Medial Ulnar Collateral Ligament Injury

                              Dr. KS Dhillon

Introduction

The medial ulnar collateral ligament (MUCL), also referred to as the medial collateral ligament (MCL), ulnar collateral ligament (UCL), and anterior bundle (AB) is the primary restraint to valgus instability of the elbow (1-5). The MUCL is one of three ligaments that comprise the “medial ulnar collateral ligament complex” of the elbow. The posterior bundle (PB) and transverse ligament (TL) are the other two (Fig 1). 

Fig 1.

The MUCL is the primary stabilizer of the elbow during valgus stress, followed by the radial head and dynamic stabilizers of the elbow such as the flexor-pronator muscle mass (6-10). The MUCL is composed of two separate bands (posterior and anterior) that provide reciprocal function with the posterior band tight in flexion, and the anterior band tight in extension. 

The MUCL is commonly injured in overhead-throwing athletes when a valgus moment is placed on the elbow during the early acceleration and late cocking phases (11-15). Incompetence or rupture of the ligament leads to valgus instability of the elbow which has varying clinical presentations. Patients may complain of instability, most however will report pain, reduced accuracy, and decreased velocity. Clinically significant pathology usually requires surgery. Appropriate graft positioning at both the humeral origin and the ulnar insertion is necessary when doing ligament reconstruction. A thorough understanding of the native anatomy of the MUCL facilitates the surgeon’s ability to restore stability and function effectively.

Morrey and An (10) in 1985 were the first to publish the quantitative analysis of the medial ulnar collateral ligament complex. They dissected 10 fresh frozen cadavers and described the dimensions of the AB and PB at various degrees of elbow flexion. Since then, multiple studies have assessed the anatomy and biomechanics of the AB (2,3,6,16,17). In the past general consensus held that the AB inserts solely and directly onto the sublime tubercle. Recent studies however have shown that the AB insertion is in fact broader, tapered, and significantly larger in terms of surface area. 

Anatomy

The MUCL (AB) is the primary restraint to valgus instability of the elbow (1-5). The PB is a soft tissue stabilizer of the elbow with greatest contributions during flexion (17). It is generally believed that the TL does not provide a significant contribution to elbow stability (10). A recent study however has revealed a direct insertion of the TL onto the AB that may potentially play a role in elbow stability (18). The AB, in particular, is the primary stabilizer of the elbow in valgus stress, with the radial head and dynamic stabilizers of the medial elbow also contributing (6-10). It originates on the anterioinferior surface of the medial epicondyle and goes on to insert on the sublime tubercle of the ulna (Fig 1).

Origin

Surface area and footprint center: The origin of the AB is posterior to the elbow’s axis of rotation. It is on the anterior, inferior, and lateral aspect of the medial epicondyle (10). The surface area of the humeral origin has been widely variable. Dugas et al (19) carried out a study in 13 fresh frozen cadavers utilizing a three-dimensional (3-D) electromagnetic tracking and digitalizing device and showed that the AB origin was round with a mean surface area of 45.5 mm2 (range of 25.9-59.4 mm2). A recent study by Camp et al (18) found a mean origin surface area of 32.3 mm2. In contrast to these two studies, Frangiamore et al (20) also studied 10 fresh frozen cadaver specimens and found the measurement to be notably smaller at 17.0 mm2 (range of 14.9-19.1 mm2). It is possible that due to differences in measurement techniques, these studies demonstrated variable results. 

Frangiamore et al (20) and Dugas et al (19) described the center of the ligament origin in different terms. This is of clinical importance when determining the location of humeral tunnel placement during MUCL reconstruction surgery. Dugas et al (19) described the center of the origin in an area on a flat surface anterior and inferior to the medial epicondyle. The mean distance they measured was 13.4 mm from the center of the medial epicondyle to the center of the origin. Camp et al (18) found a similar mean distance of 11.7 mm. Frangiamore et al (20) described this measurement in terms of two separate measurements. They reported the center of the origin to be located, on average, 8.5 mm distal (inferior) and 7.8 mm lateral (anterior) to the medial epicondyle. 

Insertion

Surface area and footprint center: The ulnar footprint of the AB inserts solely onto the sublime tubercle. It serves as the anatomical landmark for surgical repairs and reconstructions. In one early report, the mean AB insertional surface area was 66.4 mm2 (20).

Recently some authors have described the AB insertion as a longer, distally tapered area that follows the ulnar ridge. Dugas et al (19) reported that the surface area of this broader insertion has a mean surface area of 127.8 mm2. They found that the length of the ulnar footprint measured an average of 29.2 mm. Other authors have found similar lengths of tapered insertion with means of 30.2 mm and 29.2 mm (21,22). Camp et al (18) found a tapered insertion with a mean surface area of 187.6 mm2 and an ulnar footprint length averaging 29.7 mm.

Since the footprint center of a broader tapered insertion may not occur in the location previously assumed at the apex of the sublime tubercle, the optimal position of the ulnar tunnel in reconstructive surgery may still need to be elucidated. The clinical relevance of the broader tapered ulnar insertion described in studies by Camp et al (18) and Dugas et al (19) requires further investigation.

A study of 10 cadaveric specimens by Camp et al (18) has shown the mean proximal insertional width to be 9.4 mm which is greater than previously reported (18). This discrepancy in widths leaves room for further investigation. 

Overall ligament dimensions

Length: The AB is the longest ligament of the medial elbow. It spans the inferior aspect of the medial epicondyle to the sublime tubercle and extends distally along the ulnar ridge. The reported average length of AB is between 21.1 mm and 31.4 mm (2,9,10,17,20,23). These lengths were measured from the origin's center to the sublime tubercle's center, based on a direct insertion onto the sublime tubercle without a distal extension. In contrast, more recent reports measured the length from the center of the humeral origin to the most distal point of tapered insertion. They reported mean lengths of 53.9 mm (21) and 51.7 mm (22). The difference in length measured between a non-tapered sublime insertion and a tapered insertion calls for further study to evaluate native AB anatomy. The appropriate length of the ligament component has important implications for ligament reconstruction.

It is important to remember that the AB is not an isometric soft tissue stabilizer. It changes in length throughout flexion. The length of AB changes by 18%, between 2.8 mm and 4.8 mm as the elbow moves from extension to flexion (6,10,24). The dynamic length of the AB must also be kept in mind during reconstruction procedures.

Width: The width of the AB varies. It increases distally to its greatest width at the sublime tubercle before tapering to a point as it inserts distally along the ulnar ridge. Generally, there has been limited variability in widths of the AB, ranging from 4.0 to 7.6 mm (2,5,10,17,25,26).

Surface area: The reported mean surface area of the AB is between 108 mm2 to 135 mm2 (2,10) in studies that did not consider the full distal footprint. Given that Dugas et al (19) have shown the tapered ulnar footprint alone to have a mean surface area of 127.8 mm2, the overall surface area of the ligament will undoubtedly be significantly greater than previously assumed. A more recent study published by Camp et al (18) has shown the mean surface area of the entire AB to be 324.2 mm2.

Biomechanics

Valgus instability

When a valgus stress is applied the MUCL provides a vital contribution to the stability of the elbow. Morrey and An in a fresh frozen cadaveric model showed that with an intact radial head, the MUCL contributes 31% and 54% to valgus restraint at 0° and 90° of flexion, respectively (1). In this study,  varying valgus loads from 0 to 3 nm were applied at 0° and 90° of flexion in 4 fresh frozen cadavers. There was 3° of valgus laxity in full extension and 2° of laxity in flexion with the maximum force applied. There are several studies that have performed similar biomechanical testing at various degrees of flexion and various amounts of force (2,3,5,6,10,25,27). The amount of valgus laxity varies from 2° to 8° when the MUCL is intact.

Callaway et al (3) showed valgus laxity of 3.6° under a 2nm load compared to an unloaded elbow at 30° and 90° of flexion. Safran et al (5) studied 12 cadaveric specimens with a 2Nm load applied at 30 degrees of elbow flexion, and showed a mean alignment of 10.7° of valgus with a neutral forearm rotation. This study did not determine the inherent valgus alignment in an unloaded elbow. Hence it is not possible to compare these studies. With an intact MUCL and a 2 nm load applied, the amount of valgus laxity is generally greatest at 30° of flexion (5).

The effect of transecting the AB on elbow stability has been studied by several authors. In cadaveric models when the AB is disrupted, the amount of valgus instability increases until the point at which secondary osseous stabilizers such as the radial head provide stability. Callaway et al (3) demonstrated the greatest instability at 90° of flexion in the presence of AB deficiency. The study reported a gain of 1.6, 2.8, 3.2, and 3.0 degrees of valgus motion at 30, 60, 90, and 120 degrees of flexion, respectively compared to the intact state. Mullen et al (28) showed that at 90 degrees of flexion, AB transection increases valgus instability by 150%. Floris et al (25) and Søjbjerg et al (29) showed that the greatest instability occurs at 70 degrees of flexion, with recorded valgus angles of 11.8˚ and 14.2˚. Safran et al (5) produced a maximal gain of 6.3˚of laxity under 2 nm of valgus load with a transected AB at elbow flexion of 50˚. Finally, Morrey et al (4) showed a gain of laxity over baseline ranging from 3.3˚ to 4.8˚ in cadaver specimens at 20 degrees of elbow flexion. An intact AB is vital in maintaining valgus stability of the elbow throughout the flexion range.

Rotational instability

Forearm internal rotation is constrained by the soft tissue stabilizer of the medial elbow. While there is inherent internal rotation of the forearm during flexion, the degree of rotation is limited between 2.8˚-6˚ in an uninjured elbow (4,6,25). Transection of the AB allows internal rotation of the forearm to increase to 18.5˚ at 60˚ of joint flexion (25). A correct understanding of these biomechanics is important in repair and reconstruction since rotatory moment is part of the mechanism of injury.

Tissue strength

The AB is the most frequently injured ligament in overhead throwing athletes, although it has been shown to have the most inherent strength and stiffness (6,17). This shows that significant loads are placed on the medial side of the elbow during the late cocking and early acceleration phase (30,31). In a cadaveric model when each soft tissue stabilizer was evaluated under stress, the AB was found to be the strongest with an average load to failure of 260.9 N (17). During overhead throwing, the elbow experiences 64nm of mean valgus torque and 290N of tensile force on the medial side which is greater than the threshold for failure of 260.9N (30,31). A maximal mean valgus load of 90Nm has been reported (32-34). In a recent study of 81 professional baseball pitchers (MLB and MiLB), over 82000 throws showed a mean valgus torque of 60 nm with individual participant means ranging from 41 nm to 94 nm (35). Hence, it is evident why the AB fails in this subset of athletes based on the load to failure being below the force imparted on the elbow.

Conclusion

The AB of the medial ulnar collateral ligament complex plays a crucial role in elbow stability, especially as a valgus and rotational constraint. The AB originates on the humerus. It inserts onto the sublime tubercle of the ulna. Based on recent studies, the ulnar footprint has a broader insertion that is more tapered and elongated than previously thought. The data regarding the centers of the ulnar and humeral footprints guides proper tunnel placement during reconstructive procedures. 

Although the ligament is quite strong, the amount of force placed across the elbow in elite overhead-throwing athletes routinely exceeds the ligament's average load to failure. Hence it is not surprising why MUCL injuries are so common amongst baseball players and pitchers.

Understanding the native anatomy and biomechanics of the MUCL is clinically important to help understand the pathoanatomy and also to guide surgical techniques when treating MUCL injuries.

References

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4. Morrey BF, Tanaka S, An KN. Valgus stability of the elbow. A definition of primary and secondary constraints. Clin Orthop Relat Res. 1991;265:187–195. 

5. Safran M, Ahmad CS, Elattrache NS. Ulnar collateral ligament of the elbow. Arthroscopy. 2005;21:1381–1395. doi: 10.1016/j.arthro.2005.07.001.

6. Bryce CD, Armstrong AD. Anatomy and biomechanics of the elbow. Orthop Clin North Am. 2008;39:141–154, v. doi: 10.1016/j.ocl.2007.12.001. 

7. Cohen MS, Bruno RJ. The collateral ligaments of the elbow: anatomy and clinical correlation. Clin Orthop Relat Res. 2001;383:123–130. doi: 10.1097/00003086-200102000-00014. 

8. Ahmad CS, Park MC, Elattrache NS. Elbow medial ulnar collateral ligament insufficiency alters posteromedial olecranon contact. Am J Sports Med. 2004;32:1607–1612. doi: 10.1177/0363546503263149. 

9. Eygendaal D, Valstar ER, Söjbjerg JO, Rozing PM. Biomechanical evaluation of the elbow using roentgen stereophotogrammetric analysis. Clin Orthop Relat Res. 2002;396:100–105. doi: 10.1097/00003086-200203000-00017. 

10. Morrey BF, An KN. Functional anatomy of the ligaments of the elbow. Clin Orthop Relat Res. 1985;201:84–90.

11. Bruce JR, Andrews JR. Ulnar collateral ligament injuries in the throwing athlete. J Am Acad Orthop Surg. 2014;22:315–325. doi: 10.5435/JAAOS-22-05-315.

12. Jones KJ, Osbahr DC, Schrumpf MA, Dines JS, Altchek DW. Ulnar collateral ligament reconstruction in throwing athletes: a review of current concepts. AAOS exhibit selection. J Bone Joint Surg Am. 2012;94:e49. doi: 10.2106/JBJS.K.01034. [DOI] 

13. Rohrbough JT, Altchek DW, Hyman J, Williams RJ 3rd, Botts JD. Medial collateral ligament reconstruction of the elbow using the docking technique. Am J Sports Med. 2002;30:541–548. doi: 10.1177/03635465020300041401. 

14. Conway JE, Jobe FW, Glousman RE, Pink M. Medial instability of the elbow in throwing athletes. Treatment by repair or reconstruction of the ulnar collateral ligament. J Bone Joint Surg Am. 1992;74:67–83. 

15. Singh H, Osbahr DC, Wickham MQ, Kirkendall DT, Speer KP. Valgus laxity of the ulnar collateral ligament of the elbow in collegiate athletes. Am J Sports Med. 2001;29:558–561. doi: 10.1177/03635465010290050601.

16. O’Driscoll SW, Jaloszynski R, Morrey BF, An KN. Origin of the medial ulnar collateral ligament. J Hand Surg Am. 1992;17:164–168. doi: 10.1016/0363-5023(92)90135-c. [DOI] 

17. Regan WD, Korinek SL, Morrey BF, An KN. Biomechanical study of ligaments around the elbow joint. Clin Orthop Relat Res. 1991;271:170–179.

18. Camp CL, Jahandar H, Sinatro AM, Imhauser CW, Altchek DW, Dines JS. Quantitative Anatomic Analysis of the Medial Ulnar Collateral Ligament Complex of the Elbow. Orthop J Sports Med. 2018;6:2325967118762751. doi: 10.1177/2325967118762751. [DOI] 

19. Dugas JR, Ostrander RV, Cain EL, Kingsley D, Andrews JR. Anatomy of the anterior bundle of the ulnar collateral ligament. J Shoulder Elbow Surg. 2007;16:657–660. doi: 10.1016/j.jse.2006.11.009.

20. Frangiamore SJ, Moatshe G, Kruckeberg BM, Civitarese DM, Muckenhirn KJ, Chahla J, Brady AW, Cinque ME, Oleson ML, Provencher MT, et al. Qualitative and Quantitative Analyses of the Dynamic and Static Stabilizers of the Medial Elbow: An Anatomic Study. Am J Sports Med. 2018;46:687–694. doi: 10.1177/0363546517743749.

21. Farrow LD, Mahoney AJ, Stefancin JJ, Taljanovic MS, Sheppard JE, Schickendantz MS. Quantitative analysis of the medial ulnar collateral ligament ulnar footprint and its relationship to the ulnar sublime tubercle. Am J Sports Med. 2011;39:1936–1941. doi: 10.1177/0363546511406220.

22. Farrow LD, Mahoney AP, Sheppard JE, Schickendantz MS, Taljanovic MS. Sonographic assessment of the medial ulnar collateral ligament distal ulnar attachment. J Ultrasound Med. 2014;33:1485–1490. doi: 10.7863/ultra.33.8.1485. 

23. Beckett KS, McConnell P, Lagopoulos M, Newman RJ. Variations in the normal anatomy of the collateral ligaments of the human elbow joint. J Anat. 2000;197 Pt 3:507–511. doi: 10.1046/j.1469-7580.2000.19730507.x.

24. Armstrong AD, Ferreira LM, Dunning CE, Johnson JA, King GJ. The medial collateral ligament of the elbow is not isometric: an in vitro biomechanical study. Am J Sports Med. 2004;32:85–90. doi: 10.1177/0363546503258886.

25. Floris S, Olsen BS, Dalstra M, Søjbjerg JO, Sneppen O. The medial collateral ligament of the elbow joint: anatomy and kinematics. J Shoulder Elbow Surg. 1998;7:345–351. doi: 10.1016/s1058-2746(98)90021-0.

26. Timmerman LA, Andrews JR. Histology and arthroscopic anatomy of the ulnar collateral ligament of the elbow. Am J Sports Med. 1994;22:667–673. doi: 10.1177/036354659402200515. 

27. Rooker JC, Smith JRA, Amirfeyz R. Anatomy, surgical approaches and biomechanics of the elbow. Orthop Trauma. 2016;30:283–290.

28. Mullen DJ, Goradia VK, Parks BG, Matthews LS. A biomechanical study of stability of the elbow to valgus stress before and after reconstruction of the medial collateral ligament. J Shoulder Elbow Surg. 2002;11:259–264. doi: 10.1067/mse.2002.122622. [DOI] 

29. Søjbjerg JO, Ovesen J, Nielsen S. Experimental elbow instability after transection of the medial collateral ligament. Clin Orthop Relat Res. 1987;218:186–190. 

30. 30.Werner SL, Fleisig GS, Dillman CJ, Andrews JR. Biomechanics of the elbow during baseball pitching. J Orthop Sports Phys Ther. 1993;17:274–278. doi: 10.2519/jospt.1993.17.6.274. [DOI] 

31. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF. Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med. 1995;23:233–239. doi: 10.1177/036354659502300218.

32. Fleisig GS, Kingsley DS, Loftice JW, Dinnen KP, Ranganathan R, Dun S, Escamilla RF, Andrews JR. Kinetic comparison among the fastball, curveball, change-up, and slider in collegiate baseball pitchers. Am J Sports Med. 2006;34:423–430. doi: 10.1177/0363546505280431. 

33. Fleisig GS, Escamilla RF. Biomechanics of the elbow in the throwing athlete. Oper Techn Sport Med. 1996;4:62–68. 

34. Loftice J, Fleisig GS, Zheng N, Andrews JR. Biomechanics of the elbow in sports. Clin Sports Med. 2004;23:519–530, vii-viii. doi: 10.1016/j.csm.2004.06.003. 

35. Camp CL, Tubbs TG, Fleisig GS, Dines JS, Dines DM, Altchek DW, Dowling B. The Relationship of Throwing Arm Mechanics and Elbow Varus Torque: Within-Subject Variation for Professional Baseball Pitchers Across 82,000 Throws. Am J Sports Med. 2017;45:3030–3035. doi: 10.1177/0363546517719047.

 

Osteochondritis Dissecans

                             Dr. KS Dhillon

Introduction

Osteochondritis dissecans (OCD) was first described in 1888 by the German surgeon Franz König (1). Osteochondritis dissecans is also known as an osteochondral lesion. It is not a fully understood process, though it is believed to be multi-factorial in etiology. OCD is an idiopathic condition that can develop from childhood through adult life. The majority of patients present in their teenage years. The severity of these lesions can range from being asymptomatic to mild pain or in advanced cases having symptoms of joint instability and locking. The lesions can progress from stable to fragmentation of the overlying cartilage with the formation of a loose body in the joint space. Eventual early onset osteoarthritic changes of the joint can occur at any level of severity if not diagnosed and adequately treated. Therefore, early recognition and treatment are important to achieve good long-term outcomes.

Etiology

The etiology of osteochondritis dissecans has yet to be fully elucidated. It is believed to be multi-factorial. Postulated etiologies include spontaneous avascular necrosis, genetic predisposition, inflammation, and repetitive microtrauma. Originally it was believed to be related to osseous inflammation, hence the term osteochondritis. Multiple studies have failed to prove inflammation as the underlying cause. Spontaneous osteonecrosis is believed to occur during the maturation of the overlying cartilage during adolescence. At this time, the vascular supply to the subchondral bone moves from a juvenile perichondrial supply to mature supply from the medullary cavity. It is believed that during this transition period, the epiphyseal bone is predisposed to avascular necrosis. A higher prevalence of OCD in young athletes also suggests an etiology of repetitive microtrauma.  These theories have been studied with varying success in coming to a conclusion about the cause of this disease. The most commonly accepted etiology is that of repetitive microtrauma, with or without an inciting event. (2,3).

Epidemiology

The incidence of osteochondritis dissecans is approximately 15 to 29 per 100,000 patients (4). The majority of patients are 10 to 20 years of age although it can occur from childhood through adult life (5). Males are affected twice as often as females (5). There is a higher incidence in young athletes. The knee, particularly the lateral aspect of the medial femoral condyle, is the most affected joint. The elbow (capitellum) and ankle (talus) are also affected to a lesser degree (2,6).

Pathophysiology

Osteochondritis dissecans is an idiopathic focal joint disorder affecting the subchondral bone regardless of the etiology. Fragmentation of a small focus of subchondral bone creates a defect between the osteochondral lesion and the parent bone. This leads to decreased vascularization and osteonecrosis of the fragment. Fragments that are held in place by intact overlying articular cartilage are stable. Progression of the defect to involve the overlying cartilage is possible. This will lead to instability of the fragment. If lesions become unstable, they may displace from the parent site and become a loose body within the joint. In a large percentage of these affected patients, early-onset osteoarthritis occurs due to the altered articular surface caused by the osteochondral lesion.

History and Physical

Discovery and presentation of osteochondral lesions are variable. Patients can be asymptomatic. The lesion may be incidentally detected at imaging. This is true in patients who have been asymptomatic or those who never presented for evaluation but had remote chronic mild pain that resolved without treatment. Other patients present when they have chronic mild pain of the affected joint, with or without an acute injury. Typically these patients present several months to a year after the onset of symptoms. When there is a loose fragment, symptoms are generally more severe, with marked joint pain, swelling, locking, and joint instability (2,3).

Examination shows that these patients may have joint tenderness with painful or decreased range of motion of the involved joint, and swelling or effusion. Other injuries, such as ligamentous injuries and fracture has to be excluded (3).

Evaluation

Imaging plays a key role in the evaluation and treatment of these patients. Routine radiographs of the affected joint are obtained. Radiographs will show an ovoid lucency in the subchondral bone with adjacent sclerotic bone. Occasionally the bony fragment can be seen within the subchondral defect or, if displaced, elsewhere within the joint. Radiographs cannot determine the osseous fragment's stability and underestimate the lesion size. An MRI is usually used to confirm the diagnosis when an abnormality is detected on radiographs. It helps to differentiate a developmental ossification variation from OCD and aids in treatment planning, and helps to determine if the lesion is likely to be stable at the time of arthroscopy.  An MRI is highly sensitive and specific in the evaluation of fragment stability. Therefore, it is recommended for patients in whom stability is a clinical concern.

According to De Smet, the following four signs on MRI are associated with OCD lesion instability (7): 

• A discrete round focus of hyperintense signal deep to the OCD lesion measuring 5 mm or more

• Line of hyperintense signal equal to the fluid at the fragment bone interface measuring 5 mm or more in length

• Focal defect in the overlying cartilage measuring 5 mm or more

• Hyperintense signal equal to the fluid that traverses the articular cartilage and the subchondral bone which extends to the lesion.  

To evaluate for stability these same findings can be applied to any joint with an OCD lesion. These criteria have high specificity and sensitivity in the determination of OCD lesion stability.  MRI arthrography can be useful in difficult cases. Although CT arthrography is not as sensitive, it can be used in the patient when MRI is contraindicated.

MRI is also useful in monitoring treatment of the patients if conservative or surgical treatment is chosen.  The recommended time interval to perform an MRI to evaluate healing depends on the institutional protocol and surgeon. MRI findings that suggest healing following conservative management include: 

• Decrease or resolution in the surrounding bone marrow edema pattern

• A decrease in lesion size

• Decrease or the resolution of the hyperintense T2 signal rim or cyst-like foci

• Ingrowth of bone within the bed of the OCD lesion with osseous bridging.

After surgery, an MRI allows for noninvasive evaluation of the repair of the articular surface and the bone cartilage interface (7).

Treatment

The patient’s age, presentation time, severity of symptoms, and lesion stability will dictate treatment. Several systems to classify the lesions have been developed. The important feature is the degree of overlying cartilage involvement and mobility of the lesion fragment. In stable lesions, conservative management is the treatment of choice. Immobilization is carried out and protected weight-bearing is done for a length of time, depending on which joint is affected. When conservative treatment fails in patients with stable lesions they may be treated with drilling techniques (retroarticular or transarticular drilling). These drilling procedures have shown healing rates and symptom improvement in 92% to 100% of the patients. Transarticular drilling has slightly higher success rates. When lesions are displaced or unstable, surgical intervention is necessary. The drilling is typically performed arthroscopically. The knee lesions most often require surgery. Fifty-eight percent of procedures for OCD lesions are performed on the knee. There are various modalities and techniques that exist, such as debridement, fixation, microfracture, and cartilage grafting/transplantation. In situ fixation of lesions can be done using various types of bioabsorbable implants, metallic screws, or osteochondral plugs. Metallic screw fixation shows high successful healing rates of 84% to 100%. The disadvantage of using metallic screws is that there is a need for a second procedure to remove the screws. Bioabsorbable implants do not require a second procedure for removal. They show successful healing rates of around 90%. These implants however show higher rates of complications. Osteochondral autograft or allograft plugs can also be used. The clinical outcomes are “good to excellent” in 72% of patients receiving allograft plugs. The overall aim of surgery is to promote cartilage reformation and/or repair of the articular surface to prevent early-onset osteoarthritis (8).

Differential Diagnosis

Meniscus injury

Osteoarthritis

Prognosis

Stable osteochondral lesions have a better outcome as compared to unstable lesions. Spontaneous healing typically occurs when stable lesions are treated with conservative treatment alone. There is no single uniform grading scale for lesions treated surgically. Unstable lesions and those that fail conservative management undergo surgical treatment which has a success rate of 30% to 100% depending on the technique utilized (8). However, a large majority of patients treated surgically will still develop early-onset osteoarthritis. Patients presenting during adolescence tend to have a better outcome than adult patients.

Complications

Chronic pain

Arthritis

Nonunion

Conclusion

The diagnosis and management of osteochondritis dissecans is carried out by an interprofessional team that consists of a radiologist, orthopaedic surgeon, physical therapist, and primary caregiver. The treatment is dictated by the patient’s age, time of presentation, the severity of symptoms, and stability of the lesion. There are several systems that have been developed to classify the lesions. The important feature is the degree of overlying cartilage involvement and mobility of the lesion. In stable lesions, conservative management is preferred with immobilization and protected weight-bearing for a length of time, that depends on which joint is involved. When conservative treatment fails the patient can be treated with drilling techniques (retroarticular or transarticular drilling). These procedures have shown healing rates and symptom improvement ranging from 92% to 100%. Transarticular drilling has slightly higher success rates. When lesions are unstable or displaced, surgical intervention is necessary. The outcomes of stable lesions are better than unstable lesions (9,10). 

References

1. Kessler JI, Jacobs JC, Cannamela PC, Shea KG, Weiss JM. Childhood Obesity is Associated With Osteochondritis Dissecans of the Knee, Ankle, and Elbow in Children and Adolescents. J Pediatr Orthop. 2018 May/Jun;38(5):e296-e299.

2. Edmonds EW, Polousky J. A review of knowledge in osteochondritis dissecans: 123 years of minimal evolution from König to the ROCK study group. Clin Orthop Relat Res. 2013 Apr;471(4):1118-26. 

3. Zanon G, DI Vico G, Marullo M. Osteochondritis dissecans of the talus. Joints. 2014 Jul-Sep;2(3):115-23.

4. Andriolo L, Candrian C, Papio T, Cavicchioli A, Perdisa F, Filardo G. Osteochondritis Dissecans of the Knee - Conservative Treatment Strategies: A Systematic Review. Cartilage. 2019 Jul;10(3):267-277. 

5. Michael JW, Wurth A, Eysel P, König DP. Long-term results after operative treatment of osteochondritis dissecans of the knee joint-30 year results. Int Orthop. 2008 Apr;32(2):217-21. 

6. Kubota M, Ishijima M, Ikeda H, Takazawa Y, Saita Y, Kaneko H, Kurosawa H, Kaneko K. Mid and long term outcomes after fixation of osteochondritis dissecans. J Orthop. 2018 Jun;15(2):536-539.

7. Zbojniewicz AM, Laor T. Imaging of osteochondritis dissecans. Clin Sports Med. 2014 Apr;33(2):221-50.

8. Bauer KL, Polousky JD. Management of Osteochondritis Dissecans Lesions of the Knee, Elbow and Ankle. Clin Sports Med. 2017 Jul;36(3):469-487.

9. Cheng C, Milewski MD, Nepple JJ, Reuman HS, Nissen CW. Predictive Role of Symptom Duration Before the Initial Clinical Presentation of Adolescents With Capitellar Osteochondritis Dissecans on Preoperative and Postoperative Measures: A Systematic Review. Orthop J Sports Med. 2019 Feb;7(2):2325967118825059. 

10. Yamagami N, Yamamoto S, Aoki A, Ito S, Uchio Y. Outcomes of surgical treatment for osteochondritis dissecans of the elbow: evaluation by lesion location. J Shoulder Elbow Surg. 2018 Dec;27(12):2262-2270.

 Increased risk of early and medium-term revision after post-fracture total knee arthroplasty

                          Dr. KS Dhillon

Introduction

Post-traumatic osteoarthritis (PTOA) of the knee is defined as osteoarthritis that develops following an acute traumatic episode commonly associated with intra/extra-articular fracture or significant ligamentous injury (1). PTOA represents 9.8% of the overall prevalence of symptomatic knee osteoarthritis. It costs an estimated $40 billion in direct and indirect costs (2). Femoral and tibial fractures represent the major causes of PTOA of the knee (3). PTOA is caused by intra-articular fractures, which result in direct ligament and osteochondral injury, and cause joint instability and incongruity. It can be secondary to malunion of extra-articular fractures around the knee, which alters the weight-bearing axis of the lower limb and increases the joint stress, and accelerates the joint degeneration. Patients sustaining distal femur or proximal tibia fractures are around twice as likely to require total knee arthroplasty (TKA) as compared to patients with soft-tissue injuries (4,5).

TKA for PTOA is technically demanding even for experienced surgeons

due to previous surgery, retained hardware, bone defects, and the extra-articular angular deformity created by a fracture. Patients with PTOA are also susceptible to higher rates of complications, including periprosthetic joint infection, aseptic mechanical failure, wound healing problems, and higher rates of reoperation compared with TKA performed for atraumatic osteoarthritis (6,7). Bala et al (6) evaluated the impact of PTOA versus primary osteoarthritis on postoperative outcomes after TKA in a large database of Medicare patients. They found that the PTOA patients had a higher incidence of periprosthetic infection (OR 1.72, P < 0.001), knee wound complications (OR 1.80, P < 0.001), cellulitis/ seroma (OR 1.19, P < 0.001), TKA revision (OR 1.23, P = 0.01), and arthrotomy/incision and drainage (OR 1.55, P < 0.001).

The literature in the past has found several risk factors for unsatisfactory outcomes after TKA for PTOA. Shearer et al (8) found that the location of post-traumatic deformity and compromise of the soft-tissue envelope influenced the pain and functional outcomes of TKA for PTOA. Patients with isolated articular deformities have the largest improvement in pain and function while patients with combined tibial and femoral deformities as well as patients with soft-tissue compromise experienced poor outcomes. Ge et al (9) found that patients with previous site-specific fractures suffered higher surgical site complications (22% vs 4.4%) and 90-day readmissions (14.8% vs 2.2%) after TKA than patients with previous soft-tissue knee trauma. El-Galaly et al (10) reported an increased risk of early and medium-term revision of TKAs due to previous fractures in the proximal tibia and/or distal femur. There is a scarcity of literature about the risk factors for surgical site complications and reoperations after TKA in patients with PTOA secondary to prior femoral and tibial fractures.

Background and rationale

The proportion of patients with a history of previous surgery before primary total knee arthroplasty (pTKA) is highly variable (6–34%). This variability may be due to overestimation, multiple counting, underestimation, patient recall bias, incomplete chart fill, insufficient anamnesis, different current practices from one country to another, and different time periods included. It is however not clear how a history of previous surgery influences the outcome after pTKA. Patients with previous surgery have primary arthroplasty at a younger age and have a 1.5 times higher risk of subsequent revision. The risk does not substantially change when restricting the inclusion to primary OA. The difference in implant failure at 5 and 10 years is notable: about twice the risk at both time points (6.6% vs. 3.3 and 8.4% vs. 4.5%, respectively). The timing of revision is substantially higher in the short term in patients with pre-dating surgeries.

Does history of previous surgeries influence the risk of revision of primary total knee arthroplasty?

The crude risk of all-cause revision after pTKA among patients with a history of previous knee surgery is about twice as high as among those without (8.3 vs. 4.3%). Baseline differences in age, American Society of Anesthesiologists (ASA) score, sex, BMI, smoking status, patellar resurfacing, type of tibial plateau, and surgery duration partly explained the higher risk. It was, however, still 1.5 times greater after adjusting for the baseline imbalances. Subgroup analysis considering only the first pTKA implanted reveals similar results. Patients who had previous surgery are substantially younger, more often men, have fewer comorbidities including obesity, and are more often smokers. Similarly, Lim et al (11) highlighted that pTKA after previous surgery was performed at a younger age (61 vs. 66 years).

 

What is the risk of revision according to the type of previous surgery?

The risk of revision varies according to the type of previous surgery and it is lowest, with a 4.1% (CI 1.7–9.5) 5-year cumulative failure rate in the case of previous osteotomy, and higher in the case of ligamentoplasty (7.1%), arthroscopy (7.9%), or previous osteosynthesis (8.3%). However, the confidence intervals around the estimates for different types are large and overlap considerably. This kind of surgery can alter knee mechanics. Typically, previous osteotomies around the knee, or posttraumatic conditions, make TKA technically more challenging in terms of ligament balancing and implant positioning. Their effect on the revision risk however is not evident. A study by Pearse et al (12) from the New Zealand Joint Registry showed a 3-fold increased risk of early revision in patients with a history of osteotomies around the knee, compared with pTKA without previous surgery. In a more recent study by El-Galaly et al (13) from the Danish Knee Arthroplasty Registry, the 10-year survival of pTKA after HTO was inferior (91% vs. 94%).  This however could be explained by lower age and male sex rather than the osteotomy (adjusted HR of 1.2 vs. acrude HR of 1.7). 

The same group reported in another study an increased risk of early and mid-term revision of pTKA in the setting of OA after fractures around the knee (14).

How does previous surgery influence specific causes of revision and the time of revision?

The risk of revision after pTKA with previous surgery is about twice as high for any specific diagnosis, with aseptic loosening (2.1%) and infection (1.9%) being the most frequent cause of revision. The vast majority of patients are homogeneously treated making implant-related factors unlikely to explain the difference in revision rates due to aseptic loosening. Both younger age (15) and a BMI over 35 (16,17) are known patient-related risk factors for revision, due to high activity levels and a higher mechanical load across the bone–cement interface, respectively. The higher risk of infection encountered in patients with a history of previous surgery might be explained by an intrinsic risk due to previous interventions, as reported in a meta-analysis, with an RR of 3.0 (CI 1.5–5.9) (18), especially with open surgical procedures (19), as well as a history of resolved septic arthritis following surgery or prolonged surgery. Residual pain after pTKA is not unusual. High patient expectations, long chronic pain situations, and social/economic pressure to resume work might play a central role. There are substantially more short-term revisions in patients with previous surgery. There is no difference in the mid-term. In the long term, there is a higher number of revisions in those with previous surgery.

Conclusions

About 6–34% of patients undergoing pTKA have a history of previous surgery. The difference in implant failure at 5 and 10 years is notable, and baseline differences only partly explain the increased risk of revision. It is important to advise patients that their knee history adversely influences the outcome of pTKA, with a 1.5 times higher risk of revision. Future studies should analyze whether 1 vs. multiple surgeries prior to pTKA influences the survival differently and should focus on what causes of revision are related to a specific previous surgery. 

References

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