[Treatment of acute brain edema].
OBJECTIVE
To review the basic concepts and mechanisms of cerebral edema and to analyze current management of this complex clinical problem.


METHODS
Cerebral edema is a stereotyped reaction of the brain to any aggression and is a very common complication in patients with alterations of the blood-brain barrier. The cerebral edema should be recognized and treated early and aggressively to avoid disastrous results such as cerebral herniation. The most important types of edema are the vasogenic and cytotoxic. The first implies primary alterations of the blood-brain barrier, whilst in the second they are of cellular homeostasis. We have reviewed how various pro-inflammatory substances interact to stimulate the mechanisms causing edema, and also the importance of cerebrovascular autoregulation for maintenance of a normal intracranial volume. The measures necessary for good cerebral reanimation are the following: evaluation of the airway, controlled hyperventilation, maintenance of the cerebral perfusion pressure > 70 mmHg, suitable position of the head, administration of hypertonic solutions, dexamethasone, and possibly barbiturates. We have shown that a body temperature > 37.5 degrees C and blood glucose > 150 mg/dl are related to worsening of the cerebral edema. Finally, we have reviewed other experimental treatments which seem promising, such as hemicraniectomy, hypertonic saline solutions, hypothermia and other neuroprotector agents.


CONCLUSIONS
All patients with acute cerebral edema should be evaluated early and treated with therapy which will solve the underlying pathological problem. Good medical management of these patients is of vital importance to assure a satisfactory clinical outcome. Recently new, effective therapy has been evaluated which may substantially change current concepts of the treatment of patients with acute cerebral edema.
Suárez
J I
JI
University Hospitals of Cleveland/Hanna 5, 11100 Euclid Avenue, Cleveland, OH 44106, USA. jis4@po.cwru.edu
D000208:Acute Disease; D000402:Airway Obstruction / Q000628:therapy; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000927:Anticonvulsants / Q000627:therapeutic use; D001463:Barbiturates / Q000627:therapeutic use; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000502:physiology; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D019090:Case Management; D002560:Cerebrovascular Circulation; D003131:Combined Modality Therapy; D003399:Craniotomy; D003907:Dexamethasone / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D004322:Drainage; D006801:Humans; D006849:Hydrocephalus / Q000150:complications / Q000601:surgery; D006943:Hyperglycemia / Q000150:complications; D006973:Hypertension / Q000150:complications; D006982:Hypertonic Solutions / Q000627:therapeutic use; D007010:Hyponatremia / Q000150:complications; D007036:Hypothermia, Induced; D020925:Hypoxia-Ischemia, Brain / Q000150:complications; D007473:Ion Channels / Q000187:drug effects; D018696:Neuroprotective Agents / Q000627:therapeutic use; D012121:Respiration, Artificial; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
D000893:Anti-Inflammatory Agents; D000927:Anticonvulsants; D001463:Barbiturates; D004232:Diuretics; D006982:Hypertonic Solutions; D007473:Ion Channels; D018696:Neuroprotective Agents; D014662:Vasoconstrictor Agents; D003907:Dexamethasone