- Email: [email protected]
Paraplegia due to spinal subdural hematoma as a complication of posterior fossa surgery: Case report and review of the literature
Clinical Neurology and Neurosurgery 108 (2006) 590–594
Case report
Paraplegia due to spinal subdural hematoma as a complication of posterior fossa surgery: Case report and review of the literature Tufan Hicdonmez ∗ , Cumhur Kilincer, M. Kemal Hamamcioglu, Sebahattin Cobanoglu Department of Neurosurgery, Trakya University, Faculty of Medicine, Edirne, Turkey Received 19 January 2005; received in revised form 7 April 2005; accepted 11 April 2005
Abstract Although blood contamination of cerebrospinal fluid (CSF) after an intracranial operation is possible, development of a symptomatic spinal hematoma after a posterior fossa surgery has never been reported. A 43-year-old woman underwent a posterior fossa tumor removal in the prone position with no intraoperative difficulty. On the second postoperative day, she complained of severe epigastric pain and developed a rapid onset of paraplegia with anesthesia below the thoracic 5 spinal level. The emergency cranial and spinal MRIs revealed a spinal extramedullary hemorrhage spreading to the whole spinal regions, just sparing the cauda equina area. There was a prominent localized hematoma formation surrounding and compressing the spinal cord at the upper thoracic levels, which was evacuated via an urgent laminectomy. The patient showed partial neurological recovery after the decompression. Development of the spinal hematoma was explained by the movement of blood from the tumor bed into the spinal canal under the effect of gravity, during or after the operation. A 30◦ head elevation might facilitate the accumulation of blood. Localization of the hematoma formation may be caused by the fact that the upper thoracic levels constitute the apex of the kyphosis. We conclusively suggest that a spinal hematoma should be taken into consideration as a rare but potentially severe complication of a posterior fossa surgery. Meticulous hemostasis and isolation of the surgical area from the spinal spaces are essential. Overdrainage of CSF should be abandoned. Postoperatively, patients should be monitored for spinal findings as well as cranial signs. © 2005 Elsevier B.V. All rights reserved. Keywords: Complications; Magnetic resonance imaging; Paraplegia; Posterior cranial fossa; Spinal cord compression; Subdural hematoma
1. Introduction Spinal subdural hematoma (SSDH) is a rare condition usually related to trauma, lumbar puncture, coagulopathy, or vascular malformations [1–4]. Development of an SSDH after an intracranial surgery is also a rare but possible complication. A few reports have been published that point out several etiologies suggest diverse pathomechanisms [5–11]. These include the downward movement of blood from the cranial compartment by gravity [2,6,11,12], excessive decompression of intracranial space during surgery [3], and lowered cerebrospinal fluid (CSF) pressure by drainage or shunt procedures [8–10,13]. The current report presents a patient who suffered paraplegia due to an SSDH after a posterior fossa ∗
Corresponding author. Tel.: +90 284 2357641/542 2538103. E-mail address: [email protected] (T. Hicdonmez).
0303-8467/$ – see front matter © 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.clineuro.2005.04.001
surgery. To avoid this severe complication, the possible pathomechanism and its prevention are discussed in light of similar cases derived from the literature.
2. Case report A 43-year-old woman presented with a headache, vomiting, and gait disturbance of 2 months’ duration. She had mild truncal ataxia. Magnetic resonance imaging (MRI) revealed a well-circumscribed cystic posterior fossa midline tumor (Fig. 1). Dexamethasone (16 mg/day) was started, and the patient underwent an operation. In a prone and 20–30◦ reverse Trendelenburg position, a medial suboccipital craniectomy was performed. The cystic tumor was removed totally under an operating microscope. No noticeable bleeding during or at the end of the surgery was experienced. No blood
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
591
Fig. 1. Preoperative T1-weighted axial MR image showing the posterior fossa cystic midline tumor.
transfusion was required. No spinal drainage was used during the procedure. The pathological diagnosis was Pilocytic astrocytoma. The early postoperative period was uneventful. She had bed rest with the head 30◦ elevated, and there was no mobilization. On the second postoperative day, she complained of severe epigastric pain, and developed a rapid onset of complete paraplegia with anesthesia below the thoracic (Th) 5 spinal level. The emergency cranial MRI showed a small area of blood accumulation at the site of the tumor removal. However, the spinal MRI revealed a spinal extramedullary hemorrhage spreading to the whole cervical, thoracic, and lumbar levels, just sparing the cauda equina area (Figs. 2 and 3). Moreover, at the upper thoracic levels, a localized hematoma formation surrounding the spinal cord was detected (Fig. 4a–c). Coagulation tests showed no abnormality. Due to the mass-like appearance of the blood accumulation at the upper thoracic levels, which corresponded to the level of neurological deficit, Th 2–7 laminectomies were quickly performed. The epidural space was normal in appearance. The dura was tight, non-pulsatile, and, when opened, a subdural hematoma clot leading to spinal cord compression was found. At examination, no sign of any vascular abnormality was identified. The hematoma was removed from the operation site, and the dura was closed. The patient exhibited partial neurological recovery after the operation. With an intensive physiotherapy program, her neurological status progressed to paraparesis with a grade 3/5 muscle power in the lower limbs 1 year after the event, and she regained sphincteric control.
Fig. 2. Sagittal T1-weighted cervico-thoracic MR image performed on the second postoperative day after the onset of paraplegia. There was no prominent cavitary hematoma in the posterior fossa tumor bed. Excepting a small area at the posterior extramedullary area at the C2–C3 level, the entire cervical and upper thoracic regions were filled (or contaminated) by an extramedullary hematoma as depicted by the slight hyperintensity of acute blood. Also, there was an appearance of widening of the spinal cord at the thoracic 3–4 levels, caused by a surrounding isointense hematoma as demonstrated by axial views (see Fig. 4a–c).
3. Discussion Reports of spinal cord injuries after posterior fossa surgery are mainly focused on the degree of the neck flexion and whether the position was sitting, lateral oblique, or prone [14,15]. The suggested mechanisms of these cervical spinal cord injuries, the so-called midcervical flexion myelopathy, are mechanical compression of the cervical spinal cord during the extensive hyperflexion of the head, relative hypotension secondary to the sitting position, altered autoregulation due
592
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
Fig. 3. Sagittal T1-weighted emergency MR images of thoracolumbar region revealed hyperintensity of a spinal extramedullary hematoma up to the level of the conus terminalis.
to stretching of the spinal cord, and vascular compromise from either venous engorgement or tearing [14]. However, a spinal cord injury due to hyperflexion would be expected to result in an immediate postoperative deficit; thus this possibility was excluded in our case. Moreover, clear evidence of bleeding throughout the spinal canal and the mass effect of the blood accumulation at the upper thoracic levels—which corresponded to the level of neurological deficit—prompted us to think the reason for the actual neurological deficit was a hemorrhage. Whereas a relatively large number of medical reports exist regarding intraspinal hematomas, only a limited number of reports on a spinal subdural hematoma (SSDH) after an intracranial operation have been published [2,3,5–10,13]. We found three papers reporting ventriculo-peritoneal shunt cases complicated by an SSDH [8–10]. In all of those cases, accompanied cranial subdural hematomas or hygromas were described. There were three papers that reported an SSDH af-
ter aneurysm surgery: Shimizu et al. [5] reported a case of an SSDH presenting with sciatica after an uneventful aneurysm clipping. Kim et al. reported a similar case of a patient presenting low back pain 7 days after a craniotomy for the clipping of an aneurysm [2]. One other case of an SSDH reported by Yamaguchi et al. [13] had diffuse subarachnoid hemorrhage and a subdural hematoma mainly beneath the cerebellar tentorium. Intrathecal administration of urokinase and continuous cerebrospinal fluid (CSF) drainage via the cisternal route had been performed as vasospasm prophylaxis in that case. The authors proposed that low CSF pressure because of continuous drainage and intrathecal thrombolytic therapy might have played an important role in the migration of the hematoma through the spinal canal. These three cases of an SSDH after aneurysm surgery had no neurological deficit, and the patients were treated conservatively. We found three papers in the literature regarding an SSDH after an intracranial tumor operation. Marx et al. [6] reported a case of a lumbosacral subdural hematoma in a 37-yearold patient after a translabyrinthine resection of an acoustic neuroma. No surgery was performed in this case because the symptoms were limited to numbness and pain. Porto et al. [7] reported a child who developed a spinal subdural hematoma after cerebellar tumor removal. An MRI 48 h after surgery (to rule out dropping metastases) showed a large subdural hematoma extending from the thoracic to lumbar level, with compression of the spinal cord and cauda equina. The patient had neither neurological deficit nor any complaints. The authors concluded that a “silent” (i.e., without clinical symptoms) postoperative acute SSDH could occur after posterior fossa surgery. In point of fact, Cronquist et al. [11] demonstrated that the spread of blood in the cerebrospinal fluid following posterior fossa tumor surgery radiologically simulated spinal metastases in 16 of 36 patients they studied. They concluded that those changes mimicking metastases were most prominent in the posterior thoracic region, and the changes represent adhesions caused by blood from the operation. It seems that intraoperative blood contamination of CSF is frequent and may well account for the increased signal characteristics on postoperative T1-weighted MR imaging. The case presented here differs from those “silent” cases in terms of clinical presentation and, to our knowledge, constitutes a unique case that resulted in paraplegia after a posterior fossa surgery. In the literature, whether the event was after a ventriculoperitoneal shunt or aneurysm surgery, the authors explained the development of the SSDH after a cranial surgery by the movement of intracranial blood into the spinal canal under the effect of gravity. Bortolotti et al. [12] reported a case of subacute subdural hematoma at the lumbosacral level after the spontaneous resolution of a cranial subdural hematoma, suggesting the possibility that the SSDH could be related to the redistribution of cranial blood to dependent regions such as the spinal subdural space. In point of fact, the location of blood accumulation (the most bottom part of the dural sac, i.e., around the cauda equina) supports the authors’
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
593
Fig. 4. (a)–(c) Axial T2-weighted MR images at the thoracic 3–5 spinal levels showing compression of a muff-like extramedullary hematoma (mainly situated at the left-posterior of the spinal cord) with a hyperintense center and hypo-isointense rim.
explanation in those cases. However, in the presented case, the same explanation gives rise to some inconsistencies which are difficult to answer: Why did the bleeding accumulate mainly in the upper thoracic region instead of around the cauda equina? Secondly, could it be possible for the bleeding to accumulate throughout the spinal subdural area and to reach enough pressure to cause significant spinal cord injury at the upper thoracic level, without evidence of apparent hemorrhage filling the tumor bed? Two explanations could be given to answer these questions. First, it is possible that insidious venous bleeding from the tumor bed runs down to the direction of gravity. In the current case, 30◦ head elevation (during and after the operation) might facilitate the accumulation of blood, without evident hematoma formation at the operative site. A second explanation is the possibility of the unnoticed bleeding during or after the operation, which could fill the spinal canal until the critical level without noticeable symp-
toms. Then, any additional disturbance of unknown etiology (like CSF disturbance or decreased spinal blood flow) might disturb this vulnerable balance and lead the symptoms to start. The reason for the accumulation of the blood in the upper thoracic region might lie in the fact that Th 5–6 levels constitute the apex of the thoracic kyphosis. Thus, this area forms the most likely place for collecting the blood in a supine position. However, other possibilities such as spontaneous bleeding (possibly due to an undetected, mild post-op coagulopathy or a cryptic vascular malformation or tearing of a spinal subarachnoid-subdural vessel due to overdrainage of the CSF) should be kept in mind in the etiology of the SSDH in this case. Especially, the possibility of an occult vascular malformation cannot be denied, considering that the urgent MRI was suboptimal, and a spinal angiography could not been performed. Moreover, the reason for paraplegia is debatable. Even though operative findings such as tight and
594
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
non-pulsatile dura and prominent subdural blood clots consistent with the mass effect—which were well corresponded to paraplegia level—might direct us to think that the reason for the deficit was a hemorrhage, other possible reasons for the spinal cord injury such as any vascular event (i.e., anterior spinal artery thromboembolism or venous outflow obstruction) could not be definitely refused. Thus, one could argue that the SSDH was an incidental finding and might not be responsible for the paraplegia. Nevertheless, we decided that the chance of decompressive surgery was beneficial in the current case, rather than to do nothing. Although the patient’s partial recovery supports the idea that the cause of the spinal cord injury was compression of the hematoma rather than ischemia, in retrospect, it would be much more preferable to detect the hematoma earlier and operate on the patient before the paraplegia, if any subtle sign of long tract impairment could be detected before the symptoms started. To our knowledge, this is the first report of a symptomatic spinal subdural hematoma leading to paraplegia as a complication of a posterior fossa surgery. Although the mechanism of the development of the spinal subdural hematoma was not definitely proven in the presented case, the authors would like to emphasize the possibility of the blood spreading from the posterior fossa to the spinal subarachnoid and/or subdural spaces. Meticulous hemostasis and the prevention of the downward migration of the blood to the spinal spaces using surgical patties at the foramen magnum level are essential. Overdrainage of CSF should be abandoned. Postoperatively, the patient should be monitored neurologically for spinal findings as well as cranial signs. Consideration must be given to patients who have undergone posterior fossa procedures who postoperatively show inappropriate signs of pain and muscle weakness not attributable to the direct surgical procedure. These patients must be evaluated urgently, with adequate imaging including the spinal MRI. We conclusively suggest that an SSDH should be taken into consideration as a rare but potentially severe complication of a posterior fossa surgery.
References [1] Domenicucci M, Ramieri A, Ciapetta P, Delfini R. Nontraumatic acute spinal subdural hematoma. Report of five cases and review of the literature. J Neurosurg (Spine 1) 1999;91:65–73. [2] Kim MS, Chung CK, Hur JW, Lee JW, Seong SO, Lee HK. Spinal subdural hematoma following craniotomy: case report. Surg Neurol 2004;61:288–92. [3] Lee JI, Hong SC. Spinal subdural haematoma as a complication of cranial surgery. Acta Neurochir 2003;145:411–5. [4] Morandi X, Riffaud L, Chabert E, Brasier G. Acute nontraumatic spinal subdural hematomas in three patients. Spine 2001;26:547–51. [5] Shimizu S, Tachibana S, Maezawa H, Fujii K, Kan S. Lumbar spinal subdural hematoma following craniotomy—case report. Neurol Med Chir (Tokyo) 1999;39:299–301. [6] Marx SV, Roberson DW, Coates G, Langman AW. Spinal subdural hematoma after resection of an acoustic neuroma. Otolaryngol Head Neck Surg 1999;120:540–2. [7] Porto L, Kieslich M, Turowski B, Lanfermann H, Zanella FE. Spinal subdural haematoma mimicking tethered cord after posterior fossa open surgery. Neuroradiology 2002;44:415–7. [8] Ohta H, Ottomo M, Nakamura T. A case of the spinal subdural hematoma formation following ventriculoperitoneal shunting for von Recklinghausen’s disease associated with aqueductal stenosis. No Shinkei Geka 2001;29:53–7. [9] Silver JM, Wilkins RH. Spinal subdural hematoma formation following ventriculoperitoneal shunting for hydrocephalus. Case report. Acta Neurochir (Wien) 1991;108:159–62. [10] Wurm G, Pogady P, Lungenschmid K, Fischer J. Subdural hemorrhage of the cauda equina. A rare complication of cerebrospinal fluid shunt. Case report. Neurosurg Rev 1996;19:113–7. [11] Cronqvist S, Greitz D, Maeder P. Spread of blood in cerebrospinal fluid following craniotomy simulates spinal metastases. Neuroradiology 1993;35:592–5. [12] Bortolotti C, Wang H, Fraser K, Lanzino G. Subacute spinal subdural hematoma after spontaneous resolution of cranial subdural hematoma: causal relationship or coincidence. J Neurosurg (Spine 4) 2004;100:372–4. [13] Yamaguchi S, Hida K, Akino M, Yano S, Iwasaki Y. Spinal subdural hematoma: a sequela of a ruptured intracranial aneurysm? Surg Neurol 2003;59:408–12. [14] Haisa T, Kondo T. Midcervical flexion myelopathy after posterior fossa surgery in the sitting position: case report. Neurosurgery 1996;38:819–21. [15] Rau CS, Liang CL, Lui CC, Lee TC, Chen HJ, Lu K. Quadriplegia in a patient who underwent posterior fossa surgery in the prone position. Case report. J Neurosurg 2002;96:101–3.
Case report
Paraplegia due to spinal subdural hematoma as a complication of posterior fossa surgery: Case report and review of the literature Tufan Hicdonmez ∗ , Cumhur Kilincer, M. Kemal Hamamcioglu, Sebahattin Cobanoglu Department of Neurosurgery, Trakya University, Faculty of Medicine, Edirne, Turkey Received 19 January 2005; received in revised form 7 April 2005; accepted 11 April 2005
Abstract Although blood contamination of cerebrospinal fluid (CSF) after an intracranial operation is possible, development of a symptomatic spinal hematoma after a posterior fossa surgery has never been reported. A 43-year-old woman underwent a posterior fossa tumor removal in the prone position with no intraoperative difficulty. On the second postoperative day, she complained of severe epigastric pain and developed a rapid onset of paraplegia with anesthesia below the thoracic 5 spinal level. The emergency cranial and spinal MRIs revealed a spinal extramedullary hemorrhage spreading to the whole spinal regions, just sparing the cauda equina area. There was a prominent localized hematoma formation surrounding and compressing the spinal cord at the upper thoracic levels, which was evacuated via an urgent laminectomy. The patient showed partial neurological recovery after the decompression. Development of the spinal hematoma was explained by the movement of blood from the tumor bed into the spinal canal under the effect of gravity, during or after the operation. A 30◦ head elevation might facilitate the accumulation of blood. Localization of the hematoma formation may be caused by the fact that the upper thoracic levels constitute the apex of the kyphosis. We conclusively suggest that a spinal hematoma should be taken into consideration as a rare but potentially severe complication of a posterior fossa surgery. Meticulous hemostasis and isolation of the surgical area from the spinal spaces are essential. Overdrainage of CSF should be abandoned. Postoperatively, patients should be monitored for spinal findings as well as cranial signs. © 2005 Elsevier B.V. All rights reserved. Keywords: Complications; Magnetic resonance imaging; Paraplegia; Posterior cranial fossa; Spinal cord compression; Subdural hematoma
1. Introduction Spinal subdural hematoma (SSDH) is a rare condition usually related to trauma, lumbar puncture, coagulopathy, or vascular malformations [1–4]. Development of an SSDH after an intracranial surgery is also a rare but possible complication. A few reports have been published that point out several etiologies suggest diverse pathomechanisms [5–11]. These include the downward movement of blood from the cranial compartment by gravity [2,6,11,12], excessive decompression of intracranial space during surgery [3], and lowered cerebrospinal fluid (CSF) pressure by drainage or shunt procedures [8–10,13]. The current report presents a patient who suffered paraplegia due to an SSDH after a posterior fossa ∗
Corresponding author. Tel.: +90 284 2357641/542 2538103. E-mail address: [email protected] (T. Hicdonmez).
0303-8467/$ – see front matter © 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.clineuro.2005.04.001
surgery. To avoid this severe complication, the possible pathomechanism and its prevention are discussed in light of similar cases derived from the literature.
2. Case report A 43-year-old woman presented with a headache, vomiting, and gait disturbance of 2 months’ duration. She had mild truncal ataxia. Magnetic resonance imaging (MRI) revealed a well-circumscribed cystic posterior fossa midline tumor (Fig. 1). Dexamethasone (16 mg/day) was started, and the patient underwent an operation. In a prone and 20–30◦ reverse Trendelenburg position, a medial suboccipital craniectomy was performed. The cystic tumor was removed totally under an operating microscope. No noticeable bleeding during or at the end of the surgery was experienced. No blood
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
591
Fig. 1. Preoperative T1-weighted axial MR image showing the posterior fossa cystic midline tumor.
transfusion was required. No spinal drainage was used during the procedure. The pathological diagnosis was Pilocytic astrocytoma. The early postoperative period was uneventful. She had bed rest with the head 30◦ elevated, and there was no mobilization. On the second postoperative day, she complained of severe epigastric pain, and developed a rapid onset of complete paraplegia with anesthesia below the thoracic (Th) 5 spinal level. The emergency cranial MRI showed a small area of blood accumulation at the site of the tumor removal. However, the spinal MRI revealed a spinal extramedullary hemorrhage spreading to the whole cervical, thoracic, and lumbar levels, just sparing the cauda equina area (Figs. 2 and 3). Moreover, at the upper thoracic levels, a localized hematoma formation surrounding the spinal cord was detected (Fig. 4a–c). Coagulation tests showed no abnormality. Due to the mass-like appearance of the blood accumulation at the upper thoracic levels, which corresponded to the level of neurological deficit, Th 2–7 laminectomies were quickly performed. The epidural space was normal in appearance. The dura was tight, non-pulsatile, and, when opened, a subdural hematoma clot leading to spinal cord compression was found. At examination, no sign of any vascular abnormality was identified. The hematoma was removed from the operation site, and the dura was closed. The patient exhibited partial neurological recovery after the operation. With an intensive physiotherapy program, her neurological status progressed to paraparesis with a grade 3/5 muscle power in the lower limbs 1 year after the event, and she regained sphincteric control.
Fig. 2. Sagittal T1-weighted cervico-thoracic MR image performed on the second postoperative day after the onset of paraplegia. There was no prominent cavitary hematoma in the posterior fossa tumor bed. Excepting a small area at the posterior extramedullary area at the C2–C3 level, the entire cervical and upper thoracic regions were filled (or contaminated) by an extramedullary hematoma as depicted by the slight hyperintensity of acute blood. Also, there was an appearance of widening of the spinal cord at the thoracic 3–4 levels, caused by a surrounding isointense hematoma as demonstrated by axial views (see Fig. 4a–c).
3. Discussion Reports of spinal cord injuries after posterior fossa surgery are mainly focused on the degree of the neck flexion and whether the position was sitting, lateral oblique, or prone [14,15]. The suggested mechanisms of these cervical spinal cord injuries, the so-called midcervical flexion myelopathy, are mechanical compression of the cervical spinal cord during the extensive hyperflexion of the head, relative hypotension secondary to the sitting position, altered autoregulation due
592
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
Fig. 3. Sagittal T1-weighted emergency MR images of thoracolumbar region revealed hyperintensity of a spinal extramedullary hematoma up to the level of the conus terminalis.
to stretching of the spinal cord, and vascular compromise from either venous engorgement or tearing [14]. However, a spinal cord injury due to hyperflexion would be expected to result in an immediate postoperative deficit; thus this possibility was excluded in our case. Moreover, clear evidence of bleeding throughout the spinal canal and the mass effect of the blood accumulation at the upper thoracic levels—which corresponded to the level of neurological deficit—prompted us to think the reason for the actual neurological deficit was a hemorrhage. Whereas a relatively large number of medical reports exist regarding intraspinal hematomas, only a limited number of reports on a spinal subdural hematoma (SSDH) after an intracranial operation have been published [2,3,5–10,13]. We found three papers reporting ventriculo-peritoneal shunt cases complicated by an SSDH [8–10]. In all of those cases, accompanied cranial subdural hematomas or hygromas were described. There were three papers that reported an SSDH af-
ter aneurysm surgery: Shimizu et al. [5] reported a case of an SSDH presenting with sciatica after an uneventful aneurysm clipping. Kim et al. reported a similar case of a patient presenting low back pain 7 days after a craniotomy for the clipping of an aneurysm [2]. One other case of an SSDH reported by Yamaguchi et al. [13] had diffuse subarachnoid hemorrhage and a subdural hematoma mainly beneath the cerebellar tentorium. Intrathecal administration of urokinase and continuous cerebrospinal fluid (CSF) drainage via the cisternal route had been performed as vasospasm prophylaxis in that case. The authors proposed that low CSF pressure because of continuous drainage and intrathecal thrombolytic therapy might have played an important role in the migration of the hematoma through the spinal canal. These three cases of an SSDH after aneurysm surgery had no neurological deficit, and the patients were treated conservatively. We found three papers in the literature regarding an SSDH after an intracranial tumor operation. Marx et al. [6] reported a case of a lumbosacral subdural hematoma in a 37-yearold patient after a translabyrinthine resection of an acoustic neuroma. No surgery was performed in this case because the symptoms were limited to numbness and pain. Porto et al. [7] reported a child who developed a spinal subdural hematoma after cerebellar tumor removal. An MRI 48 h after surgery (to rule out dropping metastases) showed a large subdural hematoma extending from the thoracic to lumbar level, with compression of the spinal cord and cauda equina. The patient had neither neurological deficit nor any complaints. The authors concluded that a “silent” (i.e., without clinical symptoms) postoperative acute SSDH could occur after posterior fossa surgery. In point of fact, Cronquist et al. [11] demonstrated that the spread of blood in the cerebrospinal fluid following posterior fossa tumor surgery radiologically simulated spinal metastases in 16 of 36 patients they studied. They concluded that those changes mimicking metastases were most prominent in the posterior thoracic region, and the changes represent adhesions caused by blood from the operation. It seems that intraoperative blood contamination of CSF is frequent and may well account for the increased signal characteristics on postoperative T1-weighted MR imaging. The case presented here differs from those “silent” cases in terms of clinical presentation and, to our knowledge, constitutes a unique case that resulted in paraplegia after a posterior fossa surgery. In the literature, whether the event was after a ventriculoperitoneal shunt or aneurysm surgery, the authors explained the development of the SSDH after a cranial surgery by the movement of intracranial blood into the spinal canal under the effect of gravity. Bortolotti et al. [12] reported a case of subacute subdural hematoma at the lumbosacral level after the spontaneous resolution of a cranial subdural hematoma, suggesting the possibility that the SSDH could be related to the redistribution of cranial blood to dependent regions such as the spinal subdural space. In point of fact, the location of blood accumulation (the most bottom part of the dural sac, i.e., around the cauda equina) supports the authors’
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
593
Fig. 4. (a)–(c) Axial T2-weighted MR images at the thoracic 3–5 spinal levels showing compression of a muff-like extramedullary hematoma (mainly situated at the left-posterior of the spinal cord) with a hyperintense center and hypo-isointense rim.
explanation in those cases. However, in the presented case, the same explanation gives rise to some inconsistencies which are difficult to answer: Why did the bleeding accumulate mainly in the upper thoracic region instead of around the cauda equina? Secondly, could it be possible for the bleeding to accumulate throughout the spinal subdural area and to reach enough pressure to cause significant spinal cord injury at the upper thoracic level, without evidence of apparent hemorrhage filling the tumor bed? Two explanations could be given to answer these questions. First, it is possible that insidious venous bleeding from the tumor bed runs down to the direction of gravity. In the current case, 30◦ head elevation (during and after the operation) might facilitate the accumulation of blood, without evident hematoma formation at the operative site. A second explanation is the possibility of the unnoticed bleeding during or after the operation, which could fill the spinal canal until the critical level without noticeable symp-
toms. Then, any additional disturbance of unknown etiology (like CSF disturbance or decreased spinal blood flow) might disturb this vulnerable balance and lead the symptoms to start. The reason for the accumulation of the blood in the upper thoracic region might lie in the fact that Th 5–6 levels constitute the apex of the thoracic kyphosis. Thus, this area forms the most likely place for collecting the blood in a supine position. However, other possibilities such as spontaneous bleeding (possibly due to an undetected, mild post-op coagulopathy or a cryptic vascular malformation or tearing of a spinal subarachnoid-subdural vessel due to overdrainage of the CSF) should be kept in mind in the etiology of the SSDH in this case. Especially, the possibility of an occult vascular malformation cannot be denied, considering that the urgent MRI was suboptimal, and a spinal angiography could not been performed. Moreover, the reason for paraplegia is debatable. Even though operative findings such as tight and
594
T. Hicdonmez et al. / Clinical Neurology and Neurosurgery 108 (2006) 590–594
non-pulsatile dura and prominent subdural blood clots consistent with the mass effect—which were well corresponded to paraplegia level—might direct us to think that the reason for the deficit was a hemorrhage, other possible reasons for the spinal cord injury such as any vascular event (i.e., anterior spinal artery thromboembolism or venous outflow obstruction) could not be definitely refused. Thus, one could argue that the SSDH was an incidental finding and might not be responsible for the paraplegia. Nevertheless, we decided that the chance of decompressive surgery was beneficial in the current case, rather than to do nothing. Although the patient’s partial recovery supports the idea that the cause of the spinal cord injury was compression of the hematoma rather than ischemia, in retrospect, it would be much more preferable to detect the hematoma earlier and operate on the patient before the paraplegia, if any subtle sign of long tract impairment could be detected before the symptoms started. To our knowledge, this is the first report of a symptomatic spinal subdural hematoma leading to paraplegia as a complication of a posterior fossa surgery. Although the mechanism of the development of the spinal subdural hematoma was not definitely proven in the presented case, the authors would like to emphasize the possibility of the blood spreading from the posterior fossa to the spinal subarachnoid and/or subdural spaces. Meticulous hemostasis and the prevention of the downward migration of the blood to the spinal spaces using surgical patties at the foramen magnum level are essential. Overdrainage of CSF should be abandoned. Postoperatively, the patient should be monitored neurologically for spinal findings as well as cranial signs. Consideration must be given to patients who have undergone posterior fossa procedures who postoperatively show inappropriate signs of pain and muscle weakness not attributable to the direct surgical procedure. These patients must be evaluated urgently, with adequate imaging including the spinal MRI. We conclusively suggest that an SSDH should be taken into consideration as a rare but potentially severe complication of a posterior fossa surgery.
References [1] Domenicucci M, Ramieri A, Ciapetta P, Delfini R. Nontraumatic acute spinal subdural hematoma. Report of five cases and review of the literature. J Neurosurg (Spine 1) 1999;91:65–73. [2] Kim MS, Chung CK, Hur JW, Lee JW, Seong SO, Lee HK. Spinal subdural hematoma following craniotomy: case report. Surg Neurol 2004;61:288–92. [3] Lee JI, Hong SC. Spinal subdural haematoma as a complication of cranial surgery. Acta Neurochir 2003;145:411–5. [4] Morandi X, Riffaud L, Chabert E, Brasier G. Acute nontraumatic spinal subdural hematomas in three patients. Spine 2001;26:547–51. [5] Shimizu S, Tachibana S, Maezawa H, Fujii K, Kan S. Lumbar spinal subdural hematoma following craniotomy—case report. Neurol Med Chir (Tokyo) 1999;39:299–301. [6] Marx SV, Roberson DW, Coates G, Langman AW. Spinal subdural hematoma after resection of an acoustic neuroma. Otolaryngol Head Neck Surg 1999;120:540–2. [7] Porto L, Kieslich M, Turowski B, Lanfermann H, Zanella FE. Spinal subdural haematoma mimicking tethered cord after posterior fossa open surgery. Neuroradiology 2002;44:415–7. [8] Ohta H, Ottomo M, Nakamura T. A case of the spinal subdural hematoma formation following ventriculoperitoneal shunting for von Recklinghausen’s disease associated with aqueductal stenosis. No Shinkei Geka 2001;29:53–7. [9] Silver JM, Wilkins RH. Spinal subdural hematoma formation following ventriculoperitoneal shunting for hydrocephalus. Case report. Acta Neurochir (Wien) 1991;108:159–62. [10] Wurm G, Pogady P, Lungenschmid K, Fischer J. Subdural hemorrhage of the cauda equina. A rare complication of cerebrospinal fluid shunt. Case report. Neurosurg Rev 1996;19:113–7. [11] Cronqvist S, Greitz D, Maeder P. Spread of blood in cerebrospinal fluid following craniotomy simulates spinal metastases. Neuroradiology 1993;35:592–5. [12] Bortolotti C, Wang H, Fraser K, Lanzino G. Subacute spinal subdural hematoma after spontaneous resolution of cranial subdural hematoma: causal relationship or coincidence. J Neurosurg (Spine 4) 2004;100:372–4. [13] Yamaguchi S, Hida K, Akino M, Yano S, Iwasaki Y. Spinal subdural hematoma: a sequela of a ruptured intracranial aneurysm? Surg Neurol 2003;59:408–12. [14] Haisa T, Kondo T. Midcervical flexion myelopathy after posterior fossa surgery in the sitting position: case report. Neurosurgery 1996;38:819–21. [15] Rau CS, Liang CL, Lui CC, Lee TC, Chen HJ, Lu K. Quadriplegia in a patient who underwent posterior fossa surgery in the prone position. Case report. J Neurosurg 2002;96:101–3.