Lecture 24 Intra-abdominal Infections Lalji INTRA-ABDOMINAL INFECTIONS: • Appendicitis (right-sided abd. pain) • Peritonitis • Intra-abdominal abscess • Cholangitis and cholecytitis • Diverticuilitis (left-sided abd. pain) • C. difficile infection (AAD) • Food poisoning/Traveller’s Diarrhea • Helicobacter pylori (PUD) PERITONEAL CAVITY: • Extends from undersurface of diaphragm to floor of the pelvis • Contains stomach, most of small bowel, large bowel, liver, gallbladder and spleen • Duodenum, pancreas, kidneys, adrenals are in posterior peritoneum • Cavity contains 50 mL sterile serous fluid, low protein, leukocytes, and no fibrinogen NORMAL FLORA: • Reside on body surface/cavities, but normally do not invade or cause immune response • Prevent colonization, invasion, infection by other organisms • Harmless at usual sites, but may produce disease if introduced into other areas that are supposed to be sterile (opportunitists) • Understanding the pattern & density of normal flora enables prediction of microbiologic etiology of intra-abdominal infxns NORMAL GI MICROFLORA: Stomach Total bacterial count 0-10 9 log organisms/g • H. pylori, streptococci, lactobacilli Upper small intestine Total bacteria count 0-10 5 log organisms/g • Aerobes: enterococci, staphylococci, lactobacilli, E. coli, Klebsiella • Anaerobes: bacteroides BACTERIAL SYNERGISM: • Size of inoculum, number, and types of bacterial species affect outcome • Combinations of both aerobes and anaerobes increases risk of infection, and appear to be much more lethal • Facultative aerobes set-up environment conducive to anaerobes: o Consume O2 provide anaerobic environment o Produce waste used as nutrients by anaerobes o Produce enzymes that promote anaerobic tissue invasion ABDOMINAL INFECTION: 2-STAGE PROCESS 1. Days 1-5: acute, generalized gram (-) peritonitis, bacteremia, sepsis, high mortality 2. Day 5+: abscess formation, primarily by anaerobes (B. fragilis) PERITONITIS: PATHOGENESIS: • After bacteria gain entry to peritoneal cavity, humoral and cellular immune defenses respond o If there a limited number of bacteria, the immune system is able to contain the infection o Under certain conditions, bacteria disseminate throughout peritoneal cavity peritonitis 1. Large bacterial inoculum 2. Continuing bacterial contamination 3. Mixed organisms that are virulent due to synergism • With peritonitis, see outpouring of serous fluid containing leukocytes, fibrin, and proteins, which make up exudates on the peritoneal surface, and form adhesions between structures • Adhesions and ileus (paralysis of intestines) leads to confinement and collection of fluid which can cause bowel distension • Protein-rich fluid draws more water into the peritoneal space, “third spacing” from other compartments, and may lead to hypovolemia and hypotension (worsened with fever, N/V) • Inflamed peritoneal membrane permits bacteria and endotoxins to be absorbed into bloodstream and septic shock and death • Foreign objects, dead, necrotic tissue have negative effects on immune function • If body is successful in localizing contamination, abscess will form o Abscesses are formed by action of inflammatory cells, bacteria, fibrin and contain necrotic tissue, bacteria and WBCs o Abscess environment is anaerobic, hypertonic, acidic, and inhibits the action of antimicrobials PRIMARY PERITONITIS: AKA SPONTANEOUS BACTERIAL PERITONITIS (SBP): • Relatively uncommon, but most commonly in pts with chronic liver disease o SBP occurs in 10-25% of ps with ascites related to alcoholic cirrhosis • Can also be seen in patients with acute hepatitis, CHF, metastatic malignancy, or lupus (SLE), peritoneal dialysis (PD) • Source of bacteria (focus) is outside the peritoneal cavity o Thought to occur by migration of microbes through the GI wall to the mesenteric lymph nodes o Bacteria infect ascitic fluid by hematogenous or lymphatic systems • Bacterial translocation can also occur in non-cirrhotic patients whereby bacteria are transported via bloodstream, skin, lymphatics, or fallopian tubes to peritoneal cavity ETIOLOGY: often single organism • E. coli 65% • K. pneumoniae 15% • S. pneumoniae 15% • Enterococcus 5% • Anaerobes < 1% CLINICAL PRESENTATION: • Patient often not in acute distress • Fever/chills, vomiting, diffuse abdominal pain, rebound tenderness, guarding, ↓ bowel sounds o RLQ pain = appendix; LUQ = pancreas, RUQ = liver or gallbladder • May take days to weeks to develop • Peritoneal fluid: ↑ PMNs (>250/mm 3 ); pH < 7.35; + lactate, protein, gram TREATMENT PRINCIPLES: • Usually only requires antibiotics x 5 days, no surgical intervention • Primary need to cover E. coli and other gram (-) pathogens • Re-check ascitic fluid (repeat parancetesis) at 48 hours o If fluid is sterile, WBC < 250/mm 3 , protein is ↓, and patient is clinically well complete therapy TREATMENT OPTIONS: • Ceftriaxone or cefotaxime • Alternatives: o Ampicillin (or cefazolin) + gentamicin o Piperacillin/tazobactam o Ertapenem • If your hospital has resistant E. coli and K. pneumoniae (ESBL) use: o Imipenem or meropenem o Ciprofloxacin, levofloxacin, moxifloxacin PREVENTION: • Prophylactic antibiotics decrease incidence of peritonitis o Not demonstrated to reduce hospitalization or survival rates o Increase carriage of MDR organisms • 1 p prophylaxis: CTX 1-2 g daily while NPO, then TMP/SMX 1DS BID, norfloxacin 400 mg BID, or cipro 500 mg BID to complete 7 days • 2 o prophylaxis: TMP/SMX 1DS daily, norfloxacin 400 mg daily, ciprofloxacin 500 mg daily for lifetime
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Lecture 24 Intra-abdominal Infections Lalji INTRA ... · • Cholangitis and cholecytitis ... • Relatively uncommon, but most commonly in pts with chronic liver disease o SBP occurs
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Lecture 24 Intra-abdominal Infections Lalji
INTRA-ABDOMINAL INFECTIONS:
• Appendicitis (right-sided abd. pain)
• Peritonitis
• Intra-abdominal abscess
• Cholangitis and cholecytitis
• Diverticuilitis (left-sided abd. pain)
• C. difficile infection (AAD)
• Food poisoning/Traveller’s Diarrhea
• Helicobacter pylori (PUD)
PERITONEAL CAVITY:
• Extends from undersurface of diaphragm to floor of the pelvis
• Contains stomach, most of small bowel, large bowel, liver, gallbladder and spleen
• Duodenum, pancreas, kidneys, adrenals are in posterior peritoneum
• Cavity contains 50 mL sterile serous fluid, low protein, leukocytes, and no fibrinogen
NORMAL FLORA:
• Reside on body surface/cavities, but normally do not invade or
cause immune response
• Prevent colonization, invasion, infection by other organisms
• Harmless at usual sites, but may produce disease if introduced
into other areas that are supposed to be sterile (opportunitists)
• Understanding the pattern & density of normal flora enables
prediction of microbiologic etiology of intra-abdominal infxns
NORMAL GI MICROFLORA:
Stomach Total bacterial count 0-109 log organisms/g
• H. pylori, streptococci, lactobacilli
Upper small intestine
Total bacteria count 0-105 log organisms/g
• Aerobes: enterococci, staphylococci, lactobacilli, E. coli, Klebsiella
• Anaerobes: bacteroides
BACTERIAL SYNERGISM:
• Size of inoculum, number, and types of bacterial species affect outcome
• Combinations of both aerobes and anaerobes increases risk of infection, and appear
to be much more lethal
• Facultative aerobes set-up environment conducive to anaerobes:
o Consume O2 provide anaerobic environment
o Produce waste used as nutrients by anaerobes
o Produce enzymes that promote anaerobic tissue invasion
ABDOMINAL INFECTION: 2-STAGE PROCESS
1. Days 1-5: acute, generalized gram (-) peritonitis, bacteremia,
sepsis, high mortality
2. Day 5+: abscess formation, primarily by anaerobes (B. fragilis)
PERITONITIS:
PATHOGENESIS:
• After bacteria gain entry to peritoneal cavity, humoral and cellular immune defenses respond
o If there a limited number of bacteria, the immune system is able to contain the infection
o Under certain conditions, bacteria disseminate throughout peritoneal cavity peritonitis
1. Large bacterial inoculum
2. Continuing bacterial contamination
3. Mixed organisms that are virulent due to synergism
• With peritonitis, see outpouring of serous fluid containing leukocytes, fibrin, and proteins, which make up exudates on the peritoneal surface, and form
adhesions between structures
• Adhesions and ileus (paralysis of intestines) leads to confinement and collection of fluid which can cause bowel distension
• Protein-rich fluid draws more water into the peritoneal space, “third spacing” from other compartments, and may lead to hypovolemia and hypotension
(worsened with fever, N/V)
• Inflamed peritoneal membrane permits bacteria and endotoxins to be absorbed into bloodstream and septic shock and death
• Foreign objects, dead, necrotic tissue have negative effects on immune function
• If body is successful in localizing contamination, abscess will form
o Abscesses are formed by action of inflammatory cells, bacteria, fibrin and contain necrotic tissue, bacteria and WBCs
o Abscess environment is anaerobic, hypertonic, acidic, and inhibits the action of antimicrobials
PRIMARY PERITONITIS:
AKA SPONTANEOUS BACTERIAL PERITONITIS (SBP):
• Relatively uncommon, but most commonly in pts with chronic liver disease
o SBP occurs in 10-25% of ps with ascites related to alcoholic cirrhosis
• Can also be seen in patients with acute hepatitis, CHF, metastatic
malignancy, or lupus (SLE), peritoneal dialysis (PD)
• Source of bacteria (focus) is outside the peritoneal cavity
o Thought to occur by migration of microbes through the GI wall to
the mesenteric lymph nodes
o Bacteria infect ascitic fluid by hematogenous or lymphatic systems
• Bacterial translocation can also occur in non-cirrhotic patients whereby
bacteria are transported via bloodstream, skin, lymphatics, or fallopian
• No consensus on drugs of choice for empiric coverage – studies show similar cure rates if gram (-) and anaerobic coverage is included
• Antibiotic selection should always encompass host, bug and drug factors
Type Definition Single agent regimens Combination regimens Notes
Low-risk community-acquired
Mild-mod severity (including perforated appendix or appendiceal abscess) in absence of risk factors for failure of resistance
• Ertapenem
• Pip/Tazo
• Cefoxitin, moxifloxacin, clindamycin, tigecycline o Acquiring more
resistance so generally avoid
o Tigecycline = increased mortality
Cefazolin, cefuroxime, ceftriaxone, cefotaxime, ciprofloxacin, levofloxacin PLUS metronidazole
If need enterococcoal coverage, use:
Ampicillin 2 g IV q6h
PLUS
Gentamicin 5-7 mg/kg IV q24h
PLUS
Metronidazole 500 mg IV/PO BID
High-risk community-acquired
Severe infections or in patients at high risk for adverse outcomes or resistance
• Imipenem, meropenem, doripenem
• Pip/tazo
Cefepime, ceftazidime, ciprofloxacin, levofloxacin PLUS metronidazole
If need enterococcal coverage, use
Pip/Tazo PLUS gentamicin
TREATMENT FOR HEALTHCARE ASSOCIATED:
• High risk of resistant pathogens and therefore need coverage for streptococci (incl. enterococci), anaerobes (incl. B. frag) and resistant
enterobacteriaceae and P. aeruginosa
Carbapenem Pip/tazo Ceftazidime or cefepime WITH metronidazole
Aminoglycosides Vancomycin
If < 20% resistance with P. aeruginosa, Acinetobacter, or multi-drug resistant gram (-) bacilli (MDR GNB)
✔ ✔ ✔ ✔ ✖
ESBL-producing Enterobacteriaceae ✔ ✔ ✖ ✔ ✖
MRSA ✖ ✖ ✖ ✖ ✔
STEPDOWN:
• Continue IV abx until patient clinically well, including tolerate oral medications, afebrile, WBC normal, no residual fluid collections, return of GI fxn
• Oral step down:
• Amox/clav 875 mg PO BID
• 3rd/4th gen cephalosporin + metronidazole 500 mg PO BID
• TMP/SMX 1 DS BID + metronidazole 500 mg PO BID
• Ciprofloxacin 500 mg PO BID + metronidazole 500 mg PO BID o Can substitute levo/moxifloxacin
• Total duration is around 4-7 days
INTRA-ABDOMINAL ABSCESS:
• Purulent collection of fluid surrounded by a wall
(fibrinous capsule) from the surrounding tissue
• May range from a few mL to a L in volume
• Located in peritoneal cavity of within visceral organs
• Takes days to years to form
• Commonly seen in appendicitis, diverticulitis,
pancreatitis, female GU tract
• Ultrasound or CT scan may be used for evaluation
• Often need to drain abscess
• Need anaerobic coverage
ACUTE APPENDICITIS:
• Characterized by acute onset of N/V, RLQ pain, rebound tenderness, low-grade fever, anorexia
• Surgery, rather than antibiotics alone, remains gold standard (↑ recurrence with abx alone)
o Either open or laparoscopic surgery
▪ Laparoscopic surgery = fewer wound infections, less pain, shorter hospital
stay BUT higher rates of re-admission and abscess
o Antibiotics given pre-op and sometimes up to 24-hr post-op (ex// cefazolin 1-2 g)
• In patients with over 5 days of symptoms, a cooling-off approach may be used with hydration,
antibiotics, bowel rest and elective appendectomy 6-8 weeks later
• If appendix is perforated or gangrenous, or abscess seen, then treatment is surgery and
antibiotics as per mild-moderate secondary peritonitis (duration is ~ 3 days)
TREATMENT PRINCIPLES:
• Surgical: drainage of abscess/debridement; resection of perforated abdomen (colon, small intestine, ulcers); repair of trauma
• Support of vital functions: monitor BP, heart rate, urine output (0.5 mL/kg/hr)
• Antimicrobial therapy: empiric regimens should minimally cover E. coli, Klebsiella spp., Bacteriodes fragilis, Clostridium spp.
Lecture 24 Intra-abdominal Infections Lalji
ACUTE CHOLECYSTITIS AND CHOLANGITIS: inflammation of the gallbladder and ducts
CAUSES:
Gallstones • Most cholecystitis is the result of hard particles that develop in your gallbladder (= gallstones) from imbalances in the substances in bile (ex// cholesterol and bile salts)
• Gallstones can black the cystic duct (tube through which bile flows through when it leaves the gallbladder) causes bile to build up inflammation
Tumor • A tumor may prevent bile from draining out of your gallbladder properly bile buildup cholecystitis
Bile duct blockage
• Kinging or scarring of bile ducts can cause blockage that leads to cholecystitis
COMMON SYMPTOMS:
• RUQ pain
• Fever
• Leukocytosis
• Jaundice
• If severe, mental status changes and sepsis
MAIN PATHOGENS:
• Enterobacteriaceae, enterococcus, anaerobes
PATHOPHYSIOLOGY:
• A biliary system that is colonized by bacteria (it’s normally stable)
but is unobstructed typically doesn’t result in cholangitis