ACS Abdominal Compartment Syndrome

Sabiston
Acute Abdominal Compartment Syndrome Cause
Abdominal compartment syndrome (ACS) describes increasing organ
dysfunction or failure as a result of IAH. IAH is present when there is a consistent
increased IAP value higher than 12 mm Hg, determined by a minimum of three
measurements conducted 4 to 6 hours apart, measured at the end of expiration
in a relaxed patient. ACS may be primary or secondary and develops when IAP is
20 mm Hg or higher, with or without abdominal perfusion pressure (APP) less
than 50 mm Hg (at least three measurements performed 1 to 3 hours apart); it is
associated with failure of one or more organ systems that was not present
previously.
Primary ACS develops as a result of pathologic IAH caused by intraabdominal pathology and secondary ACS develops in the absence of intraabdominal primary pathology, injury, or intervention. Primary ACS is most
commonly encountered in victims of multiple trauma, especially after damage
control surgery, and develops as a result of ileus caused by bowel edema and
contamination, continued bleeding, coagulopathy, packing used to control
bleeding, capillary leak, and massive fluid resuscitation and transfusion. Closure
of a noncompliant abdominal wall under tension in these situations is associated
with IAH in 100% of cases. In nontrauma patients, IAH and possibly primary ACS
have been reported to occur in patients with ascites, retroperitoneal
hemorrhage, pancreatitis, or pneumoperitoneum and after reduction of chronic
hernias that have lost their domain, repair of ruptured abdominal aortic
aneurysm, complex abdominal procedures, and liver transplantation.
Secondary ACS is in part iatrogenic and commonly encountered in patients
with shock requiring aggressive fluid resuscitation with crystalloids, thermally
injured and shock trauma victims, critically ill hypothermic and septic patients,
and those who have sustained cardiac arrest. Shock and ischemia increase
capillary permeability; combined with excessive crystalloid resuscitation (leading
to dilution of plasma) and gut reperfusion, which further increase microvascular
permeability, exudation of fluid with resultant interstitial edema, bowel wall
edema and ascites occurs. In healthy individuals, IAP ranges from
subatmospheric to 5 mm Hg and fluctuates with respiration, body mass index,
and activity. Following uncomplicated abdominal surgery, IAP ranges from 3 to 15
mm Hg. IAP reflects intra-abdominal volume and abdominal wall compliance.
With increased volume, there is a decrease in compliance and any further
change in volume results in an increase in pressure, leading to IAH. In the early
stages of IAH, changes in organ function are not detectable and of questionable
clinical significance. With further increase in IAP, deleterious effects are observed
in the intra- and extraabdominal organs and abdominal wall.27 Upward
displacement of the diaphragm results in decreased thoracic volume and
compliance and increased intrapleural pressure. This results in an increase in
peak airway pressure (PAP), ventilation-perfusion (V-P) mismatch, hypoxia,
hypercapnia, and acidosis. When IAP reaches 25 mm Hg, there is an increase in
end-respiratory pressure to achieve a fixed tidal volume. However, modest IAH
can exacerbate acute lung injury, inhalation injury, or respiratory distress
syndrome.
Compression of the inferior vena cava and portal vein occurs and results in
decreased venous return, and therefore a decrease in preload and pooling of

blood in the splanchnic and lower extremity vascular beds, and increased
peripheral vascular resistance. Venous return decreases with IAP higher than 20
mm Hg. As a result, cardiac output (CO), cardiac index, and right atrial and
pulmonary artery occlusion pressures decrease. Increased intrathoracic pressure
also decreases left ventricular compliance, thus reducing contractility and further
decreasing the CO. Ventricular compliance is reduced when IAP is higher than 30
mm Hg. Cardiac output decreases, despite normovolemia or apparent high filling
pressures and a normal ejection when the IAP is 20 to 25 mmHg. Systemic
delivery of oxygen (O2) decreases and whole body oxygen consumption is
significantly reduced at an IAP higher than 25 mmHg.
Direct compression of the kidneys and obstruction of venous outflow, with
resultant increase in prerenal vascular resistance and shunting of blood from the
cortex to the medulla, results in a decrease in the glomerular filtration rate, renal
plasma flow, glucose reabsorption, and urine output. In the postoperative patient
admitted to the intensive care unit with an IAP higher than 18 mm Hg, renal
function is impaired by 30%, independent of prerenal circulation. With an IAP
higher than 25 mm Hg, renal output decreases in 65% of patients and in 100% of
patients with an IAP higher than 35 mm Hg. Compression of the mesenteric
vasculature leads to a decrease in splanchnic perfusion, mesenteric venous
hypertension, and decreased hepatic arterial flow. This results in severe
intramucosal acidosis, intestinal edema, and visceral swelling, increased
intestinal permeability, and possible bacterial translocation. Gastric intramucosal
acidosis develops with IAP higher than 20 to 25 cm H2O or 15 mm Hg. Elevated
central venous pressure interferes with venous cerebral outflow, with consequent
cerebral pooling and increase in intracerebral pressure. Also, with diminished CO
and increasing intracerebral pressure, cerebral perfusion pressure decreases.
Interleukin 6 (IL-6) and IL-1B levels increase in response to increased IAP. Blood
flow to the abdominal wall decreases with a progressive increase in IAP.This may
result in an increased rate of abdominal wound complications.

Diagnosis
The clinical manifestations of primary and secondary ACS are similar.
However, the effects of secondary ACS are more subtle, so the diagnosis may be
missed and the clinical deterioration of the patient is usually attributed to
severity of the primary illness or occurrence of irreversible shock. Secondary ACS
often occurs during aggressive fluid resuscitation in patients with burns,
extraabdominal injury, or sepsis. Patients with ACS have difficulty breathing or
are difficult to ventilate and exhibit rising PAP, decreased volumes, hypoxia,
worsening hypercapnia, and deteriorating compliance. Oliguria rarely occurs in
the absence of respiratory dysfunction or failure. The CO is reduced, despite
apparent high filling pressures, and vasopressor therapy is required. The
abdomen becomes distended and tense and neurologic deterioration may occur.
The central venous pressure, pulmonary capillary wedge pressure (PCWP), and
PAP become elevated and acidosis develops. Anuria, exacerbation of pulmonary
failure, cardiac decompensation, and death ultimately occur.
Use of the urinary bladder catheter has been the gold standard and is the
indirect method used to measure IAP.28 IAP is measured in the following ways:
(1) using a regular Foley catheter, disconnect from drainage tubing, directly
inject 50 mL, clamp, insert needle, and measure; (2) a three-way Foley catheter
with saline is injected into one port and IAP is measured through the other; or (3)
a regular Foley catheter is serially connected to a three-way stopcock and a

transducer. Other measurement kits have now become commercially available.

Once measured, the pressure is graded: GI (IAP < 10 to 15 cm H2O), GII (IAP <
16 to 25 cm H2O), GIII (IAP < 26 to 35 cm H2O), and GIV (IAP > 36 cm H2O).

Treatment
The prevention of primary ACS entails leaving the peritoneal cavity open
in patients at risk for IAH and after high-risk surgical procedures. Patients at risk
for secondary ACS receiving crystalloid resuscitation must be monitored closely
and, when given more than 6 liters of crystalloid in a 6-hour period, IAP must be
measured. In addition to blood pressure and urine output, monitoring APP (APP =
mean arterial pressure IAP) by continuously measuring IAP throughout
resuscitation is a helpful indicator of the resuscitation end point. Routine
measurement of IAP must also be considered in critically ill patients because IAH
is the leading cause of chest wall impairment in ARDS. Monitoring gastric pH can
detect cases of secondary ACS early after admission to the intensive care unit. A
high incidence of suspicion is paramount, especially in cases of secondary ACS in
which the onset is insidious and manifestations are subtle. Patients exhibiting the
prodromal phase of ACS benefit from timely intervention to relieve the IAH and
prevent progression to ACS (Box 13-13).
Conservative fluid resuscitation, administration of analgesia, sedatives and
pharmacologic paralysis, patient positioning, drainage of intra-abdominal fluid,
escharotomy, renal placement therapy, and diuretics are measures that may
prevent progression to ACS. Optimizing treatment and identifying patients with
IAH-ACS likely to benefit from decompression is a challenging task. The decision
to intervene surgically is not based on IAH alone but rather on the presence of
organ dysfunction in association with IAH. Few patients with a pressure of 12 mm
Hg have any organ dysfunction, whereas IAP higher than 15 to 20 mmHg is
significant in every patient. With grade III IAH, decompression may be considered
when the abdomen is tense and signs of extreme ventilatory dysfunction and
oliguria develop. In grade IV IAH, with signs of ventilator and renal failure,
decompression is indicated.
In patients with severe head injury and IAP higher than 20 mm Hg, even
without overt ACS, or intractable intracranial hypertension without obvious head
injury, abdominal decompression must be considered. Unlike primary ACS, in
which reopening of the preexisting laparotomy incision for decompression can be
easily done, there is usually reluctance to perform a formal laparotomy for
decompression in cases of secondary ACS, especially in the absence of primary
intra-abdominal pathology. If nonoperative measures (see earlier) prove
ineffective, fascial release without exposing the peritoneal cavity using minimally
invasive techniques has proven effective in lowering IAP in experimental
animals.34 Decompression (formal laparotomy) is an emergency and is
performed in the operating room. Decompression leads to reduction of IAH,
severe hypotension as a result of sudden decrease in systemic vascular
resistance, and abrupt increase in the true tidal volume delivered to the patient,
with washout of the byproducts of anaerobic metabolism from below the
diaphragm. This results in respiratory alkalosis, decrease in effective preload,
and a bolus of acid, potassium, and other

Intra-Abdominal Hypertension or Abdominal Compartment Syndrome

Complicating the Difficult Abdominal Wall
Once reexploration and staged abdominal reconstruction have been
completed, the next goal is to close the abdomen with the least amount of
physiologic stress. Intra-abdominal hypertension is known to cause ischemia to
the viscera and abdominal wall, which can progress to abdominal compartment
syndrome with organ dysfunction. In 2004, the World Congress of Abdominal
Compartment Syndrome met to develop consensus definitions for intraabdominal hypertension and abdominal compartment syndrome.7,8 These
consensus definitions are used to define intra-abdominal hypertension and
primary, secondary, and recurrent abdominal compartment syndrome.
The World Congress of Abdominal Compartment Syndrome definitions
have helped further define the disease processes of intraabdominal hypertension
and abdominal compartment syndrome (Boxes 19-2 and 19-3). Abdominal
compartment syndrome is not necessarily an end stage process but a continuum
of disease, which might be amenable to medical management at an earlier
stage. Grade III intra-abdominal hypertension (intra-abdominal pressure >20 mm
Hg) should be further monitored with intravesicular pressure monitoring. Medical
therapies should be instituted at this pointsupine positioning, judicious
crystalloid resuscitation, and drainage of intraabdominal fluid collections.9 If
these fail to improve intraabdominal hypertension or organ dysfunction develops,
serious consideration must be given to decompressive laparotomy. Other
therapies to decrease intra-abdominal hypertension may include neuromuscular
blockade, increased sedation, diuresis, evacuation of intra-luminal contents, and
hemodialysis or hemofiltration.
Abdominal decompression lowers intra-abdominal hypertension and
results in improvement in lung dynamic compliance. 10 Bladder pressures higher
than 25 mm Hg have been suggested to indicate abdominal compartment
syndrome.11 Using the definition of abdominal compartment syndrome the
development of significant respiratory compromise, including elevated
inspiratory pressure (35 cm H2O), renal dysfunction (urine <30 mL/hr),
hemodynamic instability requiring catecholamines, and a rigid or tense
abdomen, it has been found that in these patients, emergency abdominal
decompression results in a significant increase in the cardiac index, tidal volume,
and urine output, with a resultant decrease in bladder pressure, heart rate,
central venous pressure, pulmonary artery occlusion pressure, peak airway
pressure, partial pressure of arterial carbon dioxide, and lactate level. Abdominal
decompression may also be of benefit in the setting of increased intracranial
pressure.
Secondary abdominal compartment syndrome may occur after
exsanguination from an extremity injury and/or when massive volume
resuscitation is required. Recurrent abdominal compartment syndrome occurs
after damage control in a patient with an open abdomen with ongoing
hemorrhage or massive volume resuscitation. In all scenarios, intra-abdominal
pressure
should be monitored.12,13

SUMMARY
In most damage control laparotomies for trauma, vascular surgery, and/or
emergency general surgery, primary fascial closure can be achieved in 60% to
90% of the cases. Patients for whom the abdomen cannot be closed make up the
category of those with a difficult abdominal wall. This can then give rise to the
complex ventral hernia. The causes of the difficult abdominal wall share features
in commonloss of abdominal domain, risk of the development of intraabdominal hypertension and/or abdominal compartment syndrome, development
of intraabdominal abscess or fistula, systemic inflammatory response syndrome,
and a higher than 50% risk of hernia formation. When temporary coverage of the
abdomen is necessary, the technique should be easy to apply, tension-free,
atraumatic, and inexpensive and allow for a high rate of delayed primary fascial
closure.
Following normalization of physiology, reexploration and a staged repair
may be performed. It is not advisable to attempt delayed primary fascial closure
if there is undue tension on the fascia or the peak inspiratory pressure rises more
that 10 cm H2O. However, the inability to close the open abdomen by 8 days is
associated with a significant increase in complications, including
enteroatmospheric fistulas. For this reason, some surgeons have bridged an
abdominal wall defect with biologic mesh to protect the abdominal visceral.
However, this repair should be considered as a temporizing measure because
most bridging repairs will develop bulging and/or laxity within 1 year of closure.
Delayed ventral hernia repair using component separation reinforced with
biologic mesh has produced excellent results and is recommended for the
closure of the complicated abdominal wall.

Abdominal Compartment Syndrome

The abdomen is a closed space, bound by the relatively nonexpansile
fascia of the abdominal musculature and, as such, is susceptible to a
compartment syndrome analogous to that seen in the lower extremities. ACS is
fundamentally defined as increased intra-abdominal pressure (IAP) associated
with adverse physiologic consequences.40 ACS has usually been described in
patients with massive abdominal or pelvic hemorrhage, often following damage
control laparotomy, but it may be encountered in various clinical scenarios.
Circumferential torso burn eschar, reduction of a large ventral hernia, or military
antishock trousers may significantly increase IAP. Bowel distention caused by
obstruction or ileus, ascites, or pneumoperitoneum may also lead to ACS.
Pancreatitis or surgical dissection may result in profound retroperitoneal edema.
Edema of the bowel may result from prolonged evisceration during surgery,
which elongates and narrows mesenteric veins and lymphatics; it may also be
related to ischemia or reperfusion of the bowel aggravated by resuscitation with
large volumes of crystalloid solutions.
Secondary ACS refers to ACS in the absence of abdominal or pelvic
pathology and is entirely caused by edema and ascites following shock and
aggressive resuscitation. In this setting, particularly in nontrauma patients, it
may represent a state of irreversible shock, with loss of capillary integrity. The
organ systems that appear most affected by ACS are the cardiovascular,

pulmonary, and renal systems. Cardiovascular effects of increased IAP include

decreased CO because of diminished venous return and a markedly increased
systemic vascular resistance. Ensuring adequate volume status is a key feature
of ACS management and can be used to temporize the situation while
arrangements are made for urgent decompression. Increased IAP diminishes
diaphragmatic excursion, decreases pulmonary compliance, and creates high
airway pressures, with diminishing VT and resultant respiratory acidosis. Renal
dysfunction, oliguria progressing to anuria because of ACS, appears to be caused
by direct parenchymal compression and shunting of renal plasma flow. Visceral
blood flow is similarly affected, leading to intestinal necrosis, hepatic
dysfunction, and gut anastomotic breakdown. Intracranial hypertension is also
aggravated by ACS. Decompressive celiotomy can reverse these changes
immediately, but untreated ACS leads to lethal organ failure, with collective
mortality rates exceeding 50%.40
The recognition of ACS is not difficult once the diagnosis is considered.
Those at highest risk include severely injured patients who require abdominal
packing for abbreviated or staged laparotomy, particularly those with a
coagulopathy caused by core hypothermia or cirrhosis. It is prudent to screen
patients at high risk for developing ACS, particularly those acutely resuscitated
from shock, those who require vasopressors, and those who are receiving large
volumes of crystalloid fluids or blood products. The findings of a tensely
distended abdomen, progressive oliguria in spite of adequate CO, or hypoxia with
increasing airway pressures are sufficient to justify abdominal decompression.
Physical findings alone may be inaccurate in the critically ill patient; thus,
bladder pressures can be measured to determine an elevated IAP and correlate it
with physiologic parameters; therefore, bladder pressure has become the
objective measure for confirming ACS. The level of IAP at which ACS occurs is
patient-specific, so the diagnosis and treatment are based on the patients
physiologic responses to increased IAP.
Rough correlations can be made between the level of IAP elevation and
the need for decompression (Table 23-4). Although significant alterations in
physiology can be demonstrated with an IAP between 10 and 15 mm Hg (grade
I), it is doubtful that abdominal decompression is warranted at this level. With an
IAP between 15 and 25 mm Hg (grade II), the need for treatment should be
based on the patients clinical condition; however, in the absence of oliguria,
hypoxia, or significantly elevated airway pressure, abdominal decompression is
difficult to justify. Continued monitoring is clearly indicated because signs and
symptoms of intra-abdominal hypertension progress insidiously. Most patients
with an IAP between 25 and 35 mm Hg (grade III) ultimately require
decompression. All patients with an IAP higher than 35 mm Hg (grade IV) require
immediate decompression because they may deteriorate to cardiac arrest at any
time. Percutaneous drainage of ascitic fluid may be a temporizing maneuver, but
operative decompression is usually necessary.
At the time of decompression, an abdominal closure that affords additional
intra-abdominal domain is indicated. Of the various dressings described, the
most effective appears to be based on some type of vacuum, either
commercially available or home-made, so that bowel edema and lateral
retraction of the fascia are minimized and peritoneal fluid is controlled.41 Every
reasonable effort should be made to achieve definitive abdominal closure within
several days, because the lateral retractive forces of the broad flat muscles of
the abdominal wall can make primary closure difficult. If the abdomen cannot be
closed, absorbable or biologic meshes and skin grafts should be used to

minimize the risk of intestinal fistulas. Interestingly, vacuum-assisted wound

dressings may facilitate early definitive abdominal closure, as well as late closure
many weeks after the initial operation.42 Care of the patient with an open
abdomen is an evolving area of surgery but efforts should generally focus on
protecting the bowel from fistula formation, optimizing nutrition, treating
infections and organ failure, and closing the fascia as soon as possible.