“I Can’t Walk!” Acute Thrombosis of Descending Aorta Causing Paraplegia
A 50-year-old man presented to the ED after sudden onset of bilateral lower extremity weakness. The patient developed lower back pain and tingling in both lower extremities which progressed to complete paralysis within two hours after onset of the symptoms.\nHis medical history was significant for diet-controlled diabetes mellitus, systolic heart failure, hypertension, prior myocardial infarction, stroke, and prostate cancer. His medications included furosemide, digoxin, carvedilol, lisinopril, clopidogrel, and aspirin. He received hormonal therapy for his prostate cancer within the last year. His social history included 1 pack per day of cigarettes and a remote history of intravenous drug abuse.\nAt ED arrival, he was found to have a blood pressure of 127/47 mmHg (mean arterial pressure [MAP] of 74 mmHg). Upon physical exam, the patient was alert and oriented to self, time and place. Strength in lower extremities was 0/5 bilaterally, with no sensation from the distal one third of thigh and below bilaterally. Cardiovascular exam revealed regular rate and rhythm, S1, S2, and no pedal edema. However, femoral, dorsalis pedis and posterior tibialis pulses were absent bilaterally, in addition to poor rectal tone. There was mottling over the knees bilaterally, and they were cool to touch.\nLaboratory work-up revealed moderately elevated blood urea nitrogen (BUN) and creatinine, 50 and 2.5 mg/dL respectively, a creatine phosphokinase of 323 IU/L, a pH of 7.50 and a troponin of 0.7 mg/mL. Because of the physical exam findings of decreased perfusion and new onset renal failure, a serum lactate was ordered and found to be elevated to 5.6 mmol/L.\nThe history of prostate cancer led to the inclusion of acute spinal cord compression in the differential diagnosis. Consequently, contrast computed tomography (CT) of brain, thoracic and lumbar spine were ordered, all of which were unremarkable. Due to the absence of pulses in the lower extremities, additional CT angiogram was ordered, which showed a complete occlusion of the distal aorta below the inferior mesenteric artery, extending to the common iliac bifurcations (). To rule out a cardiac source for the thrombus, an echocardiogram was performed and showed an ejection fraction (EF) of 15 %, indicating severe systolic dysfunction. Clinical and laboratory evidence of global tissue hypoperfusion (shock) led to the conclusion that the patient was in need of intensive or invasive hemodynamic monitoring to guide his resuscitation.\nParalleling vascular surgery consultation, a central venous catheter was placed and a goal-directed hemodynamic optimization was performed before the necessary surgical intervention. This included optimization of preload, afterload and contractility to increase systemic oxygen delivery to meet demands and eradicate global tissue hypoperfusion. This was achieved with the use of the central venous pressure, (CVP), MAP, ScvO2 and clearance of lactate levels. During the 3 hours of ED stay prior to surgical intervention, Dobutamine was started at 2.5 mcg/kg/min and raised to 5 mcg/kg/min by the second hour. During this time, CVP decreased from 28 to12 cmH2O and ScvO2 increased from 48 to 74 %, while lactate levels decreased from 5.2 to 1.0 mmol/L. During this period MAP was maintained between 75–88 mmHg, and the heart rate ranged from 72 to 81 beats per minute. These findings indicated the initial presence of global tissue hypoxia and its resolution during the goal-directed resuscitation. Severe global tissue hypoxia was present with normal vital signs.\nAfter improvement in hemodynamic status, he underwent an open aorto-ilaic embolectomy and bilateral lower extremity 4-compartment fasciotomies to prevent the expected reperfusion injury and compartment syndrome. The patient was transferred to the surgical intensive care unit after the procedure for continued monitoring, resuscitation and systemic anticoagulation with heparin.\nHe continued to improve post-operatively and was discharged on anticoagulation. At follow-up evaluation in the vascular surgery clinic, 13 days after hospital discharge, the patient reported full return of lower extremity sensation and was able to ambulate without assistance.