Matthew J. Kruse and Bruce L. Gewertz

Introduction

Unimpeded access to the aorta and its visceral branches is essential to successful surgical treatment of mesenteric ischemia. This chapter briefly addresses clinical presentations of acute and chronic mesenteric ischemia that most often require surgery and considers the various options to achieve optimal exposure.

Clinical Presentation

Approximately half of the cases of acute mesenteric ischemia are caused by embolization of thrombus from cardiac pathology or arrhythmia. Patients present with the sudden, acute onset of epigastric pain not associated with rebound tenderness. The diagnosis is made by clinical correlation (e.g., history of cardiac arrhythmias) and angiographic findings of a focal arterial filling defect consistent with embolus. Radiographic findings of bowel ischemia (e.g., wall thickening, mesenteric edema) or bowel infarction (e.g., pneumatosis, portal venous gas) may be present.

The other primary cause of acute mesenteric ischemia is sudden thrombosis of one or more dominant mesenteric blood vessels. Although these patients frequently have symptoms similar to those with embolic events, prodromal symptoms such as postprandial abdominal pain (“intestinal angina”) and a history of atherosclerotic complications (peripheral vascular disease, myocardial infarction) are often elicited.

Chronic mesenteric ischemia is almost always caused by atherosclerosis of the mesenteric vessels; the classic symptoms are postprandial abdominal pain, weight loss, and food avoidance (“food fear”). The syndrome disproportionately affects women and heavy tobacco users. In most cases, two of the three major visceral vessels (celiac axis, superior and inferior mesenteric arteries) must be significantly narrowed or occluded for symptoms to occur. Arteriographic findings of multiple arterial plaques at the vessel origins confirm the diagnosis. Less common, nonatherosclerotic causes of chronic mesenteric ischemia include fibromuscular dysplasia, median arcuate ligament syndrome, and vasculitis.

The diagnosis of acute or chronic mesenteric ischemia requires both knowledge of the multiple clinical presentations and supporting findings from arterial imaging studies. Computed tomography angiography has an increasing role in diagnosis, with conventional angiography often reserved for potential therapeutic intervention such as fibrinolysis or angioplasty.

Surgical Anatomy

The celiac axis refers to a short arterial trunk originating from the anterior surface of the proximal abdominal aorta as it passes between the diaphragmatic crura at the level of the 12th thoracic vertebra (T12). The artery divides most often into three major branches within 2 cm of its origin: the common hepatic, splenic, and left gastric arteries (Fig. 34-1, A and B). These arterial branches and their tributaries provide the blood supply for the stomach, liver, spleen, portions of the pancreas, and proximal duodenum. The common hepatic artery gives rise to the superior pancreaticoduodenal arteries, cystic artery, and right gastric artery in addition to its left and right hepatic arteries. In approximately 18% of cases, the right hepatic artery is “replaced” and originates from the superior mesenteric artery. The splenic artery gives off the dorsal pancreatic artery, left gastroepiploic artery, and short gastric arteries before completing its tortuous course toward the spleen. The left gastric artery supplies the gastric cardia and fundus before anastomosing with the right gastric artery. A “replaced” left hepatic artery originates from the left gastric artery in approximately 12% of cases.

The next branch of the aorta, the superior mesenteric artery (SMA), provides the major arterial supply to the middle and distal small bowel as well as the ascending and transverse colon. The SMA is the major target artery for revascularization in patients with visceral ischemia caused by arterial insufficiency. The SMA typically arises about 1 cm distal to the celiac axis just inferior to the diaphragmatic hiatus at the level of the first lumbar vertebra (L1). It travels behind the neck of the pancreas, in front of the uncinate process and over the third portion of the duodenum. The SMA gives rise to the inferior pancreaticoduodenal artery, which anastomoses with the corresponding superior branch from the celiac circulation, and to the middle colic artery just before entering the base of mesentery of the small bowel.

Atherosclerotic pathology of the SMA most likely involves its origin, whereas emboli may lodge more distally in its course proximal or distal to the origin of the middle colic artery (Fig. 34-1, C and D).