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Therapeutic modalities

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: Definition : Types of physical agents Thermotherapy

Skin structure and function

Physiotherapy is a branch of medical science where physical measures such as heat, light, ultrasound, water, electricity and exercises are used in the diagnosis and treatment of orthopaedic injuries.

PHYSIOTHERAPY

PHYSIOTHERAPYPassive Physiotherapy directed toward the alleviation of symptoms

Active Physiotherapy directed toward restoration of function by activity

Aims

To treat disability and deformity. To correct disability and deformity

To prevent disability and deformity

CATEGORIESDepending on severity of the ailment

1. Short term physiotherapy

2. Long term physiotherapy

Short Term Physiotherapy Includes patients with minor neuromuscular-skeletal lesions like

Simple soft tissue injuries

Simple fractures

Non traumatic lesions

Long term physiotherapy Refers to more complicated diseases of musculoskeletal originIncludes condition like Fractures of major bonesSpinal trauma resulting in physical disability and complications like paraplegia, quadriplegia etc.Surgical procedures involving major joints Chronic conditions like RA

ModalitiesAPTAs position statement (1995): Without documentation which justifies the necessity of the exclusive use of physical agents/modalities, the use of physical agents/modalities in the absence of other skilled therapeutic or education intervention, should not be considered physical therapy.

Physical Agentsthe physical agents in use today can be classified according to their specific effects on biological tissues

Classification of physical agentsEffectsType of agentModalitiesThermalConductive heating agentsHeating by radiationHot packs, paraffin wax, cryotherapy and peloidsInfra-redThermal and non thermalDiathermy agents producing conversing heating and non thermal effectsShortwave diathermy, microwave diathermy, and ultrasonic energyStimulation of nerve and/or muscleLow frequency currentsMedium frequency currentsFaradic-type currents, long duration pulsed currents, sinusoidal currents, direct current, interferential currents, didynamic currents, acupuncture, and TENSClassification of physical agentsEffectsType of agentModalitiesStimulation of circulatory mechanismCompression units

Low frequency currentsIntermittent pressure cuffs with varyingpressure and cycleFaradic currents, sinusoidal currents. Interferential currents, didynamic currentsEffects on skin and superficial tissue for infection and skin lesionUltraviolet rays

Diathermy agentsMercury vapor lamps, fluorescent or black lighttubeskromayer or cold quartz lamps Microwave, shortwave, infrared radiation ThermotherapyModes of useConductionConvectionRadiationTypes of ApplicationsWhirlpoolsHot tubsJacuzzisMoist heat packsParaffin bathsUltrasoundPhonophoresisDiathermy heatTransfer of EnergyEnergy moves from an area of HIGH concentration to an area of LOW concentration.RadiationConductionConvectionConversionEvaporationRadiationWhen the surrounding environment is hotter that the body the radiant heat is absorbed. No-contact is made.Short-wave DiathermyMicrowave DiathermyConductionDirect transfer of energy between two objects in physical contact with each other. Energy is transferred from the area of high temp. to the area of low temp.Ice packsMoist heat packsParaffinConvectionMuch like conduction, but the medium moves across the body causing variations.FluidotherapyWhirlpoolsConversionChanges other energy forms into Heat.UltrasoundMicrowaveLiniments or BalmsEvaporationHeat is absorbed by the liquid on the skins surface and cools the skin as it turns into a gaseous state.Vapocoolant spraysAlcoholFactors Affecting Transfer of EnergyDensity of MediumReflectionRefractionAbsorptionLaw of Grotthus-DraperHealing ProcessThree Phases:1. Inflammatory2. Fibroplastic/Proliferative3. Maturation/Remodeling23The healing process is a continum. Phases of healing overlap each other.Inflammatory Response PhaseInjury Destruction of tissue Cellular injury.Cardinal Signs of Cellular injury : redness, edema, tenderness (pain), increased temperature.There is a delivery of leukocytes and other phagocytes and exudate are present at the injured tissue.Vascular Reaction involves vascular spasm, formation of a platelet plug, coagulation & growth of fibrous tissue24Purpose of cellular reaction is to localize injury,and discard byproducts.Cellular injury causes altered metabolism and liberation of the inflammatory response Cellular reaction localizes injury, disposes of injury byproducts( blood and damaged cells) through phagocytosis, sets stage for repair. In addition there are local vascular effectsVascular: immediate response is vasoconstriction of the vascular walls that lasts for 5-10 minutes. Such spasm presses the opposeing endothelial linings together to produce a local anemia that is transitory and gives way to slowing of the flow in the dialated vessels, when then can progress to stagnation and stasis. The initial effusion of bloos and plasma lasts for 24-36 hours.The amount of exeudate and swelling are limited by the chemical mediators such as histamine, leucotaxin, and necrosin.Histamine is released from the damaged mast cells causing vasodilation and increased cell permeability, owing to swelling of the endothelial cells then separation between the cells. Leukotaxin is responsible for margination in which leukocytes line up along the cell walls. It also inc. cell permeability locally causing the passage of fluid and white bl cells through the cell walls by diapedesis to form exudate.Therefore vasodilation and active hyperemia are important in exudate( plasma) formation and supplying leukocytes to the injured area . Necrosin is responsible for phagocytic activity. The amount of swelling is directly related to the extent of vessel damage.Normally, platelets do not adhere to vessel walls. With injury to a vessel, the endothelium becomes disrupted, exposing collagen fibers. Platelets adhere to the collagen fibers to create a stickymatrix on the vascular wall to which addl platelets and leukocytes adhere and eventually form a plug. Plugs obstruct local lymphatic drainage and thus localize injury response.Inflammatory Response PhaseUp to day 6Clinically should see a decrease in edema and pain is still present.Modalities are used to : Control pain and decrease edema.Cryotherapy is still appropriate25Heating too soon is a bigger mistake than using ice. When swelling subsides consider contrast baths.Intermittant compression is appropriate to use the lymphatics to reabsorb the products of inflammation.After the intiial stage the pt. can start exercise, based on the injury and tolerance of pt.Clot formationTo form a clot fibrinogen must be converted to fibrinClot formation begins around 12 hours following injury and is completed by 48 hoursSummary:during the inflammatory stage the injured area is walled off, lasts 2-4 days.26The conversion occurs because the damaged cell releases a Pr- thromboplastin. Thromboplastin causes prothrombin to be Changed into thrombin which in turn causes the conversion of fibrinogen into a very sticky fibrin clot that shuts off the blood suply to the injured area.Fibroplastic repair phaseScar formation is referred to as fibroplasia. Begins within the first few hours following injury and may last 4-6 weeks.Breakdown of the fibrin clot allows the development of granulation tissue.Development of a new scar 27During this phase of helaing proliferative aand regenerative activity leading to scar formation and repair of the injured tissue follows the vascular and exudative phenomena of inflammation. At this time many of the inflammatory signs and symptoms subside. There may be some tenderness to touch and pain with stress to the injured site.At this time there is growth of endothelial capillary buds which is caused by the lack of O2. The wound now can heal aerobically. Along with the increased o2 comes an increase in bl fl that dleivers nutrients essential for tissue regeneration in the area.Granulation tissue consists of fibroblasts, collagen and capillaries.As the capillaries continue to grow into the area fibroblasts accumulate at the wound site arranging themselves ll to the capillaries. Fibroplastic cells begin to synthesize an extracellular matrix that contains collagen elastin and ground substance that consists of nonfibrous Pr- called proteoglycans, glycosaminglycans and fluid. At about day 6 or 7 fibroblasts also begin producing collagen fibers that are deposited in a random fashion throughout the forming scar. As the tensile strength inc. the number of fibroblasts diminishes to signal the beginning of maturation phase Maturation-Remodeling PhaseCan last over 1 year.Collagen remodels or realigns in accordance with the tensile forces placed on it28Here there is an ongoing breakdown and synthesis of collagen with a steady inc. in the tensile strength of the scar matrix. With inc. stress and strain the collagen fibers realign in a position of maximum efficiency ll to the lines of tension. The tissues gradually assume a normal appearance and function, although the scar is rarely as strong as the normal uninjured tissue. Usually by the end of 3 weeks a firm strong contracted nonvascular scar existsFACTORS THAT IMPEDE HEALINGExtent of injuryEdemaHemorr-hagePoor vascular supplySeparation of tissueMuscle spasmatrophyCorticoster-oidsKeloids Hypertroph-ic ScarsInfectionHumidity,Climate,O2 tensionHealth,Age,Nutrition29Extent of injury: Microtears (overuse) Macrotears (acute Trauma).Edema: Increased pressure retards the healing process.Hemorrhage: Presence of bl produces addl tissue damage.Poor vascular supply: Likely related to a failure I the delivery of phagocytic cells and also of fibrblasts necessary for formation of scar.Separation of tissue: Wounds with jagged separated edges must heal by 2nd intention with granulation tissue filling in.Muscle spasm: causes traction, separating ends and preventing approximation ischemia may result from this.AtrophyCorticosteroids: Early phases these inhibit fibroplasia, capillary proliferation and synthesis and increases tensile strength of the healing scar.Keloids and Hypertrophic Scars: Keyloids occur when the rate of collagen production exceeds the rate of collagen breakdown during the maturation phase of healing. ThisCauses hypertrophy of scar tissue esp. around the periphery of the wound.Infection; Bacteria in the wound can delay healing and may cause excessive granulation tissue and large deformed scars.Humidity, Climate, and Oxygen Tension: Humidity affects epithelization. Occlusive dressings stimulate epthilium to migrate 2x as fast without scab formation. The formation of a scab occurs with dehydration of the wound and traps wound drainage which promote infection. Keeping the wound moist provides an advantage for the necrotic debris to go to the surface and be shed.Oxygen tension relates to the neovascularization of the wound, which translates into optimal saturation and maximal tensile strength development. Circulation to the wound can be affected by ischemia, venous stasis hematomas, and vessel trauma.12. Health Age Nutrition: Skins elasticity dec. with age. DM& Arteriosclerosis affect healing. Nutrition is important for wound healing. VitC, K, A&E ( collagen synthesis); Zn, and Amino acids play critical roles in healing.

Structure of the skinThe skin is one of the largest organs of the body. It comprises about 16% of our body mass. The skin covers the body and protects the deep tissues. Its free surface is not smooth, but is marked by delicate groove

EpidermisComposed of keratinized stratified squamous epithelium, consisting of four distinct cell types and four or five layers Cell types include keratinocytes, melanocytes, Merkel cells, and Langerhans cells Outer portion of the skin is exposed to the external environment and functions in protection

Layers of the Epidermis: 1. Stratum Basale (Basal Layer) Deepest epidermal layer firmly attached to the dermisConsists of a single row of the youngest keratinocytes Cells undergo rapid division, hence its alternate name, stratum germinativum Layers of the Epidermis:2. Stratum Spinosum (Prickly Layer) Cells contain a weblike system of intermediate filaments attached to desmosomes Melanin granules and Langerhans cells are abundant in this layer 3. Stratum Granulosum (Granular Layer) Thin; three to five cell layers in which drastic changes in keratinocyte appearance occurs Keratohyaline and lamellated granules accumulate in the cells of this layer Layers of the Epidermis:4. Stratum Lucidum (Clear Layer) Thin, transparent band superficial to the stratum granulosum Consists of a few rows of flat, dead keratinocytes Present only in thick skin Layers of the Epidermis:5. Stratum Corneum (Horny Layer) Outermost layer of keratinized cells Accounts for three quarters of the epidermal thickness Functions include: Waterproofing Protection from abrasion and penetration Rendering the body relatively insensitive to biological, chemical, and physical assaults Cells of the Epidermis Keratinocytes produce the fibrous protein keratin Melanocytes produce the brown pigment melanin Langerhans cells epidermal macrophages that help activate the immune system Merkel cells function as touch receptors in association with sensory nerve endings Dermis Second major skin region containing strong, flexible connective tissue Cell types include fibroblasts, macrophages, and occasionally mast cells and white blood cells Composed of two layers papillary and reticular The Dermis helps us to control our body temperature: N.B A. On a cold day when the body needs to conserve heat, the Blood Vessels in the Dermis NARROW.Layers of the Dermis: 1. Papillary Layer Areolar connective tissue with collagen and elastic fibers Its superior surface contains peglike projections called dermal papillae Dermal papillae contain capillary loops, Meissners corpuscles, and free nerve endings Layers of the Dermis:

2. Reticular Layer Accounts for approximately 80% of the thickness of the skin Collagen fibers in this layer add strength and resiliency to the skin Elastin fibers provide stretch-recoil properties DERMIS . The dermis is composed of two layers: the papillary layer and reticular layer . The papillary layer is closest to the epidermis. Connective tissue here is less dense than in the reticular layer. There are numerous sections of blood vessels (arterioles, venules, and capillaries) in the dermis.Hypodermis The hypodermis is the innermost and thickest layer of the skin Subcutaneous layer deep to the skin Composed of adipose and areolar connective tissue The hypodermis is used mainly for fat storage. It invaginates into the dermis and is attached to the latter, immediately above it, by collagen and elastin fibres. It is essentially composed of a type of cells specialised in accumulating and storing fats, known as adipocytes. These cells are grouped together in lobules separated by connective tissue . END OF SESSIONQ & ATHANKS