Sepsis Flashcards
Define sepsis and septic shock using the Sepsis -3 guidelines
Sepsis
- life-threatening organ dysfunction (SOFA) caused by dysregulated host response to infection
Septic shock
- sepsis with persisting hypotension requiring
vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation
What is the mortality of patients with sepsis/septic shock?
SOFA 2+ have general mortality 10%
Septic shock hospital mortality 40%
What is the qSOFA system?
Hypotension - systolic <100
Altered mental status
Tachypnoea >22/min
2+ indicates greater risk of poor outcome
Consider intensive care
What is the general pathogenesis/physiology of sepsis
Bacteria overcomes host barriers (physical, innate, adaptive)
Three phases in the pathogenesis of sepsis:
- release of bacterial toxins
- release of mediators
- effects of specific excessive mediators
Uncontrolled inflammatory response
Initial increase in inflammatory mediators
Later shift towards anti-inflammatory/immunosuppressive
What are some commonly released bacterial toxins in the first stage of sepsis?
Gram negative
- LPS
Gram positive
- MAMP (LTA, muramyl dipeptides)
- superantigens
What happens in the second stage of sepsis?
Endotoxin release
Exotoxin release - pro-inflammatory response
- small amounts of superantigens > large mediators secreted > cascade effect
What happens in the third stage of sepsis?
Pro-inflammatory vs anti-inflammatory mediators
Pro
- Promote endothelial cell-leukocyte adhesion
- Release of arachidonic acid metabolites
- Complement activation
- Vasodilatation of blood vessels by NO
- Increase coagulation by release of tissue factors and membrane coagulants
- Cause hyperthermia
Anti
- Inhibit TNF alpha
- Augment acute phase reaction
- Inhibit activation of coagulation system
- Provide negative feedback mechanisms to pro-inflammatory mediators
How does sepsis proceed depending on more pro-inflammatory vs more anti-inflammatory
Pro
- septic shock with multiorgan failure and death
Anti
- immunoparalysis with uncontrolled infection and multiorgan failure
Describe the clinical presentation of sepsis and septic shock - symptoms/signs/basic investigation results
Generalised features; example fever, hypothermia, tachycardia, altered mental status, hyperglycaemia etc
Inflammatory variables; example leucocytosis, elevated C reactive protein, elevated procalcitonin etc
Haemodynamic variables; example hypotension (systolic <90 or MAP <70), SvO2<70%, tachycardia, tachypnoea
Organ dysfunction variables; example, oliguria, coagulation abnormalities, ileus, thrombocytopenia etc
Tissue perfusion variables; example high lactate, skin mottling, etc
What host variables can affect the presentation?
Age
Co-morbidities
Immunosuppression (AIDS, drug-induced, congenital)
Previous surgery e.g. splenectomy
What organism variables can affect the presentation?
Gram + vs -
Virulence factors e.g. MRSA, toxin secretion
Bioburden
Outline the principles of clinical management of sepsis using Sepsis 6
Take 3
- blood cultures
- blood lactate
- urine output
Give 3
- IV fluid
- oxygen (aim for 94-98 sat)
- IV antibiotics
Appreciate importance of the individual components of Sepsis 6 - why is each important?
Cultures - to make microbiological diagnosis
- take two sets if spike in temperature
Lactate - marker of generalised hypoperfusion/severe sepsis/poorer prognosis
Urine output - low is a marker of renal dysfunction
When to consider HDU referral?
Low BP responsive to fluids Lactate >2 despite fluid resuscitation Elevated creatinine Oliguria Liver dysfunction, Bil, PT, Plt Bilateral infiltrates, hypoxaemia
When to consider ITU?
Septic shock
Multi-organ failure
Requires sedation, intubation and ventilation
