Abdominal Compartment Syndrome

Disease-a-Month 65 (2019) 5–19
Contents lists available at ScienceDirect
Disease-a-Month
journal homepage: www.elsevier.com/locate/disamonth
Abdominal compartment syndrome
Glenda Sosa, MD a, Narayana Gandham, MD a, Veeda Landeras, MD b,

Angela Pauline Calimag, MD c, Edgar Lerma, MD d,e,∗
a
Department of Internal Medicine, Macneal Hospital, Berwyn, IL, United States
b
Associates in Nephrology, Chicago, IL, United States
c
University of Santo Tomas, Faculty of Medicine and Surgery, Manila, Philippines
d
Section of Nephrology, University of Illinois at Chicago College of Medicine/Advocate Christ Medical Center, Oak
Lawn, IL, United States
e
Associates in Nephrology, SC, Chicago, IL, United States
a r t i c l e i n f o
Keywords:
Abdominal Compartment Syndrome (ACS)
Intra-Abdominal Hypertension (IAH)
Intra-abdominal pressure
Introduction
Intra-abdominal Hypertension (IAH) and Abdominal Compartment Syndrome (ACS) are com-
mon entities in both surgical and non-surgical critical care environments. They, however, often
remain unrecognized or underdiagnosed even though its presentation is frequently more com-
mon than imagined. The detrimental effects of high intra-abdominal pressure (IAP) in both re-
gional and global perfusion resulting in significant multiple organ failure has been associated
with increased morbidity and mortality in critically ill patients. The earliest important manifes-
tation of increasing IAP even at relatively low-level IAH is oliguria and acute kidney injury.1 IAH
prevention thru early identification by screening and monitoring of patients at risk may avoid
the development of ACS altogether. Understanding the etiology and pathophysiology of IAH and
ACS is essential in recognizing its presence and can be used as a guide in its prevention and im-
plementing appropriate therapy. This review provides a brief summary of IAH and ACS history,
∗
Corresponding author.
E-mail address: nephron0@gmail.com (E. Lerma).
https://doi.org/10.1016/j.disamonth.2018.04.003
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6 G. Sosa et al. / Disease-a-Month 65 (2019) 5–19
consensus definitions, and epidemiology with the primary emphasis on the pathophysiology, di-
agnostic technique, and consensus management algorithm.
Brief historical aspects
Multiple scientific and clinical types of research over the last century have demonstrated the
outcomes and manifestations of untreated IAH and ACS, especially in critically ill patients. Marey
was the first to document, in 1863, the impact of elevated IAP upon respiratory function. While
Burt (1870) and Henricius (1890) reiterated the notion leading to the development of the theory
that high intrathoracic pressure causes respiratory failure and death.2 In 1876, Wendt was the
first to identify the harmful effect of elevated IAP on renal function and urinary output by re-
porting oliguria in the presence of elevated IAP. It was in 1911 when Emerson demonstrated that
elevated IAP causes death by cardiovascular collapse rather than by respiratory failure.2–4 Thor-
ington and Schmidt learned in their study done in 1923, that by decompressing the abdominal
cavity, restoration of urinary output is evident.5–7
These investigations were mostly demonstrated in cat, dog and rabbit models until 1947
when Bradley and Bradley studied the effects of increased intra-abdominal pressure on renal
function in humans.8 During this clinical study, 17 subjects underwent measurement of the ve-
nous pressure in the inferior vena cava and renal vein following venous catheterization while
raising IAP to 20 mmHg. The renal plasma flow and glomerular filtration rate (GFR) were re-
duced on average by 24.4% and 27.5%, respectively. All patients showed oliguria, which was at-
tributed to the elevation in renal vein pressure that increased on average from 5.8 to 18.3 mmHg.
Later investigations have demonstrated that oliguria develops early with an IAP of 15 mmHg
and anuria at 30 mmHg.6,9 Then in 1987, Caldwell et al. used an animal study and demon-
strated that an increase of IAP to 20 and 40 mmHg causes a decrease in organ blood flow for
all intra-abdominal organs except the adrenal glands which seems to have a survival mechanism
supported by the release of catecholamines.10
The development of the ideal IAP measurement technique also went thru different modifica-
tions and reiterations. In 1872, Schatz was the first to use a manometer to measure intrauterine
pressure as an estimate of IAP, followed by Wendt in 1873 using rectal pressure as a gauge of
IAP. Then in 1875 Odebrecht used bladder pressure as an approximation of IAP.11
The term Intra-abdominal compartment syndrome was introduced in 1989 by Fietsam et al.
in their study entitled “Intra-abdominal compartment syndrome as a complication of ruptured
abdominal aortic aneurysm repair.” published in the journal The American Surgeon.3,12, 13 ACS
was however first described by Kron et al. in 1984 including the technique they used for mea-
suring IAP.14 The modified Kron technique is the most commonly referenced technique for intra-
vesical measurement of IAP in studies on IAH and ACS.
Due to the growing interest and the upsurge in studies in the last few decades involving IAH
and ACS, a group of physicians saw the need to establish The World Society of the Abdominal
Compartment Syndrome (WSACS) in 2004. From then, consensus definitions and clinical practice
guidelines, including but not limited to management guideline and treatment algorithms were
published. The society eventually evolved and updated their name in light of recent develop-
ments, into the Abdominal Compartment Society.15,16
Definitions
The consensus definition and guidelines of IAH and ACS are well defined and summarized
by the World Society of the Abdominal Compartment Syndrome (WSACS) -The Abdominal
Compartment Society. In 2013, updated IAH and ACS definitions and clinical practice guidelines
were developed to standardize and optimize management and treatment. Intra-abdominal
pressure (IAP) is defined as the pressure concealed within the abdominal cavity. In an average
adult normal IAP is within the range of 0–5 mmHg, while in critically ill adults it is typically
at 5–7 mmHg. IAH is defined by a sustained or repeated pathologic elevation of IAP greater
G. Sosa et al. / Disease-a-Month 65 (2019) 5–19 7
than or equal to 12 mmHg. Abdominal Compartment Syndrome, on the other hand, is described
as a sustained IAP greater than 20 mmHg, with or without an Abdominal Perfusion Pressure
(APP) of <60 mmHg, associated with new organ dysfunction/failure. By definition, APP is the
difference between mean arterial pressure (MAP) and the IAP. Abdominal Perfusion Pressure is
an indicator of visceral perfusion, the concept of which is likened to cerebral perfusion pressure.
According to the study done by Cheatham et al. in 20 0 0, APP was a better predictor for survival
in patients treated for IAH compared to other traditionally used endpoints.17 Moreover, an
APP less than 60 mmHg reliably predicted the necessity for surgical decompression, making it
useful both in diagnosis and treatment. The WSACS defined the normal APP at 60 mmHg or
higher. It is important to note however that the WSACS made on no account any endorsements
concerning its use as a resuscitative endpoint.1,18
A grading system has been developed by WSACS for IAH. Grading according to the level of
IAP is as follows; Grade I: IAP 12–15 mmHg, Grade II: 16–20 mmHg, Grade III: IAP 21–25 mmHg,
Grade IV: IAP > 25 mmHg. On the other hand, ACS is further classified according to the cause
and duration of IAH into primary, secondary, and recurrent. Primary ACS is a condition associ-
ated with injury or disease in the abdominopelvic region that frequently requires early surgical
or interventional radiological intervention. Secondary ACS refers to conditions that do not orig-
inate from the abdominopelvic region. Whereas recurrent ACS refers to the condition in which
ACS redevelops following previous surgical or medical treatment of primary or secondary ACS.
These grading systems and classification groupings developed by WSACS facilitate the subse-
quent management of IAH and ACS in an organized stepwise approach.19
Epidemiology
Epidemiological studies conducted in the last decades vastly differ in their report of inci-
dence and prevalence.1,20 The previous lack of consensus definitions, differing IAP measurement
techniques and the different case-mix of medical and surgical patients add to the dearth of
concurrence in incidence and prevalence data. Aside from the lack of a specific and sensitive
screening tool leading to a paucity of data for the incidence of IAH and ACS.21,22 There is an
agreement however that the occurrence of IAH during the intensive care unit stay is an inde-
pendent predictor of patients’ outcome. This was reflected in the study conducted by Malbrain
et al. comprising of 265 patients from 14 ICUs in 6 countries and found that IAH is an inde-
pendent predictor of mortality (RR = 1.85, 95% CI 1.12 to 3.06; p = 0.01).1,23 While the study
conducted by Vidal et al. showed significantly higher mortality rates and a higher incidence of
organ failure or dysfunction predominantly renal and pulmonary. Mortality rates have been re-
vealed to be as high as 60–70%.24–26 As evidenced by higher total and renal Sequential Organ
Failure Assessment (SOFA) score, lower renal filtration gradient (FG), repetitive use of mechanical
ventilation, and longer ICU stay.1,27
Predisposing conditions and risk factors
Multiple patient population characteristics, comorbidities, and therapeutic interventions con-

tribute to the development of IAH and ACS. Hence it is problematic to forecast which of these
patients will eventually develop IAH and ACS. The most common documented risk factors for
the development of IAH and/or ACS as per The Abdominal Compartment Society (WSACS) are
also commonly grouped into five categories, namely: (1) Reduced abdominal wall compliance,
(2) Increased intra-luminal contents, (3) Increased extra-luminal/intra-abdominal contents, (4)
Capillary leak/ Fluid resuscitation and (5) Others/Miscellaneous. These risk factors according to
WSACS are supported in part by primary literature. However, some of these risk factors are de-
rived from the pathophysiological rationale and clinical judgment.19,28 Several studies have cited
that the primary risk factors commonly observed in ICUs were mechanical ventilation, acute
respiratory distress syndrome, and fluid resuscitation.1,27, 29 In an effort to consolidate mixed
data from a selection of studies, Holodinsky et al., conducted a systematic review and meta-
analysis of studies involving the risk factors for IAH and ACS in ICU patients. Their research
afforded a comprehensive analysis of evidence-based risk factors for IAH and ACS.28 Compared
to the risk factors found in the WSACS consensus the results of their study were more or less
congruent.
The development of IAH in ICU patients is associated with worse clinical outcome, and
this can be observed in patients with severe acute pancreatitis where the prevalence of intra-
abdominal hypertension in this type of patients is about 40–50, which is commonly documented
as a complication of early and aggressive fluid resuscitation.30,31 In addition to major burns and
sepsis, which are some of the causes of secondary IAH/ACS, abdominal trauma and abdomi-
nal surgery are predisposing conditions that influence the development of primary IAH/ACS and
consequently post-operative renal impairment. In a prospective observational study comprised
of 263 patients, IAH (defined as an IAP greater or equal to 18 mmHg) was an independent cause
of renal impairment after abdominal surgery with an odds ratio of 2.96 (95% CI 1.62 to 5.42;
p = 0.004).1,32 A better understanding of these predisposing conditions and risk factors, associ-
ated therapeutic interventions, recognizing the clinically essential endpoints and having a high
clinical index of suspicion will aid in identifying patients ultimately at risk.
Pathophysiology
To understand the fundamentals of IAH and ACS, we can compare it over-all to compartment
syndrome wherein an increase in pressure within a relatively static compartment impairs capil-
lary blood flow eventually decreasing arteriole blood flow and decreasing venous outflow. Later
on, this causes cellular hypoxia which in turn precedes anaerobic respiration and lactic acidosis.
The human body can be viewed as having different anatomic compartments interacting with
each other, for this reason, the pathophysiology of IAH/ACS is considered to be multifactorial
and can be seen in nearly all organ systems. IAH evidently not only causes reduced perfusion to
all intra-abdominal organs but has been recognized that it also affects the intra-thoracic organs
and to some effect, it has even been shown to affect the intracranial pressure.33 Simply stated,
as the intra-abdominal pressure rises, multiple organs will progressively start to fail.Cheatham
explained, IAH has been identified to cause a series of pathophysiologic changes beginning with
regional blood flow disturbances and culminating in apparent end-organ failure and the devel-
opment of ACS.4
Aside from the level of IAP and the etiology of the patient’s IAH, pre-existing co-morbidities
is of similar importance and should be taken into consideration as this reduces the threshold of
IAP that causes clinical manifestations (Fig. 1).
Cardiovascular effects
Intra-abdominal pressure raises the intra-thoracic pressure by way of abdomino-thoracic

transmission via the cephalad displacement of the diaphragm. This phenomenon creates a di-
rect compression of the intra-thoracic organs. Direct cardiac compression causes decreased con-
tractility, cardiac filling, and right ventricular compliance. IAH likewise results in compromised
venous return as the inferior vena caval pressure increases parallel to the increase in IAP, this is
noted even at an IAP of 10 mmHg. Moreover, the cephalad deviation of the diaphragm causes
an anatomical narrowing of the vena cava at the crura hence further reducing venous return
toward the heart and eventually cardiac output. Pulmonary parenchymal compression, on the
other hand, brings about vasculature compression thereby increasing pulmonary, aortic and sys-
temic vascular resistance. Hence, in spite of decreased venous return and cardiac output, the
mean arterial pressure remains stable, making it an inaccurate hemodynamic marker.4,18, 34,35
Measurement of pressure-based intracardiac or intravascular volume such as pulmonary
artery occlusion (“wedge”) pressure (PAOP) and central venous pressure (CVP) also tend to be
Fig. 1. Pathophysiologic Implications of Intra-abdominal Hypertension. The effects of intra-abdominal hypertension

are not limited just to the intra-abdominal organs, but rather have an impact either directly or indirectly on every
organ system in the body. ICP – intracranial pressure; CPP – cerebral perfusion pressure; ITP – intrathoracic pressure;
IVC – inferior vena cava; SMA – superior mesenteric artery; pHi – gastric intramucosal pH; APP – abdominal perfusion
pressure; PIP- peak inspiratory pressure; Paw – mean airway pressure; PaO2 – oxygen tension; PaCO2 – carbon dioxide
tension; Qs/Qt – intrapulmonary shunt; Vd/Vt – pulmonary dead space; CO – cardiac output; SVR – systemic vascular
resistance; PVR – pulmonary vascular resistance; PAOP – pulmonary artery occlusion pressure; CVP – central venous
pressure; GFR – glomerular filtration rate. Copyright © 2009 Cheatham; licensee BioMed Central Ltd.
inaccurately elevated. This deviation is because both PAOP and CVP are measured proportional
to barometric pressure when in fact it is the sum of both the intravascular pressure and in-
trathoracic pressure.3,4, 13, 35–40 Other volumetric parameters that are more accurate in reflecting
intravascular volume status are the following: right ventricular end-diastolic volume(RVEDV),
global end-diastolic volume (GEDV), and stroke volume as they remain unaffected by changes in
intrathoracic pressure.4,7, 18,41
The diminished venous drainage consequently causes intestinal and mesenteric vascular ve-
nous congestion, ischemia, and edema.1,4 , 10 This results in a vicious cycle that increases IAP
creating IAH and further development of ACS.
Pulmonary effects
Similarly, elevated IAP is transmitted to the thorax mainly through direct cephalad deviation
of the diaphragm causing compression of the pulmonary parenchyma. Parenchymal compres-
sion at an IAP of 16 mmHg decreases pulmonary compliance by 50%.35,42 Parenchymal com-
pression likewise causes decreased tidal volume and functional residual capacity while peak
inspiratory, plateau and mean airway pressures are increased. The resultant alveolar atelectasis,
increased alveolar dead space, decreased pulmonary capillary blood flow leading to reduced oxy-
gen transport and reduced carbon dioxide excretion and increased intrapulmonary shunt fraction
(Qsp/Qt) leads to Ventilation-perfusion (VQ) mismatch, and ultimately hypoxemia and hypercap-
nia.18,34 , 35,37 , 42
Renal effects
Several mechanisms have been suggested as the etiology for IAH-induced renal dysfunction
and failure. Renal artery and vein compression coupled with renal tubule compression have been
suspected as the likely mechanism behind the IAH/ACS-induced renal dysfunction and failure
accompanied by reduced cardiac output.4–6 , 39,43 Various authors have suggested that direct re-
nal parenchymal compression instigates the development of a “renal compartment syndrome”
wherein renal arterial blood flow is diminished while renal venous pressure and renal vascu-
lar resistance are elevated. This causes blood to be shunted away from the renal cortex and
glomeruli leading to impaired glomerular and tubular function in effect triggering renal ischemia
and subsequent renal failure.4,43, 44 At an IAP greater than 15 mmHg oliguria is noted to oc-
cur while anuria manifests at an IAP greater than 30 mmHg. Clinically we can observe changes
in kidney function, such as a decrease in GFR, raising blood urea nitrogen (BUN) and serum
creatinine, increased in fractional excretion of sodium, decreased urinary sodium and chloride
concentrations and an increase in urinary potassium concentration.5 However, all these changes
seem to be remediable if IAH is diagnosed and managed aptly before substantial organ dys-
function happens.4,6, 18,39 Recent studies have reported that optimizing the heart function signif-
icantly (r = 0.77, p < 0.001) correlates with an improvement in renal function in patients with
IAP.45
Gastrointestinal system
High pressure within the fixed abdominal compartment causes under perfusion of the in-
testines from impaired arterial and venous blood flow. An elevation of IAP 10 mmHg has been
shown to reduce the mesenteric blood flow.46 Reduced bowel perfusion causes bowel ischemia
and eventually intestinal edema and ileus. Intestinal mucosal perfusion is compromised as well
causing decreased pH and lactic acidosis which ultimately damages the intestinal mucosal bar-
rier.7 Losing the mucosal barrier leads to intraluminal bacterial translocation resulting in sepsis
or septic shock and subsequently worsening outcomes.4,18, 47
Hepatobiliary system
Elevated IAP significantly affects the liver function by grossly decreasing hepatic arterial, hep-
atic venous and portal vein blood flow. Direct compression of the liver compromises hepatic ve-
nous and portal blood flow. Also, impingement of the hepatic veins at the level of the diaphragm
attenuates hepatic venous blood flow whereas hepatic artery flow is compromised from the re-
duced cardiac output. At the cellular level, microcirculatory blood flow is also decreased altering
the mitochondrial function by disturbing glucose metabolism causing an increase in lactate pro-
duction all the while similarly impairing the lactate clearance mechanism.7 , 48–50
Central nervous system
The mechanism that was proposed by Halverson et al. indicated that the increase in ICP oc-
curring during abdominal insufflation is caused in some part by decreased absorption of CSF
due to increasing pressure in the inferior vena cava and subsequently increased pressure in the
lumbar venous plexus.51
Sustained and prolonged increased in intra-abdominal and intrathoracic pressures is as-
sociated with increased intracranial pressure (ICP) and decreased cerebral perfusion pressure
(CPP).52 Luce et al. and Bloomfield et al. during two different studies, recognized that by in-
creasing the intrathoracic pressure the cerebral venous flow is decreased which in turn causes
intracerebral edema.39,53, 54
Diagnosis
Early identification of patients at risk is the first step in diagnosing IAH and ACS. This will
be made possible by being able to identify the different risk factors present and having a high
index of suspicion and awareness of the IAH/ACS diagnosis. WSACS recommends screening for
IAH/ACS when two or more risk factors are present. The recommendation is to assess the IAP at
baseline, and if elevated then IAP should continue to be monitored every 4–6 h.29,55, 56
Clinical examination such as palpation and measurement of abdominal circumference has
been proven to be highly inaccurate and unreliable in diagnosing IAH and/or ACS.29,55, 57 Radio-
graphic input, such as plain radiograph of the chest and/or abdomen, abdominal ultrasound, CT
scan and MRI of the abdomen has also been proven to be limited since the findings are neither
sensitive nor specific for IAH and/or ACS. However, they may demonstrate the presence of the
possible cause of IAP and can also reveal the effects of IAP such as elevated hemidiaphragm, flat-
tened inferior vena cava, compressed renal veins and increased bowel wall enhancement. When
the combination of these radiographic findings are appreciated along with concerning clinical
presentation, then the radiologist and the clinician should raise the question and bring up IAH
and/or ACS as a differential diagnosis.30
There are different methods to measure intra-abdominal pressure, it can either be direct
or indirect. Direct measurement of intra-abdominal pressure can be done using an intraperi-
toneal catheter with a pressure transducer. Indirect measurement techniques include determin-
ing either one of the following pressures such as inferior vena cava, intragastric, intracolonic,
intrauterine or intra-vesicular pressure.58 Due to the bladder’s position in the abdominal com-
partment, the intra-vesicular technique is deemed simple, precise, and minimally invasive; hence
it is a reliable and reproducible way to measure IAP.4,11, 19,59
Measuring intra-abdominal pressure via intravesicular route
Ever since the concept of IAH and ACS was identified, different studies proposed diverse tech-
niques and provided different modifications and reiterations of intra-vesical pressure measure-
ment with the aim of making it more precise, reproducible and reliable. Despite the method
used, several references must be followed: (1) Report IAP in mmHg (1 mmHg = 1.36 cm H2 O),
(2) Patient should be in a supine position to avoid incorrect elevated IAP, (3) measurements
should be taken at end-expiration during abdominal muscle relaxation,(4) Transducer should be
zeroed in the mid-axillary line at the level of the iliac crest.4,11, 29, 58–60 Described below are the
equipment needed and general steps to measuring intra-vesicular pressure via the closed system
repeated measurement techniques. Variations to these steps may be done according to protocols
and available equipment utilized per institution (Fig. 2).
Equipment required
1. Foley urine catheter with a urine bag

2. Pressure monitoring system
3. IV bag of 0.9 Normal Saline (NS)
4. Transducer cable
5. 30 ml syringe
Fig. 2. AbViser IPA Monitoring System Copyright © 2012 ConvaTec Inc.http://abviser.com/products/

abviser- iap- monitoring- device/.
Steps for measuring intra-vesicular pressure
1. Connect the transducer cable to the monitor and set up the pressure monitoring system
2. Place patient in the supine position to avoid higher IAP, a urinary catheter should be in place
3. Adjust the transducer and zero it so that atmospheric port is level with the mid-axillary line
at the iliac crest
4. Clamp the catheter distal to the port, clean the port with alcohol swab then connect the
transducer tubing to the sampling port
5. Turn the stopcock off to the patient and allow the syringe to fill to maximum of 25 ml of 0.9
NS from the IV bag
6. Turn the stopcock off to the normal saline and inject the 25 ml of 0.9 NS into the bladder
7. Release the clamp on the urinary drainage tubing to allow all air to be flushed from the
urinary catheter
8. Allow 30–60 s after installation for bladder detrusor muscle relaxation and stabilization to
occur
9. Measure IAP in the end-expiratory phase, document the pressure reading in the monitor
Management
The WSACS proposed a management algorithm based mostly on expert opinion that is based
on the principles of serial IAP monitoring, optimization of systemic organ perfusion, IAP con-
trol and reducing potential end-organ damage and surgical decompression for refractory ACS.11
The WSACS management algorithm has five medical treatment arms namely: (1) Evacuate intra-
luminal contents, (2) Evacuate intra-abdominal space-occupying lesions, (3) Improve abdominal
wall compliance, (4) Optimize fluid administration and (5) Optimize systemic/regional perfusion.
These medical interventions essentially target the 3 critical contributors to IAH which are (1)
Solid organ and hollow-viscera volume; (2) space-occupying lesions, such as ascites, blood, fluid,
or tumors; and (3) conditions that limit the expansion of the abdominal wall.61 The algorithm is
described in a tiered fashion and was part of an integrated approach that Cheatham and Safcsak
found to improve outcome and decrease hospital costs.56, 61–64 See Algorithms 1 and 2.
Algorithm 1
Management of IAH/ACS by WSACS: Adapted from World Society of the Abdominal Compartment Syndrome (WSACS)
website: http://www.wsacs.org.
Algorithm 2
Medical management of IAH/ACS by WSACS: Adapted from World Society of the Abdominal Compartment Syndrome
(WSACS) website: http://www.wsacs.org.
Evacuate intra-luminal contents
Ileus is a common finding in critically ill patients, especially those with abdominal condi-
tions such as pancreatitis, peritonitis, abdominal trauma, and postoperative patients. Nasogastric
drainage can be a simple first step to decrease IAP in these patients. When colonic ileus is most
pronounced, insertion of a rectal cannula can produce similar effects. Administration of proki-
netic agents, such as metoclopramide or erythromycin, often is used to overcome abdominal
distention and ileus and thus is a treatment option for IAH. When such pharmacologic measures
are unsuccessful in decreasing intraluminal volume, endoscopic decompression can be consid-
ered.
Evacuate intra-abdominal space occupying lesions
Ascites and blood are the most common components of space-occupying lesions; abscesses
and free air also can contribute to IAH. When located in the free intraperitoneal space, these
collections may be easy targets for percutaneous drainage, which can be performed at the
bedside in the ICU under ultrasound guidance.
Improve abdominal wall compliance
Limited abdominal wall compliance is an essential contributor to IAH. Increased abdominal

muscle tone, most often due to pain or agitation, can be relieved by adequate analgesia and
sedation if necessary. Use of restrictive bandages should be avoided. Neuromuscular blockade
repeatedly has been found to be effective in decreasing IAP in patients with IAH.52,65, 66 A trial
with neuromuscular blocking agents could be considered when more straightforward measures
are not sufficient or are ineffective, and continuous infusion of these agents could be considered
when a clinically relevant effect is shown.
Optimize fluid adminstration an systemic/regional perfusion
Fluid resuscitation also may contribute to the development of IAH, a risk that seems es-
pecially relevant in patients with capillary leakage, in which fluids accumulate in the bowel
wall and mesentery, free peritoneal cavity, retroperitoneum, and abdominal wall. This role of
fluid accumulation in IAH suggests that all efforts should be made to remove excess fluid
from a volume-overloaded patient with overt ACS. Also, when a patient’s acute illness has sub-
sided, and fluid accumulation is the cause of a more chronic form of IAH, a similar strategy
may be warranted. Depending on the clinical situation, either ultrafiltration or diuretics can be
used.67,68
Surgical decompression
If attempts to decrease IAP using medical treatment are not sufficient, formal decompressive
laparotomy should be considered. Also, in patients with rapidly progressive organ dysfunction
caused by IAH, early surgical decompression may be indicated. Although invasive, decompressive
laparotomy has been shown in studies to be effective in decreasing IAP and improving organ
function. However, if overt ACS has occurred, IAP often remains in the range of 12–20 mm Hg,
and despite dramatic improvements, normalization of organ function is rarely observed.69 The
timing of the intervention is essential; for example, Mentula et al. described poor outcomes in
patients with severe acute pancreatitis when decompression was performed more than 4 days
after admission to the ICU.70
Decompressive laparotomy may be performed in the Operating Room (OR) or at the bed-
side in the ICU. A full midline laparotomy from the xiphoid down to the pubis is the technique
most commonly used, but other less invasive modalities have been developed, with subcuta-
neous linea alba fasciotomy as one of the most promising approaches.71 Surgical decompression
means that the patient is left with an open abdomen, which can result in severe fluid losses,
infection, enterocutaneous fistulas, ventral hernia, and cosmetic concerns. Temporary abdominal
closure techniques have improved significantly in recent years, leading to lower complication
rates and earlier fascial closure rates. Minimally invasive methods are not the standard of care
at present for primary or recurrent ACS.
An understanding of the pathophysiologic mechanism would allow clinicians to choose which
treatment arm to utilize and when to escalate treatment to a different tier. Based on studies
previously conducted, it has been shown that the improvement of outcomes in these patient
populations requires an interdisciplinary, integrated, goal-directed tiered management approach.
Conclusions
It has been established that measurement of IAP bears significant prognostic value for criti-
cally ill patients as IAH and ACS are frequently associated with poor outcomes. For this reason,
early and ongoing assessment including serial IAP measurements should be monitored in any
patient who is suspected to have IAH/ACS. Early recognition is essential in management and ul-
timately patient outcome. We need to understand the pathophysiology of IAH and ACS, proceed
with higher suspicion and test for IAH in all patients presenting with risk factors. Ideally, we
would want to be able to diagnose developing IAH and ACS and intervene before the onset of
organ dysfunction and failure. Preferably, early therapeutic intervention either medical or sur-
gical attempts to decrease IAP should be considered sooner than later. The WSACS guidelines
and recommendations give clinicians a helpful understanding of IAH and ACS and their clinical
management to improve patient survival.
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Abdominal Compartment Syndrome

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Abdominal Compartment Syndrome

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Disease-a-Month 65 (2019) 5–19

Contents lists available at ScienceDirect

journal homepage: www.elsevier.com/locate/disamonth

Abdominal compartment syndrome

Glenda Sosa, MD a, Narayana Gandham, MD a, Veeda Landeras, MD b,

Brief historical aspects

Predisposing conditions and risk factors

Multiple patient population characteristics, comorbidities, and therapeutic interventions con-

Intra-abdominal pressure raises the intra-thoracic pressure by way of abdomino-thoracic

Fig. 1. Pathophysiologic Implications of Intra-abdominal Hypertension. The effects of intra-abdominal hypertension

Central nervous system

Measuring intra-abdominal pressure via intravesicular route

1. Foley urine catheter with a urine bag

Fig. 2. AbViser IPA Monitoring System Copyright © 2012 ConvaTec Inc.http://abviser.com/products/

Steps for measuring intra-vesicular pressure

Evacuate intra-luminal contents

Evacuate intra-abdominal space occupying lesions

Improve abdominal wall compliance

Limited abdominal wall compliance is an essential contributor to IAH. Increased abdominal

Optimize ﬂuid adminstration an systemic/regional perfusion

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