3. Acute Sepsis Flashcards

1
Q

Define the term ‘sepsis’.

A

Life-threatening organ dysfunction due to a dysregulated host response to infection.

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2
Q

Define the term ‘septic shock’.

A

Persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation.

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3
Q

Define the term ‘bacteraemia’.

A

Presence of bacteria in the blood (with or without clinical symptoms).

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4
Q

Which systems are used to diagnose sepsis?

A
  1. General appearance of patient - looks acutely unwell
  2. Early Warning Score (EWS) - 3 or more
  3. Clinical suspicion of infection, inc. source (e.g. UTI, pneumonia, meningitis…)
  4. Red Flags - at least 1
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5
Q

Which basic observations are included in the EWS?

A

1) Respiratory rate
2) Arterial oxygen saturation (SpO2)
3) Temperature
4) Systolic BP
5) Heart rate
6) Level of consciousness

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6
Q

Describe the 7 Red Flags.

A

1) Resp rate = 25/min or more
2) New need for O2 to keep saturations >91%
3) Systolic BP <91 mmHg (or fall of 40 from normal)
4) Heart rate >130/min
5) No urine output for 18hrs or UO <0.5ml/kg/hr
6) Responds only to voice or pain / unresponsive
7) Non-blanching rash/mottled/ashen/cyanotic

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7
Q

What action is required when a patient is diagnosed with Red Flag sepsis?

A

Complete sepsis 6 bundle within 1 hr:

  1. Give high flow oxygen
  2. Take blood cultures
  3. Give IV antibiotics
  4. Give a fluid challenge
  5. Measure lactate (if >4 mmol/L, refer to critical care)
  6. Measure urine output
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8
Q

Which investigations should urgently be performed when acute sepsis is suspected? Explain why.

A

1) Full blood count (measure of infection)
2) Assess kidney function (organ very susceptible to failure in sepsis):
- measure urea and electrolytes
- measure urine output
3) Diagnose causative agent:
- blood culture for PCR
- other microbiology samples (CSF, urine, etc.)
4) Assess metabolic function:
- measure lactate
- measure blood sugar
- liver function tests
5) Measure inflammation: C-reactive protein
6) Measure arterial blood gases (O2/CO2 saturation) - abnormally regulated in sepsis
7) Coagulation studies (very affectced in sepsis)

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9
Q

Why might X-ray/CT scans be ordered for a septic patient?

A

Identify source of infection (e.g. bowel perforation) and presence of cysts

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10
Q

Explain why sepsis leads to a decreased BP.

A
  1. Endotoxin and cytokine release… BV dilation… decreased BP.
  2. Movement of immune/inflammatory cells into tissues… decreased plasma oncotic pressure… decreased blood volume, total peripheral resistance and pressure.
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11
Q

Why do acute sepsis patients become tachycardic?

A

Low BP sensed by baroreceptors… increased HR to try and compensate and maintain organ perfusion.

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12
Q

How can endotoxin cause organ failure and death?

A
  1. Endotoxin binds to macrophages and stimulates inflammatory response - promotes wound repair and recruits reticuloendothelial system (phagocytic response).
  2. Cytokines (tissue necrosis factors and interleukins) released into circulation.
  3. Overstimulation of humoural cascades and RE system causes circulatory insult by disseminated intravascular coagulation - leads to microvascular thrombosis which blocks BVs.
  4. Organ ischaemia, dysfunction and failure.
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13
Q

How do cytokines promote the coagulation cascade?

A
  1. Initiate thrombin production

2. Inhibit fibrinolysis

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14
Q

Why can sepsis cause progressive necrosis?

A
  1. Capillary lesions coalesce - compromises blood supply to skin.
  2. Body redirects blood to essential organs

Causes necrosis, esp in hands and feet

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15
Q

How are acute sepsis patients treated?

A
  1. Antibiotics
    • agent likely to be active against meningitis-causing pathogen in patient (varies between age groups, location, etc.)
    • agents that penetrates into CSF
    • empiric choice for bacterial meningitis is ceftriaxone
  2. Supportive therapy to restore physiology
    • O2
    • fluids (for BP)
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16
Q

What are the different possible life-threatening complications of acute sepsis?

A

1- irreversible hypotension (decreased vascularisation of essential organs)
2- respiratory failure
3- acute kidney injury
4- raised intracranial pressure due to cerebral oedema
5. ischaemic necrosis of digits/hands/feet

17
Q

Name the major bacterial agent of meningitis.

  • What type of bacteria is it?
  • How is it spread?
  • How can it be classified?
A

Neisseria meningitidis

  • gram-negative diplococcus
  • spread by direct contact with respiratory secretions: aerosols and nasopharyngeal secretions
  • numerous serogroups (eg A, B, C, W-135) based on the polysaccharide capsular antigen
18
Q

Which N. meningitidis serogroup is most prevalent in UK?

A

B

19
Q

Describe the major virulence factors of N. meningitidis.

A
  1. Pilus - enhances attachment
  2. Polysaccharide capsule - promotes adherence and prevents phagocytosis
  3. Lipopolysaccharide endotoxin - triggers inflammation
20
Q

How can bacterial meningitis be prevented?

A
  1. Vaccination
    - MenC conjugate vaccine (introduced in UK in 1999 causing dramatic decrease in MenC disease)
    - ACWY vaccines (originally for immunocompromised patients and travel protection, now replacing MenC vaccine due to increase in W cases in UK)
    - Serogroup B vaccine recently introduced in UK (important as B capsule is poorly immunogenic and similar to neural tissue)
  2. Antibiotic prophylaxis
    - Is a notifiable disease (cases reported to local Health Protection Unit of Public Health England)
    - Close contacts can be given antibiotic prophylaxis and considered for vaccination
21
Q

What is a purpuric rash?

A

Rash of red spots that don’t blanch when pressure is applied