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
