Sepsis and Septic Shock Flashcards
Definition of sepsis? This isnt a clinical definition it is more about how it arises.
Systemic illness caused by microbial invasion of normally sterile parts of the body
Within the tradition model of sepsis, SIRS comes first before Sepsis, Severe Sepsis, and Septic shock. To have SIRS you need 2 or more of certain findings. What are these?
- Temp >38 or <36 degrees
- HR>90
- RR>20 or PaCO2 <32
- WBCs >12000 or <4000 or >10% bands
What defines sepsis in the model?
SIRS and infection
What defines Severe sepsis in the model?
Sepsis and end organ damage
What defines septic shock in the model?
severe sepsis and hypotension
what can cause SIRS?
- Pancreatitis
- Burns
- Trauma
Clinical definition of sepsis?
Life threatening organ dysfunction caused by dysregulated host response to infection
»Organ dysfunction identified as an acute change in total SOFA score >2 points
»SOFA score >2 reflects overall mortality risk of approx 10% in general hospital population with suspected infection
Clinical definition of septic shock?
Identified with clinical construct of sepsis with
> > persisting hypotension requiring vasopressors to maintain MAP >65mmHg
> > serum lactate of 2mmol/l despite adequate vol resus
> > hospital mortality of 40%
what 3 criteria constitute qSOFA (quick way of getting SOFA score, at least 2 suggests greater risk of poorer outcome)
> > Hypotension systolic BP <100 mmHg
altered mental status
Tachynpoea RR >22/min
Identifies patients likely to have prolonged ICU stay or die in hospital
why is quick intervention key in sepsis?
Chance of mortality increases with each hour of delay of antibiotic administering
What intervention is key in reducing mortality and cost?
SEPSIS 6
What is the bodys defences against sepsis?
> Physical barrier: skin, mucosa, epithelial lining
innate immune system: IgA in GI tract, dendritic cells/macrophages
adaptive immune system - lymphocytes, immunoglobulins
Sepsis originates from breach of host barrier. Organism enters bloodstream creating septic state
Pathophysiology of sepsis?
> > uncontrolled inflammatory response
immunosuppression features (loss of delayed hypersensitivity/unable to clear infection/predisposed to nosocomial infection)
Likely change of sepsis syndrome over time
(initial inc. in inflammatory mediators. Later shift towards anti-inflam immunosuppressive phase. Depends on patient health)
what are the 3 phases in pathogenesis of sepsis?
- release of bacterial toxins
- release of mediators
- effects of specific excessive mediators
Discuss phase 1: release of bacterial toxins?
-bacterial invasion into body tissues is source of dangerous toxins
-may/may not be neutralised and cleared by existing immune system
-commonly released toxins:
>gram -ve (lipopolysaccharide)
>gram +ve (MAMP, superantigens)
Discuss phase 2:release of mediators in response to infection?
Effects of infections due to endotoxin release
>LPS needs LPS-binding protein to bind to macrophages. LTA doesnt need a protein
Effects of infections due to exotoxin release
>pro-inflammatory response
>small amount of superantigens will cause lots of mediators to be secreted (cascade effect)
Mediator role on sepsis
>two types of mediators can be released
>pro-inflammatory mediators (eg Neutrophils, prostaglandins, TNF-a) causes inflammatory response that characterises sepsis
>compensatory anti-inflammatory reaction (interleukins, LPS-binding protein) can cause immunoparalysis
Discuss phase 3: effects of specific excessive mediators?
Pro-inflammatory mediators
- promote endothelial cell (leukocyte adhesion)
- release of arachidonic acid metabolites
- complement activation
- vasodilatiion of blood vessels by NO
- inc coagulation by release of tissue factors and membrane coagulants
- cause hyperthermia
Anti-inflammatory mediators
- Inhibit TNF alpha
- augment acute phase reaction
- inhibit activation of coagulation
- provide negative feedback mechanisms to pro-inflammatory mediators
What can over production of pro-inflammatory mediators lead to?
septic shock with multi organ failure and death
What can over production of anti-inflammatory mediators lead to?
Immunoparalysis with uncontrolled infection and multi organ failure
What are some general features of sepsis?
- Fever >38 degrees (chills, rigors, flushes, cold sweats)
- Hypothermia <36 degrees (esp in elderly/young/immunosuppressed)
- Tachycardia >90bpm
- Tachynpoea >20 breaths/min
- altered mental status (esp in elderly)
- Hyperglycaemia >8mmol/l in absence of diabetes
what are some inflammatory variables in sepsis?
- Leucocytosis (WCC>12000/ml)
- Leucopenia (WCC<4000/ml)
- Normal WCC with >10% immature forms
- high CRP
- High calcitonin
What are some haemodynamic variables in sepsis?
- Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
- SvO2 >70%
What are some organ dysfunction variables in sepsis?
-Arterial hypoxaemia (PaO2 <50mmHg)
-Oliguria (<0.5ml/kg/h)
-creatinine inc compared to baseline
-coag. abnormalities (PT>1.5/APTT>60s)
-Ileus
-Thrombocytopenia (<150000/ml)
Hyperbilirubinaemia
What are some tissue perfusion variables in sepsis?
- High lactate
- skin mottling and reduced capillary perfusion
