Journal of Critical Care 41 (2017) 275–282

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Journal of Critical Care

journal homepage: www.jccjournal.org

Intra-abdominal hypertension and abdominal compartment syndrome

in pediatrics. A review
Farah Chedly Thabet, MD a,⁎, Janeth Chiaka Ejike, MD, FAAP, FCCM b
a
Pediatric Intensive Care Unit, Prince Sultan Military Medical City, Riyadh, Saudi Arabia
b
Department of Pediatrics, Loma Linda University Children's Hospital, Loma Linda, CA, USA

a r t i c l e i n f o a b s t r a c t

Keywords: Purpose: To consolidate pediatric intensivists' understanding of the pathophysiology, definition, incidence, mon-
Intra-abdominal hypertension itoring, and management of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS);
Abdominal compartment syndrome and to highlight the characteristics related to the pediatric population.
Intensive care Methods: This is a narrative review article that utilized a systematic search of the medical literature published in
Children the English language between January 1990 and august 2016. Studies were identified by conducting a compre-
hensive search of Pub Med databases. Search terms included “intra-abdominal hypertension and child”, “intra-
abdominal hypertension and pediatrics”, “abdominal compartment syndrome and child”, and “abdominal com-
partment syndrome and pediatrics”.
Results: Intra-abdominal hypertension and ACS are associated with a number of pathophysiological disturbances
and increased morbidity and mortality. These conditions have been well described in critically ill adults. In chil-
dren, the IAH and the ACS have a reported incidence of 13% and 0.6 to 10% respectively; they carry similar prog-
nostic impact but are still under-diagnosed and under-recognized by pediatric health care providers.
Conclusions: Intra-abdominal hypertension and ACS are conditions that are regularly encountered in critically ill
children. They are associated with an increased morbidity and mortality. Early recognition, prevention and timely
management of this critical condition are necessary to improve its outcome.
© 2017 Elsevier Inc. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
2. Material and methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
3. Results and discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
3.1. Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
3.2. Intra-abdominal pressure measurement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
3.3. Pathogenesis of IAH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277
3.4. Pathophysiological implications of IAH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3.4.1. Gastrointestinal system. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3.4.2. Respiratory system. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3.4.3. Cardiovascular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3.4.4. Central nervous system. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3.4.5. Renal system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3.5. Incidence and risk factors for IAH and ACS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
3.6. Prognosis of IAH and ACS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
3.7. Management of intra-abdominal hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
3.7.1. Evacuation of intra-luminal content . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
3.7.2. Evacuation of extra-luminal content . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 280
3.7.3. Optimize fluid administration and correction of positive fluid balance: . . . . . . . . . . . . . . . . . . . . . . . . . . . . 280

⁎ Corresponding author at: Pediatric department, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.
E-mail address: Fmelaiki@psmmc.med.sa (F.C. Thabet).

http://dx.doi.org/10.1016/j.jcrc.2017.06.004
0883-9441/© 2017 Elsevier Inc. All rights reserved.
276 F.C. Thabet, J.C. Ejike / Journal of Critical Care 41 (2017) 275–282

3.7.4. Improve abdominal wall compliance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 280

Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
Funding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281

1. Introduction
There has been an increased interest in intra-abdominal hyperten-
sion (IAH) during the past decade, and the World Society of the Abdom-
inal Compartment (WSACS, www.wsacs.org) has published consensus
definitions, guidelines statements and recommendations for the screen-
ing and management of IAH and abdominal compartment syndrome
(ACS) in critically ill adult patients [1,2], with some specific consider-
ations for children in the last revised guidelines [3]. Due to increased
awareness and better defined intervention strategies, mortality due to
ACS in adults has decreased from 80 to 37% [4-6]. However, the mortal-
ity rate due to ACS in children has remained stable at 40–60% [7-9]. This
high mortality is in part attributable to poor recognition of ACS among
pediatric health care providers as demonstrated by different surveys
conducted [10-12].
In this article, we provide a narrative review of the latest reported
data on definition, incidence, monitoring, and management of IAH and
ACS in children to increase awareness among pediatric intensivists.
IAH or ACS refers to conditions that do not originate from the
abdomino-pelvic region and, recurrent IAH or ACS refers to the condi-
tion in which IAH or ACS redevelops following previous surgical or med-
ical treatment of primary or secondary IAH or ACS [3].
Abdominal perfusion pressure (APP) is the difference between the
mean arterial pressure and the IAP, it may be thought of as the abdom-
inal analogue to cerebral perfusion pressure. As APP may correlate with
visceral perfusion, this measure has been previously proposed to be
used as a resuscitation endpoint in patients with IAH [2,15]. Although
APP may have some merits, to date it is still unclear if increasing APP im-
proves outcomes. Furthermore, aiming for higher blood pressures
carries the inherent risk of excessive fluid administration, which
might ironically increase the incidence and severity of IAH and ACS.
Therefore, there is currently insufficient evidence to recommend use
of APP as a resuscitation endpoint in patients with IAH [3]. In children,
the optimum APP level is not well identified.
3.2. Intra-abdominal pressure measurement

2. Material and methods
In this narrative review article we utilized a systematic search of
Clinical trials and review papers, published in peer reviewed journals
in the English language between January 1990 and August 2016.
Given the lack of large multicenter studies in the literature, the authors
did not restrict studies based on size or particular patient cohorts, only
case reports were excluded.
Studies were identified by conducting a comprehensive search of Pub
Med databases. Search terms included “intra-abdominal hypertension
and child”, “intra-abdominal hypertension and pediatrics”, “abdominal
compartment syndrome and child”, and “abdominal compartment syn-
drome and pediatrics”. In order to identify additional citations, we also
used the Pub Med ‘related articles’ feature, and manually searched bibli-
ographies of the relevant studies. These searches yielded a total of 164 ar-
The gold standard for IAP measurement is through a peritoneal
catheter, but this method is invasive and can be associated with severe
complications such as peritonitis and bowel perforation [16]. The rec-
ommended method by the WSACS guidelines for indirectly measuring
IAP is the bladder method [3]. Indeed, the intravesical pressure closely
correlates with IAP [17], and this method was found to be the most ac-
curate indirect method of measuring IAP in children [18]. Several setups
and even IAP measuring kits exist, but the following is an example of a
simple system [19]. The aspiration port of the Foley catheter is attached
to a short 18-gauge catheter under sterile conditions, with 3 stopcocks
Table 1
Proposed pediatric specific definitions by the WSACS.
Terminology Proposed definition in children

ticles. Thirty articles were case reports and were excluded from the study, IAP The steady-state pressure concealed within the abdominal
and 88 were not selected because they were irrelevant or exclusively re- cavity (should be expressed in mmHg and measured at
end-expiration in the supine position after ensuring that
lated to adults. Hence, 44 articles pertinent to IAH and ACS in children
abdominal muscle contractions are absent and with the
were included for review. transducer zeroed at the level of the mid-axillary line)
IAP The reference standard for intermittent IAP measurement in
measurement children is via the bladder using 1 mL/kg as an instillation
3. Results and discussion volume, with a minimal instillation volume of 3 mL and a
maximum installation volume of 25 mL of sterile saline
3.1. Definitions Normal IAP 4-10 mmHg in critically ill children
APP The difference between MAP and IAP
IAH A sustained or repeated pathological elevation in IAP N10 mmHg
Normal IAP in spontaneously breathing persons is close to zero
IAH grade I IAP 10–12 mmHg
mmHg, and in mechanically ventilated children it is 7 ± 3 mmHg re- IAH grade II IAP 13–15 mmHg
gardless of the child's weight [13]. Children have lower mean arterial IAH grade III IAP 16–19 mmHg
pressures than adults; therefore multiorgan failure may occur in chil- IAH grade IV IAP ≥ 20 mmHg
dren at lower IAP thresholds than those defined for adults. Evidence of ACS A sustained elevation in IAP N10 mmHg associated with new or
worsening organ dysfunction that can be attributed to elevated IAP
organ dysfunction has been reported to occur at IAPs as low as 10–
Primary A condition associated with injury or disease in the
15 mmHg in critically ill children [8,14]. The pediatric sub-committee IAH/ACS abdomino-pelvic region that frequently requires early surgical
of the WSACS recently developed specific definitions and diagnostic or interventional radiological intervention
criteria for IAH and ACS for infants and children (Table 1). They define Secondary Refers to conditions that do not originate from the
IAH/ACS abdomino-pelvic region
IAH in children as a sustained or repeated pathological elevation in
Recurrent Refers to the condition in which IAH or ACS redevelops following
IAP N 10 mmHg. Abdominal compartment syndrome in children is de- IAH/ACS previous surgical or medical treatment of primary or secondary
fined as a sustained elevation in IAP N 10 mmHg associated with new IAH or ACS
or worsening organ dysfunction that can be attributed to elevated IAP. WSACS, world society of abdominal compartment syndrome; IAP, intra-abdominal pres-
As in adults, primary IAH or ACS is defined as a condition associated sure; APP, abdominal perfusion pressure; MAP, mean arterial pressure; IAH, intra-abdom-
with injury or disease within the abdomino-pelvic region; secondary inal hypertension; ACS, abdominal compartment syndrome.
 F.C. Thabet, J.C. Ejike / Journal of Critical Care 41 (2017) 275–282
Fig. 1. Illustration of the technique of intra-abdominal pressure monitoring.
connected to an intravenous infusion set, a syringe for flushing and
draining the tubing system, and a pressure transducer (Fig.1). The pres-
sure transducer is zeroed at the level where the mid-axillary line crosses
the iliac crest. With the patient in the supine position and the stopcock
closed to the urine collection bag and open to the bladder and transduc-
er, the appropriate volume of sterile saline is instilled into the bladder.
The IAP reading should be taken at end expiration after allowing time
for equilibration of bladder pressures and ensuring the absence of ab-
dominal muscle contractions. The appropriate instillation volume for
neonate and children is 1 mL/kg with a minimal optimal volume of
3 mL, and a maximum of 25 mL [13,20].
The WSACS recommends that IAP measurement be obtained if two
or more risk factors for IAH/ACS are present. If IAH is detected, serial
IAP measurements should be performed [3]. Several issues may be en-
countered with IAP measurement in children:
– Infants have faster respiratory rate compared with adults, mak-
ing the acquisition of measurements at end-expiration chal-
lenging.
– Abdominal breathing in a child with respiratory distress may
result in a falsely high IAP reading because of abdominal muscle
contractions. Elimination of this confounding factor can be
achieved by adequate sedation and/or neuromuscular blockade
in the mechanically ventilated child.
– Continuous bladder pressure monitoring, as described in adults,
is not applied in smaller children due to the lack of small three-
way urethral catheters [21].
3.3. Pathogenesis of IAH
Intraabdominal hypertension and ACS has been conceptualized
as having a largely mechanical pathogenesis. More contemporary
theories suggest that IAH/ACS frequently results from a two-hit,
self- perpetuating pathophysiological process initiated by bowel
277
ischemia reperfusion injury in patients with shock which produce a
vicious process that has been called ‘acute intestinal distress syn-
drome’ [22-25].
The resuscitation phase of hemorrhagic shock, septic shock and severe
burn could result in bowel ischemia-reperfusion injury, which induces a
systemic and peritoneal inflammatory response. Pro-inflammatory medi-
ators released during this response leads to neutrophil priming, increased
mesenteric capillary permeability and intestinal wall permeability, ex-
travasation of fluid into the bowel wall and mesentery, translocation of in-
testinal bacteria, and absorption of bacterial endotoxin [24]. This acute
bowel injury constitutes the first hit of the acute intestinal distress
syndrome. In the second hit, the resultant abdominal visceral
edema increases the IAH, compressing intra-abdominal lymphatics
and decreasing lymph flux out of the abdominal cavity, thereby fur-
ther increasing IAP [6]. The rising IAP decreases mucosal blood flow
to the bowel wall, results in a progressive decrease in bowel wall
perfusion, intestinal ischemia, a further increase in bowel wall per-
meability, and greater release of pro-inflammatory mediators into
systemic circulation, again further increasing intestinal permeabili-
ty, visceral edema, and IAP [26].
Excessive fluid resuscitation and capillary leak syndrome were
frequently reported as a cause of secondary abdominal compart-
ment syndrome especially in trauma, sepsis and burn resuscitation
[27–29]. Indeed the excessive fluid resuscitation during shock
management will further worsen the vicious cycle of acute intesti-
nal distress as the interstitial fluid accumulation is then further ag-
gravated by hemodilution, decreased oncotic pressure, and the
elevated hydrostatic pressure associated with massive crystalloid
infusion, contributing to more bowel edema and further increase
in the IAP [30].
In the study of Ejike et al. [7], total fluids received for initial resusci-
tation was not a predictor of ACS. However we did not use the same
goals of management as in other adult studies and they did not differen-
tiate crystalloid and blood products.
278 F.C. Thabet, J.C. Ejike / Journal of Critical Care 41 (2017) 275–282
3.4. Pathophysiological implications of IAH
3.4.1. Gastrointestinal system
Fundamental to the pathophysiology of IAH and ACS is the under-
standing of the concept of APP. The increased pressure in the abdominal
cavity is transmitted to the interstitial space and microvasculature serv-
ing as increased resistance which leads to diminished APP and blood
flow to the intra-abdominal organs, resulting in ischemia, congestion,
and edema of these organs. The organ edema further contributes to
the increased IAP, 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 per-
fusion pressure, no more blood flows to the organs, and cell death oc-
curs [31]. Intestinal ischemia and necrosis due to decreased perfusion
has been reported as one of the major causes of development of IAH
and ACS in children [8,32], but intestinal ischemia and necrosis can in
fact develop as a result of IAH and ACS. Intestinal ischemia can also
lead to bacterial translocation across the gut mucosa into the systemic
circulation, leading to bacteremia, and release of inflammatory media-
tors that further lead to deterioration in the patient's hemodynamic sta-
tus [33].
3.4.2. Respiratory system
The upward movement of the diaphragm with IAH results in
bibasilar compressive pulmonary atelectasis and ventilation-perfusion
mismatch. The transmission of elevated pressure from the abdomen to
the thoracic cavity through the diaphragm leads to increased intra-tho-
racic and airway pressure [34], reduced functional residual capacity and
low overall lung volumes, decreased chest wall and respiratory system
compliance and therefore increased work of breathing. All these mech-
anisms lead to the development of hypoxia, hypercapnia, respiratory
dysfunction and failure. In the mechanically ventilated patient, the de-
creased chest wall compliance leads to increased peak inspiratory pres-
sure and plateau pressure [35].
3.4.3. Cardiovascular system
The effects of increased IAP on cardiovascular function include a
combined negative effect on preload, afterload and contractility [36].
The preload is decreased through two main mechanisms, first, the in-
creased intra-thoracic pressure decreases blood return to the right atri-
um through the superior vena cava and limits blood return from below
the diaphragm in a pressure-dependent manner [37].Second, When IAP
increases, the cephalic deviation of the diaphragm compresses and nar-
rows the IVC as it passes through the diaphragm, further reducing ve-
nous return [36] especially if the transmural inferior vena cava (IVC)
pressure (defined as IVC pressure minus IAP) at the thoracic inlet is
below the critical closure transmural pressure. This is most often the
case in hypovolemic patients and by extension in most non-cardiogenic
shock patients [38], while those with hypervolemia and high IVC pres-
sure could have a preserved or even increased venous return. The ele-
vated IAP causes in increase an in the lower extremity hydrostatic
venous pressure leading to venous stasis and edema which could lead
to deep venous thrombosis or even limb compartment syndrome.
The elevated IAP and ITP lead to an increase in the systemic afterload
due to a direct compression of vascular beds and activation of the renin-
angiotensin-aldosterone pathway. The systemic vascular resistance can
also increase as compensation for the reduced venous return and stroke
volume.
The upward movement of the diaphragm during IAH leads to direct
compression on the heart with reduction of the right and left ventricle
end-diastolic volumes and compliance. All these mechanisms lead to
decreased cardiac output [39], and the reduced cardiac output results
in lower arterial pressures, contributing to the vicious cycle of poor
organ perfusion.
Based upon the assumption of stable ventricular compliance, pres-
sure-based parameters such as CVP have been utilized clinically as
surrogate estimates of intravascular volume. Although likely to be
valid in normal healthy individuals, the multiple assumptions necessary
to utilize CVP as estimates of right ventricular preload status, is not nec-
essarily true in the critically ill patient with IAH or ACS [36]. Indeed, be-
cause of the increase in right atrial pressures resulting from increased
intrathoracic pressure, measures of central venous pressure are inaccu-
rate estimates of preload, as they can be elevated even in the presence of
hypovolemia. Alternative methods for the evaluation of preload like
echocardiography may be needed [31].
3.4.4. Central nervous system
The increased abdominal pressure induces increased central venous
pressure which impairs the cerebral venous return contributing to in-
creased intracranial pressure and reduced cerebral perfusion pressure
especially in the presence of hemodynamic instability [40].
3.4.5. Renal system
Kidney perfusion is decreased mainly by two mechanisms: 1) the
low cardiac output affects renal perfusion, which leads to secretion of
catecholamines, angiotensin II, and aldosterone, with subsequent vaso-
constriction that results in increased systemic vascular resistance
(afterload). This further affects cardiac output and organ perfusion. 2)
Direct pressure on the kidneys decreases renal blood flow and the glo-
merular filtration rate. Clinically, this effect will be demonstrated by de-
creased renal function, and a decreased urine output that will contribute
further to fluid retention and increased IAP [41,42].
Imaging studies done in patients with ACS documented many of the
pathophysiological effect of IAH and ACS, indeed CT findings common to
these patients included narrowing of the inferior vena cava (IVC), direct
renal compression or displacement, bowel wall thickening with en-
hancement and a rounded appearance of the abdomen [43].
3.5. Incidence and risk factors for IAH and ACS
Studies following the new criteria for IAH definition in children re-
ported an incidence of 12.6% [14], and a prevalence of 43.9% [44] of
IAH in critically ill children admitted to the pediatric intensive care
units (PICU). The occurrence of ACS in pediatric patients has been previ-
ously reported as ranging from 0.6–9.8%, depending on the IAP thresh-
old used to define it (10, 12, or 15 mmHg) and on the patient
population studied, differing in surgical or medical patients [7-9,14,45,
46]. In some at-risk populations (neonates, burn patients with N40%
total body surface area burn), this incidence could exceed 30% [47,48]
(Table 2).
The WSACS suggested a wide range of risk factors that predisposes
patients to IAH and ACS based on four major pathophysiological catego-
ries [3]. Some conditions that are considered more specific to pediatric
patients include: 1) diminished abdominal wall compliance- such as
congenital abdominal wall defects [49,50], abdominal circumferential
burn, and abdominal surgery with tight closure; 2) increased intra-lu-
minal contents- for example, fecal impaction or accumulation of gas,
stool or fluid in the intestines as it can be seen in Hirschsprung disease
or toxic megacolon; 3) increased abdominal contents- for example, as-
cites, splenomegaly, hepatomegaly, intra-abdominal tumors, post kid-
ney transplant from an adult donor [51] and, post intestinal and/or
liver transplant [52,53]; and 4) capillary leak, and excessive fluid resus-
citation [27-30,54].
Conditions reported to be associated with IAH/ACS in children are
listed in Table 3. Other reported risk factors of IAH and ACS in the pedi-
atric population include: a Pediatric Risk of Mortality (PRISM) III score of
≥17 [7], abdominal distension, and a plateau pressure N 30 cm H2O for
ventilated patients [14] as well as hypothermia, and lactate level [44].
A systematic review and meta-analysis of adult literature afforded a
comprehensive description of evidence-informed risk factors for IAH
and ACS [54]. Several of these risk factors appeared to transcend across
patient populations (large-volume crystalloid resuscitation and the
 F.C. Thabet, J.C. Ejike / Journal of Critical Care 41 (2017) 275–282 279

Table 2
Reported incidence and outcome with IAH and ACS in pediatrics.

Study Type Patients n IAH IAH ACS definition ACS ACS Mortality
definition incidence incidence

Neville et al. R Patients who underwent Patch 23 NR NR Increased O2 requirements elevated PIP + NR 34.7%
(2000) [58] abdominoplasty for ACS abdominal distension and renal or cardiac
dysfunction.
Beck et al. P PICU patients 1762 NR NR IAP N 15 mmHg + abdominal distension +2 0.6% 60%
(2001) [8] new organ dysfunction
Latenser et al. P Burned patients (adults and children) 13 NR 69% IAP ≥ 30 mmHg + pulmonary or renal 31% 100%
(2002) [48] with N40% TBSA burns dysfunction
Diaz al. P PICU patients 1052 IAP N 10 NR IAP N 10 mmHg + new organ dysfunction 0.9% 40%
(2006) [45] mmHg
Ejike et al. P PICU patients b50 kg on mechanical 75 NR NR IAP N 12 mmHg + new organ dysfunction 4.7% 50%
(2007) [7] ventilation.
Hershberger R Patients who underwent 25 NR NR IAP N 12 mmHg + organ dysfunction NR 88%
et al. decompressive laparotomy for ACS
(2007) [29] (adult and children)
Pearson et al. R Children requiring an emergency 264 NR NR IAP N 12 mmHg + 1 new organ dysfunction 9.8% 58%
(2010) [9] laparotomy
Akhobadze et R Neonates with IAP monitoring 155 IAP N 10 NR IAP N 20 mmHg + 3 organ dysfunction 34% Grade I-II: 17% Grade
al. (2011) mmHg III: 37.5% Grade IV:
[47] 100%
Steinau et al. R Children who had surgical treatment 28 NR NR IAP N 12 mmHg + 1 new organ dysfunction NR 21.4%
(2011) [56] for ACS.
Fontana et al. R Pediatric patients receiving kidney 314 NR NR IAP ≥ 20 mmHg + 1 organ dysfunction. 2.9% No deaths
(2014) [51] transplants from adult donor
Thabet et al. P PICU patients 175 IAP N 10 12.7% IAP N 10 mmHg + new organ dysfunction 4% 85.7%
(2015) [14] mmHg
Horoz et al. P PICU patients 130 IAP N 10 (Prevalence: NR NR NR
(2015) [44] mmHg 43.9%)
Kuteesa J et al. P Patients requiring an emergency 192 IAP ≥ 10 20% IAP ≥ 10 mmHg + new organ dysfunction NR NR
(2015) [55] laparotomy (20 mmHg (Prevalence:
child) 25%)
Liang et al. R Patients with ACS and massive ascites 12 NR NR IAP N 10 mmHg + new organ dysfunction NR 25%
(2015) [57] treated with PCD
Divarci et al. P PICU patients 150 IAP ≥ 12 9% IAP N 15 mmHg + new organ dysfunction 4% 16%
(2016) [46] mmHg

IAH, intra-abdominal hypertension; ACS, abdominal compartment syndrome; IAP, intra-abdominal pressure; n, number of patients; R, retrospective; P, prospective; PICU, Pediatric Inten-
sive Care Unit; NR, not reported; TBSA, total body surface area; PIP, peak inspiratory pressure; PCD, percutaneous catheter drainage.

presence of shock), while many others were specific to the type of pa-
tient population under study. Interestingly, these risk factors largely
match those outlined in the pediatric-specific studies (shock, sepsis, ab-
dominal infection, ileus, abdominal surgery, pancreatitis, disease sever-
ity score, acidosis, hypothermia, high setting mechanical ventilation).
These similarities in evidence-based risk factors further highlight the
similarities in pathogenesis and pathophysiological mechanism of
IAH/ACS between adult and children and further empower these risk
factors to be considered candidate evidence-based risk factors not
only for adult but also for children until formally evaluated in a prospec-
tive multicentre observational study in these two patient populations.
3.6. Prognosis of IAH and ACS
Despite the increased morbidity and mortality associated with IAH/
ACS, it remains unknown if prevention or treatment (either surgical or
medical) of IAH/ACS among these critically ill patients improves patient
important outcomes. Therefore, some have questioned whether these
conditions are simply markers of increased critical illness severity rather
than conditions per say. Indeed a high disease severity score was signif-
icantly associated with the development of IAH and ACS in pediatric and
in adults studies [4,7,14].With our presently improved understanding of
the pathophysiology and epidemiology of IAH/ACS, future efforts in pe-
diatric studies should be focused on defining the evidence based risk
factors of development of IAH and compartment syndrome in children
and to identify whether interventions aimed at reducing IAP improve
patient mortality.

Intra-abdominal hypertension has been described in several studies
in adults as an independent predictor of ICU mortality. In a recent pro-
spective observational study in critically ill children, IAH was found to
be an independent risk factor for ICU mortality [14]. Kuteesa et al. [55]
evaluated the outcomes associated with IAH among patients scheduled
for emergency laparotomy; he found that in the pediatrics group, Pa-
tients with IAH at 6 h postoperatively were more than 24 times more
likely to die than those without IAH.
Abdominal compartment syndrome is underappreciated in children
[10,11]. Failure to recognize ACS can result in a critical delay in its man-
agement, which contributes to the resulting morbidity and mortality.
The ACS-related mortality has been reported to be 16–100% in various
studies focusing on critically ill children [7-9,14,29,44-48,51,55-58]
(Table 3).The mortality remains high even when decompression of the
abdomen is performed, a finding that highlights the importance of de-
tecting and treating IAH before end-organ damage occurs [9,59].
3.7. Management of intra-abdominal hypertension
The goal of IAH management of critically ill patients is to prevent fur-
ther organ dysfunction and to avoid progression to ACS.
Non-surgical management is an important step in the management of
patients with raised IAP. The WSACS medical management algorithm is
based on five treatment options: 1) evacuation of intra-luminal contents;
2) evacuation of intra-abdominal space occupying lesions; 3) improve-
ment of abdominal wall compliance; 4) optimization of fluid administra-
tion; and 5) optimization of systemic and regional perfusion [3].
3.7.1. Evacuation of intra-luminal content
Insertion of nasogastric, orogastric and/or rectal tubes or use of
prokinetic agents, enemas, or colonic decompression may reduce
gastro-intestinal contents and therefore intra-abdominal volume and
lead to a reduction in IAP in patients with gastric or colonic distention
280 F.C. Thabet, J.C. Ejike / Journal of Critical Care 41 (2017) 275–282
Table 3
Reported conditions associated with ACS in children.
Primary ACS
Decreased abdominal wall compliance
Gastroschesis [46,49,50]
Diaphragmatic hernia [46]
Increased intra-luminal contents
Small intestine intussusceptions [8]
Ileus [46,56]
Hirschprung's disease [58]
Increased abdominal contents
Bowel obstruction or perforation [7,56,58]
Intra-abdominal trauma (edematous viscera) [46,56,58]
Intestinal transplantation [52,53]
Kidney transplantation [51]
Intra-abdominal bleeding/retroperitoneal bleeding [56,58]
Extracorporeal membrane oxygenation [61,78,80]
Pancreatitis [56]
Acsites [57]
Wilm's Tumor [58]
Burkitt's Lymphoma [7]
Peritonitis/intra-abdominal infection [7,8,55,56]
Infectious enterocolitis [8,9,32,46,56,58]
Post abdominal surgery complication [8,9,58]
mesenteric vein thrombosis [8]
Pseudomembranous colitis [8]
Secondary ACS
Capillary leak/fluid resuscitation
Sepsis/Septic shock [7,8,46,61,79]
Cardiogenic shock/cardiac arrest [7]
Toxic shock syndrome [7]
Trauma shock [8,27,28]
Burns [14,27,29,48,56]
Capillary leak after liver or kidney transplantation [57]
Cardiac transplant rejection [61]
Hydrops fetalis [61]
[60]. However, the evidence supporting reductions in IAP with these in-
terventions is limited, and no study has yet reported improved patient
outcomes.
3.7.2. Evacuation of extra-luminal content
Intra-peritoneal fluid collections such as ascites or blood can cause
or contribute to IAH and/or ACS. Percutaneous catheter decompression
(PCD) of peritoneal fluid is an effective way to treat increased IAP in
these patients [48,57,and 61]. Bedsides sonography can assist in estab-
lishing the indication for PCD by distinguishing patients with IAH main-
ly related to intra-peritoneal fluid, from those with bowel wall edema or
a space-occupying lesion, where catheter decompression will not be
useful. PCD can prevent the progression of IAH to ACS altogether; it
may allow time to stabilize the patient for decompressive laparotomy
and it is a very useful treatment option in patients for whom decom-
pressive laparotomy is less desirable because of a high surgical risk:
PCD has successfully avoided the need to perform decompressive lapa-
rotomies in anticoagulated-patients undergoing extracorporeal life sup-
port who developed ACS [61].
3.7.3. Optimize fluid administration and correction of positive fluid balance:
Recently, an increasing awareness of the impact of fluid overload on
outcomes has been observed. Adult as well as pediatric studies have
shown a significant correlation between fluid overload and adverse out-
come in the ICU [54,62-66]. Furthermore, massive fluid resuscitation
and capillary leak syndrome are common causes of IAH in ICU. As
such, management of fluid overload and avoidance of excessive crystal-
loid resuscitation becomes an important target for intervention in criti-
cally ill patients to prevent ACS [67]. The WSACS suggests avoidance of a
positive cumulative fluid balance after the acute resuscitation has been
completed and inciting issues have been addressed [3]. Careful daily as-
sessment of the fluid balance, the use of protocolized restrictive fluid
therapy in shock and recovering critically ill patients, diuretics and con-
tinuous renal replacement therapy may be an important strategy to de-
crease the incidence and the morbidity and mortality associated with
IAH and the ACS [67]. The WSACS also suggests use of damage control
resuscitation for trauma patients with significant hemorrhage [3].
Though there is no evidence so far to support permissive hypotension
strategies nor haemostatic resuscitation in pediatrics trauma patients
with severe hemorrhage [68,69]; early hemorrhage control with bal-
anced crystalloid/transfusion therapy in hemorrhagic shock [70] may
help in reducing fluid overload and organ, tissue, and abdominal wall
edema contributing to IAH.
3.7.4. Improve abdominal wall compliance
Pain can stimulate contraction of the abdominal muscles and the mus-
cles of the trunk; the contraction of these muscles reduces the ribcage vol-
ume, pressing on the abdominal contents and increases the IAP. Using
adequate analgesia and sedation may therefore reduce IAP [71].
Neuromuscular blockade in mechanically ventilated patients can ef-
fectively reduce IAP through a reduction of abdominal muscle tone, and
an increase in abdominal wall compliance. Several case series have
shown an immediate reduction of IAP with neuromuscular blockade
use [72-74].
Positioning of a patient can impact IAP. Head of bed (HOB) elevation
significantly increased IAP values compared with those obtained in su-
pine position [75,76]. In children, Ejike et al. [77] found a 2.2 mmHg
pressure increase at 30° elevation in HOB. In addition, the prone posi-
tion in acute respiratory distress syndrome patients has been shown
to increase IAP. Hence, having a patient lie supine can be a potential con-
tributor to decreased IAP but it should be considered with caution, given
the potential risk of gastro esophageal reflux and VAP.
When medical measures fail to decrease IAP and to improve respira-
tory, renal, and cardiovascular function, one should consider prompt
surgical decompression. The specific surgical treatment for ACS is ab-
dominal decompressive laparotomy with postoperative open-abdomen
management. Decompressive laparotomy has been shown to be associ-
ated with improvement in physiologic parameters associated with ACS
[8,9,28,46,58,78,79] and in mortality [59,80]. This is further demonstrat-
ed if the surgical decompression is performed before irreversible organ
dysfunction occurs. Optimization of conservative therapies and early
decompression guided by use of a therapeutic algorithm likely contrib-
ute to improved outcomes. This was demonstrated by the studies of
Divarci et al. [46] and Steinau et al. [56]. In these two studies, a proactive
approach to abdominal decompression using IAP thresholds of
N15 mmHg and N12 mmHg respectively and only one organ dysfunc-
tion as an indication for decompressive laparotomy, was associated
with the best survival rate reported so far, at 84% and 78.6% respectively.
Decompressive laparotomy is supported by open- abdomen manage-
ment to avoid recurrence of ACS. Open-abdomen management is
achieved by leaving the fascia and the skin open, and temporarily cover-
ing the viscera (methods such as a form of negative pressure dressing,
prosthetic mesh or Wittmann patch have been reported in the literature)
[58,81,82]. The open-abdomen management with temporary abdominal
closure releases the IAP by creating a larger abdominal compartment
[83]. The goal is to reestablish intra-abdominal organ perfusion, which
is the cornerstone to reversing organ dysfunction, enabling the clinicians
to start weaning the child from cardiac, respiratory and renal support.
The medical management must continue in parallel with the surgical de-
compression. The ultimate goal of open-abdomen management is to
achieve prompt primary fascial closure without complications. Reported
complications include wound and mesh infections, entero-cutaneous fis-
tulae and hernia [9,56,58,84].
In conclusion, both, IAH and ACS are important problems in critically
ill patients, and are regularly observed in PICUs. They are associated
with high morbidity and mortality rates.
Early recognition of IAH and appropriate medical and/or surgical in-
tervention for IAH and impending ACS is the only way to ameliorate the
 F.C. Thabet, J.C. Ejike / Journal of Critical Care 41 (2017) 275–282
prognostic impact of ACS. The pediatric intensivists' knowledge of IAH
and ACS, and an awareness of patients at risk for IAH are of paramount
importance. Active IAP surveillance for at-risk patients is essential in the
early detection and management of IAH and ACS.
Conflict of interest
None.
Funding
This research did not receive any specific grant from funding agen-
cies in the public, commercial, or not-for-profit sectors.
References
[1] Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Re-
sults from the international conference of experts on intra-abdominal hypertension
and abdominal compartment syndrome. I Definitions. Intensive Care Med 2006;
32(11):1722–32.
[2] Cheatham ML, Malbrain ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Re-
sults from the international conference of experts on intra-abdominal hypertension
and abdominal compartment syndrome. II Recommendations. Intensive Care Med
2007;33(6):951–62.
[3] Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B,
et al. Pediatric guidelines sub-Committee for the World Society of the abdominal
compartment syndrome. Intra-abdominal hypertension and the abdominal com-
partment syndrome: updated consensus definitions and clinical practice guidelines
from the world Society of the Abdominal Compartment Syndrome. Intensive Care
Med 2013;39(7):1190–206.
[4] Vidal MG, Ruiz Weisser J, Gonzalez F, Toro MA, Loudet C, Balasini C, et al. Incidence
and clinical effects of intra-abdominal hypertension in critically ill patient. Crit Care
Med 2008;36:1823–31.
[5] De Waele J, Desender L, De Laet I, Ceelen W, Pattyn P, Hoste E. Abdominal decom-
pression for abdominal compartment syndrome in critically ill patients: a retrospec-
tive study. Acta Clin Belg 2010;65:399–403.
[6] Carr JA. Abdominal compartment syndrome: a decade of progress. J Am Coll Surg
2013;216:135–46.
[7] Ejike JC, Humbert S, Bahjri K, Mathur M. Outcomes of children with abdominal com-
partment syndrome. Acta Clin Belg 2007;62(Suppl. 1):141–8.
[8] Beck R, Halberthal M, Zonis Z, Shoshani G, Hayari L, Bar-Joseph G. Abdominal com-
partment syndrome in children. Pediatr Crit Care Med 2001;2:51–6.
[9] Pearson EG, Rollins MD, Vogler SA, Mills MK, Lehman EL, Jacques E, et al. Decom-
pressive laparotomy for abdominal compartment syndrome in children: before it
is too late. J Pediatr Surg 2010;45(6):1324–9.
[10] Kaussen T, Steinau G, Srinivasan PK, Otto J, Sasse M, Staudt F, et al. Recognition and
management of abdominal compartment syndrome among German pediatric
intensivists: results of a national survey. Ann Intensive Care 2012;2(Suppl. 1):S8.
[11] Ejike JC, Newcombe J, Baerg J, Bahjri K, Mathur M. Understanding of abdominal com-
partment syndrome among pediatric healthcare providers. Crit Care Res Prac 2010.
http://dx.doi.org/10.1155/2010/876013.
[12] Newcombe J, Mathur M, Bahjri K, Ejike JC. Pediatric critical care nurses' experience
with abdominal compartment syndrome. Ann Intensive Care 2012;2(Suppl. 1):S6.
[13] Ejike JC, Bahjri K, Mathur M. What is the normal intra-abdominal pressure in critical-
ly ill children and how should we measure it? Crit Care Med 2008;36:2157–62.
[14] Thabet FC, Bougmiza IM, Chehab MS, Bafaqih HA, AlMohaimeed SA, Malbrain ML. In-
cidence, risk factors, and prognosis of intra-abdominal hypertension in critically ill
children: a prospective epidemiological study. J Intensive Care Med 2015;31(6):
403–8.
[15] Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF. Abdominal perfusion
pressure: a superior parameter in the assessment of intra-abdominal hypertension.
J Trauma 2000;49:621–6.
[16] Abero K, Sequiera A. Bowel perforation during peritoneal dialysis catheter place-
ment. Am J Kidney Dis 2016;68(2):312–5.
[17] Suominen PK, Pakarinen MP, Rautiainen P, Mattila I, Sairanen H. Comparison of di-
rect and intravesical measurement of intraabdominal pressure in children. J Pediatr
Surg 2006;41(8):1381–5.
[18] Davis PJ, Koottayi S, Taylor A, Butt WW. Comparison of indirect methods of measur-
ing intra-abdominal pressure in children. Intensive Care Med 2005;31(3):471–5.
[19] Singhal J, Shanbag P. Measurement of intra-abdominal pressure in critically-ill chil-
dren. J Clin Diagn Res 2014;8(12):PC06–7.
[20] Defontaine A, Tirel O, Costet N, Beuchée A, Ozanne B, Gaillot T, et al. Transvesical
intra-abdominal pressure measurement in newborn: what is the optimal saline vol-
ume instillation? Pediatr Crit Care Med 2016;17(2):144–9.
[21] Balogh Z, De Waele JJ, Malbrain ML. Continuous intra-abdominal pressure monitor-
ing. Acta Clin Belg 2007;62(Suppl. 1):26–32.
[22] Malbrain ML, Vidts W, Ravyts M, De Waele J. Acute intestinal distress syndrome: the
importance of intra-abdominal pressure. Minerva Anestesiol 2008;74:657–73.
[23] Malbrain ML, De Laet I. It's all in the gut: introducing the concept of acute bowel in-
jury and acute intestinal distress syndrome. Crit Care Med 2009;37:365–6.
281
[24] Cheng J, Wei Z, Liu X, Li X, Yuan Z, Zheng J, et al. The role of intestinal mucosa injury
induced by intra-abdominal hypertension in the development of abdominal com-
partment syndrome and multiple organ dysfunction syndrome. Crit Care 2013;17:
R283. http://dx.doi.org/10.1186/cc13146.
[25] Roberts DJ, Ball CG, Kirkpatrick AW. Increased pressure within the abdominal com-
partment: intra-abdominal hypertension and the abdominal compartment syn-
drome. Curr Opin Crit Care 2016;22(2):174–85.
[26] Roberts DJ, De Waele J, Kirkpatrick AW, Malbrain ML. Intra-abdominal hypertension
and the abdominal compartment syndrome. In: O'Donnell JM, Flavio N, editors. Sur-
gical intensive care medicine. 3rd ed. Switzerland: Springer International Publish-
ing; 2016. p. 621–44.
[27] Jensen AR, Hughes WB, Grewal H. Secondary abdominal compartment syndrome in
children with burns and trauma: a potentially lethal complication. J Burn Care Res
2006;27(2):242–6.
[28] De Cou JM, Abrams RS, Miller RS, Gauderer MW. Abdominal compartment syn-
drome in children: experience with three cases. J Pediatr Surg 2000;35(6):840–2.
[29] Hershberger RC, Hunt JL, Arnoldo BD, Purdue GF. Abdominal compartment syn-
drome in the severely burned patient. J Burn Care Res 2007;28(5):708–14.
[30] Balogh Z, McKinley BA, Cocanour CS, Kozar RA, Holcomb JB, Ware DN, et al. Second-
ary abdominal compartment syndrome is an elusive early complication of traumatic
shock resuscitation. Am J Surg 2002;184:538–43.
[31] Carlotti AP, Carvalho WB. Abdominal compartment syndrome: a review. Pediatr Crit
Care Med 2009;10(1):115–20.
[32] Tanriverdi S, Koroglu O, Uygur O, Celik A, Dulger F, Yalaz M, et al. Serial intravesical
pressure measurements can predict the presence and the severity of necrotizing en-
terocolitis. Eur J Pediatr Surg 2013;23(3):243–8.
[33] Rezende-Neto JB, Moore EE, Melo de Andrade MV, Teixeira MM, Lisboa FA, Arantes
RM, et al. Systemic inflammatory response secondary to abdominal compartment
syndrome: stage for multiple organ failure. J Trauma 2002;53:1121–8.
[34] Cheatham ML. Abdominal compartment syndrome: pathophysiology and defini-
tions. Scand J Trauma Resusc Emerg Med 2009;17(1):10.
[35] Ejike JC, Mathur M, Moores DC. Abdominal compartment syndrome: focus on the
children. Am Surg 2001;77(Suppl. 1):S72–7.
[36] Malbrain ML, De Waele J, De Keulenaer B. What every ICU clinician needs to know
about the cardiovascular effects caused by abdominal hypertension. Anaesth Inten-
sive Ther 2015;47(4):388–99.
[37] Wauters J, Claus P, Brosens N, Mc Laughlin M, Hermans G, Malbrain M, et al. Rela-
tionship between abdominal pressure, pulmonary compliance, and cardiac preload
in a porcine model. Crit Care Res Pract 2012;2012(7631):81. http://dx.doi.org/10.
1155/2012/763181.
[38] Takata M, Wise RA, Robotham J. Effects of abdominal pressure on venous return: ab-
dominal vascular zone conditions. J Appl Physiol 1990;69:1961–72.
[39] Cheatham ML, Malbrain ML. Cardiovascular implications of abdominal compartment
syndrome. Acta Clin Belg 2007;62(Suppl. 1):98–112.
[40] De Laet I, Citerio G, Malbrain ML. The influence of intra abdominal hypertension on
the central nervous system: current insights and clinical recommendations, is it all
in the head? Acta Clin Belg 2007;62(Suppl. 1):89–97.
[41] De Waele JJ, De Laet I. Intra-abdominal hypertension and the effect on renal func-
tion. Acta Clin Belg 2007;62(Suppl. 2):371–4.
[42] Mohmand H, Goldfarb S. Renal dysfunction associated with intra-abdominal hyper-
tension and the abdominal compartment syndrome. J Am Soc Nephrol 2011;22(4):
615–21.
[43] Epelman M, Soudack M, Engel A, Halberthal M, Beck R. Abdominal compartment
syndrome in children: CT findings. Pediatr Radiol 2002;32(5):319–22.
[44] Horoz OO, Yildizdas D, Asilioglu N, Kendirli T, Erkek N, Anil AB, et al. The prevalence
of and factors associated with intra-abdominal hypertension on admission day in
critically ill pediatric patients: a multicenter study. J Crit Care 2015;30(3):584–8.
[45] Diaz FJ, Fernandez Sein A, Gotay F. Identification and management of abdominal
compartment syndrome in the pediatric intensive care unit. P R Health Sci J 2006;
25(1):17–22.
[46] Divarci E, Karapinar B, Yalaz M, Ergun O, Celik A. Incidence and prognosis of
intraabdominal hypertension and abdominal compartment syndrome in children.
J Pediatr Surg 2016;51(3):503–7.
[47] Akhobadze GR, Chkhaidze MG, Kanjaradze DV, Tsirkvadze I, Ukleba V. Identification,
management and complications of intra-abdominal hypertension and abdominal
compartment syndrome in neonatal intensive care unit (a single centre retrospec-
tive analysis). Georgian Med News 2011;192:58–64.
[48] Latenser BA, Kowal-Vern A, Kimball D, Chakrin A, Dujovny N. A pilot study comparing
percutaneous decompression with decompressive laparotomy for acute abdominal
compartment syndrome in thermal injury. J Burn Care Rehabil 2002;23(3):190–5.
[49] Tsai MH, Huang HR, Chu SM, Yang PH, Lien R. Clinical features of newborns with
gastroschisis and outcomes of different initial interventions: primary closure versus
staged repair. Pediatr Neonatol 2010;51(6):320–5.
[50] Kidd Jr JN, Jackson RJ, Smith SD, Wagner CW. Evolution of staged versus primary clo-
sure of gastroschisis. Ann Surg 2003;237(6):759–64.
[51] Fontana I, Bertocchi M, Centanaro M, Varotti G, Santori G, Mondello R, et al. Abdom-
inal compartment syndrome: an underrated complication in pediatric kidney trans-
plantation. Transplant Proc 2014;46(7):2251–3.
[52] Gupte GL, Haghighi KS, Sharif K, Mayer DA, Beath SV, Kelly DA, et al. Surgical com-
plications after intestinal transplantation in infants and children–UK experience. J
Pediatr Surg 2010;45(7):1473–8.
[53] Grevious MA, Iqbal R, Raofi V, Beatty E, Oberholzer J, Cohen M, et al. Staged approach
for abdominal wound closure following combined liver and intestinal transplanta-
tion from living donors in pediatric patients. Pediatr Transplant 2009;13(2):177–81.
[54] Holodinsky JK, Roberts DJ, Ball CG, Blaser AR, Starkopf J, Zygun DA, et al. Risk factors
for intra-abdominal hypertension and abdominal compartment syndrome among
282 F.C. Thabet, J.C. Ejike / Journal of Critical Care 41 (2017) 275–282
adult intensive care unit patients: a systematic review and meta-analysis. Crit Care
2013;17:R249. http://dx.doi.org/10.1186/CC13075.
[55] Kuteesa J, Kituuka O, Namuguzi D, Ndikuno C, Kirunda S, Mukunya D, et al. Intra-ab-
dominal hypertension; prevalence, incidence and outcomes in a low resource set-
ting; a prospective observational study. World J Emerg Surg 2015;10:57. http://dx.
doi.org/10.1186/S13017-015-0051-4.
[56] Steinau G, Kaussen T, Bolten B, Schachtrupp A, Neumann UP, Conze J, et al. Abdom-
inal compartment syndrome in childhood: diagnostics, therapy and survival rate.
Pediatr Surg Int 2011;27(4):399–405.
[57] Liang YJ, Huang HM, Yang HL, Xu LL, Zhang LD, Li SP, et al. Controlled peritoneal
drainage improves survival in children with abdominal compartment syndrome.
Ital J Pediatr 2015;41:29. http://dx.doi.org/10.1186/S13052-015-0134-6.
[58] Neville HL, Lally KP, Cox Jr CS. Emergent abdominal decompression with patch
abdominoplasty in the pediatric patient. J Pediatr Surg 2000;35(5):705–8.
[59] Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hyperten-
sion and abdominal compartment syndrome improving survival? Crit Care Med
2010;38(2):402–7.
[60] Mahajna A, Mitkal S, Krausz MM. Postoperative gastric dilatation causing abdominal
compartment syndrome. World J Emerg Surg 2008;3:7. http://dx.doi.org/10.1186/
1749-7922-3-7.
[61] Prodhan P, Imamura M, Garcia X, Byrnes JW, Bhutta AT, Dyamenahalli U. Abdominal
compartment syndrome in newborns and children supported on extracorporeal
membrane oxygenation. ASAIO J 2012;58(2):143–7.
[62] Malbrain ML, Marik PE, Witters I, Cordemans C, Kirkpatrick AW, Roberts DJ, et al.
Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: a
systematic review with suggestions for clinical practice. Anaesth Intensive Ther
2014;46:361–80.
[63] Boyd JH, Forbes J, Nakada T, Walley KR, Russell JA. Fluid resuscitation in septic shock:
a positive fluid balance and elevated central venous pressure are associated with in-
creased mortality. Crit Care Med 2011;39:259–65.
[64] Bhaskar P, Dhar AV, Thompson M, Quigley R, Modem V. Early fluid accumulation in
children with shock and ICU mortality: a matched case-control study. Intensive Care
Med 2015;41(8):1445–53.
[65] Ketharanathan N, McCulloch M, Wilson C, Rossouw B, Salie S, Ahrens J, et al. Fluid
overload in a South African pediatric intensive care unit. J Trop Pediatr 2014;
60(6):428–33.
[66] Arikan AA, Zappitelli M, Goldstein SL, Arikan AA, Zappitelli M, Goldstein SL. Fluid
overload is associated with impaired oxygenation and morbidity in critically ill chil-
dren. Pediatr Crit Care Med 2012;13(3):253–8.
[67] Regli A, De Keulenaer B, De Laet I, Roberts D, Dabrowski W, Malbrain ML. Fluid ther-
apy and perfusional considerations during resuscitation in critically ill patients with
intra-abdominal hypertension. Anaesth Intensive Ther 2015;47(1):45–53.
[68] Hughes NT, Burd RS, Teach SJ. Damage control resuscitation: permissive hypoten-
sion and massive transfusion prot ocols. Pediatr Emerg Care 2014;30(9):651–6.
[69] Cannon JW, Johnson MA, Caskey RC, Borgman MA, Neff LP. High ratio plasma resus-
citation does not improve survival in pediatric trauma patients. J Trauma Acute Care
Surg 2017 May 6. http://dx.doi.org/10.1097/TA.0000000000001549.
[70] Revell M, Greaves I, Porter K. Endpoints for fluid resuscitation in hemorrhagic shock.
J Trauma 2003;54:S63–7.
[71] Tasdogan M, Memis D, Sut N, Yuksel M. Results of a pilot study on the effects of
propofol and dexmedetomidine on inflammatory responses and intra abdominal
pressure in severe sepsis. J Clin Anesth 2009;21:394–400.
[72] De Laet I, Hoste E, Verholen E, De Waele JJ. The effect of neuromuscular blockers in
patients with intra-abdominal hypertension. Intensive Care Med 2007;33:1811–4.
[73] De Waele JJ, Benoit D, Hoste E, Colardyn F. A role for muscle relaxation in patients
with abdominal compartment syndrome? Intensive Care Med 2003;29(2):332.
[74] Chiles KT, Feeney CM. Abdominal compartment syndrome successfully treated with
neuromuscular blockade. Indian J Anaesth 2011;55(4):384–7.
[75] Cheatham ML, De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW,
et al. World society of the abdominal compartment syndrome (WSACS) clinical tri-
als working group. The impact of body position on intra-abdominal pressure mea-
surement: a multicenter analysis. Crit Care Med 2009;37:2187–90.
[76] Yi M, Leng Y, Bai Y, Yao G, Zhu X. The evaluation of the effect of body positioning on
intra-abdominal pressure measurement and the effect of intra-abdominal pressure
at different body positioning on organ function and prognosis in critically ill patients.
J Crit Care 2012;27(222):e1–6.
[77] Ejike JC, Kadry J, Bahjri K, Mathur M. Semi-recumbent position and body mass per-
centiles: effects on intra-abdominal pressure measurements in critically ill children.
Intensive Care Med 2010;36(2):329–35.
[78] Rollins MD, Deamorim-Filho J, Scaife ER, Hubbard A, Barnhart DC. Decompressive
laparotomy for abdominal compartment syndrome in children on ECMO: effect on
support and survival. J Pediatr Surg 2013;48(7):1509–13.
[79] Lam MC, Yang PT, Skippen PW, Kissoon N, Skarsgard ED. Abdominal compartment
syndrome complicating paediatric extracorporeal life support: diagnostic and thera-
peutic challenges. Anaesth Intensive Care 2008;36(5):726–31.
[80] Cheatham ML, Safcsak K. Intra-abdominal hypertension and abdominal compart-
ment syndrome: the journey forward. Am Surg 2011;77(supp 1):S1–5.
[81] Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hyperten-
sion and abdominal compartment syndrome improving survival? Crit Care Med
2010;38(2):402–7.
[82] Gutierrez IM, Gollin G. Negative pressure wound therapy for children with an open
abdomen. Langenbecks Arch Surg 2012;397(8):1353–7.
[83] Markley MA, Mantor PC, Letton RW, Tuggle DW. Pediatric vacuum packing wound
closure for damage-control laparotomy. J Pediatr Surg 2002;37(3):512–4.
[84] Ejike JC, Mathur M. Abdominal Decompression in Children. Crit Care Res Pract 2012;
2012:180797. http://dx.doi.org/10.1155/2012/180797.