The Spine Journal 3 (2003) 125–129
Delayed postoperative spinal epidural hematomas Juan Uribe, MD, Kapil Moza, MD, Omar Jimenez, MD, Barth Green, MD, Allan D.O. Levi, MD, PhD* Department of Neurosurgery, The Miami Project to Cure Paralysis, Lois Pope Life Center, 1095 NW 14 Terrace (D-4-6), University of Miami School of Medicine, Miami, FL 33136, USA Received 21 Jan 2002; accepted 19 September 2002
Background context: Symptomatic epidural hematomas after spinal surgery are uncommon and are usually diagnosed within 24 hours after surgery. Purpose: We report a series of delayed epidural hematomas in a subset of patients who awoke from surgery neurologically unchanged and then deteriorated more than 3 days after their index procedure. The goals of this report are to outline the clinical presentation, radiological characteristics and outcome of this uncommon entity. Study design/setting: We retrospectively reviewed the database of six spine surgeons over a 4-year period, looking for presence of epidural hematomas as a cause of clinical deterioration after an asymptomatic postoperative period of at least 3 days. Patient sample: We identified a subset of patients who awoke from surgery neurologically unchanged and then deteriorated more than 3 days after spinal surgery. A total of 4,018 patients were identified over the 4-year period of review. Outcome measures: Presence of spinal epidural hematoma as a cause of clinical deterioration after an asymptomatic period of at least 3 days. The medical records, including the history, physical, preoperative and postoperative neurological examinations, as well as plain radiographs and magnetic resonance images, were reviewed. Methods: We retrospectively reviewed the database of six spine surgeons over a 4-year period. We looked for delayed spinal epidural hematomas as a cause of clinical deterioration after an asymptomatic postoperative period of at least 3 days. We examined potential risk factors for spinal extradural hematomas. Results: Of 4,018 patients, we identified seven with spinal epidural hematoma who presented more than 3 days after their index procedure. The initial presenting symptom, which heralded the subsequent onset of neurological deterioration, consisted of severe sharp pain with radiation to the extremities. The average time to neurological deterioration was 5.3 days. Fifty-seven percent of the patients had multiple previous spinal surgeries at the site of the epidural hematoma. Surgical evacuation of the epidural hematomas resulted in neurological improvement in five patients. Persistent neurological deficits were observed in two patients. Conclusion: Delayed spinal epidural hematomas are an uncommon cause of delayed deterioration after spinal surgery. Previous surgery with attendant scarring that results in impairment of clot resorption may be a contributing factor in the development of the condition. © 2003 Elsevier Science Inc. All rights reserved.
Spinal epidural hematoma; Surgical management; Postoperative delayed spinal hematoma
FDA device/drug status: not applicable. Nothing of value received from a commercial entity related to this research. * Corresponding author. Department of Neurosurgery, Lois Pope Life Center 1095 NW 14 Terrace (D-4-6), Miami, FL 33136, USA. Tel.: (305) 243-2088; fax (305) 243-3337. E-mail address: [email protected]
Introduction Spinal epidural hematoma (SEH) is an uncommon clinical entity. Jackson  was the first to describe SEH in 1869, and since then, no more than 350 cases have been reported in the literature. SEH are believed to originate from the rich venous plexus of the epidural space. The most common area involved is the thoracic spine, where the epidural space is most prominent. Numerous etiologies for SEH have been
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described. The majority of hematomas occur spontaneously without a known cause, whereas others have been related to vascular anomalies such as arteriovenous malformation (AVM), vertebral hemangiomas, trauma (including vertebral fractures), obstetrical birth trauma, lumbar punctures and epidural procedures. Surgical bleeding, missile injuries, hypertension, physical exertion and abnormal bleeding tendencies, whether from hematological disorders or from anticoagulant therapy, have also been reported to result in SEH [2–12]. Postoperative hematomas after spinal surgery are an important, often remediable, cause of SEH [10,13–15, 17]. Incisional pain is an expected concomitant of invasive spinal surgeries, and occasionally patients will awake from surgery with a new or increased neurological deficit. The contribution of an epidural hematoma to pain or new neurological deficit recognized immediately after surgery is often questioned, because postoperative imaging after spinal surgery will frequently demonstrate some blood at the surgical site. We report a series of delayed SEHs in a subset of patients who awoke from surgery neurologically unchanged and then deteriorated more than 3 days after their index procedure. The goals of this article are to call attention to the clinical features of this uncommon entity and to determine if any common elements exist that predispose to the development of delayed postoperative spinal epidural hematoma (DPOSEH).
Clinical materials and methods We retrospectively reviewed the database of six spine surgeons working at the University of Miami over a 4-year period (1996 to 2000). The medical records, including the history, physical, preoperative and postoperative neurological examinations as well as plain radiographs and magnetic resonance imaging (MRI) were reviewed. We examined potential risk factors for spinal extradural hematoma, including underlying hematological conditions that predispose to bleeding (such as thrombocytopenia, coagulation factor deficiency, and so forth),
medications that predispose to bleeding, coagulation studies, the use and timing of wound drains and the presence or absence of previous surgeries. The diagnosis of DPOSEH was made on the basis of the development of a new neurological deficit in the distribution of the spinal cord or a nerve root more than 3 days after surgery resulting from the presence of a SEH seen on MRI. Neurological function was assessed using the American Spinal Injury Association (ASIA) grading system preoperatively and postoperatively and after evacuation of the extradural hematoma decompression of the spinal cord.
Results Patient population and surgery A total of 4,018 patients were identified who underwent spinal surgery over the 4-year period of review. The approximate rate of revision surgery was 18%. Nine patients were found to have postoperative epidural hematomas (0.22%). Seven patients were identified who presented with DPOSEH, as their clinical deterioration occurred more than 3 days after their index procedure (0.17%). The median age of the patients was 62 years (range, 52 to 79), and there was a 1:2 female:male ratio. All patients underwent posterior procedures, which involved, in part, performance of a laminectomy and/or laminoplasty. Four patients underwent cervical procedures, two underwent thoracic procedures, and one patient had a lumbar laminectomy. We used medium hemovac drains in four of our seven cases after the index procedure. Drains were maintained for the first 24 to 48 hours postoperatively. All patients had normal coagulation function tests at the time of the index surgical procedure. Fifty-seven percent of patients had had previous spinal surgeries at the site of the delayed spinal epidural hematoma (Patients 2, 4, 5 and 7; Table 1). Two patients had history of hepatitis C, one of whom was receiving interferon and the other had taken acetyl salicylic acid (ASA) 2 weeks prior and received two doses of tor-
Table 1 Patient profile Patient, age/sex
1. 55/F 2. 79/F
None Hepatitis C, ASA
HTN, DM, DVT on coumadin Hepatitis C
Cervical laminoplasty L2–L3 laminectomy and removal of an intradural disc Cervical laminoplasty
5. 63/M 6. 70/M 7. 69/F
Platelets 91K None None
Thoracic None Cervical
1. ACDF C7–T1 2. C5–T3 laminectomy and fusion T7–T9 laminectomy T6–T7 laminectomy Cervical laminectomy for recurrent meningioma
Interval DPOSEH/ ASIA grade
Toradol SC heparin
6 days/D 8 days/E
Heparin IV Postoperative day 3 SC heparin
SC heparin SC heparin SC heparin
No Yes No
T9 T3–T9 C5–C7
4 days/C 8 days/A 8 days/C
ACDF anterior cervical discectomy and fusion; ASA acetyl salicylic acid; ASIA American Spinal Injury Association; DM diabetes; DPOSEH delayed postoperative spinal epidural hematoma; DVT deep venous thrombosis; HTN hypertension; IV intravenous; MRI magnetic resonance imaging; PMH past medical history, SC subcutaneous heparin.
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adol for pain control (Patients 2 and 4). One patient with a history of a hypercoagulable state had stopped coumadin before surgery and was restarted on intravenous heparin 3 days postoperatively (Patient 3). Patient 5 had a platelet count of 91,000 but no prior history of thrombocytopenia. The initial postoperative examination after the index operation was unchanged. The initial presenting symptom, which heralded the onset of neurologic deterioration, consisted of a sharp, severe pain at the level of the previous surgery. This was followed by radicular symptoms consisting of dysesthesias. Soon after, motor weakness and sensory loss from spinal cord compression ensued. The ASIA neurological function grade at the time of presentation was A (Patient 6), B (Patient 3), C (Patients 4, 5 and 7), D (Patient 1) and E (Patient 2). The average time to neurological deterioration was 5.3 days (range, 3 to 8).
in the cervical region in three patients, thoracic in three patients and in the lumbar region in one patient. The hematoma was located dorsally in all patients, and the clinical level of the lesion matched the radiographic level.
The diagnosis of DPOSEH was confirmed by MRI in all patients. The signal characteristics of the lesion included increased signal intensity on both T1- and T2-weighted images. The sagittal and parasagittal images usually show a convex lens-shaped lesion (Fig. 1). The lesion was located
Surgical evacuation of DPOSEH resulted in neurological improvement in five patients. Mean follow up was 12 months postoperatively (range, 3 to 24 months) (Table 2). Two patients had no improvement in neurological function after evacuation of the hematoma. Patients 3 and 4 (ASIA B, C) returned to baseline neuroexamination within 48 hours of their surgical decompression. Patient 5 (ASIA C) had residual left hand weakness, which mildly improved at 6-month follow-up. Patient 7 (ASIA C) had right leg weakness, which mildly improved in the early postoperative period. Patients 1, 2 and 6 (ASIA D, E, A) had no change in neurological function even at 12-month follow-up.
Surgical treatment All patients were treated with emergent surgical evacuation of the hematoma. The original site of the surgery was reexplored and the clot evacuated. In many cases the hematoma was liquefied and exuded from the wound under pressure. In two cases (Patient 3 and 5), the laminectomy had to be extended inferiorly to remove blood clot, which had dissected caudally under the intact lamina. The average interval from symptom onset to surgery was 5.4 hours. On subsequent reexploration, all of the cases had drains during the immediate postoperative period.
Discussion Postoperative spinal epidural hematomas are an uncommon complication of spinal surgery occurring at a rate of 0.22% in our series. This is slightly higher than the rate published by Scavarda et al.  and Lawton et al.  (0.1%). Until now, there has been no reported series of DPOSEH-operative spinal epidural hematoma in the English literature. The incidence of DPOSEH in our series was 0.17%. Our experience suggests that the incidence of DPOSEH is higher in patients who have undergone previous spinal surgery at the same site at which the hematoma developed. Table 2 Preoperative (after diagnosis of delayed postoperative spinal epidural hematoma) and postoperative (after decompression) ASIA grades
Fig. 1. Magnetic resonance imaging scan T2-weighted sagittal image (Patient 2) demonstrates a dorsal lens-shaped lesion with increased signal intensity in the lumbar area that is compressing the thecal sac. The arrow denotes the delayed postoperative spinal epidural hematoma.
Preoperative ASIA grade
Postoperative ASIA grade
1 2 3 4 5 6 7
D E B C C A C
D E D D D A D
ASIA American Spine Injury Association.
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In our practice, the approximate rate of revision surgery is 18%. The operative site distribution was 43% cervical, 13% thoracic, 44% lumbar. The most frequent levels of involvement in our cases were the cervical and thoracic levels (four patients), and the lesion usually extended over two to four vertebral segments. The differential diagnosis of patients with severe spinal pain and progressive neurological deficit postoperatively includes intradural hemorrhage, spinal cord compression from extraxial structures, infection, inflammatory conditions, spinal cord infarction and other vascular processes [4,8,12,17,23,24]. The presenting symptom before neurological deterioration in five patients was intense, sharp pain referred to the surgical site. This was followed by dysesthesias, radicular symptoms and finally motor weakness. These are symptoms that are well described in the literature for acute SEH and did not differ for DPOSEH. The contribution of an epidural hematoma to pain or new neurological deficit recognized immediately after surgery is often questioned, because postoperative image after spinal surgery will frequently demonstrate some blood at the surgical site. In our patients with delayed neurologic deterioration after surgery, the challenge of diagnosis was even greater. All of our
Fig. 2. Magnetic resonance imaging scan T2-weighted image shows a dorsally located lens-shaped lesion with increased signal intensity in the thoracic area with associated cord displacement. The arrow denotes the delayed postoperative spinal epidural hematoma that has dissected underneath the intact most caudal lamina.
Scar tissue forms throughout the various tissue layers of the posterior spinal structures, including the epidural space, bone, ligaments, muscle, subcutaneous fat and skin after surgery. Scar tissue is less elastic than the normal host tissues; it probably (although we found no clinical or basic evidence in the literature) has reduced ability to adsorb blood and blood products and thus predisposes to DPOSEH. The use of intravenous heparin therapy soon after surgery potentiates the risk of hemorrhage as reported by others and is a well-established risk factor for SEH [1–3,5–7,9,17–20]. It is best to wait at least 12 hours before restarting anticoagulant therapy after spinal surgery . Hepatitis C infection causes acute hepatic disease that is often mild or asymptomatic, but there is a tendency for the infection to persist and lead to serious chronic liver disease. The clinical expression of hepatitis C virus infections depends on the stage of the liver disease (ie, acute hepatitis, chronic active hepatitis, cirrhosis, or end-stage chronic liver disease). A history of hepatitis C and/or low platelet counts may be a risk factor for the development of DPOSEH. However, there was not sufficient evidence to support this in our series of patients.
Fig. 3. Sagittal magnetic resonance imaging scan T2-weighted image demonstrates a lentiform thoracic epidural collection dorsal to the thecal sac, with associated cord displacement (arrow). The hyperintense hemorrhage is difficult to distinguish from cerebrospinal fluid on the T2-weighted image.
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cases awoke from surgery neurologically unchanged with an average symptom-free period of 5.3 days (range, 3.8 days). We report our cases as delayed, because there was a clear postoperative asymptomatic period of at least 3 days before the onset of the clinical symptomatology. We found that this clinical entity has some common clinical features, and there are also some elements, as mentioned above, that can predispose to the development of DPOSEH. However, it must be noted that that the sample is size is small and other factors may be implicated. MRI has replaced computed tomography myelography as the screening test for the diagnosis of SEH. The sagittal MRI and parasagittal images usually demonstrate that the lesion is present in the dorsal epidural space and in some cases extends laterally. The MRI features were quite specific for hemorrhage, including isointense signal on T1-weighted images, high signal on T2-weighted images in acute cases and increased signal intensity on both T1- and T2-weighted images in subacute cases (Figs. 1–3) [4,7,23–25]. Immediate surgical evacuation of the hematoma resulted in neurological improvement in five of our seven neurologic patients, demonstrating that the preoperative ASIA neurological grade may be helpful as a predictor of neurologic outcome. Our findings are consistent with other clinical reports describing the relationship of rapidity of surgical decompression, neurologic grade and outcome [3,6,8,9,13–15]. DPOSEH is a relatively rare entity and an uncommon cause of delayed clinical deterioration after spinal surgery. The initial presenting symptom, which heralds the subsequent onset of neurological deterioration, consists of severe pain with radiation to the extremities, followed by dysesthesias, radicular symptoms and finally motor weakness. Usually, patients have had multiple previous spinal surgeries at the site of the epidural hematoma, suggesting that scarring may be a contributing factor in the development of the condition. Diagnosis can be confirmed by MRI showing a dorsal convex, lens-shaped lesion that is iso- to hyperintense on T1-weighted images and hyperintense on T2-weighted images. Surgical evacuation resulted in neurological recovery in many instances. Conclusions In our series, DPOSEH-operative SEHs are a potential complication of spinal surgery. All cases occurred after posterior approaches to the spine, and in many cases previous surgery at the site of hematoma was observed. Immediate surgical evacuation of the hematoma resulted in recovery in many instances. Acknowledgments We acknowledge and thank the Orthospine service/University of Miami and the assistance of Gus Alameda in data management and collection (Department of Neurosurgery, University of Miami, Miami, Florida).
References  Jackson R. Case of spinal apoplexy. Lancet 1869;ii:538–9.  Avrahami E, Tadmor R, Ram Z, Feibel M, Itzhak Y. MR demonstration of spontaneous acute epidural hematoma of the thoracic spine. Neuroradiology 1989;31:89–92.  Beatty RM, Winston K. Spontaneous cervical epidural hematoma. A consideration of etiology. J Neurosurg 1984;61:143–8.  Boukobza M, Guichard JP, Boissonet M, et al. Spinal epidural hematoma: report of 11 cases and review of the literature. Neuroradiology 1994;36:456–9.  Boyd HR, Pear BL. Chronic spontaneous epidural hematoma. J Neurosurg 1972;36:239–42.  Cooper DW. Spontaneous spinal epidural hematoma. Case report. J Neurosurg 1967;25:343–5.  Cooper RG, Kenneth BH. Epidural hematoma of the lumbar spine: 18 surgically confirmed cases. Radiology 1993;187:427–31.  Dickman CA, Shedd SA, Spetzler RF, Shetter AG, Sonntag VK. Spinal epidural hematoma associated with epidural anesthesia: complications of systemic heparinization in patients receiving peripheral vascular thrombolitic therapy. Anesthesiology 1990;72:947–50.  Foo D, Rossier AB. Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas. Surg Neurol 1981; 15:389–401.  Lawton MT, Porter RW, Heiserman JE, Jacobowitz R, Sonntag VK, Dickman CA. Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome. J Neurosurg 1995;83:1–7.  Markham JW, Lynge HN, Stahlman GEB. The syndrome of spontaneous spinal epidural hematoma. J Neurosurg 1967;26:334–42.  Muller H, Schramm J, Roggendorf W, Breck M. Vascular malformations as a cause of spontaneous spinal epidural hematoma. Acta Neurochir 1982;62:297–305.  Payne DH, Fischgrund JS, Herkowitz HN, Barry RL, Kurz LT, Montgomery DM. Efficacy of closed wound suction drainage after singlelevel lumbar laminectomy. J Spinal Disord 1996;5 :401–3.  Dolan EJ, Tator CH, Endrenyi L. The value of decompression for acute experimental spinal cord compression injury. J Neurosurg 1980;53:749–55.  Grollmuss J, Hoff J. Spontaneous spinal epidural hemorrhage: good results after early treatment. J Neurol Neurosurg Psychiatry 1975;38:89–90.  McQuarrie IG. Recovery from paraplegia caused by spontaneous spinal epidural hematoma. Neurology 1978;28:224–8.  Scavarda D, Peruzzi P, Bazin A, et al. Postoperative spinal extradural hematomas: 14 cases. Neurochirurgie 1997;43:220–7.  Locke GE, Giorgio AJ, Biggers SL, Johnson AP, Salem F. Acute spinal epidural hematoma secondary to aspirin induced prolonged bleeding. Surg Neurol 1976;5:293–6.  Kearon C, Hirsh J. Management of anticoagulation before and after elective surgery. N Engl J of Med 1997;336:1506–11.  Zuccarello M, Scanarini M, D’Avella D, Andrioli GC, Gerosa M. Spontaneous spinal extradural hematoma during anticoagulant therapy. Surg Neurol 1980;14:411–3.  Mattle H, Seib JP, Rohner M, Mumenthaler M. Nontraumatic spinal epidural and subdural hematomas. Neurology 1987;37:1351–6.  Hirsh J, Dalen JE, Deykin D, Poller L, Bussey H. Oral anticoagulants mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 1995;108(suppl):231S–46S.  Bernsen PLJA, Haan J, Vielvoye GJ, Peerlinck KM. Spinal epidural hematoma visualized by magnetic resonance imaging, Neuroradiology 1988;30:280.  Pan G, Kulkarni M, Macdougall DJ, Miner ME. Traumatic epidural hematoma of the cervical spine: diagnosis with magnetic resonance imaging. J Neurosurg 1988;68:798–800.  Rothfus WE, Chedid MK, Deeb ZL, Abla AA, Maroon JC, Scherman RL. MR imaging in the diagnosis of spontaneous spinal epidural hematomas. J Comput Assist Tomogr 1987;11:851–4.