Irrespective of the dominant systemic pattern of atherosclerotic disease, the mesenteric vessels are seldom spared. Autopsy studies show that even in middle age, more than 50 per cent stenosis is present in the coeliac axis and superior mesenteric arteries of about 6 per cent of subjects studied. The inferior mesenteric artery is similarly narrowed in twice as many. Most of these lesions, in fact, neither cause chronic symptoms nor lead to acute infarction. The circumstances under which they achieve clinical importance and the nature of these events is discussed in this section.

The major arteries that supply the intra-abdominal intestinal tract are the coeliac axis, the superior mesenteric artery, and the inferior mesenteric artery. The branches of each are interconnected by one or more peripheral arcades. There are also collateral points of junction between the three major vessels. For the coeliac axis and superior mesenteric artery these are the large pancreaticoduodenal arcades and small connections between the pancreatic and proximal jejunal vessels. One or two well-developed arcades similarly join the left branch of the middle colic artery and the superior branch of the inferior mesenteric artery. Proximal collateral inflow arises from the oesophageal and inferior phrenic arteries; distal inflow arises from branches of the hypogastric arteries.

Obliterative atheromatous disease in the mesenteric arteries is seldom diffuse. The initial and most severe lesions are almost invariably at their origins, the peripheral branches and collaterals being spared. The effectiveness of these collateral channels, especially when the superior mesenteric artery is occluded, is enhanced by gradual rather than sudden development of occlusion. Anatomical variations and prior occlusive disease also influence their role. Even complete occlusion of the origin of the inferior mesenteric artery is rarely significant except in limiting its effectiveness as a collateral source. An exception is ligation during operations of the aorta. The same statements apply to the coeliac axis. Here the exception is the coeliac compression syndrome, which is, in fact, a dubious clinical entity.

The spectrum of manifestations of mesenteric artery insufficiency extends from transient episodes of visceral pain to irreversible infarction. Three points along this spectrum are clinically important: intermittent insufficiency provoked by increased demand for perfusion during digestion; sustained insufficiency, a condition that invariably proceeds to actual ischaemic injury; and infarction, either partial or full thickness. Insufficiency and infarction are also common to the presentation of a superior mesenteric artery embolus. The challenge for successful management of obliterative atheromatous disease is to recognize occlusion during the early stages. The task is made difficult by the obscure nature of signs and symptoms prior to actual infarction.

Despite the difficulty in directly measuring mesenteric blood flow in man, it is clear that there are marked increases during digestion, especially in the superior mesenteric artery. The classic presentation of intermittent ischaemia, provoked by a restriction of flow to such a degree that this increase in demand cannot be satisfied, is usually termed intestinal angina. Visceral pain, in fact, invariably accompanies small bowel ischaemia. When episodes are intermittent, however, its characteristics do not readily suggest the cause. It is aching in nature and poorly localized, being referred generally to the anterior abdomen. A useful clue in some patients is that it seems to be precipitated by meals.

A second clinical symptom of intermittent ischaemia is weight loss, usually the result of a decrease in intake rather than a loss of absorptive or digestive capacity. Even though many patients are not aware of a direct relationship between eating and pain, they progressively decrease their food intake in an effort to relieve advancing symptoms. An acute extensive ischaemic injury to the mucosa can affect absorptive capacity, but this is not generally a part of the chronic syndrome.

The third clinical manifestation of intermittent ischaemia which is even less specific, is disturbance in bowel function. Symptoms may include bloating, generalized abdominal discomfort, and a tendency toward diarrhoea or constipation.

Most patients with intestinal angina are elderly and have evidence of other obliterative atheromatous disease. An interesting physical sign is the presence of an epigastric bruit. In fact many do not have it, and most patients who do have a bruit do not have mesenteric vascular disease.

Some patients with abdominal angina are found to have multiple shallow antral gastric or post-bulbar duodenal ulcers. These are resistant to the usual therapy and are thought to reflect severe combined coeliac axis and superior mesenteric artery occlusive disease. Revascularization can allow healing.

Thrombosis of the origin of the coeliac axis or of the superior mesenteric artery is the end result of severe obliterative atheromatous lesions. It is often inconsequential, flow through the narrowed vessel origins having been restricted long enough for collateral channels to have become sufficient. This is not always the case; about one-half of the clinically significant cases of acute occlusion of the superior mesenteric artery have this aetiology. In other cases the coeliac axis or inferior mesenteric artery may represent a critical source for collateral flow in an extensively diseased system: their final occlusion may precipitate ischaemia and infarction. The site of infarction may be quite remote from the region directly supplied by the artery. Factors other than acute occlusion can also precipitate infarction in a patient with a severely compromised mesenteric circulation. These include central causes for hypotension and peripheral vasoconstriction, such as a cardiac arrhythmia or myocardial infarction, or any condition leading to hypovolaemia or shock. Hospital admission and angiographic studies may sometimes be such a factor. Nevertheless some patients with intestinal angina and no acute thrombotic lesion will have no apparent local or remote cause for infarction.

Sustained mesenteric insufficiency is characterized by persistent pain. If it is preceded by intestinal angina, the patient generally describes it as similar to that of intermittent episodes but more severe and unremitting. The majority of patients with symptomatic acute thrombosis will not have had prior mesenteric vascular symptoms: the duration of sustained insufficiency prior to infarction may vary from a few minutes to many days. The intensity of pain tends to wax and wane, and the actual severity of local ischaemia can be worsened by visceral artery spasm, bowel distension, and central factors that alter perfusion. Nevertheless, sustained mesenteric ischaemia almost always proceeds to frank infarction.

Early infarction involves only the mucosa and submucosa; sustained or profound ischaemia is associated with changes in the muscularis. The initial mucosal lesion is characterized by submucosal oedema and haemorrhage, followed by sloughing of the mucosa itself. This event releases blood into the lumen which may be detected in the gastric and rectal contents when infarction is extensive. Perforation of the bowel follows deep infarction, but may not occur for many hours.

The distribution of infarction caused by obliterative disease is variable, except when it is due to acute thrombosis of the superior mesenteric artery, when the distal small bowel and right colon are likely to be most severely affected. The infarct may also extend into areas dependent on this vessel for collateral supply, notably the left transverse and left colon. In other cases, the area of infarction may be in the distribution of the coeliac axis or patchy throughout the intestinal tract. Infarcts of the spleen, gallbladder, and liver are seen.

Intermittent ischaemia with vague pain, weight loss, and fluctuating changes in bowel function is an obscure clinical entity. When ischaemic symptoms become continuous or infarction ensues the diagnosis is no longer elusive, but survival is by then unusual. It may be necessary to evaluate a large number of patients with a suggestive history to detect the few with intestinal angina. The demonstration of gastroduodenal ulcer disease, gallstones, or other unrelated conditions can delay the discovery of the actual cause of the symptoms.

A careful history centres on the characteristics of the pain and weight loss. Perhaps the most similar presentation is that of carcinoma of the pancreas, although bowel changes sometimes lead to an initial suspicion of colon disease. A recent history of peptic ulcer disease and findings of obliterative atheromatous disease in other systems, especially if premature, are helpful. In young women there is often a history of heavy cigarette smoking. Because of the infrequent occurrence of intestinal angina, the initial evaluation often centres on other diagnoses. It is important to persist until a correct diagnosis is established in any patient with abdominal pain and weight loss.

When available, flow Doppler studies may provide a useful direct measurement of mesenteric arterial flow. The critical examination is, however, the arteriogram. A lateral projection with supracoeliac injection into the aorta gives the most useful information about the patency of the origin of the coeliac axis and superior mesenteric artery. Selective injections are also of value but must be used with caution in symptomatic patients with severely compromised circulation, as they may precipitate infarction.

Only by correlation of the history and angiographic findings can the importance of vascular lesions be determined. Intermittent ischaemia is most often associated with extensive occlusive disease of at least two, and usually all three, major vessels. Continuous ischaemia is more frequently the result of acute occlusion of the superior mesenteric artery by thrombus or an embolus. Thromboses leading to infarction can occur in the absence of other severe mesenteric lesions. Continuous ischaemia may also represent the end-stage of extensive obliterative atheromatous disease, with or without acute thrombosis. It may also be the result of impending non-occlusive infarction, venous thrombosis, or even an aortic dissection. The aortic and mesenteric angiograms may sometimes suggest or support these diagnoses in the absence of lesions of major arteries.

The disability associated with intermittent ischaemia would be sufficient to merit correction in most patients; added to this is the risk of eventual infarction. No studies have predicted the magnitude of this risk, but it must be considered high in the severely symptomatic patient.

Treatment has centred on restoration of flow to the superior mesenteric artery and a number of surgical procedures that can accomplish this have been described. These include bypass grafts from the aorta or iliac artery, reimplantation of the superior mesenteric artery after resection of its diseased origin, thromboendarterectomy, either directly or through the open aorta, and side-to-side anastomosis of the main trunk or a branch to the aorta or iliac artery. If the aorta is severely narrowed or aneurysmal, resection and grafting may be indicated at the time of revascularization. The graft can then be used for the site of origin of a bypass or reimplantation. Of all these procedures, a graft from the supracoeliac aorta is perhaps the most uniformly feasible and satisfactory technique (Fig. 1(a)) 265. Restoration of flow into the coeliac axis or one of its branches is not necessary for immediate success, but it may protect against future failure of the reconstruction because of progressive occlusive atheromatous disease. Angiodilatation provides a non-operative alternative to surgical reconstruction. The low risk in selected patients may justify the high recurrence rate.

Improvement of circulation immediately eliminates the pain of intermittent ischaemia. Recovery of normal gastrointestinal function may take months, and weight gain is slow, or non-existent in some patients.

Continuous ischaemia in patients with obliterative atheromatous disease precedes infarction, which is almost always fatal. Immediate diagnosis and intervention gives the only chance for survival. Prompt angiography can be useful, especially in patients with acute thrombosis of the superior mesenteric artery. Otherwise, and in the presence of signs of advanced infarction or peritonitis, immediate laparotomy is the best choice.

In the early stages of threatened infarction the findings are subtle. The intestine does not show discoloration or haemorrhage but is grey, and there may be areas of spasm and hyperperistalsis. Faint collateral pulses can be palpated in some cases. The surgeon should be cautious about abandoning the diagnosis because there is no infarction: to do so always leads to later infarction. With these early findings, or if infarction is limited and other areas threatened, vascular reconstruction should be attempted. A good procedure is the construction of a bypass graft from the aorta or iliac artery to the superior mesenteric artery (Fig. 1(b)) 265. A segment of saphenous vein may be superior in this circumstance. The superior mesenteric artery is exposed distal to the origin of the middle colic artery and opened to establish that no embolus is present. The arterotomy, if longitudinal, can be used for the distal anastomosis. The alternative of a thromboendarterectomy or a more complicated bypass seems less successful under these emergency conditions.

After restoration of circulation, the necessity for a bowel resection is assessed: a short period of observation should suffice. In patients with either very extensive obliterative disease or a marginal appearance of the intestine at completion of the operation, a second-look operation a few hours later has merit.

Infarction, as a terminal event in obliterative atheromatous disease, has a dismal prognosis. Many patients are old and infirm and the infarction tends to be extensive. In an unselected series more than one-half of patients were moribund at the time of admission. In a few generally more fit patients with early diagnosis and limited infarction, arterial reconstruction with a resection, or even a resection alone, can succeed. The attempt is fruitless in the presence of extensive, advanced infarction with this underlying diagnosis.

Pain relating to narrowing of the origin of the coeliac axis has been termed the coeliac axis compression syndrome. The lesion can be the result of compression of the artery by the median arcuate ligament when there is a relatively high origin of the artery or low termination of the ligament (Fig. 2) 266. Fixed narrowing by fibroses or an obliterative atheromatous plaque is frequently found at surgical exploration.

Most patients are between 20 and 40 years old. Pain, which is quite non-specific, is felt in the upper anterior abdomen and may be precipitated by eating or exercise. The mechanism of pain is unknown, but there is no evidence that it is due to actual ischaemia. Asymptomatic compression of the coeliac axis is observed on many angiograms. Occlusion in the absence of advanced disease in the superior mesenteric artery is similarly inconsequential.

Surgical management is directed towards releasing the origin of the vessel and correcting any persistent narrowing. The placebo effect of these operations may well account for their unpredictable success and its variable duration. There is no associated risk of infarction and operations for isolated coeliac axis disease are rarely advisable.

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