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Spinal epidural hematoma causing acute cauda equina syndrome KHALED M. KEBAISH, M.D., F.R.C.S.(C), AND JOHN N. AWAD, M.D. Department of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland Spinal epidural hematoma (SEH) is an uncommon cause of acute cauda equina syndrome. Most of these hematomas are caused by trauma, anticoagulation therapy, and vascular anomalies or occur following spinal epidural procedures and, rarely, spinal surgery. Spontaneous SEH is an extremely rare occurrence. The incidence of symptomatic postoperative SEH is 0.1 to 3%. Clinical evaluation is the most important tool in the early diagnosis of SEH. Once the disease is suspected clinically and confirmed on diagnostic imaging, emergency evacuation of the lesion should be performed. Prognosis depends on the rate of development of symptoms, interval to surgery, level of spinal involvement, and degree of neurological deficit.
KEY WORDS • epidural hematoma • cauda equina syndrome • epidural hematoma
Spinal epidural hematoma is an uncommon cause of acute CES. A description by Jackson11 in 1869 is credited as the first official record of an SEH. Since that time, several hundred cases with various origins have been reported in the literature.3–36 Most are the result of trauma, anticoagulation therapy, vascular anomalies, and blood dyscrasias or occur following spinal epidural procedures and, rarely, spinal surgery. INCIDENCE OF SEH Spontaneous SEH is an extremely rare occurrence and its exact incidence is unknown. Nonetheless, it should be suspected in patients who are undergoing anticoagulation therapy or thrombolysis. The incidence of postoperative SEH requiring evacuation ranges from 0.1 to 3%.8,16 In a review of 14,932 patients who had undergone spinal surgery at our institution between August 1984 and December 2002, we identified 32 who had developed this postoperative complication and required surgical intervention, revealing an overall incidence of 0.2%. A control group was selected, consisting of patients who had undergone a procedure of equal complexity, performed by the same surgeon within 1 month of the procedure. Three control patients were selected for each case of postoperative SEH. We conducted a detailed review of medical charts obtained in patients in the postoperative SEH and control groups. The variables considered were categorized. Abbreviations used in this paper: CES = cauda equina syndrome; CT = computerized tomography; DVT = deep venous thrombosis; MR = magnetic resonance; SEH = spinal epidural hematoma.
Neurosurg. Focus / Volume 16 / June, 2004
Data were analyzed using a multiple logistic regression model to determine both the significance of individual factors independent of other variables and the odds ratios for those significant factors. This method allowed us to control for the effects of other independent variables to assess the true significance of an independent variable being analyzed. A probability value less than 0.05 indicated statistical significance. Preoperative variables that were significant risks for postoperative SEH included an age older than 60 years, the use of preoperative nonsteroidal antiinflammatory drugs, and an Rh-positive blood type. Intraoperative variables that proved to be significant included more than five spinal levels subjected to surgery, hemoglobin level less than 10 g/dl, and blood loss of more than 1 L. Length of surgery, requiring fresh-frozen plasma or platelets, and the use of a cell saver were not significant risk factors of postoperative SEH. Postoperatively, significant variables included prothrombin time and international normalized ratio greater than 2 within the first 48 hours. The use of well-controlled anticoagulation therapy for DVT and/or cardiovascular prophylaxis, and subfascial drains were not directly associated with the development of postoperative SEH. Although their use is controversial, drains are commonly used in spine surgery as a prophylaxis against a hematoma that may cause neurological compromise or wound complications. A search of the literature revealed no reports supporting this hypothesis, however. In fact, Kou, et al.,15 have asserted that drains have no preventive effect on the development of postoperative SEH, and the authors of the only prospective study22 to date on the use of drains in spine surgery found that among patients who had un1
K. M. Kebaish and J. N. Awad dergone single-level lumbar laminectomies, there was no significant difference in postoperative wound infection, neurological deficits, or wound healing in a comparison of those with a drain and those without. In our study, most of the patients in the postoperative SEH and control groups had drains, and although determining the true value of drain function was not our intent, results of our analysis indicated that drain use was not a significant variable. Another concern is the use of anticoagulation therapy postoperatively. Numerous case reports feature an association between spontaneous SEH and the use of anticoagulation therapy.4,19,35 The specific use of anticoagulation agents (coumadin or low-molecular-weight heparin) for DVT prophylaxis has not been associated with the formation of a symptomatic hematoma, but patients in our study who had coagulopathy from the procedure itself or from overmedication with anticoagulant agents demonstrated a higher risk of postoperative SEH. This finding indicates that using anticoagulation postoperatively for either DVT prophylaxis or cardiovascular prophylaxis is safe as long as such use is monitored carefully. ORIGINS OF SEH Although spontaneous SEH almost always occurs following a spinal surgical procedure,34 the majority of these hematomas are clinically asymptomatic. On rare occasions, however, SEH can cause clinically significant spinal cord or nerve root compression (CES), necessitating surgical intervention.3 The literature features incidence rates of postoperative SEH requiring evacuation ranging from 0.1 to 3%.8,16 Although rare, these symptomatic postoperative SEHs can have devastating neurological consequences. PATHOPHYSIOLOGY OF SEH With regard to spontaneous SEH, some hypothesize that rupture of the internal vertebral venous plexus of Batson leads to these idiopathic hematomas.9 Extrapolating from this hypothesis to the surgical population, Kou, et al.,15 theorized that multilevel procedures increased the risk of rupture in this venous plexus, thus increasing the risk for the development of a compressive hematoma. Although this assertion has not been validated, the highly vascular nature of the spinal column can, in fact, result in high blood loss, especially during arthrodesis.10 In a series of investigations of spinal cord compression in dogs, Tarlov and colleagues29–33 concluded that recovery depended on both the magnitude and duration of cord compression. This finding was reconfirmed by data in the dog model of Delamarter, et al.5 Note, however, that studies of the effect of the magnitude and duration of cord compression on recovery in humans have produced conflicting results: Lawton, et al.,16 and McQuarrie19 showed that these findings correlated with those in humans, but other researchers6,8,14 have shown no correlation between duration of compression and functional recovery. DIAGNOSTIC EVALUATION Clinical evaluation is the most important tool in the early diagnosis of SEH. It is very important to obtain detailed 2
baseline neurological data in the immediate postoperative period, including that gathered during a rectal examination, once the patient is awake and cooperative. This will help in differentiation between neurological injury that occurred intraoperatively and that suffered postoperatively as a result of SEH, thus avoiding expensive testing and possible litigation. Often patients have few complaints initially, but significant, increasing back pain subsequently develops. This may progress to unremitting leg pain or even CES in severe cases. A complete and detailed neurological examination is mandatory and should include rectal examination and perianal pinprick sensation.37 If there is the least degree of suspicion, a careful sequential examination should be performed at short intervals. If there is new or significant neurological deterioration, emergency spinal imaging should be undertaken. Radiography and CT studies are helpful in patients with a history of acute trauma to evaluate associated fractures or dislocation preoperatively and to assess placement of instrumentation postoperatively. Magnetic resonance imaging is the preferred method in patients who do not have spinal instrumentation. The MR imaging characteristics are very specific.2 On sagittal sections, an SEH appears as a clearly outlined biconvex mass dorsal to the thecal sac, with tapering superior and inferior margins. The dura mater is visualized as a curvilinear low signal, separating the hematoma from the spinal cord. Within 24 hours of its onset, the hematoma is isointense with the cord on T1-weighted images and heterogenous on T2-weighted images. Later, it produces a high signal on both T1- and T2-weighted images.2 Myelography followed by CT scanning is indicated in patients who have spinal instrumentation, especially because the details of the spinal canal are often obscured by metal artifacts on MR images. Postmyelography CT studies with coronal and sagittal reconstruction provides a very detailed and accurate anatomical picture of the spinal canal and is the recommended method in patients with postoperative neurological deficit when instrumentation is used. The hematoma is demonstrated as a biconcave dorsal mass filling defects in the spinal canal and usually extending over more than two vertebral levels. In addition to obtaining the appropriate imaging mentioned, one should acquire a coagulation profile including the international normalized ratio, prothrombin time, activated partial thromboplastin time, and platelet count. In select cases, bleeding time might also be required. Detailed clinical evaluation remains the most valuable tool in providing early diagnosis of this serious problem. TREATMENT OF SEH Once the disease is suspected clinically and confirmed on diagnostic imaging, emergency evacuation of the hematoma in the operating room should be performed. In spontaneous SEH, posterior exposure should involve all the spinal levels affected as demonstrated on preoperative scans. Complete laminectomy is then performed and should include the entire length of the compressed spinal canal. Blood should be evacuated and any organized clot carefully peeled off the dura and the nerve roots. Rarely, active epidural bleeding is found and should be cauterized using bipolar electrocautery. Neurosurg. Focus / Volume 16 / June, 2004
Spinal epidural hematoma causing acute cauda equina syndrome Postoperative SEH usually occurs in cases in which laminectomy was part of the initial procedure. In this event, after making the original incision, blood clots should be evacuated, the laminectomy extended proximally or distally if necessary, the epidural space carefully inspected for any bone graft material that may be contributing to compression, and any offending bone graft material removed. On completion of the procedure, a small rubber catheter should be passed in the epidural space proximal and distal to the involved levels, while looking for any blockage. Although the use of subfascial drains is controversial and was not shown to provide a protective effect against SEH following posterior spinal procedures in our patient population, we do recommend the routine placement of subfascial drains following evacuation of SEH. The use of systemic steroid agents has been shown to be beneficial, although it may increase the risk of wound complications. Percutaneous CT-guided aspiration has been performed for spontaneous SEH; however, we do not recommend the procedure unless the patient’s medical condition precludes surgical intervention. PROGNOSIS OF SEH Prognosis depends on the rate of development of symptoms, time to surgery, level of spinal involvement, and degree of neurological deficit. The results are most favorable if decompression is accomplished early. In our series as well as those of others, full recovery from paraplegia with timely surgical intervention has occurred. In our review, the patients who had undergone exploration and evacuation within 6 hours of symptom onset (seven patients) experienced the greatest neurological recovery (a mean of one Frankel grade), whereas those who had decompression after 6 hours (23 patients) experienced less improvement ( one Frankel grade). Interestingly, those who were taken to the operating room within 6 hours had a more significant preevacution neurological deficit than did the patients who underwent decompression after 6 hours. A possible explanation for this is that the second group of patients developed a more insidious onset, which was noticed before significant neurological compromise, but the recovery time was shorter given the length of time the spinal cord had been compressed. CONCLUSIONS Spinal epidural hematoma is an uncommon cause of acute CES. Most of these lesions are the result of trauma, anticoagulation therapy, vascular anomalies, blood dyscrasias, spinal epidural procedures, and spinal surgery. Although rare, SEHs can cause clinically significant spinal cord and cauda equina compression, necessitating surgical intervention.3 Investigators report incidence rates of postoperative SEH requiring evacuation ranging from 0.1 to 3%.8,16 Although rare, symptomatic postoperative SEHs can have devastating neurological consequences. Clinical evaluation is the most important tool in the early diagnosis of SEH. Detailed postoperative neurological examination is mandatory and should be performed as Neurosurg. Focus / Volume 16 / June, 2004
soon as the patient is awake and cooperative. Diagnostic studies include plain radiography, MR imaging, and myelography followed by CT studies, depending on whether instrumentation is used. As soon as the diagnosis is established, emergency treatment including surgical exploration and evacuation of the hematoma should be performed without delay.
References 1. Antonacci MD, Eismont F: Neurologic complications after lumbar spine surgery. J Am Acad Orthop Surg 9:137–145, 2001 2. Boukobza M, Guichard JP, Boissonet M, et al: Spinal epidural haematoma: report of 11 cases and review of the literature. Neuroradiology 36:456–459, 1994 3. Cabana F, Pointillart V, Vital J, et al: [Postoperative compressive spinal epidural hematomas. 15 cases and a review of the literature.] Rev Chir Orthop Reparatrice Appar Mot 86: 335–345, 2000 (Fre) 4. Connolly ES Jr, Winfree CJ, McCormick PC: Management of spinal epidural hematoma after tissue plasminogen activator. A case report. Spine 21:1694–1698, 1996 5. Delamarter RB, Sherman J, Carr JB: Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg Am 77:1042–1049, 1995 6. Deyo RA, Cherkin DC, Loeser JD, et al: Morbidity and mortality in association with operations on the lumbar spine. The influence of age, diagnosis, and procedure. J Bone Joint Surg Am 74:536–543, 1992 7. Esler CN, Blakeway C, Fiddian NJ: The use of a closed-suction drain in total knee arthroplasty. A prospective, randomised study. J Bone Joint Surg Br 85:215–217, 2003 8. Foo D, Rossier AB: Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas. Surg Neurol 15:389–401, 1981 9. Groen RJ, Ponssen H: The spontaneous spinal epidural hematoma. A study of the etiology. J Neurol Sci 98:121–138, 1990 10. Gundry CR, Heithoff KB: Epidural hematoma of the lumbar spine: 18 surgically confirmed cases. Radiology 187:427–431, 1993 11. Jackson R: Case of spinal apoplexy. Lancet 2:5–6, 1869 12. Jagodzinski M, Krettek C: [Drains in trauma surgery.] Chirurg 74:115–117, 2003 (Ger) 13. Johnston RA: The management of acute spinal cord compression. J Neurol Neurosurg Psychiatry 56:1046–1054, 1993 14. Kostuik JP, Harrington I, Alexander D, et al: Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg Am 68: 386–391, 1986 15. Kou J, Fischgrund J, Biddinger A, et al: Risk factors for spinal epidural hematoma after spinal surgery. Spine 27:1670–1673, 2002 16. Lawton MT, Porter RW, Heiserman JE, et al: Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome. J Neurosurg 83:1–7, 1995 17. Manian FA, Meyer PL, Setzer J, et al: Surgical site infections associated with methicillin-resistant Staphylococcus aureus: do postoperative factors play a role? Clin Infect Dis 36:863–868, 2003 18. Markham JW, Lynge HN, Stahlman GE: The syndrome of spontaneous spinal epidural hematoma. Report of three cases. J Neurosurg 26:334–342, 1967 19. McQuarrie IG: Recovery from paraplegia caused by spontaneous spinal epidural hematoma. Neurology 28:224–228, 1978 20. Mirkovic S, Melany M: A thoracolumbar epidural hematoma simulating a disc syndrome. J Spinal Disord 5:112–115, 1992
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K. M. Kebaish and J. N. Awad 21. Mracek Z: Spontaneous spinal epidural hematoma. Experiences with four patients and a review of the literature. Zentralbl Neurochir 41:19–30, 1980 22. Payne DH, Fischgrund JS, Herkowitz HN, et al: Efficacy of closed wound suction drainage after single-level lumbar laminectomy. J Spinal Disord 9:401–403, 1996 23. Pendl G, Ganglberger JA, Horcajada J: [Spinal epidural hematoma.] Acta Neurochir 24:207–217, 1971 (Ger) 24. Rainov NG, Heidecke V, Burkert WL: Spinal epidural hematoma. Report of a case and review of the literature. Neurosurg Rev 18:53–60, 1995 25. Sasso RC, Williams JI, Dimasi N, et al: Postoperative drains at the donor sites of iliac-crest bone grafts. A prospective, randomized study of morbidity at the donor site in patients who had a traumatic injury of the spine. J Bone Joint Surg Am 80: 631–635, 1998 26. Scavarda D, Peruzzi P, Bazin A, et al: [Postoperative spinal extradural hematomas. 14 cases.] Neurochirurgie 43:220–227, 1997 (Fre) 27. Silverstein A: Neurological complications of anticoagulation therapy: a neurologist’s review. Arch Intern Med 139: 217–220, 1979 28. Spanier DE, Stambough JL: Delayed postoperative epidural hematoma formation after heparinization in lumbar spinal surgery. J Spinal Disord 13:46–49, 2000 29. Tarlov IM: Acute spinal cord compression paralysis. J Neurosurg 36:10–20, 1972 30. Tarlov IM: Spinal cord compression studies. III. Time limits for recovery after gradual compression in dogs. AMA Arch Neurol Psychiatry 71:588–597, 1954
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31. Tarlov IM, Herz E: Spinal cord compression studies. IV. Outlook with complete paralysis in man. AMA Arch Neurol Psychiatry 72:43–59, 1954 32. Tarlov IM, Klinger H: Spinal cord compression studies: II. Time limits for recovery after acute compression in dogs. AMA Arch Neurol Psychiatry 71:271–290, 1954 33. Tarlov IM, Klinger H, Vitale S: Spinal cord compression studies. I. Experimental techniques to produce acute and gradual compression. AMA Arch Neurol Psychiatry 70:813–819, 1953 34. Teplick JG, Haskin ME: Review. Computed tomography of the postoperative lumbar spine. AJR 141:865–884, 1983 35. Van Schaeybroeck P, Van Calenbergh F, Van De Werf F, et al: Spontaneous spinal epidural hematoma associated with thrombolysis and anticoagulation therapy: report of three cases. Clin Neurol Neurosurg 100:283–287, 1998 36. Wittebol MC, van Veelen CW: Spontaneous spinal epidural haematoma. Etiological considerations. Clin Neurol Neurosurg 86:265–270, 1984 37. Yonenobu K, Hosono N, Iwasaki M, et al: Neurologic complications of surgery for cervical compression myelopathy. Spine 16:1277–1282, 1991 Manuscript received April 29, 2004. Accepted in final form May 24, 2004. Address reprint requests to: Khaled M Kebaish, M.D., Department of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, 601 North Caroline Street, Suite 5244, Baltimore, Maryland 21287. email: [email protected].
Neurosurg. Focus / Volume 16 / June, 2004
Spinal epidural hematoma causing acute cauda equina syndrome KHALED M. KEBAISH, M.D., F.R.C.S.(C), AND JOHN N. AWAD, M.D. Department of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland Spinal epidural hematoma (SEH) is an uncommon cause of acute cauda equina syndrome. Most of these hematomas are caused by trauma, anticoagulation therapy, and vascular anomalies or occur following spinal epidural procedures and, rarely, spinal surgery. Spontaneous SEH is an extremely rare occurrence. The incidence of symptomatic postoperative SEH is 0.1 to 3%. Clinical evaluation is the most important tool in the early diagnosis of SEH. Once the disease is suspected clinically and confirmed on diagnostic imaging, emergency evacuation of the lesion should be performed. Prognosis depends on the rate of development of symptoms, interval to surgery, level of spinal involvement, and degree of neurological deficit.
KEY WORDS • epidural hematoma • cauda equina syndrome • epidural hematoma
Spinal epidural hematoma is an uncommon cause of acute CES. A description by Jackson11 in 1869 is credited as the first official record of an SEH. Since that time, several hundred cases with various origins have been reported in the literature.3–36 Most are the result of trauma, anticoagulation therapy, vascular anomalies, and blood dyscrasias or occur following spinal epidural procedures and, rarely, spinal surgery. INCIDENCE OF SEH Spontaneous SEH is an extremely rare occurrence and its exact incidence is unknown. Nonetheless, it should be suspected in patients who are undergoing anticoagulation therapy or thrombolysis. The incidence of postoperative SEH requiring evacuation ranges from 0.1 to 3%.8,16 In a review of 14,932 patients who had undergone spinal surgery at our institution between August 1984 and December 2002, we identified 32 who had developed this postoperative complication and required surgical intervention, revealing an overall incidence of 0.2%. A control group was selected, consisting of patients who had undergone a procedure of equal complexity, performed by the same surgeon within 1 month of the procedure. Three control patients were selected for each case of postoperative SEH. We conducted a detailed review of medical charts obtained in patients in the postoperative SEH and control groups. The variables considered were categorized. Abbreviations used in this paper: CES = cauda equina syndrome; CT = computerized tomography; DVT = deep venous thrombosis; MR = magnetic resonance; SEH = spinal epidural hematoma.
Neurosurg. Focus / Volume 16 / June, 2004
Data were analyzed using a multiple logistic regression model to determine both the significance of individual factors independent of other variables and the odds ratios for those significant factors. This method allowed us to control for the effects of other independent variables to assess the true significance of an independent variable being analyzed. A probability value less than 0.05 indicated statistical significance. Preoperative variables that were significant risks for postoperative SEH included an age older than 60 years, the use of preoperative nonsteroidal antiinflammatory drugs, and an Rh-positive blood type. Intraoperative variables that proved to be significant included more than five spinal levels subjected to surgery, hemoglobin level less than 10 g/dl, and blood loss of more than 1 L. Length of surgery, requiring fresh-frozen plasma or platelets, and the use of a cell saver were not significant risk factors of postoperative SEH. Postoperatively, significant variables included prothrombin time and international normalized ratio greater than 2 within the first 48 hours. The use of well-controlled anticoagulation therapy for DVT and/or cardiovascular prophylaxis, and subfascial drains were not directly associated with the development of postoperative SEH. Although their use is controversial, drains are commonly used in spine surgery as a prophylaxis against a hematoma that may cause neurological compromise or wound complications. A search of the literature revealed no reports supporting this hypothesis, however. In fact, Kou, et al.,15 have asserted that drains have no preventive effect on the development of postoperative SEH, and the authors of the only prospective study22 to date on the use of drains in spine surgery found that among patients who had un1
K. M. Kebaish and J. N. Awad dergone single-level lumbar laminectomies, there was no significant difference in postoperative wound infection, neurological deficits, or wound healing in a comparison of those with a drain and those without. In our study, most of the patients in the postoperative SEH and control groups had drains, and although determining the true value of drain function was not our intent, results of our analysis indicated that drain use was not a significant variable. Another concern is the use of anticoagulation therapy postoperatively. Numerous case reports feature an association between spontaneous SEH and the use of anticoagulation therapy.4,19,35 The specific use of anticoagulation agents (coumadin or low-molecular-weight heparin) for DVT prophylaxis has not been associated with the formation of a symptomatic hematoma, but patients in our study who had coagulopathy from the procedure itself or from overmedication with anticoagulant agents demonstrated a higher risk of postoperative SEH. This finding indicates that using anticoagulation postoperatively for either DVT prophylaxis or cardiovascular prophylaxis is safe as long as such use is monitored carefully. ORIGINS OF SEH Although spontaneous SEH almost always occurs following a spinal surgical procedure,34 the majority of these hematomas are clinically asymptomatic. On rare occasions, however, SEH can cause clinically significant spinal cord or nerve root compression (CES), necessitating surgical intervention.3 The literature features incidence rates of postoperative SEH requiring evacuation ranging from 0.1 to 3%.8,16 Although rare, these symptomatic postoperative SEHs can have devastating neurological consequences. PATHOPHYSIOLOGY OF SEH With regard to spontaneous SEH, some hypothesize that rupture of the internal vertebral venous plexus of Batson leads to these idiopathic hematomas.9 Extrapolating from this hypothesis to the surgical population, Kou, et al.,15 theorized that multilevel procedures increased the risk of rupture in this venous plexus, thus increasing the risk for the development of a compressive hematoma. Although this assertion has not been validated, the highly vascular nature of the spinal column can, in fact, result in high blood loss, especially during arthrodesis.10 In a series of investigations of spinal cord compression in dogs, Tarlov and colleagues29–33 concluded that recovery depended on both the magnitude and duration of cord compression. This finding was reconfirmed by data in the dog model of Delamarter, et al.5 Note, however, that studies of the effect of the magnitude and duration of cord compression on recovery in humans have produced conflicting results: Lawton, et al.,16 and McQuarrie19 showed that these findings correlated with those in humans, but other researchers6,8,14 have shown no correlation between duration of compression and functional recovery. DIAGNOSTIC EVALUATION Clinical evaluation is the most important tool in the early diagnosis of SEH. It is very important to obtain detailed 2
baseline neurological data in the immediate postoperative period, including that gathered during a rectal examination, once the patient is awake and cooperative. This will help in differentiation between neurological injury that occurred intraoperatively and that suffered postoperatively as a result of SEH, thus avoiding expensive testing and possible litigation. Often patients have few complaints initially, but significant, increasing back pain subsequently develops. This may progress to unremitting leg pain or even CES in severe cases. A complete and detailed neurological examination is mandatory and should include rectal examination and perianal pinprick sensation.37 If there is the least degree of suspicion, a careful sequential examination should be performed at short intervals. If there is new or significant neurological deterioration, emergency spinal imaging should be undertaken. Radiography and CT studies are helpful in patients with a history of acute trauma to evaluate associated fractures or dislocation preoperatively and to assess placement of instrumentation postoperatively. Magnetic resonance imaging is the preferred method in patients who do not have spinal instrumentation. The MR imaging characteristics are very specific.2 On sagittal sections, an SEH appears as a clearly outlined biconvex mass dorsal to the thecal sac, with tapering superior and inferior margins. The dura mater is visualized as a curvilinear low signal, separating the hematoma from the spinal cord. Within 24 hours of its onset, the hematoma is isointense with the cord on T1-weighted images and heterogenous on T2-weighted images. Later, it produces a high signal on both T1- and T2-weighted images.2 Myelography followed by CT scanning is indicated in patients who have spinal instrumentation, especially because the details of the spinal canal are often obscured by metal artifacts on MR images. Postmyelography CT studies with coronal and sagittal reconstruction provides a very detailed and accurate anatomical picture of the spinal canal and is the recommended method in patients with postoperative neurological deficit when instrumentation is used. The hematoma is demonstrated as a biconcave dorsal mass filling defects in the spinal canal and usually extending over more than two vertebral levels. In addition to obtaining the appropriate imaging mentioned, one should acquire a coagulation profile including the international normalized ratio, prothrombin time, activated partial thromboplastin time, and platelet count. In select cases, bleeding time might also be required. Detailed clinical evaluation remains the most valuable tool in providing early diagnosis of this serious problem. TREATMENT OF SEH Once the disease is suspected clinically and confirmed on diagnostic imaging, emergency evacuation of the hematoma in the operating room should be performed. In spontaneous SEH, posterior exposure should involve all the spinal levels affected as demonstrated on preoperative scans. Complete laminectomy is then performed and should include the entire length of the compressed spinal canal. Blood should be evacuated and any organized clot carefully peeled off the dura and the nerve roots. Rarely, active epidural bleeding is found and should be cauterized using bipolar electrocautery. Neurosurg. Focus / Volume 16 / June, 2004
Spinal epidural hematoma causing acute cauda equina syndrome Postoperative SEH usually occurs in cases in which laminectomy was part of the initial procedure. In this event, after making the original incision, blood clots should be evacuated, the laminectomy extended proximally or distally if necessary, the epidural space carefully inspected for any bone graft material that may be contributing to compression, and any offending bone graft material removed. On completion of the procedure, a small rubber catheter should be passed in the epidural space proximal and distal to the involved levels, while looking for any blockage. Although the use of subfascial drains is controversial and was not shown to provide a protective effect against SEH following posterior spinal procedures in our patient population, we do recommend the routine placement of subfascial drains following evacuation of SEH. The use of systemic steroid agents has been shown to be beneficial, although it may increase the risk of wound complications. Percutaneous CT-guided aspiration has been performed for spontaneous SEH; however, we do not recommend the procedure unless the patient’s medical condition precludes surgical intervention. PROGNOSIS OF SEH Prognosis depends on the rate of development of symptoms, time to surgery, level of spinal involvement, and degree of neurological deficit. The results are most favorable if decompression is accomplished early. In our series as well as those of others, full recovery from paraplegia with timely surgical intervention has occurred. In our review, the patients who had undergone exploration and evacuation within 6 hours of symptom onset (seven patients) experienced the greatest neurological recovery (a mean of one Frankel grade), whereas those who had decompression after 6 hours (23 patients) experienced less improvement ( one Frankel grade). Interestingly, those who were taken to the operating room within 6 hours had a more significant preevacution neurological deficit than did the patients who underwent decompression after 6 hours. A possible explanation for this is that the second group of patients developed a more insidious onset, which was noticed before significant neurological compromise, but the recovery time was shorter given the length of time the spinal cord had been compressed. CONCLUSIONS Spinal epidural hematoma is an uncommon cause of acute CES. Most of these lesions are the result of trauma, anticoagulation therapy, vascular anomalies, blood dyscrasias, spinal epidural procedures, and spinal surgery. Although rare, SEHs can cause clinically significant spinal cord and cauda equina compression, necessitating surgical intervention.3 Investigators report incidence rates of postoperative SEH requiring evacuation ranging from 0.1 to 3%.8,16 Although rare, symptomatic postoperative SEHs can have devastating neurological consequences. Clinical evaluation is the most important tool in the early diagnosis of SEH. Detailed postoperative neurological examination is mandatory and should be performed as Neurosurg. Focus / Volume 16 / June, 2004
soon as the patient is awake and cooperative. Diagnostic studies include plain radiography, MR imaging, and myelography followed by CT studies, depending on whether instrumentation is used. As soon as the diagnosis is established, emergency treatment including surgical exploration and evacuation of the hematoma should be performed without delay.
References 1. Antonacci MD, Eismont F: Neurologic complications after lumbar spine surgery. J Am Acad Orthop Surg 9:137–145, 2001 2. Boukobza M, Guichard JP, Boissonet M, et al: Spinal epidural haematoma: report of 11 cases and review of the literature. Neuroradiology 36:456–459, 1994 3. Cabana F, Pointillart V, Vital J, et al: [Postoperative compressive spinal epidural hematomas. 15 cases and a review of the literature.] Rev Chir Orthop Reparatrice Appar Mot 86: 335–345, 2000 (Fre) 4. Connolly ES Jr, Winfree CJ, McCormick PC: Management of spinal epidural hematoma after tissue plasminogen activator. A case report. Spine 21:1694–1698, 1996 5. Delamarter RB, Sherman J, Carr JB: Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg Am 77:1042–1049, 1995 6. Deyo RA, Cherkin DC, Loeser JD, et al: Morbidity and mortality in association with operations on the lumbar spine. The influence of age, diagnosis, and procedure. J Bone Joint Surg Am 74:536–543, 1992 7. Esler CN, Blakeway C, Fiddian NJ: The use of a closed-suction drain in total knee arthroplasty. A prospective, randomised study. J Bone Joint Surg Br 85:215–217, 2003 8. Foo D, Rossier AB: Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas. Surg Neurol 15:389–401, 1981 9. Groen RJ, Ponssen H: The spontaneous spinal epidural hematoma. A study of the etiology. J Neurol Sci 98:121–138, 1990 10. Gundry CR, Heithoff KB: Epidural hematoma of the lumbar spine: 18 surgically confirmed cases. Radiology 187:427–431, 1993 11. Jackson R: Case of spinal apoplexy. Lancet 2:5–6, 1869 12. Jagodzinski M, Krettek C: [Drains in trauma surgery.] Chirurg 74:115–117, 2003 (Ger) 13. Johnston RA: The management of acute spinal cord compression. J Neurol Neurosurg Psychiatry 56:1046–1054, 1993 14. Kostuik JP, Harrington I, Alexander D, et al: Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg Am 68: 386–391, 1986 15. Kou J, Fischgrund J, Biddinger A, et al: Risk factors for spinal epidural hematoma after spinal surgery. Spine 27:1670–1673, 2002 16. Lawton MT, Porter RW, Heiserman JE, et al: Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome. J Neurosurg 83:1–7, 1995 17. Manian FA, Meyer PL, Setzer J, et al: Surgical site infections associated with methicillin-resistant Staphylococcus aureus: do postoperative factors play a role? Clin Infect Dis 36:863–868, 2003 18. Markham JW, Lynge HN, Stahlman GE: The syndrome of spontaneous spinal epidural hematoma. Report of three cases. J Neurosurg 26:334–342, 1967 19. McQuarrie IG: Recovery from paraplegia caused by spontaneous spinal epidural hematoma. Neurology 28:224–228, 1978 20. Mirkovic S, Melany M: A thoracolumbar epidural hematoma simulating a disc syndrome. J Spinal Disord 5:112–115, 1992
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Neurosurg. Focus / Volume 16 / June, 2004
