doi:10.1136/pgmj.2007.064212 2008;84;293-298 Postgrad. Med. J.

  J D Hunter  

and mortality in the critically illunder-diagnosed contributory factor to morbidity Abdominal compartment syndrome: an

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Abdominal compartment syndrome: an under-diagnosed contributory factor to morbidity andmortality in the critically ill

J D Hunter

Department of Anaesthetics andIntensive Care, MacclesfieldDistrict General Hospital,Macclesfield, UK

Correspondence to:Dr J D Hunter, Department ofAnaesthetics and Intensive Care,Macclesfield District GeneralHospital, Victoria Road,Macclesfield SK10 3BL, UK;jdhunter@talk21.com

Received 23 August 2007Accepted 5 May 2008

ABSTRACTAs the abdomen is a closed cavity, it follows that anyincrease in abdominal contents will inexorably lead to arise in the intra-abdominal pressure. Normally this is lessthan 7 mm Hg, but when it persistently exceeds12 mm Hg, renal, intestinal, pulmonary, cardiovascularand central nervous system dysfunction arises. A widerange of conditions encountered in both medical andsurgical intensive care units are associated with a rise inintra-abdominal pressure. When this pressure is con-tinually above 20 mm Hg, organ system failure can occur,a condition known as abdominal compartment syndrome.Failure to recognise and treat this syndrome is associatedwith a high morbidity and mortality.

Many critically ill patients will have an increase intheir intra-abdominal pressure (IAP). This is thepressure concealed within the abdominal cavityand is determined by abdominal wall compliance,the volume of the abdominal organs and theintracompartment fluid load. Normal IAP at restis ,6.5 mm Hg, although it varies with respirationand rises with increasing body mass index.1 Intra-abdominal hypertension (IAH) is defined as asustained or repeated pathological increase in IAP>12 mm Hg.2

The term ‘‘abdominal compartment syndrome’’(ACS) was first coined by Fietsam and colleagues3

to describe the adverse physiological effects causedby massive interstitial and retroperitoneal swellingafter emergency repair of ruptured abdominalaortic aneurysm. ACS has subsequently beendefined as a sustained IAP >20 mm Hg that isassociated with new organ dysfunction or failure.2

It is characterised by a tense distended abdomen,high airway pressures, hypoxia, hypercarbia, meta-bolic acidosis and oliguria. ACS can be primary,secondary or recurrent.2 Primary ACS refers to acondition associated with injury or disease in theabdominopelvic region (box 1). Secondary ACSdevelops secondary to disease processes outwiththe abdominopelvic region, the management ofwhich requires massive fluid resuscitation (eg,septic shock, severe burns). The inflammatoryresponse associated with these conditions causescapillary leak, predisposing to bowel oedema andascites.4–8 Recurrent ACS refers to the redevelop-ment of ACS after previous surgical or medicaltreatment of primary or secondary ACS.

Until recently, IAH and ACS have been under-appreciated.9–16 The prevalence and incidence isobviously influenced by the case mix of thepopulation studied, but a recent multicentre study

of 265 consecutive patients admitted to mixedintensive care units reported that 32.1% of thepopulation had IAH and 4.2% had ACS.17 To raiseawareness of this entity, the World Society of theAbdominal Compartment Syndrome (http://www.wsacs.org) was formed in 2004.

Previously, many clinicians believed that IAHand ACS only occurred in the trauma patient.However, it is increasingly recognised that IAHand ACS can develop in critically ill patientssuffering from a wide range of both surgical andmedical conditions.18 Detection requires a highindex of suspicion and accurate measurement ofthe IAP. All critically ill patients admitted to theintensive care unit should be screened for possiblerisk factors for the development of IAH, and, if oneor more risk factors is present, a baseline measure-ment should be obtained.19 Failure to recognise andtreat IAH appropriately and in a timely mannerwill result in multiorgan failure and death.

The purpose of this review is to raise awarenessof the deleterious effects that a sustained rise inIAP has on organ function and to encourage thoseinvolved in the management of the critically ill tomonitor IAP routinely in patients with risk factorsfor the development of IAH. On the basis of thecurrent best evidence and expert opinion, recom-mendations are made for the management of IAHand ACS.

DETECTION, DIAGNOSIS AND MEASUREMENT OFIAP AND IAHRaised IAP is difficult to detect, as physicalexamination lacks sensitivity in the detection ofIAH.8 20–22 Diagnosis of IAH/ACS therefore requiresaccurate and regular measurement of IAP in thosethought to be at risk (box 2).5 8 19–23

If two or more risk factors for IAH/ACS arepresent, a baseline IAP measurement should beobtained. IAP .12 mm Hg should prompt theserial measurement of IAP throughout thepatient’s critical illness.19

Measurement of IAPAs there is poor correlation between IAP andabdominal perimeter (R2 = 0.12, p = 0.04), clini-cally significant IAH may be present withoutobvious abdominal distension.8 20 22 Detection ofIAH therefore requires accurate measurement ofIAP. Although it can be measured directly with anintraperitoneal catheter attached to a transducer,indirect methods are preferred and include rectal,uterine, inferior vena caval, gastric and urinarybladder pressure measurement.24 Regardless of the

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method used, IAP should be measured at end expiration in thecomplete supine position after the absence of abdominal musclecontractions has been ensured, and with the transducer zeroedat the level of the mid-axillary line.2

To date, the bladder method is considered the best for indirectIAP measurement.2 This technique was originally reported byKron et al,25 who described a technique to measure IAP using anindwelling Foley catheter. More recently described techniquesuse stopcocks to avoid disconnection of the urinary catheter anda maximal instillation volume of 25 ml sterile saline.24 26

Commercially available kits are now available to measureintravesical pressure (AbViser; Wolfe-Tory Medical, Salt LakeCity, Utah, USA) facilitating its measurement. Continuous IAPmonitoring has also been described allowing earlier detection ofIAH.27

When it is not possible to use the intravesical route because ofbladder trauma, pelvic haematoma, etc, IAP can be measured bymeans of an oesophageal balloon catheter inserted into thestomach.27 28

CONSEQUENCES OF RAISED IAPA sustained rise in IAP .12 mm Hg has a significant deleteriouseffect on abdominal organ perfusion and cardiac output, withsubsequent dysfunction of both abdominal and extra-abdom-inal organs. A rise in IAP decreases the abdominal perfusionpressure (APP) and hence visceral perfusion. APP is related toIAP by the formula: APP = mean arterial pressure 2 IAP. Thosefamiliar with the management of patients with traumatic braininjury will appreciate that this is analogous to the concept ofcerebral perfusion pressure (mean arterial pressure 2 intracra-nial pressure), the value of which is often used to guidemanagement.29 Likewise, APP is proving to be equally useful inthe management of patients with raised IAP. Cheatham et al30

showed that APP was significantly superior to arterial pH, basedeficit, arterial lactate, hourly urinary output, mean arterialpressure and intravesical pressure in predicting patient survivalfrom IAH and ACS. Several studies in a mixed medical/surgicalpopulation of critically ill adults suggest that maintenance ofAPP >60 mm Hg confers a survival benefit.19

Cardiovascular dysfunctionIAH leads to a reduction in cardiac output, which is exacerbatedby hypovolaemia. Direct compression of the inferior vena cavaand portal vein and an increase in intrathoracic pressure causedby elevation of the diaphragm reduces venous return.31 32

Afterload also increases because of mechanical compression ofthe vascular beds and arteriolar vasoconstriction.33 Thesechanges lead to a reduction in stroke volume with acompensatory increase in heart rate. Decompression of theabdomen leads to an immediate increase in cardiac output.31

Increased intrapleural pressure due to diaphragmatic eleva-tion reduces ventricular compliance and ventricular end-diastolic volume, causing additional haemodynamic compro-mise. This increased intrathoracic pressure is also transmitted tothe great vessels leading to spuriously raised central venouspressure, pulmonary artery pressure and pulmonary arteryocclusion pressure. High filling pressures are therefore com-monly observed in ACS despite a reduction in end-diastolicvolume, making the assessment of haemodynamic status in apatient with ACS challenging.34

IAP .12 mm Hg is associated with venous stasis and thepotential for thromboembolic disease.35

Pulmonary dysfunctionIncreased IAP leads to diaphragmatic elevation with a reductionin static and dynamic lung compliance.36 Total lung capacity,residual volume and functional residual capacity are reduced,resulting in ventilation-perfusion mismatch and hypoventila-tion.31 32 37–39 The work of breathing is increased, and mechanicalventilation is often required to overcome hypoxia and hyper-carbia.

The alteration in lung mechanics caused by raised IAP resultsin high peak airway, plateau and alveolar pressures with theattendant risks of alveolar barotrauma and volutrauma. Thehigh intrathoracic pressure is associated with an increase inpulmonary artery pressure due to hypoxic pulmonary vasocon-striction, direct compression of the lung parenchyma and itsvessels, and altered compliance of the left and right ventricles.

Raised IAP also has an adverse effect on thoracic andabdominal lymphatic flow. High intrathoracic and abdominalpressures impede the drainage of lymph from the lungs, causingan increase in extravascular lung water.37 40 Combined withsepsis-induced capillary leak, pulmonary oedema is highlylikely.41 42

Box 1 Common causes of primary abdominal compartmentsyndrome

c Massive abdominal trauma with internal bleedingc Haemorrhagic pancreatitisc Ruptured abdominal aortic aneurysmc Retroperitoneal haematomac Intestinal obstruction, ileusc Bleeding pelvic fracturesc Liver transplantation

Box 2 Risk factors for intra-abdominal hypertension/abdominal compartment syndrome

1. Diminished abdominal wall compliance– Acute respiratory failure, especially with raised

intrathoracic pressure– Abdominal surgery with primary fascial closure– Major trauma/burns– Prone positioning

2. Increased intraluminal contents– Gastroparesis– Ileus– Colonic pseudo-obstruction

3. Increased abdominal contents– Haemoperitoneum/pneumoperitoneum– Ascites/liver dysfunction

4. Capillary leak/fluid resuscitation– Acidosis (pH,7.2)– Hypotension– Hypothermia (core temperature ,33uC)– Polytransfusion (.10 units of blood/24 h)– Coagulopathy– Massive fluid resuscitation– Oliguria– Sepsis– Major trauma/burns– Damage control laparotomy

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Renal dysfunctionA rising IAP is associated with a steady reduction in renal plasmaflow and glomerular filtration rate. Oliguria is observed with IAPof 15–20 mm Hg, and pressures .30 mm Hg lead toanuria.25 31 42–47 The mechanisms responsible for this renaldysfunction are probably multifactorial. The decrease in cardiacoutput associated with IAH is only partly responsible, asrestoration of cardiac output to normal with inotropes and fluidsdoes not normalise glomerular filtration rate.45 It is likely that the

principal reason for renal dysfunction is compression of the renalparenchyma causing an increase in renal vascular resistance andthe shunting of blood away from the renal cortex.45 48

IAH also causes an increase in the release of antidiuretichormone and activation of the renin–angiotensin–aldosteronesystem, resulting in sodium and water retention and angioten-sin II-induced renal vasoconstriction.49 50

Ureteric compression and occlusion does not appear to be acontributory factor, as stenting of the ureters does not improverenal function.45

Abdominal visceral abnormalitiesIncreased IAP reduces blood flow to all abdominal viscera exceptthe adrenal glands.33 Animal experiments have shown that there isa progressive decrease in mesenteric arterial blood flow andintestinal mucosal flow above IAP of 15 mm Hg despitepreservation of a normal mean arterial pressure and cardiacoutput.51 Similar studies have reported a graded reduction inhepatic arterial, portovenous and hepatic microcirculatory bloodflow at IAP .10 mm Hg.52 Visceral oxygen delivery is compro-mised, causing intestinal ischaemia, which may predispose toproduction of oxygen free radicals and bacterial translocation.53–55

Increased IAP also has an adverse effect on the flow of bloodto the abdominal wall, increasing the risk of wound infection,poor healing and subsequent fascial dehiscence.56

Dysfunction of the central nervous systemBoth human and animal studies have shown that an acuteincrease in IAP can cause an increase in intracranial pressure.57–60

Figure 1 Suggested algorithm for apatient with abdominal compartmentsyndrome (ACS).19 APP, abdominalperfusion pressure; IAP, intra-abdominalpressure.

Figure 2 Temporary abdominal closure using a Bogota bag.

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This is thought to be caused by impedance to cerebral venousoutflow from the raised intrathoracic and central venous systempressures.61 As cerebral perfusion is compromised by intracranialhypertension, it is recommended that raised abdominal pressureis aggressively managed in those with traumatic brain injury.62

MANAGEMENTIdeally, ACS should not be allowed to develop, as prevention isbetter than cure.63 Should it occur though, systemic perfusionshould be optimised to ensure an APP >60 mm Hg, medicalprocedures should be instituted to reduce IAP, and decom-pressive laparotomy should be performed for persistently raisedIAP (fig 1).19 48

PreventionAppropriate monitoring of IAP in patients at risk of ACS allowsearly identification of IAH and the start of procedures andtactics to reduce the IAP.

Patients undergoing laparotomy for severe abdominal traumaare at high risk of developing IAH/ACS after surgery.5 64 It isincreasingly recognised that attempting to perform definitivesurgery in these patients can result in the lethal triad ofhypothermia, acidosis and coagulopathy. Instead ‘‘damagecontrol surgery’’ is performed in which uncontrollable bleedingshould be stemmed with temporary packing, devitalised tissue isresected, and damaged bowel is exteriorised.65–67 This approach isrequired in ,10% of severely injured adults requiring lapar-otomy.67 Secondary resuscitation is then performed in theintensive care unit, and definitive surgery is delayed until thepatient’s physiological status has improved. Abdominal packs,retroperitoneal haemorrhage, bowel oedema and massive fluidresuscitation make these patients highly susceptible to post-operative IAH/ACS if definitive abdominal closure is attempted.Temporary abdominal closure is therefore performed to achievea tension free, watertight coverage of the underlying viscera.Numerous methods have been described to achieve this.Probably the most widely used is the ‘‘Bogota bag’’, so calledbecause it was first described by Londoni in Bogota (fig 2).68 Asterilised 3-litre genitourinary irrigation bag is sutured over thewound, allowing a relatively water-tight transparent cover.Towel clips, various types of prosthetic mesh and ‘‘zipper’’systems have all been advocated.69–72 In recent years, vacuum-assisted closure has gained in popularity.73

Despite adoption of an ‘‘open abdomen’’ approach, IAPshould be monitored carefully after surgery, as pressure canbuild up beneath the temporary abdominal closure, causingrecurrent ACS.74

Most patients are able to undergo definitive closure within5–7 days, although a number require reconstructive surgery at alater stage. Unfortunately, the recovery of some patients iscomplicated by fistulae formation or the development oftroublesome ventral herniae.

Manoeuvres to reduce IAPPatients with mild to moderate IAH may benefit from a brieftrial of neuromuscular blockade to reduce abdominal muscletone and improve compliance.19 75 Adequate sedation andanalgesia may also beneficially influence abdominal wallmechanics.19 The head-up body position widely adopted inintensive care units to prevent ventilator-associated pneumoniaalso increases IAP, and consideration should be given to theadoption of a supine or head-down position.19 76

If possible, collections of fluid, blood, air, pus or ascites shouldbe drained percutaneously, preferably under radiological gui-dance.19 77–79 The bowels should be evacuated using laxatives andenemas, the stomach decompressed with a nasogastric tube, andprokinetics prescribed to hasten gastric transit.19 80

Diuretics may be beneficial in mobilising third-space oedemain the haemodynamically stable patient. However, as renaldysfunction is commonplace in these patients, continuous renalreplacement therapy is often required to achieve a negative fluidbalance.19

Decompressive laparotomyPersistently raised IAP refractory to the above measures withevidence of organ dysfunction warrants surgical abdominaldecompression.19 However, this procedure must be performed ina timely manner before there is irreversible visceral ischaemiaand organ damage.25 30 81 82 A thorough exploration of theabdomen should be undertaken, bleeding sources controlled,haematomas evacuated, and ascites drained. Abdominal decom-pression is associated with an immediate increase in cardiacindex, urine output, tidal volume and thoracic compliance.81

Cardiac arrhythmias and asystole have been reported immedi-ately after decompression, presumably secondary to the releaseof metabolic products on reperfusion of abdominal viscera.25

Five key references

c Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results fromthe International Conference of Experts on Intra-abdominalHypertension and Abdominal Compartment Syndrome. I.Definitions. Intensive Care Med 2006;32:1722–32.

c Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results fromthe International Conference of Experts on Intra-abdominalHypertension and Abdominal Compartment Syndrome. II.Recommendations. Intensive Care Med 2007;33:951–62.

c Sieh KM, Chu KM, Wong J. Intra-abdominal hypertension andabdominal compartment syndrome. Langenbecks Arch Surg2001;386:53–61.

c Bailey J, Shapiro MJ. Abdominal compartment syndrome. CritCare 2000;4:23–9.

c Fietsam R Jr, Villalba M, Glover JL, Clark K. Intra-abdominalcompartment syndrome as a complication of rupturedabdominal aortic aneurysm repair. Am Surg 1989;55:396–402.

Learning points

c Intra-abdominal hypertension (IAH; defined as a sustained orrepeated intra-abdominal pressure (IAP) >12 mm Hg) iscommon in the critically ill.

c Abdominal compartment syndrome (ACS) is defined as asustained IAP >20 mm Hg that is associated with new organdysfunction/failure.

c The intravesical route should be used to measure IAP.c Critically ill patients with one or more risk factors for the

development of IAH should receive IAP monitoring.c Temporary abdominal closure is advocated in those

undergoing damage control surgery for severe abdominaltrauma to prevent the development of ACS.

c Non-surgical options to reduce persistently raised IAP shouldbe attempted initially, but some patients will require adecompressive laparotomy followed by temporary abdominalclosure.

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Primary fascial closure is usually not attempted afterdecompressive laparotomy. Instead an ‘‘open abdomen’’approach is adopted with temporary abdominal closure.

SUMMARYACS can develop in a heterogeneous group of critically illpatients. It can be difficult to detect clinically, and those withtwo or more risk factors for its development should havebaseline intravesical measurement of IAP. Several relativelysimple measures are known to reduce IAP, and these should beused initially. However, persistently raised IAP with subsequentorgan dysfunction warrants timely decompressive laparotomywith temporary abdominal closure.

MULTIPLE CHOICE QUESTIONS (TRUE (T)/FALSE (F); ANSWERSAFTER THE REFERENCES)

1. Intra-abdominal pressure

A. varies with respiration

B. can be non-pathologically increased in the obese

C. is technically challenging to measure

D. is normally >12 mm Hg

E. should be measured in all critically ill adults

2. Regarding the measurement of intra-abdominal pressure,

A. it should be measured in the semi-recumbent position

B. the top of the symphysis pubis is the zero reference point

C. the intravesical route is preferred

D. results should be expressed in cm H2O

E. it should be measured at end inspiration

3. The systemic effects of raised intra-abdominal pressureinclude

A. a reduction in cardiac output

B. a vigorous diuresis

C. hypoxia and hypercapnia

D. an increase in intracranial pressure

E. a reduction in central venous pressure

4. Abdominal compartment syndrome

A. only occurs in surgical patients

B. can be reliably detected by clinical examination alone

C. is defined as a sustained intra-abdominal pressure.20 mm Hg that is associated with new organ dysfunction

D. is uniformly fatal without appropriate treatment

E. is associated with large volume resuscitation

5. Regarding the management of abdominal compartmentsyndrome,

A. surgery is always required

B. continuous renal replacement therapy may be useful

C. paracentesis may have a role

D. decompressive laparotomy should only be performed afterestablished organ failure

E. after decompression, it is no longer necessary to measureintra-abdominal pressure

Funding: None.

Competing interests: None.

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c Further study is required to establish the incidence ofabdominal compartment syndrome.

c Does routine surveillance and measurement of intra-abdominalpressure in the critically ill influence outcome?

c What is the optimal method for achieving temporaryabdominal closure?

c The relationship between positive fluid balance and the onsetof intra-abdominal hypertension should be better defined.

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Answers1. (A) T (B) T (C) F (D) F (E) F2. (A) F (B) F (C) T (D) F (E) F3. (A) T (B) F (C) T (D) T (E) F4. (A) F (B) F (C) T (D) T (E) T5. (A) F (B) T (C) T (D) F (E) F

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