- Complicated intra-abdominal infections are common problems, with appendicitis alone affecting approximately 300,000 patients/year and consuming over
1 million hospital days.
- Intra-abdominal infections are the second most common cause of infectious mortality in the intensive care unit.
- Patients should undergo rapid restoration of intravascular volume and additional measures as needed to promote physiological stability (A-II).
Initiation of Antimicrobial Therapy
- Antimicrobial therapy should be initiated once a patient is diagnosed with an intra-abdominal infection, or such an infection is considered likely. For patients in septic shock, antibiotics should be administered as soon as possible (A-III).
- Use of agents listed as appropriate for higher severity community-acquired infections and health care-associated infections is not recommended for patients with mild-to-moderate community-acquired infections since such regimens may carry a greater risk of toxicity and facilitate acquisition of more resistant organisms (B-II).
Antimicrobial TherapyâCommunity-Acquired Infection of Mild-to-Moderate Severity
- Antibiotics used for empiric treatment of community acquired intra-abdominal infection should be active against enteric Gram-negative aerobic and facultative bacilli and enteric Gram-positive streptococci (A-I).
- Coverage for obligate anaerobic bacilli should be provided for distal small bowel, appendiceal, and colon-derived infection and for more proximal gastrointestinal perforations in the presence of obstruction or paralytic ileus (A-I).
Antimicrobial TherapyâHigh Risk Community-Acquired Infection
- Use of broader-spectrum agents providing activity against some Gram-negative facultative and aerobic organisms that are occasionally isolated from such patients has the potential to improve outcomes, although this hypothesis has not been rigorously examined in clinical trials.
Antimicrobial TherapyâHealth Care-Associated Infection
- Health care-associated infection is commonly caused by a more resistant flora, which may include the nonfermenting Gram-negative P. aeruginosa and Acinetobacter species, extended-spectrum Î²-lactamase-producing Klebsiella and E. coli, Enterobacter species, Proteus species, MRSA, enterococci, and Candida species.
- Empiric antibiotic therapy for hospital-acquired intra-abdominal infections should be driven by local microbiologic results (A-II).
- An appropriate source control procedure is recommended for nearly all patients with intra-abdominal infection.
Duration of Therapy
- Antimicrobial therapy of established infections should be limited to no more than four to seven days unless it is difficult to achieve adequate source control. Longer durations of therapy have not been associated with improved outcome (B-III).For children and adults whose signs and symptoms of infection are resolved, no further antibiotic therapy is required (B-III).
Failure of Initial Therapy
- In patients who have persistent or recurrent clinical evidence of intra-abdominal infection after four to seven days of therapy, appropriate diagnostic investigation should be undertaken. This should include CT or ultrasound imaging, and antimicrobial therapy effective against the organisms initially identified should be continued (A-III).
- Extra-abdominal sources of infection and non-infectious inflammatory conditions should also be investigated if the patient is not making a satisfactory clinical response to a microbiologically adequate initial empiric antimicrobial regimen (A-II).
Table 1. Clinical Factors Predicting Failure of Source Control for Intra-Abdominal Infections
- Delay in the initial intervention (> 24 h)
- High severity of illness (APACHE II â¥ 15)*
- Advanced age
- Comorbidity and degree of organ dysfunction
- Low albumin
- Poor nutritional status
- Degree of peritoneal involvement/diffuse peritonitis
- Inability to achieve adequate debridement or control of drainage
- Presence of malignancy
*Knaus WA, Zimmerman JE, et al. APACHE - acute physiology and chronic health evaluation:
a physiologically based classification system. Crit Care Med. 1981;9:591-597.