SlideShare a Scribd company logo
Dr Rahul Gorka
M.S, M.Ch
Lecturer (Plastic Surgery)
Definition of a Burn
 “Tissue injury caused by thermal,
radiation, chemical, or electrical
contact resulting in protein
denaturation, burn wound edema,
and loss of intravascular fluid
volume due to increased vascular
permeability.”
Burn Statistics
 At least 50% of all burn accidents can
be prevented
 children playing with fire account for
more than one-third of preschool
deaths by fire
 In the US, approximately 2.4 million
burn injuries are reported each year.
 Burn injuries are second to motor
vehicle accidents as leading cause of
accidental death in the US
TYPES OF BURNS
 Flame (Thermal)
 Electrical
 AC & DC
 Lightning
 Chemical
 Steam
 Radiation
 Scald
COURTESY DAVID
EFFRON, M.D.
THIRD DEGREE BURNS
WITH ESCHAROTOMIES
Types of Burns
 Thermal Injuries (most common)
 Contact
Direct contact with hot object (i.e. pan or iron)
Anything that sticks to skin (i.e. tar, grease or
foods)
 Scalding
Direct contact with hot liquid / vapors (moist
heat)
i.e. cooking, bathing or car radiator
overheating
Single most common injury in the pediatric client
 Flame
Direct contact with flame (dry heat)
i.e. structural fires / clothing catching on fire
Types of Burns
 Chemical
 Caused by strong acids, alkalis, phenols,
cresols, phosphorus or mustard gas
 Results in necrosis
 Electrical
 Caused by electric current which may
generate heat up to 5000ºC
 May result in necrosis, respiratory paralysis, or
ventricular fibrillation
Types of Burn Injury
 Smoke & inhalation injury-inhaling hot
air or noxious chemicals
 Cold thermal injury-frostbite.
 Radiation
 Caused by prolonged or intense exposure to
ultraviolet radiation
 Examples: Sunburn, tanning beds
Classification of Burn Injury
 Treatment of burns is directly related to
the severity of injury!
 Severity is determined by:
 depth of burn
 external of burn calculated in percent of total
body surface (TBSA)
 location of burn
 patient risk factors
Location of Burns
 Has a direct relationship to the severity of
the burn.
 Face, neck & chest burns may cause
respiratory illness mechanical obstruction
secondary to edema or eschar formation
Burn Patient Severity
 Patient age
 Less than 2 or greater than 55
 Have increased incidence of complication
 Burn configuration
 Circumferential burns can cause total occlusion of
circulation to an area due to edema
 Restrict ventilation if encircle the chest
 Burns on joint area can cause disability due to scar
formation
Anatomy and Physiology of
Skin
Skin
 Largest body organ. Much more than a
passive organ.
 Protects underlying tissues from injury
 Temperature regulation
 Acts as water tight seal, keeping body fluids
in
 Sensory organ
Skin
 Injuries to skin which result in loss, have
problems with:
 Infection
 Inability to maintain normal water balance
 Inability to maintain body temperature
Skin
 Two layers
 Epidermis
 Dermis
 Epidermis
 Outer cells are dead
 Act as protection and
form water tight seal
Skin
 Epidermis
 Deeper layers divide to produce the stratum
corneum and also contain pigment to protect
against UV radiation
 Dermis
 Consists of tough, elastic connective tissue
which contains specialized structures
Skin
 Dermis - Specialized Structures
 Nerve endings
 Blood vessels
 Sweat glands
 Oil glands - keep skin waterproof, usually
discharges around hair shafts
 Hair follicles - produce hair from hair root or
papilla
 Each follicle has a small muscle (arrectus pillorum)
which can pull the hair upright and cause goose
flesh
First-Degree Burns
 Does not go below
basal layer of the
epidermis
 Dry and painful
 Appears red due to
increased blood
flow
 Heals in a few days
Second-Degree Burns
 Extends below basal
layer, but not
completely through
dermis
 Superficial
 Blister, very painful,
contains skin parts
(adnexa) which assist
in epithelialization
 Deep Partial-thickness
 Deeper in dermis,
fewer adnexa, longer
healing time, less
painful
Third-Degree Burns
 Extends completely
through dermis
 Adnexa destroyed so
can’t heal by
epithelialization
 Dermal plexus of
nerves destroyed-
less painful
 Burns can be yellow,
red, black, brown
Burn Depth
 Fourth-degree
 Full-thickness
destruction of
skin/subcutaneous
tissue
 Involves underlying
fascia, muscle, bone or
other structures
 Prolonged disability
FIRST AND SECOND DEGREE
BURNS
FIRST DEGREE BURN SECOND DEGREE BURN
THIRD DEGREE BURNS
COURTESY DAVID EFFRON,M.D.
COURTESY BONNIE
MENEELY, R.N.
CHEMICAL BURN
COURTESY ROY ALSON,
M.D.
SCALD BURN
COURTESY DAVID
EFFRON, M.D.
Initial Estimate of : “Rule of Nines”
Adult anatomical areas = 9% BSA (or multiple)
Extent of Burn
• Not accurate for
infants / children due
to larger BSA of head
& smaller BSA of legs.
Burn diagrams
illustrate adult and
child differences.
Rule of Nines
 In the adult, most areas of the body can
be divided roughly into portions of 9%, or
multiples of 9. This division, called the rule
of nines, is useful in estimating the
percentage of body surface damage an
individual has sustained in burn.
Burn Assessment Lund & Browder Chart
Thermal Burn Injury
Pathophysiology
 Emergent phase
 Response to pain  catecholamine release
 Fluid shift phase
 massive shift of fluid - intravascular 
extravascular
 Hypermetabolic phase
  demand for nutrients  repair tissue
damage
 Resolution phase
 scar tissue and remodeling of tissue
Zones of Burn Injury
 Zone of Coagulation
 Inner Zone
 Area of cellular death (necrosis)
 Zone of Stasis
 Area surrounding zone of coagulation
 Cellular injury: decreased blood flow & inflammation
 Potentially salvable; susceptible to additional injury
 Zone of Hyperemia
 Peripheral area of burn
 Area of least cellular injury & increased blood flow
 Complete recovery of this tissue likely.
ESCHAR
 The necrotic tissue resulting from a burn
is known as eschar.
 It is a good substrate for microorganisms.
If left untreated it becomes colonized,
contaminated and eventually infected.
 Topical antimicrobial agents increase the
time to eschar separation.
 systemic changes
Burn
Pathophysiology:inflammation&
Edema
 Injured tissue: capillary permeability es
 Protein leakage: resultant
hypoproteinemia, and ed osmotic
pressure in burned tissue
 Decreased cell membrane potential with
inward shift of Na+ and H2O, resulting in
cellular swelling
 Edema maximal at 24 hrs, usually resolved
by 3-5 days; capillary leak normal at 24
hrs
Burn Pathophysiology: Metabolic
 Hypermetabolic response  BSA affected;
may approach 200% of basal metabolic
rate
 catabolic response
 acute phase response
 Mediators implicated:
 stress hormones: catecholamines, steroids
 cytokines: TNF, IL-1, IL-6
 lipids: prostaglandins, thromboxane B2, PAF
Burn Pathophysiology: Metabolic
 Prostaglandins, IL-1, IL-6 implicated in:
 increase in core temperature of 1-2oC
 initiating acceleration of nitrogen catabolism
 ? inversion of T4/T8 ratios from 2:1 to 1:2
 Early enteral feeding associated with
attenuation of the hypermetabolic
response
Burn Pathophysiology:
Cardiac
 Cardiac output initially decreases
 loss of intravascular volume
 CVP and PCWP typically low-normal, even
after adequate volume resuscitation
 Cardiac output usually normalizes before
intravascular volume completely restored
  iCa++ may present as hypotension/EMD
 out of proportion to hypoalbuminemia
Burn Pathophysiology: Renal
it can result from:
 prolonged hypotension due to hypovolemia
 myoglobin release from damaged
muscle/tissue
 hemoglobinuria from heat-induced hemolysis
 Renal blood flow initially es, followed by
dramatic  in GFR, coinciding with onset
of the postburn hypermetabolic state, and
hyperdynamic circulation
Burn Pathophysiology: Renal
 Early in the postburn period, decreased
urinary Na+ and Cl-
 K+ wasting in the urine is common (up to
200 mEq/liter), secondary to the intense
adrenal response to burn injury/stress
Burn Pathophysiology: Hypertension
 May be common in pediatric patients
 up to 57% in one study
 7-10 year old boys with >20% BSA affected
 Hypertensive encephalopathy may result
 7% of hypertensive pediatric burn patients
 Mechanism may involve hypervolemia with
concomitant activation of RA SYSTEM
 ?elevated “stress” plasma renin and
aldosterone
Burn Physiology: Pulmonary
 Pulmonary dysfunction etiologies in this
setting:
 shock, inhalational injury, aspiration, sepsis,
CHF, trauma
 Upper airway injury/edema may contribute
 airway occlusion impairs flow of tidal breaths
• resolution of occlusion can cause reexpansion
Burn Physiology: Pulmonary
 Circumferential thoracic eschar or edema
may contribute to restrictive lung disease
 Hypovolemia may cause V/Q mismatch
 Inflammatory mediators released in burn
injury linked to evolution of ARDS
 therefore, expect some degree of pulmonary
capillary leak, on a continuum from mild
pulmonary edema, to frank ARDS
Burn Pathophysiology: CNS
 CNS dysfunction in up to 14% of burn pts
 most had >50% BSA involvement
 Hypoxia most common etiology
 smoke inhalation, pulm edema, pneumonia
 Hypovolemia, hyponatremia, cortical vein
thrombosis, sepsis, and gliosis due to
watershed infarct also implicated
 ? Role of neurotoxic factors
Burn Pathophysiology: GI
 Stress (curling’s) ulcer
 prophylaxis: antacids, H2 blockers, or
sucralfate
 Increased gut permeability in first 24
hours
 Acalculous cholecystitis
 fever, abdominal distention, jaundice
 bacterial seeding (ascending cholangitis)
 sterile, in patients with dehydration, ileus, or
pancreatitis
Burn Pathophysiology: GI
 Acute pseudo-obstruction of the colon
 massive colonic dilation without organic cause
Narcotic ileus
 oral narcotic antagonists may be efficacious
 hypovolemia shunt blood from the splanchnic
bed and promote mucosal atrophy and failure
of the gut barrier
Burn Pathophysiology:
Hepatic
 Modest hepatic dysfunction common early
 Persisting, or severe hepatic dysfunction,
associated with negative outcome
 larger BSA involvement (58% vs 30%)
 greater mortality (74% vs 9%)
 clinical jaundice associated with 90%
mortality
 Late onset of conjugated
hyperbilirubinemia usually related to
occult, or overt, sepsis
Burn Pathophysiology: Blood
 Initially, shortened RBC survival with intra-
vascular hemolysis/possible
hemoglobinuria
 typically resolves after the 1st week
 Anemia is common, and to be expected;
 may be masked initially by hemoconcentration
 may be exacerbated by fluid management,
occult blood loss
 typically persists until wound healing occur
 depressed erythropoietin levels documented
Burn Physiology:
Immunologic
 Skin as an organ of host defense:
 keratin layers as physical barrier to
penetration
 cycles of desquamation (“debulking” of
skin bacterial burden)
 stratum corneum: unsaturated free fatty
acid film which is bacteriostatic and
fungistatic
 colonization resistance due to normal flora
 antigen presentation to Langerhans’ cells
Burn Physiology:
Immunologic
 Cellular Immune Function
 markedly delayed allograft rejection
 ed antigen responses
 total lymphocyte count typically normal, but
T4 (helper T-cell) count , while T8
(suppressor T-cell) count  (T4/T8 ratio
inverts)
 several circulating mediators in burn patient
sera suppress normal lymphocyte function
Burn Physiology:
Immunologic
 “Immunologic Dissonance” resulting
from activation of inflammatory
cascades/SIRS
 Systemic immunosupression may therefore
occur very early in the post-burn period;
magnitude of immunocompromise  BSA
Increased gut
mucosal Permeability
Immunosuppression
Decreased Renal blood flow
Severe Burn
Vascular Permeability &
oedema
Altered haemodynamics
Hypermetabolism
Phases of Burn Care
 Emergency assessment and care (ABCs)
 Resuscitation (hours 0-48)
 Definitive care (day 3 until wounds are
closed)
 Rehabilitation (begins during resuscitation
and lasts entire lifespan)
Rescue
 A-B-C-D-E-F
 Stop the burning
 Decontaminate casualty at the scene
 Avoid injury to the rescuer
 Careful with high voltage electrical wires
 Assess for other injuries
ABCs of Emergency Burn Care
(Advanced Burn Life Support)
 A = Airway (with cervical spine assessment)
 B = Breathing
 C = Circulation
 D = Disability
 E = Exposure and Environmental Control
 F = Fluid Resuscitation based on Burn Size and
Weight Measurement
 Secondary Survey
A: Airway
 Assess the patient’s airway
 Upper airway edema due to inhalation injury
 Rapid or delayed progression
 Decision to intubate: individualized
 Mild symptoms: observe in ICU
 Pre-transport: prophylactic intubation
 When in doubt, intubate
B: Breathing
 Look, listen, feel for breath sounds and
chest movement
 Give 100% oxygen to all victims of major
burn beginning in the field
 Pulse oximetry
 Arterial blood gases
 Required for definitive diagnosis of CO
 Baseline chest x-ray
C: Circulation
 Who needs fluid resuscitation?
 All >20% total body surface area burned (TBSA)
 Young and old with >10% TBSA
 2 large bore peripheral IVs
 Unburned skin
 Burned skin
 Central access
 Cutdown
 Interosseous
D: Disability
 Assess level of consciousness: AVPU
 Alert
 Responds to verbal stimuli
 Responds to painful stimuli
 Unresponsive
 Alteration in mental status is not normal
 Pupils
 Moves extremities
E: Exposure and Environment
 Remove clothing, jewelry
 Keep warm
 blankets
 warm I.V. fluids
 heating lamps
 heat the room
 Keep Patient Dry
F: Fluid Resuscitation
(based on burn size and weight)
 Determine fluid needs based on burn size and
weight
 Burn size: include second and third degree only
 Rule of Nines
 One hand = one percent
 Lund-Browder chart
 Overestimation by referring hospitals is common
 Weight: pre-burn weight
Fluid Therapy
 1 or 2 large bore IV replacement lines (may
need jugular or subclavian)
 Cutdown if no option , increased risk of
infection & sepsis
 Fluid replacement based on: size/depth of
burn, age of pt., & individualized
considerations--ex. Dehydration in preburn
state, chronic illness
 options- RL, D5NS, dextam, albumin, etc.
 there are formula’s for replacement: Parkland
formula and Brooke formula
 Total Body Surface Area (TBSA) Burned
 Palmar Method
 A quick method to evaluate scattered or
localized burns
 Client’s palm = 1 % TBSA
 Rule of Nines
 A quick method to evaluate the extent of burns
 Major body surface areas divided into multiples
of nine
 Modified version for children and infants
 Lund-Browder Method
 Most Accurate; based on age (growth)
 Can be used for the adult, children & infants
Burns
 Parkland/Baxter Formula
 4 ml RL/kg body wt X % TBSA=ml RL for 24
hours
 eg. Pt. wt=75 kg and burned 25%
4/75/25=7500 ml/24 hours
50% 1st 8 hours=3750ml
25% 2nd 8 hours=1875 ml
25% 3rd 8 hours=1875
Formulas for Fluid Replacement
Evans Formula.
􀂋 Colloids 1 ml./kg. of body wt/%/burn.
􀂋 Saline 1 ml/kg. of b. wt./% of burn.
􀂋 free water: dependent on age &
insensible loss.
􀂋 1/2 of total is given the 1st 8 hrs. and
the remainder given the next 16 hrs.
Brooke Formula
􀂋.
􀂋 Colloids .5 ml/kg/% of body surface
burned.
􀂋 Lactated Ringers 1.5 ml/% of body wt/%
burn.
􀂋 H20 Again dependent.
􀂋 1/2 total amount given 1st 8 hrs.
􀂋 1/4 of total the 2nd 8 hrs. 1/4 the third 8
hrs.
Galveston formula
Resuscitation Formula
 1. Fluid administration-Ringers lactate
First 24 h:
 a. 5000 ml/M2 burn + 2000 ml/TBSA m2
 b. administer 1/2 in first 8 h postinjury and the 2nd half
in the next 16 h.
 Example: 15 kg child with an 87% TBSB, height 96 cm.
 Body Surface (m2) =.60
 Total Burn (m2)=.52
 2000 ml x .6 TBSAm2 = 1200 ml
 5000 ml x .52 TBSABm2 =2600 ml
 Total fluids first 24 h = 3800 ml
 Total fluids first 8 h = 1900 ml = 237 ml/h
 Total fluids next 16 h = 1900 ml = 118 ml/h
Assessment of adequacy of
fluid replacement
 Urinary output is most commonly used
parameter
 urine OP-30-50 cc/hr in an adult
 cardiopulmonary factors- BP (systolic 90-100
mmHg, pulse less than 100, resp 16-20 breaths
per min. (BP more accurate with arterial line)
 sensoruim-alert, oriented to time, place, &
person
FIRST AID
cooling the burn wound soon after the injury
(within 30minutes) is beneficial in removing heat
from the wound and limiting tissue damage.
It can also reduce early edema and protein
extravasation.
Care must be taken, as prolonged or excessive
cooling can be detrimental.
Other precautions...
 Burn too large--don’t immerse in water
due to extensive heat loss
 Never pack in ice
 Pt. should be wrapped in dry clean
material to decrease contamination of
wound and increase warmth
CRITERIA FOR ADMISSION
 Both 2nd & 3rd
degree burns
 >20% BSA any age
 >10% BSA <10 or
>50 years of age
 3rd degree only
 >5% BSA
 Burns of face,
hands, feet,
genitals, or joints
CRITERIA FOR ADMISSION
 Specialized burn
types
 Electrical &
lightning
 Chemical
 Inhalation injury
 Circumferential
chest or extremity
burns
 Significant medical
illness
 Significant other
injuries
Critical Burn Criteria
 30 > 10% BSA
 20 > 30% BSA
 >20% pediatric
 Burns with respiratory injury
 Hands, face, feet, or genitalia
 Burns complicated by other trauma
 Underlying health problems
 Electrical and deep chemical burns
Moderate Burn Criteria
 30 2-10% BSA
 20 15-30% BSA
 10-20% pediatric
 Excluding hands, face, feet, or genitalia
 Without complicating factors
Minor Burn Criteria
 30 < 2% BSA
 20 < 15% BSA
 <10% pediatric
 10 < 20% BSA
Escharotomies
—required if circumferential full thickness burns
of chest,limbs or digits are present.
 can impair circulation and cause distal
ischemia. Circumferential full-thickness chest
burns can restrict chestwall excursion and impair
ventilation.
mid-axial escharotomies performed either at
bedside or in the operating room..
An escharotomy incision will only improve
outcome without risk of harm in that situation.
INHALATION INJURIES
 Carbon monoxide poisoning
 Toxic gas inhalation
 Smoke inhalation
 Heat inhalation
 Steam inhalation
 Asphyxiation
3 types of smoke and
inhalation injuries
 1. Carbon monoxide poisoning (CO
poisoning and asphyxiation count for
majority of deaths)
 Treatment- 100% humidified oxygen-draw
carboxyhemoglobin level- can occur without
any burn injury to the skin
 2. Inhalation injury above the
glottis (caused by inhaling hot air,
steam, or smoke.)
 Mechanical obstruction can occur quickly-
True ER! Watch for facial burns, signed
nasal hair, hoarseness, painful swallowing,
and darkened oral or nasal membranes
 3. Inhalation injury below glottis
 (above glottis-injury is thermally produced)
 below glottis-it is usually chemically
produced.
 Amount of damage related to length of
exposure to smoke or toxic fumes
 Can appear 12-24 hours after burn
SIGNS OF SMOKE INHALATION
 Exposed to smoke in enclosed
space
 Unconscious while exposed to
smoke
 After exposure to smoke
 Develops cough
 Develops dyspnea
 Develops chest pain
SIGNS OF UPPER AIRWAY BURNS
 Burns of the face
 Singed eyebrows or
nasal hairs
 Burns in the mouth
 Sooty sputum
 History of being burned
while confined to an
enclosed space
COURTESY ROY ALSON, M.D.
LIP BURNS & SOOT IN
MOUTH
Inhalation Injury Management
 Airway, Oxygenation and Ventilation
 Assess for airway edema early and often
 Consider early intubation
 When in doubt oxygenate and ventilate
 High flow oxygen
 Bronchodilators may be considered if
bronchospasm present
 Diuretics not appropriate for pulmonary
edema
Inhalation Injury Management
 Circulation
 Treat for Shock (rare)
 IV Access
 LR/NS large bore, multiple IVs
 Titrate fluids to maintain systolic BP and perfusion
Inhalation Injury Management
 Other Considerations
 Assess for other Burns and Injuries
 Treat associated inhalation injury/poisoning
 Cyanide poisoning antidote kit
 Positive pressure ventilation
 Hyperbaric chamber (carbon monoxide poisoning)
Wound Care Principals
Goals
 􀂄 close wound
 􀂄 prevent infection
 􀂄 reduce scarring and contractures
 􀂄 provide for comfort
Wound cleaning
Debridement
 􀂄 mechanical
 􀂄 surgical
Topical antibacterial therapy
Cleansing and Debridement
 Can be done in tank, shower, or bed
 Debridement may be done in surgery.
(Loose necrotic skin is removed)
 bath given with with surgical detergent,
disinfectant, or cleansing agent to reduce
pathogenic organisms
Infection is the most serious
threat to further tissue injury
and possible sepsis.
 SURVIVAL is related to prevention of
wound contamination.
 Source of infection is pt’s own flora,
predominantly from the skin, resp. tract, and
GI tract.
 Prevention of cross contamination from other
patients is the priority for nurses!
2 methods used to control
infections in burn wounds...
 Open method- pt’s burn is covered with
topical antibiotic and has no dressing
 Closed method-uses sterile gauze
impregnated with or laid over a topical
antibiotic. Dressings changed 2-3 times q
24 hrs.
Wound Care continued...
 Staff should wear disposable caps, gowns,
gloves, masks when wounds are exposed
 use of sterile techniques
 keep room warm
 careful handwashing
 any bathing areas disinfected before and
after bathing
 Coverage is the primary goal for burn
wounds. Since usually not enough unburned
skin for immediate skin grafting, other
temporary wound closure methods are used
 Allograph or homograft (same species which is
usually from cadavers) is used for wound
closure-- temporary--3 days to 2 wks
 Porcine skin-heterograft or xenograft (different
species)--temporary--3 days to 2 wks
 autograft or cultured epithelial autograft- (pt’s
own skin and cell culture)- permanent
Burn Wound Closure
 Permanent Skin Grafts
 Two types:
Autografts and Cultured Epithelial Autografts
(CEA)
 Autograft
Harvested from client
Non-antigenic
Less expensive
Decreased risk of infection
Can utilize meshing to cover large area
Negatives: lack of sites and painful
Permanent Burn
Wound Closure Cont.,
 Permanent Skin Grafts Cont.,
 Cultured Epithelial Autografts (CEA)
A small piece of client’s skin is harvested and
grown in a culture medium
Takes 3 weeks to grow enough for the first
graft
Very fragile; immobile for 10 days post grafting
Great for limited donor sites
Negatives: very expensive; poor long term
cosmetic results and skin remains fragile for
years
Temporary Burn Wound Closure
 Biosynthetic Temporary Skin Grafts
 Homograft
 AKA Allograft
 Live or cadaver human donors
 Fairly expensive
 Best infection control of all biologic coverings
 Negatives:
 Risk of disease transmission (i.e. HBV & HIV)
 Antigenic: body rejects in 2 weeks
 Not always available
 Storage problems
Temporary Burn Wound Closure
 Biosynthetic Temporary Skin Grafts Cont.,
 Heterograft
AKA Xenograft
Graft between 2 different species
i.e. Porcine (pig) most common
Fresh, frozen or freeze-dried (longer shelf life)
Amendable to meshing & antimicrobial impregnation
Antigenic: body rejects 3-4 days
Fairly inexpensive
Negatives: Higher risk of infection
Temporary Burn Wound Closure
 Temporary Skin Grafting Cont.,
 Artificial Skins
Transcyte:
A collagen based dressing impregnated with
newborn fibroblasts.
Integra:
A collagen based product that helps form a
“neodermis” on which to skin graft.
 Synthetic
Any non-biologic dressing that will help
prevent fluid & heat loss
Biobrane, Xeroform or Beta Glucan collagen
matrix
Donor Site:
Wound Considerations
 The donor site is often the most painful
aspect for the post-operative client.
 We have created a brand new wound !!
 Variety of products are used for donor sites.
Most are left place for 24 hours and then left
open to air.
 Donor sites usually heal in 7-10 days
using a dermatome (left) to remove
donor skin and a mesher (right) to put
holes in it.
Example of healing burn
Other care measures include
 Face is vascular and subject to increased
edema- use open method
 eye care-use saline rinses, artificial tears
 hands &arms-extended and elevated on
pillows or in slings to minimize edema,
may need splints to keep them in
functional positions
 Ears- keep free of pressure. Ear burns-
no pillows! Neck burns should not use
pillows in order to decrease wound
contraction.
 Perineum-must be kept clean & dry.
Indwelling foley will help in this & also
to provide hourly outputs.
 Lab tests ; to monitor electrolyte
imbalance and ABGs
 Physio therapy stared immediately
Drug Therapy
 Analgesics and Sedatives
 given for pt comfort
 IV pain meds initialy due to:
 GI function is slowed or impaired because of
shock or paralytic ileus
 IM injections will not be absorbed well
Drug Therapy
 Tetanus immunization- given routinely
to all burn patients because of the
likelihood of anaerobic burn-wound
contamination
 Antimicrobial agents-usually topical
due to little or no blood supply to the burn
eschar so little delivery of the antibiotic to
wound
 Drug of choice is: Silver sulfadiazine
 Curlings ulcer prophylaxis
(Peptic Ulcer)
 An H2 blocker (cimetidine,
ranitidine,famotidine) start first 6 hours
 antacids are no longer recommended - the
patient should be kept NPO
 with burns > 15% of BSA, an NG (OG) tube
and bladder catheter should be placed
Burns (medications)
 Silver nitrate 0.5% (rarely used)
 wet dressing effectively prevents cross infection
 >0.5% injures the tissue and not effective<0.5%
 danger of electrolyte imbalance (especially Na and K)
since the electrolytes are withdrawn from the body
fluids and also from the dressing.
 Turns black in sunlight and stains clothes and hands
black
Burns (medications)
 Silvadene
 wide-spectrum antimicrobial that is
nonstaining and relatively painless
 no systemic metabolic abnormalities however
is contraindicated in pregnant women near
term and premature infants
 does not penetrate the eschar as well as
sulfamylon
Burns (medications)
 Sulfamyalon acetate
 interferes with bacterial cellular metabolism
 diffuses rapidly through burned skin and eschar
 used for gram-negative organism
 burning sensation after applied topically
 may cause metabolic acidosis and is a carbonic
andryrase inhibitor
 may cause a rash
Burns (medications)
 Furacin-nitrofurazone (gauze or cream)
 a synthetic broad-spectrum antibacterial
 inhibits enzymes required for carbohydrate
metabolism in bacteria
 Xeroform-a fine mesh gauze with
antimicrobial action
Topical antimicrobials
Advantages and Disadvantages
 Silver Sulfadiazine –Painless but Lack of
penetration
 Mafenide Acetate –Penetrates but Painful,
Carbonic anhydrase inhibitor
 Silver Nitrate- Broad spectrum but Limited
penetration
 Sodium Hypochlorite -Broad spectrum but
Impairs wound healing in high doses
 Table 7.2. Other topical agents
 Bacitracin: Gram-positive Minimal coverage
Often combined with polymyxin and neomycin
into triple ointment
 Polymyxin B :Petroleum-based Keeps grafts
moist, Often combined with mycostatin into
“Polymyco”
 Bactroban: Staphylococcal coverage ,Very
expensive
Useful for ghosted grafts
 Silvamyco:(Silvadene and mycostatin) Extended
coverage
SYSTEMIC ANTIMICROBIAL
THERAPY IN BURNS
 only after clinical suspicion of an infection
exists
 appropriate in patients with massive burns
 based on culture and sensitivities
Complications of Acute Phase
 Infection- due to destruction of body’s 1st line
of defense. Partial thickness wds can convert to
full-thickness wds with infection present.
 Signs of sepsis are: high temp., increased
pulse & resp., decreased BP, and decreased
urinary output, mild confusion, chills, malaise,
and loss of appetite. WBC bet. 10,000 and
20,000. Infections usually gram neg. bacteria
(pseudomonas, proteus)
 Obtain cultures from all possible sources: IV,
foley, wound, oropharynx, and sputum
Neurologic-possible from electrical injuries
 Musculoskeletal-has the most potential f
complications during acute phase due to
healing and scar formation making skin less
supple and pliant. contractures can occur
 Gastrointestinal-adynamic ileus results from
sepsis, diarrhea or constipation ( narcotics &
decreased mobility), gastric ulcers , stress,
occult blood in stools possible
 Endocrine-stress DM might occur-assess
glucose
Complications Cont.,
 Electrolytes Imbalances
 Hyperkalemia
 A result of cellular destruction
 Hyponatremia
 A result of fluid shifts into interstitial space
 Acid-Base Imbalances
 Metabolic Acidosis
 Failure to conserve bicarbonate
 Also, a result of fluid shifts into interstitial space
See Smeltzer & Bare pp. 1713; Table 57-3
Burn Shock
 Shock is a state of inadequate cellular perfusion
 Burn Injuries involving > 35 % TBSA
 Clinical manifestations:
 Hypotension & tachycardia
 Decreased Cardiac Output:
 Decreased preload, stroke volume & contractility
 Increased afterload
 Monitoring: PCWP & CVP values decreased
 Prevention: Early & full fluid resuscitation !!
Smeltzer & Bare pp. 1708 (Figure 57-3)
 NUTRITION
Nutritional Therapy
 Fluid replacement takes priority over
nutritional needs in the initial emergent
phase.
 NG tube is inserted and connected to
low intermittent suction for
decompression. When bowel sounds
return (48-72 hrs) after injury, start
with clear liquids and progress up to a
diet high in proteins and calories
Adult Energy Requirements
 Curreri formula
 Daily energy requirement = (25W + 40B)
 Long formula
 BEE x activity factor x injury factor
 Male BEE = 66.6 + 13.8W + 5H – 6.8A
 Female BEE = 655 + 9.6W + 1.9H – 4.7A
 Activity factors:
 1.2 if confined to bed
 1.3 if out of bed
 Injury factor:
 2.1 for severe thermal burn
 W=weight in kg, B=total burn area as % of
total body mass, H=height in cm, A=age in
years
Child Energy Requirements
 Wolfe Formula
 Energy = BMR x 2
 BMR Calculations
Age Boys Girls
0-3 years 60.9W – 54 61W – 51
4-10 years 22.7W + 459 22.5W +
499
11-18 years 17.5W + 651 12.2W + 746
 W= weight in kg
Child Energy Requirements
 Modified Galveston formula
 < 1 year: (2100 x BSA) + (1000 x burn area)
 < 12 years: (1800 x BSA) + (1300 x burn
area)
 12-18 years: (1500 x BSA) + (1500 x burn
area)
 BSA = body surface area in m2
 Burn area = surface area burned in m2
Carbohydrate Requirements
 Glucose reduces extent of hypermetabolic
response and protein breakdown
 High rates of glucose delivery:
 Causes hyperglycaemia needing insulin
 Stimulates hepatic lipogenesis & altered liver function
 Increased CO2 production
 Prevents & slow weaning from ventilator
 Adults: 5 mg/kg/min avoids complications
 Children: 5-7 mg/kg/min
 Infants: D5W 5 mg/kg/min initially then
increased to a max of 15 mg/kg/min over first few
days
Fat Requirements
 Normal diet leads to muscle wasting
with central obesity due to hepatic
steatosis
 Fat reduction prevents problems when
protein replaces lipid energy
 Adults: Minimum of 4% total energy
 15% meets essential fatty acid requirements and
provides for fat-soluble vitamins
 Vary composition of fats
 Children: Minimum of 2-3% total energy
 Infants: Maximum of 4g/kg of IBW
Protein Requirements
 Intact protein rather than amino acids
 Improved weight maintenance and survival
 Frequent estimations of nitrogen loss to
ensure adequate replacement
 TNL = TUN + 4g
 TNL = (UUN x 1.25) + 4g
 NB = TNL – NS
 6.25 g protein = 1 g nitrogen
 Adults: 2-3 g protein/kg IBW
 Children:
 < 1 year old: 3-4 g protein/kg IBW
 1-3 years old: 2.5-3 g protein/kg IBW
 >3 years old: 1.5-2.5 g protein/kg IBW
 25% energy as protein
Vitamin Requirements
 Specific requirements not established for
most
 Multivitamin supplementation
 Vitamin A
 Immune function & epithelialization
 10,000 IU/day
 < 3 years old: 5,000 IU/day
Vitamin Requirements
 Vitamin C
 Immune function
 Wound Healing
 Collagen synthesis
 Free radical scavenging properties limits tissue damage
 Ascorbic acid study
 High doses reduced resuscitation fluid volume, body
weight gain, wound edema, & severity of respiratory
dysfunction
 Adults: 500 mg twice a day
 Children up to age 10: 250 mg twice a day
Enteral vs. Parenteral Feeding
 Enteral preferred over parenteral
 Maintains integrity of GI tract
 Parenteral more expensive & increases
complications
 Hospital-made vs. commercial diets
 Hospital made diets as good as commercial
 Weight gain & protein increase similar
 Patient tolerance similar
SPECIAL CONSIDERATIONS
ELECTRICAL BURNS
 Extent of injury
depends upon
 Type of current
 Amount of current
 Path of current
 Duration of current
ELECTRICAL BURNS
 Injury from electrical
burns results from
coagulation necrosis
that is caused by
intense heat
generated from an
electric current.
Electrical injury can cause:
 Fractures of long bones and vertebra
 Cardiac arrest or arrhythmias--can be
delayed 24-48 hours after injury
 Severe metabolic acidosis--can develop in
minutes
 Myoglobinuria--acute renal tubular
necrosis- myoglobin released from muscle
tissue whenever massive muscle damage
occurs--goes to kidneys--and can
mechanically block the renal tubules due
to the large size!
ELECTRICAL INJURY
 Cardiac arrhythmias
are the most serious
immediate injury that
occurs with electrical
contact
 V-Fib
 V-Tach
ELECTRICAL BURNS
COURTESY DAVID EFFRON,
M.D.
COURTESY BONNIE
MENEELY, R.N.
Treatment of electrical
burns…
 Fluids--Ringers lactate or other fluids-
flushes out kidneys--you want 75-100
cc/hr until urine sample clear
 an osmotic diuretic (Mannitol) may be
given to maintain urine output
Electricity can instantaneously destroy tissue. This child has a
burn that resulted from biting on an electrical cord. These
burns often occur at the corners of the mouth, as seen here.
ADDITIONAL INJURIES
 Skin burns
 Entrance and
exit wounds
 Fractures
 cannot
determine the
extent of the
injury from the
surface burn
DA
Y
ON
E
DA
Y
3
LIGHTNING STRIKE
 Usually superficial
injury
 Victims die from
cardiac arrest
 Resuscitate the
“dead”
 Patients who are
breathing will usually
survive
Chemical Burn
2 types of chemical burns
 acids-can be neutralized
 alkaline- adheres to tissue, causing
protein hydrolyses and
liquefaction
 examples: cleaning agents, drain cleaners,
and lyes, etc...
Chemical Burns
 Acids
 Immediate coagulation-type ,necrosis creating
an eschar though self-limiting injury
 coagulation of protein results in necrosis in which
affected cells or tissue are converted into a dry,
dull, homogeneous eosinophilic mass without
nuclei
Chemical Burns
 Bases (Alkali)
 Liquefactive necrosis with continued
penetration into deeper tissue resulting in
extensive injury
 characterized by dull, opaque, partly or completely
fluid remains of tissue
 Dry Chemicals
 Exothermic reaction with water
CHEMICAL BURNS
 Injure the skin
 May be absorbed into the body and
damage internal organs
 May be inhaled into the lungs and cause
lung tissue damage
 May have minimal skin injury and yet
cause severe systemic injury
FACTORS CAUSING TISSUE
DAMAGE IN CHEMICAL
BURNS
 Type of chemical
 Concentration of
chemical
 Amount of chemical
 Duration of contact
 Manner of contact
 Mechanism of
action
ACID BURN
TREATMENT OF CHEMICAL EXPOSURE
 Remove and bag all contaminated
clothing
 Brush off dry chemical
 Flush with copious amounts of water
or any drinkable liquid
 Wipe or scrape any retained chemical
and irrigate again
“THE SOLUTION TO POLLUTION IS
DILUTION”
Chemical Burn to Eye
Management
 Flood the eye with copious amounts of
water only
 Never place chemical antidote in eyes
 Flush using LR/NS/H2O from medial to
lateral for at least 15 minutes
 Nasal Cannula
 IV Ad Set
 Remove contact lenses
 May trap irritants
Rehabilitation Phase
 Defined as beginning when the patient’s
burn wound is covered with skin or healed
and patient is capable of assuming some
self-care activity.
 Can occur as early as 2 weeks to as long as
2-3 months after the burn injury
 Goals for this time is to assist patient in
resuming functional role in society &
accomplish functional and cosmetic
reconstruction.
Clinical Manifestations
 Burn wd either heals by primary intention
or by grafting.
 Scars may form & contractures.
 Mature healing is reached in 6 months to
2 years
 new skin sensitive to trauma
Complications
 Most common complications of burn injury
are skin and joint contractures and
hypertrophic scarring
 Because of pain, pts will assume flexed
position. It predisposes wds to contracture
formation
 Use of physical therapy, pressure
garments, splints, etc. are used
Hypertrophic Scar Formation
 Excessive scar formation, which rises above
the level of the skin
 Management: Pressure Garments
 Elasticized garments that are custom fitted
 Maintains constant pressure on the wound
 Result: smoother skin & minimized scar appearance
 Client Considerations:
 Must be worn 23 hours a day
 Need to be worn for up to 1-2 years
 Are very hot and tight !!
Example of a pressure
garment
Contracture Formation
 Shrinkage and shortening of burned tissue
 Results in disfigurement
 Especially if burn injury involves joints
 Management is opposing force:
 Splints, proper positioning and ROM
Must begin at day one !!
Multidisciplinary approach
is essential !!
Example of Contracture
Psychosocial Considerations
 Alterations in Body Image
 Loss of Self-Esteem
 Returning to community, work or school
 Sexuality
 Supports Services
 Psychologist, social work & vocational counselors
 Local or national burn injury support organizations
 Nursing Considerations
 Encourage client & family to express feelings
 Assist in developing positive coping strategies
Prevention of Burn Injuries
 Proper education and supervision
 childproof items in electrical sockets
 keep dangerous items (matches) out of reach
 Safety measures for the elderly
 teach small children 911
 smoke detectors in house
 STOP, DROP, AND ROLL
Position of comfort after burn trauma (to be
avoided)
 1. Neck flexion
 2. Shoulder protraction
 3. Elbow flexion
 4. Metacarpal extension
 5. Interphalangeal flexion
 6. Wrist flexion
 7. Hip flexion
 8. Knee flexion
 9. Ankle plantar flexion
 Techniques available for burn
reconstruction
 1. Without deficiency of tissue
 • Excision and primary closure
 • Z-plasty
 2. With deficiency of tissue
 • Simple reconstruction
 - Skin graft
 - Transposition flaps (Z-plasty and modifications)
 • Reconstruction of skin and underlying tissues
 - Axial and random flaps
 - Myocutaneous flaps
 - Tissue expansion
 - Free flaps
Pediatric Burns
 Thin skin
 increases severity of burning relative to adults
 Large surface/volume ratio
 rapid fluid loss
 increased heat loss  hypothermia
 Delicate balance between dehydration and
overhydration
 Immature immunological response  sepsis
 Always consider possibility of child abuse
Geriatric Burns
 Decreased myocardial reserve
 fluid resuscitation difficulty
 Peripheral vascular disease, diabetes
 slow healing
 COPD
 increases complications of airway injury
 Poor immunological response - Sepsis
 % mortality ~= age + % BSA burned
Recent advances
 IV or nebulised Heparin shown to reduce
tracheobronchial cast formation in
inhalation burns
 Early near total excision and grafting
 Anabolic agents like oxandrlone
,GH,testoesterone as a nutritional
adjuvants
SUMMARY
 Protect yourself and your patient
 Maintain c-spine immobilization
 Treat burn patients as trauma patients
 Properly cool the burn
 Be alert for inhalation injuries
 Flush chemical burns adequately
 Monitor heart in electrical burn patients
BURNS
B - breathing
body image
U - urine output
R - rule of nines
resuscitation of
fluid
N - nutrition
S - shock
silvadene

More Related Content

What's hot

Burns - Embrace discomfort
Burns - Embrace discomfortBurns - Embrace discomfort
Burns - Embrace discomfort
Dona Anderson
 

What's hot (20)

Burns
BurnsBurns
Burns
 
BURN
BURN BURN
BURN
 
Burns
BurnsBurns
Burns
 
9 burn
9 burn9 burn
9 burn
 
Pediatric Burns - Handout
Pediatric Burns - HandoutPediatric Burns - Handout
Pediatric Burns - Handout
 
Burn
BurnBurn
Burn
 
Burn Injuries
Burn InjuriesBurn Injuries
Burn Injuries
 
pathophysiology of burn
pathophysiology of burnpathophysiology of burn
pathophysiology of burn
 
Burns
BurnsBurns
Burns
 
Systemic responses to burn injury
Systemic responses to burn injurySystemic responses to burn injury
Systemic responses to burn injury
 
burn seminar
burn seminarburn seminar
burn seminar
 
Burns in pediatrics
Burns in pediatricsBurns in pediatrics
Burns in pediatrics
 
BURN
BURNBURN
BURN
 
1. burn cne ppt
1. burn cne ppt1. burn cne ppt
1. burn cne ppt
 
Burns - Embrace discomfort
Burns - Embrace discomfortBurns - Embrace discomfort
Burns - Embrace discomfort
 
Burns Pathophysiology, Evaluation and Management
Burns Pathophysiology, Evaluation and ManagementBurns Pathophysiology, Evaluation and Management
Burns Pathophysiology, Evaluation and Management
 
BURN ... by Dr. Rezuan .. JIMCH , Bangladesh
BURN ... by Dr. Rezuan ..  JIMCH , BangladeshBURN ... by Dr. Rezuan ..  JIMCH , Bangladesh
BURN ... by Dr. Rezuan .. JIMCH , Bangladesh
 
Pediatric burns seminar
Pediatric burns seminarPediatric burns seminar
Pediatric burns seminar
 
Burns And ANAESTHESIA
Burns And ANAESTHESIABurns And ANAESTHESIA
Burns And ANAESTHESIA
 
Burns
BurnsBurns
Burns
 

Similar to Burns 158 slides.ppt

BURN details types and definition and all
BURN  details types and definition and allBURN  details types and definition and all
BURN details types and definition and all
TanusriBarui2
 
BURN. pptx. nursing. education. adult health
BURN. pptx. nursing. education. adult healthBURN. pptx. nursing. education. adult health
BURN. pptx. nursing. education. adult health
IpsitaBagchi1
 

Similar to Burns 158 slides.ppt (20)

Physiotherapy in burns
Physiotherapy in burnsPhysiotherapy in burns
Physiotherapy in burns
 
Burns_2_.pptx
Burns_2_.pptxBurns_2_.pptx
Burns_2_.pptx
 
evaluation and management of patient presenting with Burn.pptx
evaluation and management of patient presenting with Burn.pptxevaluation and management of patient presenting with Burn.pptx
evaluation and management of patient presenting with Burn.pptx
 
BURN CME.pptx
BURN CME.pptxBURN CME.pptx
BURN CME.pptx
 
Copy2-BURNS slides.pptx
Copy2-BURNS slides.pptxCopy2-BURNS slides.pptx
Copy2-BURNS slides.pptx
 
Burn And Scald
Burn And  ScaldBurn And  Scald
Burn And Scald
 
BURN details types and definition and all
BURN  details types and definition and allBURN  details types and definition and all
BURN details types and definition and all
 
Burns -RBXY1.ppt
Burns -RBXY1.pptBurns -RBXY1.ppt
Burns -RBXY1.ppt
 
Burns and scalds
Burns and scaldsBurns and scalds
Burns and scalds
 
Burns and scalds
Burns and scaldsBurns and scalds
Burns and scalds
 
burns ppt.pptx
burns ppt.pptxburns ppt.pptx
burns ppt.pptx
 
BURN. pptx. nursing. education. adult health
BURN. pptx. nursing. education. adult healthBURN. pptx. nursing. education. adult health
BURN. pptx. nursing. education. adult health
 
Physiotherapy in burns
Physiotherapy in burnsPhysiotherapy in burns
Physiotherapy in burns
 
BURNS REVIEW
BURNS REVIEWBURNS REVIEW
BURNS REVIEW
 
Burn
BurnBurn
Burn
 
Ohio ACEP Board Review: Environmental Emergencies I
Ohio ACEP Board Review: Environmental Emergencies IOhio ACEP Board Review: Environmental Emergencies I
Ohio ACEP Board Review: Environmental Emergencies I
 
Burn management
Burn managementBurn management
Burn management
 
SURGICAL MANAGEMENTOF BURN patient VICTIM.pptx
SURGICAL MANAGEMENTOF BURN patient VICTIM.pptxSURGICAL MANAGEMENTOF BURN patient VICTIM.pptx
SURGICAL MANAGEMENTOF BURN patient VICTIM.pptx
 
BurN baby Burn.
BurN baby Burn.BurN baby Burn.
BurN baby Burn.
 
Introduction to burns
Introduction to burnsIntroduction to burns
Introduction to burns
 

Recently uploaded

Recently uploaded (20)

Arterial health throughout cancer treatment and exercise rehabilitation in wo...
Arterial health throughout cancer treatment and exercise rehabilitation in wo...Arterial health throughout cancer treatment and exercise rehabilitation in wo...
Arterial health throughout cancer treatment and exercise rehabilitation in wo...
 
Is preeclampsia and spontaneous preterm delivery associate with vascular and ...
Is preeclampsia and spontaneous preterm delivery associate with vascular and ...Is preeclampsia and spontaneous preterm delivery associate with vascular and ...
Is preeclampsia and spontaneous preterm delivery associate with vascular and ...
 
PT MANAGEMENT OF URINARY INCONTINENCE.pptx
PT MANAGEMENT OF URINARY INCONTINENCE.pptxPT MANAGEMENT OF URINARY INCONTINENCE.pptx
PT MANAGEMENT OF URINARY INCONTINENCE.pptx
 
Why invest into infodemic management in health emergencies
Why invest into infodemic management in health emergenciesWhy invest into infodemic management in health emergencies
Why invest into infodemic management in health emergencies
 
Evaluation of antidepressant activity of clitoris ternatea in animals
Evaluation of antidepressant activity of clitoris ternatea in animalsEvaluation of antidepressant activity of clitoris ternatea in animals
Evaluation of antidepressant activity of clitoris ternatea in animals
 
Final CAPNOCYTOPHAGA INFECTION by Gauri Gawande.pptx
Final CAPNOCYTOPHAGA INFECTION by Gauri Gawande.pptxFinal CAPNOCYTOPHAGA INFECTION by Gauri Gawande.pptx
Final CAPNOCYTOPHAGA INFECTION by Gauri Gawande.pptx
 
Gauri Gawande(9) Constipation Final.pptx
Gauri Gawande(9) Constipation Final.pptxGauri Gawande(9) Constipation Final.pptx
Gauri Gawande(9) Constipation Final.pptx
 
1130525--家醫計畫2.0糖尿病照護研討會-社團法人高雄市醫師公會.pdf
1130525--家醫計畫2.0糖尿病照護研討會-社團法人高雄市醫師公會.pdf1130525--家醫計畫2.0糖尿病照護研討會-社團法人高雄市醫師公會.pdf
1130525--家醫計畫2.0糖尿病照護研討會-社團法人高雄市醫師公會.pdf
 
CURRENT HEALTH PROBLEMS AND ITS SOLUTION BY AYURVEDA.pptx
CURRENT HEALTH PROBLEMS AND ITS SOLUTION BY AYURVEDA.pptxCURRENT HEALTH PROBLEMS AND ITS SOLUTION BY AYURVEDA.pptx
CURRENT HEALTH PROBLEMS AND ITS SOLUTION BY AYURVEDA.pptx
 
Young at heart: Cardiovascular health stations to empower healthy lifestyle b...
Young at heart: Cardiovascular health stations to empower healthy lifestyle b...Young at heart: Cardiovascular health stations to empower healthy lifestyle b...
Young at heart: Cardiovascular health stations to empower healthy lifestyle b...
 
Multiple sclerosis diet.230524.ppt3.pptx
Multiple sclerosis diet.230524.ppt3.pptxMultiple sclerosis diet.230524.ppt3.pptx
Multiple sclerosis diet.230524.ppt3.pptx
 
Non-Invasive assessment of arterial stiffness in advanced heart failure patie...
Non-Invasive assessment of arterial stiffness in advanced heart failure patie...Non-Invasive assessment of arterial stiffness in advanced heart failure patie...
Non-Invasive assessment of arterial stiffness in advanced heart failure patie...
 
The POPPY STUDY (Preconception to post-partum cardiovascular function in prim...
The POPPY STUDY (Preconception to post-partum cardiovascular function in prim...The POPPY STUDY (Preconception to post-partum cardiovascular function in prim...
The POPPY STUDY (Preconception to post-partum cardiovascular function in prim...
 
Antiplatelets in IHD, Dose Duration, DAPT vs SAPT
Antiplatelets in IHD, Dose Duration, DAPT vs SAPTAntiplatelets in IHD, Dose Duration, DAPT vs SAPT
Antiplatelets in IHD, Dose Duration, DAPT vs SAPT
 
Relationship between vascular system disfunction, neurofluid flow and Alzheim...
Relationship between vascular system disfunction, neurofluid flow and Alzheim...Relationship between vascular system disfunction, neurofluid flow and Alzheim...
Relationship between vascular system disfunction, neurofluid flow and Alzheim...
 
TEST BANK For Advanced Practice Nursing in the Care of Older Adults, 2nd Edit...
TEST BANK For Advanced Practice Nursing in the Care of Older Adults, 2nd Edit...TEST BANK For Advanced Practice Nursing in the Care of Older Adults, 2nd Edit...
TEST BANK For Advanced Practice Nursing in the Care of Older Adults, 2nd Edit...
 
Impact of cancers therapies on the loss in cardiac function, myocardial fffic...
Impact of cancers therapies on the loss in cardiac function, myocardial fffic...Impact of cancers therapies on the loss in cardiac function, myocardial fffic...
Impact of cancers therapies on the loss in cardiac function, myocardial fffic...
 
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model SafeSurat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
Surat @ℂall @Girls ꧁❤8527049040❤꧂@ℂall @Girls Service Vip Top Model Safe
 
Retinal consideration in cataract surgery
Retinal consideration in cataract surgeryRetinal consideration in cataract surgery
Retinal consideration in cataract surgery
 
US E-cigarette Summit: Taming the nicotine industrial complex
US E-cigarette Summit: Taming the nicotine industrial complexUS E-cigarette Summit: Taming the nicotine industrial complex
US E-cigarette Summit: Taming the nicotine industrial complex
 

Burns 158 slides.ppt

  • 1. Dr Rahul Gorka M.S, M.Ch Lecturer (Plastic Surgery)
  • 2. Definition of a Burn  “Tissue injury caused by thermal, radiation, chemical, or electrical contact resulting in protein denaturation, burn wound edema, and loss of intravascular fluid volume due to increased vascular permeability.”
  • 3. Burn Statistics  At least 50% of all burn accidents can be prevented  children playing with fire account for more than one-third of preschool deaths by fire  In the US, approximately 2.4 million burn injuries are reported each year.  Burn injuries are second to motor vehicle accidents as leading cause of accidental death in the US
  • 4. TYPES OF BURNS  Flame (Thermal)  Electrical  AC & DC  Lightning  Chemical  Steam  Radiation  Scald COURTESY DAVID EFFRON, M.D. THIRD DEGREE BURNS WITH ESCHAROTOMIES
  • 5. Types of Burns  Thermal Injuries (most common)  Contact Direct contact with hot object (i.e. pan or iron) Anything that sticks to skin (i.e. tar, grease or foods)  Scalding Direct contact with hot liquid / vapors (moist heat) i.e. cooking, bathing or car radiator overheating Single most common injury in the pediatric client  Flame Direct contact with flame (dry heat) i.e. structural fires / clothing catching on fire
  • 6. Types of Burns  Chemical  Caused by strong acids, alkalis, phenols, cresols, phosphorus or mustard gas  Results in necrosis  Electrical  Caused by electric current which may generate heat up to 5000ºC  May result in necrosis, respiratory paralysis, or ventricular fibrillation
  • 7. Types of Burn Injury  Smoke & inhalation injury-inhaling hot air or noxious chemicals  Cold thermal injury-frostbite.  Radiation  Caused by prolonged or intense exposure to ultraviolet radiation  Examples: Sunburn, tanning beds
  • 8. Classification of Burn Injury  Treatment of burns is directly related to the severity of injury!  Severity is determined by:  depth of burn  external of burn calculated in percent of total body surface (TBSA)  location of burn  patient risk factors
  • 9. Location of Burns  Has a direct relationship to the severity of the burn.  Face, neck & chest burns may cause respiratory illness mechanical obstruction secondary to edema or eschar formation
  • 10. Burn Patient Severity  Patient age  Less than 2 or greater than 55  Have increased incidence of complication  Burn configuration  Circumferential burns can cause total occlusion of circulation to an area due to edema  Restrict ventilation if encircle the chest  Burns on joint area can cause disability due to scar formation
  • 12. Skin  Largest body organ. Much more than a passive organ.  Protects underlying tissues from injury  Temperature regulation  Acts as water tight seal, keeping body fluids in  Sensory organ
  • 13. Skin  Injuries to skin which result in loss, have problems with:  Infection  Inability to maintain normal water balance  Inability to maintain body temperature
  • 14. Skin  Two layers  Epidermis  Dermis  Epidermis  Outer cells are dead  Act as protection and form water tight seal
  • 15. Skin  Epidermis  Deeper layers divide to produce the stratum corneum and also contain pigment to protect against UV radiation  Dermis  Consists of tough, elastic connective tissue which contains specialized structures
  • 16. Skin  Dermis - Specialized Structures  Nerve endings  Blood vessels  Sweat glands  Oil glands - keep skin waterproof, usually discharges around hair shafts  Hair follicles - produce hair from hair root or papilla  Each follicle has a small muscle (arrectus pillorum) which can pull the hair upright and cause goose flesh
  • 17. First-Degree Burns  Does not go below basal layer of the epidermis  Dry and painful  Appears red due to increased blood flow  Heals in a few days
  • 18. Second-Degree Burns  Extends below basal layer, but not completely through dermis  Superficial  Blister, very painful, contains skin parts (adnexa) which assist in epithelialization  Deep Partial-thickness  Deeper in dermis, fewer adnexa, longer healing time, less painful
  • 19. Third-Degree Burns  Extends completely through dermis  Adnexa destroyed so can’t heal by epithelialization  Dermal plexus of nerves destroyed- less painful  Burns can be yellow, red, black, brown
  • 20. Burn Depth  Fourth-degree  Full-thickness destruction of skin/subcutaneous tissue  Involves underlying fascia, muscle, bone or other structures  Prolonged disability
  • 21.
  • 22. FIRST AND SECOND DEGREE BURNS FIRST DEGREE BURN SECOND DEGREE BURN
  • 23. THIRD DEGREE BURNS COURTESY DAVID EFFRON,M.D. COURTESY BONNIE MENEELY, R.N.
  • 26. Initial Estimate of : “Rule of Nines” Adult anatomical areas = 9% BSA (or multiple) Extent of Burn • Not accurate for infants / children due to larger BSA of head & smaller BSA of legs. Burn diagrams illustrate adult and child differences.
  • 27. Rule of Nines  In the adult, most areas of the body can be divided roughly into portions of 9%, or multiples of 9. This division, called the rule of nines, is useful in estimating the percentage of body surface damage an individual has sustained in burn.
  • 28. Burn Assessment Lund & Browder Chart
  • 29. Thermal Burn Injury Pathophysiology  Emergent phase  Response to pain  catecholamine release  Fluid shift phase  massive shift of fluid - intravascular  extravascular  Hypermetabolic phase   demand for nutrients  repair tissue damage  Resolution phase  scar tissue and remodeling of tissue
  • 30. Zones of Burn Injury  Zone of Coagulation  Inner Zone  Area of cellular death (necrosis)  Zone of Stasis  Area surrounding zone of coagulation  Cellular injury: decreased blood flow & inflammation  Potentially salvable; susceptible to additional injury  Zone of Hyperemia  Peripheral area of burn  Area of least cellular injury & increased blood flow  Complete recovery of this tissue likely.
  • 31. ESCHAR  The necrotic tissue resulting from a burn is known as eschar.  It is a good substrate for microorganisms. If left untreated it becomes colonized, contaminated and eventually infected.  Topical antimicrobial agents increase the time to eschar separation.
  • 33. Burn Pathophysiology:inflammation& Edema  Injured tissue: capillary permeability es  Protein leakage: resultant hypoproteinemia, and ed osmotic pressure in burned tissue  Decreased cell membrane potential with inward shift of Na+ and H2O, resulting in cellular swelling  Edema maximal at 24 hrs, usually resolved by 3-5 days; capillary leak normal at 24 hrs
  • 34. Burn Pathophysiology: Metabolic  Hypermetabolic response  BSA affected; may approach 200% of basal metabolic rate  catabolic response  acute phase response  Mediators implicated:  stress hormones: catecholamines, steroids  cytokines: TNF, IL-1, IL-6  lipids: prostaglandins, thromboxane B2, PAF
  • 35. Burn Pathophysiology: Metabolic  Prostaglandins, IL-1, IL-6 implicated in:  increase in core temperature of 1-2oC  initiating acceleration of nitrogen catabolism  ? inversion of T4/T8 ratios from 2:1 to 1:2  Early enteral feeding associated with attenuation of the hypermetabolic response
  • 36. Burn Pathophysiology: Cardiac  Cardiac output initially decreases  loss of intravascular volume  CVP and PCWP typically low-normal, even after adequate volume resuscitation  Cardiac output usually normalizes before intravascular volume completely restored   iCa++ may present as hypotension/EMD  out of proportion to hypoalbuminemia
  • 37. Burn Pathophysiology: Renal it can result from:  prolonged hypotension due to hypovolemia  myoglobin release from damaged muscle/tissue  hemoglobinuria from heat-induced hemolysis  Renal blood flow initially es, followed by dramatic  in GFR, coinciding with onset of the postburn hypermetabolic state, and hyperdynamic circulation
  • 38. Burn Pathophysiology: Renal  Early in the postburn period, decreased urinary Na+ and Cl-  K+ wasting in the urine is common (up to 200 mEq/liter), secondary to the intense adrenal response to burn injury/stress
  • 39. Burn Pathophysiology: Hypertension  May be common in pediatric patients  up to 57% in one study  7-10 year old boys with >20% BSA affected  Hypertensive encephalopathy may result  7% of hypertensive pediatric burn patients  Mechanism may involve hypervolemia with concomitant activation of RA SYSTEM  ?elevated “stress” plasma renin and aldosterone
  • 40. Burn Physiology: Pulmonary  Pulmonary dysfunction etiologies in this setting:  shock, inhalational injury, aspiration, sepsis, CHF, trauma  Upper airway injury/edema may contribute  airway occlusion impairs flow of tidal breaths • resolution of occlusion can cause reexpansion
  • 41. Burn Physiology: Pulmonary  Circumferential thoracic eschar or edema may contribute to restrictive lung disease  Hypovolemia may cause V/Q mismatch  Inflammatory mediators released in burn injury linked to evolution of ARDS  therefore, expect some degree of pulmonary capillary leak, on a continuum from mild pulmonary edema, to frank ARDS
  • 42. Burn Pathophysiology: CNS  CNS dysfunction in up to 14% of burn pts  most had >50% BSA involvement  Hypoxia most common etiology  smoke inhalation, pulm edema, pneumonia  Hypovolemia, hyponatremia, cortical vein thrombosis, sepsis, and gliosis due to watershed infarct also implicated  ? Role of neurotoxic factors
  • 43. Burn Pathophysiology: GI  Stress (curling’s) ulcer  prophylaxis: antacids, H2 blockers, or sucralfate  Increased gut permeability in first 24 hours  Acalculous cholecystitis  fever, abdominal distention, jaundice  bacterial seeding (ascending cholangitis)  sterile, in patients with dehydration, ileus, or pancreatitis
  • 44. Burn Pathophysiology: GI  Acute pseudo-obstruction of the colon  massive colonic dilation without organic cause Narcotic ileus  oral narcotic antagonists may be efficacious  hypovolemia shunt blood from the splanchnic bed and promote mucosal atrophy and failure of the gut barrier
  • 45. Burn Pathophysiology: Hepatic  Modest hepatic dysfunction common early  Persisting, or severe hepatic dysfunction, associated with negative outcome  larger BSA involvement (58% vs 30%)  greater mortality (74% vs 9%)  clinical jaundice associated with 90% mortality  Late onset of conjugated hyperbilirubinemia usually related to occult, or overt, sepsis
  • 46. Burn Pathophysiology: Blood  Initially, shortened RBC survival with intra- vascular hemolysis/possible hemoglobinuria  typically resolves after the 1st week  Anemia is common, and to be expected;  may be masked initially by hemoconcentration  may be exacerbated by fluid management, occult blood loss  typically persists until wound healing occur  depressed erythropoietin levels documented
  • 47. Burn Physiology: Immunologic  Skin as an organ of host defense:  keratin layers as physical barrier to penetration  cycles of desquamation (“debulking” of skin bacterial burden)  stratum corneum: unsaturated free fatty acid film which is bacteriostatic and fungistatic  colonization resistance due to normal flora  antigen presentation to Langerhans’ cells
  • 48. Burn Physiology: Immunologic  Cellular Immune Function  markedly delayed allograft rejection  ed antigen responses  total lymphocyte count typically normal, but T4 (helper T-cell) count , while T8 (suppressor T-cell) count  (T4/T8 ratio inverts)  several circulating mediators in burn patient sera suppress normal lymphocyte function
  • 49. Burn Physiology: Immunologic  “Immunologic Dissonance” resulting from activation of inflammatory cascades/SIRS  Systemic immunosupression may therefore occur very early in the post-burn period; magnitude of immunocompromise  BSA
  • 50. Increased gut mucosal Permeability Immunosuppression Decreased Renal blood flow Severe Burn Vascular Permeability & oedema Altered haemodynamics Hypermetabolism
  • 51. Phases of Burn Care  Emergency assessment and care (ABCs)  Resuscitation (hours 0-48)  Definitive care (day 3 until wounds are closed)  Rehabilitation (begins during resuscitation and lasts entire lifespan)
  • 52. Rescue  A-B-C-D-E-F  Stop the burning  Decontaminate casualty at the scene  Avoid injury to the rescuer  Careful with high voltage electrical wires  Assess for other injuries
  • 53. ABCs of Emergency Burn Care (Advanced Burn Life Support)  A = Airway (with cervical spine assessment)  B = Breathing  C = Circulation  D = Disability  E = Exposure and Environmental Control  F = Fluid Resuscitation based on Burn Size and Weight Measurement  Secondary Survey
  • 54. A: Airway  Assess the patient’s airway  Upper airway edema due to inhalation injury  Rapid or delayed progression  Decision to intubate: individualized  Mild symptoms: observe in ICU  Pre-transport: prophylactic intubation  When in doubt, intubate
  • 55. B: Breathing  Look, listen, feel for breath sounds and chest movement  Give 100% oxygen to all victims of major burn beginning in the field  Pulse oximetry  Arterial blood gases  Required for definitive diagnosis of CO  Baseline chest x-ray
  • 56. C: Circulation  Who needs fluid resuscitation?  All >20% total body surface area burned (TBSA)  Young and old with >10% TBSA  2 large bore peripheral IVs  Unburned skin  Burned skin  Central access  Cutdown  Interosseous
  • 57. D: Disability  Assess level of consciousness: AVPU  Alert  Responds to verbal stimuli  Responds to painful stimuli  Unresponsive  Alteration in mental status is not normal  Pupils  Moves extremities
  • 58. E: Exposure and Environment  Remove clothing, jewelry  Keep warm  blankets  warm I.V. fluids  heating lamps  heat the room  Keep Patient Dry
  • 59. F: Fluid Resuscitation (based on burn size and weight)  Determine fluid needs based on burn size and weight  Burn size: include second and third degree only  Rule of Nines  One hand = one percent  Lund-Browder chart  Overestimation by referring hospitals is common  Weight: pre-burn weight
  • 60. Fluid Therapy  1 or 2 large bore IV replacement lines (may need jugular or subclavian)  Cutdown if no option , increased risk of infection & sepsis  Fluid replacement based on: size/depth of burn, age of pt., & individualized considerations--ex. Dehydration in preburn state, chronic illness  options- RL, D5NS, dextam, albumin, etc.  there are formula’s for replacement: Parkland formula and Brooke formula
  • 61.  Total Body Surface Area (TBSA) Burned  Palmar Method  A quick method to evaluate scattered or localized burns  Client’s palm = 1 % TBSA  Rule of Nines  A quick method to evaluate the extent of burns  Major body surface areas divided into multiples of nine  Modified version for children and infants  Lund-Browder Method  Most Accurate; based on age (growth)  Can be used for the adult, children & infants
  • 62. Burns  Parkland/Baxter Formula  4 ml RL/kg body wt X % TBSA=ml RL for 24 hours  eg. Pt. wt=75 kg and burned 25% 4/75/25=7500 ml/24 hours 50% 1st 8 hours=3750ml 25% 2nd 8 hours=1875 ml 25% 3rd 8 hours=1875
  • 63. Formulas for Fluid Replacement Evans Formula. 􀂋 Colloids 1 ml./kg. of body wt/%/burn. 􀂋 Saline 1 ml/kg. of b. wt./% of burn. 􀂋 free water: dependent on age & insensible loss. 􀂋 1/2 of total is given the 1st 8 hrs. and the remainder given the next 16 hrs.
  • 64. Brooke Formula 􀂋. 􀂋 Colloids .5 ml/kg/% of body surface burned. 􀂋 Lactated Ringers 1.5 ml/% of body wt/% burn. 􀂋 H20 Again dependent. 􀂋 1/2 total amount given 1st 8 hrs. 􀂋 1/4 of total the 2nd 8 hrs. 1/4 the third 8 hrs.
  • 65. Galveston formula Resuscitation Formula  1. Fluid administration-Ringers lactate First 24 h:  a. 5000 ml/M2 burn + 2000 ml/TBSA m2  b. administer 1/2 in first 8 h postinjury and the 2nd half in the next 16 h.  Example: 15 kg child with an 87% TBSB, height 96 cm.  Body Surface (m2) =.60  Total Burn (m2)=.52  2000 ml x .6 TBSAm2 = 1200 ml  5000 ml x .52 TBSABm2 =2600 ml  Total fluids first 24 h = 3800 ml  Total fluids first 8 h = 1900 ml = 237 ml/h  Total fluids next 16 h = 1900 ml = 118 ml/h
  • 66. Assessment of adequacy of fluid replacement  Urinary output is most commonly used parameter  urine OP-30-50 cc/hr in an adult  cardiopulmonary factors- BP (systolic 90-100 mmHg, pulse less than 100, resp 16-20 breaths per min. (BP more accurate with arterial line)  sensoruim-alert, oriented to time, place, & person
  • 67. FIRST AID cooling the burn wound soon after the injury (within 30minutes) is beneficial in removing heat from the wound and limiting tissue damage. It can also reduce early edema and protein extravasation. Care must be taken, as prolonged or excessive cooling can be detrimental.
  • 68. Other precautions...  Burn too large--don’t immerse in water due to extensive heat loss  Never pack in ice  Pt. should be wrapped in dry clean material to decrease contamination of wound and increase warmth
  • 69. CRITERIA FOR ADMISSION  Both 2nd & 3rd degree burns  >20% BSA any age  >10% BSA <10 or >50 years of age  3rd degree only  >5% BSA  Burns of face, hands, feet, genitals, or joints
  • 70. CRITERIA FOR ADMISSION  Specialized burn types  Electrical & lightning  Chemical  Inhalation injury  Circumferential chest or extremity burns  Significant medical illness  Significant other injuries
  • 71. Critical Burn Criteria  30 > 10% BSA  20 > 30% BSA  >20% pediatric  Burns with respiratory injury  Hands, face, feet, or genitalia  Burns complicated by other trauma  Underlying health problems  Electrical and deep chemical burns
  • 72. Moderate Burn Criteria  30 2-10% BSA  20 15-30% BSA  10-20% pediatric  Excluding hands, face, feet, or genitalia  Without complicating factors
  • 73. Minor Burn Criteria  30 < 2% BSA  20 < 15% BSA  <10% pediatric  10 < 20% BSA
  • 74. Escharotomies —required if circumferential full thickness burns of chest,limbs or digits are present.  can impair circulation and cause distal ischemia. Circumferential full-thickness chest burns can restrict chestwall excursion and impair ventilation. mid-axial escharotomies performed either at bedside or in the operating room.. An escharotomy incision will only improve outcome without risk of harm in that situation.
  • 75.
  • 76. INHALATION INJURIES  Carbon monoxide poisoning  Toxic gas inhalation  Smoke inhalation  Heat inhalation  Steam inhalation  Asphyxiation
  • 77. 3 types of smoke and inhalation injuries  1. Carbon monoxide poisoning (CO poisoning and asphyxiation count for majority of deaths)  Treatment- 100% humidified oxygen-draw carboxyhemoglobin level- can occur without any burn injury to the skin
  • 78.  2. Inhalation injury above the glottis (caused by inhaling hot air, steam, or smoke.)  Mechanical obstruction can occur quickly- True ER! Watch for facial burns, signed nasal hair, hoarseness, painful swallowing, and darkened oral or nasal membranes
  • 79.  3. Inhalation injury below glottis  (above glottis-injury is thermally produced)  below glottis-it is usually chemically produced.  Amount of damage related to length of exposure to smoke or toxic fumes  Can appear 12-24 hours after burn
  • 80. SIGNS OF SMOKE INHALATION  Exposed to smoke in enclosed space  Unconscious while exposed to smoke  After exposure to smoke  Develops cough  Develops dyspnea  Develops chest pain
  • 81. SIGNS OF UPPER AIRWAY BURNS  Burns of the face  Singed eyebrows or nasal hairs  Burns in the mouth  Sooty sputum  History of being burned while confined to an enclosed space COURTESY ROY ALSON, M.D. LIP BURNS & SOOT IN MOUTH
  • 82. Inhalation Injury Management  Airway, Oxygenation and Ventilation  Assess for airway edema early and often  Consider early intubation  When in doubt oxygenate and ventilate  High flow oxygen  Bronchodilators may be considered if bronchospasm present  Diuretics not appropriate for pulmonary edema
  • 83. Inhalation Injury Management  Circulation  Treat for Shock (rare)  IV Access  LR/NS large bore, multiple IVs  Titrate fluids to maintain systolic BP and perfusion
  • 84. Inhalation Injury Management  Other Considerations  Assess for other Burns and Injuries  Treat associated inhalation injury/poisoning  Cyanide poisoning antidote kit  Positive pressure ventilation  Hyperbaric chamber (carbon monoxide poisoning)
  • 85. Wound Care Principals Goals  􀂄 close wound  􀂄 prevent infection  􀂄 reduce scarring and contractures  􀂄 provide for comfort Wound cleaning Debridement  􀂄 mechanical  􀂄 surgical Topical antibacterial therapy
  • 86. Cleansing and Debridement  Can be done in tank, shower, or bed  Debridement may be done in surgery. (Loose necrotic skin is removed)  bath given with with surgical detergent, disinfectant, or cleansing agent to reduce pathogenic organisms
  • 87. Infection is the most serious threat to further tissue injury and possible sepsis.  SURVIVAL is related to prevention of wound contamination.  Source of infection is pt’s own flora, predominantly from the skin, resp. tract, and GI tract.  Prevention of cross contamination from other patients is the priority for nurses!
  • 88. 2 methods used to control infections in burn wounds...  Open method- pt’s burn is covered with topical antibiotic and has no dressing  Closed method-uses sterile gauze impregnated with or laid over a topical antibiotic. Dressings changed 2-3 times q 24 hrs.
  • 89. Wound Care continued...  Staff should wear disposable caps, gowns, gloves, masks when wounds are exposed  use of sterile techniques  keep room warm  careful handwashing  any bathing areas disinfected before and after bathing
  • 90.  Coverage is the primary goal for burn wounds. Since usually not enough unburned skin for immediate skin grafting, other temporary wound closure methods are used  Allograph or homograft (same species which is usually from cadavers) is used for wound closure-- temporary--3 days to 2 wks  Porcine skin-heterograft or xenograft (different species)--temporary--3 days to 2 wks  autograft or cultured epithelial autograft- (pt’s own skin and cell culture)- permanent
  • 91. Burn Wound Closure  Permanent Skin Grafts  Two types: Autografts and Cultured Epithelial Autografts (CEA)  Autograft Harvested from client Non-antigenic Less expensive Decreased risk of infection Can utilize meshing to cover large area Negatives: lack of sites and painful
  • 92. Permanent Burn Wound Closure Cont.,  Permanent Skin Grafts Cont.,  Cultured Epithelial Autografts (CEA) A small piece of client’s skin is harvested and grown in a culture medium Takes 3 weeks to grow enough for the first graft Very fragile; immobile for 10 days post grafting Great for limited donor sites Negatives: very expensive; poor long term cosmetic results and skin remains fragile for years
  • 93. Temporary Burn Wound Closure  Biosynthetic Temporary Skin Grafts  Homograft  AKA Allograft  Live or cadaver human donors  Fairly expensive  Best infection control of all biologic coverings  Negatives:  Risk of disease transmission (i.e. HBV & HIV)  Antigenic: body rejects in 2 weeks  Not always available  Storage problems
  • 94. Temporary Burn Wound Closure  Biosynthetic Temporary Skin Grafts Cont.,  Heterograft AKA Xenograft Graft between 2 different species i.e. Porcine (pig) most common Fresh, frozen or freeze-dried (longer shelf life) Amendable to meshing & antimicrobial impregnation Antigenic: body rejects 3-4 days Fairly inexpensive Negatives: Higher risk of infection
  • 95. Temporary Burn Wound Closure  Temporary Skin Grafting Cont.,  Artificial Skins Transcyte: A collagen based dressing impregnated with newborn fibroblasts. Integra: A collagen based product that helps form a “neodermis” on which to skin graft.  Synthetic Any non-biologic dressing that will help prevent fluid & heat loss Biobrane, Xeroform or Beta Glucan collagen matrix
  • 96. Donor Site: Wound Considerations  The donor site is often the most painful aspect for the post-operative client.  We have created a brand new wound !!  Variety of products are used for donor sites. Most are left place for 24 hours and then left open to air.  Donor sites usually heal in 7-10 days
  • 97. using a dermatome (left) to remove donor skin and a mesher (right) to put holes in it.
  • 99. Other care measures include  Face is vascular and subject to increased edema- use open method  eye care-use saline rinses, artificial tears  hands &arms-extended and elevated on pillows or in slings to minimize edema, may need splints to keep them in functional positions
  • 100.  Ears- keep free of pressure. Ear burns- no pillows! Neck burns should not use pillows in order to decrease wound contraction.  Perineum-must be kept clean & dry. Indwelling foley will help in this & also to provide hourly outputs.  Lab tests ; to monitor electrolyte imbalance and ABGs  Physio therapy stared immediately
  • 101. Drug Therapy  Analgesics and Sedatives  given for pt comfort  IV pain meds initialy due to:  GI function is slowed or impaired because of shock or paralytic ileus  IM injections will not be absorbed well
  • 102. Drug Therapy  Tetanus immunization- given routinely to all burn patients because of the likelihood of anaerobic burn-wound contamination  Antimicrobial agents-usually topical due to little or no blood supply to the burn eschar so little delivery of the antibiotic to wound  Drug of choice is: Silver sulfadiazine
  • 103.  Curlings ulcer prophylaxis (Peptic Ulcer)  An H2 blocker (cimetidine, ranitidine,famotidine) start first 6 hours  antacids are no longer recommended - the patient should be kept NPO  with burns > 15% of BSA, an NG (OG) tube and bladder catheter should be placed
  • 104. Burns (medications)  Silver nitrate 0.5% (rarely used)  wet dressing effectively prevents cross infection  >0.5% injures the tissue and not effective<0.5%  danger of electrolyte imbalance (especially Na and K) since the electrolytes are withdrawn from the body fluids and also from the dressing.  Turns black in sunlight and stains clothes and hands black
  • 105. Burns (medications)  Silvadene  wide-spectrum antimicrobial that is nonstaining and relatively painless  no systemic metabolic abnormalities however is contraindicated in pregnant women near term and premature infants  does not penetrate the eschar as well as sulfamylon
  • 106. Burns (medications)  Sulfamyalon acetate  interferes with bacterial cellular metabolism  diffuses rapidly through burned skin and eschar  used for gram-negative organism  burning sensation after applied topically  may cause metabolic acidosis and is a carbonic andryrase inhibitor  may cause a rash
  • 107. Burns (medications)  Furacin-nitrofurazone (gauze or cream)  a synthetic broad-spectrum antibacterial  inhibits enzymes required for carbohydrate metabolism in bacteria  Xeroform-a fine mesh gauze with antimicrobial action
  • 108. Topical antimicrobials Advantages and Disadvantages  Silver Sulfadiazine –Painless but Lack of penetration  Mafenide Acetate –Penetrates but Painful, Carbonic anhydrase inhibitor  Silver Nitrate- Broad spectrum but Limited penetration  Sodium Hypochlorite -Broad spectrum but Impairs wound healing in high doses
  • 109.  Table 7.2. Other topical agents  Bacitracin: Gram-positive Minimal coverage Often combined with polymyxin and neomycin into triple ointment  Polymyxin B :Petroleum-based Keeps grafts moist, Often combined with mycostatin into “Polymyco”  Bactroban: Staphylococcal coverage ,Very expensive Useful for ghosted grafts  Silvamyco:(Silvadene and mycostatin) Extended coverage
  • 110. SYSTEMIC ANTIMICROBIAL THERAPY IN BURNS  only after clinical suspicion of an infection exists  appropriate in patients with massive burns  based on culture and sensitivities
  • 111. Complications of Acute Phase  Infection- due to destruction of body’s 1st line of defense. Partial thickness wds can convert to full-thickness wds with infection present.  Signs of sepsis are: high temp., increased pulse & resp., decreased BP, and decreased urinary output, mild confusion, chills, malaise, and loss of appetite. WBC bet. 10,000 and 20,000. Infections usually gram neg. bacteria (pseudomonas, proteus)  Obtain cultures from all possible sources: IV, foley, wound, oropharynx, and sputum
  • 112. Neurologic-possible from electrical injuries  Musculoskeletal-has the most potential f complications during acute phase due to healing and scar formation making skin less supple and pliant. contractures can occur  Gastrointestinal-adynamic ileus results from sepsis, diarrhea or constipation ( narcotics & decreased mobility), gastric ulcers , stress, occult blood in stools possible  Endocrine-stress DM might occur-assess glucose
  • 113. Complications Cont.,  Electrolytes Imbalances  Hyperkalemia  A result of cellular destruction  Hyponatremia  A result of fluid shifts into interstitial space  Acid-Base Imbalances  Metabolic Acidosis  Failure to conserve bicarbonate  Also, a result of fluid shifts into interstitial space See Smeltzer & Bare pp. 1713; Table 57-3
  • 114. Burn Shock  Shock is a state of inadequate cellular perfusion  Burn Injuries involving > 35 % TBSA  Clinical manifestations:  Hypotension & tachycardia  Decreased Cardiac Output:  Decreased preload, stroke volume & contractility  Increased afterload  Monitoring: PCWP & CVP values decreased  Prevention: Early & full fluid resuscitation !! Smeltzer & Bare pp. 1708 (Figure 57-3)
  • 116. Nutritional Therapy  Fluid replacement takes priority over nutritional needs in the initial emergent phase.  NG tube is inserted and connected to low intermittent suction for decompression. When bowel sounds return (48-72 hrs) after injury, start with clear liquids and progress up to a diet high in proteins and calories
  • 117. Adult Energy Requirements  Curreri formula  Daily energy requirement = (25W + 40B)  Long formula  BEE x activity factor x injury factor  Male BEE = 66.6 + 13.8W + 5H – 6.8A  Female BEE = 655 + 9.6W + 1.9H – 4.7A  Activity factors:  1.2 if confined to bed  1.3 if out of bed  Injury factor:  2.1 for severe thermal burn  W=weight in kg, B=total burn area as % of total body mass, H=height in cm, A=age in years
  • 118. Child Energy Requirements  Wolfe Formula  Energy = BMR x 2  BMR Calculations Age Boys Girls 0-3 years 60.9W – 54 61W – 51 4-10 years 22.7W + 459 22.5W + 499 11-18 years 17.5W + 651 12.2W + 746  W= weight in kg
  • 119. Child Energy Requirements  Modified Galveston formula  < 1 year: (2100 x BSA) + (1000 x burn area)  < 12 years: (1800 x BSA) + (1300 x burn area)  12-18 years: (1500 x BSA) + (1500 x burn area)  BSA = body surface area in m2  Burn area = surface area burned in m2
  • 120. Carbohydrate Requirements  Glucose reduces extent of hypermetabolic response and protein breakdown  High rates of glucose delivery:  Causes hyperglycaemia needing insulin  Stimulates hepatic lipogenesis & altered liver function  Increased CO2 production  Prevents & slow weaning from ventilator  Adults: 5 mg/kg/min avoids complications  Children: 5-7 mg/kg/min  Infants: D5W 5 mg/kg/min initially then increased to a max of 15 mg/kg/min over first few days
  • 121. Fat Requirements  Normal diet leads to muscle wasting with central obesity due to hepatic steatosis  Fat reduction prevents problems when protein replaces lipid energy  Adults: Minimum of 4% total energy  15% meets essential fatty acid requirements and provides for fat-soluble vitamins  Vary composition of fats  Children: Minimum of 2-3% total energy  Infants: Maximum of 4g/kg of IBW
  • 122. Protein Requirements  Intact protein rather than amino acids  Improved weight maintenance and survival  Frequent estimations of nitrogen loss to ensure adequate replacement  TNL = TUN + 4g  TNL = (UUN x 1.25) + 4g  NB = TNL – NS  6.25 g protein = 1 g nitrogen  Adults: 2-3 g protein/kg IBW  Children:  < 1 year old: 3-4 g protein/kg IBW  1-3 years old: 2.5-3 g protein/kg IBW  >3 years old: 1.5-2.5 g protein/kg IBW  25% energy as protein
  • 123. Vitamin Requirements  Specific requirements not established for most  Multivitamin supplementation  Vitamin A  Immune function & epithelialization  10,000 IU/day  < 3 years old: 5,000 IU/day
  • 124. Vitamin Requirements  Vitamin C  Immune function  Wound Healing  Collagen synthesis  Free radical scavenging properties limits tissue damage  Ascorbic acid study  High doses reduced resuscitation fluid volume, body weight gain, wound edema, & severity of respiratory dysfunction  Adults: 500 mg twice a day  Children up to age 10: 250 mg twice a day
  • 125. Enteral vs. Parenteral Feeding  Enteral preferred over parenteral  Maintains integrity of GI tract  Parenteral more expensive & increases complications  Hospital-made vs. commercial diets  Hospital made diets as good as commercial  Weight gain & protein increase similar  Patient tolerance similar
  • 127. ELECTRICAL BURNS  Extent of injury depends upon  Type of current  Amount of current  Path of current  Duration of current
  • 128. ELECTRICAL BURNS  Injury from electrical burns results from coagulation necrosis that is caused by intense heat generated from an electric current.
  • 129. Electrical injury can cause:  Fractures of long bones and vertebra  Cardiac arrest or arrhythmias--can be delayed 24-48 hours after injury  Severe metabolic acidosis--can develop in minutes  Myoglobinuria--acute renal tubular necrosis- myoglobin released from muscle tissue whenever massive muscle damage occurs--goes to kidneys--and can mechanically block the renal tubules due to the large size!
  • 130. ELECTRICAL INJURY  Cardiac arrhythmias are the most serious immediate injury that occurs with electrical contact  V-Fib  V-Tach
  • 131. ELECTRICAL BURNS COURTESY DAVID EFFRON, M.D. COURTESY BONNIE MENEELY, R.N.
  • 132. Treatment of electrical burns…  Fluids--Ringers lactate or other fluids- flushes out kidneys--you want 75-100 cc/hr until urine sample clear  an osmotic diuretic (Mannitol) may be given to maintain urine output
  • 133. Electricity can instantaneously destroy tissue. This child has a burn that resulted from biting on an electrical cord. These burns often occur at the corners of the mouth, as seen here.
  • 134. ADDITIONAL INJURIES  Skin burns  Entrance and exit wounds  Fractures  cannot determine the extent of the injury from the surface burn DA Y ON E DA Y 3
  • 135. LIGHTNING STRIKE  Usually superficial injury  Victims die from cardiac arrest  Resuscitate the “dead”  Patients who are breathing will usually survive
  • 136. Chemical Burn 2 types of chemical burns  acids-can be neutralized  alkaline- adheres to tissue, causing protein hydrolyses and liquefaction  examples: cleaning agents, drain cleaners, and lyes, etc...
  • 137. Chemical Burns  Acids  Immediate coagulation-type ,necrosis creating an eschar though self-limiting injury  coagulation of protein results in necrosis in which affected cells or tissue are converted into a dry, dull, homogeneous eosinophilic mass without nuclei
  • 138. Chemical Burns  Bases (Alkali)  Liquefactive necrosis with continued penetration into deeper tissue resulting in extensive injury  characterized by dull, opaque, partly or completely fluid remains of tissue  Dry Chemicals  Exothermic reaction with water
  • 139. CHEMICAL BURNS  Injure the skin  May be absorbed into the body and damage internal organs  May be inhaled into the lungs and cause lung tissue damage  May have minimal skin injury and yet cause severe systemic injury
  • 140. FACTORS CAUSING TISSUE DAMAGE IN CHEMICAL BURNS  Type of chemical  Concentration of chemical  Amount of chemical  Duration of contact  Manner of contact  Mechanism of action ACID BURN
  • 141. TREATMENT OF CHEMICAL EXPOSURE  Remove and bag all contaminated clothing  Brush off dry chemical  Flush with copious amounts of water or any drinkable liquid  Wipe or scrape any retained chemical and irrigate again “THE SOLUTION TO POLLUTION IS DILUTION”
  • 142. Chemical Burn to Eye Management  Flood the eye with copious amounts of water only  Never place chemical antidote in eyes  Flush using LR/NS/H2O from medial to lateral for at least 15 minutes  Nasal Cannula  IV Ad Set  Remove contact lenses  May trap irritants
  • 143. Rehabilitation Phase  Defined as beginning when the patient’s burn wound is covered with skin or healed and patient is capable of assuming some self-care activity.  Can occur as early as 2 weeks to as long as 2-3 months after the burn injury  Goals for this time is to assist patient in resuming functional role in society & accomplish functional and cosmetic reconstruction.
  • 144. Clinical Manifestations  Burn wd either heals by primary intention or by grafting.  Scars may form & contractures.  Mature healing is reached in 6 months to 2 years  new skin sensitive to trauma
  • 145. Complications  Most common complications of burn injury are skin and joint contractures and hypertrophic scarring  Because of pain, pts will assume flexed position. It predisposes wds to contracture formation  Use of physical therapy, pressure garments, splints, etc. are used
  • 146. Hypertrophic Scar Formation  Excessive scar formation, which rises above the level of the skin  Management: Pressure Garments  Elasticized garments that are custom fitted  Maintains constant pressure on the wound  Result: smoother skin & minimized scar appearance  Client Considerations:  Must be worn 23 hours a day  Need to be worn for up to 1-2 years  Are very hot and tight !!
  • 147. Example of a pressure garment
  • 148. Contracture Formation  Shrinkage and shortening of burned tissue  Results in disfigurement  Especially if burn injury involves joints  Management is opposing force:  Splints, proper positioning and ROM Must begin at day one !! Multidisciplinary approach is essential !!
  • 150. Psychosocial Considerations  Alterations in Body Image  Loss of Self-Esteem  Returning to community, work or school  Sexuality  Supports Services  Psychologist, social work & vocational counselors  Local or national burn injury support organizations  Nursing Considerations  Encourage client & family to express feelings  Assist in developing positive coping strategies
  • 151. Prevention of Burn Injuries  Proper education and supervision  childproof items in electrical sockets  keep dangerous items (matches) out of reach  Safety measures for the elderly  teach small children 911  smoke detectors in house  STOP, DROP, AND ROLL
  • 152. Position of comfort after burn trauma (to be avoided)  1. Neck flexion  2. Shoulder protraction  3. Elbow flexion  4. Metacarpal extension  5. Interphalangeal flexion  6. Wrist flexion  7. Hip flexion  8. Knee flexion  9. Ankle plantar flexion
  • 153.  Techniques available for burn reconstruction  1. Without deficiency of tissue  • Excision and primary closure  • Z-plasty  2. With deficiency of tissue  • Simple reconstruction  - Skin graft  - Transposition flaps (Z-plasty and modifications)  • Reconstruction of skin and underlying tissues  - Axial and random flaps  - Myocutaneous flaps  - Tissue expansion  - Free flaps
  • 154. Pediatric Burns  Thin skin  increases severity of burning relative to adults  Large surface/volume ratio  rapid fluid loss  increased heat loss  hypothermia  Delicate balance between dehydration and overhydration  Immature immunological response  sepsis  Always consider possibility of child abuse
  • 155. Geriatric Burns  Decreased myocardial reserve  fluid resuscitation difficulty  Peripheral vascular disease, diabetes  slow healing  COPD  increases complications of airway injury  Poor immunological response - Sepsis  % mortality ~= age + % BSA burned
  • 156. Recent advances  IV or nebulised Heparin shown to reduce tracheobronchial cast formation in inhalation burns  Early near total excision and grafting  Anabolic agents like oxandrlone ,GH,testoesterone as a nutritional adjuvants
  • 157. SUMMARY  Protect yourself and your patient  Maintain c-spine immobilization  Treat burn patients as trauma patients  Properly cool the burn  Be alert for inhalation injuries  Flush chemical burns adequately  Monitor heart in electrical burn patients
  • 158. BURNS B - breathing body image U - urine output R - rule of nines resuscitation of fluid N - nutrition S - shock silvadene