TY  - CHAP
M1  - Book, Section
TI  - The Pathophysiology of Critical Illness
A1  - Bagchi, Aranya
A1  - Zapol, Warren M.
A2  - Longnecker, David E.
A2  - Mackey, Sean C.
A2  - Newman, Mark F.
A2  - Sandberg, Warren S.
A2  - Zapol, Warren M.
PY  - 2017
T2  - Anesthesiology, 3e
AB  - KEY  POINTSAcute  injuries  of  various  etiologies  (such  as  trauma,  infection  and  shock)  can  cause  immediate  local  and  systemic  physiologic  and  biochemical  responses  involving  all  major  organ  systems.The  timing  and  intensity  of  the  physiologic  response  to  injury  is  affected  by  the  severity  of  the  injury  as  well  as  host  factors.  Both  pro-  and  anti-inflammatory  pathways  are  activated  in  critically  ill  patients.  Clinically,  the  initial  response  is  likely  to  be  proinflammatory,  followed  by  late  immunosuppression.The  principal  defects  in  critically  ill  patients  include  endothelial  leakage,  epithelial  barrier  dysfunction,  and  disrupted  cellular  metabolism.Organ  dysfunction  in  critical  illness  is  characterized  by  a  striking  discord  between  profound  loss  of  function  and  relatively  mild  structural  changes.  The  cellular  response  to  critical  illness  may  be  considered  analogous  to  a  “hibernation”  phenotype,  minimizing  function,  and  metabolic  needs  to  survive  the  period  of  acute  stress.Our  increased  understanding  of  the  pathophysiology  of  critical  illness  has  not  yet  translated  into  successful  biologic  therapies.  Harnessing  the  tools  of  “big  data”  in  medicine  and  using  systems  biology  approaches  may  provide  a  complementary  approach  to  traditional  reductionist  methods  in  critical  illness  research.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/19
UR  - accessanesthesiology.mhmedical.com/content.aspx?aid=1144134323
ER  -