identified on CT maybe an early indication of bowel infarction and the subsequent need for laparotomy [24].
Chronic Mesenteric Insufficiency
Chronic mesenteric ischemia (CMI) results from atherosclerotic disease of the mesenteric arteries and usually requires stenosis or occlusion of two or more mesenteric vessels. Stenosis or occlusion of a single mesenteric vessel will rarely result in abdominal pain; when it does, the SMA is usually the vessel involved. Progression to occlusion most often occurs gradually and allows development of robust collaterals in the splanchnic circulation to compensate for inflow disease. The basal circulation to the intestine is sufficient to maintain adequate blood flow at rest, but when metabolic demands increase, such as in the postprandial state, the higher resistance collateral circulation is inadequate to meet the increased oxygen requirements and symptoms of vascular insufficiency develop. The classic presentation includes a preexistent history of postprandial abdominal pain that results in food avoidance and significant
weight loss. Abdominal pain without weight loss is unusual for mesenteric ischemia and suggests an alternate diagnosis [25].
weight loss. Abdominal pain without weight loss is unusual for mesenteric ischemia and suggests an alternate diagnosis [25].
Pathophysiology
Mesenteric ischemia occurs when there is inadequate delivery of oxygenated blood to satisfy the metabolic demands of the intestines. The presence of an extensive collateral network in the splanchnic circulation maintains intestinal viability even with as much as a 75% reduction in normal blood flow [25,26]. Under normal conditions, the splanchnic circulation maintains regional blood flow to compensate for systemic changes in hemodynamics through autoregulatory mechanisms. This is achieved by altering the vasomotor tone of the arteriolar resistance vessels. Under circumstances of decreased perfusion pressure, the precapillary arterioles reflexively vasodilate to enhance regional blood flow by lowering mesenteric vascular resistance. A combination of local, humoral, and neural factors mediate the vasomotor tone of these resistance vessels in response to various pathologic conditions [25,26,27].
In the setting of acute mesenteric thrombosis or embolus, reflexive vasodilation initially occurs and transiently enhances blood flow through existing collateral circulatory pathways. As intestinal ischemia progresses, paradoxical vasoconstriction results and local blood flow is critically reduced to a point where secondary arteriolar thrombosis ensues [28].
Intestinal ischemia from mesenteric venous thrombosis results from venous outflow obstruction leading to venous hypertension resulting in reduction of capillary and arteriolar flow. The thrombosis initially begins in the small veins out in the periphery and extends proximally toward the superior mesenteric vein. Vasospasm of the mesenteric arterioles is also believed to play a major role in ischemia associated with venous thrombosis [28,29,30,31,32,33].
Early histologic evidence of intestinal ischemia can be observed after only 5 to 10 minutes of arterial occlusion [34,35,36,37,38]. When the ischemic insult is not severe and perfusion can be rapidly restored, these changes are reversible. If ischemic cellular injury persists, tissue infarction will occur, starting from the mucosal surface of the intestine where blood supply is most tenuous. With prolonged ischemia, the bowel wall becomes edematous from increased vascular permeability. Hemorrhage of the mucosal and submucosal layers follows. As infarction extends transmurally, the integrity of the intestinal wall is destroyed and risk of perforation increases. During advanced stages of ischemia, the intestine loses its protective barrier function, resulting in passage of inflammatory cells and translocation of enteric organisms into the portal circulation. Locally produced mediators are released into the circulation along with bacterial endotoxin, triggering an intense systemic inflammatory response. The resulting sepsis and physiologic stress imposed by systemic inflammatory response often leads to multiorgan dysfunction and possibly death [15,39].
Clinical Presentation
Mesenteric ischemia can manifest itself in a variety of ways depending on etiology and degree of intestinal ischemia. The signs and symptoms may be subtle, nonspecific, and insidious, especially in chronic and subacute forms of mesenteric ischemia. When ischemia develops acutely, the most common predominant symptom is sudden onset of severe abdominal pain that is often out of proportion to physical findings. However, pain is absent in 25% of individuals with acute nonocclusive ischemia [39]. Symptoms may be nonspecific, including nausea, vomiting, diarrhea, and abdominal distension. Gastrointestinal symptoms may not always dominate the clinical presentation. Acute mental status changes have been reported in 30% of elderly patients with intestinal ischemia [40].
Diagnostic Evaluation
Leukocyte count, serum lactic acid level, and arterial blood gas are the most common tests routinely ordered to screen patients for mesenteric ischemia. In patients with acute intestinal ischemia, 75% will have a leukocytosis greater than 15,000 cells per mm3 and 50% will present with a metabolic acidosis [41]. Unfortunately, abnormalities in these studies accompany other abdominal pathologies, making them nonspecific [42,43,44,45,46,47].
Plain radiographs lack specificity, and in some cases, abdominal films may even appear normal in the presence of bowel infarction [48]. Some common radiographic features observed in intestinal ischemia include presence of bowel wall thickening, intramural gas (pneumatosis), bowel distention, and mesenteric or portal venous air [49,50]. None of these findings, however, are sensitive or specific to intestinal ischemia. Pneumatosis, when present, is often a sign of advanced ischemia with bowel infarction, although it may also be associated with other acute abdominal conditions such as peptic ulcer and inflammatory bowel disease [51]. The most practical purpose of obtaining plain films in the workup of mesenteric ischemia is often to exclude other causes of acute abdominal pain, most notably gastrointestinal perforations.
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