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.
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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)