RT Book, Section
A1 Butterworth IV, John F.
A1 Mackey, David C.
A1 Wasnick, John D.
SR Print(0)
ID 1190611260
T1 Thermoregulation, Hypothermia, & Malignant Hyperthermia
T2 Morgan & Mikhail’s Clinical Anesthesiology, 7e
YR 2022
FD 2022
PB McGraw-Hill Education
PP New York, NY
SN 9781260473797
LK accessanesthesiology.mhmedical.com/content.aspx?aid=1190611260
RD 2024/04/18
AB KEY  CONCEPTS  When  there  is  no  attempt  to  actively  warm  an  anesthetized  patient,  core  temperature  usually  decreases  1°C  to  2°C  during  the  first  hour  of  general  anesthesia  (phase  one),  followed  by  a  more  gradual  decline  during  the  ensuing  3  to  4  h  (phase  two),  eventually  reaching  a  point  of  steady  state.  In  the  normal,  unanesthetized  patient,  the  hypothalamus  maintains  core  body  temperature  within  very  narrow  tolerances,  termed  the  interthreshold  range,  with  the  threshold  for  sweating  and  vasodilation  at  one  extreme  and  the  threshold  for  vasoconstriction  and  shivering  at  the  other.  Anesthetics  inhibit  central  thermoregulation  by  interfering  with  these  hypothalamic  reflex  responses.  Postoperative  hypothermia  should  be  treated  with  a  forced-air  warming  device,  if  available;  alternatively,  warming  lights  or  heating  blankets  can  be  used  to  restore  body  temperature  to  normal.  Nearly  50%  of  patients  who  experience  an  episode  of  malignant  hyperthermia  (MH)  have  had  at  least  one  previous  uneventful  exposure  to  anesthesia,  during  which  they  received  a  recognized  triggering  agent.  Why  MH  fails  to  occur  after  every  exposure  to  a  triggering  agent  is  unclear.  The  earliest  signs  of  MH  during  anesthesia  include  muscle  rigidity,  tachycardia,  unexplained  hypercarbia,  and  increased  temperature.  Susceptibility  to  MH  may  be  increased  in  several  musculoskeletal  diseases.  These  include  central-core  disease,  multi-minicore  myopathy,  and  King–Denborough  syndrome.  Treatment  of  an  MH  episode  is  directed  at  terminating  the  episode  and  treating  complications  such  as  hyperthermia  and  acidosis.  The  mortality  rate  for  MH,  even  with  prompt  treatment,  ranges  from  5%  to  30%.  First  and  most  importantly,  the  triggering  agent  must  be  stopped;  second,  dantrolene  must  be  given  immediately.  Dantrolene,  a  hydantoin  derivative,  directly  interferes  with  muscle  contraction  by  inhibiting  calcium  ion  release  from  the  sarcoplasmic  reticulum.  The  dose  is  2.5  mg/kg  intravenously  every  5  min  until  the  episode  is  terminated  (upper  limit,  10  mg/kg).  Dantrolene  should  be  continued  for  24  h  after  initial  treatment.  Propofol,  etomidate,  benzodiazepines,  ketamine,  thiopental,  methohexital,  opiates,  droperidol,  nitrous  oxide,  nondepolarizing  muscle  relaxants,  and  all  local  anesthetics  are  safe  for  use  in  MH-susceptible  patients.