Microbiology Severe Sepsis

Question 1

Infection

Answer 1

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

Question 2

SIRS (systemic inflammatory response syndrome)

Answer 2

Defined as two or more of:
• Temp >38 oc or 90 bpm
• Respiratory rate >20 or PaCo2 12 or 4 x 109 cells/L

Question 3

Sepsis

Answer 3

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

Question 4

Infection plus SIRS =

Answer 4

Sepsis

Question 5

Examples of infection plus SIRS leading to Sepsis

Answer 5

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

Question 6

Defining the severity of sepsis

Answer 6

• 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

Question 7

Sepsis Pathogenesis

Answer 7

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

Question 8

Sepsis Pathogenesis steps

Answer 8

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

Question 9

Recognition

Answer 9

Cell pathogen interaction through pattern recognition receptors

Question 10

Pathogen Complement interaction leading to Complement activation

Answer 10

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

Question 11

Lipid mediators of inflammation

Answer 11

Protaglandins
Leukatrienes
Platelets activating factor (PAF)

Question 12

Proinflammatory cytokines e.g.

Answer 12

TNFalpha
IL-1
IL-6

Question 13

Secondary Mediators

Answer 13

Complement system
Coagulation cascade
Nitric Oxide
Acute phase proteins

Question 14

Complement activation

Answer 14

Oponisatino of pathogen
Lysis of pathogen
Recruitment of inflammatory cells

Question 15

Vascular changes

Answer 15

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

Question 16

Platelet adhesion to vascular endothelium stimulated by

Answer 16

PAF

Question 17

TNFalpha and IL-1 causes

Answer 17

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

Question 18

Coagulopathy leads to

Answer 18

Occlusion of microcirculation causing hypo-perfusion then organ failure

Question 19

Cardiac Changes → Initially

Answer 19

High Cardiac Output – Classic ‘bounding pulse’ of sepsis

Question 20

Cardiac Changes → Later

Answer 20

As cardiac muscle becomes affected by organ hypoperfusion and toxic products, cardiac output falls – patient becomes cold, clammy, resembling patient with cardiogenic shock

Question 21

Toxic substances released by cells of the immune system

Answer 21

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

Question 22

Tissue damage due to

Answer 22

Toxic substances released by cells of the immune system

Question 23

Mortality

Answer 23

Severe sepsis – 30%

Septic Shock 60%

Question 24

Risk Factors for Severe Sepsis

Answer 24

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

Question 25

Defining the severity

Answer 25

Sepsis
Severe sepsis
Septic shock
Multiple Organ Failure

Question 26

Sepsis

Answer 26

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

Question 27

Severe sepsis

Answer 27

Sepsis with organ dysfunction, hypoperfusion or hypotension

Question 28

Septic shock

Answer 28

Sepsis with hypotension unresponsive to fluid resuscitation

Question 29

Systemic inflammatory response syndrome 4 criteria

Answer 29

Temp >38oC or 12 or 14)

Question 30

Other markers in Systemic inflammatory response syndrome

Answer 30

Raised CRP

Reduced platelets

Question 31

Future markers in Systemic inflammatory response syndrome

Answer 31

Procalcitonin – differentiation response to bacterial infection from response to other pathogens

Question 32

Early signs of Hypo-perfusion

Answer 32

Respiratory alkalosis – high RR blowing off Co2

Oliguria

Question 33

Oliguria in sepsis explanation

Answer 33

Renal high need blood flow bt with hypo-perfusion blood shunted – Brain/lung prioritised there renal hypo-perfused and UO decreased

Question 34

Recognition of organ dysfunction

Answer 34

• Neuro: Altered consciousness; Confusion, lethargy, combatative, psychosis
• Cardiac/Lungs: (Tachypnoea), hypoxia, ARDS
• Liver: Jaundice, increased LFT, decreased albumin, increased prothrombin time
• Renal: Oliguria, increased creatinine, increased urea (occurs acutely)
• Abdominal: pain, ileus

Question 35

Score used to look at organ dysfunction

Answer 35

• SOFA score – looks at organs o0n an individual level to assess the damage.

Question 36

Treatment

Answer 36

1. Resuscitation
2. Antibiotics
3. Treat focus to infection
4. Monitor and minimise organ damage

Question 37

Resuscitation

Answer 37

• Fluid resuscitation
• Oxygen +/- ventilation
• Vasopresser agents (in high cardiac output phase)
• Inotropic agents (in cardiac depression stage)

Question 38

Antibiotics

Answer 38

• Treat empirically according to suspected focus of infection and host factors
→ Hospital versus community acquired
→ Immunocompetent or immunosuppressed

• IV therapy

Question 39

Minimize organ damage

Answer 39

• Replace clotting factors and platelets where appropriate

Question 40

Adjunctive therapy

Answer 40

Adjunctive therapy

Question 41

Steroids

Answer 41

High dose: no benefit
Low dose
• Initial trials suggested benefit in subset with relative adrenal insufficiency