Burn Injuries

Muchtar

Definition
Injury to the skin and deeper tissues caused
by hot liquids, flames, radiant heat, direct
contact with hot solids, caustic chemicals,
electricity, or electromagnetic (nuclear)
radiation.

Incidence of Burn Injuries

Annually

in the United States:

Approximately 1 million people require medical attention from

burn injuries.

700,000 ER visits; of which 45,000 people are hospitalized

Deaths from burn / smoke inhalation injuries account for 4,500

deaths.

Most

burn injuries occur in the home

75% are victims of their own actions

Populations

at highest risk: pediatric and elderly

Burn Injuries
Potential

complications

Fluid and Electrolyte loss Hypovolemia

Hypothermia, Infection, Acidosis
Renal or hepatic failure
Formation of eschar
Complications of circumferential burn

Causes of Burn Injuries

Thermal
Electrical
Chemical
Radiation
Cold

Injuries

Inhalation

Causes of Burn Injuries

Thermal

Injuries (most common)

Contact
Direct contact with hot object (i.e. pan or iron)
Anything that sticks to skin (i.e. tar, grease or foods)
Scalding

Direct contact with hot liquid / vapors (moist heat)

i.e. cooking, bathing or car radiator overheating

Single most common injury in the pediatric client

Flame
Direct contact with flame (dry heat)
i.e. structural fires / clothing catching on fire

Causes of Burn Injuries

Electrical
Contact with an electrical current
i.e. open wiring or being struck by lightening
Pediatrics: chewing on electrical cord or placing object in
outlet
Require some different management

Chemical
Strong acids or alkaloids
i.e. household cleaning products
Management specific to chemical involved

Causes of Burn Injuries

Radiation
Prolonged exposure to ultraviolet rays of the sun
Other sources: occupational or medical therapies

Cold

Injuries

Frostbite

Dont forget all burns not from heat !!

Injury due to freezing & refreezing of intracellular fluid
Ice crystals puncture the cells and destroy tissue
Can result in amputation

Burn Classification
1st

degree/1 (Superficial burn)

2nd degree/ 2 (Partial Thickness Burn)
a. Superficial dermal burns (2a)
b. Deep dermal burns (2b)
3rd Degree/3 (Full Thickness burn)

How to classified burn depth?

Clinical

observation
Vital dyes
Laser doppler
Burn biopsy

Burn Classifications
1st

degree (Superficial burn)

Involves the epidermis

Characterized by dry & reddening
Tenderness and Pain
Increased warmth
Edema may occur, but no blistering (bullae)
Burn blanches under pressure
Example - sunburn
Usually heal in ~ 7 days

Burn Classifications

First Degree Burn

(Superficial Burn)

Burn Classifications
2nd

degree (2)

Damage extends through the epidermis and

involves the dermis.

Moist, shiny appearance
Pink to red color
Painful
Divided in 2 :

Superficial Dermal Burns (2a)

Involves

upper 1/3 of dermis

Wound Appearance:

Red to pink

Wet and weeping wounds

Thin-walled, fluid-filled blisters

Mild to moderate edema

Extremely painful

Wound Healing:

In 2 weeks (spontaneous)

Minimal scarring; minor pigment discoloration may occur

Deep Dermal Burns (2b)

Involves

larger portion of dermis (not complete)

Wound Appearance:
Mottled: Red, pink, or white area
Moist
No blisters
Moderate edema
Painful; usually less severe
Has thin eschar
Wound Healing:
May heal spontaneously 2-6 weeks
Hypertrophic scarring / formation of contractures

Wound Management:

Burn Classifications

2nd Degree Burn

(Partial Thickness
Burn)

Full-Thickness Burns (3 )
o

Involves

the entire epidermis and dermis

Wound Appearance:
Dry, leathery and rigid
+ Eschar (hard and in-elastic)
Red, white, yellow, brown or black
Severe edema
Painless & insensitive to palpation
Pain is due to intermixing of 2nd degree
May be minor bleeding
No blisters (bullae)

Full-Thickness Burns (3 )
o

Wound Healing:
No spontaneous healing;
Wound Management:
Surgical excision & skin grafting

Burn Classifications

3rd Degree Burn

(Full Thickness burn)

Burn Injuries
Often

it is not possible to predict the exact

depth of a burn in the acute phase. Some
2nd degree burns will convert to 3rd when
infection sets in. When in doubt call it 3rd
degree.

Size of a Burn Injury

Total Body Surface Area (TBSA) Burned
Palmar Method (Rule of palm)
A quick method to evaluate scattered or localized burns
Clients palm = 1 % TBSA

Rule of Nines
A quick method to evaluate the extent of burns
Major body surface areas divided into multiples of nine
Modified version for children and infants

Lund-Browder Method
Most Accurate; based on age (growth)
Can be used for the adult, children & infants

Palm Rule

1%

Adult rule of nines

Head = 9%
Chest = 9%
Abdomen = 9%
Upper back = 9%
Lower back = 9%
Right arm = 9%
Left arm = 9%
Right side, front of leg (entire length) = 9%
Right side, back of leg (entire length) = 9%
Left side, front of leg (entire length) = 9%
Left side, back of leg (entire length) = 9%
Groin = 1%
Total body = 100%

Lund & Browder Chart

Burn Patient Severity

Factors

to Consider

Depth or Classification
Body Surface area burned
Age: Adult vs Pediatric
Preexisting medical conditions
Associated Trauma
blast injury
fall injury
airway compromise
child abuse

Burn Patient Severity

Patient

age

Less than 2 or greater than 55 have increased incidence of

complication
Burn

configuration

Circumferential burns can cause total occlusion of

circulation to an area due to edema

Restrict ventilation if encircle the chest
Burns on joint area can cause disability due to scar
formation

Severity of burn (American Burn

Association 2002)
1. Critical burn
2. Moderate burn
3. Minor burn

1. Critical Burn Criteria

20 & 30 > 20% (<10yr group) & (>50yr group)

20 & 30 > 25% in other ages group
Every 30 at the hands, face, feet, or genitalia
Burns with respiratory injury
Burns complicated by other trauma
Underlying health problems
Electrical and deep chemical burns

2. Moderate Burn Criteria

20

& 30 10-20% BSA % in <10yr group &

>50yr group
20 & 30 15-25% BSA in other ages group,
with 30 <10%
30 <10% BSA, in all groups excluding
hands, face, feet, or genitalia burn

3. Minor Burn Criteria

20

& 30 <10% BSA % in <10yr group &

>50yr group
20 & 30 <15% BSA in other ages group,
20 & 30 <10% BSA, in all groups excluding
hands, face, feet, or genitalia burn

PATHOPHYSIOLOGY

Thermal Burn Injury Pathophysiology

(Jacksons Thermal Wound Theory)

Zone

of Coagulation

Inner Zone
Area of cellular death (necrosis)

Zone

of Stasis

Area surrounding zone of coagulation

Cellular injury: decreased blood flow & inflammation
Potentially salvable; susceptible to additional injury

Zone

of Hyperemia

Peripheral area of burn

Area of least cellular injury & increased blood flow
Complete recovery of this tissue likely.

Pathophysiology

Acute (Emergent) phase

ABC
Response to pain catecholamine release

Sub Acute

phase

Loss of barrier, infections, electrolyte imbalance, hyper

metabolic, & inflammatory response

Resolution

(Late) phase

scar tissue and remodeling of tissue

Acute/Emergent/
Resuscitative Phase
Lasts

from onset to 5 or more days but

usually lasts 24-48 hours
begins with fluid loss and edema formation
and continues until fluid motorization and
diuresis begins
Greatest initial threat is hypovolemic shock
to a major burn patient!

Complications during Acute

phase of burn injury are 3
major organ systems...
Respiratory
Cardiovascular
Renal systems

Respiratory System
Vulnerable

to 2 types of injury
1. Upper airway burns
obstruction of the
airway
2. Inhalation injury can show up 24 hrs later-watch for
resp. distress : increased agitation or change in rate
or character of respiration
Preexisting problem (ex. COPD) more prone to get
resp. infection
Pneumonia is common complication of major burns
Overload fluids
pulmonary edema

Respiratory System
Chest

x-rays taken within 24 hours (falsely negative

in 92%)
Require more resuscitation fluid than commonly
used formulas
Prophylactic use of high-frequency percussive
ventilation minimizes airway collapse and atelectatic
changes
The comorbid effect of moderate to severe inhalation
injury is related to both age and burn size and
increases mortality by a maximum of 20% above that
predicted on the basis of age and burn size in patients

 Respiratory compromise
secondary to circumferential eschar around the
thorax

Cardiovascular Systems

Arrhythmias, hypovolemic shock which may lead to

irreversible shock
circulation to limbs can be impaired by circumferential burns
and then the edema formation
Causes: occluded blood supply thus causing ischemia,
necrosis, and eventually gangrene.
Escharotomies (incisions through eschar) done to restore
circulation to compromised extremities.

Pathophysiology
Fluid Shift
Massive

fluid shifts out of blood vessels as a

result of increased capillary permeability.
Water, sodium, & later plasma protein (esp.
albumin) moves into interstitial spaces &
other tissues (2nd spacing). The colloidal
osmotic pressure decreases with loss of
protein from the vascular space.

Pathophysiology
Fluids

goes into areas with no fluids and

this is called third spacing (exudate and
blister formation).

Net

result is decreased volume, depletion

due to fluid shifts = edema,
blood
pressure, &
pulse

Phatophysiology
Fluid

shift usually occurs in the first 12 hr and

can continue 24 to 36 hr
Profound imbalance of fluid, electrolyte, and
acid base, hyperkalemia and hyponatremia
levels, and hemoconcentration
Fluid remobilization after 24 hr, diuretic stage
begins 48 to 72 hr after injury

Pathophysiology
Hypovolemic Shock
Occurs

when there is a loss of intravascular

fluid volume. The volume is inadequate to
fill vascular space and is unavailable for
circulation.
Also, burns have a direct loss of fluid due to
evaporation.

Renal System
Most

common renal complication of burns

in the emergent phase is ATN. Because of
hypovolemic state, blood flow decreases,
causing renal ischemia. If it continues, acute
renal failure may develop.

 Wound repair begins within the first 6-12 hours

after injury.

Sub Acute Phase

Skin

barrier destroyed and all changes make

the burn patient more susceptible to
infection, electrolyte imbalance, etc

Sub Acute Phase

Increased

capillary leak, with protein and

intravascular volume loss
Hypermetabolic response (SIRS)
loss of lean body mass, protein catabolism

Cardiac

output decreased initially, then

normalizes
depressed contractility

 Inflammatory

compensation can trigger

healing.
Sympathetic nervous system compensation
occurs when any physical or psychological
stressors are present.

SIRS (Systemic Inflammatory

Respons Syndrome)
Hyperthermia

(T > 38 oC) /hypothermia (T< 36

C)
Tachycardia (P: > 90 x/m)
Tachypnea (RR : > 20 X/m) /PaCO 2) < 32
mmHg
Leukocytosis (L >12000), Leukopenia ( <4000)
or Neutrofyl > 10 % in immature form
(2 or more days)
o

Sever
e
sepsis
Septc shock

Pathophysiology
Usual

indices (BP, CVP) of volume status

unreliable in burn patients; urine output best
surrogate marker of volume resuscitation
ARF rare unless prolonged hypotension
exception: soft tissue injury with pigmenturia
kaliuresis may require brisk K+ replacement
hypertension (with encephalopathy) may occur

Pathophysiology
Pulmonary

dysfunction results from multiple

etiologies
shock, aspiration, trauma, thoracic restriction
inhalation injury; increases mortality 35-60%
diffuse capillary leak reflected at alveolar level

CNS

dysfunction may result from

hypovolemia/hypoperfusion, hypoxia, or CO
exposure

Pathophysiology
High

risk of gastric stress ulceration

Increased gut permeability, with increased
potential for bacterial translocation
protective role of early enteral feeding

Gut

dysmotility due to drugs, or disuse

Early, mild hepatic dysfunction common; late or
severe dysfunction heralds increased morbidity

Pathophysiology
Anemia

is common

initially due to increased hemolytic tendency

later due to depressed erythropoietin levels, and

ongoing acute phase iron sequestration

may be exacerbated by occult bleeding, or
iatrogenicity related to fluid management
Thrombocytopenia

early; thrombocytosis then

supervenes as acute phase response

Pathophysiology
Immunologic

dysfunction is pleiotropic

normal barrier, immune functions of skin lost

immunoglobulin levels depressed, B-cell

response to new antigens blunted

complement components activated, consumed
impaired phagocyte function
immunologic dissonance

Late (Resolution) Phase

a. Hypertrophic scars

b. Keloids

c. contracture

TREATMENT

Pre-Hospital Care
Remove

to open & safe area, if possible

Stop the burning process
Extinguish fire - cool smoldering areas
Remove clothing and jewelry
Cut around areas where clothing is stuck to skin
Cool adherent substances (Tar, Plastic)

 If

thermal burn is large--FOCUS on the

ABCs
A=airway-check for patency, soot around nares,

or signed nasal hair

B=breathing- check for adequacy of ventilation
C=circulation-check for presence and regularity
of pulses

Other precautions...
Burn

too large--dont immerse in water due

to extensive heat loss
Never pack in ice
Patient should be wrapped in dry clean
material to decrease contamination of
wound and increase warmth

 Transport

Considerations

Appropriate Facility
Burn Center or Not
Factor to consider
Burn Patient Severity Criteria
Critical, Moderate, Minor Burn Criteria
Confounding factors
Transport resources

Treatment of minor burn

1. Alleviates pain

* water compress
* Analgesic
2. Treatment of wound
* 1st degree : - Moisturized cream
* 2nd degree: - Blister treatment

Blister: Dermal-epidermal junctions

disassembly

Treatment
Blister

management
Aspiration or multiple incisions
Non-vital epidermal layer encapsulating
blister should be retained as a biological
dressing (skin is the best wound
coverage)
Tulle: water-based
Dressing (bulky) and pressure bandage will
let the graft take

* Rest
* Diet : calorie , protein
* Medicines : - Oral Antibiotic
(second degree)
- Topical antimicrobial
- Vit. A, D, E, C & Zn

Hospitalized indications :
1. 20 > 15% for adult & > 10% for children
2. 20 or 30 at face, hand, foot, & perineum
3. 30 > 2% for adult, & every 30 for children
4. Burn with visceral trauma, fracture, &
airway problem

Initial Airway Managment

Evaluate,

and ensure airway patency

Determine the need for an artificial airway
intact airway reflexes?
risk factors for airway burns/edema?

Perioral burns, dysphagia, hoarseness or changes in phonation, soot or

singing involving mouth, nose, hair, face, facial hair,coughing, black
sputum, enclosed fire environment, unconciuous

erythema to edema transition may be rapid

Ensure

breaths

adequate air exchange, thoracic excursion with tidal

 Assist ventilations as needed

100% oxygen if:
Moderate or critical burn
Patient unconscious
Signs of possible airway burn/inhalation
injury
History of exposure to carbon monoxide or
smoke

Breathing
Assessment/Support
Ensure

adequate oxygenation

Arterial Blood Gas (ABG) with carboxyhemoglobin

level preferred
humidified 100% FiO2 emperically
Assess

for possible inhalation injury

history of an enclosed space, carbonaceous sputum,

respiratory symptoms, altered level of conciouseness

younger children at greater risk

Breathing Assessment/Support
NG

tube placement (usually 1-2 hours after

burn)
thoracic decompression; reduce aspiration risk

Ventilatory

support recommended for

circulatory insufficiency, or GCS<8
decreased airway protective reflexes
risk of inhalation injury/CO exposure
risk of concomitant injury/trauma requiring

evaluation/support

 6-12

hours later-Bronchoscopy to assess

lower resp. tact
Chest physiotherapy, suction prn

Initial Management: Circulatory

Assess

capillary refill, pulses, hydration

Evaluate sensorium
Place foley to assess urine output
Achieve hemostasis at sites of bleeding
Venous access, depending upon BSA
involvement; avoid burn sites if possible
Begin emperic volume resuscitation

 Respiratory rates are unreliable due to toxic combustion

products

May cause depressant effects

Be prepared to intubate early if patient has inhalation

injuries
Escharotomy of circumferential eschar on thorax region
Pneumothoraks or hematothoraks WSD (Water Sealed
Drainage)

Assessment & Management Circulatory

Status

Burns do not cause rapid onset of hypovolemic

shock
If shock is present, look for other injuries
Circumferential burns may cause decreased
perfusion to extremity

Indications for escharotomy

- Absence or progressive diminution of pulsatile
flow
- Delayed capillary refilling
- Cyanosis of the digits
- Progressively severe paresthesias, particularly
deep tissue pain
- Muscle compartment pressure that exceeds 30
mm Hg

Baxter (Parkland) Formula

First 24 hours : 4 ml (LR) x % of burn x weight

(Kg)

( is given in the first 8 hr

postburn & remaining volume
delivered over the next 16 hr)
Second 24 hours : 0,5 cc/kg BW/% burn
plasma (FFP) + D5W (Dextrose 5% in
Water Solution)

Evans Formula
First 24 hr : 1 ml/kg BW/% burn colloid
1 ml/kg BB/% burn NS (Normal Saline)
2000 ml D5W
( is given in the first 8 hr, remaining
delivered over the next 16 hr)
Second 24 hr : 0,5 ml/kg BW/% burn colloid
0,5 ml/kg BB/% LB NS
2000 ml D5W

Brooke Formula
First 24 hr : 0,5 ml/kg BW/% burn colloid
1,5 ml/kg BW/% burn NS (Normal Saline
2000 ml D5W
( is given in the first 8 hr, remaining
delivered in second 16 hr)
Second 24 hr : 0,25 ml/kg BW/% burn colloid
0,75 ml/kg BW/% burn NS +
2000 ml glukosa

Pediatric resuscitation
protocols
Shriners Burn Institute (Cincinnati) - 4 mL/kg per

percentage burn plus 1500 mL/m2 BSA

First 8 hours - RL solution with 50 mEq sodium bicarbonate
per liter
Second 8 hours - RL solution
Third 8 hours - RL solution plus 12.5 g of 25% albumin
solution per liter

Galveston Shriners Hospital - 5000 mL/m2 TBSA burn

plus 2000 mL/m2 BSA, using RL solution plus 12.5 g

25% albumin per liter plus D5W solution as needed for
hypoglycemia

 Consider

Fluid Therapy for

>10% BSA 30
>15% BSA 20
>30-50% BSA 10 with accompanying 20

 Monitoring
Objective
HR < 110/minute
Normal sensorium (awake, alert, oriented)
Urine output - 30-50 cc/hour (adult); 0.5-1 cc/kg/hr (pedi)
Resuscitation formulas provide estimates, adjust to individual
patient responses
CVP (< 2)
Hb/Ht

 Start through burn if necessary, upper

extremities preferred
Monitor for Pulmonary Edema

 Analgesia
Antibiotic Broad Spectrum
Morphine Sulfate
2-3 mg repeated q 10 minutes titrated to adequate
ventilations and blood pressure
0.1 mg/kg for pediatric
May require large but tolerable total doses

Burn Wound
Treatment
Low priority - After ABCs and initiation of IVs
Do not rupture blisters
Cover with sterile dressings
Moist: Controversial, limit to small areas (<10%) or
limit time of application
Dry: Use for larger areas due to concern for
hypothermia
Cover with burn sheet

Burn Wound Care

Cleanse

the wound

Pain medications as needed; 20-30 minutes prior to all

wound care procedures !!

Hydrotherapy

Shower, shower carts, bed baths or clear water spray

Maintain proper water and room temperature
Limit duration to 20-30 minutes
Treat blisters
Trim hair around wound; expect eyebrows
Dry with towel; pat dry dont rub
Dont forget about cleansing unburned skin and hair

Burn Wound Care Cont.,

Apply

an Antimicrobial Agent

Silver Sulfadiazine (Burnazin, Dermazin)

Broad spectrum; the most common agent used

Povidone Iodine (Betadine

Drying effect makes debridement of the eschar easier

Antibiotic cream/gel/zalf (Bioplacenton)

Potential to resistant

MEBO
Herbal
Stem cell activator

Burn Wound Care Cont.,

Cover

with a Sterile Dressing

Most wounds covered with several layers of sterile

gauze dressings.
Special Considerations:
Joint area lightly wrapped to allow mobility
Facial wounds maybe left open to air

Must be kept moist; prevent conversion to deep wound

Circumferential burns: wrap distal to proximal

All fingers and toes should be wrapped separately
Splints always applied over dressings
Functional positions maintained; not always comfortable

Burn Wound Care Cont.,

Debridement

of the wound

May become completed at the bedside with wound

care or as a surgical procedure.

Types of Debridement:

Natural
Body & bacterial enzymes dissolve eschar; takes a longtime

Mechanical
Sharp (scissors), Wet-to-Dry Dressings or Enzymatic Agents

Surgical
Operating room / general anesthesia

Surgical Management
Skin

Grafting

Closure of burn wound

Spontaneous wound healing would take months for even a
small full-thickness burn
Eschar is a bacteria playground and needs to be removed as
soon as possible to prevent infection
Wound needs to be covered to prevent infection, the loss of
heat, fluid and electrolytes

Therefore, skin grafting is done for most full-thickness

burns.

Can be permanent or temporary

 The

donor sites usually heal in 7-10 days

donor site is often the most painful aspect for the

post-operative client

Nutritional Support
Burn

wounds consume large amounts of energy:

Requires massive amounts of nutrition & calories to

decrease catabolism & promote wound healing.

Monitoring

Nutritional Status

Weekly pre-albumin levels

Daily weights

Nutritional Support
Routes

of Nutritional Support

High-protein & high-calorie diet

Often requiring various supplements
Routes:
Oral
Enteral
Gut is the preferred alternative route; started ASAP
i.e. G-tube or J-tube

Parenteral
i.e. TPN and PPN
Associated with an increased risk of infection

Rehabilitation Phase
Begins

day one and may last several years

Meticulous asepsis continues to be important

Major

areas of focus:

Support of adequate wound healing

Prevention of hypertrophic scarring & contractures
Psychosocial Support

Client and family

Promotion of maximal functional independence

Hypertrophic Scar Formation

Excessive

scar formation, which rises above the

level of the skin
Management: Pressure Garments
Elasticized garments that are custom fitted
Maintains constant pressure on the wound
Result: smoother skin & minimized scar appearance
Client Considerations:
Must be worn 23 hours a day
Need to be worn for up to 1-2 years
Are very hot and tight !!

Contracture Formation
Shrinkage

and shortening of burned tissue

Results in disfigurement
Especially if burn injury involves joints

Management

is opposing force:

Splints, proper positioning and ROM

Must begin at day one !!

Multidisciplinary approach
is essential !!

Psychosocial Considerations
Alterations

in Body Image

Loss of Self-Esteem
Returning to community, work or school
Sexuality
Supports Services
Psychologist, social work & vocational counselors
Local or national burn injury support organizations

Nursing Considerations
Encourage client & family to express feelings
Assist in developing positive coping strategies

Psychosocial Considerations
Nursing

Considerations

LISTEN AND PROVIDE REALISTIC SUPPORT !!

Be honest about possible scarring

Remember people come to terms with the change in

their appearance at their own pace.

Provide reassurance that skin grafts always look

worse before they look better.

Remember how a client looks at discharge is not how

they will look in 2 years.

SPECIAL BURNS

Inhalation Injuries
Suspect inhalation injury when:
Burn occurred within a closed space
Burns to face or neck
Singed nasal hair or eyebrows
Hoarseness, voice changes, wheezing or stridor
Sooty sputum
Brassy cough or drooling
Labored breathing or tachypnea
Erythema and blistering of oral or pharyngeal mucousa
Often requires intubation & mechanical ventilation

Inhalation Injuries
Carbon Monoxide Poisoning

Most common inhalation injury

May occur with or without cutaneous burns

Hemoglobins affinity for carbon monoxide is 200x greater

than that for oxygen; result = hypoxia
Diagnosis:

Serum COHb levels & ABGs

Pulse Ox: false readings !!

Management: 100% O2
Face mask or mechanical ventilation

Inhalation Injury
The pathophysiology of inhalation injury is complex
Routinely demonstrate :
1) Upper airway obstruction secondary to progressive
edema;
2) Distal airway injuries are usually caused by aerosolized
toxins rather than thermal injury
3) Reactive bronchospasm from aerosolized irritants;
4) small airway occlusion initially from edema and
subsequently from sloughed endotracheal debris and
loss of ciliary clearance mechanisms;

Inhalation Injury
5) Microatelectasis from the loss of surfactant and
alveolar edema;
6) Interstitial and alveolar edema secondary to loss of
capillary ntegrity

Inhalation Injury Management

Airway, Oxygenation

and Ventilation

Assess for airway edema early and often

Consider early intubation
When in doubt oxygenate and ventilate
High flow oxygen
Bronchodilators may be considered if

bronchospasm present
Diuretics not appropriate for pulmonary edema

Inhalation Injury Management

Other Considerations
Assess for other Burns and Injuries
Treat burn soft tissue injury
Treat associated inhalation injury/poisoning * Antidote
kit, Positive pressure ventilation,
Hyperbaric chamber (CO poisoning)
Transport considerations
Burn Center
Hyperbaric chamber

Pediatric patients
Thinner

skin; prone to more severe injury

Greater

body surface area / to weight ratio

Greater evaporative fluid losses hypovolemia

Rapid heat losses hypothermia

metabolic reserves; prone to

hypoglycemia

Reduce
Small

airways more difficult to secure

Immature

immunological response sepsis

 Delicate

balance between dehydration and

over hydration
Commonly require fluid in excess of that
predicted by several formulae
Immature immunological response
sepsis
Always consider possibility of child abuse

Geriatric Patients
Skin

is thinner; prone to more severe injury

Decreased mobility, reaction time, vision &
hearing and sensation in hands & feet.
Unable to escape or unable to detect severity
More likely to pre-existing medical conditions
(i.e. PVD, heart disease, COPD & DM); more
likely to develop complications.
Poor immunological response sepsis

ELECTRICAL INJURIES

Electrical Injury
Occurs

when electricity is converted to

heat as it travels through tissue
Divided into:
High voltage greater than 1000 V
Low voltage less than 1000

Hands

& wrists are common entrance

wounds
Feet are common exit wounds

 Adults

in workplace, children at home

Severity of injury depends on:
Intensity of electrical current (voltage of

source and resistance of victim)

Pathway through victims body
Duration of the contact with the source

Immediate death may occur from:

1) Current-induced ventricular fibrillation
2) Asystole
3) Respiratory arrest secondary to:
Paralysis of the central respiratory control

system
Paralysis of the respiratory muscles

 Electrical

injuries (excluding lightning)

are responsible for > 500 deaths/year in
the US
> 1/2 of them occur in the workplace.
4th leading cause of work-related
traumatic death
Electrocutions at home: > 200
deaths/year

 Lightning

responsible for 93 deaths/year in

US
Morbidity 5-10 times higher than that due to
other forms of electrical injury
Iatrogenic electrical injury in the ICU:
defibrillators, pacemakers, electrosurgical
devices

Principles of Electricity
Electricity:

flow of electrons (negatively

charged outer particles of an atom)
through a conductor
When the electrons flow away from this
object through a conductor they create an
electric current: amperes

 Voltage:

force that causes electrons to

flow: volts
Anything that impedes the flow of
electrons through a conductor creates
resistance: ohm

 Utility

power lines with high voltages in

sparsely populated areas
Through a succession of transformers voltage
is gradually reduced
Most homes in Indonesia (Asia), & Europe
have a 220 V. US & Canada : 120/240 V

Pathophysiologic effects of
Different Intensities of
Electrical Current

 Electrical

current exists in 2 forms:

1) AC: (Alternating Current): when

electrons flow back and forth through a
conductor in a cyclic fashion
- It is used in household and offices and
is standardized to a frequency of 60
cycles/sec (60 Hz)

2) DC: (Direct Current): when electrons

flow only in one direction
- Used in certain medical equipment:
defibrillators, pacemakers, electrical
scalpels
- AC is far more efficient and also more
dangerous than DC (~ 3 times): tetanic
muscle contractions that prolong the
contact of victim with source

Lightning is a form of DC
Occurs

when electrical difference

between a thundercloud and the ground
overcomes the insulating properties of
the surrounding air
Current rises to a peak in about 2 sec
Lasts for only 1-2 sec

 Voltage

>1,000,000 V
Currents of >200,000 A
Transformation of the electrical energy to
heat generated temperatures as high as
50,000F
Extremely short duration prevents from
melting

Determinants of Electrical Injuries

Ohms

law:
Current = Voltage/Resistance

Exposure

of different parts of the body to

the same voltage
different current
different degree of damage because
resistance varies

 The

least resistance is found in nerves,

blood, mucous membranes and muscles
The highest resistance is found in bones,
fat and tendons
Skins resistance ranging between 40,000
and 100,000 depending on thickness
Moisture of the skin; electrocution of a
person in a bathtub or swimming pool

 Moist

mucus membranes: significant

orofacial injury to infants and toddlers
Nerves and blood vessels are the best
conductors: path of least resistance for
current after it enters the body
Duration of the contact: shock caused by
AC will produce bigger injury than shock
caused by DC of the same amperage

Pathway of the current through the body:

Vertical pathway parallel to the axis of the body

is the most dangerous. It involves all the vital

organs; central nervous system, heart, respiratory
muscles, in pregnant women the uterus and fetus
Horizontal pathway from hand to hand: the heart,
respiratory muscles and spinal cord
Pathway through the lower part of the body:
local damage

Electrical Injury to Specific

Tissues & Organs
Cardiovascular System:
Pathophysiology:
Direct necrosis of the myocardium
Cardiac dysrhythmias

 Focal

or diffuse
Widespread, discrete, patchy contraction
band necrosis involving the myocardium,
nodal tissue, conduction pathways and
coronary arteries

 A current

> 50-100 mA with hand-tohand or hand-to-foot transmission --ventricular fibrillation

High-voltage current (AC or DC)
----ventricular asystole
Lightning --- cardiac standstill
Sinus rhythm may spontaneously return

 Cardiac

dysrhythmias reported in
survivors of electrical injuries
pathogenesis is rather unclear,
multifactorial

 Possible

mechanisms:

1) Arrythmogenic foci due to myocardial

necrosis (esp. SA Node injury)
2) Alterations in the Na+ - K+ adenosine
triphosphatase concentration
3) Changes in the permeability of myocyte
membranes
4) Anoxic injury (respiratory arrest precedes
the injury to the heart)

 Large

arteries not acutely affected

because their rapid flow:dissipate
heat. Medial necrosis: aneurysm
formation and rupture
Smaller vessels acutely affected
coagulation necrosis

Clinical Manifestations
Cardiac standstill, ventricular fibrillation:
most serious
Sinus tachycardia, nonspecific ST- and Twave changes: much better prognosis
Conduction defects, various degrees of
heart blocks, BBB and QT interval

 Supraventricular

tachycardias and atrial

fibrillation: usually do not cause
significant hemodynamic compromise
On echocardiogram: some depression
of the right & left ejection fractions

Cutaneous Injuries & Burns

Extensive flash and flame burns
Hemodynamic, autonomic,
cardiopulmonary, renal, metabolic and
neuroendocrine responses

Nervous System
Loss

of conciousness, confusion & impaired recall

Peripheral motor & sensory nerves ---- motor &
sensory deficits
Seizures, visual disturbances & deafness
Hemiplegia, quadriplegia, spinal cord injury
Transient paralysis, autonomic instability -----hypertension, peripheral vasospasm due to lightning
from massive release of catecholamines

Respiratory System
Direct injury to the respiratory control
center ---- cessation of respiration or
suffocation secondary to tetanic
contractions of the respiratory muscles
Acute respiratory dysfunction syndrome
secondary to ischemia, aggressive fluid
resuscitation, ventilator-associated
pneumonia

Other Systems
Kidneys

susceptible to anoxic/ischemic injury

Release of myoglobin & creatinine phosphokinase
--- renal tubular damage ---- renal failure
Fractures
Transient autonomic disturbances
fixed pupils
may be perceived as severe brain injury or even
death
Temporary sensorineural hearing loss

Electrical Burn Management

Make

sure current is off

Lightning hazards
Do not go near patient until current is off

ABCs
Ventilate and perform CPR as needed
Oxygen
ECG monitoring
Treat dysrhythmias

Electrical Burn Management

Rhabdomyolysis

Considerations

Fluid?
Dopamine?

Assess

for additional injuries

Consider transport to trauma center

Electrical Burn Management

Any patient with an electrical burn
regardless of how trivial it looks needs to go
to the hospital. There is no way to tell how
bad the burn is on the inside by the way it
looks on the outside.

Patient Monitoring
Most severe cardiac complications present
acutely
Very unlikely for a patient to develop a
serious or life-threatening dysrhythmia
hours or days later
Asymptomatic normal ECG do not need
cardiac monitoring

 Preexisting

heart disease: monitor such

patients for 24 hrs after the injury
Criteria for cardiac monitoring:
Exposure to high voltage
Loss of consciousness
Abnormal ECG at admission

Type of cardiac monitoring: (controversial)

Continuous telemetry
Serial ECGs
Serial measurement of cardiac enzymes
Prognostic value of CK-MB, noninvasive and invasive
imaging studies (echocardiography, thallium studies &
angiography): rather poor and inconsistent
Muscles injured by an electrical current can contain up
to 25% CK-MB fraction (as opposed to the normal 2-3%)
No information regarding changes in troponin

Electrical Burn Management

Electrical injury of extremities
Compartmental pressure elevation ,
secondary to edema of injured muscle
released by fasciotomy.
Usually not evident within the first few hours
after injury
Can damage even the periosseous muscles and
make amputation necessary

 Fasciotomy

Fasciotomyis to be
carried out as early as
possible to restore
deep vascular flow in
such a compartment

LIGHTNING STRIKE
Lightning
HIGH VOLTAGE!!!
Injury may result from
Direct Strike
Side Flash
Severe injuries may

result

LIGHTNING STRIKE
Usually

superficial

injury
Victims die from
cardiac arrest
Resuscitate the dead
Patients who are

breathing will usually

survive

CHEMICAL BURNS

Chemical Burns
Usually

associated with industrial exposure

First Consideration: Should you be here?
Does the patient need decontamination before

treatment?
Burning

will continue as long as the

chemical is on the skin

Chemical Burn
2 types of chemical burns

acids-can be neutralized

alkaline- adheres to tissue, causing

protein hydrolyses and liquefaction
examples: cleaning agents, drain cleaners, and

lyes, etc...

Chemical Burn

Different types of
burns
1 Outer skin layer
2 Middle skin layer
3 Deep skin layer
4 First degree burn
5 Second degree burn
6 Third degree burn

Remember.
With

chemical burns, tissue destruction may

continue for up to 72 hours afterwards.
It is important to remove the person from
the burning agent or vice versa.
The latter is accomplished by lavaging the
affected area with copious amounts of
water.

Chemical Burns
Acids
Immediate coagulation-type necrosis creating

an eschar though self-limiting injury

coagulation of protein results in necrosis in which

affected cells or tissue are converted into a dry, dull,
homogeneous eosinophilic mass without nuclei

Chemical Burns
Bases

(Alkali)

Liquefactive necrosis with continued penetration

into deeper tissue resulting in extensive injury

Dry

characterized by dull, opaque, partly or completely

fluid remains of tissue

Chemicals

Exothermic reaction with water

Chemical Burn Management

Definitive

treatment is to get the chemical

off!
Begin washing immediately - removal the
patients clothing as you wash
Watch for the socks and shoes, they trap

chemicals

Chemical Burn Management

Liquid

Chemicals

wash off with copious amounts of fluid

Dry

Chemicals

brush away as much of the chemicals as possible

then wash off with large quantities of water

Flush

for 20-30 minutes to remove all

chemicals

Chemical Burn Management

Do

not attempt neutralization

can cause additional chemical or thermal burns

from the heat of neutralization

Assess

and Deliver secondary care as with

other thermal and inhalation burns

Chemical Burn to Eye

Management
Flood

the eye with copious amounts of water only

Never place chemical antidote in eyes

Flush

using LR/NS/H2O from medial to lateral for

at least 15 minutes
Nasal Cannula
IV Ad Set

Remove

contact lenses

May trap irritants

Specific Chemical Considerations

Dry

lime

Brush off
Dry lime is water activated
Then flush with copious amounts of water

Phenol
Not water soluble
If available, use alcohol before flushing except in eyes
If unavailable, use copious amounts of water

Specific Chemical
Considerations
Sodium/Potassium

metals

Reacts violently on contact with H20

Requires large amounts of water

Sulfuric Acid
Generates heat on exposure to H2O (exothermic)
Wash with soap to neutralize or use copious amounts H 2O

Tar

Burns

Use cold packs

Do not pull off, can be dissolved

later

CHEMICAL BURNS
Injure

the skin
May be absorbed into the body and damage
internal organs
May be inhaled into the lungs and cause
lung tissue damage
May have minimal skin injury and yet cause
severe systemic injury

FACTORS CAUSING
TISSUE DAMAGE IN
CHEMICAL BURNS

Type of chemical
Concentration of
chemical
Amount of chemical
Duration of contact
Manner of contact
Mechanism of action

ACID BURN

TREATMENT OF CHEMICAL
EXPOSURE
Accident

protocol
Remove and bag all contaminated
clothing
Brush off dry chemical
Flush with copious amounts of water or
any drinkable liquid
Wipe or scrape any retained chemical
and irrigate again
THE SOLUTION TO
POLLUTION IS DILUTION

The end