journal of the american college of surgeons volume 216 issue 1 2013 [doi...

8/10/2019 Journal of the American College of Surgeons Volume 216 issue 1 2013 [doi 10.1016%2Fj.jamcollsurg.2012.09.004]

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Abdominal Compartment Syndrome: A Decadeof Progress

John Alfred Carr, MD, FCCP, FACS

Unlike many disease processes that surgeons treat inwhich progress is slow, the knowledge, denition, diag-nosis, research, and treatment of abdominal compartmentsyndrome (ACS) have undergone dramatic improvementsduring the past decade. Considering that ACS was only well characterized and physiologically dened in the labo-ratory in 1985, and better clinically dened in 1989,rapid progress has occurred in both the diagnosis andtreatment of this relatively young entity.1,2 In fact, themortality rate has dropped from 60% to between 34%and 37% in just the last 10 years.3-5

Abdominal compartment syndrome is dened as a sus-tained intra-abdominal pressure (IAP)> 20 mmHg that isassociated with new onset of organ dysfunction orfailure.6 Although often mistakenly used interchangeably, ACS is a separate and distinct entity from intra-abdominal hypertension (IAH), which is dened as a sus-tained or repeated pathologic elevation of the IAP 12mmHg. 6 Intra-abdominal hypertension does not causeorgan dysfunction, and that is the key difference betweenthe 2 disease processes. Normal or mean IAP withinthe nondiseased abdominal cavity is between 2 and5 mmHg, depending on overall body mass index (BMI), but can run as high as 12 mmHg in the obeseadult7 (Table 1). This chronic IAH does not produceorgan injury and is purely a result of visceral obesity. Itis also important to realize that normal IAP in thecritically ill, who are almost always uid overloaded andedematous, runs slightly higher, at 5 to 7 mmHg.6

Determining intra-abdominal pressureThe standardized method of determining IAP is by measuring the bladder pressure transmitted througha Foley catheter. This is correctly performed by clamping

the catheter tubing beyond the rubber or plastic dia-phragm that allows needle puncture access into the lumenof the catheter, and then instilling a maximum volume of 25 mL saline into the bladder.6 Overdistending thebladder with excessive volumes of uid will increase thebladder pressure and not reect the true IAP.8 The IAPshould be measured at end expiration with the patientsupine and relaxed or sedated, with the transducer zeroedat the mid-axillary line.6 Having the patient slightly upright at > 30 degrees has been clearly shown to produceerroneous results because IAP will increase as the head of the bed is elevated from 10 to 30 to 45 degrees.9

Once the IAP is measured, the abdominal perfusionpressure (APP) can be calculated. The APP is simply the mean arterial pressure minus the IAP. To maintainadequate perfusion to the viscera, an APP of at least60 mmHg is desired.6 For example, a critically ill patientwith a mean arterial blood pressure of 80 mmHg and anIAP of 22 mmHg, has an APP of 58 mmHg, which is justbelow the critical level. This is when end-organ dysfunc-tion can begin to occur.

Primary, secondary, and tertiary abdominalcompartment syndromeThere are 3 different types of ACS: primary, secondary,and tertiary, which is also known as recurrent ACS.Primary ACS refers to ACS that occurs due to a primary intra-abdominal (or intrapelvic) cause, such as a rupturedabdominal aortic aneurysm, abdominal trauma, or retro-peritoneal hemorrhage10 ; these are the most commoncauses. However, other rare conditions, such as malignantascites, a giant ovarian tumor, a rectus sheath hematoma,and ACS after Roux-en-Y gastric bypass, have also beenreported.11-13 Almost any pathology that creates a space-occupying or expanding lesion within the abdominal orpelvic cavity can cause ACS.

Secondary ACS (also known as extra-abdominalcompartment syndrome) refers to ACS that occurs asa result of massive bowel edema secondary to sepsis, capil-lary leak, conditions requiring massive uid resuscitation,or burns.14-16 Secondary ACS occurs most commonly after hemorrhagic shock requiring massive uid resuscita-tion or severe burn injuries requiring massive uid infu-sion. Although these situations result in total body anasarca, it is the swelling of the bowel that limits renal

CME questions for this article available athttp://jacscme.facs.org

Disclosure Information:Authorshavenothing to disclose. TimothyJ Eberlein,Editor-in-Chief, has nothing to disclose.

Received July 13, 2012; Revised August 26, 2012; Accepted September 10,2012.From the Department of Surgery, Hurley Medical Center, Flint, MI.Correspondence address: John Alfred Carr, MD, FCCP, FACS, Depart-ment of Surgery, Hurley Medical Center, One Hurley Plaza, 7th Floor, West Tower, Flint, MI 48503. email: [email protected]

135 2013 by the American College of Surgeons ISSN 1072-7515/12/$36.00Published by Elsevier Inc. http://dx.doi.org/10.1016/j.jamcollsurg.2012.09.004
http://jacscme.facs.org/mailto:[email protected]://dx.doi.org/10.1016/j.jamcollsurg.2012.09.004http://jacscme.facs.org/http://dx.doi.org/10.1016/j.jamcollsurg.2012.09.004mailto:[email protected]



perfusion and ventilation due to increased abdominalpressure. There is also an entity known as recurrent ACS (or tertiary ACS) in which ACS recurs after resolu-tion of an earlier episode of either primary or secondary ACS. Recurrent ACS is relatively uncommon and tendsto be the result of an overly aggressive attempt at abdom-inal closure in an edematous patient with an openabdomen.

Prevalence and pathophysiologyThe prevalence of ACS is difcult to quantify and varieswith the patient population that is studied and the acuity of those patients. In the general medical or surgical pop-ulation, the incidence has been reported to be around0.5% to 8%, but increases to 6% to 14% in trauma patients, depending on the classication of primary,secondary, or both.14,17,18 The incidence is even higherin burn patients, occurring in 1% to 20%, depending on severity and percentage burn.18

The various cascades of molecular and cellular eventsthat ultimately lead to ACS are multifactorial, with exten-sive interplay between the capillary membrane and inter-stitial interface, combined with neutrophil activation andhemodilution. I will now examine some of these modelsat the microvascular level. Regardless of which model isused as the example, the inciting event, whether it betrauma with hemorrhagic shock, sepsis, or burns, alllead to a capillary leak syndrome resulting in the extrav-asation of uid into the interstitium and massive bowel

wall edema. The bowel wall has an enormous capacity to hold uid, and a patient can easily sequester severalliters of uid within the bowel wall and mesentery.This edema leads to increased pressure within the abdom-inal cavity, which ultimately leads to decreased renalperfusion, decreased bowel perfusion, and loss of ventilatory capacity.

A common cause of IAH and ACS is sepsis requiring massive uid resuscitation. Clinical and basic scienceresearch has shown that interleukin-6, interleukin-8,and tumor necrosis factore a all act directly on the endo-thelial cell of the capillary beds within the bowel wall tocontribute to the capillary leak syndrome and bowel walledema.19,20 In addition, when the septic source is locatedwithin the abdomen, such as with appendicitis, the peri-toneal uid itself has been shown to contain elevatedlevels of interleukin-6 and tumor necrosis factore a ,which in turn prime neutrophils and fuel the inamma-tory cascade and capillary leak.21,22 Neutrophil priming refers to an enhanced and overly exaggerated secondary response to injury that occurs after an initial injury orstimulus.23 Priming results in the neutrophil expressing certain adhesion molecules on its surface, specically CD11b and CD18, which allows the neutrophil toadhere to the endothelial cell of the capillary andextravasate into the interstitium.24,25

Central vasodilation and shunting of blood from theperiphery during sepsis result in hypotension, which isusually managed with a combination of uid resuscitationand vasopressors. Vigorous uid resuscitation during a phase of capillary leak alters the normal hydrostaticand oncotic pressures, resulting in the formation of intes-tinal edema because of a net efux of uid into the inter-stitium.26 As the bowel edema worsens and IAP increases,upward pressure on the diaphragm increases centralvenous pressure, creating a pressure gradient againstvenous outow and causing abdominal venous hyperten-sion. The increased IAP also hinders lymphatic efux of uid from the abdomen, which only worsens theprocess.26 All of these factors combining at oncecontribute to the growing edema within the bowel walland mesentery, and IAP continues to increase. The septicpatient who has been aggressively uid resuscitated is atobvious risk for ACS.

Another common cause of IAH and ACS is abdominaltrauma, leading to hemorrhagic shock requiring massiveuid resuscitation. In this model, the initial traumaticevent leads to direct blood loss from vascular damagewithin the abdominal cavity. Whether the patientrequires surgery to control the blood loss or is managednonoperatively, the patient has lost a considerableamount of blood and requires either blood transfusion

Table 1. Grading System for Intra-Abdominal Hypertension

GradeInternal

pressure, mmHg Description

Normal < 12 This accounts for the obese1 12e 152 16e 20 Unusual to have organ dysfunction

in this range3 21e 25 Not equivalent to ACS unless organ

dysfunction occurs4 > 25 With organ dysfunction the

terminology changes to ACS ACS, abdominal compartment syndrome.

Abbreviations and Acronyms

ACS abdominal compartment syndrome APP abdominal perfusion pressureBMI body mass index IAH intra-abdominal hypertension

IAP intra-abdominal pressureICP intracranial pressureRVEDVI right ventricular end diastolic volume index

136 Carr Abdominal Compartment Syndrome J Am Coll Surg



or crystalloid resuscitation to restore their circulating blood volume. Similar to the septic model, a microvas-cular capillary leak syndrome is created in which uidextravasates from the bloodstream and into the intersti-tium of the bowel wall and mesentery creating edema,but the inciting events are different. After trauma, bloodloss followed by resuscitation or transfusion creates anischemia-reperfusion injury to the bowel, which resultsin increased capillary permeability.26 The main mediatorsof these events are interleukin-1, interleukin-6,interleukin-18, monocyte chemoattractant protein 1,and tumor necrosis factore a .27,28 With ongoing uidresuscitation, decreased oncotic pressure from crystalloiduse, and increased capillary permeability due to the medi-ators mentioned previously, all combine to cause a rapidinfusion of uid into the bowel interstitium and createedema leading to increased IAP.

The same holds true for massive uid resuscitationafter burns, but again, the molecular mediators areslightly different. After a large burn, basic science researchhas shown that there are increased systemic levels of vascular endothelial growth factor, interleukin-6, inter-leukin-8, and tumor necrosis factore a .29-31 Aftera burn, it is these systemic up-regulators of the inamma-tory response that create endothelial cell leakage from thecapillary bed and result in a net uid ux into the inter-stitium of the bowel and all the tissues of the body. Forthis reason, plasma exchange, which decreases thesystemic levels of inammatory cytokines in the blood-stream, has benecial effects after a major burn.32 But just as in the other models, the result is a capillary leak syndrome and bowel edema that increases IAP and leadsto IAH.

In summary, regardless of the inciting event, an inam-matory cascade of events and resuscitation leads toincreased hydrostatic pressure, decreased oncotic pressure,ischemia and reperfusion injury, and increased capillary permeability. This leads to interstitial edema, bowelwall edema, and increased IAP, which then leads toincreased central venous pressure, both of which causemesenteric venous hypertension and decreased lymphaticux out of the abdomen.23 The result is progressively swollen and more edematous bowel and IAH or ACS.

Risk factorsIndependent and widely substantiated risk factors fordevelopment of ACS include massive uid resuscitation,multiple transfusions (> 10 U packed RBC 24 hours),hypothermia (core temperature < 33 C), base decit/acidosis (pH < 7.2), and BMI > 306,16-18,33,34 (Table 2).High-volume uid resuscitation sufcient to cause ACShas been dened as > 3,500 mL given in 24 hours.35

However, other authors believe the risk of ACS doesnot increase substantially unless > 5,000 mL are givenwithin 24 hours.6 Abdominal trauma and abdominalsurgery also increase the risk for ACS, but the associationis weaker.33-35 The literature also cites many other risk factors, such as peritonitis, sepsis, burns, and pancreatitis,but these are risk factors for ACS only in that they allrequire uid resuscitation, which is the actual underlying risk factor itself.6

Abdominal compartment syndrome and multipleorgan failureOnce the bowel has become massively swollen and IAP isgreatly increased, organ dysfunction occurs. Comparing trauma patients with similar Injury Severity Scores, theincidence of multi-organ failure in those with andwithout ACS is 32% to 55% vs 8 to 12%, respec-tively.17,36 In addition, in the same cohort of trauma patients, the mortality rate of those with ACS is 43%to 64% vs 12% to 17% in those without ACS.17,36

Renal A well-described presentation in the trauma or septicpatient who has received massive uid resuscitation isa progressively more swollen and tense abdominal wall,followed by decreasing urine output, despite ongoing uid infusion. A bladder pressure measurement showing an IAP> 20 mmHg combined with evidence of decreasedrenal perfusion is diagnostic of ACS. The underlying pathological process that induces renal failure fromincreased IAP is increased renal venous resistance andincreased renal arteriolar resistance, which leads toreduced renal arterial ow and decreased glomerularltration rate. Rabbit, canine, and rodent studies haveall shown that renal blood ow is reduced when IAP isincreased to > 20 mmHg.37-39 Glomerular ltration ratedecreased to < 25% at a pressure of 20 mmHg anddropped to 7% when the pressure was increased to40 mmHg.38 Renal vascular resistance increased> 500%, which was 15 times higher than the systemicvascular resistance.38 Renal dysfunction from increasedIAP is due to direct renal vein compression and corticalarteriolar compression, as conrmed by these animalstudies.37-39 This was later conrmed in a human study

Table 2. Independent Risk Factors for AbdominalCompartment SyndromeMassive crystalloid uid resuscitation (> 5,000 mL in 24 h)Multiple transfusions (> 10 U packed RBC in 24 h)Hypothermia (core temperature < 33 C)Base decit/acidosis (pH < 7.2)

Body mass index (>

30)

Vol. 216, No. 1, January 2013 Carr Abdominal Compartment Syndrome 137



showing a signicantly increased resistive index in therenal arteries as well.40

In addition, the increased renal vascular resistance leadsto up-regulation of antidiuretic hormone, aldosterone,renin, and angiotensin.41-43 This worsens the entireprocess because increased levels of antidiuretic hormoneand aldosterone result in sodium and water retention,which can increase bowel edema, and increased levels of renin and angiotensin increase renal vascular resistanceeven more, and worsen renal perfusion.41-43

Respiratory Increased IAP pushes up directly against the diaphragm,limits total lung capacity, and decreases functionalresidual capacity. It also decreases pulmonary and respira-tory system static compliances and increases airway resis-tance, alveolar-arterial oxygen gradient, and respiratory dead space.44 As the diaphragm is pushed up, compressiveatelectasis of the lower lobes occurs and this impairsoxygenation, increases intrapulmonary shunting, andincreases dead-space perfusion.45 There is also a globalincrease in intrathoracic pressure, which is transmittedto the smaller airways, creating increased airway pres-sures.46-48 This reduces chest wall compliance and degreeof recoil after inspiration, creating hypercarbia and venti-latory failure.46,47 Just like in the abdomen, increasedintrathoracic pressure increases pulmonary vascular resis-tance, which worsens oxygenation.45-48

Some very interesting research in porcine models hasshown that IAH in the face of acute lung injury or acuterespiratory distress syndrome induces and worsenspulmonary edema.49,50 With intra-abdominal pressuresbetween 20 and 30 mmHg for several hours, the extravas-cular lung water content increased considerably, by up to30%.49,50 This is believed to be due to increased intratho-racic pressures impeding pulmonary venous return andincreasing pulmonary vascular resistance.

Much of the recent research has focused on the use of increased PEEP to match and overcome the abdominalpressure. In other words, have the PEEP set to matchthe abdominal pressure pushing up from below to avoidlung compression. Interestingly, high levels of PEEP( 12 mmHg) will increase IAP considerably, in bothpatients with and without IAH.51 A summary of thisresearch shows that with low levels of IAH (< 13mmHg), adding PEEP to match at the same pressurewill counterbalance the effects of IAH and maintainnormal oxygenation and hemodynamics, and preventatelectasis and loss of lung volume.52 However, withrising levels in IAP and ACS, a sufcient amount of PEEP necessary to match this pressure in the 18 to 22mmHg range results in a 26% loss of cardiac output,

decreased total respiratory compliance, decreased chestwall compliance, and did not improve arterial oxygena-tion.53 Attempts at matching the IAP with the PEEP isnot recommended because the excessive pressure createdin the chest has detrimental effects on cardiac outputand increases the risk of barotrauma, without any improvement in oxygenation.53

Cardiac To understand the effects of IAH and ACS on the heart,only 2 main factors need to be kept in mind: a decreasedvenous return and a greatly increased afterload. This isimportant to understand because increasing venousreturn (increasing the central venous pressure) andreducing afterload will restore the cardiac output in thesepatients.

Impairment of venous return from the abdominalcavity to the heart, and specically from the inferiorvena cava, begins to occur with IAPs 15 mmHg.54Once the pressure has reached 20 mmHg, there issubstantial collapse of the mesenteric and renal veins, aswell as the vena cava, which results in a considerabledrop in venous return.55 Ironically, because of theincreased abdominal pressure pushing on the vena cava and pushing upward against the diaphragm andincreasing the intrathoracic pressure as well, the centralvenous pressure will be falsely elevated. Research ina porcine model showed that an IAP of 30 mmHg willarticially increase the central venous pressure by a factorof 4.56 The novice clinician might think the patient iseuvolemic when in fact, because of continued volumeloss into the bowel interstitium, the patient is intravascu-larly volume depleted. This is evidenced by the markedimprovement in blood pressure and overall hemody-namics with intravascular volume expansion.50,57-59

The second factor that decreases cardiac output isthe elevated afterload. The afterload is elevated due toincreased systemic vascular resistance, mostly from theabdominal cavity, and increased intrathoracic pressure.54-58 Increased abdominal pressure has similar physiologicaleffects as to increased end expiratory pressure in the chestcavity. Just as increased PEEP expands the lungs, whichthen constantly apply direct pressure to the mediastinum,so too does the constant direct pressure against the dia-phragm from the swollen viscera. The direct cardiaccompression and increased intrathoracic pressure trans-mitted upward from the abdominal cavity limit ventric-ular compliance and right ventricular end diastolicvolume.51-53 In addition, there is direct compression of the arterioles within the mesentery of the bowel and otherviscera that account for a substantial increase in theafterload.




A situation is created in which there is decreasedvenous return to the heart, direct cardiac compression,and greatly increased afterload. The cardiac output willmarkedly diminish. The central venous pressure will befalsely elevated, although the patient might be volumedepleted and the right ventricle inadequately lled.Therefore, appropriate resuscitation is not guided by central venous pressure or urine output, but rather by the right ventricular end diastolic volume index, whichhas proven itself superior to the pulmonary artery occlu-sion pressure and other indices of resuscitation.60-62

Cerebral There is also a direct, although less obvious, relationshipbetween increased IAP and increased intracranial pressure(ICP). For some time, clinical observations in trauma patients with concomitant head and abdominal injurieshave shown that decompressive laparotomyfor ACSwouldalso unintentionally improve intracranial hypertension inthese patients. A substantial fall in ICP would occur assoon as the abdomen was opened in the operating room.This has been shown in both case reports and retrospectivestudies.63,64 Interestingly, in a single study in trauma patients without ACS (but mean IAP of 27 mmHg, range21 to 35 mmHg), decompressive laparotomy resulted ina rapid drop in the ICP byat least 10mmHgin all patients.In 6 patients, the improvement was transient and all6 died;in the remaining 11 patients with sustained improvementin ICP, all survived and recovered.64

Although clinically this has been shown to be true, basicscience research has not yet provided a clear explanation asto why this occurs. A prospective study performed in ICUpatients showed that increased IAP will increase ICP andhypothesized that this occurs due to increased intrathoracicpressures that create a functional obstruction to cerebralvenous outow.65 Additional research has better denedthe actual pathophysiological connection. Animal modelsin pigs and mice that articially created pneumoperito-neum and increased the IAP to 20 mmHg, resulted inincreased levels of interleukin-6 in the cerebrospinal uidand disrupted the bloode brain barrier.66,67 Anotherporcine model showed that increased IAP will narrow the inferior vena cava at the level of the diaphragm andlimit the drainage from the lumbar venous plexus andcentral nervous system.68 The combination of these eventsis likely the underlying reason that a sudden decrease inIAP, such as seen after a decompressive laparotomy, resultsin a decrease in ICP.

Splanchnic All of the structures within the abdominal cavity are alsocompressed, and this will cause regional hypoperfusion to

all of the organs in the splanchnic bed. This effect mightbe most pronounced in the liver. Animal studies haveshown that even with IAP of only 6 to 10 mmHg, portalvenous blood ow is reduced considerably, and that at20 mmHg, the portal venous ow and hepatic arterialow were reduced by 35% and 55%, respectively.69,70

Decreased blood ow can also be detected in the stomachduring times of IAH using measurements of intramucosalgastric pH.34,71,72 And the intestine itself will also show signs of decreased blood ow, especially in the regionsof the least collateral ow, as shown by elevated levelsof D-lactate and ischemia of the cecal mucosa.73,74

DiagnosisDespite IAH and ACS occurring in a variety of patientsand intensive care settings, 2 surveys among burn andpediatric physicians showed that only 47% couldcorrectly dene ACS, 25% had never measured bladderpressure, and bladder pressure was only measuredroutinely by 31%.75,76 Knowledge of the pathophysiology and a high index of suspicion are necessary to diagnoseIAH before it progresses to ACS.

Most commonly, the patient would be intubated andon mechanical ventilation in the ICU setting. The rareoccasions that IAH occurs in the awake, nonventilatedpatient are usually due to large intra-abdominal tumors,large space-occupying lesions, or ruptured abdominalaortic aneurysms.11,12,77 In addition to the tense abdomenfound on physical examination in these awake patients,continuous reports of difculty breathing due to abdom-inal pressure and lack of diaphragmatic excursion will bea prominent symptom. These patients will also reportobvious abdominal pain and feeling of fullness. They display profound orthopnea, or an inability to lay supinewithout tremendous difculty breathing, and will remainupright at all times to allow gravity to help relieve thepressure from the diaphragm.

Much more often, IAH is diagnosed in the ICU setting when the patient is already critically ill, ventilated, andsedated. The patient will have received substantialamounts of crystalloid infusion for their condition. Thepatient would be total body uid overloaded and edema-tous. Keep in mind that their underlying condition doesnot necessarily have to be of abdominal origin becausesepsis, burns, and hemorrhagic shock can also causeIAH and ACS due to large volume resuscitation.

On physical examination, the abdomen is very tenseand distended. The extremities often show considerableedema. The face and neck are also likely to be swollen,as are the penis and genitalia. Often the physician isalerted to the possibility of IAH after receiving multiplecalls about the ventilator sounding because of high airway




pressures. Additionally, a trend of decreasing urine outputor rising creatinine can signal the impending renal failure.Unfortunately, the sensitivity of the physical examinationto detect high IAP was shown to only be around 40% to60% in 2 separate prospective studies.78,79 Therefore, it isnot the most reliable diagnostic method.

As discussed previously, measuring bladder pressure isconsidered the gold standard and should be done witha maximum volume of 25 mL saline. Overdistending thebladder with excessive volumes of uid (eg, 50 to 100mL) will articially increase the bladder pressure.8 TheIAP should be measured at end expiration with the patientsupine, and relaxed or sedated, with the transducer zeroedat themid-axillary line.6 Having the patient upright at > 30degrees has been clearly shown to produce erroneousresults.9 In addition, a single measurement is not sufcient.Recommendations from an international conference of experts are that if 2 risk factors for IAH or ACS arepresent, a baseline measurement should be obtained andthen serial measurements performed during the patientscritical illness.18 Other experts have recommended thatcontinuous IAP monitoring is the best solution because itallows a more accurate trend to be determined.80

How have we improved?During the last 10 years, there have been 3 major changesin the management of the critically ill, traumatized, andburn patients that have led to a lower incidence andimprovements in the overall mortality rate of ACS.They are adoption of massive transfusion protocols and1:1 blood to plasma transfusion strategies; widespreaduse of damage control and open abdomen approachesto the polytraumatized abdominal cavity; and increaseduse of plasma and colloids in the resuscitation of burnpatients.

It has been clearly proven in both the laboratory and inclinical practice that massive resuscitation with IV crystal-loid solutions causes IAH and ACS.81 The game-changing and now widely adopted use of blood and plasma in a 1:1ratio for resuscitation, with much less reliance on crystal-loid, has dramatically reduced the prevalence of ACS intrauma centers.82-84 In addition, massive transfusionprotocols have allowed resuscitation of the exsanguinating patient to continue for hours with a dramatic reductionin the incidence of anasarca and ACS. 83,84 In fact, resus-citation with a crystalloid to packed RBC ratio of > 1.5:1had a 2-fold higher risk of ACS than for those patientsreceiving less crystalloid compared with blood.82

The same results have been found in resuscitating theburn patient. Several studies have shown that transfusionof colloids or plasma will decrease the overall amount of crystalloid required for resuscitation.85-87 One prospective

study showed that transfusion of plasma to burn patients(> 40% total body surface are) helped to maintain theIAP at< 25 mmHg, and only 1 patient in the group resus-citated with crystalloid maintained an IAP< 25 mmHg.87

And third, by simply not closing the abdominal cavity after laparotomy and using damage control and tempo-rary abdominal closure methods, the incidence of ACShas been additionally reduced.88

ManagementThe presentation and clinical severity of the critically illpatient with IAH or ACS can vary. It is important to deter-mine if and how the presence of increased IAP might ormight not be affecting each patient on an individual basis.Therefore, all guidelines that exist can be modied accord-ing to the presenting clinical scenario. For example,a patient with 30% total body surface area burn and inha-lation injury who is making good clinical progress on hisfourth hospital day, but is found to have a distendedabdomen and a bladder pressure of 18 mmHg, can bemanaged nonoperatively in ways that will be discussedhere later. On the contrary, a patient who is recovering inthe ICU just 8 hours after repair of a ruptured abdominalaortic aneurysm and has peak airway pressures of 50 mmHg, a very tight abdomen, bladder pressure of 35mmHg,andhashadminimal urineoutput sincesurgery,needs urgent decompression. Ultimately, it is importantto realize that although there are recommendations fornonoperative management of these patients, the denitivemanagement is to perform a laparotomy to release the pres-sure and provide a temporary abdominal closure until thedisease process is reversed and the swelling abates. Hesita-tiontoperformsurgerycanleadtodeath,andthemorbidity from a laparotomy in experienced hands is minimal.

A more scientic way to determine if a patient withelevated abdominal pressure but minimal signs of ACSrequires decompression is to measure the APP. Asmentioned previously, the APP is the mean arterial pres-sure minus the IAP. Although never subjected toa prospective trial, an APP of 50 mmHg was shownto improve the chances of survival in a retrospective study of surgical patients.89 Although not validated, mostauthorities now recommend attempting to maintain the APP at a level between 50 and 60 mmHg or higher, if possible, to ensure adequate blood ow to the viscera.18

Before performing a decompressive laparotomy, thenonoperative management of IAH can be divided intothe following steps: sedation and paralysis to relax theabdominal wall, evacuation of intraluminal contents,evacuation of large abdominal uid collections, optimiza-tion of APP, and correct a positive uid balance90

(Table 3).




Sedation/paralytics The rst step in the management of elevated IAP is toensure adequate sedation and, if necessary, paralysis. Anxiety and restless behavior when ghting to breathagainst mechanical ventilation will increase abdominalwall muscular activity and increase IAP.33,35 Completeparalysis will relax the abdominal wall musculature andallow additional expansion of the abdominal domain todecrease the overall IAP. A single prospective study thatexamined the effects of neuromuscular blockade onIAP found that bolus administration of cisatracuriumsignicantly decreased IAP from a mean of 18 mmHg to 14 mmHg (p 0.01) within 15 minutes; however,no change in urinary output or APP occurred.91 Intra-abdominal pressure returned to the baseline level within2 hours in all patients.

Evacuation of intraluminal contents Many critically ill patients will at some point havea gastrointestinal ileus. Gastric, small bowel, and colonicdistension can all increase IAP substantially, and simpleendoluminal decompression is a rapid and effective way to decrease an elevated IAP. Therefore, all patients withelevated IAP should have a nasogastric tube placed.Patients with colonic ileus or acute colonic pseudo-obstruction (eg, Ogilvie syndrome) should undergo eithercolonoscopic decompression or be given neostigmine.92,93

Evacuation of large abdominal uid collections Patients with ascites (eg, burns, liver failure, or malig-nancy) or those recovering from abdominal trauma canhave large collections of uid or blood within the abdom-inal cavity contributing to elevated IAP. In these cases, itis often the presence of the uid rather than swollenbowel from resuscitation that causes IAH. It wouldmake sense that simply draining the uid would alleviatethe problem. Percutaneous drainage of the uid in thesesituations has shown great success in burn and oncology patients, avoiding the need for a decompressive lapa-rotomy.94-96 However, immediate success must betempered by the fact that recurrent ACS is always possibleas the uid re-accumulates, and so continued surveillanceis necessary. One study using percutaneous drainage totreat elevated IAP in burn patients found that 44% of

the patients eventually required a decompressive lapa-rotomy.94 Unfortunately, in the trauma patient with liveror spleen injuries, the blood will quickly loculate andaggregate into pockets, which can make percutaneousdrainage difcult. In addition, ACS that develops in thetrauma patient is much more commonly due to swollenbowel from massive uid resuscitation rather than freeuid. One multi-institutional study of traumatic liverinjuries found percutaneous drainage to be effective ina small minority of the total patients.97

Optimize abdominal perfusion pressure Because IAP from swollen viscera can be relatively constant, to increase APP the mean blood pressuremust be elevated. This can be done with uid infusion.Because the central venous pressure will likely be arti-cially elevated, the right ventricular end diastolic volumeindex (RVEDVI) should be used to guide resuscitation torst ensure that the patient is euvolemic and not under-resuscitated.60-62 Random boluses or uid challengesshould be discouraged because a transient increase inblood pressure will do nothing to ameliorate the under-lying problem, and excessive uid infusion will worsenthe edema of the bowel. Multiple reports have docu-mented that excessive crystalloid resuscitation worsensIAH and ACS and can cause secondary ACS.16,73,98,99

Urine output will also be an unreliable marker of resusci-tation because the venous and arteriolar compressionwithin the renal cortex will limit urine production.100,101

The more goal-directed measures are necessary to guideresuscitation without committing over-resuscitation andworsening the bowel edema. The target for the RVEDIis debatable, but uid infusion that allows continuedincrease up to the plateau point is the goal. In other words,continue uid infusion until the right ventricle is full.Good research in this area has shown that although theoptimal right ventricular volume for each individualperson will vary and be dependent on ejection fractionand contractility, a volume < 90 mL/m2 is associatedwith a high response rate to uid administration.102

Most patients will continue to be responsive to uid infu-sion up to 130 mL/m2 .103 Other helpful measures thatsupport the RVEDVI are the base decit and lactate levels,which remain good end points to guide resuscitation.

With this in mind, uid is then given to optimize theRVEDVI and base decit and lactate are normalized.Ideally, the mean blood pressure would also rise andimprove the APP. Once the RVEDVI is optimized, addi-tional uid infusion will not be helpful and will only worsen the bowel edema. At this point, it would begood to note that one prospective, randomized study did show that colloid-based resuscitative strategies were

Table 3. Nonoperative Management of Abdominal Compart-ment SyndromeSedation and paralysis to relax the abdominal wallEvacuation of intraluminal contentsEvacuation of large abdominal uid collectionsOptimize abdominal perfusion pressure

Correct a positive uid balance




associated with a decreased incidence of ACS in burnpatients, mostly due to decreasing the total volume of uid required.86 It is a good strategy to switch to colloidinfusion for ongoing uid requirements after theRVEDVI is optimized. Another option is to use hyper-tonic crystalloid resuscitation, which, in one study, wasassociated with a substantially decreased uid require-ment and higher APP.104

Correct a positive uid balance In direct contradistinction to the previous discussion, theclinician will sometimes nd him- or herself faced witha patient who has already been grossly over-resuscitatedand not only has ACS, but also congestive heart failureand total body uid overload. In these cases, it has usually been overly aggressive resuscitation in the operating roomfor exsanguinating extra-abdominal trauma that leads toa patient succumbing to iatrogenic ACS several hourslater. In fact, several studies have shown that the under-lying events that lead to ACS might more likely be thephysician-ordered uid resuscitation rather than the trau-matic event itself.98,99,105 In these cases, the extra uidneeds to be removed without creating a situation of hypo-tension, hypoperfusion, or acidosis. Although the idea of a gentle diuresis is appealing, the reality of removing thealready third-spaced uid from the interstitium withoutcausing intravascular volume depletion and hypotensionis almost impossible in the short term, especially if thepatient shows any signs of hemodynamic instability.This difculty is compounded by the ACS-induced renalcompression and oliguria. Although diuretics can beattempted, success is unlikely. Therefore, the early institu-tion of renal replacement therapy with uid removal by continuous hemoltration or ultraltration is the mostappropriate therapy in these cases.106,107

Decompressive laparotomy Although there is a role for the nonoperative strategies just mentioned, mostly in the stable or minimally symp-tomatic patient, the denitive therapy to treat ACS isa decompressive laparotomy. This is unarguably the fast-est and most effective way to reduce elevated IAP. Onestudy that analyzed 250 patients with ACS found thatthe mean IAP changed from 35 mmHg to 16 mmHg (p < 0.001) after surgical decompression.108 Delays inperforming laparotomy are associated with excessivemorbidity and mortality rates up to 88%.92,108 The symp-tomatic patient with signs of organ distress or failureshould not be treated with nonoperative techniques.

The goals of a decompressive laparotomy are 5-fold:decrease the elevated IAP to stop organ dysfunction; allow room for continued expansion of the abdominal viscera

during ongoing resuscitation; provide temporary abdom-inal coverage/closure as the disease process resolves;prevent excessive fascial retraction, which makes subse-quent denitive abdominal closure much more difcult;and allow a means for continued evacuation of uidfrom the abdominal cavity (Table 4). No techniquecurrently in use is ideal to accomplish all of these goals,but several different techniques have been developed. Itis beyond the scope of this article to describe all of thecurrent techniques for temporary abdominal closure,but I will describe the important steps briey.

Regardless of the exact technique used, the main pointsare to perform a complete fasciotomy of the linea alba toallow evisceration, separate the underlying viscera fromthe abdominal wall with an impermeable drape/barrieror bowel bag, prevent excessive fascial retraction by suturing a prosthetic material to the fascia (or using a vacuum sponge or elastic/silicone elastomer bands),and allow ongoing evacuation of uid from the abdom-inal cavity using drains or a vacuum sponge. The rstpoint, to perform a complete fasciotomy, is very impor-tant because the degree to which the IAP decreases isa function of the degree to which the fascia is released.Interestingly, in most patients after a decompressivelaparotomy the IAP is reduced but not normalized, andcan remain high for some time after surgery.108 Inaddition, the recuperation of organ dysfunction is notimmediate and persistent organ failure can occur despitedecompression, which ultimately leads to death.108,109 Thesecond step is also crucial because the bowels will adhereand stick to the cut fascial edge within 72 hours. Afterthis time, sharply dissecting the bowel from the fascialedge is technically very difcult and places the patientat extremely high risk for enterocutaneous stula if an

Table 4. Critical Goals and Steps in Performing a Decom-pressive Laparotomy Goals

Decrease the elevated intra-abdominal pressure to stop the organdysfunction

Allow room for continued expansion of the viscera during

ongoing resuscitationProvide temporary abdominal closurePrevent excessive fascial retraction Allow a means for continued evacuation of uid from the

abdominal cavity Steps

Perform a complete fasciotomy of the linea alba to allow evisceration

Separate the underlying viscera from the abdominal wall with animpermeable drape/barrier

Suture a prosthetic mesh, vacuum sponge, or silicone elastomerto the fascia to prevent fascial retraction

Place drains or a vacuum sponge to allow ongoing removal of uid from the abdominal cavity




inadvertent enterotomy occurs. Keeping the bowels off of the fascia is critical to allow a delayed abdominal wallclosure. For this same reason, some type of preventativemeasure to keep the fascia from retracting too far laterally is necessary. Suturing mesh to the cut edge, using a vacuum sponge, silicone elastomer sheeting, or siliconeelastomer bands, all are effective.110 Finally, because theedematous bowel will continue to weep and theongoing production of peritoneal uid will continue tocollect within the abdominal cavity, a means of evacua-tion with drains or vacuum sponges is necessary, other-wise, the uid will become trapped under theimpermeable bowel drape and recurrent ACS can occur.

CONCLUSIONS Abdominal compartment syndrome is a life-threatening but treatable disease that requires good clinical skills to

diagnose and manage effectively. A high index of suspi-cion is necessary and measurements of bladder pressureshould be performed in all high-risk patients so that effec-tive intervention can be performed rapidly. Althoughnonoperative interventions have a role in the stable andminimally symptomatic patient, these techniques shouldnot be used as a surrogate for or delay a decompressivelaparotomy, which is the treatment of choice. During the last 10 years, there have been substantial improve-ments in our understanding and ability to treat ACS.The adoption of massive transfusion protocols and 1:1blood to plasma transfusion strategies in trauma, as well

as increased use of plasma and colloids for resuscitationin burn patients, has reduced the prevalence of thisdisease. In addition, the widespread use of damagecontrol and open abdomen techniques has resulted in a dramatic reduction in the mortality rate for these criti-cally ill patients. May this progress continue.

REFERENCES

1. Barnes GE, Laine GA, Giam PY, et al. Cardiovascularresponses to elevation of intra-abdominal hydrostaticpressure. Am J Physiol 1985;248:R208e R213.

2. Fietsam R Jr, Villalba M, Glover JL, Clark K. Intra-abdom-inal compartment syndrome as a complication of rupturedabdominal aortic aneurysm repair. Am Surg 1989;55:396e 402.

3. Hobson KG, Young KM, Ciraulo A, et al. Release of abdominal compartment syndrome improves survival inpatients with burn injury. J Trauma 2002;53:1129e 1133.

4. Parsak CK, Seydaoglu G, Sakman G, et al. Abdominalcompartment syndrome: current problems and new strate-gies. World J Surg 2008;32:13e 19.

5. De Waele J, Desender L, De Laet I, et al. Abdominal decom-pression for abdominal compartment syndrome in critically ill patients: a retrospective study. Acta Clin Belg 2010;65:399e 403.

6. Malbrain ML,CheathamML,Kirkpatrick A, et al.Resultsfromthe international conference of experts on intra-abdominalhypertension and abdominal compartment syndrome. I.Denitions. Intensive Care Med 2006;32:1722e 1732.

7. Lambert DM, Marceau S, Forse RA. Intra-abdominal pres-sure in the morbidly obese. Obes Surg 2005;15:1225e 1232.

8. Gudmundsson FF, Viste A, Gislason H, et al. Comparison of different methods for measuring intra-abdominal pressure.Intensive Care Med 2002;28:509e 514.

9. Yi M, Leng Y, Bai Y, et al. The evaluation of the effect of body positioning on intra-abdominal pressure measurementand the effect of intra-abdominal pressure at different body positioning on organ function and prognosis in critically illpatients. J Crit Care 2012;27:222.e1e 222.e6.

10. Leppaniemi A, Kirkpatrick AW, Salazar A, et al. Miscella-neous conditions and abdominal compartment syndrome.In: Ivatury R, Cheatham M, Malbrain M, Sugrue M, eds. Abdominal Compartment Syndrome. Austin, TX: LandesBioscience; 2006:195e 214.

11. Merlicco D, Roggia G, Lombardi M, et al. Abdominalcompartment syndrome due to a giant multilobulated ovarian

serous cystadenoma. Case report and review of the literature. Ann Ital Chir 2012 [Epub ahead of print].12. Jafferbhoy SF, Rustum Q, Shiwani MH. Abdominal compart-

ment syndromed a fatal complication from a rectus sheathhaematoma. BMJ Case Rep 2012 Apr 2. pii: bcr1220115332.http://dx.doi.org/10.1136/bcr.12.2011.5332 .

13. Huang CK, Goel R, Chang PC. Abdominal compartmentsyndrome after laparoscopic Roux-en-Y gastric bypass: a casereport. Surg Obes Relat Dis 2012 [Epub ahead of print].

14. Maxwell RA, Fabian TC, Croce MA, et al. Secondary abdominal compartment syndrome: an underappreciatedmanifestation of severe hemorrhagic shock. J Trauma 1999;47:995e 999.

15. Bif WL, Moore EE, Burch JM, et al. Secondary abdominalcompartment syndrome is a highly lethal event. Am J Surg 2001;182:645e 648.

16. Balogh Z, McKinley BA, Cocanour CS, et al. Secondary abdominal compartment syndrome is an elusive early compli-cation of traumatic shock resuscitation. Am J Surg 2002;184:538e 543.

17. Balogh Z, McKinley BA, Holcomb JB, et al. Both primary and secondary abdominal compartment syndrome can bepredicted early and are harbingers of multiple organ failure. J Trauma 2003;54:848e 859.

18. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Resultsfrom the international conference of experts onintra-abdominal hypertension and abdominal compartmentsyndrome. II. Recommendations. Intensive Care Med 2007;33:951e 962.

19. Hack CE, Hart M, van Schijndel RJ. Interleukin-8 in sepsis:relation to shock and inammatory mediators. Infect Immun1992;60:2835e 2842.

20. Chen J, Ren J, Zhang W, et al. Open versus closed abdomentreatment on liver function in rats with sepsis and abdominalcompartment syndrome. J Trauma 2011;71:1319e 1325.

21. Shah SK,JimenezF, WalkerPA, et al.Peritonealuid: a poten-tial mechanismof systemic neutrophilpriming in experimentalintra-abdominal sepsis. Am J Surg 2012;203:211e 216.

22. Schietroma M, Piccione F, Carlei F, et al. Peritonitis fromperforated appendicitis: stress response after laparoscopic oropen treatment. Am Surg 2012;78:582e 590.

http://dx.doi.org/10.1136/bcr.12.2011.5332http://dx.doi.org/10.1136/bcr.12.2011.5332


http:///reader/full/journal-of-the-american-college-of-surgeons-volume-216-issue-1-2013-doi-1010162fjjamcollsur 10/12

23. Al-Mufarrej F, Abell LM, Chawla LS. Understanding intra-abdominal hypertension: from bench to bedside. J IntensiveCare Med 2010;27:145e 160.

24. Condliffe AM, Chilvers ER, Haslett C, et al. Priming differ-entially regulates neutrophil adhesion molecule expression/function. Immunology 1996;89:105e 111.

25. Bif WL, Moore EE, Zallen G, et al. Neutrophils are primedfor cytotoxicity and resist apoptosis in injured patients at risk for multiple organ failure. Surgery 1999;126:198e 202.

26. Shah SK, Jimenez F, Letourneau PA, et al. Strategies formodulating the inammatory response after decompressionfrom abdominal compartment syndrome. Scand J Trauma Resusc Emerg Med 2012;20:25e 36.

27. Willoughby L, Dark P, Warhurst G. Investigation of systemicand mesenteric inammatory signaling and gut-derived endo-thelial toxicity in patients undergoing high-risk abdominalaortic surgery. Shock 2011;36:121e 127.

28. Victoni T, Coelho FR, Soares AL, et al. Local and remotetissue injury upon intestinal ischemia and reperfusiondependson the TLR/MyD88 signaling pathway. Med MicrobiolImmunol 2010;199:35e 42.

29. Infanger M, Schmidt O, Kossmehl P, et al. Vascular endothe-lial growth factor serum level is strongly enhanced afterburninjury and correlated with local and general tissueedema. Burns 2004;30:305e 311.

30. Csontos C, Rezman B, Foldi V, et al. Effect of N-acetylcys-teine treatment on oxidative stress and inammation aftersevere burn. Burns 2012;38:428e 437.

31. Boehm J, Fischer K, Bohnert M. Putative role of TNF-alpha,interleukin-8 and ICAM-1 as indicators of an early inam-matory reaction after burn: a morphological and immunohis-tochemical study of lung tissue of re victims. J Clin Pathol2010;63:967e 971.

32. Klein MB, Edwards JA, Kramer CB, et al. The benecialeffects of plasma exchange after severe burn injury. J BurnCare Res 2009;30:243e 248.

33. Malbrain ML, Chiumello D, Pelosi P, et al. Prevalence of intra-abdominal hypertension in critically ill patients: a multi-center epidemiological study. Intensive Care Med 2004;30:822e 829.

34. Ivatury RR, Porter JM, Simon RJ, et al. Intra-abdominalhypertension after life-threatening penetrating abdominaltrauma: prophylaxis, incidence, and clinical relevance togastric mucosal pH and abdominal compartment syndrome. J Trauma 1998;44:1016e 1021.

35. Malbrain ML, Chiumello D, Pelosi P, et al. Incidence andprognosis of intra-abdominal hypertension in a mixed popu-lation of critically ill patients: a multiple-center epidemiolog-ical study. Crit Care Med 2005;33:315e 322.

36. Raeburn CD, Moore EE, Bif WL, et al. The abdominalcompartment syndrome is a morbid complication of post-injury damage control surgery. Am J Surg 2001;182:542e 546.

37. Guler C, Sade M, Kirkali Z. Renal effects of carbon dioxideinsufation in rabbit pneumoretroperitoneum model. J Endourol 1998;12:367e 370.

38. Harman PK, Kron IL, McLachlan HD, et al. Elevated intra-abdominal pressure and renal function. Ann Surg 1982;196:594e 597.

39. Kirsch AJ, Hensle TW, Chang DT, et al. Renal effects of CO2 insufation: oliguria and acute renal dysfunction ina rat pneumoperitoneum model. Urology 1994;43:453e 459.

40. Cavaliere F, Cina A, Biasucci D, et al. Sonographic assess-ment of abdominal vein dimensional and hemodynamicchanges induced in human volunteers by a model of abdom-inal hypertension. Crit Care Med 2011;39:344e 348.

41. Bloomeld GL, Blocher CR, Fakhry IF, et al. Elevatedintra-abdominal pressure increases plasma renin activity andaldosterone levels. J Trauma 1997;42:997e 1004.

42. Hazebroek EJ, de Vos tot Nederveen Cappel, Gommers D,et al. Antidiuretic hormone release during laparoscopic donornephrectomy. Arch Surg 2002;137:600e 604.

43. Le RD, Bark H, Nyska M, et al. The effect of abdominalpressure on plasma antidiuretic hormone levels in the dog. J Surg Res 1982;32:65e 69.

44. da Silva Almeida JR, Machado FS, Schettino GP, et al.Cardiopulmonary effects of matching positive end-expiratory pressuretoabdominalpressurein concomitantabdominalhyper-tension and acute lung injury. J Trauma 2010;69:375e 383.

45. Mutoh T, Lamm WJ, Embree LJ, et al. Abdominal disten-sion alters regional pleural pressures and chest wall mechanicsin pigs in vivo. J Appl Physiol 1991;70:2611e 2618.

46. Hering R, Wrigge H, Vorwerk R, et al. The effects of prone

positioning on intraabdominal pressure and cardiovascularand renal function in patients with acute lung injury. Anesth Analg 2001;92:1226e 1231.

47. Simon RJ, Friedlander MH, Ivatury RR, et al. Hemorrhagelowers the threshold for intra-abdominal hypertension-inducedpulmonary dysfunction. J Trauma 1997;42:398e 403.

48. Kubiak BD, Gatto LA, Jimenez EJ, et al. Plateau andtranspulmonary pressure with elevated intra-abdominalpressure or atelectasis. J Surg Res 2010;159:e17e e24.

49. Quintel M, Pelosi P, Caironi P, et al. An increase of abdominalpressure increasespulmonaryedemain oleicacid-induced lung injury. Am J Respir Crit Care Med 2004;169:534e 541.

50. Schachtrupp A, Lawong G, Afy M, et al. Fluid resuscitationpreserves cardiac output but cannot prevent organ damage ina porcine model during 24 h of intra-abdominal hyperten-sion. Shock 2005;24:153e 158.

51. Verzilli D, Constantin JM, Sebbane M, et al. Positiveend-expiratory pressure affects the value of intra-abdominalpressure in acute lung injury/acute respiratory distresssyndrome patients: a pilot study. Crit Care 2010;14:R137.

52. Runck H, Schumann S, Tacke S, et al. Effects of intra-abdominal pressure on respiratory system mechanics inmechanically ventilated rats. Respir Physiol Neurobiol 2012;180:204e 210.

53. Regli A, Chakera J, De Keulenaer Bl, et al. Matching positiveend-expiratory pressure to intra-abdominal pressure preventsend-expiratory lung volume decline in a pig model of intra-abdominal hypertension. Crit Care Med 2012;40:1879e 1886.

54. Kashtan J, Green JF, Parsons EQ, et al. Hemodynamiceffect of increased abdominal pressure. J Surg Res 1981;30:249e 255.

55. Mahjoub Y, Lorne E, Maizel J, et al. Effect of intra-abdominalhypertension on left ventricular relaxation: a preliminary animal study. Br J Anaesth 2012;108:211e 215.

56. Schachtrupp A, Graf J, Tons C, et al. Intravascular volumedepletion in a 24-hour porcine model of intra-abdominalhypertension. J Trauma 2003;55:734e 740.

57. Jacques D, Bendjelid K, Duperret S, et al. Pulse pressurevariation and stroke volume variation during increasedintra-abdominal pressure: an experimental study. Crit Care2011;15:R33.




94. Latenser BA, Kowal-Vern A, Kimball D, et al. A pilotstudy comparing percutaneous decompression with decom-pressive laparotomy for acute abdominal compartmentsyndrome in thermal injury. J Burn Care Rehabil 2002;23:190e 195.

95. Parra MW, Al-Khayat H, Smith HG, Cheatham ML. Para-centesis for resuscitation-induced abdominal compartmentsyndrome: an alternative to decompressive laparotomy inthe burn patient. J Trauma 2006;60:1119e 1121.

96. Gotlieb WH, Feldman B, Feldman-Moran O, et al. Intraper-itoneal pressures and clinical parameters of total paracentesisfor palliation of symptomatic ascites in ovarian cancer.Gynecol Oncol 1998;71:381e 385.

97. Kozar RA, Moore FA, Cothren CC, et al. Risk factors forhepatic morbidity following nonoperative management:multicenter study. Arch Surg 2006;141:451e 458.

98. Madigan MC, Kemp CD, Johnson JC, Cotton BA.Secondary abdominal compartment syndrome after severeextremity injury: are early, aggressive uid resuscitation strat-egies to blame? J Trauma 2008;64:280e 285.

99. Rodas EB, Malhotra AK, Chhitwal R, et al. Hyperacute

abdominal compartment syndrome: an unrecognizedcomplication of massive intraoperative resuscitation forextra-abdominal injuries. Am Surg 2005;71:977e 981.

100. Sugrue M, Buist MD, Hourihan F, et al. Prospective study of intra-abdominal hypertension and renal function afterlaparotomy. Br J Surg 1995;82:235e 238.

101. Sugrue M, Jones F, Deane SA, et al. Intra-abdominal hyper-tension is an independent cause of post-operative renalimpairment. Arch Surg 1999;134:1082e 1085.

102. Diebel LN, Wilson RF, Tagett MG, Kline RA. End-diastolicvolume. A better indicator of preload in the critically ill. ArchSurg 1992;127:817e 821.

103. Wagner JG, Leatherman JW. Right ventricular end-diastolicvolume as a predictor of the hemodynamic response to a uidchallenge. Chest 1998;113:1048e 1054.

104. Oda J, Ueyama M, Yamashita K, et al. Hypertonic lactatedsaline resuscitation reduces the risk of abdominal compart-ment syndrome in severely burned patients. J Trauma 2006;60:64e 71.

105. Balogh Z, McKinley BA, Cocanour CS, et al. Supranormaltrauma resuscitation causes more cases of abdominalcompartment syndrome. Arch Surg 2003;138:637e 642.

106. Kula R, Szturz P, Sklienka P, et al. A role for negative uidbalance in septic patients with abdominal compartmentsyndrome? Intensive Care Med 2004;30:2138e 2139.

107. Oda S, Hirasawa H, Shiga H, et al. Management of intra-abdominalhypertension in patients withsevereacute pancreatitiswith continuous hemodialtration using a polymethyl methac-rylate membranehemolter.Ther ApherDial2005;9:355e 961.

108. De Waele JJ, Hoste EA, Malbrain ML. Decompressive lapa-

rotomy for abdominal compartment syndrome: a criticalanalysis. Crit Care 2006;10:R51.109. Hershberger RC, Hunt JL, Arnoldo BD, Purdue GF.

Abdominal compartment syndrome in the severely burnedpatient. J Burn Care Res 2007;28:708e 714.

110. Foy HM, Nathens AB, Maser B, et al. Reinforced siliconeelastomer sheeting, an improved method of temporary abdominal closure in damage control laparotomy. Am JSurg 2003;185:498e 501.


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