Professional Documents
Culture Documents
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
Layers - Epidermis
Outer layer
Dermis
Elastic connective tissue
stratigraphy Top (stratum corneum) Contains specialized
consists of dead, hardened structures
cells Nerve endings
Epidermis Lower epidermal layers Blood vessels
Dermis form stratum corneum and Sweat glands
Sebaceous (oil)
Subcutaneous
contain protective pigments
glands
Underlying Hair follicles
Structures
Fascia Subcutaneous/Muscle
Nerves Fat (protective layer)
Tendons Muscle for support,
Ligaments movement,
coordination
Muscles
Organs
Anatomy & Physiology of the Skin
Skin Functions - the largest organ of the body
Barrieragainst infection
Sensory organ
Temperature
Touch
Pain
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
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
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:
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 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%
4.5
4.5
4.5
7 7 7
Posterior trunk = 18%
Genitalia (perineum) = 1%
Prognostic index = surface area burned % x depth
of burn (grade)
P.I. under 40 : evolution is 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, or
major depending on the depth, extent, and location
MINOR BURNS
Deep partial-thickness burns <15% TBSA Full-thickness burns <2% 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
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
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)
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
Central
nervous
system
disorders
(exaltation,
depression)
acute cardio-vessel
insufficiency main Restrictive
reason of death respiratory
(develops during 1-2 insufficiency -
hours) hypoxia
In urine
cylinders,its Generalized 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
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
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 ARF may result from
wt. In kg. myoglobinuria
Escharotomy
Circumferential full
thickness burns
Chest
Arms
Legs
Medial/Lateral incision
thru burned skin
Excision & Grafting
Cool extremity, weak Removal of necrotic
pulse, decreased capillary tissue
refill, decreased pain Eschar is removed
Difficulty with ventilation until viable tissue is
in chest burns reached
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)
Clinical
Dry eschar, variable color (yellow-black), located in an
edematiated area surrounded by a congestive halo
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
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.
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