Literature Review

TWAK SHAREERAM

The description of the anatomical structure of twak, the details about the
layers, thickness are variable in various texts in Ayurveda.

Synonym--- twak, twacha, charma.

TWACHA UTPATTI (EMBRYOLOGY OF SKIN)

 “TASYA KHALWEBA PRABHRUTTASYA SUKRASHONITASYA

ABHIPACHYAMANASYAKHIRASYEVA SANTANIKA: SAPTA
TWACHO BHABANTI”. (Su.Sa.4/4)
 Sushruta had given the picture of development of cream, while explaining the
seven layer of skin. As a layer of cream develops over boiled milk, in a
similar style a layer twacha to be develops from fertilisation of ovum.
 According to Charaka, six layer of twacha are formed from mamsa
dhatu, and is a matruja bhaba.
 According to bagbhatta,twacha is formed from rakta, after paka it
gets dried and formed skin.(AH.Sa.3/8)
DOSHA
Twacha is one of the sites of vata and pitta. It is considered to be
adhisthana of sparsanendriya. Bhrajaka pitta present in twacha responsible
for reflecting varna and prabha. Snigdhata, mriduta sthirata are due to kapha.
DHATU
RASA –
Twak sara purusa is also considered as rasa sara purusa.
RAKTA-
Varna prasadana and mamsa prusthi.
MAMSA –
Twak is upadhatu of mamsa.
MALA-
Sweda is the mala of meda dhatu and is excreted by twacha.

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DIFFERENT LAYERS OF TWACHA ACCORDING TO DIFFERENT ACHARYAS:

There are some different opinions regarding different layer of twacha

according to different acharyas. These are as below-

SUSHRUTA CHARAKA ARUNADAT SARANGDHARA BHELA

TA
Avabhasini Udakadhara Bhasini Avabhasini Udakadhar
a
Lohita Asrukdhara Lohita Lohita Asrukdhara
Sweta 3rd Sweta Sweta 3rd
Tamra 4th Tamra Tamra 4th
Rohini 5th Rohini Rohini 5th
Vedini 6th Vedini Vedini 6th
Mamsadhara ---- Mamsadhara Sthula ----

LAYERS DISEASES LAYERS THICKNESS DISEASES

CHARAKA SUSHRUTA
Udakadhara ---- Avabhasini 1/18th of vrihi Sidhma, Padmakantaka

Asrukdhara ---- Lohita 1/16th of vrihi Tilakalaka, Vyanga,

Nyachha

3rd Sidhma, Sweta 1/12th of vrihi Charmadala, Ajagalika,

kilasa Mashaka
4th Dadru, Tamra 1/8th of vrihi Kilasa, Kustha
kustha

5th Alaji, Rohini 1/5th of vrihi Kustha, Visharpa

vidradhi

6th Arunshi Vedini 1 vrihi Granthi, Apachi, Arbuda,

Sleepada, Galaganda

---- ---- Mamsadhara 2 vrihi Bhagandara, Vidradhi,

Arsha

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Structure of skin

Skin is the largest organ of the body in both surface area about 20 square feet
and weight 12-15% of total body weight. Skin forms about 8% of the total body mass.
Its thickness ranges from 1.5 to 4mm according to its state of maturation, ageing and
regional specialization. The skin is thick about 5mm in sole of the foot, palm and
interscapular region. In the other area of body, the skin is thin.

Skin is the first line of defence against disease and bacterial invasion. Joseph
Lister said that, skin is also called as the best dressing of our body.

Layers of skin:-

A. Epidermis
B. Dermis
C. Subcutaneous layer

A.EPIDERMIS –

 In Latin word ‘epi’ means over/upon. It is the outermost layer of skin.it is

formed by stratified squamous (flattened) epithelium.
 The most important feature is that, it does not have blood vessels. Thickness
on palms and soles about 0.8-1.4mm and thinnest layer is epithelial layer of
tympanic membrane of ear. Epidermis mainly composed of keratinocytes.
 Its layers are made of mostly dead cells. Most of the cells of the epidermis
undergo mitotic cell division.

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 As the new cells are produced, they push older cells to the surface of the skin
and the older cells become flattened, lose their cellular contents and begin
making KERATIN.
 Eventually the keratin producing cells i.e. Keratinocytes which die and form a
tough, flexible water proof covering on the surface of the skin. The dead cells
shed or washed once in 14-28 days.

LAYERS OF EPIDERMIS:-

(From superficial to most deep)

1. Stratum corneum (Cornified layer)

2. Stratum lucidum (Clear layer)
3. Stratum granulosum (Granular layer)
4. Stratum spinosum (Spinous/prickly cell layer)
5. Stratum basale (Basal layer)

 The last three layers are metabolically active through which cells are passing
and change their form and progressively differentiate. The most superficial
layer undergoes keratinisation or cornification.
 The cellular progression from the basal layer to the skin surface takes 30 days.
The bricklike shape of keratinocytes is provided by a cytoskeleton made of
keratin intermediate filaments.

1. STRATUM CORNEUM –
 It is the outermost layer of epidermis. It is otherwise called as horny layer. It
contains cells that are completely filled with keratin and melanin units.
 Skin colour is only due to amount of melanin pigment. The melanocytes can
produce and transfer to the keratinocytes. It is called tanning of the skin due to
increased melanin production. The colour of skin reflected in this layer. Others
cells in the epidermis layer are melanocytes, Langerhans ‘cell, Markel cells.
Melanocytes are dendritic cells that distribute melanin pigment to
melanosomes and give the skin to its colour.
 The Langerhans’ cells are dendritic in nature and are originate from bone
marrow. These cells are antigen- presenting cells.
 Markel cells are derived from keratinocytes and play a role in mechano-
sensory receptors in response to touch.
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2. STRATUM LUCIDUM –
 It is called the clear layer as it is highly refractive. It contains droplets of
eledin (clear intracellular protein) is transformed to keratin. Disease which
occurs due to localised overgrowth of melanocytes and melanin.
 This layer looks like a homogenous translucent zone.

3. STRATUM GRANULOSUM –

 It is a thin layer with 2-5 rows of flattened rhomboid cells. It contains

darkly stained protein granules Keratohyaline (it is a protein structure that
involve in keratinization) converts into keratin.

4. STRATUM SPINOSUM -

 Stratum spinosum contain keratinocytes with bundle of ton filaments

(cytoplasmic protein).
 Melanocytes and Langerhans’ cells are present in this layer. At the sites of
allergic dermatitis Langerhans’ cells are taken up antigen they can react by
generation of antibodies.
 It is also called as prickly cell layer because the cell possess spine like
protoplasmic projection.

5. STRATUM BASALE –

 It is the deeper layer of epidermis adjacent to dermis. It contains tactile

receptors and free nerve endings that give rise to sensation of pain,
warmth, tickling etc. The sensory receptors are responsible for pain.
 It is also called as papillary dermis. Melanocytes are scattered between
keratinocytes produce pigment called melanin.

B. DERMIS -

 It is a layer of skin between epidermis and subcutaneous layer. On average

thick 1.0-2.0mm. It is a connective tissue layer.

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 It contains thin dermal papillae (finger prints), sensory receptors, nerve cell
processes, Blood vessels, Hair follicles, Glands.
 It consists of Irregular dense connective tissues. The dermis interlaced with
sensory nerve ending that mediate sensation of pain, heat, touch etc.
 This is also called the ‘true skin’ because most of the vital functions of the
skin are performed here.

Layers of dermis:

a. Superficial Papillary layer.

b. Deeper Reticular layer.
a. Superficial papillary layer –
 The papillary layer contains thin arrangement of collagen fibres and lower
is thicker. These layers have some pigment containing cell known as
chromatophores.
 Dermal papillae are finger like projection present in this layer. Each
papilla contains plexus of capillaries and lymphatics, which are oriented
perpendicular to the skin surface. These papillae are surrounded by rete
ridges, extending from the epidermis.
b. Deeper Reticular layer –
 The reticular layer composed of irregular connective tissue.
 Its name from dense concentration of collagenous, elastic and reticular
fibres. These fibres are found around hair bulbs, sweat gland and sebaceous
glands.
 This layer also consists of mast cell, nerve endings, lymphatic, epidermal
appendages and fibroblasts.
 It is a loose connective tissue, which connect the skin with the internal
structures of the body. Smooth muscles are present called as erector pili
around the hair follicle.

APPENDAGES OF THE SKIN –

 Hair follicles, hairs, nails, sweat gland, sebaceous gland, mammary glands are
the appendages of skin.

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COLOUR OF SKIN –

Mainly on two factors

i. Pigmentation of skin.
ii. Haemoglobin in the blood.

C.SUBCUTANEOUS LAYER –

 In Latin, ‘subcuti’ means beneath the skin. It is also called Hypodermis

(deeper to the dermis) or superficial fascia.
 It mainly consists of loose connective tissue, adipose tissue, Major blood
vessels and it is used for fat storage.

All the appendages of the skin are responsible for the re-generation of the
epidermal layer. In full-thickness burn injury, all are damaged and re-generation of the
skin impaired and re-constructive surgery is mandatory.

FUNCTION OF THE SKIN

1. Protective function.
2. Sensory function.
3. Storage function.
4. Regulation of body temperature.
5. Regulation of electrolyte imbalance.
6. Excretory function.
7. Absorptive function.
8. Secretory function.
9. Synthetic function.

AYURVEDIC REVIEW

Ayurveda is an ancient and traditional medicine system. Maharshi Sushruta

described about different methods of surgery in different diseases along with take care
of wounds which occur either due to dosha vitiation or traumatic or accidental origin.

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DAGDHA VRANA (BURN WOUND)

VEDIC PERIOD:

 In Rigveda we get the references about dagdha vrana and its management
with ghee. In Atharva Veda (Kaushika sutra) 11/31, v/23 [27/14-20, 30/120].
In v-23, where we get dagdha vrana , which is due to fault during Agnikarma.

SAMHITA KALA:

 Sushruta described in sutra-12 chpt., details about dagdha vrana, cause,

pathogenesis, its types and their management with complications.
 Other author like Chakradutta, Yogaratnakara, Bhaisajya Ratnavali also have
the same view like Sushruta.
 There is no description regarding Agni Dagdha Vrana in Charaka Samhita.

Derivation –

The word Dagdha is derived from “Dhyate sma iti” means ‘that which burn’.

“Vrana Gatra Vichurnane, Vranayati iti Vranaha”.(Su. Chi. 1/6)

 It means discontinuity, destruction of the body tissue or part of body tissues.

Etiological factors of Dagdha Vrana –

 Agni
 Sheetavarshaanila
 Atitejasa
 Ushnavataatapa
 Indravajragni

Samprapti –

 After contact the body parts with heat, blood gets vitiated along with pitta.
This causes severe pain and burning sensation.
 Immediately there will be formation of blisters on that part and later on other
complications. Patients suffer from fever and thirst.

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CLASSIFICATION OF DAGDHA VRANA

According to Aetiology –

a. Agni Dagdha Vrana

This is caused by the application of heat which is coming under the heading of
“Itharatha Dagdha”.

It is of two type’s i.e.

 Ruksha Dagdha
 Snigdha Dagdha
b. Ushnavataatapa dagdha
c. Atitejasa dagdha
d. Sheetavarshanila dagdha
e. Indravajragni dagdha
o According to depth –
A. Plustadagdha vrana -
There will be vivarna (Discolouration of skin) and atiplushyata.
B. Durdagdha vrana –
There will be sopha (Blister formation), paka, daha, teevra vedana.
C. Samyak Dagdha vrana –
Wound which is not deep seated (Anavagadha), colour like ripe palm fruit
(Talaphalavrana), and the morphology is well maintained (sushansthitam).
D. Atidagdha vrana -
The characteristics features are mamsavalambana, gatravislesa, sira-snayu-
sandhi-asthi vyapadana atimatra, jwara, daha, pipasa, murchha, vranasya
chirena ruhyati, vivarna.

CLASSIFICATION OF DAGDHA VRANA ACCORDING TO DIFFERENT EXPERTS

SL NO. SUSHRUTA VAGBHATTA SARANGDHARA

1. Plustha Tutha Plustha

2. Durdagdha Durdagdha Durdagdha
3. Samyakdagdha Samyakdagdha Samyakdagdha
4. Atidagdha Atidagdha Atidagdha

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MANAGEMENT OF DAGDHA

PLUSTA DAGDHA –

 Burn area should be burn again by agni and ushna veeryas medications. After
the fire contact the area becomes warmer and blood becomes liquefied.
 So, warm water irrigation and drinking and cold water and cold therapy should
not be used in this burn.

DURDAGDHA –

 In this type of burn both the ushna and sheeta chikitsa should be done. But
Ghee, Lepa and any medications should be sheeta veeryas.

SAMYAKDAGDHA –

 Flesh of animals belongs to Anupadesha are mix and applied externally.

 A demulcent ointment made up of tugaksiri, plaksa,red sandal wood,gairika
and ghrita should be applied.
 In case of burning sensation, the treatment described in pittaja vidradhi should
be done.
 To create the recipe beeswax, madhuka,rodhra, sarjarasa, manjishtha,
sandal wood,murva is required. They all are powdered and then cooked with
ghrita. This is a healing ointment mainly used in all types of burn described by
Maharshi Sushruta.

ATIDAGDHA –

 After the debridement of charred muscles all the cold management should be
advised.
 Paste prepared of the powder of Shali and decoction of bark of Tinduki, mixed
with milk should be applied and covered that area with leaves of Guduchi and
Lotus.
 Remaining treatment is to be followed according to the treatment described in
pittaja visarpa.

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SNEHA DAGDHA VRANA –

 Burn injury due to hot oil, ghee, and water etc. ruksha chikitsa should be
carried out.

DHOOMOPAHATA –

The characteristics features are –

 Swasa (Dyspnoea)
 Adhmana (Tympanitis)
 Kasa (Cough)
 Chakhyusa paridaha (Burning sensation in eye)
 Chakhyusa roga (Redness in eye)
 Sadhumaka nishwasiti (Smoky air expired)
 Ghreya annayatraveti (No perception of smell)
 Rasana upahanyate (Tasteless)
 Daha (Burning sensation)
 Jwara (Fever)
 Trishna (Thirsty)
 Murchha (Unconsciousness)
 Kshyabathu (Sneezing)
 Sruti upahanyate (Deafness)

MANAGEMENT –

1. Vamana Karma should be done with sugarcane juice, ghee, milk, sugar etc.
2. Kavala graha with madhura, lavan, amla, tikta dravyas
3. Nasya
4. Pathyaahara sevana.

USHNA VATAATAPA DAGDHA –

 Sheetala(Cold) chikitsa should be done.

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SHEETA VARSHANILA DAGDHA –

 Snigdha and ushna chikitsa should be employed.

ATITEJASA DAGDHA –

 In this type of dagdha, usually patient doesn’t cure after a proper treatment.

INDRA VAJRAGNI DAGDHA –

 Mortality rate is very high in this indra vajragni dagdha.

 If fortunately the patient survives then abhyanga, sneha pariseka, pradeha
should be carried out.

MANAGEMENT OF DAGDHA VRANA (ACC. TO B. Ratnabali) –

Treatment of dagdha vrana is narrated in sadyovrana chikitsaadhyaya (B.R.48/7-12)

 Treatments done as like pittaja vidradhi and pittaja visharpa.

 External application of ointment prepared from Tila bhasma( ash of Sessamum
indicum), Java, and Shyandana taila.
 Topical application of honey should be done.
 Application of Navaneet of Mahisha(Buffalo), tila reduces burning sensation.
 Dusting of Maharastri jata powder should be done.
 Dusting the powdered of java.

PREVIOUS RESEARCH STUDIES REGARDING THIS TOPIC –

 Study of dagdha and agni karma.(Vaishnav S D,BHU,1968)

 Management of dagdha vrana with indigenous medicine svatha malahara.
(Prasad km VD, Hydrabad, 1987)
 Clinical study on vansha lochanadi lepa in the management of burn. (Kasture
rupali V,Nagpur,2005)
 Management of dagdha vrana by topical application. (Kulkarni Vaivhav,
Banglore, 2005)
 To study the efficacy of patola taila for local application in burn. (Pagar vishal
V,Pune,2005)
 Study on dagdha vrana. (Sachan SC,BHU,1973)

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BURN

A burn wound is a wound in which there is coagulative necrosis of the

epidermis and underlying tissues, with the depth depends upon the area to the skin and
the duration of exposure.

A burn injury is an injury to the skin or other organic tissue primarily caused
by heat or due to radiation, radioactivity, electricity, friction or contact with
chemicals. Skin injuries due to ultraviolet radiation, radioactivity, electricity,
chemicals, as well as respiratory damage resulting from smoke inhalation, are also
considered to be burns. [W.H.O]

A burn injury is a tissue injury due to contact of heat in any form to the
external and internal body surface.

The contact of heat may be:

1. Dry heat – burns

2. Moist heat – scalds
3. Mechanical burn - friction burn
4. Chemical burn – acids, alkali and corrosive metals.
5. Electrical burn/ lightening.
6. Radiation burn – X-ray, UV rays, infrared, radium, laser.

Burn wounds which remains unhealed for longer time either due to infection or
accumulation of excess proteases for 3 to 4 weeks. Burn wound transforming to
chronic wound if not properly managed.

Causation of burn injury –

 Young infant – Scalds are more common.

 Toddlers – Again scalds are common.
 Children – Burn injuries are common due to playing with fire, games.
 Senile and epileptic persons are more prone to burn injury.
 Dowry death– More common in India.
 Radiation injury- Common in workers in different factory and during the
treatment of cancer disease or other diseases.

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Sign & symptoms of burn –

Full thickness burns may be entirely insensitive to light touch or puncture.

While superficial burns are typically red in colour, severe burn may be pink, white or
black.

Type Layers involved Appearance Texture

1st degree Epidermis Red without blisters Dry
2nd degree Extends into superficial Redness with clear Moist
( superficial) dermal papilla blister, blanches with
pressure
2nd degree (Deep) Extends into deep reticular Yellow or white. Less Fairy
dermis blanching dry
3rd degree Extend through entire Stiff or white/brown. No Leathery
dermis blanching
4th degree Extends through entire Black; charred with Dry
skin into underlying fat, eschar
muscle and bone.

Prevention and Epidemiology –

Accidents occur in kitchen. That can be avoided by simple Prevention is better

than cure. Burn injuries can take place anywhere- at home, at work, during transit;
literally anywhere. A firework injury is also very common and involves important
organs like face and hands.

In India fireworks are used on any occasions. May it be festivals of any

religion, success in sports or elections, marriages, births; almost any occasion is
suitable for burning fire crackers. Burn is a problem for everyone. The injury is
painful, cost of treatment is very high, and management is complicated due to
involvement of multiple organs, takes long time to recover and many times the
permanent marks are left behind for rest of the life.

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These injuries leave behind multiple deformities, ugly faces and crippled
hands. These are totally preventable by a little care. Burns are one of the most
devastating conditions encountered in medicine.

The injury represents an assault on all aspects of the patient, from physical to
the psychological. It affects all ages, from babies to elderly persons, and is a problem
in both developed and developing countries in the world.

Correct management requires a multidisciplinary approach that addresses all

the problems facing by a burn victim. Burn incidence rates in the developing world;
continue to be high at four to five times the rate in the United States. Two third of
burn occurs at home and commonly involve young adult men, children younger than
15 years, and elderly. 75% of burn related deaths occur at home.

Other risk factors include low socioeconomic status and unhealthy conditions.
Improvement of incidence rate in the developing world through education and
prevention programmes or through indoor awareness programmes.

MECHANISM OF INJURY

THERMAL BURN INJURY –

SCALDS – About 70% of burns in children are scalds, also often in elder persons. It

tends to cause superficial to superficial dermal burns.

FLAME – It comprises 50% of adult burns. They tend to be deep dermal or full
thickness burns.

DIRECT CONTACT– It commonly seen in the people with epilepsy or alcoholic

persons or even touch due to careless behaviour. It tends to be deep dermal or full
thickness burns.

ELECTRICAL BURN INJURY–

An electric current will travel through the body from one point to another,
creating “entry” and “exit” points. The tissue between these two points can be
damaged by the current. It results from the conversion of electrical energy into heat.

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Electrical burn injuries are deep and most of them need urgent surgical attention.
Extent of injury depends on the types of current, the path way of flow and the duration
of current. Injury at the point of exit is more severe than the point of entry. Intervening
tissues may or may not be affected.

The damage caused to the tissue is directly proportional to the resistance

caused by the tissues to the electrical current. More the resistance; more is the heat
produced and more damage is caused to the organs. The effect t of passage of
electricity in the body depends on voltage, types of current (AC or DC), duration of
contact and tissue resistance.

Electrical injuries are of 2 types

i. High voltage {>1000 volts}

ii. Low voltage {<1000 volts}

Low voltage injury is similar to thermal burn without transmission to deeper

tissues; zones of injury extend from the surface into the tissues. Most household
current [110- 220V] produces these types of injury, which causes only local damage.

The syndrome of high- voltage injury consists of varying degree of cutaneous

burn at entry and exit sites, combined with hidden destruction of deeper tissue. Initial
evaluation consists of cardiopulmonary resuscitation if ventricular fibrillation is
induced.

Thereafter, if there is a history of cardiac arrest associated with the injury,

continued cardiac monitoring is necessary. The most derangement occurs in the first
24 hours after injury. Patients with electrical injuries are at risk for other injuries, such
as being thrown by the electrical jolt or falling from heights from the electrical
current. Muscle damage results in the release of myoglobin, which are filtered in the
glomeruli and may result in obstructive nephropathy.

Therefore, patient needs vigorous hydration and infusion IV sodium

bicarbonate [5%] and mannitol [25gm every 6 hrs. For adults] are indicated to
maintain urine output if significant amounts are found in serum. Urine output is
maintained at 2ml/kg/hr.

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Delayed Effects –

Neurologic deficits may occur. So, neurological evaluations are performed as

part of the routine examination to detect any early or late neuropathology. Another
effect is the development of cataracts, which can be delayed for several years.

CHEMICAL BURN INJURY –

Most of the chemical burns are accidental and results from mishandling of
households cleaners industrial exposure. Chemical injuries may be of longer duration,
even for hours in the absence of appropriate treatment.

The degree of tissue damage, as well as the level of toxicity, is determined by

the chemical nature of the agent, the concentration of the agent, and the duration of
the skin contact.

Chemical should be removed quickly by washing with large amount of water.

This reduces the extent of burn injury, avoids the penetration of the chemical to the
deeper layers and reduces the toxic effects of the chemical due to absorption. Washing
the chemical with small amount of water should be avoided as it causes exothermic
reaction (e.g. sulphuric acid) with some chemicals and the dilution of some chemicals
(e.g. phenol) may increase absorption. Chemicals are acids, alkalis, inorganic and
organic substances.

Chemical burns occur as a result of contact of the chemical with the skin.
Chemicals cause their injury by protein destruction, with denaturation, oxidation, and
formation of protein esters or desiccation of the tissue. Some chemicals may also get
absorbed into the tissues and causes systemic poisoning. In case of chemical burns it
is not only necessary to treat the injured parts but also requires keen observation to
identify the toxic effects during their treatment.

In general; whenever possible the chemical should be neutralized with an

antidote. Deep chemical burns may be requires excision of the tissue or early skin
grafting. After this burn wounds are covered with antimicrobial agents or skin
substitutes. Skin grafting and flap coverage is performed if needed.

[A clinical study on durdagdha w.s.r to second degree superficial burn and its 20
management with indigenous drugs.]
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ALKALI –

Alkalis, such as lime, potassium hydroxide, bleach and sodium hydroxide are
among the most common agents involved in chemical injury. Accidental injury occurs
in infants and toddlers exploring cleaning cabinets.

Mechanism of alkali burn –

 Massive extraction of water from the cells causes damage because of the
hygroscopic nature of alkali.
 Alkalis dissolve and unite with the protein and it contains hydroxide ions,
these ions penetrate deeper into the tissue.

Treatment is immediate removal of the agent with lavage of huge volumes of fluid
and attempt to neutralize with weak acids. Cement [calcium oxide] burns are alkali in
nature, occur commonly and are usually work- related injury.

ACIDS –

Acid injuries are treated with copious amount of water like other chemical
injury. Acids induce protein breakdown by hydrolysis, which results in a hard eschar
that does not penetrate as deeply as alkali do. Formic acid injuries are relatively rare
and involve an organic acid used as a preservative.

Patients, who have sustained formic acid injury, electrolyte abnormalities are
of great concern with metabolic acidosis, renal failure, and pulmonary complications
being common.

Hydrofluoric acid is a toxic substance used in both industrial and domestic

setting and is a strongest inorganic acid. The treatment is also different from other
acid burns in general. Hydrofluoric acid produces corrosion of the tissue by free
hydrogen ions. So, the affected area is treated with 2.5% calcium gluconate gel. These
wounds are generally extremely painful because of calcium chelation and potassium
release.

All patients with hydrofluoric acid burns are admitted for cardiac monitoring,
with particular attention to prolongation of QT interval. Serum magnesium and
potassium are also closely monitored and replaced.
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RADIATIONAL BURN INJURY –

Radiation means a diversion of energy in all directions from a common centre.

Generally, a term is used when there is transmission of energy from one point to
another without affecting the medium through which it passes. Thermal radiation is
transmission of heat from its source to another object. The heat causes damage to the
skin causing a burn injury.

Sunburn is a commonest example which is caused by sun rays. Ionizing

radiation is caused by electrons in electromagnetic waves. The degree of ionization
depends on the intensity of ionizing energy. Radiation burn occurs after expose of the
skin to X- rays, Alpha-rays, Beta-rays, Gamma-rays, Neutrons and microwaves etc.

In clinical practice burns are seen due to damage of skin during therapeutic use
of ionizing radiation. Alpha particles do little damage, since that can be absorbed by a
layer of clothing, paper or the outer layer of skin. Beta radiation tends to be superficial
as beta particles are unable to penetrate deep into the tissues.

These burns stimulate sunburn called as ‘Nuclear tan’. Gamma rays penetrate
deep into the tissues and cause more damage. Radiation burns are common in the
patients receiving ionizing radiation during the treatment of malignancies and the staff
who work unprotected.

Radiation burns usually heals very slowly and after healing the scars have
atrophic skin with underlying fibrosis. Healing may takes from three weeks to few
months. Ionizing radiation cannot be seen, felt or heard. A specialized instrument
Geiger counter is commonly used to measure the rate of radiation as roentgens per
hour (r/hr.).

COLD INJURIES

SYSTEMIC HYPOTHERMIA –

It is not commonly seen in our country except in northern part of the country
in winter. It can be result of general cooling of the body in a cold environment as the
cool air passes over the body there is heat loss by convection. The effect is aggravated
if the clothes became wet or there is associated wind. Intense shivering, difficulty in
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speaking, muscular rigidity, amnesia, slowing of pulse and respiration and later
unconsciousness, cardiac arrhythmia and ventricular fibrillation occurs. Death occurs
due to cardio-pulmonary arrest.

TREATMENT:-

First Aid: - Do not warm the patient too rapidly. It can cause ventricular
fibrillation. Remove wet clothing and wrap the patient in blankets. Move the patient to
warm environment as soon possible. Warm the patient with heat packs, warm water
bottles, warm air, radiant warmer etc. provide oxygen and monitor vital signs.

FROST BITE –

Frost bite is the damage of the tissue caused by freezing. Skin and
subcutaneous tissues are at a risk of frost bite when exposure to cold air, liquids or
metals. Most cases of frost bites are seen in winter sports enthusiasts, climbers,
soldiers, homeless persons and those who work outdoors in cold climates. The risk of
frost bite increases with alcohol use and smoking.

The commonly affected parts are head, hand, feet, ear-pinna, cheeks, toes,
fingers and nose. When body parts are exposed to very cold air or liquids, there is
intense vasoconstriction. This leads to cutting down the blood supply in these parts.
The tissues are damaged because of combined effect of freezing and anoxia.

The ice crystals not only injure the cellular architecture but also disturb the
flux of electrolytes and water across cell membranes. Reflex vasoconstriction in the
extremities results in decreased capillary perfusion, which is aggravated by cold
induced hyper viscosity and a tendency to thrombus formation.

Clinical features –

 Painful erythema,
 Extreme pain,
 Numbness of the exposed parts,
 Loss of sensation.
 The effected skin becomes white and waxy
 Tissue necrosis occurs.
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A new method of classifying frostbite severity has been proposed: first degree,
leading to complete recovery; second degree, requiring only soft tissue amputation;
third degree, requiring bone amputation; fourth degree, requires major amputation and
effects systemic complications.

TREATMENT –

Rapid re-warming by immersion in water at 40-42 degree temperature for 20

min. is recommended. Exposure to higher temperature is contraindicated. Surgical
removal of tissue should be delayed until there is a distinct demarcation between
viable and non-viable tissue, a process that usually takes several weeks.

SUN BURN -

When the body is exposed to excessive heat in the environment or prolonged

exposure to very hot sunlight during summer it can lead to a burn injury. Usually
temperature above 400C.

When exposed for sufficient length of time can cause damage to human skin
(At 400 C in 6 hrs. Human skin can sustain full thickness burn). During the summer
many areas in our country have ambient temperature above 400C. However there is
constant evaporative heat loss from the body due to sweating which effectively cools
the skin and protects it.

The prolonged exposure to sunlight can occur in individuals after consumption

of excessive amount of alcohol or in some people who have a very sensitive skin to
sunrays. The sun burn is usually partial thickness burn and heals rapidly after adequate
closed dressing. Deep burn can occur in alcoholics when the exposure to sunlight is
too much prolonged.

Clinical features -

If the patient arrives with acute burn patient should be examined for signs of
dehydration, presence of heat cramps, increased body temperature, shallow breathing,
tachycardia, presence or absence of perspiration, semi or unconsciousness.

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TREATMENT:-

If the skin is hot skin should be cooled immediately with cold water. During
transport wrap the person with wet cloth. Closed moist dressing with appropriate anti-
bacterial agent is recommended. Suitable antibiotic agent and other supportive
treatment should be carried out.

If there is the sign of associated heat stroke patient should resuscitated and
transported to the hospital immediately. Cooling of the body should be carried out
rapidly (to reduce hyperthermia to prevent cerebral damage.) use of ice-packs if
available will be useful during the transit. Continuous monitoring of vital signs is
mandatory. Intravenous fluid replacement should be started immediately as in case of
post burn dehydration.

Classification of burn

Burns are classified into five different causal categories and depths of injury.
Causes include injury from flame, hot liquids, and contact with hot or cold objects,
chemical exposure and conduction of electricity.

The first three induce cellular damage primarily by the transfer of energy and
lead to coagulative necrosis. Chemicals and electricity cause direct injury to cellular
membranes in addition to transfer of heat.

According to cause,

 Flame – damage from superheated oxidized air.

 Scald – damage from contact with hot liquids.
 Contact – damage from contact with hot or cold solid materials.
 Chemical – damage from contact with noxious chemicals.
 Electricity – conduction of electrical current through tissue.

According to cause,

 First degree – injury localized to the epidermis.

 Second degree superficial – injury to the epidermis and superficial dermis.
 Second degree deep – injury through the epidermis and deep into the dermis.

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 Third degree – full thickness injury through the epidermis and dermis into the
sub-cutaneous fat.
 Fourth degree – injury through the skin and sub-cutaneous fat into the
underlying muscles or bone.

Burn depth -

The depth of a burn depends on the degree of tissue damage. Burn depth is
classified according to the degree of injury in the epidermis, dermis, sub-cutaneous fat
and underlying structures.

First-degree burns are, by definition, injury confined to the epidermis. These

burns are painful and erythematous, blanch to the touch, and have an intact epidermal
barrier. Examples are sunburn or a minor scald from a kitchen accident.

First- degree burns do not result in scarring, and treatment is aimed at comfort
with the use of topical soothing salves, with or without aloe, and NSAIDS agents.

Second- degree burns are divided into two types: superficial and deep. All
second-degree burns have some degree of dermal damage, and the distinction is based
on the depth of injury into this structure. Superficial dermal burns are erythematous
and painful; blanch to touch, and often blisters.

Examples include scald injury from overheated bathtub water and flash flame
burns. These wounds spontaneously re-epithelialize from the retained epidermal
structures in the rete ridges, hair follicles and sweat glands in 7-14 days.
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After healing, these burns may result in some slight skin discoloration over the
long term. Deep dermal burns into the reticular dermis appear more pale and mottled,
do not blanch to touch, but remain painful to pinprick. These burns heal in 14-35 days
by re-epithelialization from hair follicles and sweat gland keratinocytes, often with
severe scarring as a result of the loss of dermis.

Third- degree burns are full thickness through the epidermis and dermis and
are characterized by a hard, leathery eschar that is painless and black, white or cherry
red. No epidermal and dermal appendages remain; thus, these wounds must heal by
re-epithelialization from the wound edges. Deep dermal and full thickness burns
require excision and skin grafting to heal the wound in time.

Fourth- degree burns involve other organs beneath the skin, such as muscles,
bone. This is the deepest and most severe burns. They are potentially life threatening.
These burns destroy all layers of skin, bones, muscles, and tendons.

Burn size-

Determination of burn size estimates the extent of injury. Burn size is

generally accessed by the ‘Rule of Nines’. In adults, each upper extremities and the
head and neck are 9% of TBSA. The lower extremities and the anterior and posterior
aspects of the trunk are 18% each, and the perineum and genitalia are assumed to be
1% of TBSA.

In young children and babies, head and neck are 21% of TBSA, each upper
extremity are 10% of TBSA, anterior and posterior aspects of the trunk are 13% of
TBSA, each lower extremities are 13.5% of TBSA, buttocks are 5% and groin
assumed as 1% of TBSA.

The “rule of palm” is another method to estimates burn size of a burn. The
palm of the person who is burned (not fingers or wrist area) is about 1% of the body
and then transposes that measurement visually onto the wound for a determination of
its size. Use the person’s palm to measure the body surface area burned.

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RULE OF NINE

The size of a burn wound is measured as a percentage of TBSA (total body

surface area) affected by partial thickness or full thickness burns. To determine the
need for referral to specialized burn units, the American Burn Association devised a
classification system. Under this system, burns can be classified as major, moderate
and minor. This is assessed based on a number of factors, including TBSA,
involvement of specific anatomical zones, age of the person, and associated injuries.
Minor burns can typically be treated at home, moderate burns are often managed in
hospital, and major burns are managed by a burn care centre.

AMERICAN BURN ASSOCIATION SEVERITY CLASSIFICATION –

MINOR MODERATE MAJOR

Adult <10% TBSA Adult 10-20% TBSA Adult >20% TBSA
Young or old <5% Young or old 5 - 10% Young or old >10% TBSA
TBSA TBSA
<2% full thickness 2- 5% full thickness burn > 5% full thickness burn
burn
High voltage injury High voltage burn
Inhalation injury Known inhalation injury
Circumferential burn Significant burn to face, joints,
hands or feet
Other health problems Associated injuries

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General factors influencing the burn wound –

Skin lesions begin to appear after a heat exposure between 450C. and 700C.
Origin of burns can be thermal, electric or chemical. Thermal burns constitute the
major group with an incidence of 80% and present specific profile.

Electrical burns show a special feature, with two different types of lesion.
Electrical passage burns show an entry point and an exit point, mostly found on the
hand, foot, and palm of the hand. Chemical burns often present a combination of
chemical toxic effects on skin and thermal consequences.

Severe alterations of the cardiovascular function may determine the degree of

the burn shock, an abnormal physiologic state in which the tissue perfusion is
insufficient to maintain adequate delivery of oxygen and nutrients and removal of
cellular waste products.

Immediate care on burn wound –

The quality of immediate care has an important influence on the outcome of

the burn wound. A superficial second degree burn observed during the initial
evaluation can turn into a deep second degree burn. Due to poor treatment and
because of general conditions worsen the resuscitation unit. Application of systemic
antimicrobials is also of importance and has to be considered when dealing with
general infections from the burn wound.

PATHOPHYSIOLOGY:-

In second degree burns, difficulties concerning the adequate assessment and

management of the infection risk still persist. Assessment of burns is considered to be
insufficiency precise in more than 40% of the cases evaluated by the specialists,
especially during the first three days post burn. Superficial burns are characterized by
severe pain, redness of the surface.

In deep second degree burns shows a red-white aspect, a non-haemorrhagic

surface. In third degree burns, early excision and skin grafting were adopted by most
of the physicians since last decades. Dermal replacement is the real issue to prevent
functional damage and cosmetic consequences.

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Topical antimicrobials are still the first choice in the local treatment, and the
most used agent is silver sulfadiazine ointment. Size of the burn is also critical.
Increasing percentage of injury in relation to body surface area increases the mortality.
In adult 20% burn is serious and 40% burn is very serious more than 60% burns is
many times fatal.

SYSTEMIC EFFECTS OF A SEVERE BURN

Severe burns more than 40% of the TBSA are typically followed by a period
of stress, inflammation and hyper metabolism characterized by a hyper dynamic
circulatory response with increased body temperature.

Hyper-metabolic response to burn:

This hyper metabolic response to burn injury lasts for 12 months after the
initial event. Immediate post-burn patients have low cardiac output. However, 3-4
days post-burn the cardiac output is more than 1.5 times that of healthy people where
as in paediatric burn patients heart rates is 1.6 times those of non-burn children.

Post-burn muscle protein is degraded rapidly causing, loss of lean body mass
and severe muscle wasting, leading to decreased strength and failure in complete
rehabilitation. Protein degradation persists up to 1 year after severe burn injury.
Severely burn patients have a daily loss of nitrogen of 20-25gm/sq. of burned area.
Septic patients have a profound increase in metabolic rates and protein catabolism, up
to 40% more compared with those with burns of a similar size who do not develop
sepsis. Catabolic patients are more susceptible to sepsis because of change in immune
system.

Inflammation and oedema:

Significant burns are associated with massive release of inflammatory

mediators, both in the wound and in other tissues. These mediators produce
vasoconstriction and vasodilation, increased capillary permeability, and oedema
locally and in distant organs. Initially, interstitial hydrostatic pressure decreases in
burned skin. And there is an associated slight increase in interstitial pressure in non –
burned skin.

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As plasma oncotic pressure decreases and interstitial oncotic pressure

increases as a result of the protein loss induced by increased capillary permeability,
oedema forms in the burned and non-burned tissues. Oedema occurs in the burned
tissues because of lower interstitial pressure.

Effects on cardiovascular system –

There is loss of plasma volume, increased peripheral vascular resistance, and

decreased cardiac output immediately after burn. Cardiac output depressed due to
decreased blood volume and increased blood viscosity. Severely burned paediatric
patients have a marked tachycardia. Cardiac output at admission is 150% and remains
high.

Effects on renal system –

Diminished blood volume and cardiac output result in decreased renal blood
flow and glomerular filtration rate. Angiotensin, aldosterone, and vasopressin reduce
renal flow leads to oliguria, which if untreated will cause renal failure. Early
resuscitation decreases renal failure and improves the associated mortality rate.

Effects on gastro-intestinal system:

The gastrointestinal changes include mucosal atrophy, changes in digestive

absorption. Atrophy of small bowel mucosa occurs within 12 hours. Burn also causes
reduce uptake of glucose and amino acids, decrease absorption of fatty acids, and
reduction of lipase activity. Gut permeability increases even further when the burn
wounds become infected.

Effects on immune system:

Burns causes immune suppression, which is shown by allograft skin survival

on burn wounds. A great risk of numerous infections with burns of more than 20% of
TBSA, impairment of these immune functions is proportional to burn size.
Macrophages production after a burn is diminished. Total neutrophil counts are
initially increased after a burn.

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BASIC MANAGEMENT OF BURN WOUND

Burn is a complex trauma needs multidisciplinary and continuous treatment therapy.

Aim of burn wound care – To restore form, function, and feeling (psychological and
emotional recovery).

First-aid care –

The patient must be removed from the source of injury. Care must be taken to
ensure that the rescuer does not become another victim. The heat sources should be
removed. Flames should be doused in cool running water or smothered with a blanket
or by rolling the victim on the ground. Carefully remove burn clothes and quickly
assess the extent of burn.

Clothing can retain heat, even a scald burn, and should be removed as soon as
possible. Adherent materials such as nylon cloth should be left on. Tar burn should be
cooled with water, but the tar itself should not be removed. Immersion with running
tap water should be done immediately for 20 minutes because water cools the burn,
relieves pain and replace the fluid loss, removes noxious agents, and reduces oedema
by stabilising mast cells and release histamine.

In chemical injuries, clothes should be removed as soon as possible and

irrigation or immersion with copious amount of normal water. In electrical injuries,
the sources of electric current should be identified quickly and switched off, if
possible, and the victim moved from the source of the current using non-conductive
materials.

Active cooling removes heat and prevents progression of the burn. This is
effective if performed within 20 minutes of the injury. {sabiston19}

Cooling should occur for a minimum of 10 minutes and is effective up to 1

hour after the burn injury. {Bailey and loves-26}

Ice water should not be used as intense vasoconstriction can cause burn
progression. Cooling large area of skin can lead to hypothermia, especially in
children.

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Initial treatment: -

Initially, burns are sterile. Focus the treatment on speedy recovery and prevention of
infections. In every burn cases, there must be administration of tetanus toxoids
injection. Except in small burn, debride all bullae.

Excise adherent dead tissue and after debridement, gently cleanse the burned
area with 0.25% of chlorhexidine solution and 0.1% of cetrimide solution. Apply
antibiotic cream (silver sulfadiazine). Dress the burned area with petroleum gauze

Daily treatment –

Change the dressing daily (at least two times). Remove dead tissue or loose
tissue then inspect the wound carefully.

Administration of topical antibiotic daily but applied with occlusive dressing

but does not penetrate the eschar. Use Mafenide acetate which penetrates the eschar.

Monitoring of a burn patient:

Urine output is simple and well accepted methods of monitoring a fluid intake.
Good urine output indicates adequacy of visceral perfusion. Hourly nasogastric
aspiration is useful to guide the state of peristalsis.

Temperature variations are very common in burn patients. High temperature

indicates infection. Variation in heart rate or pulse rate can occur in different
situations. Tachycardia may be present in hypovolemic shock or septic shock. Central
venous pressure monitoring guides the adequacy of venous return.

High pressures are present in renal failure and low pressure indicates
inadequate resuscitation.

Blood pressure drops when the fluid replacement is inadequate for long time
and then the system compensates by peripheral vasoconstriction and increased heart
rate. Peripheral oxygen saturation (Sp02) indicates pulmonary gas exchange.
Haematocrit (PCV) if done frequently can guide rehydration of the patient.
Restlessness indicates presence of cerebral hypoxia.

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Resuscitation and electrolyte therapy:

Following a burn injury there is a loss of body fluid from a burn wound. It is
seen in the form of blister fluid. Blister fluid contains water, plasma protein and
carbohydrates as main ingredients. In severe burn this results in a deficit in circulating
blood volume leading to oligemic shock.

Body tries to compensate such discrepancy by withdrawal of fluid from

interstitial and intracellular fluid (extravascular compartment) into intravascular
compartment. This dehydration of tissue is clinically reflected as intense thirst thus,
prompting a patient to ingest fluid by oral route.

There is a peripheral vasoconstriction and increased heart rate to maintain the

blood pressure and maintain the circulation to vital organs like heart, lungs, brain
kidneys etc. Ringer’s lactate solution without dextrose is the fluid of choice, except in
children younger than 2 years, who received ringer’s lactate solution with 5%
dextrose.

The initial rate can be rapidly estimated by the TBSA burned multiplied by the
patient’s weight in kg and then dividing by 8. Thus, the rate of infusion for an 80 kg
man with a 30% of TBSA burned would be

80kg × 30% of TBSA/8 = 300Ml/hr.

The rate is continued until a formal circulation of resuscitation needs is

performed. Resuscitation fluids are broadly classified as crystalloids and colloids.

Crystalloid resuscitation –

A crystalloids fluids administration replaces the interstitial fluid deficit.

Ringer’s lactate is the most commonly used crystalloid. Crystalloids are said to be as
effective as colloids for maintaining intravascular volume.

They are also less expensive and another reason is that large protein molecules
leak out of capillaries following burn injury. Isotonic crystalloids like normal saline,
Ringer’s lactate, 5% dextrose solution are freely available.

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Colloid resuscitation –

A colloid administration maintains intravascular fluid volume. Plasma proteins

are responsible for the inward oncotic pressure that counteracts the 12 hours of burn
because, before this time, the massive fluid shifts cause protein to leak out of the cells.
Human albumin is commonly used colloid. Colloid solutions like Dextran, plasma,
human albumin.

Hypertonic saline –

Hypertonic saline has been effective in treating burn shock for many years. It
produces hyperosmolarity and hypernatremia. This reduces the shift of intracellular
fluid to extracellular space. Advantages include less tissue oedema and a decrease in
escharotomies and intubations.

Various formulae have been suggested for fluid replacement in burn patient by
many workers in the field with successful outcome.

FORMULA CRYSTALLOID COLLOID VOLUME WATER

VOLUME
PARKLAND 4mL/kg/% TBSA burn None None
EVAN 3mL/kg/% TBSA burn 0.5mL/kg/%TBSA burn None
BROOKE 1.5mL/kg/% TBSA burn 0.5mL/kg/%TBSA burn 2.0 L
GALVESTON 5000mL/m2 burned area+ None None
(paediatric) 1500mL/m2 total area

EVANS FORMULA –

One third of fluid is given in first 8 hrs. One third of the fluid should be given
in next 16 hrs. And one third in subsequent 24 hrs. He used half amount as crystalloids
and half of the amount as colloid in the form of dextran.

PARKLAND FORMULA –

Half the amount is transfused in first 8hrs. and remaining half in next 16hrs.

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Escharotomy –

It is a surgical procedure used to treat full thickness circumferential burns. In

full thickness burns, both the epidermis and dermis are destroyed along with sensory
nerves in the dermis. The tough leathery tissue remaining after a full thickness burn
has been termed as eschar. When deep second and third degree burn wound
encompass the circumference of an extremity, peripheral circulation to the limb can be
compromised causing generalized oedema beneath a non-yielding eschar impedes
venous out flow and eventually affects arterial inflow to the distal beds.

This can be recognised by numbness and tingling in the limb and increased
pain in the digits. Extremities at risk are identified either on clinical examination or by
measurement of tissue pressures greater than 40 mm Hg. If vascular compromise has
been prolonged, re-perfusion after escharotomy may cause reactive hyperaemia and
further oedema formation in the muscles, thus making continue surveillance of the
distal extremities necessary. Increased muscle compartment pressure may necessitate
fasciotomy.

Inhalation injury -

It is one of the major factors contributing to death in burn patients.

Approximately 80% of fire related deaths results not from burns, but from inhalation
of toxic products. Heat is dispersed in the upper air ways, whereas the cooled
particles of smoke and toxins are carried distally into the bronchi. Thus, the injury to
the airways is principally chemical in nature.

There is increase blood flow in the bronchial arteries to the bronchi along with
oedema formation and increases in lung lymph flow. There are increased neutrophils
in lung releasing proteases and oxygen free radicals, which can produce conjugated
dienes by lipid peroxidation.

Ciliated epithelial cells form the basement membrane is separated, followed by

exudation of proteins found in the lung lymph forming fibrin casts. Clinically, these
fibrin casts can be difficult to clear with standard airway suction techniques, and
bronchoscopy removal is required.

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Symptoms and indication of inhalation injury –

 Soot-containing airway secretions

 Coughing
 Hoarseness of voice
 Dyspnoea
 Cyanosis

Abbreviated injury score grading scale for inhalation injury on bronchoscopy.

Grade Class Description

0 No injury Absence of carbonaceous deposits, erythema, edema,
obstruction
1 Mild injury Minor or patchy area of erythema, obstruction
2 Moderate carbonaceous deposits, erythema, obstruction
injury
3 Severe injury Severe inflammation with friability, copious carbonaceous
deposits, obstruction
4 Massive Evidence of mucosal sloughing, necrosis, endo-luminal
injury obstruction
Management:-

If respiratory failure is imminent, intubation is instituted, with frequent chest

physiotherapy. Mechanical ventilation is used to provide gas exchange.

Clinical indications for intubation

CRITERIA VALUE
PaO2 (mm Hg) <60
PaCO2 (mm Hg) >50
PaO2/PaCO2 <200
Respiratory/ventilator failure impending
Upper airway edema Severe

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Physiotherapy and occupational therapy:

Initially for breathing and coughing exercises and for chest physiotherapy to
maintain clear airway, to improve air entry particularly when smoke inhalation is
suspected and later on to prevent chest complications, a physiotherapists may be
called to help. Later active or active assisted exercises under the supervision are
recommended to maintain range of movements of the joints of upper and lower
extremities and to maintain muscle bulk in order to sustain exercise tolerance later.

Occupational therapist is helpful in preparation of splints like neck-collar,

splintage for joints and for maintenance of functional positions of hand and foot. Later
on, occupational therapist is helpful to maintain patient’s activities of daily living, gait
training and to increase patient tolerance to pain. Pressure garments need to be worn at
least 22-23 hours a day for the period of 9 to 24 months. Good patient compliance
usually gives encouraging results.

Nutritional management:

Nutritional support is an important part of treatment of burn patients. Basal

metabolic rate (BMR) increases very steeply due to very large amount of loss of
water, protein and energy from the burn surface.

Well-nourished patient with minor burn can withstand this loss by endogenous
supply of nutrients. However, in patients with moderate and major burn injury a
severe catabolic status develops. Those patients who have pre-existing mal-nutrition
cannot withstand this severe catabolic state.

Without adequate nutritional supports the burn patients rapidly lose weight and
show similar to prolonged starvation in short time. Enteral nutrition is usually
preferred to parenteral nutrition because of ease of administration, cost and it is much
less associated with complications.

Nutritional care of the patient should be started very early during the course of
treatment. Preferably on admission but at least within 48 hours of the burn injury
before the state of paralytic ileus has developed.

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Whole proteins instead of Amino acids are available, cheap and convenient to
administer. When started early the body wasting is minimized, better immunological
status is achieved, healing time is reduced and overall recovery of the patient and the
period of hospitalization is greatly minimized.

Wound care –

After establishment of the airway and resuscitation, attention must be turned to the
wound. After assessment of extent and depth of the wounds, wound toilet and
debridement should be done. After the wound is dressed with an appropriate covering
it serves several functions.

1. It protects the damaged epithelium, minimizes bacterial colonization.

2. Dressing is occlusive to reduce evaporative heat loss.
3. Dressing needs to provide comfort over the wound.

First-degree wound with minimal loss requires no dressing. Second-degree burns

can be treated with daily dressing, topical antibiotics and temporary biologic or
synthetic covering to close the wound. Deep second-degree and third-degree wounds
require excision and grafting for sizable burns. Burn injury leaves behind a large
wound on the body surface. Though the burn injury is not only to the skin it
eventually leads to widespread systemic effect as a result of the fluid loss from the
circulating blood. The wound is easily contaminated due to handling and exposure.
This leads to infection and later septicaemia. There are two basic methods for the burn
wound care.

Exposure/open method-

The wound is left open to dry. The necrotic tissue dries and forms an Escher. It
is the easiest methods but it is very uncomfortable, wound contamination occurs easily
and chances of septicaemia.

Closed method:

In this method, wound is treated with a suitable anti-bacterial agent and

covered with adequate dressing. It is kept closed until the next dressing. A good
dressing should prevent wound contamination, protect from drying by retaining

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management with indigenous drugs.]
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adequate moisture, and comfortable to the patient. Extensive and deep burns will need
frequent dressing change.

ANTIMICROBIALS –

An untreated burns wound rapidly becomes colonized with bacteria and fungi
because of loss of normal skin barrier mechanisms. The antimicrobials are divided
into topical and systemic.

Topical antimicrobials:

This can be divided into two classes: slaves and soaks. Slaves are directly
applied to the wound with cotton and soaks are poured into cotton dressing on the
wound.

Topical antibiotic slaves Soaks

11% mafenite acetate 0.5% silver nitrate
1% silver sulfadiazine 0.025% sodium hypochlorite
Polymyxin B 0.25% acetic acid
Neomycin, Mupirocin, Bactiracin 5% mafenide acetate

Systemic antimicrobials:

The use of perioperative systemic antimicrobials also has a role in decreasing

burn wound sepsis until the burn wound is closed. Common organisms include S.
aureus and Pseudomonas species.

Burn wound coverage:

After burn wound excision, wound closure should be done. Various biological
and synthetic substrates have been used to replace the injured skin post burn.
Autograft from the uninjured skin remains the mainstay of treatment for many
patients. Because early wound closure using autograft may be difficult when full
thickness burn exceeds 40% of the TBSA.

Allograft frequently serves as skin substitutes for severely burned patients.

Even though these grafts provide a biologically active dermal matrix, immunological
disparities, prevents engraftment and predetermine rejection over time.

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Synthetic and biological dressings:

Synthetic and biologic dressings are an alternative to antimicrobial dressings,

stable coverage without painful dressing changes, provide a barrier to evaporative
losses, and decrease pain in the wounds.

They do not inhibit epithelialization, which is a feature of most topical

antimicrobials. These covering include allograft, xenograft (pig skin), transcyte,
biobrane, and integra. These are applied within 72 hours of the injury, before high
bacterial colonization of the wound occurs.

Biobrane sheet is placed on the wound and becomes adherent in 24-48 hours
with dried wound transudate. This sheet becomes a barrier to moisture loss, and
provides a painless wound bed.

Integra is a product of collagen matrix (dermal substitute) with silicone sheet.

The collagen matrix engrafts into the wound, and after 2 weeks the silicone layer is
removed and replaced with auto graft mainly used in full thickness burns to close the
wound.

Biologic dressing includes xenograft from swine and allograft from cadaver
donors. This human skin performs the immunologic and barrier functions of the
normal skin. Thus, these biologic dressing are the optimal wound coverage in the
absence of normal skin.

Normally, severe burned patients are immunosuppressed, and biologic

dressings that have been adherent will not be rejected for several weeks. This can be
used to cover the wound as a temporary dressing.

BIOLOGIC DRESSING

Xenograft (pig skin) Completely closes the wound; provide some

Allograft ( cadaver skin)
immunological benefits; must be removed or allowed to
slough.
Provide all the normal; functions of skin; can leave a
dermal equivalent; epithelium must be removed or
allowed to slough.

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Laboratory findings –

Changes in blood-

Haemoconcentration is due to outpouring of serum. Haemoglobin level may

rise to 150% in severe burns. Apparent increase in the number of red cells is due to
outpouring of plasma. Sludging of blood may occur due to intravascular aggregation
of R.B.Cs. There is immediate red cell destruction in the early post burn period.

Biochemical changes –

Electrolyte imbalance occurs in the form of low sodium chloride and high
potassium level in the blood. Hypoproteinaemia is due to excessive protein loss. There
will be rise in blood urea and creatinine level.

Rehabilitation –

Burn injury leaves behind many problems; physical, emotional and social.
Ideally the aim of rehabilitation should be to get the patient back to his/her original
occupation; child to go back to school, housewife to get to her home and kitchen and
worker to get back to his/her place of work.

Surgical rehabilitation:

In spite of all the care patient may develop deformities and disfigurement
leading to significant disability. There is enormous variety of these deformities. The
deformities of every patient and the requirement of their correction are different.
Surgical treatment cannot be standardized. Each situation may need a different
planning.

Psycho-social rehabilitation:

It should be start right from the beginning so that the patient is able to adjust
himself/herself to gradual and smooth recovery. There is a large variety of fear in the
patient’s mind. Fear of pain, uncertainty of recovery, development of ugly appearance,
disability. Both the patients and their relatives suffer from anxiety, due to various
problems associated with burn injury. The burn patients too need a lot of emotional
supports. It is necessary to make them understand that they should not lose their
proper concentration.

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Social rehabilitation:

It is equally important after the patient is discharged from the hospital and gets
back to the society. If there are deformities, disfigurement or disabilities there is a
strong need of understanding from the other members of the family and the work
place. They should give encouragement to get the individual back into the normal
routine in spite of their shortcoming.

COMPLICATIONS OF BURN INJURY

Endotoxins are liberated from gram-negative bacteria walls, and exotoxins are
released from both gram-positive and gram-negative bacteria.

Their release causes the initiation of a cascade of inflammatory mediators that

can result, if unchecked, in organ damage and progression to organ failure.

Curling ulcer –

Stress ulceration of the stomach and duodenum, which is known as curling’s

ulcer is come across the major thermal burn. Serial endoscopic examination has
shown that 85% of patients with burns exceeding 35% demonstrate superficial
mucosal disease within 72 hours of injury. This mucosal disease heals in majority of
patients (80%) within 1 week.

Only in 20% of the patients the disease may progress to frank gastric and
duodenal ulcers which usually become the first evident 96 hours after injury.
Curling’s ulcers are usually multiple and are found simultaneously in the stomach and
duodenum.

These lesions heal following successful resuscitation and initiation of enteral

feeding. Until the burn wound is healed, 30ml antacid is administered each hour
through nasogastric tube to maintain the gastric pH above 5. Cimetidine is usually
effective in preventing curling ulcer. In case of perforation of the ulcer, vagotomy and
gastric resection has produced for long time survival.

[A clinical study on durdagdha w.s.r to second degree superficial burn and its 43
management with indigenous drugs.]
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Acute pancreatitis –

This occurs in the patients with extensive burns with an incidence as high as
30% in those requiring treatment in intensive care unit. The peculiarity is that the
abdominal pain is often absent and this condition is only suggested by increasing fluid
requirement and new onset of hyperglycaemia. Treatment is nasogastric aspiration and
parenteral nutrition.

Acute a calculus cholecystitis –

This complication occurs occasionally in burned patients in two forms.

a. In one form, the gall bladder is infected by haematogenous seeding from a

primary source in the septic burn wound.
b. The other presentation occurs in the critically ill patients with marked
dehydration, hypernatremia, and hyper-osmolality.

Jaundice and abdominal pain may suggest this condition. Ultrasonography is

quite helpful to diagnosis by showing thickened gall bladder wall, sloughing mucosa,
and intraluminal gas in the gall bladder.

Non-occlusive ischaemic entero-colitis –

It is occasionally recognized in severely burned patients. The lesion is usually

located in the distal small bowel and colon and resembles the lesion of curling’s ulcer
in the upper G.I. tract. Nasogastric aspiration and intravenous infusion should be
started immediately.

Myocardial infarction –

This may occurs in old burned individuals. Infarction usually occurs towards
the end of the 1 week after burn. It may be due to increased cardiac output at this time
exceeding the ability of the diseased heart to meet its own perfusion and infarction
occurs. All patients with major burns should be monitored electrocardiographically.

Pulmonary dysfunction –

Pulmonary function may be severely affected leading to shallow respiration,

tachypnea, and hypoxia following oligemic shock.
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It may lead to respiratory acidosis or alkalosis. Pulmonary oedema is not

uncommon as a result of large fluid transfusion. Acute respiratory distress syndrome
(ARDS) can also occur following a burn injury. Involvement of airway mainly upper
airway affected by inhaled hot gases and smoke.

Red blood cell destruction -

This occurs as a result of direct injury by heat. The destruction of RBCs

continues for significant period of time after the injury to increased fragility. Bone
marrow depression can occur due to bacterial and tissue toxins. There may be direct
loss of blood from the granulation tissues of deep wounds and bursting of vessels in
deep burns. All these can lead to severe anaemia. Frequent haemoglobin estimation
require over a long period of time.

Immunosuppression –

Immunosuppression occurs as a result of decreased cellular and humoral immunity.

Skin grafting –

The goal of burn wound care is the timely closure of burn wound. It is the type
of skin graft surgery involving the transplantation of skin. The transplanted tissue is
called as a skin graft. It is done in extensive trauma, burns, wound. Skin graft is
employed after serious injuries when body skin is damaged.

The grafting serves 2 purposes,

 Reduce the course of treatment needed.

 Improve the function and appearance of the area of the body receives the graft.

It is of two types,

 Thin layer is removed from a healthy part of the body like peeling of a potato.
 Full thickness skin graft is risky.

The split thickness skin graft (auto graft) is directly applied to the area. During
the time interval between the eschar separation and the wound is ready for auto graft,
the open wound of granulation tissue can be temporarily covered with a heterograft or
homograft. This is called biologic or physiologic dressing.

[A clinical study on durdagdha w.s.r to second degree superficial burn and its 45
management with indigenous drugs.]
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A bilaminate membrane has been introduced which is composed,

 Temporary silastic epidermis – it remains firmly adherent but can be removed

when autograft is available.
 Porous collagen chondroitin 6-sulphate fibriller dermis –encroached with
fibroblasts and vessels from the wound bed.

A set of parallel incision is made in the sheet graft, expansion of up to 6 times

the area of the original donor site. Mesh graft is covered with occlusive dressings kept
with 0.5% silver nitrate solution. Mesh graft rapidly epithelialized within 4-8 days. It
should not be used on face, hands and feet.

Advantages of temporary biological dressing:

 Prevention and control infections.

 Preserve healthy granulation tissues.
 Decreased evaporative water loss.
 Cover exposed sensory nerve and reduced pain and Protect neurovascular
tissue and tendons.

Skin flap surgery –

It is a technique in reconstructive surgery where any type of tissue is lifted

from a donor site and moved to a recipient site with an intact blood supply.

This is the distinct from a graft, which does not have an intact blood supply
and therefore relies on growth of new blood vessels.

This is done to fill a defect such as a wound resulting from injury or surgery
when the remaining tissue is unable to support a graft, or to rebuild more complex
anatomical structures.

Classification:

Flaps can be fundamentally classified by their level of complexity, the types of

tissues present, or by their blood supply.

I. Local flaps
II. Regional flaps

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III. Distant flaps

Local flaps –

These are created by freeing a layer of tissue and then stretching the freed
layer to fill a defect. This is least complex types of flap. It includes advancement flaps,
rotation flaps, and transposition flaps, in order from the least to most complex.

With an advancement flap, incisions are extended out parallel from the wound,
creating a rectangle with one edge remaining intact. The rectangle is freed from the
deeper tissues and then stretched (advanced) forward to cover the wound.

A rotation flap is similar except instead of being stretched in a straight line, the
flap is stretched in an arc. The more complex transposition flap involves rotating an
adjacent piece of tissue, resulting in the creation of a new defect which must then be
closed.

Regional/interpolation flaps –

The freed tissue is moved over or underneath the normal tissue to reach the
defect to be filled with the blood supply still connected to the donor site via a pedicle.
This pedicle can be removed later on after new blood supply has formed.

E.X. DP for head and neck defect, TRAM for breast reconstruction.

Distant flaps –

These flaps are used when the donor site is far from the defect. Direct or tubed
flaps involve having the flap connected to both the donor and recipient sites
simultaneously forming a bridge.

This allows blood to be supplied by the donor site while a new blood supply
from the recipient site is formed.

Once this happens, the “bridge” can be disconnected from the donor site if
necessary, completing the transfer. This is the more complex types of flaps.

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Tissue types –

Here are some of the more common classifications by tissue type:

 Cutaneous flaps contain the full thickness of the skin and superficial fascia and
are used to fill small defects.
 Fascio-cutaneous flaps add subcutaneous tissue and deep fascia, resulting in a
more robust blood supply and ability to fill a larger defect.
 Musculo-cutaneous flaps further add a layer of muscle to provide bulk that can
fill a deeper defect.

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