Frequently Asked Questions
How much volume should be infused for accurate
IAP monitoring?
There must be
enough volume infused to fill the entire tubing and Foley catheter
with fluid, plus a small amount to open the bladder so it can
equilibrate with the abdominal cavity pressure and be transmitted
via the fluid column back to the transducer.
Large volumes are not required (just like you do not need to
infuse large volumes into the arterial or CVP line for accurate
pressure). The international recommendations are to infuse 25 ml or
less (children should get 1 ml/kg infused).[1, 2] With the AbViser®
AutoValve®– infuse one syringe of fluid (20 ml) in adults. In
children infuse 1 ml/kg PLUS 2 ml extra to fill the green diaphragm
(to a maximum of 20 ml).
What position should the patient be in for
pressure monitoring?
The
recommended position for accurate measurement is the supine
position, measuring the pressure at the iliac crest, midaxillary
line when the patient is relaxed without abdominal contractions.[1,
2]
It is ok to
measure the pressure in the 30 degree elevated position as long as
you are aware that this will result in a higher pressure than the
supine position.[3] As long as the pressure is normal in the upright
position there is no need to repeat it while supine. If the pressure
is significantly elevated you should reassess the patient clinically
and place the patient supine and remeasure to have an accurate
measurement before instituting any invasive or potentially dangerous
interventions.
I see the pressure fluctuates slightly over 5-10
seconds. What is the “correct” pressure to record?
The
recommended pressure to record so that everyone uses a standardized
reproducible method of measurement is the end expiratory pressure,
measured at the iliac crest, midaxillary line while the patient is
relaxed without abdominal contractions.[1, 2]
You will
typically see some increase in pressure during positive pressure
inspiration of 1 to 4 mm Hg – the degree of this change can be
helpful in predicting how rigid/non-compliant the abdominal wall is
becoming. In patients with an abdomen that is becoming tighter you
may begin to see more significant changes in inspiratory pressure –
an early warning sign of reduced abdominal wall compliance.
How often should I measure the intraabdominal
pressure?
The frequency
of IAP monitoring will depend on the stability of the patient. The
current recommendations are “at least every 4 hours” however in a
patient who is being actively resuscitated and is in a rapidly
fluctuating physiologic state more frequent monitoring every 1-2
hours may be appropriate.[1, 2] After several serial measurements in
a brief time frame – if little change has occurred then decreasing
to every 4 hours in reasonable.
I heard the patient has to be paralyzed or
significantly sedated for accurate measurement. Is this true?
No. The
recommendation is that the patient is “relaxed without abdominal
contractions.”[1] This is the baseline state of the patient and the
measured IAP is what the organs of the abdominal cavity are being
exposed. Sedation and paralysis and sedation are useful therapeutic
interventions to assist the clinician in reducing IAP if it becomes
too elevated.[4]
Isn’t the risk of CAUTI higher with IAP
monitoring – suggesting we should not be doing this monitoring?
There are two published papers that suggest IAP monitoring does not increase the risk of CAUTI – one using a homemade technique, the other using the AbViser.[5, 6] Additional research is being submitted to journals. Shuster (University Penn) prospectively measured IAP in hundreds of patients for a PhD thesis using a commercial IAP monitoring kit (AbViser) and found no evidence of CAUTI in followup monitoring of the patients.(Melanie Shuster, RN, PhD thesis) Similarly, Kimball et al prospectively collected 7 years of data on over 900 patients undergoing IAP monitoring with the AbViser and also found no increase in CAUTI. All these authors conclude that IAP monitoring is safe and does not increase the risk of UTI. (These articles provide strong evidence that aseptic technique used to "break" the urinary drain system and measure IAP does not increase CAUTI risk at all.)
Traditional teaching suggests that “breaking” the seal of the
Foley-drain tube connection increases infection risk but all
published articles that have investigated this in a randomized
controlled fashion fail to support this tradition (i.e there is no
increased risk of CAUTI with careful aseptic breaking of the urinary
drainage system).[7-11] The newest CDC guidelines published in 2009
still recommend maintaining a closed drainage system but admit this
is based on tradition and only weakly on evidence and further state
that risks versus benefits need to be applied to the decision to use
a seal on the drain connection.[12]
Since there is strong prospective evidence demonstrating that
IAH and ACS increase both mortality and cost of care[1, 13, 14], and
there is no evidence that measuring IAP leads to higher CAUTI risks
– in every patient who you consider measuring IAP you must balance
the risk of disease (and benefits of early detection) verus the risk
of CAUTI.
How does obesity impact IAP?
Obesity leads
to mild increases in baseline IAP but not typically into the range
of what would be considered intraabdominal hypertension (IAP>12 mm
Hg) though occasionally this is not the case and pressures up to 14
or 15 m Hg are seen.[15-18] For this reason, do not assume that a
high IAP is purely a baseline normal finding for an obese patient.
Its best to assume that IAH is pathologic in all patients regardless
of their BMI.[18] Since
these patients are already more complicated than non-obese patients
it is probably best to obtain baseline IAP measurements early in
their clinical course to assist with interpreting their IAP levels
and the trend.
Isn’t ACS just a traumatic surgical disease? Why
don’t you go talk to the trauma doctors?
IAH and ACS
occur due to capillary permeability in the gut from massive cytokine
release during critical illness. This pathophysiologic event occurs
in all ICU populations and is most commonly seen in severe sepsis
and pancreatitis but also is found in many other critically ill
patients including but not limited to trauma patients.[2, 19, 20]
I do not really want to measure IAP because my
surgeons won’t cut open the patient. My understanding is that
surgery is the only treatment for this complication. Is this true?
No. Many
non-surgical interventions are available and have been disseminated
by an international panel of experts.[4] Most of these interventions
can be instituted non-invasively at the bedside and if instituted
early in the patients course can reduce progression of IAP
elevation. Only in
cases of progression to full blown compartment syndrome is surgery
indicated.
Isn’t high
intraabdominal pressure just a marker of death?
It might be on
select patients, however it is clear that in many patients early
detection and protocol driven intervention can markedly improve
outcome and reduce costs of care.[4, 14]
Is the AbViser Cost effective?
Caring for
critically ill patients is very expensive.
Cost efficacy calculations in these complex patient
populations can be difficult. However, two recent studies have now
clearly documented reduced ICU lengths of stay, fewer ventilator
days, fewer operative interventions and less mortality in patients
who have early, frequent IAP monitoring instituted and who undergo
protocol driven interventions based on the measured IAP.[14, 21] Due
to speed, accuracy and simplicity of the AbViser, both of these
authors use it in their practice. Given the clear reduction in costs
(4 fewer days on the ventilator in large cohorts of patients
measured, fewer surgical interventions, faster ICU discharge) and
AbViser cost of only $85 this data is fairly compelling to suggest a
return on investment that is substantial compared to either no
measurements or delayed measurements (due to the difficulty of
making your own system).
References:
1.
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.
2.
Cheatham, M.L., Abdominal compartment syndrome. Curr
Opin Crit Care, 2009. 15(2): p. 154-62.
3.
Cheatham, M.L., et al., The effect of body position on
intra-abdominal pressure measurement: A multicenter analysis.
Acta Clinica Belgica, 2007. 62-Supplement 1: p. 246-abstract
O1.
4.
Cheatham, M.L., Nonoperative management of intraabdominal
hypertension and abdominal compartment syndrome. World J Surg,
2009. 33(6): p. 1116-22.
5.
Cheatham, M.L., et al., Intravesicular pressure monitoring
does not cause urinary tract infection. Intensive Care Med,
2006. 32(10): p. 1640-3.
6.
Ejike, J.C., K. Bahjri, and M. Mathur, What is the normal
intra-abdominal pressure in critically ill children and how should
we measure it? Crit Care Med, 2008. 36(7): p. 2157-62.
7.
DeGroot-Kosolcharoen, J., R. Guse, and J.M. Jones,
Evaluation of a urinary catheter with a preconnected closed drainage
bag. Infect Control Hosp Epidemiol, 1988. 9(2): p. 72-6.
8.
Leone, M., et al., Comparison of effectiveness of two
urinary drainage systems in intensive care unit: a prospective,
randomized clinical trial. Intensive Care Med, 2003. 29(4):
p. 551-4.
9.
Wille, J.C., A. Blusse van Oud Alblas, and E.A. Thewessen,
Nosocomial catheter-associated bacteriuria: a clinical trial
comparing two closed urinary drainage systems. J Hosp Infect,
1993. 25(3): p. 191-8.
10.
Huth, T.S., et al., Clinical trial of junction seals for
the prevention of urinary catheter-associated bacteriuria. Arch
Intern Med, 1992. 152(4): p. 807-12.
11.
Keerasuntonpong, A., et al., Incidence of urinary tract
infections in patients with short-term indwelling urethral
catheters: a comparison between a 3-day urinary drainage bag change
and no change regimens. Am J Infect Control, 2003. 31(1):
p. 9-12.
12.
Gould, C.V., et al., Guideline for Prevention of
Catheter-Associated Urinary Tract Infections 2009. Infect
Control Hosp Epidemiol.
13.
Malbrain, M.L.N.G., et al., Incidence and prognosis of
intraabdominal hypertension in a mixed population of critically ill
patients: a multiple-center epidemiological study. Crit Care
Med, 2005. 33(2): p. 315-22.
14.
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.
15.
De Keulenaer, B.L., et al., What is normal intra-abdominal
pressure and how is it affected by positioning, body mass and
positive end-expiratory pressure? Intensive Care Med, 2009.
16.
Frezza, E.E., et al., Morbid obesity causes chronic
increase of intraabdominal pressure. Dig Dis Sci, 2007. 52(4):
p. 1038-41.
17.
Parsak, C.K., T.O. Acarturk, and E. Karakoc, The
Relationship Between Increased Intra-Abdominal Pressure and Morbid
Obesity. World J Surg, 2008.
18.
Wilson, A., et al., Intra-abdominal pressure and the
morbidly obese patients: the effect of body mass index. J
Trauma, 2010. 69(1): p. 78-83.
19.
Malbrain, M.L. and I.E. De Iaet, Intra-abdominal
hypertension: evolving concepts. Clin Chest Med, 2009. 30(1):
p. 45-70, viii.
20.
Regueira, T., et al., Intraabdominal hypertension in
patients with septic shock. Am Surg, 2007. 73(9): p.
865-70.
21.
Kimball, E.J., et al., A prospective evaluation of the
protocolized managment of intra-abdominal hypertension and the
abdominal compartment syndrome. Acta Clinica Belgica, 2009.
64(3): p. 272 - Abstract 110.