title: Endocrine failure after traumatic brain injury in adults.
abstract: OBJECTIVE
  To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation.
  
  
  METHODS
  A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications.
  
  
  RESULTS
  Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary axis (HPA), neuroendocrinological effects from catecholamines and cytokines, or from systemic infection/inflammation that produces primary gland failure. Autopsy evidence of hemorrhage or ischemia in the HPA is common soon after TBI. The estimated incidence of acute hormone reduction is adrenal 15%, thyroid 5 - 15%, growth hormone 18%, vasopressin 3 - 37%, and gonadal (25 - 80%). Hyperprolactinemia occurs in more than 50% of patients. Inappropriate secretion of antidiuretic hormone (SIADH) and the euthyroid sick syndrome are common. Acute adrenal failure, central hypothyroidism, SIADH, and diabetes insipidus (DI) may cause poor neurological outcomes including death, hypo/hypernatremia, hypotension, and increased vasoactive drug requirements. Treatment of those conditions is warranted. Delayed diagnosis of hypopituitarism is often mistaken for symptoms of residual head injury. Some chronic hormone deficiency occurs in 30 - 40% of selected patients after TBI, more than one deficiency in 10 - 15%, growth hormone in 15 - 20%, gonadal hormones in 15%, and hypothyroidism in 10 - 30%. Chronic adrenal failure and DI are reported over a wide incidence. Prolactin is elevated in 30%. All clinical symptoms respond favorably to replacement therapy.
  
  
  CONCLUSIONS
  Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, hyponatremia, and/or hypotension is associated with a higher occurrence of endocrinopathy. Greater awareness of this possible complication of TBI and appropriate testing are encouraged.
authors.affiliation: Department of Neurosurgery, University of Texas Health Science Center at Houston, Houston, TX 77030, USA. david.j.powner@uth.tmc.edu
authors.forename: David J
authors.initials: DJ
authors.lastname: Powner
authors.forename: Cristina
authors.initials: C
authors.lastname: Boccalandro
authors.forename: M Serdar
authors.initials: MS
authors.lastname: Alp
authors.forename: Dennis G
authors.initials: DG
authors.lastname: Vollmer
mesh_terms: D000309:Adrenal Insufficiency / Q000453:epidemiology / Q000209:etiology; D000328:Adult; D001930:Brain Injuries / Q000150:complications*; D003937:Diagnosis, Differential; D005067:Euthyroid Sick Syndromes / Q000453:epidemiology / Q000209:etiology; D006801:Humans; D006966:Hyperprolactinemia / Q000453:epidemiology / Q000209:etiology; D007018:Hypopituitarism / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007177:Inappropriate ADH Syndrome / Q000453:epidemiology / Q000209:etiology; D010913:Pituitary-Adrenal System / Q000503:physiopathology