Burn injuries are a major health issue that can cause significant tissue damage and systemic effects. A burn occurs when skin is damaged by heat, electricity, chemicals, friction or radiation. First degree burns involve only the epidermis, while second degree burns extend deeper into the dermis. Third degree burns destroy both the epidermis and dermis. Burn depth, size, and location impact severity and treatment approach. The emergency management of burns focuses on the ABCs - airway, breathing, circulation, disability, exposure and fluid resuscitation based on burn size. Definitive burn care then focuses on wound management and rehabilitation.
2. Definition of a Burn
“Tissue injury caused by thermal,
radiation, chemical, or electrical
contact resulting in protein
denaturation, burn wound edema,
and loss of intravascular fluid
volume due to increased vascular
permeability.”
3. Burn Statistics
At least 50% of all burn accidents can
be prevented
children playing with fire account for
more than one-third of preschool
deaths by fire
In the US, approximately 2.4 million
burn injuries are reported each year.
Burn injuries are second to motor
vehicle accidents as leading cause of
accidental death in the US
4. TYPES OF BURNS
Flame (Thermal)
Electrical
AC & DC
Lightning
Chemical
Steam
Radiation
Scald
COURTESY DAVID
EFFRON, M.D.
THIRD DEGREE BURNS
WITH ESCHAROTOMIES
5. Types of Burns
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
6. Types of Burns
Chemical
Caused by strong acids, alkalis, phenols,
cresols, phosphorus or mustard gas
Results in necrosis
Electrical
Caused by electric current which may
generate heat up to 5000ºC
May result in necrosis, respiratory paralysis, or
ventricular fibrillation
7. Types of Burn Injury
Smoke & inhalation injury-inhaling hot
air or noxious chemicals
Cold thermal injury-frostbite.
Radiation
Caused by prolonged or intense exposure to
ultraviolet radiation
Examples: Sunburn, tanning beds
8. Classification of Burn Injury
Treatment of burns is directly related to
the severity of injury!
Severity is determined by:
depth of burn
external of burn calculated in percent of total
body surface (TBSA)
location of burn
patient risk factors
9. Location of Burns
Has a direct relationship to the severity of
the burn.
Face, neck & chest burns may cause
respiratory illness mechanical obstruction
secondary to edema or eschar formation
10. 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
12. Skin
Largest body organ. Much more than a
passive organ.
Protects underlying tissues from injury
Temperature regulation
Acts as water tight seal, keeping body fluids
in
Sensory organ
13. Skin
Injuries to skin which result in loss, have
problems with:
Infection
Inability to maintain normal water balance
Inability to maintain body temperature
14. Skin
Two layers
Epidermis
Dermis
Epidermis
Outer cells are dead
Act as protection and
form water tight seal
15. Skin
Epidermis
Deeper layers divide to produce the stratum
corneum and also contain pigment to protect
against UV radiation
Dermis
Consists of tough, elastic connective tissue
which contains specialized structures
16. Skin
Dermis - Specialized Structures
Nerve endings
Blood vessels
Sweat glands
Oil glands - keep skin waterproof, usually
discharges around hair shafts
Hair follicles - produce hair from hair root or
papilla
Each follicle has a small muscle (arrectus pillorum)
which can pull the hair upright and cause goose
flesh
17. First-Degree Burns
Does not go below
basal layer of the
epidermis
Dry and painful
Appears red due to
increased blood
flow
Heals in a few days
18. Second-Degree Burns
Extends below basal
layer, but not
completely through
dermis
Superficial
Blister, very painful,
contains skin parts
(adnexa) which assist
in epithelialization
Deep Partial-thickness
Deeper in dermis,
fewer adnexa, longer
healing time, less
painful
19. Third-Degree Burns
Extends completely
through dermis
Adnexa destroyed so
can’t heal by
epithelialization
Dermal plexus of
nerves destroyed-
less painful
Burns can be yellow,
red, black, brown
20. Burn Depth
Fourth-degree
Full-thickness
destruction of
skin/subcutaneous
tissue
Involves underlying
fascia, muscle, bone or
other structures
Prolonged disability
21.
22. FIRST AND SECOND DEGREE
BURNS
FIRST DEGREE BURN SECOND DEGREE BURN
26. Initial Estimate of : “Rule of Nines”
Adult anatomical areas = 9% BSA (or multiple)
Extent of Burn
• Not accurate for
infants / children due
to larger BSA of head
& smaller BSA of legs.
Burn diagrams
illustrate adult and
child differences.
27. Rule of Nines
In the adult, most areas of the body can
be divided roughly into portions of 9%, or
multiples of 9. This division, called the rule
of nines, is useful in estimating the
percentage of body surface damage an
individual has sustained in burn.
29. Thermal Burn Injury
Pathophysiology
Emergent phase
Response to pain catecholamine release
Fluid shift phase
massive shift of fluid - intravascular
extravascular
Hypermetabolic phase
demand for nutrients repair tissue
damage
Resolution phase
scar tissue and remodeling of tissue
30. Zones of Burn Injury
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.
31. ESCHAR
The necrotic tissue resulting from a burn
is known as eschar.
It is a good substrate for microorganisms.
If left untreated it becomes colonized,
contaminated and eventually infected.
Topical antimicrobial agents increase the
time to eschar separation.
33. Burn
Pathophysiology:inflammation&
Edema
Injured tissue: capillary permeability es
Protein leakage: resultant
hypoproteinemia, and ed osmotic
pressure in burned tissue
Decreased cell membrane potential with
inward shift of Na+ and H2O, resulting in
cellular swelling
Edema maximal at 24 hrs, usually resolved
by 3-5 days; capillary leak normal at 24
hrs
35. Burn Pathophysiology: Metabolic
Prostaglandins, IL-1, IL-6 implicated in:
increase in core temperature of 1-2oC
initiating acceleration of nitrogen catabolism
? inversion of T4/T8 ratios from 2:1 to 1:2
Early enteral feeding associated with
attenuation of the hypermetabolic
response
36. Burn Pathophysiology:
Cardiac
Cardiac output initially decreases
loss of intravascular volume
CVP and PCWP typically low-normal, even
after adequate volume resuscitation
Cardiac output usually normalizes before
intravascular volume completely restored
iCa++ may present as hypotension/EMD
out of proportion to hypoalbuminemia
37. Burn Pathophysiology: Renal
it can result from:
prolonged hypotension due to hypovolemia
myoglobin release from damaged
muscle/tissue
hemoglobinuria from heat-induced hemolysis
Renal blood flow initially es, followed by
dramatic in GFR, coinciding with onset
of the postburn hypermetabolic state, and
hyperdynamic circulation
38. Burn Pathophysiology: Renal
Early in the postburn period, decreased
urinary Na+ and Cl-
K+ wasting in the urine is common (up to
200 mEq/liter), secondary to the intense
adrenal response to burn injury/stress
39. Burn Pathophysiology: Hypertension
May be common in pediatric patients
up to 57% in one study
7-10 year old boys with >20% BSA affected
Hypertensive encephalopathy may result
7% of hypertensive pediatric burn patients
Mechanism may involve hypervolemia with
concomitant activation of RA SYSTEM
?elevated “stress” plasma renin and
aldosterone
40. Burn Physiology: Pulmonary
Pulmonary dysfunction etiologies in this
setting:
shock, inhalational injury, aspiration, sepsis,
CHF, trauma
Upper airway injury/edema may contribute
airway occlusion impairs flow of tidal breaths
• resolution of occlusion can cause reexpansion
41. Burn Physiology: Pulmonary
Circumferential thoracic eschar or edema
may contribute to restrictive lung disease
Hypovolemia may cause V/Q mismatch
Inflammatory mediators released in burn
injury linked to evolution of ARDS
therefore, expect some degree of pulmonary
capillary leak, on a continuum from mild
pulmonary edema, to frank ARDS
42. Burn Pathophysiology: CNS
CNS dysfunction in up to 14% of burn pts
most had >50% BSA involvement
Hypoxia most common etiology
smoke inhalation, pulm edema, pneumonia
Hypovolemia, hyponatremia, cortical vein
thrombosis, sepsis, and gliosis due to
watershed infarct also implicated
? Role of neurotoxic factors
43. Burn Pathophysiology: GI
Stress (curling’s) ulcer
prophylaxis: antacids, H2 blockers, or
sucralfate
Increased gut permeability in first 24
hours
Acalculous cholecystitis
fever, abdominal distention, jaundice
bacterial seeding (ascending cholangitis)
sterile, in patients with dehydration, ileus, or
pancreatitis
44. Burn Pathophysiology: GI
Acute pseudo-obstruction of the colon
massive colonic dilation without organic cause
Narcotic ileus
oral narcotic antagonists may be efficacious
hypovolemia shunt blood from the splanchnic
bed and promote mucosal atrophy and failure
of the gut barrier
45. Burn Pathophysiology:
Hepatic
Modest hepatic dysfunction common early
Persisting, or severe hepatic dysfunction,
associated with negative outcome
larger BSA involvement (58% vs 30%)
greater mortality (74% vs 9%)
clinical jaundice associated with 90%
mortality
Late onset of conjugated
hyperbilirubinemia usually related to
occult, or overt, sepsis
46. Burn Pathophysiology: Blood
Initially, shortened RBC survival with intra-
vascular hemolysis/possible
hemoglobinuria
typically resolves after the 1st week
Anemia is common, and to be expected;
may be masked initially by hemoconcentration
may be exacerbated by fluid management,
occult blood loss
typically persists until wound healing occur
depressed erythropoietin levels documented
47. Burn Physiology:
Immunologic
Skin as an organ of host defense:
keratin layers as physical barrier to
penetration
cycles of desquamation (“debulking” of
skin bacterial burden)
stratum corneum: unsaturated free fatty
acid film which is bacteriostatic and
fungistatic
colonization resistance due to normal flora
antigen presentation to Langerhans’ cells
48. Burn Physiology:
Immunologic
Cellular Immune Function
markedly delayed allograft rejection
ed antigen responses
total lymphocyte count typically normal, but
T4 (helper T-cell) count , while T8
(suppressor T-cell) count (T4/T8 ratio
inverts)
several circulating mediators in burn patient
sera suppress normal lymphocyte function
49. Burn Physiology:
Immunologic
“Immunologic Dissonance” resulting
from activation of inflammatory
cascades/SIRS
Systemic immunosupression may therefore
occur very early in the post-burn period;
magnitude of immunocompromise BSA
51. Phases of Burn Care
Emergency assessment and care (ABCs)
Resuscitation (hours 0-48)
Definitive care (day 3 until wounds are
closed)
Rehabilitation (begins during resuscitation
and lasts entire lifespan)
52. Rescue
A-B-C-D-E-F
Stop the burning
Decontaminate casualty at the scene
Avoid injury to the rescuer
Careful with high voltage electrical wires
Assess for other injuries
53. ABCs of Emergency Burn Care
(Advanced Burn Life Support)
A = Airway (with cervical spine assessment)
B = Breathing
C = Circulation
D = Disability
E = Exposure and Environmental Control
F = Fluid Resuscitation based on Burn Size and
Weight Measurement
Secondary Survey
54. A: Airway
Assess the patient’s airway
Upper airway edema due to inhalation injury
Rapid or delayed progression
Decision to intubate: individualized
Mild symptoms: observe in ICU
Pre-transport: prophylactic intubation
When in doubt, intubate
55. B: Breathing
Look, listen, feel for breath sounds and
chest movement
Give 100% oxygen to all victims of major
burn beginning in the field
Pulse oximetry
Arterial blood gases
Required for definitive diagnosis of CO
Baseline chest x-ray
56. C: Circulation
Who needs fluid resuscitation?
All >20% total body surface area burned (TBSA)
Young and old with >10% TBSA
2 large bore peripheral IVs
Unburned skin
Burned skin
Central access
Cutdown
Interosseous
57. D: Disability
Assess level of consciousness: AVPU
Alert
Responds to verbal stimuli
Responds to painful stimuli
Unresponsive
Alteration in mental status is not normal
Pupils
Moves extremities
59. F: Fluid Resuscitation
(based on burn size and weight)
Determine fluid needs based on burn size and
weight
Burn size: include second and third degree only
Rule of Nines
One hand = one percent
Lund-Browder chart
Overestimation by referring hospitals is common
Weight: pre-burn weight
60. Fluid Therapy
1 or 2 large bore IV replacement lines (may
need jugular or subclavian)
Cutdown if no option , increased risk of
infection & sepsis
Fluid replacement based on: size/depth of
burn, age of pt., & individualized
considerations--ex. Dehydration in preburn
state, chronic illness
options- RL, D5NS, dextam, albumin, etc.
there are formula’s for replacement: Parkland
formula and Brooke formula
61. Total Body Surface Area (TBSA) Burned
Palmar Method
A quick method to evaluate scattered or
localized burns
Client’s 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
62. Burns
Parkland/Baxter Formula
4 ml RL/kg body wt X % TBSA=ml RL for 24
hours
eg. Pt. wt=75 kg and burned 25%
4/75/25=7500 ml/24 hours
50% 1st 8 hours=3750ml
25% 2nd 8 hours=1875 ml
25% 3rd 8 hours=1875
63. Formulas for Fluid Replacement
Evans Formula.
Colloids 1 ml./kg. of body wt/%/burn.
Saline 1 ml/kg. of b. wt./% of burn.
free water: dependent on age &
insensible loss.
1/2 of total is given the 1st 8 hrs. and
the remainder given the next 16 hrs.
64. Brooke Formula
.
Colloids .5 ml/kg/% of body surface
burned.
Lactated Ringers 1.5 ml/% of body wt/%
burn.
H20 Again dependent.
1/2 total amount given 1st 8 hrs.
1/4 of total the 2nd 8 hrs. 1/4 the third 8
hrs.
65. Galveston formula
Resuscitation Formula
1. Fluid administration-Ringers lactate
First 24 h:
a. 5000 ml/M2 burn + 2000 ml/TBSA m2
b. administer 1/2 in first 8 h postinjury and the 2nd half
in the next 16 h.
Example: 15 kg child with an 87% TBSB, height 96 cm.
Body Surface (m2) =.60
Total Burn (m2)=.52
2000 ml x .6 TBSAm2 = 1200 ml
5000 ml x .52 TBSABm2 =2600 ml
Total fluids first 24 h = 3800 ml
Total fluids first 8 h = 1900 ml = 237 ml/h
Total fluids next 16 h = 1900 ml = 118 ml/h
66. Assessment of adequacy of
fluid replacement
Urinary output is most commonly used
parameter
urine OP-30-50 cc/hr in an adult
cardiopulmonary factors- BP (systolic 90-100
mmHg, pulse less than 100, resp 16-20 breaths
per min. (BP more accurate with arterial line)
sensoruim-alert, oriented to time, place, &
person
67. FIRST AID
cooling the burn wound soon after the injury
(within 30minutes) is beneficial in removing heat
from the wound and limiting tissue damage.
It can also reduce early edema and protein
extravasation.
Care must be taken, as prolonged or excessive
cooling can be detrimental.
68. Other precautions...
Burn too large--don’t immerse in water
due to extensive heat loss
Never pack in ice
Pt. should be wrapped in dry clean
material to decrease contamination of
wound and increase warmth
69. CRITERIA FOR ADMISSION
Both 2nd & 3rd
degree burns
>20% BSA any age
>10% BSA <10 or
>50 years of age
3rd degree only
>5% BSA
Burns of face,
hands, feet,
genitals, or joints
70. CRITERIA FOR ADMISSION
Specialized burn
types
Electrical &
lightning
Chemical
Inhalation injury
Circumferential
chest or extremity
burns
Significant medical
illness
Significant other
injuries
71. Critical Burn Criteria
30 > 10% BSA
20 > 30% BSA
>20% pediatric
Burns with respiratory injury
Hands, face, feet, or genitalia
Burns complicated by other trauma
Underlying health problems
Electrical and deep chemical burns
74. Escharotomies
—required if circumferential full thickness burns
of chest,limbs or digits are present.
can impair circulation and cause distal
ischemia. Circumferential full-thickness chest
burns can restrict chestwall excursion and impair
ventilation.
mid-axial escharotomies performed either at
bedside or in the operating room..
An escharotomy incision will only improve
outcome without risk of harm in that situation.
77. 3 types of smoke and
inhalation injuries
1. Carbon monoxide poisoning (CO
poisoning and asphyxiation count for
majority of deaths)
Treatment- 100% humidified oxygen-draw
carboxyhemoglobin level- can occur without
any burn injury to the skin
78. 2. Inhalation injury above the
glottis (caused by inhaling hot air,
steam, or smoke.)
Mechanical obstruction can occur quickly-
True ER! Watch for facial burns, signed
nasal hair, hoarseness, painful swallowing,
and darkened oral or nasal membranes
79. 3. Inhalation injury below glottis
(above glottis-injury is thermally produced)
below glottis-it is usually chemically
produced.
Amount of damage related to length of
exposure to smoke or toxic fumes
Can appear 12-24 hours after burn
80. SIGNS OF SMOKE INHALATION
Exposed to smoke in enclosed
space
Unconscious while exposed to
smoke
After exposure to smoke
Develops cough
Develops dyspnea
Develops chest pain
81. SIGNS OF UPPER AIRWAY BURNS
Burns of the face
Singed eyebrows or
nasal hairs
Burns in the mouth
Sooty sputum
History of being burned
while confined to an
enclosed space
COURTESY ROY ALSON, M.D.
LIP BURNS & SOOT IN
MOUTH
82. 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
83. Inhalation Injury Management
Circulation
Treat for Shock (rare)
IV Access
LR/NS large bore, multiple IVs
Titrate fluids to maintain systolic BP and perfusion
84. Inhalation Injury Management
Other Considerations
Assess for other Burns and Injuries
Treat associated inhalation injury/poisoning
Cyanide poisoning antidote kit
Positive pressure ventilation
Hyperbaric chamber (carbon monoxide poisoning)
85. Wound Care Principals
Goals
close wound
prevent infection
reduce scarring and contractures
provide for comfort
Wound cleaning
Debridement
mechanical
surgical
Topical antibacterial therapy
86. Cleansing and Debridement
Can be done in tank, shower, or bed
Debridement may be done in surgery.
(Loose necrotic skin is removed)
bath given with with surgical detergent,
disinfectant, or cleansing agent to reduce
pathogenic organisms
87. Infection is the most serious
threat to further tissue injury
and possible sepsis.
SURVIVAL is related to prevention of
wound contamination.
Source of infection is pt’s own flora,
predominantly from the skin, resp. tract, and
GI tract.
Prevention of cross contamination from other
patients is the priority for nurses!
88. 2 methods used to control
infections in burn wounds...
Open method- pt’s burn is covered with
topical antibiotic and has no dressing
Closed method-uses sterile gauze
impregnated with or laid over a topical
antibiotic. Dressings changed 2-3 times q
24 hrs.
89. Wound Care continued...
Staff should wear disposable caps, gowns,
gloves, masks when wounds are exposed
use of sterile techniques
keep room warm
careful handwashing
any bathing areas disinfected before and
after bathing
90. Coverage is the primary goal for burn
wounds. Since usually not enough unburned
skin for immediate skin grafting, other
temporary wound closure methods are used
Allograph or homograft (same species which is
usually from cadavers) is used for wound
closure-- temporary--3 days to 2 wks
Porcine skin-heterograft or xenograft (different
species)--temporary--3 days to 2 wks
autograft or cultured epithelial autograft- (pt’s
own skin and cell culture)- permanent
91. Burn Wound Closure
Permanent Skin Grafts
Two types:
Autografts and Cultured Epithelial Autografts
(CEA)
Autograft
Harvested from client
Non-antigenic
Less expensive
Decreased risk of infection
Can utilize meshing to cover large area
Negatives: lack of sites and painful
92. Permanent Burn
Wound Closure Cont.,
Permanent Skin Grafts Cont.,
Cultured Epithelial Autografts (CEA)
A small piece of client’s skin is harvested and
grown in a culture medium
Takes 3 weeks to grow enough for the first
graft
Very fragile; immobile for 10 days post grafting
Great for limited donor sites
Negatives: very expensive; poor long term
cosmetic results and skin remains fragile for
years
93. Temporary Burn Wound Closure
Biosynthetic Temporary Skin Grafts
Homograft
AKA Allograft
Live or cadaver human donors
Fairly expensive
Best infection control of all biologic coverings
Negatives:
Risk of disease transmission (i.e. HBV & HIV)
Antigenic: body rejects in 2 weeks
Not always available
Storage problems
94. Temporary Burn Wound Closure
Biosynthetic Temporary Skin Grafts Cont.,
Heterograft
AKA Xenograft
Graft between 2 different species
i.e. Porcine (pig) most common
Fresh, frozen or freeze-dried (longer shelf life)
Amendable to meshing & antimicrobial impregnation
Antigenic: body rejects 3-4 days
Fairly inexpensive
Negatives: Higher risk of infection
95. Temporary Burn Wound Closure
Temporary Skin Grafting Cont.,
Artificial Skins
Transcyte:
A collagen based dressing impregnated with
newborn fibroblasts.
Integra:
A collagen based product that helps form a
“neodermis” on which to skin graft.
Synthetic
Any non-biologic dressing that will help
prevent fluid & heat loss
Biobrane, Xeroform or Beta Glucan collagen
matrix
96. Donor Site:
Wound Considerations
The donor site is often the most painful
aspect for the post-operative client.
We have created a brand new wound !!
Variety of products are used for donor sites.
Most are left place for 24 hours and then left
open to air.
Donor sites usually heal in 7-10 days
97. using a dermatome (left) to remove
donor skin and a mesher (right) to put
holes in it.
99. Other care measures include
Face is vascular and subject to increased
edema- use open method
eye care-use saline rinses, artificial tears
hands &arms-extended and elevated on
pillows or in slings to minimize edema,
may need splints to keep them in
functional positions
100. Ears- keep free of pressure. Ear burns-
no pillows! Neck burns should not use
pillows in order to decrease wound
contraction.
Perineum-must be kept clean & dry.
Indwelling foley will help in this & also
to provide hourly outputs.
Lab tests ; to monitor electrolyte
imbalance and ABGs
Physio therapy stared immediately
101. Drug Therapy
Analgesics and Sedatives
given for pt comfort
IV pain meds initialy due to:
GI function is slowed or impaired because of
shock or paralytic ileus
IM injections will not be absorbed well
102. Drug Therapy
Tetanus immunization- given routinely
to all burn patients because of the
likelihood of anaerobic burn-wound
contamination
Antimicrobial agents-usually topical
due to little or no blood supply to the burn
eschar so little delivery of the antibiotic to
wound
Drug of choice is: Silver sulfadiazine
103. Curlings ulcer prophylaxis
(Peptic Ulcer)
An H2 blocker (cimetidine,
ranitidine,famotidine) start first 6 hours
antacids are no longer recommended - the
patient should be kept NPO
with burns > 15% of BSA, an NG (OG) tube
and bladder catheter should be placed
104. Burns (medications)
Silver nitrate 0.5% (rarely used)
wet dressing effectively prevents cross infection
>0.5% injures the tissue and not effective<0.5%
danger of electrolyte imbalance (especially Na and K)
since the electrolytes are withdrawn from the body
fluids and also from the dressing.
Turns black in sunlight and stains clothes and hands
black
105. Burns (medications)
Silvadene
wide-spectrum antimicrobial that is
nonstaining and relatively painless
no systemic metabolic abnormalities however
is contraindicated in pregnant women near
term and premature infants
does not penetrate the eschar as well as
sulfamylon
106. Burns (medications)
Sulfamyalon acetate
interferes with bacterial cellular metabolism
diffuses rapidly through burned skin and eschar
used for gram-negative organism
burning sensation after applied topically
may cause metabolic acidosis and is a carbonic
andryrase inhibitor
may cause a rash
107. Burns (medications)
Furacin-nitrofurazone (gauze or cream)
a synthetic broad-spectrum antibacterial
inhibits enzymes required for carbohydrate
metabolism in bacteria
Xeroform-a fine mesh gauze with
antimicrobial action
108. Topical antimicrobials
Advantages and Disadvantages
Silver Sulfadiazine –Painless but Lack of
penetration
Mafenide Acetate –Penetrates but Painful,
Carbonic anhydrase inhibitor
Silver Nitrate- Broad spectrum but Limited
penetration
Sodium Hypochlorite -Broad spectrum but
Impairs wound healing in high doses
109. Table 7.2. Other topical agents
Bacitracin: Gram-positive Minimal coverage
Often combined with polymyxin and neomycin
into triple ointment
Polymyxin B :Petroleum-based Keeps grafts
moist, Often combined with mycostatin into
“Polymyco”
Bactroban: Staphylococcal coverage ,Very
expensive
Useful for ghosted grafts
Silvamyco:(Silvadene and mycostatin) Extended
coverage
110. SYSTEMIC ANTIMICROBIAL
THERAPY IN BURNS
only after clinical suspicion of an infection
exists
appropriate in patients with massive burns
based on culture and sensitivities
111. Complications of Acute Phase
Infection- due to destruction of body’s 1st line
of defense. Partial thickness wds can convert to
full-thickness wds with infection present.
Signs of sepsis are: high temp., increased
pulse & resp., decreased BP, and decreased
urinary output, mild confusion, chills, malaise,
and loss of appetite. WBC bet. 10,000 and
20,000. Infections usually gram neg. bacteria
(pseudomonas, proteus)
Obtain cultures from all possible sources: IV,
foley, wound, oropharynx, and sputum
112. Neurologic-possible from electrical injuries
Musculoskeletal-has the most potential f
complications during acute phase due to
healing and scar formation making skin less
supple and pliant. contractures can occur
Gastrointestinal-adynamic ileus results from
sepsis, diarrhea or constipation ( narcotics &
decreased mobility), gastric ulcers , stress,
occult blood in stools possible
Endocrine-stress DM might occur-assess
glucose
113. Complications Cont.,
Electrolytes Imbalances
Hyperkalemia
A result of cellular destruction
Hyponatremia
A result of fluid shifts into interstitial space
Acid-Base Imbalances
Metabolic Acidosis
Failure to conserve bicarbonate
Also, a result of fluid shifts into interstitial space
See Smeltzer & Bare pp. 1713; Table 57-3
114. Burn Shock
Shock is a state of inadequate cellular perfusion
Burn Injuries involving > 35 % TBSA
Clinical manifestations:
Hypotension & tachycardia
Decreased Cardiac Output:
Decreased preload, stroke volume & contractility
Increased afterload
Monitoring: PCWP & CVP values decreased
Prevention: Early & full fluid resuscitation !!
Smeltzer & Bare pp. 1708 (Figure 57-3)
116. Nutritional Therapy
Fluid replacement takes priority over
nutritional needs in the initial emergent
phase.
NG tube is inserted and connected to
low intermittent suction for
decompression. When bowel sounds
return (48-72 hrs) after injury, start
with clear liquids and progress up to a
diet high in proteins and calories
117. Adult Energy Requirements
Curreri formula
Daily energy requirement = (25W + 40B)
Long formula
BEE x activity factor x injury factor
Male BEE = 66.6 + 13.8W + 5H – 6.8A
Female BEE = 655 + 9.6W + 1.9H – 4.7A
Activity factors:
1.2 if confined to bed
1.3 if out of bed
Injury factor:
2.1 for severe thermal burn
W=weight in kg, B=total burn area as % of
total body mass, H=height in cm, A=age in
years
118. Child Energy Requirements
Wolfe Formula
Energy = BMR x 2
BMR Calculations
Age Boys Girls
0-3 years 60.9W – 54 61W – 51
4-10 years 22.7W + 459 22.5W +
499
11-18 years 17.5W + 651 12.2W + 746
W= weight in kg
119. Child Energy Requirements
Modified Galveston formula
< 1 year: (2100 x BSA) + (1000 x burn area)
< 12 years: (1800 x BSA) + (1300 x burn
area)
12-18 years: (1500 x BSA) + (1500 x burn
area)
BSA = body surface area in m2
Burn area = surface area burned in m2
120. Carbohydrate Requirements
Glucose reduces extent of hypermetabolic
response and protein breakdown
High rates of glucose delivery:
Causes hyperglycaemia needing insulin
Stimulates hepatic lipogenesis & altered liver function
Increased CO2 production
Prevents & slow weaning from ventilator
Adults: 5 mg/kg/min avoids complications
Children: 5-7 mg/kg/min
Infants: D5W 5 mg/kg/min initially then
increased to a max of 15 mg/kg/min over first few
days
121. Fat Requirements
Normal diet leads to muscle wasting
with central obesity due to hepatic
steatosis
Fat reduction prevents problems when
protein replaces lipid energy
Adults: Minimum of 4% total energy
15% meets essential fatty acid requirements and
provides for fat-soluble vitamins
Vary composition of fats
Children: Minimum of 2-3% total energy
Infants: Maximum of 4g/kg of IBW
122. Protein Requirements
Intact protein rather than amino acids
Improved weight maintenance and survival
Frequent estimations of nitrogen loss to
ensure adequate replacement
TNL = TUN + 4g
TNL = (UUN x 1.25) + 4g
NB = TNL – NS
6.25 g protein = 1 g nitrogen
Adults: 2-3 g protein/kg IBW
Children:
< 1 year old: 3-4 g protein/kg IBW
1-3 years old: 2.5-3 g protein/kg IBW
>3 years old: 1.5-2.5 g protein/kg IBW
25% energy as protein
123. Vitamin Requirements
Specific requirements not established for
most
Multivitamin supplementation
Vitamin A
Immune function & epithelialization
10,000 IU/day
< 3 years old: 5,000 IU/day
124. Vitamin Requirements
Vitamin C
Immune function
Wound Healing
Collagen synthesis
Free radical scavenging properties limits tissue damage
Ascorbic acid study
High doses reduced resuscitation fluid volume, body
weight gain, wound edema, & severity of respiratory
dysfunction
Adults: 500 mg twice a day
Children up to age 10: 250 mg twice a day
125. Enteral vs. Parenteral Feeding
Enteral preferred over parenteral
Maintains integrity of GI tract
Parenteral more expensive & increases
complications
Hospital-made vs. commercial diets
Hospital made diets as good as commercial
Weight gain & protein increase similar
Patient tolerance similar
127. ELECTRICAL BURNS
Extent of injury
depends upon
Type of current
Amount of current
Path of current
Duration of current
128. ELECTRICAL BURNS
Injury from electrical
burns results from
coagulation necrosis
that is caused by
intense heat
generated from an
electric current.
129. Electrical injury can cause:
Fractures of long bones and vertebra
Cardiac arrest or arrhythmias--can be
delayed 24-48 hours after injury
Severe metabolic acidosis--can develop in
minutes
Myoglobinuria--acute renal tubular
necrosis- myoglobin released from muscle
tissue whenever massive muscle damage
occurs--goes to kidneys--and can
mechanically block the renal tubules due
to the large size!
130. ELECTRICAL INJURY
Cardiac arrhythmias
are the most serious
immediate injury that
occurs with electrical
contact
V-Fib
V-Tach
132. Treatment of electrical
burns…
Fluids--Ringers lactate or other fluids-
flushes out kidneys--you want 75-100
cc/hr until urine sample clear
an osmotic diuretic (Mannitol) may be
given to maintain urine output
133. Electricity can instantaneously destroy tissue. This child has a
burn that resulted from biting on an electrical cord. These
burns often occur at the corners of the mouth, as seen here.
134. ADDITIONAL INJURIES
Skin burns
Entrance and
exit wounds
Fractures
cannot
determine the
extent of the
injury from the
surface burn
DA
Y
ON
E
DA
Y
3
135. LIGHTNING STRIKE
Usually superficial
injury
Victims die from
cardiac arrest
Resuscitate the
“dead”
Patients who are
breathing will usually
survive
136. 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...
137. 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
138. Chemical Burns
Bases (Alkali)
Liquefactive necrosis with continued
penetration into deeper tissue resulting in
extensive injury
characterized by dull, opaque, partly or completely
fluid remains of tissue
Dry Chemicals
Exothermic reaction with water
139. 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
140. 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
141. TREATMENT OF CHEMICAL EXPOSURE
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”
142. 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
143. Rehabilitation Phase
Defined as beginning when the patient’s
burn wound is covered with skin or healed
and patient is capable of assuming some
self-care activity.
Can occur as early as 2 weeks to as long as
2-3 months after the burn injury
Goals for this time is to assist patient in
resuming functional role in society &
accomplish functional and cosmetic
reconstruction.
144. Clinical Manifestations
Burn wd either heals by primary intention
or by grafting.
Scars may form & contractures.
Mature healing is reached in 6 months to
2 years
new skin sensitive to trauma
145. Complications
Most common complications of burn injury
are skin and joint contractures and
hypertrophic scarring
Because of pain, pts will assume flexed
position. It predisposes wds to contracture
formation
Use of physical therapy, pressure
garments, splints, etc. are used
146. 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 !!
148. 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 !!
150. 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
151. Prevention of Burn Injuries
Proper education and supervision
childproof items in electrical sockets
keep dangerous items (matches) out of reach
Safety measures for the elderly
teach small children 911
smoke detectors in house
STOP, DROP, AND ROLL
152. Position of comfort after burn trauma (to be
avoided)
1. Neck flexion
2. Shoulder protraction
3. Elbow flexion
4. Metacarpal extension
5. Interphalangeal flexion
6. Wrist flexion
7. Hip flexion
8. Knee flexion
9. Ankle plantar flexion
153. Techniques available for burn
reconstruction
1. Without deficiency of tissue
• Excision and primary closure
• Z-plasty
2. With deficiency of tissue
• Simple reconstruction
- Skin graft
- Transposition flaps (Z-plasty and modifications)
• Reconstruction of skin and underlying tissues
- Axial and random flaps
- Myocutaneous flaps
- Tissue expansion
- Free flaps
154. Pediatric Burns
Thin skin
increases severity of burning relative to adults
Large surface/volume ratio
rapid fluid loss
increased heat loss hypothermia
Delicate balance between dehydration and
overhydration
Immature immunological response sepsis
Always consider possibility of child abuse
156. Recent advances
IV or nebulised Heparin shown to reduce
tracheobronchial cast formation in
inhalation burns
Early near total excision and grafting
Anabolic agents like oxandrlone
,GH,testoesterone as a nutritional
adjuvants
157. SUMMARY
Protect yourself and your patient
Maintain c-spine immobilization
Treat burn patients as trauma patients
Properly cool the burn
Be alert for inhalation injuries
Flush chemical burns adequately
Monitor heart in electrical burn patients
158. BURNS
B - breathing
body image
U - urine output
R - rule of nines
resuscitation of
fluid
N - nutrition
S - shock
silvadene