Atlas Lâm Sàng Về Quản Lý Và Điều Trị Bỏng (Clinical Atlas of Burn Management)

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Fig. 4.36D: Thin split skin graft applied to the raw area—
3 days postoperative picture
Fig. 4.36A: Six months old post-burn raw area scalp with
exposed skull caused by deep thermal burns. CT scan showed
normal inner cortex. The peripheral area of the wound
granulated leaving the central area where there was no
periosteum
Fig. 4.36B: The dead outer cortex could be easily removed
and there was healthy granulation tissue beneath it. Surface
of debrided dead bone seen
Fig. 4.36C: Undersurface of the removed dead bone

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Figs 4.37C to E: Two months following conservative management, the eschar gradually separated and was debrided
(C and D) gradually to reveal a healthy granulating area which could be grafted (E)
Figs 4.37A and B: Full thickness circumferential flash burns in a linesman sustained while working on high tension
wire. Escharotomy incisions in medial and lateral lines given to save the hand
A
B
C
D
E

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Fig. 4.38: Technique of harvesting thick split thickness graft
(0.018 to 0.030 inch) showing fewer and bigger bleeding
points. Thick grafts are used for covering raw areas created
after release of contractures as the secondary contraction of
these grafts is much less
Fig. 4.39: Intermediate thickness (0.012 to 0.018 inch) split
thickness skin graft being harvested and it leaves numerous
small bleeding points. It is preferred for regions like face
especially for eyelids and lips so that they contract less
postoperatively
Fig. 4.40: Thin split thickness graft (0.006 to 0.012 inch)
are most preferred for covering post-burn raw areas as their
‘take’ is the best and they also allow the donor site to be
reused more than once for procuring graft in case of extensive
burns
Fig. 4.41: Manual meshing of graft

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Fig. 4.42: Padgett’s roller skin graft mesher
Fig. 4.43A: Zimmer’s skin graft mesher
Fig. 4.43B: Graft being meshed by passing it through
the mesher
Fig. 4.43C: Meshed graft ready to be applied on raw areas

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Fig. 4.44A: Scalp as donor area—adrenaline saline
infiltration done before harvesting graft to reduce blood loss
and also to make the base firm and broad
Fig. 4.44B: Graft being harvested with Watson’s handle.
The advantage with scalp is that grafts can be harvested
repeatedly, every 10 days, as epithelialization is very fast
from the epidermal lining of the large number of hair follicles
Fig. 4.45A: Graft being harvested from the back of trunk
which is used only in extensive burns cases where the limbs
are not available for donor areas
Fig. 4.45B: Two months postoperative showing that
donor areas of the back heal fast with minimal scarring

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Fig. 4.46: Watson’s modification of Humby’s knife—most
commonly used knife
Fig. 4.47: Silver knife—used for harvesting small grafts
Fig. 4.48A: Padgett’s drum dermatome
Fig. 4.48B: Same dermatome showing the surface of the
drum on which the glue is applied when placed in contact
with the skin
Fig. 4.49: Electric dermatome

Burn Wound Infection 5

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TERMINOLOGY USED IN BURN WOUND INFECTION
Colonization
Surface culture from burn wound shows presence of
pathogenic organism and count is < 105 organisms/gm of
surface tissue.
Noninvasive wound infection
Infection is limited to eschar and sub-eschar tissues.
Bacterial count in eschar may be > 105/gm of tissue.
Burn wound infection
Invasion of normal non-burned tissues by microorganisms.
Quantitative bacterial count is > 105/gm of tissue.
Bacteremia
Presence of viable bacteria in blood.
Septicemia
Systemic illness caused by the spread of microbes or their
toxins via the blood stream
Systemic inflammatory response
If two of the following four signs are present, the patient
syndrome (SIRS)
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 < 4000/mm3
Sepsis
SIRS with proven microbial etiology in any patient
Sepsis syndrome
Sepsis and one more sign of organ dysfunction like
hypotension, metabolic acidosis, alteration of mental status,
oliguria, ARDS or platelets count < 0.1 million/mm3.
Multiple organ dysfunction syndrome
Dysfunction of more than one organ requiring intervention
(MODS)
to maintain homeostasis like ventilatory support for ARDS
and dialysis for renal failure, etc.
CLASSIFICATION OF MICROBIAL STATUS OF BURN WOUND
According to the Depth of Involvement
STAGE I is the stage of colonization
STAGE II is the stage of invasion of viable tissue
Ia. Superficial colonization: Organisms are present
IIa. Microinvasion: Microscopic foci of organism in
only on the superficial surface
viable tissue below burn wound
Ib. Microbial penetration: Microorganisms invade
IIb. Generalized invasion: Diffuse penetration into
the eschar
viable subcutaneous tissue
Ic.
Subeschar proliferation: Microorganisms
IIc. Microvascular invasion: Organisms invade into
proliferate in subeschar space
burned blood vessels and lymphatics
DIAGNOSIS OF BURN WOUND INFECTION
Local Signs of Burn Wound Infection
• Black or dark brown focal areas of discoloration
• Increasing eschars

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• 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.
Systemic Signs of Burn Wound Infection
1. Signs of gram-negative
– Rapid onset of symptoms within 8-12 hours.
septicemia
– 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.
– In untreated sepsis systolic pressure also drops (low output shock).
– Mental clouding and diarrhea.
– Multi-organ 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
– Symptoms are gradual.
septicemia
– Hyperpyrexia (temperature > 105°F) and leukocytosis.
– Hypotension, paralytic ileus and oliguria.
Fig. 5.1A: 2-year-old child with 20 percent burns with
increasing eschar indicating increasing depth of burns with
increasing inflammation and edema in normal skin indicating
burn wound sepsis
Fig. 5.1B: Same patient with hemorrhagic patches with
edema of uninvolved skin indicating patient is landing in
DIC (Disseminated intravascular coagulation)

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Fig. 5.1C: Same patient with rashes, papules and erythema
in non-burned extremities indicating invasive gram-negative
sepsis
Fig. 5.1D: Close-up view of the arm and hand of same
patient showing the changes in burn wound indicating
infection, i.e. black or dark brown focal areas of discoloration
and increasing eschar
Fig. 5.2A: Greenish discoloration of the dressing and burn
wound surface indicating pseudomonas colonization of the
wound
Fig. 5.2B: Pseudomonas invasion of the same wound
indicated by bluish purple patches appearing in the depth of
the burned area

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Fig. 5.2C: Full blown pseudomonas invasive sepsis—
hemorrhagic patches with thickening eschars, increasing
soakage from wound
Fig. 5.3A: Patient with invasive gram-negative burn wound
sepsis—hemorrhagic discoloration of entire eschar
Fig. 5.3B: Close-up view of same wound
Fig. 5.3C: Typical nodular satellite lesions in uninvolved
skin—ecthyma gangrenosum

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Fig. 5.3D: Infective gangrenous changes in thumb
indicating septic embolization
Fig. 5.3E: Nodulopapular lesions in adjacent unburned skin
over the abdomen and chest with edema of the skin with
distension abdomen
Fig. 5.3F: Patient managed with change of local antimicrobial
from SSD to mafenide and third line of systemic antibiotic—
carbapenems with aminoglycoside
Fig. 5.3G: Improving wounds—eschar penetrated by
mafenide to reach subeschar tissue, tissue edema reduced
and general condition improved

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Fig. 5.3H: Ecthyma gangrenosum reduced
Fig. 5.3I: Satellite nodules drying up
Fig. 5.3J: Healthy granulating wound after 10 days of
change in treatment
Fig. 5.3K: Same wounds grafted in stages on lower
limbs—full graft uptake

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Fig. 5.3L: Successfully grafted back of same patient
Fig. 5.3M: One month postoperative picture of the back
of same patient
Fig. 5.3N: Legs of the same patient
Fig. 5.4A: Superficial burns converted to deep burns by
pseudomonas infection which was controlled timely by
systemic antibiotics and change of local antimicrobial agent

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Fig. 5.4B: Same patient with wounds showing improvement
Fig. 5.4C: Finally grafted wounds of same patient—two
months postoperative picture
Fig. 5.5A: Streptococcal burn wound infection with
extending erythema into surrounding normal skin from burn
wound margin
Fig. 5.5B: Another patient with streptococcal erythema
involving unburnt skin of chest and abdomen

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Fig. 5.8A: Streptococcal wound infection indicated by the
hemorrhaghic bullae forming after removal of dressing
because of excessive bleeding from the granulation tissue.
Since streptococcus is still sensitive to penicillin, it responded
well to systemic penicillin
Fig. 5.8B: The granulation improved and patient was taken
up for grafting. One month postoperative picture of same
patient
Fig. 5.6: Patient in gram-positive sepsis throwing septic
emboli causing bilateral gangrenous changes in distal foot
Fig. 5.7: Burn wound showing the various signs of wound
infection, i.e. superficial wound getting converted to deep
wounds, black or dark brown focal areas of discoloration,
increasing eschar thickness, increasing inflammation and
edema of adjacent normal skin

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Fig. 5.9C: Patient responded to the treatment and the eschar
got separated gradually leaving behind granulation tissue
requiring skin grafting
Fig. 5.9D: Patient recovered completely following grafting
of the wounds
Fig. 5.9A: Superficial dermal wounds after 8 days post-
burn showing black psuedoeschar formation, inflammation
of surrounding skin with high grade fever, vomiting and
diarrhea indicating gram-negative sepsis converting the area
to deep wounds. Wound culture showed growth of Klebsiella
Fig. 5.9B: Patient was put on higher antibiotics and dressings
changed to nanocrystalline silver dressings for continous
delivery of silver ions

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Fig. 5.10: An old diabetic patient presenting with synergistic
gangrene of abdominal wall following uncontrolled burn
wound infection. The chest wall and abdominal muscles are
totally necrosed leading to exposure of underlying structures.
The patient eventually died
Fig. 5.11A: Apparently healthy granulation tissue in a
30 percent burns patient with no growth on wound swab
culture
Fig. 5.11B: Patient was taken up for skin grafting of
all areas
Fig. 5.11C: All the grafts appeared to be taken up well
till a week

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Fig. 5.11D: On third dressing (8th day) the initially taken
up graft showed islands of eaten up areas in the chest
indicative of staphylococcal infection
Fig. 5.11E: Topical antistaphylococcal antibiotic in the
form of mupirocin was started
Fig. 5.11F: In subsequent dressings the edges of the eaten
up areas appeared to be receding instead of spreading as in
a normal graft take, hence systemic antibiotic was also started
Fig. 5.11G: Three months postoperative picture. The
wounds responded to the treatment and further graft loss
could be avoided. The remaining graft eventually spread to
cover the entire raw area

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Fig. 5.12B: However, on 8th day patient developed high
grade fever and on inspection of wound there were signs of
wound infection as seen in the picture
Fig. 5.12C: Patient developed severe sepsis and went into
ARDS as seen in the X-ray
Fig. 5.11H: Hands of the same patient showing well
settled grafts with minimal hypertrophy
Fig. 5.12A: 12-year-old presenting with electrical flash and
contact burns. All areas are superficial dermal burns which
are expected to heal in 7 to 10 days (Courtesy: Dr N Jithendran,
Global Hospital, Hyderabad, Andhra Pradesh, India)

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Fig. 5.12D: Patient was taken up for debridement and there
was subeschar pus collection which was the cause of fever
Fig. 5.12E: The wounds after debridement of
all infected tissue
Fig. 5.12F: Patient immediately after grafting of the wounds
Fig. 5.12G: One-month postgrafting with
all wounds healed

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Fig. 5.13A: Patient with extensive burns presented with
necrotic patches in region of upper and lower lip (dangerous
areas of the face), edema of face and eyes, high grade fever,
headache and vomiting. These are indicative of sepsis and
there is a high probability of cavernous sinus thrombosis
with these findings which needs to be ruled out with a CT
scan brain. Prompt and vigorous treatment in the form of
higher antibiotics and other supportive treatment can only
save the patient
Fig. 5.13B: Septic thrombi in the same patient leading to
black discoloration of foot and lower leg with blistering of
the skin, finally ending in gangrene of the foot
Fig. 5.14A: 2-year-old child in sepsis with thick black
eschar over the entire burnt area
Fig. 5.14B: Patient treated with combination of higher
antibiotics and patient’s general condition improved and the
eschar gradually separated with healing of wounds at places
and granulation tissue appearing at places which were later
grafted

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Fig. 5.15: Hemorrhagic fluid filled blister in leg in a
patient in gram-negative sepsis
Fig. 5.16: Severe necrotizing fasciitis of the entire back in a
2-month-old infant with gradual separation of the eschar
Fig. 5.17: Full thickness circumferential burns of arm in a
3-year-old child who presented with separation of eschar in
burned area and extending necrotizing fasciitis in the non-
burned skin of shoulder and chest
Fig. 5.18A: Patient with 65 percent thermal burns developed
gram-negative wound infection 7 days post-burns. Greenish
discharge in the dressing and greenish yellow staining of the
eschar typical of Pseudomonas aeruginosa growth

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Fig. 5.18B: Close-up view of the abdomen of the same
patient showing the infective changes in the wound
Fig. 5.18C: Same patient went into septic shock and had
to be put on ventilator support
Fig. 5.18D: Close-up view of the thigh wounds showing
the blackened secondary eschar beginning to separate
Fig. 5.18E: Wounds of the other thigh showing infected
pseudoeschar in a stage of separation

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Fig. 5.19A: Burn wound extension following infection in
superficial burns in a severly anemic patient. Extension can
be seen going deeper to subcutaneous fat till the deep fascia
in the anterior thigh. This type of presentation is typically
seen in case of Pseudomonas infection which evolves from
intraeschar colonization to subeschar invasion. Pseudomonas
produces enzymes and other metabolic products and have
flagella which enhance their potential for invasion and rapid
spread
Fig. 5.19B: Posterior aspect of the thighs and legs of the
same patient showing separation of neoeschar following
treatment of wound infection but the underlying bed is still
not healthy as can be seen by the eaten up appearance of
the entire wound indicating a high colony count
Fig. 5.19C: Two weeks after conservative management the
wounds started to granulate and eventually became fit for
grafting
Fig. 5.20A: Bluish black necrotic skin patch in the tip of
the nose with edema in the eyelids in an otherwise healed
facial burns indicating septic embolization

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Fig. 5.20B: Typical satellite lesion in healed skin on dorsum
of hand in the same patient indicating that patient has gone
into sepsis
Fig. 5.21A: Gram-negative sepsis in a child presenting with
high grade fever, watery diarrhea and vomiting. Wound shows
signs of infection. Culture of wound was positive for multi-
drug resistant Pseudomonas. Burn wound deepening in the
form of psuedoeschar formation with signs of inflammation
in the surrounding normal skin can be seen
Fig. 5.21B: The wound dressing was changed over to
sulphamylon cream and for MDR Pseudomonas,
colistimethate sodium was started in combination with
imipenem as per sensitivity report. The general condition
improved and the pesudoeschar started drying and separating.
The signs of inflammation also subsided
Fig. 5.22: Seven days post-burn picture showing beginning
of bacterial invasion in form of multiple small hemorrhagic
spots which gradually confluence together ultimately forming
a pseudoeschar. This is the first sign of wound invasion and
aggressive management should be started immediately in
the form of change of local antimicrobial as well as higher
antibiotics to stop the further progression of wound infection

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Fig. 5.24: Macular rash over face in a 30 percent TBSA
burns child starting on the 10th day post-burn indicating
measles infection
Fig. 5.25A: Patient in fungal sepsis—the wounds appear
pale, edematous, nongranulating with exposed cheesy yellow
subeschar tissue following the debridement of the eschar.
There was no response to different combinations of higher
antibiotics. The wound biopsy showed Candida albicans.
Patient was started on antifungal therapy and responded
well
Fig. 5.25B: Healthy granulating wound after 2 weeks of
antifungal treatment
Fig. 5.23: Five-year-old child being treated for 5 percent
superficial burns with collagen dressings developed vesicular
lesions all over the body indicating varicella zoster infection

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Fig. 5.26A: Case of 60 percent electric contact and flash
burns with about 20 percent full thickness burns, developed
stress induced diabetes which remained undetected as initial
blood sugar levels were normal. He was taken up for grafting
of the deeper areas after excision but developed invasive
chest wall mucormycosis in the skin grafted site (Courtesy;
Dr N Jithendran, Global Hospital, Hyderabad, Andhra
Pradesh, India)
Fig. 5.26B: Same patient went into septicemic shock with
severe metabolic acidosis, hypotension and acute renal failure.
He was put on antifungal treatment, ventilator support,
peritoneal dialysis and insulin for stress induced diabetes
Fig. 5.25C: Same patient after first sitting of skin grafting
of the wounds
Fig. 5.25D: Two months after second sitting of skin
grafting of same patient with completely healed wounds

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Fig. 5.26C: Emergency surgical debridement was done
followed by latissimus dorsi flap cover
Fig. 5.26D: Skin grafting over the muscle flap was done in
second sitting and wound healed completely in 15 days
Fig. 5.26E: The patient made full recovery, renal function
returned back to normal and stress induced diabetes resolved
completely

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Fig. 5.27D: Twenty-four hours after second debridement
and amputation of the leg, invasive fungal growth was found
in the stump. KOH staining showed fungal hyphae and a
culture was then sent
Fig. 5.27A: Case of 10-day-old electrical contact burn treated
outside presenting late with extending myonecrosis (Courtesy:
Dr N Jithendran, Global Hospital, Hyderabad, Andhra
Pradesh, India)
Fig. 5.27B: Radical excision of wound was done, all
adductors were found necrotic and were excised exposing
the femoral vessels
Fig. 5.27C: On second debridement the necrosis was found
to be extending and therefore decision for amputation of the
limb was taken

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Fig. 5.27E: Close-up view showing fungal growth.
Unfortunately patient could not be saved
Fig. 5.28: Septic thrombophlebitis all along the length of
the great saphenous vein following venesection, with localized
abscess formation in middle third of leg. This abscess requires
drainage along with removal of the long segment of involved
superficial vein
Fig. 5.29: Another patient who developed superficial
thrombophlebitis following venesection in great saphenous
vein followed by cellulitis and increasing edema of the leg as
well as the thighs and acute tenderness in the calf indicating
involvement of the deeper veins. Color Doppler revealed
thrombosis of the long segment of femoral vein. The
involvement of deeper vein was retrograde from the
saphenofemoral junction. Treatment includes systemic
antibiotics for control of infection along with heparin and
other supportive treatment
Fig. 5.30: Another patient with septic thrombophlebitis along
the whole length of the lower limb with multiple necrotic
patches in the line of GSV. The septic focus should have
ideally been removed before abscess formation and necrosis
of skin by excision of the entire length of the vein and this
could have prevented such a severe form of presentation

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Fig. 5.31A: A case of 40 percent thermal burn in whom a
central line cannulation was done through the left femoral
vein. Patient was cured of burns and discharged at 3 weeks
but readmitted after 1 week with pain and edema of left leg
and two episodes of bleeding from the cannulation site
Fig. 5.31C: However, the swelling increased rapidly in size
and subsequent angiography revealed a leaking aneurysm
for which he was transferred to vascular surgery ward for
further management of the leaking aneurysm
Fig. 5.31B: Close-up view of the cannulation site of the
same leg showing puncture wound over a pulsatile localized
swelling in the region of the groin. Color Doppler showed a
aneurysm in the femoral artery in the region of the groin and
conservative management was advised by the vascular
surgeons

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Fig. 5.32: Necrotizing fasciitis developing in upper thigh of
a 2 months post-burn patient in whom all burnt areas had
healed except for a 1 percent raw area on the posterior aspect
of the same thigh
Fig. 5.33: Undetected extravasation of hypertonic fluids
causing blistering followed by skin necrosis at the IV drip
site. Therefore, all hypertonic fluids should be infused through
central lines and not peripheral lines
Figs 5.31D and E: Angiographic picture of the same patient showing the contrast leaking through
the pseudoaneurysm in femoral artery
D
E

Electric Burns 6

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EFFECT OF ELECTRICITY ON THE HUMAN BODY
Organ
Response of organ to electricity
Effect of electricity on organ
1. Skin
Dry skin provides resistance to current
Thermal burns
flow and converts electrical energy to
heat energy
Wet skin allows passage of current.
Local damage is minimal
2. Muscle
Allow current to flow because of their
Tetanic spasm of skeletal muscle
water content
Separation and rupture of cells
Release of myoglobins
3. Peripheral
Least resistance and maximum
Demyelinization
nerves
transmission
Rupture of axons
Nerve function impaired because of
coagulation of their nerves
Thermal burning of fibers
4. Central
Low resistance to current passage
Stimulation followed by depression
nervous
when the blood vessels of the white
system
matter coagulate
Rupture of reticular system
5. Spinal cord
Low resistance to current
Direct injury
Rupture of ascending and descending
tracts
Thrombosis of arteries of spinal cord
6. Eyes
Low resistance
Injury to cornea and lens
Cataract formation because of
ossification of proteins
7. Lungs
High resistance due to air filled alveoli
Loss of surfactant
Direct damage to pleura by contact
8. Liver
Low resistance
Rupture and thrombosis of portal system
9. Intestine
Low resistance
Direct injury or thrombosis of mesenteric
artery or vein
10. Kidney
Low resistance
Direct thrombosis of renal vessels
Blockage of renal tubules by myoglobins
11. Heart
Good conductor
Fibrillations ST and T wave changes
12. Peripheral
Intimal damage in the form of
blood vessels
Good conductors
vacuolation and separation of intimal
layers
Thrombosis of veins followed by
thrombosis of arteries
13. Bones
Maximum resistance
Damage is due to conversion of electrical
energy to heat

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Fig. 6.1: Postelectric (low voltage) burn deformity of mouth.
Oral cavity burns are mostly seen in infants and toddlers
when they try to explore the wire by taking it into their mouth
and chewing it with the gum and newly erupting teeth. Healing
of these burns usually ends in microstomia
Fig. 6.2: Arcing of current or jumping of current from wrist
to elbow to axilla following high voltage contact burns from
the hand. As the current flows through the vessels, at the
wrist, elbow and axilla, the vessels become superficial and
current transmitted through them to the overlying skin
produces heat due to resistance offered by the skin, thus
leading to full thickness skin damage at these points. In the
intervening areas because the vessels are deep and
surrounded by muscle mass, the overlying skin does not get
damaged
Fig. 6.3: Fourth degree high voltage contact injury causing
autoamputation at the level of distal forearm because of
total destruction of all structures in the forearm and complete
destruction of the bone matrix
Fig. 6.4: Complete destruction of wrist after contact with
high tension wire. The hand is completely devascularized
making amputation at wrist mandatory. A fasciotomy
incision is given in the proximal arm to relieve the
compartment pressure and prevent proximal extension of
the damage

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Fig. 6.5: High voltage current causing primary dry gangrene
of hand and forearm because of primary arterial thrombosis
of supplying vessels, with arcing at elbow and axilla causing
full thickness burns over them. Note the flexed attitude of
the hand which is due to the tetanic contraction of the forearm
muscles
Fig. 6.6: High voltage injury through contact in hand with
gangrene of hand and full thickness circumferential burns in
wrist with edema in proximal limb requiring fasciotomy to
relieve the pressure in the proximal arm so as to reduce the
level of amputation
Fig. 6.7: Entry wound due to high voltage contact injury in
the palm. It appears as a whitish yellow area with a markedly
depressed central zone surrounded by hyperemic border.
Fingers show normal circulation but since there are
circumferential deep burns in forearm and passage of current
through the muscles of forearm it is likely to lead to
compartment syndrome. Therefore, in these cases, early
fasciotomy is mandatory to save the hand. Late fasciotomy
on the other hand can cause release of pent up myoglobins
from the dead muscles into the circulation, thereby leading
to blockage of renal tubules and hence acute renal failure
Fig. 6.8: High voltage contact burn through index finger
with normal vascularity of whole hand except the index finger
which is gangrenous. Arcing effect has caused a full thickness
burn over the entire wrist and proximal forearm. In these
cases, urgent flap cover can only save the underlying structures
by reducing the venous congestion and preventing further
damage

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Fig. 6.9: Contact with high voltage current leading to
gangrenous changes in ring finger and little finger because of
primary thrombosis of ulnar artery and palmar arch on ulnar
side
Fig. 6.10: Electric contact burn in hand with damage
extending to wrist and distal forearm in the form of
circumferential full thickness burn leading to gangrene in
lateral 2/3 of hand due to primary thrombosis of radial artery
and palmar arch on radial side, but circulation apparently
appears normal in medial 1/3 of hand and fingers
Fig. 6.11A: High tension injury to hand with fasciotomy incision
given all along the arm laterally which was showing signs of
compartment syndrome. Tissues under the fascia appear normal but
with thrombosed veins. The hand however shows no signs of surviving

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Fig. 6.11B: Fasciotomy incision on medial side of arm
and forearm
Fig. 6.12A: Another patient with contact injury in hand
leading to flexor spasm in all fingers except index finger due
to tetanic contraction of flexor muscles. The entry wound
was at the base of index finger causing direct damage to the
flexor tendons thereby sparing the index finger from going
into flexion.The hand is not salvageable
Fig. 6.12B: Fasciotomy incision given in forearm and
muscles in the proximal forearm are edematous but show
normal vascularity but deeper structures in distal forearm
and wrist show lack of circulation which is not improved
after fasciotomy also. This gives a fair idea about the level
of amputation required
Fig. 6.13: Two exit wounds on plantar aspect of foot seen
as a ruptured tanned black area because of explosive release
of heat due to high voltage current coming out. Only the
area which is firmly in contact with the ground, i.e. the heel
and the head of first and second metatarsal show the exit
points of the current and the non weightbearing areas like
the instep area is spared

Electric Burns
135
Fig. 6.14A: 10-year-old boy who accidentally walked over
a high tension cable wire in which entry was through feet
show bilateral gangrenous feet in plantar flexion with extensive
necrosis of all structures above the ankles. There are deep
dermal burns in the rest of the leg and posterior thighs
Fig. 6.14B: Close-up view showing one of the foot is
partly amputated above ankle
Fig. 6.14C: Even though the legs appeared normal initially
in the same patient, he required a guillotine amputation at
the level of the knee. In electric burns, the damage is usually
progressive and extends much beyond the apparently
damaged skin so that amputation is usually done at a higher
level than what was initially anticipated. First stage of skin
grafting has been performed in the picture in the raw areas
of the stumps and posterior thighs
Fig. 6.14D: Two months postoperative picture showing
complete healing

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Fig. 6.15A: 10-year-old child sustained high tension injury
due to accidental fall of 11,000 V cable on her while
playing—entry wound in skull with loss of both tables and
brain matter coming out of the wound. These patients are
usually not salvageable
Fig. 6.15B: 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. 6.16A: Fourth degree burns due to electric contact injury
by 11,000 V wire in posterior arm and side of chest with
severe necrosis amounting to charring of all muscles of the
arm and chest exposing the humerus and ribs. In the first
look, it appeared that a life saving amputation of the arm at
shoulder level would be required
Fig. 6.16B: Anterior aspect of arm and chest of same patient
showing only a strip of skin was spared anteriorly in the arm.
The plan was to take up the patient for debridement and
flap cover with consent for amputation if required. However,
the patient’s general condition was never fit for such a major
surgery

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137
Fig. 6.16C: A fasciotomy incision was given in the forearm
because of compartment syndrome even though the
vascularity and skin of forearm was normal
Fig. 6.16D: The patient was thereafter managed
conservatively and surprisingly after the dead tissue was
debrided serially the wounds granulated in the upper arm
and chest
Fig. 6.16E: One month postgrafting for the same patient
showing all wounds healed except only a small portion of
humerus and rib was exposed
Fig. 6.17A: Case of high tension injury with gangrene of
both upper limbs requiring shoulder amputation. But prior
to amputation, the subclavian vessels have to be ligated via
supraclavicular approach in order to avoid a blowout from
the tied axillary vessels in the involved area later on

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Fig. 6.17B: Supraclavicular approach with marking of
the clavicle and vessels
Fig. 6.17C: Ligation of subclavian vessels after division
of clavicle for a better approach
Fig. 6.17D: Same patient postamputation
Fig. 6.18A: Low voltage wire contact injury over back
and side of neck showing a deep burn

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Fig. 6.18B: Patient managed conservatively, wounds healed
but patient developed severe hypertrophic scarring. Ideal
treatment would have been excision and skin grafting
Fig. 6.19A: Myoglobinuria following electric contact burns
indicated by reddish brown urine which requires vigorous
resuscitation in order to avoid blockage of renal tubules by
the myoglobins which can lead to acute renal failure
Fig. 6.19B: Gradual improvement in both color and quantity
of urine with proper resuscitation, osmotic diuresis and
alkalanization of urine
Fig. 6.20A: Contact injury on face by wire falling accidentally
causing deep injury on nose, left eye and cheek

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Fig. 6.20B: One week later picture shows necrotic nasal
bones, left maxilla and loss of left eye
Fig. 6.20C: Three months postoperative picture after
debridement of dead tissue and laterally based forehead flap
given to cover the defect. Cataract is also seen developing in
the contralateral eye
Fig. 6.21A: High voltage contact injury in the lateral side
of the neck. All neck muscles in the affected area, i.e.
trapezius, strap muscles, sternomastoid are dead which can
cause exposure and blow out of carotid vessels
Fig. 6.21B: After debridement of all dead muscles,
pectoralis major muscle is dissected and raised

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Fig. 6.21C: Pectoralis major muscle transposed into the
defect gives a good vascular cover over the vessels thus
avoiding a fatal complication
Fig. 6.21D: One month postoperative picture of
the same patient
Fig. 6.22A: Deep contact burns in axilla. If left for
conservative management, as the dead muscles slough out,
the axillary vessels can get exposed and chances of blow out
are high so early vascular flap cover is necessary
Fig. 6.22B: Pectoralis major transposed to give vascular
cover in another case involving deep burns in axilla and arm

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Fig. 6.23A: Another case with very deep contact burns in
axilla and upper arm which was managed conservatively
initially
Fig. 6.23B: After the eschar and dead muscles sloughed
out the underlying wound granulated but the axillary vessels
were also exposed
Fig. 6.23C: Parascapular flap cover given over the axillary
neurovascular bundle and rest of the area was grafted
Fig. 6.24A: Full thickness burns over wrist following
contact with current in palm

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Fig. 6.24B: Thrombosed vessels following early debridement
of electrical burn wound at wrist and lower forearm. Since
the veins are in superficial plane they tend to get involved in
circumferential deep burns around the wrist. Early
debridement and distant pedicled flap cover not only provides
cover for exposed tendons and nerves but also helps in
providing alternative venous channels which help in preventing
secondary damage due to venous congestion
Fig. 6.24C: Exposed tendons and nerves of same patient
covered by groin flap: Six months postoperative picture
Fig. 6.25A: Entry wound in fingers following contact with
high voltage line causing gangrene of ring finger and full
thickness burns over palmar aspect of other fingers and thumb
and over the wrist due to arcing
Fig. 6.25B: Following early debridement of all dead tissue,
the tendons and neurovascular bundles are exposed in the
wrist as well as the fingers

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Fig. 6.25C: Groin flap used to give cover the wrist defect
and prepucial flap for cover over the fingers. Prepucial flap
is a discovery from the author’s unit and is used extensively
as an adjunct to groin flap in cases where more than one
flap is required in upper limb
Fig. 6.25D: Two months postoperative picture of the same
patient. Prepucial flap provides a very thin skin cover which
is excellent for palmar aspect of hand and fingers
Fig. 6.26A: Falling of high tension wire on head leading to
small defect in scalp exposing outer cortex of skull. CT scan
showed intact inner cortex
Fig. 6.26B: Rotation flap done primarily to cover the
exposed skull