47 INTESTINAL ISCHEMIA
Thomas F. Rehring M.D.

1. What is the arterial supply to the gut?

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The foregut (stomach and duodenum) receives its blood supply from the celiac artery, the midgut (jejunum to the proximal descending colon) from the superior mesenteric artery (SMA), and the hindgut (the remainder of the intraperitoneal gut) from the inferior mesenteric artery (IMA).

2. Name the potential collateral pathways between the celiac axis and SMA. SMA and IMA? Iliac and IMA?

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The pancreaticoduodenal arteries form the major collaterals between the celiac artery and the SMA. The gastroduodenal artery gives off the superior pancreaticoduodenal artery that encircles the head of the pancreas and anastomoses with the inferior pancreaticoduodental artery, the first branch of the SMA.
The SMA and IMA have two main connections. The marginal artery of Drummond lies within the mesentery of the colon and is made up of branches of the ileocolic, right, middle, and left colic arteries. The arc of Riolan (meandering mesenteric artery) is more central and connects the middle colic branch of the SMA and the left colic branch of the IMA.
The internal iliac artery gives rise to the middle rectal artery, which can provide flow to the superior rectal and thus the IMA.

3. For extra credit, for whom is the marginal artery of Drummond named? What about the arc of Riolan?

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Hamilton Drummond, a British surgeon, proved the anastomotic connection that bears his name by ligating the origins of the right, middle, and left colic arteries and demonstrating flow to the sigmoidal arteries in 1913 and 1914.
Jean Riolan (1577-1657) was a well-known French anatomist who (ironically) opposed Harvey’s theory of circulation but is acknowledged to be the first person to point out the communication between the SMA and IMA.

4. Name the common causes of acute intestinal ischemia.

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Acute SMA embolism (50% of all cases), acute SMA thrombosis, nonocclusive mesenteric ischemia (NOMI), mesenteric venous thrombosis, vasculitis, and iatrogenic causes (e.g., inotropic agents, aortic surgery).

5. What is the mortality rate of patients with acute mesenteric ischemia?

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Although the prognosis of embolic occlusion is somewhat better because of the dramatic presentation, the diagnosis of acute mesenteric ischemia is often made after infarction. The result is a high mortality rate (75%), regardless of cause. Despite advances in diagnosis, intervention, and critical care, this figure has gone unchanged for more than 30 years.

6. What is a “paradoxical embolus”?

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A paradoxical embolus occurs in the setting of a venous thrombus embolizing to the arterial circulation via a cardiac defect (typically an atrial septal defect allowing right-to-left shunting).

7. What is the diagnostic triad of acute embolic intestinal ischemia?

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Sudden onset of (1) severe abdominal pain, (2) bowel evacuation (vomiting or diarrhea), and (3) a history of cardiac disease (arterial emboli). An additional hallmark is pain out of proportion to physical findings.

8. How does the presentation of patients with acute thrombotic occlusion differ?

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Thrombotic occlusion typically presents in elderly patients with diffuse atherosclerotic occlusive disease or in patients with a history consistent with chronic mesenteric ischemia (see question 25). Particularly in the former group of patients, acute embolic occlusion may be indistinguishable from thrombotic occlusion.

9. Which laboratory value is diagnostic of acute intestinal ischemia? Is acidosis?

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No laboratory values are diagnostic for acute intestinal ischemia. Metabolic acidosis is a late finding and implies advanced ischemia or infarction. Similarly, elevated lactate and elevated phosphate levels are nonspecific and frequently late findings. Although leukocytosis is found in the majority of patients, no laboratory studies are specific. The diagnosis is pursued on clinical suspicion alone.
kEY POINTS: DIAGNOSTIC TRIAD OF ACUTE EMBOLIC INTESTINAL ISCHEMIA

1. Sudden onset of severe abdominal pain out of proportion to physical exam.
2. Sudden bowel evacuation (vomiting or diarrhea).
3. History of cardiac disease (e.g., atrial fibrillation that accounts for embolic source).
4. No laboratory findings (e.g., lactate level) are diagnostic; metabolic acidosis is a late finding.
5. Emergent arteriography is indicated.

10. When acute intestinal ischemia is suspected, what study is diagnostic?

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Emergent arteriography is diagnostic. It is important to include lateral views of the aorta to visualize the visceral vessels.

11. How do the operative findings differ in patients with atherosclerotic occlusion and patients with SMA embolism?

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An SMA embolus usually lodges 3-4 cm distal to its origin, and thus beyond the proximal jejunal and middle colic arteries. Therefore, the proximal 6-10 inches of jejunum are usually spared. Thrombotic occlusion occurs directly at the ostia, where the atherosclerotic narrowing is most severe, causing ischemia of the entire midgut.

12. What is the appropriate management of an SMA embolus? Is there a role for thrombolysis?

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Immediate heparinization, urgent exploration, embolectomy, assessment of bowel viability, and resection of any infarcted bowel. Postoperative anticoagulation is essential to avoid further embolization.
Thrombolysis currently has little or no role in the treatment of acute mesenteric ischemia. Revascularization of bowel must be pursued rapidly, and bowel viability must be ascertained directly.

13. How is visceral ischemia of thrombotic origin managed?

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The general management follows that of an embolism; however, mesenteric ischemia from thrombotic occlusion is the end stage of progressive atherosclerotic occlusion. Therefore, thrombectomy alone is not sufficient; bypass or endarterectomy of the proximal diseased vessel or vessels is necessary. Again, bowel viability is assessed after reperfusion.

14. Which intraoperative tests help surgeons determine bowel viability?

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Both systemic intravenous infusion of fluorescein, which is evaluated using a Wood’s lamp, and intraoperative Doppler examination of the bowel are helpful, but ultimately the decision is based on clinical judgment.

15. When the extent of bowel viability is in question, what should be done?

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All nonviable and necrotic bowel should be resected. The surgeon should schedule a second-look operation 12-24 hours later to evaluate the bowel of marginal viability. Some segments that were initially questionable may become clearly viable or necrotic during this period.

16. How much small intestine is required to maintain adequate nutrition?

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About 100 cm of small intestine is required to maintain adequate nutrition. The distal ileum and ileocecal valve are the most important segments to retain for vital bowel absorption and function.

17. Should a second-look operation be canceled because a patient improves?

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Never. The decision is made in the operating room based on findings at the time of surgery. No clinical parameters within the ensuing 12-24 hours accurately indicate the status of the bowel in question.

18. What is NOMI?

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NOMI accounts for approximately 25% of acute ischemic cases; arterial spasm is the most common cause. This typically occurs in critically ill patients with systemic hypoperfusion. In such low-flow states, splanchnic blood flow is reduced in attempts to preserve perfusion to cardiac and cerebral beds. Pharmacologic agents such as ergot alkaloids, digitalis, and vasoconstrictors are the “usual suspects.” Cocaine-induced mesenteric ischemia has also been reported.

19. How is NOMI diagnosed and managed?

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Angiography documents vasospasm in the absence of an anatomic occlusion. The right colon is most commonly affected because of its less consistent collateral blood flow. It is associated with (and may be exacerbated by) the concomitant use of digitalis in patients with systemic hypoperfusion. In severe cases associated with multisystem organ failure, the mortality rate approaches 75%. Treatment consists of hemodynamic optimization, weaning of inotropes, and selective arterial infusion of vasodilators (papaverine) through the angiogram catheter. Surgical intervention is reserved for intestinal infarction or perforation.

20. If mesenteric vein thrombosis (MVT) is suspected, which test is best?

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The signs and symptoms of MVT are similar to those of acute intestinal ischemia, but they are often subtler. Delay in diagnosis is thought to contribute to the reported high mortality rate of 50%. Contrast-enhanced computed tomography (CT) scan remains the gold standard for diagnosis.

21. What are the risk factors for MVT? How is it treated?

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Approximately half of patients with MVT have an underlying hypercoagulable state. Other causes include splenectomy, portal hypertension, visceral infections, pancreatitis, malignancy, and blunt abdominal trauma.
Treatment of MVT includes anticoagulation, broad-spectrum antibiotics, treatment of the underlying cause, and supportive measures. Surgery is reserved for resection of nonviable bowel. Venous thrombectomy has not proven to be of effective long-term benefit. The use of thrombolytic agents has been explored but only in anecdotal reports. Furthermore, access to the splanchnic venous circulation for directed lysis is difficult.

22. What is the primary cause of chronic mesenteric ischemia?

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Atherosclerosis. In general, symptoms do not occur unless two of the three major arteries are narrowed or occluded. Bowel infarction may be forestalled by development of collaterals.

23. What is the one unique risk factor for chronic mesenteric ischemia that differs from other atherosclerotic phenomena?

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It occurs more frequently in women.

24. What are the clinical features of patients with chronic mesenteric ischemia?

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Weight loss is the most consistent sign of chronic mesenteric ischemia. Patients gradually and sometimes unknowingly become afraid to eat (food fear) because of postprandial pain (intestinal angina). In the absence of weight loss, the diagnosis of chronic intestinal ischemia is unlikely. Conversely, in patients with severe atherosclerosis and weight loss of unknown cause, mesenteric ischemia should be strongly considered. An epigastric bruit is an important sign suggestive of mesenteric occlusive disease.

25. How should patients with chronic mesenteric ischemia be evaluated?

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Noninvasive ultrasound duplex scanning may provide important physiologic information about the celiac axis and SMA. However, this procedure is technician dependent and not widely available. If unavailable or equivocal, mesenteric angiography should be performed. If surgical intervention is considered, arteriography is essential.

26. What are the goals of arterial bypass in chronic mesenteric ischemia?

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Resolution of symptoms, improved nutrition, and prevention of visceral infarction.

27. If mesenteric revascularization is entertained, what five essential decisions must be considered?

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* Surgical approach (transabdominal, retroperitoneal, thoracoabdominal)
* Which and how many vessels to revascularize
* Endarterectomy or bypass
* If bypass, antegrade or retrograde
* If bypass, what type of conduit (vein versus prosthetic)

See also question 32.

28. What is ischemic colitis?

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Ischemic colitis is circulatory insufficiency of the colon that may result from occlusive, nonocclusive, and pharmacologic (e.g., cocaine, nonsteroidal anti-inflammatory drugs) causes. Seven percent of all patients having nonemergent abdominal aortic aneurysm surgery and as many as 60% of patients who survive a ruptured abdominal aortic aneurysm suffer from ischemic colitis. Most cases are mild, typically involving only the mucosa and resulting in abdominal pain and bloody diarrhea. Severe disease (15% of cases) is characterized by transmural gangrenous infarction that presents with clear signs of peritonitis and bloody diarrhea.

29. How is ischemic colitis diagnosed and treated? What are its prognostic implications?

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The diagnosis is made by endoscopy. In idiopathic cases, angiography demonstrates patent large vessels because the responsible emboli or lesions are believed to involve peripheral, end-arterial vessels. Mild disease is typically treated conservatively with bowel rest, vigorous hydration, and broad-spectrum antibiotics. Severe disease requires surgical resection. Overall mortality rates are about 50%, but in patients requiring colon resection, the mortality rate may exceed 85%. The high mortality in the latter group is attributed to endotoxemic shock and multisystem organ failure.