burns - pathophysiology, evaluation and management
TRANSCRIPT
1
BURNS – PATHOPHYSIOLOGY, EVALUATION & MANAGEMENTDR ARUN KUMAR M GUIDE : DR S MEHROTRADR ANKIT SHARMA MS (GEN SURG),
MCH (PLASTIC SURGERY)
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
3Definition
Injuries that result from direct contact or exposure to any physical, thermal,
chemical, electrical, or radiation source are termed as Burns.
4
HISTORICAL PERSPECTIVE
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
6Historical Perspective
1607 : GF Hildanus : Pathophysiology of Burns
1797 : Edward Kentish : Chronic Burn scar Marjolin’s ulcer
7Historical Perspective
19th century : Dupuytren’s classification based on depth
1842 : Curling : Gastric & Duodenal Ulceration
Thomas Blizard CurlingBaron Guillaume Dupuytren
8Historical Perspective
1947 : Texas city disaster
Truman G. Blocker Jr: Multidisciplinary team approach of Burns.
First Burn Institute for
children in Galveston
9Historical Perspective
1951 : 45% TBSA Burns 49% mortality Present : > 70 % TBSA 49 % mortality
Focus of advance : Improved survival Rehabilitation of Burn survivors
10
STATISTICS
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
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
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)
14
CLASSIFICATION
15Classification
Based on Cause
Thermal
Electrical
Chemical
Radiation
Inhalation
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)
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
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
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
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
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
22Electrical Burns
Lightning HIGH VOLTAGE!!! Injury may result from
Direct StrikeSide Flash
Severe injuries often result
23Electrical Burns
24Electrical Burns
Manifestations:- External Burn Internal Burn Musculoskeletal injury Cardiovascular injury Respiratory injury Neurologic injury Rhabdomyolysis and Renal injury
25
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
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
28Chemical Burns
Systemic absorption of offending agents causing metabolic derangements
Formic acid – haemolysis, Haemoglobinuria Hydrofluoric acid – hypocalcemia
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
30Radiation Exposure
Gamma radiation & X-rays Most dangerous penetrating radiation May produce localized skin burns & extensive internal damage
31Classification
Based on Depth I Degree - Epidermis II Degree - Epidermis+ Dermis III Degree - Epidermis+ Dermis +
Subcutaneous tissue IV Degree - Above + Muscles/bone
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
34
35
PATHOPHYSIOLOGY
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
37Pathophysiology : Local Effects
Zone of hyperemiaViable tissue, not at risk for
further necrosis
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
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
40Clinical Significance
Formation of constricting eschars & requirement of emergency escharotomy
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
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
43Pathophysiology : Local Effects
Mediator Local effect Systemic effect
CRF Inhibitory to other factors
44Pathophysiology : Systemic Effects
> 30 % Burns in adults
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
46Pathophysiology : Systemic Effects
Hemodynamic consequences Myocardial dysfunction : O2 derived free radicals (mechanism unclear) Increased systemic vascular resistance & organ Ischemia ( Renal & GI
system)
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
48Clinical Significance
Importance of Emergency & Adequate Resuscitation
49Pathophysiology : Systemic Effects
GI system Mucosal atrophy Increased intestinal permeability Decreased absorption of glucose, amino acids & fatty acids
50Clinical Significance
Curling’s ulcer : Prophylaxis
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
52Pathophysiology : Systemic Effects
Hypermetabolic responsePhase I [ebb]First 48 hrsDecrease in
cardiac output urine outputO2 consumptionBMR
Impaired glucose tolerance with hyperglycemia
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
54Clinical Significance
Importance of Techniques of early excisionNutritional support
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)
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)
57
Carbon Monoxide
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
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
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
61Clinical Significance
Important to identify respiratory insult & Early Intubation in case required.
62
EVALUATION
63Wallace’s Rule of “9”
Head & Neck - 09
Upper limbs - 09 x 2
Trunk - 18 x 2
Lower limbs - 18 x 2
Perineum - 01
64
18
9
1
9
4.5
18
9 9
4.5
9 94 .5
7
4 .5
7
4 .5
7
18 181
65
66Lund and Browder Charts
67Palm Method
Size of Patient’s palm 1% of TBSA
Irregular wounds with scattered distribution.
68OVERVIEW
Part I Historical perspective Statistics Classification of Burns Pathophysiology Evaluation
Part II Pre-hospital Care Resuscitation & Nutritional support Burn wound care Complications Rehabilitation
MANAGEMENT OF BURNS
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.
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)
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
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
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)
PRE HOSPITAL MANAGEMENT
PRIMARY ASSESSMENT
Pulse rate better monitor than BP Spinal immobilization:
Explosion/ deceleration injury Cervical collar (Philadelphia collar)
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.
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
PRE HOSPITAL MANAGEMENT
Co-morbid conditions/ pre-existing illness
Initiate rapid transfer to hospital
Secure and protect the airway
Cervical spine immobilization; if necessary
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)
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
HOSPITAL MANAGEMENTINITIAL CARE FACILITY
C – A – B
Establish adequate airway
ET intubation – impending airway edema (post initiation of IV therapy)
Maintain cervical spine immobilization
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
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
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
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
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
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
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
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
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
OUTCOME
PROGNOSIS (Baux Score)Sum of Age in years
+
Area of burn in % TBSA
< 80 good
80-100 life threatening
>100 bad
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
PARENTERAL FLUIDS
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
Parkland Formula
Maximum applicable TBSA – 50%
Fully dilated capillaries
Maximum capillary permeability
No further mounting of inflammatory response
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
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
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
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
RESUSCITATION FAILURE
Delayed resuscitation Electric burns Inhalation injury Escharotomy Carbon monoxide poisoning Elderly patients
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
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
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
BURN WOUND CARE
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
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.
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
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
Burn Wound Care
Antimicrobial agent Bacitracin/ Neomycin/ Polymyxin B
- not broad spectrum, painless, easy to apply
Nystatin(Mycostatin) - antifungal
Mupirocin(Bactroban)- anti staphylococcal
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
Soak silver dressings and gauze in WATER (not saline).
Apply thesilver dressing.
Wrap with moist gauze.Secure with mesh, gauze or tape.
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
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
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
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
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
119Timing of surgery
“Ultraconservative” Conservative Early Acute
120Urgent surgery
High-tension electrical injury
Deep encircling burns - escharotomy limbs trunk
121For small burns
Excision and grafting as soon as possible
clearly non-healing
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
123TANGENTIAL BURN EXCISION
& EARLY SPLIT SKIN GRAFTING
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
125Early burn surgery
Superior outcomes where suitably equipped
mortality length of hospital stay morbidity during acute burn scar quality
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
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
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
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
Burn Wound Closure
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.
Types of temporary Skin Grafts
Biosynthetic- Homograft (cadaveric)/ Xenograft
(porcine)
Artificial Skins (collagen based)- Trancyte/ Integra
Synthetic – Biobrane/Opsite
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
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
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
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
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
COMPLICATIONS
Burn Wound Infection
Focal/ multi focal/ generalized
More the area of infection ↑chances of septicemia
Common org- Strep, Staph & Pseudomonas
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
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
Management
Topical anti microbial therapy
- Mafenide acetate
- Silver sulfadiazine
- Silver nitrate
Systemic antibiotics
Eschar excision & covering with biological dressings
Burn Sepsis
Host & opportunistic organism balance altered
Immunologic alteration
Defect in cell-mediated immunity Abnormal activation of complement pathway
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
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
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
Identify & document infection:
Culture positive infection
Pathologic tissue source identified
Clinical response to antimicrobials
Burn Sepsis
Clinical Manifestations
Hyperthermia, Hypothermia (later)
Tachycardia
Increased ventilation
High cardiac output
Leucocytosis
Thrombocytopenia
Hypotension & oliguria
Treatment
Definitive wound excision
Antibiotics
Supportive Care
REHABILITATION PHASE
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
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
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
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
RECENT ADVANCES
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
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
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
BURNS !!! B Breathing
U Urinary output
R Rule of Nines & Resuscitation with fluid
N Nutrition
S Shock & Silvadene
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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