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  Diagnosis of ruptured abdominal aortic aneurysm (AAA) is frequently missed or delayed. The most common misdiagnosis is renal colic.

  
  
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  AAA must be considered in any elderly patient with back, flank, or groin pain.

  
  
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  Suspected ruptured AAA requires emergent consultation, with the goal of immediate open or endovascular repair.

  
  
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  Patients with incidentally discovered AAAs must be referred for surveillance or elective repair.

Abdominal aortic aneurysm (AAA) is an increase in the diameter of the aorta of more than 50%, or an infrarenal aortic diameter greater than 3 cm. The etiology and pathogenesis of AAA is unclear, although atherosclerosis, connective tissue disorders, genetic factors, and smoking have all been implicated. A family of enzymes known as matrix metalloproteinases may be largely responsible for the inflammatory destruction of elastin and collagen fibers in the medial and adventitial layers of the aortic wall that can ultimately lead to AAA formation, enlargement, and rupture.

The rate of expansion and risk of rupture are related to tension on the wall of the aneurysm, which in turn is related to the diameter of the aneurysm and to the underlying pressure. Rupture of aneurysms smaller than 4 cm is rare, whereas the annual risk of rupture for aneurysms larger than 8 cm has been estimated at 30–50%.

AAA causes 15,000 deaths in the United States a year. It is a common cause of sudden death and is responsible for 1–2% of all deaths in men older than 65 years. The overall mortality rate of a patient with a ruptured AAA is 90%, and 50% of patients with ruptured AAA do not survive to reach the hospital. In patients who arrive at the hospital, the mortality rate improves to 60%. The mortality rate for elective open operative repair is 2–7%; recent advances in endovascular technique have mitigated early morbidity and mortality.

The incidence of AAA begins to increase in men older than 55 years. By age 80 years, 5% of men have an AAA, and 5% of women age 90 years have AAA. There is an increased incidence in smokers, whites, and those with a family history of AAA. First-degree relatives of patients with AAA have up to an 8-fold increase in the chance of developing AAA.

History

The emergency department (ED) presentation of AAA is varied, with symptoms due to expansion and rupture, distal thromboembolic complications, local mass effects, or erosion into adjacent structures. Most AAAs are asymptomatic and discovered incidentally while evaluating patients for unrelated conditions. These patients require little more than referral. At the other end of the spectrum, AAA rupture can constitute one of the most acutely life-threatening emergencies in medicine.

The classic triad of abdominal/back pain, hypotension, and a pulsatile abdominal mass is present in substantially less than one half of patients with a ruptured AAA. The vast majority of patients with ruptured AAA will have pain, typically in the abdomen, back, flank, or groin, depending on the extent and direction of rupture. Rarely, patients with rupture can present with syncope alone or with nonspecific symptoms such as vomiting, diarrhea, or dizziness.

Physical Examination

Patients with ruptured AAA may present with evidence of hemorrhagic shock: hypotension, tachycardia, and exam findings of poor perfusion. However, the patient may be normotensive or even hypertensive. Transient hypotension may also occur and can be erroneously attributed to a vasovagal etiology. Abdominal examination may detect a pulsatile mass, but this can be difficult with small aneurysms or obese patients and is subject to significant interobserver variability. Absence of a pulsatile mass on exam does not exclude the diagnosis of AAA. Lower extremity pulses should be assessed, as lower limb ischemia is present in 5% of cases.