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TAS Accidents and Poisoning ✅ > Burns and Scalds ✅ > Flashcards

Burns and Scalds ✅ Flashcards

1
Q

What can burns be caused by?

A

Usually from heat, but can also be caused by;

  • Friction
  • Electricity
  • Radiation
  • Chemicals
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2
Q

What are scalds caused by?

A

Contact with hot liquid or steam

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3
Q

Where do the vast majority of childhood burns and scalds occur?

A

Within th home

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4
Q

What are the risk factors for burn injuries?

A
  • Low and middle income countries
  • Cooking on an open fire
  • Children with underlying medical conditions such as epilepsy
  • Lower socio-economic background
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5
Q

What is the severity of burns and scalds determined by?

A
  • Length of contact

- Temperature

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6
Q

What duration of contact is required to result in epidermal injury with a contact temperature of 44 degrees?

A

6 hours

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7
Q

What duration of contact is required to result in epidermal injury with a contact temperature of 54 degrees?

A

30 seconds

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8
Q

What duration of contact is required to cause epidermal injury with a contact temperature of 70 degrees?

A

<1 second

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9
Q

What are burns classified according to?

A
  • Depth and severity of tissue damage

- Extent of body surface area

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10
Q

What are the classifications of burns?

A
  • Superficial - simple erythema
  • Superficial - partial thickness
  • Deep - partial thickness
  • Full thickness
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11
Q

What is classified as a ‘superficial - simple erythema’ burn?

A

Painful, reversible redness of the skin

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12
Q

Give an example of a ‘superficial - simple erythema’ burn

A

Milder cases of sunburn

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13
Q

What layers of the skin is affected in a ‘superficial - simple erythema’ burn?

A

Only the epidermis

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14
Q

What is the implication of a ‘superficial - simple erythema’ burn only affecting the epidermis?

A

It means there is no blistering of the skin

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15
Q

How long does a ‘superficial - simple erythema’ burn take to heal?

A

Several days

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16
Q

What may happen during healing of a ‘superficial - simple erythema’ burn?

A

There may be peeling of the skin

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17
Q

What layers of the skin does a ‘superficial - partial thickness’ burn involve?

A

Only the upper layers of the skin (epidermis and into dermis)

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18
Q

How long does a ‘superficial - partial thickness’ burn take to heal?

A

Usually heals within 2 weeks

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19
Q

Do ‘superficial - partial thickness’ burns leave scarring?

A

Usually minimal scarring

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20
Q

How do ‘superficial - partial thickness’ burns appear?

A

Erythema with blistering

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21
Q

Are ‘superficial - partial thickness’ burns painful?

A

Yes

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22
Q

What layers of the skin do ‘deep - partial thickness’ burns involve?

A

Extends into deeper layers of the dermis

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23
Q

How do ‘deep - partial thickness’ burns appear?

A

More yellow or white in colour, may be blistering

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24
Q

What may be required in the management of ‘deep - partial thickness’ burns?

A

Surgery such as skin grafting

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25
Q

What may result from ‘deep - partial thickness’ burns without surgery?

A

Usually associated with delayed healing and risk of significant scarring

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26
Q

What layers of the skin does a full thickness burn involve?

A

All layers of the skin, and extends through entire dermis

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27
Q

Are full thickness burns painful?

A

No

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28
Q

Why are full thickness burns not painful?

A

As the nerve endings have been fully damaged

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29
Q

How do full thickness burns appear?

A

White or brown in colour

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30
Q

How long do full thickness burns take to heal?

A

Months

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31
Q

What is there a high risk of if full thickness burns occur across a joint?

A

Contractures

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32
Q

Is surgery indicated in full thickness burns?

A

Usually

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33
Q

Do burn injuries cause local or systemic reactions?

A

Both

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34
Q

When is the body’s response to a burn localised to the site of the burn?

A

In small burns

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35
Q

When might a burn cause a systemic inflammatory reaction?

A
  • Burns over 30% total body surface area

- In deeper dermal burns

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36
Q

What is seen in the systemic inflammatory response to burns?

A
  • Inflammatory mediators are released into the circulation
  • Myocardial contractility may be reduced
  • Intra-abdominal vasoconstrictionocurs
  • Fluid, including electrolyte, loss
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37
Q

What inflammatory mediators are released into the circulation in burns?

A
  • Prostaglandins
  • Histamine
  • Complement
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38
Q

What is the result of the release of inflammatory mediators in burns?

A

Capillary leak increases

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39
Q

What does capillary leak in burns lead to?

A
  • Oedema in soft tissues

- Intravascular fluid depletion

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40
Q

What does the hypovolaemia caused by the inflammatory response to burns lead to?

A

Hypoperfusion

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41
Q

Why is myocardial contractility reduced in the systemic inflammatory response to burns?

A

Due to the presence of tumour necrosis factor alpha

42
Q

What is the result of intra-abdominal vasoconstriction in the systemic inflammatory response to burns?

A

Potentially compromises blood flow to organs such as the spleen, kidneys, and bowel

43
Q

How are fluids and electrolytes lost in burns?

A

Evaporation from the burn itself

44
Q

What is the cumulative effect of the changes seen in the systemic inflammatory response to burns?

A

Systemic hypotension and end organ hypoperfusion

45
Q

What happens to metabolism in major burns?

A

Catabolism is marked

46
Q

How is the increase in catabolism in major burns managed?

A

Early nutritional input to aid recovery

47
Q

Why is infection risk increased in burns?

A
  • Direct entry of micro-organisms through damaged area

- Because local immune response is compromised

48
Q

How is intravascular fluid depletion managed in burns?

A

Adequate fluid resuscitation

49
Q

What does shock in burns result from?

A
  • Hypovolaemia
  • Microcirculatory injury
  • Release of local and systemic inflammatory mediators
50
Q

What is the foundation of early burns management?

A

Treatment and prevention of shock with IV fluid administration

51
Q

What is used to determine fluid resuscitation in burns?

A

Parkland formula

52
Q

What is the Parkland formula?

A

Volume required over first 24 hours (ml) = 4x body surface area of burn x body weight

53
Q

Over what time scale is resuscitation fluid administered in the first 24 hours of a burn?

A

50% of total volume to be given in 24 hours given over first 8 hours, remained over subsequent 16 hours

54
Q

Why is 50% of the fluid resuscitation requirements given over the first 8 hours in a burn?

A

It mimics the physiological situation, as plasma losses are greatest in the first 6-8 hours after a burn with ongoing slower capillary leakage after

55
Q

When does the resuscitation period for burns begin?

A

At the time of the burn (not the time of initiating fluid resuscitation)

56
Q

What is the recommended fluid to use in burn resuscitation?

A

Crystalloid - usually Hartmann’s

57
Q

Why is Hartmann’s solution used in burns resuscitation?

A

It has the closest electrolyte composition to plasma

58
Q

What should be administered in addition to resuscitation fluid volumes in the first 24 hours of a burn?

A

Maintenance requirements

59
Q

What is the limitation of the Parkland formula?

A

It only provides a guide to fluid requirements

60
Q

What is the most important factor determining if fluid resuscitation is adequate in burns?

A

Clinical response

61
Q

How is it determined clinically if fluid resuscitation is adequate in burns?

A

Maintenance of urine output of 1ml/kg/hour

62
Q

Other than fluid management, what forms an essential element of the acute and ongoing management of burns?

A

Adequate analgesia

63
Q

What is often required to ensure adequate analgesia in the most significant burns injuries?

A

IV opiates

64
Q

What are the indications for management in a specialist burns unit?

A
  • Burns greater than 5-7% total body surface area
  • Burns to face, hands, feet, genitalia, perineum, across major joints
  • Full thickness burns
  • Electrical burns
  • Chemical burns
  • Inhalation burns
  • Circumferential burns
  • Suspicious burns
65
Q

Why should larger/more complex burns be managed in a specialist burns unit?

A
  • More likely to require surgical input, e.g. skin grafting

- More likely to require specialist monitoring or longer term complications, e.g. contractures

66
Q

How common are respiratory complications of burns sustained in house fires?

A

Relatively common

67
Q

What is the mortality of inhalation injury in combination with cutaneous burns?

A

30-90%

68
Q

What can upper airway inhalation injury lead to?

A

Obstruction

69
Q

Over what time period does inhalation injury result in obstruction?

A

The first 12 hours after exposure

70
Q

What causes upper airway injury in smoke inhalation?

A
  • Direct thermal injury

- Chemical irritation

71
Q

What causes lung parenchymal injury associated with inhalation?

A

Inhaled steam

72
Q

Is lung parenchymal injury from steam inhalation a result of direct thermal injury?

A

No

73
Q

Why does only inhaled steam cause lung parenchymal injury?

A

Only inhaled steam is capable of overcoming the heat dissipation mechanisms of the upper airways

74
Q

How does the heat carrying capacity of inhaled steam compare to that of dry air?

A

It is significantly greater

75
Q

What causes damage to the distal airways in lung parenchymal injury caused by inhalation?

A

The incomplete products of combustion, in particular aldehydes, nitrogen and sulphur oxides, and carbon monoxide

76
Q

What is the most common sequelae of inhalation injury?

A

Proximal airway damage and oedema

77
Q

What can severe causes of inhalation injury lead to?

A

RDS

78
Q

Why can severe cases of inhalation injury lead to RDS?

A

It can inactivate surfactant, leading to reduced pulmonary compliance

79
Q

Why is carbon monoxide hard to detect?

A

It is a colourless, odourless, and tasteless gas

80
Q

How is carbon monoxide produced?

A

Incomplete burning due to insufficient oxygen

81
Q

Give 2 examples of when carbon monoxide may be produced?

A
  • Older or poorly maintained gas appliances

- When solid fuel is burned in enclosed areas with inadequate ventilation

82
Q

How does carbon monoxide exert its toxic effects?

A

It has an extremely high affinity for haemoglobin

83
Q

How does the affinity of carbon monoxide to haemoglobin compare to that of oxygen?

A

230x

84
Q

What effect does the binding of carbon monoxide to one of haemoglobin’s four oxygen binding sites have?

A

It increases the affinity of the other 3 sites for oxygen

85
Q

What is the result of the increased affinity of the other 3 binding sites to oxygen when CO binds to haemoglobin?

A

It shifts the oxygen dissociation curve to the left, and impedes the release of oxygen to body tissues

86
Q

Other than haemoglobin, what does carbon monoxide bind to?

A

Other haem-containing molecules, e.g. myoglobin, mitochondrial cytochrome oxidase

87
Q

What is the result of carbon monoxide binding to other hame-containing molecules?

A

It may disrupt their function

88
Q

What are the symptoms of early carbon monoxide poisoning?

A
  • Headache
  • Nausea
  • Malaise
  • Dizziness
89
Q

What is the problem with detection of carbon monoxide poisoning in early stages?

A

The symptoms are non-specific, and can be easily attributed to common causes such as colds and flu-like illness

90
Q

What are the later symptoms of carbon monoxide poisoning?

A
  • Confusion

- Drowsiness

91
Q

What does carbon monoxide poisoning eventually lead to if untreated?

A

Loss of consciousness and death

92
Q

How is the presence of carboxyhaemoglobin levels in the blood detected?

A
  • Pulse CO-oximeter

- Blood gas analysis

93
Q

What happens to pulse oximetry readings in carbon monoxide poisoning?

A

They are normal

94
Q

Why are pulse oximetry readings normal even in significant carbon monoxide poisoning?

A

Carboxyhaemoglobin is misrepresented as oxyhemoglobin

95
Q

What happens to symptoms of carbon monoxide poisoning once carboxyhaemoglobin levels have returned to normal?

A

They may persist

96
Q

How is carbon monoxide poisoning treated?

A
  • High flow oxygen via non-rebreathe mask

- Hyperbaric oxygen

97
Q

Why is high flow oxygen given in carbon monoxide poisoning?

A

It speeds up the dissociation of carbon monoxide from carboxyhaemoglobin

98
Q

What is the rationale for hyperbaric oxygen in the treatment of carbon monoxide poisoning?

A

It may reduce the half life of carbon monoxide

99
Q

What is the limitation of hyperbaric oxygen in the treatment of carbon monoxide poisoning?

A

There is controversy over whether it offers significant clinical benefit over standard high flow oxygen

100
Q

What do the long-term effects of carbon monoxide depend on?

A

The extent of poisoning

101
Q

What are the potential long-term effects of carbon monoxide poisoning?

A

Hypoxic brain damage

102
Q

What measures are in place to prevent carbon monoxide poisoning?

A

Carbon monoxide detectors are now widely available and are recommended for use at home to detect high levels at an early stage

TAS Accidents and Poisoning ✅ (12 decks)

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