- Email: [email protected]
Delayed Posttraumatic Subacute Lumbar Subarachnoid Hematoma: Case Report and Review of the Literature
Case Report
Delayed Posttraumatic Subacute Lumbar Subarachnoid Hematoma: Case Report and Review of the Literature Thie´baud Picart1, Timothe´e Jacquesson1, Emmanuel Jouanneau1-3, Moncef Berhouma1,4
Key words Lumbar spine - Spinal hematoma - Subarachnoid hematoma - Trauma
- BACKGROUND:
Abbreviations and Acronyms MRI: magnetic resonance imaging
- CASE
-
Traumatic spinal subarachnoid hematoma, associated or not with a concurrent subdural hematoma, has rarely been described. The evolution of such hematomas is heterogeneous. This study aims at defining the most accurate management, which is currently not standardized.
Available online: www.sciencedirect.com
DESCRIPTION: A 20-year-old man, victim of a high-kinetic road accident 5 days before and with several nonneurologic nonsurgical vertebral fractures, experienced a sudden dorsolumbar pain radiating to his lower limbs. A rapidly progressive asymmetric paraparesis with loss of reflexes was noticed, associated with bilateral global hypoesthesia of the lower limbs and with acute urinary retention, whereas the anal tonicity was preserved (American Spinal Injury Association C). Magnetic resonance imaging scan revealed a conus medullaris compression at the level of the L1eL2 vertebrae by an intradural expansive mass. Immediate surgical decompression revealed a strictly subarachnoid hematoma. Venous bleeding was seen at the level of the conus medullaris and controlled. Pathologic examination of the clot excluded an underlying tumor or vascular abnormality. The complete coagulation profile was normal.
1878-8750/$ - see front matter ª 2018 Elsevier Inc. All rights reserved.
- CONCLUSION:
From the 1Department of Neurosurgery, Lyon University Hospital, Hospices Civils de Lyon, Bron; 2University Claude Bernard Lyon, Lyon; 3Signaling, Metabolism and Tumor Progression, Cancer Research Centre of Lyon, Lyon; and 4 CREATIS Laboratory, Lyon University, Lyon, France To whom correspondence should be addressed: Moncef Berhouma, M.D., M.Sc. [E-mail: [email protected]] Citation: World Neurosurg. (2018) 113:135-139. https://doi.org/10.1016/j.wneu.2018.02.035 Journal homepage: www.WORLDNEUROSURGERY.org
INTRODUCTION Traumatic spinal subarachnoid hematoma, associated or not with a concurrent subdural hematoma, has rarely been described.1-3 The evolution of such hematomas is heterogenous, opposing acute collection few hours after spinal injury and chronic collection similarly to their cranial counterparts, occurring several weeks after minor trauma.2,4,5 They are revealed by symptoms related to spinal cord compression, radicular compression, or both6,7 that can be uni- or bilateral.1,8,9 The management of such hematomas is not standardized.7 We herein report an unusual case of delayed posttraumatic purely subarachnoid subacute lumbar hematoma with a review of the literature.
CASE DESCRIPTION A 20-year-old man was referred to the intensive care unit of a peripheral hospital after a very high-kinetic automobile accident. His medical history consisted of surgically managed hematoma of the right
Six weeks after surgery, the neurologic examination revealed only a slight tactile hypoesthesia of the left thigh. With only 4 reported cases, purely subarachnoid spinal hematomas remain widely rarer than epidural hematomas. The reported case possesses a certain number of peculiarities: young age, pure subarachnoid location, lumbar location, occurrence after a car accident, subacute onset, and excellent neurologic recovery. In our opinion, a symptomatic subarachnoid spinal hematoma should be surgically evacuated at the early phase so neurologic recovery can be expected.
thigh after minor trauma a few years earlier. He was not taking any medication. Initial computed tomography of the body showed evidence of thoracic trauma with costal fractures (rib fracture, K10 and K11) and bilateral lung contusions, pelvic fracture (left obturator ring), transforaminal fracture of the sacrum, and several nonneurologic vertebral fractures (Magerl A1 for T9, T10, and L1). None of these traumatic lesions required surgical treatment. In particular, for the vertebral fractures, orthopedic treatment was ordered (immobilization with thoracolumbar corset). Five days after the accident, while the patient was at bed rest, he described sudden unbearable dorsolumbar pain
WORLD NEUROSURGERY 113: 135-139, MAY 2018
radiating to his lower limbs, which had started after a monobloc mobilization for nursing purposes. This pain was poorly relieved by morphine. A rapidly progressive asymmetric severe paraparesis with loss of reflexes was noticed (muscular strength: 2/5 for the right quadriceps, 1/5 for the left quadriceps, 0/5 for distal muscular groups), associated with a bilateral global hypoesthesia of the lower limbs and with acute urinary retention, whereas anal tonicity was preserved (American Spinal Injury Association C). Full spinal magnetic resonance imaging (MRI) revealed a conus medullaris compression at the level of the L1 and L2 vertebrae by an intradural expansive mass whose signal was isointense in
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underlying tumor or vascular malformation was excluded by pathologic examination of the hematoma. In addition, the peroperative aspect of the vessels was normal. Thus, we estimated that a medullar angiogram was not required. The postoperative course was particularly favorable, with progressive sensitive and motor recovery. Six days after surgery, while the patient was discharged to a rehabilitation center, sensation in his lower limbs was almost normal, but asymmetrical motor deficit persisted (3/5 for the right lower limb and 2/5 for the left lower limb). Six weeks after surgery, his neurologic recovery was favorable, with normal motor and sphincter functions. The neurologic examination revealed only a slight tactile hypoesthesia of the left thigh. Postoperative MRI performed 6 weeks after the surgical procedure showed no signs of residual spinal cord compression or root compression (Figures 3AeC) or signs of spine instability despite the combination of stable fracture and posterior decompression. Insofar as the patient had a history of surgically managed hematoma of the right thigh after minor trauma a few years earlier, an extensive coagulation profile was studied (blood cell count, blood clotting, blood dyscrasias, intrinsic and extrinsic factors, Von Willebrand factor, antiphospholipid antibodies) but showed no significant anomaly.
Figure 1. (A) Magnetic resonance image showing spinal cord (cauda equina) compression at the level of L1 and L2 vertebrae by a wide mass that seems to be located in the intradural space rather than the epidural space, appearing isointense in T1-weighted images. (B) Sagittal T2-weighted image showing a hyperintense aspect of the intradural mass. (C) Axial T2-weighted image showing an intradural hematoma widely extended in the spinal canal, pushing the conus medullaris on the right.
T1-weighted images and hyperintense in T2-weighted images (Figures 1AeC). A surgical evacuation was immediately planned without further exploration (notably at the vascular level) and started approximately 5 hours after the onset of the symptoms, taking into account the transfer from the peripheral hospital to our university hospital. A thoracolumbar spinolaminectomy was performed. The dura mater appeared to be bluish and completely bulged. Under the dura mater, the arachnoid was
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extremely stretched, and its opening allowed the evacuatuation of a strictly subarachnoid hematoma, organized between the cauda equina roots and pushing the conus medullaris to the right side (Figures 2AeD). After evacuation of the hematoma, the subarachnoid space was rinsed with warm saline solution. Venous bleeding was identified and rapidly controlled with gelfoam at the level of the conus medullaris. At the end of the procedure, subarachnoid fluid pulsation was restored. The existence of an
DISCUSSION Generally, the mechanisms that lead to the constitution of subdural and subarachnoid spinal hematomas can be classified into 3 categories5,8: 1) Spontaneous bleeding secondary to vascular or intravascular causes: vascular malformation, hypervascularized tumor, anticoagulant or antiplatelet medications, dyscrasia, hemophilia, collagen vascular disorders3,6,9-15; 2) major injury with sometimes subsequent vertebral fractures6 after a fall, spinal surgery,14 or a car accident4; or 3) moderate or minor injury, for instance lumbar puncture,6,14 spinal anesthesia contingently potentiated by associated intravascular causes,16,17 or acupuncture.18 To the best of our knowledge, only 4 cases of posttraumatic purely subarachnoid spinal hematomas1,14,15,19 (Table 1)
WORLD NEUROSURGERY, https://doi.org/10.1016/j.wneu.2018.02.035
CASE REPORT THIÉBAUD PICART ET AL.
DELAYED POSTTRAUMATIC SUBACUTE LUMBAR SUBARACHNOID HEMATOMA
Figure 2. (A) After spinolaminectomy, the dura mater appears bluish and completely bulged. (B) Under the dura mater, the arachnoid is extremely stretched; the hematoma is strictly subarachnoid. (C) Arachnoid opening making it possible to evacuate a strictly subarachnoid hematoma. (D) The hematoma organized to some degree with clots and pushing the conus medullaris to the right side.
Figure 3. A) Sagittal T1-weighted image 6 weeks after surgery, showing no signs of residual spinal cord or root compression. (B) Sagittal T2-weighted image 6 weeks after surgery. (C) Axial T2-weighted image 6 weeks after surgery.
WORLD NEUROSURGERY 113: 135-139, MAY 2018
have been reported, whereas spinal hematomas involving both the subdural and the subarachnoid spaces are less rare (about 200 reported cases).7 In contrast to subdural hematomas, epidural hematomas are more common,6 probably because the epidural space is relatively larger and contains more vessels with notably venous plexuses.20 The constitution of a spinal subarachnoid hematoma may result from the rupture of subarachnoid vessels resulting from the application of an indirect force or after an elevation of the intravascular pressure in case of sudden increase in abdominal or thoracic pressures.2,4,14 Given that the spinal subdural space is avascular, the bleeding source may constantly come from the subarachnoid space.8 More frequently, the volume of the bleeding might be limited and rapidly washed out by the flow of cerebrospinal fluid, thus avoiding clotting.8,14 Moreover, in cases of more important bleeding, the expansion of the hematoma is rostrocaudal rather than transversal. Consequently, the degree of spinal cord compression is relatively limited, leading to a benign course and explaining why the incidence of spinal subarachnoid hematomas is potentially underestimated.8,14 In most severe cases, blood accumulates into the subarachnoid space until the rupture of the arachnoid membrane with a subsequent spreading into the subdural space.7,8 These elements account for the common association between subdural and subarachnoid hematomas. Such traumatic hematomas seem to occur in the majority of cases at the thoracice lumbar junction (Table 1). Seventy percent of them are located at the lumbar or thoracolumbar level.7 No arterial particularity obviously justifies this preferential localization. In addition, the epidural venous plexus has a homogeneous structure all along the spinal axis.21 On the other hand, from the biomechanical point of view, it is a region that is subjected to forces important enough to cause the rupture of arachnoid veins. For mixed subdural/subarachnoid hematomas, no consensus about management is proposed in the literature. On one hand, spontaneous resolution of symptoms has been reported,22 although the exact underlying mechanisms remain unclear,8
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DELAYED POSTTRAUMATIC SUBACUTE LUMBAR SUBARACHNOID HEMATOMA
Table 1. Clinical Characteristics of Previous Similar Cases Characteristics
Current Case
Woo-Youl et al., 200714
Gupta et al., 199715
Katoh et al., 199219
Mori et al., 19871
Age (years)
20
66
6
76
43
Mechanism
Traffic accident
Fall
Traffic Accident
Fall
Fall
Symptoms
Asymetric flaccid paraparesis, hypoesthesia of lower limbs, urinary retention
Flaccid paraplegia
Flaccid paraplegia
Lumbar pain, right leg monoplegia, urinary incontinence
Left Brown-Sequard syndrome (C2eC3 level)
L1eL2
T11eT12
T11eT12
L1eL2
C2eC3
Management
T12, L1eL2 spinolaminectomy, hematoma evacuation
T11eT12 hemilaminectomy, hematoma evacuation
D8eD12 laminectomy, hematoma evacuation
L1eL2 laminectomy, hematoma evacuation
C2eC3 laminectomy, hematoma evacuation
Timing of the surgery
5 hours after onset of symptoms
Few hours after onset of symptoms
7 days after trauma
1 month after trauma
7 days after trauma
Nature of bleeding as suspected operatively
Venous bleeding
Injured radicular vein
Not found
Not found
Not found
Normal motor and sphincter functions but slight persistent tactile hypoesthesia of left thigh 6 weeks after surgery
No neurologic improvement, death 3 days after surgery resulting from multiorgan failure
No neurologic improvement
Partial improvement of symptoms
Disappearance of weakness of left leg and left anesthesia (C2 level) 6 months after surgery
Level of hematoma
Outcome
warranting conservative treatment insofar as it can be associated with a good outcome.7,9,17,23 On the other hand, more aggressive surgical management is sometimes advocated to avoid spinal cord ischemia and necrosis.5,20 A short duration of symptoms is associated with a good outcome3,4,6,11 as well as a small volume of hematoma8 or the lumbar location compared with cervical or thoracic locations.3,6 The addition of a subarachnoid component to a subdural hematoma leads to a poorer prognosis.7,13 On the MRI scan of the reported case, the precise location of the hematoma was difficult to determine. The pure subarachnoid location was confirmed only peroperatively. In addition to its unusual location, this hematoma was associated with some peculiarities. In comparison with previously published cases, our patient was particularly young (20 years against an average age of 47.75 years).1,7,14,15,19 Pure lumbar location is found only in 10% of cases of mixed subdural/subarachnoid hematomas7 and in only 1 other case of purely subarachnoid hematoma.19 The occurrence in the context of a road traffic accident is rare.4,6 The subacute onset is very uncommon.
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Thoracolumbar MRI was not performed immediately after the accident because the neurologic examination was strictly normal. Nevertheless, we hypothesize that a first transient bleeding occurred at the time of the accident and that its recurrence was triggered by the mobilization of the patient. An increase in neural edema could also be observed 5 days after the accident and involved the genesis of the symptoms by worsening the preexisting compression. CONCLUSION In comparison with other cases of purely subarachnoid spinal hematoma,1,14,15,19 the neurologic recovery of our patient was excellent, probably because he was younger, his hematoma was lower situated, and it was evacuated within a few hours after the onset of symptoms. Thus, we suggest that a symptomatic subarachnoid spinal hematoma should be promptly surgically evacuated to maximize neurologic recovery. REFERENCES 1. Mori H, Terabayashi T, Kitazawa T, Sugiyama Y, Tsukada Y. Traumatic spinal subarachnoid
hematoma presenting with Brown-Sequard syndrome. No Shinkei Geka. 1987;15:427-432. 2. Rader P. Chronic subdural hematoma of the spinal cord: report of a case. N Engl J Med. 1955;253: 374-376. 3. Zilkha A, Nicoletti JM. Acute spinal subdural hematoma: case report. J Neurosurg. 1974;41:627-630. 4. Shimada Y, Sato K, Abe E, Miyakoshi N, Tsutsumi Y. Spinal subdural hematoma. Skeletal Radiol. 1996;25:477. 5. Stewart DH Jr, Watkins ES. Spinal cord compression by chronic subdural hematoma: case report. J Neurosurg. 1969;31:80-82. 6. Paredes ES, Kishore PR, Ward JD. Cervical spinal subdural hematoma. Surg Neurol. 1981;15:477-479. 7. Domenicucci M, Ramieri A, Ciappetta P, Delfini R. Nontraumatic acute spinal subdural hematoma: report of five cases and review of the literature. J Neurosurg. 1999;91:65-73. 8. Seung-Hun O, In-Bo H, Young-Ho K, Kim OJ. Acute spinal subdural hematoma presenting with spontaneously resolving hemiplegia. J Korean Neurosurg Soc. 2009;45:390-393. 9. Wolfe AR, Faroqui RM, Visvikis GA, Mantello MT, Perel AB, Tewari SO. Spinal subarachnoid and subdural hematoma presenting as a BrownSéquard-like myelopathy following minor trauma in a patient on dabigatran etexilate. Radiol Case Rep. 2017;12:257-260.
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10. Alajouanine T, Castaigne P, Lhermitte F. L’hématome sous-dural intra-rachidien à évolution fatale, complication rare de l’hémophilie. Centenaire Soc Med Hop Paris. 1949;22:194-201. 11. Haji Mohd Yasin NA, Donato-Brown D, Taha A. Non-traumatic spontaneous spinal subdural haematoma. N Z Med J. 2012;125:77-80. 12. Han PP, Theodore N, Porter RW, Detwiler PW, Lawton MT, Spetzler RF. Subdural hematoma from a Type I spinal arteriovenous malformation: case report. J Neurosurg. 1999;90:255-257. 13. Morandi X, Riffaud L, Chabert E, Brassier G. Acute nontraumatic spinal subdural hematomas in three patients. Spine. 2001;26:E547-E551. 14. Jang WY, Lee JK, Moon KS, Kwak HJ, Joo SP, Kim IY, et al. Traumatic acute spinal subarachnoid hematoma. J Clin Neurosci. 2007;14:71-73. 15. Gupta SK, Dhir MS, Khosla MS. Traumatic spinal subarachnoid hematoma: report of a case with MRI. Surg Neurol. 1997;48:189-192.
DELAYED POSTTRAUMATIC SUBACUTE LUMBAR SUBARACHNOID HEMATOMA
16. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev. 2003;26:1-49. 17. Vidal M, Strzelecki A, Houadec M, Krikken IR, Danielli A, Souza Neto EP. Spinal subarachnoid haematoma after spinal anaesthesia: case report. Braz J Anesthesiol. 2016;66:533-535. 18. Eghbal K, Ghaffarpasand F. An acute cervical subdural hematoma as the complication of acupuncture: case report and literature review. World Neurosurg. 2016;95:11-13. 19. Katoh H, Manabe K, Shimizu A, Shima K, Chigasaki H, Tsuchiya K. A case of traumatic spinal subarachnoid hematoma causing compression of the cauda equine. No Shinkei Geka. 1992;20:1119-1123. 20. Özkan Ü, Kemaloglu MS, Aydin M, Selçuki M. Widespread post-traumatic acute spinal subdural haematoma: case report and review of the literature. Spinal Cord. 2002;40:304-306. 21. Lazorthes G, Gouaze A, Djindjian R. Vascularisation et circulation de la moelle épinière. Paris: Masson; 1973.
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22. Mavroudakis N, Levivier M, Rodesch G. Central cord syndrome due to a spontaneously regressive spinal subdural hematoma. Neurology. 1990;40: 1306-1308.
23. Kuo-Sheng H, Chun-Chung L, Cheng-Haung W, Wang CJ, Howng SL. Traumatic spinal subdural hematoma with spontaneous resolution. Spine. 2002;24:534-538.
Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 11 October 2017; accepted 6 February 2018 Citation: World Neurosurg. (2018) 113:135-139. https://doi.org/10.1016/j.wneu.2018.02.035 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2018 Elsevier Inc. All rights reserved.
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Delayed Posttraumatic Subacute Lumbar Subarachnoid Hematoma: Case Report and Review of the Literature Thie´baud Picart1, Timothe´e Jacquesson1, Emmanuel Jouanneau1-3, Moncef Berhouma1,4
Key words Lumbar spine - Spinal hematoma - Subarachnoid hematoma - Trauma
- BACKGROUND:
Abbreviations and Acronyms MRI: magnetic resonance imaging
- CASE
-
Traumatic spinal subarachnoid hematoma, associated or not with a concurrent subdural hematoma, has rarely been described. The evolution of such hematomas is heterogeneous. This study aims at defining the most accurate management, which is currently not standardized.
Available online: www.sciencedirect.com
DESCRIPTION: A 20-year-old man, victim of a high-kinetic road accident 5 days before and with several nonneurologic nonsurgical vertebral fractures, experienced a sudden dorsolumbar pain radiating to his lower limbs. A rapidly progressive asymmetric paraparesis with loss of reflexes was noticed, associated with bilateral global hypoesthesia of the lower limbs and with acute urinary retention, whereas the anal tonicity was preserved (American Spinal Injury Association C). Magnetic resonance imaging scan revealed a conus medullaris compression at the level of the L1eL2 vertebrae by an intradural expansive mass. Immediate surgical decompression revealed a strictly subarachnoid hematoma. Venous bleeding was seen at the level of the conus medullaris and controlled. Pathologic examination of the clot excluded an underlying tumor or vascular abnormality. The complete coagulation profile was normal.
1878-8750/$ - see front matter ª 2018 Elsevier Inc. All rights reserved.
- CONCLUSION:
From the 1Department of Neurosurgery, Lyon University Hospital, Hospices Civils de Lyon, Bron; 2University Claude Bernard Lyon, Lyon; 3Signaling, Metabolism and Tumor Progression, Cancer Research Centre of Lyon, Lyon; and 4 CREATIS Laboratory, Lyon University, Lyon, France To whom correspondence should be addressed: Moncef Berhouma, M.D., M.Sc. [E-mail: [email protected]] Citation: World Neurosurg. (2018) 113:135-139. https://doi.org/10.1016/j.wneu.2018.02.035 Journal homepage: www.WORLDNEUROSURGERY.org
INTRODUCTION Traumatic spinal subarachnoid hematoma, associated or not with a concurrent subdural hematoma, has rarely been described.1-3 The evolution of such hematomas is heterogenous, opposing acute collection few hours after spinal injury and chronic collection similarly to their cranial counterparts, occurring several weeks after minor trauma.2,4,5 They are revealed by symptoms related to spinal cord compression, radicular compression, or both6,7 that can be uni- or bilateral.1,8,9 The management of such hematomas is not standardized.7 We herein report an unusual case of delayed posttraumatic purely subarachnoid subacute lumbar hematoma with a review of the literature.
CASE DESCRIPTION A 20-year-old man was referred to the intensive care unit of a peripheral hospital after a very high-kinetic automobile accident. His medical history consisted of surgically managed hematoma of the right
Six weeks after surgery, the neurologic examination revealed only a slight tactile hypoesthesia of the left thigh. With only 4 reported cases, purely subarachnoid spinal hematomas remain widely rarer than epidural hematomas. The reported case possesses a certain number of peculiarities: young age, pure subarachnoid location, lumbar location, occurrence after a car accident, subacute onset, and excellent neurologic recovery. In our opinion, a symptomatic subarachnoid spinal hematoma should be surgically evacuated at the early phase so neurologic recovery can be expected.
thigh after minor trauma a few years earlier. He was not taking any medication. Initial computed tomography of the body showed evidence of thoracic trauma with costal fractures (rib fracture, K10 and K11) and bilateral lung contusions, pelvic fracture (left obturator ring), transforaminal fracture of the sacrum, and several nonneurologic vertebral fractures (Magerl A1 for T9, T10, and L1). None of these traumatic lesions required surgical treatment. In particular, for the vertebral fractures, orthopedic treatment was ordered (immobilization with thoracolumbar corset). Five days after the accident, while the patient was at bed rest, he described sudden unbearable dorsolumbar pain
WORLD NEUROSURGERY 113: 135-139, MAY 2018
radiating to his lower limbs, which had started after a monobloc mobilization for nursing purposes. This pain was poorly relieved by morphine. A rapidly progressive asymmetric severe paraparesis with loss of reflexes was noticed (muscular strength: 2/5 for the right quadriceps, 1/5 for the left quadriceps, 0/5 for distal muscular groups), associated with a bilateral global hypoesthesia of the lower limbs and with acute urinary retention, whereas anal tonicity was preserved (American Spinal Injury Association C). Full spinal magnetic resonance imaging (MRI) revealed a conus medullaris compression at the level of the L1 and L2 vertebrae by an intradural expansive mass whose signal was isointense in
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DELAYED POSTTRAUMATIC SUBACUTE LUMBAR SUBARACHNOID HEMATOMA
underlying tumor or vascular malformation was excluded by pathologic examination of the hematoma. In addition, the peroperative aspect of the vessels was normal. Thus, we estimated that a medullar angiogram was not required. The postoperative course was particularly favorable, with progressive sensitive and motor recovery. Six days after surgery, while the patient was discharged to a rehabilitation center, sensation in his lower limbs was almost normal, but asymmetrical motor deficit persisted (3/5 for the right lower limb and 2/5 for the left lower limb). Six weeks after surgery, his neurologic recovery was favorable, with normal motor and sphincter functions. The neurologic examination revealed only a slight tactile hypoesthesia of the left thigh. Postoperative MRI performed 6 weeks after the surgical procedure showed no signs of residual spinal cord compression or root compression (Figures 3AeC) or signs of spine instability despite the combination of stable fracture and posterior decompression. Insofar as the patient had a history of surgically managed hematoma of the right thigh after minor trauma a few years earlier, an extensive coagulation profile was studied (blood cell count, blood clotting, blood dyscrasias, intrinsic and extrinsic factors, Von Willebrand factor, antiphospholipid antibodies) but showed no significant anomaly.
Figure 1. (A) Magnetic resonance image showing spinal cord (cauda equina) compression at the level of L1 and L2 vertebrae by a wide mass that seems to be located in the intradural space rather than the epidural space, appearing isointense in T1-weighted images. (B) Sagittal T2-weighted image showing a hyperintense aspect of the intradural mass. (C) Axial T2-weighted image showing an intradural hematoma widely extended in the spinal canal, pushing the conus medullaris on the right.
T1-weighted images and hyperintense in T2-weighted images (Figures 1AeC). A surgical evacuation was immediately planned without further exploration (notably at the vascular level) and started approximately 5 hours after the onset of the symptoms, taking into account the transfer from the peripheral hospital to our university hospital. A thoracolumbar spinolaminectomy was performed. The dura mater appeared to be bluish and completely bulged. Under the dura mater, the arachnoid was
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extremely stretched, and its opening allowed the evacuatuation of a strictly subarachnoid hematoma, organized between the cauda equina roots and pushing the conus medullaris to the right side (Figures 2AeD). After evacuation of the hematoma, the subarachnoid space was rinsed with warm saline solution. Venous bleeding was identified and rapidly controlled with gelfoam at the level of the conus medullaris. At the end of the procedure, subarachnoid fluid pulsation was restored. The existence of an
DISCUSSION Generally, the mechanisms that lead to the constitution of subdural and subarachnoid spinal hematomas can be classified into 3 categories5,8: 1) Spontaneous bleeding secondary to vascular or intravascular causes: vascular malformation, hypervascularized tumor, anticoagulant or antiplatelet medications, dyscrasia, hemophilia, collagen vascular disorders3,6,9-15; 2) major injury with sometimes subsequent vertebral fractures6 after a fall, spinal surgery,14 or a car accident4; or 3) moderate or minor injury, for instance lumbar puncture,6,14 spinal anesthesia contingently potentiated by associated intravascular causes,16,17 or acupuncture.18 To the best of our knowledge, only 4 cases of posttraumatic purely subarachnoid spinal hematomas1,14,15,19 (Table 1)
WORLD NEUROSURGERY, https://doi.org/10.1016/j.wneu.2018.02.035
CASE REPORT THIÉBAUD PICART ET AL.
DELAYED POSTTRAUMATIC SUBACUTE LUMBAR SUBARACHNOID HEMATOMA
Figure 2. (A) After spinolaminectomy, the dura mater appears bluish and completely bulged. (B) Under the dura mater, the arachnoid is extremely stretched; the hematoma is strictly subarachnoid. (C) Arachnoid opening making it possible to evacuate a strictly subarachnoid hematoma. (D) The hematoma organized to some degree with clots and pushing the conus medullaris to the right side.
Figure 3. A) Sagittal T1-weighted image 6 weeks after surgery, showing no signs of residual spinal cord or root compression. (B) Sagittal T2-weighted image 6 weeks after surgery. (C) Axial T2-weighted image 6 weeks after surgery.
WORLD NEUROSURGERY 113: 135-139, MAY 2018
have been reported, whereas spinal hematomas involving both the subdural and the subarachnoid spaces are less rare (about 200 reported cases).7 In contrast to subdural hematomas, epidural hematomas are more common,6 probably because the epidural space is relatively larger and contains more vessels with notably venous plexuses.20 The constitution of a spinal subarachnoid hematoma may result from the rupture of subarachnoid vessels resulting from the application of an indirect force or after an elevation of the intravascular pressure in case of sudden increase in abdominal or thoracic pressures.2,4,14 Given that the spinal subdural space is avascular, the bleeding source may constantly come from the subarachnoid space.8 More frequently, the volume of the bleeding might be limited and rapidly washed out by the flow of cerebrospinal fluid, thus avoiding clotting.8,14 Moreover, in cases of more important bleeding, the expansion of the hematoma is rostrocaudal rather than transversal. Consequently, the degree of spinal cord compression is relatively limited, leading to a benign course and explaining why the incidence of spinal subarachnoid hematomas is potentially underestimated.8,14 In most severe cases, blood accumulates into the subarachnoid space until the rupture of the arachnoid membrane with a subsequent spreading into the subdural space.7,8 These elements account for the common association between subdural and subarachnoid hematomas. Such traumatic hematomas seem to occur in the majority of cases at the thoracice lumbar junction (Table 1). Seventy percent of them are located at the lumbar or thoracolumbar level.7 No arterial particularity obviously justifies this preferential localization. In addition, the epidural venous plexus has a homogeneous structure all along the spinal axis.21 On the other hand, from the biomechanical point of view, it is a region that is subjected to forces important enough to cause the rupture of arachnoid veins. For mixed subdural/subarachnoid hematomas, no consensus about management is proposed in the literature. On one hand, spontaneous resolution of symptoms has been reported,22 although the exact underlying mechanisms remain unclear,8
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CASE REPORT THIÉBAUD PICART ET AL.
DELAYED POSTTRAUMATIC SUBACUTE LUMBAR SUBARACHNOID HEMATOMA
Table 1. Clinical Characteristics of Previous Similar Cases Characteristics
Current Case
Woo-Youl et al., 200714
Gupta et al., 199715
Katoh et al., 199219
Mori et al., 19871
Age (years)
20
66
6
76
43
Mechanism
Traffic accident
Fall
Traffic Accident
Fall
Fall
Symptoms
Asymetric flaccid paraparesis, hypoesthesia of lower limbs, urinary retention
Flaccid paraplegia
Flaccid paraplegia
Lumbar pain, right leg monoplegia, urinary incontinence
Left Brown-Sequard syndrome (C2eC3 level)
L1eL2
T11eT12
T11eT12
L1eL2
C2eC3
Management
T12, L1eL2 spinolaminectomy, hematoma evacuation
T11eT12 hemilaminectomy, hematoma evacuation
D8eD12 laminectomy, hematoma evacuation
L1eL2 laminectomy, hematoma evacuation
C2eC3 laminectomy, hematoma evacuation
Timing of the surgery
5 hours after onset of symptoms
Few hours after onset of symptoms
7 days after trauma
1 month after trauma
7 days after trauma
Nature of bleeding as suspected operatively
Venous bleeding
Injured radicular vein
Not found
Not found
Not found
Normal motor and sphincter functions but slight persistent tactile hypoesthesia of left thigh 6 weeks after surgery
No neurologic improvement, death 3 days after surgery resulting from multiorgan failure
No neurologic improvement
Partial improvement of symptoms
Disappearance of weakness of left leg and left anesthesia (C2 level) 6 months after surgery
Level of hematoma
Outcome
warranting conservative treatment insofar as it can be associated with a good outcome.7,9,17,23 On the other hand, more aggressive surgical management is sometimes advocated to avoid spinal cord ischemia and necrosis.5,20 A short duration of symptoms is associated with a good outcome3,4,6,11 as well as a small volume of hematoma8 or the lumbar location compared with cervical or thoracic locations.3,6 The addition of a subarachnoid component to a subdural hematoma leads to a poorer prognosis.7,13 On the MRI scan of the reported case, the precise location of the hematoma was difficult to determine. The pure subarachnoid location was confirmed only peroperatively. In addition to its unusual location, this hematoma was associated with some peculiarities. In comparison with previously published cases, our patient was particularly young (20 years against an average age of 47.75 years).1,7,14,15,19 Pure lumbar location is found only in 10% of cases of mixed subdural/subarachnoid hematomas7 and in only 1 other case of purely subarachnoid hematoma.19 The occurrence in the context of a road traffic accident is rare.4,6 The subacute onset is very uncommon.
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Thoracolumbar MRI was not performed immediately after the accident because the neurologic examination was strictly normal. Nevertheless, we hypothesize that a first transient bleeding occurred at the time of the accident and that its recurrence was triggered by the mobilization of the patient. An increase in neural edema could also be observed 5 days after the accident and involved the genesis of the symptoms by worsening the preexisting compression. CONCLUSION In comparison with other cases of purely subarachnoid spinal hematoma,1,14,15,19 the neurologic recovery of our patient was excellent, probably because he was younger, his hematoma was lower situated, and it was evacuated within a few hours after the onset of symptoms. Thus, we suggest that a symptomatic subarachnoid spinal hematoma should be promptly surgically evacuated to maximize neurologic recovery. REFERENCES 1. Mori H, Terabayashi T, Kitazawa T, Sugiyama Y, Tsukada Y. Traumatic spinal subarachnoid
hematoma presenting with Brown-Sequard syndrome. No Shinkei Geka. 1987;15:427-432. 2. Rader P. Chronic subdural hematoma of the spinal cord: report of a case. N Engl J Med. 1955;253: 374-376. 3. Zilkha A, Nicoletti JM. Acute spinal subdural hematoma: case report. J Neurosurg. 1974;41:627-630. 4. Shimada Y, Sato K, Abe E, Miyakoshi N, Tsutsumi Y. Spinal subdural hematoma. Skeletal Radiol. 1996;25:477. 5. Stewart DH Jr, Watkins ES. Spinal cord compression by chronic subdural hematoma: case report. J Neurosurg. 1969;31:80-82. 6. Paredes ES, Kishore PR, Ward JD. Cervical spinal subdural hematoma. Surg Neurol. 1981;15:477-479. 7. Domenicucci M, Ramieri A, Ciappetta P, Delfini R. Nontraumatic acute spinal subdural hematoma: report of five cases and review of the literature. J Neurosurg. 1999;91:65-73. 8. Seung-Hun O, In-Bo H, Young-Ho K, Kim OJ. Acute spinal subdural hematoma presenting with spontaneously resolving hemiplegia. J Korean Neurosurg Soc. 2009;45:390-393. 9. Wolfe AR, Faroqui RM, Visvikis GA, Mantello MT, Perel AB, Tewari SO. Spinal subarachnoid and subdural hematoma presenting as a BrownSéquard-like myelopathy following minor trauma in a patient on dabigatran etexilate. Radiol Case Rep. 2017;12:257-260.
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CASE REPORT THIÉBAUD PICART ET AL.
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DELAYED POSTTRAUMATIC SUBACUTE LUMBAR SUBARACHNOID HEMATOMA
16. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev. 2003;26:1-49. 17. Vidal M, Strzelecki A, Houadec M, Krikken IR, Danielli A, Souza Neto EP. Spinal subarachnoid haematoma after spinal anaesthesia: case report. Braz J Anesthesiol. 2016;66:533-535. 18. Eghbal K, Ghaffarpasand F. An acute cervical subdural hematoma as the complication of acupuncture: case report and literature review. World Neurosurg. 2016;95:11-13. 19. Katoh H, Manabe K, Shimizu A, Shima K, Chigasaki H, Tsuchiya K. A case of traumatic spinal subarachnoid hematoma causing compression of the cauda equine. No Shinkei Geka. 1992;20:1119-1123. 20. Özkan Ü, Kemaloglu MS, Aydin M, Selçuki M. Widespread post-traumatic acute spinal subdural haematoma: case report and review of the literature. Spinal Cord. 2002;40:304-306. 21. Lazorthes G, Gouaze A, Djindjian R. Vascularisation et circulation de la moelle épinière. Paris: Masson; 1973.
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22. Mavroudakis N, Levivier M, Rodesch G. Central cord syndrome due to a spontaneously regressive spinal subdural hematoma. Neurology. 1990;40: 1306-1308.
23. Kuo-Sheng H, Chun-Chung L, Cheng-Haung W, Wang CJ, Howng SL. Traumatic spinal subdural hematoma with spontaneous resolution. Spine. 2002;24:534-538.
Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 11 October 2017; accepted 6 February 2018 Citation: World Neurosurg. (2018) 113:135-139. https://doi.org/10.1016/j.wneu.2018.02.035 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2018 Elsevier Inc. All rights reserved.
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