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Great Ormond Street Hospital Modular ITU Training Programme - 1 -

Burns and other Life-threatening Skin Conditions

Mary Montgomery, May 2006 Updated: Bhupinder Reel / Mary Montgomery, July 2009 Updated: Emma Borrows / Osama Hosheh, February 2015 Associated clinical guidelines/protocols:

Guideline

St Andrew’s Burn Centre (Broomfield)

Fundamental Knowledge: List of topics relevant to PIC that will have been covered in membership examinations.

Information for Year 1 ITU Training (basic):

Year 1 ITU curriculum Introduction

Classification and types of Burns

Burn pathology – local and systemic

Evaluation of extent of burn (%)

Emergency management

Specific burns management

Smoke inhalation

Wound care and prevention of infection

Burns surgery

Pharmacokinetics and pharmacodynamics

Analgesia and itch

Nutrition and metabolism

Curriculum Notes for Year 1:

Introduction

The skin is the largest organ in the body and comprises 15% of the body weight. It has a variety of functions including as a protective barrier. It is protective against injury, drying, bacterial entry, toxin absorption and excess fluid loss. It regulates body temperature by alteration of skin blood flow, sweating and pilo-erection. The skin is comprised of 3 layers: The epidermis, dermis and subcutaneous tissue

o The epidermis is composed mainly of epidermal cells, the deepest of which are immature, continually dividing and migrating towards the surface, to replace lost surface cells. As the cells mature and migrate they form keratin

Disclaimer: The Great Ormond Street Paediatric Intensive Care Training Programme was developed in 2004 by the clinicians of that Institution, primarily for use within Great Ormond Street Hospital and the Children’s Acute Transport Service (CATS). The written information (known as Modules) only forms a part of the training programme. The modules are provided for teaching purposes only and are not designed to be any form of standard reference or textbook. The views expressed in the modules do not necessarily represent the views of all the clinicians at Great Ormond Street Hospital and CATS. The authors have made considerable efforts to ensure the information contained in the modules is accurate and up to date. The modules are updated annually. Users of these modules are strongly recommended to confirm that the information contained within them, especially drug doses, is correct by way of independent sources. The authors accept no responsibility for any inaccuracies, information perceived as misleading, or the success of any treatment regimen detailed in the modules. The text, pictures, images, graphics and other items provided in the modules are copyrighted by “Great Ormond Street Hospital” or as appropriate, by the other owners of the items.

Copyright 2008-2009 Great Ormond Street Hospital. All rights reserved.


o The dermis is the deeper layer responsible for skin durability and flexibility. It contains the nerves for touch and pain, hair follicles and blood vessels. It is responsible for reforming the outer epidermis

BURNS

Incidence

o In the UK approximately 250 000 people are burnt each year, 175 000 of which attend A&E, 13 000 of which require hospital admission and 1000 require fluid resuscitation (500 of which are children <12 years)

o There are approximately 300 burn deaths a year (all ages) o 20% of all burn injuries occur in the <4 years old, 10% in 5-14 year age group o 3-10% of paediatric burns are associated with non-accidental injury o Burns in teenagers are often from illicit activities involving accelerants or electrocution

Classification of Burns 1

st degree / Superficial o Involves only the epidermis (dermis uninjured)

o Red, no blisters, dry, blanches, painful 2

nd degree / Partial Thickness o Superficial dermal (involves epidermis down to papillary dermis)

o Pink, blisters, moist, blanches, painful o Deep dermal (involves epidermis, down to reticular dermis)

o Blisters, mottled pink/white, slow capillary refill after pressure, patient complains of discomfort (pressure rather than pain)

3rd degree /Full Thickness

o Involves entire epidermis and dermis, with extension into subcutaneous tissue. o White, dry, leathery, non-blanching, painless to touch

Burn depth is proportional to the temperature (wet heat i.e scald carries more energy than dry heat ie flame, so greater tissue damage caused by the same temperature), length of contact (time) and the area affected / skin thickness (thinner skin = deeper burn, skin thickness changes with age).


Types of burn Thermal Scald

o ~70% of burns in children o Mechanisms: spilling hot drinks / liquids or being exposed to hot bathing water o Tend to cause superficial dermal burns with typical distributions

Contact o With hot surface or prolonged contact o Tend to be deep dermal or full thickness

Flame o ~50% adult burns o Often associated with inhalational injury and other trauma o Tend to be deep dermal/full thickness

Chemical o 8% of all burns, 1.1% of paediatric burns o Male>Female, Adults>children, Increasing incidence (x’s 3 in last 15 years), most common

causative agent is wet cement (calcium oxide and water → calcium hydroxide)

o Often deep dermal, severity depends on concentration, quantity of agent, duration of contact, penetration and mechanism of action

o Alkalis cause worse burns than acids and are often associated with a delayed presentation o Contaminated clothing needs to be removed and the area thoroughly irrigated (limits depth of

burn, shower NOT bath, as bathing can increase area of contact) o Use pH paper to confirm effective removal of alkali or acid o Eyes - irrigate well (with isotonic solution if possible) and refer to ophthalmologist o Diphoterine – is a sterile washing solution for chemical burns, it has polyvalent, amphoteric,

chelating properties and is 17x’s more effective than rinsing with water. For optimal benefits must be used early, often carried by paramedics or on site at chemical factories

Electrical

o Most commonly seen in young male adults, associated with high morbidity o 3 types – High voltage, low voltage, flash burns o You may see entry and exit points with tissue damage at any point between, consider other

tissue damage even if entry and exit wounds are small, may cause cardiac arrhythmias o Extent of injury is determined by the voltage, current, path of injury, duration of contact,

resistance of tissues (Nerve<vessels<muscle<skin<tendon<fat<bone) and individual susceptibility

o Low voltages (domestic source <1000 V): o Small, deep contact burns at exit and entry sites

o High voltage (tension) > 1000 V: o Extensive tissue damage +/- limb loss o Soft and bony tissue necrosis

o Muscle necrosis ⇒ rhabdomyolysis ⇒ renal failure

o Requires aggressive resuscitation o >70 000 V is invariably fatal.

o Flash burn is an electrical burn which does not pass through the body o Causes superficial burns to exposed areas such as the face and hands o Deeper burns if clothing set alight


Burn Pathology (the body’s response to a burn): Local

Three distinct zones (Jackson burn wound model 1947):

Zone of coagulation:

o Area in contact with heat source o Point of maximum damage with rapid cell death and irreversible tissue loss o Coagulative necrosis of cells that do not recover o Burn management involves the early debridement of this area exposing the underlying Zone

of Stasis

Zone of stasis: o Concentric area of lesser tissue damage around zone of coagulation o Decreased tissue perfusion but cells are viable o Additional insults such as reduced BP, infection, oedema can convert this to an area of

complete tissue loss o Fibrin deposition, vasoconstriction, and thrombosis occur as a result of continued release of

inflammatory mediators

Zone of hyperaemia: o Immediately adjacent to zone of stasis and borders unaffected tissues o Cells sustain minimal injury o Will recover unless severe additional insults o In burns >30% the zone of hyperaemia can include the whole body

Systemic Divided into acute phase (first 24-48 hours after injury) and hypermetabolic phase (can last up to 1 yr post burn) Acute Phase

o Inflammatory: Cytokines, catecholamines and other inflammatory mediators (leukotrienes, prostaglandins, oxygen free radicals and histamine) are released at burn site leading to capillary leak, peripheral/splanchnic vasoconstriction and decreased myocardial contractility

o Cardiovascular: Hypovolemia due to direct fluid loss from burns and increased capillary permeability leading to rapid oedema formation (immediate oedema occurs in the burn wound, progressive oedema over 12-24 hours occurs in the burned tissue, if TBuSA >25% oedema also seen in non-burned tissue), decreased myocardial contractility, decreased CO, increased SVR and resultant reduced peripheral blood flow. Increased haematocrit and haemoglobin concentration

o Respiratory: Bronchoconstriction +/- ARDS. Risk of bronchopneumonia / VAP o Sepsis: Loss of skin barrier function


o Thermoregulation: Loss of insulating properties of skin and increase in energy loss by latent heat of vaporisation. Effects of hypothermia include increased bleeding, CVS instability, hyper metabolism. Longer term effects are increased risk of infection and poor wound healing

o Acute Kidney injury: caused by reduced renal blood flow (secondary to hypovolaemia and

reduced cardiac output) and the effects of denatured proteins (myoglobin and unconjugated haemoglobin). Rhabdomyolysis may be secondary to direct thermal injury or compartment syndrome (common following severe electrical injury)

o Gut and nutrition: Ischaemia, Splanchnic hypo perfusion, paralytic ileus and GI ulceration (Curling’s ulcer)

Burn shock is seen when tissue perfusion is insufficient to maintain an adequate delivery of oxygen and nutrients and the removal of cellular waste products. It is a complex process that results from interplay of the effects listed above and is more common with increasing size of burn. Hyper metabolic phase (>48 hours)

o Cardiovascular: Increased catecholamine production, tachycardia, hyperdynamic circulation, increased EDV. Oedema persists secondary to increased blood flow to tissues, hypoproteinaemia and increased water permeability

o Metabolic: Increased basal metabolic rate (BMR) (% proportional to size of burn) leads to increased oxygen and glucose consumption (glycogenolysis), increased CO2 production, and pyrexia. Resulting in a catabolic state (proteolysis and lipolysis) with decreased lean body mass, muscle weakness, poor wound healing

o Nutrition: massively increased energy and nitrogen (protein) requirements o Thermoregulation: resetting of the thermoregulation ‘setpoint’ in the hypothalamus

(increased by 0.03°C / % TBuSA) due to SIRS mediators o Immunological: Non-specific down regulation of the immune system (cell mediated and

humoral pathways) o Growth: Increased central deposition of fat, decreased muscle growth, decreased bone

mineralisation, decreased longitudinal growth of body

Estimation of Extent of Burn An estimate of burn size (and depth) is necessary to guide initial fluid resuscitation, determine severity / prognosis and the need for referral to a specialist care are (Burn facility or Burn Centre). Estimation of burn size primarily relies on clinical judgements, 3 main methods of estimation are used, with varying accuracy in children

o Palmer surface: The surface area of a patients palm (including fingers) is roughly 0.8% (rounded up to 1%) of the total body surface area. Can be used as a quick estimate of burn size, best for small or very large burns (where unburnt skin is counted), innacurate for medium sized burns

o Wallace rule of nines: The body is divided into areas of 9% allowing the total burn area to be calculated (works well for adults and children >15 years with medium to large burns, doesn’t work well for younger children). Modified rule of nines can more accurately reflect the percentage of the burns in children

o Lund & Browder Chart: Most accurate method in adults and children, takes into account changes brought about by growth

Estimation of burn depth is also primarily based on clinical judgement (looking at colour, blanching with pressure, blistering etc) and though adjuncts do exists (Laser Doppler and spectrophotometric analysis) they are not widely available or used.


‘Wallace rule of nines’ ‘Lund and Browder’

Special Considerations in children o Burns greater than 10% Total Body Surface Area (TBSA) require fluid resuscitation o Burns greater than 25% TBSA +/- involving the airway are classified as a Major burn o Burns >30%TBSA, or >20% FT (15% FT if <1 yr) need referral to a specialist Burn Centre

(see childrens burn referral guidelines) o Non-accidental Injury:

o Associated with 3-10% of paediatric burns o Usually younger child (<3 years) o May be obvious pattern (cigarette/iron), distribution (soles/palms/perineum), symmetrical,

uniform, no splash marks, sparing of flexion creases, ‘tide mark’ or ‘doughnut’, or other evidence of abuse or neglect

1

o Important points in the history of non-accidental burns include an evasive or changing story, delayed presentation, no explanation or implausible mechanism given for the burn, inconsistency between the age of the burn and age given by the history, inadequate supervision

Emergency Management History

o Taking an accurate burn history is vital. Key points include the exact mechanism and timing of injury and any prehospital treatment given. The mechanism of burn will guide you to the likelihood of inhalational and other injuries. Don’t forget to ask about past medical history

Burn patients should be treated as a trauma patient unless clear history of the mechanism is confirmed. Therefore, a 1° survey (ABCDE) should be followed by a systematic 2° survey. Airway & Cervical Spine

o C-spine immobilization unless clear evidence that C-spine is not at risk o Intubation is highly recommended for:

o Airway burns: suggested if burned in enclosed space, stridor, burns to face, lips, tongue, mouth, pharynx or nasal mucosa, singed nasal hairs, soot in sputum, nose and mouth

o Inhalational injury: suggested if burned in an enclosed space, dyspnoea, hypoxaemia (SpO2 <94% in room air), increased CO level


o A large burn area: for which high levels of analgesia will be required o Circumferential chest burns o Reduced conscious level: GCS<8 or fluctuating level of consciousness

o Intubate with cuffed tube orally, do not cut the endotracheal tube: it will ride out of the mouth as the face swells

o Tube ties should be checked regularly o If unsure, discuss with a burn centre, and if in doubt, intubate

Breathing

o Respiration may be restricted by mechanical restriction of breathing, blast injury, smoke inhalation, carboxyhaemoglobin

o Administer 100% O2. Aim for saturations of >95% o CO oximeter o Chest physiotherapy o Nebulized therapy if airway involvement (see later) o Ventilation: with low T.V / protective lung strategy o Bronchoscopy: Diagnostic and therapeutic o Poor chest compliance due to deep dermal / full thickness circumferential burn may require

escharotomies (see later)

Circulation o Large bore access x2 or use intraosseous route – can go through burned tissue o Take blood for gas / FBC / U&E’s / X-match o A 12-lead ECG and continuous ECG monitoring is mandatory for all electrical burns o Volume resuscitate as necessary

o Assess extent and depth of burn on Lund & Browder Chart then use the Parkland Formula to work out fluid requirement (start from time of burn):

o 24 hour fluid requirement = 4ml / kg / %TBSA burned. Half is given over the first 8 hours, the other half over the next 16 hours (Hartmann’s solution)

This is added to the 24 hour maintenance fluids (5% Dextrose+ NACL 0.45%) calculated as normal (100mls/kg for the 1

st 10 kg + 50ml/kg for the 2

nd 10kg + 20ml/kg for each

additional kg over 24hrs) Example (22 kg child, with 30% burn): Maintenace: 1000mls + 500ls + 40mls = 1540mls as D5/0.45% Saline over 24hrs. Resuscitation fluids: 4ml × 22kg × 30(burn) = 2640mls as Hartmann solution, ½(1320mls) in the first 8hrs, and the 2

nd half(1320mls) over the next 16hrs

o Patients with burns greater 20% should have the formula used initially and then goal directed therapy using urine output, cardiovascular parameters (including invasive monitoring of CVP and BP) and haematocrit as aids to fluid resuscitation adequacy

o Catheterise all children with burns ≥20% TBSA (consider if 10-19% TBSA or perineal burn) o Aim for urine output of 1ml/kg/h (2-4ml//kg/h in rhabdomyolysis, especially with burns

secondary to electrocution) o If the urinary output is <1 ml/hr for 2 consecutive hours, check catheter first, then double the

infusion rate and re-evaluate the patient after 1 hour. If urinary output is still low, check burn size, body weight

o Extra fluids are usually needed if delayed start of resuscitation of deep burns, inhalation injuries, electrical burns, patients with malnutrition or liver disease

o Profound hypovolaemia / early large volume requirement should alert to the possibility of occult sources of blood loss such as secondary to traumatic injury (chest, abdomen and pelvis) or to cardiogenic dysfunction

Neurological Disability

o Asses level of consciousness

Exposure + Environment control o The whole of the patient should be examined (including the back) o Burn patients, especially children easily become hypothermic, therefore they should be

covered and warmed as soon as possible

Secondary survey o Head to toe examiniation looking for concomitant injuries


Referral to specialist burns care In England and Wales burn care is organised using a tiered model of care (centre, unit and facility). The most severely injured patients are cared for in services designated as centres, where patients can be offered intensive care support. Less severely injured patients will be looked after in units or facilities. The nearest regional paediatric burn centre to GOSH is St Andrews Burn Centre, Broomfield, Essex. Chelsea and Westminster hospital, East Grinstead Hospital and Stoke Mandeville Hospital are paediatric burn facilities and do not care for paediatric patients needing intensive care support. Timely referrals to a burn centre lead to reductions in patient morbidity, mortality, and length of hospital stay. The Children’s Acute Transport service (CATS) will transfer critically ill burnt children who require intensive care support.


Specific Burn Management Management of Carbon Monoxide/smoke inhalation

o Carbon monoxide (CO) has >250 X’s more affinity for haemoglobin than oxygen o Causes a left shift in the oxy-haemoglobin dissociation curve o CO displaces oxygen from haemoglobin resulting in a marked reduction in the delivery of

oxygen to peripheral tissues despite normal PaO2. o May also inhibit cytochrome oxidase and potentiate further cellular hypoxia o High levels of CO on presentation are significant, low levels do not exclude CO poisoning o Pulse oximetry cannot detect difference so measure carboxyhaemoglobin (COHb) levels in

blood o Normal COHb level 0-5% o Symptoms:

CO level % Symptoms 0-5 Normal 15-20 Headache, confusion, Visual disturbance 20-40 Disorientation, fatigue, nausea 40-60 Hallucinations, combative, coma >60 Death

o Treatment: o 100% oxygen (regardless of SpO2) reduces half-life of COHb from >5 hrs (in air) to

90 minutes. o Ventilate and other supportive measures as indicated o Continue until CO levels <10% o Hydroxycobalamine (Vit B derivative) for on scene cardiac arrest due to smoke

inhalation o Ventilate using 100% O2 until CO <10% with a pressure limited permissive

hypercarbia approach unless evidence of a head injury o National Poisons Information Service (NPIS) doesn’t currently recommend

Hyperbaric Oxygen therapy in the context of acute smoke inhalation therapy Wound care, and Prevention of Infection

o Infection worsens the inflammatory response and potentially the burn, converting it to a greater depth or greater surface area, delaying healing and worsening scarring. Wounds need to be reviewed regular, kept clean and dressed appropriately. Infection needs to be treated promptly and appropriately with microbiology advice

o In the emergency department Clingfilm should be used to cover the burn (will decrease pain, decrease heat loss and protect the area without changing the appearance until further assessment). Important to review regularly to make sure it does not become tight as tissues swell

o The subsequent mainstay of wound care is early surgical excision and wound closure with the use of skin grafts (autografts) or skin substitutes

o Wounds are reviewed, cleaned and dressed regularly (typically every 48 hours) to reduce infection, adsorb exudate, and decrease pain.

o There are a wide variety of dressings and coverings available, the choice of which is dependent on the wound (new/fresh, infected, size).

o Dressings used on non-infected wounds include synthetic tissue engineered wound dressings such as biobrane (a bilayer fabric composed of an inner layer of knitted nylon threads coated with porcine collagen and an outer layer of rubberized silicone, pervious to gases but not liquids and bacteria) or Hydrocolloid dressings such as duoderm

o Topical antimicrobials are used on Infected / colonized burns. They include: o Sodium hypochlorite – a topical antibacterial for cleansing the wound, broadspectrum

antiseptic, bactericidal against P.auruginosa, S. aureus, and other gram –‘ve / +’ve’s o Acetic acid (vinegar) o Silver sulfadiazine (Flamazine) – a water soluble cream composed of sulfadiazine

and silver. Effective against P. aeruginosa, C. albicans and S. aureus. Can delay wound colonization by gram-negative bacilli by 10 – 14 days

o Acticoat AB dressing – consists of 2 sheets of high-density polyethylene mesh coated with ionic silver with a rayon/polyester core. Provides broad spectrum antimicrobial, bactericidal cover against VRE, MRSA, P. aeruginosa and Candida sp


o Mupirocin (Bactroban) – effective against S. aureus including MRSA o Nystatin (antifungal) – works by binding to sterols in the fungal cell membrane o Gentamicin or tobramycin cream is an alternative for patients with superinfected

wounds or allergies to sulpha preparations o Polymixin E (Colistin) cream – used in resistant colonisation with P. aeruginosa

o Prophylactic antibiotics are not routinely recommended and should only be used for specific instances under microbiology guidance. Pyrexia in burns is common and is on its own not a marker of infection requiring antibiotic treatment

Surgery

o Escharotomy / Fasciotomy o Used to treat compartment syndrome and release tissue pressure / restore

circulation if signs of impaired ventilation or reduced peripheral perfusion (may be needed as part of resuscitation / emergency management)

o Under sterile conditions an incision is made through the eschar (dead tissue) until the tissue gapes such as to release the pressure particularly on the vascular supply.

o Burn excision and grafting

o Early surgical excision of the whole full thickness burn (within 24 hours) – limits infection and the hypermetabolic response and improves mortality

o Early grafting / wound closure - minimises infection, hastens wound healing4 and

maximises functional recovery o Staging of surgery

o Moderate size burns (<30%) – wound closure with partial thickness autologous skin graft in one procudeure

o Larger burns – wound closure with partial thickness meshed autograft +/- augmented with cadaveric allograft

o Very large burns – Limited donor sited available, may need staged excisions and autograft with re-harvesting of donor areas, or use of allograft / artificial skin substitutes to provide a temporary cover between autologous grafting. Initial grafting prioritised to specific areas (ie neck if tracheostomy planned)

5.

o Be aware of large blood loss associated with excision and grafting. Predicted blood loss increases with time post injury (maximum day 2-6) and if the wound is infected

Sepsis

o Burn injury is associated with a generalised loss of immunocompetence, and sepsis remains a major cause of death in burns

o Early sepsis (1-3 days post burn) is usually streptococcal or staphylococcal o Late sepsis is usually due to Pseudomonas, Acinetobacter and fungi o Prophylactic antibiotics should be avoided and instead regular cultures taken and appropriate

therapy given when indicated


o Effective topical antimicrobial therapy and early burn wound excision have significantly reduced the overall occurrence of invasive burn wound infections, but in extensive burns, with delayed excision or closure, bacterial and fungal infections are still a risk

7 Pharmacokinetics / pharmacodynamics post burn o In acute phase

o Tissue oedema formation, reduced intravascular volume, increased extracellular space. Decreased renal and hepatic blood flow. Dilution of plasma proteins.

o Volume of distribution increases for water soluble drugs o Decreased drug binding to plasma proteins (especially albumin) o Decreased renal / hepatic clearance of drugs

o In the hypermetabolic phase o Increased renal and hepatic blood flow, decreased albumin (secondary to catabolism)

and increased acute phase proteins (α-acid glycoprotein). Receptor population numbers change (often increase) as do receptor mediators and secondary cell signalling

o Increased / renal hepatic clearance (ie NDMRs)

o Decreased albumin → decreased drug binding of acid/neutral drugs ie diazepam

Increased α acid glycoprotein → increased drug binding of basic drugs ie propranolol

o Increased BMR and increased temperature → altered T½

Analgesia o Burn injuries are often very painful, the circumstances of the burn often contribute to

psychological trauma which may worsen the perceived pain. Unrelieved pain can lead to multiple problems including post traumatic stress disorder, enhanced pain/chronic pain, increased stress response, and a lack of compliance / loss of faith in the medical team

o The physical depth of the injury will influence the nociceptive pain o Deep burns are associated with dermal damage and disruption of nerve endings. Pain

may not be an early feature but will evolve with healing and atypical nerve regeneration o Partial thickness burns (ie scalds) are classically the most painful burns as the nerve is

often intact / functioning and exposed to the air o Superficial burns can be painful but this pain is usually well controlled with simple

analgesics o Management

o Treat the cause Cover wounds and reduce expose to air currents (cling film initially then biobrane

or simple dresings) Elevate Check the wound for signs of infection / compartment syndrome

o Target all 3 areas of pain control – background, breakthrough and procedural o Regular use of simple analgesia such as paracetamol and consider NSAIDs (not in

resuscitation phase and use with caution in renal failure) o Opiates are the cornerstone of pain control (potent, reliable analgesia, good range of agents,

multiple routes of delivery, high safety profiles). Disadvantaged – side effects (nausea, constipation, pruritus, sedation, respiratory depression, urinary retention), immune-modulation (increased susceptibility to infection and effect on hypothalamo-pituiatary-adrenal axis), tolerance

(receptor tolerance → desensitisation) and opiate induced hyperalgesia (pro-nociceptive

pathways activated → sensitisation)

o Consider the use of NMDA receptor antagonists (ie ketamine and gabapentin) and clonidine (α-2-agonist which works synergistically will opiates)

o Procedural pain relief – variety of options available including, those commonly used with decreasing potency are:

o general anaesthesia, IV remifentanyl, IV ketamine and midazolam, oral ketamine and midazolam, intranasal diamorphine, buccal fentanyl, and entonox.

Muscle relaxants o Neuromuscular blocking drugs (NMDAs) act mostly at the post-junctional nicotinicreceptor of the

neuromuscular junction. They may be agonists (‘depolarising’ NMBDs) or antagonists (non-depolarising NMBDs) at the nicotinic receptor

o Depolarising muscle relaxants (suxamethonium) cause widespread depolarisation and exaggerated hyperkalaemic response (can cause cardiac arrest). It is recommended to avaoid Suxamethonium 18 hours to 18 months post burn


o There is a relative resistance to NDMRs due to upregulation of the skeletal muscle nicotinic receptors and 3-5 times higher doses may be required (peaks by day 10 post burn, returns to normal by 80 days)

Burn Itch

o Healing burn injuries can be very itchy, itching can lead to local trauma and wound breakdown o St Andrews burn centre uses a 4 step anti-itch ladder

o Step 1: Moisturise and cool o Step 2: Gabapentin (Day 1 5mg/kg OD, Day 2 5mg/kg BD, Day 3 5mg/kg TDS, can be

increased to 10mg/kg if ineffective and well tolerated) o Step 3: Cetirizine and cyproheptadine o Step 4: Chlorpheniramine

Nutrition / Hypermetabolic state o Patients with severe burns (>40%) enter a hypermetabolic state that can persist for up to 12

months. Their metabolic rates can exceed twice normal. Failure to satisfy these increased energy and protein requirements can lead to impaired wound healing, organ dysfunction, susceptibility to infection, and ultimately death

o Post burn gastric stasis is common and large aspirates are normal o Early and aggressive nutritional support is an essential component of burn care (decreases

catabolism and weight loss and maintains gut integrity) o All efforts should be made to feed early using the enteral route, a naso-jejunal tube is routinely

inserted at admission to the ICU and feeding is commenced as soon as possible (within 12 hours)

o There are various formulas to calculate the nutritional requirements for paediatric patients. The Galveston formula is currently used at St Andrew’s burn centre;

Age (yrs) Daily requirements (kcal/day) = target calories 0 - 1 2100kcal/m2 SA + 1000kcal/m2 Burn SA 1 - 11 1800kcal/m2 SA + 1300kcal/m2 Burn SA

1 2 - 18 1500kcal/m2 SA + 1500kcal/m2 Burn SA SA = body surface area = √(height(cm) x weight(kg))/3600

Burn SA = burn surface area = %burn X body surface area o Some centres will add in extra protein and micronutrient (glutamine and arginine) supplements

to promote healing and growth (not current practice in paediatrics at St Andrew’s Burn Centre) o Modulation of the hypermetabolic response;

o Non-pharmacological Early excision of necrotic tissue and burn wound closure Environmental support- increasing the ambient temperature decreases the

resting energy expenditure o Pharmacological methods

Propranolol - decreases cardiac work, reduces hepatic steatosis, reduces skeletal muscle metabolism and increased lean body mass post burn

Oxandralone - enhances anabolism of muscle protein by improving the efficiency of protein synthesis. Shown to decrease loss of body weight, improves wound healing, decreases LOS


References 1. Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of burns. BMJ 2004;328(7453):1427-9. 2. Juurlink D, Buckley N, Stanbrook M, Isbister G, Bennett M, McGuigan M. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane. Database.Syst.Rev. 2005(1):CD002041. 3. Hettiaratchy S, Papini R. Initial management of a major burn: II--assessment and resuscitation. BMJ 2004;329(7457):101-3. 4. Hansbrough JF, Hansbrough W: Pediatric burns, Pediatric Rev 1999 20:117-123. 5. Henry DB, Foster RL: Burn Management in Children, Pediatric Clinic North America 2000 47:681-698. 6. Slone DS. Nutritional support of the critically ill and injured patient. Crit Care Clin. 2004;20(1):135-57. 7. Ansermino M, Hemsley C. Intensive care management and control of infection. BMJ 2004;329(7459):220-3. 8. Pegg SP. Escharotomy in burns. Ann.Acad.Med Singapore 1992;21(5):682-4. 9. Merz J, et al. Wound care of the Pediatric burn patient. AACN Clinical issues. 2003;14(4):429-41 Other sources of information: ABC of Burns – BMJ 2004 Paediatric Critical Care Medicine Textbook 2

nd ed, 2014.

Websites:

http://www.burnsurgery.org

St Andrew’s Burns Centre http://www.emedicine.com/ped/topic2702.htm

http://www.emedicine.com/plastic/topic518.htm

http://www.lsebn.nhs.uk

http://www.emedicine.com/plastic/topic518.htm

http://www.lsebn.nhs.uk/


Information for Year 2 ITU Training (advanced):

Year 2 ITU curriculum Burns:

o Management of inhalation injury o Management of burns to special areas

Medical Skin Loss:

o Stevens Johnson syndrome and Toxic epidermal Necrolysis o Erythema Multiformae o Staphylococcal scalded skin syndrome

o Necrotizing Fasciitis

Curriculum Notes for Year 2:

Advanced management of inhalation injury The degree of injury from smoke inhalation is dependent on the length of exposure (how long the patient was trapped), the smoke mass inhaled, the constituent components of the smoke (hydrogen cyanide, carbon monoxide, carbon dioxide), and the depths of respiration at the time. Smoke inhalation can lead to upper airway (typically thermal injury), lower airway (typically chemical injury) and systemic effects. o Upper airway

o Thermal injury o Heat from the smoke is absorbed in the upper airway (often limited to the supraglottic

airway and rarely extend below the vocal cords3)

o This causes an airway burn with erythema, ulceration and progressive oedema which can result in upper airway obstruction

o Symptoms and signs include – hoarse voice, stridor, facial / neck burns, intraoral burns, oedema, increased work of breathing

o Lower airways

o Chemical injury o Typically to the lower airways (below the larynx) o Caused by toxic gases in smoke and particulate matter in soot o Soot and secretions can combine to form casts which can physically block an already

bronchospastic / oedematous airway o The location of injury in the airway depends on particle size, solubility and acid base

status, and duration of exposure o Thermal injury

o Thermal injury to the mucosa results in tissue destruction and an inflammatory response, which leads to a sloughing of the mucosa and increased mucous production (often difficult to clear because of loss of ciliary activity)

o Steam has 4000 X’s the heat capacity of dry air, can retain sufficient heat to damage the alveoli and cause severe ARDS

o Symptoms and signs include cough, dyspnoea, wheeze, or respiratory distress

o Ongoing Airway Management o Early bronchoscopy (diagnostic and therapeutic to wash out soot and casts) with follow-up at

24 hours o Triple Nebulised therapy (one drug nebulised each hour):

o Heparin (5000 IU diluted with 3mls 0.9% saline 4hrly for 5-7 days) to prevent cast formation, reduce pulmonary inflammation and fibrin deposition

o Acetylcysteine (20% solution 3mls 4hrly) acts as a mucolytic and lowers the viscosity of the mucous

o Salbutamol (5mg 2 hourly) acts as a bronchodilator and aids alveolar fluid clearance


o Pulmonary toilet – minimum 4hrly, 30 minutes after acetylcysteine o Chest physiotherapy 4 times per day o Daily sputum microbiology samples o Antibiotics depending on culture results and evidence of infection only o Fluid requirements in airway burns may increase by up to 50%

o Combustible Toxins

o Consider in unexplained metabolic acidosis, with high lactate (>10) and elevated anion gap o Hydrogen Cyanide

o Produced when wool, silk, nylon and polystyrene burn o More toxic than carbon monoxide o Inhibits cellular respiration by binding to ferric ion on cytochrome a3 disrupting

mitochondrial oxygen utilization o Metabolised by the liver and renally excreted (takes >24 hours) o Treatment

Sulphur donors ie sodium thiosulphate converts to thiocyanate Cobalt compounds ie hydroxycobalamin (cyanokit) – given pre-hospital for

best effect, recommended for on scene cardiac arrest from smoke inhalation)

Methaemoglobinaemia formers ie sodium nitrite (Note - the induction of methemoglobinemia from the nitrites in addition to present carboxyhaemoglobinemia can significantly reduce the oxygen-carrying capacity of blood)

o Rubber and plastic items release ammonia, chlorine, hydrogen chloride, and oxides of sulphur which dissolve in moist mucosa of the upper airway to form alkalis and acids

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treatment is mostly supportive

Burns to special areas o Face

o Burns to the face require early specialist input o Facial swelling may make it impossible to examine the eyes for corneal burns (cornea looks

cloudy in significant burns, but may need topical fluroscein to see more superficial burns) o So if you see the patient early it is important to examine and document findings o Burns to the ears are a particular problem as they are poorly vascularised, so pressure must

not be applied. Particular care has to be taken with regard to prevention of infection (chondritis – causes liquefaction of cartilage and requires 6 weeks iv antibiotics)

o Hands

o Vital to preserve as much function as possible o High index of suspicion of potential compartment syndrome requiring escharotomies o Elevate to decrease oedema o Tend to early grafting and mobilisation

o Perineum

o Look out for urinary retention 2° pain or oedema

o High risk of infection


Other Life-threatening Skin Conditions (Medical skin loss) Stevens–Johnson syndrome (SJS) and Toxic Epidermal Necrolysis (TENS) o SJS and TEN are variants of the same process, presenting as severe mucosal erosions with

widespread erythematous, cutaneous macules/blisters o They are caused by an immunological reaction to a foreign antigen, which may be drug induced,

secondary to infection or malignancy or idiopathic. It can mimic a hypersensitivity reaction, with a delayed reaction to the initial exposure and a more rapid reaction to repeated exposure

o Drugs most commonly implicated include: antibacterials (sulphonamides), antifungals, anticonvulsant agents (carbamazepine), NSAIDs, and allopurinol

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o There are genetic associations with HLA alleles (HLA-B*15:02 and carbamazepine, HLA-B*58:01 and allopurinol) which in some places can be tested for prior to starting the medication

o Symptoms typically manifest 1-3 weeks after the drug has 1st been introduced o Patients with SJS/TENS typically have a prodromal phase (high fever, malaise and flu

like illness) which is then followed by pain, fever, erythema, conjuncitivits before the cutaneous lesions become apparent (1-2 days later for TENS, 4-8 days later for SJS)

o Cutaneous lesions start with erythema which progresses to eruptions of bullae and vesicles. This often progresses to diffuse generalized epidermal detachment and large confluent plaques

o Nikolsky sign positive o In SJS, epidermal detachment involves less than 10% of the total body skin area o Transitional SJS-TEN is defined by an epidermal detachment between 10 and 30% o TEN is defined by a detachment greater than 30% o Mucosal lesions are a significant feature of SJS/TEN with 2 or more surfaces involved. This can

lead to difficulties with swallowing, photophobia, urinary retention, respiratory distress and respiratory failure (sloughing of respiratory tract epithelium). Eye lesions can cause corneal scarring and synechiae between the eyelids and conjunctiva. Mucosal lesions are often the first to appear and last to resolve

o Typical histology shows epidermal necrosis (from keratinocyte apoptosis) with minimal dermal infiltration and dermo-epidermal separation

o Recovery is usually seen over 1-6 weeks o Mortality / morbidity is significant. With mortality rates of 5% with SJS, 30-35% with TEN and 10-

15% with transitional forms. Prognosis is worse than that of a burn victim with the same % burn o Management

o Immediate cessation of the likely causative drug is essential o Management then follows the same lines as that for burns, with emphasis on early

airway support (may require intubation and ventilation), adequate fluid administration / resuscitation (don’t use Parkland formula to estimate fluid requirements) aggressive nutritional support and pain relief

o Prophylactic antibiotics only in patients with neutropenic (known association with TENS, often self resolves in 2-5 days)

o An early skin biopsy is necessary to confirm the diagnosis followed by ongoing surgical management (debridement of necrotic areas, removal of sloughed epithelium and cover exposed dermis with biological or synthetic dressings) which is often best carried out at a Burns centre

o Regular ophthalmology review if eye involvement o Immunomodulation therapy is used to try to turn off the disease process. Early IVIG

(licensed indication, some evidence to suggest that it arrests disease progression in 24-48 hours and may decrease mortality by 6-12%7). Corticosteroids are NOT indicated in TENS / SJS

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Erythema Multiforme Major o Symmetrically distributed, erythematous, expanding macules or papules evolve into classic iris or

target lesions, with bright red borders and central petechiae, vesicles, or purpura o Typically less than 10% BSA involvement o It has a more benign course than SJS and TEN, and often occurs following an infection such as

HSV or Mycoplasma pneumoniae o Not usually associated with any mortality o Most cases are self-limited and resolve without sequelae in 2-4 weeks


Staphylococcal scalded skin syndrome o May resemble toxic epidermal necrolysis o Prodromal features include fever, malaise, irritability, impetigo, URTI o Toxin mediated disease

o 2 distinct staphylococcal exotoxins, epidermolytic toxin A (ETA) and B (ETB) which are produced by phage group 2 staphylococcus aureus

o The toxins bind to desmoglein 1 in the desomsomes, causing the desmosome to break down leading to cell separation and bullae formation with subsequent sheet like desquamation

o Cutaneous signs o Erythema (worse in flexures), blistering within 24-48 hours, sheets of skin peel away in

response to minor trauma o Nikolyski sign positive o Mucosal involvement is rare.

o Histology o Characteristic intra-epidermal splitting seen at the granular layer (stratum granulosum) o No epidermal necrosis.

o More common in infants and small children because of delayed clearance of the toxin by the immature kidney

o Usually heals within 7-10 days o Associated with low mortality 1-5% o Management comprises antistaphylococcal antibiotics (i.e flucloxacillin and gentamicin –

dependant on local protocols)

Necrotizing Fasciitis o Rare serious bacterial infection that spreads rapidly and destroys the body's soft tissue o Causative organisms include group A Streptococcus (most common cause),

Klebsiella, Clostridium, E. coli, Staphylococcus aureus, and Aeromonas hydrophila o Management

o Appropriate antibiotics (often difficult to target/reach site of infection) o Early surgical debridement of necrotic/infected tissue


References 1. Juurlink D, Buckley N, Stanbrook M, Isbister G, Bennett M, McGuigan M. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane. Database Syst Rev 2005(1):CD002041. 2. Dyer RF, Esch VH: Chemical toxicity in Fires. JAMA 1976 235:339. 3. Pruitt BA, Erickson DR, Morris A: Progressive pulmonary insufficiency and other pulmonary complications in thermal injury Trauma 2002 15:369. 4. Miller K, Chang A: Acute inhalation injury, Emerg Med Clinic North America 2003 21:533-557. 5. Bachot N, Roujeau JC. Differential diagnosis of severe cutaneous drug eruptions. Am.J Clin Dermatol. 2003;4(8):561-72. 6. Roujeau JC, Stern RS. Severe adverse cutaneous reactions to drugs. N Engl J Med 1994;331(19):1272-85. 7. Metry DW, Jung P, Levy ML. Use of intravenous immunoglobulin in children with stevens-johnson syndrome and toxic epidermal necrolysis: seven cases and review of the literature. Pediatrics 2003;112(6 Pt 1):1430-6. 8. Kaul R, McGeer A, Low DE, Green K, Schwartz B. Population-based surveillance for group A streptococcal necrotizing fasciitis: Clinical features, prognostic indicators, and microbiologic analysis of seventy-seven cases. Ontario Group A Streptococcal Study. Am.J Med 1997;103(1):18-24. 9. Sidbury R. What's new in pediatric dermatology: update for the pediatrician. Curr.Opin.Pediatr. 2004;16(4):410-4. 10. Roujeau JC, Kelly JP, Naldi L, et al. Medication use and the risk of Stevens-Johnson syndrome or toxic epidermal necrolysis. N Engl J Med 1995;333:1600-1607 11. The CDC ( Centres for Disease Control and prevention).

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