A 70-year-old woman presented to our emergency department with sudden onset of weakness in both legs, epigastric pain radiating to the back, nausea, and hematochezia. She smoked, had hypertension that had been controlled for 5 years with a ß-blocker, and had a history of myocardial infarction and decreased femoral pulses with no claudication. Two days before hospitalization, an angiotensin-converting enzyme inhibitor was prescribed as an adjunct to the ß-blocker because of blood pressure that had been fluctuating between 200/80 mm Hg and 220/90 mm Hg. She was drowsy and had a regular pulse rate (73 beats/min) and symmetrical blood pressure of 120/70 mm Hg. Clinical examination revealed cold, mottled, and pulseless lower limbs with diminished reflexes, as well as loss of sensation below the T12 level. The abdomen was tender with no palpable mass, and bowel sounds were absent. Cardiac and pulmonary auscultation were normal.

The chest radiograph was normal, and an electrocardiogram showed signs of previous inferior myocardial infarction. Blood chemistry indicated increased urea (17.8 mmol/L), creatinine (173 µmol/L), potassium (5.5 mmol/L), lactate dehydrogenase (996 U/L), and alanine aminotransferase (65 U/L) levels. Clinically significant metabolic acidosis was present (pH, 7.21; base excess, –9.3),along with an elevated blood lactate level (14 mmol/L). A thoracoabdominal computed tomographic scan without contrast showed occlusion of the distal thoracic aorta by an intraluminal calcified mass between T5 and T10 (Figure 1, top). The aorta above and below the occlusion was normal, without stenosis or aneurysmal dilatation.

View larger version (83K): [in this window] [in a new window]   Figure 1. Top. Preoperative thoracoabdominal computed tomographic scan showing a calcified mass almost completely occluding the thoracic aorta at T8. Bottom. Calcified thoracic aortic segment after surgical removal.

During surgery, the entire calcified aortic segment was resected (Figure 1, bottom) and replaced by a Dacron tube. After removal of the aortic clamp, recoloration of the liver and bowels and diuresis were marked. Histology confirmed the presence of fibrocalcifying atherosclerosis. After surgery, the patient's blood pressure returned to normal without medication.

Acute thoracic aortic occlusion occurs less frequently than acute infrarenal aortic occlusion. The literature includes reports of calcified thrombus in the region of the aortic isthmus in two cases [1, 2], thrombosis of preexisting aortitis in one case [3], and atherosclerotic obstructive disease in another case [4]. All patients presented with long-standing upper-extremity hypertension that mimicked aortic coarctation [5]. Patients who are or become unresponsive to an antihypertensive drug should be carefully investigated. The presence of diminished femoral pulses with or without claudication may justify more detailed investigation of the aorta. The combination of antihypertensive drugs may have lead to acute ischemia of the lower body in our case of an obstructive thoracic aortic lesion. The variety of clinical findings consistent with acute ischemia of the lower body and spinal cord can sometimes mislead a physician focusing on the dominating neurologic or visceral symptoms while overlooking the possibility of a vascular cause.