Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 2, 2011, pp. 281-284

Neurology India, Vol. 59, No. 2, March-April, 2011, pp. 281-284

Case Report

Spinal subdural hematoma following cranial surgery: A case report and review of the literature

Jinping Liu¹, Bo Wu¹, Hailong Feng¹, Chao You²

¹ Department of Neurosurgery, Sichuan Provincial People's Hospital, Sichuan University, Chengdu, Sichuan, China
² Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China

Correspondence Address: Chao You, Department of Neurosurgery, West China Hospital, Sichuan University, 37 Guoxuexiang Street, Chengdu, Sichuan - 610 041, China, youchao_hx@163.com

Date of Submission: 20-Dec-2010
Date of Decision: 21-Dec-2010
Date of Acceptance: 28-Dec-2010

Code Number: ni11075

PMID: 21483134

DOI: 10.4103/0028-3886.79151

Abstract

Keywords: Complication, cranial surgery, spinal subdural hematoma

Introduction

Spinal subdural hematoma (SDH) is a rare and if not treated early is associated with serious and permanent neurological deficits. ^[1] This complication usually occurs in the setting of spinal instrumentation or coagulopathy and only fewer cases have been reported as a complication of cranial surgery. ^[2],[3],[4]

Case Report

A 26-year-old man presented with 4 years history of intermittent headache and numbness of right face of 1 month duration. On neurologic examination, only slight hypoesthesia on the right side of the face was detected. Cranial magnetic resonance imaging (MRI) demonstrated a giant mass lesion at the right trigone of ventricle, suggestive of a meningioma [Figure - 1]a. Laboratory examinations, including coagulation profile were normal. Tumor was totally removed by a right parietooccipital craniotomy. Histological examination was meningioma (WHO I). A postoperative computer tomography (CT) scan showed right subdural hematoma [Figure - 1]b with mild mass effect. The patient remained asymptomatic and received no specific treatment. On the fourth postoperative day, he had a sudden onset of intolerable low back pain radiating to right thigh and was nonresponsive to analgesics. On physical examination, mild tenderness was found at the spinous process between L1 and L5. Straight leg-raising test on the right side was limited to 40 degrees. An emergency lumbosacral MRI showed an SDH at L3-S1 levels [Figure - 2]a and b. As he had no response with analgesics, surgical intervention was considered. He had a hemilaminectomy of L3-L4. At surgery, a tight, bluish, and nonpulsatile dura was found. As the dura was opened, a liquid hematoma was encountered with intact arachnoid membrane, which confirmed the diagnosis of SDH. The hematoma was totally removed. No vascular malformations or other lesions were found at operation. Postoperatively he had complete relief of symptoms. He was discharged without any neurologic deficits. Postoperative MRI revealed no residue of the hematoma [Figure - 2]c and d.

Discussion

SDH is a rare disorder with a wide etiologic spectrum. Unlike the intracranial subdural space, there are no bridging veins in the spinal subdural space, thus the origin of bleeding remains unclear. Of the nontraumatic SDHs, approximately half of them are associated with coagulopathy and iatrogenic factors, including lumbar puncture, spinal epidural anesthetic procedures, and spinal surgeries. ^[3],[4] Underlying vascular malformation is the cause of SDH in a few cases ^[1],[5] and in some cases no cause could be identified-idiopathic. ^[2] SDH rarely occurs after a cranial surgery. Silver et al. ^[6] first reported a symptomatic thoracolumbar SDH as a complication of ventriculoperitoneal shunting in 1991. With the wide use of MRI, the number of reported cases is increasing.

The details of all the 21 cases of SDH following craniotomy reported in the literature are given in [Table - 1]. One of the proposed mechanisms for the pathogenesis of SDH following cranial surgery is the migration of blood from intracranial subdural space to spinal subdural space. ^{[6],[7],[8],[9],[10],[11]} This hypothesis is further supported by the anatomical continuity between intracranial and spinal subdural space. ^[12],[13] In the case reported by Lecouvet et al, ^[14] MRI demonstrated a thin hemorrhagic collection connecting cranial and lumbar hematoma, thus giving further support to this hypothesis. The dorsal and lumbosacral location of the hematoma can be explained by the influence of gravity in lying on supine position during the postoperative period.

What factors participate in the migration of blood from intracranial subdural space to spinal counterpart is not clear. One of the explanations is that excessive drainage of cerebral spinal fluid (CSF) might play an important role in the downward movement of intracranial blood through the widened spinal subdural space. ^{[7],[8],[9],[11],[15]} The majority of the reported SDHs after the surgical procedures are associated with massive loss of CSF. Kim et al. ^[7] reported 4 cases of postcraniotomy SDHs in a series of 55 patients after intracranial aneurysm surgery. In all the 4 cases, there was overdrainage of CSF. Yamaguchi et al^[16] reported a case of SDH after intrathecal administration of urokinase in a patient with aneurysmal subarachnoid hemorrhage to prevent cerebral vasospasm. The authors proposed that the lysed blood from the intracranial space might have settled in the spinal sudural space.

In our patients there was a massive loss of CSF during the operation and this had resulted in the postoperative SDH in the infratentorial space [Figure - 1]c. The blood in the intracranial subdural space might have migrated to spinal subdural space. The MRI findings in our patient were consistent with acute hematoma. ^[17] However, intraoperative findings in our patient was liquefied blood. We speculate that probably the liquefied blood from the intracranial subdural space might have migrated to the spinal subdural space and this may account for the homogenous lower signal on the T2 sequence.

The clinical features in SDH are related to compression or chemical irritation of the neural structures. The clinical course of postcraniotomy SDH is much more benign than that of idiopathic or traumatic SDH and it has been attributed to the lumbosacral location of the SDH and also to the possible low pressure of the spinal canal in the absence of active bleeding. ^[2],[10] Possibly because of these factors, often these patients are managed conservatively and operation is indicated when there is neurologic deterioration or the initial neurologic deficits are severe. ^[18],[22]

References

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