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Diagnosis and treatment of abdominal angina

Tyson, Rev. Dr. Ronald Lee DMin, MSN, CN

doi: 10.1097/01.NPR.0000388938.08875.99
Feature: ABDOMINAL ANGINA: CE Connection
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Abdominal angina refers to abdominal pain in which perfusion to digestive tissues has been compromised, usually due to mesenteric atherosclerosis. Pathology can progress to necrosis of vital viscera, sepsis, or even death. Practitioners need to be aware of this serious medical condition, especially in the ever-growing elderly population.

Ronald Lee Tyson is an adult nurse practitioner at The Christ Hospital, Cincinnati, Ohio.

The author has disclosed that he has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.

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In the clinical setting, the term angina is almost always used to describe chest pain caused by cardiac ischemia. Yet, in the original Latin, angina literally means "to strangle or choke," and is a general idiom that can also be used to describe ischemic pain in other organs, not just the heart.

Abdominal angina (AA) refers to pain or discomfort in the gut when the blood supply to the tissues and organs of digestion has been compromised in some manner, usually due to atherosclerosis in the intestinal and mesenteric vasculature. Although the symptoms can vary from patient to patient depending on the extent of vascular compromise, in all cases the patient will consistently experience discomfort during digestion. Left untreated, underlying pathologies can progress, resulting in necrosis of vital abdominal viscera. Sequelae can range from diminished nutrient absorption to systemic sepsis and death.

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History and risk factors

In 1918, Dr. Baccelli was credited with coining the diagnostic term "abdominal angina" for the lower abdominal pain individuals were experiencing soon after eating, correctly recognizing the ischemic nature of the pain.1 Subsequent research conducted by Dunphy in 1936 linked this condition to potentially life-threatening necrosis of intestinal tissues. It was another 21 years before Mikkelson introduced the surgical treatment that could restore blood flow to the abdomen and intestine.1 Surgeons Shaw and Maynard performed the first transarterial thromboendarterectomy of the superior mesenteric artery (SMA) in 1958. This procedure was repeated in 1959 by Mikkelson and Zarro.1 Despite these early surgical successes and pioneering research efforts, in the 90-plus years since the discovery of AA, surprisingly few studies have been conducted on this serious condition.

Because AA can indicate a life-threatening situation, healthcare providers need to be aware of its implications and be able to recognize its risk factors and symptoms. Early detection increases the treatment options and the possibility of full recovery.

Current research on AA shows that gender seems to play a significant role in its development. Women are three times more likely to have the disorder than men.2 Age is also a factor. Although a recent pediatric journal describes a 5-year-old boy diagnosed with AA, the mean age of onset is over 60.3 This statistic is consistent with the vascular deterioration typically seen in the aging process. Additionally, smoking has been shown to play a key role in the development of AA. Of patients diagnosed with AA, a staggering 75% to 80% are smokers.4 Another predisposition is hypertension. Six of 10 patients who present with AA will have hypertension.5 Approximately 82% also have diabetes (type 1 or 2). Hyperlipidemia, often causing peripheral vascular disease (PVD), increases the risk of AA by 70% and is consistent with the atherosclerotic component of the disease process.6 Finally, age plays a role, with 80% to 85% of patients diagnosed being over the age of 60.4

When conducting a full medical history, it is helpful to determine whether the patient has experienced any prior atherosclerotic conditions or symptoms, as this may indicate an atherosclerotic etiology for AA. Previous pathologies such as coronary artery disease, PVD, or cerebrovascular disease signify that arterial hardening is an ongoing problem for the patient. Other risk factors include hypotension, heart failure, dysrhythmia, blood clotting disorders, hernias, prior abdominal surgery, obesity, use of oral contraceptives (increase in C-reactive protein), extensive bed rest, and certain types of cancer, especially those affecting the digestive tract.7

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AA defined

The World Health Organization (WHO) and the American Medical Association (AMA) both define the presence of AA to be abdominal pain occurring when "two or more of the major blood vessels to the mesentery have occluded or [show] stenosis."7 A diagnosis of AA is considered if postprandial pain or discomfort occurs at a fixed time (typically 15 to 30 minutes) after eating. Digestion increases circulatory demand by the intestines, and when the mesenteric arteries are unable to meet that demand, a state of ischemia develops, resulting in the sensation of pain or angina. If the blood flow continues to be interrupted, the consequence is possible necrosis of the digestive tissues, which can be fatal. AA is also known as intestinal angina, bowelgina, and intestinal ischemia.8 All nomenclature is interchangeable and generally reflects the obstructive problem of the organ system affected.

Because AA results from decreased digestive perfusion, the condition is often categorized by the location and severity of the occlusion. These distinctions establish the proper course of treatment for the patient. The four categories include:

  • colonic ischemia
  • acute mesenteric artery ischemia
  • chronic mesenteric artery ischemia
  • ischemia due to mesenteric venous thrombosis.

In each of these categories, surgery is a distinct possibility to clear an occlusion or to remove damaged or necrotic tissues.

Of the four categories, colonic ischemia is by far the most common.9 The majority of these patients will develop nongangrenous ischemia, which is transient and will resolve without treatment. A smaller, but still significant, percentage (15%) of those with colonic ischemia go on to develop gangrene of the colon, which frequently has life-threatening repercussions. Mesenteric artery ischemia can be both acute and chronic. In general, mesenteric artery ischemia refers to obstruction of one or more of the three major arteries supplying blood to the small and large intestines. In acute cases the condition is considered a surgical emergency, and these individuals should be taken to the nearest hospital for immediate reperfusion. The blockage of the artery in such cases is usually greater than 90%, and is likely to have already resulted in necrotic intestinal tissues.9

The chronic form of mesentery artery ischemia is not as high a priority because the artery is typically less than 70% to 80% occluded, but is no less life-threatening.2 Surgery will likely be required for restoration of blood flow. Finally, ischemia due to mesenteric venous thrombosis refers to the detected presence of a clot in the mesentery. The mesenteric arterial system can carry up to 40% of the cardiac output at any given time, whereas the venous system typically transports 30%.2 The instrument that initiates arterial ischemia is a large incursion of fluid into the bowel wall that results in edema and poor outflow of blood, thus impeding the inflow of arterial blood, with resultant arterial ischemia. Unlike the other forms of AA, unless damage has already occurred to mesenteric tissues, surgery is not likely necessary.10

Figure. B

Figure. B

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Pathophysiology

The most common cause of AA is atherosclerotic disease of the mesenteric arteries (see Branches of the superior and inferior mesenteric arteries). The blockage usually involves the ostia or the final few proximal centimeters of the mesenteric vessels.11 Often, aortoiliac disease is also exhibited in the patient with AA, and can be a cause of lesions of the ostia.11

The three major arteries that supply blood to the digestive tract are the celiac, superior mesenteric, and inferior mesenteric.12 Unless the blockage of two or more of these arteries is significant, it is likely that collaterals will develop among the existing vasculature, ensuring tissues are properly perfused, even though perhaps in a compromised fashion. Abdominal pain, the hallmark of AA symptomotology, occurs when the digestive processes demand increased blood flow to the gut, usually 15 to 30 minutes postprandially, but the stenotic or occluded artery is unable to provide adequate flow. The pain is caused by ischemia of the involved tissues that fail to receive necessary perfusion to carry forth digestion. The patient with AA often experiences the discomfort at almost exactly the same time after eating.

It is possible to live with AA, depending on the degree of occlusion. If the blockage is less than 50%, surgery can likely be avoided.13 The problem exists when the condition goes unchecked. With early diagnosis, the patient and provider can begin a course of medication and diet that will lower the overall low-density lipoprotein (LDL) index, thus helping alleviate further plaque buildup within the arteries. If the patient fails to receive timely diagnosis and proper treatment, the occlusion may progress from partial to complete at which point tissue necrosis occurs. If the patient then fails to obtain immediate mesenteric reperfusion, subsequent tissue necrosis will make it impossible for the digestive tract to function, and may prove fatal. Additionally, systemic sepsis due to infarction of extensive mesenteric vasculature is a dangerous possibility.

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Evaluation of the patient with potential AA

Although symptoms can vary, and usually heighten as the pathology progresses, the initial complaint of the patient experiencing AA is postprandial pain, generally in the lower abdominal quadrants (see Symptoms of AA). The abdomen is usually scaphoid and soft even during episodes of pain.4 Diarrhea is sometimes experienced by those with AA. This can cause foods to not be digested properly and nutrients to poorly absorb into the body.

Nausea is also often experienced. Consequently, some individuals will vomit, which can sometimes become so severe that it causes issues such as malnutrition due to the inability to keep food down and absorb necessary nutrients. As the disease progresses, small amounts of food in the stomach cause the same amount of pain that large amounts do. Thus, the person begins to experience weight loss. Other symptoms may include aversion to eating, or even fear of eating due to the patient's association of food with pain.

Abdominal bruits are present in 60% to 80% of patients with AA.3 Also, patients will often show classic signs of PVD, as this is a frequent comorbidity of AA. These signs might include intermittent claudication, nonhealing wounds on toes, feet, or legs, and thickened toenails. Upon examination, the abdomen is soft with palpation, even if the patient is experiencing pain. Nevertheless, physical examination alone is generally inconclusive in properly diagnosing AA because the abdominal discomfort is symptomatic of many other conditions affecting the digestive system. Thus, it is important to note when the pain happens. Discomfort that occurs regularly after every meal is a strong indicator for AA. Once other differentials have been ruled out, other diagnostic examinations should be performed, including X-ray, endoscopy, ultrasound, colonoscopy, flexible sigmoidoscopy, angiography, computed tomography (CT) scans, magnetic resonance imaging (MRI) angiography, or, in extreme cases, exploratory surgery.14 The objective is to detect the presence of necrotic digestive tissue. The angiograms should clearly indicate whether major arteries have been occluded or whether there is a thrombotic presence. The key to making an accurate diagnosis is determining whether there is an obstruction, and, if so, to what extent. Further, when evaluating patients for AA, the provider must determine whether the patient is in any of the high-risk categories, such as over age 60, female, smoker, hypertensive or hypotensive, PVD, or a history of diabetes. Blood tests alone will not be helpful in making a definitive diagnosis—although checking LDL levels may indeed lend validity to such diagnostics because high LDLs are linked to atherosclerosis.3

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Differentials

Because the common complaints pertaining to AA mimic those of several unrelated gastrointestinal (GI) tract issues, it is necessary to examine the patient for such conditions, completely ruling them out first. Strikingly similar in presentation to AA are gastric ulcers, which may be ruled out by performing an esophagogastroduodenoscopy (EGD). Another important differential is abdominal aortic aneurysms (AAAs). Conducting a CT or MRI angiogram is a conclusive diagnostic tool in determining the existence of AAA. Cancer of the colon or other GI tract organs is also a likely cause of AA-like pain, and requires a diagnostic workup to detect suspected lesions. Angiogram would be the most efficient diagnostic test for AA.

There are other, less complex diagnoses that present with abdominal pain similar to that seen in AA. Acid reflux, dietary sensitivities, and food intolerance are all potential reasons. It is therefore imperative that the provider obtain a thorough diet recall and a history of any foods that may be linked to such pain. Some patients may simply need to alter their diet to alleviate discomfort. If there appears to be a trend between particular foods and postprandial discomfort, it is preferable to explore alterations in diet before undergoing X-ray, endoscopy, angiogram, or ultrasound.

Other conditions to consider are constipation, appendicitis, pancreatitis, hepatitis, abdominal abscess, gastroenteritis, irritable bowel syndrome (IBS), or any inflammation of the GI tract. A potential complex issue here may be that the patient has AA and IBS concurrently. Constipation can be ruled out simply by obtaining a history of the patient's bowel habits. Hepatitis can be checked initially with a liver function workup. Most likely, an abdominal abscess or appendicitis would be detected during a thorough physical examination and history.

From a GI perspective, endoscopic ultrasound (EUS) can be done to evaluate the flow of the celiac artery to determine whether a patient is truly occluded.

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Diagnosis

Once other differentials have been eliminated, the actual diagnosis of AA is rather forthright, according to WHO and the AMA.7 By these strict standards, the only conclusive evidence of AA is when an angiogram or some other form of vessel imagery has been obtained that confirms at least two of these vessels are in some way occluded. Once this information has been obtained, the provider can proceed to determine how severe the blockage is, how much damage has been done to digestive tissues, and what course of treatment is required to alleviate the problem and return the patient to good health.

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Therapy options

The course of treatment for AA varies depending on the cause, the affected area, and the extent of tissue damage. For purposes of clarity, the course of treatment can be explained based on the four categories of AA.

When treating colonic ischemia, antibiotics are often the first line of defense. This will control any infections that have occurred as a result of the condition. Next, treat underlying causes of AA, such as heart failure, dysrhythmia, hyperlipidemia, or hypertension with medication, diet, or exercise as applicable. Suggest that the patient eat smaller, more frequent meals to relieve digestive load (postprandial discomfort). Also, it will be necessary to treat the patient for any conditions or behaviors that constrict blood flow to digestive vasculature (that is, hyperlipidemia, smoking). Surgery may also be indicated, depending on the extent of the arterial occlusion and tissue damage. If necrosis has occurred, it may be necessary for some tissue to be extracted surgically to prevent further vascular damage. Moreover, if the occlusion is considerable, it may be necessary for the injured artery to be bypassed to restore perfusion.

Acute mesenteric artery ischemia is almost always remedied surgically, removing or bypassing any vessel obstruction, and/or extracting intestinal sections that have been damaged by poor perfusion. Pharmaceutical therapies such as vasodilators and anticoagulants are often employed to work in conjunction with surgery to ensure recovery.3 When treating chronic mesenteric artery ischemia surgery is again the preferred course. The treatments for acute and chronic mesenteric artery ischemia are identical, except the acute condition is considered a higher priority medically and, in most cases, a medical emergency. An endovascular mesenteric revascularization procedure is an option for the patient who is unable to tolerate an open surgical procedure.15 The surgeon may also choose to insert a stent to relieve the obstruction, rather than bypassing the injured vessel.

There is no definitive medical treatment for chronic mesenteric artery ischemia.4,15 Lifestyle changes, such as eating smaller, frequent meals, may help ease abdominal discomfort. Encouraging smoking cessation and prescribing a vasodilator may help decrease vasospasm.15 The patient may also be referred to a pain center to help with pain management issues.

In the case of ischemia due to mesenteric venous thrombosis, surgery is rarely indicated. The usual course of treatment involves placing the patient on anticoagulant therapy for 3 to 6 months to prevent new clot formation.16 The only reason surgery would be considered was if impairment had occurred to mesenteric tissues.

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Provider awareness

AA is an underrecognized cause of postprandial abdominal pain, weight loss, and other commonplace GI tract disturbances. Diagnosis is frequently overlooked and requires both a careful exclusion of more general causes and a high degree of clinical impression, based on the patient's age, the coexistence of various risk factors for atherosclerosis, and the presence of vasculopathy in other regions.

Since the initial diagnosis of AA nearly a century ago, a relatively minor number of studies have been done on this potentially life-threatening disease and the repercussions it has on the health of the population, especially the elderly. Although this condition may not be seen frequently in primary care, it is nonetheless critical that NPs consider AA as a potential diagnosis when evaluating patients who present with lower abdominal pain.

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Symptoms of AA

The diagnosis of AA should be considered in a patient over age 60 who presents with recurring lower abdominal pain and no other GI condition has been identified. The symptoms of AA include the following:

  • Postprandial pain in the lower abdominal quadrants, which recurs on a regular basis within 15 to 30 minutes after a meal (usually the initial symptom)
  • Diarrhea
  • Nausea
  • Vomiting (if severe, may result in malnutrition)
  • Weight loss
  • Aversion or fear of eating (due to association of food with pain)
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REFERENCES

1. Morris GC, DeBakey ME. Abdominal Angina? Diagnosis and surgical treatment. JAMA. 1961;176(2):89–92.
2. Cline DM, Stead L. Abdominal Emergencies. New York: McGraw-Hill; 2007. Professional.
3. Dupee RM. Acute intestinal ischemia in the elderly. Ann Long Term Care. 2008;16(3):34–36.
4. Aziz F, Comerota AJ. Abdominal angina. eMedicine. December 3, 2009 .
5. Bartone G, Severino BU, Armellino MF, Maglio MN, Castriconi M. Clinical symptoms of intestinal vascular disorders. Radiol Clin North Am. 2008;46(5):887–889.
6. Kitzing B. Abdominal angina in occlusive mesenteric vascular disease: a case report. Cases J. 2009;2(1):82.
7. Levy AD. Mesenteric ischemia. Radiol Clin North Am. 2007;45(3):593–599.
8. Furrer J, Gruntzig A, Kugelmeier J, Goebel N. Treatment of abdominal angina with percutaneous dilatation of an arteria mesenterica superior stenosis. Cardiovasc Interv Radiol. 1980;3(1):43–44. doi: 10.1007/BF02551961
9. Romano S, Bartone G, Romano L. Ischemia and infarction of the intestine related to obstruction. Radiol Clin North Am. 2008;46(5):925–942.
10. Palmer ED. Abdominal angina: symptoms, signs and significance. Consultant. 1961;1(36).
11. Belohlavek J, Beran S, Linhart A. Critical ostial celiac trunk stenosis presenting as abdominal angina during massive pulmonary embolism with cardiogenic shock. J Invasive Cardiol. 2009;21(3): 139–140.
12. Pasricha PJ, Willis WD, eds. Chronic Abdominal and Visceral Pain Theory and Practice. New York: Informa Healthcare; 2006.
13. Huber FH. Ischaemic Enterocolopathies: Abdominal Angina, Ischaemic Enteritis, Colitis, Intestinal Infarction. Imaging and Intervention in Abdominal Trauma. 2004. New York: Springer; 1982.
14. Skucas J. Advanced Imaging of the Abdomen. New York: Springer; 2006.
15. Biolato M, Miele L, Gasbarrini G, et al. Abdominal angina. Am J Med Sci. 2009;338(5):389–395.
16. Paterno F, Longo WE. The etiology and pathogenesis of vascular disorders of the intestine. Radiol Clin North Am. 2008;46(5):877–885.
Keywords:

intestinal ischemia; mesenteric atherosclerosis; mesenteric ischemia

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