sodium-oxybate and Brain-Injuries

Gamma-hydroxybutyric acid (GHB) as a natural component of the mammalian brain was first introduced in clinical anaesthetic practice more than 30 years ago. Although GHB induced a reliable state of sedation and anaesthesia without depressing either respiratory or cardiocirculatory parameters or liver and kidney function, the drug was nearly displaced from clinical practice because of its prolonged duration of action. The results of recent clinical studies indicate a re-evaluation of GHB in emergency and critical care medicine. GHB is regarded as a natural neuronal transmitter with circuits which synthesise, accumulate and release GHB. Specific binding sites have also been demonstrated and identified. GHB is completely metabolized in the liver to the natural substrates carbon dioxide and water without accumulation in central or peripheral tissues. The reduction of energy metabolism and its possible properties as an "oxygen radical scavenger" may be of therapeutic benefit if tissues are exposed to hypoxia or reperfusion. Therefore, the application of GHB seems to be of advantage in states of traumatic brain injury with cerebral oedema or ischaemic lesions of brain or extraneural tissues. In hypovolaemic states or in patients with impaired cardiovascular function, the pressure effects of GHB may be beneficial for the prevention of tissue damage and may improve survival in the case of cardiocirculatory resuscitation. In the intensive care unit, GHB might be a favourable alternative to established sedative agents. Occurrence of side effects such as tolerance and withdrawal syndromes after the application of sedative drugs, an impaired metabolism with the accumulation of metabolites in the case of liver or kidney dysfunction as well as an insufficient regulation of natural sleep may be diminished by the application of GHB. The results of various clinical studies also suggest that GHB may be useful in the treatment of alcohol and opiate withdrawal syndrome. However, further studies are necessary to specify the proposed indications of GHB in anaesthesiology and critical care medicine.

Topics: Anesthesia, Intravenous; Anesthetics, Intravenous; Brain; Brain Injuries; Brain Ischemia; Cardiopulmonary Resuscitation; Conscious Sedation; Critical Care; Humans; Metabolic Clearance Rate; Sodium Oxybate

Topics: Adjuvants, Anesthesia; Brain Injuries; Child; Cognition; Humans; Magnetic Resonance Imaging; Male; Sleep; Sodium Oxybate; Thalamus

Topics: Accidents, Traffic; Adult; Brain Injuries; Diagnosis, Differential; Drug Overdose; Emergencies; Female; Humans; Illicit Drugs; Male; Sodium Oxybate

Topics: Adolescent; Adult; Aged; Barbiturates; Brain Injuries; Child; Female; Fentanyl; Humans; Intracranial Pressure; Male; Middle Aged; Monitoring, Physiologic; Prognosis; Sodium Oxybate; Tomography, X-Ray Computed

Topics: Adolescent; Adult; Brain Injuries; Child; Child, Preschool; Coma; Female; Fentanyl; Humans; Infant; Intensive Care Units; Intracranial Pressure; Male; Monitoring, Physiologic; Prognosis; Sodium Oxybate; Tomography, X-Ray Computed

Topics: Adult; Brain Injuries; Child; Humans; Hydroxybutyrates; Intracranial Pressure; Sodium Oxybate

Severe head injury often produces complex intracranial displacements of the brain, resulting in widespread, often microscopic lesions. These are responsible for two types of edema: vasogenic edema, with outflow of molecules and fluid into the extracellular spaces by rupture of the blood-brain barrier and vasoplegia, and cytotoxic edema, with swelling of astrocytes due to membrane lesions. The connexions between these two types of edema are still obscure. Alterations in membrane phospholipids may impede function of Na-K pump enzymes, causing accumulation of water in the cell. Cerebral edema is responsible for intracranial hypertension and tentorial herniation, which in turn increase edema through venous compression, ischemia, and hypoxia. The least controversial anti-edema therapeutic measures include relative fluid and salt restriction, mannitol if called for, neuroplegia, in particular with diazepam and Gamma-OH, and assisted ventilation.

Topics: Alfaxalone Alfadolone Mixture; Barbiturates; Brain Edema; Brain Injuries; Cytidine Diphosphate Choline; Diazepam; Hormones; Humans; Osmolar Concentration; Prognosis; Respiration, Artificial; Sodium Oxybate; Water-Electrolyte Imbalance

Topics: Adolescent; Adult; Aged; Blood Proteins; Brain Injuries; Female; Humans; Hydroxybutyrates; Male; Middle Aged; Phenobarbital; Prognosis; Sodium Oxybate

Topics: Adolescent; Adult; Brain Injuries; Female; Humans; Hydroxybutyrates; Male; Middle Aged; Renin-Angiotensin System; Sodium; Sodium Oxybate; Water-Electrolyte Imbalance

Topics: Brain; Brain Injuries; Coma; Electroencephalography; Humans; Hydroxybutyrates; Sodium Oxybate

Topics: Adolescent; Adult; Anesthesia, General; Brain Injuries; Child; Child, Preschool; Drug Therapy, Combination; Female; Humans; Hydroxybutyrates; Intracranial Pressure; Male; Sodium Oxybate; Thiopental