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In Practice

Intra-abdominal Hypertension and Abdominal

Compartment Syndrome
Jan J. De Waele, MD, PhD,1 Inneke De Laet, MD,1,2
Andrew W. Kirkpatrick, MD, FRCSC,3,4,5 and Eric Hoste, MD, PhD1

Increased intra-abdominal pressure (IAP), also referred to as intra-abdominal hypertension (IAH), affects
organ function in critically ill patients and may lead to abdominal compartment syndrome (ACS). Although
initially described in surgical patients, IAH and ACS also occur in medical patients without abdominal
conditions. IAP can be measured easily and reliably in patients through the bladder using simple tools. The
effects of increased IAP are multiple, but the kidney is especially vulnerable to increased IAP because of its
anatomic position. Although the means by which kidney function is impaired in patients with ACS is
incompletely elucidated, available evidence suggests that the most important factor involves alterations in
renal blood flow. IAH should be considered as a potential cause of acute kidney injury in critically ill patients; its
role in other conditions, such as hepatorenal syndrome, remains to be elucidated. Because several treatment
options (both medical and surgical) are available, IAH and ACS should no longer be considered irrelevant
epiphenomena of severe illness or critical care. An integrated approach targeting IAH may improve outcomes
and decrease hospital costs, and IAP monitoring is a first step toward dedicated IAH management. IAH
prevention, most importantly during abdominal surgery but also during fluid resuscitation, may avoid ACS
altogether. However, when ACS occurs and medical treatment fails, decompressive laparotomy is the only
Am J Kidney Dis. 57(1):159-169. © 2010 by the National Kidney Foundation, Inc.

INDEX WORDS: Intra-abdominal pressure; abdominal compartment syndrome; intra-abdominal hypertension;

acute kidney injury.

CASE PRESENTATION charged from the ICU on postoperative day 29. By this point,
kidney function had completely recovered.
A 37-year-old man was admitted to the intensive care unit (ICU)
because of alcohol-induced severe acute pancreatitis. His abdomi-
nal pain had started 2 days before presentation. On admission, the INTRODUCTION
patient was dyspneic and hypotensive and reported abdominal For several decades, increased IAP has been increas-
pain. He required massive fluid resuscitation for hemodynamic
stabilization. APACHE II (Acute Physiology and Chronic Health ingly recognized as both cause and consequence of
Evaluation II) score on admission was 20, and Ranson score after many adverse events in critically ill patients. In-
48 hours was 8. The patient required intubation 2 days after creased IAP within the closed anatomic volume of the
admission because of acute respiratory distress syndrome. Despite abdominal cavity can lead to decreased perfusion and
aggressive ventilatory strategies, his oxygenation remained tenu- ischemia of intra-abdominal organs. In addition, in-
ous and urine output progressively decreased despite aggressive
fluid therapy. Serum creatinine level at admission was 0.79 mg/dL creased IAP also leads to physiologic changes and
(69.84 ␮mol/L) and had increased to 5.05 mg/dL (446.42 ␮mol/L) organ dysfunction beyond the abdominal cavity be-
when intubation was required. cause of the close anatomic relationships with contigu-
Transvesicular intra-abdominal pressure (IAP) monitoring (us- ous cavities. Depending on the severity of increased
ing a self-assembled set based on the Cheatham technique1) was IAP and organ function, the condition is defined as
initiated shortly after admission. Initially, IAP was moderately
increased (13 mm Hg) and increased steadily, reaching a maxi- intra-abdominal hypertension (IAH) or ACS (Box 1).
mum of 27 mm Hg 3 days after admission. In the setting of
multiorgan failure, the diagnosis of abdominal compartment syn-
drome (ACS) was established. From the 1Department of Critical Care Medicine, Ghent Univer-
Because of the inability to maintain oxygenation, hemodynamic sity Hospital, Ghent; 2Intensive Care Unit, ZiekenhuisNetwerk
instability, and decreased kidney function, formal surgical abdomi- Antwerpen, Campus Stuivenberg, Antwerp, Belgium; and 3Re-
nal decompression was performed 70 hours after admission. IAP gional Trauma Services and Departments of 4Surgery and 5Criti-
immediately decreased to 14 mm Hg, and within minutes, respira- cal Care Medicine, Calgary Heatlh Region and Foothills Medical
tory and hemodynamic function improved, with urine output Centre, Calgary, Alberta, Canada.
increasing during the next few hours from 5 to 40 mL/h. Despite Received April 7, 2010. Accepted in revised form August 25,
this improved diuresis, renal replacement therapy was required and 2010.
continued for a total of 26 days. Address correspondence to Jan J. De Waele, MD, PhD, Depart-
The patient’s condition improved initially, but ongoing inflam- ment of Critical Care Medicine, Ghent University Hospital, De
mation necessitated pancreatic necronectomy 16 days after the Pintelaan 185, 9000 Gent, Belgium. E-mail:
initial decompressive laparotomy. Postoperative continuous lavage © 2010 by the National Kidney Foundation, Inc.
using abdominal drains and 2 additional surgical interventions for 0272-6386/$36.00
intra-abdominal infection were required before he could be dis- doi:10.1053/j.ajkd.2010.08.034

Am J Kidney Dis. 2011;57(1):159-169 159

De Waele et al

Box 1. Excerpts of Consensus Definitions Regarding and ACS and discuss the available medical and surgi-
IAH and ACS cal treatment options if ACS cannot be prevented.
● Definition 1: IAP is the steady-state pressure concealed Finally, the effects of IAH on the kidney are addressed
within the abdominal cavity. comprehensively.
● Definition 7: IAH is defined by a sustained or repeated
pathologic increase in IAP ⱖ12 mm Hg. DEFINITIONS AND ETIOLOGY
● Definition 8: IAH is graded as follows: grade I, IAP 12-15
mm Hg; grade II, IAP 16-20 mm Hg; grade III, IAP 21-25 mm IAH is defined as sustained or repeated IAP ⱖ12
Hg; grade IV, IAP ⬎25 mm Hg. mm Hg and is divided into 4 grades (Box 1). The
● Definition 9: ACS is defined as a sustained IAP ⬎20 mm Hg
clinical picture involving sustained IAP ⱖ20 mm Hg
(with or without APP ⬍60 mm Hg) that is associated with new
organ dysfunction/failure. with the development of new organ dysfunction or
● Definition 10: Primary ACS is a condition associated with failure constitutes ACS. ACS can be categorized as
injury or disease in the abdominal-pelvic region that fre- primary ACS (referring to an intra-abdominal cause),
quently requires early surgical or interventional radiologic secondary ACS (extra-abdominal cause), and recur-
rent ACS (recurrence despite previous treatment).2
● Definition 11: Secondary ACS refers to conditions that do
not originate from the abdominal-pelvic region. Normal IAP is ⬃5-7 mm Hg, with baseline levels
● Definition 12: Recurrent ACS refers to the condition in which in morbidly obese individuals often ranging from
ACS redevelops after previous surgical or medical treatment 9-14 mm Hg.10 Although this degree of IAH may
of primary or secondary ACS. affect organ function in other patients, it often appears
Abbreviations: ACS, abdominal compartment syndrome; APP, to be tolerated in obese individuals. Normal IAP
abdominal perfusion pressure; IAH, intra-abdominal hyperten- usually is lower in children.11 In general, an indi-
sion; IAP, intra-abdominal pressure. vidual patient’s physiologic state must be taken into
Adapted and reproduced from Malbrain et al2 with permission
account when interpreting IAP measurements. IAP
of Springer Science ⫹ Business Media.
typically is expressed in millimeters of mercury and
The harmful consequences of increased IAP ini- conversion from centimeters of water may be neces-
tially were reported more than 100 years ago, and sary (1 mm Hg ⫽ 1.36 cm H2O).
effects on the kidney were among the first described. IAH usually is associated with situations in which
In 1876, Wendt3 reported that an increase in IAP was either increased abdominal volume or decreased ab-
associated with a decrease in urine output, and in dominal compliance may predominate, and often a
1947, Bradley and Bradley4 published a comprehen- combination of the 2 is to blame. The World Society
sive experimental article describing the effect of IAP of the Abdominal Compartment Syndrome (WSACS)
on kidney perfusion and function. Several investiga- recently listed conditions associated with these situa-
tors have since noted similar effects in animal mod- tions (Box 2).2
els5 and clinical studies in the critically ill.6,7 Presum-
ably because measurement of IAP was cumbersome Box 2. Conditions Associated With IAH and ACS
and clinicians were unaware of the dangers, clinical ● Increased intra-abdominal volume
effects of IAP were not reported again until the early 〫 Gastrointestinal tract dilatation: gastroparesis and gastric
1980s. It was not until the landmark report by Kron et distention, ileus, volvulus, colonic pseudo-obstruction
al,8 which reported that IAP could be monitored 〫 Intra-abdominal or retroperitoneal masses, eg, abdominal
objectively and relatively easily through an indwell-
〫 Ascites or hemoperitoneum
ing intravesical catheter, that more clinical evidence 〫 Pneumoperitoneum, eg, during laparoscopy
was rapidly forthcoming concerning the deleterious ● Decreased abdominal wall compliance
effects of increased IAP on different organ systems. 〫 Abdominal surgery, especially with tight abdominal clo-

Since then, the clinical importance of IAH and ACS sures

〫 Abdominal wall bleeding or rectus sheath hematomas
essentially has been rediscovered, largely by physi-
〫 Surgical correction of large abdominal hernias, gastroschi-
cians and surgeons taking care of the sickest of the sis, or omphalocele
sick in the ICU. This rediscovery also reflects in part ● Combination of decreased abdominal wall compliance and
an increasing incidence of IAH and ACS in critically increased intra-abdominal volume
ill patients who were treated more aggressively than 〫 Obesity
〫 Sepsis, severe sepsis, and septic shock
ever before, both peri- and intraoperatively and in the
〫 Severe acute pancreatitis
ICU. However, changes in organ function in patients 〫 Massive fluid resuscitation
undergoing laparoscopic surgery have shown that 〫 Major burns (with or without abdominal eschars)
even at lower pressures in the range of 12-20 mm Hg, 〫 Complicated intra-abdominal infection

IAH is relevant and affects organ function.9 Abbreviations: ACS, abdominal compartment syndrome; IAH,
In this article, we review the definitions and epide- intra-abdominal hypertension
miologic and pathophysiologic characteristics of IAH Source: Malbrain et al.2

160 Am J Kidney Dis. 2011;57(1):159-169

Intra-abdominal Hypertension and AKI

IAP MEASUREMENT known risk factors, the monitoring equipment avail-

Surveys of clinicians have shown that many con- able, and nursing staff experience and should be
tinue to rely on physical examination to diagnose linked directly to a local treatment protocol.18 It is
ACS.12,13 However, studies have shown that clinical recommended that patients with any of the conditions
assessment of IAP based on either abdominal diam- associated with IAH (Box 2) are monitored using a
eter or palpation of the abdomen is unreliable; accord- transvesicular technique at least every 4 hours until
ingly, more objective measures are recommended to IAP remains ⬍12 mm Hg for at least 24 hours in the
screen for and diagnose IAH/ACS.14,15 Reliable IAP absence of organ dysfunction.
measurement is the first step in the appropriate clini-
cal management of patients with IAH/ACS. There- EPIDEMIOLOGY
fore, various methods for IAP measurement have The “rediscovery” of IAH and ACS in the early
been developed,16 which stem from the concept that 1980s was related largely to techniques used in pa-
the abdominal cavity is a closed system.2 It follows tients after emergency abdominal surgery and
that the pressure found at any point within the abdomi- trauma.20 In the setting of massive resuscitation with
nal cavity indicates the pressure throughout the cavity, crystalloid fluids, the clinical picture of IAH and ACS
in accordance with Pascal’s law,17 which states that may be dramatic, with severe and often irreversible
pressure on liquid in a container will disperse equally organ damage. In subsequent years, it has increasingly
to all parts of the container. Accordingly, IAP can be been recognized that many other patients in the ICU,
measured from any space within the abdomen. To be both adult and pediatric, are affected by IAH/ACS,
accurate in humans, pressure within the abdominal with scenarios including elective surgical procedures,
cavity also is influenced by gravity and dependent on liver transplant,21 massive fluid resuscitation for extra-
the density of the fluid within, resulting in a pressure abdominal trauma,22 septic shock,23 severe acute pan-
gradient from anterior to posterior when the patient is creatitis,24 and severe burns,25 although it is likely
in the supine position. that almost any critical illness may be a precipitant.
IAP can be measured either directly (through needle The reported incidence rates of IAH and ACS vary
puncture of the abdomen during peritoneal dialysis considerably based on the patient population, and
treatment or laparoscopy) or indirectly (using intrave- selection bias may affect these reports. Table 1 lists
sicular pressure as measured through a bladder cath- reported incidence rates. In intensive care popula-
eter or gastric pressure through a balloon catheter). tions, IAH is associated with adverse outcomes, includ-
Transvesicular measurement of IAP currently is the ing organ dysfunction and mortality,34-36 with studies
most popular technique, and several systems with or that differentiate between primary and secondary IAH
without the need for electronic equipment are avail- describing worse outcomes for patients with second-
able that allow IAP measurement in a non-ICU envi- ary ACS than with primary ACS.
ronment.18 All transvesicular IAP measurement tech- As the use of preventive strategies in the surgical
niques are based on the same principle; namely, that a and trauma setting for ACS increases, epidemiologic
fluid column in the bladder catheter and tubing to the characteristics may change significantly. This may be
collector serve as a pressure transducing medium. The especially relevant in trauma and abdominal surgery,
pressure in this closed system can be measured either in which prophylactic laparostomy (or open abdomen
by means of an electronic system using a pressure
transducer or by measuring the height of the fluid
Table 1. Reported Incidence of IAH and ACS in
column in the tubing. More information regarding the Contemporary Literature
different methods to measure IAP, including the pros
and cons of each technique, can be found in a number IAH (%) ACS (%)
of recent articles2,16,19 or on the WSACS website
Major abdominal surgery26-28 NA 33-41
Liver transplant29 NA 31
To facilitate understanding in communication and
Major trauma30-33 50 13-36
research, standardized methods and definitions are
ICU35-37 30-54 5-12
crucial. Therefore, per consensus, IAP is measured (in
Septic shock23,38 51-76 33
millimeters of mercury) at end-expiration; the patient
Severe acute pancreatitis24 59-84 25-56
should be supine and refrain from spontaneous muscle
contractions. The midaxillary line is used as the zero Note: Values shown are incidence or range (both in percent-
age). Different definitions have been used to describe both IAH
reference level for IAP measurement. Methods for
and ACS in most of the studies.
continuous IAP measurement also are available, but Abbreviations: ACS, abdominal compartment syndrome; IAH,
are not yet widely used.19 It is advised that IAP intra-abdominal hypertension; ICU, intensive care unit; NA, not
monitoring be based on a (site-specific) protocol, available.

Am J Kidney Dis. 2011;57(1):159-169 161

De Waele et al

treatment) has become the standard of care in patients sion, now considered to be an important element, was
at risk of ACS. Therefore, primary ACS probably will not always reported, the very high IAP before decom-
occur less frequently in our ICUs, and secondary pression suggests that the injurious process may have
ACS, a condition largely associated with massive been progressing for longer periods. Accordingly,
fluid resuscitation, may become more prominent. acute tubular necrosis may have developed, poten-
Whether the present evolution away from massive tially explaining the variable results. Beneficial ef-
crystalloid resuscitation fluids influences this predic- fects of nonsurgical treatment options have been de-
tion remains to be seen. scribed, including improvement after abdominal
paracentesis in patients with hepatorenal syndrome42,43
IAH AS A RISK FACTOR FOR ACUTE and after the administration of neuromuscular block-
The presence of IAH as a risk factor for acute Similar to recent consensus for a classification
kidney injury (AKI) has been shown in many clinical system for AKI, IAH now also has a more systematic
settings. After emergency abdominal surgery, IAH definition and grading system.45,46 Until 5 years ago,
occurs in 33%-41% of patients and is associated with the impact of less severe IAH on AKI was virtually
AKI and mortality.26,28 Similarly, in patients undergo- unrecognized. We are hopeful that the systematic
ing orthotopic liver transplant, Biancofiore et al21 application of both IAH severity classes, as well as
reported not only an incidence of IAH (defined as IAP AKI stages (using RIFLE or AKIN [Acute Kidney
⬎25 mm Hg) of 32%, but also a linear relationship Injury Network] criteria), may increase knowledge
between IAH and severity of decreased kidney func- and awareness of the impact of earlier phases of IAH
tion. These somewhat dated studies used definitions and less severe IAH on kidney function, as well as
with low sensitivity for both IAH and AKI. In recent lead to more early and efficacious interventions.
years, several investigators have shown similar rela-
tionships between IAH and AKI in the ICU popula- PATHOPHYSIOLOGY
tion using newer grading systems. Dalfino et al37
studied 123 consecutive patients (almost half were IAH can negatively affect the function of organs
medical patients) admitted to a general ICU for at both inside and outside the abdominal cavity. In this
least 24 hours, finding that 30% of the study popula- review, we focus on the pathologic process that has
tion developed IAH. IAP of 12 mm Hg was the most direct implications on the clinical care of the critically
optimal cutoff for AKI defined using the RIFLE (risk, ill or injured in this section, with the specific effects of
injury, failure, loss, end-stage disease) classification IAH on the kidney extensively reviewed in the next
(sensitivity, 91%; specificity, 67%; area under the section.
receiver operating characteristic curve, 0.85). In this Several factors account for the effects of IAH on
cohort of unselected ICU patients, IAH also was an the cardiovascular system, all of which ultimately
independent risk factor for the development of AKI decrease cardiac output, even if systemic blood pres-
(odds ratio, 2.44). sure is not obviously affected.47 First, reflecting cra-
More recently, IAH also has been reported to com- nial displacement of the diaphragm during IAH, in-
plicate kidney transplant. Pertek et al39 reported 4 trathoracic pressure is increased. Both animal
patients with increased IAP who developed early experiments and studies of humans show that 20%-
transplant dysfunction and subsequently were treated 80% of IAP is transferred to the thorax,48 resulting in
successfully using abdominal decompression. Simi- compression of the heart and a decrease in end-
larly, Ball et al40 described retroperitoneal compart- diastolic volume. Moreover, cardiac preload also is
ment syndrome, a subtype of secondary ACS, in 11 reduced because of a decrease in venous return from
transplant patients. Presumably because of early rec- the abdomen (and possibly also the lower limbs).17
ognition, all patients were treated successfully using Third, because of direct compression of vascular
decompression. beds, systemic afterload initially is increased. Finally,
These studies suggest a clear link between IAH and generalized vasoconstriction occurs, likely reflecting
the development of AKI. In addition, evidence regard- activation of the sympathetic nervous system and
ing the impact of IAH comes from studying the effect renin-angiotensin-aldosterone system, the latter pre-
of IAP-lowering interventions. In a review of 10 sumably caused by decreased blood flow to the kidney
studies reporting IAP before and after decompressive associated with IAH.49-52 Although mean arterial blood
laparotomy, IAP decreased from 35 to 16 mm Hg. pressure (MAP) may increase at first because of blood
Although these studies showed an inconsistent effect moving out of the abdominal cavity, it soon stabilizes
on kidney function, postdecompression urinary output or decreases.47,53 In critically ill and ventilated pa-
increased in most.41 Although the timing of decompres- tients, these cardiovascular manifestations are wors-

162 Am J Kidney Dis. 2011;57(1):159-169

Intra-abdominal Hypertension and AKI

ened by hypovolemia and use of positive end- Hemodynamic Effects

expiratory pressure.54-58 Blood flow both to and from the kidney is impaired
The increase in intrathoracic pressure also effec- in patients with IAH because IAH decreases cardiac
tively increases all manometric measurements ob- output (to a variable extent),71 leading to decreased
tained in the thorax, including central venous pres- arterial blood flow to the kidney. However, decreased
sure, pulmonary artery occlusion pressure, and cardiac output likely is not the primary cause of
pulmonary artery pressure. Thus, the measured values IAH-AKI because animal experiments have shown
may have different interpretations than they would in that correction of cardiac output by volume loading
an individual without IAH. This finding has important does not prevent IAH-AKI.72,73 However, the role of
implications if not considered. The Surviving Sepsis volume status remains unclear because one study
Campaign guidelines recommend that resuscitation showed a beneficial effect on kidney function after
target a central venous pressure of 8-12 mm Hg59; volume expansion.74 Possibly this observed benefit
based on the physiologic process discussed, higher may occur in only extreme volume depletion.
targets should be used in patients with IAH.60 The In addition to decreased cardiac output and sys-
respiratory system also is affected by the transmission temic perfusion, local arterial inflow to the kidney
of IAP to the thorax61 because IAH decreases total may be impaired by IAH. Highlighting the impor-
respiratory system compliance (by a decrease in chest tance of IAP to kidney perfusion, kidney perfusion
wall compliance) at the same time that lung compli- pressure can be defined as MAP minus IAP. There-
ance is essentially constant.62 This leads to increased fore, in theory, decreased kidney function can be
inspiratory pressures or decreased tidal volumes, de- prevented by either decreasing IAP or increasing
pending on the mode of mechanical ventilation, such MAP, either of which will increase kidney perfusion
that increased positive end-expiratory pressure may pressure.72,75 Ulyatt76 suggested that filtration gradi-
ent (FG) is a more appropriate parameter to explain
be required to adequately oxygenate patients with
AKI associated with IAH. FG reflects the balance
IAH and ACS. Moreover, both animal studies and
between hydrostatic forces in glomerular capillaries
studies of humans have suggested a direct relationship
that promote fluid transfer into Bowman space and
between IAP and intracranial pressure.53-65 A number oncotic forces that promote transfer into glomerular
of previous publications have argued that the increase capillaries. In normal physiologic states, hydrostatic
in intracranial pressure arising from IAH is explained pressure in Bowman space (and therefore in the proxi-
by increased intrathoracic pressure, which results in mal tubules) is negligible, promoting glomerular filtra-
increased central venous pressure and decreased ve- tion; accordingly, glomerular filtration pressure can
nous return from the brain and subsequent venous be approximated as equal to kidney perfusion pres-
congestion and brain edema.17 Refractory intracranial sure and thus equal to MAP – IAP. However, in the
hypertension has been treated successfully using ab- presence of IAH, Bowman space and proximal tubu-
dominal decompression or neuromuscular block- lar pressure will be close to IAP; therefore, FG can be
ers.63,66 approximated as FG ⫽ MAP – (2 ⫻ IAP), assuming
Because pressures are well transmitted through- that autoregulation of glomerular perfusion is not
out the thoracoabdominal cavities, intra-abdominal present. Although mechanistically attractive, no clini-
organs beyond the kidney also are affected: IAH cal evidence presently supports this hypothesis for the
causes diminished perfusion of all intra-abdominal development of IAH-AKI.
organs, including the gut, liver, and pancreas, and Several studies also have focused on the influence
causes mucosal acidosis.67 ACS leads to splanchnic of IAH on venous kidney blood flow. In animal
hypoperfusion that may occur without hypotension models, IAH leads to increased venous pressure and
or decreased cardiac output. As shown in animal decreased venous blood flow, which also leads to
experiments, this may lead to increased mucosal decreased renal arterial blood flow and decreased
permeability and bacterial translocation, particu- perfusion of the renal cortex.77,78
larly when it occurs with ischemia-reperfusion in-
Direct Effects on the Kidney and Ureter
Another study by Doty et al75 of the influence of
increased parenchymal pressure in the kidney found
that direct parenchymal compression had no effect on
Because of its location deep within the posterior cardiac output, MAP, renal blood flow, or inulin
retroperitoneal space, the kidney is especially vulner- clearance. Interestingly, Stone and Fulenwider79 sub-
able to the deleterious effects of increased IAP result- jected animal kidneys to ischemia by aortic cross-
ing in AKI (IAH-AKI). clamping and decapsulating 1 kidney. After 8-20 days,

Am J Kidney Dis. 2011;57(1):159-169 163

De Waele et al

the capsulated kidney had significantly less kidney func- further exacerbating kidney impairment. However,
tion than the decapsulated contralateral kidney. This led several investigators have hypothesized that IAH may
to the term renal compartment syndrome and suggests be an important contributing factor in the pathogene-
that parenchymal compression may be an important sis of hepatorenal syndrome, with observations in
contributor to AKI when it is applied in an injured small studies that paracentesis and parenteral adminis-
kidney that is subjected to ischemia-reperfusion injury tration of albumin may lead to improved kidney
(which may better reflect clinical IAH). Finally, IAH is function in critically ill patients with cirrhosis admit-
not believed to lead to postrenal AKI through ureteral ted with variceal bleeding, as well as in stable patients
compression because placement of ureteral stents has with hepatorenal syndrome.42,85 These findings war-
not resolved IAH-AKI.80 rant further study.
Unfortunately, the kidney vasculature is not readily
accessible for monitoring in a clinical setting, which MANAGEMENT OF IAH AND ACS
has been a major obstacle for both clinical research Tremendous progress has been made in the manage-
and bedside monitoring. Bedside ultrasound measure- ment of IAH and ACS. For a long time, surgical
ments of renal artery resistance index have been decompression was considered the only option for
suggested as a monitoring tool.43,81 patients who developed overt ACS and that IAH was
an irrelevant epiphenomenon of critical care. How-
IAH IN CLINICAL NEPHROLOGY PRACTICE: ever, in a prospective study, Cheatham and Safcsak86
SUMMARY POINTS found that an integrated and diligent approach to
comprehensively manage IAH/ACS led to decreased
AKI in Critically Ill Patients
mortality, earlier and higher abdominal closure rates,
Given the frequency of IAH in critically ill patients, and decreased costs. Whereas the earlier focus often
the dose-dependent effect of IAH on kidney function, was on the end stage of IAH, namely full-blown ACS,
and the identification of IAH as an independent risk this study was the first to show that aggressively
factor for AKI,37 IAH should be considered in every managing IAH in patients at highest risk can improve
patient with AKI in the ICU. When IAH is present in outcomes. Accordingly, contemporary management
an oliguric patient, fluid resuscitation can be contin- of patients with IAH/ACS is based on 4 elements (Fig
ued, but IAP should be monitored carefully and crys- 1): IAP measurement, prevention, medical manage-
talloid use should be avoided or limited. Specific ment, and surgical management.
medical treatment options to decrease IAP should be
considered (discussed later). IAP Monitoring
An essential first step in management is early
Kidney Transplant recognition of IAH.87 The only way to accomplish
As discussed, it has been reported that IAH also this is through awareness of IAH as an important
may complicate kidney transplant, but may be treated clinical condition, and then by monitoring IAP in
successfully using decompression.39,40 Mesh abdomi- patients who are at risk. The WSACS has listed a
nal closure or other techniques have been reported to number of conditions associated with IAH (Box 2)
treat or prevent this complication successfully.82-84 and recommends screening for these risk factors at
Although clinical diagnosis may be difficult, Doppler ICU admission and when organ dysfunction occurs
ultrasound is an invaluable tool to detect this compli- during an ICU stay.2,88 In at-risk patients, IAP should
cation. Reversed diastolic blood flow in interlobar and be assessed at baseline, and if there is IAH, IAP
segmental renal arteries plus minimized venous flow
have been proposed as objective criteria indicative of
retroperitoneal compartment syndrome.40

Hepatorenal Syndrome and Severe Ascites

Hepatorenal syndrome likely reflects prerenal de-
creased kidney function, occurs in patients with liver
failure and ascites, and does not respond to volume
loading. The pathophysiologic mechanism leading to
hepatorenal syndrome is believed to be splanchnic
and systemic vasodilatation leading to kidney hypoper-
fusion. Paracentesis has been performed as treatment
for hepatorenal syndrome, but generally was not advo- Figure 1. Components of intra-abdominal hypertension (IAH)
cated because of fears of inducing hypovolemia and management. Abbreviation: IAP, intra-abdominal pressure.

164 Am J Kidney Dis. 2011;57(1):159-169

Intra-abdominal Hypertension and AKI

should be monitored at least every 4-6 hours through- also may be an important contributor to IAH. In-
out the course of critical illness.18 creased abdominal muscle tone, most often due to
pain or agitation, can be relieved by adequate analge-
Prevention of IAH and ACS sia and sedation if necessary. Use of restrictive ban-
Prevention of IAH and ACS has been studied most dages should be avoided. Neuromuscular blockade
extensively in patients with primary ACS. In patients repeatedly has effectively decreased IAP in patients
with trauma and patients after ruptured abdominal with IAH.44,66,94 A trial with neuromuscular blocking
aortic aneurysms, prophylactic use of open-abdomen agents could be considered when simpler measures
strategies has proved to be beneficial, although it are not sufficient or are ineffective, and continuous
sometimes can be a complicated undertaking.89,90 infusion of these agents could be considered when a
Decreased postinterventional IAH is another benefit clinically relevant effect is shown.
of nonsurgical interventional techniques for repair of Fluid resuscitation also may contribute to the devel-
ruptured aneurysms.91 As discussed, fluid resuscita- opment of IAH, a risk that seems especially relevant
tion is an important contributor to IAH in critically ill in patients with capillary leakage, in which fluids
patients, and as discussed in the next section, there is accumulate in the bowel wall and mesentery, free
evidence in burn patients that colloid92 and hyper- peritoneal cavity, retroperitoneum, and abdominal wall.
tonic lactated saline93 lead to lower IAP incidence This mechanism was described first in trauma pa-
than crystalloid-based resuscitation. Finally, because tients,95 but numerous studies of both general ICU
ACS typically is the final stage of prolonged exposure and postoperative patients have confirmed that overall
to IAH, it may be prevented or ameliorated through positive fluid accumulation is a risk factor for IAH.35-37,96
treating IAH using medical management options. Furthermore, as mentioned, 2 randomized controlled
trials in burn patients clearly showed that limiting
Medical Management fluid resuscitation by using colloids or hypertonic
Medical interventions aimed at decreasing IAP solutions results in a lower IAP incidence than stan-
target the 3 important contributors to IAH: (1) solid- dard resuscitation schemes based on crystalloids.92,93
organ and hollow-viscera volume; (2) space occupy- Similarly, in patients with acute pancreatitis, low-
ing lesions, such as ascites, blood, fluid, or tumors; volume resuscitation is associated with a decreased
and (3) conditions that limit expansion of the abdomi- incidence of ACS.97
nal wall. When using medical management options to This role of fluid accumulation in IAH suggests that
decrease IAP, it is important to always consider indi- all efforts should be made to remove excessive fluid
vidualized pathophysiologic mechanisms leading to from a volume-overloaded patient with overt ACS. In
IAH because these may differ considerably from one addition, when a patient’s acute illness has subsided
patient to another. Critically, in patients with IAH, and fluid accumulation is the cause of a more chronic
small changes in intra-abdominal volume may have a form of IAH, a similar strategy may be warranted.
pronounced effect on IAP. Depending on the clinical situation, either ultrafiltra-
Ileus is a common finding in critically ill patients, tion or diuretics can be used.98,99
especially those with abdominal conditions such as The WSACS recently proposed a medical treat-
pancreatitis, peritonitis, and abdominal trauma, and ment algorithm based largely on expert opinion that is
postoperative patients. Nasogastric drainage can be a aimed at both decreasing IAP and optimizing fluid
simple first step to decrease IAP in these patients. resuscitation and systemic perfusion (Fig 2). The
When colonic ileus is most pronounced, insertion of a medical treatment options discussed may be applied
rectal cannula can produce similar effects. Administra- in a stepwise fashion; critically, the present level of
tion of prokinetic agents, such as metoclopramide or evidence supporting these and other elements of this
erythromycin, often is used to overcome abdominal algorithm is limited, and the separate elements are not
distention and ileus and thus is a treatment option for supported by clinical outcome data. However, this
IAH. When such pharmacologic measures are unsuc- algorithm was part of an integrated approach that
cessful in decreasing intraluminal volume, endo- Cheatham and Safcsak86 found to improve outcome
scopic decompression can be considered. and decrease hospital costs.
Ascites and blood are the most common compo-
nents of space-occupying lesions, but abscesses and Surgical Management
free air also can contribute to IAH. When located in If attempts to decrease IAP using medical treatment
the free intraperitoneal space, these collections may are not effective, formal decompressive laparotomy
be easy targets for percutaneous drainage, which can should be considered. Also in patients with rapidly
be performed at the bedside in the ICU under ultra- progressive organ dysfunction caused by IAH, early
sound guidance. Limited abdominal wall compliance surgical decompression may be indicated because,

Am J Kidney Dis. 2011;57(1):159-169 165

De Waele et al

Figure 2. Intra-abdominal hypertension (IAH)/abdominal compartment syndrome (ACS) medical management algorithm. Abbrevia-
tions: APP, abdominal perfusion pressure; IAP, intra-abdominal pressure. Reproduced from The World Society of the Abdominal
Compartment Syndrome (WSACS)100 with permission of the WSACS, originally adapted from Malbrain et al2 and Cheatham et al.89

although invasive, decompressive laparotomy is effec- infection, enterocutaneous fistulas, ventral hernia, and
tive in decreasing IAP and improving organ function. cosmetic concerns. Temporary abdominal closure tech-
However, if overt ACS has occurred, IAP often re- niques have improved significantly in recent years,
mains in the range of 12-20 mm Hg, and despite often leading to lower complication rates and earlier fascial
dramatic improvements, true normalization of organ closure rates. Several more detailed reviews of avail-
function rarely is observed.41 The timing of the inter- able surgical techniques have been published re-
vention thus also is important; for example, Mentula cently.103,104
et al101 described poor outcomes in patients with
severe acute pancreatitis when decompression was
performed more than 4 days after admission to the
ICU. IAH frequently occurs in critically ill patients, and
A full midline laparotomy from the xiphoid down multiple factors often contribute to the problem. It
to the pubis is the technique most commonly used, but may affect all organ systems, but respiratory, cardio-
other less invasive modalities have been developed, vascular, and kidney function are affected most often.
with subcutaneous linea alba fasciotomy one of the IAP monitoring is a first and essential step in the
most promising approaches.102 Obviously, decompres- diagnosis and treatment of IAH, can be performed
sion means that the patient is left with an open easily in any ICU, and also is applicable in less
abdomen, which can result in serious fluid losses, intensive hospital settings.

166 Am J Kidney Dis. 2011;57(1):159-169

Intra-abdominal Hypertension and AKI

IAH can be the sole cause of or contributing factor 14. Sugrue M, Bauman A, Jones F, et al. Clinical examination is
in AKI and other kidney-related problems, such as an inaccurate predictor of intraabdominal pressure. World J Surg.
delayed transplant function after kidney transplant
15. Malbrain ML, De Laet I, Van Regenmortel N, Schoonheydt
and hepatorenal syndrome. Therefore, it is important K, Dits H. Can the abdominal perimeter be used as an accurate
for every nephrologist and intensivist caring for pa- estimation of intra-abdominal pressure? Crit Care Med. 2009;37:
tients with acute or chronic kidney disease to be aware 316-319.
of the existence of IAH, its pathologic implications, 16. Malbrain ML. Different techniques to measure intra-
and available methods to decrease IAP. Several non- abdominal pressure (IAP): time for a critical re-appraisal. Intensive
Care Med. 2004;30:357-371.
surgical interventions are available and may avoid the
17. De Laet IE, Ravyts M, Vidts W, Valk J, De Waele JJ,
need for surgery. If medical management fails and the Malbrain ML. Current insights in intra-abdominal hypertension
patient progresses to ACS, surgical decompression and abdominal compartment syndrome: open the abdomen and
should be performed without delay. keep it open! Langenbecks Arch Surg. 2008;393(6):833-847.
18. De Waele JJ, De Laet I, Malbrain ML. Rational intraabdomi-
ACKNOWLEDGEMENTS nal pressure monitoring: how to do it? Acta Clin Belg Suppl.
Support: Dr Hoste is Senior Clinical Investigator of the Re- 19. Balogh Z, De Waele JJ, Malbrain ML. Continuous intra-
search Foundation-Flanders (Belgium) (FWO). abdominal pressure monitoring. Acta Clin Belg Suppl. 2007;(1):
Financial Disclosure: The authors declare that they have no
relevant financial interests.
20. Schein M, Wittmann DH, Aprahamian CC, Condon RE.
The abdominal compartment syndrome: the physiological and
REFERENCES clinical consequences of elevated intra-abdominal pressure. J Am
1. Cheatham ML, Safcsak K. Intraabdominal pressure: a re- Coll Surg. 1995;180:745-753.
vised method for measurement. J Am Coll Surg. 1998;186:594- 21. Biancofiore G, Bindi ML, Romanelli AM, et al. Postopera-
595. tive intra-abdominal pressure and renal function after liver trans-
2. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results plantation. Arch Surg. 2003;138:703-706.
from the International Conference of Experts on Intra-abdominal 22. Kirkpatrick AW, De Waele JJ, Ball CG, Ranson K, Widder
Hypertension and Abdominal Compartment Syndrome. I. Defini- S, Laupland KB. The secondary and recurrent abdominal compart-
tions. Intensive Care Med. 2006;32:1722-1732. ment syndrome. Acta Clin Belg Suppl. 2007;(1):60-65.
3. Wendt E. Uber den einfluss des intraabdominalen druckes 23. Regueira T, Bruhn A, Hasbun P, et al. Intra-abdominal
auf die absonderungsgeschwindigkeit des harnes. Arch Physiol hypertension: incidence and association with organ dysfunction
Heilkunde. 1876;57:525-527. during early septic shock. J Crit Care. 2008;23:461-467.
4. Bradley SE, Bradley GP. The effect of increased intra- 24. De Waele JJ, Leppaniemi AK. Intra-abdominal hyperten-
abdominal pressure on renal function in man. J Clin Invest. sion in acute pancreatitis. World J Surg. 2009;33:1128-1133.
1947;26:1010-1022. 25. Tuggle D, Skinner S, Garza J, Van Dijck D, Blot S. The
5. Thorington JM, Schmidt CF. A study of urinary output and abdominal compartment syndrome in patients with burn injury.
blood-pressure changes resulting in experimental ascites. Am J
Acta Clin Belg. 2007;62:136-140.
Med Sci. 1923;165:880-890.
26. Sugrue M, Jones F, Deane SA, Bishop G, Bauman A,
6. Shenasky JH, Gillenwater JY. The effects of external abdomi-
Hillman K. Intra-abdominal hypertension is an independent cause
nal counterpressure on renal function. Surg Forum. 1970;21:528-
of postoperative renal impairment. Arch Surg. 1999;134:1082-
7. Shenasky JH II. The renal hemodynamic and functional
27. Sugrue M, Jones F, Janjua KJ, Deane SA, Bristow P,
effects of external counterpressure. Surg Gynecol Obstet. 1972;134:
Hillman K. Temporary abdominal closure: a prospective evalua-
8. Kron IL, Harman PK, Nolan SP. The measurement of intra- tion of its effects on renal and respiratory physiology. J Trauma.
abdominal pressure as a criterion for abdominal re-exploration. 1998;45:914-921.
Ann Surg. 1984;199:28-30. 28. Sugrue M, Buist MD, Hourihan F, Deane S, Bauman A,
9. Schwarte LA, Scheeren TW, Lorenz C, De Bruyne F, Hillman K. Prospective study of intra-abdominal hypertension and
Fournell A. Moderate increase in intraabdominal pressure attenu- renal function after laparotomy. Br J Surg. 1995;82:235-238.
ates gastric mucosal oxygen saturation in patients undergoing 29. Biancofiore G, Bindi ML, Romanelli AM, et al. Intra-
laparoscopy. Anesthesiology. 2004;100:1081-1087. abdominal pressure monitoring in liver transplant recipients: a
10. De Keulenaer BL, De Waele JJ, Powell B, Malbrain ML. prospective study. Intensive Care Med. 2003;29:30-36.
What is normal intra-abdominal pressure and how is it affected by 30. Balogh Z, McKinley BA, Cocanour CS, et al. Supranormal
positioning, body mass and positive end-expiratory pressure? trauma resuscitation causes more cases of abdominal compartment
Intensive Care Med. 2009;35:969-976. syndrome. Arch Surg. 2003;138:637-642.
11. Ejike JC, Humbert S, Bahjri K, Mathur M. Outcomes of 31. Offner PJ, de Souza AL, Moore EE, et al. Avoidance of
children with abdominal compartment syndrome. Acta Clin Belg abdominal compartment syndrome in damage-control laparotomy
Suppl. 2007;(1):141-148 after trauma. Arch Surg. 2001;136:676-681.
12. De Laet IE, Hoste EA, De Waele JJ. Survey on the percep- 32. Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl
tion and management of the abdominal compartment syndrome WM. Intra-abdominal hypertension after life-threatening penetrat-
among Belgian surgeons. Acta Chir Belg. 2007;107:648-652. ing abdominal trauma: prophylaxis, incidence, and clinical rel-
13. Kimball EJ, Rollins MD, Mone MC, et al. Survey of evance to gastric mucosal pH and abdominal compartment syn-
intensive care physicians on the recognition and management of drome. J Trauma. 1998;44:1016-1021; discussion 1021-1023.
intra-abdominal hypertension and abdominal compartment syn- 33. Meldrum DR, Moore FA, Moore EE, Franciose RJ, Sauaia
drome. Crit Care Med. 2006;34:2340-2348. A, Burch JM. Prospective characterization and selective manage-

Am J Kidney Dis. 2011;57(1):159-169 167

De Waele et al

ment of the abdominal compartment syndrome. Am J Surg. 52. Malbrain ML, Cheatham ML. Cardiovascular effects and
1997;174:667-672; discussion 672-673. optimal preload markers in intra-abdominal hypertension. In: Vin-
34. Reintam A, Parm P, Kitus R, Kern H, Starkopf J. Primary cent J-L, ed. Yearbook of Intensive Care and Emergency Medicine.
and secondary intra-abdominal hypertension—different impact on Berlin, Germany: Springer-Verlag; 2004:519-543.
ICU outcome. Intensive Care Med. 2008;34:1624-1631. 53. Cheatham M, Malbrain M. Abdominal perfusion pressure.
35. Malbrain ML, Chiumello D, Pelosi P, et al. Incidence and In: Ivatury R, Cheatham M, Malbrain M, Sugrue M, eds. Abdomi-
prognosis of intraabdominal hypertension in a mixed population of nal Compartment Syndrome. Georgetown, TX: Landes Bio-
critically ill patients: a multiple-center epidemiological study. Crit science; 2006:69-81.
Care Med. 2005;33:315-322. 54. Simon RJ, Friedlander MH, Ivatury RR, DiRaimo R,
36. Vidal MG, Ruiz Weisser J, Gonzalez F, et al. Incidence and Machiedo GW. Hemorrhage lowers the threshold for intra-
clinical effects of intra-abdominal hypertension in critically ill abdominal hypertension-induced pulmonary dysfunction. J Trauma.
patients. Crit Care Med. 2008;36:1823-1831. 1997;42:398-403; discussion 404-405.
37. Dalfino L, Tullo L, Donadio I, Malcangi V, Brienza N. 55. Burchard KW, Ciombor DM, McLeod MK, Slothman GJ,
Intra-abdominal hypertension and acute renal failure in critically Gann DS. Positive end expiratory pressure with increased intra-
ill patients. Intensive Care Med. 2008;34:707-713. abdominal pressure. Surg Gynecol Obstet. 1985;161:313-318.
38. Regueira T, Hasbun P, Rebolledo R, et al. Intraabdominal 56. Pelosi P, Ravagnan I, Giurati G, et al. Positive end-
hypertension in patients with septic shock. Am Surg. 2007;73:865- expiratory pressure improves respiratory function in obese but not
870. in normal subjects during anesthesia and paralysis. Anesthesiol-
39. Pertek JP, Coissard A, Lalot JM, Renoult E, Cormier L. ogy. 1999;91:1221-1231.
Hypoperfused kidney following kidney transplantation associated 57. Sugrue M, D’Amours S. The problems with positive end
with hyperlactatemia. Ann Fr Anest Reanim. 2001;20:282-288. expiratory pressure (PEEP) in association with abdominal compart-
40. Ball CG, Kirkpatrick AW, Yilmaz S, Monroy M, Nicolaou ment syndrome (ACS). J Trauma. 2001;51:419-420.
S, Salazar A. Renal allograft compartment syndrome: an underap- 58. Sussman AM, Boyd CR, Williams JS, DiBenedetto RJ.
preciated postoperative complication. Am J Surg. 2006;191:619- Effect of positive end-expiratory pressure on intra-abdominal
624. pressure. South Med J. 1991;84:697-700.
41. De Waele JJ, Hoste EA, Malbrain ML. Decompressive 59. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis
laparotomy for abdominal compartment syndrome—a critical anal- Campaign guidelines for management of severe sepsis and septic
ysis. Crit Care. 2006;10:R51. shock. Intensive Care Med. 2004;30:536-555.
42. Umgelter A, Reindl W, Wagner KS, et al. Effects of plasma
60. Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis
expansion with albumin and paracentesis on haemodynamics and
Campaign: international guidelines for management of severe
kidney function in critically ill cirrhotic patients with tense ascites
sepsis and septic shock: 2008. Intensive Care Med. 2008;34:17-60.
and hepatorenal syndrome: a prospective uncontrolled trial. Crit
61. Pelosi P, Quintel M, Malbrain ML. Effect of intra-
Care. 2008;12:R4.
abdominal pressure on respiratory mechanics. Acta Clin Belg
43. Umgelter A, Reindl W, Franzen M, Lenhardt C, Huber W,
Suppl. 2007;(1):78-88.
Schmid RM. Renal resistive index and renal function before and
62. Mutoh T, Lamm WJ, Embree LJ, Hildebrandt J, Albert RK.
after paracentesis in patients with hepatorenal syndrome and tense
Abdominal distension alters regional pleural pressures and chest
ascites. Intensive Care Med. 2009;35:152-156.
wall mechanics in pigs in vivo. J Appl Physiol. 1991;70:2611-
44. De Waele JJ, Benoit D, Hoste E, Colardyn F. A role for
muscle relaxation in patients with abdominal compartment syn-
drome? Intensive Care Med. 2003;29:332-332. 63. Josephs LG, Este-McDonald JR, Birkett DH, Hirsch EF.
45. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P; Diagnostic laparoscopy increases intracranial pressure. J Trauma.
Acute Dialysis Quality Initiative Workgroup. Acute renal failure— 1994;36:815-818; discussion 818-819.
definition, outcome measures, animal models, fluid therapy and 64. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A,
information technology needs: the Second International Consensus Sugerman HJ. Effects of increased intra-abdominal pressure upon
Conference of the Acute Dialysis Quality Initiative (ADQI) Group. intracranial and cerebral perfusion pressure before and after vol-
Crit Care. 2004;8(4):R204-212. ume expansion. J Trauma. 1996;40:936-941; discussion 941-943.
46. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury 65. Citerio G, Vascotto E, Villa F, Celotti S, Pesenti A. Induced
Network: report of an initiative to improve outcomes in acute abdominal compartment syndrome increases intracranial pressure
kidney injury. Crit Care. 2007;11:R31. in neurotrauma patients: a prospective study. Crit Care Med.
47. Cheatham M, Malbrain M. Cardiovascular implications of 2001;29:1466-1471.
elevated intra-abdominal pressure. In: Ivatury R, Cheatham M, 66. Deeren D, Dits H, Malbrain MLNG. Correlation between
Malbrain M, Sugrue M, eds. Abdominal Compartment Syndrome. intra-abdominal and intracranial pressure in nontraumatic brain
Georgetown, TX: Landes Bioscience; 2006:89-104. injury. Intensive Care Med. 2005;31:1577-1581.
48. Wauters J, Wilmer A, Valenza F. Abdomino-thoracic trans- 67. Ivatury R, Diebel L. Intra-abdominal hypertension and the
mission during ACS: facts and figures. Acta Clin Belg Suppl. splanchnic bed. In: Ivatury R, Cheatham M, Malbrain M, Sugrue
2007;(1):200-205. M, eds. Abdominal Compartment Syndrome. Georgetown, TX:
49. Kashtan J, Green JF, Parsons EQ, Holcroft JW. Hemody- Landes Bioscience; 2006:129-137.
namic effect of increased abdominal pressure. J Surg Res. 1981;30: 68. Doty JM, Oda J, Ivatury RR, et al. The effects of hemody-
249-255. namic shock and increased intra-abdominal pressure on bacterial
50. Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ. translocation. J Trauma. 2002;52:13-17.
Cardiopulmonary effects of raised intra-abdominal pressure before 69. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic isch-
and after intravascular volume expansion. J Trauma. 1995;39:1071- emia and bacterial translocation in the abdominal compartment
1075. syndrome. J Trauma. 1997;43:852-855.
51. Richardson JD, Trinkle JK. Hemodynamic and respiratory 70. Yagci G, Zeybek N, Kaymakcioglu N, et al. Increased
alterations with increased intra-abdominal pressure. J Surg Res. intra-abdominal pressure causes bacterial translocation in rabbits.
1976;20:401-404. J Chin Med Assoc. 2005;68:172-177.

168 Am J Kidney Dis. 2011;57(1):159-169

Intra-abdominal Hypertension and AKI

71. Cheatham ML, Malbrain ML. Cardiovascular implications Hypertension and Abdominal Compartment Syndrome. II.
of abdominal compartment syndrome. Acta Clin Belg Suppl. Recommendations. Intensive Care Med. 2007;33:951-962.
2007;(1):98-112. 89. Mayer D, Rancic Z, Meier C, Pfammatter T, Veith FJ,
72. Schachtrupp A, Lawong G, Afify M, Graf J, Toens C, Lachat M. Open abdomen treatment following endovascular repair
Schumpelick V. Fluid resuscitation preserves cardiac output but of ruptured abdominal aortic aneurysms. J Vasc Surg. 2009;50:1-7.
cannot prevent organ damage in a porcine model during 24 h of 90. Rasmussen TE, Hallett JW Jr, Noel AA, et al. Early abdomi-
intraabdominal hypertension. Shock. 2005;24:153-158. nal closure with mesh reduces multiple organ failure after ruptured
73. Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, abdominal aortic aneurysm repair: guidelines from a 10-year
pulmonary, and renal effects of massively increased intra- case-control study. J Vasc Surg. 2002;35:246-253.
abdominal pressure in critically ill patients. Crit Care Med. 1989; 91. Makar RR, Badger SA, O’Donnell ME, Loan W, Lau LL,
17:118-121. Soong CV. The effects of abdominal compartment hypertension
74. Lindstrom P, Kallskog O, Wadstrom J, Persson AEG. Blood after open and endovascular repair of a ruptured abdominal aortic
flow distribution during elevated intraperitoneal pressure in the rat. aneurysm. J Vasc Surg. 2009;49:866-872.
Acta Physiol Scand. 2003;177:149-156. 92. O’Mara MS, Slater H, Goldfarb IW, Caushaj PF. A prospec-
75. Doty JM, Saggi BH, Blocher CR, et al. Effects of increased tive, randomized evaluation of intra-abdominal pressures with
renal parenchymal pressure on renal function. J Trauma. 2000;48: crystalloid and colloid resuscitation in burn patients. J Trauma.
874-877. 2005;58:1011-1018.
76. Ulyatt DB. Elevated intra-abdominal pressure. Aust Anaes. 93. Oda J, Ueyama M, Yamashita K, et al. Hypertonic lactated
1992;10:108-114. saline resuscitation reduces the risk of abdominal compartment
77. Winton FR. The control of the glomerular pressure by syndrome in severely burned patients. J Trauma. 2006;60:64-71.
vascular changes within the isolated mammalian kidney, demon- 94. De Laet I, Hoste E, Verholen E, De Waele JJ. The effect of
strated by the actions of adrenaline. J Physiol. 1931;73:151-162. neuromuscular blockers in patients with intra-abdominal hyperten-
78. Wauters J, Claus P, Brosens N, McLaughlin M, Malbrain sion. Intensive Care Med. 2007;33:1811-1814.
M, Wilmer A. Pathophysiology of renal hemodynamics and renal 95. Balogh Z, McKinley BA, Cocanour CS, et al. Secondary
abdominal compartment syndrome is an elusive early complica-
cortical microcirculation in a porcine model of elevated intra-
tion of traumatic shock resuscitation. Am J Surg. 2002;184:538-
abdominal pressure. J Trauma. 2009;66:713-719.
543; discussion 543-544.
79. Stone HH, Fulenwider JT. Renal decapsulation in the pre-
96. Serpytis M, Ivaskevicius J. The influence of fluid balance
vention of post-ischemic oliguria. Ann Surg. 1977;186:343-355.
on intra-abdominal pressure after major abdominal surgery. Medi-
80. Harman PK, Kron IL, McLachlan HD, Freedlender AE,
cina (Kaunas). 2008;44:421-427.
Nolan SP. Elevated intra-abdominal pressure and renal function.
97. Mao EQ, Tang YQ, Fei J, et al. Fluid therapy for severe
Ann Surg. 1982;196:594-597.
acute pancreatitis in acute response stage. Chin Med J (Engl).
81. Kirkpatrick AW, Colistro R, Laupland KB, et al. Renal
arterial resistive index response to intraabdominal hypertension in 98. Kula R, Szturz P, Sklienka P, Neiser J. Negative fluid
a porcine model. Crit Care Med. 2007;35(1):207-213. balance in patients with abdominal compartment syndrome—case
82. Nguan CY, Beasley KA, McAlister VC, Luke PP. Treatment reports. Acta Chir Belg. 2008;108:346-349.
of renal transplant complications with a mesh hood fascial closure 99. Kula R, Szturz P, Sklienka P, Neiser J, Jahoda J. A role for
technique. Am J Surg. 2007;193:119-121. negative fluid balance in septic patients with abdominal compart-
83. Decoster T, Vermassen FE, Peeters PC, Hoste EA, De ment syndrome? Intensive Care Med. 2004;30:2138-2139.
Waele JJ. Abdominal decompression for intra-abdominal hyperten- 100. The World Society of the Abdominal Compartment Syn-
sion after simultaneous pancreas-kidney transplantation. Clin Trans- drome. Non-operative medical management algorithm. http://
plant. 2010;24(1):118-121. Accessed September 2, 2010.
84. Losanoff JE, Reichman TW, Garfinkel MR, Testa G, Millis 101. Mentula P, Hienonen P, Kemppainen E, Puolakkainen P,
JM. Component separation to salvage a renal allograft. Transplan- Leppaniemi A. Surgical decompression for abdominal compart-
tation. 2007;83:366-367. ment syndrome in severe acute pancreatitis. Arch Surg. 2010;145(8):
85. Savino JA, Cerabona T, Agarwal N, Byrne D. Manipulation 764-769.
of ascitic fluid pressure in cirrhotics to optimize hemodynamic and 102. Leppaniemi AK, Hienonen PA, Siren JE, Kuitunen AH,
renal function. Ann Surg. 1988;208:504-511. Lindstrom OK, Kemppainen EA. Treatment of abdominal compart-
86. Cheatham ML, Safcsak K. Is the evolving management of ment syndrome with subcutaneous anterior abdominal fasciotomy
intra-abdominal hypertension and abdominal compartment syn- in severe acute pancreatitis. World J Surg. 2006;30:1922-1924.
drome improving survival? Crit Care Med. 2010;38:402-407. 103. Ivatury RR. Update on open abdomen management:
87. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, De achievements and challenges. World J Surg. 2009;33:1150-1153.
Waele J, Ivatury R. Abdominal compartment syndrome: it’s time 104. Boele van Hensbroek P, Wind J, Dijkgraaf MG, Busch
to pay attention! Intensive Care Med. 2006;32:1912-1914. OR, Carel Goslings J. Temporary closure of the open abdomen: a
88. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results systematic review on delayed primary fascial closure in patients
from the International Conference of Experts on Intra-abdominal with an open abdomen. World J Surg. 2009;33:199-207.

Am J Kidney Dis. 2011;57(1):159-169 169