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Flashcards in Microbiology Severe Sepsis Deck (41)
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1

Infection

An infection is the detrimental colonization of a host organism by a microbe

2

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

3

Sepsis

Clinical evidence of infection, plus evidence of a systemic response to infection

4

Infection plus SIRS =

Sepsis

5

Examples of infection plus SIRS leading to Sepsis

Infection – Dysuria +/- bacteruria
SIRS – Fever, tachycardia
Sepsis – Dysuria +/- bacteruria, Fever, tachycardia

6

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

7

Sepsis Pathogenesis

Bacteria/Immune csystem cells and Complement:
Mediators:
• Tissue damage
• Coagulopathy
• Immunosuppresion
• Vascular changes
• Cardiac depression
• Control of infection

8

Sepsis Pathogenesis steps

1. Invasion
2. Recognition
3. Amplification
4. End-organ effects

9

Recognition

Cell pathogen interaction through pattern recognition receptors

10

Pathogen Complement interaction leading to Complement activation

Alternative pathway, Complement binding pathogen binding
MB – Lectin pathway, Acute phase protein
Classical pathway, Antibody antigen comples

11

Lipid mediators of inflammation

Protaglandins
Leukatrienes
Platelets activating factor (PAF)

12

Proinflammatory cytokines e.g.

TNFalpha
IL-1
IL-6

13

Secondary Mediators

Complement system
Coagulation cascade
Nitric Oxide
Acute phase proteins

14

Complement activation

Oponisatino of pathogen
Lysis of pathogen
Recruitment of inflammatory cells

15

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

16

Platelet adhesion to vascular endothelium stimulated by

PAF

17

TNFalpha and IL-1 causes

Release of Tissue factor (thromboplastin) from endothelial cells leading to activation of coagulation cascade – disseminated intravascular coagulation

18

Coagulopathy leads to

Occlusion of microcirculation causing hypo-perfusion then organ failure

19

Cardiac Changes → Initially

High Cardiac Output – Classic ‘bounding pulse’ of sepsis

20

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

21

Toxic substances released by cells of the immune system

• Nitric Oxide
• Oxygen radicals
• Enzymes
• Toxic substances released by pathogens

22

Tissue damage due to

Toxic substances released by cells of the immune system

23

Mortality

Severe sepsis – 30%
Septic Shock 60%

24

Risk Factors for Severe Sepsis

Immunosuppression
Comorbidity
Age (extremes of)
Invasive devises
• Vascular
• Surgical
• Ventilatory
Use of antimicrobials

25

Defining the severity


Sepsis
Severe sepsis
Septic shock
Multiple Organ Failure

26

Sepsis

Clinical evidence of infection, plus evidence of a systemic response to infection

27

Severe sepsis

Sepsis with organ dysfunction, hypoperfusion or hypotension

28

Septic shock

Sepsis with hypotension unresponsive to fluid resuscitation

29

Systemic inflammatory response syndrome 4 criteria

Temp >38oC or 12 or 14)

30

Other markers in Systemic inflammatory response syndrome

Raised CRP
Reduced platelets

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