Microbiology Severe Sepsis Flashcards Preview

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Flashcards in Microbiology Severe Sepsis Deck (41)
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1
Q

Infection

A

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

2
Q

SIRS (systemic inflammatory response syndrome)

A

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
Q

Sepsis

A

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

4
Q

Infection plus SIRS =

A

Sepsis

5
Q

Examples of infection plus SIRS leading to Sepsis

A

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

6
Q

Defining the severity of sepsis

A
  • 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
Q

Sepsis Pathogenesis

A
Bacteria/Immune csystem cells and Complement:
Mediators:
•	Tissue damage
•	Coagulopathy
•	Immunosuppresion
•	Vascular changes
•	Cardiac depression
•	Control of infection
8
Q

Sepsis Pathogenesis steps

A
  1. Invasion
  2. Recognition
  3. Amplification
  4. End-organ effects
9
Q

Recognition

A

Cell pathogen interaction through pattern recognition receptors

10
Q

Pathogen Complement interaction leading to Complement activation

A

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

11
Q

Lipid mediators of inflammation

A

Protaglandins
Leukatrienes
Platelets activating factor (PAF)

12
Q

Proinflammatory cytokines e.g.

A

TNFalpha
IL-1
IL-6

13
Q

Secondary Mediators

A

Complement system
Coagulation cascade
Nitric Oxide
Acute phase proteins

14
Q

Complement activation

A

Oponisatino of pathogen
Lysis of pathogen
Recruitment of inflammatory cells

15
Q

Vascular changes

A
  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
Q

Platelet adhesion to vascular endothelium stimulated by

A

PAF

17
Q

TNFalpha and IL-1 causes

A

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

18
Q

Coagulopathy leads to

A

Occlusion of microcirculation causing hypo-perfusion then organ failure

19
Q

Cardiac Changes → Initially

A

High Cardiac Output – Classic ‘bounding pulse’ of sepsis

20
Q

Cardiac Changes → Later

A

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

21
Q

Toxic substances released by cells of the immune system

A
  • Nitric Oxide
  • Oxygen radicals
  • Enzymes
  • Toxic substances released by pathogens
22
Q

Tissue damage due to

A

Toxic substances released by cells of the immune system

23
Q

Mortality

A

Severe sepsis – 30%

Septic Shock 60%

24
Q

Risk Factors for Severe Sepsis

A
Immunosuppression
Comorbidity
Age (extremes of)
Invasive devises
•	Vascular
•	Surgical
•	Ventilatory
Use of antimicrobials
25
Q

Defining the severity

A

Sepsis
Severe sepsis
Septic shock
Multiple Organ Failure

26
Q

Sepsis

A

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

27
Q

Severe sepsis

A

Sepsis with organ dysfunction, hypoperfusion or hypotension

28
Q

Septic shock

A

Sepsis with hypotension unresponsive to fluid resuscitation

29
Q

Systemic inflammatory response syndrome 4 criteria

A

Temp >38oC or 12 or 14)

30
Q

Other markers in Systemic inflammatory response syndrome

A

Raised CRP

Reduced platelets

31
Q

Future markers in Systemic inflammatory response syndrome

A

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

32
Q

Early signs of Hypo-perfusion

A

Respiratory alkalosis – high RR blowing off Co2

Oliguria

33
Q

Oliguria in sepsis explanation

A

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

34
Q

Recognition of organ dysfunction

A
  • 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
35
Q

Score used to look at organ dysfunction

A

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

36
Q

Treatment

A
  1. Resuscitation
  2. Antibiotics
  3. Treat focus to infection
  4. Monitor and minimise organ damage
37
Q

Resuscitation

A
  • Fluid resuscitation
  • Oxygen +/- ventilation
  • Vasopresser agents (in high cardiac output phase)
  • Inotropic agents (in cardiac depression stage)
38
Q

Antibiotics

A

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

• IV therapy

39
Q

Minimize organ damage

A

• Replace clotting factors and platelets where appropriate

40
Q

Adjunctive therapy

A

Adjunctive therapy

41
Q

Steroids

A

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

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