Burns

The curriculum contains multiple relevant items, including the: 'pathophysiology of burn injury including thermal airway injury and smoke inhalation', 'initial assessment and management of a patient with severe burns, including electrical & chemical burns' and 'the principles of anaesthetic management of burns patients for surgery'.

A 2013 SAQ on burns (64% pass rate) was entirely airway-focused; features of inhalational injury, relevant investigations, indications for early intubation and use of suxamethonium.

The March 2017 SAQ was a carbon copy of the 2013 question.

In a new CRQ format, the March 2020 question (61% pass rate) appeared to have a similar airway slant but also included elements of fluid resuscitation i.e. the Parkland formula.

Resources

Burns are coagulative injuries of the skin and surrounding structures by energy of various origin:

Thermal: scald (40%), flame (55%), flash, contact, irradiation
Chemical: acid, alkali
Electrical inc. lightning strikes
Mechanical

90% of burns occur in low- or middle-income countries
Although scalds are the commonest mechanism of injury requiring admission, major burns more often arise from flame injuries
Injuries may be accidental, but can also arise from DSH, assaults or NAI
Paediatric patients are disproportionately represented:

20% of burns occur in those <4yrs old
Most of these are scalds due to hot liquids inc. baths

Risk factors for major burns

Low socio-economic status

Overcrowding

Cooking with kerosene

Poor safety practices

Cooking with kerosene

Pre-existing psychiatric or substance abuse problems

Extremes of age

Risk Prediction

The revised Baux score predicts mortality and length of hospitalisation in adult burns injury
It uses:

Age - increasing age strongly associated with mortality from burn injury
%TBSA - partial and full thickness burns only
Presence of inhalational injury adds 17 to the score

Baux score = age + % TBSA + 17 if inhalation injury

A Baux score of 160 represents futility i.e. 100% predicted mortality
A Baux score of 109 represents a 50% predicted mortality

Other models include:

Belgian Outcome in Burn Injury score
Abbreviated Burn Severity Index

By aetiology

Wet heat e.g. scalds carries more energy than dry heat e.g. flame

There is therefore greater tissue damage for the same temperature

By depth

Superficial burns, affect the epidermis

E.g. sunburn, simple erythema
Erythematous, painful but non-blistering
Heal in 2-3 days
Are not included in calculations of TBSA
'First degree'

Partial thickness, affect the epidermis and dermis

Painful and blister
Heal in 7 - 14 days
'Second degree'

Full thickness, affect the epidermis and dermis down to the subcutaneous fat

Hair follicles and nerve endings are lost
Are therefore painless, white, leathery
Heal by wound contracture as they have lost blood supply and cellular structure necessary to full heal
'Third degree'

By TBSA

A burn of >15% total body surface area (TBSA) affected is considered a major burn in adults (>16yrs)

Functions of the skin

Epidermis

The deepest layers continually divide and migrate to the surface to regenerate every 2 - 3 weeks
It cannot regenerate in the presence of dermal injury i.e. full thickness burn

Prevents fluid loss
Barrier to entry of micro-organisms
Major site of immune system activity
Neurosensory organ (touch, pain)
Social and psychological functions

Dermis

Contains nerves, blood vessels, exocrine glands and hair follicles

Regulation of body temperature (vascular plexus, sweating, piloerection)
Skin flexibility and duration

Local effects of burns

Local effects are divided into three zones of tissue injury:

Zone of coagulation

Occurs at the point of maximum damage
Dead tissue as a result of direct injury and protein coagulation

Zone of stasis

There is tissue hypoperfusion due to vasoconstriction of vessels in response to injury
Cells are viable, but vulnerable
Therefore the tissue is at risk of indirect injury from ischaemia, infection and necrosis

Zone of hyperaemia

Dead tissue releases inflammatory mediators, leading to vasodilation, increased vascular permeability and oedema
In the absence of fluid resuscitation, vasodilation exacerbates hypovolaemia and tissue hypoperfusion

Systemic effects

Systemically, there is an acute phase reaction for the first 48hrs post-injury
In TBSA >25%, there is a systemic inflammatory response and the whole body is a zone of hyperaemia

Respiratory	Cardiovascular	Renal	Gastrointestinal	Haematological	Endocrine
Bronchoconstriction	Hypovolaemia	AKI	Ileus	Hypercoagulability	HPA axis activation
ARDS	Myocardial depression	Tissue oedema	Stress ulceration		↑ ADH release
Pulmonary oedema	Reduced cardiac output		Abdominal compartment syndrome		Sympathetic nervous system activation
Increased O₂ consumption	Burns shock		Hypoalbuminaemia

This is followed by a hypermetabolic phase from 48hrs until up to 1yr post-injury

There are raised catecholamine, cortisol and glucagon levels with concurrent reductions in insulin levels
This leads to gluconeogenesis, glycogenolysis, lipolysis and proteolysis
There is hyperthermia, muscle weakness, weight loss, immunosuppression and impaired wound healing

Management of the patient with burns injury

First aid

On-scene first aid is vitally important and can prevent more severe injury
Burns should be run under cool or tepid running water for 20mins

Benefits up to 4hrs post-injury
Arrests tissue damage, reducing depth of injury and improving healing and scar formation

Stop the burning process and covering in non-adherent dressings e.g. cling film

Chemical burns

Remove from area of exposure
Remove all contaminated clothing
Irrigate with running water or sterile fluids (acid 45mins, alkali 1hr)

History & handover

E.g. 'AMPLE' history
Establish mechanism of injury

Explosion (shrapnel), enclosed space (inhalational injury), chemicals (protective gear required), paediatric (NAI)

Associated injuries e.g. fall from height
Timing of injury

Assessment

All burn injuries should be treated as traumatic, and should follow ATLS principles e.g. primary → secondary survey

Airway assessment (see next section) + triple immobilise C-spine as trauma often coalesces with burns

Apply 100% oxygen and assess ventilation

May need management of coalescing injuries e.g. pnuemothoraces
Circumferential chest burns or presence of eschar may restrict ventilation
May need to manage CO or cyanide poisoning (see section below)

Large bore IV access

Bloods inc. FBC, CK, U&E, LFT, VBG, G&XM blood
ECG to check for dysrhythmia esp. in presence of potassium abnormalities
Resuscitate using empiric formula e.g. Parkland formula (see below)
May require IO or CVC access
Suspect bleeding, as burns and burn-shock are not immediate causes of hypovolaemia

Polyfactorial impairments to neurological function can be present, inc. alcohol/intoxication, trauma, hypoxia, hypotension and CO poisoning

Appropriate analgesics including opioids
Trauma CT: CT head, neck, chest, abdomen, pelvis
Consider plain radiographs of areas of specific concern

Assessment of BSA burns e.g. with palmar surface method (inaccurate for medium-sized burns) Wallace's rule of 9's (not accurate in children), Mersey Burns app, Lund-Browder chart

Only areas of partial- and full-thickness burns are included
Remove clothing and jewellery, but be mindful of avoiding hypothermia

Almost all major burns patients become hypothermic
There is a resetting of the euthermic temperature to 38.5'C and excessive heat losses due to exposed tissues

Urinary catheter
Consider escharotomy of non-compliant full thickness burns:

On the chest or abdominal wall restricting ventilation
Circumferential limb burns reducing perfusion
Consider empirical antibiotics if performed

The presence of inhalational injury is associated with increased mortality
Initial assessment of the airway should particularly focus on signs of inhalalational injury ± impending airway compromise

Pathophysiology of inhalational injury

Smoke is hot vapour containing particulate matter
Particulate matter may deposited in the upper and large airways (>5μm in diameter) or small airways and alveoli (<5μm in diameter)
The hot gaseous products of combustion can cause:

Direct burn injury to the upper airway
Acute lung injury from particulate matter and chemicals entering the lower airway

E.g. from increased capillary leak, bronchoconstriction, reduced surfactant levels, ciliary dysfunction and inflammatory mediator release

Systemic toxicity from carbon monoxide or hydrogen cyanide

Inhalational injury is more common if facial burns are present

Clinical features

Clinical features of airway involvement

Burns over the face

Soot on the face

Singed eyebrows or nasal hair

Hoarse or changed voice

Stridor

Lip or oropharyngeal oedema

Drooling

Cough

Wheeze

Airway management

Consider early endotracheal intubation
RSI technique using an uncut tube as oedema may progress
Large-diameter (≥8mm) tracheal tubes are preferable to facilitate ventilation and bronchoscopy
Plan for a difficult intubation as there may be tissue erythema, ulceration or oedema distorting normal anatomy; have difficult airway trolley present
May require higher doses of non-depolarising NMBA, while suxamethonium is contraindicated after 24hrs

Indications for intubation

Actual or impending upper airway obstruction e.g. stridor, oropharyngeal burns, deep facial/neck burns or oedema

Reduced consciousness requiring airway protection

Respiratory distress from inhalation injury e.g. hypoxia, hypercapnoea

To facilitate safe transfer to a burns centre

Carbon monoxide

Oxygen saturations may be unreliable/falsely high due to presence of COHb
Use of a co-oximeter can differentiate between COHb and OxyHb
COHb levels

Normal COHb: 0.3 - 2%
Smoker COHb: 5 - 6%

Symptoms vary according to degree of COHb but there is no dose-response relationship

0 - 10% = no symptoms
10 - 20% = headache, malaise
30 - 40% = nausea, vomiting, impaired mental status
60 - 70% = cardiovascular collapse, coma, death

Half life of COHb in air is 4-5hrs
Apply 100% oxygen as it reduces time to CO washout (to 1hr)
Hyperbaric oxygen therapy can reduce this to 30mins; indicated in severe (>40%) poisoning, pregnant patients and those with either severe neurological or cardiac symptoms
Oxygen should continue until COHb level <3%
COHb >25 - 30% should be I&V

Cyanide poisoning

Cyanide poisoning from melting plastics may cause cytotoxic hypoxia

Leads to lactic acidosis and HAGMA (anaerobic metabolism)
If concerns, administer antidote:

Class	Examples	Mechanism	Product
Cobalt-containing cyanide chelators	Hydroxycobalamin Dicobalt edetate	Chelate CN^- ions	Cyanocobalamin
Sulphydryl donors	Sodium thiosulfate	Provide rhodanase substrate for SCN formation	Thiocyanate
Methaemoglobin generators	Amyl nitrite Sodium nitrite Dimethyl aminophenol	Create MetHb (contain Fe³⁺) which binds CN^-	Cyanohaemoglobin

Under-resuscitation may lead to impaired tissue perfusion, extension of burn depth and end-organ damage
Over-resuscitation can cause electrolyte disturbance, exacerbate oedema (tissue, pulmonary, cerebral) or contribute to abdominal or limb compartment syndromes

Parkland formula

The Parkland (Baxter) formula guides resuscitation fluid (Hartmann's) volume in the first 24hrs for burns >15% TBSA

4ml x actual body weight (kg) x TBSA (%)

Administer in the time since the burn was sustained
Half of this fluid in the first 8hrs since burn injury
The remaining half of the fluid in the subsequent 16hrs
Subtract fluid given already e.g. pre-hospitally
Use warmed, isotonic, balanced crystalloid

The modified formula (3ml/kg/TBSA) is advocated to limit excessive fluids being given
The subsequent 24hrs (according to the modified Parkland formula) use 0.3 - 1ml/kg/TBSA/16/hr of 5% albumin colloid
In general, titration to a urine output of 0.5 - 1ml/kg/hr IBW is as good as using other haemodynamic indices

The Brooke formula uses 2ml x actual body weight (kg) x TBSA (%)

Indications for referral	Indications for discussion
>2% TBSA in children	Burns to hands \| feet \| face \| genitalia
>3% TBSA in adults	Chemical, electrical or friction burns
Full thickness burns	Cold injuries
Circumferential burns	Co-morbidities affecting healing of burns
Burns unhealed after 2 weeks	Febrile child with a burn
Suspicion of NAI

Patients undergo a variety of surgical procedures following burn injuries:

Immediate decompressive escharotomy or fasciotomy
Surgical excision of eschar/burnt tissue in the first few days post-injury (improves mortality from removal of necrotic tissue, which fuels inflammatory responses and acts as a culture medium for pathogens)
Grafting of autografts, xenografts or synthetic dermal substitutes
Later elective cosmetic or function-restoring procedures

Surgery should take place in dedicated burns theatres

Ability to warm the theatre to reduce heat loss
Appropriate training and experience of theatre staff
Ideally close to ICU

Pre-operative assessment

History & examination

The burn: aetiology, extent and management so far
Associated injuries
Haemodynamic status, especially in wake of large-volume crystalloid resuscitation
Airway assessment inc. presence of tracheostomy

Investigations

Renal function and electrolytes, inc. CK
Clotting - there may be coagulopathy from endothelial and inflammatory changes, inc. DIC
G&XM

Peri-operative management

Keep fasting times to minimum and continue nutritional support to aid recovery
Monitoring

AAGBI
May need arterial line if no suitable site for NIBP cuff
May be difficult to attach sats probe
May be difficult to get ECG stickers to stick; needle electrodes or skin staples may be required
Core temperature monitoring and efforts to minimise heat loss

Technique

Generally GA is required

Suxamethonium is, naturally, contraindicated from 24-48hrs until 1yr post-injury
One may need higher doses of non-depolarising NMBAs (e.g. 1.2-1.5mg/kg rocuronium) and there may be a longer onset time due to altered pharmacodynamics in burns patients
Lower albumin but higher alpha-1-acid glycoprotein levels may increase or decrease (local anaesthetics, alfentanil) the free fraction of some anaesthetic drugs

Regional anaesthesia, alone or in conjunction with GA, may be useful
Caution with neuraxial anaesthesia due to increased incidence of coagulopathy and infection

Airway

Anticipate difficult airway
Have flexible bronchoscope and difficult airway trolley close-by

Ventilation

Lung-protective ventilatory strategy, especially in those with inhalational injury
Oxygen consumption and carbon dioxide production tends to be higher due to hypermetabolic response

Bleeding risk

Estimate 3.4% total blood volume for each 1% TBSA excised, higher if tissue is infected, burn is deeper or operation is longer
Use of tourniquets, topical adrenaline and compression may reduce bleeding
Use of visco-elastic haemostatic assays may be more useful in detecting clotting abnormalities and directing blood product use

Respiratory

Lung-protective ventilation as at risk of ARDS
Consider bronchial lavage

Cardiovascular

Invasive arterial monitoring, especially if no suitable site for NIBP cuff
Central venous access
Fluid therapy as per Parkland formula initially, titrated to haemodynamic indices thereafter

Neurological

Pain may be excruciating, difficult to manage and be associated with poorer long-term psychological outcomes
Management should involve a specialist pain service
Pain may arise from:

Burn injury
Non-burn injuries
Skin autograft sites
Invasive lines/tubes/catheters
Pressure areas

Non-pharmacological measures such as appropriate dressings, comfortable positioning and therapies including music and CBT can aid management of background pain
Multimodal background analgesia should be used, but other agents may be needed to combat:

Breakthrough pain e.g. boluses of rapid-acting agents, increased background infusion rates, anticipatory doses
Procedural pain e.g. opioid boluses, inhaled nitrous oxide or methoxyflurane, ketamine (which may reduce chronic pain development) or dexmedetomidine

Renal

Aim urine output 0.5 - 1ml/kg/hr
Check renal function inc. CK daily as high risk of developing rhabdomyolysis and acute renal failure

Gastrointestinal inc. nutrition

Ulcer prophylaxis: increased risk of Cushing's ulcers

NGT and GI feeding as patients are catabolic

Nutritional support should be started ASAP, ideally within 6 - 12hours immediately after injury
BMR more-than-doubles in patients with >40% TBSA
The aim is to meet the substantially increased caloric requirements whilst avoiding harmful overfeeding

Macronutrient mix may differ slightly from standard ICU regimens, with greater protein and lower carbohydrate content:

55% carbohydrate maximum - more than this can lead to hyperglycaemia
15-30% lipids maximum - more than this can cause hepatic accumulation and impaired immune function
1.5-2g/kg/day protein - to prevent negative nitrogen balance

There is a direct correlation between loss of lean body mass and adverse events/complications; aim is to lose no more than 10% total body weight during admission
Perhaps unsurprisingly supplementing extra glutamine doesn't improve outcome

Thermoregulation

In major burn injuries, there is thermal dysregulation
Initial propensity to hypothermia due to heat and fluid loss from the burn injuries
Subsequently there is often a raised core temperature

Due to altered hypothalamic setpoint by IL-1 and TNF
Once >39.5°C may need interventions such as debulking dressings, anti-pyretic medications, ice, cooled fluid, visceral irrigation or intravascular heat exchange catheters

Haematological

Increased risk of VTE so chemical ± mechanical thromboprophylaxis

Infection

No need for prophylactic antibiotics

Loss of skin barrier and relative immunosuppression means there's an increased risk of infectious complications

Infection is a major source of morbidity and accounts for 42 - 65% of deaths following burn injury
Colonisation or infection, often with MDR-organisms, can occur

It may be difficult to distinguish markers of infection from that of the post-burn inflammatory response
Potential markers of infection include: temp >39, HR >110, RR >25, Plt <100 (3 days' post injury), intolerance of NG feed, Glu >11 or insulin >7units/hr
There may be post-burn leukopaenia

In the case of infection, antibiotic choice should be Microbiology-led and organism-targeted

Commonest organisms in early admission are Staph. aureus, Streptococci or Enterococci inc. VRE
Pseudomonas can translocate and thrive in burn wounds, leading to invasive infection; Acinetobacter, E.coli and Klebsiella may do likewise

Fungal colonisation can also occur and is associated with increased mortality; Candida albicans is the most common pathogen

Toxic shock syndrome may arise from strains of toxin-producing S. aureus or Group A Strep.
Antibiotics that directly reduce exotoxin production such as clindamycin or linezolid should be considered, as should IVIg

Other measures in the management of infection include:

Surgical debridement of infected tissue
Special wound dressings impregnated with antimicrobials
May need to consider tetanus depending on mechanism of injury