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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