Antimicrobial Approach To Intra-Abdominal Infections in Adults

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Antimicrobial approach to intra-abdominal infections in adults

AUTHOR: Miriam Baron Barshak, MD
SECTION EDITOR: Stephen B Calderwood, MD
DEPUTY EDITOR: Keri K Hall, MD, MS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2024.

This topic last updated: Dec 01, 2023.
INTRODUCTION
Infections within the abdominal cavity typically arise because of inflammation or disruption of the gastrointestinal tract. Less commonly,
they can arise from the gynecologic or urinary tract. Abdominal infections are usually polymicrobial and result in an intra-abdominal
abscess or secondary peritonitis, which may be generalized or localized (phlegmon).
The approach to antimicrobial selection and administration for intra-abdominal infections in adults is discussed here. The general and
surgical management of these infections are discussed in detail elsewhere. (See "Management of acute appendicitis in adults" and
"Acute colonic diverticulitis: Medical management" and "Acute colonic diverticulitis: Surgical management" and "Acute cholangitis:
Clinical manifestations, diagnosis, and management" and "Treatment of acute calculous cholecystitis" and "Acalculous cholecystitis:
Clinical manifestations, diagnosis, and management" and "Overview of gastrointestinal tract perforation".)
The approach to management of abscesses within specific intra-abdominal organs (such as the liver or kidney) are also discussed in
detail separately. (See "Pyogenic liver abscess" and "Invasive liver abscess syndrome caused by Klebsiella pneumoniae" and "Renal and
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perinephric abscess" and "Management and complications of tubo-ovarian abscess" and "Posthysterectomy pelvic abscess".)
Spontaneous peritonitis and peritonitis associated with peritoneal dialysis are also discussed elsewhere. (See "Spontaneous bacterial
peritonitis in adults: Treatment and prophylaxis" and "Microbiology and therapy of peritonitis in peritoneal dialysis".)
MICROBIOLOGY
Intra-abdominal infections usually arise after a breach in the intrinsic mucosal defense barrier that allows normal bowel flora to
inoculate the abdominal cavity. The precise microbiological spectrum depends on the precise gastrointestinal source (ie, small versus
large bowel).
Colonic flora is especially common in intra-abdominal infections, reflecting the frequency of associated diseases at this anatomic site,
including appendicitis, diverticulitis, carcinoma of the colon, inflammatory bowel disease, and previous colon surgery. Thus, the
predominant bacteria involved in such infections are coliforms (mainly Escherichia coli, Klebsiella spp, Proteus spp, and Enterobacter spp)
streptococci, enterococci, and anaerobic bacteria ( picture 1). However, while colonic flora consists of approximately 400 species, an
average of only four to six species are generally recovered from these intra-abdominal infections. The dominant isolates in most series
are Bacteroides fragilis and E. coli ( table 1) [1-6]. The probable factors contributing to this phenomenon include the limited ability of
clinical laboratories to isolate all the different organisms as well as the ability of specific organisms to cause infection and survive based
upon their virulence factors and capacity to adapt to new environmental conditions. For example, the capacity of B. fragilis to tolerate
small amounts of oxygen contributes to its emergence as a highly invasive anaerobic pathogen in abdominal infections [7]. Experimental
animal studies of intra-abdominal sepsis suggest that both anaerobes and coliforms contribute to the pathogenesis although they play
different roles, with coliforms contributing to early sepsis and anaerobes implicated in the late sequelae with abscess formation [8]. (See
"Anaerobic bacterial infections", section on 'Intra-abdominal infections'.)
Perforation of the proximal bowel, as with perforated peptic ulcer, results in an infection that is microbiologically distinct, reflecting the
flora of the upper gastrointestinal tract. The predominant microbial species in such cases often include aerobic and anaerobic gram-
positive bacteria or Candida spp. (See "Overview of complications of peptic ulcer disease", section on 'Perforation'.)
Prior antimicrobial therapy and health care exposures are associated with microbiologic changes in the bowel flora, and intra-abdominal
infections in such settings are thus more likely to involve nosocomial pathogens, such as Pseudomonas aeruginosa and other drug-
resistant organisms. Enterococci are most likely to be clinically relevant in health care-associated infections, particularly postoperative
infections, in contrast to community-acquired infections, in which they are frequently isolated but are often not important pathogens
[9,10]. Candida spp are also more common, in both small and large bowel processes, among patients with hospital-acquired infection,
prior antibiotic exposure, immunocompromising conditions, or with recurrent infection [11]. (See 'Considerations for specific pathogens'
below.)
SOURCE CONTROL AND DRAINAGE
Surgical intervention and/or percutaneous drainage are usually critical to the management of intra-abdominal infections other than
spontaneous peritonitis [12]. Surgical intervention may be required to close an anatomic breach or debride infected necrotic tissue, and
drainage is usually necessary for clearance of an abscess. When feasible, percutaneous abscess drainage is preferred [11]. Most clinical
treatment failures are due to failure to achieve such source control.
Surgical or percutaneous intervention also affords the opportunity for collection of primary specimens for microbiologic analysis (Gram
stain, aerobic and anaerobic cultures, and if appropriate, fungal and mycobacterial studies). This is particularly important for those
patients with intra-abdominal abscesses or otherwise complicated infections, with prior antibiotic exposure, or with a high risk of
infection with resistant organisms. Gram stain of the specimen can provide early guidance for antibiotic selection and may be the only
source of information if cultures do not grow. Inoculating the specimen directly into blood culture bottles can increase the microbiologic
yield, but this approach has several drawbacks [11,13,14]. It forfeits the ability to obtain Gram stain results, unless a separate specimen is
collected for Gram stain, and in polymicrobial infections, competitive growth in blood culture bottles can hinder identification of all
important pathogens, so cultures with routine media are also important in such cases.
The surgical management of intra-abdominal processes is discussed in detail elsewhere. (See "Management of acute appendicitis in
adults" and "Acute cholangitis: Clinical manifestations, diagnosis, and management", section on 'Biliary drainage' and "Treatment of
acute calculous cholecystitis" and "Acalculous cholecystitis: Clinical manifestations, diagnosis, and management", section on
'Management' and "Overview of gastrointestinal tract perforation", section on 'Indications for abdominal exploration' and "Acute colonic
diverticulitis: Surgical management".)
EMPIRIC ANTIMICROBIAL THERAPY
Timing — Patients who are critically ill should receive empiric antimicrobial therapy as soon as possible, ideally once blood and urine
samples have been obtained for culture. In patients who are not critically ill, delaying antibiotic therapy until samples from the site of
abdominal infection have been obtained for culture can be helpful to optimize the microbiologic yield that guides subsequent antibiotic
selection.
Approach to empiric antibiotic selection — In general, empiric regimens for intra-abdominal infections include antimicrobial activity
against enteric streptococci, coliforms, and anaerobes. Studies evaluating the relative efficacy of different antibiotic regimens with these
spectra of activity have generally demonstrated equivalent efficacy (see 'General principles of regimen selection' below). The precise
antimicrobial regimen and indications for broader antimicrobial coverage depend upon several factors ( table 2):
● Whether the infection is community-acquired versus health care-associated.
● Whether there are individual risk factors for infection with resistant bacteria (such as recent travel to areas of the world that have
high rates of antibiotic-resistant organisms or known colonization with such organisms).
● Whether the patient is considered to be at high risk for adverse outcomes. High-risk features that are associated with poor
outcomes after intra-abdominal infection are advanced age (>70 years), delay in initial intervention >24 hours, inability to achieve
adequate debridement or control of infection with drainage, other comorbidity (eg, renal or liver disease, malignancy),
immunocompromising condition (eg, poorly controlled diabetes mellitus, chronic high-dose corticosteroid use, use of other
immunosuppressive agents, neutropenia, advanced HIV infection, B or T lymphocyte defects), organ dysfunction, severe peritoneal
involvement or diffuse peritonitis, low albumin level, and poor nutritional status [11,15-17].
Patients with community-acquired infections of mild to moderate severity who have none of these risk factors may not warrant very
broad coverage, as the likelihood of resistant bacteria is low and the consequences of not covering them empirically are less. In contrast,
broad coverage is appropriate in patients who are at risk for infection with resistant bacteria or who are at risk for adverse outcomes and
mortality should empiric antibiotic therapy not be adequate. Thus, regimen selection is somewhat different for these different
populations. (See 'Low-risk community-acquired infections' below and 'High-risk community-acquired infections' below and 'Health care-
associated infections' below.)
Other factors that influence the choice of regimen include the location or type of infection (ie, gram-negative anaerobes are generally
not critical pathogens in infections arising from the upper gastrointestinal tract), whether there is a plan for surgical intervention, the
local rates of antibiotic-resistant Enterobacteriaceae, and expected patient tolerance. Rates of antibiotic resistance in Enterobacteriaceae
are high in certain parts of the world, including east Asia, Africa, and the Middle East, and are especially high in southeast Asia [18].
Travelers from these areas are at risk for colonization with resistant bacteria; this risk generally lasts a few weeks but can be prolonged in
those with diarrhea or antibiotic exposure during travel [18-21].
Overarching these considerations are goals for antibiotic stewardship, which generally favor narrower rather than broader coverage
when possible.
The suggested regimens in the following sections are intended to provide general guidance and may need to be altered to cover
emerging resistance patterns that are specific to the hospital or region; this is more likely to be necessary for the aerobic component but
could also apply to the anaerobic component.
These recommendations are also generally in keeping with the joint Surgical Infection Society (SIS) and the Infectious Diseases Society of
America (IDSA) guidelines on the management of complicated intra-abdominal infections, which were published in 2010. The SIS
published updated guidelines in 2017, while the IDSA guidelines are in the process of revision [11,22]. There are some exceptions based
on updated in vitro susceptibility data. As examples, although clindamycin and cefotetan were previously considered acceptable options
for intra-abdominal infections involving anaerobes, these drugs are no longer recommended due to escalating rates of resistance in the
B. fragilis group. As detailed in those guidelines, ampicillin-sulbactam is also not recommended due to high rates of resistance among
community-acquired E. coli.
Regimens
Low-risk community-acquired infections — For patients with mild to moderate community-acquired intra-abdominal infections (eg,
perforated appendix or appendiceal abscess) who have no risk factors for antibiotic resistance or treatment failure ( table 2), coverage
of streptococci, nonresistant Enterobacteriaceae, and (in most cases) anaerobes is generally sufficient. The following initial empiric
regimens are appropriate, and dosages are listed in the table ( table 3):
● Single-agent regimens – Piperacillin-tazobactam
● Combination regimens – Cefazolin, cefuroxime, ceftriaxone, cefotaxime, ciprofloxacin, or levofloxacin, each in combination with
metronidazole (although for most uncomplicated biliary infections of mild to moderate severity, the addition of metronidazole is
not necessary)
When piperacillin-tazobactam or one of the above combination regimens cannot be used, ertapenem is a reasonable alternative but we
try to preserve this agent for more resistant infections whenever possible.
An oral regimen (for example, a fluoroquinolone plus metronidazole or monotherapy with amoxicillin-clavulanic acid) is a reasonable
choice for empiric therapy for patients with mild-moderate community-acquired infection who have no risk factors for infection with
antibiotic-resistant organisms and when the prevalence of E. coli susceptibility to the chosen regimen exceeds 90 percent in the
community and hospital. Oral regimens can still be used if the prevalence of E. coli susceptibility to oral options is less than 90 percent,
but clinicians and patients should be aware of the greater risk of regimen failure in this case.
For these community-acquired infections, an empiric antimicrobial regimen does not have to include specific activity against enterococci
or Pseudomonas. In several trials, clinical outcomes for community-acquired intra-abdominal infections have been similar with empiric
regimens that have enterococcal and/or pseudomonal activity and those that do not [9,23-27].
The SIS/IDSA 2010 guidelines also list cefoxitin, moxifloxacin, and tigecycline as options, but we generally avoid using these agents in
this setting [11]. This is because of substantial rates of in vitro resistance to cefoxitin and fluoroquinolones among Bacteroides spp and
coliforms [28,29] and concern for increased mortality associated with tigecycline compared with other antibiotics for various infections,
including intra-abdominal infections [30,31]. (See "Anaerobic bacterial infections", section on 'Antimicrobial resistance'.)
The SIS 2017 guidelines also list cefoperazone-sulbactam as an alternative, but we generally avoid using this agent in the interest of
antimicrobial stewardship, as it provides coverage for resistant Pseudomonas spp that is typically not needed for this patient population
[22]. These guidelines also suggest against cefazolin for empiric therapy of intra-abdominal infections because of the lack of trial data
informing its use in such infections; we continue to use cefazolin as an option for low-risk community-acquired infections as long as the
risk of resistance is not high (eg, local prevalence of cefazolin resistance in Enterobacteriaceae <10 percent, no recent antibiotic use).
High-risk community-acquired infections — For community-acquired intra-abdominal infections that are severe or in patients at high
risk for adverse outcomes or resistance, broader coverage is warranted in an attempt to minimize the risk of inadequate empiric
treatment. We generally include an agent with gram-negative activity broad enough to cover P. aeruginosa and Enterobacteriaceae that
are resistant to nonpseudomonal cephalosporins in addition to coverage against enteric streptococci and (in most cases) anaerobes
( table 4). For community-acquired infections that clearly have an abdominal source, coverage for MRSA is generally not warranted,
even in those individuals known to be MRSA-colonized. Empiric antifungal therapy is usually not warranted, but it is reasonable in some
patients, as discussed below [22]. (See 'Health care-associated infections' below.)
The following initial empiric regimens are appropriate in areas where the local rates of resistance to these antibiotics are <10 percent
(dosages are listed in the table ( table 2)):
● Single-agent regimens – Piperacillin-tazobactam
● Combination regimens – Cefepime or ceftazidime, each administered with metronidazole.
If a cephalosporin is used, the SIS 2017 guidelines recommend adding vancomycin or ampicillin to provide enterococcal coverage, but
we do not routinely employ empiric coverage of Enterococcus spp for community-acquired infections.
For patients who cannot tolerate beta-lactams, a carbapenem (imipenem or meropenem) should be chosen. For patients who cannot
tolerate beta-lactams or carbapenems, combination therapy with vancomycin plus aztreonam plus metronidazole is an alternative
regimen.
For patients at risk for infection with an extended-spectrum beta-lactamase (ESBL)-producing organism (eg, known colonization or prior
infection with an ESBL-producing organism), a carbapenem (imipenem or meropenem) should be chosen. Alternatives include
monotherapy with tigecycline or eravacycline, but there is less clinical information on their efficacy and we typically reserve these agents
for infections unable to be treated with other agents [32,33].
When beta-lactams or carbapenems are chosen for patients who are critically ill or are at high risk of infection with drug-resistant
pathogens, we favor a prolonged infusion dosing strategy, which is also endorsed by the World Society of Emergency Surgery (WSES)
[34]. (See "Prolonged infusions of beta-lactam antibiotics".)
Empiric antifungal coverage is usually unnecessary but is appropriate for specific patients (eg, critically ill patients with an upper
gastrointestinal source), as discussed below. (See 'Health care-associated infections' below.)
Health care-associated infections — For patients with health care-associated infections, the likelihood of drug resistance is high. Thus,
to achieve empiric coverage of likely pathogens, in addition to coverage against streptococci and anaerobes, regimens should at least
include agents with expanded spectra of activity against gram-negative bacilli (including P. aeruginosa and Enterobacteriaceae that are
resistant to nonpseudomonal third-generation cephalosporins and fluoroquinolones). We also usually use an empiric regimen that has
anti-enterococcal activity for patients with health care–associated intra-abdominal infection, particularly those with postoperative
infection, those who have previously received cephalosporins or other antimicrobial agents selecting for Enterococcus species,
immunocompromised patients, and those with valvular heart disease or prosthetic intravascular materials. Local rates of resistance
should inform antibiotic selection (ie, agents for which there is >10 percent resistance among Enterobacteriaceae should be avoided).
Single-drug regimens that have expanded activity against gram-negative aerobic and anaerobic bacilli include piperacillin-tazobactam,
meropenem, and imipenem-cilastatin. Combination regimens include ceftazidime or cefepime plus metronidazole. The combination of
vancomycin, aztreonam, and metronidazole is an alternative for those who cannot use beta-lactams or carbapenems (eg, because of
severe reactions). See table for details regarding dosing ( table 5).
Cephalosporin-based regimens lack anti-enterococcal activity, so ampicillin or vancomycin can be added to these regimens for
enterococcal coverage until culture results are available. Empiric coverage for vancomycin-resistant enterococci (VRE) is generally not
recommended.
When beta-lactams or carbapenems are chosen for patients who are critically ill or are at high risk of infection with drug-resistant
pathogens, we favor a prolonged infusion dosing strategy, if feasible. (See "Prolonged infusions of beta-lactam antibiotics".)
Additions or modifications to the regimen may be indicated if other risk factors are present:
● For patients with health care-associated intra-abdominal infection who are known to be colonized with MRSA or who are at risk of
having an infection due to this organism because of prior treatment failure and significant antibiotic exposure, empiric
antimicrobial coverage directed against MRSA, typically with vancomycin, should be provided. (See "Methicillin-resistant
Staphylococcus aureus (MRSA) in adults: Treatment of bacteremia".)
● For patients at risk for infection with an extended-spectrum beta-lactamase (ESBL) -producing organism (eg, known colonization or
prior infection with an ESBL-producing organism), a carbapenem (imipenem or meropenem) should be chosen. (See "Extended-
spectrum beta-lactamases", section on 'Preferred agents'.)
We avoid tigecycline and eravacycline due to lack of clinical data for health care-associated infections, lack of pseudomonal
coverage, and in the interest of antibiotic stewardship. If these agents are used for such infections, additional antipseudomonal
coverage should be added while awaiting culture results [32,33].
● For patients who are known to be colonized with highly resistant gram-negative bacteria, the addition of an aminoglycoside,
polymyxin, or novel beta-lactam combination (ceftolozane-tazobactam or ceftazidime-avibactam) to an empiric regimen may be
warranted. These agents should be combined with an agent that has activity against anaerobes (eg, metronidazole). We typically
avoid tigecycline and eravacycline in this population for the same reasons we avoid them when ESBL organisms are suspected, as
stated in the above bullet. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on
'Management of multidrug-resistant organisms' and "Acinetobacter infection: Treatment and prevention", section on 'Second-line
antibiotics' and "Carbapenem-resistant E. coli, K. pneumoniae, and other Enterobacterales (CRE)", section on 'Approach to
treatment'.)
● Empiric vancomycin-resistant Enterococcus (VRE) coverage is not generally recommended, except for patients who are at very high
risk for infection due to VRE. These include liver transplant recipients with a hepatobiliary infection and patients known to be
colonized with VRE. In such cases, including a VRE-active agent (such as linezolid or daptomycin) in the empiric regimen is
reasonable. [11]. For those known to be colonized with ampicillin-sensitive VRE, ampicillin, piperacillin-tazobactam, or imipenem
can be used for coverage. (See "Treatment of enterococcal infections".)
● Empiric antifungal coverage is appropriate for patients at risk for infection with Candida spp, including those with upper
gastrointestinal perforations, recurrent bowel perforations, surgically treated pancreatitis, heavy colonization with Candida spp,
and/or yeast identified on Gram stain of samples from infected peritoneal fluid or tissue [22]. Fluconazole can be used for patients
who are not severely ill and have no history of infection with a fluconazole-resistant isolate; otherwise, an echinocandin should be
used. (See "Management of candidemia and invasive candidiasis in adults".)
TARGETED ANTIMICROBIAL THERAPY
General principles of regimen selection — Targeted antimicrobial therapy is chosen based on the results of culture and susceptibility
testing from appropriate specimens. Most antibiotic regimens that cover coliforms and anaerobes have comparable efficacy [35-37].
One meta-analysis evaluated 40 randomized or quasi-randomized controlled trials of antibiotic regimens in the treatment of secondary
peritonitis in adults [35]. All antibiotics (16 different comparative regimens) showed equivalent clinical success. A subsequent systematic
review identified 16 trials that compared various regimens for complicated intra-abdominal infections, including ceftriaxone plus
metronidazole, piperacillin-tazobactam, ertapenem, imipenem, meropenem, ceftolozane-tazobactam plus metronidazole, and
ceftazidime-avibactam plus metronidazole [37]. Clinical success ranged from 75 to 97 percent and comparators were generally of
comparable efficacy.
Assessment of culture data — The source and timing of collection of culture material are critical to the utility of culture results in
guiding selection of antibiotics. Specifically, culture of a specimen that is collected prior to starting antibiotics, from a site that should be
sterile, is the most informative. In the critically ill patient who requires antibiotic treatment prior to collection of cultures from the site of
infection, cultures that are collected early in the course (eg, within a few hours of antibiotic initiation) are more meaningful than those
that are collected after longer periods of antibiotic exposure.
Culture of a specimen collected days after starting antibiotics, especially if collected from a chronic drain, is more likely to reflect
colonizing bacteria that may have developed resistance to the treatment regimen but are not necessarily causing infection in the patient.
For this reason, it is advisable to avoid collecting cultures from chronic drains/fistulae, and results of all such cultures should be assessed
carefully for clinical relevance before decisions are made to target results of these cultures with antibiotic therapy [11].
Antibiotic stewardship — In the interests of preserving antibiotic efficacy over time for individual patients and populations, narrowing
of antibiotics is advisable once a patient has improved and/or results of reliable cultures are available. Lower-risk patients with
community-acquired intra-abdominal infection likely do not warrant alteration of therapy if a satisfactory clinical response to source
control and initial therapy occurs, even if unsuspected and untreated pathogens are later reported [11].
Anaerobic coverage — The anaerobic bacterial component of intra-abdominal infections is often not determined but assumed and
treated empirically. Coverage for anaerobes is often continued for the duration of the antibiotic course even when anaerobes are not
isolated from cultures, particularly if the cultures were obtained only after initiation of antibiotics that are active against anaerobes.
Susceptibility of anaerobic pathogens is rarely known at the time that a decision about the appropriate antibiotic regimen is made since
results take a long time, laboratory methods for isolating anaerobes are not well standardized, and activity is usually predictable based
on in vitro susceptibility testing from reference laboratories [38], clinical trials, and the site of infection [8,39].
Parenteral versus oral therapy — For patients who are able to eat and tolerate oral medications and whose relevant organisms are
not resistant to oral agents, an intravenous regimen can be transitioned to an oral regimen once the patient has demonstrated clinical
improvement. Reasonable oral regimens that cover common gut aerobic and anaerobic bacteria include levofloxacin (750 mg once daily)
or ciprofloxacin (500 mg twice daily), each with metronidazole (500 mg three times daily), or monotherapy with amoxicillin-clavulanate
(875/125 mg two to three times daily), depending on susceptibility testing.
Considerations for specific pathogens
● Enterococcus spp – These are commonly present in intra-abdominal infections and often are not covered in the recommended
empiric regimens for community-acquired infections. We agree with the recommendation from the joint Surgical Infection Society
and IDSA guidelines that coverage for Enterococcus is not necessary unless it is either recovered from the blood or is the only isolate
recovered in culture from the infected site [11].
● Candida spp – Antifungal coverage is warranted if there is growth of Candida spp from a sterile site. Fluconazole is appropriate for
Candida albicans; an echinocandin is appropriate for fluconazole-resistant Candida spp and as empiric antifungal coverage in the
critically ill patient while awaiting yeast identification and susceptibility testing results. (See "Management of candidemia and
invasive candidiasis in adults".)
● Resistant gram-negative bacilli – Isolation of resistant strains of P. aeruginosa, Acinetobacter spp, extended spectrum beta-
lactamase (ESBL), or carbapenemase-producing Enterobacteriaceae may warrant specific adjustment of the antibiotic regimen. The
novel cephalosporin-beta-lactamase inhibitor combinations, ceftazidime-avibactam and ceftolozane-tazobactam, when combined
with metronidazole for anaerobic coverage [40,41], may have niche roles in intra-abdominal infections caused by mixed flora that
include P. aeruginosa resistant to other antibiotics or ESBL-producing organisms, as long as susceptibility to these agents is
confirmed. Ceftazidime-avibactam has activity against many Klebsiella pneumoniae carbapenemase (KPC)-producing isolates as well.
Management of infections due to these organisms is discussed elsewhere. (See "Principles of antimicrobial therapy of
Pseudomonas aeruginosa infections" and "Acinetobacter infection: Treatment and prevention" and "Extended-spectrum beta-
lactamases", section on 'Treatment options' and "Carbapenem-resistant E. coli, K. pneumoniae, and other Enterobacterales (CRE)",
section on 'Approach to treatment'.)
● Actinomyces – Actinomyces are slow-growing filamentous gram-positive anaerobic bacteria and are part of the normal flora of the
mouth and gastrointestinal tract. If they breach the mucosal surface, these organisms can cause actinomycosis, an uncommon
granulomatous disease that is indolent and sometimes mistaken for malignancy because of local spread across tissue planes. In
the abdomen, actinomycosis most commonly involves the appendix and ileocecal region. Classic actinomycosis generally warrants
prolonged antibiotic therapy (ie, 6 to 12 months). (See "Abdominal actinomycosis".)
In patients who present clinically with a syndrome more typical of an abscess caused by gram-negative organisms and anaerobes
(acute presentation, fevers, septic physiology), the isolation of actinomyces on culture of the infected site is of uncertain clinical
significance. In such cases, we generally include an antibiotic that is active against actinomyces in the regimen (eg, penicillins) and
continue for one to two months, longer than the duration typically warranted for intra-abdominal infections. We also monitor
closely for symptoms suggestive of classic actinomycosis with a low threshold for repeat imaging if there is concern for
recrudescent infection following antibiotic discontinuation.
Infectious disease consultation — Consultation with an expert in infectious diseases can be especially helpful in the setting of
diagnostic uncertainty, for assessment of culture results to guide narrowing of empiric antibiotics, and in specific complex situations.
These include neutropenic, organ transplant, or otherwise-immunocompromised patients and patients with antibiotic allergies,
potentially infected foreign material (eg, mesh), intra-abdominal malignancy, inflammatory bowel disease, fistulae, or severe obesity.
Duration of therapy — The appropriate duration of antimicrobial therapy depends on whether the presumptive source of the intra-
abdominal infection has been controlled.
When adequate source control has been achieved and the contaminated material cleared from the intra-abdominal space, we generally
limit antimicrobial therapy to four to five days [11]. The efficacy of such a short course of antimicrobial therapy was demonstrated in the
Study To Optimize Peritoneal Infection Therapy (STOP-IT) trial, in which 518 patients with complicated intra-abdominal infection and
adequate source control were randomly assigned to receive either a fixed course of antibiotics for 4±1 days (experimental group) or
antibiotics until two days after resolution of fever, leukocytosis, and ileus, with a maximum of 10 days of antimicrobial therapy (control
group) [42]. The median duration of antibiotics was four days in the experimental group versus eight days in the control group. The
composite primary outcome of surgical site infection, recurrent intra-abdominal infection, or death occurred in a similar percentage of
patients in both groups (21.8 in the experimental group versus 22.3 percent in the control group). No significant between-group
differences were observed in the individual rates of the components of the primary outcome. Similarly, in a trial of critically ill patients
with postoperative intra-abdominal infections and adequate source control, the 45-day mortality rate was not different with a short
versus longer antibiotic course (8 versus 15 days) [43].
However, there are several situations in which a longer course of antibiotic therapy is appropriate.
● For patients in whom source control is known to be suboptimal, the optimal duration of antibiotic treatment is uncertain and
decisions on treatment duration must be made on a case-by-case basis.
● For those patients with uncomplicated appendicitis who do not undergo immediate surgery, we generally continue antibiotic
therapy for approximately 10 days, as in several trials which suggested the safety of this approach in select patients [44]. (See
'Source control and drainage' above.)
● In some cases, an indwelling catheter is required for ongoing drainage and removal of infected material. We generally continue
antibiotics in such cases until the efficacy of catheter drainage is established, for example, until an infected hematoma is liquefied
well enough to drain effectively via catheter. This may require two to three weeks for a peritoneal abscess. Liver abscess is typically
treated for four to six weeks (see "Pyogenic liver abscess", section on 'Treatment'). If there is chronic active drainage through the
catheter from an ongoing bowel or biliary leak without accumulation in the peritoneal cavity, discontinuation of antibiotics is
usually reasonable as long as the patient has clinically improved.
Patients with undrained abscesses, uncontrolled ongoing bowel leak, or other unresolved mechanical problems often develop worsening
clinical signs and symptoms of infection after antibiotics are stopped. We generally refer such patients for repeat surgical or
percutaneous intervention for source control. For patients in whom source control cannot be achieved, long-term antibiotics are unlikely
to be helpful.
In uncertain cases, declining inflammatory markers (such as C-reactive protein [CRP], erythrocyte sedimentation rate [ESR], and, if
available, procalcitonin) can be used cautiously, in addition to clinical resolution, to support antibiotic discontinuation with clinical follow-
up to assess for signs or symptoms of recurrent infection. Evidence to support this practice remains indirect.
Several studies have evaluated the utility of inflammatory markers to assist in guiding antibiotic discontinuation, but most of these have
been performed with procalcitonin, which is not widely available. In one study of patients with secondary peritonitis who underwent
emergency surgery, antibiotic discontinuation based on procalcitonin thresholds (level <1.0 ng/mL or >80 percent decrease compared
with the first postoperative day), in addition to resolution of clinical signs, was associated with a shorter duration of antibiotic use and
similar adverse events compared with historical controls [45]. In a separate retrospective study, procalcitonin guidance was associated
with a 50 percent reduction in antibiotic duration (5 versus 10 days) among intensive care unit patients with secondary peritonitis (both
with and without septic shock) [46]. However, in another study of patients with perioperative septic shock in the setting of intra-
abdominal infections, the rate and degree of procalcitonin decrease failed to accurately predict treatment response [47].
Evidence from randomized trials supporting antibiotic discontinuation based on procalcitonin levels is mainly from other populations,
and these studies have excluded individuals with intra-abdominal abscesses [48]. Additional studies in patients with intra-abdominal
infections are warranted.
CLINICAL FAILURE
Patients, particularly those with uncertain source control, should be assessed clinically during antibiotic therapy and after
discontinuation for treatment failure, which is suggested by persistent or recurrent signs and/or symptoms of infection, including fever,
hypotension, nausea, abdominal pain, organ dysfunction, or leukocytosis. In such cases, the possibility of inadequate source control (eg,
an undrained abscess, active bowel leak, retained infected mesh) should be assessed with repeat imaging. The original microbiologic
data and the antibiotic regimen should also be reviewed to ensure that the clinically relevant pathogens have been appropriately
covered. As noted, most clinical treatment failures are due to failure to achieve source control; cultures from chronic drains, surface
wounds, or other nonsterile sites cannot be relied upon to identify organisms requiring targeted antibiotics.
Other considerations in patients with ongoing infectious symptoms or signs include other nosocomial infections (eg, Clostridioides
[formerly Clostridium] difficile colitis, health care-associated pneumonia or urinary tract infection, or catheter-associated bloodstream
infection). For patients with persistent clinical symptoms and signs but in whom no evidence of a new or persistent infection is
uncovered after a careful investigation, discontinuation of antimicrobial therapy is warranted [11]. Noninfectious processes such as
thromboembolic disease, drug reaction, and pancreatitis are potential mimickers of infection.
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately.
(See "Society guideline links: Intra-abdominal infections in adults".)
SUMMARY AND RECOMMENDATIONS
● Pathogenesis – Intra-abdominal infections usually arise after a breach in the normal mucosal defense barrier that allows normal
bowel flora to inoculate the abdominal cavity.
● Microbiology – The predominant bacteria involved are coliforms (eg, Escherichia, Klebsiella spp, Proteus spp, Enterobacter spp),
streptococci, and anaerobic bacteria. Although enterococci are frequently isolated, their clinical relevance is generally limited to
health care-associated infections. (See 'Microbiology' above.)
● Importance of surgical intervention or percutaneous drainage – These procedures are usually critical to the management of
intra-abdominal infections (other than spontaneous peritonitis) since most clinical treatment failures are due to failure to achieve
source control. Specimens should be obtained during the procedure for microbiologic stain and culture. (See 'Source control and
drainage' above.)
The surgical management of intra-abdominal processes is discussed in detail elsewhere. (See "Management of acute appendicitis in
adults" and "Acute cholangitis: Clinical manifestations, diagnosis, and management", section on 'Biliary drainage' and "Treatment of
acute calculous cholecystitis" and "Acalculous cholecystitis: Clinical manifestations, diagnosis, and management", section on
'Management' and "Overview of gastrointestinal tract perforation", section on 'Indications for abdominal exploration' and "Acute
colonic diverticulitis: Surgical management".)
● Antibiotic therapy
• Empiric antibiotic selection – Critically ill patients should receive empiric antimicrobial therapy as soon as possible, ideally once
blood and urine cultures have been obtained. For patients who are not critically ill, antibiotic therapy should be delayed until
after collection of culture samples from the site of infection.
- Mild to moderate community-acquired infections with no risk factors for antibiotic resistance or poor outcome
( table 2) – Antibiotics for these infections should cover enteric streptococci, nonresistant Enterobacteriaceae, and
anaerobes ( table 3). Examples of infections in this category include perforated appendix or appendiceal abscess. (See
'Low-risk community-acquired infections' above.)
- Severe community-acquired infections or infections in patients at high risk for resistance or poor outcome
( table 2) – For these infections, we generally include antibiotic coverage against Pseudomonas aeruginosa,
Enterobacteriaceae, enteric streptococci, and anaerobes ( table 4). Empiric antifungal coverage is not typically necessary,
but is reasonable for some patients (eg, critically ill patients with an upper gastrointestinal source). (See 'High-risk
community-acquired infections' above.)
- Health care-associated infections – For these infections, we generally include coverage against P. aeruginosa, resistant
Enterobacteriaceae, streptococci, enterococci, and anaerobes ( table 5). Empiric antifungal coverage is reasonable for
patients with upper gastrointestinal perforations, recurrent bowel perforations, surgically treated pancreatitis, heavy
colonization with Candida spp, or microbiologic evidence of yeast on intra-abdominal specimens. (See 'Health care-
associated infections' above.)
• Targeted antibiotic selection – Depending on the results of culture and susceptibility testing, antibiotic adjustments may be
necessary. Regardless of culture results, coverage for Enterobacteriaceae and anaerobes is often continued for the full duration
of therapy, even if they did not grow in culture. (See 'Targeted antimicrobial therapy' above.)
Cultures from a chronic indwelling drain more likely reflect colonizing bacteria rather than clinically relevant pathogens. (See
'General principles of regimen selection' above.)
• Duration of antibiotic therapy – For patients who have adequate source control, we suggest limiting antibiotic therapy to four
to five days (Grade 2B). Longer courses are often appropriate if source control is suboptimal or uncertain. (See 'Duration of
therapy' above.)
Use of UpToDate is subject to the Terms of Use.
REFERENCES
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2000; 49:827.
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3. Brook I, Frazier EH. Microbiology of subphrenic abscesses: a 14-year experience. Am Surg 1999; 65:1049.
4. Sabbaj J, Sutter VL, Finegold SM. Anaerobic pyogenic liver abscess. Ann Intern Med 1972; 77:627.
5. Stone HH, Strom PR, Fabian TC, Dunlop WE. Third-generation cephalosporins for polymicrobial surgical sepsis. Arch Surg 1983;
118:193.
6. Lucasti C, Jasovich A, Umeh O, et al. Efficacy and tolerability of IV doripenem versus meropenem in adults with complicated intra-
abdominal infection: a phase III, prospective, multicenter, randomized, double-blind, noninferiority study. Clin Ther 2008; 30:868.
7. Baughn AD, Malamy MH. The strict anaerobe Bacteroides fragilis grows in and benefits from nanomolar concentrations of oxygen.
Nature 2004; 427:441.
8. Bartlett JG, Onderdonk AB, Louie T, et al. A review. Lessons from an animal model of intra-abdominal sepsis. Arch Surg 1978;
113:853.
9. Harbarth S, Uckay I. Are there patients with peritonitis who require empiric therapy for enterococcus? Eur J Clin Microbiol Infect Dis
2004; 23:73.
10. Sitges-Serra A, López MJ, Girvent M, et al. Postoperative enterococcal infection after treatment of complicated intra-abdominal
sepsis. Br J Surg 2002; 89:361.
11. Solomkin JS, Mazuski JE, Bradley JS, et al. 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; 50:133.
12. Reitz KM, Kennedy J, Li SR, et al. Association Between Time to Source Control in Sepsis and 90-Day Mortality. JAMA Surg 2022;
157:817.
13. Baron EJ, Miller JM, Weinstein MP, et al. A guide to utilization of the microbiology laboratory for diagnosis of infectious diseases:
2013 recommendations by the Infectious Diseases Society of America (IDSA) and the American Society for Microbiology (ASM). Clin
Infect Dis 2013; 57:e22.
14. Simor AE, Scythes K, Meaney H, Louie M. Evaluation of the BacT/Alert microbial detection system with FAN aerobic and FAN
anaerobic bottles for culturing normally sterile body fluids other than blood. Diagn Microbiol Infect Dis 2000; 37:5.
15. Wacha H, Hau T, Dittmer R, Ohmann C. Risk factors associated with intraabdominal infections: a prospective multicenter study.
Peritonitis Study Group. Langenbecks Arch Surg 1999; 384:24.
16. Torer N, Yorganci K, Elker D, Sayek I. Prognostic factors of the mortality of postoperative intraabdominal infections. Infection 2010;
38:255.
17. Inui T, Haridas M, Claridge JA, Malangoni MA. Mortality for intra-abdominal infection is associated with intrinsic risk factors rather
than the source of infection. Surgery 2009; 146:654.
18. Woerther PL, Burdet C, Chachaty E, Andremont A. Trends in human fecal carriage of extended-spectrum β-lactamases in the
community: toward the globalization of CTX-M. Clin Microbiol Rev 2013; 26:744.
19. Peirano G, Laupland KB, Gregson DB, Pitout JD. Colonization of returning travelers with CTX-M-producing Escherichia coli. J Travel
Med 2011; 18:299.
20. Tham J, Odenholt I, Walder M, et al. Extended-spectrum beta-lactamase-producing Escherichia coli in patients with travellers'
diarrhoea. Scand J Infect Dis 2010; 42:275.
21. Tängdén T, Cars O, Melhus A, Löwdin E. Foreign travel is a major risk factor for colonization with Escherichia coli producing CTX-M-
type extended-spectrum beta-lactamases: a prospective study with Swedish volunteers. Antimicrob Agents Chemother 2010;
54:3564.
22. Mazuski JE, Tessier JM, May AK, et al. The Surgical Infection Society Revised Guidelines on the Management of Intra-Abdominal
Infection. Surg Infect (Larchmt) 2017; 18:1.
23. Röhrborn A, Wacha H, Schöffel U, et al. Coverage of enterococci in community acquired secondary peritonitis: results of a
randomized trial. Surg Infect (Larchmt) 2000; 1:95.
24. Ohlin B, Cederberg A, Forssell H, et al. Piperacillin/tazobactam compared with cefuroxime/ metronidazole in the treatment of intra-
abdominal infections. Eur J Surg 1999; 165:875.
25. Cohn SM, Lipsett PA, Buchman TG, et al. Comparison of intravenous/oral ciprofloxacin plus metronidazole versus
piperacillin/tazobactam in the treatment of complicated intraabdominal infections. Ann Surg 2000; 232:254.
26. Malangoni MA, Song J, Herrington J, et al. Randomized controlled trial of moxifloxacin compared with piperacillin-tazobactam and
amoxicillin-clavulanate for the treatment of complicated intra-abdominal infections. Ann Surg 2006; 244:204.
27. Worden LJ, Dumkow LE, VanLangen KM, et al. Antipseudomonal Versus Narrow-Spectrum Agents for the Treatment of Community-
Onset Intra-abdominal Infections. Open Forum Infect Dis 2021; 8:ofab514.
28. Brook I, Wexler HM, Goldstein EJ. Antianaerobic antimicrobials: spectrum and susceptibility testing. Clin Microbiol Rev 2013; 26:526.
29. Goldstein EJ, Citron DM, Warren YA, et al. In vitro activity of moxifloxacin against 923 anaerobes isolated from human intra-
abdominal infections. Antimicrob Agents Chemother 2006; 50:148.
30. Prasad P, Sun J, Danner RL, Natanson C. Excess deaths associated with tigecycline after approval based on noninferiority trials. Clin
Infect Dis 2012; 54:1699.
31. FDA Drug Safety Communication: Increased risk of death with Tygacil (tigecycline) compared to other antibiotics used to treat simila
r infections. http://www.fda.gov/Drugs/DrugSafety/ucm224370.htm (Accessed on May 21, 2013).
32. Eckmann C, Montravers P, Bassetti M, et al. 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; 68 Suppl 2:ii25.
33. Eljaaly K, Ortwine JK, Shaikhomer M, et al. Efficacy and safety of eravacycline: A meta-analysis. J Glob Antimicrob Resist 2021; 24:424.
34. Sartelli M, Catena F, Abu-Zidan FM, et al. Management of intra-abdominal infections: recommendations by the WSES 2016 consensus
conference. World J Emerg Surg 2017; 12:22.
35. Wong PF, Gilliam AD, Kumar S, et al. Antibiotic regimens for secondary peritonitis of gastrointestinal origin in adults. Cochrane
Database Syst Rev 2005; :CD004539.
36. Goldstein EJ, Solomkin JS, Citron DM, Alder JD. Clinical efficacy and correlation of clinical outcomes with in vitro susceptibility for
anaerobic bacteria in patients with complicated intra-abdominal infections treated with moxifloxacin. Clin Infect Dis 2011; 53:1074.
37. Golan Y. Empiric therapy for hospital-acquired, Gram-negative complicated intra-abdominal infection and complicated urinary tract
infections: a systematic literature review of current and emerging treatment options. BMC Infect Dis 2015; 15:313.
38. Snydman DR, Jacobus NV, McDermott LA, et al. Update on resistance of Bacteroides fragilis group and related species with special
attention to carbapenems 2006-2009. Anaerobe 2011; 17:147.
39. Tally FP, Gorbach SL. Therapy of mixed anaerobic-aerobic infections. Lessons from studies of intra-abdominal sepsis. Am J Med 1985;
78:145.
40. Lagacé-Wiens P, Walkty A, Karlowsky JA. Ceftazidime-avibactam: an evidence-based review of its pharmacology and potential use in
the treatment of Gram-negative bacterial infections. Core Evid 2014; 9:13.
41. Snydman DR, McDermott LA, Jacobus NV. Activity of ceftolozane-tazobactam against a broad spectrum of recent clinical anaerobic
isolates. Antimicrob Agents Chemother 2014; 58:1218.
42. Sawyer RG, Claridge JA, Nathens AB, et al. Trial of short-course antimicrobial therapy for intraabdominal infection. N Engl J Med
2015; 372:1996.
43. Montravers P, Tubach F, Lescot T, et al. Short-course antibiotic therapy for critically ill patients treated for postoperative intra-
abdominal infection: the DURAPOP randomised clinical trial. Intensive Care Med 2018; 44:300.
44. Livingston E, Vons C. Treating Appendicitis Without Surgery. JAMA 2015; 313:2327.
45. Huang TS, Huang SS, Shyu YC, et al. A procalcitonin-based algorithm to guide antibiotic therapy in secondary peritonitis following
emergency surgery: a prospective study with propensity score matching analysis. PLoS One 2014; 9:e90539.
46. Maseda E, Suarez-de-la-Rica A, Anillo V, et al. Procalcitonin-guided therapy may reduce length of antibiotic treatment in intensive
care unit patients with secondary peritonitis: A multicenter retrospective study. J Crit Care 2015; 30:537.
47. Jung B, Molinari N, Nasri M, et al. Procalcitonin biomarker kinetics fails to predict treatment response in perioperative abdominal
infection with septic shock. Crit Care 2013; 17:R255.
48. Quenot JP, Luyt CE, Roche N, et al. Role of biomarkers in the management of antibiotic therapy: an expert panel review II: clinical use
of biomarkers for initiation or discontinuation of antibiotic therapy. Ann Intensive Care 2013; 3:21.
Topic 101694 Version 30.0
GRAPHICS
Mixed flora in peritoneal fluid from a ruptured viscus
Gram stain of peritoneal fluid (x1000) shows several different organisms, including gram-positive cocci in chains, gram-positive rods, plump enteric
gram-negative bacilli, and thinner gram-negative rods. Mixed fecal flora grew from this specimen.
Courtesy of Harriet Provine.
Graphic 77736 Version 3.0
Bacteriology of intraabdominal sepsis
Cases studied 759
Bacteriology
Aerobes only 132 (17)*
Anaerobes only 7 (1)*
Anaerobes plus aerobes 620 (82)*
Bacterial isolates Number of isolates ¶
Aerobes 1256
Escherichia coli 306
Pseudomonas aeruginosa 121
Klebsiella 119
Other gram-negative bacilli 270
Enterococcus 277
Staphylococcus aureus 111
Other gram-positive cocci 62
Anaerobes 1187
Bacteroides species 443
Bacteroides fragilis 133
Clostridium species 306
Peptostreptococcus 220
Fusobacterium 35
Miscellaneous 116
* Number of isolates (percent).
¶ Numbers of isolates are greater than numbers of cases since the majority of cases had more than one microorganism isolated.
Data from Stone HH et al. Arch Surg 1983.
Risk factors that warrant broad empiric antimicrobial coverage for intra-abdominal infections
Factors associated with mortality
Age >70 years
Medical comorbidity (eg, renal or liver disease, presence of malignancy, chronic malnutrition)
Immunocompromising condition (eg, poorly controlled diabetes mellitus, chronic high-dose corticosteroid use, use of other immunosuppressive
agents, neutropenia, advanced HIV infection, B or T leukocyte deficiency)
High severity of illness (ie, sepsis)
Extensive peritoneal involvement or diffuse peritonitis
Delay in initial intervention (source control) >24 hours
Inability to achieve adequate debridement or drainage control
Factors associated with infection with antibiotic-resistant bacteria

Health care-acquired infection
Travel to areas with higher rates of antibiotic-resistant organisms* within the few weeks prior to infection onset or if antibiotics were received during
travel
Known colonization with antibiotic-resistant organisms
* High rates of antibiotic resistance have been reported from southeast Asia, east Asia, the Middle East, and Africa.
References:
1. Solomkin JS, Mazuski JE, Bradley JS, et al. 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; 50:133.
2. Woerther PL, Burdet C, Chachaty E, Andremont A. Trends in human fecal carriage of extended-spectrum β-lactamases in the community: toward the globalization of CTX-M. Clin
Microbiol Rev 2013; 26:744.
Empiric antibiotic regimens for low-risk community-acquired intra-abdominal infections in adults
Dose
Single-agent regimen
Piperacillin-tazobactam* 3.375 g IV every 6 hours
Combination regimen with metronidazole*
One of the following:
Cefazolin 1 to 2 g IV every 8 hours
or
Cefuroxime 1.5 g IV every 8 hours
or
Ceftriaxone 2 g IV once daily
or
Cefotaxime 2 g IV every 8 hours
or
Ciprofloxacin 400 mg IV every 12 hours or
500 mg PO every 12 hours
or
Levofloxacin 750 mg IV or PO once daily
Plus:
Metronidazole¶ 500 mg IV or PO every 8 hours
For empiric therapy of low-risk community-acquired intra-abdominal infections, we cover streptococci, Enterobacteriaceae, and anaerobes. Low-risk
community-acquired intra-abdominal infections are those that are of mild to moderate severity (including perforated appendix or appendiceal
abscess) in the absence of risk factors for antibiotic resistance or treatment failure. Such risk factors include recent travel to areas of the world with
high rates of antibiotics-resistant organisms, known colonization with such organisms, advanced age, immunocompromising conditions, or other
major medical comorbidities. Refer to other UpToDate content on the antimicrobial treatment of intra-abdominal infections for further discussion of
these risk factors.
The antibiotic doses listed are for adult patients with normal renal function. The duration of antibiotic therapy depends on the specific infection and
whether the presumptive source of infection has been controlled; refer to other UpToDate content for details.
IV: intravenously; PO: orally.
* When piperacillin-tazobactam or one of the combination regimens in the table cannot be used, ertapenem (1 g IV once daily) is a reasonable
alternative.
¶ For most uncomplicated biliary infections of mild to moderate severity, the addition of metronidazole is not necessary.
Empiric antibiotic regimens for high-risk community-acquired intra-abdominal infections in adults
Dose
Imipenem-cilastatin 500 mg IV every 6 hours
Meropenem 1 g IV every 8 hours
Doripenem 500 mg IV every 8 hours
Piperacillin-tazobactam 4.5 g IV every 6 hours
Combination regimen with metronidazole
ONE of the following:
Cefepime 2 g IV every 8 hours
OR
Ceftazidime 2 g IV every 8 hours
PLUS:
Metronidazole 500 mg IV or orally every 8 hours
High-risk community-acquired intra-abdominal infections are those that are severe or in patients at high risk for adverse outcomes or antimicrobial
resistance. These include patients with recent travel to areas of the world with high rates of antibiotics-resistant organisms, known colonization with
such organisms, advanced age, immunocompromising conditions, or other major medical comorbidities. Refer to the UpToDate topic on the
antimicrobial treatment of intra-abdominal infections for further discussion of these risk factors.
For empiric therapy of high-risk community-acquired intra-abdominal infections, we cover streptococci, Enterobacteriaceae resistant to third-
generation cephalosporins, Pseudomonas aeruginosa, and anaerobes. Empiric antifungal therapy is usually not warranted but is reasonable for
critically ill patients with an upper gastrointestinal source.
Local rates of resistance should inform antibiotic selection (ie, agents for which there is >10% resistance among Enterobacteriaceae should be
avoided). If the patient is at risk for infection with an extended-spectrum beta-lactamase (ESBL)-producing organism (eg, known colonization or prior
infection with an ESBL-producing organism), a carbapenem should be chosen. When beta-lactams or carbapenems are chosen for patients who are
critically ill or are at high risk of infection with drug-resistant pathogens, we favor a prolonged infusion dosing strategy. Refer to other UpToDate
content on prolonged infusions of beta-lactam antibiotics.
The combination of vancomycin, aztreonam, and metronidazole is an alternative for those who cannot use other beta-lactams or carbapenems (eg,
because of severe reactions).
The antibiotic doses listed are for adult patients with normal renal function. The duration of antibiotic therapy depends on the specific infection and
IV: intravenous.
Empiric antibiotic regimens for health care-associated intra-abdominal infections in adults
Dose
Imipenem-cilastatin 500 mg IV every 6 hours
Meropenem 1 g IV every 8 hours
Doripenem 500 mg IV every 8 hours
Piperacillin-tazobactam 4.5 g IV every 6 hours
Combination regimen
ONE of the following:
Cefepime 2 g IV every 8 hours
OR
Ceftazidime 2 g IV every 8 hours
PLUS:
Metronidazole 500 mg IV or orally every 8 hours
PLUS ONE of the following (in some cases*):
Ampicillin 2 g IV every 4 hours
OR
Vancomycin 15 to 20 mg/kg IV every 8 to 12 hours
For empiric therapy of health care-associated intra-abdominal infections, we cover streptococci, enterococci, Enterobacteriaceae that are resistant to
third-generation cephalosporins and fluoroquinolones, Pseudomonas aeruginosa, and anaerobes. We include coverage against methicillin-resistant
Staphylococcus aureus (MRSA) with vancomycin in those who are known to be colonized, those with prior treatment failure, and those with significant
prior antibiotic exposure. Empiric antifungal coverage is appropriate for patients at risk for infection with Candida spp, including those with upper
gastrointestinal perforations, recurrent bowel perforations, surgically treated pancreatitis, heavy colonization with Candida spp, and/or yeast
identified on Gram stain of samples from infected peritoneal fluid or tissue. Refer to other UpToDate content on treatment of invasive candidiasis.
If the patient is at risk for infection with an extended-spectrum beta-lactamase (ESBL)-producing organism (eg, known colonization or prior infection
with an ESBL-producing organism), a carbapenem should be chosen. For patients who are known to be colonized with highly resistant gram-negative
bacteria, the addition of an aminoglycoside, polymyxin, or novel beta-lactam combination (ceftolozane-tazobactam or ceftazidime-avibactam) to an
empiric regimen may be warranted. In such cases, consultation with an expert in infectious diseases is advised.
When beta-lactams or carbapenems are chosen for patients who are critically ill or are at high risk of infection with drug-resistant pathogens, we favor
a prolonged infusion dosing strategy. Refer to other UpToDate content on prolonged infusions of beta-lactam antibiotics.
The combination of vancomycin, aztreonam, and metronidazole is an alternative for those who cannot use other beta-lactams or carbapenems (eg,
because of severe reactions).
The antibiotic doses listed are for adult patients with normal kidney function. The duration of antibiotic therapy depends on the specific infection and
IV: intravenous.
* We add ampicillin or vancomycin to a cephalosporin-based regimen to provide enterococcal coverage, particularly in those with postoperative
infection, prior use of antibiotics that select for Enterococcus, immunocompromising condition, valvular heart disease, or prosthetic intravascular
materials. Coverage against vancomycin-resistant enterococci (VRE) is generally not recommended, although it is reasonable in patients who have a
history of VRE colonization or in liver transplant recipients who have an infection of hepatobiliary source.

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Literature review current through: Feb 2024.

SOURCE CONTROL AND DRAINAGE

EMPIRIC ANTIMICROBIAL THERAPY

● Whether the infection is community-acquired versus health care-associated.

● Single-agent regimens – Piperacillin-tazobactam

● Single-agent regimens – Piperacillin-tazobactam

● Combination regimens – Cefepime or ceftazidime, each administered with metronidazole.

TARGETED ANTIMICROBIAL THERAPY

Considerations for specific pathogens

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

Use of UpToDate is subject to the Terms of Use.

Mixed flora in peritoneal fluid from a ruptured viscus

Courtesy of Harriet Provine.

Graphic 77736 Version 3.0

Bacteriology of intraabdominal sepsis

Cases studied 759

Aerobes only 132 (17)*

Anaerobes only 7 (1)*

Anaerobes plus aerobes 620 (82)*

Bacterial isolates Number of isolates ¶

Escherichia coli 306

Pseudomonas aeruginosa 121

Other gram-negative bacilli 270

Staphylococcus aureus 111

Other gram-positive cocci 62

Bacteroides species 443

Bacteroides fragilis 133

Clostridium species 306

* Number of isolates (percent).

Data from Stone HH et al. Arch Surg 1983.

Graphic 79147 Version 5.0

Factors associated with mortality

Age >70 years

High severity of illness (ie, sepsis)

Extensive peritoneal involvement or diffuse peritonitis

Delay in initial intervention (source control) >24 hours

Inability to achieve adequate debridement or drainage control

Factors associated with infection with antibiotic-resistant bacteria

Known colonization with antibiotic-resistant organisms

Graphic 105865 Version 3.0

Empiric antibiotic regimens for low-risk community-acquired intra-abdominal infections in adults

Piperacillin-tazobactam* 3.375 g IV every 6 hours

Combination regimen with metronidazole*

One of the following:

Cefazolin 1 to 2 g IV every 8 hours

Cefuroxime 1.5 g IV every 8 hours

Ceftriaxone 2 g IV once daily

Cefotaxime 2 g IV every 8 hours

Ciprofloxacin 400 mg IV every 12 hours or

500 mg PO every 12 hours

Levofloxacin 750 mg IV or PO once daily

Metronidazole¶ 500 mg IV or PO every 8 hours

IV: intravenously; PO: orally.

Graphic 106948 Version 13.0

Empiric antibiotic regimens for high-risk community-acquired intra-abdominal infections in adults

Imipenem-cilastatin 500 mg IV every 6 hours

Meropenem 1 g IV every 8 hours

Doripenem 500 mg IV every 8 hours

Piperacillin-tazobactam 4.5 g IV every 6 hours