title: [Deleterious role of hyperthermia in neurocritical care].
abstract: Fever is a secondary brain injury and may worsen neurological prognosis of neurological intensive care unit (NICU) patients. In response to an immunological threat, fever associates various physiological reactions, including hyperthermia. Its definition may vary but the most commonly used threshold is 37.5 degrees C. In animal studies, hyperthermia applied before, during or after cerebral ischemia may increase the volume of ischemic lesions. The mechanism of this effect may include increase in blood brain barrier permeability, increase in excitatory amino acid release and increase in free radical production. In NICU patients, fever is frequent, occurring in up to 20-30% of patients. Moreover, after haemorrhagic stroke, fever has been reported in 40-50% of patients. In half of the patients, fever may be related to an infectious cause but in more than 25% of patients, hyperthermia may be of central origin. After ischemic stroke, hyperthermia during the first 72 hours is associated with an increase in infarct size and increase in morbidity and mortality. This holds true also after subarachnoid haemorrhage. After traumatic brain injury, fever is not related to mortality but may increase morbidity. Whereas no causal link has been established between fever and unfavourable outcome, it seems reasonable to treat hyperthermia in patients suffering from brain injuries. In such patients, antipyretics have a moderate efficacy. In case of failure, they should be replaced by physical cooling techniques.
authors.affiliation: Service d'anesthésie-réanimation, hôpital Central, CHU de Nancy, 29, avenue du Maréchal-de-Lattre-de-Tassigny, 54000 Nancy, France. g.audibert@chu-nancy.fr
authors.forename: G
authors.initials: G
authors.lastname: Audibert
authors.forename: A
authors.initials: A
authors.lastname: Baumann
authors.forename: C
authors.initials: C
authors.lastname: Charpentier
authors.forename: P-M
authors.initials: PM
authors.lastname: Mertes
mesh_terms: D018712:Analgesics, Non-Narcotic / Q000627:therapeutic use; D000818:Animals; D001812:Blood-Brain Barrier; D001925:Brain Damage, Chronic / Q000209:etiology / Q000517:prevention & control*; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology; D003422:Critical Care; D018846:Excitatory Amino Acids / Q000378:metabolism; D005334:Fever / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D006323:Heart Arrest / Q000150:complications / Q000503:physiopathology; D006801:Humans; D007036:Hypothermia, Induced; D007239:Infections / Q000150:complications; D011379:Prognosis; D051381:Rats; D012151:Resuscitation; D020521:Stroke / Q000150:complications / Q000503:physiopathology; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology
chemical_list: D018712:Analgesics, Non-Narcotic; D018846:Excitatory Amino Acids