Sepsis and Septic Shock Flashcards
Sepsis definition [2]
- Life threatening organ dysfunction
- Caused by a dysregulated host response to infection
What defines septic shock in the model? [2]
- severe sepsis and hypotension
Clinical definition of septic shock [2]
What is hospital mortality of patients with septic shock?
Criteria of septic shock:
> > 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?
How many criteria is associated with greater risk of poor outcome?
> > Hypotension systolic BP <100 mmHg
altered mental status - confusion
Tachypnoea RR >22/min
- at least 2 suggests greater risk of poorer outcome)
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 sepsis associated mortality and cost? [6]
SEPSIS 6 Give 3 Oxygen IV Ab IV fluid challenge
Take 3
Bloods
Lactate
Urine output
What is the bodys defences against sepsis?
3 main headings
> Physical barrier: skin, mucosa, epithelial lining
> innate immune system: IgA in GI tract, dendritic cells/macrophages
> adaptive immune system - lymphocytes, immunoglobulins
Pathophysiology of sepsis [4]
Sepsis originates from breach of host barrier.
Organism enters bloodstream creating septic state
»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?
Define [1]
Name commonly released toxins by gram +ve [1] bacteria
Name 2 commonly released toxins by gram -ve bacteria
-bacterial invasion into body tissues is source of dangerous toxins
-commonly released toxins:
>gram +ve (lipopolysaccharide)
>gram -ve (MAMP, superantigens)
Discuss phase 2: release of mediators in response to infection?
Endotoxin vs Exotoxin release
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)
Discuss phase 3: effects of specific excessive mediators?
Name 6 effects of pro-inflammatory mediators
Name 4 effects of anti-inflammatory mediators
Pro-inflammatory mediators
- promote endothelial cell (leukocyte adhesion)
- release of arachidonic acid metabolites
- complement activation
- vasodilation 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? [2]
- Immunoparalysis with uncontrolled infection
- multi organ failure
What are some general features of sepsis? [6]
- 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 inflammatory variables in sepsis? [5]
- 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? (3)
- Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
- SvO2 >70%