Abdominal Aortic Aneurysm Clinical Presentation

Updated: Jan 08, 2019
  • Author: Saum A Rahimi, MD, FACS; Chief Editor: Vincent Lopez Rowe, MD  more...
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Presentation

History

As noted (see 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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