TY  - CHAP
M1  - Book, Section
TI  - Adrenal Insufficiency
A1  - Malcolm, William F.
Y1  - 2015
N1  - 
T2  - Beyond the NICU: Comprehensive Care of the High-Risk Infant
AB  - DefinitionAdrenal  insufficiency  in  preterm  newborns  and  to  a  lesser  extent  in  late  preterm  and  term  newborns  is  due  to  a:Transient  adrenocortical  insufficiency  of  prematurity  (TAP):  an  “immature”  hypothalamic-pituitary-adrenal  (HPA)  axis  with  reduced  capability  of  the  adrenal  glands  to  produce  cortisol  secondary  to  intermediate  enzyme  deficiency  in  the  steroidogenesis  pathway,  but  with  rapid  recovery  of  the  hormonal  axis  in  early  (∼14  days)  postnatal  lifeRelative  adrenal  insufficiency:  failure  to  produce  adequate  quantity  of  stress  hormone  resulting  in  inappropriately  low-circulating  cortisol  concentration  for  the  degree  of  stress  or  illness  experienced  (a  condition  similar  to  that  observed  in  critically  ill  adults  with  seemingly  normal  adrenal  function)Adrenal  insufficiency  due  to  congenital  adrenal  hyperplasia  (CAH)  is  a  different  condition  and  not  covered  in  this  chapter.IncidenceThe  exact  incidence  of  TAP  and  adrenocortical  insufficiency  in  late  preterm  or  term  newborns  is  not  known.  This  is  because  the  normal  range  of  serum  cortisol  concentration  in  this  age  group  is  difficult  to  define,  and  the  level  that  constitutes  clinical  adrenal  impairment  has  not  been  ascertained  (see  Diagnosis).The  earlier  the  gestation  (primarily  in  those  born  <30  weeks),  the  higher  is  the  chance  of  developing  this  condition.It  is  fallacious  to  assume  that  all  preterm  infants  with  improvement  of  blood  pressure  after  receiving  systemic  corticosteroids  are  due  to  TAP,  because  corticosteroids  per  se  can  also  elevate  the  blood  pressure  in  adrenal  competent  subjects.Those  infants  with  genuine  cortisol  deficiency  will  respond  promptly  and  dramatically  to  a  “replacement”  or  “stress”  dose  of  corticosteroids.PathophysiologyTAP  is  most  likely  due  to  delay  in  maturation  of  the  HPA  axis,  resulting  in  decreased  ability  of  the  adrenal  glands  to  produce  adequate  amount  of  cortisol.Adrenocortical  insufficiency  is  likely  related  to  ineffective  adrenal  steroidogenesis  secondary  to  immature  intermediate  enzymes,  eg,  11β-hydroxylase  and  3β-hydroxysteroid  dehydrogenase  activity  of  the  glucocorticoid  pathway  and  manifests  as  increased  cortisol  precursors/cortisol  ratios.This  may  be  associated  with  normal  fetal  development  of  the  adrenal  glands  that  generally  do  not  synthesize  cortisol  de  novo  until  30  weeks'  gestation,  and  utilize  placental  progesterone  for  production  of  cortisol,  thereby  bypassing  the  intermediate  enzymes  during  the  process.Although  the  use  of  antenatal  corticosteroids  has  been  shown  to  suppress  the  adrenal  glands  in  preterm  infants,  no  significant  association  has  been  reported  between  antenatal  corticosteroids  usage  and  TAP.  However,  prolonged  use  of  steroids  during  the  neonatal  period  may  contribute  to  the  relative  adrenal  insufficiency  seen  in  infants  following  their  NICU  course.Inadequate  circulating  cortisol  can  have  two  major  clinical  consequences  in  preterm  infants.Chronic  lung  disease:  Reduced  ability  to  suppress  inflammation  can  lead  to  exaggeration  of  inflammatory  responses  in  the  lungs,  giving  rise  to  increased  risks  of  developing  chronic  lung  disease.Cardiovascular  instability:  Decreased  ability  to  maintain  hemodynamic  stability  resulting  in  refractory  hypotension  and  cardiovascular  collapse.Transient  adrenocortical  insufficiency  in  late  preterm  or  term  infants  may  be  related  to  the  above  described  mechanism,  and  in  addition,  transitional  changes  of  hormone  production  from  intrauterine  to  extrauterine  life  in  the  HPA  axis.During  intrauterine  life,  CRH  produced  by  the  placenta  plays  a  key  role  in  determining  the  timing  of  parturition  and  maintaining  homeostasis  of  the  fetus.  The  sequence  of  events  is  as  follows:↑  CRH  production  by  ...
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/20
UR  - accesspediatrics.mhmedical.com/content.aspx?aid=1105545078
ER  -