SUBJECT SEMINAR ON BURNS IN PEDIATRICS

Chairperson: Dr.Shivasharanappa Presenter: Dr.Mohan.T.Shenoy

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1. 2. 3. 4. 5. 6. 7. 8. 9.

Nelson Textbook of Pediatrics, 18th ed. Roger's Textbook of Pediatric Intensive Care, 4th edition Medical Emergencies in Children ² Meherban Singh Pediatric and Neonatal emergencies - Sachdev Short Practice of Surgery ² Bailey & Love 25th edition Clinical Surgery ² Cuschieri ² 2nd edition Sabistons textbook of surgery 18th ed Pediatric surgery ² Ashcraft and Holcomb ² 4th edition Current Topics in Burn Care ²Wachtel & Kahn

10.CME ON MODERN MANAGEMENT OF PAEDIATRIC BURNS MARCH 2010 11.MANAGEMENT OF BURNS - STANDARD TREATMENT GUIDELINES MOHFW (GOVT. OF INDIA) 12.AMERICAN BURN ASSOCIATION PRACTICE 2 GUIDELINES 2008

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vaio, 7/27/2010

1. Incidence 2. Introduction 3. Types of burns 4. Grades of burns 5. Pediatric age group 6. Pathophysiology 7. Assessment of wound 8. Criteria for admission & referral 9. MANAGEMENT ABCDE & first aid 10. Fluid resuscitation guidelines 11. Complications & morbidities 12. Skin grafting & surgical measures 13. Recent research in burns care 14. Preventive strategy

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One of the most physically & psychologically devastating forms of injury in children. 

Burn wounds occur when there is contact between tissue and an energy source, such as
heat, chemicals, electrical current, or irradiation. 

The term ¶injury· by definition is ³a body lesion due to an external cause, either
intentional or unintentional, resulting from a sudden exposure to energy (mechanical, electrical, thermal, chemical or radiant) generated by agent±host interaction.´ 

In India => 2,000,000 burns reported/year During 2001, 32,509 persons died in India - 27% of total injury deaths. The high incidence makes burns an endemic health hazard The major causes of death were resuscitation failure, inhalation injury or infections.
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In India => 2,000,000 burns reported/year
Burns-related injuries are frequent during festival of lights (Diwali).

Hospital admissions 70,000/year Burns-related death 8500/year 21-40 yrs => MC age group affected Vulnerable section Extremes of Age Ages 1-5 => Scald injuries Elderly (>60ys) => Scalds, Contact and Flame burns Special group = Alcoholics, Epileptics & Psychiatric patients Only 3% to 5% of all burns in children are life-threatening.
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Journal of Clinical and Diagnostic Research. 2009June;(3)1608-1610

¤Burns & related injuries are 2nd leading cause of death in childhood, killing approximately 2,500 children/year. ¤Most burns are minor scalds, accounting for about 85 % of all thermal injuries. ¤Flames produce 10% of burns and, with associated smoke inhalation, result in the majority of deaths. ¤Electrical or chemical burns account for 2% to 3% of injuries and pose special challenges in management.

Approximately 50% of burn deaths occur within 1st 10 days

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Skin = Largest body organ
Epidermis
± Outer cells are dead ± Protect to form water-tight seal ± Melanin to protect against UV radiation

Dermis

Brunner, 2008, Figure 55.1. anatomic structures of the skin

± Tough, elastic connective tissue which contains specialized structures
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‡ ‡ ‡ ‡

Protects against bacteria Initiates immune response Prevents fluid loss Regulates temperature

‡ Sensation ‡ Aesthetic & psychological importance
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TYPES OF BURN INJURIES
2%

3%
10%

Scalds

Open Flame
Chemicals Electrical

85%
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Types of Burn Injuries
y Thermal burn
y Skin injury y Inhalation injury

y Chemical burn
y Skin injury y Inhalation injury y Mucous membrane injury

y Electrical burn
y Lightning

y Radiation burn
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First Degree Burns
‡ ‡ ‡ ‡ Tissue damage is minimal Blanches with pressure Erythematous Often painful

‡ Sunburn is a classic example
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Second Degree Burns
‡ Epidermis & portions of dermis are involved ‡ Adnexal structures (sweat glands, hair follicles) often involved ‡ The burned area is characterized by blisters and is very painful

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Third Degree Burns
‡ ‡ ‡ ‡ These burns are generally leathery in consistency, dry, and waxy Painless surface - May be red and does not blanch with pressure Healing is very slow Often associated with extensive scarring

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Grades of Burns
Depth
First degree

Characteristics
Erythema, pain, absence of blisters Heals by 3-6 days Red or mottled; flash burns Heals by 2-4 weeks depending on depth

Cause
Sunburn, Flash burns

Second degree (partial thickness)

Flame Contact with hot liquids Chemicals, Fire Electric or lightning Prolonged contact with hot liquids/objects

Third degree (full thickness)

Dark and leathery parchment-like Dry with thrombosed blood vessels Requires skin grafting

A single burn wound can have all three degrees!
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PEDIATRIC AGE GROUP SPECIAL PHYSIOLOGY 
Larger Body surface relative to weight ‡ rapid fluid loss ‡ increased heat loss hypothermia ‡ Thin skin increases severity of burning relative to adults  Delicate balance between dehydration and overhydration  Immature renal function = osmotic imbalance  Impaired pulmonary function = early ventilatory16 assistance

PATHOPHYSIOLOGY Zones of Injury = local response (Jackson±1947)

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LOCAL CHANGES

Orgill D. NEJM 2009;360:893-901

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PATHOPHYSIOLOGY
‡ Once 30% burns reached, systemic effect due to release of cytokines.

‡ ‡ ‡ ‡ ‡

Circulatory changes and Evaporative losses Hematological changes CardioPulmonary changes Metabolic changes and immune dysfunction Renal effects

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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
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Systemic Response
Cardiovascular = Reduced Myocardial contractility Metabolic = BMR (3 ×) Splanchnic hypoperfusion Respiratory = Bronchoconstriction ,ARDS Immunological = Non-specific downregulation

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CHANGES AFTER LOWER AIRWAY BURN INJURY
Hypermetabolism

Inflammatory Mediators
Thomboxanes, Cytokines, Prostoglandins

Immune Dysfunction

Ciliary loss

Capillary leak
(oedema)

Burn Injury
Myocardial Dysfunction

Oedema Alveolar injury

Renal Dysfunction
q perfusion of burn wound

LUNG INJURY
Sepsis

Surfactant loss

Burn Shock

V/Q mismatch Pneumonia Obstruction

q perfusion of gut

MOD

Hypoxia

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TYPES OF BURNS

Flame

Scalds

Chemical

Electrical

Anhydrous Ammonia Burns
Neonate with scalds

Caustic soda burns 25
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TYPES OF BURN INJURIES 

THERMAL

Scald: damage from contact with hot liquid Flame: damage from superheated oxidized heat 

CHEMICAL

Alkalies cause liquefactive necrosis with deeper wounds 

Electrical
Low voltage ± domestic electrocution deep burns at contact & exit sites. High voltage >1000 V : severe injury with tissue loss, renal failure due to rhabdomyolysis. 

Irradiation exposure to high energy electromagnetic waves

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SCALD BURNS
Age group: 6 months to 2 years Aetiology: hot water heaters & spillage of hot foods liquids
Soft tissue is burned when exposed to temperatures above 115ºF (46°C). The extent of damage depends on surface temperature & contact duration. At 120°F. Within 3 seconds Accidental scalds often show a pattern of splashing, with burns separated by patches of uninjured skin. In contrast, intentional scalds often involve the entire extremity, appearing in a circumferential pattern with a line that marks the liquid surface.

FLAME BURNS
‡Contact with open flame causes direct injury to tissue. ‡Flame may ignite clothing. ‡Natural fibers like cotton tend to burn, synthetic fibers (like nylon) may melt or ignite, adding a contact burn component to the injury ‡If occurs in an enclosed area at risk for
CO poisoning and cyanide poisoning inhalational injury from the smoke and heat.

‡Flash burns are a subset of flame burns and are a result of rapid ignition of a flammable gas or liquid.

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CONTACT BURNS
Contact burns result from direct contact with a hot object. Burn injury is confined to the point of contact. Eg: Burns from cigarettes & tools (soldering irons, cooking appliances, curling irons).

With the exception of concentrated / fuming sulfuric acids, thermal injury rarely plays a role in chemical injury. The main mechanisms of action on living tissue: (1) reduction, (2) oxidation, (3) corrosion, (4) protoplasmic poisons. Mode of damage: Protein destruction Alkalis dissolve lipid of cell wall; penetrate to cause lysosomal release to produce systemic effects

ALKALI INJURIES 3 FACTORS
a. Bind with tissue proteins to form alkaline proteinates b. Dissolve lipid of cell wall; Saponification of fat causes loss of function with increased damage due to heat reaction. 
Systemic effects by lysosomal release due to penetratation

c.

Extraction of water from cells => Dessication

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MECHANISMS OF ACTION

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MANAGEMENT
Speed is most essential in the management of chemical burns. 
If chemicals were ingested

‡ Upper GI tract and oropharynx may also be at risk ‡Circumoral burns may be present ‡Airway edema. 
Lavage with copious quantities of clean water Antidote Correction of metabolic disturbances

ELECTRICAL INJURIES
‡ Definition:
Tissue injury following exposure to electrical current or forces
Produce heat injury by passing through tissue. Includes direct contact, arc injuries, flash & flame burns

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ELECTRICAL BURNS
True electrical injuries can be due to:
1) High Voltage 2) Low Voltage 3) Alternating current 4) Direct current

Entrance & exit wounds

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» Tissues with the lowest resistance to current » Generally the nerves, blood vessels, and muscles » Muscle is most damaged tissue

» Low voltage burns:
» Similar to thermal burns only local damage.

» High voltage burns:
» Hidden destruction of deep tissue -fasciotomies may be required » Ventricular fibrillation, » Violent tetanic muscular contractions- fractures and dislocations » Late effects: Neurologic deficits, cataracts can occur
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DIFFERENCES BETWEEN TRUE HIGH TENSION AND FLASH BURN

ALTERNATING CURRENT
Š Alternating current is more harmful because it causes tetanic muscle spasm that may fix the victim to current source Š High Tension Voltage: 1) Takes a direct path between entrance and exit points 2) Charring at the point of entrance and explosion at the point of exit is linked to Firtree appearance o Cardiac injury is prominent, and monitored for 4-72 hours depending on the strength of the voltage and the age of the patient. o Check for Visceral injuries, long bone and spine fractures, myoglobinuria, and compartment syndromes.

ARC BURNS

Heat generated may be as high as 20,000 °C and depth depends on proximity of current to skin Flexor aspect of wrist, cubital fossa and axilla along anterior folds

Radiation Exposure
Waves or particles of energy that are emitted from radioactive sources

Alpha radiation
large, travel a short distance, minimal penetrating ability can harm internal organs if inhaled, ingested or absorbed

Beta radiation
small, more energy, more penetrating ability usually enter through damaged skin, ingestion or inhalation

Gamma radiation & X-rays
most dangerous penetrating radiation may produce localized skin burns & extensive internal damage
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MANAGEMENT

GENERAL POINTS & FIRST AID 
Put off the cause and limit the damage 
Extinguish fire/ Put off mains/ Washing under running tap water  Remove clothing that is hot/burned/exposed to chemicals  Remove constrictive clothing, jewellery 

Perform rapid primary survey 
Burns victims rarely die immediately due to the burn!  Immediate death due to associated trauma/airway compromise 

Register medicolegal case 
An important step is to determine depth and extent of damage to44 44 determine where and how the patient should be treated

TRIAGE ASSESSMENT OF BURNS
‡ Brief history
² ² ² ² Age of child Site of burns Exact time, agent, cause/mechanism, place of occurrence Associated injuries ² Concomitant & Non-accidental

‡ Quick assessment
² Extent - Area involved in relation to total body area ² Depth ² temp. of agent and duration of contact
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SITE INVOLVED

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GOALS IN ASSESSMENT
1. Classify the wound 2. Criteria for hospitalisation 
Minor burns  Moderate burns  Major burns

3. Calculate fluid requirement 4. Communication ² prognosis (survival/surgery)

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ESTIMATING THE DEPTH OF BURN
A) Causative agent: ‡ ‡ ‡ ‡ Scalds & UV light ± superficial Flame, electricity & molten metals ± deep Acid ± deep (depending on conc.) Alkali ± deep

B) Duration of contact C) Location of burn wound a) deep in delicate skin ± eyelids b) superficial in thick skin ± palms & soles

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ESTIMATING THE DEPTH OF BURN

ESTIMATING THE DEPTH OF BURN
BURN DEPTH RESPONSE TO NEEDLE PRICK (21 G needle) BLEEDING SENSATION APPEARANCE

SUPERFICIAL

BRISK

PAIN

RED GLISTENING BLANCHES

DEEP DERMAL

DELAYED

TOUCH BUT NO PAIN

PALE NOT MOIST BLANCHES

FULL THICKNESS

NONE

NONE

DRY LEATHERY HARD

Wallace¶s Rule of Nines and Lund±Browder Charts

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Orgill D. N Engl J Med 2009;360:893-901

Exact Assessment :Lund Browder Chart

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RULE OF FIVES

Lynch & Blocker 1963

INFANT

CHILD
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Who Needs Admission
2 2 2 2 2 2 > 10%

, /

,

,

‡ Suspicion of abuse
± ± ± ± ± ± Frequently changing history Absence of splash marks Stocking glove distribution Sharply demarcated burns Burns on soles, palms, cigarette ash burns Stated mechanism inconsistent with developmental age

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CRITERIA IN 2nd OR 3rd DEGREE BURN PATIENT FOR REFERRAL TO A REGIONAL BURN CENTER 

   

Any burn > 9% TBSA in those 5 yrs age Any burn > 15% TBSA Any 3rd degree burn > 5% TBSA Any burn inv . critical body parts eye/face/hands/feet/ear/genital area Any burn in those with preexisting disease that may complicate or retard recovery.  Inhalational/Electrical & burns injuries complicated by underlying fractures/other trauma.

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GROSS WORKABLE GUIDE
‡ Isolate the patient as far as possible in separate ward/cubicle ‡ Appropriate fluid replacement therapy ‡ Medication for pain ‡ Early enteral feeds with additional nutrition ‡ Nasogastric tube to decompress the stomach ‡ H2 receptor antagonists to prevent stress ulcers/erosions ‡ Tetanus Prophylaxis and systemic antibiotics
± Antibiotics not indicated in early post-burn period as colonisation of resistant organisms 58 ± Ceftazidime + Amikacin + Metronidazole after 48 hrs based on

A : Airway (above vocal cords) with cervical spine control

Evidence of inhalational injury
‡Flame burns, singed nasal hair, ‡Full-thickness/deep dermal wounds to face/neck/upper torso, ‡Carbonaceous sputum/carbon particles in orophaynx

Indications for intubation
‡Erythema/edema in oropharynx, ‡Voice change-hoarseness/stridor ‡Dyspnoea
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B : Breathing ( below vocal cord)
o 100 % O2 simple face mask/ nasal cannula o Artificial ventilation if required

‡ Mechanical restriction : Circumferential chest burns Escharotomy ‡ Blast injury : ‡

LUNG CONTUSIONS, TENSION PNEUMOTHORAX, ARDS Smoke inhalation: Direct irritants - bronchospasm,
Atelectasis,hypostatic pneumonia
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‡ Carbon Monoxide poisoning

Circulation
Peripheral Venous Access PREFERABLY THROUGH UNBURNT TISSUE AT 2 SITES No compromise with IV access Ringers lactate solution Calculate volume from time of injury not time of admission Central venous access [If extensive (>30%)] ,venous cut-down and invasive measures best avoided. Unless in severe shock, oral fluids started
within 1st 24 hrs and 1/4th of normal daily requirement
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INVESTIGATIONS
‡ ‡ ‡ ‡ ‡ ‡ ‡ Blood grouping & typing Hemogram Coagulation profile Random blood sugar Renal function tests Urine routine ABG
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Fluid Calculation
‡ Parkland Formula
± Isotonic crystalloid (RL) ± 4 ml/kg/ % TBSA over 1st 24
hrs

‡ Shriners - Galveston Formula
± 5000 ml/m2/ % TBSA + 2000 ml/m2/ 24 hrs maintenance ± ½ in 8 hrs, ½ in next 16 hrs ± RL for 24 hrs, then D5RL
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± ½ in 8 hrs, ½ in next 16 hrs ± Maintenance fluid in addition

SPECIAL CONSIDERATIONS
Body Surface area calculation formulae used Deduct fluid already given Hyponatremia in aggressive fluid resuscitation. Central pontine myelinolysis in rapid correction

D5RL esp. in <2yrs child (due to limited glycogen stores) Colloid formula: Roughly 1 plasma volume (5% of body
weight) for every 15% burn + Normal daily requirements

Assessment of adequacy of fluid replacement
‡ Urinary output is most commonly used parameter
± At least 0.5ml/kg/hr is suggestive of adequate renal perfusion

‡ Cardiopulmonary factors- Pulse,BP,RR,SpO2,,CFT ‡ Arterial Blood pH and Base deficit ‡ Sensorium-alert, oriented to time, place, & person
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COMPLICATIONS IN FLUID RESUSCITATION

Measurement

Comment

Goal

Signs of Underresuscitation
Low Urine output

Signs of Overresuscitation
Urine output > 30ml/hr ; hyperosmolar diuresis from hyperglycemia must be excluded

Fluid Volume

Fluid input generally exceeds output during early postburn period as edema develops Accuracy needed to extimate fluid requirements Hyperthermia may indicate hyperdynamic state

Urine output : 30ml/hr in >30kg 1-1.5 ml/kg/hr in <30 kg

Body weight

Weight will increase due to intravascular leak and resuscitation volume Normothermia

Weight approaches dry weight

Massive weight gain from anasarca

Body temperature

-

-

Electro cardio- Dysrythmias graphic status are uncommon

Normal sinus rhythm

Tachycardia may reflect intravascular contraction

Dysrythmias may indicate poor oxygenation, electrolyte 67 imbalance or pH 67 abnormality 67

BROOKE FORMULA
1st 24 hours : 1.5 ml/kg/TBSA Ringer s Lactate + Colloid 0.5 ml/kg/TBSA 2ND 24 hours: Fluid replacement is half of the 1st 24 hr period
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EVANS FORMULA
1st 24 hours Colloids : 1ml/kg/TBSA Normal Saline: 1ml/kg/TBSA 5%D in water : 2000 cc in adults; proportionately less in children 2ND 24 HOURS Fluid replacement is half of the 1st 24 hr period
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MUIR AND BARCLAY FORMULA
» The resuscitating fluid is plasma. » This formula is so planned as to provide 6 rations during the first 36 hours » Each ration is calculated as follows:

% burns x Kg bodyweight/ 2 = ml of fluid required
» The first 3 rations are administered at 4 hr intervals followed by 2 rations at 6 hr intervals and the last ration over 12 hrs.

» If at the end of 4 hrs , the progress is satisfactory, the same volume of ration is administered for the next period. Otherwise it is altered depending upon the response.
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FLUID RESUSCITATION FORMULAE
‡ Colloids
± 5% Albumin [Given after 24hrs,if S.proteins < 4 gm%] ± Fresh-frozen plasma [Given early in respiratory burns]

‡ Blood & Blood products
± Whole blood ± Packed cell
‡ After 24 hrs, attention to be given for Potassium balance ± Add Potassium chloride to infusate or Oral supplements

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Fluid resuscitation formulae -SUMMARY
Crystalloid formulae Parkland Modified Brooke Colloid formulae Evans Brooke Slater Modified Hypertonic saline formulae Monafo Fluid contains Na 250 mmol/L Maintain UO at 30 ml/h Colloid 1.0 ml/kg/ %TBSA Colloid 0.5 ml/kg/%TBSA Colloid 0.5 ml/kg/%TBSA + Normal saline 1.0 ml/kg/%TBSA + Lactated Ringer's 1.5 ml/kg/%TBSA Lactated Ringer's 2 L/ 24 hours Lactated Ringer's Lactated Ringer's 4 ml/kg/%TBSA 2 ml/kg/%TBSA

Demling

Dextran 40 in saline í Lactated Ringer's PLUS 2 ml/kg/h for 8 h FFP í 0.5 ml/kg/h for 18 h beginning 8 h post burn

DISABILITY
‡ ‡ ‡ ‡ Alteration in mental status is not normal Determine Glasgow Coma Scale Pupils size and reactivity Check for any focal finding

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EXPOSURE WITH ENVIRONMENT CONTROL
‡ Remove all clothes for complete examination including back ‡ Avoid hypothermia ± deepening of wound & hypoperfusion ‡ The secondary survey continues in ahead to toe examination

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SECONDARY SURVEY
» This is a comprehensive history and head to toe examination after life-threatening conditions have been diagnosed and treated. » Mechanism of injury how ,when , where

» AMPLE : Allergies, Medications, Past medical history, Last meal, Events/Environment related to injury » head to toe physical examination
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WOUND CARE/FIRST AID
T DRENCH THE BURN THOROUGHLY WITH COOL WATER (NOT ICE) TO PREVENT FURTHER DAMAGE AND REMOVE ALL BURNED CLOTHING T IF THE BURN AREA IS LIMITED, IMMERSE THE SITE IN COOL WATER FOR 30 MINUTES TO REDUCE PAIN AND OEDEMA T IF THE AREA IS LARGE, AFTER IT HAS BEEN DOUSED WITH COOL WATER, APPLY CLEAN WRAPS ABOUT THE BURNED AREA TO PREVENT SYSTEMIC HEAT LOSS AND HYPOTHERMIA T HYPOTHERMIA IS A PARTICULAR RISK IN YOUNG CHILDREN T FIRST 6 HOURS FOLLOWING INJURY ARE CRITICAL,

INITIAL TREATMENT
‡ Consists mainly of cooling, simple cleansing and appropriate dressing
² Burn wound should be cleaned, but use of disinfectant is discouraged as it can inhibit healing. ² Growing support for washing the wound using mild soap and water.

‡ Debridement
² Sloughed or necrotic skin including ruptured blisters, is debrided. ² Extensive debridement is generally not required immediately and may be deferred until the initial follow up visit.

‡ Blisters
² Ruptured blisters should be removed, but management of clean intact blisters is controversial. ² Needle aspiration should never be performed, as it increases risk of infection.

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TREATMENT
‡ Pain management
² Small burn injuries : Paracetamol & NSAIDs, alone or in combination with opioids ² Sustained burns & significant pain : IV narcotics. ² Elevation of foot and hand burns above heart level reduce pain & swelling for several days following the injury

‡ Psychologic support for rehabilitation ‡ Pruritus is common & treated with Syst. Antihistamines/moisturizing lotions ‡ Tetanus immune globulin should be given to patient who have not received a complete
immunization, particularly for any burns deeper than than superficial thickness.

‡ Dressing
± superficial burns do not require dressings. ± Partial and full thickness burns should be dressed.
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Hypermetabolism can be as high as 200% of the normal metabolic rate (returns to normal only with the complete closure of the wound.)  HarrisBenedict formula: multiply the basal energy (1500 kcal) expenditure by 2 in 40% burns of TBSA.  Curreri formula: 25 kcal/kg/day plus 40 kcal per percent TBSA burned per day.  Anabolic agents: growth hormone, insulin-like growth factor, insulin, oxandrolone, testosterone, and propranolol.  Total parenteral nutrition is reserved only for those patients who cannot 79 tolerate enteral feedings.

ENERGY & PROTEIN REQUIREMENTS OF BURN PATIENTS Age
0-1 year 1-11 years > 12 years

Calories
2100 kcal/m2 + 1000 kcal/m2 burn 1800 kcal/m2 + 1300 kcal/m2 burn 1500 kcal/m2 + 1500 kcal/m2 burn

Age
0-1 year 1-3 years 4-15 years

Calories
RDA + 15 kcal/% burn RDA + 25 kcal/%burn RDA + 40 kcal/%burn

Age
0-6 months 6-24 months > 2 years

Proteins
4.5 g/kg 4 g/kg 3.5 g/kg
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BURN WOUND MANAGEMENT 
Topical agents  Early wound excision  Early wound closure 
  

Autologous graft Allogenic skin Autologous keratinocytes Skin substitutes
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TOPICAL ANTIBIOTICS IN BURN CARE
Agent Antimicrobiological coverage Advantages Disadvantages

Bacitracin

Gram positive

Mupirocin Silver Sulfadiazine

Anti-MRSA Broad Spectrum

No deeper wound Soothing penetration Moisturizes; Facial care Effective against Narrow Gram MRI neg. coverage Soothes, Painless, Excellent coverage Poor Eschar Penetration, Leukopenia Can impede epithelialization
Painful application, Met. Acidosis

Mafenide

Broad Spectrum & AntiClostridial

Good eschar penetration

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‡ Chlorhexidine ‡ Povidone-Iodine
± Wide antibacterial spectrum ± Half-life of 12 hrs (twice daily application) ± Inactivated by wound exudates

‡ Triple ointment ‡ Framycetin-based

ROLE OF BACTIGRAS TM
‡Antiseptic, soft paraffin dressing ‡ 0.5% chlorhexidine - active agent against a wide range of bacteria ‡Soothes and protects the wound ‡Reduce wound infection and inflammation.

‡Low adherence => allows the wound to drain freely into an absorbent secondary dressing.
‡ Suitable for covering wounds upto 10% of body area ‡ minor burns ‡ lacerations ‡ abrasions ‡ graft sites ‡ leg ulcers. ‡Sterile open-weave gauze presentation in a wide range of sizes
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DEBRIDEMENT
Debridement is the most important factor contributory to improve survival after major burn.
Types of debridement: 1. Auto debridement. 2. Tangential excision (at the end of 1st week). 3. Staged primary debridement (1-3 days post burn) done early to interrupt & attenuate systemic inflammatory response; normalize immune function.

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Early surgical excision is one of the major advances led to decreased morbidity and mortality in pediatric burns

3rd to 5th Post-Burns day

ESCHAROTOMY
For deep circumferential burn, urgent escharotomy is done

To avoid vascular compromise, emergency escharotomy along medial & lateral aspects of extremity For hand, medial and lateral digits and on dorsum
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‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡

COMPARTMENT SYNDROME SMOKE INHALATION Acute respiratory distress syndrome (ARDS) STRESS ULCER (Curling·s) ACUTE RENAL FAILURE LOCAL WOUND INFECTION SEPSIS SHOCK DEATH
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BURN INFECTION 
All burn patients are infected and immunocompromised  Infection is commonest cause of death following burn injury

Bacterial surveillance Vs empirical treatment Nosocomial infection common Initial G+ve replaced with G-ve then fungi burn size systemic infection Early wound closure essential

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SEPSIS
Temperature > 38.5º C or < 36º C. Tachycardia > 2 SD above normal. Tachypnea > 2 SD for age Incr./ Decr. W.B.C. count .Or >10% immature neutrophils

SEVERE SEPSIS
Organ dysfunction. Hypo perfusion. Hypotension.

MULTI ORGAN DYSFUNCTION SYNDROME
Altered organ function

SEPTIC SHOCK
Sepsis with hypotension Lactic acidosis, Oliguria Alteration in mental state

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SEPSIS
» Burn sepsis continues to be major cause of mortality after a burned patient survives the period of resuscitation.
» Meticulous antiseptic techniques can lessen colonization of burns with potential pathogens. » Topical antibiotics further reduce bacterial number. » Broad-spectrum antibiotics should not be used prophylactically
» Do not significantly reduce the incidence of infections, » Increase the likelihood of acquiring resistant organisms. » Specific antibiotic therapy for documented infections » Frequent examination of healing burns » Cultures to monitor colonization

» Pediatric patients greater risk than adults, so some pediatric burn centers administer IV penicillin for first 3 to 5 days. 91 91

Sites of infection

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INFECTION Burns impetigo

DIAGNOSTIC POINTS
‡Loss of epithelium from previously epithelialized surface ‡Not related to local trauma

TREATMENT STRATEGIES
2 2 2 &

Burnsrelated surgical wound infection Burns wound cellulitis Invasive burn wound

‡Infection in surgically created wound which has not yet epithelialized ‡Includes loss of any overlying graft or membrane

2 2 &

&

2
‡ Infection in uninjured skin surrounding a wound ‡ Signs of local infection progress beyond expected from burns related inflmmn ‡ Infection in unexcised burn and invades underlying tissue ‡ Diagnosis confirmed by

2 2

2
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SEPTIC SHOCK
‡ ‡ ‡ ‡ ‡ ‡ ‡ Fever Macular rash Hypotension Hypoxemia Low WBC Low platelets MSOF

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Significant Morbidity
‡ Cosmetic problems ² Scar hypertrophy ² Contractures ‡ Deformities ‡ Chronic pain syndrome ‡ Psychological ‡ Malignancy ² Marjolin·s ulcer
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Classically deeper partial-thickness and full-thickness injuries allowed to heal by primary intention. Delayed excision and pigmented individuals are at an increased risk. In donor sites : graft thickness, donor site infection, and patient characteristics. Most successful approach: initial pressure therapy until the wound matures, followed by subsequent excision & grafting if necessary. Intralesional injection of triamcinolone acts by decreasing collagen synthesis and increasing collagen degradation.
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Contractures
‡ ‡ ‡ ‡ Physiotherapy Splinting Contracture release Alphabet surgery.

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GOAL OF PHYSIOTHERAPY:
1. Prevent, minimize or correct deformity. 2. Protect weak muscles from over stretching. 3. Maintain range of motion. 4. Provide positional function. 5. Protect any exposed joints or tendons. 6. Provide immobilization across joints after grafting. 7. Minimize scarring with pressure garment. 8. Develop functional skills.
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Chronic ulceration of old burn scars was noted by Marjolin to predispose to malignant degeneration.
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Squamous cell carcinoma is most common, although basal cell carcinomas occasionally occur, and rare tumors such as malignant fibrous histiocytoma, sarcoma, and melanoma have been reported Burn scar carcinomas can metastasize, typically to regional nodal basins. Prophylactic regional lymph node dissection has not improved survival, but sentinel lymph node biopsy is a promising modality to direct therapeutic node dissection and awaits validation in this population. Malignancy mandates wide excision, with potential amputation if the lesion is on an extremity. On a selected basis, adjuvant radiation may be warranted. Generally, outcome is good with prompt diagnosis and resection
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SKIN GRAFT
‡ Definition:
³segment of dermis & epidermis which has been completely separated from its blood supply & donor site attachment before being transplanted to another area of body, its recipient site.´

100 100

SKIN GRAFT

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STORAGE OF SKIN GRAFTS
‡ Donor site: simple,effective,removed easily w/o anaesthesia
upto 10 days.

‡ Refrigeration: upto 21 days; 4 C; cover with gauze moistened with
saline.

Viability can be maintained for a longer period by storing in Hank·s tissue culture fluid that has plasma and Neomycin. ‡ Don·t immerse graft in any other solution as it can macerate. ‡ Longer the storage ²less likely its chance to take.
102

DERMATOME (left) to remove donor skin MESHER (right) to put holes in it

103
103 103

SKIN GRAFT 
Burns: STSG for cover. 

2nd choice is stored viable allograft when sufficient autograft is not available.These are temporary covers and will be rejected in few weeks 

Closure of donor sites of flaps and FTSG defects  Mucosal replacements-STSG for mucosa of mouth,pharynx, nose,vagina & urinary bladder  Disadvantages- contraction of grafts; so use of molds/prosthesis, Hair 104 104 follicles transplanted may grow hair so choose Non-hair bearing skin for

TYPES SKIN GRAFT TYPES
T 1. DEPENDING

ON SOURCE

‡ AUTOGRAFT-one location to another in same animal ‡ ALLOGRAFT/HOMOGRAFT-between genetically
separate individuals of the same species

‡ XENOGRAFT/HETEROGRAFT- between different
species
105

‡ ISOGRAFTS/SYNGENIC-between genetically identical

SKIN GRAFT TYPES 2.DEPENDING ON THICKNESS
1.Split thickness consists of epidermis and portion of dermis 2.Full thickness consists of epidermis & whole of dermis

106

BIOLOGICAL DRESSINGS
Temporary skin covers derived from various human and anima tissues Trying to restore few of the lost functions of skin Advantages: Pain control, Less frequent change of dressings, Prevention of evaporative losses , Control of infection

1. Epidermal cultured cells
Autologous keratinocytes - costly alternative ;not always successful.

2. Collagen Sheets
3. Amnion

commercially available, economical

and devoid of risk of transmission of Hep B and HIV
107

SYNTHETIC COVERINGS
EXAMPLE of SKIN SUBSTITUTE ADVANTAGES DRAWBACKS

BIOBRANE INTEGRA

Provides wound barrier with minimal pain

Accumulation of exudate No Antimicrobial properties

Complete wound closure Sporadic take rates with dermal equivalence No Antimicrobial properties

OPSITE

Inexpensive Frequent accumulation of Provides moisture barrier transudate/exudate Decreased wound pain No Antimicrobial properties

TRANSCYTE

Accelerated wound Accumulation of exudate healing Complete wound No Antimicrobial properties closure with dermal 108 equivalence

ROLE OF DUODERM
» » » » » » »

TM

Hydrocolloid dressing, made from a fruit pectin derivative Reliable, skin-friendly adhesive Latex free dressing - triple hydrocolloid matrix with a viral & bacteria barrier. Can stay in place for up to 7 days. Provides a moist environment - ensures re-epithellalizationbut no maceration Autolyte debridement effect Treatment of superficial and deep partial thickness burns

109

RECENT RESEARCH IN BURNS TREATMENT
Orcel
TM

dressing helps treat graft donor sites on burn patients.

MEBO TM (Moist exposed burn ointment ) may reduce hypertrophic scarring. Full thickness skin grafts are helpful in treating burn wounds on the face. AllodermTM : Human dermis acts as scafffold for a new dermis Integra TM Dermal Regeneration Template for deep hand burns. Porcine wound models for skin substitution and burn treatment Papain-Urea (Accuzyme TM ) = Chemical debridement Thymus oil may be helpful in burn wound healing. Aquacel Ag is a primary wound dressing made from sodium carboxymethylcellulose
(NaCMC) containing 1.2% silver in an ionic form.effective against many pathogens MRSA and VRE
111

TREATMENT OF AIRWAY BURNS
WHAT¶S NEW?
Pressure controlled ventilation High frequency ventilation Percussive ventilation Nitric Oxide Partial liquid ventilation Surfactant replacement ECMO

‡ Prevention is the key as it s the most preventable of all injuries. ‡Triple tragedy pain & cost , visible scars , psychological problems.

Exercise is important in preventing contractures. ‡Collaborate with local fire service to develop burn prevention programs ‡Children should not be allowed to play with lighters or fireworks. ‡Proactive approach in the community by discussing burn injury & prevention with organizations such as local media, school officials

‡Need for Individualized guidelines for management. ‡Varying capabilities for Hospitals, physicians, and parents ‡The prognosis varies from excellent to poor depending on the severity of the burn.
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Care of
B - breathing
body image

BURNS

U - urine output R - rule of nines
resuscitation of fluid

N - nutrition S - shock
63

silver sulfadiazine
114

THANK YOU
115

First degree

Second degree

Third de ree

hird degree

Grades of Burns

First degree

Second degree

Third degree
Reed, o er ntz: ergency

Third degree
117

n ge ent of pedi tric urns. edi tr

erg

re 1 (2); 2005117

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