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Spinal epidural hematoma associated with cocaine abuse
Spinal Epidural Hematoma Associated With Cocaine Abuse J. STEPHEN HUFF, MD A 41-year-old man rapidly developed quadriparesis moments after injactins cocaine. Investigation discovered a cervical spinal epidural hematoma. This complication of cocaine abuse has not been previously reported. (Am J Emerg Med 1994;12:350-352. Copyright 0 1994 by W.9. Saunders Company) Cocaine abuse is associated with many central nervous system (CNS) abnormalities, including ischemic strokes, in-
tracerebral hemorrhages, subarachnoid hemorrhage, seizures, and vasculitis. ‘-lo Most of these symptoms are secondary to involvement of the brain or vasculature. Spinal cord syndromes are less frequently reported.‘,” An intravenous (IV) user of cocaine suffered spinal cord compression from an extra-axial hematoma moments after injection. This potentially reversible condition should be considered in patients who develop quadriparesis associated with cocaine abuse. CASE REPORT A 41-year-old man was transferred from a rural hospital by air ambulance for evaluation of a possible spinal cord injury. Occult trauma was suspected. The patient was an IV drug user. After selfadministration of an injection of cocaine, he became weak. He initially had felt warm throughout his body and then immediately performed several stretching maneuvers that he described as standing push-up type exercises. He then experienced some pain in the neck radiating to his upper back as if something “pulled.” Weakness in the lower extremities developed as he walked toward a couch to recline; he was then unable to get up. Upper and lower extremities “lost all feeling.” The time from injection to severe weakness of the extremities and loss of sensation was 1 or 2 minutes. Additional history was remarkable for a 4-year history of ankylosing spondylitis. The patient was not taking anticoagulants. The patient had a history of episodic ethanol abuse. The outlying hospital noted weakness in the legs and variable strength in the upper extremities before transfer. A cervical collar was applied. Cervical spine radiographs were unremarkable except for changes consistent with ankylosing spondylitis. The clinical course during air transport was unremarkable. At arrival to the referral center 4 hours after the onset of weakness, the patient was awake and alert. Blood pressure was 110/70 mm Hg, and pulse was 70 beats/min. There were no signs of trauma. Neurological examination showed the absence of pin prick and proprioception below the C4 to C5 level. The patient could shrug his From the Department of Emergency Medicine, Eastern Virginia Graduate School of Medicine, Norfolk, VA. ManuscriDt received Julv 2, 1993; revision accented November 10, 1993. Address reprint requests to Dr Huff, Department of Emergency Medicine, Eastern Virginia Graduate School of Medicine. 600 Gresham Dr, Raleigh gldg, Room 204, Norfolk, VA 23507. Key Words: Cocaine, drug abuse, epidural hematoma, hematoma, quadriplegia, spinal cord. Copyright 0 1994 by W.B. Saunders Company 07356757/94/1203-0024$5.00/O
shoulders. The patient had weak contractions of the left biceps but was unable to resist any oppositional force to that muscle group. The right upper extremity was flaccid and without motor activity. There was no motor activity in the flaccid lower extremities. Muscle stretch reflexes were absent in all extremities. Rectal tone was lax. Priapism was present. Laboratory work included PT 13 (1 I- 13) and PTT 24 (20-35), both in the normal range. Immediate neurosurgical consultation was requested. A vascular injury to the spinal cord was suspected and a working diagnosis of spinal cord infarction was entertained. Arrangements were made for magnetic resonance imaging (MRI) later that day. MRI performed approximately 12 hours after arrival showed a mass posterior to the spinal cord extending from Cl to T3 with spinal cord compression between spaces C3-C4 and CS-C6 (Figure 1). This was thought to possibly represent dural thickening or an epidural mass. Computerized tomographic scan (CT) confirmed the epidural mass and spinal cord compression (Figure 2). The patient was taken to the operating room approximately 20 hours after the onset of weakness. A cervical laminectomy from C3 to C6 was performed. A liquified epidural hematoma was evacuated. Intraoperative ultrasound demonstrated cord decompression. There was no evidence of vascular malformation discovered during exploration. The patient made little neurological recovery postoperatively and was discharged quadriplegic to a rehabilitation facility.
DISCUSSION Cocaine is thought to cause injury to the CNS by several mechanisms. On the cellular level, cocaine causes interference with the normal functioning of sodium channels and also disrupts normal neurotransmitter functions. Hypertension and vasospasm associated with increased adrenergic stimulation are thought to be the mechanisms associated with most subarachnoid and intracerebral hemorrhages associated with cocaine abuse.‘s4 Stroke after cocaine use may be related to intracranial aneurysms or arteriovenous malformations in a few patients.6 Cerebral vasculitis has been documented in some cocaine users, but its role in cocainerelated stroke is unclear.‘.” Hemorrhage into a CNS tumor temporally related to cocaine use has also been reported.‘* Nervous system complications have been described after all of the different routes of cocaine administration. Levine et al found that cerebral infarction was more common after alkaloidal cocaine (crack) use than with cocaine hydrochloride users.’ With crack use, stroke seems evenly divided between ischemic and hemorrhagic forms. Hemorrhagic stroke occurs approximately twice as frequently as ischemic stroke in nasal (snorting) cocaine hydrochloride users. Only hemorrhagic stroke has been reported with IV cocaine use.‘*13 Seizures, altered mental status, subarachnoid hemorrhage, and headache are other frequently reported complications.‘-5 Spinal cord symptoms are rarely reported in association with cocaine use. Ischemic stroke of the spinal cord does occur.‘,” Anterior spinal artery syndrome’ and a complete syndrome with quadriplegia pattern have been reported.”
J. STEPHEN HUFF
m
351
SPINAL EPIOURAL tiEhd~~0MA
FIGURE 1. MRI showing an epidural mass with cord compression. The hematoma is shown as a dark mass impinging on the spinal canal.
The presence of a spinal cord syndrome in an IV drug abuser should raise the possibility of an epidural abscess. The onset of weakness with this condition is usually progressive over a period of hours or days. There may or may not be associated fever.14-16 Other diagnostic possibilities with nontraumatic spinal cord compression include transverse myelitis, metastatic tumors, spondylosis, herniated discs, rheumatic atlanto-axial dislocations, and spinal canal hemorrhages-epidural, subdural, subarachnoid, and intramedullary . ” Nontraumatic spinal epidural hematomas and subdural hematomas are unusual. Most frequently, they are associated with anticoagulant use. Another identified risk group are patients with liver disease and associated coagulopathy. However, spontaneous hematomas are reported. Sudden cervical or back pain followed by onset of neurological deficit in a spinal cord injury pattern are the characteristic clues toward
this diagnosis. The spinal cord injury may be from direct compression by the hematoma or result from vascular compromise to the spinal cord. Treatment is immediate surgical decompression. The preoperative state of the patient seems to correlate well with neurological recovery. If an incomplete sensorimotor syndrome is present, good recovery may be expected. If complete paraplegia or quadriplegia is present before decompression, the outlook for functional recovery is poor.‘8-20 This case is remarkable for the temporal association of cocaine use and the development of weakness from the epidural hematoma. Although CNS cerebrovascular complications are frequent with cocaine use, extra-axial hematomas have not been reported. The possibility of an occult vascular malformation cannot be excluded in this case, but this seems unlikely with the unremarkable surgical exploration. Spontaneous spinal epidural hematomas are at times associated with effort, l9 this patient’s stretching exercises may have had a contributing part. A pathophysiological mechanism involving increased adrenergic activity after cocaine use may have played a role. It is also possible that this patient by chance evolved a spinal epidural hematoma moments after injection of cocaine, but this seems unlikely in view of the very close temporal relationship of the events. In this case, a decision was made to defer neuroimaging until MRI was available later in the day. In another recently reported case of acute spinal epidural hematoma, a delay in neuroimaging also occurred while waiting for MRI availability.21 MRI is generally felt to be more sensitive in detecting intramedullary lesions such as infarction of the spinal cord. However, the clinical syndrome of spinal cord compression from an epidural hematoma may be identical to that of spinal cord ischemia. A basic principle in emergency management is to rapidly exclude the existence of a reversible process. CT was readily available at the time of this patient’s presentation, but was not ordered initially to avoid unnecessary duplication of tests. Either CT or myelography would most likely have demonstrated spinal cord compression and could have been performed more quickly. Assuming an irreversible lesion is present when the possibility of a reversible lesion has not been excluded may lead to clinical error. However, the fact that quadriplegia had been present for several hours makes the likelihood of recovery small even if decompression had occurred earlier. SUMMARY A 41-year-old man rapidly developed quadriparesis from a cervical epidural hematoma temporally related to cocaine injection. This association of spinal epidural hematoma with cocaine abuse has not been reported previously. The possibility of this potentially reversible lesion should be considered in patients with a new spinal cord syndrome and a recent history of cocaine use. REFERENCES
FIGURE 2. CT showing a dorsal epidural mass compressing cervical spinal cord.
the
1. Spivey WI-i, Euerle B: Neurologic complications of cocaine abuse. Ann Emerg Med 1990;19:1422-1428 2. Derlet RW, Albertson TE: Emergency department presentation of cocaine intoxication. Ann Emerg Med 1989;18:182-186 3. Rich JA, Singer DE: Cocaine-related symptoms in patients presenting to an urban emergency department. Ann Em&g Med 1991;20:616-621
352
AMERICAN JOURNAL OF EMERGENCY MEDICINE n Volume 12, Number 3 n May 1994
4. Brody SL, Slovis CM: Recognition and management of complications related to cocaine abuse. Emerg Med Rep 1988; 9:41-48 5. Holland RW, Marx JA, Earnest MP, et al: Grand mal seizures temporally related to cocaine use: Clinical and diagnostic features. Ann Emerg Med 1992;21:772-778 8. Klonoff DC, Andrews BT, Obaba WG: Stroke associated with cocaine use. Arch Neurol 1989;46:989-993 7. Levine SR, Brust JCM, Futrell N, et al: Cerebrovascular complications of the use of the “crack” form of alkaloidal cocaine. New Engl J Med 1990;323:699-704 8. Mody CK, Miller BL, McIntyre HB, et al: Neurologic complications of cocaine abuse. Neurology 1988;32:1189-1193 9. Krendel DA, Ditter SM, Frankel MR, et al: Biopsy-proven cerebral vasculitis associated with cocaine use. Neurology 1990; 40:1092-1094 10. Kaye BR, Fainstat M: Cerebral vasculitis associated with cocaine use. JAMA 1987;258:2104-2106 11. Sawaya GR, Kaminski MJ: Spinal cord infarction after cocaine use. Southern Med J 1990;83:601-602 12. Yapro WV, Gutierrez FA: Cocaine-induced intratumoral hemorrhage: Case report and review of the literature. Neurosurgery 1992;30:288-291
13. Levine SR, Brust JCM, Futrell N, et al: A comparative study of the cerebrovascular complications of cocaine: Alkaloidal versus hydrochloride-A review. Neurology 1991;41 :1173-1177 14. Koppel BS, Tuchman AH, Mangiardi JR, et al: Epidural spinal infection in intravenous drug users. Arch Neurol 1988;45: 1331-1337 15. Siao P, Yagnik P: Spinal epidural abscess. J Emerg Med 1988;6:391-396 16. Lasker BR, Harter DH: Cervical epidural abscess. Neurology 1987;37:1747-1753 17. Schmidt RD, Markovchick V: Nontraumatic spinal cord compression. J Emerg Med 1992;10:189-199 18. Mattle H, Sieb JP, Rohner M, et al: Nontraumatic spinal epidural and subdural hematomas. Neurology 1987;37:13511356 19. Demierre B, Unger P, Bongioanni F: Sudden cervical pain: Spontaneous cervical epidural hematoma. Am J Emerg Med 1991;9:54-56 20. Tomarken JL: Spinal subdural hematoma: A case report and literature review. Am J Emerg Med 1987;5:123-125 21. Joseph AP, Vinen JD: Acute spinal epidural hematoma. J Emerg Med 1993;11:437-441
tracerebral hemorrhages, subarachnoid hemorrhage, seizures, and vasculitis. ‘-lo Most of these symptoms are secondary to involvement of the brain or vasculature. Spinal cord syndromes are less frequently reported.‘,” An intravenous (IV) user of cocaine suffered spinal cord compression from an extra-axial hematoma moments after injection. This potentially reversible condition should be considered in patients who develop quadriparesis associated with cocaine abuse. CASE REPORT A 41-year-old man was transferred from a rural hospital by air ambulance for evaluation of a possible spinal cord injury. Occult trauma was suspected. The patient was an IV drug user. After selfadministration of an injection of cocaine, he became weak. He initially had felt warm throughout his body and then immediately performed several stretching maneuvers that he described as standing push-up type exercises. He then experienced some pain in the neck radiating to his upper back as if something “pulled.” Weakness in the lower extremities developed as he walked toward a couch to recline; he was then unable to get up. Upper and lower extremities “lost all feeling.” The time from injection to severe weakness of the extremities and loss of sensation was 1 or 2 minutes. Additional history was remarkable for a 4-year history of ankylosing spondylitis. The patient was not taking anticoagulants. The patient had a history of episodic ethanol abuse. The outlying hospital noted weakness in the legs and variable strength in the upper extremities before transfer. A cervical collar was applied. Cervical spine radiographs were unremarkable except for changes consistent with ankylosing spondylitis. The clinical course during air transport was unremarkable. At arrival to the referral center 4 hours after the onset of weakness, the patient was awake and alert. Blood pressure was 110/70 mm Hg, and pulse was 70 beats/min. There were no signs of trauma. Neurological examination showed the absence of pin prick and proprioception below the C4 to C5 level. The patient could shrug his From the Department of Emergency Medicine, Eastern Virginia Graduate School of Medicine, Norfolk, VA. ManuscriDt received Julv 2, 1993; revision accented November 10, 1993. Address reprint requests to Dr Huff, Department of Emergency Medicine, Eastern Virginia Graduate School of Medicine. 600 Gresham Dr, Raleigh gldg, Room 204, Norfolk, VA 23507. Key Words: Cocaine, drug abuse, epidural hematoma, hematoma, quadriplegia, spinal cord. Copyright 0 1994 by W.B. Saunders Company 07356757/94/1203-0024$5.00/O
shoulders. The patient had weak contractions of the left biceps but was unable to resist any oppositional force to that muscle group. The right upper extremity was flaccid and without motor activity. There was no motor activity in the flaccid lower extremities. Muscle stretch reflexes were absent in all extremities. Rectal tone was lax. Priapism was present. Laboratory work included PT 13 (1 I- 13) and PTT 24 (20-35), both in the normal range. Immediate neurosurgical consultation was requested. A vascular injury to the spinal cord was suspected and a working diagnosis of spinal cord infarction was entertained. Arrangements were made for magnetic resonance imaging (MRI) later that day. MRI performed approximately 12 hours after arrival showed a mass posterior to the spinal cord extending from Cl to T3 with spinal cord compression between spaces C3-C4 and CS-C6 (Figure 1). This was thought to possibly represent dural thickening or an epidural mass. Computerized tomographic scan (CT) confirmed the epidural mass and spinal cord compression (Figure 2). The patient was taken to the operating room approximately 20 hours after the onset of weakness. A cervical laminectomy from C3 to C6 was performed. A liquified epidural hematoma was evacuated. Intraoperative ultrasound demonstrated cord decompression. There was no evidence of vascular malformation discovered during exploration. The patient made little neurological recovery postoperatively and was discharged quadriplegic to a rehabilitation facility.
DISCUSSION Cocaine is thought to cause injury to the CNS by several mechanisms. On the cellular level, cocaine causes interference with the normal functioning of sodium channels and also disrupts normal neurotransmitter functions. Hypertension and vasospasm associated with increased adrenergic stimulation are thought to be the mechanisms associated with most subarachnoid and intracerebral hemorrhages associated with cocaine abuse.‘s4 Stroke after cocaine use may be related to intracranial aneurysms or arteriovenous malformations in a few patients.6 Cerebral vasculitis has been documented in some cocaine users, but its role in cocainerelated stroke is unclear.‘.” Hemorrhage into a CNS tumor temporally related to cocaine use has also been reported.‘* Nervous system complications have been described after all of the different routes of cocaine administration. Levine et al found that cerebral infarction was more common after alkaloidal cocaine (crack) use than with cocaine hydrochloride users.’ With crack use, stroke seems evenly divided between ischemic and hemorrhagic forms. Hemorrhagic stroke occurs approximately twice as frequently as ischemic stroke in nasal (snorting) cocaine hydrochloride users. Only hemorrhagic stroke has been reported with IV cocaine use.‘*13 Seizures, altered mental status, subarachnoid hemorrhage, and headache are other frequently reported complications.‘-5 Spinal cord symptoms are rarely reported in association with cocaine use. Ischemic stroke of the spinal cord does occur.‘,” Anterior spinal artery syndrome’ and a complete syndrome with quadriplegia pattern have been reported.”
J. STEPHEN HUFF
m
351
SPINAL EPIOURAL tiEhd~~0MA
FIGURE 1. MRI showing an epidural mass with cord compression. The hematoma is shown as a dark mass impinging on the spinal canal.
The presence of a spinal cord syndrome in an IV drug abuser should raise the possibility of an epidural abscess. The onset of weakness with this condition is usually progressive over a period of hours or days. There may or may not be associated fever.14-16 Other diagnostic possibilities with nontraumatic spinal cord compression include transverse myelitis, metastatic tumors, spondylosis, herniated discs, rheumatic atlanto-axial dislocations, and spinal canal hemorrhages-epidural, subdural, subarachnoid, and intramedullary . ” Nontraumatic spinal epidural hematomas and subdural hematomas are unusual. Most frequently, they are associated with anticoagulant use. Another identified risk group are patients with liver disease and associated coagulopathy. However, spontaneous hematomas are reported. Sudden cervical or back pain followed by onset of neurological deficit in a spinal cord injury pattern are the characteristic clues toward
this diagnosis. The spinal cord injury may be from direct compression by the hematoma or result from vascular compromise to the spinal cord. Treatment is immediate surgical decompression. The preoperative state of the patient seems to correlate well with neurological recovery. If an incomplete sensorimotor syndrome is present, good recovery may be expected. If complete paraplegia or quadriplegia is present before decompression, the outlook for functional recovery is poor.‘8-20 This case is remarkable for the temporal association of cocaine use and the development of weakness from the epidural hematoma. Although CNS cerebrovascular complications are frequent with cocaine use, extra-axial hematomas have not been reported. The possibility of an occult vascular malformation cannot be excluded in this case, but this seems unlikely with the unremarkable surgical exploration. Spontaneous spinal epidural hematomas are at times associated with effort, l9 this patient’s stretching exercises may have had a contributing part. A pathophysiological mechanism involving increased adrenergic activity after cocaine use may have played a role. It is also possible that this patient by chance evolved a spinal epidural hematoma moments after injection of cocaine, but this seems unlikely in view of the very close temporal relationship of the events. In this case, a decision was made to defer neuroimaging until MRI was available later in the day. In another recently reported case of acute spinal epidural hematoma, a delay in neuroimaging also occurred while waiting for MRI availability.21 MRI is generally felt to be more sensitive in detecting intramedullary lesions such as infarction of the spinal cord. However, the clinical syndrome of spinal cord compression from an epidural hematoma may be identical to that of spinal cord ischemia. A basic principle in emergency management is to rapidly exclude the existence of a reversible process. CT was readily available at the time of this patient’s presentation, but was not ordered initially to avoid unnecessary duplication of tests. Either CT or myelography would most likely have demonstrated spinal cord compression and could have been performed more quickly. Assuming an irreversible lesion is present when the possibility of a reversible lesion has not been excluded may lead to clinical error. However, the fact that quadriplegia had been present for several hours makes the likelihood of recovery small even if decompression had occurred earlier. SUMMARY A 41-year-old man rapidly developed quadriparesis from a cervical epidural hematoma temporally related to cocaine injection. This association of spinal epidural hematoma with cocaine abuse has not been reported previously. The possibility of this potentially reversible lesion should be considered in patients with a new spinal cord syndrome and a recent history of cocaine use. REFERENCES
FIGURE 2. CT showing a dorsal epidural mass compressing cervical spinal cord.
the
1. Spivey WI-i, Euerle B: Neurologic complications of cocaine abuse. Ann Emerg Med 1990;19:1422-1428 2. Derlet RW, Albertson TE: Emergency department presentation of cocaine intoxication. Ann Emerg Med 1989;18:182-186 3. Rich JA, Singer DE: Cocaine-related symptoms in patients presenting to an urban emergency department. Ann Em&g Med 1991;20:616-621
352
AMERICAN JOURNAL OF EMERGENCY MEDICINE n Volume 12, Number 3 n May 1994
4. Brody SL, Slovis CM: Recognition and management of complications related to cocaine abuse. Emerg Med Rep 1988; 9:41-48 5. Holland RW, Marx JA, Earnest MP, et al: Grand mal seizures temporally related to cocaine use: Clinical and diagnostic features. Ann Emerg Med 1992;21:772-778 8. Klonoff DC, Andrews BT, Obaba WG: Stroke associated with cocaine use. Arch Neurol 1989;46:989-993 7. Levine SR, Brust JCM, Futrell N, et al: Cerebrovascular complications of the use of the “crack” form of alkaloidal cocaine. New Engl J Med 1990;323:699-704 8. Mody CK, Miller BL, McIntyre HB, et al: Neurologic complications of cocaine abuse. Neurology 1988;32:1189-1193 9. Krendel DA, Ditter SM, Frankel MR, et al: Biopsy-proven cerebral vasculitis associated with cocaine use. Neurology 1990; 40:1092-1094 10. Kaye BR, Fainstat M: Cerebral vasculitis associated with cocaine use. JAMA 1987;258:2104-2106 11. Sawaya GR, Kaminski MJ: Spinal cord infarction after cocaine use. Southern Med J 1990;83:601-602 12. Yapro WV, Gutierrez FA: Cocaine-induced intratumoral hemorrhage: Case report and review of the literature. Neurosurgery 1992;30:288-291
13. Levine SR, Brust JCM, Futrell N, et al: A comparative study of the cerebrovascular complications of cocaine: Alkaloidal versus hydrochloride-A review. Neurology 1991;41 :1173-1177 14. Koppel BS, Tuchman AH, Mangiardi JR, et al: Epidural spinal infection in intravenous drug users. Arch Neurol 1988;45: 1331-1337 15. Siao P, Yagnik P: Spinal epidural abscess. J Emerg Med 1988;6:391-396 16. Lasker BR, Harter DH: Cervical epidural abscess. Neurology 1987;37:1747-1753 17. Schmidt RD, Markovchick V: Nontraumatic spinal cord compression. J Emerg Med 1992;10:189-199 18. Mattle H, Sieb JP, Rohner M, et al: Nontraumatic spinal epidural and subdural hematomas. Neurology 1987;37:13511356 19. Demierre B, Unger P, Bongioanni F: Sudden cervical pain: Spontaneous cervical epidural hematoma. Am J Emerg Med 1991;9:54-56 20. Tomarken JL: Spinal subdural hematoma: A case report and literature review. Am J Emerg Med 1987;5:123-125 21. Joseph AP, Vinen JD: Acute spinal epidural hematoma. J Emerg Med 1993;11:437-441