Inappropriate secretion of antidiuretic hormone after cerebral injury.
A case has been presented in which a patient sustained a closed head injury with concomitant maxillofacial injuries; early signs of water intoxication and ISADH developed six days after injury. This disorder was corrected by restricting free water intake for six days until equilibration occurred. Successful reduction of the facial fractures was accomplished after stabilization of the patient's neurological condition and correction of her metabolic disorder. The ISADH and resulting hyponatremia have been documented in a variety of disease states including trauma to the central nervous system. Disruption or irritation to the hypothalamic-neurohypophyseal system has been proposed as the mechanism of dysfunction after cerebral injury. The results of the secretion of inappropriate amounts of ADH relative to renal function and homeostatis have been discussed. Clinical and laboratory diagnosis as well as the elective and emergency management of ISADH have been reviewed. The fact that the sequelae of this abnormal metabolic state may mimic or mask the neurological deterioration which may follow cerebral injury is significant. This may contribute to the difficulty in making a correct diagnosis and designing proper therapy. The problem is basically one of differentiating a correctable metabolic disorder from a lesion that can be fatal unless surgically removed.
D000328:Adult; D001769:Blood; D001810:Blood Volume; D001930:Brain Injuries / Q000503:physiopathology*; D005110:Extracellular Space; D005260:Female; D006801:Humans; D007010:Hyponatremia / Q000209:etiology; D007031:Hypothalamus / Q000502:physiology; D007668:Kidney / Q000378:metabolism; D009994:Osmolar Concentration; D012964:Sodium / Q000378:metabolism; D014667:Vasopressins / Q000378:metabolism*; D014882:Water-Electrolyte Balance
D014667:Vasopressins; D012964:Sodium