Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 52, Num. 2, 2004, pp. 284-286

Neurology India, Vol. 52, No. 2, April-June, 2004, pp. 284-286

Letter To Editor

Death following Ventricular cerebrospinal fluid shunting in supratentorial malignant tumor associated with hydrocephalus

Muzumdar DP, Bhatjiwale MG, Goel A

Department of Neurosurgery, King Edward VII Memorial Hospital and Seth G. S. Medical College, Parel, Mumbai

Correspondence Address:Department of Neurosurgery, King Edward VII Memorial Hospital and Seth G. S. Medical College, Parel, Mumbai
dmuzumdar@hotmail.com

Code Number: ni04101

Sir
A 26-year-old male presented (in 1996) with complaints of headaches and right focal motor seizures for two years. The patient was dull and drowsy but had no higher function disturbance or focal neurological deficit. There was bilateral florid papilledema. Computerized tomography (CT) scan showed a large, anterior corpus callosal tumor and moderate hydrocephalus [Figure - 1]. A biventriculoperitoneal shunt was performed. The cerebrospinal fluid pressure was high and it flowed out like a ′jet′ through the cannula used during the shunt. Following surgery, the patient could not be reversed from anesthesia. Neurological examination three hours after surgery revealed that the patient was deeply unconscious and the left pupil was dilated and fixed. Within an hour, the right pupil also dilated and was unresponsive to light. Cerebral decongestants proved to be of no benefit. CT scan showed that both the ventricular catheters were in-situ and the ventricles were collapsed [Figure - 2]. The cerebral hemispheres showed extensive edema. The patient succumbed on the third postoperative day. Post-mortem examination showed swollen cerebral hemispheres and generalized cerebral edema.

Discussion

Supratentorial intra-axial tumors lead to a rise in the intracranial pressure by virtue of the tumor mass and its surrounding edema. Occasionally, there is a ventricular dilatation as a result of direct or indirect compression of the cerebrospinal fluid pathways[1],[2]. In large hemispheric tumors, which result in a significant rise in the intracranial pressure, contralateral ventricular enlargement is frequently seen. Ventricular dilatation and cerebral edema are often considered to be a part of the pathological process. In our case an unconventional treatment strategy was adopted. A biventricular shunt was done. The aim of such a procedure was to attempt to reduce the intracranial pressure, relieve the patient of his symptoms, to normalize the altered cerebral blood flow and to ′relax′ the brain that would assist the surgeon in the definitive surgical procedure planned through an interhemispheric approach at a later date. The strategy was unsuccessful and the patient worsened dramatically after the shunt.

We attempted to analyze the cause of the fatal outcome in an otherwise well preserved patient and reviewed the relevant literature. As the shunt surgery in itself was uneventful and the postoperative scan did not show any evidence of hemorrhage, direct trauma by the shunt assembly appeared unlikely. It is known that ventricular tapping and shunt insertion in the presence of a large posterior fossa tumor may result in upward or reverse herniation or may result in subtle movements in the tumor due to a change in the naturally adjusted pressure dynamics following drainage of cerebrospinal fluid from lateral ventricles.[3],[4],[5]

Such movements may be the cause of hemorrhage in some tumors.[4],[6] Spinal tumor movement and impaction in the spinal canal and neurological worsening following a lateral ventricular shunt surgery has been recorded.[7] Posterior fossa, suprasellar and thalamic tumor patients have been recorded to worsen neurologically following a shunt operation.[3],[8] Tumor movement and alteration of the delicately balanced intracranial pressure have been implicated as the cause of the clinical worsening.[8],[9]

Our patient had a large tumor mass. The intraventricular pressure was high as was observed during the ventricular tapping whilst performing the shunt surgery. Both these factors contributed to a significantly high intracranial pressure. The neurological worsening following the ventricular tapping in our case suggests that the rise in the intraventricular pressure was in some manner maintaining or balancing the intracranial dynamics. Following the ventricular cannulation and rapid drainage of the cerebrospinal fluid, there could have been movements within the tumor or of the tumor as a whole. The large tumor could have probably impacted on to the hypothalamus or the internal capsule, or could have resulted in a subtle but definitive midline shift that initiated a chain of events that resulted in increased cerebral edema and later transtentorial herniation. There was no obvious hypoxic event during the induction of the anesthesia. Despite the fact that the cause of worsening in our case could not be actually confirmed, it appears that any form of ventricular drainage prior to surgery on large cerebral tumors associated with hydrocephalus is detrimental and should be avoided. The role of ventricular dilatation and the impact of a rise in the intraventricular cerebrospinal fluid pressure in the presence of a large intracranial tumor need to be evaluated further.

References

Copyright 2004 - Neurology India

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