Sepsis Flashcards
What are the 4 stages of sepsis?
SIRS-systemic inflammatory response syndrome
Sepsis
Severe sepsis
Septic shock
Define sepsis
SIRS+infection
Systemic illness caused by microbial invasion of normally sterile parts of the body.
Define severe sepsis
Sepsis with organ dysfunction
What is septic shock?
Sepsis with sustained hypotension (low BP) not improved by fluids, vasopressors required to maintain MAP>65mmHg and serum lactate >2mmol.
What are the qSOFA criteria?
2 or more needed of:
Hypotension (systolic BP< 100mmHg)
Altered mental state
Tachypnea RR>22/min
What is an antimicrobial delay and what does it mean?
This is the time it takes to give the patient antibiotics, the longer the antimicrobial delay the worse the prognosis.
Every hour increases mortality by 7.6%
How does sepsis occur?
Pathogens breach the host barrier (either physically or immunologically) and enter the blood stream. Any patient is then not able to clear the infection and there is an uncontrolled response.
1st bacterial toxins are released which causes inflammation, then mediators released then specific excessive mediators are released causing anti-inflammatory immunosuppressive phase.
What are the potential features of sepsis?
Fever (>38) or hypothermia (<36) tachycardia (>90bpm) tachypnoea (>22/min) altered mental state hyperglycaemia (>8mmol/l) in absence of diabetes) jaundice increase creatinine high or low wcc (>12000 or <4000), high CPR, high procalcitonin Hyperbilirubinemia high lactate
What is the treatment of sepsis?
IV Antibiotics
IV fluids
Oxygen (aim for 94-98%)
Take blood cultures, blood lactate and measure urine output.
What 3 do you give in sepsis treatment?
IV fluids
IV antibiotics
Oxygen (aim for 94-98%)
What 3 things do you take in Sepsis treatment? why are they taken?
Blood cultures- make microbial diagnosis
Blood lactate- marker of generalised hypoperfusion/severe sepsis/poorer prognosis
Measure urine output- low urine output is marker or renal dysfunction
A definition of sepsis.
Sepsis - a life-threatening organ dysfunction caused by dysregulated host response to infection.
What are the effects of pro-inflammatory specific excess mediators?
Promote adhesion of endothelial cells and leukocytes
Release of arachidonic acid metabolites
Complement activation
Vasodilation of blood vessels by NO
Increase coagulation by release of tissue factors and membrane coagulants
Hyperthermia
What do anti-inflammatory specific excessive mediators cause?
Inhibit TNF-alpha so reduce temp
Augment acute phase reaction
Inhibit activation of coagulation system
Provide negative feedback mechanisms to pro-inflammatory mediators