Abdominal aortic aneurysm: A ticking time bomb Capt. Christopher M. Howell, USAF, DSc, MPAS, PA-C, MBA, FAAPA, MACEMPA; Capt. Michael J. Rabener, USAF, DSc, MMS, PA-C, BS, FAAPA, EMPA

ABSTRACT Abdominal aortic aneurysm (AAA) is a clinical challenge in risk assessment, recognition, treatment, and prevention. This article explores the pathogenesis, presentation, diagnosis, treatment, and prevention of AAA. Keywords: abdominal aortic aneurysm, AAA, rupture, dilation, pulsatile mass, beta-blockers

Learning objectives


Describe the etiologic factors and key clinical risk factors associated with AAA. Differentiate the classical clinical presentation of patients with AAA from more commonly encountered presentations. Discuss the role of ultrasound in routine screening and diagnosis of patients with AAA. List evidence-based interventions for prevention of AAA and risk reduction. Differentiate clinical factors that support nonsurgical versus surgical management of a patient with AAA.


bdominal aortic aneurysm (AAA) is the 13th leading cause of death in the United States, so prompt recognition and management of symptomatic patients is key, as is prevention in at-risk patients.1 Asymptomatic patients are far more commonly encountered than symptomatic patients in clinical practice.2 All clinicians must recognize the presenting signs and symptoms consistent with AAA and an imminent or active rupture as well as factors that contribute to AAA. Clinical indications are nonspecific and the physical examination has little sensitivity, with little prognostic indication of a positive outcome.2 Because symptom development is a late clinical finding, prevention focuses on targeting risk factors and reducing modifiable ones. This article provides a brief overview of AAAs for general practitioners. Most patients are asymptomatic until the Christopher M. Howell practices in the ED at Wright-Patterson Air Force Base in Dayton, Ohio. Michael J. Rabener practices in the ED at Keesler Air Force Base in Biloxi, Miss. The authors have disclosed no potential conflicts of interest, financial or otherwise. DOI: 10.1097/01.JAA.0000480855.07045.50 Copyright © 2016 American Academy of Physician Assistants


AAA expands or ruptures. By recognizing risk factors, including contributing family, medical, and social history, clinicians can intervene appropriately and reduce patient morbidity and mortality. PATHOGENESIS AND RISK FACTORS For details on normal aortic anatomy, see Figure 1. An AAA, like any aneurysm, occurs when the media’s extracellular matrix of elastin and collagen is eroded by proteolytic degradation properties and the artery irreversibly dilates.2 Ninety percent of all AAAs occur at a focal area in the infrarenal aspect within the abdomen.1,2 A normal aortic diameter, infrarenally, is 1.7 cm in men and 1.5 cm in women. A diameter greater than 3 cm is clinically significant for an aneurysm.1 Yet, the aneurysmal size neither dictates the clinical manifestations of disease nor absolute medicinal or surgical intervention. Other contributing factors to AAA are biomechanical wall stress and inflammation, which can be caused by Volume 29 • Number 3 • March 2016

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Abdominal aortic aneurysm: A ticking time bomb

Key points

hypertension and hyperlipidemia.3 Targeting factors that contribute to the endothelial damage and oxidative stress of the arterial wall remain the cornerstone of preventive management. Risk factors for AAA include advanced age, tobacco use, hypertension, hyperlipidemia, atherosclerosis, history of coronary artery disease, greater physical height of the patient, and having a first-degree relative with a history of AAA. Advanced age and smoking, at any time in the patient’s past, pose the greatest risks. Patients who use tobacco are at seven times the risk of AAA compared with nonsmokers; the longer the smoking history, the greater the risk.4 AAAs occur almost exclusively in older adults, with the mean age between 65 and 75 years.1 However, consider AAA in any patient, regardless of age or sex, who has appropriate risk factors, signs and symptoms, and presentation.1 AAA is more common in men but women with AAAs are four times more likely than men to develop a rupture.4 Although collagen vascular diseases such as Marfan and Ehlers-Danlos syndromes have been linked to aneurysmal development, AAAs have been reported in fewer than 5% of established cases.1,2 HISTORY AND PHYSICAL EXAMINATION Patient presentations can be variable and nonspecific, and too often misleading, mimicking other conditions such as appendicitis, cholelithiasis, diverticular disease, and bowel obstruction.1 AAAs may produce symptoms of flank pain and hematuria, which appear consistent with renal colic but can occur when the renal artery dissects in response to an expanding aneurysm.1,2 Some patients have an abrupt onset of fatigue or even syncope before presentation, as well as severe abdominal, back, flank, or groin pain; patients also may have signs and symptoms of shock.1 Symptoms suggesting AAA are nebulous at best and mimic other conditions, including appendicitis, cholelithiasis, diverticular disease, gastritis and peptic ulcer disease, nephrolithiasis, ischemic bowel, pyelonephritis, perforated ulcer, large and small bowel obstruction, myocardial infarction, and urinary tract infection.1


AAA is the 13th leading cause of death in the United States, so prompt recognition and management of symptomatic patients is key, as is prevention in at-risk patients. Asymptomatic patients are far more commonly encountered than symptomatic patients in clinical practice. Symptoms suggesting AAA are nebulous at best and mimic other conditions, including appendicitis, cholelithiasis, and diverticular disease. Smoking cessation and control of hypertension are key interventions to reduce patient risk for AAA.

FIGURE 1. Aortic anatomy1,4

The abdominal aorta begins at the level of the diaphragm, running just anterior to the spine in the retroperitoneal space before bifurcating into the left and right iliac arteries at the level of the umbilicus. Like other arteries, the aorta comprises three layers: the tunica intima, media, and adventitia. The strength, structure, and elasticity of this vessel are defined predominantly by the media, or middle layer, which consists of elastin, collagen, and proteoglycans surrounding one layer of smooth muscle.

The classic presentation of AAA includes the finding of a palpable pulsatile abdominal mass in the epigastric and left hypochondriac regions of the abdomen; however, this is only discovered in fewer than half of critical patients presenting to the ED, making it unreliable as an exclusive diagnostic tool.1,4 In fact, presence of a palpable pulsatile abdominal mass largely depends on the size of the aneurysm and the patient’s body habitus. On average, only 40% of AAAs in patients who are not obese are discovered when relying on this physical examination finding. Although as many as 76% of AAAs are discovered when larger than 5 cm, only 29% are discovered at 3 cm.4,5 In patients with an established diagnosis of AAA, up to 25% of AAAs were not palpable even by the vascular surgeon who was preparing the patient for surgery. A palpable pulsatile mass typically is a late finding, with the palpability most common when a rupture had already occurred and prognosis is poor; mortality for patients with a ruptured AAA approaches 90%.1,2 Clinicians need not be concerned about the technique used to palpate the abdomen because no clinical evidence supports provider manipulation causing aneurysm rupture.1 A patient with a ruptured AAA may be in shock and have hypotension, tachycardia, altered mental status,

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mottling and/or in some cases cyanosis—symptoms that neither support nor refute AAA as a diagnosis.1 Patients may have no symptoms and those with symptoms may have a normal physical examination. DIAGNOSTICS For symptomatic patients, the most useful noninvasive diagnostic tool is bedside ultrasonography. In the hands of a skilled clinician, ultrasound has a sensitivity of about 100% and specificity of about 96% for AAA, making it one of the most valuable and practical tools for confirming or ruling out AAA; a diagnosis can be confirmed in less than 60 seconds.1,6 Limitations to ultrasound include patient obesity, significant bowel gas, being unable to visualize significant portions of the aorta, and operator skill.1 The US Preventive Services Task Force (USPSTF) recommends a one-time ultrasound when clinically appropriate (that is, in men over age 65 years with a history of smoking), and reports a detection sensitivity of 95% and a specificity of 100%.5,7 Ultrasound is the only recommended diagnostic screening tool for asymptomatic patients (Figures 2 and 3). Symptomatic patients may be evaluated via abdominal CT, MRI, and angiography, depending on patient presentation, hemodynamic stability, availability of the test, and clinician preference. The abdominal CT is 100% sensitive and is more reliable than ultrasound at determining size and extent of involvement, and visualizing adjacent structures, and is not impaired by bowel gas or obesity. However, CT is more expensive, takes longer (delaying treatment), and is invasive if contrast is used—an issue for older adults with comorbidities, particularly chronic kidney disease.1 Obtaining a CT also requires patients to be out of the presence of the management team, posing risk if the patient’s clinical condition deteriorates.1 MRI is an option in stable patients unable to tolerate CT contrast media.1 Angiography provides the best visualization of aortic anatomy, but is invasive, time-consuming, and poses the risks of embolization, perforation, and bleeding. For these reasons, angiography is not a recommended first-line diagnostic tool for asymptomatic or symptomatic patients.1 TREATMENT The nonsurgical approach is only appropriate in asymptomatic patients with aneurysms less than 5.5 cm in diameter, or patients whose aneurysms dilate less than 0.8 cm per year as documented by serial imaging.2 The United Kingdom Small Aneurysm Trial (UKSAT) and the Aneurysm Detection and Management (ADAM) trial randomly assigned 1,090 and 1,136 patients, respectively, with AAAs 4 cm to 5.4 cm in diameter to immediate elective open repair or periodic imaging surveillance leading to repair when an AAA enlarged beyond 5.5 cm or became symptomatic.8-10 The primary outcome, all-cause mortality, was the same in both intervention groups in both trials, as 34

FIGURE 2. Transverse view of an AAA in an asymptomatic

patient over age 65 years with a history of smoking.

FIGURE 3. Transverse view of a small AAA.The size is the char-

acteristic finding; otherwise the gross appearance is the same as non-aneurysmal vessels. Volume 29 • Number 3 • March 2016

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Abdominal aortic aneurysm: A ticking time bomb

was quality of life, suggesting that elective repair of AAA smaller than 5.5 cm did not change health outcomes. Because of these influential trials, elective repair is usually reserved for AAAs larger than 5.5 cm.5 In patients who are candidates for nonsurgical management, targeting risk factors is paramount to effective risk reduction. Pharmacologic therapy is used for nonsurgical management, as a way to slow the progression of an established aneurysm. This therapy is described in the section on prevention. If conservative management fails or the patient develops concerning symptoms, treatment focuses on the patient’s presenting signs and symptoms. Initial stabilization typically consists of: • administering supplemental oxygen • establishing continuous cardiac monitoring • obtaining large-bore IV access at two sites to administer fluid and analgesia (and medications if the patient’s condition deteriorates). Morphine often is used because it reduces ventricular contraction as well as the rate and rise of arterial pressure that may proceed rupture. • cautiously reducing BP to 100 to 120 mm Hg systolic, or the lowest reasonable pressure that maintains vital organ perfusion. Once the patient is stabilized, symptomatic patients, regardless of aneurysm size, and patients with aneurysms greater than 5.5 cm should undergo open surgical or endovascular repair. PREVENTION AND RISK REDUCTION Identifying and treating modifiable risk factors before they develop is key to preventing future AAAs. Smoking cessation The initial, and by far the most significant, lifestyle change for patients at risk for AAA is to stop smoking.11 The American Lung Association (ALA) estimated in 2009 that nearly 47 million adults in the United States smoke.12 At every visit, encourage patients to consider smoking cessation as a significant investment in their overall health. Although many clinicians consider discussing smoking cessation both futile and time-consuming, 40% of smokers have tried to quit in the past and 70% persist in their desire to quit.13 Talking to a patient about smoking cessation can be done in as little as 3 to 5 minutes and can have an overwhelming effect on patient’s health and risk reduction.13 The ALA endorses combining pharmacotherapy and counseling for optimal success because smokers may make many attempts to quit before being successful.13 Hypertension Initial aneurysm development correlates directly with a history of hypertension. Antihypertensive drugs can reduce the progression of aneurysm diameter and the risk of rupture.14 Hypertension should be managed using the Joint National Committee 8 (JNC 8) guidelines.15 Although beta-blockers, particularly propranolol, have been used the most, no evidence suggests that propranolol is superior as an antihypertensive agent over calcium channel blockers, diuretics, or angiotensin-converting enzyme

(ACE) inhibitors.3 Some literature supports the use of ACE inhibitors and/or angiotensin receptor blockers (ARBs), especially when coupled with a statin; however, more studies supporting mortality reduction are needed before this can be recommended.3 No one agent is preferred for every patient; therapy depends on the patient’s laboratory results, ethnicity, comorbid conditions, and other drugs. We favor labetalol for stable patients, but have found esmolol better for emergent patients whose BP and heart rate may be labile. Esmolol’s fast onset of action and short half-life make it easy to titrate in critically ill patients. Where appropriate, patients also should continue lifestyle modifications to reduce BP, such as exercise and a lowsodium diet. Encourage patients to take control of their health and reduce their risk for disease. Hyperlipidemia and atherosclerosis These conditions play less of a direct role in the formation of AAAs but are widely accepted as contributors to arterial wall oxidative stress. A diet high in soluble fiber and 20 to 30 minutes of exercise 3 to 5 days per week are essential contributions to cholesterol management. However, when these measures fail to control cholesterol levels, patients should be started on statins, which target low-density lipoprotein (LDL) cholesterol. A direct correlation between LDL cholesterol reduction and cardiovascular event reduction is widely accepted, and reducing LDL cholesterol may also reduce the growth rate of existing AAAs and mortality from AAAs.16 A 5-year double-blind study of simvastatin versus placebo revealed a 22% risk reduction in first major vascular events among patients on simvastatin, but any statin for cholesterol management would be appropriate.16 CONCLUSION Patients must be encouraged to know their personal and family health risk factors and to visit their primary care provider for regular examinations, including BP and cholesterol screenings. Patients at risk for AAAs should be encouraged to make lifestyle changes to deal with modifiable risk factors, particularly smoking. Through lifestyle changes and medications, patients at risk for AAAs can significantly reduce their risk. JAAPA Earn Category I CME Credit by reading both CME articles in this issue, reviewing the post-test, then taking the online test at Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of March 2016.

REFERENCES 1. Rahimi SA. Abdominal aortic aneurysm. http://emedicine. Accessed November 5, 2015. 2. Upchurch GR Jr, Schaub TA. Abdominal aortic aneurysm. Am Fam Physician. 2006;73(7):1198-1204. 3. Guessous I, Periard D, Lorenzetti D, et al. The efficacy of pharmacotherapy for decreasing the expansion rate of

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CME abdominal aortic aneurysms: a systematic review and metaanalysis. PLoS One. 2008;3(3):e1895. pmc/articles/PMC2267254. Accessed December 2, 2015. 4. Chaikof EL, Brewster DC, Dalman RL, et al. The care of patients with an abdominal aortic aneurysm: the Society for Vascular Surgery practice guidelines. J Vasc Surg. 2009;50(4 suppl):2S-49S. 5. Lederle FA. In the clinic. Abdominal aortic aneurysm. Ann Intern Med. 2009;150(9):ITC5-1-ITC5-14. 6. Pregerson B. Imaging options for patients with acute abdominal pain. Clinical Advisor. 2010:21-26. 7. US Preventive Services Task Force. Abdominal aortic aneurysm: screening. UpdateSummaryFinal/abdominal-aortic-aneurysm-screening?ds= 1&s=abdominal_aortic_aneurysm. Accessed December 2, 2015. 8. The UK Small Aneurysm Trial Participants. Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet. 1998;352:1649-1655. 9. Powell JT, Brown LC, Forbes JF, et al. Final 12-year follow-up of surgery versus surveillance in the UK Small Aneurysm Trial. Br J Surg. 2007;94(6):702-708.


10. Aneurysm Detection and Management Veterans Affairs Cooperative Study Group. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med. 2002;346(19):1437-1444. 11. Golledge J, Norman PE. Pathophysiology of abdominal aortic aneurysm relevant to improvements in patients’ management. Curr Opin Cardiol. 2009;24(6):532-538. 12. American Lung Association. Trends in tobacco use. www.lung. org/assets/documents/research/tobacco-trend-report.pdf. Accessed December 2, 2015. 13. Covino J. Tobacco dependence: how should a busy physician assistant intervene? JAAPA. 2010;23(2):22-25. 14. Kleinschmidt D, Plestis K, Housits P. Indications and surgical strategy for thoracic aortic aneurysm repair. JAAPA. 2010;23 (2):44-48. 15. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311(5): 507-520. 16. Stalenhoef AF. The benefit of statins in non-cardiac vascular surgery patients. J Vasc Surg. 2009;49(1):260-265.

Volume 29 • Number 3 • March 2016

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Abdominal aortic aneurysm: A ticking time bomb.

Abdominal aortic aneurysm (AAA) is a clinical challenge in risk assessment, recognition, treatment, and prevention. This article explores the pathogen...
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