Burns and Scalds ✅ Flashcards
(102 cards)
1
Q
What can burns be caused by?
A
Usually from heat, but can also be caused by;
- Friction
- Electricity
- Radiation
- Chemicals
2
Q
What are scalds caused by?
A
Contact with hot liquid or steam
3
Q
Where do the vast majority of childhood burns and scalds occur?
A
Within th home
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
5
Q
What is the severity of burns and scalds determined by?
A
- Length of contact
- Temperature
6
Q
What duration of contact is required to result in epidermal injury with a contact temperature of 44 degrees?
A
6 hours
7
Q
What duration of contact is required to result in epidermal injury with a contact temperature of 54 degrees?
A
30 seconds
8
Q
What duration of contact is required to cause epidermal injury with a contact temperature of 70 degrees?
A
<1 second
9
Q
What are burns classified according to?
A
- Depth and severity of tissue damage
- Extent of body surface area
10
Q
What are the classifications of burns?
A
- Superficial - simple erythema
- Superficial - partial thickness
- Deep - partial thickness
- Full thickness
11
Q
What is classified as a ‘superficial - simple erythema’ burn?
A
Painful, reversible redness of the skin
12
Q
Give an example of a ‘superficial - simple erythema’ burn
A
Milder cases of sunburn
13
Q
What layers of the skin is affected in a ‘superficial - simple erythema’ burn?
A
Only the epidermis
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
15
Q
How long does a ‘superficial - simple erythema’ burn take to heal?
A
Several days
16
Q
What may happen during healing of a ‘superficial - simple erythema’ burn?
A
There may be peeling of the skin
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)
18
Q
How long does a ‘superficial - partial thickness’ burn take to heal?
A
Usually heals within 2 weeks
19
Q
Do ‘superficial - partial thickness’ burns leave scarring?
A
Usually minimal scarring
20
Q
How do ‘superficial - partial thickness’ burns appear?
A
Erythema with blistering
21
Q
Are ‘superficial - partial thickness’ burns painful?
A
Yes
22
Q
What layers of the skin do ‘deep - partial thickness’ burns involve?
A
Extends into deeper layers of the dermis
23
Q
How do ‘deep - partial thickness’ burns appear?
A
More yellow or white in colour, may be blistering
24
Q
What may be required in the management of ‘deep - partial thickness’ burns?
A
Surgery such as skin grafting
25
What may result from 'deep - partial thickness' burns without surgery?
Usually associated with delayed healing and risk of significant scarring
26
What layers of the skin does a full thickness burn involve?
All layers of the skin, and extends through entire dermis
27
Are full thickness burns painful?
No
28
Why are full thickness burns not painful?
As the nerve endings have been fully damaged
29
How do full thickness burns appear?
White or brown in colour
30
How long do full thickness burns take to heal?
Months
31
What is there a high risk of if full thickness burns occur across a joint?
Contractures
32
Is surgery indicated in full thickness burns?
Usually
33
Do burn injuries cause local or systemic reactions?
Both
34
When is the body's response to a burn localised to the site of the burn?
In small burns
35
When might a burn cause a systemic inflammatory reaction?
- Burns over 30% total body surface area
| - In deeper dermal burns
36
What is seen in the systemic inflammatory response to burns?
- Inflammatory mediators are released into the circulation
- Myocardial contractility may be reduced
- Intra-abdominal vasoconstrictionocurs
- Fluid, including electrolyte, loss
37
What inflammatory mediators are released into the circulation in burns?
- Prostaglandins
- Histamine
- Complement
38
What is the result of the release of inflammatory mediators in burns?
Capillary leak increases
39
What does capillary leak in burns lead to?
- Oedema in soft tissues
| - Intravascular fluid depletion
40
What does the hypovolaemia caused by the inflammatory response to burns lead to?
Hypoperfusion
41
Why is myocardial contractility reduced in the systemic inflammatory response to burns?
Due to the presence of tumour necrosis factor alpha
42
What is the result of intra-abdominal vasoconstriction in the systemic inflammatory response to burns?
Potentially compromises blood flow to organs such as the spleen, kidneys, and bowel
43
How are fluids and electrolytes lost in burns?
Evaporation from the burn itself
44
What is the cumulative effect of the changes seen in the systemic inflammatory response to burns?
Systemic hypotension and end organ hypoperfusion
45
What happens to metabolism in major burns?
Catabolism is marked
46
How is the increase in catabolism in major burns managed?
Early nutritional input to aid recovery
47
Why is infection risk increased in burns?
- Direct entry of micro-organisms through damaged area
| - Because local immune response is compromised
48
How is intravascular fluid depletion managed in burns?
Adequate fluid resuscitation
49
What does shock in burns result from?
- Hypovolaemia
- Microcirculatory injury
- Release of local and systemic inflammatory mediators
50
What is the foundation of early burns management?
Treatment and prevention of shock with IV fluid administration
51
What is used to determine fluid resuscitation in burns?
Parkland formula
52
What is the Parkland formula?
Volume required over first 24 hours (ml) = 4x body surface area of burn x body weight
53
Over what time scale is resuscitation fluid administered in the first 24 hours of a burn?
50% of total volume to be given in 24 hours given over first 8 hours, remained over subsequent 16 hours
54
Why is 50% of the fluid resuscitation requirements given over the first 8 hours in a burn?
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
When does the resuscitation period for burns begin?
At the time of the burn (not the time of initiating fluid resuscitation)
56
What is the recommended fluid to use in burn resuscitation?
Crystalloid - usually Hartmann's
57
Why is Hartmann's solution used in burns resuscitation?
It has the closest electrolyte composition to plasma
58
What should be administered in addition to resuscitation fluid volumes in the first 24 hours of a burn?
Maintenance requirements
59
What is the limitation of the Parkland formula?
It only provides a guide to fluid requirements
60
What is the most important factor determining if fluid resuscitation is adequate in burns?
Clinical response
61
How is it determined clinically if fluid resuscitation is adequate in burns?
Maintenance of urine output of 1ml/kg/hour
62
Other than fluid management, what forms an essential element of the acute and ongoing management of burns?
Adequate analgesia
63
What is often required to ensure adequate analgesia in the most significant burns injuries?
IV opiates
64
What are the indications for management in a specialist burns unit?
- 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
Why should larger/more complex burns be managed in a specialist burns unit?
- More likely to require surgical input, e.g. skin grafting
| - More likely to require specialist monitoring or longer term complications, e.g. contractures
66
How common are respiratory complications of burns sustained in house fires?
Relatively common
67
What is the mortality of inhalation injury in combination with cutaneous burns?
30-90%
68
What can upper airway inhalation injury lead to?
Obstruction
69
Over what time period does inhalation injury result in obstruction?
The first 12 hours after exposure
70
What causes upper airway injury in smoke inhalation?
- Direct thermal injury
| - Chemical irritation
71
What causes lung parenchymal injury associated with inhalation?
Inhaled steam
72
Is lung parenchymal injury from steam inhalation a result of direct thermal injury?
No
73
Why does only inhaled steam cause lung parenchymal injury?
Only inhaled steam is capable of overcoming the heat dissipation mechanisms of the upper airways
74
How does the heat carrying capacity of inhaled steam compare to that of dry air?
It is significantly greater
75
What causes damage to the distal airways in lung parenchymal injury caused by inhalation?
The incomplete products of combustion, in particular aldehydes, nitrogen and sulphur oxides, and carbon monoxide
76
What is the most common sequelae of inhalation injury?
Proximal airway damage and oedema
77
What can severe causes of inhalation injury lead to?
RDS
78
Why can severe cases of inhalation injury lead to RDS?
It can inactivate surfactant, leading to reduced pulmonary compliance
79
Why is carbon monoxide hard to detect?
It is a colourless, odourless, and tasteless gas
80
How is carbon monoxide produced?
Incomplete burning due to insufficient oxygen
81
Give 2 examples of when carbon monoxide may be produced?
- Older or poorly maintained gas appliances
| - When solid fuel is burned in enclosed areas with inadequate ventilation
82
How does carbon monoxide exert its toxic effects?
It has an extremely high affinity for haemoglobin
83
How does the affinity of carbon monoxide to haemoglobin compare to that of oxygen?
230x
84
What effect does the binding of carbon monoxide to one of haemoglobin's four oxygen binding sites have?
It increases the affinity of the other 3 sites for oxygen
85
What is the result of the increased affinity of the other 3 binding sites to oxygen when CO binds to haemoglobin?
It shifts the oxygen dissociation curve to the left, and impedes the release of oxygen to body tissues
86
Other than haemoglobin, what does carbon monoxide bind to?
Other haem-containing molecules, e.g. myoglobin, mitochondrial cytochrome oxidase
87
What is the result of carbon monoxide binding to other hame-containing molecules?
It may disrupt their function
88
What are the symptoms of early carbon monoxide poisoning?
- Headache
- Nausea
- Malaise
- Dizziness
89
What is the problem with detection of carbon monoxide poisoning in early stages?
The symptoms are non-specific, and can be easily attributed to common causes such as colds and flu-like illness
90
What are the later symptoms of carbon monoxide poisoning?
- Confusion
| - Drowsiness
91
What does carbon monoxide poisoning eventually lead to if untreated?
Loss of consciousness and death
92
How is the presence of carboxyhaemoglobin levels in the blood detected?
- Pulse CO-oximeter
| - Blood gas analysis
93
What happens to pulse oximetry readings in carbon monoxide poisoning?
They are normal
94
Why are pulse oximetry readings normal even in significant carbon monoxide poisoning?
Carboxyhaemoglobin is misrepresented as oxyhemoglobin
95
What happens to symptoms of carbon monoxide poisoning once carboxyhaemoglobin levels have returned to normal?
They may persist
96
How is carbon monoxide poisoning treated?
- High flow oxygen via non-rebreathe mask
| - Hyperbaric oxygen
97
Why is high flow oxygen given in carbon monoxide poisoning?
It speeds up the dissociation of carbon monoxide from carboxyhaemoglobin
98
What is the rationale for hyperbaric oxygen in the treatment of carbon monoxide poisoning?
It may reduce the half life of carbon monoxide
99
What is the limitation of hyperbaric oxygen in the treatment of carbon monoxide poisoning?
There is controversy over whether it offers significant clinical benefit over standard high flow oxygen
100
What do the long-term effects of carbon monoxide depend on?
The extent of poisoning
101
What are the potential long-term effects of carbon monoxide poisoning?
Hypoxic brain damage
102
What measures are in place to prevent carbon monoxide poisoning?
Carbon monoxide detectors are now widely available and are recommended for use at home to detect high levels at an early stage
