Pathophysiology

At rest the gut receives approximately 20% of the cardiac output. This amount increases to 35% after meal intake. Three major vessels supply the intestines including the celiac axis, superior mesenteric artery, and the inferior mesenteric artery. Major branches of the celiac artery include the left gastric artery which supplies the stomach and duodenum. The remainder of the small bowel, right colon, and transverse colon are supplied by the superior mesenteric artery. The descending colon, sigmoid, and proximal rectum are supplied by the three branches of the inferior mesenteric artery. An extensive array of collaterals exist which protect the bowel from ischemic injury. These develop rapidly in response to a period of ischemia, and provide adequate perfusion for a variable period of time. Collateral pathways include the gastroduodenal artery which represents an important potential connection between the celiac axis and the superior mesenteric artery. The marginal artery of Drummond and the arc of Riolan provide important collaterals between the superior mesenteric artery (SMA) and the inferior mesenteric artery. In addition to this, a network of intramural submucosal vessels exists which allows preservation of bowel segments even in the face of reduced blood flow. However, there are areas which remain particularly vulnerable to an ischemic injury. The branches off the SMA form a series of arcades from which straight end arteries enter the intestinal wall limiting collateral flow. Also two “watershed” areas exist in the colon. These are Griffiths point, at the splenic flexure between the superior and inferior mesenteric arteries, and Sudeck point in the rectosigmoid between the inferior mesenteric and the hypogastric arteries. These areas are vulnerable secondary to incomplete anastomoses of the marginal artery in these areas.

This article reviews the clinical spectrum of mesenteric ischemia in the elderly with particular emphasis on the varied presentations, evaluation, and management of ischemic disorders of the intestines.

Acute mesenteric ischemia

AMI remains a potentially lethal disorder with little improvement in survival in the past 70 years. Average mortality approaches 71% with a range of 59% to 93%. The lack of progress relates to the delay in diagnosis with only one third of patients properly diagnosed before surgical intervention or death. This suggests that mortality may even be higher as many fatal cases may go unrecognized. It is essential then to maintain a high index of suspicion in an elderly patient who presents with acute abdominal pain and has associated risk factors for vascular disease. Classically the pain at presentation is out of proportion to the physical findings. In fact any development of peritoneal signs suggests the onset of transmural infarction which portends a dismal prognosis. Other presenting complaints include nausea and vomiting, abdominal distention, or forceful diarrhea which may be dark or test positive for blood. However, in the elderly the presentation may differ somewhat with less frequent abdominal pain and more often symptoms such as tachypnea or mental status changes. These are nonspecific symptoms, but when coupled with the clinical history, should alert the clinician to the diagnosis. Patients at particular risk for AMI include those over the age of 60 with a history of cardiomyopathy, cardiac arrhythmias, myocardial infarction, renal failure (hemodialysis), hypotension, hypovolemia, ventricular aneurysms, hypercoagulable state, or use of vasoactive drugs.

The mortality rate is entirely dependent on early diagnosis. In one series, survival decreased from 100% to 18% if the diagnosis were delayed from less than 12 hours to greater than 24 hours. Distinguishing this condition from a differential diagnosis which includes inflammatory bowel disease, diverticulitis, small bowel obstruction, acute pancreatitis, peptic ulcer disease, appendicitis, cholecystitis, or infectious gastroenteritis may be difficult as these conditions are far more common than mesenteric ischemia. Early on, the laboratory assessment is of little value in distinguishing among these diagnoses. Common findings include leukocytosis, hemoconcentration, elevated amylase levels, abnormal liver enzymes (aspartate aminotransferase [AST], alkaline phosphatase), hyperphosphatemia, and metabolic acidosis. Unfortunately none of these findings is specific for ischemia and more characteristic abnormalities such as elevated lactic acid levels appear later in the course, after the onset of infarction. d -Dimer may have value in detecting early ischemia, but remains to be confirmed.

A plain film of the abdomen is typically normal early on, with less than 40% of patients demonstrating the characteristic findings of “thumbprinting” or thickening of bowel loops. As with the laboratory results, changes on the flat plate occur later, indicating a poorer outcome. In one study, a normal flat plate was associated with a mortality of 29%, compared with 78% if pathologic changes were seen.

Acute mesenteric ischemia

AMI remains a potentially lethal disorder with little improvement in survival in the past 70 years. Average mortality approaches 71% with a range of 59% to 93%. The lack of progress relates to the delay in diagnosis with only one third of patients properly diagnosed before surgical intervention or death. This suggests that mortality may even be higher as many fatal cases may go unrecognized. It is essential then to maintain a high index of suspicion in an elderly patient who presents with acute abdominal pain and has associated risk factors for vascular disease. Classically the pain at presentation is out of proportion to the physical findings. In fact any development of peritoneal signs suggests the onset of transmural infarction which portends a dismal prognosis. Other presenting complaints include nausea and vomiting, abdominal distention, or forceful diarrhea which may be dark or test positive for blood. However, in the elderly the presentation may differ somewhat with less frequent abdominal pain and more often symptoms such as tachypnea or mental status changes. These are nonspecific symptoms, but when coupled with the clinical history, should alert the clinician to the diagnosis. Patients at particular risk for AMI include those over the age of 60 with a history of cardiomyopathy, cardiac arrhythmias, myocardial infarction, renal failure (hemodialysis), hypotension, hypovolemia, ventricular aneurysms, hypercoagulable state, or use of vasoactive drugs.

The mortality rate is entirely dependent on early diagnosis. In one series, survival decreased from 100% to 18% if the diagnosis were delayed from less than 12 hours to greater than 24 hours. Distinguishing this condition from a differential diagnosis which includes inflammatory bowel disease, diverticulitis, small bowel obstruction, acute pancreatitis, peptic ulcer disease, appendicitis, cholecystitis, or infectious gastroenteritis may be difficult as these conditions are far more common than mesenteric ischemia. Early on, the laboratory assessment is of little value in distinguishing among these diagnoses. Common findings include leukocytosis, hemoconcentration, elevated amylase levels, abnormal liver enzymes (aspartate aminotransferase [AST], alkaline phosphatase), hyperphosphatemia, and metabolic acidosis. Unfortunately none of these findings is specific for ischemia and more characteristic abnormalities such as elevated lactic acid levels appear later in the course, after the onset of infarction. d -Dimer may have value in detecting early ischemia, but remains to be confirmed.

A plain film of the abdomen is typically normal early on, with less than 40% of patients demonstrating the characteristic findings of “thumbprinting” or thickening of bowel loops. As with the laboratory results, changes on the flat plate occur later, indicating a poorer outcome. In one study, a normal flat plate was associated with a mortality of 29%, compared with 78% if pathologic changes were seen.

Mesenteric venous thrombosis

MVT is the least common cause of mesenteric ischemia, accounting for approximately 10% of cases. However, mortality remains high at between 20% and 50%. Most cases have an identifiable cause with only 10% now characterized as idiopathic. These causes include cirrhosis with portal hypertension, a hypercoagulable state due to inherent clotting disorders including factor V Leiden mutation, protein C or protein S deficiency, malignancy, or recent surgery. Up to 50% of cases have had a deep venous thrombosis or pulmonary embolism before. Bowel involvement in MVT is usually segmental with edema and hemorrhage of the bowel wall with focal exfoliation of the mucosa. Its presentation may be acute or chronic, generally presenting for evaluation 1 to 2 weeks after onset of symptoms. The diagnosis is difficult as the symptoms are often nonspecific. Most patients will have abdominal pain (90%), but the onset is variable and location is inconsistent. Patients typically do not experience the classic symptoms of postprandial pain and sitophobia seen in arterial thrombosis. Nausea and vomiting are present in 60% to 75% of patients and 30% will have altered bowel habits with either constipation or diarrhea. The diarrhea infrequently is bloody, but more than one half of patients are positive for occult blood. Fever is a common finding along with abdominal tenderness, distention with decreased bowel sounds, but peritoneal signs are seen in only two thirds of patients.

As with AMI, the laboratory parameters are nonspecific. Plain films of the abdomen often are normal at presentation or simply show a nonspecific ileus. These factors all contribute to the difficulty in making this diagnosis, but do not lessen the importance. Mortality is directly related to timing of diagnosis and institution of prompt therapy, as discussed in this article.

Nonocclusive mesenteric ischemia

NOMI accounts for 20% to 30% of acute mesenteric ischemic events, and, as with other types of AMI, carries a high mortality rate of 50% to 90%. NOMI refers to ischemia secondary to a low flow state in the absence of arterial or venous occlusion. The decrease in cardiac output is associated with a diffuse mesenteric vasoconstriction which further reduces flow, leading to ischemia and ultimately necrosis. Clinical symptoms are often missed as the patients with NOMI may be critically ill and the onset of symptoms is often insidious. Any condition associated with reduced cardiac output may cause NOMI, for example, MI, congestive heart failure, hypovolemia, or hypotension. Use of alpha-adrenergic agonists, digoxin or beta-receptor blocking agents may also increase risk. NOMI is also seen in the setting of major abdominal or cardiovascular surgery. The risk increases further if the patients are receiving enteral nutrition. The increased demand generated by the enteral feedings may exceed the capacity of blood flow to meet the metabolic requirements. Incidence of NOMI in this setting has been reported to be 0.3% to 8.5%.

A series of autopsies were reviewed to assess the incidence of NOMI, the extent of involvement, and the potential risk factors. The incidence was rare, yet increased in octogenarians from 2/100,000 person-years before age 80 to 40/100,000 person-years after age 80. Only 29% were correctly diagnosed before death, again verifying the difficulty in making an early diagnosis. The 3 major potential causes in this series were heart failure, atrial fibrillation, and recent major surgery. Forty percent of fatal cases of NOMI were found to have mesenteric stenosis which further contributed to the low flow state.

As with other forms of AMI, early laboratories and the abdominal flat plate show little change or are nonspecific. A high index of suspicion is required and NOMI should be considered in those patients who develop unexplained clinical deterioration or failure to thrive while recovering from a cardiac event or major surgery.

Diagnosis

Early diagnosis is critical to improving mortality or preventing the dire consequences of a short bowel syndrome secondary to massive small bowel infarction. Choosing the appropriate diagnostic studies at presentation, therefore, is essential as clinical deterioration is rapid and does not allow the luxury of multiple studies.