Tennis Elbow - Everything You Need to Know

Tennis Elbow

Written by Devon Patel with Dr. Ebraheim

Lateral epicondylitis, also known as tennis elbow, is an overuse injury that results in inflammation, tendinosis, and lateral elbow pain. It is the most common cause of pain in the lateral elbow, affecting between 1 and 3% of the general population (1). The primary structure impacted in tennis elbow is the extensor carpi radialis brevis, which originates at the lateral epicondyle (2). This condition is primarily seen in middle-aged individuals, especially those between the ages of 40 and 50 (3). Tennis players (up to 50% of regular players) and workers who engage in heavy lifting or repetitive gripping are more likely to develop tennis elbow (2). Other conditions, such as rotator cuff pathology or De Quervain’s diseases, and lifestyle factors, such as smoking, are associated risk factors for lateral epicondylitis (4). Rotator cuff pathology could be a risk factor because lateral epicondylitis can also be caused by biomechanical stress, but it is unclear exactly why it and other conditions are associated with each other (4). In terms of histology, disorganized collagen, dense fibroblasts, and vascular hyperplasia are primarily seen (2). Immature fibroblastic and vascular infiltration of the origin of the extensor carpi radialis brevis has consistently been identified during surgery (5). A physical exam and history are typically used to diagnose this condition. Clinical tests to assist in diagnosis include grip strength, Cozen’s, Maudsley’s, and Mill’s tests (3). Lateral epicondylitis is indicated if the previous tests are positive along with reduced grip strength or reproduced pain (3). If necessary, diagnostic scans can be obtained. Majority of patients show altered signal around the lateral epicondyle on MRI scans and hot focus on infrared thermography (6, 7). Radial tunnel syndrome is a differential diagnosis of tennis elbow. This syndrome is seen in 5% of patients who have compression of the posterior interosseous nerve. The pain associated with radial tunnel syndrome is approximately 3-4 cm distal and anterior to the lateral epicondyle, which differentiates it from tennis elbow.

Non-surgical treatments are the primary mode of treatment and there is a 95% success rate with treatments to relieve pain. The most frequently used treatment is corticosteroid injection (2). Oral or topical non-steroidal anti-inflammatory drugs (NSAIDs) can also be prescribed, but their effectiveness is variable (8). Patients can also undergo physical therapy to relieve their symptoms. Eccentric exercises have been shown to be especially effective in pain management (9). Using an inelastic, nonarticular proximal forearm brace could also be recommended (10). Two relatively newer treatments for tennis elbow are ultrasonic (US) and extracorporeal shock wave therapy (ESWT). There are minimal side effects to US and ESWT, thus making them preferable for patients and clinicians (11). Even though there is no difference between US and ESWT in elbow function evaluation scores, ESWT has been shown to have greater efficacy in pain relief (12). Surgical procedures are a last resort for treatment of tennis elbow and only indicated if patients are unresponsive to conservative treatments after an extended period of time. Debridement is the most common surgical intervention, but it can result in injury of the lateral collateral ligament and subsequent posterolateral rotary instability of the elbow.

           

References

1.         Shiri R, Viikari-Juntura E, Varonen H, Heliovaara M. Prevalence and Determinants of Lateral and Medial Epicondylitis: A Population Study. American Journal of Epidemiology. 2006;164(11):1065-74. doi: 10.1093/aje/kwj325.

2.         Cutts S, Gangoo S, Modi N, Pasapula C. Tennis elbow: A clinical review article. Journal of Orthopaedics. 2020;17:203-7. doi: 10.1016/j.jor.2019.08.005.

3.         Speers CJ, Bhogal GS, Collins R. Lateral elbow tendinosis: a review of diagnosis and management in general practice. British Journal of General Practice. 2018;68(676):548-9. doi: 10.3399/bjgp18x699725.

4.         Titchener AG, Fakis A, Tambe AA, Smith C, Hubbard RB, Clark DI. Risk factors in lateral epicondylitis (tennis elbow): a case-control study. Journal of Hand Surgery (European Volume). 2013;38(2):159-64. doi: 10.1177/1753193412442464.

5.         Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. The Journal of bone and joint surgery American volume. 1979;61(6A):832-9. PubMed PMID: 479229.

6.         Steinborn M, Heuck A, Jessel C, Bonel H, Reiser M. Magnetic resonance imaging of lateral epicondylitis of the elbow with a 0.2-T dedicated system. European Radiology. 1999;9(7):1376-80. doi: 10.1007/s003300050851.

7.         Thomas D, Siahamis G, Marion M, Boyle C. Computerised infrared thermography and isotopic bone scanning in tennis elbow. Annals of the Rheumatic Diseases. 1992;51(1):103. doi: 10.1136/ard.51.1.103.

8.         Pattanittum P, Turner T, Green S, Buchbinder R. Non‐steroidal anti‐inflammatory drugs (NSAIDs) for treating lateral elbow pain in adults. Cochrane Database of Systematic Reviews. 2013(5). doi: 10.1002/14651858.CD003686.pub2. PubMed PMID: CD003686.

9.         Croisier J-L, Foidart-Dessalle M, Tinant F, Crielaard J-M, Forthomme B. An isokinetic eccentric programme for the management of chronic lateral epicondylar tendinopathy. British Journal of Sports Medicine. 2007;41(4):269. doi: 10.1136/bjsm.2006.033324.

10.       Johnson GW, Cadwallader K, Scheffel SB, Epperly TD. Treatment of lateral epicondylitis. Am Fam Physician. 2007;76(6):843-8. Epub 2007/10/04. PubMed PMID: 17910298.

11.       Coombes BK, Connelly L, Bisset L, Vicenzino B. Economic evaluation favours physiotherapy but not corticosteroid injection as a first-line intervention for chronic lateral epicondylalgia: evidence from a randomised clinical trial. British Journal of Sports Medicine. 2016;50(22):1400-5. doi: 10.1136/bjsports-2015-094729.

12.       Yan C, Xiong Y, Chen L, Endo Y, Hu L, Liu M, et al. A comparative study of the efficacy of ultrasonics and extracorporeal shock wave in the treatment of tennis elbow: a meta-analysis of randomized controlled trials. Journal of Orthopaedic Surgery and Research. 2019;14(1). doi: 10.1186/s13018-019-1290-y.

Ehlers-Danlos Syndrome

 Ehlers-Danlos Syndrome

Written by Drew Gryczewski with Dr. Nabil Ebraheim

Ehlers-Danlos Syndrome (EDS) is a family of inherited connective tissue disorders that impacts collagen and manifests as a wide spectrum of symptoms ranging from joint hypermobility to severe vascular defects, such as arterial aneurysms and dissections. It currently is classified into thirteen subtypes. The defects in collagen can be separated into either a direct mutation in the genes encoding collagen or a mutation in the enzymes involved in the synthesis of collagen. Collagen is fibrillar structure that provides support and strength for the extracellular matrix and is found in essentially all the organs and tissues in the body (1). Collagen is synthesized from three subunits that follow the general form Glycine-X-Y where X is typically proline and Y is 4-hydroxyproline. Each individual chain is then used to form a triple helix which is the functional structure of collagen. The 4-hydroxyprolines are important for maintaining the triple helix. Most subtypes of Ehlers-Danlos Syndrome follow an autosomal dominant inheritance, however there are also subtypes that follow an autosomal recessive inheritance pattern (2). Ehlers-Danlos Syndrome is divided into 6 major subtypes (13 subtypes total) including: classic, hypermobile, vascular, kyphoscoliosis, arthrochalasia, and dermatosparaxis. The most common subtypes being the hypermobile and classical (3). Classic Ehlers-Danlos Syndrome (cEDS) is associated with a mutation in the COL5A1 and COL5A2 genes which encode type V collagen. Typical clinical finding with classic Ehlers-Danlos Syndrome include skin hyperextensibility, widened atrophic scars, and easy bruising. These signs are all major criteria for the diagnosis of classical Ehlers-Danlos syndrome. Molecular testing for a variant of type V collagen is helpful for making the diagnosis (1). 

One of the consequences experienced by individuals with hypermobile Ehlers-Danlos Syndrome (hEDS) is recurrent joint dislocations and subluxations. The incidence of joint dislocation is closely related to the severity of the hypermobility of the joints. The ligamentous and capsular laxity have been attributed as the cause for dislocation and subsequent joint instability. The recurrence and burden of these frequent dislocations and subluxations tends to increase with age (1, 4). Joint dislocations occur in 75% of all cases of Ehlers-Danlos Syndrome with the most being seen in the hypermobile subtype with 95% reporting dislocations (5). Later in life, individuals who suffer from recurrent dislocations and sprains usually develop chronic pain that is difficult to treat (1). Vascular Ehlers-Danlos Syndrome (vEDS) is caused by a mutation in type III collagen specifically the COL3A1 gene. This type of collagen is commonly found in the walls of arteries and hollow organs. A defect in this collagen carries severe complications including aortic
aneurysms and dissections, intestinal perforations, spontaneous pneumothorax, and uterine rupture during pregnancy (6). A way that the vascular and classical Ehlers-Danlos Syndrome are
differentiated is by the associated skin manifestations. In classical Ehlers-Danlos, the skin is normally smooth and velvety and is hyperextensible. The vascular type of Ehlers-Danlos however, is not associated with hyperextensible skin but the skin is thinner and more transparent. This subtype has the worst prognosis due to the relative frequency of arterial rupture (1). 

Making the diagnosis of Ehlers-Danlos Syndrome in infants can be difficult as they present as a “floppy baby”, and this can be a sign of more devastating pathology (4). Treatment can include both conservative and surgical interventions, although surgery isn’t recommended unless it is absolutely required, due to the risk of surgery incision dehiscence, poor wound healing, and other increased risks. In conservative treatment, the goal is the stabilize the muscles and the joint. The glenohumeral joint which is frequently involved requires strengthening of the rotator cuff muscles to improve stability. This should be done along with strengthening the deltoids and scapular stabilizer muscles to further decrease scapular dyskinesia. A barrier in surgical treatment is the abnormalities in the connective tissue that is characteristic of Ehlers-Danlos Syndrome.
The goal of surgical intervention is to correct capsular laxity by augmentation of the ligaments and bony structures. While these procedures tend to yield satisfactory outcomes in the general
population, there has not been sufficient data collected on individuals with Ehlers-Danlos Syndrome and thus each plan of care should be individualized (5). Most people with Ehlers-Danlos Syndrome spend years searching for the diagnosis, due to lack of awareness and understanding throughout the healthcare system. It also can be difficult to recognize due to the wide range of comorbidities associated with it. Treatment typically requires treating individual symptoms by a team of different healthcare specialists.

References

1. De Paepe A, Malfait F. The Ehlers–Danlos syndrome, a disorder with many faces. Clin Genet. 2012 Feb 13;82(1):1-11. 

2. Myllyharju J, Kivirikko KI. Collagens, modifying enzymes and their mutations in humans, flies and worms. Trends Genet. 2004 Jan;20(1):33-43. 

3. Scheufler O, Andresen JR, Andresen R. Surgical treatment of abdominal wall weakness and lumbar hernias in Ehlers-Danlos syndrome – Case report. International Journal of Surgery Case Reports. 2020 Sep 21;76:14-18. 

4. Beighton P, Horan F. Orthopaedic Aspects of Ehlers-Danlos Syndrome. J Bone Joint Surg. 1969 Aug 1;51 B(3):444-53

5. Broida SE, Sweeney AP, Gottschack MB, Wagner ER. JSES Reviews, Reports, and Techniques. 2021 Mar 23;1(3):155-64

6. Sage L, Russo ML, Byers PH, Demasi J, Morris SA, Puryear LN, Fulton DS, Shalhub S; Vascular Ehlers-Danlos Syndrome Research Collaborative. Setting a research agenda for vascular Ehlers-Danlos syndrome using a patient and stakeholder engagement model. J Vasc Surg. 2020 Oct;72(4):1436-1444

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