Publication Type Review
Authors Berger S, Schürer L, Dautermann C, Härtl R, Murr R, Röhrich F, Baethmann A
Journal Zentralbl Chir
Volume 118
Issue 5
Pagination 237-43; discussion 243-4
Date Published 01/01/1993
ISSN 0044-409X
Keywords Brain Injuries, Hypertonic Solutions, Intracranial Pressure, Pseudotumor Cerebri
Abstract Administration of hypertonic solutions is the method of choice for acute treatment of intracranial hypertension. Recording of the intracranial pressure during treatment facilitates adjustment of the dosis to the actual ICP-response, avoiding thereby administration of an excessive osmotic load as a basis to prolong therapeutical efficacy. The mechanisms underlying reduction of the intracranial pressure by hypertonic solutions are still controversially discussed. Dehydration of normal probably also of edematous brain parenchyma and constriction of cerebral resistance vessels as an autoregulatory response causing reduction of the intracranial blood volume are the most likely options. Administration of hypertonic/hyperoncotic solutions has regained attention on account of its unmatched therapeutical efficacy to reestablish normal conditions in severe hemorrhagic shock. Administration of, e.g. 7.2% NaCl/10% Dextran 60 in an amount equivalent of only 10% of the shed blood volume is immediately normalizing cardiac output and improving the microcirculation in peripheral organs. These therapeutical properties are relevant in head injury, since inflicted patients quite often are suffering from peripheral trauma and consequently from hemorrhagic shock. No evidence has been obtained in a variety of experimental studies that hypertonic/hyperoncotic solutions have adverse effects on the brain in the presence of a cerebral lesion. To the contrary, the fluid mixture has been found to lower the increased intracranial pressure. Administration of hypertonic/hyperoncotic solutions appears therefore appropriate in acute cerebral insults from head injury and impending circulatory failure from shock in order to inhibit development of secondary brain damage.
PubMed ID 8322535
Back to Top