Transcript ABDOMINAL INFECTIONS AND PUERPURAL SEPSIS

Samuel Mwaniki
OBJECTIVES
 Describe pathogenesis & clinical characteristics of
intra-abdominal infections
 Identify most likely etiologic organism(s)
 Review appropriate drug therapy
INTRA-ABDOMINAL INFECTIONS
Infections contained within the peritoneum or
retroperitoneal space.
Peritoneal cavity contains:
 Stomach
 Jejunum, Ileum
 Appendix
 Large intestine (colon)
 Liver, gallbladder and spleen
Retroperitoneal space:
 Duodenum
 Pancreas
 Kidneys
Intra-abdominal Infections
 Appendicitis
 Peritonitis
 Intra-abdominal Abscess
 Diverticulitis
 Antibiotic-Associated Diarrhea - Clostridium difficile
 Food Poisoning/Traveler’s Diarrhea – E. Coli
 PUD - Helicobacter pylori
 Pelvic Inflammatory Disease
GI Microflora
Stomach:
 H. Pylori, Lactobacilli
Upper Intestine:
 Streptococci, Enterococci, Staphylococci, E. Coli, Klebsiella,
Bacteroides
Ileum:
 Streptococci, Staphylococci, Escherichia coli, Klebsiella,
Enterobacter, Bacteroides, Clostridium
Colon:
 Bacteroides, Peptostreptococci, Clostridium,
Bifidobacterium, Escherichia coli, Klebsiella, Enterobacter,
Enterococci, Staphylococci
Peritonitis
Inflammation of the serous lining of the peritoneal
cavity due to:
 Microorganisms
 Chemicals
 Irradiation
 Foreign body injury
Primary (Spontaneous Bacterial Peritonitis)
 No focus of disease is evident
 Arises without a breach in the peritoneal cavity or GIT
 Bacteria transported from blood stream to peritoneal
cavity (Cirrhosis, CAPD)
 Usually monomicrobial
Secondary
 Acute perforation of the GI tract (diverticulitis - ),
appendix (appendicitis), gallbladder, tumor
perforations)
 Community acquired or nosocomial
 Usually polymicrobial
 Post-operative peritonitis
 Post-traumatic peritonitis
Tertiary
 Peritonitis in a critically ill patient which persists or
recurs at least 48 h after apparently adequate
management of primary or secondary peritonitis
Clinical Symptoms
 Abdominal pain
 Anorexia (N/V)
 Fever (38-40 ºC)
 Abdominal distention and tenderness
 Hypoactive or faint bowl sounds
 Leukocytosis
Normally:
 20 to 50 mL transudate
 Peritoneal membrane measures approx. 1.7 metres square
 WBC < 300 cells/mm3
 Protein: <3 g/dL
Bacterial peritonitis:
 300 to 500mL inflow/hr resulting in hypovolemia.
 WBC > 300 cells/mm3
 Gram stain + for bacteria
Microbiology
 Blood cultures often –ve
 Peritoneal fluid used (parecentesis)
 Health care associated intra-abdominal infection
usually due to nosocomial organisms particular to the
site of the operation and specific hospital and unit
 Community acquired infections
 infections derived from stomach, duodenum, biliary
system and proximal small bowel:
 Gram positive and Gram negative aerobic and
facultative bacteria
 distal small bowel:
 Gram negative facultative and aerobic bacteria
 Anaerobes
 large bowel:
 Facultative and obligate anaerobic bacteria
 Streptococi and enterococci commonly present
Aerobes:
 GN Bacilli: E. Coli, Klebsiella,Enterobacter, Proteus
mirabilis, Pseudomonas aeruginosa
 GP Cocci: Enterococcus spp e.g. E. faecalis,
Streptococcus, S.aureus, Coagulase –ve Staphylococcus
Anaerobes:
 GN Bacilli : B.fragilis, Prevotella, Pophyromonas
 GP Cocci: Clostridium spp, Peptostreptococcus.
Fungi:
 C. albicans
Appendicitis
 Highest incidence 10-19y/o
 Male > female
 Pathophysiology: Relationship to onset of sx
0-24h after sx onset: obstruction within appendix , inflammation &
occlusion of vascular & lymphatic flow, bacterial overgrowth then
necrosis.
>48h after sx onset: perforation, abscess/peritonitis
Early sx: dull, non-localized pain, indigestion,bowel irregularity,
flatulence
Later sx: pain/tenderness more localized, N/V, Fever > 39 degrees
celcius, leukocytes >15000: perforation likely
Management
Acute, non-perforated appendicitis
 cefazolin + metronidazole
Perforated appendicitis
 Cover enteric gram – rods and anaerobes
(2nd/3rd generation ceph or FQ) + metronidazole, Cefoxitin,
piperacillin/tazobactam, ampicillin/sulbactam, imipenem
 Antibiotics are started before surgery, continued for 7- 10 days
 Switch to PO based on patient status
Intra – abdominal Abscess
 Abscess: purulent collection of fluid, necrotic debris, bacteria,
inflammatory cells that is walled off/encapsulated by adjacent
healthy cells in an attempt to keep pus from infecting
neighboring structures.
 Encapsulation can prevent immune cells/abx from attacking
contained bacteria, low O2 in capsule, anaerobes thrive
here!
 A Result of chronic inflammation, develop over days-yrs
 Located within peritoneal cavity or visceral organs
 May range from a few milliliters to a liter in volume
Ruptured abscess
 Spread of bacteria + toxins into peritoneum - peritonitis
 Spread of bacteria + toxins into systemic circulation –
sepsis, multi-organ failure, death
Presentation:
 Nonspecific low grade or spiking fever, abdominal
pain/discomfort +/- distension
Labs:
 Leukocytosis, +/- positive blood cultures, +/-hyperglycemia
 Ultrasound, GI contrast study, or CT scan may be used for
evaluation
Microbiology
 Usually mixed infection: aerobes & anaerobes within
the same abscess
 E. coli
 Klebsiella
 Enterococci
 B. fragilis
 Clostridium
Management
Combination of modalities:
 Surgical: Prompt drainage of abscess (secondary
peritonitis) and/or debridement, Resection of perforated
colon, small intestine, ulcers, Repair of trauma.
 Support of Vital functions: Blood pressure/fluid
replacement, Monitor heart rate, Monitor urine out put
(0.5 ml/kg/hr)
 Appropriate antimicrobial therapy
Empiric Antibiotic Therapy
MUST include aerobic/anaerobic coverage
Agents with Aerobic and Anaerobic activity:
 Ampicillin/sulbactam - (enterococci)
 Piperacillin/tazobactam - (enterococci)
 Imipenem/cilistatin
 Meropenem
 Ertapenem
 Aminoglycoside + clindamycin or metronidazole
 Tigecycline
 Moxifloxacin - (active against 83% of Bacteroides strains) +
metronidazole
Antibiotic Associated Diarrhoea
 Antibiotic therapy (broad spectrum agents:
clindamycin, ampicillin, 3rd generation
cephalosporins are most common)
 Disruption of normal colonic flora
 C. difficile colonization (gram +, spore forming
anaerobe)
 Release of toxins A (enterotoxin), B (cytotoxin), &
binary toxin
 CDT (associated w/ recent outbreaks)
 Damage to colonic mucosa (pseudomembranous
plaques),inflammation, intestinal fluid secretion
Treatment
FIRST LINE:
 Metronidazole (Treatment of Choice)
 250mg PO QID or 500mg PO/IV TID x 10-14 days
ALTERNATIVE: (if pregnant, not responding to
metronidazole or
recurrences)
 Vancomycin
 125mg PO QID x 10-14 days +/- rifampin 600mg PO BID
Always stop the drug responsible for causing the infection as
soon as possible!
PUERPURAL SEPSIS
Definition of Puerpurum
1. The time from the delivery of the placenta through
the first few weeks after the delivery.
2. 6 weeks in duration.
3. By 6 weeks after delivery, most of the changes of
pregnancy, labor, and delivery have resolved and the
body has reverted to the non pregnant state.
Puerperal Infection
Any bacterial infection of the genital tract after
delivery. Incidence: 6%. The most important cause of
maternal death.
Puerperal Morbidity
Temperature 38.0℃ or higher, the temperature to
occur on any 2 of the first 10days postpartum, exclusive
of the first 24 hours, and to be taken by mouth by a
standard technique at least four times daily.
Risk factors
1. Anaemia
2. Hemorrhage
3. Episiotomy and CS
4. Placenta retention
5. Hospital contamination
Common pathogens
1. Aerobes
 Group A, B, and D streptococci
 Gram-negative bacteria: Escherichia coli, Klebsiella
 Staphylococcus aureus
2.
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3.
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Anaerobes
Peptostreptococcus species
Bacteroides fragilis group
Clostridium species
Other
Chlamydia trachomatis
Mycoplasma species
Manifestation
 Acute vulvitis, vaginitis, cervicitis and endometritis
 Uterine infection
 Adnexal infections
 Septic pelvic thrombophlebitis
 Sapremia (blood poisoning resulting from
absorption of putrefaction matter from the uterus)
MERCI BEACOUP,
MADAME
MADEMOISELLE ET
MESSRS!