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Sepsis 3 2016 update

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Pollyanna Kellett

on 31 January 2017

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Transcript of Sepsis 3 2016 update

Describe updated sepsis definition
Understand significance of sepsis treatment
Understand and have skills to
screen
for sepsis
Define
actions
for patients with sepsis
Apply knowledge and understanding to clinical scenarios to enhance practice
Treating sepsis
Assessment: A to E, plan, monitoring, re-assessment and evaluation
Escalation: SBAR to appropriate team
Treatment: oxygen, fluids, antibiotics, vasopressors (drugs that cause vasoconstriction leading to increased SVR & BP eg noradrenaline, vasopressin)
inotropes (drugs that increase myocardial contractility eg adrenaline, dobutamine)
What is sepsis?
a life threatening condition arising when the body's response to an infection injures its own tissues and organs.
learning objectives
Screen, Recognise, Act
Sepsis UK
1) is NEWS 3 or above?
2) Could this be due to infection?
3) Is ONE red flag present?
VPU only
systolic <90 mmHg
hr >130 pm
rr >25 pm
needs oxygen to keep SpO2 >92%
non-blanching rash, mottled/ashen/cyanotic
no urine output > 18 hours
UO <0.5ml/kg/hr
lactate > 2 mmo/l
recent chemo
3 'in'
1) Administer oxygen
2) Give IV antibiotics
3) Give IV fluids
Learning about sepsis
Screening for sepsis
Action
Sepsis 3 2016 update
Marx G (2003) Fluid therapy in sepsis with capillary leakage. European Journal of Anaesthesiology. 20 (6) pp.426-442

Sepsis Trust (2016) Information for Professionals. Available at:Sepsistrust.org [accessed 20/08/16]

NICE (2016) Nice Guidelines NG51

JAMA (2016) Consensus Definition for Sepsis and Septic Shock. Available at: [accessed 20/11/16]
References
3 'out'
1) Take blood cultures
2) Check serum lactate
3) Measure urine output
JAMA: q sofa
Quick Sepsis-related Organ Failure Assessment
GCS < 15
SBP < 100
RR > 22
red flags:
Oxygen
An exaggerated inflammatory response throughout the body
Normal immune response to infection or trauma: vasodilation, leaky capillaries and clot formation
Inflammatory mediators released (histamine, cytokines, prostaglandins) into circulation causing widespread vasodilation
Blood vessels dilate causing blood pressure to plummet
Capillaries become increasingly permeable, allowing fluid to leak out of the circulation – produces hypovoleamia and therefore more hypotension
Coagulation system becomes activated forming micro-thrombi in small blood vessels – restricted blood flow to vital organs and tissues.
Clotting cascade inhibited: normally body breaks down clots by fibrinolysis and releases anti-inflammatory mediators BUT is sepsis the fibrinolysis is inhibited so patient bleeds.

Pathophysiology
Sepsis – an immune system-mediated collection of physiological responses to infection.
Common clinical signs: pyrexia, tachycardia, hypotension
BUT clinical course depends on the type and resistance of the infectious organism, the site and size of insult, and the genetically determined or acquired properties of patients immune system (BMJ, 2014)

Microbes:
Bacteria
Fungi
Viruses
(NIH 2014)

Blood cultures,treat with appropriate antimicrobials

Activation of the innate immune system results in complex series of responses, each amplifying further:
1) Pro-inflammatory cytokines (tumour necrosis factor (TNF), interleukins 1 and 6 are released – activate immune cells
2) proteases and nitric oxide (NO) are released – kill bacteria, cause vasodilation and increase capillary permeability, stop mitochondria from working
3) complement system is activated, activates leukocytes, attracting them to site of infection – directly attack the organism(phagocytes, cytotoxic T lymphocytes)

Vascular endothelium has major role in defence against invading organisms – it allows migration and adhesion of stimulated immune cells BUT also becomes porous to larger molecules eg proteins – causing tissue oedema
Clotting – increase in procoagulation factors eg plasminogen and tissue factor, plus the reduced circulating levels of natural anticoagulants

Endothelium & coagulation
Tissue oedema
Because of tissue and peri-capillary oedema, oxygen delivery is impaired -oxygen has to travel further to diffuse. Capillary diameter is reduced because of oedema, and because of the pro-coagulant state, capillary microthrombi form
Therefore organs become hypoxic – leading to lactic acidosis, cellular dysfunction and multi-organ failure

Organ Dysfunction

Due to vasodilation and increased capillary permeability, sepsis results in reduction in circulating volume
Initially increased heart rate causes cardiac output to increase to compensate and maintain perfusion pressures BUT as compensatory mechanism is exhausted, Hypovoleamia is compounded by reduced left ventricular contractility causing hypotension, hypo perfusion and shock

Shock

1. Initial: Hypoperfusion causes hypoxia. This leads to mitochondrial dysfunction. The cells become leaky and switch to anaerobic metabolism. This switch produces lactic acid and a resultant metabolic acidosis.
2. Compensatory: During this phase the body employs several mechanisms in an attempt to correct the metabolic upset of shock:
a. Hyperventilation: This will create a respiratory alkalosis in an attempt to neutralize the metabolic acidosis of shock returning the body to a normal pH or hydrogen ion concentration. Clearly if lung function or respiratory drive mechanisms are impaired this compensation will be less effective.
b. Catecholamine response: In response to hypotension, noradrenaline and adrenaline will be released in an attempt to maintain both SVR and CO (see formulaA and B.
c. Renin-angiotensin response: Vasopressin excretion is increased leading to fluid retention (to maintain circulating volume) and vasoconstriction.
3. Progressive: The mechanisms listed above can only compensate for worsening shock for so long. Eventually they will begin to fail. At this point cellular dysfunction begins to spiral out of control, metabolic acidosis worsens and the arteriolar and precapillary sphincters constrict such that blood remains in the capillaries. The pressure within the capillaries will increase. This, combined with membrane dysfunction, will lead to fluid loss into the extravascular interstitial spaces. This will further worsen the intravascular volume status.
4. Refractory: At this stage organs fail and the shock can no longer be reversed. Death normally occurs rapidly.
http://www.scottishintensivecare.org.uk/education/icm%20induction/shock/shock08.htm

NICE guidelines:
https://www.nice.org.uk/guidance/indevelopment/ng51/documents

Sepsis screening and sepsis 6
http://sepsistrust.org/wp-content/uploads/2016/07/Inpatient-adult-NICE-Final-1107-2.pdf
Conclusion

Describe updated sepsis definition
Understand significance of sepsis treatment
Understand and have skills to
screen
for sepsis
Define
actions
for patients with sepsis
Apply knowledge and understanding to clinical scenarios to enhance practice

Questions?
Why is sepsis important?

Sepsis kills 44,000 lives a year in UK
Sepsis costs NHS £2.5 billion a year
Early intervention saves lives, reduces length of stay and ICU admission
If YOU work with your Trust, together you could save 100 lives a year and £1.25 million a year for a typical DGH, just by getting the basics right!
UK sepsis trust screening tool templates: http://sepsistrust.org/wp-content/uploads/2016/07/Inpatient-adult-NICE-Final-1107-2.pdf
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