Abdominal Compartment Syndrome: Complication of Critical Illness

2 Nursing CEs

Written by: Brooke Baldwin-Rodriguez, RN, MSN, WCC

Date: July 24^th, 2007

Updated: September 11, 2009

Course Description

This course is designed to provide and overview of abdominal compartment syndrome, a complication of critical illness, and present the different levels of severity. Definitions will be provided in order to clarify concepts associated with abdominal compartment syndrome. The pathophysiologic process of the syndrome will be outlined and signs and symptoms will be discussed so that nurses can provide early identification of increased pressure within the abdominal compartment. Emphasis will be given to the most accepted method for monitoring pressure within the abdominal compartment. The final focus of this course will describe both non-surgical and surgical alternatives for management of abdominal compartment syndrome.

Course Objectives

Upon completion of this course the student will be able to:

• Define Abdominal Compartment Syndrome
• Outline the 5 grades of Intra-abdominal Hypertension
• Review the pathophysiology of abdominal compartment syndrome
• List at least 4 contributing causes of abdominal compartment syndrome
• State the effects of abdominal compartment syndrome on the renal, cardiovascular, and respiratory systems
• Discuss the diagnosis and assessment of intra-abdominal hypertension and abdominal compartment syndrome
• Identify direct and indirect measurements of intra-abdominal pressure
• Describe surgical and non-surgical management of intra-abdominal hypertension and abdominal compartment syndrome
• Identify the role of nurses in the prevention, care and treatment of intra-abdominal hypertension, measuring intra-abdominal pressure, and treatment of abdominal compartment syndrome

What is Abdominal Compartment Syndrome?

The syndrome of abdominal compartment syndrome can be looked at as part of a continuum that ranges from increase in intra-abdominal pressure to intra-abdominal hypertension to abdominal compartment syndrome.

Defining Abdominal Compartment Syndrome:

More focus has been places on IAH and ACS during the last 10 years as a serious consequence of critical illness, however the syndrome remains largely under recognized and under diagnosed and has traditionally been largely associated with traumatic injury. Definitions associated with IAH and ACS include:

• Intra-abdominal pressure (IAP): The steady-state pressure concealed within the abdominal cavity. IAP should be expressed in millimeters of mercury (mmHg).
• Abdominal perfusion pressure (APP): Abdominal perfusion pressure (APP) = mean arterial pressure (MAP) – intra-abdominal pressure (IAP)
• Intra-abdominal hypertension (IAH): A sustained or repeated pathological elevation in IAP > 12 mmHg. Grades of IAH are:

o       Grade I: IAP 12-15mmHg

o       Grade II: IAP 16-20mmHg

o       Grade III: IAP 21-25mmHg

o       Grade IV: IAP > 25mmHg

o       Normal IAP = 5 to 7 mmHg

• Abdominal compartment syndrome (ACS): A sustained IAP > 20 mmHg (with or without an APP < 60 mmHg) that is associated with new organ dysfunction.

Classification of IAH/ACS:

o       Primary ACS is a condition associated with injury or disease in the abdominopelvic region that frequently requires early surgical or interventional radiological intervention.

o       Secondary ACS refers to conditions that do not originate from the abdominopelvic region.

o       Recurrent ACS refers to the condition in which ACS redevelops following previous surgical or medical treatment of primary or secondary ACS.

Note: The definitions above were developed as part of an international consensus group for ACS in 2004, so that consistent definitions and recommendations in treatment help provide consistent evidence-based care for critically ill patients at risk for IAH and ACS.

Etiology:

An increase of pressure within an enclosed anatomical space is a hallmark sign of a compartment syndrome. When the pressure increases within an enclosed space normal cellular function is interrupted. Most nurses have familiarity with extremity compartment syndrome, but abdominal compartment syndrome may be a relatively new concept. As nurses increase their knowledge of this syndrome early recognition and intervention is possible. True numbers of patients who develop IAH and ACS are unknown since there are no established guidelines in most critical care units about when to begin monitoring IAP.            Any condition that elevates pressure in the abdominal cavity and lead to IAH and ACS. Common conditions leading to increased abdominal pressure include:

Ø      Bleeding

Ø      Ileus

Ø      Visceral edema

Ø      Noncompliant abdominal wall, as in blunt abdominal trauma

Ø      Pancreatitis

Ø      Fluid resuscitation

Post injury ACS may happen as early as 6 to 8 hours after the patient is admitted to the ICU Below is a chart with a comprehensive list of conditions associated with intra-abdominal hypertension and abdominal compartment syndrome.

Pathophysiology of IAH and ACS:

The pathophysiology of IAH and ACS begins with either a physiologic insult (i.e. trauma) or as a result of general critical illness (i.e. pancreatitis). Either of these initial insults leads to ischemia and/or systemic inflammatory response (SIRS). Cellular mechanisms lead to the release of proinflammatory cytokines. The release of cytokines leads to increased capillary permeability and edema. With capillary leak, patients are often resuscitated with fluid. Or, a patient may have bleeding, which leads to excess fluid in the abdominal cavity. As a result of edema, capillary leak, and fluid resuscitation (or bleeding into the intra-abdominal space), intra-abdominal pressures rise. As pressure rises in the enclosed abdominal space, perfusion in the gut is impaired. Impaired gut perfusion continues the cycle of hypoxia and cell death throughout the body.

Clinical Manifestations:

Clinical manifestations of ACS are not only seen in the abdominal cavity, but are evident in all organ systems of the body. The pulmonary, cardiovascular, renal, gastrointestinal, neurological, and immune systems can all exhibit signs of dysfunction when IAH/ACS as develops.

Ø      Pulmonary Manifestations

Increased IAP creates a restrictive effect on the lungs. The restrictive effect on the lung leads to reduces ventilation, decreased lung compliance, increase in airway pressures, and reduction in tidal volumes; the end result being respiratory acidosis.

Ø      Cardiovascular manifestations

Increased IAP reduces cardiac output, increases central venous pressure, increases systemic vascular resistance, increases pulmonary artery pressure, and increasing pulmonary artery wedge pressure. The rises in pressures can be misleading as the rises in pressure are not necessarily due to increased volume.

Ø      Renal manifestations

Increased IAP can cause reduction in renal plasma flow and glomerular filtration rate. Most likely this is due to increases in renal vascular resistance and decreases in cardiac output, oliguria develops.

Ø      Gastrointestinal manifestations

IAP decreases abdominal perfusion pressure, decreases celiac blood flow, decreases superior mesenteric artery blood flow, decreases the blood flow to all intra-abdominal organs, and decreases mucosal blood flow. Enteral feeding becomes difficult, intestinal permeability increases and bacterial translocation can occur. There is an increased risk for gastrointestinal bleeding.

Ø      Neurological manifestations

Increased IAP can cause obstruction of cerebral venous outflow, leading to vascular congestion and increased intracranial pressure. Decreased cardiac output, in combination with increased intracranial pressure and lead to decreased cerebral perfusion pressure.

Nurses are at a distinct advantage for monitoring for the clinical signs of increased intra-abdominal pressure since they are performing serial nursing assessments on each patient at risk for ACS at least every four hours in the ICU. The signs of ACS may develop slowly over time so the symptoms may be subtle. The nursing assessment is also particularly important since the signs of ACS mimic other clinical conditions like acute respiratory distress syndrome, acute renal failure, congestive heart failure, and intracranial hypertension. The nurse has a distinct advantage of catching the early signs and can aide in the distinction between other clinical conditions and ACS.

Nurse must assess for signs of:

·        Decrease in blood pressure and cardiac output

·        Oliguria or anuria

·        Increase in peak inspiratory pressures

·        Hypoxia and hypercarbia

·        Elevated intracranial pressure (ICP)

·        Increase in abdominal girth

·        Increase in the tenseness of the abdominal wall

Note: These signs should prompt suspicion that intra-abdominal pressure may be rising and that the patient has IAH and/or ACS.

Diagnosis of IAH/ACS and Nursing Management

Diagnosis of IAH/ACS requires measurement of IAP. Nurses generally monitor IAP since they are at the bedside and can measure the IAP as frequently as needed. Current methods for measuring IAP include:

• Rectal routes
• Direct intraperitoneal measurement (using a peritoneal dialysis catheter) Intragastric method (via a nasogastric tube)
• Measurement via urinary catheter in the bladder

Direct measurement via a peritoneal dialysis catheter is the most accurate measurement, but is not a realistic method for the majority of ICU patients since it is invasive and involves the insertion of an intraperitoneal catheter into the abdomen. The “gold standard” measurement in the ICU has been the urinary catheter connected to a pressure transducer monitoring set in order to get a bladder pressure measurement. Bladder pressure measurement is reflective of IAP and is measured in millimeters of mercury (mmHg).

Equipment needed for IAP measurement includes:

·        Nonsterile gloves

·        Cardiac monitor and pressure cable for interface with the monitor

·        500 or 1000ml bag of normal saline (NS) solution with appropriate-size pressure bag

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

·        60-ml Leurer-Lok syringe

·        Clamp

·        Provodine-iodine pads or swab-sticks

·        18-guage needle or angiocatheter (not needed if the Foley catheter has a leur-lock connection port)

The procedure for measuring IAP is as follows:

·        Assemble the pressure system and connect the transducer to the monitoring system and connect the needle to the end of transducer (the transducer can be directly connected to the Foley catheter without the needle if the Foley catheter has a leur-lock connection).

·        Attach a 60-ml syringe to the distal stopcock and the bladder drainage system and then clamped just distal to the catheter and drainage bag connection on the drainage bag tubing.

·        The measurement is obtained when a needle, attached to the pressure system, is inserted into the sampling port.

·        The needle method is generally used for intermittent access, while the angiocatheter method remains in place continuously.

·        In order to obtain a pressure measurement the stopcock should be turned off to the pressure bag and open to the syringe and patient.

·        Once opened to the patient, 50 mls of saline is instilled into the bladder

·        (The fluid-filled bladder acts as a passive diaphragm and accurate pressure can be obtained).

·        The patient should ideally be placed in the supine position with the zero reference point at the mid-axillary line.

·        The supine position will reduce falsely elevated pressures as a result of downward pressure from abdominal organs.

·        If the head of bed must be maintained at a higher elevation due to due to conditions such as head injury or risk of aspiration, it is important that all subsequent reading be taken at the same head of bed elevation.

·        Keeping the volume of saline at 50 mls will prevent bladder over distension and false elevation of bladder pressure and, thus, IAP reading.

·        The IAP reading should be done during end expiration to minimize the effects of pulmonary pressure.

·        Remember that the drainage system should be unclamped between readings. The 50mls of saline instilled for the measurement should be subtracted from the hourly urine output calculation.

·        Serial measurements, taken every 2 to 4 hours will help to detect early rises in IAP. As the IAP rises, the risk of the patient developing ACS increases.

·        Since the urinary catheter is repeatedly accessed, the signs and symptoms of urinary tract infection should be monitored closely.

·        Effective hand hygiene, standard precautions, and good cleansing technique of the catheter are critical to ensure that microorganisms are not introduced into the system. The chance of a patient developing a nosocomial urinary tract infection should be eliminated.

·        The patient should be informed that there will be a feeling of fullness when the 50mls of normal saline is instilled into the bladder.

Recent trials utilizing continuous measurement via a three way catheter has shown several potential advantages. Continuous IAP monitoring via a urinary catheter allows for monitoring without the potential for introduction of microorganisms into the catheter since the sterile connection between catheter and drainage bag does not have to be broken. The time that is needed to perform the procedure is reduced as well.

Treatment/Nursing Care

The best way to treat ACS is to prevent it. Recognizing early signs and symptoms is the best form of treatment for ACS. As critical care nurses our constant vigilance at the patient beside is really the best way to identify this syndrome. Anticipation of this complication associated with critical illness and monitoring for the early manifestations can mean potential life saving interventions for a patient. Management and treatment of IAH and ACS is varied due to the different etiologies of t

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