KEY NOTES CHAPTER 8: BURNS - Surgery, Dressings, Complications, Referral Guidelines, Acute Management, Secondary Reconstruction, Chemical Burns, Electrical Burns, Cold Injury, Conditions Causing Burn-like Wounds.

Question 0

How do you classify the timings of burns surgery?

Answer 0

Emergency
Immediate
Early
Intermediate
Late

Question 1

What is classified as emergency surgery?

Answer 1

Tracheostomy
Surgical decompression

Question 2

What is immediate burn wound excision?

Answer 2

Within 24hrs.
SPT - temporary skin substitutes.
DD & FT - excised and grafted (auto or allograft until donor sites heal for recropping).
Advantages
- modulate hypermetabolic and SIRS response by removing nonviable tissue.
- less blood loss.
Disadvantages
- resource intensive (multiple surgeons and experienced anaesthetist and theatre staff, ICU)
- high demand for blood products.
- patient may not be fit.

Question 3

What is early serial burn wound excision?

Answer 3

Within 72hrs.
~25% excision per theatre visit in 48hrs intervals.
Advantages:
- decreases risk of excising potentially viable tissue
- less physiological ‘hit’.
Disadvantages:
- prolongs hypermetabolic response
- increased risk of colonisation, bacteraemia.

Question 4

Intermediate burns excision.

Answer 4

Within 3wks
- Sometimes non-life-threatening indeterminant depth burns are treated this way.
- Dressing applied, wait for 10-14 days to assess healing potential. If it doesn’t heal by 3 wks, excise and graft.
- 78% of wounds not healed by 3 weeks will become hypertrophic.

Question 5

Late burns excision.

Answer 5

> 3weeks
- may be due to medical optimisation or
- lack of resources, delayed presentation.

Question 6

What are the different methods of burns excision?

Answer 6

Tangential
Fascial
Amputation

Question 7

What signs are present to determine whether tangential excision is adequate?

Answer 7

Inadequate: yellow grey dermis, pink-brown fat, thrombosed vessels.
Adequate: bleeding bed, yellow fat, white glistening dermis.

Question 8

When is fascial excision indicated?

Answer 8

Deep/massive burns, where blood loss is of concern. Cutting diathermy is used and perforators are cauterised.
Advantages: more predictable wound bed, less blood loss.
Disadvantages: longer op time, poor cosmesis, denervation, distal limb oedema, exposure of non-graftable structures.

Question 9

What techniques are used for minimising blood loss?

Answer 9

Tumescent infiltration with 1:1,000,000 adrenaline.
Topical adrenaline soaks.
Tourniquets on limbs.
Permissive hypotension.
Tranexamic acid.
Systemic terlipressin (vasopressin analogue), recombinant factor VIIa (NonoSeven)
Topical surgical sealants (Tiseel - human fibrinogen and thrombin, bovine aprotinin.)

Question 10

How do you classify wound cover in burns?

Answer 10

Temporary
- Biological - organic or synthetic

Permanent
- autograft
- skin substitutes

Question 11

Give examples of temporary biological organic dressings.

Answer 11

Allograft, Xenograft (porcine).
(Cadaveric allograft can be stored in glycerol / cryopreserved (-80 degrees) / irradiated).

Human amnion (developing countries)

Question 12

What is the Alexander technique?

Answer 12

‘sandwich grafting’
Widely meshed autograft covered by meshed allograft.

Question 13

Give examples of temporary biological synthetic dressings.

Answer 13

Biobrane - bilaminate dressing of thin semipermeable silicone film with partially embedded nylon fabric and porcine dermal collagen 3D matrix.
Used in confluent SPT paediatric burns, donor sites.
Provides good pain relief

TransCyte - nylon mesh, porcine dermal collagen on thin silicone layer and neonatal human fibroblast cells. Frozen.

Question 14

Permanent wound cover with autograft skin.

Answer 14

SSG - meshed, sheet (face, hands)
FTSG - e.g. eyelids, secondary recon.

Question 15

What skin substitutes do you know of?

Answer 15

Integra - bilaminar dermal template composed of outer silicone sheet and inner layer of bovine collagen and shark cartilage GAG. Inner acts like ECM that organises fibroblasts and collagen into a neodermis. After 3 wks silicone layer is peeled off and thin SSG is applied.

Matriderm - single layer dermal template consisting of bovine dermal collagen and nuchal ligament elastin. Used in single stage reconstruction (SSG applied directly over Matriderm).

Cultured epithelial autograft - comes in suspension in spray form or sheets. Involves harvesting postage stamp sized SSG and culture for 3wks.

Question 16

What is the Cuono technique?

Answer 16

Application of spray cells on allograft dermal bed.
Allograft is applied for temporary wound closure whilst cell culture takes place. Allograft epidermis is dermabraded and cells are sprayed onto remaining dermis. (graft rejection is primarily mediated by epidermal Langerhans cells).

Question 17

What complications can be encounters with burns?

Answer 17

Systemic inflammatory response syndrome and sepsis
Toxic shock syndrome
Cardiovascular and respiratory impairment
Renal impairment
Gastrointestinal impairment
Electrolyte imbalance
Neurological complications
Musculoskeletal complications

Question 18

How is SIRS diagnosed?

Answer 18

2 or more of
- Temp >38 or <36 deg C
- HR >90bpm
- RR >20/min or PaCO2<32mmHg
- WBC >12,000 or <4000/microL

Question 19

What is infection?
What is sepsis?
What is septic shock?
What is MODS?

Answer 19

Infection = >10-5 per gram of tissue.
Sepsis = 2+ SIRS criteria.
Septic shock = sepsis with persistent hypotension despite adequate fluid resus.
MODS = altered organ function in acutely ill patient necessitating intervention.

Question 20

What is toxic shock syndrome?

Answer 20

Toxin-mediated acute life-threatening illness.
Young children at risk, usually caused by S. aureus (TSST-1) or Group A Streptococcus (pyrogenic exotoxins).
Superantigens (toxins) directly active T cells and trigger massive cytokine production.
Features: pyrexia, rash, vomiting, diarrhoea, myalgia, headache, hypotension, MODS.
ITU - systemic antibiotics, FFP, supportive therapies.
50% mortality if septic shock is established.

Question 21

What is the aetiology of renal impairment in burns?

Answer 21

SIRS.
Hypotension.
Pulmonary dysfunction -> SIRS and MODS.
Nephrotoxic drugs (antibiotics, NSAIDs).
Sepsis.
Myoglobinuria.

Question 22

How is myoglobinuria treated to prevent acute tubular necrosis?

Answer 22

UO >1-2ml/kg/hr.
Mannitol.
(Na bicarbonate alkalinisation controversial).

Question 23

What GI complications may occur?

Answer 23

Gastic stasis, paralytic ileus.
Curling’s ulcers (duodenal stress ulcers in burns).
Small bowel ischaemia (& bacterial translocation).
Minimised by early enteral feeding and PPI.

Question 24

What neurological complications may occur?

Answer 24

Global weakness, neuropathy following prolonged ITU.
Neuropsychiatric - anxiety, depression, PTSD.

Question 25

What musculoskeletal complications may occur?

Answer 25

Osteoporosis.
Heterotopic ossification.

Question 26

What are the referral guidelines used in UK?

Answer 26

UK National Burn Care Referral Guidance (2012)
- Burns >= 2% TBSA in children or >=3% in adults
- Full thickness burns
- Circumferential
- Burns not healed in 2 weeks
- Suspicion of NAI

Requiring discussion with Burns Consultant:
- Burns to hands, feet, face, perineum, genitalia.
- Chemical, electrical, friction burns.
- Cold injury
- Unwell febrile child with burn
- Concerns with co-morbidities that may affect treatment or healing.

Question 27

How are non-accidental injuries categorised?

Answer 27

1. Acts - intentional e.g. forced hot water immersion, cigarette burns (<0.1% of all paediatric burns).
2. Omissions - inadequate supervision (~20%).

NAI may occur in elderly / vulnerable adults.

Question 28

What evidence in the history may point towards NAI?

Answer 28

Mechanism of burn is
- inconsistent with exam findings or
- child’s developmental stage.

Weaker evidence
- delayed presentation.
- vague inconsistent history.
- inadequate supervision.
- sibling blame.
- lack of guilt.
- lack of engagement / co-operation with team.

Question 29

What evidence in the examination may point towards NAI?

Answer 29

• behavioural changes (frozen watchfulness).
• obvious patterns (cigarette, clear demarcation, uniform depth, symmetrical, donut sign on buttock).
• restraint injuries (finger mark bruises).
• bruises of varying age, fractures, poor hygiene, lack of engagement with health visitor / GP.
• background of social issues.
• immediate admission, contact local child protection nurses and paediatric consultant.

Question 30

Tell me how you would advise A&E to manage a child (or adult) with a 40% burn?

Answer 30

First aid: stop burning process, cool wound with tap water.
History: time, mechanism, clothing (removed?), inhalation, associated injuries? Tetanus status, PMH.
Examination and concomitant treatment.
- Airway, c-spine control.
- Breathing & ventilation, adminster O2.
- Circulation: control haemorrhage, monitor BP&HR, 2 wide bore cannulae, bloods.
- Disability: GCS / AVPU.
- Exposure: remove all clothing, assess TBSA and depth (send them age appropriate Lund and Browder chart),
need for escharotomies / fasciotomies, cover with cling film, weigh patient, blanket, warming.

Resuscitate
- fluid resuscitation (Parklands + maintenance).
- analgesia.
- ABG.
- tetanus.

reassess
- ABCs, HR, BP, UO, core temp.
- Urinary catheter.
- NG tube.
- Anaesthetic review before transfer to burns unit.

Question 31

Tell me how you would manage an adult with a major burn once he arrives in the burns unit?

Answer 31

Burns & anaesthetic team, theatre team and ITU team should be informed.
Warm theatres and prepare surgical instruments.
Weigh patient on weigh bridge.
Handover - history and examination, fluids administered, analgesia, intubated?, vital signs stable? Lines (venous, arterial, central, urinary catheter). Estimated TBSA, family members.
Intubate +/- lines +/- bronchoscopy.
Shave head if indicated.
Social scrub with betadine then saline.
Assess and document TBSA and potential donor sites on Lund and Browder chart.
Calculate accuracy of A&E estimates, alter resus fluids accordingly.
Assess adequacy of escharotomies / fasciotomies.
Dress with jelonet, gauze, gamgee, crepe.
Plan excision.

Question 32

How do you manage a major burns patient at first excision?

Answer 32

Anaesthetised, supine, arm boards, warming, induction antibiotics, blood products and allograft ordered.
Liaise with anaesthetic team - operation time is reduced if patient unstable, cold, coagulopathic, acidotic, hypotensive.

Logical sequence of excision. Prep,drape.
Anterior trunk: mark excision margins, harvest donor autograft. Tangentially excise burns, haemostasis, pack with adrenaline soaks.
Reposition prone, mark burns, harvest SSG, excise tangentially, haemostasis, sandwich graft to back and secure with staples, Acticoat, gamgee dressings, temporary drapes to avoid soiling dressings.
Reposition supine. Haemostasis should be achieved with adrenaline soaks and tamponade in prone position. Apply sandwich / allograft.
Sheet graft to neck if tracheostomy anticipated in 7-10 days.
Limbs excised with tourniquet control. Allograft / sandwich graft. Splint hands in POSI.
Area least likely to take = buttock, only autograft if spare, otherwise allograft.

Nursing team preparing autografts, allografts (meshed 1:1.5), and then dressings during excision.

Later on - consider bowel management system.

Question 33

How is secondary burns contracture minimised?

Answer 33

• early excision and grafting.
• thick sheet grafts to hand, face.
• respecting facial aesthetic subunits.
• early scar management - splints, face masks, silicone.

Question 34

How can burns scarring be assessed?

Answer 34

Vancouver Scar Scale.
- Vascularity.
- Pigmentation.
- Pliability.
- Height.
Visual Analog Scale.
Manchester Scar Scale.

Doesn’t assess function, pain, itch.

Question 35

What are Potokar’s 5 P’s in burn reconstruction?

Answer 35

1. Problems (FFPIP)
   - form (appearance)
   - function (restrictions on ADLs)
   - pain
   - itch
   - psychological issues (daily life)
2. Priorities
   - urgent: e.g. ectropion eyelid, lip, joint / neck contractures.
   - patient’s ranking of importance.
3. Possibilities
   - treatment options / donor sites?
4. Perceptions
   - patient’s expectations of treatment and outcomes.
5. Plan
   - devise with patient, start with a ‘winner’.

Question 36

How is burns reconstruction prioritised?

Answer 36

Acute
Eyelid: exposure keratitis.
Neck: airway problems.
Mouth: ectropion, incontinence, microstomia.
Nerve compression.

Intermediate
- e.g. joints, tension on tight scars during physiotherapy may cause cracks, pain, further hypertrophy.

Late
- uncomfortable scars, cosmesis.

Question 37

What is intrinsic and extrinsic burn contractures?

Answer 37

Intrinsic - scarring within affected area causing contracture.

Extrinsic - scarring remote from tight area creating tension.

e.g. eyelid ectropion may be either or both.

Question 38

What are the treatment options for contracture release?

Answer 38

Incisional
Excisional
Resultant defects are reconstructed with vascularised tissue (preferred esp in growing children) or grafts.

Question 39

What options are there for burns reconstruction?

Answer 39

Local flaps
- z plasty
- w plasty
- Y-V plasty
- 4 or 5 flap z plasty

Regional flaps
- pedicled, free FC or MC flaps

Skin substitutes
- Integra
- Matriderm

Tissue expansion

Skin grafts

+/- joint release

Question 40

What is the mainstay of scar management?

Answer 40

Pressure therapy (15-40mmHg, limits blood supply, decreases collagen synthesis, increases apoptosis in scar)
Massage
Silicone (occlusion and hydration of scar)

Question 41

What treatments are available for abnormal scars?

Answer 41

Intralesional corticosteroid injections
- reduce inflammation
- reduce collagen and GAG synthesis
- increased collagen degradation
- inhibit fibroblast proliferation

Laser
- Vascular lasers: PDL, KTP
- destroys blood vessels, localised ischaemia and causes breakdown and realignment of collagen fibres.
- reduces scar colour, height and firmness.
- Fractional CO2 lasers: releases contracted hypertrophic scars.

Cryotherapy
- liquid N2 +/- intralesional steroids.

Surgical excision
- usually combined with pressure therapy, steroids or DXT

Radiotherapy
- given within 48hrs of excision, inhibits neovascular buds and fibroblasts (collagen production). Carcinogenesis risk.

5 Fluorouracil
- used off-license after years of safe intraocular use.
- inhibits fibroblast proliferation?
- minimal systemic absorption, but contraindicated during pregnancy.
- Mixed with Adcortyl 1:1 (? 5FU=25mg/ml?), use finest bore needle to minimise bruising, haematoma, pain and ulceration.

Question 42

How do chemical agents cause burns?

Answer 42

1. Oxidation: denaturation by adding oxygen / sulphur ion to proteins, e.g. sodium hypochlorite, potassium permanganate.
2. Reduction: bind free electrons e.g. HCL, nitric acids.
3. Corrosion: denaturation on contact e.g. phenol, sodium hypochlorite, white phosphorous.
4. Protoplasmic poisons: bind Ca or other ions necessary for tissue function e.g. HF and formic acids.
5. Vesicants: ischaemia and anoxic necrosis, e.g. DMSO dimethyl sulfoxide, mustard gas.
   Dessicants: e.g. sulphuric and concentrated hydrochloric acids.

Question 43

What are alkali burns?

Answer 43

• cause liquefactive necrosis and deep penetration.
• e.g. household cleaning solutions, oven cleaners, fertilisers, cement.

Question 44

What are acid burns?

Answer 44

• cause coagulative necrosis.
• N.B. hydrofluoric acid buns.

Question 45

How is hydrofluoric acid burns managed?

Answer 45

• H+ ions cause coagulative necrosis, F- ions cause liquefactive necrosis and systemic hypocalcaemia and hypomagnesaemia.
• F- poisons Na-K ATPase and efflux of K+ from cells.
• ECG monitoring required for prolonged QT interval.
• Even trivial burns require treatment.
• Apply topical 10% calcium gluconate gel to inactivate free F ions.
• May require subcut 0.5ml 10% Ca gluconate per cm2.
• Intra-arterial Ca solutions may be considered.

Question 46

Where is phosphorus found? How do you treat phosphorus burns?

Answer 46

• Fertilisers, fireworks, firearms, insecticides.
• It ignites in air, therefore copious irrigation required.
• 0.5% copper sulphate solution impedes oxidation, turns phosphorous black, to help identification and removal.

Question 47

How is Na, K, Li burns treated?

Answer 47

• ignites with water.
• extinguish, then cover with oil.

Question 48

How is phenol burns treated?

Answer 48

• Water insoluble, therefore wipe off with 50% polyethylene glycol.

Question 49

How do you manage a chemical burn?

Answer 49

• remove clothing.
• remove chemical.
• irrigate copiously with water.
• consider Diphoterine (can be used on skin and eyes).
• treat systemic toxicity.
• examine nails, hair web spaces for residual
• toxicology for specific antidotes.
• treat as per thermal burns (early excision etc).

Question 50

Classify electrical burns.

Answer 50

Voltage
- low <1000V
- high >1000V
- extremely high: lightning strikes.

Current
- DC: single muscle spasm and throws body away from source (blunt trauma).
- AC: continuous muscle tetany, difficult for victim to release from source, more likely to develop arrhythmias.

Mechanism
- direct contact: electrothermal heating.
- indirect contact: arc, flame, flash.

Question 51

What are the different mechanisms of injury from lightning?

Answer 51

1. Direct strike - massive current impulse, often fatal.
2. Side flash or ‘splash’ - when lightning strikes a structure e.g. tree and then discharges current through the air or ground to the victim.
3. Contact - victim touches part of current pathway.
4. Ground current or ‘step voltage’ - current spreads radially through the ground and preferentially flows through the legs and body of victim (body is better conductor than earth).

Lichtenberg figures - pathognomonic sign of lightning injury. Disappears in a few hours.
Burns and deep muscle damage rare, but systole, respiratory arrest and neurological damage common.

Question 52

What is the pathophysiology of a low voltage electrical injury?

Answer 52

• burn injury usually small.
• more likely to die from cardiac arrhythmia / asystole.
• if ECG is normal, no need to monitor.

Question 53

What is the pathophysiology of a high voltage electrical injury?

Answer 53

• injury caused by heat, and severity of injury is dependent on current, resistance and duration of contact.

Resistance
- nerve, muscles, blood vessels: low.
- fat, tendons, bone: high.
- skin: intermediate (lowered if wet).

Current pathway: through
- chest -> myocardial problems.
- brain -> respiratory arrest, seizures.
- orbits -> cataracts.

Be vigilant: entry and exit wounds with extensive underlying damage, compartment syndrome and myoglobinuria.

Question 54

How should high voltage electrical injuries be treated?

Answer 54

cardiac monitoring
fluid resuscitation
renoprotection
early fasciotomy

Question 55

How are cold injuries classified?

Answer 55

Freezing
- Frostnip
- Frostbite

Non-freezing
- Trench foot

Question 56

What is frostnip?

Answer 56

• mildest form of cold injury, full recovery expected.
• acral areas: fingers, toes, nosetip, ears become white and insensate.
• rewarming: skin becomes hyperaemic and anaesthetic.

Question 57

What is frostbite?

Answer 57

• As skin cools to 0 degrees, extracellular ice crystals form.
• Ischaemia results from shunting of peripheral blood to maintain core temp
• Extracellular crystals draw fluid out of cells, causing intracellular hyperosmolarity, leading to cell damage and protein denaturation.
• Microvascular endothelial damage and vascular stasis leads to thrombosis and gangrene.
• Treatment of hypothermia in hospital is required.
• Extremities are rewarded in 37-39 degree circulating water for 1hr, until skin is red-purple colour and pliable.
• dressings are applied to protect from infection and minor trauma.
• Ibuprofen: anti-inflammatory and analgesic.
• Thrombolytic therapy may be beneficial.
• Fasciotomy may be required.
• Amputation usually delayed after demarcation.

Question 58

What is trench foot?

Answer 58

• prolonged exposure to wet environment.
• superficial, moist, liquefactive necrosis.
• combination of: near-freezing temp, wet, dependancy, constriction by shoes and clothing.

Question 59

What is the pathogenesis and treatment of trench foot?

Answer 59

Pathogenesis
1. Pre-hyperaemic phase
- limb is cold, swollen, discoloured, numb.
2. Hyperaemic phase
- red, swollen, bounding circulation.
3. Post-hyperaemic phase
- warm, cold sensitivity.

Treatment
- washing, air-dry feet, rewarming, bed rest, elevation.

Question 60

What is toxic epidermal necrolysis?

Answer 60

• rare, acute, potentially fatal skin reaction.
• characterised by epidermal skin and mucosal loss.
• most cases are attributable to a particular drug, most commonly allopurinol, co-trimoxazole, other antibiotics, anti-convulsants, NSAIDs.
• pathogenesis is believed to be immune-mediated.

Question 61

What are the signs of TEN?

Answer 61

• erythematous macules, Nikolsky sign.
• epidermal detachment, blisters.
• mucosa: eyes, mouth , oesophagus, URT, GIT, GUT.
• histopathology: keratinocyte apoptosis and necrosis (causing epidermal detachment).

Question 62

What is the difference between SJS and TEN?

Answer 62

SJS <10% TBSA.
TEN >35% TBSA.
SJS-TEN overlap diagnosis in between.

Question 63

How can prognosis be predicted?

Answer 63

SCORTEN: validated illness severity score.
1 point for each:
- Age > 40
- Malignancy
- HR >120 bpm
- >30% TBSA initial epidermal detachment
- Urea > 10mmol/L
- Glucose > 14
- Bicarb >20

Mortality
1 = 3.2%
5+ = 90%
3+ should be managed in ITU

Question 64

What is the management of TEN?

Answer 64

stop causative drug
SCORTEN
Burns unit supportive care
survival rates higher if earlier transfer (29.8% vs 51.4% if within 7days)
Ophthamology review
Fluid electrolyte balance
No consensus with treatment
- Deroofing vs leaving blisters
- Biobrane vs conventional dressings
- Possible benefit from ivIg, cyclosporin, anti-TNFalpha antibodies, plasmapheresis.

Question 65

What are the complications of TEN?

Answer 65

Ocular: symblepharon, conjuctival synechiae, entropion, trichiasis.
Cutaneous: scarring, irregular pigmentation.
Mucosal: persistent erosions, phimosis, vaginal synechiae, nail dystrophy, diffuse hair loss.

Question 66

What is staphylococcal scalded skin syndrome?

Answer 66

• red blistered skin.
• caused by staphylococcal exotoxins (exfoliative toxins A&B).
• localised toxins cause bullous impetigo.
• systemic dissemination causes SSSS.
• usually seen in <5yr old, childhood mortality 5%, up to 60% in adults with co-morbities.
  Histology:
• SSSS: superficial epidermal blistering.
• SJS/TEN: subepidermal blistering & necrotic keratinocytes.

Management:
- supportive.
- anti-staph antibiotics: flucloxacillin.
- usually heals in 1 wk.