Acute. Chronic. Tendinopathy: Acute vs. Chronic Differences in Anatomy, Symptoms & Treatment

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1 Tendinopathy: Acute vs. Chronic Differences in Anatomy, Symptoms & Treatment Science and Management Symposium SAM 2018 Marlene Reid, DPM FACFAS, FACFAO, FASPS Tendinopathy Tendinopathy is a failed healing response of the tendon, with haphazard proliferation of tenocytes, intracellular abnormalities in tenocytes, disruption of collagen fibers, and a subsequent increase in noncollagenous matrix. The term tendinopathy is a generic descriptor of the clinical conditions (both pain and pathological characteristics) associated with overuse in and around tendons. Acute Overuse Sudden/gradual onset pain Edema, erythema Superficially tender Tendinitis Chronic Long term Deeper pain Aching pain Less related to activity Tendonosis Acute vs. Chronic: Understanding the differences 1

2 Tendonitis: Acute Reaction to excessive force or load beyond its capacity to bear causing traumatic strain or tear Recent onset of pain with localized edema, erythema due to inflammation History of acute injury or repetitive injury Pain from passive ROM Pain with motion against resistance Tendonitis: Basic Clinical Presentation is not enough for effective treatment! Phase of Healing: Determines Treatment I. Acute Inflammatory Response Cellular Response: First hours to days Hemostasis: vasoconstriction, platelets, coagulation, clot formation Inflammatory Reaction: vasodilation and cellular infiltration, degradation and phagocytosis Acute Symptoms: Edema, erythema Decrease muscle function from splinting pain with palpation from cellular rxn pain from muscle spasms pain with ROM pain with stretching pain with or without resistance Phase of Healing: Determines Treatment II. Subacute/Regeneration/Repair Collagen Proliferation: Day 2-4 thru 2 to 3 weeks Angiogenesis, granulation, collagen Granulation tissue forms Subacute Symptoms: Decrease edema and tenderness Decrease muscle function from guarding and weakness Easily reinjured due to fragile granulation tissue Pain with stretching initially then decreases as collagen builds Fills defect and produces new capillaries Fibroblasts produce collagen Early granulation tissue is very fragile Collagen (type III) increases tensile strength 2

3 Acute Presentation typical to ER or PCP Subacute Presentation typical to podiatrist Standard Treatment: RICE Reduce edema Reduce mobility of tendon and muscle Considerations: NSAID use - controlling vs. allowing inflammation When does the subacute phase end and the remodeling phase begin?? Phase of Healing: Determines Treatment Phase III: Remodeling and Maturation Chronic Inflammation Scar Tissue Formation and maturation 2-3 Weeks to years Chronic phase of healing no inflammation Collagen Type III remodeled into Type I Collagen fibers realign Tensile Strength increases Scar tissue has 80% strength of normal due to irregular arrangement of fibers When to encourage mobilize?? Wolff s Law Bone grows in response to mechanical stress and tissue remodeling is dependent on the forces it is subjected to. Proper amounts of mobilization are required for normal healing and prevention of adhesions, BUT Excessive immobilization can cause excessive amounts of collagen, forming crosslinks that adhere to adjoining structures and cause further pain and degenerative changes. Do Some Immobilize Too Much? Do Some Immobilize Too Little? When is the proper time to start physical therapy? 3

4 When to Immobilize??? Mobilization too early in the rehabilitation (during Phase 2 of healing) program can interfere with healing if the tissue is reinjured before it is properly healed causing chronic irritation and a prolonged inflammatory response Mobilization too late in rehabilitation can cause adhesions, scar tissue and continued pain with resistance as the tendon can no longer bear its original load. Chronic Inflammation develops! Tendonosis is most commonly thought of as chronic tendonitis. Tendonosis is a relatively new diagnosis with much confusion. It is not known whether substages of tendonosis exist and whether it is an ongoing process or an end-stage. Rheumatology 2001; 40: Tendonosis is a term referring to intratendinous degeneration due to atrophy Tendinopathy=failed healing response, Lower Extremity Review 2013;Vol 5: Defining Tendonosis Tendonosis Intratendinous hypertrophyic collagen degeneration Non-inflammatory avascular Fatty degeneration atrophy Fiber disorientation Scattered vascular ingrowth local necrosis or calcification Very different from tendonitis!! Decreased function of the tissue Continued pain with use Palpable nodule Pain with after resistance or fatigue Persistent pain Duration of symptoms 4

5 Could it be caused by over healing - limiting inflammation and mobilization? Or is it caused by under healing and not allowing the enough supportive measures? Is it actually incomplete healing that needs a kick start? Tendonosis : Leftover tenopathy Other Considerations in Tendon Injury Lower Extremity Review, 2013 Volume 5: Genetic factors Family history of Achilles x5 risk for injury Specific genes over or under expressed-9 studies representing collagen protein encoding, matrix metaloproteinases (MMPs) and inflammatory signaling molecules COL5A gene encodes type 1 collagen fibrils Metabolic Considerations Diabetes>advanced glycation end products links with collagen fibers>increase degeneration Hormonal Influences in SFT Injury Conflicting Findings: Increased estrogen > lower collagen synthesis which may change structure and function Estrogen may>dec. firoblast biosynthesis>may decrease collagen density ACL rupture decreased with inc. estrogen Estrogen limits skeletal muscle fiber diameter 5

6 Fatty Degeneration of Tendonosis Heel Pain: Fasciitis vs. Fasciosis Symptoms drastically change after a few months Acute must be treated differently from chronic! Plantar Fasciitis: A Degenerative Process (Fasciosis) Without Inflammation, Harvey Lemont, et al. JAPMA, May/June 2003 Histiological Findings from heel spur surgery cases show no evidence of inflammation in all samples examined. Many samples showed fiber fragmentation and myxoid degeneration Podiatry Today September 2007 Steroid Injections: Are They Over-utilized in Athletes?..uses cortisone for chronic inflammatory conditions inflammatory conditions with a long, ongoing history will not have healthy tissue and the corticosteroid t id injection will cause further tissue degradation and possible rupture. Cortisone Controversy 6

7 Tendonosis is chronic pain characterized by hypovascularity and collagen degeneration that requires a treatment option designed specifically for these conditions. Treatments must Address Collagen Repair and Vascularity NOT inflammation Treating Tendonosis: Treatment should kick start an inflammatory process to convert chronic to acute Traumeel Injections: Homeopathy Prolotherapy: Proliferation of tissue with dextrose solution injection inflammatory response to the irritant Needling ESWT Coblation - Bipolar Radiofrequency (RF) Electrosurgery Platelet Rich Plasma (PRP) Amniotic Tissue injections Open Debridement and excision of necrotic tissue Identify the stage of healing the tendon is in. Providing supportive measures to allow the normal inflammatory response to occur. Initiating mobilization to tolerance allowing the tendon to function to the ability it is able to while encourage proper tissue modeling and repair. Recognizing when healing is chronic and needs to be converted back to active healing. Prevention of Tendonosis: Using What We Already Know 7

8 Tendonosis vs. Tendonitis: Understanding the difference between acute and chronic tendinopathy! Thank you 8