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YEAR 3 - SEMESTER 1 > CASE 10 - BURNS > Flashcards

CASE 10 - BURNS Flashcards

1
Q

Which layers of the skin are vascularised?

A

Dermis and hypodermis

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2
Q

In which layer of the skin are adipocytes located?

A

Hypodermis (subcutaneous layer)

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3
Q

What are the differences between thick and thin skin? (Location, histology, thickness)

A

THICK skin is located on the palms and soles of the hands and feet, contains 5 different layers, and the epidermis is about 5mm thick.
NO sweat glands or hair follicles. YES sebaceous glands.

THIN skin is located everywhere else on the body, contains 4 different layers (lacking a stratum lucidum), and the epidermis is ~0.1mm thick.
YES sweat glands, hair follicles, and sebaceous glands.

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4
Q

Name the 5 TYPES of cells in the epidermis

A
  1. Stem cells (located in stratum basal)
  2. Keratinocytes
  3. Dendritic/Langerhans cells
  4. Merckel/tactile cells
  5. Melanocytes (also in stratum basale)

look @ a diagram

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5
Q

What is the function of the STEM cells within the epidermis?

A

Undifferentiated cells that give rise to keratin, which comprise the majority of the epidermis

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6
Q

What is the function of the KERATINOCYTES within the epidermis?

A

Synthesise keratin (which offers protection and acts as a moisture barrier)

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7
Q

What is the function of the MERCKEL/TACTILE cells within the epidermis?

A

Touch receptor cells

Prominent in areas such as the lips and oral cavity

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8
Q

What is the function of the DENDRITIC/LANGERHANS cells within the epidermis?

A

Present pathogens (that have penetrated through the epidermis) to the immune system

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9
Q

What is the function of the MELANOCYTES within the epidermis?

A

Protects mitotically active cells from DNA damage by producing melanin

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10
Q

What is the thickest layer of skin? Which cell type is found here?

A

Stratum spinosum; keratinocytes.

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11
Q

Name 5 functions of the skin

A
  1. Protection (against pathogens and UV light)
  2. Thermoregulation (adipose, sweat glands, hair)
  3. Metabolism (vitamin D production)
  4. Cutaneous sensation
  5. Physiological
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12
Q

Name 5 factors which make burn sites an ideal environment for infection

A
  1. Loss of intact skin barrier
  2. Necrotic skin provides great culture medium
  3. Oedema reduces blood supply to the area
  4. Reduced immunoglobulin levels right after the burn
  5. Hypovolemia –> hypotension –> hypoxia (natural response)
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13
Q

What is the most effective method of preventing infection in burns? Why?

A

Debridement/escharotomy - gets rid of dead tissue/culture medium

(following patient stabilisation and burns demarcation)

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14
Q

Describe what is involved in the infection control procedures for burns patients

A
  1. Single-patient rooms (for >20% open wounds)
  2. Hand hygiene
  3. PPE
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15
Q

Describe what is involved in the surveillance policies for burns patients

A
  1. Routine wound, sputum, and urine cultures
  2. Identifying episodes of cross contamination

This helps guide empiric antibiotic treatment, e.g. if the patient does develop an infection days-weeks later, we know what organisms were present

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16
Q

What is the gold-standard investigation in un-excised burns?

A

Histology

Tissue biopsy is graded from 0-IV

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17
Q

What are the most common causative organism in burns infections for:

  • Early infections
  • Mid-term infections
  • Late infections
A

EARLY: gram-positive organisms such as Staph aureus, streptococcus pyogenes

MIDDLE: gram-negative Ps. Aeruginosa

LATE: multi-resistant organisms & fungal infections (e.g. candida, aspergillus)

https://www-uptodate-com.proxy.library.adelaide.edu.au/contents/burn-wound-infection-and-sepsis?search=burns%20infection&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H372573676

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18
Q

Name 4 other non-local infection complications

A
  1. Bloodstream infections
  2. Pneumonia (e.g. inhalation injury)
  3. Endocarditis
  4. UTI
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19
Q

Name the 2 factors that affect burn severity

A
  1. Depth of burn

2. Surface area

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20
Q

Give an example of thermal and non-thermal burns

A

THERMAL: contact with fire

NON-THERMAL: electrical burn, radiation burn, chemical burn

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21
Q

How can burns cause compartment syndrome?

A

Circumferential burns or eschars cause loss of skin elasticity, impairing blood flow

This can then cause compartment syndrome due to fluid accumulation

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22
Q

How can the surface area of burns (TBSA) be calculated?

A
  1. Lund-Browder chart (for adults and children) - note that superficial/first-degree burns are not included in percentage TBSA assessment
  2. Wallace’s rule of 9s (for adults)
  3. Palm method (least accurate)
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23
Q

Time frame when cool running water is still effective?

A

<1 hour

but evidence is not conclusive

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24
Q

What are the major threats to life in a severely-burned patient? (name 5)

A
  • Shock/Hypovolemia
  • Infection
  • Hypothermia
  • Pneumonia (from inhalation injury)
  • Systemic inflammatory response –> compromises organ perfusion
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25
Q

How is the depth of burns assessed?

A

1st, 2nd, 3rd, 4th degree classification was replaced by a system reflecting the need for surgical intervention:

Superficial/epidermal
Superficial partial-thickness
Deep partial-thickness
Full-thickness
Deeper injury

(figure 1: https://www-uptodate-com.proxy.library.adelaide.edu.
au/contents/assessment-and-classification-of-burn-injury?search=burns&source=search_
result&selectedTitle=2~150&usage_
type=default&display_rank=2#H10)

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26
Q

When is surgical intervention required? (according to depth of burn)

A

Deep partial-thickness and beyond

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27
Q

Describe the appearance of a superficial/epidermal burn

1st-degree

A

Dry, red
Blanches when touched
Painful

https://www.nature.com/articles/s41572-020-0145-5

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28
Q

Describe the appearance of a superficial partial-thickness burn
(2nd-degree)

A

Moist, red, weeping
Blisters
Blanches with pressure
Painful to temperature, air, and touch

Only affects the dermal papillary layer

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29
Q

Describe the appearance of a DEEP partial-thickness burn

2nd-degree

A 
Blisters (easily unroofed)
Waxy/wet
Variable in colour from red to white
Blanching with pressure may be sluggish
Painful to pressure ONLY

Affects the dermal papillary AND reticular layer

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30
Q

Describe the appearance of a FULL-thickness burn

3rd-degree

A

Waxy white to leathery gray to charred and black
Dry and inelastic
No blanching with pressure
Painful to DEEP pressure ONLY (no pinprick or light touch sensation)

Epidermis AND dermis affected

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31
Q

Describe the appearance of a deeper injury burn

4th-degree

A

Extends into fascia and/or muscle and bone (hypodermic layer)
Sensation: deep pressure only

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32
Q

What is a pressure garment used for?

A

Maintaining alignment of collagen fibres whilst the burn is healing.

Helps reduce scarring.

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33
Q

When is airway management/intubation indicated?

A
  • If an inhalation injury is suspected

- If burns involve >30-40% of the body surface

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34
Q

Prolonged cooling of a larger TBSA (>9%) can cause…?

A

Hypothermia

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35
Q

What are the 3 components of inhalation injury?

A
  1. Upper airway swelling (occurs 12-24 hours after initial burn injury)
  2. Acute respiratory failure
  3. CO intoxication (due to smoke inhalation)
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36
Q

List 4 signs of inhalation/upper airway injury that would prompt intubation.

A
  • Voice changes!
  • Cough
  • Stridor
  • Inspiratory grunting
  • Tachypnoea
  • Wheezing
  • Burn distribution: i.e. above the clavicles, involving the face, burns to the nose, nasal hairs, mouth, pharynx
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37
Q

Why is intubation recommended as opposed to observation for upper airway injury?

A

Natural Hx of upper airway injury: it causes oedema and narrowing of the airway within 12-24 hours

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38
Q

There are many systemic effects of large (>30% TBSA) burns injuries. List 5 of these.

A
  1. Systemic inflammatory response
  2. Evaporative fluid loss leading to hypovolemia and hypothermia
  3. Haemolysis & muscle damage
  4. Immunosuppression
  5. Hypermetabolic state
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39
Q

Outline the pathophysiology and consequences of systemic inflammatory response syndrome

A
  1. Release of cytokines & inflammatory mediators
  2. Increased vascular permeability
  3. Extravasation of intravascular proteins and fluid into interstitial tissue

RESULTS: tissue oedema, hypovolemic shock, acute respiratory distress syndrome, paralytic ileus, disseminated intravascular coagulation (DIC)

40
Q

Describe 3 clinical features that may be present in a severely-burned person

A
  1. Clinical features of SHOCK: hypotension, tachycardia, poor urine output, prolonged cap refill
  2. Clinical features of ARDS: dyspnoea
  3. Clinical features of inhalation injury / upper airway injury: tachypnoea, wheeze, stridor
  4. Compartment syndrome / acute limb ischaemia: 5 P’s (pallor, pulselessness, parasthesia, paralysis, pain)
41
Q

Outline the acute/immediate management of severe burns

A
  1. AIRWAY: intubation and high-flow oxygen (if indicated)
  2. Fluid resuscitation
  3. Management of burn area (e.g. removing burnt clothing, cooling and covering the burn area)
  4. Analgesia
  5. Tetanus prophylaxis
42
Q

Fluid resuscitation is adjusted to maintain urine output at…?

A
  1. 0 mL/kg/hour for children

0. 5 - 1 mL/kg/hour for adults

43
Q

What is an escharotomy?

A

A surgical procedure used to treat full-thickness (third-degree) circumferential burns

Incision down to the subcutaneous fat in order to allow underlying structures to expand - prevents further tissue injury

44
Q

Why is a burn a ‘dynamic’ injury?

A

It can change in size and depth over time (explained by the theory of Jackson’s burn wound model)

45
Q

Describe Jackson’s burn would model

A

https://www.racgp.org.au/afp/2017/march/burns-dressings/

3 zones:

  1. Zone of coagulation (dead: irreversible coagulative necrosis)
  2. Zone of stasis (damaged but viable tissue with decreased perfusion. The target area for burns treatment; prevent progression to coagulation)
  3. Zone of hyperaemia (inflammation and increased blood flow)
46
Q

How can burns cause asphyxiation?

A

Compressive eschar around the neck or chest –> restricts chest excursion –> asphyxia

47
Q

What is Postburn hypermetabolism and when does it occur?

A

Initial hypometabolism (ebb state) followed by hypermetabolic state (flow state): occurs in patients with moderate-severe injuries

Hypermetabolic state onset ~5-7 days post-injury and can last for up to three years

48
Q

What is the hypermetabolic flow phase characterised by?

A
  • Hyperdynamic circulation
  • Insulin resistance
  • Protein & lipid catabolism
  • Increased resting energy expenditure
  • Increased body temp
  • Muscle wasting
  • Simulated synthesis of acute-phase reactants

BASICALLY JUST A CATABOLIC STATE

49
Q

In the first 48 hours following a burn injury, pathogens from which areas colonise and cause infection?

A

Staphylococci from the sweat glands and hair follicles

50
Q

In the 5-7 days following a burn injury, pathogens from which areas colonise and cause infection?

A

GIT
Upper respiratory tract
Hospital environment

51
Q

What are the 2 methods of wound healing? Describe what is involved in each.

A
  1. Regenerative (primary intension): tissue replaced with parenchymal tissue (e.g. fracture)
  2. Non-regenerative (secondary intension): healing occurs by replacement with connective tissue scar (e.g. MI). Tissue is NOT replaced with functional parenchymal cells.
52
Q

Using the ABCDE primary survey, outline the concerns and treatments that can be implemented in someone with significant burns.

A

ATTS = analgesia, tests, tubes (e.g. NG, indwelling catheter), secondary survey

https://trauma.reach.vic.gov.au/guidelines/burns/primary-survey

53
Q

When can you use glad wrap?

A

Within the first 12-24 hours as a transfer dressing

DON’T USE IT ON THE FACE YOU’LL SUFFOCATE THEM LOL

54
Q

Difference between an escharotomy vs. a escherectomy?

A

Escharotomy: cutting into the skin for decompression

Escharectomy: removing the entire thing

55
Q

What is the Parkland formula? How is it used?

A

Parkland formula: 3-4mL/kg/% of burn/24 hours

1/2 in the first 8 hours from the time of injury

1/2 in the next 16 hours

E.g. in an 80kg person with 25% TBSA burns: 4mL x 80 x 25 = 8000mL (8L): 4L in first 8 hours, 4L in next 16 hours.

However it is important to note that there may be an increased risk/exacerbation of laryngeal oedema or compartment syndrome if present. In this case the modified Parkland formula may be used where instead of 4mL, the volume is calculated using 2 or 3 mL.

56
Q

Oedema occurs in all burned areas. When does oedema occur in NON-BURNED areas?

A

When TBSA of burns exceeds 25%

57
Q

Explain the changes that occur at a capillary level when someone suffers a burn. How does this cause oedema?

A

INFLAMMATORY METABOLITES and DAMAGE FROM THE BURN = leaky capillaries

Na+, proteins, and fluid shift from the intravascular into the interstitial space.

58
Q

TISSUE COMPLIANCE:

Proteins become denatured. When the proteins are damaged in the ICM, there is a vacuum that draws fluid OUT and you leak fluid.

Burned tissue will swell dramatically but whole body will swell more because the capillary is leaking ADDITIONAL fluid. It SUCKS fluid out of the adjacent capillary bed.

A

TISSUE COMPLIANCE:

Proteins become denatured. When the proteins are damaged in the ICM, there is a vacuum that draws fluid OUT and you leak fluid.

Burned tissue will swell dramatically but whole body will swell more because the capillary is leaking ADDITIONAL fluid. It SUCKS fluid out of the adjacent capillary bed.

59
Q

How can circumferential burns be treated (initially and later in management)?

A

Start with ELEVATION to reduce oedema

THEN an escharotomy (especially if you are a few hours away from more advance help)

60
Q

Factors that increase the time of exposure to a burn and increase the depth of burn

A
  • Intoxication
  • Clothing
  • Viscosity (e.g. hot oil vs. flame)
61
Q

What percentages make up wallace’s rule of 9s

A 
Head & neck = 9%
Arms (2 x 9) = 18%
Trunk = 18%
Trunk (Back) = 18%
Legs (18 x 2) = 36%
Perineum = 1%
62
Q

What is Hartmann’s solution and how does it differ from saline?

A

Hartmann’s solution is a crystalloid solution that is closely isotonic with plasma.

It contains electrolytes and lactate (which helps generate alkalising bicarbonate). It is more ‘physiological’ than saline.

63
Q

What issues are caused by an eschar?

A

Leaving dead tissue in a deep burn facilitates bacterial colonisation and drives deterioration/deepening of the burn.

Removal helps address the negative hydrostatic pressure across into the interstitial space –> less oedema

64
Q

How is burn depth assessed?

A

insert some flow chart

Epidermal integrity –> slippery –> colour or blister thickness, etc.

It’s in ur screenshots

65
Q

What is Nikolsky’s sign?

A

Dislodgement of intact superficial epidermis by a shearing force.

If the sign is positive, the first layer of skin will shear off.

66
Q

When is Hartmann’s Solution preferred over normal saline in IV resuscitation for burns?

A

When TBSA > 20%

67
Q 
Name one (1) Gram positive and one (1) Gram negative microorganism that cause multi-drug resistant
infections of burns.
A

Gram-positive: staphylococcus aureus

Gram-negative: pseudomonas aeruginosa

68
Q

Outline the primary survey to be undertaken for a burns patient.

A

AIRWAY: inhalation injury (soot, facial burns, hoarse voice, singed nasal hairs, etc.), contaminants in the mouth, airway patency

BREATHING: work of breathing, effectiveness of breathing, stridor, wheeze, circumferential burns that may be inhibiting chest wall movement, ARDS

CIRCULATION: signs of shock/hypovolemia (HR, BP, temperature, cap refill), carbon monoxide poisoning

DISABILITY: AVPU, altered mental status (e.g. due to CO inhalation), head injury

ENVIRONMENT/EXPOSURE: check how much of the body is burned (calculate %TBSA)

69
Q

Why is IV fentanyl the preferred analgesia for severe burns?

A

Fast-acting pain relief (1-2 minutes)

Also less likely to induce NV

Morphine is renally-cleared and may not be suitable if a burns patient is suffering AKI from hypoperfusion

70
Q

What should be carefully monitored in patients receiving opioids?

A

Respiratory depression
CNS depression
Dependence

71
Q

Outline the investigations that would be required for a burn injury

A

PULSE OXIMETRY - monitor for hypoxemia (CO inhalation will not affect pulse oximetry)

BLOOD GASES - monitor for hypoxemia and respiratory or metabolic acidosis

SERUM ELECTROLYTES - hyperkalemia and hyponatremia in the acute phase

CXR: rule out ARDS

CARBOXYHAEMOGLOBIN LEVELS: check for CO poisoning

SERUM PROTEIN AND ALBUMIN: hypoalbuminaemia in the acute phase after a burn

72
Q

Why are pulse oximetry values unaffected (or falsely high) in carbon monoxide poisoning?

A

Complexes of Hb and oxygen and complex of Hb and carbon monoxide are indistinguishable.

73
Q

What is ARDS?

A

A severe inflammatory response of the lungs to pulmonary damage

74
Q

Name a defining laboratory feature of ARDS and explain what it represents

A

PaO2/FiO2 ratio <300mmHg

This is the ratio of arterial oxygen partial pressure (measured by ABG) to fractional inspired oxygen (FiO2).

75
Q

What is a normal PaO2/FiO2 ratio?

A

PaO2/FiO2 ratio >500mmHg

76
Q

What is the pathophysiology behind ARDS?

A
  1. Pulmonary damage
  2. Inflammatory response
  3. Neutrophils move into alveoli
  4. Excessive release of neutrophilic mediators
  5. Diffuse alveolar damage

Clinical manifestations: decreased pulmonary compliance, hypoxemia, respiratory distress, hyperventilation

77
Q

What are the clinical features of ARDS?

A

Acute dyspnoea, tachycardia, tachypnoea

Cyanosis

Diffuse crackles

Possible: fever, cough, chest pain

78
Q

What acute findings may be present on the CXR of someone with ARDS?

A

Diffuse bilateral symmetrical infiltrates

note that CXR may be normal in the first 24 hours

79
Q

How can a CXR resembling ARDS be distinguished from CHF?

A
  • History

- Other investigations: ABG, echocardiography, CT chest, etc.)

80
Q

Why are serum protein levels low after a significant burn injury?

A

Higher vascular permeability (at the site of the wound and possibly also due to SIRS) produces exudation

81
Q

What measures can be taken to prevent the patient from losing heat during surgery?

A

Warm IV fluid

Heated operating theatre

82
Q

Why does gentamicin require such careful monitoring of renal function and gentamicin concentrations?

A

Ear toxicity - can get hearing loss

Reversible kidney damage (100% really cleared) but irreversible ototoxicity

83
Q

What is biobrane?

A

A biosynthetic skin dressing that mimics the properties of skin and doesn’t tear.

Stretchable, provides temporary cover for clean partial thickness burns or over split skin grafts.

84
Q

What is a split skin graft?

A

A split skin graft (SSG) is where a very thin shaving of normal, healthy skin is used to cover an area of skin that has been damaged or cannot heal because of an injury (e.g. a severe burn).

85
Q

What does meshing of a split skin graft involve?

A

Poking holes in the skin graft so that it can be stretched over a larger surface area (for larger injuries)

86
Q

Which factors contribute to hypovolemic shock and potentially end-organ damage in a burns patient? (3 things)

A
  1. Loss of fluid through evaporation (no skin barrier)
  2. SIRS or inflammatory factors –> increased capillary permeability –> fluid leakage into interstitial and third space
  3. Potential infection –> sepsis –> increased capillary permeability
87
Q

Why do burns patients develop hyperkalemia?

A

Ischaemia and necrosis of muscle cells –> release of intracellular contents (potassium)

88
Q

Why is intubation performed before commencing fluid resuscitation?

A

Because fluid resuscitation can worsen laryngeal edema, intubation should be performed before fluid resuscitation!

89
Q

Initial management and management of complications

A 
INITIAL MANAGEMENT:
Pain control
Debridement/Escharectomy
Intubation
Fluid management

MANAGING COMPLICATIONS:
Hypovolaemia and Shock [Potential end organ failure]
Lungs – respiratory failure
Local oedema and protein loss
Fluid and electrolyte changes and requirements in treatment
Renal adjustments and consequences in burns patients
Infection and infection control
Nutritional requirements
Trace element needs

90
Q

Why do burns patients develop raised creatinine levels?

A

Acute kidney injury

91
Q

A slippery burn indicates which burn thickness?

A

Superfichttps://www.brainscape.com/l/dashboardial dermal

Mid-dermal

(will have blisters)

92
Q

A non-slippery burn indicates which burn thickness?

A

Deep dermal

Full thickness

93
Q

Name the predominant Gram-positive and Gram-negative organisms cultured from burn sites.

A

Gram-positive: staphylococcus aureus

Gram-negative: pseudomonas aeruginosa

94
Q

Where do infective organisms arise from? (group according to timeline of burn)

A

EARLY: commensal skin organisms (e.g. staphylococcus aureus, strep progenies), respiratory tract, environment

2-4 DAYS POST-BURN: Gram-negative organisms (e.g. p. aeruginosa, E. Coli). Skin, upper respiratory tract, GIT, hospital.

Gram-negatives dominate after day 5.

95
Q

The development of which type of vitamin deficiency can occur in full-thickness burn injury?

A

Vitamin D deficiency

YEAR 3 - SEMESTER 1 (15 decks)

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