Abdominal Compartment Syndrome

Published on 22/03/2015 by admin

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Last modified 22/03/2015

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201 Abdominal Compartment Syndrome

image 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).

image 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.1215 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.

image 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

image 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

Increased Abdominal Contents Decreased Abdominal Volume
Ascites Reduction of large long-standing hernia
Hemoperitoneum Direct closure of large, long-standing abdominal wall defect
Visceral edema Circumferential abdominal-wall burnContinuous positive-pressure ventilation
Abdominal packs
Peritonitis
Retroperitoneal edema (pancreatitis) Retroperitoneal edema (pancreatitis)
Large pelvic, retroperitoneal hematoma Large pelvic, retroperitoneal hematoma
Intestinal obstruction  
Ileus  
Gastric distention (esophageal ventilation)  
Abdominal aortic aneurysm  
Severe constipation  
Large abdominal tumor (chronic)  
Morbid obesity (chronic)  
Pregnancy (chronic)  

image Pathophysiologic Response of Specific Organs

Cardiac Function

Increased IAP impedes venous return to the heart, causing sequestration of blood in the lower extremities. High intrathoracic pressure increases central venous pressure and pulmonary capillary wedge pressure but does not increase right or left ventricular end-diastolic volume. In other words, when intrathoracic pressure is increased, central venous and pulmonary capillary wedge pressures are not reliable indices for assessing the adequacy of preload. Simultaneously, left ventricular afterload increases owing to increased systemic vascular resistance. Increased intrathoracic pressure can increase right ventricular afterload, potentially leading to right ventricular failure and dilation, with consequent leftward displacement of the ventricular septum and impairment of left ventricular filling.3134 Cardiac failure with elevated pulmonary capillary wedge pressure, increased systemic vascular resistance, and decreased cardiac index is a typical finding in profound intraabdominal hypertension and defines ACS. The cardiac index usually does not respond to fluid challenges, which can be detrimental if the underlying cause (ACS) is not treated. The cardiac index’s response to decompression is predictive of outcome; patients who survive have a significantly greater increase in cardiac index after decompression than those who subsequently die.5

Respiratory Function

Increased IAP pushes the diaphragm into the thoracic cavity. Thoracic compliance decreases, and increased airway pressure is required for mechanical ventilation. Additionally, functional residual capacity decreases, and ventilation/perfusion mismatching increases, leading to impaired oxygenation.34,35 In the setting of massive resuscitation, these changes can be misinterpreted as being caused by acute lung injury. Historically, ACS was diagnosed by the presence of a firm abdomen in the setting of oliguria and increased airway pressures. Although airway pressure promptly decreases in response to abdominal decompression, this finding does not differentiate survivors from nonsurvivors.5 The peak airway pressure is an important parameter to monitor during attempted primary fascial closure after laparotomy when ACS is a possible complication.

Renal Function

Oliguria or anuria despite aggressive fluid resuscitation is a typical sign of ACS. Mechanisms responsible for decreased renal function include direct compression of the renal parenchyma, decreased perfusion of the kidneys due to decreased cardiac index, and increased water and sodium retention due to activation of the renin-angiotensin system.3638 The usual threshold for defining acute oliguria—urinary output less than 0.5 mL/kg/h—should be used cautiously and considered in the context of the magnitude of the resuscitation. Among patients who require massive resuscitation, the index of suspicion for ACS should be high when urinary output is less than 1 mL/kg/h.5

Gut Function

Increased IAP impairs splanchnic perfusion by decreasing the cardiac index and increasing splanchnic vascular resistance. When severe, tissue ischemia can result.3942 Intestinal perfusion can be assessed objectively using gastric tonometry. Decreased gastric intramural pH (pHi), increased gastric regional partial pressure of carbon dioxide (PCO2), and a wide gap between gastric regional PCO2 and end-tidal PCO2 are all indicators of impaired abdominal visceral perfusion. Combined with urinary bladder pressure measurements, the newer semicontinuous tonometers are an excellent adjunct for the early identification of impending ACS.3 Moreover, the physiologic response to decompression can be evaluated by assessing changes in pHi and related parameters using gastric tonometry.5

Microcirculation

Laboratory studies have shown that decompression of ACS causes circulating neutrophils to increase CD11b adhesion receptor expression.44 Decompression of ACS is also associated with the release of cytokines into the portal circulation and increased lung permeability, similar in degree to that seen after hemorrhagic shock and resuscitation.44,45 Moreover, when ACS decompression is appropriately sequenced with hemorrhagic shock, it can serve as a “second hit” (i.e., ACS decompression 8 hours after hemorrhagic shock causes more intense acute lung injury than does ACS decompression 2 or 18 hours after shock).4446

image 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

Basis of Classification Subcategories
Time frame Acute
Chronic
Relation to peritoneal cavity Primary
Secondary
Etiology Trauma
Burn
Postoperative
Pancreatitis
Bowel obstruction
Ileus
Abdominal aortic aneurysm
Oncologic
Gynecologic

Primary Versus Secondary

Irrespective of cause, the presence of intraperitoneal pathology defines primary ACS. A typical case is one in which the damage-control paradigm was followed and perihepatic packing, combined with temporary closure of the abdominal wall, was used to tamponade bleeding from the liver.48 As time progressed, intraabdominal bleeding and bowel edema (secondary to resuscitation) caused the volume of the intraabdominal contents to increase, precipitating ACS. Recognition of this problem has prompted trauma surgeons to leave the abdominal incision open after many damage-control procedures, reducing but not eliminating the risk of ACS. Primary ACS can also occur in patients who fail nonoperative management of abdominal organ injuries because of ongoing bleeding.49

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