title: Osmoregulation of vasopressin secretion is altered in the postacute phase of septic shock.
abstract: OBJECTIVE
  To determine whether septic shock patients have an abnormal reponse to increasing osmolarity.
  
  
  METHODS
  Prospective interventional study.
  
  
  METHODS
  Intensive care unit at Raymond Poincaré and Etampes Hospitals.
  
  
  METHODS
  Normonatremic patients at > 72 hrs from septic shock onset.
  
  
  METHODS
  Osmotic challenge consisting of infusing 500 mL of hypertonic saline solution (with cumulative amount of sodium not exceeding 24 g) over 120 mins.
  
  
  RESULTS
  Plasma arginine vasopressin levels were measured 15 mins before the test and then four times every 30 mins. A slope of the relation between arginine vasopressin and plasma sodium levels of < 0.5 pg/mEq defined nonresponders. Among the 33 included patients, 17 (52%) were nonresponders. During osmotic challenge, variations throughout the test in plasma sodium levels, blood pressure, and central venous pressure were comparable between the two groups. Arginine vasopressin increased from 4.8 pg/mL [3.3-6.4 pg/mL] to 14.4 pg/mL [11.2-23.3 pg/mL] in responders but only from 2.8 pg/mL [2.3-4.0 pg/mL] to 4.0 pg/mL [3.1-5.3 pg/mL] in nonresponders (p < .0001). Responders had a higher plasma arginine vasopressin levels at baseline and a more severe hematosis alteration. Nonresponders had more frequently bacteremia and liver dysfunction, been referred from the ward and undergone surgery. Critical illness severity, hemodynamic alteration, hydroelectrolytic disturbances, treatment, and outcome did not differ between the two groups.
  
  
  CONCLUSIONS
  Osmoregulation is dramatically altered in half of patients with prolonged septic shock.
authors.affiliation: Department of Intensive Care Medicine, Sud-Essonne Hospital, Etampes, France.
authors.forename: Shidasp
authors.initials: S
authors.lastname: Siami
authors.forename: Juliette
authors.initials: J
authors.lastname: Bailly-Salin
authors.forename: Andrea
authors.initials: A
authors.lastname: Polito
authors.forename: Raphael
authors.initials: R
authors.lastname: Porcher
authors.forename: Anne
authors.initials: A
authors.lastname: Blanchard
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Haymann
authors.forename: Kathleen
authors.initials: K
authors.lastname: Laborde
authors.forename: Virginie
authors.initials: V
authors.lastname: Maxime
authors.forename: Catherine
authors.initials: C
authors.lastname: Boucly
authors.forename: Robert
authors.initials: R
authors.lastname: Carlier
authors.forename: Djillali
authors.initials: D
authors.lastname: Annane
authors.forename: Tarek
authors.initials: T
authors.lastname: Sharshar
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000368:Aged; D001127:Arginine Vasopressin / Q000097:blood / Q000378:metabolism* / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002116:Calcitonin / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011498:Protein Precursors / Q000097:blood; D012720:Severity of Illness Index; D012772:Shock, Septic / Q000097:blood / Q000503:physiopathology*; D012964:Sodium / Q000097:blood; D014882:Water-Electrolyte Balance / Q000502:physiology*
chemical_list: D015850:Interleukin-6; D011498:Protein Precursors; D001127:Arginine Vasopressin; D016753:Interleukin-10; D000324:Adrenocorticotropic Hormone; D002116:Calcitonin; D012964:Sodium; D006854:Hydrocortisone