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Acute Mesenteric Ischemia Moshe Schein · Paul N. Rogers

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Moshe Schein · Paul N. Rogers

“Vascular surgery is peculiar because, above all, it is mainly surgery of ruins.”

(Cid dos Santos)

“Occlusion of the mesenteric vessels is regarded as one of those conditions of which the diagnosis is impossible, the prognosis hopeless, and the treatment almost useless.” (A. Cokkins, 1921)

Acute mesenteric ischemia usually involves the region supplied by the superior mesenteric artery (SMA). Thus the small intestine is predominantly affected but the right colon, which is also supplied by the SMA, can be involved as well. Isolated ischemia of the colon, which is much less common, will be discussed separately under the heading of ischemic colitis in > Chap. 24.

The Problem

The problem is a sudden reduction in arterial perfusion of the small bowel, which quickly leads to central abdominal pain. If left untreated, the process pro- gressively involves the muscular layer of the intestines and it is only after some hours, when the serosa is affected, that peritoneal signs appear. In an attempt to simplify matters let us divide acute mesenteric ischemia (AMI) into three types, which are almost equally common:

Thrombotic: due to an acute arterial thrombosis, which usually occludes the orifice of the SMA,resulting in massive ischemia of the entire small bowel plus the right colon – the area supplied by the SMA.

Embolic: due to a shower of embolic material originating proximally – from the heart (atrial fibrillation, post myocardial infarction, diseased valve) or an aneurysmal or atherosclerotic aorta. Emboli usually lodge in the proximal SMA, but beyond the exit of the middle colic artery; therefore – as a rule – the most proximal segment of proximal small bowel is spared, along with the transverse and (probably) the right colon. Emboli tend to fragment and re-embolize distally, producing a patchy type of small bowel ischemia.

Non-occlusive: due to a “low-flow state”,in the absence of documented arterial thrombosis or embolus. Note, however, that an underlying mesenteric athero- sclerosis may be a precipitating/contributory factor. The low-flow state is a product of low cardiac output (e.g. cardiogenic shock), reduced mesenteric

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flow (e.g. intra-abdominal hypertension) or mesenteric vasoconstriction (e.g. administration of vasopressors) – usually, however, it is due to a com- bination of these factors, developing in the setting of a pre-existent critical illness.

Mesenteric venous thrombosiscan also produce small bowel ischemia. The features and management of this entity differ drastically from the other three.It will be discussed separately below.

The problem is that in clinical practice, outside the textbook, mesenteric ischemia is usually recognized when it has already led to intestinal gangrene.At that stage the Pandora’s box of SIRS (systemic inflammatory response syndrome) has been opened and even removal of the entire gangrenous intestine will not always stop the progression to organ failure and death. Even if such physiologic con- sequences can be overcome the patient commonly becomes an “intestinal cripple”, suffering from the short bowel syndrome.

Assessing the Problem

Typically, the early clinical picture is non-specific – the patient complains of severe abdominal pain – if he is able to complain at all – and the doctor finds little on physical examination.

There may have been preceding symptoms of a similar sort of pain developing with meals and accompanied by weight loss, suggesting pre-existing mesenteric angina. History or evidence of systemic atherosclerotic vascular disease is almost the rule in patients with mesenteric thrombosis while a source for emboli, such as atrial fibrillation,is usually present in patients with mesenteric embolism.Low-flow state patients are commonly moribund due to underlying critical disease.

Nausea, vomiting, diarrhea and hematochezia come late, if ever. You must resist the natural temptation to ascribe patients’ non-specific symptoms to some other benign condition such as gastroenteritis, unless the associated history and symptoms for the alternate explanation are fully present.And by the way – in the elderly – the diagnosis of “acute gastroenteritis” is very rarely the final diagnosis.

Physical examination in the early stages of the process is treacherously benign; peritoneal irritation appears too late, when the bowel is already dead.

Plain abdominal X-raysearly in the course of the illness are normal. Later there may be a pattern of adynamic ileus, with visible loops of small bowel and fluid levels, but with gas and feces seen within the normal colon and rectum. Likewise, laboratory studiesusually are normal until the intestine loses viability; only then do leukocytosis, hyperamylasemia, and lactic acidosis develop.

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The bottom line is that initially in acute mesenteric ischemia the physical examination and all commonly available X-rays and blood tests may be normal.

At this stage, entertaining the diagnosis of mesenteric ischemia, you have two options: the first is to enter in the chart “abdominal examination normal; mesen- teric ischemia cannot be ruled out; will re-assess later”.The second option is to order a CT scan, which has replaced mesenteric angiography as the initial, “screening”

imaging modality in AMI. Although angiography is more specific and accurate, surgeons have been reluctant to offer such an invasive procedure in patients with a non-specific clinical picture. Unfortunately, the first option is the still common in the community – leading to procrastination,late diagnosis and treatment,and a very high mortality rate.

Computed Tomography

To be diagnostic the examination should include oral contrast and intravenous contrast (“CT angio”), with the focus on two areas: the bowel wall and mesenteric vessels. The commonest finding is bowel wall thickening, which is, however, non- specific. The bowel wall may appear low in attenuation due to edema or, when sub- mucosal hemorrhage is present, it may appear of high attenuation due to the blood products. Visualization of the dynamic enhancement pattern of the affected bowel loops may improve diagnosis. Affected bowel loops may demonstrate absence of enhancement,delay in enhancement,or persistent enhancement when compared to unaffected loops. Pneumatosis is an uncommon but specific sign. It is due to intra- luminal gas dissecting into the friable bowel wall. “CT angio” can also visualize emboli within the SMA or thrombosis of the latter at its origin. From this descrip- tion one can easily appreciate that even the CT findings in this condition are subtle and easy to miss.

Mesenteric Angiography

To be beneficial the angiogram should be performed before the bowel has become gangrenous.The clock is ticking; every minute passing reduces the chances of the bowel and the patient surviving.Note that an “acute abdomen”with peritoneal signs is a contra-indication to angiography. The radiologist should start with biplanar angiography (i.e. including a lateral view to show the origins of the SMA and the celiac axis).An occluded ostium of the SMA denotes thrombosis and calls for an immediate operation – unless there is evidence of a good collateral inflow – the angiography providing the road map for vascular reconstruction.When the ostium is patent the radiologist advances the catheter into the SMA. Emboli lodge distal to

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the takeoff of the middle colic artery, produce a smooth filling defect on the back- ground of a normal SMA, and can be multiple.

Non-operative Treatment

In the absence of peritoneal signs attempts at non-operative treatment are justified – tailored to the clinical/CT/angiographic findings. The selective diagnos- tic angiography can now become therapeutic – infusing a thrombolytic agent to lyse the thrombus or embolus with or without adding papaverine1to relieve the associated mesenteric vasospasm. Cessation of abdominal symptoms together with angiographic resolution means that the emergency is over; pre-existing mesenteric artery stenoses can be addressed electively – if indicated.

In the event of non-occlusive mesenteric ischemia the approach involves attempts at restoring compromised hemodynamics. To relieve associated arterio- spasm, a selective intra-arterial infusion of a vasodilator, such as papaverine2, has been advocated. The few champions of this method have reported “favorable responses”. When emboliare the cause, after successful trans-catheter therapy, long-term anticoagulation is indicated. A final point – while rushing to the arterio- graphy suite remember to ensure adequate hydration of your patient to oppose the nephrotoxic effect of the contrast media, which may be used in large quantities.

Operative Treatment

As we told you above – peritoneal signs are an indication not to do arteriog- raphy but to operate; the same applies to the failure of the non-operative regimen discussed above. Through a midline incision assess the viability of the intestine.

In general there are two main possible scenarios: one is the bowel being frankly gangrenous (“dead”), the second when the bowel appears ischemic (“dusky”) and of questionable viability.

 Frank gangrene.Frank gangrene of the entire small bowel is usually combined with the same problem of the right colon and signifies SMA thrombosis. Theoreti- cally, a sporadic patient could survive resection of his entire small bowel and right colon. He may even tolerate a duodenocolic anastomosis while being nutritionally supported at home with total parenteral nutrition (TPN). But the eventual mortal-

1That intra-arterial papaverine infusion is beneficial is a myth – originating in a retrospective study from one New York hospital more than 20 years ago, and since perpetuated in reviews and texts, but never further corroborated by a meaningful clinical experience.

2See previous footnote.

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ity of such an exercise in the average elderly vasculopath approaches 100% and the cost is immense. Our recommendation to you when involved in a similar situation is to walk out to talk to the family, explain that anything done will only increase the suffering of their beloved, return and close the abdomen over the dead bowel.

Provide a lot of morphine and comfort.Frank gangrene of a shorter segment of small bowel or multiple segments-usually denotes embolism. After excising all dead segments carefully examine the remaining bowel. Measure it: how long it is? Only about half of patients left with less than 1 meter (3 feet) of small bowel will live without TPN (saving the ileocecal valve improves the prognosis).Now, observe the remaining bowel. Is it truly non-compromised? Are the mesenteric arcades pulsat- ing well? Feel the SMA at its root – is it vigorously pulsating?

 Dusky bowel.When you are not happy with the remaining bowel, or when the bowel is not dead but appears ischemic and of questionable viability from the start, proceed as follows. Wrap the bowel in warm, saline-moistened sponges and wait 15 minutes. Unscrub and have a coffee; surgeons cannot stare at an inactive field for that long without starting to fiddle. Failure of the bowel to pink-up mandates its resection.When the length of remaining normal-looking bowel reduces towards 1.5 meters (5 feet) it may be advisable to leave the doubtful bowel in situ, to be re- examined during a re-look operation (see below). Saving even a short segment of small bowel may improve the chances of a reasonable life quality. Some authors recommend the use of hand-held Doppler to examine the perfusion of the anti- mesenteric side of the bowel; others use intra-operative fluorescein angiography.

Fig. 23.1. How much should I resect?”

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You may choose to use such modalities if available to you but your clinical judgment should be just as good as any gimmick (> Fig. 23.1).

Adjunctive Vascular Procedures

The ideal setting surgically to improve the perfusion of ischemic small bowel is when the operation follows emergency arteriography (plus failed angiographic therapy) and the bowel is viable or doubtful. Obviously, when the bowel is dead it cannot be revived! Arteriography serves as a road map; when the SMA is occluded – thrombosed at its origin – a vein or graft bypass, antegrade or retrograde, is indi- cated to re-perfuse the SMA. Such a scenario is, however, extremely rare; more commonly you’ll encounter a picture of SMA embolism. Palpate for the SMA just at the base of the mesocolon; if non-pulsatile you’ll find it, after incising the perito- neum, to the right of the large/blue superior mesenteric vein. After obtaining con- trol, open the artery transversely and pass up and down a small Fogarty embolec- tomy balloon catheter. You may conclude the procedure with a shot of urokinase injected distally to lyse the clots in the distal branches,which are inaccessible to your embolectomy balloon catheter.

To Anastomose or Not?

You should be very selective in attempting an anastomosis following any resection of devitalized intestine.The patient has to be hemodynamically stable and his nutritional status at least fair. To be hooked-up the remaining bowel has to be unquestionably viable and the peritoneal cavity free of established infection. Most crucially, the cause of ischemia has to be solved.Another factor strongly bearing on your decision is the length of the remaining bowel and its predicted postoperative function. When more than half of the small bowel is resected, the resection is considered “massive”. Restoring intestinal continuity in such cases would lead to poorly tolerated and intractable diarrhea. And finally, the chief reason not to anas- tomose the bowel is the possibility that further ischemia may develop.

We recommend, therefore, that whenever the above-mentioned favorable factors are absent,or when resection is “massive”,the two ends of the resected bowel should be exteriorized as an end-enterostomy and mucus fistula – if possible via one abdominal wall site (this would allow a subsequent re-anastomosis without a major laparotomy). The postoperative appearance of the stomas will accurately reflect the status of the remaining bowel.

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Second-Look Operations?

A routine planned “second-look” re-operation allows direct re-assessment of intestinal viability at the earliest possible stage, before additional mediators of SIRS have been released, and in a way that aims to preserve the greatest possible length of viable intestine.This concept,which in theory at least is attractive,motivates many surgeons to re-explore their patients routinely after 24 to 48 hours. The finding of completely normal bowel at re-operation is of course reassuring but the anastomosis may still leak 5 days after it has been observed to be intact.If you plan a “second look”

operation there is no need to close the abdomen at the end of the first procedure;

instead,treat the abdomen as a laparostomy (> Chap.38) until re-exploration; reliev- ing any intra-abdominal hypertension to further improve mesenteric blood flow.

An alternative option is to close the abdomen,leaving a few laparoscopic ports adjacent to the bowel, through which a laparoscope may subsequently be inserted to assess the status of the bowel.

To sum up – it appears that in most patients who at the end of the operation do not have stomas,a second-look procedure is indicated.Those with viable stomas, who are otherwise well, can be observed.

Mesenteric Venous Thrombosis

This is a rare condition, which occludes the venous outflow of the bowel.

The clinical presentation is entirely non-specific, with abdominal pain and varying gastrointestinal symptoms that may last a few days until eventually the intestines are compromised and peritoneal signs develop. Mesenteric venous thrombosis may be idiopathic (i.e. the doctor is an idiot – ignorant of the underlying reason) but commonly an underlying hypercoagulable state (such as polycythemia rubra vera) or sluggish portal flow due to hepatic cirrhosis, are present.

Typically, many of these patients are admitted to “medicine” with a surgeon consulted much later – to operate for non-viable bowel. However, an early trip to a contrast-enhanced CT scan may achieve an earlier diagnosis, helping to avoid an operation altogether and improve survival.

Characteristic findings on CT represent a triad of:

 A hypodensity in the trunk of the superior mesenteric vein

 Associated intra-peritoneal fluid

 Thickened segment of small bowel

With the above findings, and in the absence of peritoneal signs, full systemic anticoagulation with heparin may result in a spontaneous resolution of the process.

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The role of systemic thrombolysis is not clear.Failure to improve or the development of peritoneal signs mandate an operation.

At surgery, you’ll find some free serosanguinous peritoneal fluid; the small bowel will be thick, edematous, dark-blue but not frankly “dead”, with the involved intestinal segment poorly demarcated. Arterial pulsations will be present and thrombosed veins seen. You’ll need to resect the affected bowel. As to whether to anastomose or not and considerations about the need for a “second look” – apply the same judgement as discussed above for arterial ischemia. Postoperative anti- coagulation is mandatory to prevent progression of the thrombotic process.Adding a venous thrombectomy is advocated by some, so is intra-operative thrombolysis;

the real benefits of these controversial approaches are unknown.

Conclusion

In most places the mortality rate of acute mesenteric ischemia is still prohib- itive. Why? Because surgeons fail to do the following:

 Suspect ischemia before intestinal gangrene develops

 Proceed with diagnostic/therapeutic angiography

 Improve intestinal perfusion during laparotomy

 Exteriorize the bowel or execute a second-look operation

If you wish to see survivors of this horrendous condition – be aggressive.

On the other hand, the presentation of these patients is so non-specific and the CT findings so subtle that if an aggressive approach is taken, many patients with self-limiting minor abdominal complaints will have unnecessary investigations and operations, and yet cases will still be missed. Furthermore these patients rarely have simple pathology. They commonly suffer from multisystem disease and even in receipt of optimal care they will have a high mortality. Regrettably, in the majority of patients this condition seems likely to remain an agonal complaint.

It is almost impossible to increase the current M & M associated with acute mesenteric ischemia.

“The man is as old as his arteries.” (Thomas Sydenham, 1662–1689)

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