Mesenteric ischemia is a condition characterized by high mortality. It does not occur very frequently but when it foes the diagnosis is often made too late. Several new approaches have been suggested but mortality still remains in the same high range for the last decades.
Definition, pathogenesis and epidemiology
Mesenteric ischemia is defined as a condition in which the supply of oxygen is too small to satisfy the needs of the intestines.
Ischemia can affect the small intestine, the colon or both. It can be acute and chronic.
Most often mesenteric ischemia is classified as occlusive or non-occlusive.
Probably the most common cause of acute occlusive mesenteric ischemia is strangulation. This variant will, however, not be dealt with in this chapter. Other common causes of occlusive intestinal ischemia are arterial emboli, arterial thrombosis, complications of aortoiliac surgery and venous thrombosis. Unusual causes of occlusive mesenteric ischemia include trauma and small vessel disease. Acute non-occlusive mesenteric ischemia occurs as a consequence of other critical diseases such as shock and heart failure. Non-occlusive intestinal ischemia can also be induced pharmacologically by e.g. digitalis and vasoactive drugs. Chronic ischemia can be caused by atherosclerosis, fibromuscular dysplasia, inflammatory disease (Takayasu), and be a consequence of radiation injury. It can also be congenital as a part of aortic coarctation.
The pathogenesis in occlusive ischemia is most often an abrupt occlusion of a major vessel resulting in a significant reduction in intestinal blood flow. It is, however, not unusual that one finds two of the three supplying major arteries to be occluded without signs of mesenteric ischemia. That probably requires that the process has taken some time to allow collateral blood flow to develop and that the remaining vessels are healthy. In the elderly patient with atherosclerotic vessels, which is a common situation in the western world, sudden obstruction of blood flow by an embolus in the superior mesenteric artery is likely to impair blood flow enough to cause bowel infarction. If ischemia is total or near total it takes 8–16 hours to develop transmural infarction. This is, thus, the time frame during which the diagnosis has to be made and appropriate actions started in order to allow measures to prevent bowel infarction. After this period removal of dead bowel is all that can be achieved surgically and the prognosis is then dependent on the extent of bowel necrosis.
In the non-occlusive forms time course and extent of bowel injury is less easy to predict. Small intestinal blood flow can be reduced to about half of normal and the bowel can compensate for this reduction in oxygen delivery by increased oxygen extraction. (As a consequence the liver might become quite hypoxic). If blood flow is about 5% of normal or less then ischemia is total or near total. In between, e.g., reduction down to 10–40% of the normal level, ischemia causes mucosal injury but not transmural infarction even if it becomes quite prolonged. This mucosal injury is considered important in the sense that it further exaggerates the underlying shock situation by release of various toxic factors from the intestine including bacteria and endotoxin - a process often referred to as translocation. Impairment of the intestinal immune function and the associated liver ischemia may also contribute to the aggravation of the underlying disease. The mucosal injury caused by this degree of intestinal ischemia, is likely to be exacerbated at reperfusion by increased generation of oxygen free radicals.
The colon seems to be affected less often by ischemia than the small intestine. One exception is focal non-occlusive colonic ischemia affecting the splenic flexure. The ischemic episode often remains undiscovered and these patients later are found to have a stricture at barium enema. This stricture sometimes can be mistaken for a neoplastic one. Colon is also affected in ischemia caused by surgery for abdominal aortic aneurysm.
The frequency of acute mesenteric ischemia is low. It has been reported that less than 1% of all acute laparotomies are performed because of acute mesenteric ischemia. Arterial thrombosis and embolus make up the two most common occlusive causes of acute mesenteric ischemia (approximately 50 and 33%, respectively). Most often the patient with a mesenteric embolus has an atrial fibrillation as the source of the embolus. Venous mesenteric thrombosis is the cause of acute mesenteric ischemia in about 10–15% of all cases. The onset of ischemia may be significantly prolonged in some patients with venous thrombosis.
Irrespective of etiology four clinical stages are usually recognized. As mentioned above in arterial embolism the onset of symptoms is often very quick and the progression of symptoms rapid while the process can take several days following venous thrombosis.
The first stage is the hyperactive stage. This is characterized by the intermittent severe pain which starts immediately after occlusion of the vessel. Frequently there is passage of loose stools, sometimes with blood, and vomiting. Usually there is a discrepancy between the often very severe pain and the few findings on physical abdominal examination. Ischemia causes hyperperistalsis reflected in hyperactive bowel sounds on auscultation.
The paralytic stage. The pain is usually diminishing but becomes more continuous and diffuse. During this stage the size of the abdomen increases and it becomes more generally tender and there is no bowel sounds at auscultation.
The stage of disarranged fluid balance. Fluids containing proteins and electrolytes start to leak through the mucosal as well as the serosal side of the gut. When the bowel becomes necrotic peritonitis develops. The fluid loss is usually massive. In this stage the patient does not differ much from other patients suffering from peritonitis of other causes.
The Shock stage. In this stage patients are rapidly deteriorating with severe alterations in the fluid balance and the situation soon goes over into irreversible shock.
Rapid diagnosis is essential in order to improve the high rate of detrimental outcome in acute mesenteric ischemia. A high degree of suspicion is the single most important factor in order to achieve diagnosis while treatment still could be corrective.
When the patient is in the hyperactive symptomatic stage at laparotomy the gut could still be saved if an embolectomy, thrombectomy or a reconstruction could be performed.
Plain X-ray is unspecific until very late when gas can be seen in the bowel wall and in the mesenteric veins.
Duplex ultrasonography can be diagnostic in the hyperactive stage but in the later stages there is usually too much gas to allow reliable readings.
Angiography can be diagnostic and has been advocated strongly by some. Others have argued angiography may cause unacceptable delays in the handling of these patients. If angiography is performed and if there is non-occlusive disease the catheter can be used for local infusion of vasodilating drugs as papaverin as advocated by Boley and co-workers (6). They have reported significantly lower mortality following this treatment modality compared with what is generally found in the literature but the evidence supporting this concept is still grade C.
Ischemia following aortoiliac reconstructive surgery constitutes a special situation. Clinical colonic ischemia occurs in 2.3% of all cases increasing to 7.3% after surgery for ruptured aortic aneurysm with the patient in shock (1). If the patients are routinely followed up by endoscopy mucosal ischemia is seen in about 10% of the cases.
Early passage of stools postoperatively, especially if bloody, is an important sign of warning. Other signs that might indicate ischemia include failure to improve as expected, increasing creatinine concentrations in serum and extensive thrombocytopenia. The vast majority of the ischemic lesions following surgery for aortic aneurysm is within reach by the sigmoidoscope. If continuous monitoring of intramucosal pH using the tonometric technique has been employed values below 7.1 without a trend of normalization should arouse suspicion of bowel ischemia.
If the diagnosis is made before bowel gangrene has developed (or if there is a only a minor localized gangrenous area which could be resected although surrounded with ischemic but not yet gangrenous intestine) and if there is a localized obstruction an embolectomy or an thrombectomy is the best treatment, although not supported by RCTs.
If there is a central stenosis in the superior mesenteric artery with low flow after thrombectomy this is best treated by implanting the infrapancreatic part of the artery end to side in the infrarenal aorta or by a short bypass. Reconstruction of the superior mesenteric artery close to the aorta is warned against because of the difficult anatomic position.
Following this type of surgery, with or without simultaneous bowel resection, the rule should be to perform a second look 12–24 - hours later. This decision should be made at the time of the first operation and should basically not be discussed thereafter.
Mortality following second look surgery is generally 65–85%. It is, however, 100% if nothing is done. (Grade A.)
In transmural colonic ischemia following aortic aneurysm surgery resection of the affected bowel segment should be performed. Closing the distal end of the colon blindly and an end colostomy (the Hartmann procedure) is then a safe operation. If the bowel segment is removed before signs of peritonitis are visible the prognosis is excellent.
If there is significant bowel infarction at the time of surgery all that could be done is removal of the dead gut.
In case that the remaining part of the gut would allow oral nutrition and a normal life, resection should be performed. It is often advised to perform a second look 24 hours later and this decision should be made at the time of primary surgery, as stated above. If, however, the entire small intestine is gangrenous and the patients has peritonitis it is most often too late to save the life of the patient and often nothing is done at laparotomy in such cases.
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Ulf Haglund, M.D.
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