Intra-abdominal Hypertension and Abdominal Compartment ...€¦ · intra-abdominal hypertensiona Grade I II III IV Intra-abdominal pressure, mm Hg 12-15 16-20 21-25 ≥25 a Based

The concept of IAH was proposedin the late 1800s, forgotten afterWorld War I, and rediscovered nearthe end of the 20th century.1 In 2004,a group of international physiciansand surgeons formed the World Soci-ety of the Abdominal CompartmentSyndrome (WSACS).2 The goal of thisnew organization was to develop acohesive approach to the managementof IAH and ACS, foster educationand research, and develop consensusstatements and definitions. WSACShas developed evidence-based defi-nitions, guidelines, and treatmentalgorithms and has identified evidence-based devices and methods to meas-ure intra-abdominal pressure (IAP).

DefinitionsIntra-abdominal Pressure

IAP is the steady-state pressurewithin the abdominal cavity.2 In

Intra-abdominalHypertension andAbdominal Compartment SyndromeA Comprehensive Overview

Cover Article

This article has been designated for CE credit. A closed-book, multiple-choice examination fol-lows this article, which tests your knowledge ofthe following objectives:

1. Define intra-abdominal hypertension andabdominal compartment syndrome

2. Describe 2 methods of measuring intra-abdominal pressure

3. Discuss the management of intra-abdominal hypertension

Rosemary Koehl Lee, DNP, ARNP, CNS, ACNP-BC, CCNS, CCRN

CEContinuing Education

©2012 American Association of Critical-Care Nurses doi: 10.4037/ccn2012662

Collaborative managementof acute and critically illpatients may result incomplications associatedwith therapeutic meas-

ures. This article provides a compre-hensive overview of intra-abdominalhypertension (IAH) and abdominalcompartment syndrome (ACS), thenurse’s role in assessing and moni-toring patients with these entities,and collaborative management ofpatients who have IAH and ACS.

www.ccnonline.org CriticalCareNurse Vol 32, No. 1, FEBRUARY 2012 19

Intra-abdominal hypertension has a prevalence of at least 50% in the critically illpopulation and has been identified as an independent risk factor for death. Yet, manyof the members of the critical care team do not assess for intra-abdominal hypertensionand are unaware of the consequences of untreated intra-abdominal hypertension.These consequences can be abdominal compartment syndrome, multisystem organfailure, and death. This article provides an overview of the pathophysiology of intra-abdominal hypertension and abdominal compartment syndrome. In addition, theevidence-based definitions, guidelines, and recommendations of the World Societyof the Abdominal Compartment Syndrome are presented. (Critical Care Nurse.2012;32[1]:19-32)

http://ccn.aacnjournals.org

healthy persons, IAP is 0 to 5 mm Hg3

and varies inversely with intratho-racic pressure during normal breath-ing. Various factors, such as coughing,sneezing, and loud singing, can causeIAP to increase drastically for shortperiods and then return easily tobaseline. IAP is also increased inpersons who are morbidly obese,have chronic ascites, or are pregnant.In these chronic forms, the increasedevelops slowly and the body adjuststo the change. Patients with chroni-cally increased IAP do not experiencethe systemic effects of IAH. The meanIAP in critically ill adults is approxi-mately 5 to 7 mm Hg.4

Intra-abdominal HypertensionIAH is a sustained or repeated

pathological elevation of IAP of 12mm Hg or greater.2 WSACS hasdeveloped grades of IAH (Table 1).

Abdominal Perfusion PressureAbdominal perfusion pressure

(APP) is a measure of the relative

adequacy of abdominal blood flow.APP is calculated by subtracting theIAP from the mean arterial pressure(MAP): MAP-IAP=APP. The APP inpatients with IAH or ACS should bemaintained at 60 mm Hg or higher.2-4

Abdominal Compartment SyndromeACS is a sustained IAP greater

than 20 mm Hg (with or without anAPP <60 mm Hg) associated withnew organ dysfunction or failure.2-4

Causes of ACSWSACS categorizes conditions

that cause ACS as primary (surgical),secondary (medical), and recurrent4

(Table 2). Primary conditions areones that need surgical or interven-tional radiological treatment. Second-ary conditions are due to medicalcauses that do not require surgery or

radiological intervention as an initialtherapy. Recurrent conditions areones in which ACS redevelops aftersurgical or medical treatment of pri-mary or secondary causes of ACS.

Incidence and Prevalence Prevalence is a 1-day snapshot of a

particular issue or concern. Malbrain etal5 conducted a prevalence study in 13intensive care units (ICUs) and assessed97 patients. The overall prevalence ofIAH was 58.8% (IAP >12 mm Hg).Prevalence was 65% in surgical patientsand 54.4% in medical patients. How-ever, the medical patients had a higherprevalence of an increased IAP (>15mm Hg) than did the surgical patients(29.8% vs 27.5%). Also, the medicalpatients had a higher prevalence ofACS than did the surgical patients(10.5% vs 5%). Differences in IAHprevalence between the medical andsurgical patients were not significant.

Incidence is the occurrence of aparticular issue or concern over time.Vidal et al6 studied the incidence ofIAP in 83 critically ill patients in a sin-gle ICU. A total of 31% of the patientshad IAH at the time of admission to

Rosemary Koehl Lee is a clinical nurse specialist for the critical care and progressive caredepartments at Homestead Hospital, Homestead, Florida. She is also an adjunct facultymember at Barry University in Miami Shores, Florida.

Author

Corresponding author: Rosemary K. Lee, Critical Care Dept, Homestead Hospital, 975 Baptist Way, Homestead,FL 33033 (e-mail: [email protected]).

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

20 CriticalCareNurse Vol 32, No. 1, FEBRUARY 2012 www.ccnonline.org

Table 1 Grading system forintra-abdominal hypertensiona

Grade

I

II

III

IV

Intra-abdominal pressure, mm Hg

12 -15

16 -20

21 -25

≥25

a Based on information from the World Societyof the Abdominal Compartment Syndrome,2

Muckart et al,3 and Malbrain et al.4

Table 2 Primary and secondary conditions that cause intra-abdominal hypertension and abdominal compartment syndromea

Primary

Blunt/penetrating trauma

Liver transplantation

Ruptured abdominal aortic aneurysm

Postoperative bleeding

Retroperitoneal hemorrhage

Mechanical intestinal obstruction

Postoperative closure of the abdomenunder tension

Bleeding pelvic fractures

Secondary

Severe intra-abdominal infection

Large-volume fluid replacement

Ascites

Pancreatitis

Ileus

Sepsis

Major burns

Continuous ambulatory peritoneal dialysis

Morbid obesity

Pregnancy

a Based on information from Muckart et al3 and Malbrain et al.4


the unit, and the condition developedin another 33% after admission.Compared with patients without IAH,patients with IAH were sicker andhad a higher mortality rate (53% vs27%; P = .02). According to logisticregression, IAH was an independentpredictor of mortality (P = .003). ACSdeveloped in 10 patients (12%), and8 of the 10 (80%) died.

Reintam et al7 performed a studyto identify the differences in inci-dence, course, and outcome of pri-mary and secondary IAH and todetermine if IAH is an independentrisk factor for death. A total of 257patients receiving mechanical venti-lation were enrolled in the study.IAP was measured repeatedly. IAHdeveloped in 95 of the patients; 60had primary IAH and 35 had sec-ondary IAH. During the first 3 days,mean IAP decreased in the patientswith primary IAH and increased sig-nificantly (P=.05) in those with sec-ondary IAH. The patients with IAHhad a significantly higher mortalitythan did patients without IAH. ICUmortality was 37.9% for patients withIAH and 19.1% for patients withoutIAH (P=.001). The 28-day mortalitywas 48.4% vs 27.8% (P = .001), andthe 90-day mortality was 53.7% vs35.8% (P =.004). Patients with sec-ondary IAH had a significantly highermortality than did patients with pri-mary IAH (P =.03). Reintam et al7

concluded that development of IAHis an independent risk factor fordeath. They further concluded thatcompared with primary IAH, sec-ondary IAH does not occur as often,has a different development course,and has worse outcomes.

These 3 studies5-7 indicate thatIAH occurs frequently and mayworsen patients’ outcome. Health

care practitioners tend to be awareof the development of IAH in surgi-cal patients and in patients withobviously distended abdomens.However, the team must also beaware of the implications of IAH inmedical patients.

Pathophysiological Effectsof IAH and ACS

The abdomen can be considereda compartment with the spine, pelvis,

and costal arch as its inflexible edgesand the diaphragm and abdominalwall as its more pliable edges.8 Theinternal contents of this compart-ment consist of the stomach, largeand small intestine, omentum, liver,spleen, pancreas, gall bladder, kid-neys, adrenal glands, ureters, blad-der, and, in females, the uterus(Figures 1 and 2). Major blood ves-sels also course through this com-partment. The abdominal aorta,


Figure 1 Abdominal anatomy–gastrointestinal. Reprinted from Saladin,9 with permission from The McGraw-Hill Companies.

Oral cavity

Submandibular gland

Diaphragm

Liver

Gallbladder

Small intestine

CecumAppendix

AnusAnal canalRectum

Sigmoidcolon

Descendingcolon

Transversecolon

Stomach

Esophagus

Pharynx

Parotidgland

Pancreas

Bile duct

Ascendingcolon

Sublingual gland

Tongue

Teeth


with its branches of the celiac axisand the superior and inferior mesen-teric arteries, perfuses the gut andthe accessory organs. All the venousblood from the gut drains into theportal vein to the liver and leavesthe liver via the hepatic vein to bedrained into the inferior vena cava.The abdominal compartment con-tains solid organs, hollow organs,fluid, gas, solids, and adipose tissue.When a condition arises that persist-ently increases pressure in the abdom-inal cavity to 12 mm Hg or greater,not only the gut but all major bodysystems can be affected, and theeffects can lead to multisystem organfailure and death.

Gastrointestinal SystemThe effect of IAH on the splanch-

nic organs leads to diminished gutperfusion. The consequences of thischange lead to ischemia, acidosis ofthe mucosal bed, capillary leak,

intestinal edema, and translocationof gut bacteria.10 As IAP increases,pressure is placed on the arteries,capillaries, and veins in the abdomi-nal cavity. This increased pressurecauses diminished arterial blood flowto the organs and resistance todrainage into the veins.

The diminished oxygenation to thegut leads to intramucosal acidosis.10,11

The ischemic intestine loses its pro-tective mucosal barrier and becomesmore permeable to the intestinal con-tents. Edema develops in the intestinalwall and further increases the IAP.The increased permeability allowsthe intestinal flora to translocate viathe villi into the lymph and vascularsystems. This microbial translocationsets the stage for the development ofsepsis.12 Patients with IAH are also athigh risk for stress ulcers because ofthe loss of the mucosal barrier.8

An IAP of up to 20 mm Hg candecrease mesenteric perfusion by

40%, and pres-sures up to 40 mm Hg candecreasemesentericperfusion by70%.12 The cor-rection of IAHcan lead toischemia-reperfusioninjury and sendinflammatorycytokines toother organs,setting theground workfor multisystemorgan failure.12

IAH affectsthe abdominalwall by impos-

ing pressure directly on the vesselsfeeding the wall. The pressure leadsto edema and ischemia of abdominalwall tissues. Distention of the abdom-inal wall by IAH leads to decreasedcompliance of the wall, further com-pounding the IAH. The decreasedblood flow leads to poor healing andpossible dehiscence of abdominalsurgical wounds.11

The vascular liver is extremelysusceptible to IAH. Persistent pres-sures as low as 10 mm Hg can decreasehepatic perfusion and impair liverfunction.10,12 If varices are present, thissame pressure can lead to increasedvariceal stress and possible rupture.13

With increased IAP, blood flowdecreases in both the hepatic arteryand the portal vein. This change inblood flow leads to decreased glucosemetabolism, mitochondrial malfunc-tion, and decreased lactate clearanceby the liver.12 Diminished lactateclearance leads to lactic acidosis.


Figure 2 Abdominal anatomy –renal. Reprinted from Saladin,9 with permission from The McGraw-Hill Companies.

Anterior view Posterior view

Diaphragm11th and 12th ribs

Adrenal glandRenal arteryRenal veinKidney

Vertebra L2Aorta

Inferior vena cava

Ureter

Urinary bladder

Urethra


Renal SystemIAH leads to impaired renal

function.14 Persistent pressures of15 mm Hg or greater have beenindependently associated withrenal impairment.14 The acute kid-ney injury that accompanies IAHis multifactorial. The primary fac-tor is decreased renal perfusion.Other factors are decreased APP(<60 mm Hg), decreased cardiacoutput, and increased systemicvascular resistance.14 The renalimpairment, as indicated by anelevated serum level of creatinine,may not appear until 2 to 3 daysafter the incident of IAH.14

Pulmonary SystemAs the abdomen distends with

intestinal gas, fluid, or edematousorgans, the diaphragm is pushedupward, impinging on the tho-racic cavity. Approximately 50%of the IAP is dispersed across thediaphragm and affects respirationand ventilation.11 Pulmonary dys-function may be one of the earli-est signs of ACS.15 Because thelungs cannot expand fully, respira-tory excursion is limited, therebyreducing inhaled tidal volume,leading to hypoxemia. Conversely,carbon dioxide is retained, caus-ing hypercarbia and respiratoryacidosis. Compression atelectasisadds to the ventilation-perfusionmismatch and decreases the ratioof PaO2 to fraction of inspiredoxygen. Hospital- or ventilator-acquired pneumonia associatedwith the compression atelectasismay develop.

IAH can cause increases inpeak airway and plateau pressuresin patients treated with mechani-cal ventilation. The increases can

increases the workload of the rightventricle and decreases the ability ofthe left ventricle to fill. The increasedworkload increases myocardial oxy-gen demand. Through the compen-satory measures of the sympatheticnervous system to maintain arterialpressure, systemic vascular resist-ance increases. In addition, the directcompression of the abdominalaorta, due to IAH, further increasessystemic vascular resistance and theworkload on the left ventricle.11,17

IAH also causes pressure on thefemoral veins. This pressure increasesvenous stasis and the developmentof deep vein thrombosis. When theIAH is resolved, the risk of pulmonaryemboli increases.11

Central Nervous SystemStudies in animals and humans

have correlated the effects of IAHon intracranial pressure.18,19 TheMunro- Kellie hypothesis statesthat the cranium is a nondistensiblevault filled with brain tissue, cere-brospinal fluid, and blood.20 If 1 ofthe vault’s substances increases insize, the other 2 substances adjusttheir volume to compensate andmaintain equilibrium. Cerebro -spinal fluid and the brain’s venousdrainage both leave the brain viathe jugular vein.20 Elevations in IAPare transferred into the thoraciccompartment. Increased intratho-racic pressure puts back pressureon the jugular veins and decreasesdrainage of cerebrospinal fluid andblood, leading to increased intracra-nial pressure.18,20 In patients withincreased intracranial pressure, theeffects of IAH can cause a furtherincrease in the pressure in the cra-nium and decrease cerebral perfu-sion pressure.

be suggestive of acute lung injuryand lead to a shift to lung protectivestrategies and low tidal volumes.When acute lung injury is not pres-ent, but ACS is, low tidal volumes willnot improve the respiratory picture.16

However, in patients with ACS, acutelung injury or acute respiratory dis-tress syndrome can be a sequela.15

Cardiovascular SystemOne conundrum of IAH is the

effect of the abnormality on the car-diovascular system. The increasedintrathoracic pressure compressesthe heart and major vessels, causinga tamponade-like picture, especiallywith the higher grades of IAH. Cen-tral venous pressures (CVPs) andpulmonary artery wedge pressures(PAWPs) are fictitiously elevatedbecause of the effects of IAH.17 Theseelevations may lead clinicians tosurmise that a patient is volumeloaded or overloaded.

The components of cardiac out-put (ie, preload, afterload, and con-tractility) are all adversely affectedby increased IAH.17 Compression ofthe inferior vena cava causes adecrease in venous return to theheart, affecting preload and causinga decrease in cardiac output. Con-tractility is affected mainly by changesin right ventricular mechanics.17

The elevated intrathoracic pressurecaused by IAH also increases pul-monary vascular resistance andright ventricular afterload. The rightventricle is a thin-walled chamberthat normally acts as a passive con-duit in pumping blood to the leftside of the heart. In adapting to theincreased pulmonary vascular resist-ance, the right ventricle dilates andpushes the intraventricular septuminto the left ventricle. This situation



SummaryIn summary, IAH can affect

almost all body systems. IAH hasbeen proposed as the initial fall ofthe dominoes on the pathway ofmultisystem organ failure.11,21 ManuMalbrain,22 a past president ofWSACS from Belgium, states thatjust as researchers and clinicianshave focused on acute kidney injuryand acute kidney failure and onacute lung injury and acute respira-tory distress syndrome, they needto raise the concepts of IAH andACS to “acute bowel injury andacute intestinal distress syndrome.”

Measuring Intra-abdominalPressure

To manage patients with IAHappropriately, nurses must be cog-nizant of the proper procedure forIAP measurement. Hands-on assess-ment of the abdomen and serialmeasurements of abdominal girthare not sensitive or specific enoughto detect IAH.23,24 A distendedabdomen that has increased slowlyover time, as in chronic ascites orpregnancy, will not necessarily havean elevated IAP.23 Conversely, clini-cally important IAH can occur in theabsence of a distended abdomen withthe onset of an acute condition.23

Various methods are used fordirect and indirect measurementsof IAP.22 The gold standard of indi-rect measurement is measurementvia a urinary bladder catheter.2,11,23

Either a transducer technique or amanometer technique can be used.The tools to measure IAP are readilyavailable in any ICU,19,21 and special-ized kits can be purchased. Thetechniques and tools described herehave been deemed acceptable by theWSACS.4 The society does not

promote one device over another.The qualities a clinician should lookfor in a device for measuring IAPare reproducibility of results,patient and staff safety, effective-ness, ease of use, and cost. Accord-ing to Michael Cheatham, past

president of the WSACS, “The besttechnique is the one that you andyour nursing staff will use.”23

Transducer TechniqueFigure 3 is an illustration of the

transducer technique,25 and Table 3


Figure 3 Setup for transducer technique for measuring intra-abdominal pressure.The current guidelines recommend no more than 25 mL be instilled in the bladder. A 60-mL syringe is not recommended. Abbreviation: IV, intravenous.

Reprinted from Malbrain,25 with permission from Springer Science+Business Media.

IV Infusion Bag

To IV Infusion Bag

A

B

60 mL Syringe

60 mL Syringe

Ramp with 3 stopcocks

C CMM

1 2 3

To Monitor

PressureTransducer

PressureTubing

PressureTubing

FoleyCatheter

To Foley Catheter

UrineDrainage

Urine Drainage

NormalTubing


provides a list of the equipmentneeded and the procedure for setup.(Of note, Figure 3 was publishedbefore the recommendation wasmade to use only 25 mL at the mostfor instillation.) Figure 4 and Table4 provide information about analternative setup method. Theadvantages of the transducer tech-nique include no need for special-ized equipment, cost-effectiveness,and safety. Once the initial setup iscompleted, the system remains

to remove the clamp after the meas-urement to ensure flow of urine.

Two commercial kits are avail-able for the transducer method.The AbViser AutoValve (Wolfe ToryMedical, Inc, Salt Lake, Utah; Fig-ure 5) has a valve that automati-cally opens 1 to 3 minutes after thesaline has been instilled, adding ameasure of safety to this device.Another IAP transducer kit is theBard intra-abdominal pressuremonitoring device (Bard MedicalDivision, Covington, Georgia).Regardless of the transducer setupused, the way in which an IAPmeasurement is obtained shouldremain the same. WSACS recom-mends the procedure2,25,27 given inTable 5 and Figure 6.

Manometer TechniqueThe manometer technique is

similar to the method of measuringCVP with a fluid column. The patientshould have a urinary catheter inplace; the only equipment needed isa centimeter ruler. This technique iscalled the U-tube technique (Figure7) and is a modification of a tech-nique first developed by an emer-gency department nurse.23,25,28,29

Table 6 gives the steps for using thetechnique. The clinical validationwith the U-tube technique is poor,and the method is recommendedprimarily for screening.

Holtech Medical (Charlotten-lund, Denmark) has developed aurinary manometry tool (Figures 8and 9) that is simple to use and ismarked in millimeters of mercuryinstead of centimeters of water, sono conversion is needed. Studies23,25

with the Holtech device indicate thatit can provide reproducible, consis-tent, and accurate measurements.

closed, with minimal risk for urinarytract infection.26 Each measurementrequires less than 2 minutes of nurs-ing time, and the setup can be usedfor repetitive measurements for 2 to3 weeks.13,23,25 One drawback is thatthe stopcock system can be confus-ing, and if stopcock 3 is left in theoff-to-drainage position after a meas-urement is obtained, urinary drainagewill be obstructed. A patient safetyconcern with the specimen-portsetup is that nurses must remember


Table 3 Procedure for transducer setup with a manifold

Equipment needed

Indwelling urinary catheter with drainage bag

A manifold ramp with 3 stopcocks or 3 stopcocks connected to one another

Conical connectors for each end of the manifold

Sterile scissors

Disinfectant (povidone-iodine solution, chlorhexidine, or alcohol)

Sterile gloves

Sterile drape

Standard intravenous setup with a 500-mL container of normal saline

20- to 25-mL syringe

Transducer and pressure tubing

Setup

Using aseptic technique, set up the manifold system, container of normal saline, the 20-mL to 25-mL syringe, and the pressure tubing and transducer as shown inFigure 3.

A pressure bag connected to the pressure tubing is not required.

Open the intravenous fluid and flush the system.

Don sterile gloves and place the sterile drape so it is centered under the area wherethe catheter connects to the drainage tubing.

Cleanse the drainage tubing with an appropriate disinfectant from the connection tothe catheter to about 60 cm down the drainage tubing.

With the sterile scissors, cut the drainage tubing about 40 cm after the culture aspira-tion port and insert the stopcock ramp into the drainage tubing as shown in Figure 3.

To work the stopcocks to obtain a measurement, turn the first stopcock off to thepatient and on to the intravenous bag, and open the second stopcock to the syringe.

Aspirate 20 to 25 mL of the normal saline.

Turn the first stopcock off to the intravenous bag and on to the patient.

Turn the third stopcock on to the patient and transducer and off to the drainage tub-ing; instill the 20 mL of saline into the bladder.

After the measurement is obtained, ensure that stopcocks are turned so that urine canflow from the patient to the urinary drainage bag.


The advantage of the manome-try method is that it can be usedoutside the ICU. One concern is thatreinstillation of urine and salineinto the bladder can cause a urinarytract infection.30

The preceding techniques areused for intermittent measurements.A validated continuous techniquewith a 3-way urinary catheter hasbeen deemed acceptable byWSACS.23,25,31,32 Although the meas-urements with this third techniquemay be continuous, they would notbe considered accurate unless thepatient were supine with the headof the bed flat, and the abdominalmuscles relaxed. In essence, with thiscontinuous method, measurementscould only be obtained “intermit-tently,” because patients do need tobe turned, repositioned, and so on.


Infusionport

Normalsaline

Cableto monitor

Regularintravenous

tubing

TransducerAir

Flush

Clamp

Balloonport

To patient→

→

→

→

→

→

→

→

→

Catheter

To urinecollection bag

3-waystopcock

Pressuretubing

Urinespecimen

port

20-mLsyringe

→

→

→

→→ →

Table 4 Procedure for transducer setup with a specimen port

Equipment needed

Indwelling urinary catheter with drainage bag and needleless specimen port

Disinfectant (povidone-iodine solution, chlorhexidine, or alcohol)

Standard intravenous setup with 500 mL of normal saline

20- to 25-mL syringe

Transducer and pressure tubing

Clamp for urinary drainage tubing

Setup

Using aseptic technique, set up the manifold system, intravenous container of normalsaline, the 20- to 25-mL syringe, and the pressure tubing and transducer as shown inFigure 4.

A pressure bag connected to the pressure tubing is not required.

Open the intravenous fluid and flush the system.

Connect the pressure system setup to the needleless specimen port.

To obtain a measurement, clamp the urinary drainage tubing distal to the specimen port.

Aspirate 20 to 25 mL of the normal saline.

Instill 20 to 25 mL of normal saline.

After the measurement, ensure that the clamp is removed from the tubing.

Figure 4 Transducer setup with a specimen port.Sketch by Teri Weiser, RN.


Clinicians can check the WSACSWeb site (http://www.wsacs.org)for new evidence on acceptablemethods and devices for measuringIAP. Trying out the do-it-yourselfpressure-measuring devices andmanufacturers’ ready-made kits isalso recommended, so a consensusamong the collaborative team canbe made on which device to use forconsistency of practice.

Several caveats are associatedwith use of IAP monitoring via aurinary catheter. This method maybe contraindicated in patients whohave bladder surgery or trauma andmay not be reliable in patients whohave neurogenic bladder.25 In patientswith anuria, bladder pressure moni-toring can still be done if at least 20to 25 mL of saline is in the bladder.25

The difficulties of inserting a uri-nary catheter into a patient withanuria must be weighed against thebenefits of information that may beneeded to prevent ACS.25

Screening and Monitor ingOnce an IAP measuring device

has been decided on and put intopractice, nurses must know how tointerpret the measurements. Thecritical IAP can vary from patient topatient; an IAP of 15 mm Hg maybe tipping one patient over the edge,whereas another patient may toler-ate a persistent IAP of 20 mm Hg.The APP is a better marker ofabdominal organ perfusion than isIAP alone.4,33 Calculation of APP issimilar to that for cerebral perfusionpressure: MAP - IAP = APP. WSACS2

recommends that the APP be main-tained at greater than 60 mm Hg inpatients with IAH or ACS.

WSACS has developed guide-lines for screening and monitoring


Figure 5 AbViser Autovalve.Image courtesy Wolfe Tory Medical Inc, Salt Lake City, Utah.

Table 5 Procedure for measuring intra-abdominal pressure with the transducermethod

Position the patient supine with the head of the bed flat.

The patient should be quiet, not agitated, restless, coughing, or talking; ensure thatabdominal muscle contractions are absent.

Level transducer at the iliac crest in line with the midaxillary line and zero the trans-ducer. The transducer can be secured to the patient’s thigh or on a pole with a trans-ducer holder.

Draw up 20 to 25 mL of sterile normal saline via the intra-abdominal pressure moni-toring system, and instill it into the bladder. Instill for 10-15 seconds.

Wait 30 seconds before obtaining a measurement so that the bladder detrusor musclecan relax and the monitor can equilibrate.

Obtain the measurement at end expiration (which corresponds to the trough on theventilator patient’s respiration waveform, and the peak in a nonventilator patient'srespiration waveform) and record.

When measurement is completed, reposition patient to appropriate position for thepatient’s condition.

Deduct the amount of instilled saline from the patient’s urinary output.

Figure 6 Intra-abdominal pressure measurement by using the transducermethod. The top waveform is the central venous pressure (CVP) waveform of apatient undergoing mechanical ventilation. End expiration would be at the end ofthe CVP trough and is approximately 5 mm Hg. The intra-abdominal pressure islabeled as P2, and is approximately 22 to 24 mm Hg.


patients for IAH (Figure 10–availableonline only). In summary, any patientadmitted to a critical care unit or inwhom new organ failure developsshould be screened for risk factorsfor IAH and ACS. If a patient has atleast 2 of the risk factors, a baseline

IAP measurement should beobtained. In the study by Vidal et al,6

almost one-third of patients had IAHat the time of admission to the ICU,and the abnormality developed inanother one-third after admission.Perhaps, initially the U-tube method

could be used as a screening tool,and then once the IAP is greaterthan 12 mm Hg for 2 consecutivemeasurements, a more reliablemeasuring device should be used.Patients at risk for IAH or ACSshould have IAP measured at leastevery 4 to 6 hours.11 Patients withunstable hemodynamic status andpatients with rapidly deterioratingorgan dysfunction should have IAPmeasured hourly.11 IAP measure-ments can be discontinued once thecondition causing IAH has resolvedand the IAP has remained at 10 to12 mm Hg or less for 24 to 48 hours.11

A few of the risk factors identi-fied by WSACS need to be studiedmore closely. The Institute forHealthcare Improvement34 has rec-ommended the use of a sepsis bun-dle. Sepsis is already a risk factor forIAH. The goal-directed fluid therapythat is a part of this bundle addsanother risk factor (ie, >5 L of intra-venous fluid in 24 hours). Largeblood transfusions (>10 units ofpacked red blood cells in 24 hours)required by patients with trauma,ruptured abdominal aortic aneurysm,or gastrointestinal bleeding areanother risk factor. Burn patients,especially those with large areas ofabdominal eschar, are at risk forIAH because of the restriction ofthe abdominal wall by the escharand the large volumes of fluidneeded for fluid replacement.Therapeutic hypothermia for coma-tose survivors of cardiac arrest alsoputs patients at risk for IAH; boththe hypothermia and the fluidreplacement add to the possibilityof IAH. Adding measurement ofIAH as a part of protocols specifi-cally for these comatose patientsshould be considered.


Figure 7 U-tube technique. Used with permission of Demetrios Demetriades, MD.

Ruler raised 90°to patient

Foleycatheter

Zero

Level ofurine

To collectionchamber

Meniscus(height of the columnof urine from themeniscus to

symphysis pubis)

Ruler placed at levelof symphysis pubisand parallel to floor

Table 6 U tube method for the manometer technique

Obtain a centimeter ruler.

Position the patient supine with the head of the bed flat.

The patient should be quiet, not agitated, restless, coughing, or talking. Ensure that abdominal muscle contractions are absent.

Raise the urinary catheter above the patient, allowing a U-shaped loop to develop.

Level the connection site (the zero level) where the catheter meets the drainage tubing in line with the symphysis pubis.

The urine in the tubing should fluctuate with respirations.

Allow the fluid column to settle, and using the centimeter ruler, measure from the “zero” connection site to the meniscus of the fluid column.

Convert from centimeters of water to millimeters of mercury (1.00 cm H2O=0.74 mm Hg).

When measurement is completed, reposition patient to appropriate position for patient’s condition.


unconscious, or sedated should bechecked daily for fecal impactions.Abdominal radiographs and com-puted tomography reports shouldbe reviewed for evidence of impactedfeces. Maintaining the patency ofthe nasogastric tube and the rectaltube, if used, is important. Patients’tolerance to enteral feedings shouldbe assessed, and if residuals aregreater than accepted levels, theamounts administered should bedecreased or feedings should be dis-continued. IAH should be reevalu-ated as a possible cause of increasesin residual volumes. For patients whoare able to eat, gas-producing foodsshould be minimized or eliminated.Recommendations for evacuatingintra-abdominal space-occupyinglesions are part of the purview ofphysicians or advanced practicenurses. Bedside nurses ensure thatthe diagnostic studies are safely car-ried out and assist with any bedsideinterventional procedures.

Positioning patients to achievestability has been a mainstay ofacute and critical care nurses’ prac-tice. Recommendations to improveabdominal wall compliance includeavoiding the prone position andelevating the head of bed more than20º.36,37 Raising the head of the bedis a conflict with the recommenda-tions of the ventilator bundle toprevent ventilator-associated pneu-monia, which calls for elevating thehead of the bed at least 30º. Oneway to compromise is to placepatients in a reverse Trendelenbergposition. However, when IAP ismeasured, patients must be supinewith the head of the bed flat.

The recommendations to improveabdominal wall compliance are inter-disciplinary. Debriding of abdominal

CollaborativeManagement

Once IAH hasbeen detected ina susceptiblepatient, the goalis to decrease theIAP to 15 mm Hgor less, maintainthe APP at 60 mmHg or greater, andprevent ACS.2,11,13

The WSACS hasdeveloped a med-ical managementalgorithm2,35 basedon the causes ofIAH and thecondition of thepatient. The algo-rithm is set up inan escalating step-wise approach(Figure 11–avail-able online only).Many of the rec-ommendationsare specifically forphysicians andadvanced practicenurses, but manyare within thedomain of bed-side nurses.

Recommenda-tions for evacuat-ing intraluminalcontents includemonitoring andrecording dailybowel movementsand implementinga bowel protocolbefore a patientbecomes consti-pated. Patientswho are paralyzed,


Figure 8 Urinary manometry tool. Used with permission of Holtech Medical, Charlottenlund, Denmark.

Figure 9 Urinary manometry tool. Used with permission of Holtech Medical, Charlottenlund, Denmark.



eschar and removal of constrictiveabdominal dressings are advised.Patients who are in pain or are agi-tated should be given adequatedoses of analgesics and sedativesand should be assessed for relief.As a last resort, patients may needto be intubated and given paralyticagents to decrease the effects ofmuscle contraction on IAP.

Fluid replacement is a knownrisk factor for IAH, especially if apatient has capillary leak. Monitor-ing and recording daily intake andoutput and assessing cumulativefluid balance are important nursingactions in managing these patients.The recommendations for optimiz-ing fluid administration are toavoid excessive fluid administrationand to aim for a goal of an equal ornegative fluid balance by the thirdday in the ICU. If nurses have afluid replacement protocol to followand the protocol includes an optionto use colloids or crystalloids; thecolloids should be chosen. Mem-bers of the health care team shoulddiscuss possible use of hypertonicsaline in patients who have boweledema. Compared with crystal-loids, colloids and hypertonic salineappear to provide a better responsein patients with IAH and capillaryleak.11,38-40 Diuresis, continuousrenal replacement therapy, andhemodialysis are stepwise escalat-ing recommendations according tothe medical management algorithm(Figure 11–available online only).2

The last category in the medicalmanagement algorithm is optimiz-ing systemic and regional perfusion.Again, goal-directed fluid replace-ment is recommended. If the APPcannot be maintained at 60 mm Hgor greater with fluids, inotropes orvasopressors can be given. This cat-egory includes the need for hemo-dynamic monitoring to guide fluidreplacement. IAH causes fictitiouselevations in the CVP and PAWP. Tonegate this effect, the WSACS2 rec-ommends using the following cor-rection formula:

CVPcorrected = CVPmeasured – (IAP/2)PAWPcorrected = PAWPmeasured – (IAP/2)An example is as follows:

A patient has a measured CVP of15 mm Hg and an IAP of 20 mm Hg

CVPcorrected = 15 – (20/2) = 5 mm Hg

A patient has a measured PAWP of22 mm Hg and an IAP of 12 mm Hg

PAWPcorrected =22 – (12/2)=16 mm Hg

Because of the inaccuracies associ-ated with using these pressure val-ues, the WSACS2,41 recommendsusing volumetric indices such asstroke volume variation or pulsepressure variation.

If the escalating medical interven-tions do not decrease IAH or preventACS, a decompressive laparotomy isrecommended2 (Figure 12–availableonline only). Nurses need to preparepatients and patients’ family mem-bers for this emergent procedure,which may need to take place at thebedside. After the surgery, patientsoften have an open abdomen untilbowel edema subsides. IAP meas-urements should still be obtained.

It Is TimeWe are well into a new century.

The members of WSACS will not letthe concepts of IAP and ACS fade

away again. WSACS has been theimpetus to coalesce the critical carecommunity to identify and act onIAH and ACS. CCN

AcknowledgmentsThe author thanks Teri Weiser, RN, and SophieBoudreau, RN, BSN, CCRN, for their assistance inpreparing this manuscript.

Financial DisclosuresNone reported.

References1. Schein M. Abdominal compartment syn-

drome: historical background. In: Ivatury RR,Cheatham ML, Malbrain M, Sugrue M, eds.Abdominal Compartment Syndrome. George-town, TX: Landis Bioscience; 2006:1-7.

2. World Society of the Abdominal Compart-ment Syndrome. Mission statement. WorldSociety of the Abdominal CompartmentSyndrome Web site. http://www.wsacs.org.Accessed October 27, 2011.

3. Muckart DJJ, Ivatury RR, Leppaniemi A,Smith RS. Definitions. In: Ivatury RR,Cheatham ML, Malbrain M, Sugrue M, eds.Abdominal Compartment Syndrome. George-town, TX: Landis Bioscience; 2006:8-18.

4. Malbrain M, Cheatham M, Kirkpatrick A,et al. Results from the International Confer-ence of Experts on Intra-abdominal Hyper-tension and Abdominal CompartmentSyndrome, I: definitions. Intensive Care Med.2006;32(11):1722-1732.

5. Malbrain M, Chiumello D, Pelosi P, et al.Prevalence of intra-abdominal hypertensionin critically ill patients: a multicentre epi-demiological study. Intensive Care Med.2004;30:822-829.

6. Vidal MG, Weisser JR, Gonzalez F, et al. Inci-dence and clinical effects of intra-abdominalhypertension in critically ill patients. CritCare Med. 2008;36(6):1823-1831.

7. Reintam A, Parm P, Kitus R, Kern H,Starkopf J. Primary and secondary intra-abdominal hypertension—different impacton ICU outcome. Intensive Care Med. 2008;34(9):1624-1631.

8. Malbrain M. The Pathophysiologic Implica-tions of Intra-abdominal Hypertension in theCritically Ill. Antwerp, Belgium: KatholiekeUniversiteit Leuven; 2007.

9. Saladin K. Anatomy and Physiology: TheUnity of Form and Function. 4th ed. NewYork, NY: McGraw-Hill; 2007.

10. Ivatury RR, Diebel LN. Intra-abdominalhypertension and the splanchnic bed. In:Ivatury RR, Cheatham ML, Malbrain M,Sugrue M, eds. Abdominal CompartmentSyndrome. Georgetown, TX: Landis Bio-science; 2006:129-137.

11. Malbrain M, De Iaet IE. Intra-abdominalhypertension: evolving concepts. Clin ChestMed. 2009;30:45-70.

12. Wendon J, Biancofiore G, Auzinger G.Intra-abdominal hypertension and the liver.

To learn more about intra-abdominal pres-sure measurement, read “Revision of theProcedure for Monitoring Intra-abdominalPressure” by Rhonda Anderson in CriticalCare Nurse, October 2007;27:67-70. Availableat www.ccnonline.org.

Now that you’ve read the article, create or contributeto an online discussion about this topic using eLetters.Just visit www.ccnonline.org and click “Submit aresponse” in either the full-text or PDF view of thearticle.



In: Ivatury RR, Cheatham ML, Malbrain M,Sugrue M, eds. Abdominal CompartmentSyndrome. Georgetown, TX: Landis Bio-science; 2006:138-143.

13. Malbrain M, Deeren D, De Potter T. Intra-abdominal hypertension in the critically ill:it is time to pay attention? Curr Opin CritCare. 2005;11:156-171.

14. Sugrue M, Hallal A, D’Amours S. Intra-abdominal hypertension and the kidney. In:Ivatury RR, Cheatham ML, Malbrain M,Sugrue M, eds. Abdominal CompartmentSyndrome. Georgetown, TX: Landis Bio-science; 2006:119-128.

15. Mertens zur Borg IRAM, Verbrugge SJC,Olvera CI. Intra-abdominal hypertensionand the respiratory system. In: Ivatury RR,Cheatham ML, Malbrain M, Sugrue M, eds.Abdominal Compartment Syndrome. George-town, TX: Landis Bioscience; 2006:105-118.

16. Lui F, Sangosanya A, Kaplan LJ. Abdominalcompartment syndrome: clinical aspects andmonitoring. Crit Care Clin. 2007;23:415-433.

17. Cheatham ML, Malbrain M. Intra-abdomi-nal hypertension and the cardiovascularsystem. In: Ivatury RR, Cheatham ML, Mal-brain M, Sugrue M, eds. Abdominal Com-partment Syndrome. Georgetown, TX:Landis Bioscience; 2006:89-104.

18. Citerio G, Berra L. Intra-abdominal hyper-tension and the central nervous system. In:Ivatury RR, Cheatham ML, Malbrain M,Sugrue M, eds. Abdominal CompartmentSyndrome. Georgetown, TX: Landis Bio-science; 2006:144-156.

19. Scalea TM, Grant BV, Habashi N et al.Increased intra-abdominal, intrathoracic,and intracranial pressure after severe braininjury: multiple compartment syndrome.J Trauma. 2007;62 (3):647-656.

20. Ropper AH, Samuels MA. Disturbances ofcerebrospinal fluid and its circulationincluding hydrocephalus, pseudotumorcerebri, and low-pressure syndromes. In:Adams and Victor’s Principles of Neurology.9th ed. New York, NY: McGraw-Hill Med-ical; 2009:529-545.

21. Raeburn CD, Moore EF. Abdominal com-partment syndrome provokes multipleorgan failure: animal and human support-ing evidence. In: Ivatury RR, Cheatham ML,Malbrain M, Sugrue M, eds. AbdominalCompartment Syndrome. Georgetown, TX:Landis Bioscience; 2006:157-169.

22. Malbrain M, De Iaet I. AIDS is coming toyour ICU: be prepared for acute bowel injuryand acute intestinal distress syndrome . . .Intensive Care Med. 2008;34(9):1565-1569.

23. Malbrain M, Jones F. Intra-abdominal pres-sure measurement techniques. In: Ivatury RR,Cheatham ML, Malbrain M, Sugrue M, eds.Abdominal Compartment Syndrome. George-town, TX: Landis Bioscience; 2006:19-68.

24. Malbrain M, De Iaet I, Van Regenmortel N,Schoonheydt K, Dits H. Can the abdominalperimeter be used as an accurate estimateof intra-abdominal pressure? Crit Care Med.2009;37(1):316-319.

25. Malbrain M. Different techniques to meas-ure intra-abdominal pressure (IAP): timefor a critical re-appraisal. Intensive Care Med.2004;30:357-371.

26. Cheatham ML, Sagraves SG, Johnson JL,White MW. Intravesicular pressure moni-toring does not cause urinary tract infection.Intensive Care Med. 2006;32:1640-1630.

27. De Waele JJ, De Iaet I, De Keulenaer B, et al.

The effect of different reference transducerpositions on intra-abdominal pressuremeasurement: a multicenter analysis. Inten-sive Care Med. 2008;34:1299-1303.

28. Harrahill M. Intra-abdominal pressure mon-itoring. J Emerg Nurs. 1998;24(5):465-466.

29. Asensio JA, Ceballos J, Forno W, Sava J.Intra-abdominal pressure monitoring. In:Shoemaker W, Velmahos GC, DemetriadesD, eds. Procedures and Monitoring for theCritically Ill. Philadelphia, PA: WB SaundersCo; 2002:99-103.

30. Lo E, Nicolle L, Classen D, et al. Strategies toprevent catheter-associated urinary tract infec-tions in acute care hospitals. Infect ControlHosp Epidemiol. 2008;29(suppl 1):S41-S50.

31. Zengerink I, McBeth P, Zygun DA, et al.Validation and experience with a simplecontinuous intra-abdominal pressure meas-urement technique in a multidisciplinarymedical/surgical critical care unit. J Trauma.2008;64:1159-1164.

32. Balogh Z, Jones F, D’Amours S, Parr M,Sugrue M. Continuous intra-abdominalpressure measurement technique. Am JSurg. 2004;188:679-684.

33. Cheatham M, Malbrain M. Abdominal per-fusion pressure. In: Ivatury RR, CheathamML, Malbrain M, Sugrue M, eds. Abdomi-nal Compartment Syndrome. Georgetown,TX: Landis Bioscience; 2006:69-81.

34. Institute for Healthcare Improvement. Sep-sis resuscitation bundle: fluid management.Institute for Healthcare Improvement Website. http://www.ihi.org/knowledge/Pages/Changes/TreatHypotensionandorElevatedLactatewithFluids.aspx. Accessed Novem-ber 28, 2011.

35. Cheatham M. Nonoperative managementof intra-abdominal hypertension andabdominal compartment syndrome. WorldJ Surg. 2009;33(6):1116-1122.

36. McBeth PB, Zygun DA, Widder S, et al.Effect of patient positioning on intra-abdominal pressure monitoring. Am J Surg.2007;193:644-647.

37. Cheatham ML, De Waele JJ, De Laet I, et al.The impact of body position on intra-abdominal pressure measurement: a multi-center analysis. Crit Care Med. 2009;37(7):2187-2190.

38. Oda J, Ueyama M, Yamashita K, et al. Hyper-tonic lactated saline resuscitation reduces therisk of abdominal compartment syndrome inseverely burned patients. J Trauma. 2006;60:64-71.

39. O’Mara MS, Slater H, Goldfarb IW, et al. Aprospective randomized evaluation of intra-abdominal pressure with crystalloid andcolloid resuscitation in burn patients.J Trauma. 2005;58:1011-1018.

40. Cheatham ML, Malbrain M, Kirkpatrick A.Results from the International Conferenceof Experts on Intra-abdominal Hyperten-sion and Abdominal Compartment Syn-drome, II: recommendations. Intensive CareMed. 2007;33(6):951-962.

41. Renner J, Gruenewald M, Quaden R, et al.Influence of increased intra-abdominalpressure on fluid responsiveness predictedby pulse pressure variation and stroke vol-ume variation in a porcine model. Crit CareMed. 2009;37(2):650-658.


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