Overview: Intra-abdominal hypertension and abdominal compartment syndrome
FREE CME Lecture – 1 hour:
Intra-abdominal hypertension – the ARDS of
the Gut, By Dr. Tim Wolfe
Audio-video
overview of the topic – click here to view
Click here for a medical review article on the topic from 2009
Click here for a surgical review article on the topic from 2009
Introduction:
Compartment
syndrome occurs when the pressure within a closed anatomic space (a
compartment) becomes so elevated that capillary perfusion is
compromised and tissue ischemia develops. Compartment syndromes are
classically thought of as complications associated with orthopedic
trauma, occurring when muscular compartments of extremities develop
elevated pressures requiring decompressive fasciotomies.
However, any closed anatomic space, including the abdominal
cavity, is at risk of developing a compartment syndrome.[1]
Abdominal compartment syndrome is a clinical disease spectrum that
results from elevated intra-abdominal pressure (IAP) due to tissue
edema or free fluid collecting in the abdominal cavity.[1-6]
Elevated pressure in the abdomen is referred to as intra-abdominal
hypertension (IAH) while the spectrum of pathophysiologic
derangements that occur as a result of increasing IAH is referred to
as the abdominal compartment syndrome (ACS).
This clinical spectrum dramatically impacts patient
outcome:
The end result of ACS, if undetected and untreated, is multisystem
organ failure and patient death.[4-7]
Pathophysiology of increased
intra-abdominal pressure:
Critically ill
patients requiring resuscitation with fluids and/or vasopressors
suffer tissue ischemia/reperfusion injuries.[6, 8] This cycle of
ischemia/reperfusion results in microvascular permeability,
capillary leakage of fluid and tissue edema.[8] An especially
susceptible organ to tissue ischemia/reperfusion injury, capillary
leak and edema is the bowel. Since the abdominal wall limits the
total volume of intra-abdominal space, as bowel expands the pressure
within the abdomen also increases. This causes occlusion of
capillary blood flow and ultimately ends in compromise of venous
return and arterial flow. The resulting ischemia triggers a vicious
cycle of further inflammation, capillary leak, bowel edema and
increasing intra-abdominal pressure. Normal intra-abdominal pressure
is 0-5 mm Hg. Physiologic compromise begins when the pressure rises
above 8-10 mm Hg. Once the pressures increase beyond 20 mm Hg
irreversible tissue injury occurs, ultimately resulting in ACS and
multiple organ failure. Early recognition of rising abdominal
pressure is critically important when it is still relatively occult
(intraabdominal hypertension) because it allows prompt intervention
which will prevent ACS from developing, leading to a much better
prognosis for the patient.
Figure: Pathophysiologic impact of IAH on the organs
(Click
here for a high resolution 8 MB document of this figure)
Traditionally,
ACS was considered a traumatic surgical disease. However, ACS is a
problem in many critically ill patients who have suffered no trauma,
especially those suffering systemic inflammatory response syndromes
(SIRS) (click here to
see the section on prevalence and risk factors). Table 1 lists a
number of clinical conditions associated with ACS development.
While this list is a helpful reminder of conditions that can
be complicated by ACS, recognizing a clinical pattern is more
useful. Biffl et al and
others point out such a pattern: Any patient with an inflammatory
response causing capillary leak and requiring volume resuscitation
or vasopressor support is at risk for developing bowel edema,
intra-abdominal hypertension
and ACS.[6, 8, 9] Intra-abdominal pressure monitoring should be
strongly considered in all patients with this clinical
presentation.[3, 10] Peruse this web site and there is a large
amount of additional information discussing risk factors,
interventions, pathophysiology and outcome data regarding this still
relatively infrequently recognized disease that is occurring daily
in most ICU’s across the world.
Table 1: Risk Factors associated with intra-abdominal hypertension
and abdominal compartment syndrome
Click here for the PDF of the document
References:
1.
Schein, M., et al., The
abdominal compartment syndrome: the physiological and clinical
consequences of elevated intra-abdominal pressure. J Am Coll
Surg, 1995. 180(6): p. 745-53.
2.
Morken, J. and M.A. West,
Abdominal compartment syndrome
in the intensive care unit. Curr Opin Crit Care, 2001.
7(4): p. 268-74.
3.
Cheatham, M.L., et al.,
Results from the International Conference of Experts on
Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II.
Recommendations. Intensive Care Med, 2007.
33(6): p. 951-62.
4.
Malbrain, M.L. and I.E. De laet,
Intra-abdominal hypertension:
evolving concepts. Clin Chest Med, 2009.
30(1): p. 45-70, viii.
5.
Cheatham, M.L., et al.,
Criteria for a diagnosis of abdominal compartment syndrome. Can
J Surg, 2009. 52(4): p. 315-316.
6.
Cheatham, M.L.,
Abdominal Compartment Syndrome: pathophysiology and definitions.
Scand J Trauma Resusc Emerg Med, 2009.
17(1): p. 10.
7.
Cheatham, M.L.,
Intra-abdominal hypertension and abdominal compartment syndrome.
New Horiz, 1999. 7: p. 96-115.
8.
Biffl, W.L., et al.,
Secondary abdominal compartment syndrome is a highly lethal event.
Am J Surg, 2001. 182(6):
p. 645-8.
9.
Ivatury, R.R., H.J. Sugerman, and A.B. Peitzman,
Abdominal compartment
syndrome: Recognition and management, in
Advances in Surgery, J.L. Cameron, Editor. 2001, Mosby. p. 1-19.
10.
Cheatham, M.L.,
Nonoperative management of intraabdominal hypertension and abdominal
compartment syndrome. World J Surg, 2009.
33(6): p. 1116-22.