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TAS Emergencies and Critical Care ✅ > Sepsis ✅ > Flashcards

Sepsis ✅ Flashcards

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
Q

What has caused the reduction in hospital mortality of meningococcal sepsis?

A
  • Improvements in public awareness

- Early recognition and management

26
Q

What is most of the pathophysiology of sepsis caused by?

A

Activation of host immune mechanisms triggered by numerous bacterial factors

27
Q

How long can the activation of host immune mechanisms continue for after eradication of causative micro-organisms by appropriate antibacterial therapy in sepsis?

A

For days or weeks

28
Q

How do bacterial factors activate the immune system in sepsis?

A

Bacterial cell wall components bind to and stimulate inflammatory and vascular endothelial cells via a variety of mechanisms

29
Q

What happens when monocytes are stimulated in sepsis?

A

They produce a range of pro-inflammatory cytokines, including tumour necrosis factor alpha

30
Q

What are cytokine levels closely correlated with in sepsis?

A

Disease severity and risk of death

31
Q

What happens when neutrophils are stimulated in sepsis?

A

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
Q

What is the main pathophysiological event occurring in bacterial septicaemia?

A

The change in the vascular endothelial surface

33
Q

What is the normal function of the vascular endothelial surface?

A
  • Regulates vascular permeability

- Presents a thromboresistant, non-reactive surface to circulating blood cells

34
Q

What happens to the normal functions of the vascular endothelial surface in sepsis?

A

They are lost

35
Q

What processes affecting the microvasculature occur in sepsis?

A
  • Increased vascular permeability
  • Pathological vasoconstriction and vasodilation
  • Loss of thromboresistance and intravascular coagulation
  • Myocardial dysfunction
36
Q

What is the consequence of increased vascular permeability in sepsis?

A
  • Hypovolaemia

- Oedema in organ and tissues

37
Q

How is hypovolaemia initially compensated for in sepsis?

A

Homeostatic mechanisms, including vasoconstriction of both arterial and venous vascular beds

38
Q

What happens as capillary leak progresses past what can be compensated for with homeostatic in mechanisms in sepsis?

A

Venous return to the heart is impaired and cardiac output falls

39
Q

What is the most important component of resuscitation in hypovolaemia caused by sepsis?

A

Restoration of circulating volume

40
Q

What is the problem with restoring circulating volume in hypovolaemia caused by sepsis?

A

It can increase the risk of increasing oedema in all tissues and organs as a result of persistent capillary leak

41
Q

Where might fluid accumulate due to increased vascular permeability in sepsis?

A
  • Tissue and muscle compartments
  • Peritoneal space
  • Pleural space
  • In alveoli
42
Q

What acts as an early protective measure in sepsis?

A

Compensatory vasoconstriction

43
Q

What is the purpose of compensatory vasoconstriction in sepsis?

A

To maintain tissue and organ perfusion in the face of diminished cardiac output

44
Q

Does vasoconstriction always improve following resuscitation in sepsis?

A

No, it may persist

45
Q

What is cold shock?

A

When patients with severe vasoconstriction develop cold, pale, and ischaemic limbs

46
Q

What is warm shock?

A

When patients develop profound vasodilatation following resuscitation, with bounding pulses, warm peripheries, and hypotension

47
Q

Who usually develops warm shock?

A

Older children

48
Q

What management does warm shock usually respond to?

A

Fluid resuscitation and vasopressors such as noradrenaline

49
Q

What is the hallmark of severe meningococcal sepsis?

A

Widespread purpura fulminans with thrombosis and haemorrhagic necrosis in the skin

50
Q

What can haemorrhagic necrosis cause in extreme cases of severe meningococcal sepsis?

A

Infarction and gangrene of limbs and digits

51
Q

What causes the purpura, thrombosis, and haemorrhagic necrosis in severe meningococcal sepsis?

A

Disruption of the normal anti-thrombotic properties of the vascular endothelial surface and impairment of natural anticoagulant pathways and fibrinolysis

52
Q

What abnormalities are found on blood tests due to disruption of normal coagulation pathways in severe meningococcal sepsis?

A
  • Profound thrombocytopenia

- Prolonged coagulation

53
Q

Why do you get profound thrombocytopenia and prolonged coagulation in severe meningococcal meningitis?

A

As platelets and clotting factors are consumed as clot is formed in small vessels

54
Q

What further increases the likelihood of thrombosis in the skin and peripheries in severe meningococcal sepsis?

A

Sluggish capillary circulation and intense vasoconstriction

55
Q

What causes the low cardiac output seen in sepsis?

A
  • Hypovolaemia

- Decrease in myocardial contractility

56
Q

What causes the hypovolaemia leading to low cardiac output in sepsis?

A
  • Capillary leak

- Loss of circulating volume

57
Q

Does the decrease in myocardial contractility seen in sepsis persist after correction of circulating volume?

A

Yes

58
Q

What causes the development of myocardial dysfunction in meningococcal sepsis?

A

The negative inotropic effect of pro-inflammatory mediators, especially IL-6

59
Q

What factors common to all types of sepsis can adversely affect myocardial function?

A
  • Hypoxia
  • Acidosis
  • Hypoglycaemia
  • Hypokalaemia
  • Hypocalcaemia
  • Hypophosphataemia
60
Q

What may be required to manage the myocardial dysfunction in sepsis?

A

Very high doses of inotropes

61
Q

What is the long term impact of myocardial dysfunction in sepsis?

A

Most patients recover without any long-term consequences

TAS Emergencies and Critical Care ✅ (8 decks)

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