Burn Injury Classification, Assessment and Management
1. Burns
Dr Janai A. M. Ondieki
For Clinical Medicine Diploma Class
yr 2
2. Definitions
• Burns are caused by transfer of energy from a
heat source to the body. Heat may be transferred
through conduction or electromagnetic radiation.
• Burns are defined as a wound caused by
exogenous agent leading to coagulative necrosis
of tissue
• Tissue destruction results from coagulation,
protein denaturation, or ionization of cellular
contents.
4. Thermal Burns
– Heat changes the molecular structure of tissue causing
denaturing of proteins
– The extent of burn damage depends on
• Temperature
• Amount of heat
• Duration of contact
For example, in the case of scald burns in adults, 1 second of contact
with hot tap water at 68.9°C (156°F) may result in a burn that
destroys both the epidermis and the dermis, causing a fullthickness
(third-degree) injury.
Fifteen seconds of exposure to hot water at 56.1°C (133°F) results in a
similar full-thickness injury.
5. • The effects of thermal burns are influenced by
– Intensity of the energy
– the duration of exposure
– the type of tissue injured
6. Pathophysiology of burns
•Burns that do not exceed 25% TBSA produce a primarily local
response.
•Burns that exceed 25% TBSA may produce both a local and a
systemic response and are considered major burn injuries.
•The incidence, magnitude, and duration of pathophysiologic
changes in burns are proportional to the extent of burn injury,
with a maximal response seen in burns covering 60% or more
TBSA
•These systemic responses are due to the release of cytokines
and other mediators into the systemic circulation
7. • Fluid shift
– period of inflammatory response
– Vessels adjacent to burn injury dilate, increased
capillary hydrostatic pressure and permeability
– Continous leak of plasma from intravascular space
into interstitial space
– associated imbalences in fluids, electrolytes and
acid-base occur
– Haemoconcentration
– Lasts 24-36 hours
8. • Fluid mobilization
– capillary leak ceases and fluid shifts back into the
circulation
– Restores fluid balance and renal perfusion
• increased urine formation and diuresis
– continued electrolyte imbalances
• hypokalaemia
• Hyponatremia
– Haemodilution
9. • Systemic Changes
• Cardiac
– decreased cardiac output
• Pulmonary
– Respiratory insufficiency as a secondary process
– can lead to respiratory failure
• Gastrointestinal
– Decreased or absent motility
– Stress Ulcer formation ( Curlings Ulcer)
10. • Metabollic
– Hypermetabolic state
– increased oxygen and calorie requirements
– increased in core body temperature
• Immunological
– loss of protective barrier
– increased risk of infection
– suppression of humoral and cell-mediated immune responses
11. Acute Phase
• Clinical issues
• External loss of Plasma
• Loss ofd circulating red cells
• Burn oedema
12. Sub Aute Phase
• Diuresis
• Clinical Anaemia
• Accelerated metabolic rate
• Nitrogen Disequilibrium
• Bone and joint changes
• Endocrine disturbances
• Electrolyte and chemical imbalance
• circulatiry derangements
• loss of function of skin as an organ
13. Body's response to Burns
• Emergent Phase (stage 1)
– Pain response
– Catecholamine release
– tachycardia, tachypnoea, mild Hypertension, mild anxiety
• Fluid Shift Phase (stage 2)
– Length 8-24 hours
– Begins after emergent phase
• reaches peak in 6-8 hours
– damaged cells initiate inflammatory response
• increased blood flow to cells
• Shift of fluid from intravascular to extra vascular space
– MASSIVE OEDEMA
14. • Hypermetabolic Phase (stage 3)
– Lasts for days to weeks
– Large increase in the body's need for nutrients as
it repairs itself
• Resolution phase(stage 4)
– scar formation
– general rehabilitation and progression to normal
function
15. Jackson's theory of Thermal Burns
• Zone of coagulation
– Area nearest to the heat
source that suffers the most
damage as evidenced by
clotted blood and
thrombosed blood vessels
• Zone of Stasis
– Area surrounding zone of
coagulation characterized by
decreased blood flow
• Zone of Hyperemia
– Peripheral area around burn
that has increased blood flow
16.
17. • Severity of burns is determined by
– depth of the burn
– Extent of the burn/total Burn Surface A (TBSA)
– Location of the burn
– Patient risk factors
18. Grading of burn according to depth
• First Degree - Injury to the
Epidermis
• Superficial Second Degree -
injury to epidermis and
Superficial Papillary dermis
• Deep secondary Degree -
Injury from epidemis to
reticular dermis
• Third degree -full thickness
burn through epidermis and all
layers of dermis
• Fourth degree - injury trhough
skin, subcutaneous fat into
underlying muscle or bone
19. • Burn Depth
• Burn depth determines whether epithelialization will occur.
• Determining burn depth can be difficult even for the
experienced burn care provider.
• The following factors are considered in determining the
depth of the burn:
– How the injury occurred
– Causative agent, such as flame or scalding liquid
– Temperature of the burning agent
– Duration of contact with the agent
– Thickness of the skin
20. 1st Degree Burn
• Involves only the epidermis
• Reddening/Darkening of the
skin
• Pain at burn site
• Blanch to touch
• Have an intact epidermal
barrier
• Do not result in scarring
• Examples: Sun Burn, Minor
Scald from Kitchen accident
• Treatment aimed at comfort
21. 2nd degree Superficial
Burn
• Involves the epidermis
and papillary dermis
• Intense pain
• Blisters
• reddening/darkening
• Spares hair follicles ,
sweat glands etc
• erythematous & blanch
to touch
• Very painful/sensitive
• No/Minimal Scaring
• Spontaneously re-
epithelialize from
retained epidermal
structures in 7-14 days
22. 2nd degree deep burn
• Involves the epidermis and
reticular dermis
• less pain, remain painful to
pin prick
• Appears pale and mottled
• do not blanch to touch
• capillary return sluggish or
absent
• takes 14-35 days to heal by
epithelialisation from hair
follicles & sweat glands
often with severe scaring
• Contractures possible
• may require excision & skin
grafting
23. 3rd degree burns
• dry, leathery skin(white,
dark, brown or charred)
• Loss of sensation
• All dermal layers are
invovled
• will require surgery
26. Assessing Total Burn Surface Area
• Rule of Nines
– best used for large surface areas
– Expedient tool to measure extent of burn
– Modified to Rule of Sevens for pediatric age group
• Rule of palms
– best used for burns< 10% BSA
• Lund and Browder Chart
31. Criteria for Classifying the Extent of Burn
Injury(American Burn Association)
Minor Burn Injury
• Second-degree burn of less than 15% total body
surface area(TBSA) in adults or less than 10%
TBSA in children
• Third-degree burn of less than 2% TBSA not
involving special care areas (eyes, ears, face,
hands, feet, perineum, joints)
• Excludes electrical injury, inhalation injury,
concurrent trauma, all poor-risk patients (eg,
extremes of age, concurrent disease) 31
32. Criteria for Classifying the Extent of Burn
Injury(American Burn Association)
Moderate, Uncomplicated Burn Injury
• Second-degree burns of 15%–25% TBSA in
adults or10%–20% in children
• Third-degree burns of less than 10% TBSA not
involving special care areas
• Excludes electrical injury, inhalation injury,
concurrent trauma, all poor-risk patients (eg,
extremes of age, concurrent disease) 32
33. Criteria for Classifying the Extent of Burn
Injury(American Burn Association)
Major Burn Injury
• Second-degree burns exceeding 25% TBSA in adults
or 20% in children
• All third-degree burns exceeding 10% TBSA
• All burns involving eyes, ears, face, hands, feet,
perineum, joints
• All inhalation injury, electrical injury, concurrent
trauma, all poor-risk patients 33
34. Pre Hospital care for burn victims
• Ensure rescuer safety
• Stop the burning process: Stop, drop and roll
• Check for other injuries
– Standard ABC (airway, breathing, circulation)followed by a rapid
secondary survey
• Cool the burn wound
– Analgesia
– Slows the delayed microvascular damage
– minimum of 10 min
– effective up to 1 hour after the burn injury
• give oxygen
• elevate
35. Management of the Patient With a
Burn Injury
35
• Burn care must be planned according to the burn
depth and local response, the extent of the injury,
and the presence of a systemic response.
• Burn care then proceeds through three phases:
– Emergent/resuscitative phase (on-the-scene care),
– Acute/intermediate phase, and
– Rehabilitation phase.
• Although priorities exist for each of the phases, the
phases overlap, and assessment and management
of specific problems and complications are not
limited to these phases but take place throughout
burn care.
36. Table: phases of burn care
36
Phase Duration Priorities
Emergent or
immediate
resuscitative
From onset of injury to
completion
of fluid resuscitation
First aid
Prevention of shock
Prevention of respiratory distress
Detection and treatment of concomitant
injuries
Wound assessment and initial care
Acute From beginning of diuresis
to near
completion of wound
closure
Wound care and closure
Prevention or treatment of
complications, including infection
Nutritional support
Rehabilitatio
n
From major wound closure
to return
to individual’s optimal level
of physical
and psychosocial
adjustment
Prevention of scars and contractures
Physical, occupational, and vocational
rehabilitation
Functional and cosmetic reconstruction
Psychosocial counseling
37. • Criteria for admission to hospital/Burns Unit
• suspected airway/inhalational injury
• any burn requiring fluid resuscitation (>15% in adults and 10% in
children)
• any burn requiring surgery
• burns to special areas; face, hands, feet perineum
• pts with psychiatric or social circumstance making it inadvisable to
send them home
• any suspicion of non-accidental Injury
• Any burn in a patient at extremes of age
• any burn associated with potentially serious sequelae
• high tension electrical burns
• Chemical burns
38. Emergent/resuscitative phase mgt
• Emergency Medical Management
• A: Airway Control
• B: Breathing and ventilation
• C: Circulation
• D: Disability - neurological status
• E: Exposure with environmental control
• F: Fluid resuscitation
38
39. • Airway Recognition of the
potentially burned airway
– A history of being trapped in
the presence of smoke or hot
Gases
– Burns on the palate or nasal
mucosa, or loss of all the
hairs in the nose
– burns around the mouth and
neck
40. Burned airway
• Early elective intubation is
safest
• Delay can make intubation
very difficult because of
Swelling
• Be ready to perform an
emergency cricothyroidotomy
if intubation is delayed
41. Upper Airway Injury
• Injury above the glottis
• Results from direct heat (hot air) or edema
• Manifested by mechanical obstruction of the
upper airway, including the pharynx and the
larynx
• Assess patients for facial burns, erythema,
swelling, tachypnea, dyspnea, hoarsness, and
singed nasal hairs.
• Treatment: early endotracheal or nasotracheal
intubation
42. Lower Airway Injury
• Injury below the glottis
• Results from inhaling toxic gases and chemical
contained in inhaled smoke
• When these substances come in contact with
pulmonary mucosa, irritation and inflammation
reaction occurs, resulting in hypersecretion, severe
mucosal edema, ciliary action , and possibly
bronchospasm
• Pulmonary surfactant is reduced, causing atelectasis
• Assess patient for expectoration of sputum with
carbon particles
43. Carbon Monoxide (CO) Poisoning
• CO is a colorless, odorless
gas that is a by-product of
the combustion of organic
materials.
• The affinity of hemoglobin
for CO is 200X greater than
that for O₂
• CO combines with
hemoglobin to form
carboxyhemoglobin and
blocks the uptake of O₂ and
causing tissue hypoxia
• Treatment: early intubation
and mechanical ventilation
with 100% O₂
44. Fluids for resuscitation
• In children with burns over 10% TBSA and adults with burns
over 15% TBSA, consider the need for intravenous fluid
resuscitation
• Fluids needed can be calculated from a standard formula
• Parkland Formula: Total percentage body surface area ×
weight(kg) × 4 = volume (ml)
– Half this volume is given in the first 8 hours, and
– the second half is given in the subsequent 16hours.
45. • Crystalloid : Ringer’s lactate
• Hypertonic saline
• Human albumin solution
• Colloid resuscitation
Not Routinely
Used in Our set
up !!
46. Management of fluid loss and shock
Fluid Replacement Therapy:
• The total volume and rate of intravenous fluid
replacement are gauged by the patient’s
response.
• The adequacy of fluid resuscitation is determined
by:
– urine Output totals of 30 to 50 mL/hour
–systolic blood pressure exceeding 100 mm Hg
and/or
– pulse rate less than 110/minute. 46
48. Acute Phase management
• Hemodynamically stable through diuresis
• Capillary permeability is restored
• 48-72 hours after injury
• Goal is restorative therapy
• Focus on infection control, wound care and
closure, nutritional support, pain management,
PT
• Concluded when the burned area is completely
covered by skin grafts or when the wounds are
healed 48
49. Full to deep partial
thickness HWB
Skin graft
Day 1
3 weeks
Day 12
50. Acute Phase management
Pathophysiology
• Diuresis from fluid mobilization occurs, and the
patient is no longer grossly edematous
• Bowel sounds return
• Healing begins
• Formation of granulation tissue
• A partial-thickness burn wound will heal from
the edges
• Full-thickness burns must be covered by skin
grafts 50
51. Acute Phase management
• Wound Care
• Daily observation
• Assessment
• Cleansing
• Debridement
• Appropriate coverage of the burn
51
52. TREATING THE BURN WOUND
• Escharotomy Circumferential
full-thickness burns to the limbs
require emergency surgery.
• The tourniquet effect of this
injury is easilytreated by incising
the whole length of full-
thickness burns..
• Escharotomy•
– Incise along medialand/or
lateral surfaces.
– Avoid bonyprominences.
– Avoid tendons, nerves,major
vessels.
53. • Debridement•
• Types of debridement:
– 1. Auto debridement.
– 2. Tangential excision (at the
end of 1st week)
– 3. Staged primary
debridement (1-3 days
postburn).
• This early debridement of
dead tissue interrupts and
attenuates the systemic
inflammatory response and
normalize immune function
– .4. For deep circumferential
burn, urgent escharotomy is
done
54. • Superficial burns expected to heal by
epitheliaization are managed by either
Exposure Method or by Closed Dressing
55. Acute Phase management
Excision and Grafting
• Eschar is removed down to the subcutaneous
tissue or fascia and skin grafts done
55
59. Acute Phase management
Pain Management
• Opioids
• Several drugs in combination ( MULTIMODAL
ANALGESIA)
• Non pharmacologic strategies
• Relaxation tapes
• Visualization, guided imagery
• Meditation
59
60. Acute Phase management
• Nutrition
– Burns patients need extra feeding
– A nasogastric tube should be used in allpatients with
burns over 15% of TBSA
– Removing the burn and achieving healing stops the
catabolic drive.
• Nutrition Sutherland formula
– Children: 60 kcal/ kg + 35 kcal% TBSA
– Adults: 20 kcal /kg + 70 kcal% TBSA
– Protein20% of energy1.5 to 2 g/kg protein/day
61. Acute Phase management
Infection Prevention
• Tetanus prophylaxis
– Tetanus toxoid, 0.5 mL intramuscularly, if thelast booster dose was
more than 5 years beforethe injury.
– If immunization status is unknown,human tetanus immunoglobulin
250 to 500units, I.M. plus tetanus toxoid in opposite side
• Monitoring and control of infection
– Burns patients are immunocompromised
– They are susceptible to infection from manyroutes
– Sterile precautions must be rigorous
– Swabs should be taken regularly
– A rise in white blood cell count,thrombocytosis and increased
catabolism are warnings of infection
62. • Topical treatment of deep burns
– 1% silver sulphadiazine cream
– • 0.5% silver nitrate solution
– Mafenide acetate cream•
– Serum nitrate, silver sulphadiazine and
ceriumnitrate
63. Rehabilitation Phase
• The rehabilitation phase is defined as
beginning when the patient’s burn wounds
are covered with skin or healed and the
patient is able to resume a level of self-care
activity
• Complications
– Skin and joint contractures
– Hypertrophic scarring
63
64. Rehabilitation Phase
• Both patient and family actively learn how to
care for healing wounds
• Cosmetic surgery is often needed following
major burns
• Role of exercise (physiotherapy) cannot be
overemphasized
• Constant encouragement and reassurance
• Address spiritual and cultural needs
• Maintain a high-calorie, high-protein diet
• Occupational therapy 64
65. Complications of Burns
• Emergent phase
– Shock and multi organ failure
• Renal failure
– Respiratory failure (inhalational Injury)
– Hypothermia
70. Chemical Burns
Chemical Burns
Acids
• Protein injury by hydrolysis.
• Thermal injury is made with skin contact.
Alkali
• Saponification of fat
• Hygroscopic effect- dehydrates cells
• Dissolves proteins by creation of alkaline
proteinates (hydroxide ions)
71. Electrical Burns
• Greatest heat occurs at the points
of resistance
• –Entrance and Exit wounds
• –Dry skin = Greater resistance
• – Wet Skin = Less resistance
• Longer the contact, the greater the
potential of injury
– Increased damage inside body
• Smaller the point of contact, the
more concentrated the energy, the
greater the injury.
72. • Electrical Current Flow
• –Tissue of Less Resistance
• • Blood vessels
• • Nerve
– –Tissue of Greater Resistance
• • Muscle
• • Bone
• Results in………..
• –Serious vascular and nervous injury
• –Immobilization of muscles
• –Flash burns
• Late complications: cataracts, progressive
demyelinating neurologic loss
73.
74. • Assess patient
• Entrance & Exit wounds
• Remove clothing, jewelry, and leather items
• Treat any visible injuries– Thermal burns
• ECG monitoring– Bradycardia, Tachycardia, VF or
Asystole– Treat cardiac & respiratory arrest– Aggressive
airway, ventilation, and circulatory management.
• Consider Fluid bolus for serious burns– 20 ml/kg
• Look out for compartment syndrome – prohylactic
fasciotomy
• Myoglobinuria – leads to renal failure
Editor's Notes
CO poisoning is the most common cause of inhalation injury because it is a byproduct of the combustion of organic materials and therefore present in smoke
The pathophysiologic effects of CO poisoning is hypoxemia
100% O₂ is essential to accelerate the removal of CO from hemoglobin molecules
