Complete Nonsurgical Resolution of a Spontaneous Spinal Epidural Hematoma STEVEN H. SILBER, DO Spontaneous spinal epidural hematomas (SSEH) are heralded by spinal pain and progressive cord compression syndromes which may lead to permanent neurological disability or death if emergent neurosurgical intervention is delayed. It therefore must be considered early in the differential diagnosis of acute spinal cord compression syndrome. A case of spontaneous spinal epidural hematoma presenting as an acute myelopathy in a clarinet player who chronically used a nonsteroidal antiinflammatory medication is presented. The case was remarkable for the rare complete spontaneous resolution of neurological function. Approximately 250 cases of SSEH have been reported in the medical literature, although only a handful of these patients have recovered spontaneously. This is the sixth report of such an event. The etiologies, contributing factors, disease progression, and treatment recommendations are discussed. (Am J Emerg Med 1996;14:391-393. Copyright © 1996 by W.B. Saunders Company) Spontaneous spinal epidural hematomas (SSEH) are heralded by spinal pain and progressive cord compression syndromes which may lead to permanent neurological disability or death if emergent neurosurgical intervention is delayed. ~-5 It therefore must be considered early in the differential diagnosis of acute spinal cord compression syndrome. Approximately 250 cases of SSEH have been reported in the medical literature. Only five of these patients had permanent spontaneous resolution. 6-1°This is the sixth report of such an event.
CASE REPORT A 51-year-old male professional clarinet player was in good health until he experienced sudden, mild nonradiating upper back pain after performing his usual daily morning routine of yoga, light weight-lifting exercises, and playing the clarinet. He had no significant medical history, no recent illness, and had been taking up to 400 mg ibuprofen daily for over 1 year. Over the subsequent 2 hours, he developed progressive numbness and weakness of his lower extremities beginning in his toes and progressing proximally to his mid-chest. He also complained of the loss of fine motor coordination of his right hand and an inability to urinate. On presentation to the emergency department (ED), the patient was awake, alert, and oriented, but was unable to ambulate unassisted because of his extreme lower extremity weakness. His temperature was 36.6°C, pulse was 66 beats/min and regular, respirations were 20 breaths/min, and blood pressure was 130/80 nun Hg. There was no facial asymmetry and his cranial nerves were
From the Department of Emergency Medicine, New York Methodist Hospital, Brooklyn. Manuscript received April 20, 1995; accepted June 1, 1995. Address reprint requests to Dr Silber, Department of Emergency Medicine, New York Methodist Hospital, 506 Sixth Street, Brooklyn, New York 11215. Key Words:Spinal cord compression; hematoma, epidural. Copyright © 1996 by W.B. Saunders Company 0735-6757/96/1404-001455.00/0
intact. His pupils were equal and reactive and the fundiscopic examination was unremarkable. There was no spinal tenderness, nuchal rigidity, or bruits. Cardiac examination was normal and peripheral pulses were present and symmetrical. The sensory examination revealed diminished pinprick sensation to the right gluteal region and both lower extremities. Vibratory sense was intact and there were occasional joint position sense errors in his toes bilaterally. There was moderate paraparesis of the hip girdle musculature and almost complete bilateral lower extremity paralysis. The patient was unable to dorsiflex his feet. He also exhibited coordination deficits of his fight arm and diminished grip strength of his right hand. No sensory deficits were appreciated. His deep tendon reflexes were equal and normal in the upper extremities and equal but slightly brisk in the lower extremities. There was no clonus and the plantar reflexes were neutral. Rectal sphincter tone was normal and the bladder did not appear distended. Catheter insertion revealed 200 mL of clear urine. A diagnosis of acute myelopathy secondary to spinal cord compression of undetermined etiology was made. An immediate omnipaque myelogram with computerized tomography (CT) scanning was requested. Neurology and neurosurgery consultation concurred with the ED assessment, and the patient was administered 75 mg of dexamethasone intravenouslyon their recommendation. The myelogram with CT scan showed a posterolateral epidural defect on the right from the level of C5 to T4 with slight cord compression (Figure 1). Laboratory analyses, including complete blood count, serum chemistry levels, PT, PTT sedimentation rate, and ¥DRL, were normal. Subsequent cerebrospinal fluid (CSF) analysis revealed 144 red blood cells per high-power field and an elevated protein of 96.5 mg/dL. The CSF was negative for culture, acid fast bacilli, India ink, fungus, and oligoclonal banding. Magnetic resonance imaging (MRI) performed the next day showed an area of intermediate signal density that did not enhance following contrast, commencing at C6 and extending to the level of T3 with mild to moderate cord compression, most prominent at T1 (Figure 2). This most likely represented a spinal epidural hematoma. While undergoing the initial radiographic procedures, the patient's symptoms began to spontaneously resolve, beginning with the recovery of sensation and motion in his toes. Emergent neurosurgical intervention was recommended but the patient refused. He was maintained on dexamethasone for the duration of his hospital stay. His hospital course was remarkable for almost complete neurological recovery within 96 hours after the onset of symptoms. He was able to walk with assistance within 24 hours and independently at 48 hours. His Foley catheter was removed in 72 hours and he had no problem urinating. He was discharged from the hospital 4 days after initial presentation with only mild lower extremity coordination defecits. He was advised to give up playing the clarinet, to refrain from any strenuous physical activities, and to avoid the use of aspirin, nonsteroidal anti-inflammatory drugs, and any other anticoagulant medications. A follow-up examination 1 month after discharge revealed resolution of the coordination defecits. MRI at that time showed no 391
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AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 14, Number 4 • July 1996
FIGURE 1. Myelogram with CT shows compression of spinal cord (a) by an epidural mass (b). evidence of epidural blood or spinal cord compression. As of follow-up 7 months later, he had had no further incidents.
DISCUSSION Spontaneous spinal epidural hematomas are unusual causes of spinal cord compression. The differential diagnosis includes transverse myelitis, acute ruptured intravertebral disc, epidural abscess or neoplasia, and pathological vertebral fractures. The clinical presentation is usually that of initial spinal pains at the level of the hemorrhage, 11 which may be followed by radicular pain. Varying degrees of motor and sensory defecits with urinary retention then develop. The symptoms are usually progressive and may be fatal, depend-
ing on the level of the hemorrhage and degree of cord compression. Respiratory failure is the most common cause of death. ~2The symptoms have been reported to progress to acute paraplegia, 13-18 quadraplegia, ~9 an anterior cord syndrome, 2° Brown Sequard syndromes, 21,22and a cauda equina syndrome. 23 The symptoms have been reported to have begun after episodes of apparently incidental trauma such as straining at stool, 19 micturation, 24,25 bending forward, 11 sneezingy and lifting. 26 In a review of the world literature by Foo and Rossier, 5 however, no probable cause for the development of SSEH could be found in a majority of cases. Factors reported to contribute to the development of this entity have been reported to be inherited bleeding disorders such as hemophilia, 6,27 factor XI deficiency, 21 and yon Willebrand's disease, 28 drug-induced bleeding disorders such as from the use of coumadin, 7,15,29-32 streptokinase and heparin, 33 dipyrimdamole and ticlopidine, 34 aspirin, 35 and naproxyn, ~2and other acquired bleeding disorders. 36,~v Anatomic predispositions include arteriovenous malformations, 16,2°,38-41 arterial aneurysms, 23 vascular neoplasms, 42 and Paget's DiseaseY In those cases found to have no underlying vascular abnormality the bleeding is believed to be venous in origin, 14,44 although an arterial etiology has been suggested. 12 Permanent spontaneous symptom resolution is extremely rare. Only five such cases have been reported. 6-a°A potential sixth case suffered a relapse 2 hours after initial symptom resolution. 45 Spontaneous spinal epidural hematomas should be considered immediate neurosurgical emergencies, z The risk of permanent neurological disability has been shown to be directly related to the rapidity with which the paralysis developed, the force of compression, the duration of paralysis, 2"4 and the severity of the neurological defecits prior to surgical decompression. 5
CONCLUSION Acute spontaneous spinal epidural hematomas are rare acute neurosurgical emergencies that must be considered early in the differential diagnosis of spinal cord compression to prevent permanent neurological disability or even death. Although rare cases have been known to undergo spontaneous resolution, others have been shown to relapse. A case of spontaneous spinal epidural hematoma with spinal cord compression and complete spontaneous resolution has been presented, along with a discussion of the etiologies, contributing factors, disease progression, and treatment recommendations.
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FIGURE 2. MRI shows compression the spinal cord (a) at Tl by the epidural hematoma (b).
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STEVEN H. SILBER • SPONTANEOUS SPINAL EPIDURAL HEMATOMA
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