Acute Cerebral Infarction Caused by Aortic Dissection: Caution in the Thrombolytic Era
To the Editor:
The National Institute of Neurological Disorders and Stroke (NINDS) Acute Ischemic Stroke Trial1 has brought treatment of acute ischemic stroke into the thrombolytic era.2 The inclusion and exclusion criteria were established to provide guidelines for the safe treatment of ischemic stroke within the first 3 hours.
Case: A 72-year-old woman was noted to drive off the road at 9:45 pm, with her car traveling at approximately 10 miles per hour. When they arrived minutes later, emergency medical services noted that the woman had a left facial droop and left hemiparesis. She arrived at the emergency department 20 minutes later. On initial evaluation, her temperature was 36.1°C, blood pressure 130/80 mm Hg, and pulse 54 and regular. She alerted to voice and could follow simple commands intermittently. She had minimal verbal output, except for perseveration of the word “hello.” Cranial nerve examination was significant for a left upper motor neuron facial droop and right gaze preference. She had a left hemiplegia with reduced reflexes on the left and a Babinski sign. Heart auscultation revealed a regular rate and rhythm with no murmurs. Lungs were clear to auscultation bilaterally. Carotid pulses were diminished but present bilaterally, and no bruits were heard. Radial pulses were also present but diminished bilaterally (right greater than left). Femoral and distal pedal pulses were normal. There were no external signs of trauma.
Laboratory studies, including complete blood count, electrolytes, glucose, prothrombin time, and partial thromboplastin time, were within normal limits. An electrocardiogram revealed sinus rhythm at a rate of 52. A head CT without contrast revealed subtle sulcal effacement frontally on the right but no hypodensity or hemorrhage. Intravenous tissue plasminogen activator was considered at this point; however, a chest x-ray revealed a widened superior mediastinum (Figure 1⇓), and intravenous tPA was not given. A CT scan of the chest with and without contrast revealed dilatation of the ascending aorta, with dissection beginning at the lateral aortic root (Figure 2⇓). Only a thin crescent of contrast was seen in the brachiocephalic trunk, with opacification of the right subclavian artery. There was no flow in the left or right common carotid artery.
During evaluation in the emergency department, the patient’s heart rate and blood pressure dropped, requiring atropine and fluid resuscitation. She was not considered a surgical candidate for aortic repair secondary to profound neurological deficits. She was admitted for medical management and died the next day.
The inadvertent administration of thrombolytics to patients with aortic dissection has been a concern for cardiologists since the advent of the thrombolytic therapy for acute myocardial infarction. Patients with aortic dissection may present with symptoms or signs consistent with an acute myocardial infarction. When these patients are given intravenous tPA, the majority have poor outcomes.3
The aggressiveness in screening for aortic dissection in patients meeting thrombolytic therapy criteria for myocardial infarction has been debated.4 The incidence of myocardial infarction far exceeds that of aortic dissection, and most feel it would be a disservice to delay thrombolytic therapy for a large number of patients who could benefit in order to protect the minority of those with aortic dissection.
A comprehensive review of the literature with a Medline database from 1966 to the present reveals no cases of tPA given intravenously to a person with acute ischemic stroke resulting from aortic dissection. It is likely that similar poor outcomes would occur in ischemic stroke if tPA were administered intravenously to such patients. Not only might intravenous tPA contribute to early death by worsening hemothorax or hemopericardium, but it also may delay potential surgical procedures and interfere with hemostasis. Therefore, it is important to clinically recognize this possibility. Because aortic dissection is a rare cause of ischemic stroke, the aggressiveness of screening for this entity is also questioned. Chest CT scanning and transesophogeal echocardiography, while very sensitive for aortic dissection, are time consuming and expensive. Up to 20% of chest x-rays may be negative in patients with aortic dissection5 ; however, this is a relatively simple, quick study that is a routine part of a stroke mechanism evaluation.
An emergent chest x-ray should be considered as part of acute ischemic stroke protocols and should be completed in ischemic stroke patients before administration of intravenous tPA or other thrombolytic therapy. In the unusual setting in which chest x-ray would significantly delay emergent use of thrombolysis, it should be completed when history (chest or back pain or significant trauma immediately before the cerebral infarction) or physical examination (hypotension, reduced peripheral pulses, aortic regurgitation murmur) findings are suggestive of aortic dissection or when communication is impaired.
- Copyright © 1999 by American Heart Association
Chiu D, Krieger D, Villar-Cordova C, Kassner SE, Morgenstern LB, Bratina PL, Yatsu FM, Grotta JC. Intravenous tissue plasminogen activator for acute ischemic stroke: feasibility, safety, and efficacy in the first year of clinical practice. Stroke.. 1998;29:18–22.
Fann JI, Sarris GE, Miller DC, Mitchell RS, Oyer PE, Stinson EB, Shumway NE. Surgical management of acute aortic dissection complicated by stroke. Circulation. 1989;80 (suppl I):I-257–I-263.