case report: anesthetic challenges in patient with known ... · case report: anesthetic challenges...

3
Case Report: Anesthetic challenges in patient with known inter-atrial shunt undergoing re-do sternotomy for CABG and MVR Rowena Lui , M.D. , Aymen Alian, M.D. Department of Anesthesiology, Yale University School of Medicine, New Haven, CT Background (cont.) References 79yearold male with PMHx coronary artery disease, severe mitral regurgitaCon, s/p thymectomy with radiaCon to chest presented for redo sternotomy for CABG and MVR. Preop CT chest was concerning for adhesions between mediasCnal structures and posterior table of the sternum. IntraoperaCve echo was posiCve for severe mitral regurgitaCon and leMtoright inter atrial shunt. Upon chest dissecCon, a copious amount of blood was encountered along with a decrease in blood pressure. Emergent right femfem bypass was iniCated to decompress the right heart and chest dissecCon was completed. Once the chest was open, laceraCon of the right ventricle was discovered. During TEE examinaCon to check venous cannula posiCon, numerous air bubbles were detected on both sides of the heart and in the aorta. Surgeon was noCfied, and due to concern for air emboli stroke, paCent was placed in Trendelenberg posiCon, cooled to 20°C, his head was packed in ice, and corCcosteroids were administered The right ventricle was repaired with a pericardial patch and planned procedure was aborted. PaCent followed postop, was AAOx3 without any focal neurological deficits and normal minimental state examinaCon Case: This was a case complicated by many issues. The paCent unfortunately had previous thoracic surgery causing significant scarring and adhesions between mediasCnal structures, and radiaCon therapy resulCng in severe radiaConinduced vasculiCs. This caused the iniCal chest dissecCon to be challenging requiring a sagiYal saw, which resulted in damage to the right ventricle. The damaged right ventricle likely caused entrained air, which involved the leM heart through his interatrial shunt aMer bypass was iniCated. With the large amount of air in his leM heart, the paCent was at a high risk for an air embolic stroke. Fortunately the paCent did not suffer any neurologic sequelae. There are several case reports of paCents on bypass who did have an air embolic event with subsequent CT findings and neurologic deficits. In all of the cases, the paCents were given steroids and placed under deep hypothermic circulatory arrest. In one case, the paCent was placed in a hyperbaric oxygen chamber and improved over the course of a few days. Another report menConed placing the paCent in a barbiturate coma to further decrease cerebral metabolic funcCon; however, this paCent did not improve. But these examples can certainly be taken into consideraCon for our paCent, had he had neurologic deficits. Conclusions: 1. Recognize the risks of reopening a sternotomy incision complicated by prior radiaCon therapy 2. Interpret the finding of intracardiac air in the leM heart and realize the associated risks 3. Demonstrate knowledge of how to minimize damage from possible cerebral ischemia intraoperaCvely 1. Van der Zee, M; Koene, B; Mariani, M. Fatal air embolism during cardiopulmonary bypass: analysis of an incident and prevenCon measures. InteracCve Cardiovascular and Thoracic Surgery. 2014, 1–3 2. Tian, DH et al. A metaanalysis of deep hypothermic circulatory arrest alone versus with adjuncCve selecCve antegrade cerebral perfusion. Ann Cardiothorac Surg. 2013, May;2(3):26170 3. Moon RE. Bubbles in the brain: what to do for arterial gas embolism? Crit Care Med 2005;33:909910 4. Shrinivas VG, Sankarkumar R, Rupa S. Retrograde cerebral perfusion for treatment of air embolism aMer valve surgery. Asian Cardiovasc Thorac Ann 2004;12:8182. Figure 2: Mid esophageal 4chamber view. Air visible in the leM atrium and right atrium Figure 3: Mid esophageal 4chamber view with air in the LA and LV Background Discussion Arterial air embolism during cardiac surgery is a complicaCon requiring expediCous acCon before significant cerebral damage occurs. The most likely causes of an embolic event include a reversed vent line, ruptured arterial tubing, introducCon of air during administraCon of cardioplegia, inadequate removal of air from the arterial circuit, and a defect in the oxygenator (1). Outside the context of cardiac surgery, arterial air embolism can also be caused by venous gas entering the arterial circulaCon via a righttoleM shunt (e.g. a patent foramen ovale or an atrial septal defect). Because the brain receives about 20% of cardiac output, an arterial air embolism can cause major cerebral injury; direct occlusion can cause sudden ischemia, clinically manifesCng as a stroke (altered mental status, loss of consciousness, focal neurologic deficits), which is difficult to assess in the semng of general anesthesia. Thus, it is important to have a high index of suspicion and take appropriate acCon. The literature menCons several measures to treat an air embolic stroke (or at least miCgate the cerebral damage it may cause) which include: placing the paCent in steep Trendelenberg posiCon, iniCaCng deep hypothermic circulatory arrest, administering corCcosteroids, retrograde brain perfusion, and administraCon of hyperbaric oxygen. Trendelenberg posiConing and hyperbaric oxygen aims to reduce the amount and volume of the actual air bubbles while the other treatments are targeted to brain funcCon (2, 3). Hypothermic circulaCon lowers cerebral metabolic rate and corCcosteroids serve to minimize inflammaCon and edema. Retrograde cerebral perfusion is not in common use, but is an established technique during aorCc surgery along with deep hypothermic circulatory arrest for cerebral protecCon (2, 4). Figure 2: Figure 1: Mid esophageal bicaval view with shunt visible between RA and LA LA RA shunt LA LA LV RA

Upload: trandien

Post on 16-May-2018

215 views

Category:

Documents


2 download

TRANSCRIPT

Case Report: Anesthetic challenges in patient with known inter-atrial shunt undergoing re-do sternotomy for CABG and MVR

Rowena Lui, M.D., Aymen Alian, M.D. Department of Anesthesiology, Yale University School of Medicine, New Haven, CT

Background  (cont.)  

References  

79-­‐year-­‐old   male   with   PMHx   coronary   artery   disease,   severe   mitral  regurgitaCon,     s/p   thymectomy   with   radiaCon   to   chest   presented   for  redo  sternotomy  for  CABG  and  MVR.    •  Pre-­‐op   CT   chest   was   concerning   for   adhesions   between  mediasCnal  structures   and  posterior   table  of   the   sternum.     Intra-­‐operaCve  echo  was   posiCve   for   severe   mitral   regurgitaCon   and   leM-­‐to-­‐right   inter-­‐atrial  shunt.    

•  Upon   chest  dissecCon,   a   copious   amount  of   blood  was  encountered  along   with   a   decrease   in   blood   pressure.   Emergent   right   fem-­‐fem  bypass   was   iniCated   to   decompress   the   right   heart   and   chest  dissecCon  was  completed.    Once  the  chest  was  open,  laceraCon  of  the  right  ventricle  was  discovered.    

•  During  TEE  examinaCon  to  check  venous  cannula  posiCon,  numerous  air  bubbles  were  detected  on  both  sides  of  the  heart  and  in  the  aorta.    Surgeon   was   noCfied,   and   due   to   concern   for   air   emboli   stroke,  paCent  was  placed  in  Trendelenberg  posiCon,  cooled  to  20°C,  his  head  was  packed  in  ice,  and  corCcosteroids  were  administered  

•  The  right  ventricle  was  repaired  with  a  pericardial  patch  and  planned  procedure  was  aborted.      

•  PaCent   followed  post-­‐op,  was  AAOx3  without   any   focal   neurological  deficits  and  normal  mini-­‐mental  state  examinaCon  

Case:   This   was   a   case   complicated   by   many   issues.   The   paCent  unfortunately  had  previous  thoracic  surgery  causing  significant  scarring  and   adhesions   between   mediasCnal   structures,   and   radiaCon   therapy  resulCng   in   severe   radiaCon-­‐induced   vasculiCs.     This   caused   the   iniCal  chest   dissecCon   to   be   challenging   requiring   a   sagiYal   saw,   which  resulted   in   damage   to   the   right   ventricle.   The   damaged   right   ventricle  likely   caused   entrained   air,   which   involved   the   leM   heart   through   his  inter-­‐atrial  shunt  aMer  bypass  was  iniCated.  With  the  large  amount  of  air  in  his  leM  heart,  the  paCent  was  at  a  high  risk  for  an  air  embolic  stroke.        Fortunately  the  paCent  did  not  suffer  any  neurologic  sequelae.  There  are  several  case  reports  of  paCents  on  bypass  who  did  have  an  air  embolic  event  with  subsequent  CT  findings  and  neurologic  deficits.    In  all  of  the  cases,   the   paCents   were   given   steroids   and   placed   under   deep  hypothermic  circulatory  arrest.    In  one  case,  the  paCent  was  placed  in  a  hyperbaric  oxygen  chamber  and  improved  over  the  course  of  a  few  days.    Another  report  menConed  placing  the  paCent   in  a  barbiturate  coma  to  further  decrease  cerebral  metabolic  funcCon;  however,  this  paCent  did  not   improve.     But   these   examples   can   certainly   be   taken   into  consideraCon  for  our  paCent,  had  he  had  neurologic  deficits.    Conclusions:  1.  Recognize  the  risks  of  re-­‐opening  a  sternotomy  incision  complicated  

by  prior  radiaCon  therapy  2.  Interpret  the  finding  of  intra-­‐cardiac  air  in  the  leM  heart  and  realize  

the  associated  risks  3.  Demonstrate  knowledge  of  how  to  minimize  damage  from  possible  

cerebral  ischemia  intra-­‐operaCvely  

1.  Van  der  Zee,  M;  Koene,  B;  Mariani,  M.  Fatal  air  embolism  during  cardiopulmonary  bypass:  analysis  of  an  incident  and  prevenCon  measures.  InteracCve  Cardiovascular  and  Thoracic  Surgery.  2014,  1–3  

2.  Tian,  DH  et  al.  A  meta-­‐analysis  of  deep  hypothermic  circulatory  arrest  alone  versus  with  adjuncCve  selecCve  antegrade  cerebral  perfusion.  Ann  Cardiothorac  Surg.  2013,  May;2(3):261-­‐70  

3.  Moon  RE.  Bubbles  in  the  brain:  what  to  do  for  arterial  gas  embolism?  Crit  Care  Med  2005;33:909-­‐910  4.  Shrinivas  VG,  Sankarkumar  R,  Rupa  S.  Retrograde  cerebral  perfusion  for  treatment  of  air  embolism  aMer  valve  surgery.  

Asian  Cardiovasc  Thorac  Ann  2004;12:81-­‐82.  

Figure  2:  Mid  esophageal  4-­‐chamber  view.    Air  visible  in  the  leM  atrium  and  right  atrium  

Figure  3:  Mid-­‐esophageal  4-­‐chamber  view  with    air  in  the  LA  and  LV  

Background  

Discussion  

Arterial  air  embolism  during  cardiac  surgery   is  a  complicaCon  requiring  expediCous  acCon  before  significant  cerebral  damage  occurs.    The  most  likely  causes  of  an  embolic  event  include  a  reversed  vent  line,  ruptured  arterial  tubing,  introducCon  of  air  during  administraCon  of  cardioplegia,  inadequate   removal  of  air   from  the  arterial   circuit,  and  a  defect   in   the  oxygenator  (1).      Outside  the  context  of  cardiac  surgery,  arterial  air  embolism  can  also  be  caused  by  venous  gas  entering  the  arterial  circulaCon  via  a  right-­‐to-­‐leM  shunt  (e.g.  a  patent  foramen  ovale  or  an  atrial  septal  defect).      

Because  the  brain  receives  about  20%  of  cardiac  output,  an  arterial  air  embolism   can   cause   major   cerebral   injury;   direct   occlusion   can   cause  sudden   ischemia,   clinically   manifesCng   as   a   stroke   (altered   mental  status,  loss  of  consciousness,  focal  neurologic  deficits),  which  is  difficult  to   assess   in   the   semng   of   general   anesthesia.   Thus,   it   is   important   to  have  a  high  index  of  suspicion  and  take  appropriate  acCon.        The  literature  menCons  several  measures  to  treat  an  air  embolic  stroke  (or   at   least  miCgate   the   cerebral  damage   it  may   cause)  which   include:  placing   the   paCent   in   steep   Trendelenberg   posiCon,   iniCaCng   deep  hypothermic  circulatory  arrest,  administering  corCcosteroids,  retrograde  brain   perfusion,   and   administraCon   of   hyperbaric   oxygen.    Trendelenberg   posiConing   and   hyperbaric   oxygen   aims   to   reduce   the  amount  and  volume  of  the  actual  air  bubbles  while  the  other  treatments  are   targeted   to   brain   funcCon   (2,   3).     Hypothermic   circulaCon   lowers  cerebral   metabolic   rate   and   corCcosteroids   serve   to   minimize  inflammaCon   and   edema.     Retrograde   cerebral   perfusion   is   not   in  common  use,  but  is  an  established  technique  during  aorCc  surgery  along  with  deep  hypothermic  circulatory  arrest  for  cerebral  protecCon  (2,  4).          

Figure  2:      

Figure  1:  Mid  esophageal  bicaval  view  with  shunt  visible  between  RA  and  LA  

LA  

RA  

shunt  LA   LA  

LV  RA  

Abstract  

Effect of changes in tidal volume on plethysmographic variability in pediatric patients Rowena Lui, M.D., Aymen Alian, M.D.

Department of Anesthesiology, Yale University School of Medicine, New Haven, CT

IntroducCon   Results  

References  

The   pulse   oximeter   is   widely   used   as   a   standard   for   intra-­‐operaCve   monitoring   of   oxygenaCon   during   anesthesia.    Studies   have   looked   into   expanding   its   uClity   by   using   the  respiratory   induced   variaCon   of   the   photoplethysmography  (PPG)  waveform  as  a  dynamic  index  of  preload  (1,2).    It  has  also  been  shown  that  shown  that  different  respiratory  paYerns  can  affect  the  waveform  variability.    In  adults,  a  Cdal  volume  of  at  least   8cc/kg   is   necessary   to   cause   significant   circulatory  changes  (4).  Reviews  of   studies  done   in  children  have  been  equivocal  with  regard   to   the   use   of   respiratory-­‐induced   PPG   variaCon   to  predict   preload   condiCons   (5).     None   of   the   studies  standardized   the   venClator   semngs   used.     AddiConally,  compared  to  adults,  children  have  higher  chest  wall  compliance  and  more  compliant  arterial  vasculature.    The  aim  of  this  study  is   to   invesCgate   whether   or   not   pediatric   paCents   require  higher   than  8cc/kg  Cdal  volume  to   induce  respiratory   induced  variaCons  due  to  their  physiology.    

StaCsCcally   significant   changes   were   seen   in   PPG   waveform  parameters   in   Group   1   between   the   baseline   Cdal   volume   of  8cc/kg  and  25%  above  (10cc/kg),  but  not  between  baseline  and  25%  below.    This  suggests  that  within  that  age  group,  at   least  10cc/kg   is   required   to   induce   circulatory   changes   that   would  produce   respiraCon-­‐induced   variability   in   the   PPG   waveform.    In   Group   2,   however,   there   was   a   significant   difference  between   baseline   Cdal   volume   and   25%   below;   this   suggests  that  in  that  age  group,  8cc/kg  is  adequate.    

Methods  

Conclusion/Discussion  

We  included  paCents  age  0  day  to  17  years,  ASA  classificaCon  1  and   2  who  were   intubated  with   posiCve   pressure   venClaCon.    They   were   grouped   according   to   the   NICHD   Pediatric  terminology.     In   these   results,  we   included   12   paCents   age   1  month  -­‐  1  year  (Group  1),  22  paCents  age  1-­‐6  years(Group  2).    Tidal  volume  was  maintained  at  baseline,  altered  to  25%  above  then  25%  below  baseline  while   respiratory   rate  held   constant  for  5-­‐minute  intervals.    Vital  signs  and  basic  hemodynamic  data  were  recorded,  in  addiCon  to  conCnuous  recording  of  the  PPG  and  airway  pressure  waveforms  at  100Hz.    Waveforms  were  

In  Group  1  there  was  a  staCsCcally  significant  difference  in  the  PPG   DC%   between   baseline   Cdal   volume   of   8cc/kg   and   25%  above   (p   =   0.02)   and   in   the   PPG   AC%   between   baseline   and  25%   above   (p   =   0.03).     In   Group   2,   there   was   staCsCcally  significant   difference   in   the   PPG   DC%   between   baseline   and  25%  below  (p  =  0.017).      

Figure  2   Figure  3  

Figure  4   Figure  5  

analyzed   using   frequency   domain   analysis   at   baseline   Cdal  volume,   and   at   25%   below   and   25%   above   baseline.     PPG  waveform   measurements   were   divided   by   their   respecCve  cardiac  pulse  amplitude  to  generate  normalized  DC%  and  AC%  values.   Results   are   presented   as   median   and   inter-­‐quarCle  range  (IQR).    Friedman  ANOVA  and  Wilcoxon  tests  were  used,  p  <  0.05  is  considered  staCsCcally  significant.  

Methods,  cont.  

1.  Charron,  C.,  C.  Fessenmeyer,  et  al.  (2006).  "The  Influence  of  Tidal  Volume  on  the  Dynamic  Variables  of  Fluid  Responsiveness  in  CriCcally  Ill  PaCents."  Anesthesia  &  Analgesia  102(5):  1511-­‐1517Michard,    2.  F.,   J.  L.  Teboul,  et  al.   (2003).  "Influence  of  Cdal  volume  on  stroke  volume  variaCon.  Does   it  really  maYer?"  Intensive  Care  Med  29(9):  1613.  3.  Perner,  A.  and  T.  Faber  (2006).  "Stroke  volume  variaCon  does  not  predict  fluid  responsiveness   in  paCents   with   sepCc   shock   on   pressure   support   venClaCon."   Acta   Anaesthesiol   Scand   50(9):  1068-­‐1073  4.  De  Backer,  Daniel,  et  al.  "Pulse  pressure  variaCons  to  predict  fluid  responsiveness:  influence  of  Cdal  volume."  Intensive  care  medicine  31.4  (2005):  517-­‐523  5.   Cannesson,   M.   et   al   (2013).   “PredicCng   fluid   responsiveness   in   children:   a   systemaCc   review.”  Anesthesia  &  Analgesia  Vol  116  No  6,  December  2013.    

Figures  2  and  3:  TV  and  PPG  AC%,  TV  and  PPG  DC%  for  Group  1  paCents  

Figures  4  and  5:  TV  and  PPG  AC%,  TV  and  PPG  DC%  for  Group  2  paCents  

Effect of changes in respiratory rate on plethysmographic variability in pediatric patients Rowena Lui, M.D., Aymen Alian, M.D.

Department of Anesthesiology, Yale University School of Medicine, New Haven, CT

IntroducCon  

Results   References  

The   pulse   oximeter   is   widely   used   as   a   standard   for   intra-­‐operaCve   monitoring   of   oxygenaCon   during   anesthesia.    Studies   have   looked   into   expanding   its   uClity   by   using   the  respiratory   induced   variaCon   of   the   photoplethysmography  (PPG)  waveform   as   a   dynamic   index   of   preload.     It   has   been  shown   in  several  meta-­‐analyses  and  systemic  reviews  of  adult  studies   and   some   animal   studies   that   these   indices   have  excellent  predicCve  value  of  preload  condiCons.    AddiConally,  there   have   been   studies   showing   that   different   respiratory  paYerns   can   affect   the   variaCon.     In   studies   involving   adult  paCents,  high  respiratory  rates  have  been  shown  to  abolish  the  variaCons  in  some  dynamic  indices  of  preload.    Reviews  of   studies  done   in  children  have  been  equivocal  with  regard   to   the   use   of   respiratory-­‐induced   PPG   variaCon   to  predict  preload  condiCons.    None  of   the   studies   standardized  the  venClator  semngs  that  were  used.    AddiConally,  compared  to   adults,   children   have   higher   chest   wall   compliance,   and  more  compliant  arterial  vasculature.    The  aim  of  this  study  is  to  invesCgate  whether  or  not  changes  n  respiratory  rate  have  an  effect  on  the  PPG  waveform  variability.  

StaCsCcally   significant   changes   were   seen   in   only   PPG  waveform  parameters  in  Group  2  between  baseline  respiratory  rate  and  25%  below  baseline,  and  no  changes  were  seen  in  the  other   group.     Further   studies   in   other   age   groups   would   be  useful  for  comparison.    The  normal  range  for  respiratory  range  varies   widely   within   the   pediatric   populaCon   from   neonates  (35-­‐40)   to   adolescents   (10-­‐14).     Another   parameter   that  was  studied   in   adults   and   could  be   a   useful   addiCon   to   looking   at  respiratory  rate  is  heart  rate  to  respiratory  rate  raCo.    

Methods  

Conclusion/Discussion  

In  Group  2  there  was  a  staCsCcally  significant  difference  in  the  PPG  DC  (p=0.008)  and  PPG  DC%  (p  =  0.0002)  between  baseline  respiratory  rate  and  25%  below  baseline  

above   then   25%   below   baseline   while   Cdal   volume   held  constant   for   5-­‐minute   intervals.     Vital   signs   and   basic  hemodynamic   data   were   recorded,   in   addiCon   to   conCnuous  recording  of  the  PPG  and  airway  pressure  waveforms  at  100Hz.    Waveforms  were  analyzed  using   frequency  domain  analysis  at  baseline   respiratory   rate,   and   at   25%   below   and   25%   above  baseline.    PPG  waveform  measurements  were  divided  by  their  respecCve  cardiac  pulse  amplitude  to  generate  normalized  DC%  and  AC%  values.  Results  are  presented  as  median  and  inter-­‐quarCle   range   (IQR).     Friedman   ANOVA   and   Wilcoxon   tests  were  used,  p  <  0.05  is  considered  staCsCcally  significant.  

Methods,  cont.  

1.  Charron,  C.,  C.  Fessenmeyer,  et  al.  (2006).  "The  Influence  of  Tidal  Volume  on  the  Dynamic  Variables  of  Fluid  Responsiveness  in  CriCcally  Ill  PaCents."  Anesthesia  &  Analgesia  102(5):  1511-­‐1517Michard,    2.  F.,   J.  L.  Teboul,  et  al.   (2003).  "Influence  of  Cdal  volume  on  stroke  volume  variaCon.  Does   it  really  maYer?"  Intensive  Care  Med  29(9):  1613.  3.  Perner,  A.  and  T.  Faber  (2006).  "Stroke  volume  variaCon  does  not  predict  fluid  responsiveness   in  paCents   with   sepCc   shock   on   pressure   support   venClaCon."   Acta   Anaesthesiol   Scand   50(9):  1068-­‐1073  4.  De  Backer,  Daniel,  et  al.  "Pulse  pressure  variaCons  to  predict  fluid  responsiveness:  influence  of  Cdal  volume."  Intensive  care  medicine  31.4  (2005):  517-­‐523  5.   Cannesson,   M.   et   al   (2013).   “PredicCng   fluid   responsiveness   in   children:   a   systemaCc   review.”  Anesthesia  &  Analgesia  Vol  116  No  6,  December  2013.    

We  included  paCents  age  0  day  to  17  years,  ASA  classificaCon  1  and   2  who  were   intubated  with   posiCve   pressure   venClaCon.    They  were  grouped  according  to  the  NICHD  (NaConal  InsCtute  of   Child   Health   and   Human   Development)   Pediatric  terminology.     In   this   study,   we   included   12   paCents   age   1  month  -­‐  1  year  (Group  1),  20  paCents  age  1-­‐6  years(Group  2).    Respiratory  rate  was  maintained  at  baseline,  altered  to  25%  

Results,  cont.