CV
Matthew C. Bozeman
Charles B. Ross
Division of Vascular Surgery and Endovascular Therapeutics, Department
of Surgery, University of Louisville
intra-abdominal hypertension
and abdominal compartment
syndrome in association with
ruptured abdominal aortic aneurysm in the endovascular era:
vigilance remains critical
Abstract
Intra-abdominal hypertension (IAH)
and abdominal compartment syndrome (ACS) are common complications of ruptured abdominal aortoiliac
aneurysms (rAAAs) and other abdominal vascular catastrophes even in the
age of endovascular therapy.
Morbidity and mortality due to
systemic inflammatory response
syndrome (SIRS) and multiple organ
failure (MOF) are significant. Recognition and management of IAH are key
critical care measures which may decrease morbidity and improve survival
in these vascular patients.
Two strategies have been utilized:
expectant management with prompt
decompressive laparotomy upon diagnosis of threshold levels of IAH versus
prophylactic, delayed abdominal
closure based upon clinical parameters
at the time of initial repair.
Competent management of the abdominal wound with preservation of
abdominal domain is also an important component of the care of these
patients.
1. Introduction
Patients who survive an initial operation for an intra-abdominal catastrophic event, such as a ruptured abdominal aortic aneurysm (rAAA) or other abdominal vascular
catastrophes such as complicated mesenteric revascularization, often suffer from severe physiologic derangements.
In this review, we describe published
experience with IAH and ACS complicating abdominal vascular catastrophes, experience with ACS complicating endovascular repair of rAAAs,
and techniques for management of the
abdominal wound.
Vigilance and appropriate management of IAH and ACS remains critically important in decreasing morbidity
and optimizing survival following
catastrophic intra-abdominal vascular
events.
Kron et al. [7] in 1984 described ACS and end-organ failure
emphasizing oliguria managed successfully with decompressive laparotomy following an initial operation for repair
of rAAA. Fietsam et al. [8] first described delayed abdominal closure and subsequent management in 1989. Since
that time, further experiences and lessons learned from diagnosing and treating ACS have been reported [1, 4, 9–20].
Factors contributing to their critical illness include hemodynamic instability, massive fluid resuscitation, transfusion of blood products, hypothermia, acidosis, and lengthy
operations with resultant fluid shifts. ACS is recognized
as a major cause of death after treatment for rAAA with
short-term mortality rates as much as 5 times greater than
observed in patients without ACS even in patients treated
by endovascular techniques [1].
2. The Physiologic Basis of Abdominal Compartment Syndrome
Although endovascular repair of rAAA (REVAR) has shown
promise in reducing these challenges and improving survival in patients with suitable anatomy [2], a reported 10–20%
of patients treated by endovascular techniques still develop
ACS [1–6]. Recognition and management of IAH and ACS
complicating open or endovascular repairs is critically
important in decreasing morbidity and improving survival
from rAAA.
IAH is defined as an intra-abdominal pressure (IAP) greater than 12 mmHg in consecutive, standardized measurements with the risk of progression to overt ACS, defined as
IAP greater than 20 mmHg or abdominal perfusion pressure less than 60 mmHg with end-organ dysfunction [21],
increasing as IAP increases.
CV DIRECTIONS VOL. 2, NO. 2
The end result of intra-abdominal hypertension is impaired
organ perfusion resulting in MOF. A relationship exists as a
continuum between IAH and ACS. IAH is evaluated with a
grading system reported in 2006 by the World Conference
on Abdominal Compartment Syndrome (Table 1) [21].
Early in the disease process, prior to stage III, patients
develop oliguria, elevat ed end-inspiratory pressures, and
9