Burns

-transfer of energy from heat source to the body

-cell destruction of the layers of the skin

Patients at High risk for Burns
1. Very Old (60yrs and above)
2. Very Young (3-5 yrs of age)
3. People who live in manufactured homes and rural areas

Patients at greater risk of Mortality due to Burns
1. Patients <5yrs of age
2. Patients >40 yrs old

Prevention
1. Keep all matches and lighters away from children
2. Do not leave children alone around fires
3. Install and maintain smoke detectors
4. Set water heater temperature no higher than 120F (48.9C)
5. Do not smoke in bed or fall asleep while smoking
6. Use caution when cooking
7. Keep a working fire extinguisher at home

Types of Burns:
1. Thermal
>exposure to hot substances (e.g. exposure to flames, hot liquids, steam or hot objects)
> e.g. Scald Burns
-wet burns
- injury to the skin by touching a very hot liquid or steam
-most frequent thermal injury
2. Electrical
>contact with live current
>caused by heat generated by electrical energy as it passes through the body
>electricity travels through areas of least resistance and destroys everything in its path
(nerves and blood vessels first.
>internal damage maybe more severe than expected from external injury
>Principles:
-the stronger the current=the longer the contact
-the longer the contact=the more severe the injury
>important to note: voltage, type of current, contact site and duration of contact
>e.g.
a. High Voltage burns
-1000Volts
-can cause tissue and bone destruction causing amputation
-can cause death by cardiac and respiratory abnormalities
b. True Electrical Injury
-when the current of electricity travels through the body and exits to the ground
itself
-there is an entrance wound and an exit of wound
c. Arc injury
-result of electricity travelling outside of the body and arcing around it
-clothes often catch fire because of high energy
-patient gets a flame burn and often small spider-like markings that make a path
on the skin
d. Cutaneous injury
-usually small compared with the damage under the surface of the skin
3. Chemical
>caused by contact with strong acids or strong bases or prolonged contact with most
chemicals
>systemic toxicity may occur from cutaneous absorption
4. Radiation
>exposure to high doses of radioactive material, ultraviolet light or X-ray

Classification of Burns:
A. According to Depth
>determines whether epithelialization will occur
>factors
+how the injury occurred
+causative agent such as flame or scalding liquid
+temperature of burning agent
+duration of contact with agent
+thickness of skin
Depth of Burn Injury
Characteri
stic First Degree
Second Degree
Third
degree
Superficial Partial-
thickness
Deep Partial-
thickness
Full
thickne
ss
Morpholog
y
Destruction
of the
dermis only
Destruction of
epidermis and
some dermis
Destruction of
epidermis and dermis,
leaving only skin
appendages
Destru
ction of
epider
mis,
and
underly
ing
subcut
aneous
tissue
Skin
function
Intact Absent Absent Absent
Tactile and
pain
sensors
Intact Intact Intact but diminished Absent
Blisters Present
only after
first 24 hrs
Present within
minutes; thin-
walled and fluid
filled
May or may not
appear as fluid-filled
blisters; often is layer
of flat, dehydrated
tissue paper that lifts
off in sheets
Blisters
rare;
usually
is a
layer of
flat,
dehydr
ated
tissue
paper
that
lifts off
easily
Appearanc
e of wound
after initial
debrideme
nt
Skin peels
at 24-48 hr;
normal or
slightly red
underneath
Red to pale ivory,
moist surface
Mottled with areas of
waxy, white, dry
surface
White,
Cherry
red or
black;
may
contain
visible
thromb
osed
veins;
dry,
hard,
leather
y
surface
Healing
time
3-5 days 21-28 days 30 days to many
months
Will not
heal;
may
close
from
edges
as
second
ary
healing
if
wound
is small
Scarring None May be present;
low incidence
influenced by
genetic
predesposition
Highest incidence
because of slow
healing rate promoting
scar tissue
development; also
influenced by genetic
predesposition
Skin
graft;
scarrin
g
minimiz
ed by
early
excisio
n and
grafting
;
influen
ced by
genetic
predes
positio
n

B. According to extent
>estimating Total Body Surface Area (TBSA) affected by burns
a. Rule of Nines
-quick away to estimate extent of burns
-system where body parts are assigned with percentages in multiples of 9
b. Lund and Broweder chart
-more precise method of estimating extent of burn
-recognizes the percentage surface area of various anatomic parts especially
the head, legs and thighs which vary according to age
-divide the body into very small areas providing estimate of the proportion of
TBSA
c. Palm Method
-scattered burns
-principle: the size of the patients palm is approximately 1% of TBSA























C. Palm method


Pathophysiology of burns

Modifiable Non-modifiable
>Occupation >age
>Place of living >voltage (e.g. lightning)
>Contact with burn agents >duration of contact (e.g.lightning)
>Duration of contact with source



Coagulation, Protein Denaturation,
Ionization of cellular contents



Burned Tissue/TISSUE DESTRUCTION INHALATION
OF GAS


CV F&E Renal Immunologic Cellular/ Thermoreg. GI Pulmo
Metabolic

A. Cardiovascular changes
-Complications:
>BURN SHOCK -> CNS release of catecholamines -> peripheral
resistancePR->
C.O. -> myocardial depressant factor-> SUPPRESSED
MYOCARDIALCONTRACTILITY
*Capillary Seal
-term used to indicate end of burn shock period
>Anemia
>thrombocytopenia
> prolonged clotting and prothrombin time

B.
C. Fluid and electrolyte Changes
-complications:
>Edema
>Hyponatremia
>Hypekalemia- after burn injury
>Hypokalemia- occurs with fluid shifts, and inadequate potassium replacements

D. Pulmonary Alterations
Inhalation injury
-prolonged hospitalization
-major cause of morbidity and mortality in pts c burn injury
-can occur in people trapped inside a burning structure
-categories:
>Upper airway injury
-caused by direct heat or edema
-manifested by mechanical obstruction of the upper airway
>Inhalation injury below the glottis
-results from inhaling the product of incomplete combustion of noxious gases
>restrictive defects
-Arise when edema develops under full thickness burns encircling the neck and
thorax
-complications
1. ARDS
2. Acute Respiratory Failure

E. Renal Alterations
-complications
1. Acute tubular necrosis
2. renal failure

F. Immunologic Alterations
-risk for infection

G. Cellular and Metabolic Changes
-hyper metabolism

H. Thermoregulatory Alterations
T-during early hours after injury
T-due to hypermetabolism during healing process

I. Gastrointestinal Alterations
-complications:
1. paralytic ileus
2. curlings ulcer
3. Abdominal compartment syndrome



Management of Burn Injury
Three phases:
Emergent/ Resuscitative phase
Acute/ Intermediate phase
Rehabilitation phase
Emergent/ Resuscitative phase
Duration : from onset of injury to completion of fluid resuscitation
Priorities:
- First aid
- Prevention of shock
Prevention of respiratory distress
Detection and treatment of concomitant injuries
Wound assessment and initial care
- Paralytic Ileus
- Curlings ulcer
Nursing Management: Acute/Intermediate Phase
Duration: From beginning of diuresis to near completion of wound closure
Begins 48 to 72 hours after the burn injury.
Priorities:
- Wound care and closure
- Prevention or treatment of complications
- Nutritional support
Focus on hemodynamic alterations, wound healing, pain and psychosocial responses,
and early detection of complications.
Measure vital signs frequently.
Assess peripheral pulses frequently for first few days after the burn for restricted blood
flow.
Closely observe hourly fluid intake and urinary output, blood pressure, and cardiac
rhythm.
For patient with inhalation injury, regularly monitor level of consciousness, pulmonary
function, and ability to ventilate, frequent suctioning and assessment of the airway are
priorities.
Rehabilitation Phase


CONSENSUS FORMULA. Lactated Ringer's solution (or other balanced saline solution): 2-4 mL
x kg body weight x % total body surface area (TBSA) burned. Half to be given in first 8h;
remaining half to be given over next 16h.

EVANS FORMULA. 1. Colloids: 1mL x kg body weight x %TBSA burned. 2. Electrolytes (saline):
1mL x bodyweight x %TBSA burned. 3. Glucose (5% in water): 2000mL for insensible loss.
Day1: Half to be given in first 8h; remaining half over next 16h.
Day 2: Half of previous day's colloids and electrolytes; all of insensible fluid replacement.
Maximum of 10,000 mL over 24h. Second and thirddegree (partial and full thickness) burns
exceeding 50% TBSA are calculated on the basis of 50% TBSA.

BROOKE ARMY FORMULA. 1. Colloids: O.5mL x kg body weight x %TBSA burned. 2.
Electrolytes (Lactated Ringers solution): 1.5mL x kg bodyweight x %TBSA burned. 3. Glucose
(5% in water): 2000mL for insensible loss. Day1: Half to be given in first 8h; remaining half over
next 16h.
Day 2: Half of colloids; half of electrolytes electrolytes; all of insensible fluid replacement.
Second and third degree (partial and full thickness) burns exceeding 50% TBSA are calculated
on the basis of 50% TBSA.

PARKLAND/BAXTER FORMULA.
Lactated Ringers solution: 4mL x kg bodyweight x %TBSA burned.
Day1: Half to be given in first 8h; half to be given over next 16h.
Day 2: Varies. Colloid is added.

HYPERTONIC SALINE SOLUTION.
Concentrated solutions of sodium chloride (NaCl) and lactate with concentration of 250-300
mEq of sodium per liter, administered at a rate sufficient to maintain a desired volume of urinary
output. Do not increase the infusion rate during the first 8 postburn hours. Serum sodium levels
must be monitored closely. Goal: Increase serum level and osmolality to reduce edema and
prevent pulmonary complications.