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Abdominal Aortic Aneurysm Clinical Presentation

  • Author: Saum A Rahimi, MD, FACS; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Sep 28, 2015
 

History

As noted (see Overview, Etiology), patients at greatest risk for abdominal aortic aneurysms (AAAs) are those who are older than 65 years and have peripheral atherosclerotic vascular disease. Accordingly, a history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension is often elicited. Less frequent causes include Marfan and Ehlers-Danlos syndromes, collagen vascular diseases, and mycotic aneurysm. Patients who have a first-degree relative with AAA are at increased risk.

AAAs are usually asymptomatic until they expand or rupture. Patients may experience unimpressive back, flank, abdominal, or groin pain for some time before rupture. Isolated groin pain is a particularly insidious presentation. This occurs with retroperitoneal expansion and pressure on either the right or left femoral nerve. This symptom may be present without any other associated findings, and a high index of suspicion is necessary to make the diagnosis.

At times, AAAs may cause symptoms from local compression, including early satiety, nausea, vomiting, urinary symptoms, or venous thrombosis from venous compression. Back pain can be caused by erosion of the AAA into adjacent vertebrae. Other symptoms include abdominal pain, groin pain, embolic phenomena affecting the toes (eg, livedo reticularis, or blue toe syndrome; see the image below), and fever. Occasionally, small AAAs thrombose, producing acute claudication.

Atheroemboli from small abdominal aortic aneurysms Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of feet (ie, blue toe syndrome).

Patients may describe a pulse in the abdomen and may actually feel a pulsatile mass.

It is important to note progressive symptoms, which should alert the clinician to the possibility of expansion with imminent rupture. An expanding AAA commonly causes sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the chief complaint, with pain less prominent.

Symptoms of ruptured AAA

Persons with AAAs that have ruptured may present in many ways. The most typical manifestation of rupture is abdominal or back pain with a pulsatile abdominal mass. However, the symptoms may be vague, and the abdominal mass may be missed. Symptoms may include groin pain, syncope, paralysis, and flank mass. The diagnosis may be confused with renal calculus, diverticulitis, incarcerated hernia, or lumbar spine disease.

Transient hypotension should prompt consideration of rupture because this finding can progress to frank shock over a period of hours. Temporary loss of consciousness is also a potential symptom of rupture.

Patients with a ruptured AAA may present in frank shock, as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension. As many as 65% of patients with ruptured AAAs die of sudden cardiovascular collapse before arriving at a hospital.

AAAs may rupture into the vena cava, producing large arteriovenous fistulae. In this case, symptoms include tachycardia, congestive heart failure (CHF), leg swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral ischemia. Finally, an AAA may rupture into the fourth portion of the duodenum. These patients may present with a herald upper gastrointestinal bleed followed by an exsanguinating hemorrhage.

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Physical Examination

Most clinically significant AAAs are palpable upon routine physical examination; however, the sensitivity of palpation depends on the experience of the examiner, the size of the aneurysm, and the size of the patient. In one study, 38% of AAA cases were detected on the basis of physical examination findings, whereas 62% were detected incidentally on radiologic studies obtained for other reasons.

Abdominal examination includes palpation of the aorta and estimation of the size of the aneurysm. AAAs are palpated in the upper abdomen; the aorta bifurcates into the iliac arteries just above the umbilicus. The clinician need not be afraid of properly palpating the abdomen, because there is no evidence to indicate that aortic rupture can be precipitated by this maneuver.

Whereas the abrupt onset of pain due to rupture of an AAA may be quite dramatic, the associated physical findings may be very subtle. Patients may have normal vital signs in the presence of a ruptured AAA as a consequence of retroperitoneal containment of hematoma.

The presence of a pulsatile abdominal mass (see the image below) is virtually diagnostic of an AAA but is found in fewer than 50% of cases. It is more likely to be noted with a ruptured aneurysm. In an obese abdomen, an AAA is more difficult to palpate. Even in patients known to have an aneurysm, vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery in 25% of cases.

Pulsatile abdominal mass. Pulsatile abdominal mass.

Occasionally, an overlying mass (pancreas or stomach) may be mistaken for an AAA. An abdominal bruit is nonspecific for an unruptured aneurysm, but the presence of an abdominal bruit or the lateral propagation of the aortic pulse wave can offer subtle clues and may be more frequently found than a pulsatile mass. Bruits may also indicate the presence of renal or visceral artery stenosis; a thrill is possible with aortocaval fistulae. Patients with popliteal artery aneurysms frequently have AAAs (25-50% of cases).

Misdiagnosis is fairly common because the classic presentation of pain associated with hypotension, tachycardia, and a pulsatile abdominal mass is present in less than 30-50% of cases. The leading misdiagnosis is renal colic; dissection of the renal artery may produce flank pain and hematuria.

Normally, systolic blood pressures are higher in the thigh than in the arm. In patients with AAA, this relation may be reversed. Bilateral upper-extremity blood pressures should be measured in patients with AAAs. Upper-extremity blood pressures that differ from each other by more than 30 mm Hg indicate subclavian artery stenosis, and perioperative monitoring is important. Cervical bruits may indicate carotid artery stenosis. Hypertension may trigger a workup for renal artery stenosis.

Femoral/popliteal pulses and pedal (dorsalis pedis or posterior tibial) pulses should be palpated to determine if an associated aneurysm (femoral/popliteal) or occlusive disease exists. Flank ecchymosis (Grey Turner sign) represents retroperitoneal hemorrhage.

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Complications

The following are potential complications of AAAs:

  • Death (1.8-5% mortality for elective open repair, <1% for endovascular repair, and 50% if the AAA has ruptured, though studies are showing that this last figure is decreased with endovascular repair)
  • Pneumonia (5%)
  • Groin infection (<5%)
  • Graft infection (<1%)
  • Colon ischemia (<1% for elective repair, 15-20% if the AAA has ruptured)
  • Renal failure related to preoperative creatinine level, intraoperative cholesterol embolization, and hypotension
  • Incisional hernia (10-20%)
  • Bowel obstruction
  • Amputation from major arterial occlusion
  • Blue toe syndrome and cholesterol embolization to feet
  • Impotence in males - Erectile dysfunction and retrograde ejaculation (>30%)
  • Paresthesias in thighs from femoral exposure (rare)
  • Lymphocele in groin (~2%)
  • Late graft enteric fistula
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Contributor Information and Disclosures
Author

Saum A Rahimi, MD, FACS Interim Chief, Assistant Professor of Surgery, Division of Vascular Surgery, Rutgers Robert Wood Johnson Medical School

Saum A Rahimi, MD, FACS is a member of the following medical societies: American College of Surgeons, Society for Vascular Surgery, Eastern Vascular Society, Vascular Society of New Jersey

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

Acknowledgements

Suman Annambhotla, MD Fellow in Vascular Surgery, Northwestern University, The Feinberg School of Medicine

Suman Annambhotla, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

Jeffrey Lawrence Kaufman, MD Associate Professor, Department of Surgery, Division of Vascular Surgery, Tufts University School of Medicine

Jeffrey Lawrence Kaufman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society for Artificial Internal Organs, Association for Academic Surgery, Association for Surgical Education, Massachusetts Medical Society, Phi Beta Kappa, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

William H Pearce, MD Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University, The Feinberg School of Medicine

William H Pearce, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, New York Academy of Sciences, Society for Vascular Surgery, Society of Critical Care Medicine, Society of University Surgeons, andWestern Surgical Association

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Radiograph shows calcification of abdominal aorta. Left wall is clearly depicted and appears aneurysmal; however, right wall overlies spine.
On radiography, lateral view clearly shows calcification of both walls of abdominal aortic aneurysm, allowing diagnosis to be made with certainty.
CT demonstrates abdominal aortic aneurysm (AAA). Aneurysm was noted during workup for back pain, and CT was ordered after AAA was identified on radiography. No evidence of rupture is seen.
Arteriography demonstrates infrarenal abdominal aortic aneurysm. This arteriogram was obtained in preparation for endovascular repair of aneurysm.
Lateral arteriogram demonstrates infrarenal abdominal aortic aneurysm. Demonstration of superior mesenteric artery, inferior mesenteric artery, and celiac artery on lateral arteriogram is important for complete evaluation of extent of aneurysm.
Arteriogram after successful endovascular repair of abdominal aortic aneurysm.
Ultrasonogram from patient with abdominal aortic aneurysm (AAA). This aneurysm was best visualized on transverse or axial image. Patient underwent conventional AAA repair.
MRI of 77-year-old man with leg pain believed to be secondary to degenerative disk disease. During evaluation, abdominal aortic aneurysm was discovered.
Age is risk factor for development of aneurysm.
Inflammation, thinning of media, and marked loss of elastin.
Pulsatile abdominal mass.
Aneurysm with retroperitoneal fibrosis and adhesion of duodenum.
Aortic endoprosthesis (Cook aortic and aortobi-iliac endograft).
Endoaneurysmorrhaphy
Endovascular grafts.
Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of feet (ie, blue toe syndrome).
Enhanced spiral CT scans with multiplanar reconstruction and CT angiogram.
Angiography is used to diagnose renal area. In this instance, endoleak represented continued pressurization of sac.
Table 1. Operative Mortality Risk of Open Repair of Abdominal Aortic Aneurysm
Lowest Risk Moderate Risk High Risk
Age < 70 y Age 70-80 y Age 80 y
Physically active Active Inactive, poor stamina
No clinically overt cardiac disease Stable coronary disease; remote MI; LVEF >35% Significant coronary disease; recent MI; frequent angina; CHF; LVEF < 25%
No significant comorbidities Mild COPD Limiting COPD; dyspnea at rest; O2 dependency; FEV1 < 1 L/sec
... Creatinine 2.0-3.0 mg/dL ...
Normal anatomy Adverse anatomy or AAA characteristics Creatinine >3 mg/dL
No adverse AAA characteristics ... Liver disease (↑ PT; albumin < 2 g/dL)
Anticipated operative mortality, 1%-3% Anticipated operative mortality, 3%-7% Anticipated operative mortality, at least 5%-10%; each comorbid condition adds ~3%-5% mortality risk
AAA—abdominal aortic aneurysm; CHF—chronic heart failure; COPD—chronic obstructive pulmonary disease; FEV1 —forced expiratory volume in 1 second; LVEF—left ventricular ejection fraction; MI—myocardial infarction; PT—prothrombin time.
Table 2. Abdominal Aortic Aneurysm Size and Estimated Annual Risk of Rupture
AAA Diameter (cm) Rupture Risk (%/y)
< 4 0
4-5 0.5-5
5-6 3-15
6-7 10-20
7-8 20-40
>8 30-50
AAA—abdominal aortic aneurysm.
Table 3. Factors Affecting Risk of Abdominal Aortic Aneurysm Rupture
  Low Risk Average Risk High Risk
Diameter < 5 cm 5-6 cm >6 cm
Expansion < 0.3 cm/y 0.3-0.6 cm/y >0.6 cm/y
Smoking/COPD None, mild Moderate Severe/steroids
Family history No relatives One relative Numerous relatives
Hypertension Normal blood pressure Controlled Poorly controlled
Shape Fusiform Saccular Very eccentric
Wall stress Low (35 N/cm2 Medium (40 N/cm2 High (45 N/cm2)
Sex ... Male Female
COPD—chronic obstructive pulmonary disease.
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