Info
🌱 來自: Huppert’s Notes
Intra-Abdominal Infections🚧 施工中
Intra-Abdominal Infections
Peritonitis/intra-abdominal abscess
• Pathogenesis: Disruption of or inflammation in the GI tract may allow normal bowel flora to enter the abdominal cavity and cause frank peritonitis and/or the development of intra-abdominal abscesses
• Pathogens:
- These infections are almost always polymicrobial
- Colonic organisms are the predominant pathogens, which include: E. coli, Klebsiella spp., Proteus spp., Enterobacter spp., Enterococcus spp., anaerobic organisms, such as B. fragilis
• Clinical features:
- Abdominal pain, nausea, vomiting, or bloating +/– fever, tachycardia, hypotension. Some patients may appear relatively stable, while others may have florid shock
- Patients age 65+ yr, immunocompromised, or those on chronic steroids may have especially occult presentations of severe intra-abdominal infections with less pronounced pain
• Diagnosis:
- If unstable, consult general surgery to determine the need for immediate surgical intervention vs. whether to first obtain diagnostic imaging studies (typically CT abdomen/pelvis with contrast)
• Treatment:
- Procedural interventions: Surgical intervention or percutaneous drainage are key aspects of management for complicated intra-abdominal infection. Consult general surgery and/or interventional radiology. Obtain cultures from drained material to guide antimicrobial management
- Antibiotic therapy:
• Start antibiotics ASAP to cover enteric Gram-positive, Gram-negative, and anerobic organisms
• Patients with certain risk factors are considered high-risk (age >70 yr, diffuse peritonitis, severe sepsis, immunocompromising conditions, health care–acquired infections) and warrant coverage of multidrug-resistant (MDR) organisms
• Regimens include:
- Low-risk community acquired infections:
• Ertapenem
• Ciprofloxacin or ceftriaxone + metronidazole
- High-risk community acquired infections or hospital-acquired infections:
• Piperacillin-tazobactam
• Meropenem
• Cefepime + metronidazole
Clostridium difficile
• Pathophysiology:
- C. difficile colitis can occur as a result of either community-acquired or nosocomial infections
- Not all strains of C. difficile cause infection; only toxin producing strains cause diarrhea and colitis.
- Risk factors for C. difficile infection include:
• Recent antibiotic use (commonly implicated antibiotics include clindamycin, fluoroquinolones, and cephalosporins)
• Age ≥65 yr
• Suppression of gastric acid with PPIs or H2-blockers is also associated with an increased risk of C. difficile infection, though the exact mechanism for this is unknown
• Clinical features:
- Range from mild diarrheal illness to a severe, fulminant, and potentially fatal colitis
- Criteria for severe C. difficile infection:
• More frequent diarrhea and more severe abdominal pain
• Very high leukocytosis, often ≥15K cells/μL
• Hypotension and lactic acidosis due to hypovolemia and sepsis
• AKI with Cr ≥1.5 mg/dL
• Colonic ileus with little to no diarrhea, which is known as “toxic megacolon”
• Diagnosis:
- Perform C. difficile stool testing in patients with a diarrheal illness (e.g., ≥3 watery stools in a day) and no alternative reason to have loose stools (e.g., laxative use)
- Consider CT abdomen/pelvis if concern for severe or fulminant disease
• Treatment:
- First-line treatment: Vancomycin 125 mg PO QID ×10 days or fidaxomicin 200 mg PO BID ×10 days. Add metronidazole 500 mg IV TID only if fulminant disease.
- Recurrent disease: Defined by resolution of symptoms with therapy followed by return of symptoms within 2 months of treatment completion. Requires longer course of antibiotics.