EDUBRIEFS in CCTC

Abdominal Compartment Pressure Monitoring

What is it?

It is the measurement of the pressure inside the abdominal compartment. 

How can it be done?

It can be measured directly by inserting a catheter into the abdominal compartment, or indirectly, by monitoring the pressure in the bladder, stomach or other cavities.

Why is it done?

The pressure inside the abdominal compartment can increase following trauma, as a result of the accumulation of blood, fluid or edema.  Non-traumatic bowel ischemia/infarction or gastrointestinal hemorrhage can also lead to increased pressure in the abdominal compartment as ischemic cells swell or fluids collect.  Coagulopathies with abdominal bleeding, cirrhosis, or profound hypothermia are other potential causes.  Once the pressure in the abdominal compartment overcomes the pressure inside the capillaries that are responsible for perfusing the organs, ischemia and infarction of organs can occur. 

Abdominal compartment pressure monitoring is done to help recognize life threatening elevations in pressure before ischemia or infarction of the abdominal organs occurs.  When a patient exhibits a distended and taut abdomen, the measurement of abdominal compartment pressure can provide direction regarding the need for decompressive surgery. 

What values are important?

Normal intra-abdominal pressure is 0 - 5 mmHg.  Pressures > 13 mmHg may be sufficient to restrict perfusion to the organs of the gut.  If the abdominal compartment pressures is between 16-25 mmHg, hypervolemic volume expansion therapy can be used to maintain the perfusion pressure gradient for the abdominal organs.  When compartment pressures exceed  25 mmHg, decompression surgery should be considered to prevent organ damage. 

Pressure may rise rapidly with active bleeding. Edema (which occurs with any ischemic insult) will generally result in a later rise in the pressure (27 hours or more post insult). 

What findings are clinically significant?

Patients with abdominal compartment syndrome should be monitored for the following:

    • oliguria due to renal ischemia

    • increased peak airway pressures/reduced tidal volumes/hypoxemia/hypercarbia due to restriction of the diaphragm

    • hypotension and decreased cardiac output as a result of decreased venous return and/or volume loss into the abdominal compartment

    • gastrointestinal bleeding due to ischemia of the bowel

    • impaired distal extremity circulation secondary to pressure on the aorta


     

The most common findings of abdominal compartment syndrome are renal and cardiopulmonary complications. In head injury, increased abdominal compartment pressure can increase ICP. 

Monitoring Techniques

Bladder pressure is measured as a surrogate of intra-abdominal pressure. Intra-abdominal pressure will be transmitted to the bladder, and will generally correlate well with intra-abdominal pressures.  The pressure trend can also provide information regarding the clinical progression. 

Some patients may experience gut ischemia prior to elevation of the compartment pressure.  It is also possible that bladder pressure may not capture an elevation of the abdominal compartment pressure if there is a loculated area.  While abdominal compartment pressure monitoring via the bladder may provide valuable information regarding patients with abdominal hypertension, abdominal compartment syndrome should not be ruled out in the presence of a normal pressures if persistent clinical findings exist. 

How can I measure pressure quickly?

Abdominal compartment syndrome pressure can be measured very quickly, by hooking a pressure monitoring system up to the Foley catheter. 

Ideally, a 3 - way Foley catheter is desirable.  This allows pressure to be monitored via the irrigation limb.  Use of the irrigation limb avoids the need to repeatedly access a closed system.  When initially choosing a catheter for a patient at risk for abdominal compartment syndrome, consider inserting a 3 - way catheter to facilitate future monitoring, should it become necessary. 

Alternatively, if a 2-way catheter is already insitu connect the pressure tubing into the luer lok of the rubber sampling port of the urinary drainage bag.  

 

The equipment, plus diagrams of the set-up for both 2-way and 3-way Foley catheters are displayed below. 

 

Set-up 
Using 2 - Way Foley Catheter
Set-up 
Using 3 - Way Foley Catheter
  • non-sterile gloves  
  • 1 litre bag of normal saline
  • one set of pressure tubing with transducer and arterial line extension 
  • 1 kelly clamp 
  • 1 60 cc luer lock syringe 
  • 1 urinary drainage bag with a sampling port close to the catheter connection 
  • non-sterile gloves
  • 1 litre bag of normal saline 
  • one set of pressure tubing with transducer and arterial line 
  • 1 kelly clamp
  • 1 STERILE feeding tube Y - connector 
  • 1 - 60 cc luer lock syringe 
  • 1 urinary drainage bag
click to view set-up for 3 - way catheter

 

 

Method


1.  Prime the pressure circuit with the normal saline (the flush solution does not require heparin or pressurization).

2.  Connect the pressure tubing (leave the arterial line extension with stopcock in place) to the Foley as follows:

  • for the 2 - way Foley catheter -  connect the pressure tubing into the luer lok of the rubber sampling port of the urinary drainage bag

  • for the 3 - way Foley catheter - connect a feeding tube Y - connector to the end of the pressure tubing

3.  Prior to measuring bladder pressure, the catheter remains open to continuous drainage, therefore, the bladder should be empty.  Perform hand hygiene and don non-sterile gloves. .Clamp the drainage bag as shown in the diagrams.

4.  Fill the bladder with 25 ml of normal saline using the 60 cc syringe.  This ensures that the volume of fluid in the bladder is constant for each measurement.  Fluid is required to transmit the pressure to the transducer.

5.  Ensure that the transducer is level with the bladder ((which should be approximately mid axillary line). Level the transducer to the mid-axillary line WITH THE HEAD OF BED FLAT. Flattening the HOB ensures that the mid-axillary line and bladder are approximated, and helps to relax the abdominal wall.

6.  Close the stopcock off to the syringe, and obtain the mean pressure reading.  The abdominal blood flow should produce fluctuations in the waveform with the heart beat. Should the waveform (displayed in a small scale) fail to produce fluctuations, flush the line and transducer as you would to troubleshoot dampening of any pressure waveform. Remove non-sterile gloves and perform hand hygiene.

 

7.  Monitor pressure q 2 - 4 hours, document findings on patient flowsheet.

 

 

Brenda Morgan
Clinical Educator, CCTC
September 1999
Revised: May 8, 2008, July 23, 2010

Reviewed: March 19, 2010.
 
References:

Bloomfield, G., Saggi, B., Blocher, C, & Sugerman, H.  (1999).  Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension.  Journal of Trauma: Injury, Infection and Critical Care.  Jun; 46(6): 1014-6.

Diebel, L., Dulchavsky & S., Brown, W.  (1997).  Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome.  Journal of Trauma: Injury, Infection and Critical Care.  Nov; 43(5): 852-5.

Ivatury, R., et al.  (1998). Intra-abdominal hypertension after life-threatening penetrating abdominal trauma:  prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome.  Journal of Trauma: Injury, Infection and Critical Care.  Jun; 44(6): 1016-23.

Offner, P. & Burch, J. (1998).  Abdominal compartment syndrome, part 1:  presentation and workup: cardiopulmonary and renal findings are among the most prominent signs. Journal of Critical Illness. Oct; 13(10): 634-8.

Offner, P. & Burch, J. (1998).  Abdominal compartment syndrome, part 2:  management guidelines: which patients will require abdominal decompression? Journal of Critical Illness.  Oct 13(10): 639-42.

Williams, M. & Simms, H. (1997). Abdominal compartment syndrome:  case reports and implications for management in critically ill patients.  American Surgeon.  Jun; 63(6): 555-8.

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Last Updated July 23, 2010 | © 2007, LHSC, London Ontario Canada