Ruptured Abdominal Aortic Aneurysm
An obese 61-year-old man with a history of heroin abuse was brought to the hospital after he had fallen onto his buttocks on a sidewalk. He was able to stand initially, but weakness and numb-ness in his legs rendered him suddenly unable to walk or prevent himself from voiding. He denied abdominal or back pain. His medical history included asthma, chronic obstructive pulmonary disease, and hypertension.
An obese 61-year-old man with a history of heroin abuse was brought to the hospital after he had fallen onto his buttocks on a sidewalk. He was able to stand initially, but weakness and numb-ness in his legs rendered him suddenly unable to walk or prevent himself from voiding. He denied abdominal or back pain. His medical history included asthma, chronic obstructive pulmonary disease, and hypertension.
The patient was alert and well-oriented. He was afebrile; heart rate was 105 beats per minute; blood pressure, 130/81 mm Hg; and respiration rate, 16 breaths per minute. Chest and cardiac findings were unremarkable. His abdomen was soft and nontender, without distention, pulsatile masses, or bruits. Cranial nerves were intact. Motor strength was decreased in the right lower extremity; the other extremities were normal. Deep tendon reflexes were normal. Two-point discrimination and sensation were intact. Sphincter tone was diminished; there was no saddle anesthesia. No midline spinal deformities or tenderness was noted; femoral and dorsalis pedis pulses were intact and equal bilaterally.
White blood cell count was 19,100/µL, with 92% segmented neutrophils; blood urea nitrogen was 22 mg/dL; creatinine was 1.4 mg/dL; and hemoglobin was 13.7 g/dL. An ECG showed normal sinus rhythm at 93 beats per minute. Results from cardiac enzyme studies and a CT scan of the head were negative. A radiograph of the spine showed a large calcified mass in the abdomen (A). A CT scan of the abdomen and pelvis with intravenous contrast revealed a large (8 cm) infrarenal abdominal aortic aneurysm (AAA) with a right-sided retroperitoneal hematoma (B). The patient was brought to the operating room, but he became hypotensive and died during surgery.
The incidence of ruptured AAA has increased over the past 3 decades, despite elective repair.1 One theory cites the increased life expectancy in the Western world as a possible cause.2
AAA has a wide variety of presenting symptoms. Spinal cord ischemia and cauda equina syndrome are rare presentations of atherosclerotic aortic disease; they have been reported as presenting complaints of AAA in only a small number of cases, usually with a poor outcome.3 Although the exact mechanism is unknown, local dissection may interrupt the blood supply to the artery of Adamkiewicz, with thrombosis of the lumbar vessels.2
The classic presenting symptoms of AAA-abdominal pain, back pain, and a palpable aortic mass-occur in only 49% of cases, and the misdiagnosis rate is estimated to be as high as 16%.4 The diagnosis requires a high index of suspicion in all patients with risk factors, including male sex; old age; and a history of hypertension, smoking, or dyslipidemia (specifically a low serum high-density lipoprotein cholesterol level).5
Ruptured AAA is a true vascular emergency. Mortality is about 60% for patients who experience out-of-hospital ruptures and 41% to 50% for those who are admitted.6 Mortality is directly related to the timeliness of diagnosis and surgery; most delays are caused by a misleading, atypical presentation.6
There are no formal screening guidelines for asymptomatic AAA.7,8 However, patients with newly diagnosed AAA should undergo ultrasonographic imaging every 6 months; surgical or endovascular repair is advisable for aneurysms larger than 5.5 cm. Smoking cessation therapy and treatment of hypertension and hypercholesterolemia are also recommended, although there is no evidence that they slow the growth of the aneurysm.9
References:
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