RT Book, Section
A1 Boucher, Bradley A.
A1 Wood, G. Christopher
A2 DiPiro, Joseph T.
A2 Yee, Gary C.
A2 Posey, L. Michael
A2 Haines, Stuart T.
A2 Nolin, Thomas D.
A2 Ellingrod, Vicki
SR Print(0)
ID 1182446446
T1 Acute Management of the Brain Injury Patient
T2 Pharmacotherapy: A Pathophysiologic Approach, 11e
YR 2020
FD 2020
PB McGraw-Hill Education
PP New York, NY
SN 9781260116816
LK accesspharmacy.mhmedical.com/content.aspx?aid=1182446446
RD 2024/04/19
AB KEY  CONCEPTS  Cerebral  ischemia  is  the  key  pathophysiologic  event  triggering  secondary  neuronal  injury  following  severe  traumatic  brain  injury  (TBI).  Intracellular  accumulation  of  calcium  is  postulated  to  be  a  central  pathophysiologic  process  in  amplifying  and  perpetuating  secondary  neuronal  injury  via  inhibition  of  cellular  respiration  and  enzyme  activation.Guidelines  for  the  Management  of  Severe  Brain  Injury,  4th  edition,  published  by  the  Brain  Trauma  Foundation  (BTF)/American  Association  of  Neurological  Surgeons  (AANS),  serve  as  the  foundation  on  which  clinical  decisions  in  managing  adult  neurotrauma  patients  are  based;  comparable  guidelines  for  infants,  children,  and  adolescents  have  also  been  published.  Correcting  and  preventing  early  hypotension  (systolic  blood  pressure  [SBP]  less  than  100  to  110  mm  Hg  depending  on  age)  with  an  SBP  goal  of  120  to  140  mm  Hg  and  reversal  of  hypoxemia  are  primary  goals  during  the  initial  resuscitative  and  intensive  care  of  patients  with  severe  TBI.  Nonpharmacologic  management  of  intracranial  hypertension  includes  raising  the  head  of  the  bed  30°,  and  ventricular  drainage  if  an  extraventricular  drain  (EVD)  is  present.  The  principal  monitoring  parameter  for  patients  with  severe  TBI  within  the  intensive  care  environment  is  increased  intracranial  pressure  (ICP).  Cerebral  perfusion  pressure  (CPP)  is  also  a  critical  monitoring  parameter  and  should  be  maintained  between  60  and  70  mm  Hg  (8.0  and  9.3  kPa)  (greater  than  40  mm  Hg  [5.3  kPa]  in  pediatric  patients)  through  the  use  of  fluids,  vasopressors,  and/or  ICP  normalization  therapy.  Nonspecific  pharmacologic  management  of  intracranial  hypertension  should  include  analgesics,  sedatives,  and  antipyretics;  paralytics  may  be  advantageous  under  selected  circumstances.  Specific  pharmacologic  management  of  intracranial  hypertension  includes  mannitol,  hypertonic  saline,  furosemide,  and  high-dose  pentobarbital.  Neither  routine  use  of  corticosteroids  nor  aggressive  hyperventilation  (ie,  PaCO2  less  than  25  mm  Hg  [3.3  kPa])  should  be  used  in  the  management  of  intracranial  hypertension.  Numerous  investigational  strategies  targeted  at  limiting  injury  and/or  stimulating  axonal  repair  following  severe  TBI  have  been  employed;  however,  no  proven  therapeutic  benefits  have  been  identified.  Use  of  phenytoin  (alternatively  levetiracetam)  for  the  prophylaxis  of  posttraumatic  seizures  generally  should  be  discontinued  after  7  days  if  no  seizures  are  observed.