Sepsis and Septic Shock

Question 1

Define sepsis

Answer 1

Life threatening organ dysfunction caused by dysregulated host response to infection

Question 2

Define septic shock

Answer 2

Clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation

Question 3

What is the mortality rate of those with septic shock?

Answer 3

40%

Question 4

What are the body’s defences against sepsis?

Answer 4

Physical barrier - skin, mucosa or epithelial lining

Innate immune system - IgA in GI tract, dendritic cells/macrophages

Adaptive immune system - lymphocytes and immunoglobulins

Question 5

How does sepsis occur?

Answer 5

Breach of host barrier, whether physical or immunological. Organism enters bloodstream creating a septic state

Question 6

What is the pathophysiology of infection?

Answer 6

Uncontrolled inflammatory response. They have features consistent with immuosuppression such as loss of delayed hypersensitivity, inability to clear infection, predisposition to nosocomial infection

Question 7

What are the three phases in the pathogenesis of sepsis?

Answer 7

1, Release of bacterial toxins

2. Release of mediators
3. Effects of specific excessive mediators

Question 8

What occurs during bacterial toxin release?

Answer 8

Bacterial invasion into body tissue = toxin release

Question 9

What are the two types of mediators released?

Answer 9

Pro-inflammatory mediators which cause inflammatory response that characterises sepsis

Compensatory anti-inflammatory reaction that causes immunoparalysis

Question 10

What are the effects of pro-inflammatory mediators?

Answer 10

Promote endothelial cell-leukocyte adhesion
Release of arachidonic acid metabolites
Complement activation
Vasodilation of blood vessels by NO
Increase coagulation by release of tissue factors and membrane coagulants
Causes hyperthermia

Question 11

What are the effects of anti-inflammatory mediators ?

Answer 11

Inhibit TNF alpha, augment acute phase reaction, inhibit activation of coagulation system, provide negative feedback mechanisms to pro-inflammatory mediators

Question 12

What occurs when there is more pro inflammatory mediators to anti inflammatory mediators?

Answer 12

Septic shock with multiorgan failure and death

Question 13

What occurs when there is more compensatory anti-inflammatory mediators?

Answer 13

Immunoparalysis with uncontrolled infection and multiorgan failure

Question 14

What are the clinical features of sepsis?

Answer 14

Host, organism and environment

Question 15

What are the symptoms of organ dysfunction?

Answer 15

Altered consciousness, confusion, psychosis, tachypnoea, jaundice, tachycardia, hypotension, oliguria, anuria, fever, rigors, chill, cold sweats, night sweats, hypothermia, tachycardia, tachypnoea, hyperglycaemia

Question 16

What tests should be performed?

Answer 16

Blood cultures, blood lactate and measure urine output

Question 17

What treatment should be given?

Answer 17

Oxygen sats, IV antibiotics, IV fluid challenge

Question 18

How much IV fluids should be given ?

Answer 18

30ml/kg

Question 19

When should HDU referral be considered?

Answer 19

Low BP responsive to fluids, lactate >2 despite fluid resuscitation, elevated creatinine, oliguria, liver dysfunction

Question 20

When should ITU referral be considered?

Answer 20

Septic shock, multi-organ failure, requires sedation, intubation and ventilation

Question 21

Sepsis 6

Answer 21

Take blood cultures, serum lactate levels and monitor urine levels
Give supplemental O2, IV antibiotics and IV fluids

Question 22

qSOFA scoring for Sepsis?

Answer 22

Altered mental state
RR>22/Min
SBP <100mmHg

2/3 = Poor outcome