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Sepsis and Septic Shock presentation 2021

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Sepsis and
Septic Shock
Module 4
Recognising and Responding to the
Deteriorating Patient
This Photo by Unknow Author is licensed under CC BY-SA
Learning outcomes
At the end of this session students will be able to:
•
•
•
•
Recognise the burden of sepsis
Examine the pathophysiology of sepsis
Examine the pathophysiology of shock
Differentiate between different types of shock, with
special focus on septic shock
• Discuss the treatment guidelines relating to the
management of septic shock
Session structure
Pre-session
work
Presentation
Post-session
work
Pre-session work (10’)
Watch Video 1 on Canvas
Sepsis is real
Sepsis mortality over the years
250,000 admission 2015 in UK
NCEPOD (2015) reported mortality was 28.9%
Sepsis Trust (2018) sepsis claims more live than lung cancer, bowel, breast
and prostate cancer combined.
Criteria and definitions over time
• Sepsis continuum 1991, 2004, 2008, 2012
• Red flags (Sepsis Trust 2015)
• Sepsis 3 consensuses (February 2016) Singer et al (2016)
• NICE mild, moderate and high risk criteria (August 2016)
• Surviving sepsis campaign (2016)
• Royal College of Physician (2017) NEWS 2
• Sepsis Trust (2018) Sepsis Manual
RCP 2017 and Sepsis Trust 2018
Definition of sepsis
“Sepsis is characterized by a dysregulated host response to infection
mediated by the immune system and resulting in organ dysfunction,
potentially multi-organ failure, shock and death”.
Sepsis identification criteria
1. Adult patient with suspect infection
2. Aggregate NEWS score of 5 and above
Let’s break it down
• Dysregulated host response to infection
• Mediated by the immune system
• Results in organ dysfunction
• Potentially multi-organ failure
• Potentially shock
• Potentially death
Let’s break it down
• Dysregulated host response to infection
• Mediated by the immune system
• Results in organ dysfunction
• Potentially multi-organ failure
• Potentially shock
• Potentially death
SEPSIS: Dysregulated host
response to infection
Dysfunction
Immune
system
Risk factors
Excessive
Systemic
activation of
inflammation
Overcompensation
Body response
Risk Factors for sepsis
•
•
•
•
•
•
•
•
•
•
Underlying malignancy
Age <65 years
Haemodialysis
Alcoholism
Diabetes mellitus
Recent surgery or other invasive
procedure
Breach of skin integrity
Indwelling lines or catheters
Intravenous drug use
Pregnancy or recent pregnancy
This Photo by Un under CC BY
Most “popular” causes of sepsis
Sepsis Trust Manual 2018
Let’s break it down
• Dysregulated host response to infection
• Mediated by the immune system
• Results in organ dysfunction
• Potentially multi-organ failure
• Potentially shock
• Potentially death
Intensive
Care
Sepsis criteria
2016- Sepsis 3
qSOFA calculator
Let’s break it down
• Dysregulated host response to infection
• Mediated by the immune system
• Results in organ dysfunction
• Potentially multi-organ failure
• Potentially shock
• Potentially death
Need a break?
good vessel capacity
How does
our body
maintain
blood
pressure?
Healthy cardiac function
appropriate blood
volume
Normal response to hypotension
(Woodrow, 2019)
• Baroreceptors in major arteries identify hypotension – hypothalamus/ pituitary/
adrenal axis is stimulated, causing a fight or flight response
• ACTH (Adrenocorticothrophic hormone) released from Pituitary gland,
stimulating adrenal production of adrenaline and noradrenaline, causing
vasoconstriction and increased heart rate, increasing BP.
• Increased glucocorticoid secretion
• Intrarenal hypotension initiates the renin-angiotensin- aldosterone system (RAAS)
• Renin (Kidney) activates Angiotensin (Liver) 1 – A1 causes mild vasoconstriction
and turns into A2 in the lungs
• A2 is a powerful vasoconstrictor and increases adrenal production of Aldosterone
• Aldosterone (adrenal glands) increases renal sodium reabsorbtion
• Intrarenal hypotension initiates the renin-angiotensin- aldosterone system (RAAS)
• Pituitary gland releases antidiuretic hormone (vasopressin), increasing water
reabsorption.
Vasoconstriction – reducing blood
vessel capacity
Body adjusts
to
hypotension!
Increased heart rate – increase
blood volume
Increased sodium reabsorption +
antidiuretic hormone – increase
blood volume
Stages of shock:
Initial (hypodynamic – poor cardiac output
causes systemic hypoperfusion and
kickstarts anaerobic metabolism)
Compensation (sympathetic nervous system
– fight of flight: tachycardia, tachypnoea,
oliguria, agitation, hyperglycaemia)
Progression (Hypotensive – parasympathetic
nervous system)
Refractory (multiorgan failure, no response
to treatments)
Perfusion and system failures due to shock
Perfusion failure (causes
depend on type of shock)
System failure
• Insufficient circulation
volume
• Inadequate cardiac output
• Excessive peripheral
vasodilatation
• Perfusion issues cause
anaerobic metabolism,
metabolic acidosis and
increased lactate, which in
turn lead to
• Multi-organ failure
Septic Shock
A subset of sepsis
• Characterised with profound circulatory,
cellular and metabolic abnormalities
Clinically can be identified by:
1. the need for vasopressors to keep
MABP>65mmHg
2. Lactate> 2 mmol/l
• The presence of 1 and 2 in the absence of
hypovolaemia (or despite adequate fluid
resuscitation)
• Associated with hospital mortality is
greater than 40%
Septic Shock
A severe and potentially fatal condition that occurs
when sepsis progresses to life threatening low blood
pressure.
This in turn can lead to respiratory or heart failure,
stroke, failure of other organs such as Kidneys, Bowel
and liver and can lead ultimately to death.
Signs
• Low blood pressure
• Decreased urine output
• Acute confusion
• Dizziness
• Issues with breathing in the regulation and the rate
• Cyanosis of the lips, fingers, toes etc.
How does the body react to Septic shock
Early
intervention
is key
The red flags of the Sepsis 6
• Objective evidence of new or altered mental state Systolic BP ≤ 90 mmHg (or
drop of >40 from normal)
• Heart rate ≥ 130 per minute
• Respiratory rate ≥ 25 per minute Needs O2 to keep SpO2 ≥ 92% (88% in COPD)
• Non-blanching rash / mottled / ashen / cyanotic
• Lactate ≥ 2 mmol/l
• Recent chemotherapy
• Not passed urine in 18 hours
(0.5mls?kg/hr if catheterised)
The Amber Flags for the Sepsis 6
(send blood, senior review within 1 hour)
• Relatives concerned about mental status
• Acute deterioration in functional ability
• Immunosuppressed
• Trauma / surgery / procedure in last 8 weeks
• Respiratory rate 21-24
• Systolic BP 91-100 mmHg
• Heart rate 91-130 or new dysrhythmia
• Temperature
• Clinical signs of wound infection
Treatment of sepsis and septic shock (nursing
perspective)
prevention
• When possible,
prevent
infection
infection
management
initial
resuscitation
hemodynamic
supporting
supportive
nursing care
• control of the
infection source
and
transmissionbased
precautions.
• Early
recognition of
the
deteriorating
patient,
diagnosis of
severe sepsis,
seeking further
assistance, and
initiating early
resuscitation
measures.
• improving both
tissue
oxygenation
and circulation
• nutrition,
mouth and eye
care, and
pressure ulcer
prevention and
management.
Post-session activities
• Complete Activity 1 and 2 on Canvas
• Read the NICE guidelines on sepsis
• Read the Sepsis Manual
• Read the Nursing Considerations for the SSC
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