title: Hypocortisolism in noncomatose patients during the acute phase of subarachnoid hemorrhage.
abstract: BACKGROUND
  Hypopituitarism represents a common long-term complication of subarachnoid hemorrhage (SAH). The incidence of hypocortisolism may be higher during the acute phase of SAH. Although hypocortisolism may be harmful in critically ill SAH patients, data are still lacking. The primary objective of this study was to investigate the incidence of hypocortisolism during the acute phase of SAH (15 days). Secondary objectives included an analysis of the relationship between hypocortisolism and outcome and the computation of the cortisol-time secretion curve.
  
  
  METHODS
  Clinical data of a consecutive series of 26 noncomatose patients with aneurysmal SAH were collected prospectively. The sample size was calculated considering an expected proportion of hypocortisolism of 30%, a confidence level of 95%, and a total width of confidence interval of 0.35. The definition of hypocortisolism (as taken from a statement from the critical care medicine task forces) includes random total cortisol <10 μg/dL or a Δtotal serum cortisol <9 μg/dL after 1 μg of corticotrophin hormone.
  
  
  RESULTS
  Hypocortisolism was diagnosed in 11 patients (42.3%). Cortisol increment after stimulation test was always >9 μg/dl, suggesting a hypothalamic-pituitary impairment. Hypocortisolism was independently associated with a higher risk of poor outcome (P = .046) even after adjusting for age and Hunt and Hess grade. The cortisol-time secretion curve showed a peak at day 5 and a minimum at day 8. The peak at day 5 correlated with the risk of delayed cerebral ischemia (P = .001), and the cortisol concentration slope between days 1 and 8 correlated with the risk of poor outcome (P = .033).
  
  
  CONCLUSIONS
  Patients with SAH are at high risk of secondary hypocortisolism during the first 15 days after bleeding. Hypocortisolism independently increases the risk of poor outcome. The acute phase of hypothalamo-pituitary dysfunction, as reflected by an abnormal day-by-day cortisol secretion pattern, may affect the risk of delayed cerebral ischemia.
authors.affiliation: Department of Neuroscience and Surgery of the Nervous System, Ospedali Riuniti, Bergamo, Italy. Electronic address: l.lanterna@gmail.com.
authors.forename: Luigi A
authors.initials: LA
authors.lastname: Lanterna
authors.forename: Veronica
authors.initials: V
authors.lastname: Spreafico
authors.forename: Paolo
authors.initials: P
authors.lastname: Gritti
authors.forename: Flavia
authors.initials: F
authors.lastname: Prodam
authors.forename: Antonio
authors.initials: A
authors.lastname: Signorelli
authors.forename: Francesco
authors.initials: F
authors.lastname: Biroli
authors.forename: Gianluca
authors.initials: G
authors.lastname: Aimaretti
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007018:Hypopituitarism / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D015994:Incidence; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000097:blood / Q000150:complications* / Q000453:epidemiology
chemical_list: D006854:Hydrocortisone