Sepsis ✅ Flashcards

(61 cards)

1
Q

What is sepsis?

A

The systemic response to infection

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2
Q

What is SIRS defined as?

A

The presence of at least 2 of the following criteria, one of which must be abnormal temperature or leukocyte count;

  • Temperature abnormalities
  • Respiratory rate abnormalities
  • Heart rate abnormalities
  • White cell count abnormalities
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3
Q

What is tachycardia defined as in the definition of SIRS?

A

Mean heart rate >2SD above normal for age in the absence of external stimulus, chronic drugs or painful stimuli, or otherwise unexplained elevation over a 0.5-4 hour time period

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4
Q

What is classified as a heart rate abnormality in SIRS?

A

Tachycardia, or in children <1 year old bradycardia

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5
Q

What is bradycardia defined as in the definition of SIRS?

A

Mean heart rate <10th percentile for age in the absence of external vagal stimulus, beta-blocker drugs, or congenital heart disease, or otherwise unexplained persistent depression over a 0.5hour time period

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6
Q

What is classified as a respiratory rate abnormality in SIRS?

A

Raised respiratory rate, or mechanical ventilation for an acute process not related to underlying neuromuscular disease or general anaesthesia

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7
Q

What is raised respiratory rate defined as in the definition of SIRS?

A

Mean respiratory rate >2SD above normal for age

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8
Q

What is classified as white blood cell abnormalities in SIRS?

A

Leukocyte elevated or depressed for age (not secondary to chemotherapy-induced leukopenia) or >10% immature neutrophils

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9
Q

Give 4 causes of SIRS

A
  • Infection
  • Trauma
  • Burns
  • Pancreatitis
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10
Q

What is infection defined as?

A

Suspected or proven infection caused by any pathogen, or clinical syndrome associated with high probability of infection

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11
Q

How can an infection be proven?

A

Positive culture, tissue stain, or PCR test

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12
Q

Give 5 examples of evidence of infection

A
  • Positive findings on clinical exam
  • White blood cels in normally sterile body fluid
  • Perforated viscus
  • Chest radiograph consistent with pneumonia
  • Petechial or purpuric rash, or purport fulminans
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13
Q

What is sepsis defined as?

A

SIRS in the presence of or as a result of suspected or proven infection

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14
Q

What is severe sepsis defined as?

A

Sepsis plus one of;

  • Cardiovascular organ dysfunction
  • Acute respiratory distress syndrome
  • Two or more other organ dysfunctions
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15
Q

What is the characteristic pattern of severe sepsis?

A

Worsening cardiovascular, respiratory, and subsequently other organ system dysfunction

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16
Q

What is septic shock defined as?

A

Sepsis and cardiovascular dysfunction

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17
Q

What is classified as a temperature abnormality in SIRS?

A

Core temperature >38.5 or <36

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18
Q

What has led to a change in the causative agents of septicaemia in children?

A

Introduction of conjugate vaccinations

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19
Q

What pathogens causing septicaemia has there been a major reduction in since the introduction in vaccines?

A
  • N. meningitidis
  • Vaccine serotypes of S pneumonia
  • Hib
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20
Q

What pathogens have increased in incidence since vaccine introduction?

A
  • Non vaccine serotypes of S. pneumonia
  • E. coli
  • S. aureus
  • Group A streptococcus
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21
Q

What is toxic shock syndrome?

A

An acute febrile illness caused by S. aureus or Group A streptococcus

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22
Q

What is toxic shock syndrome characterised by?

A
  • Hypotension

- Multi-organ function

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23
Q

What causes hypotension and multi-organ dyfunction in toxic shock syndrome?

A

Bacterial exotoxins that act as superantigens

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24
Q

By how much has the hospital mortality of meningococcal sepsis fallen?

A

From over 90% in the mid 20th century to around 10% currently

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25
What has caused the reduction in hospital mortality of meningococcal sepsis?
- Improvements in public awareness | - Early recognition and management
26
What is most of the pathophysiology of sepsis caused by?
Activation of host immune mechanisms triggered by numerous bacterial factors
27
How long can the activation of host immune mechanisms continue for after eradication of causative micro-organisms by appropriate antibacterial therapy in sepsis?
For days or weeks
28
How do bacterial factors activate the immune system in sepsis?
Bacterial cell wall components bind to and stimulate inflammatory and vascular endothelial cells via a variety of mechanisms
29
What happens when monocytes are stimulated in sepsis?
They produce a range of pro-inflammatory cytokines, including tumour necrosis factor alpha
30
What are cytokine levels closely correlated with in sepsis?
Disease severity and risk of death
31
What happens when neutrophils are stimulated in sepsis?
They undergo a respiratory burst with the production of reactive oxygen species, as well as degranulation and the release of a range of inflammatory proteins, proteases, and other enzymes. They also contribute to the damage seen at the endothelial surface
32
What is the main pathophysiological event occurring in bacterial septicaemia?
The change in the vascular endothelial surface
33
What is the normal function of the vascular endothelial surface?
- Regulates vascular permeability | - Presents a thromboresistant, non-reactive surface to circulating blood cells
34
What happens to the normal functions of the vascular endothelial surface in sepsis?
They are lost
35
What processes affecting the microvasculature occur in sepsis?
- Increased vascular permeability - Pathological vasoconstriction and vasodilation - Loss of thromboresistance and intravascular coagulation - Myocardial dysfunction
36
What is the consequence of increased vascular permeability in sepsis?
- Hypovolaemia | - Oedema in organ and tissues
37
How is hypovolaemia initially compensated for in sepsis?
Homeostatic mechanisms, including vasoconstriction of both arterial and venous vascular beds
38
What happens as capillary leak progresses past what can be compensated for with homeostatic in mechanisms in sepsis?
Venous return to the heart is impaired and cardiac output falls
39
What is the most important component of resuscitation in hypovolaemia caused by sepsis?
Restoration of circulating volume
40
What is the problem with restoring circulating volume in hypovolaemia caused by sepsis?
It can increase the risk of increasing oedema in all tissues and organs as a result of persistent capillary leak
41
Where might fluid accumulate due to increased vascular permeability in sepsis?
- Tissue and muscle compartments - Peritoneal space - Pleural space - In alveoli
42
What acts as an early protective measure in sepsis?
Compensatory vasoconstriction
43
What is the purpose of compensatory vasoconstriction in sepsis?
To maintain tissue and organ perfusion in the face of diminished cardiac output
44
Does vasoconstriction always improve following resuscitation in sepsis?
No, it may persist
45
What is cold shock?
When patients with severe vasoconstriction develop cold, pale, and ischaemic limbs
46
What is warm shock?
When patients develop profound vasodilatation following resuscitation, with bounding pulses, warm peripheries, and hypotension
47
Who usually develops warm shock?
Older children
48
What management does warm shock usually respond to?
Fluid resuscitation and vasopressors such as noradrenaline
49
What is the hallmark of severe meningococcal sepsis?
Widespread purpura fulminans with thrombosis and haemorrhagic necrosis in the skin
50
What can haemorrhagic necrosis cause in extreme cases of severe meningococcal sepsis?
Infarction and gangrene of limbs and digits
51
What causes the purpura, thrombosis, and haemorrhagic necrosis in severe meningococcal sepsis?
Disruption of the normal anti-thrombotic properties of the vascular endothelial surface and impairment of natural anticoagulant pathways and fibrinolysis
52
What abnormalities are found on blood tests due to disruption of normal coagulation pathways in severe meningococcal sepsis?
- Profound thrombocytopenia | - Prolonged coagulation
53
Why do you get profound thrombocytopenia and prolonged coagulation in severe meningococcal meningitis?
As platelets and clotting factors are consumed as clot is formed in small vessels
54
What further increases the likelihood of thrombosis in the skin and peripheries in severe meningococcal sepsis?
Sluggish capillary circulation and intense vasoconstriction
55
What causes the low cardiac output seen in sepsis?
- Hypovolaemia | - Decrease in myocardial contractility
56
What causes the hypovolaemia leading to low cardiac output in sepsis?
- Capillary leak | - Loss of circulating volume
57
Does the decrease in myocardial contractility seen in sepsis persist after correction of circulating volume?
Yes
58
What causes the development of myocardial dysfunction in meningococcal sepsis?
The negative inotropic effect of pro-inflammatory mediators, especially IL-6
59
What factors common to all types of sepsis can adversely affect myocardial function?
- Hypoxia - Acidosis - Hypoglycaemia - Hypokalaemia - Hypocalcaemia - Hypophosphataemia
60
What may be required to manage the myocardial dysfunction in sepsis?
Very high doses of inotropes
61
What is the long term impact of myocardial dysfunction in sepsis?
Most patients recover without any long-term consequences