Principles and Practice of Burn Care

Keratinocyte Culture
237
the cell culture, the holoclones progressively become
meroclones and paraclones. As a result only second and
third passages are used for grafting. Each colony of the
cultured cells expands by the peripheral cells dividing and
moving outwards. After 8-10 days when cultures are nearly
confluent, all the cultures are seeded/reseeded with
attenuated 3T3 cells.
The cultures are maintained by the same conditions
until confluence and differentiation into multicellular
epithelium is obtained (Figs 19.1 and 19.2). The epithelium
is enzymatically detached from the culture flask or dish by
Dispase and rinsed in PBS. The epidermis is taken on to
Vaseline gauze of smaller mesh size by preserving the
orientation of the graft in such a way that the basal cells are
applied on to the wound bed (Figs 19.3 to 19.5). Cultured
epithelial autografts usually take about 2-3 weeks time. The
detached epithelium is assessed for cell viability (Green et
al, 1979).5
Fig. 19.2: Confluent keratinocyte on culture
Fig. 19.1: Cell suspension of keratinocyte
Fig. 19.3: Sheet of cultured keratinocytes on vaseline gauze before
transfer
Fig. 19.4: Cultured keratinocyte sheet spread out on hand
Fig. 19.5: Multilayered cultured keratinocyte under high power
magnification

238
Principles and Practice of Burn Care
During this intervening period when the keratinocytes
are being cultured, the patient’s wounds are serially debrided
to remove all the dead tissues after the patient’s general
condition stabilizes, usually after the third day post burn.
The excision is done every 2-3 days and can vary from
tangential to fascial depending on the depth of burns. The
excised areas are covered either with a dermal skin substitute
like biobrane or integra or if possible by cadaveric
homograft.
The cultured graft material is transported in aseptic
conditions in petridishes containing DMEM under 5% CO2
to the operation theater, where the patient is prepared for
surgery.
Grafting Procedure and Post Grafting Care
The grafting is carried out as soon as the cultured graft
material arrives in the OT. The graft material with carrier
gauze is applied on to the wound bed after debridement
without friction, air bubbles and hematoma formation
underneath the graft (Figs 19.6 to 19.8). The carrier gauze
is covered with saline soaked gauze followed by thick dry
gauze dressing. The first dressing change is done after the
initial 5 days and every 2 days thereafter. The carrier gauze
is removed between day 6 and 8. The other management
procedures are same as those routinely followed for skin
grafting. Limitation of cultured epithelial autografts for full
thickness loss is the failure of this approach to reconstitute
dermal layer. Epidermal replacement also ignores the
fundamental importance of the dermis in providing the skin
with its integrity and durability. Clinical problems of poor
durability, scarring and wound contraction often are
encountered. Graft ‘take’ can be improved by placing
cultured keratinocytes autografts on a pre-grafted cadaver
dermis.
Disadvantages
Many of the drawbacks associated with cultured
keratinocyte autografts can be attributed to the absence of
dermal element. The keratinocyte culture contains no dermal
matrix tissue and is placed on debrided full thickness burns
that lack any dermal elements. Since it is the dermis that
provides the elastic quality to the skin, healed wounds that
lack dermis are thin and stiff. Cultured keratinocyte grafts
placed directly on the muscles or subcutaneous tissues form
the basement membrane very gradually. The basement
membrane serves as an important attachment function and
epidermis lacking a well formed basement membrane,
Fig. 19.6: Burn wound on forehead—Preoperative
Fig. 19.7: Healed burn wound on forehead covered with cultured
keratinocyte sheet after 2 weeks of application
Fig. 19.8: Burn wound on forehead covered with cultured
keratinocyte sheet

Keratinocyte Culture
239
blisters and shears off easily. Graft fragility results in ‘delayed
losses’. However, even a partial ‘take’ of epidermal cultured
grafts can lead to complete wound healing by gradually
progressing epithelialization from the islets. In the long term,
it has been observed that these grafted areas tend to contract
in the same manner as an autograft, though at the same
time, the inflammatory reactions are weak and hypertrophic
scarring rarely develops in these areas. The above drawbacks
have limited their clinical applications and emphasize the
need to develop keratinocyte culture methods on surfaces
that mimic the human dermis or dermal equivalent.
There are reports of using various dermal equivalents
with different compositions.16-19 Even though they do
increase the possibility of graft ‘take’, the high cost of these
materials preclude their use for extensively burned patients
who would require a large skin resurfacing in a short period
of time. There have also been a lot of studies on using
acellular fibrin gels as a biological support medium for
keratinocyte cultures.20,21 It has been observed that the
keratinocytes cultured on fibrin gels are easier to handle
and can be easily detached when prepared without using
any enzymes so that the continuity of the layer of cells is
preserved as use of enzymes reduces the adhesion potential
of the cells. Also this method reduces the culture time to 15
days for producing sheet grafts. Currie et al22 have also
reported the use of keratinocyte cell sprays though the
culture time remained at 5 weeks.
Epidermal Allograft Culture
Several centers have used cultured keratinocyte allograft to
treat burn wounds with varying success. The cultured
epidermal allograft can be available at all times and are much
less expensive to produce. However, they undergo rejection
similar to cadaveric homograft. The cells work best as
temporary coverage where a supply of autologous
keratinocytes is available to replace the allograft after
rejection. The concept is that it will prevent the desiccation
of underlying wounds and there is release of unknown
growth stimulating substances by the cells as they die which
will stimulate native wound healing.
SUMMARY
When Rheinwald and Green described the cultivation of
strains of human epidermal keratinocytes with the formation
of colonies of these cells from one single cell, there were
claims by scientists that it had revolutionized the burn care
of the future since it provided quick and easy cover of burn
wounds following excision. Unfortunately this is far from
reality as it is clear that cultured epidermis can in no way
replace the classical autogenous skin grafting. Though it
was thought that autologous keratinocyte culture was a boon
for coverage of an extensively burnt patient but it is not
universally accepted because of many of the imperfections
associated with it, which are mainly unstable wound
coverage, high cost, time consuming and sophisticated
technology. It requires a close co-operation between the
burn surgeons as well as cell culture biologists and all other
personnel involved in patient care. The absence of dermal
component produces frequent disruptions of overlying
epithelium. Therefore, efforts to find suitable dermal
component to be used along with epidermal cells are
underway. Once the limitations of this technology are
overcome by future research, acceptability of the same will
increase manifold. At the same time the concept of tissue
engineering using ‘stem cells’ is being explored and
researched and if successful would have a dramatic impact
on burn wound care and it may even take over the skin
culture in the near future. However, further in depth studies
will only tell about the real clinical potential of the method.
REFERENCES
1. Pickeril HP. On the possibility of establishing skin banks. Br J Plast
Surg 1951;4:157-65.
2. Basset C, Evans V, Earle W. Characteristics and potentials of long
term culture of human skin. Plast Reconstr Surg, 1956;17:421-29.
3. Karaseck MA. Growth and differentiation of transplanted epithelial
cell cultures. J Inves Dermatol 1968;51:247-52.
4. Rheinwald JG, Green H. Serial cultivation of human epidermal
Keratinocytes: The formation of keratinizing colonies from single
cells. Cell 1975;6:331-44.
5. Green H, Kehinde O, Thomas J. Growth of cultured human
epidermal cells into multiple epithelial suitable for grafting. Proc.
Natl. Acad. Sci USA 1979;76:5665-68.
6. O’Connor NE, Mulliken JB, Banks –Sclegel S, et al. Grafting of
burns with cultured epithelium prepared from autologus epidermal
cells. Lancet i, 1981;75.
7. Gallico GG, O’Connor NE, Crompton CC, et al. Permanent coverage
of large burn wounds with autologus cultured human epithelium. N
Engl J. Med 1985; 311:448-51.
8. Cuono C, Langdon R, Mc Guire J. Use of cultured epidermal
autografts and dermal allografts as skin replacement after burn
injury. Lancet I, 1986:1123.
9. DeLuca M, Bondanza S, Canceeda R, Tamisani AM, et al. Permanent
coverage of full thickness burns with autologus cultured epidermis
and re-epithelialization of partial thickness lesions induced by
allogenic cultured epidermis: A multicentre study in the treatment
of children. Burns 1992;88:S16-S19.

240
Principles and Practice of Burn Care
10. Paddle-Ledinek JE, Cruickshank DG, Masterton, JP. Skin
replacement by cultured Keratinocytes grafts: An Australian
experience BURNS 1997;86:204-211.
11. Hefton JM, Caldevell D, Bizoes DG, Balin AK, Carter DM. Grafting
skin ulcers with cultured autologous epidermal cells. J Am Acad-
Dermatol. 1986;14:399-405.
12. Plott RT, Brysk MM, Newton RC, Raimer SS, Rajaraman., S. A
surgical treatment for vitilgo: Autologus cultured epithelial grafts.
J. Dermatol. Surg. Oncol 1989;15:1161-66
13. Lontz W, Olsson MJ, Moellmann G, Lerner AB. Pigment cell
transplantation for treatment of vitiligo: A Progress report. J Am
Acad Dermatol 1994;30:591-97.
14. Green, H. Cultured cells for treatment of diseased. Scient. Amer
1991;11:64-70.
15. Hefemann B. Heltich R, Ennslen S, Kowol B, Zuhlke A, Ebert R,
Konigs M, Kirkpatrick CJ. Treatment of skin defects using
suspensions of in vitro cultured keratinocytes. Burns 1994;20:
168-72.
16. Kamolz LP, Luuehmair M, Wick N et al. The Vietnamese culture
method: cultured human epithelium obtained on a dermal matrix
based on fibroblast containing fibrin glue gels. Burns 2005;31:25-9.
17. Maraguchi T, Maraguchi Y, Suzuki S, Matsuda K et al. A new skin
equivalent: keratinocytes proliferated and differentiated on
collagen sponge containing fibroblast. Plast Recons Surg
1994;93:537-44.
18. Boyce S, Hansbrough J. Biologic attachment, grow and
differentiation of cultured human epidermal keratinocytes on a
graftable collagen and chondroitin-6-sulphats substrate.Surgery
1988;103:421-31.
19. Saintigny G, Bonnard M, Damour O, Collombel C. Reconstruction
of epidermis on a chitosan cross linked collagen –GAG lattice:
effect of fibroblast. Acta Dermatl Venerol 1993;73:175-80.
20. Kaiser HW, Stark GB, Kopp J et al. Cultured autologous
keratinocytes in fibrin glue suspension ,exclusively and combined
with STS –allograft (preliminary clinical and histological report of
a new technique). Burns 1994; 20:23-9.
21. Currie LJ, Sharpe JR, Martin R. The use of fibrin glue in skin grafts
and tissue engineered skin replacements: a review. Plast Reconstr
Surg 2001;108:1713-26.
22. Currie JL, Martin R, Sharpe JD, James SE. A comparison of
keratinocyte cell sprays with and without fibrin glue. Burns
2003;29:677-85.

Burn Wound Infection
241
Burn Wound Infection
20
VK Tiwari, Sujata Sarabahi
Chapter
INTRODUCTION
The management of patients with extensive burns has
improved drastically over the years, greatly improving their
survival rate. Yet microbial infections and resultant
complications are the most important factors in burns
mortality. Extensively burnt patients are immuno-
compromised and far more susceptible to infection than
normal individuals despite the use of systemic and topical
antimicrobials. Burn wounds at the onset are considered
sterile. The amount of heat sufficient to cause damage to
skin kills the microorganisms in and around the burnt area
as well. Colonization by patient’s normal skin flora, i.e.
Staphylococcus aureus and Streptococcus pyogenes occurs
within 48 hours following a burn injury as these organisms
are located deep within the sweat glands and hair follicles
surviving the thermal insult. Subsequent contamination of
wound either by endogenous (gut flora) or by exogenous
sources occurs shortly thereafter, usually within 5-7 days.1-3
Blisters and eschar represent superficial and deep burn
respectively and are part of dead and devitalized tissue and
they are potential sites for colonization and bacterial invasion.
The pattern of bacterial and fungal colonization is related in
part to the topical or systemic antibiotic(s) used for
prophylaxis and treatment of infection and varies with the
area burnt. For example, burns of lower limbs are more
frequently contaminated with enteric flora.
ETIOPATHOGENESIS OF BURN WOUND
INFECTION
Simple colonization of the burned surface does not
necessarily indicate infection but it can be dangerous as it
can be followed by rapid proliferation of bacteria which
eventually invade healthy tissues. Though the bacteria
proliferate at the interface between the burn eschar and the
underlying healthy normal tissues, invasion of latter manifests
only at concentrations of 10 5 organisms/gm of tissue. With
tissue invasion, local arteritis and thrombosis occurs
producing characteristic satellite lesions around the burn
wound. Septic emboli eventually also enter the blood stream
producing abscesses in the liver, kidney and brain. The blood
borne bacterial dissemination can be documented through
positive blood cultures although this is true for gram-positive
bacteria only. The absence of bacteria in blood cultures
with clinical signs of sepsis indicates gram-negative toxemia.
This is due to exotoxins liberated from the primary site of
infection rather than the circulating bacteria per se.4
Older literature emphasized on Streptococcus and
Staphylococcus as the most commonly isolated organisms
in the burn wound. However, the frequency of these
infections were gradually exceeded by gram-negative
infections including those due to Pseudomonas, E. coli,
Klebsiella, Enterobacter, Citrobacter, Proteus and
Bacteroides.5 With increasing use of topical and systemic
antimicrobial agents over the past five decades, the fungal
infection of burn wounds has becoming a growing problem
and even viral infections have also gained significance.
Staphylococcus aureus, especially MRSA (methicillin
resistant) is again emerging as the most common cause of
burn wound infection in many centers at present.6-9
Pseudomonas aeruginosa has been reported to be the second
most frequent agent followed by Acinetobacter, Klebsiella,
etc. One of the most dangerous aspects of post burn infection
by Pseudomonas and Acinetobacter spp. is the multi-drug

242
Principles and Practice of Burn Care
resistance (MDR) of these organisms which is fast becoming
a therapeutic problem. Even the bacteremia caused by gram-
negative organisms is associated with a high mortality in
burn patients.10
The incidence of invasive infection depends on the type
of organisms present in the eschar.11,12 Pseudomonas
produces enzymes and other metabolic products and have
flagella which enhance their potential for invasion and rapid
spread. On the other hand, gram-positive organisms form
different sized micro-abscesses in the eschar and
subcutaneous tissues but rarely invade more deeply. Candida
sp. also rarely invades deeper tissues. On the other hand,
filamentous fungi like Aspergillus are more aggressive
invaders of the subcutaneous tissues.
The most distinct pathologic response in burn wound is
demonstrated in Pseudomonas infection which evolves from
intra-eschar colonization to subeschar invasion. The
diagnosis may be suspected when areas of hemorrhagic
discoloration are seen in and around the burn wound though
the actual infective focus may be hidden by the thick eschar.
On histopathology of necrotic hemorrhagic tissues, it can
be seen invaded by scores of bacilli. The reason for these
lesions is attributed to vasculitis and effects of bacterial
endotoxins. Typical colonization of bacilli seen in the walls
of the blood vessels in case of Pseudomonas infection is far
in excess of what is seen in infection with Proteus and
other gram-negative bacteria.
MICROORGANISMS AND THEIR SOURCES IN
BURN WOUND CONTAMINATION
Microorganisms can contaminate a burn wound from either
endogenous or exogenous sources.
A. Endogenous—Bacterial source is patient’s own body.
1. Patient’s normal skin flora –Streptococcus and
Pseudomonas
2. Upper respiratory tract—Staphylococcus
3. Faecal flora—E. coli and other enteric bacteria.
B. Exogenous can be from:
1. Community acquired infection—This is caused by
Streptococcus and other less virulent bacteria that
are sensitive to first line of antibiotics.
2. Hospital acquired (Nosocomial) Infection— Existing
bacterial flora of ICU/ Ward contaminates the burn
wound. Staphylococcus (MRSA), Pseudomonas,
Acinetobacter and Klebsiella are the common
organisms which are usually resistant to the first
line of antibiotics. The nosocomial transmission of
microorganisms to the burn wound occurs by
transfer from the hands of health care personnel or
through immersion hydrotherapy13,14 or through
contaminated surfaces such as patient’s mattresses,
blankets, etc. In many of the burn units, immersion
hydrotherapy treatment was a standard practice till
the 1990’s. It was found to increase the risk of
nosocomial infections and cross infections among
the burn patients. Thereafter, showering with a hand
held sprayer gradually replaced hydrotherapy tanks
for cleaning and debridement of burn wounds. This
has diminished the risk of transfer of bacteria from
one patient to another.
The various routes for invasion of pathogens into the
wound are as follows:
1. Burn wound: The burn wound with its exudates and
necrotic tissue makes an excellent nutrient medium which
favors growth of microorganisms. Because of the large
surface area involved in major burns, it is constantly
susceptible to contamination by bacteria from the
environment as well as patient’s own endogenous flora
till the healing is complete. Patients suffering from
electrical burns with massive muscle necrosis, which
produces an anaerobic environment, tend to get infected
with Clostridium tetani and Clostridium perfringens and
may manifest the disease frankly. With regular use of
tetanus immunization in the pediatric age group and
following trauma, the incidence of tetanus has now
reduced greatly.
2. Pulmonary: Infection of the lower respiratory tract is
an important cause of death from sepsis in burns. This
is common in patients with inhalational injury, especially
those requiring endotracheal intubation or tracheostomy
and patients who do not receive proper chest
physiotherapy.
3. Indwelling cannulae: Intravenous cannulations and
venesections, if not carried out with proper aseptic and
antiseptic precautions or if performed through the burnt
skin or if kept for a prolonged period of time, may lead
to suppurative thrombophlebitis and multiple abscesses
along the length of the vein. This is an important cause
for sepsis as well as sudden thromboembolic deaths in
burn patients. The superficial cutaneous peripheral veins
of the burned areas represent a strategic route whereby
focal invasion quickly leads to disseminated sepsis.
Therefore, veins cannulated beneath or adjacent to burn
wounds are more readily infected than those from
unburned areas.

Burn Wound Infection
243
4. Urinary tract: Prolonged catheterization, which very
often is unnecessary, can lead to urinary tract infection.
However, prolonged catheterization may be imperative
in children and female patients to prevent soilage of
dressings on thighs and perineum.
5. Gastrointestinal tract: Translocation of bacteria through
the gut is a very frequent occurrence in burn patients
who have not been resuscitated well and are hypovolemic
for a long time after sustaining burns. This is due to the
sustained splanchnic vasoconstriction leading to gut
mucosal erosions and migration of bacteria and their
toxins through the gut wall into the peritoneum. This is
an important cause for sepsis in burn patients.
6. Miscellaneous: Escharotomy incisions, burned areas
which involve cartilage, e.g. the burns of pinna, are
particularly susceptible to infection. Suppurative
chondritis, endocarditis, arthritis also form a focus of
infection in a burn patient which can, in rare cases, lead
to sepsis.
TYPES OF ORGANISMS IN BURN
WOUND CONTAMINATION
Since 1960 till date, Pseudomonas aeruginosa has remained
the commonest organism isolated from the burn wound.
Prevalence of this organism is around 60% in most of the
burn units. Average distribution of different microorganisms
is given in Table 20.1.
TERMINOLOGY USED IN BURN
WOUND INFECTION
There are many terms used while defining different stages
in burn wound infection. They are as follows:
Colonization
Surface culture from burn wound shows presence of
pathogenic organism and count is <105 organisms / gm of
surface tissue. This is also termed as supra-eschar
colonization. This supra-eschar colonization through dead
hair follicles, may invade eschar tissue usually termed as
non-invasive wound infection.
Non-invasive Wound Infection
Infection is limited to eschar and sub-eschar tissues. Bacterial
count in eschar may be >105/gm of tissue. Sub-eschar
infection helps in early eschar separation. In extensive burns
and low resistance individuals this sub-eschar colonization
may lead to invasion of healthy tissues and burn wound
infection.
Burn Wound Infection
Invasion of normal non-burned tissues by microorganisms
is known as burn wound infection. Quantitative bacterial
count is > 105/gm of tissue.
Bacteremia
Presence of viable bacteria in blood is known as bacteremia.
Septicemia
Systemic illness caused by the spread of microbes or their
toxins via the bloodstream is known as septicemia.
Systemic Inflammatory Response
Syndrome (SIRS)
If two of the following four signs are present, the patient is
labeled as having SIRS.
1. Oral temperature is >38 °C or is < 36 °C.
2. Respiratory rate of >20 breaths/minute or PaCO2 < 32
Torr.
3. Heart rate > 90 beats/minute.
4. Total leucocytes count >12000/mm3 or < 400/mm3
Sepsis
SIRS with proven microbial etiology in any patient is termed
as sepsis.
Sepsis Syndrome
Sepsis and one more sign of organ dysfunction like
hypertension, metabolic acidosis, alteration of mental status,
oliguria, ARDS or Platelets count < 0.1 million/mm3.
Multiple Organ Dysfunction Syndrome (MODS)
Dysfunction of more than one organ requiring intervention
to maintain homeostasis like ventilatory support for ARDS
and dialysis for renal failure, etc.
The microbial status of burn wound can be further
classified according to the depth of involvement into:
Stage I is the stage of Colonization—
a. Superficial colonization: Organisms are present only on
the superficial surface

244
Principles and Practice of Burn Care
Table 20.1: Showing the various types of microorganisms isolated from burn wound, their incidence
and sensitivity in the authors’ unit
Type of
Name
%
Source
Antibiotic
Remarks
organisms
Incidence
susceptibility
Gm +ve
Staphylococcus
1 to 2
Community
Amoxicillin and
Present in burn wound of patients
Cocci
MSSA
acquired
Cephalexine
treated at other hospital for 5 to
7 days before coming to burns unit
Staphylococcus
10 to12
Nosocomial
Vancomycin and
Cause of fulminant sepsis in
MRSA
Teicoplanin
extensive burns
Streptococcus
0.5 to1
Endogenous
Crystalline
100% graft failure if present in burn
β Haemolyticus
Penicillin
wound
Streptococcus
0.5 to1
Endogenous
Crystalline
In immunocompromised extensive
Faecalis
Penicillin
burns patient, can cause fulminant
sepsis
Gm. –ve
Pseudomonas
65 to 70
Nosocomial
Beta Lactamase producing
Rapidly develops multi-drug resistance
Bacilli
Aerugenosa
Sensitive to Cefperazone
by efflux pump mechanism
+ Sulbactam and
Piperacillin + Tazobactam.
ESBL Sensitive to
Carbapenems (second
generation)
Klebsciela
10 to 12
Nosocomial
Gr.2 Beta Lactamase and
More likely to cause fulminant
Extended Spectrum Beta
lung infection
Lactamase producing,
Sensitive to Cefperazone +
Sulbactam, Piperacillin +
Tazobactam, Amino
glycosides and
Carbapenems (second
generation)
Proteus
2 to 5
Nosocomial
Gr. 2 Beta lactamase
Usually respond to proper timely
producing, sensitive to
intervention
Amino glycosides,
Cefperazone + Sulbactam,
Piperacillin + Tazobatum,
Carbapenems
Acinetobacter
2 to 5
Nosocomial
ELBS producing, Sensitive
Fulminant pulmonary complication
to Carbapenems (Also
known as Gm –ve bacilli
equal to MRSA)
Fungal
Candida sp.
50 to 60
Endogenous
Azoles, Caspofungin
Mainly in patients on prolonged
infection
antibiotic combinations, TPN, diabetics
b. Microbial penetration: Microorganisms invade the eschar
c. Subeschar proliferation: Microorganisms proliferate in
subeschar space
STAGE II is the stage of invasion of viable tissue—
a. Microinvasion: Microscopic foci of organism in viable
tissue below burn wound
b. Generalized invasion: Diffuse penetration into viable
subcutaneous tissue
c. Microvascular invasion: Organisms invade into burned
blood vessels and lymphatics
IMMUNE PROFILE OF EXTENSIVELY BURNT
PATIENT15-20
The natural resistance of human body to infection in any
kind of wound is primarily a function of the innate immune
system. Following burns, the innate immune system

Burn Wound Infection
245
responds by stimulating localized and systemic inflammatory
reaction. But in extensive burns, patients are usually immuno-
compromised due to:
a. Alteration in the function of neutrophils, lymphocytes
and macrophages.
b. Alteration in Immunoglobulin kinetics.
This results in depression of both cellular and humoral
immunity. As a result, the burn victim gets predisposed to
infectious complications. The host response to thermal injury
is mediated to some extent by arachidonic acid and cytokinin
cascade and the combined effect of this cascade being
release of various endotoxins, like Prostaglandin E2 (PGE),
Thromboxenase, α2-vasoconstrictor, TNF (Tumor
necrosing factor) etc. The alteration in the immune system
has a combined effect of increasing the burn patient’s
exposure to pathogens and decreasing the natural defenses
responsible for counteracting them. Because of impaired
function of the neutrophils, natural killer cells and
macrophages, the body’s immune system is unable to
eradicate the pathogens to which the wounds are exposed.
Thus, burn patients are more susceptible to wound infections,
sepsis and multi-organ failure. Even the reduction of levels
of circulating immunoglobulins like IgG and IgM have been
associated with high burn wound infection rate and mortality.
Briefly, there is a marked diminution of serum IgG
concentration, total and all subclasses. The maximum fall
occurs at 2-3 days after injury when the mean concentration
of IgG, IgA, IgM, IgD and IgE have been shown to be 30,
44, 49, 35 and 22% respectively of the level found in healthy
controls. Their concentration returns to normal level after
19, 9, 7, 30 and 11 days respectively.
CLINICAL FEATURES
Early Diagnosis of Burn Wound Infection (Figs 20.1A to
20.3)
Local Signs of Burn Wound Infection
•
Black or dark brown focal areas of discoloration.
•
Increasing eschars
•
Increase in the depth of burn injury.
•
Increasing inflammation and edema in normal skin
adjacent to burn margin.
•
Increased bleeding from granulation tissue during
dressing.
•
Rashes or papule in skin surrounding burn wound and/
or distant part of body.
Fig. 20.1B: Same patient with hemorrhagic patches with edema of
uninvolved skin indicating patient is landing up in DIC ( Disseminated
intravascular coagulation)
Fig. 20.1A: A 2-year-old child with 20% burns with increasing eschar
indicating increasing depth of burns with increasing inflammation and
edema in normal skin
Fig. 20.1C: Same patient with rashes, papules and erythema in
non-burned extremities indicating invasive gram-negative sepsis

246
Principles and Practice of Burn Care
Systemic Signs of Burn Wound Infection
1. Signs of gram-negative septicemia –Rapid onset of
symptoms within 8-12 hours characterized by
hyperthermia (100-103°F), tachycardia and tachypnea.
Patient is well perfused with bounding pulse. Systolic
blood pressure is initially normal or raised (high output
shock). Pulse pressure is usually varied as vasodilatation
may reduce diastolic pressure to a considerably low limit.
Later on, if sepsis remains untreated systolic pressure
also drops (low output shock). Mental clouding and
diarrhea are sometimes presenting symptoms of burn
wound infection leading to sepsis. Multiorgan failure in
late stage may involve any system causing renal failure,
paralytic ileus, Acute Respiratory Distress Syndrome
(ARDS). Jaundice and disseminated intravascular
coagulation (DIC) are very late manifestations and
usually have very poor prognosis. Decrease in platelet
counts is another diagnostic sign of beginning of sepsis.
2. Signs of gram-positive septicemia—Symptoms are
gradual and usually start with hyperpyrexia (temp.
>105°F) and leucocytosis. Hypotension, paralytic ileus
and oliguria are common with initial gram-positive
septicemia.
The most reliable clinical sign of an invasive burn wound
infection is the conversion of an area of partial thickness
injury to full thickness necrosis (Fig. 20.4). Any change in
wound appearance mandates immediate biopsy of the area
for histopathology and culture sensitivity as wound biopsy
is the only reliable way of differentiating microbial
colonization from invasive infection. Beta hemolytic
streptococcal infection may be manifested by an increase
in erythema at the margins of the burn wound, like in cellulitis,
with inflamed and edematous burn wound (Figs 20.5 and
20.6).
Colonization of burn wound by Pseudomonas is
evidenced by bluish green discoloration of the wound which
is due to pyocyanin or there can be erythematous, violaceous
or necrotic escharified nodular lesions in the unburned skin,
called as Ecthyma gangrenosum (Figs 20.7A to C). When
there is a foul smelling odor with purulent discharge, Proteus
organism should be suspected.
Following excision of a burn wound, if the surface is
left exposed, the wound surface undergoes desiccation
which creates a neoeschar. This should not be mistaken for
infection-related necrosis. Therefore, excised areas should
always be covered immediately either by autograft or
homograft.
Fig. 20.3: Patient in gram-positive sepsis throwing septic emboli
causing bilateral gangrenous changes in distal foot
Fig. 20.2B: Neglected patient showing deepening of burn wound up
to ribcage with exposed pleura
Fig. 20.2A: Synergistic gangrene of abdominal wall following
uncontrolled burn wound infection. The chest wall and abdominal
muscles are totally necrosed which is likely to expose the underlying
structures

Burn Wound Infection
247
Fig. 20.4: Superficial burns converting to deep burns indicating burn
wound infection—Black areas of discoloration, thickening eschar
Fig. 20.5: Streptococcal burn wound infection with extending
erythema into surrounding normal skin from burn wound margin
Fig. 20.6: Another patient with streptococcal erythema involving
unburnt skin of chest and abdomen
Fig. 20.7C: Full blown Pseudomonas invasive sepsis–Hemorrhagic
patches with thickening eschars, increasing soakage from wound
Fig. 20.7A: Greenish discoloration of the dressing and burn wound
surface indicating Pseudomonas colonization of the wound
Fig. 20.7B: Pseudomonas invasion of the same wound indicated by
bluish purple patches appearing in the depth of the burned area

248
Principles and Practice of Burn Care
FUNGAL INFECTION IN BURNS
Although fungal growths were noticed in burn wounds prior
to the use of topical antimicrobial therapy, with their
extensive use for burn dressings, the incidence of fungal
colonization in burn wounds has increased. In fact after the
introduction of Mafenide for burn dressing there was a four
fold increase in the incidence of fungal burn wound
infection.21 This trend continued with incidence of bacterial
infections decreasing over the years till such a period when
fungi represented the most common burn wound infection.22
The fungi most frequently isolated include Candida, Mucor,
Rhizopus, Aspergillus and Alternaria sp.
The fungal involvement of burn wound is classified into
fungal wound colonization (FWC) and fungal wound
infection (FWI).
Fungal wound colonization (FWC) is defined as presence
of fungus in the burn eschar without penetration to the
level of viable tissues. Fungal wound infection (FWI) is
defined as invasion into viable tissue below the eschar.
The fungi can be grouped into 3 categories:
a. Aspergillus like morphology
b. Mucor like morphology (Zygomycosis/ mucormycosis)
c. Yeast like morphology (Candida)
Candida albicans has been reported as the most frequent
pathogenic species causing nosocomial fungal infection in
burn patients with an incidence of 3%6, with mortality
ranging from 38 to 50%.23,24 The incidence of candidiasis
increases as the duration of stay in the hospital increases. It
has been reported from the authors’ unit that the incidence
of candidiasis is 5% in less than 7 days post burn patients
and it increases to 58% in more than 7 days post burn.25
This is attributed to long term use of systemic antibiotics,
central lines, use of total parenteral nutrition,
immunosuppression and ventilatory support.
The earliest gross findings of fungal infection are
hemorrhagic area(s) of discoloration in burn wound. Some
of the fungi especially Mucor and Aspergillus have a
preference for vascular invasion and therefore, produce
widespread ischemic necrosis of soft tissues which may
be so severe as to produce gangrene of an entire limb.
Necrosis and saponification of subeschar fat beneath the
burn wound is also characteristic of fungal infection and
this is seen as a cheesy yellow appearance of subeschar
tissues when the burn wound is debrided (Figs 20.8 and
20.9A to C). Histopathologic examination of wound biopsy
is required for differentiating fungal infection from the other
bacterial infection.
Fig. 20.8: Close up view of Invasive fungal sepsis due to
Aspergillus infection
VIRAL INFECTION IN BURNS
Viral infection in burn patients has not received much
attention in the past but burn wound infection by Herpes–
Varicella viruses and Cytomegalovirus has been reported.26
The reason given for this is the lowered immune status of
the patient which allows the latent viruses to manifest
themselves. The lesions usually occur in the area of healing
second degree burns and present as vesicles and superficial
erosions with secondary bacterial infection. Extensive
cutaneous herpetic infection or varicella zoster (Chicken pox)
infection may develop in some burn patients and the systemic
dissemination to liver, adrenals, respiratory and gastrointestinal
system along with secondary bacterial infection of cutaneous
lesions may be quite fatal (Figs 20.10 A to C). Only biopsy
of an early lesion will manifest signs of infection by Herpes-
Varicella group because rapid colonization by Staphylococcus
and Pseudomonas later can obscure the viral nature of the
lesions. Usually shave biopsy of entire vesicle provides
adequate tissue for diagnosis. Diagnosis can also be
established by measuring neutralizing or complement fixing
antibodies in acute and convalescent phase sera because
viruses cannot be isolated from older lesions.
MANAGEMENT OF BURN WOUND INFECTION
There are three levels of management of burn wound
infection:
a. Prevention of burn wound contamination from exogenous
source (Primary line of management).
b. Prevention of burn wound infection and septicemia in
wounds which are already contaminated by

Burn Wound Infection
249
Fig. 20.9A: A 3-year-old child with fungal sepsis—Wounds are pale,
edematous, nongranulating with exposed subeschar fat
Fig. 20.9B: Same patient’s typical septic look
Fig. 20.9C: Close up of the same invasive fungal wound
Fig. 20.10C: Distribution of lesions on the back in uninvolved skin
Fig. 20.10B: Same patient with vesicular lesions on the face—
Varicella zoster infection
Fig. 20.10A: Typical varicella infective lesions in a healing burned
patient

250
Principles and Practice of Burn Care
microorganisms from exogenous or endogenous sources
(Secondary line of management).
c. Early diagnosis and treatment of infected burn wound
(Tertiary line of management).
Primary Line of Management
(Aseptic Techniques)
The saying, “An Ounce of prevention is better than tons of
cure”, holds true when dealing with burn wound infection.
The principles are same as what we follow and practice in
any surgical discipline for wound care management,
comprising of aseptic and antiseptic techniques.
1. Primary line of management for burn wound starts as
soon as the patient enters the casualty or even earlier at
the site of accident. Wounds are essentially sterile at the
time of burns. Prevention of wound contamination is,
therefore, of utmost importance. The public should be
taught to cover the burn wounds with cleanest sheet
available. In the casualty, the first dressing should not
be done in hospital’s main casualty, unless the hospital
has a separate burns casualty manned by proper trained
staff. If extensive burns are being received in hospitals
main casualty, they should be wrapped in sterile sheet
with sterile McIntosh placed underneath the victim and
transported to burns unit for dressing. Practice of
applying coloring agents like Gentian violet and
Mercurochrome creates problems in burn assessment;
hence, should be discouraged.
2. Dressing stations—The dressing stations are an important
site for transmission of infection from health care
workers to the wound as well as from one patient to
another. During dressing of any extensive burn, there is
heavy contamination of the air inside the room. There
should be a gap of at least 30 minutes between two
dressings. The ideal burn dressing room should have
total exchange of sterile air between two dressings.
Room air can be decontaminated within minutes by the
use of laminar airflow system with bacterial filters and
fixed air aseptisizers. HEPA filter (High efficiency
particulate air filter) fitted laminar airflow rooms,
providing sterile environment, are the ideal dressing
station and patient care cubicles. Plenum ventilated
dressing stations are now replaced by fixed air
aseptisizers to get round the clock sterile environment.
3. Dressing technique — “No Touch Technique” is a must
in treating the burn wound. Burn dressing is a highly
skilled job and should be carried out by the person well
trained in that. Three teams are responsible for change
of one dressing only, which includes doctors, nurses
and dressers. First team which involves a nurse and
dresser is for dressing removal only and is usually known
as “dirty” or “unsterile” nurse. Second team is the main
dressing team who does the sterile dressing work. Third
team is responsible for floor work, known as “floor
nurse”. Once the dressing of one patient is completed,
the entire team changes for next dressing. Minimum of
two to three such teams should be there in a “heavy”
burns unit, where 8 to 10 extensive dressings are being
performed daily. In minimal touch technique instruments
are mainly used for doing dressings, burns wounds are
not at all touched by hands. Priority of dressing should
be for clean, less extensive and pediatric dressings first,
extensive and ‘dirty’ dressings to be done later. All
workers in the dressing room should follow strict
operation theater norms.
4. Invasive procedure like urethral catheterization and
venesections or CVP(central venous pressure ) cannula
insertion is often found to be major source of
septicemia. Ideally peripheral cannulae should be
changed every three days. Prolonged use of catheters
and long lines require proper maintenance for avoiding
major source of infection, especially infective deep vein
thrombosis which often is the triggering point of burn
septicemia.
5. Prevention of infection in Burn ICU—Extensive burns
patient require isolation as well as maximum nursing
care and monitoring in a burn ICU. Barrier nursing,
patient isolation and environmental sterilization are few
methods to prevent cross infection. All health care
personnel should be appropriately gowned and gloved
at each entry into the patient’s room. Simple hand wash
during ward rounds, before and after seeing the burn
patient is the simplest way to prevent cross
contamination. Bacillocid spray 30 minutes before
receiving the patient is equally effective and less toxic
than fumigation. All equipment in each patient’s room
should be regularly cleaned with appropriate
disinfectants.
6. Culture of environment of burn ward, burn ICU and all
other burn stations by exposing culture disc for 15
minutes and culture from beds, monitors and other
equipments is done every 3 weeks . If found positive
their remedial process is very important aspect of burn

Burn Wound Infection
251
wound prevention. Formalin fumigation and
carbolization of bed and equipment have largely been
replaced by modern environment friendly safe procedures
like Bacillocid spray of walls and equipments. Ultraviolet
light can be installed to reduce bacterial count in vacant
areas (without patient). Usually a combination of the
following procedures is used to minimize environment
and fomite contamination.
Procedures that predispose the patient to cross–
contamination, such as hydrotherapy tanks, are kept to a
minimum. Cohort nursing care is another component of
environmental control in a burn unit. Nurses and other health
workers are assigned to work as a team for one specific
patient or a group of patients and the movement between
patients is strictly limited. Patients convalescing are kept
separate from the acute patients since they form a reservoir
of more antibiotic resistant organisms which are acquired
during their hospital stay. Thus, after the ICU, there is a
step down ICU where the patient is shifted after he/she is
fully resuscitated and stabilized and thereafter, there should
be a chronic ward where patients are prepared for skin
grafting of the raw areas.
a. Physical
1. Laminar-air flow system with HEPA filters (high
efficiency particulate air filters).
2. Fixed or mobile air aseptisizer (Fig. 20.11)
3. UV light exposures
b. Chemical
1. Formalin fumigation, carbolisation, bacillocid spray.
Secondary Line of Burn Wound Management
(Antiseptic Methods)
A. Prophylactic antibiotics
B. Local chemotherapeutic agents
C. Biological dressings
D. Early wound closure
E. Immunotherapy
Prophylactic antibiotics: Role of prophylactic antibiotics in
burns is debatable. Healthy adults up to 30% burns may not
require any prophylactic antibiotic. Extensive burn patients
are usually immunocompromised and may require
prophylactic antibiotics. A diabetic burn patient and the one
coming late to a burn center from far-flung areas with open
wounds have fair chances of wound contamination and
invasion. Prophylactic first line of antibiotics has a definite
role in such types of community acquired infection.
Crystalline penicillin in combination with an aminoglycoside
usually takes care of community acquired infections and
Clostridium tetani as well, if patient is not previously
immunized for tetanus.
Local chemotherapeutic agents: 1% Silver sulfadiazine
cream for extensive burns usually takes care of surface
contaminants or endogenous contamination from hair
follicles with painless acceptable eschar penetration and
minimal toxicity. Therefore, it is the ideal topical antimicrobial
cream for extensive burns.
Biological dressings: Collagen dressings and other biological
dressings seal the wound from external environment and
thereby reduce the chances of wound contamination.
Excision of deep dermal and full thickness burns with
immediate skin grafting reduces the morbidity. Elimination
of the necrotic tissues and raw areas, in turn, reduces the
chances of infection and septicemia.
Immunoprophylaxis: Apart from active and passive tetanus
prophylaxis many other vaccines are available for gram-
negative and gram-positive bacteria. Their efficacy is
debatable. However, there is a definite role of
immunoglobulins in prevention and management of burn
wound infection and septicemia. The availability of much
refined preparations of immunoglobulins and widespread
increase in prevalence of multi-drug resistant bacteria has
brought immunoglobulins to the forefront during the last
decade. The role of intravenous gamma globulin factor in
burn patients has been studied extensively in the past.17,18
Recently, the use of IgM enriched immunoglobulins to
Fig. 20.11: Fixed air aseptisizer at the entrance of Burns ICU and
wards to reduce bacterial count

252
Principles and Practice of Burn Care
enhance the humoral response has emerged as a valuable
tool in the management of burn patients with infection.
Experimental in vitro and animal studies on IgM enriched
immunoglobulins have demonstrated that elevated titre of
anti-endotoxin antibodies correlate significantly with
decreased mortality due to gram-negative sepsis. Besides
neutralizing antigen, IgM enriched immunoglobulin also
activate compliment factor like opsonins. To enhance
immune response against bacteria, IgM immunoglobulin has
been shown to have a synergistic action with beta-lactam
antibiotics as well as a beneficial immunomodulating
effect.19,20
Tertiary Line of Management of Burn
Wound Infection
Early Diagnosis and Treatment
(Figs 20.12A to N)
Early diagnosis of burn wound infection and septicemia
and specific treatment for the same is the key for decreasing
mortality in extensive burns. Going by the definition of
SIRS(systemic inflammatory response syndrome), almost
all extensive burn patients are in SIRS. They have to be
regularly observed for signs of septic syndrome. Patients
with diabetes or other immunocompromised conditions are
more likely to land in septic complications. Following local
signs and symptoms, if present, are the starting point for
invasive infection:
1. Unexplained pain or discomfort in burn wound
2. Excessive soakage
3. Unexplained fever
4. Inflamed burn wound margins are the starting point of
wound infection. In facial burns especially if ears are
involved, increased cephaloconchal angle is the first sign
of inflammation.
5. Gastrointestinal symptoms in the form of loose motions
and or abdominal distension
6. Abnormal behavior, intermittent irrelevant talks and
oliguria despite adequate perfusion are sometimes the
presenting features of sepsis.
Investigations
Investigations along with these preliminary signs and
symptoms help in diagnosing the specific organism invading
the burn wound.
1. Leukocyte count and platelet count –Importance of total
leukocyte count in relation to infection is well
documented. Leucocytosis in early sepsis and leucopenia
in late sepsis is often diagnostic. Persistently decreasing
platelet count is often the first sign of impending septic
syndrome in extensive burns.
2. Invasive burn wound infection usually starts after the
5th post burn day in extensive burns. Initial surface
culture report, if available, is the best guide for the type
of organism and its antibiotic sensitivity.
3. Blood culture is usually non-informative as 75% cases
are in gram-negative septicemia in which only the toxins
are present in blood. In gram-positive septicemia blood
culture report is usually more informative.
4. Wound biopsies –Quantitative wound analysis is helpful
in some cases not responding to treatment as bacterial
counts more than 105 organisms/gm of tissue demand
for a multipronged approach for burn sepsis. Serial
biopsies are essential to follow the progress of infection.
Any change from stage Ia to stage Ic (as mentioned
earlier) demands immediate change in wound care
management. If stage II is diagnosed, excision of the
eschar and underlying infected tissues should be carried
out as soon as possible. If gram-negative invasion is
present, the topical antimicrobial agent being used is
stopped and mafenide cream should be used till excision
is performed. Wound biopsy is also indicated for fungal
infection, usually superimposed, once bacterial infection
is being successfully treated with advanced antibiotics.
Treatment
Depending on extent of body surface area burnt, the type
of infecting organism and the general condition of the host,
the treatment should be planned against the infecting
microorganism using
a. Local and systemic antimicrobial agents
b. Increasing the host resistance to infection by using
Immunoglobulin
c. Enteral and parenteral nutrition including albumin and
blood transfusions
d. Controlling concomitant diseases like diabetes,
hypertension, etc.
Local Wound Dressings
Early burn wound infection requires change of antimicrobial
agent to the one which is effective against the suspected
organism(s). Unfortunately, very few agents are available
for use in extensive burns with good eschar penetration. If
1% silver sulfadiazine (SSD) cream is being used and
subsequently Pseudomonas infection is suspected, change

Burn Wound Infection
253
Fig. 20.12F: Patient managed with change of local antimicrobial from
SSD to mafenide and third line of systemic antibiotic—Carbapenems
with aminoglycoside
Fig. 20.12E: Nodulopapular lesions in adjacent unburned skin over the
abdomen and chest with edema of the skin with distension abdomen
Fig. 20.12D: Infective gangrenous changes in thumb indicating
septic embolization
Fig. 20.12A: Patient with invasive gram-negative burn wound
sepsis—Hemorrhagic discoloration of entire eschar
Fig. 20.12B: Close up view of same wounds
Fig. 20.12C: Typical nodular satellite lesions in uninvolved skin—
Ecthyma gangrenosum

254
Principles and Practice of Burn Care
Fig. 20.12L: Successfully grafted back of same patient
Fig. 20.12K: Same wounds grafted in stages on lower limbs—
Full graft uptake
Fig. 20.12G: Improving wounds—Eschar penetrated by mafenide to
reach subeschar tissue,tissue edema reduced and general condition
improved
Fig. 20.12H: Ecthyma gangrenosum reduced
Fig. 20.12I: Satellite nodules drying up
Fig. 20.12J: Healthy granulating wound after 10 days of
change in treatment

Burn Wound Infection
255
Fig. 20.12M: One month postoperative picture of
the back of same patient
Fig. 20.12N: Legs of the same patient
over to 11.1% mafenide cream is advised (Figs 20.13A
to C). This should be applied twice a day. If MRSA
(methicillin resistant Staph. aureus) is the causative agent,
silver ion is more effective and a thick coating of SSD is to
be applied and dressing needs to be changed every 8 hours.
Systemic Antibiotics
In stage IIc, hematogenous and lymphatic dissemination
demands systemic antibiotic therapy. Ideally systemic
antibiotics should have been started much earlier so as to
prevent progression to this stage which may ultimately lead
to multi-organ failure.
Fig. 20.13B: Same patient with wounds showing improvement
Fig. 20.13A: Superficial burns converted to deep burns by
Pseudomonas infection which was controlled timely by systemic
antibiotics and change of local antimicrobial agent
Fig. 20.13C: Finally grafted wounds of same patient–2 months
postoperative picture

256
Principles and Practice of Burn Care
Appropriate systemic antibiotics should be started
depending on the culture sensitivity report. If however, the
sensitivity report is not available, empirical antibiotic therapy
has to be started as per the ward antibiogram. Every burn
unit should formulate its own antibiotic policy according to
which the treatment can be started. In the authors’ unit, it
is a standard practice to use Cefoperazone + Sulbactam or
Piperacillin + Tazobactam and Amikacin for beta lactamase
producing Pseudomonas and Klebsiella and vancomycin for
MRSA. Extended spectrum beta lactamases (metalloenzyme)
producing Pseudomonas and Klebsiella require second
generation Carbapenems i.e. Imipenem + Cilastin or
Meropenem along with Aminoglycosides.
It is important to diagnose the type of fungal infection
accurately because no antifungal provides optimal coverage
for all fungi. Because of this varying spectrum of activity
of each antifungal agent it is important to identify the
infecting fungi accurately, often down to the species level.
Intravenous Amphotericin B still has the broadest antifungal
spectrum especially Candida and Aspergillus sp. The older
azole agents, fluconazole and Itraconazole cover most
Candida species but have limited action against moulds.
The newer broad spectrum azole, voriconazole has improved
mould coverage as well as Fusarium and P. boydii but no
action against Zygomycetes. The newer agents like
Caspofungin, micafungin and Echinocandin have good
action against Candida and Aspergillus but do not cover
Zygomycetes, moulds and Cryptococcus.
Antimicrobial resistance—There is a worldwide emergence
of antimicrobial resistance amongst the majority of human
bacterial and fungal burn wound pathogens which makes
the therapeutic options limited for effective treatment of
burn wound infection.27,28 MRSA and Methicillin resistant
coagulase negative Staphylococcus, vancomycin resistant
enterococci and multiple resistant gram-negative bacteria
which have several types of beta lactamases including ESBL,
amp-C beta lactamases and metallobeta lactamases are
emerging as serious pathogens in hospitalized burn
patients.27-29 The risk factors for acquisition of antibiotic–
resistant organisms include treatment with antibiotics prior
to the development of infection, prolonged hospital stay,
previous hospitalization, invasive procedures and advancing
age. The antibiotic utilization should be rotated or changed
on a regular basis as per the changing antibiotic resistance
and sensitivity patterns.
Even fungi especially Candida sp. has become an
important opportunistic pathogen due to widespread
inappropriate use of broad spectrum topical and systemic
antibacterial agents in burn patients and are now showing
increasing degree of antifungal drug resistance.30,31
Strict infection control practices and appropriate
empirical antimicrobial therapy is essential for reducing
incidence of infection by these resistant organisms.
The use of subeschar clysis32 with a broad spectrum
antipseudomonal agent has also been recommended with
no. 20 spinal needle (half of the dose mixed in 1000 cc
saline) to fight the infection locally. This can be repeated
just before excision to reduce intraoperative dissemination
of viable bacteria and toxins.
Burn Unit Antibiogram
All burn units should routinely determine the specific pattern
of burn wound microbial colonization and the changes in
the microbial flora with time and the susceptibility profiles
of the organisms. This information can be obtained by
periodic sampling of burn wounds and other anatomic sites
and with a proper liaison between the treating clinician and
the microbiologist, a yearly antibiogram data can be analyzed
periodically. This can then help in selecting and administering
appropriate empirical systemic antibiotic, at the slightest
sign of sepsis, even before the microbiological culture and
sensitivity report is available. This saves precious time
required to control invasive infection.
Surgical Treatment of Infected Burn Wound
The excision of infected wound should be done under
general anesthesia, with a scalpel and all tissues above deep
fascia should be excised. In case there is involvement of
fascia or subfascial tissues, they also need to be excised. If
it is definite that all the infected tissue has been excised, the
resulting wounds should be split skin grafted or covered
with skin substitute or biological dressing. However, if there
is any doubt regarding the depth of excision, the wounds
should be dressed with gauze soaked in 5% mafenide or
0.5% silver nitrate solution. The wounds should be
reexamined 24-48 hours later for further excision.
Fungal infection (Figs 20.14A to E): Candida infected burn
wounds do not require surgical excision as they rarely invade
healthy tissue. For these cases dressing with topical
antifungal agent such as Clotrimazole cream is usually
effective. If infection is not controlled with the above
treatment and involves more tissues locally, excision may

Burn Wound Infection
257
Fig. 20.14E: Same patients upper limb healed with skin
graft in two weeks
Fig. 20.14A: Fungal infected wounds on lower limb—Patient started
on systemic antifungal agents and local clotrimazole cream dressing
Fig. 20.14B: Same patient’s wounds on upper limb
Fig. 20.14C: The wounds improved with local dressing with
systemic treatment and prepared for grafting
Fig. 20.14D: Raw areas successfully grafted on lower limb –2
weeks postoperative picture
be necessary. Invasion of the wound is usually seen in
filamentous fungi as previously stated, the most aggressive
being Phycomycetes followed by Aspergillus sp. and merits
a complete excision of the infected wound followed by twice
daily application of topical Clotrimazole cream. Extensive
involvement or systemic invasion requires systemic
Amphotericin B or other antifungal agents as per sensitivity
pattern. In some of these cases if muscles are also involved,
an amputation of the limbs may be necessary.
Viral infection26: If a patient has unexplained hypotension
or other signs of systemic sepsis with no other source and
rapidly spreading cutaneous herpetic lesions, the possibility
of systemic herpes simplex virus should be entertained and
Acyclovir therapy should be instituted.

258
Principles and Practice of Burn Care
BURN WOUND IMPETIGO
It is characterized by multiple small superficial abscesses,
the causative organism being Staphylococcus. If not
controlled in time, it can cause extensive destruction of
grafted areas or even healed partial thickness burns and
donor areas (Figs 20.15A and B). Treatment for this
condition involves de-roofing of all abscesses and application
of topical antibacterial ointments like Mupirocin (T-bact®,
Bactroban®) or Fusidic acid (Fucidin®) twice a day.
Vancomycin is required if there is a disproportionate systemic
response to this infection.
time with an impairment of host defenses due to burn injury.
The incidence of catheter associated infections has been
found to be inversely proportional to the distance of the line
insertion site from the burn wound. Catheter infections in
burn patients usually arise from the adherence and migration
of burn wound flora microorganisms along the catheter
surface to the tip.6,33 Though peripheral and central venous
catheters should ideally be inserted through normal skin,
this may not be possible in case of extensive burns. At times,
it may be necessary to cut down into a vein through the
burn wound itself if other veins have been exhausted in a
patient with extensive burns. All veins which have been
cannulated have to be examined. Usually there is a red streak
seen along the length of infected vein with tenderness
indicating thrombophlebitis. If the vein is incised and there
is a brisk flow of blood from proximal segment this condition
can be excluded as the cause for sepsis. But if there is pus
in the vein, culture of the pus should be taken and the entire
involved vein till the point where it is grossly normal should
be excised completely. Systemic antibiotics are also essential
at the same time. To avoid this condition, the I/V site should
be changed every 3 days.
TETANUS IN BURNS
Despite the widespread use of tetanus toxoid which is till
date the most effective vaccine, tetanus is still a problem in
most developing countries. The actual incidence of tetanus
associated with burn injury is not reported in Indian literature,
although American literature has quoted an incidence of 2-
6.6%.34,35 Since tetanus prophylaxis is an integral part of
management of all patients with burns, the incidence of
tetanus in patients admitted with thermal burns is very rare.
In the author’s unit, tetanus is noticed mostly in electric
burn patients and patients who are referred late from other
units not receiving proper tetanus prophylaxis.
In addition to tetanus, gas gangrene and mixed clostridial
infections are also seen in burn patients especially with full
thickness burns or electric burns with extensive muscle
necrosis which is a suitable environment for anaerobic
organisms.
Tetanus Prophylaxis
For burn patients who have history of being previously
immunized by basic immunization series plus a booster dose,
0.5 ml of tetanus toxoid (TT) given I/M at initial treatment
of burn is usually adequate prophylaxis. In case, interval
from last booster dose is more than 10 years or if there is a
delay from time of burning to treatment, 500 units of Human
Fig. 20.15B: Same patients grafted chest showing graft eaten up by
Staphylococcus—Required change of local antimicrobial agent to
mupirocin and systemic antibiotics with antistaphylococcal action
Fig. 20.15A: Staphylococcal infection postgrafting—Typical eaten
up appearance of graft applied on hands and arm
SUPPURATIVE THROMBOPHLEBITIS
(FIGS 20.16 AND 20.17)
Very often, thrombophlebitis is a cause for septicemia in
burn patients as these patients require intravenous (I/V) fluids
and frequent parenteral hyper alimentation fluids for a long

Burn Wound Infection
259
tetanus globulin should be given I/M in addition to tetanus
toxoid with a different syringe at a different site. Patients
who have not received basic immunization as per schedule
should receive initial 0.5 ml tetanus toxoid at time of burns
followed by 2 injections of 0.5 ml TT at 4 weeks interval
and then a booster dose at 6 months to 1 year after the last
injection. In addition to this schedule, 500 units of human
tetanus immunoglobulin should be also given I/M with a
different syringe at a different site.
Tetanus organisms are sensitive in vitro to penicillin
and tetracycline. Earlier when the incidence of tetanus used
to be high, routine antibiotic prophylaxis for tetanus was
given in the form of crystalline penicillin for the first 7 days
following burns. This was, supposedly, to give protection
against tetanus till active immunity by tetanus toxoid takes
over which is usually from 7-10 days. Topical therapy
with mafenide also gives protection against Clostridial
infection.
Treatment of Tetanus in Burns
There are 3 stages of tetanus–first stage is the ‘focus of
infection’ stage, wherein there is deposition of Clostridial
tetani in the burn wound. This infection is well localized as
the organism does not have strong invasive powers. During
this stage only local wound care is sufficient, failing which
the second stage sets in. This is the stage where the organism
releases highly diffusible neurotoxin into the body fluids.
Treatment during this stage is by neutralization of the toxin
with tetanus antitoxin which may be present in the body
from active immunization or should be administered
passively. If this stage is not controlled in time, the third
stage or neurological stage sets in wherein the toxin fixes to
the neuromotor cells in the central nervous system. At this
stage the antitoxin has no effect on the tetanus neurotoxin.
The neurological or clinical tetanus is diagnosed on
clinical signs and symptoms and can be mild, severe or
fulminating depending upon the amount of toxin combined
with the nervous system cells. Tetanus typically begins with
increase in tone of various muscle groups especially spasm
of masseter muscle leading to difficulty in opening mouth
or clenching of teeth with a fixed smile called ‘ risus
sardonicus’. The patient is irritable and complains of inability
to swallow, i.e. dysphagia. As the disease progresses there
will be stiffness of neck, back and abdominal muscles.
Violent contractions of muscles or tetanospasms produce
opisthotonus, abdominal rigidity and extension of extremities
and these can be initiated with the slightest stimulus. These
can even lead to difficulty in respiration which may manifest
with hypoxia, cyanosis and even sudden death.
Fig. 20.16A: Deep vein thrombosis in a patient on prolonged central
venous line in left lower limb showing gross edema of lower limb and
color Doppler showed thrombous extending in popliteal V, femoral
vein till external iliac V
Fig. 20.17: Septic thrombophlebitis all along the length of the great
saphenous vein with abscesses presenting superficially at multiple
sites with overlying skin necrosis—Required drainage of pus with
excision of the entire length of vein
Fig. 20.16B: Grossly edematous left thigh of same patient

260
Principles and Practice of Burn Care
Treatment of established tetanus involves the following
steps:
1
Neutralization of circulating toxin by administering 3000
units (1500-10,000 U) of human tetanus immunoglobulin
once only at different sites deep intramuscular.
2. Removal of source of toxin, by excision of presumed
site of entry which is the burn wound, is possible only
in small burns. Excision of major burns for treating
tetanus is not recommended.
3. Antibiotics in the form of Penicillin or Tetracycline also
help in eliminating tetanus organisms.
4. Sedation to control tetanic spasms in the form of
diazepam is useful though toxic doses should be avoided.
5. Maintenance of respiration – All patients with tetanus
should undergo tracheostomy and ventilator should be
kept ready, if needed.
6. Supporting care: Fluid electrolyte balance, renal function,
ventilation, nutrition and prophylaxis for pulmonary and
urinary tract infections have to be looked into as well.
REFERENCES
1. LeVoyer T, WG Cioffi Jr. Pruitt L, Shipper R, Mc Manus WF,
Mason AD Jr, Pruitt BA Jr. Alterations in intestinal permeability
after thermal injury, Arch Surg 1992;127:26-29.
2. Manson WL, Klasen HJ, Saver EW, Olieman A. Selective intestinal
decontamination for prevention of wound colonization in severely
burned patients: a retrospective analysis. Burns 1992;18:98-102.
3. Ryan CM, Bailey SH, Carter EA, Schoenfeld DA, Tompkins RG.
Additive effects of thermal injury and infection on gut permeability.
Arch Surg 1994;129:325-328.
4. Teplitz C. Pathology of burns and the fundamentals of burn wound
sepsis. In CP Artz; JA Moncreif; BA. Pruitt (Eds). Burns: A team
approach. Philadelphia. WB Saunders, 1979, 69.
5. Mac Millan BG, Local care and infection in burns, J. of Trauma,
1965;5:292-306.
6. Santucci SG, Gobara S, Santos CR, Fontana CA, Levin AS. Infections
in a burn intensive care unit: Experience of 7 years. Journal of
hospital infections 2003;53:6-13.
7. Taylor GD, Kibsey P, Kirkland T, Burroughs E, Tredget E.
Predominance of staphylococcal organisms in infection occurring
in a burns ICU. Burns 1992;18:332-335.
8. Gang RK, Sanyal SC, Bang RL, Mokaddas E, Lari AR. Staphylococcus
septicemia in burns. Burns 2000;26:359-366.
9. Wisplinghoff H, Perbix W, Seifert H. Risk factors for nosocomial
bloodstream infection due to Acinetobacter baumanni: a case
control study of adult burns patients. Clin. Infect Dis. 1999;28:
59-66.
10. Mason AD Jr, McManus AT, Pruitt BA Jr. Association of burn
mortality and bacteremia. Arch Surg 1986,121: 1027-32.
11. Pruitt BA Jr. Infections of burns and other wounds caused by
Pseudomonas aeruginosa. In: Doggett RG, editor. Pseudomonas
aeruginosa. New York: Academic, 1979: 339-66.
12. Pruitt BA Jr., Mc Manus AT. The changing epidemiology of
infections in burn patients. World J Surg. 1992 ; 16: 57-67.
13. Cardamy CR, Rodeheaver GT, Horowitz, Kenny JG and RF Edlich.
Influence of hydrotherapy and antiseptic agents on burn wound
bacterial contamination. J Burn care Rehabilitation 1985;6:230-
32.
14. Mayhall CG. The epidemiology of burn wound infections: then and
now. Clin. Infec Dis 2003;37:543-50.
15. Arturson G, Hogman CF, Johansson SGO, Killander J. Changes in
immunoglobulin level in severely burned patients. Lancet
1969;1:546-48.
16. Munster AM, Hoacland HC, Pruitt BA Jr. The effect of thermal
injury on serum immunoglobulin. Ann Surg 1971; 172: 965-69.
17. Dominioni L, Dionigi R, Zanello M, Chiaranda M, et al. Effect of
high dose IgG on survival of surgical patients with sepsis score of
20 or greater. Arch Surg 1991; 126: 236-40.
18. Rodriguez A, Rello J, Neira J, Maskin B, et al. Effect of high dose of
I/V immunoglobulin and antibiotics on survival for severe sepsis
undergoing surgery. SHOCK 2005; 23 (4): 298-304.
19. Stephen W, Dichtelmuller H, Schedel I. Properties and efficacy of
a human Ig M preparation for Intravenous administration. Arzneim
Forsch/Drug Res 1985;35(1):933-36.
20. Balikcioglu S, Schedel I, Berger D. Rationale of anti-endotoxin
therapy of sepsis and septic shock with polyclonal immunoglobulin.
Third International Congress on the immunomechanics and
therapeutic approaches; 2-5 March; 1995; vol 20. Munich edited
by: Eugeu Fairst, Artheu EB, Lambert T.
21. Nash G, Foley FD, Goodwin MN, Bruck HM, Greenwald KA, Pruitt
Jr BA. Fungal burn wound infection. JAMA 1971; 215: 1664-6.
22. Becker WK, Cioffi WG, McManus AT, et al. fungal burn wound
infection. Arch Surg, 1991; 126: 44-48.
23. Robert F, Lebreton F, Bougnoux ME, Pangam A, Wasserman D,
et al . Use of random amplified polymorphic DNA as a typing
method for .albicans in epidemiological surveillance of a burn unit.
J. Clin Microbiol 1995: 33, 2369-71.
24. Mac Millan BG. The control of burn wound sepsis. Intensive care
med 1981;7:63-69.
25. Gupta N, Haque A, Latiff AA, Narayan RP, Mukhopadhyay G,
Prasad R. Epidemiology and molecular typing of Candida isolates
from burn patients. Mycopathologia 2004;158:397-405.
26. Foley FD, Greenwald KA, Nash G, Pruitt BA Jr. Herpes virus
infection in burned patients. New England J of medicine
1970;282:652.
27. Clark Nm, Patterson J, Lynch JP. Antimicrobial resistance among
gram negative organism in the ICU. Curr. Opin. Crit Care
2003;9:413-23.
28. Heggars JP, McCoy L, Reisner B, Smith M, Edgar P, Ramirez RJ.
Alternate microbial therapy for vancomycin resistant enterococci
burn wound infections. J Burn Care Rehabilit 1998;19:399-403.
29. Embil JM, McLeod JA, Al- Barrak AM, Thompson GM, Aoki FY,
et al . An outbreak of MRSA on a burn unit: potential role of
contaminated hydrotherapy equipment, Burns 2001;27:681-688.
30. Mac Manus WG, Mason AD Jr. Subeschar antibiotic infusion in the
treatment of burn wound infection. J Trauma 1980;20:1021.
31. Baddley JW and Moser SA. Emerging fungal resistance. Clin. Lab
Med 2004;24:721-735,vii
32. Mousa HA, AL –Bader SM. Yeast infection in burns. Mycoses
2001;44:147-49.
33. Ramose GE, Bolgiani AN, Patino O, et al. Catheter infection risk
related to the distance between insertion site and burned area. J .Burn
Care Rehabil 2002;23:266-71.
34. Altemeier WA, Culbertson WR, Gonzalez LL. Clinical experiences
in the treatment of tetanus. Arch Surg 1960; 80:977.
35. Christensen NA, Thurber DL. Clinical experience with tetanus: 91
case. Proc Mayo Clin, 1957;32:146.

Electrical Burns
261

(Trang không có chữ)

Electrical Burns
21
SP Bajaj
Chapter
INTRODUCTION
Electricity is known to mankind since time immemorial.
Thales of Miletus in 6th century BC wrote that rubbing fur
on amber would cause attraction between the two
substances. This is probably what we understand as static
electricity today. The word ‘electricity’ is derived from Latin
“electricus”, meaning amber-like.
Luigi Galvani (1781) demonstrated that electricity was
the medium by which nerve cells pass signals. In 1821,
Michael Faraday invented the electric motor. Commercial
use of electricity became possible only in mid-eighteenth
century. Electricity is probably the most dangerous
commodity which we use everyday and in every moment
of our lives. Development of electricity drastically affected
social thinking. During the age of mechanization, there was
an emphasis on splitting the work into many sections and
then creating a sequence of completing each section
separately. With the development of electricity there was
emphasis on work being done in “totality, simultaneously
and instantly.”
EPIDEMIOLOGY
With the widespread use of electricity its dangers also started
showing its effects. First recorded death from an electric
current was in Lyons, France in 1879, where electricity
was used to lighten a stage for opera. In US, Samuel Smith
was the first person who died from electrocution from a
generator in 1881 in Buffalo, New York.1
With the continued growth of the electrical industry,
there was a simultaneous rise in number of electrical injuries
and deaths. Today in US 0.8 to 1% accidental deaths2 are
caused by electricity. Electricity causes around 1000 deaths
each year in industrial workers.3 Between 1992 and 1998,
2287 people died from electricity at their place of work.
32807 people sustained different degrees of burns and burn
shock, keeping them away from work. In US, roughly one
person dies everyday at his place of work by an electrical
injury and over 13 days of work are lost per electrical injury.
No such detailed data is available from Europe, Indian sub-
continent, Africa or Asia.
All over the world, electrical injuries are the second most
important cause for admission to a burns unit. The
percentage varies from 6% in US to 20% at many Asian
and African burns units. 40% of these patient’s with serious
electrical injuries die.4,5 There are two age groups which
are frequently involved in electrical injuries. The first is that
of children less than 6 years age who have a high incidence
of oral electrical burns because of oral contact with electric
cords or when they come in contact with electric poles or
wires while playing. The incidence decreases in teenage
years and then increases in adults as they start working.6,7
Approximately one third of electrical injuries involve electrical
workers and one third affect construction workers. Male
to female ratio in childhood electrical injuries ranges from
1:1 to 2:1 with male predominance. Amongst adults, 93%
of the victims are men.
Electrical burns are often regarded as equivalent to
thermal burns, as electrical energy is converted to thermal
energy when it comes in contact with the body. However,
many effects of electricity on the human body are other
than that of heat. For its complete understanding, some
basic knowledge of electrical physics is essential.

264
Principles and Practice of Burn Care
PHYSICS OF ELECTRICITY8,9
Electric Current
Electron, Proton and Charge: Movement of electric charge
is known as electric current. Charge on electron and proton
is same and is expressed as negative or positive. This concept
of negative and positive charge was given by Benjamin
Franklin. Symbol “Q” is used to express the amount of
charge and is expressed in Coulombs. Each electron or proton
has a charge of 1.602 × 10-19 coulombs. Electron is
negatively charged while proton is positively charged.
Unit of Current
Ampere: Passage of electrons at a given point in one second
is expressed in amperes. When 6.242 × 1015 electrons are
passed from a given point in one second, it is called passing
of 1 ampere of current.
Voltage
In all conductors electron move in a random fashion until
driving forces (electromotive force) are applied to them.
This is expressed in Volts. A large volt exerts a large force
which makes electron to move in a short period thus more
current to flow in a short period. Thus, in all transmission
cables high voltage is used. More the voltage less is the
safety to the human body. High voltage is also used to move
electric train and underground metro. In UK and some
European countries this is 11,000 volts. In India, it is 25,000
volts. House-hold current in American sub-continent is
supplied at 110-120 volts. In Indian sub-continent, Europe,
Australia and most of Africa it is 210-220 volts.
Resistance
All substances have some resistance to the flow of current.
Substances which have low resistance are called good
conductors while substances with high resistance are called
bad conductors. In a substance which is a bad conductor
electrons are fixed and have hardly any movement while in
a good conductor electrons are loosely placed. Substances
which have no resistance are called super conductors. Human
skin provides high resistance which may be as high as one
million ohm/cm2. Resistance in human skin decreases in
summer because of sweating. It is less whenever it is wet.
Resistance is also low in children and at extremes of age
because of thinness of skin epidermis. In the skin, dermis
has lesser resistance as compared to epidermis. Resistance
is also related to the circumference. Thus, chest and
abdomen with greater circumferences provide lesser
resistance while a finger with lesser circumference provides
greater resistance. Similarly, current flow in the large vessels
with bigger circumference provides less resistance while
smaller vessels provide more resistance and hence are more
likely to get thrombosed.
Further, current density increases in smaller vessels while
it is reduced in larger structures. Current density has further
effect in the human body. With arteries having rapidly moving
blood, current density at any given point and at any given
time becomes less because of flow of blood. While current
density is more in the veins because of slower flow of blood.
Therefore, thrombosis and stoppage of blood flow is high
in veins and comparatively less in arteries.
Ohm’s Law
There is a definite relationship between flow of current
(ampere), force of current flow (voltage) and resistance to
flow (ohm). This relationship was best described by Ohm
and is called Ohm’s law. Ohm’s law states
Current (I) = Voltage (E)/Resistance (R)
It means current is directly proportional to voltage and
inversely proportional to resistance, more the voltage more
the current, more the resistance less is the flow of current.
Joule’s Law
Further, with greater resistance, greater numbers of electrons
collides with each other and generate more heat. This was
described by Joule and is explained mathematically by Joule’s
Law.
Power (P) = Voltage (E) × Current (I)
Further E = I × R
Therefore P = I2 × R
Heat generated in a current source due to flow of current
is the indicator of power. Watt is the unit of electrical power.
1 ampere of current flow through 1 Ohm of resistance in 1
second is one Watt of energy generated. One Watt per second
produces 0.24 calories of heat.
Type of Current
Direct current (DC) or Alternate Current (AC).
There were great discussion about safety and cost of
current supply between DC (invented by Edison) and AC
(invented by Tesla) in 19th and early 20th centuries. At
present, Alternate Current (AC) has entirely superseded
Direct Current (DC). It is cheaper and easy to transform

Electrical Burns
265
into any desired voltage. Direct Current is restricted to the
chemical and metallurgical industry. It is also used in the
automobiles. However, it is believed that AC current is more
dangerous to life as compared to DC current. There is no
‘let go’ effect in AC current while in DC current a person is
thrown out after a short muscle contraction. AC current
flow regularly reverses its direction and thus creates a sign
wave. Direct current flows in a constant direction. All
batteries deliver Direct Current. Use of UPS and alternators
are based on Direct Current.
Electric Arc10,11
An electric arc is formed between the two substances of
high potential difference. In humans, it is high voltage power
source and grounded body of the man. Arc is made up of
ionized particles which are driven by high electromagnetic
force (Voltage) between the source and human body with
air space in between. Temperature of the ionized particles
may reach as high as 3-4 thousand degree Celsius. Such
high temperatures can melt any metal. Arc is seen around
for a distance of many centimeters even in case of few
thousands volts.
Burn occurs at the point where arc strikes the human
body. Electric arc remains an important cause in high voltage
electrical injuries.
EFFECT OF CURRENT SUPPLY ON
HUMAN BODY (FLOW CHART 21.1)
Effects of current on human body are well described.
However, the mechanism(s) of action is (are) not equally
well understood. Most often, this effect is described on the
basis of conversion of electrical energy into the heat energy.
Therefore, it is justifiable to think about the resistance offered
by the body to the flow of current. Different body tissues
provide different resistance to the flow of current. Maximum
resistance is provided by the deepest structure i.e. bones
and the most superficial structure i.e. epidermis of skin.
However, there is an alternative view also which says that
human body works like a volume conductor and there is no
effect of resistance of individual tissue. The latter part
appears to be correct. Because of bigger volume of chest
and abdomen lesser damage is seen to these structures as
the heat dissipates over a larger area. Because of smaller
volume of fingers and limbs more damage is seen at these
points12 (Fig. 21.1).
In humans and in the animal kingdom as a whole, the
mechanical energy is converted to chemical energy which
is converted into electrical energy. All final commands in
the body tissues and cells are by electrical signals only.
From the conduction point of view best conductors are
nerves followed by blood vessels and muscle. Tendon,
tendon-sheath, deep fascia, dermis, epidermis and
subcutaneous tissue have the resistance in this ascending
order.
Unfortunately not much has been explained about how
the current affects the cells and tissues which are permitting
the current to flow. We must remember while gravitational
forces keep the cells and masses pulled towards each other,
electromagnetic force is 1042 times stronger than the
gravitational force and pushes the electron apart. This
electromagnetic force is responsible for creating vacuolation
in the cell membrane, separating the cells and detaching
from each other, blocking the sodium pump, leading to entry
of sodium into the cell, stopping the cell function and finally
death. At any given time, cell may remain in a hibernation
period and once the effect of current has gone may recover
fully. Unfortunately, these effects are not fully understood
and its mechanism remains debatable. Effect on brain and
the heart muscle show considerable period of hibernation
hence often complete recovery after initial sign of infarct
or hemorrhage.
Classic work of Kouwenhoven (1949)13 provides the
basic understanding about the effect of electricity on the
human body. According to him effects of the current depends
on the following factors.
1. Type of current used i.e. AC or DC
2. Voltage of circuit
3. Resistance
4. Amperage or amount of current.
5. Pathway of current
6. Duration of contact.
Fig. 21.1: Electrical contact burn in a young patient who was standing
next to a wall and holding a pole with both his hands which accidentally
touched a high tension wire causing severe burn in both the hands–
Gangrene of both hands and exit wound in lower chest and abdomen
which is less than the limb injury because of the larger circumference
of the chest

266
Principles and Practice of Burn Care
Flow chart 21.1: Effect of electrical current of human body

Electrical Burns
267
To this a seventh factor can be added and that is area of
contact. He also confirmed that the main mechanism of
immediate death from electricity was by induction of
ventricular fibrillation.
Type of current causes significantly different effects
on the human body. Skin offers greater resistance to the
Direct Current than to Alternate Current. 3-4 times more
Direct Current is required in producing the same effect as
alternate current. Direct Current does not produce muscle
contraction as produced by the Alternate Current. With
increasing alternating current the magnitude of muscles
contraction keeps on increasing and subjects hold on the
contact point becomes so intense that he/she cannot release
the conductor. Maximum current a person can hold and still
release on one’s will is called “Let go” current. Such strong
muscle contraction may lead to fractures and/or dislocation
of joints. Threshold for ‘let go’ effect in both sexes is
different, probably because of different muscle strength. It
is 15.87 mA in men and 10.5 mA in women with normal
commercial supply of 60 cycles of alternating current.
In contrast to low voltage, high voltage direct current is
more lethal than alternating current (Flow chart 21.2).
Alternating current of 60 cycles with as low voltage as 60-
65 volts has resulted in fatal accidents. However, the
threshold of 24 volts has been described as safe. Lower
volts than this in any circuit have been found to have no
lethal effects on the human body.
Actually it is the total current entering the human body
which is of concern. All effects are based on the total amount
which has entered into a human body. This was best
described by Hodgkin BC14 in 1974. According to him 1
mA of current leads to just tingling or perception which
becomes painful when increased to 5 mA. At 60 mA, it
leads to cardiac fibrillation, burns at 5000 mA and respiratory
arrest at 10,000 mA. A person with high voltage injury
develops respiratory arrest and is more likely to revive,
compared to low voltage injury where the heart goes into
fibrillation and is less likely to be revived.
Pathway(s) of current in the human body is (are) of
extreme importance.14 When heart or brain comes in the
path of a current, it is more likely to be lethal. Further,
longer the duration of contact, greater are the chances of
damage to the vital structures. Thus, a current passing from
skull to feet is more lethal than a current passing from right
upper limb to the right lower limb (Figs 21.2A to C). Similar
current passing from left hand to right hand will have more
lethality because of involvement of heart in its path.
From a practical point of view, an electrical injury will
have more local effects (burns) when skin provides higher
Fig. 21.2C: Third area of contact in same patient below the axilla
exposing pleura requiring chest tube drainage for pneumothorax
Fig. 21.2B: Another area of contact with wire in the neck causing a
deep wound exposing the carotid vessels , with deep flash burns in
the surrounding area on face and chest
Fig. 21.2A: A 10-year-old child sustained high tension injury due to
accidental fall of 11000 V cable falling on her while playing—Entry
wound in skull with loss of both tables and brain matter coming out of
the wound

268
Principles and Practice of Burn Care
resistance and will have more severe systemic effects when
the skin has lower resistance.
One must understand that during short-circuiting
electrons randomly collide with each other producing intense
heat and flash. This intense heat and flash leads to burns
(Fig. 21.14). This intense heat or flash is for fraction of a
second. Contact with human body will produce extensive
burns. These are mostly superficial burns. Sometimes
clothes catch fire from these intense flashes and produce
deeper burns. These burns are truly thermal burns although
the causative agent is electricity. In these injuries, there are
no systemic or local effects of electric current on the human
body.
TYPES OF ELECTRICAL INJURIES
(FLOW CHART 21.3)
There are five types of presentation seen in electrical injury.
1. True electrical injury: In which body becomes a part of
the circuit and injury by the passage of current through
the body is manifested by entry and exit wounds. This
can be either low voltage (< 1000 V) or High voltage
(> 1000V) injury (Figs 21.2 and 21.3).
2. Flash burns: These are surface thermal injuries involving
exposed areas of the body like face, forearm and hands.
These are sustained by flashes produced during sparking
which come in contact with the skin and the heat
produced during the process causes burns.The current
does not enter the body at all. The temperature in the
spark may be as high as 4000°C and though it lasts for
a fraction of a second, it can produce full thickness
burns (Figs 21.4 and 21.5).
Flow chart 21.2: Types of electrical contact burns depending on voltage
Fig. 21.3: High voltage contact injury causing autoamputation at the
level of forearm because of necrosis till bone
Fig. 21.4: Full thickness flash burns

Electrical Burns
269
3. Flame injuries: These are caused by spontaneous
combustion of victim’s clothes when they come in
contact with an electric arc. This is also a pure thermal
injury.
4. Lightning:15,16 Consists of hundreds of million volts
lasting from a fraction of a second, often resulting in a
flashover phenomenon in which majority of the electrical
energy flows over the victim’s body rather than through
it. The burn due to lightning can vary from minor burns
to major burns from ignition of the victim’s clothes or
heating of the metallic objects on the victim’s body like
jewellery, coins or dental fillings. The cutaneous burns
from lightning are seen as feathery or arborescent, linear
or punctate pattern. Respiratory arrest or cardiac arrest
with unconsciousness may occur and requires prompt
resuscitation with cardiac massage and ventilation.
5. Electric shock or electrocution9: It is usually suffered
by electricians who describe the feeling as balls of light
when the current passes through the body followed by
trembling, pallor, sweating and feeling of apathy or
euphoria. The patient may become unconscious because
of cerebral edema and raised intracranial pressure. Many
a times there may be cardiac and respiratory arrest
requiring cardiac massage and artificial respiration. There
may be temporary deafness or blindness with auditory
hallucinations and stiffness or paralysis of limbs. These
can last for a few minutes to hours. Altered sensorium
may also be temporary.
LOW VOLTAGE INJURY (FIGS 21.6 TO 21.9B)
These injuries usually take place at home. Malfunctioning
lawn mower, electric kettle, iron etc. are the causative agents
for these injuries. Here the current involved is 110-120 volts
(American sub-continent) and 210-240 volts (European,
Indian, African and Asian sub-continent). Where three phase
electrical current is used as in industries, it may be 440
volts. In all these instances, usually hands are involved and
the injury is local. There is practically no systemic effect of
electrical current. However, sometimes ECG changes are
seen in the form of elevated ST segment/T-wave depression.
Oral Cavity Burns (Figs 21.10A and B)
These injuries are seen in infants and toddlers. An inquisitive
child tries to explore the wire by taking it into the mouth
Flow chart 21.3: Types of electrical injury
Fig. 21.5: Typical deep dermal injury in flash burns

270
Principles and Practice of Burn Care
and chewing it with the gum or newly erupting teeth. In
majority of these cases both the wires, positive as well as
negative, are taken into the child’s mouth. Salty watery
contents of the mouth allow the current to flow out through
the same wire (contact burn in series). Here child’s mouth17
works like a resistance added in the flow of current. The
current is converted to heat energy (1000-1500°C) leading
to extensive local damage of the oral cavity involving lips,
mucous membranes of oral cavity and tongue. An occasional
complication is a secondary hemorrhage from labial artery
which may occur even many days later when the scab over
the artery is dislodged by the child.18
In the 2nd type of contact burn (contact in parallel)
current passes out from the body to the ground from child’s
wet diaper, feet or buttocks. This invariably led to serious
cardiac problem and may prove fatal (around 5% of the
cases).
In most cases, upper lips, lower lips and angle of mouth
are involved either alone or in different combinations.
Sometime tongue and cheeks are also involved resulting in
massive edema. Usually it does not lead to any respiratory
problem or any difficulty in swallowing. Excessive salivation
and dribbling are seen.
Management
First aid at site of injury: Whenever a victim of electric
injury has to be rescued, the safety of the rescuer is of
prime consideration. First, the electrical supply should be
turned off or the patient should be removed from the
electrical source with the help of a well insulated, wooden
or rubber coated tool. Next, attention has to be directed
towards airway, breathing and circulation of the patient and
steps for basic life support have to be taken. It is highly
desirable that the general public should be conversant with
this basic first aid knowledge.The patient should then be
shifted immediately to the closest hospital. Within few
minutes of resuscitation, if possible, cardiac monitoring of
the patient is essential because most arrhythmias occur
within the first few minutes to an hour after an electrical
injury. Defibrillation at the scene of injury or as soon as
possible may save a patient’s life who is having arrhythmias.
Therefore, all patients must have an ECG done and should
be monitored for 48-72 hours for cardiac status. It becomes
more important if there are some changes in the ECG initially.
A venous line is kept ready for management and the
drug administration for cardiotropic drugs. Usually, no
intravenous fluids may be required for resuscitation in very
small and localized electric burns. In fingers and hands proper
assessment must be made of the circulation as fingers are
closed compartments and similarly at wrist a tight
compartment may develop because of tight carpal tunnel.
These may require urgent release.
After the initial resuscitation patient needs to be shifted
to a specialized burn unit where decision regarding further
management of the burn wound can be taken. As all burns
are deep in contact burns, excision of burn can be undertaken
once patient appears to be stable from the cardiopulmonary
point of view. However, person performing these surgeries
should be well trained in providing flap cover to the excised
regions. Sometime at the wrist and dorsum of hand level
there may be damage to flexor or extensor tendons or may
be direct injury to the median or ulnar nerve. If injury to the
nerve is seen excision of nerve is done and nerve grafting
can be undertaken once one is confident that he has
successfully excised all the dead tissues. This must be
associated with flap cover, especially areas where burns
are excised at the wrist level or carpal and ulnar tunnels are
opened (Figs 21.7A to F).
Similarly hand burns are seen in infants and toddlers
due to putting the fingers into the electric sockets. However,
with the development of better and safe childproof sockets
these electric burns in children have become much less.
Electrical burns in children because of soft pliability of skin
accumulate lots of fluids and are more likely to develop
ischemic changes or median and ulnar nerve damage if burn
involve wrist. An early surgery should always be considered
in children and one must release the carpal and ulnar tunnel
and also provide a flap cover. In fingers, a cross finger
flap, flag flap or meta-carpal artery flaps can be used to
cover the fingers (Figs 21.8 and 21.9).
Fig. 21.6. Low voltage electrical burns of fingers treated by primary
excision and grafting. No involvement of tendon and nerves

Electrical Burns
271
Figs 21.7A to F: Low voltage electrical injury involving extensor surface of the hand. Showing different levels of involvement with in between
normal tissue while deeper necrosis of tendon or thrombosis of veins. Total reconstruction by providing tendon and cover. Cover by pedicle
groin flap preferred over free flap
Management of Oral Cavity Burn
All these burns are confined to infants and children hence
management should take into consideration, growth and
further development. Electrical burns of mouth extend from
angle of mouth to the lower lip with injury to the gum, bone
and developing teeth. There are two opposing views of
thought in the management of mouth burn. One believes in
early excision and primary cover. This provides sufficient
vascularised tissue for the growth of bones and tooth buds.
The other view is that while trying to do the early excision
one may excise too much of tissues which may recover on
their own. As mouth is a specialized structure, no
A
B
C
E
F
D

272
Principles and Practice of Burn Care
Fig. 21.8: A case of electrical socket injury involving index finger and
dorsum of hand. Dorsum primarily excised and closed. Finger covered
by pedicle groin flap
Fig. 21.9B: Electrical burn in a child from domestic electric current
220-240 volts with involvement of extensor surface of hands and
wrist
Fig. 21.9A: Domestic electrical burn involving inner aspect of the ring
finger. An electrical socket injury. Exposed tendon treated by cross
finger flap cover
Fig. 21.10B: Defect after removal of eschar exposing both alveoli
and teeth requiring flap cover
Fig. 21.10A: A 8-year-old with oral cavity burns due to accidental fall
of high tension wire over face, leading to necrosis of both upper and
lower lips and left cheek

Electrical Burns
273
reconstruction can be as perfect to take up all the normal
functions. The consensus today is towards initial
conservative management and early release of all tight
contracting bands including tight oral commissure.
Conservative management includes proper mouth care,
topical antibacterial creams and providing splintage for
6-12 months. This provides a practically invisible scar but
with a defect or deformity (Fig. 21.11).
Fig. 21.11: Post electric burn deformity of mouth (Microstomia)
HIGH VOLTAGE BURN INJURIES
(FIGS 21.12 TO 21.18)
Arc injuries from high voltage live wire are not an uncommon
injury. Here the current passes to the individual and to the
ground with no direct contact. Ionized particles in the air
work like conductor.10,11 These arc burns are mostly seen
on the palmer surface of hand, flexor aspect of wrists,
forearm, and flexor surface on the elbow joint. Usually there
is little or no systemic effect. Current takes the path of
maximum conductivity. There is maximum damage to nerves
which are burnt out at the site of the injury and where
current passes, the veins get thrombosed (Fig. 21.19).
Tendons are charred and muscles show typical pale lusterless
appearance with no contractibility and become dead. Early
excision and flap cover is needed. In the author’s opinion
as there is far more damage to the venous system, a pedicled
flap helps in providing alternative venous channels which
help in preventing any further damage by venous congestion.
Fig. 21.12: High tension electrical burn in female (Electric arc). This
young girl sustained arc burns while drying wet dupatta close to high
tension wires passing near the balcony. Her both hands were involved,
involving both median and ulnar nerves. Thrombosis of both ulnar
arteries. Damage to most of the flexor tendons. Both hands were
saved by pedicled extended groin flaps
Fig. 21.13: High voltage electrical injury involving all four limbs,
scalp and back. Patient died from severity of injury

274
Principles and Practice of Burn Care
Fig. 21.14: Electrical contact burn on the right hand with full
thickness burns on the left leg from clothes catching fire
Fig. 21.15: Electrical contact burns of right lower limb showing patchy
areas of normal skin with proximal and distal full thickness burns and
flame burns of the lower extremity from clothes catching fire
Fig. 21.16: High tension electrical burn involving left groin. The
patient was on a pole holding the pole by both the thighs
Fig. 21.17: Electrical contact burns on left thigh in an electrician
sustained while working on an electrical pole with extensive muscle
damage exposing hip joint
Fig. 21.18: Electrical flash burn
Fig. 21.19: Thrombosed radial vessels following early debridement
of electrical burn wound at wrist and lower forearm

Electrical Burns
275
High Voltage Contact Burn19
Practically all high voltage contact burns are contact in
parallel (as the current passes out from the human body to
the ground). There is reduction in the cumulative resistance
(resistance of the individual and that of current source).
Thus, more current can flow through the human body to
the ground leading to more damage to the body tissues.
Extent of damage, as previously stated, is related to the
duration of current flow, amount of resistance offered to
flow, voltage or magnitude of force of current or in
summary, the amount of current flown and the rate at which
it flows in the human body.
Resistance offered by the skin generates enormous
amount of heat leading to evaporation of water content of
the skin and underneath tissue. Current flow rises after the
initial resistance and peaks up within seconds with complete
drying of skin. Current ceases to flow because of
carbonization of the skin. This cessation of current is
heralded with a flash or arc. Thus, entry point of electric
current (high-voltage) appears charred or whitish yellow
area with a leathery texture, with markedly depressed central
zone surrounded by hyperemic border (Fig. 21.20A). Exit
wounds, which can be in lower limb or opposite hand can
be multiple and appear ruptured tanned black because of
explosive release of heat due to high-voltage current coming
out (Fig. 21.20B). Thus, two places show maximum
resistance; hence, maximum local damage is seen at these
two sites. Once the current crosses the initial resistance
and enters the body, current flows through the structure
which provides least resistance to current flow. Thus, more
current flows through the muscles. This excessive load on
the muscle cells which they cannot handle leads to
breakdown of muscle cells. This damage is further increased
by venous obstruction caused by venous thrombosis and
ultimately muscle death from damage to the arterial blood
supply. These damages are usually seen in one group or
one compartment of muscles. Sometimes these damages
are segmental. These segmental muscle damages are seen
when the current suddenly moves from one muscle group
to another muscle group or where the muscles have multiple
points of origin.
It is not common to see deep muscle damage much
beyond the point of entry with no superficial muscle damage.
In the case of upper limbs where entry point of current is
the finger, skin damage is seen at wrist, elbow and at the
axilla. This type of patchy skin damage is often described
as “arcing of current” from finger to wrist and from wrist
Fig. 21.20A: Entry wounds in fingers due to contact with low voltage
current and arc injury at wrist causing full thickness burn at wrist
Fig. 21.20B: Exit wound in feet
to elbow because of muscle contraction (Fig. 21.21). It
means these damages are indirect damage where current
has flown from outside with air pocket in between, i.e.
‘jumping of current’ across a flexed joint. As the current
exits and re-enters the skin, a tremendous amount of heat is
generated and the cutaneous injury in flexor creases can
vary from minor erythema to explosive charring. However,
in the author’s opinion, after examining more than sixty
cases of high tension burns, this injury is because of flow
of current through the blood vessels and at these points i.e.
at the wrist, elbow and axilla, the blood vessels become
superficial and these vessels give perforating vessels to the
skin. Current transmitted through the blood vessels reach
the superficial tissues in the skin and again resistance of
skin leads to the heat production and full thickness skin
damage occurs. Here, damage to the skin is based on
changing direction and flow of current.

276
Principles and Practice of Burn Care
Further damage to the bones and cuff of periosteum
has been described. But in a study done by the author on 30
lower extremity high tension burns and 40 upper extremity
burns, no such damage was seen, except initially at the
point of entry or exit where more damage was seen. From
this work, it appears that current flows in a linear axis
through the most conductive areas. Nerve damage is seen
at the point of entry of current. More often, it is charred
and divided. No further nerve damage is seen. However,
distant damage is seen in muscles, arteries and veins. More
current flows through the muscle because of larger muscle
mass and diameter with more water content. Blood vessels
because of smaller diameter have more resistance. In
arteries, because of rapid flow of blood, there is reduction
in current density at any given point while in the veins
because of slow flow of blood the current density is high.
Therefore, chances of thrombosis of veins are higher which
lead to increase in edema and rise in compartmental pressure
leading to further damage to the muscles and compression
of the arterial supply. The latter may also ultimately get
thrombosed leading to complete death of the muscle. It
appears that most of the damage in electrical burn is
secondary to vascular damage20 (Figs 21.22 to 21.24).
Electric current can cause tetanic contractions of skeletal
muscles or rupture of tendons and at times dislocation and
multiple fractures. The heat generated from the passage of
current through the bone can cause aseptic necrosis, burns
to periosteum or complete destruction of bone matrix leading
to autoamputation (Fig. 21.25). The rate of auto-amputation
is reported to be as high as 35=60%.21
Sometimes, in alternate current with inability to “let go”
effect, a limb or a person as a whole may be completely
charred from the electrical current and one may not be in a
Fig. 21.21: Arcing of current or jumping of current from wrist to
elbow to axilla with contact in the fingers
Fig. 21.22: High tension injury showing extent of damage to deeper
structures beyond the apparently damaged skin.Though the line of
demarcation is till elbow, the muscles are seen necrosed much more
proximally, thus requiring a higher level of amputation
Fig. 21.23: high voltage contact burn in palmar surface of hand with
arcing causing full thickness circumferential burns in wrist and lower
forearm causing compartment syndrome leading to ischemic damage
to all fingers
Fig. 21.24: High voltage current causing primary gangrene of hand
with arcing at elbow causing full thickness burns over elbow

Electrical Burns
277
Damaged muscles release pigment so do the damaged
red cells. These pigments enter into the blood and can block
the renal tubular system leading to acute renal failure.
Another mechanism, which is not well understood, is the
release of substances by ischemic muscles which enter into
the blood. These substances have a depressive effect on
the myocardium. This is well seen by improvement in cardiac
functions once an injured muscle or limb is removed by
amputation.
DIAGNOSTIC MODALITIES24,25
Though many diagnostic modalities have been suggested to
diagnose the muscle damage which includes various enzyme
levels, SGOT, SGPT but all these are non-specific as these
Fig. 21.25: Primary forearm autoamputation following high voltage
injury with visible proximal damage of elbow extending till axilla
condition to identify anything separately. Some peculiar
injuries are seen in electrical burns from the point of entry
of electrical current. These are hollow-viscous or solid
viscous injuries. Usually intra-abdominal injury is prevented
by a comparatively avascular peritoneum. However, when
current enters through the abdomen one gets direct injury
to the intestine and colonic injuries are the most common
(Fig. 21.26). Similarly, injuries to the urinary bladder and
penis also take place from direct current damage.22 Fatal
injuries to the liver in a similar fashion have been described23
(Fig. 21.27).
Thus, anatomical positions have great bearing as direct
damage to any organ can be affected by the electrical injuries.
It is not necessary that structures are involved between
entry and exit points as path taken by the current may
markedly vary and many structures may completely survive
as current may jump from one group of anatomical structure
to the other which is in close proximity.
SEQUELAE OF SECONDARY EFFECTS
AFTER INJURIES
Because of an electrical injury there is marked extravasation
of fluid from the muscles leading to rise in intra-
compartmental pressure leading to further decrease in the
venous outflow, which impairs arterial inflow and causes
further devascularization of muscles and other tissues. If
this compartment pressure is not released quickly, damage
to the muscles and other structures becomes irreversible
leading to gangrene of the limbs.
Fig. 21.26: A 14-year-old boy with electric contact burn over lower
abdomen exposing the bowel with loss of external genitalia
Fig. 21.27: Deep high voltage injury in trunk with extensive damage
of all abdominal muscles exposing underlying viscera

278
Principles and Practice of Burn Care
may be elevated without muscle damage also. Presence of
pigment in the urine is the single most important indicator
of muscle damage.
The patient should be placed on a cardiac monitor and a
12 lead ECG should be obtained. MRI can be used to detect
edema but is not necessarily of much help.26
A Technetium Tc 99m Stannus Pyrophosphate (99m
Tc Pyp)27 muscle scan can be safe, sensitive, noninvasive
and reliable diagnostic tool in defining the viability of muscles.
Areas of muscle unable to show uptake of isotopes (cold
spot) are indicative of dead muscle. However, the test is
extremely sensitive and many false positive effects may be
seen when there is increase in compartmental pressure. In
case of severely mummified tissue requiring amputation,
the exact level of vascular occlusion can be localized by
preoperative arteriography and the approximate level of
surgical amputation can be decided.28
Exploration, direct visualization of muscle, its
contractility and bleeding on cutting are the practical tools
in deciding the level of muscle damage.
TREATMENT
In the emergency department, attention to the protocol of
basic life support and advanced life support should be
followed as per requirement. Tetanus prophylaxis is essential
for all electrical burn patients. Hydration should be started
with ringer lactate. Surface damage in electrical injury may
not necessarily reflect the severity of deeper tissue damage
so fluid replacement may be grossly underestimated.
Resuscitation of electrical burn patient from the point of
view of hypovolemia using conventional skin burns formula
may not be correct as most of the fluid is lost in the muscles.
Here, fluid should be titrated so that one can get a urine
output of 2 ml/kg body weight/hour. The fluid required in
an electrical burn may be 2-3 times more as compared to
thermal burns. The objective of aggressive early rehydration
is to avoid renal failure secondary to myoglobinuria as there
is release of myoglobins from damaged muscle cells and
small amount of hemoglobin from damaged red blood cells
and unidentified intracellular substances which can produce
severe metabolic acidosis.
In the presence of pigments in the urine, alkalinization
of urine should be done and mannitol should be give so that
tubules can clear the pigments. Initial dose of 25 gm of
mannitol followed by 12.5 gm/hour for several hours usually
produces urine volume of 200-300 ml/hour. This further
forces more fluid to be infused in electrical burns. The
Local Wound Management
In electrical flash burns, where there are only surface
thermal burns, the standard treatment of cleaning,
debridement and topical dressings using antimicrobial agents
is sufficient. When deeper structures are involved, there
may be significant limb edema predisposing the patient to
the danger of compartment syndrome. In these patients, it
is necessary to perform a fasciotomy as early as possible to
persistence of reddish black urine once the urine flow is >
50 ml/hour indicates massive muscle damage (Figs 21.28A
and B).
In these cases, the arterial pH may remain below 7.30
after volume repletion. Slow intravenous administration of
80-120 ml of 8.4% soda bicarbonate/hour is continued till
pH is stabilized to above 7.35.
Fig. 21.28B: Gradual improvement in both color and quantity of urine
with proper resuscitation, osmotic diuresis and alkalanization of urine
Fig. 21.28A: Myoglobinuria indicated by reddish black urine requires
vigorous resuscitation

Electrical Burns
279
salvage the limb (Figs 21.29A to 21.30B). This is because,
if the underlying necrotic muscle masses go undetected,
there are chances of gangrene of distal extremities as well
as early toxicity (within 3-5 days) and later infected abscess
formation producing lethal sepsis. Likewise in
circumferential full thickness limb burns, an escharotomy
may be necessary to eliminate the constricting effect of the
circumferential injury. It is important to resuscitate the patient
well prior to fasciotomy. Once the fasciotomy is done, the
tourniquet effect of deep fascia due to underlying edematous
tissue is released and the venous return is established from
the distal tissues, the myoglobin pigment from these ischemic
distal tissues enters into the circulation. The pigments then
go on to block the renal tubules and the patient may end up
in renal failure.
Surgical exploration is the only reliable method of
identifying the presence of muscle damage. Early excision
or debridement should be done to prevent further damage
and to reduce the immediate depressive effect of dead tissues
on the myocardium. Many workers have suggested a policy
of ‘wait and watch’ for development of line of demarcation.
This policy may lead to an increase in the secondary damage
while early surgical interventions have no side effect other
than the one that the patient may require a second excisional
surgery.
Amputation: The large necrotic muscle mass and dead tissue
resulting from the passage of electrical current should be
removed early. The initial fasciotomy often limits further
ischemic damage to distal tissues by removing the effects
of vascular compression and thus lowers the site of
amputation and ensures least number of complications and
better survival of body parts and life as well. In general,
necessary amputations can be done safely after 48-72 hours
of injury once the patient has been thoroughly resuscitated
and line of demarcation is established. These early
amputations should be preferably done under regional blocks
as the myocardium remains sensitized to various drugs for
5-7 days following passage of electrical current through
the heart (Fig. 21.31). General anesthesia should be avoided.
At times the level of amputation may be higher than the
cutaneous line of demarcation because the underlying muscle
damage extends more proximal than the skin damage. Infact
for several inches proximal to the line of demarcation, the
skin may appear normal and yet the underlying muscles
may be dead. Hence, they may require revision more than
once to a higher level.
Fig. 21.29A: Contact injury to hand and wrist causing proximal
compartment syndrome in forearm and tight carpal tunnel
Fig. 21.29B: Dorsum of same hand showing circumferential injury at
wrist with edematous dorsum
Fig. 21.29C: Early fasciotomy done to release compartment syndrome
and opened carpal tunnel showing thrombosed ulnar vessels

280
Principles and Practice of Burn Care
Ligation of subclavian vessels may be essential in case
the entire length of upper limb is gangrenous and requires
amputation at shoulder level so as to avoid blow out from
axillary vessels at amputated site if the damage extends till
axilla or more proximal (Figs 21.32A to 21.34).
Fig. 21.30B: Fasciotomy incision extending into foot
Fig. 21.30A: Early fasciotomy in lower limb to release
compartment syndrome
Fig. 21.31: Guillotine amputation done in midarm level showing
residual dead muscles requiring revision of amputation
Fig. 21.32A: Gangrene of entire length of upper limb because of high
voltage contact burns requiring amputation at the level of shoulders.
Prior to amputation the subclavian vessel ligation was required so as
to prevent their blowout postoperatively
Fig. 21.32B: Marking for locating subclavian vessels
Fig. 21.32C: Subclavian vessels exposed beneath the clavicle

Electrical Burns
281
Fig. 21.32D: Bilateral subclavian ligation achieved after which both
the gangrenous limbs can be disarticulated safely at the shoulder
Fig. 21.33: A case of arm to arm transmission of high voltage electricity
leading to above elbow amputation of both the upper limbs
Fig. 21.34: Electric contact burns in series, no wound of exit or
grounding. Maximum local damage by production of heat
COMPLICATION OF ELECTRIC BURNS
Some specific complications/effects of electrical burns43
are as follows:
Neurological Complications29-32
Many neurological complications have been described in
electrical burn. Some are understandable while others are
not fully understood. Electrical current can cause acute and
delayed injury to the central and peripheral nervous systems.
Acute central nervous system symptoms include altered
mental status like confusion, impaired concentration, and
disorientation. More severe cases may have paralysis,
seizures, coma, loss of consciousness and depression of
respiratory center. Injury or effects on peripheral nerve,
median, ulnar or radial and sometimes compound global
brachial plexus injuries can also take place because of severe
muscle contraction pulling the brachial plexus. Mostly,
injuries to the nerves are confined to the local site where a
nerve is directly damaged from the electrical current. In
some cases the nerve damage is secondary to increased
intra-compartmental pressure. The effects revert to normal
once the pressure is released. When irreversible damage
occurs, nerve grafting may be required. However, results
of nerve grafting may not be good because of intense
scarring in the region of damage and also because of the
associated muscle damage.
Damage to brain and spinal cord has also been
described39-43 (Fig. 21.35). The cause of this damage is not
well understood. Often, a hemorrhagic infarct is seen in
brain especially in the area of thalamus and internal capsule.
These are the areas where blood vessels are less protected
in the white matter and are more likely to have flow of
current outside leading to damage. These cases develop
extra-pyramidal symptoms.31,32 Probably similar effect is
seen in the spinal cord leading to paraplegia or quadriplegia.
Delayed effects in the spinal cord have also been described
which develop months and years after an electrical insult.
In these patients, motor symptoms are more pronounced
than the sensory involvement. Mechanism of its development
is not fully understood but appears to be due to slow
development of cord ischemia.
Cardiovascular and Pulmonary Complications
Both heart and lungs are well protected by comparatively
avascular structures, i.e. pericardium and pleura.
Different conduction abnormalities are seen in the heart.
Cardiac arrest can be either complete standstill (asystole)

282
Principles and Practice of Burn Care
or ineffective overactivity (ventricular fibrillation). Different
levels of heart block have also been described. Most
common types of conductive anomalies are sinus
tachycardia, ST elevation and T-wave depression. Most of
these revert to normal in due course of time. Multiple
extrasystoles and atrial fibrillation can also develop requiring
administration of different cardiotropic drugs. Most of the
cardiac effects recover spontaneously, long-term
consequences being very rare.
Enzymatic assessment of cardiac damage may not be
helpful because most of these are elevated due to striated
muscle damage and may not be cardio-specific. LDH level
changes may also be seen without ischemic changes in the
heart as slight damage of cardiac muscle recovers
spontaneously and may not be of any consequence.
Delayed vascular damage has also been described.33
Whether one should describe them as true electrical cause
or secondary hemorrhage is a point of individual perception.
However, one must remember that small vessels are likely
to be affected because they provide more resistance to the
flow, produce more heat and develop thrombosis. If there
is extensive necrosis over large blood vessels, there is always
a danger of delayed hemorrhage from these large vessels.
This can be minimized by providing early vascularized muscle
flap cover over these areas which gives additional blood
supply to the vessel wall.
Lung tissues are usually not involved. The most serious
pulmonary sequel from an electrical injury is respiratory
arrest. Usually, it is the pleura which gets damaged leading
to effusion or collapse of lung necessitating intercostal
drainage.34 Rarely atelectasis, pneumonia, hemopneumo-
thorax, pulmonary contusion and laryngeal injuries may be
seen.
Eye
Different eye changes have been described which include
damage to cornea, retina or optic nerve. The most common
involvement is of the lens leading to early development of
cataract.35 It may be on one side or both eyes may be
involved. It usually manifests in 6 months to 1 year after
electrical injury to head. An ophthalmologist’s intervention
is required. One must remember that phacoemulsification
may not be an easy procedure in these cases (Figs 21.36
and 21.37).
Bone and Joint
Bone and joint injuries may be associated with electrical
burns. These may be secondary to fall or because of severe
and strong muscle contraction. An orthopedic consultation
is required for optimum management. However, all the dead
tissue must be excised if fracture site is in the area of burns
and/or areas must be covered with vascularized flap (either
regional flap or a free flap). Free flap must be carefully
planned and anastomotic site should be placed away from
the site of injury.
Fig. 21.35: CT Scan showing hemorrhagic infarct in the area of
internal capsule following electric contact burns
Fig. 21.36: Cataract development after electrical contact
burn near zygoma

Electrical Burns
283
Gas Gangrene and Tetanus
Apart from damage and destruction of tissues of the body,
infection of the wound may occur leading to sepsis
especially if the gangrenous limb or tissue is not removed
timely. Gas gangrene and tetanus due to clostridial infection
in the dead tissue has been reported following electric burns.
Gas gangrene require urgent management, i.e. amputation
of the involved limb in order to save the patient’s life along
with medical management in the form of appropriate
antibiotics (Penicillin) and anti-gas gangrene serum.
BURNS OF SPECIAL SITES
Scalp (Figs 21.38A to 21.39B)
Scalp is third most common site involved in electrical burns
after upper and lower limbs. All scalp burns are full thickness.
Invariably, there is involvement of calvarium as well.
However, involvement of dura is the least common. These
burns may have different degrees of brain involvement. Most
commonly when brain is involved there is a localized
hemorrhagic infarct especially in the white matter areas like
internal capsule or thalamus as vessels of these sites are
comparatively unprotected.
Management
When localized to scalp with no other injuries like cardiac,
renal and pulmonary involvement and the patient is otherwise
stable, they are treated by primary excision of burned scalp
and covering the defect by transposition flap or rotation
flap or by the free flap (latissimus dorsi flap with skin graft).
These vascularized flaps provide vascularity to the bone
underneath and may allow it to regenerate. Alternatively all
obvious dead bone is removed till bleeding areas or both
tables are removed. Reconstruction is done with either bone
substitute or by split calvarial bone or rib graft covered
with a flap.
In more serious patients, who cannot be taken up for
surgery early, these areas are permitted to granulate and
later skin graft is applied over the granulating area.
Abdomen (Fig. 21.40)36,37
These burns involve major portions of abdominal wall
because of the low water content of the peritoneum.
Abdominal contents are normally saved by the resistance
of the peritoneum. However, in case of direct prolonged
contact, local damage to the hollow-viscous may be seen.
There can be necrosis of intestines and small bowel
perforations or even direct electrical damage to liver,
pancreas, gallbladder, etc. which can be fatal. Stress ulcers,
Curling’s ulcers and gastrointestinal bleeding have also been
reported. Treatment consists of excision and exploratory
laparotomy in case where there are signs of intra-abdominal
injury which is confirmed by ultrasonography and CT scan.
Injured hollow-viscous are treated by colostomy or
exteriorization of the colon or small bowel. In case there is
severe injury in perineal region, it can lead to loss of male
external genitalia as well as bladder injury. These have to be
reconstructed using local or regional flaps.38-40 There are
Fig. 21.37A: Contact injury on face by wire falling accidentally causing
deep injury on nose, left eye and cheek with total loss of left eye
Fig. 21.37B: Following debridement laterally based forehead flap cover
given to cover the defect and cataract seen to have developed in the
contralateral eye

284
Principles and Practice of Burn Care
Fig. 21.38A: Dead exposed skull bone due to high
voltage injury to skull
Fig. 21.38B: Dead outer and inner table debrided exposing the dura
Fig. 21.38C: Bony defect covered with artificial bony material
Fig. 21.38D: Adjacent scalp flap transposed to cover the defect
Fig. 21.38E: Donor area grafted
various reports of successful treatment of such rare injuries
and reconstructing abdominal wall defects using different
flaps e.g. free latissimus dorsi flap, tensor fascia lata flap
etc41 (Figs 21.41A to D).
Upper Extremity and Lower Extremity
(Figs 21.42A to 21.46B)
Involvement of upper extremity is the most common injury
of the electrical burns. Linear flow of electrical current may
cause muscle damage right up to axilla, however this damage
may be to a particular group of muscles only. These group
of muscles should be excised primarily and all areas should
be covered with a vascularized flap. In the author’s opinion
this probably prevents further damage to the other group of

Electrical Burns
285
In the case of lower extremity with larger muscle mass,
more dead muscles produce a greater effect on the heart.
Therefore, one should not hesitate to amputate the lower
extremity to save the patient as good lower limb prostheses
are available for patient rehabilitation.
Electrical Burns and Pregnancy
95% of electrical burns are in men. Therefore, involvement
of pregnant women is very rare. However, whenever it
happens, invariably there is death of the fetus. It is not
known whether it is because of the direct current on the
fetus or due to secondary effect from burns to the mother.
It is a well known that nature always gives priority to the
mother over the fetus and the latter is expelled out to save
the mother. Thus, pregnant women with electrical burn abort
or expel their fetuses in natural way.
SUMMARY
This chapter summarizes the current concepts in the
management of patients with electrical injuries. Apart from
understanding the pathophysiology of manifestations of these
burns, both local and systemic, an early diagnosis of the
extent of underlying tissue damage is equally important. An
aggressive program of prompt and adequate resuscitation,
timely fasciotomy, and early debridement including
amputations and vascularized flap cover can decrease the
incidence of renal failure, early toxemia and septicemia
reducing the morbidity and mortality. The importance of
progressive destruction of tissues in electric burns cannot
be overlooked and necessitates repeated assessment and
frequent debridements. Following healing of all wounds,
Fig. 21.39A: Post electric burn exposed skull and neck tissues
Fig. 21.39B: Transposition flap cover from adjacent scalp
muscles by providing alternating venous channels for venous
return. Most commonly used flap is latissimus dorsi muscle
flap which is invariably not involved in upper limb electrical
injury. However, when all muscles with their neurovascular
bundles are involved, a prompt amputation should be
preformed. Unfortunately upper limb amputation is 2-3 times
more common than the lower limb despite reconstructive
procedures to salvage the limb.
Fig. 21.40: High tension electrical burn of abdomen wall. Patient
climbed on the roof top of electrified train