Burns - Pathophysiology, Evaluation and Management
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Transcript of Burns - Pathophysiology, Evaluation and Management
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1
BURNS – PATHOPHYSIOLOGY, EVALUATION & MANAGEMENTDR ARUN KUMAR M GUIDE : DR S MEHROTRADR ANKIT SHARMA MS (GEN SURG),
MCH (PLASTIC SURGERY)
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2OVERVIEW
Part I Historical perspective Statistics Classification of Burns Pathophysiology Evaluation
Part II Management Pre-hospital Care Resuscitation & Nutritional support Burn wound care Complications Rehabilitation
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3Definition
Injuries that result from direct contact or exposure to any physical, thermal,
chemical, electrical, or radiation source are termed as Burns.
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4
HISTORICAL PERSPECTIVE
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5Historical Perspective
First direct evidence of treatment for burns - Cave paintings of Neanderthal man
1500 BC : Egyptian Smith Papyrus – Resin & Honey
Ambroise Pare ( AD 1510 – 1590) : Technique of early excision of burn wounds
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6Historical Perspective
1607 : GF Hildanus : Pathophysiology of Burns
1797 : Edward Kentish : Chronic Burn scar Marjolin’s ulcer
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7Historical Perspective
19th century : Dupuytren’s classification based on depth
1842 : Curling : Gastric & Duodenal Ulceration
Thomas Blizard CurlingBaron Guillaume Dupuytren
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8Historical Perspective
1947 : Texas city disaster
Truman G. Blocker Jr: Multidisciplinary team approach of Burns.
First Burn Institute for
children in Galveston
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9Historical Perspective
1951 : 45% TBSA Burns 49% mortality Present : > 70 % TBSA 49 % mortality
Focus of advance : Improved survival Rehabilitation of Burn survivors
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10
STATISTICS
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11Problem Statement : Global
An estimated 265000 deaths every year are caused by burns.
One of leading causes of disability-adjusted life-years (DALYs) lost in low- and middle-income countries.
In 2004, nearly 11 million people worldwide were burned severely enough to require medical attention.
WHO Apr 14
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12Problem Statement: US
Burn Injuries Receiving Medical Treatment : 486,000 Fire/Smoke Inhalation Deaths : 3,275 Hospitalizations Related to Burn Injury : 40,000
Survival Rate : 96.8%
American Burn Association, 2016
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13Problem Statement : India
70 lakh burn injury cases annually Over 10,00,000 people are moderately or severely burnt every year 1.4 lakh people die of burn every year. Around 70% of all burn injuries occur in most productive age group (15-35
years). Around 4/5 are women & children. As many as 80% of cases admitted are a result of accidents at home (kitchen-
related incidents)
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14
CLASSIFICATION
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15Classification
Based on Cause
Thermal
Electrical
Chemical
Radiation
Inhalation
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16Thermal Injuries
Most common Types : Dry & wet
ContactDirect contact with hot object (i.e. pan or iron)Anything that sticks to skin (i.e. tar, grease or
foods)
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17Thermal Injuries
FlameDirect contact with flame (dry heat)structural fires / clothing catching on fire
ScaldingDirect contact with hot liquid / vapours (moist
heat)Cooking, bathing or car radiator overheatingSingle most common injury in the paediatric pt
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18Electrical Burns
Usually follows accidental contact with exposed object conducting electricity Electrically powered devices Electrical wiring Power transmission lines
Can also result from Lightning
Damage depends on intensity of current
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19Electrical Burns
Severity depends upon: what tissue current passes through (Low voltage/ High voltage) width or extent of the current pathway AC or DC duration of current contact
Tissues with the lowest resistance eg. nerves, blood vessels & muscles Heat generation during passage of the current injures the tissues Skin has a relatively high resistance, hence is mostly spared
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20Electrical Burns
Low-tension injuries(<1000 V) Low energy burns Minimal damage to subcutaneous tissue Entry & Exit points – fingers small deep burns AC Tetany within muscles, cardiac arrest due to interference with normal
cardiac pacing
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21Electrical Burns
High-tension injuries(>1000V)Flash/ Flame / CurrentEarthed high tension lines Arc
over the patient Flash burnHeating of the surrounding air
Explosion Flame burnDirect contact patient acts as
conduction rod huge subcutaneous damage
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22Electrical Burns
Lightning HIGH VOLTAGE!!! Injury may result from
Direct StrikeSide Flash
Severe injuries often result
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23Electrical Burns
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24Electrical Burns
Manifestations:- External Burn Internal Burn Musculoskeletal injury Cardiovascular injury Respiratory injury Neurologic injury Rhabdomyolysis and Renal injury
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25
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26Chemical Burns
Usually associated with industrial exposure Accidental mishandling of household cleaners
Degree of tissue damage determined by
- Chemical nature of the agent
- Concentration of the agent
- Duration of skin contact
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27Chemical Burns
Acids Immediate coagulation necrosis creating an eschar; self-limiting
Bases (Alkali) Liquefactive necrosis with continued penetration into deeper tissue resulting
in extensive injury Eg. Lime, potassium hydroxide, cement
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28Chemical Burns
Systemic absorption of offending agents causing metabolic derangements
Formic acid – haemolysis, Haemoglobinuria Hydrofluoric acid – hypocalcemia
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29Radiation 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
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30Radiation Exposure
Gamma radiation & X-rays Most dangerous penetrating radiation May produce localized skin burns & extensive internal damage
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31Classification
Based on Depth I Degree - Epidermis II Degree - Epidermis+ Dermis III Degree - Epidermis+ Dermis +
Subcutaneous tissue IV Degree - Above + Muscles/bone
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32Classification
Degree of Burn
1st Degree 2nd DegreePartial Thickness
2nd Degree Deep Burns
3rd Degree 4th Degree
Involvement Epidermis Epidermis + Dermis E+ D E+D+Subcut tissue E+D+S+muscles, tendons & bone
Appearance
Symptoms & Signs
Pain ++ Pain ++++ Painful -less severe Painless,insensitive, Severe Edema
No Edema
Healing 3-5 days , spontaneousNo Scarring
2 weeks, min scarring, minimal discolouration
2-6 weeksHypertrophic scarring / formation of contractures
No spontaneous healing
No spontaneous healing
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34
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35
PATHOPHYSIOLOGY
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36Pathophysiology : Local Effects
Zone of coagulation Necrotic area with cellular disruption Irreversible tissue damage
Zone of stasis Moderate insult with decreased tissue
perfusion Can survive or go on to coagulative
necrosis depending on wound environment
JACKSON’s burn zones
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37Pathophysiology : Local Effects
Zone of hyperemiaViable tissue, not at risk for
further necrosis
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38Pathophysiology : Local Effects
Burn wound edema Biphasic pattern
Burn shock : >1/3rd of TBSA
Hypovolemia + Rapid edema formation
1st Hr 12-24 Hrs
Immediate & Rapid increase in edema
Gradual increase
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39Pathophysiology : Local Effects
Edema in non-burned tissue Loss of capillary endothelial integrity Reduced transmembrane potentials of skeletal muscle at the site of
injury as well as away from the site of damage [-90mv -70 to -80mv] Increase in intracellular Na & water leading to edema
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40Clinical Significance
Formation of constricting eschars & requirement of emergency escharotomy
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41Pathophysiology : Local Effects
Inflammatory MediatorsMediator Local effect Systemic effect
Histamine Increased microvascular permeabilityArteriolar dilatation & Venular contraction
Reduced BPHypovolemia
Prostaglandins (PGE2)
Local Vasodilatation (increased blood flow & increased permeability)
Reduced systemic & pulmonary arterial BP
Prostacycline (PGI2)
Increased capillary permeability Reduced BP
Leukotrienes (LB4 & LD4)
Pulmonary HTN
Thromboxane A2 & B2
Vasoconstriction Ischaemia of wound Increasing depth of burn
GI IshcaemiaPulmonary HTN
Kinins (Bradykinin) Increased microvascular permeabilityVasodialatation
Reduced BPHypovolemia
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42Pathophysiology : Local Effects
Mediator Local effect Systemic effect
Serotonin Increased permeability of large blood vessels
Catecholamines Epinephrine Nor-epinephrine
Vasoconstriction (a1 receptors)Vasodialatation (b1 receptors)Antiistaminic & BradykininReduce permeability
Increased PR, BP, Metabolism
O2 RadicalsO2-, H2O2, OH-, ONOO-
Tissue damage & Increased permeability Cardiac dysfunction
PAF Increased permeability
Angiotensin II & Vasopressin
Vasoconstriction GI IshcaemiaIncreased BP
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43Pathophysiology : Local Effects
Mediator Local effect Systemic effect
CRF Inhibitory to other factors
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44Pathophysiology : Systemic Effects
> 30 % Burns in adults
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45Pathophysiology : Systemic Effects
Hemodynamic consequences Reduced cardiac output
Initial phase• Impaired electrical activity of muscle• Vasoconstriction of peripheral vessels
Delayed phase• Hypovolemia • Reduced venous return
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46Pathophysiology : Systemic Effects
Hemodynamic consequences Myocardial dysfunction : O2 derived free radicals (mechanism unclear) Increased systemic vascular resistance & organ Ischemia ( Renal & GI
system)
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47Pathophysiology : Systemic Effects
Renal systemDecreased cardiac output, decreased blood flow
Stress induced hormones & mediators (angiotensin, aldosterone, vasopressin)
Decreased renal blood flow & GFR
Oliguria & renal failure
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48Clinical Significance
Importance of Emergency & Adequate Resuscitation
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49Pathophysiology : Systemic Effects
GI system Mucosal atrophy Increased intestinal permeability Decreased absorption of glucose, amino acids & fatty acids
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50Clinical Significance
Curling’s ulcer : Prophylaxis
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51Pathophysiology : Systemic Effects
Immune system Global depression in immune function Diminished production of macrophages Increased neutrophil count (dysfunctional) followed by decrease after 48-
72 hrs Impaired cytotoxic T cell activity
Increase risk of infections
Depressed Th function
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52Pathophysiology : Systemic Effects
Hypermetabolic responsePhase I [ebb]First 48 hrsDecrease in
cardiac output urine outputO2 consumptionBMR
Impaired glucose tolerance with hyperglycemia
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53Pathophysiology : Systemic Effects
Hypermetabolic response Metabolic variables gradually increase within first five days post injury to reach a plateau Phase II [flow] Increase in metabolic rate
Urine cortisol Serum catecholamines Basal energy expenditure Serum cytokines
Hyperdynamic state – increase in cardiac output Insulin resistance Persists for upto 3 years
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54Clinical Significance
Importance of Techniques of early excisionNutritional support
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55Pathophysiology : Systemic Effects
Inhalational Injury 80% of fire-related deaths due to inhalation of toxic gases Synergestic effect of inhaled toxic gases (CO + HCN)
Agents: Carbon Monoxide Hydrogen Cyanide Hydrogen chloride (PVC) Nitrogen oxides Aldehydes & Acrolein (Wood & Kerosene)
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56Pathophysiology : Systemic Effects
Carbon Monoxide Most frequent cause of death in smoke induced inhalational injury Pathology : 0.1% of CO 50% Carboxy Hb Hb affinity of CO 200-250 times that of O2 Mechanism: Competitive inhibition of Cyt P450
Free radical formation
(Xanthine dehydrogenase Xanthine
Oxidase)
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57
Carbon Monoxide
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58Pathophysiology
Hydrogen cyanide Fires involving N2 containing
compounds Mechanism :
Inhibition of cellular oxygenation with resultant tissue anoxia
Reversible inhibition of Cyt oxidase (Fe 3+) by CN
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59Pathophysiology : Oropharynx
HeatDenaturation of proteins Complement Activation
Histamine releaseFormation of Xanthine
OxidaseConverts Uric acid to ureaRelease
of O2 free
radicals
Edema
formation
Release of
Eicosanoids
Attract PMNs to the site
(Amplify
effects)
Massive
Edema
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60Pathophysiology : Tracheo-bronchial areas
Chemical Injury to airway
Seperation of ciliated epi-cells from BMIncreased Circulation to lung & bronchial
circulationEdema formation
Diffuse transudate in early changes
Bronchoconstriction Fibrin castsObstructio
n of smaller airwaysCulture media
for infectio
ns
Pneumonia
, Sepsi
s & Death
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61Clinical Significance
Important to identify respiratory insult & Early Intubation in case required.
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62
EVALUATION
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63Wallace’s Rule of “9”
Head & Neck - 09
Upper limbs - 09 x 2
Trunk - 18 x 2
Lower limbs - 18 x 2
Perineum - 01
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64
18
9
1
9
4.5
18
9 9
4.5
9 94 .5
7
4 .5
7
4 .5
7
18 181
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65
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66Lund and Browder Charts
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67Palm Method
Size of Patient’s palm 1% of TBSA
Irregular wounds with scattered distribution.
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68OVERVIEW
Part I Historical perspective Statistics Classification of Burns Pathophysiology Evaluation
Part II Pre-hospital Care Resuscitation & Nutritional support Burn wound care Complications Rehabilitation
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MANAGEMENT OF BURNS
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PHASES OF TPT
Phase 1: Treatment at the scene and tpt to initial care facility
Phase 2: Assessment and stabilization at initial care facility and tpt to burn ICU.
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PRE HOSPITAL MANAGEMENT
Rescuer to avoid injuring himself
Remove patient from source of injury
Stop burn process
Burning clothing; jewelry, watches, belts to be removed
Pour ample water on burnt area (not ice/ ice packs – skin injury &
hypothermia)
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PRE HOSPITAL MANAGEMENT
Chemical burns: Remove saturated clothing Brush skin if agent is powder Irrigation with copious amount water to be started and continued in
hospital
Electrical burns: Turn off the current Use non-conductor item to separate from source
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PRE HOSPITAL MANAGEMENT
PRIMARY ASSESSMENT
A – B – C – Cervical spine immobilization
Respiratory tract: Edema of upper airway sets in very fast Upper airway obstruction 100% humidified O2 if no obvious resp distress
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PRE HOSPITAL MANAGEMENT
PRIMARY ASSESSMENT ET intubation + assisted ventilation with 100% O2 if:
Overt signs and symptoms of airway obstruction (Progressive hoarseness) Suspected inhalational injury (smoke/ carbon monoxide intoxication) Unconscious patient/ rapidly deteriorating patient Acute respiratory distress Burns of face & neck Extensive Burns (> 40% TBSA)
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PRE HOSPITAL MANAGEMENT
PRIMARY ASSESSMENT
Pulse rate better monitor than BP Spinal immobilization:
Explosion/ deceleration injury Cervical collar (Philadelphia collar)
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PRE HOSPITAL MANAGEMENT
Ice/ice cold water causes numbness, intense vasoconstriction, hypothermia
causing further damage. Do not break blisters. Do not apply lotions, powders, grease, ghee, gentian violet, calamine lotion,
toothpastes, butter and other sticky agents over the burn wound. Prevent contamination: Wrap burn part in clean dry sheet /cloth. Assess for life threatening injuries.
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PRE HOSPITAL MANAGEMENT
NO I/M or S/C inj (Capillary leakage results in unpredictable absorption)
I/V morphine to allay anxiety
Pain relief and reassurance
Withhold oral intake
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PRE HOSPITAL MANAGEMENT
Co-morbid conditions/ pre-existing illness
Initiate rapid transfer to hospital
Secure and protect the airway
Cervical spine immobilization; if necessary
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PRE HOSPITAL MANAGEMENT
SECONDARY ASSESSMENT
Performed only if no immediate life threatening injury/ hazard present
Thorough head to toe evaluation
Medical history, medication, allergies, mechanism of injury
Start IV line (not reqd in hospital <60 min away)
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PRE HOSPITAL MANAGEMENT
SECONDARY ASSESSMENT RL infusion:
≥ 14 yrs – 500mL/hr 6-14 yrs – 250mL/hr ≤ 5yrs – 125mL/hr
Apply clean dressing/ sheet to protect area and minimize heat loss IV Tramadol to relieve pain No topical antimicrobial
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HOSPITAL MANAGEMENTINITIAL CARE FACILITY
C – A – B
Establish adequate airway
ET intubation – impending airway edema (post initiation of IV therapy)
Maintain cervical spine immobilization
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INITIAL CARE FACILITY
History Mechanism of injury Time of injury Surroundings (closed space/ chemicals)
Physical examination Head to toe assessment Careful neurological examination (cerebral anoxia) Corneal fluorescent examination in facial burns Labs: CBC, electrolytes, BUN Pulmonary assessment: ABG, CXR, carboxyhemoglobin
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INITIAL CARE FACILITY
Pulse in extremities: manual/ doppler Loss of distal circulation
Pallor/coolness/absent pulse/loss capillary refill/decreased oxygen saturation
Pain on passive extension Deep pain at rest Absent pulse: emergency escharotomy to release constrictive, unyielding
eschar
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ESCHAROTOMY
Deep 2nd & 3rd degree circumferential burns Chest: To allow respiratory movement Limb: To restore circulation in limb with excess swelling under rigid eschar
Bedside, IV sedation, cautery Midaxial incision into eschar, Across joints Caution at elbow, wrist, fibular head, medial ankle, neck Not in SC tissue Exposes SC fat
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ESCHAROTOMY
Elevate limbs above level of heart
Monitor pulses for 48 hrs
Chemical escharotomy if pulses +nt but feeble.
Useful in hand burns.
Enzyme – collagenase
Complications : bleeding, infection
Antimicrobial prophylaxis must to prevent sepsis
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INDICATIONS FOR ADMISSION
>15% burns in adults 10% burns in children Airway and inhalation injury. Significant burn involving face, hands, feet and perineum. Extremes of age. Suspected non-accidental burns. Burns that require early surgery (deep partial thickness / full thickness) Patients deficient of nursing care by attendants at home Severe electric and acid burns that is likely to have serious sequelae
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RECEPTION
• Resuscitation –ensure ABC
• Large gauge I.V catheter
• Central line Insertion
• Venesection
• Foleys catheter and NG tube placement
• Quick assessment of extent
• Tetanus prophylaxis (the only IM administered inj)
• Weigh the patient
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Respiratory Care
Assess airway, respiration & breath sounds
Removal of pulmonary secretions O2 Humidification Chest physiotherapy, deep breathing & coughing Frequent position changes and suction
Pharmacologic Considerations: Bronchodilators and mucolytics
Circumferential chest burns can impair ventilation Escharotomy may be required
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Cardiovascular Care
Increase capillary permeability “Capillary Leakage Syndrome” Fluid shift intravascular to interstitial space blistering and massive
edema
Excessive insensible loss via burn wound 3-5 lit/d !!
Finally hypovolemia untreated BURNS’ SHOCK
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Severity of Burn Injuries
Treatment of burns as per severity of injury
Severity is determined by: Depth of burns TBSA involved Site - face, hands, feet, face or perineum Age Associated injuries
N Engl J Med 1996;335:1581 J Trauma 1994;36;59
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OUTCOME
PROGNOSIS (Baux Score)Sum of Age in years
+
Area of burn in % TBSA
< 80 good
80-100 life threatening
>100 bad
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Resuscitation Phase
First 24-48 hours after initial burn injury or until spontaneous diuresis occurs. Resuscitation phase characterized by:
Life-threatening airway problems Cardiopulmonary instability Hypovolemia
Goal: Maintain vital organ function and perfusion
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PARENTERAL FLUIDS
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Parkland Formula Fluid of Choice
Lactated Ringer’s (RL) NS can produce hyperchloremic acidosis
4 ml x % of burn x weight (Kg) in 24 hours First ½ of total volume given in the first 8 hours Remaining ½ of total volume given over following 16 hours
NEXT 24 HRS Total volume ½ of first day Colloids ( 0.5 ml / kg / % ) 5 % glucose to make up the rest
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Parkland Formula
Maximum applicable TBSA – 50%
Fully dilated capillaries
Maximum capillary permeability
No further mounting of inflammatory response
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Adult Fluid Resuscitation
Evan’s formula:
Requirement for first 24 hrs Colloids : 1ml/kg/% burn Saline : 1ml/kg/% burn D5 : 2000ml
Requirement for second 24 hrs ½ of first 24 hrs
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Adult Fluid Resuscitation
Brooke formula
Requirement for first 24 hrsColloids : 0.5ml / kg /% burnRL : 1.5ml / kg / %burnD5 : 2000ml in adults
Requirement for second 24 hrs ½ of first 24hrs
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Pediatric age group
Carvajal Formula
5000cc x m2 x % BSA initial + 2000cc x m2 maint /d
Change to 5%D+RL with albumin after 6 hrs Urine output 1-2 cc/ kg/h
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Assessment of Adequacy ofFluid Resuscitation
Monitor Urinary Output
Adult: > 1 ml/ kg/ hr Daily Weight Vital Signs
Heart rate and blood pressure CVP Level of Consciousness
Laboratory values
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RESUSCITATION FAILURE
Delayed resuscitation Electric burns Inhalation injury Escharotomy Carbon monoxide poisoning Elderly patients
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Nutritional Support
Burn wounds consume large amounts of energy: Requires massive amounts of nutrition to promote wound healing
Monitoring Nutritional Status Weekly albumin levels Daily weight EMR (Estimated metabolic requirement) (Curreri formula)
=25kcal x body weight (kg) + 40 kcal x % BSA
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Routes of Nutritional Support
High-protein & high-calorie diet Often requiring various supplements Routes:
ORAL (BEST)Enteral
Gut is the preferred alternative route G-tube or J-tube (Head injury/ surgery/ unconscious)
Parenteral TPN and PPN Associated with an increased risk of infections
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Nutritional Support
Formulas to Predict Caloric Needs in Severely Burned Children
Age group Maintenance needs Burn wound needs
Infants (0-12 mo) 2100 KCal/ %TBSA/ 24hr 1000 KCal/ %TBSA/ 24hr
Children (1-12 yr) 1800 KCal/ %TBSA/ 24hr 1300 KCal/ %TBSA/24 hr
Adolescents (12-18 yr) 1500 KCal/ %TBSA/ 24hr 1500 KCal/ %TBSA/ 24hr
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BURN WOUND CARE
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Burn Wounds
Risk for Infection
Skin first line of defense Necrotic tissue bacterial growth
Management Burn wounds are frequently monitored for bacterial colonizationWound swab cultures and invasive biopsies
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Role of burn wound cultures
Early cultures positive/ high counts early contamination of the burn wound
Routine cultures aid in empiric antimicrobial coverage if the patient subsequently becomes ill
Increasing colony counts change topical antimicrobial agents.
Colonization by virulent or resistant organisms predictor of impending invasive burn wound infection.
Wound colony counts >106 high risk of infectious & graft failure.
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Burn Wound Care
Hydrotherapy
Shower, bed baths or clear water sprayMaintain appropriate water and room temperatureLimit duration to 20-30 minutes Don’t burst blisters, aspirate them!!! Trim hair around wound; except eyebrowsDry with towel; pat dry, don’t rub! Clean unburned skin and hair
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Burn Wound Care
Antimicrobial Agent Silvadene (silver sulfadiazine)
Broad spectrum; the most common agent used Painless & easy to use Doesn’t penetrate eschar Leaves black tattoos from silver ion
Sulfamylon (mafenide acetate) Penetrates eschar Painful for approximately 20 minutes after application Metabolic acidosis
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Burn Wound Care
Antimicrobial agent Bacitracin/ Neomycin/ Polymyxin B
- not broad spectrum, painless, easy to apply
Nystatin(Mycostatin) - antifungal
Mupirocin(Bactroban)- anti staphylococcal
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Burn Wound Care
Betadine
Drying effect makes debridement of the eschar easier
Acticoat (antimicrobial occlusive dressing)
A silver impregnated gauze that can be left in place for 5 days Moist with sterile water only; remoisten every 3-4 hours
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Soak silver dressings and gauze in WATER (not saline).
Apply thesilver dressing.
Wrap with moist gauze.Secure with mesh, gauze or tape.
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Burn Wound Care
Antimicrobial (SOAKS) 0.5% Silver nitrate
Effective against all micro-organism Stains contacted area, leaches sodium from wound Methemoglobinemia
5% Mafenide acetate Painful metabolic acidosis
0.025 Sodium hypochlorite - Gram Positive organism
0.25% Acetic acid - Gram Negative organism
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Closed Dressing
Advantages• Less wound desiccation• Decreased heat loss• Decreased cross
contamination• Debriding effect• More comfortable
• Disadvantages• Time consuming• Expensive• Increase chances of
infection if not changed frequently
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Burn Wound Care
Cover with a Sterile Dressing Most wounds covered with several layers of sterile gauze dressings.
Special Considerations: Joint area lightly wrapped to allow mobility Facial wounds may be left open to air Circumferential burns: wrap distal to proximal All fingers and toes should be wrapped separately Splints over dressings
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Burn Wound Care
Debridement of the wound May be completed at the bedside or as a surgical procedure. Types of Debridement:
Natural Body & bacterial enzymes dissolve eschar; takes a long time
Mechanical Sharp (scissors), Wet-to-Dry Dressings or Enzymatic Agents
Surgical
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Why excise the burn?
Burn wound is a focus for sepsis
Burn stimulates inflammatory mediators
Deep burns cannot heal without grafts
Possible effect on future scar quality
118
Non full-thickness burns may heal spontaneously
Superficial burns heal with acceptable scars
Excised burn wound must be closed
Major burn surgery is hazardous
but
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119Timing of surgery
“Ultraconservative” Conservative Early Acute
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120Urgent surgery
High-tension electrical injury
Deep encircling burns - escharotomy limbs trunk
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121For small burns
Excision and grafting as soon as possible
clearly non-healing
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122Early excision of burns
Tangential excision to
viable tissue on day 2-3
Janzekovic (1970)
Jackson & Stone (1972)
Current concept – within hours Hardly any bleed Upto 60% burns
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123TANGENTIAL BURN EXCISION
& EARLY SPLIT SKIN GRAFTING
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124TANGENTIAL BURN EXCISION
& EARLY SPLIT SKIN GRAFTING
Early wound closure; shorter hospital stay No increase in morbidity Significant ↓ in mortality Reduced bacterial colonization Tissue preservation Maintenance of function Less scaring
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125Early burn surgery
Superior outcomes where suitably equipped
mortality length of hospital stay morbidity during acute burn scar quality
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126Desirable surgical management
Excision of all non-shallow burns as soon as practicable in as few stages as possible
Closure of excised wounds with autograft, allograft or artificial material
Definitive wound closure
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Surgical Management
Skin Grafting Closure of burn wound
Spontaneous wound healing would take months for even a small full-thickness burn
Eschar is removed as soon as possible to prevent infection Wound needs to be covered to prevent infection, loss of heat, fluid and
electrolytes Therefore, skin grafting is done for most full-thickness burns.
Can be permanent or temporary
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Burn Wound Closure
Permanent Skin Grafts Two types:
Autografts and Cultured Epithelial Autografts (CEA) Autograft
Harvested from pt Non-antigenic Less expensive Decreased risk of infection Can utilize meshing to cover large area Disadvantage : lack of sites and painful
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Burn Wound Closure
Cultured Epithelial Autografts (CEA)
A small piece of pt’s skin is harvested and grown in a culture medium (PDGF impregnated)
Takes 3 weeks to grow enough for the first graft
Very fragile; immobile for 10 days post grafting
Useful for limited donor sites
Disadvantage : very expensive; poor long term cosmetic results and skin remains fragile for years
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Burn Wound Closure
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Burn Wound Closure
Temporary Skin Grafts
Why temporary ??
Available donor sites are used first, but in large burns not enough donor sites.
While waiting for donor site to heal it can be reused as a temporary covering.
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Types of temporary Skin Grafts
Biosynthetic- Homograft (cadaveric)/ Xenograft
(porcine)
Artificial Skins (collagen based)- Trancyte/ Integra
Synthetic – Biobrane/Opsite
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Burn Wound Closure
Biosynthetic Temporary Skin Grafts Homograft
Allograft Live or cadaver human donors Fairly expensive/ all the function of skin Best infection control of all biologic coverings Disadvantage :
Disease transmission (HBV & HIV) Antigenic: body rejects in 2 weeks Not always available Storage problems
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Biosynthetic Temporary Skin Grafts
Heterograft Xenograft Graft between 2 different species
Porcine most common Fresh, frozen or freeze-dried (longer shelf life) Amenable to meshing & antimicrobial impregnation Antigenic: body rejects in 3-4 days Fairly inexpensive Disadvantage : Higher risk of infection
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Biosynthetic Temporary Skin Grafts
Artificial SkinsTranscyte:
A collagen based dressing impregnated with newborn fibroblasts. Integra:
A collagen based product that helps to form a “neodermis”no anti-microbial property
SyntheticAny non-biologic dressing that will help prevent fluid & heat loss
Biobrane, Xeroform, OpSite or Beta Glucan collagen matrix
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Biobrane
Artificial dressing has elastic property Bilayer fabric Inner layer - knitted nylon threads
coated with porcine collagen Outer layer - rubberized silicone Pervious to gases but not to liquids
and bacteria Epithelialization takes place under
the dressing in partial thickness wound in 1-2 wks
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Donor Site: Wound Considerations
The donor site is often the most painful aspect for the post-operative pt brand new wound !! Variety of products are used for donor sites
Most are left in place for 24 hours and then left open to air
Donor sites usually heal in 3 wks
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COMPLICATIONS
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Burn Wound Infection
Focal/ multi focal/ generalized
More the area of infection ↑chances of septicemia
Common org- Strep, Staph & Pseudomonas
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Monitoring Wound Infection
Definite diagnosis wound biopsy
More than 100,000 organisms is highly suggestive of burn wound infection
Concomitant positive blood culture is a reliable indicator
Children & burns > 30% TBSA are more likely to develop burn sepsis
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Clinical Signs of Burn Wound Infection
2nd degree burn full-thickness necrosis
Focal dark-brown or black discoloration
Wound degeneration “neo-eschar” formation
Unexpectedly rapid eschar separation
Hemorrhagic discoloration of sub-eschar fat
Erythematous or violaceous edematous wound margin
Septic lesions in unburned tissue
Crusted serrations of wound margin
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Management
Topical anti microbial therapy
- Mafenide acetate
- Silver sulfadiazine
- Silver nitrate
Systemic antibiotics
Eschar excision & covering with biological dressings
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Burn Sepsis
Host & opportunistic organism balance altered
Immunologic alteration
Defect in cell-mediated immunity Abnormal activation of complement pathway
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Sepsis in burn pt concern for infection.
Age-dependent definition with adjustments for children.
The trigger includes at least three of the following:
I. Temperature >39° or <36.5°C II. Progressive tachycardia
Adults >110 bpm Children >2 SD above age-specific norms (85% age-adjusted max
heart rate)
Burn Sepsis
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III. Progressive tachypnea Adults >25 /min not ventilated
Minute ventilation >12 L/min ventilated Children >2 SD above age-specific norms
(85% age- adjusted max respiratory rate)
IV. Thrombocytopenia (only 3 days after initial resuscitation) Adults <100 000/mcl Children <2 SD below age-specific norms
Burn Sepsis
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V. Hyperglycemia (in the absence of pre-existing diabetes mellitus) Untreated plasma glucose >200 mg/dL or equivalent mM/L Insulin resistance – examples include
>7 units of insulin/h intravenous drip (adults) Resistance to insulin (>25% increase in insulin requirements over 24 hours)
VI. Inability to continue enteral feedings >24 hours Abdominal distension Enteral feeding intolerance (residual >150 mL/h in children or 2× feeding rate in adults) Uncontrollable diarrhoea (>2500 mL/d for adults or >400 mL/d in children)
Burn Sepsis
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Identify & document infection:
Culture positive infection
Pathologic tissue source identified
Clinical response to antimicrobials
Burn Sepsis
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Clinical Manifestations
Hyperthermia, Hypothermia (later)
Tachycardia
Increased ventilation
High cardiac output
Leucocytosis
Thrombocytopenia
Hypotension & oliguria
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Treatment
Definitive wound excision
Antibiotics
Supportive Care
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REHABILITATION PHASE
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Begins day one and may last several years Nursing care Meticulous asepsis continues to be important
Major areas of focus: Support for adequate wound healing
Prevention of hypertrophic scarring & contractures
Psychosocial Support Patient and family
Promotion of maximal functional independence
Rehabilitation
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Hypertrophic Scar Formation
Excessive scar formation, which rises above the skin Management: Pressure Garments
Elasticized garments that are custom fitted Maintains constant pressure on the wound
Result: smoother skin & minimized scar appearance
Pt Considerations: Must be worn 2-3 hours a day Up to 1-2 years Jobst garments, foam sponge, foam tape, silicon gel sheet
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Contracture Formation
Shrinkage and shortening of burned tissue
Results in disfigurement Especially if burn injury involves joints
Management is application of opposing force: Splints, proper positioning, mobilisation
Must begin at day oneMultidisciplinary approach is essential
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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 orgs
Psy Considerations Encourage pt & family to express feelings Assist in developing positive coping strategies
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RECENT ADVANCES
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RAs (grafts)
Liposomal gene transfer Branski L, Pereira CT, Herndon DN, Jeschke MG. Gene therapy in wound healing: Present Status and Future Directions. Gene Therapy, 2006 Aug 24
cationic cholesterol-containing liposomal constructs (best so far)
Naked DNA application, Viral transfection, High-pressure injection Liposomal delivery
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RAs (grafts)
ARTIFICIAL SKIN SUBSTRATES Dermal matrices with epidermal components Boyce ST, Kagan RJ, Yakuboff KP, Meyer
NA, Rieman MT, Greenhalgh DG, Warden GD. Cultured skin substitutes reduce donor skin harvesting for closure of excised, full-thickness burns. Ann surg, 2002 Feb; 235(2):269-279
Amniotic wound coverage devices . Branski LK, Herndon DN, Masters OE, Celis M, Norbury WB, Jeschke MG. Amnion in the treatment of pediatric partial-thickness facial burns. Burns, 2007 Oct 4.
Dermal component matrices Schulz JT 3rd, Tompkins RG, Burke JF. Artificial skin. Ann Rev Med, 2000; 51:231-244
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CONCLUSION
Early, aggressive, controlled fluids Monitor urine output as a guide to resuscitation Prevent extension of injury Maintain high suspicion for inhalation injury & low thresh hold for intubation Always rule out co-incident trauma Frequent reassessment of extremities Seek out & treat CO poisoning Liberal use of analgesia Prevent hypothermia Provide for increased metabolic demands
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BURNS !!! B Breathing
U Urinary output
R Rule of Nines & Resuscitation with fluid
N Nutrition
S Shock & Silvadene
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160References
Total Burn Care; David N Herndon 4th Ed Bailey And Love's Short Practice of Surgery 26th Ed 2013 Schwartz’s Principles of Surgery, 10th Ed Sabiston Textbook of Surgery 19th ed 2012
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161
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