106: Intraabdominal Pressure Monitoring

Published on 06/03/2015 by admin

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PROCEDURE 106

Intraabdominal Pressure Monitoring

John J. Gallagher

PURPOSE:

Intraabdominal hypertension and abdominal compartment syndrome occur when the abdominal contents expand in excess of the capacity of the abdominal cavity, compromising abdominal organ perfusion and resulting in organ dysfunction or failure and associated mortality.³^,⁵^,⁹^,¹³^,¹⁴^,¹⁷^,²⁰^,²³^,²⁵

PREREQUISITE NURSING KNOWLEDGE

• Understanding of gastrointestinal anatomy and physiology is necessary.

• Knowledge of aseptic technique is essential.

• Intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS) occur when the abdominal contents expand in excess of the capacity of the abdominal cavity, compromising abdominal organ perfusion and resulting in organ dysfunction or failure and associated mortality.³^,⁵^,⁹^,¹³^,¹⁴^,¹⁷^,²⁰^,²³^,²⁵

• Four major categories of risk are associated with the development of IAH and ACS (Table 106-1).³^,¹⁷ They include:

Table 106-1

Patients at Risk for Development of Intraabdominal Hypertension and Abdominal Compartment Syndrome ³^,¹⁷ (Levels C, D, E*)

^*Level C: Qualitative studies, descriptive or correlational studies, integrative reviews, systematic reviews, or randomized controlled trials with inconsistent results

^*Level D: Peer-reviewed, professional organizational standards with clinical studies to support recommendations

^*Level E: Multiple case reports, theory-based evidence from expert opinions, or peer-reviewed professional organizational standards without clinical studies to support recommendations

Diminished abdominal wall compliance

Increased intestinal intraluminal contents

Increased peritoneal cavity contents

Capillary leakage into the bowel wall and mesentery/fluid resuscitation

• IAH is defined as a sustained or repeated pathologic elevation of intraabdominal pressure (IAP) to more than or equal to 12 mm Hg.³^,¹⁷

• IAH is graded by severity ³^,¹⁷:

Grade I: IAP, 12 to 15 mm Hg

Grade II: IAP, 16 to 20 mm Hg

Grade III: IAP, 21 to 25 mm Hg

Grade IV: IAP, >25 mm Hg

• ACS is defined as IAP more than or equal to 20 mm Hg that is associated with new organ dysfunction or failure.¹^,³^,¹⁷^,²⁰^,²¹^,²⁵ ACS is categorized into three types³^,¹²^,¹⁷:

Primary ACS: Associated with injury or disease of the abdominopelvic region.

Secondary ACS: Associated with disease outside the abdominopelvic region (sepsis, burns, fluid resuscitation).

Recurrent ACS: ACS that redevelops after previous medical or surgical treatment of primary or secondary ACS.

• Both IAH and ACS may compromise perfusion to the visceral organs represented by the parameter: abdominal perfusion pressure (APP).³^,^6–8^,¹⁷ APP is derived as:

• APP should be maintained at more than 50 to 60 mm Hg to maintain adequate perfusion to the abdominal organs and reduce the chance of organ dysfunction.³^,⁶^,⁷^,¹⁷

• Measurement of bladder pressure via an indwelling urinary bladder catheter is considered the reference standard for the measurement of IAP and may be performed with equipment readily available in the critical care environment (Fig. 106-1).²^,³^,⁸^,¹⁵^,¹⁷^,²² Commercially prepared kits designed for measurement of IAP are also available and may provide advantages in efficiency, standardization of measurement technique, and data reproducibility. Instructions for specific setup and operation of commercially prepared devices are provided by the manufacturer. Note that regardless of the device used, a standardized procedure for measurement should be used to prevent measurement variability between practitioners.¹²^,¹⁵^,²²

Figure 106-1 Bladder pressure monitoring setup. (Illustration by John J. Gallagher.)

• The bladder acts as a passive reservoir and accurately reflects IAP when intravesicular volumes of 25 mL or less are used. Larger volumes previously suggested (50 to 100 mL) are not necessary and may in fact overdistend the bladder, falsely elevating measured bladder pressure (IAP).³^,¹¹^,¹⁸

• Normal IAP is 0 mm Hg and may even be subatmospheric. In patients who are critically ill, it may rise to 5 to 7 mm Hg.³^,¹⁷

• IAP should be measured with the patient in the supine position. The transducer should be leveled or zeroed at the iliac crest in the midaxillary line (Fig. 106-2).²^,³^,¹⁷^,²⁴

Figure 106-2 Correct position of the transducer for bladder pressure measurement. (Illustration by John J. Gallagher.)

• IAP should be measured at end expiration. Wait an appropriate time (10 to 60 seconds) after saline solution instillation to allow for equilibration of the monitor to a steady state pressure reading.³^,¹⁷

• IAP should be expressed in millimeters of mercury (mm Hg; 1 mm Hg = 1.36 cm H₂O).³^,¹⁷

• Serial monitoring of bladder pressures is useful in detection of the onset of IAH and the progression to the more severe condition of ACS. Recommendations are that measurements be repeated every 2 to 4 hours in patients with IAP more than or equal to 12 mm Hg so a trend may be established and increases in pressure are detected.³^,¹⁷

• Bladder pressure measurement may be contraindicated in certain conditions, such as bladder trauma, bladder surgery, and neurogenic bladder. Risks and benefits of measurement should be discussed with the physician before the procedure is performed in these patients.

• In patients who do not have a urinary catheter in place, the risks and benefits of catheter placement for the purpose of bladder pressure measurement should be considered.

EQUIPMENT

• Nonsterile gloves

• Cardiac monitor and pressure cable for interface with the monitor

• 500- or 1000-mL intravenous (IV) bag of normal saline (NS) solution

• Pressure transducer system, including pressure tubing with flush device, transducer, and two stopcocks

• 25-mL Luer-Lok syringe

• Clamp

• Chlorhexidine swab sticks

Note: Commercial bladder pressure monitoring system may be substituted for the previous list.

PATIENT AND FAMILY EDUCATION

• Explain the procedure of bladder pressure measurement and its purpose to the patient and family. Rationale: Patient and family anxiety may be decreased. Understanding of how the procedure is performed may promote the patient’s ability to cooperate.

• Inform the patient that fullness may be felt in the bladder when saline solution is injected into the bladder during the procedure. Rationale: Patient anxiety may be decreased. Patient is prepared for what to expect.

PATIENT ASSESSMENT AND PREPARATION

Patient Assessment

• Obtain a patient health history to uncover risk factors that may predispose the patient to IAH or ACS. These conditions are outlined in Table 106-1. Rationale: Patients with these conditions may experience an increase in abdominal cavity fluid collection or tissue edema, placing them at risk for IAH and ACS.³^,¹⁷

• Assess the patient for signs of IAH through serial bladder pressure measurement.³^,¹⁷ Rationale: IAH may be detected early through IAP measurement.

• Assess the patient for signs of progression of IAH to ACS. These findings include decreased cardiac output and blood pressure, oliguria and anuria, increased peak inspiratory pressures (PIPs), hypercarbia and hypoxia, and increased intracranial pressure (ICP);(Table 106-2).^1–5,⁷^,⁹^,¹³^,¹⁶^,¹⁷^,²⁵^, Rationale: These physical findings indicate pathophysiologic organ system changes associated with the progression of IAH to ACS.³^,^5–7^,⁹^,¹³^,¹⁶^,¹⁷^,²⁵

Table 106-2

Physiologic Changes Associated with Intraabdominal Hypertension and Abdominal Compartment Syndrome ³^,^5–7^,⁹^,¹³^,¹⁶^,¹⁷^,²⁵ (Levels C, D, E*)

Organ System	Rationale
Cardiovascular ↑ CVP, PAP, PCWP, SVR ↓ CO (more pronounced with hypovolemia) ↓ Venous return from lower extremities (risk for DVT)	Increased abdominal pressure prevents venous return (preload reduction) and impedes arterial outflow (increase in afterload). Transmitted backpressure from the abdominal cavity falsely elevates CVP, PAP, PCWP, PVR, and SVR. CVP and PCWP may be corrected for the influence of increased IAP as follows⁵: CVP corrected = CVP measured – IAP/2 PCWP corrected = PCWP measured – IAP/2
Renal ↑ Renal blood flow → ↓GFR → ↓urine output	Increased IAP reduces cardiac output to the kidney, thereby reducing perfusion pressure to the glomerulus. Simultaneously IAP increases the pressure within the renal parenchyma, leading to reduction in filtration. The combination leads to a marked reduction in GFR and urine production.
Pulmonary ↑ Intrathoracic pressures ↑ Peak inspiratory pressures ↓ Tidal volume → hypercarbia + ↓PaO₂ ↓ Compliance	Increased IAP causes an increase in intrathoracic pressure and limits diaphragm excursion, resulting in hypoventilation and hypoxia.
Neurologic ↑ICP ↓CPP	Increased IAP impedes venous outflow from the brain, increasing cerebral venous congestion.
Gastrointestinal/hepatic effect ↓Celiac and portal blood flow ↓Lactate clearance ↓Mucosal blood flow → ↓ pHi	Increased IAP reduces perfusion to the abdominal organs. Capillary blood flow becomes obstructed as the IAP rises. When the IAP achieves and surpasses the venous capillary pressure, capillary blood flow is reduced or ceases. Transfer of oxygen/nutrients stops leading to anaerobic metabolism.