Abdominal  Compartment  Syndrome  

Diane  Cobble  M.D.,  FACS  Professor,  ETSU  Dept.  of  Surgery  

7th  Annual  Rural  Trauma  Symposium  August  27,  2015  

Disclosure Statement of Financial Interest

I DO NOT have a financial interest/arrangement or affiliation with one or

more organizations that could be perceived as a real or apparent

conflict of interest in the context of the subject of this presentation.

Trauma  Scenario  

•  A  32yof  was  stabbed  in  the  liver.  She  arrived  in  the  ER  hypotensive  &  unresponsive  to  pain.  AKer  she  had  a  massive  transfusion  &  emergent  ex  lap,  she  was  admiMed  to  the  ICU.  During  the  next  6°,  mechanical  venQlaQon  became  progressively  more  difficult.  Although  cvp  remained  slightly  é,  her  CO  ê’d  markedly  

General  Surgery  Scenario  

•  An  87yo  NH  resident  had  severe  abd  pain.  His  care  providers  reported  that  he  had  recently  experienced  several  episodes  of  protracted  vomiQng  progressing  to  êbp,  éhr  &  êLOC.  Transfer  for  tests  to  determine  if  he  had  sepsis  was  arranged  &  he  was  admiMed  to  ICU.  Despite  administraQon  of  mulQple  fluid  boluses,  he  remained  hypotensive  &  anuric.  ConQnuous  ngt  sucQoning  produced  large  amt  of  green-­‐brown  fluid  &  abd  CT  revealed  complete  sbo  

History  

•  Recognized  clinically  19th  century  when  Marey  &  Burt  observed  its  assoc  w/declines  in  respiratory  fxn  

•  ForgoMen  aKer  WWI  &  rediscovered  near  end  20th  century  

•  More  recently,  Kron  (1984)  developed  simple  method  of  accurately  measuring  IAP  which  led  to  beMer  understanding  of  relaQonship  btwn  IAP  &  ACS  

•  2004  group  of  internaQonal  physicians  &  surgeons  developed  World  Society  of  ACS  (WSACS)  

definiQons  

•  Nl  IAP:  0-­‐5  mmHg  •  IAH:  sustained  IAP  ≥  12mmHg  •  ACS:  sustained  IAP  >  20mmHg  w/new  organ  dysfxn  

•  Morbidly  obese  &  pregnant  pts  can  have  chronically  é  IAP  10-­‐15  mmHg  w/o  adverse  sequelae  

categories  

•  Primary  (surgical):  intra-­‐abd  pathology  is  directly  &  proximally  responsible  for  the  ACS  

•  Secondary  (medical):  no  visible  intra-­‐abd  injury  is  present  but  injuries  outside  the  abd  cause  fluid  accumulaQon  

•  Recurrent:  ACS  redevelops  aKer  surgical/medical  tx  of  1°  or  2°  causes  

Risk  factors  

Primary  •  Major  trauma  •  Liver  transplantaQon  •  Ruptured  AAA  •  Mechanical  bowel  obst  •  Retroperitoneal  

hemorrhage  •  Postop  bleeding/abd  

closure  under  tension  •  Bleeding  pelvic  fxs    

Secondary  •  Obesity  or  é  BMI  •  Pregnancy  •  Major  burns/sepsis  •  Ileus/pancreaQQs/ascites  •  Large  vol  fluid  replacement  •  Severe  intra-­‐abd  infexn  •  CAPD  

Typical  scenarios  Abdominal  injury  w/ongoing  intra-­‐abd  bleeding  

A8er  DCL  2°  packing  therefore  vac  closure  

pathophysiology  •  Begins  @  organ  level  w/direct  compression  

•  Hollow  systems  (GI  tract  &  portal-­‐caval  system)  collapse  

•  Immediate  effects  (thrombosis  or  bowel  wall  edema)  è  translocaQon  of  bacterial  products  èaddiQonal  fluid  accumulaQon  è éIAP  

•  Cellular  level:  O2  impaired  è  ischemia  &  anaerobic  metabolism  

•  VasoacQve  substances  (histamine  &  serotonin)  é  endothelial  permeability  –  Further  capillary  leak  impairs  rbc  transport  &  ischemia  worsens  

 

Cellular  hypoxia  sequelae  Release  of  cytokines  FormaQon  of  O2  free  radicals  ê  Cellular  producQon  of  ATP  

Systems  Most  Affected  

•  Cardiovascular  •  Pulmonary  •  Renal    

CV  Effects  é  Intrathoracic  pressure  compresses  heart/great  vessels  ê  CO  due  to  ê  venous  return  éé  SVR  CVP/PCWP  falsely  é  IAH  causes  pressure  on  femoral  veins  è  stasis  è  DVT.  When  resolved,  risk  of  PE  é    

Pulmonary  

•  May  be  one  of  the  earliest  signs  

•  ê  excursion  of  diaphragm  •  ê  pulmonary  compliance  •  é  airway  pressure  w/ê  Qdal  volume  &  respiratory  acidosis  2°  to  é  pCO2  

•  Hypoxemia    

Other  System  DysfuncQon  

Renal    •  Oliguria  è  anuria  2°  direct    

parenchymal  compression  &  shunQng  of  renal  plasma  flow  

•  é  Cr  may  not  be  seen  for  2-­‐3d  

Visceral  •  ê  blood  flow  w/subsequent  

intesQnal  necrosis  •  HepaQc  dysfuncQon  w/ê  

glucose  metabolism  &  lactate  clearance  

•  Gut  anastomoQc  breakdown  

brain  

•  ObstrucQon  of  cerebral  venous  ouolow  

•  é  ICP  •  ê  CPP  

Organ  DysfuncQon  

Grading  ACs  

•  Grade  I:  10-­‐14  mmHg  •  Grade  II:  15-­‐24  mmHg  •  Grade  III:  25-­‐35  mmHg  •  Grade  IV:  >35  mmHg    

Abdominal  perfusion  pressure  

•  Measure  of  visceral  organ  perfusion  – Suggested  as  a  guide  by  some  authors  

•  APP  =  MAP-­‐IAP  •  More  accurate  predictor  of  abd  organ  perfusion  &  more  effecQve  guide  for  resuscitaQon  measures  

•  Ideal  level  is  anything  >  60  mmHg  

app  

•  Cheatham et al J Trauma 2000– Concluded  that  APP  60  mmHg  in  pts  w/ACS  98%  sensiQve  in  predicQng  survival  compared  to  APP  40  mmHg  being  70%  sensiQve  in  populaQon  largely  comprised  of  trauma  pts  (n=144)  

•  Also  concluded  APP  more  accurate  predictor  of  resuscitaQon  than  lactate,  MAP,  arterial  pH,  base  deficit,  IAP  

•  RetrospecQve  study  5/97-­‐6/99  

Bladder  pressure  

•  Can  be  measured  intermiMently  or  conQnuously  if  foley  connected  to  pressure  transducer  w/recording  device  

•  InsQll  ~25cc  NS  in  bladder  &  clamp  foley  •  18  gauge  needle  inserted  into  aspiraQon  port  &  aMached  to  pressure  transducer  

•  Pressure  obtained  @  end-­‐expiraQon  &  zeroed  @  mid-­‐axillary  line  

Measuring  Bladder  Pressure  May  not  be  accurate  w/morbid  obesity,  massive  ascites,  pelvic  hematoma,  adhesions  or  neurogenic  bladder  Can  use  intragastric,  intracolonic  or  IVC  catheters  

Frequency  of  monitoring  

•  Pts  @  risk  should  have  IAP  measured  q4-­‐6°  •  Pts  HD  unstable  or  w/rapidly  deterioraQng  organ  dysfxn  should  be  measured  q1°  

•  D/C  aKer  condiQon  resolved  &  IAP  remains  ≤10-­‐12  for  24-­‐48°  

epidemiology  

•  5-­‐15%  freq  in  trauma  ICU  adm  according  to  recent  lit  

 •  1%  gen  trauma  admissions  

prevalence  

•  Malbrain et al Intensive Care Medicine 2004:– Prevalence  study  in  13  ICU’s  involving  97  pts  

•  Overall  rate  IAH  58.8%  – 65%  surgical,  54.4%  medical  pts  

•  Medical  pts  é  prevalence  IAP  >15  – 29.8%  vs  27.5%  

•  Medical  pts  é  prevalence  ACS    – 10.5%  vs  5%  

prevalence  

•  Reintam et al Intensive Care Medicine 2008:– 257  venQlated  pts    

•  IAH  developed  in  95  pts    – 60  primary,  35  secondary  

•  During  1st  3  days,  IAP  ê  w/primary  &  éé  w/secondary  

Mortality  rates  

w/IAH  •  ICU  mortality  37.9%  •  28d  mortality  48.4%  •  90d  mortality  53.7%  •  Independent  risk  fx  for  

death  •  Secondary  ê  common,  

different  dev  course  &  worse  outcome  

w/o  IAH  •  ICU  mortality  19.1%  •  28d  mortality  27.8%  •  90d  mortality35.8%  

incidence  

•  Vidal et al Critical Care Medicine 2008:•  Studied  incidence  of  IAP  in  83  criQcally  ill  pts  in  single  ICU  

•  31%  pts  had  IAH  @  ICU  adm  &  33%  developed  it  aKer  adm  

•  Pts  w/IAH  were  sicker  w/é  mortality  rate    53%  vs  27%  

•  IAH  independent  predictor  of  mortality    – ACS  developed  in  10  pts    w/80%  mortality                  

           

Treatment  (physician)  

•  Burn  pts  may  respond  to  escharotomy  alone  •  Grade  I:  douboul  abd  decompression  warranted  

•  Grade  II:  need  for  tx  based  on  pts  clinical  condiQon  – Absence  of  oliguria,  hypoxia  or  sig  é  airway  pressure  difficult  to  jusQfy  abd  decompression  

•  Grade  III:  most  req  decompression  •  Grade  IV:  all  req  immed  decompression  b/c  may  è  cardiac  arrest  @  any  Qme  

Treatment  (nursing)  

•  Maintain  patency  of  NGT  &  rectal  tube  if  used  •  Monitor    &  record  daily  BM’s  

–  Check  qd  for  fecal  impacQon  if  pt  unconscious,  sedated  or  paralyzed  

•  Assess  tolerance  to  enteral  TF’s  &  adjust  accordingly  if  residuals  too  high  

•  For  pts  able  to  eat,  minimize/eliminate  gas-­‐producing  foods  

•  Avoid  prone  posiQon  &  place  pt  in  reverse  Trendelenberg  – Must  be  supine  to  measure  bladder  pressure  

mortality  

•  Early  decompression  improves  survival  •  Mortality  rates    range  from  25-­‐75%  •  High  rate  even  w/tx  reflects  fact  that  condiQon  affects  mulQple  organ  systems  

•  Furthermore  oKen  a  sequelae  to  severe  injuries  that  independently  carry  high  morbidity/mortality  

•  Assoc  w/éLOS,  éé  costs  &  further  dev  of  comorbidiQes  

World  society  acs  

•  Updated  consensus  definiQons  &  clinical  pracQce  guidelines  published  in  2013  Intensive Care Medicine  (prev  2006)  

•  PaQent  (P)  •  IntervenQons  (I)  •  Comparison  (C)  •  Outcome  (O)  

Wsacs  definiQons  

IAP  ~5-­‐7  mmHg  in  criQcally  ill  pts  •  Max  of  25ml  NS  insQlled  to  

determine  bladder  pressure  

IAH  •  Grade  I:  12-­‐15  mmHg  •  Grade  II:  16-­‐20  mmHg  •  Grade  III:  21-­‐25  mmHg  •  Grade  IV:  >25  mmHg  

recommendaQons  

•  Measuring  IAP  when  any  known  risk  fx  for  IAH/ACS  is  present  in  a  criQcally  ill/injured  pt  

•  Studies  should  adopt  the  trans-­‐bladder  technique  as  std  IAP  measurement  technique  

•  Use  of  protocolized  monitoring  &  mgmt  of  IAP  vs  not  

•  Efforts  &/or  protocols  to  avoid  sustained  IAH  as  compared  to  inaMenQon  to  IAP  among  criQcally  ill  or  injured  pts  

Cont,d    

•  Decompressive  lap  in  cases  of  overt  ACS  compared  to  strategies  that  do  not  use  DL  in  criQcally  ill  adults  w/ACS  

•  Among  ICU  pts  w/open  abdominal  wounds,  conscious  &/or  protocolized  efforts  be  made  to  obtain  an  early  or  @  least  same-­‐hospital-­‐stay  abd  fascial  closure  

•  Among  criQcally  ill/injured  pts  w/open  abdominal  wounds,  strategies  uQlizing  NPW  therapy  should  be  used  vs  not  

suggesQons  

•  Enhanced  raQo  plasma/prbc’s  for  massive  hemorrhage  

•  Perc  catheter  drainage  to  remove  fluid  when  technically  possible  (may  alleviate  need  for  DL)  

•  ProphylacQc  use  of  open  abd  when  undergoing  lap  for  physiologic  exhausQon  

•  Not  rouQnely  using  open  abd  for  pts  w/severe  abd  contaminaQon  

•  BioprostheQc  meshes  not  rouQnely  used  in  early  closure  open  abd  vs  alt.  strategies  

No  recommendaQons  

•  Use  of  APP  •  Use  of  diureQcs  or  RRT  •  Albumin  administraQon  •  ProphylacQc  use  of  open  abd  in  non-­‐trauma  acute  care  surg  pts  

•  Acute  component  separaQon  technique  to  facilitate  fascial  closure  

quesQons