Fluid mobilization and ventilator weaning in the face of elevated IAP
Why should
intra-abdominal hypertension be detected and treated even if it does
not progress to the abdominal compartment syndrome?
Editorial by
Tim Wolfe, MD
If one
carefully reads the references provided on this web site, considers
the pathophysiology of IAH and observes its impact and its therapy
in a clinical setting – it becomes apparent that simple
interventions can impact morbidity in many patients who only have
IAH and never develop ACS. Here is what I think is occurring:
As IAH develops
and pressures in the abdomen exceed the CVP (or about 12 mm Hg) the
syndrome becomes somewhat self-perpetuating:
High IAP compresses the vena cava, reduces preload and
subsequently reduces cardiac output. This reduces perfusion of the
gut and nephron. Simultaneously, high circulating cytokines cause
capillary permeability induced gut edema to occur. This edema leads
to a distended abdomen that stiffens the thoracoabdominal wall and
pushes the diaphragms into the chest. The result is pulmonary
compromise and an increase in the work of breathing.
If IAP is high
enough or present for long time periods it causes ischemia that
exacerbates cytokine formation leading to persistent cytokine levels
in the plasma. These cytokines maintain at least some level of
capillary permeability syndrome and persistent edema in the tissues
of the body – specifically the bowel wall and mesentery. Eventually
this cascade will stabilize in most patients and the patient will
eventually mobilizes their fluids, clear the edema and get
extubated. However, this may take many days to occur and until the
patient mobilizes that edema from the gut they cannot overcome the
IAP during ventilatory weaning trials and therefor cannot be
extubated.
I believe that
the research demonstrating reduced time on the ventilator and
shorter ICU stays when IAH is directly addressed and treated is due
to this phenomenon.[1-4]
By implementing relatively simple bedside interventions that
reduce intraabdominal pressure, renal perfusion is improved and
cytokine production is reduced. The result is an early improvement
in urine output and mobilization of some of the gut edema that is
leading to the high IAP.
As this progresses the IAP drops and the work of breathing
improves. Once the
patient is able to breath against a lower IAP – they have a better
chance of successfully being extubated. Once extubated they have
less risk of VAP and better chances for mobilization and eventual
discharge from the ICU. By helping this process along with therapies
focuses specifically on IAP reduction, ill patients with IAH tend to
get off the ventilator 3-5 days earlier than those who are not
actively treated.
In my opinion
you should actively and aggressively measuring IAP and intervene
early in all high-risk patients. However, if you are not there yet
and are looking for a great return on time and investment that will
convince you of the value – then start measuring IAP and treating
IAH in any patient who is difficult to wean off the ventilator or
who seems to have excess edema and marginal urine production.
References:
1.
Mullens, W., et al.,
Prompt reduction in intra-abdominal pressure following large-volume
mechanical fluid removal improves renal insufficiency in refractory
decompensated heart failure. J Card Fail, 2008.
14(6): p. 508-14.
2.
Mullens, W., et al.,
Elevated intra-abdominal pressure in acute decompensated heart
failure: a potential contributor to worsening renal function? J
Am Coll Cardiol, 2008. 51(3): p. 300-6.
3.
Cheatham, M.L. and K. Safcsak,
Is the evolving management of
intra-abdominal hypertension and abdominal compartment syndrome
improving survival? Crit Care Med, 2010.
38(2): p. 402-7.
4.
Kimball, E.J., et al.,
A Prospective Evaluation of the Protocolized Management of
Intra-abdominal Hypertension and the Abdominal Compartment Syndrome
Acta Clinica Belgica, 2009.
64(3): p. 272 (Abstract 110).