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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
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
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.