(See also Acute Abdominal Pain Acute Abdominal Pain Abdominal pain is common and often inconsequential. Acute and severe abdominal pain, however, is almost always a symptom of intra-abdominal disease. It may be the sole indicator of the need... read more .)
The intestinal mucosa has a high metabolic rate and, accordingly, a high blood flow requirement (normally receiving 20 to 25% of cardiac output), making it very sensitive to the effects of decreased perfusion. Ischemia disrupts the mucosal barrier, allowing release of bacteria, toxins, and vasoactive mediators, which in turn leads to myocardial depression, systemic inflammatory response syndrome (see Sepsis and Septic Shock Sepsis and Septic Shock Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, there is critical reduction in tissue perfusion; acute failure... read more ), multisystem organ failure, and death. Mediator release may occur even before complete infarction. Necrosis can occur as soon as 6 hours after the onset of symptoms.
Three major vessels serve the abdominal contents:
Celiac trunk: Supplies the esophagus, stomach, proximal duodenum, liver, gallbladder, pancreas, and spleen
Superior mesenteric artery (SMA): Supplies the distal duodenum, jejunum, ileum, and colon to the splenic flexure
Inferior mesenteric artery (IMA): Supplies the descending colon, sigmoid colon, and rectum
Collateral vessels are abundant in the stomach, duodenum, and rectum; these areas rarely develop ischemia. The splenic flexure is a watershed between the SMA and IMA and is at particular risk of ischemia. Note that acute mesenteric ischemia is distinct from ischemic colitis Ischemic Colitis Ischemic colitis is a transient reduction in blood flow to the colon. Diagnosis is by CT or colonoscopy. Treatment is supportive with IV fluids, bowel rest, and antibiotics. Necrosis may occur... read more , which involves only small vessels and causes mainly mucosal necrosis and bleeding.
Mesenteric blood flow may be disrupted on either the venous or arterial sides. In general, patients > 50 are at greatest risk and have the types of occlusions and risk factors shown in table Causes of Acute Mesenteric Ischemia Causes of Acute Mesenteric Ischemia Acute mesenteric ischemia is interruption of intestinal blood flow by embolism, thrombosis, or a low-flow state. It leads to mediator release, inflammation, and ultimately infarction. Abdominal... read more . However, many patients have no identifiable risk factors.
The early hallmark of mesenteric ischemia is severe pain but minimal physical findings. The abdomen remains soft, with little or no tenderness. Mild tachycardia may be present. Later, as necrosis develops, signs of peritonitis appear, with marked abdominal tenderness, guarding, rigidity, and no bowel sounds. The stool may be heme-positive (increasingly likely as ischemia progresses). The usual signs of shock develop and are frequently followed by death.
Sudden onset of pain suggests but is not diagnostic of an arterial embolism, whereas a more gradual onset is typical of venous thrombosis. Patients with a history of postprandial abdominal discomfort (which suggests intestinal angina) may have arterial thrombosis.
Early diagnosis of mesenteric ischemia is particularly important because mortality increases significantly once intestinal infarction has occurred. Mesenteric ischemia must be considered in any patient > 50 with known risk factors or predisposing conditions who develops sudden, severe abdominal pain.
Patients with clear peritoneal signs should proceed directly to the operating room for both diagnosis and treatment. For others, selective mesenteric angiography or CT angiography is the diagnostic procedure of choice. Other imaging studies and serum markers can show abnormalities but lack sensitivity and specificity early in the course of the disease when diagnosis is most critical. Plain abdominal x-rays are useful mainly in ruling out other causes of pain (eg, perforated viscus), although portal venous gas or pneumatosis intestinalis may be seen late in the disease. These findings also appear on CT, which may also directly visualize vascular occlusion—more accurately on the venous side. Doppler ultrasonography can sometimes identify arterial occlusion, but sensitivity is low. MRI is very accurate in proximal vascular occlusion, less so in distal vascular occlusion. Serum markers (eg, creatine kinase, lactate) rise with necrosis but are nonspecific findings that are seen later.
If diagnosis is made during exploratory laparotomy, options are surgical embolectomy, revascularization, and resection. A “second look” laparotomy may be needed to reassess the viability of questionable areas of bowel. If diagnosis is made by angiography, infusion of the vasodilator papaverine through the angiography catheter may improve survival in both occlusive and nonocclusive ischemia. Papaverine is useful even when surgical intervention is planned and is sometimes given during and after surgical intervention as well. In addition, for arterial occlusion, thrombolysis or surgical embolectomy may be done. The development of peritoneal signs at any time during the evaluation suggests the need for immediate surgery. Mesenteric venous thrombosis without signs of peritonitis can be treated with anticoagulation.
Patients with arterial embolism or venous thrombosis require long-term anticoagulation. Patients with nonocclusive ischemia may be treated with antiplatelet therapy.
Early diagnosis is critical because mortality increases significantly once intestinal infarction has occurred.
Initially, pain is severe, but physical findings are minimal.
Surgical exploration is often the best diagnostic measure for patients with clear peritoneal findings.
For other patients, mesenteric angiography or CT angiography is done.
Treatment options include embolectomy, revascularization, and resection.