Acute aortic occlusion (AAO) is a relatively rare vascular emergency. The actual incidence of AAO is unknown but has been variously reported to be 1% to 4%, and the incidence of AAO secondary to infrarenal abdominal aortic aneurysm is reported to be about 2%.1 Acute aortic occlusion may present with acute onset of neurologic deficits as a consequence of spinal cord ischemia from thrombotic or embolic etiology. Risk factors for thrombosis include hypertension, tobacco smoking, and diabetes mellitus; heart disease and female gender are associated with embolism.2 Spinal cord infarction accounts for only 1% to 2% of all strokes and is characterized by acute onset of paralysis, bowel and bladder dysfunction, and loss of pain and temperature perception. Proprioception and vibratory sense are typically preserved.3 The authors present the case of a patient with acute onset of lower limb paralysis and urinary incontinence who was later found to have AAO due to thrombosis and consequent spinal cord infarction.
An 80-year-old white woman presented to the emergency department of Jefferson Regional Medical Center in Pine Bluff, Arkansas, with the sudden onset of severe lower back pain, bilateral leg paralysis and paresthesia, and urinary incontinence. The patient stated that she had been watching television when her legs began to tingle and feel numb. Within 10 to 20 minutes she was unable to move her legs and became incontinent of urine. She reported no injury or previous history of back pain. Her medical history was significant for “irregular heartbeat my whole life,” hypertension, hyperlipidemia, and bladder cancer. She was not receiving systemic anticoagulation therapy. She reported a previous 15 pack-year smoking history but reported that she had quit cigarette smoking and usually drank 1 glass of wine daily. She had previously completed 3 rounds of chemotherapy for bladder cancer and received her first radiation treatment earlier that day. The symptoms began about 8 hours later that evening.
On examination the patient was noted to be in acute distress due to pain. Her vital signs in triage were blood pressure (BP) 122/71 mm Hg, pulse 54 beats per min (BPM), respirations 18 breathes per min, temperature 98° F, and pulse oximetry 90% on 2 L/min oxygen via nasal cannula. Laboratory evaluation was remarkable only for serum sodium 132 mEq/L, potassium 2.8 mEq/L, and thrombocytosis with platelets 697 × 103/μL. A neurologic examination showed normal motor function, strength of the upper extremities, and paralysis of the lower extremities, which were insensate to blunt or sharp touch and with decreased skin temperature from the groin distally. Pedal pulses were absent bilaterally. She was incontinent of urine and had anal sphincter laxity.
Magnetic resonance imaging showed bulging lumbar intervertebral discs and foraminal narrowing, which the consulting neurosurgeon did not feel explained her presentation and suggested that a vascular etiology was more likely. A contrast-enhanced computed tomography (CT) scan of the abdomen and pelvis showed occlusion of the infrarenal abdominal aorta, bilateral common, and external iliac arteries. The proximal inferior mesenteric artery was occluded, and there was 90% stenosis of the proximal superior mesenteric artery with noncalcified plaque. There was no abdominal aortic aneurysm or dissection demonstrated. A chest CT was unremarkable.
The patient was started on IV heparin 800 U/h and transferred via ambulance to the University of Arkansas for Medical Sciences in Little Rock, Arkansas, for vascular surgery. On arrival her vital signs were BP 108/69 mm Hg, pulse 123 BPM, respirations 18 breathes per min, temperature 98° F, and pulse oximetry 94% on 2 L/min oxygen via nasal cannula. The patient’s electrocardiogram demonstrated atrial fibrillation with rapid ventricular response with premature ventricular complexes. On examination the bilateral lower extremities were cyanotic and cold to the touch. The pedal pulses were nonpalpable, and decreased distal sensation with dense paralysis was noted.
The patient was taken emergently to the operating room (OR) for left axillary bifemoral bypass. Severe atherosclerotic disease was noted at surgery. She was transferred to the surgical intensive care unit (SICU) for postoperative hemodynamic monitoring. Her clinical course became complicated by mesenteric ischemia from chronic superior mesenteric artery (SMA) occlusion. On postoperative day 2, she became progressively more hypotensive, and she was placed on vasopressin 0.04 U/min and amiodarone 0.5 mg/min infusions.
Bedside echocardiography showed diffuse ventricular hypokinesis and a left ventricular ejection fraction (LVEF) of about 30% but no mural thrombus. The patient developed altered mental status and respiratory distress, and her serum lactate increased to 6.1 mg/dL. She was emergently intubated and taken to the OR to attempt recanalization of the SMA occlusion, which was unsuccessful. She was returned to the SICU for continued resuscitation and monitoring. She continued to decline with hypotensive pressures, increasing serum creatinine and lactate, and worsening metabolic acidosis. Management options and goals of care were discussed with the family, and it was decided to honor her do not resuscitate status and pursue comfort care. She was extubated and expired a short time after this was done.