Abstract
Subarachnoid hemorrhage (SAH) implies an immediate potential catastro-phy but also a high risk of later complications with fatal outcome or lasting morbidity. Raised intracranial pressure (ICP) after SAH has been frequently observed (2, 6, 7, 8). The cause is usually obvious in cases with intracerebral hematomas (5) and/or massive invasion of blood into the ventricular system. In some cases the high ICP is explained by ischemic lesions due to arterial spasm, causing focal cerebral edema. In the long run the development of so-called normal pressure hydrocephalus (NPH) is well known. However, except for this late manifestation of cerebrospinal fluid (CSF) absorptive difficulties, problems appertaining to the CSF dynamics in SAH have been given comparatively little consideration until recent years. It has been shown (1) that posthemorrhagic ventricular dilatation roentgenologically is a frequent finding. Apparently clinically manifest NPH is much more unusual. Several investigators (3, 8, 10) have recently published their experiences with ventricular drainage (VD) early after SAH.
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References
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Sundbärg, G., Pontén, U. (1976). ICP and CSF Absorption Impairment After Subarachnoid Hemorrhage. In: Beks, J.W.F., Bosch, D.A., Brock, M. (eds) Intracranial Pressure III. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66508-0_25
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DOI: https://doi.org/10.1007/978-3-642-66508-0_25
Publisher Name: Springer, Berlin, Heidelberg
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