60 patients were included in a prospective study to evaluate the effectiveness of hyperbaric oxygenation (OHP) as a treatment of head injury coma. They were assigned to nine subgroups according to age, level of consciousness and eventual neurosurgical procedure, and then selected randomly for OHP or standard therapy. OHP was administered in one or several series of daily exposure at 2.5 ATA. However, the OHP therapy protocol was to be interrupted in 11 cases developing pulmonary, hyperoxic, or infectious complications. Overall mortality and mean duration of coma in survivors were not different in both groups, indicating that OHP was either ineffective or too intermittently applicated. Analysis of results in subgroups revealed that, in one subgroup (18 patients), the rate of recovered consciousness at 1 month was significantly higher when OHP was used. These patients were under 30 and had a brain stem contusion without supraten-torial mass lesion. The view is defended that, besides its toxic action on the normal nervous tissue, OHP can counteract edema and ischemia in the zones of brain injuries.
A series of head-injured patients, in coma, were treated with hyperbaric oxygen (OHP) at 2.5 atm. Cerebral blood flow (CBF), cerebral metabolic rates of oxygen (CMRO2), glucose (CMRGL), and lactate (CMRL act), and various cerebrospinal fluid (CSF) parameters were measured before and 2 h after the treatment. Pre-OHP and post-OHP average values of arterial blood and CSF lactate, and CMRL act were higher than normal, while CBF, CMRO2 and CSF oxygen pressure (PO2) were lower. CBF tended to increase after OHP in some patients and to decrease in others. This discrepancy and the conflicting results of the literature can be tentatively explained in assuming that there is a different effect of OHP on normal brain circulation as compared to impaired brain circulation. Changes of cerebral metabolic rates were inconsistent and did not relate to changes of CBF, except with repeated studies of the same patient. A correlation was found between the variations of CMRGL and those of arterial blood and CSF glucose content. CSF PO2, CSF acid-base balance, and CSF lactate content did not vary, and arterial PO2 showed a consistent fall. In two patients who were neurologically improved after OHP exposure, the CBF and metabolic changes were not the same.
A controlled double-blind evaluation of the effects of Dextran 40 at different concentrations on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2) and cerebral lactate production (CMRLact) was carried out. We studied 40 patients in coma due to recent head injury. Concentrations of Dextran solution were not significantly related to variations in CBF and metabolic rate over the period of infusion. The lack of effect of the Dextran infusion may be explained by the absence of global brain ischemia in these patients at the time of the study. The very low initial CBF values were a consequence of brain metabolic depression and not a sign of global ischaemia. The rheological benefits of treatment with Dextran 40 in head injured patients should preferably be investigated using techniques which permit detection of local changes in CBF and metabolism.
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