Burn and Scald

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 Burn & Scald
Etiology
 A burn injury occurs as a result of destruction of
the skin from direct or indirect thermal force.
 Burn are caused by exposure to heat, electric
current, radiation or chemical.

 Scald burn result from exposure to moist heat

(steam or hot fluids) and involve superficial.

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 Types of burn injury

1. Thermal burns.
2. Chemical burns
3. Electrical burns
4. Radiation burns.

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 Types of burn injury
 Thermal burns
-exposure to dry heat (flames) or moist heat
(steam and hot liquids).
-Most common burn injuries
 Chemical burns
-Direct skin contact with either acid or alkaline
agents
-destroys tissue protein, leading to necrosis.
-Burn cause by alkalis are more difficult to
neutralize than are burns caused by acid.
-Alkalis tends to have deeper penetration.
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Chemical burns

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 Types of burn injury
 Electrical burns.
-severity depends on the type and duration
of current, and amount of voltage.
-difficult to assess, due to electrical
insulator.
 Radiation burns.
-sunburn or radiation treatment of cancer.
-involve outermost layers tends to be
superficial.
-all function skin is intact.
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Electrical hand burn.

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 Burn & Scald:Epidemiology
 1 million people suffer thermal injury each
year in U.S.
 45,000 persons are admitted to hospital.
 ↑45,000 persons die as a result of burn
injury.
 The direct cost of treating a burn injury
can be high.
 Cost are higher for large burns.

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 Burn
• The depth of a burn is dependent on the
temperature of the burning agent and the length
of time.
• Tissue damage may occur at temperatures of
48°c.
• Irreversible damage to the dermis occurs at 70°.
• Burn injuries are described as:-
1.Superficial (first-degree burns)
2.Superficial or deep partial thickness (second-
degree burns).
3.Full thickness (third-degree burn)
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 Burn:Classification
1. Superficial (first-degree burns)
• Involve only the epidermal layer of the skin.
• sunburns are commonly first-degree burns.

2. Superficial or deep partial thickness (second-

degree burns).
• Destruction of the epidermis and varying depths
of the dermis.
• Usually painful because nerve endings have
been injured & exposed.
• Ability to heal because epithelial cells is not
destroyed.

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1° burn

2° burn

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Superficial burn (1° burn)

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Partial thickness (2°burn)

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 Burn:Classification
• Present of blisters indicates superficial
partial-thickness injury.
• Blister may ↑size because continuous
exudation and collection of tissue fluid.
• Healing phase of partial thickness, itching
and dryness because ↑vascularization of
sebaceous glands, ↓reduction of
secretions and ↑perspiration.
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Blister may ↑size because continuous
exudation and collection of tissue fluid

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 Burn:Classification
3.Full thickness (third-degree burn)
• Destruction of the epidermis and the entire
dermis, subcutaneous layer, muscle and bone.
• Nerve ending are destroyed-painless wound.
• Eschar may be formed due to surface
dehydration.
• Black networks of coagulate capillaries may be
seen.
• Need skin grafting because the destroyed tissue
is unable to epithelialize.
• Deep partial-thickness burn may convert to a
full-thickness burn because of infection, trauma
or ↓blood supply.
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3° burn

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Eschar:composed of
denatured protein
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Full thickness (3°burn)

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 Burn and scald
Function of the skin.  As a result of burns &
 Protection scald normal skin
 Body temperature structure and function are
regulation impaired.
 Cutaneous sensation. -sweat and sebaceous
 Metabolic functions (vit glands are destroyed.
D) -sensory receptors is ↓.
 Blood reservoir -body fluids escape,
 Excretion. -lack of temperature control.

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Pathopysiology

 Local tissue response

 Systemic response to burn injury.

Local tissue response

 Damage to skin from thermal injury cause tissue
changes know as zone of injury.
 If the heat is severe, a zone of coagulation is
formed, in this area protein has been coagulated
and the damage is irresversible.

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Local tissue response
 Therefore, blood vessels are damage, resulting
in ↓perfusion.

Zon of statis
 Poor blood flow and tissue edema will cause
risk for death over a few hours or days.
 Further necrosis can happen, because other
factors e.g dehydration and infection.
 Due to these wound have to be clean/care,
hydration and prevention of infection are
essential to limit further destruction.

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Local tissue response

 Zone of hyperemia or inflammation is at

the outer edge of the burn.
 Here blood flow is ↑because of
vasodilation.
 Vasodilation because of the release of
vasoactive substances.
 ↑blood flow brings leukocytes and
nutrients to promote wound healing.

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Zon of injury

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Thermal injury Vasoactive substance

Vasodilatation
Inflammation & ↑blood flow

Leukocyctes
& nutrient promote
healing
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Normal Vasodilatation

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Systemic response to burn injury:
severe burn
• Every organ system is affected by
a major burn injury.
• Systemic changes known as burn
shock develop with a burn greater
than 25% of the total body surface
area (TBSA)-major burn injury.
• Damaged tissue released cellular
mediators and vasoactive
substances. E.g, histamine,
serotonin & prostaglandins
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Systemic response to burn injury
• These substances induce a systemic
inflammatory response and cause
vasoconstriction & capillary
permeability
• Vasoconstriction occur for a short
period due to vascular system attempts
to compensate for fluids loss.
• Vascular permeability, resulting in
hypovolemia and edema.
• This phase begins at injury, peaks in
12-24 hours, and last for 48 to 72 hours
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Osmotic pressure ↓, Edema
Due to protein plasma
Escape out to interstitial
•↓blood flow & hypovolemia
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Intravascular
Normal

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Burn
Shock
First 24
hours

Burn
Shock
after 24
hours

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 Thermal injury

Inflammation

Histamine release

↑capillary permeability ↑Protein

Vasoconstriction
leakage
Fluids leakage and
↑blood pressure Loss from injury Hypoproteinemia
Site (edema)

↓intravascular fluid
↑blood flow to injury ↓Plasma osmotic
pressure 35
Hypovolemic shock
 Factors determining severity of
burns
• Size of burn
• Depth of burn
• Age of victim
• Body part involved
• Mechanism of injury
• History of cardiac, pulmonary, renal, or
hepatic disease
• Injuries sustained at time of burn.
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Effects of a severe burn

1. Cardiovascular
2. Respiratory
3. Immune
4. Integumentary
5. Gastrointestinal
6. Urinary

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 Cardiovascular system
 Blood pressure falls-fluid leaks from
intravascular to interstitial (sodium and protein)
 When blood pressure is low, pulse rate ↑.
 Blood flow in intravascular is concentrated and
cause static.
 Cardiac output ↓,
 Due to that tissue perfusion ↓,

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 Hematologic changes

 Some RBC is destroys to the burn injury.-

anemia
 Thrombocytopenia, abnormal platelet
function, depressed fibrinogen levels,
deficit plasma clotting factors.
 Life span ↓RBC.
 Blood loss during diagnostic and
therapeutic procedure.
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 Respiration system
 Majority of deaths from fire are due to smoke
inhalation.
 Pulmonary damage can be from direct inhalation
injury or systemic respond to the injury.
 Damage to cilia and cell in the airway-
inflammation.
 Mucociliary transport mechanism not
functioning-bronchial congestion and infection.
 Pulmonary edema, fluids escape to interstitial.
 Airway obstruction.

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 Factors determining inhalation injury or
potential airway obstruction

 Burns to face and neck

 Singed hairs, nasal hair, beard, eyelids or
eyelashes
 Intraoral charcoal, especially on teeth and gums
 Hoarseness
 Smell of smoke on victims clothes or on victim.
 Respiratory distress.
 Copious sputum production.

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Features of respiratory failure
 Inability to speak due to dyspnea
 Sweating
 Apparent exhaustion/tired
 Tachycardia
 Tachypnea [R. Rate > 40 /min in adults ]

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 Management
 Anaesthetic consultation
 High flow oxygen
 Tracheobronchial [ bronchoscopy]
 Physiotherapy
 Close monitoring [preferably ICU ]
 Ventilatory support
 Hemodynamic support, when required

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 Gastrointestinal
 Burn >20% experience ↓peristalsis, gastric
distention and ↑risk of aspiration.
 Paralytic ileus due to secondary to burn trauma.
 Stress ulcer (stomach/duodenum) due to burn
injury.
 Indication of stress ulcer-malena stool or
hematemesis.
 These signs suggest gastric or duodenal erosion
(Curling`s ulcer)
 Gastric distention and nausea may lead to
vomiting.
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 Urinary system
 Hypovolemic state, blood flow to kidney ↓,
causing renal ischemia.
 If this continues, acute renal failure may
develop.
 Full thickness and electrical burns, myoglobin
(from muscle breakdown) and heamoglobin
(from RBC breakdown) are released into the
bloodstream and occlude renal tubules.
 Adequate fluid replacement and diuretics can
counteract this obstruction.

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Myoglobinuria

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 Immunologic changes

 Skin barrier to invading organisms s destroyed,

circulating levels of immunoglobulins are ↓
 Changes in WBC both quantitative and
qualitative.
 Depression of neutrophil, phagocytic and
bactericidal activity is found after burn injury.
 All this changes in the immune system can make
the burn patient more susceptible to infection.

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 Complications
Early
 Hypovolemia
 Fluid overload  Pulmonary
 Renal dysfunction dysfunction
 Hemoglobinuria
 Stress  Local / systemic
gastroduodenal ulcers sepsis

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 Complications

Late
 Scarring –
hypertrophic, keloid  Disfigurement
 Contractures – limbs,  Functional disability
neck  Posttraumatic stress

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 Extent of surface area burned
 Rule of nines-An estimated
of the TBSA involved as a
result of a burn.

 The rule of nines measures

the percentage of the body
burned by dividing the body
into multiples of nine.

 The initial evaluation is

made upon arrival at the
hospital.

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Rule of nines

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 Lund and Browder
 More precise method of estimating
 Recognizes that the percentage of BSA of
various anatomic parts.
 By dividing the body into very small areas and
providing an estimate of proportion of BSA
accounted for by such body parts
 Includes, a table indicating the adjustment for
different ages
 Head and trunk represent larger proportions of
body surface in children.
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 Lund and Browder chart
Age in years 0 1 5 10 15 Adult

A-head (back or 9½ 8 6½ 5½ 4½ 3½
front) ½
B-1 thigh (back or 2¾ 3 4 4¼ 4½ 4¾
front) ¼
C-1 leg (back or 2½ 2 2¾ 3 3¼ 3½
front) ½

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 Review
 Types of burn injury
 Burn: Classification
 Pathophysiology:-
 local tissue respond (zon of injury)
 systemic respond to burn injury.
 surface area burned:-
 Rule of nines and Lund & Bruder Browder

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 Prehospital patient management
 Rescuers must ensure their own safety,
ones safety is establish:-
 Eliminate the heat source.
 Stabilizing the victim condition.
 Identify the type of burn.
 Preventing heat loss.
 Reducing wound contamination.
 Restrict jewelry and clothing is removed
 Preparing for emergency transport.
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 Stop the burning process:Thermal
burns.
 Stop the flame: extinguish the flame/lavage with
water.
 Cool the burn
 Do not used ice water for cooling it causes
vasoconstriction and may result in further injury.
 Cover the wound to minimize bacteria
contamination
 Cover victim to prevent hypothermia.
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 Chemical burns
 Immediately remove the clothing and a hose or shower
to lavage the involved area for a minimum 20 minutes.
Electrical burns
-Serious harm to victim and rescuer.
-Ensure source of electrical has been disconnected.
-Use non conductive device to remove victim.
-If victim unresponsive, assess respiration and pulse.
-Commenced CPR (cardiopulmonary resuscitation) if no
pulse.

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 Radiation burn

 Usually minor, involved epidermal layer of skin.

 Helping the normal body mechanism to
promote wound healing
 Shielding, establishing distance.
 Limit time of exposure to radioactive source.

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 Phases of treatment
 3 phases of treatment can be identified
in the care of the severely burned
patient.
2. The emergent phase refers to the first 24
to 48 hours after a burn.
3. Acute phase
4. Rehabilitation phase.

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Burn bedspace

1. Plastic sheet top

2. bottom sterile Microdon sheeting
3. Caps, masks, sterile gloves, gowns
4. Intravenous fluids/equipment
5. Intubation equipment
6. Oxygen therapy
7. Cardiac monitoring
8. Catheter, syringes, needles
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 Isolation
 Reverse Isolation is designed to prevent
transmission of microorganisms to patient.
 Burn patient are protected from infection
from other patients, visitors, and health
care providers.
 Universal precautions, apply to all burn
patients.
 The minimum requirements: Universal
Precautions are……………..
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 Universal Precautions

1. All patients have a private room

2. Handwashing is required before entering
and after leaving the patient's room.
3. Gowns, gloves and masks,
4. Health care provider having URTI are not
allowed to enter room

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 Assessment Vital signs
History

Intravenous
Nasogastric line
tube
ER
Indwelling
Neurological
assessment catheter
Physical
examination
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 Emergency department
Management: Emergent/immediate
phase
1. Assessment
-Health history, how, when, duration of contact, location,
age, medical history.
2. Physical examination
 Respiration, patent airway, sign of inhalation injury.

 Listen for hoarsenes and crackle. Need intubation.

 Observe for upper body burned, erythema or blistering

of lips or buccal mucosa or pharynx
 Area of body burned-face, hands, feet, perineum.
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 Emergency department
Management: Emergent/immediate
phase
 Cardiac monitoring, is indicated for cardiac
history, electrical injury or respiratory problems.
 Vital signs-BP, PR. For severe burn an arterial
catheter is used for blood pressure.
 Large bore intravenous lines and an indwelling
urinary catheter are inserted to assess and
monitor fluid intake and output.
 May assist in determining the extent of preburn
renal function and fluids status.
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 Emergency department
Management: Emergent/immediate
phase
 Nurse needs to know the maximal volume of
fluid the patient should receive.
 Infusion pumps and rate controller are useful
devices for correctly delivery.
 Insert nasogastric tube to remove gastric juice,
which can prevent aspiration and vomiting.
 The neurologic assessment focuses on the
pateint`s levels of consciousness, psychologic s
status, pain, behavior and anxiety.
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 Support vital sign
 If the patient has no pulse and not
breathing, begin CPR.
 Establish airway-nasotracheal suction and
endotracheal intubation.-oxygen 100% via
face mask.
 Connect to cardiac monitor and observe
for arrhytmia.
Pulse oximeter-assessment for patient oxygen
saturation.
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 Pulse oximeter
 The pulse oximeter probe contains two
electrodes, which emit light of specific
wavelength through a cutaneous vascular
bed, such as that of the digits or the ear
lobe.

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Pulse oximeter

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 Support vital sign; pulse rate
1. Following a burn, tachycardia is inevitable,
 due to hypovolemia as a result of tissue trauma and pain.

2. A pulse rate lower than 120 beats/min

 usually indicates adequate volume.
 Whereas a pulse rate higher than 130 beats/min
 usually suggests inadequate resuscitation

3. Beware that in the elderly or those with

 preexisting heart disease, the heart rate may not be able
to increase in proportion to the stimulus.

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 Support vital sign
 Continue assess heart output.
 A minimal mean arterial pressure of
-90mmHg should be maintained for adequate
tissue perfusion.
 If the patient is hemodynamically unstable,
-the extremities are burned or if frequent
measurement of arterial blood gases are
required, insertion of an arterial catheter may be
necessary.
 Obtain Arterial blood gases,
carboxyheamoglobin.
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 Arterial blood gases

PH ↓ 7.35-7.45

PCO2 ↑ 35-45 mmHg

PO 75-100mmHg

*To assess acid-base balance due

to a respiratory disorder, respiratory acidosis.
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 Support vital sign
 Cover patient to maintain body
temperature and to prevent wound
contamination
 Initiate fluids replacement
 Urine output, this is the single best monitor
of fluid replacement.
 Weight should be measured daily, as
changes in weight from admission allow
an assessment of fluid balance
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 Insert Foley catheter
1.Foley catheter should be placed in all patients
undergoing resuscitation for severe burns and in
patients with smaller burns with a history of
difficulty voiding.
2. A loose-fitting catheter should be placed to
prevent urethral stricture.
3.The catheter should remain in place throughout
resuscitation.
4. Acceptable values are 0.5ml/kg/hr in an adult
and at least 1ml/kg/hr in a child

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Summary; Emergent
phase

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 Emergency Management

 Site

-Maintain clear airway

-Remove from source of injury
-Prevent ongoing thermal injury
-Keep others safe
-Arrange prompt transfer to Burns Unit

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 Emergency Management

 Hospital Priorities
-Airway
-IV access – large bore peripheral line
-Analgesia – diluted opioids,
-intravenously, large bore.
Catheterise bladder
Investigations [ see box below]

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 Diagnostic test
Initial
Essential Optional
Full Blood Count CXR
Urea & electrolytes ECG
Blood sugar Carboxyhemoglobin
Grouping & typing ABGs
Urinalysis
Later
PCV until stable ABGs
Daily FBC
Daily urea , electrolytes
Swabs for culture
&sensitivity
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 Emergency Management

 History of accident
 General Examination
 Estimate the Area and the depth of the burn.
Look for signs of inhalational burns
• Stridor
• Respiratory distress
• Cough
• Sooty sputum
• Singed nasal hair
• Nasolabial burns
• Airway swelling
• Document all findings
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 Estimation of Total Body Surface
Area Burned [ TBSA]
 Major Burns : >10 % BSA deep burn in a
child
>25% BSA deep burn in an
adult
All major burns WILL need parenteral fluid
resuscitation , since the main cause of
early mortality is Burns Shock.

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 Pathophysiology: Fluids
replacement

A. Four major processes are thought to contribute to the

major loss of intravascular fluid.

1. change in microvascular membrane integrity

2. change in tissue forces

3. cellular shock

4. evaporative losses

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B.Changes in microvascular integrity

1. Following a burn there is a massive release of

inflammator
mediators.

2. Histamine is released early,which increase

capillary permeability

3. Polymorphonuclear leukocytes adhere to the

endothelium.
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 C. Changes in tissue forces

1.The capillary leak causes fluid and plasma

proteins to shift from the intravascular
to the interstitial space.
2. This causes hypoproteinemia, decreased
intravascular osmotic pressure and
increased interstitial osmotic pressure.
3.Edema results when the volume of
interstitial fluid exceeds the capacity of
the lymphatics to remove it.
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 E. Evaporative losses

 Additional evaporative losses through the

burn wound can be between 4 and 20
times greater than normal and persist until
complete wound closure is obtained.

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 Fluids resuscitation

 Lactated Ringer’s (LR) solution is the most

popular resuscitation fluid used.
 There are numerous formula that can be
used for fluid resuscitation.
 No fluid resuscitation formula has proven
to be superior.
 All formulas are only a starting point.
 Administered fluids through 2 large bore
needle.
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 Fluids resuscitation
 Fluid prescription for adults commonly uses the
Parkland Formula which is:
 4cc X weight (kg) X %TBSA burn = cc’s for 1st
24 hours (Ringer's Lactated)
 First half of this total is administered over the
first 8 hours,
 And the second half over the next 16 hours.
 Over 24 hours, >30% burn, provide 5% dextrose

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 Exampel: Parkland
 4cc X weight (kg) X %TBSA burn
 4cc x 50kg x25% = 5000cc

5000 ÷ 500mls = 10 bottles.

 50% to be administer = 2500 cc x 8 Per
hours ~ 312.5cc.
 Second half to be administer = 2500cc x
16 hours.
Per hour~156.25cc
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Fluids resuscitation; Over 24 hours

 4cc X weight (kg) X %TBSA burn

 4cc x 50kg x25% = 5000cc
 5000cc of Ringer's Lactated + 2000cc 5%
Dextrose water.

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 Fluids resuscitation

 Calculate fluid deficit and decide fluid

requirement
 2 types of fluids –Crystalloids and Colloids

Crystalloids [e.g. –Ringer’s Lactate]

-Several formulas: Evans, Brookland etc.
3 – 4 ml / Kg. bodyweight / % Burn during the
first 24 hours,
-half of which is to be given in the first 8 hrs [from
the time of injury]
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 Crystalloid Solutions
Plasma 0.9% Ringer’s
Saline lactate
Na 141 154 130 mEq/L
Cl 103 154 109 mEq/L
K 4-5 -- 4 mEq/L
Ca/Mg 5/2 -- 3/0 mEq/L
Buffer Bicarb. -- Lactate mEq/L
(26) (28)
pH 7.4 5.7 6.7
Osmolality 289 308 273
(mosm/k
g)
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 Colloids [e.g. Human Albumin Solution ]
1.Proteins in plasma generate osmotic pressure
and serve to maintain the intravascular volume.
-The administration of colloid compensates for this
protein lost.

2. Much debate exists as to when capillary integrity

is established and when or if colloid should be
given

3. Early infusion of colloid solutions may decrease

overall fluid requirements and reduce edema.
However, excessive use of colloid risks
iatrogenic pulmonary complications.
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 Colloids

4.Guidelines for adding colloid to crystalloid

regimen:
a.patients with burns less than 30% TBSA
do not usually require colloid
b.patients with burns greater than 30%
TBSA should receive colloid eight hours
after injury
c.patients with inadequate urine output
d.colloid is administered by adding 50g of
albumin to each liter of crystalloid
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 Rate of infusion
 Adult formula: Fluid  if shock present give
first 24 hours = 4cc x bolus of fluid until
perfusion restored
% total body surface x
body weight (one half
in first 8 hours)
 then use constant rate,
adjusting as needed
after 10 to 12 hrs.

 gradually decrease
infusion rate to avoid
excess edema while
maintaining perfusion

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 Intravenous Access

 A peripheral vein catheter through

nonburn tissue is the route preferred for
fluid administration.
 A central line or pulmonary artery line is
only occasionally needed to monitor the
patient during the initial resuscitation
period and is removed as soon as it is no
longer needed.
 The possibilities for intravenous access
are:
97
 Choices For Access

 First choice: Peripheral vein; nonburn

area

 Second choice: Central vein; nonburn

area

 Third choice: Peripheral vein; burn

area

 Worst choice: Central vein; burn area

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 Choices For Access
Central venous access

1. subclavian vein- most desirable site due

to lowest infection rate
2. internal jugular vein
3. femoral vein

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 Interventions:Ineffective airway
clearance
 Baseline assessments respiratory status.
 Chest x-ray, ABG, vital signs.
 Intubation for burns of chest, face or
neck.
4. Maintain the head of the bed at 30°.
5. Turn patient side to side every 2 hours to
prevent hypostatic pneumonia.

100
 Ineffective airway clearance
 Encourage coughing and deep breathing
exercise promote airway clearance of mucus
and fibrin.
 Chest physiotherapy - via percussion and
vibrations, assists with bronchial drainage
 Positioning - patients are shaken and turned
side to side every two hours to aid in secretion
mobilization
 Early ambulation - allows adequate air exchange
in lung regions that are normally hyperventilated
while the patient is recumbent
101
 Ineffective airway clearance

 To keep airway clear, suction the client

frequently, removes accumulated secretions that
cannot be removed by spontaneous cough.
 Caring of patient with nasotracheal tube
placement and orotracheal-more than 3 week
tracheostomy performed.
 Aseptic procedure for suctioning.
 Patients should be hyperoxygenated with 100%
oxygen prior to suctioning. This should not be
continued for more than 15 seconds without
further oxygenation.
 Vagal stimulation and bradycardia are possible
complications.
102
 Ineffective airway clearance

 Medication to dilate constricted bronchial

passages.-via intravenous/inhalants to
control bronchospasms and wheezing.
 Proper positioning to ↓the work of
breathing and promote chest expansion.
 Ensure adequate tissue oxygenation-
pulse oxymeter.
 Oxygenation therapy, ↓oxygenation
saturation.
103
Burn victim

104
Endotracheal tube

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Tracheostomy

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