title: The effects of supraphysiological doses of corticosteroids in hypotensive liver failure.
abstract: BACKGROUND
  In septic shock, supraphysiological doses of corticosteroids reduce norepinephrine requirements. We reviewed our experience of this treatment in hypotensive liver failure.
  
  
  METHODS
  We retrospectively analysed 20 patients with liver failure who were treated with supraphysiological doses of hydrocortisone because of norepinephrine dependence. We compared their norepinephrine requirements, outcome, microbiology and incidence of gastrointestinal bleeding to an historical control group treated with norepinephrine but not corticosteroids.
  
  
  RESULTS
  After 48 h of steroid treatment, the median norepinephrine dose was reduced (0.14 microg/kg/min to 0.08 microg/kg/min; P < 0.05) while the blood pressure over the same period of time did not change significantly (67.3 mm Hg to 70 mm Hg). Duration of ITU stay was longer in the steroid treated group (13.5 days vs 3 days; P < 0.05) but survival was similar in both groups. There were 23 episodes of positive bacterial cultures after norepinephrine was started in the steroid treated group, compared with 18 episodes in the control group. More of the positive cultures were due to resistant organisms in the steroid treated group (65% vs 17% in the control group; P < 0.002). There was no significant bleeding due to gastrointestinal inflammation in either group.
  
  
  CONCLUSIONS
  Supraphysiological doses of corticosteroids reduce norepinephrine requirements in hypotensive liver failure. They do not improve survival but may extend time to find a suitable donor in those awaiting urgent liver transplantation.
authors.affiliation: Liver Intensive Care Unit, Kings College Hospital, SE5 9RS, London, UK.
authors.forename: Rachael
authors.initials: R
authors.lastname: Harry
authors.forename: Georg
authors.initials: G
authors.lastname: Auzinger
authors.forename: Julia
authors.initials: J
authors.lastname: Wendon
mesh_terms: D000305:Adrenal Cortex Hormones / Q000008:administration & dosage*; D000309:Adrenal Insufficiency / Q000139:chemically induced; D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004351:Drug Resistance / Q000502:physiology; D005500:Follow-Up Studies; D006801:Humans; D007022:Hypotension / Q000401:mortality / Q000628:therapy*; D015994:Incidence; D008107:Liver Diseases / Q000209:etiology / Q000401:mortality / Q000628:therapy; D017114:Liver Failure, Acute / Q000209:etiology / Q000401:mortality / Q000628:therapy*; D016031:Liver Transplantation; D008875:Middle Aged; D009638:Norepinephrine / Q000008:administration & dosage; D010343:Patient Admission; D012189:Retrospective Studies; D016019:Survival Analysis; D013997:Time Factors; D016896:Treatment Outcome; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D000305:Adrenal Cortex Hormones; D000316:Adrenergic alpha-Agonists; D009638:Norepinephrine