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Surgical Neurology 70 (2008) 213 – 216 www.surgicalneurology-online.com
“Migration” of traumatic subarachnoid hematoma? A case report Hsien-Chih Chen, MDa,b,⁎, Peng-Wei Hsu, MD a , Wen-Ching Tzaan, MD a,b a
Department of Neurosurgery, Chang Gung Memorial Hospital, Keelung 204, Taiwan b School of Medicine, Chang Gung University, TaoYuan 333, Taiwan Received 26 February 2007; accepted 9 April 2007
Background: Traumatic spinal SAH with neurologic deficits is rare and easily misdiagnosed, especially after traumatic intracranial hemorrhage. Case Description: We report a case of spinal SAH with root compression occurring after a scooter accident. Conclusions: Physicians should be aware of descending migration of intracranial SAH as a possible cause of spinal cord or root compression, especially in the patient with late onset spinal symptoms. © 2008 Elsevier Inc. All rights reserved.
Subarachnoid hematoma; Traumatic; Spinal
1. Introduction Most traumatic spinal SAHs have associated coagulation disorders, or occur as spinal procedure complications [1,5,7,8,12]. Only 5 reported cases were caused by “real” traumatic injury (trivial trauma, falling accident, stab injury, etc) [3,4,10,11,14]. This report presents a case that developed spinal SAH after a scooter accident. Spinal SAH in this case was not associated with any coagulation abnormality. The patient recovered after surgical drainage. This report also discusses the possible causes of this rare problem.
Chang Gung Memorial Hospital. Her medical history showed no noteworthy event, that is, no lumbar puncture, blood disease, or anticoagulant therapy. Initially, she was treated
2. Case description 2.1. History This 41-year-old woman fell off her scooter while riding on a bumpy road. She lost consciousness initially and regained consciousness in the emergency department at
Abbreviations: CSF, cerebrospinal fluid; CT, computed tomography; MRI, magnetic resonance imaging; SAH, subarachnoid hematoma. ⁎ Corresponding author. Chang Gung Memorial Hospital, Keelung 204, Taiwan. Tel.: +886 2 24313131x2670; fax: +886 2 24332655. E-mail addresses: [email protected]
, [email protected]
(H.-C. Chen). 0090-3019/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.surneu.2007.04.003
Fig. 1. Brain CT showed some SAHs within the left sylvian fissure and left temporal sulci.
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under the impression of traumatic intracranial SAH (left sylvian fissure and left temporal sulci) identified by brain CT (Fig. 1) and right clavicle fracture demonstrated by x-ray. 2.2. Examination After admission, the patient complained of left posterior thigh numbness and heavy sensation, as well as headache and constipation. Seven days later, her headache subsided. However, numbness extended to the bilateral buttock and
radiated to the bilateral posterior calves. Lower back progressive soreness and pain were noted. The patient was only able to walk and lie down by frequently changing her position and was unable to sit for more than 1 minute. Prothrombin and partial thromboplastin times and platelet count were all within normal limits. Lumbar x-ray was normal. Lumbar MRI demonstrated a fusiform lesion (largest dimension, 35.3 mm) with hyperintensity on T1WI, hypointensity on T2WI, located at the lower end of the
Fig. 2. Magnetic resonance imaging demonstrated a fusiform lesion at the lower end of the lumbar thecal sac. The lesion had hyperintensity on T1WI, hypointensity on T2WI, and was not suppressed with a fat suppression technique. A: Sagittal T2; B: sagittal T1; C: fat suppression T1.
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No hematoma was noted over the epidural or subdural spaces. After an incision was made in the arachnoid membrane, considerable brownish fluid gushed out. An old blood clot was identified within nerves and vessels, and no definite bleeding point was detected. No tumor or vascular abnormality was found (Fig. 3). Pathologic examination showed fragments of blood and fibrin clots with scattered acute and chronic inflammatory cells. Few hemosiderinladened histiocytes and fibroblasts were present, a finding compatible with that for an old hematoma. 2.4. Postoperative course The pain and radiating numbness disappeared immediately after surgery. The patient was discharged after 1 week and returned to work symptom-free 2 weeks after discharge. At 1-year follow-up, the patient had no neurologic deficit or pain. 3. Discussion
Fig. 3. Intraoperative photographs: brownish fluid and blackish blood clots located beneath the arachnoid. A: Before arachnoid incision; B: after arachnoid opening.
lumbar thecal sac (Fig. 2A and B). Lipoma was not likely, because the lesion was not suppressed with a fat suppression technique (Fig. 2C). Hemorrhage or calcification was suspected. 2.3. Operation Because of worsening symptoms, a partial lower L5 and upper S1 laminectomy was performed for surgical exposure.
A circumscribed collection of blood in the spinal subarachnoid space is a very uncommon scenario. Most traumatic spinal SAHs have a blood coagulation defect (anticoagulant therapy, thrombocytopenia, etc), or occur as a complication of spinal procedures (spinal anesthesia, myelography, acupuncture, etc) [1,5,7,8,12]. A literature review found only 5 cases of “real” traumatic injury [3,4,10,11,14] (Table 1). This case is the first reported, except for those cases after lumbar spinal tap traumatic spinal SAHs located at the end of the spinal canal. This patient developed this condition after a fall and has had no history of coagulation disorders or iatrogenic spinal procedures. The migration of intracranial SAH in this case could lead to a suspicion of the bleeding source of spinal SAH and it could not be completely disproved. However, there is no existing report elucidating this relationship. Conversely, rapid changes in intraabdominal and intrathoracic pressures secondary to trauma elevate intraluminal pressures within vessels traversing the spinal subarachnoid space. When CSF pressure momentarily drops lower than intravascular pressure, it is possible that vessels rupture and produce spinal subarachnoid bleeding [2,11]. As a rule, the fibrinolytic action of CSF and its diluent and continuous “washing” action prevent clot formation.
Table 1 Reviewed cases of traumatic spinal SAH Literature
Mori et al  Thakur et al  Pau et al  Katoh et al  Gupta et al  Present case
Recovered 6 mo later Good
M F M F
Hyperextension injury Stab injury Receiving recoil of shotgun Fell down Hit by a tractor Fell down
60 76 6 41
C1-C2 L1-L2 T3-T7 L1-L2 T11-T12 L5-S1
1 mo 7d 7d
Operation Operation Operation
Improved partially No improvement Good
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Consequently, a situation retarding normal liquid circulationproducing stasis and, thus, causing sufficient blood accumulation (such as a spinal neoplasm or preexisting arachnoiditis) might be reasonably suspected . In this case, location of the hematoma at the spinal canal tail could be 1 more reason predisposing to further clotting, likely due to gravity sedimentation and reduced “washing” action. The most effective diagnostic modality for spinal SAH is MRI, even though differentiating between subdural or subarachnoid sites is difficult. Surgical intervention is indicated for cases with neurologic deterioration, although 1 case achieved a good outcome without surgery . Outcome of spinal SAH is related to its location level, duration of compression, and clot volume. In addition, a possibility of arachnoid adhesions, which can adversely affect long-term outcomes, should be considered . 4. Conclusion A literature review showed that this case is extremely pathologically rare. Only 5 other cases of traumatic spinal SAHs have been reported, and all—like this case—were without a history of a blood coagulation disorder or spinal tap. The possibility of downward tracking of intracranial blood could not be excluded; neurosurgeons should be aware of descending migration of intracranial SAH as a possible cause of spinal cord or root compression, especially in the patient with late-onset spinal symptoms. References  Brem SS, Hafler DA, Van Uitert RL, Ruff RL, Reichert WH. Spinal subarachnoid hematoma: a hazard of lumbar puncture resulting in reversible paraplegia. N Engl J Med 1981;304(17):1020-1.  Calhoun JM, Boop F. Spontaneous spinal subdural hematoma: case report and review of the literature. Neurosurgery 1991;29(1):133-4.  Gupta SK, Dhir JS, Khosla VK. Traumatic spinal subarachnoid hematoma: report of a case with MRI. Surg Neurol 1997;48(2):189-92.  Katoh H, Manabe K, Shimizu A, Shima K, Chigasaki H, Tsuchiya K. A case of traumatic spinal subarachnoid hematoma causing compression of the cauda equina. No Shinkei Geka 1992;20(10):1119-23.  Keane JR, Ahmadi J, Gruen P. Spinal epidural hematoma with subarachnoid haemorrhage caused by acupuncture. AJNR Am J Neuroradiol 1993;14(2):365-6.  Khosla VK, Kak VK, Mathuriya SN. Chronic spinal subdural hematomas. Report of two cases. J Neurosurg 1985;63(4):636-9.
 Koehler PJ, Kuiters RR. Brown-Sequard syndrome caused by a spinal subarachnoid hematoma due to anticoagulant therapy. Surg Neurol 1986;25(2):191-3.  Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev 2003;26(1): 1-49.  Masdeu JC, Breuer AC, Schoene WC. Spinal subarachnoid hematomas: clue to a source of bleeding in traumatic lumbar puncture. Neurology 1979;29(6):872-6.  Mori H, Terabayashi T, Kitazawa T, Sugiyama Y, Tsukada Y. Traumatic spinal subarachnoid hematoma presenting with BrownSequard syndrome. No Shinkei Geka 1987;15(4):427-32.  Pau A, Brambilla M, Cossu M, Francaviglia N, Siccardi D, Silvestro C. Spinal subarachnoid hematoma of unknown etiology. A case report. Neurochirurgia (Stuttg) 1991;34(5):151-3.  Scott EW, Cazenave CR, Virapongse C. Spinal subarachnoid hematoma complicating lumbar puncture: diagnosis and management. Neurosurgery 1989;25(2):287-92 [discussion 292-93].  Swann KW, Ropper AH, New PF, Poletti CE. Spontaneous spinal subarachnoid haemorrhage and subdural hematoma. Report of two cases. J Neurosurg 1984;61(5):975-80.  Thakur RC, Mittal RS, Khosla VK. Spinal subarachnoid hematomas after stab injury of the cauda equina. South Afr J Surg 1990;26:21-3.
Commentary The authors have carefully presented a very unusual and thought-provoking case, and the scarce literature has been well reviewed. Not mentioned in their review is the possibility that the expected hypercoagulability after head injury might have contributed to the stability of a subarachnoid clot that might normally not have formed a stable coagulum. Also, one might speculate that the specific pathophysiology of the neurologic deficit was related less to the compression from the clot and more to the late developing inflammatory byproducts of the clot as it began to lyse at the 7- to 10-day period. Overall, this case describes a rare clinical entity that will only be discovered if considered in a differential diagnosis. The authors have done a service by presenting this case. Charles David Hunt, MD Marquette General Neurosurgery, Marquette, MI 49855, USA