Mesenteric Artery Ischemia 

Patients with mesenteric ischemia have a rare, potentially life-threatening disease and may present to the primary care or emergency medicine physician. Acute and chronic forms of mesenteric ischemia share many similarities and have many differences (see images below). This article discusses mesenteric artery ischemia in general. Acute Mesenteric Ischemia, Chronic Mesenteric Ischemia, Mesenteric Artery Thrombosis, and Mesenteric Venous Thrombosis discuss the specific types of mesenteric ischemia.

First described by Antonio Hodgson in the latter part of the 15th century, the medical profession did not become interested in this condition until the middle of the 19th century. By the turn of this century, many review articles and texts were written describing the advances in the characterization and treatment of mesenteric ischemia.

In 1901, Schnitzler described a patient with a long history of postprandial pain who was found to have an atherosclerotic plaque with overlying thrombus of the superior mesenteric artery (SMA). Schnitzler concluded that if patients could develop pain of their lower extremities secondary to atherosclerosis, patients could also develop postprandial pain as a result of atherosclerosis of the mesenteric vessels. By the middle of the 20th century, Dunphy correctly hypothesized that mesenteric ischemia was a manifestation of visceral atherosclerosis.

In 1958, Shaw and Maynard described the first thromboendarterectomy of the SMA for the treatment of acute and chronic mesenteric ischemia. Several other surgical techniques have been used to revascularize obstructed mesenteric vessels, including reimplantation of the mesenteric vessels into the adjacent aorta, transaortic visceral thromboendarterectomy first described by Stoney and Wylie in 1972, and aortovisceral bypass with vein or prosthetic grafts.

While acute mesenteric ischemia is a surgical emergency, patients with chronic mesenteric ischemia typically present with a more benign process. The specific causes of mesenteric ischemia include the following:

• Acute thrombotic and acute embolic mesenteric artery ischemia
• Visceral venous thrombosis
• Chronic mesenteric ischemia
• Nonocclusive mesenteric ischemia

Whatever the cause, the result is a decreased blood supply to the small and/or large bowel resulting in ischemia, bowel infarction, necrosis, sepsis, and, ultimately, death.

Frequency

Mesenteric ischemia accounts for 0.1% of all hospital admissions. Risk factors for this disease include atherosclerosis, arrhythmias, hypovolemia, congestive heart failure, recent myocardial infarction (MI), valvular disease, advanced age, and intra-abdominal malignancy.^{[1, 2]} Mesenteric artery stenosis is found in 17.5% of independent elderly adults.

Etiology can be divided into acute and chronic obstructive and nonobstructive causes.

Acute mesenteric arterial embolism usually occurs when emboli from the heart lodge in the mesenteric arteries. The sources of such emboli can be from blood stasis secondary to atrial fibrillation or from a mural thrombus after an MI.

Valvular lesions can also result in emboli to the mesenteric system. Rarely, an embolus may be composed of atherosclerotic debris that may be dislodged during arteriography or surgery, such as aortic aneurysm resection. Most emboli lodge in the SMA, just distal to the origin of the middle colic artery.

Thrombosis typically occurs at the artery origin, resulting in more structures affected by the occlusion. Embolization, unlike thrombosis, causes less ischemic disease and is associated with better survival. Mesenteric emboli account for 50% of all cases of mesenteric ischemia.

Nonocclusive mesenteric ischemia can occur without any arterial or venous abnormalities. Typically, patients have some degree of atherosclerosis of the mesenteric vessels and report symptoms when external forces such as intra-abdominal tumors compress the vessel or when they have poor perfusion secondary to congestive heart failure, MI, or hypovolemia. It is generally a syndrome of vasospasm and constriction that typically occurs in critically ill patients who are in low-flow states (eg, from septic shock, cardiac shock, burns, or hypovolemic shock).

Low-flow states cause peripheral vasodilation and shunting of the blood from the gut to the periphery. Even treatment of mesenteric insufficiency by revascularization can result in vasospasm and an ischemic episode. Cases of patients without atherosclerotic disease of their mesenteric arteries having ischemia have been reported, but this is rare and occurs in patients with profound hypovolemic shock.

Finally, digitalis has been found to cause vasoconstriction of arterial and venous smooth muscle cells in the mesenteric vasculature. Of patients with acute mesenteric ischemia, 20-30% have nonocclusive disease.

Chronic mesenteric ischemia can be the precursor to any of the above conditions. When the arterial lumen is narrowed secondary to atherosclerosis, any increase in demand of the gut (eg, eating) or a decrease in supply (eg, hypovolemia) can result in severe abdominal pain and possibly infarction. The risk factors for atherosclerosis are therefore pertinent to the development of chronic mesenteric ischemia.

Acute insufficiency of the splanchnic blood flow can result from an arterial or venous occlusive process or a nonocclusive process such as vasospasm. The splanchnic blood flow normally ranges from 10-40% of the cardiac output depending on the state of the patient. This wide variation in flow through the mesenteric system is caused by local and regional control mechanisms. Adenosine, a metabolic byproduct of ischemia, causes dilation of the splanchnic vessels, as does nitric oxide. The sympathetic system antagonizes these vasodilatory effects and causes redirection of the blood from the gut to the more vital brain and heart during times of stress. Activation of the renin-angiotensin pathway is also known to cause vasoconstriction of the splanchnic bed. During times of hypovolemia, a patient may experience nonobstructive mesenteric ischemia because of the low-flow state. The mechanism by which a patient experiences pain because of the ischemia is poorly understood.

The consequences of vascular occlusion depend on the vessels involved. A patient with chronic mesenteric ischemia with atrial fibrillation who has an embolism to a branch of the SMA may experience mild or no symptoms because of adequate collateral flow. The patient with acute thrombosis loses perfusion from the origin of the SMA, resulting in a greater amount of dead bowel. Tissue injury can result from one of 2 mechanisms: (1) ischemic injury to the bowel or (2) reperfusion injury.

Within 4 hours after ischemia begins, the mucosal villi become necrotic. As early as 6 hours, full-thickness infarction can be observed (see the first 2 images below). Submucosal hemorrhage and edema in the colon produce a characteristic thumbprinting that is depicted in the third image below. If left untreated, patients can hemorrhage into their bowel, experience perforation, and, ultimately, become septic and die.

Reperfusion injury occurs when ischemic bowel regains its blood flow. The result is a release of oxygen free radicals by leukocytes. Other factors, such as phospholipase A2, up-regulate prostaglandins and leukotrienes, which causes more injury.

Patients with mesenteric ischemia have a very typical presentation. However, the diagnosis may be overlooked because of the vague nature of the patients' symptoms.^[3] Depending on the type of mesenteric ischemia, patients may present with a variety of signs and symptoms. Patients may present with a history of postprandial pain, typically starting 20-30 minutes after their last meal, that may last up to 60-90 minutes. Because of this, they develop food fear and experience subsequent weight loss. Patients may be severely malnourished upon presentation.

Some patients may present with an acute onset of severe abdominal pain without a history of previous postprandial pain. These patients may report blood in their stool as their bowel begins to die. The classic patient with chronic mesenteric ischemia may provide a history of postprandial pain between 10 minutes and 3 hours after a meal. The pain can become so severe that the patient may develop a fear of eating and report recent weight loss. Patients may report diarrhea or constipation, and occult testing of stool may return positive results because of the sloughing of dead ischemic bowel.

Patients with acute mesenteric ischemia provide a history of sudden onset of symptoms. Further exploration may reveal a history similar to persons with chronic ischemia. Review of the past medical history may reveal other manifestations of atherosclerotic disease such as MI, stroke, or peripheral vascular disease.

Upon physical examination, the patient is thin and writhing in pain. Palpation of the abdomen reveals no peritoneal signs (pain out of proportion to examination), and auscultation of the abdomen may reveal a bruit.

Once a diagnosis of acute mesenteric ischemia is confirmed, the patient should undergo surgery because of the risk of weight loss, pain, bowel infarction, and possible death. If chronic mesenteric ischemia is diagnosed, patients should be evaluated for cardiopulmonary and renal disease before surgery is considered.

Mastery of the anatomy of the mesenteric vessels is essential to understanding and treating patients with mesenteric artery ischemia. Unfortunately, the endless array of vascular variations can make this difficult.

• The celiac axis, the SMA, and the inferior mesenteric artery supply the foregut, midgut, and hindgut, respectively.
• The celiac axis arises from the ventral surface of the aorta at the T12-L1 vertebral body. It courses anteroinferior before branching into the common hepatic, splenic, and left gastric arteries. Variations to this have been observed but are too numerous to describe here.
• The hepatic artery gives off the gastroduodenal artery, which branches further to the right gastroepiploic artery and the anterosuperior and posterosuperior pancreaticoduodenal arteries.
• The right gastroepiploic artery has a communication with the left gastroepiploic artery, which is an immediate branch of the splenic artery.
• The anterosuperior and posterosuperior pancreaticoduodenal arteries communicate with the corresponding inferior branches from the SMA.
• The splenic artery gives off the left gastroepiploic artery and the dorsal pancreatic artery, which supplies the body and tail of the pancreas and communicates with the anterosuperior pancreaticoduodenal and gastroduodenal arteries and, sometimes, the middle colic artery or SMA.
• The third important branch of the celiac artery is the left gastric artery, which communicates with the right gastric artery along the posterior aspect of the lesser curvature of the stomach.
• The celiac artery supplies most of the blood to the lower esophagus, stomach, duodenum, liver, pancreas, and spleen.
• The SMA comes off of the ventral aorta and supplies the midgut by giving off the inferior pancreaticoduodenal artery and the middle colic, right colic, and jejunal and ileal branches.
• The inferior pancreaticoduodenal artery gives rise to the corresponding anteroinferior and posteroinferior branches that anastomose with the superior counterparts as described above. This communication is but one important connection that helps maintain bowel perfusion in times of ischemia of the mesenteric vessels.
• The ileocolic artery supplies the ileum, cecum, and ascending colon, while the middle colic artery supplies the transverse colon and communicates with the inferior mesenteric artery.
• The right colic artery typically branches at the same level as the middle colic artery.
• The right and middle colic arteries are important suppliers of blood to the marginal artery of Drummond and give rise to the terminal vasa recta, which provide blood to the colon.
• The inferior mesenteric artery is the smallest mesenteric vessel and comes off the anterior aorta. The inferior mesenteric artery provides blood to the distal transverse, descending, and sigmoid colon and the rectum.
• Many communications exist within the mesentery to the SMA, and rectal branches offer communication of the visceral blood supply with the common blood supply.
• The watershed area, near the splenic flexure, is thought to be more susceptible to ischemia secondary to poor arterial flow. Because this area is poorly developed, it has an increased propensity for ischemia.

Because of the multiple areas of potential collateral flow in the mesenteric system, at least 2 of the 3 vessels must be occluded to produce chronic ischemia.

• Acute mesenteric ischemia is deemed an emergency because of the poor outcomes of untreated patients. It should be treated without reservation.
• Surgical treatment may be contraindicated if the risks caused by comorbid conditions preclude surgery.
• If the ischemia is thought to be caused by vasospasm, surgery is not indicated. Medical management with anticoagulants and intra-arterial vasodilators is appropriate.