Sepsis Flashcards

1
Q

What is sepsis?

A

Life-threatening organ dysfunction caused by dysregulated host response to infection i.e. host response leads to injury of hosts own tissues

Considered a syndrome rather than a specific disease

Interaction between pathogen and immune system rather than only the pathogen effect itself

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2
Q

What is the pathophysiology of sepsis?

Which immune molecules are involved?

A

Immune system has complex interaction with pathogen= CYTOKINE RELEASE:

  • vasodilation
  • increased vascular permeability
  • migration of WBC
  • mitochondrial dysfunction

Dysregulation of haemostasis due to stimulation of coagulation

Endothelial barrier compromised

Vasodilation and increase permeability leads to hypotension and tissue hypoperfusion leading to change to anaerobic metabolism

TNF-alpha, IL-18 and IL1b

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3
Q

Why does septic shock occur?

What might a blood test show to indicate a patient is experiencing toxic shock?

A

Due to sepsis not responding to treatment resulting in cardio-circulatory failure:

  • DROP IN BLOOD PRESSURE due to profound circulatory, cellular and metabolic abnormalities I.e. Leads to multiple organ failure
  • persistent hypotension which requires vasopressors to be maintained =>65mmHg

Serum lactate >2mmol/L = sign of organ underperfusion and consequent switch to anaerobic respiration

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4
Q

What are the examples of end-organ failure which occur in sepsis?

A
ARDs
Cardiomyopathy 
AKI
Cholestasis 
Coagulopathy 
Delirium/encephalopathy 
Bone marrow suppression 
Myopathy
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5
Q

What are the most common sources of sepsis?

A
Pneumonia 
Blood stream infection 
Abdominal infection i.e. appendicitis/infectious diarrhoea/gall bladder infection 
UTI
Catheter-related infection 
Skin or soft tissue infection 
Meningitis 

I.e. bacteria most commonly compared with viruses/fungi/parasites

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6
Q

Who is at risk of developing sepsis?

What are clinical signs that someone is at risk of developing sepsis?

A

People at the extremes of life i.e. <1 or >65
Immunosuppressed
Chronic disease i.e. diabetes, COPD and CKD
Post surgery i.e. damage to normal mucosal barrier
Post-partum i.e. damage to normal mucosal barrier

Temp >38 or <36 
Pulse >90 BPM
RR >20
New confusion/drowsiness
WBC >12 or <4 10^9
Blood glucose >7.7
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7
Q

How would you recognise a possible case of sepsis?

A

Possible infection in conjunction with circulatory compromise +/- unexplained deterioration

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8
Q

What is the clinical method of detecting sepsis? When should patients be escalated for query of sepsis based on this method?

A

NEWS/NEWS2

Resp rate 
SpO2 (2 scales i.e. one for those with respiratory disorder) 
-scale 2 used when COPD patients have hypoxic drive due to loss of CO2 sensitivity 
Oxygen administration 
Blood pressure 
Pulse
Consciousness 
Temperature

When score =<5 OR when scores 3 in any of the sections

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9
Q

How is the qSOFA score used to assess whether patient suffering from sepsis?

A
Defines organ failure due to sepsis 
Diagnosis of sepsis requires 2(+) of the following:
-Tachypnoea= RR>22 
-hypotension= SBP<100
-Altered mentation= GCS<15
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10
Q

How might a patient with sepsis present?

A

Hypotension

High or low temp

Tachypnoea

Confusion

Shivering
-due to rigor

Low urine
-indicator of poor kidney perfusion

Drowsiness

Sweating

Skin mottling
-due to hypoperfusion

Cool peripheries

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11
Q

How do you manangement sepsis?

A

SEPSIS 6= do within first 1hr
I.e. 3 treatments and 3 investigations = 3 in, 3 out

Give IV fluids

  • Resusitation= IV bolus crystalloid (200-250ml)
  • maintenance dose= 125ml per hour i.e. 70kg person= 2500ml IV Hartmans solution per day

Give IV antibiotics
-within 1 hour
-empirical antibiotics to treat source of infection or unknown source if not clear
I.e. narrower spectrum antibiotics can be used when results from blood culture indicate the source of the infection and the possible resistance

Give oxygen (high flow)- if appropriate

  • > 92% target
  • need to be conscious of COPD

Measure lactate via VBG

  • measure of tissue perfusion as indicates how much of tissue has switched to anaerobic respiration
  • > 2 mmol/L = concerned

Blood cultures
-determining the pathogen acting as source of infection so can target Ab

Measure urine output (should be 30ml per hour) i.e. might need to catheritise

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12
Q

What investigation should be done for sepsis?

A

Bedside:

  • urine analysis
  • swabs
  • ECG

Bloods:

  • FBC
  • U+E
  • LFT
  • coagulation
  • CRP
  • lactate via VBG
  • cultures

Imaging:
-CXR

Invasive:
-lumbar puncture

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13
Q

How is sepsis monitored?

A

Hourly observations

Urine output and GCS

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14
Q

What are the complications asscociated with recovery from sepsis?

A

ITU admission to support respiratory and vaso support
- can lead to healthcare associated infections and myopathy

Prolonged immune-suppressive phase which leads to increase risk of secondary infection

Psychology effects
I.e. anxiety/difficulty concentration/clouded thinking/poor memory

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15
Q

What measures can be taken to prevent sepsis?

A

Vaccinations such as meningococcal vaccination

Hand hygiene

Prevention of hospital-associated infection
-mouth hygiene in ICU as can be main cause of hospital acquired pneumonia

Public awareness
-calling ambulance when there is change in consciousness or new onset confusion

Clean water

Safe childbirth

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16
Q

What level of lactate is a sign for concern? What does this indicate?

A

> 2

Increased lactate is a hallmark for hypoperfusion and anaerobic metabolism

17
Q

How is a younger person experiencing sepsis most likely to present? Why is this?

A

Tachycardia with increase resp rate before fall in BP

BP can be maintained in normal range for longer in younger patients with sepsis meaning this is not a very sensitive way of identifying patient suffering from sepsis

18
Q

What is the difference between sepsis and septic shock?

A

Sepsis is diagnosed as NEWS of =>5

Septic shock is diagnosed AFTER treatment has been commenced as it is the development of cardio-circulatory failure due to a failure to respond to treatment

19
Q

How can you differentiate sepsis from a normal infection?

A

Sepsis is defined by the addition of ORGAN DYSFUNCTION in the presence of infection

20
Q

Why is a systems review important for sepsis?

A

Used to determine the source of infection

Chest= cough or SOB
Urine= dip stick or analysis (if >65 y/o due to dip stick giving false positives)
GI
CNS= headache/neck stiffness
Skin= rashes
Recent surgery i.e. post-operative infection

21
Q

What is fluid challenge and how is it used as part of the fluid resuscitation phase in sepsis management?

A

Fluid challenge involves giving patient a IV bolus and measure BP response
Can give 2-3 fluid challenges if no initial response
Need to refer to ICU if no response after 2 litres fluids= indicates vasopressors required to try and raise BP

22
Q

What is the Portsmouth/seagull sign and what is it a red flag for?

A

Where SBP falls below heart rate i.e. BP on downwards trend and HR on upwards trends

Indicative of hypovolaemia in association with SEPSIS

23
Q

What is AVPU and what role does it have in NEWS2?

A

Awake
Voice
Pain
Unresponsive

Used as quicker alternative to GCS to assess patients consciousness

24
Q

What are the red flags for sepsis?

A
Systolic BP < 90mmHg 
Lactate >2 mmol/L
Heart rate >130 BPM
RR > 25 
Oxygen required to maintain SpO2 >92%
Only response to voice or pain or is unresponsive 
Non-blanching rash 
Not passed urine in last 18 hours 
Urine output <0.5 ml/kg/hr
25
Q

Which inflammatory mediators are involved in the pathiophysiology of sepsis?

A

Nitric oxide
-causes and maintains vasodilation-> leaky capillaries

Bradykinin

  • pain at site of inflammation
  • vasodilation

Complement proteins
-neutralise pathogens and mobilise WBC

Thrombin
-helps clot to form

Interleukins
-aid with WBC function and attracting them to site of inflammation

TNF
-pro-inflammatory cytokine

26
Q

What is the mechanism behind the swelling/oedema associated with sepsis?

A

Mediators cause vasodilation and increased capillary permeability leading to increase transcapillary loss of albumin
Leads to shift in osmotic pressure and oedema