2. • Background: Compartment syndrome occurs when a
fixed compartment, defined by myofascial elements or
bone, becomes subject to increased pressure, leading to
ischemia and organ dysfunction. Well recognized to
occur in the extremities, it also occurs in the abdomen,
and some believe, in the intracranial cavity. The exact
clinical conditions that define abdominal compartment
syndrome (ACS) are controversial; however, organ
dysfunction caused by intra-abdominal hypertension
(IAH) is considered to be ACS. The dysfunction may be
respiratory insufficiency secondary to compromised tidal
volumes, decreased urine output caused by falling renal
3. • ACS was recognized clinically in the 19th century when
Marey and Burt observed its association with declines in
respiratory function. In the early 20th century, Emerson's
animal experiments demonstrated mortality associated
with ACS. Initially, cardiorespiratory compromise was
thought to be the cause; however, renal failure was
hypothesized by Wendt and was later studied by
Thorington and Schmidt. More recently, Kron and Iberti
developed a simple method of accurately measuring
intra-abdominal pressure, leading to a better
understanding of the relationship between IAH and ACS.
4. • ACS can be divided into the following 3
categories, which are explained in greater detail
• Primary or acute ACS: This occurs when intra-
abdominal pathology is directly and proximally
responsible for the compartment syndrome.
• Secondary ACS: This occurs when no visible
intra-abdominal injury is present but injuries
outside the abdomen cause fluid accumulation.
• Chronic ACS: This occurs in the presence of
cirrhosis and ascites, often in the later stages of
5. • The abdominal compartment syndrome represents the
pathophysiologic consequence of a raised intra-abdominal pressure.
The normal intra-abdominal pressure ranges between 0 and 5
mmHg. When it is mildly increased to between 10 and 15 mmHg,
cardiac index is usually maintained or even increased because
abdominal viscera are mildly squeezed and venous return
increases. Respiratory and renal symptoms are unlikely to occur.
Hepatosplanchnic blood flow may decrease . At this point,
intravascular volume optimization will probably correct these
alterations. When intra-abdominal pressure is moderately increased
to between 15 and 25 mmHg the full syndrome may be observed,
but usually responds to aggressive fluid resuscitation, and surgical
decompression should be considered. At high pressures (< 25
mmHg) surgical decompression associated with fluid resuscitation
and transient use of vasoconstrictive agents is mandatory.
6. • Various clinical conditions are associated
with this syndrome and include massive
intra-abdominal or retroperitoneal
hemorrhage, severe gut edema or
intestinal obstruction, and ascites under
7. • Pathophysiology: Organ dysfunction with ACS is a product of the
effects of IAH on multiple organ systems. ACS follows a destructive
pathway similar to compartment syndrome of the extremity.
Problems begin at the organ level with direct compression; hollow
systems such as the intestinal tract and portal-caval system collapse
under high pressure. Immediate effects such as thrombosis or bowel
wall edema are followed by translocation of bacterial products
leading to additional fluid accumulation, further increasing intra-
abdominal pressure. At the cellular level, oxygen delivery is
impaired leading to ischemia and anaerobic metabolism. Vasoactive
substances such as histamine and serotonin increase endothelial
permeability, further capillary leakage impairs red cell transport, and
8. • Although the abdominal cavity (ie, peritoneal and, to a
lesser extent, retroperitoneal cavities) are much more
distensible than an extremity, they reach an endpoint at
which the pressure rises dramatically. This is less
apparent in chronic cases because the fascia and skin
slowly stretch and thus tolerate greater fluid
accumulation. As pressure rises, ACS impairs not only
visceral organs, but also the cardiovascular and the
pulmonary systems; it may also cause a decrease in
cerebral perfusion pressure. Therefore, ACS should be
recognized as a possible cause of decompensation in
any critically injured patient.
9. • Frequency:
• In the US: According to recent literature, frequency in trauma ICU admissions is
anywhere from 5-15% and is 1% of general trauma admissions.
• Internationally: Much of the recent literature on ACS has originated from outside the
United States, where frequency and morbidity appear to be the same.
• Mortality/Morbidity: The morbidity of ACS is attributed to its effects on multiple
organ systems. Because of this, ACS has a high mortality rate even with treatment.
Furthermore, ACS is often a sequela to severe injuries that independently carry high
morbidity and mortality rates.
• In the early 1990s Eddy and Morris documented an ACS mortality rate of 68%, this
has been reflected in the subsequent literature, with similar mortality rates of 25-75%.
• Race: Nothing has been published indicating a racial or gender difference in the
incidence or mortality of abdominal compartment syndrome.
• Age: ACS has been documented in all age groups. The intra-abdominal pressure
(IAP) that leads to morbidity (>25 mm Hg) appears to be similar in the pediatric
10. • First, the increased intra-abdominal pressure is transmitted to the
pleural space so that lung compliance decreases. Hypoventilation
and alteration of ventilation/perfusion distribution lead to hypoxemia
and hypercapnia. When mechanical ventilation is applied, very high
inspiratory pressures are often required to deliver tidal volume.
Second, the combined increase in abdominal pressure and pleural
pressure leads to a decrease in venous return, direct compression
of the heart, and increased afterload (especially in the right
ventricle). Third, perfusion to the intra-abdominal organs can be
critically reduced by the combined effects of the decreased cardiac
output, increased interstitial pressure, and increased outflow
pressure. This can lead to oliguria and renal failure. Splanchnic
ischemia can also occur as reflected by a decreased mucosal pH
[1,2], decreased liver metabolism , and bacterial translocation .
In addition, perfusion of the abdominal wall may be decreased, so
that wound healing may be impaired. Finally, intracranial pressure
may also be increased due to the decrease in cerebral venous
11. • History: The history varies depending upon the cause of
ACS, but abdominal pain is commonly present.
Abdominal pain may precede the development of ACS
and be directly related to a precipitating event, such as
blunt abdominal trauma or pancreatitis.
• Syncope or weakness may be a sign of hypovolemia.
Although abdominal pain and distension are commonly
present, patients may not experience abdominal pain;
difficulty breathing or decreased urine output may be the
first signs of IAH.
• Furthermore, patients who develop abdominal
compartment syndrome may be unable to communicate
because they are often intubated and critically ill.
12. • Increase in abdominal girth
• Difficulty breathing
• Decreased urine output
• Nonsteroidal anti-inflammatory drug (NSAID)
• Alcohol abuse
• Nausea and vomiting
• History of pancreatitis
13. • Physical: Compartment syndrome in the
abdomen is usually suggested by an increased
abdominal girth. If this change is acute, the
abdomen is tense and tender. Although this may
be difficult to recognize in patients with morbid
obesity, other patients often have an abdomen
clearly out of proportion to their body habitus.
This may be easier to visualize with the patient
standing or sitting upright. Look for the
secondary effects of ACS.
15. • Causes: ACS occurs when the IAP is too high, similar to
compartment syndrome in an extremity. The 3 types of
ACS have different and sometimes overlapping causes.
• Primary (ie, acute)
– Penetrating trauma
– Intraperitoneal hemorrhage
– External compressing forces, such as debris from a motor
vehicle collision or after a large structure explosion
– Pelvic fracture
– Rupture of abdominal aortic aneurysm
– Perforated peptic ulcer
16. • Secondary: Secondary ACS may occur in patients
without an intra-abdominal injury, when fluid
accumulates in volumes sufficient to cause IAH.
– Large-volume resuscitation: The literature shows a significantly
increased risk when more than 3 L are infused.
– Large areas of full-thickness burns: In 2002, Hobson
demonstrated ACS within 24 hours in burn patients who had
received an average of 237 mL/kg over a 12-hour period.
– Penetrating or blunt trauma without identifiable injury
– Packing and primary fascial closure, which increases incidence
Pediatrics, Bacteremia and Sepsis
Pediatrics, Child Sexual Abuse
Pediatrics, Foreign Body Ingestion
Pediatrics, Gastrointestinal Bleeding
Pelvic Inflammatory Disease
Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum
Pneumothorax, Tension and Traumatic
Respiratory Distress Syndrome, Adult
Spinal Cord Injuries
Spontaneous Bacterial Peritonitis
Superior Vena Cava Syndrome
Trauma, Lower Genitourinary
Trauma, Upper Genitourinary
Esophageal Perforation, Rupture and Tears
Foreign Bodies, Gastrointestinal
Foreign Bodies, Rectum
Hantavirus Cardiopulmonary Syndrome
Hyperosmolar Hyperglycemic Nonketotic Coma
Hypothyroidism and Myxedema Coma
Inflammatory Bowel Disease
21. • Lab Studies:
• Comprehensive metabolic panel (CMP)
• Complete blood cell count (CBC)
• Amylase and lipase assessment
• Prothrombin time (PT), activated partial thromboplastin
time (aPTT) if the patient is heparinized
• Test for cardiac markers
• Urinalysis and urine drug screen
• Measurement of serum lactate levels: At many
institutions, the sample must be kept on ice.
• Arterial blood gas (ABG): This is a quick way to measure
the pH, lactate, and base deficit.
22. • Imaging Studies:
• Examine the abdominal series for evidence of free air or bowel obstruction.
– Realize plain abdominal radiographic studies are often useless in identifying
abdominal compartment syndrome.
• Abdominal CT scanning can reveal many subtle findings. In 1999, Pickhardt
found the following in patients with ACS:
– Round-belly sign - Abdominal distention with an increased ratio of
anteroposterior-to-transverse abdominal diameter (ratio >0.80; P <0.001)
– Collapse of the vena cava
– Bowel wall thickening with enhancement
– Bilateral inguinal herniation
• Abdominal ultrasonography
– An aortic aneurysm, particularly when large, may be detected.
– Bowel gas or obesity makes performing the study difficult.
23. • Other Tests:
• Intraluminal bladder pressure measurement, which is
described by Ivatury in a 1997 report as follows:
• Measurement of intraluminal bladder pressure consists
of instilling about 50 mL of saline into the urinary bladder
through the Foley catheter. The tubing of the collecting
bag is clamped, and a needle is inserted into the
specimen-collecting port of the tubing proximal to the
clamp and is attached to a manometer. Bladder pressure
measured in mm Hg is the height at which the level of
the saline column stabilizes with the symphysis pubis as
the zero point.
24. • The diagnosis of this syndrome is difficult
because it usually occurs in critically ill patients
with other causes of circulatory or respiratory
failure. One should always consider the
abdominal compartment syndrome when
confronted with acute circulatory failure with
wide systolic-diastolic pressure variation and
elevated filling pressures. After exclusion of
cardiac tamponade and increased pleural
pressure (tension pneumothorax, status
asthmaticus, etc), the intra-abdominal pressure
should be measured.
25. • Current methodology for intra-abdominal
pressure assessment relies on the
measurement of bladder pressure. Alternative
methods include indirect estimations of inferior
vena cava pressure, rectal and gastric pressure
measurements, and direct measurement of the
intra-abdominal pressure by direct puncture. In
experimental conditions, bladder pressure is
closely related to abdominal pressure .
Indeed, Yol et al  found good agreement
between bladder pressure and intra-abdominal
26. • In this issue, Johna et al  challenged the value of bladder
pressure measurements. During laparoscopic cholecystectomy, the
authors simultaneously measured intra-abdominal pressure by direct
puncture and bladder pressure. The two pressures were clearly not
identical, because bladder pressure systematically overestimated
the true abdominal pressure; this could lead to an over-diagnosis of
intra-abdominal compartment syndrome. Although these data were
obtained using a rigorous methodology (and the authors rightly point
out that the amount of fluid used to prime the Foley catheter should
be limited to 50 ml in order to avoid bladder distension), one should
be aware of some limitations. First, although ethical considerations
precluded the application of intra-abdominal pressures higher than
15 mmHg, it is, however, dangerous to extrapolate these results to
higher pressure levels, at which clinical manifestations of the intra-
abdominal compartment syndrome are much more serious. Second,
bladder pressure may be higher than the abdominal pressure in
27. • When patients are lying in a flat position, the bladder pressure will
represent the sum of the exogenously applied pressure (gas
pressure) and the pressure exerted by the viscera (which can be
roughly estimated as the height of these viscera), whereas the
directly measured intra-abdominal pressure only takes into account
the pressure of the insufflated gas. Third, bladder pressure
increments reflected increments in intra-abdominal pressure on an
individual basis, which could advocate the use of very early bladder
pressure monitoring in patients at risk of developing an intra-
abdominal compartment syndrome. Finally, most clinical studies
have used bladder pressure measurements [2,11], so that clinical
manifestations have been classified according to bladder pressure
levels rather than to directly measured intra-abdominal pressure
levels. The study by Johna et al  highlights that bladder pressure
measurements require cautious interpretation, but we still think that
they remain an easy, safe, and valuable tool for diagnosing the
abdominal compartment syndrome in critically ill patients.
28. • Prehospital Care: If ACS is suspected,
the focus of prehospital care is to
immediately transport the patient to the
• Remove any constricting garments.
• Do not place anything on the patient's
abdomen (eg, life packs, bundles of
blankets, oxygen tanks).
29. • Emergency Department Care: The first
priority of the emergency medicine
physician is to determine the diagnosis. In
any patient with the aforementioned
mechanisms of injury or pathology, ACS is
missed unless it is in the differential
diagnosis. Therapy should include fluid
resuscitation, transfusion if needed, and
30. • Measure IAP if ACS is suspected. In an excellent group
of articles in 1996, Burch et al developed a grading
system. Patients with higher-grade ACS are shown to
have end-organ damage, which is evidenced by splenic
hypercarbia and elevated lactate levels, even if they
appear clinically stable. The following grading system
has become accepted if IAH is present:
– Grade I, 10-15 cm H2O
– Grade II, 15-25 cm H2O
– Grade III, 25-35 cm H2O
– Grade IV, greater than 35 cm H2O
31. • End-organ damage has been observed with IAP as low as 10 cm
H2O, and multiple studies have found damage at values ranging
from 20-40 cm H2O. Disparity exists because ACS never occurs as
an isolated event.
• In 1997, Simon demonstrated a significantly lowered threshold for
injury from IAH in pigs after hemorrhage and fluid resuscitation.
Oxygen delivery may play an important role.
• In 2000, Cheatham found abdominal perfusion pressure (APP) to be
a much better predictor of end-organ injury than lactate, pH, urine
output, or base deficit. The APP is equal to the mean arterial
pressure minus the IAP.
• Pharmacologic therapy is less effective than mechanical drainage.
Pressors have a role but may not be equally effective in treating
• Dobutamine was shown to be superior to dopamine in restoring
intestinal mucosal perfusion in a porcine mo
32. • Consultations:
• General surgeon
• Orthopedic surgeon
• Obstetrician and gynecologist (OB/GYN)
• Vascular surgeon