Abstract
Many patients with subarachnoid hemorrhage (SAH) from ruptured aneurysms develop vasospasm and ischemic neurological deficits which progress relentlessly despite agressive measures to improve cerebral perfusion. In such situations barbiturate coma may prevent infarction from occurring by decreasing the metabolic needs of the brain to approximate the availability of substrates provided by the compromised circulation. Furthermore, intracranial hypertension is common in these patients (1) and the decrease in ICP which results from barbiturate therapy should improve cerebral blood flow (2,3).
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References
Kassell NF, Peerless SJ, Reilly PL (1976) ICP, aneurysms and subarachnoid hemorrhage. In: Beks JWF, Bosch DA, Brock M (eds) Intracranial Pressure III. Springer, Berlin Heidelberg New York p. 147
Marshall LF, Bruce DA, Bruno L et al (1977) The role of intracranial pressure monitoring and barbiturate therapy in malignant intracranial hypertension. Case report. J Neurosurg 47:481–485
Shapiro HM, Galindo A, Wyte SR et al (1973) Rapid intra-operative reduction of intracranial pressure with thiopentone. Br J Anaesthesiol 45:1057–1062
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© 1980 Springer-Verlag Berlin Heidelberg
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Kassell, N.F., Peerless, S.J., Drake, C.G. (1980). Cerebral Vasospasm, ICP and Barbiturate Coma. In: Shulman, K., Marmarou, A., Miller, J.D., Becker, D.P., Hochwald, G.M., Brock, M. (eds) Intracranial Pressure IV. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67543-0_141
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DOI: https://doi.org/10.1007/978-3-642-67543-0_141
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