Burns

Aetiology

• Fire/flame 41%
  • Common in young adults
  • Damage from super-heated oxidised air by convection and radiation
• Scalds 33%
  • Damage from contact with hot liquids
  • Common in children
• Contact burns 9%
  • Damage from contact with hot or cold solids
• Chemical burns 3%
• Electrical burns 3%
  • Conduct of electrical current through tissues
• Always consider NAI in infants/children

Pathophysiology

• Thermal burns cause damage to skin and occasionally underlying structures through abrupt temperature change that exceeds biological tolerance. This leads to membrane disruption, protein denaturation, and necrosis.  The injury extends from the skin surgace to deeper structures in a first-order logarithmic distribution depending on the temperature of the burning agent and duration of exposure.
• Flame, scald and contact burns induce injury by transfer of energy, causing coagulative necrosis. Chemical and electrical burns also cause direct injury to cellular membranes.
• Zones of injury - 'Jackson levels' - has been questioned recently, but helpful paradigm for now.
  • Zone of coagulation - necrotic area of burn, where cells are directly disrupted. Irreversibly damaged at the time of injury.
  • Zone of stasis - moderate degree of insult, with decreased perfusion. Can either survive or go on to coagulative necrosis.
  • Zone of hyperaemia - vasodilation from inflammation surrounding the burn wound. Contains the clearly viable tissue from which the healing process begins. Generally not at risk for further necrosis.
• Systemic effects
  • Systemic inflammatory response to the burn - many mediators involved
  • Generalised oedema in both burned and unburned skin
  • Pre-renal AKI common, sometimes bad enough to lead to ATN
  • Global depression in immune function - higher risk of bacterial wound infection, pneumonia, and fungal and viral infections. With burns >20% TBSA, this impairment is proportional to burn size.
  • Hyper-metabolism - tachycardia, increased oxygen consumption, and massive proteolysis/lipolysis. Can be sustained for months, leading to massive weight loss and decreased strength.
• Inhalation injury
  • Damage primarily from chemical burns associated with inhaled toxins
  • Heat is dispersed in the upper airways, so direct thermal lung injury is rarely seen, except in high-pressure steam inhalation
  • Smoke inhalation leads to immediate airway oedema and increased lymph flow, which is high in inflammatory mediators, and may cause further lung injury. Also leads to exudate formation within airways, which eventually coalesces into fibrin casts, which are difficult to clear with standard airway suction techniques.
  • Three phases of inhalation injury

• • 1. Acute pulmonary insufficiency
    2. Increased extravascular lung water, hypoxia, and diffuse lobar infiltrates (72-96 hours post-injury); similar to ARDS
    3. Clinical bronchopulmonary pneumonia (generally 3-10 days post-injury). Early pneumonias are generally staph, whereas gram negative organisms come later.

Burn depth

• Depth of injury is best assessed by experienced practitioners, although imaging may help in the future
• If unsure whether superficial or deep partial-thickness, assume deep

Depth	Appearance	Sensation	Healing time
Superficial (epidermal)	Dry, red Blanches with pressure	Painful	3 to 6 days Won't scar. Topical salves and NSAIDs.
Superficial partial-thickness (epidermis and papillary dermis)	Blisters (within 24 hours) Moist, red, weeping Blanches with pressure Retention of hairs to gentle pulling.	Painful to temperature and air	Spontaneously re-epithelialize in 7 to 21 days. May have some slight discolouration and textural differences.
Deep partial-thickness (epidermis and reticular dermis)	Blisters (easily unroofed) Wet or waxy dry Variable color (patchy to cheesy white to red) Does not blanch with pressure	Perceptive of pressure only. Painful to pin-prick.	Re-epithelialize in 15-21 days from deep hair follicles and sweat gland keratinocytes, often with severe scarring.
Full-thickness (into subcutaneous fat)	Waxy white to leathery gray to charred and black Dry and inelastic No blanching with pressure	Deep pressure only	Rare, unless surgically treated. No keratinocytes remain - so must heal by re-epithelialization from wound edges. Benefit from excision of eschar and autologous grafting to minimise contractures.
Deeper injury (ie, fourth degree)	Extends into fascia and/or muscle	Deep pressure	Never, unless surgically treated

Burn size

• Rule of 9s. Alternatively, take palm of hand as 1%.
• Use Berkow formula to determine burn size in children/infants
• Don't include superficial burns in TBSA
• Baux score: age + TBSA
• Modified Baux score: Per Cent Mortality = Age + Percent Burn + [17 x (Inhalation Injury, 1= yes, 0= no)]

Indications for referral to a burns centre

• Partial-thickness burns involving >10% TBSA
• Burns involving face, hands, feet, genitalia, perineum or major joints
• Any full-thickness burn
• Electrical burns, including lightning injury
• Chemical burns
• Inhalation injury
• Burns in patients with pre-existing medical disorders that could complicate management, prolong recovery, or affect outcome
• Any patient with burns and concomitant trauma in which the burn injury poses the greater immediate risk of morbidity and mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially transferred to a burn unit. Physician judgment is necessary in such situations and should be in concern with the regional medical control plan and triage protocols.
• Burned children in hospitals without qualified personnel or equipment to care for children
• Burns in patients who will benefit from special social, emotional or long-term rehabilitative intervention.

Initial assessment, resus and treatment of burns patients

Pre-hospital

• • Suspect inhalation injury, and give 100% oxygen if required
  • Remove all jewellery
  • 20 minutes of cool running water is beneficial within 3 hours of injury, but don't cool the wound, as it can lead to hypothermia
  • Transport to emergency
  • Dry dressings or clean sheet to avoid maceration
  • Warm with blankets
  • Don't use IM or S/C analgaesia - impaired absorption from vasoconstriction

Initial treatment of burn

• • Remove clothing and debris (don't peel off adherent clothing)
  • Cooling
    • Cool/room temp water
    • Alternatively cover with wet gauze
    • Avoid ice or very cold water
    • Avoid macerating wound - max five minutes
  • Simple cleansing
    • Gently clean with gauze and normal saline, or 0.1% aqueous chlorhexidine
    • Remove loose skin/debris
    • A clean flannel can be substituted if gauze is unavailable
    • Shave burns to a 2cm border at initial cleaning, and with subsequent dressing changes
  • Debride
    • Remove sloughed or necrotic skin, ruptured blisters
    • Management of intact blisters is controversial. Indications for debriding them:
      • Thick-walled blisters
      • Blisters over joints or dependent areas
      • >2cm in diameter
  • Appropriate dressing
    • Superficial and superficial partial thickness do not need chemoprophylaxis - use moisturiser cream
    • Deep partial or full thickness should have a topical antibiotic
    • Do not use systemic antibiotics prophylactically
    • No role for topical steroids
    • If transferring, dry gauze is appropriate
    • For longer-term dressings, use gauze with a non-stick layer or hydrocolloid eg duoderm
  • Pain management
    • Simple stuff
    • Elevation may help
    • Itching - use antihistamines
  • Tetanus prophylaxis

Moderate to severe burns: initial assessment and treatment

• • Trauma ABCD assessment
    • Can be hard to take BP due to charred extremities - need invasive arterial monitoring in this setting, with peripheral pulses being used as a proxy of perfusion in the meantime
  • Basics
    • Cover burns with clingfilm (can give a rinse if possible)
    • Bloods (?G+H)
    • IV access - prefer peripheral veins in unburned skin, but IVC through burned skin is better than no access at all
    • BSL
    • Pregnancy test
    • Check for compartment syndrome
      • Especially high-voltage electrical injuries, circumferential burns, delayed resus, or high-volume resus
      • Typically evolves over 12-72 hours following burn and resus
      • Hands, feet, legs, forearms, abdomen, eyes
      • Check for acute nerve compression syndromes
      • Serum CK and myoglobin can assist diagnosis
    • Remove jewellery
    • NGT if vomiting or TBSA>20%, according to Sabiston, as high-risk for aspiration
    • Tetanus if >10% TBSA
    • Consider deliberate burns
      • Burns on soles of feet
      • Buttocks
      • Other injuries present
      • Poor nutritional/developmental/psychologic state
  • Assess for inhalation injury
    • Generally occurs above vocal cords
    • Can be catastrophic
    • Tends to worsen over the course of hours, not minutes
    • Signs of inhalation injury: (all individually non-sensitive, need to use clinical context as a whole, and bronchoscopy)

• • • • Persistent cough, stridor, wheezing
      • Hoarseness - impending airway obstruction
      • Deep facial or circumferential neck burns
      • Singed nares/inflammation
      • Carbonaceous sputum
      • Obvious blistering/oedema of oropharynx
      • Elevated carbon monoxide or cyanide levels
      • Hypoxia/hypercapnia

• • • AIS grading of inhalation injury by bronchoscopy is as follows:

• • • • 0 (no injury) – Absence of carbonaceous deposits, erythema, edema, bronchorrhea, or obstruction
      • 1 (mild injury) – Minor or patchy areas of erythema or carbonaceous deposits in the proximal or distal bronchi
      • 2 (moderate injury) – Moderate degree of erythema, carbonaceous deposits, bronchorrhea, or bronchial obstruction
      • 3 (severe injury) – Severe inflammation with friability, copious carbonaceous deposits, bronchorrhea, or obstruction
      • 4 (massive injury) – Evidence of mucosal sloughing, necrosis, endoluminal obliteration

• • • Cyanide inhalation

• • • • Cyanide toxicity can occur with burns in enclosed spaces - anaerobic metabolism -> hyperlactataemia or unexplained metabolic acidosis.
      • Treat with hydroxycobalamin.

• • • Carbon monoxide exposure

• • • • Presume in all suspected inhalation injuries
      • Most commonly causes dizziness, altered mental status, arrhythmias or even MI
      • HbCO levels:
        • <20% asymptomatic
        • 20-30% headache/nausea
        • 30-40% dyspnoea, confusion
        • 40-60% syncope, seizures, obtundation
        • >60% death
        • Also look for cherry-red skin but this is rare
        • If exposure has occurred, give 100% O2 via non-rebreather. Half-life is expected to be 40 mins with this, or 4 hours without O2.

• • • Intubate if:

• • • • Deep burns to face and neck
      • Blisters/oedema of oropharyns, burns inside mouth
      • Stridor (late)
      • Use of accessories
      • Resp distress or signs of compromise (fatigue, inability to clear secretions)
      • Sub/suprasternal retractions
      • Hypoventilation
      • TBSA >40% - often intubated prophylactically for impending oedema
      • Needing emergent transfer
      • Carboxyhaemoglobin >10% is a relative indication
      • May require bronchoscopy later - prefer size 8mm internal diameter tube (4.5mm in child)

• • • If not intubated:

• • • • Aim sats >90% with humidified high-flow
      • Coughing/deep breathing q2h
      • Chest physio
      • Saline nebs
      • Bronchodilator if wheezing
      • Mobilise if possible
      • Prophylactic antibiotics are not needed for inhalation injury

Fluid resuscitation

• • • Burn shock - rapid fluid shifts leading to decreased intravascular volume
    • Therefore aggressive and early resuscitation is necessary
    • Use CSL for all >2yo. Use CSL with 5% dextrose for <2yo.
    • Recommended formal fluid resus if TBSA >15%
    • Hourly UO should be maintained at 0.5ml/kg/hr
    • Be aware that over-resus may worsen airway oedema
    • 2-4xTBSA % per kg for second/third degree burns

• • • • Half in first 8 hours, half during subsequent 16
      • Under-resus leads to hypoperfusion and end-organ injury. Over-resus leads to oedema (burn depth progression, compartment syndrome, airway oedema).
      • Initial rate given by TBSA x10, plus 100mL/hr for every additional 10kg of weight above 80kg. Continue this rate until a formal calculation has been done.

• • • Generally start introducing colloids after 24 hours

Escharotomies

• • Required when compromised circulation may be present due to the combination of unyielding eschar and generalised oedema (initially venous, then arterial)
    • Assess as for compartment syndrome
    • Generally don't do prophylactic escharotomy at a peripheral site if transfer is planned same day, because the problem usually arises after 12 hours of resuscitation causing third-spacing
    • Required more often with circumferential burns, but can be needed with non-circumferential too
  • Can also occur on trunk, with restriction of ventilation
  • Perform at bedside or OT by incising the lateral and medial aspects of the extremity, completely through the eschar, with a scalpel or diathermy. Must incise the entire constricting eschar longitudinally.
    • Stop once healthy fat is seen and the tissue springs about 1cm apart - don't need to go down to fascia
  • For upper limb, carry incision down onto thenar/hypothenar eminences, and sometimes even fingers.
  • Reperfusion injury can occur afterwards

Principles of dressings:

• Protect the damaged epithelium
• Minimise bacterial and fungal colonisation
• Provide splinting action to preserve function, as needed
• Should be occlusive to reduce evaporative heat loss and minimise cold stress
• Should provide comfort over the painful wound

Superficial

• Usually need an absorptive dressing for first 72 hours

Superficial partial thickness:

• Cover with either
  • Daily dressings with topical antibiotics, gauze, tubigrip OR
  • Longer-lasting silver dressings (ActiCoat)
    • More useful in contamination, clinical infection, deeper burns, or burns with large surface area
• Wounds expected to take >3 weeks for re-epithelialisation would benefit from surgical excision and grafting
• Partial thickness scald burns, especially in children, generally can have a trial of conservative management, although they should be reviewed at 24 hours in case of worsening. Gentle debridement of dead skin in bath, solugel or paraffin on top maybe, and good oral analgaesia.

Deep partial thickness/full thickness:

• "There is no advantage to unexcised eschar"
• Will need prompt surgical excision and wound closure, usually with autograft
• Depth of excision is below the dermis. Absence of bleeding identifies necrotic subcutis.
• True invasive burn wound infection with bacteria or mould may require amputation/wide debridement
• Initial dressing is aimed at holding bacterial proliferation in check, and completely occluding until the operation is performed

Operative principles

• Spend no more than 2 hours operating, excise no more than 20% TBSA, and lose no more than 2 units of blood.
• Good to cover posterior trunk and buttocks early, to allow supine positioning later in recovery
• Coverage generally proceeds proximal to distal when future amputation is a possibility
• Aim to graft dorsal and digits within first three weeks
• Tangential excision - remove skin layer by layer until viable tissue is reached, followed by immediate application of STSG
• STSG harvested with powered dermatome at 0.008 to 0.01 inch (0.1 to 0.2mm)
• Meshing the graft can allow haematoma/seroma to drain. If haematoma/seroma forms under an un-meshed graft, use a needle to remove the fluid. Meshing also expands the graft.
• Use cadaver allografts when limited by amount of skin available for autograft. One practice is to use widely expanded autografts coered with cadaver allografts. The 4:1 autografts heals in about 3 weeks, and the cadaver skin falls off.

Unique burns

• Electrical
  • Clenched hand with small entrance point means a likely extensive deep injury
  • ECG and monitoring esp if >1000 volts ('high voltage')
  • Consider rhabdo - ?dark red urine - IV fluid stat
  • Consider spinal injury
  • Resus
    • ABCD
    • Full spinal immobilisation
    • Define path of current through body - locate contact points
    • Check ECG, troponins, consider TTE (if no arrhythmia in ED, no need for 24 hour monitoring)
    • Consider compartment syndromes
    • Fluid resus if rhabdo is a possibility
    • Wounds often devolve over time, so serial debridement with VAC is often used
    • Consider cataract and tympanic exam
• Frostbite
  • Produced by freezing temperatures
  • Grading
    • First-degree: hyperaemia and oedema, no necrosis. Heals spontaneously in 1-2 weeks.
    • Second: large clear vesicle formation, partial-thickness necrosis, numbness, oedema. Heals in 2-4 weeks. Can heal as thin, atrophic skin if deeper injury.
    • Third: Full thickness and subcutaneous necrosis, haemorrhagic vesicles. Reactive hyperaemia for first 48-72 hours followed by a black eschar that separates slowly in 1-3 months unless infection occurs.
    • Fourth: Full thickness, including muscle and bone. Black, mummified tissues are present at first. If the mummified area becomes infected, it softens and becomes swollen and macerated at the margin with viable tissue.
    • Final surgical management depends on eventual level of demarcation
  • Initial management:
    • Warm - ideally circulating water at 40 degrees until pink colour and perfusion return (normally 20-30 mins)
    • Watch for rewarming syndrome (acidosis, hyperkalaemia, local swelling)
• Trench foot
  • Produced by prolonged exposure to above-freezing temperatures, along with the presence of moisture
• Immersion hand and foot
  • Prolonged exposure to cold but not freezing water
  • Can be a/w major nerve paralysis, in addition to chronic vasospastic cold sensitivity and pain
• Chilblains
  • Mildest form of cold injury, with prolonged exposure
  • Burning, itching, mild dermatitis
  • Can see vesicles and haemorrhagic lesions
  • Does not produce tissue loss
• Chemical
• Toxic epidermal necrolysis, Stevens-Johnson Syndrome, etc
  • Usually superficial partial-thickness injuries
  • Sulfa drugs, anti-epileptic drugs and allopurinol
  • Need to examine eye

Prognosis

• Deaths from burns occur in a bimodal distribution - either immediately after the injury or several weeks later as a result of multi-organ dysfunction
• 55% TBSA burn has a 50% chance of death, with higher surface area giving a higher mortality and vice versa. Baux score gives a 50% chance of death at 105, and 90% death rate at 130.