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The abdominal compartmentsyndrome (ACS) is a recentlyrecognized pattern of altered

cardiovascular hemodynamics, respi-ratory mechanics and renal function,occurring secondary to a sustained in-crease in intra-abdominal pressure(IAP). Typically, patients with thesyndrome are critically ill and depen-dent on ventilatory support in an in-tensive care unit. Although an analogywith the extremity compartment syn-drome is frequently made, this anal-ogy is not entirely valid because theACS has profound systemic effectsthat are not part of the extremity com-partment syndrome.Recently, awareness of the ACS has

increased for 2 primary reasons. First,

the increased use of laparoscopyamong general surgeons has broughtwith it an appreciation of IAP as areadily quantifiable entity. Second, themore frequent use of planned repeatlaparotomy for trauma has allowedboth surgeon and intensivist to appre-ciate the beneficial effects of abdomi-nal decompression upon removal ofpacking or evacuation of hematoma.Elevations in IAP have broad sys-

temic as well as local effects. Severalclinical and experimental studies haveprovided evidence that most adverseeffects of ACS are due to mechanicalfactors and their subsequent influenceon the intra-abdominal, retroperi-toneal or thoracic compartments. It isconceivable that neurohumoral re-

sponses may play a role in the patho-genesis of ACS; however, there arecurrently little data to support thisconcept.

INCREASED IAP

Systemic effects

The effects of increased IAP on sys-temic hemodynamics are complex.1-4

A graded increase in IAP from 10 to40 mm Hg lowers cardiac output ow-ing to a reduction in stroke volume.Stroke volume decreases because of adrop in preload and an increase in af-terload. Preload is reduced as a resultof pooling of blood in splanchnic andlower extremity vascular beds from

Surgical Biology for the ClinicianBiologie chirurgicale pour le clinicien

THE ABDOMINAL COMPARTMENT SYNDROME

Avery B. Nathens, MD, PhD; Frederick D. Brenneman, MD; Bernard R. Boulanger, MD

From the Department of Surgery, Sunnybrook Health Science Centre and the University of Toronto, Toronto, Ont.

Correspondence to: Dr. Bernard R. Boulanger, Rm. H-170, Sunnybrook Health Science Centre, 2075 Bayview Ave., North York ON M4N 3M5

© 1997 Canadian Medical Association (text and abstract/résumé)

The abdominal compartment syndrome refers to the alterations in respiratory mechanics, hemodynamicparameters and renal function that occur as a result of a sustained increase in intra-abdominal pressure. Thesyndrome may follow a diverse series of insults, including laparotomy for severe abdominal trauma, rup-tured abdominal aortic aneurysm and intra-abdominal infection. Diagnosis depends on recognizing theclinical picture in patients at risk, followed by an objective measurement of intra-abdominal pressure. Suc-cessful management may require abdominal decompression with temporary abdominal closure. Despite ur-gent decompression, the death rate is high because of the severity of the patients’ underlyingillness.

Le syndrome du compartiment abdominal désigne les modifications de la mécanique respiratoire, desparamètres hémodynamiques et de la fonction rénale qu’entraîne une augmentation soutenue de la pres-sion intra-abdominale. Le syndrome peut découler d’une série diverse d’atteintes, y compris une laparo-tomie à la suite d’un traumatisme abdominal grave, une rupture d’un anévrisme de l’aorte abdominale etune infection intra-abdominale. Le diagnostic dépend de l’identification du tableau clinique chez les pa-tients à risque, suivie d’une mesure objective de la pression intra-abdominale. Un traitement réussi peut ex-iger une décompression abdominale avec fermeture temporaire de l’abdomen. Malgré les décompressionsd’urgence, le taux de mortalité est élevé à cause de la gravité de la maladie sous-jacente des patients.

marked increases in portal venous andinferior vena caval pressures. Addi-tionally, elevated intrathoracic pres-sures reduce left ventricular compli-ance, thus impairing ventricular filling.In spite of the reduced preload, mea-surements of central venous and pul-monary capillary wedge pressures arefactitiously increased, a reflection ofthe elevated intrathoracic pressure. Atthe same time, high IAPs increase af-terload by elevating systemic vascularresistance, an effect that is mediatedby mechanical compression of capil-lary beds. This increase in systemicvascular resistance functions to main-tain a relatively normal blood pressuredespite the reduction in cardiac out-put. Thus, the clinical picture is oneof low cardiac output and high sys-temic vascular resistance in the con-text of high central venous and pul-monary capillary wedge pressures.Even in the face of these high fillingpressures, patients will respond to in-travascular volume loading, whichfunctions to augment preload, albeitat the cost of supranormal left ventric-ular end diastolic pressures.Elevations in IAP have profound

effects on respiratory mechanics andultimately limit effective ventilation.Passive elevation of the diaphragms al-lows the transmission of high IAP intothe pleural cavity, reducing both staticand dynamic lung compliance.1,2 Thisreduction in compliance results in theneed for very high inspiratory airwaypressures to maintain effective ventila-tion. Elevations of peak airway pres-sures are evident at IAPs as low as 15mm Hg.3 Arterial blood-gas analysisdemonstrates a rising partial pressureof carbon dioxide in arterial blood, areflection of the decreased lung com-pliance and ineffective ventilation.The partial pressure of oxygen in arte-rial blood may also be reduced as a re-sult of basal atelectasis and decreasedcardiac output. Plain chest radi-

ographs in patients with ACS typicallyshow clear but very small lung fieldsand elevated hemidiaphragms.1

The systemic effects of elevatedIAPs are not limited to cardiorespira-tory dysfunction, as adverse effects oncerebral perfusion have also been doc-umented. This is a critical point whenone considers that one of the mostcommon events leading to the devel-opment of ACS is major abdominaltrauma and that 50% of such patientshave coexistent serious head injuries.Reduced cerebral perfusion is primar-ily due to a decrease in cerebral venousoutflow, secondary to the elevation inintrathoracic pressure.5 Although vol-ume expansion may be a useful meansto maintain or increase mean arterialpressure and thus cerebral perfusionpressure, it may also serve to exacer-bate cerebral edema.6 These data sug-gest that unchecked increases in IAPmay adversely effect neurologic out-come.

Local effects

All intraperitoneal and retroperi-toneal viscera demonstrate a markedreduction in blood flow at IAPsgreater than 20 mm Hg. The one ex-ception is the adrenal gland for whichmeasures of perfusion clearly indicatea paradoxical increase in blood flow atIAPs as high as 40 mm Hg.7

Oliguria is a common manifesta-tion of ACS. The cause of renal dys-function in ACS is multifactorial. Al-though ureteric compression has beenconsidered as a possible mechanism,both clinical and experimental inser-tions of ureteric stents do not mitigatethis phenomenon.8,9 A reduction incardiac output and hence renal bloodflow is in part responsible. Addition-ally, elevated IAP significantly in-creases renal vein pressure owing todirect compressive forces, resulting inrenal vein hypertension and increased

local pressures within the renalparenchyma. The combined effect ofincreased renal parenchymal pressures(and hence elevated proximal tubularpressures) and a reduction in renalblood flow decreases the pressure gra-dient across the glomerular membraneand thus markedly reduces theglomerular filtration rate (GFR).10 Inexperimental studies carried out in eu-volemic subjects, an IAP of 20mm Hg resulted in a 75% reduction inGFR and a pressure of 40 mm Hg re-sulted in anuria. The reduction inGFR is refractory to volume loading,suggesting that the reduction in renalblood flow is of lesser importance thanthe increase in renal vein pressures.8

Increases in IAP also have adverseeffects on splanchnic blood flow inde-pendent of the reduction in cardiacoutput. At IAPs exceeding 15mm Hg, there is reduced superiormesenteric artery blood flow, result-ing in impaired mucosal blood flowand mucosal oxygen delivery. Mucosalacidosis consistent with ischemiaeventually ensues.11,12 Even at pres-sures of 10 mm Hg, marked changesin hepatic blood flow are detectable.Hepatic artery and portal venousblood flow are reduced by 40% and30% respectively and portal venouspressures rise in parallel with IAP.13

Small-bowel ischemia and elevatedportal venous pressure cause visceraledema, an event that may further in-crease the volume of contents in theperitoneal cavity and thus aggravateany increase in IAP.The local effects of elevated IAP

extend beyond the intra-abdominalcompartment and affect abdominalwall blood flow. Complications ofwound healing, particularly wound in-fection and fascial dehiscence, arecommon in patients with ACS. Thereis evidence to suggest that these ad-verse events may be in part related toa reduction in abdominal wall perfu-

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sion. For example, blood flow to therectus sheath as measured by laserDoppler flowmetry is reduced by al-most 60% at an IAP of 10 mm Hg.14

As collagen deposition and resistanceto infection are directly related to tis-sue perfusion and oxygenation, it isplausible that elevated IAP over pro-longed periods may adversely effectwound healing.

DIAGNOSIS OF ACS

A diagnosis of the ACS requires therecognition of patients at risk, identi-fication of the clinical syndrome andultimately measurement of IAPs. Sev-eral clinical scenarios have been iden-tified as potential precursors to thesyndrome (Table I). The 2 common-est scenarios follow emergent repair ofa ruptured abdominal aortic aneurysmand abdominal trauma. In both cases,retroperitoneal hematomas combinedwith massive fluid resuscitation andconsequent visceral and abdominalwall edema set the stage for the syn-drome. In patients who undergo anabbreviated laparotomy for trauma tocontain hemorrhage, intra-abdominalpacking with or without ongoingbleeding also contributes to the devel-opment of elevated IAPs.15

The classic clinical clues to the pres-ence of ACS are as follows: a tense ordistended abdomen, massive intra-

venous fluid requirements, elevatedcentral venous and pulmonary capil-lary wedge pressures, decreased car-diac output, elevated peak airway pres-sures and oliguria. Importantly, apatient may have mild to moderate el-evation in IAP that is not evident onabdominal examination. Also, patientsjudged to have elevated IAP by physi-cal examination may actually have anormal measured IAP. Thus, in a pa-tient with a clinical presentation sug-gestive of ACS, an objective evalua-tion of IAP is necessary.16

MEASUREMENT OF IAP

A variety of experimental studieshave utilized direct measurements ofIAP by connecting an intraperitonealcatheter to a pressure transducer. Al-though this method is accurate overall ranges of IAP, it is impractical forroutine use in the intensive care unit.The most widely used method in-volves transurethral measurement ofurinary bladder pressure using a Foleycatheter.17,18 The bladder acts as a pas-sive diaphragm at volumes of 50 to100 mL and thus accurately reflectsIAPs over a wide range (0 to 70mm Hg). In the supine position, a Fo-ley catheter is passed into the bladderand clamped distal to the culture aspi-ration port after the bladder has beenemptied. An 18-gauge needle is in-serted into the aspiration port and 50to 100 mL of sterile saline is instilledinto the bladder. The clamp is releasedto allow the proximal drainage tubingto fill with saline from the bladder.The needle is then connected to anelectronic central venous pressuretransducer or water manometer withthe reference point being the symph-ysis pubis. Alternatively, a 3-way stop-cock can be inserted into the Foleycatheter and the stopcock connectedto a pressure transducer. In the supineposition the normal IAP is less than

10 mm Hg. After abdominal surgery,pressures are typically in the range of3 to 15 mm Hg.18 In patients having aneurogenic bladder or in those havinga small contracted bladder (e.g., afterradiotherapy), measurements may beinaccurate. The incidence of IAPshigh enough to alter local and sys-temic hemodynamics and respiratorymechanics is significant. In one study,38% of patients admitted to an inten-sive care unit after major abdominalsurgery had IAPs greater than 20mm Hg.19

The level of IAP at which the ACSoccurs is variable. Clearly, variabilityin the physiologic response to agraded increase in pressure depends inpart on the intravascular volume sta-tus of the patient as well as underlyingpulmonary or renal dysfunction.Therefore, the diagnosis and need fortreatment depend on the clinical sta-tus of the individual patient. Burchand associates20 have proposed a grad-ing system for ACS, which may helpin guiding the need for therapy. In pa-tients with pressures less than 15mm Hg (i.e., grade I) treatment israrely indicated. The need for treat-ment in patients with grade II ACS(15 to 25 mm Hg) depends largely onthe clinical status of the patient. Pa-tients without oliguria and elevatedairway pressures probably warrantclose observation. Grade III ACS (25to 35 mm Hg) usually requires inter-vention. In these patients, hemody-namic and renal dysfunction often de-velop slowly, frequently leading to adelay in both diagnosis and therapy.Patients with IAPs greater than 35mm Hg (grade IV) are usually ingrave clinical condition and requireimmediate treatment.

MANAGEMENT OF ACS

Abdominal decompression is theonly definitive management for the

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Clinical Scenarios Associated With theDevelopment of the Abdominal CompartmentSyndrome

Abdominal aortic aneurysm repair(emergency)

Abdominal trauma

Traumatic retroperitoneal hematoma

Severe intra-abdominal infection

Pancreatitis

Liver transplantation

Massive ascites

Table I

syndrome. Although administrationof fluids may transiently restore urineoutput and paralysis may minimizeairway pressures, these efforts shouldonly be considered temporizing mea-sures until decompression can beachieved. Optimally, decompressioninvolves either reopening a laparo-tomy incision or, in patients withoutrecent laparotomy, opening the peri-toneal cavity through a midline inci-sion. If the patient is in extremis andcannot tolerate transport to the oper-ating room, decompression in the in-tensive care unit may be necessary.Characteristically, decompression isfollowed by an immediate drop in air-way pressures, brisk diuresis and im-provement in hemodynamic measure-ments. Fig. 1 presents the profile of

cardiorespiratory derangements andtheir reversal after decompression in arepresentative patient. Less frequently,hypotension may follow rapid decom-pression because of the abrupt drop incentral filling pressures and systemicvascular resistance. Supraventriculararrhythmias and episodes of asystolehave also been reported.1,21 One po-tential mechanism for these adverseevents is the rapid washout and sys-temic circulation of acid and metabo-lites from the reperfused viscera andlower extremities.1 At the time of ab-dominal decompression, it is impera-tive that intravascular volume is opti-mized. Inotropic agents must beavailable in case of sudden cardiovas-cular collapse, and it may be necessaryto administer sodium bicarbonate tominimize reperfusion acidosis.The details of the decompressive la-

parotomy depend on the clinical pic-ture. In a patient with severe intra-abdominal injuries in whom packshave been left in situ to tamponadebleeding, definitive management ofhemorrhage and removal of the packsshould be a priority. In other clinicalscenarios, the laparotomy for abdomi-nal decompression may be limited toopening up the wound and evacuat-ing hematoma and any ascites. Occa-sionally, removal of packs alone maysufficiently decrease the volume ofperitoneal contents such that primaryfascial closure can be accomplished. Inmost cases, however, the developmentof marked visceral edema precludesclosure of the abdominal wall, requir-ing the use of some form of temporaryabdominal closure.There are several options for man-

agement of the abdominal wound af-ter decompression. Absorbable ornonabsorbable mesh may be used tobridge the fascial defect, with sutureof the prosthesis to the fascial edges orskin. Our preference is a piece ofpolyglycolic acid mesh with Op-site

(Smith and Nephew, Lachine, Que.)adherent to either side in the form ofa sandwich. Op-site prevents adher-ence to the viscera at the time of meshremoval and lessens evaporative fluidlosses. We prefer to suture the meshdirectly to the skin to maintainstrength and integrity of the fascialedges, thus saving them for the defin-itive closure. Others advocate the useof sterile 3-L genitourinary irrigationbags. They are sutured to each otherto create an appropriate sized prosthe-sis and to the wound edges with a run-ning monofilament suture.2 Wheneverpossible, the omentum should be in-terposed between the viscera andprosthesis to minimize adherence tobowel and to prevent fistula forma-tion.Definitive abdominal closure

should be attempted once the follow-ing criteria have been met. First, theremust be evidence of a global improve-ment in the clinical picture along withrestoration of tissue oxygenation, re-versal of coagulopathy and restorationof euvolemia. Second, there must be ahigh likelihood of fascial approxima-tion. This is most likely to occur 3 to4 days after abdominal decompressiononce mobilization of interstitial fluidand a brisk diuresis have reduced pe-ripheral and visceral edema. Finally,the likelihood of subsequent repeat laparotomy for bleeding or sepsisshould be extremely low.When these criteria have been met,

primary fascial closure should be at-tempted with nonabsorbable suturematerial and retention sutures if nec-essary. If at the time of closure it be-comes apparent that fascial approxi-mation cannot be achieved withouttension, it is worthwhile to trim theprosthesis to bridge whatever gap re-mains and then attempt definitive clo-sure at the earliest possible opportu-nity. If abdominal wall closure cannotbe achieved within 2 weeks, a split-

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FIG. 1. Hemodynamic and respiratory parame-ters in a patient with abdominal compartmentsyndrome and the response to abdominal de-compression. Prior to decompression, the car-diac index (CI) drops, whereas both pulmonarycapillary wedge pressure (PCWP) and systemicvascular resistance (SVR) increase. Peak inspi-ratory pressures are high and the patient is olig-uric. All parameters improve upon decompres-sion and a brisk diuresis ensues. IAP =intra-abdominal pressure, MAP = mean arterialpressure.

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thickness skin graft may provide ade-quate coverage over the granulatingsurface; definitive abdominal wall re-construction can then be deferred for6 to 12 months.22

PROGNOSIS

The death rate in patients withACS is extremely high. Several smallseries have reported death rates rang-ing from 42% to 71%.1,2,18,22,23 Thesehigh rates must be considered in thecontext of the patients’ underlyingdisease. The majority of these patientsare critically ill and are admitted to theintensive care unit with severe intra-abdominal sepsis, intra-abdominal in-juries or after repair of a ruptured ab-dominal aortic aneurysm. Even withprompt recognition and abdominaldecompression, the frequency of mul-tiple organ dysfunction and death ishigh because of the severity of the ini-tial physiologic insult. However, inthe face of elevated IAP and a clinicalpicture consistent with ACS, thechance of survival is extremely lowwithout urgent abdominal decom-pression.1,18

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