CASE REPORT
Spinal-Epidural Hematoma Presenting as Paraplegia Following Mitral Valve Surgery: A Case Report Anil Karlekar, MD,* Devesh Dutta, MD, FNB,* Kapil Dev Arora, MD, FNB,* and Y.K. Mishra, PhD†
S
PINAL-EPIDURAL HEMATOMA (SEH) is an uncommon entity, and could be acute, chronic, spontaneous, posttraumatic, or iatrogenic, the occurrence following cardiac surgery being even more rare. Although cases of paraplegia following cardiac surgery as a consequence of spinal cord infarction are reported in the literature,1 spinal-epidural hematomas presenting as paraplegia after heart valve surgery only are sporadic.2 The authors herein describe a patient who developed paraplegia in the immediate postoperative period as a consequence of a spinal-epidural hematoma. CASE REPORT A 57–year-old male patient (height 182 cm, weight 66.7 kg, body mass index 20.14) with a history of diabetes mellitus and hypothyroidism presented to the hospital with recurrent episodes of breathlessness on exertion for further evaluation and management. He also gave a history of palpitations and ocassional giddiness. Apart from an irregular pulse, the rest of his physical examination was unremarkable. Echocardiography revealed severe mitral stenosis (mitral valve area 0.9 cm2), dilated left atrium, a suspected clot in the left atrial appendage, and normal left ventricular function. In addition, spontaneous echo contrast in the left atrium, moderate tricuspid regurgitation, and right ventricular systolic pressure of 55 mmHg also were reported. Coronary angiography revealed normal coronaries. Preoperatively, the patient was getting oral warfarin, metoprolol, furosemide, and thyroxin supplement. Warfarin was stopped 7 days before the scheduled day of surgery, and on the day of surgery, prothrombin time (PT) and INR were normal, 13 seconds and 1.08, respectively. Platelet count was 115 103/mm3, and other values were within normal limits. He underwent mitral valve replacement (29-mm Hancock II tissue valve; Medtronic, Minneapolis, MN) and left atrial appendage clot removal through a standard median sternotomy under hypothermic (321C) cardiopulmonary bypass. Institutional protocol of desired anticoagulation of ACT 4480 seconds was maintained with Heparin (loading dose 25,000 IU followed by 1 supplemental dose of 6,000 IU). No epidural catheter was placed, and the patient did not require an intraaortic balloon pump perioperatively. The patient remained hemodynamically stable and was weaned successfully from cardiopulmonary bypass with epinephrine, 0.025 mg/kg/min, and dobutamine, 3 mg/kg/min, respectively. Cardiopulmonary bypass time and cross-clamp time were 103 and 78 minutes, respectively. After termination of cardiopulmonary bypass, heparin was neutralized with protamine in 1:1 ratio, and ACT following heparin reversal was 130 seconds. Since the surgical field appeared “wet” despite normal ACT, the patient was transfused 2 units each of fresh frozen plasma and platelet concentrates. Initial neurologic assessment 2 hours after arrival in the recovery room was reported normal, and there was minimal bleeding (total drainage 310 mL in the first 12 hours) in the early postoperative period. Tracheal extubation was carried out successfully after overnight elective ventilation. Three hours following tracheal extubation, the patient first complained of weakness of both lower
limbs. Neurologic examination revealed loss of motor power (grade 0/5) of both lower limbs although sensory functions appeared preserved. An urgent neurology consultation was sought, and magnetic resonance imaging (MRI) of the head was obtained. Once the MRI of the brain was reported as normal, suspicion turned towards the possibility of a spinal pathology, resulting in a delay of another 6 hours by the time the MRI of the spine eventually was done and the diagnosis of spinalepidural hematoma established. The MRI revealed a large epidural collection extending from the lower thoracic region to the S1 vertebra (Fig 1 and Fig 2). A neurosurgical consult was sought, and a few more crucial hours were lost in seeking the patient’s and family’s consent for surgical intervention to treat an uncommon complication of a cardiac surgical procedure. Eventually, the patient underwent decompressive laminectomy and evacuation of the spinal-epidural hematoma approximately 40 hours after he had first complained of weakness in the lower limbs. Intraoperatively, there was no evidence of a tumor mass or any vascular malformation. After laminectomy, the patient did not improve clinically and was discharged on the fifteenth postoperative day and remained on supportive treatment. The importance of timely detection and intervention cannot be overemphasized as is obvious in the present case. DISCUSSION
SEH, an uncommon cause of spinal cord compression, was first described by Jackson in 1869. Although SEH has been reported in all age groups, it appears to occur more often in the sixth and seventh decade with slight male preponderance, and of all the regions of the spine, cervicothoracic and thoracolumbar junction are the most commonly affected.3 SEH can be associated with traumatic spinal injuries, blood dyscrasia, anticoagulation therapy, spinal and epidural anesthesia, lumbar puncture, and arteriovenous malformation. In the absence of any predisposing factor, the hematoma is referred to as spontaneous spinal-epidural hematoma (SSEH), accounting for almost 40-50% of cases. However, the term “spontaneous”
From the Departments of *Anaesthesiology and Intensive Care and †Cardiothoracic Surgery, Fortis Escorts Heart Institute, New Delhi, India. Address reprint requests to Devesh Dutta, MD, FNB, Fortis Escorts Heart Institute, Department of Anaesthesiology and Intensive Care, New Delhi, India, New Delhi-110025, India. E-mail: drdeveshdutta@ yahoo.co.uk © 2013 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2013.07.012 Key words: spinal-epidural, hematoma, cardiac surgery, paraplegia, mitral, valve surgery, complications
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2013: pp ]]]–]]]
1
2
has been expanded to include hematomas associated with hypertension, pregnancy, and anticoagulation or even ordinary activities like coughing, sneezing, or physical exertion.4 Anticoagulant therapy is the most common known cause of SSEH, but prothrombin time or INR values do not seem to correlate with the risk of hemorrhage.5 The definite underlying pathology of a spinal-epidural hematoma remains unclear but most probably results from ruptured veins in the epidural venous plexus.6 Paraplegia after cardiac surgery may be related to formation of a spinal or epidural hematoma or hypoperfusion of the spinal cord due to hypotension. Use of an intraaortic balloon catheter, aortocoronary grafts, and microemboli also are considered contributing factors for the development of paraplegia.1 Warfarin therapy after valve replacement, streptokinase, or heparin after acute coronary syndrome are the possible causes of an epidural hematoma as a complication of anticoagulant therapy.7 However, the etiology of the spinal-epidural hematoma is not clear in the authors’ patient; changes in venous pressure, a minor injury, or an unremarkable event after heparinization during cardiopulmonary bypass surgery could have been causative factors in isolation or collectively. The classic presentation of spinal hematoma is a sudden onset of severe spinal pain with or without radicular radiation, followed by variable degrees of motor and sensory deficit and bladder involvement. However, in some patients, radicular pain may be one of the first presenting symptoms.8 In cardiac surgery, patients remain under the effect of analgesics and sedatives in the immediate postoperative period rendering early identification often a difficult challenge.
Fig 1. Mid-sagittal T2-weighted MRI of the spine demonstrating a biconvex spinal-epidural hematoma (white arrow) extending from the lower thoracic region to the S1 vertebra, compressing the spinal cord.
KARLEKAR ET AL
Fig 2. Axial T2-weighted MRI showing spinal-epidural hematoma (white arrow), compressing the spinal cord.
Magnetic resonance imaging (MRI) is the preferred modality for early detection of SEH as it provides precise information about its location as well as extent. It also gives an accurate measure of the degree of cord compression and also may help in excluding conditions like arteriovenous malformation that could have pre-existed but present only postoperatively. Furthermore, the pattern of T1 and T2 signal intensity on MRI can help to date the hematoma as signal intensity depends upon the age and oxygenation status of the hematoma. In addition, the hematoma image partially may be enhanced with intravenous gadolinium contrast.9 However, although the MRI is decidedly more sensitive than a CT for early diagnosis of a spinal pathology, challenges like availability of MR-compatible equipment (syringe pumps, monitors, ventilators) and presence of metallic prosthetic implants (prosthetic heart valve, sternal wires, pacemakers, and stents) may restrict its commissioning universally. In addition, an MRI takes much longer time for completing imaging cycles than CT, and it often may pose a challenge to manage patients in the MR suite, particularly if they have unstable hemodynamics requiring supportive ventilation and/or inotropes. However, increasing awareness about its edge over CT in acute situations and easy availability of MR-compatible equipment apart from most prosthetic heart valves and other implants being made of MR-compatible metals, use of MR imaging is now commonplace in similar situations, enabling early and precise diagnosis. On sagittal sections, the hematoma appears as a biconvex mass dorsal to the thecal sac with tapering superior and inferior margins. The MRI scan of the authors’ patient showed similar findings. SEH is a neurologic emergency, and it requires urgent intervention. The spectrum of treatment for SEH ranges from conservative management to immediate surgical decompression. Surgery is the preferred treatment, regardless of etiology, especially in patients with extensive hematomas and neurologic deficits.10 However, in certain settings, like improvement in
3
SPINAL-EPIDURAL HEMATOMA
clinical condition or overall poor medical condition with comorbidities including advanced age, it may be prudent to consider conservative treatment after proper risk evaluation.3 In a subset of patients like those fully anticoagulated immediately after myocardial infarction or patients on heparin therapy in the early postoperative period after valve surgeries, operative morbidity and mortality can be unacceptably high. In these cases, operative risk must be weighed against the severity and evolution of neurologic deficit before arriving at a decision to intervene surgically or manage conservatively. In a similar case of paraplegia, a consequence of a spinal epidural hematoma was reported by Hayashiet al.2 However, the patient was managed conservatively as the paraplegia was not progressive although it took a month for the hematoma to resolve, and the patient did ultimately regain sufficient muscle strength. Prognosis depends on the speed of diagnosis, time of intervention, neurologic status, and the rate at which the neurologic deficit progresses.2 Early decompression (o8 hours)
promises the highest probability of neurologic recovery; but on the other hand, delayed surgery after total loss of spinal cord function does not completely exclude the possibility of some recovery.11 Delay in the surgical decompression may have been the contributing factor for non-recovery in the present patient; however, in about 60% of patients, early laminectomy also failed to relieve paraplegia.12 The present case report illustrates that SHE, although rare, must be suspected as a cause of neurologic deficit postoperatively after cardiac surgery. The diagnosis of such an entity can be delayed because sedation and analgesics can mask the classic symptoms in the immediate postoperative period. It is important to include SEH in the differential diagnosis of the acute neurologic deficit after cardiac surgery, and involvement of the spine always should be considered when faced with such a situation. Prompt MRI scanning in suspected cases can be helpful as early diagnosis and treatment is the key deciding factor for neurologic outcome in these cases.
REFERENCES 1. Scheer K, Urquhart G, Eichorst C, et al: Paraplegia after coronary artery bypass graft surgery: Case report of a rare event. Crit Care Nurse 26:34-45, 2006 2. Hayashi I, Shimamura Y, Maehara M: Paraplegia due to spinal epidural hematoma after mitral valve surgery: Report of a case. Surg Today 41:704-706, 2011 3. Groen RJ, Ponssen H: The spontaneous spinal hematoma: A study of the etiology. J Neurol Sci 98:121-138, 1990 4. Parman SC: Spontaneous spinal epidural hematoma. Ann Emerg Med 9:368370, 1980 5. Zuccarello M, Scanarini M, D’Avella D, et al: Spontaneous spinal extradural hematoma during anticoagulant therapy. Surg Neurol 14: 411413, 1980 6. Maingi M, Glynn MF, Scully HE, et al: Spontaneous spinal epidural hematoma in a patient with a mechanical aortic valve taking warfarin. Can J Cardiol 11:429-432, 1995 7. Mustafa MH, Gallino R: Spontaneous spinal epidural hematoma causing cord compression after streptokinase and heparin
therapy for acute coronary artery occlusion. South Med J 81: 1202-1203, 1988 8. Chan KM, Law KL, Chung CH: Case report: Thoracic spinal epidural hematoma an unusual cause of chest pain. J Emerg Med 13: 217-220, 2006 9. Jamjoom ZA: Acute spontaneous spinal epidural hematoma: The influence of magnetic resonance imaging on diagnosis and treatment. Surg Neurol 46:345-349, 1996 10. Lawton MW, 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 11. Wulf H: Epidural anaesthesia and spinal haematoma. Can J Anaesth 43:12601271, 1996 12. Biglioli P, Roberto M, Cannata A, et al: Paraplegia after iatrogenic extrinsic spinal cord compression after descending thoracic aorta repair: Case report and literature review. J Thorac Cardiovasc Surg 124:407-410, 2002
Spinal-Epidural Hematoma Presenting as Paraplegia Following Mitral Valve Surgery: A Case Report Anil Karlekar, MD,* Devesh Dutta, MD, FNB,* Kapil Dev Arora, MD, FNB,* and Y.K. Mishra, PhD†
S
PINAL-EPIDURAL HEMATOMA (SEH) is an uncommon entity, and could be acute, chronic, spontaneous, posttraumatic, or iatrogenic, the occurrence following cardiac surgery being even more rare. Although cases of paraplegia following cardiac surgery as a consequence of spinal cord infarction are reported in the literature,1 spinal-epidural hematomas presenting as paraplegia after heart valve surgery only are sporadic.2 The authors herein describe a patient who developed paraplegia in the immediate postoperative period as a consequence of a spinal-epidural hematoma. CASE REPORT A 57–year-old male patient (height 182 cm, weight 66.7 kg, body mass index 20.14) with a history of diabetes mellitus and hypothyroidism presented to the hospital with recurrent episodes of breathlessness on exertion for further evaluation and management. He also gave a history of palpitations and ocassional giddiness. Apart from an irregular pulse, the rest of his physical examination was unremarkable. Echocardiography revealed severe mitral stenosis (mitral valve area 0.9 cm2), dilated left atrium, a suspected clot in the left atrial appendage, and normal left ventricular function. In addition, spontaneous echo contrast in the left atrium, moderate tricuspid regurgitation, and right ventricular systolic pressure of 55 mmHg also were reported. Coronary angiography revealed normal coronaries. Preoperatively, the patient was getting oral warfarin, metoprolol, furosemide, and thyroxin supplement. Warfarin was stopped 7 days before the scheduled day of surgery, and on the day of surgery, prothrombin time (PT) and INR were normal, 13 seconds and 1.08, respectively. Platelet count was 115 103/mm3, and other values were within normal limits. He underwent mitral valve replacement (29-mm Hancock II tissue valve; Medtronic, Minneapolis, MN) and left atrial appendage clot removal through a standard median sternotomy under hypothermic (321C) cardiopulmonary bypass. Institutional protocol of desired anticoagulation of ACT 4480 seconds was maintained with Heparin (loading dose 25,000 IU followed by 1 supplemental dose of 6,000 IU). No epidural catheter was placed, and the patient did not require an intraaortic balloon pump perioperatively. The patient remained hemodynamically stable and was weaned successfully from cardiopulmonary bypass with epinephrine, 0.025 mg/kg/min, and dobutamine, 3 mg/kg/min, respectively. Cardiopulmonary bypass time and cross-clamp time were 103 and 78 minutes, respectively. After termination of cardiopulmonary bypass, heparin was neutralized with protamine in 1:1 ratio, and ACT following heparin reversal was 130 seconds. Since the surgical field appeared “wet” despite normal ACT, the patient was transfused 2 units each of fresh frozen plasma and platelet concentrates. Initial neurologic assessment 2 hours after arrival in the recovery room was reported normal, and there was minimal bleeding (total drainage 310 mL in the first 12 hours) in the early postoperative period. Tracheal extubation was carried out successfully after overnight elective ventilation. Three hours following tracheal extubation, the patient first complained of weakness of both lower
limbs. Neurologic examination revealed loss of motor power (grade 0/5) of both lower limbs although sensory functions appeared preserved. An urgent neurology consultation was sought, and magnetic resonance imaging (MRI) of the head was obtained. Once the MRI of the brain was reported as normal, suspicion turned towards the possibility of a spinal pathology, resulting in a delay of another 6 hours by the time the MRI of the spine eventually was done and the diagnosis of spinalepidural hematoma established. The MRI revealed a large epidural collection extending from the lower thoracic region to the S1 vertebra (Fig 1 and Fig 2). A neurosurgical consult was sought, and a few more crucial hours were lost in seeking the patient’s and family’s consent for surgical intervention to treat an uncommon complication of a cardiac surgical procedure. Eventually, the patient underwent decompressive laminectomy and evacuation of the spinal-epidural hematoma approximately 40 hours after he had first complained of weakness in the lower limbs. Intraoperatively, there was no evidence of a tumor mass or any vascular malformation. After laminectomy, the patient did not improve clinically and was discharged on the fifteenth postoperative day and remained on supportive treatment. The importance of timely detection and intervention cannot be overemphasized as is obvious in the present case. DISCUSSION
SEH, an uncommon cause of spinal cord compression, was first described by Jackson in 1869. Although SEH has been reported in all age groups, it appears to occur more often in the sixth and seventh decade with slight male preponderance, and of all the regions of the spine, cervicothoracic and thoracolumbar junction are the most commonly affected.3 SEH can be associated with traumatic spinal injuries, blood dyscrasia, anticoagulation therapy, spinal and epidural anesthesia, lumbar puncture, and arteriovenous malformation. In the absence of any predisposing factor, the hematoma is referred to as spontaneous spinal-epidural hematoma (SSEH), accounting for almost 40-50% of cases. However, the term “spontaneous”
From the Departments of *Anaesthesiology and Intensive Care and †Cardiothoracic Surgery, Fortis Escorts Heart Institute, New Delhi, India. Address reprint requests to Devesh Dutta, MD, FNB, Fortis Escorts Heart Institute, Department of Anaesthesiology and Intensive Care, New Delhi, India, New Delhi-110025, India. E-mail: drdeveshdutta@ yahoo.co.uk © 2013 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2013.07.012 Key words: spinal-epidural, hematoma, cardiac surgery, paraplegia, mitral, valve surgery, complications
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2013: pp ]]]–]]]
1
2
has been expanded to include hematomas associated with hypertension, pregnancy, and anticoagulation or even ordinary activities like coughing, sneezing, or physical exertion.4 Anticoagulant therapy is the most common known cause of SSEH, but prothrombin time or INR values do not seem to correlate with the risk of hemorrhage.5 The definite underlying pathology of a spinal-epidural hematoma remains unclear but most probably results from ruptured veins in the epidural venous plexus.6 Paraplegia after cardiac surgery may be related to formation of a spinal or epidural hematoma or hypoperfusion of the spinal cord due to hypotension. Use of an intraaortic balloon catheter, aortocoronary grafts, and microemboli also are considered contributing factors for the development of paraplegia.1 Warfarin therapy after valve replacement, streptokinase, or heparin after acute coronary syndrome are the possible causes of an epidural hematoma as a complication of anticoagulant therapy.7 However, the etiology of the spinal-epidural hematoma is not clear in the authors’ patient; changes in venous pressure, a minor injury, or an unremarkable event after heparinization during cardiopulmonary bypass surgery could have been causative factors in isolation or collectively. The classic presentation of spinal hematoma is a sudden onset of severe spinal pain with or without radicular radiation, followed by variable degrees of motor and sensory deficit and bladder involvement. However, in some patients, radicular pain may be one of the first presenting symptoms.8 In cardiac surgery, patients remain under the effect of analgesics and sedatives in the immediate postoperative period rendering early identification often a difficult challenge.
Fig 1. Mid-sagittal T2-weighted MRI of the spine demonstrating a biconvex spinal-epidural hematoma (white arrow) extending from the lower thoracic region to the S1 vertebra, compressing the spinal cord.
KARLEKAR ET AL
Fig 2. Axial T2-weighted MRI showing spinal-epidural hematoma (white arrow), compressing the spinal cord.
Magnetic resonance imaging (MRI) is the preferred modality for early detection of SEH as it provides precise information about its location as well as extent. It also gives an accurate measure of the degree of cord compression and also may help in excluding conditions like arteriovenous malformation that could have pre-existed but present only postoperatively. Furthermore, the pattern of T1 and T2 signal intensity on MRI can help to date the hematoma as signal intensity depends upon the age and oxygenation status of the hematoma. In addition, the hematoma image partially may be enhanced with intravenous gadolinium contrast.9 However, although the MRI is decidedly more sensitive than a CT for early diagnosis of a spinal pathology, challenges like availability of MR-compatible equipment (syringe pumps, monitors, ventilators) and presence of metallic prosthetic implants (prosthetic heart valve, sternal wires, pacemakers, and stents) may restrict its commissioning universally. In addition, an MRI takes much longer time for completing imaging cycles than CT, and it often may pose a challenge to manage patients in the MR suite, particularly if they have unstable hemodynamics requiring supportive ventilation and/or inotropes. However, increasing awareness about its edge over CT in acute situations and easy availability of MR-compatible equipment apart from most prosthetic heart valves and other implants being made of MR-compatible metals, use of MR imaging is now commonplace in similar situations, enabling early and precise diagnosis. On sagittal sections, the hematoma appears as a biconvex mass dorsal to the thecal sac with tapering superior and inferior margins. The MRI scan of the authors’ patient showed similar findings. SEH is a neurologic emergency, and it requires urgent intervention. The spectrum of treatment for SEH ranges from conservative management to immediate surgical decompression. Surgery is the preferred treatment, regardless of etiology, especially in patients with extensive hematomas and neurologic deficits.10 However, in certain settings, like improvement in
3
SPINAL-EPIDURAL HEMATOMA
clinical condition or overall poor medical condition with comorbidities including advanced age, it may be prudent to consider conservative treatment after proper risk evaluation.3 In a subset of patients like those fully anticoagulated immediately after myocardial infarction or patients on heparin therapy in the early postoperative period after valve surgeries, operative morbidity and mortality can be unacceptably high. In these cases, operative risk must be weighed against the severity and evolution of neurologic deficit before arriving at a decision to intervene surgically or manage conservatively. In a similar case of paraplegia, a consequence of a spinal epidural hematoma was reported by Hayashiet al.2 However, the patient was managed conservatively as the paraplegia was not progressive although it took a month for the hematoma to resolve, and the patient did ultimately regain sufficient muscle strength. Prognosis depends on the speed of diagnosis, time of intervention, neurologic status, and the rate at which the neurologic deficit progresses.2 Early decompression (o8 hours)
promises the highest probability of neurologic recovery; but on the other hand, delayed surgery after total loss of spinal cord function does not completely exclude the possibility of some recovery.11 Delay in the surgical decompression may have been the contributing factor for non-recovery in the present patient; however, in about 60% of patients, early laminectomy also failed to relieve paraplegia.12 The present case report illustrates that SHE, although rare, must be suspected as a cause of neurologic deficit postoperatively after cardiac surgery. The diagnosis of such an entity can be delayed because sedation and analgesics can mask the classic symptoms in the immediate postoperative period. It is important to include SEH in the differential diagnosis of the acute neurologic deficit after cardiac surgery, and involvement of the spine always should be considered when faced with such a situation. Prompt MRI scanning in suspected cases can be helpful as early diagnosis and treatment is the key deciding factor for neurologic outcome in these cases.
REFERENCES 1. Scheer K, Urquhart G, Eichorst C, et al: Paraplegia after coronary artery bypass graft surgery: Case report of a rare event. Crit Care Nurse 26:34-45, 2006 2. Hayashi I, Shimamura Y, Maehara M: Paraplegia due to spinal epidural hematoma after mitral valve surgery: Report of a case. Surg Today 41:704-706, 2011 3. Groen RJ, Ponssen H: The spontaneous spinal hematoma: A study of the etiology. J Neurol Sci 98:121-138, 1990 4. Parman SC: Spontaneous spinal epidural hematoma. Ann Emerg Med 9:368370, 1980 5. Zuccarello M, Scanarini M, D’Avella D, et al: Spontaneous spinal extradural hematoma during anticoagulant therapy. Surg Neurol 14: 411413, 1980 6. Maingi M, Glynn MF, Scully HE, et al: Spontaneous spinal epidural hematoma in a patient with a mechanical aortic valve taking warfarin. Can J Cardiol 11:429-432, 1995 7. Mustafa MH, Gallino R: Spontaneous spinal epidural hematoma causing cord compression after streptokinase and heparin
therapy for acute coronary artery occlusion. South Med J 81: 1202-1203, 1988 8. Chan KM, Law KL, Chung CH: Case report: Thoracic spinal epidural hematoma an unusual cause of chest pain. J Emerg Med 13: 217-220, 2006 9. Jamjoom ZA: Acute spontaneous spinal epidural hematoma: The influence of magnetic resonance imaging on diagnosis and treatment. Surg Neurol 46:345-349, 1996 10. Lawton MW, 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 11. Wulf H: Epidural anaesthesia and spinal haematoma. Can J Anaesth 43:12601271, 1996 12. Biglioli P, Roberto M, Cannata A, et al: Paraplegia after iatrogenic extrinsic spinal cord compression after descending thoracic aorta repair: Case report and literature review. J Thorac Cardiovasc Surg 124:407-410, 2002
