Week 7- Management Of Acute Burns Flashcards

1
Q

What are the layers of the skin

A

-Epidermis
• Superficial protective layer
• Keratin which toughens and waterproofs
• Melanin (melanocytes) produce pigment for UV protection
• Rete pegs for attachment /adherence to dermis
• No blood vessels in epidermis

-Dermis
• 2 layers – Papillary layer (closer to epidermis) and Reticular layer
• Network of blood and lymph vessels, nerves, elastin fibres and collagen
• Provides mechanical strength of the skin
• Ground substance - surrounds all the structures in dermis – semi-fluid matrix that lubricates cells during
stretch and acts as a buffer during recoil (made up of glycosaminoglycans and proteoglycans)

-Epidermal Appendages
• Hair follicles, sweat glands, sebaceous glands
• All are surrounded by epidermal cells & a rich network of capillaries
• Centre for regeneration of the epidermis

-Hypodermis
• Subcutaneous fat and fascia

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2
Q

What are skin types

A

-Skin Thickness
• Epidermal and dermal thickness varies throughout the body
• Thinnest skin – eyelids (0.5mm epidermis, 0.6mm dermis)
• Thickest skin
-Palms of hands (1.5mm epidermis)
-Soles of feet (1.5mm epidermis, 3mm dermis)
-Back (3mm+ dermis)

-Hairy skin
• Thin epidermis
• Contains hair follicles

Glabrous Skin
• Thick epidermis – additional layer within the epidermis (stratum lucidum)
• Devoid of hair
• Palms, soles of feet, lips, genitals

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3
Q

What is the Fitzpatrick Skin Type Scale

A

• Numerical classification for skin colour
• Rating considers
1) the amount of melanin in the skin (white, brown, black)
2) the skin’s tolerance to sunlight and tendency to tan or burn (Score = 0-40)- Q’s attached

Type I - Pale white, very fair skin; blond or red hair; blue eyes; freckles; always burns, never tans (Score 0-6) – High risk of scarring
Type II - White; fair skin; blond or red hair; blue, green, or hazel eyes; usually burns easily, tans minimally (Score 7-13)
Type III - Cream white skin; fair with medium to dark hair, varied eye colour; quite common; burns moderately, tans uniformly (Score 14-20)
Type IV - Moderate brown; typical Mediterranean olive skin tone; rarely burns, always tans well (Score 21-27)
Type V - Dark brown; Middle Eastern skin types; very rarely burns, darkens and tans very easily (Score 28-34) (Very high risk of scarring)
Type VI – Very dark skin, Deeply pigmented dark brown to black; Dark eyes, dark hair, never burns (Score 35+) (Very high risk of scarring)

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4
Q

What are skin functions and implications for skin loss

A
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5
Q

How are burn wounds classified

A

1) Type of burn or mechanism of injury
Thermal burn, chemical burn, electrical burn

2) Depth of burn
Partial thickness vs Full thickness burn

3) Size or Area of the burn
Surface area percentage of burn

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6
Q

Types of burns

A

Flame Burns
• Most common type of injury in adults

Scald Burns
• Most common injury in paediatrics and the elderly

Work related incidents
• Flame / Chemical / Electrical

Other injuries
• Friction / Contact / Radiant heat / Pressurised gas

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7
Q

Classifying depth of burn

A

-Superficial Burn
-Partial Thickness Burn (Dermal Burn)
• Superficial Partial Thickness or Superficial Dermal Burn
• Deep Partial Thickness or Deep Dermal Burn
-Full Thickness Burn

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8
Q

Describe a superficial burn

A
  • Areas Destroyed: Epidermis only destroyed
  • Appearance: Red and blistered
  • Sensation: Sensation intact, hypersensitive
  • Blanching / Capillary return: Rapid capillary return / blanching
  • Wound Closure: Wound closure spontaneously in 7 - 10 days
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9
Q

Describe superficial partial thickness burn

A
  • Area Destroyed: Epidermis and superficial part of dermis
  • Appearance: Red to pink appearance, blistered
  • Sensation: Sensation intact, hypersensitive and painful
  • Blanching / Capillary Return: Rapid capillary return / blanching
  • Wound Closure: Wound closure spontaneously in 14 days
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10
Q

Describe deep partial thickness burn

A
  • Areas Destroyed: Epidermis and deeper into the dermis
  • Appearance: Creamy moist white appearance, pseudomembrane may be present, oedematous
  • Sensation: Sensation intact but may have decreased sensation to light touch in some areas (some nerve endings damaged)
  • Blanching / Capillary Return: Delayed capillary return / blanching but present
  • Wound Closure: From wound edge and epidermal appendages in >14 days
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11
Q

Describe full thickness burn

A
  • Areas Destroyed: Epidermis,dermis&underlyingstructures
  • Appearance: white, tan, black, brightred; dry leathery appearance
  • Sensation: No light touch sensation to skin
  • Blanching / Capillary Return: Nil blanching/capillary return
  • Wound closure: Takes >3weeks for closure -requires grafting
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12
Q

How to classify the size or area of the burn

A

• Total Body Surface Area affected (% TBSA)
• Usually calculated on the Lund & Browder chart
– Accounts for body proportion changes with growth and development
• %TBSA essential for accurate calculation of fluid replacement requirement
• Rule of nines gives a quick estimate of percentage burn

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13
Q

What are the ANZBA referral guidelines

A

The following criteria are endorsed by ANZBA in assessing whether burns require treatment in a specialised burns unit (ANZBA 2004)
• Burns greater than 10% of total body surface area (TBSA);
• Burns of special areas—face, hands, feet, genitalia, perineum, and major joints;
• Full-thickness burns greater than 5% of TBSA;
• Electrical burns;
• Chemical burns;
• Burns with an associated inhalation injury;
• Circumferential burns of the limbs or chest;
• Burns in the very young or very old;
• Burns in people with pre-existing medical disorders that could complicate management, prolong recovery, or increase mortality; and
• Burns with associated trauma.

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14
Q

What are the wound healing stages

A
  • Inflammatory phase - (1 to 5 days)
  • Cell Proliferation phase - (3-5 days - 3 weeks)
  • Remodelling phase - (3 weeks - 12- 18mths)
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15
Q

Explain the cell proliferation phase (3-5 days to 3 weeks)

A

• Fibroblasts begin synthesising collagen and ground substance
– gives the wound tensile strength and provides a matrix for new cells to migrate and proliferate
• Fibroblasts differentiate into myofibroblasts
• Myofibroblasts cause wound contraction
– first appear Day 3-5
– are contractile and pull the edges of the wound together: contracture
• Keratinocytes proliferate and become mobile across wound surface —> epithelialisation of wound
• At end of proliferation phase the wound is closed with the formation of scar tissue
– dermis of disoriented collagen
– epidermis that lacks interconnection with dermis
– prone to abrasion and minor trauma

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16
Q

Explain the remodelling phase (3 weeks to 12-18 months)

A
  • Collagen forms cross links to increase tensile strength of scar tissue
  • Tensile strength continues to increase for up to 1 year following injury
  • Ground substance is often more dense and bony like
  • Continual collagen synthesis and degradation during remodelling phase (synthesis outways degradation)
  • Orientation of collagen becomes less random and more parallel with mechanical stress
  • Myofibroblasts peak in number at 4 to 5 months post burn
  • Scars are adaptable to rehabilitation during this phase until scar maturation
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17
Q

Summarise the wound healing

A
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18
Q

What is a hypertrophic scar?

A

A thick raised scare, an abnormal response to wound healing in which extra connective tissue forms within the original wound area.

  • Remains within border of injury (vs Keloid – outside border of injury)
  • Excessive collagen deposition into whorl-like haphazard collagen bundles
  • Reduced amount of highly cross linked collagen (reduced skin strength)
  • Develops within 1 – 3 months post-injury, progresses for 3 to 6 months, gradual regression over time
  • Increased blood supply in scar (highly vascular/ red in appearance)
  • Build up of granulation tissue (thick and raised)
  • Overabundant collagen deposition by fibroblasts (2 – 3 x rate of normal skin fibroblasts)
  • No significant difference in collagen degradation
  • Minimal regeneration of elastin fibres
  • Changes in ground substance (“bony like”)
  • Significantly reduced skin stretch
  • Constant contraction through myofibroblast activity
  • Adhesion to underlying structures
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19
Q

What are clinical signs of a hypertrophic scars

A

• Colour / Vascularity
– (purple ➢ red ➢ pink)

• Height / Thickness
– Thickened texture of scar
– Bumpy & irregular scar texture

• Pliability / Hardness
– Hard, non supple or pliable feel –  ROM & function

• Sensation
– Altered sensation, hypersensitivity, itch, pain

• Associated Oedema

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20
Q

What are risk factors for scarring

A
  • Race lead to dark skinned, skin type V and VI, Asian and African skin types
  • Genetic predisposition – keloid > hypertrophic scar
  • Site of scar – head, hands, neck and axilla, across joints
  • Depth of wound – deeper the wound lead to longer to heal
  • Prolonged inflammatory stage and increased granulation
  • Skin grafting – decrease scar vs wounds left to heal conservatively > 21 days
  • Type of grafting procedure - SSG > full thickness grafts
  • TBSA, no. of surgical procedures and anatomical location – increase scar risk
  • Age – children and adolescents > adults > elderly
  • Female gender
  • Compliance or access to early treatment
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21
Q

What is appropriate first aid after a burn

A
• Stop the burning
– Stop drop roll / Wrap in blanket / water irrigation
– Remove heat source
• Copious water irrigation
– 20 mins
– Running water
– Avoid hypothermia 
• Avoid dirt or dirty water if possible

Note do not use ice as will increase burn depth

22
Q

What is medical management after a burn

A

• Assessment of size and depth of burn
• Fluid Resuscitation
• Management of airway +/- inhalation injury
• Escharatomies
• Prevention and management of infection
– Tetanus injection
• Nutritional support
– Early enteral feeding reduced morbidity (<24 hours) - shorter ICU stay and reduced wound infections
– >15% TBSA burn should have supplemental feeding via oral route
• Wound Management – conservative vs Skin grafting
– Early debridement and grafting blunts SIRS response and reduces risk of infection (< 48hours)
– Priority areas – line sites, trache site
• Pain management
– Long acting (MS Contin), Short acting for procedures (Morphine)
– Gabapentin – burning pain
– Others – entonox, anti-anxiety medications
• DVT and ulcer prophylaxis

23
Q

What is an escharotomy

A

• Incision through eshar to relieve pressure and improve tissue perfusion in muscle compartment
• Usually done when circumferential full thickness burns
• Limbs, chest, abdo (rarely neck/digits)
• Assessment
– Pain / paraesthesia / loss of function
– Cap refill / pulse oximeter < 90% O2
– Peripheral pulse / doppler pulses
– Compartments feel tight (compartment pressures >25mmHg)
– Increased ventilatory pressures
• Abdominal and chest escharotomy – may be necessary to improve ventilation
• Can extend to Fasciotomy if pressures not corrected – more common in electrical injury

24
Q

What’s included in conservative wound management

A
  • Silver Based Dressings – acticoat, Mepilex Ag, Silvazine / Flamazine
  • Provides antibacterial effects
  • Promotes wound healing
  • Acticoat and Mepilex Ag can stay intact for 3 - 7 days
  • Silvazine / Flamazine cream changed daily
25
Q

What are surgical management

A
  • Autograft
  • Cultured autologous keratinocytes
  • Homograft – Cadaver allograft
  • Skin Substitutes– Integra / Biobrane / BTM
  • Flaps
26
Q

Explain autographs

A
  • Burn wound bed is debrided to viable tissue
  • Donor skin taken - absolute thickness is variable (8/1000 - 24/1000 inch)
  • Skin graft secured (usually with staples but also use glue or sutures)
  • Surrounding joints immobilised with splints initially to allow take of the graft
  • Split thickness vs Full Thickness
  • Meshed vs Non Meshed
27
Q

Explain a graft take

A

• Appearance
– skin appears pink, securely adhered and blanches with pressure

• Adherence
– fibrin is responsible in first 48 hours

• Revascularisation
– complete at Day 5-6
– first 48 hrs - plasmic imbibition 
– 48-72hrs
• anastomoses of vessels in graft and wound bed 
• growth of new endothelial buds
28
Q

What are split thickness grafts

A
  • epidermis and varying amounts of the dermis depending on depth of donor
  • donor site will heal on its own
29
Q

Explain thickness grafts

A

-thick donor site to allow transfer of dermis and epidermis (needs a split thickness graft to cover the defect left at donor site)

30
Q

What are meshed grafts

A

– Graft put through meshing device to allow greater spread of graft
– Better earlier take of graft
– Mesh allows exudate to be evacuated from under graft
– Cosmetically always left with a mesh pattern

31
Q

What are non-meshed grafts

A

– Better aesthetically as no mesh pattern – usually used for face or hands
– More fragile in earlier stages as no mesh to allow escape of exudate from under graft
– Nurses may need to prick graft and roll exudate or haematoma out from under graft to improve graft take

32
Q

What are cultured autologous keratinocytes

A
  • Biopsy of epidermal cells taken
  • Cells cultured in lab to form skin sheets (2 - 3 weeks) or cell suspension (5 days)

• Advantages
– allows large %TBSA burns to be covered without need for donor sites
– nil rejection (patient’s own skin)

• Disadvantages
– skin remains fragile - lack of dermal attachments
– inflammation can cause blistering and sloughing off of cells

33
Q

What are homograft- cadaver allograft

A
  • Tissue donation from human donor - cryopreserved
  • Temporary cover
  • Rejection occurs in 7 - 14 days

• Used as biological bandaid
– Over debrided wound bed
– Over widely meshed SSG – sandwich graft

  • Can have problems with transmission of viruses / infection – screened as per blood donation etc
  • Expensive and in short supply
34
Q

What are skin substitutes

A
  • integra
  • biobrane
  • BTM (biodegradable Temporizing Matrix)
35
Q

Explain integra

A

• 2 layer skin substitute
– dermal replacement layer
– epidermal substitute-silicone layer

• Artificial dermis is allowed to vascularise (14 - 21 days) then silicone layer is removed and replaced with a thin epidermal autograft

• Advantages
– early wound closure without donor sites
– large TBSA covered in one operation
– less hypertrophic scarring
– thinner donor sites needed for coverage - less donor site pain, faster healing, frequent reharvesting
– no rejection
– grows with children

• Disadvantages
– poor resistance of dermis to infection
– less drainage of exudate through solid sheet of silastic
– need for a second operation in smaller burns

36
Q

Explain biobrane

A
  • Synthetic nylon mesh fabric covered with silicone rubber membrane
  • Semi-permeable to water
  • Protective barrier to micro-organisms
  • Temporary cover for partial thickness burns
  • Used as a staging procedure for full thickness burns
  • If deeper burn, it may still require grafting after removal of biobrane
37
Q

BTM

A

• Biodegradable Temporizing Matrix
• 2 layer system
– Dermal replacement – synthetic sponge
– Epidermal replacement – silicone
• Dermis proliferates along sponge matrix
• Product stays in place for 4-5 weeks for granulation to occur
• Removal of silicone layer and skin graft

38
Q

Explain flaps

A

• Performed when a simple skin graft is not enough to cover a wound / defect
• Used to cover exposed bone, tendon or other structures.
• Flaps are classified as either
-Skin flaps (skin and subcutaneous tissue with or without underlying fascia)
-Muscle flaps (flap created from muscle with or without attached overlying skin).
• The main difference between a flap and a graft
-Flap usually transferred with its own blood supply
-Skin graft blood supply has to come from the underlying wound bed
• Free flap vs Pedicle flap vs Rotational flap
• More prolonged immobilisation – 10 days

39
Q

What is the inhalation injury

A

• Upper respiratory Tract damage
– Direct thermal injury
– Upper airway oedema

• Lower Respiratory Tract damage
– Due to interactions of chemical compounds contained in the inhaled smoke
– Limited cases of direct thermal damage
• Due to efficient cooling and fast glottic reflexes
• High pressurised steam causes direct thermal damage to the lungs

• Results in
– damage to mucosal lining
– mucosal oedema
– de-epithelialisation
– pseudomembrane formation - airway plugging and compromised alveolar ventilation
– deactivation of surfactant
40
Q

Signs/ symptoms of inhalation injury

A
• Burn injury occurred in enclosed space
• Lowered consciousness at time of fire
– Alcohol use
– Drug use
– Pre-existing condition eg HI, CP
• Facial / oral burns
• Singed nasal hairs
• Soot in mouth or nose
• Hoarse voice
• Respiratory distress
– increase RR, increase accessory muscle use, SOB
• Bronchospasm / stridor
• Carbonaceous / sooty sputum
• Auscultation - wheezes initially and then fine crackles
• ABGs - high levels of carboxyhaemoglobin, decreased PaO2
• Chest Xray - patchy atelectasis and pulmonary oedema
41
Q

How to confirm a diagnosis inhalation injury

A
Bronchoscopy
– airway oedema
– airway inflammation
– mucosal necrosis
– pseudomembranous plugs 
– soot or char in the airways
42
Q

What are the clinical stages

A

• Acute pulmonary insufficiency
– (first 36 hours post injury)
– fire consumes available oxygen
– CO disturbs O2 carrying capacity
– atelectasis compounded by laryngeal spasm and coughing
• Pulmonary oedema
– (6 - 72 hours post injury - peaks at 12 hours)
– Presence of pulmonary oedema and deactivation of surfactant leads to decreased lung compliance
• Bronchopneumonia
– (3 - 10 days post injury)

43
Q

What are bronchopeumonia

A

*De-epithelialisation of mucosa
*Pseudomembrane forms on airway wall
*Separation of pseudomembrane
– obstruct / plug airway
– prevention of normal mucous clearance
– pooling of secretions
– distal atelectasis and bronchopneumonia

44
Q

What is medical management of inhalation injuries

A
  • oxygen
  • intubation and ventilation
  • therapeutic bronchoscopy
  • high PEEP/ CPAP/ use of BiPAP
  • Escharotomies to chest wall
  • Bronchodilators
  • Humidification
  • nebuliser heparin
  • regular chest Physiotherapy
45
Q

What are Physiotherapy respiratory Techniques

A

• Ventilated Patients
– Manual hyperinflation / Ventilator Hyperinflation
– Percussion and Vibration
– Suctioning
– Positioning
– Passive / Active assisted demand ventilation

• Non Ventilated Patients
– Staged basal expansion ex with inspiratory holds
– Incentive spirometry
– Demand ventilation and mobility
– Positive pressure devices
• NIV eg BiPAP, PEP masks, flutter
– percussion, vibration, postural drainage

46
Q

Timing of respiratory techniques

A

-Prior to grafting
• Can perform percussion / vibrations over burns to anterior chest

-Post grafting
• Initially cease manual techniques over newly grafted chest wall
• Recommence manual techniques dependent on grafting technique

-Considerations for treatment timing
• Ensure use of humidification (if not requiring oxygen then use on room air)
• Nebulised heparin – time physiotherapy for 20-30minutes after neb
• Positive pressure techniques are helpful to assist with recruitment of distal alveoli and consequently assists with secretion removal

47
Q

What is Physiotherapy management for the acute phase

A

• Appropriate subjective / objective assessment
– Dependent on level of consciousness of the patient
• Develop Rapport with patient / family
• Education
– Importance of exercise program
– Protocols for management
• Respiratory management
• Oedema management
– Elevation, compression bandaging, ROM exercises
• Exercise Prescription
– ROM, resistance / strength, CV fitness
– Early mobility / Promote functional independence
– Need to address fear of movement, Pain, Bulk of dressings, direction of contracture (combined stretches)
• Positioning / splinting / protective footwear

48
Q

What’s included in the subjective assessment

A

From the Medical Chart and patient interview
• Mechanism of injury – how burn occurred, people involved in incident, damage to home
• Area of burn and Burn depth
• Current medical management to date eg escharotomy, fluid resuscitation, oxygen requirement
• All relevant injuries and treatment to date eg associated fractures / trauma
• Patient’s age

Past History
• Mental health history – anxiety / depression, diagnosed mental health conditions
• History of diabetes, vascular disease, long term steroid use
• History of respiratory conditions, smoking history

Social History
• Who patient resides with, who are their potential supports, where do they live (regionally vs metropolitan)
• Nature of residence – high set vs low set, stairs, slopes

Pre-morbid Function
• Work status and occupation / school level
• Level of independence with mobility and ADLs, what they have been able to do since the injury
• Leisure / hobbies

49
Q

What’s included in the objective assessment

A

Pain Assessment
• Rating at rest and with movement

Respiratory Assessment
• Observation / Palpation / Auscultation

Musculoskeletal Assessment
• If possible initial assessment with dressings removed (time with dressing change)
-Note location of burn injury and depth of burn injury over joints
-Potential risk areas eg neck, axilla, hands
-Potential exposed tendons eg achilles, dorsum of the hands
• Assessment of Range of motion of all affected joints / areas
-Resting position of the joint (position of rest = position of contracture)
-Active vs assisted active vs passive ROM
-What is the limitation to the ROM – pain vs skin tightness vs oedema
• Presence of blanching with movement – early signs of skin tightness
• Can it be improved by exercise
• Assessment of strength / functional ability at subsequent reviews (usually with dressings intact)

Assessment of Oedema
• Circumferental measure vs observation

Mobility Assessment
• Bed mobility / transfers / mobility
• Mobility aids required
• Appropriate bandaging and protective footwear required

50
Q

Respiratory management

A

High Risk of Respiratory Complications due to
– Presence of Inhalation Injury
– Effects of prolonged bed rest
• Reduced FRC
• Increased risk of pneumonia
– Multiple anaesthetics for surgical management

Respiratory Physiotherapy management based on assessment findings
– Physiotherapy techniques to increase air entry
– Physiotherapy techniques to improve secretion clearance
– Techniques to improve cardiovascular endurance and exercise tolerance

51
Q

What is oedema management?

A

• Acute oedema occurs immediately after burn injury
• Peaks at 1-2 days, plateau at day 4
• Presence of oedema increases the diffusion distance between capillaries and cells
-Delays exchange of nutrients and oxygen to the cells
-May lead to burn wound depth conversion and delayed healing
• Main aims of oedema management
-To promote appropriate wound healing
- To promote function / range of motion

What we can do: