Definitions

To date, the most common way to measure intraabdominal pressure (IAP) is the intravesical technique via a urinary catheter (often referred to as urinary bladder pressure).^1–3 The mean value of IAP in hospitalized nontrauma patients is 6.5 mm Hg (range, 0.2-16.2 mm Hg).⁴ In critically ill ICU patients or trauma patients with shock and subsequent resuscitation, IAP is typically higher (12-16 mm Hg).⁵

Intraabdominal hypertension (IAH) is defined as IAP greater than 12 mm Hg without pathophysiology of ACS. IAH is graded from I to IV based on the IAP value (grade I: 12-15 mm Hg; grade II: 16-20 mm Hg; grade III: 21-25 mm Hg; grade IV: above 25 mm Hg).

Abdominal compartment syndrome (ACS) is defined as a sustained IAP greater than 20 mm Hg that is associated with new organ dysfunction/failure.

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

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

Damage Control

Patients undergoing laparotomy for major abdominal bleeding or sepsis are at risk for entering a “vicious circle” of acidosis, hypothermia, and coagulopathy; selected patients benefit from an abbreviated laparotomy (“damage-control” strategy).^6,7 The goals are to quickly control bleeding and prevent further contamination or spillage from hollow viscus perforations. The abdomen is temporarily closed without fascial approximation, and the patient is triaged to the intensive care unit (ICU), where resuscitation can be optimized and the vicious-circle physiology corrected. Damage control has saved the lives of severely injured and septic patients who otherwise would have died. Nevertheless, use of damage control has created new challenges for clinicians, including recognition and management of ACS, management of the open abdomen, and early multiple organ failure (MOF).

Historical Perspective

After 2 decades of re-recognition, ACS is still a heavily investigated critical care topic. Before the most recent description, IAP measurement, intraabdominal hypertension and ACS-related pathophysiology were investigated and published more than 150 years ago in both animal and human studies.^8,9 Initially, IAP was thought to be negative (subatmospheric), but by the beginning of the 20th century, animal studies verified that IAP is generally positive and if significantly increased can cause cardiac failure.¹⁰ These laboratory observations had little impact on clinical practice until the 1950s, when pediatric surgeons recognized the catastrophic consequences of acutely closing large congenital abdominal defects. Silo closure with gradual reduction of the abdominal defect was recommended to prevent fulminant organ failures.¹¹ In the 1980s, vascular surgeons described ACS after abdominal aortic aneurysm surgery. Additionally, they described the present technique of IAP measurement and used high IAP as a criterion for re-exploration.¹ However, it was not until the 1990s, when trauma surgeons adopted the liberal use of the damage-control strategy, that sufficient numbers of patients were available to define the epidemiology and pathophysiology of this previously rare and elusive complication.^12–15 Early observational case descriptions and retrospective series allowed for development of appropriate prospective epidemiologic characterization. These clinical observations stimulated laboratory investigations which have revealed some surprising and potentially important immunologic consequences of decompressive laparotomy of ACS after traumatic shock resuscitation (i.e., it may serve as a “second hit” in the systemic inflammatory response that causes early MOF).¹⁵ Parallel with these advances in understanding postinjury ACS is the recognition that ACS occurs in a variety of clinical scenarios such as extreme constipation,¹⁶ ovarian hyperstimulation,¹⁷ noninvasive ventilation,¹⁸ pancreatitis,¹⁹ and severe burns.²⁰ Since 2004, the World Society of the Abdominal Compartment Syndrome has offered leadership in consensus definitions, regular conferences, educational material, and organization of clinical trials.

Intraabdominal Pressure Measurement

Clinical examination of the abdomen is inaccurate for determining the presence of intraabdominal hypertension.^21,22 A standardized measurement of IAP is fundamental to the definition of intraabdominal hypertension and ACS.^1,2 IAP has been measured in virtually all parts of the abdominal cavity. The intravesical technique using a standard urinary catheter seems to be the most reliable and least invasive method. The rationale is that IAP is transmitted to the urinary bladder, which serves as a pressure transducer when filled with normal saline. Traditionally, a larger volume of saline was recommended, but recent studies showed that as little as 20 mL of instilled normal saline is enough for accurate measurement. Pressure is conducted by the fluid in the bladder to fluid in the urinary catheter, which is clamped during the interval when pressure is being measured. Pressure in the catheter tubing can be measured by inserting a sterile needle into the sample port of the catheter tube. Alternatively, a T-piece with three-way stopcock can be inserted into the catheter tube, connecting one limb to a strain-gauge pressure transducer.²³ The intravesical technique has been shown to correlate well with IAP measured directly using a laparoscopic insufflator.²⁴ The vesical route is more accurate than the use of rectal and gastric probes, which tend to provide different readouts, depending on the position of the patient.²⁴ Animal studies have shown that the pressure in the inferior vena cava correlates well with the vesical pressure,²⁵ but the inferior vena caval and direct peritoneal routes are more invasive. The urinary bladder pressure technique for IAP measurement was originally described by Kron et al.³ and validated by Iberti et al.²⁶ The technique was simplified by Sugrue et al., who described the insertion of a T-connector into the drainage tubing.²³ This modification eliminated the need for multiple needle insertions into the sample port and minimized the risk of needlestick injury and microbial contamination of the bladder. This technique is relatively simple and can be performed in any ICU where a pressure transducer is available. Several proprietary devices are available for clinicians. Unfortunately, obtaining an accurate measurement requires about 7 minutes of nursing time, limiting the frequency with which measurements can be obtained. Even when personnel are highly aware of the possible consequences of ACS, screening measurements of IAP are rarely obtained more often than every 4 hours. ACS can develop 4 to 6 hours after ICU admission in patients who are at high risk.⁵ The standard protocol for intermittent measurements of IAP does not provide information about the duration of intraabdominal hypertension. To address these shortcomings (labor intensity, intermittent nature), a continuous IAP measurement technique was developed and is currently being validated. The IAP can be continuously measured without clamping the tubing and instilling fluid into the bladder. For this new method, a standard three-way catheter is inserted, and the pressure transducer is connected to the saline-filled irrigation port. Once the setup is zeroed, the continuous IAP trace can be monitored without any further intervention or interference with the urine flow or tubing; this is the Balogh-Sugrue technique.²⁷

Pathophysiology

The pathophysiologic effects of increased pressure in a closed body compartment are well described in other regions (e.g., tension pneumothorax, pericardial tamponade, increased intracranial pressure, extremity compartment syndromes) and are taught in the basic medical curriculum. The abdominal cavity is a “neglected” compartment (see Historical Perspective). The volume of the abdominal cavity is limited by its least tensile component, the fascia. Increased pressure can be due to an increase in the volume of the abdominal contents or to a decrease in the volume of the “container” (Table 201-1). After IAP increases to greater than 20 mm Hg, the abdominal cavity is on the steep portion of its pressure-volume curve, and as a result, small increases in content volume or decreases in cavity volume can cause dramatic increases in IAP. This is when close monitoring of IAP (preferably continuously) and organ function is essential for timely intervention.

TABLE 201-1 Causes of Intraabdominal Hypertension and Abdominal Compartment Syndrome

Pathophysiologic Response of Specific Organs

Classification

ACS can be classified based on the duration of the syndrome, the presence or absence of intraperitoneal pathology, and the cause of the raised IAP (Table 201-2).

TABLE 201-2 Classification of Abdominal Compartment Syndrome