Abdominalcompartmentsyndrome

MarilynJ.Borst,M.D.*,AndrewB.Peitzman,M.D.*
*

TheDepartmentofSurgery,UniversityofPittsburghSchoolofMedicine.
Address correspondence to: Andrew B. Peitzman, M.D. Room A1010, Presbyterian
UniversityHospital,Pittsburgh,PA15213.

SUMMARY
AnIAPgreater than25mmHginapatient withadequate bloodvolume andoliguriais an
indicationfordecompressivelaparotomy.RenalandsplanchnicdysfunctionoccurwithIAPof
1015mmHg.Forcedfascialorskinclosureoverswollenbowelorintraabdominalpacksmust
beavoided.ThiswilloftenpreventthedevelopmentofACSinthepatientathighriskafter
laparotomy.
SurgeonscaringforpatientsatriskfordevelopmentofACSmustbecognizantofthemultiple
organ systems affected by an increasing IAP. Surgeons caring for multiply injured trauma
patients,especiallythosewithcombinedabdominalandheadtrauma,mustbeparticularlyaware
oftheeffectsofincreasedIAPupontheCNS.
Keyword:Abdominalcompartmentsyndrome.Abdominalhypertension.
Theabdominalcompartmentsyndrome(ACS),alsoknownasintraabdominalhypertension,is
thedevelopmentofphysiologicdysfunctioninintraabdominalandextraabdominalorgansas
theresultofincreasedintraabdominalpressure(IAP) 15.TheelevatedIAPisafunctionofthe
rateoffluidaccumulationwithintheabdominalcavityandthecomplianceoftheabdomen.The
pressurevolumecurvefortheabdominalcavityisnonlinear 6.Duetothedecreasingcompliance
of the abdomen, as fluid within the peritoneal cavity progressively accumulates, a greater
increaseinIAPresults.TheACSmayoccurinpatientswithavarietyofconditionsinwhich
increasedIAPoccurs.Clinicalsettingswhichhavebeenassociatedwiththesyndromeinclude
ruptured abdominal aortic aneurysm, ascites, intraperitoneal hemorrhage, abdominal trauma,
ovariantumors,livertransplantation,andhemorrhagicpancreatitis1,4,5,714.
Traumapatientswithhepaticorintraabdominalvascularinjuriesareparticularlysusceptibleto
the development of ACS. The increased IAP in these patients develops from increasing
hemoperitoneumcompoundedbyhypothermiaandcoagulopathy.Increasingbowelwalledema
andthirdspacefluidlossesduetolargevolumesofbloodproductsandnonsanguinoussolutions
usedinresuscitationalsocontributetotheincreasedIAP.
OtherfactorswhichmaycontributetothedevelopmentofincreasedIAPinthetraumapatient
include retroperitoneal bleeding, pneumatic antishock garments, abdominal closure under
excessivetension,ongoingsurgicalbleeding(missedinjuries),orbleedingcontrolledwithintra
abdominal packs (damage control laparotomy). On rare occasion, abdominal compartment
syndrome may occur in the patient who has been massively fluid resuscitated without an
associatedintraabdominalinjury.
SYSTEMICMANIFESTATIONSOFINCREASEDINTRAABDOMINALPRESSURE

Increased IAP results in dysfunction of the respiratory, cardiovascular, and renal systems.
Elevationinintracranialpressure(ICP)anddepressionofcerebralperfusionpressure(CPP)may
alsoresultfromincreasedIAP.
Respiratorysystem.ThehemidiaphragmsareelevatedduetotheincreasedIAP.Adecreasein
thoracic volume and compliance results. Peak inspiratory pressure and pulmonary vascular
resistance increase. Higher pressures are required to deliver a set tidal volume. Ventilation
perfusionabnormalitiesoccur.Increasingpositiveendexpiratorypressure(PEEP)isrequiredto
oxygenate the patient. The use of increasing PEEP can exacerbate cardiovascular and
hemodynamic abnormalities in the patient with elevated IAP. Continued impairments in
ventilationandoxygenationresultinhypercarbia,acidosis,andprogressivehypoxemia15.
Cardiovascularsystem.AstheIAPincreases,centralvenouspressure(CVP),pulmonaryartery
wedgepressure(PAWP),andsystemicvascularresistanceincrease15. TheCVPandPAWPare
elevated due to an increased pleural pressure secondary to the increased IAP.The measured
PAWPandCVPareeachthesumofpleuralpressureandtheintravascularfillingpressuresand
thusspuriouslyelevated17.
Cardiac output (CO) decreases progressively as the IAP increases 15. The magnitude of the
depressionofCOisdependentontheintravascularvolumestatus.Inaninterestinglaboratory
study,theimpactofintravascularvolumestatusondepressionofCOinACSwasassessed.In
hypovolemic animals, CO declined 53%; in euvolemic animals, CO declined 17%; and in
hypervolemicanimals,COincreased50%inthesettingofACS 18. AlleffectsofACS,including
depressionofcardiacoutput,areexacerbatedbyhypovolemia.Intravenousvolumeexpansion
willincreasethecardiacoutputandcentralfillingpressuresinACS,butwillnotcorrecttheother
manifestationsofACS,includingdepressedrenalfunctionandsplanchnicbloodflow.Anactual
depressionofmyocardialfunctionoccurswithACSduetomarkedincreaseinafterload,aswell
asimpairmentofvenousreturn18.
Renalsystem.OliguriadevelopsdespitemeasurednormalormildlyelevatedCVPandPAWP.
OliguriaoccurswithIAP>15mmHg,andanuriaresultswithIAP>30mmHg.Bloodflowand
glomerular filtration in the kidney are diminished. In an animal study, renal bloodflow and
glomerularfiltrationratewere25%ofnormalatanIAPof20mmHgandonly7%ofnormalat
anIAPof40mmHg19.Therenalveinandinferiorvenacavaarecompressed.Inaddition,renal
vascularresistanceincreasesseveralfoldinACS.Directcompressionoftherenalparenchyma
alsocontributestotherenaldysfunction.OliguriaisoftentheearliestsignofACSandanuria
followsiftheIAPisnotreduced15.
Inaswinemodel,elevatedIAPwasfoundtodecreaseurineoutputandupregulatethehormonal
outputofthereninangiotensinaldosteronesystem.Abdominaldecompressionincombination
withintravascular volume expansionreversedtheeffects uponrenal functionandtherenin
angiotensinaldosteronesystem20.
Abdominal and visceral effects. Clinically, the abdominal girth increases and the abdomen
becomesmoretenseastheIAPincreases.SplanchnicbloodflowdecreasesasACSdevelops.

Usingadogmodel,CaldwellandRicotta21demonstratedadecreasedorganbloodflowindex
(organbloodflow/cardiacoutput)withincreasedIAPinallmajorabdominalorgans,exceptthe
adrenal glands. In a pig model, hepatic arterial, portal venous, and hepatic microcirculatory
bloodflowdecreasedsignificantlywithincreasingIAP 22.Inarabbitmodel,decreasedhepatic
bloodflowresultingfromincreasedIAPwasfoundtoimpairhepaticenergyproductionand
reducethehepaticenergylevel23.
IlealandgastricmucosalbloodflowaredecreasedwithincreasedIAP 2426.Smallboweltissue
oxygenation is decreased in ACS27. Bacterial translocation has been demonstrated in rat
models24,28.Thesestudieshaveidentifiedphysiologicderangements thatoccurwithincreased
IAPwhichmayplayaroleinthedevelopmentofsepsisandsystemicinflammatoryresponse
syndrome(SIRS)inpatientswithACS.
Centralnervoussystem. Inaporcinemodel,Bloomfield etal havedemonstratedsignificant
effects of elevated IAP upon the central nervous system (CNS); elevated IAP resulted in
increasedintracranialpressure(ICP)anddecreasedcerebralperfusionpressure(CPP)2931. The
proposedmechanismisfunctionalobstructionofjugularvenousdrainageduetotheelevated
pleuralpressuresandCVP.DuetotheMonroeKelliedoctrine,thisincreaseinintracranialblood
volumeresultsinelevationoftheICP.Abdominaldecompressionresultedinareturntoward
baselineforICPandanimprovementintheCPP 30.Withthecommonassociationofabdominal
injuryandclosedheadinjury,thisobservation(confimedclinically)isimportant.Decompressive
laparotomyinthispatientresultedinadramaticreductioninICP32.
Eyes.IncreasedIAPhasbeenassociatedwiththeruptureofretinalcapillaries,resultinginthe
sudden onset of decreased central vision (valsalva retinopathy). It has been described in a
numberofsettingsinwhichasuddenincreaseinIAPorintrathoracicpressurehasoccurred.
The retinal hemorrhage usually resolves within days tomonths and nospecific treatment is
necessary33. If a patient with ACS develops visual changes, valsalva retinopathy should be
consideredandanappropriateophthalmicexaminationperformed.
DIAGNOSIS
To diagnose and intervene early in the course of ACS, a high index of suspicion must be
maintained34.Clinically,thesyndromeconsistsoftheassociationofabdominaldistentionwith
increasing peak inspiratory pressures, increased central venous pressure (if the patient is
euvolemic),oliguria,andhypercarbia15,35.
Often,adiagnosisofACSshouldbemadeonthebasisofclinicalsuspicionanddecompressive
laparotomyperformedwithoutattemptsatmeasuringIAP 35.IntheearlyphasesofACS,when
oliguriamaybetheonlysign,measurementofIAPisuseful.MethodsofmeasuringIAPinclude
measurementofbladderpressure,measurementofthegastricpressure,ormeasurementofthe
IAPusingalongfemoralvenouscatheterplacedintheinferiorvenacava36.
As mentioned earlier, an IAP greater than 1525 mmHg has been found to induce renal
dysfunction. Therefore, an IAP greater than 25 mmHg in a postoperative patient with an
adequatebloodvolumeandoliguriaisanindicationfordecompressivelaparotomy1.

MeasurementofIAP.ThemostaccurateandsimplewaytodeterminetheIAPisindirectlyby
measurementofthebladderpressureusingaFoleycatheter.Thebladderpressureisessentially
equivalenttotheIAP.
Tomeasurethebladderpressure,inject50100mlofsterilesalineintotheFoleycatheterviathe
aspirationport;crossclampthesteriletubingoftheurinarydrainagebagjustdistaltotheculture
aspirationport;connecttheendofthedrainagebagtubingtotheindwellingFoleycatheter;
releasetheclampjustenoughtoallowthetubingproximaltotheclamptofillwithfluidfromthe
bladderthenreapplytheclamp;Yconnectapressuretransducertothedrainagebag,viathe
culture aspiration port of the tubing, using a 16gauge needle; determine the IAP from the
transducerusingthetopofthesymphysispubisboneasthezeropointwiththepatientsupine.A
handheldmanometerconnectedtotheFoleycatheterviathecolumnoffluidinthetubingmay
beusedtodeterminethepressure,insteadofatransducer1,10,37.
TREATMENT
IfACSispresentbasedonthemeasuredIAPorclinicalsuspicion,adecompressivelaparotomy
shouldbeperformed.Duringdecompressionoftheabdomen,thefollowingactionsshouldbe
taken to prevent hemodynamic decompensation: restoration of the intravascular volume;
maximization of oxygen delivery; correction of hypothermia; and correction of coagulation
defects15.
Theabdomenmaybeopenedinthesurgicalintensivecareunit(SICU),however,theoperating
roomispreferable.IftheabdomenisopenedintheSICU,theoperatingroommustbeprepared
toacceptthepatientifsurgicallycorrectablebleedingisidentifiedatthetimeofdecompressive
laparotomy35.
Afterdecompression,promptdiuresisoccursandpolyuriaoftendevelops.Peakairwaypressure
decreasesastheabdomenisopened,necessitatingsimultaneousadjustmentsoftheventilator35.
Immediateaystolemayoccuruponopeningtheabdomen.Twopossibleetiologieshavebeen
proposed for this phenomenon. Decompression of the abdomen results in acute, dramatic
decrease in systemic vascular resistance and increase in cardiac output; an acute drop in
bloodpressure results14,15. The second mechanism proposes a reperfusion syndrome from the
releaseofacidandmetabolitesfromreperfusedtissues15,35.Thisreperfusionsyndromemaybe
ameliorated by using a solution containing mannitol and sodium bicarbonate for the initial
volumeresuscitationfollowingdecompressivelaparotomy.A2lsolutionispreparedconsisting
of0.45%normalsalinewith50gofmannitoland50mEqofsodiumbicarbonate33.
After decompressive laparotomy, a temporary abdominal closure is performed, followed by
permanentabdominalclosureatalaterdate.
Temporary abdominal closure. Several methods of temporary abdominal closure may be
utilized.Thefirstdecisiontobemadeiswhethertoclosethefasciawithsyntheticmaterialor
leavethefasciaopen.Thefasciashouldnotbeclosedprimarily;thisisassociatedwithahigh
reoccurrenceofACS.

Ifthefasciaisclosedwithsyntheticmaterial,avarietyofmaterials(absorbable/nonabsorbable;
porous/nonporous)maybeused15.Varioustypesofmeshmaybeused,includingpolyglycolic
acid (Vicryl)35,38, polypropylene (Marlex)5,38, or polytetrafluoroethylene (PTFE) 38. An
absorbable material is preferred. Closure with an artificial burr (Velcrolike) device 15,39,
intravenousfluidbag(Bogotbag)38,40,sterilexraycassettebags38,andSilasticsheets41have
beenused.
Ifthefasciaisleftopenandtheabdomenpacked,theskinmaybeclosedorleftopen.Theskin
may be closed using sutures, towel clips 42,43, Esmarch latex bandage44, or mesh. If mesh is
suturedtotheskin,itiscoveredwithmoist,steriledressingsandanadhesivedrape(Vidrape
orSteriDrape).Suturingthesyntheticmaterialtotheskin,ratherthantothefascia,preserves
thefasciaforlaterdefinitiveclosure.
IfclosureoftheskinalonecausesanincreaseintheIAP,theskinisleftopen.Thebowelis
coveredwithanonadhesive,nonporousmaterial(suchasabowelbagoradhesivedrapefolded
uponitselfsothattheadhesivesidestickstoitself).Theedgesofthenonadhesive,nonporous
material are tucked under the edges of the anterior abdominal wall in order to prevent
eviscerationofthebowel.Next,steriletowelsareplaced,followedbyanadhesivedrape(Vi
drapeorSteriDrape)whichstickstotheabdominalwallandfurtherpreventsevisceration,
desiccationofthebowel,andfluidlossesfromtheopenabdomen.Directapplicationofthe
adhesivedrapetothebowelincreasestheriskofenterocutaneousfistulaandisnotadvised.
Permanentabdominalclosure. Permanentabdominalclosureisperformedafterhypovolemia,
hypothermia,coagulapathy,andacidosishavebeencorrected;whichisusuallythreetofourdays
afterabdominaldecompression15,35.Severalmethodsofabdominalclosurehavebeendescribed.
Primaryclosureofthefasciamaybeperformedoraskingraftmaybeplacedfollowedby
delayedabdominalwallreconstruction.
Aftersignificantmobilizationoffluids,itmaybepossibletoclosethefasciawithoutsignificant
tension. However, a separation of parts technique may be required to reapproximate the
fascia38,45,46.
Ifmeshwasplacedasthetemporaryabdominalclosure(preferablyanabsorbablematerial),the
meshmaybeleftinsitufortwoweeksthencoveredwithpartialthicknessskingraftstothe
underlyinggranulationtissue.Themeshwillusuallybeincorporatedintothegranulationtissue
atthispointintime.
Ifthefasciawasnotclosedandthepatientisleftwithanabdominalwalldefect,abdominalwall
reconstruction may be performed six to twelve months later 15,36. Various methods of
reconstruction have been described, including bilateral medial advancement of the rectus
abdominusmuscleanditsfasciawithorwithoutskinrelaxationincisions 32,38,45,46.Subcutaneous
tissueexpandersfollowedbybilateralmyocutaneousadvancementflapshavealsobeenused 47.
Midline abdominal defects may require flap reconstruction or reconstruction with
nonabsorbablemesh38,48.
PREVENTION

Prevention of the ACS must be the goal of surgeons caring for patients at risk for the
development of this syndrome. In an interesting animal model in which sternotomy and
pleuropericardiotomy were performed , the majority of the systemic effects of abdominal
compartmentsyndromewerepreventableinthesettingofincreasedintraabdominalpressure.
Only depression of the cardiac output persisted 31. Thus, a means for decompression of the
abdominalcompartmentinourpatientscanpreventthesystemicconsequencesinourpatients.
Looseclosureoftheabdomenisthemostdirectmeanstoaccomplishthis.Thefollowingactions
shouldbetakentopreventthedevelopmentofincreasedIAPandACS.Theabdominalfascia
shouldnotbeclosedinpatientswhoarehypothermic,coagulopathic,oronwhomadamage
controllaparotomywasrequired.Theskinshouldusuallybeleftopenaswell.Ongoingnon
surgicalbleedingcanleadtoanincreasedIAPeveninpatientsinwhomthefasciawasleftopen
buttheskinclosed.
Aforcedfascialclosureoftheabdomenshouldbeavoided,suchasinpatientswithmassive
retroperitoneal hematoma, visceral edema, orintraabdominal packs. Hypothermia should be
prevented.Bloodwarmersshouldbeusedforadministrationofbloodproductsandintravenous
fluids.Patientsshouldbeexternallywarmedusingwarminglightsandspecialwarmingblankets.
Theresuscitationareaandoperatingroomshouldbewarm.
Coagulopathy should be corrected by restoration of normal temperature and replacement of
coagulationfactors36.
MORBIDITYANDMORTALITY
Morbidity in patients with ACS is often due to sepsis and multiple organ failure. The
developmentoftheseclinicalconditionsmaybeassociatedwiththesplanchnichypoperfusion
resultingfromincreasedIAP,aspreviouslydiscussed.
HighmortalityratesarefoundinpatientswhodevelopACS;40to62.5%ofpatientswithACS
willdie15,35.Mostpatientssufferlatedeathsresultingfromtheunderlyinginsultandmultiple
organdysfunctionsyndrome.
RESUMEN
Unapresinintrabdominalmayorde25mmHgenunpacienteconoliguriayvolumensaguneo
adecuadoesunaindicacinparaunalaparotomadecompresiva.Ladisfuncinrenalyesplnica
ocurreconunapresinintrabdominalde1015mmHg.Sedebeevitarelcierreforzadodefascia
opielsobreintestinosedematizadosocompresasintrabdominales.Estoamenudovaaevitarel
desarrollo del sndrome de compartimiento abdominal en los pacientes de alto riesgo. Los
cirujanos encargados del manejo de los pacientes con riesgo de desarrollar un sndrome de
compartimientoabdominaldebenconocerelefectosistmicoymultiorgnicodeunapresin
intrabdominalelevada.Loscirujanosquemanejanpacientescontraumamltiple,especialmente
lostraumacombinadodeabdomenycrneo,debenestarenteradosdelosefectosdelapresin
intrabdominalelevadasobreelsistemanerviosocentral.
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