inta-abdominal infections Flashcards
secondary peritonitis etiology
Results from a focal disease process within the abdomen
Bacteria usually enter the peritoneum as a result of disruption of the integrity of the GI tract by diseases, injuries, surgery, or from local lesions of the female genital tract
microbiologic characteristic sof secondary peritonitis
different organs/areas of the GI tract have different commonly found bacteria
sometimes conc are up to 10^11
causative organisms in patients with complicated intra-abdominal infections
gram negative: E. Coli 74%, klebsiella, enterobacter, P. mirabilis, P. aeruginosa (not normal GI flora - host acq)
also gram positive gram pos bacteria, anaerobic bacteria, fungi
Average of 4.5 isolates/case of peritonitis (2.5 anaerobes, 2 aerobes or facultatives)
normal peritoneal fluid
sterile**, low in protein and leukocytes, contains no fibrinogen
bacteria in peritoneal cavity
immediate response to contain the insult If inoculum is not handled by host defenses, bacteria disseminate → peritonitis More likely to occur if: -Foreign body (bullet) -Large bacterial inoculum -Continuing bacterial contamination -Contamination involving a mixture of organisms -Impaired host defenses
pathophyiology of secondary peritonitis
Serous fluid containing leukocytes, high protein concentration (>3g/dl), and fibrinogen move into peritoneum → fibrinogen polymerizes forming plaques of fibrinous exudates on the inflamed peritoneal surface and begins to form adhesions
-Fluid and protein shift (“third-spacing”) may cause decreased circulating blood volume, decreased cardiac output, and hypotension
Mortality secondary to multiple organ dysfunction**
systemic responses of secondary peritonitis
Gastrointestinal tract – initially hypermotility, followed by bowel paralysis; accumulation of fluid in the lumen of the bowel → distention
Cardiovascular – fluid shifts result in decreased circulating blood volume, decreased venous return, decreased cardiac output, hypotension; evidence of increased adrenergic activity (tachycardia, vasoconstriction)
Respiratory – inflamed peritoneum results in high, fixed diaphragm and pain on ventilation; atelectasis with intrapulmonary shunting of blood → hypoxemia; pulmonary edema due to increased pulmonary capillary leakage secondary to hypoalbuminemia or direct effect of bacterial toxins (ARDS)
Renal – decreased renal perfusion → acute renal failure
Metabolic – increased energy demands deplete glycogen stores → catabolism of muscle and fat → weight loss
bacterial synergy
Combination of aerobic and anaerobic organisms are more lethal than infections caused by either alone.
role of factultative bacteria - enterobacteriaceae - early mortality, environment conductive to obligate anaerobes
role of anaerobes - responsible for abcess formation, virulence factors (enzymes, polysaccharide capsule, B-lactamase production, succinic acid)
sxs of secondary peritonitis
Abdominal pain, aggravated by any motion, and distention, Anorexia, Nausea/vomiting, Fever ± chills, Thirst, Decreased urination, Inability to pass flatus or feces
physical findings in secondary peritonitis
Lie very still in bed, supine with knees flexed (movement is very painful), Frequent, limited** intercostal respirations, Fever (up to 42°C), Tachycardia, Hypotension, Marked abdominal tenderness to palpation → voluntary** guarding, Rebound tenderness, Muscular rigidity of the abdominal wall → involuntary** guarding, Hypoactive or absent bowel sounds
diagnostic studies of secondary peritonitis
Peripheral leukocytosis (> 15,000 to 20,000/mm^3) with left shift*
Elevated hematocrit and BUN (2° to dehydration**) - if hct is not elevated, must be bleeding
X-ray – abdominal distention with adynamic loops of bowel; pneumoperitoneum (free air may be visible, indicating perforation)
CT scan, ultrasound
Blood cultures are not routinely recommended for community-acquired intra-abdominal infections unless patient appears to be septic
Exploratory laparotomy – definitive
treatment of secondary peritonitis
surgery or antimicrobial therapy
surgery for secondary peritonitis
Source control – stop continuing bacterial contamination by repairing perforations and resection or removal of infected organs; remove foreign material
Drain purulent collections
COLLECT AEROBIC AND ANAEROBIC SPECIMENS FOR GRAM STAIN,
CULTURE, SUSCEPTIBILITY TESTING!
antimicrobial therapy overview for secondary peritonitis
Begin empiric IV** therapy immediately after obtaining appropriate cultures
Broad spectrum antimicrobial therapy required to cover facultative aerobic and anaerobic organisms – Enterobacteriaceae** and Bacteroidaceae**
Resistance in enteric gram-negative pathogens – study of 1,442 gram-negative aerobes from intraabdominal infections in USA –12.7% of K. pneumoniae and 9.7% of E. coli were ESBL** producers
Risk factors for resistant pathogens: healthcare acquisition, corticosteroid use, organ transplantation, underlying pulmonary or hepatic disease, duodenal infection source
Mortality rates in non-transplant patients 8.4% with susceptible pathogens vs. 14.0% with resistant pathogens (p=0.008)
Susceptibility testing of anaerobes not routinely recommended* (anaerobes universally susceptible to metronidazole, carbapenems, β-lactam/β-lactamase inhibitors
Regimens for initial empiric treatment of community-acquired, extra-biliary complicated intra-abdominal infections
single agent for mild-to-moderate secondary peritonitis severity: perforated or abscessed appendicitis and other infections of mild-to moderate severity***
Cefoxitin
Ertapenem
Ticarcillin-clavulanate
single agent High-risk or severity secondary peritonitis: severe physiologic disturbance, advanced age, or immunocompromised state***
Imipenem
Meropenem
Doripenem
Piperacillin/tazobactam
combination therapy in Mild-to-moderate severity secondary peritonitis:* perforated or abscessed appendicitis and other infections of mild-to moderate severity***
Cefazolin, cefuroxime, ceftriaxone, cefotaxime, ciprofloxacin, or levofloxacin, each in combination with metronidazole**
combination therapy in High-risk or severity secondary peritonitis: severe physiologic disturbance, advanced age, or immunocompromised state***
Cefepime, ceftazidime, ciprofloxacin, or levofloxacin, each in combination with metronidazole**
empiric therapy for healthcare-associated* intra-abdominal infections
Meropenem, doripenem, imipenem, piperacillin/tazobactam, ceftazidime + metronidazole, cefepime + metronidazole
Aminoglycosides or colistin may be required
Therapy should be tailored when C&S results are known
Empiric antienterococcal therapy*** is recommended in patients receiving previous cephalosporin therapy, in patients who are immunocompromised, if the biliary tract is the source, and in patients with valvular heart disease or prosthetic intravascular material (ampicillin, piperacillin/tazobactam, vancomycin)
Empiric coverage for MRSA in patients who are known to be colonized with MRSA or in patients at risk for MRSA due to prior treatment failure or significant antibiotic exposure (vancomycin)
duration of therapy for secondary peritonitis
Established infections – 4 to 7 days** (unless difficulty achieving source control)
For acute stomach and proximal jejunum perforations, in the absence of acid-reducing therapy or malignancy and when source control is achieved within 24 hours** – prophylactic antibiotics directed at aerobic gram-positive cocci for ≤ 24 hours**
Bowel injuries attributable to penetrating, blunt, or iatrogenic trauma that are repaired within 12 hours** should be treated for ≤ 24 hours** (contaminated, not infected)
Acute appendicitis without evidence of perforation, abscess, or local peritonitis - prophylactic therapy only (discontinue within 24 hours)
Cholecystitis without evidence of perforation – up to 24 hours
Diverticulitis – no antibiotics if uncomplicated; 4-7 days** if moderate to severe
Transition to oral therapy** in established infections – ciprofloxacin + metronidazole; levofloxacin + metronidazole; amoxicillin-clavulanate
abscesses diagnosis
Leukocytosis
May have positive blood cultures (Bacteroides – indicates intraabdominal process)
Exploratory laparotomy – definitive
X-ray – collection of gas or air-fluid level in peritoneum
Contrast studies – displacement of structures
Ultrasound
Radionuclide studies – Gallium 67, Indium111
CT/MRI
abscess treatment
Drainage – surgical or percutaneous catheter
Antimicrobial therapy – cover Enterobacteriaceae and Bacteroidaceae
