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Smoking and vascular disease.

The incidence of acute intestinal infarction approximates to the reported death rate-some 600 deaths a year in the United Kingdom. Though it may be theoretically possible to restore the intestinal circulation, late diagnosis of cases with additional cardiac, respiratory, and renal abnormalities precludes a successful outcome in the majority, and the patient is usually doomed from the start. Though the classical description is of a patient who develops sudden severe abdominal colic, passes blood and mucus per rectum, and rapidly develops peripheral circulatory failure, A. Marston' rightly emphasizes that the mode of presentation is usually atypical. The onset is often insidious with only vague abdominal pain, and the patient may remain apparently well for hours or even days. At this stage, when the diagnosis must be made or laparotomy undertaken for treatment to be effective, the patient may have mild abdominal distension with generalized tenderness but no rigidity. Bowel sounds are normal or increased until the stage when peritonitis ensues, the abdomen is silent, and irreversible gangrene is present. It requires a high degree of suspicion on the physician's part to consider a diagnosis of intestinal infarction at this stage, and the surgeon will often hesitate to undertake laparotomy for vague symptoms when the patient's general condition gives rise to doubts about the anaesthetic risk. As the ischaemic process continues, vast quantities of fluid and blood are lost, and the patient rapidly deteriorates. Marston points out that, when florid physical signs have appeared, the point of recovery for the patient has probably been passed. Investigation of the acute case yields disappointing results. Plain films of the abdomen may show intestinal distension, and aortography is of doubtful value. Leucocytosis occurs early and may be of value, but other laboratory investigations merely reflect the severity of the underlying changes. Before surgical operation resuscitation by intravenous fluids, correction of metabolic acidosis by bicarbonate, and administration of antibiotic may help to prepare the patient. Administration of heparin is unlikely to be rewarding. Though total midgut necrosis is lethal, it is sometimes possible to undertake a limited resection, the removal of a mesenteric embolus by Fogarty catheter, or revascularization of the superior mesenteric artery by bypass graft or by direct anastomosis to aorta or common iliac. Routine reoperation 24 hours later is strongly advised to assess the success of revascularization and to resect any bowel which has subsequently become gangrenous. Chronic intestinal ischaemia is a different problem, but, if the diagnosis can be made, successful revascularization may avert acute infarction. The classical history of severe, persistent, postprandial pain ("intestinal angina"), vomiting, severe loss of weight, and alteration in bowel habit is seen only infrequently, and the patient is more likely to present with vague abdominal pain and moderate loss of weight. Early enthusiasm for the investigation and treatment of cases due to atherosclerosis has waned because many patients develop a good collateral blood supply and do not require surgery.2 Recently attention has been paid to the coeliac axis compression syndrome. American reports3 are encouraging in that patients with abdominal pain, weight loss, and bowel upset have been shown to have stenosis of the coeliac axis caused by external compression from the median arcuate ligament of the diaphragm or from periarterial fibrosis. Simple division of the constricting fibres brings relief of symptoms in 70-80% of cases. J. A. Edwards and his colleagues4 are not so convinced, and there is certainly a need for further study of this problem.