Purpose of the reviewThere has been an exponentially increasing interest in intra-abdominal hypertension (IAH). Comparison of the published data however is difficult due to the lack of consensus definitions. This review will focus on the available literature from the last 2 years. A Medline and PubM

Intra-abdominal hypertension in the critically ill: it is time to pay attention.

In response to infectious and, in some instances, noninfectious insults, the affected tissues/cells of the host undergo inflammation. However, uncontrolled inflammation could be detrimental to the host, resulting in inflammatory disease, such as inflammatory lung disease. Although the etiology of the disease is well defined, the underling pathogenesis is still incompletely understood. The renin-angiotensin system (RAS), one of the primary cardiovascular regulatory systems, has been proposed to be involved in the pathogenesis of inflammatory lung disease. In particular, the RAS has been implicated as advances in the understanding of the multifunctionality of individual components of the system have been made, and by the fact that the RAS acts not only systemically, but also locally in a variety of tissues, including the lung. Angiotensin-converting enzyme 2 (ACE2), a relatively new member of the RAS, has drawn extensive attention since 2003, because of the findings that ACE2 is the receptor for SARS Corona virus and that maintenance of normal ACE2 levels in the lung is beneficial for the host to combat inflammatory lung disease. Nevertheless, the mechanism through which ACE2 plays a role in inflammatory lung disease has not been clearly identified. In an attempt to summarize current literature findings and progress made in uncovering the role of ACE2 in inflammatory lung disease, this review will focus on recent studies examining pulmonary ACE2 biology, its roles in inflammatory lung disease pathogenesis and possible underlying mechanisms. Finally, we will discuss pulmonary ACE2 as a potential therapeutic target for inflammatory lung disease.

Pulmonary Angiotensin-Converting Enzyme 2 (ACE2) and Inflammatory Lung Disease.

Abdominal compartment syndrome (ACS) has emerged to be a significant problem in patients who develop postinjury multiple organ failure (MOF). Current laboratory research suggests that ACS could be a second hit for the development of MOF. Recent studies demonstrate that ACS is an independent predictor of MOF and that the prevention of ACS decreases the incidence of MOF. The Trauma Research Centers at the University of Colorado and the University of Texas-Houston Medical School are focused on defining the role of the gut in postinjury MOF. Because ACS is a plausible modifiable risk factor, our interest has been to 1) describe the epidemiology of ACS, 2) build prediction models, 3) provide strategies for prevention and treatment of ACS, and 4) develop relevant laboratory models. This review summarizes our findings.

Abdominal compartment syndrome: the cause or effect of postinjury multiple organ failure.

Once considered mostly a postsurgical condition, intra-abdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) are now thought to increase morbidity and mortality in many patients receiving medical or surgical intensive care. Animal data and human observational studies indicate that oliguria and acute kidney injury are early and frequent consequences of IAH/ACS and can be present at relatively low levels of intra-abdominal pressure (IAP). Among medical patients at particular risk are those with septic shock and severe acute pancreatitis, but the adverse effects of IAH may also be seen in cardiorenal and hepatorenal syndromes. Factors predisposing to IAH/ACS include sepsis, large volume fluid resuscitation, polytransfusion, mechanical ventilation with high intrathoracic pressure, and acidosis, among others. Transduction of bladder pressure is the gold standard for measuring intra-abdominal pressure, and several nonsurgical methods can help reduce IAP. The role of renal replacement therapy for volume management is not well defined but may be beneficial in some cases. IAH/ACS is an important possible cause of acute renal failure in critically ill patients and screening may benefit those at increased risk.

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Renal Dysfunction Associated with Intra-abdominal Hypertension and the Abdominal Compartment Syndrome

PURPOSE OF REVIEW This review focuses on the available literature published in the past 2 years. MEDLINE and PubMed searches were performed using intraabdominal pressure, intraabdominal hypertension, and abdominal compartment as search items. The aim was to find an answer to the question: "Is it wise not to measure or even not to think about intraabdominal hypertension in ICU?" RECENT FINDINGS It is difficult to find a good gold standard for intraabdominal pressure measurement. Bladder pressure can be used as an intraabdominal pressure estimate provided it is measured in a reproducible way. Automated continuous intraabdominal pressure monitoring has recently become available. Key messages are (1). body mass index and fluid resuscitation are independent predictors of intraabdominal hypertension; (2). intraabdominal hypertension increases intrathoracic, intracranial, and intracardiac filling pressures; (3). transmural or transabdominal filling pressures combined with volumetric parameters better reflect preload; (4). volumetric target values need to be corrected for baseline ejection fractions; (5). intraabdominal hypertension decreases left ventricular, chest wall and total respiratory system compliance; (6). best positive end-expiratory pressure can be set to counteract intraabdominal pressure; (7). acute respiratory distress syndrome definitions should take into account best positive end-expiratory pressure and intraabdominal pressure but not wedge pressure; (8). lung protective strategies should aim at deltaPplat (plateau pressure - intraabdominal pressure); (9). intraabdominal hypertension causes atelectasis and increases extravascular lung water; (10). intraabdominal hypertension is an independent predictor of acute renal failure; (11). monitoring of abdominal perfusion pressure can be useful; and (12). intraabdominal hypertension triggers bacterial translocation and multiple organ system failure. SUMMARY The answer is that it is unwise not to measure intraabdominal pressure in the ICU or even not to think about it.

Is it wise not to think about intraabdominal hypertension in the ICU

Background The abdominal compartment syndrome (ACS) has been implicated in the pathogenesis of postinjury multiple organ failure. The ACS is defined as intra-abdominal hypertension causing adverse physiologic response. This study was designed to determine the effects of IAH on the production of interleukin-1b (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and the effects on remote organ injury. Methods IAH was induced in Sprague-Dawley rats which were divided into 5 groups, 10 animals each. Intra-abdominal pressure (IAP) was increased to 20 mm Hg for 60 and 90 minutes in two different groups. In a third group following IAP of 20 mm Hg the abdomen was decompressed for 30 minutes before samples were collected. The other animals were used as controls. Hemodynamic response was monitored throughout the procedure. Cytokine levels were assessed in the plasma. Remote organ injury was assessed by histopathology and myeloperoxidase activity. Results IAH caused a significant decrease in MAP. After abdominal decompression MAP returned to baseline levels. A significant decrease in arterial pH was also noted. Increase in the levels of TNF-alpha and IL-6 was noted 30 minutes after abdominal decompression. Plasma concentration of IL-1b was elevated after 60 minutes of IAH. Abdominal decompression, however, did not cause a significant increase in the levels of this cytokine. Lung neutrophil accumulation was significantly elevated only after abdominal decompression. Histopathological findings showed intense pulmonary inflammatory infiltration including atelectasis and alveolar edema. Conclusions IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF.

Jose Rennan da Cunha-Melo

Papers

Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure.