BURNS DR. EDITH H. TERNA-YAWE MBBS,FWACS - PowerPoint Presentation

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BURNS

DR. EDITH H. TERNA-YAWE MBBS,FWACS

CONSULTANT PLASTIC AND RECONSTRUCTIVE SURGEON

National Hospital Abuja

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OUTLINE

INTRODUCTION

CAUSES

PATHOPHYSIOLOGY

BURN CARE

INHALATION INJURY

WOUND CARE

CHEMICAL BURN

ELECTRICAL BURN

COMPLICATIONS

PREVENTION

CONCLUSION

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INTRODUCTION

Devastating trauma

Largely

PREVENTABLE

Multidisciplinary treatment

Requires proper understanding of pathology for treatment and good outcome

Slide4

ANATOMY /FUNCTIONS OF SKIN

1.Epidermis – outer layer

2.Dermis

3.Subcutaneous tissue

FUNCTIONS

-Protective Barrier

-Regulation of Temperature

-Sensation

etc

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FUNCTIONS OF THE SKIN/BURN INJURY

SKIN FUNCTION

CONSEQUENCE OF BURN INJURY

INTERVENTION

Thermoregulation

Prone to lose body heat

Must keep patient covered and

warm

Control of fluid loss

Loss of large amounts of water and protein from the skin and other body tissues

Adequate fluid resuscitation

Mechanical barrier to bacterial invasion and immunological organ

High risk of infection

Antibiotic ointments. Systemic antibiotics if signs of specific infection present.

TT prophylaxis if necessary

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CAUSES OF BURN

HOT FLUIDS(SCALDS)- commonest in children

Hot water

Soups

Oils

Drinks

FLAME(NAKED FIRE)- commonest in adults

House fires- fuel, kerosene, gas explosion, electrical faults

Camp fires

Burning of trash, leaves

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CAUSES OF BURN

CONTACT BURN

Hot objects

eg

metals, plastics, coal

Usually deeper burns

ELECTRICAL BURN

CHEMICAL BURN

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PATHOPHYSIOLOGY OF THE BURN WOUND

Amount of tissue destruction is based on

Temperature

Time of exposure

Specific heat of the causative agent

IMMERSION TIME TO PRODUCE FULL-THICKNESS BURNS

TIME

TEMPERATURE(

0

F

)

1

second

158

2 seconds

150

10 seconds

140

30

seconds

130

1 minute

127

10 minutes

120

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PATHOPHYSIOLOGY

Jackson(1953) described zones of injury

ZONE OF COAGULATION

No blood flow

Irreversible cell damage

Cellular death/necrosis

ZONE OF STASIS(

oedema

)

Decreased perfusion

Microvascular

sludging

and thrombosis of vessels results in progressive tissue necrosis

Cellular death in 24-48hr without proper treatment

N/B: factors

favouring

cell survival: moist,

asceptic

environment, rich blood supply

Zone where appropriate early intervention has most profound effect in minimizing injury

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PATHOPHYSIOLOGY

ZONE OF HYPERAEMIA

Vasodilatation from inflammation

Entirely viable

Cells recover within 7 days

Contributes to systemic consequences seen with major burns

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PATHOPHYSIOLOGY

SEVERE BURNS

Vascular permeability,

oedema

Altered

haemodynamics

(decreased cardiac output, increased vascular resistance)

Hypermetabolism

Progressive pulmonary insufficiency

Increased gut mucosal permeability(GI bleed risk)

Immunosuppression

Renal failure(decreased renal blood flow)

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American Burn Association Burn Centre TRANSFER Criteria

2

nd

or 3

rd

degree burns greater than 10% TBSA in patients younger than 10yrs or older than 50yrs

2

nd

or 3

rd

degree burns greater than 20% TBSA in persons of other age groups

2

nd

or 3

rd

degree burns that involve the face, hands, feet, genitalia, perineum or major joints

3

rd

degree burns greater than 5% TBSA in persons of any age

Electrical burns including lightening injury

Chemical burns

Inhalational burns

Burn injury in patients of pre-existing medical disorders that could complicate management, prolong recovery, or affect mortality

Any patient with burns or concomitant trauma (e.g. fracture) in which the burn injury poses the greatest risk or morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be treated initially in a Trauma Centre until stable before transfer to a Burn Centre

Lack of qualified personnel or equipment for the care of children (transfer to facility with these qualities)

Burn injury in patients who require social/emotional and/or long-term rehabilitative support, including cases involving suspected child abuse or substance abuse

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EXTENT OF BURNS(TBSA)

Wallace’s rule of nines

Lund and Browder chart

Patient’s palm = 1%

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BURN EXTENT

Rule of Nines

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The Lund and Browder Chart

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Lund and Browder chart

Area

Birth 1yr

1-4 yr

5-9 yr

10-14 yr

15yr

Adult

Partial thickness 2

O

Full thickness 3

O

Total

Head

19

17

13

11

9

7

Neck

2

2

2

2

2

2

Anterior trunk

13

13

13

13

13

13

Posterior trunk

13

13

13

13

13

13

Right buttock

2 ½

2 ½

2 ½

2 ½

2 ½

2 ½

Left buttock

2 ½

2 ½

2 ½

2 ½

2 ½

2 ½

Genitalia

1

1

1

1

1

1

Right upper arm

4

4

4

4

4

4

Left upper arm

4

4

4

4

4

4

Right lower arm

3

3

3

3

3

3

Left lower arm

3

3

3

3

3

3

Right hand

2 ½

2 ½

2 ½

2 ½

2 ½

2 ½

Left hand

2 ½

2 ½

2 ½

2 ½

2 ½

2 ½

Right thigh

5 ½

6 ½

8

8 ½

9

9 ½

Left thigh

5 ½

6 ½

8

8 ½

9

9 ½

Right leg

5

5

5 ½

6

6 ½

7

Left leg

5

5

5 ½

6

6 ½

7

Right foot

3 ½

3 ½

3 ½

3 ½

3 ½

3 ½

Left foot

3 ½

3 ½

3 ½

3 ½

3 ½

3 ½

Total

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BURN DEPTH

DETERMINATION OF BURN DEPTH

Inspection – most reliable by experienced burn surgeon

Fluorescein dyes

Ultrasound

Laser Doppler

Magnetic Resonance Imaging

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Burn depth

NOMENCLATURE

TRADITIONAL NOMENCLATURE

DEPTH

CLINICAL FEATURES/APPEARANCE

Erythema/Superficial

1

st

degree

Epidermis

Painful, sensation intact, erythema

blanchable

Superficial partial thickness

2

nd

degree

Superficial (papillary) dermis

Painful, sensation intact, erythema, blisters with clear fluid, erythema,

blanchable

, hair follicles present

Deep partial thickness

2

nd

degree

Deep (reticular) dermis

Insensate, difficult to

distinquish

from full thickness, does not blanch, some hair follicles still attached

Full thickness

3

rd

degree

Insensate,nerve

endings

destroyed,hard,leathery

eschar that is

black,grey,white

or cherry red in

colour.Hairs

do not stay

attached,may

see thrombosed veins

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MANAGEMENT

Pre-hospital care

First aid

Primary Survey/Assessment

- Airway

- Breathing

- Circulation

Secondary Survey

Mechanism of injury

Evaluation for presence/absence of inhalation injury/carbon monoxide poisoning

Consider possibility of abuse

Detailed assessment of burns wound

Detailed history documented

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MANAGEMENT

Prevent and/or treat burn shock – 2 wide bore IV cannula

Identify and treat immediate life-threatening conditions

eg

inhalation injury, CO poisoning

Determine TBSA affected

Depth – difficult to determine initially, easier to determine after 24hrs

Tetanus prophylaxis – 0.5ml IM, also give 250 units of tetanus Ig if prior immunization absent or unclear or last booster >10yrs ago

Baseline lab studies: FBC, urinalysis, EUC, RBS, GXM

Cleanse, debride and apply antimicrobial dressing

Early excision and grafting important for good outcome in deeper burns

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FLUID THERAPY

Parkland formula: 4ml Ringers lactate/kg/%TBSA

½ of total in 0-8hrs

½ of total next 16hrs

EXTRA FLUID IS REQUIRED IN THE FOLLOWING

Burn>80%TBSA

4

0

burns

Associated traumatic injury

Inhalational injury

Electrical injury

Delayed start of resuscitation

Paediatric

burns

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MONITORING

Urine output – best measure for adequate fluid resuscitation. Maintain at 0.5ml/kg/

hr

for adults, then 1ml/kg/

hr

for children <12yrs

Maintain a clear sensorium,

HR<120/min, mean BP>70mmHg

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INHALATIONAL INJURY

Closed-space fire incidents

Soot in the

nares

and mouth

Facial burns

Singed nasal hairs

Cough, hoarseness of voice, difficulty in breathing

Carbon monoxide intoxication

Probable in persons injured in structural fires, particularly if they are obtunded

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INHALATION INJURY 2

Bronchoscopy

Carbonaceous debris

Ulceration/erythema

Clinical consequences

Upper airway

oedemia

Bronchospasm

Small airway occlusion

Increased dead space and intrapulmonary shunting

Decreased lung and chest wall compliance

Infection

Management

- Largely supportive

- Oxygen

- Intubation and ventilation

- Airway toileting

- Vasodilators

- Pneumonia/

tracheobronchitis

occur in 30% of these patients

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BURN WOUND MANAGEMENT

Out-patient (Majority)

In-patient

FOUR PHASES

Initial evaluation & resuscitation

Initial wound excision & biologic closure

Definitive wound closure

Rehabilitation & reconstruction

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MEDICATION AND MEMBRANE

MEDICATIONS

Silver sulfadiazine

Aqueous 0.5% silver nitrate

Mafernide

acetate

Petrolatum

Various

debriding

enzymes

Honey

Various antibiotic ointments

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SKIN COVER SUBSTITUTES

Split thickness human allograft

Epidermal

Amniotic membrane

Dermal analogues

Intergra

R

Alloderm

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MEMBRANES

Porcine

xenograft

Amniotic membrane

Split thickness allograft

Various hydrocolloid dressings

Various impregnated gauzes

Various semi-permeable membrane

Acticoat

Biobrane

Transcyte

Alloderm

R

Intergra

R

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CHEMICAL BURNS

Acid

Alkaline

Phosphorus

Chemical injection injuries

COMMON AGENTS

Cement

Hydrofluoric acid

Phenol

Tar

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CHEMICAL BURNS

MECHANISM OF INJURY

Chemical solutions coagulate tissue leading to necrosis

ACIDS – coagulative necrosis

ALKALI – saponification followed by liquefactive necrosis

SEVERITY DEPENDS ON

Type of chemical

Temperature

Volume

Concentration

Contact time

Site affected

Mechanism of chemical reaction

Degree of tissue penetration

N/B: burns are deeper than they initially appear and may progress with time

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CHEMICAL BURNS

Immediate removal of clothes and chemical

First responders need to protect themselves from injury

Copious irrigation with tap water for at least 30mins

Some agents are associated with irritating fumes which can result in airway compromise

Inspect and irrigate eyes if affected with normal saline

Correct metabolic abnormalities and tetanus prophylaxis if necessary

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CHEMICAL BURN

HYDROFLUORIC ACID

Water irrigation

Topical Calcium gel

+/- subcutaneous injection of Calcium gluconate

+/- 10% IV Calcium gluconate depending on amount of exposure and pain

SULFURIC ACID

Treat with soap/lime prior to irrigation as direct water exposure produces heat

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ELECTRICAL BURNS

Low voltage

Mid-voltage (200 to 1,000V)

Can have destructive injuries

High voltage (> 1,000V)

Associated with cardiac arrhythmias,

myoglobinuria

, loss of consciousness, falls, fractures

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ELECTRICAL BURN

System-specific damages associated with electrical burns

Abdominal – intraperitoneal damage

Bone – fractures and dislocations

Cardiopulmonary – anoxia, ventricular fibrillation, arrhythmias

Muscle –

myoglobinuria

indicates significant muscle damage/compartment syndrome

Neurological – seizures, spinal cord damage

Ophthalmic – cataract formation

Renal – acute tubular necrosis

Vascular – vessel thrombosis

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ELECTRICAL BURNSTreatment

Primary and secondary survey

Treat associated injuries

Monitor

colour

of urine, compartment syndrome and urine output

WOUND MANAGEMENT

Topical agents with good penetrating ability(Silver sulfadiazine or

Mafenide

acetate)

Debride non-viable tissues early and repeat PRN(every 48hrs) to prevent sepsis

Amputations frequently required

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BURNS REHABILITATION

Physiotherapy should commence from a critical care setting

Range of motion exercise

Splinting

Anti-deformity positioning

Minimize

oedema

Reconstructive surgeries

Scar management

Compression garments

Topical silicon

Steroid injections

Management of

pruritus

Slide37

PROGNOSIS

TBSA

Age

Depth

Location

Inhalation injury

Associated injuries

Comorbid factors

Slide38

PREVENTION

Patients, personnel and community education

Speed limits

Not carrying inflammable substances in passenger vehicles

Fire extinguishers in vehicles, etc

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REFERENCES

1. Robert L. Sheridan MD et al. Initial evaluation & management of the burn. Emedicine.medscape.com (2015)

2. Matthew B. Klein. Thermal, chemical and electrical injuries. Chapter 17 Grab & Smith’s plastic surgery. 6

th

edition (2007)

3. Brett D.

Amolda

et al. Electrical Injuries. Chapter 38. Total Burns Care 4

th

edition (2012)

4. Ronald P.

Mlcak

et al. Pre-hospital Management, transportation and emergency care. Chapter 7. Total Burns Care 4

th

edition (2012)

Nigerian Burn Society. Handbook on Prevention of Burns in our Environment/Society.

Charles H. Thorne:

Grabb

and Smith’s Plastic Surgery. 6

th

Ed.(2007). Lippincott Williams and Wilkins.

Ryan Austin et. al. Toronto notes of Plastic Surgery. 2011