BURNS

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Epidemiology
Tissue injury caused by thermal, electrical, or chemical agents Can be fatal, disfiguring, or discapacitating About 1.25 million burn injuries per year

45,000 hospitalized each year 4500 die per year

Third largest cause of death

Anatomy & Physiology of Skin

Largest body organ

Protects underlying tissue from injury
Temperature regulation Acts as a water tight seal, keeping body

fluids in Sensory organ

Skin

Injuries to the skin which result in loss, have problems with:

Infection Inability to maintain normal water balance

Inability to maintain body temperature

Skin

Two layers
Epidermis Dermis

Epidermis
Outer cells are dead
Act as protection Forms water tight seal Deeper layers divide to protect

the stratum corneum and also contain pigment to protect against UV radiation

Skin

Dermis
Consists of tough, elastic connective tissue

which contains specialized structures

Nerve endings Blood vessels

Sweat glands
Oil glands Keep skin waterproof, usually discharges around hair shafts Hair follicles Each follicle has a small muscle which can pull the hair upright and cause goose flesh

A burn injury is a type of injury that is caused by heat, cold, electricity, chemicals, light, radiation, friction

Potential Complications
Fluid & Electrolyte loss -- hypovolemia Hypothermia Infection Acidosis Catecholamine release vasoconstriction Renal or hepatic failure Formation of eschar

Types of Burn Injuries

Thermal Burns Chemical Burns Electrical Burns Radiation Burns

Thermal Burns

Caused by
Exposure to flame
Hot liquids Steam

Any hot object

Injury
Skin

Inhalation

Chemical Burn

Caused by
Contact with strong acids, alkalis, or organic

compounds Injury
Skin
Inhalation Mucous membrane

Electrical Burns

Caused by
Exogenous electric shock that that passes through the

body
Lightning AC or DC, low voltage, high voltage

Important to identify
Type of current Alternating current is associated with cardiopulmonary arrest, ventricular fibrillation, titanic muscle contraction and bone fracture Duration of contact Contact site

Injury
Muscle and tissue damage

Radiation Burns

Caused by
Exposure to UV rays (sunlight) Most common
X-ray

Other radiation sources

Injury
Burns

Burn Injuries

An important step in management is to determine depth and extent of damage to determine where and how the patient is to be treated

Superficial-thickness Burn (First Degree)

Involves the epidermis Characterized by reddening Tenderness and pain Increased warmth Edema may occur, but no blistering Burn blanches under pressure Usually heal in about 7 days

First Degree Burn

Partial-thickness Superficial Burn (Second Degree)

Damage extends through the epidermis and into the dermis Does not interfere with the regeneration of the epithelium Moist shiny appearance Salmon pink to red appearance Painful Blisters ( though not always) Usually heal in 1-3 weeks

Second Degree Burns

Full-thickness Burn (Third Degree)

Both epidermis and dermis are destroyed, with burning into the SQ fat Thick, dry appearance Pearl gray or charred black color Painless nerve endings are destroyed Pain is due to intermixing of second degree burns May be minor bleeding Cannot spontaneously heal and require grafting Recovery takes weeks to months

Third Degree Burns

Deep Full-thickness Burn ( Fourth Degree)

Involves injury to the muscle and bone Black appearance No edema No blisters No pain Eschar is hard and inelastic Grafts are required

Fourth Degree Burns

Rule of Nines

The body surface is divided into areas representing 9% or multiples

Head and neck: 9% Anterior trunk: 18% Posterior trunk: 18 % Arm (9% each): 18% Legs (9% each): 18% Perineum: 1%

Palm rule

The patients palm represents 1% of the body surface area

Lund & Browder Chart

More accurate Allows for differing proportions of body in those of different ages

Burn Severity

Factors to consider

Depth or classification Body surface area burned Age: adult vs. pediatric Preexisting medical conditions Associated trauma
Fall injury Blast injury Airway compromise Child abuse

Burn Severity

Age
Less than two or greater than fifty-five Increased incidence of complication

Burn configuration
Circumferential burns can cause total

occlusion of circulation to an area due to edema Restrict ventilation if encircle the chest Burns on joint area can cause disability due to scar formation

Critical Burn Criteria

Third degree >10% BSA Second degree >20% BSA

Pediatrics > 10%

Burns with respiratory injury Hands, face, feet, or genitalia Burns complicated by other trauma Underlying health problems Electrical and deep chemical burns

Moderate Burn Criteria

Third degree 2-10% BSA Second degree 15-30% BSA

10-20% pediatric

Excludes hand, face, feet, or genitalia Without complicating factors

Minor Burn Criteria

Third degree
< 2% BSA

Second degree
< 15% BSA < 10% pediatrics

First degree
< 20%

Jacksons Thermal Wound Theory

Zone of Coagulation

Area nearest to the burn Cell membranes rupture Clotted blood Thrombosed vessels Ischemia Point of maximum damage Irreversible tissue loss d/t coagulation

Zone of Stasis

Edema Inflammation Decreased blood flow Decreased tissue perfusion

Potentially salvageable

Zone of Hyperemia

Peripheral area of burn Tissue perfusion increased

Increased blood flow

Limited inflammation Tissue will recover, unless there is prolonged severe hypoperfusion

Eschar Formation

Skin denaturing
Hard and leathery

Skin constricts over wound

Increased pressure underneath Restricts blood flow

Respiratory compromise
Secondary to circumferential eschar around

thorax

Circulatory compromise
Secondary to circumferential eschar around

extremity

Systemic Response

The release of cytokines and inflammatory mediators at the site of injury will cause systemic effects once the burn covers about 30% of total body surface area

Cardiovascular
Increased capillary permeability leading to loss of intravascular proteins and fluids Peripheral and splanchnic vasoconstriction Myocardial contractility is decreased All these factors result in systemic hypotension and end-organ hypoperfusion

Respiratory

Inflammatory mediators cause bronchoconstriction which may progress to ARDS.

Metabolic
Basal metabolic rate is increased up to threefold Splanchnic vasoconstriction Early and aggressive enteral feeding is necessary to maintain gut integrity

Immunologic

Non-specific down regulation of both cell mediated and humoral pathways

Inhalation Injury
Important determinant of morbidity & mortality Manifests within the first 5 days after injury Present in 20-50% of pts admitted to burn centers Present in 60-70% of pts who die in burn centers

Inhalation Injury Above the Glottis

Most common inhalation injury Results from heat dissipation into tissues Commonly leads to obstruction Edema lasts for 2-4 days Dx by visualization of upper airways

Indicators of Inhalation Injury

Burned

in closed space Facial or intra-oral burns Singed nasal hairs Soot in mouth, nostrils, larynx Hoarseness or stridor Respiratory distress Signs of hypoxemia

Types of Inhalation Injury

Carbon Monoxide Poisoning Inhalation Injury Above the Glottis Inhalation Below the Glottis

Carbon Monoxide Poisoning

Colorless, odorless gas Binds to hemoglobin 200 times more than oxygen Most immediate threat to life in survivors with severe inhalation injury Toxicity related directly to percentage of hemoglobin it saturates

Signs of CO Poisoning

Cherry red coloration Normal or pale skin with lip coloration Hypoxic with no apparent cyanosis PaO2 is unaffected Essential to determine carboxyhemoglobin levels !

CO Poisoning: Treatment

100% oxygen until carboxyhemoglobin levels less than 15

Increases rate of CO diffusion from 4 hours

to 45 minutes

Hyperbaric oxygen is of unproven value

May be useful in isolated CO intoxication but

complicates wound care

Inhalation Injury Above the Glottis

Most common inhalation injury Results from heat dissipation into tissues Commonly leads to obstruction May result in edema of pharynx and larynx
Lasts for 2-4 days

Dx by visualization of upper airways Symptoms

Brassy cough Stridor Hoarseness Facial burns Carbonaceous sputum

Inhalation Injury Above the Glottis: Treatment

Intubate!!!

Inhalation Injury Below the Glottis

Rare injury Injury to lung parenchyma Chemical pneumonitis caused by toxic products of combustion

Ammonia, chlorine, hydrogen chloride, phosgene,

aldehydes, sulfur & nitrogen oxides Related to amount and type of volatile substances inhaled

Onset of symptoms is unpredictable

Close monitoring for first 24 hours

Inhalation Injury Below the Glottis: Treatment

Prior to transfer to burn center Intubation

to clear secretions relieve dyspnea deliver PEEP Improve oxygenation

Steroids not indicated Prophylactic antibiotics unjustified Circumferential chest burns: escharotomies

Phases of Burn Management

Pre-hospital care Emergent (resuscitative) Acute (wound healing) Rehabilitative (restorative)

Prehospital Care

Electrical injuries
Remove patient from contact with source.

Chemical injuries
Brush solid particles off the skin. Use water lavage.

Prehospital Care

Small thermal burns

Cover with clean, cool, tap water

dampened towel.

Large thermal burns

Airway, breathing, and circulation

Prehospital Care

Large thermal burns

Do not immerse in cool water or pack with

ice. Remove burned clothing. Wrap in clean, dry sheet or blanket.

Pre-hospital Phase

Inhalation injury
Observe for signs of respiratory distress or

compromise. Treat quickly.

Copyright 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

A Airway B Breathing C Circulation / C-spine / Cardiac status D Disability / Neurologic Deficit E Exposure and Examination F Fluid Resuscitation

Emergent Phase

Emergent phase is the period of time required to resolve immediate problems resulting from the injury.

Emergent Phase
Usually lasts up to 72 hours Primary concerns are onset of hypovolemic shock and edema. Phase begins with fluid loss and edema formation and continues until fluid mobilization and diuresis begin.

Emergent Phase Pathophysiology

Fluid and electrolyte shifts

Greatest threat is hypovolemic shock,

caused by a massive shift of fluids out of blood vessels as a result of increased capillary permeability. Colloidal osmotic pressure decreases, resulting in more fluid shifting out of the vascular space into the interstitial spaces.

Emergent Phase Pathophysiology

Fluid and electrolyte shifts (contd)

The net result of the fluid shift is

intravascular volume depletion.

Edema Blood pressure Pulse

Normal insensible loss: 30 to 50 mL/hr Severely burned patient: 200 to

400 mL/hr

Emergent Phase Pathophysiology

Fluid and electrolyte shifts (contd)

RBCs are hemolyzed by a circulating factor

released at the time of the burn. Thrombosis Elevated hematocrit Na+ shifts to the interstitial spaces and remains until edema formation ceases. K+ shift develops because injured cells and hemolyzed RBCs release K+ into extracellular spaces.

Emergent Phase Pathophysiology

Inflammation and healing

Neutrophils and monocytes accumulate at

the site of injury. Fibroblasts and collagen fibrils begin wound repair within the first 6 to 12 hours after injury.

Emergent Phase Pathophysiology

Immunologic changes
Burn injury causes widespread impairment of the

immune system. Skin barrier is destroyed. Bone marrow is depressed. Circulating levels of immune globulins are decreased. WBCs develop defects.

Emergent Phase Clinical Manifestations

Shock from pain and hypovolemia Blisters Adynamic ileus Shivering Altered mental status

Emergent Phase Complications

Cardiovascular system

Dysrhythmias and hypovolemic shock Impaired circulation to extremities Tissue ischemia Necrosis

Emergent Phase Complications

Cardiovascular system (contd)

Impaired microcirculation and

viscosity sludging

Emergent Phase Complications

Respiratory system
Upper respiratory tract injury Edema formation Mechanical airway obstruction and asphyxia Pneumonia Pulmonary edema

Emergent Phase Complications

Urinary system
Blood flow to kidneys causes renal

ischemia. Acute tubular necrosis (ATN)

Emergent Phase
Nursing and Collaborative Management

Airway management

Early endotracheal intubation Escharotomies of the chest wall Fiberoptic bronchoscopy Humidified air and 100% oxygen

Emergent Phase
Nursing and Collaborative Management

Fluid therapy
Two large-bore IV lines for >15% TBSA Type of fluid replacement based on

size/depth of burn, age, and individual considerations Parkland (Baxter) formula for fluid replacement Colloidal solutions

Fluid Resuscitation

Parkland Formula

Total fluid requirement in 24 hours =

4 ml(total burn surface area (%)) (body weight

(kg)) 50% given in first 8 hours 50% given in next 16 hours

Children receive maintenance fluid in addition, at hourly rate of

4 ml/kg for first 10 kg of body weight plus 2 ml/kg for second 10 kg of body weight plus 1 ml/kg for > 20 kg of body weight

End point
Urine output of 0.5-1.0 ml/kg/hour in adults Urine output of 1.0-1.5 ml/kg/hour in children

Emergent Phase Nursing & Collaborative Management

Wound care
Should be delayed until a patent airway,

adequate circulation, and adequate fluid replacement have been established Cleansing
Can be done in a cart shower, shower, or bed

Debridement May need to be done in the OR Loose necrotic skin is removed.

Emergent Phase
Nursing and Collaborative Management

Wound care (contd)

Shower Tap water not exceeding 104 F is acceptable. Once-daily shower Dressing change in morning and evening Infection is the most serious threat to further

tissue injury.
Source of infection is the patients own flora

Emergent Phase
Nursing and Collaborative Management

Wound care (contd)

Open method Burn is covered with a topical antibiotic with no dressing over the wound. Multiple dressing changes or closed method Sterilized gauze dressings are laid over a topical antibiotic. Dressings may be changed from every 12 to 24 hours to once every 14 days

Emergent Phase
Nursing and Collaborative Management

Other care measures

Facial care Performed by the open method Eye care for corneal burns Antibiotic ointment is used. Periorbital edema may frighten patient Hands and arms should be extended and

elevated on pillows or slings. Ears should be kept free of pressure.

No use of pillows

Emergent Phase
Nursing and Collaborative Management

Other care measures (contd)

Perineum must be kept as clean and dry as

possible. Routine laboratory tests Early ROM exercises

Emergent Phase
Nursing and Collaborative Management

Drug therapy
Analgesics and sedatives Morphine Hydromorphone (Dilaudid) Haloperidol (Haldol) Lorazepam (Ativan) Midazolam (Versed) Tetanus immunization Given routinely to all burn patients

Emergent Phase
Nursing and Collaborative Management

Drug therapy (contd)

Antimicrobial agents Topical agents
Silver sulfadiazine (Silvadene)
Mafenide acetate (Sulfamylon)

Systemic agents are not usually used in controlling

burn flora.
Initiated when diagnosis of invasive burn wound sepsis is

made

Emergent Phase
Nursing and Collaborative Management

Drug therapy (contd)

VTE prophylaxis Low-molecular-weight heparin or low-dose unfractionated heparin is started. Those at high bleeding risk, with mechanical VTE prophylaxis with sequential compression devices

Emergent Phase
Nursing and Collaborative Management

Nutritional therapy
Fluid replacement takes priority over

nutritional needs. Early and aggressive nutritional support within hours of burn injury
Decreases mortality and complications Optimizes wound healing Minimizes negative effects

Emergent Phase
Nursing and Collaborative Management

Nutritional therapy (contd)

Hypermetabolic state Resting metabolic expenditure may be increased by 50% to 100% above normal. Core temperature is elevated. Caloric needs are about 5000 kcal/day. Early, continuous enteral feeding promotes optimal conditions for wound healing. Supplemental vitamins and iron may be given.

Acute Phase
The acute phase begins with the mobilization of extracellular fluid and subsequent diuresis. The acute phase is concluded when the burned area is completely covered by skin grafts, or when the wounds are healed.

Acute Phase Pathophysiology

Diuresis from fluid mobilization occurs, and the patient is less edematous. Bowel sounds return. Healing begins when WBCs surround the burn wound and phagocytosis occurs.

Acute Phase Pathophysiology

Necrotic tissue begins to slough. Granulation tissue forms. A partial-thickness burn wound heals from the edges. Full-thickness burns must be covered by skin grafts.

Acute Phase Clinical Manifestations

Partial-thickness wounds form eschar.

Once eschar is removed,

re-epithelialization begins.

Full-thickness wounds require debridement.

Acute Phase Laboratory Values

Sodium
Hyponatremia can develop from Excessive GI suction Diarrhea Water intoxication Hypernatremia may develop following Successful fluid replacement Improper tube feedings Inappropriate fluid administration

Acute Phase Laboratory Values

Potassium
Hyperkalemia noted if patient has Renal failure Adrenocortical insufficiency Massive deep muscle injury Hyperkalemia can cause Cardiac dysrhythmias and ventricular failure Muscle weakness ECG changes Hypokalemia can be caused by Lengthy IV therapy without potassium Vomiting, diarrhea Prolonged gastrointestinal suction

Acute Phase Complications

Infection
Localized inflammation, induration, and

suppuration Partial-thickness burns can become fullthickness wounds in the presence of infection. Wound infection may progress to transient bacteremia. Patient may develop sepsis.
Condition becomes critical

Acute Phase Complications

Cardiovascular and respiratory systems

Same complications can be present in the

emergent phase and may continue into the acute phase.

Acute Phase Complications

Neurologic system
Usually no problems unless severe hypoxia

or complications from electrical injuries occur. Disorientation Combative Hallucinations Delirium Transient state Variety of causes have been considered

Acute Phase Complications

Musculoskeletal system
Decreased ROM Contractures

Gastrointestinal system

Paralytic ileus Diarrhea Constipation Curlings ulcer

Acute Phase Complications

Endocrine system
Blood glucose levels Insulin production Hyperglycemia

Acute Phase
Nursing and Collaborative Management
Wound care Excision and grafting Pain management Physical and occupational therapy Nutritional therapy Psychosocial care

Acute Phase
Nursing and Collaborative Management

Wound care

Daily observation Assessment Cleansing Debridement Dressing reapplication Enzymatic debridement

Speeds up removal of dead tissue from

healthy wound bed

Acute Phase
Nursing and Collaborative Management

Wound care (contd)

Appropriate coverage of the graft: Gauze next to the graft followed by middle and outer dressings Unmeshed sheet grafts used for facial grafts
Grafts are left open. Complication: Blebs

Acute Phase
Nursing and Collaborative Management

Excision and grafting

Eschar is removed down to the

subcutaneous tissue or fascia. Graft is placed on clean, viable tissue. Wound is covered with autograft. Donor skin is taken with a dermatome. Choice of dressings varies.

Acute Phase
Nursing and Collaborative Management

Excision and grafting (contd)

Cultured epithelial autographs (CEAs) Grown from biopsies obtained from the patients own skin Used in patients with a large body surface burn area or those with limited skin for harvesting

Acute Phase
Nursing and Collaborative Management

Excision and grafting

Artificial skin Life-threatening full-thickness or deep partialthickness wounds where conventional autograft is not available or advisable

Acute Phase
Nursing and Collaborative Management

Pain management
Patients experience two kinds of pain. Continuous background pain Treatment-induced pain Several drugs in combination Morphine with haloperidol Treatment-induced pain managed with

potent, short-acting analgesic

Acute Phase
Nursing and Collaborative Management

Pain management (contd)

Nonpharmacologic strategies Relaxation strategies Visualization, guided imagery Hypnosis Biofeedback Music therapy

Acute Phase
Nursing and Collaborative Management

Physical and occupational therapy

Good time for exercise is during wound

cleaning. Passive and active ROM Splints should be custom-fitted.

Acute Phase
Nursing and Collaborative Management

Nutritional therapy
Meeting daily caloric requirements is crucial. Caloric needs should be calculated by

dietitian. High-protein, high-carbohydrate foods Favorite foods from home Patients should be weighed regularly.

Acute Phase
Nursing and Collaborative Management
Psychosocial care
Social worker Nursing staff Pastoral care

Rehabilitation Phase

The rehabilitation phase begins when

Burn wounds are healed Patient is able to resume a level of self-care

activity

Rehabilitation Phase
Pathophysiologic Changes
Burn

wound heals either by primary intention or by grafting. Layers of epithelialization begin to rebuild the tissue structure. Collagen fibers add strength to weakened areas.

Rehabilitation Phase
Pathophysiologic Changes
In

approximately 4 to 6 weeks, the area becomes raised and hyperemic. Mature healing is reached in 6 months to 2 years. Skin never completely regains its original color.

Rehabilitation Phase
Pathophysiologic Changes
Discoloration

of scar fades with time. Pressure can help keep scar flat. Newly healed areas can be hypersensitive or hyposensitive to cold, heat, and touch. Healed areas must be protected from direct sunlight for 1 year.

Rehabilitation Phase Complications

Skin and joint contractures

Most common complications during rehab

phase Positioning, splinting, and exercise should be used to minimize contracture.

Rehabilitation Phase
Nursing and Collaborative Management
Both

patient and family actively learn how to care for healing wounds. An emollient water-based cream should be used. Cosmetic surgery is often needed following major burns.

Rehabilitation Phase
Nursing and Collaborative Management
Role

of exercise cannot by overemphasized. Constant encouragement and reassurance Address spiritual and cultural needs.

Gerontologic Considerations

Normal aging puts the patient at risk for injury because of:

Unsteady gait Failing eyesight Diminished hearing The fact that wounds take longer to heal

Emotional Needs of the Patient and Family

A common emotional response is regression. Early psychiatric intervention Assess psychoemotional cues. Issue of sexuality must be met with honesty. Family and patient support groups

Special Needs of the Nursing Staff

You may find it difficult to cope with burn injuries. Know you provide care that makes a critical difference. Practice good self-care.

Frostbite

Localized Hypothermia Injuries Freezing injuries: Frostbite Frostnip Non-freezing injuries: Trench foot Chilbain (Pernio)

Definition
Local freezing of tissues with ice formation mostly in the extra-cellular space Cellular dehydration and tissue destruction by ice crystals Vascular thrombosis Alternation of vasoconstriction and vasodilatation

Pathophysiology
Peripheral vasoconstriction specific to humans (20mL/min-8000mL/min) Nose, ears, hands and feet are the most vulnerable 2nd to numerous AV anastomoses capable of shunting Predisposing factors include nicotine, tight garments, previous cold injury, PVD and Raynauds phenomena

Symptoms and Signs

Pain and numbness, worse with thawing Waxy white initially With thawing: hyperemia, edema, blebs, vesicles, thrombosis Late: Severe ischemia, gangrene, autonomic dysfunction Non-blanching cyanosis and no edema are poor prognostic signs

Frostbite Classification
First degree: central pallor and anesthesia with surrounding edema Second degree: blisters (serous or milky) surrounded by edema and erythema Third degree: deeper with hemorrhagic blisters progressing to black eschar Fourth degree: necrosis down to muscles and bones

Second Degree Frostbite

Third Degree Frostbite

Treatment
Initial: rewarming in warm water (100104 degrees), prevent further injury by air drying Elevation Daily dressing like burns Non weight bearing, early AROM Tetanus vaccination update No need for antibiotics Narcotics/NSAIDS

Treatment
Trental and heparinization for cases of thrombosis Catheter directed TPA within 4-6 hours to achieve thrombolysis within 24 hours Local care by deflating blisters gentle cleaning with soap/ water or whirlpool if available, pad between toes, antibiotic ointment non-stick dressing, elevate, pad pressure points

Surgical Debridement
Tissue damage is chronic and insidious May take up to 4 weeks to demarcate non-viable tissue Earlier debridement if life threatening necrosis/infection Fasciotomy for compartment syndrome Debride clearly necrotic, non-functional tissue