samuel mwaniki. objectives describe pathogenesis & clinical characteristics of intra-abdominal...

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Samuel Mwaniki

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Samuel Mwaniki

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)

MERCI BEACOUP, MADAME

MADEMOISELLE ET MESSRS!