Sepsis and Septic Shock Flashcards
SIRS criteria
temp <36 or >38
HR > 90
RR > 22 or PaCO2 <32
WBC >12,000 or <4,000 or 10% bands
sepsis =
SIRS + infection
severe sepsis =
sepsis + end organ damage
septic shock =
severe sepsis + hypotension
sepsis definition
life threatening organ dysfunction caused by dysregulated host response to infection
how can organ dysfuction be identified?
acute change in total SOFA score > 2 points consequent ot the infection
how can septic shock be identified?
Septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP > 65 mmHg and having a serum lactate of >2 mmol/l despite adequatevolume resuscitation.
what is the hospital mortality of patients with septic shock?
40%
how to calculate SOFA score
hypotension, systolic BP < 100
altered mental status
tachypnoea RR > 22
body defence mecahnisms
physical barrier - skin mucosa, epithelial lining
innate immune system - IgA in GIT, dendritic cells/macrophages
adaptive immune system - lymphocytes, immunoglobulins
patients with sepsis have an uncontrolled inflammatory response. what features are consistent with immunosuppression?
loss of delayed hypersensitivity
inability to clear infection
predisposition to nosocomial infection
change in sepsis syndrome over time
increase in inflammatory mediators then there is a shift to an anti-inflammatory immunosuppressive phase
name the 3 phases in the pathogenesis of sepsis
release of bacterial toxins
release of mediators
effects of specific excessive mediators
bacterial invasion of the body tissues is a source of what?
dangerous toxins
name the commonly released gram negative toxins
lipopolysaccharide (LPS)
name the commonly released gram positive toxins
microbial associated molecular pattern: lipoteichoic acid, muramyl dipeptides
super antigens: staphylococcal toxic shock syndrome, streptococcal exotoxins
name the 3 components of the release of mediators in sepsis
effects of infections due to endotoxin release
effects of infections due to exotoxin release
mediator role on sepsis (Th1 vs Th2)
draw a diagram showing effects of infections due to endotoxin release
LPS needs an LPS-binding protein to bind to macrophages
LTA do not need these
draw a diagram to show the effects of infections due to exotoxin release
pro-inflammatory response
small amounts of super antigens will cause a large number of mediators to be secreted: cascade effect
what is the mediator role on sepsis?
pro-inflammatory
causes inflammatory response that characterises sepsis
compensatory anti-inflammatory reaction can cause immunoparalysis
describe the effects of pro-inflammatory mediators
- Promote endothelial call – 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
describe the effects of anti-inflammatory mediators
- Inhibit TNF alpha
- Augment acute phase reaction
- Inhibit activation of coagulation system
- Provide negative feedback mechanisms to pro-inflammatory mediators
clinical features of sepsis: nervous system
altered consciousness
confusion
psychosis
clinical features of sepsis: respiratory
tachypneoa
PaO2 <70
<90%
clinical features of sepsis: liver
jaundice
increased liver enzymes
decreased albumin
increased prothrombin
clinical features of sepsis: blood
decreased plateletes
increased PT/APTT
decreased protein C
increased d-dimer
clinical features of sepsis: cardiac
tachycardia
hypotension
clinical features of sepsis: renal
oliguria
anuria
increased creatinine
clinical features of sepsis: general
fever >38
hypothermia <36
hyperglycaemia > 8 mmol/l
inflammatory variables in sepsis
leucocytosis WCC > 12,000/ml leucopoenia WCC < 4,000/ml normal WCC with >10% immature high CRP high procalcitonin
haemodynamic variables in sepsis
arterial hypotension - systolic < 90 or MAP < 70
SvO2 > 70%
organ dysfunction variables in sepsis
arterial hypoxaemia PaO2/FiO2 < 50mmHg oliguria < 0.5ml/kg/h creatinine increase coagulation abnormalities PT > 1.5 or APTT > 60s ileus thrombocytopaenia <150,000/ml hyperbilirubinaemia
tissue perfusion variables in sepsis
high lactate
skin mottling and reduced capillary perfusion
how can the host affect sepsis presentation?
• Age
• Co-morbidities
o COPD, DM, CCF, CRF, disseminated malignancy
• Immunosuppression
o Acquired – HIV/AIDS
o Drug induced – steroids, chemotherapeutic agents, biologics
o Congenital – agammaglobulinaemia, phagocytic defects, defects in terminal
complement component
• Previous surgery – splenectomy
how can the organism affect sepsis presentation?
gram positive vs gram negative
virulence factors - MRSA, toxin secretion, ESBL, KPC, NDM-1
bioburden
how can the environment affect sepsis presentation?
occupation
travel
hospitalisation
sepsis 6
high flow oxygen IV antibiotics IV fluids Blood cultures Serum lactate Urine output
antibiotic guidance in sepsis 6
o Based on working diagnosis from history and examination
o Local antibiotic guidelines
o Consider allergy
o Consider previous MRSA, ESBL, CPE
o Consider antibiotic toxicity/interactions
IV fluids in sepsis 6
30ml/kg
in sepsis, if there is a spike in temperature what should you do?
take another set of blood cultures
what is serum lactate a marker of?
generalised hypoperfusion/sever sepsis/poorer prognosis
type A serum lactate shows?
hypoperfusion
type B serum lactate shows?
mitochondrial toxins
alcohol
malignancy
metabolism errors
of the available biomarkers which one has the most support to identify adverse outcomes in sepsis?
lactate
what is urine output a measure of?
renal dysfunction
when would you consider a HDU referral in a septic patient?
- Low BP responsive to fluids
- Lactate > 2 despite fluid resus
- Elevated creatinine
- Oliguria
- Liver dysfunction, bil, PT, Plt
- Bilateral infiltrates, hypoxaemia
when would you consider a ITU referral in a septic patient?
When to Consider ITU Referral
• Septic shock
• Multi-organ failure
• Requires sedation, intubation and ventilation
