Neurologia medico-chirurgica
Online ISSN : 1349-8029
Print ISSN : 0470-8105
ISSN-L : 0470-8105
Treatment of Increased Intracranial Pressure by Hyperbaric Oxygenation
Hidenori OHTAShingo KAWAMURAMasahito NEMOTOKouichi KITAMINobuyuki YASUIYoshitaka HINUMAEiichi SUZUKI
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1986 Volume 26 Issue 5 Pages 385-391

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Abstract

The authors evaluated the effect of hyperoxia including hyperbaric oxygenation (HBO) on increased intracranial pressure (ICP). Seventeen postoperative cases of subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysm in an acute stage were studied. The intervals from the onset to ICP studied ranged from 3 to 17 (average±SD: 7±4) days. ICP was monitored through a ventricular drainage (CVD) tube using a Statham pressure transducer P-50. In the hyperbaric chamber, ICP was monitored during the resting state [before HBO, 1 atmosphere absolute-air breathing (1ATA-air)], before HBO 1ATA-pure oxygen inhalation (1ATA-O2), 2ATA-O2, after HBO 1ATA-O2, after HBO 1ATA-air and 200 ml glycerol administration. Mean ICP showed a 20% decrease in the period before HBO 1ATA-O2 and 23 to 27% decrease during HBO and return to the resting state after decompression. A notable finding was 18% rebound increase after oxygen inhalation ceased. Glycerol lowered ICP about 50% and was more effective in reducing ICP than HBO. Changes of PaO2 were as follows: at rest; 82±12 mmHg, before HBO 1ATA-O2; 406±73 mmHg, 2ATA-O2; 761±167 mmHg, and after HBO 1ATA-air; 79±13 mmHg (mean±SD). The somatosensory evoked potential (SEP) test revealed improved parietal N1 (P1-N1 peak to peak) amplitude in 43% during HBO, in 17% after HBO and in 12.5% after the administration of glycerol. Causes of ICP decrease during hyperoxia are considered to be vasoconstriction and a slight hypocapnia. The authors propose to name the vasoconstriction caused by hyperoxia “O2 response”. “O2 response” may be one of the regulating mechanisms of cerebral blood flow like autoregulation and CO2 response. ICP decrease caused by hyperoxia in intracranial hypertension may depend upon the capacity of the “O2 response” of patients. Two main causes of the rebound phenomenon after decompression in SAH patients may be rebound vasodilatation after HBO and the natural worsening of hydrocephalus. Brain function evaluated by SEP tests suggested the beneficial effect of HBO. This may be due to the improved oxygen supply to the brain in addition to the ICP decrease during HBO. The effect of HBO is temporary and there exists a rebound increase of ICP after HBO. In the management of increased ICP, other methods to control ICP such as ventricular drainage and administration of dehydrating agents should be used together with HBO.

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© The Japan Neurosurgical Society
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