E S Connolly1, C J Winfree, P C McCormick. 1. Department of Neurological Surgery, Columbia-Presbyterian Medical Center, New York, New York, USA.
Abstract
STUDY DESIGN: This case report illustrates a patient with a spontaneous epidural hematoma after tissue plasminogen activator therapy who presented 10 days after the incident with a resolving Brown-Sèquard syndrome. OBJECTIVES: The treatment of this patient involves the principles of conservative follow-up directed by an improving examination and an understanding of the pathophysiology of coagulopathy-induced spontaneous epidural bleeds. SUMMARY OF BACKGROUND DATA: The use of tissue plasminogen activator therapy for thrombolysis in patients with early acute myocardial infarction is becoming increasingly routine. Use is limited most significantly by bleeding complications. Recently, several groups have drawn attention to the neurologic complications associated with intracranial hemorrhage after tissue plasminogen activator therapy. Spontaneous spinal epidural hemorrhage has, by comparison, received little attention. The authors report the second case in the literature and the first without a history of antecedent trauma. METHODS: The onset of the painful myelopathy in this patient was missed in the acute setting because of low suspicion. When the diagnosis was made, coadministered heparin had already been discontinued without reversal, and the patient's examination had already improved. Careful follow-up by neurologic examination and magnetic resonance imaging was obtained without spinal angiography being performed. RESULTS: The patient regained his prehemorrhage neurologic status, experienced no further bleeding, and his coronary ischemia remained subclinical. CONCLUSIONS: Spinal epidural hemorrhage secondary to thrombolytic therapy is becoming increasingly common. Urgent surgical decompression is generally warranted to preserve neurologic function. In cases where the deficit is minimal or resolving, a conservative approach may be warranted with magnetic resonance imaging but not angiographic follow-up.
STUDY DESIGN: This case report illustrates a patient with a spontaneous epidural hematoma after tissue plasminogen activator therapy who presented 10 days after the incident with a resolving Brown-Sèquard syndrome. OBJECTIVES: The treatment of this patient involves the principles of conservative follow-up directed by an improving examination and an understanding of the pathophysiology of coagulopathy-induced spontaneous epidural bleeds. SUMMARY OF BACKGROUND DATA: The use of tissue plasminogen activator therapy for thrombolysis in patients with early acute myocardial infarction is becoming increasingly routine. Use is limited most significantly by bleeding complications. Recently, several groups have drawn attention to the neurologic complications associated with intracranial hemorrhage after tissue plasminogen activator therapy. Spontaneous spinal epidural hemorrhage has, by comparison, received little attention. The authors report the second case in the literature and the first without a history of antecedent trauma. METHODS: The onset of the painful myelopathy in this patient was missed in the acute setting because of low suspicion. When the diagnosis was made, coadministered heparin had already been discontinued without reversal, and the patient's examination had already improved. Careful follow-up by neurologic examination and magnetic resonance imaging was obtained without spinal angiography being performed. RESULTS: The patient regained his prehemorrhage neurologic status, experienced no further bleeding, and his coronary ischemia remained subclinical. CONCLUSIONS: Spinal epidural hemorrhage secondary to thrombolytic therapy is becoming increasingly common. Urgent surgical decompression is generally warranted to preserve neurologic function. In cases where the deficit is minimal or resolving, a conservative approach may be warranted with magnetic resonance imaging but not angiographic follow-up.