abdominal compartment syndrome

R.Phillip Dellinger,MD,FCCM,Section EditorConcise Definitive Review Abdominal compartment syndrome:A concise clinical reviewGary An,MD;Michael A.West,MD,PhDThere has been an increased awareness of the presence and clinical importance of abdom-inal compartment syndrome(ACS)over the past decade.Whereas this condition was formerly recognized pre-dominately in blunt trauma victims,it is now appreciated that elevations of ab-dominal pressure occur in a wide variety of critically ill patients.Critical care prac-titioners need to be familiar with the signs and symptoms of ACS and under-stand how to treat this increasingly com-mon condition (1).This review provides a current,clinically focused approach to the diagnosis and management of ACS,with a particular emphasis on care in the intensive care unit (ICU).Full-blown abdominal compartment syndrome is a clinical syndrome charac-terized by progressive intra-abdominal organ dysfunction resulting from ele-vated intra-abdominal pressure (IAP).The term abdominal compartment syn-drome was coined by Kron et al.(2)in 1984,when they described the patho-physiology following a ruptured abdomi-nal aortic aneurysm.The classic descrip-tion of ACS included a tense distended abdomen,increased IAP,decreased renal function,elevated peak airway pressure,hypoxia,and inadequate ventilation.Im-provement of all variables was seen after decompressive laparotomy.DefinitionsElevated IAP with progression to ACS has been described in a wide variety of clinical conditions (3–25).A number of authors have promulgated a wide variety of sometimes subtly different definitions and classification schemes (26–28).The World Society of the Abdominal Com-partment Syndrome met in 2004to try to bring order to this chaotic situation via an international consensus conference.The goal was to produce a consensus statement (accessible at )related to the definition,diagnosis,and treatment of ACS (29,30).The con-sensus statement defines intra-abdominal hypertension (IAH)as an IAP Ն12mmHg and ACS as a sustained IAP Ն20mm Hg that is associated with new organ dys-function or failure.The society also de-fined another variable,abdominal perfu-sion pressure (APP),which may be useful in discussing ACS.This value,which is equal to the mean arterial pressure (MAP)minus the IAP (APP ϭMAP ϪIAP)is a measure of the net pressure available for perfusion of intra-abdominal organs (31).Clinicians can think of APP in the same way that cerebral perfusion pressure is used when discussing brain perfusion in the face of intracranial hypertension.Table 1compares the current World So-ciety of the Abdominal Compartment Syndrome grading classification of ele-vated IAP to the previously widely used Burch/Meldrum classification (4,32).The consensus conference also redefined the zero point for pressure measurements (29,30).The updated zero point,the mid-axillary line,is the same reference point used for most other hemodynamic mea-surements in the critically ill.IAP should be measured in reference to this point,expressed in mm Hg,and measured at end-expiration in the complete supine position after ensuring that abdominal muscular contractions are absent.From the Department of Surgery,Feinberg School of Medicine,Northwestern University,Chicago,IL.For information regarding this article,E-mail:mwest@Copyright ©2008by the Society of Critical Care Medicine and Lippincott Williams &Wilkins DOI:10.1097/CCM.0b013e31816929f4Objective:There has been an increased awareness of the presence and clinical importance of abdominal compartment syn-drome.It is now appreciated that elevations of abdominal pres-sure occur in a wide variety of critically ill patients.Full-blown abdominal compartment syndrome is a clinical syndrome char-acterized by progressive intra-abdominal organ dysfunction re-sulting from elevated intra-abdominal pressure.This review pro-vides a current,clinically focused approach to the diagnosis and management of abdominal compartment syndrome,with a par-ticular emphasis on intensive care.Methods:Source data were obtained from a PubMed search of the medical literature,with an emphasis on the time period after 2000.PubMed “related articles”search strategies were likewise employed frequently.Additional information was derived from the Web site of the World Society of the Abdominal Compartment Syndrome ().Summary and Conclusions:The detrimental impact of elevated intra-abdominal pressure,progressing to abdominal compart-ment syndrome,is recognized in both surgical and medical in-tensive care units.The recent international abdominal compart-ment syndrome consensus conference has helped to define,characterize,and raise awareness of abdominal compartment syndrome.Because of the frequency of this condition,routine measurement of intra-abdominal pressure should be performed in high-risk patients in the intensive care unit.Evidence-based interventions can be used to minimize the risk of developing elevated intra-abdominal pressure and to aggressively treat intra-abdominal hypertension when identified.Surgical decompression remains the gold standard for rapid,definitive treatment of fully developed abdominal compartment syndrome,but nonsurgical measures can often effectively affect lesser degrees of intra-abdominal hypertension and abdominal compartment syndrome.(Crit Care Med 2008;36:1304–1310)K EY W ORDS :intra-abdominal hypertension;intra-abdominal pressure;compartment syndrome;massive resuscitation;damage control;decompressive laparotomy;temporary abdominal closureAbdominal compartment syndrome can be classified as either primary ACS (33–35),due to the presence of intra-abdominal and/or retroperitoneal pathol-ogy,or secondary ACS(17,35–37),due to generalized capillary leak with massive fluid resuscitation leading to edema of otherwise normal bowel or development of tense ascites.Examples of primary ACS include those associated with damage control laparotomies for trauma or large retroperitoneal hematomas.Secondary ACS is often seen in the postresuscitation phase for septic shock,hemorrhagic shock,or burn injury.Recurrent ACS re-fers to situations in which ACS redevel-ops after treatment for either primary or secondary ACS(26,33).It is vital to identify and recognize the underlying pathophysiologic conditions, whether primary or secondary(or even tertiary)(38),that produce elevated IAP and that may progress to ACS.In many cases the pathogenesis of ACS is multi-factorial,such as primary ACS following abdominal trauma being exacerbated by secondary ACS resulting from massive fluid resuscitation.IAH and ACS share the same pathophysiology,and the clini-cal distinctions represent points along a continuum.Therefore,when dealing with an individual patient it is critical to iden-tify which pathophysiologic processes are involved in the evolution of IAH/ACS. PathophysiologyThe abdominal compartment is bounded inferiorly by the pelvicfloor,circumfer-entially by the abdominal wall,and supe-riorly by the diaphragm,which separates the abdomen from the thorax.Although the diaphragm anatomically divides the chest and abdomen,the diaphragm is not a rigid barrier to transmission of in-creased pressures within the torso(39), although the tendency is more for intra-abdominal processes to affect intratho-racic measurements than in the other direction.The underlying pathophysiol-ogy of ACS is consistent with the patho-genesis of compartment syndrome inother body regions(40–42).The funda-mental abnormality,increased pressurewithin a(relatively)nonexpandable com-partment,leads to aberrations in thebloodflow of intracompartmental tissues,initially at the microvascular(capillary)level but eventually progressing to affectthe venous return and arterial inflow.In contrast to extremity compart-ment syndromes,the organ dysfunctionfrom sustained IAH usually becomesclinically significant before actual in-tra-abdominal organ infarction(e.g.,bowel necrosis).However,as with ex-tremity compartment syndromes,thereis a threshold of IAH at which the cycleof microvascular derangement becomesself-propagating.This point is reachedwhen elevations in IAP increase venousoutflow resistance,leading to venouscongestion and further increases of in-tracompartmental pressures.At thepoint where IAP is greater thanف20mm Hg,there is a significant reductionin effective perfusion of the capillarybeds,leading to tissue ischemia andactivation of inflammatory mediators.This in turn leads to increased extravas-cularfluid loss via capillary leak,pro-ducing more tissuefluid influx,a fur-ther net increase in intra-abdominalvolume,and additional elevation of IAP,perpetuating the cycle.An additionalcontributing factor in the cycle of IAH/ACS is the impairment of lymphaticflow and subsequent increase in intes-tinal edema(43,44).The systemic and clinical manifesta-tions of ACS are related to the conse-quences of IAH at the organ level.Expan-sion of the abdominal cavity fromelevated IAP results in a cephalad dis-placement of the diaphragm with reduc-tion in dynamic pulmonary complianceand a requirement for increasing positiveairway pressure to deliver the same tidalvolume(45).The cycle of impaired out-flow,decreased capillary perfusion,andincreasing pressure also leads to de-creased hepatosplanchnicflow(withimpaired liver function)(46–48),de-creased renal bloodflow(resulting inlow urine output,progressing from ol-iguria to anuria)(49–51),compressionof the inferior vena cava,and decreasedvenous return to the heart(with result-ant decreased cardiac output,progress-ing to shock)(52).DiagnosisThe diagnosis of ACS can be dividedinto three components:1)identifying pa-tients at risk;2)recognizing the clinicalsigns associated with the transition ofIAH to ACS;and3)proactively carryingout diagnostic measures to confirm thesuspected diagnosis.Elevations in IAP,and even the presence of ACS,may besuspected based on computed tomogra-phy radiographicfindings(53–55).Riskfactors for ICU patients can be seen inTable2.A variety of means of measuringIAP have been reported,such as gastricpressure via a nasogastric tube(56),in-ferior vena cava pressure(57),rectalpressure,direct IAP via direct puncture,or use of bedside ultrasound to assess thecaliber and respiratory variation of theinferior vena cava(58),but measurementof IAP using the bladder is the currentmainstay of diagnosis(59).The currentlyrecommended technique involves instil-lation of25–50mL of sterile saline intothe bladder via a Foley catheter(29,60).The catheter tubing is clamped,and aneedle is inserted via the specimen-collection port proximal to the clamp andattached to a calibrated pressure trans-ducer.Variation in IAP with gentle ab-dominal pressure confirms that there isgoodfidelity of pressure transduction.Toensure accuracy and reproducibility,IAPshould be measured at end-expirationwith the patient completely supine(30).Abdominal muscle contractions shouldbe absent and the transducer is zeroed atthe level of midaxillary line.Modifica-tions of this system allow continuousmeasurement(57,61,62).Patients who are at risk for possibledevelopment of ACS(35,63–66)(Table3)should have baseline measurement of IAPat admission to the ICU.The most com-mon risk factor associated with ACS is ahistory of massivefluid resuscitation,usually with a significant crystalloid com-ponent.In this context,massive is definedasϾ5L of intravenousfluid resuscitationwithin a24-hr period.Experienced clini-cians will quickly recognize that such aTable1.Grading schemes for elevated intra-abdominal pressureGrade WSACS Definition(30),mm Hg a Burch(4)/Meldrum(32)Classification,mm Hg b I12–1510–15II16–2016–25III21–2526–35IVϾ25Ͼ35WSACS,World Society of the Abdominal Compartment Syndrome.a Pressure measured with zero at midaxillary line;b pressure measured with zero at pubic symphysis.definition of massive resuscitation encom-passes a large number of ICU patients,un-derscoring the importance of always con-sidering the possibility of ACS development and proactively assessing IAP.Clinical Signs of ACSThe classic constellation of clinical findings associated with ACS includes in-creased airway pressure,decreased urineoutput,and a tense abdomen on physicalexam(2).Unfortunately,from a practicalstandpoint,these signs and symptoms areextremely nonspecific in critically ill pa-tients.For example,patients undergoinglarge-volumefluid resuscitation fre-quently have impaired tissue perfusion,hypotension,and oliguria.These samepatients are at risk for acute lung injuryor pulmonary edema,either of whichmay result in increased airway pressure(67,68).In many cases the only way todetect ACS is via active monitoring ofIAP.This is especially important for theconditions delineated in Table4.Factorsinvolved in determining the subsequentinterval and duration of IAP monitoringinclude the baseline pressure measure-ment,the ability to alter etiologic andrisk factors,and the dynamic evolution ofthe patient’s course.TreatmentTo a great extent,the best treatmentfor ACS is prevention.Increased recogni-tion regarding the risk factors,setting,and pathogenesis of ACS allows earlieridentification of at-risk patients.This inturn prompts earlier,more aggressivemonitoring of IAP and facilitates the in-stitution of corrective/preventive mea-sures before full-blown ACS develops.Prevention of ACS also involves accuratedetermination of appropriate end pointsof resuscitation(69–74)in order to avoidexcessfluid administration.While thespecific variables used to determine endpoints of resuscitation may always be de-bated,the adage that“if some urine isgood,more urine is better”is clearly ob-solete.Furthermore,development of ACSis just one of the adverse clinical conse-quences of overly vigorousfluid adminis-tration.In the setting of IAH,traditionalmeasures of preload may be insufficientdue to a concomitant increase in in-trathoracic pressure.In these cases,moreprecise measures of ventricular preload,such as those obtained via global end-diastolic volume(obtained via transpul-monary thermodilution)or continuousright ventricular end-diastolic volume,may be used(75,76).Once goal-directedresuscitation end points(i.e.,decrease inlactate,adequate mixed venous oxygensaturation,decrease in base deficit)areachieved,ongoing aggressive resuscita-tion should be stopped just as aggres-sively.Finally,primary ACS can be fore-stalled by the recognition of patients atrisk while still in the operating room.Inhigh-risk patients it may be safest for thesurgeon to use prophylactic measures,such as temporary abdominal closure,toallow the abdominal contents to expandmore freely(77–80).However,when pa-tients return to the ICU with a temporaryabdominal closure,it is still imperativethat the ICU team avoid overresuscita-tion.Monitoring the APP during this pe-riod may provide guidance in determin-ing the trends during resuscitation,and ifit is not possible to maintain an APPϾ60,then additional surgical interventionshould be considered.The definitive treatment for fully man-ifested ACS is surgical decompression viaa laparotomy(1,81–83).When per-formed appropriately,surgical decom-pression is almost always effective,oftenimmediately and dramatically,with rapidresolution of hypotension,oliguria,andelevated airway pressure.Surgical de-compression requires the presence of asurgeon and usually requires general an-esthesia.Numerous reports attest to thefact that surgical decompression can besafely performed at the bedside in the ICU(84,85),an important factor to consider,since many patients with ACS are clini-cally unstable.Surgical decompressionalso involves a surgical stress that mayserve as a second hit with respect to theimmunoinflammatory status of the pa-tient(86,87).Additionally,the rapid res-olution of the hemodynamic conse-quences of ACS may lead to ischemia-reperfusion injury to the visceral organs(88).Successful surgical decompressionof ACS creates another problem:how todeal with the open abdominal wound.The rate of unsuccessful reclosure of theabdomen has been reported between20%and78%(89–91).A substantial numberof these patients represent major chal-lenges with respect to coverage of thebowel,prevention and management of en-terocutaneousfistulas,and management oflarge ventral hernias.Because of these poten-tial consequences to an open abdomen,at-tempts should be made to close the abdomenas soon as the underlying cause of the ACShas been addressed,since the incidence offailed closure and additional complicationsincreases as time passes.This timeframe canbe short but varies greatly from patient topatient,and actual timing depends greatly onthe assessment of the abdomen by the sur-geons involved.While surgical decompression is un-questionably a rapid and definitive treat-ment,given the consequences of this pro-Table2.Intensive care unit conditions that may predispose to intra-abdominal hypertension(29, 35,64–66)Acidosis(arterial pH,Յ7.2)Hypothermia(core temperature,Յ33°C) Polytransfusion(transfusion,Ն10units of PRBCs in24hrs)Coagulopathy(platelets,Յ55,000/mm3;PTT,Ͼ2ϫnormal;or an INR,Ͼ1.5)Sepsis(American-European Consensus Conference definition)Bacteremia(positive blood cultures)Liver dysfunction(cirrhosis with ascites,portal vein thrombosis,ischemic hepatitis)Need for mechanical ventilationUse of PEEP or the presence of auto-PEEP PneumoniaPRBCs,packed red blood cells;PTT,partial thromboplastin time;INR,international normal-ized ratio;PEEP,positive end-expiratory pres-sure.mon etiologic factors for intra-abdominal hypertension(29,33,110,111) Abdominal surgeryMassivefluid resuscitation(Ͼ5L in24hrs) Ileus(paralytic,mechanical,or pseudo-obstructive)Intra-abdominal infection Pneumoperitoneum(can include pneumoperitoneum for laparoscopy) Hemoperitoneummon clinical conditions that war-rant prospective monitoring of intra-abdominal hypertensionPostoperative from abdominal surgeryBlunt or penetrating abdominal traumaPelvic fractures with retroperitoneal bleeding Mechanically ventilated ICU patients with other organ dysfunction(increased SOFA or MOF score)Abdominal packing after temporary abdominal closure for multiple trauma or liver transplantationOpen abdomen(may still develop ACS,especially if early postoperative)Large-volumefluid resuscitation(e.g., pancreatitis,septic shock,trauma)ICU,intensive care unit;SOFA,Sepsis-related Organ Failure Assessment;MOF,multiple organ failure;ACS,abdominal compartment syndrome.cedure there is increasing enthusiasm for nonsurgical treatment options of elevated IAH,IAP,and ACS(Table5).Many of these measures are employed relatively routinely(e.g.,nasogastric decompres-sion and sedation)in critically ill pa-tients.Prokinetic agents,enemas,or placement of a rectal decompression tube will seldom dramatically change IAP and should be used very cautiously in cases where toxic megacolon or inflammatory bowel syndrome is suspected.Likewise, the impact of body positioning should not be underestimated as a potentially con-founding variable.Avoiding acuteflexion at the hips(even though this is counter to the current ICU guideline to maintain a30–45°elevation of the head of the bed) and/or employing reverse Trendelenburg can relieve pressure on the abdomen. Neuromuscular blockade may dramati-cally decrease IAP and can be adminis-tered quickly and safely to intubated ICU patients(28,29,92–96).Even small amounts of tension in the abdominal muscles can have a large impact on IAP, and this component can easily be re-moved with neuromuscular blockade.In many cases,decreases in IAP with neuro-muscular blockade may provide sufficient time for other nonoperative measures, such as removal of excessfluid,to be effective.Excessfluid can and should be aggres-sively removed(by diuretics or ultrafiltra-tion);however,it is absolutely crucial to ensure thatfluid removal does not result in impaired oxygen delivery or systemic or local perfusion.In our practice we often employ invasive hemodynamic monitoring(e.g.,pulmonary artery cath-eter)with continuous measurements of cardiac output and mixed venous oxygen saturation to avoid hypoperfusion and ex-acerbation of shock.If accessible free fluid is present in the abdomen,percuta-neous catheter drainage has been re-ported to be a successful treatment forACS(31,81,97–100).Even with primaryACS there may be moderately large pock-ets of accessiblefluid,and removal ofeven small volumes can significantlylower IAP(100).Bedside ultrasound canbe useful for identifying a safe window forplacing the drainage catheter in the set-ting of abdominal distension and ACS(97).Generally,success with catheterdrainage is early and dramatic.Therefore,if ACS persists after catheter drainage,definitive treatment(i.e.,surgical decom-pression)should not be delayed in thehope that repositioning the drainagecatheter will improve the situation(81).Management of the open abdomenfollowing surgical decompression is anarea of controversy and ongoing re-search.There are many modifications ofthe classic Bogota bag abdominal clo-sure(78,79,101–103);the most impor-tant consideration when performing atemporary abdominal closure is to al-low for additional bowel swelling,thereby avoiding recurrent ACS.WhenACS and elevated IAP have resolved,aneffort to close the abdomen with autog-enous tissue should be made as soon asthe capillary leak and edema have re-solved(34,90,103,104).In this phase,aggressive,deliberate diuresis and/orultrafiltration can be used to removeexcess total body water.While the win-dow of opportunity for primary fascialclosure may vary from patient to pa-tient,in general it isف7days;beyondthis time the development of adhesionsand early granulation tissue often leadsto a“frozen abdomen”that precludesfascial closure.The chances of successcan be further augmented by progres-sive incremental closure or increasedtension of the temporary closure(80,105–107).Additionally,the use of vac-uum-assisted wound devices may aid inclosing the abdomen or at least poten-tially reduce the size of any residualventral hernia(81,89).Cliniciansshould remain vigilant for the possibil-ity of recurrent ACS during these ef-forts.Abdominoplasty,in the form ofcomponent separation and closure,hasalso been reported(80,108,109),al-though these sometimes extensive pro-cedures are usually limited to more sta-ble patients.An excellent review ofissues related to management of theopen abdomen has been recently pub-lished(90).CONCLUSIONSThe detrimental impact of elevatedIAP,progressing to ACS,is recognizedmore frequently in both surgical andmedical ICUs.Because of the frequencyof this condition and the subtle clinicalfindings,routine measurement of IAPshould be performed in all high-riskICU patients.A number of measures canbe employed to minimize the risk ofdeveloping elevated IAP and to aggres-sively treat IAH when identified.Non-surgical measures can effectively treatlesser degrees of IAH and ACS,but sur-gical decompression remains the goldstandard for rapid,definitive treatmentof fully developed ACS.The recent in-ternational ACS consensus conferencehas helped to define,characterize,andraise awareness of this condition.Wehope that this review will assist in un-derstanding and recognizing ACS 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