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Download MBBS Burns and Plastic Surgery PPT 2 Burns Epidemiology Extent Pathophysiology And Prevention Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Burns and Plastic Surgery PPT 2 Burns Epidemiology Extent Pathophysiology And Prevention Lecture Notes

This post was last modified on 07 April 2022


Burns: Epidemiology,

Pathophysiology and

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Prevention

Introduction

A burn is an injury to the skin or other organic tissue primarily caused by heat

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or due to radiation, radioactivity, electricity, friction or contact with

chemicals.

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Thermal (heat) burns occur when some or all of the cells in the skin or other

tissues are destroyed by:

hot liquids (scalds)

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hot solids (contact burns), or
flames (flame burns).
Epidemiology of Burns

The global scenario

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Burns are a global public health problem, accounting for an estimated 265 000

deaths annually. The majority of these occur in low- and middle-income countries

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and almost half occur in the WHO South-East Asia Region.

Non-fatal burns are a leading cause of morbidity, including prolonged hospitalization,

disfigurement and disability, often with resulting stigma and rejection.

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Burns are among the leading causes of disability-adjusted life-years (DALYs) lost in low-

and middle-income countries.

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In 2004, nearly 11 million people worldwide were burned severely enough to require

medical attention.


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India
Who is at risk?

Gender

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Females and males have broadly similar rates for burns. according to the most

recent data. (In contrast to other injuries where males have a higher rate)

Age

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children are particularly vulnerable to burns. Burns are the 11th leading cause of

death of children aged 1?9 years and are also the fifth most common cause of

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non-fatal childhood injuries.

Regional factors

There are important regional differences in burn rates.

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Children under 5 in the WHO African Region have almost 3 times the incidence of

burn deaths than infants worldwide

Socioeconomic factors

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People living in low- and middle-income countries are at higher risk for burns than

people living in high-income countries.

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Within all countries however, burn risk correlates with socioeconomic status.

Other risk factors

occupations that increase exposure to fire;

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poverty, overcrowding and lack of proper safety measures;
placement of young girls in household roles such as cooking and care of small

children;

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underlying medical conditions, including epilepsy, peripheral neuropathy, and

physical and cognitive disabilities;

alcohol abuse and smoking;

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easy access to chemicals used for assault (such as in acid violence attacks);
use of kerosene (paraffin) as a fuel source for non-electric domestic appliances;
inadequate safety measures for liquefied petroleum gas and electricity.
In which settings do burns occur?

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Burns occur mainly in the home and workplace.

Community surveys in Bangladesh and Ethiopia show that 80?90% of burns occur at home.

Children and women are usually burned in domestic kitchens, from upset receptacles containing

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hot liquids or flames, or from cookstove explosions.

Men are most likely to be burned in the workplace due to fire, scalds, chemical and electrical

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burns.

Classification of Burn Injuries


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By mechanism of cause

1. thermal
2. Electrical
3. Chemical

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4. Inhalational
result of breathing in superheated gases, steam, hot liquids or noxious

products of incomplete combustion.

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cause thermal or chemical injury to the airways and lungs.

Thermal Burns

Thermal burns involve the skin and

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may present as: ?

a) scalds ? hot liquid or steam
b) contact burns ? hot solids or items

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such as hot pressing irons and

cooking utensils, as well as lighted

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cigarettes

c) flame burns ? flames or

incandescent fi res, such as those

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started by lighted cigarettes,

candles, lamps or stoves

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Electrical Burns

caused by an electrical current passing from an electrical outlet, cord or

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appliance through the bodyfrom one point to another, creating "entry"

and "exit" points.

The tissue between these two points can be damaged by the current.

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Can be high voltage or low voltage injuries
High voltage injuries:

Flash burns
True high tension injury

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Electrocardiogram after electrocution

showing atrial fibril ation

Chemical Burns

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caused by exposure to reactive

chemical substances such as

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strong acids or alkalis

These burns tend to be deep, as

the corrosive agent continues to

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cause coagulative necrosis until

completely removed.

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Alkalis tend to penetrate deeper

and cause worse burns than acids.

Cement is a common cause of

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alkali burns.


By the degree and depth of a burn

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First degree
Second Degree
Third degree
Fourth degree

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First degree Burn

Cause: Flash flame.

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ultraviolet(sunbum)

Surface appearance: Dry, no

blisters, no or minimal edema

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Colour: Erythematous
Pain level: Painful


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Second Degree Burn(Superficial partial

thickness)

Cause: Contact with hot liquids or

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solids, flash flame to clothing,

direct flame, chemical. Ultraviolet

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Surface appearance: Moist blebs,

blisters

Colour: Mottled white to pink,

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cherry red

Pain level: Very Painful

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Third degree Burns (Deep Partial

thickness)

Cause: Contact with hot liquids or

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solids, flame. chemical, electrical

Surface appearance:Dry with

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leathery eschar until

debridement; charred vessels

visible under eschar

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Colour:Mixed white, waxy. pearly;

dark, khaki, mahogany; charred

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Pain level: Little or no pain; hair

pulls out easily


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Fourth degree Burn

Cause: Prolonged contact with

flame, electrical

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Surface appearance:Same as

third degree, possibly with

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exposed bone, muscle, or tendon

Colour: Same as third degree
Pain level: Same as third degree

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Currently burn depth assessment is

done clinically

Future: multisensor heatable laser

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Doppler flowmeter


Assessing the extent of burn

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This is calculated as a percentage of Total body surface area(TBSA)

Rule of 9

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Lund and Browder chart

The Rule of 9's provides a simple

method of estimating

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total body surface area burned.

Due to differences in body

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proportions,

the percentage for each body

area is different in adults and

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children.


The Lund and

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Browder chart

provideo a more

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precise estimate of

bum TBSA for each

body part based on

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the individual's age.

Pathophysiology of Burn
Body's response to burn injury

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Burn injuries result in both local and systemic responses.

Local response

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The three zones of a burn were described by Jackson in 1947.
Zone of coagulation--This occurs at the point of maximum damage. In this

zone there is irreversible tissue loss due to coagulation of the constituent

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proteins.

Zone of stasis--The surrounding zone of stasis is characterised by decreased

tissue perfusion. The tissue in this zone is potentially salvageable. The main

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aim of burns resuscitation is to increase tissue perfusion here and prevent

any damage becoming irreversible. Additional insults--such as prolonged

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hypotension, infection, or oedema--can convert this zone into an area of

complete tissue loss.

Zone of hyperaemia--In this outermost zone tissue perfusion is increased.

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The tissue here will invariably recover unless there is severe sepsis or

prolonged hypoperfusion.

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These three zones of a burn are three dimensional, and loss of tissue in the

zone of stasis will lead to the wound deepening as well as widening.


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Clinical image of burn

zones. There is central

necrosis, surrounded by

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the zones of stasis and of

hyperaemia
Systemic response

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The release of cytokines and other inflammatory mediators at the site of

injury has a systemic effect once the burn reaches 30% of total body

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surface area.

Cardiovascular changes

Capillary permeability is increased, leading to loss of intravascular proteins

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and fluids into the interstitial compartment.

Peripheral and splanchnic vasoconstriction occurs.
Myocardial contractility is decreased, possibly due to release of tumour

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necrosis factor .

These changes, coupled with fluid loss from the burn wound, result in

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systemic hypotension and end organ hypoperfusion.
Respiratory changes

Inflammatory

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mediators cause

bronchoconstriction,

and in severe burns

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adult respiratory

distress syndrome

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can occur.

Gastrointestinal changes

Atrophy of the small bowel mucosa occurs within 12 hours of injury in

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proportion to the burn size

reduced uptake of glucose and amino acids, decreased absorption of

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fatty acids, and a reduction in brush border lipase activity

Intestinal permeability to macromolecules, which are normally repelled by

an intact mucosal barrier, increases after a burn.

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splanchnic hypoperfusion occurs
early and aggressive enteral feeding to decrease catabolism and maintain

gut integrity.

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Metabolic changes

The basal metabolic rate increases up to three times its original rate.
A stress such as a severe burn induces the release of inflammatory

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hormones, which results in

gluconeogenesis,
lipolysis, and
proteolysis.

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Inflammatory changes

Non-specific down regulation of the immune response occurs, affecting

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both cell mediated and humoral pathways.


Prevention
BURNS ARE PREVENTABLE

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Prevention strategies: forming a burn

prevention plan

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Prevention strategies should address the hazards for specific burn injuries, education for vulnerable

populations and training of communities in first aid.

An effective burn prevention plan should be multisectoral and include broad efforts to:

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improve awareness

develop and enforce effective policy

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describe burden and identify risk factors

set research priorities with promotion of promising interventions

provide burn prevention programmes

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strengthen burn care

strengthen capacities to carry out all of the above.
Recommendations for individuals,

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communities and public health officials

1. Enclose fires and limit the height of open flames in domestic environments.
2. Promote safer cookstoves and less hazardous fuels, and educate regarding

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loose clothing.

3. Apply safety regulations to housing designs and materials, and encourage

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home inspections.

4. Improve the design of cookstoves, particularly with regard to stability and

prevention of access by children.

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5. Lower the temperature in hot water taps.
6. Promote fire safety education and the use of smoke detectors, fire

sprinklers, and fire-escape systems in homes.

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7. Promote the introduction of and compliance with industrial safety

regulations, and the use of fire-retardant fabrics for children's sleepwear.

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8. Avoid smoking in bed and encourage the use of child-resistant lighters.

9. Promote legislation mandating the production of fire-safe cigarettes.

10.Improve treatment of epilepsy, particularly in developing countries.

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11.Encourage further development of burn-care systems, including the training

of health-care providers in the appropriate triage and management of

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people with burns.

7. Support the development and distribution of fire-retardant aprons to be

used while cooking around an open flame or kerosene stove.

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Thank You