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12 Cards in this Set

  • Front
  • Back
T or F
The mortality of septic shock approaches 50% globally

Gram neg organisms are more common than gram pos in septic shock

Pathogens are identified in 30% of pts

Primary source of infection is respiratory
T
F (S aureus is commonest)
F (70%)
T (36%, followed by bloodstream 20% then intraabdo 19%)
What is the definition of SIRS

How does sepsis differ from SIRS

How does sepsis differ from severe sepsis
Two or more of the following:
Temp >38 or <36
HR >90
RR>20 or PCO2 <32
WCC>12 or <4 or >10% immature band cells

Sepsis = SIRS + documented infection site

Severe sepsis = sepsis + hypoperfusion (hypotension or lactate elevation)
Define septic shock
Severe sepsis with PERSISTENT hypotension despite adequate fluid resuscitation
T or F
Regarding septic shock, elevated lactate level is correlated with higher mortality rate

Abdo CT is helpful in septic shock in the absence of identified focus

If there is an altered mental state, LP should never be undertaken

Standardised ED guidelines focussing on haemodynamic resuscitation and early ab therapy have not reduced mortality
T
T
F (this would be an indication for LP unless contraindicated by clinical status)
F (mortality is reduced and compliance with recommended therapy improves)
What are the components of early goal directed therapy
adequate vol replacement followed by vasopressor and inotropic therapy aimed at maintaining:
- MAP >65mmHg
- U/O>0.5ml/kg/hr
- +/- SCVO2 >70%
When should you consider central lines and art pressure monitoring in severe sepsis

When is fluid resuscitation adequate
Pt who remain hypotensive, acidotic or oliguric after 2L of crystalloid

Fluid resus should continue til a CVP = 8-12mmHg
Should vasopressor therapy with NA ever be commenced concurrently with fluid resus
yes, in the presence of profound hypotension. Also when fluid resus fails to restore tissue perfusion eg MAP, lactate and U/O do not normalise
With regards to the EGDT study by RIvers, which is incorrect:
Red cell transfusion to HCT >30% and dobutamine infusion to improve C/O in pts who fail to achieve SCVO2>70% with other measures improved mortality

Mortality rate for sepsis was equivalent to Australian rate
T (other studies have not demonstrated survival benefit and have shown potential harm; RBC transfusion only recommended if Hb 7-9)
F (rates were substantially higher)
Why is intubation and ventilation with sedation and paralysis beneficial in septic shock
Minimises O2 consumption, should be considered early in pts with resp acidosis, hypoxia or persistent haemodynamic compromise
Low tidal vol 6ml/kg with PEEP <30cmH2O recommmended
With regards to ab therapy, T or F
Ab admin w/in one hr of onset of hypotension is associated with increased survival

For every hr after the onset of hypotension, the mortality rate rises by 3% for each hr of delay of commencement of ab

Unknown source should be treated with fluclox 2g QID + gentamicin 4-6mg/kg daily

Neutropenic pts should be treated with fluclox, gent and vanc
T
F (8% per hr for 6 hrs)
T
F (ceftaz and vanc) - follow local guidelines
Source control is an important part of the management of sepsis/septic shock. Give examples of for which it is immediate and urgent.
1. necrotising fasciitis
2. GI perforation (except contained diverticulitis)
3. Biliary tract obstruction (ERCP or percutaneous cholecystostomy)
4. Ureteric obstruction (perc nephrostomy)
Regarding additional therapies in the management of sepsis/septic shock, which is incorrect
1. IV steroids are beneficial in pts with severe septic shock
2. activated protein C has been shown to reduce mortality in septic patients with organ dysfunction
3. glycaemic control may be relevant
1. False - only pt with relative adrenal insufficiency (e.g. those on regular steroid) have been shown to improve survival - in this group give 100mg hydrocort early
2. T - it is indicated in those at high risk of death with LOW risk of bleeding/need for surgery