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S.Y. 2016-2017

This written report on

RESPIRATORY THERAPY S.Y. 2016-2017 This written report on MEDICAL BACKGROUND: BURNS Is submitted to the COLLEGE


Is submitted to the


In partial fulfillment to the requirements on the subject



Mr. Bernardo Tayaban Jr., PTRP, MDA

Maverick Kaypee A. Colet, PTRP



Novemeber 14, 2016



ST segment changes) secondary to alterations in electrical conductivity of the heart, myocardial contusion or infarction, or heart wall or papillary muscle rupture.

Types of Burns


Thermal Burns

As a result of the high risk of fatal arrhythmias in

Thermal burns are the result of conduction or convection, as in contact with a hot object, liquid, chemical, flame, or steam. In order of frequency, the common types of thermal burns are scalds, flame burns, flash burns, and contact burns

Electrical Burns

An electrical burn is caused by exposure to a low- or highvoltage current and results in varied degrees of visible cutaneous tissue destruction at the contact points, as well as less visible but massive damage of subcutaneous tissue, muscle, nerve, and bone. Tissue necrosis of these deeper structures occurs from the high heat intensity of the current and the electrical disruption of cell membranes. Tissue damage occurs along the path of the current, with smaller distal areas of the body damaged most severely. This pattern of tissue damage accounts for the high incidence of amputation associated with electrical injury. The severity of an electrical burn depends primarily on the duration of contact with the source, the voltage of the source, the type and pathway current, and the amperage and resistance through the body tissues.

Electrical burns are characterized by deep entrance and exit wounds and arc wounds. The entrance wound is usually an obvious necrotic and depressed area, whereas the exit wound varies in presentation. The exit wound can be a single wound or multiple wounds located where the patient was grounded during injury. An arc wound is caused by the passage of current directly between joints in close opposition. For example, if the elbow is fully flexed and an electrical current passes through the arm, burns may be located at the volar aspect of the wrist, antecubital space, and axilla. Complications specific to electrical injury include:

• Cardiovascular: Cardiac arrest (ventricular fibrillation for electric current or systole for lightning), arrhythmia (usually sinus tachycardia or nonspecific

this population, the American Burn Association (ABA) recommends an electrocardiogram (ECG) be performed on all patients who sustain electrical injuries, and those with a documented loss of consciousness or presence of arrhythmia following injury should be admitted for telemetry monitoring.18 • Neurologic: Headache, seizure, brief

loss of consciousness or coma, peripheral nerve injury (resulting from ischemia), spinal cord paralysis (from demyelination), herniated nucleus pulposus, or decreased attention and concentration.

• Orthopedic: Dislocations or fractures secondary to

sustained muscular contraction or from a fall during the electrical injury.

• Other: Visceral perforation or necrosis, cataracts, tympanic membrane rupture, anxiety, depression, or posttraumatic stress disorder.


Lightning, considered a form of very high electrical current, causes injury via four mechanisms:

1. Direct strike, in which the person is the grounding


2. Flash discharge, in which an object deviates the

course of the lightning current before striking the


3. Ground current, in which lightning strikes the ground and a person within the grounding area creates a pathway for the current

4. Shock wave, in which lightning travels outside the

person and static electricity vaporizes moisture in the skin

Chemical Burns

Chemical burns can be the result of reduction, oxidation, corrosion, or desecration of body tissue with or without an associated thermal injury.The severity of the burn depends on the type and concentration of the chemical, duration of contact, and mechanism of action. Unlike thermal burns, chemical burns significantly alter systemic tissue pH and metabolism. These changes can cause serious pulmonary complications (e.g., airway obstruction from bronchospasm, edema, or epithelial sloughing)

and metabolic complications (e.g., liver necrosis or renal dysfunction from prolonged chemical exposure). Ultraviolet and Ionizing Radiation Burns

A nonblistering sunburn is a first-degree burn from

the overexposure of the skin to UV radiation. More severe burns can also occur due to UV exposure and would . Ionizing radiation burns with or without thermal injury occur when electromagnetic or particulate radiation energy is transferred to body tissues, resulting in the formation of chemical free radicals.2Ionizing radiation burns usually occur in

laboratory or industrial settings, but can also be seen

in the medical setting following radiation treatment,

most often for cancer. The severity of the ionizing radiation burn depends on the dose, the dose rate, and the tissue sensitivity of exposed cells. Often referred to as acute radiation syndrome, complications of ionizing radiation burns include • Gastrointestinal: Cramps, nausea, vomiting, diarrhea, and bowel ischemia • Hematologic: Pancytopenia (decreased number of red blood cells, white blood cells, and platelets), granulocytopenia (decreased number of granular leukocytes), thrombocytopenia (decreased number of platelets), and hemorrhage • Vascular: Endothelium destruction

classification of burn

Epidermal Burn

An epidermal burn, as the name implies, causes cell damage only to the epidermis (Fig. 24.2). This depth of burns correlates to practice pattern 7B, Impaired Integumentary Integrity Associated with Superficial Skin Involvement, in the Guide to Physical Therapist Practice. The classic “sunburn” is the best example of an epidermal burn. Clinically, the skin appears red or erythematous.The erythema is a result of epidermal damage and dermal irritation, but there is no injury to the dermal tissue. There is diffusion of inflammatory mediators from sites of epidermal damage and

there is no injury to the dermal tissue. There is diffusion of inflammatory mediators from sites
there is no injury to the dermal tissue. There is diffusion of inflammatory mediators from sites

release of vasoactive substances from mast cells. The surface of an epidermal burn is dry. Blisters will be absent, but slight edema may be apparent. After an epidermal burn, there is usually a delay in the development of pain, at which point the area becomes tender to the touch. Following epidermal damage, the injured epidermal layers will peel off or desquamate in 3 to 4 days. Epidermal healing is spontaneous; that is, the skin will heal by itself, and no scar tissue will form.

Superficial Partial-Thickness Burn

blanch, which means if pressure is exerted against the tissue with a finger, a white spot appears as a result of displacement of blood in the capillaries under pressure. On release of pressure, the white area will demonstrate brisk capillary refill. Edema can be moderate. This type of burn is extremely painful secondary to irritation of the nerve endings contained in the dermis. When the wound is open, the patient will be highly sensitive to temperature changes, exposure to air, and light touch. In addition to pain, fever may be present if areas become infected. Some topical antimicrobial creams will cause the wound to develop a gelatin-like film that eventually will peel off, similar to the desquamation that occurs with sunburn. This exudate is a coagulum of the topical antibiotic used to prevent infection and serum that seeps from the wound as a result of the insult to capillary integrity. Superficial partial-thickness burns heal without surgical intervention, by means of epithelial cell production and migration from the wound’s periphery and surviving skin appendages. Coverage by new epithelium resumes the barrier function of the skin, and complete healing should occur in 7 to 10 days. There may be some residual skin color change owing to destruction of melanocytes, but scarring is minimal.

to destruction of melanocytes, but scarring is minimal. With a superficial partial-thickness burn (Fig 24.3) damage

With a superficial partial-thickness burn (Fig 24.3) damage occurs through the epidermis and into the papillary layer of the dermis. The epidermal layer is destroyed completely, but the papillary dermal layer sustains only mild to moderate damage. This depth of burn corresponds to practice pattern 7C, Impaired Integumentary Integrity Associated with Partial- Thickness Skin Involvement and Scar Formation, in the Guide to Physical Therapist Practice. The most common sign of a superficial partial-thickness burn is the presence of intact blisters over the area that has been injured. Although the internal environment of a blister is considered sterile, it has been shown that blister fluid contains substances that increase the inflammatory response and retard the healing process, and it is recommended that blisters be evacuated. Healing will occur more rapidly if the damaged skin is removed and an appropriate topical agent and wound dressing applied. Once blisters have been removed, the surface appearance of the burn area will be moist. The wound will be bright red because the dermis is inflamed. The wound will

be bright red because the dermis is inflamed. The wound will Deep Partial-Thickness Burn A deep

Deep Partial-Thickness Burn

A deep partial-thickness burn (Fig. 24.4) involves destruction of the epidermis and papillary dermis with damage down into the reticular dermal layer. As this burn nears the deepest dermis it begins to resemble a full-thickness burn, and the depth best

matches practice pattern 7C, Impaired Integumentary Integrity Associated with Partial-Thickness Skin Involvement and Scar Formation, in the Guide to Physical Therapist Practice.21 Most of the nerve endings, hair follicles, and sweat ducts will be injured because most of the dermis is destroyed. Deep partial-thickness burns appear as a mixed red or waxy white color. The deeper the injury, the more white it will appear. Capillary refill will be sluggish after the application of pressure on the wound. The surface usually is wet from broken blisters and alteration of the dermal vascular network, which leaks plasma fluid. Marked edema is a hallmark sign of this burn depth. There is a large amount of evaporative water loss (15 to 20 times normal) because of tissue and vascular destruction. An area of deep partial-thickness burn has diminished sensation to light touch or sharp/dull discrimination but retains the sense of deep pressure due to the location of the Pacinian corpuscle deep in the reticular dermis. Healing occurs through scar formation and re-epithelialization. By definition, the dermis is only partially destroyed; therefore, some viable epidermal cells may remain within the surviving epidermal appendages and serve as a source for new skin growth. The depth of a deep partial-thickness injury is sometimes difficult to determine, so allowing the wound to demarcate (between normal and damaged tissue) during the first few days is necessary. Demarcation becomes evident after several days as the dead tissue begins to slough. Hair follicles that penetrate into the deeper dermal regions below the burn level remain viable. Preservation of hair follicles and new hair growth will indicate a deep partialthickness burn rather than a full-thickness injury, and there is a corresponding greater potential for spontaneous healing. Particularly important factors that determine which epidermal structures survive and which die include the thickness of the skin in a particular location and/or the distance of the area from the source of heat. Deep partial-thickness burns that are allowed to heal spontaneously will have a thin epithelium and may lack the usual number of sebaceous glands to keep the skin lubricated. New tissue usually appears dry and scaly, is itchy, and is easily abraded. Creams are necessary to artificially lubricate the new surface. Sensation and the number of active sweat ducts will be diminished. A deep partial-thickness burn generally will heal in 3 to 5 weeks if it does not become infected. It is critical to keep the wound free of infection, because

infection can convert a deep partial-thickness burn into a deeper injury. The development of hypertrophic and keloid scars is a frequent consequence of a deep partial-thickness burn.

Full-Thickness Burn

In a full-thickness burn (Fig. 24.5) all of the

epidermal and dermal layers are destroyed completely. In addition, the subcutaneous fat layer may be damaged to some extent. This burn depth is

fat layer may be damaged to some extent. This burn depth is consistent with practice pattern

consistent with practice pattern 7D, Impaired Integumentary Integrity Associated with Full-

Thickness Skin Involvement and Scar Formation, in the Guide to Physical Therapist Practice.

A full-thickness burn is characterized by a

hard, parchment-like eschar covering the area. Eschar is devitalized tissue consisting of desiccated coagulum of plasma and necrotic cells. Eschar feels dry, leathery, and rigid. The color of eschar can vary from black to deep red to white; the latter indicates total ischemia of the area. Frequently, thrombosis of superficial blood vessels is apparent and no blanching of the tissue is observed. The deep red color of the tissue results from hemoglobin fixation liberated from

destroyed red blood cells. Hair follicles are completely destroyed, so body hairs pull out easily. All nerve endings in the dermal tissue are destroyed so the wound will be insensate (without feeling); however, a patient still may experience a significant amount of pain because adjacent areas of partial-thickness burn usually surround a full-thickness injury.

A major problem that arises from deep burns is the damage to the peripheral vascular system. Because large amounts of fluid leak into the interstitial space beneath unyielding eschar, the pressure in the extravascular space increases, potentially constricting the deep circulation to the point of occlusion (see later discussion of cardiovascular complications in the section titled Complications of Burn Injury). Because eschar does not have the elastic quality of normal skin, edema that forms in an area of a circumferential burn can cause compression of the underlying vasculature. If this compression is not relieved, it may lead to eventual occlusion with possible necrosis of tissue distal to the site of injury. To maintain vascular flow, an escharotomy may be necessary. An escharotomy is a midline lateral incision of the eschar the length of an

is a midline lateral incision of the eschar the length of an extremity or chest wall.

extremity or chest wall. Figure 24.6 shows an escharotomy and the result of pressure that forces the incision to gape. Following an escharotomy, pulses are frequently examined to monitor restoration of circulation. If the escharotomy is successful, there will be an immediate improvement in the peripheral blood flow, demonstrated by normal pulses distal to the wound and by return of normal temperature and capillary refill of the distal extremity. Although at times it may be difficult to differentiate a deep-partial from a full-thickness burn in the early postburn period, the differences will become evident after several days. With a full- thickness burn, there are no sites available for re- epithelialization of the wound. All epithelial cells have been destroyed, and skin grafting will be necessary. Grafting is discussed in detail in the section titled Surgical Management of the Burn Wound.

Subdermal Burn

titled Surgical Management of the Burn Wound. Subdermal Burn An additional category of burn, the subdermal

An additional category of burn, the subdermal burn, involves complete destruction of all tissue from the epidermis down to and through the subcutaneous tissue (Fig. 24.7). This depth of injury correlates with practice pattern 7E, Impaired Integumentary Integrity Associated with Skin Involvement Extending into Fascia, Muscle, or Bone and Scar Formation, in the Guide to Physical Therapist Practice.21 Muscle and bone are subject to necrosis when burned. This type of burn occurs with prolonged contact with a heat source and routinely occurs as a result of contact with electricity. Extensive surgical and therapeutic management is necessary to return a patient to some degreeof function.

Allograft (or homograft): skin used for temporary coverage of a burn wound;the skin is taken from the same species(usually cadaver skin). Autograft: skin taken from an unburned area of a patoent, which is then transplanted to cover a wound Blanch: a white spot seen in the skin when pressure is applied. This is an indication of the presence of viable capillary beds; and the blanched area will become pink when pressure is released if capillary bed is perfused. Closed technique: the wound care technique of covering a wound from the outside environment with an appropriate dressing. Contact inhibition: inhibition of the migration of epithelial cells when they are in contact with other epithelial cells on all sides. Debribement: the removal of escar and or any loose tissues from burn wound. Sharp debridement: use of sterile scissors and forceps to remove eschar. Dermal healing: the process whereby the dermis is repaired via scar formation.

Dermatome: device used to harvest then slices of skin for skin grafting. Dermis: deep layer of skin that contais bloodvessels, lymphatics, nerve endings, collagen, and elastin, and that encloses the sweat glands, sebaceous glands, and hair folicles. Desquamation: peeling of the outer layers of the epidermis. Donor site: site from which a skin graft is taken. Electrical burn: injury sustained from the passage of electric current through the tissues of the body. Epidermis: the outer most layer of the skin, which provides the body with a barrier to the environment. Epithelial healing: the process of regeneration of the epidermis through epithelial cell migration, proliferation, and differentiation. Epithelial islands: surviving tissue from which new epithelial cell growth will originate. Eschar: the dead, necrotic tissue from a burn wound. Eschartomy: midlateral incision of the burned eschar used to relived pressure in an extremity or on the trunk. Fibroblast: a connective tissue cell that forms the fibrous tissues in the body. Full thickness burn: burn involving the entire dermis. Full thickness skin graft: graft containig epidermis and full dermal thickness. Heterotopic oddification: abnormal bone growth in soft tissues. Hypertrophy: increase in size or bulk. Inhalation injury: injury sustained by the lungs due to breathing hot and or toxic gases. Usually occurs when individual is burned in a closed space. Keloid scrar: raised scar that extends beyond the boundaries of the original burn wound. Mesh graft: proces whereby the donor skin is placed through a device that increases the surface area of the graft. Open technique: absence of dressings: often used after skin grafting to the face Partial thicness burn: burns involving the epidermis and parrt of the dermis. Subcategories are superficial partial thickness and deep partial thickness burns, depending on the amount of dermis involved. Primary excision: surgical removal of eschar. Rule of nines: estimation used to dtermis the amount of total body surface area that has been burned. It divides the body into segments that are approximately 9 percent of the total. Sheet graft: autograft that is aplied in a single sheet without alteration. May be split-thickness or full thciness in depth.

Skin substitutes; tissues engineeres in a laboratory which are used to restore the essential funtions of the skin, provide a barrier to the environment, and control evaporative water loss. Split-thickness sin graft: graft containing epidermis and only the superficial layers of the dermis. Subdermal burn: burn involving only the epidermial layer. Wound contraction: movement of the wound margins toward the center of the defect. Thought to be caused by the active movement of the fibroblat in the wound bed. Xenograft or heterograft: skin used as a temporary wound cover; which is harvested from another species of animal, usually a pic. z-plasty: procedure used to surgically lengthen a burn scar contracture to allow for greater ROM. Zone of coagulation: cells are irreversible damage. And skin death occurs. Zone of hyperemia: site of minimal cell damage. Tissue should recover within several days. Zone of stasis: site of injured cells that may die without specialized treatment


•approximately 90% of all burn deaths worldwide occurring in low- and middle-income countries.

•Intentional burn injuries, rare in the United States but seen most commonly in young men, are more common in young women in India and middle-aged men in Europe.

Unintentional burn injuries are also more common

in girls than boys, in low- to middle-income countries. Changing burn mortality in the future may be focused on improved treatments for inhalation injury and preventing burns in the elderly and in low- to middle-income countries.

•braddom •It is estimated that 1.25 million people experience burn injuries each year. Of those, approximately 500,000 receive some form of medical treatment and 40,000 are hospitalized. •Burns predominantly affect young men (mode age:

20 to 40; male: 70%). •Two thirds of burn injuries affect adults and onethird affect children. •Most burns occur by fire/flame (43%) or scald injuries (36%) •Other etiologies that comprise the minority of burns include electrical, contact, chemical, tar, radiation, and grease injuries as well as skin diseases. • Approximately one third of burn injuries are associated with concomitant alcohol or drug use. A large majority of burn survivors have less than or equal to a high-school education (82%).

• Most injuries (65%) are result of an accident that is not work related. •A minority of burn injuries (17%) occur at work. •Approximately 5% of burn injuries are the result of child abuse or adult assault or abuse. •Among children less than 2 years old, burn injuries represent the most common cause of accidental death; most of these deaths are a result of abuse. •Overall, the survival rate is approximately 95%.

• The risk of death is increased for those at the

extremes of age, with inhalation injury and with larger burns



Functions of the Integumentary System

Protection against injury and infection

Regulates body temperature

Sensory perception

Regulates water loss

Chemical synthesis

Protection covers and protects the entire body against injury and infection

Physical barriers - continuity of the skin and hardness of keratinzed cells

• Due to the skin’s physical characteristics such as the keratinized cells and waterproofing properties of the glycolipids.

Keratin helps waterproof the skin and protects from abrasions and bacteria

Glycolipids prevent diffusion of water and water-

soluble substances between cells

Continuity prevents bacterial invasion

Substances that are able to penetrate the skin:

• Substances that are able to penetrate the skin: Lipid-soluble substances (i.e., oxygen, carbon dioxide,

Lipid-soluble substances (i.e., oxygen, carbon dioxide, steroids, and fat-soluble vitamins) Oleoresins of certain plants (ex. poison ivy and poison oak) Organic solvents (ex. acetone, dry cleaning fluid, and paint thinner)

(ex. acetone, dry cleaning fluid, and paint thinner) Salts of heavy metals (ex. lead, mercury, and
(ex. acetone, dry cleaning fluid, and paint thinner) Salts of heavy metals (ex. lead, mercury, and
(ex. acetone, dry cleaning fluid, and paint thinner) Salts of heavy metals (ex. lead, mercury, and

Salts of heavy metals (ex. lead, mercury, and nickel) Topical medications as motion sickness patch

Penetration enhancers Chemical barriers - (skin secretion and melanin) Skin secretions such as sebum, human defensins (antimicrobial peptides), acid mantle of the skin retards bacteria growth and/or kills them

Melanin provides protection from UV damage

Skin secretions (acid mantle)

Low pH and sebum slow bacterial growth on skin surface

Human defensin natural antibiotic

Cathelicidins proteins that prevent Strep A infection in wounded skin

Melanin chemical pigment that prevents UV

damage Biological Barriers

• Langerhans’ cells, macrophages, and DNA

• Langerhans’ cells in epidermis present antigens to lymphocytes

Dermal macrophages (2nd line of defense) attack bacteria and viruses that have penetrated the epidermis

• Langerhan’s cells and macrophages present in the skin helps activate the body’s immune system.

DNA structure the electrons in DNA absorb UV radiation and converts it to heat Temperature regulation

Production of copious amounts of sweat to dissipate heat

When body temperature rises and is hotter than the

external environment the blood vessels in the dermal area dilates and sweat glands are stimulated into activity.

• Evaporation of the sweat from skin’s surface helps

dissipate heat from the body.

Constriction of dermal blood vessels to retain heat

When it is cold outside, the dermal blood vessels

constrict and pull the blood away from the skin and keeps it close to the body core to protect crucial internal organs. Cutaneous Sensations

- cutaneous sensory receptors (see - nervous system)

• Meissner’s corpuscles: light touch

Merkel discs: light touch

Pascinian receptors lies in deeper

dermis/hypodermis & detect deep pressure contacts

Hair root plexus: sensations from movement of hairs

Hair follicle receptors movement across the surface of the skin

Bare nerve endings: painful stimuli (chemicals, heat, cold) Excretion/Absorption

Elimination of nitrogen-containing wastes

(ammonia, urea, uric acid), sodium chloride, and water. It regulates water loss

Metabolic Functions Synthesis of Vitamin D increases calcium absorption in the body

Vitamin D is a fat-soluble vitamin that may be

absorbed from the intestines or may be produced by the skin when the skin is exposed to ultraviolet light (particularly sunlight).It is converted to its active form by the body in 2 steps, occurring first in the liver and completed in the kidneys. In its active form, vitamin D acts as a hormone to regulate calcium absorption from the intestine and to regulate levels of calcium and phosphate in the bones. Vitamin D deficiency causes Rickets

When the body is deficient in vitamin D, it is unable

to properly regulate calcium and phosphate levels. If the blood levels of these minerals becomes

low, the other body hormones may stimulate release of calcium and phosphate from the bones to the bloodstream.

Chemical conversion of many substances

Blood Reservoir preferential shunting of blood as needed

Types of Membranes - thin sheet-like structures that protect parts of the body Serous Membranes

• Line body cavities that have no opening to the


• Secrete a watery fluid called serous fluid that lubricates surfaces.

Mucous Membranes

• Line cavities and tubes that open to the outside Synovial Membranes

• Form the inner lining of joint cavities

• Secrete a thick fluid called synovial fluid

Cutaneous Membrane also known as skin Characteristics of Skin The integument covers the entire body and is the largest organ ~ 2 meters and heaviest organ 16% of body mass of the body. Composed of the epidermis and dermis Pliable, yet durable Thickness: 1.5 to 6.0 mm Types of Skin Thin - 1-2 mm on most of the body and 0.5 mm in eyelids •Hairy •Covers all parts of the body except palms of hands and soles of feet •Thin epidermis and lacks stratum lucidum •Lacks dermal papillae •Has more sebaceous glands •Fewer sweat glands, sensory receptors than thick skin Thick - up to 6 mm thick on palms of hands and soles of feet •Hairless •Covers palms of hands and soles of feet •Thick epidermis and a distinct stratum lucidum •Epidermal ridges are present due to well developed, numerous dermal papillae. •Lacks sebaceous glands, has more sweat glands •Sense receptors are also more densely packed. Layers of the Skin


Types of Cells Keratinocytes 90 % of epidermal cells are keratinized contains keratin (fibrous protein) •protects and waterproofs the skin Melanocytes 8% of the epidermal cells produces melanin contributes to skin color and absorbs UV light Langerhans cells Arise from red bone marrow and migrate to the epidermis •Constitute small portion of epidermal cells •Participate in immune responses •Easily damaged by UV light Merkel cells Least numerous of the epidermal cells •Found in the deepest layer of the epidermis •Along with tactile discs, they function in sensation of touch Layers of epidermis

Stratum corneum 25-30 layers of dead flat keratinocytes Shed continuously and replaced by cells from the deeper strata Serves as a water, microbe, injury barrier

Stratum lucidum Present only in thick skin 3-5 layers of clear, flat, dead keratinocytes Dense packed intermediate filaments Thick plasma membranes

Stratum granulosum Located above the stratum spinsosum 3-5 layers of flattened keratinocytes undergoing apoptosis Organelles begin to disintegrate becomes nonliving cells Marks the transition between deeper metabolically active strata and the dead cells of the superficial strata. Contains lamellar granules Secretes lipid-rich secretion that acts as a water sealant

Stratum spinosum Located above the stratum basale 8-10 layers of keratinocytes Some cells retain their ability for cell division Cells have spinelike projections (bundles of

filaments of the cytoskeleton) tightly joins cells to each other. Provides skin both strength and flexibility

Infants and elderly have less of this than adults and are therefore more sensitive to cold

Stratum basale Also referred to as stratum germinatum because this is where new cells are formed Deepest layer of the epidermis

Skin Appearances Epidermis appears translucent when there is little melanin or carotene White skin appears pink to red depending on amount and oxygen content of blood moving

Single row of cuboidal or columnar keratinocytes


the capillaries of the dermis.

Growth of epidermis Newly formed cells in the stratum basale undergo keratinazation as they are pushed to the surface. They accumulate more keratin during the process Then they undergo apoptosis

Albinism is an inherited trait where a person can’t produce melanin. The have melanocytes but are unable to make tyrsinase (the enzyme which initiates melanin production) so. melanin is missing in their hair, eyes, and skin.

Eventually they slough off and are replaced

Skin color as diagnostic clues for medical conditions

The process takes about 4 weeks


Cyanotic (cyan = blue) Ex: someone who has

Rate of cell division in the stratum basale increases

stopped breathing and the skin appears bluish

during injury


because the hemoglobin is depleted of oxyen

Dermis Second deepest part of the skin

Jaundice (jaund = yellow) - Buildup of bilirubin (yellow pigment) in the blood gives a yellowish


Blood vessels, nerves, glands and hair follicles are embedded here

appearance of eyes and skin indicating liver disease Bilirubin is produced when red blood cells

Composed mainly of connective tissues (collagen


old and are broken down by the body. Normally it

and elastic fibers)


processed in the liver and then deposited

Collagen fibers make up 70% of the dermis and give


the intestine so it can come out in the stool.

structural toughness and strength. Elastin fibers are


Erythema (ery = red) - Engorgement of capillaries in

loosely arranged in all directions and give elasticity to


dermis indicating skin injury,

the skin

infection, heat exposure, inflammation, allergies,

Has two layers Papillary Layer and Epidermal layer.

emotional state, hypertension

Papillary layer

Pallor - paleness, emotional state, anemia, low blood pressure


Superficial portion of the dermis


Bronzing - Addison’s disease, adrenal cortex

Consist of areolar connective tissue containing


Bruising (hematoma)- escaped blood has

elastic fiber

clottedhematomas , deficiency in Vitamin C or

Surface area is increased due to projections called


dermal papillae


leathery skin - overexposure clumping of elastin

which contains capillaries or tactile receptors

fibers depressed immune system

Epidermal ridges conforms to the dermal papillae


can alter DNA to cause skin cancer


photosensitivity - to antibiotics & antihistamines

Reticular layer Deeper portion of the dermis Consist of dense irregular connective tissue containing collagen/elastic fibers Provides skin with strength and elasticity Contains hair follicles, nerves, sebaceous and sudoriferous glands

Hypodermis (subcutaneous) Attaches the skin to underlying organs and tissues Not part of the skin - lies below the dermis Contains connective tissue and adipose tissues (subcutaneous fat) for insulation

Skin Color genetic factors, environmental factors and volume

of blood

Skin Pigments - three pigments are responsible for

skin color- melanin, carotene, hemoglobin

Melanin Located mostly in epidermis

Number of melanocytes are about the same in all


Difference in skin color is due to the amount of pigment that melanocytes produce and disperse to keratinocytes. Freckles are caused by the accumulation of melanin

in patches

Liver spots are also caused by the accumulation of melanin Melanocytes synthesize melanin from an amino acid called tyrosine along with an enzyme called tyrosinase. All this occurs in the melanosome which is an organelle in the melanocyte. Two types of melanin: eumelanin which is brownish black and pheomelanin which is reddish yellow Fair-skinned people have more pheomelanin and dark skinned people have more eumelanin

Environmental Factors UV light increases enzymatic activity in the melanosomes and leads to increased melanin production. A tan is achieved because the amount of melanin has increased as well as the darkness of the melanin. (Eumelanin provides protection from UV exposure while pheomelanin tends to break down with too much UV exposure) The melanin provides protection from the UV radiation but prolonged exposure may cause skin cancer. Carotene (carot = carrot) yellow-orange pigment precursor for Vitamin A which is used to make pigments needed for vision found in stratum corneum and fatty areas of dermis and hypodermis layer Hemoglobin Oxygen-carrying pigment in red blood cells Skin Markings - skin is marked by many lines, creases and ridges friction ridges: markings on fingertips characteristic of primates allow us to manipulate objects more easily - fingerprints are friction ridge skin impressions flexion lines: on flexor surfaces of digits, palms, wrists, elbows etc skin is tightly bound to deep fascia at these points freckles: flat melanized patches vary with heredity or exposure to sun moles: elevated patch of melanized skin, of the with hair mostly harmless, beauty marks

Derivatives of skin - during embryonic development thousands of small groups of epidermal cells from stratum basale push down into dermis to form hair follicles and glands Skin receptors:

Your skin and deeper tissues contain millions of sensory receptors.

Most of your touch receptors sit close to your skin's surface. Light touch Meissner's corpuscles are enclosed in

a capsule of connective tissue

They react to light touch and are located in the skin of your palms, soles, lips, eyelids, external genitals and nipples These areas of your body are particularly sensitive Heavy pressure Paccinian corpuscules sense pressure and vibration changes deep in your skin. Every square centimeter of your skin contains around 14 pressure receptors Pain skin receptors register pain pain receptors are the most numerous each square centimeter of your skin contains around 200 pain receptors Temperature Skin receptors register warmth and cold Each square centimeter of your skin contains 6 receptors for cold and 1 receptor for warmth Cold receptors start to perceive cold sensations when the surface of the skin drops below 95 º F. They are most stimulated when the surface of the skin is at 77 º F and are no longer stimulated when the surface of the skin drops below 41 º F. This is why your feet or hands start to go numb when they are submerged in icy water for a long period of time.

Hot receptors start to perceive hot sensations when the surface of the skin rises above 86 º F and are most stimulated at 113 º F. Beyond 113 º F, pain receptors take over to avoid damage being done to the skin and underlying tissues. Thermoreceptors are found all over the body, but cold receptors are found in greater density than heat receptors most of the time our environment is colder than our body temperature The highest concentration of thermoreceptors can be found in the face and ears so your nose and ears

always get colder faster than the rest of your body on

a chilly winter day

Skin Glands Sudoriferous - sweat glands (sudori = sweat) (ferous

= bearing)

3- 4 million glands in your body empties onto the skin thru pores or into hair follicles Two main types of sweat glands Eccrine sweat glands

An in depth knowledge of pathophysiology of burns, and their effects both locally and systemically is necessary to ensure effective management of a patient with a burn injury.


Secretes cooling sweat


Secretes directly onto the skin

Zones of Injury and Wound Conversion


Began to function soon after birth

The local effect involves three burn zones:


Sweat is composed of 98 percent water and two

(Hettiaratchy and Dziewulski 2004)

percent dissolved salts and nitrogenous wastes, such as urea and uric acid

o Helps regulate body temperature/aids in waste


Appocrine sweat glands

Zone of Coagulation:

the point of maximum damage

Irreversible tissue loss due to coagulation of constituent proteins.


Stimulated during emotional stress/excitement


Secretes into hair folicle

Zone of Stasis:


Begins to function at puberty

Characterised by decreased tissue perfusion


Slightly more viscous than eccrine secretions

Potential to rescue the tissue in this zone


Composed of the same components as eccrine

Problems such as prolonged hypotension, infection


or oedema can convert this area into one of complete


tissue loss


lipids and proteins.


Referred to as “cold sweat”.

Zone of Hyperaemia:

Sebaceous - oil glands (sebace = grease) They are mostly connected to hair follicles. Sebaceous glands are embedded in the dermis over most of the body. Absent in the palms and soles. Vary in size, shape and numbers in other areas of the

body. Secrete an oily substance called sebum. which lubricates the hair and skin

Mixture of fats, cholesterol, proteins, inorganic salts, pheromones. Coats surface of hair Prevents excessive evaporation of water from skin Keeps skin soft and pliable Inhibits growth of some bacteria. Sebaceous gland activity increases with puberty, due

to the male and female hormone activity

Accumulation of sebum in the ducts = white pimples if the sebum darkens -black heads form

Acne - inflammation of sebaceous gland ducts

Ceruminous - modified sweat glands of the external ear that produce ear wax (cer = wax) Open directly onto the surface of the external auditory canal (ear canal) or into ducts of sebaceous glands. Earwax is the combination of secretion of ceruminous and sebaceous glands. Earwax and the hair combine to provide a sticky barrier against foreign items. Physiology of Burns

The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion.

The depth of the wound develops over time: The burn process peaks at approximately three days. Progression is 3D- zone of coagulation both increases in depth and width (Ever et al 2010).

at approximately three days. Progression is 3D- zone of coagulation both increases in depth and width

or car fires is exacerbated by the inhalation of toxic gases from burning household furniture, leading to severe inhalation injuries as well as burns.

Contact burns from contact with molten metal or

plastic are common in industry. An unconscious patient may sustain burns from contact with a cooker or a hot radiator.

Electrical burns due to electrical current from plugs, sockets and wiring. Deep structures can be involved at the current entry and exit sites on the body. The patient’s cardiac status requires close monitoring. •Elsevier


Thermal burns, the most common type, frequently result from:

•residential fires •automobile accidents •playing with matches •improper handling of firecrackers •scalding accidents and kitchen accidents (such as a child climbing on top of a stove or grabbing a hot iron) •parental abuse of (in children or elders) •clothes that have caught on fire.

children or elders) •clothes that have caught on fire.  Chemical burns result from contact, ingestion,

Chemical burns result from contact, ingestion, inhalation, or injection of acids, alkalis, or vesicants.

Electrical burns usually result from contact with faulty electrical wiring or high-voltage power lines. Sometimes young children chew electrical cords. •Friction or abrasion burns occur when the skin rubs harshly against a coarse surface. •Sunburn results from excessive exposure to sunlight.

• Burns can be caused by

excessive heat or cold, by chemicals, ultraviolet light or radiation.

• The most common causes of burns requiring

hospital treatment are:

Scalds from hot fluids or steam are common in the

under fives and the elderly. -Explosions, flash flame or steam, bonfires, fireworks, barbeques and the use of flammable liquids such as

petrol. Flash burns tend to be partial-thickness burns, but can be deeper if the patient’s clothes ignite.

Flame burns occur when the patient’s clothes, hair

or skin catch light. The effect of damage from house


Pathophysiology of Burns Skin and body tissue destruction occurs from the absorption of heat energy and results in tissue coagulation. This coagulation is depicted in zones (Figure 12-2). The zone of coagulation, located in the center of the burn, is the area of greatest damage and contains nonviable tissue referred to as eschar. Although eschar covers the surface and may appear to take the place of skin, it does not have any of the characteristics or functions of normal skin. Instead, eschar is constrictive, attracts microorganisms, houses toxins that may circulate throughout the body, and prevents progression through the normal phases of healing.3 The zone of stasis, which surrounds the zone of coagulation, contains marginally viable tissue which can easily be further damaged from processes such as hypoperfusion, edema, or infection. Proper wound care can minimize this conversion and preserve the integrity of the viable tissue in this zone. The zone of hyperemia, the outermost area, is the least damaged and heals rapidly unless additional tissue injury occurs.7-9 The depth of a burn can be described as superficial, moderate partial thickness, deep partial thickness, or full thickness (Figure 12-3). Each type has its own appearance, sensation, healing time, and level of pain, as described in Table 12-2. First-degree burns have no significant structural damage and therefore no zone of stasis or coagulation. Differentiation between moderate and deep second- degree burns can be made based on the presence of the zones of coagulation, stasis, and hyperemia in the deeper burns while moderate second-degree burns will only have zones of stasis and hyperemia. Third- degree burns contain a significant and easily identifiable zone of coagulation as well.

of stasis and hyperemia. Third- degree burns contain a significant and easily identifiable zone of coagulation
of stasis and hyperemia. Third- degree burns contain a significant and easily identifiable zone of coagulation


Signs and symptoms Signs and symptoms depend on the type of burn and may include:

localized pain and erythema, usually without blisters in the first 24 hours (first-degree burn) chills, headache, localized edema, and nausea and vomiting (more severe first-degree burn) thin-walled, fluid-filled blisters appearing within minutes of the injury, with mild to moderate edema and pain (second-degree superficial partial-thickness burn) white, waxy appearance to damaged area (second- degree deep partial-thickness burn) white, brown, or black leathery tissue and visible thrombosed vessels due to destruction of skin elasticity (dorsum of hand most common site of thrombosed veins), without blisters (third-degree burn) silver-colored, raised area, usually at the site of electrical contact (electrical burn) singed nasal hairs, mucosal burns, voice changes, coughing, wheezing, soot in mouth or nose, and darkened sputum (with smoke inhalation and pulmonary damage). •OkDoKeY

Potential impairment

Body area



Facial disfigurement (contractures of eyelids, nose, mouth, ears, and adjacent facial skin) Inability to close eyes Loss of facial expression Teeth malalignment Drooling and inability to close lips Lower lip eversion


Loss of normal cervical spine range of motion Limited visual fields Difficulties with anesthesia, due to decreased neck range of motion


Protraction of shoulders Kyphosis Functional scoliosis


Decreased respiratory function Breast entrapment Perineal banding


Type 1: either anterior or posterior contracture Type 2: anterior and posterior contracture with sparing of dome Type 3: anterior and posterior contracture and axillary dome

Hands Metacarpophalangeal extension deformities Wrist extension deformities Proximal interphalangeal flexion deformities Interdigital web contractures Clawing of fourth and fifth digits Thumb contractures (adduction, opposition, flexion, or extension)

Arms and legs

Antecubital banding and flexion Posterior popliteal banding and flexion Anterior hip banding and flexion Medial and lateral malleolar scarring

Foot and ankle

Hyperextension metatarsophalangeal joints Equinovarus Cavus foot Rocker bottom deformity


Systemic Complications of Burn Injury

Body System



Inhalation injury, restrictive pulmonary pattern (which may OCCur with a burn on the trunk), atelectasis, pneumonia, microthrombi, and adult respiratory distress syndrome


Hypovolemiaihypotension, pulmonary hypertension, subendocardial ischemia, anemia, and disseminated intravascular coagulopathy


Stress ulceration, hemorrhage, ileus, ischemic co\iris, cholesrasis, liver failure, and urinary rract infection



Edema, hemorrhage, acute tubular necrosis, acure renal failure



Electrical burns Complications specific to electrical injury include the following"s:

Cardiovascular: Cardiac arrest (ventricular fibrillation for electric current or asystolic for lightning), arrhythmia (usually sinus tachycardia or nonspecific ST changes) secondary to alterations in electrical conductivity of the heart, myocardial contusion or infarction, or heart wall or papillary muscle rupture Neurologic: Headache, seizure, brief loss of consciousness or coma, peripheral nerve injury (resulting from ischemia), spinal cord paralysis (from demyelination), herniated nucleus pulposus, or decreased attention and concentration

Orthopedic: Dislocations or fractures secondary to

sustained muscular contraction or from a fall during the burn injury

Other: Visceral perforation or necrosis, cataracts, tympanic

burn shock (due to fluid shifts out of the vascular compartments, possibly leading to kidney damage and renal failure) peptic ulcer disease (due to decreased blood supply in the abdominal area) disseminated intravascular coagulation (more severe burn states)

membrane rupture, anxiety, depression, or post- traumatic stress disorder

Chemical Burns

pulmonary complications (e. g. , airway obstruction from bronchospasm, edema, or epithelial sloughing) and metabolic complications (e. g., liver necrosis or renal dysfunction from prolonged chemical exposure).

Ultraviolet and Ionizing Radiation Burns

Gastrointestinal: Cramps, nausea, vomiting, diarrhea, and bowel ischemia

Hematologic: Pancytopenia (decreased number of

red blood cells, white blood cells, and platelets),

granulocytopenia (decreased number of granular leukocytes), thrombocytopenia (decreased number of platelets), and hemorrhage •paz

Complications Possible complications of burns include:

loss of function (burns to face, hands, feet, and genitalia) total occlusion of circulation in extremity (due to edema from circumferential burns) airway obstruction (neck burns) or restricted respiratory expansion (chest burns) pulmonary injury (from smoke inhalation or pulmonary embolism) adult respiratory distress syndrome (due to left- sided heart failure or myocardial infarction) greater damage than indicated by the surface burn (electrical and chemical burns) or internal tissue damage along the conduction pathway (electrical burns) cardiac arrhythmias (due to electrical shock) infected burn wound stroke, heart attack, or pulmonary embolism (due to formation of blood clots resulting from slower blood flow)

added pain, depression, and financial burden (due to psychological component of disfigurement).

Vascular: Endothelium destruction •OkDoKeY









Pink to red With or without edema Dry appearance without blisters Blanches Sensation intact Skin intact when rubbed





Tenderness to



tOuch or


epithelialization Skin appears intact




Pink ro mortied red or red with edema Moist appearance with blisters Blanches with slow capillary refill Sensation intact


days to 3 wks by

Very painful

thickness (second degree)-superficial dermis injured

epithelialization Pigmentation changes are likely




Pink ro pale ivory Dry appearance with blisters May blanch wirh slow capillary refill Decreased sensation ro pinprick Hair readily removed


wks to mas by

Very painful



granulation tissue formation and epithelialization Scar formation likely




injured with hair follicles and sweat




Full-thickness-entire dermis injured (third degree) or fat, muscle, and bone injured (fourth degree)

White, red, brown, or black (charred if fourth degree) Dry appearance without blanching May be blistered Insensate to pinprick Depressed wound

Not able to regenerate

No pain, perhaps an ache

Source: Data from P Wiebelhaus, SL Hansen, Burns: handle with care. RN 1999;62:52-75.

Systemic effects

Once the burn covers more than 30% of TBSA, the injury has a systemic effect due to •Molecular structural alterations

(Jeschke et al 2007; Grisbrook et al 2012a; Hurt et al


This hyper metabolic state leads to energy substrate release from protein and fat stores Protein



Release of toxic metabolites

•Loss of lean muscle mass and wasting


Release of antigen and immunomodulatory agents

Release of antigen and immunomodulatory agents

•Potentially fatal if structure and function of organs

Histamine, Serotonin, Bradykinin, Nitric oxide, etc.

are compromised (Jeschke et al 2007; Hurt et al 2000)

Causes systemic shock, cardiovascular, respiratory and renal failure, immunosuppression and hypermetabolism. (Evers et al 2010)

In adults with burns of 25% TBSA, metabolic rate

ranges from 118-210% that of predicted values. At 40% TBSA, the resting metabolic rate in a thermoneutral environment is


Cardiovascular Changes


180% at acute admission

Myocardial depression


150% at full healing


Myocardial contractility decreased


140% post 6 months

Oedema formation


120% at 9 months


Capillary permeability is increased


110% at 10 months

o leads to loss of intravascular proteins and fluids to the interstitial compartment •Hypovolemia

o Secondary to oedema and rapid fluid loss from

surface of wound

(Jeschke et al 2007; Herndon and Tomkins 2004)

Gastrointestinal Changes

•Impaired gastrointestinal motility •Impaired digestion and absorption

Peripheral and splanchnic vasoconstriction occurs

Increased intragastric pH


May cause renal failure

• Feeding difficulties exacerbate effects of hyper

These changes may lead to systemic hypotension and end organ hypoperfusion. (Evers et al, 2010)

Respiratory Changes

Inflammatory mediators cause bronchoconstriction and pulmonary oedema •severely burnt adults acute respiratory distress syndrome (ARDS) can occur •Exacerbated in the case of inhalation injury (Evers et al 2010)

Metabolic Changes

Hypermetabolism begins approximately five days post burn

o Metabolic state is initially suppressed by the effects of acute shock

o Can persist for up to two years post injury

Inflammatory, hormonal and cytokine milieu cause •Increased body temperature

• Increased oxygen and glucose consumption

•Increased CO2 and minute ventilation •Increased heart rate for up to 2 years post burn

metabolism (Evers et al 2010)

Immunological Changes

(Hettiaratchy and Dziewulski 2004)

• Immune deficiency occurs despite the activation of the immune system. High risk of infection, particularly while wounds are open.





Physiotherapy Assessment of the Burn Patient

had a reduced level of consciousness aggressive respiratory treatment to commence immediately

The physiotherapist must be aware of the importance of an early and adequate assessment of Burn patients for optimal functional and cosmetic outcomes to minimise the impact of the trauma long term. They must have a concise knowledge of the assessment procedure through from Accident and Emergency to the ward, onto the rehabilitation setting and out in the community. The following information is gathered through assessment, and a treatment plan is formulated, constantly reassessed and revised.


Papini 2004)



Physiotherapy aims

1. Prevent respiratory complications

2. Control Oedema

3. Maintain Joint ROM

4. Maintain Strength

5. Prevent Excessive Scarring

Patients are at high risk due to:


burn area - systemic inflammatory reaction syndrome involving the

lungs; depth of burn and scarring

2. Patient factors - Reduced

ambulation and mobility; increased bed rest; increased Pain; pre-existing co- morbidities 3. Iatrogenic factors Skin reconstruction surgery; invasive monitoring and

procedures, management in critical care

Injury factors - Inhalation injury;


Eisenmann-Klein 2010)






Total Body Surface Area (TBSA)

o The rule of nine or the Lund and Brower chart are used to assess the TBSA o The Lund and Brower Charts are considered to be more accurate than rule of nines,


but both are commonly used.

Database/Subjective Assessment

The following pieces of information should be included in the physiotherapists’ database.

Presenting Complaint

Inhalation injury There should be a high index of suspicion if the patient was injured in an enclosed space and / or

•Measure burn wound areas by mapping wound – 1% TBSA patient’s hand (palm and fingers included) •Note: when calculating burn size area, oedema should not be included. •A burn of > 20 – 25% TBSA creates a global or systemic inflammatory reaction affecting all body organs and indicates a significant risk for the respiratory system

Burn Type and Depth

monitor extent of tissue

destruction as it alters for at least 48 hours post

burn injury

• It




o Jacksons’ burn wound model.

•It is rare that a burn will present with a single depth.

• Likely to change depending on the early

management e.g. appropriate first aid and other

patient factors. (ANZBA 2007; British Burn Association 2005; Eisenmann-Klein 2010)

Burn Site and Impact

• Develop awareness of the implication of burn to special areas of the body. the following require specialised treatment









This is in consideration of the complexity of the post burn reconstruction and potential functional impact of inappropriate management of these important body areas.

History of Presenting Complaint

•History of the incident with specific attention paid to the mechanism of injury. •First aid – was adequate first aid given? - If not, suspect deeper burn injury •Falls – was there any indication that the patient fell? From what height? possible head injury, sprains or fractures •Electrical injury – voltage involved? Parts of body in contact with earth? suspect nerve and deep muscle injury with high voltage current •Explosions – falls, high velocity injuries, possible tympanic membrane injury loss of hearing and difficulty communicating •Passage to hospital and time to admission ANZBA 2007; British Burn Association 2005; Eisenmann-Klein 2010;

Medical and Surgical History

Any surgical or medical management


Pain medication
















ANZBA 2007; British Burn Association 2005; Hettiaratchy et al 2004

Past Medical/ Drug History

Social History


Eisenmann-Klein 2010


























stairs, reaching, lifting








endurance, balance

Social support and home Situation


Particularly important for hand burns

Psychosocial/ Yellow Flags


Coping style

Mental health

Emotional behaviour

ANZBA 2007; British Burn Association 2005; Hettiaratchy et al 2004

Considerations for the Assessment of Hand Burns

The area of the hand that is injured has a huge impact on recovery. A burn on the hand can have detrimental effects for ADLs and functioning. Dependant on the area and depth of the burn, it may lead to significant deformity.


Evaluation and classification of the size and depth of the burn of the hand

Post burn Hand Deformities

o First web adduction contractures


Web space contractures


Dorsal skin contractures


Digital flexion contracture


Boutonniere deformity


Dorsal skin deficiency


Digital loss secondary to ischemia


Median and ulnar nerve compression



skin deficiency o Digital loss secondary to ischemia o Median and ulnar nerve compression o Syndrome

o Surgical managementremoval of eschar, transplantation of skin grafts, flap

Early postoperative physical therapy

Functional rehabilitation

Secondary and tertiary corrections if necessary

Objective Assessment

Inspection and Palpation









Chest x-ray changes (ANZBA 2007; British Burn Association 2005)

Oedema Assessment

To assist with treatment planning, pertinent data

that can be gathered from the direct observation of a patient or palpation include the following:

• Level of consciousness

• Presence of agitation, pain, and stress

• Location of the burn or graft, including the

proximity of the burn to a joint

• Presence and location of dressings, splints, or

pressure garments

• Presence of lines, tubes, or other equipment

• Presence and location of edema

• Posture

• Position of head, trunk, and extremities

• Heart rate and blood pressure, respiratory rate and pattern, and oxygen saturation

Overview An acute burn injury creates inflammation and swelling. After wound healing is complete, scar tissue maturation and contraction may lead to sub- acute and chronic states of oedema formation. With time, oedema fluid changes in its composition and creates greater stiffness and resistance to movement within the tissues. This is particularly notable when surgical reconstruction is required and if the burn is circumferential around limbs or other structures. See table 4 for clinical stages of oedema.


Eisenmann-Klein 2010)






Mobility Assessment

Pain Intensity Assessment

Observational behavioural pain assessment scales should be used to

Measure pain in children aged 0 to 4 years e.g. The FLACC scale

Faces pain rating scale can be used in children

aged 5 years and older. E.g. The Wong-Baker FACES

pain rating scale

VAS can be used in children aged 12 years and older and adults.

Inhalation Assessment

Physical signs to observe:

Hoarse vocal quality

Singed facial / nasal hair


Erythema (Superficial reddening of

the skin, usually in patches, as a result of injury or irritation causing

dilatation of the blood capillaries)

Soot stained sputum

The assessment and treatment of mobility can be separated into two aspects - the limbs & trunk, and general functional mobility (e.g. transferring and ambulation). A physiotherapist must also consider factors such as increased bed rest, increased pain and pre-existing co-morbidities.

(ANZBA 2007; Hettiaratchy et al 2004; Settle 1986; Siemionow and Eisenmann-Klein 2010)

Limb and Trunk

Assessment of limbs and trunk should include joint ROM and strength. Limiting factors may include pain, muscle length, trans-articular burns, scar contracture and the individual specificity of the burn.

may include pain, muscle length, trans-articular burns, scar contracture and the individual specificity of the burn.

General Functional Mobility

Assessment of general mobility is two-fold, prevention of complications associated with prolonged bed rest and the restoration of function & independence. All functional transfers, gait, endurance and balance should be assessed once the patient is medically stable. Factors to consideration when assessing mobility:


Demands of vocational roles and ADLs

Cardiovascular response to mobilisation

Neurological status


Concomitant injuries/weight-bearing status



Pharmacological Pain Management

an analgesia.

Regular and repeated pain assessments are used to monitor the effectiveness of analgesia. Thus there is no standard treatment of burns patients, each requires individual assessment. Opioids: the cornerstone of pain management in burns, and are available in a variety of potencies, methods of administration and duration of action. Opioids used to effectively manage background pain, with well-timed and effective doses of opioids used separately to manage

During the first 48 hours

Decreased organ blood supply alters the clearance of drugs

The body then enters a hyper metabolic state, o Associated with increased clearance of analgesia. Variations in levels of acute phase plasma and total body water volume further impact upon effectiveness


Side Effects

Examples of Opioids


Pain relief

Respiratory distress







Nausea and vomiting Opioid tolerance requiring increasing doses Opioid induced hyperalgesia (OIH) increased sensitivity, throughout the body following opioid exposure Provide poor defence against central sensitisation Physical dependence common in long term use

Fentanyl: potent, rapid onset, short acting opioid. Used for procedural pain management. Remifentaril: ultra-short acting opiate. Alfentaril: short acting, used for post-procedural analgesia.






stress disorder

to reduced Post- traumatic stress disorder procedural pain Simple analgesics : paracetamol can be used

procedural pain



paracetamol can be used in conjunction with opioids, to give a


comparable to a higher opioid dose. Paracetamol is an effective anti- pyretic and has few contra-indications. NSAIDS: synergistic with

opioids and can reduce opioid dose and thus

reduce side-effects. Not used in wide spread burns due to already increased risk of renal failure and peptic ulceration. There is potential to increase bleeding in large burns also, due to the anti-platelet effect.




- Drowsiness

- Adverse reaction

- Nausea and increased risk of aspiration









- Postural hypotension, and fainting

Non- Pharmacological Pain Management

The following is a synthesis of information form the following articles: Summer et al (2007), Richardson and Mustard (2009), ANZBA (2007) and de Jong et al (2007) Overall, the levels of evidence to support the use of alternative therapies for pain relief are of poor quality. However, no negative side effects were reported in the literature reviews and these therapies are all used in conjunction with pharmacological management to optimize pain relief for the individual.

Psychological techniques:

beneficial for reducing anxiety and providing patients with coping methods for pain levels and durations. These include relaxation, distraction and cognitive behavioural therapy (CBT). CBT is beneficial in the management of complex pain problems and can reduce fear and anxiety associated with activities or environments.


a state of “increased suggestibility, attention and relaxation”. In the burn patient hypnosis is used in the management of procedural pain and anxiety. The use of hypnosis clinically is increasing but its usefulness is dependent on the individual’s hypnotic susceptibility, high baseline pain and the skill of the practitioner. The current best available evidence for management of procedural pain was found for active hypnosis, rapid induction analgesia and distraction relaxation.

Virtual Reality:

immersing the patient in a virtual world has shown some effect on procedural pain control and is better than hand-held gaming devices. However, the equipment is costly and bulky and not always suitable for paediatric intervention. A paediatric intervention, using hand-held game devices which provide augmented reality was trialled among 3-14 year olds. This has shown significantly lower pain scores than standard distraction and relaxation when undergoing dressing changes (Mott et al 2008).

Sleep Normalisation:

disrupted sleep occurs in up to 50% of burn patients and links have been established between poor sleep quality and pain severity, as well as pain and prolonged experiences of sleep disturbance. Normalisation of the 24hour day, with a bedtime routine, within the limits of the hospital environment is aimed for to promote sleep, with the use of analgesics and night sedation.

Music therapy:

this is thought to target pain via the gate control theory. This suggests that music serves as a distraction from noxious stimuli. Also, the anxiety related to the rehabilitation of burns can increase the activation of the sympathetic nervous system. Music uses all three cognitive strategies employed in pain and anxiety management (imagery envisioning events that are inconsistent with pain, self-statements and attention- diversion devices to direct attention away from the pain ad redirects it to another event) (Ferusson and Voll 2004; Presner et al 2001). A systematic review of music therapy among pregnant women, medical- surgical patients and critical care patients showed statistically significant reductions in pain scores. Of the seventeen studies reviewed by Cole and LoBiondo- Wood (2012), 13 studies demonstrated the positive effects of music on pain. Other positive findings of the studies included reduced anxiety, muscle tension, blood pressure and heart rate. A burn specific study included showed reduced pain levels during and after the debridement, reduced anxiety and decreased muscle tension during and after dressing changes. The Cochrane Review of music as an adjunct to pain relief concluded that “music and other non- pharmacological therapies could have a synergistic effect to produce clinically important benefits on pain intensity or analgesic requirements” and thus requires further study. This is based on the studies indicating that music resulted in reduced pain intensity and reduced opioid requirements. The reported changes in both of these outcomes were small however, and their clinical importance is unclear (Cepeda et al 2006).

Paediatric Burn Pain

(Richardson and Mustard 2009) •children 0-4 years represent approx. 20% all hospitalised burn patients •In preschool aged children the half-life of opioids (morphine and alfentanyl) are 50% those in adults. Higher dosage required.

• Risk of accidental overdose due to difficulties with pain evaluation resulting in overestimation of child’s pain

•Childs environment has huge effect on pain perception. Parents’ presence and aid during dressing change can have beneficial for procedural pain and reducing anxiety.

Medical and surgical Management

Reconstruction Post Burn Injury

The impact of reconstructive surgery post burn injury has a major impact on a patient. As an allied health professional, we must work as part of an MDT in order to ensure successful surgery while at the same time ensuring long term health and function. Timely burn wound excision and skin grafting form the cornerstone for acute burn surgical management (Klein 2010).Surgery for burned patients is not normally indicated until 48 hours after injury, when the depth of the burn has been established. The only exception is when necrotic tissue is evident then early excision may be required. A plastic surgeon must reconstruct the injured body part in

a way that is extensible, sensate and cosmetically acceptable

(Glassey 2004). In addition to this, they must rebuild or replace muscles, tendons, joints and nerves

to ensure they are appropriately intact.


1. Achieve would closure

2. Prevent infection

3. Re-establish the function and properties of an intact




5. Reduce the extent of a cosmetically unacceptable scar









(Glassey 2004; BBA Standard 6 2005)

Choosing the Correct Method of Reconstruction

The simplest management involves conservative wound care and dressings, while the most complex is free-flap reconstruction. When deciding on the most appropriate intervention, a surgeon must consider the extent of the missing tissue and the structures effected (Glassey 2004). Generally, a superficial partial thickness burn will heal with conservative treatment (secondary intention) in 10 days to 3 weeks, unless infection occurs. Primary intention occurs if a wound is of such size that it can be closed directly without producing undue tension at the wound site. Delayed primary closure occurs once a

suspected infection has been cleared. Deep partial and full thickness burns both require surgical intervention. Surgery normally takes place within the first 5 days post injury to prevent infection which could extend the depth of the tissue loss (Glassey 2004).

Skin Grafts

“A skin graft is the transportation of skin from one area of the body to another.” (Glassey 2004)

A graft is an area of skin that is separated from its own blood supply and requires a highly vascular recipient bed in order for it to be successful. Prior to grafting, the process of wound debridement must take place. Wound debridement involves removing necrotic tissue, foreign debris, and reducing the bacterial load on the wound surface (Cardinal et al 2009).This is believed to encourage better healing. The following are the methods available for grafting onto a debrided wound to obtain closure:

•Autograft (‘split skin graft’) (own skin)

• Allograft (donor skin)

• Heterograft or xenografts (animal skin)

• Cultured skin

• Artificial skin

(Glassey 2004) Meshed vs. Sheet Grafts

Sheet grafts are those which are not altered once they have been taken from the donor site.

Meshed grafts are those which are passed through a machine that places fenestrations (small holes)

Meshed grafts are those which are passed through a machine that places fenestrations (small holes) in the graft. Meshed grafts have advantages over sheet grafts of 1) allowing the leakage of serum and blood which prevents haematomas and seromas and 2) they can be expanded to cover a larger surface area. (Klein 2010)







Diagnosis of DEEP tissue loss

Patient is systemically fit for surgery


no coagulation abnormalities










streptococcus (Glassey 2004)

The Donor Site

The thigh is the most common donor site for split thickness skin grafts (STSG). A split thickness graft involves a portion of the thickness of the dermis while a full thickness skin graft (FTSG) involves the entire thickness of the dermis (Klein 2010). The most common site for full thickness skin grafts is the groin. Cosmetic areas such as the face should be avoided for graft donation. The donor site should just be left with a superficial or a superficial partial thickness wound which will heal in 10-14 days and may be reused if necessary. Often, the donor site can be more painful than the recipient due to exposure of nerve endings (Glassey 2004).

Skin Substitutes

“Skin Substitutes are defined as a heterogeneous group of wound cover materials that aid in wound closure and replace the functions of the skin either temporarily or permanently” (Halim et al 2010) Conventionally, STSG and FTSG have been found to be the best option for burn wound coverage (Halim et al 2010). However, in cases of extensive burn injury, the supply of autografts is limited by additional wound or scarring at donor sites. For this reason, skin substitutes will be required. Skin substitutes require higher cost, expertise and experience than autografts. However, they also offer numerous advantages in the form of rapid wound coverage requiring a less vascularised wound bed, an increase in the dermal component of a healed wound, reduced inhibitory factors of wound healing, reduced inflammatory response and reduced scarring (Halim et al 2010). Currently, there are various skin substitutes on the market but scientists and engineers are working

(Halim et al 2010). Currently, there are various skin substitutes on the market but scientists and

towards producing the optimal skin substitute. As a general rule, skin substitutes are classified as either temporary or permanent and synthetic or biological. A very clear and concise overview of the different skin substitutes available for burn injuries is provided in Halim et al (2010).

•Tendon without paratenon

•Cartilage without perichondrium (Glassey 2004) Categorisation of Skin Flaps

Based on three factors:

The Recipient Site

1. Vascularity


2. Anatomical composition


The graft should take within 5 days and will provide a permanent covering of the injury. A graft should always be placed over bleeding, healthy tissue to ensure it is vascularised for survival (Glassey 2004). Post-operatively the graft site is dressed to ensure pressure is created over the graft to limit haematoma formation. The body part is immobilised in an anti- deformity position at first in order to prevent shearing forces that could disrupt the graft (Edgar and Brereton 2004). Some very mobile body parts, such as the hand, may require splinting to ensure joint immobility.

3. Method of relocation (Glassey 2004)



















Process of Graft ‘Take’

• Serum Inhibition (24-48hrs): fibrin layer formation and diffusion of fluid from the wound bed Inoscultation (day 3): capillary budding from the wound bed up into the base of the graft •Capillary in-growth and remodelling (Glassey 2004)

Reasons for Graft Failure

• Inadequate blood supply to wound bed

• Graft movement

• Collection of fluid beneath graft (e.g. haematoma)

• Infection (e.g. streptococcus)

• The grafts properties (e.g. vascularity of donor site) (Glassey 2004)

Skin Flaps

The difference between a skin graft and a skin flap is that “a skin flap contains its own vasculature and therefore can be used to take over a wound bed that is avascular”. A skin graft does not have this ability (Glassey 2004). When speaking about grafts and flaps in the research, skin flaps is often incorporated into the term ‘skin grafts’. Tissues which a skin graft will not take over include and which a skin flap will include:

•Bone without periosteum

vascularity. Random pattern flaps are not raised on any particular major blood vessel, but instead are raised on smaller branches of these blood vessels known as the subdermal plexus. These flaps are limited in size to ensure distal parts do not become ischemic (Glassey 2004). Examples of these flaps include Z-plasty, V-Y advancement flap, rotation flap and transposition flap. Axial flaps, on the other hand, are raised upon a specific blood vessel which allows them to be lifted on a narrow pedicle and ensures greater perfusion for survival.

Flap anatomical Composition

Flaps are also classified depending on their composition, i.e. which layers of the skin they contain. The composition is often clear from the name of the flap.

The composition is often clear from the name of the flap. Skin Flap- epidermis, dermis and

Skin Flap- epidermis, dermis and superficial fascia

• Fasciocutaneous Flap- epidermis, dermis and both superficial and deep fascia


• Myocutaneous Flap-muscle belly with the overlying skin

• Osseous Flap- bone

Flap-muscle belly without overlying


• Osseomyocutaneous Flap-bone, muscle, skin

• Composite Flap- Contains a no. Of different tissues

such as skin, fascia, muscle and bone. (Glassey 2004)

Relocation of Flaps

The third way in which flaps are classified is by their method of relocation. Flaps are defined as either ‘local’ or ‘distant’ depending on the distance between the donor and recipient sites (Glassey 2004).

•Local Flaps:

Rotation or transpositional flaps are tissue that is lifted and manipulated to cover the local defect, maintaining their connection with the body. Therefore, they are never fully excised. Advancement flaps are those in which the tissue is moved directly forward to cover the defect, e.g. V-Y flaps used to cover finger-tip injuries (Glassey 2004). •Distant Flaps:

Pedicled flaps are those which are transferred to another area of the body but the vascular attachment is always maintained and so the distance it can travel depends on the length of the pedicle. Free flaps are those in which the tissue is completely separated from the body and transferred to another area and the vascular supply is re-established by anastomising the blood vessels (Glassey 2004).

Rehabilitation Post Burn Injury

•Rehabilitation requires a prolonged, dedicated and multidisciplinary effort to optimise patient outcomes, as inpatients and outpatients. (Schneider et al 2012; Disseldorp et al 2007; Esselman,


The aims of the multidisciplinary rehabilitation of a burn include:

Prevention of additional/deeper injuries

Rapid wound closure

Preservation of active and passive ROM

Prevention of infection

Prevention of loss of functional structures

Early functional rehabilitation (Kamolz et al


• Early functional rehabilitation (Kamolz et al 2009) The physiotherapist may only have a role in

The physiotherapist may only have a role in achieving some of these goals.

Above all cause no harm.

Significant improvements in the medical and surgical management of burns has occurred in the last century.

Increased survival rates mean that focus is turning to achieving optimal functional outcomes.

• Burn survivors often suffer from o permanent scarring, reduced range of motion, weakness, and impaired functional capacity

o psychological and social problems, which significantly affect their ability to resume their normal activities post discharge

Early initiation of rehabilitation is essential to maximise functional outcomes for the patient

The pain and psychological distress of a burn

has a massive impact on compliance o An empathetic, encouraging and understanding approach is necessary The urgency and importance of beginning early rehabilitation should be communicated in a clear

but gentle manner (Procter 2010).

Role of the Physiotherapist in the Rehabilitation of the Acute Burn Pa

For the purpose of clarity, the following section has been divided into acute, sub acute and chronic rehabilitation. However, rehabilitation is a continuum, and significant crossover may occur. All of the following concepts apply to burns on any part of the body, with specialised treatment addressed for the hand where necessary. Depending on the size and the severity of the injury this stage may last from a few days to a few months (Procter 2010) Patient

Acute phase of inflammation


2010) Patient • Acute phase of inflammation • Pain • Oedema increasing for up to 36

Oedema increasing for up to 36 hours post injury

Hypermetabolic response, peaking at five days post injury

Early synthesis and remodelling of collagen

Aims Reduce risk of complications

o Reduce oedema, particularly where it poses

a risk for impinging on peripheral circulation or

it poses a risk for impinging on peripheral circulation or airways Predisposition to contractures • Prevent


Predisposition to contracturesa risk for impinging on peripheral circulation or airways • Prevent deformities/loss of range • Protect/promote

Prevent deformities/loss of range

Protect/promote healing

Common treatment techniques




Bed rest




Rationale for Immobilisation

Positioning in the Acute Stage

*Modify according to burn area, patient pain and medical status.*

1mmobilisation post skin reconstruction surgery

Stopping movement and function of the body parts involved should be enforced after skin reconstruction for a burn has taken place. When a body part must be immobilised, it should be splinted or positioned in an anti-deformity position for the minimum length of time possible (Edgar and Brereton 2004; ANZBA 2007)

The following is a table drawn up using current literature on the recommended immobilisation times for the various skin grafts:

The times frames for mobilisation post-surgery outlined in this booklet are merely a guide taken from an analysis of current literature and are NOT a replacement for the specific time frames directed by the operating surgeon or consultant (ANZBA 2007). For a physiotherapist the most important concepts to grasp are:

• What is the minimum timeframe of immobilisation


• What structures MUST be immobilised

• Special considerations for movement, function and ambulation dependent on

(Boscheinen-Morrin 2004) Donor sites and the structures repaired or excised during surgery. Static Splinting •

(Boscheinen-Morrin 2004)

Donor sites and the structures repaired or excised during surgery.

Static Splinting

repaired or excised during surgery. Static Splinting • A serial static splint is a device with

A serial static splint is a device with no moving parts designed to be remoulded as a contracture improves. The most common serial static splint you will come across is a thermoplastic palmar splint moulded in the position of safe immobilisation.

A static progressive splint is a device designed to

• A static progressive splint is a device designed to stretch contractures through the application of

stretch contractures through the application of incrementally adjusted static force to promote lengthening of contracted tissue (Smiths 2009). There are various types of static progressive splints available depending on the area affected. One such static progressive splint is a finger flexion strap splint. This type of splint is used in the treatment of MCP extension contractures. The flexion straps serially stretch scar bands along the dorsum of hand and wrist causing extension contracture. The stretching force is

Immobilisation of the hand

Deformity Prevention The most common deformity associated with burns is the ‘claw’ deformity. It involves extension of the MCP joints, flexion of the PIP joints, adduction of the thumb and flexion of the wrist (Kamolz 2009). This position is also referred to as the intrinsic minus position. Position of Safe Immobilisation

The position of safe immobilisation of the burned hand is essentially the opposite of the above claw deformity position. This position involves: 20-30 wrist extension, 80-90 degrees flexion MCP joints, full extension PIP and DIP joints and palmar abduction of the thumb (Boscheinen-Morrin 2004).


Physiological rationale for splinting (Kwan 2002) Scar tissue is visco-elastic. It will elongate steadily within a certain range. When this stretching force is released, there is an immediate decrease in the tissue tension but a delay in the retractions of the tissue to a shorter length. These stress relaxation properties of visco elastic scar tissue means it can accommodate to stretching force overtime. Dynamic and static splinting provide this prolonged low stretching force.

Categories of Splints

Static or Dynamic

Supportive or Corrective

Rigid or soft

Dorsal or Volar

Digit, hand or forearm based

Static or Dynamic • Supportive or Corrective • Rigid or soft • Dorsal or Volar •

localised to the MCP joints by applying the straps via a wrist extension splint. This stabilises the wrist providing static support below the MCP joint (Kwan 2002). Dynamic Splinting

A dynamic splint is one which aids in initiating and

performing movements by controlling the plane and range of motion of the injured part. It applies a mobile force in one direction while allowing active motion in the opposite direction. This mobile force is usually

Precaution must be taken to ensure that splints do not product friction causing unnecessary trauma to the soft tissues (Duncan et al 1989).

Precaution must be taken to ensure that splints do

not produce excessive pressure. There is particular risk

of pressure injury to skin after burn injuries due to potential skin anaesthesia

(Leong 1997).

Splinting should not be used in isolation but as an adjunct to a treatment regime

be used in isolation but as an adjunct to a treatment regime applied with rubber bands,
be used in isolation but as an adjunct to a treatment regime applied with rubber bands,

applied with rubber bands, elastics and springs (Smith


Dynamic extension splints are most commonly used

in the treatment of palmar and / or finger burns (i.e.

flexion contractures). All the finger joints including the MCP, PIP and DIP joints are in full extension (Smith


MCP, PIP and DIP joints are in full extension (Smith 2009). A type can • Dynamic




Dynamic flexion splints are used in the treatment of dorsal hand burns. During wound healing and subsequent scar maturation, the skin on the dorsal aspect of the hand can markedly contract limiting digit

flexion. A dynamic flexion splint in the sub-acute stage

of dorsal hand burns can aid in the prevention of MCP

joint extension contractures (Kwan 2002).

Splinting Precautions

Splints need to be cleaned regularly to prevent colonization by microbes which may lead to wound infection

(Wright et al 1989; Faoagali et al 1994)

Unnecessary use of splinting may cause venous and lymphatic stasis, which may result in an increase in oedema

(Palmada et al 1999)

Management of Oedema Elevation

Elevation of the hand above heart level is the most simple and effective ways to prevent and decrease oedema (Kamolz




used to facilitate






to facilitate elevation. of facilitates elevation • be This sling both and protection of wound area





protection of wound area while still allowing movement. Its foam design also reduces the risk of the development of pressure points or friction (Glassey


When a patient is admitted with severe burns of a large TBSA they are at risk of systemic inflammation. Therefore, not only must the affected limb be placed in elevation,

the following precautions should also be taken Elevation of the head: This aids chest clearance, reduces swelling of head, neck and upper airways. It is important not place a pillow underneath the head in the case of anterior neck burns as there is a risk of neck flexion contractures

Elevate all limbs effected

Feet should be kept at 90

Neutral position of hips

Care must be taken to reduce the risk of pressure sores. (Procter 2010) Coban

Coban wrap can be used to decrease hand oedema. The main advantage of Coban wrap is that it does not stick to underlying tissue, making it suitable for use in the acute stages of burns (Lowell 2003). There is currently limited quantity of evidence to support the use of Coban wrap in the treatment of Oedema. In 2003 Lowell et al carried out a case study involving a subject with dorsal hand burns.

Oedema Glove/Digi Sleeve

These are hand specific oedema management products. There is currently no specific evidence available to support the efficacy of oedema gloves or digi sleeves in the reduction of oedema. However it is common practice in Irish hospital to provide these products to patients with excessive hand and finger oedema. Their use is based on the principle of compression to reduce oedema which is heavily supported by evidence (Latham and Radomski 2008).

Role of the Physiotherapist in the Rehabilitation of the Sub Acute Burn Patient

Beyond the acute stage of immobilisation, inpatient and outpatient rehabilitation typically consists of a variety of interventions including pressure garment therapy, silicone therapy, scar massage, range of motion and mobilisation techniques, strengthening, functional and gait retraining, and balance and fine motor retraining ( Schneider et al, 2012). Interventions should be tailored according to a full patient assessment. As it would be unethical to withhold treatment, physiotherapy intervention as a whole is not well investigated. Schneider et al (2012) found a significant improvement in contractures; balance and hand function with inpatient rehabilitation, through a longitudinal observational study of eleven people. However, in the following section, we will attempt to display the evidence for commonly used modalities. The patient

Primary closure of wound

Scar remodelling

Scar contraction


Optimise scar appearance

Limit effects of scar contraction/prolonged positioning on range of motion and function

Address effects of prolonged bed rest

Common modalities



Scar management adjuncts o Pressure garments, silicone, massage Continuation of oedema/ positioning management where necessary






Mobilisation The advantages of general mobilisation for a burns patient to counteract the effects of prolonged bed rest are no different to that of a surgical or medical patient. Burns patients should be mobilised as early as possible to avoid deconditioning and possible respiratory complications associated with prolonged bed rest (Esselman 2007).

As outlined in the above introduction, due to the ethical issues surrounding withdrawal or modification of treatment the evidence surround the optimal duration, frequency and methods of physiotherapy interventions in the treatment of burn patients is unclear. Despite this lack of clarify surrounding these issues it is clear that both active and passive mobilisation plays a key role throughout the stages of burn recovery. Below is a summary of the recommendations from the currently literature on passive and active mobilisation of burns.

Active ROM

Depending on the need for immobilisation gentle active ROM exercises is the preferred treatment during the acute stage of injury as it is the most effective means of reducing oedema by means of active muscle contraction (Glassey 2004). If this is not possible due to sedation, surgical intervention etc. then positioning the patient is the next best alternative (see immobilisation and position).

Passive ROM

Passive ROM exercises in the acute stage are contraindicated as applying passive stretching forces may result in future damage to the burned structures

(Boscheinen-Morrin 2004). Applying these passive manoeuvres in the acute stage will result in increased oedema, haemorrhage and fibrosis of the burned tissues (Cooper 2007).

The biomechanical principle of creep when passive stretching. A slow sustained stretch is more tolerable for patient and more effective for producing lengthening (Kwan 2002).

Passive joint mobilisations can begin during the scar maturation phase once the scar tissue has adequate tensile strength to tolerate friction caused by mobilisation techniques (Boscheinen-Morrin and Connolly 2001).

Frequency, Duration Recommendations

Physiotherapy intervention should be twice daily with patients prescribed frequent active exercises in between sessions.

For the sedated patient gentle passive range of motion exercises should be done 3 times a day once indicated (Boscheinen-Morrin and Connolly 2001).

Dependent on the severity of the burn active and

very gentle passive range of motion exercises for the hand and fingers are begun from day one of injury.


Active or Passive range of motion exercises should

not be carried out if there is suspected damage to extensor tendons (common occurrence with deep dermal and full thickness burns). Flexion of the PIP joints should be avoided at all costs to prevent extensor tendon rupture. The hand should be splinted in the position of safe immobilisation or alternatively a volar PIP extension splint until surgical intervention

(Boscheinen-Morrin and Connolly 2001) is discussed.

Range of motion exercises are also contraindicated post skin grafting as a period of 3-5 days immobilisation is required to enable graft healing (Boscheinen-Morrin and Connolly 2001).

Practical factors to consider when mobilising

Be aware of dressing clinic/daily dressing changes.

Mobilisation should coincide with this as it is important

to monitor the wound during AROM frequently.















treatment sessions.

Observe the patient carrying out the AROM and PROM exercises prior to beginning treatment. Also observe the patient taking on/off splints.

Always monitor for post exercise pain and wound breakdown.


compromise vascularity.

The patient may present with a reduced capacity for exercise secondary to increased metabolic rate, altered thermoregulation and increased nutritional demands.








Postural hypotension may be present due to prolonged bed rest and low haemoglobin. (ANZBA 2007)

Scar Management

Abnormal scarring is the most common complication of burn injuries, with the estimated prevalence of > 70% of those who suffer burn injuries (Anzarut et al, 2009). Not only do hypertrophic scars cause psychosocial difficulties through their cosmetic appearance, they may also be painful, pruritic, and they may limit range of motion where they occur on or near a joint (Morien et al 2009; Polotto 2011). Hypertrophic scars require a continuum of dedicated and specialised treatment from the acute stage to many years post treatment (Procter, 2010, ANZBA 2007).

The following is an examination of the evidence and recommendations for use in the most common of these, including silicone gel, pressure garment therapy, and massage. The positioning and mobilisation advice above is all applicable, and should be continued in the management of hypertrophic scars where necessary.

Scar Outcome Measures

1. Vancouver Burn Scar Scale (VBSS/VSS)

2. Patient and Observer Scar Assessment Scale (POSAS)

Vancouver Burn Scar Scale (VBSS/VSS)

Use: Most familiar burn scar assessment. Measures:

pigmentation, pliability, thickness and vascularisation (Fearmonti et al 2010). Reliability: Not enough evidence to make it a ‘gold standard’ OCM. Moderate to high overall inter rater reliability. Test- Retest and intra rater reliability has not been assessed for burn scars to date (Durani et al 2009).

Validity: When compared with POSAS scale, validity was evident (Durani et al 2009) Sensitivity: Most Scar OCM rely on categorical/ordinal data with few levels which provides limited sensitivity and can only identify considerable differences between scars (Fearmonti et al 2010).

Patient and Observer Scar Assessment Scale (POSAS)

Use: Measures pigmentation, vascularity, thickness, relief, pliability and surface area. Also includes assessment of patient pain, itching, colour, stiffness, thickness and relief. The only scale to measure subjective aspects of pain and pruritus (severe itching) (Fearmonti et al 2010). Reliability: Good internal consistency and reliability (Durani et al 2009) Validity: Good concurrent validity (Durani et al 2009) Sensitivity: Like the VBSS/VSS above, limited sensitivity due to categorical/ordinal data (Fearmonti et al 2010) Further studies are required to validate the reliability and validity of these scales as they are considered to be very subjective measures (Durani et al 2009). Scar scales like the Vancouver Burn Scar Scale (VBSS/VSS) and the Patient and Observer Scar Assessment Scale (POSAS) are cost effective and can be easily transferred within a clinical setting. To optimise the scar scales, photographic evidence of the scar at timed intervals is of great value also to the clinician (Brusselaers et al 2010) Silicone

Silicone Overview The use of silicone gel or sheeting to prevent and treat hypertrophic scarring is still relatively new. It began in 1981 with treatment of burn scars (O’Brien & Pandit 2008). The physiological effects of silicone in the treatment of scarring remain unclear. Below is a summary of the current hypotheses surrounding the physiological effects of silicone. This summary has been adapted from the most recently published literature on this topic. 1) Hydration Effect: Hydration can be caused by the occlusion of the underlying skin. It decreases capillary activity and collagen production, through inhibition of the proliferation of fibroblasts

2) Increase in temperature: A rise in temperature increases collagenase activity thus increased scar breakdown.

3) Polarized Electric Fields: The negative charge within silicone causes polarization of the scar tissue, resulting in involution of the scar.

4) Presence of silicone oil: The presence of silicone has been detected in the stratum corneum of skin exposed to silicone. However other researchers suggest occlusive products without silicone show similar results.

5) Oxygen tension: After silicone treatment the hydrated stratum corneum is more permeable to oxygen and thus oxygen tension in the epidermis and upper dermis rises. Increased oxygen tension will inhibit the ‘‘hypoxia signal’’ from this tissue. Hypoxia is a stimulus to angiogenesis and tissue growth in wound healing, as a consequence removing the hypoxia stops new tissue growth. This theory has been contraindicated by other researchers.

6) Mast cells: It is suggested that silicone results in an increase of mast cells in the cellular matrix of the scar with subsequent accelerated remodelling of the tissue.

7) Static electricity: Static electricity on silicone may influence the alignment of collagen deposition (negative static electric field generated by friction between silicone gel/sheets and the skin could cause collagen realignment and result in the involution of scars. (Bloemen et al 2009; Momeni et al 2009)

Pressure Garment Therapy (PGT)

Though the effectiveness of PGT has never been proven, it is a common treatment modality for reducing oedema and managing hypertrophic scars (Procter, 2010). Aims


Reduce scarring by hastening maturation


Pressure decreases blood flow


Local hypoxia of hypervascular scars


Reduction in collagen deposition




Decreases scar thickness


Decreases scar redness


Decreases swelling


Reduces itch

o Protects new skin/grafts

o Maintains contours (Procter 2010)

The exact physiological effects of how pressure positively influences the maturation of hypertrophic scars remain unclear. Below is a summary of the current hypotheses surrounding the physiological effects of pressure garments. This summary has been adapted from the most recently published literature on

1) Hydration effect: decreased scar hydration results in mast cell stabilization and a subsequent decrease in neurovascularisation and extracellular matrix production. However this hypothesis is in contrast with a mechanism of action of silicone, in which an increase of mast cells causes scar maturation.

2) Blood flow: a decrease in blood flow causes excessive hypoxia resulting in fibroblast degeneration and decreased levels of chondroitin-4-sulfate, with a subsequent increase in collagen degradation.

3) Prostaglandin E2 release: Induction of prostaglandin E2 release, which can block fibroblast proliferation as well as collagen production (MacIntyre & Baird 2006)







Pressure: 15 mmHg has been noted as the minimum to elicit change, and pressures of above 40 mmHg have been found to cause complications. Both Anzarut et al (2009) and Engrav et al (2010) used pressures of between 15 and 25 mmHg. Time: It is recommended that garments are worn for up to 23 hours a day, with removal for cleaning of the wound and garment, and moisturisation of the wound.

(Procter 2010; Anzarut et al 2009 and Bloeman et al


Duration: garments can be worn as soon as wound closure has been obtained, and the scar is stable enough to tolerate pressure. Post grafting, 10-14 days wait is recommended, at the discretion of the surgeon (Bloeman et al 2009).

Garments should be worn for up to one year, or until scar maturation (Anzarut et al 2009; Engrav et al 2010 and Bloeman et al 2009). Possible complications/ confounding factors for use of PGT

Lack of a scientific evidence to established optimum pressure



Heat and perspiration

Swelling of extremities caused by inhibited venous return

Skin breakdown






Web space discomfort


Personal hygiene difficulties possibility of infection

Allergies to material (MacIntyre & Baird 2006; Glassey 2004) Massage

Five principles of scar massage:

1. Prevent adherence

2. Reduce redness

3. Reduce elevation of scar tissue

4. Relieve pruritus

5. Moisturise (Glassey 2004)

Scar Massage Techniques

Retrograde massage to aid venous return, increase lymphatic drainage, mobilise fluid

Effleurage to increase circulation

massage to aid venous return, increase lymphatic drainage, mobilise fluid • Effleurage to increase circulation

Static pressure to reduce pockets of swelling

Finger and thumb kneading to mobilise the scar and surrounding tissue

Skin rolling to restore mobility to tissue interfaces








collagenous remodelling


Frictions to loosen adhesions


(Holey and Cook 2003)








Insufficient consistency in literature with regards to protocols on frequency or duration of treatment. Suggestions for practice include (Shin and Bordeaux, 2012, Morien et al, 2008)

Clean hands essential










Modify practice according to patient stage of healing, sensitivity and pain levels.


Shin and Bordeaux 2012

Compromised integrity of epidermis

Acute infection


Wound dehiscence,

Graft failure

Intolerable discomfort

Hypersensitivity to emollient

The Role of the Physiotherapist in the Rehabilitation of the Chronic Burn Patient.

The patient Healing process may continue for up to two years, as scar tissue remodels and matures

May require functional retraining and integration back into the community and activities.

It is important to note that though scar management is initiated in the sub-acute phase, it may need to be continued long term, as many patients suffer from continuing limitation to range of motion

(Procter 2010).

Aerobic and Resistance Training Post Burn

Rationale for Aerobic and Resistance Training

Low cardiorespiratory endurance has been found to be a concern for all

(Willis et al 2011)

Aerobic capacity as measured by VO2 peak and time to fatigue has been found to be lower in adults and children of >15% TBSA at one year post burn, compared to age matched healthy controls

(Willis et al 2011; McEntine et al 2006)

Muscular strength and lean body mass has been found to be significantly less in patients suffering from burns of >30% TBSA, particularly in exercises requiring a high velocity (Disseldorp et al 2007; Ebid et al 2012). The systemic effects caused by large surface area burns means that weakness may be global, not just local to the site of the injury

(Grisbrook et al 2012b)

Reduced lean body mass, endurance and strength has been associated with limited standing/walking tolerance, reduced upper limb function and lower health related QOL and ability to participate in activities

(Grisbrook et al 2012b).

This has been found to persist beyond discharge from hospital despite routine physiotherapy and occupational therapy in hospital (Disseldorp et al 2007). Though protein metabolism begins to normalise 9-12 months post burn, patients are still found

All found a decrease of up to 20% in lean muscle mass compared to age matched controls

Adults with a TBSA >30% suffered a significant decrease in torque, work and power in the quadriceps muscles compared to age matched controls. (De Lauter et al 2007) Exercise and Hypermetabolism

Though exercise requires an increase in energy expenditure and metabolism for a short period of time no adverse effects have been found with regard to exacerbating hypermetabolism or protein catabolism.

o All studies investigating the effects of exercise on

lean body mass found it to increase, particularly with resistance training

( Grisbrook et al 2012b; Suman and Herndon 2007; Suman et al 2001; Przkora et al 2007)

o Suman et al, 2001, found an increase of 15% in

resting energy expenditure in children with burns of >40% TBSA who were not treated with resistance and aerobic exercise, while the REE of those who participated in the intervention remained stable. o Suggested that exercise may have sympathetic nervous system attenuating effects

A balance of resistance and aerobic exercise may cause a decrease in SNS activity, decreasing catabolic effects.

o Exercise is required to integrate dietary amino acids into lean muscle mass (Herndon and Tomkins 2004)


Human skin produces sweat to dissipate heat in

response to thermal stress (McEntine et al 2006). A proper sweat response requires functional integrity of


Sweat glands

Skin circulation

Neural control of the skin (McEntine et al 2006)

Full thickness burns damage the dermal appendages including sweat glands. These are not replaced by grafting. There is also a decreased density of sweat glands in the donor site post grafting (Esselman et al 2007). However, McEntine et al 2006 found that in 15 children with an average of 55% TBSA there was No significant difference in core temperature, measured tympanically, pre or post 20 minutes of treadmill exercise at room temperature compared to age matched healthy controls.

No significant difference in average skin temperature between burned and healthy children.

Significantly increased skin temperature in healthy versus burned skin per child.

Austin et al, 2003 studied 3 adults with > 60% TBSA, 3 with between 30-40 TBSA and 2 unburned patients post 1 hr cycling at 35 degrees and 60% humidity

None showed significant intolerance for heat as measured by heart rate and core temperature, measured rectally

No significant difference in whole body sweat rate

Overcompensation by healthy skin in the burned patients.

Suggested physical history was a factor in determining patients’ ability to thermoregulate. Therefore adaptations may occur through training.

However, studies involving heat loads of 40 degrees have found a significant inability to maintain adequate thermoregulation. Due to the small study numbers of the above, and the controversy surrounding the efficacy of measuring core temperature accurately, it is advised that patients are closely monitored initially during aerobic exercise for signs of heat intolerance.

***Inhalation injury and pulmonary insufficiency

Long term pulmonary function is compromised in some patients post severe burn

Lasts several years

Documented in both children and adults (Grisbrook et al 2012a)

Caused by


Smoke inhalation


Direct thermal damage to airways


Pulmonary oedema


Respiratory tract infection


Complications from intubation


Recurrent infection leading to chronic


Less likely to cause dysfunction in <30% TBSA,

no injury over torso, and no inhalation injury

(Willis et al 2011) Evidence for impact on aerobic and exercise capacity conflicting (Grisbrook et al 2012a). However Willis et al (2011) studied 8 males post > 15% TBSA burns at one year post injury, and found

Significantly decreased FEV1, peak VO2 and time to fatigue, in the burned patients

No significant decrease in SpO2 at baseline or peak VO2- however, the SpO2 of burned patients took









Resistance Training Summary and Recommendations for Practice

No significant difference in participation levels in physical activity, though burn survivors were more likely to participate in work rather than leisure activity.

Burns survivors were less likely to participate in vigorous intensity exercise over 9 METs

Therefore, decreased pulmonary function did not prevent them from participating

The lower relative intensity of their exercise may have caused their decreased aerobic capacity.

All of the above factors must be considered as both a contributor to the patients’ loss of strength and aerobic capacity, and a potential limiter of their ability to participate in therapy. Careful monitoring and modification of treatment according to individual response is advised.

Aerobic Training Summary and Recommendations for Practice

Exercise prescription:

Frequency: The majority of papers which investigated an aerobic intervention used 3 times per week as their frequency (De Lauteur et al 2007; Grisbrook et al 2012). These obtained significant improvements. However, Przkora et al (2007) used a frequency of 5 times per week with children. There have been no studies investigating optimal frequency. Intensity: All studies used between 65 and 85% predicted heart rate max, with one study using interval training of 120 seconds 85% HRM and 120 seconds of 65-70 HRM. All studies obtained positive effect, with none directly comparing intensities to determine the optimum. De Lauteur et al (2007), concluded that whether the patient gradually increased their intensity by working to a specific quota each week, or if they simply worked at their target heart rate for as long as they could tolerate, there was no significant difference in gains in aerobic capacity. Type: All interventions used treadmill training, whether walking or running. Time: All studies recommended the duration of treatment be 12 weeks, with the exception of Paratz et al, 2012, who investigated a high intensity six week programme. However, the specific results of this are unknown. Sessions were 20-40 minutes in length, with the majority using 30 minutes (Grisbrook et al 2012; De Lauteur et al 2007; Przkora et al 2007)

Exercise prescription: Post two years, Grisbrook et al (2012b) found that burned patients responded to resistance exercise similarly to controls. Therefore, normal guidelines may be adequate. Frequency: All studies investigating the effects of resistance training used a frequency of three times per week. There have been no studies to investigate the optimum frequency for resistance training in this population. Suman et al (2001), suggested that a break of more than 48 hrs must be given between bouts of resistance training. o Resistance exercise causes microtrauma to muscles already in a compromised state.

o Resistance exercise in burned patients stimulates protein synthesis as in unburned subjects- However; a longer period of recovery may be required for optimum results.

Type/ Intensity: Children: using free weights or resistive machines: 1 set of 50-60% of the patients 3 RM week 1, followed by a progression to 70-75% for week 2-6 (4-10 repetitions), and 80-85% week 7-12, (8- 12 repetitions) (Suman et al 2001; Suman and Herndon


Isokinetic training: 10 reps at 150 degrees per second, using 1-5 sets for the 1st -5th session,6 sets for the 6th -24th session, and 10 sets from 25th to 36th session, with three minute rests between sets. (Ebid et al 2012). Mixed and functional strength training: Grisbrook et al (2012b) commenced on the biodex, targeting specific muscle groups for the desired functional goal, and progressed to resistive machine and finally free weight training using functional items. Intensity was 50-60% of 1 RM initially, for 10-15 reps, adjusting as 1 RM increased. While no studies have compared the optimum type/intensity of exercise, this may be the optimum approach. Providing functional exercises may also increase motivation and compliance. Time: All the studies used a protocol of 12 weeks. There were no studies comparing the efficacy of shorter or longer time frames, however, given that loss of lean body mass is a possible cause of strength loss post burn, an exercise programme of longer than eight weeks is probably required to ensure hypertrophy and optimum gains in the burn patient (Suman et al 2001)








Initiating aerobic and strength training:

studies stipulated a minimum of six months to two years post burn before initiation of programmes, though many subjects were included who had been burned many years before. These participants all benefited from the interventions.

Suman and Herndon (2007) suggested that the time frame of 6 months post burn was chosen based on clinical experience because by this time paediatric patients with >40% TBSA burns were


95% healed




had had the opportunity to return home

Therefore, more favourable psychological status There were no studies investigating early training o With extensive burns, adequate healing of wounds and medical stability required before initiating aerobic/strength exercise

Other safety considerations:

Though exercise has been shown to increase lean body mass, liaison with doctors concerning anabolic steroids and medication and with dieticians regarding optimal nutrition is recommended in order to ensure correct management of hypermetabolisim.

Caution should be used with regard to impaired thermoregulation. Monitoring of heart rate and blood

pressure may be advisable, particularly on initiation of exercise and when exercising with additional thermal stress. Manage the environment to minimise thermal stress initially in particular.

Particularly those at risk of reduced pulmonary function post burn (i.e., >30% TBSA, injury to torso, or inhalation injury), monitor SpO2 and RPE during exercise. Allow additional rest periods to allow SpO2 to return to normal levels post exercise, as this has been shown to be delayed.

additional rest periods to allow SpO2 to return to normal levels post exercise, as this has


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