CV
hypoperfusion due to decreasing cardiac output [22]. With
unabated progression of the clinical syndrome, high peak
inspiratory pressures with hypercarbia, impaired venous
return, marked oliguria to anuria unresponsive to fluid
challenge, altered levels of consciousness, and respiratory
failure are encountered [23].
Table 1: Grading of intra-abdominal hypertension (WSACS
consensus definitions, 2004).
At or above an intra-abdominal pressure of 25 mmHg,
extensive bowel necrosis, frequently involving the left
colon, is observed. Malperfusion of the gut in this clinical
continuum may be particularly threatening when vascular
operations have altered mesenteric blood supply, that is,
coverage of a previously patent inferior mesenteric artery,
hypogastric artery, or both.
IAP = Intra-abdominal pressure.
From the WSACS consensus definitions, 2004 [21], major
risk factors for the development of ACS in patients suffering from acute intra-abdominal vascular catastrophe are
listed in Table 2. Knowledge of these risk factors combined
with calculation of IAP or abdominal perfusion pressure
(abdominal perfusion pressure = mean arterial pressure-intra-abdominal pressure) may guide management.
The WSACS defined an abdominal perfusion pressure
(APP) of 60 mmHg or less to be consistent with poor perfusion and an increased risk for ischemia. Cheatham et al.
[24] found the abdominal perfusion pressure (target of 50
mmHg) to be superior to intra-abdominal pressure measurements, arterial pH, urinary output, lactate, and base
deficit measurements as an endpoint of resuscitation and a
better predictor of survival in patients with IAH and ACS.
3. Measuring Intra-Abdominal Pressure
Various methods have been described for the accurate
measurement of intra-abdominal pressure. Puncture of the
abdominal wall for pressure measurement carries unacceptable risk, making indirect techniques necessary.
Most commonly, intra-cystic pressures are used as a surrogate for intra-abdominal pressure. Djavani Gidlund [4]
described inflation of 50 mL of sterile saline into the aspiration port of a Foley catheter, clamping the tube distal to the
port, and connecting a 16-gauge needle to a transducer to
measure the pressure transmitted across the bladder wall.
Because of the potential for spuriously elevated pressures,
current protocols specify inflation of the Foley balloon with
only 25 mL of saline [25].
The midaxillary line is used as the zero point for the supine
patient. Intermittent indirect measurement methods have
been described, and Balogh et al. [26] detailed a continuous
measurement technique based on a three-way Foley catheter and irrigation. A standardized algorithm was published
in 2007 by WSACS assessing IAH [25] (Figure 1).
Another technique to measure bladder pressure is the
Foleymanometer [27] system (Holtech Medical, Copenhagen Denmark), which can be applied to both ICU patients
as well as patients in noncritical care settings. This system
uses the patient’s own urine as the pressure transducing
medium. A 50 mL container filled with biofiller that is able
to be vented is inserted between the Foley catheter and the
drainage bag.
10
Grade I
Grade II
Grade III
Grade IV
IAP 12-25 mmHg
IAP 16-20 mmHg
IAP 21-25 mmHg
IAP > 25 mmHg
Table 2: Established risk factors for IAH/ACS in acute abdominal vascular catastrophe.
Adapted from WSACS consensus definitions, 2004 [21]
Hemoperitoneum and retroperitoneal hematoma
Massive fluid resuscitation (>5 L colloid or crystalloid/24 h)
Polytransfusion (>10 U packed red blood/24 h)
Coagulopathy (platelets <55,000/mm3 or activated
patial thromboplastin time two times notmal or higher or
prothrombin time <50% or international standardized
ratio >1.5)
Hypothermia (core temperature <330 C)
Acidosis (pH < 7.2)
Lengthy cross-clamp time or balloon-occlusion time
Lengthy operative times
Bozeman, Ross
During normal drainage, this container fills with urine, but
once elevated, 50 mL of urine flows back into the patient’s
bladder creating a pressure transducing column. The tubing
is clear and marked to allow easy reading of the patients’
IAP. Malbrain [28] found excellent correlation between this
technique and those previously described.
4. Incidence of Abdominal Compartment Syndrome after rAAA
Vascular surgeons have not always recognized the significance of ACS as a determinate of survival in rAAA patients.
In a survey of practicing vascular surgeons in Australia
reported in 2008, Choi et al. [29] found that only 30% routinely measured intra-abdominal pressure in postoperative
rAAA patients and that only 17% would consider prophylactic delayed abdominal wound closure in rAAA patients
meeting criteria making them high risk for postoperative
development of ACS.
It follows that the true incidence of ACS as a contributing
factor to MOF and death following repair of rAAA may be
underappreciated due, in part, to failure to monitor for its
occurrence. Another factor contributing to the under recognition of ACS in these patients is that, prior to 2004, no
consensus definition existed to define IAH and ACS and to
guide management.
Fietsam et al. [8] reported a retrospective review from
1978–1988 in which 4/104 (5.8%) patients surviving an
rAAA repair developed ACS, apparent to the authors even
without a standardized definition at that time. Two of these
patients were managed with an open abdomen at the con-
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