Flashcards in 27 Intra-Abdominal Infections Deck (44):
What is the definition of Intra-Abdominal Infections (IAI)?
Infection of the peritoneal space and/or the viscera contained inside. Classification: Primary peritonitis, Secondary peritonitis, Abscess, Cholangitis/Cholecystitis
What is the Peritoneum normally like?
Normally lined by a highly permeable serous membrane with a surface area approximately that of skin. Cavity contains 50ml of serous fluid normally sterile. Low in protein and leukocytes, no fibrinogen
What is inflammation of the Peritoneum (peritonitis) like?
Inflammation secondary to bacteria. Outpouring into the peritoneum serous fluid containing leukocytes, fibrin, other proteins. Fluid and protein collect in bowel --> distention, 3rd spacing. Intravascular volume depletion, fever, vomiting, diarrhea --> septic shock
What is Primary Peritonitis?
Infection of peritoneal cavity without an evident source
What is the etiology of Primary Peritonitis?
Cirrhosis with ascites (spontaneous bacterial peritonitis, SBP)
What is the pathogenesis of Primary Peritonitis?
Source of infection is usually the GI tract. Route of infection usually not apparent but presumed to be: Hematogenous, Lymphogenous, Transmural migration through an intact gut wall. Reduced bacterial clearance from blood secondary to liver disease. Ascitic fluid favorable for aerobic bacterial growth
What is the microbiology of Primary Peritonitis like?
Usually caused by a SINGLE organism. Gram-neg bacilli - 70% (mainly E. coli). Gram-positive cocci - 30% (mainly Streptococcus). Anaerobes are RARE causes of primary peritonitis
What is the clinical presentation of Primary Peritonitis?
May develop over a period of days to week. Presents as an acute febrile illness. Others Sxs may include: Abdominal pain, Rebound tenderness, Increased WBC, N/V/D, Hypoactive or absent bowel sounds. Patients with cirrhosis may have other features of end-stage liver disease: Hepatorenal syndrome, Encephalopathy, Variceal hemorrhage
What tests are run for the diagnosis of Primary Peritonitis?
Paracentesis (aspirate of ascites fluid). Cultures (results may take 24-72h)
What is done in Paracentesis in the diagnosis of Primary Peritonitis?
Check for WBC, lactate, pH, bacteria. WBC > 500 (best single predictor). Lactate > 25. pH < 7.4. Gram stain for organisms (often negative)
What is done in Cultures for the diagnosis of Primary Peritonitis?
Check blood cultures (75% positive). Check ascites cultures (22-77% positive)
What are your first line empiric Rx regimens for Primary Peritonitis?
Mainly suspect GNR & Strep: Cephalosporins (2nd or 3rd gen). Cefoxitin, cefotetan or cefuroxime. Cefotaxime or ceftriaxone. Add clinda or metronidazole if suspect anaerobes. Vancomycin + Aztreonam for PCN and CEPH allergic pts (Tigecycline is an alternative)
Why are FQs not used first line in Primary Peritonitis?
Concerns for increased resistance secondary to overuse. Reserve for Pseudomonas infections
Why are Aminoglycosides (Gent) + Ampicillin or Penicillin G not primarily used for Primary Peritonitis?
Proven efficacy but increased risk of nephrotoxicity and ototoxicity especially in patients with hepatorenal syndrome
What is the response to therapy like in Primary Peritonitis?
Clinical improvement should occur after 24-48hrs of treatment. If no improvement observed, other DX should be considered. Use Culture and Sensitivity results to streamline therapy. Duration of Rx: 10-14 days (shorter 5-7 days have been effective)
What is the Etiology of Secondary Peritonitis?
Preceded by a primary intra-abdominal event that allows bacteria to enter the peritoneal cavity. Disease or injuries of the GI tract (i.e. appendicitis, diverticulitis, etc.). Gangrene of the bowel (bowel obstruction). Other (pancreatitis, operative contamination, lesions of female genital tract, etc)
What is the Microbiology like in Secondary Peritonitis?
Most cases caused by normal flora of GI tract. POLYMICROBIAL (both aerobes + anaerobes). Aerobes (E. coli most common, Klebsiella, Proteus, Enterococci). Anaerobes (B. fragilis most common)
What is the pathogenesis of Secondary Peritonitis?
Size of the bacterial inoculum, number and types of species significantly affect patient outcomes (virulence of bacteria may be enhanced when certain microorganisms are combined --> bacterial synergy). Inflammatory response caused by intraperitoneal fluid + fibrin entering the peritoneal cavity. Bacteria may become trapped beneath fibrin layers --> abscess formation. Anaerobic bacteria requirements met by devitalized tissue as a consequence of ischemia, trauma or neoplastic growth
What is the clinical presentation of Secondary Peritonitis?
Patients are usually in acute distress. Abdominal pain. Fever or hypothermia (shock). Shallow-rapid respirations. Decreased or absent bowel sounds. Decreased BP, increased HR. Anorexia/N/V. Altered mental status. Increase WBC with left shift
What is done for the Diagnosis of Secondary Peritonitis?
Exploratory laporatomy. Needle aspiration of peritoneal cavity. Imaging studies: abdominal X-Rays, CT, MRI, WBC scans. Blood cultures. Peritoneal cavity aspirate cultures
What are the different treatment routes that can be taken for Secondary Peritonitis?
Surgery - usually necessary to correct underlying pathology (stop contamination, remove foreign material, provide drainage of purulent collections). Antimicrobial agents - adjunctive therapy (control bacteremia, prevent local spread of existing infection, prevent abscess formation)
What is the selection of ABx based upon for Secondary Peritonitis?
Based upon: severity of infection, community-acquired vs. health-care associated (CA use narrower spectrum (monotherapy), HCA more resistant (may need multi-drug regimens)). Local susceptibility patterns
What are the empiric Rx Regimens used for Secondary Peritonitis?
3rd Gen CEPH + Metronidazole. Ertapenem. Pip/Tazo +/- AG (aminoglycoside useful in cases of bacteremia/septic shock but poor penetration into abscess)
What are some alternative treatment options in Secondary Peritonitis for patients allergic to PCN and CEPH?
Aztreonam + Metronidazole (need to add GPC coverage). Tigecycline (no Pseud coverage, NOT for patients with positive blood cultures)
What are some Abx regimens that are NOT recommended for Secondary Peritonitis?
Amp/Sulbactam NOT recommended d/t high rates of E. coli resistance. Cefotetan/Cefoxitin or Clindamycin NOT recommended d/t high rates of resistance with B. fragilis
What are some treatment considerations for Secondary Peritonitis?
Anti-Enterococci Coverage (NOT routinely needed for Community-acquired except in high-risk. NEED for Hospital-acquired particularly in patients: post-op infection, received prior CEPH therapy, immunocompromised, have valvular heart disease or prosthetic intravascular materials). Anti-MRSA coverage (empiric for HCA-IAI in patients: known colonizer, prior treatment failure and significant abx exposure)
What are the Abx choices for Anti-Enterococci coverage in Secondary Peritonitis?
Ampicillin, Pip/Tazo, Vanco
What is the Abx choice for Anti-MRSA coverage in Secondary Peritonitis?
Vancomycin treatment of choice
When is Antifungal coverage needed in Secondary Peritonitis?
Candida. NEED coverage when isolated, in: Severe community-acquired, Healthcare-associated infection, Neonates as empiric therapy if suspected
What are the agents used for Antifungal coverage in Secondary Peritonitis?
Fluconazole; Echinocandin if critically ill
What is the treatment response like for Secondary Peritonitis?
Use C&S results to streamline therapy. Oral step-down therapy when S/Sxs resolving, subsequent drainage procedures not likely to be required and able to tolerate an oral diet
What is the duration of Rx like for Secondary Peritonitis?
Usually 4-7 days, unless difficult to achieve adequate source control. 24h for acute appendicitis w/o perforation, local abscess or peritonitis. 24h for acute stomach and proximal jejunum perforations in the absence of acid-reducing therapy or malignancy and source control is achieved w/in 24h
What should be done if patient does not improve after 4-7 days of therapy for Secondary Peritonitis?
Consider: Resistance, superinfection, Presence of undrained focus of infection, CT or ultrasound imaging
What are some clinical factors predictive of failure of source control in Peritonitis?
Delay of initial intervention (> 24h). High severity of APACHE II (> 15). Advanced age. Comorbidity and degree of organ dysfunction. Low albumin level. Poor nutritional status. Degree of peritoneal involvement or diffuse peritonitis. Inability to achieve adequate debridement or control of drainage. Presence of malignancy
What is Intra-Abdominal Abscess?
Complication of either primary or secondary peritonitis. Appendicitis, perforated peptic ulcer, abdominal surgery, diverticulitis, pancreatitis, trauma, etc.
What is the microbiology of Intra-Abdominal Abscess like?
Usually POLYMICROBIAL; anaerobes predominate (secondary to low O2 tension). Organisms similar to secondary peritonitis (Aerobes: GNRs (PEK). Anaerobes: B. fragilis)
What is the pathogenesis of Intra-Abdominal Abscess?
Contamination followed by localization of infection. Location depends on site of primary focus. May take several days to evolve. Abscess environment: hypertonic & acidic, contains neutrophils & bacteria, fibrinous capsule. Can rupture leading to diffuse peritonitis
What is the clinical presentation of Intra-Abdominal Abscess?
Course if more indolent than w/ primary or secondary peritonitis. Patient may or may not have dramatic presentation: fever, abdominal pain, abdominal distention, tenderness, hyperglycemia (diabetics)
What is the diagnosis of Intra-Abdominal Abscess like?
R/o other causes. Non-invasive imaging studies (ultrasound, CT, MRI). Laparotomy
What is the treatment like for Intra-Abdominal Abscess?
Surgery: to provide drainage. Antimicrobials: adjunctive therapy (Regimens similar to secondary peritonitis. Aminoglycoside - less desirable agent d/t poor penetration, inactivation by decrease in pH)
What are the Biliary Tract Infections?
What is Cholecystitis?
> 90% associated w/ gallstones impacted in the cystic duct. Obstruction --> gallblader distention --> compromised blood supply lymphatic drainage --> tissue necrosis + bacterial proliferation (infection develops in 50% of cases). Abx treatment to d/c w/in 24h in pts undergoing cholecystectomy if no evidence of infection outside of gallbladder wall
What is Cholangitis?
Inflammation/infection involving hepatic and common bile ducts. Surgery may be needed to decompress the common bile duct. Enterococcal coverage NOT needed except liver transplant pts.