Lateral and Medial Epicondylitis Ian S Rice MD Sports Medicine Orthopedic Surgeon

Outline Epidemiology Anatomy Biomechanics Pathophysiology Diagnosis Treatment Research

Lateral Epicondylitis Tennis Elbow

History First described in 1873 by Runge Tendinosis not inflammatory condition Affects common attachment of extensor muscles of forearm to lateral epicondyle of humerus Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64 Van Hofwegen, C., et al. (2010) Clin Sports Med 29: 577-97

Epidemiology Incidence 1%-3% adults per year in UK 10-50% of people who play tennis regularly, Male > Female Lateral 4-7 times more common than Medial 35 – 55 years of age Male = Female in general population Dominant arm > Non-dominant Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64 Van Hofwegen, C., et al. (2010) Clin Sports Med 29: 577-97

Anatomy Common Extensors: Radial  superficial sensory + deep  PIN Extensor Carpi Radialis Brevis* Extensor Carpi Radialis Longus Extensor Digitorum Extensor Carpi Ulnaris Radial  superficial sensory + deep  PIN Ulnaris is reported to vary in origin-most likely originate more proximally along anterior aspect of supracondylar ridge Lateral Collateral Ligament: lateral ulnar collateral ligament, radial collateral ligament PIN inters Supinator muscle (Radial Tunnel): compression in refractory cases of lateral epicondylitis = Radial Tunnel Syndrome; coexist in up to 5% Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64 Van Hofwegen, C., et al. (2010) Clin Sports Med 29: 577-97

Anatomy Radial Collateral Ligament Lateral Ulnar Collateral Ligament Annular Ligament

Biomechanics: Extensor Group Eccentric contraction of ECRB Excessive/repetitive use extensors or supinator Tennis, typing, piano, manual work Risk factors in racquet sports: Incorrect technique Extended duration of play Frequency of play Size of handle Racquet weight Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Pathophysiology Paucity of inflammatory cells Gross: Grayish, homogenous, edematous and friable tissue Tendinosis  degenerative process Rate of stretching exceeds tolerance  microtears  tendinosis Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64 Van Hofwegen, C., et al. (2010) Clin Sports Med 29: 577-97

Histologic Stages of Microtrauma 1: Acute inflammatory response Sometimes resolves 2: Angiofibroblastic hyperplasia (increased concentration of fibroblasts, vascular hyperplasia, disorganized collagen) Hypercellularity in both organized and unorganized fasion Most common stage of presentation for treatment 3: Structural failure of tendon with partial of complete rupture 4: Features of stage 2 or 3 plus fibrosis, soft calcification within collagen and hard osseous calcification Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Pathophysiology: Microscopy A: Normal Tendon w/ uniform collagen B: Diseased tendon: Neovascularization, , disordered collagen, mucoid degeneration Normal Tendon Kraushaar, BS, et al. (1999) J Bone Joint Surg. 81A(2): 1158-64

Pathophysiology: Microscopy A: Normal Tendon w/ uniform collagen B: Diseased tendon: Neovascularization, , disordered collagen, mucoid degeneration Tendinosis of ECRB with some normal tendon and some disorganized tendon Kraushaar, BS, et al. (1999) J Bone Joint Surg. 81A(2): 1158-64

Pathophysiology: Microscopy A: Normal Tendon w/ uniform collagen B: Diseased tendon: Neovascularization, , disordered collagen, mucoid degeneration Angiofibroblastic hyperplasia meets normal tendon Kraushaar, BS, et al. (1999) J Bone Joint Surg. 81A(2): 1158-64

Pathophysiology: Other Theories Stress shielding certain sections of tendon leading to structural weakening Shear forces leading to fibrocartilaginous composition of ECRB attachment  weak attachment  tendinosis Long muscle contraction rendering tendon avascular  free radicals Hyperthermic injury Protein kinase  apoptosis Altered gene expression and imbalance of matrix metalloproteinases and growth factors Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Pathophysiology: Neurologic Changes High variability of patient’s symptoms Increased concentration neurotransmitters (glutamate), which sensitize pain response and direct irritation by lactate Cascade of changes in PNS neurons, which leads to sensitization of CNS May explain associated neck pain in 56% of patients Could be other overuse or altered biomechanics Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Diagnosis: History Pain at lateral epicondyle Insidious onset Radiates down extensor mass, occasionally proximally Exacerbated by contraction of extensor mass Insidious onset History of repetitive activity or overuse Inability to hold items Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Diagnosis: Physical Examination Tenderness ECRB origin or more diffuse centered about lateral epicondyle Resisted extension Full elbow/wrist ROM Sensation normal Wrist Extensor weakness 2º pain Decreased grip strength Conjoined tendon origin: 2-5mm anterior and distal to midpoint of epicondyl Resisted wrist and finger extension with elbow in FULL EXTENSION VERY IMPORTANT to examine and evaluate neck, entire upper extremity (cervical disease with radiculopathy, radial nerve compression at the elbow, intra-articular disease=plica, osteochondral disease) Limited Shoulder internal rotation requires ECRB compensation  0veruse Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Differential Diagnosis Cervical radiculopathy Elbow overuse compensating for frozen shoulder PIN entrapment Radiocapitellar degenerative changes or OCD Inflammation of anconeus Infection Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Diagnosis: Imaging Plain film: 22%-25% calcification within soft tissue Otherwise normal Calcification about the lateral epicondyl in 20% of those requiring surgery Probably No prognostic implications May disappear after treatment *Must correlate with physical exam-very common in unsymptomatic elbows (intra-articular lesions, radial collateral ligament, extent of tearing of extensor tendon). US: Very dependant on operator: hypoexhoic areas, intrasubstance tears, peritendinous fluid, thickening of common extensor origin. Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Diagnosis: Imaging MRI: Presence of degenerative tissue, tears in tendon More reproducible than US Intra-articular pathology Poor correlation with symptoms Generally not necessary Clinical diagnosis Calcification about the lateral epicondyl in 20% of those requiring surgery Probably No prognostic implications May disappear after treatment *Must correlate with physical exam-very common in unsymptomatic elbows (intra-articular lesions, radial collateral ligament, extent of tearing of extensor tendon). US: Very dependant on operator: hypoexhoic areas, intrasubstance tears, peritendinous fluid, thickening of common extensor origin. Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Treatment: Nonsurgical 80% + Improve within 1 year Relative rest Ice NSAIDs Steroid Injection: Short-term relief Counterforce Bracing (decrease tension on extensors) and wrist splint PT/Rehab: range of motion, eccentric strengthening Complete immobilization may lead to disuse atrophy NSAIDs for synnovitis and other local inflammation despite this not being a non-inflammatory process: improved pain, but no functional improvement + GI concerns Although typically non-inflammatory process, Substance P and increased glutamate (excitatory NT) is commonly found (mechanism for neurogenic pain generation) which is responsive to steroids. Must be injected deep to the tendons in the fatty subaponeurotic recess (anterior and distal to lateral epicondyle). Pain relief in 55-89%, but return of symptoms in 18%-54% Counterforce brace: inhibits full muscular expansion) No real proof yet of advantage over controls. Also concerns of extensions lag. No difference in grip strength, no difference in pain, no difference in physical function Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Treatment: Alternative Ultrasound/Extracorporeal shock waves (ECSW’s) Acupuncture/dry needling Platelet-rich plasma: growth factors Single-pulsed sonic waves dissipate energy at substance interface-may induce a reparative response. Light: not proven effective Manipulation: turns microtear into complete tear to allow healing in an elongated state. Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64

Treatment: Surgical 4%-11% require surgery Extra-articular extensor tendon debridement Intra-articular: excise synovial fringe and portion of orbicular ligament Tendon excision with origin reattachment Up to 25% of referral clinic patients my require surgery

Surgical: Open Debridement 8-10 cm incision over lateral epicondyle Subperiosteal detachment of common tendon Tendon debridement Decortication of epicondyle with rongeur Drill 2 v-shaped tunnels with horizontal mattress reattachment Splint 7-10 days with progressive mobilization Fascial incision over epicondyle down to radiocapitellar articulation Reflex back common extensor tendon Debridement: granulation tissue and fibrillated edges  excised Decortication  bleeding surface 5/64-inch drillbit Side to side fascial closure 85-90% return to full activity without pain. 10-12% improve but some pain. 2-3% no improvement Complications: excessive debridement instability and weakness; neuroma of posterior cutaneous branch of forearm; cutaneous branch radial nerve damage (1.5 cm anterior to epicondyle)

Surgical: Open Limited Incision Ahmed, Z., et al. (2013) Bone Joint J. 95-B: 1158-64 Van Hofwegen, C., et al. (2010) Clin Sports Med 29: 577-97

Randomized to injection with PRP, steroid or saline 60 patients Randomized to injection with PRP, steroid or saline Neither PRP no steroid superior to saline Pain at 3 months Steroid decreased pain at 1 month, hypervascularity, and tendon thickness

Steroid injection worse than placebo Therapy did no change outcome 165 patients Randomized to 1. steroid injection, 2. placebo injection, 3. steroid plus therapy, 4. placebo plus therapy Steroid injection worse than placebo Therapy did no change outcome JAMA 2013

PRP vers Placebo PRP versus placebo (AJSM 2013) No change 12 weeks PRP improved 24 weeks Pain

Medial Epicondylitis Golfer’s Elbow

Epidemiology Prevalence <1% 3.8 – 8.2% occupational settings 10-20% of epicondylitis patients Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Anatomy Pronator Teres* Flexor Carpi Radialis Palmaris Longus Flexor Digitorum Superficialis Flexor Carpi Ulnaris Medial Collateral Ligament PT and FCR originate supracondylar ridge Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Anatomy Common flexor tendon attaches to medial humeral epicondyle anteriolrly and attaches proximally to anterior bundle of ulnar collateral ligament, becomes confluent with hyperplastic section of anteromedial joint capsule PT and FCR originate supracondylar ridge Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Biomechanics Repetitive eccentric loading Valgus stress at elbow Wrist flexion, forearm pronation Valgus stress at elbow Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Pathophysiology Peritendinous inflammation Angiofibroblastic hyperplasia Irreparable fibrosis or calcification Ulnar collateral ligament Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

History Sports: overhead throwing, golf, tennis, football, weightlifting, bowling Occupational Forceful grip Loads >44lbs Constant vibratory force at elbow 84% have concomitant work-related disorder Carpal tunnel, lateral epicondylitis, rotator cuff tendinitis Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Diagnosis Pain along medial elbow Radiation to proximal forearm Increased pain with resisted pronation and wrist flexion Tenderness 5-10mm distal and anterior to epicondyle Normal ROM Normal Sensation Resisted wrist flexion, forearm pronation, grip may be weak Valgus Stress  Ligamentous pain X-rays usually normal Concomitant ulnar neuritis X-rays: may have medial ulnar traction spurs and MCL calcification. Must rule out ulnar neuropathy Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Imaging MRI is standard of care when imaging needed Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Treatment: Non-surgical Similar to Lateral Epicondylitis Rest 6-12 weeks off throwing NSAIDs Wrist flexor and forearm pronator stretching Night splinting Therapy: ROM, eccentric strengthening Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Treatment: Surgical Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55 Open: 86+% had no limitations; excellent or good results (97% results) Nirav, HA, et al. (2015) JAAOS. 23.6: 348-55

Research No RCT in last 3 years