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Diagnosis and Surgical Management of the Visceral Ischemic Syndromes
Although the causal relationship between mesenteric vascular occlusion and intestinal gangrene was suspected in the 15th century, the first successful case of intestinal resection for infarction was not reported until 1895. Recognition of the chronic form soon followed, with the term angina abdominis applied by Goodman to illustrate the similarities to the newly described angina pectoris. Indisputable evidence was provided in 1936 by Dunphy, a surgical resident at the Peter Bent Brigham Hospital in Boston, who described the clinical course of a 47-year-old man with weight loss and periumbilical pain out of proportion to the findings on physical examination. The patient died suddenly in the hospital, and postmortem examination revealed chronic mesenteric disease with fresh thrombus completely occluding the celiac trunk. Dunphy reviewed twelve other deaths from mesenteric vascular occlusion and found an antecedent history of chronic recurrent abdominal pain in seven.
The first successful reports of mesenteric revascularization for chronic mesenteric ischemia appeared in 1958. In that year, Shaw and Maynard from the Massachusetts General Hospital reported two cases of superior mesenteric artery (SMA) thrombosis superimposed on atherosclerotic occlusive disease. Both patients were treated with SMA thromboendarterectomy and survived. The surgeons made the astute observation that although the responsible atherosclerotic lesions involved all three mesenteric arteries, they were confined to the proximal segments, such that vascular reconstruction was technically feasible.
Since that time, intestinal ischemic disorders have been recognized as uncommon but clinically important causes of abdominal pain. Although their incidence is estimated at only a few cases per 100,000 population, their lethal nature requires vigilance and a high index of clinical suspicion to avoid catastrophe. This chapter reviews the pathophysiology, clinical presentation, diagnostic evaluation, and treatment of both acute and chronic intestinal ischemic disorders. The surgical and endovascular techniques of treatment and outcomes are discussed in detail.
Vascular Anatomy
The mesenteric circulation consists primarily of three branches of the abdominal aorta ( Fig. 25.1 ): the celiac axis, the SMA, and the inferior mesenteric artery (IMA). The mesenteric vascular bed is “privileged”—that is, it exhibits very low resistance to both mean and oscillatory blood flow and has the potential for extensive collateralization when its main trunks are compromised. Their multiple branch points and interconnections form such a rich anastomotic network that compromises two of the three major arteries that are usually required for the development of chronic ischemic symptoms. Knowledge of the normal and variant anatomy is essential for surgical diagnosis and revascularization.
Celiac Axis
The celiac axis supplies the foregut including the stomach, liver, spleen, portions of the pancreas, and the proximal duodenum. It originates from the ventral portion of the abdominal aorta, near the level of T12 to L1, between the diaphragmatic crura. Its origin is encased in the median arcuate ligament, a dense, fibrous portion of the central posterior diaphragm draped across the aortic hiatus. In most patients, the celiac axis branches soon after its origin into the common hepatic, splenic, and left gastric arteries. In 1% of cases, the SMA arises from the celiac axis as well, forming a common celiomesenteric trunk.
The hepatic artery is usually the first branch of the celiac axis. It may also arise from the SMA (the so-called replaced right hepatic artery) in approximately 12% of cases. Additional variants include the replaced common hepatic artery (approximately 2.5%) and direct origin of the common hepatic artery from the aorta (approximately 2%). The common hepatic artery gives rise to the right gastric artery and the gastroduodenal artery, which further divides into the right gastroepiploic and superior pancreaticoduodenal arteries. The remaining proper hepatic artery gives rise to the cystic, right hepatic, and left hepatic arteries, which serve the gallbladder, the right and caudate hepatic lobes, and the middle and left hepatic lobes, respectively.
The second branch of the celiac axis is the splenic artery. Its first named branch is the dorsal pancreatic artery, supplying the posterior body and tail of the pancreas. Just before entering the splenic hilum, the splenic artery gives rise to the left gastroepiploic artery and multiple short gastric arteries, providing blood flow to the gastric fundus.
The final branch of the celiac axis is the left gastric artery. It courses cephalad and to the left to supply the gastric cardia and fundus along the lesser curvature of the stomach, joining centrally with the right gastric artery from the hepatic artery. In approximately 12% of the population, the left hepatic artery originates from the left gastric artery.
Superior Mesenteric Artery
The SMA arises from the aorta just distal to the celiac axis at the level of L1 to L2. It passes behind the neck of the pancreas, in front of the uncinate process, and over the third portion of the duodenum. Its first branch, the inferior pancreaticoduodenal artery, courses superiorly to join the superior pancreaticoduodenal artery (from the gastroduodenal artery) and forms the most proximal collateral pathway with the celiac axis. The central branches of the SMA supply the midgut from the ligament of Treitz to the midtransverse colon. These include the middle colic (serving the proximal two-thirds of the transverse colon), right colic (mid-ascending and distal ascending colon), and ileocolic (distal ileum, cecum, appendix, and proximal ascending colon).
Inferior Mesenteric Artery
The IMA arises from the left side of the aorta 8 to 10 cm distal to the SMA at the level of L3. It travels caudad and to the left before dividing into the left colic and sigmoid arteries. The IMA supplies the distal third of the transverse colon, the descending and sigmoid colons, and the proximal rectum. It has anastomotic communications with the left branch of the middle colic from the SMA and with portions of the middle and inferior rectal arteries from the internal iliac.
Collateral Circulation
The mesenteric circulation has a redundant collateral network that serves to maintain perfusion, even with compromise of the proximal main channels. The celiac axis and SMA communicate primarily via the superior and inferior pancreaticoduodenal arteries (via the gastroduodenal artery). The SMA and IMA communicate via the centrally located arch of Riolan (often referred to as the meandering mesenteric artery ), and by the multiple communications at the periphery of the colon called the marginal arteries of Drummond . In addition to these collateral pathways, muscular branches of the aorta may contribute to intestinal perfusion, including the lumbar arteries, internal mammary arteries (via the deep epigastric arteries), middle sacral artery, and internal iliac arteries (via collaterals between the inferior and superior rectal arteries). Because of this plentiful collateral network, it is understandable that in most instances of gradual occlusion, at least two of the three major mesenteric artery orifices must be blocked to produce the clinical syndromes of chronic intestinal ischemia. In contrast, sudden occlusion of one widely patent vessel can cause acute ischemia because collaterals may be underdeveloped.
Acute Ischemia
Pathophysiology
Acute mesenteric ischemia (AMI) is caused by an abrupt reduction in or cessation of the delivery of oxygen to the intestine. This can result from an occlusion of the mesenteric arterial supply or venous drainage as well as hypoperfusion during shock states. The most common pathophysiologic mechanisms include acute embolization to the SMA (approximately 50% of all cases), in situ SMA thrombosis of a preexisting atherosclerotic lesion at the origin of the vessel (20%), nonocclusive mesenteric ischemia (20%), most often associated with low-flow states such as shock and/or mesenteric vasospasm, and mesenteric venous thrombosis (10%). In earlier series, the phenomenon of nonocclusive mesenteric ischemia was not well appreciated and was frequently misdiagnosed as acute venous occlusion. For example, Cokkinis reported in 1935 that acute mesenteric venous thrombosis accounted for the majority of cases of AMI.
Other unusual arteriopathies, such as Takayasu arteritis, fibromuscular dysplasia, and polyarteritis nodosa, may first present with intestinal ischemia. Isolated dissections of the SMA also have been reported, although the more common mechanism is extension of dissections of the descending thoracic aorta into the SMA and celiac axis.
If untreated, acute intestinal ischemia commonly leads to intestinal infarction. Tissue loss may result from both hypoxia during flow interruption and reperfusion injury once intestinal arterial blood flow is restored. Reperfusion injury is principally mediated by activation of the enzyme xanthine oxidase and the recruitment and activation of circulating polymorphonuclear neutrophils (PMNs). In the presence of oxygen and hypoxanthine (a by-product of adenosine triphosphate metabolism), xanthine oxidase produces oxygen-derived free radicals that cause severe local tissue injury through lipid peroxidation, membrane disruption, and increased microvascular permeability. PMNs are attracted to reperfused tissue by the local secretion of cytokines (tumor necrosis factor-α, interleukin-1, platelet-derived growth factor) by ischemic endothelium. Subsequent rolling, adherence, and activation of the PMNs in the microcirculation result in the secretion of myeloperoxidase, collagenases, and elastases that can further injure the already ischemic and vulnerable tissue. Activation of the inflammatory cascade may also have systemic effects, with cardiac, pulmonary, and other organ system dysfunction.
Acute Mesenteric Arterial Embolism
Most mesenteric arterial emboli originate from left atrial or ventricular mural thrombi or cardiac valvular lesions. These thrombi are usually associated with cardiac dysrhythmias such as atrial fibrillation or hypokinetic regions from previous myocardial infarctions. The majority of mesenteric emboli lodge in the SMA because of its high baseline flow rate and nearly parallel course to the abdominal aorta. Only 15% of SMA emboli remain impacted at the origin of the vessel. The majority of emboli progress distally 3 to 10 cm to the tapered segment of the SMA just past the origin of the middle colic artery ( Fig. 25.2 ). The middle colic and ileocolic branches may remain patent and the resulting pattern of bowel ischemia may be less extensive, with the proximal jejunum and transverse colon being spared, than after in situ thrombosis, where the ascending colon and more of the small bowel are involved. A substantial fraction (10% to 15%) of mesenteric emboli are associated with concurrent emboli to another arterial bed. Intestinal ischemia due to embolic arterial occlusion can be compounded by reactive mesenteric vasoconstriction, which further reduces collateral flow and aggravates the ischemic insult.
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