Burns and Rehabilitation
Detroit Receiving Hospital
Burn Incidence

The Numbers
• How often?
• How many injuries?
• How many
hospitalizations?
• How many “major”
injuries?
• How many deaths?
Gender*
Male
69.9%
Female
30.1%

*Total N=126,642
Race/Ethnicity*
Missing
2.9%
Caucasian
62.3%
Native
American
0.6%
African
American
18.0%
Other
1.8%
Asian
2.0%
*Total N = 126,642
Hispanic
12.4%
Age Group*
18,000
16,000
14,000
No. of Cases
12,000
10,000
8,000
6,000
4,000
2,000
0
0 - 1.9
2 - 4.9
5 - 19.9
20 - 29.9
30 - 39.9
40 - 49.9
50 - 59.9
60 - 69.9
≥ 70
Age Group

*Total N=107,685 (Excludes Unknown/Missing)
Etiology*
Other
2.2%
Chemical
3.2%
Scald
32.5%
Electrical
4.3%
Skin Disease
1.4%
Contact with Hot
Object
8.1%
Unknown
1.0%
Other Burn
0.7%
Radiation
0.3%
Fire/Flame
46.0%

Inhalation Only
0.3%
*Total N=76,659 (Cases Where Etiology
Was Included)
Place of Occurrence
Other Specified
4.6%
Industrial
8.4%
Recreation/Sport
4.2%
Public Building
(school)
1.8%
Street/Highway
16.8%
Unspecified
19.2%
Residential Institution
1.0%
Farm
0.7%
Home
43.2%
Mine/Quarry
0.1%
Circumstances of Injury*
Other
5.1%
Accid-recreation
4.9%
Accid-unspecified
3.2%
Accid-work related
17.0%
Accid-non work
related
64.8%
Suspected: SelfInflicted; Child
Abuse;
Assault/Abuse;
Arson
5.0%
*Total N=72,324 (Excludes
Unknown/Missing)
Hospital Disposition*
Lived
94.6%
Died
5.4%

*Total N=126,645
What are the functions of skin?







Conservation of body
fluids
Temperature
regulation
Excretion of sweat and
electrolytes
Secretion of oils that
lubricate the skin
Vitamin D synthesis
Sensation
Cosmetic appearance
and sexual identity

Burn
injuries
cause loss
to some or
all of these
functions
Types of Burn Injury

Thermal burns

Chemical burns

Electrical burns

Radiation burns
Thermal Burns

Two factors are related to
the extent of thermal injury:
•1) Degree of temperature
•2) Length of exposure
Scald Burns

Common particularly in children

Accidental versus Abuse
Chemical Burns


Caused by exposure of the skin to
noxious substances
Amount of tissue damage is
dependent upon:



1) Concentration of the agent
2) Length of exposure
3) Mechanism of chemical reaction
Chemical Burns


Caused by acids and alkalis
Chemical agents continue to cause
injury until inactivated

1) Inactivated by local tissue reaction

2) Neutralized by external agent

3) Diluted by water
Electrical Burns

Thermal injury incurred via electrical
contact depends on:
• 1) Type of current-AC more damaging
• 2) Pathway of current
• 3) Local tissue resistance
• 4) Duration of contact
Electrical Burns


Death rate and voltage are variable
Electrical current follows a path of
least resistance
Electrical Burns

Severity of injury can be deceptive

Complications often occur:

1) Tetanic muscle contractions

2) Fractures/ dislocations from falling

3) Cardiac dysfunction

4) Internal organ injuries
Radiation Burns

Occurs as a result of a local accident
• Laboratory
• Exposure to therapeutic radiation (cancer)
Dimensions of Burn Injury

Zone of
coagulation
(necrosis)

Zone of stasis

Zone of hyperemia
Degrees of Burn Injury




First Degree
Second Degree (Superficial and Deep Partial
Thickness)
Third Degree (Full Thickness)
Fourth Degree (Subdermal)
First Degree Burns

Cell damage

Epidermis only

Perfect example: Classic sunburn

Red in color

Skin is dry

Delayed onset to pain

Desquamation=peeling

Heals spontaneously
Superficial Second Degree Burns

Cell damage

through epidermis and upper dermis

Epidermis completely destroyed

Mild-moderate damage to the dermis

Blisters are common sign=superficial
2nd degree
Superficial Second Degree Burns

Blisters removed for applying
antibiotics

Bright red in color

Blanching occurs

Edema is usually minimal
Superficial Second Degree Burns

Extremely painful

Highly sensitive

Heals spontaneously

Color change from destruction of
melanocytes

Scarring is minimal
Deep Second Degree Burns

Cell damage


Through epidermis
Deep layers of dermis

Mixed red or waxy white color

Surface is usually wet=interstial fluid

Edema is moderate
Deep Second Degree Burns

Painful

Sensation


Intact to pressure
Diminished to light touch

Healing occurs with scar formation and
reepithelialization

Epidermal cells (follicular) assist with
reepithelialization
Deep Second Degree Burns

Surgery or no surgery?

Spontaneous healing often results in:
• 1) Thin epithelium
• 2) Dry, scaly skin
• 3) Decreased sensation
• 4) Lack of thermoregulation
Deep Second Degree Burns




Healing in 3 to 5 weeks (if NO
infection)
Wound care is critical to avoid
conversion (getting worse to 3rd)
Hypertrophic scarring (raised scar,
confined to area of wound) is
common
Will still have hair follicles.
Third Degree Burns

Cell damage


Complete through epidermis
Complete through dermis

Characterized by eschar

Hair follicles completely destroyed

Nerve endings are destroyed- What is the
result of this?
Third Degree Burns


Pain from surrounding areas that are
only partial thickness burns
Characterized with complete vascular
occlusion and edema
• Occlusion of blood flow of even deep
vascular branches
• Distal pulses must be monitored, because
edema can occuled.
Third Degree Burns

Highly susceptible to infection

Wound care is extremely important

No sites for new skin growth

Skin grafting is required
Fourth Degree Burns

Cell damage
• Complete destruction tissues from epidermis to
subcutaneous layers
• Muscle and bone may be damaged

Occurrence
• Prolonged contact with flames or hot liquids
• Result of contact with electricity

Extensive surgical
management=amputation
Extent of Burn Injury



Rule of Nines
developed by Pulaski
and Tennison
Segments are
approximately 9
percent of total body
surface area (TBSA)
Rapid assessment of
TBSA injured
Extent of Burn Injury




Altered the
percentages of body
surface for children
Accommodates for
growth body
segments with age
Permits for higher
accuracy
Feasibility in emergent
care?
Wound Debridement

Purpose:
• Remove dead tissues
• Prevent infection
• Promote revascularization/
epithelialization

Mechanical
• Whirlpool (non-selective)
• Sharp (selective)

Enzymatic
• Santyl
Burn Wound Dressing
Purpose:
 Comfort
 Maintain a moist, healing
environment
 Protective barrier towards microorganisims
 Debridement of eschar/necrotic
tissue.
Burn Wound Dressing

Topicals:
• Bacitracin (triple antibiotic)
• Silvadene (inappropriate to be applied,
outdated)

Gauze/Film
• Xeroform
• Aquacel Ag (gel Matrix)=great stuff, comes in
rolls, has petroleum so wont stick
• Acticoat Ag

Foam:
• Aquacel foam
• Mepilex=for ulcers/wounds
Burn Wound Dressings

Superficial burns
• Use an occlusive dressing


Xeroform gauze=mosit, does not stick.
Dressing to cover
• No need for antibacterial agent
• Silvadene only used for minor burns
Burn Wound Dressings

Mild to Deep Dermal Burns
• Most common treatment:


Use a topical antibacterial cream such as a
triple antibiotic (Bacitracin) or Santyl (use
till there less the 50-40% necrotic tissue)
Cover with a dry occlusive dressing once or
twice a day (to absorb interstial)
• Skin substitutes provide best protection


Ie: Alloderm, Epicel, Integra (~Shark Skin),
Oasis (Pig Intestines)
More expensive
Burn Wound Dressings

Full Thickness Burn
• Topical antibiotic cream for protection
• Skin substitutes also used for coverage
until surgery
• Surgical excision and grafting
Surgical Management

Skin Grafting:
• Autograft
• Allograft (Homograft)
• Xenograft (Heterograft)
• Cultured epidermal autograft
Surgical Management

Skin Grafting
• Extent and depth of injuries determine grafting
needs
• Donor site
• Split-thickness skin graft (STSG)-take
epidermis and top layer of dermis.
• Full-thickness skin graft:
Surgical Management

Sheet graft: Applied to recipient
without alteration of donor skin
• Cosmetically the best results

Mesh graft: Donor skin is stretched
prior to placement on the wound bed
Surgical Management

Survival of the skin graft depends
upon:
• 1) Circulation
• 2) Inosculation=penetration of vessels
into graft
• 3) Penetration of host vessels into graft
Surgical Management




Deeply burned areas will develop
eschar
Eschar has poor elastic quality of
normal skin
Edema forms in areas under eschar
Escharotomy may be necessary
Surgical Management


Escharotomy:
Surgical incisions made across joint
lines

Depth penetrates the eschar

Done without anesthesia
Z-Plasty



P.T. management
Z- shaped incision- to open up and
allow better cervical mobility.
Grafting post procedure
SPECIAL TOPICS
INHALATION INJURY
3 Types of Inhalation Injury
1.
Damage from Heat
Inhalation
2. Damage from Smoke
Inhalation
3. Damage from Systemic Toxins
Damage from Heat Inhalation



Caused by hot air or flame, or from
a forceful high pressure source
The thermal injury is usually in the
upper airway only
If steam is inhaled, patient can have
secondary airway involvement
because the steam has a higher
thermal capacity than dry air.
Damage from Smoke Inhalation



Can be hidden in patients without
obvious burn injury
Can be overlooked in patients with
burn injury
In 1997, 4675 firefighters suffered
burn injury as part of their duties.
Of those, 3770 also suffered an
inhalation injury. (National Fire
Protection Association)
Damage from Systemic Toxins



Systemic toxins impede our ability to
absorb oxygen
Symptoms include confusion or
unconsciousness
A primary example is Carbon
Monoxide Poisoning
Indications of Inhalation Injury
1.
2.
3.
4.
5.
6.
Patient is confused or becomes
unconscious
Patient is found, or evidence of, smoke
and/or fire in a small or enclosed area
Soot is found in, or around, the nose and
upper airway
Eyebrows, eyelashes or nose hairs have
been singed
Facial or neck burns
Patient exhibits upper airway distress
(stridor)
Carboxyhemoglobin (COHgb) Test



Blood test to measure the amount of
COHgb in the blood
Carbon Monoxide (CO) replaces
oxygen on red blood cells forming
COHgb
This causes oxygen deficiency
COHgb Values





Less than 2.3 %:
normal adults
2.1 – 4.2 %:
adult smokers
8.0 – 9.0 %:
heavy smokers (2 packs
plus/day)
15.0 – 20.0 %: critical value (toxic
signs/symptoms)
More than 40 %:
shock
Treatment of Inhalation Injury
Elevated COHgb levels: Hyperbaric
Oxygen treatment (HBOT)
 Evidence of possible airway
involvement: early intubation
 Bronchoscopy: irrigates soot and
toxins from the airway

Hyperbaric Oxygen Tx (HBOT)



Enclosed environment, monitored by
specially trained staff
Can be single bed (critical patients)
or full room size (multiple patients)
Oxygen delivered at high
concentration, higher than 1.0 atm
pressure
Bronchoscopy Video
http://www.youtube.com/wat
ch?v=esjI3jzXO7Y
SPECIAL TOPICS
STEVENS JOHNSON SYNDROME
TOXIC EPIDERMAL NECROLYSIS SYNDROME
(TENS)
SJS: Characteristics






Presence of purpuric macules
Full thickness epidermal necrosis
Mucous membrane involvement
Less than 10 % TBSA involved
Most often caused by medication
reaction
Mortality approximately 5%
TENS: Characteristics






Presence of erythmatous macules
Full thickness epidermal necrosis
Mucous membrane involvement
Greater than 30% TBSA involved
Nearly always caused by medication
reaction
Mortality can near 40%
Pathophysiology


SJS and TENS are drug induced,
pathophysiology remains unknown
Theories:
• Genetic

Possibly a predisposition for toxic metabolic
accumulation
• Apoptosis



Possibly a cell-mediated cytotoxic reaction of
keratinocytes (keratinocyte apoptosis is known
in TENS)
Apoptosis = programmed cell death
Necrosis = uncontrolled cell death (inflammatory
septic response)
Drug Induced

Short Term Exposure (1-3 weeks)
• Sulfonamide Abx (Trimethoprim,
Prontosil)
• Aminopenicillins (Amoxicillin, Ampicillin)
• Quinolones (Cipro, Levaquin)
• Cephalosporins (Ancef, Keflex, Ceclor)
• Allopurinol (Zyloprim)=Gout

Allopurinol most associated with SJS
and TENS development
Drug Induced

Long Term Exposure (first 2 months
of use)
• Carbamazepine (Tegretol)
• Phenobarbitol
• Phenytoin (Dilantin)
• Valproic Acid (Depakote)
• Corticosteriods (Prednisone,
Methylprednisolone)
• NSAIDS (Advil, Motrin)
Mortality and Morbidity

Mortality
• SJS: approx. 5%
TENS: up to 40%
• Sepsis, respiratory distress,
complications
• Inc. TBSA involvement = Inc. mortality

Morbidity
• Disease course can be completed in
days but usually up to 3 weeks
Mortality and Morbidity

Long Term Sequelae
• Eye disorders



Photophobia
Corneal and conjunctival revascularization problems
As many as 40% TENS survivors may have some
blindness
• Hyper- or Hypo- pigmentation of the skin post
healing
• Finger and toe nail regrowth abnormalities
• Internal mucosal abnormalities (respiratory,
GI, genito-urinary)
Prognosis

Specific prognosticators
• Increased age

Although reported in all age groups
• Increased TBSA % involved
• Abnormal lab values

SCORTEN
• Severity of illness score (reliable and
validated)
• Calculated within 24 hours of admission
SCORTEN
Treatment


Discontinuation of causative agent
(medication)
Burn Unit Admission
• Fluid replacement
• Wound care with sterile technique

Avoid sulfonamide inciting drugs/dressings
(Silvadene)
• Opthomology consult
• Critical care as medical status warrants
SPECIAL TOPICS
FROSTBITE
Frostbite

Cold related injury, actual freezing of
the tissue seen in:
• Homeless
• People who work outside in the cold
• Athletes who are outside for training or
competition
• People who enjoy outdoor winter
activities
Frostbite:
Pathophysiology

Cold exposure leads to:
• Ice crystal formation
• Cellular dehydration
• Protein changes
• Capillary damage
Frostbite:
Pathophysiology

Re-warming leads to:
• Cell swelling and edema
• Platelet aggregation
• Endothelial cell damage
• Thrombosis
• Tissue edema and compartment
syndrome
• Local ischemia
• Tissue death
Frostbite

Long term damages:
• Parasthesias and sensory deficits
• Vasospasm
• Cold sensitivity
• Joint pain and stiffness
• Phantom pain of amputated extremities
or digits
Frostbite

Signs and Symptoms
• Coldness and firm tissue
• Stinging, burning and numbness
• Clumsiness of digits/extremities

On re-warming:
• Pain, throbbing and burning
Frostbite:
Degrees of Injury

First degree: “frost nip”
• Erythema
• Edema
• Hard white “plaques”
• Sensory deficit
Frostbite:
Degrees of Injury

Second degree:
• Clear or milky blisters
• Blisters appear within 24 hours
• Erythema
• Edema
Frostbite:
Degrees of Injury

Third degree:
• Blood filled blisters
• Blisters turn into black eschar within a
few weeks

Fourth degree:
• Full thickness, involving muscle, bone
Frostbite:
Treatment





Initiate re-warming, no rubbing or
trying to thaw with snow
Once under medical care: fluid
resuscitation
Thawing can take 20-40 minutes
Debride clear blisters, leave
hemhorragic blisters alone
Admit to a burn unit if necessary
Frostbite




Demarcation can take 1-3 months to
complete
Tissue often heals or mummifies
without surgery, so delay amputation
Lower extremity injury and those
who delay treatment have a higher
incidence of surgical intervention
HBO: studies are still case specific
Frostbite

Complications:
• Infection
• Tissue loss
• Gangrene
Frostbite:
Prognostic Indicators

Good prognosis
• Early sensory return with good pinprick
• Healthy looking tissue
• Clear blisters

Poor prognosis
• Cyanosis
• Hemorrhagic blisters
• Skin has frozen appearance
Topics Requested






1.
2.
3.
4.
5.
Stretching and scar management
Mobility training
Pressure garments
Positioning
Splinting/Orthotics
All topics are related across the
continuum of care!
Rehabilitation Services for Burns:
Who needs Therapy?

Acute Hospital
•
•

Inpatient Rehab
•

Patients who meet Burn Unit criteria
Patients with decreased mobility
Patients who require functional re-training
Outpatient
•
•
Patients with scar/contracture
evidence/potential
Patients who require pressure garments
Burn Unit Admission Requirements








1. 2nd and 3rd degree burns > 10% TBSA in
patients under the age of 10 or over 50.
2. 2nd and 3rd degree burns > 20% TBSA in all
other patients.
3. 2nd and 3rd degree that involve face, hands,
feet, genitalia/perineum and major joints.
4. 3rd degree > 5% TBSA in any age group.
5. Electrical burns, including electrocution.
6. Chemical burns.
7. Inhalation injury.
8. Patients with burns and concomitant
trauma.
Rehabilitation Management Team



Physical Therapist (PT)
• Lower extremity splinting
• Lower extremity ROM
exercises
• Functional activity

• Ensures oral motor skills are
adequate for speech and
swallowing
• Treats concurrent injury
issues (i.e. head injuries)
Occupational Therapist (OT)
• Upper extremity splinting
• Upper extremity ROM
exercises
• ADLs training and
management
• Functional activity
Nursing (RN, LPN)
• Medical management
• Direct wound care-dressing
changes, debridement
• Hydrotherapy
Speech-Language
Pathologist (SLP)

Orthotist (CO)
• Performs fitting for custom
pressure garments for scar
management
• Evaluates and treats patient
for advanced orthosis needs
(dynamic splints, custom
lower extremity orthotics,
face masks)
Rehab Management

Rehabilitation occurs concurrently with wound
healing
Rehab Management: Acute

Early stages consist of:
• 1) Positioning and control of edema
• 2) Maintenance of normal ROM and
strength (prevent contractures)
• 3) Prevent functional loss
• 4) Maintenance of cardio-pulmonary
system
Rehab Management: Acute

Edema control
• Elevation
• Early, frequent
active motion
• Prop extremities
correctly
Rehab Management: Acute

Positioning in Bed
• Position of Comfort = Position of
Deformity
• Contractures and neuropathies
• Individualized to patient needs
• Sustained stretch positions
• Pressure Relief Ankle Foot Orthosis
(PRAFO)
Positioning: Acute Burn
Rehab Management: Acute

Maintain ROM and Contracture Prevention
• Encourage early AROM whenever possible
• Assist with PROM/AAROM for patients unable
to complete full range themselves
• Splinting early encourages proper positioning
• Discontinue active exercise 3-5 post graft
• Self-stretching for donor site areas: ok to
begin 24 hours post op.
Early Splinting: Acute
Early Splinting: Acute
No splints: loss of function
Rehab Management: Mobility

Bed Mobility
• Can be very painful, especially with
back or buttock burns
• Exudry utilized for comfort
• Bridging on heels

Transfers
• OOB as soon as possible
• Use of cardiac chairs
• Abdominal and anterior thigh burns can
impact sit-stand
Rehab Management: Mobility

Ambulation
• Use ACE wrap on LE’s to control edema
and decrease pain
• Discourage flexed posture: trunk
positioning, use of AD

Exercises for posture
• Trunk rotation and extension
• LE self stretches for donor sites
Scar Management: Healing

Healing in 2 weeks:
• Minimal to no scarring
• Superficial second degree burns

Healing in 3 weeks:
• Minimal to no scar except in high risk groups
(AA or Asians)

Healing in > 4 weeks:
• Hypertrophic scarring in more than 50% of
patients
• Due to prolonged inflammatory phase,
increased histamine (fibrous tissue growth)
Scar Management: Healing





Early grafting = less scar
Thicker graft leads to less scar
Mesh grafts leave more scarring than
sheet grafts
The wider the mesh (increased ratio)
the more scarring
Scars will develop at the edge of a
graft in high risk patient groups
Scar Management: Stretching

Stretching with Burn Patient
•
•
•
•
•
Slow, long manual stretch: up to 60 seconds
Contract-relax techniques
Lubrication: deep-prep or cocoa butter
Blanching of wound: “if it’s white, it’s tight”
Contraindications:


1) Exposed joints or tendons
2) Joints with heterotrophic bone formation
• Elbow most common in burn population


3) Possible fractures
4) Joints with osteopenia, osteoporosis or
osteomyelitis
Burn Stretching:
Virtual Reality Video
www.youtube.com
Scar Management: Hypertrophy



Occurs in approximately 50% of healed
deep burns
Males and Females both affected, only
seen in humans
Characteristics of the Hypertrophic Scar
•
•
•
•
•
Surface erythema
Raised from original wound
Lack of elasticity
Increased collagen
Painful and itchy
Scar Management: Hypertrophy
Scar Management: Hypertrophy



Hypertrophic scar development
peaks at approximately 3 - 6 months
post burn
Scar is partially resolved by 12 – 18
months post burn
Treatment: 3 categories
• Biophysical
• Surgical
• Pharmocologic
Burn Wound Healing

Hypertrophic
scar
• 1) Red, itchy,
elevated
• 2) Confined to
original area of
injury
Burn Wound Healing

Keloid scar
• 1) Type of hypertrophic
scar
• 2) Red, itchy, painful
• 3) Extends outside the
area of original injury
• 4) Tumor-like appearance
• 5) More common in
African-American and
Asian-American
populations
Scar Management: Treatment

Biophysical Treatments
• Compression: pressure garments
• Ultrasound or microwave heat: possibly
increases collagenase acivity
• Gel sheeting: silicon sheets held in place
by ACE wraps
• Scar massage: break down of the scar
matrix
Scar Management: Compression

Pressure Garments
• Custom fitted to the
patients
• Used as soon as wound
closure is achieved
• Continuum from acute
care to outpatient
Scar Management: Compression

Pressure Garments
• Theory




1) Decrease scar blood flow
2) Decrease protein
deposition
3) Increase lysis
4) Decrease edema
• Goals







1) Decreasing redness
2) Flattening raised areas
3) Increasing scar pliability
4) Preventing contractures
5) Decreasing itching
6) Relieving hyperesthesia
7) Speeding up healing
process
Scar Management: Compression

Pressure Garments
• Wearing Schedule


1) Progressive up to
23 hours per day
2) Continue process
for up to 2 years until
Maturation Phase
completed
Scar Management: Compression

Pressure Garments
• Maintenance




Monitored frequently
at outpatient clinics
Measured/refitted
with muscle growth
and weight changes
Observed for skin
breakdown
2 sets so that 1 set
is always clean
Scar Management: Compression

Transparent Facial Orthoses (TFOs)
• Work under the same theory and goals
as pressure garments
• Can be utilized prior to complete wound
closure
• Worn for a progressive schedule up to
23 hours per day
• Covers areas of injury only
• Conventional vs. Computer generated
Scar Management

Conventional Method
• Petroleum jelly placed
directly over face in OR
or bedside
• Plaster or casting
material placed over
face
• Plaster negative is
allowed to dry and
filled with plaster to
create positive mold
• Plastic mask vacuumformed to the mold
• Mask fit and trimmed
to the patient

Computer Scanning
• Facial features scanned
by computer (15
seconds)
• Scanner catches
topographic data
• Mold created via
stereolithography in
plastic
• Plastic vacuum-formed
to mold
• Patient is fit and
trimmed to the mask
Scar Management: Compression

Examples of the use of a TFO in a child
and a Transparent Neck Orthosis (TNO)
for an anterior neck burn injury
Scar Management: Surgery

Excision
• Small scars
• High recurrence rate, more than 50% return

Laser
• Thermal tissue reaction occurs
• Improves elasticity, less redness and less itching
• 50% improvement in half the cases

Cryo-therapy
• Similar to laser, causes microcirculatory changes
that damage fibroblasts
• 50 to 70% of patients report some improvement
Cold Laser Video
Berns Triplets
http://www.youtube.com
Scar Management: Pharmacologic

Corticosteriods
• Reduces histamine and reduces itching
• Injected into the scar itself

Interferon
• Reduces scar forming growth factor
TGF-beta
• IV or injected into the scar

Protein kinase C inhibitors
• Calcium channel blockers reduce protein
deposited into wound
Questions?

E-mail: lhall3@dmc.org