Abdominal Compartment Syndrome in Children

Abdominal Compartment Syndrome in Children
Jennifer Newcombe, Mudit Mathur and J. Chiaka Ejike

Crit Care Nurse 2012;32:51-61 doi: 10.4037/ccn2012761
2012 American Association of Critical-Care Nurses
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Pediatric Care
Abdominal Compartment
Syndrome in Children
Jennifer Newcombe, MSN, CNS, CPNP
Mudit Mathur, MD
J. Chiaka Ejike, MD
Abdominal compartment syndrome is defined as sustained intra-abdominal

pressure greater than 20 mm Hg (with or without abdominal perfusion pressure
<60 mm Hg) associated with new organ failure or dysfunction. The syndrome is
associated with 90% to 100% mortality if not recognized and treated in a timely
manner. Nurses are responsible for accurately measuring intra-abdominal pressure
in children with abdominal compartment syndrome and for alerting physicians
about important changes. This article provides relevant definitions, outlines risk
factors for abdominal compartment syndrome developing in children, and discusses an instructive case involving an adolescent with abdominal compartment
syndrome. Techniques for measuring intra-abdominal pressure, normal ranges, and
the importance of monitoring in the critical care setting for timely identification of
intra-abdominal hypertension and abdominal compartment syndrome also are discussed. (Critical Care Nurse. 2012;32[6]:51-61)
bdominal compartment
syndrome (ACS) is
defined as sustained
intra-abdominal pressure (IAP) greater than
20 mm Hg (with or without abdom-
CNEContinuing Nursing Education

This article has been designated for CNE credit.
A closed-book, multiple-choice examination
follows this article, which tests your knowledge
of the following objectives:
1. Define abdominal compartment syndrome
in children
2. Describe techniques for obtaining accurate
intra-abdominal pressure measurements
3. Identify medical and surgical strategies for
decreasing intra-abdominal pressure
2012 American Association of Critical-Care Nurses
doi: http://dx.doi.org/10.4037/ccn2012761
www.ccnonline.org
inal perfusion pressure <60 mm Hg)

associated with new organ failure or
dysfunction.1,2 ACS is associated with
90% to 100% mortality if not recognized and treated promptly.3 The
results of a recent survey4 suggest
that pediatric health care providers
are not as familiar as their counterparts who provide care to critically
ill adults with the definition, monitoring, and treatment of ACS. Only
46.8% of pediatric providers correctly
defined ACS, 24.2% had never measured IAP before, and only half (51%)
reported that they had ever managed
a child with ACS.4
In this article, we provide relevant
definitions, outline risk factors for
ACS in children, and discuss an

instructive case of ACS in an adolescent. We also describe techniques
for measuring IAP, normal IAP
ranges, and the importance of IAP
monitoring for timely detection of
intra-abdominal hypertension (IAH)
and ACS.
Definitions
The World Society of Abdominal
Compartment Syndrome (WSACS)
recently developed definitions and
diagnostic criteria for IAH and ACS
and outlined standards for IAP
measurement in adults1-3,5,6 (Table 1).
Currently, no standardized definitions specific for infants and children
are available.
Children have lower mean arterial pressures than adults do, so multiorgan failure may occur in children
at lower IAP thresholds than those
defined by WSACS. As a result, lower
IAP cutoff values of 12 and 15 mm Hg
have been used to define ACS in children.7,8 For an individual child, the
actual IAP value may be less important than the impact of the pressure
on organ function. Normal IAP is 7
(SD, 3) mm Hg in children,5 so ACS
in a child may be more appropriately
CriticalCareNurse Vol 32, No. 6, DECEMBER 2012 51

Table 1
Important definitions
Term
Intra-abdominal pressure
Definition
(IAP)a
Pressure concealed within the abdominal cavity1,2
Abdominal perfusion pressure (APP)b

Intra-abdominal hypertension
(IAH)c
The difference between the mean arterial pressure and IAP2

Sustained or repeated elevation in IAP 12 mm Hg1,2
Grade I: IAP 12-15 mm Hg
Grade II: IAP 16-20 mm Hg
Grade III: IAP 21-25 mm Hg
Grade IV: IAP >25 mm Hg
Abdominal compartment syndrome
(ACS)d
Sustained IAP >20 mm Hg (with or without APP <60 mm Hg) associated with new
organ dysfunction or failure1,2
Primary ACS
Condition associated with injury or disease in the abdominopelvic region1,2
Secondary ACS
Condition that does not originate from the abdominopelvic region1,2
Recurrent ACS
Condition in which ACS redevelops after previous surgical or medical treatment of

primary or secondary ACS1,2
a Mean
IAP reference values range from 0 mm Hg in healthy persons, to 5-7 mm Hg in critically ill adults, 7 (SD, 3) mm Hg in critically ill children (0-18 years old),
and 1-8 mm Hg in children after cardiopulmonary bypass.3,5,6
b APP = mean arterial pressure IAP.
c The grades better define severity of IAH, may guide management and facilitate research; for example, comparing outcomes by using patients with more comparable severities of IAH.
d ACS may be classified as primary, secondary, or recurrent according to its cause and duration.
defined as an IAP of greater than

10 mm Hg with evidence of new
organ dysfunction or failure.4
Incidence, Risk Factors,

and Indications for
IAP Monitoring
IAH and ACS occur in a wide
variety of patients, including infants,
children, and adults who require
medical or surgical treatment or
treatment for burns, and is associated with a variety of diagnoses.7,9-12
The reported incidence of ACS varies
from less than 1% to 60%, depending
on the definitions used and the different populations of patients studied.7,8,12-14 Many health care providers
think ACS may be underrecognized
and thus underreported.
According to WSACS,15 risk factors for IAH and ACS can be categorized into conditions associated with
certain clinical characteristics (Figure 1). Examples of conditions in
children include the following:
Diminished abdominal wall
compliance: gastroschisis,
omphalocele, third-degree
circumferential abdominal wall
Authors
Jennifer Newcombe is a pediatric nurse practitioner, Pediatric Cardiothoracic Surgery,
School of Nursing, Loma Linda University, Loma Linda, California.
Mudit Mathur is a pediatric intensivist, Department of Pediatrics, Division of Pediatric
Critical Care, School of Medicine, Loma Linda University.
J. Chiaka Ejike is a pediatric intensivist, Department of Pediatrics, Division of Pediatric
Critical Care, School of Medicine, Loma Linda University.
Corresponding author: Jennifer Newcombe, RN, NP, 11234 Anderson St, Rm 5827, Loma Linda, CA 92354 (e-mail:
jnewcomb@llu.edu).
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, reprints@aacn.org.
burns, and abdominal surgery

with tight closure
Increased intraluminal contents:
constipation, Hirschsprung
disease
Increased abdominal contents:
splenomegaly, hepatomegaly,
intra-abdominal tumors (Wilms
tumor), ascites, intraperitoneal
or retroperitoneal bleeding
Capillary leak/fluid replacement: systemic inflammatory
response syndrome, sepsis
As a result of the favorable riskbenefit ratio of IAP monitoring and
the marked associated morbidity
and mortality of IAH and ACS, the
WSACS recommends measuring
IAP if a patient has 2 or more risk
factors for IAH or ACS. If IAH is
detected, serial IAP measurements
should be performed (Figure 1).
Pathophysiology of ACS
ACS is due to persistently elevated pressure in the abdominal
52 CriticalCareNurse Vol 32, No. 6, DECEMBER 2012
www.ccnonline.org
Patients should be screened for IAH/ACS risk factors upon admission and with new or progressive organ failure.
If two or more risk factors are present, a baseline IAP measurement should be obtained.
If IAH is present, serial IAP measurements should be performed throughout the patients critical illness.
Patient has TWO or more risk factors
for IAH/ACS upon either ICU admission
or in the presence of new or
progressive organ failure
Measure patients IAP to eastablish baseline pressure

IAP measurements
1. Expressed in mm Hg (1 mm Hg = 1.36 cm H2O)
2. Measured at end-expiration
3. Performed in the supine position
4. Zeroed at the iliac crest in the mid-axilliary line
5. Performed with an instillation volume of no
greater than 25 mL of saline [1 mL/kg for children
up to 20 kg] (for bladder technique)
6. Measured 30-60 seconds after installation to
allow for bladder detrusor muscle relaxation
(for bladder technique)
7. Measured in the absence of active abdominal
muscle contractions
Sustained IAP
12 mm Hg?
YES
NO
Patient has IAH
Patient does not

have IAH
Notify patients doctor of

elevated IAP.
Proceed to IAH/ACS
management algorithm.
Risk Factors for IAH/ACS

1. Diminished abdominal wall compliance
Acute respiratory failure, especially with elevated intrathoracic
pressure
Abdominal surgery with primary fascial or tight closure
Major trauma/burns
Prone positioning, head of bead >30 degrees
High body mass index (BMI), central obesity
2. Increased intra-luminal contents
Gastroparesis
Ileus
Colonic pseudo-obstruction
3. Increased abdominal contents
Hemoperitoneum/pneumoperitoneum
Ascites/liver dysfunction
4. Capillary leak/fluid resuscitation
Acidosis (pH <7.2)
Hypotension
Hypothermia (core temperature <33C)
Polytransfusion (>10 units of blood/24 hr)
Coagulopathy (platelets <55000/mm3 OR prothrombin time (PT)
>15 seconds OR partial thromboplastin time (PTT) >2 time
normal OR international standardised ratio (INR) >1.5)
Massive fluid resuscitation (>5 L/24 hr)
Pancreatitis
Oliguria
Sepsis
Major trauma/burns
Damage control laparotomy
Observe patient.
Recheck IAP if patient
deteriorates clinically.
IAH Grading
Grade I
Grade II
Grade III
Grade IV
IAP 12-15 mm Hg
IAP 16-20 mm Hg
IAP 21-25 mm Hg
IAP > 25 mm Hg
Abbreviations
IAH - intra-abdominal hypertension

ACS - abdominal compartment syndrome
IAP - intra-abdominal pressure
Adapted from Intensive Care Medicine 2006;32(11):1722-1732 & 2007;33(6):951-962

2007 World Society of the Abdominal Compartment Syndrome. All rights reserved.
World Society of the Abdominal Compartment Syndrome (WSACS)

ZNA Stuivenberg, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium
Tel: +32 3 2177092 Fax: +32 3 2177279 e-mail: info@wsacs.org
Website: http://www.wsacs.org
Figure 1 Intra-abdominal hypertension assessment algorithm.a

a Reprinted
from World Society of the Abdominal Compartment Syndrome,15 with permission.
www.ccnonline.org

compartment.16 The increased pressure can be due to increased volumes

within the fixed space, a decrease in
the volume of the compartment
itself, or a combination of both.17
The underlying pathophysiology of
all compartment syndromes is inadequate perfusion and oxygenation
of the organ or tissues within the
confined space due to an elevation
in pressure.18 Most likely, cellular
anoxia is the final pathway leading
to death from compartment syndromes.19 Sustained elevation of IAP
has multisystem adverse effects
because of the size and central location of the abdominal compartment
and the number of vital organs
located within the compartment17,20
(Figure 2). Preexisting comorbid
conditions such as renal failure or
cardiomyopathy play an important
role in aggravating the effects of
IAH and may reduce the threshold
of IAH that causes clinical manifestations of ACS. The underlying
cause of a patients IAH is also of
vital importance.20
Effects of IAP
In normal physiological conditions, perfusion of an organ requires

flow of oxygen and nutrient-rich
blood to the organ along a pressure
gradient from the heart to the capillaries in the organ. This blood flow
is opposed by venous and interstitial
pressures, which typically do not
exceed the perfusion pressure to the
organ, allowing blood to flow to the
organ.17 The elevated pressure in the
abdominal compartment is transmitted to the interstitial space and
microvasculature, leading to diminished flow of oxygen and nutrient-rich
blood to the intra-abdominal organs,
resulting in ischemia, congestion,
Pulmonary
compliance
PIP
Paw
PaO2
PaCO2
Qs/Qt
Vd/Vt
atelectasis
Central Nervous System

ICP
CPP
Thoracoabdominal
elevated diaphragm
ITP
IVC distortion
chest wall compliance
abdominal wall compliance
abdominal wall blood flow
Cardiovascular
hypovolemia
CO
venous return
IVC blood flow
SVR
PVR
PAOP
CVP
Hepatic
portal blood flow
lactate clearance
Gastrointestinal
celiac blood flow
SMA blood flow
mucosal blood flow
pHi
APP
Renal
renal blood flow
urinary output
GFR
Figure 2 Pathophysiological implications of intra-abdominal hypertension.a

Abbreviations: APP, abdominal perfusion pressure; CO, cardiac output; CPP, cerebral perfusion pressure;
CVP, central venous pressure; GFR, glomerular filtration rate; ICP, intracranial pressure; ITP, intrathoracic
pressure; IVC, inferior vena cava; PaCO2, carbon dioxide tension; PaO2, oxygen tension; PAOP, pulmonary
artery occlusion pressure; Paw, mean airway pressure; pHi, gastric mucosal pH; PIP, peak inspiratory pressure; PVR, pulmonary vascular resistance; Qs/Qt, intrapulmonary shunt; SMA, superior mesenteric artery;
SVR, systemic vascular resistance; Vd/Vt, pulmonary dead space.
a Reprinted
from Cheatam,20 with permission.
and swelling of those organs. The

swelling further encroaches on the
intra-abdominal space, worsening
the IAP and setting up a vicious cycle
of worsening compression of the
vascular structures with worsening
perfusion of the organs and subsequent progressive organ dysfunction.
When IAP exceeds the perfusion
pressure, blood flow to the organs is
completely cut off, and cell death
and necrosis occur.3,6
The effect of sustained elevations
in IAP also compromises respiratory,
cardiovascular, renal, gastrointestinal,
hepatic, and central nervous system
homeostasis.3,20
Respiratory System. Elevated IAP
causes increased pressure and upward
displacement of the diaphragm,
thereby diminishing the intrathoracic
compartment and leading to

increased intrathoracic pressure.
Elevated intrathoracic pressure
affects the lungs by decreasing lung
compliance, causing atelectasis and
ventilation-perfusion mismatch, all
of which lead to hypoxia and
hypercarbia. All these changes are
manifested as increased oxygen
requirements and the need for
increased mechanical ventilation.20-22
Cardiovascular System. Elevations
in intrathoracic pressure affect the
heart adversely by direct compression, causing transmission of elevated pressures across the atria.
Consequently, higher filling pressures are needed to establish adequate preload to support cardiac
output. This mechanical pressure
also causes decreased end-diastolic
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volume and decreased stroke volume,

changes that lead to decreased cardiac output.20,22 The lower cardiac
output results in lower arterial pressures, contributing to the vicious cycle
of poor perfusion, fueling further
organ swelling and worsening IAP.
Intra-abdominal Structures.
Within the abdomen, elevated IAP
causes direct compression of organs.
This compression results in collapse
of the inferior vena cava, portal vein,
and mesenteric vessels, leading to
decreased venous return and, subsequently, decreased cardiac output.
The low cardiac output and renal
plasma flow lead to secretion of
catecholamines, angiotensin II, and
aldosterone, with subsequent vasoconstriction, which results in
increased systemic vascular resistance (afterload) and adversely
affects cardiac output and organ
perfusion. Ischemia of the intestines
due to decreased perfusion may result
in translocation of bacteria across
the gut mucosa into the systemic
circulation, leading to bacteremia,
sepsis, and release of inflammatory
mediators, changes that adversely
affect patients overall hemodynamic status. Direct pressure on the
kidneys results in decreased perfusion to the kidneys, thereby decreasing renal blood flow and glomerular
filtration rate.22,23 The low cardiac
output and renal plasma flow in
turn cause increased secretion of
catecholamines, angiotensin II, and
aldosterone, with subsequent renal
vasoconstriction. The vasoconstriction exacerbates the decrease in renal
blood flow and glomerular filtration
rate, alterations that are manifested
clinically as decreased urine output
and worsening fluid retention, compounding the swelling of intra- and
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extra-abdominal organs3 and further elevating the IAP.

Central Nervous System. Intracranial pressure is increased by elevation in IAP. The higher pressures in
the superior vena cava and right
atrium are transmitted via the elevated intrathoracic pressure, impeding venous return from the head.20,24
Involvement of
Multiple Organ Systems
The multisystem effects of IAP

leads to ACS-related organ dysfunction. If left uncontrolled, the organ
dysfunction may become irreversible
and lead to death. However, ACSrelated dysfunction can be difficult
to separate from the organ damage
caused by the underlying diagnosis.
Medical and surgical interventions can be used to interrupt the
cascade of events related to ACS, but
once ACS is established, mortality
remains as high as 30% to 60% even
with intervention.25-27 Thus, the best
course of treatment remains early
recognition and management of elevated IAP, before ACS develops.
Diagnosis of ACS
The clinical manifestations of
ACS are as variable as the multiple
organ systems affected and the many
underlying diagnoses associated
with the syndrome. This characteristic makes ACS difficult to recognize
on the basis of a constellation of
signs and symptoms alone. ACS can
be diagnosed at the bedside, without the need for elaborate laboratory
or radiological tests, by simply measuring IAP. All patients at risk for
IAH should have routine IAP measurements until the IAP becomes
normal and risk factors for IAH
resolve. Because IAP monitoring is
simple, a high index of suspicion and

broad indications for IAP monitoring may help clinicians diagnose IAH
and ACS early, with few drawbacks.
IAP Measurements
Methods
IAP can be measured directly or

indirectly. With the direct method, a
catheter or needle is placed into the
peritoneal space, and IAP is determined by using a fluid column or
pressure transducer system (Figure 3).
With the indirect method, IAP is
measured indirectly via the pressure
transmitted to the lumen of an intraabdominal structure or organ (Figure 3). Indirect measurements include
those determined by using intragastric, intrarectal, venacaval, intrauterine, and intravesical methods.8,28,29
The gold standard for IAP measurement is the direct method, but this
method is invasive and can be associated with complications such as
bowel perforation and peritonitis.30
The most accepted standard for indirectly measuring IAP is the bladder
method.5,28 The pressure transducer
is leveled at the cross-section between
the iliac crest and the midaxillary
line. Appropriate volumes of saline
are instilled into the bladder via a
urethral catheter, and the pressure is
measured after allowing time for
equilibration of bladder pressures.2,5
In adults, the current recommended
volume of saline instilled varies from
10 to 25 mL.2,31,32 In children, the minimum volume recommended is 3 mL;
however, 1 mL/kg up to a maximum
of 25 mL can be used to obtain an
accurate IAP.5,28
Factors That Affect Measurements
IAP increases with inspiration

and decreases with expiration

Peritoneal drain
3
5
4
3
4
To drain
bag
Figure 3 Intra-abdominal pressure (IAP) measurement setup. A, Setup for indirect measurement. B, Setup for direct measurement.
1, Normal saline bag. 2, Syringe for accurately drawing up appropriate instillation volumes. 3, Transducer (zeroed at the intersection of the iliac crest and the mid-axillary lines). 4, Stopcock (the stopcock in the direct IAP setup [B] must be opened to the
transducer and closed to the drain bag during IAP measurements). 5, Automatic valve (Abviser Autovalve) allows instilled volume
to dwell in the bladder for a short period during which the IAP is measured and then that instilled volume is automatically released
and drainage of urine continues (this valve can be replaced by a simple stopcock that would need to be opened to the bladder and
transducer and closed to the urine bag during IAP measurement; one must remember to open the stopcock to the urine bag
immediately after the measurement to prevent iatrogenic urinary retention). 6, Urethral catheter. 7, Urine bag.
because of diaphragmatic contraction

and relaxation3,33 (Table 2). Higher
body mass index is correlated with
higher IAP in adults,6,34 but not in
children.35 Body position also affects
IAP. Patients tend to have higher IAP
in prone and semirecumbent positions than in the supine position.3,6,35-37
Other factors that affect IAP measurements obtained via the intravesical method include tense abdominal
muscles,38 volume of fluid instilled
into the bladder for measurements,5,28,39 temperature of the fluid
instilled,6,40 presence of air bubbles
in the fluid column, and position of
the transducer.41
Recommendations
Before dissemination of the

WSACS guidelines, the recommended
position for the transducer was at
the level of the symphysis pubis. IAP

measurements obtained at this level
are lower than those obtained with
the transducer at the midaxillary
position, the current recommended
position.41 According to the WSACS,
IAP should be expressed in millimeters of mercury. Measurements
should be taken with patients in the
supine position and at end expiration. The transducer should be
zeroed at the level of the iliac crest
in the midaxillary line. The instillation volume should be 3 mL of
physiological saline for children who
weigh less than 50 kg or 1 mL/kg
up to a maximum of 25 mL. IAP
should be measured 30 to 60 seconds after instillation to allow relaxation of the detrusor muscle and in
the absence of abdominal muscle
contractions (Figure 1).
Prognosis of ACS
Mortality associated with ACS is
40% to 90%, depending on the population of patients studied,7,14,42,43 and
can be as high as 80% to 90% if the
syndrome is unrecognized and
untreated.3 Most deaths from ACS
are attributed to sepsis and multisystem organ failure.3 Elevated IAP
is an independent predictor of mortality among critically ill patients.6,14
Mortality remains high even when
decompression of the abdomen is
performed, a finding that validates
the importance of detecting and
treating IAH before end-organ damage occurs.3,25-27
Medical Management
Optimal management of ACS is
contingent on early recognition of
IAH and prevention of ACS. Initially,
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Table 2
Factors that affect measurements of intra-abdominal pressure

Effect on measurement
Factors to consider
Higher body mass index
Increases in adults
No correlation found in children
Elevation of the head of the bed above 0
Increases
Respiration
Increases with inspiration

Decreases with expiration
Increases
Contraction of abdominal muscles (agitation, valsalva maneuver, coughing)

Transducer below the reference
pointa
Increases
Transducer above the reference
pointa
Decreases
Midaxillary line as reference point for placement of transducer compared with the symphysis pubis
Increases
Presence of air bubbles in the fluid column
Is unreliable
Larger instilled volume (>50 mL) in the bladder for measurement
Increases
Temperature of fluid instilled into the bladder for measurement
Very cold water may increase
a Reference
point refers to the cross-section at the level of the iliac crest and the midaxillary line.
nonsurgical options should be tried

in an attempt to control IAH. The
goal of medical management is to
decrease the IAP by using one of the
following interventions:
Evacuate the intraluminal contents of the intestines by using
gastric suctioning, rectal enemas, and gastroprokinetic and
coloprokinetic agents.44
Evacuate the intra-abdominal
space-occupying abnormalities
to treat extraluminal pathological changes such as ascites,
hemoperitoneum, or pneumoperitoneum, which may
require procedures such as
paracentesis.20,44
Optimize fluid administration
by using goal-directed therapies.
Use of diuretics and continuous
renal replacement therapy may
be helpful in reducing fluid
overload and organ, tissue,
and abdominal wall edema
contributing to IAH.23,44,45 These
strategies could also be helpful
in controlling capillary leak
syndrome.
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Improve abdominal wall compliance by using adequate

analgesia, sedation, and neuromuscular blockade. A maneuver
as simple as body positioning
(ie, having a patient lie more
supine) can decrease IAP.22,35,44
If these nonoperative measures
are not successful, the specific surgical treatment for ACS is abdominal
decompression by laparotomy with
postoperative open-abdomen management.7,20,27,44,46 The vacuum pack
technique, also known as negativepressure dressing for temporary
abdominal closure, has been associated with good outcomes in adults
and children.25,47 In a retrospective
study in neonates,47 use of the vacuum pack technique resulted in
85.7% successful primary fascial
closure in a median of 4 days.
Surgical decompression and
temporary abdominal closure release
the IAP by creating a larger abdominal compartment; the goal is to
reestablish intra-abdominal organ
perfusion. Successful early management of ACS may reverse organ
dysfunction, as evidenced by
improved urine output and more
stable hemodynamic status and
ventilatory parameters, enabling
clinicians to start weaning the child
from cardiac and respiratory support. Although it is a lifesaving
strategy, the open abdomen has
been associated with morbidity in
some cases. Abdominal abscesses,
fistulas, and major herniations of
the abdominal wall have all been
reported.43 Patients with planned
ventral hernias after open-abdomen
management require major reconstructive procedures several months
after the initial precipitating factor.43
The complications of ACS can
decrease when a comprehensive
evidence-based management strategy is used that includes early use
of open-abdomen management in
patients at risk. In a recent study25
in adults, overall survival improved
from 50% to 72% between 2002 and
2007, the ability to achieve successful primary fascial closure increased
from 59% to 81%, and the number
of patients with complications

CASE STUDY
13-year-old boy was brought to the emergency

department via ambulance after a horse kicked
him in the left flank and left upper abdominal
quadrant. Vital signs were heart rate 69/min, blood
pressure 117/72 mm Hg, respirations 16/min, and oxygen
saturation 100%. Abdominal computed tomography
revealed no free fluid and a mild splenic contusion. The
boy was admitted by the pediatric surgery team for observation and serial abdominal examinations. Within 24
hours, he began having increased pain, nausea, and vomiting. Repeat abdominal computed tomography showed
free intraperitoneal fluid. The patient was taken to the
operating room for an exploratory laparotomy. A perforation in the jejunum was found and repaired, and primary closure of the fascia was achieved. However, within
24 hours of surgery, the boy had altered mentation, tachycardia to 160/min, and hypotension (blood pressure as
low as 33/24 mm Hg). He was emergently given 4 L of
physiological saline, and inotropic support was started
during transfer to the pediatric intensive care unit.
Vital signs upon admission to the unit were heart rate
165/min, respirations 60/min, blood pressure 90/25 mm Hg.
He had worsening abdominal distention, decreased urine
output, and decreased perfusion to his lower extremities. His
IAP was measured by using the indirect intravesical method
with appropriate instillation volumes for his weight: 25 mL
for a weight of 69 kg. The initial IAP was 30 mm Hg. This
value with the new development of organ failure was indicative of ACS. Because the underlying cause of ACS was within
the abdomen, the syndrome was defined as primary ACS.
The boy was taken back to the operating room for
emergent abdominal decompression and reexploration. He
returned to the intensive care unit with his abdomen open
and a negative-pressure wound dressing in place to further
manage the ACS. The IAP decreased to 19 mm Hg after this
intervention. Serial IAP monitoring indicated ongoing IAH
with increasing IAP. The patient was returned to the operating room once more for another decompressive laparotomy to treat recurrent ACS (IAP 32 mm Hg) that occurred
despite leaving the abdomen open. The dressing was reexpanded to increase the volume of the abdominal compartment, thereby decreasing the IAP. The open abdomen was
again managed with a negative-pressure wound dressing.
The patient subsequently had 4 more trips to the operating
room for irrigation, debridement, and dressing

changes until postoperative day 28, when the abdominal fascia was closed with a soft-tissue graft. The
abdominal wound was allowed to heal by secondary
intention.
The multiorgan dysfunction caused by ACS gradually resolved. The patient had been treated with highfrequency oscillator ventilation for respiratory failure
complicated by acute respiratory distress syndrome.
The boy was successfully weaned from mechanical
ventilation after 19 days. Continuous renal replacement
therapy was used to support the patients renal failure
for 3 days until return of optimal urine output. The
patient was eventually discharged home on postoperative day 50; he was receiving parenteral nutrition and
required wound dressing management. His subsequent
course was complicated by development of a gastrocutaneous fistula, which was managed with parenteral
nutrition, application of a negative-pressure wound
dressing, and subsequent surgical excision of the fistula
after 3 months. He eventually had reconstructive surgery of the abdominal wall and was functioning as a
normal teenager, 5 years after the injury.
This case highlights the importance of IAP monitoring in a patient at risk for ACS. Perhaps, if the IAP had
been monitored immediately after the initial exploratory
laparotomy, evidence of increasing pressures might
have prompted the physicians to explore the abdomen
or decompress it before the IAP reached 30 mm Hg
and the patient had multiorgan dysfunction. Other lessons learned from this patient include the need to continue monitoring IAP despite surgical intervention for
ACS, because of the potential for recurrent ACS even
when the abdomen is left open. IAP management can
be used to determine timing for reexploration and
decompression. Support of organ dysfunction during
management of ACS is vital for survival. For example,
in this case pulmonary function was supported by
using high-frequency oscillator ventilation, cardiac
function with inotropes, and renal function with continuous renal replacement therapy.
Complications of the open abdomen, such as the
development of an enterocutaneous fistula, can be
managed with good outcomes.
www.ccnonline.org
associated with an incisional hernia

decreased from 41 to 19. In a retrospective study26 in 26 children undergoing decompressive laparotomy for
ACS, all survivors eventually had
closure of the abdominal wall. Time
to definitive closure was 8.6 days
(range, 1-61), and the mean number
of separate operations before final
closure was achieved was 3.2. Specific complications related to openabdomen management included
fascial dehiscence (n=1) and enterocutaneous fistula (n=1). Overall mortality was 58%, and mortality was
higher in children who had higher
preoperative serum lactate levels.
Nursing Management
Detection of ACS requires close
surveillance of IAP in patients at risk
for IAH. Nursing management
should focus on risk assessment for
IAH and routine IAP monitoring.
Nurses should be proficient in obtaining accurate IAP measurements by
the method used at their institution
and should understand the clinical
factors that affect IAP measurements.
A clear understanding of the definitions of IAH and ACS can guide
bedside nurses in the early detection
of IAH and potentially lead to early
medical interventions and prevention
of ACS. Nurses should also be familiar with simple measures that can be
taken to decrease IAP, such as aspiration of gastric contents or suctioning,
rectal decompression, and use of
To learn more about abdominal compartment syndrome in the critical care setting,
read Intra-abdominal Hypertension and
Abdominal Compartment Syndrome:
A Comprehensive Overview by Lee in
Critical Care Nurse, 2012;32:19-31.
Available at www.ccnonline.org.
www.ccnonline.org
adequate levels of sedation and neuromuscular blockade to discourage

voluntary abdominal muscle contractions. These interventions ultimately
would improve patients outcomes.
Conclusion
ACS is associated with a high
mortality rate and can cause significant morbidity in survivors.7,8,48,49
Thus, ACS is a clinically important
problem in critically ill patients that
can be ameliorated by early recognition of IAH and appropriate medical
or surgical intervention for IAH and
impending ACS. Bedside critical care
nurses are responsible for accurately
measuring IAP and alerting physicians about important observed
changes. Nurses knowledge of IAH
and ACS, awareness of the patients at
risk for IAH, and recognition of IAH
and progression to ACS are important. A high index of suspicion and
active IAP surveillance for at-risk
patients are essential in early detection and management of ACS. CCN
Now that youve read the article, create or contribute
to an online discussion about this topic using eLetters.
Just visit www.ccnonline.org and click Submit a
response in either the full-text or PDF view of the
article.
Financial Disclosures
None reported.
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Vasquez DG, Berg-Copas GM, Wetta-Hall R.
Influence of semi-recumbent position on intraabdominal pressure as measured by bladder
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Shafik A, El-Sharkawy A, Sharaf WM. Direct
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various conditions. Eur J Surg. 1997;163(12):
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The effect of different reference transducer
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measurement: a multicenter analysis.

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www.ccnonline.org
CNE Test Test ID C1262: Abdominal Compartment Syndrome in Children

Learning objectives: 1. Define abdominal compartment syndrome in children 2. Describe techniques for obtaining accurate intra-abdominal pressure
measurements 3. Identify medical and surgical strategies for decreasing intra-abdominal pressure
7. How is a diagnosis of ACS usually established?
a. Clinical signs and symptoms
b. Radiological examination
c. Laboratory tests
d. IAP monitoring
1. Which of the following is the definition of abdominal compartment

syndrome (ACS)?
a. Intra-abdominal pressure (IAP), 0-10 mm Hg
b. IAP, 10-15 mm Hg
c. IAP, 15-25 mm Hg
d. Multisystem organ dysfunction with evidence of elevated IAP
2. Which of the following statements differentiates ACS in children from
ACS in adults?
a. Children are less likely to experience multiorgan failure from ACS.
b. Higher IAP values are used to define ACS in children.
c. Standardized definitions for ACS are not available for infants and children.
d. IAP values are the best predicator of organ damage in children.
3. Which statement best describes the pathophysiology of compartment
syndrome?
a. Increased pressure occurs as a result of increased volume within a compartment.
b. Increased pressure occurs as a result of decreased size of the compartment.
c. Increased pressure occurs from a combination of increased volume and
decreased space.
d. Decreased tissue perfusion occurs secondary to increased pressure within
a confined space.
4. Which of the following is important when considering the clinical
sequelae of ACS?
a. Cardiac arrhythmias are the leading cause of death.
b. The effects of elevated pressure are usually limited to the gastrointestinal tract.
c. Comorbid conditions may aggravate the effects of intra-abdominal hypertension.
d. The underlying cause of intra-abdominal hypertension is of little importance.
5. Sustained elevation in IAP has which of the following impacts on the
respiratory system?
a. Downward displacement of the diaphragm
b. Increased intrathoracic pressure
c. Increased lung compliance
d. Alveolar expansion and rupture
8. Clinical conditions in children that increase risk for ACS include all
except which of the following?
a. Cystic fibrosis
b. Hirschprung disease
c. Gastroschisis
d. Sepsis
9. Current recommendations for performing IAP monitoring include
which of the following?
a. Obtaining measurements with the patient in the supine position
b. Positioning the transducer at the level of the symphysis pubis
c. Using a maximum of 50 mL of normal saline
d. Obtaining measurements at end inspiration
10. Which of the following therapies may help control capillary leak
syndrome in patients with ACS?
a. Adequate sedation
b. Gastric suctioning
c. Continuous renal replacement therapy
d. Neuromuscular blockade
11. Surgical decompression of the abdomen results in all except which
of the following?
a. Larger abdominal compartment
b. Decreased IAP
c. Improved intra-abdominal organ perfusion
d. 100% survival
12. Medical strategies to decrease IAP include which of the following?
a. Patient positioning with head of bed >30 degrees
b. Liberal fluid replacement
c. Adequate sedation and analgesia
d. Constrictive abdominal dressings
6. Increased IAP produces which of the following cardiovascular effects?

a. Increased venous return
b. Decreased cardiac output
c. Ventricular arrhythmias
d. Hypertension
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. q a
qb
qc
qd
2. q a
qb
qc
qd
3. q a
qb
qc
qd
4. q a
qb
qc
qd
5. q a
qb
qc
qd
6. q a
qb
qc
qd
7. q a
qb
qc
qd
8. q a
qb
qc
qd
9. q a
qb
qc
qd
10. q a
qb
qc
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11. q a
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qc
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12. q a
qb
qc
qd
Test ID: C1262 Form expires: December 1, 2015 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP Category A
Test writer: Joni L. Dirks, RN-BC, MS, CCRN
Program evaluation
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Aliso Viejo, CA 92656.
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Abdominal Compartment Syndrome in Children

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Abdominal Compartment Syndrome in Children

Jennifer Newcombe, Mudit Mathur and J. Chiaka Ejike

Downloaded from ccn.aacnjournals.org by guest on December 19, 2012

Abdominal compartment syndrome is defined as sustained intra-abdominal

CNEContinuing Nursing Education

inal perfusion pressure <60 mm Hg)

ACS in children, and discuss an

CriticalCareNurse Vol 32, No. 6, DECEMBER 2012 51

Pressure concealed within the abdominal cavity1,2

Abdominal perfusion pressure (APP)b

The difference between the mean arterial pressure and IAP2