Physical Agents and Modalities Lecture Notes PDF

PHYSICAL AGENTS AND MODALITIES Physical Agents are consist of energy and EFFECTS OF PHYSICAL AGENTS materials applied to patients to assist in their rehabilitation 1. Inflammation and healing (thermal) It includes heat, cold, water, p...

PHYSICAL AGENTS AND MODALITIES Physical Agents are consist of energy and EFFECTS OF PHYSICAL AGENTS materials applied to patients to assist in their rehabilitation 1. Inflammation and healing (thermal) It includes heat, cold, water, pressure, modify by changing the rates of circulation sound and electromagnetic radiation. and chemical reactions. (mechanical) control motion and alter fluid f low, and CATEGORIES OF PHYSICAL AGENTS electromagnetic agents alter cell function, particularly membrane permeability and 1. Thermal Agents transport. transfer energy to a patient to 2. Pain PAs can control pain by modifying pain increase or decrease tissue transmission or perception or by changing temperature. (hot packs, ice packs, the underlying process that is causing the ultrasound, whirlpool, diathermy) sensation. Using of hot and cold increases 3. Collagen extensibility and motion transfer of energy the skin will adapt restrictions collagen must be stretched to to the hot and cold packs so it must return soft tissue to its normal functioning be check every 5 mins. length. Therapeutic Ultrasound the px must 4. Muscle Tone alter muscle tone directly by not feel any heat or pain, the px altering nerve conduction, nerve sensitivity, must feel a vibration pero dapat wala or biomechanical properties of muscle or mafeel yung px in general. indirectly by reducing pain or underlying 2. Mechanical agents cause of pain. apply force to increase or decrease pressure on the body. (water, traction, compression, sound). Traction this uses force outside of the body (pulley force) 3. Electromagnetic Agents apply energy in the form of electromagnetic radiation or an electrical current. (UV radiation, infrared radiation, laser (light applied stimulation emission), diathermy, electrical current.) TENS ( Transcutaneous Electrical Nerve Stimulation) NMES ( Neuromuscular emission stimulation ) - AS, TENS, FES - Setting of ultrasound ( pulse, continuous, intermittent) - SWT (shortwave therapy) RAINE LEGASPI 1  Agonist muscles- prime movers Antagonist muscles - opposing to the agonists GENERAL CONTRAINDICATIONS AND PRECAUTIONS FOR PHYSICAL AGENT USE PREGNANCY- energy produced by the agent or its physiologic effects may reach the fetus. - These types of energy on fetal development usually are unknown and fetal development is adversely affected by many influences MALIGNANCY- if the energy produced by the agent may reach malignant tissue or alter the circulation to such tissue. PACEMAKER OR OTHER IMPLANTED Bawal ang heat sa cancer px kasi pwede DEVICES- the energy may alter functioni ng mag metastasis or dumami yung cancer of the device. cell. IMPAIRED SENSATION OR MENTATION- If mag increase yung temp tataas rin ang the limit for application of these agents is collagen. the patient’s report of the sensation of heat as comfortable or painful is used to guide TYPE 1 collagen- muscle, skin, bones, tendons, the intensity of treatment. Patient must be ligaments evaluated first. TYPE 2 collagen- Cartilage EVALUATION AND PLANNING FOR THE USE OF PHYSICAL AGENTS One should first check the physician’s referral, for a medical diagnosis of the patient’s condition and necessary precautions. Examination should include but not limited to, the patient’s history (information about the history of the current complaint, relevant medical history) and information about current and expected levels of activity and participation RAINE LEGASPI 2  INFLAMMATION PHASE SKIN ANATOMY Begins when the normal physiology of 1. Epidermis - outer layer that provides a tissue is altered by disease or trauma. protective barrier to injury. It is avascular. It Hyperemia - accounts for increased also prevents dehydration of underlying temperature and redness in the area od tissue acute inflammation. It is controlled by 2. Dermis - vascularized layer. Composed of neurogenic and chemical mediators. collagen and elastin fibers tissues. Nerve Vascular response - damaged vessels endings are located here. respond rapidly with transient constriction in 3. Hypodermis - aka the subcutaneous an attempt to minimize blood loss. layer/superficial fascia. Consists of well Edema - accumulation of fluid within the vascularized, loose areolar connective extravascular space and interstitial tissues. tissue and adipose tissue. Fat storage for Swelling is the clinical manifestation. insulation and cushioning. Transudate fluid first forms edema during inflammation with low protein, lipid and cellular debris. Exudate fluid are cloudy, 1. INFLAMMATION PHASE ( 1 - 6 DAYS ) An with high lipids and cellular debris. immediate protective response to injury. Hemostatic response - controls blood loss Hyperemia - increased temperature at the when vessels are damaged or ruptured site of injury. Marks the beginning of the inflammatory responses. 2. PROLIFERATION PHASE (3 - 20 DAYS ) The wound is covered, and the injured site starts to regain initial strength 3 3. MATURATION PHASE ( DAY 9 - ONWARDS ) Longest phase in the process. Scar becomes whiter as collagen matures predominantly collagen I PROLIFERATION PHASE In this phase, the wound is covered and the injured site starts to regain initial strength. 1. Epithelialization - re-establishment of the epidermis; 48 hours if wound is superficial, but can last longer for deeper wounds 2. Collagen production RAINE LEGASPI 3  3. Wound contraction - mechanism for EFFECTS OF PHYSICAL AGENTS repairing an injured area; begins at 5 days and peaks at 2nd week. Pulls edges of injured site which is then replaced by scar Generally assist during the inflammation tissue. If uncontrolled, can result into a phase (lasts for 1 to 6 days) by reducing contracture. circulation, reducing pain, reducing 4. Neovascularization - development of new enzyme activity rate, controlling motion blood supply to the injured area. Occurs as and promoting progression to the a result of angiogenesis(formation of new proliferation phase blood vessels). Assist in the proliferation phase (starts within 1st 3 days, lasts for 20 days) by MATURATION PHASE Longest phase. Scar increasing circulation and the enzyme becomes whiter as collagen matures; activity rate by promoting collagen predominantly collagen I because type I is stronger deposition and progression to the and tensile strength increases faster than mass. remodeling phase. In the maturation phase (starts 9 days PHAGOCYTOSIS- cell eating after initial injury, lasts to 2 years), PINOCYTOSIS- cell drinking generally assist by altering the balance of Ca3, C5a, PAf- sila nagppipigil para magka inflammation. collagen deposition and resorption and improving the alignment of new collagen CLOTTING FACTORS fibers. First Person Told Cancer Leads PHYSICAL AGENTS FOR TISSUE HEALING Sickness, Another Chap Said Protein High Fat 1. Factor I: Fibrinogen (First) Initial injury - goal is to prevent further 2. Factor II: Prothrombin (Person) injury or bleeding and to clean away 3. Factor III: Tissue thromboplastin or wound contaminants if the skin has been Tissue factor (Told) broken. 4. Factor IV: Calcium (Cancer) Cryotherapy helps control bleeding by 5. Factor V: Labile factor (Leads), limiting blood flow to the injured area by Proaccelerin constricting vessels and increasing the 6. Factor VI: Accelerin (Remember: blood’s viscosity. has been eliminated as it plays no Thermotherapy is contraindicated role in blood coagulation) because it can increase bleeding. Non 7. Factor VII: Stable factor (Sickness), Immersion can be used to clean the Proconvertin injured area if the skin has been broken 8. Factor VIII: Anti-hemophilic factor A and the wound has become (Another) contaminated. Only neutral-warm or 9. Factor IX: Christmas factor (Chap), cooler water should be used. Anti-hemophilic factor B Acute inflammation - goal is to control 10. Factor X: Stuart power factor (Said), edema, pain, bleeding and the release Autoprothrombin III and activity of inflammatory mediators. 11. Factor XI: Plasma Thromboplastin Thermotherapy, intermittent traction, and Antecedent or PTA (Protein) motor-level ES are contraindicated. 12. Factor XII: Hageman factor (High), Contrast baths can be used to control or Glass or contact factor reduce edema. 13. Factor XIII: Fibrin stabilizing factor or Cryotherapy and compression can also Fibrinase (Fat) help control bleeding. Chronic inflammation - goals are to prevent or decrease joint stiffness, control Edema - pitting is palpable, Non-pitting is hindi pain, increase circulation, and promote palpable. progression of healing. Most effective are RAINE LEGASPI 4  thermotherapy and motion. Cryotherapy is Vascular Supply Movement generally not recommended because it Immobilization may be used to aid early can increase the associated joint stiffness. healing and repair because early movement Proliferation - to control scar tissue of a newly injured area may delay healing. formation, ensuring adequate circulation, Continuous passive motion with strictly maintaining strength and flexibility. controlled parameters is often used to Thermotherapy, electrotherapy, remobilize and restore function safely. compression, water immersion, exercise or contrast baths. The water environment SYSTEMIC FACTORS reduces loading thus may decrease potential trauma to weight bearing structures. Age Wound closure occurs more rapidly in Maturation - to regain or maintain pediatric patients than in adult patients strength and f lexibility and to control the because the physiological changes and formation of scar tissue. Treatment should cumulative sun exposure that occur with focus on reversing any adverse effects. aging can reduce the healing rate. Strengthening may be more effective with Disease For example, poorly controlled ES, EMG biofeedback, and water diabetes mellitus impairs collagen synthesis exercise. which increases the risk of infection as a result of a dampened immune response. Immunocompromised patients are prone to FACTORS AFFECTING THE wound infection because they have an inadequate inflammatory response. HEALING PROCESS Medications For example, antibiotics can prevent or fight off infection, which can help speed healing but they may have toxic LOCAL FACTORS effects that inhibit healing. Nutrition Deficiency of important nutrients can result in delayed or impaired healing. Type, Size, and Location of the Injury This occurs because physiological stress Injuries located in well-vascularized tissue from the injury induces a hypermetabolic heal faster than injuries in poorly state. Hence, the slower healing. vascularized areas. Those injuries that may be caused by arterial obstruction or excessive pressure may heal more slowly PAIN AND PAIN MANAGEMENT as well. Smaller wounds heal faster and surgical incisions. Pain is the most common reason patients Soft tissue injuries over bones tend to seek medical attention and rehabilitation. adhere to the bony surfaces, preventing Managing pain using physical agents and contraction and adequate opposition of the restoring function through active therapy are edges sometimes seen as competing priorities in Infection Can reduce collagen production rehabilitation. and increase collagen lysis, prevent or Nociception is “the neural process of delay healing, and encourage excessive encoding noxious stimuli granulation tissue formation. There are three dimensions of pain Vascular Supply Depends largely on the experience: availability of a sufficient vascular supply. Sensory discriminative, Decreased oxygen tension resulting from a motivational-affective, and cognitive compromised blood supply can result in evaluative. inhibition of fibroblast and collagen The dimensions and characteristics of pain synthesis leading to decreased tensile experiences are influenced by contextual, strength of the injured area. emotional, environmental and cognitive External Forces factors. RAINE LEGASPI 5  Gate control theory of pain by Melzack & ACUTE PAIN Wall Direct result of actual injury. Treatment is u Melzack and Wall proposed that a gating sual ly pharmacological. Non mechanism exists within the dorsal horn of pharmacological may be patient education. the spinal cord which explains why thoughts Chronic pain Management should begin and emotions influence pain and perception. with identifying and weighing the Small nerve fibers (pain receptors) and pathophysiological pain mechanisms. large nerve fibers (normal receptors) synapse on projection cells (P), which go the spinothalamic tract to the brain, and Preventing acute pain from becoming chronic inhibitory interneurons (i) within the dorsal horn. Physical agents or other non pharmacological techniques that help reduce pain intensity may also be helpful. Signs that certain sensitivity are not resolving yet, immediate address should happen. Chronic pain Management should begin with identifying and weighing the pathophysiological pain mechanisms. Preventing acute pain from The interplay among interconnections becoming chronic determines when painful stimuli go to the brain: When no input comes in, the inhibitory Primary chronic nociceptive pain neuron prevents the projection neuron from sending signals to the brain (gate is closed) Normal somatosensory input happens when This will usually be felt at or near the site of there is more or only large-fiber stimulation. injury although it may be referred to other Both the inhibitory neuron and the projection areas of the body. Pain may be use as a are stimulated, but the inhibitory neuron guide to when the tissue needs to rest. prevents the projection neuron from sending signals to the brain (gate is closed) Nociception (pain receptors) happens when Peripheral neuropathic pain there is more small-fiber stimulation or only small-fiber stimulation. This inactivates that Arises as a direct consequence of a lesion inhibitor neuron, and the projection neuron or disease affecting the peripheral nerves. sends signals to the brain of pain (gate is Typically manifests as nerve trunk pain and open) dysesthetic pain. Descending pathways from the brain close the gate by inhibiting the projection neurons and diminishing pain and perception. Central sensitization This theory does not tell us everything about pain perception, but it does explain some things. If you rub or shake your hand after Often has no clear anatomical correlation. you bang your finger, you stimulate the Frequently associated with fatigue and normal somatosensory input to the projector sleep disturbance, etc. The approach to this neurons. This closes the gate and reduces can be simplified to “desensitization the perception of pain. RAINE LEGASPI 6 Psychosocial pain 4. Radiation- reheating a cold w/o direct contact , energy transferred the electromagnetic wave Cognition, emotion, context and 5. Evaporation- Changes heat due to loss of environment play a dominant role in heat. triggering a patient's pain. The distinguishing factor between CS and PP is that allodynia and hyperpathia are not THERMOTHERAPY- THE THERAPEUTIC provoked by psychosocial factors. APPLICATION OF HEAT. PAIN MANAGEMENT EFFECTS OF HEAT Visual analog and numerical scales HEMODYNAMIC EFFECTS Semantic differential scales NEUROMUSCULAR EFFECTS METABOLIC EFFECTS Other measures ALTERED TISSUE EXTENSIBILITY Physical Agents Pharmacological Approaches Cognitive-Behavioral Therapy CLINICAL INDICATIONS FOR SUPERFICIAL HEAT Comprehensive Pain Management Programs PAIN CONTROL INCREASED RANGE OF MOTION AND DECREASED JOINT STIFFNESS INTRODUCTION TO THERMAL ACCELERATED HEALING AGENTS INFRARED RADIATION FOR PSORIASIS The therapeutic application of thermal CONTRAINDICATIONS FOR THERMOTHERAPY agents results in the transfer of heat to or from a patient’s body and between tissues RECENT OR POTENTIAL HEMORRHAGE and fluids of the body THROMBOPHLEBITIS Heat transfer occurs by conduction, IMPAIRED SENSATION OR IMPAIRED convection, conversion, radiation or MENTATION evaporation. Heating agents transfer heat MALIGNANT TISSUE away from the body INFRARED IRRADIATION OF THE EYES Specific heat - amount of energy required to raise PRECAUTIONS FOR THERMOTHERAPY the temperature of a unit mass of a material by one degree. ACUTE INJURY OR INFLAMMATION PREGNANCY Modes of heat transfer: IMPAIRED CIRCULATION OR POOR THERMOREGULATION EDEMA METAL IN THE AREA 7. OVER AN OPEN 1. Conduction - The transfer of heat thru WOUND direct contact, pag nag init ng water mag OVER AREAS WHERE TOPICAL transfer yung heat sa pot then it will reach COUNTERIRRITANTS HAVE RECENTLY the water. BEEN APPLIED 2. Convection - Transfer of heat from one CARDIAC INSUFFICIENCY place to another due to mvmt of fluid gas or DEMYELINATED NERVES air. 3. Conversion- process of turning non-thermal into heat. RAINE LEGASPI 7 ADVERSE EFFECTS OF THERMOTHERAPY BURNS FAINTING BLEEDING SKIN AND EYE DAMAGE FROM INFRARED Application techniques Evaluate and set goals Determine whether thermotherapy is the most appropriate intervention Determine that thermotherapy is not contraindicated Select the heating agent Apply the agent Inspect treated area Document Explain the procedure and reason for application RAINE LEGASPI 8