RT Book, Section
A1 Furtado, Nicholas
A2 Schafermeyer, Robert
A2 Tenenbein, Milton
A2 Macias, Charles G.
A2 Sharieff, Ghazala Q.
A2 Yamamoto, Loren G.
SR Print(0)
ID 1105684154
T1 Adrenal Insufficiency
T2 Strange and Schafermeyer's Pediatric Emergency Medicine, 4e
YR 2014
FD 2014
PB McGraw-Hill Education
PP New York, NY
SN 978-0-07-182926-7
LK accesspediatrics.mhmedical.com/content.aspx?aid=1105684154
RD 2024/04/18
AB Adrenal  insufficiency  (AI)  results  from  deficiency  of  glucocorticoid  (cortisol)  and  mineralocorticoid  (aldosterone)  secreted  by  the  adrenal  cortex.Glucocorticoid  deficiency  impairs  gluconeogenesis  and  glycogenolysis,  resulting  in  fasting  hypoglycemia.Aldosterone  deficiency  results  in  decreased  sodium  retention  by  the  kidney  and  distal  renal  tubular  exchange  of  potassium  and  hydrogen  ions  for  sodium,  resulting  in  osmotic  diuresis,  hyponatremia,  hypovolemia,  hyperkalemia,  acidosis,  and  prerenal  azotemia.AI  is  classified  into  primary  (adrenocortical  failure  itself),  secondary  (pituitary),  or  tertiary  (hypothalamic)  types.  AI,  because  of  withdrawal  from  exogenous  steroid  administration,  is  the  most  common  cause  of  adrenal  crisis.Symptoms  of  AI  are  usually  nonspecific  such  as  fatigue,  anorexia,  abdominal  pain,  nausea,  or  diarrhea  but  it  can  present  as  cardiovascular  collapse  or  shock  and  hence  a  high  index  of  suspicion  is  required.The  most  common  cause  of  primary  AI  in  infants  is  congenital  adrenal  hyperplasia  (CAH).Acquired  causes  of  primary  AI  in  children  are  less  common  than  congenital  disorders.Acquired  AI  results  from  autoimmune,  infectious,  infiltrative,  hemorrhagic,  or  toxic  causes.Acute  management  consists  of  rapid  fluid  resuscitation,  correction  of  hypoglycemia,  hyperkalemia,  and  acidosis  and  stress  doses  of  hydrocortisone  (50–75  mg/m2  IV).