Acute burn pathophysiology and classification.

1. ACUTE BURNS -
CLASSIFICATION &
PATHOPHYSIOLOGY
Dr. Varun Kashyap

2. LEARNING OBJECTIVE
• Pathophysiology of local & systemic effect in acute burn injury.
• Etiology & its effects
• To classify burn injury based on severity.

3. INTRODUCTION
• Annual burn incidence of 6-7 million in India.
• Second largest group of injuries after road accidents.
• Nearly 10% of these are life threatening and require hospitalization.
• Approximately 50% of those hospitalized succumb to their injuries.
• Nearly 1 to 1.5 lac people get crippled and require multiple surgeries
and prolonged rehabilitation

4. ANATOMY OF SKIN

5. Skin receptors
• Meissner receptors detect light touch.
• Pacinian corpuscles perceive deep pressure and vibrational changes.
• Ruffini endings detect deep pressure and stretching of the skin’s collagen
fibers.
• Free nerve endings located in the epidermis respond to pain, light touch,
and temperature variations.
• Merkel receptors associated with the Merkel cells respond to sustained
light touch induction over the skin.

6. Classifications of Burns
• Etiology
• Severity
• Depth
• Size

7. Mechanisms of injury
• Thermal
• Chemical
• Electrical
• Cold injury
• Radiation.

8. Thermal injuries
• Scalds—About 70% of burns in children are caused by scalds. The common
mechanisms are spilling hot drinks or liquids or being exposed to hot bathing
water. Scalds tend to cause superficial to superficial dermal burns.
• Flame—Flame burns comprise 50% of adult burns. They are often associated
with inhalational injury and other concomitant trauma. Flame burns tend to be
deep dermal or full thickness.
• Contact—In order to get a burn from direct contact, the object touched must
either have been extremely hot or the contact was abnormally long. Contact
burns tend to be deep dermal or full thickness.

9. Electrical injuries
• Some 3-4% of burn unit admissions are caused by electrocution
injuries.
• The tissue between “entry” and “exit” points can be damaged by the
current.
• The amount of heat generated, and hence the level of tissue damage,
is equal to 0.24×(voltage)²×resistance.
• Low voltage, domestic current and high voltage currents

10. • Voltage
• Current (amperage)
• Type of current (alternating or direct)
• Path of current flow
• Duration of contact
• Resistance at the point of contact
• Individual susceptibility

11. (1) True electrical injury caused by the flow of current
(2) Arc injury
(3) Flame injury
(4) Lightning strikes.

13. Domestic electricity—Low voltages tend to cause small, deep contact burns at the
exit and entry sites. The alternating nature of domestic current can interfere with
the cardiac cycle, giving rise to arrhythmias.
“True” high tension injuries occur when the voltage is 1000 V or greater.
• There is usually a large amount of soft and bony tissue necrosis.
• Muscle damage gives rise to rhabdomyolysis, and renal failure may occur with
these injuries. This injury pattern needs more aggressive resuscitation and
debridement than other burns.
“Flash” injury can occur when there has been an arc of current from a high
tension voltage source. The heat from this arc can cause superficial flash burns to
exposed body parts, typically the face and hands. However, clothing can also be
set alight, giving rise to deeper burns.

14. • Electroporation - aqueous pores in lipid bilayers exposed to a
supraphysiologic electrical field.
• Electrochemical interactions - calcium influx into the cytoplasm and
triggers apoptosis.
• Thermal interactions.
Cells of long length (skeletal muscle and nerve) are more vulnerable to
electroporation

15. Chemical injuries
• Industrial accidents or household chemical products.
• These burns tend to be deep, as the corrosive agent continues to
cause coagulative necrosis until completely removed.
• Alkalis tend to penetrate deeper and cause worse burns than acids.
Cement is a common cause of alkali burns.

16. ∘ Oxidation, e.g. sodium hypochlorite
∘ Reduction, e.g. hydrochloric acid
∘ Corrosion, e.g. phenol
∘ Protoplasm poisoning, e.g. formic acid
∘ Vesiculation, e.g. dimethylsulfoxide
∘ Desiccation, e.g. sulphuric acid.

17. Alkali burns
• Cause liquefactive necrosis.
• deeper penetration of the alkali.
∘ Household cleaning solutions
∘ Oven cleaners
∘ Fertilisers
∘ Cement.
Acid burns
• Cause coagulative necrosis.
• Should be irrigated within 10 minutes to minimise deep damage.
• Hydrochloric acid fumes can cause airway oedema and pneumonitis.

18. Management of chemical burns
• All contaminated clothing must be removed
• Area thoroughly irrigated.
• This limits the depth of the burn.
• Litmus paper can be used to confirm removal of alkali or acid.
• Eye injuries should be irrigated copiously

19. Cold injury
• Frostnip
• Frostbite
extracellular ice crystals formation
intracellular hyperosmolarity causes cell damage and protein
denaturation

22. Classification by Size
• The Rule of Nine
• The Lund-Browder Method
• The Palmar Surface

24. Lund-Browder Method

25. Pathophysiology of Burns

26. Local and systemic effects
• Local Effect
Zone of coagulation: point of maximum damage and this zone is
characterised by irreversible tissue damage due to coagulation of proteins.
Zone of stasis or zone of ischemia: moderate degree of damage associated
with vascular leakage, elevated concentration of vasoconstrictors, and local
inflammatory reactions resulting in compromised tissue perfusion.
Zone of hyperemia: This is the outermost zone, characterised by the
increased blood supply and inflammatory vasodilation. The tissue here will
recover unless there is severe sepsis or prolong hypoperfusion.

28. Inflammatory Mediators of Burn Injury
• HISTAMINE
• PROSTAGLANDINS - PGE2, PGI2 and leukotrienes(LB4 and LD4)
• THROMBOXANE A2 & B2
• KININS
• SEROTONIN
• CATECHOLAMINES
• REACTIVE OXYGEN SPECIES
• PLATELET AGGREGATION FACTOR

30. Hypovolemia and Rapid Edema Formation

31. CONCEPT OF GLYCOCALYX IN BURN EDEMA
• Glycoprotein and polysaccharides layer
on the luminal side of endothelial cells.
• Maintains barrier
• Reduces osmotic gradient and thereby
reducing filtration.
• thickness of the glycocalyx
• varies from 20 nm in capillaries to 3000
nm
• Revised starling law
Jv = Kf [(Pc − Pif )− (p − g )]

34. Systemic Response
• Severe burn injury, >30% TBSA complex reaction occurs both from the
burn area and in the area distant to the burn.
• Cytokines, chemokines and other inflammatory mediators are
released in excess resulting in extensive inflammatory reactions
within a few hours of injury.
• The initial response of the burn injury is similar to the inflammation
that is triggered after tissue destruction such as trauma or major
surgery.

35. Different factors contribute to the magnitude of the host response,
they include:
• Burn Severity (Percentage TBSA And Burn Depth)
• Burn Cause
• Inhalation Injury
• Exposure To Toxins & Other Traumatic Injuries
• Patient-related Factors Such As Age, Pre-existing Chronic Medical
Conditions, Drug Or Alcohol Intoxication
• Timing Of Presentation To Medical Aid

44. THANK YOU