title: Prophylactic management of excessive natriuresis with hydrocortisone for efficient hypervolemic therapy after subarachnoid hemorrhage.
abstract: OBJECTIVE
  Hyponatremia caused by excessive natriuresis is common in patients with aneurysmal subarachnoid hemorrhage (SAH). Natriuresis decreases the total blood volume through osmotic diuresis and increases the risk of symptomatic cerebral vasospasm. In such patients, hypervolemic therapy is difficult to achieve without causing hyponatremia because sodium replacement provokes further natriuresis and osmotic diuresis. We examined the effects of hydrocortisone, which promotes sodium retention, in patients with SAH.
  
  
  METHODS
  Twenty-eight SAH patients were randomized into 2 groups after direct surgery: group 1 patients without hydrocortisone treatment (n=14) and group 2 patients with hydrocortisone treatment (1200 mg/d for 10 days; n=14). Both groups underwent hypervolemic therapy by aggressive sodium and water replacement. The goal of the hypervolemic therapy was to maintain the serum sodium level >140 mEq/L and the central venous pressure (CVP) within 8 to 12 cm H2O.
  
  
  RESULTS
  Group 2 demonstrated a lower sodium excretion (P<0.05) and higher serum sodium level (P<0.05) compared with group 1. Hyponatremia developed in 6 patients (43%) in group 1 and 0 patients in group 2 (P<0.05). Group 2 also demonstrated a lower urine volume, lower infusion volume (P<0.05) required for hypervolemic therapy, and higher CVP (P<0.05). Failure to maintain CVP was observed in 12 patients (86%) in group 1 and 3 patients (21%) in group 2 (P<0.05). Hydrocortisone caused no serious side effects.
  
  
  CONCLUSIONS
  Hydrocortisone clearly attenuates excessive natriuresis. Prophylactic hydrocortisone administration appears to have a therapeutic value in inducing hypervolemia efficiently after SAH.
authors.affiliation: Department of Neurological Surgery, Nihon University School of Medicine, 30-1 Oyaguchi-kamimachi, Itabashi-ku, Tokyo 173-8610, Japan. moro@med.nihon-u.ac.jp
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Moro
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Katayama
authors.forename: Jun
authors.initials: J
authors.lastname: Kojima
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Mori
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Kawamata
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis / Q000187:drug effects; D001798:Blood Proteins / Q000032:analysis; D001810:Blood Volume / Q000187:drug effects; D005260:Female; D023261:Glasgow Outcome Scale; D006801:Humans; D006854:Hydrocortisone / Q000009:adverse effects / Q000627:therapeutic use*; D007010:Hyponatremia / Q000150:complications* / Q000188:drug therapy* / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D009318:Natriuresis / Q000187:drug effects*; D009997:Osmotic Pressure / Q000187:drug effects; D011188:Potassium / Q000097:blood / Q000652:urine; D012964:Sodium / Q000097:blood / Q000652:urine; D012982:Sodium, Dietary; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000601:surgery; D016896:Treatment Outcome; D020301:Vasospasm, Intracranial / Q000517:prevention & control; D014882:Water-Electrolyte Balance / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D001798:Blood Proteins; D012982:Sodium, Dietary; D012964:Sodium; D011188:Potassium; D006854:Hydrocortisone