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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. 3. 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!