MANAGEMENT OF SPINAL EPIDURAL HEMATOMA AFTER TISSUE-PLASMINOGEN ACTIVATOR - A CASE-REPORT

Citation
Es. Connolly et al., MANAGEMENT OF SPINAL EPIDURAL HEMATOMA AFTER TISSUE-PLASMINOGEN ACTIVATOR - A CASE-REPORT, Spine (Philadelphia, Pa. 1976), 21(14), 1996, pp. 1694-1698
Citations number
29
Categorie Soggetti
Orthopedics,"Clinical Neurology
ISSN journal
03622436
Volume
21
Issue
14
Year of publication
1996
Pages
1694 - 1698
Database
ISI
SICI code
0362-2436(1996)21:14<1694:MOSEHA>2.0.ZU;2-O
Abstract
Study Design. This case report illustrates a patient with a spontaneou s epidural hematoma after tissue plasminogen activator therapy who pre sented 10 days after the incident with a resolving Brown-Sequard syndr ome. Objectives. The treatment of this patient involves the principles of conservative follow-up directed by an improving examination an und erstanding of the pathophysiology of coagulopathy-induced spontaneous epidural bleeds. Summary of Background Data. The use of tissue plasmin ogen activator therapy for thrombolysis in patients with early acute m yocardial 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. Sp ontaneous spinal epidural hemorrhage has, by comparison, received litt le 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 sett ing because of low suspicion. When the diagnosis was made, coadministe red heparin had already been discontinued without reversal, and the pa tient's examination had already improved. Careful follow-up by neurolo gic examination and magnetic resonance imaging was obtained without sp inal angiography being performed. Results. The patient regained his pr ehemorrhage neurologic status, experienced no further bleeding, and hi s coronary ischemia remained subclinical. Conclusions. Spinal epidural hemorrhage secondary to thrombolytic therapy is becoming increasingly common. Urgent surgical decompression is generally warranted to prese rve neurologic function. In cases where the deficit is minimal or reso lving, a conservative approach may be warranted with magnetic resonanc e imaging but no angiographic follow-up.