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

2. Outline Epidemiology Anatomy Biomechanics Pathophysiology Diagnosis
Treatment
Research

3. Lateral Epicondylitis
Tennis Elbow

4. 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:
Van Hofwegen, C., et al. (2010) Clin Sports Med 29:

5. 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:
Van Hofwegen, C., et al. (2010) Clin Sports Med 29:

6. 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:
Van Hofwegen, C., et al. (2010) Clin Sports Med 29:

7. Anatomy Radial Collateral Ligament Lateral Ulnar Collateral Ligament
Annular Ligament

8. 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:

9. 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:
Van Hofwegen, C., et al. (2010) Clin Sports Med 29:

10. 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:

11. 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):

12. 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):

13. 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):

14. 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:

15. 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:

16. 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:

17. 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:

18. 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:

19. 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:

20. 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:

21. 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:

22. 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:

23. 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

24. 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 % 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)

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

26. 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

27. 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

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

29. Medial Epicondylitis
Golfer’s Elbow

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

31. 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:

32. 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:

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

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

35. 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:

36. 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:

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

38. 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:

39. 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:

40. Research
No RCT in last 3 years