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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
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/mm3); 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/mm3, 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
• 1p 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
• 2o prophylaxis: TMP/SMX 1DS daily, norfloxacin 400 mg daily,
ciprofloxacin 500 mg daily for lifetime
Lecture 24 Intra-abdominal Infections Lalji
PERITONITIS (CONTINUED):
PD-RELATED PERITONITIS:
PD-RELATED PERITONITIS:
• Source of bacteria (focus) is outside the peritoneal cavity
• 60% of all patients on chronic ambulatory peritoneal dialysis (CAPD) will
have at least one episode in 1st year
• Average incidence in CAPD patients is 1.3 – 1.4 eps/year
• Catheter connecting abdominal cavity to exterior body is a major risk factor
• Submit first cloudy effluent to lab for gram stain & culture
ETIOLOGY:
• S. epidermis 8%
• S. aureus 4%
o More likely if nasal carrier, immunocompromised, or diabetic
• Enterobacteriacae 3%
TREATMENT PRINCIPLES:
• Empiric therapy should cover both gram + organisms (with
vancomycin if there is a lot of MRSA or cefazolin) and gram –
organisms (with 3rd/4th gen cephalosporins or aminoglycosides)
• Can use intra-peritoneal (IP) or intra-venous (IV)
o IP is preferred due to high local concentrations: can be
dosed intermittently or continuous dosing
• Total duration is at least 2 weeks
o Sometimes 3 weeks if severe infections and those with
P. aeruginosa or S. aureus
• Narrow therapy when C&S results are back
• High relapse rate, watch for abscess, consider catheter removal
(esp. if keep having repeat infections with same pathogens)
TREATMENT OPTIONS:
• IP > IV
o Cefazolin 15 mg/kg IP + gentamicin 0.6 mg/kg IP once per day (6 hours dwell time) synergistic combination
o Vancomycin 15-30 mg/kg IP q7days + gentamicin 0.6 mg/kg IP once per day
o May also use IV vancomycin or cefazolin, as well as the IP
• Instead of AMG, can use ceftazidime, cefepime, carbapenem
o Use of cefazolin + ceftazidime NOT optimal as the 2 beta-lactams are antagonistic promotes resistance
o Ciprofloxacin no longer recommended due to high resistance plus not active for Staph
SECONDARY PERITONITIS:
BACKGROUND:
• Source of bacteria (focus) is within the peritoneal
cavity, usually from the GIT
o Bowel perforation trauma OR neoplasms,
mechanical problems
o Ruptured appendix
• Often complicated with abscess
o Harder to treat infection
o Often need to control source through surgery
and drain abscess
ETIOLOGY:
• Microbiologic etiology depends on location of infection, but is commonly polymicrobial
Gram-negative bacilli Anaerobes
• E. coli 71%
• Klebsiella sp 14%
• P. aeruginosa 14%
• Proteus spp. 5%
• B. fragilis 35%
• Other bacteriodes spp. 71%
• Prevotella 12%
• Peptostreptocci 17%
• Clostridium spp. 29%
• Fusobacterium spp. 9% Candida may be present
Gram-positive cocci
• Enterobacter spp. 5%
• Streptococci (incl. Enterococci) 12-38%
• Staphylococci 4%
RISK FACTORS ASSOCIATED WITH MORTALITY:
• Age > 70 years
• Comorbid conditions
o Renal/liver disease
o Malignancy
• Immunocompromised
• Severe illness (i.e. sepsis)
• Diffuse peritonitis/extensive peritoneal involvement
• Delay in source control > 24 h
• Inability to achieve adequate drainage/debridement
RISK FACTORS ASSOCIATED WITH ABX RESISTANCE:
• Healthcare acquired infection
• Travel to areas with high resistance rates within a
few weeks prior to getting ill
• Known colonization with MDR
ENTEROCOCCUS: likely only pathogenic (and therefore coverage is necessary) in:
• Health-care associated infxn
• Distal colon surgery
• Hepatobiliary/pancreatic infxn
• Chronic illness
• Immunocompromised
• Valvular disease
• Prosthetic heart valve
• Previous txt with cephalosporins
• Enterococcus is predominant organism on culture
CANDIDA: only treat when yeast/candida on gram stain/culture AND one of the following:
• Yeast seen intracellularly
• Presence of hyphae
• Immunocompromised
• Multiple previous antibiotics
• Upper GI perforation
• Post-operative IA infection
• Recurrent IA infection
► If C. albicans: add fluconazole (or micafungin if fluconazole-resistnat)
► If non-albicans: add echinocandin
TREATMENT GOALS:
• Control bacteremia & prevent metastatic foci
(gram negative)
• Reduce suppurative complications (anaerobes)
• Prevent local spread of existing infection
o Surgery + antibiotics
• Prevent morbidity and mortality
CLINICAL PRESENTATION:
General Look “toxic”, acute distress, lying still, dehydrated
CNS Febrile, may increase rapidly; ↓ LOC if “septic”
HEENT Grimacing, diaphoretic, dry mucous membranes
RESP ↑ RR, rapid, shallow breathing
CVS ↓BP, ↑ HR, may require fluid/vasopressors for septic shock
GI/GU Bowel sounds initially faint, may disappear; voluntary guarding; abdominal pain/tenderness; N/V
ABD X-RAY Bowel distension, “free air” = perforation surgical emergency
LABS ↓ urine output, ↑ BUN, ↑ SCr, ↑Hb/Hct, alkalosis then acidosis
MSK/DERM ↓ skin turgor, cool, clammy extremities
Lecture 24 Intra-abdominal Infections Lalji
PERITONITIS (CONTINUED):
SECONDARY PERITONITIS:
TREATMENT FOR COMMUNITY-ACQUIRED:
• 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
• Biliary obstruction diminishes host antibacterial defenses, causes
immune dysfunction, and subsequently increases small bowel
bacterial colonization
o Bacteria gain access to the biliary tree by retrograde ascent
from the duodenum or from portal venous blood
o Infection ascends into hepatic ducts, causing serious infxn
o Increased biliary pressure pushes infection into biliary
canaliculi, hepatic veins, and perihepatic lymphatics
bacteremia (25-45%)
o The infection can be suppurative in the biliary tract
TREATMENT:
• Initial supportive care with hydration, pain control & bowel rest
• Same as treatment of appendicitis: surgery > antibiotics alone
o Antibiotics given pre-op and sometimes up to 24-hr post-op
(ex// cefazolin 1-2 g)
• If gallbladder is perforated or gangrenous, or abscess seen, then
treatment is surgery and antibiotics as per secondary peritonitis
(short-course: 3-5 days)
DIAGNOSIS:
• DDx: ultrasound and CT scan
• Consult: GI and surgery