title: Neuroendocrine dysfunction in pediatric critical illness.
abstract: BACKGROUND
  The extent of neuroendocrine dysfunction (NED) has not been well defined in critically ill children and likely varies significantly from that in adults. We sought to define the prevalence of neuroendocrine dysfunction in a group of children in a multidisciplinary pediatric intensive care unit and determine the relationship of neuroendocrine dysfunction with severity of illness and presence of sepsis.
  
  
  METHODS
  Prospective observational study in a pediatric intensive care unit at a referral childrens hospital. Blood samples were evaluated within 12 hrs of admission for serum cortisol, thyroid stimulating hormone, total triiodothyronine (T3), reverse triiodothyroine (rT3), free thyroxine, and arginine vasopressin. Pediatric risk of mortality, pediatric logistic organ dysfunction scores, and length of stay were calculated.
  
  
  RESULTS
  Seventy-three children were enrolled over a 13-month period. Median patient age was 72 months (range, 3-228 months). Overall prevalence of absolute adrenal insufficiency ranged from 7% to 58% based on cortisol cutoff chosen. Presence of absolute adrenal insufficiency, low T3 syndrome (LT3S), or vasopressin insufficiency did not differ between septic or nonseptic patients. NED did not correlate with pediatric logistic organ dysfunction, Pediatric Risk of Mortality Score III, length of stay, or mortality. Prevalence of multiple NED was 62% (28 of 45 children), where 62% had 2 neurohormonal deficiencies and 24% had 3 neurohormonal deficiencies.
  
  
  CONCLUSIONS
  NED is common in both septic and nonseptic critically ill children in a single pediatric intensive care unit. Larger scale studies are necessary to determine whether presence of NED, or specific combinations of neurohormonal dysfunction, is important in predicting outcomes or benefit of early hormonal replacement therapies in critically ill children.
authors.affiliation: Divisions of Critical Care, Department of Pediatrics, Emory University School of Medicine, Atlanta GA, USA. kiran.hebbar@choa.org
authors.forename: Kiran
authors.initials: K
authors.lastname: Hebbar
authors.forename: Mark R
authors.initials: MR
authors.lastname: Rigby
authors.forename: Eric I
authors.initials: EI
authors.lastname: Felner
authors.forename: Kirk A
authors.initials: KA
authors.lastname: Easley
authors.forename: James D
authors.initials: JD
authors.lastname: Fortenberry
mesh_terms: D018806:APACHE; D000293:Adolescent; D000367:Age Factors; D002423:Cause of Death; D016009:Chi-Square Distribution; D002648:Child; D002675:Child, Preschool; D016638:Critical Illness / Q000401:mortality; D004700:Endocrine System Diseases / Q000097:blood / Q000175:diagnosis* / Q000401:mortality*; D005260:Female; D017052:Hospital Mortality / Q000639:trends*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007223:Infant; D015278:Intensive Care Units, Pediatric; D008297:Male; D009102:Multiple Organ Failure / Q000097:blood / Q000401:mortality; D009490:Neurosecretory Systems / Q000503:physiopathology*; D011446:Prospective Studies; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D018805:Sepsis / Q000097:blood / Q000401:mortality; D012737:Sex Factors; D018709:Statistics, Nonparametric; D016019:Survival Analysis; D013972:Thyrotropin / Q000097:blood; D014667:Vasopressins / Q000097:blood
chemical_list: D014667:Vasopressins; D013972:Thyrotropin; D006854:Hydrocortisone