Mesenteric ischemia

This is the diagnosis that keeps general surgeons up at night, and it deserves a careful explanation because it is both uncommon and frequently missed.

Three arteries supply the entire gastrointestinal tract: the celiac artery to the stomach, liver and spleen; the superior mesenteric artery to the small intestine and the right side of the colon; and the inferior mesenteric artery to the left colon and rectum. At rest, the gut receives roughly a quarter of everything the heart pumps, and after a meal that rises substantially.

These three vessels are connected to each other by collateral pathways, which is genuinely fortunate. It means one of them can gradually narrow or close over years and the other two can compensate. It also means that when disease is chronic and gradual, symptoms appear late; and when the loss of blood flow is sudden, the collaterals have no time to develop and the consequences are immediate.

Mesenteric ischemia means the bowel is not receiving enough blood. Left uncorrected, the bowel dies.

The four ways this happens

Embolism to the superior mesenteric artery. The most common form. A clot forms somewhere else — most often in the heart, in the setting of atrial fibrillation, a recent heart attack, or valvular disease — breaks off, travels, and lodges in the SMA. The onset is abrupt, and patients can often tell you the exact minute it started.

Thrombosis of the superior mesenteric artery. Here the vessel was already narrowed by atherosclerosis over years, and it finally closes off. These patients frequently have a history of the chronic symptoms described below, and because the blockage tends to sit at the very origin of the vessel, the length of bowel affected is often greater than with an embolus.

Non-occlusive mesenteric ischemia. The vessels are open, but flow through them is inadequate. This occurs in patients who are profoundly ill for other reasons — cardiogenic shock, sepsis, high-dose vasopressor requirements, dialysis. In shock, the body preferentially shunts blood to the brain and heart and constricts the splanchnic circulation, and the gut is the organ that pays for that decision. This form has the worst outcomes, largely because the patients are already critically ill and the diagnosis is easily attributed to their other problems.

Mesenteric venous thrombosis. Here the problem is drainage rather than supply. Blood cannot leave the bowel, so the bowel becomes congested and edematous and eventually cannot receive fresh blood either. These patients are typically younger, often have an inherited or acquired clotting disorder, portal hypertension, or a recent abdominal inflammatory process. The course is more gradual, over days rather than hours, and a substantial number are treated with anticoagulation alone without ever needing an operation.

The one thing to remember

Pain out of proportion to the physical examination.

Early in acute mesenteric ischemia the patient is in severe, unremitting pain and cannot get comfortable, while the abdomen on examination is soft and often barely tender. That mismatch is the entire diagnosis, and it is unlike almost everything else in general surgery, where the exam tracks the severity.

The reason is anatomical. The pain of ischemic bowel is initially visceral, carried by autonomic fibers, and is diffuse and poorly localized. The peritoneum lining the abdominal wall, which is what produces tenderness and guarding on examination, is not yet involved. It becomes involved once the bowel wall dies through its full thickness and inflammation reaches the peritoneal surface. So by the time the abdomen is rigid and exquisitely tender — by the time it finally looks the way the patient has been feeling — the bowel is dead.

This is why the disease is missed. A patient in severe pain with a benign abdomen and normal initial bloodwork is easy to reassure, and reassurance is the wrong answer.

What about lab tests?

An elevated lactate is often cited, and it is real, but it is a late finding. A normal lactate early in the course does not exclude the diagnosis and should never be used to do so. The same goes for the white blood cell count.

The test is CT angiography of the abdomen, and the practical point is that this must be requested specifically. A routine abdominal CT without arterial-phase imaging can look unremarkable in the early hours of this disease. If mesenteric ischemia is on the list of possibilities, someone has to say so out loud and order the right study.

Chronic mesenteric ischemia

This is the slow version, and it has a distinctive story. Blood flow is adequate at rest but insufficient after a meal, when demand rises. Patients describe cramping pain beginning fifteen to thirty minutes after eating and lasting an hour or two. They start eating smaller meals, then start avoiding food altogether because eating hurts, and lose a great deal of weight.

That combination — postprandial pain, food avoidance, and weight loss in a patient with atherosclerosis elsewhere — is frequently worked up for months as a possible malignancy before anyone images the mesenteric vessels. It is treated with stenting or bypass, and patients often describe the relief afterward in fairly dramatic terms.

Almost all of these patients are or were heavy smokers.

Treatment of the acute form

Two problems must be solved: restore blood flow, and deal with bowel that has already died.

Restoring flow may mean removing the clot directly through an incision in the artery, stenting or aspirating it through a catheter, or bypassing the blockage. Which approach depends on the cause, the anatomy, and how sick the patient is.

Bowel that is frankly dead is resected. Bowel that looks marginal presents a genuine dilemma, because the surgeon is being asked to judge viability at a single moment in time, in tissue that has just had its blood supply restored and has not yet declared itself. Resecting too much creates a patient dependent on intravenous nutrition for life. Resecting too little leaves dead bowel behind, which is fatal.

The standard answer to that dilemma is the second-look operation: the surgeon deliberately plans to return to the operating room in twenty-four to forty-eight hours to reassess, often leaving the abdomen temporarily open in the interval. This is not a sign that something went wrong the first time. It is a planned strategy that exists precisely because viability is impossible to judge reliably in the moment, and it is one of the more honest things surgery does.

Outcomes

I will not soften this. Acute mesenteric ischemia carries a high mortality — historically over half, and in the non-occlusive form higher still. The single largest determinant of outcome is how much time passed between the onset of pain and the restoration of blood flow.

The patients who do well are the ones in whom someone considered the diagnosis early, in a patient who did not look that sick, and ordered the right scan anyway.

If a very large length of small intestine has to be removed, the result is short bowel syndrome, in which there is not enough intestine remaining to absorb adequate nutrition, and patients require intravenous nutrition either temporarily or permanently. The bowel does adapt over months to years, and some patients regain significant function, but this is a major and lasting change.