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

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 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

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

and hydraulic conductivity of the capil ary wal

Pc is the capil ary hydrostatic pressure

Pif is the interstitial fluid hydrostatic pressure

p is the colloid osmotic pressure of plasma

if is the colloid osmotic pressure of interstitial fluid

is the osmotic reflection coefficient.

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

increased Jv
Landis Starling Equation
Skin Biology & Response to Burns

Epidermis

? Derived from ectoderm so is capable of

regenerative healing.

? Keratinocytes proliferate from dermal

appendages leading to re-epithelialization.

? Depleted melanocytes regenerate slowly

leading to pigmentary changes

? Loss of anchoring collagen fibrils (type7) leads

to blister formation
Skin Biology & Response to Burns

Dermis

? Superficial papil ary

? Deep reticular

? Fibroblasts produce col agen fibrils and elastic

fibers

? Dermal appendages lined by keratinocyte derived

epidermal cel s

? Contain capil ary plexus and sensory nerves

? Derived from mesoderm so heal by scarring

Patho-phyisological changes

Jackson Zones
? Temperature and duration of contact have a

synergestic effect

? 1s at 69OC / 1 hour at 45oC
? Zone of coagulation? Centre of the wound
? 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
? Protection of zone of stasis is achieved with

adequate fluid resuscitation, avoidance of

vasoconstrictors and prevention of infection

Depth of Burn

1st Degree
? Burns involving only the epidermis.
? Erythematous and very painful but do not

form blisters.

? Sunburns fit this category of superficial,

epidermal injury.

? Within 3?4 days, the dead epidermis sloughs

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

? Extend into the papil ary dermis and characteristical y

form blisters.

? Appearance is pink, wet and hypersensitive to touch.

? Painful as uncovering the wound al ows currents of air

to pass over it.

? These wounds blanch with pressure as the blood flow

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

operation.
3rd degree (Deep Dermal Burns)

? Extend into the reticular dermis and general y wil take

3 or more weeks to heal.

? They also blister, but the wound surface appears

mottled pink and white

? The patient complains of discomfort and pressure

rather than pain.

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

slowly

? Partial-thickness burns that are predicted not to heal

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

? Ful -thickness burns involve the entire dermis and

extend into subcutaneous tissue.

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

depressed when compared to adjoining normal skin.

? These wounds are insensitive to light touch and

pinprick.

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

they may have a mottled appearance

? Must be excised and grafted early
SCALD INJURY
Scald Injury

? The depth of scald injury depends on the water

temperature, the skin thickness and the duration of

contact.

? Boiling water often causes a deep dermal burn, unless

the duration of contact is very short.

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

remain in contact longer with the skin and invariably

cause deep dermal burns.

? Exposed areas tend to be burned less deeply than

clothed areas.

? Clothing retains the heat and keeps the liquid in

contact with the skin longer.

Scalds are a mosaic of dermal burns

? A common example is a toddler who reaches

above head level and spills hot water on

himself. His face bears a superficial burn, his

trunk burn is of indeterminate thickness, and

his skin under his diaper has a deep dermal

burn.
Immersion Scalds

? Immersion scalds are often deep because of the

prolonged skin exposure.

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

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

in hot water)

? Those who are not able to escape from the hot

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

with physical and cognitive disabilities).
Atypical Scalds

? Grease and cooking oils cause deep dermal and

full thickness injuries

? Tar and asphalt are `special scald' injuries

because they have to be first removed before the

depth of wound can be assessed

? Tar can be removed by application of petroleum-

based ointment under a dressing.

? The dressing is changed and ointment reapplied

every 2?4 h until the tar has dissolved

RADIATION BURN
Radiation Injuries

? Damage to biological tissue by ionizing

radiation is due to

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

gamma rays)

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

particles or neutrons).

? The severity of tissue damage is determined

by the energy deposited per unit track length,

known as Linear Energy Transfer (LET).

How to measure Radiation Injury

? Electromagnetic radiation passes through tissue

almost unimpeded by the skin and are cal ed low

LET since little energy is left behind.

? Neutron exposure has high-LET, resulting in

significant energy absorption within the first few

centimeters of the body.

? Alpha and low-energy beta particles do not

penetrate the skin, and represent a hazard only

when internalized by inhalation, ingestion or

absorption through a wound.
How to measure Radiation Injury

? The biological effect of radiation is measured by rad

( Radiation Absorbed Dose)

? 1 Gy= 100 rad

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

? rem(Roentgen Equivalent Man)= dose in

rads*Quality Factor(QF)

? QF takes into account linear energy transfer so

QF for X ray=1 & neutron=10

? 1 (Sv) Seivert= 100 rem

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

Incidence of radiation injury

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

radiography.

3) Radioisotope accidents involving radioactive

materials which are unsealed, such as tritium,

fission products, radium and free isotopes

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

Radiation accident is defined as

? Whole body doses >25 rem (0.25 Sv)

? Skin doses > 600 rem (6 Sv)

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

or organs from an external source

? Internal contamination >one-half the maximum

permissible body burden (MPBB) as defined by

the International Commission on Radiological Protection

( different for each radionuclide)

Radiation Effect

? Ionizing radiation causes formation of free

radicles which injure DNA, nuclear and cel ular

membrane

? Cel s are most sensitive when undergoing mitosis

so that those that divide rapidly such as bone

marrow, skin and the gastrointestinal tract are

more susceptible to radiation damage.

? 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

connective tissue and microcirculation.
Localized Injury-Skin

? Erythema is equivalent to a first-degree thermal

burn and occurs in two stages.

1) Mild erythema appears within minutes or hours

fol owing the initial exposure and subsides in 2?

3 days.

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

after exposure and is accompanied by dry

desquamation of the epidermal keratinocytes.

? 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.

Localized Injury-Skin

? Moist desquamation is equivalent to a second-

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

doses.

? Blisters form, which are susceptible to infection if

not treated.

? Full-thickness skin ulceration and necrosis are

caused by doses in excess of about 25 Gy
ARS

? Physiological effects of whole-body radiation are

described as the acute radiation syndrome (ARS).

? Prodromal symptoms include nausea, vomiting,

diarrhea, fatigue, fever and headache.

? There then fol ows a latent period, the duration

of which is related to the dose.

? Hematopoietic and gastrointestinal complications

fol ow this.

ARS

Three Sub Syndromes of ARS-

? Hematopoietic syndrome

Opportunistic infections result from the granulocytopenia and

spontaneous bleeding results from thrombocytopenia.

? Gastrointestinal syndrome

Epithelial damage results in loss of transport capability, bacterial

translocation with sepsis, bowel ischemia and bloody diarrhea.

? Neurovascular syndrome

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

mediators.

This leads to neurological symptoms, respiratory distress,

cardiovascular collapse and death.
Treatment

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

counter shows minimum radiation count

? Exposures >100 rem require full evaluation in

hospital.

? Patients with exposures >200 rem or who have

symptoms of ARS should preferably be sent to

specialist centers with facilities to treat bone

marrow failure.

Treatment..

? Burn wound is managed as per the depth of

wound

? Pain is severe and can be treated by opiates

? Radiation injury causes severe nausea and

vomiting which can be managed by

ondensetaron ( safe in children)

? Diethylene triamine pentaacetic acid (DTPA)

and intravenous administration of DTPA for

workers exposed to plutonium
FROSTBITE

Frostbite

? Traumatic injury caused by the failure of normal

protective mechanisms against the thermal

environment, resulting in local tissue

temperatures fal ing below freezing

? At risk populations are

Mental y il

Homeless

Alcohol and Drug Intoxications

Wilderness activities( Treking /Camping)

? Acral areas are typical y affected
Pathophysiology

Direct Cellular Damage

? Intracel ular formation of Ice crystals

D/t rapid cooling and leads to severe cel injury

Histamine release occurs which causes flushing and

formation of blisters

? Extracel ular formation of Ice crystals

D/t slow cooling and leads to injury to cel

membrane

Leads to gradual dehydration of cel as osmotic

imbalance occurs

Pathophysiology

Microvascular Occlusion

? Cold injury causes vasoconstriction

? With rewarming capil ary blood flow resumes but

with presence of microemboli

? Certain areas close to injury wil have complete

cessation of blood flow within 20 min

? The remaining area is at risk due to endothelial

injury and accumulation of inflamatory mediators

similar to Jackson Model
Classification

? First-degree injury

It is superficial, without formation of vesicles or blebs.

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

? Second-degree

Partial dermal involvement with general y favourable prognosis

Associated with light-colored blisters and subsequent epidermal

sloughings.

? Third-degree

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

over 1?2 weeks.

? Fourth-degree

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

loss.

Management

? Rewarming in the field should not be pursued

unless the ability to maintain the affected tissue

in a thawed state is certain

? Injured areas should be mechanical y protected

from trauma because they are typical y insensate

and are at high risk for further injury

? Management of Hypothermia (Temp<32) should

be started before Management of frostbite
Management

? Rewarming is done with the help of water

bath at temperatures of 40- 42oC

? Duration of rewarming is usually 30 min

? Clinically until sensation returns and flushing

in the most distal part of tissue

? Blisters may be debrided as they help in

assessment of the deeper tissue

? Blisters contain high amount of PGF2Aalpha

&TXA2

Non Surgical Management

? Systemic NSAIDs and topical aloe vera to

address the inflammatory chemokines

coupled with systemic penicillin as prophylaxis

against Gram-positive infection

? Pentoxifylline improves red blood cell

flexibility, which may limit microvascular

sludging and thereby diminish thrombus

formation in small vessels.
Role of Thrombolytics

? Use of Thrombolytic therapy can enhance survival

of digits

? t-PA only appears to be efficacious within 24

hours of thaw, meaning that this may not be an

option for patients who are injured in extremely

remote environments.

? Additional y, although digit salvage has been

improved with thrombolytics, the actual long-

term functional results of this salvage have not

been documented.

HBO

? Studies of hyperbaric oxygen are limited but

have some of the most promising functional

results of an adjunctive therapy for frostbite.

? One of the early documented uses of HBO for

therapy in frostbite involved four Alpine

mountaineers, all of whom presented 10 or

more days following injury and all of whom

demonstrated good tissue preservation with

HBO
Management

? Prevalent clinical practice remains to time

surgery anywhere from 4 weeks to 3 months

following injury, once tissues have clearly

demarcated to an experienced clinical eye.

CHEMICAL BURNS
Chemical Burns

? The 3D structure of biological proteins depends

on hydrogen bonding and weak Van der wal s

forces

? Chemicals substances can destabilize a protein

and alter its function by changing the pH or

dissolving the lipids thus altering the hydrogen

bonding

? Thermal injury also occurs by breaking the

hydrogen bonds and causing protein

denaturation

Severity of Chemical Burn

? Quantity of Chemical Agent

? Concentration of Chemicals

? Manner and Duration of skin contact

? Extent of penetration

? Mechanism of action
Mechanism Of Action

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

denaturation.

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

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

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

surrounding tissue.

Eg Sodium hypochlorite, Potassium permanganate, Peroxide.

3. Corrosive agents: Corrosive substances denature tissue proteins on

contact and form eschar and a shal ow ulcer.

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

sulphuric acid, and hydrochloric acid, Alkalis .

Mechanism Of Action

4. Protoplasmic poisons: These agents produce their

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.

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

site of contact.

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.

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

? Acids cause coagulation necrosis with

precipitation of protein, whereas the reaction

to alkali is `liquefaction' necrosis allowing the

alkali to penetrate deeper into the injured

tissue.

? The presence of hydroxyl ions within these

tissues increases their solubility, allowing

alkaline proteinates to form when the alkalis

dissolve the proteins of the tissues.

Treatment

Removal of the Chemical

? This requires removal of al contaminated

clothing and copious irrigation.

? Irrigation of chemical burns requires protection

of healthcare providers to prevent additional

injuries.

? Wounds should not be irrigated by placing the

patient into a tub, thereby containing the

chemical and spreading the injurious material.

? Irrigation should be large volume and drained `to

the floor,' or out of an appropriate drain
Treatment

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

further thermal damage

? Protect from hypothermia as unwarmed

lavage fluid is being used

? Most of these patients require excision with

grafting as the chemical burn wound tend to

be deeper than they appear

Management of Hydrofluoric Acid

Burn

? HF is used as cleaning agent in petroleum

industry, for glass etching and removal of rust

? Acid component causes coagulation necrosis

? Fluoride ion then gains a portal of entry that

chelates calcium and magnesium, resulting in

hypocalcemia and hypomagnesemia.

? Efflux of intracellular calcium down

concentration gradient occurs with resultant

cell death.
HF Burn Management.....

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

duration of exposure is prolonged Calcium

gluconate injections are to be given topically,

subcutaneously and intra Arterially

? 10% Calcium Gluconate 0.5ml/cm2
? 10 ml of 10% Calcium Gluconate in D5 to be

infused over 2-4 hrs

Vesicant Chemical Warfare agents

? Lewisite, Mustard gas ? Affect all epithelial

tissue including eyes and respiratory

epithelium

? Cause burning in eyes & throat along with

blister formation on skin

? Dimercaprol is used as Cheliating agent for

Lewisite

? Sodium thiosulfate & N-Acetylcysteine for

management of Mustard gas poisoning
ELECTRIC BURN

Electric Burn

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

with deep extension and tissue damage like

crush injury

? Low Voltage(<1000V) cause injury mostly

around the area of contact point

? Current = Voltage / Resistance
Pathophysiology

Burn severity is determined by
? voltage
? current (amperage),
? type of current (alternating or direct),
? path of current flow,
? duration of contact,
? resistance at the point of contact

Pathophysiology...

? Alternating current causes tetanic muscle

contractions, which may either throw victims

away from the contact or draw them into

continued contact with the electrical source ? the

`no-let-go' phenomenon

? This phenomenon occurs because both flexors

and extensors of the forearm are stimulated by

current flow.

? However, the muscles of flexion are stronger,

making the person unable to let go voluntarily
Pathophysiology...

Electrical Injury is divided into

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

? Tissue resistance is from lowest to highest in

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

< bone

? Severity of injury is inversely proportional to the

cross-sectional area of the body part involved.

? Thus the most severe injuries are often seen at

the wrist and ankle

Pathophysiology...

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

bilayers exposed to a supraphysiologic

electrical field.

? The formation of these pores allows calcium

influx into the cytoplasm and triggers a

subsequent cascade leading to apoptosis
Pathophysiology...

3) Electroconformational denaturation
? The transmembrane proteins change in

polarity of amino acids in response to

exposure to electrical fields.

? Voltage-gated channel proteins were found to

change their conductance and ion specificity

after exposure to a powerful pulsed field

Pathophysiology...

? Low voltage alternating current injury is

usually localized to the points of contact,

? On prolonged contact, tissue damage may

extend into deep tissues with little lateral

extension, as seen in high-voltage wounds.

? These wounds are treated by excision to viable

tissue and appropriate coverage based on

wound depth and location.
Management

? Besides the ATLS guidelines 3 points are to be

considered

1) Identify patients who wil require ECG

monitoring

2) Fluid therapy for Myoglobinurea

3) Identify patients at risk for compartment

syndrome

ECG Abnormality

? Due to skeletal muscle injury along with injury

to myocardium it is problematic to use cardiac

biomarkers such as CK-MB

? Non-specific ST-T changes are the most

common ECG abnormality and atrial

fibrillation is the most common dysrhythmia

? Low voltage injury patients normally do no not

require ECG monitoring
Criteria for 24 ECG monitoring

(1) Loss of consciousness

(2) ECG abnormality

(3) Documented dysrhythmia either before or

after admission to the emergency room

(4) CPR in the field.

Myoglobinurea

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

output>100ml/hr

? Alkalinization of the urine with a sodium

bicarbonate

? Osmotic Diuresis with Mannitol
Compartment Syndrome

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

the extremity, may increase pressures to the point

where muscle blood flow is compromised.

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

syndrome, unlike the early loss of pulses occurring in a

circumferential y burned extremity requiring

escharotomy.

? A high index of suspicion is paramount for an early

diagnosis, usual y by serial examinations.

? Compartment pressure measurement is general y not

necessary and may even be misleading

Compartment Syndrome

? Four compartment fasciotomies of the lower

leg

? Anterior as well as posterior fasciotomies of

the upper extremity are performed in the

operating room under general anesthesia.

? Upper extremity decompression will generally

always include a carpal tunnel release, as this

is usually the location of the most severe

injury.
Low Voltage Injuries

? Burns of the oral cavity are the most common

type of serious electrical burn in young children.

? Injuries involving only the oral commissure are

almost never excised, as the extent of injury is

difficult to predict

? Gentle stretching and the use of oral splints gives

good cosmetic and functional results in most

patients, with reconstructive surgery being

reserved for the remainder
Low Voltage Injuries

? Most cases require excision and grafting at the

point of contact only

? Burns to the fingers are also mostly seen in

children as they insert their fingers in power

sockets

Problem Areas

? Scalp Injury where loss of outer table has occurred

? Costal chondritis is the most frequent complication of

deep chest wal burns, often becoming a source of long

-term morbidity, requiring multiple debridements.

? Abdominal wounds provide the potential for internal

injuries, both directly under contact points and

remotely as the result of late ischemic necrosis.

? Changes in their abdominal examination and/or

feeding tolerance mandates investigation &

laparotomy.



Lightning Strike..

? Neurologic complications are relatively common

and include unconsciousness, seizures,

paresthesias and paralysis, which may develop

over several days after injury

? Surgical y treatable lesions, including epidural,

subdural and intracerebral hematomas, may

occur, mandating a high index of suspicion for

altered levels of consciousness.

? Prognosis of many lightning-caused neurologic

injuries is general y better than for other types of

traumatic cause

Lightning Strike

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

fern-like branching erythematous pattern on the skin.

? Lichtenberg figures (also known as keraunographic

markings), consist of extravasation of blood in the

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

also been reported as characteristic.

? Lightning may cause both respiratory and cardiac stand-

still, for which CPR is especially effective when promptly

initiated.
Thank You