BURNSEarly management issues

Epidemiology

• Approx 135 000 total burn injuries in Oz in 2001. • 2% of all injury hospitalisations• 6000 children to A&E with burns each year

– 20-25 children die each year from burns• 13 000 hosp. in NSW between 95 and 99, 40% children. • Declining trend of burn-related deaths in NSW from 90s

to early 2000s. • Gender 60% men• Age – death higher among the elderly; late teens to mid

40s most commonly affected.

Types of burns

• Thermal• Chemical• Radiation• Electrical

Thermal burns

• Fire (46%)– Flash, flame

• Scalding (32%)– Liquids, grease, stream

• Contact (8%)• (Electrical – voltage > 1000 V) (4%)

Simple applied physics

• Temperature (energy)• Duration / exposure time• Medium• Skin thickness (age) (intrinsic structure of

tissue)• Heat dissipation (blood flow)

Depth of burn injury• Classified in degrees of injury based on the amount of epidermis and

dermis injured. At present, depth is estimated by physical appearance, pain, and skin texture or pliability.

• First-degree burn involves only the thin outer epidermis and is characterized by erythema and mild discomfort, healing rapidly.

• Second-degree burns are defined as those in which the entire epidermis and variable portions of the dermis are destroyed. Subdivided into superficial second-degree burn and deep dermal(or deep second-degree) burn

• Full-thickness (or third-degree) burn occurs with destruction of the entire epidermis and dermis, leaving no residual epidermal cells to repopulate the burned area. The portion of the wound not closed by wound contraction will require skin grafting.

Rule of 9s

Prognosis

• Overall survival rates from all burns 95%• Greatly improved survival over last 50 years– Shock Sepsis Inhalation / pneumonia

• Pneumonia now greatest cause of mortality• % TBSA burnt + age = mortality• Multidisciplinary approach and specialised

burns centres

Indicators of poor prognosis• Extremes of age• %TBSA• Severe inhalation injury and ventilator dependency• Combination of inhalation injury with cutaneous

burn• Co-existent trauma• Acute renal injury / elevated creatinine • Poor pre-morbid health status• Sepsis / pneumonia (mortality increased with 40%)• Thrombocytopenia (< 20 000)• Elevated serum lactate and / or base deficit.

NSW Referral centres

• Concorde• Royal North Shore • Westmead (under 16 years of age)

Who to refer?• Partial/full thickness burns in adults >10% TBSA.• Partial/full thickness burn in children > 5% TBSA.• Burns to the face, hands, feet, genitalia, perineum and

major joints. • Chemical burns• Electrical burns• Burns with concomitant trauma• Burns in patients with pre-existing medical conditions that

could adversely affect patient care and outcome• Children with suspected non-accidental injury• Pregnancy with cutaneous burns

Who to retrieve?

• Any intubated patients• Head and neck burns• Partial and full thickness burns > 10% in children / >

20% in adults• Burns with significant co-morbidities• Associated trauma• Significant pre-existing medical disorder• Electrical conduction injury with cutaneous burns• Chemical injury with cutaneous burns

Management

• Trauma team• Handover from paramedics– Details important – when, where, how, what etc.– First aid / treatment this far– Vital signs

Trauma call

A burn patient is a trauma patient; therefore, other injuries should be expected and sought

• Dramatic physiologic and metabolic changes over the course of the injury state.

• Three phases of burns:1) Resuscitation phase (0 to 36 hours)

characterised by cardiopulmonary instability

2) Post resuscitation phase (2 to 6 days) 3) Inflammation / infection phase (7 days to wound closure)

Airways & BreathingPathophysiology of early changes1) Inhalation injury complex

- Toxic compounds absorbed- Upper airway obstruction- Chemical irritation / injury to airways and lung

parenchyma

2) Burn injury (external) to face and neck3) Burn injury (external) involving the thorax

Smoke inhalation injury complex• Pulmonary insufficiency caused by the inhalation of heat and smoke is

the major cause of mortality in the fire-injured person, accounting for more than 50% of fire-related deaths. Acute upper airway obstruction occurs in 20-33% of hospitalised burn patients with inhal. injury.

• Many new synthetics in home furnishings and clothing have resulted in a much more complex form of injury, due to the extremely toxic combustion products of these advances in technology.

• A closed space fire can result in a severe hypoxic insult as well as lung damage from the inhalation of toxic fumes.

• The exposure time, the concentration of fumes, the elements release and the degree of concomitant body burn are critical variables.

• These factors cause a very complex injury with morbidity and mortality risks, especially when combined with a body burn.

Carbon monoxide toxicity• One of the leading causes of death in fires.• Basic by-product of (incomplete) combustion. • Rapidly transported across the alveolar membrane.

Preferentially binds with the haemoglobin molecule in place of oxygen (*200). Shifts the Hb-oxygen curve to the left, thereby impairing oxygen unloading at tissue level.

• Tissue hypoxia. Also binds to myoglobin. Can also saturate the cell, bind to cytochrome oxidase and thereby impair mitochondrial function and ATP production.

Carbon Monoxide Toxicity

How to diagnose?• ABG

– High COHb– Unexplained metabolic acidosis– Low SpO2 for PO2

Carboxy-Hb level % Symptoms0-5 Normal value15-20 Headache, confusion20-40 Disorientation, fatigue, nausea, visual disturb.

40-60 Hallucination, agitation, coma, shock state

60 or above Mortality 50%+

Cyanide toxicity• Cyanide toxicity presents in a very similar fashion

to carbon monoxide, with severe metabolic acidosis and obtundation in severe cases.

• Normal levels < 0.1 mg/L• Binds to cytochrome c oxidase and disrupts the

electron transport chain, inhibiting aerobic metabolism and depleting cells from ATP.

• Diagnosis is more difficult because cyanide levels are not always readily available or very reliable.

Treatment CO toxicity• Oxygen and supportive care. • Hyperbaric oxygen• T1/2 room air – 90 minutes. T1/2 FiO2 1.00 – 30 minutes.

Treatment cyanide toxicity• Cardiopulmonary support is usually sufficient treatment,

since the liver via the enzyme rhodenase will clear the cyanide from the circulation.

• Sodium nitrite is used (300mg intravenously over 5 to 10 minutes) in severe cases (confirm levels).

• Hydroxycobalmin and thiosulphate.

Upper airway obstruction from tissue oedema• Direct heat injury caused by the inhalation of air heated to a temperature of

150O C or higher ordinarily results in burns to the face, oropharynx, and upper airway (above the vocal cords).

• Heat immediate injury to the airway mucosa with oedema, erythema, and ulceration. Anatomically these changes may be present shortly after the burn, but clinical signs may not occur till 12-18 hours after injury.

• Inhalational injury + body burn much higher risk of oedematous airway obstruction due to fluid resuscitation given and the release of inflammatory mediators from the burned skin.

• Burn to face or neck marked anatomic distortion and, in the case of the deep neck burn, external compression on the larynx. Third degree burn of the neck is particularly bad

Minimal external oedema due to the non-elastic burnNo external expansion. Massive intraoral / pharyngeal oedema

• Increased secretions• Oedema resolves around day 4-5 unless there is extensive and deep injuries.

Symptoms & signs of obstruction• Upper airway noise (turbulent airflow), dyspnoea,

increased work of breathing, anxiety, stridor and eventually cyanosis.

• Difficult to distinguish noise from a narrowed airway from that caused by increased oral and nasal secretions due to smoke irritation.

• The airway oedema and the external burn oedema process have a parallel time course so that by the time symptoms of airway oedema develop, external and internal anatomic distortion will be extensive.

How to confirm airway involvement if in doubt?How to determine degree of involvement?• Signs of facial burn / erythema, swollen lips, singed

facial hair, carbonaceous sputum. • Serial fibreoptic bronchoscopies/ laryngoscopies. – Remember oedema is progressive up until 18 hours post

injury.

Treatment• Intubate early if indicated• Otherwise close monitoring and regular

reviews are essential while...– Positioning the patient to minimise head/neck

swelling– Careful not to overhydrate and promote oedema– Analgesia

• Escharotomy (patient usually intubated by this stage)

• More to follow...

CHEMICAL BURN TO UPPER AND LOWER AIRWAYS

• Generally much more serious than that produced by heat alone.

• Exposure to toxic gases contained in smoke PLUS carbon particles coated with irritating aldehydes and organic acids

• Injury to both upper and lower airways.• The location of injury will depend on the

duration of exposure, the size of the particles, and the solubility of the gases.

Toxic elements in house fire smokeGas Source Effects

Carbon monoxide Any organic matter Tissue hypoxia

Nitrogen dioxide Wallpaper, wood Bronchial irritation, dizziness, pulm oedema

Hydrogen chloride Plastics (PVC) Severe mucosal irritation, pulm oedema

Hydrogen cyanide Wool, silk, nylons, polyurethane

Headaches, respiratory failure, coma

Benzene Petroleum plastics Mucosal irritation, coma

Aldehydes Wood, cotton, paper Severe mucosal damage, extensive lung damage

Ammonia Nylon Mucosal irritation

• The unconscious patient loses airway protective mechanisms, resulting in a more severe injury to the lower airways when continuing to inspire.

• Water-soluble gases such as ammonia, sulphur dioxide and chlorine react with water in the mucous membranes to produce strong acids and alkalies irritation, bronchospasm, mucous membrane ulceration and oedema. Severe impairment of the ciliary mechanism impaired removal of particles and mucus.

• Lipid-soluble compounds, e.g. nitrous oxide, phosgene, hydrogen chloride, and various toxic aldehydes, are transported to the lower airways on carbon particles that, in turn, adhere to the mucosa. All these agents produce cell membrane damage.

• Alveolar oedema is not a major component of the early disease state.

• Symptoms may be absent on admission. The magnitude of the degree of injury evident after 24 to 48 hours.

• Early symptoms usually consist of bronchospasm manifested as wheezing and bronchorrhoea. Coughing. Sometimes confused with pulmonary oedema.

• Marked decrease in lung compliance and increased work of breathing. Impaired clearance of secretions. – V/Q mismatch with increased A-a gradient.

• Injury at the alveolar level is usually fatal.

Diagnosis• History – exposure, confined space? • Symptoms & signs• High HbCO• Laryngoscopy – Absence of upper airways injury (serial reviews)

usually means absence of lower airway injury. • Bronchoscopy (if intubated)• Xenon scan (not in acute settings)

Treatment• Aggressive approach to upper airway maintenance and pulmonary

support, which includes maintenance of small airways patency and removal of soot and the mucopurulent secretions.

• I.e. very likely to need intubation. • PEEP to maintain small airway patency and an adequate FRC. Prevention

easier than treating. • Early intubation and PEEP have been reported to decrease pulmonary

deaths after severe burns and smoke inhalation.• Tube size – minimal 7 mm for adults.• Humidified oxygen • Elevation of the patient’s head and chest 20 to 300 is also helpful.• Careful well-monitored fluid resuscitation • Bronchodilators for bronchospasms.• Anticholinergics to minimize bronchorrhoea + bronchodilator effect? • No role for AB and steroids.

IMPAIRED CHEST WALL COMPLIANCE

• Respiratory excursion can be markedly impaired by a burn to the chest wall. Most evident with a circumferential third degree burn with loss of elasticity in the chest wall due to the burn tissue . Increased WOB to maintain functional residual capacity and an adequate tidal volume.

• Oedema from a second degree burn is also sufficient to alter lung mechanics (axillae and lateral chest walls).

• Compressed intrathoracic volume significant V/Q mismatch, atelectasis, and hypoventilation. Maximum respiratory effort is required just to maintain adequate gas exchange.

• Symptoms may not be clearly evident until oedema formation peaks at about 10 to 12 hours.

• In the combined chest burn and inhalation injury it is very difficult to distinguish the degree of impairment in total lung compliance due to the increased airway oedema and bronchospasm compared with that due to the impaired chest wall.

Treatment• Positioning and judicious fluid resuscitation. • NIV or mechanical ventilation.• Escharotomy (early if circumferential 3rd degree).

A&B Summary of early management- High flow 70-100% oxygen to all patients- Assess airway and surrounding tissues

- Intubate (RSI) if indicated - ? In-line immobilisation of neck- Risk factors for (early) intubation:

- Unconsciousness at scene- Fire in confined space- Facial burns singed facial hair, soot in nostrils or sputum, facial erythema.- Voice changes or “lump in throat”- Elevated carbon monoxide levels on ABG or respiratory failure.

- Assess breathing and thorax- Intervention?

- Continue primary survey and obtain monitoring and ABG results. CXR

Secondary survey• If not intubated yet– Other injuries identified?– Time, equipment and appropriate staff for

laryngoscopy?– Positioning of patient– Assist with clearance of secretions– Fluid management– Chest wall excursion– ?Role of NIV– Bronchodilators if wheezing

Criteria for intubation (NSW Health)

• Clinical evidence of possible airway compromise:– Head and neck burns/scalds with increased swelling– Stridor, hoarse voice, swollen lips– Carbonaceous material around or in the mouth, nose or sputum– Singed facial, head or nasal hairs.

• Intubate early– If patient unconscious – If there are head and neck burns with obvious swelling– If the patient is to be transported and meets any of the above

criteria. – If there are other clinical symptoms and signs and ABG results are

indicative of respiratory dysfunction.

Post resuscitation phase (day 2-6)

Potentially five major pulmonary problems:1. Continued Upper Airway Obstruction 2. Decreased Chest Wall Compliance3. Tracheobronchitis from Inhalation Injury4. Pulmonary Oedema 5. Surgery - and Anaesthesia-Induced Lung

Dysfunction 30-70% of patients with inhalational injury will develop ventilator-associated pneumonia.

Continued upper airway obstructionPathophysiology

– Continued airways oedema – Mucosal damage with slough – Increased oral secretions – Bacterial colonization

Treatment– Keep intubated until oedema resolves – Head elevated position – Avoid excessive tube motion – Vigorous oral hygiene (+/- Nystatin if on antibiotics) – Avoid cuff over-inflation– Consider tracheostomyWhen can the patient be extubated?

Decreased chest wall compliance• Not completely eliminated by escharotomy• Continuous swelling for days• High PEEP can affect haemodynamics• More difficult to manage during GA

Treatment• Continue supportive care and mechanical

ventilation.• Care with fluid adm. • Early surgical management of full thickness burns

Tracheobronchitis Pathophysiology– Ongoing mucosal injury (degree and duration

depending on chemical exposure)– Increased secretions / bronchorrhoea and

impaired ciliary function– Bronchospasm– Interstitial oedema– Necrosis and slough– Airway plugging, atelectasis and hypoxaemia – Increased risk of infection (colonisation inevitable) • Tracheobronchitis bronchopneumonia

Clinical findings– Sputum changing from loose to purulent – Evidence of necrotic tissue in sputum – Wheezing, ronchi, creps +/- bronchial breathing– Increased work of breathing – Altered gas exchange – Bronchoscopic findings– Infiltrates on radiographs: Late finding

Treatment– Aggressive pulmonary toilet with frequent postural drainage (consider rotation

bed) ; physiotherapy.– Infection surveillance (daily sputum/ETT samples) – Antibiotics when indicated (not prophylactic ) – Inhaled bronchodilators – Inhaled N-acetylcysteine?– Positive pressure to maintain FRC – Aggressive diuresis to correct airways oedema not shown to work

Pulmonary oedema• High pressure pulmonary oedema.

ARDS (low pressure) typically occurs later (after the 1st week).

• Fluid shifts and overload.• Severe hypoalbuminaemia / proteinaemia• Stress response and reduced ANP• More likely with underlying heart disease and renal

impairment. • May progress to alveolar oedema and cause shunting

and worsening gas exchange. • CXR and wedge pressure / PICCO.

Inflammation / infection phase (1 week to wound closure)

• Pneumonia and sepsis (VAP, nosocomial)• Hypermetabolism –induced respiratory failure– 50-100% increase in CO2 production– Catabolism and muscle weakness

• ARDS

Cardiovascular systemPathophysiology of initial changes- Unique combination of distributive and

hypovolaemic shock. - Intravascular volume depletion and low PA wedge

pressure- Poor cardiac output- Increased systemic vascular resistance.

Cardiac• Reduced myocardial contractility – aetilogy

thought to be multifactorial e.g. Circulating inflammatory markers, impaired cellular calcium utilisation, myocardial oedema...

Vascular • Local and systemic effects• Microcirculation loses its wall integrity. • Protein, electrolyte and fluid losses dramatic

changes in the balance between osmotic forces and hydrostatic pressures

• loss of circulating plasma volume, heamoconcentration, oedema formation, decreased urine output, depressed C.O.

• Most oedema occurs locally at the burn site and is maximal at 24 hours post injury.

• Oedema increased tissue pressure with poor tissue perfusion and hypoxia fluid therapy used to correct the hypovolaemia but further accentuate the oedema.

• Leakiness returns towards normal within the first 24 hours or so. Fluid requirements change. Oedema remains for several days.

Cardiovascular system

Early management• Anticipate and prevent rather than treat shock.• Peripheral venous access +/- central access.– Site ?

• Challenge to find balance between optimising filling pressures / volume and preventing fluid overload and consequently pulmonary oedema, pump failure, poor wound healing and extension of burn, ACS and risk of escharotomies.

• Monitoring:– HR/ECG (<110 vs >120 b/min)– BP via arterial line– SpO2

– +/- central venous pressure for trend and SpvO2

– IDC for urine output monitoring– ABGs incl. lactate and base deficit• No evidence to recommend the use of these markers to

guide treatment or to use as independent predictors of outcome.

• What end points are we aiming for?

Fluids

• Universally accepted that aggressive fluid therapy greatly improves outcome in burns >15-20% TBSA / shock.

• WARM fluids to avoid hypothermia• Multiple formulas and “local recipes”. • Multiple suggested “best fluids” but no evidence that

one type improves morbidity / mortality vs. others. • Formulas should be regarded as resuscitation guidelines

only. Has to be adjusted to individual patient needs.

• Modified Parkland formula (Consensus formula):24 hour fluid requirement = 3-4 ml/kg * body wt * %TBSA burnt.

First half to be adm. over initial 8 hours after injury. Consider deficits. Hartmann’s solution / Ringer’s.

• Children:Modified Parkland (Hartmann’s)+Maintenance fluids (4%D 1/5 NS)

• Fluid requirements increased with late presentations, inhalational injuries, electrical burns, associated injuries / trauma, ETOH intox.....

• Limitation with the above formula:– Based on pt wt (NB! Children)– Based on estimate of TBSA injury (over- vs.

underestimation of extent)Great variations in fluid management

• Once urine output established, can use this to guide further fluid management.

• Non-responders: Consider patient groups known to require more fluids +/- commence vasopressors/inotropes.

• Evaporation from the surface of the burn becomes a major source of water loss that persists until the wound is closed. This loss is related to the water vapour pressure at the surface. A reasonable estimate of loss can be obtained from the following formula:

EVAPORATIVE WATER LOSS = ( 25 + % TBSA burnt ) * TBSA in m2

Cardiovascular system post resuscitation phase

• Blood volume can be restored more effectively as the leakage decreases at about 24 to 36 hours.

• Since non-burnt tissue appears to regain normal permeability very shortly after injury, and since hypoproteinaemia may accentuate the oedema in non-burnt tissue, protein restoration beginning at about 8 to 12 hours with 4% albumin seems appropriate if oedema in non-injured tissue and total fluid requirements are to be minimized.

• Pulm. congestion• Hypermetabolic phase over the next 3 to 5 days.

Tachycardia, ranging from modest to significant (100 to 120 beats per minute), is seen frequently and results partly from persistent elevation of catecholamine levels. Systemic vascular resistance begins to decrease. The vasodilatation results in an increase in the capacity of the vascular space and, therefore, an increased need for colloid and red blood cells.

D

• Head trauma• Underlying disease• Respiratory failure• Carbon monoxide poisoning• Cyanide poisoning

E

Hypothermia

Other acute issues

• Gastro• Analgesia• Wound care incl escharotomy and

compartment pressure monitoring• Minimise exposure to bugs

From day 2-7

• Infection / sepsis• Anaemia / haematological• Compartment syndromes• Nutrition / metabolism• Surgery / plastics• Dvt prophylaxis (incidence 1-23%)

Controversial issues

• Antibiotics• Steroids• Blood transfusion• Surfactant and other inhaled therapies• Vitamin C superdoses.