[Current status of treatment of the cerebral edema].
The treatment of cerebral edema has changed during recent years. On the one hand, knowledge of the pathophysiology of brain swelling has expanded; on the other, the analysis of biodata such as intracranial pressure, cerebral blood flow, and blood volume has become routine. The methods of measuring intracranial pressure (nowadays without risk due to the use of microtipepidural probes, e.g. Gaeltec) in particular, make it possible to monitor the effects of therapy and enable us to evaluate the different therapeutic measures individually for each patient. Regarding drug treatment, osmotherapy deserves first mention, especially the polyvalent alcohols mannitol and sorbitol, but in spite of possible side effects, glycerin as well. Knowledge of the mechanism of osmotic therapy leads to the proper concept of treatment with bolus administration under control of serum osmolarity and intracranial pressure. Corticosteroids only effectively influence the cerebral edema caused by tumor. The treatment of posttraumatic (and postoperative) cerebral edema is described controversally in the literature. As the side-effects of cortisone therapy are under control, corticosteroids may also be included in the treatment of therapy-resistant cerebral edema. Acting together with sedative drugs, procaine derivatives help to reduce intracranial pressure peaks during intensive care measures. Barbiturates are used as sedatives or in a loading dose until burst suppression is seen in the EEG. The risk of hemodynamic side effects such as reduced cardiac output and cerebral perfusion pressure is decreased by measuring pulmonary arterial pressure and the use of catecholamines. The acidotic impairment of cerebral autoregulation can be regulated using THAM (thrometamine) and the response of the vascular system to hypocapnia can be improved.(ABSTRACT TRUNCATED AT 250 WORDS)
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D001463:Barbiturates / Q000627:therapeutic use; D001508:Bed Conversion; D001929:Brain Edema / Q000188:drug therapy* / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D003131:Combined Modality Therapy; D005665:Furosemide / Q000627:therapeutic use; D006801:Humans; D007427:Intracranial Pressure / Q000187:drug effects; D008012:Lidocaine / Q000627:therapeutic use; D008353:Mannitol / Q000627:therapeutic use; D009994:Osmolar Concentration; D013012:Sorbitol / Q000627:therapeutic use; D013318:Stroke Volume; D014325:Tromethamine / Q000627:therapeutic use
D000305:Adrenal Cortex Hormones; D001463:Barbiturates; D014325:Tromethamine; D002245:Carbon Dioxide; D008353:Mannitol; D013012:Sorbitol; D005665:Furosemide; D008012:Lidocaine
Der gegenwärtige Stand in der Behandlung des Hirnödems.