Flashcards in Microbiology Severe Sepsis Deck (41)
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Infection
An infection is the detrimental colonization of a host organism by a microbe
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SIRS (systemic inflammatory response syndrome)
Defined as two or more of:
• Temp >38 oc or 90 bpm
• Respiratory rate >20 or PaCo2 12 or 4 x 109 cells/L
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Sepsis
Clinical evidence of infection, plus evidence of a systemic response to infection
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Infection plus SIRS =
Sepsis
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Examples of infection plus SIRS leading to Sepsis
Infection – Dysuria +/- bacteruria
SIRS – Fever, tachycardia
Sepsis – Dysuria +/- bacteruria, Fever, tachycardia
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Defining the severity of sepsis
• Infection plus SIRs leading to Sepsis
• Plus Hypoperfusion or organ dysfunction or hypotension leads to severe sepsis
• Severe sepsis plus hypotension refractory to fluid leads to septic shock
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Sepsis Pathogenesis
Bacteria/Immune csystem cells and Complement:
Mediators:
• Tissue damage
• Coagulopathy
• Immunosuppresion
• Vascular changes
• Cardiac depression
• Control of infection
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Sepsis Pathogenesis steps
1. Invasion
2. Recognition
3. Amplification
4. End-organ effects
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Recognition
Cell pathogen interaction through pattern recognition receptors
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Pathogen Complement interaction leading to Complement activation
Alternative pathway, Complement binding pathogen binding
MB – Lectin pathway, Acute phase protein
Classical pathway, Antibody antigen comples
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Lipid mediators of inflammation
Protaglandins
Leukatrienes
Platelets activating factor (PAF)
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Proinflammatory cytokines e.g.
TNFalpha
IL-1
IL-6
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Secondary Mediators
Complement system
Coagulation cascade
Nitric Oxide
Acute phase proteins
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Complement activation
Oponisatino of pathogen
Lysis of pathogen
Recruitment of inflammatory cells
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Vascular changes
1. PAF causes increased platlet activation and adhesion
2. TNFapha and C5a cause increased vascular permeability
3. Nitric oxide causes loss of contractility f vascular smooth muscle
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Platelet adhesion to vascular endothelium stimulated by
PAF
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TNFalpha and IL-1 causes
Release of Tissue factor (thromboplastin) from endothelial cells leading to activation of coagulation cascade – disseminated intravascular coagulation
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Coagulopathy leads to
Occlusion of microcirculation causing hypo-perfusion then organ failure
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Cardiac Changes → Initially
High Cardiac Output – Classic ‘bounding pulse’ of sepsis
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Cardiac Changes → Later
As cardiac muscle becomes affected by organ hypoperfusion and toxic products, cardiac output falls – patient becomes cold, clammy, resembling patient with cardiogenic shock
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Toxic substances released by cells of the immune system
• Nitric Oxide
• Oxygen radicals
• Enzymes
• Toxic substances released by pathogens
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Tissue damage due to
Toxic substances released by cells of the immune system
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Mortality
Severe sepsis – 30%
Septic Shock 60%
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Risk Factors for Severe Sepsis
Immunosuppression
Comorbidity
Age (extremes of)
Invasive devises
• Vascular
• Surgical
• Ventilatory
Use of antimicrobials
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Defining the severity
Sepsis
Severe sepsis
Septic shock
Multiple Organ Failure
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Sepsis
Clinical evidence of infection, plus evidence of a systemic response to infection
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Severe sepsis
Sepsis with organ dysfunction, hypoperfusion or hypotension
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Septic shock
Sepsis with hypotension unresponsive to fluid resuscitation
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Systemic inflammatory response syndrome 4 criteria
Temp >38oC or 12 or 14)
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