title: Blood arginine vasopressin, adrenocorticotropin hormone, and cortisol concentrations at admission in septic and critically ill foals and their association with survival.
abstract: BACKGROUND
  Sepsis is an important cause for neonatal foal mortality. The hypothalamic-pituitary-adrenal axis (HPAA) responses to sepsis are well documented in critically ill humans, but limited data exist in foals. The purpose of this study was to evaluate the HPAA response to sepsis in foals, and to associate these endocrine changes with survival.
  
  
  OBJECTIVE
  Blood concentrations of arginine vasopressin (AVP), adrenocorticotropin hormone (ACTH), and cortisol will be higher in septic foals as compared with sick nonseptic and healthy foals. The magnitude of increase in hormone concentration will be negatively associated with survival.
  
  
  METHODS
  Fifty-one septic, 29 sick nonseptic, and 31 healthy foals of < or =7 days of age were included.
  
  
  METHODS
  Blood was collected at admission for analysis. Foals with positive blood culture or sepsis score > or =14 were considered septic. Foals admitted with disease other than sepsis and healthy foals were used as controls. AVP, ACTH, and cortisol concentrations were measured using validated immunoassays.
  
  
  RESULTS
  AVP, ACTH, and cortisol concentrations were increased in septic foals. Septic nonsurvivor foals (n = 26/51) had higher plasma ACTH and AVP concentrations than did survivors (n = 25/51). Some septic foals had normal or low cortisol concentrations despite increased ACTH, suggesting relative adrenal insufficiency. AVP, ACTH, and cortisol concentrations were higher in sick nonseptic foals compared with healthy foals.
  
  
  CONCLUSIONS
  Increased plasma AVP and ACTH concentrations in septic foals were associated with mortality. Several septic foals had increased AVP : ACTH and ACTH : cortisol ratios, which indicates relative adenohypophyseal and adrenal insufficiency.
authors.affiliation: Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210, USA. Samuel.Hurcombe@cvm.osu.edu
authors.forename: S D A
authors.initials: SD
authors.lastname: Hurcombe
authors.forename: R E
authors.initials: RE
authors.lastname: Toribio
authors.forename: N
authors.initials: N
authors.lastname: Slovis
authors.forename: C W
authors.initials: CW
authors.lastname: Kohn
authors.forename: K
authors.initials: K
authors.lastname: Refsal
authors.forename: W
authors.initials: W
authors.lastname: Saville
authors.forename: M C
authors.initials: MC
authors.lastname: Mudge
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood*; D016022:Case-Control Studies; D016638:Critical Illness; D005260:Female; D006734:Horse Diseases / Q000097:blood* / Q000401:mortality; D006736:Horses; D006854:Hydrocortisone / Q000097:blood*; D008297:Male; D018805:Sepsis / Q000097:blood* / Q000401:mortality; D016019:Survival Analysis
chemical_list: D001127:Arginine Vasopressin; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone