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.

Bursitis of the Knee, Hip, Elbow and Shoulder - Everything You Need to Know

 Bursitis of the Knee, Hip, Elbow and Shoulder - Everything You Need to Know
Written by Andrew Kelley with Dr. Nabil Ebraheim

Prepatellar Bursitis of the Knee
Prepatellar bursitis, also known as housemaid’s, carpet layer’s, and carpenter’s knee, is a superficial bursitis caused by inflammation of the bursa separating the patellar bone and the skin (1). Patients with prepatellar bursitis will normally present with knee pain and swelling (2). Prepatellar bursitis is mostly caused by long-term repetitive mini trauma from kneeling and crawling on hard surfaces. Other causes include acute injury, infection, gout, and rheumatoid arthritis (2). Its annual incidence is 10/100,000 per year with 80% of those affected being males age 40-60 (1). In cases of non-traumatic prepatellar bursitis, treatment is dependent on resolution of the underlying condition. Early differentiation between septic and non-septic bursitis is important in the early presentation in order to improve patient outcomes. Acute bursitis normally responds well to conservative treatment such as rest, ice, activity modification, NSAIDs, and fluid aspiration. Chronic bursitis due to mini traumas is treated similarly but may require additional corticosteroid therapy (1).

Olecranon Bursitis of the Elbow
Olecranon Bursitis, also known as student’s elbow and plumber’s elbow, is caused by inflammation of the bursa overlaying the olecranon process of the ulnar bone at the tip of the elbow. This bursa allows for smooth motion of the olecranon process against the superficial tissue at the tip of the elbow. Affected patients normally present with swelling at the bend of the elbow. A characteristic “golf ball” shape of swelling can be seen, and a fully intact range of motion of the elbow can differentiate it from elbow joint injuries (3). Olecranon Bursitis most commonly affects men age 30-60. Most cases are due to repeated minor trauma and sports (4). Treatment is focused on resolving the underlying cause of inflammation. Conservative treatment includes ice and rest along with NSAIDs for symptomatic relief are indicated. While aspiration and corticosteroid injection are proven relief interventions, they carry an increased risk for infection (4).

Greater Trochanteric Bursitis of the Hip
Greater trochanteric bursitis, or greater trochanteric pain syndrome (GTPS), is caused by inflammation of the bursa laying deep to the iliotibial band and superficial to the greater trochanter of the femur. It acts as a lubricant for the gluteal tendons. Patients with hip bursitis normally present with chronic intermittent pain of the lateral hip, thigh, and buttock (6). This bursitis normally affects women age 40-60. The increased pelvic width of women relative to their body may predispose them to increased iliotibial band tension on the bursa (6). The cause of hip bursitis can be repetitive microtrauma, blunt trauma, or idiopathic. Movements requiring repetitive hip abduction like stair climbing and bicycling, direct traumatic falls, and sedentary lifestyles are common causes of this condition (5).  Common treatments for this bursitis include NSAIDs, physical therapy, and corticosteroid injection. Surgery is a rare treatment option for bursitis resistant to conservative treatment options (5).

Subacromial Bursitis of the Shoulder
Subacromial bursitis is caused by inflammation to the bursa just below the acromion process. The subacromial bursa acts as a lubricating medium between the acromion process superiorly and the muscles of the rotator cup inferiorly.  Subacromial bursitis normally presents as anterolateral shoulder pain, especially during overhead activities. This chronic inflammation of the shoulder bursa can eventually lead to weakness and rupture of the surrounding ligaments and tendons (7). Older individuals are more likely to experience shoulder bursitis due to years of overuse. Most patients present due to direct trauma to the shoulder or repetitive overhead activities (7). Treatment includes rest, NSAIDs, physical therapy, and corticosteroid injections. Surgical therapy is reserved for cases unresponsive to conservative therapy (7).
 
 
 

References:  
1.  Rishor-Olney CR, Pozun A. Prepatellar Bursitis. [Updated 2021 Sep 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.
2.  J. Dean Cole MD. Causes of knee bursitis (prepatellar bursitis) [Internet]. Arthritis. Arthritis-health; [cited 2021Oct28]. Available from: https://www.arthritis-health.com/types/bursitis/causes-knee-bursitis-prepatellar-bursitis
3.  Pangia J. Olecranon bursitis [Internet]. StatPearls [Internet]. U.S. National Library of Medicine; 2021 [cited 2021Oct28]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470291/
4.  Blackwell JR, Hay BA, Bolt AM, Hay SM. Olecranon bursitis: a systematic overview. Shoulder Elbow. 2014 Jul;6(3):182-90. doi: 10.1177/1758573214532787. Epub 2014 May 6. PMID: 27582935; PMCID: PMC4935058.
5.  Seidman AJ. Trochanteric bursitis [Internet]. StatPearls [Internet]. U.S. National Library of Medicine; 2021 [cited 2021Oct28]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538503/
6.  Reid D. The management of Greater Trochanteric pain syndrome: A systematic literature review [Internet]. Journal of orthopaedics. Elsevier; 2016 [cited 2021Oct28]. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4761624/
7.  Faruqi T. Subacromial bursitis [Internet]. StatPearls [Internet]. U.S. National Library of Medicine; 2021 [cited 2021Oct29]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK541096/

Fractures of the Calcaneus: Everything You Need to Know

Fractures of the Calcaneus: Everything You Need to Know

Written by Dominic Ruwe and Dr. Nabil Ebraheim

Fractures of the calcaneus can be open or closed.¹ Open fractures are more serious than closed fractures.¹ The primary fracture line is caused by an axial load injury.¹ The primary fracture line goes from anterolateral to posteromedial.¹ The primary fracture line divides the calcaneus into two main fragments: the superomedial fragment which is also called the constant or sustentacular (SAS) fragment and the superolateral or tuberosity fragment.¹ The superomedial fragment includes the sustentaculum tali and is stabilized to the talus by ligaments. So, the talus is attached to the constant fragment.¹ The sustentacular fragment is a useful reference point for fracture reduction.² The flexor hallucis longus tendon lies underneath the sustentaculum. If screw placement to the sustentacular fragment is too long, the flexor hallucis longus tendon could be affected, causing fixed flexion of the big toe.³

                The Essex-Lopresti classification system is a useful way to differentiate between different joint fractures. There are two types of Essex-Lopresti fractures: a tongue-type fracture and a joint depression type fracture.¹ In the tongue-type, the posterior facet is attached to the tuberosity. In the joint depression type, the posterior facet is not attached to the tuberosity.⁴ In the tongue-type, the primary fracture line exits anterolaterally and posteromedially.⁵ The secondary fracture line appears beneath the posterior facet and exits posteriorly through the tuberosity.⁵ The superolateral fragment and posterior facet are attached to the tuberosity. The tongue-type fracture can be treated with open reduction and internal fixation.⁶

                In the joint depression type, the primary fracture line splits the calcaneus obliquely through the posterior facet and exits anterolaterally and posteromedially.¹ The secondary fracture line exits superiorly just behind the posterior facet.¹ The posterior facet is a free fragment. The lateral portion of the posterior facet is usually involved and depressed.⁴

The Sander’s classification of calcaneal fractures is used to guide the treatment and predict the outcome of the treatment. This classification system is based on the number of posterior facet fracture fragments seen on a coronal CT scan.⁷ Type I is a nondisplaced fracture which requires nonoperative treatment.⁷ Type II is a two-part fracture of the posterior facet.⁷ Type III is a three-part fracture of the posterior facet.⁷ Type II and III calcaneal fractures benefit from surgery of reduction and fixation.¹ Type III fractures normally result in more arthritis because it has more fracture fragments and may end by fusion.⁸ Type IV fractures are highly comminuted.⁹ They may require primary subtalar arthrodesis.¹

Calcaneal avulsion fractures are typically serious. These types of fractures require urgent reduction and internal fixation to prevent skin complications.¹⁰ In joint depression fractures of the calcaneus, the swelling must go down before surgery. Avulsion fractures of the calcaneus are emergencies, so emergency surgery is performed before the swelling goes down. Open reduction and internal fixation of the calcaneus is generally delayed for 1-2 weeks to allow for improvement of the soft tissue swelling, except with avulsion fractures.¹ Avulsion fractures can cause skin tenting and urgent reduction is recommended.¹⁰

There are many associated conditions with calcaneal fractures. Ten percent are associated with spinal fractures.¹¹ Ten percent are associated with compartment syndrome of the foot.¹² If this is neglected, it will lead to claw toes due to contracture of the intrinsic flexor muscles.¹² Approximately ten percent are associated with bilateral fractures.¹³ Sixty percent are associated with calcaneocuboid joint fractures.¹⁴ Calcaneal fractures may also be associated with peroneal tendon subluxation. Peroneal tendon subluxation may be detected on axial CT scans or it may be seen as an avulsion fracture of the fibula on x-rays.¹⁵

                Complication rates for calcaneal fractures are high. Factors associated with poor outcomes are age greater than 50, smoking, early surgery, history of a fall, heavy manual labor, males, bilateral injury, workman’s compensation, and peripheral vascular disease.^1,16,17 Men do worse with calcaneal fractures than women. Calcaneal fractures in men are normally associated with workman’s compensation, heavy labor, and a 0˚ Bohler angle.¹ These fractures typically need subtalar fusion.¹⁸ Calcaneal fractures in females have a simple fracture pattern. Since calcaneal fractures in males are usually more severe, it follows that better outcomes are seen in females with calcaneal fractures.¹⁹

                The Bohler angle is measured on lateral x-rays.¹ This angle is normally between 20˚-40˚.¹ The Bohler angle is formed by a line drawn from the highest point of the anterior process of the calcaneus to the highest point of the posterior facet and a line drawn tangential to the superior edge of the tuberosity.¹ A decrease in this angle indicates a collapse of the posterior facet.¹ When viewing calcaneal fractures with the Harris view, the calcaneus appears to be shortened and widened with varus.¹ When viewing calcaneal fractures through CT scans, the axial cut shows the calcaneocuboid joint and peroneal tendon subluxation.^1,20 The sagittal view shows the subtalar joint and its depression.²¹ The coronal view shows the displacement of the posterior facet.²² Coronal CT scans can also show the number of the joint fracture fragments.¹ The surgical outcome of calcaneal fractures correlate with the number of the joint fracture fragments and the quality of reduction.¹ MR imaging shows stress fractures of the calcaneus and the integrity of the peroneal tendons.^23,24

Stress fractures of the calcaneus may be misdiagnosed as plantar fasciitis.²⁵ Stress fractures usually occur in female runners.²⁶ It is characterized by swelling and tenderness with medial and lateral compression of the hindfoot during the squeeze test.²⁷ If the X-ray is negative, an MRI should be obtained. The fracture will be seen in T1 MR imaging as a linear streak or a band of low signal intensity in the posterior calcaneal tuberosity.²⁸ In T2 imaging, the signal will be increased.²⁸

                There are several complications with calcaneal fractures. Wound-related complications are the most common complication.²⁹ Wound-related complications occur more in smokers, diabetics, and patients with open fractures.¹ Open fractures of the calcaneus is another common complication. Open fractures of the calcaneus can lead to amputation.³⁰ There is also a high risk of infection with open fractures.³⁰ Grade I and Grade II open fractures have wounds that open medially. Open reduction and internal fixation (ORIF) can be done to treat this complication.³⁰ Open reduction and internal fixation should not be done in Grade III medial wounds and in most lateral wounds.³⁰ Another complication is malunion of the calcaneus.³¹ This is characterized by widening of the heel, varus deformity, and loss of height.³¹ The talus is dorsiflexed, limiting dorsiflexion of the ankle.³¹ Peroneal tendon irritation and impingement from the lateral wall is another complication.³²

                Surgery on the calcaneus decreases the risk of post-traumatic arthritis.³³ Tongue-type and joint depression type fractures may benefit from open reduction and internal fixation.⁶ Subtalar distraction arthrodesis is a good operation to treat calcaneal fractures associated with loss of height and limited dorsiflexion of the ankle.³¹ This operation improves talar inclination and decreases anterior ankle impingement.³¹ Additionally, it takes care of arthritis in the subtalar joint.³¹ Another surgical approach is extensile lateral approach. The lateral calcaneal artery provides blood supply to the lateral flap associated with the calcaneal extensile approach.³⁴ It is important to be aware that the Sural nerve is in the vicinity of the surgical area.³⁵ Delayed wound healing is a common complication in the extensile lateral approach.³⁵

 

References:

1. Trompeter A, Razik A, Harris M. Calcaneal fractures: Where are we now? Strategies in Trauma and Limb Reconstruction. 2017;13(1):1–11.

2. Berberian W, Sood A, Karanfilian B, Najarian R, Lin S, Liporace F. Displacement of the SUSTENTACULAR fragment in INTRA-ARTICULAR CALCANEAL FRACTURES. Journal of Bone and Joint Surgery. 2013;95(11):995–1000.

3. Carr JB. Complications of CALCANEUS fractures entrapment of the Flexor hallucis longus. Journal of Orthopaedic Trauma. 1990;4(2):166–8.

4. Rothberg DL, Yoo BJ. Posterior facet cartilage injury in OPERATIVELY Treated Intra-articular CALCANEUS FRACTURES. Foot & Ankle International. 2014;35(10):970–4.

5. White EA, Skalski MR, Matcuk GR, Heckmann N, Tomasian A, Gross JS, et al. Intra-articular tongue-type fractures of the calcaneus: Anatomy, injury patterns, and an approach to management. Emergency Radiology. 2018;26(1):67–74.

6. Chhabra N, Sherman SC, Szatkowski JP. Tongue-type calcaneus fractures: a threat to skin. The American Journal of Emergency Medicine. 2013;31(7).

7. Jiménez-Almonte JH, King JD, Luo TD, Aneja A, Moghadamian E. Classifications in Brief: Sanders classification OF INTRAARTICULAR fractures of the calcaneus. Clinical Orthopaedics & Related Research. 2018;477(2):467–71.

8. Rammelt S, Marx C. Managing severely malunited calcaneal fractures and fracture-dislocations. Foot and Ankle Clinics. 2020;25(2):239–56.

9. Piovesana LG, Lopes HC, Pacca DM, Ninomiya AF, Dinato MC, Pagnano RG. Assessment of reproducibility of sanders classification for calcaneal fractures. Acta Ortopédica Brasileira. 2016;24(2):90–3.

10. Berringer R. Avulsion fracture of the calcaneus. Canadian Medical Association Journal. 2018;190(45).

11. Rowe CR. Fractures of the os calcis. JAMA. 1963;184(12):920.

12. Myerson Mark, Manoli Arthur. Compartment syndromes of the foot after calcaneal fractures. Clinical Orthopaedics and Related Research. 1993;&NA;(290).

13. Popelka V. Súčasné trendy v liečbe intraartikulárnych zlomenín pätovej kosti [Current Concepts in the Treatment of Intra-Articular Calcaneal Fractures]. Acta Chir Orthop Traumatol Cech. 2019;86(1):58-64. Slovak. PMID: 30843515.14.

14. Kinner B, Schieder S, Müller F, Pannek A, Roll C. Calcaneocuboid joint involvement IN CALCANEAL FRACTURES. Journal of Trauma: Injury, Infection & Critical Care. 2010;68(5):1192–9.

15. Park C-H, Gwak H-C, Kim J-H, Lee C-R, Kim D-H, Park C-S. Peroneal tendon Subluxation and dislocation In CALCANEUS FRACTURES. The Journal of Foot and Ankle Surgery. 2021;60(2):233–6.

16. Su J, Cao X. Can operations achieve good outcomes in elderly patients with SANDERS II–III calcaneal fractures? Medicine. 2017;96(29).

17. Clare MP, Crawford WS. Managing complications of CALCANEUS FRACTURES. Foot and Ankle Clinics. 2017;22(1):105–16.

18. Csizy M, Buckley R, Tough S, Leighton R, Smith J, McCormack R, et al. Displaced Intra-articular CALCANEAL FRACTURES. Journal of Orthopaedic Trauma. 2003;17(2):106–12.

19. Barla J, Buckley R, McCormack R, Pate G, Leighton R, Petrie D, et al. Displaced intraarticular calcaneal fractures: Long-term outcome in women. Foot & Ankle International. 2004;25(12):853–6.

20. Toussaint RJ, Lin D, Ehrlichman LK, Ellington JK, Strasser N, Kwon JY. Peroneal tendon DISPLACEMENT Accompanying INTRA-ARTICULAR CALCANEAL FRACTURES. Journal of Bone and Joint Surgery. 2014;96(4):310–5.

21. Badillo K, Pacheco JA, Padua SO, Gomez AA, Colon E, Vidal JA. Multidetector CT evaluation Of CALCANEAL FRACTURES. RadioGraphics. 2011;31(1):81–92.

22. Buckley R. Displaced fracture of the calcaneus body [Internet]. AO Foundation Surgery Reference. [cited 2021Sep29]. Available from: https://surgeryreference.aofoundation.org/orthopedic-trauma/adult-trauma/calcaneous/displaced-body-fractures/definition

23. Kato M, Warashina H, Kataoka A, Ando T, Mitamura S. Calcaneal insufficiency fractures following ipsilateral total knee arthroplasty. Injury. 2021;52(7):1978–84.

24. Park HJ, Cha SD, Kim HS, Chung ST, Park NH, Yoo JH, et al. Reliability of MRI findings OF PERONEAL Tendinopathy in patients with LATERAL CHRONIC Ankle Instability. Clinics in Orthopedic Surgery. 2010Nov5;2(4):237.

25. Weber JM, Vidt LG, Gehl RS, Montgomery T. Calcaneal stress fractures. Clinics in Podiatric Medicine and Surgery. 2005;22(1):45–54.

26. Labronici P, Pires RE, Amorim L. Calcaneal stress fractures in civilian patients. Journal of the Foot & Ankle. 2021;15(1):54–9.

27. Kiel J, Kaiser K. Stress Reaction and Fractures. 2021 Aug 4. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 29939612.

28. Lawrence DA, Rolen MF, Morshed KA, Moukaddam H. MRI of heel pain. American Journal of Roentgenology. 2013Apr18;200(4):845–55.

29. Ding L, He Z, Xiao H, Chai L, Xue F. Risk factors for postoperative wound complications of calcaneal fractures following plate fixation. Foot & Ankle International. 2013;34(9):1238–44.

30. Heier KA, Infante AF, Walling AK, Sanders RW. Open fractures of THE Calcaneus: Soft-tissue Injury DETERMINES OUTCOME. The Journal of Bone and Joint Surgery-American Volume. 2004;86(11):2569.

31. Guang-Rong Y, Xiao Y. Surgical management Of Calcaneal Malunion. Journal of Orthopaedics, Trauma and Rehabilitation. 2013;17(1):2–8.

32. Davis D, Seaman TJ, Newton EJ. Calcaneus Fractures. 2021 Aug 9. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 28613611.

33. Vilá-Rico J, Ojeda-Thies C, Mellado-Romero MÁ, Sánchez-Morata EJ, Ramos-Pascua LR. Arthroscopic posterior subtalar arthrodesis for salvage of posttraumatic arthritis following calcaneal fractures. Injury. 2018;49.

34. Mehta CR, An VV, Phan K, Sivakumar B, Kanawati AJ, Suthersan M. Extensile lateral versus sinus Tarsi approach For displaced, intra-articular Calcaneal Fractures: A meta-analysis. Journal of Orthopaedic Surgery and Research. 2018;13(1).

35. Buckley R. Extended lateral approach to the calcaneus [Internet]. AO Foundation Surgery Reference. [cited 2021Sep29]. Available from: https://surgeryreference.aofoundation.org/orthopedic-trauma/adult-trauma/calcaneous/approach/extended-lateral-approach-to-the-calcaneus

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

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Layers of Articular Cartilage - Everything You Need To Know

Layers of Articular Cartilage - Everything You Need To Know 

 Dr. Nabil Ebraheim

https://www.youtube.com/watch?v=9g0TG249BDI

The articular cartilage is made up of many layers.  If you look at the joint, this will be the top of the articular cartilage.  If you magnify the joint, this is the articular surface, the subchondral bone and the cancellous bone.

 

How many layers are in the articular cartilage?

There are 4 layers in the articular cartilage.

1. Superficial zone

2. Middle zone

3. Deep zone

4. Calcified zone

In every layer there will be some changes.  These layers will differ in the chondrocytes, the morphology, size and in the orientation of the collagen bundles, and in the amount of water and proteoglycan present.

We start with the superficial zone which is about 10 to 15%.  Another name for the articular cartilage layer is the tangential layer.  The superficial zone is really a thin layer, but it is an important layer.  You find that the cartilage fibers are parallel to the surface.  The chondrocytes are elongated and parallel to the axis of the articular cartilage.  It has the highest concentration of collagen, which means it has the highest tensile strength, the highest concentration of water and the lowest concentration of proteoglycans.  It has less cells than the deep zone.  You do not want proteoglycans here because it will swell (do not want the cartilage to swell in this area).  This is the area connected to the motion of the articular cartilage, so you have to have a high tensile strength.  You have to have some collagen and some water, but you do not need proteoglycans because you do not need the cartilage to swell.  Both the cells and the collagen fibers are pounded by the pressure, becoming flattened and elongated along the long axis of the joint.

The middle zone is the transition zone (zone between the superficial and the deep zones).  The chondrocytes and the collagen fibers are oriented randomly.  In the middle cartilage layer, you will find the collagen in an oblique orientation.  You can see the disparity between the arrangement of the structures in the superficial zone and the arrangement of the structures in the deep zone.  You can imagine the transition zone is really disorganized because they do not know which zone they belong to.

The deep zone is about 30%.  The collagen fibers are perpendicular to the surface.  There are more cells, they are round and they are arranged in columns perpendicular to the joint.  The deep zone has the highest concentration of proteoglycans and the lowest concentration of water.  You do not need water inside of the cartilage.  In the deep zone, the chondrocytes are arranged in columns and the collagen fibers are oriented vertical to the articular cartilage.  The deep layer is strong in compression.

The fourth layer is the calcified cartilage and then the cancellous bone.  The calcified cartilage will start at the tidemark and it has Type X collagen (it is a transition zone to the bone).  The calcified zone is the transitional zone between the cartilage and the subchondral bone.  There is a tidemark that goes over the calcified zone.  The tidemark is the boundary between the calcified and uncalcified layers of articular cartilage. The tidemark separates the deep zone from the calcified zone.  The tidemark is seen mainly in the mature articular cartilage of the joint (for example: not cartilage of osteochondroma).