LOCALIZED HEAT INJURY -

BURNS (COMBUSTIO)
 LOCALIZED HEAT INJURY -
BURNS (COMBUSTIO)
Patients with burns compose 2% of surgical
patients. Burns may be caused with the action of
heat (thermal burn), chemical agents (acids,
alkalis, phosphorus), electricity and ionizing
radiation (radiation burn), X-ray, flash, insolation
(solar burn).
Most large hospitals have specialized burn units.
There is burn centre, (founder and chief surgeon
prof. B.Iashvili) in Tbilisi (Georgia), designed to
address the specific problems arising in the
management of burnt patients.
 Mechanism of thermal
trauma
inflammation of benzine (petrol, gasoline), lasting
few parts of secunds, causes the overheating of the
tissues, during minutes. Vapor action during 20sec
causes overheating of the tissues, lasting 3min.
Overheating of the tissues, below the 58°C causes-
humid necrosis, above the 65°C – coagulation necrosis.
Long-term action (6h) of 42°C leads to the skin necrosis
(the same situation occurs in case of applying of
heater) to the skin of the unconscious patient). The
threshold temperature for the epidermis is 50°C
(during 3min), for the leucocytes, osteoblasts - 44-46°C.
 Fig 134. Zones of thermal injury
The severity of
burn is
determined by
the several factors
(depth, surface
area, site, smoke
inhalation and etc
/fig. 134/).
 Estimation of percentage
of burnt surface
1. The rule of “nines” /fig. 135/ -which is distributed in the
following way: head and neck-9%,upper extremity - 9%,trunk
(front) - 18%, trunk (posterior surface) - 18%, lower extremity -
18% (hip - 9%, chin and foot - 9%) genitalia and perineum-1%,
whole skin surface composes 1600-2000 cm2, thickness of the skin
is 1mm.
2. The rule of palm: surface of he palm composes 1% of whole
surface. The loss of protein-rich fluid from the surface of the
burn may be so great, that hypoproteinemia and hypovolemia
occur, which may lead to the shock, when more, than 10% of body
surface area is injured with full - thickness burns. Treatment in
burn centers has improved survival rates dramatically and even
patients with burns over 75% of their bodies may recover.
Fig 135. The rule of “nines”
 Estimation of percentage
of burnt surface
3. Site: burns of clean areas, which can be
immobilized, heal better, than similar burns in more
difficult or contaminated areas (eg. perineal and groin
burns).
4. Smoke inhalation: most frequently deaths in fires
are caused by smoke inhalation and not actual burning.
Thermal damage of the respiratory tract causes alveolar
necrosis, hemorrhage, pulmonary edema (lung
swelling) and leads to respiratory distress syndrome.
Burning of the body usually occurs after the death.
 Classification of burns according to the
depth of necrosis
Burns are divided on superficial (non-
problematic) and deep (problematic) types.
Superficial burns include I, II, IIIa degrees, deep - IIIb
and IV degrees. Superficial burns heels
spontaneously (epithe­li­sa­tion).
First degree burns (Combustio erithematosa)
/fig. 136/ are associated with focal epidermal
necrosis, but no blistering. Dilation of dermal
capillaries leads to erythema. Healing is uneventful,
with epidermal regeneration, occurring from the
basal layer. There is no scarring .
 Fig 136. Classification of burns
according to the depth of necrosis
 Classification of burns according to the
depth of necrosis
Second-degree burns (Combustio bullosa) are
associated with separation (detachment) of the
epidermis with blistering (vesiculation) in addition to
erythema and edema. Healing without scarring, but
more slow.
Third - “a” degree burns (Combustio escharotica
cutis partialis) are associated with necrosis of
epidermis and upper derma with maintaining of
papillary layer and adnexal residual epithelium (from
hair follicle, fatty and sweat gland).
 Classification of burns according
to the depth of necrosis
Third - “b” degree burns (Combustio escharotica
cutis totalis) are associated with necrosis of the epidermis,
derma and adnexal structures. Third-degree burns heal very
slowly by regeneration of epithelium from unburned skin at
the edges. Dermal scarring is usually severe. Skin is pallor,
touching or pricking with needle of the burned areas isn’t
painful, because of death of nervous receptors. Only on 7-
14th days is possible to determine the degree of burn precisely
/fig. 137/.
Forth degrees burns involves skin, subcutaneous fat,
fascia, sometimes-muscles and bones.
 The rule of "hundred". It is necessary to add
Estimation of severity of burns

age (years) of adult patient to the burned surface

(in %). Prognosis is favorable, if sum is less than
60, less favorable, - 60-80, doubtful - 81-100,
unsuccessful - 101 and more.
Index of Frank: This index is composed with
sum of superficial burns surface (in %) + 3 x
surface of deep burns surface (%). Prognosis is
good if Frank's index is less than 30, relatively
good - 30-60, doubtful- 61-90 and bad - more
than 90.
 Burn severity classification
Major burn injury:
II and IIIa degree burn of >25% of body surface
in adults;
II and IIIa degree burn of >20% of body surface
in children;
IV and IIIb degree burn of >10% body surface;
Most burns involving hands, face, eyes, ears, feet
or perineum;
Most patients with the inhalation injury,
electric injury, burn injury complicated by the
other major trauma, high-risk patients with
 Burn severity classification
Moderate uncomplicated burn injury:
II and IIIa degree burn of 15-25% of body surface in
adults;
II and IIIa degree burn of 10-20% of body surface in
children;
IV and IIIb degree burn of < 10% of body surface.
Minor burn injury:
II degree burn of <15% of body surface in adults;
II degree burn of <10% of body surface in children;
III degree burn of <2% of body surface.
 Complications of the burns
1. Hypovolemia is the result of fluid exudation on the
surface of the burn. Urgent i.v. infusion of plasma and
blood substitute liquids is necessary in aim to avoid the
shock and renal damage;
2. Necrosis of erythrocytes occurs in the burnt blood
vessels and free hemoglobin and cell destruction product
may cause acute renal failure;
3. The black crust (slough) hardens (after coagulative
necrosis of epidermis and derma) and contracts over the
first few days. Contraction of the crust may prevent blood
flow (as a tourniquet), requiring surgical relief, when a
circumferential burns of the limb occurres;
 Complications of the burns
4. Burnt skin no longer serves as barrier to infection and
actually promotes the growth of microbes (pseudomonas,
species, fungi as Candida Albicans and Aspergillus);
5. Curling's ulcers (acute peptic ulcers of the stomach and
duodenum) may occur the following major burn injury and
cause severe gastrointestinal bleeding. Excessive adrenal
corticosteroid secretion during the acute stress of the burn
has been implicated;
6. Scarring: when large areas of the body are burnt, severe
scarring occurs during healing and often requires cosmetic
plastic surgery. Scars may also cause contractures, that limits
function /fig. 138/. Burn scars may be transformed into
squamous carcinoma many years later.
 Burn disease
Burn disease occurs in case of superficial (I, II, IIIa
degree) burn of more than 15% of body surface, or 10% in
case of deep (IIIb, IV degree) burn. Burn disease is divided
on 4 periods:
1. Burn shock: hypotension, hypothermia and
oligoanuria, hypovolemia, excitation at first, then
depressed condition, thirst, nausea, vomiting. Duration 2-
72 h;
2. Acute burn toxemia lasts 7-8 days. Return of the
liquids into the blood circulation leads to the restoration
of the hemodynamic indexes, but to the intoxication at the
same time (tachycardia, dullness of the heart sounds,
hypo- and dysproteinemia, dysfunction of liver and
 Burn disease
3. Septicopiemia usually starts from the 10th day.
Infectious agents are: staphylococcus, B.Aeruginosa
(B.Pyocyaneus), E.coli. Pushing away of burn eschar
(crust) starts from the 7-10th days and purulent infectious
complications as pneumonia, decubitus, sepsis occurre.
In case of extensive deep burns, septicopiemia is
accompanied with burn depletion (body mass loss,
pallor, muscle atrophy, contracture of joints).
4. Reconvalescention is accompanied with restoration
of damaged functions, but the heart, liver and kidney
disturbance may be stay during 2-4 years after the
trauma.
 The first emergency aid in
case of burn
It is necessary to avoid the thermal agent (flame) and
cool the burnt surface with the help of cold water, ice
bag, snow, during 10-15min, not less to give the
antipyretic drugs and apply the aseptic bandage, give to
drink alkaline (sodium bicarbonate) mineral waters as
“Borjomi”, tea. Patient must be dressed warm.
Analgesics, antihistamine drugs, neuroleptics must be
injected before transportation, which must last 1h,not
more. In other way blood and plasma substitute solutions
must be infused i.v., oxygen therapy, cardiotonics and
nitrous oxide inhalation (N2O) must be applied.
 The local treatment of burns
There are two methods of treatment of burns: 1. closed; 2. opened.
1. Closed method includes the applying of bandages with various emulsious
and ointments (Mafenid, Furagin, Iodopiron, Propolis, Thurmanidze’s
ointment for the treatment of burns).
2. Opened method is based on the drying effect of warm air, ultraviolet and
infrared insolation, also on the effect of the abacterial environment, what
makes the economy of banding materials. Usually, it is used in case of face,
neck, perineal burns. Usually, burns of II degree heel with spontaneous
epithelisation during 7-12 days, IIIa degree-to the end of 3-4 weeks. The crust
formation lasts 3-7days in the type of humid or dry (coagulative) necrosis, in
case of deep burns. Marked purulent process and intoxication occurs in the
first case, crust pushing away starts from 7-10 days and granulative border
formation finishes on the 4-7th week. Chemical treatment of the crust
includes drying of the surface with the solar lamp, ultrasonic radiation,
treatment with potassium permanganate (KMNO4). Chemical necrectomy
means the applying of proteolytic enzymes, 40-50% Salycilic or Benzoic
acids.
 Surgical treatment of the Burns
It includes early operations (necrotomy and necrectomy),
also autodermoplasty (skin grafting), limb amputation and
restorative-recon­structive operations.
Necrotomy is indicated in case of circumference burn of
extremity, in aim to avoid the compression of limb.
Necrectomy must be performed as soon as possible (1-3
days) after the successful treatment of shock. Excessive
necrotomy must be performed 0n 4-7th days. The surface of
necrectomy mustn’t be more, than 25-30%in one moment.
Autodermoplasty is the single method of treatment of IIIb-
IV degrees of burns. The graft with 0.2-0.4mm thickness must
be taken from the healthy regions of the body by the help of
dermatome under the local (topical) or general anesthesia.
The surface of the graft must be not more, than 800-1500cm 2.
 General principles and
intensive care of burns
It is necessary to provide first aid before
hospitalization:
1. Quite, applying of aseptic bandages;
2. Injection of analgesic and antihistamine drugs, in case
of excessive burns-injection of Phentanyl and
Droperidole, inhalation anesthesia;
3. Fight against the hypothermia (warm cloth, heaters,
hot tea);
4. Replacement of plasma loss (drinking of alkaline
waters, as “Borjomi”, i.v infusion of blood and plasma
substituents).
 General principles and
intensive care of burns
In the hospital patient must be placed in the antishock
ward in aim to reach following goals:
1. Giving analgesics, antihistamine drugs;
2. Cardiotonic drugs;
3. Improvement of microcirculation;
4. Corticosteroid preparations;
5. Oxygen inhalation;
6. Diuretic drugs;
7. Bacteriophage and staphylococcal anatoxin, antitetanic
immunization;
8. Infusion-transfusion therapy: blood, plasma, albumin, protein,
fibrin, Macrodex, Rheomacrodex, Gelofusin, Neokempensan, 10%
sol. of Glucose, Lactasol, sodium Bicarbonate (4%), Trisamin;
 General principles and
intensive care of burns
It is necessary to keep in mind, that most grave plasma (6-8
L/per 24h) and protein loss (70-80g/24h) occurs in the first 8-
12h and lasts for 2days.Volume of transfused liquids mustn’t
be more, than 10% of body mass. It is necessary to infuse ½ or
2/3 of daily volume of liquids in the first 8h after the burn.
Infused liquid mass composes not more, than 5% of body
mass on the second and third day after the burn.
Brocka’s formula for estimation of infused liquid mass: 1ml
X body mass X burned surface (first degree isn’t in count) +
2000ml of 5% sol. of Glucose.
Monitoring values: central venous pressure, Hb, Ht,
diuresis/per hour.
 Chemical Burns
They are caused with the action of concentrated
solutions of acids (acid burn), alkalis (alkali burn), some
heavy metal salts, phosphorus (phosphorus burn), toxic airs
(Iprit, Luisit). Action of some chemical agents may cause not
only the damage of skin and mucosa membranes, but general
toxic action (eg. phenol, mercury salts), kidney and liver
injury may be caused with the action of phosphorus and
phosphoric acid. The action of the acids and heavy metal
salts on tissues, cause the coagulation of proteins and
coagulation necrosis with formation of hard and superficial
crust (slough). The concentrated of alkalis pe­netrate into
deeper layers, than acids, cause colliquation (humid)
necrosis.
 Chemical Burns
Morbid anatomy: there is a picture of inflammation in case
of superficial (I-II degree) and necrosis in case of deep (III-IV
degree) chemical burns. In case of alkalis burns histological
picture at first is normal, but Karyolysis, karyorhexis and
cytolysis occurs a little later. Coagulation necrosis,
hyperchromatosis and karyopiknosis occurs from the very
beginning of acid burns. The clinical picture of traumatic and
hemorrhagic shock occur in case of severe and massive
chemical burns. Most frequent is the chemical burns with
sulfuric acid (H2SO4). In this case the crust is grey, dark brown
or black. Crust is yellow in case of burn with nitric acid
(H2NO3), grey-yellow - in case of burn with hydrochloric acid
(HCl) and green - in case of burn with acetic acid (CH3COOH).
 Chemical Burns
I degree chemical burn: patient feels burning pain. Skin
is swelled, redness (hyperemia) is noted .Swelling is more
advanced in case of alkali burn. Sense is maintained
,sensitivity to pain is increased.
II degree: superficial dry (in case of acid burn) or gel or
soap form (in case of alkali burn) crust occurs, which is
very thin and mobile.
III-IV degree: crust is thick, hard and fixed. Sense is
absent. Only after 3-4 weeks is possible to make
differential diagnosis between III (full-thickness skin
necrosis) and IV degree (necrosis of the skin and deep
tissues, up to the bones) burns.
 Radiation Burn (Ionizing
radiation injury)
Tissues, exposed to radiation, show the damage
of collagen that results in dense hyalinization.
Blood vessel changes vary, from the development
of teleangiectatic vessels formation to thickening
and hyalinization of the walls. Fibroblasts and
endothelial cells are enlarged and demonstrate
nuclear abnormalities, including hyperchomatism
and abnormal chromatin clumping. Karyotypic
analysis shows aneuploidy and polyploidy with
various chromosomal abnormalities.
 Skin alterations
erythema, swelling and epidermal desquamation (acute
radiodermatitis) are seen In the first 2-6weeks after radiation
exposure. Later chronic radiodermatitis occurs (epidermal
atrophy with atypical cytological pictures in the cells, dermal
fibrosis, teleagiectatic and hyalinized vessels formation). The
skin becomes blotchy and atrophic with irregular surface and
ulceration, depigmentated areas, hair loss. Chronic
radiodermatitis persists for years. Cancer of squamous
epithelium may occur many years after exposure.
 Skin alterations
The radiation burn includes following periods:
1. Primary (early) reaction starts few hours after the
exposure and lasts 1-2days (erythemal formation, skin
tension, itch);
2. Occult period, without marked (pronounced) clinical
signs;
3. Period of acute inflammation (from 2-3weeks up to
few months) with hyperemia, swelling, blistering,
necrosis, erosions and ulcer formation /fig. 139 /;
4. Period of recover with tissue restoration. Regeneration
is very slow, lasts for many time with scar formation,
residual erosions and ulcers with dry, necrotic bottom.
Fig 139. Local Radiation injury (ulcer
formation) of lower third of thigh
 Treatment
removal of radioactive substance from the
skin with stream of water. In case of pain-
narcotic analgesics, Novocain blockade.
Infusion of blood and blood substitute
liquids, vitamins, calcium chloride, Dimedrol,
bandings with stimulation action ointments,
skin grafting, sometimes grafting with tissue
complex (skin, subcutaneous tissues, muscles
with feeding blood vessel) grafts.
 Localized cold injury -
Frostbite (Congelatio)
The severity of focal cold injury depends on temperature,
the rate of chilling and duration of exposure. The factors,
determining the severity of frostbite:
1. Meteorolgic factors (humidity, wind);
2. Factors, impairing blood circulation (tight cloth, boots,
clenching with force the handle of gun, growl, prolonged
staying in immovable and uncomfortable position;
3. Factors, decreasing the local resistance of tissues (traumas,
blood supply and innervation impairment);
4. Factors, decreasing general resistance of the organism
(shock, woun­ding, blood loss, fatigue, depletion, alcoholism,
avitaminosis).
 Classification of Frostbite
Classification according to clinical duration:
a) Latent (pre-reactive) period;
b) Reactive (after getting warm) period.
Latent period: the tissues are in the condition of
hypothermia, frostbite occurs unnoticeably, without marked
clinical signs. Pallor of skin, piercing (stabbing) pain (slight)
hypothermia and loss of sense.
Reactive period starts after the warming of frostbitten
tissues and marked pain, progressive swelling, paresthesias -
creeping, burning or cold sensation occurs, than - signs of
necrosis and reactive inflammation. Only after 5-7days is
possible to determine borders of pathologic process, its depth
and degree.
 Classification of frostbites
according to its depth/fig. 140 /
I degree frostbite: circulation and innervation disturbance
occurs without necrosis of tissues. Clinical signs:
itch,paresthesia,cyanosis of skin, swelling, which disappears after
3-7days. Epidermis desorganization and hypersensitivity on cold
occurs later.
II degree frostbite: blistering with transparent hemorrhagic gel
consistence content occurs on the purpure-cyanotic skin. Necrosis
don’t attaches the papillary layer (the bottom of the blisters),
which is sensitive on mechanical irritation and alcohol (positive
test on alcohol). The II degree heals without granulation and
scarring. New nails grew instead of lost ones. Limited wideness of
movement in joints may last during few months/ fig. 141 /. 
 Classification of frostbites
according to its depth
III degree frostbite: necrosis of whole
skin and subcutaneous fatty tissue occurs.
Blisters contain dark-hemorrhagic liquid,
their bottom is purpur-blue with lost
sensation on pain and alcohol. Healing
with granulation and scar formation lasts
1-2 months. Sometimes it is necessary to
perform skin grafting.
 Fig 140. Classification of frostbites according to
its depth. 1. Epidermis; 2. Papillary; 3. Derma; 4.
Soft tissues and bone.
II degree frostbite
 Classification of frostbites
according to its depth
IV degree: necrosis of all deep layers, up to the bones occurs.
Blistering with dark-hemorrhagic content. Swelling decreases
on 5-7days, demarcation of necrotic tissues occurs, Billroth’s
test is positive (absence of pain and blood in case of piercing
of injured tissues with the needle). Moist and humid gangrene
occur /fig. 142/. Demarcation of necrotic tissues occurs on 2-3rd
week, wound heeling lasts a few months. Full thickness or
tissue complex grafting of skin is indicated. Purulent
complications may occur (phlegmonas, tendovaginitis,
arthritis, osteomyelitis, septic condition). Late complications
are: obliteration endarteritis, poly and mononeuritis, trophic
ulcers.
Fig 142. Zones of frostbitten foot. 1. zone of
necrosis; 2. zone of irreversible alteration of
tissues; 3. zone of reversible alteration of
tissues; 4. healthy tissues
 Classification of frostbite,
according to their etiology
a) Frostbite due to the action of cold air is most common
type. Distal segments of extremity are frostbitten in 90-97%
(fingers, hands, foot), rarely – nose, ears, cheeks. Two or more
limbs are frostbitten at one and the same time, but not
proximally than wrist and ankle-joint.
b) Trench foot is the result of long, continued (3-4 days)
action of high humidity, mud cold, and nonfreezing (above
0°) temperatures on the extremity. It was common
complication of warfare during World War I. Cooling of the
foot is changed with short and incomplete warming. First
symptom is loosening of sense of pain, than swelling ,multiple
hemorrhagic blisters necrotic crust formation, in grave cases-
humid gangrene, septic condition;
 Classification of frostbite,
according to their etiology
c) Immersion foot means frostbite, as a result of action of cold
water. It happens in case of shipwrecks. The initial response of tissue
to cold water is vasoconstriction, which causes ischemic damage of
muscles and nerves. Vasomotor paralysis occurs after several hours of
continued immersion, leading to fixed vasodilatation and damage of
the microcirculation. The involved area becomes swollen and blue
and is often extensively blistered. Thrombosis ultimately occurs,
after several days of exposure, leading to gangrene. Swelling, pain
and hyperemia disappears after 10-12 days in case of I degree.
Swelling lasts upto the knee-joint, with multiple blistering, pain,
paresthesia, muscle weakness, lasting 2-5 months in case of II
degree. III-IV degree: skin is swollen, blue-green, with
mummification, humid gangrene, lymphangitis, lymphadenitis,
thrombophlebilitis, intoxication, obliteration of peripheral arteries.
 Classification of frostbite,
according to their etiology
d) Contactive frostbite occurs in case of direct
contact with metallic objects, cooled down to –40°C
and more. Latent period is absent. Usually, frostbite of
III degree occurs, on fingers, face, ears, nose.
e) Chilling (pernio) means chronic first-degree
frostbite and usually impairs the young people which
regularly stay at the cold in the winter, spring or
autumn under the repeated, not prolonged action of
not pronounced cold.
Clinical picture: swelling, itch, fissures, ulceration,
dermatitis.
 Treatment of frostbite: first aid includes getting warm, giving hot
meal or drink, treatment of the nose, ears with alcohol and applying of
the aseptic bandage. In case of generalized cold injury (hypothermia) and
dyspnea - artificial pulmonary ventilation and hospitalization. Injection
of antitetanic anatoxin. It is necessary to put the patient into the bath
with 36°C water and heat the water upto 38-40°C during 15-20 min, in
case of generalized cold injury. Warming must last 1-1.5h.It is necessary
to infuse Trental, Nicosphan, Glucose, Reomacrodex, Calcium Chloride,
4% sol. of Sodium Bicarbonate, Fibrinolysin, Heparin, vitamins,
Neocompensan, analgesics, antibiotics, perform Novocain blockade. It is
preferable not to open blisters, as in case of II degree frostbite
epithelisation goes on better under them. Necrectomy is necessary in
aim to avoid humid gangrene and infection in case of III degree frostbite.
Necrotomia and necrectomia must be done on 8-14 days, after the
formation of demarcation line. The treatment is the same, as in case of
simple wounds after the granulation tissue formation. It is necessary to
perform necrectomy in case of IV degree frostbite, in several cases –
amputation of the extremity and grafting with tissue complexes.
 Electric burns and Electric trauma
(Electrocution)
It is possible occurrence of electric burns in case of current
with 24v and more voltage. Electric traumas compose 2-2.5%
of whole traumas. Thermal action of electric current according
to the rule of Joule: Q=I2RT (Q=warmth, I=forth of current in
amperes, R=impedance of tissues in Om, T=exposure of
action). Water containing tissues have less impedance (are
good conductors) and better pass the current. Eg., impedance
(resistance) of muscles is 1500 Om/cm2, skin’s - 50.000-
700.000 Om/cm2. bone’s - 800.000 Om/cm2, dry callous skin -
1.000.000 Om/cm2.
Electric burns and Electric trauma
Electrochemical action of electric current includes
polarization, intracellular gel formation from the
proteins and occurrence of coagulation necrosis, blood
vessels thrombosis and secondary necrosis. General
biological action includes: heart damage (fibrillation),
unconsciousness, respiratory standstill. Electric burns are
absolutely not painful because of death of nervous
receptors, moist necrosis with slow pushing away of
necrotic tissues (in comparison with thermal burns).
Appr. 1000 deaths occur annually in U.S.A., as a result of
electrocution and 200 death – as a result of lightning
strike /fig. 143/.
Fig 143. Lightning strike
 Electric burns and Electric trauma
Injury occurs when the human body becomes a part of
electric circuit. Severe electrical injuries are more common
in countries, that use a 220-240v domestic supply, than
those, that use a 110v supply. The exact path taken by the
current through the body and the organs is the pathway,
eg., the earth is the exit point, a current that enters the body
in the lag and leaves through the foot will be much less
harmful, than one which enters the hand, since in the latter
instance cardiac arrhythmias may develop as the current
passes across the heart. Very important is also duration of
contact with the source of current. Alternating current (AC)
is more dangerous then direct current (DC), because it
causes tetanic contraction of muscles, that may prevent the
victim from letting go of the contact source.
 Electric burns and Electric trauma
In case of contact with the metallic bodies impregnation
of the tissues with metallic microcorpuscles (metallization
to tissues) occurs. Exploding of phosphorus and calcium
salts, so called “pearl” appears in the bones because of
electrolysis, steam and air formation.
Skin is necrotic in the place of entrance and exit points,
but deep layers are impaired more, than skin, because of
thrombosis of blood vessels, which can cause the gangrene
of extremity. “Current marks” /fig. 144/ (burn wounds) on
the skin is typical for electrocution. “Lightening figures”
are dark-brown branch form stripes on the skin.
Fig 144. Current marks, caused by DC
 Electric burns and Electric trauma
The first aid in case of electrocution includes
disconnection of the injured person from the source of
current, provide resuscitation measures in case of
necessity. They must be transported to the hospital after
the applying of aseptic bandings on the burned surface.
General treatment of electric burns is the same, as in
case of thermal burns. In case of anuria, hemodyalisis
must be used. Necrotomia must be performed step by
step (not in one moment). Amputation must be
performed in case of bone injury. Early amputation is the
prophylaxis of complications (bleeding, renal
impairment, sepsis). Plastic operations (grafting) and
prosthetics must be done later.