RT Book, Section
A1 Chwals, Walter J.
A2 Goday, Praveen S.
A2 Mehta, Nilesh M.
SR Print(0)
ID 1105178408
T1 The Acute Metabolic Response to Injury in Children
T2 Pediatric Critical Care Nutrition
YR 2015
FD 2015
PB McGraw-Hill Education
PP New York, NY
SN 978-0-07-179852-5
LK accesspediatrics.mhmedical.com/content.aspx?aid=1105178408
RD 2024/04/23
AB In  response  to  a  variety  of  injurious  stimuli,  such  as  trauma,  sepsis,  and  acute  inflammatory  conditions,  a  series  of  metabolic  changes  occur  that  characterize  the  acute  metabolic  stress  (AMS)  response  in  humans  (Figs.  1-1A  and  1-1B).  This  response  is  basically  stereotypical  in  nature  in  all  patient  populations  (children  and  adults).1-4  This  response  may  vary  to  some  degree  with  respect  to  the  nature  (e.g.,  sepsis,  burn,)  and  severity  of  the  insult,  as  well  as  factors  that  impact  the  endogenous  metabolic  reserve  and/or  reserve  mobilization  capacity  (e.g.,  malnutrition,  recent  previous  tissue  injury,  underlying  systemic  disease,  age,  pharmacologic  intervention,)  of  the  acutely  injured  host.  In  infants,  especially  those  born  prematurely,  functional  immaturity  is  a  particularly  important  response-modifying  variable.5  Among  the  early  features  of  the  injury  response  is  the  release  of  cytokines,  followed  rapidly  by  important  alterations  in  the  hormonal  environment.  Increased  counter-regulatory  hormone  concentrations  are  associated  with  insulin  and  growth  hormone  (GH)  resistance.  As  a  result  of  this  response,  a  sequence  of  metabolic  events  is  initiated  that  includes  the  catabolism  of  endogenous  stores  of  protein,  carbohydrate,  and  fat  to  provide  essential  substrate  intermediates  and  energy  necessary  to  fuel  the  ongoing  response  process.  Amino  acids  from  catabolized  proteins  flow  to  the  liver  where  they  provide  substrate  for  the  synthesis  of  acutephase  proteins  and  glucose  (gluconeogenesis).  Therefore,  the  AMS  response  represents  a  hypermetabolic,  hypercatabolic  state  that  results  in  the  loss  of  endogenous  tissue  stores  with  associated  increases  in  glucose  and  free  fatty  acid  (FFA)  production  and  oxidation,  increased  energy  expenditure,  and  increased  protein  turnover  and  breakdown.  Growth,  which  is  an  anabolic  process,  is  thought  to  be  inhibited  during  periods  of  AMS.  As  the  AMS  response  resolves,  adaptive  anabolic  metabolism  ensues  to  restore  catabolic  losses.  In  children,  this  phase  is  characterized  by  the  resumption  of  somatic  growth.