Physical Therapy Foundation II week 1 [Physical agents, inflammation, and tissue repair]

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4 cardinal signs of Inflammation phase 4 simultaneous processes of proliferation phase A-delta fibers peripheral nerve pathways Acute pain characteristics

heat and redness(increased vascularity), swelling (blockage of lymphatic drainage) pain (physical pressure, chemical irritation of pain sensitive structures). epithelialization, collagen production, wound contracture, neovascularization.

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Chronic inflammation cellular response

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primary cells present are mononuclear cells (lymphocytes, macrophages, & monocytes), results of immunological and nonimmunological factors, results in increased fibroblast proliferation, collagen production, and scar tissue and adhesion formation. the simultaneous progression of active inflammation, tissue destruction, and healing. Result following acute inflamm. Caused by cumulative trauma and/or immune repose to an altered host tissue or foreign object, or the resulting from an autoimmune disease (RA). persist beyong the normal time for tissue healing, usually the result of activation of dysfunctional neurological or psychological responses. May start as acute pain, lasting longer than 3-6 months, 1/3 of US population has this type of pain. Nociceptive pain: mechanical, chemical, or thermal stimuli and associated ongoing tissue damage (arthritis). Neuropathic pain: result of peripheral or CNS dysfunction without ongoing tissue damage (diabetic neuropathy). Mixed pain: multiple or uncertain pathophysiology (recurrent HA's). made of fibroblasts, provides increased strength to the wound, facilitates the movement of other cells (endothelial cells, macrophages) in the wound healing process. 21, 6 weeks), day 7- significant amount of collagen, day 21- maximal production of collagen, but only 20% strength, 6 weeksabout 80% of long term strength. goal of treatment, effects of a particular PA, review contraindications/precautions, evidence, cost/convenience/ and availability, most effective treatment parameters, properly integrate into the rehab program, assess and modify as indicated. location, quality, severity, timing, factors better or worse, setting, quantifies, assessment of how pain affects function, activities, and participation.

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20% afferent nerve fibers (conduct impulses from periphery toward CNS), Group III fferents, small myelinated, fast transmission of pain, high intensity of mechnial stimulation, heat, cold, or sharp. less than 6 months duration for which an underlying pathology can be identified. Combo of unpleasant sensory, perceptual, and emotional experiences. Viewed as biologically meaningful, useful, and timelimited. Mediated through rapidly conducting pathways. usually related to degree of tissue inflammation, damage/ destruction in area where pain is felt. Generally well-localized and defined. Pain from skin (superficial) is more well-localized and accurate. Pain from muscles is more diffuse. with autonomic, psychological, emotional and behavioral reactions. With increased: muscle tone. HR, BP, skin conductance, and sympathetic nervous system activity. Felt in response to actual or potential tissue damage that resolves when tissue damage or the threat of damage passes. Response to noxious stimuli provoked by actue injury or disease. afferent nerve fibers (conduct impulses from periphery toward CNS), 80%, Group IV afferents, small unmyelinated, slow transmission of pain, noxious levels of mechanical, thermal, and chemical stimulation. Dull, long-lasting, aching. delivery of leukocytes to injured area to rid of bacteria and debris of phagocytes, Macrophages (the most important cell in the inflammatory process) produce a number of products critical to the healing process (e.g collagenase, coagulation factors, box 3-1).
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Chronic inflammation results

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Chronic pain characteristics

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Acute pain intensity and location

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Chronic pain pathophysiology

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Acute pain is associated

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Acute Pain Response

Collagen production consists of and purpose Collagen production timeline (Day 7 Considerations when choosing a physical agent

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C fibers peripheral nerve pathways

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Cellular response (inflammation phase days 16)

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Documenting pain

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Effects of physical agents Effusion

inflammation and healing, pain, collagen extensibility and motion restrictions (fig 14.), muscle tone. swelling of fluid in a joint. All effusion are swelling but not all swelling is an effusion. electromagnetic fields (ultraviolet, laser), electric currents the process of leukocyte migration from the blood vessels into the perivascular tissues. pain is modulated at the peripheral, spinal cord, and cortical levels by endogenous neurotransmitters, have same effects of opiates. the reestablishment of the epidermis is active early with a superficial wound, occurs late in deep wound, provides protective barrier (prevents fluid and electrolyte loss, decrease risk of infection,) local factors, external factors, and systemic factors. pain is modulated at the spinal cord level by inhibitory effects of innocuous afferent input, severity of pain is determined by balance of excitatory and inhibitory input to T cells, TENS devices. early movement of an acute injured area may delay healing, more often controlled early movement is recommended to avoid the adverse effects of the immobilization, continuous passive motion (CPM). thermal, electromagnetic, mechanical, etc and used to impact the healing process. soft tissue injuries over boney areas tend to develop more adhesions and impacts contraction and healing. smaller wounds heal faster than larger wounds, surgical incisions heal faster than wounds caused by blunt trauma. well vascular zed tissue heals faster than poorly vascularized tissues, injuries in areas of ischemia (excessive pressure) heal more slowly. the most problematic local factor that affects healing, 50% are due to local infection, affects collagen metabolism which reduces collagen production and increased lysis, prevents / delays healing which causes excessive granulation tissue formation (fibrous connective tissue).

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Healing Local factors vascular supply Healing of cartilage timeframe

decreased O2 tension due to compromised blood supply, can result in inhibition of fibroblast migration and collagen synthesis (decreased tensile strength, increased risk of infection). within 2 weeks, differentiation of granulation tissue into chondrocytes. Within 2 months , normal appearing cartilage can be seen. The new cartilage has a low proteoglycan content and is predisposed to degenerative and erosive changes. inflammation 1st 72 hours, collagen synthesis 1 week, fibroblasts predominant 2 weeks, alignment: early on perpendicular orientation to the tendon's long axis. At day 10, more parallel and over the next 2 months continued gradual transition of parallel alignment. Control mobilization of repaired tendons accelerates and increases the strength of the repair. capsular and extracapsular ligaments stimulate an adequate repair process. Intracapsular ligaments do not stimulate the same effect (synovial environment, limited neovascularization, fibroblast migration), mature repaired ligamentous tissue is 30-50% weaker than uninjured tissue but is larger. direct trauma and myositis ossificans: calcification of muscle. in older individuals wounds heal more slowly, decreased density and cross-bridging of collagen (reduced tensile strength), the elderly have a decreased # of mast cells and fibroblasts and a lower rate of epithelialization. DM leads to impaired collagen synthesis. PVD leads to decreased local blood supply. Neuropathies lead to increased risk of trauma, decreased ability to heal. Corticosteroids (prednisone) block the inflammatory cascade, inhibiting many pathways involved in inflamm. NSAIDS (IB) less of an impact on the inflammatory process, can cause vasoconstriction and suppress the inflammatory response. deficiencies can result in delayed or impaired healing. Injury creates a hypermetabolic state, if an insufficient amount of "fuel" is available, the healing process is slowed.

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Electromagnetic agents Emigration The Endogenous Opiod system Epithelization

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Healing of tendons

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Factors affecting the healing process Gate control theory

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Healing on ligaments

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Healing external factors movement

Healing on skeletal muscle Healing systematic factor AGE

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Healing external factors physical agents Healing local factor location Healing local factor size Healing local factor type

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Healing systemic factors DISEASE Healing systemic factors MEDS

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Healing local factors infection

Healing systemic factors NUTRITION

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Hemostatic response occurs in what phase and consists of Hemostatis response reactions Highest to lowest priority

Inflammation phase (day 1-6), hematomaaccumulation of blood in a tissue or organ, hemarthrosis- bloody fluid in a joint .

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Maturation phase orientation of fiber theories

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retraction and sealing off of blood vessels, platelets form clots, assit in forming fibrin lattice, fibrin lattice serves as a source of tensile strength of the wound. 1A. Primary underlying problem, 1B. Problem most likely to respond to treatment, 2. Treatments that address more than one problem simultaneously, 3. Symptomatic treatment only. mediated by cellular an humoral factors (e.g antibodies, hormones, cytokines), activation of the complement system resulting in increased vascular permeability, stimulation of phagocytes, and acts as a chemotatic (cell movement away from chemicals) stimuli for leukocytes. acute: lasts no more than 2 weeks, subacute: more than 4 weeks, chronic: lasts months or years. restore function by eliminating the pathology or physical insult, replace damaged or destroyed tissue, and promote regeneration of normal tissue structure. limited ability to heal due to lack of lympahtics, blood vessels, and nerves. Injuries to the articular cartilage alone: limited response to injury generally fails to heal the defect and rarely resolve. Injuries to articular cartilage and subchondral bone: the vascularization of the subchondral bone allows for the formation of a fibrin clot (fibrin-fibronectin gel) allowing the inflammatory cells access. the lining of blood vessel walls by neutrophils (white blood cells). over 27 different types on collagen, type Iprimary collagen in bone, skin, tendon, and mature scars, type II- predominant collagen in cartilage, also found in gastrointestinal tract and adult blood vessels, collagen synthesis and lysis can last up to 12-24 months after injury. the longest phase in the healing process, goal is to restore the prior function of the injured tissue, the rate of maturation and the final physical characteristics of the scar is determined by (fiber orientation, balance of collagen synthesis and lysis).

induction theory- scar attempts to mimic the tissue it is healing, dense tissue leads to dense, highly crosses linked scar. Tension theoryinternal/external stresses during this phase determine final structure. visual analog and numeric scales, comparison with a predefined stimulus semantic differentiated scales, other measures. traction, compression, water (whirlpool), sound (ultrasound) pain receptors, peripheral nerve pathways, sympatheic nervous system influences, the role of substance P. based on biopsychosocial model of pain, address multiple facets of chronic pain with multidisciplinary approach, overall results in increased functional activity levels, reduced pain behaviors, and decreased use of medical interventions. generation of new vascular network, anastomosis (connection of normally separate parts of spaces so they intercommunicate to exiting vessels), coupling of vessels in the injured area. development of new blood supply, this occurs as a result of angiogenesis (the growth of new blood vessels). free, peripheral nerve endings, different conc around body, present in almost all types of tissue, activated by intense thermal, mechanical or chemical stimuli, when activated release neuropeptides including substance P. an experience bases on a complex interaction of physical and psychological processes. An unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such damage. parhmocological, physical agents, multidisciplinary pain treatment programs. Warning sign, protect the body from damage, activation of noxious receptors of noxious stimuli (nociception) and the sensory experiences, suffering, and alteration in behavior.

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Measuring pain

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Mechanical agents Mechanisms of pain reception and transmission Multidisciplinary pain treatment programs

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Immune reponse (inflammation phase days 16)

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Inflammation categories Inflammation phase goals

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Neovascularization 3 mechanisms

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Limited healing on cartilage

Neovascularization is and occurs Nociceptors

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Margination Maturation phase (Day 9 and on) consists of

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Pain definitions

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Pain management approaches Pain purpose

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Maturation phase (Day 9 and on) purpose

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Pain types Pavementing Pharmacological approaches

acute, chronic, referred. the layering of cells on the endothelial lining of vessels. systemic analgesics, nonsteroidal antiinflammatory drugs (NSAIDS), acetaminophen, opoids, antidepressants, spinal analgesia, local injection, other. inflammation phase (1-6 days), proliferation (3-20 days), maturation (day 9 and on). relive pain directly, moderate inflammatory mediators (timing/control), modulating pain at spinal cord level, alternating nerve conduction (slow process), increasing endorphin levels, indirectly reduce pain (traction), help to restore underlying cause of pain. thermal, mechanical, electromagnetic pregnancy, malignancy, pacemakers, impaired sensation and mentation. to cover the wound and impart strength to the injury site, involves both epithelial cells and connective tissues, connective tissue is made up of fibroblast, ground substance, and fibrous strands- provides structure for other tissues.

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Role of Substance P

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Phases of inflammation & healing Physical agents

neurotransmitter, involved in transmission of neuropathic and inflammatory pain, cane xcite pain transmitting neurons, appears to be involved in sensitization of pain transmitting neurons and in the development of hyperalgesia (increased sensitivity to noxious stimulation), meds to control pain can inhibit sunstance P or using antagonists (poor results). Vitamin A- slowed epithelialization, collagen synthesis & cross linking. Vitamin B- decreased collagen formation (B1), decreased tensile strength and reduced fibroblast number (B5). Vitamin C impaired collagen synthesis, increased capillary rupture and increased risk of infection. 1. Impaction, 2. Induction, 3. Inflammation, 4. Soft callus, 5. Hard callus, 6. Remodeling. a component of autonomic nervous system (ANS), "fight or flight", increases in HR, BP, sweating , etc., Normally activated by acute pain or injury, abnormal activation leading to hyperactive response (may increase or maintain pain), RSD (reflex sympathetic dystrophy) CRPS: complex regional pain syndrome. deep heating, superficial heating, and cooling agents, hyperemia (increase of blood in an area), vasoconstriction followed by vasodilation (capillaries, postcapillary venules & lymphatics), vasodilation mediated by chemical mediators (histamine, bradykinin, prostaglandins), Slowing of blood flow, Margination, pavementing, and emigration of leukocytes, Accumulation of fluid in interstitial tissues leads to edema. final mechanism for injury repair, pulls edges of wound together (shrinks defect), begins 5 days after injury and peaks after about 2 weeks, myofibroblasts are the primary cells responsible for this process, "picture frame" theory of wound healing (fig 3-13), uncontrolled wound contracture leads to contracture.

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Specific nutritional deficiencies

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Physical agents Precautions for PA use Proliferation phase purpose (days 3-20)

Stages of bone fracture healing Sympathetic nervous system influences

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Referred pain 3 ways

1. Nerve to its innervation, 2. One area to another from same dermatome, 3. One area to another from same embryonic segment. felt at a location distance from its source, can be referred from one joint to another (Hip OA to knee), Peripheral nerve to distal innervation (L5S1 nerve root to lateral leg), Internal orga to area of MS tissue (spleen to left shoulder). assess and analyze the presenting problem. Know when Pas can be an effective component of treatment. Know the level of skill required for the application of different physical agents. Optimize the use of the skill levels of different practitioners. Use home programs when appropriate. Treat in groups when appropriate. Reassess pateitns regularly to determine the efficacy of the treatment provided. Adjust the plan of care according to the finding of reassessments.

Thermal agents Vascular response (inflammation phase day 1-6)

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Referred pain characteristics

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Requirements for cost-effective use of physical agents

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Wound contracture