title: Effect of barbiturate coma on adrenal response in patients with traumatic brain injury.
abstract: BACKGROUND
  Barbiturate coma is the second tier measure recommended by guidelines to treat post-traumatic refractory intracranial pressure. Systemic hypotension is its most important side effect. Recent evidence suggests that low-dose corticosteroid therapy may be used in a subset of patients with traumatic brain injury (TBI) to avoid hypotension. We evaluated adrenal function in TBI patients undergoing barbiturate coma, as treatment of their refractory intracranial hypertension.
  
  
  METHODS
  We prospectively studied 40 patients with moderate to severe TBI. Group A (17 patients) were treated with barbiturate coma. Group B (23 patients) presented intracranial hypertension controlled with first tier measures, and acted as a control. Adrenal function was evaluated by using the high-dose corticotropin stimulation test within 24 h after brain injury and after barbiturate coma induction.
  
  
  RESULTS
  Within 24 h after TBI, adrenal function was similar in both groups. Once barbiturate coma was induced, patients in group A treated with barbiturate coma presented a higher incidence of adrenal insufficiency compared with the control group B (53% vs 22%, p=0.03). Patients treated with barbiturates, who developed adrenal impairment, required higher doses of norepinephrine to maintain cerebral perfusion pressure than patients treated with barbiturates without adrenal impairment (1.07+/-1.04 microg/kg/min vs 0.31+/-0.32 mug/kg/min, p=0.03).
  
  
  CONCLUSIONS
  Patients with TBI treated with barbiturate coma are at higher risk of developing adrenal insufficiency. This subset of patients presented higher requirements of vasoactive support to avoid hypotension. In these patients corticosteroid therapy may have potential therapeutic implications to treat hemodynamic instability.
authors.affiliation: Intensive Care Medicine Service, Son Dureta University Hospital, Palma de Mallorca, Spain. jallompart@hsd.es
authors.forename: J A
authors.initials: JA
authors.lastname: Llompart-Pou
authors.forename: J
authors.initials: J
authors.lastname: Pérez-Bárcena
authors.forename: J M
authors.initials: JM
authors.lastname: Raurich
authors.forename: B
authors.initials: B
authors.lastname: Burguera
authors.forename: J I
authors.initials: JI
authors.lastname: Ayestarán
authors.forename: J M
authors.initials: JM
authors.lastname: Abadal
authors.forename: J
authors.initials: J
authors.lastname: Homar
authors.forename: J
authors.initials: J
authors.lastname: Ibáñez
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects*; D000309:Adrenal Insufficiency / Q000139:chemically induced* / Q000188:drug therapy / Q000378:metabolism; D000328:Adult; D001463:Barbiturates / Q000008:administration & dosage* / Q000009:adverse effects*; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism; D003128:Coma / Q000139:chemically induced*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007022:Hypotension / Q000517:prevention & control; D019586:Intracranial Hypertension / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000627:therapeutic use; D011446:Prospective Studies; D013566:Sympathomimetics / Q000627:therapeutic use; D015599:Trauma Severity Indices
chemical_list: D001463:Barbiturates; D013566:Sympathomimetics; D006854:Hydrocortisone; D009638:Norepinephrine