Organ and tissue damage due to shock may take one of two forms. Primary injury is the result of direct traumatic or ischemic insult and is characterized by either physical tissue destruction or acute vascular occlusion or thrombosis. This injury may be permanent and complete before the patient seeks medical care. Secondary injury follows the primary injury and is a result of cytokine release and the systemic inflammatory response process. This inflammatory cascade is characterized by a cycle of edema, capillary compression, inadequate cellular oxygenation, anaerobic metabolism, worsening intracellular acidosis, tissue hypoxia, intravascular thrombosis, and organ failure. Appropriate and timely resuscitation clearly modulates and can ameliorate secondary injury, reducing its associated morbidity and mortality. Minimizing secondary injury must be the goal of every critical care practitioner. Compartment syndrome represents a significant cause of morbidity and mortality in the ICU. It is frequently caused by secondary injury due to disease progression, systemic inflammatory response syndrome, or fluid resuscitation. Unfortunately, timely recognition of these syndromes in the critically ill patient may be confounded by injury, altered sensorium, sedation, pharmacological paralysis, or the distraction of other more obvious life-threatening conditions. As a result, successful prevention and management of compartment syndrome requires a high index of suspicion, serial physical examinations, liberal measurement of intercompartmental pressures in patients at risk, and meticulous goal-directed resuscitation to avoid secondary injury. At the cellular level, compartment syndromes occur when the pressure within an anatomic compartment increases to the point that tissue perfusion and cellular oxygenation are compromised. This initiates a cycle of progressive tissue injury, edema formation, inadequate oxygen delivery, anaerobic metabolism, metabolic acidosis, and ultimately cellular death and organ failure. At the macro level, both primary and secondary injury cause swelling of tissues, organs, or extremities. In the absence of a constricting envelope, such as fascia, skin, or bone, this edema is generally well-tolerated if appropriate resuscitation maintains adequate tissue perfusion. When such tissue edema occurs within the confines of a closed, non-compliant anatomic space, however, the organ or tissue can expand only to the volume of the anatomic compartment. After this point, further edema is translated into a rapidly increasing intercompartmental pressure. Initially, venous outflow from the compartment is impeded, while arterial inflow remains unimpaired, further accentuating edema formation, cellular anoxia, and secondary injury. As intercompartmental pressure increases to critical levels, arterial inflow and tissue oxygen delivery cease, leading to organ failure. As intensivists, we encounter a variety of compartment syndromes in the ICU every day. Extremity compartment syndrome is perhaps the most well-known, but compartment syndromes of the chest, such as tension hemothorax, tension pneumothorax, and pericardial tamponade, as well as compartment syndrome of the head, better known as intracranial hypertension, are also common. Today, however, we will be focusing on compartment syndrome of the abdominal cavity. There are a number of urban legends that we should dispel regarding abdominal compartment syndrome. Abdominal compartment syndrome is not solely a disease of trauma patients. In reality, it is more prevalent in medical patients, but is significantly under-recognized. There are a host of interventions that we can implement to improve patient outcome, all of which begin with measuring intra-abdominal pressure. Surgeon willingness to open the abdomen in the patient with abdominal compartment syndrome has increased over the decades, especially when they are provided with objective measurements, such as intra-abdominal pressure. Abdominal compartment syndrome is encountered in pediatric patients also. In fact, the surgical management of abdominal compartment syndrome was initially based upon pediatric surgeons' experience with gastroschisis and omphalocele. Patient survival from abdominal compartment syndrome continues to increase with earlier detection and intervention. Finally, studies have shown no difference in long-term disability in patients who require an open abdomen. The fact is that while intra-abdominal hypertension and abdominal compartment syndrome are associated with significant morbidity and mortality, early recognition and appropriate medical and surgical management significantly improves patient survival and results in very good long-term outcomes. The severity and injury potential of elevated intracompartmental pressure are correlated with four key factors. First, the rapidity of onset. Second, the duration of intracompartmental hypertension. Third, the adequacy of compartmental perfusion pressure. And fourth, the rapidity of decompression. Prolonged intracompartmental hypertension and inadequate compartmental perfusion pressure, defined as inflow pressure minus intracompartmental pressure, uniformly lead to cellular hypoxia, progressive secondary injury, and permanent tissue damage. Rapid recognition of elevated pressure with expedient resolution of the compartment syndrome through decompression is associated with improved patient outcome. So what is intra-abdominal pressure? The World Society of the Abdominal Compartment Syndrome has defined it as the steady state pressure within the abdominal cavity. Intra-abdominal pressure is commonly elevated in the critically ill as a result of three factors, increased solid organ or visceral volume, the presence of space-occupying lesions such as ascites, blood, fluid, or tumors, and conditions which limit abdominal wall expansion, such as burn scars or third space edema. Normally, intra-abdominal pressure ranges from zero to five millimeters of mercury, but is increased by critical illness, recent surgery, or shock. An intra-abdominal pressure of 15 millimeters of mercury or greater can cause significant end-organ dysfunction and failure, and if unrecognized or untreated, patient death. The impact of elevated intra-abdominal pressure extends well outside the abdominal cavity with negative effects upon virtually every organ system. It is for this reason that elevated intra-abdominal pressure plays such a role in the development of multi-system organ failure. Unfortunately, physical examination is notoriously poor in detecting elevated intra-abdominal pressure. Intra-abdominal pressure measurements are therefore essential to detecting elevated pressures and guiding resuscitation to restore patient organ perfusion and function. Intra-abdominal pressure is most commonly measured using intravesicular or bladder pressure as a surrogate. Such measurements can be performed in any ICU using commonly available supplies. Intra-abdominal pressure should be measured using a consistent technique to ensure accuracy between measurements. This illustrates one example of a simple setup for measuring intravesicular pressure that can be created using readily available supplies. Commercial kits for measuring intra-abdominal pressure are also available. I am frequently asked, what number should I keep the intra-abdominal pressure under? The critical intra-abdominal pressure, unfortunately, varies from patient to patient. There is thus no single threshold number that can be globally applied to all patient resuscitation. It is the perfusion pressure of the compartment that is most important. Abdominal perfusion pressure is defined as mean arterial pressure is defined as mean arterial pressure minus intra-abdominal pressure. Analogous to cerebral perfusion pressure, APP assesses not only the severity of intra-abdominal pressure, but also the relative adequacy of abdominal blood flow. Abdominal perfusion pressure has been demonstrated to be superior to intra-abdominal pressure, arterial pH, base deficit, and arterial lactate in predicting organ failure and patient outcome. Studies have demonstrated that failure to maintain an APP greater than 60 millimeters of mercury predicts patient survival. When intra-abdominal pressure is sustained at 12 millimeters of mercury or more, the patient has intra-abdominal hypertension. This is the level at which we begin to see renal, hepatic, cardiac, pulmonary, and gastrointestinal dysfunction. As the intra-abdominal pressure continues to increase above this level, the severity of organ dysfunction increases. The possibility of intra-abdominal hypertension should be considered in any patient who presents with one or more of the following risk factors. The World Society has defined abdominal compartment syndrome as a sustained intra-abdominal pressure greater than 20 millimeters of mercury with or without an abdominal perfusion pressure less than 60 millimeters of mercury that is associated with new organ dysfunction or failure. The most common organ dysfunctions are metabolic acidosis despite resuscitation, oliguria despite volume repletion, elevated peak airway pressures, hypercarbia refractory to increased mechanical ventilation, hypoxemia refractory to oxygen and positive end-expiratory pressure, and intracranial hypertension. There are three types of abdominal compartment syndrome. Primary abdominal compartment syndrome develops due to conditions associated with the abdominal pelvic region requiring surgical or angiographic intervention such as blunt abdominal trauma, bleeding pelvic fractures, massive retroperitoneal hematoma, secondary peritonitis, abdominal tumor, or recent liver transplant. Secondary abdominal compartment syndrome represents the sequelae of shock resuscitation and interstitial edema formation and typically develops due to conditions outside the abdominal cavity such as sepsis, capillary leak, major burns, or other conditions requiring significant fluid resuscitation. Primary abdominal compartment syndrome is most commonly seen in young trauma patients with blunt abdominal injury. It tends to appear early following injury and generally has a lower mortality as it is recognized earlier. Secondary abdominal compartment syndrome is most common in medical, surgical, and burn patients due to sepsis, ischemia, and iatrogenic fluid resuscitation. It tends to occur in older patients and has a higher mortality as it frequently is underrecognized. Recurrent abdominal compartment syndrome is a second hit phenomenon after the initial recovery from either primary or secondary abdominal compartment syndrome. It is typically due to premature or inappropriate abdominal closure or worsening of the patient's intraabdominal process. In any of the three forms of abdominal compartment syndrome, survival depends on prompt recognition and rapid intervention to reduce intraabdominal pressure and restore end-organ perfusion. The management of intraabdominal hypertension and abdominal compartment syndrome has evolved dramatically over the past 30 years. Improved survival is correlated with earlier recognition, intraabdominal pressure-guided therapy, multimodality medical and surgical management, prophylactic decompression in patients at risk, and earlier abdominal closure once intraabdominal pressure has decreased. In 2004, the World Society of the Abdominal Compartment Syndrome held a consensus conference and proposed an evidence-based resuscitation algorithm for intraabdominal hypertension and abdominal compartment syndrome that has been updated over the years. It emphasizes the importance of intraabdominal pressure measurements in patients at risk followed by multimodality medical management options when intraabdominal hypertension is present. Prompt surgical decompression is advocated when intraabdominal pressure fails to respond to medical interventions. We performed a prospective study of the impact of this resuscitation algorithm compared to historical controls and demonstrated its benefit in improving patient survival following intraabdominal hypertension and abdominal compartment syndrome. While severity of illness remained unchanged, use of the algorithm significantly reduced hospital length of stay, improved primary fascial closure rate, and increased patient survival. In this study, abdominal compartment syndrome was associated with a greater than five-fold increase in mortality, while a prophylactic open abdomen reduced mortality more than three-fold. This emphasizes the importance of avoiding abdominal compartment syndrome whenever possible through prophylactic efforts to reduce intraabdominal pressure and restore organ perfusion. The recent incidents, risk factors, and outcomes of intraabdominal hypertension study, a prospective international multicenter trial, identified that almost half of all critically ill medical and surgical patients admitted to the ICU develop intraabdominal hypertension. Over 6% of patients at risk for intraabdominal hypertension developed abdominal compartment syndrome. The presence of intraabdominal hypertension predicted the need for mechanical ventilation, increased intensive care unit and hospital length of stay, and both increased 28-day and 90-day mortality. Admission variables that independently predicted the development of intraabdominal hypertension included abdominal distension, body mass index greater than or equal to 27, PEEP greater than or equal to 7 centimeters of water, and absence of bowel sounds. Smit et al. studied 503 critically ill patients with risk factors for intraabdominal hypertension. They managed these patients according to the World Society algorithm. One-third of the patients developed intraabdominal hypertension, while almost 4% developed abdominal compartment syndrome. The highest prevalences of intraabdominal hypertension and abdominal compartment syndrome were seen in patients with pancreatitis, liver transplant, aortic surgery, and traumatic injury. Medical patients were almost 9 times and emergent surgery patients almost 3 times more likely to develop intraabdominal hypertension and abdominal compartment syndrome compared to elective surgery patients. Electively ventilated patients were 3.5 times more likely. Patients with intraabdominal hypertension or abdominal compartment syndrome had significantly longer intensive care unit length of stay, need for renal replacement therapy, duration of mechanical ventilation, and both intensive care unit and 90-day mortality. In response to concerns over long-term patient outcome following the development of intraabdominal hypertension or abdominal compartment syndrome, we performed two studies evaluating physical and mental health following abdominal decompression. Both studies found that long-term physical and mental health among patients who develop intraabdominal hypertension or abdominal compartment syndrome are identical to the United States general population once they have recovered from their critical illness. Further, we identified that abdominal decompression does not prevent a patient's return to gainful employment. So what are the key management points with regard to patients with intraabdominal hypertension and abdominal compartment syndrome? Intraabdominal pressure should be measured early and often to both diagnose the presence of intraabdominal hypertension as well as guide resuscitation. Medical management strategies to reduce elevated intraabdominal pressure should be instituted early. When such interventions fail, early surgical decompression improves survival. Once open, the patient's abdomen should be closed as early as reasonable based upon decreasing intraabdominal pressures. In summary, intraabdominal hypertension and abdominal compartment syndrome are causes of significant morbidity and mortality in the critically ill. A high index of suspicion for elevated intraabdominal pressure is essential. Serial intraabdominal pressure measurements are necessary to detect intraabdominal hypertension and abdominal compartment syndrome as well as guide therapeutic resuscitation. Implementation of a comprehensive medical and surgical management strategy significantly improves patient survival, decreases length of stay, and reduces hospital cost. Finally, abdominal decompression does not result in long-term disability.

organ damage

compartment syndrome

abdominal pressure

surgical decompression

intra-abdominal hypertension

mortality