Transcript BURNS Early management issues

BURNS
Early 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
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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
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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
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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 & Breathing
Pathophysiology of early changes
1) Inhalation injury complex
- Toxic compounds absorbed
- Upper airway obstruction
- Chemical irritation / injury to airways and lung
parenchyma
2) Burn injury (external) to face and neck
3) 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
Carboxy-Hb level %
Symptoms
0-5
Normal value
15-20
Headache, confusion
20-40
Disorientation, fatigue, nausea, visual disturb.
40-60
Hallucination, agitation, coma, shock state
60 or above
Mortality 50%+
How to diagnose?
• ABG
– High COHb
– Unexplained metabolic acidosis
– Low SpO2 for PO2
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
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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 burn
No 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 smoke
Gas
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:
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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:
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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 Compliance
3. Tracheobronchitis from Inhalation Injury
4. Pulmonary Oedema
5. Surgery - and Anaesthesia-Induced Lung
Dysfunction
30-70% of patients with inhalational injury will
develop ventilator-associated pneumonia.
Continued upper airway obstruction
Pathophysiology
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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 tracheostomy
When can the patient be extubated?
Decreased chest wall compliance
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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
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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 system
Pathophysiology 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)
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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.
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Head trauma
Underlying disease
Respiratory failure
Carbon monoxide poisoning
Cyanide poisoning
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Hypothermia
Other acute issues
• Gastro
• Analgesia
• Wound care incl escharotomy and
compartment pressure monitoring
• Minimise exposure to bugs
From day 2-7
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Infection / sepsis
Anaemia / haematological
Compartment syndromes
Nutrition / metabolism
Surgery / plastics
Dvt prophylaxis (incidence 1-23%)
Controversial issues
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Antibiotics
Steroids
Blood transfusion
Surfactant and other inhaled therapies
Vitamin C superdoses.