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O'Connor OJ, Maher MM. Imaging of cholecystitis. A]R Am

] Roentgenol 201 1;1 96:W367-W374.

Strasberg SM. Clinical practice. Acute calculous cholecystitis.

N Eng! ] Med 2008;358:2804S-281 1S.

Abdominal Aortic

Aneu rysm

Alex de Ia Fuente, MD

Key Points

• Diagnosis of ruptured abdominal aortic aneurysm (AM)

is frequently missed or delayed. The most common

misdiagnosis is renal colic.

• AM must be considered in any elderly patient with

back, flank, or groin pain.

INTRODUCTION

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 em. The etiology and patho ­

genesis of AAA is unclear, although atherosclerosis, c onnective 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 ulti -

mately 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 em is

rare, whereas the annual risk of rupture for aneurysms

larger than 8 em 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.

• Suspected ruptured AAA requires emergent consu ltation, with the goal of immediate open or endovascular

repair.

• Patients with incidentally discovered AAAs must be

referred for surveillance or elective repair.

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.

CLINICAL PRESENTATION

..... History

The emergency department (ED) presentation of AAA is varied, with symptoms due to expansion and rupture, distal

thromboembolic complications, local mass eff ects, 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 r uptured 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.

1 25

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