Peritonitis (acute and chronic pancreatitis) .ppt

Ppt

1. Samuel Mwaniki

2. OBJECTIVES
Describe pathogenesis & clinical characteristics of
intra-abdominal infections
Identify most likely etiologic organism(s)
Review appropriate drug therapy

3. 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

4. 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

5. 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

6. Peritonitis
Inflammation of the serous lining of the peritoneal
cavity due to:
Microorganisms
Chemicals
Irradiation
Foreign body injury

7. 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

8. 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

9. Tertiary
Peritonitis in a critically ill patient which persists or
recurs at least 48 h after apparently adequate
management of primary or secondary peritonitis

10. Clinical Symptoms
Abdominal pain
Anorexia (N/V)
Fever (38-40 ºC)
Abdominal distention and tenderness
Hypoactive or faint bowl sounds
Leukocytosis

11. Normally:
20 to 50 mLtransudate
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

12. 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

13. 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
Streptocociand enterococcicommonly present

14. 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

15. Anaerobes:
GN Bacilli : B.fragilis, Prevotella, Pophyromonas
GP Cocci: Clostridium spp, Peptostreptococcus.
Fungi:
C. albicans

16. Appendicitis
Highest incidence 10-19y/o
Male > female
Pathophysiology: Relationship to onset of sx
0-24h after sxonset: obstruction within appendix , inflammation &
occlusion of vascular & lymphatic flow, bacterial overgrowth then
necrosis.
>48h after sxonset: perforation, abscess/peritonitis
Early sx: dull, non-localized pain, indigestion,bowelirregularity,
flatulence
Later sx: pain/tenderness more localized, N/V, Fever >39 degrees
celcius, leukocytes >15000: perforation likely

17. Management
Acute, non-perforated appendicitis
cefazolin+ metronidazole
Perforated appendicitis
Cover enteric gram –rods and anaerobes
(2nd/3rd generation cephor 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

18. 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
neighboringstructures.
Encapsulation can prevent immune cells/abxfrom 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 millilitersto a literin volume

19. 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

20. Microbiology
Usually mixed infection: aerobes & anaerobes within
the same abscess
E. coli
Klebsiella
Enterococci
B. fragilis
Clostridium

21. 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

22. 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+ clindamycinor metronidazole
Tigecycline
Moxifloxacin-(active against 83% of Bacteroidesstrains)+
metronidazole

23. 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

24. 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
metronidazoleor
recurrences)
Vancomycin
125mg PO QID x 10-14 days +/-rifampin600mg PO BID
Always stop the drug responsible for causing the infection as
soon as possible!

25. 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.

26. 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.

27. Risk factors
1.Anaemia
2.Hemorrhage
3.Episiotomy and CS
4.Placenta retention
5.Hospital contamination

28. Common pathogens
1.Aerobes
Group A, B, and D streptococci
Gram-negative bacteria: Escherichia coli, Klebsiella
Staphylococcus aureus

29. 2.Anaerobes
Peptostreptococcusspecies
Bacteroides fragilis group
Clostridium species
3.Other
Chlamydia trachomatis
Mycoplasmaspecies

30. Manifestation
Acute vulvitis, vaginitis,cervicitisand endometritis
Uterine infection
Adnexalinfections
Septic pelvic thrombophlebitis
Sapremia(blood poisoning resulting from
absorption of putrefaction matter from the uterus)

31. MERCI BEACOUP,
MADAME
MADEMOISELLE ET
MESSRS!