Postoperative Imaging of Sports Injuries [1st ed.] 9783030545901, 9783030545918

Table of contents :
Front Matter ....Pages i-xii
Shoulder: Rotator Cuff Repair (Vivek Kalia, Jon A. Jacobson)....Pages 1-19
Post Op Imaging of the Shoulder: Stabilization Surgery (Klaus Woertler)....Pages 21-40
Elbow (David A. Rubin)....Pages 41-76
Post-operative Imaging of the Hand and Wrist (Bouke Boden, Abishek Jain, Doug Campbell, Rob Campbell)....Pages 77-125
Postoperative Imaging of the Hip (Franca Boldt, Reto Sutter)....Pages 127-149
Knee: Ligament Reconstruction (James P. Baren, Emma Rowbotham, Scott D. Wuertzer, Andrew J. Grainger)....Pages 151-199
Post-operative Imaging: The Menisci (Tom Magee, Emma Rowbotham)....Pages 201-219
Postoperative Imaging of Sports Injuries: Foot and Ankle (Joyce HM Cheng, Steven Lange, William B. Morrison)....Pages 221-255
Imaging Following Cartilage Repair Surgery (Emma L. Gerety, David A. Rubin, Andrew J. Grainger)....Pages 257-296

Citation preview

Postoperative Imaging of Sports Injuries Emma Rowbotham Andrew J. Grainger Editors

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Postoperative Imaging of Sports Injuries

Emma Rowbotham  •  Andrew J. Grainger Editors

Postoperative Imaging of Sports Injuries

Editors Emma Rowbotham Consultant Musculoskeletal Radiologist Leeds Teaching Hospitals NHS Trust Leeds UK

Andrew J. Grainger Consultant Musculoskeletal Radiologist Cambridge University Hospitals Cambridge UK

ISBN 978-3-030-54590-1    ISBN 978-3-030-54591-8 (eBook) https://doi.org/10.1007/978-3-030-54591-8 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Foreword

It is an honor and a privilege to have been asked to write the Foreword for this outstanding book. The editors, Dr. Andrew J. Grainger and Dr. Emma Rowbotham, are both Fellows of the Royal College of Radiologists and are recognized as world authorities in the field of sports medicine and musculoskeletal imaging. Both editors provided imaging services to the 2012 London Olympics. I worked with Dr. Grainger when he was a Clinical Research Fellow at UCSF and have great regard for his intelligence and sense of humor. Since then, he has become an excellent researcher, clinician, and educator. Dr. Grainger has recently taken a Consultant post at Cambridge University Hospital following his time as a Consultant at Leeds Teaching Hospitals NHS Trust, where he worked with co-editor Dr. Rowbotham. Prior to taking up her post in Leeds she was a Consultant Musculoskeletal Radiologist in Bath, where she developed her interest in sports imaging, in particular working with colleagues and athletes from the English Institute of Sport. Both of the authors provide diagnostic and interventional support to many professional athletes and are popular lecturers in sports imaging. The editors have gathered other luminaries from Britain, Europe, and the United States to author various chapters on imaging of joint surgeries. Most of the radiologists who have written in this book, including the editors, are members of the prestigious International Skeletal Society as well as the Society of Skeletal Radiology and the European Society of Musculoskeletal Radiology. They have written the scientific articles and reviews on their designated subjects in many of the top journals and have lectured about them throughout the world. This review of postoperative imaging of joints is a timely, important, and valuable resource to all radiologists who read musculoskeletal imaging studies. Specifically, the chapters cover rotator cuff repair, shoulder stabilization surgery, elbow, hand, and wrist surgery, as well as knee ligament and meniscal surgery. Foot and ankle surgery and imaging of cartilage repair round out the topics. When faced with increasing and different types of surgery being performed for musculoskeletal ailments, it can be challenging to read these postoperative imaging studies. This authoritative book takes on that challenge to provide a background of the procedures, their normal appearance, as well as the complications in an organized and concise manner. The surgical procedures are discussed in just the right detail to make it easier to understand what we are seeing. Key points and tables are given to guide the technical planning of the study along with a review of v

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postoperative findings and complications. Up-to-date references are included for further reading. Importantly, the chapters contain a wealth of state-of-the-art imaging examples of the normal postoperative appearance and the complications. Kudos to the editors and authors for providing a practical go-to source that contains crucial and unique information that we can really use in our practices!  Francisco, CA, USA San

Lynne Steinbach, MD, FACR

Preface

Imaging has become a crucial part of the pathway in both the diagnosis and treatment of sports injuries, not only for the elite athletic population but also for the far greater number of people sustaining musculoskeletal injuries either through amateur sport or through their everyday activities. In elite sport, there is increasing pressure to return the athlete to their original level of play as quickly as possible, even following surgery. Consequently, an understanding of the normal post-operative imaging appearances and the potential issues that can arise is of paramount importance. The idea for this book came about because we often struggled to find a concise description of surgical techniques appropriate to the radiologist. Whilst there are plenty of in-depth texts on surgical procedures in the athlete, we felt there was a general lack of the more specific radiological descriptions required to report on post-operative cases, but not to actually perform the surgery! We also wanted to draw on the information that is available in individual articles on the post-operative imaging of specific joints and surgical procedures into a single volume. Whilst this book is not exhaustive in terms of post-operative diagnoses, a large number of the most common injuries encountered are covered. Each chapter contains concise descriptions of the most commonly performed surgical procedures, enough to help recognise which technique has been performed in any particular case, followed by normal and abnormal imaging appearances. We hope the book will act as a source of reference to all radiologists involved in post-operative sports imaging, where imaging studies can be complicated and challenging to interpret. We are indebted to all the authors and contributors who have been so generous in contributing their time expertise and wealth of experience to put together such outstanding chapters, and we hope that readers will find this book both interesting and helpful in their daily practice. Leeds, UK Cambridge, UK 

Emma Rowbotham Andrew J. Grainger

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Contents

1 Shoulder: Rotator Cuff Repair����������������������������������������������������������������   1 Vivek Kalia and Jon A. Jacobson 2 Post Op Imaging of the Shoulder: Stabilization Surgery����������������������  21 Klaus Woertler 3 Elbow����������������������������������������������������������������������������������������������������������  41 David A. Rubin 4 Post-operative Imaging of the Hand and Wrist��������������������������������������  77 Bouke Boden, Abishek Jain, Doug Campbell, and Rob Campbell 5 Postoperative Imaging of the Hip ������������������������������������������������������������ 127 Franca Boldt and Reto Sutter 6 Knee: Ligament Reconstruction�������������������������������������������������������������� 151 James P. Baren, Emma Rowbotham, Scott D. Wuertzer, and Andrew J. Grainger 7 Post-operative Imaging: The Menisci������������������������������������������������������ 201 Tom Magee and Emma Rowbotham 8 Postoperative Imaging of Sports Injuries: Foot and Ankle�������������������� 221 Joyce HM. Cheng, Steven Lange, and William B. Morrison 9 Imaging Following Cartilage Repair Surgery ���������������������������������������� 257 Emma L. Gerety, David A. Rubin, and Andrew J. Grainger

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Contributors

James P. Baren  Department of Radiology, Leeds Teaching Hospitals, Leeds, UK Bouke Boden  Department of Radiology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands Franca Boldt  Balgrist University Hospital, Zurich, Switzerland Doug  Campbell  Department of Orthopedic Surgery, Spire Leeds Hospital, Leeds, UK Rob  Campbell  Department of Radiology, Royal Liverpool University Hospital, Liverpool, UK Joyce  HM. Cheng  Department of Radiology, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong Emma  L.  Gerety  Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK Andrew  J.  Grainger  Consultant Musculoskeletal Radiologist, Cambridge University Hospitals, Cambridge, UK Jon  A.  Jacobson  Department of Radiology, University of Michigan Health System, Ann Arbor, MI, USA Abishek  Jain  Department of Radiology, Royal Liverpool University Hospital, Liverpool, UK Vivek  Kalia  Department of Radiology, University of Michigan Health System, Ann Arbor, MI, USA Steven  Lange  Department of Radiology, Thomas Jefferson University Hospital, Philadelphia, PA, USA Tom  Magee  NSI, University of Central Florida College of Medicine, Orlando, FL, USA William  B.  Morrison  Department of Radiology, Thomas Jefferson University Hospital, Philadelphia, PA, USA

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Contributors

Emma  Rowbotham  Department of Radiology, Leeds Teaching Hospitals, Leeds, UK David A. Rubin  Radsource, Brentwood, TN, USA Department of Radiology, Grossman NYU School of Medicine, New York, NY, USA All Pro Orthopedic Imaging Consultants, LLC, St Louis, MO, USA Reto Sutter  Balgrist University Hospital, Zurich, Switzerland Klaus Woertler  Technische Universität München, Munich, Germany Scott D. Wuertzer  Department of Radiology, Wake Forest Baptist Medical Center, Winston-Salem, NC, USA

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Shoulder: Rotator Cuff Repair Vivek Kalia and Jon A. Jacobson

1.1

Introduction

Imaging evaluation of the postoperative rotator cuff remains challenging despite advancements in both our understanding of the normal evolution of the postoperative rotator cuff appearance with time and the imaging techniques themselves. It is critical that radiologists and other musculoskeletal care providers understand the normal procedures for operative repair of the rotator cuff, so that they have a baseline of what a “normal” repaired cuff should look like and develop an understanding of when to call a re-tear vs. normal expected postoperative findings. Furthermore, it is important to understand advantages and disadvantages of both MRI and ultrasound for evaluation of the cuff in the normal non-injured state, normal postoperative state, and postoperative state with new injury suspicious for re-tear. This chapter aims to provide such context.

1.2

Operative Management of Rotator Cuff Repairs

Radiologists’ familiarity with conventional approaches to operative repair of a rotator cuff tendon or tendons is critical for optimal postoperative evaluation. Before MRI evaluation or live scanning with ultrasound, it is ideal if the operative report for the initial repair can be reviewed, so that any particular modifications or deviations from the standard cuff repair procedure are not misconstrued as new injury. For example, alterations in a patient’s anatomy due to tendon transfer procedures (commonly performed with massive rotator cuff tears) can create a perplexing situation for the interpreting radiologist. Many cases of rotator cuff tear can be managed conservatively, especially in patients with lower demands. However, where patients have persistent symptoms or functional V. Kalia (*) · J. A. Jacobson Department of Radiology, University of Michigan Health System, Ann Arbor, MI, USA e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2020 E. Rowbotham, A. J. Grainger (eds.), Postoperative Imaging of Sports Injuries, https://doi.org/10.1007/978-3-030-54591-8_1

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deficit or in patients with high level of demand on their shoulder such as athletes, operative repair may be required. While both degenerative and traumatic tears can be repaired, it has been suggested that better results are achieved in younger patients with traumatic tears [1]. Rotator cuff repair is most commonly performed arthroscopically or, if more visualization and access is required, through a mini-open technique requiring a deltoid split. Although subscapularis repair is more technically challenging arthroscopically compared to conventional open repair, recent studies show better patient outcomes in terms of range of motion and pain with arthroscopic approaches. The mini-open repair technique seems to be associated with more postoperative complications and is thus less preferred to fully arthroscopic repair, which is associated with decreased short-term pain and is considered the standard of care for most tears [2]. Typical indications for repair are: 1 . Acute full-thickness tendon tears 2. Bursal-sided tears >25% in depth 3. Articular-sided tears >50% in depth 4. Partial articular supraspinatus tendon avulsion (PASTA) lesions with >7 mm of exposed bony footprint between the articular surface and intact tendon A variety of repair techniques are available to reattach the torn tendon to the bone. Initial open repair techniques used bone tunnels to pass suture material through from the greater tuberosity anchor point to the lateral aspect of the tuberosity where they are tied. This can be a problematic technique when bone quality is poor and currently repair is normally accomplished with suture anchors. These can be placed as a single row or a double row with the intention of recreating the footprint of the tendon. The double row technique is intended to maximize the contact area between the torn tendon and tuberosity, recreating the medial to lateral footprint. While the clinical and functional outcome of the double-row technique over the single row is not clearly shown, there is evidence that the double-row technique speeds up tendon healing and reduces re-tear rates. The majority of available studies in the literature also favor double-row repair vs. single row with regard to tensile strength, construct failure, gap formation, and footprint coverage [3–5]. Another described technique known as the suture bridge technique or transosseous equivalent technique uses a row of medially placed suture anchors at the articular margin to anchor the tendon at a point 10–12 mm medial to the lateral edge of the torn tendon. The suture material is then passed over the bursal surface of the tendon lateral to this anchor point and fastened with a row of anchors lateral to the edge of the torn tendon. The suture material therefore acts to compress the tendon repair against the bone in the footprint area. If this technique is used, the radiologist can expect to see suture anchors lateral to the tendon repair site and this should not be misinterpreted as tendon having pulled away from the anchors. The typical recovery period takes about 8–12 weeks for adequate healing of the cuff tendon to the greater tuberosity. In the case of massive rotator cuff tears, tendon transfer from the pectoralis major (for chronic subscapularis tendon tears) or latissimus dorsi (for large supraspinatus and infraspinatus tendon tears) may be performed. However, tendon transfer procedures require a longer period of rigid immobilization. In some centers an augmented repair may be used for the treatment of large rotator cuff tears, particularly if there is substantial retraction of the torn tendon or the tendon

1  Shoulder: Rotator Cuff Repair

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is of poor quality. In these cases an allograft or a synthetic graft, made from material such as Teflon, is used to augment the repair. Use of a graft has been shown to reinforce primary repairs in massive rotator cuff tears by enhancing biologic tendon healing and overall biomechanical integrity of the repair [6–8]. This can be achieved through a patch graft augmentation after completion of primary repair of the torn tendon or a patch graft bridge, performed for an irreparable defect >1 cm in size with inadequate excursion of the retracted tendon [9]. In the latter, the graft replaces the native rotator cuff tendon as a bridge between the torn tendon and bony footprint [10]. Other procedures which may be performed in addition to suture anchor placement in a repaired cuff at the time of initial surgery include subacromial decompression and rotator cuff debridement, both performed in patients with low-grade partial articular-sided tears. The most common cause of a failed rotator cuff repair is inadequate healing of the cuff tissue to native bone, which results in suture pullout from the repaired tissue. Risk factors for repair failure include: • • • • •

Age > 65 years Tear size >5 cm in length Muscular atrophy History of diabetes mellitus Retraction of torn tendon medial to the glenoid

Lastly, superior capsular reconstruction (SCR) may be performed in certain cases (Fig.  1.1a, b), indicated in patients with intolerable pain and/or significant functional deficits (based on the patient’s lifestyle) who have failed nonoperative therapies and who a

b

Fig. 1.1  61-year-old male with surgical repair of massive rotator cuff tear involving supraspinatus and a portion of the infraspinatus. Coronal (a) and sagittal (b) T2-weighted fat-saturated MR images show intact low signal intensity superior capsular reconstruction with dermal allograft. T2 signal hyperintensity at the glenoid attachment represents a suture hole. The sagittal image demonstrates the graft covering the entire superior humeral head. The side-to-side attachment with the infraspinatus tendon is intact

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1 . have massive, irreparable rotator cuff tears 2. do not have moderate or severe rotator cuff arthropathy 3. have an intact/reparable subscapularis tendon 4. have functional, preserved deltoid musculature [11] It is contraindicated in patients with moderate to severe rotator cuff arthropathy, patients with glenohumeral osteoarthritis, and in patients with an irreparably torn subscapularis. After successful SCR typically using an acellular dermal allograft, there is passive constraint to superior humeral head translation which helps improve shoulder functionality.

1.3

Imaging Evaluation of the Cuff After Cuff Repair

The mainstays of evaluation of the postoperative rotator cuff are MRI and ultrasound. It is important to note that recurrent tear rates are higher as judged by MRI compared to ultrasound though MRI does offer higher sensitivity [12]. Direct MR arthrography is the most sensitive and specific technique for the diagnosis of partial-­thickness or full-thickness rotator cuff tears and post-repair re-tears [13–15], though it may overestimate the failure of healing of repaired cuffs compared to conventional MRI [13]. With optimal protocols and scanning techniques, common re-tear patterns and other complications following rotator cuff repair can be readily identified. In this chapter we will define the expected appearance of the postoperative (i.e., repaired) rotator cuff and the imaging appearance of a range of complications, predominantly focusing on re-tears of a repaired rotator cuff. Both MRI and ultrasound are highly sensitive and specific for detecting rotator cuff tears of the native cuff [15–18], though the sensitivity and specificity drop in the postoperative setting for both modalities.

1.3.1 MRI Using MRI, the early postoperative period presents a particularly challenging period when evaluating patients with reinjury following rotator cuff repair. This is partly because the repaired tendon(s) can be expected to have a heterogeneous and irregular appearance for a period of about 3–6  months following surgery which can significantly complicate interpretation.

1.3.1.1 Normal Nonoperative RC Tendon On MRI, the entire length of the supraspinatus and infraspinatus tendons is usually best seen on coronal oblique images, whereas the anterior fibers of the supraspinatus tendon are often best seen on sagittal oblique images. The teres minor tendon is best evaluated on sagittal oblique images, and the subscapularis tendon is best evaluated on axial and sagittal oblique images. The normal tendons should be uniformly hypointense on all pulse sequences on both arthrographic and non-­arthrographic MRI exams (Fig. 1.2a, b). Though no strict cutoffs for tendon thickening are routinely used in clinical practice, thickening as well as increased MRI signal are features of tendinosis.

1  Shoulder: Rotator Cuff Repair

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b

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Fig. 1.2  27-year-old male football player with right arm weakness and shoulder pain. The rotator cuff was found to be normal in this patient. (a) Coronal T2-weighted fat-saturated MR image shows normal low signal intensity, fibrillar architecture of the supraspinatus tendon (white arrows), with normal appearance of the footprint on the greater tuberosity. (b) Coronal T1-weighted fat-­ saturated MR image after intra-articular injection of gadolinium contrast in this arthrogram shows no penetration of contrast into the supraspinatus tendon (white arrows) to suggest tear. No contrast was seen in the subacromial-subdeltoid bursa to suggest full-thickness rotator cuff tear. (c) Long-­ axis grayscale static ultrasound image of the supraspinatus tendon (white arrows) demonstrates the normal fibrillar and echogenic appearance of a healthy tendon

1.3.1.2 Normal Postoperative (Repaired) RC Tendon MRI evaluation of the repaired rotator cuff can be inherently challenging due to distortion of normal anatomy and variable degrees of surrounding soft tissue abnormality [19]. In addition, introduced hardware such as suture anchors and, if

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applicable, graft material may introduce additional artifacts which make interpretation difficult. Fortunately, most implanted rotator cuff hardware used today is made of titanium or plastic and results in minimal metal-related artifact. The normal MRI appearance of the postoperative rotator cuff (Fig. 1.3) is highly variable, both due to variable healing patterns and due to variations in surgical technique, including a varying number of anchors, number of sutures, and type of sutures used. The factors influencing the postoperative cuff appearance include the extent and chronicity of the native rotator cuff disease, the exact procedure performed, and the time interval between repair and imaging. About 90% of repaired tendons show signal hyperintensity on postoperative MRI [20]. However, there can be significant variability in the postoperative tendon thickness, with tendon thickening due to secondary fibrosis or tendon thinning, as a result of the formation of granulation tissue, both occurring. Repaired rotator cuff tendon(s) demonstrates intermediate/high signal intensity in the early postoperative period [13, 21]. This appearance reflects postoperative edema, inflammatory change, and/or the formation of granulation tissue. This increased intratendinous signal may persist for several months to years [22] and is considered to be part of the normal spectrum of the postoperative appearance of the rotator cuff tendons [20]. Associated marrow edema may also persist long after rotator cuff repair and should not be routinely interpreted as reflective of fracture [22]. It is critical for radiologists to review operative reports following rotator cuff repairs as operative techniques and thus expected postoperative imaging findings vary considerably, even so much so that in some cases portions of a torn tendon may be left unrepaired due to poor tissue or edge quality or an inadequate length of

Fig. 1.3  56-year-old male with right shoulder pain but no functional deficit following rotator cuff repair 3 months prior. Coronal oblique T2-weighted fat-saturated MR image shows the expected postoperative appearance of the repaired supraspinatus tendon (white arrows). Despite a small amount of signal hyperintensity at the supraspinatus footprint, no tendon fiber discontinuity or clefts were seen, so no tear was called. Incidentally noted were findings of a small glenohumeral joint effusion and small volume subacromial-subdeltoid bursal fluid

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tendon to achieve repair. Such diligence can help prevent errors such as unknowingly calling re-tears of intact repairs [23]. Another critical postoperative finding to be aware of reflects the fact that rotator cuff tendon repair procedures do not necessarily produce a “watertight” repair, so postoperative MR arthrography may show contrast material communicating from the glenohumeral joint to the subacromialsubdeltoid bursa without a full-thickness tear present [24, 25]. The radiologist needs to be aware of whether a graft has been used to augment the repair. Graft material will generally show low signal on conventional MRI sequences. There may be an apparent gap at the tendon tear site simulating a re-tear which is in fact bridged by the graft material. Postoperatively, it is not uncommon to see new T2 signal hyperintensity of the glenohumeral joint capsule and pericapsular soft tissues at the axillary recess [26] which may reflect synovial proliferation and capsular hypervascularity [27]. This new T2 signal hyperintensity in the axillary recess may coincide with limited range of motion of internal and external rotation in some patients at 4-month follow-up [26], findings commonly associated with adhesive capsulitis.

1.3.1.3 Torn Postoperative RC Tendon Re-tear after surgical repair of the rotator cuff remains a significant problem [28, 29] despite advances in surgical approaches, technique, instrumentation, and imaging techniques. Re-tear rates are reported in the range of 11–68% [30, 31]. The significance of a re-tear is determined by considering the type of surgical repair undertaken, imaging findings, and clinical assessment. Taken together, this information may inform whether further surgery is likely to be successful. Symptomatic smaller partial-thickness tears are sometimes debrided without repair, whereas higher-grade partial-thickness (>50%) and full-thickness tears are commonly repaired with either a single or double row of suture anchors at the greater tuberosity footprint [32]. The double-row suture anchor technique and the suture bridge technique have been reported as having lower tendon re-tear rates [33–36]. Despite these and other advancements in surgical technique for rotator cuff repair over many years, a certain percentage of patients will inevitably succumb to structural failure of the repair [28, 37–40]. Risk factors for rotator cuff tendon re-tear following surgical repair include advanced age, smoker status, longer time interval between initial tear and surgical repair, larger tear size, poor tendon quality, and muscle atrophy [41–43]. It should be noted that MR arthrography performed after rotator cuff repair is thought to result in overcalling of re-tears due to the appearance of pseudo-tears that are a part of the normal healing process [13]. Timing of MRI after rotator cuff repair strongly influences the expected appearance of the repair, and recent data suggest that 6  months postoperatively may be the ideal time to assess and predict for future structural failure after arthroscopic rotator cuff repair [44]. The quality of the underlying bone, repaired tendon, and the muscle must all be considered when assessing the potential for a successful re-operation.

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A re-tear of a repaired rotator cuff will typically show a fluid signal intensity cleft at the repair site (Fig. 1.4), along with absence of the heterogeneous repaired tendon at the expected site. As with the native cuff, a re-tear of a repaired rotator cuff may be partial-thickness (Fig. 1.5a, b) or full-thickness or, if involving multiple tendons, may be described as a massive re-tear (Fig. 1.6a–c). The stump of re-torn tendon is typically visible and is often proximally retracted to a variable degree. It is critical to note the absence of tendon bulk (Fig. 1.7a–d) at the expected tendon footprint on the greater tuberosity, as intervening intermediate-signal granulation tissue and scar may create the appearance of a partial-thickness or incomplete re-­ tear. It is critical to assess both the repair site and the musculotendinous junction in all available planes to assess for changes in the configuration of the repaired tendon which may provide a subtle indication that a re-tear has occurred. When examined in the early postoperative period after surgery (e.g., 3 months), the repaired rotator cuff typically appears disorganized and heterogeneous on MRI, though this appearance gradually improves and becomes more homogeneous through remodelling and repair from 3 to 12 months [13, 45]. Hyperintense granulation tissue may mimic a re-tear of a repaired rotator cuff tendon, and though these changes tend to decrease with time, they can persist for several months to years and create challenges in interpretation of postoperative MR imaging [46]. A systematic review by Saccomanno and colleagues in 2015 showed that structural integrity of the repaired rotator cuff, dichotomized by the Sugaya classification [40] into intact versus re-tear, was the only one of many variables measured in 120 different analyzed studies that showed good intra- and inter-observer reliability [47]. Other variables analyzed included footprint coverage, tendon thickness, tendon signal intensity, partial re-tear, full-thickness re-tear location, tear size, number of tendons involved, tendon retraction, fatty infiltration, marrow edema and/or cysts in the humeral head, presence of a glenohumeral joint effusion, and the acromiohumeral (AH) interval.

Fig. 1.4  42-year-old male with persistent right shoulder pain, now 1.5 years status-post rotator cuff repair. Coronal T2-weighted fat-saturated MR image shows a focal bursal-sided re-tear (white arrow) at the supraspinatus footprint with mild diffuse thinning/ attenuation of the tendon. A small amount of fluid is also noted in the subacromial-­subdeltoid bursa

1  Shoulder: Rotator Cuff Repair

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Fig. 1.5  65-year-old female with left shoulder pain and weakness 5  months after rotator cuff repair. (a) Sagittal T2-weighted fat-saturated MR image shows marked heterogeneity in the region of both the supraspinatus and anterior infraspinatus tendons (white arrows) without discernible tendon fibers, suggestive of at least a partial re-tear. (b) Coronal T2-weighted fat-saturated MR image shows a high-grade bursal-sided rotator cuff re-tear (white arrows) involving the supraspinatus tendon several centimeters medial to the footprint. There is fluid in the glenohumeral joint as well as in the subacromial-subdeltoid bursa

Independent predictive factors for re-tear after rotator cuff repair include the degree of tendon retraction [48–50] and the degree of narrowing of the AH interval preoperatively [50]. Specifically, patients who experienced re-tears tended to have narrower AH intervals (6.8 ± 2.1 mm) compared to those without re-tears (8.7 ± 1.2, p = 0.000). This same study [50] of predictive factors of re-tear after repaired fullthickness supraspinatus tendon tears showed the following variables to not be independent predictive factors for re-tear: the type of rotator cuff tear (e.g., full-­thickness full-width versus full-thickness partial-width), presence of signal intensity near the tear edge, degree of supraspinatus muscle fatty infiltration, and the anteroposterior (AP) dimension of the torn tendon. However, it is important to note that other studies have shown the AP dimension of rotator cuff tears and fatty infiltration of the rotator cuff musculature predispose patients to greater re-tear rate [28, 51, 52].

1.3.2 Ultrasound As is the case with MRI, the postoperative cuff presents a challenge for ultrasound evaluation given the expected heterogeneity seen in the postoperative state, especially in the first 6 months. Ultrasound faces additional challenges as well—that the sound beam must travel through superficial soft tissues to reach the deeper cuff

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c

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Fig. 1.6  44-year-old male with severely limited motion and pain since an injury to his shoulder at work 4 months prior. History of rotator cuff repair. (a) Coronal T2-weighted fat-saturated MR image shows no discernible tendon fibers attaching at the greater tuberosity. There is free communication of fluid from the glenohumeral joint into the subacromial-subdeltoid bursa through the large full-thickness rotator cuff rear. The torn tendon edge/stump (white arrows) is seen retracted to the level of the glenoid. (b) Sagittal T2-weighted fat-saturated MR image shows no discernible tendon fibers attaching at the greater tuberosity. (c) Coronal T2-weighted fat-saturated MR image again shows no discernible tendon fibers attaching at the greater tuberosity. Also depicted here is the classic “geyser sign” (white arrow), an eruption of synovial fluid through this chronic full-­thickness rotator cuff tear and through the degenerated acromioclavicular joint. This often results in a palpable lump

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a

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d

Fig. 1.7  64-year-old female with prior rotator cuff repair, now with 12-month follow-up evaluation for progressive weakness and loss of range of motion. (a) External rotation radiographic view of the right shoulder shows three suture anchors in the right humeral head, significant cortical irregularity at the greater tuberosity, and a high-riding humeral head. The patient has also undergone prior distal clavicular resection. (b) Scapular Y radiographic view of the right shoulder shows congruency of the humeral head with the glenoid. (c, d) Sagittal T2-weighted fat-saturated MR images show a discontinuous rotator cuff with a prominent fluid-filled gap where the anterior supraspinatus tendon should reside (white arrow)

tendons and musculature means that if there is any fatty infiltration of the deltoid or other echogenic soft tissue overlying the rotator cuff, visualization of the cuff is limited. In some cases, artifact from suture material may obscure areas of interest to a greater extent than on MRI. Some of the advantages of ultrasound evaluation of the postoperative rotator cuff include dynamic assessment, fast execution, low cost, and less artifact associated with sutures, suture anchors, micrometallic debris (which may cause obscuring blooming artifact on MRI), and knots [53]. Several studies suggest that ultrasound may be the preferred modality to evaluate for repair integrity in the early postoperative period (e.g., 3 months postoperatively) due to its high sensitivity and specificity [28, 39, 54, 55]. However, ultrasound is operator-dependent and offers only a limited field of view, necessitating knowledge of anatomic landmarks

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to a greater extent than MRI [56, 57]. It has been reported that assessing rotator cuff repairs in patients serially at 3 months and then at 6 months has a high sensitivity and specificity for predicting future structural failure [44]. These authors concluded that all patients, even those who are asymptomatic at 6 months, should undergo ultrasound at 6 months because of the utility of predicting future functional outcomes based on these imaging findings and to provide a baseline for future studies.

1.3.2.1 Normal Nonoperative RC Tendon Ultrasound evaluation of the intact native rotator cuff requires knowledge of the detailed anatomy of the various structures of the rotator cuff. The supraspinatus tendon typically measures 23  mm in anterior-to-posterior width and inserts onto both the superior and middle facets of the greater tuberosity [58]. The infraspinatus tendon measures approximately 22  mm in anterior-to-posterior width and inserts onto the middle facet of the greater tuberosity, its anterior fibers overlapping with the supraspinatus tendon’s posterior fibers at a junctional zone measuring about 10 mm. The supraspinatus footprint, a common site for rotator cuff tears, measures approximately 12  mm in medial to lateral dimension. The teres minor tendon attaches onto the inferior facet of the greater tuberosity, located posteriorly. The subscapularis tendon attaches to the lesser tuberosity. In the healthy state, rotator cuff tendons appear fibrillar and hyperechoic on ultrasound (Fig. 1.2c) and demonstrate anisotropy. In addition, for example with the supraspinatus tendon, the superior (bursal-sided) surface of the tendon should be convex without areas of discontinuity or concavity. The tendons should be smooth and without hypoechoic or anechoic defects. Care must be taken during ultrasound examination of the cuff to ensure the entire width of each tendon is evaluated (for example, the full anterior to posterior width of the supraspinatus tendon and the full craniocaudal extent of the subscapularis tendon anteriorly). In short-axis evaluation, the multiple tendon slips of the subscapularis tendon should be visible as discrete hyperechoic bundles, each demonstrating the expected sonographic features of tendons described above. 1.3.2.2 Normal Postoperative (Repaired) RC Tendon Ultrasound evaluation of the postoperative cuff allows for excellent dynamic assessment of the repaired cuff’s continuity, tendon position and thickness, and for the presence of secondary complications such as bursitis or infection [23]. The normal early postoperative (i.e., first 6 months after surgery) repaired cuff typically shows hypoechogenicity with loss of normal fibrillar tendon architecture (Fig.  1.8a, b). Most commonly, echogenicity of repaired tendons increases with time as healing continues. Suture anchors may be seen as hyperechoic foci with associated reverberation artifact, and there is often cortical irregularity of the greater tuberosity at the tendon reattachment site. If subacromial decompression was performed, cortical irregularity may also be seen at the lateral acromial undersurface. It is critical for interpreting radiologists to know that it is not uncommon to see an apparent full-thickness defect or focal clefting at a repair site in the early postoperative period. This is hypothesized to reflect reparative scar formation rather than a true re-tear [59] and has been corroborated by histological studies [45, 60]. Serial

1  Shoulder: Rotator Cuff Repair

a

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b

Fig. 1.8  50-year-old male with history of rotator cuff repair 6 months prior. Patient is currently asymptomatic. (a) Long-axis ultrasound image of the supraspinatus tendon demonstrates heterogeneous diffuse hypoechogenicity with hyperechoic suture material and minimal anechoic fluid in the subacromial-subdeltoid bursa. (b) Short-axis ultrasound image of the supraspinatus tendon demonstrates heterogeneity of the postoperative supraspinatus and infraspinatus tendons. Postoperative changes in the humeral head at the site of suture anchor insertion are also seen

imaging by ultrasound will often show fill-in of these apparent clefts and irregular areas of the repaired cuff. It is therefore critical to dynamically assess the repaired tendons during postoperative sonographic evaluation to look for true gapping at a suspected tear site. The variable and heterogenous ultrasound appearance of the repaired cuff may persist for years after surgery [58, 61, 62]. Interestingly, up to 20–50% of repaired cuffs may show postoperative cuff defects even up to 5  years after surgery [63]. Other findings such as subacromial-subdeltoid bursitis and increased vascularity of the repaired tendon have been shown to decrease serially over time [64].

1.3.2.3 Torn Postoperative RC Tendon Sonographic evaluation of a potentially re-torn rotator cuff offers advantages of dynamic imaging properties, easy accessibility, high spatial resolution, and high sensitivity, specificity, and accuracy, measuring 91%, 86%, and 89% in one study, respectively [62]. Most structural failures after arthroscopic rotator cuff repair, up to 74% [65], occur within the first 3 months postoperatively [39]. Few tears occur after 26 weeks post-repair [66]. The ultrasound appearance of a rotator cuff re-tear after initial repair shows a tendon defect or tendon non-visualization at its expected location (Fig. 1.9). These re-tears usually occur at the site of repair on the greater tuberosity. Indirect ultrasound findings of a tear in the native rotator cuff, such as tendon thinning and cortical irregularity at the supraspinatus tendon footprint, cannot be applied after surgical repair. In addition, small or equivocal tendon defects may become less apparent over time. A follow-up ultrasound examination should be considered with any equivocal tendon finding to help determine its significance and whether its appearance on initial postoperative scan may reflect normal evolution of the healing process.

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Fig. 1.9  61-year-old female with limited range of motion of her left shoulder. Longitudinal ultrasound image of the posterior aspect of the humeral head shows no discernible tendon fibers at the infraspinatus footprint on the middle facet of the greater tuberosity

1.4

Displacement of Suture Anchors

The majority of rotator cuff repairs involve the placement of suture anchors and these can dislodge (Fig. 1.10a–d). While this may or may not result in failure of the cuff repair, the displaced anchor in itself can generate synovitis and become a cause of pain or chondral damage. The displaced anchor may also lead to catching or locking of the joint [67]. One study has suggested that pain following rotator cuff repair is not uncommonly associated with dislodged suture anchors [68]. In this small study all cases presented within the first 6 months after surgery. While dislodged metallic suture anchors may be readily visualized on conventional radiographs (Fig. 1.10c), bioabsorbable anchors are not easily seen. However, MRI can identify the displacement and location of any displaced anchor which can help with surgical planning (Fig.  1.10a, b). Ultrasound is also able to identify anchor displacement and has the ability to demonstrate suture material as well (Fig. 1.10d). The latter when seen unrelated to the cuff may in itself indicate breakdown of the repair.

1.5

Other Complications

As noted above, subacromial bursitis is a frequent finding in the immediate postoperative period and may be seen in asymptomatic individuals [20]. However, when a large bursal collection is seen in a symptomatic patient, consideration should be given to the possibility of infection or a reaction to suture anchors [69]. In patients who undergo open rotator cuff repair or mini-open technique, the deltoid muscle is divided to access the joint. Although rare, deltoid dehiscence as a result of failure of the closing sutures can be difficult to manage and is often associated with a poor outcome [70]. A similar problem can also occur as a complication of acromioplasty and arthroscopic decompression. The dehiscence can be detected on MRI and ultrasound by the presence of retraction of the deltoid at the site of

1  Shoulder: Rotator Cuff Repair

a

15

b

c d

Fig. 1.10  Case 1 (a, b) 61-year-old female with prior arthroscopic rotator cuff repair 11 months ago. Case 2 (c, d) 78-year-old female with prior arthroscopic rotator cuff repair 4 months ago. Coronal (a) and sagittal (b) T2-weighted fat-saturated MR images show medial displacement of a suture anchor previously embedded in the humeral head at the supraspinatus footprint. The suture anchor is now seen oriented horizontally above the humeral head and is seen in the region of the supraspinatus/infraspinatus overlap on sagittal images, clearly displaced from its insertion site (arrows). Frontal neutral radiograph (c) of the left shoulder and long-axis ultrasound image of the supraspinatus tendon (d) demonstrate a displaced metallic suture anchor projecting in the subacromial space above the humeral head (arrow). An additional metallic anchor is seen on the radiograph at the greater tuberosity

breakdown, with the gap being filled with fluid. Depending on the chronicity there may also be associated atrophy and fatty infiltration of the deltoid musculature [67]. Other postoperative complications following rotator cuff repair include acromial fracture, injury to the suprascapular or axillary nerve and biceps tendon subluxation or rupture. When imaging the shoulder following rotator cuff repair in patients with ongoing pain, careful inspection of the biceps tendon should be made. However, as ever it is important to review the operative notes as surgery may have also involved biceps tenotomy or tenodesis [67].

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Conclusion

MRI and ultrasound are both effective imaging modalities for evaluating a repaired rotator cuff tendon for potential re-tear. In the early postoperative period (less than 6 months), the repaired tendon often has a heterogeneous appearance, and it evolves in a predictable manner with time. Serial imaging is very helpful to evaluate for re-­ tears after a new injury or new symptom development. The diagnosis of a tendon re-tear should rely on the unequivocal identification of a tendon defect rather than simply heterogeneity or small cleft. Since small tendon defects may disappear over time, any equivocal imaging finding of the rotator cuff after repair can be followed up with imaging to determine its clinical significance.

References 1. Braune C, von Eisenhart-Rothe R, Welsch F, et al. Mid-term results and quantitative comparison of postoperative shoulder function in traumatic and non-traumatic rotator cuff tears. Arch Orthop Trauma Surg. 2003;123:419–24. 2. Depres-Tremblay G, Chevrier A, Snow M, et al. Rotator cuff repair: a review of surgical techniques, animal models, and new technologies under development. J Shoulder Elbow Surg. 2016;25:2078–85. 3. Hohmann E, Konig A, Kat CJ, et al. Single- versus double-row repair for full-thickness rotator cuff tears using suture anchors. Eur J Orthop Surg Traumatol. 2018;28:859–68. 4. Jancuska J, Matthews J, Miller T, et al. A systematic summary of systematic reviews on the topic of the rotator cuff. Orthop J Sports Med. 2018;6:2325967118797891. 5. Rossi LA, Rodeo SA, Chahla J, et al. Current concepts in rotator cuff repair techniques: biomechanical, functional, and structural outcomes. Orthop J Sports Med. 2019;7:2325967119868674. 6. Bedi A, Dines J, Warren RF, et al. Massive tears of the rotator cuff. J Bone Joint Surg Am. 2010;92:1894–908. 7. Derwin KA, Badylak SF, Steinmann SP, et al. Extracellular matrix scaffold devices for rotator cuff repair. J Shoulder Elbow Surg. 2010;19:467–76. 8. Samim M, Walsh P, Gyftopoulos S, et al. Postoperative MRI of massive rotator cuff tears. AJR Am J Roentgenol. 2018;211:146–54. 9. Barber FA, Burns JP, Deutsch A, et al. A prospective, randomized evaluation of acellular human dermal matrix augmentation for arthroscopic rotator cuff repair. Arthroscopy. 2012;28:8–15. 10. Wong I, Burns J, Snyder S. Arthroscopic GraftJacket repair of rotator cuff tears. J Shoulder Elbow Surg. 2010;19:104–9. 11. Frank RM, Cvetanovich G, Savin D, et al. Superior capsular reconstruction: indications, techniques, and clinical outcomes. JBJS Rev. 2018;6:e10. 12. Collin P, Yoshida M, Delarue A, et al. Evaluating postoperative rotator cuff healing: prospective comparison of MRI and ultrasound. Orthop Traumatol Surg Res. 2015;101:S265–8. 13. Crim J, Burks R, Manaster BJ, et al. Temporal evolution of MRI findings after arthroscopic rotator cuff repair. AJR Am J Roentgenol. 2010;195:1361–6. 14. Duc SR, Mengiardi B, Pfirrmann CW, et al. Diagnostic performance of MR arthrography after rotator cuff repair. AJR Am J Roentgenol. 2006;186:237–41. 15. Tudisco C, Bisicchia S, Savarese E, et al. Single-row vs. double-row arthroscopic rotator cuff repair: clinical and 3 tesla MR arthrography results. BMC Musculoskelet Disord. 2013;14:43. 16. de Jesus JO, Parker L, Frangos AJ, et al. Accuracy of MRI, MR arthrography, and ultrasound in the diagnosis of rotator cuff tears: a meta-analysis. AJR Am J Roentgenol. 2009;192: 1701–7.

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17. Gazzola S, Bleakney RR.  Current imaging of the rotator cuff. Sports Med Arthrosc Rev. 2011;19:300–9. 18. Sipola P, Niemitukia L, Kroger H, et  al. Detection and quantification of rotator cuff tears with ultrasonography and magnetic resonance imaging—a prospective study in 77 consecutive patients with a surgical reference. Ultrasound Med Biol. 2010;36:1981–9. 19. Peh WC, Chan JH. Artifacts in musculoskeletal magnetic resonance imaging: identification and correction. Skeletal Radiol. 2001;30:179–91. 20. Spielmann AL, Forster BB, Kokan P, et al. Shoulder after rotator cuff repair: MR imaging findings in asymptomatic individuals—initial experience. Radiology. 1999;213:705–8. 21. Zlatkin MB. MRI of the postoperative shoulder. Skeletal Radiol. 2002;31:63–80. 22. Magee TH, Gaenslen ES, Seitz R, et al. MR imaging of the shoulder after surgery. AJR Am J Roentgenol. 1997;168:925–8. 23. Barile A, Bruno F, Mariani S, et al. What can be seen after rotator cuff repair: a brief review of diagnostic imaging findings. Musculoskelet Surg. 2017;101:3–14. 24. Beltran LS, Bencardino JT, Steinbach LS. Postoperative MRI of the shoulder. J Magn Resonan Imag. 2014;40:1280–97. 25. von Engelhardt LV, von Falkenhausen M, Fahmy U et  al. [MRI after reconstruction of the supraspinatus tendon: MR-tomographic findings]. Z Orthop Ihre Grenzgeb. 2004;142:586–91. 26. Kim JN, Kwon ST, Kim KC. Early postoperative magnetic resonance imaging findings after arthroscopic rotator cuff repair: T2 hyperintensity of the capsule can predict reduced shoulder motion. Arch Orthop Trauma Surg. 2018;138:247–58. 27. Sofka CM, Ciavarra GA, Hannafin JA, et al. Magnetic resonance imaging of adhesive capsulitis: correlation with clinical staging. HSS J. 2008;4:164–9. 28. Galatz LM, Ball CM, Teefey SA, et  al. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J Bone Joint Surg Am. 2004;86:219–24. 29. Kim JR, Cho YS, Ryu KJ, et al. Clinical and radiographic outcomes after arthroscopic repair of massive rotator cuff tears using a suture bridge technique: assessment of repair integrity on magnetic resonance imaging. Am J Sports Med. 2012;40:786–93. 30. Mellado JM, Calmet J, Olona M, et al. MR assessment of the repaired rotator cuff: prevalence, size, location, and clinical relevance of tendon rerupture. Eur Radiol. 2006;16:2186–96. 31. Tashjian RZ, Hollins AM, Kim HM, et al. Factors affecting healing rates after arthroscopic double-row rotator cuff repair. Am J Sports Med. 2010;38:2435–42. 32. Matava MJ, Purcell DB, Rudzki JR.  Partial-thickness rotator cuff tears. Am J Sports Med. 2005;33:1405–17. 33. Mihata T, Fukuhara T, Jun BJ, et al. Effect of shoulder abduction angle on biomechanical properties of the repaired rotator cuff tendons with 3 types of double-row technique. Am J Sports Med. 2011;39:551–6. 34. Mihata T, Watanabe C, Fukunishi K, et al. Functional and structural outcomes of single-row versus double-row versus combined double-row and suture-bridge repair for rotator cuff tears. Am J Sports Med. 2011;39:2091–8. 35. Park MC, Elattrache NS, Ahmad CS, et al. “Transosseous-equivalent” rotator cuff repair technique. Arthroscopy. 2006;22(1360):e1–5. 36. Park MC, Tibone JE, ElAttrache NS, et al. Part II: biomechanical assessment for a footprint-­ restoring transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg. 2007;16:469–76. 37. Bishop J, Klepps S, Lo IK, et  al. Cuff integrity after arthroscopic versus open rotator cuff repair: a prospective study. J Shoulder Elbow Surg. 2006;15:290–9. 38. DeFranco MJ, Bershadsky B, Ciccone J, et al. Functional outcome of arthroscopic rotator cuff repairs: a correlation of anatomic and clinical results. J Shoulder Elbow Surg. 2007;16:759–65. 39. Miller BS, Downie BK, Kohen RB, et al. When do rotator cuff repairs fail? Serial ultrasound examination after arthroscopic repair of large and massive rotator cuff tears. Am J Sports Med. 2011;39:2064–70.

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40. Sugaya H, Maeda K, Matsuki K, et al. Functional and structural outcome after arthroscopic full-thickness rotator cuff repair: single-row versus dual-row fixation. Arthroscopy. 2005;21:1307–16. 41. Mallon WJ, Misamore G, Snead DS, et al. The impact of preoperative smoking habits on the results of rotator cuff repair. J Shoulder Elbow Surg. 2004;13:129–32. 42. McFarland EG, O’Neill OR, Hsu CY. Complications of shoulder arthroscopy. J South Orthop Assoc. 1997;6:190–6. 43. Romeo AA, Hang DW, Bach BR, Jr. et al. Repair of full thickness rotator cuff tears. Gender, age, and other factors affecting outcome. Clin Orthop Relat Res 1999;(367):243–55. 44. Oh JH, Kim JY, Kim SH, et  al. Predictability of early postoperative ultrasonography after arthroscopic rotator cuff repair. Orthopedics. 2017;40:e975–81. 45. Cohen DB, Kawamura S, Ehteshami JR, et al. Indomethacin and celecoxib impair rotator cuff tendon-to-bone healing. Am J Sports Med. 2006;34:362–9. 46. Jost B, Zumstein M, Pfirrmann CW, et al. Long-term outcome after structural failure of rotator cuff repairs. J Bone Joint Surg Am. 2006;88:472–9. 47. Saccomanno MF, Cazzato G, Fodale M, et  al. Magnetic resonance imaging criteria for the assessment of the rotator cuff after repair: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2015;23:423–42. 48. Kim JH, Hong IT, Ryu KJ, et al. Retear rate in the late postoperative period after arthroscopic rotator cuff repair. Am J Sports Med. 2014;42:2606–13. 49. Meyer DC, Wieser K, Farshad M, et  al. Retraction of supraspinatus muscle and tendon as predictors of success of rotator cuff repair. Am J Sports Med. 2012;40:2242–7. 50. Shin YK, Ryu KN, Park JS, et al. Predictive factors of retear in patients with repaired rotator cuff tear on shoulder MRI. AJR Am J Roentgenol. 2018;210:134–41. 51. Gulotta LV, Nho SJ, Dodson CC, et  al. Prospective evaluation of arthroscopic rotator cuff repairs at 5 years: part II–prognostic factors for clinical and radiographic outcomes. J Shoulder Elbow Surg. 2011;20:941–6. 52. Kim SJ, Kim SH, Lee SK, et al. Arthroscopic repair of massive contracted rotator cuff tears: aggressive release with anterior and posterior interval slides do not improve cuff healing and integrity. J Bone Joint Surg Am. 2013;95:1482–8. 53. Toyoda H, Ito Y, Tomo H, et  al. Evaluation of rotator cuff tears with magnetic resonance arthrography. Clin Orthop Relat Res. 2005;439:109–15. 54. Meyer M, Klouche S, Rousselin B, et al. Does arthroscopic rotator cuff repair actually heal? Anatomic evaluation with magnetic resonance arthrography at minimum 2 years follow-up. J Shoulder Elbow Surg. 2012;21:531–6. 55. Teefey SA, Hasan SA, Middleton WD, et al. Ultrasonography of the rotator cuff. A comparison of ultrasonographic and arthroscopic findings in one hundred consecutive cases. J Bone Joint Surg Am. 2000;82:498–504. 56. Sofka CM, Adler RS. Original report. Sonographic evaluation of shoulder arthroplasty. AJR Am J Roentgenol. 2003;180:1117–20. 57. Sugaya H, Maeda K, Matsuki K, et  al. Repair integrity and functional outcome after arthroscopic double-row rotator cuff repair. A prospective outcome study. J Bone Joint Surg Am. 2007;89:953–60. 58. Jacobson JA.  Shoulder US: anatomy, technique, and scanning pitfalls. Radiology. 2011;260:6–16. 59. Fealy S, Adler RS, Drakos MC, et al. Patterns of vascular and anatomical response after rotator cuff repair. Am J Sports Med. 2006;34:120–7. 60. St Pierre P, Olson EJ, Elliott JJ, et al. Tendon-healing to cortical bone compared with healing to a cancellous trough. A biomechanical and histological evaluation in goats. J Bone Joint Surg Am. 1995;77:1858–66. 61. Adler RS. Postoperative rotator cuff. Semin Musculoskelet Radiol. 2013;17:12–9. 62. Prickett WD, Teefey SA, Galatz LM, et al. Accuracy of ultrasound imaging of the rotator cuff in shoulders that are painful postoperatively. J Bone Joint Surg Am. 2003;85:1084–9.

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63. Gulotta LV, Nho SJ, Dodson CC, et  al. Prospective evaluation of arthroscopic rotator cuff repairs at 5 years: part I—functional outcomes and radiographic healing rates. J Shoulder Elbow Surg. 2011;20:934–40. 64. Yoo HJ, Choi JY, Hong SH, et al. Assessment of the postoperative appearance of the rotator cuff tendon using serial sonography after arthroscopic repair of a rotator cuff tear. J Ultrasound Med. 2015;34:1183–90. 65. Kluger R, Mayrhofer R, Kröner A, et  al. Sonographic versus magnetic resonance arthrographic evaluation of full-thickness rotator cuff tears in millimeters. J Shoulder Elbow Surg. 2003;12:110–6. 66. Iannotti JP, Deutsch A, Green A, et al. Time to failure after rotator cuff repair: a prospective imaging study. J Bone Joint Surg Am. 2013;95:965–71. 67. Thakkar RS, Thakkar SC, Srikumaran U, et al. Complications of rotator cuff surgery-the role of post-operative imaging in patient care. Br J Radiol. 2014;87:20130630. 68. Magee T, Shapiro M, Hewell G, et al. Complications of rotator cuff surgery in which bioabsorbable anchors are used. AJR Am J Roentgenol. 2003;181:1227–31. 69. Gusmer PB, Potter HG, Donovan WD, et al. MR imaging of the shoulder after rotator cuff repair. AJR Am J Roentgenol. 1997;168:559–63. 70. Chebli CM, Murthi AM.  Deltoidplasty: outcomes using orthobiologic augmentation. J Shoulder Elbow Surg. 2007;16:425–8.

2

Post Op Imaging of the Shoulder: Stabilization Surgery Klaus Woertler

2.1

Soft Tissue and Bone Lesions in the Unstable Shoulder

The soft tissue and bone lesions, which result from a single or from multiple dislocations, are the patho-anatomic cause of traumatic shoulder instability and will be the target of the surgical treatment which is usually required to correct the instability. Disruption of the anterior or posterior labro-ligamentous complex, the main passive joint stabilizers, is the typical underlying soft tissue injury, with the classic Bankart lesion and its variants (glenoid-sided labral avulsion) representing the most common type. The antero-inferior labro-ligamentous complex might also be avulsed together with an osseous fragment of variable size (bony Bankart lesion). Deficiency of the glenoid represents another important factor for joint instability once the bony fragment reaches a critical size. Loss of glenoidal bone substance may occur in the absence of acute fracture as a result of chronic wear resulting from multiple shoulder dislocations. The normal glenoid usually shows a slight retroversion of less than 10°. Abnormal retroversion (>5°) can contribute to the development of posterior glenohumeral instability [1–8]. The Hill Sachs lesion is a compression fracture of the posterolateral humeral head, which is created by forceful impaction of the humeral head against the antero-­inferior glenoid during anterior shoulder dislocation. The lesion can considerably vary in size and depth ranging from a shallow chondral defect to a deep osteochondral impaction fracture and is seen in 40–100% of patients with traumatic anterior shoulder dislocations. After posterior shoulder dislocation a similar, often wedge-­shaped defect can be found at the anteromedial aspect of the humeral head. This finding has been called the reverse Hill Sachs or McLaughlin lesion [1, 2, 6–9].

K. Woertler (*) Technische Universität München, Munich, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 E. Rowbotham, A. J. Grainger (eds.), Postoperative Imaging of Sports Injuries, https://doi.org/10.1007/978-3-030-54591-8_2

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Whereas shoulder surgeons used to focus on glenoid-sided soft tissue and bone lesions in former years, more recently a bipolar concept considering both, lesions of the glenoid and the humeral head, has developed (Fig.  2.1). With the use of the “glenoid track” method, patients at risk of failure following Bankart repair (reattachment of the labro-ligamentous complex) can be identified. In the presence of bipolar bone loss, the remaining glenoid track can be calculated by drawing a best fit circle to encompass the full anteroposterior diameter of the inferior glenoid on a sagittal CT or MR image, multiplying the diameter with 0.83, and subtracting the size of the glenoid defect as measured from the anterior aspect of the circle perpendicular to the anterior border of the remaining glenoid. Next, the Hill Sachs interval is determined by measuring the largest transverse diameter of the Hill Sachs defect and adding the distance from its lateral margin to the insertion of the rotator cuff. If the Hill Sachs interval is less than the glenoid track, the Hill Sachs lesion is considered “on-track”, if it is greater than the glenoid track, it is considered “off-track”. “Off-track” lesions are more likely to cross and engage the anterior border of the glenoid in abduction and external rotation and, consequently, to cause shoulder dislocation than “on-track” lesions [8, 10–12]. Superior labral anterior to posterior (SLAP) lesions are commonly associated injuries in athletes with shoulder instability. Superior extension of an antero-inferior labro-ligamentous injury, caused by the anterior shoulder dislocation, leads to the classic combination of a Bankart or Bankart variant lesion and a SLAP type 2 or type 4 lesion with an unstable biceps anchor. SLAP lesions however may also be seen in athletes with microinstability or as an isolated injury in athletes with stable shoulders [7, 13]. a

b

Fig. 2.1  Glenoid track method. (a) Determination of the glenoid track by measuring the full AP diameter of the glenoid (D) on a sagittal oblique image, multiplying the measured value with 0.83 and subtracting the measured size of the bony defect (d): glenoid track  =  0.83  ×  D  −  d. (b) Determination of the Hill Sachs interval by adding the largest diameter of the Hill Sachs defect (white line) and its distance from the insertion of the rotator cuff (red line) on an axial image. In this example, sagittal and axial CT reformation images were used for measurements. The Hill Sachs defect is considered “off track”, because the Hill Sachs interval is greater than the glenoid track

2  Post Op Imaging of the Shoulder: Stabilization Surgery

2.2

23

Soft Tissue Reconstruction Procedures

Traumatic shoulder instability without a significant glenoid bone defect is usually treated by primary anatomic repair of the labro-ligamentous complex (Fig. 2.2). The original surgical technique described by Bankart was an open procedure with reattachment of the torn labrum using transosseous sutures; however, nowadays the majority of anatomic repair procedures are performed arthroscopically (arthroscopic Bankart repair). Most shoulder surgeons reattach the antero-inferior labro-­ ligamentous complex with the use of three suture anchors placed at the 2, 4–5 and 5 o’clock positions of the glenoid. The two inferior anchors should be located proximally and distally to the origin of the inferior glenohumeral ligament. The configuration and composition of these anchors has repeatedly changed over the years and is still an area of continued development. At present, bioabsorbable and non-­ resorbable plastic (PEEK) anchors are favoured by many surgeons, but metallic (titanium) anchors are also still in use. Similar procedures are performed to repair the posterior labrum in patients with posterior instability. Reduction of the capsular volume (capsulorrhaphy) might be indicated in atraumatic shoulder instability or in combination with Bankart repair in individuals with a

b

3′ Glenoid

4-5′ W OE

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5′ Labrum

IGHL

Fig. 2.2  Suture anchor Bankart repair. (a) Schematic drawing shows preoperative finding with avulsion of antero-inferior labrum and inferior glenohumeral ligament (IGHL) from underlying glenoid. (b) Schematic drawing demonstrates postoperative situation after refixation of the antero-­ inferior labro-ligamentous complex with the use of suture anchors (Bankart repair). In the schematic they are indicated at the 3, 4–5 and 5 o’clock positions

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traumatic instability. Open capsular shift and rotator interval closure have been widely replaced by arthroscopic suture capsular plication. Overall, capsulorrhaphy procedures are relatively rarely performed today [6, 8, 14–17].

2.2.1 Normal Postoperative Findings Following arthroscopic Bankart repair (Figs. 2.3 and 2.4), the correct suture anchor position can be best assessed on sagittal MR or CT reformation images through the glenoid. The reattached glenoid labrum can appear plump, slightly irregular and enlarged and may show increased signal intensity on MR imaging, but it should be located in a normal anatomic position closely attached to the underlying glenoid. Partial clefts under the labrum, which may be seen on MR arthrography, do not correlate with a poor functional outcome. Irregularity and thickening of the inferior glenohumeral ligament and joint capsule are common postoperative findings. Following surgical capsular reduction, the axillary recess may appear shortened. The integrity of the repaired antero-inferior labro-ligamentous complex is however often difficult to assess, because scar tissue and metallic abrasion artefacts can obscure the anatomic structures on MR images or MR arthrograms obtained in the neutral position. MR arthrograms in the ABER (abduction and external rotation) position are very helpful in this situation, because the IGHL becomes taut and the entire labro-ligamentous complex can be followed from the glenoid to its humeral insertion. On ABER images the repaired complex should be in close contact with the humeral head without pooling of contrast media between the IGHL and the cartilage surface [6, 16, 18].

2.2.2 Recurrent or Persistent Instability A retear of the repaired labro-ligamentous complex is the expected morphologic finding if recurrent instability following Bankart repair is initiated by a traumatic shoulder redislocation or subluxation. The criteria to diagnose a repeat labral tear on MR imaging are similar to those used in the preoperative setting. The overall accuracy of MR arthrography in identifying recurrent labral tears has been reported to be greater than 90% [5, 18]. MR arthrograms can demonstrate partial or complete detachment of the labrum from the glenoid, capsular stripping with medial or inferior displacement of the labrum on the scapular neck, tearing of the inferior glenohumeral ligament, or complete destruction of the entire labro-ligamentous complex (Fig.  2.5). Images obtained in the ABER position are valuable for defining the exact site and extent of the recurrent labro-ligamentous injury, for detecting non-displaced labral tears and for identifying defects otherwise obscured by scar tissue [4, 6, 16, 19]. Insufficient surgical reduction of capsular volume can cause persistent or recurrent shoulder instability in the absence of a repeat labro-ligamentous tear (Fig. 2.6). Capsular volume may be estimated on MR or CT arthrograms. A wide anterior joint recess and a wide rotator interval should raise suspicion for a redundant anterior

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Fig. 2.3  Bankart repair: normal postoperative findings. (a, b) Axial T1-weighted MR arthrograms obtained following arthroscopic Bankart repair in a patient with stable shoulder but suspected to have a pulley lesion (not shown) reveal anatomic reconstruction of the antero-inferior glenoid labrum (arrow) and the IGHL (arrowhead). (c) Corresponding MR arthrogram in ABER position demonstrates perfect continuity of the labro-ligamentous complex in close contact with the humeral head. Remnant of bioabsorbable suture anchor is seen within glenoid (asterisk)

capsule, whereas overtightening may lead to a relative widening of the posterior recess, posterior subluxation of the humeral head and premature osteoarthritis. MR arthrograms obtained in the ABER position typically demonstrate redundancy signs with a patulous or sigmoid-shaped inferior glenohumeral ligament and pooling of contrast media between the anterior capsule and the humeral head [6, 20].

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Fig. 2.4  Bankart repair: normal postoperative findings. (a) Axial T1-weighted MR arthrogram obtained following arthroscopic Bankart repair with the use of three titanium anchors shows seemingly enlarged antero-inferior labro-ligamentous complex obscured by susceptibility artefacts and scar tissue (arrow). (b) Corresponding MR arthrogram in ABER position depicts integrity of the restored labro-ligamentous complex without evidence of a repeat tear. The IGHL appears slightly thickened and irregular (arrowheads)

Bone defects of the glenoid as a cause for failed Bankart surgery are best depicted on cross-sectional images in the sagittal plane (Fig. 2.7). Classically, CT has been recommended to assess the exact extent of glenoid bone loss, but MR imaging with the use of 2D or 3D pulse sequences has been shown to be able to provide comparable results [10, 21, 22].

2.2.3 Postoperative Complications Suture anchors can cause mechanical complications due to malpositioning, loosening or displacement into the joint space. Proud or loose anchors can become symptomatic with pain, locking, limited range of motion and joint effusion. They may lead to damage to the cartilage surface of the humeral head and glenoid. Osteolysis around suture anchors may be induced by biodegradable material but is not necessarily associated with fixation failure or unfavourable clinical outcome. Loose bioabsorbable anchors displaced into the joint space induce severe synovitis and arthropathy and should be immediately removed by the surgeon. Whereas the position of metallic anchors can easily be identified on radiographs and CT images, the non-radiopaque bioabsorbable anchors are only depicted on

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Fig. 2.5  Traumatic retear of the antero-inferior labro-ligamentous complex following arthroscopic Bankart repair. (a, b) Axial and (c) coronal T1-weighted MR arthrograms show antero-inferior labrum in a normal anatomic position but undermined by contrast media (arrows). Dislodged bioabsorbable suture anchors can be seen in the subcoracoid recess and interposed between the glenoid rim and the detached labrum (arrowheads). (d) In addition to a recurrent labral tear (arrow), MR arthrogram obtained in the ABER position demonstrates discontinuity of the IGHL (asterisk)

ultrasound or MR imaging (Fig.  2.5). Biodegradable material does not exhibit any MR signal and therefore is indirectly visualized within bone marrow or, in the case of displacement, within the surrounding joint fluid or soft tissues [6, 23, 24]. Osteolysis caused by bioabsorbable anchors can contain granulation tissue or may appear entirely cystic on MR imaging [2, 4, 6]. Other postoperative complications are quite rare and correspond to the general complications of arthroscopic surgery, including infection, adhesive capsulitis, nerve injury and osteoarthritis [6].

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Fig. 2.6  Arthroscopic Bankart repair: insufficient capsular reduction. (a, b) Axial T1-weighted MR arthrograms obtained in a patient with persistent anterior instability after Bankart repair reveal thickened antero-inferior labrum and IGHL in a normal anatomic position (arrows). The anterior capsular recess appears relatively wide. (c) Corresponding MR arthrogram in ABER position shows a redundant IGHL (arrowhead) and pooling of contrast media between the ligament and the humeral head in the absence of a retear suggesting insufficient surgical tightening

2.3

Bone Reconstruction Procedures and Remplissage

Acute bony Bankart lesions are usually treated by screw fixation of the osseous fragment to the glenoid or with the use of the “bony Bankart bridge” technique. The latter technique involves an arthroscopic procedure during which the lesion is reduced and reattached using suture anchors placed medial to the fracture on the scapular neck and on the glenoid face connected by a suture around the bony fragment. Further anchors are placed superior and inferior to the bony fragment in order to repair the labrum and joint capsule [15].

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Fig. 2.7  Failed arthroscopic Bankart repair: glenoid bone defect. (a) Coronal and (b) axial intermediate-­weighted MR images from a patient with recurrent shoulder instability after Bankart repair show a recurrent tear of the postoperatively enlarged antero-inferior labrum associated with capsuloperiosteal stripping (arrows). Glenoid bone loss can already be suspected on MR images. (c) Axial and (d) sagittal CT reformation images verify a significant osseous defect of the anterior glenoid (arrowheads)

Patients with anterior instability who have undergone unsuccessful arthroscopic Bankart repair and with chronic glenoid defects of a significant size are currently treated surgically with the Bristow and Latarjet or other bone block procedures (Fig.  2.8). In the modified Bristow procedure, augmentation of the glenoid is achieved by removing the tip of the coracoid process and fixing it to the antero-­ inferior glenoid in a standing position with the use of a screw. In the Latarjet procedure, a larger portion of the coracoid is transferred together with the attached conjoined tendon of the biceps brachii and coracobrachialis muscles and fixed to the antero-inferior glenoid with two screws in a lying position. In addition to augmentation of the glenoid, the Latarjet procedure provides anterior stabilization by a

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Fig. 2.8  Coracoid transfer procedures. (a) Schematic drawing of the shoulder shows transfer of the resected coracoid process together with its tendinous attachments to the antero-inferior glenoid through a horizontal slit incision within the subscapularis muscle (SSC). (b) Bristow procedure: the tip of the coracoid is fixed to the glenoid in a standing position with the use of a screw. (c) Latarjet procedure: the coracoid is resected at its base and secured at the glenoid in a lying position with two screws

dynamic sling effect caused by the conjoined tendon weaved through an intramuscular split in the subscapularis muscle [4, 6, 8, 12, 25]. The J-bone graft procedure (Resch procedure) is an alternative technique for anatomical reconstruction of the glenoid. During this procedure, a J-shaped bone graft harvested from the iliac crest is inserted into a slot in the scapular neck created approximately 5 mm medial to the articular surface. The bone block is introduced with a press-fit-technique without using fixation devices [26]. Both, coracoid transfer and J-bone graft procedures, can nowadays be performed arthroscopically and are typically used to treat glenoid defects with up to 35% loss of surface area [14, 25]. In cases with more extensive defects the glenoid may be augmented with screw fixation of larger bone grafts from the iliac crest. An abnormal retroversion of the glenoid can be corrected by glenoid osteotomy and insertion of a wedge-shaped bone graft harvested from the scapular spine or iliac crest [1]. Off-track Hill Sachs lesions represent an indication for surgery dependent on their location, depth and aetiology. More superficial defects can be addressed by remplissage, an arthroscopic procedure involving transfer of the infraspinatus tendon and posterior joint capsule into the Hill Sachs lesion with the use of suture anchors for fixation. The procedure reduces the risk of engaging and resultant further anterior dislocations by excluding the Hill Sachs defect from the joint and by decreasing anterior translation and external rotation of the humeral head [8, 12]. Larger defects might require filling with a bone graft. In rare cases, extensive Hill Sachs lesions are treated by partial resurfacing of the humeral head with bone grafts or metallic implants (partial prosthesis).

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The modified McLaughlin procedure is an arthroscopic remplissage technique which can be performed to address reverse Hill Sachs lesions by filling the defect of the humeral head with the subscapularis tendon [1, 9].

2.3.1 Normal Postoperative Findings MR imaging is less useful than CT or CT arthrography for evaluating the morphologic result after bone reconstruction procedures; patients may however undergo MR imaging for other reasons, such as assessment of the rotator cuff. The Bristow/ Latarjet procedure may induce variable amounts of scar tissue formation at the anterior glenoid and associated with the subscapularis muscle. The muscle belly often shows signs of atrophy and fatty infiltration [4, 6]. CT is best suited for depicting the exact position of reattached bony Bankart fragments, bone grafts and screws. In patients who have undergone coracoid transfer, the coracoid process will show an osseous defect, which involves the tip in case of the Bristow procedure and a larger portion in case of the Latarjet procedure. The ideal position of the transposed graft is flush with the articular surface on axial images and below the equator of the glenoid on sagittal images [8, 27] (Fig. 2.9). Following J-bone graft procedures or glenoid osteotomies, CT should show integration of the intraosseous bone graft without signs of fracture of the glenoid and, in the case of osteotomy, correction of glenoid version [1] (Fig. 2.10).

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Fig. 2.9  Latarjet procedure: normal postoperative findings. (a) Postoperative AP radiograph shows transferred coracoid process fixed with two screws (arrow). Note Hill Sachs defect of the humeral head (arrowhead). (b) Axial CT image obtained on follow-up reveals osseous fusion of the graft (arrow) with the underlying glenoid in a correct position flush with the articular surface

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Fig. 2.10  Glenoid osteotomy: normal postoperative findings. (a) Axial CT image shows correct intraosseous position of bone graft (arrow) following posterior glenoid osteotomy performed for correction of abnormal retroversion in a patient with posterior shoulder instability. (b) Axial CT image obtained at the level of the scapular spine depicts bone defect at the donor site (arrowhead)

If a remplissage procedure has been performed, MR imaging should show firm attachment of the tendon (infraspinatus or subscapularis) to the humeral head in direct contact with the suture anchor(s) used for fixation. The bony defect (Hill Sachs or reverse Hill Sachs lesion) is however not always entirely filled with tendon tissue. The corresponding muscle belly can show various grades of muscle atrophy and fatty infiltration [4, 12, 28].

2.3.2 Complications The Bristow/Latarjet and J-bone graft procedures have a low rate of recurrence. Persistent shoulder instability may occur if the bone block is placed too medial relative to the glenoid surface. All bone reconstruction procedures may be complicated by malpositioning, dislocation, non-union, resorption of fragments or grafts, and, if screw fixation is performed, fracture, loosening and migration of screws. A complication rate of up to 30% has been reported after the Bristow/Latarjet procedure. Non-union, fracture or resorption of the graft are however not necessarily associated with an unfavourable clinical outcome [4, 6, 25, 27] (Fig. 2.11). Further complications include postoperative infection and nerve injury due to intraoperative tissue retraction or direct laceration, which might affect the axillary, musculocutaneous or, rarely, the suprascapular nerve. The suprascapular nerve might also be damaged by transglenoidal screws protruding into the spinoglenoid notch. On MR imaging, injury to the axillary nerve can be diagnosed, if denervation oedema of the deltoid

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Fig. 2.11  Latarjet procedure: postoperative complications. (a, b) Axial and sagittal CT reformation images demonstrate osseous non-union and migration of the graft (arrows) as well as loosening and dislocation of screws. (c, d) Axial CT images show fracture of the transferred coracoid process with fragment dislocation (arrowheads)

and/or teres minor muscles is seen (Fig. 2.12). Suprascapular nerve palsy leads to denervation of the supraspinatus and infraspinatus muscle or the infraspinatus muscle alone, depending on the site of injury. Subsequent muscular changes include atrophy and fatty infiltration [4, 6, 12, 27, 29]. Osteoarthritis is a typical sequel of long-standing glenohumeral instability and a frequent complication of stabilization surgery, equally common after the Bristow/ Latarjet and other bone block procedures. Technical errors, such as lateral overhanging of the bone graft or intra-articular screw placement, pre-existing degenerative joint changes, older age, preoperative fracture of the glenoid, large Hill Sachs lesions, and high-demand sports are all positive predictors for the development of osteoarthritis in patients who have undergone the Latarjet procedure [4, 6, 12, 25, 27] (Fig. 2.13).

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Fig. 2.12  Postoperative axillary nerve palsy. (a, b) Coronal fat-suppressed intermediate-weighted MR images of the shoulder show denervation oedema of the deltoid (D) and teres minor (TM) muscles in a patient with injury of the axillary nerve during stabilization surgery

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Fig. 2.13  Latarjet procedure: osteoarthritis. (a) AP radiograph and (b) axial CT image show early degenerative changes of the anterior glenohumeral joint (arrows) in a young patient with anterior shoulder instability who had undergone a Latarjet procedure. Note lateral overhang of the bone graft in contact with the humeral head

Complications after arthroscopic remplissage are rare. Abnormal MR imaging findings indicative of fixation failure are poor filling of the osseous defect at the humeral head with tendon tissue, fluid or contrast media extending between the tendon and the bone defect, lack of tendon tissue at the suture anchor, and anchor pull-out [12] (Fig. 2.14).

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Fig. 2.14 Remplissage: fixation failure. Axial T1-weighted MR arthrogram of the shoulder demonstrates extension of contrast media (arrow) between the surface of a large Hill Sachs defect and the frayed infraspinatus tendon (ISP) in a patient after arthroscopic remplissage. There is no contact between the suture anchor (arrowhead) and tendon tissue

2.4

SLAP Repair and Biceps Tenodesis

The concept of surgical treatment of patients with SLAP lesions has changed, as anatomical repair is no longer recommended in athletes older than 25 years. The majority of patients are nowadays treated by biceps tenodesis. For anatomical SLAP repair the biceps anchor and superior labrum are refixed to the glenoid with the use of one or two suture anchors. If tenodesis is performed, the intra-articular portion of the long head of biceps tendon is resected and the extra-articular portion is fixed either to the surrounding soft tissues by sutures or to the proximal humerus with the use of a drill hole and an interference screw or with a suture anchor [2, 18, 30].

2.4.1 Normal Postoperative Findings Following SLAP repair, the superior labrum and biceps anchor should have a smooth contour, and there should be no fluid or contrast media entering the labrum or interposed between the labrum and the glenoid on MR imaging, MR or CT arthrography [2, 4, 6]. If two suture anchors are used, they should be seen posterior and anterior to the biceps anchor at the 10–11 o’clock and 1–2 o’clock position on the glenoid [6]. Following biceps tenodesis, the intra-articular portion of the tendon is absent, and the superior glenoid labrum may appear shortened or truncated (Fig. 2.15). The site of reattachment is typically seen on the head or proximal shaft of the humerus.

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Fig. 2.15  Biceps tenodesis: normal postoperative findings. (a) Sagittal T2-weighted MR image shows intact tenodesis of the long head of biceps tendon (arrows) at the level of the intertubercular groove with the use of a bioabsorbable interference screw (asterisk). (b) Coronal fat-suppressed intermediate-weighted MR image demonstrates shortening of the superior glenoid labrum (arrowhead) and absence of the intra-articular biceps tendon

With fixation to bone, MR imaging may show metallic abrasion artefacts from drilling. Metallic or bioabsorbable fixation devices should have an entirely intraosseous position and should be in direct contact with the tendon. The integrity of the tenodesis can be assessed by ultrasound or MR imaging. Radiographs may show an apparent “lytic lesion” caused by the drill hole if a bioabsorbable interference screw is used for fixation [4, 6, 12, 26].

2.4.2 Recurrent Lesions Fixation failure, anchor pull-out and recurrent tears after SLAP repair are probably best visualized on MR or CT arthrography, although scientific data supporting this assumption have so far not been obtained (Fig. 2.16). The development of a paralabral ganglion cyst must be interpreted as an indirect sign of a retear. Pull-out or tears after tenodesis result in discontinuity, retraction or non-visualization of the biceps tendon [6] (Fig. 2.17).

2.4.3 Complications Both, SLAP repair and biceps tenodesis, harbour a low risk of postoperative complications. Anatomic reattachment of the biceps anchor can lead to adhesive capsulitis

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Fig. 2.16 Repeat tear following SLAP repair. (a) Sagittal T1-weighted and (b) coronal fat-­ suppressed T1-weighted MR arthrograms show correct position of two suture anchors (arrowheads) after anatomic refixation of the biceps anchor. Contrast media is seen extending under the superior labrum to the supraglenoid tubercle (arrow) indicative of a recurrent SLAP lesion

Fig. 2.17  Fixation failure of biceps tenodesis. Sagittal fat-suppressed intermediate-weighted MR image of the shoulder reveals pull-out of the bioabsorbable interference screw (arrowhead) in the early postoperative phase after biceps tenodesis. The tendon (arrows) is only mildly retracted and still in contact with the screw

with shoulder stiffness. Biceps tenodesis may be complicated by infection, haematoma, fracture, neurologic compromise and reflex sympathetic dystrophy [2, 12, 31]. Complications related to metallic or bioabsorbable screws and anchors are similar to those described with Bankart repair (Fig. 2.18).

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Fig. 2.18  Osteolysis after SLAP repair with bioabsorbable anchors. (a) Axial and (b) sagittal T1-weighted MR arthrograms and (c) coronal fat-suppressed intermediate-weighted MR arthrogram depict a sharply delineated lesion around the anterior suture anchor at the superior glenoid (arrows). Bioabsorbable material is readily identified within the cyst-like osteolytic area. The reattached biceps insertion appears intact (arrowhead)

References 1. Antosh IJ, Tokish JM, Owens BD. Posterior shoulder instability: current surgical management. Sports Health. 2016;8:520–6. 2. Beltran LS, Bencardino JT, Steinbach LS. Postoperative MRI of the shoulder. J Magn Reson Imaging. 2014;40:1280–97. 3. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16:677–94. 4. Pierce JL, Nacey NC, Jones S, et al. Postoperative shoulder imaging: rotator cuff, labrum, and biceps tendon. Radiographics. 2016;36:1648–71. 5. Probyn LJ, White LM, Salonen DC, Tomlinson G, Boynton EL.  Recurrent symptoms after shoulder instability repair: direct MR arthrographic assessment—correlation with second-look surgical evaluation. Radiology. 2007;245:814–23.

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6. Woertler K. Multimodality imaging of the postoperative shoulder. Eur Radiol. 2007;17:3038–55. 7. Woertler K, Waldt S.  MR imaging of sports-related glenohumeral instability. Eur Radiol. 2006;16:2622–36. 8. Younan Y, Wong PK, Karas S, Umpierrez M, Gonzalez F, Jose J, Singer AD.  The glenoid track: a review of the clinical relevance, method of calculation and current evidence behind this method. Skeletal Radiol. 2017;46:1625–34. 9. Martetschläger F, Padalecki JR, Millet PJ. Modified arthroscopic McLaughlin procedure for treatment of posterior instability of the shoulder with an associated reverse Hill-Sachs lesion. Knee Surg Sports Traumatol Arthrosc. 2013;21:1642–6. 10. Gyftopoulos S, Beltran LS, Bookman J, Rokito A. MRI evaluation of bipolar bone loss using the on-track off-track method: a feasibility study. AJR. 2015;205:848–52. 11. Shaba JS, Cook JB, Rowles DJ, Bottoni CR, Shaba SH, Tokish JM.  Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98:1918–23. 12. Smith CR, Yoon JT, Long JR, Friedman MV, Hillen TJ, Stensby JD. The radiologist’s primer to imaging of noncuff, nonlabral postoperative shoulder. Radiographics. 2018;38:149–68. 13. Snyder SJ, Karzel RP, Del-Pizzo W, Ferkel RD, Friedmann MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6:274–9. 14. John R, Wong I.  Innovative approaches in the management of shoulder instability: current concept review. Curr Rev Musculoskelet Med. 2019;12:386–96. 15. Millett PJ, Braun S. The “bony Bankart bridge” procedure: a new arthroscopic technique for reduction and internal fixation of a bony Bankart lesion. Arthroscopy. 2009;25:102–5. 16. Sugimoto H, Suzuki K, Mihara K, Kubota H, Tsuitsui H. MR arthrography of shoulder after suture-anchor Bankart repair. Radiology. 2002;224:105–11. 17. Zhu M, Young SW, Pinto C, Poon PC.  Functional outcome and the structural integrity of arthroscopic Bankart repair: a prospective trial. Shoulder Elbow. 2015;7:85–93. 18. Wagner SC, Schweitzer ME, Morrison WB, Fenlin JM, Bartolozzi AR. Shoulder instability: accuracy of MR imaging performed after surgery in depicting recurrent injury—initial findings. Radiology. 2002;222:196–203. 19. Tiegs-Heiden CA, Rhodes NG, Collins MS, Fender QA, Howe B. MR arthrogram of the postoperative glenoid labrum: normal postoperative appearance versus recurrent tears. Skeletal Radiol. 2018;47:1475–148. 20. Schaeffeler C, Waldt S, Bauer JS, Kirchhoff C, Haller B, Schroeder M, Rummeny EJ, Imhoff AB, Woertler K. MR arthrography including abduction and external rotation images in the assessment of atraumatic multidirectional instability of the shoulder. Eur Radiol. 2014;24:1376–85. 21. Lee RK, Griffith JF, Tong MM, Sharma N, Yung O. Glenoid bone loss: assessment with MR imaging. Radiology. 2013;267:496–502. 22. Stillwater L, Koenig J, Maycher B, Davisdon M. 3D-MR vs. 3D-CT of the shoulder in patient with glenohumeral instability. Skeletal Radiol. 2017;46:325–31. 23. Major NM, Banks MC. MR imaging of complications of loose surgical tacks in the shoulder. Am J Roentgenol. 2003;180:377–80. 24. Park HB, Keyurapan E, Harpreet SG, Selhi HS, McFarland EG. Suture anchors and tacks for shoulder surgery. Part II: the prevention and treatment of complications. Am J Sports Med. 2006;34:136–44. 25. Longo UG, Loppini M, Rizzello G, Ciuffreda M, Maffuli N, Denaro V. Latarjet, Bristow, and Eden-Hybinette procedures for anterior shoulder dislocation: systematic review and quantitative synthesis of the literature. Arthroscopy. 2014;30:1184–211. 26. Auffahrt A, Schauer J, Matis N, Kofler B, Hitzl W, Resch H. The J-bone graft for anatomical glenoid reconstruction in recurrent posttraumatic anterior shoulder dislocation. Am J Sports Med. 2008;36:638–47. 27. Domos P, Lunini E, Walch G. Contraindications and complications of the Latarjet procedure. Shoulder Elbow. 2017;10:15–24.

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28. Park MJ, Garcia G, Malhotra A, Major N, Tjoumakaris FP, Kelly JD 4th. The evaluation of arthroscopic remplissage by high-resolution magnetic resonance imaging. Am J Sports Med. 2012;40:2331–6. 29. Perlmutter GS. Axillary nerve injury. Clin Orthop Relat Res. 1999;368:28–36. 30. Braun S, Imhoff AB.  Modern treatment strategies for the long head of the biceps tendon. Orthopade. 2018;47:113–20. [article in German]. 31. Virk MS, Nicholson GP.  Complications of proximal biceps tenotomy and tenodesis. Clin Sports Med. 2016;35(1):181–2.

3

Elbow David A. Rubin

3.1

Ligament Injuries

Athletic injuries to the elbow ligaments range from temporarily disabling to career-­ ending. Initial diagnosis typically relies on MR or ultrasound to supplement physical examination. Both conservative and operative management have roles. Recognizing surgical complications and reinjuries requires a basic knowledge of the common operative techniques.

3.1.1 Ulnar Collateral Ligament The main ligament stabilizing the medial elbow is the ulnar collateral ligament (UCL), which is composed of anterior and posterior bundles and an intervening transverse portion. Biomechanically, the anterior bundle is most important, serving as the primary restraint against valgus forces [1]. It extends from the distal surface of the medial humeral epicondyle to the sublime tubercle on the medial surface of the proximal ulna, distal to the coronoid process. The more dorsally positioned posterior bundle forms the floor of the cubital tunnel. The normal ligament is best visualized on coronal MR images, where it appears as a taut, continuous low-signal-­ intensity structure, homogeneous in thickness. Distally a small recess may exist between the sublime tubercle and ligament insertion [2]. Contrast should not enter the substance of the ligament when MR arthrography is performed [3]. On ultrasound imaging, the normal ligament is of uniform thickness and echotexture; during

D. A. Rubin (*) Radsource, Brentwood, TN, USA Department of Radiology, Grossman NYU School of Medicine, New York, NY, USA All Pro Orthopedic Imaging Consultants, LLC, St Louis, MO, USA © Springer Nature Switzerland AG 2020 E. Rowbotham, A. J. Grainger (eds.), Postoperative Imaging of Sports Injuries, https://doi.org/10.1007/978-3-030-54591-8_3

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dynamic examination performed with applied valgus stress, a 1 mm difference in medial humeroulnar widening between the injured and normal elbow correlates with UCL tears requiring surgery in baseball players [4]. An UCL rupture may occur (usually together with other injuries) after an elbow dislocation from a single violent injury. Isolated acute ligament injuries occur in sports like judo and gymnastics that produce sudden valgus stress in the elbow [5, 6]. In throwing sports like baseball, UCL tears are associated with the repetitive extreme forces that occur during the late cocking phase of overhand pitching [7]. Ligament tears in these athletes are one manifestation of valgus extension overload—a condition that also encompasses compressive bone injuries on the lateral side of the joint (e.g., osteochondral lesions of the capitellum) and degenerative arthritis posteriorly between the olecranon process of the ulna and the humeral olecranon fossa. Treatment options for athletic UCL injuries include nonoperative measures (primarily prolonged, enforced rest), ligament reconstruction, and primary ligament repair. Nonoperative management has an excellent success rate for injuries where MR shows a partial ligament tear (especially a low-grade tear involving the proximal ligament) even in professional baseball players [8, 9]. For players with symptomatic complete UCL tears, or those who fail conservative management, ligament reconstruction is indicated. The first successful UCL reconstruction in a professional baseball pitcher was performed in 1974; the procedure is often called “Tommy John surgery” after that initial player, who was able to return to the sport following surgery [10, 11]. The original approach involved drilling converging tunnels in the humeral medial epicondyle and using a tendon graft (most often an autologous palmaris) passed through the tunnels across the joint, through a tunnel in the proximal medial ulna, then back again and sutured in a figure of 8 pattern. Exposure involved taking down the flexor-pronator origin, which risked ulnar nerve injury unless a nerve transposition was also performed [11, 12]. Later modifications of the technique employed a flexor muscle splitting approach that made ulnar nerve transposition optional, changing the tunnel configuration in the humerus to a Y-shape that allowed docking of the tendon graft within the tunnels, and using doubled tendon grafts that resulted in three or four strands of tendon crossing the joint for added stability [13–15]. The key to recognizing any of these procedures on radiographs is the identification of the drilled tunnels in both the humeral medial epicondyle and the ulna just distal to the sublime tubercle (Fig. 3.1). On MR images, the tendon graft will appear thicker than the native ligament (Fig. 3.2a). Most intact grafts are low signal intensity on both T1- and T2-weighted sequences; however, a graft that has higher signal (usually proximally) but still identifiable fibers and uniform thickness is likely intact. Because the ulnar tunnel is normally drilled a few millimeters distal to the articular surface, a small recess containing joint fluid or injected contrast (a distal “T-sign”) may be present in normally functioning reconstructions [16]. At the donor site within the forearm, a small, edematous muscle belly of the palmaris longus surrounding its central tendon

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Fig. 3.1  Ulnar collateral ligament reconstruction in a baseball pitcher. AP radiograph shows three-pronged, “Y-shaped” docking tunnel in medial humeral epicondyle and single surgical tunnel drilled in ulnar sublime tubercle (arrows)

should not be interpreted as abnormal if the distal tendon has been harvested for the reconstruction (Fig. 3.2b). In addition, focal edema involving a portion of the proximal flexor carpi ulnaris muscle may be present, especially if a concomitant ulnar nerve transposition was performed (Fig. 3.2c), likely representing subacute denervation due to injury or sacrifice of one of the motor branches supplying a portion of the muscle. Failed reconstructions either show discontinuity of the fibers (Fig. 3.3), contrast entering the substance of the graft (on an MR arthrogram), or severe tissue degeneration where no discernable graft fibers can be identified [16]. Associated heterotopic ossification identified on radiographs or MR may be symptomatic but does not automatically mean a failed reconstruction, even though ossification of a native UCL usually indicates a chronic tear [16–18]. Fractures and stress fractures through the tunnels in the medial humeral epicondyle or the proximal ulna can occur (Fig. 3.4) and require open reduction and internal fixation if displaced; however, these fractures also do not necessarily correlate with failure and recurrent instability [14, 15, 19]. Ultrasound evaluation of an intact tendon graft shows an echogenic, compact, cord-like structure of uniform thickness deep to the proximal flexor tendons [20, 21]. In cases with imaging findings that are

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Fig. 3.2  Successful ulnar collateral ligament reconstructions in three different athletes. (a) Coronal T2-weighted MR image shows intact graft (arrows) that is predominantly low signal intensity, uniform in thickness, and contiguous between two tunnels. (b) Decreased bulk and edema in palmaris longus muscle (arrow) on transverse T2-weighted image is related to harvest of distal tendon for graft and subsequent retraction of proximal muscle belly. (c) Transverse T2-weighted image shows flexor carpi ulnaris muscle (within contour) with decreased size and edema in posterior portion, likely due to subacute denervation in this player who underwent concomitant ulnar nerve transposition

ambiguous or discordant with the clinical presentation, a stress ultrasound examination showing asymmetric joint widening on the operated side supports the diagnosis of a failed operation (Fig. 3.5). Professional and high-level throwers requiring surgery for UCL insufficiency typically have diffuse, attritional damage to the ligament due to repetitive microtrauma. Even when these athletes suffer an acute-on-chronic tear, the poor tissue quality usually necessitates reconstruction using a tendon graft. However primary UCL repair may be possible in younger patients whose ligaments have little underlying degeneration [22]. Only proximal or distal ligament avulsions, not mid-­ substance ruptures, are eligible for repair (Fig. 3.6). Recent refinements in surgical technique—including incorporating a fiber tape “internal brace” and expanding the indications to include partial-thickness tears—now make repair a viable alternative for selected injuries in elite athletes, potentially allowing for accelerated rehabilitation and faster return to competition (6  months or less for repair compared to a

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Fig. 3.3  Failed ulnar collateral ligament reconstruction. (a) Coronal T1-weighted image shows position of bone tunnels (arrows) but no continuous graft tissue along ulnar side of joint. (b) On fat-suppressed, T2-weighted image, graft has torn at entrance of humeral tunnel (arrow), with marrow edema in underlying medial epicondyle

minimum of 9–12 months for reconstruction in elite baseball pitchers) [14, 23–25]. No published studies have reported the normal and abnormal postoperative appearances following UCL repair or internal augmentation.

3.1.2 Lateral Ligaments On the lateral (radial) side of the elbow, stability is maintained by the interplay of three ligaments [26]. The annular ligament is anchored at both ends to the dorsal and volar lips of the proximal ulna forming a sling around the radial head and neck, preventing subluxation of the proximal radioulnar joint [27]. The radial collateral ligament (RCL) originates on the lateral humeral epicondyle and inserts into the fibers of the annular ligament. A lateral ulnar collateral ligament (LUCL) lies posterior to the RCL, sharing its origin from the humeral lateral epicondyle. The LUCL then passes dorsal to the radial head and inserts on the supinator crest of the proximal ulna, creating a hammock that prevents posterior subluxation of the radiocapitellar joint [28]. Note that none of the lateral ligaments directly insert on the radius, which allows it to freely rotate for forearm supination and pronation. Like the UCL, the lateral ligament complex can be injured in sports-related falls and collisions, either as an isolated injury, or together with fractures often of the radial head and/or coronoid process of the ulna (a pattern called the “terrible triad” because of its propensity for recurrent instability and/or postoperative stiffness) [29,

46 Fig. 3.4  Ulnar collateral ligament reconstruction complicated by tunnel fracture. (a) coronal T1-weighted and (b) transverse fat-suppressed, T2-weighted images show fractured cortical fragment of humeral tunnel (dotted arrows) adjacent to tendon graft (solid arrows). Injury was associated with recurrent ligament insufficiency (not always the case with tunnel fractures) and required revision surgery

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30]. Severe fracture-dislocations may also include UCL tears, and/or musculotendinous injuries. Not uncommonly after initial reduction of one of the injuries, persistent posterior radiocapitellar subluxation will be present on a lateral radiograph or sagittal MR (Fig. 3.7). This finding usually accompanies clinical posterolateral rotatory elbow instability due to a ruptured LUCL [31]. If recognized acutely, primary suture repair of the RCL and LUCL can be performed following avulsion injuries at their origins [26, 32]. Associated radial head fractures are reduced and internally fixated or managed by hemiarthroplasty; coronoid fractures may also be managed operatively depending on their extent and

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Fig. 3.5  Dynamic ultrasound examination of failed right ulnar collateral ligament reconstruction in professional baseball pitcher with normal left side for comparison. Graft fibers appear discontinuous (arrows). Cursors mark edges of medial humerus and ulna while valgus stress was applied to elbows. Bone gapping measures 4.7 mm on postoperative side compared to 2.2 mm on contralateral normal side

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Fig. 3.6  Repairable acute ulnar collateral ligament tear in 14-year-old boy. (a) Coronal and (b) sagittal fat-suppressed, T2-weighted images show robust, normal-appearing ligament (arrows) avulsed from distal attachment. Based on MR appearance and young age primary repair was performed instead of reconstruction

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Fig. 3.7 Posterolateral rotatory instability after initial reduction of posterior elbow dislocation. A nondisplaced coronoid fracture was also present (not shown). Sagittal intermediate-weighted image from an MR arthrogram shows the radial head (R) remaining posteriorly subluxated with respect to the capitellum (C). Distal end of torn lateral ulnar collateral ligament lies posteriorly (arrow)

morphology [29, 33]. Concurrent UCL injuries are usually left to heal by scarring, unless persistent valgus instability is evident after the initial lateral ligament repair [33, 34]. The main complication of open repair is development of heterotopic ossification, which can be associated with postoperative stiffness; arthroscopic techniques to acutely repair the ligament complex and address intra-articular fractures are now available to allow for faster rehabilitation and fewer complications compared with open surgery [31, 35]. A new technique using a nonabsorbable tape as an internal brace to augment lateral ligament repairs has been developed [36], similar to recent advances for UCL tears. When lateral ligament injuries are not recognized early, chronic posterolateral rotatory instability may develop [37], which requires formal ligament reconstruction, typically using an autologous tendon graft anchored into surgically created tunnels, similar to UCL reconstruction [38–40]. A recent cadaver study suggested that the initial strength of an internally braced lateral ligament injury using synthetic tape was equivalent to that of tendon-graft reconstruction [41] and is therefore a viable alternative in some patients.

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Postoperative imaging following primary ligament repair might only show ferromagnetic artifact or evidence of a suture anchor in the lateral humeral epicondyle. An intact, repaired ligament should be taut and continuous. When a reconstruction or augmentation has been performed, tunnels with or without anchors will be evident in the lateral humeral epicondyle and supinator crest of the proximal ulna (Fig. 3.8). The tissue spanning the joint will appear wider than the native ligaments but should be homogeneous in thickness and not disrupted (Fig. 3.9). Heterogeneous signal intensity in the graft is an expected finding that should decrease over time [42]. Any laxity, thinning, or discontinuity of the repaired or reconstructed tissues suggest re-tear [43]. Secondary findings of failure include widening of the radiocapitellar joint and posterior radiocapitellar subluxation. Recurrent instability is the most common long-term complication, occurring in 8–11% of patients [44, 45]. Large fluid collections, hematomas, and fractures related to the surgical anchor sites may also occur. For both repairs and reconstructions, the presence, amount, and maturity of heterotopic ossification should be noted. Osteolysis within the lateral distal humerus related to the surgical tunnels, graft, or implants may impact decision-­making in cases where a revision is contemplated; bone loss is best evaluated by CT [46].

3.2

Tendon Injuries

Sports-related tendon injuries in the elbow include both acute tendon avulsions and chronic attritional tears related to repetitive injury and overuse, where degeneration (tendinosis) progresses to partial- and full-thickness tears. The former, typified by biceps ruptures, are usually repaired in the acute setting. Lateral epicondylitis is an example of the latter, where multiple nonsurgical and operative management options are available. Similar to ligament injuries, an understanding of the surgical techniques and expected imaging appearances of tendon injuries is needed to recognize abnormal outcomes.

3.2.1 Biceps Tendon Sports-related distal biceps tendon ruptures occur during resisted concentric contraction with the elbow flexed (e.g., in arm wrestling) or accompany sudden eccentric contractions, like during weight training. The injury primarily affects men, with anabolic steroid use a recognized risk factor. Tears typically involve the distal 1–2 cm of the tendon and may be either complete or partial [47]. Nonoperative management frequently results in decreased flexion and supination strength as well as functional limitations, and so is usually reserved for low-demand patients [48, 49]. Surgical repair is associated with better outcomes compared to conservative management, in both acute and chronic complete ruptures [49, 50]. Historically, tenodesis of the torn tendon to the distal brachialis was an option [51], but now preferred treatment is anatomic reinsertion to the radial tuberosity using

50 Fig. 3.8  Lateral ulnar ligament reconstruction. (a) AP and (b) lateral radiographs show proximal and distal ends of tunnel drilled through ulnar supinator crest (solid arrows) through which tendon graft was passed. Larger diameter tunnel in posterior humeral lateral epicondyle (dashed arrows) accommodates both proximal tendon limbs. Smaller drill holes in more proximal humerus are where sutures in proximal graft were pulled through and tied

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Fig. 3.9  Intact lateral ulnar ligament reconstruction. Coronal T1-weighted images through (a) distal humerus and (b) proximal ulna show graft anchor sites (arrows). (c) Coronal fat-suppressed, T2-weighted image demonstrates intact graft fibers (arrows)

suture anchors or screw fixation, or via a trans-osseous tunnel and cortical button (Fig.  3.10). Occasionally a tendon interposition graft will be needed for chronic tears with difficult mobilization or poor tissue quality [52]. Partial tears that fail conservative therapy also benefit from direct repair, after either suture reinforcement of the remaining intact tendon or conversion to a complete tear [53, 54]. A two-incision surgical approach has higher incidence of heterotopic ossification compared to a single incision anterior method [52], but with decreased risk of

52 Fig. 3.10  Distal biceps repair. (a) AP and (b) lateral radiographs demonstrate two trans-­ osseous drill sites (arrows) in radial tuberosity where direct suture repair of avulsed distal biceps tendon was performed

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traction nerve injury [55]. The overall complication rate of biceps repair is approximately 25%, with neuropraxia affecting the lateral antebrachial cutaneous nerve most common (approximately 10%); posterior interosseous nerve palsy, which may be transient or permanent, occurs less frequently [56]. Postoperatively, radiographs are useful to detect complications like heterotopic ossification, implant migration, or fractures associated with a proximal radius tunnel [57]. As is the case with the native tendon, the entire repaired tendon is often not visible on a single sagittal or coronal MR image, so its continuity should be confirmed on sequential transverse images that include the entire radial tuberosity. In uncertain cases, repositioning the patient with the arm elevated above the head, the elbow flexed, and the forearm supinated reorients the anatomy, allowing depiction of the entire distal tendon from the myotendinous junction through its insertion on a single long axis image (Fig. 3.11) [58, 59]. The intact repaired tendon is typically thicker than the native tendon, and may be heterogeneous in signal intensity especially on intermediate-weighted images, but should maintain a fibrillar architecture (Fig. 3.12) [58–60]. Approximately 1–4% of repairs re-rupture, appearing as a gap between the tendon and radial insertion site (Fig. 3.13), sometimes associated with loss of fixation [61, 62]. A hematoma or fluid collection in the antecubital fossa frequently accompanies acute, recurrent tears and should initiate a close examination of the reinsertion site (Fig. 3.14). For both intact and ruptured repairs, the location, amount, and maturity of any ectopic bone formation should be noted. Foci of mature heterotopic ossification within the tendon or distal muscle belly are common and do not necessarily Fig. 3.11  Elbow MR examination performed with elbow flexion, shoulder abduction, and forearm supination. Oblique T1-weighted image acquired in this position demonstrates entire length of native biceps (arrows) from myotendinous junction to insertion on radial tuberosity. Same maneuver can be used in evaluation of repaired tendons. R radius, U ulna

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Fig. 3.12  Intact distal biceps repair. (a) Sagittal T2-weighted image shows continuous tendon fibers (solid arrows) to reinsertion site (dotted arrow) on radial tuberosity. Visualizing entire length of repaired tendon is unusual on single long axis image. More commonly sequential transverse images (b, c) need to be interrogated to confirm repaired tendon (arrows) extends to insertion site on radius (R). Repaired tendon is thicker than native tendon. U ulna

correlate with poor outcome [59, 60]. However, ossification between the proximal radius and ulna may limit forearm pronation and supination or even form a synostosis requiring resection (Fig. 3.15). Diffuse muscle edema or atrophy involving the supinator and extensor muscles suggests denervation and injury to the posterior interosseous branch of the radial nerve (Fig. 3.16).

3.2.2 Triceps Tendon Distal triceps tears occur with sudden, acute trauma. Usual mechanisms in athletes are falls and direct blows, or forceful eccentric contraction of the muscle to resist elbow flexion (e.g., while blocking in American football) [63]. Anabolic steroid use, prior local steroid injections, and olecranon bursitis have been implicated as risk

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Fig. 3.13  Recurrent biceps tendon rupture. (a) Sagittal fat-suppressed, T2-weighted images show retracted tendon stump (arrow) superficial to brachialis muscle (Br). Site of avulsion from tendon reinsertion site at radial tuberosity (arrows) is confirmed on (b) sagittal image located more radially and (c) transverse image

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Fig. 3.14  Recurrent biceps tendon rupture. Transverse (a) T1-weighted and (b) fat-suppressed, T2-weighted images show subacute hematoma (asterisks) in antecubital fossa. No repaired tendon fibers are present at radial tuberosity anchor site (arrow) Fig. 3.15 Symptomatic heterotopic ossification. AP radiographs obtained 11 months after distal biceps tendon repair shows mature heterotopic ossification (arrows) between proximal radius and ulna forming near synostosis. Severely limited forearm supination and pronation required resection of ectopic bone

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Fig. 3.16  Chronic muscle denervation. Transverse T1-weighted image shows intact distal biceps tendon repair (arrow). Fatty atrophy of entire supinator muscle (S) suggests injury to branch of radial nerve resulting in chronic denervation

factors for injury [64, 65]. The tendon usually avulses from the olecranon tip, sometimes accompanied by a small, crescentic fracture fragment; myotendinous tears are uncommon [66]. For complete tears, results of nonoperative management are poor with debilitating loss of extension power [67]. Incomplete tears with preserved active extension can be successfully managed either conservatively or surgically in athletes depending on the extent of injury [68, 69]. Surgery consists of primary tendon repair to the olecranon using sutures with anchors or trans-osseous tunnels [66, 70]. Very little has been published on the postoperative appearances of triceps tendon repairs, but by analogy with other sites in the body, the repaired tendon is expected to be hypertrophied and heterogeneous in signal intensity compared to the native tendon, but with intact fibers. On MR imaging, sagittal images usually suffice for evaluation. Re-rupture is the most frequently reported complication, occurring in 11–21% of repairs [67, 70]. Recurrent tears can be complete (Fig. 3.17) or partial (Fig. 3.18) and involve just the superficial (lateral and long head) tendon, the deeper muscular insertion of the medial head, or both. Additionally, like the biceps, recurrent triceps tendon ruptures may be associated with failed fixation (Fig. 3.19).

3.2.3 Medial and Lateral Tendons Avulsion of either the extensor tendon origin from the lateral humeral epicondyle or the common flexor-pronator tendon from the medial epicondyle can occur with

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Fig. 3.17 Complete re-rupture of distal triceps tendon in bodybuilder 3 weeks after tendon repair. Sagittal fat-­ suppressed, T2-weighted image shows avulsed, retracted tendon end (arrow) with no tissue attached to edematous olecranon (asterisk). Patient had been noncompliant with prescribed limitations and began weight training prematurely

severe acute trauma, and these are normally managed with open surgical repair if the torn tendons are retracted. However, these traumatic tendon injuries are unusual in sports. More commonly, chronic repetitive injury to these tendons leads to tendinosis characterized histologically by micro-tears and angiofibroblastic degeneration, a condition called “epicondylitis” even though the insult is not to the epicondyle and does not involve inflammation [71]. Tendinosis of the medial or lateral (most commonly the extensor carpi radialis brevis) tendon origins is often painful, and eventually can weaken the tendons leading to partial- or full-thickness tearing. Lateral epicondylitis, also known as “tennis elbow,” because it affects many recreational players, is much more common than medial epicondylitis, sometimes called “golfer’s elbow.” Both MR imaging and ultrasound (Fig. 3.20) are moderately sensitive to associated pathologic changes—tendon thickening, increased signal and echogenicity, and hypervascularity (with intravenous contrast administration or color Doppler interrogation)—although imaging findings may not correlate with pain severity [72, 73].

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Fig. 3.18  Partial re-tear of repaired triceps tendon. (a) Sagittal STIR image shows no intact tendon attached to olecranon (O). (b) Image located more laterally demonstrates some intact tendon fibers (arrow) anchored in bone. In both images deeper muscular insertion (m) of medial triceps head remains intact Fig. 3.19  Failed distal triceps repair. Associated with recurrent distal triceps tear on sagittal fat-­ suppressed, T2-weighted image is orthopedic implant (arrow) that has lost bone purchase and is both pulled out and bent

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Fig. 3.20  Lateral epicondylitis. (a) Long-axis ultrasound image shows heterogeneity in extensor tendon origins (arrow) adjacent to lateral humeral epicondyle (H). R radial head. (b) Corresponding power Doppler image demonstrates severe hyperemia in diseased tendon. Dry needling was subsequently performed

Conservative measures for these conditions include rest, non-steroidal anti-­ inflammatory medications, physical therapy, and counterforce bracing [74]; percutaneous steroid and/or anesthetic injections may also be used [75, 76]. Mounting evidence supports the effectiveness of ultrasound-guided tenotomy (also called “dry needling”)—essentially passing a small needle repeatedly through the diseased tendon to incite a healing response characterized by neovascularity and organized collagen formation (Fig.  3.20) [77, 78]. Many practitioners combine percutaneous needling with injection of anesthetic, steroid, or platelet-rich plasma although current evidence suggests that none of these is superior to the others (or to saline) for long-term relief [73, 77, 79]. Following percutaneous treatment, there is variable resolution of abnormal MR imaging and ultrasound findings, which may not necessarily correlate with clinical improvement [72, 73]. Chronic, refractory cases of medial or lateral epicondylitis may require surgery. On the lateral side, open debridement of the diseased tissue with tendon release or repair is an option. Percutaneous and arthroscopic techniques for

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Fig. 3.21  Intact extensor tendon origin 5 years after debridement and repair for severe tendinosis. Coronal T1-weighted image shows low-signal-intensity tendon fibers (arrow) firmly attached to lateral humeral epicondyle. Soft tissue structure superficial to tendons (asterisk) was reason for study and proved to be a ganglion cyst on T2-weighted images (not shown)

tendon release have also been developed [80, 81]. Medially, the proximity of the ulnar nerve is a hazard for arthroscopic or percutaneous approaches, so surgery is typically performed open [82]. Suture anchors are usually employed in cases where a partly torn, completely torn, or debrided tendon is reattached [83]. While surgery effectively reduces both rest and activity-related pain in most patients, a recent randomized, controlled trial found no advantage of tendon debridement compared to sham (placebo) surgery in patients with chronic lateral epicondylitis [84]. Postoperative appearances vary depending on the procedure performed. Cases managed with only debridement or tendon release are expected to show focal discontinuity of the treated portions of the affected tendon, while a successfully repaired tendon should be attached to its respective epicondyle (Fig. 3.21). MR images in the coronal plane are most useful. Failed repairs will demonstrate a tendon gap and distal retraction, with or without fractured or displaced anchors (Fig.  3.22). Surgical complications have been most extensively studied for cases of treated lateral disease. Persistent pain may be as a result of inadequate debridement of diseased tissue, which will be hard to distinguish from normal postoperative changes on imaging studies. Radial tunnel syndrome

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Fig. 3.22  Failed extensor tendon repair. Coronal fat-suppressed, T2-weighted image shows distally retracted tendon stump of previously repaired tendon (solid arrow) avulsed from humeral lateral epicondyle (H). Note associated rupture of lateral ulnar collateral ligament (dotted arrow), which was diseased but unrecognized at the time of original operation. Patient now has symptomatic posterolateral rotatory instability

(posterior interosseous nerve compression) has been reported as a postoperative complication, but as it can mimic or coexist with lateral epicondylitis, it is difficult to know if this is truly a complication or an unrecognized initial condition. Denervation changes in the proximal forearm extensor muscles and supinator will typically be present if the motor branches of the nerve are involved. Posterolateral rotatory instability (See 3.1.2) is a clinically important condition to recognize after surgical treatment of lateral epicondylitis. Abnormalities of the LUCL are common in patients with moderate to severe extensor tendinosis [85, 86] and if unrecognized may lead to instability after steroid injections or tendon debridement done for symptomatic tennis elbow (Fig. 3.22). Heterotopic ossification formation has also been reported as a complication following surgery for refractory epicondylitis [87, 88].

3.3

Nerve Injuries

Sports-related neuritis can occur as an isolated entrapment, can coexist with ligament, tendon, bone, or osteochondral injuries, or can develop as a treatment complication of other conditions. Both conservative and operative treatments are available. An understanding of surgical approaches aids in the evaluation of subsequent imaging studies.

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3.3.1 Ulnar Nerve In athletes, like the general population, disorders affecting the ulnar nerve are most commonly seen around the elbow. The nerve is particularly vulnerable in the cubital tunnel, a canal along the posteromedial elbow between the olecranon and dorsal trochlea, whose floor is composed of the posterior bundle of the UCL. A retinaculum (also called Osborne’s ligament) connecting the medial humeral epicondyle and medial olecranon forms the tunnel’s roof, although the retinaculum may be abnormally thickened or replaced by an anomalous muscle—the anconeus epitrochlearis—that can predispose to nerve compression (Fig.  3.23) [1, 89]. When a

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Fig. 3.23  Preoperative transverse T1-weighted images in three different patients with ulnar neuritis. (a) Cubital tunnel retinaculum (arrow) is thicker than normal. (b) Accessory muscle (anconeus epitrochlearis, asterisk) replaces normal retinaculum and compresses ulnar nerve (arrow) in floor of tunnel. (c) Hypoplastic retinaculum (black arrow) incompletely attached to humeral epicondyle allows ulnar nerve (white arrow) to sublux medially. Images in (b) and (c) were performed after intra-articular contrast injection into joint

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the retinaculum is congenitally lax or absent, the nerve may intermittently sublux anteromedially from the cubital tunnel (Fig.  3.23c) [90]. In other patients, nerve subluxation may be asymptomatic or painful, and can be accompanied by a sudden “snap,” sometimes followed by a second one in instances where the medial head of the triceps also displaces [91]. Posterior olecranon osteophytes in players with valgus extension overload can extend into the tunnel and compress the nerve. Furthermore, the nerve is exposed to high traction and friction forces from valgus stress during overhead activities [92]. Thus, not uncommonly, ulnar neuritis will coexist with UCL insufficiency in throwing athletes. Ulnar neuritis sometimes also accompanies medial epicondylitis [93]. Other regions of compression include the arcade of Struthers or a hypertrophied triceps muscle cranial to the elbow, or between the heads of the flexor carpi ulnaris in the proximal forearm [1]. Iatrogenic nerve injury can also occur during UCL surgery or arthroscopy [94, 95]. In cases where nerve compression is the primary issue and conservative measures have failed, simple decompression or nerve transposition is effective treatment. Decompression consists of removing offending lesions (e.g., olecranon osteophytes), releasing a tight cubital tunnel retinaculum, excising an anconeus epitrochlearis muscle, and/or decompressing the space between the heads of flexor carpi ulnaris [96]. A second approach is to decompress the nerve by removing bone, either via a partial medial epicondylectomy or deepening of the tunnel by resecting bone at its base (Fig. 3.24) [97, 98]. For nerve transposition, release is followed by surgically moving the nerve from the cubital tunnel to a less vulnerable position anterior to the medial humeral epicondyle. Transfer to a subcutaneous or submuscular position is most common [98, 99]. Athletes with symptomatic nerve subluxation or snapping are also managed with transposition. Finally, some surgeons routinely perform an ulnar nerve transposition as part of UCL reconstruction. Fig. 3.24  Ulnar neuritis managed by cubital tunnel deepening. Transverse T1-weighted image shows bone removed from posterior aspect of medial humeral epicondyle (black arrows) decompressing the ulnar nerve (white arrow) within cubital tunnel

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Fig. 3.25  Patient with no ulnar nerve symptoms 10  years after cubital tunnel decompression. Transverse (a) T1-weighted and (b) fat-suppressed, T2-weighted images show absence of retinaculum overlying ulnar nerve (arrows). Relative hyperintensity of nerve on T2-weighted image is a normal finding

Imaging changes may be minor after isolated nerve decompression, showing only artifact related to the overlying incision and absence of the previously present retinaculum or accessory muscle (Fig.  3.25). New ulnar nerve subluxation is a potential complication after cubital tunnel decompression [90], but analogous to cases with intermittent subluxation not precipitated by surgery, the nerve can reside normally within the tunnel when the elbow is extended for a typical MR imaging examination. Re-examination with elbow flexion (either after repositioning for MR imaging or using dynamic ultrasound examination) may be required for diagnosis. If a partial medial epicondylectomy is performed, the associated surgical dissection may weaken the flexor-pronator origin or UCL, increasing the risk for postoperative failure of either structure [100]. After transposition, it is easiest to trace the new course of the nerve on sequential transverse MR imaging or sonographic images beginning either above or below the elbow. Some surgeons will employ a fascial sling from the flexor carpi ulnaris to help stabilize the nerve when transposing it subcutaneously (Fig. 3.26). Submuscular transfers are typically done deep to the pronator teres [101]. The nerve’s new course should be relatively smooth, without kinks or angulation, and the nerve should not change suddenly in caliber [42, 101]. Scar tissue distorting or tethering the transposed nerve may be a cause of recurrent symptoms (Fig. 3.27) [90]. The normal ulnar nerve may be hyperintense compared to skeletal muscle on T2-weighted images both before and after surgery (Fig.  3.25) [89]; the signal intensity of the nerve tends not to be particularly useful, unless it is nearly isointense to fluid. Most of the muscles supplied by the ulnar nerve reside in the hand, but denervation involving a portion of the flexor carpi ulnaris or flexor digitorum profundus can occur due to injury of the proximal motor branches in the proximal forearm after transposition (Fig. 3.2c).

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Fig. 3.26 Subcutaneous ulnar nerve transposition. Transverse T1-weighted MR arthrogram image shows ulnar nerve (arrow) transferred to subcutaneous position anterior to humerus. Note thin fascial sling created superficial to nerve to help stabilize it

Fig. 3.27  Recurrent ulnar neuritis following combined ulnar collateral ligament reconstruction and ulnar nerve transposition. Transverse T1-weighted image shows very low signal intensity scar adherent to transposed ulnar nerve (arrow). Posterior humeroulnar arthritis is also present in this professional baseball pitcher with valgus extension overload

3.3.2 Other Peripheral Nerves In athletes, entrapment of other nerves around the elbow occurs less frequently compared to ulnar nerve compression. Muscle activation potentially affects the median nerve during several phases of the throwing cycle, while sports that involve repetitive forearm supination and pronation may irritate the radial nerve [102]. Diagnosis is usually based on clinical evaluation supplemented by electrodiagnostic

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testing; imaging is indicated only when a mass is suspected (which is rare) or to exclude other conditions [103]. The radial nerve is most vulnerable at the cranial edge of the supinator muscle sometimes due to a variably present fibrous band (an arcade of Frohse) but can be entrapped anywhere from the volar aspect of the radiocapitellar joint to the distal edge of the supinator. Compression of the posterior interosseous (motor) branch affects the supinator and extensor muscles, which may demonstrate changes of denervation on MR as the only finding suggesting radial nerve entrapment. In radial tunnel syndrome, concomitant involvement of the sensory branches produces elbow and forearm pain similar to that from lateral epicondylitis [1, 104]. Median nerve compression involving its distal anterior interosseous branch affects the pronator quadratus, flexor digitorum profundus, and flexor pollicis longus muscles resulting in hand weakness. When the nerve is affected more proximally, as may happen with hypertrophy of the pronator teres muscle in throwing athletes, pronator syndrome results, which can lead to denervation of the pronator teres, flexor carpi radialis, flexor digitorum superficialis, and palmaris longus in addition to muscles innervated by the more distal anterior interosseous branch. Pain and paresthesia due to median nerve compression around the elbow may mimic symptoms of carpal tunnel syndrome [1, 103]. Various normal variants of both muscles and ligaments are risk factors for median nerve compression [89, 103]. Injuries to both the median and radial nerve have also been reported as complications following elbow arthroscopy [94, 95]. Additionally, iatrogenic injury to the posterior interosseous nerve is a known risk factor during distal biceps tendon repair (Fig. 3.16) [56]. If conservative management fails, operative treatment for either median or radial nerve compression consists of local decompression. Surgery for the median nerve will typically begin cranial to the elbow (to release a ligament of Struthers and resect a supracondylar process, if either is present). In the proximal forearm, release of the lacertus fibrosus and proximal edge of the flexor digitorum superficialis may be accompanied by a lengthening tenotomy of the pronator teres. Any accessory muscles along the course of the nerve will also be resected [105]. Several different surgical exposures are available for radial nerve release but will typically include exploration of the entire course of the nerve throughout its atrisk zone [104]. Following successful median or radial nerve decompression, release of the surrounding structures will result in increased fat surrounding the nerve, which may be easiest to appreciate when compared to preoperative imaging (Fig. 3.28). Like the case for the ulnar nerve, when symptoms persist or progress, postoperative images should be evaluated for incomplete decompression, abrupt angulation, or perineural scarring. Subacute denervation (muscle edema) in the affected distribution can reverse once nerve entrapment is relieved; chronic denervation (muscle atrophy) is usually irreversible and might increase even after successful surgery (Fig. 3.28).

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Fig. 3.28  Radial nerve decompression. (a) Transverse T1-weighted image shows radial nerve (long arrow) deep to superficial supinator muscle (short arrows) anterior to radius (R). (b) Two years later, radial nerve (long arrow) has been decompressed by sectioning proximal supinator (short arrows). Note progressive fatty atrophy of extensor muscles (asterisks) representing chronic denervation

3.4

Bone, Chondral, and Osteochondral Injuries

Postoperative imaging of treated fractures in athletes follows the same principles as in non-athletes and will not be covered here. However, injuries due to compression of the lateral elbow bones (chiefly the capitellum of the distal humerus) are strongly associated with baseball and gymnastics, with unique surgical considerations, especially in the throwing population [106]. As previously discussed, valgus extension overload from stretching and tearing of the medial elbow constraints leads to increased compressive forces between the radial head and capitellum, especially if activities like throwing continue. With acute UCL injuries bone contusions or even fractures can occur laterally. In adults, subacute and chronic UCL insufficiency may lead to wear of the lateral-side articular cartilage with subsequent osteophyte and/or loose body formation. The same forces in adolescents are thought to result in osteochondritis dissecans (OCD)—primarily affecting the anterior capitellum—from repetitive trauma with or without vascular insults to the subchondral plate. These lesions are normally visible on radiographs or ultrasound [107, 108]. Capitellar OCD staging with MR imaging is similar to that in the skeletally immature knee, with an empty crater or loose body diagnostic of fragment instability, and disruption of the subchondral bone plate, defects in the overlying cartilage, or a hyperintense rim at the crater base statistically more common in unstable lesions compared to stable ones [109].

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Stable lesions with an intact subchondral bone plate have the potential to heal with rest, especially in patients with open physes and preserved range of motion [108, 110]. Arthroscopic drilling or pinning may be used to stimulate healing when a separate fragment is present in the crater that is not mobile or ballotable [111]. When possible, unstable lesions with in situ or displaced fragments are treated by debridement of the fragment and underlying bone followed by internal fixation with bone pegs, internal fixation, or absorbable implants [108]. Loose body removal with debridement and marrow stimulation (e.g., by microfracture) of the underlying bone is an alternative, but data suggest that this approach may result in future limitations of movement affecting sports participation [112, 113]. Osteochondral autograft transplantation harvested from the distal femur or rib is now an option for cases with larger lesions, failed fragment integration after pinning, or with extensive subchondral bone loss [114, 115]. Postoperative radiographs may show enlargement of the radial head and secondary osteoarthritis following debridement of large OCD lesions in patients with open growth plates [116]. MR image after successful microfracture should show filling­in of the crater by fibrocartilage, despite continued flattening of the underlying subchondral bone plate (Fig. 3.29) [117]. A high-signal-intensity interface surrounding osteochondral autografts has been reported as an expected finding for up to 6 months a

b

Fig. 3.29  Successfully treated capitellar osteochondritis dissecans. (a) Preoperative sagittal fat-­ suppressed, T2-weighted image shows unstable osteochondral lesion of anterior capitellum with high-signal-intensity interface at the base of lesion (arrow). Following arthroscopic removal of unstable fragments, the base of lesion was treated by microfracture to stimulate healing. (b) Four months later elbow effusion persists but crater has completely filled with reparative tissue resulting in congruent articular surface

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a

b

Fig. 3.30  Failed treatment of capitellar osteochondritis dissecans. (a) Preoperative sagittal T1-weighted image shows nondisplaced osteochondral lesion of capitellum. At arthroscopy lesion was soft but stable and managed by drilling through lesion into underlying bone. Patient ignored instructions and began throwing early after surgery with new intermittent pain and catching. (b) On follow-up MR imaging, osteochondral fragment (arrow) is now separated from underlying bone with disruption of subchondral bone plate

after implantation, with most grafts going on to heal at 12 months [118]. Similar to the knee, successful autografts should show bone incorporation of the deep portions of the plugs and congruence of the articular cartilage cap with the surrounding capitellum [119]. Regardless of treatment, any new fragment separation from the crater or displacement, incomplete defect filling, or persistent gaps between the lesion and surrounding normal articular surface are signs indicative of failure of incorporation (Fig. 3.30).

3.5

Summary

Athletic elbow injuries include lesions of the ligaments, tendons, nerves, and osteochondral surfaces. A variety of operative procedures exist to address each of these. Radiographs, CT, and ultrasound have important roles in postoperative evaluation, although as is the case for other joints, MR imaging typically provides the most complete evaluation. A basic understanding of the treatment principles and surgical techniques is essential to correctly identify expected postsurgical findings, and to recognize imaging findings of complications and treatment failures.

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4

Post-operative Imaging of the Hand and Wrist Bouke Boden, Abishek Jain, Doug Campbell, and Rob Campbell

4.1

Introduction

Hand and wrist injuries commonly occur in a wide spectrum of sporting activities. They can be divided into three broad categories: bony injuries, injuries of ligaments and other supporting soft tissue structures and chronic impingement disorders. Imaging is frequently performed to aid diagnosis and management of hand and wrist injury. The radiological findings are well documented for the majority of conditions. However, post-operative imaging of the wrist can represent a challenge for the radiologist, in part due to the limited amount of data in the radiology literature. This is particularly true for reconstructive surgery of soft tissue injuries. Frequently the nature of surgery that has been performed may be unfamiliar to the reporting radiologist. This chapter discusses the indications for surgery and reviews the normal and abnormal post-operative imaging findings in the most common hand and wrist soft tissue reconstructive procedures. Where there is a lack of supporting evidence in the literature, the advice given in this chapter represents the considered opinion of the authors. Complications may include failure of the soft tissue reconstruction, inadequate primary reconstruction, restriction of movement due to post-­ operative adhesions, post-operative infection and secondary osteoarthritis. The Electronic Supplementary Material The online version of this chapter (https://doi. org/10.1007/978-3-030-54591-8_4) contains supplementary material, which is available to authorized users. B. Boden Department of Radiology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands e-mail: [email protected] A. Jain · R. Campbell (*) Department of Radiology, Royal Liverpool University Hospital, Liverpool, UK D. Campbell Department of Orthopedic Surgery, Spire Leeds Hospital, Leeds, UK © Springer Nature Switzerland AG 2020 E. Rowbotham, A. J. Grainger (eds.), Postoperative Imaging of Sports Injuries, https://doi.org/10.1007/978-3-030-54591-8_4

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radiologist should also remember to identify any other joint or soft tissue pathology in the region of interest that may be unrelated to the primary injury or that has previously been overlooked.

4.2

Ulnar-Sided Wrist Surgery

The cause of ulnar-sided wrist pain may be multi-factorial and can therefore present difficulties for surgeons and radiologists because of the complex anatomy. Pain can be related to acute trauma or chronic overuse. The possible affected structures include the triangular fibrocartilage complex (TFCC), which is the primary stabilizer of the distal radioulnar joint (DRUJ), the DRUJ itself, the lunotriquetral ligament and the extensor carpi ulnaris (ECU) tendon. Injury to these structures can cause pain and instability and impair athletic performance.

4.2.1 TFCC The TFCC lies at the distal aspect of the ulna and comprises several components: the dorsal and volar radioulnar ligaments, the triangular fibrocartilage disc (TFC), the meniscal homologue and the tendon subsheath of the ECU [1]. TFCC pathology can be subdivided into acute traumatic (type I) and chronic degenerative (type II) tears. Traumatic injuries of the TFCC usually result from forced axial load, such as a fall on an outstretched hand [2]. According to the location of a tear they can be classified into four different types (A to D) [3]. Type IB consists of a tear involving the ulnar aspect of the TFCC and is one of the most common types to be associated with DRUJ instability. Other traumatic tear types are central perforations (type IA), distal avulsions at the carpal attachment (type IC) and radial avulsions (type ID). Degenerative defects are more often seen in older patients, especially in patients over the age of 40, and may be associated with ulnocarpal impaction. Conventional MRI may be used to diagnose defects of the TFCC but may miss peripheral ulnar-sided tears. MR arthrography is often the preferred imaging modality, particularly in younger patients involved in sports [4]. Surgical options for managing TFCC tears include repair, debridement, ulnar shortening and ulnar head resection, all depending upon symptoms, tear type, ulnar variance and DRUJ stability [5]. Type II tears, often a result of ulnocarpal impaction, are usually treated by debridement in combination with ulnar shortening osteotomy or ulnar head resection [6, 7].

4.2.1.1 Normal Post-operative Imaging Findings TFC repair or debridement will result in post-operative changes on MRI in the TFCC and surrounding area, which may change over time. Following TFC debridement granulation tissue will initially form and this will be seen on MRI as low to intermediate signal intensity (SI) on T1 weighted images and high SI on T2 weighted images. These signal changes may persist for many years and therefore should not be considered to be abnormal (Fig. 4.1). The central perforation present before debridement surgery will be seen as a larger defect post-operatively, and it is important not to interpret this finding

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as a recurrent tear or defect (Fig. 4.2). Arthrography will consequently show a persistent communication between the radiocarpal joint and the DRUJ.  Homogeneous enhancement of granulation tissue is expected following administration of intravenous contrast. The TFC has irregular and poorly defined margins, which will be most pronounced on T1 weighted images, with associated loss of fat planes. Ulnar-sided tears (type IB) are best suited for surgical repair, because this is the most vascular zone of the TFC. They are also most frequently associated with DRUJ instability. In central TFC defects with a stable DRUJ, debridement is the preferred treatment [8]. When the TFC is repairable, suturing or reattachment are treatment

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Fig. 4.1  Coronal T1 (a) and T2 FS (b) MR images of a patient post-TFC debridement. The TFC has irregular and poorly defined margins with a persistent central defect filled in by high T2 signal (white arrow) representing a combination of fluid and granulation tissue. There is also a small amount of fluid in the DRUJ (black arrow). Ulnar variance is normal

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Fig. 4.2  Pre-operative coronal T1 FS arthrogram (a) and post-operative coronal T2 FS (b) MR images acquired following TFC debridement. The pre-operative image shows only minor central attenuation of the TFC disc (white arrow). Post-operatively there is a larger central defect (black arrow) which was considered to be a normal expected finding in a patient with new onset radial pain, but no recurrent ulnar wrist pain

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options, depending upon tear type. Ulnar-sided tears limited to the dorsal surface may be repaired with arthroscopic suturing. Larger ulnar-sided avulsion injuries may be treated with either open or arthroscopic reattachment. The TFC will be secured with bony anchors or sutures at the fovea of the ulna (Fig. 4.3). MRI shows the reattachment site which often is surrounded by granulation tissue usually decreasing over time (Fig. 4.4). MRI susceptibility artefacts are often present and are typically more pronounced on gradient echo and spectral fat saturated sequences (Fig. 4.5). The extent of artefact will depend on the type of suture material or implant. It is important to look a

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Fig. 4.3  Illustration (a) of TFC reattachment. Conventional radiograph (b) of a normal TFC reattachment showing the anchor site in the ulnar fovea (white arrow). The anchor is non-radiopaque

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Fig. 4.4  Radiograph (a) and coronal gradient echo (b) MR image in a patient after TFC reimplantation. The TFC reimplantation demonstrates minor susceptibility artefact and granulation tissue at the periphery of the ulnar repair site (white arrow), but is normally positioned and intact

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Fig. 4.5  Images of a patient after reattachment of an ulnar-sided TFC tear. Axial T1 (a), coronal T1 (b) and coronal gradient echo (c) images show low to intermediate signal intensity areas surrounding the reattachment site (white arrows) representing a combination of granulation tissue and susceptibility artefacts caused by suture material. These susceptibility artefacts are more pronounced on the gradient echo image (white curved arrow). There is TFC disc material present (black arrows) and on contiguous coronal PD FS images (d–f) there is no obvious recurrent TFC injury. There is a small degenerative central TFC perforation (white arrowhead) which was considered not to be significant. Axial sonographic (g) and axial T2 FS (h) MR images of the same patient demonstrate a tendinopathic and subluxed ECU (black arrowhead) complicating the TFC reattachment in this case which was a more likely cause of this patient’s recurrent ulnar wrist pain. No primary tendon stabilization had been performed

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Fig. 4.6  Patient with an un-united ulnar styloid fracture (a) (white arrow) for which resection and TFC reimplantation was performed for DRUJ instability. The post-operative T1 FS MR arthrogram image (b) shows susceptibility artefact in the region of the peripheral TFC repair site (white open arrow). The TFC repair appears intact and there is no communication between the radiocarpal and DRU joint

for signs of commonly occurring associated injuries like ECU or DRUJ instability, and if present, compare these to pre-operative images when available (Fig. 4.5). There is no current data in the literature that documents whether a persistent TFC defect or communication between the DRUJ and the radiocarpal joint on wrist arthrography following TFC repair or reattachment is a normal or abnormal finding. The absence of a communication is likely to be reassuring for confirming integrity of the TFC repair (Fig. 4.6). However, it is the author’s opinion that contrast in both

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Fig. 4.7  Pre-operative coronal T1 FS (a) and post-operative PD (b) MR arthrogram images in a patient with an ulnar-sided TFC tear and subsequent repair. Pre-operatively there is leakage of contrast into the DRUJ with a full-thickness defect at the ulnar attachment of the TFC (black arrow). The post-operative image shows an intact TFC repair, but persistent leakage of contrast into the DRUJ (white arrow) which was considered a normal finding

joints as an isolated finding should also be considered a normal finding (Fig. 4.7). Comparison with the pre-operative imaging may help in image analysis. A defect of a similar or larger size than the pre-operative scan is more likely to be a significant finding in patients with recurrent ulnar-sided wrist pain. TFC debridement in type II defects is commonly performed in combination with an ulnar shortening procedure (USP), especially when positive ulnar variance is present. In patients with normal ulnar length and failed conservative therapy for a TFC defect, or in patients with ulnar-sided pain after TFC repair or debridement, an USP may also be performed to off-load the ulnocarpal joint. Post-operative imaging findings depend upon the procedure performed. A commonly performed ulnar shortening procedure is the Wafer osteotomy (Fig. 4.8). Ulnar shortening of 2–3 mm can be combined with TFC debridement or repair in a single procedure which is considered a major advantage (Fig. 4.9). A Wafer osteotomy is performed either through an open dorsal surgical approach via the floor of the fifth extensor compartment or arthroscopically using a small power burr through the central degenerative defect of the TFC. The benefit of a Wafer osteotomy over other USP’s is that the mechanics of the DRUJ are not disturbed. Patients with a positive ulnar variance of less than 4  mm and no DRUJ instability or DRUJ osteoarthritis are eligible for this procedure [9]. Various ulnar osteotomy shortening procedures have been described and choice is largely based on surgeon preference. Disadvantages of an open ulnar osteotomy include the more invasive nature of the surgery, longer immobilization period, bigger scar, risk of non-union and metalware complications. Advantages of open procedures are the ability to keep the distal articular structures intact and there is less restriction on the length of ulnar shortening that can be achieved (Fig. 4.10) [10].

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Fig. 4.8  Schematic illustrations of a Wafer procedure (a) before and (b) after surgery. This arthroscopic procedure preserves ligamentous attachments and function of the DRU joint and can be combined with TFC debridement or repair

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Fig. 4.9  Pre-operative (a) and post-operative (b) radiographs of a successful Wafer procedure. Approximately 2–3 mm has been shaved off from the ulnar head with a drill (white arrow). DRUJ alignment is preserved

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Fig. 4.10  Pre-operative (a) and post-operative (b) radiographs of a patient after a successful open ulnar shortening procedure. Positive ulnar variance (white arrow) has been appropriately corrected (black arrow)

4.2.1.2 Abnormal Post-operative Imaging Findings Complications of TFC repair include suture rupture or detachment, potentially causing recurrent DRUJ instability, and suture knot irritation causing tendinosis or tenosynovitis of adjacent tendons [11]. Suture rupture or detachment may be demonstrated on imaging as a recurrent defect in the TFC, with possible displacement of anchor or suture material. However, this diagnosis will be difficult in the absence of access to pre-operative imaging. As indicated previously, a communication between the DRUJ and RC joint at arthrography may not necessarily be an abnormal finding, and correlation with the patient’s symptoms and the nature of the surgery is therefore necessary (Fig. 4.11). Further research on the accuracy of diagnosis of failed TFC repair is needed. Neuropraxia of the dorsal sensory branch of the ulnar nerve is a relatively frequent complication, but this is a clinical diagnosis and imaging is usually not required, although small post-traumatic neuromata might be visible on US. Features of ulnocarpal impaction may be seen if positive ulnar variance is not corrected at the time of TFC surgery. This can occur in patients after distal radial fractures with radial shortening, with or without associated TFC injury, or after TFC debridement in patients with type II TFC tears (Fig. 4.12). Complications of ulnar shortening procedures include insufficient - or over-shortening with DRUJ incongruity, non-union, failure of metalware and extensor carpi ulnaris

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Fig. 4.11  Images of a patient with a history of a foveal detachment of the TFC (not shown) which was treated with subsequent reattachment. Post-operative coronal T1 FS MR arthrogram image (a) shows an intact TFC repair (white arrow). The patient sustained a new trauma and the subsequent PD MR arthrogram image (b) demonstrated a new post-traumatic central defect in the TFC disc (white open arrow) representing a recurrent tear. Leakage of contrast material into the DRUJ is also seen (white curved arrow). The foveal attachment repair site remains intact

instability (Figs.  4.13 and 4.14). CT may be required to assess the status of delayed or non-union of ulnar osteotomy and any associated metalware complications (Fig.  4.15). Post-­operative wrist stiffness may be due to secondary osteoarthritis or arthrofibrosis (Fig. 4.16).

4.2.2 DRUJ The distal radioulnar joint (DRUJ) is a complex joint responsible for forearm rotation, ulnocarpal motion and stability [12]. DRUJ stability depends on bony contact between the distal radius and ulna, but also relies on surrounding soft tissues. These soft tissue stabilizers comprise the intrinsic stabilizers (TFC disc, dorsal and volar radioulnar ligaments) and the extrinsic stabilizers of the distal forearm (interosseous ligament and joint capsule). Injuries to the TFCC that involve the dorsal and volar radioulnar ligaments are most likely to result in DRUJ instability. The periphery of the TFCC is relatively vascular, and tears at this site are amenable to arthroscopic repair. DRUJ instability can occur in combination with ECU

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Fig. 4.12  Coronal T1 (a), coronal T2 FS (b), axial PD FS (c) MR images and longitudinal ultrasound (d) image of a patient with persistent ulnar-sided wrist pain post-radial fracture, subsequent TFC debridement and volar plate removal. Screw-tracts from the previous volar plate fixation of the distal radius are visible (black arrows). There is marked central attenuation of the TFC following debridement (white arrow). The patients’ symptoms were caused by ulno-triquetral impingement due to secondary positive ulnar variance resulting from radial shortening due to fracture. There is irregular low signal intensity at the ulnar styloid representing sclerosis, which is seen best on the coronal T1 image (white open arrow), due to bony impingement. There is also severe thickening of the ECU consistent with tendinopathy (white curved arrow) caused by impingement of the ECU tendon and hypertrophic bone formation on the triquetrum secondary to ulno-triquetral impingement which is best seen on the ultrasound image (white arrowhead)

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Fig. 4.13  Pre-operative (a) and post-operative (b) radiographs of a Wafer procedure. The patient experienced residual symptoms due to undershortening of the ulna. Pre-operatively there is marked positive ulnar variance present (white arrow) which was insufficiently corrected (black arrow) and caused persistent symptoms of ulnocarpal abutment

instability, ulnocarpal impaction and DRUJ osteoarthritis. All these factors should be assessed on imaging prior to surgery. TFCC injury and DRUJ instability are commonly seen in combination with fractures and non-union through the base of the ulnar styloid. When DRUJ instability is due to fracture malunion, a corrective osteotomy is indicated. TFC repair is the preferred treatment for DRUJ instability in the presence of a normal skeleton, but when repair has failed or native tissue is not repairable, an anatomic DRUJ reconstruction can be performed. Several reconstruction techniques have been described in the literature [13–16]; the distal radioulnar ligament reconstruction using a tendon graft as described by Adams is a popular technique (Fig. 4.17) [13].

4.2.2.1 Normal Post-operative Imaging Findings Post-operative radiographs will demonstrate the surgical tunnels and status of ulnar variance (Fig.  4.18). CT is more reliable for assessment of DRUJ congruity and precise tunnel location when radiographs are indeterminate. MRI may also be used to assess DRUJ congruity and tunnel location, and may aid in visualization of the tendon graft to confirm its integrity. However, there are no studies documenting the post-operative MRI appearances of DRUJ stabilization surgery. It is likely that high T2 SI changes in and around the graft will be present in the early post-operative

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Fig. 4.14  Radiograph (a) showing non-union of an ulnar osteotomy (white arrow) after an ulnar shortening procedure. The patient underwent an additional ulnar shortening procedure with bonegrafting and post-operative image (b) shows over-shortening of the ulna (black arrow) and secondary degenerative changes of the DRU and radiocarpal joint (white open arrows)

period, and will normally resolve over months. A well-incorporated graft is likely to demonstrate low signal intensity on T1- and T2 weighted images similar to other healthy tendons. The TFCC is expected to be very abnormal post-DRUJ stabilization because ligament reconstruction is only performed when TFCC damage is extensive and beyond repair.

4.2.2.2 Abnormal Post-operative Imaging Findings The commonly encountered complications following DRUJ reconstruction are persistent or recurrent instability, progressive osteoarthritis, neuropraxia and neuroma formation [17]. Progressive osteoarthritis is diagnosed on radiographs, but for instability and other complications cross-sectional imaging may be required. CT and MRI can complement the clinical suspicion of DRUJ instability (Figs.  4.19 and 4.20). Dynamic CT can be performed with scans in both pronation and supination. MRI is able to demonstrate most graft-related complications such as graft-rupture, dislocation, tunnel-cyst formation and infection, all of which may be a cause for recurrent DRUJ instability (Fig. 4.21). Traumatic neuroma formation can be diagnosed with US or MRI.

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Fig. 4.15  Radiograph (a) and coronal CT image (b) of a patient after ulnar shortening osteotomy. The radiograph suggested incomplete bony union (white arrow) and subsequent CT confirmed non-union (white arrowhead). Radiographic bony lucency around the distal screws is also present (white open arrows), indicating loosening of the implant probably related to micromotion

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Fig. 4.16  Coronal T2 FS MR images before (a) and after (b) TFC debridement in a patient with persistent wrist pain. The post-operative image shows loss of cartilage (white arrow) and subchondral bone marrow oedema (white open arrow) in the distal radius due to early secondary OA. This finding was not appreciated on radiographs

4  Post-operative Imaging of the Hand and Wrist Fig. 4.17  Illustrations (a, b) of radioulnar ligament reconstruction according to the Adams procedure using a tendon graft (typically palmaris longus). Location of radial and ulnar tunnels are indicated with dotted lines

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Fig. 4.18  Radiographs of two different patients after DRUJ reconstruction according to Adams. Radial and ulnar tunnels are indicated with white and black arrows. There is a positive (a) and a negative (b) ulnar variance post-operatively which was of no clinical significance in either patient, both with otherwise good clinical outcome

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Fig. 4.19  Coronal (a, b) and axial (c, d) CT images in a patient with forearm fractures and failed DRUJ repair. Ligament reconstruction according to Adams was performed showing tunnels in the radius (white arrow) and ulna (black arrow). There is persistent dorsal DRUJ subluxation and there are secondary OA changes (white open arrows). There is also delayed union of the radial fracture (white arrowhead). The patient eventually proceeded to have a distal ulnar prosthesis (e) to treat OA-related pain. The radial fracture has subsequently healed

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Fig. 4.20  Patient who had fixation of the radius for a Galeazzi fracture but presented shortly after with DRUJ subluxation (white arrows) demonstrated on radiographs (a, b). The DRUJ subluxation is also seen on the axial PD MR image (black arrow) (c). There also is an ECU tendon dislocation (white arrowhead), but there is no associated tendinopathy. A subsequent osteotomy of the sigmoid notch was performed (white open arrow) to create a more congruent socket; however this procedure failed with persistent dorsal subluxation of the DRUJ demonstrated on CT (d). DRUJ fusion and radial osteotomy was subsequently performed. The follow-up radiograph (e) shows failure of the DRUJ fusion with lucency around the K-wire (white curved arrow). There is also non-union of the radial osteotomy (black curved arrow). The patient developed progressive secondary OA in the DRUJ

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4.2.3 ECU The ECU tendon normally lies in the ECU groove of the distal ulna. It is stabilized by the ECU subsheath and the extensor retinaculum (Fig. 4.22). ECU tendon pathology includes ECU instability, tenosynovitis, tendinosis and tendon rupture. These conditions may occur in combination or in isolation [18]. Instability of the ECU results from injury to the ECU subsheath. It may be encountered as an acute traumatic event, particularly in contact sports such as rugby, or may be seen as chronic habitual subluxation, and is common in golf and tennis. A spectrum of tendon displacement can occur ranging from complete tendon dislocation to dynamic subluxation as the wrist moves from pronation into supination. Chronic habitual tendon subluxation is often asymptomatic, but when associated with tendon snapping it can be a cause of ulnar-sided wrist pain, particularly when associated with tendinopathy [19]. Ultrasound is the primary imaging modality to evaluate ECU instability and is able to assess the integrity of the ECU subsheath. US performed during pronation and supination of the wrist is able to detect dynamic tendon subluxation more easily than static MRI or CT. MRI has the advantage of assessing for structural changes in the DRUJ and TFCC which are not amenable to evaluation with US. Immobilization is the initial choice of treatment in the majority of patients. When symptoms persist, surgery may be considered. Surgical techniques include anatomical and non-anatomical repair. Anatomical repair of the ECU subsheath consists of suturing the torn edges of the subsheath or reattaching the subsheath to the ulna

4  Post-operative Imaging of the Hand and Wrist Fig. 4.21  Radiograph (a) and axial PD FS MR image (b) of a failed Adams procedure with persistent volar subluxation of the ulna (white arrow). No tendon graft is visible in the ulnar tunnel (white arrowhead), although a portion of the tendon graft is visible deep to the ECU tendon (white curved arrow). A portion of the radial tunnel is also visible (black arrow) (Reprinted from ‘Imaging the post-operative wrist’ Campbell RSD & Campbell DA in Imaging of the hand & Wrist: ed, Davies AM, Grainger AJ and James SJ. Pub Springer ISBN:978-3-642-11146-4)

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Fig. 4.22  Illustration showing the ECU tendon (in blue) which is maintained in position by the subsheath (yellow) and the extensor retinaculum (red) in the normal situation (a) and ECU tendon subluxation following a subsheath tear (b). NB: there are a variety of different patterns of subsheath tears dependent on the exact site of the tear

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Fig. 4.23  Illustration of a non-anatomical repair of the ECU subsheath. The tendon is externalized to the retinaculum and stabilized using a radial flap of the extensor retinaculum. The tendon may also be sutured on the internal surface of the retinaculum

using anchors, and is often the technique of choice in acute injuries. Alternatively, a non-anatomical repair may be utilized in both acute and chronic ECU tendon instability, and associated ECU or other ulnocarpal pathology can be concomitantly treated [20]. In this procedure, the ECU is externalized to the extensor retinaculum and a flap of tissue from the retinaculum is used to maintain the ECU tendon in a dorsal location (Fig. 4.23). Return to sports is possible between 8 and 10 weeks after surgery in the majority of cases.

4.2.3.1 Normal Post-operative Imaging Findings The normal (pre-operative) ECU subsheath on ultrasound is a thin hyperechoic structure, which maintains the tendon within the ulnar groove. It is not consistently seen. On MRI the healthy subsheath is seen as a thin band-like structure with low signal intensity on all sequences (Fig. 4.24). In a non-anatomic reconstruction, the tendon will not normally be expected to lie within the groove on the distal ulna but should be stabilized in a position relative to the dorso-ulnar aspect of the distal ulna. It is also expected that the tendon will be contained within a band of low SI material representing the flap of extensor retinaculum (Fig. 4.25). After anatomic repair the ECU tendon should lie within the ulnar groove, but post-operative low SI thickening of the subsheath on MRI is likely (Fig. 4.26). In both procedures, the ECU tendon should ideally be stable on dynamic US between wrist pronation and supination. Persistent imaging features of ECU tendinopathy may be seen in patients with good outcomes. It is therefore important to look for other causes of ulnar-sided wrist pain.

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Fig. 4.24  Axial sonographic (a) and PD FS (b) images showing the normal ECU subsheath which appears as a thin linear structure (white arrows) holding the ECU into its desired position

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Fig. 4.25  Axial T2 FS image (a) following a non-anatomic ECU repair. The tendon (black arrow) no longer lies within the groove on the distal ulna but does lie in an acceptable position that is dorsal to the ulna. It is contained by a thickened low signal intensity sleeve of tissue from the re-­ fashioned extensor retinaculum (white arrow). There is no tendinopathy, although a small amount of fluid is present within the tendon sheath. Peri-operative photo (b) of a different patient after a non-anatomic subsheath repair using a flap of the local extensor retinaculum (white arrow). The ECU (black arrow) is positioned in its groove

4.2.3.2 Abnormal Post-operative Imaging Findings Complications of anatomical and non-anatomical repair include failure of stabilization, either with dislocation or dynamic subluxation, although persistent tendon dislocation is not always symptomatic. In primary anatomic repair, overtightening of the subsheath may occur because of inadequate residual subsheath tissue available for repair. This may predispose to a type of stenosing tenosynovitis (Fig.  4.26). Ultimately, tendon failure can occur on a background of chronic tendinosis.

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Fig. 4.26  Axial (a, b) and coronal (c) T2 FS weighted MR images in a golfer who underwent an anatomical repair of the ECU subsheath. The pre-operative image (a) shows disruption of the subsheath (white arrow) and minor tendinosis of the ECU tendon (white arrowhead). The post-­ operative images (b, c) show a normal appearance of the repaired subsheath which is evident as a thick low signal intensity structure on both the axial and coronal images (white arrows). There is minor persistent tendinosis, but there also is prominent tenosynovitis (black arrow) due to overtightening of the subsheath contributing to residual ulnar-sided wrist pain. An axial sonographic image (d) shows a heterogeneously thickened ECU (white arrow) consistent with tendinosis, and also echogenic thickening (black arrow) of the post-operative subsheath repair. Synovial thickening within the tendon sheath is also seen (white curved arrow). The patient was treated with ultrasound-­guided tendon sheath injection and had good clinical outcome

4.3

Carpal Instability Surgery

The intrinsic and extrinsic wrist ligaments are important structures with a key role in carpal stability. Intrinsic ligaments originate and insert within the same carpal row. Extrinsic ligaments originate in one row and insert in a different row. The most important intrinsic ligaments of the wrist are the scapholunate (SL) and lunotriquetral (LT) ligaments. The extrinsic wrist ligaments also contribute to stability of the carpus but their precise role is more complex and less well known. It is beyond the scope of this chapter to fully describe the biomechanics of wrist stability and instability.

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Injury to the intrinsic or extrinsic ligaments (or both) may lead to carpal instability. If untreated, patients may develop secondary OA.  The time from trauma to development of secondary OA is related to the severity of initial injury, the ligaments involved, and the presence of concomitant fractures or dislocations. Pain, limited grip strength and reduced range of motion are common presenting symptoms. Co-existing injuries, such as a distal radial fracture, are not infrequently present and carpal ligament injury may not always be diagnosed at initial presentation.

4.3.1 Scapholunate Ligament The SL ligament is a horse-shoe-shaped ligament comprising three components: dorsal, interosseous and volar. The dorsal portion is the thickest and functionally most important part of the ligament and symptomatic individuals most often present with injury of this part of the ligament [21]. When patients present in the acute phase (4 weeks) is usually followed by SL ligament reconstruction or a salvage procedure. Radiographs are the initial imaging investigation of choice when SL injury is suspected. In patients with an isolated SL injury, no abnormalities are seen on static images. Dynamic SL instability may be visible with additional stress-views or cineradiography. When secondary stabilizers, especially the extrinsic ligaments, are also injured, a static SL instability will develop with diastasis (≥3  mm) between the scaphoid and lunate on PA radiographs. Further damage will result in a dorsal intercalated segment instability (DISI) deformity which is seen as dorsal tilting/extension of the lunate on a lateral view, with an increased scapholunate angle. If left untreated, secondary OA with scapholunate advanced collapse (SLAC) will develop. MRI or MR arthrography are more sensitive imaging techniques for detecting SL-tears and additional injuries and they are often used when radiography findings are equivocal or when surgery is considered. Primary repair techniques in patients with acute injury include ligament reattachment using bone anchors with or without additional capsulodesis. Temporary K-wire fixation is often performed to stabilize carpal alignment during healing and, if present, to fixate other important fractures. Results of primary SL repair vary significantly and factors contributing to unfavourable outcome include (unrecognized) extrinsic ligament injury, chondral damage and arthrofibrosis. Patients with partial SL tears can be treated with arthroscopic debridement only and outcome is generally more favourable. In patients with chronic SL injuries, soft tissue reconstruction can be performed before the development of a SLAC wrist. Several reconstruction techniques have been described in literature. The modified Brunelli technique, including additional modifications to this technique, is a popular method at the present time [22]. This procedure aims to restore the extended position of the scaphoid and also to partly reconstruct the SL ligament itself by using a strip of the flexor carpi radialis (FCR) tendon which is pulled through a tunnel from the palmar surface of the distal pole

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Fig. 4.27  Illustration of the modified Brunelli technique (a, b). The FCR tendon strip runs obliquely through a tunnel in the scaphoid and loops around the radiolunotriquetral ligament (RLTL) to be sutured onto itself

of the scaphoid to exit on the dorsal surface of the proximal scaphoid, and is then passed around the dorsal radiolunotriquetral ligament to be sutured onto itself, or alternatively fixated onto the lunate or scaphoid (Fig. 4.27). In patients with chronic SL injuries and a SLAC wrist, ligament reconstruction is contra-indicated and salvage procedures are the treatment of choice. The two most commonly performed procedures are scaphoidectomy with 4-corner arthrodesis and proximal row carpectomy. Both techniques have proven to be beneficial in terms of pain relief and adequate function.

4.3.1.1 Normal Post-operative Imaging Findings Conventional radiography is the primary imaging modality for follow-up of post-­ operative SL repair or reconstruction. The distance between the scaphoid and lunate will decrease in the majority of patients after SL repair or reconstruction (Fig. 4.28). However, a persistent diastasis between the scaphoid and lunate, or even an increase in diastasis on follow-up, is not necessarily associated with a higher risk of developing secondary osteoarthritis and this should not be interpreted as an abnormal finding in isolation (Fig. 4.29) [23]. Possible explanations for persistent or increasing widening are ligament laxity or stretching of a tendon graft. Persistent increased scapholunate angle on lateral radiographs can also be seen post-operatively in successful SL repair or reconstruction (Fig. 4.30). Therefore, CT or MRI with or without arthrography are useful adjuncts to radiographs in patients with recurrent post-operative symptoms. CT with multi-planar reconstruction best demonstrates the exact course and orientation of the graft-tunnel and identifies any bony abnormality. MRI is able to assess graft integrity and associated soft tissue abnormalities (Figs. 4.31 and 4.32).

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Fig. 4.28  Images from a patient with a clinically successful SL repair. A coronal PD FS MR image (a) shows a normal SL interval (white arrow) with bone anchor (white open arrow) in the lunate. A sagittal CT image (b) demonstrates a normal lunocapitate alignment (white arrow), with no dorsal rotation of the lunate Fig. 4.29  Radiograph of a patient with a clinically successful SL repair, with anchor in lunate (white arrow) but showing persistent diastasis (black arrow) between scaphoid and lunate which was stable over time and reflects an acceptable post-operative finding

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Fig. 4.30  Coronal (a) and sagittal (b) CT images in an asymptomatic patient after SL repair. There is persistent diastasis between scaphoid and lunate on the coronal image (white arrow) which was stable on follow-up. The sagittal image also shows dorsal rotation (black arrow) of the lunate. This was considered an acceptable post-operative finding as there were no features of secondary OA or other complications

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Fig. 4.31  SL reconstruction according to modified Brunelli technique. Immediate post-operative (a) image shows supporting stabilizing K-wires (white arrow) in situ which were removed after 6 weeks (b). In this patient an anchor (black arrow) is seen in the lunate reflecting the FCR strip fixation point. The FCR tunnel in the scaphoid (white arrowhead) is also visible

4  Post-operative Imaging of the Hand and Wrist Fig. 4.32  Axial (a) and sagittal (b) PD weighted MRI images of the same patient as shown in previous figure. The tendon graft is seen passing through the radial tunnel to pass over the dorsal surface of the lunate (black arrow) deep to the extensor tendons. The fixation point is visible as an area of susceptibility artefact (white arrow) on the dorsal aspect of the lunate. Residual dorsal tilt of the lunate is seen, which was considered to be an acceptable finding (Reprinted from ‘Imaging the post-operative wrist’ Campbell RSD & Campbell DA in Imaging of the hand & Wrist: ed, Davies AM, Grainger AJ and James SJ. Pub Springer ISBN:978-3-642-11146-4)

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Fig. 4.33  Failed SL repair. There is dynamic instability of the SL joint with an increase in diastasis between scaphoid and lunate on radiographs in the neutral position (white arrow) (a), compared with the clenched fist view (black arrow) (b). There is also negative ulnar variance and secondary DRUJ OA (white arrowhead), which may be a contributing factor to wrist pain, and which requires clinical correlation

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Fig. 4.34  Patient with an isolated SL injury who underwent attempted SL fusion with bone graft harvested (white arrow) from the distal radius (a). Proximal carpal row resection and arthroplasty (black arrow) was performed subsequently due to failure fusion and development of DISI deformity (b)

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Fig. 4.35  Patient with successful SL repair. Radiograph (a) showing persistent diastasis between the scaphoid and lunate (white arrow) which was considered to be an unremarkable finding. There is however development of early onset radiocarpal OA, with joint space narrowing (black arrow). A coronal PD FS MR image (b) confirms the integrity of the repaired SL ligament with repair tissue visible within the SL joint (white arrowhead). There is loss of articular cartilage and bone marrow oedema (black arrowhead) in the radiocarpal joint confirming secondary OA changes

symptomatic and determining the relevance of this finding may be difficult in the absence of other secondary complications. Hardware-related complications, progressive OA, non-union and delayed union can all be seen in the variety of salvage procedures.

4.3.2 Lunotriquetral Ligament The LT ligament stabilizes the LT joint and comprises three different components, similar to the SL ligament. These are the dorsal, membranous and volar bundles, but unlike the SL ligament, the volar region is thickest and most important in stabilizing the joint. Isolated LT injury is an uncommon injury and often results from a fall on an outstretched hand. Ulnar-sided wrist pain and decreased grip strength are the most frequently presenting symptoms. Radiographs in patients with an isolated LT injury may show no abnormal findings in the majority of cases, although there may be disruption of the arc of Gilula between the lunate and triquetrum, especially in stress radiographs. Diastasis between lunate and triquetrum is rarely seen. A volar intercalated segment instability (VISI) deformity occurs when additional extrinsic ligament injury is present [25]. Treatment options for isolated LT injury vary depending on injury severity and chronicity. For acute injuries immobilization,

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Fig. 4.36  Radiograph (a), coronal T1 FS (b) and coronal PD weighted MR arthrogram images (c, d) in a patient who underwent SL reconstruction (white arrows) according to the modified Brunelli technique. The graft was intact, but there is secondary OA change primarily in the midcarpal joint (black arrows) with cartilage loss and reactive bone marrow oedema (white arrowhead) (Reprinted from ‘Imaging the post-operative wrist’ Campbell RSD & Campbell DA in Imaging of the hand & Wrist: ed, Davies AM, Grainger AJ and James SJ. Pub Springer ISBN:978-3-642-11146-4)

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Fig. 4.37  Coronal T1 (a), coronal T2 FS (b) and sagittal PD (c, d) MR images performed in a patient after Brunelli procedure who had an acute injury and a suspected undisplaced radial fracture. The graft is intact with normal SL interval (white arrow) and normal lunatocapitate alignment (black arrow). However, there is advanced secondary OA with loss of articular cartilage (white open arrow) and reactive bone marrow oedema (white arrowheads) around the radiocarpal joint

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Fig. 4.38  PA (a) and lateral (b) radiographs following a recent SL ligament repair in a Boxer with a recurrent injury and fifth metacarpal fracture. The anchor site (black arrow) is visible in the scaphoid and there is no SL diastasis. However, there is joint space narrowing between the lunate and capitate, associated with new onset of flexion of the lunate and extension of the capitate demonstrated on the lateral view (white arrow). The coronal PD FS (c) MR image shows the graft site which was intact, with narrowing of the midcarpal joint, reactive bone marrow oedema and joint effusion (white open arrow). The sagittal PD (d) MR image confirms the abnormal lunatocapitate alignment (white arrowhead). This was due to a tear of the volar extrinsic ligaments subsequently confirmed at arthroscopy. PA (e) and lateral (f) radiographs show satisfactory reduction of midcarpal alignment following manipulation and k-wire fixation, performed in an attempt to allow healing of the volar ligaments and delay further progression of OA. A k-wire through the scapho-capitate joint has already been removed

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arthroscopic debridement and ligament repair are commonly performed. In patients with chronic injury soft tissue reconstruction, LT-arthrodesis and ulnar shortening are recognized treatment options (Fig. 4.43) [26, 27]. Complications after LT surgery are similar to those encountered following SL surgery and include graft failure, hardware-related complications, infection and development or progression of OA. Delayed or non-union can be seen in several salvage procedures. Normal and abnormal post-operative imaging findings are not separately discussed in this section since these are comparable to previously described findings.

4.4

UCL of the Thumb Surgery

The ulnar collateral ligament (UCL) of the first MCP joint functions as one of the most important stabilizers of the thumb restricting excessive valgus movement. Injury of the UCL was initially described as a chronic stretching injury in Scottish gamekeepers and is also seen as a common acute skiing injury, but often occurs from other traumatic injuries. The mechanism of injury consists of hyperabduction accompanied by varying degrees of hyperextension. Patients often present in the

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Fig. 4.39  Images of a patient following SL repair who subsequently developed pain, swelling and inflammation in the post-operative period. Radiographs show erosions of the scaphoid and radius (white arrows) (a) with progression on follow-up imaging a few weeks later (black arrows) (b). Axial T1 (c) and coronal T2 FS (d) MR images show joint effusion, synovitis (white open arrow), bone marrow oedema, erosions and cartilage loss (black open arrow). Infection was suspected but never proven, and this was assumed to be a reactive but sterile synovitis. No progressive bone erosion was documented on subsequent radiographs

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Fig. 4.40  PA (a) and lateral (b) radiographs of a patient who sustained a complex carpal injury that included lunate dislocation (white arrow), radial translation of the wrist and a radial styloid (black arrow) fracture. This was treated with reduction and K-wire fixation, but no SL ligament repair. The initial post-operative image (c) shows a satisfactory position and alignment of the K-wires and the carpus. However, a radiograph performed at 5 weeks post-procedure (d) shows widening between scaphoid and lunate (white open arrow) and rapid development of radiocarpal and intercarpal OA (white arrowheads). PA (e) and lateral (f) radiographs demonstrate the subsequent proximal row carpectomy and wrist arthrodesis performed to treat intractable wrist pain

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acute phase and experience pain, swelling and reduced hand grip strength, particularly pinch strength. Clinical examination will reveal joint instability with stress testing. Untreated UCL injuries may lead to chronic instability, chronic pain and early osteoarthritis.

4.4.1 UCL The UCL originates at the ulnar side of the first metacarpal head and inserts on the medial tubercle of the proximal phalanx running in a dorsopalmar oblique orientation. There are three main types of UCL injury. The first type is an avulsion fracture at the base of the proximal phalanx. The degree of displacement can be seen on a standard PA radiograph and additional imaging is usually not needed. In the acute setting surgical reduction and fixation is performed when a fracture fragment is significantly displaced (≥2 mm). The second type of injury is a non-displaced ligament tear with a spectrum varying from strain to complete rupture. The ligament most often tears at the distal insertion, but mid- and proximal tears also occur. This type of injury can be treated non-operatively by immobilization. The length of immobilization depends on injury severity and varies between approximately 10 days for strains and 6 weeks for complete ruptures. The third type of injury is a distally torn ligament with retraction and displacement over the proximal edge of the adductor pollicis aponeurosis, also called a ‘Stener lesion’ [28]. Differentiation between a non-displaced UCL tear and a Stener lesion is of critical importance since the latter is an indication for surgery because the two torn edges of the injured

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Fig. 4.41  Pre-operative (a) and post-operative (b) radiographs of a patient who underwent a 4-corner arthrodesis (white arrow) due to a SLAC wrist with secondary radiocarpal and intercarpal OA (black arrows). Coronal CT image (c) shows a normal post-operative appearance with complete bony fusion (white open arrow)

ligament are separated by the interposed adductor aponeurosis and will never heal. Ultrasound and MRI can both be used to evaluate for UCL injury and reliably differentiate between a non-displaced UCL tear and a Stener lesion. In most acute injuries a primary repair can be performed. In chronic injuries (>6 weeks), or when tissue quality or length is insufficient, a reconstruction will be performed if there is no secondary osteoarthritis of the MCP joint. Reconstructions of the UCL are

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Fig. 4.42  Patient with persistent wrist pain after SL repair. Conventional arthrography image (a) and coronal T1 FS MR image (b) demonstrate contrast in the radiocarpal joint (white arrow), but not in the ulnocarpal joint in keeping with arthrofibrosis. The intact SL repair (white open arrow) is also demonstrated. (Courtesy of Laura Bancroft, University of South Florida College of Medicine)

performed by using a tendon graft. The palmaris longus tendon, if present, is used most frequently. Outcomes for both repair and reconstruction are generally good to excellent. Patients with combined MCP instability and osteoarthritis are best managed with a joint arthrodesis.

4.4.1.1 Normal Post-operative Imaging Findings Imaging after UCL repair is not routinely undertaken, but may be requested in patients with persistent or recurrent pain and instability. Radiographs are best to evaluate the status and position of bone anchors and joint subluxation. Radiographs are also used to identify secondary OA. Ultrasound and MRI can assess the integrity of the UCL repair or reconstruction. US is able to dynamically test the UCL. MRI may be affected by a variable degree of image degradation due to susceptibility artefacts. The post-operative UCL will normally be thicker, less well defined and more heterogeneous in appearance than a native ligament (Fig. 4.44). Suture material may be evident on US as echogenic areas, and should be differentiated from small bony fragments by correlation with radiographs (Fig. 4.45).

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Fig. 4.43  Images in a patient with chronic LT instability for which a soft tissue reconstruction using part of the ECU was performed. In this procedure part of the ECU is harvested with its distal attachment preserved. The harvested tendon is looped through the triquetrum, and the bone tunnels (white arrows) are visualized on the axial (a) and coronal (b) CT arthrogram images, the tendon is sutured back onto itself distally. No VISI deformity (black arrow) is seen on the sagittal CT arthrogram image (c). Coronal PD (d) MR arthrogram image acquired at the same attendance as the CT scan shows both components of the ECU with the anchor site on the triquetrum (white open arrow). There are no secondary OA changes

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Fig. 4.44  Radiograph (a) following UCL repair demonstrating radiolucent anchor sites at the base of the proximal phalanx (black arrow) and the metacarpal head (white arrow). A longitudinal ultrasound image (b) shows a thickened and heterogeneous UCL (white open arrow) which is intact. The linear echogenic structure at the base of the proximal phalanx represents suture material (white arrowhead)

4.4.1.2 Abnormal Post-operative Imaging Findings UCL repair and reconstruction procedures both have excellent clinical outcomes and complications after UCL surgery are rare [29]. Complications which do occur include failure of the primary repair or graft stiffness due to overtightening or the presence of adhesions between the UCL and adductor aponeurosis (Fig.  4.46). Dynamic imaging with US by flexing the terminal phalanx of the thumb can show limitation of the normal excursion of the adductor aponeurosis over the UCL graft/repair site (Video 4.1). Infection, radial sensory nerve injury with neuroma formation and development of secondary OA, may also occur. Unexpected concomitant soft tissue pathology in the area of interest which has been previously overlooked may be present that may be a cause for residual symptoms (Fig. 4.47).

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Fig. 4.45  Longitudinal sonographic image of a thickened but otherwise intact UCL after repair. Cortical irregularity at the head of the metacarpal (white arrow) corresponds to suture fixation site of the UCL, and a small echogenic area at the base of the proximal phalanx is also compatible with suture material (no bony avulsion was seen on radiographs). The adductor aponeurosis (white open arrow) is visible lying superficial to the UCL repair (white arrowhead)

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Fig. 4.46  Longitudinal ultrasound images, in sagittal plane, (a, b) in a patient after UCL repair who experienced recurrent instability. The patient had laxity on dynamic imaging and evidence of repair failure. The heterogeneous echogenicity is the failed UCL repair (white arrow) with the echogenic material (white open arrow) represents the retracted anchor

4.5

Wrist Tendon Repair

Tendon rupture may lead to variable function loss and deformity, dependent on the functional importance of the affected tendon. Injuries may be acute, chronic, or acute-on-chronic, and are caused by either direct or indirect trauma. Direct trauma, due to laceration or contusion, affects the mid-portion of the tendon. Indirect

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Video 4.1  Patient after UCL repair with suture in situ (white arrow) showing restricted movement of the adductor aponeurosis (white open arrow) due to adhesions

traumas are associated with avulsion injuries of the distal tendon insertion [30]. Extensor tendons on the dorsum of the hand and wrist are located more superficially and are therefore more vulnerable to direct trauma than flexor tendons. Chronic or acute-on-­chronic injuries are seen in patients with underlying tendon disease and other predisposing causes and often occur without any preceding trauma. Rheumatoid arthritis and chronic friction over bony prominences or hardware from previous surgery are common causes of spontaneous tendon rupture. Repair can be performed in most acute injuries (25% of the articular surface, >2  mm displacement, or persistent posterior subluxation of the talus, posterior malleolar fixation may be performed with lag screw or plate. Intraoperatively, it is also crucial to assess for any tibiofibular syndesmosis instability, and to perform fixation in the same setting. Screw fixation currently remains the gold standard. Commonly used are cortical screws (3.5 mm or 4.5 mm) or a syndesmotic screw. Another option is the button technique, in which a non-biodegradable wire is held in place by two cortical metal buttons at either end. Postoperative imaging is helpful in the assessment of the initial hardware placement and whether anatomical alignment is restored. A step-off or gap of >3 mm at the fracture site is considered poor alignment [3]. Radiological signs of complication should also be evaluated, including malunion, non-union, lucency at hardware interfaces, post-traumatic arthritis, synostosis of the tibia and fibula, loss of reduction or fixation, and hardware-related complications such as fracture or impingement on soft tissue. Other sport-related fractures of the foot and ankle are treated with similar principles, restoration of normal anatomic alignment, apposition of the fracture fragments and fixation to assist healing (Fig. 8.2). Avulsion injuries are typically treated conservatively and nonoperatively.

8.3

Stress Fracture

Stress fractures are extremely common in athletes, especially during the early phase of a new training regimen. Stress injuries involving the foot and ankle can be seen in running and contact sports as well as dance. Stress fractures are most commonly treated using conservative measures including offloading, controlled ankle motion (CAM) boot, and change in activity. Imaging may initially be with plain film

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Fig. 8.1  Professional football player with Maisonneuve fracture suffered during a game. Axial T2-weighted MR image above the ankle (a) shows scarring of the syndesmotic interosseous membrane (arrows) with edema (arrowheads) representing recent injury. Coronal STIR MR image of the tibia/fibula (b) shows the associated proximal fibular fracture (arrow). Syndesmotic screws were placed. AP radiograph (c) shows syndesmotic screws were placed subsequently, and the plater returned to the field in 4 weeks. Subsequently screws were removed; axial T2-weighted MR image (d) shows prior screw tract (arrows) with additional syndesmosis scarring (arrowheads)

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Fig. 8.2  Professional hockey player with non-displaced acute first metatarsal fracture. AP radiograph (a) and axial CT image (b) of the foot show the fracture line (arrows). Postoperative AP radiograph (c) shows placement of screws across the fracture

radiographs; these may be normal in the case of bone stress without fracture, or may show either periosteal reaction or fracture. MRI, however, is the most useful imaging modality and will show both bone stress and stress fracture. However, some stress injuries can persist and require surgical intervention to return the athlete to their activity. Fifth metatarsal stress fractures and navicular fractures are especially common in basketball players. Non-healing stress fractures can lead to non-union, with persistent pain and imaging findings of rounded, sclerotic margins and low intervening T2 signal (fibrous union) or fluid signal (cartilaginous non-union). Screw fixation is standard of care for non-healing stress fractures and non-unions (Fig. 8.3). Augmentation can be performed with a calcium phosphate bone substitute material (subchondroplasty) injected into an area with stress-­related bone marrow edema to reduce pain and speed up the healing process (Fig. 8.4).

8.4

Ligament Repair

8.4.1 Lateral Reconstruction Lateral ankle injury is one of the most frequent lower limb injuries, comprising up to one-third of sports injuries [5]. The lateral ankle ligament complex consists of the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the

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Fig. 8.3  Professional basketball player with stress fracture of the navicular bone. (a) Axial T2-weighted fat-suppressed MR image of the hindfoot shows intense bone marrow edema of the navicular bone (arrows) with a small low signal fracture line (arrowhead). Subsequent coronal CT image (b) shows screws (arrows) traversing the fracture site and sclerosis (arrowheads) representing healing

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Fig. 8.4  Persistent, painful bone marrow edema of the medial and lateral malleolus in a gymnast and treatment with subchondroplasty. Coronal T2-weighted fat-suppressed MR image of the ankle (a) shows bone marrow edema in the medial and lateral malleoli (arrows) presumptively representing stress response. Axial proton density MR image (b): bone substitute material injection (arrows) was performed resulting in resolution of symptoms

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posterior talofibular ligament (PTFL). Among these, the ATFL is the most frequently injured ligament, often in isolation. It commonly occurs upon inversion of a plantar flexed ankle. The CFL is rarely injured alone, more often associated with the ATFL injuries and occurs in 50–75% in the more severe cases. It is commonly injured when the ankle is in inversion and dorsiflexion. The PTFL is the most robust ligament among the three and is rarely injured, apart from in association with ankle dislocation [5]. Lateral ankle injury may progress to chronic ankle instability, which refers to persistent symptoms of “giving way,” repetitive sprains, and ligamental laxity lasting for more than 6 months [6]. Ligamentous laxity can be interpreted as anterior drawer test of ≥10 mm on physical examination. Radiologically, although there is no absolute cutoff, an increase of talar tilt >10°, or >5° more than the contralateral side on stress radiographs, is considered as abnormal [5]. Initial treatment is conservative, such as bracing and functional rehabilitation. In about 10–30% cases where conservative treatment fails, operative treatment is considered [6, 7]. To date, many different surgical approaches have been described, which can be broadly classified into anatomic repairs and non-anatomic repairs (Fig. 8.5). The wide variability of operative techniques results in the complexity of postoperative MR appearances. Understanding the different techniques for lateral ankle ligament repair is crucial for interpretation and assessment of the ligament reconstruction on imaging exams [8–11].

8.4.1.1 Anatomic Repair and Reconstruction Anatomic repair restores normal anatomy and joint mechanics by in situ repair of the injured ligament, while non-anatomic reconstruction uses tendon grafts to replicate anatomic positions of the ligaments to restore joint biomechanics [8, 9]. The Brostrom procedure is the prototypical technique of anatomic repair, in which physiologic anatomy is restored by directly suturing the ATFL to bone. Direct repair of CFL injury may also be performed (Fig.  8.5a). Reinforcement by also tacking down the extensor retinaculum, lateral talocalcaneal ligament, or a periosteal flap of the fibula can be performed if necessary, which is a modification known as the Brostrom-­Gould procedure (Fig. 8.5b). Providing an augmented buttress to tibiotalar and subtalar laxity, it is now considered the operation of choice for lateral ankle instability. Alternatively, synthetic grafts, tendon autografts, or allografts have also been described for anatomic reconstruction with satisfactory results. The plantaris, semitendinosus, or peroneus longus are frequently used as tendon grafts. Metallic suture anchors at the attachments of the ATFL can be appreciated on radiographs, with artifact on MR imaging (Fig. 8.6). However, the standard is now to use bioabsorbable anchors which are radiolucent. A lucent channel for the anchor can be seen on radiographs; on MRI the absorbable anchor will show low signal without artifact, the repaired ligament appearing dark and thickened, with adjacent fascial scarring if the repair was reinforced using the extensor retinaculum. On ultrasound, the repaired ligament generally appears diffusely thickened, intermingled with acoustic shadowing casted by suture material [12].

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Fig. 8.5  Schematics demonstrating the common anatomical and non-anatomical lateral ligaments reconstructions describe in the text. (a): Brostrom repair (b): Modified Brostrom (Brostrom-Gould) procedure (c): Modified Evans procedure (d): Lee Procedure (e): Watson-Jones procedure (f): Chrisman-Snook procedure

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Fig. 8.6  Primary (anatomic) repair of anterior talofibular ligament (ATFL) and calcaneofibular ligament (CFL) tear. Sagittal T1-weighted MR image (a), and axial and coronal proton density MR images (b, c) of the ankle show suture anchors (arrows) and surgical artifact along the ATFL and CFL (arrowheads) representing direct ligament re-attachment. AP radiograph (d) of a different patient shows tracts from absorbable, radiolucent anchors (arrows) in the fibula

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Fig. 8.7  Non-anatomic reconstruction of the lateral ankle ligaments. Axial proton density MR image (a) and sagittal STIR MR image (b) of the ankle shows a tunnel (arrows) through the fibula representing tendon transfer and rerouting, used to reconstruct the ATFL and CFL (Chrisman-­ Snook procedure in this example). Note tendon exiting tunnel and extending toward talus (arrowheads). Axial proton density MR image (c) at the level of the calcaneus shows fixation anchor at the insertion site of the native CFL (arrow)

8.4.1.2 Non-anatomic Repair In situations where there is failure of prior anatomic repair, or if the ligaments are severely attenuated precluding direct repair, non-anatomic repair is considered (Fig. 8.7). It involves rerouting of adjacent tendons to augment ligament repair [10, 11]. However, as demonstrated by a recent meta-analysis, non-anatomic repairs are found to be associated with less favorable outcomes (e.g., persistent instability, increased inversion stiffness at the subtalar level), and are mostly superseded by anatomic repairs using either native ligaments or allograft tendons. Peroneus Brevis Tendon Rerouting The first described technique was the Evans procedure, which involves rerouting of the peroneus brevis (PB) tendon to reconstruct the ATFL, attaching it along the course of the native ligament [13]. The modified version of the Evans procedure is more commonly practiced in recent times: the peroneus brevis is transected above the ankle distal to the musculotendinous junction, passed posterosuperiorly through a surgically created oblique tunnel through the distal fibula and reattached to the initial transected site (Fig. 8.5c) [10]. On MR, the oblique vertical fibular tunnel can be demonstrated, and the PB tendon can be traced from its distal attachment at the fifth metatarsal base, entering the osseous tunnel at the fibular tip, coursing within the tunnel posterosuperiorly and exiting at the posterior end, attaching to the muscle belly. Again, suture materials manifest as artifact on MR imaging [12]. Peroneus Brevis Tendon Loop The Lee procedure is a variation of Evans technique. As in the Evans procedure, the PB tendon is transected above the ankle and a tunnel through the distal fibula is created. However, the tunnel is orientated anteroposteriorly and the tendon is looped through the osseous tunnel from backward to forward, followed by suturing distally back to

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itself and to the sheath of peroneus longus (Fig. 8.5d). A flap of fascia harvested from the distal fibula may be sutured onto the neo-ligament to further strengthen the construct. The proximal muscle fibers are sutured to the peroneus longus to preserve the eversion action. On cross-sectional imaging, the PB tendon can be traced from the base of fifth metatarsal base, coursing along the lateral aspect of the lateral malleolus, entering the posterior opening of osseous tunnel, exiting from the anterior opening and sutured onto itself near the fibular tip, where suture material-related artifacts may be seen [12]. Watson-Jones is another non-anatomic reconstruction technique, described in 1940, with various modifications proposed subsequently. It consists of drilling of two osseous tunnels in the lateral malleolus orientated posteroanteriorly and another vertical osseous tunnel in the talus. The graft is passed through the superior fibular tunnel, down the talar tunnel, through the inferior fibular tunnel and sutured back to itself posterior to the lateral malleolus (Fig. 8.5e). Peroneus Brevis Tendon Split and Rerouting Chrisman-Snook is a technique described for combined ATFL and CFL reconstruction. The PB tendon is divided longitudinally, half of which is separated proximally at the musculotendinous junction. The separated tendon is routed beneath the periosteum of the talus (with periosteal patches), through an anteroposteriorly oriented fibular osseous tunnel, beneath the periosteum of the calcaneus, coursing anteriorly and sutured back onto itself near the fifth metatarsal base. Half of the PB tendon is preserved for maintaining the dynamic function of the muscle belly (Fig. 8.5f) [11]. On cross-­sectional imaging, the split PB tendon can be traced along its course with artifacts from suture material on MR imaging [12].

8.4.2 Lisfranc Reconstruction/Fixation The Lisfranc joint or tarsometatarsal joint complex is a polyarticular system consisting of complicated capsuloligamentous and osseous structures, providing stress transduction and stability to the midfoot [14, 15]. Lisfranc injuries are relatively common in contact sports including football and rugby [16, 17]. They are typically classified as low-grade and high-grade injuries, referred to as Lisfranc (or midfoot) sprains and Lisfranc fracture-dislocations, respectively. The differentiation of the injury type is important for treatment planning. Fracture-dislocations are uncommon from athletic injury, more typically seen following conventional high-energy mechanical trauma. Regardless of the severity of injury, restoration of anatomic alignment is crucial, and this is the most important factor in achieving satisfactory outcome. Up to 50–95% of patients with anatomic alignment achieve good or excellent results, in contrast to only 17–30% of patients with non-anatomic alignment. Other factors including cartilage damage and associated soft tissue injuries will also influence the treatment result [18, 19]. Patients with low-grade and stable Lisfranc injuries are often treated conservatively initially. Non-weight-bearing and immobilization in a controlled ankle motion

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(CAM) boot or short leg cast for 6–8 weeks is usually recommended as the first-line treatment. Subsequent gradual weight-bearing as tolerated, physiotherapy and follow-­up weight-bearing radiographs in 2–3 weeks to ensure stable alignment should be followed. These patients usually have good recovery with minimal long-term morbidity; however, prolonged recovery time is often required [18, 19]. For displaced or unstable Lisfranc injuries, including pure ligamentous, osseous, or combination injuries, operative management is indicated. Ideally, surgery should be performed within the first 2 weeks of injury and after the soft tissue swelling subsides; this optimal timing is associated with better outcomes. Closed reduction under fluoroscopy may be sufficient to achieve anatomic alignment in some cases, which may be followed by Kirschner wire (K-wire) fixation. However, this is associated with higher failure risk, which can be related to entrapment of osseous fragments, anterior tibialis, or peroneus longus tendons [18, 19]. If closed anatomic reduction has failed or cannot be performed, or if fractures are comminuted, surgical options include open reduction and internal fixation (ORIF) and primary arthrodesis (Fig. 8.8) [20]. ORIF may be performed by cortical screw a

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Fig. 8.8  Lisfranc injury and fixation in a fitness performer with twisting injury. Axial T2-weighted fatsuppressed MR image (a) shows a Lisfranc ligament tear (arrowheads) and associated fractures of the tarsal bones and metatarsal bases. AP radiograph (b) shows metallic fixation spanning the Lisfranc joint

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or K-wire fixation of the medial and middle tarsometatarsal compartments. The choice of screw or K-wire for fixation is controversial: while some authors prefer screws for a more rigid and stable fixation, others prefer K-wires particularly in patients with comminuted metatarsal base fractures. Some complications of ORIF include hardware failure (e.g., screw breakage, migration, loosening), symptomatic need for removal, and risk of infection. Recently, Lisfranc joint ligament complex reconstruction has been proposed for young active patients with missed or delayed pure ligamentous injury (>6 weeks after injury) without osteoarthritic change. This involves creation of a horizontal osseous tunnel through the medial cuneiform to the second metatarsal, screw fixation of the first and third tarsometatarsal joints, and harvesting and passage of gracilis tendon graft through the tunnel [21]. Imaging is not only helpful in assessing the postoperative anatomical alignment, which is the major determinant for subsequent post-traumatic osteoarthritis development. It is also important in evaluation of any short and long-term complications [22]. The most well-recognized complication, midfoot osteoarthritis, occurs in about 50% radiographically; however, only 8% are symptomatic. Other post-­ traumatic and postoperative complications include delayed or non-union, compartment syndrome, deep vein thrombosis, infection, hardware failure, and planovalgus deformity.

8.5

Achilles Tendon Repair

The Achilles tendon, formed by merging of the gastrocnemius and soleus tendons, is the largest and strongest tendon in the body. The Achilles tendon does not have a tendon sheath; however, there is a double-layered paratenon surrounding it. Treatment of Achilles tendon injury depends on the acuity and degree of injury. Knowledge of expected postoperative MRI appearances allows accurate interpretation of the repaired Achilles tendon, which varies with different surgical techniques.

8.5.1 Acute Achilles Tendon Rupture The incidence of acute Achilles tendon rupture is approximately 2.1 to 24 per 100,000 persons per year in the general population. This injury is particularly common in athletes, occurring more commonly in an older athletic population reflecting underlying chronic tendinosis. Mechanisms of injury include sudden forceful plantar flexion, unexpected or violent dorsiflexion. Acute Achilles tendon rupture most commonly occurs at the watershed zone, which is relatively hypovascular and located approximately 5–6 cm proximal to the calcaneal insertion [23–25]. Operative treatment was previously considered as gold standard due to high re-­ rupture rates associated with conservative treatment (Fig.  8.9). However, there is paradigm shift to nonoperative management with early rehabilitation in recent years. Multiple randomized controlled trials and meta-analyses show comparable

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Fig. 8.9  Achilles tendon primary repair. Sagittal T1-weighted MR image shows diffuse thickening of the proximal and mid-Achilles tendon (arrows) with surgical artifact (arrowheads) representing prior suturing

re-rupture rates with fewer complications, including infection, adhesion formation, and sural nerve injury in the nonoperative group. Functional outcomes are also comparable, except that surgery offers early restoration and maintenance of calf muscle strength [26–28]. Conservative treatment usually comprises splinting with functional brace or cast, followed by early rehabilitation. In physically active patients with greater demand of function, operative treatment may be considered for expedited recovery. Surgical approaches can be categorized into open repair, percutaneous repair, and mini-open repair with or without augmentation [28]. Type of repair Open

Technique Simple end-to-end apposition of the tendon stumps for defect 3 cm) or there is inadequate fiber substance for direct repair. However, there is no clear evidence of better outcomes compared with non-augmented repair. Commonly used tendon grafts include plantaris, flexor hallucis longus (FHL), and peroneal tendons (Fig. 8.10). Homogeneous integration of the transferred tendon may be demonstrated in half of the cases, while others may show a change of the presumed course of orientation. In particular, if the FHL tendon is used, it is resected distally and attached to the undersurface of the Achilles tendon, which is reattached to the posterior calcaneus. It is followed by tenodesis of the distal portion of FHL to FDL for preservation of big toe flexion. On postoperative MRI, atrophy of gastrocnemius and soleus with hypertrophy of FHL muscle are expected. a

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Fig. 8.10  Achilles tendon repair with flexor hallucis longus (FHL) augmentation; wound breakdown with soft tissue infection. Sagittal T1-weighted MR image (a) demonstrates the course of the rerouted FHL (long arrows) with an anchor (arrowheads) at the posterosuperior calcaneus. Ulceration is present along the surgical site (short arrows). Axial T1-weighted fat-suppressed post-­ contrast MR image (b) shows skin ulceration (arrows) with underlying soft tissue enhancement (arrowheads) representing cellulitis

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Re-rupture is the most concerning complication of Achilles tendon repair, occurring in 5–7% of cases. Other common complications include wound complications, infections (e.g., abscesses, suture granuloma, osteomyelitis), deep vein thrombosis, and sural nerve injury. If FHL tendon transfer is performed, attention should also be paid to the tendon anchor for any loosening or displacement.

8.5.2 Chronic Achilles Tendinopathy Chronic Achilles tendinopathy is a primarily degenerative condition commonly resulting from repetitive overuse injury, commonly seen in ballet dancers and jumping athletes. This condition can be categorized into insertional and non-insertional (2–6  cm proximal to the insertion). Conservative management is the first line of treatment, which include NSAIDs, injections (e.g., corticosteroids, platelet-rich plasma, hyperosmolar dextrose), activity modifications, splintage, extracorporeal shockwave therapy, topical nitroglycerin, and low-level laser therapy. Surgical treatment is reserved for a minority of patients who are recalcitrant to nonoperative treatment, typically after 3–6 months of conservative management with high success rates reported [29, 30]. In non-insertional Achilles tendinopathy, the aim of surgery is to rest degenerative tissue and stimulate tendon healing with or without graft augmentation of the tendon. Surgical options include percutaneous longitudinal tenotomy, minimally invasive tendon stripping, open tenosynovectomy with or without paratenon resection, open debridement and tubularization, and augmentation with tendon transfer or graft in cases of >50% debridement of the diseased tendon [31]. For insertional Achilles tendinopathy, in addition to the above, removal of associated calcification and resection of inflamed retrocalcaneal bursa may be performed as required. Calcaneoplasty, which refers to resection of a prominent posterior superior calcaneal tuberosity (Haglund deformity), may also be performed where appropriate (Fig. 8.11) [29]. Complications include wound necrosis, superficial and deep infections, seroma or hematoma formation, sural nerve injury, re-rupture, and deep venous thrombosis. Reported re-operation rate in a series of 432 patients was 3% [30]. On postoperative imaging, the repaired Achilles tendon typically shows diffuse fusiform tendon thickening, which appears diffusely hypoechoic with loss of normal fibrillations on US and ill-defined T2-weighted hyperintense signal on MRI, with the presence of suture materials. On dynamic US, reduced tendon gliding motion may be observed. Visualization of a residual tendon gap at the site of anastomosis is expected, or may be even more apparent due to granulation, which can overestimate the actual tendon gap. Associated contrast enhancement may be present, which could be due to a combination of granulation tissue and fibrovascular

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Fig. 8.11  Haglund resection and Achilles tendon repair; follow-up with recurrent tear. Sagittal STIR MR image of the ankle in a runner (a) reveals insertional pathology of the Achilles tendon with thickening (long arrows) as well as underlying partial tear (arrowhead) and bone marrow edema (short arrow). Postoperative sagittal STIR MR image (b) with new pain shows recurrent tear (arrowheads) of the tendon at the suture anchors (arrows). Lateral radiograph of a different patient (c) shows resection of the posterosuperior calcaneus (arrow) from previous Haglund deformity and Achilles tendon re-attachment with metallic suture anchor (arrowhead)

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scar and is largely resolved by 12 weeks. Ring-shaped contrast enhancement representing the paratenon may also be visible around the tendon and persist beyond 12 weeks. The tendon gap at the site of anastomosis eventually disappears approximately 12 weeks postoperatively, earlier on T2- than T1-weighted sequences. The intra-tendinous heterogeneous T2-weighted signal intensity and tendon thickening may persist for up to 1–3 years after the operation. Focal intra-tendinous T2 and PD-high signal intensity, however, raises the suspicion of tendon re-tear. Peritendinous edema is also atypical if present a few months after the operation. Intra-tendinous ossification, which is seen as marrow signal within the tendon, may predispose to or indicate underlying re-tear [32–34].

8.6

Osteochondral Injuries

Osteochondral injuries are common in the athletic population. The tibio talar joint has been reported to be the third most frequently affected joint, after the knee and elbow [35]. The majority of osteochondral lesions (OCLs) of the talus are located over the centromedial and centrolateral zones, resulting from different injury mechanisms and direction of applied force [36]. Trauma history is more commonly associated with lateral lesions than medial lesions. In addition, medial lesions are usually larger, deeper, and more commonly involve subchondral bone. However, lateral OCLs are more likely to be displaced and result in osteoarthritis. OCLs may be observed in other locations depending on activity, including the navicular bone in basketball players and at the first metatarsal head in ballet dancers. Treatment of OCL is guided by the staging, chronicity of the lesion, associated symptoms, patient’s age, and severity at the onset of symptoms [37–41]. For patients with asymptomatic lesions and symptomatic non-displaced lesions, conservative management and serial radiographs monitoring for progression are usually recommended. About 45–50% of the patients respond to nonoperative treatment. Operative treatment is generally recommended for patients with acute displaced lesions or those who failed conservative management. Surgical options for OCLs can be classified into cartilage repair, cartilage regeneration, and cartilage replacement techniques. The choice of treatment usually depends on the lesion size: cartilage repair techniques for smaller lesions, and cartilage replacement or regenerative cell techniques for larger lesions or failed cartilage repair.

8.6.1 Bone Marrow Stimulation (BMS) Bone marrow stimulation (BMS) is a major technique of articular cartilage repair, often considered the first-line operative treatment typically in younger patients (