Transcript Infection and sepsis - NUS

INFECTION AND SEPSIS
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Surrounded by pathogens
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Infection is the exception
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Protective from infection
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Physical barriers
Chemical barriers
Immunological function
Physical and Chemical
Barriers to Infection
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Skin
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stronger in hands and feet
sebaceous secretions lower pH
Mucous membranes
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ciliary function
mucous barrier
acid mileu in stomach
Barriers breached in Surgery
Barriers Breached in Trauma
Immune Defense
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Humoral defense
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antibodies
complement
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Cellular defense
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Cytokines
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potential for deleterious effects
Interaction of mechanisms
Breakdown of Host Defense
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Physical, chemical and immunological
breakdown -act synergistically
e.g. patient with
diabetes
 immunosuppresion
 surgery
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Potential for deleterious effects
Fourniers Gangrene
Commensal Microbial Flora
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Important for immune development
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Occupy binding sites for pathogens
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Provide mucobacterial barrier
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Anerobic bacteria
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present in greatest quantity in GIT
Greatest diversity
Prevent invasion by gram neg. aerobes
Breakdown of Host Defense
- GIT Flora
Transmigration of bacteria
Lack of feeding
 Overuse of antibiotics
 Absence of bile
 Protein malnutrition
 Immune deficiency
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ICU patient fed enteraly
To preserve GIT integrity
Infection Manifestation
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Local signs
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Systemic signs
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Fever, somnolence, confusion, ileus,
hypotension
Lab tests
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pain,redness,swelling, warmth loss of
function
TW,polymorphs, Cultures
Non infective- causes may manifest as
infection
Common Infections
Wound infection
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Initial inoculum overwhelms host defense
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Occurs at 5 - 7 days post op
Factors
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host - immune suppression, DM, renal failure
surgeon - technique
environment - contamination
Common Infections
Types of Wounds
1. Clean - no viscus, no sterile breach
2. Clean contaminated - controlled entry into
viscus
3. Contaminated - emergency bowel resection,
perforated appendix
4. Dirty - heavy contamination / long duration
Antibiotics used
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type 2 as prophylaxis
type 3,4 as treatment
Wound Closure
Wounds
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Closure by
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primary intention
secondary intention
Timing of closure
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delayed primary closure
secondary closure
Closure by Secondary Intention
Intraabdominal Infection
Defense
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Bacterial clearance - stomata between
mesothelial cells under diaphragm lead to
lymph vessels
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Phagocytosis - both resident and recruited
phagocytes
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Sequestration - by fibrin rich inflammatory
exudate, with omentum/viscera
Intraabdomianal Infection
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Signs of peritonitis
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Pain
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Posture
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sharp in character, well localised at first
spreads to surrounding areas
involuntary guarding, rigidity
absent bowel sounds
lying still, rapid breathing ,no movement
General condition
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ill, septic, dehydrated, hypotension
Intraabdominal Infection
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Usually viscus perforation
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Isolates
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colon worse than upper GIT
aerobic - E. Coli, klebsiella other
enterobacter, strep, enterococci,
proteus, pseudomonas
anaerobic - bacteroides, Clostridium
Treatment is surgical and aggressive
antibiotic treatment
Enterocutaneous Fistula
Common Post Surgical
Infections
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Pneumonia
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Protein malnourished
upper abdominal wounds ® poor cough
bed bound - atelectasis
elderly
ventilator
Occurs from 3 days post op
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careful clinical exam,CXR
Routine chest physiotherapy
Common Post Surgical
Infections
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Urinary Tract Infection
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catheters
dehydration
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Remove catheters early
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Ensure hydration
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Antimicrobial therapy
Common Post Surgical
Infections
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Catheter and prosthetic devices
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I/v canulas
central lines
mesh
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Skin organisms- S aureus, S epidermidis
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Aseptic technique
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Remove if infected
Less Common Post
Surgical Infections
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Necrotising soft tissue infection
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Parotitis
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Sinusitis
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Tonsillitis
Treatment of Infection
General principles
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incise and drain pus
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antibiotics as needed
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debride dead tissue
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remove foreign bodies
Antibiotic Therapy
Prophylaxis
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Short course to prevent infection
Must be on board before contamination
Antibiotics with activity against expected
inoculation organisms
Avoid extended spectrum agents
Post op benefit not proven
Topical antibiotics - not proven
Antibiotic Therapy
Empirical therapy
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based on clinical information
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search for source must continue
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limit duration of empirical therapy
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use known institution pattern of infection
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multi agent vs broad agent
Antibiotic Therapy
Directed therapy
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target identified pathogens
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choose suitable efficacy /minimal
toxicity agent
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cover aerobic and anaerobic if
likelihood exist for both
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extended spectrum as last resort
Multiple System
Organ Failure
AKA - Gram neg. bacterial sepsis
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30% mortality
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Healthy and compromised host
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3-13 cases per 1000 admissions
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Nosocomial
Multiple System Organ Failure
Factors
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Host compromise
Elderly, disability
Malnutrition
Antimicrobial therapy
Major surgery
Cavity manipulation
Immunosuppression e.g. steroids
MSOF
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Fever
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Acidosis, hypoxemia
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Disordered oxygen and substrate use
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Hyperglycaemia
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Decreased systemic vascular resistance
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Elevated cardiac output
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Hypotension
MSOF
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Evidence for LPS - endotoxin
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LPS
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O antigen - specific for each organism
core LPS
membrane lipid A
LPS - EFFECTS
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non specific polyclonal b cell proliferation
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macrophage activation, cytokine release
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hypotension, hypoxemia
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bacterial translocation
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complement and coagulation activation
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platelet and white cell margination
LPS - Mechanism
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Direct effect of bacteria
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Indirect (mediated) effect
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trigger macrophages to release TNFa, IL-1,
IL-6, aIFN
TNFa, IL-1, - primary mediators but may
be deleterious in large amounts
aIFN- causes continued activation of
macrophages
Permeability defects in microcirculation
ARDS, GUT, Hepatic, renal failure
Problem
A 23 year old man
had a perforated
appendix. Three
days post op this
was his temperature
chart. What is your
interpretation.
Problem
What is your choice for antibiotic
prophylaxis for
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colorectal surgery
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biliary surgery
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upper GI surgery
Problem
A 75 year old diabetic had an operation for
perforated diverticular disease. His wound
was found to be infected on the 5th POD.
What factors may have contributed to this?