Current concept of abdominal sepsis: WSES position paper

World Journal of Emergency Surgery, Mar 2014

Although sepsis is a systemic process, the pathophysiological cascade of events may vary from region to region. Abdominal sepsis represents the host’s systemic inflammatory response to bacterial peritonitis. It is associated with significant morbidity and mortality rates, and is the second most common cause of sepsis-related mortality in the intensive care unit. The review focuses on sepsis in the specific setting of severe peritonitis.

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Current concept of abdominal sepsis: WSES position paper

World Journal of Emergency Surgery Current concept of abdominal sepsis: WSES position paper Massimo Sartelli 0 Fausto Catena Salomone Di Saverio Luca Ansaloni Mark Malangoni Ernest E Moore Frederick A Moore Rao Ivatury Raul Coimbra Ari Leppaniemi Walter Biffl Yoram Kluger Gustavo P Fraga Carlos A Ordonez Sanjay Marwah Igor Gerych Jae Gil Lee Cristian Tran 0 Federico Coccolini Francesco Corradetti James Kirkby-Bott 0 Department of Surgery, Macerata Hospital , Macerata , Italy Although sepsis is a systemic process, the pathophysiological cascade of events may vary from region to region. Abdominal sepsis represents the host's systemic inflammatory response to bacterial peritonitis. It is associated with significant morbidity and mortality rates, and is the second most common cause of sepsis-related mortality in the intensive care unit. The review focuses on sepsis in the specific setting of severe peritonitis. - Introduction Abdominal sepsis is associated with significant morbidity and mortality rates. Results of prospective trials have often overestimated the outcomes of patients with severe peritonitis [1]. Treatment of patients who have complicated intra-abdominal infections (IAIs) by adequate management, has generally been described to produce satisfactory results; recent clinical trials have demonstrated an overall mortality of 2% to 3% among patients with complicated IAIs [1,2]. However, results from published clinical trials may not be representative of the true morbidity and mortality rates of such infections. Patients who have perforated appendicitis are usually over represented in clinical trials [1]. Furthermore patients with intra-abdominal infection enrolled in clinical trials have often an increased likelihood of cure and survival. In fact trial eligibility criteria often restrict the inclusion of patients with co-morbid diseases that would increase the death rate of patients with intra-abdominal infections. After excluding patients with perforated appendicitis, Merlino et al. [3] found that the cure rate among patients who had intra-abdominal infections and were enrolled in clinical trials, was much higher than that of patients who were not enrolled (79% versus 41%) and that the mortality rate was much lower (10% versus 33%). Epidemiological studies of patients with intra-abdominal infections including severely ill subjects, have demonstrated higher mortality rates [4]. In the CIAO study the overall mortality rate was 7.7% (166/2152) [5]. Analyzing the subgroup of patients with severe sepsis or septic shock at admission to hospital the mortality rate reached 32.4% (89/274). In patients with severe sepsis or septic shock in the immediate postoperative period, the mortality rate was 42.3% (110/266). Abdominal sepsis represents the hosts systemic inflammatory response to bacterial or yeast peritonitis. In the event of peritonitis gram-negative, gram-positive, as well as anaerobic bacteria, including common gut flora, such as Escherichia coli, Klebsiella pneumoniae, Streptococcus spp. and Bacteroides fragilis, enter the peritoneal cavity. Sepsis from an abdominal origin is initiated by the outer membrane component of gram-negative organisms (e.g., lipopolysaccharide [LPS], lipid A, endotoxin) or gram-positive organisms (e.g., lipoteichoic acid, peptidoglycan), as well anaerobe toxins. This lead to the release of proinflammatory cytokines such as tumor necrosis factor (TNF-), and interleukins 1 and 6 (IL-1, IL-6). TNF- and interleukins lead to the production of toxic mediators, including prostaglandins, leukotrienes, platelet-activating factor, and phospholipase A2, that damage the endothelial lining, leading to increased capillary leakage [6]. Cytokines lead to the production of adhesion molecules on endothelial cells and neutrophils. Neutrophil-endothelial cell interaction leads to further endothelial injury through the release of neutrophil components. Activated neutrophils release nitric oxide, a potent vasodilator that leads to septic shock. Cytokines also disrupt natural modulators of coagulation and inflammation, activated protein C (APC) and antithrombin. As a result, multiple organ failure may occur. Early detection and timely therapeutic intervention can improve the prognosis and overall clinical outcome of septic patients. However, early diagnosis of sepsis can be difficult; determining which patients presenting with signs of infection during an initial evaluation, do currently have, or will later develop a more serious illness is not an easy or straightforward task. Sepsis is a complex, multifactorial syndrome which can evolve into conditions of varying severity. If left untreated, it may lead to the functional impairment of one or more vital organs or systems [7]. Severity of illness and the inherent mortality risk escalate from sepsis, through severe sepsis and septic shock up multi-organ failure. Previous studies have demonstrated that mortality rates increase dramatic (...truncated)


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Massimo Sartelli, Fausto Catena, Salomone Di Saverio, Luca Ansaloni, Mark Malangoni, Ernest E Moore, Frederick A Moore, Rao Ivatury, Raul Coimbra, Ari Leppaniemi, Walter Biffl, Yoram Kluger, Gustavo P Fraga, Carlos A Ordonez, Sanjay Marwah, Igor Gerych, Jae Lee, Cristian TranĂ , Federico Coccolini, Francesco Corradetti, James Kirkby-Bott. Current concept of abdominal sepsis: WSES position paper, World Journal of Emergency Surgery, 2014, pp. 22, 9, DOI: 10.1186/1749-7922-9-22