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SUBJECT SEMINAR SUBJECT SEMINAR ON ON BURNS IN PEDIATRICS BURNS IN PEDIATRICS Chairperson: Dr.Shivasharanappa Presenter: Dr.Mohan.T.Shenoy

Picu Protocols-Dr.mohan Shenoy_2.8.2010

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Page 1: Picu Protocols-Dr.mohan Shenoy_2.8.2010

SUBJECT SEMINAR SUBJECT SEMINAR ONON

BURNS IN BURNS IN PEDIATRICS PEDIATRICS

Chairperson: Dr.Shivasharanappa

Presenter: Dr.Mohan.T.Shenoy

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1. Nelson Textbook of Pediatrics, 18th ed. 2. Roger's Textbook of Pediatric Intensive Care, 4th

edition3. Medical Emergencies in Children – Meherban

Singh4. Pediatric and Neonatal emergencies - Sachdev5. Short Practice of Surgery – Bailey & Love 25th

edition6. Clinical Surgery – Cuschieri – 2nd edition7. Sabistons textbook of surgery 18th ed8. Pediatric surgery – Ashcraft and Holcomb – 4th

edition9. Current Topics in Burn Care – Wachtel & Kahn10.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 Guidelines 2008

13.“Injuries in India: A national perspective” - NCMH Background Papers· Burden of

Disease in India

vaio
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1. Incidence2. Introduction3. Types of burns4. Grades of burns5. Pediatric age group6. Pathophysiology7. Assessment of wound 8. Criteria for admission & referral9. MANAGEMENT – ABCDE & first aid10.Fluid resuscitation guidelines11.Complications & morbidities12.Skin grafting & surgical measures13.Recent research in burns care14.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 “a 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.

Journal of Clinical and Diagnostic Research. 2009June;(3)1608-1610

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¤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.

ApproximatApproximately 50% of ely 50% of burn deaths burn deaths occur occur within 1within 1stst 10 days10 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

– Tough, elastic connective tissue which contains specialized structures

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

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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

9

85%

10%

2%3%

Scalds

Open Flame

Chemicals

Electrical

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Types of Burn InjuriesThermal burn

Skin injuryInhalation injury

Chemical burnSkin injuryInhalation injuryMucous membrane injury

Electrical burnLightning

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 Characteristics Cause

First degreeErythema, pain, absence of blisters

Heals by 3-6 daysSunburn, Flash burns

Second degree (partial thickness)

Red or mottled; flash burns Heals by 2-4 weeks depending on

depth

FlameContact with hot liquids

Third degree (full thickness)

Dark and leathery parchment-likeDry with thrombosed blood vessels

Requires skin grafting

Chemicals,Fire

Electric or lightningProlonged contact with hot

liquids/objects

A single burn wound can have all three degrees!

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PEDIATRIC AGE GROUPPEDIATRIC AGE GROUPSPECIAL PHYSIOLOGYSPECIAL 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 ventilatory assistance Immature immunological response sepsis Immature thermoregulation centre (< 6 months age)

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Zones of Injury = local response (Jackson–1947)

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PATHOPHYSIOLOGY

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LOCAL CHANGES

Orgill D. NEJM 2009;360:893-901 18

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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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Burn Injury

LUNGINJURY

Burn Shock

Myocardial

Dysfunction

Inflammatory MediatorsThomboxanes, Cytokines,

Prostoglandins

Renal Dysfunctio

n

perfusion of burn wound

perfusion of gut

Capillary leak

(oedema)

Hypermetabolism

Hypoxia

Sepsis

MOD

Immune Dysfunction

V/Q mismatch

Obstruction

Pneumonia

Ciliary loss

Oedema

Alveolar injury

Surfactant loss

CHANGES AFTER LOWER AIRWAY BURN CHANGES AFTER LOWER AIRWAY BURN INJURYINJURY

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TYPES OF BURNS

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FlameFlame ScaldsScalds ChemicalChemical Electrical Electrical

Neonate with scalds

Anhydrous

Ammonia

Burns

Anhydrous

Ammonia

BurnsCaustic soda burnsCaustic soda burns

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THERMAL

Scald: damage from contact with hot liquidFlame: 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 26

TYPES OF BURN INJURIES

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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.

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FLAME BURNS 

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•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).

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• 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

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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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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

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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

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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

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ALTERNATING CURRENTALTERNATING CURRENT Alternating current is more harmful because it causes tetanic

muscle spasm that may fix the victim to current source

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.

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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

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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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MANAGEMENMANAGEMENTT

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GENERAL POINTS & FIRST AIDPut 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 to determine where and how the patient should be treated 44

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TRIAGE ASSESSMENT OF BURNS

• Brief history

– Age of child– Site of burns– Exact time, agent, cause/mechanism, place of

occurrence– Associated injuries – Concomitant & Non-accidental

• Quick assessment

– Extent - Area involved in relation to total body area– Depth – 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 – prognosis (survival/surgery)484848

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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

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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

PALENOT MOIST BLANCHES

FULL THICKNESS NONE NONE DRY LEATHERY HARD

ESTIMATING THE DEPTH OF BURN

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Wallace’s Rule of Nines and Lund–Browder Charts

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

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Exact Assessment :Lund – Browder Chart

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RULE OF FIVES – Lynch & Blocker 1963

INFANT CHILD

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Who Needs Admission

• Burns > 10% TBSA in a child• Any burn in the very young• Any full thickness burn• Burns of hands, feet, face, perineum• Circumferential burns• Inhalation injury/Electrocution

• 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 55

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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

– Ceftazidime + Amikacin + Metronidazole after 48 hrs based on wound sensitivity pattern

• Initial Wound Care with sterile precautions• Escharotomy

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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

• Carbon Monoxide poisoning60

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CCirculationirculation• 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

– ½ in 8 hrs, ½ in next 16 hrs

– Maintenance fluid in addition

• 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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SPECIAL CONSIDERATIONS

Body Surface area calculation formulae used

Deduct fluid already givenHyponatremia 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

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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

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Measurement Comment Goal Signs of Underresuscitatio

n

Signs of Overresuscitati

on

Fluid Volume Fluid input generally exceeds output during early postburn period as edema develops

Urine output : 30ml/hr in >30kg

1-1.5 ml/kg/hr in <30 kg

Low Urine output Urine output > 30ml/hr ; hyperosmolar diuresis from hyperglycemia must be excluded

Body weight Accuracy needed to extimate fluid requirements

Weight will increase due to intravascular leak and resuscitation volume

Weight approaches dry weight

Massive weight gain from anasarca

Body temperature

Hyperthermia may indicate hyperdynamic state

Normothermia - -

Electro cardio-graphic status

Dysrythmias are uncommon

Normal sinus rhythm

Tachycardia may reflect intravascular contraction

Dysrythmias may indicate poor oxygenation, electrolyte imbalance or pH abnormality

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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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• 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

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Fluid resuscitation formulae -SUMMARYCrystalloid formulae

Parkland Lactated Ringer's 4 ml/kg/%TBSA

Modified Brooke Lactated Ringer's 2 ml/kg/%TBSA

Colloid formulae

Evans Colloid 1.0 ml/kg/ %TBSA + Normal saline 1.0 ml/kg/%TBSA

Brooke Colloid 0.5 ml/kg/%TBSA + Lactated Ringer's 1.5 ml/kg/%TBSA

Slater Colloid 0.5 ml/kg/%TBSA Lactated Ringer's 2 L/ 24 hours

Modified Hypertonic saline formulae

Monafo Fluid contains Na 250 mmol/L

Maintain UO at 30 ml/h

Demling Dextran 40 in saline − 2 ml/kg/h for 8 h

Lactated Ringer's PLUSFFP − 0.5 ml/kg/h for 18 h beginning 8 h post burn

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• Alteration in mental status is not normal

• Determine Glasgow Coma Scale

• Pupils size and reactivity

• Check for any focal finding

DISABILITY

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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• Drench the burn thoroughly with cool water (not ice) to

prevent further damage and remove all burned clothing

• If the burn area is limited, immerse the site in cool water for 30 minutes to reduce pain and oedema

• 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

• Hypothermia is a particular risk in young children

• First 6 hours following injury are critical, transport the patient with severe burns to hospital as soon as possible.

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INITIAL TREATMENT• Consists mainly of cooling, simple cleansing and appropriate

dressing

– Burn wound should be cleaned, but use of disinfectant is discouraged as it can inhibit healing.

– Growing support for washing the wound using mild soap and water.

• Debridement

– Sloughed or necrotic skin including ruptured blisters, is debrided.– Extensive debridement is generally not required immediately and may

be deferred until the initial follow up visit.

• Blisters

– Ruptured blisters should be removed, but management of clean intact blisters is controversial.

– Needle aspiration should never be performed, as it increases risk of infection.

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TREATMENT• Pain management

– Small burn injuries : Paracetamol & NSAIDs, alone or in combination with opioids– Sustained burns & significant pain : IV narcotics. – 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 tolerate enteral feedings.

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Age Calories

0-1 year 2100 kcal/m2 + 1000 kcal/m2 burn

1-11 years 1800 kcal/m2 + 1300 kcal/m2 burn

> 12 years 1500 kcal/m2 + 1500 kcal/m2 burn

ENERGY & PROTEIN REQUIREMENTS OF BURN PATIENTS

Age Calories0-1 year RDA + 15 kcal/% burn

1-3 years RDA + 25 kcal/%burn

4-15 years RDA + 40 kcal/%burn

Age Proteins0-6 months 4.5 g/kg

6-24 months 4 g/kg

> 2 years 3.5 g/kg

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BURN WOUND BURN WOUND MANAGEMENTMANAGEMENT

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 Soothing Moisturizes; Facial care

No deeper wound

penetration

Mupirocin Anti-MRSA Effective against MRI

Narrow Gram neg. coverage

Silver Sulfadiazin

e

Broad Spectrum Soothes, Painless, Excellent coverage

Poor Eschar Penetration, Leukopenia

Can impede

epithelialization

Mafenide Broad Spectrum & AntiClostridial

Good eschar penetration

Painful application, Met. Acidosis

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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

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•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

ROLE OF BACTIGRAS TM

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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

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ESCHAROTOMY

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To avoid vascular compromise, emergency escharotomy along medial & lateral aspects of extremity

For hand, medial and lateral digits and on dorsum

For deep circumferential burn, urgent escharotomy is done

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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

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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 ageIncr./ Decr. W.B.C. count .Or >10% immature neutrophils

SEVERE SEPSIS Organ dysfunction. Hypo perfusion.Hypotension.

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

Altered organ function

MULTI ORGAN DYSFUNCTION

SYNDROME

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» 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.

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SEPSIS

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Sites of infection

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INFECTION

DIAGNOSTIC POINTS

TREATMENT STRATEGIES

Burns impetigo

•Loss of epithelium from previously epithelialized surface •Not related to local trauma

•Regular cleaning of debris & exudate •Topical Antistaphylococcal antibiotics •Grafting of chronically unstable areas

Burns-related surgical wound

infection

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

•Regular cleaning of debris & exudate •Systemic & Topical Antistaphylococcal antibiotics •Grafting of unstable areas of epithelium

Burns wound

cellulitis

• Infection in uninjured skin surrounding a wound • Signs of local infection progress beyond expected from burns related inflmmn

•Systemic antibiotics against Streptococcus pyogenes•Proper treatment of the primary wound

Invasive burn

wound infection

• Infection in unexcised burn and invades underlying tissue• Diagnosis confirmed by histopathology or tissue cultures

•Systemic antibiotics against presumed pathogen•Wound excision and biological closure wherever possible

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SEPTIC SHOCK

• Fever• Macular rash• Hypotension• Hypoxemia• Low WBC• Low platelets• MSOF

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Significant Morbidity• Cosmetic problems

– Scar hypertrophy – Contractures

• Deformities

• Chronic pain syndrome

• Psychological

• Malignancy – 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. 96

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Contractures

•Physiotherapy•Splinting•Contracture release•Alphabet surgery.

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GOAL OF PHYSIOTHERAPY: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.

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 resection99

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• Definition:

“segment 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

SKIN GRAFTSKIN GRAFT

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101101

SKIN GRAFTSKIN GRAFT

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• Donor site: simple,effective,removed easily w/o anaesthesia upto 10 days.

• Refrigeration: upto 21 days; 4 WC; 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 –less likely its chance to take. 102

Storage of Skin grafts

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DERMATOME (left) to remove donor skin

MESHER (right) to put holes in it

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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 follicles transplanted may grow hair so choose Non-hair bearing skin for transplantation. 104

SKIN GRAFTSKIN GRAFT

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• 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

• ISOGRAFTS/SYNGENIC-between genetically identical individuals [identical twins/highly inbred strains]

TYPES SKIN GRAFT TYPESSKIN GRAFT TYPES

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1.Split thickness consists of epidermis and portion of dermis

2.Full thickness consists of epidermis & whole of dermis

106

SKIN GRAFT TYPESSKIN GRAFT TYPES 2.DEPENDING ON

THICKNESS

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

107

2. Collagen Sheets commercially available, economical and devoid of risk of transmission of Hep B and HIV

3. Amnion

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

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SYNTHETIC COVERINGS

108

EXAMPLE of SKIN EXAMPLE of SKIN SUBSTITUTESUBSTITUTE

ADVANTAGESADVANTAGES DRAWBACKSDRAWBACKS

BIOBRANE Provides wound barrier with minimal pain

Accumulation of exudateNo Antimicrobial properties

INTEGRA Complete wound closure with dermal equivalence

Sporadic take ratesNo Antimicrobial properties

OPSITE InexpensiveProvides moisture barrier Decreased wound pain

Frequent accumulation of transudate/exudate No Antimicrobial properties

TRANSCYTE Accelerated wound healing Complete wound

closure with dermal equivalence

Accumulation of exudateNo Antimicrobial properties

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» 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-epithellalization

but no maceration

» Autolyte debridement effect » Treatment of superficial and deep partial thickness

burns109

ROLE OF DUODERM TM

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111

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

Page 112: Picu Protocols-Dr.mohan Shenoy_2.8.2010

TREATMENT OF AIRWAY BURNS WHAT’S NEW?

• Pressure controlled ventilation• High frequency ventilation• Percussive ventilation• Nitric Oxide• Partial liquid ventilation• Surfactant replacement• ECMO

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• 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. 113

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Care of Care of BB UU RR NN SSBB - - breathing

body image

UU - urine output

RR - rule of nines resuscitation of fluid

NN - - nutrition

S S - shock silver sulfadiazine

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THANK

YOU

Page 116: Picu Protocols-Dr.mohan Shenoy_2.8.2010

First degree Second degree

Third degree Third degree

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Grades of BurnsGrades of Burns

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First degree Second degree

Third degree Third degree

Reed, Pomerantz: Emergency management of pediatric burns. Pediatr Emerg Care 21 (2); 2005