Mesenteric ischaemia and infarction results from interruption of arterial or venous perfusion of all or part of the intestinal tract. The major causes are acute occlusion of the superior mesenteric artery, mesenteric venous thrombosis, and non-occlusive infarction. In general, the prognosis for survival is poor.

Acute superior mesenteric artery occlusion may be the result of either thrombosis or an embolus. Emboli account for about 20 per cent of all cases of acute ischaemia or infarction and about one-half of the cases of acute occlusion of the mesenteric artery. With early diagnosis and proper management, survival with preservation of most or all of the small intestine is readily achieved.

Three vessels constitute the major arterial supply to the intra-abdominal intestine. These are the coeliac axis for the stomach and duodenum, the superior mesenteric artery for the jejunum, ileum, and right and transverse colon, and the inferior mesenteric artery for the left and sigmoid colon. It is unusual for an embolus to either the coeliac axis or the inferior mesenteric artery to produce infarction, because of the obtuse angle of the coeliac axis to the aorta, the small size of the inferior mesenteric artery, and the adequacy of collateral inflow to both. The superior mesenteric artery, in contrast, originates at an acute angle, is large and, at least when acute occlusion is proximal, seldom has the sufficient collateral flow to preserve viability of the entire area of intestine which it supplies. This artery is one of the most frequent sites of clinically apparent emboli to visceral vessels.

The first branches of the superior mesenteric artery are small, supplying the duodenum, pancreas, and proximal jejunum. The initial branch of any size is the middle colic artery. The superior mesenteric artery tapers rather rapidly distal to it, terminating in the arteries to the distal ileum. The usual sites at which an embolus lodges are at the origin of the middle colic artery, where it may or may not cause occlusion, and in the main trunk of the artery, within 5 cm distal to the origin of the middle colic artery. (Fig. 1) 352,353. Occlusion at the origin of the superior mesenteric artery is almost invariably the result of thrombosis, not an embolus.

As with other peripheral emboli, most mesenteric emboli come from the heart. Common sources of emboli are atrial fibrillation, infarction of the ventricle with mural thrombus, and valvular excrescences. A few emboli come from the aortic wall itself, and some are iatrogenic, following aortic surgery or catheterization.

When occlusion of the superior mesenteric artery occurs gradually, collateral inflow from the other visceral vessels usually protects the intestine from ischaemic injury. When occlusion is acute, this collateral supply is not sufficient. Depending on the site at which an embolus lodges, the resulting ischaemic injury may extend from the proximal jejunum to the left transverse colon or, with a more peripheral site of occlusion, may involve only the ileum and right colon. Anatomical variation in collaterals and the presence of fragments of emboli peripherally mean that the ischaemic injury may be patchy and variable in its severity, especially in the early stages. However, the central area of supply, the ileum and caecum, usually sustains the most profound injury. A small embolus that enters a branch of the superior mesenteric artery may lead to a segmental infarct or to no ischaemic injury.

The mucosa is the only layer of the intestinal wall to have little resistance to ischaemic injury, becoming damaged rapidly by even relatively mild degrees of ischaemia. The first gross evidence of damage is submucosal oedema. This proceeds to haemorrhage and sloughing of the mucosa, with a small amount of intraluminal bleeding. If the deeper layers remain viable, or if arterial perfusion is restored, the mucosa regenerates: this may take several weeks, during which there is usually diarrhoea and sometimes a degree of malabsorption. In a few patients, the presence of deep ulcers leads to major haemorrhage from regenerating areas.

The initial response of the muscularis propria to ischaemia is spasm. Depending on the severity and duration of ischaemia, atony, infarction, and perforation can follow. Full thickness, irreversible infarction produces a characteristic foul-smelling bloody, peritoneal exudate. With restoration of arterial perfusion the viability of the outer layers may be preserved and chronic ulceration may lead to the development of strictures, which may take several weeks to become apparent.

Visceral pain is an invariable symptom of mesenteric ischaemia. Only in the obtunded or otherwise mentally impaired patient will it not suggest the diagnosis. In its absence, the diagnosis can be confidently excluded. Other symptoms and signs are less definite and depend on the extent, severity, and location of the ischaemic injury.

The course of ischaemic injury caused by an embolus is also variable. Short of removal of the embolus, the only factor likely to improve perfusion is remission of arterial spasm and the gradual enlargement of collateral vessels. Conversely, the ischaemic injury may be worsened by factors that further decrease perfusion, including hypoperfusion due to systemic hypotension and visceral artery spasm. Local factors, including oedema, haemorrhage, and distension, can also cause extension of the infarct. Although a superior mesenteric artery embolus can lead to immediate infarction and perforation within a few hours, this is not the usual course. Many patients will have symptoms for hours or even days before the development of irreversible infarction.

The collateral flow tends initially to lead to a gradient of severity of ischaemic injury, the peripheral areas being most spared. There is a tendency for areas of full thickness infarction to extend to include the marginal areas with the passage of hours. Eventually the initial patchy involvement will usually become an extended area of full thickness infarction.

Patients with mesenteric emboli almost always present with abdominal pain which tends to be steady and, being visceral in origin, poorly localized and referred generally to the mid-abdomen. Although traditionally thought to be sudden in onset and remarkably severe, this is not always true. There may be a vague onset and variable intensity, even with intermittent disappearance. Pain may have been present for several hours or even a few days.

The history may include vomiting, diarrhoea, or even tenesmus. Since signs of peritonitis are present only after perforation, there are initially no positive findings on physical examination. The gastric or rectal contents may contain gross or occult blood. At later stages, although the findings are non-specific, an intra-abdominal catastrophe is obvious, as is the need for laparotomy.

Diagnosis is most elusive during the early stages, when the chance for successful management is high. The decision to proceed with either angiography or laparotomy must be made on the basis of suspicion, not certainty. The diagnosis must be seriously entertained in any patient with unexplained abdominal pain, especially in those over 60 years old.

Laboratory tests are not so specific as to be useful in a positive way. Many patients, but not all, have a leucocytosis which may be extreme, counts exceeding 20000/mm³. The serum amylase is slightly elevated in 50 per cent of victims. Plain radiographs show no, or only non-specific, findings in most cases.

Arteriography is especially helpful in the patient with either a superior mesenteric artery embolus or thrombosis, but is less so in those with venous or non-occlusive infarction, though it may still yield useful indirect findings. The major application of arteriography is in the patient with a history suggesting an embolus, but without systemic or local findings to herald the later stages of infarction. In these patients, arteriography establishes the diagnosis, leading direct to an expeditious laparotomy. When the embolus is small and in a branch, arteriography may also eliminate the need for surgery, although this is quite an unusual site of embolism. As well as providing a certain diagnosis, the arteriogram provides the surgeon with useful information about the site of occlusion and patency of other visceral vessels.

Other radiographic studies, such as computer augmented tomography and indirect flow studies using a Doppler device show promise in helping to reach a diagnosis. They have not reached a level of development and application where they are generally useful or available.

Even with the availability of angiographic therapeutic techniques, immediate laparotomy is the best approach for the management of the embolus and injured bowel. The ideal operation consists of an embolectomy followed by resection of any segment of non-viable bowel.

The surgeon must first confirm the diagnosis, then make an estimate of the extent and severity of ischaemic injury. In the early stages there may be no gross evidence of bowel injury, and there may even be faint peripheral pulses from collateral inflow. The diagnosis of superior mesenteric artery embolism should be abandoned only after the presence of a strong pulse in the main trunk is confirmed. In these early cases, an embolectomy can allow preservation of all of the intestine. Failure to perform an embolectomy invariably leads to infarction and a poor prognosis.

In the usual clinical setting, many patients have extensive infarction that is clearly irreversible. Experience and judgement are needed to decide whether a resection of most of the small bowel, with or without an embolectomy, should be performed. This decision should reflect the age and general condition of the patient and the amount of viable jejunum. Parenteral nutrition solutions have made a major contribution to management of patients with very extensive resections, and permanent home hyperalimentation is a measure to be considered. A successful outcome can be achieved in carefully selected patients with extensive infarction.

If the extent of injury is limited, decisions regarding resection or embolectomy must take into account the site of the embolus. Here, arteriography is helpful (Fig. 2) 354. In a few cases, the embolus is in a peripheral vessel and perfusion to adjacent segments of bowel is normal: resection alone is all that is needed. A delayed reanastomosis may be selected for the colon. If the embolus is located centrally, even though the extent of the infarction is limited, resection alone is almost certain to fail. Further infarction can be anticipated, and an embolectomy is indicated.

The technical demands for an embolectomy of the superior mesenteric artery are within the skills of the general surgeon. The approach to the vessel is at the base of the mesocolon, lifting the transverse colon in an anterior superior direction. The vein is usually to the right of the artery and most of its left branches pass posterior to it (Fig. 3) 355. The perivascular nerve plexus makes exposure somewhat more tedious than that for an extremity artery. This approach will lead to exposure just distal to the middle colic artery. A longitudinal arteriotomy is easier to close, especially in an atherosclerotic vessel, and can also serve as a site for bypass anastomosis if the diagnosis proves to be thrombosis at the origin of the superior mesenteric artery. In the presence of an embolus the pulse will be noted to end at or just beyond the middle colic artery. Embolectomy catheters can be used if the embolus is proximal to the arteriotomy and if there is distal propagation of thrombosis. The mesenteric vessels are fragile, and catheters should be used with care. The arteriotomy can usually be closed directly; eversion is neither necessary nor desirable. Rarely, a local endarterectomy or patch graft may be required.

After mesenteric flow is restored, a period of observation is needed to determine which ischaemic segments of bowel are viable. Although fluorescein injections with observation under an ultraviolet light, and determination of pulsatile flow in the bowel wall by a Doppler device make objective assessment possible, these are usually unavailable, and the observation of an experienced surgeon carries the same degree of accuracy. If no doubt exists, non-viable segments should be resected. Depending on the apparent adequacy of arterial circulation, anastomosis may be performed, or stomas should be established.

When doubt continues after observation, clearly infarcted segments should be extirpated and a second-look operation scheduled. The second operation can be done at a convenient time, a few hours later, when there should be a clear demarcation of infarcted areas. The decision about reoperation should be made during the first operation, as the clinical course over the next few hours cannot serve as an indication that all is well. There is evidence that supports a policy of routine second-look operations after embolectomy.

Postoperative measures to prevent recurrence or extension of thrombus may be appropriate. These include the infusion of antispasm drugs, using angiographic techniques. More important is attention to the management of the cardiovascular system: hypovolaemia and peripheral vasospasm must be avoided. Anticoagulants prevent the formation of further emboli but must be used with caution for the first 24 h in the patients with a mesenteric artery suture line.

A number of specific postembolectomy complications can be described, all of which are relatively uncommon. Occlusion of the artery by thrombus or a new embolus will cause the original symptoms to recur and this is suggested in the patient who notes recurrence of pain. Early bleeding from the suture line follows anticoagulation; late bleeding usually means sepsis. Diarrhoea, often severe, is common, and parenteral nutrition can make an important contribution to survival. This subsides as the mucosal injury heals: persistence is indicative of extensive ulceration and stricture formation and a further resection will be needed. During the healing phase, mild bleeding is usual. Massive bleeding from deep ulcers may indicate the need for a resection. Angiography is often helpful in detecting the site of bleeding.

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