samuel mwaniki. objectives describe pathogenesis & clinical characteristics of intra-abdominal...
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OBJECTIVESDescribe pathogenesis & clinical
characteristics of intra-abdominal infectionsIdentify most likely etiologic organism(s)Review appropriate drug therapy
INTRA-ABDOMINAL INFECTIONSInfections contained within the peritoneum orretroperitoneal space.
Peritoneal cavity contains: Stomach Jejunum, Ileum Appendix Large intestine (colon) Liver, gallbladder and spleen
Retroperitoneal space: Duodenum Pancreas Kidneys
Intra-abdominal InfectionsAppendicitisPeritonitisIntra-abdominal AbscessDiverticulitisAntibiotic-Associated Diarrhea - Clostridium
difficileFood Poisoning/Traveler’s Diarrhea – E. ColiPUD - Helicobacter pyloriPelvic Inflammatory Disease
GI MicrofloraStomach: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:MicroorganismsChemicalsIrradiationForeign body injury
Primary (Spontaneous Bacterial Peritonitis)
No focus of disease is evidentArises without a breach in the peritoneal
cavity or GITBacteria transported from blood stream to
peritoneal cavity (Cirrhosis, CAPD)Usually monomicrobial
SecondaryAcute perforation of the GI tract
(diverticulitis - ), appendix (appendicitis), gallbladder, tumor perforations)
Community acquired or nosocomialUsually polymicrobialPost-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 painAnorexia (N/V)Fever (38-40 ºC)Abdominal distention and tendernessHypoactive or faint bowl soundsLeukocytosis
Normally: 20 to 50 mL transudatePeritoneal membrane measures approx. 1.7 metres
squareWBC < 300 cells/mm3Protein: <3 g/dL
Bacterial peritonitis: 300 to 500mL inflow/hr resulting in hypovolemia.WBC > 300 cells/mm3Gram stain + for bacteria
MicrobiologyBlood cultures often –vePeritoneal 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 infectionsinfections derived from stomach, duodenum,
biliary system and proximal small bowel:Gram positive and Gram negative aerobic and
facultative bacteriadistal small bowel:
Gram negative facultative and aerobic bacteriaAnaerobes
large bowel:Facultative and obligate anaerobic bacteriaStreptococi and enterococci commonly present
Aerobes:GN Bacilli: E. Coli, Klebsiella,Enterobacter,
Proteus mirabilis, Pseudomonas aeruginosaGP 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
AppendicitisHighest incidence 10-19y/oMale > femalePathophysiology: 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 appendicitisCover 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 AbscessAbscess: 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 thrivehere!
A Result of chronic inflammation, develop over days-yrsLocated within peritoneal cavity or visceral organsMay range from a few milliliters to a liter in volume
Ruptured abscessSpread of bacteria + toxins into peritoneum -
peritonitisSpread 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, +/-
hyperglycemiaUltrasound, GI contrast study, or CT scan may be used
for evaluation
MicrobiologyUsually mixed infection: aerobes & anaerobes
within the same abscessE. coliKlebsiellaEnterococciB. fragilisClostridium
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 ErtapenemAminoglycoside + clindamycin or metronidazoleTigecycline Moxifloxacin - (active against 83% of Bacteroides
strains) + metronidazole
Antibiotic Associated DiarrhoeaAntibiotic therapy (broad spectrum agents:
clindamycin, ampicillin, 3rd generation cephalosporins are most common)
Disruption of normal colonic floraC. difficile colonization (gram +, spore forming
anaerobe)Release of toxins A (enterotoxin), B (cytotoxin),
& binary toxinCDT (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)Vancomycin125mg PO QID x 10-14 days +/- rifampin 600mg
PO BID
Always stop the drug responsible for causing the infection as soon as possible!
PUERPURAL SEPSISDefinition of Puerpurum1. 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 InfectionAny bacterial infection of the genital tract after delivery. Incidence: 6%. The most important cause of maternal death.
Puerperal MorbidityTemperature 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 factors1. Anaemia2. Hemorrhage3. Episiotomy and CS4. Placenta retention5. Hospital contamination
Common pathogens1. Aerobes Group A, B, and D streptococci Gram-negative bacteria: Escherichia coli,
Klebsiella Staphylococcus aureus
2. Anaerobes Peptostreptococcus species Bacteroides fragilis group Clostridium species
3. 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)