Author of Lecture: Milliss, David (Dr)

Title of Lecture: Burns Patient

(Problem 1, Lecture 1, 2009)

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 Burn Management

Dr David Milliss
FANZCA FJCICM

Head of Department, ICU, CRGH

Clinical Senior Lecturer, Concord Clinical School
 Introduction
Epidemiology of burn injuries

Pathophysiology of burn injuries

Acute burn management

Medium to long term issues

Severe electrical injuries

 Burns - Incidence

1% Australia and New Zealand per year

250,000 people per year

50% Restriction Daily Living Activities

10% Hospital

10% of Hospital admissions are Severe Burns

EMSB
 Burn Admissions (%)
Adult Children

Explosion & Flame 48 25

Scald - oil & water 33 60
Contact 8 10
Electrical 5 1
Chemical 3 2
Friction 2 1
Sun 1 1

EMSB
 Place of Burn

Home 61%
Work 17%
Roadway 10%
Outdoors 8%
Institution 4%
Elsewhere 2%

EMSB
 Childrens Burns

> 75% at Home

Kitchen

Bathroom

EMSB
 Pathophysiology
Jackson Burn Wound Model

Zone of Survival
Slide
Zone of Damage
Zone of Necrosis

Coagulation

Stasis
Hyperaemia
EMSB
Pathophysiology
 ZONE OF STASIS
Compromised but viable cells;
Impaired blood flow:
Platelet aggregation; stiff heat-injured rbcs;
white cells adhere to vessel walls; fibrin
deposition

Endothelial swelling; vasoconstriction

Cells are susceptible to:

hypovolaemia, dehydration, low perfusion
pressure, oedema, cold
infection
 LARGE BURNS (>20-25%)
Large quantity of inflammatory mediators
released from zone of hyperaemia -> leaky
capillaries -> whole body oedema

Fall in plasma volume

Fall in cardiac output

Hypovolaemic shock

EMSB
General Response
 Early Care
First aid
Stop the burning

Cool the burn injury

Untreated,intense local
response causes progression of
depth over 48 hours
 First Aid
Cool the burn.
ASAP

Any fluid: 8 - 25 C (15o)

Continue >20 minutes

Effective up to 3 hours

Avoid hypothermia
 Immediate Management
Airway & C-spine

Breathing & O2

Circulation & haemorrhage control

Disability (neurological)

Exposure the patient & control environment

Fluids

Immediate surgery if necessary

NB: 2ndary survey: history, head to toe exam

 Assess the burn size
Size
Rule of nines
Patient palm
Chart
Assess Burn Depth
 Epidermal

Eg. Sunburn
Red
Painful
No blisters
Healing in less than
one week
No scarring
Superficial
Dermal
Red
Painful
Blisters
Capillary refill
present
Healing slower,
over a few weeks
May be some
scarring
 Deep
Dermal
Dark red
Not Painful
Blisters may be
seen
No capillary refill
Minimal or no
healing
Scarring will
occur
 Full Thickness
White, waxy, charred
No sensation
No blisters
No capillary refill
No healing
Initial Assessment - Depth
Classic progression
Erythema
Blistering
Pink, blanching
Red, non-blanching
Leathery or charred.

Early appearances are deceptive

The burn wound
is:

Mixed

Dynamic
 Progression in a Burn Wound
4 hours after injury 4 days later
Note early rigidity of deep All areas have become
burn around waist deep.
 Fluid Resuscitation
Which type?
Na containing, Hartmanns solution, albumin

How much
Size and depth: not epidermal
Parkland formula: 3-4 ml/kg/%TBSA burnt
Administration: in first 8 hrs; in next 16 hrs

How do we monitor our efforts?

Urine
PR, BP, Perfusion, acidosis

Burn wound oedema

 Fluid resuscitation
INCREASED NEEDS IN:
Late resuscitation

Inhalation injury

Electrical burns

Associated trauma

Other factors
Dehydration
Drugs
 Dressings
Dry clean linen

Glad wrap

Paraffin based dressings eg bactigras

Special dressings and Skin substitutes

 Medium to long term issues
Infection:
Burn wound
Lines and tubes
Immunosuppression
Surgery
Nutrition:
Stress response, hypercatabolic
Lasts weeks to months
Loss of muscle mass
Chronic pain, rehabilitation
Electrical Injuries
 Basic Principles: physics
Electricity is the movement of negatively
charged electrons along a conductor
(current/amperage)

Voltage is the electric pressure that causes

current to flow

Resistance is the opposing force to flow of

current; or the tendency for matter to resist the
flow of current

I=V/R
 Basic Principles
Resistance of body tissues (least greatest)
nerves
blood
mucus membranes
muscle
dry skin
tendon
fat
bone

Heat is produced when current

flow meets resistance
 Basic Principles: pathophysiology
Effects of current flow:
Electrophysiological
Depolarisation of cells

Cardiac injury

Heat production (major cause of injury)

Joules Law

P (heat) = I2 x R x t
 Basic Principles: pathophysiology
Damage to the tissues
in the body:
Strength of the current
Voltage difference

Resistance of the tissues

Duration of the flow of current

Pathway of the current

 Classification
Low voltage:
< 1000
Home: 240 volts at 50 Hz (AC)

High voltage:
>1000
Power lines, utilities, industry (AC)
Typically: 11,000 / 33,000 volts, may be more

Lightning:
>1 million volts
DC
 Low voltage injuries

Commonly seen in
children
Produce local
contact wounds
Usually mouth
(80%) or hands
May produce
cardiac problems
 Low voltage injuries
Documented rate of arrhythmia following
electrical injury is about 8-15%
most occur within the first few hours
sudden cardiac death can occur
asystole (DC)
ventricular fibrillation (AC)
other arrhythmias include sinus tach,
transient ST elevation, reversible QT
prolongation, PVCs, AF, BBB
 Low voltage injuries
Indications for cardiac monitoring
cardiac arrest
Reduced LOC
abnormal ECG
documented dysrhythmia
history of cardiac disease or risk factors
concomitant severe injury
suspicion of conductive injury through thorax
chest pain
hypoxia
 Low voltage injuries
Asymptomatic patients who have suffered
a 110 V or 240 V electrical injury and have
a normal initial ECG, do not need
admission for cardiac monitoring

Overall, low voltage injuries have the

lowest mortality rates
 High voltage injuries

> 1000 volts; 11,00

33,000 or more
Injury from:
Current transmission
Estimate only
Heat produced

Arc flash burns, clothing

Associated trauma
 High voltage injuries
Clinically:
Entrance and exit wounds (usually F/T)
+/- other cutaneous burns
Unknown internal tissue damage
Need to look for it
Cardiac

Muscle

Vascular

Renal, Neural

Other injuries
Trauma
High voltage injuries
 High voltage injuries
Mostly work related
Some due to risk taking behaviour
Usually male, adults, some adolescents

More operations
More complications
Muscle damage: fasciotomy, amputations
Associated injury: brain, orthopaedic
Increased length of stay, higher mortality
 High voltage injuries
Cardiac:
Not common
Arrhythmias
Cardiac arrest: asystole, VF
Early dysfunction, cardiomyopathy
Vascular:
Thrombosis, vessel rupture, spasm
Compartment syndromes
 High voltage injuries
Neural:
Peripheral:
direct, myelin sheath vascular supply,
compartment syndrome
Spinal cord:
Immediate evidence of damage
Delayed presentation, prolonged recovery

Brain:
Transient loss of consciousness
Prolonged coma with eventual recovery, cataracts

Head trauma
 High voltage injuries
Muscle and other tissue damage
Direct coagulation necrosis, vessel
damage, compartment syndrome
Damage is erratic
Damage can be deep
 High voltage injuries
Muscle damage:
Direct coagulation necrosis, vessel
damage, compartment syndrome
Myoglobin released; Renal impairment

Fasciotomy
Amputations
 High voltage injuries
Management:
Usual
Remove patient from danger
Protect self
ABC
Knowledge of the event
Burns
Deep tissue damage
Other injuries
 High voltage injuries
Fluid resuscitation:
Formula: plus more than calculated from
cutaneous injury due to deep injuries
Myoglobinuria

Trauma approach to imaging:

Plain films: Cxal spine, chest, pelvis
CT head and spine
Others as indicated
 Lightning Injuries

A lightning strike exposes a person to

>10 million V of DC that lasts
1/10,000 to 1/1000 s
20,000-100 million amps
In comparison: little energy delivered
10,000,000 V x 1/1000 sec = 10,000 W-
sec
15,000 V x 120 sec = 1,800,000 W-sec
 Lightning Injuries

Tend to cause asystole

Cardiac automaticity may re-establish a rhythm

However, respiratory arrest is usually longer and

leads to a secondary hypoxic cardiac arrest

NB: neurological, skeletal, skin injuries, eye, ear

NB: deep tissue damage is unusual

 Lightning Injuries

Skin
less than 5% have deep burns (exit wound)
superficial burns
Linear
Punctate

Feathering

Thermal

requires standard burn care treatment

 Lightning Injuries

Mechanisms of injury
Direct strike, orifices
Contact
Side flash, splash
Blunt trauma

Highest mortality: 7-15%

But not a common injury)
Lightning Injuries
 Lightning Injuries

Management:
Usual
Remove patient from danger
Protect self
ABC
Burns