EEG CHANGES DURING SEDATION WITH GAMMA-HY DROXYBUTYRIC ACID

Gamma-hydroxybutyric acid (GHB) is a naturally occurring transmitter i n the mammalian brain, related to sleep regulation and possibly to ene rgy balance in diving or hibernating animals. It has been used for alm ost 35 years as an intravenous agent for induction of anaesthesia and for long-term sedation. Its convincing pharmacological properties? wit hout serious adresse effects on circulation or respiration, are compro mised by its unpredictable duration of action. This is not a major pro blem with long-term sedation during ICU treatment. GHB has been used w ith good results for sedation of patients with severe brain injury, wh ere it compares favourably with barbiturates. In animal studies, it se ems to possess a protective action against hypoxia on a cellular and w hole organ level. However, in some experimental animals GHB has been s hown to produce seizure-like activities, and the compound is being use d to produce absence-like seizures. GHB has been used in our ICU for y ears to provide adequate sedation for patients under controlled ventil ation or for patients figthing the respirator during spontaneous respi ration. No serious side effects were observed in these patients? while in some patients under haemodialysis hypernatraemia and metabolic alk alosis developed: both were reversible after discontinuation of GHB an d restriction of additional sodium input (Somsanit, the commercially a vailable GHB preparation in Germany, contains 9.2 mmol sodium/g the da ily dose averages 20-40 g GHB, i.e. 180-370 mmol sodium). Patients and Methods. In 31 patients after major abdominal surgery, sedation was e stablished with GHB 50 mg/kg BW injected via perfusion pump over a 20- min period. No centrally acting medication had been given for at least 2 h, A computer-based multichannel EEG system (CATEEM, MediSyst, Lind en) was used, allowing for fast Fourier transformation, spectral analy sis and topographical brain mapping. EEG during induction of sedation was followed after a baseline EEG (10 min) had been recorded. Patients receiving long-term sedation were studied daily for an additional 15- min period. Corresponding well to the clinical findings. EEG pattern c hanged to a slow delta-theta or delta-only rhythm within 10 min of the start of Injection. Alpha and beta power decreased, while delta activ ity exhibited an increase. All changes were most obvious in frontal an d central areas of the brain. In about one out of three patients, a bu rst - suppression pattern developed. Sines automatic processing of EEG may fail to detect special patterns like the looked-for 3/s spikes an d waves, the raw EEG was analysed visually by an expert neurologist. B oth processed and conventionally analysed EEG were free of any seizure -like electrical activity. Conclusion. We conclude that animal data ma y not apply to the use of GHB in humans, provided the dose is limited to the clinical needs. GHB is used in clinical practice in doses twice as high, or even higher, than the one wt: use Tor induction. without obvious side effects. However, the suppression of theta rhythm we obse rved in about half of the patients studied may indicate that even less than 50 mg/kg BW might be sufficient for adequate sedation.