Principles and Practice of Burn Care

Electrical Burns
287
Figs 21.43A to D: (A) High voltage injury on the back of chest. (B) Wound debrided and exposed ribs with raised latissimus dorsi flap.
(C) Latissimus dorsi flap covering the defect. (D) Skin graft applied over muscle flap
Fig. 21.44A: Exposed knee joint following electric
contact burns
Fig. 21.44B: Covering knee joint by superiorly based
fasciocutaneous flap
A
B
D
C

288
Principles and Practice of Burn Care
Fig. 21.45A: Exposed axillary vessels following debridement of
eschar from electric burns
Fig. 21.45B: Cover over exposed vessels by latissimus dorsi
musculocutaneous flap
Fig. 21.46B: Reconstruction of hand after electrical burn – functional
gracilis muscle transfer for finger flexion with groin flap cover over
exposed vessels and tendons in wrist
Fig. 21.46A: Reconstruction to save the involved neurovascular bundle
in elbow by providing muscle cover (Latissimus dorsi muscle)
Fig. 21.47: A girl, who lost all her four limbs after 11,000-volt power
line fell on her, paints with her mouth

Electrical Burns
289
rehabilitation of the patient, both physical/occupational and
psychological, particularly if patient has undergone
amputations, is very important in order to successfully
rehabilitate the patient (Fig. 21.47).
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and by lightning. Be Med J.1913, 1: 425-30,492-98,548-52,
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2. James CC, Gerald TH. Occupational electrical injuries in the United
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3. Fish RM. Electric injury, part I. Treatment priorities, subtle
diagnostic factors, and burns. J Emerg Med. 1999;17:977-83.
4. Luce EA, Gottleib SE. True high tension electric injuries. Ann Plast
Surg 1984,12: 321.
5. Wright RK, Davis JH. The investigation of electrical deaths: a
report of 220 fatalities. J Forensic Sci 1980, 25;514-21.
6. Baker MD, Chianello C. Household electrical injuries in children:
epidemiology and identification of avoidable hazards. Am J Dis
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7. Burke JF, Quinby WC, Bondoc C. Patterns of high tension electrical
injury in children and adolescents and their management. AM J
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8. Fish R. Electrical shock, part I: Physics and pathology. The J of
Emer Med 1993; 11:309-12.
9. Hodgkin BC. Some consequences of electric shock. J. Maine Med.
Assoc 1974; 65:1.
10. Fish R. Electrical shock, part II: Nature an mechanisms of injury.
The J of Emer Med 1993; 11:457-62.
11. Fish R. Electric shock, part III. Deliberately applied electrical
shocks and treatment of electric injuries. The J of Emer Med
1993;11:599-603.
12. Hunt JL, Mason AD, Masterson TS, et al. The pathophysiology of
acute electrical injury. J Trauma 1976,16:335-40.
13. Kouwenhoven WB. Effects of electricity on the human body.
Electrical Engineering 1949;68:199.
14. Hodgkin BC. Some consequences of electric shock. J.Maine Med.
Assoc 1974;65:1.
15. Hanson GC, Mcllwraith GR. Lightning injury: Two case histories
and a review of management. Br. Med. J. 1973; 4:271.
16. Apfelberg DB, Masters FW, Robinson DW. Pathophysiology and
treatment of lightning injuries. J. Trauma 1974;14:453.
17. American National Standard Protective headwear for industrial
workers. ANSI Z89.1-1986 [database online]. New York: American
National Standards Institute 1986.
18. Orgel MG. Electrical burns of the mouth in children: a method for
assessing results. J Trauma 1975, 15;285.
19. Reddy SC. Electric cataract: A case report and the view of the
literature. Eur J Ophthalmol 1999;9:134-8.
20. Rijhwani A, Sunil I. Colonic fistula complicating electric burns—A
case report. J Pediatr Surg 2003;38:1232-3.
21. Laborde TC, Meir RH III: Amputations resulting from electrical
injury. A review of 22 cases. Arch Phy Med Rehabil 197 8, 59; 134.
22. Affleck DG, Edelman L, Morris SE, Saffle JR. Assessment of tissue
viability in complex extremity injuries: utility of the pyrophosphate
nuclear scan. J Trauma 2001; 50:263-9.
23. Koumbourlis AC. Electric injuries. Crit Care Med 2006; 30:S319-30.
24. Hammond J, Ward CG. Myocardial damage and electrical injuries:
significance of early elevation of CPK-MB isoenzymes. South Med
J 1986;79:414-6.
25. Chandra NC, Siu CO, Munster AM. Clinical predictors of myocardial
damage after high voltage electrical injury. Crit Care
Med 1990;18:293-7.
26. Nettelblad H, Thuomas KA, Sjoberg F. Magnetic resonance imaging:
a new diagnostic aid in the care of high-voltage electrical
burns. Burns 1996;22:117-9.
27. Hammond J, Ward CG. The use of Technietium-99 pyrophosphate
scanning in management of high voltage electrical injuries. Am
Surg 1994;60:886-8.
28. Hunt JL, McManus, Hary WP, Pruitt BA. Vascular lesions in acute
electrical injuries. J of Trauma 1974;14(6);461-73.
29. Cherington M. Central nervous system complications of lightning
and electrical injuries. Semin Neurol 1995;15:233-40.
30. Wilbourn AJ. Peripheral nerve disorders in electrical and lightning
injuries. Semin Neurol 1995;15:241-55.
31. Husetin C, Sevil AY, Ismill D, Dursun O, Yasar C, Ahmet D. Right
thalamic hemorrhage resulting from high-voltage electrical injury:
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32. Parasher A, Chittoria R, Nanda V. Extrapyramidal symptoms
following electrical burns – a case report. Burns. 2004;30:402-04
33. Chuang SS, Yu CC. Delayed obturator artery rupture: a complication
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34. Lai CC, Lin CM, Xiao QC, Ding LW. Pneumothorax: A rare
complication of electric injury. Burns 2008; 34:125-26.
35. Adams AL, Klein M. Electrical cataract: Notes on case and review
of literature. Br J Ophthalmol 1945,29;169-75.
36. Sinha JK, Roy SK. Perforation of the caecum caused by an electrical
burn. Br J Plast Surg 1976;29:179-81.
37. Kumar S, Thomas S, Lehri S. Abdominal wall and stomach
perforation following accidental electrocution with high-tension
wire: a unique case. J Emerg Med 1993;11:141-5.
38. Muir IKF, Morgan BDG. Burns of the genitalia and perineum. In:
Horton CE, editor, Plastic and Reconstructive surgery of the genital
area. Boston. Little brown 1973:443.
39. Mc Dougal WS, Peterson HD, Pruitt BA et al. The thermally
injured perineum. J Urolo 1979,121:320.
40. Bajaj SP, Pande Sujata, Ahmed I, Arora S. Abdominoperineal electrical
injury involving urogenital organs. Burns 2000;26:664-8.
41. Honda T, Yamamoto Y, Mizuno M, et al. Successful treatment of a
case of electric burns with visceral injury and full thickness loss of
abdominal wall. Burns 2000; 26:587-92.
42. Levine NS, Atkins A, McKeel DW, Peck SD, Pruitt BA. Spinal cord
injury following electrical accidents: Case reports. J Trauma
1975;15:459.
43. Varghese G, Mani MM, Redford JB. Spinal cord injuries following
electrical accidents. Paraplegia 1986;24:159-66.
44. Esses SI, Peters WJ. Electrical burns; pathophysiology and
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J. 27 1982;61:318-21.

290
Principles and Practice of Burn Care
Industrial and Chemical Burns
22
Mamta Sikroria
Chapter
INTRODUCTION
Industrial burns are similar to any other burns. The only
major difference is labor and union problems and one must
be fully aware of the labor laws and compensation. Also
emphasis on safety measures is a must as the treatment of
burn is a painful and prolonged process and also involves a
lot of expenditure. Besides the loss to the company in terms
of substantial man power loss, the cost of treatment and
subsequent compensation involved puts a tremendous
burden on the company. Any type of burn can occur
depending on the type of industry the worker is employed
with.
EPIDEMIOLOGY
The exact statistics of burn and cost of treatment is not
available in India. In America a fatal injury occurs every
103 minutes and a disabling work place injury occurs every
8 seconds. Work place injuries cost Americans $ 125 billion
in a year that’s equivalent to nearly triple the combined profit
reported by the top 5 fortune 500 companies in the same
year. Work related burns account for 20-25%1 of all serious
burns. In India approximately 1 million burns occur every
year. Percentage of industrial burns is not exactly known in
India. However, in a steel industry like ours the work related
burns which need admission account for 10-15% of total
burn admissions.2
Except major disasters which occur once in a while,
these burns are usually not very extensive and mortality is
accordingly very low. Most of the work related burns are
seen in welders where flash burns and explosions are the
most common injury producing events. Other common form
of injury is contact with hot metal (sometime molten metal).
These burns are very deep and cause severe morbidity but
are rarely fatal.
Chemical burns again are quite frequently reported at
work place but they are rarely fatal. The greatest risk of
phenol injury is associated with manufacturing of dyer,
fertilizer, plastics and explosive and in hospitals where it is
used as a disinfectant. Workers involved with glass etching
process, petroleum refining and air conditioner cleaning are
exposed to the risk of hydrofluoric acid injury.
Anhydrous ammonia injury commonly occurs in
agricultural workers. White phosphorus and mustard gas
injuries mostly inflict military personnel.3 Risk of injury due
to strong acids occurs in persons who are involved in plating
process and fertilizer manufactures. The greatest risk of
strong alkali injury in the work place is associated with
soap manufacturing.
Flame burns are less common in factories; usually occur
in restaurant workers but rarely serious to warrant hospital
admissions.
Electrical current injuries are very common in line man
working on high tension wires. They usually present with
very deep burns and even gangrene leading to multiple
amputations. They are commonly associated with injuries
like head injury or spinal injuries.
Electric flash burns are usually seen in workers who
are checking transformers or electrical switch boards.
Employees of utility companies, electricians,
construction workers (particularly those working with
cranes), farm workers moving irrigation pipe, oil field

Industrial and Chemical Burns
291
workers, truck drivers and individuals installing antennae
are at great risk of high voltage electric injury.4 Hot tar burn
is common in workers involved in building and road
construction. Cement burns (due to lime in it) though
reported in Western literature are very rarely seen in India.
Acid burns in Indian subcontinent are usually homicidal
and only few cases are accidental. Accidents are usually
domestic because of improper storage of chemicals used
for cleaning toilets and drains. Work related acid burns are
seen very often in jewelers who use sulfuric acid for
cleaning purpose. Phenol burns are commonly seen in
hospitals where it is used for carbolization of wards and
operation theaters.5-8
PATHOPHYSIOLOGY
Pathophysiology of thermal burns and electrical burn is
discussed in detail in chapters dealing with them. Contact
burns with hot metal are thermal burns and so
pathophysiology remains same. Here, we will only dwell
upon the chemical burns. There are similarities between
chemical and thermal burns, namely, both involve protein
denaturing and produce wounds which look superficially
alike. On the other hand, important differences do occur.
Thermal burns are typically produced by very short term
exposure to intense heat which is relatively quickly stopped.5
Chemical injuries are more likely produced by longer
exposure to chemical and this exposure may still be
continuing in an emergency room. In thermal injuries, there
is a rapid coagulation of protein due to irreversible cross-
linking reaction, whereas with chemical burn the protein
destruction is continued by other mechanisms. The
commonest mechanism is hydrolysis which is driven by
pH disturbances. Thus, there is an additional problem of
restoring tissue pH in order to stop cellular damage. These
mechanisms may continue so long as traces of the offending
agent are present, especially in the deeper layers. The degree
of tissue damage as well as the level of systemic toxicity is
determined by the chemical nature of the agent, its
concentration, the duration of skin contact and the
mechanism of action. Chemical injuries are classified either
by the mechanism of action on skin or by the chemical
class of the offending agent.
MECHANISM OF ACTION
With the exception of concentrated or fuming sulfuric acids,
thermal injury rarely plays more than a minor role in chemical
injury. The main mechanisms of action on living tissue can
be placed into six categories. The cells may be damaged by:
1. Reduction
2. Oxidation
3. Corrosion
4. Protoplasmic poisons
5. Desiccation or
6. Vesicant activity
Reduction: Protein denaturation is caused by the reduction
of the amide linkages following exposure to reducing agents.
Heat may also be a product of a chemical reaction, thereby
causing a mixed picture. Reducing agents are rather rare
and highly reactive chemicals, e.g. Alkyl mercuric
compounds, diborane, lithium, aluminum hydride and other
metallic hydrides.
Oxidation: Some agents cause damage by inserting oxygen,
sulfur or halogen (most often chlorine) atom to otherwise
viable body proteins. In general, this destroys a protein’s
ability to function. Sometimes, the oxidation product can
have very untoward effects as it becomes a competitor for
active metabolic sites. Common examples are sodium
hypochlorite, potassium permanganate, all peroxides and
chromic acid.
Corrosive agent: Some agents corrode the skin and cause
massive protein denaturation. As a class they act in a variety
of ways but they tend to produce a soft eschar which may
progress to shallow indolent ulceration. Phenols are the
commonest corrosive agents encountered. The hydroxides
of sodium, potassium, ammonium and calcium follow as
close second.
Protoplasmic poisons: Some poisons produce their effects
by causing the formation of esters with proteins or by the
binding or inhibition of the inorganic ions which are necessary
for normal healthy cellular function. Ester formers are
typified by formic and acetic acids while metabolic
competitors or inhibitors include oxalic and hydrofluoric
acids.
Desiccants: The damage by desiccants is caused by water
being extracted from tissues by hygroscopic agents. The
damage is often exacerbated by heat production as these
reactions are usually exothermic. Concentrated or fuming
sulfuric acid is the best known desiccant.
Vesicants: These are characterized by their ability to
produce cutaneous blisters and are potent chemical warfare
agents. They include mustards, arsenicals and halogenated
oximes. Mustards are alkylating agents and the damage to

292
Principles and Practice of Burn Care
DNA renders them toxic to proliferating cells. Following
death of the basal cells proteases are released from
lysosomes causing the epidermis to separate from the
dermis. The result is a blister with the basement membrane
on its dermal side.10
Chemical Classes
The chemical class of a noxious agent is based on the
chemical reactions which the agent is prone to initiate.
Acidity/alkalinity or the ability to influence pH is one of the
most important characteristics of all injurious chemicals
and one which must be considered in effective wound
management. It should also be noted that concentration plays
an important role in the reactivity of a chemical. In general,
concentrated solution (>70% wt) are more viscous, more
reactive, more hygroscopic and liberate more heat during
lavage or neutralization. The strength of an acid is defined
by how easily it gives up the proton; the strength of a base
is determined by how avidly it binds the proton. The strength
of acids and bases is defined by using the pH scale, which
ranges from 1-14 and is logarithmic. A strong acid has a pH
of 1, and a strong base has a pH of 14. A pH of 7 is neutral.
The severity of a chemical burn is related to a number
of factors, including the pH of the agent, the concentration
of the agent, the length of the contact time, the volume of
the offending agent and the physical form of the agent. The
ingestion of solid pellets of alkaline substances results in
prolonged contact time in the stomach, thus, more severe
burns. In addition, concentrated forms of some acids and
bases generate significant heat when diluted, resulting in
thermal and caustic injury. 11
The long-term effect of caustic dermal burns is scarring
and depending on the site of the burn, scarring can be
significant. Ocular burns can result in opacification of the
cornea and complete loss of vision (Fig. 22.1). Esophageal
and gastric burns can result in stricture formation.
Acids
Acids are proton donors and so they release hydrogen ions
and reduce pH from a neutral 7 down to values as low as 0.
Hydrogen ions are reactive and protonate any amine or
carboxylic site. This causes a protein structure to collapse.
After sometime, hydrogen ions catalyze protein hydrolysis
into constituent amino acids. Most acids produce a
coagulation necrosis by denaturing proteins, forming a
coagulum (e.g., eschar) that limits the penetration of the
acid. Mineral acids may also have other effects as seen in
concentrated sulfuric acid injuries where there is heat
generation and desiccation, producing a mixed injury.
Phosphoric acid for instance, can produce a similar mixed
injury by chelating calcium as well. Hydrofluoric acid is
somewhat different from other acids in that it produces a
liquefaction necrosis.
Bases
Bases are proton acceptors. The major types to cause injury
are mineral alkalis. Bases strip hydrogen ions from
protonated amine groups and carboxylic groups. This causes
protein structure to collapse and in common with acids,
bases catalyse protein hydrolysis. Bases can also cause a
mixed injury by forming salts and soaps, causing tissue
destruction as seen in the corrosive group. Bases typically
produce a more severe injury known as liquefaction
necrosis. This involves denaturing of proteins as well as
saponification of fats, which does not limit tissue penetration.
Ammonia, the hydroxides of sodium and potassium and
lime are the most common agents of this type to cause
injury.
A large number of industrial and commercial products
contain potentially toxic concentrations of acids, bases or
other chemicals that can cause burns. Some of the more
common products are listed as follows:
Acids
•
Sulfuric acid is commonly used in toilet bowl cleaners,
drain cleaners, metal cleaners, automobile battery fluid,
munitions and fertilizer manufacturing. Concentrations
Fig. 22.1: Deep acid burns of face and scalp in a 4-year-old child
involving both eyes with complete loss of vision

Industrial and Chemical Burns
293
range from 8% acid to almost pure acid. The concentrated
acid is very viscous and denser than water. It also
generates significant heat when diluted. These attributes
make sulfuric acid an effective drain cleaner. Concentrated
sulfuric acid is hygroscopic. Thus, it produces dermal
injuries by dehydration, thermal injury and chemical
injury. It rapidly produces carbon from glucose in the
tissues and thus typically produces a brownish black
slough (Figs 22.2 to 22.4).
•
Nitric acid is commonly used in engraving, metal refining,
electroplating, and fertilizer manufacturing. It causes a
typical orange yellow discoloration of the skin due to
xanthoprotein reaction.
•
Hydrochloric acid is commonly used in toilet bowl
cleaners, metal cleaners, soldering fluxes, dye
manufacturing, metal refining, plumbing applications,
swimming pool cleaners and laboratory chemicals.
Concentrations range from 5-44%. Hydrochloric acid
is also known as muriatic acid and it produces yellow
brown discoloration of skin (Fig. 22.5).
•
Hydrofluoric acid is commonly used in rust removers,
tire cleaners, tile cleaners, glass etching, dental work,
tanning, semiconductors, refrigerant and fertilizer
manufacturing and petroleum refining. This is actually
a weak acid and in dilute form, it does not cause
immediate burning and pain on contact..
•
Phosphoric acid is commonly used in metal cleaners,
rust proofing, disinfectants, detergents and fertilizer
manufacturing.
•
Acetic acid is commonly used in printing, dyes, rayon
and hat manufacturing, disinfectants and hair wave
neutralizers. Vinegar is dilute acetic acid.
•
Formic acid is commonly used in airplane glue, tanning
and cellulose manufacturing.
•
Chloroacetic acids:
–
Monochloroacetic acid is used in the production of
carboxymethylcellulose, phenoxyacetates, pigments
and some drugs. It has significant systemic toxicity
because it enters and blocks the tricarboxylic acid
cycle, inhibiting cellular respiration. It is highly
corrosive.
–
Dichloroacetic acid is used in manufacturing
chemicals. It is a weaker acid than trichloroacetic
acid and it does not inhibit cellular respiration.
–
Trichloroacetic acid is used in laboratories and in
chemical manufacturing. It is highly corrosive and
“fixes” tissues it contacts. It does not inhibit cellular
respiration.
Fig. 22.4: Full thickness burns due to concentrated sulfuric acid
with discoloration of sclera and black eschar on face
Fig. 22.3: Case of homicidal acid burns with brownish color eschar
and involvement of left eye
Fig. 22.2: Case of homicidal acid burns with superficial and deep
dermal burns of face due to sulfuric acid showing brownish
discoloration of skin and total loss of right ear

294
Principles and Practice of Burn Care
Bases
•
Sodium hydroxide and potassium hydroxide are used in
drain cleaners, oven cleaners, Clinitest tablets and denture
cleaners. They are extremely corrosive. Clinitest tablets
contain 45-50% sodium hydroxide (NaOH) or potassium
hydroxide (KOH). Solid or concentrated NaOH or KOH
is denser than water and generates significant heat when
diluted. Both the heat generated and the alkalinity
contributes to burns (Figs 22.6A to C).
•
Calcium hydroxide is also known as slaked lime. It is
used in mortar, plaster and cement. It is not as caustic
as NaOH, KOH or calcium oxide.
•
Sodium and calcium hypochlorite are common
ingredients in household bleach and pool chlorinating
solution. Pool chlorinators also contain NaOH and have
a pH around 13.5, making them very caustic. Household
bleach has a pH around 11 and is much less corrosive.
•
Calcium oxide, also known as lime, is the caustic
ingredient in cement. It generates heat when diluted with
water and can produce a thermal or caustic burn (Fig.
22.7). Lime is very often used in our country for removal
of moles and warts..
•
Ammonia is used in cleaners and detergents. The dilute
form is not very corrosive. Gaseous anhydrous ammonia
is used in a number of industrial applications, particularly
in fertilizer manufacturing. It is very hygroscopic (has
a high affinity for water). It produces injury by
desiccation and heat of dilution in addition to causing a
chemical burn. It can cause severe skin burns as well
as pulmonary injury.
Fig. 22.5: Case of homicidal acid burns due to hydrochloric acid
showing yellowish brown discoloration of skin
Fig. 22.6B: Same patient’s hand as in Figure 22.6A–Dorsal aspect
Fig. 22.6A: Accidental alkali burns of hand while using alkali in
laboratory–Palmar aspect
Fig. 22.6C: Patient with alkali burns due to Drainex(NaOH)

Industrial and Chemical Burns
295
•
Phosphates are commonly used in many types of
household detergents and cleaners. Substances include
tribasic potassium phosphate, trisodium phosphate and
sodium tripolyphosphates.
•
Silicates include sodium silicate and sodium metasilicate.
They are used to replace phosphates in detergents.
Dishwashing detergents are alkaline, primarily to builders
such as silicates and carbonates. They are moderately
corrosive.
•
Sodium carbonate is used in detergents. It is moderately
alkaline, depending on the concentration.
•
Lithium hydride is used to absorb carbon dioxide in space
technology applications. It vigorously reacts with water
to generate hydrogen and lithium hydroxide. It can
produce thermal and alkaline burns.
Organic Compounds
A wide range of organic compounds damage protein by
direct chemical reactions and heat production. They may
also act as solvents and disrupt the protein structure. Such
agents include phenol and petroleum based compounds.
–
Phenol, also known as carbolic acid, is a weak organic
acid used in the manufacture of resins, plastics,
pharmaceuticals and disinfectants.
–
Cresols are dihydroxybenzenes that are used as wood
preservatives, de-greasing agents and chemical
intermediates. These substances are very irritating to
the skin and can be absorbed through the skin to produce
systemic toxicity.
Inorganic Agents
Apart from the mineral acid and alkalis referred to above,
highly reactive elements damage skin by direct binding and
salt formation as well as heat production. Sodium,
phosphorus, lithium and chlorine are excellent examples
(Figs 22.8 and 22.9). Some salts especially fluoride can
also cause damage.
Oxidants
•
Bleaches: Chlorates are the primary chemicals used as
bleaches in the United States. Household bleach is alkaline
with a pH of 11-12, but it is dilute enough to be minimally
irritating to the skin. More concentrated, industrial
strength chlorates may be more damaging to the skin.
Fig. 22.7: Lime burn of face (lime used for ‘treating’ a mole)
Fig. 22.9: Phosphorus burns of face due to accidental
bursting of fire cracker
Fig. 22.8: Burns of face due to blast from a mixture of sodium and
potassium that the patient was grinding

296
Principles and Practice of Burn Care
•
Peroxides: Household-grade hydrogen peroxide (3%)
produces minimal-to-no skin irritation. Concen-
trations of 10% may cause paresthesias and blanching
of the skin. Concentrations of 35% or more cause
immediate blistering.
•
Chromates: Potassium dichromate and chromic acid
are common industrial chemicals used in tanning,
waterproofing fabrics, corrosion inhibitor, painting
and printing and they are also used as an oxidizing
agent in chemical reactions. Chromates can result in
severe skin burns and subsequent systemic toxicity,
including renal failure.
•
Manganates: Potassium permanganate is a strong
oxidizing agent that is used in dilute solutions as a
disinfectant or sanitizing agent. In dilute solutions, it
is minimally irritating to the skin. In concentrated
form or pure crystals, it can cause severe burns,
ulcerations and systemic toxicity (Figs 22.10A
and B).
•
Other common Corrosives which have been seen
to cause burns are concentrated Savlon (Fig. 22.11).
MANAGEMENT
Starts with on site care and transfer to a specialized burn
unit.
On Site Emergency Care of Burn Victims
Thermal burns caused by flame, steam, hot liquid or
contact with a hot surface before the medical help arrives:
1. Stop the burning processes by using low pressure water
2. Provide first aid measures as needed (CPR etc)
3. Control bleeding (Burns do not bleed and if it is present
there is another cause)
4. Have someone call for emergency medical assistance
5. Keep the victim warm using blanket
6. Stay with victim until help arrives
For tar burn cool the tar with water. Do not try to remove
the tar at the accident site.
Electric burn: Caused by contact with electric current.
Before medical help arrives:
1. If the victim is being held by the source, turn the current
off or use a non-conductive item (like wooden stick) to
knock the victim away from the source before
attempting rescue.
2. If clothing has got ignited use low pressure water to
extinguish the flame.
3. Provide first aid measures and CPR as indicated.12
Fig. 22.10B: Same patient after complete healing of
wounds in 2 weeks
Fig. 22.10A: Perineal burns due to potassium permanganate
used for sitz bath
Fig. 22.11: Superficial burns caused by Savlon cleaning during
dilatation and curettage operation in a female

Industrial and Chemical Burns
297
Chemical burn: Caused by contact with a hazardous
chemical. Before medical help arrives:
1. If in the powder form brush off as much as possible
before using water13
2. Immediately use low pressure water (safety shower) to
wash off the chemical 14
3. Remove contaminated clothing, jewelry and contact lens
while under water
4. Make the patient stay in shower for at least 30 minute to
1 hour before leaving for the hospital15
5. Take the MSDS sheet for the chemical to the hospital
with the person
6. Do not use neutralizing agent.
If the eyes are involved:
1. Flush the eyes thoroughly using eye wash station
2. Hold the eyelid open while flushing and remove contact
lenses while flushing with water
3. Do not use neutralizing agent
Once the Patient Reaches the Hospital
In the emergency take the history preferably from patient,
if not possible, the accompanying person(s) can give the
history. It is important to know the mode of burn and any
associated injuries so that treatment can be instituted
accordingly.
History
•
Type of burn
–
Thermal
•
Scald
•
Flame
•
Contact
•
Flash
–
Non thermal
•
Electric
•
Chemical
•
Radiation
•
Duration of exposure or contact with hot object
•
In case of chemical burns concentration of the offending
agent should also be known, the type of chemical (acid,
base etc) and whether it was ingested or only dermal
exposure should also be known.
•
In case of electric burn one should know whether it
was electric flash or high or low voltage contact electric
burn
•
Next important thing to know is whether patient had
any fall from a height or whether any heavy object has
fallen on the patient (common in case of steel industry)
in case of hot furnace blast in which patient sustains
flame burns as well as soft tissue and bony injury as
well (Figs 22.12A to C).
•
Other important point is to know whether water has
been used to extinguish the flames or cool down the
skin surface or to wash off the chemical from the skin
surface as it definitely reduces the depth of burn.
After taking history, patient should be thoroughly
examined to know:
1. The airway and circulation status
2. Extent and depth of burn
3. Presence of any head injury or spinal injury which takes
priority over burn treatment
4. Any ocular exposure (specially in chemical or electric
flash burn)
5. Presence of any long bone fracture.
Treatment in Emergency Room
1. Ensure airway patency and breathing
2. Establish good intravenous line and start IV infusion
with ringer lactate
3. Intravenous analgesics and/or sedation (if head injury is
ruled out)
4. Stabilize fracture(s) with splint
5. If chemical burn, then thorough washing with water
must be done for at least 30 minutes to 1 hour and
further confirmation for whether adequate washing has
been done is by litmus test.
6. CT scan for head injury and spinal injury should be done
7. ECG should be done if there is history of electric current
injury
After this patient should be transferred to burn ward.
In the burn ward the patient should be examined in detail.
History is taken again in detail. Any history of an associated
illness like diabetes mellitus, hypertension, ischemic heart
disease, etc. must be taken as this affects the prognosis. In
female patients history of pregnancy and lactation must be
taken. Physical examination should be done in detail again
to know the extent and depth of burn and any other
associated injury.
If a good intravenous access has not been already set
up in emergency room, it must be started now.
Patient should be catheterized. Analgesics and/or
sedatives should be given.
If patient is having any associated inhalation injury,
bronchodilators and oxygen by mask should be given. If
these measures do not suffice, endotracheal intubation or

298
Principles and Practice of Burn Care
tracheostomy can be done. Intravenous fluids should be
given using the Parkland formula or modified Brooke formula
aiming to keep the urine output at 0.5-1ml/hour/kg. In electric
burn more intravenous fluids (as much as 6-7 ml/kg/% burn)
are required to flush out the pigments released by damage
to RBC or muscles. If need be, mannitol can be given to
increase urine output.
Once the patient is stabilized with sufficient intravenous
fluids and analgesics and the urine output is satisfactory,
the wound should now be dressed and the investigations
are sent.
Investigations
Routine: Complete hemogram, biochemistry (urea, sugar,
creatinine, electrolytes, etc.) serum protein and albumin level
and sometimes serum transferrin level, if available. In case
of electric burn, samples for serum creatinine phosphokinase
and lactic dehydrogenase should also be sent.
If required, serum bilirubin, SGOT, SGPT, alkaline
phosphatase etc. should be sent specially in chemical burns.
In tribal areas and in certain communities like Sahu in
Chhattisgarh, sickling test must be done routinely and if
required complete Hb electrophoresis should be done.
Blood grouping should be done routinely.
Fig. 22.12A: 80% flame burns sustained during a hot furnace blast
Fig. 22.12B: Same patient after complete healing
from front
Fig. 22.12C: Same patient from back showing the hypertrophic
scarring in lower limbs and upper limbs

Industrial and Chemical Burns
299
ECG should be done routinely in all electric burn patients
and in elderly patients.
X-ray chest should be done to rule out any hemothorax
or pneumothorax in electric burn patients or in any other
patient, if required.
Radiography of spine and long bones should be done if
there is history of fall.16
Computerized tomography and radiography of skull
should be done again to rule out head injury in suspected
cases.12
Gastrografin contrast studies may be indicated for a
suspected perforated viscera.
Wound Management
In case of thermal burns (scald, flame, contact, flash, etc.)
wound is first washed thoroughly with any soapy solution
(surgiscrub or savlon) to remove all dirt or grease, etc. All
blisters are punctured, large blisters should be debrided.
The wound should be washed with saline or distilled water.
Second degree superficial and deep dermal burn wounds
are dressed with antimicrobial creams, nonadherent and
absorbent dressings. Skin substitutes may be used depending
on their availability in a particular hospital.
Various biological dressings available in India are amniotic
membrane, collagen, etc. Integra17 which is a double layered
biological dressing (outer Silastic epidermis and inner
artificial dermis) is available but very costly. Other skin
substitutes like porcine skin and cadaver skin are not easily
available for use in India.
Biological dressings reduce the number of dressings
thereby reducing the work load on the burn team. Other
important advantages of biological dressings are that they
reduce evaporative water loss from denuded body surface
thereby reducing fluid requirement, reduce pain as the
exposed nerve endings are covered and also reduce the need
for antibiotics by preventing bacterial invasion of wound.
Sometimes, in second degree deep dermal burns the
biological dressing is rejected. Still the wound healing is
enhanced as initial prevention of wound desiccation (because
of evaporative loss) and bacterial invasion prevents
conversion of second degree deep dermal wound into third
degree burn. After the initial biological dressing wound is
opened after 48 hours and reviewed. If the dressing is
adherent and patient is stable he/she can be discharged with
advice to come for out patient treatment.
If burns are very extensive, especially in circumferential
burns, biological dressings become too costly and we opt
for conventional dressings. Again for the same reason
because the biological dressing does not adhere it is not
used for third degree burns.
We go for conventional dressing in extensive
circumferential burns and in third degree burns. After
cleaning with surgiscrub and saline a final wash with 5%
povidone iodine lotion is done (optional) and then dressing
is done with 1% silver sulfadiazine ointment. The author is
using silver sulfadiazine ointment mixed with 30% Aloe vera
juice for dressing in their setup. It is known that silver
sulfadiazine inhibits the wound epithelization 18and aloe vera
enhances epithelization by increasing wound circulation and
enhancing collagen formation.19
Aloe vera acts as an antimicrobial also as it prevents
bacterial growth. Ointment like mafenide acetate is very
good for burn wound as it has very good penetration of
eschar but it is not available in India and is also very toxic.20
Other ointments like povidone iodine, nitrofurazone,
Neosporin, etc. are also in use but they are better used for
small wounds as their antimicrobial spectrum is very limited.
For extensive burns, silver sulfadiazine is the best.21
In third degree circumferential burns escharotomy
should be done once the patient is adequately resuscitated
as distal circulation may be compromised or in case of burns
of the trunk, respiration may be compromised.
In electrical burns fasciotomy must be done
immediately.12 Other resuscitative measures are same as
for thermal burns.
Chemical Burns
The management of chemical burns differs a little from
other burns.22-24
Management Guidelines for Chemical Burns
1. Evaluate ABC (Airway, Breathing, Circulation)
2. Start decontamination:
A. Ensure medical personnel are protected
B. Remove all clothing (undress to access)
C. Wipe away or debride all solid chemical particles
D. Inspect hair, nails and web spaces for collections of
the chemical
E. Remove caked compounds with green soap solution
(liquid soap and 10% Isopropyl alcohol)
3. Obtain history
A.
Type and concentration of chemical
B.
Nature and duration of exposure
C.
Concomitant traumatic injuries

300
Principles and Practice of Burn Care
D.
Pre-existing medical illnesses
E.
Tetanus immunization and allergies
4. Physical examination
A. Exposure by ingestion may lead to esophageal edema,
stridor, use of accessory muscles, etc.
B. Dermal exposure: Size, depth, location, circum-
ferential burns, etc.
C. Ocular exposure
D. Visual acuity
E. Presence of periorbital dermal lesion
5. In case the nature of the agent is not known, litmus
paper test can be done to find out whether agent was
acid or alkali (Fig. 22.13).
6. Start treatment with specific antidotes if applicable (only
after initial thorough irrigation with water
7. Identify hospitalization criteria
8. Check effectiveness of irrigation, use pH/litmus paper;
if the pH is not neutral, continue irrigating for an
additional hour (Dilution is the solution to chemical
pollution).
Caustic Ingestions
•
Gastric emptying is contraindicated. Activated charcoal
is not useful and may interfere with subsequent
endoscopy. Dilution with milk or water is contraindicated
if any degree of airway compromise is present. Milk
may interfere with subsequent endoscopy. Water is
benign. Some substances, such as drain cleaners
containing sulfuric acid or sodium hydroxide, generate
heat when diluted with water. Local areas of heat
generation can be minimized by diluting with a moderate
quantity of fluid (250-500 ml).
•
Do not attempt to neutralize the caustic agent.
Neutralizing the caustic agent may generate excessive
heat from the exothermic reaction of neutralization.
Endoscopy for Ingestions
•
Perform esophagoscopy and gastroscopy on all patients
with symptomatic ingestions and on patients who are
asymptomatic but have a history of a significant ingestion
of a substance with the potential to cause major injury.
•
Findings on esophagoscopy do not correlate well with
physical signs and symptoms. Of patients with
esophageal injuries, 2-15% have no oral burns.
•
Burn findings are classified as superficial, transmucosal,
or transmural.
•
Esophagoscopy findings are used to guide further
treatment. The presence of full-thickness or
circumferential burns is associated with future stricture
formation.
–
The issue of whether to extend the endoscopic
examination past the first site of injury is
controversial.
–
Esophageal and gastric burns can result in stricture
formation.
Ocular Exposures to Chemicals25
•
The goal for decontamination should be to achieve a pH
(of the eye wash) of at least 7.2, preferably 7.4.
•
If pH paper is not available, an adequate guideline is
decontamination with 1-2 L of irrigation fluid over 30-
60 minutes.
•
Ocular burns can result in opacification of the cornea
and complete loss of vision (Fig. 22.14).
Fig. 22.13: Litmus paper test to identify the chemical (blue litmus
turning red indicated acid and red paper turning blue indicating alkali)
Fig. 22.14: Ocular chemical burns showing complete corneal
opacification

Industrial and Chemical Burns
301
•
Indications for hospitalization of patients with chemical
burns are almost same as other burns like:
–
High risk patients (concurrent illnesses)
–
Burns of hand, foot, face, eye or perineum
–
Burns of greater than 15% total body surface
–
Deep burns (second degree deep dermal or third
degree)
–
Burns with substances that have systemic toxicity.
SPECIFIC AGENTS
In case of an industrial setting the causative agent is usually
known. The following list of chemical is not definitive but
it provides an inventory of the commonest agents to cause
chemical burns.
Acetic Acid
This acid is a protoplasmic poison. Glacial acetic acid nearly
100% pure is the usual offender. Vinegar, a 5% solution of
acetic acid, is usually benign unless scalding hot.
Alkali (Strong)
Multiple chemical agents are involved in caustic alkali burns.
Lime, potassium hydroxide and sodium hydroxide are the
most common agents causing chemical injury. Accidental
injury occurs in infants and toddlers. The mechanism by
which these alkali injuries are caused is due to three factors:
1. Saponification of fat causes fatty tissue to lose its
function with increased damage due to heat reaction
2. Extraction of considerable water from cells cause
damage because of an alkali’s hygroscopic nature; and
3. Alkalis dissolve and unite with the proteins of the tissues
to form alkaline proteinates, which are soluble and
contain OH ions and these ions cause further chemical
reactions which initiate deeper injury of the tissues.
As with other chemical burns alkalis are capable of deep
penetration and can cause severe pain. For treatment it is
necessary to remove the causative substance as quickly as
possible by washing with large volumes of water. Washing
is presumed to cause dilution and elimination of a chemical
substance, attenuation of the chemical reaction and
suppression of any raised tissue metabolism to have an anti-
inflammatory action, to suppress the hygroscopic action
and to return skin pH levels to normal. In lime burns the dry
lime must be brushed away before washing in order to
minimize the production of heat.
It is very difficult to determine the depth of tissue damage
on admission to a hospital because chemical burns are
different from thermal burns. Because the corrosive material
blackens the skin, rapidly converting it to a firmly adherent,
firm, dry eschar, a true assessment of the depth of an injury
can only be made in retrospect as spontaneous healing or
non-healing occurs.
Ocular damage is a common sequel to alkali injury.
Damage is related to the pH: the higher the pH, the greater
the damage to the eye, with the most significant injury
occurring around pH 11-11.5. Alkali penetrates quickly and
with little resistance, saponifies plasma membranes,
denatures collagen and causes vascular thrombosis in the
conjunctiva, the episclera and even in the anterior uvea.
Very small volumes of alkali material can cause significant
damage. Such damage may be made worse by repeated
attempts to wipe off the chemical agent with the hands or
inadequately washing the eyes. The policy is to treat with
topical anesthetics followed by copious irrigation, induction
of cycloplegia and mydriasis as soon as possible. Antibiotics
such as gentamicin and chloramphenicol are effective.
Topically cysteine, a collagenase inhibitor is applied every 2
hours in order to prevent perforation. Topical steroids are
applied four times a day after complete epithelization has
taken place.
Assorted Acids
Tungstic, picric, sulfosalicylic, trichloroacetic and cresylic
acid are all strong protoplasmic poisons. They form firm
eschars which may help spare underlying tissue from
damage. Tannic acid has been used in the past as a treatment
for thermal injury. These acids are absorbable and cause
metabolic symptoms and are both renal and hepatic toxic.
Most have pungent, suffocating odors and have wide
industrial usage.
Cement
Cement is really an alkali but warrants a separate mention
as it differs in many ways. When mixed with water, sand
and gravel, it becomes more abrasive and is known as
concrete. Injuries are not infrequently found in construction
workers and do it yourself enthusiasts.26 Cement (calcium
oxide) penetrates clothing and reacts with sweat and an
exothermic reaction takes place. The dry powder is very
hygroscopic and causes a desiccation injury if not exposed
to moisture. Hydrated calcium oxide becomes calcium
hydroxide. An injury progresses as with a strong alkali. The
critical substance responsible for skin damage is the hydroxyl
ion.27 A victim may not know until many hours later that a

302
Principles and Practice of Burn Care
burn has been sustained as it is often a painless occurrence
under clothing. Treatment consists of removal of
contaminated clothing and washing the affected area with
soap and water. Surgical excision is likely to be required as
these injuries are often deeper than they appear.
Chromic Acid
A powerful oxidizing agent, chromic acid is used in the
cleaning of other metals. The active chemical is chromic
trioxide (CrO3) in a solution of strong sulfuric acid. If a
sample is examined it is a pungent viscid yellow liquid.
Contact with skin causes protein coagulation, blister
formation and ulceration. Ingestion leads to gastroenteritis
which becomes severe very rapidly with vertigo, muscle
cramps, peripheral vascular collapse and coma. This is
followed by nephritis and is associated with glycosuria. The
lethal dose is from 5 to 10 gm. Primary treatment of contact
areas comprises water lavage to dilute the acid. Washing
with a dilute solution of sodium hyposulfite followed by a
rinsing with a buffered phosphate solution is the treatment
of choice and should be available if this agent is in common
use (70 gm monobasic potassium phosphate and 180 gm
dibasic sodium phosphate to 850 ml of water). Systemic
manifestations are to be treated with Dimercaprol 4 mg/kg
by deep intramuscular injection every 4 hours for 2 days,
followed by 2-4 mg/kg daily for about a week along with
support for the failing organ system.
Formic Acid
Despite the common use of this organic acid for industrial
de-scaling and as hay preservative28, dermal injury is rare.
All patients injured by formic acid should be hospitalized, if
only for observation because cutaneous absorption from
the injured area can cause metabolic acidosis, intravascular
hemolysis, hemoglobinurea and renal failure as well as
pulmonary complications, including ARDS. Vomiting and
abdominal pain are usually common and although the cause
is unknown, necrotizing pancreatitis has been described as
a complication of formic acid ingestion. However, elevated
serum amylase has not been reported in formic acid
poisoning. Acidosis should be corrected with intravenous
sodium bicarbonate. Minor hemolysis requires no treatment,
but diuresis with mannitol is recommended where hemolysis
occur after deep burns. Where extensive absorption of formic
acid has occurred, hemodialysis should be considered. The
wound has a greenish hue and is followed within 48 hours
by gross edema and blister formation. Wounds tend to be
deeper than they initially appear and are best treated by surgical
excision.
Hydrocarbons
Petrol burns are seen in patients trapped under vehicles
following road traffic accidents. The solvent properties of
hydrocarbons promote cell membrane injury and dissolution
of lipids, resulting in skin necrosis. Symptoms present with
erythema and blistering. Burns tend to be superficial and
heal spontaneously 29, grafting is usually not necessary
although full thickness burns do occur. If absorbed
systemically, toxicity can cause respiratory depression. If
ignited deep thermal injury is common.
Exposure to gasoline may be complicated by the leading
agents that are used to improve the performance
characteristics. Significant lead absorption and subsequent
neurological damage may ensue from gasoline exposure.
Tetraethyl lead is more toxic than elemental lead in this
regard.
Common complications from the contact effects of
gasoline and other light petroleum products such as kerosene
include toxic effects from inhalation and ingestion. In
addition to the skin burn, the patient often may have serious
multi-system effects, including organ system failure.
Inhalation or absorption of gasoline produces symptoms
similar to those of ethanol in descaling, including ataxia,
mental confusion and blurred speech. High concentrations
of gasoline vapors may lead to coma and death. Once far
more common, the gasoline snifter is much less frequently
found now.
Cardiovascular complications include sudden death when
inhalation is followed by strenuous exercise or stressful
situations. Spontaneous and severe cardiac arrhythmias are
the causes of death in these cases. Catecholamine release
appears to increase the toxic potential of the petroleum
distillate.
Gasoline absorption has produced renal damage to include
glomerulonephritis and renal tubular acidosis. The
hydrocarbon hepatitis is secondary to vascular endothelial
damage and is usually a reversible lesion without long term
sequel.
Initial treatment of the gasoline immersion burn is to
remove the clothing and cleanse the skin surfaces. Further
emergency treatment of a petroleum distillate burn should
include low pressure irrigation with water for at least 1
hour. The patient should be admitted to the hospital and
observed for at least 24 hours. A monitored bed is appropriate

Industrial and Chemical Burns
303
for these patients. Serum lead levels should be obtained and
treatment initiated if the lead level is greater than 30 to 40
nanogram per 100 ml. Dimer caprol (British Anti-lewisite)
and calcium EDTA followed by penicillamine therapy for
15 to 20 days has proved efficacious in these cases.
Hydrofluoric Acid Burns
Hydrofluoric acid (HF) is a colorless liquid or gas that is
manufactured by allowing sulfuric acid to react with
fluorospar in heated ovens. HF was first manufactured by
an English glassworker in about 1720.21 It is produced as a
gas, purified and then condensed in a liquid form. An
aqueous solution will fume when the concentration is greater
than about 50%. HF is a weak acid and is 1000 times less
dissociated than hydrochloric acid. It means that HF can be
absorbed or penetrate through the skin without dissociating
into the constituent hydrogen and fluoride ions.
Hydrofluoric acid is used in glass and semiconductor
industries as an etching agent, in the plastic industries in
production of various plastic materials and in the nuclear
industries as a solvent for uranium. Many rust removal agents
contain hydrofluoric acid. Most hydrofluoric acid burns
appear to come from either the semiconductor or the glass
industry.
Hydrofluoric acid is very damaging to tissues even at
low concentrations.30 An HF solution of greater than 50%
concentration produces immediate pain and tissue
destruction. Solutions of less than 20% may cause burns
delayed as long as 24 hours after the exposure while
intermediate strength solutions can cause symptoms as long
as 8 hours after exposure. The fluoride ions may enter the
body through the skin or any mucous membrane, including
the respiratory and gastrointestinal system.
The fluoride ion causes a breakdown in all calcium-
dependent processes in the cell membrane. This destruction
of the cell membrane causes liquefaction necrosis of the
skin and subcutaneous tissues. The salts formed by HF are
soluble and permeate through the tissues with continued
destruction. The fluoride ion is also a cellular poison and
causes cell death by blocking glycolysis.
As the salts continue to be bioactive, the fluoride ions
must be inactivated. Without specific treatment, the injury
is progressive and potentially fatal. Calcium and magnesium
ions form insoluble salts with the fluoride ions. All other
salts are soluble and dissociate completely allowing the
continued diffusion of ions into the tissues.
HF = H+ + F– (Toxic)
Immediately after the exposure, the area should be
flooded with copious amounts of water at low pressures.
While in the shower, the worker should remove all clothing
and shoes to decrease the possibility of further
contamination. After the area has been flooded with water
for at least 30 minutes, the remaining fluoride ions can be
fixed in insoluble salts with the application of topical
magnesium oxide ointment or calcium chloride/calcium
gluconate solutions. Of these, calcium holds the most promise
for skin burns from HF.
Ca++ + F– = CaF2 (Nontoxic)
Some authorities also recommend the use of quaternary
ammonia compounds such as Hibclens or Zephiran. These
ammonia compounds have a dubious effect upon fluoride
skin poisoning. They may also tend to irritate sensitive skin
like that of the face.
Initial Presentation
The initial presentation is usually pain at the site of the
exposure. Local erythema and edema may be present. The
pain is uniformly described as excruciating, particularly after
exposure to solutions of greater than 20% concentration.
Also, the pain is often described as deep, throbbing or
burning. Regional nerve blocks may be required for relief.
Exposure to concentrated HF over as little area of skin as
2.5% of TBSA has produced fatal systemic fluoride
poisoning.
As the injury progresses, erythema and edema progress
to blanching. Bullae denote a more severe burn that requires
aggressive treatment. A grossly necrotic area may develop
with a subsequent sloughing of tissues and slow healing
wound. In severe cases, bony injury may manifest and severe
decalcification may be noted. Hydrofluoric acid burns have
caused systemic hydrofluorosis with subsequent death.
Initial Treatment
If there is evidence of skin damage, even in the form of
erythema, the skin has been penetrated by fluoride ions and
these must be inactivated. It is probably appropriate and
safe to assume that all spills are contaminated and that the
patient will develop an injury, if not treated. Before
proceeding, the provider must ensure that adequate
protection against this agent is available and being used.
Butyl rubber or nitryl gloves and apron are worn as a
minimum precaution. Shoe covers decrease both “tracking”
and contamination of the provider’s shoes. All contaminated

304
Principles and Practice of Burn Care
clothing and bedding should be placed in heavy plastic
garbage bags and prominently labeled to ensure that there is
no spill.
The area should be copiously flushed with running water
while materials and further preparations are in progress. All
bullae and vesicles should be aspirated to remove fluoride-
containing fluids. Care must be taken not to spill the aspirate
on any other part of the skin. The lesions must then be
debrided.
Local Infiltrating Therapy
After debridement of the lesions, 10% calcium gluconate is
injected into the burn to further bind the fluoride ions. About
0.5 ml of solution should be injected intradermally for every
square centimeter of tissue damage.31 The injection is
extended about 0.5 cm into the margins of the burn to bind
ions that may have already migrated there. To ease the pain
of injection, a 27 or 30 gauge needle is used and the area
slowly infiltrated. The calcium gluconate injection is usually
effective in relieving the pain of the burn. Unfortunately,
the volume of the calcium chloride is limited to only 0.5 ml
per injection. This severely restricts the amount of calcium
that can be injected therapeutically in one sitting. Recurrence
of the pain is an indication of further fluoride ion migration
and another injection is needed.
Intra-arterial Injection
Intra-arterial calcium may provide better tissue distribution
and less tissue distention than injection into the burnt area.
The arterial catheter should be placed in the distribution
system, of course. Arterial injection of calcium may provide
relief from burns to the finger tips without loss of either
nail or distal finger. The calcium may be injected as either
gluconate or chloride over four hours. If the patient
complains of continued pain, additional calcium may be
infused. Intravenous administration of calcium has not been
effective as the concentration of calcium salts is limited by
systemic calcium toxicity.
Eye Injuries
HF solution or vapor in the eye causes a more extensive
damage than other acids in similar concentrations. The
deeper penetration and liquefaction necrosis makes HF more
destructive to the eye. Eye burns should be treated with
immediate and copious irrigation of the eye immediately
after exposure. If available, a morgan contact irrigating lens
may be ideal for this. Eyelid spasm may be decreased by
use of tetracaine or other ophthalmic anesthetic solutions.
Following this irrigation, a 1% calcium gluconate solution
in isotonic sodium chloride can be used as drops and instilled
every 2-3 hours. Some workers feel that only irrigation
with water, isotonic saline solution or magnesium chloride
solution offer any therapeutic benefit. Other therapies that
have been used on skin have been associated with increased
rates of ocular injuries. Prompt ophthalmologist’s
consultation is essential.
Dressings
After the injection of calcium, the area may be covered
with either calcium or magnesium oxide dressings.
Magnesium oxide dressings are less expensive and easier to
obtain but not as effective as calcium-based dressings.
Calcium chloride soaks may also be used. Some authors
recommend 2.5% calcium gluconate in a gel vehicle but
further clinical trials are indicated before advocating this
more costly therapy. A mixture of 2.5 to 5.0% calcium
gluconate in KY jelly may be used as an inexpensive alternate.
The wound must be inspected frequently to determine
if there is any further damage. Recurrence of pain is an
indication for re-inspection and re-injection. A fluoride burn
should always be re-inspected at 24-hour intervals, no matter
how small or innocuous it seems.
Hydrofluoric acid can rapidly penetrate the nail bed and
destroy the underlying nail bed and matrix. Infiltration of
calcium ions into the subungual spaces is extremely painful
and may cause vascular compromise in the restrictive space
between nail and nail bed. When ungual areas are involved
in a hydrofluoric acid burn, the affected nail must usually
be excised under regional anesthesia. Removal of the nail
allows regeneration after the injury.
Treatment that has been proposed in the past includes
steroids and early surgical excision of the lesion. Steroids
have not shown any beneficial effect and surgical therapy
may be unnecessarily mutilating.
Complications
Skin burns with hydrofluoric acid may be associated with
significant systemic absorption of fluoride ions. The fluoride
ion can cause decalcification of bone and systemic
hypocalcemia as a result of the formation of poorly soluble
calcium fluoride complexes. This precipitous drop in serum
calcium has been implicated in fluoride-induced sudden

Industrial and Chemical Burns
305
death. The mechanism of death is usually intractable
ventricular fibrillation but this dysrhythmia does not respond
to usual doses of intravenous calcium.32 Several authors
have reported use of massive doses of calcium salts with
relief of the hypocalcemia. This profound hypocalcemia is
often not associated with tetany.
Other authors feel that the leak of potassium from
fluoride-damaged cells causes a fatal hyperkalemia. This
hyperkalemia is mediated by calcium-dependent channels
and has been blocked in dogs by quinidine. There are no
reported trials of quinidine in fluoride toxic humans with
hyperkalemia, hypocalcemia, and ventricular dysrhythmias.
However, in view of the poor response to extant therapies,
quinidine may be appropriate in these selected patients.
If there is any evidence of systemic fluorosis or the
possibility of inhalation injury, the patient should be admitted
to the hospital and observed for at least 24 hours. In these
patients, monitoring of liver function studies, renal function
studies, electrolytes and serial serum calcium levels in
indicated.
Elemental Sodium, Potassium and Lithium Burns
Sodium, potassium and to a lesser extent lithium
spontaneously ignite when in contact with water, including
water vapor in the air or on the skin (Fig. 22.8). Using
water to irrigate these burns only intensifies the combustion
effects. When these metals combine with water, sodium,
potassium and lithium hydroxides are formed. These are
among the strongest of alkalies and capable of causing severe
caustic burns.
To extinguish these burning metals, the oxygen and water
must be removed from the area. A class D fire extinguisher
or sand may be used to smother the fire. After the fire is
extinguished, the area should be covered with oil, such as
mineral oil or cooking oil to isolate the metal from water.
Small metal pieces should be removed by debridement to
healthy tissues. Embedded pieces must be removed
surgically. Following debridement and ensuring that all pieces
are removed, the area must be irrigated with water, using
the same techniques as for an alkali burn.
Light Metals
Water is generally contraindicated for extinguishing burning
light metal fragments because of the hydroxides and
hydrogen gases that are produced when water is added to
hot metals. Particularly injurious are burning fragments of
elemental magnesium, which produces magnesium oxide.
If the pieces of magnesium are not removed, the small ulcers
that form slowly enlarge and become extensive lesions. After
these fragments of burning metal are removed, the resultant
wound must be treated as alkali burns.
Phosphorus Burns
White phosphorus is a waxy translucent substance that
ignites spontaneously on contact with air. It is usually
preserved under water and becomes a liquid at 44oC. White
phosphorus is used in the construction of military weapons
and fireworks and is a component in insecticides and rodent
poisons.33 White phosphorus is the most common form of
phosphorus found in chemical burn (Fig. 22.9).
Phosphorous pentachloride is a yellowish white fuming
crystalline mass with a pungent odor. It is widely used as a
catalyst, a chlorinating and a dehydrating agent. There is
only one report of phosphorus pentachloride chemical burn
in the literature, so this agent is not extensively discussed.
Following an explosion of white phosphorus munitions,
flaming droplets of white phosphorus are flung about widely
and dense clouds of white smoke with a typical “garlic-
like” smell are produced. The flaming pieces of phosphorus
cause primarily thermal tissue damage but may also cause
high-speed projectile injuries. The smoke is made by the
oxidation of phosphorus to phosphoric acid, which can
damage the lungs as well as the skin. Some “tracer” bullets
have white phosphorus as a major component. This may
lead to absorption of retained phosphorus fragments after
either an explosion of a phosphorus-based shell or after a
bullet wound with a tracer bullet.
White phosphorus is highly fat soluble and is easily
absorbed from phosphorus particles driven into the
subcutaneous lipid tissues or from the gastrointestinal tract
if ingested. The two most common systemic effects are
hepatotoxicity and renal damage, but changes in blood
phosphorus and calcium levels are also noted. ECG changes
with prolongation of the QT interval, ST segment
depression, T-wave changes and bradycardia are also noted.
Sudden death34 has been reported in patients with reversed
calcium-phosphorus ratios but is fortunately rare. Monitoring
for electrocardiographic abnormalities and changes in serum
calcium and phosphorus is appropriate for patients with
significant wounds. In cases where systemic absorption is
suspected, BUN, creatinine, serum phosphorus and liver
enzymes should be assessed frequently.

306
Principles and Practice of Burn Care
Flaming white phosphorus is extinguished by immersing
the pieces in water. Surface particles and particles embedded
in clothing should be promptly removed. During transport,
the emergency medical team should cover the burned areas
with moistened cloths to prevent further burning. This is
the same method that the armies of Israel and the United
States recommend for transport of the patient burned by
white phosphorus. Irrigation may help to remove surface
particles, but is not effective against those particles driven
deep into tissue by blast effects.
The wound may then be washed with one percent copper
sulfate solution. The copper sulfate solution combines with
phosphorus to form copper phosphate, which can be readily
identified as black particles. These black pieces can be easily
debrided. If the particles are not debrided, they are absorbed
and systemic effects ensue. This is a controversial step
and some investigators feel that it is not required and may
even be detrimental to the patient. Certainly, once
debridement is completed, no further copper sulfate solution
is needed.
The copper sulfate solution should not be used for a
prolonged period, because of the risk of systemic copper
poisoning. Systemic copper poisoning can be manifested
by vomiting, diarrhea, oliguria, intravascular hemolysis,
hematuria, hepatic necrosis and cardiovascular collapse. The
hemolysis is thought to be due to copper’s inhibition of the
erythrocyte hexose monophosphate shunt. This results in a
hemolysis similar to that found in G6PD deficiency disease.
To minimize copper absorption, the wound may be
irrigated with a solution of 5% sodium bicarbonate and 3%
copper sulfate suspended in 1% hydroxyethyl cellulose. Wet
dressings of copper sulfate in any form should never be
applied to the wound. Following debridement, the wound is
irrigated with copious amounts of water to remove the
copper salts. Unfortunately, in the animal studies performed
by Eldad and Simon, mortality was not decreased by use of
this gel.
Other investigators irrigate the wound with sodium
bicarbonate in order to neutralize the effects of the phosphoric
acids. This also had no appreciable decrease in mortality in
the experimental model.
Metabolic derangements have been noted with white
phosphorus injuries. Hypocalcemia, hyperphosphatemia and
ECG abnormalities are all noted. The electrocardiographic
abnormalities include prolongation of the QT interval,
bradycardia, and nonspecific ST-T wave changes.
Sulfur Mustard Gas
Sulfur mustard is a vesicant gas used primarily for warfare.
It is a close relative of the cytotoxic nitrogen mustard
compounds used for cancer chemotherapy. Sulfur mustard
goes by several names: H, HD in the United States Military
classification system, mustard, mustard gas or even Yperite
(for the battle of Ypres where the first formal chemical
warfare took place in 1915).
The toxic reactions of mustard occur when it forms
highly reactive and unstable “onium” compounds that further
cause inhibition of cellular glycolysis, alkylation of DNA
purine bases (guanine and adenine) and breakdown of DNA.
These effects occur within an hour of exposure to 19-33
mg/m3 concentrations.35
Phenol Burns
Phenol is an aromatic acid alcohol that is a highly reactive
and corrosive contact poison. The phenols have been used
as bactericidal agents and are used in industry as bases for
plastics and organic polymers. In the form of creosote, it is
also used as a preservative for wood.
Phenols were first used as antiseptics by Lister in 1867
and their effects on tissues have been well studied. In either
the vapor or the liquid form, phenol is rapidly absorbed
through the skin surfaces. Phenol vapors are easily absorbed
by the lungs. If the skin absorption is significant, the
exposure may result in toxic effects on the cardiovascular
and central nervous systems. These include:
•
Central nervous system depression
•
Hypotension
•
Intravascular hemolysis
•
Pulmonary edema
•
Shock
•
Death
The most common manifestation of systemic phenol
poisoning is a profound fulminant central nervous system
depression with coma, hypothermia, loss of vasomotor tone
and respiratory arrest. In many cases, loss of consciousness
may be noted within 30 minutes of skin contact.
Cardiopulmonary collapse frequently accompanies this CNS
presentation and is due to the cardiac depressant effects of
phenol. In animal studies, as little as 0.625 mg/kg of phenol
has caused death.
Phenol skin burns are characterized by initial pain,
followed by numbness as the nerve endings are anesthetized.
The skin then blanches and an eschar forms over the burned

Industrial and Chemical Burns
307
area during a period of hours. Phenols in strong
concentrations rapidly produce a whitish slough, which
turns to a greenish-black or copper-colored eschar.
Coagulation necrosis of the dermis delays the absorption,
but this delay is only temporary.
Treatment must be initiated immediately. Before washing
the contaminated area, remove any liquid on the skin. Swabs,
gauze pads or even clothing is acceptable for this. If
polyethylene glycol is not available, glycerol may aid in the
removal. Removal of the liquid should not wait until these
materials are available.
Water irrigation is not recommended by some authorities.
In severe phenol burns, the necrotic tissues may act as a
temporary barrier that does not allow penetration of the
water into the deeper layers of the injury. The water may
also dilute the phenol and allow more rapid penetration into
the skin.
Although water irrigation is effective for phenol burn,
wiping the skin with undiluted polyethylene glycol 300 or
400 dissolves and removes the phenols more quickly36 than
water alone. Alcohols and glycerol are also effective in
removal of the phenols. Polyethylene glycol solution is not
irritating to the tissues and may safely be used to irrigate
facial burns and eye injuries.
Alcohol Burns
Isopropyl alcohol is a commonly used disinfectant in hospital
settings and is used for cleaning in home and industry. In
infants and small children, it can be associated with skin
burns. The mechanism of action is thought to be desertification
of the skin. The degree of burn is related to the concentration
of the alcohol, the duration of the exposure and the condition
of the skin to which the alcohol has been applied. Premature
infants are at most risk. Burns occur most often in areas of
pressure and where the alcohol can pool, such as around the
diapers.
Coal Tar Burns (Figs 22.15A to 22.16B)
Coal tar or bitumen is used for making roads and roofs.
They are composed of different aliphatic, aromatic and
heterocyclic compounds. They are used in molten form at
very high temperatures (292°C). Whenever, the skin comes
in contact with bitumen it rapidly cools down and adheres
tightly to the skin. The heat contained within this layer of
tar can continue to damage the underlying skin and cause
deeper burns if not acted upon very quickly. However, if an
attempt is made to peel off the bitumen it can cause further
damage to the epidermis to which it bonds tightly. In case of
small areas the tar is best left as such because the skin under
it is usually sterilized by the heat and the layer of tar acts as a
‘dressing’ under which the skin heals spontaneously and the
tar separates slowly in 2-3 weeks.
It is advisable to cool the skin with water for 30 minutes
as a first aid measure to limit the damage to the skin. For
extensive areas or if patient’s face or limbs are involved
circumferentially, the tar can be safely removed by wiping
with swabs soaked in cooking oil or fat or butter or paraffin
oil. It can be a time consuming and messy procedure and
may not remove the entire material. The remaining bitumen
Fig. 22.15B: Same patient with completely healed face, arms and
chest in 10 days indicating superficial burns
Fig. 22.15A: Coal tar burns involving face, chest
and both arms

308
Principles and Practice of Burn Care
can be trimmed away as it separates spontaneously over 3
weeks as the skin heals.
Many organic solvents like carbon tetrachloride, kerosene
and petrol can readily dissolve bitumen but there is always
a danger of the solvent causing chemical damage to the skin
or being absorbed through the skin and poisoning the patient.
Molten Plastic Burns
Burns with molten plastic are seen in the plastic industry
and like coal tar tend to adhere to the skin and may produce
deep burns. It has to be removed surgically only.
Hot Metal Burns (Figs 22.17A to 22.18)
Molten metal burns are seen in furnace men, moulders and
casters in the iron, steel, brass or aluminium industries.
Since iron and steel have very high melting points
(approaching 1500°C), the molten iron and steel usually
produce full thickness burns. Aluminium has a lower melting
point comparatively (650 °C); it produces deep dermal burns.
Sometimes, if the temperatures are very high as it falls
directly from the furnace on to a body part like dorsum of
foot, the molten metal may even penetrate through and
through like a bullet wound.
Fig. 22.15D: Same patient’s feet with deep burns
Fig. 22.15C: Same patient’s legs with deep burns
due to coal tar
Fig. 22.16B: Same hand palmar aspect
Fig. 22.16A: Patient with deep burns of hands
due to coal tar

Industrial and Chemical Burns
309
Majority of these burns are due to accidental stumbling
of the worker into a molten metal container or due to an
explosion in the furnace. The main reason for explosion is
water getting into the molten metal accidentally following
which the molten metal splatters on to the workers’ body
parts or clothes which catch fire. The commonest body
part involved are the feet as it may trickle down from the
trousers inside the boots.
Molten metals typically produce full thickness burns
which demand primary full thickness excision and grafting
for best results. Molten aluminium burns may be deep dermal
and for these cases tangential excision and grafting suffices.
Some of the burns in which bones get exposed, may require
flap cover.
SURGICAL TREATMENT IN CHEMICAL AND
INDUSTRIAL BURNS
Small deep burns sustained from hot metal or slag is very
common especially in steel industry. Though they are usually
too small to cause serious threat to life or limb, they cause
loss of huge man hours.37 These small deep burns are best
treated by excision of slough and skin grafting at the earliest
under local anesthesia.
For moderate burns, early excision and skin grafting is
the treatment of choice. However, it is not always feasible
in Indian scenario because of constraints like non-availability
of blood, shortage of operating time, etc. Patient should be
taken for surgery after 48 to 72 hours after the patient is
well resuscitated and adequate blood is arranged. Early
excision and grafting is reserved only for those cases, which
are full thickness burns. If the burns are of mixed nature or
if there is any doubt regarding the depth it is better to wait
for two weeks as by that time partial thickness burns start
healing (Fig. 22.19). This reduces the area requiring grafting
and thereby the blood transfusions required are also reduced.
In extensive burns also because of paucity of donor
area, delayed excision and grafting (in third week post burn)
is the treatment of choice, as by this time second degree
superficial and some third degree deep burns heal. Healed
second degree superficial areas can be utilized for harvesting
skin graft in addition to the small available donor area in
extensive burns. In metal burns with crush injuries also it is
better to delay the grafting until third post burn week as the
poly trauma is to be taken care of first (Figs 22.17A and B).
Cadaver skin and porcine skin is not available in India
and cultured skin is still in its budding stage. So the preferred
method is delayed skin grafting instead of early excision
Fig. 22.17B: Same patient with completely healed wounds after
grafting
Fig. 22.17A: Deep burns of lower half of body and arms with crush
injury of thigh due to fall of a hot metal box
Fig. 22.18: Deep burns due to hot coal dust

310
Principles and Practice of Burn Care
and grafting in extensive burns. We like to take the patient
for grafting in third week post burn. Usually by this time
the partial thickness burns have either healed or they are in
healing phase.
We prefer to give antibiotics as per the wound culture
sensitivity reports to take care of both gram-positive and
gram-negative bacteria. Antibiotics are started a day prior
to surgery and continued till fifth postoperative day when
primary dressing is done. Subsequently injectable antibiotics
are stopped and switched over to oral antibiotics for another
3-5 days, if required. After the first dressing, subsequent
dressings are done every alternate day or as per requirement
till the wounds heal. Accordingly patient is asked to take
bath around 11th to 14th postoperative day.
Subsequently patient is asked to do massage of the
grafted and donor areas with a corticosteroid ointment twice
a day. Physiotherapy, which is a continuous ongoing
process, is continued during recovery phase. After massage
and physiotherapy, patient is asked to use either pressure
bandage or pressure garments. After two to three weeks,
corticosteroid ointment is replaced with bland oils or creams.
The duration varies in individual cases (4-6 months). Plain
coconut oil massage is continued till scar matures (1-2
years). If there is extensive hypertrophy it is advisable to
use silicon gel sheet lined pressure garments. For smaller
hypertrophic areas intralesional triamcinolone injections are
very effective at 4 weeks interval.
Surgical Procedure
Usually thin split thickness grafts are preferred. Donor areas
are simply dressed using Vaseline gauze, dry gauze, cotton
and pressure bandage in that order. Readymade available
collagen sheets are used for donor areas, which are in near
vicinity of burn wounds (In patients where separate donor
areas like leg, thigh or back are not available). Donor
dressings are not changed. They are opened after 11 to 14
days, when patient is asked to take bath. In extensive burns
when grafting is to be done in multiple sittings same donor
area can be used for graft harvesting after 3 weeks. In the
authors unit burn wound is injected with saline adrenaline
and gentamicin for proper hemostasis in the beginning at
least 10 minutes prior to excision. (1 ampoule adrenaline
and 80 mg. of gentamicin is added to 500 ml of saline). 5
ml of this solution is injected every 5 cm square area. If
patient is sensitive to adrenaline or anesthetist has some
objections adrenaline 1 ampoule is added to 1000 ml of
saline. While one surgeon harvests skin graft another one
prepares the burn wound. The operating nurse prepares the
graft for application by meshing it in a ratio of 1:2. We do
not spread the meshed graft to its fullest unless the available
graft is very less. The burn wound is excised tangentially
using a Watson’s modification of Humby’s skin grafting
knife or a silver knife (for small areas) till healthy bleeding
surface is reached. After excision of slough, the bleeding
surface is covered with wet saline soaked gauze pieces and
pressure is applied. Any big bleeder is cauterized. If bleeding
is not controlled by these methods we sometimes use
hemostatic solution soaked gauze pieces on the bleeding
surface and wait for 5 minutes. Meshed graft is then applied
over these raw surfaces. Pressure is again applied with wet
gauze to remove any clots beneath the graft. The wound is
covered with a very thin layer of Vaseline gauze. Over this
4-6 layers thick Povidone iodine solution soaked gauze is
applied. These gauzes are squeezed nicely before application
and they help to soak any discharge from the wound. Over
this, dry gauze and then a very thin layer of cotton is applied.
Pressure bandage is then applied and Plaster of Paris splints
are used for immobilizing the grafted area. Subsequent
dressing changes are done as mentioned earlier.
In electrical burns immediate fasciotomy is done over
limbs or trunk. Subsequently, debridement and wound
Fig. 22.19: Deep acid burns of back showing separation of eschar
in the middle and healing of superficial burn from the periphery

Industrial and Chemical Burns
311
coverage is done according to the situation. There are two
schools of thoughts for dealing with high tension electric
current injury of limbs (Entry wound). Some surgeons
immediately debride and cover the wound with flap. Others
wait for line of demarcation before undertaking surgery.
Many studies have shown that early debridement and flap
cover only increases the morbidity. Majority of patients end
up with amputation(s) of the limb. In our hospital we wait
for one or two weeks before taking the wound for final
closure. If the hand or foot is totally gangrenous at the time
of admission or if patent shows signs of uremia with
hemoglobinuria and myoglobinuria without any signs of
improvement with resuscitation, the amputation is done
within 2-3 days with stump coverage immediately, if feasible,
or later on. Every case should be weighed individually and
dealt with accordingly. All exposed vital areas must be
covered with locally available flaps or free flaps. Surgical
treatment of chemical burns remains the same as of flame
or scald burn.
SUMMARY
Burns is the severest form of injury the body sustains. It is
more serious than road traffic accidents. However, its
seriousness is often overlooked, as the patient remains
conscious till the end. Burns is one of the causes of systemic
inflammatory response syndrome (other causes being
polytrauma, septicemia, etc.) involving most of the organs
because of the various inflammatory mediators released. If
septicemia occurs in burns patients, it becomes almost
impossible to save the patient. All efforts must be directed
to achieve three goals simultaneously, that is, prevention of
infection, maintenance of nutrition and rehabilitation. All
these three objectives go hand in hand; laxity in any one
part may lead to loss of patient. The metabolism in burn
patients may be as high as 150% of the normal individual.
So the nutritional requirements of a burn patient are
tremendously high to maintain the immunocompetence.
Also, there is tremendous loss of protein from the denuded
body surface so that the extra requirement should be added
to the daily requirement (We use Curreri formula to calculate
the calorie requirement in burn patient (25 kcal/kg + 40
kcal/% burn).
The calorie nitrogen ratio is kept as 120:1 to 100:1
Protein administration is usually 1 gm/kg + 3 gm %
BSA burnt.
Enteral route is preferred over parenteral unless the
patient is not cooperative or burn is more than 40% where
parenteral is added to enteral to supplement extra
requirement, or where gut is not functioning properly. The
maximum permissible dose of antibiotic and the maximum
permissible dosage schedule is to be started in burn patient
because of the high metabolism. The exact bacteria and
their spectrum must be known before starting the antibiotic
and is better to use target specific antibiotics in combination
to cover both gram-positive as well as gram-negative
bacteria.
Physiotherapy is another very important component of
therapy. It should start from 2nd day, continued throughout
treatment and carried over to post healing phase to take
care of respiratory problems, infective problems, prevention
of various contractures and prevention of bed sores
development, etc.
Summary of Treatment Measures for Specific
Chemical Burns
Irrigation with Water
Chromic acid, cantharides, lyes and alkalies, hydroxides of
potassium, sodium, barium, calcium etc, sulfosalicylic acid,
acetic acid, cresylic acid, potassium permanganate,
demethyl sulfoxide (DMSO), sodium hypochlorites, phenol,
hydrofluoric acid, dichromate salts, tungstic acid, picric
acid, trichloroacetic acid, formic acid and gasoline.
Calcium Salt Irrigation or Injection
Hydrofluoric acid.
Cover Burn with Oil
Sodium metal, lithium metal, potassium metal and mustard
gas.
Cover with Water
Phosphorous metal.
Special Measures for Certain Chemicals
Sodium, potassium and lithium metals: Pieces must be
excised.
Phenol: Polyethylene glycol wipes
White phosphorus: Copper sulfate irrigation
Alkyl mercury agent: Debride and remove vesicle fluid.
For Electrical burns: More IV fluids per percent burn, keep
urine alkaline to dissolve the pigments, if required give

312
Principles and Practice of Burn Care
mannitol. Immediate fasciotomy to release the compartment
tightness, flap cover for coverage of vital structures like
vessels, tendons, bones, etc. Amputation of limbs if damage
is too extensive because better prosthesis are more useful
than a non-functional natural limb.
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4. Pruitt B A Jr, Mason A D Jr, Goodwin CW. Epidemiology of burn
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Problems in Gen Surgery. Vol 7, No2, Philadelphia: J B Lippincott,
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8. Occupational Burns among restaurant workers – Colorado and
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9. Stephen M. Milner, Lindsey T A. Rylah, Thuan T. Nguyen, Robert
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11. Jelenko C 3d. Chemicals that burn. J Trauma 1974; 14(1):65-72.
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Jurkiewicz MJ, Krizek TJ, Mathes SJ, Ariyan S (Eds.) Plastic surgery:
Principles and Practice. St Louis: C V Mosby Company 1990:
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13. “Beyond The Road” Chemical Skin Burn Charles Stewart.
14. Bromberg BF, Song IC, Walden RH. Hydrotherapy of chemical
burn. Plast. Reconstr. Surg 1965; 35:85-95.
15. Leonard LG, Scheulen JJ, Munster AM. Chemical burns: Effect of
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16. Baxter CR. Present concepts in the management of major electrical
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21. Flood S. Hydrofluoric acid burns. Am Fam Physician 1988;
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22. Currerie PW, Asch MJ, Pruitt BA. The treatment of chemical
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workers in an oil industry. Burn 2001; 27:475-80.

Radiation Burns
23
BC Shankar, PR Bongirwar, Hemant Haldavnekar
Chapter
INTRODUCTION
Radioactivity was discovered by a French physicist Henri
Becquerel in 1896 and soon it was observed that biological
damage can be produced by absorption of energy from this
radiation in living organisms.
Though the word ‘Radiation’ encompasses the entire
spectrum of emissions from gamma rays and X-rays
(ionizing radiations) to the ultra violet, visible and infra red
light, microwave and Radio waves (non-ionizing radiations),
only in this chapter it is used to describe the effects of
ionizing radiation only.
World has witnessed one of the worst effects of radiation
following the bombing of Hiroshima and Nagasaki in 1945.
Thereafter, more than 400 accidents have taken place in
different settings ranging from a nuclear reactor accident
and tele-therapy equipments to stolen radioactive sources
with resultant deaths and radiation burns in several people.
With increasing use of radiation in diverse fields like
agriculture, medicine, industry and power generation, the
chances of coming across radiation burns, although remote,
is not impossible. It is, therefore prudent to gain an insight
into the management of injuries arising out of radiation
exposures.
International Basic Safety Standards defines an accident
as “any unintended event, including operating errors,
equipment failures or other mishaps, the consequences or
potential consequences of which are not negligible from
the point of view of protection or safety” and a radiological
accident as “an unforeseen event involving overexposure
or contamination of person(s) and/or the environment by
radioactive material”.
The accidents at Chernobyl, Ukraine (April 1986),
Goiânia, Brazil (September 1987), San Salvador, El Salvador
(1989) and several others provided important information
for the diagnosis, monitoring and treatment of radiation
injuries.
TYPES OF ACCIDENT
An accident is called a nuclear accident when it involves
nuclear fission especially in a nuclear reactor. A radiological
accident, on the other hand, involves a release of ionizing
radiation (X-ray equipment or sealed sources like Cobalt 60
(60 Co), Cesium137 (137 Cs) or Iridium 192(192 Ir) in
tele-therapy equipments, industrial radiography cameras or
irradiators) or discharge of radioactive materials (unsealed
sources used in nuclear medicine and scientific research)
into the environment.
Accidents may occur in the following situations:
a. A radioactive source (in tele-therapy equipments or
industrial radiography cameras) may be stolen, lost or
misplaced and may come into the possession of people
thereby exposing them and possibly others to radiation.
b. A radioactive source (in tele-therapy equipments,
industrial radiography cameras or irradiators) may fail
to get retracted after use and may remain unshielded,
exposing the operator to high levels of radiation.
c. A vial containing radioactive material may leak and the
material may get dispersed exposing and often resulting
in external and internal contamination of the person.
BASICS OF RADIATION
Radioactive materials emit energy in the form of alpha (α)
particles, beta (β) particles and gamma (γ) rays. These

314
Principles and Practice of Burn Care
radiations may interact with matter and give rise to the
emission of X-rays and neutron particles. Certain machines
operated at high voltages can generate X-rays and neutrons.
The shorter wavelength of the neutrons or X-rays gives
them a higher energy and ability to penetrate matter.
β particles are emitted by radionuclides such as
hydrogen-3 (3H) and phosphorus-32 (32P) and neutron
particles in general travel more slowly than beta particles,
but being heavier particles they consequently have higher
energies.
As radiation travels through human tissue, it collides
and interacts with the component atoms and molecules
resulting in the atom or molecule to be altered and becoming
an ion. The radiation leaves a trail of ionized atoms and
molecules in its course.
Alpha (α) particles are heavy particles (nuclei of Helium
atom) and carry a positive charge. They can travel within a
few cm in air or about 50 micron (millionth of a meter, μm)
in human soft tissue and can be easily stopped by a thin
sheet of paper. Thus, they do not even penetrate the outer
horny layer of skin and therefore do not cause any external
radiation damage. However, they can cause great damage if
they get incorporated in the body following inhalation,
ingestion or through open wounds due to the intense
ionization they give rise to.
Beta (β) particles are light particles (electrons) and can
travel several meters in air and about a cm in tissues and
can be stopped by a thin sheet of aluminium or 1 cm of
plastic. As they deposit their energy in a smaller thickness
of tissue, they can cause greater damage to the superficial
layers of the skin giving rise to burns (also called burns).
Gamma (γ) and X-rays have a range of many meters in
air and many cm in tissues and eventually pass through a
human body and can be attenuated by about 20 cm of
concrete. As they penetrate deeper into the body, they cause
harm to the deeper structures and vital organs, including
the bone marrow, giving rise to systemic effects of “Acute
radiation syndrome (ARS)” apart from causing skin damage.
Neutrons interact with atoms and molecules in complex
ways causing ionization indirectly through the charged
particles (α, β, γ) they release upon interaction. They have
a range of many meters in air and many cm in the tissues
and eventually get absorbed or pass through a human body
(Table 23.1).
RADIATION BIOLOGY
Ionizing radiation can have a direct action on the DNA within
the cell by breaking the bonds between the atoms. Indirectly,
ionization of water molecules produces free radicals which
are capable of attacking the coded genetic information in
the cell nucleus, disrupting the cell’s chemistry and function
or physically rupturing membranes containing the digestive
enzymes. Natural repair mechanisms can limit the damage
and improve the cell’s chance of survival. However, if the
repair is incomplete, the cell may become incapable of
dividing and may eventually die or may behave abnormally
leading to development of cancers.
The sensitivities of different tissues of the body is different,
being the highest in lymphocytes, the fast dividing cells of
the bone marrow and the cells lining the intestinal villi. The
nerve tissue, by contrast, is the most radio resistant tissue.
RADIATION UNITS
The unit of radiation dose is defined as energy absorbed per
unit mass of matter with which radiation reacts (measured
in Joules/kg). The SI unit of the absorbed dose is Gray
(Gy), the earlier unit for which was rad (1 Gy = 100 rad).
The biological damage (cell killing, transformation,
chromosomal damage) caused by different radiations may
vary and hence a quantity called “Relative Biological
Effectiveness (RBE)” was introduced. The ICRP
(International commission for radiation protection) has
recommended a quantity called “Quality factor (Q)” or
“Radiation weighting factor (WR)” to find the dose-equivalent
(Table 23.2).
Table 23.1: Characteristics of different types of radiation
Type of Radiation
Relative mass in
Range in air
Absorber material which can be used as a shield
amu(atomic mass
unit) and charge
Alpha
4 amu; (+2)
Few cm.
Paper
Beta
Negligible; ( -1)
Few meters
Plastic or Aluminum
Gamma
Zero; ( 0 )
Very Large
Lead, water or concrete
Neutrons
1 amu; ( 0 )
Very Large
Cadmium or Boron for Thermal Neutrons;
Paraffin followed by Cadmium or Boron for Fast Neutrons

Radiation Burns
315
The dose-equivalent is derived by multiplying the dose
with the Radiation weighting factor. The SI unit for dose-
equivalent is Sievert (Sv), the earlier unit for which was
rem (1 Sv = 100 rem).
RADIATION INJURIES
Radiation injuries may manifest as a localized or whole body
exposure or as external deposition or incorporation (internal
contamination) of radioactive material in the body. The
effects may be dependent on the dose and type of radiation
received and the area of the body involved. Careful history
and early clinical findings may guide the treating physician.
ACUTE RADIATION SYNDROME
Whole-body Exposure
A single acute high dose (>1 Gy) exposure of penetrating
radiation like radiation or X-rays to the major portion of the
body can give rise to a clinical entity of “Acute Radiation
Syndrome (ARS)”. The condition is heralded by a prodromal
phase which may be marked by nausea, vomiting
(Hematopoietic involvement), diarrhea (Gastrointestinal
involvement), prostration, hypotension (Cardiovascular
involvement), ataxia and convulsions (Central nervous
system involvement) in increasing order of severity. The
time of onset and severity may give an indication of the
system involved (Tables 23.3 to 23.5).
The prodromal period may be followed by a latent period
of 2-3 weeks during which the person may feel better (at
higher doses the latent period may be absent) only to be
followed by a stage of manifest illness.
ARS may be classified according to the system most
affected as:
Hematopoietic syndrome (1-10 Gy): The injury to bone
marrow results in thrombocytopenia and granulocytopenia
with resultant hemorrhages and infections needing blood
component therapy and treatment of opportunistic
infections. Hematopoietic Growth Factors—-G-
CSF(Granulocyte colony stimulating factor), rhGMCSF
(recombinant human granulocyte macrophage colony
stimulating factor), rhIL6 (recombinant human interleukin
-6) have been used to stimulate the residual bone marrow.
Doses higher than 9 Gy may require a Bone Marrow
Transplant (BMT) or Peripheral Blood Stem Cell Transplant
(PBSCT).
Gastrointestinal syndrome (10-20 Gy): The injury to
intestinal mucosal stem cells gives rise to death due to severe
diarrhea, electrolyte disturbances, and sepsis.
Cardiovascular syndrome (> 30 Gy) and CNS syndrome
(> 30-50 Gy): The hypotension and cerebral edema and
injury to various other vital organs results and only terminal
care remains possible.
Table 23.2: Radiation weighting factor for different radiations
Type of radiation
Radiation weighting factor: WR
Gamma
1
Beta
1
X-rays
1
Alpha
20
Heavy Ions
20
Neutrons
5 to 20 depending on the energy of the neutrons.
Protons
5
Table 23.3: Dose-effect relation after acute whole-body radiation from gamma rays or X-rays
Whole-body
Effect*
absorbed dose
0.05 Gy
No symptoms
0.15 Gy
No symptoms, but possible chromosomal aberrations in cultured peripheral-blood lymphocytes
0.5 Gy
No symptoms (minor decreases in white-cell and platelet counts in a few persons)
1 Gy
Nausea and vomiting in approximately 10 percent of persons within 48 hour after exposure
2 Gy
Nausea and vomiting in approximately 50% of persons within 24 hour, with marked decreases in white-cell and platelet
counts
4 Gy
Nausea and vomiting in 90% of persons within 12 hr, and diarrhea in 10% within 8 hour; 50% mortality in the absence of
medical treatment
6 Gy
100% mortality within 30 days due to bone marrow failure in the absence of medical treatment.
10 Gy
Approximate dose that is survivable with the best medical therapy available
>10-30 Gy
Nausea and vomiting in all persons in less than 5 minutes; severe gastrointestinal damage; death likely in 2 to 3 weeks in the
absence of treatment
>30 Gy
Cardiovascular collapse and central nervous system damage, with death in 24 to 72 hour
*Data are from Gusev et al.

316
Principles and Practice of Burn Care
Localized Exposure
Handling of highly radioactive sources (e.g. placing a hand
in the beam of industrial radiography camera) may give rise
to a very high dose locally. However, the torso being spared,
the dose may not give rise to symptoms of whole body
exposure or ARS and the systemic manifestations may be
absent. The signs of radiation burn may take several days
to appear. The vascular insufficiency caused by endarteritis
obliterans may result in breaking down of previously healed
skin.
INVESTIGATIONS
For Dose Estimation
History of exposure to radiation in the form of X-rays or
gamma rays from teletherapy/industrial radiography source
may be elicited. Absence of contact with corrosives, heat
or insect bites should arouse suspicion of a radiation injury.
Physical Dosimetry
1. If the person has a personal thermo luminescent
dosimeter (TLD), it should be collected and sent for
reading to give an indication about the dose received by
the person.
2. Accident reconstruction—A detailed history of the
accident should be recorded. The exposure geometry
which includes activity of the source, the distance from
the source and the approximate time of exposure can
give an idea of the dose received by the person.
3. The use of electron spin resonance method can be helpful
to estimate the dose incurred. This can be used with
samples like dental enamel, clothes, buttons, earrings or
any organic substance exposed to radiation.
Biological Dosimetry
1. 6 hourly peripheral blood counts for absolute lymphocyte
counts when plotted on a graph called ‘Andrew’s
nomogram’ give an accurate indication of the dose.
2. Chromosomal analysis of cultured lymphocytes
3. Semen analysis – Estimation of sperm counts
immediately after exposure (as a base line reading) and
40-60 days thereafter.
4. Slit-lamp examination of eyes.
Investigative Modalities for Assessing the
Severity of Cutaneous Radiation Injury
1. Serial color photographs– Even a detailed description is
not enough to give a proper indication about the progress
of the lesion as a function of time. While assessing the
damage, serial color photographs (calibrated by using a
piece of white paper) may be valuable.
2. Ultrasound (7.5-20 MHz B-scan sonography)– A 20 MHz
probe is used for evaluating epidermis, dermis and
subcutaneous fat tissue up to the depth of 10 mm
whereas a 7.5 MHz probe can be used for evaluation of
dermis, subcutaneous fat tissue, muscle fascia and
musculature. It is also useful for assessing the depth of
ulcers and the extent of radiation fibrosis.
3. Vascular scintigraphy is a radio-isotopic method in which
99mTc pertechnate is injected intravenously to record
the vascular circulation.
4. CT scan for assessing damage to deeper structures.
5. MRI– This non-invasive investigation can reveal fluid in
the tissues (as a result of inflammation, edema or
necrosis). The extent of ulcer can be estimated as also
the extent of necrotic tissue and this can influence the
decision about conducting a conservative necrectomy
or a more radical amputation.
Table 23.5: Time of onset of clinical signs of skin injury-depending
on the dose received
Stage/symptoms
Dose range
Time of onset
(Gy)
(days)
Erythema (Transient)
3
Hours to days
Erythema (Fixed)
6-10
14-21
Epilation
>3
14-18
Dry desquamation
8-12
25-30
Moist desquamation
15-20
20-28
Blister formation
15-25
15-25
Ulceration (within skin)
>20
14-21
Necrosis (deeper penetration)
>25
>21
Gangrene
>30
Table 23.4: Skin changes after single acute localized exposure*
Absorbed Dose
Change
3-4 Gy
Epilation in 2–3 weeks
10-15 Gy
Threshold for erythema; appears 18-20 days after
exposure at lower doses but may appear within a
few hours at higher doses
20 Gy
Moist desquamation with possible ulceration
25 Gy
Ulceration with slow healing
30-50 Gy
Blistering and necrosis at 3 weeks
100 Gy
Blistering and necrosis at 1-2 weeks
*Data are from Gusev et al.

Radiation Burns
317
6. Thermography– The heat emitted by the skin is directly
dependent on the surface temperature of the skin, which
in turn is dependent on the cutaneous vascularity.
Significantly lower skin temperatures are seen in
necrosis. The different techniques available are liquid
crystal contact thermography, infrared and microwave
telethermovision.
7. Capillary microscopy– The capillaries of the stratum
papillare can be evaluated by using this non-invasive
method, the capillaries of the nail fold of the fingers or
toes being dilated in the manifest stage whereas they are
few and smaller in the chronic phase of cutaneous
syndrome.
8. Profilometry
9. Histology– In the manifest stage, dilated blood vessels,
edema and neutrophilic and eosinophilic infiltration is
observed whereas the chronic/late stage is set apart by
epidermal atrophy/hypertrophy, dermal fibrosis, dilated
blood and lymphatic vessels, pigmentary changes like
hypo/hyperpigmentation and a deficit of hair follicles.
Investigations required for effective treatment are:
I. Peripheral blood counts
II. Bacterial culture and antibiotic sensitivity tests
MEDICAL TREATMENT
As the cutaneous injury may be associated with ARS, the
following care may be required
1. Supportive care –
a. Antiemetics
i.
Antihistaminics (dimenhydrinate) – Poor efficacy.
ii.
Serotonin selective 5-HT3 receptor antagonists
(e.g., ondansetron, tropisetron, granisetron) – High
effectiveness.
iii.
Dopamine-D2 receptor antagonists (e.g.,
metaclopramide) – Good efficacy.
b. Analgesics
i.
Analgesics (paracetamol).
ii.
Non-steroidal anti-inflammatory drugs (ibuprofen,
diclofenac, meloxicam). Aspirin is avoided as it
can cause bleeding in thrombocytopenia.
iii.
Opiates (codeine, tramadol, pethidine, morphine,
buprenorphine in increasing order of
effectiveness). These may be combined with
antiemetics to offset the emesis caused by opiates.
c. Nutrition – Severe nausea may necessitate use of
parenteral nutrition in the form of prefabricated
solutions or total parenteral nutrition through a central
venous line.
d. Antibiotics, antifungals, antivirals – In case of
associated ARS with attendant leucopenia and
thrombocytopenia, infection of the respiratory tract,
mucous membranes, skin ulcers and internal organs
can take place. Mostly, these infections are a result
of preexisting endogenous organisms. This has to
be adequately countered by use of oral drug
combinations like metronidazole and ciprofloxacin
for sterilization of the gut. Antibiotics can be
administered as per the results of the antibiotic
sensitivity tests. Empirically, broad spectrum
penicillins combined with third generation
cephalosporins or carbapenems alone can be given.
If there is an evidence of an infection not responding
to antibiotics, antifungals like fluconazole should be
considered. Antivirals like acyclovir or ganciclovir
may have to be employed in herpes simplex or
cytomegalovirus infections respectively.
2. Skin treatment
i.
Anti-inflammatory cream – Linoleic acid cream
ii.
Non-atrophogenic local steroid/ Systemic steroid
(equivalent to prednisolone 0.5-1.0 mg/kg body
weight)
iii.
Analgesics (as above)
iv.
Non-sedative mast-cell stabilizer – Loratadine
v.
Antibiotic creams / Systemic antibiotics
vi.
Heparin
vii.
Argon laser for ablation of telangiectasias
viii.
Lioxasol cream increases cell proliferative activity
in the skin
ix.
Tretinoin cream
x.
Topical / Systemic superoxide dismutase (SOD)
xi.
Systemic pentoxiphylline
xii.
Systemic alpha-tocopherol
xiii.
Systemic proteinase inhibitors like Aprotininum
(Gordox)
xiv.
Systemic interferon gamma
xv.
Topical tetrachlorodecaoxide (TCDO)
xvi.
Solcoseril gel has regenerative properties
xvii.
Actovegin is obtained by ultra-filtration of calf
blood. It contains inositol phospho-oligosac-
charides (IPOs), which are known to increase
uptake and utilization of oxygen by hypoxic tissues
and cells by promoting mitochondrial respiratory
function, decreasing the formation of lactate, and
in turn, protecting hypoxic tissue.

318
Principles and Practice of Burn Care
xviii.
Hydrocolloid dressings
xix.
Topical thrombocytic growth factors
xx.
Semi-synthetic skin equivalent - Integra
The various degrees of radiation burns described are as
follows:
Erythema and dry desquamation: Treatment is purely
symptomatic. Severe erythema associated with edema is
treated with lotions or sprays containing hydrocortisone to
relieve the symptoms. Tight clothing should not be worn
over the affected part.
Moist desquamation needs daily sterile protective
dressings and bathing of the affected skin in antiseptic
solutions. Antibiotic creams can also be used to prevent
bacterial infections.
Ulceration requires isolation of the limb in a sterile
environment. A daily dressing and bathing of the ulcer in
antiseptic solutions is recommended. Analgesics or stronger
opioids may be necessary. Topical or systemic antibiotic
therapy should be considered if secondary infection is
suspected or verified by bacterial culture.
Necrosis needs excision followed by skin grafts or other
types of skin cover. Unless the underlying vasculature is
intact, skin grafting may not be possible and a
myocutaneous flap or pedicle flap may be required. Surgery
in the form of ulcerectomy, necrectomy and amputation
may be needed, the extent, timing and type of surgical
intervention being determined on a case to case basis as the
lesion progresses.
Indications for amputation depend on the following
determinants:-
a. Intractable pain
b. Size and location of the injury
c. Degree of control of infection
d. Very severe destruction of underlying tissues with
vascular damage
e. Value of the part
Not only does the latent period for development of signs
and symptoms but also the intensity and duration of lesions
depend on the dose and the type of radiation received. Thus,
at a high dose (>100 Gy) the manifestations may develop
early (within a week), whereas with a low dose they may
take weeks to develop.
CUTANEOUS RADIATION SYNDROME
(FIGS 23.1A TO 23.5B)
The basal cells of the epidermis including those cells situated
within the canal of the hair follicle are the cells, which are
damaged resulting in denudation of the epidermis resulting
in manifestations of Cutaneous Radiation Injury syndrome
(CRI). The erythema is a result of dilatation of superficial
blood vessels due to an inflammatory reaction (Table 23.6).
Grading
Grade 1
Prodromal stage may start with itching and a brief transient
erythema usually subsiding within 36 hours of exposure.
The true erythema (a second wave of erythema also referred
to as fixed erythema) appears around 5 days post-exposure
and lasts a few weeks. Damage to sweat and sebaceous
glands may give rise to a dry, scaly desquamation of the
skin in 20-30 days, which resolves within a few weeks.
Treatment: Outpatient Care
Topical anti-inflammatory, anti-proliferative, non-
atrophogenic glucocorticoids.
Systemic non-sedative anti-histamines.
Investigations: Ultrasound to determine changes in thickness
of the skin and a basal thermography may show
hyperthermic and hypothermic areas, which could serve as
a reference for long-term follow-up.
Grade 2
Skin surface affected < 10% body surface. This phase
consists of blisters which generally form around 4 weeks
post exposure and can result in moist desquamation which
can even occur without prior blisters due to depletion of
epidermal stem cells. This may be associated with transient
hair loss (around 2 weeks).
Treatment: Outpatient Care
Topical anti-inflammatory, anti-proliferative, non-
atrophogenic glucocorticoids.
Systemic non-sedative anti-histamines
Linoleic acid creams
Puncture of blisters
Non-adherent dressings
Prevention of infections as per antibiotic sensitivity tests
Investigations: 20 MHz sonography to determine changes
in thickness of the skin
Thermography to detect hyperthermic and hypothermic
areas as a reference for regular follow-ups.

Radiation Burns
319
Table 23.6: Grades of cutaneous radiation injury (CRI)
Grade Skin dose*
Prodromal stage
Latent stage
Manifest illness stage
Third wave of erythema†
Recovery
Late effects
I
> 2 Gy
1-2 days
no injury evident
• 2–5 weeks postexposure, lasting
Not seen
Complete healing
• Possible slight
(200 rads) ‡ postexposure
for 2–5 weeks post-
20-30 days: redness of skin,
expected 28-40
skin atrophy
or not seen
exposure§
slight edema, possible increased
days after dry
• Possible skin
pigmentation
desquamation
cancer decades
• 6-7 weeks postexposure, dry
(3-6 months
after exposure
desquamation
postexposure)
II
> 15 Gy
6-24 hours post-
No injury evident for • 1-3 weeks postexposure; redness
• 10-16 weeks
Healing depends on
• Possible skin
(1,500 rads) exposure with
1-3 weeks post-
of skin, sense of heat, edema,
postexposure,
size of injury and
atrophy or ulcer
immediate sensation exposure
skin may turn brown
injury of blood
the possibility of
recurrence
of heat lasting 1-2
• 5-6 weeks postexposure, edema
vessels, edema,
more cycles of
• Possible
days

of subcutaneous tissues and
and increasing pain
erythema
telangiectasia (up
blisters with moist desquamation
• epilation may
to 10 years
• Possible epithelialization later
subside, but new
postexposure)
ulcers and necrotic
• Possible skin
changes are possible
cancer decades
after exposure
III
> 40 Gy
4-24 hours post-
None or less than
• 1-2 weeks postexposure: redness
• 10-16 weeks post-
Can involve ulcers
• Possible skin
(4,000 rads) exposure, with
2 weeks
of skin, blisters, sense of heat,
exposure: injury of
that are extremely
atrophy,
immediate pain or
slight edema, possible increased
blood vessels,
difficult to treat and
depigmentation,
tingling lasting
pigmentation
edema, new ulcers,
that can require
constant ulcer
1-2 days
• Followed by erosions and
and increasing pain
months to years to

recurrence, or
ulceration as well as severe pain
• possible necrosis
heal fully
deformity
• Possible occlusion
of small vessels
with subsequent
disturbances in
the blood supply,
destruction of
the lymphatic
network, regional
lymphostasis, and
increasing fibrosis
and sclerosis of
the connective
tissue
Contd.

320
Principles and Practice of Burn Care
Contd.
Grade Skin dose*
Prodromal stage
Latent stage
Manifest illness stage
Third wave of erythema†
Recovery
Late effects
• Possible telangiectasia
• Possible skin
cancer decades
after exposure
IV
> 550 Gy
Occurs minutes to
None
• 1-4 days postexposure
Does not occur due
Recovery possible
• Continued plastic
(55,000 rads) hours postexposure,
accompanied by blisters
to necrosis of skin
following amputation
surgery may be
with immediate pain
• Early ischemia (tissue turns
in the affected area
of severely affected
required over
or tingling,
white, then dark blue or black
areas and possible
several years
accompanied by
with substantial pain) in most
skin grafts
• Possible skin
swelling
severe cases
cancer decades
• Tissue becomes necrotic within
after exposure
2 weeks following exposure,
accompanied by substantial pain
*Absorbed dose to at least 10 cm2 of the basal cell layer of the skin
†Especially with beta exposure
‡The Gray (Gy) is a unit of absorbed dose and reflects an amount of energy deposited in a mass of tissue (1 Gy = 100 rads).
§Skin of the face, chest, and neck have a shorter latent phase than the skin of the palms of the hands and the skin of the feet.

Radiation Burns
321
Myocutaneous flap done 9 months
following exposure
Fig. 23.1C: Ulceration and partial healing 6 weeks postexposure
Fig. 23.1B: Ulceration 5 weeks postexposure
Fig. 23.1A: Evolution of cutaneous radiation syndrome following
accidental exposure to an industrial radiographic device showing
fixed erythema and blistering 4 weeks postexposure. Erythema is
best appreciated in fair skinned individuals. The transient erythema
cannot be appreciated in the dark skinned. In the dark skinned, fixed
erythema appears darkly pigmented
Fig. 23.1F: Even after 9 months with surgical cover few areas of
ulceration still remain
Fig. 23.1E: Same wound 14 weeks postexposure showing
deepening of ulceration up to the fascia and muscle
Fig. 23.1D: Ulceration with central necrosis 8 weeks postexposure

322
Principles and Practice of Burn Care
Fig. 23.1H: Close up view of the flap on forearm
Fig. 23.1G: Same patient with abdominal flap cover following
radiation burn wound over forearm
Fig. 23.2: Acute radiation burn of left hand following a 20 Gy
exposure to a Co-60 source
Fig. 23.4B: Erythema 11 days after exposure
Fig. 23.3: Hand exposed to a radiographic unit showing changes in
middle finger and thumb 6 weeks after exposure
Fig. 23.4A: Iridium-192 source (185 GBq, 5 Ci) mounted in a pen-size
source holder for industrial radiography was placed in the pocket of
the worker’s overall and kept there for about two hours (Courtesy:
Figure 23.4A to C from How to recognize and initially respond to an
accidental radiation injury (pamphlet), IAEA, Vienna, Austria, 2000)
showing early erythema 5 days after the exposure

Radiation Burns
323
Fig. 23.4C: Desquamation and skin necrosis 21 days after
exposure
Fig 23.5B: TRAM flap done for cover of the same defect
(Courtesy: Editor)
Fig. 23.5A: Non-healing ulcer on right chest following radiotherapy
given postmastectomy (Courtesy: Editor)
Grade 3
Skin surface affected 10-40% body surface. This phase
consists of severe swelling, which is caused by increased
vascular permeability and loss of fluids in the third space.
Blisters form around 5 days postexposure resulting in ulcer
or necrosis. Recovery may follow. However, it is incomplete
and the sequelae may be alopecia, fibrosis, contractures,
pigment changes, increased vulnerability to trauma and
repeated breakdown of healed areas.
Treatment: Inpatient care
Topical antibacterial agents
Linoleic acid creams
Systemic anti-inflammatory, anti-proliferative, non-
atrophogenic glucocorticoids to reduce edema.
Analgesia
Aspiration of fluid from blisters
Debridement of necrotic tissues
Non-adherent dressings
Prevention of infections as per antibiotic sensitivity tests
Investigations: 7.5 MHz sonography to determine
changes in thickness of the skin
Doppler ultrasound to assess damage to underlying larger
vessels
Sonography to assess the depth of the lesion
MRI to detect damage to underlying muscles
Surgery may be required in the form of full-thickness
skin grafts/flaps.
Grade 4
Skin surface affected >40% body surface. This phase
consists of severe damage to not only epidermis and dermis
but also to subcutaneous tissues, underlying muscles and
perhaps bones. This is associated with severe swelling,
which is caused by increased vascular permeability and loss
of fluids in the third space. Bullae form within a few days
post-exposure and can result in acute necrosis. Recovery
is unlikely and leaves deficits like alopecia, fibrosis,
contractures, pigment changes and increased vulnerability
to trauma, thermal and pressure changes, subcutaneous
sclerosis and keratosis. Amputation of extremities may have
to be considered.
Because of the extensive exposure, this may be
associated ARS with resultant granulocytopenia (causing
opportunistic infections) and thrombocytopenia (causing
hemorrhages).

324
Principles and Practice of Burn Care
Treatment: Inpatient intensive care
Topical antibacterial agents
Linoleic acid creams
Systemic anti-inflammatory, anti-proliferative, non-
atrophic glucocorticoids to reduce edema.
Analgesia
Aspiration of fluid from bullae
Debridement of necrotic tissues
Necrectomy and full thickness skin graft
Amputation
Prevention and treatment of infections as per antibiotic
sensitivity tests
Investigations: 7.5 MHz sonography to determine
changes in thickness of the skin
Doppler ultrasound to assess damage to underlying larger
vessels
Sonography to assess the depth of the lesion
MRI to detect deeper damage to underlying muscles
The percentage of the surface area of burns can be
calculated by the rule of nine. The fluid and electrolyte/
colloid requirements vary according to the grade/depth of
burns. It is simpler to calculate the fluid requirement for
partial burns wherein various formulae used in thermal
burns may serve as a useful guide for maintenance of
fluid and electrolyte balance. However, in case of whole
body burns with concomitant ARS and also in deep burns
as a result of irradiation, the hemodynamic stability needs
measurement of central venous pressure (CVP), electrolytes,
renal profile and associated management of ARS as
mentioned earlier.
The management of radiation burns needs a team of:
a. Physician trained in handling radiation injuries
b. Health physicist to help arrive at the dose received and
to ascertain the type of radiation (β, γ) using various
dosimetric techniques
c. Hematologist (for management of ARS) when radiation
burns are associated with partial or whole body
exposure.
d. Plastic and reconstructive surgeon
Unlike the thermal, chemical or other forms of burns
injuries, there are no physical symptoms at the time of
exposure to radiation sources. The full extent of tissue
damage can take a few days, weeks and even years to evolve
and hence early decision regarding the type of surgical
intervention has to be avoided. The only early intervention
would be in the form of maintenance of fluid, electrolyte
balance and life saving measures.
SURGICAL MANAGEMENT
Surgical management depends on:
a. Type of burns (β and γ)
b. The extent of surface area of burns
c. The depth of burns
The accident rate world over in atomic power reactors
is extremely low as there is a well-structured radiation
protection setup for man and machine. Most accidents
leading to burns are reported from those using industrial
radiography and some from radiological procedures in
medical field like tele-radiotherapy because of inadvertent
exposure to a naked (exposed) source and in interventional
radiography due to non-adherence to periodic maintenance
and calibration checks.
1st degree burns heal with conservative treatment
spontaneously just as in the case of thermal burns. However,
the recovery may take a longer time. Extensive 2nd degree
burns may require split thickness skin grafting to reduce
the morbidity and to expedite healing. 3rd or 4th degree
burns (γ, X-rays) require investigations directed at the
vascular viability of the affected tissues and procedures
such as rotation flap, myocutaneous and neurovascular flaps
have to be employed. Deep burns adjacent to torso and
limbs have a potential to cause associated injury to hollow
viscera (bladder, intestines etc.) and to the underlying bone
giving rise to radionecrosis requiring additional major surgical
procedures for fecal and urinary fistulae thus carrying a
high mortality and poor outcome. Special mention must be
made about hand injury (especially injury to digits) as this is
a common form of accident. Having a hand surgeon would
be a vital addition to the list of experts to help in the
reconstruction treatment and rehabilitation. A timely decision
regarding partial or total amputation would reduce morbidity
in those injured.
Even after recovery, a possibility exists for development
of late sequelae like radiation fibrosis and squamous cell
carcinoma of the skin.
RADIATION PROTECTION PROGRAMS
Radiation protection involves restriction of exposure or
potential exposure. This may be achieved by:

Radiation Burns
325
a. Engineering controls employing reducing the time of
operation, increasing the distance from the source by
use of remote handling operations and provision of good
shielding and suitable containment to prevent the spread
of unsealed radioactive materials to restrict external
exposure.
b. Administrative methods such as documented
procedures, good working practices, adequate
supervision and restricted exposure times
c. Personal protective equipment such as lead aprons for
work with X-rays, laboratory wear and industrial suits
to protect against body contamination and devices such
as respiratory protective equipment.
The radiation protection program works on the
philosophy of ALARA (As Low As Reasonably Achievable)
and contributes by preventing accidents which cause acute
exposures with resultant deterministic effects and also by
reducing routine exposures and the risks of stochastic
effects.
Personal dosimeters are worn by individual employees
and the actual doses received are measured. Personal air
samplers (PAS) can measure the air activity that might
contribute to an internal dose. Organ and whole body
monitoring for internal exposure and biological assessments
of intakes of radioactivity are used to determine internal
doses.
It is important to note that everybody who deals with
intervention radiological and therapeutic procedures, e.g.
those undertaken by urologist, cardiologist or orthopeadicians
should compulsorily use TLD (Thermoluminescent protection
dosimeter) badges and stay out of the field of radiation as
far as possible to prevent delayed radiation response.
BIBLIOGRAPHY
1. AERB Safety Guide - Medical Management of Persons Exposed in
Radiation Accidents, Atomic Energy Regulatory Board, Mumbai,
1990.
2. AERB Safety Manual—Handbook of Medical Management of
Persons Exposed in Radiation Accidents, Atomic Energy Regulatory
Board, Mumbai, 1989.
3. Cutaneous Radiation Injury: Fact Sheet for Physicians,

4. Fred A. Mettler Jr, George L. Voelz, Major Radiation Exposure —
What To Expect And How To Respond, New England Journal of
Medicine, Vol. 346, No. 20, May 16, 2002.
5. Gusev IA, Guskova AK, Mettler FA, Jr, (Eds). Medical Management
of Radiation Accidents. 2nd.ed. New York: CRC Press, Inc.; 2001.
6. How to recognize and initially respond to an accidental radiation
injury (pamphlet), International Atomic Energy Agency, Vienna,
Austria, 2000.
7. IAEA Safety Series No. 88—Medical Handling of Accidentally
Exposed Individuals, International Atomic Energy Agency, Vienna,
1988.
8. International Basic Safety Standards for Protection against Ionizing
Radiation and for the Safety of Radiation Sources, Safety Series No
115, IAEA, Vienna 1996:295.
9. Medical Response To Radiation Incidents and Radionuclear Threats,
István Turai, Katalin Veress, Bengül Günalp, Gennadi Souchkevitch;
BMJ Volume 328, 6 March 2004.
10. One decade after Chernobyl, summing up the consequences of the
accident: proceedings of an international conference, Vienna, 1996
April;8-12. International Atomic Energy Agency, Vienna, Austria
1996.
11. Practical Radiation Technical Manual - Health Effects and Medical
Surveillance, International Atomic Energy Agency, Vienna, 2004.
12. Safety Reports Series No. 2—Diagnosis and Treatment of Radiation
Injuries jointly sponsored by the International Atomic Energy
Agency and the World Health Organization, Vienna, 1998.
13. The Radiological Accident In Gilan, International Atomic Energy
Agency, Vienna, Austria 2002.
14. The Radiological Accident In Goiania, International Atomic Energy
Agency, Vienna, Austria 1988.

(Trang không có chữ)

326
Principles and Practice of Burn Care
Friction Burns
24
Karoon Agrawal
Chapter
INTRODUCTION
Historically fire was produced by friction between two
stones. The Olympic lamp was lit by rubbing stones and
this tradition is still followed. Friction can generate a large
amount of heat, so much so that it can melt stones and
burn meteors in space. When rockets and space ships enter
the earth’s atmosphere, there is a danger of their burning
due to the extreme heat produced by friction with the
atmospheric air.1 The greatly talked about Discovery space
shuttle accident in which the India born astronaut Kalpana
Chawla was killed along with other colleagues, is an example
of the high magnitude of heat generated due to friction in
space.
Burns due to friction are one of the commonest non-
thermal burns. Very often, they are not reported and are
overlooked in our practice as well as in literature. This is
probably because in the majority of patients friction causes
partial thickness burn in a small body surface area which is
ignored. Usually, it is associated with mechanical injury
which may be more severe than the burns. Whenever there
is friction between two objects, the relatively delicate object
bears the brunt of the mechanical trauma in the form of
abrasion, laceration or avulsion. Hence most often the burn
takes a back seat and the mechanical injury becomes the
priority.
PATHOGENESIS
Friction is generated as mechanical energy when two
surfaces rub against one another, out of which at least one
is moving. The kinetic energy is converted into thermal
energy or heat. When the delicate body surface comes in
contact with this heat energy, it causes burn. As it is always
associated with kinetic energy, friction burn and mechanical
injury are seen together in various combinations and
proportions.
The quantity of energy produced following friction is
determined by the coefficient of friction which depends
mainly upon the material of the surface causing friction,
for example, stainless steel has a very low friction coefficient
as compared to rubber on a pavement. Similarly when a
part of the human body rubs against any hard object, the
high coefficient of friction produces a large amount of heat
energy causing body surface burn.
EPIDEMIOLOGY
Epidemiological studies of friction burns are difficult.
Majority of these studies available in literature are hospital
based, which have their inherent deficiencies. To know the
correct incidence, community based studies are required
which are neither available, nor feasible. Trying to quantitate
the reported cases of friction burn is only the tip of the
iceberg. A vast majority of these cases are ignored or
managed with first aid or household care. Only relatively
major burns or burns associated with other trauma report
to the hospital, hence the fallacy of the reported incidence
and degree of burn reported due to friction.
In a retrospective epidemiological study on childhood
burns conducted in New Zealand in1981, 14% children had
friction burns and it was the third commonest burn after
scalds (40%) and contact burns (20%).2
In an epidemiological study from Ahmedabad, India, 60
patients of friction burns were reported over a period of
two years. Majority of the patients were males in 21-30

Friction Burns
327
years age group. Lower limb was affected in the majority
of patients due to road side accidents. Split thickness skin
graft was required in 41.7% and a flap cover was performed
in 10% of patients.3
In an American review of 1211 children younger than 6
years over a period of 6 years there were 48 patients (4%)
with friction burns because of household treadmill (Fig.
24.1). Palmar surface of the hand was the most common
site.4 Maguina et al reported 10 patients of treadmill related
friction burn over a period of 4 years.5
In a similar retrospective study from Korea, records of
25 children with treadmill-induced friction burn were
analysed. Friction burns constituted 1.4% of total number
of pediatric burn injury. All lesions affected the hands and
forearm. Majority affected the volar surface.6
The database of patients over 20 years from Brisbane
and Queensland was analyzed. Out of 4523 patients admitted
in the hospital, friction burn constituted 1%.7
ETIOLOGY
A friction burn is a non-conventional burn injury and is not
reported to the hospital unless it is unusually large or else
associated with other injuries. The etiological factors are
very interesting and worth enlisting here (Table 24.1).
In an Indian epidemiological study of 60 friction burn
patients, the Road Traffic Accidents constituted 93% and
the rest were equally contributed by fall and sports.3
Sports activities are the commonest cause of friction
burn. These are usually small, superficial and localized
injuries which are mostly managed on the spot and hence,
not recorded in hospital statistics. It can occur while skidding
over a synthetic turf. Rope seems to be a common etiological
factor in rope based sports like rope climbing, water
skidding, tug of war, etc. Running causes burn over soles
especially, if one runs bare-foot or with ill-fitting shoes.
Aerobic dancing causes burns over the soles. The water
slides in water sports cause burn due to friction against the
railing and the floor of the slides, especially if the flow of
water is inadequate.8
Increased popularity of physical fitness in modern society
has brought many mechanized equipments into our homes.
Presence of such equipment at home increases the hazard
for friction burn of the hands in young children.4-7, 9-11 A
review of 1211 pediatric patients of less than six years from
USA revealed treadmill friction injuries in 48 (4%) patients.
The mean burnt area reported was 0.5%, mostly over the
volar surface of the hand.4 In another study, 14 injuries in
nine patients were recorded. The average age of the children
was 3-4 years.10 An American study reported six hands
Treadmill related friction burns at an average age of 31
months. These were mostly on the palmar aspect of the
fingers.9
Till now all the friction burn reports were from American
centers. In a retrospective study, treadmill injury from Seoul,
Korea constituted 1.4% of all the pediatric burn admissions.
The mean age was 3.9 + 3.2 years. 9 This indicates the
spread of treadmill related pediatric friction burn to other
countries.
Fig. 24.1: A photograph of a household treadmill for exercising
Table 24.1: List of etiological factors of friction burn
Sports
Skidding over turf
Rope based sports8
Bare foot trekking23
Water slides,
Aerobic dancing
Road Traffic
Car-tyre friction12
Accidents
Bicycle spoke injuries13
Air bag friction15-17
Loose clothing getting caught
in automobile22
House hold and
Treadmill4-7,9-11
industrial machines
• Child activates the machine
• Accidentally an unsupervised
child comes in contact with
the moving belt
Washing machine2
Domestic vacuum cleaner17,18
Rolling belt in industries and
agriculture
Medical equipments
Tourniquet applied over bare skin20
Reaming of bone21
Miscellaneous
As a part of pathomimia24

328
Principles and Practice of Burn Care
There are two ways by which a child can get friction
burn due to treadmills at home: one is when a child activates
the machine in the absence of an adult and secondly when
a child accidentally comes in contact with the moving belt
of the treadmill causing trauma and friction.10
Road side accidents are the cause of a large number of
friction burns especially in hospital based studies. Al-Qattam
(2000) reported 25 cases of car-tyre friction injuries of
foot in children. These injuries occurred while trying to
stop the car.12 In an Indian study (2006) the incidence of
friction burn reported due to Road Traffic Accidents was
as high as 93.33 % 3 (Fig. 24.2).
In a Japanese study, 26% of their study patients of lower
limb trauma caused by bicycle spoke injuries were abrasion
and friction burn from the shearing effects of the spokes
causing partial to full-thickness skin defect.13 Occasionally
the friction burn may be severe enough to cause full
thickness loss of chest wall.14
Modern technology brings some unexpected problems
with it. Airbags are effective and a well accepted safety
device to reduce the impact of motor vehicle accidents
and morbidity and mortality associated with it. Rapid
deceleration due to an impact causes the ignition of sodium
azide cartridge, thereby releasing nitrogen to inflate the
nylon rubber bag. Most of the airbags inflate in 0.01 second
at a speed of >160 km/hour15 (Figs 24.3A and B). The
physical contact with rapidly inflating airbags causes
friction burn. Also direct thermal burns from high
temperature gases, indirect injuries due to the melting of
clothing or chemical burns due to direct contact are possible
with airbags.16,17
There are many other interesting etiological factors
causing friction burn reported in literature. These are caused
Fig. 24.2: A large full thickness burn over thigh following friction with
the truck tyre. The presence of thick eschar indicates the occurrence
of deep burn due to friction. There is evidence of avulsion injury
laterally
Figs 24.3A and B: A line diagram showing the inflation of car airbag
after impact. The airbag inflates with nitrogen after the crash sensor
activates the inflator
A
B
by common machines used in day-to-day life and are
commonly ignored. There are reports of friction burn caused
by washing machine wringers 2 and domestic vacuum
cleaners18,19 (Fig. 24.4). Among the medical equipments,
tourniquet applied over the thigh without padding causes
friction burn20 and the reaming of bone significantly increases
the temperature inside the bone. Rolling belts in industries
are hazardous as these cause friction burns.21
Loose clothes around the body may get caught in a
revolving machine or in automobiles and can snare the neck
or other parts of the body. In a freak accident, a 17-year-old
girl had friction burn over the neck due to her ‘Chunni’ (also
called, ‘dupatta’), a traditional Indian clothing, wrapped round
the neck caught in a three wheeler auto wheel.22 Bare Foot
Mountain trekking can cause friction/frost burn.23

Friction Burns
329
Friction blisters may be a manifestation of pathomimia,
which can be produced by nails, razor, blades, cigarettes,
chemicals etc. These are not true friction burns, but resemble
them; hence, we should be aware of them.24
Apart from these etiological factors environmental factors
play a very important role in the occurrence of and in
determining the degree of friction burn. In summer season
the incidence and magnitude of friction burns is more.
Inadequate clothing in summer also increases the risk. Pegg
and Mayzee (1982) have pointed out that only 9% of friction
burns occurred during winters, due to adequate clothing.
On the other hand, the incidence was much more in summer
because of inadequate clothing like use of shorts and thin
flimsy shirts.7
TYPE OF BURNS
The burns inflicted with friction are mostly minor and
superficial (Figs 24.3 and 24.4) However, there are a few
reports of deeper friction burns too.3,14 In an Indian study
of sixty burn patients 31.66% had first degree (Fig. 24.5),
20% had second degree (Figs 24.6 to 24.8C) and 48.33 %
had third degree burns 3 (Figs 24.9 and 24.10). This is a
hospital based study; hence, a large number of more severe
burns. Majority of small, superficial first and second degree
burns may have taken treatment at home or from private
clinics and hence, not reported.
Majority of the accidental friction burns in children take
place at home. Although the burn is small, it should be taken
seriously in children.
Fig. 24.4: Friction burns over dorsum of fingers because of hand
coming in the pressing machine, showing full thickness loss in the
center surrounded by zone of partial thickness skin loss
Fig. 24.5: A typical superficial friction burn over face after road side
accident in a child
Fig. 24.6: A deep partial thickness friction burn over the right zygomatic
region following road side accident requiring closure of wound by
grafting
Fig. 24.7: Deep friction burns with associated avulsion injury in
thigh of a young man following road traffic accident

330
Principles and Practice of Burn Care
MANAGEMENT
It is simple and straight forward because of the limited extent
of burn in the majority of patients. The principles of
management of friction burns are the same as for thermal
burns. Majority of the friction burns are managed as minor
burn with tetanus prophylaxis, local wound care, systemic
antibiotics and analgesics. Sometimes, it requires surgical
management with tangential excision and split thickness skin
grafting. In treadmill related injuries 46% of children with
friction burn had full thickness burn requiring surgical
management.5 In another study 33% of Treadmill related
friction burn cases required skin grafting.9 Major friction
burns are associated with other injuries which should be
managed simultaneously. In an Indian study 35% had hand
fractures, 10% had head injury and 5% had associated
tendon and nerve injury.3
Majority of the airbag friction burns are minor and partial
thickness and do not require hospitalization.17 Though the
majority of airbag lesions are minor, correct diagnosis of
Fig. 24.8C: Close up view after 4 days showing some remanant of
dermis in the center with superficial burn in the periphery in healing
phase, requiring skin grafting in the center
Fig. 24.8B: Same case showing the tyre marks with intermixed
superficial and deep dermal burn with total loss of skin in the proximal
thigh (extreme left)
Fig. 24.8A: Typical friction burn over lower limb because of truck
tyre running over the limb
Fig. 24.10: Full thickness friction burn over dorsum of foot by car
tyre running over it
Fig. 24.9: A large full thickness burn over thigh following friction with
truck tyre. The presence of thick eschar indicates deep burn due to
friction. There is evidence of avulsion distally

Friction Burns
331
Fig. 24.12B: Fasciocutaneous flap raised from opposite
leg for cover
Fig. 24.12A: Exposed tibia after removal of thick eschar following
deep friction burn over leg in road traffic accident
Fig. 24.11: Combination of friction burn and avulsion due to road side
accident. The Proximal and distal parts of the raw areas are following
the separation of eschar. Central area with exposed muscle is due to
associated avulsion injury. These areas can be covered with split skin
graft alone
Fig. 24.12C: Inset cross leg flap covering the same defect
completly
not be totally preventable in a large number of cases.
However, appropriate preventive habits, prevention of road
side accidents and specific precautions observed while
dealing with etiological factors may reduce the incidence of
friction burn.
Benever et al predict that the incidence of friction burn
injury with treadmill like domestic machines is likely to
increase in future unless protective modification of exercise
machine is done. 9 Additional safety measures, warning labels
and parental education can prevent friction burns due to
domestic and industrial causes.
Proper use of seat belts through shoulder and lap reduces
the overall injury to the car riders. The airbag friction burn
is also less when the riders have their seat belts on.
type of burn is necessary as it may be a friction or chemical
burn or mechanical trauma. Based on the type of trauma,
the appropriate treatment is instituted. The benefit of airbags
far outweighs the risks of the burns and hence are
acceptable.
In the Indian study, 41.66% required split thickness skin
graft (Fig. 24.11) and 10% required major flap procedures3
(Figs 24.12A to C). A full thickness defect of the
chest-wall has been reported requiring multiple flap
reconstructions.14
Early recognition and appropriate management result in
excellent functional outcome with minimum morbidity.
PREVENTION
Majority of unreported and reported friction burns occur
during sports and routine activities and hence, these may

332
Principles and Practice of Burn Care
SUMMARY
To conclude, the friction burn is an interesting trauma
associated with day-to-day active life. One has to accept
the occurrence of friction burn as a part of life. Modern
gadgets have become a part of today’s lifestyle, which may
increase the possibilities of friction burn. There are a few
areas where preventive measures and watchful lifestyle may
significantly reduce the incidence of friction burn.
REFERENCES
1. cat=technology
2. Langley J, Tobin P. Childhood Burns. N Z Med J. 1983 Sep 14;
96(739):681-4.
3. Agrawal A, Vora HJ, Raibagkar SC. Friction Burn: Epidemiology
and prevention. Indian J Burns 2006; 14(1):20-22.
4. Collier ML, Ward RS, Saffle JR, Edelman LS, Morris SE, Lundy C
Home treadmill friction injuries: a five-year review. J. Burn Care
Rehabil. 2004 Sep-Oct; 25(5):441-4.
5. Maguine P, Palmieri TL, Greenhalgh DG. Treadmills: A preventable
source of pediatric friction burn injuries. J. Burn Care Rehabil.
2004 Mar-Apr; 25(2):201-4.
6. Han T, Han K, Kim J, Lee G, Choi J, Lee J, Jang Y, Oh S. Pediatric
hand injury induced by treadmill. Burns 2005 Nov; 31(7):906-9.
Epub 2005 Jun 28.
7. Pegg S P. Burn epidemiology in the Brisbane and Queensland area.
Burns 2005 Jan; 31 Suppl 1:S27-31.
8. Wright JB. Wild water rapid burns. Br J Sports Med. 1995
Sep;2993):208-9.
9. Benever GT Moriarty KP, Sachs BF, Courtney RA, Konefal SH Jr,
Barbeau L. Pediatric hand treadmill injuries. J Craniofac Surg 2003
Jul; 14(4):487-90; discussion 491-2.
10. Borschel GH, Wolter KG, Cederna PS, Franklin GA. Acute
management of exercise treadmill-associated injuries in children. J.
Trauma 2003 Jul; 55(1):130-4.
11. Marshall J. Lourie GM. Pediatric hand Friction Burn injuries
secondary to treadmills. J. Pediatr. Orthop. 2003 May-Jun;
23(3):407-9.
12. Al-Qattan MM. Car-tyre friction injuries of the foot in children.
Burns 2000 Jun; 26(4):399-408.
13. Mine R, Fukui M, Nishimura G. Bicycle spoke injuries in the lower
extremity. Plast Reconstr Surg 2000 Dec; 106(7):1501-6.
14. Ono I, Tateshita T. Reconstruction of a full-thickness defect of the
chest wall caused by friction burn using a combined myocutaneous
flap of teres major and latissimus dorsi muscles. Burns, 2001 May;
27(3):283-8.
15. Baruchin AM, Jakim I, Rosenberg L, Nahlieli O. On burn injuries
related to airbag deployment. Burns 1999; 25:49-52.
16. Ulrich D, Noah EM, Fuchs P, Pullua N. Burn injuries caused by air
bag deployment. Burns, 2001 Mar; 27(2):196-9.
17. Corazza M, Trincone S, Virgili A. Effects of airbag deployment:
lesions, epidemiology and management. Am J Clin Dermatol. 2004;
595):295-300.
18. Rubin P, Starley I, Jones RP. The revolutionary dual cyclone vacuum
cleaner - a new cause of digital friction burn in children. Burns
1998Feb; 24(1):78-9.
19. Macgegor D. Hand injuries in young children from contact with
vacuum cleaners. Emerg med J. 2002 Jan; 19(1):80-1.
20. Choudhary S, Koshy C, Ahmed J, Evans J. Friction burns to thigh
caused by tourniquet if applied over bare limb skin. Br J Plast Surg
1998 Mar;51(2):142-3.
21. Giannoudis PV, Snowden S, Matthews SJ, Smye SW, Smith RM.
Friction burns within the tibia during reaming. Are they affected by
the use of a tourniquet? J Bone Joint Surg Br 2002 May; 84(4):
492-6.
22. Mehrotra S, Nanda V, Chittoria R, Ksharma R. “Chunni burn”: a
rare mode of clothing-induced friction burn. Plast Reconstr Surg
2004 Jul; 114(1):282-3.
23. Mahahan AL, Regan PJ. Tolls of a trek up Croagh Patrick: a case of
friction/frost burns to the feet. Burns 2004 May; 30(3):283-5.
24. Brehmer-Andersson E, Goransson K. Friction blisters as a
manifestation of pathomimia. Acta Derm Venereol 1975;55(1):
65-71.

Firework and Firecracker Injuries
333
Firework and Firecracker Injuries
25
Arun Goel, Sameek Bhattacharya
Chapter
INTRODUCTION AND HISTORY
Fire, which changed the face of human civilization, has
been man’s fascination since its discovery. Among the
modalities of its use, ranging from highly beneficial to highly
destructive, fire has been central to numerous occasions of
celebration. Initial uses were limited to decorative illumination
but later, with the evolution of ordnance technology,
developed the art of manufacturing and setting off of
fireworks (Pyrotechnics). The earliest documentation of
“fireworks” is from China during Han dynasties (200 BC)
which dates even before the discovery of gunpowder.
Burning of green bamboo led to expansion of trapped air
resulting in loud bang. The bursting bamboo or “pao chuk”
in Chinese, were part of Lunar New Year celebrations and
other festive moments for about a thousand years till
gunpowder was invented during Sui and Tang dynasties
(600-900 AD). The precursor to the discovery of
gunpowder was a chance finding of a sulfurous mixture by
Chinese alchemists during the course of their experiments,
which burst into illuminating flame on burning. “Hao yao”
or fire dung as they called it were packed in bamboo tubes
and burned as firecrackers. The knowledge of pyrotechnics
reached the West only in 1200 AD when Marco Polo brought
the Chinese know-how to Italy. It was the Italians who
added the esthetic dimension to the fireworks by adding
metal powder to gunpowder in order to produce colorful
sparkles. With further advances in chemistry, some more
metal salts were added to produce multi-colored
pyrotechnic-effects.
The new age pyrotechnic devices are broadly classified
as incendiary fireworks and explosive firecrackers. A
firework is a low explosive pyrotechnic device used primarily
for esthetic illumination and entertainment in the form of
light, sparkles and floaters, noise being secondary. A
firecracker, on the other hand, is a relatively higher explosive
device designed primarily to produce noise in the form of a
loud bang and visual effect is incidental. Both firecracker
and fireworks are basically explosives wrapped in heavy
paper casing with a long fuse to ignite.
FIREWORK/FIRECRACKER SCENARIO
IN MODERN TIMES
In modern times, social events like marriage, religious
functions and state functions, e.g. Independence Day all
involve display of fireworks and bursting of firecrackers.
So much so that even fireworks competitions are being
organized at a number of places in the world, for example,
the annual Montreal Fireworks Festival in Canada and World
Pyro Olympics held in Philippines. Many major cities around
the globe begin the New Year with fireworks and firecrackers.
The opening and closing ceremony of Beijing Olympics in
2008 were marked by one of the greatest firework display.
The fireworks/firecrackers have also been known for their
use to exorcise evil spirits with their loud sound. Firecrackers
are even utilized by farmers as a modality to scare away
wild animals and birds from farms.
Its use in festivities is universal all over the world, be it
a developed or under-developed nation. In India, widespread
and large scale use of firecrackers and fireworks during
“Diwali” (‘festival of lights’) is unparalleled in the world.
“Diwali” or “Deepawali” is celebrated to mark the victorious
return of Lord Rama (an incarnation of Lord Vishnu, a Hindu

334
Principles and Practice of Burn Care
God) to his kingdom in Ayodhya after killing the evil Ravana
(the demon king) of Lanka (now Sri Lanka). During this
festive night of victory of good over evil, the houses are
adorned with small earthen oil lamps, candles and colorful
electric lights. After offering the prayers, the entire family
participates in the bursting of firecrackers. Twenty days
preceding “Diwali”, “Dussehera” is celebrated by burning
the towering effigies of Ravana, his brother Kumbhakarna
and son Meghnada. These are packed with massive amounts
of various types of firecrackers and fireworks and this
public display is attended by thousands of onlookers in every
locality. “Diwali” is also celebrated in many other countries
of South East Asia having large population of Indian origin.
Thrissur Pooram, a two century old festival to mark
the end of caste supremacy is celebrated in Kerala, southern
India. The festivities are attended by millions of people from
across the state and even international visitors. The
spectacular fireworks display, biggest in India, starts in the
early hours (0230 Hours IST) and lasts for 3-4 hours.
During marriages in India, firecrackers are burst and
fireworks are arranged with complete disregard to safety
measures. The area may be a congested, narrow road with
vehicles, children surrounding the site at close range as
onlookers and ladies wearing synthetic, inflammable free
flowing dresses. The make-shift “pandals” (tents) are also
made of inflammable cloth. In India, even victory in
international cricket matches, whether played in or out of
country, is celebrated by cricket fans at home by bursting
crackers.
Hari Raya Puasa, marking the culmination of”Ramadan”,
the holy month of fasting is celebrated in Malayasia by
Muslims. Shab-e-Barat in Pakistan, Independence Day in
USA and Halloween season in Ireland and elsewhere are all
celebrated with fireworks and firecrackers.
Presently fireworks/firecrackers are billions of dollar
industry giving employment to millions from manufacturing
to retail sale. China is the largest manufacturer and exporter
in the world. Sivakasi city in Tamil Nadu is the leading
producer in India.It has a great share in world market as
well. Thus, it is clear that despite their immense harmful
potential, it may not be possible to effectively ban their
manufacturing and use. From time to time different nations
have tried partial or total ban on them which only led to
illegal manufacture and smuggling. Such illicit firecrackers,
obviously devoid of standard safety features, posed greater
risk ultimately lifting of ban allowing restricted use. For
example, in Singapore, a partial ban on firecrackers was
imposed in 1970 and converted to complete ban in 1972.
However, in 2003 firecrackers were allowed to be set off
during festival seasons under controlled conditions by
Singapore Tourism Board. Similarly, in United States in 1973,
the National Society for the Prevention of Blindness
proposed to The US Consumer Product Safety Commission
(responsible for regulating fireworks under Govt. Act) a
total ban on the sale of fireworks for personal use and a
temporary ban was imposed. Despite this ban having the
support of American Academy of Pediatrics, American
Public Health Association and National Fire Protection
Association, etc. the ban had to be lifted the same year. At
present, although firecrackers are not illegal in US, there
are strict regulations regarding their sale, possession and
use.
The fireworks/firecrackers are so much ingrained in
the Indian psyche and socio-cultural fabric that imposition
of a total/partial ban by the authorities is next to impossible.
Whatever laws are in place, the slackness in their execution
allows rampant violations in manufacture, storage, sale and
individual use by the public leading to a large number of
cracker-related burns, blast injuries, deaths and disablement
apart from economic loss and loss of property. The sale of
fireworks is largely unrestricted in India and people have
access to a variety of fireworks including illicit and poorly
standardized ‘make’ and light them in densely populated
parts of cities and towns without a hint of safety concern.
Improper use of fireworks may be dangerous, both to the
person operating them as well as to the bystander(s).
TYPES OF FIRECRACKERS
The various types of firecrackers available are:
1. Phooljhari or “Sparkler” (Fig. 25. 1): This is commonly
used in lighting most of the other firecrackers. It consists
of a metal stick with one-half covered with pyrotechnic
compounds and the other half acts as a handle.
2. Anar or “fountain” or “flowerpetal” (Fig. 25.2). It
emerges as a big sparkling fountain of fire when lit. In
addition, “Anar” is unique to our country and many
people make its crude form at home, which poses grave
risk while preparing as well as igniting them.
3. Zameen Chakri or Ground spinner (Fig. 25.3): It is a
spinning circle of fire with sparks coming out of it.
4. Rocket (Fig. 25.4A): When fired, goes in the sky and
bursts into myriad of colors and designs. They may
prove dangerous when they change their course and
enter into residential buildings. In addition, they may
start fires after landing on inflammable material.