Download MBBS Burns and Plastic Surgery PPT 6 Scalds Chemical Burn Radiation Burn Frostbite Electric Burn Injury Lecture Notes

Scalds Electrical Burns, Chemical Burns,

Radiation Burns, Frostbite

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Dept. Of Burns & Plastic Surgery

Jv is the volume of fluid that crosses the microvasculature barrier.

Kf is the capil ary filtration coefficient, which is the product of the surface area

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and hydraulic conductivity of the capil ary wal

Pc is the capil ary hydrostatic pressure

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Pif is the interstitial fluid hydrostatic pressure

p is the colloid osmotic pressure of plasma

if is the colloid osmotic pressure of interstitial fluid

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is the osmotic reflection coefficient.

Edema occurs when the lymphatic drainage (JL) does not keep pace with the

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increased Jv
Landis Starling Equation
Skin Biology & Response to Burns

Epidermis

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? Derived from ectoderm so is capable of

regenerative healing.

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? Keratinocytes proliferate from dermal

appendages leading to re-epithelialization.

? Depleted melanocytes regenerate slowly

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leading to pigmentary changes

? Loss of anchoring collagen fibrils (type7) leads

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to blister formation
Skin Biology & Response to Burns

Dermis

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? Superficial papil ary

? Deep reticular

? Fibroblasts produce col agen fibrils and elastic

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fibers

? Dermal appendages lined by keratinocyte derived

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epidermal cel s

? Contain capil ary plexus and sensory nerves

? Derived from mesoderm so heal by scarring

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Patho-phyisological changes

Jackson Zones
? Temperature and duration of contact have a

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synergestic effect

? 1s at 69OC / 1 hour at 45oC
? Zone of coagulation? Centre of the wound

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? Zone of stasis ? At risk area with mix of viable

and non viable cel s along with vasoconstriction

? Zone of hyperemia- Viable cel s with vasodialtion

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? Protection of zone of stasis is achieved with

adequate fluid resuscitation, avoidance of

vasoconstrictors and prevention of infection

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Depth of Burn

1st Degree
? Burns involving only the epidermis.

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? Erythematous and very painful but do not

form blisters.

? Sunburns fit this category of superficial,

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epidermal injury.

? Within 3?4 days, the dead epidermis sloughs

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and is replaced by regenerating keratinocytes.
2nd degree (Superficial dermal burns)

? Extend into the papil ary dermis and characteristical y

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form blisters.

? Appearance is pink, wet and hypersensitive to touch.

? Painful as uncovering the wound al ows currents of air

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to pass over it.

? These wounds blanch with pressure as the blood flow

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to the dermis is increased due to vasodilation.

? Superficial dermal burns usual y heal within 2?3 weeks

without risk of scarring and therefore do not require

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operation.
3rd degree (Deep Dermal Burns)

? Extend into the reticular dermis and general y wil take

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3 or more weeks to heal.

? They also blister, but the wound surface appears

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mottled pink and white

? The patient complains of discomfort and pressure

rather than pain.

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? When pressure is applied to the burn, capil aries refil

slowly

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? Partial-thickness burns that are predicted not to heal

by 3 weeks should be excised and grafted.
4th Degree (Ful Thickness)

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? Ful -thickness burns involve the entire dermis and

extend into subcutaneous tissue.

? Their appearance may be charred, leathery, firm, and

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depressed when compared to adjoining normal skin.

? These wounds are insensitive to light touch and

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pinprick.

? Non-charred ful -thickness burns can be deceptive as

they may have a mottled appearance

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? Must be excised and grafted early
SCALD INJURY
Scald Injury

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? The depth of scald injury depends on the water

temperature, the skin thickness and the duration of

contact.

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? Boiling water often causes a deep dermal burn, unless

the duration of contact is very short.

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? Soups and sauces, which are thicker in consistency, wil

remain in contact longer with the skin and invariably

cause deep dermal burns.

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? Exposed areas tend to be burned less deeply than

clothed areas.

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? Clothing retains the heat and keeps the liquid in

contact with the skin longer.

Scalds are a mosaic of dermal burns

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? A common example is a toddler who reaches

above head level and spills hot water on

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himself. His face bears a superficial burn, his

trunk burn is of indeterminate thickness, and

his skin under his diaper has a deep dermal

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burn.
Immersion Scalds

? Immersion scalds are often deep because of the

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prolonged skin exposure.

They occur in individuals who
? Cannot perceive the discomfort of prolonged

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immersion (i.e. a diabetic patient soaking his foot

in hot water)

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? Those who are not able to escape from the hot

water (i.e. young children, the elderly, or people

with physical and cognitive disabilities).

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Atypical Scalds

? Grease and cooking oils cause deep dermal and

full thickness injuries

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? Tar and asphalt are `special scald' injuries

because they have to be first removed before the

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depth of wound can be assessed

? Tar can be removed by application of petroleum-

based ointment under a dressing.

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? The dressing is changed and ointment reapplied

every 2?4 h until the tar has dissolved

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RADIATION BURN
Radiation Injuries

? Damage to biological tissue by ionizing

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radiation is due to

1) Electromagnetic radiation (e.g. X-rays and

gamma rays)

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2) Particulate radiation (e.g. alpha and beta

particles or neutrons).

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? The severity of tissue damage is determined

by the energy deposited per unit track length,

known as Linear Energy Transfer (LET).

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How to measure Radiation Injury

? Electromagnetic radiation passes through tissue

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almost unimpeded by the skin and are cal ed low

LET since little energy is left behind.

? Neutron exposure has high-LET, resulting in

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significant energy absorption within the first few

centimeters of the body.

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? Alpha and low-energy beta particles do not

penetrate the skin, and represent a hazard only

when internalized by inhalation, ingestion or

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absorption through a wound.
How to measure Radiation Injury

? The biological effect of radiation is measured by rad

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( Radiation Absorbed Dose)

? 1 Gy= 100 rad

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? Is 1Gy of X Ray = 1 Gy of Neutron?

? rem(Roentgen Equivalent Man)= dose in

rads*Quality Factor(QF)

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? QF takes into account linear energy transfer so

QF for X ray=1 & neutron=10

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? 1 (Sv) Seivert= 100 rem

? So now 1Sv of X ray= 1Sv of neutron

Incidence of radiation injury

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The majority of radiation accidents are from
1) Radiation devices such as accelerator
2) Highly radioactive sources used for industrial

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radiography.

3) Radioisotope accidents involving radioactive

materials which are unsealed, such as tritium,

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fission products, radium and free isotopes

used for diagnosis and therapy.
How does Radiation Injury Occur?

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Radiation accident is defined as

? Whole body doses >25 rem (0.25 Sv)

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? Skin doses > 600 rem (6 Sv)

? Absorbed dose > 75 rem (0.75 Sv) to other tissues

or organs from an external source

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? Internal contamination >one-half the maximum

permissible body burden (MPBB) as defined by

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the International Commission on Radiological Protection

( different for each radionuclide)

Radiation Effect

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? Ionizing radiation causes formation of free

radicles which injure DNA, nuclear and cel ular

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membrane

? Cel s are most sensitive when undergoing mitosis

so that those that divide rapidly such as bone

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marrow, skin and the gastrointestinal tract are

more susceptible to radiation damage.

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? Radiation to an organ such as brain or liver, which

has parenchymal cel s with a slow turnover rate,

results in damage to the more sensitive

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connective tissue and microcirculation.
Localized Injury-Skin

? Erythema is equivalent to a first-degree thermal

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burn and occurs in two stages.

1) Mild erythema appears within minutes or hours

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fol owing the initial exposure and subsides in 2?

3 days.

2) The second onset of erythema occurs 2?3 weeks

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after exposure and is accompanied by dry

desquamation of the epidermal keratinocytes.

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? Epilation may occur as soon as 7 days post injury.

? It is usual y temporary with doses less than 5 Gy

but may be permanent with higher doses.

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Localized Injury-Skin

? Moist desquamation is equivalent to a second-

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degree thermal burn and develops after a latent

period of about 3 weeks with a dose of 12?20 Gy.

? The latency period may be shorter with higher

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doses.

? Blisters form, which are susceptible to infection if

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not treated.

? Full-thickness skin ulceration and necrosis are

caused by doses in excess of about 25 Gy

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ARS

? Physiological effects of whole-body radiation are

described as the acute radiation syndrome (ARS).

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? Prodromal symptoms include nausea, vomiting,

diarrhea, fatigue, fever and headache.

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? There then fol ows a latent period, the duration

of which is related to the dose.

? Hematopoietic and gastrointestinal complications

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fol ow this.

ARS

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Three Sub Syndromes of ARS-

? Hematopoietic syndrome

Opportunistic infections result from the granulocytopenia and

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spontaneous bleeding results from thrombocytopenia.

? Gastrointestinal syndrome

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Epithelial damage results in loss of transport capability, bacterial

translocation with sepsis, bowel ischemia and bloody diarrhea.

? Neurovascular syndrome

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Due to endothelial injury there is release of NO and other vasodilator

mediators.

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This leads to neurological symptoms, respiratory distress,

cardiovascular collapse and death.
Treatment

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? First aid (airway, breathing , circulation)
? Irrigation with running water until Geiger Muller

counter shows minimum radiation count

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? Exposures >100 rem require full evaluation in

hospital.

? Patients with exposures >200 rem or who have

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symptoms of ARS should preferably be sent to

specialist centers with facilities to treat bone

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marrow failure.

Treatment..

? Burn wound is managed as per the depth of

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wound

? Pain is severe and can be treated by opiates

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? Radiation injury causes severe nausea and

vomiting which can be managed by

ondensetaron ( safe in children)

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? Diethylene triamine pentaacetic acid (DTPA)

and intravenous administration of DTPA for

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workers exposed to plutonium
FROSTBITE

Frostbite

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? Traumatic injury caused by the failure of normal

protective mechanisms against the thermal

environment, resulting in local tissue

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temperatures fal ing below freezing

? At risk populations are

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Mental y il

Homeless

Alcohol and Drug Intoxications

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Wilderness activities( Treking /Camping)

? Acral areas are typical y affected
Pathophysiology

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Direct Cellular Damage

? Intracel ular formation of Ice crystals

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D/t rapid cooling and leads to severe cel injury

Histamine release occurs which causes flushing and

formation of blisters

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? Extracel ular formation of Ice crystals

D/t slow cooling and leads to injury to cel

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membrane

Leads to gradual dehydration of cel as osmotic

imbalance occurs

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Pathophysiology

Microvascular Occlusion

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? Cold injury causes vasoconstriction

? With rewarming capil ary blood flow resumes but

with presence of microemboli

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? Certain areas close to injury wil have complete

cessation of blood flow within 20 min

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? The remaining area is at risk due to endothelial

injury and accumulation of inflamatory mediators

similar to Jackson Model

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Classification

? First-degree injury

It is superficial, without formation of vesicles or blebs.

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There may initial y be an area of pal or with surrounding erythema.

? Second-degree

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Partial dermal involvement with general y favourable prognosis

Associated with light-colored blisters and subsequent epidermal

sloughings.

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? Third-degree

Has dark or hemorrhagic blisters that evolve into thick, black eschar

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over 1?2 weeks.

? Fourth-degree

Injury involves bone, tendon or muscle and uniformly results in tissue

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loss.

Management

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? Rewarming in the field should not be pursued

unless the ability to maintain the affected tissue

in a thawed state is certain

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? Injured areas should be mechanical y protected

from trauma because they are typical y insensate

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and are at high risk for further injury

? Management of Hypothermia (Temp<32) should

be started before Management of frostbite

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Management

? Rewarming is done with the help of water

bath at temperatures of 40- 42oC

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? Duration of rewarming is usually 30 min

? Clinically until sensation returns and flushing

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in the most distal part of tissue

? Blisters may be debrided as they help in

assessment of the deeper tissue

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? Blisters contain high amount of PGF2Aalpha

&TXA2

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Non Surgical Management

? Systemic NSAIDs and topical aloe vera to

address the inflammatory chemokines

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coupled with systemic penicillin as prophylaxis

against Gram-positive infection

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? Pentoxifylline improves red blood cell

flexibility, which may limit microvascular

sludging and thereby diminish thrombus

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formation in small vessels.
Role of Thrombolytics

? Use of Thrombolytic therapy can enhance survival

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of digits

? t-PA only appears to be efficacious within 24

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hours of thaw, meaning that this may not be an

option for patients who are injured in extremely

remote environments.

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? Additional y, although digit salvage has been

improved with thrombolytics, the actual long-

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term functional results of this salvage have not

been documented.

HBO

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? Studies of hyperbaric oxygen are limited but

have some of the most promising functional

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results of an adjunctive therapy for frostbite.

? One of the early documented uses of HBO for

therapy in frostbite involved four Alpine

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mountaineers, all of whom presented 10 or

more days following injury and all of whom

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demonstrated good tissue preservation with

HBO
Management

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? Prevalent clinical practice remains to time

surgery anywhere from 4 weeks to 3 months

following injury, once tissues have clearly

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demarcated to an experienced clinical eye.

CHEMICAL BURNS
Chemical Burns

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? The 3D structure of biological proteins depends

on hydrogen bonding and weak Van der wal s

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forces

? Chemicals substances can destabilize a protein

and alter its function by changing the pH or

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dissolving the lipids thus altering the hydrogen

bonding

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? Thermal injury also occurs by breaking the

hydrogen bonds and causing protein

denaturation

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Severity of Chemical Burn

? Quantity of Chemical Agent

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? Concentration of Chemicals

? Manner and Duration of skin contact

? Extent of penetration

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? Mechanism of action
Mechanism Of Action

1.Reduction: Act by binding free electrons in tissue proteins, causing

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denaturation.

Eg Alkyl mercuric compounds, Ferrous iron, and Sulphite compounds.

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2. Oxidation: Oxidizing agents are oxidized on contact with tissue

proteins. Byproducts are often toxic and continue to react with the

surrounding tissue.

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Eg Sodium hypochlorite, Potassium permanganate, Peroxide.

3. Corrosive agents: Corrosive substances denature tissue proteins on

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contact and form eschar and a shal ow ulcer.

Eg. Phenols, Cresols, White phosphorus, sodium metals, lyes,

sulphuric acid, and hydrochloric acid, Alkalis .

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Mechanism Of Action

4. Protoplasmic poisons: These agents produce their

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effects by binding or inhibiting calcium or other organic ions necessary

for tissue viability and function.

Eg. Acetic acid, Formic acid, Oxalic, Hydrofluoric, and hydrazoic acid.

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5. Vesicants: Vesicant agents produce ischemia with necrosis at the

site of contact.

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Eg. Mustard gas (sulphur and nitrogen), and Lewisite.

6. Desiccants: cause damage by dehydrating tissues and exothermic

reactions causing the release of heat into the tissue.

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Eg. Calcium sulphate , Silica gel
Alkalis more dangerous than Acids

? Acids cause coagulation necrosis with

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precipitation of protein, whereas the reaction

to alkali is `liquefaction' necrosis allowing the

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alkali to penetrate deeper into the injured

tissue.

? The presence of hydroxyl ions within these

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tissues increases their solubility, allowing

alkaline proteinates to form when the alkalis

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dissolve the proteins of the tissues.

Treatment

Removal of the Chemical

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? This requires removal of al contaminated

clothing and copious irrigation.

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? Irrigation of chemical burns requires protection

of healthcare providers to prevent additional

injuries.

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? Wounds should not be irrigated by placing the

patient into a tub, thereby containing the

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chemical and spreading the injurious material.

? Irrigation should be large volume and drained `to

the floor,' or out of an appropriate drain

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Treatment

? Do not use neutralizing agents
? They cause exothermic reactions causing

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further thermal damage

? Protect from hypothermia as unwarmed

lavage fluid is being used

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? Most of these patients require excision with

grafting as the chemical burn wound tend to

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be deeper than they appear

Management of Hydrofluoric Acid

Burn

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? HF is used as cleaning agent in petroleum

industry, for glass etching and removal of rust

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? Acid component causes coagulation necrosis

? Fluoride ion then gains a portal of entry that

chelates calcium and magnesium, resulting in

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hypocalcemia and hypomagnesemia.

? Efflux of intracellular calcium down

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concentration gradient occurs with resultant

cell death.
HF Burn Management.....

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? Death is mostly due to systemic toxicity
? When concentration of exposure is >20% or

duration of exposure is prolonged Calcium

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gluconate injections are to be given topically,

subcutaneously and intra Arterially

? 10% Calcium Gluconate 0.5ml/cm2

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? 10 ml of 10% Calcium Gluconate in D5 to be

infused over 2-4 hrs

Vesicant Chemical Warfare agents

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? Lewisite, Mustard gas ? Affect all epithelial

tissue including eyes and respiratory

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epithelium

? Cause burning in eyes & throat along with

blister formation on skin

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? Dimercaprol is used as Cheliating agent for

Lewisite

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? Sodium thiosulfate & N-Acetylcysteine for

management of Mustard gas poisoning
ELECTRIC BURN

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Electric Burn

Pathophysiology
? High Voltage burns (>1000V) are associated

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with deep extension and tissue damage like

crush injury

? Low Voltage(<1000V) cause injury mostly

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around the area of contact point

? Current = Voltage / Resistance
Pathophysiology

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Burn severity is determined by
? voltage
? current (amperage),
? type of current (alternating or direct),

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? path of current flow,
? duration of contact,
? resistance at the point of contact

Pathophysiology...

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? Alternating current causes tetanic muscle

contractions, which may either throw victims

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away from the contact or draw them into

continued contact with the electrical source ? the

`no-let-go' phenomenon

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? This phenomenon occurs because both flexors

and extensors of the forearm are stimulated by

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current flow.

? However, the muscles of flexion are stronger,

making the person unable to let go voluntarily

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Pathophysiology...

Electrical Injury is divided into

1) Joule Heating (J) =I2(Current)?R(Resistance)

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? Tissue resistance is from lowest to highest in

nerves<blood vessels< muscle< skin< tendon< fat

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< bone

? Severity of injury is inversely proportional to the

cross-sectional area of the body part involved.

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? Thus the most severe injuries are often seen at

the wrist and ankle

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Pathophysiology...

2) Electroporation
? It is the formation of aqueous pores in lipid

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bilayers exposed to a supraphysiologic

electrical field.

? The formation of these pores allows calcium

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influx into the cytoplasm and triggers a

subsequent cascade leading to apoptosis
Pathophysiology...

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3) Electroconformational denaturation
? The transmembrane proteins change in

polarity of amino acids in response to

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exposure to electrical fields.

? Voltage-gated channel proteins were found to

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change their conductance and ion specificity

after exposure to a powerful pulsed field

Pathophysiology...

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? Low voltage alternating current injury is

usually localized to the points of contact,

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? On prolonged contact, tissue damage may

extend into deep tissues with little lateral

extension, as seen in high-voltage wounds.

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? These wounds are treated by excision to viable

tissue and appropriate coverage based on

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wound depth and location.
Management

? Besides the ATLS guidelines 3 points are to be

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considered

1) Identify patients who wil require ECG

monitoring

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2) Fluid therapy for Myoglobinurea

3) Identify patients at risk for compartment

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syndrome

ECG Abnormality

? Due to skeletal muscle injury along with injury

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to myocardium it is problematic to use cardiac

biomarkers such as CK-MB

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? Non-specific ST-T changes are the most

common ECG abnormality and atrial

fibrillation is the most common dysrhythmia

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? Low voltage injury patients normally do no not

require ECG monitoring
Criteria for 24 ECG monitoring

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(1) Loss of consciousness

(2) ECG abnormality

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(3) Documented dysrhythmia either before or

after admission to the emergency room

(4) CPR in the field.

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Myoglobinurea

? Light pink urine indicates myogloninurea
? Recussitation with RL to maintain urine

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output>100ml/hr

? Alkalinization of the urine with a sodium

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bicarbonate

? Osmotic Diuresis with Mannitol
Compartment Syndrome

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? Damaged muscle, and swel ing in the investing fascia of

the extremity, may increase pressures to the point

where muscle blood flow is compromised.

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? Loss of pulses is one of the last signs of a compartment

syndrome, unlike the early loss of pulses occurring in a

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circumferential y burned extremity requiring

escharotomy.

? A high index of suspicion is paramount for an early

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diagnosis, usual y by serial examinations.

? Compartment pressure measurement is general y not

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necessary and may even be misleading

Compartment Syndrome

? Four compartment fasciotomies of the lower

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leg

? Anterior as well as posterior fasciotomies of

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the upper extremity are performed in the

operating room under general anesthesia.

? Upper extremity decompression will generally

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always include a carpal tunnel release, as this

is usually the location of the most severe

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injury.
Low Voltage Injuries

? Burns of the oral cavity are the most common

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type of serious electrical burn in young children.

? Injuries involving only the oral commissure are

almost never excised, as the extent of injury is

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difficult to predict

? Gentle stretching and the use of oral splints gives

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good cosmetic and functional results in most

patients, with reconstructive surgery being

reserved for the remainder

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Low Voltage Injuries

? Most cases require excision and grafting at the

point of contact only

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? Burns to the fingers are also mostly seen in

children as they insert their fingers in power

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sockets

Problem Areas

? Scalp Injury where loss of outer table has occurred

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? Costal chondritis is the most frequent complication of

deep chest wal burns, often becoming a source of long

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-term morbidity, requiring multiple debridements.

? Abdominal wounds provide the potential for internal

injuries, both directly under contact points and

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remotely as the result of late ischemic necrosis.

? Changes in their abdominal examination and/or

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feeding tolerance mandates investigation &

laparotomy.

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Lightning Strike..

? Neurologic complications are relatively common

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and include unconsciousness, seizures,

paresthesias and paralysis, which may develop

over several days after injury

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? Surgical y treatable lesions, including epidural,

subdural and intracerebral hematomas, may

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occur, mandating a high index of suspicion for

altered levels of consciousness.

? Prognosis of many lightning-caused neurologic

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injuries is general y better than for other types of

traumatic cause

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Lightning Strike

? The pathognomonic sign of a lightning strike is a dendritic,

fern-like branching erythematous pattern on the skin.

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? Lichtenberg figures (also known as keraunographic

markings), consist of extravasation of blood in the

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subcutaneous tissue which appears within an hour of injury

and fades rapidly, much like a wheal and flare reaction.

? Full-thickness isolated burns on the tips of the toes have

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also been reported as characteristic.

? Lightning may cause both respiratory and cardiac stand-

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still, for which CPR is especially effective when promptly

initiated.
Thank You