id000057
10.3205/id000057
urn:nbn:de:0183-id0000570
Leitlinie
Guideline
Kalkulierte parenterale Initialtherapie bakterieller Infektionen: Intraabdominelle Infektionen
Calculated parenteral initial treatment of bacterial infections: Intra-abdominal infections
Eckmann
Eckmann
Christian
C
Prof. Dr.
Klinik für Allgemein-, Viszeral- und Thoraxchirurgie, Klinikum Hannoversch-Münden, Vogelsang 105, 34346 Hannoversch-Münden, DeutschlandKlinik für Allgemein-, Viszeral- und Thoraxchirurgie, Klinikum Hannoversch-Münden, Deutschland
Klinik für Allgemein-, Viszeral- und Thoraxchirurgie, Klinikum Hannoversch-Münden, Vogelsang 105, 34346 Hannoversch-Münden, GermanyKlinik für Allgemein-, Viszeral- und Thoraxchirurgie, Klinikum Hannoversch-Münden, Germany
c.eckmann@khmue.de
author
Isenmann
Isenmann
Rainer
R
Allgemein- und Visceralchirurgie, St. Anna-Virngrund-Klinik Ellwangen, Deutschland
Allgemein- und Visceralchirurgie, St. Anna-Virngrund-Klinik Ellwangen, Germany
author
Kujath
Kujath
Peter
P
Chirurgische Klinik, Medizinische Universität Lübeck, Deutschland
Chirurgische Klinik, Medizinische Universität Lübeck, Germany
author
Pross
Pross
Annette
A
Klinik und Poliklinik für Chirurgie, Universitätsklinikum Regensburg, Deutschland
Klinik und Poliklinik für Chirurgie, Universitätsklinikum Regensburg, Germany
author
Rodloff
Rodloff
Arne C.
AC
Institut für Medizinische Mikrobiologie und Infektionsepidemiologie, Universitätsklinikum Leipzig, Deutschland
Institut für Medizinische Mikrobiologie und Infektionsepidemiologie, Universitätsklinikum Leipzig, Germany
author
Schmitz
Schmitz
Franz-Josef
FJ
Institut für Laboratoriumsmedizin, Mikrobiologie, Hygiene, Umweltmedizin und Transfusionsmedizin Johannes Wesling Klinikum Minden, Deutschland
Institut für Laboratoriumsmedizin, Mikrobiologie, Hygiene, Umweltmedizin und Transfusionsmedizin Johannes Wesling Klinikum Minden, Germany
author
German Medical Science GMS Publishing House
Düsseldorf
610
Calculated parenteral initial therapy
Kalkulierte parenterale Initialtherapie
20200326
germ
engl
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung).
2195-8831
8
GMS Infectious Diseases
GMS Infect Dis
13
Dies ist das siebte Kapitel der von der Paul-Ehrlich-Gesellschaft für Chemotherapie e.V. (PEG) herausgegebenen S2k Leitlinie „Kalkulierte parenterale Initialtherapie bakterieller Erkrankungen bei Erwachsenen – Update 2018“ in der 2. aktualisierten Fassung.Es behandelt die empirische und gezielte antimikrobielle Therapie komplizierter intraabdominaler Infektionen und enthält Empfehlungen für die antibakterielle und antimykotische Behandlung.
This is the seventh chapter of the guideline “Calculated initial parenteral treatment of bacterial infections in adults – update 2018” in the 2nd updated version. The German guideline by the Paul-Ehrlich-Gesellschaft für Chemotherapie e.V. (PEG) has been translated to address an international audience.The chapter deals with the empirical and targeted antimicrobial therapy of complicated intra-abdominal infections. It includes recommendations for antibacterial and antifungal treatment.
Indikation zur antimikrobiellen TherapieIntraabdominelle Infektionen (IAI) sind häufig. Die Diagnose akute Peritonitis ist sehr häufig. Im Institut für das Entgeltsystem im Krankenhaus (InEK) wurden im Jahr 2014 in 30.000 Fällen eine Peritonitis im Bereich der Viszeralchirurgie (MDC 6–7) kodiert. Nationale und internationale Datenbanken zeigen, dass ca. 30% aller Fälle einer schweren Sepsis oder eines septischen Schocks sich auf IAI zurückführen lassen , , . Fast 90% aller intraabdominellen Infektionen bedürfen primär einer chirurgischen Herdsanierung (z.B. Überernährung einer Magenperforation). Der Wert einer Antibiotika-Therapie gegenüber Placebo ist dennoch auch in dieser Krankheitsgruppe gesichert . Eine initial inadäquate Antibiotika-Therapie von IAI verschlechtert die Prognose der betroffenen Patienten substanziell und führt zu einem erheblichen finanziellen Schaden , , , .Empfehlungen zur Antibiotika-Therapie bei intraabdominalen Infektionen werden von einer Vielzahl von prospektiv randomisierten und kontrollierten Studien abgeleitet. Da das Ziel fast aller Studien der Nachweis einer therapeutischen Äquivalenz ist, reichen die Ergebnisse derzeit nicht aus, um einer Substanz oder einem Substanzregime den Vorzug zu geben . Einschränkend muss hinzugefügt werden, dass bei allen randomisierten Studien die Ein- und Ausschlusskriterien so gewählt wurden, dass Patienten mit eher leichteren IAI (APACHE II Score ca. 6) rekrutiert wurden. Dies erschwert die Beurteilung der Wirksamkeit der angegebenen Substanzen bei lebensbedrohlichen Peritonitiden. Bei der Auswahl des geeigneten Antibiotikums sollten der individuelle Patient (z.B. Immunsuppression, Vorbehandlung), das zu erwartende Erregerspektrum, die lokale Erreger- und Resistenzstatistik, ein einfacher Applikationsmodus, eine geringe Toxizität der Substanzen und die Kosten in die Entscheidung mit einfließen.Komplizierte IAI liegen definitionsgemäß vor, wenn die Infektion das betroffene Organ überschreitet und entweder einen Abszess oder eine Peritonitis (lokal oder diffus) auslöst . Diese Differenzierung ist aber klinisch nicht eindeutig. So ist z.B. eine phlegmonöse Appendizitis mit geringer Umgebungsreaktion (Letalität unter 0,5%) eine komplizierte IAI, wohingegen eine schwere Clostridium difficile-induzierte Kolitis (Letalität bei Ribotyp 027 bis zu 40%) eine unkomplizierte IAI nach der obigen Definition darstellt. Klinisch akkurater lassen sich drei verschiedene Formen der Peritonitis differenzieren, die sich kausal pathogenetisch, bezüglich des Erregerspektrums und der chirurgischen und antimikrobiellen Therapie substanziell voneinander unterscheiden .
Indications for antimicrobial treatmentIntra-abdominal infections (IAI) are common. Diagnosis of acute peritonitis is very common. The Institute for the Hospital Remuneration System (InEK) recorded 30,000 cases of peritonitis in the area of visceral surgery (MDC 6–7) in 2014. National and international databases show that about 30% of all cases of severe sepsis or septic shock are due to IAI , , . Nearly 90% of all intra-abdominal infections primarily require surgical infectious source rehabilitation (e.g. hyperalimentation of a gastric perforation). Nevertheless the value of antibiotic treatment versus placebo is confirmed even in this disease group . An initially inadequate antibiotic treatment of IAI substantially worsens the prognosis of the affected patients and leads to considerable economic damage , , , . Recommendations for antibiotic treatment in intra-abdominal infections are derived from a variety of prospective randomized and controlled trials. Since the goal of almost all studies is to demonstrate therapeutic equivalence, the current results are insufficient and don’t allow identification of a preferred substance or a substance regimen . It should be added that in all randomized studies the inclusion and exclusion criteria were chosen so that patients with a less severe IAI (APACHE II score around 6) were recruited. This complicates the assessment of the effectiveness of the specified substances in life-threatening peritonitis. When selecting an appropriate antibiotic, the individual patient (e.g. immunosuppression, prior treatment), expected pathogen spectrum, local pathogen and resistance statistics, a simple mode of application, low toxicity of the substances and costs should be considered in the decision-making process.By definition, complicated IAIs occur when the infection moves beyond the affected organ and causes an abscess or peritonitis (local or diffuse) . However, clinically this differentiation is not clear. For example, phlegmonous appendicitis with low environmental response (lethality below 0.5%) constitutes a complicated IAI, whereas severe Clostridium difficile-induced colitis (lethality up to 40% in case of ribotype 027) represents an uncomplicated IAI as per the above definition. Clinically speaking, three different forms of peritonitis can be differentiated, which are causally pathogenetic, substantially different in terms of the spectrum of pathogens and surgical and antimicrobial treatment .
PeritonitisPrimäre PeritonitisDie primäre (spontan bakterielle) Peritonitis (SBP) betrifft nur ca. 1% aller Peritonitis-Fälle. Bei der juvenilen Form handelt es sich um eine hämatogen entstandene Infekti<![CDATA[o</PlainText></TextGroup>n, die durch Streptokokken, Pneumokokken oder in selteneren Fällen durch <Mark2>Haemophilus influenzae</Mark2> ausgelöst wird. Beim Erwachsenen sind vorwiegend Patienten mit Aszites bei alkoholischer Leberzirrhose (ca. 70%) oder einer reduzierten Abwehrlage aus anderer Ursache (ca. 30%) betroffen <TextLink reference="10"></TextLink>, <TextLink reference="11"></TextLink>. Meist handelt es sich um eine Monoinfektion. In realitätsnahen Arbeiten gelingt nur in etwa 35% der Fälle ein Erregernachweis, wobei sich <Mark2>Escherichia coli</Mark2>, <Mark2>Klebsiella</Mark2> spp., Staphylokokken, Enterokokken oder Streptokokken, gelegentlich auch pathogene Gastroenteritis-Erreger wie <Mark2>Aeromonas</Mark2> spp. oder <Mark2>Salmonella</Mark2> spp. nachweisen lassen <TextLink reference="10"></TextLink>. Bei der primären Peritonitis, die im Rahmen einer Tuberkulose auftreten kann, handelt es sich um eine hämatogene Streuung.</Pgraph><Pgraph>Randomisierte Studien zur Behandlung der SBP sind rar. Meist handelt es sich um retrospektive Arbeiten. Eingesetzte Substanzen waren Ceftriaxon, Cefotaxim, Ceftazidim, Ampicillin/Sulbactam, Ampicillin + Tobramycin sowie Amoxicillin/Clavulansäure <TextLink reference="12"></TextLink>, <TextLink reference="13"></TextLink>, <TextLink reference="14"></TextLink> (Tabelle 1 <ImgLink imgNo="1" imgType="table"/>). Damit ließen sich zusammen mit der Gabe von Albumin klinische Heilungsraten von ca. 80% erzielen <TextLink reference="15"></TextLink>. Bezüglich der Behandlung von primären Peritonitiden, die durch resistente Erreger verursacht werden, siehe auch <TextGroup><PlainText>Tabelle 1 </PlainText></TextGroup><ImgLink imgNo="1" imgType="table"/>.</Pgraph><SubHeadline>Peritonitis bei CAPD</SubHeadline><Pgraph>Eine Peritonitis bei CAPD wird in der Regel durch Kontamination des Schlauch- oder Kathetersystems verursacht. Häufigste Erreger sind Koagulase-negative Staphylokokken und <Mark2>Staphylococcus aureus</Mark2>. Seltener werden <Mark2>Escherichia coli</Mark2>, Enterokokken, Streptokokken, <Mark2>Pseudomonas aeruginosa</Mark2>, Anaerobier, <Mark2>Enterobacter</Mark2> spp., oder <Mark2>Candida</Mark2>-Arten nachgewiesen <TextLink reference="16"></TextLink>. Unkomplizierte Fälle können lokal durch Zugabe antimikrobieller Substanzen zur Dialysierflüssigkeit behandelt werden. Nur bei den selteneren schweren Verlaufsformen wird neben der intraperitonealen auch eine parenterale Therapie notwendig. Dabei müssen die Besonderheiten der Antibiotika-Dosierung bei Niereninsuffizienz beachtet werden. </Pgraph><Pgraph>Zur kalkulierten Therapie wird Cefotaxim, Cefuroxim oder Ceftriaxon (in Monotherapie oder in Kombination mit Ciprofloxacin) empfohlen <TextLink reference="17"></TextLink>. Die Therapie sollte nach den Ergebnissen der mikrobiologischen Diagnostik gezielt fortgeführt werden. Bei Nachweis von MRSA, MRSE und Enterokokken (inkl. VRE) stehen die Antibiotika gemäß Tabelle 2 <ImgLink imgNo="2" imgType="table"/> zur Verfügung. Wird die Infektion nicht binnen einer Woche durch die antimikrobielle Therapie beherrscht, sollte der Peritoneal-Dialyse-Katheter entfernt werden <TextLink reference="18"></TextLink>.</Pgraph><SubHeadline>Sekundäre Peritonitis</SubHeadline><Pgraph>Die sekundäre Peritonitis, bei der eine Perforation des Gastrointestinaltrakts vorliegt, ist mit etwa 80–90% die mit Abstand häufigste IAI. Definitionsgemäß muss eine chirurgische Fokuskontrolle (Herdsanierung, z.B. Appendektomie bei perforierter Appendizitis) oder interventionelle Therapie (z.B. CT-gesteuerte Drainage eines Abszesses) stattfinden. Im Sinne eines Drei-Säulen-Modells ist bei diffuser Peritonitis eine chirurgische, antimikrobielle und intensivmedizinische Therapie erforderlich <TextLink reference="18"></TextLink>. Zunehmend setzt sich die primäre Herdsanierung mit anschließendem definitivem Verschluss des Abdomens und klinischer Verlaufskontrolle des Patienten durch <TextLink reference="19"></TextLink>. Die sekundäre Peritonitis kann differenziert werden in eine ambulant erworbene (ca. 60%) und eine postoperative (ca. 40%) Form.</Pgraph><SubHeadline>Ambulant erworbene sekundäre Peritonitis</SubHeadline><Pgraph>Bei der ambulant erworbenen sekundären Peritonitis liegt stets eine Mischinfektion vor. Das Erregerspektrum entstammt der Flora des Magen-Darm-Trakts und ist abhängig von der Pathogenese und der Lokalisation der Perforation bzw. Leckage. Leiterreger sind <Mark2>Escherichia coli</Mark2>, <Mark2>Bacteroides fragilis</Mark2>, Enterokokken und <Mark2>Candida</Mark2> spp. Resistente Spezies müssen nur bei ambulant mit Antibiotika vorbehandelten Patienten und anderen speziellen Risikofaktoren (siehe Tabelle 3 <ImgLink imgNo="3" imgType="table"/>) berücksichtigt werden. Die vorliegenden Empfehlungen berücksichtigen die Dauer der Erkrankung und das Erregerspektrum in Abhängigkeit von der Krankheitsursache <TextLink reference="18"></TextLink>. Zur Antibiotika-Therapie von lokal begrenzten, akuten Peritonitiden können Cefuroxim, Cefotaxim, Ceftriaxon oder Ciprofloxacin, jeweils in Kombination mit Metronidazol, sowie Ampicillin/Sulbactam oder Amoxicillin/Clavulansäure eingesetzt werden. Piperacillin/Tazobactam sowie Ertapenem, die in dieser Indikation ebenfalls zugelassen und geprüft worden sind, sollten eher bei schwereren IAI eingesetzt werden (Tabelle 4 <ImgLink imgNo="4" imgType="table"/>). </Pgraph><Pgraph>Zur Therapie einer bereits mehr als 2–4 Stunden andauernden, diffusen Peritonitis sollten Substanzen oder Kombinationen mit einem breiten Wirkungsspektrum eingesetzt werden. Zur kalkulierten Therapie können Piperacillin/Tazobactam, Moxifloxacin, Tigecyclin oder Ertapenem angewendet werden. Alternativ können Kombinationen von Metronidazol mit Ceftriaxon oder Cefepim verwendet werden. Die Berücksichtigung von Enterokokken bei der Substanzauswahl wird nur im Ausnahmefall bekannter Kolonisation empfohlen <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. </Pgraph><Pgraph>Die Hinzufügung von Aminoglykosiden zeigte in Metaanalysen keine verbesserte Wirkung und gilt aus diesem Grund nicht mehr als Therapie der Wahl <TextLink reference="24"></TextLink>. Variable kinetische Parameter sowie die Oto- und Nephrotoxizität erfordern zudem eine regelmäßige Serumspiegel-Kontrolle.</Pgraph><SubHeadline>Postoperative, posttraumatische und postinterventionelle Peritonitis</SubHeadline><Pgraph>Die postoperative Peritonitis ist eine nosokomial erworbene sekundäre Peritonitisform und wird definiert als infektiöse abdominelle Komplikation, die auf einen operativen Eingriff folgt (z.B. Anastomoseninsuffizienz nach anteriorer Rektumresektion). Bei der postoperativen Peritonitis liegt im Gegensatz zur tertiären Peritonitis ein chirurgisch oder interventionell (z.B. Endo-VAC-Einlage in eine Insuffizienzhöhle) behandlungsbedürftiges Krankheitsbild vor <TextLink reference="9"></TextLink>. Die meisten Patienten sind zum Zeitpunkt der Erkrankung bereits antimikrobiell vorbehandelt. Daher zeichnet sich die postoperative Peritonitis durch ein selektioniertes Erregerspektrum mit Enterokokken (inklusive VRE), gramnegativen Problemerregern („Exte<TextGroup><PlainText>nd</PlainText></TextGroup>ed-Spektrum“-Beta-Lactamase [ESBL]-Bildner) und Pilzen aus. <Mark2>Pseudomonas</Mark2> spp. und Carbapenemase-Bildner werden eher selten nachgewiesen.</Pgraph><Pgraph>Als Antibiotika mit einem breiten Wirkungsspektrum können Imipenem/Cilastatin, Meropenem, Ertapenem, Tigecyclin und Fosfomycin eingesetzt werden <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, wobei letzteres aufgrund der schnellen Resistenzentwicklung nicht in Monotherapie verwendet werden sollte. Ceftolozan/Tazobactam steht seit kurzem als neues ESBL-wirksames Medikament zur Verfügung. In der Zulassungsstudie für IAI, bei der Ceftolozan/Tazobactam in Kombination mit Metronidazol eingesetzt wurde, wurde speziell diese Patientengruppe unter kontrollierten klinischen Bedingungen sehr erfolgreich behandelt <TextLink reference="25"></TextLink>, <TextLink reference="26"></TextLink>. Eine weitere Therapieoption in diesem Indikationsbereich stellt das ebenfalls kürzlich zugelassene Ceftazidim/Avibactam in Kombination mit Metronidazol dar. Ggf. müssen auch Pilzinfektionen in der empirischen antiinfektiven Therapie berücksichtigt werden (siehe <TextGroup><PlainText>Tabelle 5 </PlainText></TextGroup><ImgLink imgNo="5" imgType="table"/><TextGroup><PlainText>).</PlainText></TextGroup></Pgraph><SubHeadline>Tertiäre Peritonitis</SubHeadline><Pgraph>Bei der tertiären Peritonitis (wie die postoperative Peritonitis eine nosokomiale Peritonitisform) persistiert die Infektion der Abdominalhöhle ohne chirurgisch sanierbaren Fokus, nachdem zuvor die chirurgische Herdsanierung einer sekundären Peritonitis abgeschlossen worden ist <TextLink reference="9"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>. Die Übergänge von der sekundären zur tertiären Peritonitis können fließend sein. In diagnostisch unklaren Situationen kann nur durch eine Relaparotomie bewiesen werden, dass kein chirurgisch behandlungsbedürftiger Fokus vorliegt <TextLink reference="21"></TextLink>. Meist handelt es sich um wenig virulente Erreger, die wegen der anhaltenden Immunsuppression des betroffenen Patienten zu einer anhaltenden Infektion führen. Diese Form der nosokomialen Peritonitis weist aufgrund der antimikrobiellen Vorbehandlung ein ähnliches Erregerspektrum wie die sekundäre postoperative Peritonitis auf. Es finden sich häufig Enterokokken inkl. VRE, Staphylokokken inkl. MRSA, Enterobacteriaceae inkl. ESBL-Bildnern sowie Anaerobier. Bei der tertiären Peritonitis werden auch <Mark2>Pseudomonas</Mark2> spp. und <Mark2>Candida</Mark2> spp. häufiger nachgewiesen <TextLink reference="9"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>. Für die Antibiotika-Therapie stehen Tigecyclin (ggf. in Kombination mit einer <Mark2>Pseudomonas</Mark2>-wirksamen Substanz) sowie Imipenem/Cilastatin, Meropenem, Ceftolozan/Tazobactam mit Metronidazol oder Ceftazidim/Avibactam mit Metronidazol (ggf. jeweils in Kombination mit Linezolid) zur Verfügung <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="27"></TextLink>.</Pgraph></TextBlock>
<TextBlock language="en" linked="yes" name="Peritonitis">
<MainHeadline>Peritonitis</MainHeadline><SubHeadline>Primary peritonitis</SubHeadline><Pgraph>Primary (spontaneous bacterial) peritonitis (SBP) affects only about 1% of all peritonitis cases. The juvenile form is a hematogenous infection caused by streptococci, pneumococci or, more rarely, <Mark2>Haemophilus influenzae</Mark2>. In adults, predominantly patients with ascites through alcoholic liver cirrhosis (ca. 70%) are affected or patients with a reduced immune status from another cause (ca. 30%) <TextLink reference="10"></TextLink>, <TextLink reference="11"></TextLink>. Mostly it is a mono-infection. In realistic studies, it is only possible to detect pathogens in about 35% of cases, with <Mark2>Escherichia coli</Mark2>, <Mark2>Klebsiella</Mark2> spp., Staphylococci, enterococci or streptococci, and occasionally pathogenic gastroenteritis pathogens such as <Mark2>Aeromonas</Mark2> spp. or <Mark2>Salmonella</Mark2> spp. being detected <TextLink reference="10"></TextLink>. Primary peritonitis, which can occur as part of tuberculosis, is spread hematogenously.</Pgraph><Pgraph>Randomized studies on the treatment of SBP are rare. Most of them are retrospective studies. Substances used were ceftriaxone, cefotaxime, ceftazidime, ampicillin/sulbactam, ampicillin + tobramycin and amoxycillin/clavulanic acid <TextLink reference="12"></TextLink>, <TextLink reference="13"></TextLink>, <TextLink reference="14"></TextLink> (Table 1 <ImgLink imgNo="1" imgType="table"/>). Using these alongside administration of albumin, clinical cure rates of about 80% were achieved <TextLink reference="15"></TextLink>. Regarding treatment of primary peritonitis caused by resistant pathogens, see also <TextGroup><PlainText>Table 1 </PlainText></TextGroup><ImgLink imgNo="1" imgType="table"/>.</Pgraph><SubHeadline>Peritonitis under CAPD</SubHeadline><Pgraph>CAPD peritonitis is usually caused by contamination of the tubing or catheter system. The most common pathogens are coagulase-negative staphylococci and <Mark2>Staphylococcus aureus</Mark2>. <Mark2>Escherichia coli</Mark2>, enterococci, streptococci, <Mark2>Pseudomonas aeruginosa</Mark2>, anaerobes, Enterobacter spp., or <Mark2>Candida</Mark2> species are detected less commonly <TextLink reference="16"></TextLink>. Uncomplicated cases can be treated locally by adding antimicrobial substances to the dialysis fluid. In addition to intraperitoneal treatment, parenteral treatment also becomes necessary in the rarer severe forms. The peculiarities of antibiotic dosing in cases of renal insufficiency must be taken into account. </Pgraph><Pgraph>Cefotaxime, cefuroxime or ceftriaxone (in monotherapy or in combination with ciprofloxacin) is recommended for calculated treatment <TextLink reference="17"></TextLink>. Once the results of microbiological diagnostics have been obtained, treatment should continue in a targeted fashion. If MRSA, MRSE and enterococci (including VRE) are detected, the antibiotics in Table 2 <ImgLink imgNo="2" imgType="table"/> are available. If the infection is not under control after one week of antimicrobial treatment, the peritoneal dialysis catheter should be removed <TextLink reference="18"></TextLink>.</Pgraph><SubHeadline>Secondary peritonitis</SubHeadline><Pgraph>Secondary peritonitis, with perforation of the gastrointestinal tract, is by far the most common IAI, at around 80–90%. By definition, surgical source control must be carried out (infectious source rehabilitation, for example appendectomy for perforated appendicitis) or interventional treatment (for example CT-controlled drainage of an abscess). In terms of a three-pillar model, diffuse peritonitis requires surgical, antimicrobial and intensive care treatment <TextLink reference="18"></TextLink>. Increasingly, primary infectious source rehabilitation is followed by definitive closure of the abdomen and clinical progress monitoring of the patient <TextLink reference="19"></TextLink>. In secondary peritonitis, a distinction can be made between a community-acquired (ca. 60%) and a post-operative form (ca. 40%).</Pgraph><SubHeadline>Community-acquired secondary peritonitis</SubHeadline><Pgraph>In community-acquired secondary peritonitis there is always a mixed infection. The pathogen spectrum derives from the flora of the gastrointestinal tract and is dependent on the pathogenesis and the location of the perforation or leakage. Key pathogens are <Mark2>Escherichia coli</Mark2>, <Mark2>Bacteroides fragilis</Mark2>, Enterococci and <Mark2>Candida</Mark2> spp. Resistant species need only be considered in patients treated with antibiotics on an out-patient basis and other specific risk factors (see Table 3 <ImgLink imgNo="3" imgType="table"/>). The present recommendations take into account the duration of the illness and the pathogen spectrum depending on the cause of the disease <TextLink reference="18"></TextLink>. For antibiotic treatment of localized acute peritonitis, cefuroxime, cefotaxime, ceftriaxone or ciprofloxacin, in combination with metronidazole, as well as ampicillin/sulbactam or amoxicillin/clavulanic acid can be used. Piperacillin/tazobactam and ertapenem, which have also been approved and tested in this indication, should be used in cases of more severe IAI (Table 4 <ImgLink imgNo="4" imgType="table"/>).</Pgraph><Pgraph>For the treatment of diffuse peritonitis, which persists for more than 2–4 hours, substances or combinations with a broad action spectrum should be used. Piperacillin/tazobactam, moxifloxacin, tigecycline or ertapenem can be used for calculated treatment. Alternatively, combinations of metronidazole with ceftriaxone or cefepime can be used. Considering enterococci in substance selection is recommended only in the exceptional case of known colonization <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. </Pgraph><Pgraph>Addition of aminoglycosides did result in improved effectiveness in meta-analyzes and is therefore no longer considered the treatment of choice <TextLink reference="24"></TextLink>. Variable kinetic parameters as well as ototoxicity and nephrotoxicity also require regular serum-level control.</Pgraph><SubHeadline>Post-operative, post-traumatic and post-interventional peritonitis</SubHeadline><Pgraph>Post-operative peritonitis is a nosocomially acquired secondary form of peritonitis and is defined as an infectious abdominal complication following surgery (for example anastomotic leakage following anterior rectal resection). In post-operative peritonitis, in contrast to tertiary peritonitis, a surgical or interventional (such as an endo-VAC insert into an insufficiency cavity) is a condition in need of treatment <TextLink reference="9"></TextLink>. Most patients will already have had antimicrobial treatment at the time of illness. Post-operative peritonitis is thus characterized by a selective pathogen spectrum with enterococci (including VRE), Gram-negative pathogens (“extended spectrum” beta-lactamase [ESBL]) and fungi. <Mark2>Pseudomonas</Mark2> spp. and carbapenemase producers are rarely detected.</Pgraph><Pgraph>Imipenem/cilastatin, meropenem, ertapenem, tigecycline and fosfomycin can be used as antibiotics with a broad action spectrum <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, the latter not being used in monotherapy because of the rapid development of resistance. Ceftolozane/tazobactam has recently become available as a new ESBL-effective drug. In the approval study for IAI, which used ceftolozane/tazobactam in combination with metronidazole, this group of patients in particular was treated very successfully under controlled clinical conditions <TextLink reference="25"></TextLink>, <TextLink reference="26"></TextLink>. Another treatment option in this indication range is the recently approved ceftazidime/avibactam in combination with metronidazole. The possibility of fungal infections in empirical anti-infective treatment must also be considered (see Table 5 <ImgLink imgNo="5" imgType="table"/>).</Pgraph><SubHeadline>Tertiary peritonits</SubHeadline><Pgraph>In tertiary peritonitis (such as post-operative peritonitis, a nosocomial form of peritonitis), infection of the abdominal cavity persists without a focus that can be remedied surgically, after previously completed infectious source rehabilitation of secondary peritonitis <TextLink reference="9"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>. The transitions from secondary to tertiary peritonitis can be fluid. In diagnostically unclear situations, relaparotomy is the only way of proving there is no need for a surgical intervention <TextLink reference="21"></TextLink>. Most are low-virulence pathogens, which lead to a sustained infection because of the sustained immunosuppression of the affected patient. This form of nosocomial peritonitis has a similar pathogen spectrum to secondary post-operative peritonitis due to prior antimicrobial treatment. There are often enterococci including VRE, staphylococci incl. MRSA, Enterobacteriaceae incl. ESBL producers and anaerobes. In tertiary peritonitis, <Mark2>Pseudomonas</Mark2> spp. and <Mark2>Candida</Mark2> spp. are detected more frequently <TextLink reference="9"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>. For antibiotic treatment, tigecycline (possibly in combination with a <Mark2>Pseudomonas</Mark2>-active substance) as well as imipenem/cilastatin, meropenem, ceftolozane/tazobactam with metronidazole or ceftazidime/avibactam with metronidazole (if necessary in combination with linezolid) are available <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="27"></TextLink>.</Pgraph></TextBlock>
<TextBlock language="de" linked="yes" name="Nekrotisierende Pankreatitis mit infizierten Nekrosen">
<MainHeadline>Nekrotisierende Pankreatitis mit infizierten Nekrosen</MainHeadline><Pgraph>Etwa 80% aller Todesfälle bei akuter Pankreatitis werden durch septische Komplikationen verursacht. Die Translokation von Erregern aus dem Kolon in das peripankreatische Gewebe ist die häufigste Ursache sekundär infizierter Pankreasnekrosen <TextLink reference="28"></TextLink>, <TextLink reference="29"></TextLink>, <TextLink reference="30"></TextLink>. Infizierte Pankreasnekrosen können vermutet werden, wenn Fieber, Leukozytose, Anstieg der CRP-Serumkonzentration und eine unerwartete klinische Verschlechterung auftreten. Der Nachweis von Gaseinschlüssen innerhalb nekrotischen Pankreasgewebes in der Abdomen-CT gilt als beweisend für infizierte Nekrosen <TextLink reference="31"></TextLink>. Die interventionelle Behandlung infizierter Pankreasnekrosen umfasst konservative Maßnahmen (endoskopisch geführte transgastrale Drainage, CT-gesteuerte Ableitung) sowie eine operative Behandlung. Gegenwärtig wird davon ausgegangen, dass der optimale Zeitpunkt für die operative Behandlung (offen oder minimal invasiv) nach Ablauf von mehr als drei Wochen gegeben ist <TextLink reference="32"></TextLink>. Metaanalysen kamen bereits 2004 und 2006 zu der Erkenntnis, dass eine generelle Gabe von Antibiotika keinen signifikant positiven Effekt auf den Verlauf einer nekrotisierenden Pankreatitis hat, sondern eher resistente Erreger und <Mark2>Candida</Mark2> spp. selektioniert <TextLink reference="33"></TextLink>, <TextLink reference="34"></TextLink>, <TextLink reference="35"></TextLink>, <TextLink reference="36"></TextLink>, <TextLink reference="37"></TextLink>, <TextLink reference="38"></TextLink>. In der rezenten Leitlinie des American College of Gastroenterology wird empfohlen, prinzipiell keine Antibiotika-Therapie durchzuführen <TextLink reference="39"></TextLink>. </Pgraph><Pgraph>Eine sichere Indikation für eine Antibiotika-Therapie besteht bei nachgewiesenen infizierten Nekrosen, infizierten Pseudozysten, Abszessbildung, Cholangitis und anderen extrapankreatischen Infektionen. Die wichtigsten Erreger bei infizierten Pankreasnekrosen sind Enterobacteriaceae, Enterokokken, Staphylokokken, Anaerobier und <Mark2>Candida</Mark2> spp. Bei der Auswahl geeigneter Antibiotika ist auch die Pankreasgängigkeit der Medikamente zu berücksichtigen (Tabelle 5 <ImgLink imgNo="5" imgType="table"/>). Untersuchungen mit verlässlichen Daten für eine gute Penetration in das Pankreasgewebe existieren für Fluorchinolone (Ciprofloxacin, Moxifloxacin), Carbapeneme (Imipenem/Cilastatin, Meropenem, Ertapenem), Tigecyclin und Piperacillin/Tazobactam. Eine unzureichende Gewebepenetration ist für Aminoglykoside belegt <TextLink reference="18"></TextLink>, <TextLink reference="24"></TextLink>. Alle oben genannten Substanzen können in seltenen Fällen selbst eine Pankreatitis auslösen.</Pgraph></TextBlock>
<TextBlock language="en" linked="yes" name="Necrotizing pancreatitis with infected necroses">
<MainHeadline>Necrotizing pancreatitis with infected necroses</MainHeadline><Pgraph>About 80% of all deaths from acute pancreatitis are caused by septic complications. The translocation of pathogens from the colon into the peripancreatic tissue is the most common cause of secondarily infected pancreatic necrosis <TextLink reference="28"></TextLink>, <TextLink reference="29"></TextLink>, <TextLink reference="30"></TextLink>. Infected pancreatic necroses can be suspected if fever, leukocytosis, CRP serum elevation and unexpected clinical deterioration occur. Detection of gas inclusions within necrotic pancreatic tissue in abdominal CT is considered to be evidence of infected necroses <TextLink reference="31"></TextLink>. Interventions in cases of infected pancreatic necrosis includes conservative measures (endoscopically guided transgastric drainage, CT-guided drainage) as well as surgical intervention. Currently, it is assumed that the optimal time for surgical treatment (open or minimally invasive) is after more than three weeks <TextLink reference="32"></TextLink>. Meta-analyzes already concluded in 2004 and 2006 that a general administration of antibiotics has no significant positive effect on the course of necrotizing pancreatitis and instead leads to a selection of resistant pathogens and <Mark2>Candida</Mark2> spp. <TextLink reference="33"></TextLink>, <TextLink reference="34"></TextLink>, <TextLink reference="35"></TextLink>, <TextLink reference="36"></TextLink>, <TextLink reference="37"></TextLink>, <TextLink reference="38"></TextLink>. The recent guideline of the American College of Gastroenterology recommends that in principle no antibiotic treatment should be carried out <TextLink reference="39"></TextLink>. </Pgraph><Pgraph>A safe indication for antibiotic treatment is proven infected necrosis, infected pseudocysts, abscess formation, cholangitis, and other extra-pancreatic infections. The most important pathogens in infected pancreatic necroses are Enterobacteriaceae, enterococci, staphylococci, anaerobes and <Mark2>Candida</Mark2> spp. When selecting appropriate antibiotics, pancreatic mobility of the drugs should also be considered (Table 5 <ImgLink imgNo="5" imgType="table"/>). Studies with reliable data for good penetration into the pancreatic tissue exist for fluoroquinolones (ciprofloxacin, moxifloxacin), carbapenems (imipenem/cilastatin, meropenem, ertapenem), tigecycline and piperacillin/tazobactam. Inadequate tissue penetration has been demonstrated for aminoglycosides <TextLink reference="18"></TextLink>, <TextLink reference="24"></TextLink>. All the above-mentioned substances can in rare cases cause pancreatitis.</Pgraph></TextBlock>
<TextBlock language="de" linked="yes" name="Invasive intraabdominelle Mykosen">
<MainHeadline>Invasive intraabdominelle Mykosen</MainHeadline><Pgraph>Die meisten intraabdominellen invasiven Mykosen (IIM) werden durch <Mark2>Candida</Mark2> spp. ausgelöst. Insgesamt werden bis zu 18% aller schweren Sepsis-Fälle in Deutschland auf <Mark2>Candida</Mark2> spp. zurückgeführt <TextLink reference="3"></TextLink>. Der einmalige Nachweis im intraoperativ gewonnenen Material bei einer ambulant erworbenen sekundären Peritonitis (z.B. perforiertes Magenulcus) bedarf beim postoperativ stabilen und immunkompetenten Patienten keiner antimykotischen Therapie. Risikokollektive aus chirurgischer Sicht sind Patienten mit einer schweren postoperativen (z.B. Nahtinsuffizienz nach Ösophagojejunostomie) oder tertiären Peritonitis <TextLink reference="40"></TextLink>, <TextLink reference="41"></TextLink>, <TextLink reference="42"></TextLink>, <TextLink reference="43"></TextLink>, <TextLink reference="44"></TextLink>, <TextLink reference="45"></TextLink>, <TextLink reference="46"></TextLink>. Die prophylaktische Gabe von Fluconazol hat zwar zu einer Reduktion von <Mark2>Candida</Mark2>-Infektionen geführt, die Letalität aber nicht verändert und wird daher nicht empfohlen <TextLink reference="40"></TextLink>, <TextLink reference="47"></TextLink>. </Pgraph><Pgraph>Die Anzahl von <Mark2>Candida</Mark2>-Stämmen mit eingeschränkter Empfindlichkeit gegenüber Fluconazol liegt in Deutschland bei ca. 40% <TextLink reference="27"></TextLink>, <TextLink reference="40"></TextLink>. Daher wird vor dem Hintergrund der Ergebnisse neuerer Multicenterstudien die Anwendung eines Echinocandins (Anidulafungin, Caspofungin, Micafungin) präferiert, wenn der Patient instabil ist oder wenn kürzlich eine Azol-Therapie oder -Prophylaxe durchgeführt worden ist. Alternativ kann bei Empfindlichkeit gegenüber Azolen und Kreislaufstabilität der Einsatz von Fluconazol und, bei Verfügbarkeit eines therapeutischen Drug Monitorings, auch der von Voriconazol erwogen werden. Eine Initialtherapie mit (liposomalem) Amphotericin B ist unter individueller Abwägung der potenteillen Nebenwirkungen (glomeruläre und tubuläre Nephrotoxizizät) ebenfalls eine Option. Zu Isavuconazol oder Posaconazol liegen keine Studiendaten zur Behandlung invasiver <Mark2>Candida</Mark2>-Infektionen vor (kein Grading). Die Therapiedauer beträgt mindestens 14 Tage <TextLink reference="40"></TextLink>, <TextLink reference="47"></TextLink>. Insgesamt liegen speziell bei intraabdominellen Mykosen wenige kontrollierte Daten vor. Die publizierten Kollektive sind bezüglich wesentlicher Basisparameter sehr heterogen <TextLink reference="48"></TextLink>. Die Prognose einer IIM ist bei verzögerter Therapie schlecht <TextLink reference="40"></TextLink>, <TextLink reference="41"></TextLink>, <TextLink reference="42"></TextLink>, <TextLink reference="43"></TextLink>, <TextLink reference="44"></TextLink>, <TextLink reference="45"></TextLink>, <TextLink reference="46"></TextLink>, <TextLink reference="47"></TextLink>, <TextLink reference="48"></TextLink>.</Pgraph></TextBlock>
<TextBlock language="en" linked="yes" name="Invasive intra-abdominal mycoses">
<MainHeadline>Invasive intra-abdominal mycoses</MainHeadline><Pgraph>Most intra-abdominal invasive mycoses (IIM) are triggered by <Mark2>Candida</Mark2> spp. In total, up to 18% of all severe sepsis cases in Germany were found to be due to <Mark2>Candida</Mark2> spp. <TextLink reference="3"></TextLink>. One-off detection in surgically-obtained material in cases of community-acquired secondary peritonitis (for example perforated gastric ulcer) does not require anti-fungal treatment in the post-operative care of stable and immunocompetent patients. From a surgical point of view, at-risk groups are patients with severe post-operative (for instance suture insufficiency following esophagojejunostomy) or tertiary peritonitis <TextLink reference="40"></TextLink>, <TextLink reference="41"></TextLink>, <TextLink reference="42"></TextLink>, <TextLink reference="43"></TextLink>, <TextLink reference="44"></TextLink>, <TextLink reference="45"></TextLink>, <TextLink reference="46"></TextLink>. Although the prophylactic administration of fluconazole has led to a reduction of Candida infections, it does not alter the lethality and is therefore not recommended <TextLink reference="40"></TextLink>, <TextLink reference="47"></TextLink>. </Pgraph><Pgraph>The number of Candida strains in Germany with limited sensitivity to fluconazole is approximately 40% <TextLink reference="27"></TextLink>, <TextLink reference="40"></TextLink>. Therefore, against the backdrop of the results of recent multi-center studies, the use of an echinocandin (anidulafungin, caspofungin, micafungin) is preferred when the patient is unstable or when azole therapy or prophylaxis has recently been carried out. Alternatively, in cases of sensitivity to azoles and cardiovascular stability, the use of fluconazole and, if therapeutic drug monitoring is available, that of voriconazole may also be considered. Initial therapy with (liposomal) amphotericin B is also an option, taking into account the potential side effects (glomerular and tubular nephrotoxicity). There are no data available on isavuconazole or posaconazole in the treatment of invasive <Mark2>Candida</Mark2> infections (no grading). The duration of treatment is at least 14 days <TextLink reference="40"></TextLink>, <TextLink reference="47"></TextLink>. Overall, there are few controlled data, especially for intra-abdominal mycoses. The published collectives are very heterogeneous as regards basic parameters <TextLink reference="48"></TextLink>. Prognosis of IIM is poor in delayed treatment <TextLink reference="40"></TextLink>, <TextLink reference="41"></TextLink>, <TextLink reference="42"></TextLink>, <TextLink reference="43"></TextLink>, <TextLink reference="44"></TextLink>, <TextLink reference="45"></TextLink>, <TextLink reference="46"></TextLink>, <TextLink reference="47"></TextLink>, <TextLink reference="48"></TextLink>.</Pgraph></TextBlock>
<TextBlock language="de" linked="yes" name="Schwer therapierbare und multiresistente Erreger (MRE)">
<MainHeadline>Schwer therapierbare und multiresistente Erreger (MRE)</MainHeadline><Pgraph>Während Mitte der 90er Jahre noch 95–97% aller bei IAI nachgewiesenen bakteriellen Erreger gegenüber häufig verwendeten Antibiotika (z.B. Cefotaxim oder Ciprofloxacin + Metronidazol) sensibel waren, hat in den letzten Jahren, insbesondere bei der postoperativen Peritonitis sowie der tertiären Peritonitis, der Anteil resistenter Stämme (MRSA, VRE, ESBL-Bildner, (multi)resistente <Mark2>Pseudomonas</Mark2> spp.) weltweit deutlich zugenommen <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="27"></TextLink>, <TextLink reference="49"></TextLink>, <TextLink reference="50"></TextLink>, <TextLink reference="51"></TextLink>, <TextLink reference="52"></TextLink>, <TextLink reference="53"></TextLink>. Gerade bei den von resistenten Erregern verursachten, lebensbedrohlichen Krankheitsbildern ist es wichtig, mit der initialen Antibiotika-Therapie das zu erwartende Erregerspektrum möglichst vollständig zu erfassen. Findet sich nach der mikrobiologischen Untersuchung kein Nachweis von resistenten Erregern, sollte eine Deeskalation der Therapie erfolgen. </Pgraph><Pgraph>Eine Übersicht der resistenten Erreger und ihrer Häufigkeit bei intraabdominellen Infektionen, die zugleich als Entscheidungsmatrix für eine empirische Therapie genutzt werden kann, gibt Tabelle 6 <ImgLink imgNo="6" imgType="table"/> modifiziert wider <TextLink reference="23"></TextLink>. Die folgenden Abschnitte sind resistenten Erregern gewidmet, die wegen ihrer besonderen Bedeutung einer gesonderten Betrachtung bedürfen. Hinweise zur kalkulierten Therapie bei IAI durch diese Erreger finden sich in Tabelle 2 <ImgLink imgNo="2" imgType="table"/>.</Pgraph><SubHeadline>MRSA</SubHeadline><Pgraph>Eine Infektion der Abdominalhöhle mit MRSA ist beim immunkompetenten Patienten selten. Meist handelt es sich um eine MRSA-Kolonisation bei offenem Abdomen, z.B. nach abdominellem Kompartmentsyndrom. Eine Indikation zur Antibiotika-Therapie ergibt sich bei nicht immunsupprimierten Patienten, wenn lokale und systemische Infektionszeichen sowie ein persistierender Nachweis vorliegen. Bei immunsupprimierten Patienten nach Transplantation sollte jeder Nachweis von MRSA als behandlungsbedürftig erachtet werden. Tigecyclin besitzt als einziges MRSA-wirksames Antibiotikum eine Zulassung zur Behandlung von IAI <TextLink reference="54"></TextLink> und erfasst auch das zu erwartende gramnegative und anaerobe Erregerspektrum. Vancomycin zeichnet sich durch eine vergleichsweise schlechte Penetration in das abdominelle Kompartiment aus. Für Linezolid liegen klinische Daten über die Behandlung von IAI vor <TextLink reference="55"></TextLink>, <TextLink reference="56"></TextLink>. Linezolid, Daptomycin und Vancomycin sollten mit einem Antibiotikum kombiniert werden, das gegen gramnegative Erreger wirksam ist <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. </Pgraph><SubHeadline>Enterokokken inklusive VRE</SubHeadline><Pgraph>Die Rolle der Enterokokken als primärer pathogener Erreger in einer polymikrobiellen IAI wird kontrovers beurteilt <TextLink reference="57"></TextLink>, <TextLink reference="58"></TextLink>. Enterokokken der Spezies <Mark2>Enterococcus faecalis</Mark2> und <Mark2>Enterococcus faecium</Mark2> sind wichtige Erreger nosokomialer Infektionen. Sie stehen in Deutschland hinsichtlich ihrer Häufigkeit an dritter Stelle <TextLink reference="27"></TextLink>. <Mark2>Enterococcus faecium</Mark2> verfügt über ein breites Spektrum an intrinsischen und erworbenen Antibiotikaresistenzen und hat dadurch zunehmende Bedeutung als Erreger von nosokomialen Infektionen bei immunsupprimierten und intensivmedizinisch versorgten multimorbiden Patienten erlangt <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="27"></TextLink>. Insbesondere bei Patienten mit postoperativer Peritonitis, tertiärer Peritonitis, schwerer abdomineller Sepsis sowie Antibiotika-Vorbehandlung oder bei Endokarditis-gefährdeten Patienten (Peritonitis und Herzklappenersatz) sollten Enterokokken-wirksame Antibiotika eingesetzt werden <TextLink reference="18"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. Im europäischen Vergleich findet sich in Deutschland ein vergleichsweise hoher Anteil an VRE<Mark2>nterococcus faecium</Mark2> <TextLink reference="27"></TextLink>. Nur wenige Antibiotika sind gegenüber VRE<Mark2>nterococcus faecium</Mark2> wirksam, nämlich Tigecyclin <TextLink reference="59"></TextLink>, Linezolid <TextLink reference="60"></TextLink>, und z.T. auch Daptomycin (keine kontrollierten klinischen Daten). Kasuistiken über Linezolid- bzw. Tigecyclin-resistente Enterokokken-Stämme liegen vor, z.B. <TextLink reference="61"></TextLink>.</Pgraph><SubHeadline>Resistente Enterobacteriaceae </SubHeadline><Pgraph>ESBL-bildende Enterobacteriaceae können viele der zur kalkulierten Initialtherapie eingesetzten Penicilline und Cephalosporine inaktivieren. Häufig findet sich auch eine Resistenz gegenüber den Beta-Lactamase-Inhibitor-ge<TextGroup><PlainText>s</PlainText></TextGroup>chützten Kombinationen Amoxicillin/Clavulansäure, Ampicillin/Sulbactam und (seltener) Piperacillin/Tazobactam sowie eine Parallelresistenz gegenüber weiteren Antibiotika-Klassen, einschließlich Fluorchinolonen und Aminoglykosiden <TextLink reference="62"></TextLink>, <TextLink reference="63"></TextLink>. Es ist davon auszugehen, dass es mittlerweile weltweit ein riesiges Reservoir an Personen gibt, die mit ESBL-bildenden Erregern kolonisiert sind <TextLink reference="27"></TextLink>, <TextLink reference="63"></TextLink> und dies kein nosokomiales Phänomen ist. Erschwerend kommt hinzu, dass der Anteil ESBL-bil<TextGroup><PlainText>d</PlainText></TextGroup>ender Bakterien auch bei Tieren deutlich zunimmt und die Erreger auch auf Lebensmitteln und im Wasser nachgewiesen werden. In der PEG-Resistenzstudie 2013 betrug der Anteil von Isolaten mit dem „Extended-Spektrum“-Beta-Lactamase (ESBL)-Phänotyp bei <Mark2>Escherichia coli</Mark2> 15,4% und bei <Mark2>Klebsiella</Mark2> pneumoniae 17,8%. Weiterhin hat auch der Anteil von Carbapenemasen-bildenden Enterobakteraiceae zugenommen <TextLink reference="27"></TextLink>. Eine weiterführende Bearbeitung dieses wichtigen Themenkomplexes findet sich in Kapitel 16 <TextLink reference="64"></TextLink>.</Pgraph><Pgraph>Als Therapie der Wahl werden Carbapeneme, Fosfomycin (keine Monotherapie wegen der Gefahr der schnellen Resistenzentwicklung) und Tigecyclin empfohlen <TextLink reference="18"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="27"></TextLink>. Letzteres wurde unter „real-life“ Bedingungen in einer europaweiten Studie bei ca. 75% der Patienten mit IAI klinisch erfolgreich eingesetzt <TextLink reference="59"></TextLink>. Ceftolozan/Tazobactam steht seit kurzem als neues ESBL-wirksames Medikament zur Verfügung. In der Zulassungsstudie für IAI wurde speziell die Patientengruppe der ESBL-verursachten IAI unter kontrollierten Bedingungen erfolgreich behandelt <TextLink reference="25"></TextLink>, <TextLink reference="26"></TextLink>. Des Weiteren kommt der Einsatz des ebenfalls kürzlich für dieses Indikationsgebiet zugelassene Ceftazidim/Avibactam in Betracht <TextLink reference="65"></TextLink>.</Pgraph><Pgraph>Mittlerweile sind Enterobacteriaceae auch in der Lage, Carbapenemasen (KPC, NDM) zu produzieren, wodurch Carbapenem-Antibiotika unwirksam werden. Carbapenemasen sind am häufigsten bei <Mark2>Klebsiella pneumoniae</Mark2> anzutreffen (<Mark2>Klebsiella-pneumoniae</Mark2>-Carbapenemasen, KPC), können aber auch bei <Mark2>Escherichia coli</Mark2> und anderen gramnegativen Erregern, wie z.B. <Mark2>Acinetobacter</Mark2> spp., vorkommen. Für eine gezielte adäquate Therapie stehen hier nur noch wenige Optionen zur Verfügung. Empfohlen werden Kombinations-Antibiotikaregime, die Tigecyclin, Meropenem und Colistin beinhalten. Als neue, in diesem Indikationsbereich zugelassene Substanz kommt auch der Einsatz von Ceftazidim/Avibactam in Betracht <TextLink reference="66"></TextLink>, <TextLink reference="67"></TextLink>, <TextLink reference="68"></TextLink>.</Pgraph><SubHeadline>Pseudomonas spp., Acinetobacter spp.</SubHeadline><Pgraph><Mark2>Pseudomonas</Mark2> spp. werden in ca. 8–15% aller IAI nachgewiesen, wobei der Anteil kausal pathogenetisch relevanter Stämme deutlich niedriger liegen dürfte <TextLink reference="9"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="69"></TextLink>. Resistenzen gegen 3 oder 4 der zur Verfügung stehenden Antibiotikaklassen (3MRGN, 4MRGN) werden auch bei IAI immer häufiger beobachtet. Gleiches gilt für Carbapenem-resistente Acinetobacter spp., wobei sich hier in Einzelfällen noch Tigecyclin als wirksam erweisen kann. Als Besonderheit ist hier gelegentlich auch Sulbactam in Monotherapie wirksam (Testergebnis beachten).</Pgraph></TextBlock>
<TextBlock language="en" linked="yes" name="Difficult to treat and multidrug-resistant pathogens (MDROs)">
<MainHeadline>Difficult to treat and multidrug- resistant pathogens (MDROs)</MainHeadline><Pgraph>While in the mid-1990s 95–97% of all bacterial pathogens detected in IAI were still sensitive to common antibiotics (such as cefotaxime or ciprofloxacin + metronidazole), in recent years, especially in post-operative and tertiary peritonitis, the proportion of more resistant strains (MRSA, VRE, ESBL producer, (multi)resistant <Mark2>Pseudomonas</Mark2> spp.) have increased significantly worldwide <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="27"></TextLink>, <TextLink reference="49"></TextLink>, <TextLink reference="50"></TextLink>, <TextLink reference="51"></TextLink>, <TextLink reference="52"></TextLink>, <TextLink reference="53"></TextLink>. It is important to cover the expected pathogen spectrum as completely as possible with the initial antibiotic treatment, particularl<TextGroup><PlainText>y in</PlainText></TextGroup> the case of life-threatening clinical scenarios caused by resistant pathogens. If no evidence of resistant pathogens is found after microbiological examination, treatment should be de-escalated. </Pgraph><Pgraph>An overview of the resistant pathogens and their frequency in intra-abdominal infections, which can also be used as a decision matrix for empirical treatment, is given in Table 6 <ImgLink imgNo="6" imgType="table"/> in modified form <TextLink reference="23"></TextLink>. The following sections deal with resistant pathogens, which require special considerations because of their particular importance. Information on the calculated treatment of IAI caused by these pathogens can be found in Table 2 <ImgLink imgNo="3" imgType="table"/>.</Pgraph><SubHeadline>MRSA</SubHeadline><Pgraph>An infection of the abdominal cavity with MRSA is rare in immunocompetent patients. It is usually MRSA colonization due to an open abdomen, for example after abdominal compartment syndrome. In non-immunosuppressed patients an indication for antibiotic treatment results if local and systemic signs of infection and persistent evidence are present. In immunosuppressed patients after transplantation, any detection of MRSA should be considered as requiring treatment. Tigecycline is the only MRSA-active antibiotic approved for the treatment of IAI <TextLink reference="54"></TextLink> and also covers the expected Gram-negative and anaerobic pathogen spectrum. Vancomycin is characterized by a relatively poor penetration into the abdominal compartment. There is clinical data on linezolid for the treatment of IAI <TextLink reference="55"></TextLink>, <TextLink reference="56"></TextLink>. Linezolid, daptomycin and vancomycin should be combined with an antibiotic effective against Gram-negative pathogens <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. </Pgraph><SubHeadline>Enterococci including VRE</SubHeadline><Pgraph>The role of enterococci as the primary pathogen in a polymicrobial IAI is controversial <TextLink reference="57"></TextLink>, <TextLink reference="58"></TextLink>. Enterococci of the species <Mark2>Enterococcus faecalis</Mark2> and <Mark2>Enterococcus faecium</Mark2> are important pathogens of nosocomial infections. They rank third in Germany in terms of frequency <TextLink reference="27"></TextLink>. <Mark2>Enterococcus faecium</Mark2> has a broad spectrum of intrinsic and acquired antibiotic resistance and has become increasingly important as a pathogen for nosocomial infections in immunosuppressed and intensive care multi-morbid patients <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="27"></TextLink>. Enterococci-effective antibiotics should be used particularly in patients with postoperative peritonitis, tertiary peritonitis, severe abdominal sepsis and prior antibiotic treatment or endocarditis-prone patients (peritonitis and heart valve replacement), <TextLink reference="18"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. Compared to the rest of Europe, a comparatively high proportion of VRE<Mark2>nterococcus faecium</Mark2> is found in Germany <TextLink reference="27"></TextLink>. Only a few antibiotics are active against VRE<Mark2>nterococcus faecium</Mark2>. These are tigecycline <TextLink reference="59"></TextLink>, linezolid <TextLink reference="60"></TextLink>, and also to some extent daptomycin (no controlled clinical data). Cases of linezolid or tigecycline-resistant enterococci strains have been documented, for instance <TextLink reference="61"></TextLink>.</Pgraph><SubHeadline>Resistant Enterobacteriaceae </SubHeadline><Pgraph>ESBL-producing Enterobacteriaceae can inactivate many of the penicillins and cephalosporins used for calculated initial treatment. In many cases there is also resistance to the beta-lactamase inhibitor-protected combinations amoxicillin/clavulanic acid, ampicillin/sulbactam, and (more rarely) piperacillin/tazobactam, as well as parallel resistance to other antibiotic classes, including fluoroquinolones and aminoglycosides <TextLink reference="62"></TextLink>, <TextLink reference="63"></TextLink>. It can be assumed that there is now a huge reservoir of people worldwide who are colonized with ESBL-producing pathogens <TextLink reference="27"></TextLink>, <TextLink reference="63"></TextLink> and that this is not a nosocomial phenomenon. To make matters worse, the proportion of ESBL-producing bacteria is also increasing significantly in animals and the pathogens are also detected on food and in water. In the PEG resistance study in 2013, the proportion of isolates with the extended spectrum beta-lactamase (ESBL) phenotype was 15.4% for <Mark2>Escherichia coli</Mark2> and 17.8% for <Mark2>Klebsiella pneumoniae</Mark2>. Furthermore, the proportion of carbapenemase-producing Enterobacteriaceae has also increased <TextLink reference="27"></TextLink>. Further work on this important topic can be found in chapter 16 <TextLink reference="64"></TextLink>.</Pgraph><Pgraph>Carbapenems, fosfomycin (no monotherapy because of the risk of rapid development of resistance) and tigecycline are recommended as treatment of choice <TextLink reference="18"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>, <TextLink reference="27"></TextLink>. The latter was used clinically in approximately 75% of patients with IAI under real-life conditions in a Europe-wide study <TextLink reference="59"></TextLink>. Ceftolozan/tazobactam has recently become available as a new ESBL-effective drug. In the IAI licensing study, the ESBL-induced IAI group of patients was treated successfully under controlled conditions <TextLink reference="25"></TextLink>, <TextLink reference="26"></TextLink>. Furthermore, the use of ceftazidime/avibactam, which was also recently approved for this type of indication, can also be considered <TextLink reference="65"></TextLink>.</Pgraph><Pgraph>By now, Enterobacteriaceae are also able to produce carbapenemases (KPC, NDM), thereby rendering carbapenem antibiotics ineffective. Occurrences of carbapenemases are most commonly found in <Mark2>Klebsiella pneumoniae</Mark2> (<Mark2>Klebsiella pneumoniae</Mark2> carbapenemases, KPC) but can also be found in <Mark2>Escherichia coli</Mark2> and other Gram-negative pathogens, for example <Mark2>Acinetobacter</Mark2> spp. Only a few options remain for adequate targeted treatment. Combination antibiotic regimens containing tigecycline, meropenem and colistin are recommended. The use of ceftazidime/avibactam, a new substance approved for this type of indication, can also be taken into consideration <TextLink reference="66"></TextLink>, <TextLink reference="67"></TextLink>, <TextLink reference="68"></TextLink>.</Pgraph><SubHeadline>Pseudomonas spp., Acinetobacter spp.</SubHeadline><Pgraph>Pseudomonas spp. are detected in about 8–15% of all IAI, although the proportion of causally pathogenetically relevant strains is likely to be much lower <TextLink reference="9"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="69"></TextLink>. Resistance to 3 or 4 of the available antibiotic classes (3MRGN, 4MRGN) is also being observed more frequently in IAI. The same applies to carbapenem-resistant <Mark2>Acinetobacter</Mark2> spp., where in some cases tigecycline can still prove to be effective. As a special feature here occasionally sulbactam in monotherapy is also effective (note test result).</Pgraph></TextBlock>
<TextBlock language="de" linked="yes" name="Dauer der empirischen Antibiotika-Therapie intraabdomineller Infektionen">
<MainHeadline>Dauer der empirischen Antibiotika-Therapie intraabdomineller Infektionen</MainHeadline><Pgraph>Sehr häufig müssen Kliniker mit der antimikrobiellen Therapie empirisch beginnen, d.h. bevor ein Erregernachweis erfolgt ist Empfehlungen für die empirische Therapie von IAI nach einem Stufenmodell finden sich in <TextGroup><PlainText>Tabelle 4 </PlainText></TextGroup><ImgLink imgNo="4" imgType="table"/>. Je lokaler die Infektion begrenzt ist, desto kürzer kann die Therapiedauer sein. Zur Therapie ambulant erworbener lokaler Peritonitiden ohne Risikofaktoren (Stufe 1: Therapiedauer 1 Tag; Stufe 2: Therapiedauer 3 Tage) sollten Substanzen wie Cephalosporine der Gruppen 2 oder 3a (z.B. Cefuroxim, Cefotaxim) oder Fluorchinolone (z.B. Ciprofloxacin), jeweils in Kombination mit Metronidazol, zum Einsatz kommen. Alternativ können auch Aminopenicilline in Kombination mit einem Beta-Lactamase-Inhibitor (z.B. Amoxicillin/Clavulansäure) eingesetzt werden (siehe Tabelle 3 <ImgLink imgNo="3" imgType="table"/>) <TextLink reference="18"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. </Pgraph><Pgraph>Mit Anstieg der lokalen und systemischen Ausbreitung der Infektion sowie bei möglichem Vorliegen von Risikofaktoren (siehe Tabelle 3 <ImgLink imgNo="3" imgType="table"/>) kommen Piperacillin/Tazobactam, Ertapenem und eingeschränkt auch Moxifloxacin in Frage (Stufe 3: Therapiedauer 5 Tage). Bei fortgeschrittener lokaler Peritonitis ist bei adäquater Herdsanierung ein Behandlungszeitraum von 4–5 Tagen nicht schlechter als eine 8- bis 10-tägige Antibiotika-Therapie, wie unlängst im Rahmen einer großen randomisierten, doppelblinden Studie gezeigt wurde <TextLink reference="70"></TextLink>. Bei nosokomialen Peritonitiden und bei hämodynamisch instabilen Patienten im septischen Schock ist die Wahrscheinlichkeit allerdings sehr hoch, dass resistente Erreger die Infektion mitauslösen. Hier sollten lediglich Meropenem, Imipenem, Tigecyclin (ggf. in Kombination mit einer Pseudomonas-wirksamen Substanz) oder auch Ceftolozan/Tazobactam + Metronidazol bzw. Ceftazidim/Avivactam + Metronidazol eingesetzt werden (Stufe 4: 7–10 Tage Therapiedauer). Stellt sich nach 7–10 Tagen kein Behandlungserfolg ein, ist ein Absetzen der antimikrobiellen Therapie und eine anschließende erneute Probengewinnung einer unklaren, resistente Erreger selektionierenden Fortsetzung der möglicherweise toxischen Therapie vorzuziehen.</Pgraph></TextBlock>
<TextBlock language="en" linked="yes" name="Duration of empirical antibiotic treatment of intra-abdominal infections">
<MainHeadline>Duration of empirical antibiotic treatment of intra-abdominal infections</MainHeadline><Pgraph>Very often clinicians must begin antimicrobial treatment empirically, i.e. prior to pathogen detection. Recommendations for the empirical treatment of IAI according to a level model can be found in Table 4 <ImgLink imgNo="4" imgType="table"/>. The more local the infection is, the shorter the duration of treatment can be. For the treatment of community-acquired local peritonitis without risk factors (level 1: treatment duration 1 day; level 2: treatment duration 3 days), substances such as cephalosporins of groups 2 or 3a (for example cefuroxime, cefotaxime) or fluoroquinolones (for example ciprofloxacin), in each case in combination with metronidazole, should be used. Alternatively, aminopenicillins may be used in combination with a beta-lactamase inhibitor (for example amoxycillin/clavulanic acid) (see <TextGroup><PlainText>Table 3 </PlainText></TextGroup><ImgLink imgNo="3" imgType="table"/>) <TextLink reference="18"></TextLink>, <TextLink reference="20"></TextLink>, <TextLink reference="21"></TextLink>, <TextLink reference="22"></TextLink>, <TextLink reference="23"></TextLink>. </Pgraph><Pgraph>With increased local and systemic spread of the infection and possible risk factors (see Table 3 <ImgLink imgNo="3" imgType="table"/>), piperacillin/tazobactam, ertapenem and, to a lesser extent, moxifloxacin may be considered (level 3: treatment duration 5 days). For advanced localized peritonitis, a <TextGroup><PlainText>4–5 day</PlainText></TextGroup> treatment period is not inferior to an 8 to 10-day course of antibiotics with adequate infectious source rehabilitation, as recently demonstrated in a large randomized, double-blind study <TextLink reference="70"></TextLink>. However, in nosocomial peritonitis and hemodynamically unstable patients in septic shock, the likelihood is high that resistant pathogens will co-trigger the infection. Only meropenem, imipenem, tigecycline (possibly in combination with a Pseudomonas-active substance) or ceftolozane/tazobactam + metronidazole or ceftazidime/avibactam + metronidazole should be used (level 4: treatment duration 7–10 days). If no treatment success occurs after 7–10 days, discontinuation of antimicrobial treatment and taking new samples is preferable to continuation of an unclear, resistant pathogen-selecting, potentially toxic therapy.</Pgraph></TextBlock>
<TextBlock language="de" linked="yes" name="Anmerkung">
<MainHeadline>Anmerkung</MainHeadline><Pgraph>Dies ist das siebte Kapitel der von der Paul-Ehrlich-Gesellschaft für Chemotherapie e.V. (PEG) herausgegebenen S2k Leitlinie „Kalkulierte parenterale Initialtherapie bakterieller Erkrankungen bei Erwachsenen – Update 2018“ in der 2. aktualisierten Fassung.</Pgraph></TextBlock>
<TextBlock language="en" linked="yes" name="Note">
<MainHeadline>Note</MainHeadline><Pgraph>This is the seventh chapter of the guideline “Calculated initial parenteral treatment of bacterial infections in adults – update 2018” in the 2<Superscript>nd</Superscript> updated version. The German guideline by the Paul-Ehrlich-Gesellschaft für Chemothe<TextGroup><PlainText>ra</PlainText></TextGroup>pie e.V. (PEG) has been translated to address an international audience.</Pgraph></TextBlock>
<TextBlock language="de" linked="yes" name="Interessenkonflikte">
<MainHeadline>Interessenkonflikte</MainHeadline><Pgraph>Die Autoren erklären, dass sie keine Interessenkonflikte in Zusammenhang mit diesem Artikel haben.</Pgraph></TextBlock>
<TextBlock language="en" linked="yes" name="Competing interests">
<MainHeadline>Competing interests</MainHeadline><Pgraph>The authors declare that they have no competing interests.</Pgraph></TextBlock>
<References linked="yes">
<Reference refNo="1">
<RefAuthor>Bader FG</RefAuthor>
<RefAuthor>Schröder M</RefAuthor>
<RefAuthor>Kujath P</RefAuthor>
<RefAuthor>Muhl E</RefAuthor>
<RefAuthor>Bruch HP</RefAuthor>
<RefAuthor>Eckmann C</RefAuthor>
<RefTitle>Diffuse postoperative peritonitis – value of diagnostic parameters and impact of early indication for relaparotomy</RefTitle>
<RefYear>2009</RefYear>
<RefJournal>Eur J Med Res</RefJournal>
<RefPage>491-6</RefPage>
<RefTotal>Bader FG, Schröder M, Kujath P, Muhl E, Bruch HP, Eckmann C. Diffuse postoperative peritonitis – value of diagnostic parameters and impact of early indication for relaparotomy. Eur J Med Res. 2009 Nov;14(11):491-6. DOI: 10.1186/2047-783X-14-11-491</RefTotal>
<RefLink>https://doi.org/10.1186/2047-783X-14-11-491</RefLink>
</Reference>
<Reference refNo="2">
<RefAuthor>Kumar A</RefAuthor>
<RefAuthor>Roberts D</RefAuthor>
<RefAuthor>Wood KE</RefAuthor>
<RefAuthor>Light B</RefAuthor>
<RefAuthor>Parrillo JE</RefAuthor>
<RefAuthor>Sharma S</RefAuthor>
<RefAuthor>Suppes R</RefAuthor>
<RefAuthor>Feinstein D</RefAuthor>
<RefAuthor>Zanotti S</RefAuthor>
<RefAuthor>Taiberg L</RefAuthor>
<RefAuthor>Gurka D</RefAuthor>
<RefAuthor>Kumar A</RefAuthor>
<RefAuthor>Cheang M</RefAuthor>
<RefTitle>Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>Crit Care Med</RefJournal>
<RefPage>1589-96</RefPage>
<RefTotal>Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S, Suppes R, Feinstein D, Zanotti S, Taiberg L, Gurka D, Kumar A, Cheang M. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006 Jun;34(6):1589-96. DOI: 10.1097/01.CCM.0000217961.75225.E9</RefTotal>
<RefLink>https://doi.org/10.1097/01.CCM.0000217961.75225.E9</RefLink>
</Reference>
<Reference refNo="3">
<RefAuthor>Engel C</RefAuthor>
<RefAuthor>Brunkhorst FM</RefAuthor>
<RefAuthor>Bone HG</RefAuthor>
<RefAuthor>Brunkhorst R</RefAuthor>
<RefAuthor>Gerlach H</RefAuthor>
<RefAuthor>Grond S</RefAuthor>
<RefAuthor>Gruendling M</RefAuthor>
<RefAuthor>Huhle G</RefAuthor>
<RefAuthor>Jaschinski U</RefAuthor>
<RefAuthor>John S</RefAuthor>
<RefAuthor>Mayer K</RefAuthor>
<RefAuthor>Oppert M</RefAuthor>
<RefAuthor>Olthoff D</RefAuthor>
<RefAuthor>Quintel M</RefAuthor>
<RefAuthor>Ragaller M</RefAuthor>
<RefAuthor>Rossaint R</RefAuthor>
<RefAuthor>Stuber F</RefAuthor>
<RefAuthor>Weiler N</RefAuthor>
<RefAuthor>Welte T</RefAuthor>
<RefAuthor>Bogatsch H</RefAuthor>
<RefAuthor>Hartog C</RefAuthor>
<RefAuthor>Loeffler M</RefAuthor>
<RefAuthor>Reinhart K</RefAuthor>
<RefTitle>Epidemiology of sepsis in Germany: results from a national prospective multicenter study</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Intensive Care Med</RefJournal>
<RefPage>606-18</RefPage>
<RefTotal>Engel C, Brunkhorst FM, Bone HG, Brunkhorst R, Gerlach H, Grond S, Gruendling M, Huhle G, Jaschinski U, John S, Mayer K, Oppert M, Olthoff D, Quintel M, Ragaller M, Rossaint R, Stuber F, Weiler N, Welte T, Bogatsch H, Hartog C, Loeffler M, Reinhart K. Epidemiology of sepsis in Germany: results from a national prospective multicenter study. Intensive Care Med. 2007 Apr;33(4):606-18. DOI: 10.1007/s00134-006-0517-7</RefTotal>
<RefLink>https://doi.org/10.1007/s00134-006-0517-7</RefLink>
</Reference>
<Reference refNo="4">
<RefAuthor>Wong PF</RefAuthor>
<RefAuthor>Gilliam AD</RefAuthor>
<RefAuthor>Kumar S</RefAuthor>
<RefAuthor>Shenfine J</RefAuthor>
<RefAuthor>O’Dair GN</RefAuthor>
<RefAuthor>Leaper DJ</RefAuthor>
<RefTitle>Antibiotic regimens for secondary peritonitis of gastrointestinal origin in adults</RefTitle>
<RefYear>2005</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage>CD004539</RefPage>
<RefTotal>Wong PF, Gilliam AD, Kumar S, Shenfine J, O’Dair GN, Leaper DJ. Antibiotic regimens for secondary peritonitis of gastrointestinal origin in adults. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD004539. DOI: 10.1002/14651858.CD004539.pub2</RefTotal>
<RefLink>https://doi.org/10.1002/14651858.CD004539.pub2</RefLink>
</Reference>
<Reference refNo="5">
<RefAuthor>Edelsberg J</RefAuthor>
<RefAuthor>Berger A</RefAuthor>
<RefAuthor>Schell S</RefAuthor>
<RefAuthor>Mallick R</RefAuthor>
<RefAuthor>Kuznik A</RefAuthor>
<RefAuthor>Oster G</RefAuthor>
<RefTitle>Economic consequences of failure of initial antibiotic therapy in hospitalized adults with complicated intra-abdominal infections</RefTitle>
<RefYear>2008</RefYear>
<RefJournal>Surg Infect (Larchmt)</RefJournal>
<RefPage>335-47</RefPage>
<RefTotal>Edelsberg J, Berger A, Schell S, Mallick R, Kuznik A, Oster G. Economic consequences of failure of initial antibiotic therapy in hospitalized adults with complicated intra-abdominal infections. Surg Infect (Larchmt). 2008 Jun;9(3):335-47. DOI: 10.1089/sur.2006.100</RefTotal>
<RefLink>https://doi.org/10.1089/sur.2006.100</RefLink>
</Reference>
<Reference refNo="6">
<RefAuthor>Barie PS</RefAuthor>
<RefTitle>The cost of failure</RefTitle>
<RefYear>2008</RefYear>
<RefJournal>Surg Infect (Larchmt)</RefJournal>
<RefPage>313-5</RefPage>
<RefTotal>Barie PS. The cost of failure. Surg Infect (Larchmt). 2008 Jun;9(3):313-5. DOI: 10.1089/sur.2007.9964</RefTotal>
<RefLink>https://doi.org/10.1089/sur.2007.9964</RefLink>
</Reference>
<Reference refNo="7">
<RefAuthor>Davey PG</RefAuthor>
<RefAuthor>Marwick C</RefAuthor>
<RefTitle>Appropriate vs. inappropriate antimicrobial therapy</RefTitle>
<RefYear>2008</RefYear>
<RefJournal>Clin Microbiol Infect</RefJournal>
<RefPage>15-21</RefPage>
<RefTotal>Davey PG, Marwick C. Appropriate vs. inappropriate antimicrobial therapy. Clin Microbiol Infect. 2008 Apr;14 Suppl 3:15-21. DOI: 10.1111/j.1469-0691.2008.01959.x</RefTotal>
<RefLink>https://doi.org/10.1111/j.1469-0691.2008.01959.x</RefLink>
</Reference>
<Reference refNo="8">
<RefAuthor>Nathens AB</RefAuthor>
<RefAuthor>Cook CH</RefAuthor>
<RefAuthor>Machiedo G</RefAuthor>
<RefAuthor>Moore EE</RefAuthor>
<RefAuthor>Namias N</RefAuthor>
<RefAuthor>Nwariaku F</RefAuthor>
<RefTitle>Defining the research agenda for surgical infection: a consensus of experts using the Delphi approach</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>Surg Infect (Larchmt)</RefJournal>
<RefPage>101-10</RefPage>
<RefTotal>Nathens AB, Cook CH, Machiedo G, Moore EE, Namias N, Nwariaku F. Defining the research agenda for surgical infection: a consensus of experts using the Delphi approach. Surg Infect (Larchmt). 2006 Apr;7(2):101-10. DOI: 10.1089/sur.2006.7.101</RefTotal>
<RefLink>https://doi.org/10.1089/sur.2006.7.101</RefLink>
</Reference>
<Reference refNo="9">
<RefAuthor>Kujath P</RefAuthor>
<RefAuthor>Rodloff AC</RefAuthor>
<RefTitle></RefTitle>
<RefYear>2005</RefYear>
<RefBookTitle>Peritonitis</RefBookTitle>
<RefPage>13-5</RefPage>
<RefTotal>Kujath P, Rodloff AC. Peritonitis. 2nd ed. Heidelberg: Uni-Med Verlag; 2005. p. 13-15.</RefTotal>
</Reference>
<Reference refNo="10">
<RefAuthor>Gerbes AL</RefAuthor>
<RefAuthor>Gülberg V</RefAuthor>
<RefAuthor>Sauerbruch T</RefAuthor>
<RefAuthor>Wiest R</RefAuthor>
<RefAuthor>Appenrodt B</RefAuthor>
<RefAuthor>Bahr MJ</RefAuthor>
<RefAuthor>Dollinger MM</RefAuthor>
<RefAuthor>Rössle M</RefAuthor>
<RefAuthor>Schepke M</RefAuthor>
<RefTitle>S3-Leitlinie „Aszites, spontan bakterielle Peritonitis, hepatorenales Syndrom“</RefTitle>
<RefYear>2011</RefYear>
<RefJournal>Z Gastroenterol</RefJournal>
<RefPage>749-79</RefPage>
<RefTotal>Gerbes AL, Gülberg V, Sauerbruch T, Wiest R, Appenrodt B, Bahr MJ, Dollinger MM, Rössle M, Schepke M. S3-Leitlinie „Aszites, spontan bakterielle Peritonitis, hepatorenales Syndrom“ [German S 3-guideline “ascites, spontaneous bacterial peritonitis, hepatorenal syndrome”]. Z Gastroenterol. 2011 Jun;49(6):749-79. DOI: 10.1055/s-0031-1273405</RefTotal>
<RefLink>https://doi.org/10.1055/s-0031-1273405</RefLink>
</Reference>
<Reference refNo="11">
<RefAuthor>Rimola A</RefAuthor>
<RefAuthor>García-Tsao G</RefAuthor>
<RefAuthor>Navasa M</RefAuthor>
<RefAuthor>Piddock LJ</RefAuthor>
<RefAuthor>Planas R</RefAuthor>
<RefAuthor>Bernard B</RefAuthor>
<RefAuthor>Inadomi JM</RefAuthor>
<RefTitle>Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document. International Ascites Club</RefTitle>
<RefYear>2000</RefYear>
<RefJournal>J Hepatol</RefJournal>
<RefPage>142-53</RefPage>
<RefTotal>Rimola A, García-Tsao G, Navasa M, Piddock LJ, Planas R, Bernard B, Inadomi JM. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document. International Ascites Club. J Hepatol. 2000 Jan;32(1):142-53. DOI: 10.1016/S0168-8278(00)80201-9</RefTotal>
<RefLink>https://doi.org/10.1016/S0168-8278(00)80201-9</RefLink>
</Reference>
<Reference refNo="12">
<RefAuthor>Felisart J</RefAuthor>
<RefAuthor>Rimola A</RefAuthor>
<RefAuthor>Arroyo V</RefAuthor>
<RefAuthor>Perez-Ayuso RM</RefAuthor>
<RefAuthor>Quintero E</RefAuthor>
<RefAuthor>Gines P</RefAuthor>
<RefAuthor>Rodes J</RefAuthor>
<RefTitle>Cefotaxime is more effective than is ampicillin-tobramycin in cirrhotics with severe infections</RefTitle>
<RefYear>1985</RefYear>
<RefJournal>Hepatology</RefJournal>
<RefPage>457-62</RefPage>
<RefTotal>Felisart J, Rimola A, Arroyo V, Perez-Ayuso RM, Quintero E, Gines P, Rodes J. Cefotaxime is more effective than is ampicillin-tobramycin in cirrhotics with severe infections. Hepatology. 1985 May-Jun;5(3):457-62. DOI: 10.1002/hep.1840050319</RefTotal>
<RefLink>https://doi.org/10.1002/hep.1840050319</RefLink>
</Reference>
<Reference refNo="13">
<RefAuthor>Javid G</RefAuthor>
<RefAuthor>Khan BA</RefAuthor>
<RefAuthor>Khan BA</RefAuthor>
<RefAuthor>Shah AH</RefAuthor>
<RefAuthor>Gulzar GM</RefAuthor>
<RefAuthor>Khan MA</RefAuthor>
<RefTitle>Short-course ceftriaxone therapy in spontaneous bacterial peritonitis</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Postgrad Med J</RefJournal>
<RefPage>592-5</RefPage>
<RefTotal>Javid G, Khan BA, Khan BA, Shah AH, Gulzar GM, Khan MA. Short-course ceftriaxone therapy in spontaneous bacterial peritonitis. Postgrad Med J. 1998 Oct;74(876):592-5. DOI: 10.1136/pgmj.74.876.592</RefTotal>
<RefLink>https://doi.org/10.1136/pgmj.74.876.592</RefLink>
</Reference>
<Reference refNo="14">
<RefAuthor>Mowat C</RefAuthor>
<RefAuthor>Stanley AJ</RefAuthor>
<RefTitle>Review article: spontaneous bacterial peritonitis – diagnosis, treatment and prevention</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Aliment Pharmacol Ther</RefJournal>
<RefPage>1851-9</RefPage>
<RefTotal>Mowat C, Stanley AJ. Review article: spontaneous bacterial peritonitis – diagnosis, treatment and prevention. Aliment Pharmacol Ther. 2001 Dec;15(12):1851-9. DOI: 10.1046/j.1365-2036.2001.01116.x</RefTotal>
<RefLink>https://doi.org/10.1046/j.1365-2036.2001.01116.x</RefLink>
</Reference>
<Reference refNo="15">
<RefAuthor>Sort P</RefAuthor>
<RefAuthor>Navasa M</RefAuthor>
<RefAuthor>Arroyo V</RefAuthor>
<RefAuthor>Aldeguer X</RefAuthor>
<RefAuthor>Planas R</RefAuthor>
<RefAuthor>Ruiz-del-Arbol L</RefAuthor>
<RefAuthor>Castells L</RefAuthor>
<RefAuthor>Vargas V</RefAuthor>
<RefAuthor>Soriano G</RefAuthor>
<RefAuthor>Guevara M</RefAuthor>
<RefAuthor>Ginès P</RefAuthor>
<RefAuthor>Rodés J</RefAuthor>
<RefTitle>Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>N Engl J Med</RefJournal>
<RefPage>403-9</RefPage>
<RefTotal>Sort P, Navasa M, Arroyo V, Aldeguer X, Planas R, Ruiz-del-Arbol L, Castells L, Vargas V, Soriano G, Guevara M, Ginès P, Rodés J. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999 Aug;341(6):403-9. DOI: 10.1056/NEJM199908053410603</RefTotal>
<RefLink>https://doi.org/10.1056/NEJM199908053410603</RefLink>
</Reference>
<Reference refNo="16">
<RefAuthor>Stuart S</RefAuthor>
<RefAuthor>Booth TC</RefAuthor>
<RefAuthor>Cash CJ</RefAuthor>
<RefAuthor>Hameeduddin A</RefAuthor>
<RefAuthor>Goode JA</RefAuthor>
<RefAuthor>Harvey C</RefAuthor>
<RefAuthor>Malhotra A</RefAuthor>
<RefTitle>Complications of continuous ambulatory peritoneal dialysis</RefTitle>
<RefYear>2009</RefYear>
<RefJournal>Radiographics</RefJournal>
<RefPage>441-60</RefPage>
<RefTotal>Stuart S, Booth TC, Cash CJ, Hameeduddin A, Goode JA, Harvey C, Malhotra A. Complications of continuous ambulatory peritoneal dialysis. Radiographics. 2009 Mar-Apr;29(2):441-60. DOI: 10.1148/rg.292085136</RefTotal>
<RefLink>https://doi.org/10.1148/rg.292085136</RefLink>
</Reference>
<Reference refNo="17">
<RefAuthor>Lima RC</RefAuthor>
<RefAuthor>Barreira A</RefAuthor>
<RefAuthor>Cardoso FL</RefAuthor>
<RefAuthor>Lima MH</RefAuthor>
<RefAuthor>Leite M Jr</RefAuthor>
<RefTitle>Ciprofloxacin and cefazolin as a combination for empirical initial therapy of peritoneal dialysis-related peritonitis: five-year follow-up</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Perit Dial Int</RefJournal>
<RefPage>56-60</RefPage>
<RefTotal>Lima RC, Barreira A, Cardoso FL, Lima MH, Leite M Jr. Ciprofloxacin and cefazolin as a combination for empirical initial therapy of peritoneal dialysis-related peritonitis: five-year follow-up. Perit Dial Int. 2007 Jan-Feb;27(1):56-60.</RefTotal>
</Reference>
<Reference refNo="18">
<RefAuthor>Bodmann KF</RefAuthor>
<RefAuthor>Grabein B</RefAuthor>
<RefAuthor> Expertengruppe der Paul-Ehrlich Gesellschaft</RefAuthor>
<RefTitle>Empfehlungen zur kalkulierten parenteralen Initialtherapie bakterieller Erkrankungen bei Erwachsenen</RefTitle>
<RefYear>2010</RefYear>
<RefJournal>Chemother J</RefJournal>
<RefPage>179-255</RefPage>
<RefTotal>Bodmann KF, Grabein B; Expertengruppe der Paul-Ehrlich Gesellschaft. Empfehlungen zur kalkulierten parenteralen Initialtherapie bakterieller Erkrankungen bei Erwachsenen. Chemother J. 2010;19(6):179-255.</RefTotal>
</Reference>
<Reference refNo="19">
<RefAuthor>van Ruler O</RefAuthor>
<RefAuthor>Mahler CW</RefAuthor>
<RefAuthor>Boer KR</RefAuthor>
<RefAuthor>Reuland EA</RefAuthor>
<RefAuthor>Gooszen HG</RefAuthor>
<RefAuthor>Opmeer BC</RefAuthor>
<RefAuthor>de Graaf PW</RefAuthor>
<RefAuthor>Lamme B</RefAuthor>
<RefAuthor>Gerhards MF</RefAuthor>
<RefAuthor>Steller EP</RefAuthor>
<RefAuthor>van Till JW</RefAuthor>
<RefAuthor>de Borgie CJ</RefAuthor>
<RefAuthor>Gouma DJ</RefAuthor>
<RefAuthor>Reitsma JB</RefAuthor>
<RefAuthor>Boermeester MA</RefAuthor>
<RefAuthor> Dutch Peritonitis Study Group</RefAuthor>
<RefTitle>Comparison of on-demand vs planned relaparotomy strategy in patients with severe peritonitis: a randomized trial</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>JAMA</RefJournal>
<RefPage>865-72</RefPage>
<RefTotal>van Ruler O, Mahler CW, Boer KR, Reuland EA, Gooszen HG, Opmeer BC, de Graaf PW, Lamme B, Gerhards MF, Steller EP, van Till JW, de Borgie CJ, Gouma DJ, Reitsma JB, Boermeester MA; Dutch Peritonitis Study Group. Comparison of on-demand vs planned relaparotomy strategy in patients with severe peritonitis: a randomized trial. JAMA. 2007 Aug;298(8):865-72. DOI: 10.1001/jama.298.8.865</RefTotal>
<RefLink>https://doi.org/10.1001/jama.298.8.865</RefLink>
</Reference>
<Reference refNo="20">
<RefAuthor>Solomkin JS</RefAuthor>
<RefAuthor>Mazuski JE</RefAuthor>
<RefAuthor>Bradley JS</RefAuthor>
<RefAuthor>Rodvold KA</RefAuthor>
<RefAuthor>Goldstein EJ</RefAuthor>
<RefAuthor>Baron EJ</RefAuthor>
<RefAuthor>O’Neill PJ</RefAuthor>
<RefAuthor>Chow AW</RefAuthor>
<RefAuthor>Dellinger EP</RefAuthor>
<RefAuthor>Eachempati SR</RefAuthor>
<RefAuthor>Gorbach S</RefAuthor>
<RefAuthor>Hilfiker M</RefAuthor>
<RefAuthor>May AK</RefAuthor>
<RefAuthor>Nathens AB</RefAuthor>
<RefAuthor>Sawyer RG</RefAuthor>
<RefAuthor>Bartlett JG</RefAuthor>
<RefTitle>Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America</RefTitle>
<RefYear>2010</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>133-64</RefPage>
<RefTotal>Solomkin JS, Mazuski JE, Bradley JS, Rodvold KA, Goldstein EJ, Baron EJ, O’Neill PJ, Chow AW, Dellinger EP, Eachempati SR, Gorbach S, Hilfiker M, May AK, Nathens AB, Sawyer RG, Bartlett JG. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Clin Infect Dis. 2010 Jan;50(2):133-64. DOI: 10.1086/649554</RefTotal>
<RefLink>https://doi.org/10.1086/649554</RefLink>
</Reference>
<Reference refNo="21">
<RefAuthor>Eckmann C</RefAuthor>
<RefAuthor>Dryden M</RefAuthor>
<RefAuthor>Montravers P</RefAuthor>
<RefAuthor>Kozlov R</RefAuthor>
<RefAuthor>Sganga G</RefAuthor>
<RefTitle>Antimicrobial treatment of “complicated” intra-abdominal infections and the new IDSA guidelines? a commentary and an alternative European approach according to clinical definitions</RefTitle>
<RefYear>2011</RefYear>
<RefJournal>Eur J Med Res</RefJournal>
<RefPage>115-26</RefPage>
<RefTotal>Eckmann C, Dryden M, Montravers P, Kozlov R, Sganga G. Antimicrobial treatment of “complicated” intra-abdominal infections and the new IDSA guidelines? a commentary and an alternative European approach according to clinical definitions. Eur J Med Res. 2011 Mar;16(3):115-26. DOI: 10.1186/2047-783X-16-3-115</RefTotal>
<RefLink>https://doi.org/10.1186/2047-783X-16-3-115</RefLink>
</Reference>
<Reference refNo="22">
<RefAuthor>Eckmann C</RefAuthor>
<RefTitle>Antibiotikatherapie intraabdomineller Infektionen im Zeitalter der Multiresistenz</RefTitle>
<RefYear>2016</RefYear>
<RefJournal>Chirurg</RefJournal>
<RefPage>26-33</RefPage>
<RefTotal>Eckmann C. Antibiotikatherapie intraabdomineller Infektionen im Zeitalter der Multiresistenz [Antibiotic therapy of intra-abdominal infections in the era of multiresistance]. Chirurg. 2016 Jan;87(1):26-33. DOI: 10.1007/s00104-015-0106-9</RefTotal>
<RefLink>https://doi.org/10.1007/s00104-015-0106-9</RefLink>
</Reference>
<Reference refNo="23">
<RefAuthor>Eckmann C</RefAuthor>
<RefAuthor>Shekarriz H</RefAuthor>
<RefTitle>Antimicrobial management of complicated intra-abdominal infections caused by resistant bacteria</RefTitle>
<RefYear>2012</RefYear>
<RefJournal>Eur Infect Dis</RefJournal>
<RefPage>22-7</RefPage>
<RefTotal>Eckmann C, Shekarriz H. Antimicrobial management of complicated intra-abdominal infections caused by resistant bacteria. Eur Infect Dis. 2012;6:22-7.</RefTotal>
</Reference>
<Reference refNo="24">
<RefAuthor>Paul M</RefAuthor>
<RefAuthor>Silbiger I</RefAuthor>
<RefAuthor>Grozinsky S</RefAuthor>
<RefAuthor>Soares-Weiser K</RefAuthor>
<RefAuthor>Leibovici L</RefAuthor>
<RefTitle>Beta lactam antibiotic monotherapy versus beta lactam-aminoglycoside antibiotic combination therapy for sepsis</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage>CD003344</RefPage>
<RefTotal>Paul M, Silbiger I, Grozinsky S, Soares-Weiser K, Leibovici L. Beta lactam antibiotic monotherapy versus beta lactam-aminoglycoside antibiotic combination therapy for sepsis. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD003344. DOI: 10.1002/14651858.CD003344.pub2</RefTotal>
<RefLink>https://doi.org/10.1002/14651858.CD003344.pub2</RefLink>
</Reference>
<Reference refNo="25">
<RefAuthor>Solomkin J</RefAuthor>
<RefAuthor>Hershberger E</RefAuthor>
<RefAuthor>Miller B</RefAuthor>
<RefAuthor>Popejoy M</RefAuthor>
<RefAuthor>Friedland I</RefAuthor>
<RefAuthor>Steenbergen J</RefAuthor>
<RefAuthor>Yoon M</RefAuthor>
<RefAuthor>Collins S</RefAuthor>
<RefAuthor>Yuan G</RefAuthor>
<RefAuthor>Barie PS</RefAuthor>
<RefAuthor>Eckmann C</RefAuthor>
<RefTitle>Ceftolozane/Tazobactam Plus Metronidazole for Complicated Intra-abdominal Infections in an Era of Multidrug Resistance: Results From a Randomized, Double-Blind, Phase 3 Trial (ASPECT-cIAI)</RefTitle>
<RefYear>2015</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>1462-71</RefPage>
<RefTotal>Solomkin J, Hershberger E, Miller B, Popejoy M, Friedland I, Steenbergen J, Yoon M, Collins S, Yuan G, Barie PS, Eckmann C. Ceftolozane/Tazobactam Plus Metronidazole for Complicated Intra-abdominal Infections in an Era of Multidrug Resistance: Results From a Randomized, Double-Blind, Phase 3 Trial (ASPECT-cIAI). Clin Infect Dis. 2015 May;60(10):1462-71. DOI: 10.1093/cid/civ097</RefTotal>
<RefLink>https://doi.org/10.1093/cid/civ097</RefLink>
</Reference>
<Reference refNo="26">
<RefAuthor>Eckmann C</RefAuthor>
<RefAuthor>Solomkin J</RefAuthor>
<RefTitle>Ceftolozane/tazobactam for the treatment of complicated intra-abdominal infections</RefTitle>
<RefYear>2015</RefYear>
<RefJournal>Expert Opin Pharmacother</RefJournal>
<RefPage>271-80</RefPage>
<RefTotal>Eckmann C, Solomkin J. Ceftolozane/tazobactam for the treatment of complicated intra-abdominal infections. Expert Opin Pharmacother. 2015 Feb;16(2):271-80. DOI: 10.1517/14656566.2015.994504</RefTotal>
<RefLink>https://doi.org/10.1517/14656566.2015.994504</RefLink>
</Reference>
<Reference refNo="27">
<RefAuthor>Pletz MW</RefAuthor>
<RefAuthor>Eckmann C</RefAuthor>
<RefAuthor>Hagel S</RefAuthor>
<RefAuthor>Heppner HJ</RefAuthor>
<RefAuthor>Huber K</RefAuthor>
<RefAuthor>Kämmerer W</RefAuthor>
<RefAuthor>Schmitz FJ</RefAuthor>
<RefAuthor>Wilke M</RefAuthor>
<RefAuthor>Grabein B</RefAuthor>
<RefTitle>Multiresistente Erreger – Infektionsmanagement 2015</RefTitle>
<RefYear>2015</RefYear>
<RefJournal>Dtsch Med Wochenschr</RefJournal>
<RefPage>975-81</RefPage>
<RefTotal>Pletz MW, Eckmann C, Hagel S, Heppner HJ, Huber K, Kämmerer W, Schmitz FJ, Wilke M, Grabein B. Multiresistente Erreger – Infektionsmanagement 2015 [Current strategies against multi-drug resistant organisms]. Dtsch Med Wochenschr. 2015 Jun;140(13):975-81. DOI: 10.1055/s-0041-102452</RefTotal>
<RefLink>https://doi.org/10.1055/s-0041-102452</RefLink>
</Reference>
<Reference refNo="28">
<RefAuthor>Balthazar EJ</RefAuthor>
<RefAuthor>Robinson DL</RefAuthor>
<RefAuthor>Megibow AJ</RefAuthor>
<RefAuthor>Ranson JH</RefAuthor>
<RefTitle>Acute pancreatitis: value of CT in establishing prognosis</RefTitle>
<RefYear>1990</RefYear>
<RefJournal>Radiology</RefJournal>
<RefPage>331-6</RefPage>
<RefTotal>Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990 Feb;174(2):331-6. DOI: 10.1148/radiology.174.2.2296641</RefTotal>
<RefLink>https://doi.org/10.1148/radiology.174.2.2296641</RefLink>
</Reference>
<Reference refNo="29">
<RefAuthor>Larvin M</RefAuthor>
<RefAuthor>McMahon MJ</RefAuthor>
<RefTitle>APACHE-II score for assessment and monitoring of acute pancreatitis</RefTitle>
<RefYear>1989</RefYear>
<RefJournal>Lancet</RefJournal>
<RefPage>201-5</RefPage>
<RefTotal>Larvin M, McMahon MJ. APACHE-II score for assessment and monitoring of acute pancreatitis. Lancet. 1989 Jul 22;2(8656):201-5. DOI: 10.1016/S0140-6736(89)90381-4</RefTotal>
<RefLink>https://doi.org/10.1016/S0140-6736(89)90381-4</RefLink>
</Reference>
<Reference refNo="30">
<RefAuthor>Whitcomb DC</RefAuthor>
<RefTitle>Clinical practice. Acute pancreatitis</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>N Engl J Med</RefJournal>
<RefPage>2142-50</RefPage>
<RefTotal>Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med. 2006 May;354(20):2142-50. DOI: 10.1056/NEJMcp054958</RefTotal>
<RefLink>https://doi.org/10.1056/NEJMcp054958</RefLink>
</Reference>
<Reference refNo="31">
<RefAuthor>Banks PA</RefAuthor>
<RefAuthor>Gerzof SG</RefAuthor>
<RefAuthor>Langevin RE</RefAuthor>
<RefAuthor>Silverman SG</RefAuthor>
<RefAuthor>Sica GT</RefAuthor>
<RefAuthor>Hughes MD</RefAuthor>
<RefTitle>CT-guided aspiration of suspected pancreatic infection: bacteriology and clinical outcome</RefTitle>
<RefYear>1995</RefYear>
<RefJournal>Int J Pancreatol</RefJournal>
<RefPage>265-70</RefPage>
<RefTotal>Banks PA, Gerzof SG, Langevin RE, Silverman SG, Sica GT, Hughes MD. CT-guided aspiration of suspected pancreatic infection: bacteriology and clinical outcome. Int J Pancreatol. 1995 Dec;18(3):265-70. DOI: 10.1007/BF02784951</RefTotal>
<RefLink>https://doi.org/10.1007/BF02784951</RefLink>
</Reference>
<Reference refNo="32">
<RefAuthor>Besselink MG</RefAuthor>
<RefAuthor>Verwer TJ</RefAuthor>
<RefAuthor>Schoenmaeckers EJ</RefAuthor>
<RefAuthor>Buskens E</RefAuthor>
<RefAuthor>Ridwan BU</RefAuthor>
<RefAuthor>Visser MR</RefAuthor>
<RefAuthor>Nieuwenhuijs VB</RefAuthor>
<RefAuthor>Gooszen HG</RefAuthor>
<RefTitle>Timing of surgical intervention in necrotizing pancreatitis</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Arch Surg</RefJournal>
<RefPage>1194-201</RefPage>
<RefTotal>Besselink MG, Verwer TJ, Schoenmaeckers EJ, Buskens E, Ridwan BU, Visser MR, Nieuwenhuijs VB, Gooszen HG. Timing of surgical intervention in necrotizing pancreatitis. Arch Surg. 2007 Dec;142(12):1194-201. DOI: 10.1001/archsurg.142.12.1194</RefTotal>
<RefLink>https://doi.org/10.1001/archsurg.142.12.1194</RefLink>
</Reference>
<Reference refNo="33">
<RefAuthor>Bassi C</RefAuthor>
<RefAuthor>Larvin M</RefAuthor>
<RefAuthor>Villatoro E</RefAuthor>
<RefTitle>Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage>CD002941</RefPage>
<RefTotal>Bassi C, Larvin M, Villatoro E. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev. 2003;(4):CD002941. DOI: 10.1002/14651858.CD002941</RefTotal>
<RefLink>https://doi.org/10.1002/14651858.CD002941</RefLink>
</Reference>
<Reference refNo="34">
<RefAuthor>Villatoro E</RefAuthor>
<RefAuthor>Bassi C</RefAuthor>
<RefAuthor>Larvin M</RefAuthor>
<RefTitle>Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>Cochrane Database Syst Rev</RefJournal>
<RefPage>CD002941</RefPage>
<RefTotal>Villatoro E, Bassi C, Larvin M. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD002941. DOI: 10.1002/14651858.CD002941.pub2</RefTotal>
<RefLink>https://doi.org/10.1002/14651858.CD002941.pub2</RefLink>
</Reference>
<Reference refNo="35">
<RefAuthor>Mazaki T</RefAuthor>
<RefAuthor>Ishii Y</RefAuthor>
<RefAuthor>Takayama T</RefAuthor>
<RefTitle>Meta-analysis of prophylactic antibiotic use in acute necrotizing pancreatitis</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>Br J Surg</RefJournal>
<RefPage>674-84</RefPage>
<RefTotal>Mazaki T, Ishii Y, Takayama T. Meta-analysis of prophylactic antibiotic use in acute necrotizing pancreatitis. Br J Surg. 2006 Jun;93(6):674-84. DOI: 10.1002/bjs.5389</RefTotal>
<RefLink>https://doi.org/10.1002/bjs.5389</RefLink>
</Reference>
<Reference refNo="36">
<RefAuthor>Huber W</RefAuthor>
<RefAuthor>Schmid RM</RefAuthor>
<RefTitle>Akute Pankreatitis: Evidenzbasierte Diagnostik und Therapie</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Dtsch Arztebl</RefJournal>
<RefPage>A1832-42</RefPage>
<RefTotal>Huber W, Schmid RM. Akute Pankreatitis: Evidenzbasierte Diagnostik und Therapie. Dtsch Arztebl. 2007;104(25):A1832-42.</RefTotal>
</Reference>
<Reference refNo="37">
<RefAuthor>Isenmann R</RefAuthor>
<RefAuthor>Rünzi M</RefAuthor>
<RefAuthor>Kron M</RefAuthor>
<RefAuthor>Kahl S</RefAuthor>
<RefAuthor>Kraus D</RefAuthor>
<RefAuthor>Jung N</RefAuthor>
<RefAuthor>Maier L</RefAuthor>
<RefAuthor>Malfertheiner P</RefAuthor>
<RefAuthor>Goebell H</RefAuthor>
<RefAuthor>Beger HG</RefAuthor>
<RefAuthor> German Antibiotics in Severe Acute Pancreatitis Study Group</RefAuthor>
<RefTitle>Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: a placebo-controlled, double-blind trial</RefTitle>
<RefYear>2004</RefYear>
<RefJournal>Gastroenterology</RefJournal>
<RefPage>997-1004</RefPage>
<RefTotal>Isenmann R, Rünzi M, Kron M, Kahl S, Kraus D, Jung N, Maier L, Malfertheiner P, Goebell H, Beger HG; German Antibiotics in Severe Acute Pancreatitis Study Group. Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: a placebo-controlled, double-blind trial. Gastroenterology. 2004 Apr;126(4):997-1004. DOI: 10.1053/j.gastro.2003.12.050</RefTotal>
<RefLink>https://doi.org/10.1053/j.gastro.2003.12.050</RefLink>
</Reference>
<Reference refNo="38">
<RefAuthor>Teich N</RefAuthor>
<RefAuthor>Leinung S</RefAuthor>
<RefAuthor>Jonas S</RefAuthor>
<RefAuthor>Mössner J</RefAuthor>
<RefTitle>Akute Pankreatitis</RefTitle>
<RefYear>2009</RefYear>
<RefJournal>Chirurg</RefJournal>
<RefPage>245-52; quiz 253-4</RefPage>
<RefTotal>Teich N, Leinung S, Jonas S, Mössner J. Akute Pankreatitis [Acute pancreatitis]. Chirurg. 2009 Mar;80(3):245-52; quiz 253-4. DOI: 10.1007/s00104-009-1682-3</RefTotal>
<RefLink>https://doi.org/10.1007/s00104-009-1682-3</RefLink>
</Reference>
<Reference refNo="39">
<RefAuthor>Tenner S</RefAuthor>
<RefAuthor>Baillie J</RefAuthor>
<RefAuthor>DeWitt J</RefAuthor>
<RefAuthor>Vege SS</RefAuthor>
<RefAuthor> American College of Gastroenterology</RefAuthor>
<RefTitle>American College of Gastroenterology guideline: management of acute pancreatitis</RefTitle>
<RefYear>2013</RefYear>
<RefJournal>Am J Gastroenterol</RefJournal>
<RefPage>1400-15; 1416</RefPage>
<RefTotal>Tenner S, Baillie J, DeWitt J, Vege SS; American College of Gastroenterology. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013 Sep;108(9):1400-15; 1416. DOI: 10.1038/ajg.2013.218</RefTotal>
<RefLink>https://doi.org/10.1038/ajg.2013.218</RefLink>
</Reference>
<Reference refNo="40">
<RefAuthor>Bassetti M</RefAuthor>
<RefAuthor>Marchetti M</RefAuthor>
<RefAuthor>Chakrabarti A</RefAuthor>
<RefAuthor>Colizza S</RefAuthor>
<RefAuthor>Garnacho-Montero J</RefAuthor>
<RefAuthor>Kett DH</RefAuthor>
<RefAuthor>Munoz P</RefAuthor>
<RefAuthor>Cristini F</RefAuthor>
<RefAuthor>Andoniadou A</RefAuthor>
<RefAuthor>Viale P</RefAuthor>
<RefAuthor>Rocca GD</RefAuthor>
<RefAuthor>Roilides E</RefAuthor>
<RefAuthor>Sganga G</RefAuthor>
<RefAuthor>Walsh TJ</RefAuthor>
<RefAuthor>Tascini C</RefAuthor>
<RefAuthor>Tumbarello M</RefAuthor>
<RefAuthor>Menichetti F</RefAuthor>
<RefAuthor>Righi E</RefAuthor>
<RefAuthor>Eckmann C</RefAuthor>
<RefAuthor>Viscoli C</RefAuthor>
<RefAuthor>Shorr AF</RefAuthor>
<RefAuthor>Leroy O</RefAuthor>
<RefAuthor>Petrikos G</RefAuthor>
<RefAuthor>De Rosa FG</RefAuthor>
<RefTitle>A research agenda on the management of intra-abdominal candidiasis: results from a consensus of multinational experts</RefTitle>
<RefYear>2013</RefYear>
<RefJournal>Intensive Care Med</RefJournal>
<RefPage>2092-106</RefPage>
<RefTotal>Bassetti M, Marchetti M, Chakrabarti A, Colizza S, Garnacho-Montero J, Kett DH, Munoz P, Cristini F, Andoniadou A, Viale P, Rocca GD, Roilides E, Sganga G, Walsh TJ, Tascini C, Tumbarello M, Menichetti F, Righi E, Eckmann C, Viscoli C, Shorr AF, Leroy O, Petrikos G, De Rosa FG. A research agenda on the management of intra-abdominal candidiasis: results from a consensus of multinational experts. Intensive Care Med. 2013 Dec;39(12):2092-106. DOI: 10.1007/s00134-013-3109-3</RefTotal>
<RefLink>https://doi.org/10.1007/s00134-013-3109-3</RefLink>
</Reference>
<Reference refNo="41">
<RefAuthor>Blot SI</RefAuthor>
<RefAuthor>Vandewoude KH</RefAuthor>
<RefAuthor>De Waele JJ</RefAuthor>
<RefTitle>Candida peritonitis</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Curr Opin Crit Care</RefJournal>
<RefPage>195-9</RefPage>
<RefTotal>Blot SI, Vandewoude KH, De Waele JJ. Candida peritonitis. Curr Opin Crit Care. 2007 Apr;13(2):195-9. DOI: 10.1097/MCC.0b013e328028fd92</RefTotal>
<RefLink>https://doi.org/10.1097/MCC.0b013e328028fd92</RefLink>
</Reference>
<Reference refNo="42">
<RefAuthor>Blot S</RefAuthor>
<RefAuthor>Dimopoulos G</RefAuthor>
<RefAuthor>Rello J</RefAuthor>
<RefAuthor>Vogelaers D</RefAuthor>
<RefTitle>Is Candida really a threat in the ICU?</RefTitle>
<RefYear>2008</RefYear>
<RefJournal>Curr Opin Crit Care</RefJournal>
<RefPage>600-4</RefPage>
<RefTotal>Blot S, Dimopoulos G, Rello J, Vogelaers D. Is Candida really a threat in the ICU? Curr Opin Crit Care. 2008 Oct;14(5):600-4. DOI: 10.1097/MCC.0b013e32830f1dff</RefTotal>
<RefLink>https://doi.org/10.1097/MCC.0b013e32830f1dff</RefLink>
</Reference>
<Reference refNo="43">
<RefAuthor>León C</RefAuthor>
<RefAuthor>Ruiz-Santana S</RefAuthor>
<RefAuthor>Saavedra P</RefAuthor>
<RefAuthor>Almirante B</RefAuthor>
<RefAuthor>Nolla-Salas J</RefAuthor>
<RefAuthor>Alvarez-Lerma F</RefAuthor>
<RefAuthor>Garnacho-Montero J</RefAuthor>
<RefAuthor>León MA</RefAuthor>
<RefAuthor> EPCAN Study Group</RefAuthor>
<RefTitle>A bedside scoring system (“Candida score”) for early antifungal treatment in nonneutropenic critically ill patients with Candida colonization</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>Crit Care Med</RefJournal>
<RefPage>730-7</RefPage>
<RefTotal>León C, Ruiz-Santana S, Saavedra P, Almirante B, Nolla-Salas J, Alvarez-Lerma F, Garnacho-Montero J, León MA; EPCAN Study Group. A bedside scoring system (“Candida score”) for early antifungal treatment in nonneutropenic critically ill patients with Candida colonization. Crit Care Med. 2006 Mar;34(3):730-7. DOI: 10.1097/01.CCM.0000202208.37364.7D</RefTotal>
<RefLink>https://doi.org/10.1097/01.CCM.0000202208.37364.7D</RefLink>
</Reference>
<Reference refNo="44">
<RefAuthor>Pelz RK</RefAuthor>
<RefAuthor>Hendrix CW</RefAuthor>
<RefAuthor>Swoboda SM</RefAuthor>
<RefAuthor>Diener-West M</RefAuthor>
<RefAuthor>Merz WG</RefAuthor>
<RefAuthor>Hammond J</RefAuthor>
<RefAuthor>Lipsett PA</RefAuthor>
<RefTitle>Double-blind placebo-controlled trial of fluconazole to prevent candidal infections in critically ill surgical patients</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Ann Surg</RefJournal>
<RefPage>542-8</RefPage>
<RefTotal>Pelz RK, Hendrix CW, Swoboda SM, Diener-West M, Merz WG, Hammond J, Lipsett PA. Double-blind placebo-controlled trial of fluconazole to prevent candidal infections in critically ill surgical patients. Ann Surg. 2001 Apr;233(4):542-8. DOI: 10.1097/00000658-200104000-00010</RefTotal>
<RefLink>https://doi.org/10.1097/00000658-200104000-00010</RefLink>
</Reference>
<Reference refNo="45">
<RefAuthor>Eggimann P</RefAuthor>
<RefAuthor>Francioli P</RefAuthor>
<RefAuthor>Bille J</RefAuthor>
<RefAuthor>Schneider R</RefAuthor>
<RefAuthor>Wu MM</RefAuthor>
<RefAuthor>Chapuis G</RefAuthor>
<RefAuthor>Chiolero R</RefAuthor>
<RefAuthor>Pannatier A</RefAuthor>
<RefAuthor>Schilling J</RefAuthor>
<RefAuthor>Geroulanos S</RefAuthor>
<RefAuthor>Glauser MP</RefAuthor>
<RefAuthor>Calandra T</RefAuthor>
<RefTitle>Fluconazole prophylaxis prevents intra-abdominal candidiasis in high-risk surgical patients</RefTitle>
<RefYear>1999</RefYear>
<RefJournal>Crit Care Med</RefJournal>
<RefPage>1066-72</RefPage>
<RefTotal>Eggimann P, Francioli P, Bille J, Schneider R, Wu MM, Chapuis G, Chiolero R, Pannatier A, Schilling J, Geroulanos S, Glauser MP, Calandra T. Fluconazole prophylaxis prevents intra-abdominal candidiasis in high-risk surgical patients. Crit Care Med. 1999 Jun;27(6):1066-72. DOI: 10.1097/00003246-199906000-00019</RefTotal>
<RefLink>https://doi.org/10.1097/00003246-199906000-00019</RefLink>
</Reference>
<Reference refNo="46">
<RefAuthor>Pfaller MA</RefAuthor>
<RefAuthor>Diekema DJ</RefAuthor>
<RefTitle>Epidemiology of invasive candidiasis: a persistent public health problem</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Clin Microbiol Rev</RefJournal>
<RefPage>133-63</RefPage>
<RefTotal>Pfaller MA, Diekema DJ. Epidemiology of invasive candidiasis: a persistent public health problem. Clin Microbiol Rev. 2007 Jan;20(1):133-63. DOI: 10.1128/CMR.00029-06</RefTotal>
<RefLink>https://doi.org/10.1128/CMR.00029-06</RefLink>
</Reference>
<Reference refNo="47">
<RefAuthor>Pappas PG</RefAuthor>
<RefAuthor>Kauffman CA</RefAuthor>
<RefAuthor>Andes DR</RefAuthor>
<RefAuthor>Clancy CJ</RefAuthor>
<RefAuthor>Marr KA</RefAuthor>
<RefAuthor>Ostrosky-Zeichner L</RefAuthor>
<RefAuthor>Reboli AC</RefAuthor>
<RefAuthor>Schuster MG</RefAuthor>
<RefAuthor>Vazquez JA</RefAuthor>
<RefAuthor>Walsh TJ</RefAuthor>
<RefAuthor>Zaoutis TE</RefAuthor>
<RefAuthor>Sobel JD</RefAuthor>
<RefTitle>Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America</RefTitle>
<RefYear>2016</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>e1-50</RefPage>
<RefTotal>Pappas PG, Kauffman CA, Andes DR, Clancy CJ, Marr KA, Ostrosky-Zeichner L, Reboli AC, Schuster MG, Vazquez JA, Walsh TJ, Zaoutis TE, Sobel JD. Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2016 Feb 15;62(4):e1-50. DOI: 10.1093/cid/civ933</RefTotal>
<RefLink>https://doi.org/10.1093/cid/civ933</RefLink>
</Reference>
<Reference refNo="48">
<RefAuthor>Montravers P</RefAuthor>
<RefAuthor>Leroy O</RefAuthor>
<RefAuthor>Eckmann C</RefAuthor>
<RefTitle>Intra-abdominal candidiasis: it’s still a long way to get unquestionable data</RefTitle>
<RefYear>2015</RefYear>
<RefJournal>Intensive Care Med</RefJournal>
<RefPage>1682-4</RefPage>
<RefTotal>Montravers P, Leroy O, Eckmann C. Intra-abdominal candidiasis: it’s still a long way to get unquestionable data. Intensive Care Med. 2015 Sep;41(9):1682-4. DOI: 10.1007/s00134-015-3894-y</RefTotal>
<RefLink>https://doi.org/10.1007/s00134-015-3894-y</RefLink>
</Reference>
<Reference refNo="49">
<RefAuthor>Kresken M</RefAuthor>
<RefAuthor>Hafner D</RefAuthor>
<RefAuthor>Schmitz FJ</RefAuthor>
<RefAuthor>Peters G</RefAuthor>
<RefAuthor>von Eiff C</RefAuthor>
<RefTitle>Resistenz bei häufig isolierten Enterobacteriaceae gegenüber Breitspektrumantibiotika</RefTitle>
<RefYear>2006</RefYear>
<RefJournal>Chemother J</RefJournal>
<RefPage>179-90</RefPage>
<RefTotal>Kresken M, Hafner D, Schmitz FJ, Peters G, von Eiff C. Resistenz bei häufig isolierten Enterobacteriaceae gegenüber Breitspektrumantibiotika. Chemother J. 2006;15(6):179-90.</RefTotal>
</Reference>
<Reference refNo="50">
<RefAuthor>Chromik AM</RefAuthor>
<RefAuthor>Meiser A</RefAuthor>
<RefAuthor>Hölling J</RefAuthor>
<RefAuthor>Sülberg D</RefAuthor>
<RefAuthor>Daigeler A</RefAuthor>
<RefAuthor>Meurer K</RefAuthor>
<RefAuthor>Vogelsang H</RefAuthor>
<RefAuthor>Seelig MH</RefAuthor>
<RefAuthor>Uhl W</RefAuthor>
<RefTitle>Identification of patients at risk for development of tertiary peritonitis on a surgical intensive care unit</RefTitle>
<RefYear>2009</RefYear>
<RefJournal>J Gastrointest Surg</RefJournal>
<RefPage>1358-67</RefPage>
<RefTotal>Chromik AM, Meiser A, Hölling J, Sülberg D, Daigeler A, Meurer K, Vogelsang H, Seelig MH, Uhl W. Identification of patients at risk for development of tertiary peritonitis on a surgical intensive care unit. J Gastrointest Surg. 2009 Jul;13(7):1358-67. DOI: 10.1007/s11605-009-0882-y</RefTotal>
<RefLink>https://doi.org/10.1007/s11605-009-0882-y</RefLink>
</Reference>
<Reference refNo="51">
<RefAuthor>Mazuski JE</RefAuthor>
<RefTitle>Antimicrobial treatment for intra-abdominal infections</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Expert Opin Pharmacother</RefJournal>
<RefPage>2933-45</RefPage>
<RefTotal>Mazuski JE. Antimicrobial treatment for intra-abdominal infections. Expert Opin Pharmacother. 2007 Dec;8(17):2933-45. DOI: 10.1517/14656566.8.17.2933</RefTotal>
<RefLink>https://doi.org/10.1517/14656566.8.17.2933</RefLink>
</Reference>
<Reference refNo="52">
<RefAuthor>De Waele JJ</RefAuthor>
<RefAuthor>Hoste EA</RefAuthor>
<RefAuthor>Blot SI</RefAuthor>
<RefTitle>Blood stream infections of abdominal origin in the intensive care unit: characteristics and determinants of death</RefTitle>
<RefYear>2008</RefYear>
<RefJournal>Surg Infect (Larchmt)</RefJournal>
<RefPage>171-7</RefPage>
<RefTotal>De Waele JJ, Hoste EA, Blot SI. Blood stream infections of abdominal origin in the intensive care unit: characteristics and determinants of death. Surg Infect (Larchmt). 2008 Apr;9(2):171-7. DOI: 10.1089/sur.2006.063</RefTotal>
<RefLink>https://doi.org/10.1089/sur.2006.063</RefLink>
</Reference>
<Reference refNo="53">
<RefAuthor>Roehrborn A</RefAuthor>
<RefAuthor>Thomas L</RefAuthor>
<RefAuthor>Potreck O</RefAuthor>
<RefAuthor>Ebener C</RefAuthor>
<RefAuthor>Ohmann C</RefAuthor>
<RefAuthor>Goretzki PE</RefAuthor>
<RefAuthor>Röher HD</RefAuthor>
<RefTitle>The microbiology of postoperative peritonitis</RefTitle>
<RefYear>2001</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>1513-9</RefPage>
<RefTotal>Roehrborn A, Thomas L, Potreck O, Ebener C, Ohmann C, Goretzki PE, Röher HD. The microbiology of postoperative peritonitis. Clin Infect Dis. 2001 Nov;33(9):1513-9. DOI: 10.1086/323333</RefTotal>
<RefLink>https://doi.org/10.1086/323333</RefLink>
</Reference>
<Reference refNo="54">
<RefAuthor>Babinchak T</RefAuthor>
<RefAuthor>Ellis-Grosse E</RefAuthor>
<RefAuthor>Dartois N</RefAuthor>
<RefAuthor>Rose GM</RefAuthor>
<RefAuthor>Loh E</RefAuthor>
<RefAuthor> Tigecycline 301 Study Group</RefAuthor>
<RefAuthor> Tigecycline 306 Study Group</RefAuthor>
<RefTitle>The efficacy and safety of tigecycline for the treatment of complicated intra-abdominal infections: analysis of pooled clinical trial data</RefTitle>
<RefYear>2005</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>S354-67</RefPage>
<RefTotal>Babinchak T, Ellis-Grosse E, Dartois N, Rose GM, Loh E; Tigecycline 301 Study Group; Tigecycline 306 Study Group. The efficacy and safety of tigecycline for the treatment of complicated intra-abdominal infections: analysis of pooled clinical trial data. Clin Infect Dis. 2005 Sep;41 Suppl 5:S354-67. DOI: 10.1086/431676</RefTotal>
<RefLink>https://doi.org/10.1086/431676</RefLink>
</Reference>
<Reference refNo="55">
<RefAuthor>Takatsuki M</RefAuthor>
<RefAuthor>Eguchi S</RefAuthor>
<RefAuthor>Yamanouchi K</RefAuthor>
<RefAuthor>Hidaka M</RefAuthor>
<RefAuthor>Soyama A</RefAuthor>
<RefAuthor>Miyazaki K</RefAuthor>
<RefAuthor>Tajima Y</RefAuthor>
<RefAuthor>Kanematsu T</RefAuthor>
<RefTitle>The outcomes of methicillin-resistant Staphylococcus aureus infection after living donor liver transplantation in a Japanese center</RefTitle>
<RefYear>2010</RefYear>
<RefJournal>J Hepatobiliary Pancreat Sci</RefJournal>
<RefPage>839-43</RefPage>
<RefTotal>Takatsuki M, Eguchi S, Yamanouchi K, Hidaka M, Soyama A, Miyazaki K, Tajima Y, Kanematsu T. The outcomes of methicillin-resistant Staphylococcus aureus infection after living donor liver transplantation in a Japanese center. J Hepatobiliary Pancreat Sci. 2010 Nov;17(6):839-43. DOI: 10.1007/s00534-010-0273-5</RefTotal>
<RefLink>https://doi.org/10.1007/s00534-010-0273-5</RefLink>
</Reference>
<Reference refNo="56">
<RefAuthor>Salzer W</RefAuthor>
<RefTitle>Antimicrobial-resistant gram-positive bacteria in PD peritonitis and the newer antibiotics used to treat them</RefTitle>
<RefYear>2005</RefYear>
<RefJournal>Perit Dial Int</RefJournal>
<RefPage>313-9</RefPage>
<RefTotal>Salzer W. Antimicrobial-resistant gram-positive bacteria in PD peritonitis and the newer antibiotics used to treat them. Perit Dial Int. 2005 Jul-Aug;25(4):313-9.</RefTotal>
</Reference>
<Reference refNo="57">
<RefAuthor>Cercenado E</RefAuthor>
<RefAuthor>Torroba L</RefAuthor>
<RefAuthor>Cantón R</RefAuthor>
<RefAuthor>Martínez-Martínez L</RefAuthor>
<RefAuthor>Chaves F</RefAuthor>
<RefAuthor>García-Rodríguez JA</RefAuthor>
<RefAuthor>Lopez-Garcia C</RefAuthor>
<RefAuthor>Aguilar L</RefAuthor>
<RefAuthor>García-Rey C</RefAuthor>
<RefAuthor>García-Escribano N</RefAuthor>
<RefAuthor>Bouza E</RefAuthor>
<RefTitle>Multicenter study evaluating the role of enterococci in secondary bacterial peritonitis</RefTitle>
<RefYear>2010</RefYear>
<RefJournal>J Clin Microbiol</RefJournal>
<RefPage>456-9</RefPage>
<RefTotal>Cercenado E, Torroba L, Cantón R, Martínez-Martínez L, Chaves F, García-Rodríguez JA, Lopez-Garcia C, Aguilar L, García-Rey C, García-Escribano N, Bouza E. Multicenter study evaluating the role of enterococci in secondary bacterial peritonitis. J Clin Microbiol. 2010 Feb;48(2):456-9. DOI: 10.1128/JCM.01782-09</RefTotal>
<RefLink>https://doi.org/10.1128/JCM.01782-09</RefLink>
</Reference>
<Reference refNo="58">
<RefAuthor>Nichols RL</RefAuthor>
<RefAuthor>Muzik AC</RefAuthor>
<RefTitle>Enterococcal infections in surgical patients: the mystery continues</RefTitle>
<RefYear>1992</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>72-6</RefPage>
<RefTotal>Nichols RL, Muzik AC. Enterococcal infections in surgical patients: the mystery continues. Clin Infect Dis. 1992 Jul;15(1):72-6. DOI: 10.1093/clinids/15.1.72</RefTotal>
<RefLink>https://doi.org/10.1093/clinids/15.1.72</RefLink>
</Reference>
<Reference refNo="59">
<RefAuthor>Eckmann C</RefAuthor>
<RefAuthor>Montravers P</RefAuthor>
<RefAuthor>Bassetti M</RefAuthor>
<RefAuthor>Bodmann KF</RefAuthor>
<RefAuthor>Heizmann WR</RefAuthor>
<RefAuthor>Sánchez García M</RefAuthor>
<RefAuthor>Guirao X</RefAuthor>
<RefAuthor>Capparella MR</RefAuthor>
<RefAuthor>Simoneau D</RefAuthor>
<RefAuthor>Dupont H</RefAuthor>
<RefTitle>Efficacy of tigecycline for the treatment of complicated intra-abdominal infections in real-life clinical practice from five European observational studies</RefTitle>
<RefYear>2013</RefYear>
<RefJournal>J Antimicrob Chemother</RefJournal>
<RefPage>ii25-35</RefPage>
<RefTotal>Eckmann C, Montravers P, Bassetti M, Bodmann KF, Heizmann WR, Sánchez García M, Guirao X, Capparella MR, Simoneau D, Dupont H. Efficacy of tigecycline for the treatment of complicated intra-abdominal infections in real-life clinical practice from five European observational studies. J Antimicrob Chemother. 2013 Jul;68 Suppl 2:ii25-35. DOI: 10.1093/jac/dkt142</RefTotal>
<RefLink>https://doi.org/10.1093/jac/dkt142</RefLink>
</Reference>
<Reference refNo="60">
<RefAuthor>Birmingham MC</RefAuthor>
<RefAuthor>Rayner CR</RefAuthor>
<RefAuthor>Meagher AK</RefAuthor>
<RefAuthor>Flavin SM</RefAuthor>
<RefAuthor>Batts DH</RefAuthor>
<RefAuthor>Schentag JJ</RefAuthor>
<RefTitle>Linezolid for the treatment of multidrug-resistant, gram-positive infections: experience from a compassionate-use program</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>159-68</RefPage>
<RefTotal>Birmingham MC, Rayner CR, Meagher AK, Flavin SM, Batts DH, Schentag JJ. Linezolid for the treatment of multidrug-resistant, gram-positive infections: experience from a compassionate-use program. Clin Infect Dis. 2003 Jan;36(2):159-68. DOI: 10.1086/345744</RefTotal>
<RefLink>https://doi.org/10.1086/345744</RefLink>
</Reference>
<Reference refNo="61">
<RefAuthor>Werner G</RefAuthor>
<RefAuthor>Gfrörer S</RefAuthor>
<RefAuthor>Fleige C</RefAuthor>
<RefAuthor>Witte W</RefAuthor>
<RefAuthor>Klare I</RefAuthor>
<RefTitle>Tigecycline-resistant Enterococcus faecalis strain isolated from a German intensive care unit patient</RefTitle>
<RefYear>2008</RefYear>
<RefJournal>J Antimicrob Chemother</RefJournal>
<RefPage>1182-3</RefPage>
<RefTotal>Werner G, Gfrörer S, Fleige C, Witte W, Klare I. Tigecycline-resistant Enterococcus faecalis strain isolated from a German intensive care unit patient. J Antimicrob Chemother. 2008 May;61(5):1182-3. DOI: 10.1093/jac/dkn065</RefTotal>
<RefLink>https://doi.org/10.1093/jac/dkn065</RefLink>
</Reference>
<Reference refNo="62">
<RefAuthor>Witte W</RefAuthor>
<RefAuthor>Mielke M</RefAuthor>
<RefTitle>Beta-Laktamasen mit breitem Wirkungsspektrum: Grundlagen, Epidemiologie, Schlussfolgerungen für die Prävention</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Bundesgesundheitsbl Gesundheitsforsch Gesundheitssch</RefJournal>
<RefPage>881-90</RefPage>
<RefTotal>Witte W, Mielke M. Beta-Laktamasen mit breitem Wirkungsspektrum: Grundlagen, Epidemiologie, Schlussfolgerungen für die Prävention. Bundesgesundheitsbl Gesundheitsforsch Gesundheitssch. 2003;46:881-90. DOI: 10.1007/s00103-003-0693-3</RefTotal>
<RefLink>https://doi.org/10.1007/s00103-003-0693-3</RefLink>
</Reference>
<Reference refNo="63">
<RefAuthor>Dinubile MJ</RefAuthor>
<RefAuthor>Friedland I</RefAuthor>
<RefAuthor>Chan CY</RefAuthor>
<RefAuthor>Motyl MR</RefAuthor>
<RefAuthor>Giezek H</RefAuthor>
<RefAuthor>Shivaprakash M</RefAuthor>
<RefAuthor>Weinstein RA</RefAuthor>
<RefAuthor>Quinn JP</RefAuthor>
<RefTitle>Bowel colonization with resistant gram-negative bacilli after antimicrobial therapy of intra-abdominal infections: observations from two randomized comparative clinical trials of ertapenem therapy</RefTitle>
<RefYear>2005</RefYear>
<RefJournal>Eur J Clin Microbiol Infect Dis</RefJournal>
<RefPage>443-9</RefPage>
<RefTotal>Dinubile MJ, Friedland I, Chan CY, Motyl MR, Giezek H, Shivaprakash M, Weinstein RA, Quinn JP. Bowel colonization with resistant gram-negative bacilli after antimicrobial therapy of intra-abdominal infections: observations from two randomized comparative clinical trials of ertapenem therapy. Eur J Clin Microbiol Infect Dis. 2005 Jul;24(7):443-9. DOI: 10.1007/s10096-005-1356-0</RefTotal>
<RefLink>https://doi.org/10.1007/s10096-005-1356-0</RefLink>
</Reference>
<Reference refNo="65">
<RefAuthor>Mazuski JE</RefAuthor>
<RefAuthor>Gasink LB</RefAuthor>
<RefAuthor>Armstrong J</RefAuthor>
<RefAuthor>Broadhurst H</RefAuthor>
<RefAuthor>Stone GG</RefAuthor>
<RefAuthor>Rank D</RefAuthor>
<RefAuthor>Llorens L</RefAuthor>
<RefAuthor>Newell P</RefAuthor>
<RefAuthor>Pachl J</RefAuthor>
<RefTitle>Efficacy and Safety of Ceftazidime-Avibactam Plus Metronidazole Versus Meropenem in the Treatment of Complicated Intra-abdominal Infection: Results From a Randomized, Controlled, Double-Blind, Phase 3 Program</RefTitle>
<RefYear>2016</RefYear>
<RefJournal>Clin Infect Dis</RefJournal>
<RefPage>1380-9</RefPage>
<RefTotal>Mazuski JE, Gasink LB, Armstrong J, Broadhurst H, Stone GG, Rank D, Llorens L, Newell P, Pachl J. Efficacy and Safety of Ceftazidime-Avibactam Plus Metronidazole Versus Meropenem in the Treatment of Complicated Intra-abdominal Infection: Results From a Randomized, Controlled, Double-Blind, Phase 3 Program. Clin Infect Dis. 2016 06;62(11):1380-9. DOI: 10.1093/cid/ciw133</RefTotal>
<RefLink>https://doi.org/10.1093/cid/ciw133</RefLink>
</Reference>
<Reference refNo="66">
<RefAuthor>Bergamasco MD</RefAuthor>
<RefAuthor>Barroso Barbosa M</RefAuthor>
<RefAuthor>de Oliveira Garcia D</RefAuthor>
<RefAuthor>Cipullo R</RefAuthor>
<RefAuthor>Moreira JC</RefAuthor>
<RefAuthor>Baia C</RefAuthor>
<RefAuthor>Barbosa V</RefAuthor>
<RefAuthor>Abboud CS</RefAuthor>
<RefTitle>Infection with Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae in solid organ transplantation</RefTitle>
<RefYear>2012</RefYear>
<RefJournal>Transpl Infect Dis</RefJournal>
<RefPage>198-205</RefPage>
<RefTotal>Bergamasco MD, Barroso Barbosa M, de Oliveira Garcia D, Cipullo R, Moreira JC, Baia C, Barbosa V, Abboud CS. Infection with Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae in solid organ transplantation. Transpl Infect Dis. 2012 Apr;14(2):198-205. DOI: 10.1111/j.1399-3062.2011.00688.x</RefTotal>
<RefLink>https://doi.org/10.1111/j.1399-3062.2011.00688.x</RefLink>
</Reference>
<Reference refNo="67">
<RefAuthor>Hirsch EB</RefAuthor>
<RefAuthor>Tam VH</RefAuthor>
<RefTitle>Detection and treatment options for Klebsiella pneumoniae carbapenemases (KPCs): an emerging cause of multidrug-resistant infection</RefTitle>
<RefYear>2010</RefYear>
<RefJournal>J Antimicrob Chemother</RefJournal>
<RefPage>1119-25</RefPage>
<RefTotal>Hirsch EB, Tam VH. Detection and treatment options for Klebsiella pneumoniae carbapenemases (KPCs): an emerging cause of multidrug-resistant infection. J Antimicrob Chemother. 2010 Jun;65(6):1119-25. DOI: 10.1093/jac/dkq108</RefTotal>
<RefLink>https://doi.org/10.1093/jac/dkq108</RefLink>
</Reference>
<Reference refNo="68">
<RefAuthor>Di Carlo P</RefAuthor>
<RefAuthor>Pantuso G</RefAuthor>
<RefAuthor>Cusimano A</RefAuthor>
<RefAuthor>D’Arpa F</RefAuthor>
<RefAuthor>Giammanco A</RefAuthor>
<RefAuthor>Gulotta G</RefAuthor>
<RefAuthor>Latteri AM</RefAuthor>
<RefAuthor>Madonia S</RefAuthor>
<RefAuthor>Salamone G</RefAuthor>
<RefAuthor>Mammina C</RefAuthor>
<RefTitle>Two cases of monomicrobial intraabdominal abscesses due to KPC-3 Klebsiella pneumoniae ST258 clone</RefTitle>
<RefYear>2011</RefYear>
<RefJournal>BMC Gastroenterol</RefJournal>
<RefPage>103</RefPage>
<RefTotal>Di Carlo P, Pantuso G, Cusimano A, D’Arpa F, Giammanco A, Gulotta G, Latteri AM, Madonia S, Salamone G, Mammina C. Two cases of monomicrobial intraabdominal abscesses due to KPC-3 Klebsiella pneumoniae ST258 clone. BMC Gastroenterol. 2011 Sep;11:103. DOI: 10.1186/1471-230X-11-103</RefTotal>
<RefLink>https://doi.org/10.1186/1471-230X-11-103</RefLink>
</Reference>
<Reference refNo="69">
<RefAuthor>Driscoll JA</RefAuthor>
<RefAuthor>Brody SL</RefAuthor>
<RefAuthor>Kollef MH</RefAuthor>
<RefTitle>The epidemiology, pathogenesis and treatment of Pseudomonas aeruginosa infections</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Drugs</RefJournal>
<RefPage>351-68</RefPage>
<RefTotal>Driscoll JA, Brody SL, Kollef MH. The epidemiology, pathogenesis and treatment of Pseudomonas aeruginosa infections. Drugs. 2007;67(3):351-68. DOI: 10.2165/00003495-200767030-00003</RefTotal>
<RefLink>https://doi.org/10.2165/00003495-200767030-00003</RefLink>
</Reference>
<Reference refNo="70">
<RefAuthor>Sawyer RG</RefAuthor>
<RefAuthor>Claridge JA</RefAuthor>
<RefAuthor>Nathens AB</RefAuthor>
<RefAuthor>Rotstein OD</RefAuthor>
<RefAuthor>Duane TM</RefAuthor>
<RefAuthor>Evans HL</RefAuthor>
<RefAuthor>Cook CH</RefAuthor>
<RefAuthor>O’Neill PJ</RefAuthor>
<RefAuthor>Mazuski JE</RefAuthor>
<RefAuthor>Askari R</RefAuthor>
<RefAuthor>Wilson MA</RefAuthor>
<RefAuthor>Napolitano LM</RefAuthor>
<RefAuthor>Namias N</RefAuthor>
<RefAuthor>Miller PR</RefAuthor>
<RefAuthor>Dellinger EP</RefAuthor>
<RefAuthor>Watson CM</RefAuthor>
<RefAuthor>Coimbra R</RefAuthor>
<RefAuthor>Dent DL</RefAuthor>
<RefAuthor>Lowry SF</RefAuthor>
<RefAuthor>Cocanour CS</RefAuthor>
<RefAuthor>West MA</RefAuthor>
<RefAuthor>Banton KL</RefAuthor>
<RefAuthor>Cheadle WG</RefAuthor>
<RefAuthor>Lipsett PA</RefAuthor>
<RefAuthor>Guidry CA</RefAuthor>
<RefAuthor>Popovsky K</RefAuthor>
<RefTitle>Trial of short-course antimicrobial therapy for intraabdominal infection</RefTitle>
<RefYear>2015</RefYear>
<RefJournal>N Engl J Med</RefJournal>
<RefPage>1996-2005</RefPage>
<RefTotal>Sawyer RG, Claridge JA, Nathens AB, Rotstein OD, Duane TM, Evans HL, Cook CH, O’Neill PJ, Mazuski JE, Askari R, Wilson MA, Napolitano LM, Namias N, Miller PR, Dellinger EP, Watson CM, Coimbra R, Dent DL, Lowry SF, Cocanour CS, West MA, Banton KL, Cheadle WG, Lipsett PA, Guidry CA, Popovsky K. Trial of short-course antimicrobial therapy for intraabdominal infection. N Engl J Med. 2015 May;372(21):1996-2005. DOI: 10.1056/NEJMoa1411162</RefTotal>
<RefLink>https://doi.org/10.1056/NEJMoa1411162</RefLink>
</Reference>
<Reference refNo="64">
<RefAuthor>Grabein B</RefAuthor>
<RefAuthor>Ebenhoch M</RefAuthor>
<RefAuthor>Kühnen E</RefAuthor>
<RefAuthor>Thalhammer F</RefAuthor>
<RefTitle>Kalkulierte parenterale Initialtherapie bakterieller Infektionen: Infektionen durch multiresistente gramnegative Stäbchen – ESBL-Bildner, Carbapenemase-bildende Enterobacteriaceae, Carbapenem-resistente Acinetobacter baumannii</RefTitle>
<RefYear>2020</RefYear>
<RefJournal>GMS Infect Dis</RefJournal>
<RefPage>Doc04</RefPage>
<RefTotal>Grabein B, Ebenhoch M, Kühnen E, Thalhammer F. Kalkulierte parenterale Initialtherapie bakterieller Infektionen: Infektionen durch multiresistente gramnegative Stäbchen – ESBL-Bildner, Carbapenemase-bildende Enterobacteriaceae, Carbapenem-resistente Acinetobacter baumannii [Calculated parenteral initial treatment of bacterial infections: Infections with multi-resistant Gram-negative rods – ESBL producers, carbapenemase-producing Enterobacteriaceae, carbapenem-resistant Acinetobacter baumannii]. GMS Infect Dis. 2020;8:Doc04. DOI: 10.3205/id000048</RefTotal>
<RefLink>https://doi.org/10.3205/id000048</RefLink>
</Reference>
</References>
<Media>
<Tables>
<Table format="png">
<MediaNo>1</MediaNo>
<MediaID language="de">1de</MediaID>
<MediaID language="en">1en</MediaID>
<Caption language="de"><Pgraph><Mark1>Tabelle 1: Therapieempfehlungen zur Initialtherapie der verschiedenen Formen der primären Peritonitis</Mark1></Pgraph></Caption>
<Caption language="en"><Pgraph><Mark1>Table 1: Therapy recommendations for the initial treatment of different forms of primary peritonitis</Mark1></Pgraph></Caption>
</Table>
<Table format="png">
<MediaNo>3</MediaNo>
<MediaID language="de">3de</MediaID>
<MediaID language="en">3en</MediaID>
<Caption language="de"><Pgraph><Mark1>Tabelle 3: Evidenzbasierte Risikofaktoren für das Vorhandensein multiresistenter Erreger (MRE) bei Bauchrauminfektionen</Mark1></Pgraph></Caption>
<Caption language="en"><Pgraph><Mark1>Table 3: Evidence-based risk factors for the presence of multidrug-resistant pathogens (MDROs) in abdominal infections</Mark1></Pgraph></Caption>
</Table>
<Table format="png">
<MediaNo>4</MediaNo>
<MediaID language="de">4de</MediaID>
<MediaID language="en">4en</MediaID>
<Caption language="de"><Pgraph><Mark1>Tabelle 4: Empfehlungen zur Initialtherapie der verschiedenen Formen der sekundären und tertiären Peritonitis</Mark1></Pgraph></Caption>
<Caption language="en"><Pgraph><Mark1>Table 4: Recommendations for the initial treatment of the different forms of secondary and tertiary peritonitis</Mark1></Pgraph></Caption>
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<MediaNo>5</MediaNo>
<MediaID language="de">5de</MediaID>
<MediaID language="en">5en</MediaID>
<Caption language="de"><Pgraph><Mark1>Tabelle 5: Kalkulierte Antibiotika-Therapie bei nekrotisierender Pankreatitis und intraabdominellen Mykosen</Mark1></Pgraph></Caption>
<Caption language="en"><Pgraph><Mark1>Table 5: Calculated antibiotic therapy for necrotizing pancreatitis and intra-abdominal mycoses</Mark1></Pgraph></Caption>
</Table>
<Table format="png">
<MediaNo>6</MediaNo>
<MediaID language="de">6de</MediaID>
<MediaID language="en">6en</MediaID>
<Caption language="de"><Pgraph><Mark1>Tabelle 6: Matrix für die Wahrscheinlichkeit des Nachweises resistenter Erreger bei verschiedenen Peritonitisformen (modifiziert nach [23])</Mark1></Pgraph></Caption>
<Caption language="en"><Pgraph><Mark1>Table 6: Matrix for the probability of detecting resistant pathogens in various forms of peritonitis (modified according to [23])</Mark1></Pgraph></Caption>
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<Table format="png">
<MediaNo>2</MediaNo>
<MediaID language="de">2de</MediaID>
<MediaID language="en">2en</MediaID>
<Caption language="de"><Pgraph><Mark1>Tabelle 2: Kalkulierte Antibiotika-Therapie bei intra- abdomineller Infektion mit Verdacht auf resistenten Erreger</Mark1></Pgraph></Caption>
<Caption language="en"><Pgraph><Mark1>Table 2: Calculated antibiotic treatment for intra-abdominal infection suspected of resistant pathogens</Mark1></Pgraph></Caption>
</Table>
<NoOfTables>6</NoOfTables>
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