Burns

Local and general surgical disease

Multiple vulnerable agents

Evolution stage Prognostic - local lesion

amplitude
- severity of
complications
- precocity of the
treatment
IOB 2015
 Introduction - Burn Injuries
1.25-2 million Americans treated for burns annually
50,000 require hospitalization
3-5% considered life threatening
2nd leading cause of death for children <12
Half of all tap-water burns occur to children < 5

Greatest risk
Very young & very old
Infirm
Firefighters
Metal smelters
Chemical workers
 Anatomy & Physiology of the Skin
Adult skin surface 1.5-2.0 m2 (0.2-0.3 in newborns); largest organ
Skin thickness 1-2 mm; peaks age 30-40; M> F

Epidermis Dermis
Layers Elastic connective tissue
Outer layer
-stratigraphy Top (stratum corneum) Contains specialized
consists of dead, hardened structures
cells Nerve endings
Epidermis
Lower epidermal layers Blood vessels
Dermis Sweat glands
form stratum corneum and
Subcutaneous contain protective pigments Sebaceous (oil)
glands
Underlying
Hair follicles
Structures
Fascia
Nerves Subcutaneous/Muscle
Tendons Fat (protective layer)
Ligaments Muscle for support,
Muscles movement,
Organs coordination
 Anatomy & Physiology of the Skin
Skin Functions - the largest organ of the body
Barrier against infection
Sensory organ
Temperature
Touch
Pain

Prevention of fluid loss by evaporation -maintenance of

fluid/electrolyte homeostasis
Thermoregulation
Protection against environment provided by sensory
information
Immunologic function
Metabolic organ (i.e., Vit D synthesis)
 Types of Burn Injury
Pathophysiologic point of view

Thermal
Chemical
Electrical
Radiation
 Thermal Burns
Caused by the action of physical agents that transmit
heat energy to skin and tissue
dry heat (flame) - the most common cause of the
thermal burns 37%
hot liquids (water, oil, producing large burns,
irregular, variable depth in relation to temperature
and degree of viscosity)
gas and superheated steam as a result of explosions
(boilers, bombs)
other flammable materials, caloric radiation (solar,
ultraviolet)
incandescent solids (molten metal, coal, producing
limited area burns, but deep burns, with eschars
viscous molten substances (bitumen, wax)
The causative agent of the injury affects both the prognosis and the treatment
Heat changes the molecular structure of tissue

The main effects of the heat induced in the skin

are:
enzymatic degradation more than 46 C
coagulative necrosis and caramelization of
carbohydrates more than 100 C
carbonization at 600 C
calcination at above 1000 C

Temperatures above 80 C are rapidly fatal by

proteins cell coagulation
 Thermal Burns
Extent of burn damage depends on :
Thermal Gradient temperature difference between the
tissue and the vulnerable agent
Temperature of agent
Concentration of heat
Duration of contact

Main criterions for clasification of burns :

area (%)
depth (I,II,III,IV)
severity (units)
Threshold depth in relation to:
injury of the vascular plexus of skin
skin regeneration possibilities

Three thresholds:
- germinative basal layer of the epidermis which is irrigated by
dermal capillary superficial plexus - Basal membrane is not
harmed, making it possible to "restitutio ad integrum" -
epithelialization regardless of the cellular damage
- dermal layer contains intermediate capillary plexus, hair follicles
and sweat gland ducts (epithelialization resources)
- deep dermal layer with deep dermal capillary plexus, glomeruli
sweat glands
 Classification of burns according to the depth - 4 degrees of depth

Gr I - I stage epidermal burn

hyperemia and edema by
- lesions of keratin cells and
pellucid
- irritation of intraepithelial nerve
endings
Gr II II stage dermal superficial
burn blisters containing serous fluid
- destruction of epidermice
layer+ plasma extravasation
Gr III III stage dermal deep burn -
blisters containing sero hemorrhagic
fluid
- epidermis + dermis + destroy
intermediate capillary plexus
Gr IV - IV stage under fascia burn
- necrosis - by destroying
completely dermis and epidermis
 Jacksons Theory of
Thermal Wounds extension of area
burns
Zone of Hyperemia

Zone of Stasis

Zone of Coagulation
Local lesion burning - at this level, produce fluid
leaks out (plasmoragy) both circulating mass and
interstitial spaces. Its describe (in terms of anatomical
pathology) three concentric zones:

I. Zone of Coagulation (burning wound area ) : devitalized,

necrotic, white, no circulation
irreversible damage by heat effect of all structures, including
capillary
capillary blood flow absent
depth is determined by the temperature and duration of exposure

.
II Zone of Stasis : circulation ,sluggish, may covert to full thickness,
mottled red
capillary blood flow slowed
major tissue damage, but not irreversible
vascular occlusion by microthrombosis may occur, with secondary
enlargement of injuries

III. Zone of Hyperemia, in peripheral area :

dynamic and hyperpermeability capillary disorders
fluid extravasations
release of specific mediators of inflammation
Superficial Burn:
1 st Degree Burn
- involves only the upper layers of the
epidermis It is an irritation of the living cells
in this region and results in some pain,
minor edema, tenderness, and erythema
- typical, sunburn - a very superficial
lesion, also UV light, mild radiation
- tissue will blanch with pressure, possible
mild swelling, no blisters

- symptoms disappear in 24-48

hours , expect peeling in a few days and
discreet pigmentation (by stimulating
melanocytes)
- heals in 3-6 days- generally no scaring and
require only local wound care
Partial-Thickness Burn: 2nd
Degree Burn
- affected all layers of the epidermis, even
some germinal cells in the basal layer, but
basal lamina remains intact
- sebaceous glands, sweat glands and
pilosebaceous unit unaffected; all of these will
form epithelialization islands that will promote
healing
- blistering second degree by subdermal
vascular plexus damage and important plasma
extravasation : content sero-citrine fluid, never
haemorrhagic
-septic risk, due to the opening of the
sebaceous glands and sweat ducts in closed
environment, non-aerated, of the blistering
- per primam healing, impaired pigmentosa,
without sequelae in approximately 14 days
Full Thickness Burn (Third degree) -
fully involve the epidermis and dermis in
varying degree, without to overcome
III 1) The burn affects only the upper dermis
(served by intermediate dermal capillary
plexus)
- damaged tissue thickness is not too big
and edema fluid hydraulic force can deploy,
forming blisters Grade III: sero-
hemorrhagic content or bloody franc due to
destruction of the capillaries in the dermis;
- hair follicles and sweat gland ducts are
destroyed and there are no epithelial
barrier Healing is secondary ("per
secundam intentionem) by
III 2) Burning destroys almost completely
eccentric proliferation of
dermis respecting only one blade deep
piloglandular stumps
dermal (served by deep dermal capillary
(epithelialization lasts more than
plexus)
three weeks), , creating scars (often
- affected tissue layer is too thick, it can
vicious) and installation of major
not force hydraulic lift to form an
functional sequelae
Intradermal blistering, appears an eschar
thin, elastic and hydrated white Nerve endings destroyed - little
or no pain
Full thickness Burn (4th degree) - damage to the
entire thickness of the skin (epidermis and dermis
in full) and even deeper tissues (subcutaneous fat,
fascia, muscles)
- the wound resources of epithelialization are
destroyed, "restitutio ad integrum" is impossible
- eschar lesion is characteristic of the fourth
degree (white or brown)
a. eschar soft white: the background of intense
edema, which can lead to ischemic, in inextensibil
regions between fascias, in extremities
b. eschar bear, brown (brown, dark red or black) as
a result of tissue coagulation complete
Spontaneous evolution I of 4th degree lesions is to
repair only marginal proliferation, concentric slow,
retractile scars or keloids leaves deep,
dysfunctional and mutilating.
Spontaneous epithelisation is theoretically possible
only if the distance between the wound edges is
less than 5 cm. Healing is possible only by skin
grafting, often complicated with sequelae.
 Burns prognosis depends on
multiple factors

Extent of Burns
Depth of Burns
Location of Burns
Age of patient
Possible complications of the burn
State of health of the patient prior to the
accident
Location of the trauma associated
(particularly lung lesions)
Earliness and quality of treatment
Burned area is expressed as a percentage of total
body surface - Calculation of Burned Body Surface Area

Rule of Nines 9 Wallace

Rapid assessment tool for large
burns extension - Easy to remember,
quick method

Rule of Palm
Good for estimating small patches
of burn wound < 10% BSA
A burn equivalent to the size of
the patients hand is equal to
1% body surface area (BSA)
 Rule of Nines 9 Wallace
4 .5
4 .5 Head & Neck = 9%
Each upper extremity
18 18 (Arms) = 9%
9 9 Each lower extremity
1
4 .5 4 .5 4 .5
(Legs) = 18%
18 18 Anterior trunk= 18%
9 9 9 9 1

7 7 7
Posterior trunk = 18%
Genitalia (perineum) = 1%
Prognostic index = surface area burned % x depth
P.I. under 40 : evolution
ofisburn (grade)
without shock, without complications,
survival is the rule
P.I. between 40-60 : general phenomena are mandatory, post-
combustion shock occurs, complications can begin to appear, but
survival and cure are the rule
P.I. between 60-80 : complicated cases are equal to those
uncomplicated; complications can cause serious conditions, even
deadly; cure and survival remain the rule
P.I. between 80-100: complications are the majority and deaths
occur, but healing outnumber deaths
P.I. between 100-140: Complications are usually chronic shock
occurs and the number of deaths increases
P.I. between 140-160: deaths are equal or exceed the healings, that
are sequelae
P.I. over 160 : survival and cure are very rare
P.I. over 200: cure and survival are exceptional
 Quick Evaluation of Burn Injury - The American
Burn Association (ABA) describes burns as minor,
moderate,
MINOR BURNS or major depending on the depth,
Deep partial-thickness burns <15% TBSA Full-thickness burns <2% TBSA No
extent,
burns of eyes, ears, face, and
hands, feet, location
or perineum No electrical burns No
inhalation injury No complicated concomitant injury
Patient is under 60 yr and has no chronic cardiac, pulmonary, or endocrine
disorder
MODERATE BURNS
Deep partial-thickness burns 15%-25% TBSA Full-thickness burns 2%-10% TBSA
No burns of eyes, ears, face, hands, feet, or perineum No electrical burns No
inhalation injury No complicated concomitant injury
Patient is under 60 yr and has no chronic cardiac, pulmonary, or endocrine
disorder
MAJOR BURNS
Partial-thickness burns >25% TBSA
Full-thickness burns >10%
Any burn involving the eyes, ears, face, hands, feet, perineum
Electrical injury
Inhalation injury
Client over 60 yr of age
Burn is complicated with other injuries (e.g., fractures)
Client has cardiac, pulmonary, or other chronic metabolic disorders
 Burns more than just another soft tissue injury
Pathophysiology of Burns - a series of physiological
disturbances, whose intensity depends on the severity
of aggression and functional reserve of the body, local
and general level

Local disturbances - vasodilatation

(Jacksonian phenomena ) - edema
- blood suffusions
- small vessels
thrombosis

coagulation necrosis + eschars

sealing burn
 Burns more than just another soft tissue injury

The tissue destruction caused by a burn injury can

cause many local and systemic problems, including fluid
and protein losses, sepsis, and disturbances of the
metabolic, endocrine, respiratory, cardiac, hematological,
and immune systems. Complex of these disturbances is
called burn disease

Burn disease
appears in case of burns of more than 10-15% of body area in
adults and 5-7% in children
Burn shock (24-72 hours and more)
Acute burn toxemia
Burn septic toxemia (lasts till the all wounds will be closed
by autografts)
Changes From Burn Injury include:
Cardiac / Pulmonary / GI (Curlings ulcer)/ Metabolic /
Immunologic
Clinical signs of shock burn - several syndromes,
confounding and amplifying each other

A. Circulatory Syndrome:
hypovolemia
haemoconcentration
hemodynamic disturbances

Circulatory disruption occurs at the burn site immediately after a burn injury, blood
flow decreases and blood vessel thrombosis may occur, causing necrosis
FLUID SHIFT - Occurs after initial vasoconstriction, then dilation - blood vessels
dilate and leak fluid into the interstitial space ( known as third spacing or
capillary leak syndrome) - causes decreased blood volume and blood pressure -
Occurs within the first 12 hours after the burn and can continue to up to 36
hours
FLUID IMBALANCES - Occur as a result of fluid shift and cell damage
Hypovolemia, Metabolic acidosis, Hyperkalemia, Hyponatremia -
Hemoconcentration (elevated blood osmolarity, hematocrit/hemoglobin) due to
dehydration
The vascular capillary response to burn injury
- fluid shift (capillary leak syndrome)
POSTBURN BLOOD
NORMAL BLOOD CAPILLARY
CAPILLARY

Water molecule Protein molecule

Water is the smallest molecule

that can pass through the Permeability is increased, which
capillary pores. allows large molecules such as
proteins to pass through the
capillary pores easily.
 Clinical signs of shock burn
B. Respiratory syndrome dominated by
phenomena of hypoxia :
hypoxic hypoxia caused by lack of oxygen
anemic hypoxia - by reducing the number of oxygen-
carrying red blood cells
histotoxic hypoxia - caused by substances reabsorbed from
the burning area

Pulmonary Changes
Respiratory failure
Inhalation injury
Sloughing
Pulmonary insufficiency and infection
 Clinical signs of shock burn
C. Hematologic syndrome, initially masked by
hemoconcentration consecutive extravasation of
fluid includes:
anemia
leukocytosis
decreased platelets

D. Metabolic syndrome :
affecting all sectors of intermediary metabolism
metabolic acidosis caused by hypoxia
immediate postagresiva phase, catabolism predominates, with
high consumption of energy reserves, high fluid loss and
severe malnutrition that will shock the chronic phase
Increases metabolism
Caloric needs double or triple depending on the extend of injury.
Increased core body temperature
 Clinical signs of shock burn

E. Neuroendocrine Syndrome :
initial effects of hypovolemia compensation - increased
release of catecholamines (adrenalin and noradrenalin),
ACTH and glucocorticoids
subsequent depletion phenomena release ADH, thyroid
hormones and aldosterone

All these initial neuroendocrine changes

rebounds on:
circulation (tachycardia, hypertension)
breathing (tachypnea, hipercapnee)
renal function (oliguria, glycosuria)
 Clinic of burn shock

Central
nervous
system
disorders
(exaltation,
depression)

acute cardio-vessel
insufficiency main Restrictive
reason of death respiratory
(develops during 1-2 insufficiency -
hours) hypoxia
Slow or no gastric motility.
Concentration Decreased bowel sounds. Abdominal
distention Nausea and vomiting
of blood, hyper Beginning ulceration of
gastrointestinal mucosa.
coagulation, Translocation of microorganisms to
DVS on 2-3 day vessels

In urine Generalized
cylinders,its edema
dark red,
anuria
Progress of the postagresive reaction
in severe burns
Post-combustion shock installed
at more than 15% area burned,
is franc to 25%, and is serious to
50% of the surface, when may
appear death

Evolution course : 4 Stage

Stage I During the first 3 days

(1-3 days) (post-combustion
shock) or the immediate
postagresive period

The period of postcombustional shock

and possible organ insufficiencies,
and its end, if evolution is favorable,
the patient should be afebrile and
vital functions restored
Pathogenesis of the development of burn
shock

traumatic

hypovolemic

hypercoagulative
pain
 Stage I
The main causes of shock are:
hypovolemia (fluid loss from the burn area)
hypoxia (hypoxic, anemic, stasis and cytotoxic)
pain (intense in I-II degree burns, less the ones lll
degree and even absent in the IV degree, due to
destruction of dermal nerve endings)
superinfection injuries (always possible II-III degree
burns)
toxins present in the bloodstream
increased levels of catecholamines (increased
catabolism and energy deposits depletion)
Major clinical signs characteristic of
Stage I:
large electrolyte losses (thirst)
respiratory failure (dyspnea, tachypnea, hypoxia
phenomena)
anemia
cardiovascular disorders (tachycardia, hypotension,
arrhythmia)
neurological signs due to hypoxia (agitation or
sleepiness)
digestive disorders (nausea, vomiting)
oliguria
Stage II. During the first three weeks (4-21
days) (metaagresive dysmetabolic period) -
intense metabolic disorders caused by a
continuous catabolism, by overloading organs
and systems due metabolites and toxins
affecting the cardiovascular system: tachycardia,
arrhythmias or myocardial ischaemia
dyspnea varying degrees by hypoxia or shock lung
ARDS (Acute Respiratory Distress Syndrome)
thrombosis due to the release of large quantities of
thromboplastin tissue
varying degrees of anemia due to hemolysis caused by
toxins and extravasation of fluid
severe renal failure (oliguria worsening, consequence
of hypovolemia and toxemia, with tubular necrosis)
 Stage II
hyposecretion and hypomotility
gastrointestinal associated with
gastric mucosal lesions that will lead
to ulceration (Curling ulcer) and
bleeding
metabolism disorders
decreased of general immunity

Possible evolutionary pathways

correct rebalancing
overcoming post-combustion shock / worsening installation of
toxic-septic shock
occurs resorption edema and polyuria crisis, which will
improve electrolyte disorders
The local evolution of the burn
spontaneous healing (if lesions grade I, II and part III grade)
elimination of escars and ready for grafting, with granular bed
formation (in lesions of III and IV degree)
Stage III. The period up to 2 months (21-60
days) - (conversion period from catabolism -
anabolism )
strengthening spontaneous epithelization and healing
surgical coverage areas (also called epithelization period or
surgery period )
recovery phase of patients correctly cared
metabolism begins to be dominated by anabolism
gradual return to normal biological constants and functions
of the various systems
Good progress metabolic balance correct grafting
between days 21-28
Losing operator momentum or severe burn Serious
large areas wounds granulation chronic shock
Stage IV - The period of " chronic
shock
occurs in cases with severe burns, with P.I. over 120,
patients with depleted biological resources
candidates for chronic shock installation presents
anemia, cachexia, hypoproteinemia with
dysproteinemia, sepsis, chronic anorexia, sleepiness,
fever, behavioral disorders, wound granulation (lack
of epithelialization) stagnant

biological constants are the lower limit of normal

at this stage, they have to be grafted quickly improve

the general health status
 BURNS COMPLICATIONS
Functional disorders reversible damage
Uncompensated functional disorders worsening
irreversible degenerative lesions MSOF
Septic :
Local complications Urinary : hemolysis and rhabdomyolysis
AKF
Tracheobronchial
Kidney shock
Pulmonary CRD
Urinary
Septicemia Hepatic :
Digestiv: Toxic Jaundice
Transaminases
Gastrointestinal bleeding
Gastric dilatation Neuropsychiatric :
Changes in behavior
Stress ulcers
Neuroses
Enterocolitis , etc.
Psychosis
Come
Tromboembolic :
Delirium
thrombophlebitis
pulmonary embolisms

(tissue thromboplastin , prolonged bed rest)

 BURNS SEQUELAE
Cicatricial:
Scars :
Hypopigmented

Hyperpigmented
Hypertrophic
Keloid
Retractions:
Skin in the folds of flexion
Tendinitis

Malignancy post-combustion scars (Marjolin

ulcer) vicious scars, retractile,
hyperkeratosis prophylactic surgical
ablation
Organic late sequelae
Liver
Kidney
Deformities hole ear, nose, lips
 The treatment of thermal burns:
Burns treatment is complex, general and local is an
immediate surgical emergency
1. First aid measures at the accident place Rapid
evacuation of patient Transport to specialized
units
Removing the patient from the accident scene
Stop Burning Process!
Remove patient from source of injury
Remove clothing unless stuck to burn
Cut around clothing stuck to burn, leave in place
Initial patient treatment
Consider burn patient as a multiple trauma patient until
determined the real status
Perform ABCDE assessment / Avoid hypothermia!
Remove constricting clothing and jewelry
 Criteria for burn center
admission
Full-thickness > 5% BSA Circumferential burns
Partial-thickness > 10%
BSA
Any full-thickness or
partial-thickness burn
involving critical areas
(face, hands, feet,
genitals, perineum, skin
over major joint)
Children with severe
burns
of thorax or extremities
Significant chemical
injury, electrical burns,
lightening injury, co-
existing major trauma
or significant pre-
existing medical
conditions
Presence of inhalation
injury
 The treatment of thermal burns :

2. On burn center
admission :
- Providing a peripheral or
central venous access
- Emergency analysis
- Bladder Catheterization to
monitorization urine output
- Tetanus prophylaxis with
ATPA im dose of 0.5 ml;
- Pain relief
- Oxygen therapy nasal
probe
- As needed, can practice
oro-tracheal intubation
3. General treatment of burn - Assess
Circulation
Rebalancing hydroelectrolytic - prompt and early for
preventing hypovolemic shock and kidney failure
The amount of liquid required within 24 hours after the accident is
in relation to the patient's weight and degree burn , area burned
and is calculated as follows:
2 x % burn area x weight kg + 2000 ml
Infusion solutions are:
- Crystalloid micromolecular (50%) - saline, isotonic glucose,
lactate Ringer
- Macromolecular (50%) - plasma, dextran 40 (colloids), mannitol,
Blood
The minimum value of diuresis: 40-60 ml / h in adults and 1 ml /
kg / h in children below 30 kg.
Exception ELECTRIC SHOCK : accompanied by myoglobinuria,
which require a diuresis of 100-150 ml / h to avoid paralysis and
tubular renal failure
 Parkland Formula
4 cc R/L x % burn x
body wt. In kg.
of calculated fluid is
administered in the first
8 hours
Balance is given over
the remaining 16 hours.
Maintain urine output at
0.5 cc/kg/hr.
ARF may result from
myoglobinuria
Increased fluid volume,
mannitol bolus and
NaHCO3 into each liter
of LR to alkalinize the
urine may be indicated
Lactated Ringers - preferred
solution
Contains Na+ - restoration of
Na+ loss is essential
Free of glucose high levels of
circulating stress hormones may
cause glucose intolerance
 Rebalancing haematological mandatory in
severe burns that induce severe anemia
transfuse blood izogrup izoRh . Blood is half of
macromolecular fluids transfused (25% of total
liquids) calculation by approximately :
500 ml for every 3 units of hematocrit lost

- by
Rebalancing the acid-base balance
the administration of Na bicarbonate
8.3%
Colloid osmotic pressure normalization
Infection prevention
Respiratory reanimation
 Assess Airway/Breathing
Start oxygen if:
Moderate or critical burn
Decreased level of consciousness
Signs of respiratory involvement
Burn occurred in closed space
History of CO or smoke exposure

Assist ventilations as needed

Inhalation Injury
Provide high-flow O2 by NRB (non-rebreather
mask)
Consider intubation if swelling /
tracheostomy
 Treatment of renal disorders
mannitol 20% (2 x 250 ml), furosemide (5-10
ampoules / 24 hours) and, as a last resort, dialysis
Preventing possible digestive
complications

insert a nasogastric probe

by i.v. H2-receptor blockers

Pain Treatment is done with specific

medication iv
Other treatments:
anticoagulants (heparin 20,000 IU / day infusion,
administered subcutaneously calciparina)
vitamin therapy (C, B1, B2, B6, B12, A, E)

Nutritional support (nutritional rebalance)

Burn Injury: Wound
Management
removal of exudates and
necrotic tissue
cleaning the area,
stimulating granulation
and revascularization Decompressing incisions
The first dressing to a
applying dressings. maximum of 24 hours in a
special room
debridement may be

At 72 hours the first

needed balance of the damage and
appreciation indication
excision graft
Regarding attitudes
toward the burned
wound in the coming
days, there are 2 ways
of approach:
a) closed method:
involves covering the burned
wound with sterile dressing
extremity immobilization in
functional position

b) open method:
wound exposure to air under
sterile tents
formation of a crust under appear
epithelial regeneration
crusts take off, will be removed
 1ST Degree Burn
skin gentle embrocations with alchool
Bioxiteracor type sprays

2ND Degree Burn

excision of blisters
skin gentle embrocations with alchool
3RD Degree Burn
superficial: the same treatment as 2ND Degree Burn
and epithelialization up to 3 weeks
deep: graft after excision or removal eschar

4TH Degree Burn - after primary processing of the

wound, there are two possible treatment options:
a) early excision-grafting (modern)
b) grafting after granulation of the wound (classical)
 Burn Injury: Wound
Management
Escharotomy/fasciotomy may be
necessary within hours
neurovascular compression; chest wall motion
Surgery for wound closure is necessary
for full thickness injury, or areas of deep
partial thickness that would heal with
delay or scar
In life threatening burns, urgency to graft
before substantial colonization occurs
 Dressing the Burn Wound
Standard wound dressings
Biologic dressings:
Homografthuman skin
Heterograftskin from other species
Amniotic membrane
Cultured skin
Artificial skin
Biosynthetic dressings
Synthetic dressings
Surgical Management
Surgical excision
Wound covering:
Skin graft

Escharotomy
Circumferential full
thickness burns
Chest
Arms
Legs
Medial/Lateral
incision
thru burned skin
Excision & Grafting
Cool extremity, weak Removal of
pulse, decreased
necrotic tissue
capillary refill,
Eschar is removed
decreased pain
until viable tissue
Difficulty with ventilation
is reached
in chest burns
Early excision-grafting

Aims
reduce patient suffering
removes source of harmful
substances generated by
general disorders
remove the source of the
germs
shorten hospitalization
decrease the functional
and aesthetic sequelae
 Rehabilitative Phase
Rehabilitation begins with wound closure
and ends when the patient returns to the
highest possible level of functioning.
Emphasis during this phase is on
psychosocial adjustment, prevention of
scars and contractures, and resumption
of preburn activity.
This phase may last years or even a
lifetime if patient needs to adjust to
permanent limitations.
 Chemical Burns
Injury different thermal burn, through both trigger
mechanism (irritating, toxic, necrotic) and through
individualized treatment according to noxa; Frequency
5-8%
Pathogenic pathways :
dehydrating action on tissues affected (acids)
Saponification action of fats (bases)
Phenomena of systemic intoxication (hepatic and
renal lesions) - Absorption of chemical; systemic toxic
effects
These chemical reactions are generally exothermic, it sums the
chemical effect with the caloric effect, consequence of heat
release
 Etiopathogeny of chemical burns
A. Acids:
strong mineral acids (hydrochloric, sulfuric, nitric,
hydrofluoric, phosphoric acid )
weak organic acids (acetic, oxalic, carbonic)
B. Bases :
strong(sodium and potassium hydroxide)
weak (calcium hydroxide )

C. White (or yellow) phosphorus

D. Organic peroxides : The most
commonly hydrogen peroxide
E. Photosensitizing substances:
aniline
Mineral acids
brutal tissues dehydration, protein precipitation with
exothermic reaction; coagulation necrosis with limited
effect

Clinical
Dry eschar, variable color (yellow-black), located in
an edematiated area surrounded by a congestive halo

Hydrogen fluoride is the most corrosive:

coagulation necrosis
form salts with calcium and magnesium, potentially
damaging in depth until consumption of all ions of
fluorine (iv injections neutralized with Ca gluconate).
Organic acids (acetic, oxalic, carbonic, etc.) and their
derivatives (phenol, cresols):
acts similar to mineral, but slower
lead to torpid lesions with soft and pale eschars
allow systemic absorption of toxic, with severe necrotic lesions,
especially liver and kidney (liver failure, renal failure acute
tubular necrosis

Strong mineral acids:

Fast severe cellular dehydration
HCl Dry eschar, paperboard, insensitive (gray, yellow,
H2SO4 etc.) - Finally black
HNO3 Eschar limited action acid and systemic absorption
H3PO4

Weak organic acids:

Evolutionary soft eschar
ac. Acetic
Evolves slowly due to sepsis
ac. Oxalic
ac. Carbonic Allows systemic resorption
Burns caused by alkaline substances
Pathogenic pathways
dehydration
degradation of proteins and fat saponification
resulting wet eschars, quickly liquefy but slowly and
incompletely deleted
Strong bases lead to liquefaction necrosis without limitation
barrier, with potential of extensive and infectious
Weak bases lead to dehydration and burn lesion

Burns caused by other toxic substances -

phosphorus and magnesium
produce highly exothermic reactions
phosphorus is absorbed systemically, causing liver
and kidney damage. (high lipophilicity )
 Chemical Burns treatment

General treatment
similar to treatment of the thermal burns
relieve pain by administering analgesics
(Mialgin), monitoring of vital parameters
great attention should be given liver and
kidney functions, especially for chemicals
that absorb, producing systemic toxic effects
If anuria persist in the context of a suitable
electrolyte balancing, can use dialysis
 Chemical Burns treatment
Local burned wound treatment
Removal of the chemical agent and wash with running
water in large quantities in the area concerned, both at
the accident scene, and later at the hospital.
excepting burns lime (CaO) where dry cleaning of skin is
recommended
In the case of burns with hydrogen fluoride,
recommended infiltrations with diluted calcium
gluconate or iv injected (2%)
The phosphor burn area was washed with 1% CuSO4 for
short periods (liver toxicity) and recommended excision-
grafting procedure immediate
After primary wound toilet, burned wound bandaged or
exposed to air
In deep burns, III-IV degree, recommended early
excision-grafting
 Frostbite
Freezing of a distal or
small body part from
prolonged cold
exposure
Cold air / Contact
with a cold object
/Wind and/or water
chill
Local cooling injuries to
extremities
Feet and toes
/Hands and fingers /
Face: nose and
cheeks / Ears
All morpho-functional modifications limited to
organs exposed to cold
 Frostbite
A result of prolonged cold exposure, outdoors as
well as indoors, constricting blood vessels in
the extremities, which diverts warm blood flow
and oxygen to central vital organs
Constriction cycles with dilation to preserve
functions of extremities

As the body temperature continues to drop, the

brain permanently constricts vessels in
extremities to maintain warmth in vital organs:
frostbite begins
Cell death due to exposure
Ice crystals form in the space outside cells
Cells become dehydrated
 Frostbite
Predisposing Factors
Low external temperatures/ Wind (convective
loss)
Humidity (conductive loss) /Skin wetness
Poor hydration / Hypoxia

Frostbite Risk Factors

Nicotine
Alcohol / Psychiatric/mental incapacity
Motor vehicle failure or trauma
 Frostbite
Besides low temperature some additional
factors play role in appearing of frostbite:
Mechanical factors that lead to disorders of
microcirculation tight shoes or close, long
lasting forced position.

Factors that decrease local tissue resistance

frostbites and traumas in the past, increased
perspiration of feet, neuro-trophic disorders.

Factors that decrease general resistance of the

organism trauma and blood lose, inflammation,
fatigue, lack of vitamins, drank stage, lose of
consciousness, hypoxia in the mountains.
 Frostbite Post-Rewarming
Classification
Difficult to predict the severity
of
injury when frostbite is first
seen
Severity established only after
re-warming has occurred
3-4 days usually needed to know

if superficial or deep
 Frostbite of the I stage
Superficial Duration of cold action is short.
Paleness changes into
Only the skin has been
frozen hyperemia. Sensitiveness is
saved. Moves of fingers of
Large blisters filled
with clear or yellow hand and feet are active.
fluid develop in about Edema is progressing. Pain is
12 hours severe. Full recovery in 5-7
Erythema with days.
rewarming; persistent
increased skin
sensitivity Frostbite of the II stage
During first days severe pain and
itching. Edema of tissues is
bigger than injured area. Main
sign is formation of blisters
with plasma like transparent
liquid. Blisters appear on 2 day
after the injury. Derivates of
skin are saved that is why full
restoring of skin cover is
possible and it takes 1-2
 Deep
Complete anesthesia (lack of sensation)
Hemorrhagic (blood-filled) blisters
Edema proximal to frostbite in 5-7 days
Frostbite of the III stage
Necrosis of all skin layers sometimes even injury of
subcutaneous tissue. Blisters with hemorrhage liquid.
Decreasing of sensitiveness. Skin in reactive period is
red and cyanotic. Cold on touch. If proper treatment
with autoplastic is not used, big connective tissue
scars appear.

Deep Progressive
Completely through dermis
Subcutaneous tissue, muscle, bone
Causes eventual mummification
Frostbite of the IV stage
Injury includes destroying of bones and joints.
Temperature of skin in bfore reactive period is
extremely decreased. Edema appears during first 1-2
hours, than - dry or wet gangrene of injured areas.
Demarcation line appears after 1-2 weeks. Edema
takes much larger area than gangrene.
 Frostbite
Known by several names
Frostnip
Immersion foot (trench
foot): Injury to skin, blood
vessels, and nerves of the feet
from continuous immersion in
water, even in above freezing
conditions
Chilblains (pernio):
Inflammation of the hands and
feet from repeated exposure to
cold and moisture
 Frostnip
Frostnip is the mildest form of a freezing cold injury.
Only the very outer layers of the skin freeze, usually
on the cheeks, earlobes, fingers, and toes, and also
nose and chin.

Usually occurs at about 29F

Generally reversible, no tissue injury or
permanent damage
Skin turns white, top layer of skin feels hard
but deeper tissue still feels normal (soft)
May feel tingling or numbness
 Frostnip - Treatment
Gently re-warm affected area by blowing warm
air on it or placing it against a warm body part
Do not use very hot objects such as hot water
bottles to re-warm the area or person.
Do not rub the affected part - ice crystals in
the tissue can cause damage if the skin is
rubbed.

Frostnip can be prevented by wearing

warm clothing, gloves and insulated footwear.
 Chilblains
Chilblains is caused by prolonged and repeated
exposure of bare skin to air temperatures above
freezing (0C)
0C to 15C,
15C accompanied by high humidity
or wet conditions. It can develop in only a few hours.

The most commonly affected areas are the cheeks, ears,

nose, fingers, and toes.

Affected area appears as red, swollen skin which is

tender, hot to the touch, and may itch

Can worsen to aching, prickly (pins and needles)

sensation, then numbness.

In severe cases, open sores or bleeding lesions may

result from continued exposure.
 Chilblains - Treatment
Warm affected area gently with direct body heat:
Put bare hands over the affected area on the face
Put affected areas against armpits or stomach of
another person

Do not massage or rub affected areas.

Do not wet the area or rub it with snow or ice.

Do not expose affected area to open fire, stove, or any

other intense heat source.

Seek medical attention to evaluate for tissue damage.

Signs and symptoms of tissue damage may be slow to
appear.
 Immersion Injury (Trench
foot)
Immersion injury (trench foot) results from prolonged exposure
of the feet to wet or damp cool conditions, such as in cold water,
mud, or wet fields, or wearing damp socks. A similar condition of
the hands can occur if a person wears wet gloves for a
prolonged period under cold conditions.

Usually develops slowly, over hours to

days and at temperatures from 0C to
9C.
Can occur at temperatures as high as
15C if the feet are constantly wet
The primary injury is to nerve and muscle
tissue. There is no formation of ice
crystals in the tissues but immersion
injury can cause permanent damage.
 Immersion Injury (Trench
foot)
Note the cyanosis (blueness
of skin) around the nail beds;
redness and swelling; and
blisters.
Symptoms
Initially reddened skin, then turns
pale and mottled, finally purple, grey,
or blue
Tingling pain, itching, burning
sensation, or numbness may occur,
followed by leg cramps and swelling
May cause permanent damage to
the circulatory system so person is
more sensitive and prone to cold-
related injuries in that area
May develop blisters, ulcers, and
gangrene. Amputation may be
necessary
 Immersion Injury (Trench
foot)
Treatment
Remove wet clothing and replace with dry, warm clothing.

Warm affected area slowly at room temperature. Carefully

clean, dry, and wrap loosely with sterile dressing, taking
care not to break the blisters. This can lead to infection.

Elevate feet to reduce swelling.

Do not walk on injured feet.

Seek prompt medical attention; trench foot can cause

severe disability.
 Immersion Injury (Trench
foot)
Prevention
Keep feet clean and dry.

Check them regularly; if they get wet from

water or sweat, dry them and replace with
dry socks.

Change socks at least every 8 hours or

whenever wet and apply foot powder.
Foot powder with aluminum hydroxide can help.

Dont wear tight socks; this can further impair circulation.

Dont sleep with wet socks.

 Frostbite - SURGICAL
TREATMENT
1. Necrotomy cutting through necrotic tissues
for decreasing of edema and circulatory
disorders ( first 3 days after the trauma).
2. Necrectomy cutting off the necrotic tissues
:
) early ( 1st day ). In case of gangrene, total
injury of big segments of extremities, toxemia,
risk of sepsis;
b) delayed (15-30th day after the trauma )
in case of gangrene with clear limits;
c) late (more than 1 month) in case of
gangrene with osteolisis or osteonecrosis.
 Frostbite - SURGICAL
3. AmputationTREATMENT
of injured segment - besides cases
that can be decided during necrectomy, and
formation of functionally good stump. Always
should be provided proximally than demarcation
line.

4. Surgical restoring of the skin cover. In case of

granulation wounds with size of more than 1,5
sm2. Terms of providing depending on wounds.

5. Reconstructive operations increase functional

capacities of stumps and future cosmetic aims.
Terms of providing more than 2 months.
 First aid in case of frostbites
To dress the victim into dry close, not to make additional injury
during dressing and changing of footwear.

To warm injured extremity in the bath. The temperature should

be increasing from +37 till +40. At the same time, by hands
and soft soap sponge make gentle massage of the extremity
from periphery to center.

Grinding of skin by camphor alcohol, glycerin, or just by wet

hand for stimulation and restoring of blood circulation

After the extremity become warmer and pink (30-40 min), it

should be dried and handled by alcohol or strong antiseptic
solution, dressed with antiseptic bandage, wraped by thick layer
of grey gauze (thermal isolating dressing). This method stops
cooling of tissues from the outside and gradual warming from
inside, parallel to restoring of normal blood circulation. This
dress should not be taken off during 8-20 hours.

Victims with frostbites should get warm drinks ( tea, coffee),

warm food.
Voltaire
..the art of
medicine is to
amuse the patient
while nature heals
the disease

Je le pansai,
Dieu le gurit

Ambroise
Par