Shoulder Arthroscopy: Principles and Practice [2 ed.] 366266867X, 9783662668672

Citation preview

Giuseppe Milano Andrea Grasso Roman Brzóska Ladislav Kovačič Editors

Shoulder Arthroscopy Principles and Practice Second Edition

Shoulder Arthroscopy

Giuseppe Milano  •  Andrea Grasso Roman Brzóska  •  Ladislav Kovačič Editors

Shoulder Arthroscopy Principles and Practice Second Edition

Editors Giuseppe Milano Department of Joint and Bone Surgery University of Brescia Brescia, Brescia, Italy Roman Brzóska Shoulder and Upper Limb Department St. Luke's Hospital Bielsko-Biała, Poland

Andrea Grasso Department of Orthopaedics and Traumatology Casa di Cura Villa Valeria Rome, Roma, Italy Ladislav Kovačič Department of Traumatology University Medical Centre Ljubljana Ljubljana, Slovenia

This work contains media enhancements, which are displayed with a “play” icon. Material in the print book can be viewed on a mobile device by downloading the Springer Nature “More Media” app available in the major app stores. The media enhancements in the online version of the work can be accessed directly by authorized users. ISBN 978-3-662-66867-2    ISBN 978-3-662-66868-9 (eBook) https://doi.org/10.1007/978-3-662-66868-9 © Springer-Verlag GmbH Germany, part of Springer Nature 2023 This work is subject to copyright. All rights are solely and exclusively licensed 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-Verlag GmbH, DE, part of Springer Nature. The registered company address is: Heidelberger Platz 3, 14197 Berlin, Germany

G.M.: “To Adriana, thank you for walking by my side during this incredible journey together.” R.B.: “To my beloved family.” L.K.: “To my family, place of joy and love. Thank you for your commitment, support and dedication.”

Contents

1 Anatomy  of the Shoulder����������������������������������������������������������������   1 Francesc Soler, León Ezagüi, and Angel Calvo 2 Biomechanics  of the Shoulder��������������������������������������������������������  17 Lennard Funk 3 Biology  of Injury and Repair of Soft Tissues of the Shoulder ��������������������������������������������������������������������������������  33 James B. Carr II and Scott A. Rodeo 4 Principles  of Shoulder Arthroscopy Rehabilitation����������������������  55 Giovanni Di Giacomo, Todd S. Ellenbecker, and Mattia Pugliese 5 Instrumentation in Shoulder Arthroscopy������������������������������������  67 Emmanouil Brilakis and Angelos Trellopoulos 6 Operating  Room Setup and Patient Positioning ��������������������������  81 Andreas Voss and Robert Lawton 7 Anesthesia in Shoulder Arthroscopy����������������������������������������������  93 Stefano Santoprete, Angelo Chierichini, Giulia Concina, Carlotta Rubino, and Federica Marchetti 8 Portal  Placement and Related Anatomy���������������������������������������� 107 Gonzalo Samitier and Eduard Alentorn-Geli 9 Diagnostic Shoulder Arthroscopy�������������������������������������������������� 119 Antonio Cartucho 10 Anchors and Sutures������������������������������������������������������������������������ 127 F. Alan Barber and Michael S. Howard 11 Arthroscopic Suture Management ������������������������������������������������ 147 Alessandra Scaini, Marco Adriani, and Maristella F. Saccomanno 12 Arthroscopic Knot Tying���������������������������������������������������������������� 159 Selim Ergün, Fatih Yuvacı, and Umut Akgün 13 Complications in Shoulder Arthroscopy���������������������������������������� 169 Randelli Pietro, Compagnoni Riccardo, and Zanini Beatrice

vii

viii

14 Shoulder  Instability: Diagnosis and Classification ���������������������� 181 Ángel Calvo Díaz, Pablo Carnero Martín de Soto, and Néstor Zurita Uroz 15 Acute Traumatic Anterior Shoulder Instability���������������������������� 193 Yiğit Umur Cırdı, Selim Ergün, and Mustafa Karahan 16 Recurrent Anterior Shoulder Instability �������������������������������������� 205 Liam A. Peebles, Petar Golijanin, Annalise M. Peebles, Mary K. Mulcahey, and Matthew T. Provencher 17 Posterior Shoulder Instability�������������������������������������������������������� 229 Philipp Moroder, Victor Danzinger, and Doruk Akgün 18 Multidirectional  Instability of the Shoulder���������������������������������� 245 Christopher L. Antonacci, Brandon J. Erickson, and Anthony A. Romeo 19 SLAP Lesions ���������������������������������������������������������������������������������� 259 Michael E. Hantes and Georgios Komnos 20 Arthroscopic  Treatment of HAGL and Reverse HAGL Lesions���������������������������������������������������������������������������������� 273 Philip-C. Nolte, Bryant P. Elrick, and Peter J. Millett 21 Arthroscopic  Treatment of Bony Bankart Lesions ���������������������� 287 Hiroyuki Sugaya 22 Arthroscopic Treatment of Hill-­Sachs Lesions������������������������������ 299 Francesco Franceschi, Edoardo Giovannetti de Sanctis, Giovanni Perricone, and Edoardo Franceschetti 23 Arthroscopic  Treatment of Glenoid Bone Loss: Bone Block Grafting������������������������������������������������������������������������ 309 Ettore Taverna, Vincenzo Guarrella, and Carlo Perfetti 24 Arthroscopic  Treatment of Glenoid Bone Loss: Distal Clavicle Grafting ������������������������������������������������������������������ 317 Katarzyna Herman, Adam Kwapisz, and John M. Tokish 25 Arthroscopic Latarjet Procedure �������������������������������������������������� 329 Berte Boe and Geoffroy Nourissat 26 Advanced  Soft Tissue Procedures for Glenohumeral Instability: The BLS Technique������������������������������������������������������ 337 Roman Brzoska and Hubert Laprus 27 Advanced  Soft Tissue Procedures for Glenohumeral Instability: The ASA Technique������������������������������������������������������ 343 Marco Maiotti, Giuseppe Della Rotonda, Cecilia Rao, and Raffaele Russo 28 Advanced  Soft Tissue Procedures for Glenohumeral Instability: Labral Augmentation�������������������������������������������������� 351 Maristella F. Saccomanno, Jacopo Maffeis, and Giuseppe Milano

Contents

Contents

ix

29 Failed  Glenohumeral Instability Surgery�������������������������������������� 361 Nuno Sampaio Gomes, Mikel Aramberri, and Helder Fonte 30 Neuropathies  and Nerve Entrapments Around the Scapula and the Shoulder���������������������������������������������������������������� 379 Marcello Motta, MacDonald Tedah Djemetio, and Giuseppe Milano 31 The Overhead Athlete���������������������������������������������������������������������� 405 W. Ben Kibler and Aaron Sciascia 32 Scapulothoracic Arthroscopy���������������������������������������������������������� 427 Ladislav Kovačič 33 Rotator  Cuff Tears: Diagnosis and Classification������������������������ 445 Emilio Calvo, Carlos Rebollón Guardado, Diana Morcillo, and Guillermo Arce 34 Impingement Syndromes���������������������������������������������������������������� 453 Nobuyuki Yamamoto and Eiji Itoi 35 Partial-Thickness Rotator Cuff Tears�������������������������������������������� 463 Brady T. Williams, Theodore S. Wolfson, Amar Vadhera, and Nikhil N. Verma 36 Full-Thickness Rotator Cuff Tears������������������������������������������������ 483 Andrew J. Sheean and Stephen S. Burkhart 37 Large  to Massive Rotator Cuff Tears �������������������������������������������� 497 Brandon D. Bushnell and Jeffrey S. Abrams 38 Rotator  Interval and Biceps Tendon Disorders���������������������������� 515 Lukas N. Muench, Colin Uyeki, Knut Beitzel, and Augustus D. Mazzocca 39 Subscapularis Tendon Tears������������������������������������������������������������ 529 Jae Chul Yoo and Su Cheol Kim 40 Augmentation  in Rotator Cuff Repair: Improving Biology���������������������������������������������������������������������������������������������� 551 Claudio Rosso and Patrick Vavken 41 Augmentation  in Rotator Cuff Repair: Improving Biomechanics������������������������������������������������������������������������������������ 557 Olaf Lorbach and Mike H. Baums 42 Patch  Graft Augmentation in Rotator Cuff Repair���������������������� 563 Roger G. Hackney and Ofer Levy 43 Arthroscopic  Suprascapular Nerve Release���������������������������������� 573 Andres Muniz, Florian Grubhofer, and Jon J. P. Warner 44 Treatment  Options for Irreparable Rotator Cuff Tears: Arthroscopic Tendon Transfers���������������������������������� 587 Jean Kany

x

45 Treatment  Options for Irreparable Rotator Cuff Tears: Superior Capsule Reconstruction�������������������������������������� 601 Clara de Campos Azevedo and Ana Catarina Ângelo 46 Treatment  Options for Irreparable Rotator Cuff Tears: Biceps Autograft Augmentation������������������������������������������������������ 617 John Swan, Achilleas Boutsiadis, Manuel Ignacio Olmos, and Johannes Barth 47 Treatment  Options for Irreparable Rotator Cuff Tears: Subacromial Spacer ������������������������������������������������������������������������ 631 Ladislav Kovačič and Vladimir Senekovič 48 Treatment  Options for Irreparable Rotator Cuff Tears: Reverse Total Shoulder Arthroplasty �������������������������������������������� 643 Rolf Michael Krifter 49 Failed  Rotator Cuff Surgery ���������������������������������������������������������� 655 Barrett J. Hawkins and Felix H. Savoie III 50 Acromioclavicular  Joint Instability: Diagnosis and Classification ���������������������������������������������������������������������������� 667 Alexander Themessl, Andreas Voss, and Andreas B. Imhoff 51 Treatment  of Acute Acromioclavicular Joint Dislocations���������� 673 Lucca Lacheta and Frank Martetschläger 52 Treatment  of Chronic Acromioclavicular Joint Dislocation�������� 685 Daniel P. Berthold, Lukas N. Muench, Andreas B. Imhoff, and Knut Beitzel 53 Acromioclavicular Joint Osteoarthritis ���������������������������������������� 695 Emmanouil Antonogiannakis, Stefania Kokkineli, and Dimitrios Mantakos 54 Osteolysis  of the Distal End of the Clavicle ���������������������������������� 703 Christos K. Yiannakopoulos 55 Calcific Tendonitis���������������������������������������������������������������������������� 727 Emre Bilgin, Mehmet Kapicioglu, and Kerem Bilsel 56 Adhesive Capsulitis�������������������������������������������������������������������������� 743 Cristina Rossi, Daniela Battisti, Fabrizio Mocini, and Andrea Grasso 57 Early Glenohumeral Osteoarthritis ���������������������������������������������� 755 Philipp Heuberer, Leo Pauzenberger, and Werner Anderl 58 Arthroscopic  Management of Glenohumeral Arthritis���������������� 765 Andrew R. Jensen, Donald W. Hohman, Thomas Duquin, and John W. Sperling 59 Arthroscopic  Management of Tuberosity Fractures�������������������� 777 Mark Tauber

Contents

Contents

xi

60 Arthroscopic  Management of Glenoid Fractures ������������������������ 787 Nestor Zurita, Pablo Carnero, Carlos Verdu, and Angel Calvo 61 Outcome  Measurement Tools for Functional Assessment of the Shoulder������������������������������������������������������������ 797 Justin D. Khoriaty and Warren R. Dunn 62 Patient  Education and Patient Expectation in Shoulder Surgery������������������������������������������������������������������������ 817 Berte Bøe and Ragnhild Ø. Støen 63 Animal  Models in Shoulder Research�������������������������������������������� 827 Leonardo Cavinatto and Leesa M. Galatz

1

Anatomy of the Shoulder Francesc Soler, León Ezagüi, and Angel Calvo

Abstract

1.1 Glenohumeral Joint

The authors present an accurate description of the different anatomical structures of the shoulder, including the glenohumeral joint (capsoligamentous structures, glenoid, glenoid labrum, and humeral head), the acromioclavicular joint, the extraarticular/subacromial space (acromion and spine of the scapula, coracoacromial ligament, coracoid, coracohumeral ligament, synovial bursae, rotator cuff muscles and tendons, long head of biceps, lastissimus dorsi muscle), and neurovascular structures, focusing on the relationships between anatomic features and the most common arthroscopic shoulder portals and procedures.

1.1.1 Capsuloligamentous Structures

Keywords

Shoulder · Anatomy · Arthroscopy · Anatomical description

F. Soler (*) Traumadvance Orthopaedic Group, Aptima Centre Clinic, Terrassa, Spain e-mail: [email protected] L. Ezagüi Shoulder and Elbow Surgery Unit, Hospital Egarsat, Barcelona, Spain A. Calvo Arthrosport Zaragoza, Zaragoza, Spain e-mail: [email protected]

The shoulder joint has a wide capsule; the posterior part is thinner than the anterior part. The capsule originates from the scapular neck and inserts into the anatomical neck of the humerus. The anterior part of the capsule is reinforced by ligaments: the glenohumeral ligaments (GHLs) and the coracohumeral ligament (CHL). The GHLs are variable in size and thickness. Three ligaments have been described: –– Superior glenohumeral ligament (SGHL): is present in 97% of the population [1]. It originates from the upper aspects of the glenoid and inserts to the fovea capitis, cranial to the lesser tuberosity. Biomechanical studies have shown that SGHL contributes little to the stability of the shoulder [2]. Arthroscopically, SGHL is part of the medial pillar of the articular entrance of the bicipital groove. –– Middle glenohumeral ligament (MGHL): originates just below the SGHL and inserts to the humerus medial to the lesser tuberosity. It is the most variable and its function depends on its size and shape; it may be a secondary restraint to anterior

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_1

1

F. Soler et al.

2

translation and external rotation of the humerus [2]. The MGHL is mostly firmly connected with the subscapularis muscle tendon, as we can see in the arthroscopic articular view. –– Inferior glenohumeral ligament (IGHL): It is a hammock-like structure, which is composed of an anterior band and a posterior band (generally thinner than the anterior one). Between anterior and posterior bands, the shoulder capsule forms the axillary pouch or recess. The IGHL arises from the inferior labrum and inserts close to the anatomical neck of the humerus. This ligament is the main static stabilizer of the abducted arm [3] (Fig. 1.1). –– Rotator interval: is the space between the upper border of the subscapularis tendon and the anterior margin of the supraspinatus tendon; it has a triangular shape with its apex above to the bicipital groove. The rotator interval (RI) consists of four layers [4]: the superficial layer of the CHL, supraspinatus and subscapularis fibers, the deep layer of the CHL, and the SGHL.  Its function is still debated: some authors defined its function as a control of the external rotation with the arm at the side [4]; other authors showed that RI stabilizes the shoulder posterorinferiorly and anteroinferiorly in a 60° abducted arm position [5]; others reported that RI acts as a medial stabilizer of the long head of biceps tendon [6].

Fig. 1.1  Inferior glenohumeral ligament. Arthroscopic vision of axillary pouch

1.1.2 Glenoid It is the part of the scapula that articulates with the humeral head, thus creating the glenohumeral joint (GHJ). The glenoid has a flat, slightly concave surface that measures 6–8  cm2 and has an oval- or pear-shaped outline, depending on the absence or presence of a concave notch in its anterosuperior aspect, well defined in 55% of the population [7]. Three types of glenoid shapes have been described: pear-shaped with notch, pear-shaped without notch, and oval contour [8]. The articular surface of the humeral head is approximately three or four times larger than the glenoid. The depth of the glenoid is increased by the glenoid labrum and varies between individuals. The curvature of the glenoid is nearly equivalent to the curvature of the humeral head (Fig. 1.2). The glenoid surface is covered by hyaline cartilage, and in its center, the cartilage is thinner than peripherally; this area is called the “bare area.” The glenoid could be either anteverted or retroverted: it is retroverted by about 7.5° in 75% of the population and anteverted by about 2°–10° in 25% of cases. It is angled at an average of 15° medially with regard to the scapular plane [9].

1.1.3 Glenoid Labrum The glenoid is completely rounded by the labrum, a circular rim that slightly increases glenoid concavity and depth. It has commonly a triangular section, but it may also be rounded, crescent-­

Fig. 1.2  The humeral head and the glenoid

1  Anatomy of the Shoulder

shaped, or blunted [10]. It consists of dense fibrous tissue with a few elastic fibers; fibrocartilage can be found only in a small transitional zone between the labrum and the glenoid. The clinical significance of this circular joint lip relies on the frequency of labral injuries after dislocations of the shoulder joint. Two important anatomical variants of labrum insertion have been described: –– Buford complex: It is detected in 1.5% of cases; the absence of the anterosuperior labrum is associated with a cord-like middle glenohumeral ligament originating anteriorly to the LHB and running over the subscapularis tendon. It should not be confused with a labrum tear or a SLAP lesion [11]. –– Sublabral hole: It is detected in 12% of cases; in the anterosuperior area, there is a hole beneath the labrum insertion [12] (Fig. 1.3).

1.1.4 Humeral Head The proximal epiphysis of the humerus is formed by the head of the humerus, which is separated from the diaphysis by the anatomical neck. Below these structures, branches of anterior and posterior circumflex humeral arteries penetrate the bone for the nutrition of the humeral head. Injury to those vessels may cause aseptic humeral head necrosis in patients with severely dislocated fractures of the anatomical neck [13].

3

The humeral head is medially and proximally bent with an inclination angle of about 137° [14]. Laterally and anteriorly the proximal end of the humeral diaphysis bears two independent ossifying apophyses: the greater tuberosity and the lesser tuberosity. The two tubercles are separated by the intertubercular groove, which is covered with fibrocartilage and serves as slide bearing for the long head of biceps tendon [15]. The greater tuberosity serves as insertion for the supraspinatus, infraspinatus, and teres minor tendons and for a part of the subscapularis tendon. The major part of the subscapularis tendon inserts onto the lesser tuberosity. The articular surface of the humeral head is spheroid and has a radius of curvature of about 2.25 cm [16]. The surface is covered with articular cartilage 1.5–2  mm thick. Because of the shape of the humerus and glenoid, the shoulder joint is regarded as a ball-and-socket joint, although there is a little deviation from the exact form of a sphere. The humeral head is characterized by two “bare areas”: one is located in the posterior aspect of the head, between the posterior insertion of the rotator cuff and articular surface, and it is 2–3 cm long and usually cannot be seen in young patients; it is probably associated with age-related degenerative processes and must not be confused with the Hill–Sachs lesions. The second is anterior, between the subscapularis footprint and the articular surface, and has a trapezoidal shape [17].

1.2 Acromioclavicular Joint

Fig. 1.3  Sublabral hole (arrow)

The acromioclavicular (AC) joint is a diarthrodial joint that allows gliding, shearing, and rotational motion. It is enveloped by the articular capsule that is thinner inferiorly; meanwhile, the posterior and superior portions of the capsule play the most important part in limiting anterior and posterior translation of the distal clavicle. It is also stabilized by both static and dynamic stabilizers. The static stabilizers include the AC ligaments (superior, inferior, anterior, and posterior), the coracoclavicular (CC) ligaments (trapezoid and conoid), and the CAL. The superior AC ligament

F. Soler et al.

4

and the capsule are continuous with the aponeuroses of the deltoid and trapezius muscles and therefore are consistently thicker than the inferior AC ligament [18]. These muscle attachments are important in strengthening the AC ligaments and adding stability to the AC joint [19]. The two CC ligaments attach to the coracoid and to the distal end of the clavicle and have an average length of 1.3  cm [20] (Fig.  1.4). The conoid ligament originates from the conoid tubercle and is characterized by an inverted cone shape, with a base wider than the surface where the ligament inserts. On its more frequent variation, it inserts on the most posterior part of the dorsal aspect of the coracoid process, behind the insertion of the trapezoid ligament. The trapezoid ligament originates from the trapezoid line of the clavicle which is three times thicker than the ligament insertion surface on the most posterior aspect of the horizontal part of the coracoid. The distance from the lateral edge of the clavicle to the center of the trapezoid and conoid tuberosities reported is 25.9 ± 3.9 mm and 35 ± 5.9 mm, respectively [21]. Other recent studies also reported the mean most lateral insertion of the coracoclavicular ligaments on the clavicle from the AC joint was 15.7 mm. The distance between the mean most medial to the most lateral point of the coracoclavicular ligaments on the clavicle was 25.6  mm, which accounted for a mean of 18.2% of the clavicle length [22]. The function of the CC ligaments, reported in several biomechanical studies [23, 24], is to sta-

Fig. 1.4 Acromioclavicular capsule (asterisk) and coraco-­clavicular ligaments: conoid (C) and trapezoid (T)

bilize the clavicle at the scapula, with the conoid ligament primarily preventing anterior and superior clavicular displacement and the trapezoid ligament being the primary constraint against compression of the distal clavicle into the acromion. Because of the small area of the AC joint and the high compressive loads transmitted from the humerus to the chest by muscles such as the pectoralis major, the stresses on the AC joint can be very high. As a result, the articular surface of the distal clavicle is prone to compressive failure, as seen in osteolysis of the distal clavicle in weightlifters. Failure of the disc to accommodate both articular surfaces congruently may explain the high rate of early degenerative changes observed in this joint [25]. The dynamic stabilizers of the AC joint include the deltoid and trapezius muscles. Fibers from the superior AC ligament blend with the fascia of the trapezius and deltoid muscles, adding stability to the joint when they contract or stretch. Blood supply to the AC joint derives mainly from the acromial artery. Innervation is supplied by the pectoral, axillary, and suprascapular nerves [26].

1.3 Extraarticular/Subacromial Space 1.3.1 Acromion and Spine of the Scapula The acromion is a scapular structure projected anteriorly from the lateral border of the scapular spine, which can be easily identified as a landmark for arthroscopic portal orientation and positioning. Placed in the upper part of the shoulder is the rectangular extension of the scapular spine. In its antero-medial part, it joins with the clavicle, being part of the acromioclavicular joint. It presents superior and inferior surfaces and medial and lateral borders. The inferior lip of the crest of the spine is continued with the lateral acromion border, and the medial border corresponds to a prolongation of the scapular crest of the upper lip of the scapula spine. Both acromial

1  Anatomy of the Shoulder

borders join anteriorly, forming a triangle called acromial angle. The superior acromial surface is subcutaneous, covered only by skin and the superficial fascia [27]. The principal muscle and ligament insertions are the mid portion of the deltoid muscle, which originates along the lateral border of the acromion, and the coracoacromial ligament (CAL), a triangular fibrous lamina attached on the apex and the undersurface of the acromion and to the lateral border of the coracoid process. The spine of the scapula is an oblique process that runs from the medial margin to the upper lateral part of the scapula and becomes gradually thicker, making it very easy to identify by palpation and useful as a landmark. It is the boundary between the infraspinatus fossa and the supraspinatus fossa and functions as part of the insertion of the trapezius and the posterior deltoid [28]. According to Bigliani et al., the slope of the acromion appears in three different shapes: type I “flat,” type II “curved,” and type III “hooked.” The prevalence described in the literature for each type depends upon the analized population, but in general, the evidence shows a higher frequency of type II (near 50–55%), followed by type III (25–30%) and type I (15– 20%) [29]. Classically, type III has been associated with rotator cuff lesions in 70% of the cases [30, 31]. However, later studies performed have not been able to show such an association [32, 33]. The mean distance between the acromion and humerus is 9–10  mm (6.6–13.8  mm for males and 7.1–11.9  mm for females) [34]. Under the acromion, and above the humeral head, is the supraspinatus tendon (superior part of the rotator cuff), which is the bottom of the subacromial space (and the ceiling of glenohumeral joint). During the arthroscopic procedure, we can see the undersurface of the acromion by looking into the subacromial space from the posterior or lateral portal. Anatomical variations, known as “os acromiale,” can be originated by an incomplete fusion of the secondary acromial ossification centers, thus resulting in an epiphyseal fragment

5

that is separated from the rest of the bone structure [35]. The prevalence in cadaveric studies is reported at 7.6% and in radiological studies 4.2%. The most usual location reported is the meso-acromion type (76.6%); other variables and locations are less frequent. A significant association has been reported with black ancestry and a nonsignificant relationship with gender and side, and a high rate of acromial degenerative signs associated with this anomaly [36].

1.3.2 Coracoacromial Ligament The coracoacromial ligament (CAL) runs from the superior part of the coracoid tip to the anterior part of the acromion and defines the supraspinatus outlet. It has different parts: the principal one consists of fibers from the conjoint tendon, the clavipectoral fascia, and the rotator interval. The most lateral aspect originates at the lateral edge of the rotator interval and inserts on the conjoint tendon forming a structure called “falx” [37]. Biomechanical studies have shown a tension-­ band wiring function of this ligament: after a complete lesion, the acromion experiences a ten times higher bending force [38]. From the arthroscopic posterior view, we can see the posterior part of the CAL and its superior attachment on the anterior part of the acromion in front of us, as the anterior “wall” of the subacromial space.

1.3.3 Coracoid The coracoid process is a fundamental landmark for shoulder arthroscopy, it marks the medial limit the arthroscopic instruments should reach in most procedures, since just medial to it, under the pectoralis minor tendon, there are important neurovascular structures such as the axillary artery and the brachial plexus. Originating at the upper base of the neck of the glenoid it passes anteriorly with an ascending portion, before hooking to a more lateral position. Its smooth apex is the insertion surface of the conjoint tendon anteriorly, the hori-

F. Soler et al.

6

zontal portion gives attachment to the pectoralis minor medially and the CAL laterally. Studies reported on the coracoid insertion of the CAL, coming from the single consistent acromial attachment, bifurcates into two bundles, anterior and posterior, inserting separately on the lateral aspect of the coracoid, with footprint mean areas of 54.4 mm2 and 30.6 mm2, respectively [22]. At its base, the coracoid attaches the conoid ligament, and running from it obliquely on to the horizontal portion, the trapezoid ligament. The conoid and the trapezoid attach the coracoid to the distal end of the clavicle and have an average length of about 1.3 cm [20]. The average length of the coracoid process reported is 4.26 ± 0.26 cm, and its width and height at the tip were 2.11 ± 0.2 and 1.49  ±  0.12  cm, respectively. The average distance from the apex to the most anterior part of the trapezoid ligament reported is 3.33 ± 0.38 cm. A study that reported on the safety margin for osteotomy, with correlation with the insertion of the posterior border of the pectoralis minor, found a safety margin of 2.64  cm [39]. More recent studies reported a mean minimum distance between the coracoid apex and the trapezoid ligament of 25.1 mm and was noted to be different in males (28.1 mm) and females (22.0 mm), indicating the minimal distance from the apex of the coracoid a osteotomy should be made for graft purposes [22]. Also, an individual height and the distance from the coracoid tip to the anterior CAL have been associated with the length of the available coracoid bone graft and suggested as valuable measures for predicting a sufficient length for coracoid transfer of >25 mm [40]. Regarding the vascular supply, the vertical portion is supplied by a branch of the suprascapular artery, and the horizontal portion is supplied by a branch of the acromial branch of the thoracoacromial artery, which runs beneath the CAL and enters next to the insertion of this ligament. A direct branch from the second portion of the axillary artery, behind the pectoralis minor muscle, can rarely be found [41].

1.3.4 Coracohumeral Ligament It originates from the proximal third of the horizontal part of the coracoid process, it courses through the rotator interval and forms two bands distally: –– Lateral band: formed by superficial fibers that insert at the greater tuberosity; only 15–50% of the fibers insert at the lesser tuberosity; they blend into muscular fibers of the supraspinatus and subscapularis tendons. –– Medial band: formed by deep fibers that blend into expansions of the subscapularis tendon; only a few fibers run over LHB tendon and insert into the lesser tuberosity [42], forming an anterior cover around the biceps tendon, where it blends with the fibers of the subscapularis tendon [43]. Anterior border of the CHL is well-defined medially, while it blends with the capsule laterally. The posterior border is normally difficult to distinguish. Although it has been considered as a ligament, histological features are more similar to capsular tissue [42]. Some authors have shown that the CHL is key on keeping the LHB tendon aligned within the bicipital groove [44], basically in its medial pillar, which we can recognize at the intraarticular arthroscopic view.

1.3.5 Synovial Bursae Many bursae are described in the shoulder. They are totally avascular hollow spaces. The most important are: –– Subacromial bursa: lubricates motion between the rotator cuff and the acromion.; it is not usually connected with the glenohumeral joint [15]. –– Subdeltoid bursa: mostly communicates with the subacromial bursa; this connection varies: sometimes one can observe a narrow transi-

1  Anatomy of the Shoulder

7

tion close to the insertion site of the supraspinatus muscle. Mostly the two bursae are fused in such a way that the border between them is no longer visible [45]. –– Subscapularis bursa: lubricates motion between the subscapularis tendons and the coracoid. –– Coracobrachialis bursa: not always detachable

lar supply of the deltoid is largely derived from the posterior circumflex humeral artery (middle and posterior portions of the deltoid). The thoracoacromial artery, branched from the axillary artery, with its branches to the deltoid, and the acromial artery also provides a supply to the deltoid muscle. Also, the anterior circumflex humeral artery sends a branch to the anterior portion in 63% of cadaveric specimens [48].

1.4 Muscles

1.4.2 Rotator Cuff

1.4.1 Deltoid

1.4.2.1 Supraspinatus Macroscopic anatomy The supraspinatus muscle originates from the supraspinatus fossa and the superior surface of the spine of the scapula, and it passes laterally. Two portions are described, an anterior portion that originates at the supraspinatus fossa, with its internal tendon found at the center of the muscle belly, and the posterior portion wider, smaller and with no intramuscular tendon, described as “straplike” [49], that originates from the spine of the scapula and the glenoid neck. Although the wider, “straplike” posterior tendon may offer greater coverage of the humeral head, the anterior supraspinatus tendon transmits the majority of the contractile load, and abduction and humeral head depression actions of the supraspinatus are best affected by its contractile function, thus suggesting that surgical repair of the anterior tendon should be achieved whenever possible to obtain the best functional outcome [50, 51]. Both of these portions are divided into superficial, middle, and deep sections, based on fiber orientation and insertion [52, 53]. The supraspinatus runs beneath the coracoacromial arch and inserts into the greater tuberosity of the humerus. The mean anteroposterior dimension of the supraspinatus insertion reported is 25  mm. The mean tendon thickness at the rotator interval is 11.6  mm, 12.1  mm at mid-tendon, and 12  mm at the posterior edge [54]. The upper surface of the greater tuberosity has been generally described as being marked by three facets: the highest, the middle, and the low-

The deltoid is a large and triangular muscle, which covers the humeral head and the rotator cuff. Typically, the deltoid is divided into three anatomical portions: the anterior deltoid originates from the lateral third of the clavicle and from the anterior edge of the acromion; the middle deltoid originates from the lateral acromion; and posterior deltoid originates at the posterior edge of the acromion and the spine of the scapula. These three portions converge and insert to the deltoid tubercle on the lateral aspect of the humeral shaft. The arrangement of the muscle fibers differs among these three portions. The anterior and posterior portions have parallel fibers with long excursion, whereas the middle portion has oblique fibers in a multipennate fashion with short excursion. The superficial fascia of the proximal deltoid continues to the fascia of the trapezius muscle and forms the deltotrapezial fascia. Sakoma et al. [46] identified seven segments, each one characterized by an intramuscular tendon: three posterior, three anterior, and a middle one. Each segment is proximally separated from the others by precise landmarks. In other words, it has three origins and three insertions that do not match each other. The anterior insertion has three (A1, A2, and A3), the middle insertion has one (M1), and the posterior insertion has three (P1, P2, and P3) intramuscular tendons [47]. Innervation of the deltoid is supplied by the axillary nerve (C5 and C6) branched from the posterior cord of the brachial plexus. The vascu-

8

est. The supraspinatus tendon inserts at the anteromedial area of the highest facet. The insertional footprint has a trapezoidal or triangular shape with a major proximal base; at the insertion, it has an average maximum length and width of 23 mm (range: 18–33 mm) and 16 mm (range: 12–21 mm), respectively [55]. According to most classic anatomical texts, the rotator cuff tendon insertions are described as being clearly distinct and separate from one another with tendons inserting separately onto the humeral tubercles: however, more recent studies have shown a clear fusion and interdigitation between tendon fibers [56]. Minagawa et al. [57] reported overlapping areas of the supraspinatus and infraspinatus tendons on the footprint and claimed the footprint of the supraspinatus to have a wider area than had been previously described. This interdigitation and overlapping between fibers creates a common insertion on the humeral tubercles, that together with the capsule, should be regarded as one complete unit with a more singular insertional area on the tubercles [58, 59]. Anatomical and biomechanical studies on the insertional portion of the cuff tendons describe a specialized structure capable of adapting at different joint angles. Burkhart et al. [60] described a structure called the “rotator crescent,” as a thin, crescent-shaped sheet of rotator cuff comprising the distal portions of the supraspinatus and infraspinatus insertions, bounded on its proximal margin by a thick bundle of fibers called the “rotator cable,” reported to average 2.59 times the thickness of the rotator crescent, and acting as a suspension bridge. Nakajima et al. [61] reported four structurally independent subunits: the tendon proper, the attachment fibrocartilage, the rotator cable, and the capsule. The densely packed unidirectional collagen fibers of the rotator cable extend from the coracohumeral ligament (CHL) posteriorly to the infraspinatus, running both superficial and deep to the tendon. Arthroscopic anatomy From the arthroscopic intraarticular view, the supraspinatus tendon is quite difficult to distinguish from the articular capsule; it is provided

F. Soler et al.

with a synovial sheath, which merges into the capsule of the shoulder joint. The superior shoulder capsule is a thin membranous structure beneath the rotator cuff that is attached to a substantial area of the greater tuberosity [59, 62]. Patients with rotator cuff tears have a defect of the superior capsule, which creates discontinuity of the shoulder capsule in the transverse direction. This effect has been studied as one of the causes underlying shoulder instability after rotator cuff tears [63, 64]. The crescent and rotator cable structures can be identified next to the insertion on the greater tuberosity. The distance from the articular cartilage margin to the bony tendon insertion reported is 1.5–1.9 mm, with a mean of 1.7 mm. Arthroscopic measurement of the exposed bone between the articular margin and the supraspinatus tendon insertion can be useful as a way to estimate a tear depth and provide a reliable guideline for treatment [54]. From the subacromial view, after the CHL and synovium in the undersurface of the acromion is evaluated, the bursa is identified. There is often a shelf-like bursal band extending from anterior to posterior, separating the bursa into two spaces: subacromial and subdeltoid. After removal of the bursa, the rotator cuff attachment and footprint are seen, and the connection with the infraspinatus posteriorly and rotator interval anteriorly.

1.4.2.2 Infraspinatus Macroscopic anatomy The infraspinatus is a thick triangular muscle, which occupies most part of the infraspinatus fossa. In cadaveric studies, the muscle originated in the infraspinatus fossa by three pinnate origins (80%), or bipinnate and monopinnate muscle origins (20%) [65]. The infraspinatus fascia covers and separates the infraspinatus muscle from the teres major and teres minor. The muscle converges into a tendon, which passes over the lateral border of the spine of the scapula and, crossing the posterior part of the capsule of the shoulder joint, inserts into the middle facet on the greater tuberosity of the humerus.

1  Anatomy of the Shoulder

The insertional area (footprint) of the infraspinatus is the second in size after that of the subscapularis, and in cadaveric studies it interdigitated and wrapped superiorly around the posterior aspect of the supraspinatus tendon. Its trapezoidal shape has an average maximum length of 29 mm (range: 20–45 mm) and width of 19 mm (range: 12–27 mm) [55]. Arthroscopic anatomy From the intraarticular arthroscopic view, the infraspinatus tendon does not insert at the articular margin, and a portion of the head lacking articular cartilage is seen. Within this bare area, deep pits representing vascular channels are found. The bare area is an important anatomic point for the identification of the infraspinatus footprint, and care should be taken not to be misled to think of it as a pathologic finding. From the subacromial view, the infraspinatus attachment on the footprint can be evaluated. Posterior bursa under the posterior border of the subacromial space is identified, sometimes can be thick and must be removed for visualization. The infraspinatus muscle belly, covered by a thin fascial layer, lies just under the bursa.

1.4.2.3 Teres Minor The teres minor is a focused topic on the treatment of massive rotator cuff tears and it has encouraged recent investigation on its anatomy and function, as its function becomes more important in large or massive tears of the rotator cuff, especially those involving the infraspinatus [66]. In cadaveric studies, the teres minor originated from the dorsal surface of the lateral edge of the scapula, running superolaterally, and inserting into the inferior portion (posteroinferior area) of the greater tuberosity and linearly into the surgical neck of the humerus. The muscle consisted of two distinct and independent bundles: the upper and lower portions. The upper portion originated from the lateral edge of the scapula as tendinous attachment and the lower portion arose from the fascia between the teres minor and infraspinatus and the inferior surface of the lateral edge of the scapula as muscular attachment. In the area of distal

9

insertion, the upper portion had a round-shaped attachment in the posterior facet of the greater tuberosity, with an average length and width of 14 ± 2 mm and 11 ± 3 mm, respectively, and the lower portion had a linear shaped insertion on the surgical neck of the humerus with an average length of 17  ±  6  mm. The upper portion was situated inferiorly in the origin and superiorly in the distal insertion; hence, the two portions changed their relationship in the origin and insertion. In addition, the lower portion was located on the inferior and dorsal side of the upper portion and ran toward the distal insertion. The muscle architecture was fusiform in the lower portion and pennate in the upper portion [67].

1.4.2.4 Subscapularis Macroscopic anatomy The subscapularis is a triangular-shaped multipennate muscle. Origin arises from the subscapularis fossa as the largest muscle attached to the scapula. The majority of the subscapularis inserts into the lesser tuberosity, with some differences between reports regarding insertion shape and width. Most studies described a wider tendinous insertion superiorly, representing the superior two-thirds of the insertion, that tapers inferiorly to end as a purely musculocapsular attachment in a trapezoidal form [55, 68–70] (Fig. 1.5). In the study by Curtis et al. [55], the average maximum length was 40 mm (range: 35–55 mm), and the average maximum width was 20  mm (range: 15–25 mm). It inserted along the medial aspect of the biceps groove, and its distance from the articular surface tapered from 0 mm superiorly to 18  mm inferiorly. Another anatomical study [70] reported that about one-fifth of the superior part of the tendon, not covered by the capsule, presented the widest area of the tendon footprint with maximum transverse length mean value of 9.36 ± 3.68 mm. At the superior border, a group of tendon fibers formed a “slip”, creating the floor of the bicipital groove. At the inferior end, the tendon became tapered and its tendinous part reached its minimal transverse length of a mean value: 7.14 ± 3.16 mm followed by purely

10

Fig. 1.5  Shoulder anterior view: Supraspinatus (SS) and subscapularis (SSC) tendons

muscular attachment. The maximum longitudinal length mean value of the subscapularis tendon footprint was 29.17 ± 12.28 mm. Passing the lesser tuberosity, continuous tissue over the bicipital groove covers the entire biceps tendon and extends across to the greater tuberosity, thus blending with the supraspinatus over the greater tuberosity [71]. Arthroscopic anatomy Arthroscopic examination of the glenohumeral joint via a posterior portal allows visualization of a distinct upper part of the subscapularis tendon, more exactly the region confined to the lateral portion of its cephalad border. The majority of the posterior surface of the subscapularis tendon is veiled by the MGHL and IGHL, and no portion of the caudal margin of the subscapularis is arthroscopically visible (Fig.  1.6). The visible portion represents only a small percentage (26 ± 11%) of the entire tendon [72]. To visualize a greater part of the tendon, it is necessary to put the scope into the subacromial space, by following the course of the coracoacromial ligament, which leads to the coracoid. Once reached the coracoid, one goes further, following the conjoined tendon under which the subscapularis tendon is located [73].

F. Soler et al.

Fig. 1.6  Intraarticular subscapularis tendon (SSC), with the MGHL (asterisk) and the SGHL (arrow)

1.4.2.5 Rotator Cuff Innervation and Vascular Supply The arterial supply of the rotator cuff muscles is generally provided by the subscapular, circumflex scapular, posterior circumflex humeral, and suprascapular arteries. In a cadaveric study [74], the subscapularis muscle was supplied by the subscapular, suprascapular, and circumflex scapular arteries. The supraspinatus and infraspinatus muscles were supplied by the suprascapular artery. The infraspinatus and teres minor muscles were found to be supplied by the circumflex scapular artery. In addition to the branches of these arteries, the rotator cuff muscles were found to be supplied by the dorsal scapular, lateral thoracic, thoracodorsal and posterior circumflex humeral arteries. Innervation of the rotator cuff comes from the suprascapular nerve for the supraspinatus and infraspinatus, the axillary nerve for the teres minor, and the subscapular nerve for the subscapularis.

1.4.3 Long Head of the Biceps The long head of the biceps (LHB) originates from the glenoid labrum and the supraglenoid tubercle of the scapula with an intraarticular portion that passes over the humeral head before entering the bicipital groove, then becoming

1  Anatomy of the Shoulder

Fig. 1.7  Entrance of long head biceps tendon into the bicipital groove (arrow)

extraarticular. The tendon is approximately 9 cm long and 5–6 mm in diameter, but the size of the tendon varies, and the articular portion is flatter and larger than the groove extraarticular portion which is rounded and smaller [75] (Fig. 1.7). The intraarticular portion is extrasynovial and is essentially static within the joint as the groove slides over the biceps during abduction and ­rotation. The synovial sheath reflects on itself to form a visceral sheath that encases the biceps tendon; it communicates directly with the glenohumeral joint and ends in a blind pouch at the level of the bicipital groove. Once out of the groove, the tendon continues down to the ventral portion of the humerus and becomes musculotendinous near the insertion of the deltoid and the pectoralis major [76]. Dierickx et al. [77] suggested a classification based on the anatomy of the LHB and its dynamic

11

behavior during the arthroscopy, with a differentiation into four major families, mesotenon, adherent, split, and absence. Each divided into 1–5 subgroups, resulting in a classification of 12 variations of the intra-articular portion of the tendon. The biceps pulley is a capsuloligamentous complex that acts to stabilize the LHB tendon in the bicipital groove, built by fibers of the CHL, SGHL, and parts of the subscapularis tendon [78]. Walch et  al. [79] observed that the SGHL and CHL act as a pulley system for the LHB. The most superior part of the subscapularis tendon was found attached to the upper margin of the lesser tuberosity and extended as a thin tendinous slip to the fovea capitis of the humerus, and supports the LHB from behind the SGHL. This superior insertion point has been considered by some authors as the most important structure to serve as a restraint to keep the LHB from dislocating [44]. The SGHL from its origin at the superior glenoid tubercle, just anterior to the LHB, forms laterally a U-shaped “sling” that crosses underneath the biceps tendon and inserts into the lesser tuberosity, where it blends with the CHL [43]. The SGHL attaches to the tendinous slip of the subscapularis insertion as a fold of loose connective tissue and directly supports the LHB. Meanwhile, the CHL, which is also a part of the same loose connective tissue, is considered to provide tension to SGHL [44]. Arterial supply for the LHB comes from three origins: branches of the brachial artery crossing the musculotendinous junction, branches of the thoracoacromial artery crossing the osteotendinous junction, and branches of the anterior circumflex humeral artery traveling in a mesotenon, less frequently according to anatomical studies. This supply divides the LHB tendon into either two or three vascular territories, with a zone of hypovascularity consistently found in an area 1.2–3 cm from the tendon origin, extending from midway through the glenohumeral joint to the proximal inter-tubercular groove. Considering LHB pathology, this is the region of the LHB tendon most frequently prone to rupture [80].

F. Soler et al.

12

1.4.4 Latissimus Dorsi The latissimus dorsi has an origin on the thoracic spinous processes of T7–T12, the lower ribs, and through the thoracolumbar fascia on the lumbar and sacral vertebrae and iliac crest. The muscle fibers converge superolaterally covering the inferior angle of the scapula. The musculotendinous junction is approximately at the entrance of the axillary region [81]. The tendon inserts onto the intertubercular groove of the proximal humerus between the pectoralis major anteriorly and the teres major posteriorly. The average distance reported from the inferior angle of the scapula to the insertion was 18.2 ± 3.4 cm, with a distance from scapula to musculotendinous junction of 12.3 ± 2.3 cm [82]. The thoracodorsal nerve (C6–C8) from the posterior cord of the brachial plexus innervates the latissimus dorsi, while the thoracodorsal artery provides the blood supply. The neurovascular pedicle enters the muscle approximately 2-cm medial to the musculotendinous border [83].

1.5 Neurovascular Structures 1.5.1 Axillary Nerve The axillary nerve (C5–C6) originates in approximately 80% of cases from the posterior cord of the brachial plexus. Can pass through the subscapularis muscle and participates in innervating this muscle. Moreover, a branch of the axillary nerve innervates the teres minor and infraspinatus muscles and the long head triceps muscle [84]. The main branch of the axillary nerve and the posterior humeral circumflex artery and vein pass the quadrilateral space, which is bounded by the subscapularis and teres minor muscle above, by the teres major muscle below and medially by the long head triceps. The nerve curves around the humeral surgical neck and divides into three main branches. The posterior branch supplies the spinal part of the deltoid muscle and the teres minor; the middle branch innervates the lateral part of the pars spinalis of

the deltoid muscle and the acromial part of the deltoid muscle; the anterior branch passes adjacent to the deltoid muscle in a horizontal direction anteriorly, and supplies the acromial and clavicular parts of deltoid muscle [15].

1.5.2 Suprascapular Nerve The suprascapular nerve is a mixed motor and sensory nerve that typically arises from the fifth and sixth cervical roots [85], and only in approximately 25% of individuals, receives contributions from the C4 nerve root [86]. It exits the upper trunk of the brachial plexus approximately 3 cm above the clavicle to run laterally and parallel to the muscle belly of the omohyoid muscle and deep to the anterior border of the trapezius along the posterior cervical triangle, then travels along the posterior border of the clavicle to reach the superior border of the scapula and diving into the suprascapular notch under the transverse scapular ligament (TSL). The TSL is about 9–11.5 mm long and about 3.5 mm thick [87]. Is thin and flat, being narrower at the middle than at its insertions. Is also missing in 1.5–9.5% of cases [87, 88], and ossification of the TSL has been reported to occur in approximately 25% of clinical cases [89]. Three variations of the TSL have been described in cadaveric studies, the majority of specimens exhibited either a fan-shaped ligament (54.6%) or band-shaped ligament (41.9%); however, a bifid ligament was also found in 3.5% of specimens [90]. In most cases, the suprascapular artery takes an anterior position and enters the suprascapular notch over the TSL. The suprascapular nerve as it enters the supraspinatus fossa gives off two motor branches to the supraspinatus muscle belly. The nerve also gives off sensory and sympathetic branches to two-thirds of the GHJ, the CC ligament, the CHL, the subacromial bursa, as well as the posterior capsule of the AC joint [91, 92]. The nerve then travels along the supraspinatus fossa and laterally around the scapular spine to descend into the infraspinatus fossa only to pass under the spinoglenoid ligament, also known as the inferior TSL,

1  Anatomy of the Shoulder

and gives off 2–4 branches to the infraspinatus muscle belly. The suprascapular nerve is approximately 2.5  cm away from the glenoid rim and approximately 4 cm from the posterior corner of the spine of the scapula [93]. The suprascapular notch is about 6  mm high and about 8  mm wide [87]. Multiple variations have been described, type I (U-shaped) being the most common (43.7%) [94]. While hypertrophy of the TSL can lead to stenosis of the suprascapular notch, the variation in the geometry of the suprascapular notch itself, specifically a reduction in the height of the notch, may also cause compression of the nerve, leading to neuropraxia.

1.5.3 Musculocutaneous Nerve The musculocutaneous nerve (C5–C7) arises from the infraclavicular part of the brachial plexus. The nerve originates at the upper rim of the pectoralis minor muscle from the lateral fascicle and runs within a distance of 5–6 cm to the coracoid process through the axilla to the coracobrachialis muscle, penetrates it and passes distally between the biceps muscle and brachial muscle. It supplies the coracobrachialis muscle, the biceps muscle and the brachialis muscle with its muscular branches [15].

1.5.4 Anterior Humeral Circumflex Artery The anterior circumflex humeral artery is weaker than the posterior humeral circumflex artery. It arises below the coracobrachialis and passes in front of the humerus to the bicipital groove, where it ramifies into an ascending and descending branch supplying the deltoid muscle of the long biceps tendon and the shoulder joint.

1.5.5 Posterior Humeral Circumflex Artery This artery generally arises above the lastissimus dorsi tendon from the axillary artery, passing

13

through the lateral axillary space together with the axillary nerve. It passes around the surgical neck of the humerus in a posterior medial direction, supplying large portions of the deltoid muscle and branching to the lateral triceps head, the teres major and teres minor muscles and the articular capsule.

References 1. De Palma AF, Callery G, Bennet GA. Shoulder joint: variational anatomy and degenerative lesions of the shoulder joint. Instr Course Lec. 1949;6:255–81. 2. Schwartz RE, O’Brien SJ, Warren RF.  Capsular restraints to anterior-posterior motion of the abducted shoulder: a biomechanical study. Orthop Trans. 1988;12:727. 3. Steinbeck J, Liljenqvist U, Jerosch J.  The anatomy of the glenohumeral ligamentous complex and its contribution to anterior shoulder stability. J Shoulder Elbow Surg. 1998;7:122–6. 4. Jost B, Koch PP, Gerber C. Anatomy and functional aspects of the rotator interval. J Shoulder Elbow Surg. 2000;9:336–41. 5. Harryman DT II, Sidles JA, Harris SL, Matsen FA III. The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg. 1992;74A:53–66. 6. Slätis P, Aalto K.  Medial dislocation of the tendon of the long head of the biceps brachii. Acta Orthop Scand. 1979;50:73–7. 7. Prescher A, Klümpen T.  The glenoid notch and its relation to the shape of the glenoid cavity of the scapula. J Anat. 1997;190:457–60. 8. AnetzbergerH PR.  The scapula: principles of construction and stress. Acta Anat. 1996;156:70–80. 9. Saha A.  Theory of the shoulder mechanism: descriptive and applied. Springfield: Charles C Thomas; 1961. 10. De Maeseneer M, Van Roy F, Lenchik L, Shahabpour M, Jacobson J, Ryu KN, et al. CT and MR arthrography of the normal and pathologic anterosuperior labrum and labral-bicipital complex. Radiographics. 2000;20 Spec No:S67–81. 11. Williams MM, Snyder SJ, Buford D Jr. The Buford complex  – the “cord-like” middle glenohumeral ligament and absent anterosuperior labrum complex: a normal anatomic capsulolabral variant. Arthroscopy. 1994;10:241–7. 12. Snyder S. Shoulder arthroscopy. New York: McGraw Hill; 1994. 13. Kunner E, Schlosser V.  Traumatologie. Stuttgart: Thieme; 1995. 14. Hertel R, Knothe U, Ballmer FT.  Geometry of the proximal humerus and implications for prosthetic design. J Shoulder Elbow Surg. 2002;11:331–8.

14 15. Ellis V.  The diagnosis of shoulder lesions due to injuries of the rotator cuff. J Bone Joint Surg. 1953;35B:72–4. 16. Perry J. Biomechanics of the shoulder. In: Rowe CR, editor. The shoulder. New York: Churchil Livingstone; 1988. p. 1–15. 17. Ide J, Tokiyoshi A, Hirose J, Mizuta H.  An anatomic study of the subscapularis insertion to the humerus: the subscapularis footprint. Arthroscopy. 2008;24:749–53. 18. Renfree KJ, Wright TW. Anatomy and biomechanics of the acromioclavicular and sternoclavicular joints. Clin Sports Med. 2003;22:219–38. 19. Rockwood CA Jr, Young DC.  Disorders of the acromioclavicular joint. In: Rockwood Jr CA, Matsen III FA, editors. The shoulder. Philadelphia, PA: Saunders; 1990. p. 413–76. 20. Renfree KJ, Riley MK, Wheeler D, et al. Ligamentous anatomy of the distal clavicle. J Shoulder Elbow Surg. 2003;12(4):355–9. 21. Rios CG, Arciero RA, Mazzocca AD.  Anatomy of the clavicle and coracoid process for reconstruction of the coracoclavicular ligaments. Am J Sports Med. 2007;35:811–7. 22. Chahla J, Marchetti DC, Moatshe G, Ferrari MB, Sanchez G, Brady AW, et al. Quantitative Assessment of the Coracoacromial and the Coracoclavicular Ligaments With 3-Dimensional Mapping of the Coracoid Process Anatomy: A Cadaveric Study of Surgically Relevant Structures. Arthroscopy. 2018;34(5):1403–11. https://doi.org/10.1016/j. arthro.2017.11.033. Epub 2018 Feb 1 23. Harris RI, Wallace AL, Harper GD, Goldberg JA, Sonnabend DH, Walsh WR.  Structural properties of the intact and reconstructed coracoclavicular ligament complex. Am J Sports Med. 2000;28:103–8. 24. Motamedi AR, Blevins FT, Willis MC, McNally TP, Shahinpoor M. Biomechanics of the coracoclavicular ligament complex and augmentations used in its repair and reconstruction. Am J Sports Med. 2000;28:380–4. 25. Ernberg LA, Potter HG.  Radiographic evaluation of the acromioclavicular and sternoclavicular joints. Clin Sports Med. 2003;22:255–75. 26. Hollinshead W.  Anatomy for surgeons, vol. III. 3rd ed. Philadelphia: Harper & Row; 1982. 27. Standring S. The anatomical basis of clinical practice. In: Gray’s anatomy. 39th ed. London: Elsevier; 2005. 28. Jobe M. Gross anatomy of the shoulder. In: Rockwood CA, Matsen FA, editors. The shoulder. Philadelphia: Saunders; 1990. 29. Collipal E. The acromion and its different forms. Int J Morphol. 2010;28(4):1189–92. 30. Bigliani LU, Ticker JB, Flatow EL, Soslowsky LJ, Mow VC. The relationship of acromial architecture to rotator cuff disease. Clin Sports Med. 1991;10:823–38. 31. Bigliani L, Morrison D, April EW. The morphology of the acromion in its relationship to rotator cuff tears. Orthop Trans. 1986;10:228. 32. Hamid N, Omid R, Yamaguchi K, Steger-May K, Stobbs G, Keener JD.  Relationship of radiographic

F. Soler et al. acromial characteristics and rotator cuff disease: a prospective investigation of clinical, radiographic, and sonographic findings. J Shoulder Elbow Surg. 2012;21(10):1289–98. 33. Gill TJ, McIrvin E, Kocher MS, Homa K, Mair SD, Hawkins RJ.  The relative importance of acromial morphology and age with respect to rotator cuff pathology. J Shoulder Elbow Surg. 2002;11(4):327–30. 34. Petersson CJ, Redlund-Johnell I.  The subacromial space in normal shoulder radiographs. Acta Orthop Scand. 1984;55:57–8. 35. Edelson JG, Zuckerman J, Hershkovitz I.  Os acromiale: anatomy and surgical implications. J Bone Joint Surg Br. 1993;75(4):551–5. 36. Yammine K.  The prevalence of Os acromiale: a systematic review and meta-analysis. Clin Anat. 2014;27(4):610–21. 37. Bellato E, Blonna D, Castoldi F.  Anatomy of the shoulder. In: Milano G, Grasso A, editors. Shoulder arthroscopy. London: Springer; 2014. 38. Putz R, Liebermann J, Reichelt A.  Funktion des ligamentum coracoacromiale. Acta Anat. 1988;131:140–5. 39. Terra BB, Ejnisman B, de Figueiredo EA, et  al. Anatomic study of the coracoid process: safety margin and practical implications. Arthroscopy. 2013;29:25–30. 40. Shibata T, Izaki T, Miyake S, Doi N, Arashiro Y, Shibata Y, et  al. Predictors of safety margin for coracoid transfer: a cadaveric morphometric analysis. J Orthopaedic Surg Res. 2019;14:174. https://doi. org/10.1186/s13018-­019-­1212-­z. 41. Hamel A, Hamel O, Ploteau S, Robert R, Rogez JM, Malinge M.  The arterial supply of the coracoid process. Surg Radiol Anat. 2012;34:599–607. 42. Yang HF, Tang KL, Chen W, Dong SW, Jin T, Gong JC, et  al. An anatomic and histologic study of the coracohumeral ligament. J Shoulder Elbow Surg. 2009;18:305–10. 43. Nakata W, Katou S, Fujita A, Nakata M, Lefor AT, Sugimoto H.  Biceps pulley: normal anatomy and associated lesions at MR arthrography. Radiographics. 2011;31(3):791–810. 44. Arai R, Mochizuki T, Yamaguchi K, Sugaya H, Kobayashi M, Nakamura T, et al. Functional anatomy of the superior glenohumeral and coracohumeral ligaments and the subscapularis tendon in view of stabilization of the long head of the biceps tendon. J Shoulder Elbow Surg. 2010;19:58–64. 45. Tillman B, Petersen W. Clinical anatomy. In: Wülker N, Mansat M, Fu FH, editors. Shoulder surgery. London: Martin Dunitz; 2001. 46. Sakoma Y, Sano H, Shinozaki N, Itoigawa Y, Yamamoto N, Ozaki T, et  al. Anatomical and functional segments of the deltoid muscle. J Anat. 2011;218:185–90. 47. Leijnse JN, Han SH, Kwon YH.  Morphology of deltoid origin and end tendons  – a generic model. J Anat. 2008;213:733–42.

1  Anatomy of the Shoulder 48. Hue E, Gagey O, Mestdagh H, Fontaine C, Drizenko A, Maynou C. The blood supply of the deltoid muscle. Application to the deltoid flap technique. Surg Radiol Anat. 1998;20(3):161–5. 49. Vahlensieck M, Pollack M, Lang P, Grampp S, Genant HK. Two segments of the supraspinatus muscle: cause of high signal intensity at MR imaging? Radiology. 1993;186:449–54. 50. Howell SM, Imobersteg AM, Seger DH, Marone PJ.  Clarification of the role of the supraspinatus muscle in shoulder function. J Bone Joint Surg Am. 1986;68:398–404. 51. Soslowsky LJ, Carpenter JE, Bucchieri JS, Flatow EL.  Biomechanics of the rotator cuff. Orthop Clin North Am. 1997;28:17–30. 52. Roh MS, Wang VM, April EW, Pollock RG, Bigliani LU, Flatow EL.  Anterior and posterior musculotendinous anatomy of the supraspinatus. J Shoulder Elbow Surg. 2000;9:436–40. 53. Kim SY, Boynton EL, Ravichandiran K, Fung LY, Bleakney R, Agur AM.  Three-dimensional study of the musculotendinous architecture of supraspinatus and its functional correlations. Clin Anat. 2007;20:648–55. 54. Ruotolo C, Fow JE, Nottage WM. The supraspinatus footprint: an anatomic study of the supraspinatus insertion. Arthroscopy. 2004;20:246–9. 55. Curtis AS, Burbank KM, Tierney JJ, Scheller AD, Curran AR.  The insertional footprint of the rotator cuff: an anatomic study. Arthroscopy. 2006;22:603–9. 56. Clark JM, Harryman DT.  Tendons, ligaments, and capsule of the rotator cuff. Gross and microscopic anatomy. J Bone Jt Surg. 1992;74-A:713–25. 57. Minagawa H, Itoi E, Konno N, Kido T, Sano A, Urayama M, et  al. Humeral attachment of the supraspinatus and infraspinatus tendons: an anatomic study. Arthroscopy. 1998;14:302–6. 58. Vosloo M, Keough N, De Beer MA.  The clinical anatomy of the insertion of the rotator cuff tendons. Eur J Orthop Surg Traumatol. 2017;27(3):359–66. https://doi.org/10.1007/s00590-­017-­1922-­z. Epub 2017 Feb 16 59. Nimura A, Kato A, Yamaguchi K, Mochizuki T, Okawa A, Sugaya H, et al. The superior capsule of the shoulder joint complements the insertion of the rotator cuff. J Shoulder Elbow Surg. 2012;21(7):867–72. 60. Burkhart SS, Esch JC, Jolson RS.  The rotator crescent and rotator cable: an anatomic description of the shoulder’s “suspension bridge”. Arthroscopy. 1993;9:611–6. 61. Nakajima T, Rokuuma N, Hamada K, Tomatsu T, Fukuda H.  Histologic and biomechanical characteristics of the supraspinatus tendon: reference to rotator cuff tearing. J Shoulder Elbow Surg. 1994;3:79–87. 62. Ishihara Y, Mihata T, Tamboli M, Nguyen L, Park KJ, McGarry MH, et  al. Role of the superior shoulder capsule in passive stability of the glenohumeral joint. J Shoulder Elbow Surg. 2014;23:642–8.

15 63. Mihata T, McGarry MH, Pirolo JM, Kinoshita M, Lee TQ.  Superior capsule reconstruction to restore superior stability in irreparable rotator cuff tears: a biomechanical cadaveric study. Am J Sports Med. 2012;40:2248–55. 64. Paxton ES, Dodson CC, Lazarus MD.  Shoulder instability in older patients. Orthop Clin North Am. 2014;45:377–85. 65. Holibka R, Holibková A, Laichman S, Růzicková K.  Some peculiarities of the rotator cuff muscles. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2003;147:233–7. 66. Gartsman G. Massive, irreparable tears of the rotator cuff. J Bone Joint Surg Am. 1997;79:715–21. 67. Hamada J, Nimura A, Yoshizaki K, Akita K.  Anatomic study and electromyographic analysis of the teres minor muscle. J Shoulder Elbow Surg. 2017;26(5):870–7. https://doi.org/10.1016/j. jse.2016.09.046. Epub 2017 Jan 10 68. Richards DP, Burkhart SS, Tehrany AM, Wirth MA.  The subscapularis footprint: an anatomic description of its insertion site. Arthroscopy. 2007;23(3):251–4. 69. Arai R, Sugaya H, Mochizuki T, Nimura A, Moriishi J, Akita K.  Subscapularis tendon tear: an anatomic and clinical investigation. Arthroscopy. 2008;24(9):997–1004. 70. Kordasiewicz B, Kicinski M, Pronicki M, Małachowski K, Brzozowska M, Pomianowski S. A new look at the shoulder anterior capsuloligamentous complex complementing the insertion of the subscapularis tendon-Anatomical, histological and ultrasound studies of the lesser tuberosity enthesis. Ann Anat. 2016;205:45–52. 71. Boon J, de Beer M, Botha D, Maritz N, Fouche A. The anatomy of the subscapularis tendon insertion as applied to rotator cuff repair. J Shoulder Elbow Surg. 2004;13:165–9. 72. Wright JM, Heavrin B, Hawkins RJ, Noonan T.  Arthroscopic visualization of the subscapularis tendon. Arthroscopy. 2001;17:677–84. 73. Paribelli G, Boschi S. Complete subscapularis tendon visualization and axillary nerve identification by arthroscopic technique. Arthroscopy. 2005;21:1016. e1–5. https://doi.org/10.1016/j.arthro.2005.05.031. 74. Naidoo N, Lazarus L, De Gama BZ, Ajayi NO, Satyapal KS.  Arterial supply to the rotator cuff muscles. Int J Morphol. 2014;32(1):136–40. 75. Ahrens PM, Boileau P.  The long head of biceps and associated tendinopathy. J Bone Joint Surg Br. 2007;89:1001–9. 76. Di Giacomo G, Constantini A, De Vita A, de Gasperis N, Piscitelli L.  The anatomy of the biceps pulley. In: Imhoff AB, Savoie III FH, editors. Rotator cuff across the life span. https://doi. org/10.1007/978-­3-­662-­58729-­4_25. 77. Dierickx C, Ceccarelli E, Conti M, Vanlommel J, Castagna A.  Variations of intraarticular portion of the long head of the biceps tendon: a classification

16 of embryologically explained variations. J Shoulder Elbow Surg. 2009;18(4):556–65. 78. Werner A, Mueller T, Boehm D, Gohlke F.  The stabilizing sling for the long head of the biceps tendon in the rotator cuff interval. A histoanatomic study. Am J Sports Med. 2000;28:28–31. 79. Walch G, Nove-Josserand L, Levigne C, Renaud E. Tears of the supraspinatus tendon associated with “hidden” lesions of the rotator interval. J Shoulder Elbow Surg. 1994;3:353–60. 80. Cheng NM, Pan WR, Vally F, Le Roux CM, Richardson MD. The arterial supply of the long head of biceps tendon: anatomical study with implications for tendon rupture. Clin Anat. 2010;23:683–92. 81. Pouliart N, Di Giacomo G. Functional anatomy of the Latissimus Dorsi. In: Paribelli G, editor. Latissimus Dorsi Transfer. Cham: Springer; 2017. 82. Elhassan B, Christensen TJ, Wagner ER.  Feasibility of latissimus and teres major transfer to reconstruct irreparable subscapularis tendon tear: an anatomic study. J Shoulder Elbow Surg. 2014;23(4):492–9. https://doi.org/10.1016/j.jse.2013.07.046. 83. Clark NJ, Elhassan BT.  The role of tendon transfers for irreparable rotator cuff tears. Curr Rev Musculoskeletal Med. 2018;11:141–9. 84. Bergman RA, Thompson SA, Afifi AK.  Catalog of human variation. Baltimore: Urban & Schwarzenberg; 1984. 153 85. Cummins CA, Messer TM, Nuber GW. Suprascapular nerve entrapment. J Bone Joint Surg. 2000;82A:415–24. 86. Yan J, Horiguchi M.  The communicating branch of the 4th cervical nerve to the brachial plexus: the double constitution, anterior and posterior, of its fibers. Surg Radiol Anat. 2000;22(3–4):175–9.

F. Soler et al. 87. Yang HJ, Gil YC, Jin JD, Ahn SV, Lee HY.  Topographical anatomy of the suprascapular nerve and vessels at the suprascapular notch. Clin Anat. 2012;25:359–65. 88. Rengachary SS, Burr D, Lucas S, Hassanein KM, Mohn MP, Matzke H.  Suprascapular entrapment neuropathy: a clinical, anatomical, and comparative study. Part 2: Anatomical study. Neurosurgery. 1979;5:447–51. 89. Ticker JB, Djurasovic M, Strauch RJ, April EW, Pollock RG, Flatow EL, et  al. The incidence of ganglion cysts and other variations in anatomy along the course of the suprascapular nerve. J Shoulder Elbow Surg. 1998;7(5):472–8. 90. Polguj M, Jedrzejewski K, Podgorski M, Majos A, Topol M. A proposal for classification of the superior transverse scapular ligament: variable morphology and its potential infl uence on suprascapular nerve entrapment. J Shoulder Elbow Surg. 2013;22(9):1265–73. 91. Aszmann OC, Dellon AL, Birely BT, McFarland EG.  Innervation of the human shoulder joint and its implications for surgery. Clin Orthop Relat Res. 1996;330:202–7. 92. Ebraheim NA, Whitehead JL, Alla SR, Moral MZ, Castillo S, McCollough AL, et al. The suprascapular nerve and its articular branch to the acromioclavicular joint: an anatomic study. J Shoulder Elbow Surg. 2011;20(2):e13–7. 93. Plancher KD, Peterson RK, Johnston JC, Luke TA.  The spinoglenoid ligament. Anatomy, morphology, and histological findings. J Bone Joint Surg Am. 2005;87(2):361–5. 94. Edelson JG.  Bony bridges and other variations of the suprascapular notch. J Bone Joint Surg. 1995;77B:505–6.

2

Biomechanics of the Shoulder Lennard Funk

Abstract

The shoulder is not a joint, but a complex of articulations, bones, muscles, and ligaments. These all interplay in a well-orchestrated manner to allow movement and function of the hand in space, allowing us to perform many activities that are unique to humans. The shoulder complex in humans has mainly evolved for throwing, which was important for hunting. Overhead sports have replaced traditional hunting. Each of the five joints of the shoulder has unique biomechanics, thus unique injuries. In this chapter we will cover the biomechanical properties of each joint, as well as the important muscle-tendon movers and stabilizers of the shoulder complex. We will focus on how these relate to injuries, disease, and arthroscopic surgery. Keywords

Biomechanics · Kinematics · Shoulder complex · Instability · Kinetic chain · Scapula · Moments · Forces · Muscles · Tendons · Articulations

L. Funk (*) Upper Limb Unit, Wrightington Hospital, Wigan, UK e-mail: [email protected]

2.1 Kinematics of the Shoulder Complex The human shoulder is specialized from the primitive mammalian model. It is inherited from a tree-swinging quadrupedal ancestor to the bipedal human. The shoulder complex follows Williston’s concept of evolution: “in the course of evolution the number of structural parts becomes reduced and the remaining parts become more specialized.” The human shoulder complex has evolved predominantly for throwing and manipulating tools in space, as opposed to walking, swimming, flying, or swinging. In that regard, it is unique among mammals. Unlike the lower extremity, in which most functional and sport-specific movements occur in a closed kinetic chain environment, the upper extremity functions almost exclusively in an open kinetic chain format [1]. The throwing motion, volleyball spike, tennis serve, and tennis ground stroke are all examples of open kinetic chain activities of the upper extremity. This movement is facilitated by the combined and synchronous motion of the shoulder complex articulations. Shoulder complex movements represent carefully orchestrated motion of all of its components. The humerus rotates around the scapula within the glenohumeral joint, the scapula rotates around the clavicle at the acromioclavicular joint, and the clavicle rotates around the sternum at the sternoclavicular joint [2]. Movement of all of

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_2

17

L. Funk

18

these components must occur for the arm to achieve 180 degrees of humeral elevation. (The term elevation is frequently used in the literature without differentiation between abduction and flexion.) The movement of the upper limb can be described in many ways. The most typical is scapulohumerothoracic rhythm, which recognizes the role played by the scapula in the chain forming an intermediate link between humerus and thorax. Various ratios of scapula to humeral motion (scapulohumeral rhythm) have been reported, thus it is likely that it is variable and changes with load, function, and velocity of movement [3]. The shoulder complex has a unique anatomy, providing the largest range of motion within mammalian joint assemblies, while antagonized by a high load carrying capacity. This motion and function can be subdivided into the individual articulations. The complex has three true independent articulations—Glenohumeral, Acromioclavicular, and Sternoclavicular, with and two false articulations (Scapulothoracic and Acomiohumeral). Each joint, while capable of independent motion, contributes to the normal function of the upper extremity, participating in a simultaneous, rather than successive, manner of overall motion. This motion is only possible via the foundation of the linkage to the trunk. The arm is linked to the trunk anteriorly via the clavicle through the acromioclavicular and sternoclavicular joints. Posteriorly there are no true joints, so the muscular attachments of the scapula to the thorax are of major importance in maintenance of that integrity. The ability of the shoulder to position the arm in space is dependent on the individual joint stabilizers and large muscle groups to ensure that the balance between mobility and stability is optimal for the intended task.

2.2 Kinesiology of the Shoulder Complex The evolution from quadruped to plantigrade mammals has necessitated alteration of the upper limb from one used primarily for stability in weight-bearing to one used primarily as a mobile

structure. This has led to evolution in the variable demands and functions of the muscles. Many muscles that are large and important in the quadruped animal are less important in the biped human. The muscles of the shoulder complex can be divided into three groups: (1) Muscles that originate on the trunk and insert on the scapula; (2) Muscles that originate on the trunk and insert on the humerus; (3) Muscles that originate on the scapula and insert on the humerus (Table 2.1) [4]. Although it is comprised of three distinct segments, movement of any one of those segments may produce movement in other segments. For example, movement of the humerus through action of the latissimus dorsi or pectoralis major (both of which originate on the trunk) will produce movement of the scapula and clavicle as well. Thus, the shoulder complex functions as a kinematic chain. Muscles almost always act in combinations to produce motion. A prerequisite for normal function is for all relevant muscles to act synchronously and appropriately. Table  2.2 shows the primary actions of the muscles of the shoulder complex [5]. For any muscle to be primarily responsible for a given motion, other muscles provide supportive stability (either as an agonist or antagoTable 2.1  Muscles of the shoulder complex 1. From the trunk to the shoulder girdle: Serratus anterior Trapezius Rhomboids Pectoralis minor Levator scapulae Subclavius 2. From the trunk to the humerus: Latissimus dorsi Pectoralis major 3. From the shoulder girdle to the humerus, radius, or ulna: Supraspinatus Infraspinatus Subscapularis Teres Major Teres minor Coracobrachialis Biceps Triceps

X

X

X

X

X

X

X

X

X X

X X

X

X X

X

X

X

X

X

X X X

X

X

X

X

X X

b

a

Biceps brachii long head may abduct the humerus if the humerus is externally rotated The joint angle will determine whether posterior deltoid can adduct the humerus c The joint angle will determine whether teres major abducts or adducts the limb d The joint angle will determine whether the lower trapezius upwardly or downwardly rotates the scapula

Biceps—short head Biceps—long heada Biceps—long head Triceps—long head Supraspinatus Deltoid     Anterior     Middle     Posteriorb Coracobrachialis Latissimus Dorsi Pectoralis major     Upper fibers     Lower fibers Subscapularis Teres majorc Infraspinatus Teres minor Pectoralis minor Rhomboids Levator scapulae Trapezius     Upper     Middle     Lowerd Serratus anterior     Upper fibers     Lower fibres X

X

X

X

X X X

X

X X

X

X

X X

X

X

X X

X

X

X

Internal External Horizontal Downward Upward Anterior Flexion Extension rotation rotation Abduction Adduction adduction Elevation Depression rotation rotation Protraction Retraction tilt X X X

Table 2.2  Prime mover muscles

2  Biomechanics of the Shoulder 19

20

nist), or synergistically as a secondary mover. For motion to occur normally, the relevant antagonist must lengthen appropriately and the stabilizers must act coordinately to provide a stable base throughout the remainder of the body. The postural muscles provide stability of the body for upper extremity movement. The action of postural muscles varies depending on body position in space. The muscles that maintain stability will depend on the relationship of body alignment to the line of gravity at any given time. This gives rise to the kinetic chain concept in shoulder function.

2.3 Scapula The scapula is a flat bone whose primary function is to provide a site for the muscle attachments of the shoulder. A total of 15 major muscles acting at the shoulder attach to the scapula [6, 7]. In quadrupedal animals the scapula is long and thin and rests on the lateral aspect of the thorax. In primates, there is a gradual mediolateral expansion of the bone along with a gradual migration from a position lateral on the thorax to a more posterior location. This mediolateral expansion broadens the attachment area for the rotator cuff muscles [4]. These changes in location and structure of the scapula reflect the gradual change in the function of these muscles from weight bearing to position and support a scapula and glenohumeral joint that is free to move through a much larger excursion. The plane of the scapula is oriented approximately 30–45° from the frontal plane (Fig. 2.1). This position directs the glenoid anteriorly with respect to the body. However, the glenoid fossa is retroverted, or rotated posteriorly, with respect to the neck of the scapula. Thus, the gle-

L. Funk

Fig. 2.1  Position of the scapula and glenoid orientation on the thorax. Note the narrow dashed line demonstrating retroversion of the glenoid on a scapula that lies anteriorly directed on the thorax

noid fossa is directed anteriorly (with respect to the body) and at the same time is retroverted (with respect to the scapula). The degrees of version and tilt of the glenoid vary significantly from individual to individual [8]. These variations have been implicated as predisposing to various acquired pathologies, such as instability direction (related to version) [9, 10], rotator cuff disease (upward tilt) [11], and osteoarthritis (downward tilt) [12, 13]. Normal movement of the scapula comprises of three motions: (1) upward/downward rotation around a horizontal axis perpendicular to the plane of the scapula; (2) internal/external rotation around a vertical axis through the plane of the scapula; and (3) anterior/posterior tilt around a horizontal axis in the plane of the scapula. The clavicle acts as a strut for the shoulder complex, connecting the scapula to the axial skeleton. Normality of this linkage enables two translations: (1) upward/downward translation on the thoracic wall and (2) retraction/protraction around the rounded thorax [14].

2  Biomechanics of the Shoulder

The coupling of scapular external rotation, posterior tilt, upward rotation, and medial translation is called retraction. The coupling of internal rotation, angular tilt, downward rotation, and lateral translation is called protraction. The coupling of upward translation, anterior tilt, and internal rotation is seen as a shrug. The scapula fulfils important functions in dynamic and static modes. In addition to upward rotation, the scapula is required to tilt posteriorly and externally rotate to clear the acromion from the moving arm in elevation and abduction. In addition, the scapula must be able to internally/externally rotate in a synchronous manner to maintain the glenoid as a congruent socket for the arm in motion, thereby maximizing concavity compression and ball and socket kinematics. The scapula must be dynamically stabilized in a position of retraction during use of the arm to achieve maximal activation of all of the muscles that originate on the scapula. The upper and lower trapezius muscles in addition to the serratus anterior muscles are the main contributors to scapular stability and mobility (Fig.  2.2). The trapezius and serratus anterior muscles initiate upward rotation and posterior tilt of the scapula. Activation of the lower trapezius muscle plays an important role in the stability of the arm in the overhead position and in descent of the arm from a position of maximum elevation. The rhomboids assist the trapezius in stabilizing the scapula contributing to control of medial and lateral scapular translation. Latissimus dorsi and pectoralis minor, which are both extrinsic shoulder girdle muscles, affect scapular motion in their role as prime movers of the arm. These muscles act mainly as force couples. The appropriate force couples for scapular stabilization include the upper and lower portions of the trapezius muscle working

21

Fig. 2.2  Prime movers and stabilizers of the scapula: upper and lower trapezius with serratus anterior

together with the rhomboid muscles, paired with the serratus anterior muscle (Fig.  2.3). The appropriate force couples for acromial elevation are the lower trapezius and the serratus muscles working together paired with the upper trapezius and rhomboid muscles. Another important role of the scapula in the normal shoulder is as a link in the proximal to distal sequencing of velocity, energy, and forces of shoulder function, thus contributing to the kinetic chain. This linkage is essential for the transference of force for throwing, lifting, and all overhead activities. In most cases, sequencing begins at ground level and individual body segments are coordinated by muscle activation and body position to generate, summate, and transfer forces through these segments to the terminal link. This sequence is termed the kinetic chain (Fig. 2.4).

L. Funk

22

a

b

c

d

Fig. 2.3  Force couples for scapula motion: in early elevation (a, b), the upper and lower trapezius and serratus anterior muscles have long lever arms, being effective rotators and stabilizers. With higher arm elevation (c), the upper trapezius moment arm is shorter, whereas the lower trapezius and serratus anterior moment arms remain long,

continuing to rotate the scapula. With maximum arm elevation (d), the lower trapezius maintains scapula position and the instant center of rotation moves from the medial border of the spine to the acromioclavicular joint (adapted from Bagg SD, Forrest W)

2  Biomechanics of the Shoulder

23

bility, in particular for extremes of the range of motion, the major passive soft tissue stabilizers include the glenoid labrum and capsuloligamentous components. Negative intra-articular pressure [16] generated by an interaction between capsule and synovial fluid is a further physiological mechanism of stability (Fig. 2.5).

2.4.1 Glenoid Labrum

Fig. 2.4  The kinetic chain—the chain linkage for force production of arm movement and shoulder function. To generate arm forces, the force initiation starts at the ground and is transferred to the arm via the trunk and scapula

2.4 Glenohumeral Joint The articulation between the glenoid and the humerus is a large unconstrained synovial ball and socket joint. The ball (humeral head) is 3–4 times larger than the socket (glenoid), with only 25–30% of the humeral head articulating with the glenoid socket at any one time. Thus, for the glenoid and humerus to remain in contact through range of motion, the soft tissue structures need to contain the glenohumeral joint. Loss of this containment leads to glenohumeral joint instability. Glenohumeral joint stability is maintained through an intricate interplay between a number of static and dynamic structures and physiological mechanisms. Dynamic stability of the joint may be coordinated by higher cortical control of local musculotendinous units providing direct stability by generating a joint reaction force and maintenance of optimal scapulohumeral balance [15] through proprioceptive feedback. The end effectors of such control are the rotator cuff musculotendinous units and associated periscapular and shoulder girdle musculature. Although the viscoelastic properties of the shoulder musculature may infer a significant degree of passive sta-

The glenoid labrum is a fibrous rim that serves to slightly deepen the glenoid fossa and allows for the attachment of the glenohumeral ligaments to the glenoid. The vast majority of the labrum consists of dense fibrous tissue with few elastic fibers. A small amount of fibrocartilage exists at the junction of the glenoid and fibrous capsule. The labrum receives a blood supply to its periphery. The superior and anterosuperior portions of the labrum are less vascular than the ­posterosuperior and inferior portions [17]. The labrum is well attached to the glenoid anteroinferiorly, inferiorly and posteriorly, but variably and loosely attached anterosuperiorly. The superior labrum is often loose and resembles the mobility of the meniscus in the knee, with a frequent sublabral recess. The role of the labrum as a stabilizing structure has been debated in the literature. The labrum functions to deepen the glenoid, from 2.5 to approximately 5 mm. The labrum may function in combination with joint compression forces to stabilize the joint within the midrange of glenohumeral motion where the ligamentous capsular structures are lax. Biomechanical studies have indicated that resection of the labrum can reduce the effectiveness of the compression stabilization by 20% [18]. The labrum appears to serve as a buttress assisting in controlling glenohumeral translation, similar to a chock-block, which would prevent the wheel of a tractor from rolling downhill. Additionally, Bowen et  al. have stated that the labrum may also contribute to stability by increasing the surface area and acting as a load-­ bearing structure for the humeral head [19]. Overall, failure of the labrum alone is insufficient

L. Funk

24

a

b

c

d

Fig. 2.5 Mechanisms of Glenohumeral Stability: (a) demonstrates the effect of the concavity depth on stability, (b) the angular range of stability resulting from glenohumeral balance, (c) demonstrates the effect of limited vol-

to cause anterior dislocation unless accompanied by disruption of the anterior capsule and ligamentous structures [20]. In fact, Bankart emphasized the importance of an obvious anterior capsular detachment in instability and stated that the labrum could be excised so long as the capsule was firmly attached to bone [21].

ume and negative intra-articular pressure, while (d) the role of articular compression due to soft tissue tensioning during rotation

assists in providing joint stability. Distractive force leads to an increase in longitudinal stretching of the capsule and, thus, constriction of the cylinder, resulting in greater joint compression and enhanced effects of negative intra-articular pressure, similar to a Chinese finger trap mechanism [22]. The capsular ligaments are regions of thick densely organized collagen fibers, with the thick2.4.2 Capsule and Ligaments est being in the anteroinferior capsule. These contribute greatly to joint stability when the joint The glenohumeral joint capsule is large, loose, is placed in extremes of motion. The anterior and redundant, thereby allowing for the large band of the inferior glenohumeral ligament range of glenohumeral motion. It is composed of (IGHL) complex has been identified as critical in multilayered collagen fiber bundles of differing resisting anterior translation of the humeral head strength and orientation. The joint capsule colla- with increased abduction and external rotation gen fiber orientation is comprised of radial fibers [23]. At lower degrees of abduction, the middle that are linked to each other by circular elements. glenohumeral ligament (MGHL) plays a more Thus, rotational forces produce tension within significant role. The posterior band of the IGHL the fibers, which leads to compression of the joint has been shown to constrain the humeral head at surfaces but also a centering of the joint. The cir- 30 degrees of flexion. However, capsular cutting cular collagen fibers appear to play a significant studies have shown the synergistic ability of the role in absorbing stress and tension. The spiral-­ capsule to stabilize the joint, and as such, the posshaped, cross-linked capsular collagen structure terior capsule also has a role to play in the main-

2  Biomechanics of the Shoulder

tenance of anterior stability, as the anterior capsule does in posterior stability [24, 25]. This supports the ‘circle stability concept’ [26], which suggests a combination of different structural failures result in joint instability. As such, this symptomatic translation is indicative of a significant number of complex interacting pathologies. However, in conceptual terms, in order for dislocation to occur, damage to the capsule must occur on both the same and opposite side to the direction of dislocation [27] (Fig. 2.6). We can classify the structures in the direction of the translation as the primary restraints and the structures on the opposite side of the joint as the secondary restraints. The constraints to inferior translation of the humeral head on the glenoid vary based on arm position and degree of rotation. Selective tissue cutting studies have demonstrated that the ­primary and secondary restraints preventing inferior translation with the arm in the adducted position are the superior glenohumeral ligament (SGHL) and the coracohumeral ligament (CHL) [28]. When the arm is abducted to 45 degrees and neutrally rotated, the anterior band of the IGHL complex is the primary restraint to inferior trans-

25

lation. At 90 degrees of abduction, the posterior band of the IGHL complex is the primary stabilizer against inferior motion of the humeral head on the glenoid. The MGHL plays a significant role in limiting anterior translation within the midrange of shoulder abduction. The constraints to posterior translation are also based on arm position. The IGHL complex (with the posteroinferior capsule) is the primary passive stabilizer against posterior instability with the arm in 90 degrees of abduction [29]. When the arm is positioned below 90 degrees of abduction, the posterior capsule provides the primary restraint to any posterior force. With abduction and external rotation, the anterior band of the IGHL complex fans out and surrounds the anteroinferior aspect of the humeral head much like a hammock, thus, restraining anterior displacement, while the posterior band prevents inferior displacement. With internal rotation and abduction, the anterior band of the IGHL complex moves inferiorly to resist inferior translation as the posterior band shifts posterosuperiorly to prevent posterior translation [30] (Fig.  2.7). With the shoulder in 90 degrees of abduction and 30 degrees of extension, the anterior band of the IGHL complex becomes the primary stabilizer against both anterior and posterior translation. The amount of strain present within the glenohumeral ligaments varies with arm position, with a maximum concentration of strain in the IGHL complex at 90 degrees of glenohumeral abduction. The strain is concentrated within the superior and middle glenohumeral ligaments at 0 degrees of abduction [31]. As a general rule, the superior capsular structures play significant roles in joint stability when the arm is adducted. Conversely, the inferior structures are p­ redominant in joint stability from 90 degrees of abduction toward full elevation.

2.4.3 Dynamic Stabilizers of the Glenohumeral Joint Fig. 2.6  The ‘circle stability’ concept: in order for dislocation to occur, damage to the capsule must occur on both the same and opposite side to the direction of dislocation (adapted from Pagnani and Warren [27])

The dynamic stabilizers contribute several active mechanisms to the inherent stability of the shoulder joint. The primary active stabilizers of the

26

L. Funk

Fig. 2.7  The reciprocal effect of the IGHLC. The image demonstrates accentuation of the reciprocal role of the inferior glenohumeral ligaments at 90° of abduction (adapted from Warner et al. [28])

glenohumeral joint include the rotator cuff muscles (supraspinatus, infraspinatus, teres minor, subscapularis), the deltoid, and the long head of the biceps brachii. Secondary stabilizers include the teres major, latissimus dorsi, and pectoralis major muscles. The primary role of the muscles is through combinations of muscular contraction which enhances the stability of the humeral head during active arm movements. These muscles act together in an agonist/ antagonist relationship to provide movement of the arm but also to stabilize the glenohumeral joint. In the past, these muscles were thought to function as part of a force couple relationship [32]. A force couple, by definition, occurs when two parallel forces of equal magnitude but opposite direction are applied to a structure at equal distances from the center of the mass. The two force couples most commonly described at the shoulder are the subscapularis counterbalanced by the infraspinatus/teres minor in the transverse plane and the deltoid counterbalanced by the inferior rotator cuff muscles in the coronal plane [32]. However, dynamic electromyography studies have shown that the rotator cuff muscles act to counteract the shearing force generated by the deltoid muscles [33, 34]. This combined effect of

Fig. 2.8  Dynamic stability of the glenohumeral joint from the compressive forces of the rotator cuff muscles— ‘balance of forces’

the rotator cuff synergistic action creates humeral head compression within the glenoid, which is a major contributor to joint stability (Fig.  2.8). Thus, a more appropriate term for the counterbalancing action of the rotator cuff and deltoid muscles would be a “balance of forces,” rather than a force couple relationship. The second method of active glenohumeral joint stability is provided through the blending of the rotator cuff tendons into the shoulder capsule. As the rotator cuff muscles contract, tension is

2  Biomechanics of the Shoulder

produced within the capsular ligaments, actively tightening the glenohumeral ligamentous capsule, again promoting a centering of the humeral head within the glenoid fossa [35]. The third component contributing to dynamic shoulder stability has been termed “neuromuscular control”. This concept refers to the continuous interplay of afferent input and efferent output. Thus, it is the individual’s awareness of joint position (proprioception) and the ability to produce a voluntary muscular contraction to stabilize the joint and/or to alter the joint position. The glenohumeral capsulolabral structures are rich in Ruffinian and Pacinian corpuscles and Golgi mechanoreceptors, particularly inferiorly. These stretch-sensitive mechanoreceptors could be activated by tension, thus, producing a muscular contraction to protect the ligaments at the extremes of motion [25]. Advanced exercises, such as plyometrics, proprioceptive neuromuscular facilitation movements, and reactive muscular training drills, may assist in reestablishing the reactive neuromuscular control abilities at the shoulder joint [36]. The scapulothoracic musculature also plays a significant role in shoulder stability by providing a stable base of support for the glenohumeral muscles to function from. One of the primary roles of the scapulothoracic joint is to dynamically maintain a consistent length-tension relationship for the shoulder girdle muscles [36]. Scapulothoracic joint stability is greatly dependent on the scapulothoracic musculature. Weakness of these muscles or muscle groups contributes to a lack of functional stability of the scapula, which directly affects the ultimate function of the glenohumeral joint musculature. This implies a direct link between weak scapular musculature and multidirectional shoulder instability [37].

2.5 Acromioclavicular Joint The acromioclavicular joint is generally regarded as a gliding joint. Although gliding joints allow only translational movements, many authors describe rotational movement about specific axes

27

of motion at the acromioclavicular joint. While the clavicle and scapula move together, their contributions to whole shoulder motion require that they also move somewhat independently of one another. This independent movement requires motion at the acromioclavicular joint. When analyzing relative motion of the scapula with respect to the clavicle, the scapula rotates about a specific screw axis, passing through the insertions of both the acromioclavicular and the coracoclavicular ligaments on the coracoid process [38] (Fig. 2.9). This screw axis describes the total rotation and translation, with a total of 35 degrees of rotation with full shoulder abduction. This suggests that the acromioclavicular joint allows significant motion between the scapula and clavicle. The acromioclavicular joint is supported by a capsule that is reinforced superiorly and inferiorly by strong acromioclavicular ligaments. The acromioclavicular ligaments appear to provide important limitations to posterior glide of the acromioclavicular joint regardless of the magnitude of displacement or load, contributing approximately 90% of the ligamentous constraint [39]. The inferior acromioclavicular ligament also provides substantial resistance to excessive anterior displacement of the clavicle on the scapula [40]. The anteroinferior ligaments contribute significantly to the rotational stability of the acromioclavicular joint [41]. Nakazawa et  al. [42] described the acromioclavicular ligaments as two separate bundles (superoposterior and anteroinferior structures). They reported a higher quality structural composition of the superoposterior bundle by macroscopic inspection and microscopic investigation. Their findings suggested that the anteroinferior segment of the AC capsule is inconsistent and appeared only thin and narrow while proposing an important role for horizontal instability. From this, we can conclude that with damage to the acromioclavicular joint capsule, the amplitude of the clavicle’s motion in relation to the acromion would be highly increased when the arm is moved. Therefore, the strut function of the clavicle to support the physiological scapulothoracic motion will be severely limited by relative instability of the joint.

L. Funk

28

a

b

Fig. 2.9  The acromioclavicular joint screw axis (Sahara et al. [38]): demonstrating the relative motion of the scapula to the clavicle from 0 degrees of abduction to maximum abduction. (a) View from the front and (b) from above

The other major support to the acromioclavicular joint is the extracapsular coracoclavicular ligament that runs from the base of the coracoid process to the inferior surface of the clavicle. This ligament provides critical support to the acromioclavicular joint, particularly against large excursions and medial displacements. Mechanical tests reveal that it is substantially stiffer than the acromioclavicular, coracoacromial, and superior glenohumeral ligaments [43]. The ligament is composed of two parts, the conoid ligament that runs vertically from the coracoid process to the conoid tubercle on the clavicle and the trapezoid ligament that runs vertically and laterally to the trapezoid line. The conoid ligament limits excessive superior glides at the acromioclavicular joint, while the acromioclavicular ligaments limit smaller superior displacements. The trapezoid ligament protects against the shearing forces that can drive the acromion inferiorly and medially under the clavicle. Dynamic stability and mobility of the acromioclavicular joint is provided via an interplay between the anterior deltoid and the upper trapezius muscles. The anterior fibers of the deltoid muscle and the upper trapezius muscle attach to

the anterior and posterior aspect of the distal end of the clavicle, respectively. At 90 degrees of abduction, the insertion of the deltoid muscle is located in the lateral side of the clavicle, and the traction force of this muscle is directed laterally. Thus, the anterior component of the traction force of this muscle may become smaller than the posterior component of the traction force of the upper trapezius, causing the clavicle to translate posteriorly. At maximum abduction, the deltoid insertion is located in the anterolateral side of the clavicle. Thus, the anterior component of the traction force of this muscle may become larger than the posterior component of the upper trapezius, causing the clavicle to translate anteriorly [38].

2.6 Sternoclavicular Joint The sternoclavicular joint has been described as either a ball-and-socket joint or saddle joint. Both types of joints are triaxial, so there is little functional significance to the distinction. The joint is enclosed by a synovial capsule attaching to the sternum and clavicle beyond the articular sur-

2  Biomechanics of the Shoulder

faces. The capsule is relatively weak inferiorly but is reinforced anteriorly, posteriorly, and superiorly by accessory ligaments that are thickenings of the capsule itself (Fig.  2.10). The ligaments serve to limit anterior and posterior glide of the sternoclavicular joint. They also provide some limits to the joint’s normal transverse plane movement, known as protraction and retraction. The articular surface of the clavicle is much larger than that of the sternum, with the superior part of the clavicular head projecting superiorly above the sternum. This disparity of the articular surfaces results in an inherent instability, which allows the clavicle to slide medially over the sternum. An intra-articular disc also blocks medial movement of the clavicle. The disc is attached inferiorly to the superior aspect of the first costal cartilage and superiorly to the superior border of the clavicle’s articular surface dividing the joint into two separate synovial cavities. The clavicle is anchored to the underlying first costal cartilage by the intra-articular disc resisting any medial movement of the clavicle. The disc may also

Fig. 2.10  Anatomy of the sternoclavicular joints

29

serve as a shock absorber between the clavicle and sternum. Another important stabilizing structure of the sternoclavicular joint is the costoclavicular ligament, an extracapsular ligament lying lateral to the joint itself. It runs from the lateral aspect of the first costal cartilage superiorly to the inferior aspect of the medial clavicle. Its anterior fibers run superiorly and laterally, while the posterior fibers run superiorly and medially. Consequently, this ligament provides significant limits movements of the clavicle in all directions. Despite being an inherently unstable joint, the supporting structures of the sternoclavicular joint together limit medial, lateral, posterior, anterior, and superior displacements of the clavicle on the sternum. Inferior movement of the clavicle is limited by the interclavicular ligament and by the costal cartilage itself. Thus, it is clear that the sternoclavicular joint is so reinforced that it is quite a stable joint. Few studies are available that investigate the motion of the sternoclavicular joint [44, 45]. The total excursion of elevation and depression is report-

30

edly 50–60 degrees, with depression being less than 10 degrees of the total. Elevation is limited by the costoclavicular ligament, and depression by the superior portion of the capsule and the interclavicular ligament. Protraction and retraction appear to be more equal in excursion, with a reported total excursion ranging from 30 to 60 degrees. Protraction is limited by the posterior sternoclavicular ligament limiting the backward movement of the clavicular head and by the costoclavicular ligament limiting the forward movement of the body of the clavicle. Retraction is limited similarly by the anterior sternoclavicular ligament and by the costoclavicular ligament. The interclavicular ligament assists in limiting both motions. Upward and downward rotations appear to be more limited than the other motions, with estimates of upward rotation that vary from 25 to 55 degrees. Downward rotation appears to be much less than upward. Regardless of the exact amount of excursion available at the sternoclavicular joint, it is well understood that motion at the sternoclavicular joint is intimately related to motions of the other joints of the shoulder complex, particularly the acromioclavicular joint via the strut mechanism of the clavicle.

Fig. 2.11  The strut linkage of the clavicle between the sternoclavicular joint and acromioclavicular joint, with the linkage to the scapula via the conoid part of the coracoclavicular ligament allows for the upward rotation of the scapula with supplementary movements at both ends of the clavicular strut

L. Funk

2.6.1 Sternoclavicular and Acromioclavicular Motion With the upward rotation of the scapula during arm elevation, there must be concomitant elevation of the clavicle to which the scapula is attached. The sternoclavicular joint elevates 15–40 degrees during arm elevation. The joint also retracts and upwardly rotates during elevation. Total scapular upward rotation is 60 degrees and the total clavicular elevation is approximately 40 degrees. This disparity of motion suggests that the scapula moves away from the clavicle, causing motion at the acromioclavicular joint. As the scapula is pulled away from the clavicle by upward rotation, the conoid ligament is pulled tight and pulls on the conoid tubercle situated on the inferior surface of the crank-shaped clavicle. The tubercle is drawn toward the coracoid process, causing the clavicle to be pulled into upward rotation (Fig. 2.11). The crank shape of the clavicle allows the clavicle to remain close to the scapula as it completes its lateral rotation, without using additional elevation at the sternoclavicular joint. The sternoclavicular joint thus elevates less than its full available motion, which

2  Biomechanics of the Shoulder

is approximately 60°. Therefore, full shoulder flexion or abduction can still be augmented by additional sternoclavicular elevation in activities that require an extra-long reach, such as reaching to the very top shelf. This sequence of events demonstrates the significance of the crank shape of the clavicle and the mobility of the ­acromioclavicular joint to the overall motion of the shoulder complex. This description of sternoclavicular and acromioclavicular motion reveals the remarkable synergy of movement among all four joints of the shoulder complex necessary to complete full flexion and abduction. The scapulothoracic joint must rotate upward to allow full glenohumeral flexion or abduction. The clavicle must elevate and upwardly rotate to allow scapular rotation.

2.7 Summary This chapter examines the mechanics of the shoulder complex, which allow considerable mobility and possess inherent challenges to stability. The primary limits to normal shoulder motion are the capsuloligamentous complex and the surrounding muscles of the shoulder. The normal function of the shoulder complex depends on the integrity of four individual joint structures and their coordinated contributions to arm motion. The glenohumeral joint contributes over 50% of the motion in arm elevation. The remaining elevation comes from upward rotation of the scapula. The scapula also undergoes posterior tilting and lateral rotation about a vertical axis during elevation. In addition to glenohumeral and scapulothoracic contributions to elevation, the sternoclavicular and acromioclavicular joints contribute important motions to allow full elevation. Each of these joints has unique soft tissue structures that work synchronously to allow the extensive range of motion of the shoulder complex, while maintaining stability. The relevance of the kinetic chain to providing a stable base and force generation system is key to allowing power and function of the arm. Impairment or injury to any of the individual joints or structures can pro-

31

duce altered movement and affect the other structures of the shoulder complex. The current chapter is an update of the one published in the previous edition and authored by Michael O. Schär and Scott A. Rodeo.

References 1. Palmitier RA, An KN, Scott SG, Chao EY.  Kinetic chain exercise in knee rehabilitation. Sports Med. 1991;11(6):402–13. 2. Steindler A.  Kinesiology of the human body under normal and pathological conditions. Springfield, IL: Charles C. Thomas; 1955. 3. Sugamoto K, Harada T, Machida A, Inui H, Miyamoto T, Takeuchi E, Yoshikawa H, Ochi T. Scapulohumeral rhythm: relationship between motion velocity and rhythm. Clin Orthop Relat Res. 2002;401:119–24. 4. Inman JT, Saunders M, Abbott L.  Observations on the function of the shoulder joint. J Bone Joint Surg. 1944;26:1–30. 5. Shenkman M, De Cartaya VR.  Kinesiology of the shoulder complex. JOSPT. 1987;8(9):438–50. 6. Lucas D.  Biomechanics of the shoulder joint. Arch Surg. 1973;107:425–32. 7. Williams P, Bannister L, Berry M, et  al. Gray’s Anatomy, The anatomical basis of medicine and surgery. Br. ed. London: Churchill Livingstone; 1995. 8. Churchill RS, Brems JJ, Kotschi H.  Glenoid size, inclination, and version: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):327–32. 9. Brewer BJ, Wubben RC, Carrera GF.  Excessive retroversion of the glenoid cavity. A cause of non-­ traumatic posterior instability of the shoulder. JBJS. 1986;68(5):724–31. 10. Semogas V, Granville-Chapman J, Mackenzie TA, Funk L.  Glenoid version as a contributing factor to shoulder instability. Shoulder Elbow. 2015;7:309–32. 11. Hughes RE, Bryant CR, Hall JM, Wening J, Huston LJ, Kuhn JE, Carpenter JE, Blasier RB. Glenoid inclination is associated with full-thickness rotator cuff tears. Clin Orthop Relat Res. 2003;407:86–91. 12. Moor BK, Bouaicha S, Rothenfluh DA, Sukthankar A, Gerber C. Is there an association between the individual anatomy of the scapula and the development of rotator cuff tears or osteoarthritis of the glenohumeral joint? A radiological study of the critical shoulder angle. Bone Joint J. 2013;95(7):935–41. 13. Ricchetti ET, Hendel MD, Collins DN, Iannotti JP. Is premorbid glenoid anatomy altered in patients with glenohumeral osteoarthritis? Clin Orthop Relat Res. 2013;471(9):2932–9. 14. Roche SJ, Funk L, Sciascia A, Kibler WB. Scapular dyskinesis: the surgeon’s perspective. Shoulder Elbow. 2015;7(4):289–97.

32 15. Lippitt SB, Matsen FA III. Mechanisms of glenohumeral joint stability. Clin Orthop. 1993;291:20–8. 16. Gibb TD, Sidles JA, Harryman DT 2nd, McQuade KJ, Matsen FA III.  The effect of capsular venting on glenohumeral laxity. Clin Orthop Relat Res. 1991;268:120–7. 17. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, Dicarlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am Vol. 1992;74(1):46–52. 18. Vanderhooft E, Lippett S, Harris S, Sidles J, Harryman DT, Matsen FA.  Glenohumeral stability from concavity-­compression: a quantitative analysis. Orthop Trans. 1992;l6:774. 19. Bowen MK, Deng XH, Hannafin JA, O’Brien SJ, Altchek DW, Warren RF. An analysis of the patterns of glenohumeral joint contact and their relationship to the glenoid “bare area”. Trans Orthop Res Soc. 1992;l7:496. 20. Townley CO.  The capsular mechanism in recurrent dislocation of the shoulder. J Bone Joint Surg. 1950;32A:370–80. 21. Bankart ASB. Discussion on recurrent dislocation of the shoulder. J Bone Joint Surg. 1948;30B:46–7. 22. Gohlke F, Essigkrug B, Schmitz F.  The pattern of the collagen fiber bundles of the capsule of the glenohumeral joint. J Shoulder Elbow Surg. 1994;3:111–28. 23. Turkel SJ, Panio MW, Marshall JL, Girgis FG.  Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg. 1981;63-A:1208–17. 24. Blasier RB, Goldberg RE, Rothman ED.  Anterior shoulder stability: contributions of rotator cuff forces and the capsular ligaments in a cadaver model. J Shoulder Elbow Surg. 1992;1:140–50. 25. Terry GS, Hammon D, France P, Norwood LA. The stabilizing function of passive shoulder restraints. Am J Sports Med. 1991;19:26–34. 26. Warren RF.  Subluxation of the shoulder in athletes. Clin Sports Med. 1983;2(2):339–54. 27. Pagnani MJ, Warren RF.  Stabilizers of the glenohumeral joint. J Shoulder Elbow Surg. 1994;3:173–90. 28. Warner JJP, Deng XP, Warren RF, Torzilli PA. Static capsular ligamentous constraints to superior-inferior translation of the glenohumeral joint. Am J Sports Med. 1992;20:675–85. 29. O’Brien SJ, Schwartz RE, Warren RF, Torzilli PA. Capsular restraints to anterior/posterior motion of the shoulder. Orthop Trans. 1988;12:143. 30. O’Brien SJ, Neves MC, Arnoczky SP, Rozbruch SR, DiCarlo EF, Warren RF, Schwartz R.  The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med. 1990;18:449–56.

L. Funk 31. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E.  The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med. 1991:18579–84. 32. Inman VT, Saunders JR, Abbott JC. Observations on the function of the shoulder joint. J Bone Joint Surg. 1994;26(A):1–30. 33. Perry J.  Muscle control of the shoulder. In: Rowe CR, editor. The shoulder. New  York: Churchill Livingstone; 1988. p. 17–34. 34. Wuelker N, Wirth CJ, Plitz W, Roetman B. A dynamic shoulder model: reliability testing and muscle force study. Biomech. 1995;28(5):489–99. 35. Clark M, Harryman DT.  Tendons, ligaments and capsule of the rotator cuff. J Bone Joint Surg. 1992;74A:713–25. 36. Wilk KE, Voight ML, Keirns MA, Gambetta V, Andrews JR, Dillman CJ. Stretch-shortening drills for the upper extremities: theory and clinical application. J Orthop Sports Phys Ther. 1993;17:225–39. 37. Wilk KE, Arrigo CA, Andrews JR. Current concepts: the stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther. 1997;25(6):364–79. 38. Sahara W, Sugamoto K, Murai M, Tanaka H, Yoshikawa H. 3D kinematic analysis of the acromioclavicular joint during arm abduction using vertically open MRI. J Orthop Res. 2006;24(9):1823–31. 39. Fukuda KI, Craig EV, An KN, Cofield RH, Chao EY. Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am Vol. 1986;68(3):434–40. 40. Lee K, Debski RE, Chen C, et al. Functional evaluation of the ligaments at the acromioclavicular joint during anteroposterior and superoinferior translation. Am J Sports Med. 1997;25:858–62. 41. Dyrna FG, Imhoff FB, Voss A, Braun S, Obopilwe E, Apostolakos JM, Morikawa D, Comer B, Imhoff AB, Mazzocca AD, Beitzel K.  The integrity of the acromioclavicular capsule ensures physiological centering of the acromioclavicular joint under rotational loading. Am J Sports Med. 2018;46(6):1432–40. 42. Nakazawa M, Nimura A, Mochizuki T, Koizumi M, Sato T, Akita K. The orientation and variation of the acromioclavicular ligament: an anatomic study. Am J Sports Med. 2016;44(10):2690–5. 43. Costic RS, Vangura A, Fenwick JA, et al. Viscoelastic behaviour and structural properties of the coracoclavicular ligaments. Scand J Med Sci Sports. 2003;13:305–10. 44. Steindler A.  Kinesiology of the human body under normal and pathological conditions. Springfield, IL: Charles C. Thomas; 1959. 45. Oatis CA. Kinesiology: the mechanics and pathomechanics of human movement. Lippincott Williams & Wilkins; 2009.

3

Biology of Injury and Repair of Soft Tissues of the Shoulder James B. Carr II and Scott A. Rodeo

Abstract

Soft tissue injuries in the shoulder, especially to the rotator cuff tendons, are a common source of shoulder pain and dysfunction. Intrinsic pathological changes in the rotator cuff tendon often lead to diminished tendon quality and eventual rotator cuff tendinosis and tearing. Understanding the native biology of the rotator cuff, the effect of aging on tendon quality, the intrinsic and extrinsic factors that may play a role in tendon degeneration, and the biology of tendon healing is critically important for a comprehensive approach to the management of rotator cuff disease. Specifically, common hormones, proteins, and growth factors that affect degeneration and healing of the rotator cuff may offer potential targets for biological treatments. The current chapter provides an in-depth review of the biological processes during injury and repair of the soft tissues about the shoulder joint with a special emphasis on the rotator cuff. Keywords

Shoulder pathology · Rotator cuff disease · Growth factors · Soft tissue injury · Soft tissue healing J. B. Carr II (*) · S. A. Rodeo Department of Sports Medicine and Shoulder Surgery, Hospital for Special Surgery, New York, NY, USA e-mail: [email protected]; [email protected]

3.1 Introduction Pathologies of the shoulder, especially rotator cuff (RC) tears, are increasing in the aging population. The underlying biologic mechanisms of different shoulder pathologies are complex and remain poorly defined. However, improved understanding of the mechanisms that lead to pathologic changes and healing can lead to better approaches for treating pathologies of the shoulder. Many factors have been implicated in both the development of degenerative changes and the healing process within the shoulder joint. This chapter will outline current understanding of the biology of different shoulder pathologies, including the rotator cuff, the long head of the biceps, and the glenoid labrum.

3.2 Biology of the Intact Rotator Cuff 3.2.1 Four Zones of the Intact Tendon-Bone Interface The tendon-bone attachment in the RC represents a biomechanical challenge since the force must be transferred from the soft tendon tissue with low stiffness to the relatively stiff bone. In the RC, this problem is solved with a special transitional area between the tendon and the bone called the “enthesis” (Fig. 3.1). In this area, the

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_3

33

34

J. B. Carr II and S. A. Rodeo

3.2.2 Fetal Development of the Native Tendon and the Tendon-Bone Junction

Fig. 3.1  Normal ACL insertion with bone blending into tendon substance via a calcified and an uncalcified fibrocartilage zone (Hematoxylin-eosin stain)

stiffness increases gradually from the tendon to the bone and enables an effective transfer of the mechanical load from the tendon to the bone. The fully formed enthesis is generally described as having four zones: (1) the tendon, (2) the uncalcified fibrocartilage, (3) calcified fibrocartilage, and (4) bone. In these zones, the different collagens and proteoglycans, such as aggrecan, decorin, and biglycan, are not distributed uniformly. There are no sharp boundaries between these zones [1]. This continuous change from the bone to tendon enables a transfer of the load between the bone and the tendon. The transition of these four zones occurs approximately over a distance of 1 mm in length. The mechanisms that regulate development of the complex series of tissue gradations are not yet clear. During tendon-bone healing, the normal enthesis with its four distinctive zones is not restored properly, which results in a relatively high incidence of repair failure. Recurrent tears following rotator cuff repair are likely due to the inferior material properties of the healing enthesis. Understanding the natural development of the tendon and its enthesis during embryogenesis may provide insight into basic mechanisms that could inform development of new approaches to improve the healing rate and to reestablish the four zones that connect the bone with the tendon.

The mechanisms that govern formation of the four zones of the enthesis are incompletely understood. The tendon and bone of the RC complex is formed 15.5 days postconception during fetal development. The transitional zone does not develop until 7 days postnatally and remodels into a mature fibrocartilaginous enthesis after 21 days postnatally [2]. Fibroblasts of the tendon (zone 1) are active throughout development. Collagen I is expressed by fibroblasts in zone I and II, whereas collagen II is expressed in zone III and IV by chondrocytes. In zone IV, it is expressed up to 14 days postnatally. Close to the insertion, chondrocytes become hypertrophic and start expressing collagen X beginning 14 days postnatally. These hypertrophic chondrocytes possibly mature into the fibrocartilaginous transition zone. It is hypothesized that collagen X might sustain the transition between the unmineralized and mineralized zones [3]. Several transcription factors play an important role in the development of the tendon-bone junction in the RC. Scleraxis (Scx) is a basic helix-­ loop-­helix protein which is a key transcription factor in tenogenesis [4–6], while chondrocyte differentiation is induced by the transcription factor Sox-9 [7]. The size of the developing tendon is regulated by how many cells are expressing Scx. Scleraxis and Sox-9 [8] also appear to play an important role in enthesis formation [4]. The expression of Scx has been detected in the developing insertion site, but Sox9 might also be expressed in the developing enthesis [9]. Both transcription factors are expressed during fetal development as early as 10.5 days postconception [4]. At 15.5 days postconception, scleraxis was more restricted to tendons. Lastly, proteins such as parathyroid hormone-related protein (PTHrP) and Indian hedgehog (Ihh) protein might not only play an important role in the development of the growth plate, but also in the

3  Biology of Injury and Repair of Soft Tissues of the Shoulder

development of the tendon-bone enthesis by regulating chondrocyte differentiation [10, 11]. Various members of the bone morphogenetic protein (BMP) family of proteins, in particular BMP-12, BMP-13, and BMP-14 (GDF-7, GDF-­ 6, and GDF-5), also have an influence on tendon development. Mice that are deficient in BMP-12, BMP-13, or BMP-14 show biomechanical, biological, and/or structural abnormalities in the tendon [12, 13]. BMP-4 seems to be another important factor. Its expression in tendons is necessary for the initiation of bone ridges. Blockade of BMP-4 during embryologic development did not abrogate insertion formation, suggesting that other pathways play an important role [14]. Other factors include members of the transforming growth factor beta (TGF-β) protein superfamily. These proteins have been shown to have a positive effect on the expression of Scx. For example, in the TGF-β 2/TGF-β 3 double mutant or type II TGF-β receptor null mice, most of the tendons were lost [15]. However, the induction of Scx-expressing tendon progenitors was not affected in these embryos. Fibroblast growth factors (FGF) also influence gene expression in early development. Scleraxis was highly upregulated when an FGF-8-soaked bead was applied in somites [16, 17]. The inhibition of FGF signaling, on the other hand, caused loss of Scx expression. However, the precise mechanism(s) underlying the interaction between members of the FGF family and Scx is currently unclear. Tendon and cartilage emerge from the same precursor cells, and BMP and FGF appear to have antagonistic roles in regulation of the process of differentiation. BMP-2 stimulated chondrogenesis in chicken embryos and inhibits tendon development [5, 18, 19]. Inhibition of BMP leads to tendon differentiation, whereas the inhibition of FGF induces chondrogenesis. Signals from muscle may also play a role in RC tendon. Several studies suggest that signals from myogenic cells are not necessary to initiate the expression of Scx. In a mouse knockout model, in which mice without muscle were bred,

35

Scx was expressed in progenitor cells in similar amounts as in normal mice [11, 20]. However, the expression of Scx was not sustained in the setting of a continuous absence of myogenic cells [20, 21]. Scx seems to be regulated by ectodermal signals [5]. Mechanical cues may also play a role in enthesis formation, although little is known about its mechanism [3, 22]. For example, the expression of Scx has been shown to be mechanosensitive, as mesenchymal stem cells that are cyclically loaded responded with an upregulation of the expression of Scx [23]. Further studies are necessary to understand the complex pathways involved in tendon and insertion site development.

3.3 Biology of Rotator Cuff Degeneration in Adults The underlying pathogenesis of RC tendon degeneration is multifactorial and remains an area that is incompletely understood, although recent research has begun to elucidate the cellular and molecular mechanisms of tendinopathy. The etiologic factors for RC tendon degeneration can be divided into intrinsic and extrinsic causes.

3.3.1 Extrinsic Causes for Rotator Cuff Degeneration Subacromial impingement, resulting in damage to the supraspinatus tendon, was first described as an extrinsic cause of RC tendon degeneration [24]. In this situation the tendon impinges on the overlying coracoacromial arch, leading to degeneration and eventual rupture of the tendon. This model is supported by the fact that 72% of patients with stage I and II impingement syndrome in one study showed good to excellent results after subacromial decompression [25]. While extrinsic RC degeneration is a generally accepted mechanism, intrinsic degeneration is likely to play a more prominent role in RC degeneration.

36

3.3.2 Intrinsic Causes for Rotator Cuff Degeneration A widely accepted intrinsic model is the degenerative microtrauma model [26], where age-­related degeneration and accumulated microinjury lead to increased mucoid deposition, fatty infiltration, a shift from collagen type I to III, and hydroxyapatite microcalcification [27, 28]. The basic cellular and molecular processes that lead to these changes are currently not well defined. All of these changes adversely affect the material properties of the tendon, leading eventually to a partial- or full-thickness RC tear. Current data suggest that metabolic dysfunction and genetic predisposition may accelerate this process [29, 30]. It is generally believed that intrinsic damage to the enthesis can lead to an inflammatory reaction within the articular sided synovium and/ or the subacromial bursal tissue, leading to production and accumulation of matrix-­degrading molecules and increased proliferation of osteoclasts [31–35]. Tendon hypovascularity is another intrinsic factor that likely contributes to RC degeneration. Two studies show that there is a critical hypovascular zone within 10  mm of the supraspinatus tendon insertion [36, 37]. Interestingly, in the infraspinatus tendon, this zone was only found in the superior portion, which may explain the preponderance for supraspinatus tendon tears. This hypovascularity could lead to cumulative degeneration and impaired tendon healing. A recent study reveals evidence that hypoxic damage in the RC may lead to a loss of cells by apoptosis [38]. It has been shown that cytokines such as IL-1β and enzymes such as matrix metalloproteinases (MMP)-3 are important contributors to the pathology of tendinopathies [39]. Cytokines also play a key role in oxidative stress-induced cellular apoptosis. The role of apoptosis in degeneration of tendon cells has recently been studied. Excessive apoptosis has been noted in the edges of the torn RC tendons. Yuan et al. [40] reported that the number of apoptotic cells in degenerative RC tendon was significantly higher than that in the control group. These apoptotic cells are also

J. B. Carr II and S. A. Rodeo

found in perivascular areas. This oxidative stress-­ induced apoptosis is mediated by the release of caspase 3 and the cytochrome C pathway [41]. Conversely, heat shock proteins seem to protect tendon cells from the cytotoxic effects of apoptotic mediators and cytokines [42]. Occasionally, the intrinsic degenerative process can lead to delamination of the supraspinatus tendon as the RC tear progresses. Delamination likely occurs due to separation between the superficial and deep layers of the rotator cuff tendon during tear progression [43]. This may be due to differing shear forces and vascularity between the layers. Delamination is largely viewed as a sign of a chronic tear, and it has been found to be more prevalent in the elderly population and in smokers [43, 44].

3.4 Biology of the Rotator Cuff Tear Natural history data suggest that degenerative processes likely predispose to RC tears during the aging process. However, high-energy trauma in patients without degenerative changes in the RC can also lead to RC tears. After an RC tear, the histopathological changes in the tendon are not restricted to the end of the tendon. One study compared the histopathological changes after RC tears in the intact part of the supraspinatus tendon with an intact tendon control group [45]. The tendon in the tear group showed changes of the collagen with an increased collagen type III content and a loss of collagen alignment. A decrease in tenocyte number with associated alterations of the shape of the nucleoli was also reported. Furthermore, increased vascularization was observed. Since these changes were not only limited to the tendon end but also to the intact third of the tendon, the authors advise against extensive debridement of the tendon end during repair. The authors did not correlate the pathological changes with the tear size [46]. Matthews et  al. [29] found a decrease in the fibroblast number with increased tear size. The number of newly formed vessels and inflammatory cells, which are important for the healing

3  Biology of Injury and Repair of Soft Tissues of the Shoulder

process, was also reduced in massive tears. In smaller RC tears, they found a thickened synovial layer, which normally indicates an attempt at healing. In massive tears these findings were absent [29].

3.5 Biology of Rotator Cuff Healing The healing process can be roughly divided into three phases. In the initial inflammatory phase, there is infiltration of inflammatory cells to the injury site. Within the first 24  h, macrophages and monocytes remove necrotic tissue and release cytokines that initiate early vascularization, cell migration, proliferation, and differentiation. This phase lasts for several days and is then followed by the proliferative phase. Cells, including tenocytes and fibroblasts, are recruited to the repair site. Early collagen type III production begins in this phase. This phase lasts several weeks and is then followed by the remodeling phase. During the remodeling phase, collagen III is replaced by collagen type I, and the cellularity of the tissue gradually decreases. In this process, the tendon-bone interface is repaired by reactive scar formation (Fig.  3.2). Predictable recreation of the four zones of the native insertion site does not occur. This scar tissue has inferior material properties compared to

Fig. 3.2  Histology of the healing enthesis after a rotator cuff repair containing interposed fibrovascular tissue. This tissue is gradually remodelled (Hematoxylin-eosin stain)

37

the native insertion site, placing the repaired site at a mechanical disadvantage compared to the native enthesis. In order to achieve a physiological reconstruction of the enthesis, new biological treatment strategies are required. These strategies should address all the requisites that are necessary for healing, including: (1) intrinsic and extrinsic cells, (2) different growth factors released in the optimal concentration at the right time, (3) extracellular matrix (ECM) proteins, and (4) the optimal amount of load and mobilization. Biologic agents are becoming increasingly popular within the field of orthopedic surgery. Regarding RC tears, they offer the possibility of improved healing, but such promise has not been reliably proven in clinical studies. Furthermore, inconsistent terminology and consumer-driven demands create a confusing environment for physicians and consumers alike. Briefly, the most popular biologic agents currently available include platelet-rich plasma (PRP) and cell-based therapies, such as bone marrow aspirate concentrate (BMAC) or adipose tissue from lipo-aspiration. Recent meta-analyses investigating the effect of PRP on RC repair healing have shown mixed results. Zhao et  al. reviewed eight randomized controlled trials that investigated the outcomes of arthroscopic rotator cuff repairs with or without concomitant PRP injections [47]. No difference was found in any outcome scores or healing rates. Similarly, Saltzman et al. found no difference in clinical outcomes after PRP administration following RC repair [48]. Conversely, Hurley et al. investigated 18 randomized controlled studies with 1147 patients and found that PRP injection improved healing rates for small and medium RC tear repairs while also improving pain scores and clinical outcome scores [49]. The heterogeneity of conclusions is likely due to the wide variability in the studies included in each analysis as well as the high amount of variability between individual studies. The role of BMAC in augmentation of RC healing is equally conflicting with many clinical studies lacking a control group [50–52]. Perhaps the most compelling study to support the use of

J. B. Carr II and S. A. Rodeo

38

BMAC was performed by Hernigou et al. [53]. A total of 45 patients underwent RC repair that was augmented by concentrated cells from bone marrow and 45 patients underwent isolated repair without augmentation. Patients who received the cell preparations demonstrated superior tendon healing and enhanced quality of repaired tendon on postoperative advanced imaging with 100% of patients in the treatment group demonstrating healing compared to 67% of patients in the control group. At 10-year follow-up, repairs remained intact in 87% of the treatment group compared to 44% of the control group. Long-term maintenance of the tendon repair integrity was directly correlated with a higher number of implanted cells. In general, caution should be used when drawing conclusions about the role of biologics in RC biology augmentation. While some basic science data and limited clinical data are compelling, the overall body of work is very mixed with inconclusive results. Biologic agents merit further investigation with more rigorous testing with the hope that more clearly defined formulations and approaches can be elucidated in the future. A brief summary of the most commonly used biologic agents in shoulder pathology can be found in Table 3.1.

3.5.1 Influence of Cells on Healing The hypocellular nature of the tendon and the enthesis may contribute to the poor healing potential of the repaired rotator cuff. Two different cell sources are likely important for healing: (1) intrinsic cells including tenocytes and osteoblasts and (2) extrinsic cells including inflammatory cells and mesenchymal stem cells. Hirose et al. [46] reported that intrinsic cells derived from the epitenon of the bursal surface of the tendon migrate into the repair site. Tenocytes synthesize and secrete ECM proteins [54]. Because these cells exhibit very low proliferative capacities [55], one possible approach to improve tendon healing is to augment the enthesis with extrinsic cells, such as mesenchymal stromal cells (MSCs). These cells have the unique prop-

Table 3.1  Positive features and drawbacks for commonly used biologic agents in the management of shoulder pathology Biologic agent Bone marrow aspirate concentrate (BMAC)

Positives – Autologous agent that is relatively easy to harvest in office or operating room – FDA approved because minimally manipulated – Contains more growth factors and nucleated cells than PRP Platelet-rich – Autologous agent plasma that is harvested (PRP) from peripheral blood draw – Easy to obtain with minimal pain to the patient, making it ideal for the office setting – Different formulations (i.e., leukocyte-rich and leukocyte-poor) can be generated based on desired end-product Lipo-­ – Autologous agent aspiration of readily found in stromal cells most patients – Aspiration of subcutaneous fat is relatively painless and may be performed in clinic or the operating room – Contains mesenchymal stromal cells

Drawbacks – Contains very small amounts of mesenchymal stromal cells and progenitor cells – Harvesting can be painful for patient – Currently there is limited clinical data to support its regular use – Not currently covered by insurance, so often expensive for the patient – Does not contain any mesenchymal stromal cells – Currently there is limited clinical data to support its regular use despite promising basic science data

– Requires manipulation (not FDA approved) to maximize amount of stromal cells. – May not be a viable option in skinny patients or extremely fit athletes with low body fat percentage. – Currently there is limited clinical data to support its regular use

erties of multi-lineage differentiation capacity and self-renewal. Furthermore, they can be harvested relatively easily from the bone marrow. Recently, the subacromial bursa has also been identified as a potentially rich source of mesenchymal stromal cells [56–58]. This is particularly

3  Biology of Injury and Repair of Soft Tissues of the Shoulder

39

appealing as harvest of MSCs from the subacromial bursa would require less morbidity to the patient and would also have the convenience of being a local site to the shoulder. However, preliminary work in a rat RC repair model found that mesenchymal stromal cells did not improve the biomechanical and histological properties [59]. One possible explanation may be that the repair site may lack the signals necessary

to induce appropriate differentiation of the transplanted MSCs. This is supported by further work in this model in which MSCs that were transduced with the transcription factor Scleraxis before implantation led to improved tendon healing (Fig. 3.3). Similarly, MSCs genetically modified to overexpress the developmental gene MT1-MMP have also been shown to improve early RC healing by the production of more fibro-

Fig. 3.3  Histology images of cartilage at the insertions site. Slides were prepared with safranin-O/fast green stains that stain the proteoglycans in cartilage a magenta color. There was a greater area of metachromasia found in

the Ad-Scx as compared with the mesenchymal stem cell (MSC) group at 4 weeks. Scx scleraxis. (Magnification ×100). (From [39]. Copyright: Dr Scott A.  Rodeo. Reproduced with permission)

40

cartilage at the insertion and improved biomechanical strength [60]. Leukocytes, including lymphocytes, neutrophils, and macrophages, represent another extrinsic cell source that is involved in the early cellular events following tendon repair. These inflammatory cells act in the initial stage of the tendon repair process by secreting growth factors and other soluble mediators, which initiate the repair cascade [61].

3.5.2 Influence of Growth Factors on Healing The healing response in RC tears is highly dependent on a coordinated sequence of growth factor expression. Migration of cells into the defect is mediated by growth factors and is important for the healing of the tendon. In the proximal site of the myotendinous insertion, growth factors appear earlier than at the distal defect of the tendon, although they are detectable in the lesion for a longer period [62]. Several studies show that most growth factors return to normal levels 3–8 weeks after the injury [62, 63]. Cytokines involved in tendon healing include TGF-β1, fibroblast growth factor (FGF), BMP, interleukins (IL), plateletderived growth factors (PDGF), and vascular endothelial growth factors (VEGF). The interplay of these factors is complex.

3.5.2.1 Transforming Growth Factor-Beta Transforming growth factor-beta (TGF-β) is produced by all the cells that are involved in the healing process, whereas normal tendons show low concentrations of TGF-β [64, 65]. The TGF-β 1 isoform is involved in adult wound healing and leads to the formation of scar tissue. In contrast, in early fetal “scarless” wound healing, TGF-β 3 is increased. TGF-β 1 remains highly upregulated for the first 8 weeks following tendon injury and repair in the adult wound [63, 65]. It is active in the healing process during all phases [62, 65]. The potential negative effect of the TGF-β 1 isoform was shown in a study where TGF-β 1 was delivered via an osmotic pump in a rat supraspi-

J. B. Carr II and S. A. Rodeo

natus tendon tear model. An increase in type III collagen production was seen, indicative of scar-­ mediated response [66]. Kovacevic et  al. [32] reported that RC reconstructions that were augmented with an osteoconductive calcium phosphate matrix containing TGF-β 3 showed a significantly improved strength of the repair at 4 weeks postoperatively and resulted in a more favorable collagen I/collagen III ratio when compared to the group with augmentation performed with only calcium phosphate matrix (Table 3.1). Manning et al. [67] also reported similar results.

3.5.2.2 Fibroblast Growth Factor Members of the fibroblast growth factor family may affect tendon-bone healing. FGF-2, which is also known as bFGF, has a role in formation of granulation tissue. bFGF is produced not only by leukocytes, but also by tenocytes and fibroblasts [64, 65]. It remains highly upregulated during the entire healing process, but has its peak between the seventh and the ninth day. This factor stimulates the proliferation of RC tendon cells (RCTC) in a dose-dependent manner and suppresses the secretion of collagens from RCTC in vitro [68]. Several authors reported improved tendon healing after the addition of bFGF [69, 70]. Local application of bFGF using an acellular dermal matrix graft led to a significant increase in strength and tendon maturity at 6 and 12 weeks postoperatively [71, 72]. On the other hand, Thomopoulos et al. [73] showed in an intrasynovial flexor tendon canine model that the administration of bFGF failed to produce improvements in either the mechanical or the functional properties of the repair. They also found an increased vascularity, cellularity, and adhesion with an increase in peritendinous scar formation. 3.5.2.3 Bone Morphogenetic Protein It has been proposed that the formation of the enthesis bears some similarity to the process of enchondral ossification [74]. It has been shown that ingrowth of bone into the tendon is fundamental in the tendon-bone healing process [75]. For this reason, the augmentation of RC reconstructions using osteoinductive growth factors has been proposed. The prototypical

3  Biology of Injury and Repair of Soft Tissues of the Shoulder

o­ steoinductive factors are members of the bone morphogenetic protein (BMP) family. Except for BMP-1, which is a metalloprotease, all BMPs belong to the TGF-β superfamily. BMP-2, for example, increased the collagen I production in an in vitro study on the tenocyte-­ like cells isolated from human RC tissue samples [76]. An increase in collagen type I production and expression, as well as increased cell activity, was observed for BMP-7. The combination of BMP-2 and BMP-7 resulted in smaller changes compared to the use of BMP-7 alone [76]. The application of BMP-2  in an injectable hydrogel into a ruptured RC resulted in a significantly higher maximum pullout load at 4 and 8 weeks postoperatively [77]. BMP-14 can be localized to the bursal side of the tendon and tendon edge in the histologic examination of full-thickness RC tears in humans [78]. When adipose-derived or bone-marrow-­ derived MSC were treated with BMP-14  in an in  vitro model, a higher proliferation rate was observed, along with an increased differentiation towards a tenocyte phenotype [79, 80]. In contrast, MSCs that were treated BMP-13 differentiated into chondrocytes [81]. The addition of rhBMP-12, rhBMP-13, and rhBMP-14 induced neotendon formation when implanted at ectopic sites in vivo [82]. In an animal model, the application of rhBMP-12 and rhBMP-13 enhanced RC tendon-bone healing [83, 84].

3.5.2.4 Matrix Metalloproteinases and Tissue Inhibitor Metalloproteinases Matrix metalloproteinases (MMPs) belong to the super family of proteases and are catabolic enzymes. They can degrade all components of the extracellular matrix (ECM) such as collagen. In normal healthy tissue, there is a balance between MMPs and tissue inhibitors of metalloproteinases (TIMPs). An imbalance between these two factors produces dysregulation in collagen turnover and matrix remodeling with subsequent adverse effects on matrix material properties. Data from unloaded flexor tendons of rats suggest that MMP-9 and MMP-13 mediate tissue degradation during the early phase of heal-

41

ing, whereas MMP-2, MMP-3, and MMP-14 (MT1-MMP) mediate tissue degradation and later remodeling [85]. The time course of the expression of MMPs and TIMPs during RC healing was first reported by Choi et al. [86]. In a clinical study performed with patients who had undergone recent RC reconstruction, a significantly higher expression of MMP-1 and MMP-9 was found in the supraspinatus tendon in the non-healed group compared to the healed group [87]. Also, MMP-13 protein levels were increased in torn RC tendons, and they showed a proportional correlation with the patients’ pain score [88]. However, the balance between MMPs and their inhibitors is complex and requires further study. Specific MMPs delivered at a certain time point may have a positive effect on healing. For example, MSCs that were genetically manipulated to overexpress MT1-MMP (MMP-14) improved the RC healing in a rat model [60]. There are many unanswered questions about the optimal doses and combinations of various cytokines, timing of delivery, and the ideal delivery vehicle. Furthermore, the complexity of wound healing, including inflammation, cell proliferation, matrix synthesis, and remodeling, suggests that healing may be best optimized by a combination of factors.

3.5.3 Influence of the Extracellular Matrix on Healing Proteoglycans and collagens are the structural components of the ECM in tendon and enthesis. Ninety-five percent of all the collagen in tendons is type I collagen. In the rest of the enthesis (zone II-III), the collagen organization is less parallel than in the tendon itself [89]. Type I collagen is found mainly in zones I and IV (tendon and bone) [2]. It is also found temporarily in the stage of remodeling [65]. Type II collagen is found during fetal development in zone IV and postnatally in zones II and III (fibrocartilage zones) [2, 90]. Type III collagen is found in zones I and IV [91]. It is present during the early stages of the healing process [92]. In the healing of tendons and bone, collagen type III is associated with early scar

42

t­issue formation [92, 93]. It is not yet clear to what extent excessive levels of collagen III can impair insertion site quality. The fibril diameter of collagen type I is regulated by type V collagen [92], and therefore, type V collagen can be found predominantly in zones I and IV [94, 95]. The fibril-­related type IX collagen is located predominantly on the osseous side of the insertion and connects mainly with type II collagen. Collagen type X is produced during human development by hypertrophic chondrocytes in the mineralized fibrocartilaginous transitional zone III [2, 94]. Collagen X seems to play an important role in the conversion of unmineralized to mineralized tissue because it persists in zone III (mineralized fibrocartilage region), even if the hypertrophic chondrocytes are no longer present. It is interesting to note that collagen X is not present in adult enthesis healing [2, 94]. It is in fact not produced until zones II and III have been developed. The role of mechanical stimulus in the expression and production of collagen X is supported by the fact that in tendons of patients with paralyzed shoulders, the formation of a fibrocartilaginous transitional zone is disturbed [96]. Collagen XII is situated on both sides of the insertion [97] and belongs, like collagen type IX, to the fibril-associated group. It binds to collagen type I [94]. Proteoglycans also contribute to the tissue regulation of the ECM. Biglycan, for example, is a tendon-specific ECM protein. It is only found in zone I of the enthesis area [91, 94, 98]. Biglycan forms bridges between the collagen fibrils and increases their stability. By influencing fibrillogenesis, it also determines their structure [97]. Biglycan is involved in organizing the niche for tendon stem/progenitor cells in mammalian tendon. In double null mice lacking both biglycan and fibromodulin, a local increase of BMP signaling was detected, which favors local chondrocytic/osteoblastic differentiation. It also promotes ectopic endochondral bone formation and impairs tendon formation in the young adult [99]. Aggrecan is a cartilage-specific ECM protein analogous to versican, which is only found in the unmineralized fibrocartilage region of the enthesis [90, 91, 94, 98]. The production of aggrecan is triggered by compressive stress [2], which is why

J. B. Carr II and S. A. Rodeo

this protein predominates in zone III [94]. Aggrecan also strongly binds water [94]. Decorin is another important proteoglycan, which regulates the collagen fibril diameter, like type V collagen. It is found mainly in zone I and II of the intact insertion [92, 94, 97]. During the healing process, decorin is found at reduced levels, but can still be detected. It contributes to the stabilization of the collagen structure by building bridges between collagen fibrils and by influencing fibrillogenesis through inhibition of collagen type I formation [94, 97]. It also regulates the activity of TGF-β [94].

3.5.4 Influence of Load and Mobilization on Healing Several studies show that load has a profound effect on tendon and enthesis healing. It is well established that mechanical stress improves the tensile strength, stiffness, and cross-sectional area of tendons [100, 101]. This is most probably caused by an increase in collagen and ECM synthesis by tenocytes [101]. If collagen is stress-­ shielded during the proliferative and remodeling phase, it is weaker and less organized compared to collagen under tensile load. Repetitive motion increases DNA content and protein synthesis in human tenocytes [102]. At the same time, application of strain to tenocytes produces stress-­ activated protein kinases, which in turn triggers apoptosis, demonstrating the complexity of the tenocyte response to load [103, 104]. Although stress-shielding of tendon may have a negative effect, excessive mechanical load may also adversely affect the biologic events in tendon healing. Further study is required to determine the optimal magnitude, type, and timing of mechanical load on healing tendon.

3.5.5 Influence of Muscle Changes on Rotator Cuff Healing After an RC tear, the muscle retracts, atrophies, and is infiltrated by fat. These muscle changes have significant effects on rotator cuff tendon

3  Biology of Injury and Repair of Soft Tissues of the Shoulder

healing and represent important prognostic factors for the success of an RC reconstruction.

3.5.5.1 Retraction The retraction of the musculotendinous unit is generally considered to be an important pathophysiological consequence after an RC tear. Several studies show that pronounced tendon retraction is associated with a higher rate of failed healing [105–108]. Fatty infiltration, especially of the supraspinatus and infraspinatus muscle, has been shown to be a negative prognostic factor for RC healing after repair [108–110]. Furthermore, successful healing after RC repair has been associated with reversal of fatty infiltration of the supraspinatus up to 2 years after surgery [111]. It has been shown that continuous elongation of a retracted, fatty infiltrated, and atrophied musculotendinous unit is technically feasible in the sheep infraspinatus model [112]. There is evidence that up to Goutallier stage III, retraction of the supraspinatus muscle is caused mainly by the muscle. In advanced stages, the retraction results also from shortening of the tendon tissue itself [113]. Due to this shortened tendon stump, the muscle must be stretched beyond its physiological length in order to compensate for the tendon retraction. When the muscle retracts, the pennation angle increases and therefore gaps form between the single muscle fibers. As a result, fat is deposited into these gaps. 3.5.5.2 Fatty Infiltration It is currently unclear if fatty infiltration is part of the normal age-related degenerative process of tendinopathy or appears due to the failed biological repair mechanism. Fatty infiltration is found after RC tears and as a result of denervation. It is found in different areas of the musculotendinous unit, including the intramuscular compartments [114]. The accumulation of fat leads to a reduction in the mechanical properties of the muscle [115]. Fatty infiltration is also found in the extramuscular space and in the torn tendon [116]. It is notable that fat is deposited not only around the muscle fibers, but also accumulates in type 1 muscle within the sarcoplasm [114]. Even though

43

fatty infiltration has an important effect on the outcome of RC repairs, little is known about the etiology of this process. Understanding the pathophysiological mechanisms that lead to fatty degeneration is critical in order to determine potential strategies that may ultimately be able to halt or even reverse these adverse changes. Several theories have been proposed to explain the mechanism of fatty infiltration. Peroxisome proliferator-activated receptor gamma (PPARγ) is one of the central regulators of adipogenesis. PPARγ is a ligand-activated transcription factor that plays an important and central role in adipose cell differentiation [117] and in the control of macrophage function, immunity, and cell proliferation [118]. Studies show that PPARγ is not only necessary, but also sufficient for fat cell differentiation [119]. The adipogenic transcription factor CAAT/ enhancer-binding protein β (C/EBPβ) also plays an important role in the process of fatty infiltration. It is induced during early adipocyte differentiation and can transactivate adipocyte genes. Furthermore, like PPARγ, it is able to inhibit MYf5, a myogenic transcription factor [117]. A neurogenic cause for fatty infiltration is also discussed in the literature. Vad et al. showed that 25% of the 28 patients with a complete RC tear had an abnormal electromyogram, which is suggestive for a peripheral neuropathy [120]. The tensile stress on the suprascapular nerve after an RC tear may promote atrophy and fatty degeneration due to denervation. This is supported by the fact that in tears of the supraspinatus tendon, the intact infraspinatus muscle can also show fatty degeneration [121]. Other authors suggest that the change in the muscle architecture after an RC tear may make the muscle vulnerable to fatty changes. These changes were documented in animal studies. When the muscle retracts, the muscle fibers shorten, the pennation angle increases, and as a result, interstices are formed between the muscle fibers. This enlargement of the space between the muscle fibers could be perceived as an injury with the result that fat is deposited into these interstices [115]. The force of the supraspinatus muscle is directly proportional to the degree of fatty infil-

44

tration [113]. This suggests that the loss of the contractile force is not only caused by muscle atrophy, but also by the degree of fatty infiltration. The change of the pennation angle and subsequent integration of fat into the gaps reduces the load-transfer ability since the force vector is almost perpendicular to the muscle fiber axis.

3.5.5.3 Atrophy After an RC rupture, in addition to fatty infiltration, asymmetric muscle atrophy also develops [122]. The reduction of the muscle diameter after tenotomy is established as an important factor in treatment of an RC lesion [123]. However, the slow-twitch type 1 muscle fibers are more affected than the fast-twitch fibers (type 2A), whereas the type 2B fibers atrophy the least [115, 124]. Furthermore, intramuscular fibrotic tissue also increases following tenotomy [124]. After a short time period, the muscle shortens and starts to lose the capability to develop tension [125]. Sixteen weeks after a tenotomy in sheep, the infraspinatus muscle was retracted 29  mm, corresponding to the physiological range of motion in the muscle. As a result, the muscle fibers were shortened and the pennation angle increased from 30° to 55°. The muscle diameter decreased to 57% compared to the healthy opposite side. Due to the chronic retraction, the muscle fibers were shortened up to 50% by the breakdown of serially arranged sarcomeres. While the muscle length decreases, the diameter remains unchanged because the amount of fibers remains the same. The degeneration of the muscle is in reality more a reduction of healthy functional muscle tissue rather than degeneration per se [115]. This was confirmed by another study where it was shown that the cause of atrophy in RC tears greater than 3 cm is not caused by muscle fiber death, but by a decrease in the absolute myofibril volume [114]. At the gene expression level, key regulators like muscle RING-finger protein-1 (MuRF1) and Atrogin-1, which are able to induce muscle atrophy, are upregulated shortly after tenotomy and return to normal shortly thereafter [126, 127]. On the other hand, several genes that are involved in

J. B. Carr II and S. A. Rodeo

muscle atrophy are massively upregulated in large RC tears compared to smaller tears, for instance, cathepsin B (CTSB), calpain, ubiquitin-­ conjugated enzyme-E2B (UBE2B) and ubiquitin-­ conjugated enzyme-E3A (UBE2A), and Forkhead box protein O1A (FOXO1A). These transcriptional changes likely contribute to the poorer healing rates in larger tears.

3.5.6 Exogenous Factors That Affect Rotator Cuff Healing This section investigates some of the exogenous factors that impair or improve the healing of the rotator cuff.

3.5.6.1 Nonsteroidal Anti-­ inflammatory Drugs Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed after RC repair. Although the inflammatory process contributes to healing by formation of reactive scar tissue, inflammation is a fundamental response to injury. Thus, blockade of the inflammatory process may have an adverse effect on healing. Indomethacin and celecoxib both significantly inhibited tendon-­ bone healing in a rat supraspinatus repair model [128]. There were significant differences in collagen organization and load to failure between the nonsteroidal anti-inflammatory and the control groups [128]. However, the clinical relevance of NSAIDs on tendon healing is unknown. A clinical study reported an increased risk of RC healing failure (37%) after selective COX-2 inhibitor use compared to nonselective NSAID use (7% failure rate) [129]. A recent meta-analysis revealed no clear deleterious effect on healing rates following rotator cuff repair with NSAID therapy in the postoperative period [130]. 3.5.6.2 MMP Inhibition with Doxycycline Matrix metalloproteinases (MMPs) may adversely affect development of new tissue at the healing tendon-bone junction. In one study, doxycycline, which is a broad-spectrum inhibitor of

3  Biology of Injury and Repair of Soft Tissues of the Shoulder

MMPs, was administered orally in rats after RC repair. Rats treated with doxycycline showed a reduced MMP-13 activity 8 days postoperatively, improved collagen fiber organization, and an increased load to failure after 2 weeks [131]. These data suggest the possibility of modulation of MMP activity to improve tendon healing.

3.5.6.3 Diabetes Bedi et  al. [132] found that sustained hyperglycemia impairs tendon-bone healing after RC repair in a rodent model. Diabetic animals demonstrated significantly less-organized collagen and less fibrocartilage with a decreased ultimate load to failure (Fig. 3.4) [132].

b

a

c

45

Metachromasia

80000 *

70000

*

Diabetic Control

Metachromasia (um2)

60000 50000 40000 30000 20000 10000 0

1 week

2 weeks Postoperative Duration

Fig. 3.4  Fibrocartilage formation. (a) Control enthesis (2 weeks, 40× magnification). (b) Diabetic enthesis (2 weeks, 40× magnification). (c) Quantitative histomorphometry revealed that the diabetic animals had significantly reduced fibrocartilage at the healing enthesis compared to control animals at both 1 and 2 weeks post-

operatively (17,254 ± 14,957 μm2 vs. 61,724 ± 10,493 μm2 and 25,025 ± 14,705 μm2 vs. 61,000 ± 9175 μm2 for 1 and 2 weeks, respectively) (*P 30  bpm in 70 years) population [7, 8]. As a result of a primary injury mechanism, acute posterior dislocation with fracture dislocation is a very rare condition and has been identified to affect only 2–4% of all shoulder dislocations with an annual incidence of 0.6 in 100.000 [9, 10].

17.3.3 Static PSI Constitutional static posterior subluxation of the humeral head has been observed in case series of young patients, who did not experience any history of trauma preceding the static PSI at presentation. Epidemiologic occurrence and risk factors are still poorly understood and their entities still have to be discovered [13]. In contrast to a consti-

17  Posterior Shoulder Instability

tutional pathomechanism, static PSI may also develop due to an acquired structural defect with the glenohumeral head in a permanent decentered position. Static-acquired PSI can be observed among young children (90°) warranting surgical treatment [38]. In the case of an engaging reverse Hill-Sachs defect, acute surgery in terms of defect disimpaction should be considered within 2 weeks after trauma. In subacute cases, the tendon of the subscapularis can be used to fill the defect arthroscopically in a McLaughlin technique [39]. If conservative treatment is chosen in the acute setting, immobilization in neutral rotation is recommended to prevent redislocation. Acute posterior glenoid rim fractures should be treated surgically in terms of either indirect suture anchor repair (small fragment) or direct fixation (large fragment).

17.7.2 Dynamic PSI Surgical treatment often fails to restore stability in patients with functional PSI (B1) due to pathological muscle activation patterns and lack of structural deficiencies, and sometimes results in worsening pain and limited function [40]. Targeted conservative treatment including core stabilization, coordination exercises, and strengthening is the warranted therapy in these patients. A new method of treatment is the so-­ called Shoulder Pacemaker therapy which has shown to be effective even in severe cases of functional PSI [41]. In patients with painful and functionally restricting dynamic posterior instability with structural defects (B2) surgical treatment should be considered depending on the severity of the soft tissue and bony defects. Over time, significant increase in the rate of surgical interventions was observed mostly due to the introduction of suture anchors and developments in arthroscopic capsulolabral repair techniques [42]. In patients with relevant reverse Hill-Sachs defects a soft tissue coverage or bone grafting should be considered. In a systematic review DeLong et al. were able to show that arthroscopic stabilization procedures using suture anchors result in fewer recurrences and superior patient outcomes compared to open procedures [43]. However, patients with large bony defects are likely to be at a higher risk for recurrence of instability after arthroscopic

capsulolabral repair. Although the size of this defect which is considered critical remains controversial, Nacca et al. were able to demonstrate in a cadaveric study that osseous defects >20% of the posterior glenoid width may be critical and isolated Bankart lesion repairs fail to restore stability [44]. In these cases and in cases with failed previous soft tissue stabilization, bony reconstructive procedures, including bone block augmentation with auto- or allograft are indicated [45]. It is important to know that a posterior glenoid defect can turn a non-engaging reverse Hill-­ Sachs lesion into an engaging defect. Therefore, in all cases of bone defects in structural dynamic posterior shoulder instability, the additive effect of reverse Hill-Sachs lesions and glenoid defects needs to be accounted for [46].

17.7.3 Static PSI In patients with constitutional static posterior instability (C1) nonsurgical management with physical therapy incorporating scapulothoracic stabilization and strengthening of the external rotators to re-center the humeral head can be applied to reduce symptoms mostly due to posterior labral tears with concomitant cartilage defects and degenerative chances. Surgical options include reconstruction of the posterior capsulolabral tissue with coverage of the posterior glenoidal cartilage defect, posterior open-­ wedge osteotomy, posterior bone block procedures, and arthroplasty in severe arthritic changes. Soft tissue reconstruction or bony procedures to restore the articulating surface are considered in acquired static posterior instability (C2). In cases with chronic locked posterior dislocation with severe reverse Hill-Sacs defects and or glenoid defect bone grafting is a viable joint preserving option. Arthroplasty can be performed in elderly patients with advanced osteoarthritic changes.

17.7.4 Decision-Making Algorithm The treatment decision between conservative versus operative management of patients with

17  Posterior Shoulder Instability

235

Table 17.1  Algorithm for choosing the appropriate treatment option for PSI based on the ABC classification

Posterior shoulder instability (PSI)

Static PSI (C)

Dynamic PSI (B)

Acute PSI (A)

Consitutional static PSI (C1)

Acute posterior Subluxation (A1)

Acute posterior dislocation (A2)

Functional dynamic PSI (B1)

-Conservative therapy to re-center the humeral head

-Surgical options include

-Conservative treatment, if no softtissue or bony defects -Otherwise arthroscopic labral repair (in athletes)

Arthroscopic labral/bony glenoid rim repair with disimpaction of reverse Hill-Sachs if Gamma angle >90°

Conservative treatment, including Scapulothoracic stabilization and strengthening of the external rotators; Shoulder Pacemaker

Acquired static PSI (C2)

Structural dynamic PSI (B2)

Glenoid bone loss < 20%, soft tissue pathology, cartilage defect

Arthroscopic capsulolabral repair and coverage of reverse Hill-Sachs, if Gamma angle >90°

PSI should be made on a case-by-case scenario based on the etiology and structural defects and of course while keeping in mind patient-specific factors (i.e., activity level) (Table 17.1).

17.8 Surgical Technique 17.8.1 Arthroscopic Reduction and Defect Disimpaction of an Acute Reverse Hill-Sachs Defect in a Patient with Acute Posterior Dislocation (A2) 17.8.1.1 Setup and Patient Positioning The patient is placed in a beach-chair position. Standard posterior, anterosuperior, anteroinferior, and lateral portals are used during the case. An initial diagnostic arthroscopy of the shoulder is performed with attention being paid to the posterior labrum and glenoid surface. In case of a posterior labral tear, a capsulolabral repair is performed as described in case 2. 17.8.1.2 Step-by-Step Procedure After performing the diagnostic arthroscopy attention is paid to the reverse Hill-Sachs lesion.

Posterior glenoid bone loss > 20%

capsulolabral repair, posterior open-wedge osteotomy, posterior bone block

Capsulolabral repair, posterior open-wedge osteotomy, posterior bone block, humeral head autograft or allograft

Bony augmentation with autograft and coverage of reverse Hill-Sachs, if Gamma angle >90°

The area of the injury is arthroscopically visualized via the anterolateral or anterosuperior viewing portal using a 30° arthroscope in this left shoulder. Under arthroscopic visualization a drill guide is then introduced through the anteroinferior portal and placed on the reverse Hill-Sachs defect to accurately drill the guide pin (Fig. 17.2). The drill guide is then placed on the lateral aspect of the humeral head after blunt dissection of the deltoid muscle. A k-wire is advanced into the drill guide and perforates through the impacted articular surface (Fig. 17.3). The correct position of the instruments is controlled and confirmed by a combination of intraoperative fluoroscopy and direct arthroscopic visualization. After removing the drill, a pushing rod is inserted through the drill hole towards the subchondral bone of the reverse Hill-Sachs defect. A reduction of the humeral articular surface is then achieved by soft hammer taps against the pushing rod. An arthroscopic elevator can be inserted to ensure that the fragment is not over-­ reduced (Fig. 17.4).

17.8.1.3 Postoperative Care The patients are immediately immobilized in a neutral rotation brace for 6  weeks. During this 6-week period only limited passive shoulder

P. Moroder et al.

236

Fig. 17.2  View from an anterolateral/anterosuperior portal in a left shoulder showing drill guide insertion through the anteroinferior portal and placement on the reverse Hill-Sachs defect

a

Fig. 17.3  View from an anterolateral/anterosuperior portal in a left shoulder showing the passage of the k-wire through the impacted part of the articular surface with the help of the drill guide

b

Fig. 17.4  View from an anterolateral/anterosuperior portal in a left shoulder showing (a) the use of an arthroscopic elevator to avoid over-reduction of the fragment and (b)

the final reduction of the impacted fragment with reconstruction of the articular surface

ROM and pendulum exercises without internal rotation are permitted. After 6 weeks the brace is discontinued and free active ROM is permitted.

After achieving free active ROM strengthening of the rotator cuff and especially scapulothoracic musculature can be initiated.

17  Posterior Shoulder Instability

17.8.2 Arthroscopic Capsulolabral Repair in a Patient with Structural Dynamic PSI (B2) with Posterior Labral Tear 17.8.2.1 Patient Positioning Arthroscopic posterior shoulder stabilization can be performed with patients in either beach-chair (BC) or lateral decubitus (LD) position. Recently, two systematic reviews were published identifying similar patients’ satisfaction and failure rates. Thus, current data prevent any conclusion being made regarding the superiority of one approach over another [47, 48]. The authors prefer to perform the procedure with the patient in lateral decubitus position due to better visualization of the posteroinferior glenoid as increased joint separation can be achieved by traction and axillary suspension (Fig. 17.5).

237

rectly identifying and managing all associated pathologies, remains a fundamental step in achieving the best treatment outcome and reducing complication rates. Unidirectional posterior instability involves a spectrum of both bone and/ or soft tissue pathologies such as posterior labral tears, SLAP tears, cartilage defect of the posterior glenoid, reverse Hill-Sachs defects, posterior glenoid bone loss, and/or increased glenoid retroversion [48, 49]. An anteroinferior portal as a working portal just superior to the subscapularis tendon and an anterosuperior portal just anterior to the long head of the biceps tendon as a viewing portal is established using a spinal needle. Furthermore, a 7 o’clock posterolateral accessory portal is needed in most of the cases to assist in a better suture anchor placement in the posteroinferior glenoid (Fig. 17.6).

17.8.2.2 Portals and Diagnostic Arthroscopy A standard posterior portal is established to perform a comprehensive diagnostic arthroscopy in order to identify intra-articular pathologies including bony or soft tissue defects. Both, cor-

Fig. 17.5  Lateral decubitus (LD) positioning to perform arthroscopic shoulder stabilization. Using axillary suspension (a) and traction (b) may lead to better visualization of the posteroinferior glenoid rim during the procedure

Fig. 17.6  Lateral decubitus (LD) positioning and portals used for posterior stabilization (a: Anteroinferior portal; b: anterosuperior portal; c: posterolateral accessory portal; d: standard posterior portal

238

17.8.2.3 Step-by-Step Procedure After performing the diagnostic arthroscopy attention is paid to preparation of the torn labrum and affected posterior glenoid rim. The area of the injury is arthroscopically visualized via the anterosuperior viewing portal using a 30° arthroscope in this right shoulder. After evaluation of the labrum and cartilage defect with a hook, debridement and preparation with the shaver is performed. Degenerative labral tissue and loose bodies are debrided to get healthy labral tissue to enhance healing after repair (Fig. 17.7). It is also important to use traction in order to reach the posteroinferior part of the glenoid rim (Fig. 17.8). A shaver or curette is used to debride the cartilage defect and prepare a bleeding bony surface for the healing of the repaired labrum (Fig. 17.9). An all-suture anchor is placed via the posterolateral accessory portal and a suture passing device is used to pass the sutures through the labrum (Fig.  17.10). Then, both ends of the sutures are knotted and the labrum is fixed on the glenoid rim. The number of anchors used (usually 2–4) depends on the size of the labral pathology. Finally, a mattress stitch-type knotted labral repair construct is established after cutting the sutures using an arthroscopic suture cutter (Fig. 17.11).

Fig. 17.7  View from the anterosuperior portal in a right shoulder showing the posterior chondral defect and labral detachment from the glenoid rim. A shaver is used for debridement

P. Moroder et al.

Fig. 17.8  View from the anterosuperior portal in a right shoulder. Access to the inferior part of the joint can be improved via lateral traction of the arm

17.8.2.4 Tips and Tricks The accessory posterolateral portal gives easy access to the posteroinferior glenoid rim for excellent anchor placement and also for suture passing devices. Avoid axillary nerve damage by avoiding incision of the capsule with a scalpel. Use blunt dissection with scissors after skin incision. The most inferior aspect of the posterior glenoid rim should be addressed first due to volume reduction after each capsulolabral repair stitch, which makes further stitches more difficult. A proper debridement and preparation of the bleeding bony glenoid and torn labrum using shaver and rasp is the key to improve the healing rate and consequently postoperative outcome. Three anchors are usually sufficient for labral pathology but the amount of anchors used mainly depends on the size of the labral pathology. 17.8.2.5 Postoperative Care All patients are immobilized in a brace in neutral rotation for 6 weeks postoperatively (Fig. 17.12). During this 6-week period only limited passive shoulder ROM and pendulum exercises without internal rotation are permitted. After 6 weeks the brace is discontinued and free active ROM is permitted. After achieving free active ROM strength-

17  Posterior Shoulder Instability

a

239

b

Fig. 17.9  View from the anterosuperior portal in a right shoulder showing the use of (a) a curette and (b) a shaver to debride the cartilage defect and create a bleeding bone surface to improve healing of the labrum

a

b

Fig. 17.10  View from the anterosuperior portal in a right shoulder showing the posteroinferior placement of (a) an all-suture anchor via a posterolateral portal and (b) the use

of a suture passing device to pass the sutures through the labrum

ening of the rotator cuff and especially scapulothoracic musculature may be initiated. In our own experience, we use the Shoulder Pacemaker concept to strengthen external rotators and scapula retractors which has proven to be crucial to regain stability. A return to sport depends on the patients’ functional status and is typically permitted 6 months after surgery.

17.8.3 Arthroscopic Coverage of a Reverse Hill-Sachs Defect with Modified Arthroscopic McLaughlin Type Procedure 17.8.3.1 Patient Positioning The authors prefer to perform the procedure with the patient in lateral decubitus position due to

240

better visualization of the posteroinferior glenoid to perform a concomitant posterior capsulolabral repair as outlined in Case 2.

17.8.3.2 Portals and Diagnostic Arthroscopy A standard posterior portal is established to perform a comprehensive diagnostic arthroscopy in

Fig. 17.11  View from the anterosuperior portal in a right shoulder showing the reinsertion of the posterior labrum via mattress stitches

Fig. 17.12  Postoperative placement of the arm in a neutral rotation brace

P. Moroder et al.

order to identify intra-articular pathologies including bony or soft tissue defects. A standardized anteroinferior portal as a working portal and an anterosuperior viewing portal is used in this case. An initial diagnostic arthroscopy of the shoulder is performed with attention being paid to the posterior labrum and glenoid surface. In the case of a posterior labral tear, a capsulolabral repair is performed as described in case 2.

17.8.3.3 Step-by-Step Procedure The reverse Hill-Sachs defect is visualized and debrided with a shaver. Two suture anchors are then inserted into the defect (Fig. 17.13). A suture retriever is then used to pass the sutures through the subscapularis tendon in a mattress configuration (Fig.  17.14). Attention must be paid not to pass the sutures too medially as this tightens the subscapularis. The sutures are then tied and the subscapularis tendon is inserted into the reverse Hill-Sachs defect (Fig. 17.15). It is important to tie the subscapularis sutures after completing the posterior labral repair not to overtighten the joint, which can make the labral repair difficult. Very large reverse Hill-Sachs defects should not be treated with this procedure as too much of the articular

Fig. 17.13  View from an anterosuperior/suprabicipital portal in a left shoulder showing two suture anchors inserted into the reverse Hill-Sachs defect

17  Posterior Shoulder Instability

241

17.8.3.4 Postoperative Care All patients with a concomitant repair of the posterior labrum are immobilized in a brace in neutral rotation for 6 weeks postoperatively. During this 6-week period only limited passive shoulder ROM and pendulum exercises are permitted. Patients should avoid internal rotation during this period. After 6  weeks the brace is discontinued and free active ROM is permitted. After achieving free active ROM strengthening of the rotator cuff and especially scapulothoracic musculature may be initiated.

References Fig. 17.14  View from an anterosuperior/suprabicipital portal in a left shoulder showing suture shuttling through the subscapularis tendon using a suture passing device

Fig. 17.15  View from an anterosuperior/suprabicipital portal in a left shoulder showing coverage of the reverse Hill-Sachs defect with the subscapularis tendon in terms of a modified McLaughlin procedure

surface will be covered by the subscapularis tendon and patients tend to become stiff. Instead, a transposition of the lesser tuberosity (Neer procedure) or filling of the defect with a bone graft should be performed.

1. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB.  The incidence and characteristics of shoulder instability at the United States military academy. Am J Sports Med. 2007;35(7):1168–73. 2. Song DJ, Cook JB, Krul KP, Bottoni CR, Rowles DJ, Shaha SH, et al. High frequency of posterior and combined shoulder instability in young active patients. J Shoulder Elb Surg. 2015;24(2):186–90. 3. Antosh IJ, Tokish JM, Owens BD. Posterior shoulder instability. Sports Health. 2016;8(6):520–6. 4. Hawkins RJ, Koppert G, Johnston G. Recurrent posterior instability (subluxation) of the shoulder. J Bone Joint Surg Am. 1984;66(2):169–74. 5. Provencher MT, LeClere LE, King S, McDonald LS, Frank RM, Mologne TS, et al. Posterior instability of the shoulder: diagnosis and management. Am J Sports Med. 2011;39(4):874–86. 6. Moroder P, Scheibel M.  ABC classification of posterior shoulder instability. Obere Extrem. 2017;12(2):66–74. 7. Robinson CM, Seah M, Akhtar MA. The epidemiology, risk of recurrence, and functional outcome after an acute traumatic posterior dislocation of the shoulder. J Bone Joint Surg Am. 2011;93(17):1605–13. 8. Zacchilli MA, Owens BD.  Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg Am. 2010;92(3):542–9. 9. Robinson CM, Akhtar A, Mitchell M, Beavis C.  Complex posterior fracture-dislocation of the shoulder. Epidemiology, injury patterns, and results of operative treatment. J Bone Joint Surg Am. 2007;89(7):1454–66. 10. Bock P, Kluger R, Hintermann B. Anatomical reconstruction for reverse hill-Sachs lesions after posterior locked shoulder dislocation fracture: a case

242 series of six patients. Arch Orthop Trauma Surg. 2007;127(7):543–8. 11. Danzinger V, Schulz E, Moroder P.  Epidemiology of functional shoulder instability: an online survey. BMC Musculoskelet Disord. 2019;20(1):281. 12. Malone A, Jaggi A, Calvert P, Lambert S, Bayley I.  The prevalence of inappropriate muscle sequencing in recurrent shoulder instability. Orthopaed Proc 2005;87-B(SUPP_II):163. 13. Walch G, Ascani C, Boulahia A, Nove-Josserand L, Edwards TB.  Static posterior subluxation of the humeral head: an unrecognized entity responsible for glenohumeral osteoarthritis in the young adult. J Shoulder Elb Surg. 2002;11(4):309–14. 14. Dahlin LB, Erichs K, Andersson C, Thornqvist C, Backman C, Duppe H, et al. Incidence of early posterior shoulder dislocation in brachial plexus birth palsy. J Brachial Plex Peripher Nerve Inj. 2007;2:24. 15. Buhler M, Gerber C.  Shoulder instability related to epileptic seizures. J Shoulder Elb Surg. 2002;11(4):339–44. 16. Ketenci IE, Duymus TM, Ulusoy A, Yanik HS, Mutlu S, Durakbasa MO. Bilateral posterior shoulder dislocation after electrical shock: a case report. Ann Med Surg (Lond). 2015;4(4):417–21. 17. Schliemann B, Muder D, Gessmann J, Schildhauer TA, Seybold D.  Locked posterior shoulder dislocation: treatment options and clinical outcomes. Arch Orthop Trauma Surg. 2011;131(8):1127–34. 18. Diklic ID, Ganic ZD, Blagojevic ZD, Nho SJ, Romeo AA. Treatment of locked chronic posterior dislocation of the shoulder by reconstruction of the defect in the humeral head with an allograft. J Bone Joint Surg Br. 2010;92(1):71–6. 19. Moroder P, Danzinger V, Maziak N, Plachel F, Pauly S, Scheibel M, et al. Characteristics of functional shoulder instability. J Shoulder Elbow Surg. 2019; 29(1):68–78. 20. Akgün D, Siegert P, Danzinger V, Plachel F, Minkus M, Thiele K, Moroder P. Glenoid vault and humeral head alignment in relation to the scapular blade axis in young patients with pre-osteoarthritic static posterior subluxation of the humeral head. J Shoulder Elb Surg. 2021;30(4):756–62. https://doi.org/10.1016/j. jse.2020.08.004. PMID: 32853792. 21. Gurzi MD, De Meo D, Pugliese M, Di Giorgio L, Persiani P, Villani C.  Bilateral posterior fracture-­ dislocation of the shoulder after epileptic seizure. Trauma Case Rep. 2018;13:35–41. 22. Moukoko D, Ezaki M, Wilkes D, Carter P. Posterior shoulder dislocation in infants with neonatal brachial plexus palsy. J Bone Joint Surg Am. 2004;86(4):787–93. 23. Plachel F, Akgün D, Imiolczyk J-P, Minkus M, Moroder P.  Patient-specific risk profile associated with early-onset primary osteoarthritis of the shoulder: is it really primary? Arch Orthop Trauma Surg. 2023;143(2):699–706. https://doi.org/10.1007/ s00402-021-04125-2. PMID: 34406506. PMCID: PMC9925503.

P. Moroder et al. 24. Jaggi A, Noorani A, Malone A, Cowan J, Lambert S, Bayley I. Muscle activation patterns in patients with recurrent shoulder instability. Int J Shoulder Surg. 2012;6(4):101–7. 25. Kibler WB.  The role of the scapula in athletic shoulder function. Am J Sports Med. 1998;26(2): 325–37. 26. Cameron KL, Duffey ML, DeBerardino TM, Stoneman PD, Jones CJ, Owens BD.  Association of generalized joint hypermobility with a history of glenohumeral joint instability. J Athl Train. 2010;45(3):253–8. 27. Saccomanno MF, Fodale M, Capasso L, Cazzato G, Milano G.  Generalized joint laxity and multidirectional instability of the shoulder. Joints. 2013;1(4):171–9. 28. Baum J, Larsson LG.  Hypermobility syndrome--new diagnostic criteria. J Rheumatol 2000;27(7):1585–1586. 29. Jia X, Ji JH, Petersen SA, Freehill MT, McFarland EG. An analysis of shoulder laxity in patients undergoing shoulder surgery. J Bone Joint Surg Am. 2009;91(9):2144–50. 30. Coudane H, Walch G, Sebesta A. [Chronic anterior instability of the shoulder in adults. Methodology]. Rev Chir Orthop Reparatrice Appar Mot. 2000;86 Suppl 1:94–5. 31. Gagey OJ, Gagey N. The hyperabduction test. J Bone Joint Surg Br. 2001;83(1):69–74. 32. Hawkins R, Bokor DJ.  In: Rockwood CA, Matsen FA, editors. Clinical evaluation of shoulder problems. Philadelphia: Saunders; 1990. 33. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder--a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188–92. 34. Owen JM, Boulter T, Walton M, Funk L, Mackenzie TA.  Reinterpretation of O’Brien test in posterior labral tears of the shoulder. Int J Shoulder Surg. 2015;9(1):6–8. 35. Weishaupt D, Zanetti M, Nyffeler RW, Gerber C, Hodler J.  Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skelet Radiol. 2000;29(4):204–10. 36. Edwards BT, Lassiter TE Jr, Easterbrook J.  Immobilization of anterior and posterior glenohumeral dislocation. J Bone Joint Surg Am. 2002;84(5):873–4. author reply 4 37. Jaggi A, Alexander S.  Rehabilitation for shoulder instability  - current approaches. Open Orthop J. 2017;11:957–71. 38. Moroder P, Runer A, Kraemer M, Fierlbeck J, Niederberger A, Cotofana S, et  al. Influence of defect size and localization on the engagement of reverse Hill-Sachs lesions. Am J Sports Med. 2015;43(3):542–8. 39. Kelly BJ, Field LD. Arthroscopic transfer of the subscapularis tendon for treatment of a reverse hill-Sachs lesion. Arthrosc Tech. 2017;6(5):e2061–e4.

17  Posterior Shoulder Instability 40. Kuroda S, Sumiyoshi T, Moriishi J, Maruta K, Ishige N. The natural course of atraumatic shoulder instability. J Shoulder Elb Surg. 2001;10(2):100–4. 41. Moroder P, Plachel F, Van-Vliet H, Adamczewski C, Danzinger V. Shoulder-pacemaker treatment concept for posterior positional functional shoulder instability: a prospective clinical trial. Am J Sports Med. 2020;48(9):2097–104. 42. Woodmass JM, Lee J, Wu IT, Desai VS, Camp CL, Dahm DL, et  al. Incidence of posterior shoulder instability and trends in surgical reconstruction: a 22-year population-based study. J Shoulder Elb Surg. 2019;28(4):611–6. 43. DeLong JM, Jiang K, Bradley JP. Posterior instability of the shoulder: a systematic review and meta-­ analysis of clinical outcomes. Am J Sports Med. 2015;43(7):1805–17. 44. Nacca C, Gil JA, Badida R, Crisco JJ, Owens BD. Critical glenoid bone loss in posterior shoulder instability. Am J Sports Med. 2018;46(5):1058–63. 45. Lacheta L, Singh TSP, Hovsepian JM, Braun S, Imhoff AB, Pogorzelski J. Posterior open wedge glenoid osteotomy provides reliable results in young patients with

243 increased glenoid retroversion and posterior shoulder instability. Knee Surg Sports Traumatol Arthrosc. 2019;27(1):299–304. 46. Moroder P, Plachel F, Tauber M, Habermeyer P, Imhoff A, Liem D, et al. Risk of engagement of bipolar bone defects in posterior shoulder instability. Am J Sports Med. 2017;45(12):2835–9. 47. Moeller EA, Houck DA, McCarty EC, Seidl AJ, Bravman JT, Vidal AF, et al. Outcomes of arthroscopic posterior shoulder stabilization in the beach-chair versus lateral decubitus position: a systematic review. Orthop J Sports Med. 2019;7(1):2325967118822452. 48. de Sa D, Sheean AJ, Morales-Restrepo A, Dombrowski M, Kay J, Vyas D.  Patient positioning in arthroscopic management of posterior-inferior shoulder Instability: a systematic review comparing beach chair and lateral decubitus approaches. Arthroscopy. 2019;35(1):214–24 e3. 49. Galvin JW, Parada SA, Li X, Eichinger JK. Critical findings on magnetic resonance arthrograms in posterior shoulder instability compared with an age-matched controlled cohort. Am J Sports Med. 2016;44(12):3222–9.

Multidirectional Instability of the Shoulder

18

Christopher L. Antonacci, Brandon J. Erickson, and Anthony A. Romeo

Abstract

Shoulder instability is one of the most common pathologies treated by orthopedic sports medicine and shoulder surgeons. While the primary direction of instability is anteroinferior, there are patients who suffer from posterior instability as well as multidirectional instability (MDI). MDI indicates the patient has shoulder instability in two or more directions (anterior, inferior, posterior), and occurs when the static and dynamic restraints of the shoulder are not providing adequate stability. MDI is often seen in young adults and can present with shoulder instability, but more commonly presents as shoulder pain. The mainstay of treatment for MDI is nonoperative management with physical therapy aimed at scapular stabilization as well as rotator cuff and deltoid strengthening. Patients who have failed at least 6–12  months of conservative treatment can be considered for operative intervention such as arthroscopic capsular plication, rotator interval closure, or labral augmentation. However, every effort should be made to avoid surgical treatment of these C. L. Antonacci · B. J. Erickson (*) Rothman Orthopaedic Institute, New York, NY, USA e-mail: [email protected] A. A. Romeo Duly Health and Care, Elmhurst, IL, USA Duly Health and Care, Elmhurst, IL, USA

patients when possible as the outcomes following surgery are variable. Keywords

Shoulder · Instability · Multidirectional · Laxity · Arthroscopic treatment

18.1 Epidemiology Multidirectional instability (MDI) represents a wide spectrum of disease but is defined as symptomatic, involuntary, and uncontrollable subluxation or dislocation of the glenohumeral joint in two or more directions (anterior, inferior, and/or posterior). Patients have difficulty maintaining the head of the humerus centered within the glenoid fossa as the static, and occasionally dynamic, stabilizers of the glenohumeral joint are not functioning properly [1]. When discussing multidirectional instability, it is imperative to differentiate instability (where the patient is symptomatic) from laxity, in which no symptoms are present. Due to its inconsistent definition in the literature, it is difficult to reliably determine the actual incidence of MDI. MDI certainly represents a less common clinical entity than anterior traumatic instability, representing 7–10% of all instability cases [2, 3]. Among sedentary individuals, the condition is more common in young women with poor

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_18

245

246

muscular development and patients with large rotator cuff tendon tears. Among athletes or active individuals, MDI can develop in individuals who participate in activities involving repetitive overhead movements, such as gymnasts, tennis players, and throwers [4, 5]. MDI is also seen in patients with generalized ligamentous laxity secondary to connective tissue disorders such as Marfan and Ehlers-Danlos syndromes.

18.2 Pathophysiology MDI occurs when the static and dynamic restraints of the glenohumeral joint are not providing adequate stability. This lack of stability can stem from a variety of causes. However, the essential lesion in MDI is an enlarged, lax glenohumeral joint capsule [6]. This “patulous” capsule fails to provide adequate stabilization to the glenohumeral joint [7, 8]. The glenohumeral ligaments, specifically the anterior and posterior bands of the inferior glenohumeral ligament, often become incompetent and no longer provide adequate stability when the shoulder reaches 90° of abduction. If the middle and superior glenohumeral ligaments are incompetent, the shoulder will become unstable in lesser degrees of abduction. A litany of other pathologic lesions may be found in conjunction with a patulous capsule that contributes to the instability. Both anterior and posterior labral lesions are commonly identified from repeat subluxations/dislocations [7–9]. The biceps tendon, which is thought to provide dynamic stability to the glenohumeral joint, has been found to be more anterior compared with normal controls [10]. Some patients demonstrate Hill-Sachs lesions from prior instability events or articular-sided partial-thickness rotator cuff tears from internal impingement where the humeral head rides slightly superior and catches the articular side of the rotator cuff between the glenoid and humeral head. Some authors suggest the rotator interval is widened in MDI, although this finding remains controversial. The etiology of multidirectional instability is likely due to a combination of factors including anatomic, biologic, and neuromuscular patholo-

C. L. Antonacci et al.

gies. Repetitive episodes of microtrauma to the capsule and other stabilizers, secondary to subacromial bursitis or rotator cuff impingement, for example, may be a significant contributor to the progression of this clinical entity [11–13]. Clinical as well as histopathologic data have suggested that patients with MDI may have an underlying connective tissue disorder that predisposes them towards instability [10]. Biologically, patients with MDI demonstrate an increase in collagen cross-linking, collagen fiber diameter, cysteine content, as well as elastin content when compared to normal shoulders. These likely represent adaptive changes [6, 14]. Although patients often have bilateral laxity, most are only symptomatic on one side. This suggests that factors beyond biology play a role in the development of instability. Anatomically, static stabilizers of the joint include the glenoid concavity, the labrum, and the glenohumeral ligaments. The glenoid/labrum complex is relatively shallow and provides little inherent stability. Nonetheless, some studies have demonstrated that patients with MDI demonstrate shallower glenoid cavities relative to normal controls [14]. The glenohumeral ligaments provide the stability in varying degrees of humeral abduction with the superior glenohumeral ligament providing maximal stability in 0° of abduction and the inferior glenohumeral ligament providing maximal stability in 90° of abduction. These ligaments are an extremely important part of glenohumeral stability. Furthermore, the dynamic stabilizers of the shoulder, which include the rotator cuff, biceps, deltoid, and scapula rotators, are also critical for stability, specifically midrange stability. The dynamic stabilizers compress the humeral head against the glenoid and increase the contact pressure of the glenohumeral joint to provide concavity compression [15]. Impaired coordination of the dynamic stabilizers of the shoulder girdle has been suggested as a possible contributor to MDI.  Electromyography performed in patients with MDI demonstrated altered activation of the anterior and posterior deltoid muscles compared to normal subjects [16, 17]. Scapulothoracic

18  Multidirectional Instability of the Shoulder

dysfunction is also considered a contributor to MDI.  Failure of the scapula to rotate through shoulder range of motion (ROM) may force abnormal translation of the humeral head and contribute to the progression of instability [18]. Diminished proprioception has been suggested as a contributor to MDI. Barden et al. showed that patients with MDI demonstrated significantly higher error rates with hand positioning in space compared with normal controls. They suggest that the failure of proprioceptive feedback may play a role in humeral head instability [19].

18.3 Clinical Diagnosis 18.3.1 History MDI can be challenging to diagnose as it represents a wide spectrum of pathology, and the reported symptoms may be nonspecific unless the condition is preceded by specific trauma or complicated by subacromial impingement or rotator cuff pathology [12]. MDI is often found in young adults who present with primary complaints of pain, rather than frank instability [19]. Nonetheless, over 25% of patients with MDI present with radiographic evidence of previous dislocation (Hill-Sachs lesion, anterior or posterior labral tear, etc.). Patients often complain of constant diffuse background pain that is exacerbated with lifting or sleeping. Many complain of “loose” shoulders that may have associated popping, clicking, or snapping. Athletes may complain of decreased strength or performance. The threshold for inducing symptoms may be lower than that associated with traumatic dislocations. Consequently, MDI patients may be more limited in their daily activities. Many patients report transient neurological complaints such as numbness or tingling. Patients with a history of repetitive overhead activity may be predisposed to MDI through microtrauma. Symptoms of shoulder instability often occur with glenohumeral motion, eventually leading patients to avoid the extremes of glenohumeral motion [12]. If frank instability is suggested by history, it is important to delineate the frequency and mechanisms by which instability occurs.

247

Arm position at the time of dislocation may suggest the direction of instability. Many patients with MDI cite a history of low-demand activities inciting dislocations, which require minimal effort to reduce. Some authors have suggested that patients who dislocate during sleep represent a subset of difficult-to-treat “decompensated shoulders” [12]. A detailed history may suggest the direction of instability. Pain and numbness while carrying heavy objects suggest inferior instability. Discomfort with pushing (e.g., bench press, pushups, pushing a door open, etc.) may indicate posterior pathology. Pain with the arm in abduction and external rotation, such as a throwing motion, implies anterior pathology [13]. This information is critical in guiding therapy or, in some cases, operative intervention. Patients should be questioned about previous joint sprains or patellar instability. As noted above, patients with MDI have been noted to demonstrate connective tissue disorders, and workup for these diseases may be warranted. Furthermore, if a connective tissue disorder is suspected, a referral to the appropriate medical specialist is essential to monitor for other sequelae of these disorders (cardiac abnormalities, ophthalmologic issues, etc.). All patients with a history of voluntary dislocation should be evaluated closely for underlying psychiatric disorders. Patients with ongoing mental health issues respond poorly to operative and nonoperative management until those pathologies have been resolved. A subset of voluntary dislocators without underlying emotional problems however may respond to operative treatment; patients who demonstrate positions that reproduce instability but who subsequently avoid these positions generally respond well to surgical intervention and should not be included in the subset of patients who demonstrate willful dislocation [1]. It is critical to elicit previous treatment history including injections, physical therapy, or operative intervention. Patients should be questioned about the quality and length of their physical therapy treatment as this is often the mainstay of treatment for MDI, and patients will often state they have tried physical therapy, but upon further

248

questioning the patients disclose they only went to two or three therapy visits. This does not constitute prior therapy treatment. MDI is often misdiagnosed as unilateral instability, impingement, brachial plexitis, cervical neck pathology, or thoracic outlet syndrome. A history of failed previous treatments may suggest MDI.

18.3.2 Clinical Examination A careful clinical examination is essential in differentiating MDI from other causes of shoulder pain. Furthermore, identification of incompetent structures on exam will elucidate appropriate, directed treatment. It is important to first visually inspect the shoulders, neck, and torso to identify important findings such as muscle asymmetry or atrophy, scapular winging, or surgical scars. Visual inspection of the shoulder may reveal a protracted scapula or muscle atrophy. The lateral acromion may appear squared secondary to inferior humeral head subluxation. After visual inspection, the patient can be asked to demonstrate voluntary instability if they have previously described this ability. They may be able to voluntarily dislocate or subluxate their shoulder; findings such as this would demonstrate increased laxity of the glenohumeral joint [20, 21]. The patient should then be assessed for hyperlaxity, including patellar laxity, elbow hyperextension, thumb-for-forearm test, or genu recurvatum [20, 21]. Clinical suspicion for a connective tissue disorder such as Marfan syndrome, Ehlers-Danlos syndrome, or benign joint hypermobility syndrome merits further workup with the Beighton scoring system as surgical outcomes are very poor in this patient population [22, 23]. Active ROM may reveal scapular dyskinesia. Often patients with MDI will have altered scapular mechanics including medial scapular winging, inferior tip rotation, and poor scapular protraction against the chest wall [24]. The pectoralis minor muscle may become contracted secondary to prolonged scapular malposition, and the patient may exhibit point tenderness over the coracoid. MDI patients may exhibit pain with manual strength

C. L. Antonacci et al.

testing as they can develop rotator cuff tendonitis and/or subacromial impingement. The key diagnostic finding for MDI is the reproduction of symptoms with provocative maneuvers. The load-and-shift test assesses the degree of humeral instability. With the patient supine, the clinician stabilizes the elbow while attempting to translate the humeral head anteriorly or posteriorly. Subluxation of the head over the glenoid rim is abnormal, and the magnitude and direction of instability were assessed. While patients may have multi-planar laxity, they may be primarily symptomatic in just one direction. Patients with painful posterior jerk test have a higher rate of failure with nonoperative management [25]. Internal rotation strength may be decreased by up to 30% in patients with MDI [25]. An abnormal sulcus sign, in which there is increased translation with inferior traction on the adducted arm suggests laxity (Fig. 18.1). A complementary test to the sulcus sign is to see if the inferior translation reduces as the shoulder is externally rotated. With a competent rotator interval, the sulcus should decrease as the arm is externally rotated. Failure of the sulcus to decrease suggests significant laxity. Traction may occasionally provoke neurologic symptoms. An isolated sulcus sign in the absence of symptoms does not suggest MDI. The Gagey test evaluates the competency of the inferior capsule. The test is considered positive when the shoulder can be passively abducted more than 105° with concomitant stabilization of the scapula. In addition to the standard bilateral shoulder strength, ROM,

Fig. 18.1  Sulcus sign with arm in 30 degrees of external rotation indicating rotator interval laxity

18  Multidirectional Instability of the Shoulder

and instability tests, the exam must include a thorough cervical and neurologic exam.

18.4 Imaging Although patients with MDI may have normal radiographs, a complete instability series of X-rays should always be obtained at the initial visit. This series consists of anteroposterior, axillary, scapular Y, West Point axillary (to evaluate for anterior glenoid bony defects), and Stryker notch (to evaluate for a Hill-Sachs defect) views. These views allow for the evaluation of humeral head displacement on the glenoid, Hill-Sachs lesions, bony Bankart pathology, fractures of the lesser and greater tuberosities, glenoid hypoplasia, or rim defects and fractures. In addition, the AP radiograph can reveal inferior subluxation of the humerus on the glenoid. In patients with suspected glenoid hypoplasia, bone loss, and retroversion, a CT scan with 3  mm cuts with and without humeral head subtraction should be ordered. In addition to radiographs for patients with suspected MDI, the authors’ preferred choice of advanced imaging is magnetic resonance imaging (MRI) or MR arthrogram to further delineate soft tissue pathology involving the rotator interval, biceps, capsulolabral structures, and the rotator cuff (Fig.  18.2). Some authors

Fig. 18.2 Axial cut of MDI patient demonstrating anterior labral pathology and patulous pouch

249

have suggested a widened rotator interval is present in most cases of MDI.  While Warner et  al. demonstrated that MRI arthrography comparing normal and instability patients failed to demonstrate a difference, recent studies suggest that the inferior labro-capsular distance on MRI arthrography can be used as an effective screening method for atraumatic MDI of the shoulder [24, 26, 27].

18.5 Treatment Nonoperative management is the mainstay of treatment for patients with MDI. A comprehensive physical therapy program directed at scapular stabilization, rotator cuff, and deltoid strengthening exercises is often effective in treating patients with MDI [28]. While there is a lack of direct, comparative evidence to determine the relative benefits of physical therapy-based management compared to surgery, most patients with true MDI will have decreased pain and improved stability with a rigorous strengthening and rehabilitation program designed to strengthen the stabilizing muscles of the shoulder and improve neuromuscular coordination of glenohumeral and scapulothoracic movement [29, 30]. Patients with MDI perform at least 6–12 months of supervised therapy before any surgical intervention is considered. One randomized controlled study recently compared two different therapy programs for patients with MDI and found the Watson program was more effective than the Rockwood program at 12 and 24  weeks [31]. However, patients in both programs saw improvements in pain and clinical outcome scores. It is crucial to evaluate progress with a focused scapular retraining program prior to embarking on any surgical intervention. Young, athletic patients with instability or generalized ligamentous laxity due to a traumatic event however are less likely to respond to therapy compared to patients whose pathology stems from repetitive microtrauma or atraumatic ligamentous laxity [10]. Although patients with a traumatic etiology to shoulder instability are likely to have concomitant glenohumeral pathol-

250

ogy, such as a Bankart lesion, this does not preclude a trial of conservative treatment. Increased awareness and understanding of clinical symptoms and exam findings in patients with voluntary versus involuntary MDI have led to more appropriate patient selection criteria for surgical stabilization. In particular, patients with a history of voluntary shoulder dislocation and psychiatric issues should not be treated surgically in lieu of higher failure rates [6].

18.5.1 Decision-Making Algorithm Surgical options include open and arthroscopic capsular plication, rotator interval closure, and labral augmentation [32–36]. Improvements in arthroscopic techniques have led to a shift from open to arthroscopic stabilization, which allows for an outpatient procedure with potentially decreased risk of complications such as subscapularis rupture or postoperative subscapularis insufficiency. With improvements in current implants and arthroscopic techniques, a successful stabilization procedure for patients with MDI can be attained, as patients treated in this manner have been shown to have a high rate of return to sport or activity [32, 37]. The actual repair technique and implants used will be dictated by findings from clinical exam and diagnostic arthroscopy. Treatment of lesions that do not correspond to any physical exam findings may result in overtightened shoulders. Failure to recognize all directions of instability on clinical exam may lead to persistent symptoms postoperatively. The decision to perform a rotator interval closure is controversial. Provencher et  al. suggest in a recent editorial commentary that while interval closure continues to be a challenge, clinical indications for rotator interval closure include: multidirectional instability with increased capsular volume; anterior instability, and especially a failed arthroscopic instability repair, that could benefit from imbrication of the coracohumeral ligament; a sulcus that persists in external rotation in the setting of symptomatic instability; and posterior instability with a multidirectional component [38].

C. L. Antonacci et al.

Successful clinical outcomes can be achieved with and without rotator interval closure [7–9]. Patients who demonstrate a sulcus sign with the arm in external rotation should be considered for rotator interval closure.

18.5.2 Clinical Case/Example C.V., an 18-year-old right-hand-dominant female, had a 5-year history of bilateral shoulder instability. The initial dislocations were atraumatic but painful in nature. The patient has described multiple instability episodes without the need for closed reduction in the emergency room. On exam, the patient has a positive sulcus sign and exhibits a positive apprehension sign when the right arm is positioned in abduction and external rotation. Her shoulder could be moved through a full ROM with no neurovascular deficits. The patient did have evidence of hypermobility bilaterally with hyperextension of the elbows and metacarpophalangeal joints of the fingers (Fig. 18.3). Radiographic examination revealed a small Hill-Sachs lesion on both the Stryker notch and AP views of the glenohumeral joint. The axillary view demonstrated minimal anterior glenoid bone loss. MRI revealed anterior and posterior labral lesions. After evaluation in clinic, the patient was placed in a therapy program with focus on scapular, cuff, and deltoid strengthening. After 12  months of conservative treatment,

Fig. 18.3  Clinical evidence of hypermobility including elbow hyperextension

18  Multidirectional Instability of the Shoulder

the patient continued to complain of shoulder instability and noted that these symptoms occurred with greater frequency. Given the history of recurrent instability, physical exam findings consistent with MDI, and failure of conservative treatment, the patient opted to proceed with arthroscopic stabilization.

18.6 Surgical Technique 18.6.1 Exam Under Anesthesia We prefer interscalene block for patients undergoing surgical treatment for MDI as it enhances postoperative pain control. Careful examination of the patient under anesthesia prior to surgical skin preparation will confirm the diagnosis as well as guide treatment. A load-andshift test as well as sulcus sign should be performed. The magnitude of instability should be evaluated with the patient’s preoperative symptomatology kept in mind. A patient with preoperative symptoms and a sulcus sign that remains 2+ or greater in external rotation is pathognomonic for MDI. Both the beach chair and lateral positions can be used for the arthroscopic treatment of MDI. However, the lateral decubitus position has been shown to offer improved visualization of the posterior and inferior aspects of the shoulder where the significant pathologic lesions may be located and therefore is the authors’ preferred position [39].

18.6.2 Patient Positioning The lateral decubitus position is maintained with a bean bag and careful padding of the peroneal and axillary nerves. The arm is placed in 5–10 lb. of longitudinal traction with a traction sleeve at 15° of forward flexion and 65° of abduction. This position maximizes access to the posterior and inferior shoulder joint. We prefer to rotate the bed approximately 180° to provide unobstructed access to the anterior and posterior portals. A bump may be used in the axilla to create more

251

space in the posterior-inferior region. It may be helpful to place the arm in 90° of external rotation to prevent overtightening of the anterior shoulder structures.

18.6.3 Portals Portal placement should be tailored to address the pathologic findings identified on physical exam and diagnostic arthroscopy. Many surgeries can be performed through four portals, although more may be required. Surgeons should not hesitate to create accessory portals when needed to ensure adequate fixation. All surgeries begin with a posterior portal placed approximately 1  cm inferior and just medial to the lateral border of the acromion. Compared to a standard posterior portal, a more lateral position for this portal permits improved access to the posterior glenoid. An anterior-superior portal is made with the aid of an 18-gauge spinal needle, placed percutaneously through the rotator interval to ensure satisfactory trajectory. An anterior portal is then made just above the subscapularis using 18-gauge spinal needle localization. A percutaneous accessory posterolateral portal at the 7 o’clock position should be made approximately 1 cm lateral and 2 cm distal to the posterior portal. Placement of this portal is critical to allow access to the posterior-­inferior glenoid [40] (Fig. 18.4). When making the accessory portals, a switching stick (Wissinger rod) is used to penetrate the capsule in the exact location where the cannula should be placed. This allows for more accurate placement of the cannulas. 8.25  mm clear cannulas are placed in through these portals to accommodate repair, instrumentation, and anchor placement. For anteroinferior pathology, a small percutaneous incision through the subscapularis may be made to allow satisfactory trajectory for the anterior anchors.

18.6.4 Diagnostic Arthroscopy Diagnostic arthroscopy should be performed to evaluate the labrum in its entirety, rotator cuff,

C. L. Antonacci et al.

252

a

Fig. 18.4  a Portal placement for multidirectional instability. Standard posterior and anterior portals are established. 5 o’clock and 7 o’clock portals used to

b

achieve a satisfactory trajectory for inferior anchors. b View from anterior portal demonstrating posteriorsuperior and posterior-­inferior portals

Fig. 18.6  Abrasion of the capsule with a rasp to stimulate the healing response Fig. 18.5  Skybox View

capsule, articular surfaces, as well as rotator interval. Often there is a “drive-through” sign and “skybox” view with posterior-inferior laxity (Fig.  18.5). Careful examination may reveal a patulous capsule, labral splitting, 360° labral pathology, under-surface partial tears of the ­rotator cuff, and widening of the rotator interval. Careful examination of the posterior structures should be performed from the anterior-superior portal. The fibers of the infraspinatus muscle may be visible through the thin posterior capsular tissue. The posterior labrum should be meticulously probed to identify any crack or tear. If such pathology is visualized, the labrum should be taken down and prepared for anchor repair. Three hundred and sixty degree labral pathology may

be identified in MDI patients. In areas where no labral pathology can be identified, the labrum can be used to anchor the capsular plication.

18.6.5 Step-by-Step Procedure (Box 18.1) After diagnostic arthroscopy, the posterior and inferior structures are addressed first. The posterior capsule should be gently abraded with a rasp to stimulate a healing response (Fig. 18.6). If disrupted, the posterior labrum should be fully elevated from the glenoid rim. Preparation of the posterior chondrolabral junction should be performed from an anterior portal, which allows the appropriate trajectory to minimize the chance of traumatic injury to the labrum or articular sur-

18  Multidirectional Instability of the Shoulder

Fig. 18.7  View from the anterior portal. Initial anchor placement in the inferior glenoid at the 6 o’clock position, through the 7 o’clock portal, approximately 2 mm central to the glenoid rim

face. A bleeding bony surface is created at the glenoid rim with an arthroscopic burr or rasp. The essential lesion to address is the patulous capsule. Optimal repair strategy includes shifting the capsular tissue from an inferior to superior position. Each plication reduces the available working area. Therefore, anchors should be sequentially placed and fixed from inferior to superior along the rim of the glenoid. Up to five anchors may be required to adequately address pathology from the 6 o’clock to approximately 10 o’clock position posteriorly. With the camera in the anterosuperior portal, the first anchor should be placed at the 6 o’clock position through the posterior-lateral 7 o’clock portal. The anchor should be placed 2 mm onto the glenoid rim to create a stable bumper (Fig.  18.7) We prefer a 3-mm double-loaded suture anchor. All sutures should be brought through the posterior-superior portal. A curved capsulolabral device should be used through the posterior-lateral portal to penetrate the capsule approximately 1 cm inferior to the labrum. The capsule should become taut when it is brought to the level of the glenoid. It is important that the entry point for the suture hook is inferior to the placement of each anchor in order to shift the tissue superiorly. The device can then be used to penetrate the labrum. A PDS suture is passed through the capsulolabral device into the joint.

253

Fig. 18.8  View from the anterior portal. The suture is shuttled through the capsule and labrum with a capsulolabral device and tied. The entry point for the capsulolabral device should be approximately 1 cm interior to the anchor on the glenoid

An arthroscopic grasper can be used to bring one limb of the suture as well as the PDS shuttle through the posterior portal. The sutures are tied outside the cannula, and the suture limb is shuttled through the capsulolabral tissue (Fig. 18.8). Both ends of the suture are brought through the posterior-lateral portal. The suture is tied with a non-sliding knot backed up with three alternating half hitches, ensuring that the post-limb remains away from the articular surface to avoid damage to the humeral chondral surface from the knot. The other suture is passed and tied in a similar fashion to provide additional plication. Subsequent anchors can be placed along the posterior glenoid up to the 9 o’clock position using the 7 o’clock and posterior portals for proper anchor trajectory (Fig.  18.9). Knotless anchors are typically used for the remainder of the posterior labral repair to minimize the risk of chondral damage from the knot stacks. For areas without frank labral tears, simple plication sutures through the capsule and labrum are passed and tied. Once the posterior and inferior structures have been repaired, the anterior capsulolabral structures should be addressed. With the arthroscope in the posterior portal, the anterior glenoid can be prepared with a burr after the labrum has been liberated from the glenoid. The anterior capsule

254

Fig. 18.9  View from the anterior portal. Multiple double-­ loaded anchors are placed approximately 8 mm apart posteriorly from the 6 o’clock to 9 o’clock position

C. L. Antonacci et al.

Fig. 18.11  View from the posterior portal demonstrating satisfactory glenoid bumper without capsular redundancy

Fig. 18.12  View from the posterior portal. PDS suture used to close the rotator interval Fig. 18.10  View from the posterior portal. In order to place an anterior inferior anchor, a small percutaneous incision through the subscapularis is made through which an anchor trocar can be passed

should be abraded with a rasp and can be safely performed from the posterior-lateral portal. An 18-gauge spinal needle is used to identify a satisfactory trajectory for a 5 o’clock anchor, which is placed through a small percutaneous incision through the subscapularis tendon (Fig. 18.10). A curved capsulolabral device is used through the posterior-lateral portal to capture approximately 1 cm of tissue inferior to this anchor. The capsule should become taut when brought to the level of the anchor. The PDS shuttle and one limb of the suture are brought through the posterior-lateral portal where they are tied outside the body. The

suture limb is shuttled through the capsulolabral tissue and tied away from the glenoid surface. Knotless anchors should be progressively placed superiorly along the glenoid as needed. In general, we place no fewer than three anchors from 6 o’clock to 3 o’clock positions. The final repair construct should produce a glenoid bumper providing sufficient tension along the tissue without capsular redundancy (Fig. 18.11). The rotator interval should then be assessed clinically. If persistent laxity is identified with the sulcus sign in 30° of external rotation, the surgeon should consider rotator interval closure. Arthroscopic determination of rotator interval closure is difficult, but the displacement of the biceps tendon may suggest pathology. An 18-gauge spinal needle is

18  Multidirectional Instability of the Shoulder

passed through the supraspinatus tendon 1  cm medial to the humeral head. A PDS suture is threaded through this needle into the joint and retrieved through the superior aspect of the subscapularis (Fig.  18.12). The PDS limbs are retrieved in the subacromial space where they are tied. This technique may need to be repeated with more medial stitches to adequately close the rotator interval.

18.7 Postoperative Care In general, the postoperative rehabilitation protocol for patients undergoing arthroscopic treatment of multidirectional instability should be individualized for each patient, depending on the location of intra-articular pathology, the direction of primary instability, and the type of surgical treatment used. Immediately after surgery, patients are immobilized in a sling with a 30° abduction pillow. The arm should be in neutral rotation. Patients are instructed to begin passive pendulums at 1 week postoperatively. In addition, they are allowed to perform active ROM of their wrist, hand, and elbow. The average immobilization period is 4–6 weeks, with timing of progression dictated largely by the magnitude of the injury and the extent of the repair. Active-assisted glenohumeral ROM is generally instituted at the 4–6-week mark. In cases that involve repair of posterior instability, internal rotation, and cross-body (horizontal) adduction are restricted for a full 6  weeks postoperatively. Along with progression from active-assisted to active ROM protocol, the patient may begin rotator cuff strengthening and scapular stabilization program at this time. Patients progress to pulleys and weights to improve deltoid and rotator cuff strength and endurance. Sport-specific training programs are then initiated prior to return to play. The majority of patients may return to play or return to manual labor approximately 6  months postoperatively. Range of motion and strength should be at least 80–90% of their opposite extremity prior to being cleared for full activities. After completion of formal rehabilitation, it is usually necessary for a

255

• Portal placement is critical. Ideal placement should be localized w 18-gauge spinal needle. This should be used to touch all are planned repair, ensuring appr position and trajectory. • Begin the case with the pump pr set at 30 mmHg and attempt to m

patient to maintain shoulder stability and strength through a home exercise program approximately two to three times per week.

18.8 Literature Review Many patients diagnosed with MDI can be treated successfully with nonoperative management. A comprehensive physical therapy program directed at scapular stabilization, rotator cuff, and deltoid strengthening exercises is often effective in treating patients with MDI. Watson et al. evaluated the effectiveness of a physiotherapy-led exercise program for participants with MDI and reported large effects between pre- and post-­ rehabilitation scores on all functional instability questionnaires used [28]. However, Misamore et  al. demonstrated that 70% of patients with MDI treated conservatively opted for surgical treatment or had fair or poor ratings for their shoulders at 7- to 10-year follow-up [41]. Warby et  al. suggested in a systematic review that the effect of exercise-based management compared with surgery for MDI is difficult to determine, due in large part to participant heterogeneity and a high level of bias across included studies; however, the authors found that surgery was superior to exercise therapy for shoulder kinematics and return to sport or work, whereas exercise therapy was superior to surgical treatment in patient satisfaction scores [29]. Patients with instability due to shoulder trauma and athletes who participate in overhead sports often have a less favorable outcome with nonoperative management and require surgical repair [1, 12, 42]. Arthroscopic treatment of MDI successfully improves pain and function in most patients [7,

C. L. Antonacci et al.

256

37, 43, 44]. The two most common surgical techniques for MDI include open capsular shift (OCS) and arthroscopic capsular plication (ACP). The most common complication of multidirectional instability treatment is persistent or recurrent instability. Additionally, aggressive capsular plication may result in postoperative stiffness, especially with external rotation [45]. A recent meta-analysis suggests that while no difference was observed between OCS and ACP groups in regard to recurrent postsurgical instability (9.9% versus 6.0%, respectively) and reoperation rates (5.2% versus 4.8%, respectively), OCS caused more postoperative stiffness than ACP, losing 7.0° versus 2° in external rotation, respectively [46]. Even patients with large labral lesions of greater than 270° can be successfully treated, although they may have some mild persistent instability [7]. Although most patients improve in terms of pain and function, Baker et al. reported that only 65% of athletes were able to return to the same level of sport after arthroscopic treatment [37]. Postoperative axillary nerve palsy has not been reported, but its proximity to the operative field puts this structure at risk.

18.9 Summary Multidirectional instability presents a difficult clinical entity to diagnose and treat as it represents a wide spectrum of disease. Conservative management with physical therapy remains the mainstay of initial treatment. If surgical intervention is warranted, satisfactory patient outcomes can be achieved when pathologic lesions that correlate with preoperative findings are addressed during surgery. Successful surgery is dependent upon successful volume reduction and restoration of balanced capsulolabral attachments. Acknowledgments  This chapter is an update of the one published in the previous edition and authored by Anthony A. Romeo and Benjamin Bruce.

References 1. Gaskill TR, Taylor DC, Millett PJ.  Management of multidirectional instability of the shoulder. J Am Acad Orthop Surg. 2011;19:758–67. 2. Blomquist J, Solheim E, Liavaag S, Schroder CP, Espehaug B, Havelin LI. Shoulder instability surgery in Norway: the first report from a multicenter register, with 1-year follow-up. Acta Orthop. 2012;83:165–70. 3. Owens BD, Duffey ML, Nelson BJ, De Berardino TM, Taylor DC, Mountcastle SB.  The incidence and characteristics of shoulder instability at the United States military academy. Am J Sports Med. 2007;35:1168–73. 4. Borsa PA, Sauers EL, Herline DE.  Patterns of glenohumeral joint laxity and stiffness in healthy men and women. Med Sci Sports Exerc. 2000;32:1685–90. 5. Zemek MJ, Magee DJ. Comparison of glenohumeral joint laxity in elite and recreational swimmers. Clin J Sport Med. 1996;6:40–7. 6. Neer CS 2nd, Foster CR.  Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg. 1980;62A:897–908. 7. Gartsman GM, Roddey TS, Hammerman SM.  Arthroscopic treatment of bidirectional glenohumeral instability: two- to five-year follow-up. J Shoulder Elb Surg. 2001;10:28–36. 8. Kim SH, Ha KI, Yoo JC, Noh KC.  Kim’s lesion: an incomplete and concealed avulsion of the posteroinferior labrum in posterior or multidirectional posteroinferior instability of the shoulder. Arthroscopy. 2004;20:712–20. 9. Provencher MT, Dewing CB, Bell SJ, McCormick F, Solomon DJ, Rooney TB, et al. An analysis of the rotator interval in patients with anterior, posterior, and multidirectional shoulder instability. Arthroscopy. 2008;24:921–9. 10. Bahu MJ, Trentacosta N, Vorys GC, Covey AS, Ahmad CS.  Multidirectional instability: evaluation and treatment options. Clin Sports Med. 2008;27:671–89. 11. Guerrero P, Busconi B, Deangelis N, Powers G.  J Orthop Sports Phys Ther. 2009;39:124–34. 12. Schenk TJ, Brems JJ.  Multidirectional instability of the shoulder: pathophysiology, diagnosis, and management. J Am Acad Orthop Surg. 1998;6:65–72. 13. Alpert JM, Verma N, Wysocki R, Yanke AB, Romeo AA.  Arthroscopic treatment of multidirectional shoulder instability with minimum 270 degrees labral repair: minimum 2-year follow-up. Arthroscopy. 2008;24:704–11. 14. Rodeo SA, Suzuki K, Yamauchi M, Bhargava M, Warren RF. Analysis of collagen and elastic fibers in shoulder capsule in patients with shoulder instability. Am J Sports Med. 1998;26:634–43. 15. von Eisenhart-Rothe R, Mayr HO, Hinterwimmer S, Graichen H.  Simultaneous 3D assessment of glenohumeral shape, humeral head centering, and

18  Multidirectional Instability of the Shoulder scapular positioning in atraumatic shoulder instability: a magnetic resonance-based in  vivo analysis. Am J Sports Med. 2010;38:375–82. 16. Lippitt S, Matsen F.  Mechanisms of glenohumeral joint stability. Clin Orthop Relat Res. 1993;291:20–8. 17. Morris AD, Kemp GJ, Frostick SP.  Shoulder electromyography in multidirectional instability. J Shoulder Elb Surg. 2004;13:24–9. 18. Illyés Á, Kiss R.  Electromyographic analysis in patients with multidirectional shoulder instability during pull, forward punch, elevation and overhead throw. Knee Surg Sports Traumatol Arthrosc. 2007;15:624–31. 19. Barden JM, Balyk R, Raso VJM, Moreau M, Bagnall K.  Dynamic upper limb proprioception in multidirectional shoulder instability. Clin Orthop ­ Relat Res. 2004;420:181–9. 20. Cameron KL, Duffey ML, DeBerardino TM, et  al. Association of generalized joint hypermobility with a history of glenohumeral joint instability. J Athl Train. 2010;45:253–8. 21. Cooper RA, Brems JJ.  The inferior capsular-shift procedure for multidirectional instability of the shoulder. J Bone Joint Surg Am. 1992;74:1516–21. 22. Beighton P, Horan F.  Orthopaedic aspects of the Ehlers-Danlos syndrome. J Bone Joint Surg Br. 1969;51:444–53. 23. Ogston JB, Ludewig PM.  Differences in 3-­dimensional shoulder kinematics between persons with multidirectional instability and asymptomatic controls. Am J Sports Med. 2007;35:1361–70. 24. Warner JJ, Micheli LJ, Arslanian LE, Kennedy J, Kennedy R. Patterns of flexibility, laxity, and strength in normal shoulders and shoulders with instability and impingement. Am J Sports Med. 1990;18:366–75. 25. Kim SH, Park JC, Park JS, Oh I.  Painful Jerk test. A predictor of success in nonoperative treatment of postero-­ inferior instability of the shoulder. Am J Sports Med 2004: 32:1849–1855. 26. Lim CO, Park KJ, Cho BK, Kim YM, Chun KA. A new screening method for multidirectional shoulder instability on magnetic resonance arthrography: labro-­ capsular distance. Skelet Radiol. 2016;45:921–7. 27. Saba L, De Filippo M. MR arthrography evaluation in patients with traumatic anterior shoulder instability. J Orthop. 2017;14:73–6. 28. Watson L, Balster S, Lenssen R, Hoy G, Pizzari T. The effects of a conservative rehabilitation program for multidirectional instability of the shoulder. J Shoulder Elb Surg. 2018;27:104–11. 29. Warby SA, Pizzari T, Ford JJ, Hahne AJ, Watson L.  Exercise-based management versus surgery for multidirectional instability of the glenohumeral joint: a systematic review. Br J Sports Med. 2016;50:1115–23. 30. Burkhead WZ Jr, Rockwood CA Jr. Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg. 1992;74:890–6. 31. Warby SA, Ford JJ, Hahne AJ, Watson L, Balster S, Lenssen R, Pizzari T.  Comparison of 2 exercise

257 rehabilitation programs for multidirectional instability of the glenohumeral joint: a randomized controlled trial. Am J Sports Med. 2018;46:87–97. 32. Gartsman GM, Roddey TS, Hammerman SM.  Arthroscopic treatment of multidirectional glenohumeral instability: 2- to 5-year follow-up. Arthroscopy. 2001;17:236–43. 33. Kim SH, Kim HK, Sun JI, Park JS, Oh I. Arthroscopic capsulolabroplasty for posteroinferior multidirectional instability of the shoulder. Am J Sports Med. 2004;32:594–607. 34. Karas SG, Creighton RA, DeMorat GJ. Glenohumeral volume reduction in arthroscopic shoulder reconstruction: cadaveric analysis of suture plication and thermal capsulorrhaphy. Arthroscopy. 2004;20:179–84. 35. Provencher MT, Verma N, Obopilwe E, Rincon LM, Tracy J, Romeo AA, Mazzocca A. A biomechanical analysis of capsular plication versus anchor repair of the shoulder: can the labrum be used as a suture anchor? Arthroscopy. 2008;24:210–6. 36. Van der Reis W, Wolf EM.  Arthroscopic rotator cuff interval capsular closure. Orthopedics. 2001;24:657–61. 37. Baker CL 3rd, Mascarenhas R, Kline AJ, Chhabra A, Pombo MW, Bradley JP.  Arthroscopic treatment of multidirectional shoulder instability in athletes: a retrospective analysis of 2- to 5-year clinical outcomes. Am J Sports Med. 2009;37:1712–20. 38. Provencher MT, Peebles LA.  Editorial commentary: rotator interval closure of the shoulder continues to be a challenge in consensus on treatment. Arthroscopy. 2018;34:3109–11. 39. Hewitt M, Getelman MH, Snyder SJ.  Arthroscopic management of multidirectional instability: pancapsular plication. Orthop Clin North Am. 2003;34:549–57. 40. Cvetanovich GL, McCormick F, Erickson BJ, et  al. The posterolateral portal: optimizing anchor placement and labral repair at the inferior glenoid. Arthrosc Tech. 2013;2:201–4. 41. Misamore GW, Sallay PI, Didelot W. A longitudinal study of patients with multidirectional instability of the shoulder with seven- to ten-year follow-up. J Shoulder Elb Surg. 2005;14:466–70. 42. Bois AJ, Wirth MA.  Revision open capsular shift for atraumatic and multidirectional instability of the shoulder. J Bone Joint Surg Am. 2012;94:748–56. 43. Choi C, Ogilvie-Harris D.  Inferior capsular shift operation for multidirectional instability of the shoulder in players of contact sports. Br J Sports Med. 2002;36:290–4. 44. Voigt C, Schulz AP, Lill H.  Arthroscopic treatment of multidirectional glenohumeral instability in young overhead athletes. Open Orthop J. 2009;3:107–14. 45. Provencher MT, Mologne TS, Hongo M, Zhao K, Tasto JP, An KN.  Arthroscopic versus open rotator interval closure: biomechanical evaluation of stability and motion. Arthroscopy. 2007;23:583–92. 46. Chen D, Goldberg J, Herald I, Critchley A. Effects of surgical management on multidirectional instability

C. L. Antonacci et al.

258 of the shoulder: a meta-analysis. Knee Surg Sports

Traumatol Arthrosc. 2016;24:630–9.

19

SLAP Lesions Michael E. Hantes and Georgios Komnos

Abstract

SLAP lesions belong to capsulolabral lesions and can appear isolated or in conjunction with rotator cuff (RC) tears, instability, or/and impingement. The main clinical manifestations include shoulder pain, instability, and functional impairment. It is not a common entity and its prevalence is estimated to be 5% of all shoulder injuries. Thorough knowledge of the anatomy of the labrum, especially the superior, is necessary for correct diagnosis and treatment. Macro-trauma and micro-­ trauma, usually from repetitive use of the shoulder are the main causes of SLAP lesions. Clinical diagnosis of a SLAP lesion is extremely challenging since no specific examination test exists, and those that are utilized have questionable effectiveness. From the imaging aspect, magnetic resonance imaging (MRI) and magnetic resonance arthrography (MRA) are the most helpful tools to set the diagnosis. No absolute indications for surgical treatment exist. The persistence of pain and symptoms, which do not resolve after conservative treatment, is the leading cause of applying an operative treatment. Debridement and repair are the preferable means of operative M. E. Hantes (*) · G. Komnos Department of Orthopedics, Faculty of Medicine, University of Thessaly, Larisa, Greece e-mail: [email protected]

management. Tenodesis instead of repair is applied to middle-aged and older patient groups, though. Postoperative rehabilitation is extremely essential with the main goal being to avoid stiffness. Keywords

SLAP · Capsulolabral lesions · Shoulder arthroscopy · Labrum · Debridement · Repair · Tenodesis

19.1 Introduction SLAP (Superior Labrum Anterior to Posterior) lesions are a specific pattern of injury belonging to capsulolabral lesions and characterized by disruption of the superior labrum. They may appear as an isolated entity or can be associated with rotator cuff (RC) tears, instability, or/and impingement. They usually lead to shoulder pain, instability, and functional impairment.

19.2 Epidemiology The incidence of SLAP lesions remains in doubt. They are relatively uncommon and correspond to 5% of all shoulder injuries. The incidence increases with age, overhead activity, and trauma. In a series of shoulder arthroscopies, the inci-

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_19

259

260

dence of SLAP lesions varies from 5.4% to more than 10% [1–4]. Type II lesions are considered to be the most common ones [5, 6]. Snyder et al. evaluated 2375 shoulder arthroscopies and reported that 140 (6%) of them revealed a SLAP lesion, with type II being the most prevalent one [2]. In a similar study, Maffet et al. reported an incidence of 12% in 712 patients undergoing shoulder arthroscopy [7], and Handelberg et al. a 6% in 530 patients [8]. In a population of elite professional athletes (355 shoulder arthroscopies), the incidence of SLAP lesions was found to be 9.9% [9]. Moreover, Weber et al [4]. reported an incidence of 12.4% of SLAP repairs among athlete population undergoing shoulder operation in contrast to 9.2% of the general population. Furthermore, military personnel has been found to be at an increased risk for SLAP tears with a reported incidence of as high as 38% [10]. In a prospective study, type I lesions were present at an amazingly high rate, and in contrast to the majority of published data, estimated to correspond to 74% of the total incidence, 21% to type II, 1% to type III, and 4% to type IV [11]. SLAP lesions are frequently associated with other intra-articular pathologies, such as Bankart lesions or rotator cuff tears. Bankart lesion has been demonstrated to be the most common concomitant injury (37%) in elite athletes, followed by partial cuff tear (25%) [9]. In the same study, isolated SLAP lesions represented 17% of total injuries. Association between SLAP lesions and chondral injuries at the humerus, the glenoid, or both has been also documented in the literature [3]. The anterosuperior part is the most common localization of humeral and glenoidal chondral lesions in type II SLAP lesions, while the central part is the most common one in any other type than type II. Surgical repair of SLAP lesions seems to be on the rise during the last decades. Onyekwelu et al. [12] demonstrated an increase of 464% in the number of arthroscopic SLAP repairs between 2002 and 2010 in the USA. One of the main reasons for this huge increase is probably a better awareness of this pathology.

M. E. Hantes and G. Komnos

19.3 Pathophysiology The glenohumeral joint (GHJ) consists of the humeral head, the glenoid, and the labrum. Anatomically, the labrum is a ring of fibrocartilaginous tissue that surrounds the glenoid rim and serves as the glenoid attachment for the GH ligaments (GHLs) and for the long head of the biceps tendon (LHBT). Glenoid labrum consists of two parts: One fibrous peripheral layer, which acts as an anchor for the LHBT and GHL, and a fibrocartilaginous transitional zone which plays the role of the stabilizer of the peripheral layer to a deeper layer of the glenoid. The superior glenoid labrum and the insertion complex of the LHBT are passive stabilizers of the GHJ [3, 13, 14]. The anterior and the superior parts of the labrum have inferior vascularity than the rest of the labrum, which predisposes them to injuries and lowers healing ability. The superior labrum is more mobile and more loosely adherent to the glenoid compared to anterior-inferior labrum [13]. Biceps tendon insertion to the superior labrum is complex. Fifty percent of its fibers insert into the labrum and 50% into supraglenoid tubercle [15]. Four types of proximal LHBT attachment in relation to the glenoid labrum have been described [15]. Type I is characterized by entire LHBT attachment to the posterior labrum, Type II by attachment mainly to posterior labrum and less to anterior, Type III by equal insertion to both posterior and anterior labrum, and Type IV by attachment mainly to anterior labrum. It is important for the orthopedic surgeon to acknowledge the different variants of the superior labrum to distinguish between an anatomic variant and pathology. Many anatomic variations of the glenoid labrum have been described in the literature [16, 17]. In a cadaveric study by Cooper et al. [13], it was demonstrated that the superior and anterosuperior portions of the labrum are loosely attached to the glenoid and they have a menisci-type macroscopic anatomy. Additionally, they found that these parts have less vascularity than the rest of the labrum. Some well-­recognized variants of the superior part of the labrum include the superior sub-

261

19  SLAP Lesions

Typ I

Typ II

Typ III

Typ IV

Fig. 19.1  Types I–IV illustrated according to Snyder classification. Reproduced with permission from Braun, S., Feucht, M. & Imhoff, A. Anatomie und Ätiologie von

SLAP- und Bizeps-Pulley-Läsionen. Obere Extremität 9, 2–8 (2014). https://doi.org/10.1007/s11678-013-0242-0

labral recess, the sublabral foramen and the “Buford complex” [18]. The superior sublabral recess is located beneath the LHBT anchor [19]. Sublabral foramen is a groove located between the normal anterosuperior labrum and the anterior cartilage border of the glenoid. “Buford complex is characterized by a thick, cord-like middle glenohumeral ligament (MGHL) that attached to the superior part of the labrum accompanied with the absence of anterosuperior labral tissue [20]. These anatomic variations are correlated to superior labrum lesions. More specifically, patients with the sublabral foramen and the Buford complex have been found more prone to SLAP type II lesions [18]. The exact pathophysiology of the SLAP tears is still under investigation. Traction on LHBT can end up in SLAP tear [21]. Snyder et al. classified SLAP lesions into four types [22]: Type I (degenerative fraying), Type II (avulsion of biceps-­labral complex), Type III (bucket handle with partial biceps tear), and Type IV (bucket handle with biceps split) (Fig.  19.1). Maffet et  al. [7] expanded this classification system incorporating three more types (types V–VII) (Table 19.1).

Table 19.1  Maffet expanded classification Type V

An anterior-inferior Bankart lesion continues superiorly to include separation of the biceps tendon Type VI An unstable flap tear of the labrum is present in addition to biceps tendon separation Type VII The superior labrum-biceps tendon separation extends anteriorly beneath the middle glenohumeral ligament

19.4 Clinical Diagnosis 19.4.1 History Natural history of SLAP tears is unknown. It was first described by Andrews et al. [23] in throwing athletes. Macro-trauma and micro-trauma can both cause SLAP injury. The patient usually reports direct trauma or overuse of his/her shoulder before the onset of the symptoms. Compression or traction injuries are the main types responsible for these lesions. Nevertheless, SLAP tears are usually overuse injuries. Professional overhead athletes usually suffer from symptomatic type II SLAP lesions [24]. Recurrent clicking or mechanical symptoms may be present. The mechanism of injury is usually related to a fall on an outstretched arm, with the

262

shoulder in abduction and slight forward flexion. Degenerative tears are also probable and mostly responsible for SLAP tears in throwing athletes. The onset of the symptoms may be insidious or following an injury. The main symptoms include pain, increasing with overhead activity and painful “catching” or “popping” in the shoulder.

19.4.2 Clinical Examination Clinical tests are a key element in diagnosing shoulder pathology. However, the clinical diagnosis of a SLAP lesion is extremely challenging. One of the main reasons is that the clinical tests used for the diagnosis have questionable effectiveness [25, 26]. Another reason is the absence of unique clinical findings associated with SLAP lesions since this condition is frequently associated with concomitant shoulder pathology. Complete and detailed history taken is obligatory and a thorough physical examination of the shoulder is always necessary. There is no clinical test considered as the gold standard for diagnosing a SLAP lesion. Several tests are used during the clinical evaluation of the patient.

19.4.2.1 O’Brien Test (Active Compression Test) The patient stands with his/her shoulder in 10 degrees adduction, 90 degrees forward flexion, and maximal pronation. Pain with resistance indicates a positive test (SLAP lesion). 19.4.2.2 Speed Test With the patient seated, he/she is instructed to resist forward flexion in scapular plane. Pain in the shoulder and especially in the bicipital groove indicates bicipital tendinitis. 19.4.2.3 Kibler Test (Anterior Slide Test) The patient is seated with hand on the hip. Joint loading is applied. Pain with resistance indicates SLAP lesion.

M. E. Hantes and G. Komnos

19.4.2.4 Crank Test The patient is supine and the shoulder is in full abduction. Humeral loading is applied along with internal and external rotation. Click and pain indicates SLAP lesion. 19.4.2.5 Kim Test (Biceps Load Test) The patient is supine and the shoulder in full abduction, with the elbow in 90 degrees flexion and the forearm in supination. Pain during external rotation and resisted flexion of the elbow provokes a positive test. 19.4.2.6 O’Driscoll Test (Dynamic Labral Shear Test) With the patient seated and the elbow 90 degrees flexion, external rotation 90 degrees, and 90 degrees abduction. Pain in abduction from 90 degrees to 120 indicates a positive test. 19.4.2.7 Labral Tension Test With the patient supine and full abduction, the arm is fully externally rotated. Pain provoked when the patient supinates the forearm against resistance indicates a positive test. Biceps load test has been demonstrated useful in identifying patients with isolated SLAP lesion [25]. There is no consistency in the literature regarding the sensitivity and specificity values of the aforementioned tests. Sensitivity of speed test has been reported to be 32% and specificity 61% for diagnosing SLAP lesions [27]. Dynamic labral shear test was evaluated in a prospective study and found to be sensitive but not specific for detecting isolated SLAP tears [28]. In a meta-­analysis by Meserve et al. [29] active compression test was found to be the most sensitive and speed test the most specific one. Moreover, anterior slide test was proven to have the most inferior accuracy. Kibler et  al. [30] published that the combination of dynamic labral shear test and O’Brien test is the most appropriate to identify labral tears.

19  SLAP Lesions

263

19.5 Imaging

Diagnosis is usually set when abnormal morphology of the superior labrum is identified. The most Correct diagnosis and prediction of the proper common finding, indicative for SLAP lesion, is candidates for operative or conservative treat- high signal extending anterior and posterior to ment are very essential for the physician. Since the biceps anchor. clinical evaluation can never certainly diagnose MRA with dilute gadolinium is superior to the specific shoulder pathology, imaging and conventional MRI in revealing the anatomy and especially magnetic resonance imaging (MRI) pathology of the glenoid labrum and GHLs [31]. and magnetic resonance arthrography (MRA) It has the highest accuracy for the detection of are very helpful tools (Fig. 19.2). Nevertheless, SLAP lesions [32], with high sensitivity and plain radiographs should always be obtained, specificity, reaching 90% [1, 6]. Sagittal plane is although their role is limited on contributing to the most appropriate one to detect SLAP lesions. differential diagnosis and identifying concomi- Bencardino et  al. [1] reported a sensitivity of tant pathology. These are usually normal in 89% and specificity of 91% in their study, compatients with isolated SLAP lesions. bining MRA and shoulder arthroscopy for SLAP The imaging modality of choice is MRI. MRI tear diagnosis. Similar results were demonis demonstrated to have moderate sensitivity and strated by Jee et  al. [33] and Igbal et  al. [5]. specificity. Knowledge of labrum anatomy and According to a systematic review by its variants is of great importance for interpreting Arirachakaran et  al. [34] MRA proved to be correctly the MRI scans. Physicians should more accurate than MRI in the diagnosis of always be aware of the normal anatomic variants SLAP lesions types II–VII. and MRI findings should always be evaluated in 3-Tesla (3-T) MRI and MRA for detecting conjunction with clinical examination. labral injuries are on the merge in recent years. Fibrocartilaginous labrum more often has a trian- Magee et  al [35]. reported a sensitivity of 90% gular structure, but may also be round, crescent-­ and a specificity of 100% using 3-T MRI for the shaped, or blunted on coronal sections [19]. diagnosis of SLAP tears, while in another study he demonstrated that 3-T MRA has increased accuracy compared to 3-T MRI in detecting SLAP tears [36]. When MRA is contraindicated, computed tomography arthrography (CTA) can be performed. Sensitivity and specificity values are slightly inferior, but high enough reaching 86% and 90%, respectively [37]. Diagnostic findings suggestive of the diagnosing SLAP lesion either by MRI or MRA are the following [38–40] (Fig. 19.3).

Fig. 19.2  A type II SLAP lesion in MR arthrography

• Laterally curved, linear signal in the labrum on coronal plane • Multiple lines of high density on coronal plane • Full-thickness detachment with high signal density and/or wide separation between labrum and glenoid on coronal plane • A glenolabral cyst extending from the superior labrum

264

M. E. Hantes and G. Komnos

When the question arises for SLAP repair or LHBT procedure (e.g., tenodesis), then some of the indications in favor of the last, are age over 35 years old, stable shoulder, tears also in the tendon, and associated pathology. Absolute contraindications do not exist, but age >35  years, alcohol and/or tobacco use, and heavy lifting at work are considered to be negative prognostic factors for success of SLAP repair. In addition, associated pathology, such as degenerative osteoarthritis, RC tear, and acromioclavicular joint pathology may exclude many patients from operative management.

19.6.1 Decision-Making Algorithm Fig. 19.3  A type IV SLAP lesion in MR arthrography

19.6 Treatment Since SLAP lesions are not blamed to lead to severe degenerative changes in the shoulder there are no absolute indications for surgical treatment. The main indication for surgical intervention remains the persistence of pain and symptoms, which do not resolve after conservative treatment. Published data propose anatomic alternations or excessive labral activity as the main indications-causes for operative treatment [41– 43]. In terms of surgical management, it seems that repair is not indicated for middle-aged and older patient groups, who would better benefit from tenodesis instead of repair [44, 45]. When arthroscopy is performed as a diagnostic tool, there are some arthroscopic findings that could set the indications for SLAP tear. These include [46–48]: • Loss of attachment from the glenoid (type II or more) • A peel-back phenomenon, showing labral detachment • Glenoid articular cartilage damage, as a result of possible translation • Loss of capsular tension • Increased posterior labral thickness

Rarely do the findings from a single test (in the absence of patient history or other clinical findings) provide enough information for necessary decision-making. Final decision for surgical treatment is very controversial. However, when there is high clinical suspicion of SLAP tear, then the best way of patient management is to perform a shoulder arthroscopy. Conservative treatment will not lead to tear healing, but symptoms and function may improve. If nonoperative treatment is advised to the patient, the physician should bear in mind that it may have good results in terms of pain relief and arm use especially in young, active patients [49]. Nonoperative treatment includes anti-inflammatory drugs, rest, and physical therapy including strengthening of the RC and exercises for stretching the posterior capsule. However, history of trauma or the presence of mechanical symptoms is negative prognostic factors for the success of nonoperative treatment [50]. Regarding surgical management of SLAP lesions, this remains disputable. Debridement is usually proposed as the best means of treatment in types I and III, but controversy exists in surgical management of type II [51]. Operation options for type II SLAP include debridement, labral repair, biceps tenodesis or tenotomy, and/ or a combination of these. Tenodesis may lead to better results and functional outcomes in older patients with excessive degeneration of the

19  SLAP Lesions Table 19.2  Brockmeyer’s proposed treatment algorithm Type I: Conservative treatment or arthroscopic debridement Type II: SLAP repair or biceps tenotomy/tenodesis Type III: Resection (repair as required) Type IV: SLAP repair (repair/resection if 50% of BT is affected) Type V: Bankart-repair and SLAP repair Type VI: Resection (repair as required) Type VII: Refixation of anterosuperior labrum and SLAP repair

labrum and younger patients with overhead activity demands. Published data support the superiority of tenodesis against repair even in high-level overhead athletes with better clinical results and higher success rates in returning to pre-injury level [52]. Type III SLAP lesions are usually treated with excision of bucket-handle labral tear along with labral repair if the surgeon judges so [53]. Type IV lesions are treated depending on the size of biceps tendon tear. If this is more than 50%, then excision of the fragment and repair is performed, whereas in less than 50%, tenotomy or tenodesis of the tendon is indicated [54]. If repair is not indicated, then the dilemma that arises is whether to perform a tenodesis or tenotomy. Age of the patient is essential in deciding the final treatment strategy. Provencher et  al. [55] demonstrated a higher failure rate after ­surgical treatment in patients older than 36 years old. In conclusion, selection of proper candidates for SLAP repair is essential for the success of the operation. Patient history taking, physical examination and imaging investigations are the tools that should be used before taking the final decision. Brockmeyer et al. [51] proposed a treatment algorithm based on the type of lesion and concomitant injuries, patient’s age, and sport activity level (Table 19.2).

265

in the outpatient clinic. The affected shoulder was the dominant one. She mentioned that the problem started 1 month ago without recalling a severe injury. After complete history taking, she mentioned that she might have had a minor fall at her right outstretched hand slightly before the symptoms’ onset. A thorough clinical examination showed a reproduction of the symptom attempted a full abduction and rotation of the shoulder, with the patient lying. Clinical tests for all other shoulder pathologies were negative. Plain X-rays were obtained and were normal. The patient was given rehabilitation exercises for strengthening and stretching. However, 3 weeks later, came back with the persistence of the symptoms, which had a serious impact on her athletic activities. An MRA was ordered, and SLAP II tear diagnosis was set (Fig. 19.4). An arthroscopy was proposed and performed 1  week later. Diagnostic arthroscopy was initially performed and the diagnosis of a SLAP type II tear was confirmed (Fig.  19.5). Debridement was performed and then repair was decided, and two anchors were used. The patient was discharged the next day with an immobilization sling. Follow-up took place at 2 weeks, 1 month, 2 months, 3, and then 5 months. She returned to full sports activity at 6  months with no pain or other symptoms reported since then.

19.6.2 Clinical Case/Example A 28-years old female volleyball player with “clicking” symptoms in her right shoulder came

Fig. 19.4  Type II Slap, SGHL tear in the female athlete

266

M. E. Hantes and G. Komnos

Fig. 19.5  Intraoperative view of the lesion. Probing of the type II tear

19.7 Surgical Technique

Fig. 19.6  Evaluation of the lesion and the biceps tendon with the probe

19.7.1 Patient Positioning

19.7.3 Diagnostic Arthroscopy

The patient may be in a beach chair position or in lateral decubitus position, depending on the surgeon’s preference and experience. However, lateral decubitus position is more often used for SLAP tears. In both positions, the arm is placed in a traction sleeve and then connected to a traction device. In beach chair position the head and neck should be in neutral position and the table flexed at 45–60 degrees with the back elevated. In lateral position, the patient should be placed that way so as the glenoid is parallel to the floor. The arm is in 25–45 degrees of abduction and 10–20 degrees of forward flexion. Head and neck should have a neutral position.

Before initiating the arthroscopy, the patient is examined under anesthesia to evaluate joint mobility. The arthroscopy begins with the insertion of the arthroscope into the glenohumeral joint through the posterior portal. The whole joint and the subacromial space are evaluated. Rotator interval is examined to see the status of biceps tendon, for possible inflammation, tear, etc. With the use of the probe the attachment of the LHBT, along with the attachment of the labrum are assessed for possible SLAP or Bankart lesion (Fig.  19.6). GHLs should also be evaluated. Supraspinatus, infraspinatus, and subscapularis are examined for partial- or full-thickness tears or fatty infiltration. Anterior axillary pouch is checked for loose bodies or synovitis. Furthermore, articular cartilage is evaluated for degenerative changes. More specifically, for identifying SLAP lesions the probe is used to palpate the superior labrum and evaluate its mobility. The labrum may be found torn, frayed, detached, or with degenerative changes. Knowledge of the anatomic variants is essential. After visualization and palpation, the SLAP lesion is categorized again. When degenerative changes are recognized but the labrum is still attached to the gle-

19.7.2 Portals Portals used maybe two or three depending on the surgeon’s preference. Two portals are usually enough, but a third portal can be used if necessary. The standard posterior portal is used to initiate the procedure. Next, an anterior superior or a superolateral portal is used as an accessory portal. If there is a posterior extending SLAP, then the port of Wilmington can be helpful and is necessary most of the time.

19  SLAP Lesions

noid then it is a type I lesion. Degenerative changes accompanied by detachment of the labrum from the glenoid rim and instability of biceps tendon attachment are indicative of type II lesion. Finding of a displaced part of the labrum into the joint categorizes the pathology as type III which is further categorized as type IV if there is also recognized LHBT injury.

19.7.4 Step-by-Step Procedure (Box 19.1)

267

(Fig. 19.7). If the lesion needs only debridement, this is performed with a 4.0  mm shaver by smoothening the labrum. If fixation is needed, fixation techniques include transosseous sutures, staples, screws, arthroscopic sutures, and bioabsorbable tacks [2, 56, 57]. Bioabsorbable tacks are not frequently used nowadays though, due to increased rate of complications [58, 59]. On the other hand, use of bioabsorbable anchors loaded with nonabsorbable sutures is on the merge [60, 61]. Multiple-point fixation with the use of multiple anchors improves labral stability (Fig. 19.8).

As aforementioned, direct visualization and evaluation of labral injury and mobility, and capsular tension are initially performed. Excessive mobility to probing is indicative of SLAP lesion

Box 19.1 Tips and Tricks

• Posterolateral portal (port of Wilmington) is useful for labral and SLAP tears. • Always perform initially a diagnostic arthroscopy. “Peel back” test shows “peel back of the labrum with 900 of external rotation and abduction. • When ready for the fixation, be sure that there is an adequate footprint on the glenoid. • Placement of enough posterior-superior anchors to eliminate the peel-back phenomenon. • Always evaluate biceps mobility after suture placement to ensure tendon motion during shoulder rotation. Be careful with the anchor placed anterior to the biceps. This has a greater effect on external rotation. Loss of external rotation may be devastating for throwing athletes [64]. • Always treat the concomitant pathology of the shoulder. • Select the proper candidate for surgery and perform the right operation (Consider tenodesis instead of repair in patients older than 35 years old).

Fig. 19.7  Utilization of the probe for evaluating the mobility of the labrum

Fig. 19.8  Placement of a 2nd anchor to repair the lesion

268

One or two anchors may be used [43, 62, 63] or for better stability two or more [42, 58, 60]. Anchor placement is of crucial importance in joint stability after surgery. After insertion of the anchors, sutures are passed through the soft tissues. Simple sutures with high-strength material or mattress sutures can be used. Mattress sutures help to spread the repair over a larger area. Finishing, the sutures are tied, and the portals are closed, after evaluating again the labrum and the fixation. Postoperative complications include postoperative stiffness, humeral head lesion by the anchors, especially metallic ones, capsulitis, and chondrolysis. Complications related to SLAP surgical management include failure of proper anchor placement or failure of proper diagnosis (coexisting lesions or anatomic variants).

19.8 Postoperative Care The most important issue in postoperative rehabilitation is the early start of motion to avoid postoperative stiffness. An important goal is to restore the internal and external rotation deficits and gain safe total range of motion (ROM). Patient compliance is very essential for achieving the best result after surgery. When SLAP repair has been performed the patient is usually advised to sling immobilization for 3 weeks and isometric exercises to 45 degrees until 6 weeks. Patients are encouraged to perform pendulums almost immediately postoperatively. ROM is gradually increased over 6–8 weeks with the final goal to achieve full ROM in 3 months. Resistance training starts after 2  months and return to sports is anticipated at 5–6 months.

19.9 Literature Review Several studies, especially retrospective ones have reported promising results in the operative treatment of SLAP lesions. In the absence of significant prospective studies, systematic ­ reviews have tried to shed more light on this subject.

M. E. Hantes and G. Komnos

Gorantla et al. [65] evaluated the outcome of arthroscopic repair of type II SLAP lesions in a minimum 2-year follow-up. They found that excellent reports results vary from 40 to 94%. Even wider was the variety of the reported return to sports (20–94%), with overhead athletes having smaller chance of returning (22–64%). The difficulty of overhead athletes to return to their pre-injury level is also emphasized by Huri et al. [44]. They also demonstrated the superiority of biceps tenodesis against SLAP repair in non-­ athletic population because of the high failure of SLAP repair. In one of the few prospective studies, Brockmeier et al. [60] evaluated 47 patients with type II SLAP lesion, treated with arthroscopic suture anchor fixation. At a minimum 2-year follow-­up, 74% of them were able to return to their pre-injury level, while in total, 87% rated the result as good or excellent. Remarkably, they found that patients with traumatic mechanism of injury were more likely to return to previous level of competition (92%). Refractory stiffness was the most significant complication among total group. Furthermore, Schroeder et  al. [66] prospectively assessed the long-term results after isolated superior labral repair and reported a satisfaction rate of 88% at 5  years. Postoperative stiffness was remarkable (13.1%), while results were proved to be independent of age at a cut-off of 40 years old. Boesmueller et al. [67] prospectively evaluated the functional outcome and pain after arthroscopic repair of isolated SLAP II tears and found that there was a significant improvement in the functional scores and a decrease in pain at about 6 months after surgery. Subsequently, they defined this timeline as the cut-off for returning to sports activity. Extensive labral tears (type>IV) were treated arthroscopically with capsulolabral reconstruction, with good functional outcome scores and clinical results in a study by Huang et al. [68]. Although most studies have reported good to excellent results after SLAP repair failure rates in some studies reach 37% [55], especially in older patients. Franceschi et al. [69] evaluated patients older than 50 years with type II SLAP tear and coexisting RC tears and reported better clinical outcome

19  SLAP Lesions

after a biceps tenotomy than SLAP repair. Erickson et  al. [70] attempted to determine the trends in SLAP repairs and found that over the decade between 2004 and 2014 the number of biceps tenodesis has significantly increased. Another trend demonstrated in the published literature is the decreasing average age of patients that undergo arthroscopic SLAP repair [70].

19.10 Summary SLAP lesions are quite uncommon but existing entity. Injury mechanism is multifactorial, and symptoms include in most cases pain, “snapping” and functional impairment. Concomitant lesions are often present. Accurate diagnosis is extremely challenging and mainly based on clinical examination and MRI findings. Occasionally, diagnosis can even be one of exclusion. It is usually found in recreational or professional athletes involved in overhead activities. Controversy exists regarding the treatment strategy for patients with SLAP lesions. In general, conservative treatment is usually initially proposed. In the case of persistent pain and symptoms, operative treatment is suggested. The type of surgical procedure mainly depends on the intraoperative findings and the type of lesion. In general, SLAP repair is reserved for young overhead athletes, while tenodesis is a viable option in older patients (>35  years). Postoperative rehabilitation protocols are very important for achieving the best result since stiffness remains the most important complication after surgery.

References 1. Bencardino JT, Beltran J, Rosenberg ZS, Rokito A, Schmahmann S, Mota J, et  al. Superior labrum anterior-­posterior lesions: diagnosis with MR arthrography of the shoulder. Radiology. 2000; https://doi. org/10.1148/radiology.214.1.r00ja22267. 2. Snyder SJ, Banas MP, Karzel RP.  An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elb Surg. 1995; https://doi.org/10.1016/ S1058-­2746(05)80015-­1. 3. Patzer T, Lichtenberg S, Kircher J, Magosch P, Habermeyer P. Influence of SLAP lesions on chondral

269 lesions of the glenohumeral joint. Knee Surg Sport Traumatol Arthrosc. 2010; https://doi.org/10.1007/ s00167-­009-­0938-­2. 4. Weber SC, Martin DF, Seiler JG, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery Part II candidates. Am J Sports Med. 2012; https://doi. org/10.1177/0363546512447785. 5. Iqbal HJ, Rani S, Mahmood A, Brownson P, Aniq H.  Diagnostic value of MR arthrogram in SLAP lesions of the shoulder. Surgeon. 2010; https://doi. org/10.1016/j.surge.2010.06.006. 6. Waldt S, Burkart A, Lange P, Imhoff AB, Rummeny EJ, Woertler K.  Diagnostic performance of MR arthrography in the assessment of superior labral anteroposterior lesions of the shoulder. Am J Roentgenol. 2004; https://doi.org/10.2214/ ajr.182.5.1821271. 7. Maffet MW, Gartsman GM, Moseley B.  Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med. 1995; https://doi. org/10.1177/036354659502300116. 8. Handelberg F, Willems S, Shahabpour M, Huskin JP, Kuta J. SLAP lesions: a retrospective multicenter study. Arthroscopy. 1998; https://doi.org/10.1016/ S0749-­8063(98)70028-­3. 9. Beyzadeoglu T, Circi E. Superior labrum anterior posterior lesions and associated injuries: return to play in elite athletes. Orthop J Sport Med. 2015; https://doi. org/10.1177/2325967115577359. 10. Kampa RJ, Clasper J.  Incidence of SLAP lesions in a military population. J R Army Med Corps. 2005; https://doi.org/10.1136/jramc-­151-­03-­07. 11. Kim TK, Queale WS, Cosgarea AJ, McFarland EG. Clinical features of the different types of SLAP lesions: an analysis of one hundred and thirty-nine cases. J Bone Jt Surg  - Ser A. 2003; https://doi. org/10.2106/00004623-­200301000-­00011. 12. Onyekwelu I, Khatib O, Zuckerman JD, Rokito AS, Kwon YW. The rising incidence of arthroscopic superior labrum anterior and posterior (SLAP) repairs. J Shoulder Elb Surg. 2012; https://doi.org/10.1016/j. jse.2012.02.001. 13. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, DiCarlo E, Allen AA.  Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Jt Surg  - Ser A. 1992; https://doi. org/10.2106/00004623-­199274010-­00007. 14. Burkart A, Debski RE, Musahl V, McMahon PJ.  Glenohumeral translations are only partially restored after repair of a simulated type II superior labral lesion. Am J Sports Med. 2003; https://doi.org/ 10.1177/03635465030310012101. 15. Vangsness CT, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Jt Surg - Ser B. 1994; 16. Ilahi OA, Cosculluela PE, Ho DM. Classification of anterosuperior glenoid labrum variants and their asso-

270 ciation with shoulder pathology. Orthopedics. 2008; https://doi.org/10.3928/01477447-­20080301-­18. 17. Rao AG, Kim TK, Chronopoulos E, McFarland EG. Anatomical variants in the anterosuperior aspect of the glenoid labrum: a statistical analysis of seventy-­ three cases. J Bone Jt Surg - Ser A. 2003; https://doi. org/10.2106/00004623-­200304000-­00011. 18. Kanatli U, Ozturk BY, Bolukbasi S.  Anatomical variations of the anterosuperior labrum: prevalence and association with type II superior labrum anterior-­ posterior (SLAP) lesions. J Shoulder Elb Surg. 2010; https://doi.org/10.1016/j.jse.2010.07.016. 19. De Maeseneer M, Van Roy F, Lenchik L, Shahabpour M, Jacobson J, Ryu KN, et al. CT and MR arthrography of the normal and pathologic anterosuperior labrum and labral-bicipital complex. Radiographics. 2000; 20. Williams MM, Snyder SJ, Buford D.  The buford complex—the “cord-like” middle glenohumeral ligament and absent anterosuperior labrum complex: a normal anatomic capsulolabral variant. Arthroscopy. 1994; https://doi.org/10.1016/ S0749-­8063(05)80105-­7. 21. Bey MJ, Elders GJ, Huston LJ, Kuhn JE, Blasier RB, Soslowsky LJ. The mechanism of creation of superior labrum, anterior, and posterior lesions in a dynamic biomechanical model of the shoulder: the role of inferior subluxation. J Shoulder Elb Surg. 1998; https:// doi.org/10.1016/S1058-­2746(98)90031-­3. 22. Snyder SMD, Karzel RMD, Pizzo D, Wilson MD, Ferkel RMD, Friedman MD.  SLAP lesions of the shoulder. Arthrosc J Arthrosc Relat Surg. 1990; 23. Andrews JR, Carson WG, Mcleod WD.  Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985; https://doi. org/10.1177/036354658501300508. 24. Barber FA, Field LD, Ryu RKN. Biceps tendon and superior labrum injuries: decision making. Instr Course Lect. 2008; 25. Cook C, Beaty S, Kissenberth MJ, Siffri P, Pill SG, Hawkins RJ. Diagnostic accuracy of five orthopedic clinical tests for diagnosis of superior labrum anterior posterior (SLAP) lesions. J Shoulder Elb Surg. 2012; https://doi.org/10.1016/j.jse.2011.07.012. 26. Nørregaard J, Krogsgaard MR, Lorenzen T, Jensen EM.  Diagnosing patients with longstanding shoulder joint pain. Ann Rheum Dis. 2002; https://doi. org/10.1136/ard.61.7.646. 27. Hegedus EJ, Goode A, Campbell S, Morin A, Tamaddoni M, Moorman CT, et al. Physical examination tests of the shoulder: a systematic review with meta-analysis of individual tests. Br J Sports Med. 2008; https://doi.org/10.1136/bjsm.2007.038406. 28. Sodha S, Srikumaran U, Choi K, Borade AU, McFarland EG.  Clinical assessment of the dynamic labral shear test for superior labrum anterior and posterior lesions. Am J Sports Med. 2017; https://doi. org/10.1177/0363546517690349. 29. Meserve BB, Cleland JA, Boucher TR. A meta-­analysis examining clinical test utility for assessing superior

M. E. Hantes and G. Komnos labral anterior posterior lesions. Am J Sports Med. 2009; https://doi.org/10.1177/0363546508325153. 30. Kibler WB, Sciascia AD, Hester P, Dome D, Jacobs C.  Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009; https://doi. org/10.1177/0363546509332505. 31. Chandnani VP, Yeager TD, DeBerardino T, Christensen K, Gagliardi JA, Heitz DR, et al. Glenoid labral tears: prospective evaluation with MR imaging, MR arthrography, and CT arthrography. Am J Roentgenol. 1993; 32. Holzapfel K, Waldt S, Bruegel M, Paul J, Heinrich P, Imhoff AB, et al. Inter- and intraobserver variability of MR arthrography in the detection and classification of superior labral anterior posterior (SLAP) lesions: evaluation in 78 cases with arthroscopic correlation. Eur Radiol. 2010; https://doi.org/10.1007/ s00330-­009-­1593-­1. 33. Jee WH, McCauley TR, Katz LD, Matheny JM, Ruwe PA, Daigneault JP.  Superior labral anterior posterior (SLAP) lesions of the glenoid labrum: reliability and accuracy of MR arthrography for diagnosis. Radiology. 2001; https://doi.org/10.1148/radiology.2 18.1.r01ja44127. 34. Arirachakaran A, Boonard M, Chaijenkij K, Pituckanotai K, Prommahachai A, Kongtharvonskul J. A systematic review and meta-analysis of diagnostic test of MRA versus MRI for detection superior labrum anterior to posterior lesions type II–VII. Skelet Radiol. 2017; https://doi.org/10.1007/s00256-­016-­2525-­1. 35. Magee TH, Williams D. Sensitivity and specificity in detection of labral tears with 3.0-T MRI of the shoulder. Am J Roentgenol. 2006; https://doi.org/10.2214/ AJR.05.0338. 36. Magee T. 3-T MRI of the shoulder: is MR arthrography necessary? Am J Roentgenol. 2009; https://doi. org/10.2214/AJR.08.1097. 37. Oh JH, Kim JY, Choi JA, Kim WS. Effectiveness of multidetector computed tomography arthrography for the diagnosis of shoulder pathology: comparison with magnetic resonance imaging with arthroscopic correlation. J Shoulder Elb Surg. 2010; https://doi. org/10.1016/j.jse.2009.04.012. 38. Jung JY, Jee WH, Park MY, Lee SY, Kim YS. SLAP tears: diagnosis using 3-T shoulder MR arthrography with the 3D isotropic turbo spin-echo space sequence versus conventional 2D sequences. Eur Radiol. 2013; https://doi.org/10.1007/s00330-­012-­2599-­7. 39. Boutin RD, Marder RA.  MR imaging of SLAP lesions. Open Orthop J. 2018; https://doi.org/10.217 4/1874325001812010314. 40. Kessler MA, Stoffel K, Oswald A, Stutz G, Gaechter A. The SLAP lesion as a reason for glenolabral cysts: a report of five cases and review of the literature. Arch Orthop Trauma Surg. 2007; https://doi.org/10.1007/ s00402-­006-­0154-­1. 41. Kibler WB, Sciascia A. Current practice for the surgical treatment of SLAP lesions: a systematic review.

19  SLAP Lesions Arthrosc  - J Arthrosc Relat Surg. 2016; https://doi. org/10.1016/j.arthro.2015.08.041. 42. Coleman SH, Cohen DB, Drakos MC, Allen AA, Williams RJ, O’Brien SJ, et  al. Arthroscopic repair of type II superior labral anterior posterior lesions with and without acromioplasty: a clinical analysis of 50 patients. Am J Sports Med. 2007; https://doi. org/10.1177/0363546506296735. 43. Kanatli U, Ozturk BY, Bolukbasi S.  Arthroscopic repair of type II superior labrum anterior posterior (SLAP) lesions in patients over the age of 45 years: a prospective study. Arch Orthop Trauma Surg. 2011; https://doi.org/10.1007/s00402-­011-­1348-­8. 44. Huri G, Hyun YS, Garbis NG, Mcfarland EG.  Treatment of superior labrum anterior posterior lesions: a literature review. Acta Orthop Traumatol Turc. 2014; https://doi.org/10.3944/ AOTT.2014.3169. 45. Patterson BM, Creighton RA, Spang JT, Roberson JR, Kamath GV.  Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American board of orthopaedic surgery certification examination database. Am J Sports Med. 2014; https://doi. org/10.1177/0363546514534939. 46. Kibler WB, Kuhn JE, Wilk K, Sciascia A, Moore S, Laudner K, et  al. The disabled throwing shoulder: Spectrum of pathology - 10-year update. Arthrosc - J Arthrosc Relat Surg. 2013; https://doi.org/10.1016/j. arthro.2012.10.009. 47. Burkhart SS, Morgan CD, Kibler WB.  The disabled throwing shoulder: Spectrum of pathology part I: Pathoanatomy and biomechanics. Arthrosc - J Arthrosc Relat Surg. 2003; https://doi.org/10.1053/ jars.2003.50128. 48. Snyder SJ, Karzel RP, Pizzo WD, Ferkel RD, Friedman MJ.  SLAP lesions of the shoulder. Arthrosc  - J Arthrosc Relat Surg. 2010; https://doi.org/10.1016/j. arthro.2010.06.004. 49. Edwards SL, Lee JA, Bell JE, Packer JD, Ahmad CS, Levine WN, et al. Nonoperative treatment of superior labrum anterior posterior tears: improvements in pain, function, and quality of life. Am J Sports Med. 2010; https://doi.org/10.1177/0363546510370937. 50. Jang SH, Seo JG, Jang HS, Jung JE, Kim JG. Predictive factors associated with failure of nonoperative treatment of superior labrum anterior-posterior tears. J Shoulder Elb Surg. 2016; https://doi.org/10.1016/j. jse.2015.09.008. 51. Brockmeyer M, Tompkins M, Kohn DM, Lorbach O.  SLAP lesions: a treatment algorithm. Knee Surg Sport Traumatol Arthrosc. 2016; https://doi. org/10.1007/s00167-­015-­3966-­0. 52. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R.  Arthroscopic treatment of isolated type II slap lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009; https://doi. org/10.1177/0363546508330127. 53. Gartsman GM, Hammerman SM.  Superior labrum, anterior and posterior lesions: when and how to treat

271 them. Clin Sports Med. 2000; https://doi.org/10.1016/ S0278-­5919(05)70299-­4. 54. Rames RD, Karzel RP. Injuries to the glenoid labrum, including slap lesions. Orthop Clin North Am. 1993; 55. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D.  A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013; https://doi. org/10.1177/0363546513477363. 56. Abrams GD, Safran MR.  Diagnosis and management of superior labrum anterior posterior lesions in overhead athletes. Br J Sports Med. 2010; https://doi. org/10.1136/bjsm.2009.070458. 57. Pagnani MJ, Deng XH, Warren RF, Torzilli PA, Altchek DW.  Effect of lesions of the superior portion of the glenoid labrum on glenohumeral translation. J Bone Jt Surg  - Ser A. 1995; https://doi. org/10.2106/00004623-­199507000-­00005. 58. Cohen DB, Coleman S, Drakos MC, Allen AA, O’Brien SJ, Altchek DW, et  al. Outcomes of isolated type II SLAP lesions treated with arthroscopic fixation using a bioabsorbable tack. Arthrosc  - J Arthrosc Relat Surg. 2006; https://doi.org/10.1016/j. arthro.2005.11.002. 59. Sassmannshausen G, Sukay M, Mair SD.  Broken or dislodged poly-L-lactic acid bioabsorbable tacks in patients after SLAP lesion surgery. Arthrosc  - J Arthrosc Relat Surg. 2006; https://doi.org/10.1016/j. arthro.2006.03.009. 60. Brockmeier SF, Voos JE, Williams RJ, Altchek DW, Cordasco FA, Allen AA. Outcomes after arthroscopic repair of type-II SLAP lesions. J Bone Jt Surg - Ser A. 2009; https://doi.org/10.2106/JBJS.H.00205. 61. Ozbaydar M, Elhassan B, Warner JJP.  The use of anchors in shoulder surgery: a shift from metallic to bioabsorbable anchors. Arthrosc  - J Arthrosc Relat Surg. 2007; https://doi.org/10.1016/j. arthro.2007.05.011. 62. Friel NA, Karas V, Slabaugh MA, Cole BJ. Outcomes of type II superior labrum, anterior to posterior (SLAP) repair: prospective evaluation at a minimum two-year follow-up. J Shoulder Elb Surg. 2010; https://doi.org/10.1016/j.jse.2010.03.004. 63. Maier D, Jaeger M, Ogon P, Bornebusch L, Izadpanah K, Suedkamp NP.  Suture anchors or transglenoidal sutures for arthroscopic repair of isolated SLAP-2 lesions? A matched-pair comparison of functional outcome and return to sports. Arch Orthop Trauma Surg. 2013; https://doi.org/10.1007/s00402-­012-­1657-­6. 64. McCulloch PC, Andrews WJ, Alexander J, Brekke A, Duwani S, Noble P. The effect on external rotation of an anchor placed anterior to the biceps in type 2 SLAP repairs in a cadaveric throwing model. Arthrosc  - J Arthrosc Relat Surg. 2013; https://doi.org/10.1016/j. arthro.2012.06.021. 65. Gorantla K, Gill C, Wright RW. The outcome of type II SLAP repair: a systematic review. Arthrosc  - J Arthrosc Relat Surg. 2010; https://doi.org/10.1016/j. arthro.2009.08.017.

272 66. Schroder CP, Skare O, Gjengedal E, Uppheim G, Reikerås O, Brox JI.  Long-term results after SLAP repair: a 5-year follow-up study of 107 patients with comparison of patients aged over and under 40 years. Arthrosc  - J Arthrosc Relat Surg. 2012; https://doi. org/10.1016/j.arthro.2012.02.025. 67. Boesmueller S, Tiefenboeck TM, Hofbauer M, Bukaty A, Oberleitner G, Huf W, et al. Progression of function and pain relief as indicators for returning to sports after arthroscopic isolated type II SLAP repair - a prospective study. BMC Musculoskelet Disord. 2017; https://doi.org/10.1186/s12891-­017-­1620-­3. 68. Huang H, Zheng X, Li P, Shen H.  Arthroscopic reconstruction of shoulder’s labrum with extensive

M. E. Hantes and G. Komnos tears. Int J Surg. 2013; https://doi.org/10.1016/j. ijsu.2013.07.015. 69. Franceschi F, Longo UG, Ruzzini L, Rizzello G, Maffulli N, Denaro V.  No advantages in repairing a type II superior labrum anterior and posterior (SLAP) lesion when associated with rotator cuff repair in patients over age 50: a randomized controlled trial. Am J Sports Med. 2008; https://doi. org/10.1177/0363546507308194. 70. Erickson BJ, Jain A, Abrams GD, Nicholson GP, Cole BJ, Romeo AA, et al. SLAP lesions: trends in treatment. Arthrosc - J Arthrosc Relat Surg. 2016; https:// doi.org/10.1016/j.arthro.2015.11.044.

Arthroscopic Treatment of HAGL and Reverse HAGL Lesions

20

Philip-C. Nolte, Bryant P. Elrick, and Peter J. Millett

Abstract

This chapter discusses humeral avulsions of the glenohumeral ligament (HAGL) lesions, both anterior and posterior. While injuries of the anteroinferior glenoid labrum (Bankart lesions) and of the posteroinferior glenoid labrum (posterior Bankart lesions) are well-­ recognized, common injuries following traumatic shoulder dislocations and subluxations, HAGL, and posterior HAGL lesions are uncommon and less well-recognized. Although pathophysiology and associated risks are similar, injuries to the capsuloligamentous attachments on the humeral side of the shoulder joint have received less attention when compared to labral injuries. An anterior shoulder dislocation with avulsion of the anterior band of the inferior glenohumeral ligament (IGHL) was first described by Nicola as early as 1942, and it was not until 1995 that

P.-C. Nolte Department of Trauma and Orthopedic Surgery, BG Trauma Center, Ludwigshafen, Germany e-mail: [email protected] B. P. Elrick Steadman Philippon Research Institute, Vail, CO, USA e-mail: [email protected] P. J. Millett (*) Steadman Philippon Research Institute, The Steadman Clinic, Vail, CO, USA e-mail: [email protected]

Wolf et al. established the term HAGL. Due to advancements in arthroscopy and improved imaging, anterior and posterior HAGL lesions have become increasingly recognized throughout the last decade, leading to a better understanding and treatment of these injuries. Keywords

Shoulder instability · Arthroscopic · Humeral avulsion · Glenohumeral ligament · Shoulder stabilization · HAGL · Posterior HAGL

20.1 Introduction This chapter discusses humeral avulsions of the glenohumeral ligaments (HAGL) lesions, both anterior and posterior. Although the pathophysiology and associated risks are similar, injuries to the capsuloligamentous attachments on the humeral side of the shoulder joint have received less attention when compared to labral injuries. An anterior shoulder dislocation with avulsion of the anterior band of the inferior glenohumeral ligament (IGHL) was first described by Nicola as early as 1942 [1], and it was not until 1995 that Wolf et al. established the term humeral avulsion of the glenohumeral ligament (HAGL) [2]. Even though the typical anterior HAGL lesion with an avulsion of the anterior band of the IGHL

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_20

273

P.-C. Nolte et al.

274

is more common, posterior HAGL lesions (PHAGL), sometimes also known as reverse HAGL lesions, involving the posterior band of the IGHL, occur as well. Due to advancements in arthroscopy and improved imaging, anterior and posterior HAGL lesions have become increasingly recognized throughout the last decade, leading to a better understanding and treatment of these injuries.

20.2 Epidemiology HAGL and PHAGL lesions occur in 1–9% of patients with shoulder instability [3–5] but can reach up to 18% in patients needing revision procedures [3]. Although this pathology can be seen in isolation, it is commonly associated with other injuries such as Bankart and reverse Bankart lesions, Hill-Sachs lesions, rotator cuff tears, superior labrum anterior to posterior (SLAP) lesions, and long head of the biceps tendon tears [4, 6–9]. As one would expect with traumatic glenohumeral instability, Bankart lesions (14–41%) and Hill-Sachs lesions (13– 81%) are the most frequently observed copathologies that occur in conjunction with HAGL lesions [9, 10]. Most of the patients are male [8, 10, 11] and in their second or third decade of life [9, 10]. Although the patient’s history typically involves high-energy trauma with hyperabduction, external rotation, and subsequent shoulder dislocation [7, 9, 12], repetitive microtrauma in overhead and throwing athletes has also been described as a potential cause for this pathology, specifically in females [9, 13]. While HAGL lesions are usually associated with anterior instability, PHAGL lesions have been reported in association with posterior instability [14]. HAGL lesions are more common than PHAGL lesions, with a reported incidence of 52–93% for HAGL, and 7–37% for PHAGL lesions [5, 9, 15]. The combination of HAGL and PHAGL lesions can occur in 11% of cases [15], and bony HAGL lesions are seen in 8% of cases [9].

20.3 Pathophysiology The shoulder joint is the most mobile joint in the human body and serves to position the hand in space. To achieve this degree of mobility, the shoulder joint has less bony restraints and relies on static and dynamic soft tissue stabilization. However, with these anatomic features there comes a higher risk of dislocation making the shoulder joint the most frequently dislocated diarthrodial joint [16]. Static components comprise of the glenohumeral labrum, ligaments, and the capsule, while dynamic stabilizers include all the musculature surrounding the shoulder, but most importantly the rotator cuff [4]. The capsuloligamentous complex represents the coracohumeral ligament (CHL), the superior glenohumeral ligament (SGHL), the middle glenohumeral ligament (MGHL), and the inferior glenohumeral ligament (IGHL), which is divided into respective anterior (aIGHL) and posterior (pIGHL) parts that are interconnected via the axillary pouch (Fig. 20.1) [17]. This architecture

Fig. 20.1 Glenohumeral ligament anatomy. Note the anterior (aIGHL) and posterior (pIGHL) bands of the IGHL complex interconnected with the axillary pouch [18]

20  Arthroscopic Treatment of HAGL and Reverse HAGL Lesions

of the IGHL complex results in a “hammock-­ like” structure [18–20]. Furthermore, it conforms to different shapes with various arm positions, allowing it to statically stabilize the humeral head within the glenoid throughout the glenohumeral range of motion [18, 20, 21]. When the shoulder is abducted to 90 degrees and externally rotated, the IGHL serves as the main anterior stabilizer [4, 22, 23]. The IGHL complex arises from the glenohumeral labrum. More specifically, the aIGHL originates between 2 and 4 o’clock and the pIGHL originates between 7 and 9 o’clock, assuming a right shoulder clock face [6]. The insertion on the humeral side has been described as either “collar-like” with its attachment below the inferior articular margin of the humeral head, or “V-shaped” with the aIGHL and pIGHL attaching close to the cartilaginous rim. In reference to the latter, the attachment lies more distal on the humeral metaphysis, mimicking the shape of the letter V [5, 6, 19–21, 24]. When an anterior shoulder dislocation is sustained, this can result in a disruption of the IGHL at the anteroinferior glenoid (i.e., Bankart lesion), the mid-substance, or at the humeral insertion (HAGL lesion) (Fig. 20.2). In the case of posterior shoulder dislocations, a PHAGL lesion can

275

result, either with “floating” PIGHL or without a posterior Bankart lesion (Fig.  20.3) [14]. Additionally, the combination of a HAGL and PHAGL lesion is possible. It has been demonstrated that in the setting of PHAGL lesions, 50% of cases can have concomitant anterior capsuloligamentous injuries [11]. These findings are in support of the “circle concept” [25]: when a significant injury to one area of the capsule is ­sustained, the opposite side is likely to be injured as well [11, 25]. Bui-Mansfield et al. established the West Point classification for describing anterior (HAGL) and posterior (PHAGL) injuries to the IGHL (Table 20.1) [5]. Furthermore, Ames and Millett contributed to the better understanding of

Fig. 20.3 Axial MRI of a floating posterior IGHL (PIGHL) lesion in a 19-year-old male rugby player who sustained a forceful hyperabduction and external rotation injury Table 20.1  West Point classification of HAGL lesions according to Bui-Mansfield et al. [6]

Fig. 20.2  Arthroscopic visualization through a posterior viewing portal of a right shoulder displaying a humeral avulsion of the glenohumeral ligament (HAGL) lesion. Note the bleeding and fraying of the avulsed inferior glenohumeral ligament (IGHL)

Anterior Anterior humeral avulsion of the glenohumeral ligament (AHAGL) Anterior bony humeral avulsion of the glenohumeral ligament (ABHAGL) Floating AHAGL

Posterior Reverse humeral avulsion of the glenohumeral ligament (PHAGL) Posterior bony humeral avulsion of the glenohumeral ligament (PBHAGL) Floating PHAGL

P.-C. Nolte et al.

276 Fig. 20.4 Floating PIGHL subtypes as described by Ames and Millett [15]. Type 1 represents a PHAGL with a concomitant posterior Bankart lesion. Type 2 is a PHAGL with a posterior bony Bankart lesion. Type 3 comprises of a PHAGL with an additional posterior Bankart lesion. Type 4 is a bony PHAGL with a posterior bony Bankart lesion

Type 1

Type 2

Type 3

Type 4

PHAGL lesions by adding a classification of floating PIGHL subtypes (Fig. 20.4) [14].

20.4 Clinical Diagnosis 20.4.1 History In order to diagnose HAGL lesions the physician must be aware of this entity as a differential diagnosis for shoulder pain and instability, as these injuries are commonly overlooked. The patient’s history is key in the evaluation of suspected HAGL lesions. In most cases, shoulder complaints are nonspecific, and patients report pain, weakness, and discomfort [9]. Interestingly, patients with magnetic resonance imaging (MRI) diagnosed HAGL lesions had pain in 85% of cases and presented with instability in only 15% of cases [15]. Although a history of shoulder dislocation or subluxation is typically attainable, repetitive microtrauma due to overhead or throwing activities should also be investigated [9, 13]. If a distinct injury (i.e., dislocation) was sustained, the patient should be questioned about the direction of instability and if there is recurrence. The arm position at the time of injury is also critical as hyperabduction and external rotation are

most commonly observed in HAGL lesions, while the external rotational component is not always necessary for a Bankart lesion [7, 9, 12]. Most importantly, a high index of suspicion for an undetected or untreated HAGL or PHAGL lesion during the index surgery should be raised for patients who present with recurrent instability following a previous Bankart repair [4, 9].

20.4.2 Clinical Examination Unfortunately, there are no specific tests to reliably identify glenohumeral avulsion lesions to the IGHL complex (HAGL or PHAGL lesions) and findings may vary widely [15]. Therefore, it is crucial to rule out other shoulder pathology. The physician should focus on a complete examination of the active and passive range of motion, as well as strength, compared to the asymptomatic shoulder. Since HAGL lesions are commonly associated with instability, pertinent provocative maneuvers should be performed. These include the load and shift test, the jerk test, anterior and posterior apprehension test, as well as the relocation test. Furthermore, the rotator interval should be checked for a sulcus sign and a hyperabduction test (Gagey-test) should be performed in order to assess hyper-

20  Arthroscopic Treatment of HAGL and Reverse HAGL Lesions

277

laxity and multidirectional instability [26]. Although these maneuvers are indicative of instability, none are sensitive or specific for HAGL or PHAGL lesions [9].

20.5 Imaging Since the patient’s history and clinical examination can often be vague for the detection of HAGL and PHAGL lesions, imaging contributes extensively to the diagnosis of these injuries. Diagnostic imaging has improved over recent years, mostly due to better recognition, understanding, and treatment of IGHL complex pathology. Plain radiographs are the first step in the diagnostic chain, evaluating for HAGL lesion, and should be performed in at least three planes: anteroposterior (AP), scapular “Y” and axillary films. AP views are utilized to assess for fractures, especially those of the lesser and greater tuberosities, as they are often encountered in the setting of instability following previous trauma. Furthermore, AP films can show avulsed bony fragments in projection to the humeral insertion of the IGHL [3, 6, 24, 27]. Scapular “Y” views are used to evaluate glenohumeral alignment and assess the integrity of the glenoid, while axillary films help in the diagnosis of injuries to the humeral head, such as Hill-Sachs lesions, and glenoid pathology. Care should be taken to evaluate the subchondral sclerosis line of the glenoid for interruptions, as these can be indicative of fractures or chronic bone loss causing instability. When osseous injuries are suspected, computed tomography can help in further classification, although the role for the diagnosis of HAGL and PHAGL lesions is little. MRI with or without contrast enhancement is the imaging modality of choice in detecting HAGL and PAHGL lesions; however, there is a wide divergence in the reliability of MRI [28]. T2-weighted fat-suppressed images should be obtained. Coronal oblique and sagittal oblique views are most likely to lead to the diagnosis, although axial images prove to be useful sometimes (Figs. 20.3, 20.5, and 20.6) [5, 6].

Fig. 20.5  Coronal MRI of a humeral avulsion of the glenohumeral ligament (HAGL) lesion in an 18-year-old male who sustained an anterior shoulder dislocation. Note the “J-sign”

A specific finding is the direct visualization of the ruptured ligament, less specific findings include contrast extravasation and the “J-sign” (Fig. 20.5) [4, 6, 28]. The axillary pouch of the shoulder contains fluid and usually displays a U-shape in sagittal oblique MRI images. The “J-sign” can occur when there is an injury to the IGHL complex, leading to a low-lying axillary pouch in the shape of a “J” [28]. In the acute setting, enhancement is usually not necessary, since hemarthrosis serves as an excellent contrast. Alternatively, chronic, more subtle cases may require contrast enhancement. Furthermore, extra-articular contrast extravasation has been demonstrated to serve as a valid and reliable sign of HAGL and PHAGL lesions (83% of arthroscopically positive cases) with the high interobserver agreement [28]. Finally, findings that support the diagnosis of instability, such as Hill-Sachs, Bankart, and reverse Bankart lesions, should raise suspicion and lead the physician to closely evaluate for HAGL and PHAGL lesions, respectively. Vice versa, if a HAGL lesion is identified on MRI, one should be alert and look for concomitant injuries as they occur in the majority of cases [11].

P.-C. Nolte et al.

278

a

b

Fig. 20.6  Posterior humeral avulsion of the glenohumeral ligament (PHAGL) lesion in a 23-year-old male ice hockey player who sustained a posterior shoulder dislocation. a Sagittal MRI. b Axial MRI

20.6 Treatment An initial course of nonoperative management can be performed in low-demand patients, especially with mid-substance tears of the anterior and posterior IGHL. Here, care should be taken to account for the high possibility of concomitant pathologies that may necessitate a surgical intervention [11]. As with other causes of instability, nonoperative treatment of HAGL lesions involves physical therapy. The goal of therapy is to strengthen the rotator cuff and surrounding musculature, aiming to center the humeral head in the glenoid fossa. Interestingly, there has been a paradigm shift in recent treatment strategies. Whereas historically an initial course of nonoperative treatment was suggested, this has been shown to result in poor outcomes [9, 10]. Despite only evaluating a small subset of 42 shoulders with HAGL lesions, a systematic review demonstrated a recurrence rate of instability in 90% of cases, while operative treatment resulted in no recurrence [9]. Since the typical patient with an injury to the IGHL complex is between 20 and 30  years of age, and recurrent instability can lead to arthropathy over time [29], repair is especially recommended in younger patients.

Biomechanical data have shown that large HAGL lesions (6–9 o’clock on the right humeral head clock face; 36.8 mm in length) increase glenohumeral range of motion (ROM), translation in the anteroinferior, posterior, and inferior direction and caused an abnormal shift of the humeral head in abduction, whereas these changes did not occur in small HAGL lesions (6–7:30 o’clock; 18.4 mm in length) [30]. The abnormal biomechanics in large HAGL lesions were reversible when repaired with three single-loaded suture anchors [30]. In a similar cadaveric study, a consistent kinematic pattern in terms of increased translation was observed from the intact state to medium HAGL lesions (4:30– 5:30 o’clock) and large HAGL lesions (3:30–6:30 o’clock) [22]. Furthermore, a juxta-chondral repair (2 suture anchors placed at the chondral margin) proved to restore passive ROM more similar to the intact state, compared to a repair on the humeral neck (2 suture anchors placed 1 centimeter (cm) distal from the chondral margin) [22]. Operative treatment options for the repair of HAGL and PHAGL lesions comprise open, mini-­ open, and arthroscopic techniques (Fig. 20.7) [8, 15, 31–33]. Both, open and arthroscopic procedures result in good functional outcomes, and there is no recent literature in favor of the former

20  Arthroscopic Treatment of HAGL and Reverse HAGL Lesions

a

b

279

c

Fig. 20.7  Posterior humeral avulsion of the glenohumeral ligament (PHAGL) lesion in a left shoulder of a 23-year-old male ice hockey player. a PHAGL. b Repair sutures applied. c Repair

or the latter [10]. The contraindications for surgical management are similar to those of any open or arthroscopic shoulder surgery.

20.6.1 Decision-Making Algorithm As mentioned previously, presenting symptoms can often be nonspecific thus it is imperative that patients undergo a thorough history, physical examination, and imaging studies, to establish the correct diagnosis. Clinically, especially preoperatively, the differentiation between small, medium, and large HAGL lesions remains difficult. High clinical suspicion for HAGL ­ lesions must be maintained in patients who have failed previous instability surgery [34]. In some instances, conservative management may be considered to rehabilitate the shoulder [34], although current literature suggests it should probably be pursued with caution [9, 10]. If conservative measures fail or in cases of failed stabilization surgery with recurrent instability, surgical treatment is indicated [10, 34]. Younger, athletic patients are highly encouraged to undergo surgical repair. HAGL lesions found as concomitant pathology during diagnostic arthroscopy should be surgically repaired to prevent chronic instability and limit revision surgery [35].

20.6.2 Clinical Case/Example A 23-year-old male professional hockey player suffered traumatic dislocation of his left shoulder with

subsequent recurrent posterior dislocations. The initial injury occurred during a game when he was checked into the boards with his left arm abducted and extended. He immediately felt his shoulder posteriorly dislocate before reducing spontaneously. Despite the injury, he continued to play and suffered a secondary posterior dislocation shortly after. Initially, he was managed conservatively and was given a brace to wear during games; however, after discontinuing the brace as a result of improved symptoms, he suffered a third dislocation. Prior to the initial injury, he reported no significant history of shoulder injury or dislocation. Upon presentation, the patient reported 2/10 pain at rest and 8/10 at its worst. He noted the pain occasionally disturbed his sleep, is exacerbated when he checks opponents during games, and was alleviated with rest and activity modification. He denied neck pain, elbow pain, weakness, and paresthesia. Physical examination revealed normal inspection without tenderness to palpation. Neurovascular examination was normal. Range of motion and strength were full. His shoulder was notably unstable with grade 2 posterior translation but was stable anteriorly with an insignificant sulcus sign ( GT, the shoulder is off-track while if the HSI  25% high demanding sport / work patient Latarjet +/-remplissage

Glenoid bone loss < 25% or low sport / work activity patient Bankart +/-remplissage

ISIS = /> 4

Glenoid bone loss > 12% Latarjet +/-remplissage

Glenoid bone loss < 12% or low sport / work activity patient Bankart +/-remplissage

Fig. 25.1  Treatment algorithm for recurrent anterior traumatic instability. If the Hill-Sachs lesion is on track or engages when tested intraoperatively “remplissage” should be considered

25  Arthroscopic Latarjet Procedure

The Latarjet procedure is also contraindicated in hyperlax patients with voluntary dislocations and in patients with epilepsy without efficient treatment of their seizures.

25.3 Surgical Technique Latarjet procedure consists of transferring the coracoid with the conjoint tendon to the anterior aspect of the glenoid. To date, it is not possible to achieve under arthroscopy the “triple locking effect” initially described by Patte [1, 11]. In fact, it is not possible to fix the capsule to the remnant of the coracoacromial (CA) ligament attached to the lateral side of the coracoid, albeit labral repair can be accomplished. Arthroscopic Latarjet procedure prevents anterior dislocation by treating the bony defect and increasing the bony stability of the glenoid. The primary stabilizing effect is obtained by the increase of the anteroposterior width of the glenoid. At the same time, the conjoint tendon crosses the lower anterior aspect of the subscapularis muscle thus performing a ­hammock effect during abduction and external rotation. This effect is considered as one of the main stabilizing effects of the Latarjet procedure [14]. There are two main surgical techniques to perform the arthroscopic Latarjet procedure according to the hardware used for coracoid fixation: screws or buttons. The technique with screws is the authors’ preferred one and is described in this chapter.

25.3.1 Patient Positioning We prefer beach-chair for arthroscopic Latarjet even though we use lateral decubitus for most of the other arthroscopic shoulder procedures. An examination under anesthesia should be performed to confirm instability. We always start with the scope in the posterior portal and we perform a diagnostic arthroscopy initially. If the operating time gets long it is possible to lower the head and back of the patient when you move the camera to the front of the patient.

331

25.3.2 Portals Make the portals you need but try to limit their size to avoid leakage. Our standard portals are adopted from Lafosse’s description of arthroscopic Latarjet. The standard posterior portal (A) is used for initial visualization and for a switching stick to guide the orientation of the glenohumeral joint line. The anterolateral portal through the rotator interval (D) gives access to the glenohumeral (GH) joint and the coracoid. The anterior superior portal, also through the rotator interval (E), gives access to the GH joint and coracoid and supplements when the D portal is occupied. The anterior superior portal above the coracoid (H) is used to drill the tunnels in the coracoid and to make the osteotomy. Anterior portal (I) is used for visualization and chiseling underneath the coracoid before making the osteotomy. Anterior inferior portal (J) is used for visualization and preparation of the coracoid. The anterior medial portal (M) is used for the double plastic cannula to drill the guide wires and fixation of the coracoid with screws.

25.3.3 Diagnostic Arthroscopy A diagnostic arthroscopy is mandatory before you start with your arthroscopic Latarjet procedure. In the patient group scheduled for Latarjet most of them have a Hill-Sachs lesion. In some patients the bone loss is of a certain amount that you need to do a remplissage in addition to anterior stabilization. We prefer to place the suture anchors for the remplissage and to pass the sutures through the infraspinatus at the beginning of the surgical procedure. The sutures will then be tied at the end after performing the anterior stabilization. Other concomitant lesions should also be diagnosed and addressed if necessary.

25.3.4 Step-by-Step Procedure For the Latarjet we start with the camera from posterior. Second portal is D, anterolateral through the rotator interval. The anterior labrum

332

B. Boe and G. Nourissat

is assessed and in most cases removed. In case of revision, anchors and sutures of the previous surgery are removed. The 3 o’clock position of the glenoid is marked by electrocautery. A blunt incision is made in the posterior part of the subscapularis muscle to prepare the split and to decide the height of the split, which is usually performed between the lower third and the upper two third of the muscle and corresponds to the inferior half of the glenoid (below the 3 o’clock mark) (Fig.  25.2). Soft tissue from the rotator interval and underneath the coracoid is removed. The conjoined tendon and the CA ligament are then identified. The ligament is released, and it is possible to develop the space underneath the deltoid and pectoralis major muscles. At this point the camera is moved to the front. The soft tissue superior to the coracoid is removed to the base where the coracoclavicular ligaments are seen. To make a split between the conjoined tendon and the pectoralis minor the anterior part of the pectoralis minor is released from the coracoid. With careful dissection in the fat layer between the muscles, the musculocutaneus nerve can be identified. With the aim of a guide, two pins are placed into the coracoid through the H portal close to

the clavicle (Fig. 25.3). The pins are over drilled and a top hat might be used (Fig. 25.4). After the coracoid is prepared a chisel is used for osteotomy. If the chisel is used from underneath before you go all the way through the coracoid from the top formation of a spike underneath can be avoided (Fig. 25.5). After the osteotomy we look for the axillary nerve between the con-

Fig. 25.2  Working with the camera from posterior portal the 3 o’clock position is marked on the glenoid and the level of the split in m. Subscapularis is marked from posterior. Making a weakness in the tendon at desired height will make it easier to perform the split from anterior later in the procedure

Fig. 25.4  Top hat. We use top hat in the inferior tunnel. Osteolysis often develops in the superior part of the graft meaning the screw and top hat can be more prominent with time. Without top hat the superior screw can be placed deeper into the bone and hopefully not cause irritation later

Fig. 25.3  Two long Kirchner pins are drilled in the center of the coracoid at least 5  mm from the tip. A coracoid guide is used to secure parallelism and 10  mm distance between the pins

25  Arthroscopic Latarjet Procedure

Fig. 25.5  Chisel underneath coracoid. To avoid a spike formation on the lower part of the glenoid the chisel can be used through cortical bone from inferior before you perform the osteotomy from superior

Fig. 25.6 Axillary nerve. To avoid the serious complication of axillary nerve injury we highly recommend visualizing the nerve and protecting it during certain steps of the procedure

joined tendon and the subscapularis muscle (Fig.  25.6). We think visualization and protection of the axillary nerve is mandatory to perform this procedure to avoid a complication that will be a disaster for the patient. When the nerve is visible the split through subscapularis can be made safely. A switching rod is placed through the joint from posterior to anterior to guide the height of the split.

333

Fig. 25.7  Stabilizing coracoid fragment. The coracoid fragment sometimes has spikes or seems unnecessarily large after osteotomy. The shape is easier to form with the shaver if threading it onto the guide pin stabilizes the fragment

With the plastic guide through the subscapularis split from anterior and the 3 o’clock mark on the glenoid, a guide pin is drilled through the lower glenoid aiming the same direction as the joint surface. The guide is over drilled and the trumpet is placed from posterior to measure screw length. The graft is fixed to the plastic cannula with 3.5mm metal sleeves. To stabilize the graft, in case you need to reshape it with the shaver blade, it is helpful to thread the sleeve onto the guide pin (Fig. 25.7). This step also facilitates pushing the graft through the subscapularis split. Before you fix the graft with both screws the switching rod through the joint can be helpful to make sure the graft is not lateralized. Graft positioning should be evaluated both from anterior and posterior before finishing the procedure. Along with the evaluation the arm can be released and the range of motion intraoperatively tested.

25.3.5 Tips and Tricks • Be friends with your anesthesiologist. Hypotensive anesthesia is necessary to avoid bleeding and extensive soft tissue swelling. Tranexamic acid might be used. • Use switching rods to push tissue and expand the room where you are working.

334

• For the upper hole in the coracoid, the top hat might be prominent and the patient develops osteolysis over time. For this reason, we only use top hat in the distal hole. • The osteotomy sometimes leads to fracture of the coracoid. Be meticulous when positioning the drill holes and make sure there is at least 3  mm from the upper hole to the osteotomy line. Most fractures will need to be converted to open surgery, but sometimes it is possible to achieve arthroscopic graft fixation with non-­ resorbable sutures and suture anchors (Fig. 25.8). • With the switching rod through the subscapularis muscle, the arm can be rotated to make a blunt dissection where the split is planned. • The surface of the anterior glenoid and the under surface of the coracoid should be prepared to optimize healing. • Drilling the Kirschner wires to position the screws is easier if you do it without the pull from the coracoid/conjoined tendon. We recommend drilling with the plastic cannula guide through the subscapularis before you fasten the coracoid to the cannula.

Fig. 25.8 Coracoid fracture. One of the pitfalls in Latarjet procedure is the fracture of the coracoid fragment. In this case, we were able to stabilize two pieces anatomically with three different non-resorbable sutures around the graft arthroscopically. Sutures from anchors in the glenoid also secured the graft and conjoined tendon

B. Boe and G. Nourissat

25.4 Postoperative Care One of the benefits of arthroscopic procedures compared to open surgery is thought to be less painful postoperatively. This is still our impression and has been demonstrated by a simple visual analog scale [15]. Less pain is an advantage when it comes to the length of hospital stay; however, the difference has not been proven to be significant after 30 days. The postoperative rehabilitation protocol might differ between countries and hospitals. For most surgeons, early mobilization is allowed to avoid stiffness. For the first 4 weeks a sling might be useful to get rest. Strengthening exercises are normally not allowed for the first 6 weeks. The most important goal after surgery is the progression of passive range of motion. Contact sports are not recommended before 6  months postoperatively. Repeated radiographs are performed to assess the position of the graft. Postoperative CT scan is useful to surgeons at the beginning of their learning curve to assess graft placement.

25.5 Literature Review Since the first description by Lafosse et  al. [3], many authors have reported results of arthroscopic Latarjet procedure. Several surgical tricks have been described with different fixation techniques to improve the reliability and safety of the procedure. However, papers reporting clinical results raised some concerns about the complication rate. Marion et  al. first compared the results of open versus arthroscopic Latarjet procedure [16] and found less pain 3  days after surgery in the arthroscopic group, but no difference at a 2-year follow-up. The French arthroscopy society conducted a prospective multicentre study comparing arthroscopic and open Latarjet procedures performed by experts [12, 17]. The authors analyzed 390 cases at a minimum 2-year follow-up and found no significant differences between groups for shoulder scores and bone graft positioning.

25  Arthroscopic Latarjet Procedure

Graft positioning is a critical step of the Latarjet procedure. If the graft is positioned too high there is a risk of recurrent inferior instability and injury to the suprascapular nerve because of screw penetration [18, 19]. If the graft is too low the lower screw has a risk of poor fixation into the glenoid and the reconstruction depends on one screw alone. Lateral overhang is a serious concern that has to be avoided knowing this to be significantly associated with postoperative osteoarthritis [20]. Medial placement is more contentious. As long as the patient feels safe and stable it is hard to argue that the graft is medial. In other cases, with medial placement the patient feels unsecure and will experience subluxations or recurrence of luxation. It has been argued that graft positioning is better achieved with arthroscopic technique, as the surgeon can visualize the graft from different portals. However, on comparing open and arthroscopic techniques, Neyton et al. found that the positioning of the graft was more lateral in the arthroscopic group [12]. After the operation, there will always be some degree of swelling and hematoma. As arthroscopic Latarjet is a challenging and timeconsuming procedure, most surgeons experience voluminous swelling in some of their early cases. Postoperative infection rate is low in arthroscopic surgery, but a feared complication anyway, sometimes leading to the necessity of hardware removal Nevertheless, the literature review demonstrated no difference in terms of complications or benefits for the arthroscopic versus open procedure [17].

25.6 Summary Since its first description by Lafosse more than 10 years ago, arthroscopic Latarjet procedure has become more popular and was developed by many surgeons. Unfortunately, its future is rather unclear, as it is a technically demanding procedure that can only be carried out by experienced surgeons with advanced arthroscopic skills. Trying to improve clinical results is a good reason for innovation, but the improvement has to be

335

demonstrated. To date, arthroscopic Latarjet did not demonstrate its superiority compared to the open procedure and there is still controversy about which method to perform. Natural evolution is likely to develop more and more advanced all-arthroscopic procedures; however, more benefits should be brought by the arthroscopic technique to recognize it as a first choice. Concerns still exist regarding the overall outcome [21] and the current techniques have to improve to reach adequate reliability and safety.

References 1. Young AA, Maia R, Berhouet J, Walch G.  Open Latarjet procedure for management of bone loss in anterior instability of the glenohumeral joint. J Shoulder Elb Surg. 2011;20(2 Suppl):S61–9. 2. Nourissat G, Nedellec G, O’Sullivan NA, Debet-­ Mejean A, Dumontier C, Sautet A, et  al. Mini-­ open arthroscopically assisted Bristow-Latarjet procedure for the treatment of patients with anterior shoulder instability: a cadaver study. Arthroscopy. 2006;22(10):1113–8. 3. Lafosse L, Lejeune E, Bouchard A, Kakuda C, Gobezie R, Kochhar T.  The arthroscopic Latarjet procedure for the treatment of anterior shoulder instability. Arthroscopy. 2007;23(11):1242e1–5. 4. Boileau P, Saliken D, Gendre P, Seeto BL, d’Ollonne T, Gonzalez JF, et  al. Arthroscopic Latarjet: suture-­ button fixation is a safe and reliable alternative to screw fixation. Arthroscopy. 2019;35(4):1050–61. 5. Kordasiewicz B, Malachowski K, Kicinski M, Chaberek S, Boszczyk A, Marczak D, et  al. Intraoperative graft-related complications are a risk factor for recurrence in arthroscopic Latarjet stabilisation. Knee Surg Sports Traumatol Arthrosc. 2019;27(10):3230–9. 6. Valenti P, Maroun C, Wagner E, Werthel JD.  Arthroscopic Latarjet procedure combined with Bankart repair: a technique using 2 cortical buttons and specific glenoid and coracoid guides. Arthrosc Tech. 2018;7(4):e313–e20. 7. Olds M, Ellis R, Donaldson K, Parmar P, Kersten P. Risk factors which predispose first-time traumatic anterior shoulder dislocations to recurrent instability in adults: a systematic review and meta-analysis. Br J Sports Med. 2015;49(14):913–22. 8. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-­ track” lesion. Arthroscopy. 2014;30(1):90–8. 9. Burkhart SS, Debeer JF, Tehrany AM, Parten PM. Quantifying glenoid bone loss arthroscopically in shoulder instability. Arthroscopy. 2002;18(5):488–91.

336 10. Chuang TY, Adams CR, Burkhart SS.  Use of preoperative three-dimensional computed tomography to quantify glenoid bone loss in shoulder instability. Arthroscopy. 2008;24(4):376–82. 11. Gowd AK, Liu JN, Cabarcas BC, Garcia GH, Cvetanovich GL, Provencher MT, et al. Management of recurrent anterior shoulder instability with bipolar bone loss: a systematic review to assess critical bone loss amounts. Am J Sports Med. 2019;47(10):2484–93. 12. Neyton L, Barth J, Nourissat G, Metais P, Boileau P, Walch G, et al. Arthroscopic Latarjet techniques: graft and fixation positioning assessed with 2-dimensional computed tomography is not equivalent with standard open technique. Arthroscopy. 2018;34(7):2032–40. 13. Neviaser RJ, Neviaser TJ, Neviaser JS.  Concurrent rupture of the rotator cuff and anterior dislocation of the shoulder in the older patient. J Bone Joint Surg Am. 1988;70(9):1308–11. 14. Clavert P, Kempf JF, Kahn JL.  Biomechanics of open Bankart and coracoid abutment procedures in a human cadaveric shoulder model. J Shoulder Elb Surg. 2009;18(1):69–74. 15. Nourissat G, Neyton L, Metais P, Clavert P, Villain B, Haeni D, et  al. Functional outcomes after open versus arthroscopic Latarjet procedure: a prospective comparative study. Orthop Traumatol Surg Res. 2016;102(8S):S277–S9.

B. Boe and G. Nourissat 16. Marion B, Klouche S, Deranlot J, Bauer T, Nourissat G, Hardy P.  A prospective comparative study of arthroscopic versus mini-open Latarjet procedure with a minimum 2-year follow-up. Arthroscopy. 2017;33(2):269–77. 17. Metais P, Clavert P, Barth J, Boileau P, Brzoska R, Nourissat G, et  al. Preliminary clinical outcomes of Latarjet-Patte coracoid transfer by arthroscopy vs. open surgery: prospective multicentre study of 390 cases. Orthop Traumatol Surg Res. 2016;102(8S):S271–S6. 18. Ladermann A, Denard PJ, Burkhart SS. Injury of the suprascapular nerve during latarjet procedure: an anatomic study. Arthroscopy. 2012;28(3):316–21. 19. Shishido H, Kikuchi S.  Injury of the suprascapular nerve in shoulder surgery: an anatomic study. J Shoulder Elb Surg. 2001;10(4):372–6. 20. Mizuno N, Denard PJ, Raiss P, Melis B, Walch G.  Long-term results of the Latarjet procedure for anterior instability of the shoulder. J Shoulder Elb Surg. 2014;23(11):1691–9. 21. Minkus M, Wolke J, Fischer P, Scheibel M. Analysis of complication after open coracoid transfer as a revision surgery for failed soft tissue stabilization in recurrent anterior shoulder instability. Arch Orthop Trauma Surg. 2019;139(10):1435–44.

Advanced Soft Tissue Procedures for Glenohumeral Instability: The BLS Technique

26

Roman Brzoska and Hubert Laprus

Abstract

Arthroscopic Bankart repair in the treatment of shoulder instability is associated with high prevalence rate of instability recurrence. The extracapsular stabilization of the glenohumeral joint with enhancement of anterior wall soft tissues could be an alternative and more efficient procedure especially in case of anterior glenoid bone loss or anterior wall insufficiency. Following this point of view novel anterior extracapsular stabilization technique “Between glenohumeral Ligaments and Subscapularis tendon” (BLS) was introduced. In authors’ experience, the BLS technique has been shown to be an effective way of treatment of anterior shoulder instability for patients without significant glenoid bone loss. It was also shown that this technique does not decrease shoulder range of motion.

26.1 Introduction Treatment of anterior shoulder instability is currently a subject of debate. Several different operative techniques, with various effectiveness, have been proposed and there is yet no consensus of which technique provides the best outcome. For many years, open or arthroscopic Bankart repair procedure was the proposed treatment for every case [1, 2]. Unfortunately, studies showed that approximately one-third of patients had instability recurrence after arthroscopic Bankart repair and among patients younger than 21 years, the risk of failure was shown to be even higher, with a reported failure rate of more than 50% [2–4]. In the pursuit for a surgical technique that could prevent recurrent anterior shoulder instability, the authors developed a new arthroscopic technique which can be considered as a modification of the classic Bankart procedure [5, 6].

Keywords

Anterior instability · Glenoid bone loss · Arthroscopic treatment · BLS · Bankart repair

R. Brzoska · H. Laprus (*) St Luke’s Hospital, Bielsko-Biala, Poland

26.2 Surgical Rationale This non-anatomic technique relies on augmentation of the damaged anterior wall soft tissues by a part of the subscapularis muscle and was named “between glenohumeral ligaments and subscapularis muscle stabilization” (BLS). This technique enables restoration of the original capsulolabral footprint while protecting the

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_26

337

R. Brzoska and H. Laprus

338

articular surface by extracapsular knots placement, thus, reducing the risk of future articular damage by abrasion.

In case of arthroscopically confirmed engaging Hill-Sachs lesion [7], remplissage standard technique was performed [8]. Viewing through the posterior portal, the glenoid labrum pouch (GLP) and ligament subscapularis pouch (LSP) are 26.3 Indications marked with electrothermal cautery inserted and Contraindications through the anterolateral portal. The GLP is prepared first in the standard fashion, using a rasp to The indications for BLS treatment are similar to approximately the 6 o’clock position. The LSP is the traditional indications for Bankart treatment. then marked through the direct anterior portal, They include patients with instability, usually viewing through the anterolateral portal first-time instability, without significant glenoid (Fig. 26.1). To create this space, the capsule must bone loss (GBL) estimated on 11% [6], and with- be separated from the overlying subscapularis, out significant degeneration of anterior soft tissue and this delicate dissection is carried out medistabilizers such as the labrum and MGHL what is ally and inferiorly until subscapularis muscle crucial to perform BLS according to the proper fibers are visualized. Care must be taken to orient technical description. the electrothermal cautery toward subscapularis Contraindications are significant GBL, and away from the anterior capsule, which might defined as ≥11%, previous shoulder stabilization, otherwise become injured. Because the anterior multidirectional instability, voluntary instability, capsular tissues are usually deficient, a lower moderate or severe osteoarthritis and drug-­ third or fourth tendinous cord of subscapularis resistant epilepsy. muscle is separated with a grasper in order to augment the repair without affecting motion (Fig.  26.2). Double-loaded suture anchor is 26.4 Surgical Technique inserted into the glenoid rim at the 5:30. The sutures from anchor must pass through the center The patient is placed in the beach chair position of the labrum, anterior capsule and glenohumeral under general anesthesia following interscalene ligaments and finally attach a silver cord of subblock. The standard posterior portal is performed. scapularis tendon to augment the repaired anteTwo additional portals, anterolateral and anterior, rior stabilizers. Using the grasper through the are created. During the initial arthroscopic exam- posterior portal to pull up the anterior wall comination, a Hill-Sachs lesion should be identified. plex and hold it in position, a second double-­ a

b

Fig. 26.1 (a) Arthroscopic view of marked glenoid labrum pouch (GLP) and ligament subscapularis pouch (LSP). (b) Arthroscopic view of LSP through the anterolateral portal

26  Advanced Soft Tissue Procedures for Glenohumeral Instability: The BLS Technique

a

339

b

Fig. 26.2 (a) Subscapularis muscle tendinous cords in MRI imaging—white arrow indicates proper cord used for anterior wall augmentation. (b) Lower cord of subscapularis muscle used in anterior wall augmentation

a

b

Fig. 26.3 (a) Cord of subscapularis muscle used for anterior wall augmentation. (b) Cadaveric view of subscapularis muscle tendinous cord

loaded suture anchor is placed at 4 o’clock, and two additional mattress sutures are placed. Previously dissected third or fourth tendinous cord of subscapularis muscle has to be surrounded and stitched by sutures from the lowest anchor (Fig. 26.3). It should be underlined, that suture passing through the tendon and knot tying should be performed with the shoulder in external rotation, so that after fixing this part of the

subscapularis muscle, there is no restriction in external rotation. If necessary, another anchor is placed like in the standard arthroscopic Bankart procedure (Fig. 26.4). After knot tying, tendinous cord dissected previously from subscapularis muscle is parallel to the inferior glenohumeral ligament, thus strengthening the anterior capsuloligamentous complex. The use of mattress sutures helps to position the suture material away

340

R. Brzoska and H. Laprus

tion (IR) exercises were performed twice a day. Active movements within painless range of motion were introduced from 6th week. Starting from week 12, gradually forced active movements were introduced to restore muscle strength and full range of motion. A majority of the patients were allowed to return to daily activities after 3  months and to the previous sport after 6  months postoperatively, in case of negative apprehension sign.

26.6 Literature Review

Fig. 26.4  BLS technique before knot tying

Fig. 26.5  Final intraarticular view after BLS technique

from the articular surface, and the knots used to control the LSP are truly extracapsular, lying between the capsule and subscapularis (Fig. 26.5).

26.5 Postoperative Care Patients were immobilized in a shoulder sling for the first 6  weeks, postoperatively. During the time in the sling, isometric deltoid exercises and passive external rotation (ER) and internal rota-

The authors reported on a study cohort consisting of 100 patients [6]. There were 74 men and 26 women with a mean age of 27.5 + 10.3 years. The dominant shoulder was affected in 62 cases. The mean follow-up was 82.9 + 29.4 months. At follow-up, 86 patients had full restoration of joint stability. The mean Constant score significantly increased from mean 82.9 + 9.1 preoperatively to 88.2 + 10.3 (p 90% very promising. The underlying pathology is usually neuropraxia of the nerve leading to full recovery after a couple of weeks or some months. The initial finding is inferior humeral head subluxation on a true antero-posterior X-ray corresponding to weakness in shoulder flexion and abduction. Hypoesthesia in the area of the sensitory branch of the axillary nerve at the deltoid muscle is not always present. Neurological evaluation and follow-­up by EMG of the deltoid muscle is mandatory in order to exclude a complete and severe lesion of the nerve and its recovery over time in case of spontaneous recovery.

59.6 Literature Review Since introduction of arthroscopic techniques into fracture treatment, comparison with open procedures as gold standard must prove their reliability and validity.

783

Liao et  al. [16] compared 17 patients after ORIF with 15 patients after arthroscopic double-­ row fixation of isolated displaced greater tuberosity fractures. They found a significant longer surgical time for arthroscopic management (95 vs. 62 min) with bone union in all patients after 3  months. Functional outcome was superior in the arthroscopic group (ASES score 92 vs. 87 points, forward flexion 153° vs. 138°, and abduction 146° vs. 132°, p  DR > TS). Mean force of cyclic loading to create 5 mm of displacement and ultimate failure load were not significantly different between the suture anchor groups (SB vs DR); however, both groups were significantly superior to the TS group. The authors concluded that suture anchor constructs provide stronger fixation than screws for GT fractures. Thus, arthroscopic techniques seem to provide sufficient primary fracture stability allowing for bone union.

59.7 Summary Arthroscopic management of tuberosity fractures provides convincing functional results. Based on the principles of arthroscopic rotator cuff repair, bony avulsions of the tendons are fixed with suture anchors, usually following a double-row configuration. Arthroscopic screw fixation in solid fractures of the tuberosities is feasible, as well. Even if technically demanding, the results are satisfying, and the overall complication rate is low. An appropriate postoperative protocol has to be followed to ensure a reliable functional recovery and to avoid the most feared postoperative complication, secondary fragment displacement.

References 1. Kim E, Shin HK, Kim CH. Characteristics of an isolated greater tuberosity fracture of the humerus. J Orthop Sci. 2005;10(5):441–4. 2. Green A, Izzi J Jr. Isolated fractures of the greater tuberosity of the proximal humerus. J Shoulder Elb Surg. 2003;12(6):641–9. 3. Park SE, et  al. Arthroscopic-assisted plate fixation for displaced large-sized comminuted greater tuberosity fractures of proximal humerus: a novel surgical technique. Knee Surg Sports Traumatol Arthrosc. 2016;24(12):3892–8. 4. Lill H, et  al. All-arthroscopic intramedullary nailing of 2- and 3-part proximal humeral fractures: a new arthroscopic technique and preliminary results. Arch Orthop Trauma Surg. 2012;132(5):641–7. 5. Wafaisade A, et  al. Arthroscopic Transosseous suture button fixation technique for treatment of large anterior glenoid fracture. Arthrosc Tech. 2019;8(11):e1319–26. 6. Tauber M, et  al. Arthroscopic screw fixation of large anterior glenoid fractures. Knee Surg Sports Traumatol Arthrosc. 2008;16(3):326–32. 7. Motta P, et al. Acute lateral dislocated clavicular fractures: arthroscopic stabilization with TightRope. J Shoulder Elb Surg. 2014;23(3):e47–52. 8. Metwaly RG, Edres K. Biplanar fixation of acromio-­ clavicular joint dislocation associated with coracoid process fracture: case report. Trauma Case Rep. 2018;15:4–7. 9. Müller ME, et al. The comprehensive classification of fractures of long bones. Springer; 1990. p. 120–1. 10. Bahrs C, et al. Mechanism of injury and morphology of the greater tuberosity fracture. J Shoulder Elb Surg. 2006;15(2):140–7. 11. Mutch J, et al. A new morphological classification for greater tuberosity fractures of the proximal humerus: validation and clinical implications. Bone Joint J. 2014;96-B(5):646–51. 12. McLaughlin HL.  Dislocation of the shoulder with tuberosity fracture. Surg Clin North Am. 1963;43:1615–20. 13. Park TS, et al. A new suggestion for the treatment of minimally displaced fractures of the greater tuberosity of the proximal humerus. Bull Hosp Jt Dis. 1997;56(3):171–6. 14. van Laarhoven HA, te Slaa RL, van Laarhoven EW.  Isolated avulsion fracture of the lesser tuberosity of the humerus. J Trauma. 1995;39(5): 997–9. 15. Ogawa K, Takahashi M. Long-term outcome of isolated lesser tuberosity fractures of the humerus. J Trauma. 1997;42(5):955–9. 16. Liao W, et  al. Is arthroscopic technique superior to open reduction internal fixation in the treatment of isolated displaced greater tuberosity fractures? Clin Orthop Relat Res. 2016;474(5):1269–79.

59  Arthroscopic Management of Tuberosity Fractures

785

17. Kim SH, Ha KI. Arthroscopic treatment of symptomatic shoulders with minimally displaced greater tuberosity fracture. Arthroscopy. 2000;16(7):695–700. 18. Ji JH, et  al. Arthroscopic fixation technique for comminuted, displaced greater tuberosity fracture. Arthroscopy. 2010;26(5):600–9. 19. Tsikouris GD, et  al. Arthroscopic reduction and fixation of fractures of the greater humeral tuberosity in athletes: a case series. Br J Sports Med. 2013;47(10):e3.

20. Braunstein V, et  al. Operative treatment of greater tuberosity fractures of the humerus–a biomechanical analysis. Clin Biomech. 2007;22(6):652–7. 21. Seppel G, et  al. Single versus double row suture anchor fixation for greater tuberosity fractures–a biomechanical study. BMC Musculoskelet Disord. 2017;18(1):506. 22. Lin CL, et al. Suture anchor versus screw fixation for greater tuberosity fractures of the humerus–a biomechanical study. J Orthop Res. 2012;30(3):423–8.

Arthroscopic Management of Glenoid Fractures

60

Nestor Zurita, Pablo Carnero, Carlos Verdu, and Angel Calvo

Abstract

Keywords

Glenoid fractures represent approximately 10–20% of scapula fractures, and relatively, little is known about their mechanism, fracture pattern, and optimal treatment strategies. If untreated, displaced glenoid fractures may lead to persistent pain, malunion, development of early glenohumeral osteoarthritis, and chronic shoulder instability. It is therefore of utmost importance to properly diagnose, analyze, and treat these fractures. Computed tomography (CT) has improved the quality in the evaluation of glenoid fractures and has proven to be a very useful tool to diagnose the extent of the lesion and the relationship of the humeral head with the main fragment of the glenoid. Arthroscopic surgery has made considerable progress in the treatment of fractures of the anterior glenoid edge with a reduction in complications and reoperation rates. This arthroscopic approach is used in combination with percutaneous fixation with screws. However, it should not be forgotten that the open surgical approach is still necessary for some fractures.

Glenoid · Fracture · Treatment · Arthroscopy · Surgery

N. Zurita (*) Arthrosport, IMED Hospital, Elche, Spain P. Carnero · A. Calvo Arthrosport, Zaragoza, Spain C. Verdu Elche General Hospital, Elche, Spain

60.1 Introduction Glenohumeral (GH) joint has a great mobility but rather poor intrinsic stability, and this is determined by a relatively small surface of the glenoid joint. Iannotti et  al. [1] found that the anteroposterior dimension of the glenoid fossa had a pear or oval shape, the lower half being larger than the upper half. It was also shown that the radius of curvature of the glenoid, measured in the coronal plane, was on average 2.3  mm larger than that of the humeral head, indicating incongruity in the normal GH joint. The low depth of the glenoid cavity and its multiple morphologies also contribute to instability [2]. In this context, the stability of the glenohumeral joint is determined by the presence of a fibrous labrum, a structure that surrounds the glenoid and increases its articular surface. In addition, the ligaments of the shoulder and the rotator cuff are inserted into the humeral head to maintain stability [3]. Glenoid fractures are rare [4] and relatively little is known about their mechanism, fracture pattern, and optimal treatment strategies. Fractures of the glenoid cavity are often

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_60

787

N. Zurita et al.

788

observed in association with various patterns of shoulder instability, especially when these fractures affect the most peripheral part of the glenoid [5]. Fractures of the glenoid fossa are often associated with other injuries and are the result of closed trauma or high-speed sports injuries where the humeral head impact heavily on the glenoid fossa [6]. If untreated, displaced glenoid fractures may lead to persistent pain, malunion, development of early glenohumeral osteoarthritis, and chronic shoulder instability. It is therefore of utmost importance to properly diagnose, analyze, and treat these fractures. Limited studies on glenoid fractures make diagnosis and treatment rather difficult. However, management of these fractures is progressively evolving with the improvement of image quality, the development of new classification systems, and advanced surgical techniques. In this context, it is important to highlight that non-surgical treatment is included in the current options for the treatment of glenoid fractures.

60.2 Pathophysiology Glenoid fractures represent approximately 10–20% of scapula fractures [7]. Glenoid avulsions and rim injuries are more common and usually occur in association with an anterior shoulder dislocation and generally do not require a great impact to occur, as commonly happens in sports injuries or low-impact trauma. In this line, avulsions and fractures of the rim can also be secondary to high traction in the capsule-labral-ligament complex secondary to indirect force or to external force in abduction rotation [6]. Scapular fractures, including the glenoid fossa, are secondary to high-energy trauma and are often associated with other injuries [8]. The fracture mechanism is not always clear, but glenoid fractures are mostly observed after a direct impact of the humeral head onto the glenoid fossa. These fractures are typically transverse and occur along the direction of force impact [6].

60.3 Classification Existing classification systems are purely descriptive without therapeutic implications. They are based on the mechanism of injury, the location, and severity of the fracture pattern. In addition, none of them provide prognostic information about fractures, except the location and severity of the fracture pattern that are prognostic for GH instability [9]. The most commonly used classification system for this type of fracture has been performed based on intra-articular fracture patterns published by Ideberg in 1995 [10]. This classification was only developed on the basis of standard radiographs and was later modified by other authors, such as Goss [7] and May [11]. This classification identifies six main fracture patterns (Table 60.1 and Fig. 60.1). Classifications based on the radiographic examination are not very useful for describing the fracture and the degree of displacement. Computed tomography (CT) has improved the quality in the evaluation of glenoid fractures and has proven to be a very useful tool to assess fracture pattern, the extent of the injury, and the relationship of the humeral head with the main fragment of the glenoid [4]. Particularly, three-­ dimensional (3D) analysis is useful to accurately assess fractures that involve the glenoid fossa (Fig. 60.2). Isolated glenoid fossa fractures were first classified by Bigliani et  al. in 1998 [12]. The authors identified four types, depending on the binding to the capsule and the size of the fragment Table 60.1 Ideberg classification of glenoid fossa fractures as modified by Goss [7] Type Ia Type Ib Type II Type III Type IV Type Va Type Vb Type Vc Type VI

Anterior rim fracture Posterior rim fracture Fracture line through glenoid fossa exiting scapula laterally Fracture line through glenoid fossa exiting scapula superiorly Fracture line through glenoid fossa exiting scapula medially Combination of types II and IV Combination of types III and IV Combination of types II, III, and IV Severe comminution

60  Arthroscopic Management of Glenoid Fractures

Fig. 60.1  Ideberg classification of glenoid fossa fractures as modified by Goss [7] (Reproduced with permission from Lasanianos, N.G., Panteli, M. (2015). Glenoid

789

Fractures. In: Lasanianos, N., Kanakaris, N., Giannoudis, P. (eds) Trauma and Orthopaedic Classifications. Springer, London. https://doi.org/10.1007/978-­1-­4471-­6572-­9_5)

Table 60.2 Bigliani classification of glenoid fossa fractures [12] Type I

Displaced avulsion fracture with attached capsule Type II Medially displaced fragment malunited to the glenoid rim Type Erosion of the glenoid rim with less than 25% IIIA Type Erosion of the glenoid rim greater than 25% IIIB Table 60.3 AO/OTA classification for glenoid fossa fractures

Fig. 60.2  CT Three-dimensional (3D) analysis where the characteristics of the glenoid fracture and associated bone injuries are observed with precision

(Table  60.2). In fractures of the glenoid edge, Bartoníček et al. [13] suggested a modified version based on the size of the avulsed fragment, the course of the fracture line, and the location of the fragment.

Scapula: 14; Glenoid fossa: F 14F0 Extra-articular fracture running along the glenoid neck 14F1 Intra-articular simple fracture 14F1.1 Anterior rim fractures 14F1.2 Posterior rim fractures 14F1.3 Transverse fractures 14F2 Intra-articular multifragmentary fractures 14F2.1 Glenoid fossa fractures 14F2.2 Central fracture dislocation

In 2012, the AO Foundation developed a comprehensive classification of scapular fractures with three main groups described based on anatomical parts [14]. The glenoid is one of these parts and includes extra-articular and intra-­ articular fractures (Table 60.3). This ­classification

N. Zurita et al.

790

system has been validated by Harvey et al. [15] and has been found reliable for simple radiographs and especially when CT is used.

60.4 Diagnosis Accurate history is essential to help determining the mechanism of injury. The physical exam includes an exam of the humerus, clavicle, scapula, and shoulder joint. The range of active and passive movement, strength, and neurovascular

status should be evaluated. Ecchymosis is, among the clinical findings, the one that has the highest correlation with a glenoid fracture. Signs such as pain and an alteration of the range of movement of the shoulder are also present [16]. Scapular fractures may be diagnosed using plain radiographs (Fig.  60.3); combination of true anteroposterior (scapular plane) and axillary views provide the best view of the glenoid fossa [6]. CT scan is very useful to define the fracture (Fig. 60.4), assess the extent of the injury, as well as its displacement, and establish the relationship of the humeral head with the glenoid fossa [17].

60.5 Surgical Technique

Fig. 60.3 Anteroposterior X-ray image of the left shoulder with comminuted scapula fracture that includes the glenoid

a

b

Fig. 60.4  Coronal (3a) and axial (3b) view of different types of glenoid fracture. The morphological characteristics of the fracture can be observed, as well as its relation-

Arthroscopic surgery has made considerable progress in the treatment of fractures of the anterior glenoid edge with a reduction in complications and reoperation rates [18]. This arthroscopic approach is used in combination with percutaneous fixation with screws. For glenoid fractures that involve less than 21% of the joint area, several arthroscopic procedures using suture anchors or transcutaneous screws have been established in recent years. In the case of fractures of the glenoid fossa, the introduction of arthroscopically assisted treatment has been described for an Ideberg type I pattern, or a fracture of the lower anterior glenoid [10]. Type III and IV patterns are also c

ship with the humeral head. The 3D images (3c) give us a very interesting vision of the joint set

60  Arthroscopic Management of Glenoid Fractures

now treated routinely. Using arthroscopic techniques [19]. However, it should not be forgotten that the open surgical approach is still necessary for some fractures. Traditionally, an anatomical and concentric joint restoration should be the goal of surgical treatment for a better functional outcome [20]. As general indications of treatment, it can be established that avulsion fractures of less than 5 mm and stable can be treated conservatively with immobilization. However, unstable or displaced fractures with poor alignment with the head of the humerus are usually indication of surgical stabilization to avoid poor results such as malunion and/or instability [6]. In any case, fractures that affect more than 25% of the lower diameter of the glenoid cavity should be repaired due to the high risk of dislocation [21]. More recent studies support the need to repair glenoid defects of more than 15% [22]. Yamamoto and Itoi [23], in a biomechanical study, identified a critical point for GH stability in a glenoid defect greater than 21%. In this context, it can be asserted that the indications for surgical treatment of glenoid fractures may increase in the future due to the development of new techniques of arthroscopic fixation. The surgery can be performed both in a beach chair (Fig.  60.5) and in lateral decubitus (Fig. 60.6). Basically, three portals are created: a standard posterior portal, a superior and anterior portal, through the rotator interval, and an anterior portal superior to the subscapular (Fig. 60.7). Depending of the moment during surgery, the portals can be used as viewing or working portals. After performing a characteristic arthroscopic diagnostic path, we will look for the main bone fragment that is usually found in the capsule-­ labral complex at the medial and inferior levels (Fig. 60.8). We can use different instrumentation to raise and reduce the fragment from the anterior superior portal. Subsequently, the glenoid surface is prepared to obtain a bleeding surface and facilitate the consolidation of the bone fragment (Fig. 60.9).

791

Fig. 60.5  Beach chair position

Fig. 60.6  Lateral decubitus position

Fig. 60.7  These portals can be used in a standardized way both in the beach chair position and in the lateral decubitus position. We can use accessory portals according to the needs of the surgery

792

N. Zurita et al.

Fig. 60.8  Arthroscopic image of the right shoulder with vision located in the anterosuperior portal where a glenoid fracture is observed with the main fragment attached to capsulolabral structures

Fig. 60.10  View from the anterosuperior portal in the right shoulder where a Kirschner wire is observed through an accessory anterior portal introduced for the fixation of the bone fragment once reduced

Fig. 60.9  Arthroscopic vision from the anterosuperior portal during motorized osteoplasty of the glenoid to obtain a bleeding surface that facilitates bone healing

Fig. 60.11 Cannulated screw placement through the Kirschner wire after reduction of the glenoid fragment

For the fixation of the bone fragment, cannulated screws or suture anchors can be employed following the technique described by Sugaya [24]. During the performance of the osteosynthesis technique with cannulated screws, the glenoid fragment is fixed by K-wires once reduced. The

K-wires should go parallel to the glenoid surface. Therefore, it is necessary to create an anterior accessory portal located about 2 cm medial to the conventional anterior portal that usually crosses the subscapular tendon (Fig. 60.10). Cannulated AO screws are used for the synthesis (Fig. 60.11). The number of screws will depend on the size of the glenoid bone fragment. Ideally, the technique should be done with two

60  Arthroscopic Management of Glenoid Fractures

793

Fig. 60.12  We perform an adequate liberation of the bone fragment that is generally attached to capsulolabral structures. After obtaining a bleeding surface of the glenoid, we reduce the fragment whose fixation we carried

out through anchors, always starting from the lowest one. We will place a number of anchors according to the magnitude of the injuries. The final vision must reproduce the normal arrangement of the joint

screws; in case of using a single fixation point, it is useful to place a second K-wire temporarily to stabilize the fragment and avoid its rotation during the introduction of the screw. In the technique of Sugaya [24], once the bone fragment has been reduced and the glenoid prepared, we will place a variable number of anchors starting with the lowest one. The guide for the placement of the anchors is introduced through the anteroinferior portal. We can help each other with a clamp through the anterosuperior portal to maintain the reduction by pulling the labrum while passing the sutures and maintaining the

vision from the posterior portal. After the placement of the sutures, we will check the final reduction (Fig. 60.12).

60.6 Postoperative Care After surgery, most of the studies and clinical guidelines recommend an immobilization period of 4.8 ± 1.8 weeks [25]. There is no scientific evidence on the proper position of immobilization [26]. It must be maintained the whole day except for activities such as personal hygiene and to

N. Zurita et al.

794

on the activity they wish to achieve. In this line, there are specific programs based on the requirements of each activity to get the normalization of strength, endurance, neuromuscular control, and power. In this way, we obtain a gradual return to activities of daily life, work, and recreational and/or sports activities [30].

60.7 Summary The development of the possibilities of arthroscopic fixation results in an increase in the surgical indications of this technique that allows repairs of increasingly complex glenoid fractures. In addition, good clinical and radiological results after arthroscopic repair of large fragments and displaced glenoid fossa fractures and displaced glenoid neck fractures have been described in the literature.

References Fig. 60.13  In the lower image, a retracted scapular position is observed after the contraction of the periscapular muscles

p­ erform exercises with restricted and progressive ranges of mobility that are safe and that protect the osteosynthesis effectuated [27]. When the immobilization period ends, it can begin with passive mobility associating active mobility that it can be started as required in all planes [28]. It is important to take into account the scapulo-­ thoracic limitations. Thus, the rehabilitation program should be focused to allow working with the scapula in a retracted position (Fig.  60.13), starting with stretching exercises. Later, with a stable scapular base, where the activation of the periscapular muscles is more effective, carry out strengthening exercises that involve the entire kinetic chain [29]. The recovery of complete muscle strength and the re-education of the mobility pattern (in the case of athletes) must be performed individually according to the goals of each patient depending

1. Iannotti JP, Gabriel JP, Schneck SL, Evans BG, Misra S. The normal glenohumeral relationships. An anatomical study of one hundred and forty shoulders. J Bone Joint Surg Am. 1992;74-A:491–500. 2. Gilbert F, Eden L, Meffert R, Konietschke F, Lotz J, Bauer L, Staab W. Intra- and interobserver reliability of glenoid fracture classifications by Ideberg, Euler and AO. BMC Musculoskelet Disord. 2018;19(1):89. 3. Van Oostveen DP, Temmerman OP, Burger BJ, van Noort A, Robinson M. Glenoid fractures: a review of pathology, classification, treatment and results. Acta Orthop Belg. 2014;80(1):88–98. 4. Armitage BM, Wijdicks CA, Tarkin IS, et  al. Mapping of scapular fractures with three-­dimensional computed tomography. J Bone Joint Surg Am. 2009;91-A:2222–8. 5. Surace PA, Boyd AJ, Vallier HA. Case series evaluating the operative and nonoperative treatment of scapular fractures. Am J Orthop. 2018;47(8):ajo.2018.0067. 6. Zamani A, Sharifi MD, Farzaneh R, Disfani HF, Kakhki BR, Hashemian AM.  The relationship between clinical findings of shoulder joint with bone damage of shoulder joint in patients with isolated shoulder blunt trauma. Open Access Maced J Med Sci. 2018;6(11):2101–6. 7. Goss TP.  Fractures of the glenoid cavity. JBJS. 1992;74(2):299–305. 8. Südkamp NP, Jaeger N, Bornebusch L, Maier D, Izadpanah K.  Fractures of the scapula. Acta Chir Orthop Traumatol Cechoslov. 2011;78(4):297–304.

60  Arthroscopic Management of Glenoid Fractures 9. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82-A:35–46. 10. Ideberg R, Grevsten S, Larsson S.  Epidemiology of scapular fractures. Incidence and classification of 338 fractures. Acta Orthop Scand. 1995;66:395–7. 11. Mayo KA, Benirschke SK, Mast JW.  Displaced fractures of the glenoid fossa. Results of open reduction and internal fixation. Clin Orthop Relat Res. 1998;347:122–30. 12. Bigliani LU, Newton PM, Steinmann SP, Connor PM, Mcllveen SJ.  Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med. 1998;26:41–5. 13. Bartoníček J, Kozánek M, Jupiter JB. Early history of scapular fractures. Int Orthop. 2016;40:213–22. 14. Jaeger M, Lambert S, Südkamp NP, et  al. The AO Foundation and orthopaedic trauma association (AO/ OTA) scapula fracture classification system: focus on glenoid fossa involvement. J Shoulder Elb Surg. 2013;22:512–20. 15. Harvey E, Audigé L, Herscovici D Jr, et  al. Development and validation of the new international classification for scapula fractures. J Orthop Trauma. 2012;26:364–9. 16. Varacallo M, Mair SD.  Rotator cuff tendonitis. StatPearls; 2019. 17. Königshausen M, Coulibaly MO, Nicolas V, Schildhauer TA, Seybold D. Results of non-operative treatment of fractures of the glenoid fossa. Bone Joint J. 2016;98-B:1074–9. 18. Maruvada S, Varacallo M.  Anatomy, rotator cuff. StatPearls; 2018. 19. Yang HB, Wang D, He XJ.  Arthroscopic-assisted reduction and percutaneous cannulated screw fixation for Ideberg type III glenoid fractures: a minimum 2-year follow-up of 18 cases. Am J Sports Med. 2011;39:1923–8. 20. Jones CB, Cornelius JP, Sietsema DL, Ringler JR, Endres TJ. Modified Judet approach and minifragment

795 fixation of scapular body and glenoid neck fractures. J Orthop Trauma. 2009;23:558–64. 21. Burkhart SS, De Beer JF.  Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs. Arthroscopy. 2000;16(7):677–94. 22. Bonnevialle N, Clavert P, Arboucalot M, Bahlau D, Bauer T, Ehlinger M, et  al. Contribution of arthroscopy in the treatment of anterior glenoid rim fractures: a comparison with open surgery. J Shoulder Elb Surg. 2019;28(1):42–7. 23. Yamamoto N, Itoi E. Osseous defects seen in patients with anterior shoulder instability. Clin Orthop Surg. 2015;7:425–9. 24. Sugaya H, Kon Y, Tsuchiya A. Arthroscopic repair of glenoid fractures using suture anchors. Arthroscopy. 2005;21(5):635. 25. DeFroda SF, Mehta N, Owens BD. Physical therapy protocols for arthroscopic Bankart repair. Sports Health. 2018;10(3):250–8. 26. Whelan DB, Kletke SN, Schemitsch G, Chahal J. Immobilization in external rotation versus internal rotation after primary anterior shoulder dislocation: a meta-analysis of randomized controlled trials. Am J Sports Med. 2016;44(2):521–32. 27. McEleney ET, Donovan MJ, Shea KP, Nowak MD. Initial failure strength of open and arthroscopic Bankart repairs. Arthroscopy. 1995;11(4):426–31. 28. Harryman DT 2nd, Sidles JA, Clark JM, McQuade KJ, Gibb TD, Matsen FA 3rd. Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am. 1990;72(9):1334–43. 29. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of 127 pathology part III: the SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy. 2003;19:641–61. 30. Chang ES, Bishop ME, Baker D, West RV.  Interval throwing and hitting programs in baseball: biomechanics and rehabilitation. Am J Orthop (Belle Mead NJ). 2016;45(3):157–62.

Outcome Measurement Tools for Functional Assessment of the Shoulder

61

Justin D. Khoriaty and Warren R. Dunn

Abstract

The impact of shoulder injuries and treatments on patients is mostly measured during the clinical evaluation. Initially, simple questions inquire about pain, other symptoms, influence on function, and treatment satisfaction. Next, a physical examination assesses the shoulder’s range of motion, strength, and stability before performing different provocative maneuvers evaluating for different pathologies. Finally, diagnostic imaging data are obtained and appraised first for injuries and deformity, and then later for signs of healing and prosthetic alignment and stability. The physician deciphers through all the clinical information to evaluate how the shoulder pathology is affecting the patient, determine treatment, and then gauge the effectiveness of their treatment on the patient. Keywords

Rotator cuff · Minimal clinically important difference · Constant score · Rotator cuff repair · Western Ontario Rotator Cuff

J. D. Khoriaty · W. R. Dunn (*) Fondren Orthopedic Research Institute (FORI), Houston, TX, USA

61.1 Introduction The impact of shoulder injuries and treatments on patients is mostly measured during the clinical evaluation. Initially, simple questions inquire about pain, other symptoms, influence on function, and treatment satisfaction. Next, a physical examination assesses the shoulder’s range of motion, strength, and stability before performing different provocative maneuvers evaluating for different pathologies. Finally, diagnostic imaging data are obtained and appraised first for injuries and deformity, and then later for signs of healing and prosthetic alignment and stability. The physician deciphers through all the clinical information to evaluate how the shoulder pathology is affecting the patient, determine treatment, and then gauge the effectiveness of their treatment on the patient. This modality of physician-based outcome measurements has demonstrated some inconsistent results. A study comparing self-reported and observer-reported disability in an orthopedic trauma population found that disability level rating varied greatly, with observers consistently rating disability levels lower than participants [1]. Two other studies evaluating anterior cruciate ligament reconstruction one-year postoperatively found the patients’ ratings of satisfaction, activity level, and function on their self-­ administered questionnaire to be significantly lower than the surgeons’ rating after patient

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_61

797

798

­interviews [2, 3]. Indeed, whenever an observer questions a patient with regard to function and then records a response, the possibility of observer bias is introduced [4]. In addition, several studies have demonstrated unreliable results in “objective” measures such as range of motion [5–8], rotator cuff function tests [9], and shoulder instability tests [10]. Such “objective” measures correlate poorly with patient satisfaction when compared with outcome measures that focus on subjective symptoms and function [11]. Overall, physician-directed outcome measures have inherent biases and inconsistencies that adversely affect their results, as well as ignore or marginalize the patients’ perspective. Patient-directed outcome measures focus mostly on domains that directly impact the health and quality of life of the patient. These domains include pain and physical symptoms, sports and recreational function, occupational function, mental health, social issues, emotional issues, and impact on general health. As the health care system of the twenty-first century continues to evolve, the utilization of these outcome measures is becoming increasingly important. Progressively more focus is being placed on health care interventions in terms of their effectiveness, their impact on the general health of patients, and their overall cost-effectiveness. Consequently, the use of patient-directed outcome measures that can evaluate these criteria are increasing in the orthopedic literature [12], with some publications making their inclusion a requirement [13]. Furthermore, the orthopedic community has placed emphasis on the utilization of these outcome measures in clinical practice as well as research [14].

61.2 Categories of Shoulder Outcome Measures There are a multitude of different shoulder outcome measures available for patient evaluation, each with specific strengths and weaknesses. These shoulder instruments can be subdivided into two broad categories: general health outcome measures and shoulder-specific outcome

J. D. Khoriaty and W. R. Dunn

measures. Improvements in the development and utilization of these measures have resulted in an increased and improved number of tools. Consequently, outcome measures assessing the shoulder can be further sub-divided into limb-­ specific outcome instruments, joint-specific outcome instruments, and disease-specific outcome instruments (Table 61.1). General health outcome measures appraise the impact of any medical condition on general health, including physical, mental, and emotional parameters. Its utilization across different medical disciplines allows shoulder pathologies to be compared to other major medical conditions, such as hypertension, congestive heart failure, acute myocardial infarction, diabetes mellitus, and clinical depression [15]. However, its broad multidisciplinary application lacks content specific to the shoulder and upper extremity, so changes to shoulder function may go undetected. Additionally, general health outcome scores tend to be affected more by lower extremity function than upper extremity function [13]. Because the upper extremity operates as part of the kinetic chain, its function is predicated by the concerted effort of the shoulder, elbow, wrist, and hand. Thus, any ailment affecting one of these joints will have an impact on upper extremity function. Limb-specific outcome instruments evaluate the influence of a single or multiple disorders of the upper limb on physical function, symptoms, and psychosocial issues. These types of questionnaires are specially designed to better detect changes in upper extremity function when compared with general health outcome instruments. Additional advantages include its utilization when more than one part of the upper extremity is involved, or when the diagnosis is less certain. The evaluation of limb-specific instruments has found a close correlation with general health, joint-specific, and condition-­ specific outcome measures; however, they are less sensitive to changes in shoulder function compared with joint-specific and condition-­ specific instruments [4, 12, 16]. Joint-specific and condition-specific outcome measures concentrate on factors directly related to the shoulder or a particular condition of the

61  Outcome Measurement Tools for Functional Assessment of the Shoulder

799

Table 61.1  Categories of outcome measures to evaluate the shoulder Category General health

Definition Evaluate the impact of any medical condition on physical, mental, and emotional aspects of general health

Limb-­ specific

Evaluates the physical function, symptoms, and psychosocial factors of a single or multiple disorders of the upper extremity

Joint-­ specific

Questionnaires specific to shoulder symptoms, function, and their impact on different activities

Condition-­ Assess specific conditions specific to the shoulder

Advantages Disadvantages Examples • Determines impact on • Outcome scores Medical outcomes quality of life affected more by lower 36-item short form • Allows comparison of extremity function than (SF-36) different diseases and upper extremity Medical outcomes conditions across a function 12-item short form medical spectrum • Limited responsiveness (SF-12) to changes in shoulder Patient-reported function outcomes measurement information system (PROMIS) • More specific • Less responsive than Disabilities of the questionnaires to shoulder-specific or arm, shoulder, and upper extremity than condition-specific hand (DASH) general health measures QuickDASH outcome instruments • Evaluation of a single or multiple disorders • Useful if diagnosis to upper extremity unknown • Allows comparison between different upper extremity conditions • More sensitive than • Less able to evaluate American shoulder general health and effect on overall health and elbow surgeons limb-specific outcome • Unable to compare (ASES) measures outcome across Constant-Murley different conditions, simple shoulder test populations or interventions • Most sensitivie to • Limited usefulness in Western Ontario small changes in the comparing outcomes rotator cuff index condition being across different (WORC) evaluated disorders, anatomic Western Ontario sites, and population shoulder instability • Need several outcome index (WOSI) measures to assess all Western Ontario conditions affecting the osteoarthritis of the shoulder shoulder index (WOOS) Rotator cuff: quality-of-life (RCQOL)

shoulder, respectively. These specialized questionnaires are best able to detect small changes in shoulder function, with condition-specific outcome measures being the most sensitive to small changes in the condition for which they were designed. However, as these questionnaires become more specific toward a particular joint or pathology, they become less valuable in apprais-

ing overall health and function, especially the more mental and emotional aspects. Also, the evaluation of a narrowed patient population prevents comparisons between different conditions, anatomic sites, and interventions. A general health outcome measure should always be included as part of the patient evaluation because of its ability to evaluate the impact

J. D. Khoriaty and W. R. Dunn

800

of a shoulder condition or treatment on the overall health of a patient. In addition, the instrument’s ability to compare a shoulder condition to other systemic diseases is an advantage. Because of its limited upper extremity content, the clinical evaluation of a shoulder patient should also include either a limb-specific or joint-specific outcome measure. The addition of a condition-­ specific outcome measure is usually only needed for research purposes, in which a very specific patient population is being evaluated.

61.3 Measurement Properties of Outcome Measures Once the appropriate categories of shoulder outcome measures have been decided, the next step is determining which specific outcome measure to employ. With over forty different instruments for functional assessment of the shoulder, several factors are involved in the decision-making process of which outcome measurement tool to use. Each unique measure has specific strengths depending on the population being assessed and the reason for using the instrument. An outcome measurement tool must be context-specific, and selection should be based on evidence that the instrument has the necessary measurement properties in the population being sampled for a study or assessment. The quality of an outcome measure can be assessed objectively and given the plethora of outcome measures that have been developed, it is advisable to use an outcome measure for which there are data on its measurement properties. The measurement properties of an outcome measure that are important to clinicians are reliability, validity, responsiveness, and level of measurement (Table 61.2). Reliability describes the repeatability of an outcome score taken at different settings from patients with a stable condition. Shoulder outcome instruments should be sufficiently reliable such that the score derived from the instrument does not change if the patient’s clinical problem has remained the same, even if the questionnaire is completed on different occasions. Quantifying this measurement property is accomplished

through test-retest analysis, in which individuals complete the same questionnaire on more than one occasion and the difference in scores is statistically analyzed [17]. Most problems with test-­ retest reliability occur because of the wording of the items, and as such there is sometimes difficulty when a questionnaire is developed in one country and used in another [18]. Moreover, some patients with certain conditions have problems with consistency in their questionnaires [19]. Therefore, an outcome measure can only be considered reliable for the specific condition evaluated. Validity is the degree to which an outcome score accurately reflects or assesses the condition being measured [17, 20]. Validity has several different facets, and thus cannot be appraised by a single statistic, instead requiring a body of evidence demonstrating a relationship between the true functional status of the patient and the score Table 61.2  Measurement properties of outcome measurement tools Property Reliability

Validity

Responsiveness

Level of measurement

Computerized adaptive testing

Definition An outcome instrument generating similar scores for a patient with a stable condition. The accuracy of an instrument regarding the impairment of a patient’s condition.

Examples Test-retest reliability

Face validity Content validity Criterion-­ related validity Construct validity The ability of an Minimal instrument to detect a clinically change in a patient’s important condition. difference Ceiling effect Floor effect The measurement Yes-or-no scales used for Likert scale responses to the Visual questionnaires. analog scale Computer-based ASES CAT testing where PROMIS PF questions are adapted CAT to individuals based on prior answers

61  Outcome Measurement Tools for Functional Assessment of the Shoulder

obtained from the instrument. Face validity is the degree to which a test appears to measure what it is intended to measure. The extent to which an outcome measure covers all the important domains of the condition being measured is referred to as content validity. An outcome measure evaluating shoulder instability would lack content validity without questions regarding apprehension and overhead activity. Both face validity and content validity are considered lower levels of validity, as they cannot be examined experimentally and can only be evaluated subjectively. The higher forms of validity, namely ­criterion and construct, can be objectively examined with different statistical measures. Criterion-­ related validity compares the accuracy of the instrument to a gold standard or another outcome score that has been previously validated for the specific condition. Construct validity assesses the instrument’s ability to measure the underlying concept of interest [17, 20]. Shoulder outcome measures with construct validity demonstrate scores that compare with patient-derived and physician-derived assessments of the severity of the shoulder impairment, the level of pain, the ability to perform normal activities of daily living, and responses to other contemporary patient-­ completed questionnaires [4]. Collectively, evidence demonstrating that an outcome measure has validity for a specific shoulder condition indicates the resultant score will yield an accurate account of its impact on a patient’s symptoms and function. The ability of an outcome measurement tool to detect a true change in a patient’s condition defines responsiveness [21]. One of the primary roles of an outcome instrument is to evaluate the changes in the condition of patients following different therapy modalities. As such, several authors believe that responsiveness is the most important property of an outcome tool. Responsiveness is calculated by defining a cohort of patients whose health condition has changed between testings. The minimal clinically important difference (MCID) of an outcome measure is the minimum change in a score that indicates a change in disability. An understanding of MCID is critical for

801

an accurate appraisal of orthopedic literature, as well as when selecting appropriate instruments for research. A statistically significant improvement in an outcome score following a certain therapy would not be clinically significant if the improvement is not greater than the MCID.  Therefore, when deciding between outcome measures, the smaller the MCID, the more sensitive the instrument in picking up small changes in a patient’s outcome. Additionally, outcome measures may have ceiling or floor effects, which would adversely affect the responsiveness of the instrument. The ceiling effect occurs when patients score so high on the scale that improvements in their impairments cannot be detected. The floor effect occurs when patients score so low on the scale that declines in their disability cannot be detected. The potential for ceiling or floor effects, together with MCID, are important properties when evaluating outcome instruments as measures of change in a patient’s condition. Outcome measurement tools utilize different levels of measurement, or measurement scales, in their questionnaires. Among shoulder outcome measures, responses to questions can be yes-or­no answers, Likert scales or visual analog scales. With increasing complexity to the response methodology, the more difficult the questionnaire is to complete by the patient and to be analyzed by the clinician. However, these more complex modalities allow for an improvement in the responsiveness of the instrument [4]. Yes-or-no answers limit the number of possible responses by the patient, making completing and analyzing the questionnaire relatively easy, but also limiting the instrument’s responsiveness (Fig.  61.1A). The Likert scale is an ordinal scale of responses to a question or statement ordered in a hierarchical sequence (Fig.  61.1B). The number of responses can vary from two responses to seven, but typically has four or five responses. The increasing complexity adds to the instrument’s responsiveness but may be more difficult for patients to complete and for the clinician to analyze. Finally, the visual analog scale displays a scale as a straight line without any discrete choices, differentiating it from the Likert scale

J. D. Khoriaty and W. R. Dunn

802

61.4 Computerized Adaptive Testing

A. Are you satisfied with the results of your shoulder surgery? Yes

No

B. Please rate your level of satisfaction regarding your shoulder surgery. Excellent

Good

Fair

Poor

C. Please rate your level of satisfaction regarding your shoulder, with 0 being completely unsatisfied, and 100 being completely satisfied

0 Completely Unsatisfied

100 Completely Satisfied

Fig. 61.1  Measurement scales in shoulder outcome measurement tools. (A) Yes-or-no scale. (B) Likert scale. (C) Visual analog scale. The same question with different responses increases the responsiveness of the item, but also increases the complexity for the patient answering the question and the clinician quantifying the answers

(Fig.  61.1C). Patients respond to questions by indicating a position along a continuous line in between two end-points. Evidence has shown that a visual analog scale has superior metrical characteristics than discrete scales, thus a wider range of statistical methods can be applied to the measurements [22]. As illustrated with the levels of measurements, increasing the complexity of the questionnaire can increase the level of data and information obtained. However, it also increases the difficulty from both the physician and patient perspective. The evaluation process for outcome ­measurement instruments needs to be based on both the measurement properties of the outcome score, as well as the practicality of the questionnaire. Given the increasing paperwork demands being placed on both patients and physicians, the administration of these questionnaires needs to be feasible for both parties. From the patient’s perspective, the questionnaire needs to be easy to understand, simple to answer, and not too time-­consuming. Different factors the physician must account for include the time required to administer and score the questionnaire, the potential training or staff required to manage the outcome scores, and the availability of normative data. These factors can establish whether an outcome measurement tool is seamlessly integrated into a clinical practice, or inundates it with increasing workload and more paperwork.

Computerized Adaptive Testing (CAT) is a form of computer-based testing whereby the patient takes a test, and the computer then tailors the test to that individual based on responses already provided thus eliminating redundant or irrelevant questions [98]. This is designed to increase the efficiency of gathering data while maintaining validity and responsiveness of the testing modality. For example, the American Shoulder and Elbow Surgeons (ASES) Outcome Score had the question burden decreased by 40% while maintaining score integrity [103]. Likewise, DASH and QuickDASH scores showed a similar ability to decrease question burden with CAT while maintaining score integrity [104]. In patients undergoing primary total shoulder arthroplasty, PROMIS PF CAT decreases question burden on patients and has no ceiling effects, increasing the usefulness of the measurement tool [105].

61.5 General Health Outcome Measurement Tools 61.5.1 Medical Outcomes Study 36-Item Short Form (SF-36) The medical outcomes study 36-item short form (SF-36) is the most popular general health outcome measure [23]. It is a shortened version of a 149 validated health-related questionnaire originally reported as part of a medical outcomes study of more than 22,000 patients [24]. The questionnaire consists of 35 items in eight health domains and one general overall health status question that assesses the patient’s perception of changes in health (Table  61.3). The SF-36 is designed to be a self-administered paper or computer questionnaire, taking an average of 5 to 10 min to complete. Each health domain is scored from 0 (worst possible health, severe disability) to 100 (best health, no disability), with normative population data available for comparison [25]. An alternative scoring system consolidates these

General health Limb-­ specific Joint-­ specific

Limb-­ specific

DASH

Category General health

PROMIS

Outcome instrument SF-36

Upper extremity disorders

General health Physical health Mental health

Target population All medical disciplines Health domains Physical functioning General health Emotional well-being Vitality Physical role Emotional role Pain Social functioning Varies depending on Physical functioning system being General health measured Emotional well-being Vitality Physical role Emotional role Pain Social functioning 30 Physical function (+8 optional) Symptoms Social/role function Work activities (optional) Sport/music activities (optional)

Items/Time to administer 31

Table 61.3  Outcome measurement instruments for functional assessment of the shoulder

Likert scale

Likert scale

Measurement scale Primarily Likert scale, also yes-or-no scale

100 to 0

0 to 100

Score (worst to better) 0 to 100

(continued)

Different for each system being examined

10.2 18–65 yo Glenohumeral osteoarthritis Rotator cuff tendonitis Total shoulder arthroplasty Rotator cuff repair Psoriatic arthritis

Yes

Validated parameters Yes

Minimal clinically important difference Not defined

61  Outcome Measurement Tools for Functional Assessment of the Shoulder 803

Joint-­ specific

Joint-­ specific

Joint-­ specific

Joint-­ specific

ASES

SPADI

SST

Category Joint-­ specific

Constant

Outcome instrument UCLA

Table 61.3 (continued)

Shoulder disorders

Shoulder disorders

Shoulder disorders

Shoulder disorders

Target population Shoulder disorders

12

13

10

8 items (6 clinician-based, 2 patient-based)

Items/Time to administer 5 items (3 patient-based, 2 clinician-based)

Likert scale

Pain function Range of motion

Yes-or-no scale

Visual analog scale Pain Activities of daily living

Pain Instability Activites of daily living

Health domains Measurement scale Likert scale Pain function Forward flexion Motion Forward flexion Strength Patient satisfaction Likert scale Pain Activities of daily living Range of motion Strength

0 to 100

100 to 0

0 to 100

0 to 100

Score (worst to better) 00–35

14–85 yo General shoulder patient RCR, Adhesive capsulitis, prox humerus fx 20–81 yo General shoulder patient Rotator cuff disease Glenohumeral osteoarthritis Shoulder instability Shoulder arthroplasty General shoulder patient Rotator cuff disease Glenohumeral osteoarthritis Glenohumeral rheumatoid arthritis Adhesive capsulitis Total joint arthroplasty General shoulder patient Glenohumeral osteoarthritis Rotator cuff disease

Validated parameters Not validated

17.1–25.0

8–13

6.4

Not determined

Minimal clinically important difference Not determined

804 J. D. Khoriaty and W. R. Dunn

Joint-­ specific

Joint-­ specific Condition-­ specific

Condition-­ specific

Condition-­ specific

Condition-­ specific

SANE

Shoulder activity level WOOS

WOSI

WORC

RCQOL

Rotator cuff tears

Rotator cuff tears

Shoulder instability

Shoulder disorders Osteoarthritis

Shoulder disorders

34

21

21

19

7

1

Shoulder percentage of normal Five different functional tasks Pain and physical symptoms Sports, recreation, and work Lifestyle function Emotional function Physical symptoms Sports, recreation, and work Lifestyle emotions Pain and physical symptoms Sports and recreation Work function Social function Emotional function Symptoms and physical complaints Sports and recreation Work Lifestyle Social issues Emotional issues Visual analog scale

Visual analog scale

Visual analog scale

Visual analog scale

Likert scale

0 to 100

2100 to 0

2100 to 0

1900 to 0

0 to 20

0 to 100

25–83 yo Rotator cuff disease

Rotator cuff disease

Shoulder instability

OA, TSA

RCR, OA, instability

Not determined

245.26

220

Not determined

Not determined

All shoulder diagnoses 15

61  Outcome Measurement Tools for Functional Assessment of the Shoulder 805

806

eight health domains into two components, a physical component summary (PCS) and a mental component summary (MCS) score. No single, total score is quantified for the SF-36. A scoring manual is available for the SF-36 that provides information regarding its measurement properties and provides normative data for the eight health domains and two component summary subscales [25]. A multitude of studies have demonstrated a high level of reliability among patients with similar medical conditions [26, 27], as well as validity across a wide number of medical disciplines [13]. Validation studies have found the SF-36 able to differentiate psychiatric and physical illnesses, as well as discriminate several major medical illnesses from moderately ill or healthy individuals [25, 28]. However, the SF-36 is limited in its responsiveness, with limited data describing the instrument’s ability to detect changes in clinical status on all eight subscales of the questionnaire [29]. The SF-36 has been employed in a number of different ways for the functional assessment of the shoulder. One main advantage of the SF-36 is its ability to determine the impact of a condition on a patient’s quality of health. Gartsman et  al. [15] demonstrated that 544 patients with five common shoulder conditions compared closely in quality of health with five major medical conditions: hypertension, congestive heart failure, acute myocardial infarction, diabetes mellitus, and clinical depression. The SF-36 can also be utilized to evaluate the outcomes of different treatment options. McKee et  al. [30] exhibited improvements in SF-36 scores for pain, physical role functioning, and vitality following an open acromioplasty and subacromial bursectomy in 71 patients. A prospective study evaluating rotator cuff repair for chronic rotator cuff tears found a significant difference in SF-36 scores between workers’ compensation patients and nonworkers’ compensation patients [31]. Overall, SF-36 scores have been found to correlate well with shoulder-specific scores, despite being less responsive and reliable [32–34]. Because of its

J. D. Khoriaty and W. R. Dunn

lack of shoulder function content, most authors would agree that an SF-36 questionnaire should be used in combination with another more shoulder-­specific questionnaire for a more complete assessment of the shoulder patient.

61.5.2 Patient-Reported Outcomes Measurement Information System (PROMIS) The Patient-Reported Outcomes Measurement Information System (PROMIS) was developed by the National Institute of Health to validate patient-reported outcomes (PROs) for clinical research and practice. The aim was to create a tool that could be used widely and provided information that was highly reliable and concise while decreasing the burden on both the patient and provider. It consists of a set of person-­centered questions that evaluate physical, mental, and social health in both adults and children. System-specific versions of PROMIS have been developed, including the PROMIS Physical Function (PROMIS PF) and the PROMIS Upper Extremity (PROMIS UE) questionnaires. The PROMIS Physical function test is also available with computerized adaptive testing (PROMIS PF CAT) increasing its efficiency. Both the PROMIS PF CAT and the PROMIS UE have been investigated for validity in a number of shoulder conditions including rotator cuff tear, total shoulder arthroplasty, and shoulder instability [98–101]. These studies have shown a strong correlation between the PROMIS PF and the PROMIS UE scores and legacy patient-reported outcome (PROs) scores. Schwarz et al. concluded that PROMIS PF or PROMIS UE can be used in place of legacy PRO measures with a lower number of questions and a higher generalizability compared to legacy measurements [99]. PROMIS PF forms were shown to have significantly fewer questions and be completed in significantly less time than legacy PROs without sacrificing reliability [102].

61  Outcome Measurement Tools for Functional Assessment of the Shoulder

61.6 Limb-Specific Outcome Measurement Tools 61.6.1 Disabilities of the Arm, Shoulder, and Hand (DASH) Score The Disabilities of the Arm, Shoulder, and Hand (DASH) score was developed for the evaluation of single or multiple disorders of the entire upper extremity. The DASH evaluates the physical function (21 items), symptoms (six items), and social or role functions (three items) of the upper extremity in this self-administered, 30-item questionnaire. Two optional sections are also ­ included that assess work activities (four items) and sports and/or performing arts activities (four items). Interestingly, the questionnaire does not differentiate which arm, the injured or uninjured, is needed to perform the activity. Rather, the questionnaire produces a score of patient function employing both upper extremities. This feature is both an advantage and disadvantage of this instrument. The DASH score ranges from 0 to 100, with a higher score reflecting greater disability [35] and normative data available for comparison [36]. The DASH questionnaire is intended to be used for any upper extremity condition, including all shoulder conditions. However, this outcome instrument has been specifically validated for glenohumeral arthritis, rotator cuff tendonitis, total shoulder arthroplasty, rotator cuff repair, and psoriatic arthritis [37–41]. Although no specific age limit has been set for this instrument, it is recommended in patients between the ages of 18 and 65 years old. The minimal clinically important difference was calculated to be 10 for the shoulder, and 17 for more distal joints of the upper extremity [42]. As a limb-specific outcome measurement tool, the DASH questionnaire has demonstrated improved responsiveness with fewer ceiling or floor effects than the SF-36 [16]. These results are not surprising given the increased emphasis on upper extremity function rather than general

807

health. However, the broad scope of the DASH encompassing upper extremity function as a whole limits its usefulness to shoulder-specific conditions. In fact, Dowrick et al. demonstrated the DASH score does not exclusively assess disability in the upper extremity and is affected in patients with lower extremity injuries [43]. Furthermore, many of the items within the questionnaire are irrelevant to patients with shoulder complaints, limiting the test’s usefulness for shoulder-specific patients. The validity of the DASH score in intercollegiate athletes may be limited by a ceiling effect because of the high overall function of this population [35]. Beaton et al. also showed a general lack of validity and responsiveness of the DASH score when compared with disease-specific outcome measures of the shoulder. In general, the DASH questionnaire is a useful outcome measure for patients presenting with general upper extremity complaints without a specific diagnosis, rather than patients with specific shoulder complaints in which a shoulder-specific or condition-specific outcome instrument has demonstrated improvement measurement properties.

61.7 Joint-Specific Outcome Measurement Tools 61.7.1 UCLA Shoulder Score One of the first outcome measurement tools created primarily for the shoulder is the UCLA shoulder score [44]. This outcome instrument evaluates shoulder pain, function, forward flexion motion, forward flexion strength, and overall satisfaction with the shoulder. Since its inception in 1981, this instrument has been utilized for nearly every shoulder condition [45–49] and continues to be popular given its historic standing. However, it has never been formally validated because there were no comparable tests at the time of its development. Also, the combination of self-administered, subjective evaluations with “objective” physical examination findings

808

increases the inaccuracies and biases that can adversely affect the score results. As such, recent comparison studies have identified poor reliability, validity, and responsiveness associated with this score [50, 51].

61.7.2 Constant Score Originally published as a master’s thesis, the Constant score is the most commonly used shoulder evaluation instrument in Europe [50] and has been recommended by the European Society for Surgery of the Shoulder and Elbow (SECEC) and the Journal of Shoulder and Elbow Surgery to be a mandatory evaluation tool for all shoulder publications and presentations [52]. The Constant score comprises a patient self-assessment portion evaluating pain and activities of daily living, as well as a physical examination component that attempts to assess active range of motion and strength of the shoulder [53]. This measure has a 100-point scale, with 100 points being the best score; 35 points are derived from the patient’s self-assessment while 65 are generated from the physical examination. Similar to the UCLA score, the combination of a physician-based and physical examination domain increases the risk of bias and measurement error, generating instrument imprecision and inaccuracy. An original validation study was performed for 25 patients with a wide variety of shoulder conditions including arthritis, instability, and impingement [54]. The score was easy to use, but was not very reliable and demonstrated a ceiling effect in instability patients. Further studies evaluating the Constant score raised several concerns regarding its reliability, correlation with other shoulder scores, scoring methods that increase the risk for bias, and variability in objective testing measures [52, 54–57]. In addition, age-related declines in scores and strength occur for both sexes [57–59]. Despite these limitations, the Constant score has been validated for total shoulder arthroplasty [37], rotator cuff repair, adhesive capsulitis [60], and proximal humerus fractures [61]. To improve upon the inherent weakness associated with objective testing measures, the Constant score has attempted to better define the

J. D. Khoriaty and W. R. Dunn

methodology and measurements of strength and range of motion to produce more consistent results [52].

61.7.3 American Shoulder and Elbow Surgeons (ASES) Outcome Score The American Shoulder and Elbow Surgeons (ASES) society developed their own questionnaire in 1994 with the goals of creating a scoring system that would allow consistent communication between physicians, stimulate the undertaking of multicenter trials, encourage validity testing of shoulder outcome measures, and create a scoring system that could be utilized in all patients with any shoulder condition [51, 62]. The ASES outcome score consists of a 10-item patient self-assessment containing domains in pain, instability, and activities of daily living, as well as a physician-directed domain which is rarely used. The questionnaire takes about 3 to 5 min to complete, and about 2 min to score [63, 64]. The raw score is converted to a 100-point scale, with 100 points being the best score, and normative data are available to compare [65]. The ASES outcome score has demonstrated reasonable reliability, responsiveness, and validity for patients aged 20 to 81 years old with a wide variety of shoulder diagnoses managed both operatively and nonoperatively [64]. More specifically, the ASES outcome score has been validated for rotator cuff disease, glenohumeral osteoarthritis, shoulder instability, and shoulder arthroplasty [37, 66]. The MCID has been quantified to 6.4 for general shoulder problems [64], and has also been estimated to be 12 for rotator cuff disease [67]. The ASES correlated well with other shoulderspecific outcome measures, but often times did not correlated with the SF-36 [68–70].

61.7.4 Shoulder Pain and Disability Index (SPADI) The Shoulder Pain and Disability Index (SPADI) was developed by a group of rheumatologists to measure the pain and disability associated with

61  Outcome Measurement Tools for Functional Assessment of the Shoulder

“the clinical syndrome of the painful shoulder” of musculoskeletal, neurogenic or undetermined origin [71]. This questionnaire consists of five items related to pain symptoms and eight items related to physical function and disability, and takes between 2 and 5 min to complete. The score is converted to a 100-point scale, with zero points being the best score and 100 being the worst score. The SPADI, together with the DASH and ASES, are the three most studied shoulder outcome measurement tools in terms of their measurement properties [72]. The reliability and responsiveness have been found to be acceptable in a variety of patient populations and in patients with improving and deteriorating conditions [69, 72, 73]. Early validation studies focused in the primary care settings on heterogeneous populations with a wide variety of shoulder conditions [69, 71]. More recently, the SPADI has been validated for rotator cuff disease [74], osteoarthritis, rheumatoid arthritis [75], adhesive capsulitis [76, 77], and joint replacement surgery [78]. The MCID has been reported to be between 8 and 13 [64, 79]. Overall, the SPADI was found to be more responsive and reliable than general health outcome measures, and correlate well with other shoulder-specific outcome tools [72, 80].

61.7.5 Simple Shoulder Test (SST) The Simple Shoulder Test (SST) was designed to be a simple and efficient instrument to characterize the severity of a condition and functional improvement seen after a surgical procedure. The questionnaire focuses on 12 different functional tasks that focus on pain, function/strength, and range of motion [81]. Response items employ the yes-or-no scale, allowing the questionnaire to be completed in less than 3 min. This dichotomous response option allows for excellent reliability [82, 83]; however, its simplicity does impact the validity and responsiveness. Criterion-related validity is lacking for this instrument, as there is no gold standard for comparison and most other shoulder outcome instruments use different scales for their responses. Several evaluations of the SST have found the questionnaire to have a high degree

809

of reliability, as well as acceptable content and construct validity [72, 83, 84] for a wide variety of shoulder conditions treated both nonoperatively and operatively. In general, the responsiveness of the SST is weaker compared to other shoulder outcome measures because of its binary response choices. Several authors illustrated that the SST cannot be used to differentiate patients with varying degrees of the same condition [50, 85]. Godfrey et al. [83] found decreasing responsiveness in younger patients and patients with instability. Limited data are available regarding MCIDs for different conditions, but recent studies have calculated the MCID to be 17.1 for rotator cuff disease [67] and 25.0 for shoulder arthroplasty [86], which are substantially higher than other shoulder outcome tools. Therefore, despite being highly reliable and valid for most nonoperative and operative shoulder conditions, most authors are cautioning the use of the SST for clinical use given its decreased responsiveness.

61.7.6 Single Assessment Numeric Evaluation (SANE) The simplest outcome measure, the Single Assessment Numeric Evaluation (SANE), attempts to quantify the shoulder function into one question: “How would you rate your shoulder today as a percentage of normal (0% to 100%, with 100% being normal)?” [87]. This outcome measure is inherently used in most clinical offices in evaluating patient progress. Several studies have reported its use for a variety of shoulder conditions [87–90]. The SANE score has been validated by several studies for conditions such as rotator cuff repair, total shoulder replacement, and physical therapy for impingement or adhesive capsulitis [106]. It correlates positively with ASES score and Western Ontario Rotator Cuff Index (WORC) in patients undergoing rotator cuff repair [106–108]. Additionally, SANE has been correlated with ASES and Constant scores for clinically significant outcomes with regard to total shoulder arthroplasty [109]. These validation studies show that SANE can be used as a quick and simple measurement of patient outcomes.

810

61.7.7 Shoulder Activity Level Most shoulder outcome measurement tools evaluate some aspect of pain and function in their questionnaire. Patients can artificially elevate their scores by decreasing their activity level, which decreases their pain while still allowing them to accomplish most activities of daily living. This is especially evident in outcome measures susceptible to the ceiling effect, in which high level athletes are able to score high on questionnaires despite having significant disability in their sport or activity. Thus, the shoulder activity level was developed as a supplementary tool to evaluate their current activity level associated with their other outcome measures [91]. The test evaluates five different activities: carrying weights ≥8  lbs by hand, handling objects overhead, weight lifting or weight training with the arms, executing a swinging motion (e.g., golf, baseball, etc.) and lifting objects weighing ≥25 lbs. Each task is graded from 0 to 4 in terms of frequency performed per month: never or once per month (zero points), once per month (one point), once per week (two points), more than once per week (three points), or daily (four points). Validation studies have been performed in patients with rotator cuff disease, glenohumeral osteoarthritis, and glenohumeral instability [92], but an MCID is not known.

61.8 Condition-Specific Outcome Measurement Tools 61.8.1 Western Ontario Shoulder Outcome Instruments Three condition-specific outcome measurement tools for the shoulder were developed at the University of Western Ontario from 1998 to 2003. Outcome measures for shoulder instability (Western Ontario Shoulder Instability Index, WOSI), glenohumeral osteoarthritis (Western Ontario Osteoarthritis of the Shoulder Index, WOOS), and rotator cuff pathology (Western Ontario Rotator Cuff Index, WORC) were established by reviewing the literature and preexisting

J. D. Khoriaty and W. R. Dunn

scoring systems, interviewing orthopedic surgeons and physical therapists, and interviewing patients with the specific condition [51]. The goal for these disease-specific instruments was utilization as a primary outcome measure in clinical trials evaluating treatments. The WOSI and WORC are 21-item questionnaires, while the WOOS is a 19-item questionnaire. All outcome instruments are subdivided into health domains concerning physical symptoms, sport/recreation/work function, lifestyle function, and emotional function. The response items used a 100-mm visual analog scale, with the score summations from the items ranging from 0 to 2100 for WOSI and WORC and 0 to 1900 for WOOS, with higher raw scores representing worse function. Each test takes about 10 min to complete. The measurement properties of the WOSI, WOOS, and WORC have been evaluated by the developers of the instrument. As characteristic of condition-specific outcome measures, all three instruments demonstrated the most responsiveness to small changes in their respective condition compared to all other outcome measurement tools [50]. The estimated MCID for WOSI is 220 and for WORC is 245 [26, 50]. No MCID has been established for the WOOS. The developers also concluded that their outcome instruments were reliable and valid for their specific condition [93–95]. Overall, the homogeneity of the population studies and the use of the visual analog scale help to make these measurement properties the strongest of any outcome tool. However, other than the developers’ data, there is not much evidence evaluating the reliability, validity, and responsiveness of these tools. Due to this lack of testing data, caution is necessary for measurement at an individual patient level.

61.8.2 Rotator Cuff Quality-of-Life (RCQOL) The Rotator Cuff Quality-of-Life (RCQOL) score was developed for the evaluation of large and massive rotator cuff tears [96]. It consists of a 34-item questionnaire with health domains evaluating symptoms and physical complaints,

61  Outcome Measurement Tools for Functional Assessment of the Shoulder

sports and recreation, work function, lifestyle, social issues, and emotional issues. The responses are recorded using the visual analog scale, with scores ranging from a low, worst outcome of 0 and a high, best outcome of 100. It has been validated for patients aged 25 to 83 years old with different forms of rotator cuff pathology [97]. The MCID has not been determined.

61.9 Summary Patient-based outcome measurement tools are becoming increasingly popular as the modality of choice for patient evaluation. Utilization of these tools allows for an unbiased and accurate account of a condition’s impact on a patient’s health, including pain and physical symptoms, sports and recreational function, occupational function, mental health, social issues, emotional issues, and impact on general health. The functional assessment of the shoulder typically involves a general health outcome measurement tool along with a shoulder-specific or disease-specific outcome measurement tool. Scientific evidence of an instrument’s measurement properties, including reliability, validity, and responsiveness for the condition of interest, are appraised when deciding on which specific instrument to utilize. The goal is choosing an outcome measurement tool that is able to accurately appraise the disease state, as well as recognize any change in that state. Ultimately, these quantifiable values can be utilized as critical feedback for treating physicians, provide transparency of different treatment options to patients, and give values to surgical procedures for third-party payers. Acknowledgment  The current chapter is an update of the one published in the previous edition and authored by Warren R. Dunn and James P. Leonard.

References 1. Dowrick AS, Gabbe BJ, Williamson OD, Wolfe R, Cameron PA.  A comparison of self-reported and independently observed disability in an orthopedic trauma population. J Trauma. 2006;61:1447–52.

811

2. Roos EM.  Outcome after anterior cruciate ligament reconstruction - a comparison of patients’ and surgeons’ assessments. Scand J Med Sci Sports. 2001;11:287–91. 3. Hoher J, Bach T, Munster A, Bouillon B, Tiling T. Does the mode of data collection change results in a subjective knee score? Self-administration versus interview. Am J Sports Med. 1997;25:642–7. 4. Richards RR. Effectiveness evaluation of the shoulder. In: Rockwood Jr C, Matsen III F, Wirth M, editors. The shoulder. 4th ed. Philadelphia: Saunders Elsevier; 2009. p. 267–78. Chapt 7. 5. Hayes KWJ, Szomor ZR, Murrel GA. Reliability of five methods for assessing shoulder range of motion. Aust J Physiother. 2001;47:289–94. 6. Terwee CB, de Winter AF, Scholten RJ, Jans MP, Devillè W, van Schaardenburg D, et al. Interobserver reproducibility of the visual estimate of range of motion of the shoulder. Arch Phys Med Rehabil. 2005;86:1356–61. 7. Rudiger HA, Fuchs B, von Campe A, Gerber C.  Measurements of shoulder mobility by patient and surgeon correlate poorly: a prospective study. J Shoulder Elbow Surg. 2008;17:255–60. 8. Hickey BW, Milosavljevic S, Bell ML, Milburn PD.  Accuracy and reliability of observational motion analysis in identifying shoulder symptoms. Man Ther. 2007;12:263–70. 9. Ostor AJ, Richards CA, Prevost AT, Hazleman BL, Speed CA.  Interrater reproducibility of clinical tests for rotator cuff lesions. Ann Rheum Dis. 2004;63:1288–92. 10. Tzannes A, Paxinos A, Callanan M, Murrell GA. An assessment of the interexaminer reliability of tests for shoulder instability. J Shoulder Elbow Surg. 2004;13:18–23. 11. Kocher MS, Steadman JR, Briggs KK, Sterett WI, Hawkins RJ.  Relationships between objective assessment of ligament stability and subjective assessment of symptoms and function after anterior cruciate ligament reconstruction. Am J Sports Med. 2004;32:629–34. 12. Beaton DE, Schemitsch E.  Measures of health-­ related quality of life and physical function. Clin Orthop Rel Res. 2003;413:90–105. 13. Patel AA, Donegan D, Albert T.  The 36-item short form. J Am Acad Orthop Surg. 2007;15: 126–34. 14. Swiontkowski MF, Buckwalter JA, Keller RB, Haralson R. The outcomes movement in orthopaedic surgery: where we are and where we should go. J Bone Joint Surg. 1999;81A:732–40. 15. Gartsman GM, Brinker MR, Khan M, Karahan M.  Self-assessment of general health status in patients with five common shoulder conditions. J Shoulder Elbow Surg. 1998;7:228–37. 16. SooHoo NF, McDonald AP, Seiler JG 3rd, McGillivary GR. Evaluation of the construct validity of the DASH questionnaire by correlation to the SF-36. J Hand Surg. 2002;27:537–41.

812 17. Portney L, Watkins M, editors. Foundations of clinical research: application to practice. 2nd ed. Upper Saddle River: Prentice Hall Inc; 2000. 18. Beaton DE, Bombardier C, Guillemin F, Ferraz MB.  Guidelines for the process of cross-­ cultural adaptation of self-report measures. Spine. 2000;25:3186–91. 19. Roach K.  Measurement of health outcomes: reliability, validity and responsiveness. J Pros Orth. 2006;18:8–12. 20. Finch E, Brooks D, Stratford P, Mayo N, editors. Physical rehabilitation outcome measures: a guide to enhanced clinical decision making. 2nd ed. Hamilton: Canadian Physiotherapy Association; 2002. 21. Beaton DE, Bombardier C, Katz JN, Wright JG. A taxonomy for responsiveness. J Clin Epidemiol. 2001;54:1204–17. 22. Reips UD, Funke F.  Interval-level measurement with visual analogue scales in Internet-based research: VAS Generator. Behav Res Methods. 2008;40:699–704. 23. Wright RW. Knee injury outcomes measures. J Am Acad Orthop Surg. 2009;17:31–9. 24. Tarlov AR, Ware JE Jr, Greenfield S, Nelson EC, Perrin E, Zubkoff M. The Medical Outcomes Study. An application of methods for monitoring the results of medical care. JAMA. 1989;262:925–30. 25. Naughton MJ, Anderson RT. Outcomes research in orthopaedics: health-related quality of life and the SF-36. Arthroscopy. 1998;14:127–9. 26. Stewart AL, Hays RD, Ware JE Jr. The MOS short-­ form general health survey. Reliability and validity in a patient population. Med Care. 1988;26:724–35. 27. Brazier JE, Harper R, Jones NM, O’Cathain A, Thomas KJ, Usherwood T, et  al. Validating the SF-36 health survey questionnaire: new outcome measure for primary care. BMJ. 1992;305:160–4. 28. Garratt AM, Ruta DA, Abdalla MI, Buckingham JK, Russell IT. The SF36 health survey questionnaire: an outcome measure suitable for routine use within the NHS? BMJ. 1993;306:1440–4. 29. Anderson RT, Aaronson NK, Wilkin D.  Critical review of the international assessments of health-­ related quality of life. Qual Life Res. 1993;2:369–95. 30. McKee MD, Yoo DJ. The effect of surgery for rotator cuff disease on general health status. Results of a prospective trial. J Bone Joint Surg. 2000;82A:970–9. 31. Henn RF 3rd, Kang L, Tashjian RZ, Green A. Patients with workers’ compensation claims have worse outcomes after rotator cuff repair. J Bone Joint Surg. 2008;90A:2105–13. 32. Smith KL, Harryman DT 2nd, Antoniou J, Campbell B, Sidles JA, Matsen FA 3rd. A prospective, multipractice study of shoulder function and health status in patients with documented rotator cuff tears. J Shoulder Elbow Surg. 2000;9:395–402. 33. Crane PK, Hart DL, Gibbons LE, Cook KF.  A 37-item shoulder functional status item pool had

J. D. Khoriaty and W. R. Dunn negligible differential item functioning. J Clin Epidemiol. 2006;59:478–84. 34. Gartsman GM, Brinker MR, Khan M.  Early effectiveness of arthroscopic repair for full-thickness tears of the rotator cuff: an outcome analysis. J Bone Joint Surg. 1998;80A:33–40. 35. Beaton DE, Katz JN, Fossel AH, Wright JG, Tarasuk V, Bombardier C.  Measuring the whole or the parts? Validity, reliability, and responsiveness of the Disabilities of the Arm, Shoulder and Hand outcome measure in different regions of the upper extremity. J Hand Ther. 2001;14:128–46. 36. Hunsaker FG, Cioffi DA, Amadio PC, Wright JG, Caughlin B.  The American academy of orthopaedic surgeons outcomes instruments: normative values from the general population. J Bone Joint Surg. 2002;84A:208–15. 37. Angst F, Pap G, Mannion AF, Herren DB, Aeschlimann A, Schwyzer HK, et al. Comprehensive assessment of clinical outcome and quality of life after total shoulder arthroplasty: usefulness and validity of subjective outcome measures. Arthritis Rheum. 2004;51:819–28. 38. McConnel S, Beaton DE, Bombardier C, editors. Disabilities of the Arm, Shoulder and Hand: The DASH Outcome Measure User’s Manual. Toronto: Institute for Work & Health; 1999. 39. MacDermid JC, Solomon P, Prkachin K.  The Shoulder Pain and Disability Index demonstrates factor, construct and longitudinal validity. BMC Musculoskeletal Disord. 2006;7:12. 40. Getahun T, MacDermid JC.  Concurrent validity of patient rating scales in assessment of outcome after rotator cuff repair. J Musculoskeletal Res. 2000;119:27. 41. Navsarikar A, Gladman DD, Husted JA, Cook RJ.  Validity assessment of the disabilities of arm, shoulder, and hand questionnaire (DASH) for patients with psoriatic arthritis. J Rheum. 1999;26:2191–4. 42. Schmitt JS, Di Fabio RP.  Reliable change and minimum important difference (MID) proportions facilitated group responsiveness comparisons using individual threshold criteria. J Clin Epidemiol. 2004;57:1008–18. 43. Dowrick AS, Gabbe BJ, Williamson OD, Cameron PA.  Does the disabilities of the arm, shoulder and hand (DASH) scoring system only measure disability due to injuries to the upper limb? J Bone Joint Surg. 2006;88B:524–7. 44. Amstutz HC, Sew Hoy AL, Clarke IC. UCLA anatomic total shoulder arthroplasty. Clin Orthop Rel Res. 1981;155:7–20. 45. Wright RW, Heller MA, Quick DC, Buss DD.  Arthroscopic decompression for impingement syndrome secondary to an unstable os acromiale. Arthroscopy. 2000;16:595–9. 46. Romeo AA, Mazzocca A, Hang DW, Shott S, Bach BR Jr. Shoulder scoring scales for the evalu-

61  Outcome Measurement Tools for Functional Assessment of the Shoulder ation of rotator cuff repair. Clin Orthop Rel Res. 2004;427:107–14. 47. O’Connor DA, Chipchase LS, Tomlinson J, Krishnan J. Arthroscopic subacromial decompression: responsiveness of disease-specific and health-related quality of life outcome measures. Arthroscopy. 1999;15:836–40. 48. Krepler P, Wanivenhaus AH, Wurnig C.  Outcome assessment of hemiarthroplasty of the shoulder: a 5-year follow-up with 4 evaluation tools. Acta Orthop. 2006;77:778–84. 49. Fealy S, Kingham TP, Altchek DW.  Mini-open rotator cuff repair using a two-row fixation technique: outcomes analysis in patients with small, moderate, and large rotator cuff tears. Arthroscopy. 2002;18:665–70. 50. Kirkley A, Griffin S, Dainty K.  Scoring systems for the functional assessment of the shoulder. Arthroscopy. 2003;19:1109–20. 51. Wright RW, Baumgarten KM.  Shoulder outcomes measures. J Am Acad Orthop Surg. 2010;18:436–44. 52. Constant CR, Gerber C, Emery RJ, Sojbjerg JO, Gohlke F, Boileau P. A review of the Constant score: modifications and guidelines for its use. J Shoulder Elbow Surg. 2008;17:355–61. 53. Constant CR, Murley AH.  A clinical method of functional assessment of the shoulder. Clin Orthop Rel Res. 1987;214:160–4. 54. Conboy VB, Morris RW, Kiss J, Carr AJ. An evaluation of the Constant-Murley shoulder assessment. J Bone Joint Surg. 1996;78B:229–32. 55. Bankes MJ, Crossman JE, Emery RJ.  A standard method of shoulder strength measurement for the Constant score with a spring balance. J Shoulder Elbow Surg. 1998;7:116–21. 56. Fialka C, Oberleitner G, Stampfl P, Brannath W, Hexel M, Vecsei V.  Modification of the Constant-­ Murley shoulder score-introduction of the individual relative Constant score Individual shoulder assessment. Injury. 2005;36:1159–65. 57. Walton MJ, Walton JC, Honorez LA, Harding VF, Wallace WA. A comparison of methods for shoulder strength assessment and analysis of Constant score change in patients aged over fifty years in the United Kingdom. J Shoulder Elbow Surg. 2007;16:285–9. 58. Brinker MR, Cuomo JS, Popham GJ, O’Connor DP, Barrack RL.  An examination of bias in shoulder scoring instruments among healthy collegiate and recreational athletes. J Shoulder Elbow Surg. 2002;11:463–9. 59. Katolik LI, Romeo AA, Cole BJ, Verma NN, Hayden JK, Bach BR. Normalization of the Constant score. J Shoulder Elbow Surg. 2005;14:279–85. 60. Othman A, Taylor G.  Is the constant score reliable in assessing patients with frozen shoulder? 60 shoulders scored 3 years after manipulation under anaesthesia. Acta Orthop Scand. 2004;75:114–6. 61. Baker P, Nanda R, Goodchild L, Finn P, Rangan A. A comparison of the Constant and Oxford shoul-

813

der scores in patients with conservatively treated proximal humeral fractures. J Shoulder Elbow Surg. 2008;17:37–41. 62. Richards RR, An KN, Bigliani LU, Friedman RJ, Gartsman GM, Gristina AG, et  al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3:347–52. 63. Michener LA, Leggin BG.  A review of self-report scales for the assessment of functional limitation and disability of the shoulder. J Hand Ther. 2001;14:68–76. 64. Michener LA, McClure PW, Sennett BJ. American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, patient self-report section: reliability, validity, and responsiveness. J Shoulder Elbow Surg. 2002;11:587–94. 65. Sallay PI, Reed L.  The measurement of normative American Shoulder and Elbow Surgeons scores. J Shoulder Elbow Surg. 2003;12:622–7. 66. Kocher MS, Horan MP, Briggs KK, Richardson TR, O’Holleran J, Hawkins RJ.  Reliability, validity, and responsiveness of the American Shoulder and Elbow Surgeons subjective shoulder scale in patients with shoulder instability, rotator cuff disease, and glenohumeral arthritis. J Bone Joint Surg. 2005;87A:2006–11. 67. Tashjian RZ, Deloach J, Green A, Porucznik CA, Powell AP. Minimal clinically important differences in ASES and simple shoulder test scores after nonoperative treatment of rotator cuff disease. J Bone Joint Surg. 2010;92A:296–303. 68. Angst F, Goldhahn J, Drerup S, Aeschlimann A, Schwyzer HK, Simmen BR. Responsiveness of six outcome assessment instruments in total shoulder arthroplasty. Arthritis Rheum. 2008;59:391–8. 69. Beaton DE, Richards RR.  Measuring function of the shoulder. A cross-sectional comparison of five questionnaires. J Bone Joint Surg. 1996;78A: 882–90. 70. Placzek JD, Lukens SC, Badalanmenti S, Roubal PJ, Freeman DC, Walleman KM, et  al. Shoulder outcome measures: a comparison of 6 functional tests. Am J Sports Med. 2004;32:1270–7. 71. Roach KE, Budiman-Mak E, Songsiridej N, Lertratanakul Y. Development of a shoulder pain and disability index. Arthritis Care Res. 1991;4:143–9. 72. Roy JS, MacDermid JC, Woodhouse LJ. Measuring shoulder function: a systematic review of four questionnaires. Arthritis Rheum. 2009;61:623–32. 73. Williams JW Jr, Holleman DR Jr, Simel DL.  Measuring shoulder function with the Shoulder Pain and Disability Index. J Rheumatol. 1995;22:727–32. 74. Ekeberg OM, Bautz-Holter E, Tveita EK, Keller A, Juel NG, Brox JI. Agreement, reliability and validity in 3 shoulder questionnaires in patients with rotator cuff disease. BMC Musculoskeletal Dis. 2008;9:68. 75. Christie A, Dagfinrud H, Engen Matre K, Flaatten HI, Ringen Osnes H, Hagen KB.  Surgical inter-

814 ventions for the rheumatoid shoulder. Cochrane Database Syst Rev. 2010;20:CD006188. 76. Staples MP, Forbes A, Green S, Buchbinder R.  Shoulder-specific disability measures showed acceptable construct validity and responsiveness. J Clin Epidemiol. 2010;63:163–70. 77. Tveita EK, Ekeberg OM, Juel NG, Bautz-Holter E. Responsiveness of the shoulder pain and disability index in patients with adhesive capsulitis. BMC Musculoskeletal Disord. 2008;9:161. 78. Angst F, Goldhahn J, Pap G, Mannion AF, Roach KE, Siebertz D, et al. Cross-cultural adaptation, reliability and validity of the German Shoulder Pain and Disability Index (SPADI). Rheumatology (Oxford). 2007;46:87–92. 79. Paul A, Lewis M, Shadforth MF, Croft PR, Van Der Windt DA, Hay EM. A comparison of four shoulder-­ specific questionnaires in primary care. Ann Rheum Dis. 2004;63:1293–9. 80. Breckenridge JD, McAuley JH.  Shoulder Pain and Disability Index (SPADI). J Physiother. 2011;57:197. 81. Roddey TS, Olson SL, Cook KF, Gartsman GM, Hanten W.  Comparison of the University of California-Los Angeles Shoulder Scale and the Simple Shoulder Test with the shoulder pain and disability index: single-administration reliability and validity. Phys Ther. 2000;80:759–68. 82. Beaton D, Richards RR.  Assessing the reliability and responsiveness of 5 shoulder questionnaires. J Shoulder Elbow Surg. 1998;7:565–72. 83. Godfrey J, Hamman R, Lowenstein S, Briggs K, Kocher M.  Reliability, validity, and responsiveness of the simple shoulder test: psychometric properties by age and injury type. J Shoulder Elbow Surg. 2007;16:260–7. 84. Angst F, Schwyzer HK, Aeschlimann A, Simmen BR, Goldhahn J.  Measures of adult shoulder function: Disabilities of the Arm, Shoulder, and Hand Questionnaire (DASH) and its short version (QuickDASH), Shoulder Pain and Disability Index (SPADI), American Shoulder and Elbow Surgeons (ASES) Society standardized shoulder assessment form, Constant (Murley) Score (CS), Simple Shoulder Test (SST), Oxford Shoulder Score (OSS), Shoulder Disability Questionnaire (SDQ), and Western Ontario Shoulder Instability Index (WOSI). Arthritis Care Res. 2011;63:S174–88. 85. Cook KF, Gartsman GM, Roddey TS, Olson SL. The measurement level and trait-specific reliability of 4 scales of shoulder functioning: an empiric investigation. Arch Phys Med Rehabil. 2001;82:1558–65. 86. Roy JS, Macdermid JC, Faber KJ, Drosdowech DS, Athwal GS. The simple shoulder test is responsive in assessing change following shoulder arthroplasty. J Orthop Sports Phys Ther. 2010;40:413–21. 87. Williams GN, Gangel TJ, Arciero RA, Uhorchak JM, Taylor DC.  Comparison of the Single Assessment Numeric Evaluation method and two shoulder rating scales. Outcomes measures after shoulder surgery. Am J Sports Med. 1999;27:214–21.

J. D. Khoriaty and W. R. Dunn 88. Barber FA.  Long-term results of acromioclavicular joint coplaning. Arthroscopy. 2006;22:125–9. 89. Kerr BJ, McCarty EC.  Outcome of arthroscopic debridement is worse for patients with glenohumeral arthritis of both sides of the joint. Clin Orthop Relat Res. 2008;466:634–8. 90. Jones KJ, Wiesel B, Ganley TJ, Wells L. Functional outcomes of early arthroscopic bankart repair in adolescents aged 11 to 18 years. J Pediatr Orthop. 2007;27:209–13. 91. Brophy RH, Beauvais RL, Jones EC, Cordasco FA, Marx RG.  Measurement of shoulder activity level. Clin Orthop Relat Res. 2005;439:101–8. 92. Brophy RH, Levy B, Chu S, Dahm DL, Sperling JW, Marx RG.  Shoulder activity level varies by diagnosis. Knee Surg Sports Traumatol Arthrosc. 2009;17:1516–21. 93. Lo IK, Griffin S, Kirkley A. The development of a disease-specific quality of life measurement tool for osteoarthritis of the shoulder: The Western Ontario Osteoarthritis of the Shoulder (WOOS) index. Osteoarthritis Cartilage. 2001;9:771–8. 94. Kirkley A, Griffin S, McLintock H, Ng L. The development and evaluation of a disease-specific quality of life measurement tool for shoulder instability. The Western Ontario Shoulder Instability Index (WOSI). Am J Sports Med. 1998;26:764–72. 95. Kirkley A, Alvarez C, Griffin S.  The development and evaluation of a disease-specific quality-of-life questionnaire for disorders of the rotator cuff: The Western Ontario Rotator Cuff Index. Clin J Sport Med. 2003;13:84–92. 96. Hollinshead RM, Mohtadi NG, Vande Guchte RA, Wadey VM.  Two 6-year follow-up studies of large and massive rotator cuff tears: comparison of outcome measures. J Shoulder Elbow Surg. 2000;9:373–81. 97. Mohtadi NG, Hollinshead RM, Sasyniuk TM, Fletcher JA, Chan DS, Li FX. A randomized clinical trial comparing open to arthroscopic acromioplasty with mini-open rotator cuff repair for full-thickness rotator cuff tears: disease-specific quality of life outcome at an average 2-year follow-up. Am J Sports Med. 2008;36:1043–51. 98. Patterson BM, Orvets ND, Aleem AW, Keener JD, Calfee RP, Nixon DC, Chamberlain AM. Correlation of Patient-Reported Outcomes Measurement Information System (PROMIS) scores with legacy patient-reported outcome scores in patients undergoing rotator cuff repair. J Shoulder Elbow Surg. 2018;27(6S):S17–23. 99. Schwarz I, Smith JH, Houck DA, Frank RM, Bravman JT, McCarty EC.  Use of the Patient-Reported Outcomes Measurement Information System (PROMIS) for Operative Shoulder Outcomes. Orthop J Sports Med. 2020;8(6):2325967120924345. 100. Anthony CA, Glass N, Hancock K, Bollier M, Hettrich CM, Wolf BR. Preoperative performance of the patient-reported outcomes measurement infor-

61  Outcome Measurement Tools for Functional Assessment of the Shoulder mation system in patients with rotator cuff pathology. Arthroscopy. 2017;33(10):1770–1774.e1. 101. Anthony CA, Glass NA, Hancock K, Bollier M, Wolf BR, Hettrich CM.  Performance of PROMIS instruments in patients with shoulder instability. Am J Sports Med. 2017;45(2):449–53. 102. Ziedas AC, Abed V, Swantek AJ, Rahman TM, Cross A, Thomashow K, Makhni EC.  PROMIS physical function instruments compare favorably to legacy patient-reported outcome measures in upper and lower extremity orthopedic patients: a systematic review of the literature. Arthroscopy. 2021:S0749-8063(21)00517-X. 103. Plummer OR, Abboud JA, Bell JE, Murthi AM, Romeo AA, Singh P, Zmistowski BM.  A concise shoulder outcome measure: application of computerized adaptive testing to the American ­ Shoulder and Elbow Surgeons Shoulder Assessment. J Shoulder Elbow Surg. 2019;28(7):1273–80. 104. Kane LT, Abboud JA, Plummer OR, Beredjiklian PT.  Improving efficiency of patient-reported outcome collection: application of computerized adaptive testing to DASH and QuickDASH Outcome Scores. J Hand Surg Am. 2021;46(4):278–86. 105. Dowdle SB, Glass N, Anthony CA, Hettrich CM.  Use of PROMIS for patients undergoing pri-

815

mary total shoulder arthroplasty. Orthop J Sports Med. 2017;5(9):2325967117726044. 106. Thigpen CA, Shanley E, Momaya AM, Kissenberth MJ, Tolan SJ, Tokish JM, Hawkins RJ.  Validity and responsiveness of the single alpha-numeric evaluation for shoulder patients. Am J Sports Med. 2018;46(14):3480–5. 107. Retzky JS, Baker M, Hannan CV, Srikumaran U.  Single Assessment Numeric Evaluation scores correlate positively with American Shoulder and Elbow Surgeons scores postoperatively in patients undergoing rotator cuff repair. J Shoulder Elbow Surg. 2020;29(1):146–9. 108. Wickman JR, Lau BC, Scribani MB, Wittstein JR. Single Assessment Numeric Evaluation (SANE) correlates with American Shoulder and Elbow Surgeons score and Western Ontario Rotator Cuff index in patients undergoing arthroscopic rotator cuff repair. J Shoulder Elbow Surg. 2020;29(2):363–9. 109. Gowd AK, Charles MD, Liu JN, Lalehzarian SP, Cabarcas BC, Manderle BJ, Nicholson GP, Romeo AA, Verma NN.  Single Assessment Numeric Evaluation (SANE) is a reliable metric to measure clinically significant improvements following shoulder arthroplasty. J Shoulder Elbow Surg. 2019;28(11):2238–46.

Patient Education and Patient Expectation in Shoulder Surgery

62

Berte Bøe and Ragnhild Ø. Støen

Abstract

Postoperative patient satisfaction, an important quality outcome measure, is highly influenced by preoperative patient education and expectations. Lately, the patients have been more and more involved in the decision-­ making process related to their care. Patient satisfaction is often associated with improved function and decreased disability postoperative. It is an aim to improve the efficiency and quality of health care, and patient-related outcome scores are frequently used to evaluate the outcomes from the patient’s perspective. Literature investigating the influence of patient education and expectations and the importance of comorbidity on the postoperative outcome has recently caught increased attention from orthopedic surgeons. Keywords

Patient education · Patient expectation · Outcome · Preoperative counseling · Patient satisfaction

B. Bøe (*) · R. Ø. Støen Division of Orthopaedic Surgery, Oslo University Hospital, Oslo, Norway e-mail: [email protected]

62.1 Introduction Patients’ rights are lately gaining increased status in the medical community and as part of health legislation [1]. This is true both for research and for treatment. In the outpatient clinic when time is limited and history and examination is finished, the doctor very often has an opinion on what should be the further treatment. It can be difficult to find time to discuss the pros and cons with the patient. However, a well-informed patient that is actively taking part in his or her treatment is likely to have a better result [2]. An understanding of the condition is an important base for the patient to comply with the extensive rehab necessary before and after shoulder surgery. Furthermore, a well-educated patient believing in the treatment will also benefit of the placebo effect in addition to the mechanical-anatomical effect of the treatment. Expectations play an important role for the outcome of medical procedures. It is widely accepted that this is also true for surgical and arthroscopic procedures, and it is the reason for sham studies to be conducted [3]. A consultation in the outpatient clinic should consist of a thorough shoulder history together with general medical history. There should be performed an examination and laboratory tests and radiology should be ordered. The findings should then be summarized to the patient in a face-to-face consultation before information

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_62

817

818

about possible treatment options and risks and results associated with the actual procedure are given. Information should be tailored to the patient and as complete as possible. One should emphasize what part of the recommendations is the doctor’s own opinion and what is actually documented in the literature, e.g., educate the patient in what we know and what we believe as professionals. Many doctors will equal patient education with preoperative information about side effects and complications of a treatment. This information has important medicolegal consequences and should also be documented in the patient chart or by written informed consent according to local routine. The information about side effects is important together with realistic information about expected outcome because they are base for the patient’s choice of further treatment. Shoulder surgery is rarely strictly indicated, but the indication can be strong or weak, and patient preference, comorbidity, and life situation could be important factors that can pull the choice in one or the other direction. Information about treatment reassures the patient that the doctor is able and confident, and lack of information is a major factor in diminished compliance from the patients, including interruption of treatment and rehabilitation [1], for example, will educating the patient about what to expect of wound healing increase the chance of early recognition of an infection, which could be decisive for whether shoulder prosthesis could survive or needs to be revised.

62.2 Measures Patient-related outcome measurements (PROMs) are used by clinicians to measure the patient’s development over time and general satisfaction after treatment and are being increasingly important outcome measures in orthopedic surgery. The preoperative score can be used to assess the indication for surgery and in some cases give information of what we can expect of results after surgery. In some cases, the difference from preoperative to postoperative value is the most

B. Bøe and R. Ø. Støen

important, and in other cases, the absolute value of a PROM postoperative is more interesting. Musculoskeletal Outcomes Data Evaluation and Management System (MODEMS) questionnaire asks patients questions on a Likert scale of 1 to 5, with 1 corresponding to the lowest level of expectations (i.e., not likely at all) and 5 corresponding to the highest level (i.e., extremely likely).

62.3 Survey of Expectations and Concerns Patient often presents to orthopedic surgeons with very limited knowledge about their injury or disease. Even though there are unlimited resources available on the Internet for everybody to read, these publications are unsorted and might be filled of medical terms difficult for patients to understand. After reading on the Internet, patients often have misunderstood and are confused about their condition. Misconceptions can be difficult to clear out and information from the physicians can also be difficult to retain. The mixture of a need of information and the fear of upcoming surgery can be overwhelming. The goal and driving factors of orthopedic surgery must be to reduce pain and/or enhance function to improve the patient’s quality of life. Patients have variable expectations of the level of improvement they will achieve after surgery. There have been reported over-optimistic expectations from patients in knee surgery leading to poor postoperative satisfaction [4]. From the patients view, it is probably unthinkable that the result after surgery might be even worse than before an operation. It is mandatory for surgeons to inform all patients about possible complications of surgery, both before acute and planned procedures. Most people have a tendency to think that possible complications like infection, nerve injury, and wound rupture do happen to everybody else but themselves. To avoid misperceptions, the surgeon must make sure that the patient understands the preoperative information. For conditions without pain, operated because of decreased function, it is especially important to inform the patient of possible pain and tenderness after surgery.

62  Patient Education and Patient Expectation in Shoulder Surgery

The psychological status of our patients might be a predictor of outcome after shoulder surgery and should be taken into consideration preoperatively. A psychological distress can influence selfassessed pain, disability, and quality of life. The Hospital Anxiety and Depression Scale (HADS) is correlated with visual analog scale (VAS) for pain and negatively correlated with American Shoulder and Elbow Surgeons (ASES) scale in patients scheduled for rotator cuff repair [5].

62.4 Patient Education Educational status is closely related to health. This is well established and consistent through time and countries [6]. The mechanisms for this are not well understood. Two theories are frequently reproduced; the higher educated patients understand the doctor better and use existing medical care more efficient. The other hypothesis is that educated people do better health choices and avoid illness [7]. It is probable that both hypotheses are valid, and it is an assumption that educated people are more eligible to do the right choices faced with proper information. However, proper information in a proper way is crucial for the correct choices. This is not new thinking. Already in a leading article in BMJ in 1947, the editor called for patient education in the meeting with the doctor to break down in advance the reserve, which during illness often delays the doctor's efforts and the patient's recovery [8]. Fig. 62.1 Minimal content of an office consultation

819

Medical curricula include patient communication and education. But many other health ­professionals are also trained in patient education. Patient information and education are not a task for the doctor herself, but a task for the whole team, and parts of the patient education can be handed over to other health professionals. It is, however, the doctor’s responsibility to decide what kind of information to be given, ensure that the patient has received the information and decide if there is need to involve family or caretakers in the patient education. The information should be given in a calm atmosphere where the patient has enough time to receive and process the information and ask questions. There should be room to repeat the information if needed. Furthermore, information needs to be revised if the condition has changed, for example long time between consultation and surgery or if complications occur after surgery [1].

62.4.1 Doctor and Patient Dialog The consultation starts at the waiting room. The conditions should be clean and reassuring. Magazines or other ways to consume time should be provided. Toys should be present if pediatric patients are frequent in the office. The consultation room should be professional and put the doctor and the department in a good light. Waiting time at the waiting room before seeing the surgeon is important for patient satisfaction [9].

History of shoulder injury and disease General history Examination X-ray Explaining the pathology Present treatment options Information on the exact procedure planned with risks and benifits

B. Bøe and R. Ø. Støen

820

Meeting the patient with interest is mandatory (Fig. 62.1).

62.4.2 Posters and Models The use of posters and models will reinforce the dialog and makes it easier for the patient to understand the relevant anatomy and procedures. The use of 3D printing of patient-specific anatomy further adds to the relevance in patient (and intern) education [10].

62.4.3 Information Letter Information letter is used everywhere in health care. Patients are informed about time for consultation, preparation before surgery, and contact information to the hospital. It is also very common to have procedure-specific information letters as part of the patient education.

62.4.4 App Everyone has a smart telephone, and applications are cheap and can be used to reach many patients. It gives the possibility of interaction and is always available. However, the use and effect should be monitored, as shown by Ledford and co-workers. They found in a randomized controlled trial on prenatal patient education that changing from a spiral notebook with information to an app reduced the active participation of the pregnant woman in prenatal choices regarding for example induction of labor [11]. We therefore recommend the use of mobile telephone apps in addition to other ways of educating the patients.

62.4.5 Web Based Information on a website can complement other sources of information. It would also reach

patients that is not already in contact with the health care and is therefore a good way of communicating and guiding patients with shoulder problems.

62.4.6 Standardized Information or Need-Based Too little and too much information can increase patient anxiety. A randomized, controlled trial by Wongkietkachorn et  al. showed that in a day-­ surgery setting, patient-tailored information decreased anxiety and increased satisfaction significantly compared to standardized information in a day-surgery unit. In addition, the time spent for patient education was decreased [12].

62.4.7 Decision Aids A decision aid can be useful where there are different treatment options that either is regarded equal or where different people would value risk and benefits differently. A decision aid could be a pamphlet, videos, or an app. A Cochrane review found that there is high-quality evidence that use of decision aids improves patients’ knowledge of the options and feel better informed and more clear about what matters most to them [13]. However, local decision aids should be validated for desired outcome in the actual patient group.

62.5 Patient Expectations 62.5.1 Subacromial Pain Syndrome The importance of psychological factors in influencing the outcome after surgery is now emerging in elective orthopedic procedures. Subacromial pain syndrome (SAPS) is a common problem that represents almost half of all shoulder pathologic processes presenting to general practice [14]. In the initial phase,

62  Patient Education and Patient Expectation in Shoulder Surgery

treatment is nonoperative with physiotherapy, analgesics, and corticosteroid injection. The patient's general practitioner (GP) or physiotherapist should initiate this treatment. In most countries, it will be easier and cheaper for the patient to get this information from the firstline health service compared to an orthopedic surgeon. Surgery is considered when patients fail to improve after 3–6 months of conservative measures. Even after failed conservative treatment, there is not always recommended to move on with a surgical p­ rocedure. The surgeon has to do a thorough examination of the shoulder and the indication for acromioplasty has become more narrow with new critical studies published, one of them including sham surgery [15–17]. For several years, surgical acromial decompression has been the solution to many of these patients’ problems. And surgery has also been an easy solution for the doctors, both the GP and the surgeon. A small arthroscopic operation, in and out of clinic the same day, seems like efficient treatment. After a long period with this treatment recommendation, it takes time to turn the patients’ expectation of surgical treatment. A quick operation will for many patients seem like an easier solution than several months of exercises and physiotherapy. The knowledge of recent research about this patient group has to be communicated to the first-­ line health service. Because if the patient come to the orthopedic surgeon with an expectation of surgical treatment for their diagnosis, it may be extremely difficult for the surgeon to convince them otherwise.

62.5.2 Rotator Cuff Repair Rotator cuff repair surgery is one of the most common orthopedic procedures and the incidence increases rapidly [18–21]. The superiority of operative treatment over nonoperative can be questioned since there are no convincing evidence. There are several reports on the quality of patient education when it comes to rotator cuff surgery [22]. Even though the quality of patient education materials is high, this is not necessarily

821

positive because the information has to be presented in an appropriate reading grade level. The mean readability levels of American Academy of Orthopaedic Surgeons (AAOS) articles are higher than generally recommended. Henn et  al. evaluated patients’ preoperative expectations before surgical treatment of chronic rotator cuff repair [23]. The parameters asked for were ability to do household or yard activities, ability to sleep at night, return to work, to exercise, and do recreational activities. Symptom relief and future disability prevention were also asked for. More than 85% expected surgery to be “very likely” or “extremely likely” to improve in all areas questioned meaning they had high expectations of rotator cuff repair. The purpose of their work was to assess if the patients’ preoperative expectations affected the postoperative outcome. In a rigorous multivariate analysis, controlling for age, gender, smoking, Workers’ Compensation status, symptom duration, number of previous operations, number of comorbidities, tear size, and repair technique greater preoperative expectations were a significant independent predictor of better performance at one year and greater improvement on the SST, the DASH, visual analog scale, and the SF-36. In knee and hip surgery, there has been a growing concern that patients with a high level of anxiety and depression respond poorly to surgical treatment [24, 25]. For rotator cuff tears, the results have been different. Even though anxiety and depression have negatively influenced self-­ assessed preoperative pain, function and quality of life depression have not predicted poor outcome after rotator cuff surgery [26]. Surprisingly, the symptoms of anxiety and depression have turned out to improve after rotator cuff surgery [27] For patients operated because of rotator cuff tears surgical variables including debridement of massive, irreparable cuff tears, presence of subscapularis tear, and comparatively larger supraspinatus and infraspinatus tears are reported to be associated with decreased satisfaction [28].

822

62.6 Factors Influencing Patient Satisfaction

B. Bøe and R. Ø. Støen

patients, physicians, and employers and to identify opportunities for improvement. Outcomes in patients with work-related musculoskeletal disorMany factors can influence the patient’s self-­ ders, including those with a workers’ compensaassessed pain, function, and general health status. tion claim, appear to be significantly worse Lower educational level, workers’ compensation compared to workers. status, preoperative disability, anxiety and PROMS can be used as a tool for doctors to depression, persistence of pain, and reduced better counsel their patients about their function are more frequently seen in patients ­expectations of surgery. This is important in furwith poor satisfaction after surgery. In the other thering the doctor–patient relation and increase direction factors like being employed and mar- patient satisfaction. In some situations, the scorried and being of older age predict higher ing forms are filled out after the patient is schedsatisfaction. uled for surgery. When the patient has been In most cases, a patient with low scores informed that their condition is in need for surpreoperative will end up with a lower score than gery, this may influence patient-perceived funca patient who started out with a high score. Even tional outcomes. The patient is affected to believe though the patient with a low score might be that the function is worse because the condition more satisfied than the other patient after the requires an operation. treatment [29]. For some conditions, this can be Comorbidity is always to be assessed before explained by a minimal demand of function to the patient is set up for surgery. Tashjihan et al. perform daily activities. The patient with the low found a correlation between the number of score initially might reach a threshold making comorbidities and self-assessed preoperative easy daily tasks possible. This can make a great baseline pain, function, and general health status difference for the individual. For the patient with for patients with chronic rotator cuff tears [31]. a higher score, initially the result might be good Comorbidities had a significant negative impact enough for daily living, but if the goal was return on preoperative data and should therefore be to sport, which they are not able to, he or she will expected to influence the outcome data after surnot be satisfied. Patients who desire a higher level gery as well. of activity may report lower PROMs and satisfacDekker et  al. investigated the influence of tion as they become functionally limited by deg- anxiety and depression on the outcome after radation of their surgery, whereas a less active arthroscopic subacromial decompression (ASD) individual may be able to perform all activities of in shoulder surgery [32]. They found a strong daily living and report a good outcome as a result. negative correlation between preoperative Whether a person is able to work or not is a Hospital Anxiety and Depression Scale (HADS) significant factor in most people’s life. Workers’ and clinical results. HADS>11 before ASD had compensation status has been studied as a factor worse outcomes postoperatively, and this should possible influencing the outcome after health be taken into account in preoperative planning. treatment, both surgical and nonoperative. In a Although different types of shoulder surgery study of patients with lumbar intervertebral disk are effective in treating patients for their herniation (IDH), there was no added benefit shoulder complains, the benefit patients derive associated with surgical treatment for patients from this treatment varies widely for reasons with workers’ compensation at 2 years while not fully understood. Postoperative patientthose in the nonworkers’ compensation group reported outcomes are affected by a variety of had significantly greater improvement with sur- psychosocial factors, including the patient’s gical treatment [30]. Understanding how work- expectations, sense of self-efficacy, and mental ers’ compensation affects outcomes among health. Even the patient’s confidence in his or various treatments is important in order to advise her ability to recover to the expected postop-

62  Patient Education and Patient Expectation in Shoulder Surgery

erative level will probably influence the outcome. Total shoulder arthroplasty is well-accepted treatment for painful osteoarthritis of the shoulder, but the surgical procedure and recovery are nevertheless stressful for the patients. It is essential to understand and address patients’ individual concerns and goals for treatment. Tokish et  al. studied how resilience, characterized by an ability to bounce back or recover from stress, increasingly recognized as a psychometric property, affected traditional orthopedic outcome scores [33]. Patients with high resilience demonstrated shoulder arthroplasty outcomes that were up to 40 points higher than patients with low resilience on a 0–100 scale. After shoulder arthroplasty, mid-term outcome is of great importance. Jacobs et al. compared satisfied and not satisfied patients

823

after 2–5 years [34]. Nearly 90% were satisfied with their procedure. Dissatisfied patients had lower pre- and postoperative ASES score as well as significantly lower pre- to postoperative change. A low change in ASES score (55 years old

ASA class 1

Better outcome

No prior surgery on shoulder

Being employed

Being married

Low initial Simple Shoulder Test score

824

B. Bøe and R. Ø. Støen

7. Muurinen JM.  Demand for health: a generalised Grossman model. J Health Econ. 1982;1(1):5–28. PubMed PMID: 10263949. Epub 1982/04/11. eng. 8. British Medical Journal. 1947;1(1):494. 9. Teunis T, Thornton ER, Jayakumar P, Ring D.  Time seeing a hand surgeon is not associated with patient satisfaction. Clin Orthop Relat Res. 2015;473(7):2362–8. PubMed PMID: 25475717. Pubmed Central PMCID: 4457762. 10. Powers MK, Lee BR, Silberstein J.  Three-­ dimensional printing of surgical anatomy. Curr Opin Urol. 2016;26(3):283–8. PubMed PMID: 26825651. Epub 2016/01/31. eng. 11. Ledford CJW, Womack JJ, Rider HA, Seehusen AB, Conner SJ, Lauters RA, et  al. Unexpected 62.7 Summary effects of a system-distributed mobile application in maternity care: a randomized controlled trial. Health More confident patients experience better Educ Behav. 2018;45(3):323–30. PubMed PMID: functional outcomes after shoulder surgery. An 28918669. Epub 2017/09/19. eng. important factor to surgeons’ best possible results 12. Wongkietkachorn A, Wongkietkachorn N, Rhunsiri P.  Preoperative needs-based education to reduce could be feasibility of modifying a patient’s preanxiety, increase satisfaction, and decrease time spent operative expectations by education. in day surgery: a randomized controlled trial. World J Surg. 2018;42(3):666–74. PubMed PMID: 28875242. Epub 2017/09/07. eng. 13. Stacey D, Legare F, Lewis K, Barry MJ, Bennett CL, References Eden KB, et al. Decision aids for people facing health treatment or screening decisions. Cochrane Database 1. Gleyze P, Coudane H. Patient information in orthopedic Syst Rev. 2017;4:CD001431. PubMed PMID: and trauma surgery. Fundamental knowledge, 28402085. Pubmed Central PMCID: 6478132. legal aspects and practical recommendations. 14. Dorrestijn O, Stevens M, Winters JC, van der Meer Orthop Traumatol Surg Res: OTSR. 2016;102(1 K, Diercks RL. Conservative or surgical treatment for Suppl):S105–11. PubMed PMID: 26826803. subacromial impingement syndrome? A systematic 2. Moyer R, Ikert K, Long K, Marsh J.  The value of review. J Shoulder Elbow Surg. 2009;18(4):652–60. preoperative exercise and education for patients PubMed PMID: 19286397. undergoing total hip and knee arthroplasty: a 15. Paavola M, Malmivaara A, Taimela S, Kanto K, Inkinen systematic review and meta-analysis. JBJS Rev. J, Kalske J, et al. Subacromial decompression versus 2017;5(12):e2. PubMed PMID: 29232265. Epub diagnostic arthroscopy for shoulder impingement: 2017/12/13. eng. randomised, placebo surgery controlled c­ linical trial. 3. Wartolowska K, Judge A, Hopewell S, Collins GS, BMJ. 2018;362:k2860. PubMed PMID: 30026230. Dean BJ, Rombach I, et  al. Use of placebo controls Pubmed Central PMCID: 6052435 at http://www. in the evaluation of surgery: systematic review. BMJ. icmje.org/coi_disclosure.pdf (available on request 2014;348:g3253. PubMed PMID: 24850821. Pubmed from the corresponding author) and declare: no Central PMCID: PMC4029190. Epub 2014/05/23. support from any organisation for the submitted work eng. other than those described above; ST reports personal 4. Pihl K, Roos EM, Nissen N, JoRgensen U, fees from Evalua group of companies, personal fees Schjerning J, Thorlund JB.  Over-optimistic patient from DBC group of companies, and personal fees expectations of recovery and leisure activities after from insurance companies, outside the submitted arthroscopic meniscus surgery. Acta Orthopaedica. work; KK reports an honorarium for a lecture from 2016;87(6):615–21. PubMed PMID: 27622598. Linvatec, outside the submitted work; TLNJ reports Pubmed Central PMCID: 5119445. an honorarium for a lecture on osteoporosis from 5. Cho CH, Seo HJ, Bae KC, Lee KJ, Hwang I, Warner AMGEN (donated to AllTrials campaign); no other JJ.  The impact of depression and anxiety on self-­ relationships or activities that could appear to have assessed pain, disability, and quality of life in patients influenced the submitted work. scheduled for rotator cuff repair. J Shoulder Elbow 16. Brox JI, Staff PH, Ljunggren AE, Brevik Surg. 2013;22(9):1160–6. PubMed PMID: 23594716. JI.  Arthroscopic surgery compared with supervised 6. Hanushek EA, Machin SJ, Woessmann L. Handbook exercises in patients with rotator cuff disease (stage II of the economics of education. Elsevier; 2016. impingement syndrome). BMJ. 1993;307(6909):899– 903. PubMed PMID: 8241852. Pubmed Central PMCID: 1679023.

Younger age is associated with higher level of activity and secondary higher expectations of postoperative outcome after surgery. Henn et al. found that younger patients both had a greater number of expectations as well as greater expectations for relief of night pain, improved ability to interact with others, and improved ability to exercise or participate in sports after shoulder arthroplasty (Fig. 62.2).

62  Patient Education and Patient Expectation in Shoulder Surgery 17. Beard DJ, Rees JL, Cook JA, Rombach I, Cooper C, Merritt N, et  al. Arthroscopic subacromial decompression for subacromial shoulder pain (CSAW): a multicentre, pragmatic, parallel group, placebo-­controlled, three-group, randomised surgical trial. Lancet. 2018;391(10118):329–38. PubMed PMID: 29169668. Pubmed Central PMCID: 5803129. 18. Colvin AC, Egorova N, Harrison AK, Moskowitz A, Flatow EL. National trends in rotator cuff repair. J Bone Joint Surg Am Vol. 2012;94(3):227–33. PubMed PMID: 22298054. Pubmed Central PMCID: 3262185. 19. Judge A, Murphy RJ, Maxwell R, Arden NK, Carr AJ.  Temporal trends and geographical variation in the use of subacromial decompression and rotator cuff repair of the shoulder in England. Bone Joint J. 2014;96-B(1):70–4. PubMed PMID: 24395314. 20. Ensor KL, Kwon YW, Dibeneditto MR, Zuckerman JD, Rokito AS.  The rising incidence of rotator cuff repairs. J Shoulder Elbow Surg. 2013;22(12):1628– 32. PubMed PMID: 23466172. 21. Paloneva J, Lepola V, Aarimaa V, Joukainen A, Ylinen J, Mattila VM.  Increasing incidence of rotator cuff repairs--a nationwide registry study in Finland. BMC Musculoskelet Disord. 2015;16:189. PubMed PMID: 26265152. Pubmed Central PMCID: 4531533. 22. Roberts H, Zhang D, Dyer GS.  The readability of AAOS patient education materials: evaluating the progress since 2008. J Bone Joint Surg Am Vol. 2016;98(17):e70. PubMed PMID: 27605695. 23. Henn RF 3rd, Kang L, Tashjian RZ, Green A.  Patients’ preoperative expectations predict the outcome of rotator cuff repair. J Bone Joint Surg Am Vol. 2007;89(9):1913–9. PubMed PMID: 17768186. 24. Blackburn J, Qureshi A, Amirfeyz R, Bannister G. Does preoperative anxiety and depression predict satisfaction after total knee replacement? Knee. 2012;19(5):522–4. PubMed PMID: 21846588. 25. Rolfson O, Dahlberg LE, Nilsson JA, Malchau H, Garellick G.  Variables determining outcome in total hip replacement surgery. J Bone Joint Surg Br Vol. 2009;91(2):157–61. PubMed PMID: 19190046. 26. Potter MQ, Wylie JD, Granger EK, Greis PE, Burks RT, Tashjian RZ. One-year patient-reported outcomes after arthroscopic rotator cuff repair do not correlate

825

with mild to moderate psychological distress. Clin Orthop Relat Res. 2015;473(11):3501–10. PubMed PMID: 26293222. Pubmed Central PMCID: 4586226. 27. Cho CH, Song KS, Hwang I, Warner JJ. Does rotator cuff repair improve psychologic status and quality of life in patients with rotator cuff tear? Clin Orthop Relat Res. 2015;473(11):3494–500. PubMed PMID: 25791445. Pubmed Central PMCID: 4586231. 28. O’Holleran JD, Kocher MS, Horan MP, Briggs KK, Hawkins RJ.  Determinants of patient satisfaction with outcome after rotator cuff surgery. J Bone Joint Surg Am Vol. 2005;87(1):121–6. PubMed PMID: 15634822. 29. Chen RE, Papuga MO, Nicandri GT, Miller RJ, Voloshin I.  Preoperative Patient-Reported Outcomes Measurement Information System (PROMIS) scores predict postoperative outcome in total shoulder arthroplasty patients. J Shoulder Elbow Surg. 2019;28(3):547–54. PubMed PMID: 30473243. 30. Atlas SJ, Tosteson TD, Blood EA, Skinner JS, Pransky GS, Weinstein JN.  The impact of workers’ compensation on outcomes of surgical and nonoperative therapy for patients with a lumbar disc herniation: SPORT.  Spine. 2010;35(1):89–97. PubMed PMID: 20023603. Pubmed Central PMCID: 2828633. 31. Tashjian RZ, Henn RF, Kang L, Green A. The effect of comorbidity on self-assessed function in patients with a chronic rotator cuff tear. J Bone Joint Surg Am Vol. 2004;86(2):355–62. PubMed PMID: 14960682. 32. Dekker AP, Salar O, Karuppiah SV, Bayley E, Kurian J.  Anxiety and depression predict poor outcomes in arthroscopic subacromial decompression. J Shoulder Elbow Surg. 2016;25(6):873–80. PubMed PMID: 27068379. 33. Tokish JM, Kissenberth MJ, Tolan SJ, Salim TI, Tadlock J, Kellam T, et al. Resilience correlates with outcomes after total shoulder arthroplasty. J Shoulder Elbow Surg. 2017;26(5):752–6. PubMed PMID: 28190668. 34. Jacobs CA, Morris BJ, Sciascia AD, Edwards TB. Comparison of satisfied and dissatisfied patients 2 to 5 years after anatomic total shoulder arthroplasty. J Shoulder Elbow Surg. 2016;25(7):1128–32. PubMed PMID: 26897317.

Animal Models in Shoulder Research

63

Leonardo Cavinatto and Leesa M. Galatz

Abstract

Animal models represent a very important tool for the advancement of orthopedic research. These models enhance the understanding about the natural history of diseases, contribute to the development of new clinical treatments and surgical techniques, and serve as a bridge between in vitro studies and human clinical trials. The use of animal models permits testing of emerging theories and concepts in a coherent and controlled environment, with consistent approaches at specific time points. Keywords

Rotator cuff · Rotator cuff repair · Large animal model · Rotator cuff tendon · Shoulder pathology

L. Cavinatto (*) Department of Orthopaedic Surgery, Corewell Health, Royal Oak, MI, USA e-mail: [email protected] L. M. Galatz Leni and Peter W. May Department of Orthopaedic Surgery, Icahn School of Medicine at Mount Sinai, New York, NY, USA e-mail: [email protected]

63.1 Introduction Animal models represent a very important tool for the advancement of orthopedic research. These models enhance the understanding about the natural history of diseases, contribute to the development of new clinical treatments and surgical techniques, and serve as a bridge between in vitro studies and human clinical trials. The use of animal models permits testing of emerging theories and concepts in a coherent and controlled environment, with consistent approaches at specific time points. In orthopedic research, there are many well-­ established animal models that closely reproduce human conditions. Several shoulder conditions have been the subject of experiments using animal models, including shoulder contracture [1], shoulder arthroplasty [2, 3], shoulder instability and joint capsule injury [4, 5], shoulder infection [6], rotator cuff tear arthropathy [7], and neonatal brachial plexus palsy [8, 9]. In recent years, most shoulder experiments using animal models focus on rotator cuff disease, the most prevalent shoulder orthopedic condition (Table 63.1). Cadaveric studies provide an appropriate tool to study some of the basic concepts of the shoulder, such as anatomy and biomechanics. Regarding rotator cuff disease, cadaveric studies precisely test muscle function, shoulder biomechanics, strength of various repair techniques, but are not suitable for analyzing the healing process

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 G. Milano et al. (eds.), Shoulder Arthroscopy, https://doi.org/10.1007/978-3-662-66868-9_63

827

L. Cavinatto and L. M. Galatz

828 Table 63.1  Comparative analysis of reported models for shoulder research Mouse Rat Rabbit Dog Sheep Primate

Bony anatomy +++ +++ ++ + + +++

Biologic reagents +++ +++ + – –

Rotator cuff repair No Difficult Yes Yes Yes Yes

after rotator cuff repair. A biological scenario is necessary to study tendon-to-bone healing tissue, bone morphometry, gene expression, extracellular matrix production, and tissue viscoelastic properties. In order to try to identify the best animal model for the study of rotator cuff disease, Soslowsky et al. [10] compared 33 animals using 34 different criteria. As a result, they suggest the rat as the most appropriate animal model for the study of rotator cuff disease, although the mouse was not included in the analysis. This chapter will review the various models used for the study of shoulder disorders and discuss their strengths and weaknesses with regards to clinical relevance.

63.2 Rat Model The rat is the most used animal model for the study of rotator cuff disease. As shown by Soslowsky et al. [10], the rat has numerous similarities to the human in terms of both bone and soft tissue anatomy (Fig. 63.1). In fact, the rat is one of the rare animals that has a well-developed acromion that orients anteriorly and articulates with the clavicle, forming an enclosed bony arch over the supraspinatus and infraspinatus tendons. When the rat walks, burrows, or reaches overhead, there is an excursion of these tendons under the coracoacromial arch. This particular anatomy, similar to the human condition, makes this a relevant model to study extrinsic mechanisms involved in rotator cuff disease, such as impingement and overuse [11, 12]. A wide variety of different biologic reagents are available for the rat, making broad categories

Cost $ $ $$ $$$ $$$ $$$$

Ease of handling ++++ ++++ +++ ++ ++ Very challenging

Arthroplasty No No No Yes Yes Potential

of biological analysis feasible [13]. Because of the large number of primers and antibodies already commercially available, gene expression, protein quantification, and immunohistochemistry assays are easily accessible. The rat is one of the animals with the greatest percentage of genetic similarity to humans. One study of comparative genomics showed an 80 to 90% of genetic semblance between the rat and the human [14]. This similarity enables the rat to provide very useful translational data. The rat is also one of the rare animals that can tolerate bilateral surgery. This unique characteristic makes paired analysis possible, which enhances the statistical power of the study. Additionally, rats have a short gestational period with multiple offspring, a rapid growth rate, and a short life span [13]. As opposed to many other animals used in shoulder research, rats rarely get infected or sick, tolerate anesthesia well, are relatively inexpensive, and are very docile. However, the rat and the human rotator cuff have considerable differences. In the rat, the tendons are not interdigitated together, and they are blended to the underlying joint capsule only very close to their bone attachment. In the human shoulder, the rotator cuff tendons are interdigitated together and blended to the capsule throughout the whole trajectory [15]. Additionally, rodents have a growth plate at the proximal humerus that remains open well into maturity. The clinical significance of this is unknown but suggests a higher capacity for certain remodeling and regenerative processes compared to humans. Another obvious disadvantage of the rat model for shoulder research is the small size of the rotator cuff tendons, making standard-of-care repair

63  Animal Models in Shoulder Research

829

Fig. 63.1  The bony anatomy of the human and the rat shoulder is very similar. A well-developed acromion and coracoacromial ligament forms a rigid arch over the rotator cuff. [From ref 61. Copyright: Journal of Shoulder and Elbow Surgery; published by Elsevier 1996. Reproduced with permission] Human

Human

techniques virtually impossible. The rat, like all other animals used for shoulder research, generates a massive scar response between the stump of the tendon and the bone where the tendon was previously attached. Therefore, the rat generates scar tissue even in the absence of repair [16, 17]. However, unlike large animal models, tendon repairs rarely fail in the rat, making the study of repaired tendon-to-bone insertion sites possible [18–20]. In the following sections, the important contributions from rodent models concerning shoulder pathology and development will be briefly described.

Rat

Rat

63.2.1 Mechanobiology The rat model has opened new avenues for studying mechanobiology during tendon development and rotator cuff disease and has provided insight for clinical application. Muscle paralysis during tendon development in neonatal rodents, either by botulinum toxin injection or superior trunk neurotomy, results in delayed tendon formation, delayed fibrocartilage maturation, and impaired mineralization of the enthesis as well as shoulder contracture [8, 9, 21]. For the first two weeks of life, the effects of paralysis are minimal, and the effects escalate

L. Cavinatto and L. M. Galatz

830

beyond that time point. These findings suggest that early development is under genetic control, while later changes are greatly influenced by the mechanical environment. These experiments lead the way for developing a useful animal model for future research examining musculoskeletal changes secondary to neonatal nerve injury, including Neonatal Brachial Plexus Palsy (NBPP). The rat model has been instrumental in studying tendon-to-bone healing of the rotator cuff. This model has been used to develop and improve repair and rehabilitation strategies. In an acutely repaired rat rotator cuff, immobilizing the operated limb leads to improved mechanical properties, smaller volume of scar tissue, and greater collagen organization, when compared to the rats that were allowed normal cage activity or exercised on a treadmill [22, 23]. These data ­ show a potential negative effect of excessive motion and force at the repair site. Similarly, another study demonstrated that high load and excessive motion across the repair site during tendon healing leads to inferior mechanical properties and poor healing outcomes. Passive motion and exercise following tendon-to-bone repair led to a significant decrease in the mechanical, structural, and compositional properties at the repair site. Exercise and passive motion also led to reduced range of motion compared with rats exposed to immobilization or regular cage activity [22, 24, 25]. Although some stress deprivation by immobilization or short-term paralysis can potentially benefit recovery and enhance the mechanical properties of the enthesis in certain scenarios [26, 27], complete unloading has also been shown to be detrimental for tendon-to-bone healing. In two experiments where rat supraspinatus muscles were injected with botulinum toxin after repair, biomechanical testing demonstrated significantly inferior structural properties, specifically ultimate stress and stiffness, in experimental rats compared to controls [18, 28]. Therefore, like other musculoskeletal tissues, some controlled force is beneficial to healing. There is an optimal level of tension for tendon-

to-bone healing, and both the complete lack of force as well as excessive loads are detrimental [29]. This research provides insight for rehabilitation protocols in clinical practice.

63.2.2 Biological Studies The rodent model has enabled the study of biological adjuvants with respect to the repaired rotator cuff, in an effort to improve healing. Augmentation of the tendon-to-bone environment with growth factors [30], stem cells [31, 32] or bioengineered scaffolds [33–35] has been used to enhance healing of the rotator cuff to bone. Although some improvement could be seen with the addition of some specific growth factors, the biological process is complex and involves a multitude of growth and transcription factors. Ideal timing for delivery and maximally effective agent is still under investigation [29]. Cellular and gene transfer approaches have shown to promote some improvement in the rotator cuff repair. Although mesenchymal stem cells (MSC) alone delivered at the repair site did not result in improvement [36], MSCs transfected with scleraxis, a transcription factor involved in tendon development, resulted in improved structural properties of the newly formed repair [37]. A similar study with MSCs transfected with type-1 matrix metalloproteinase (MMP-1) also resulted in a significant improvement in rat rotator cuff healing compared to controls [32].

63.2.3 Scaffolds The rat provides a live model to test bioengineered scaffolds. Newer scaffolds that recreate the native tissue mineral gradation in composition, structure, mechanical properties between the compliant tendon and the stiff bone are beginning to be tested in the rat shoulder [29, 38]. These scaffolds are either being implanted alone, with MSCs, or with MSCs transfected with bone morphogenic protein-1 (BMP-1). Further studies are ongoing but still several challenges need to be addressed.

63  Animal Models in Shoulder Research

63.2.4 Chronic Model For the rat model of rotator cuff tears, isolated supraspinatus or infraspinatus transection resulted in an initial degeneration of the musculotendinous units followed by reversal of the degenerative changes as a result of the restoration of tendon tension caused by adherence in the neighboring tissues. Recently, the rat was validated as a model for massive, chronic rotator cuff tear. It was shown that the detachment of both the supraspinatus and infraspinatus from the greater tuberosity alone or combined with suprascapular neurotomy resulted in fatty muscular degeneration, atrophy, and stiffness of the musculotendinous unit, similar to the findings in humans [39, 40]. All of these changes are the clinical characteristics of chronic degenerated rotator ­ cuff. A study comparing early repair with late repair of massive rotator tears (supraspinatus and infraspinatus ruptures) favored the early repair considering the biomechanical properties of the healed tendon-to-bone attachment and the morphometry of the humeral head [17]. A study investigated the role of biceps tenotomy in the setting of a chronic and massive rotator cuff tear [41]. Rats that underwent biceps tenotomy showed improved gait parameters, suba

Fig. 63.2  Mouse supraspinatus (a) and infraspinatus (b) muscles at 8 weeks after tenotomy of the 2 tendons (supraspinatus and infraspinatus) and neurotomy of the suprascapular nerve shows substantial muscle degenera-

831

scapularis tendon mechanical properties and histological scores of the glenoid cartilage as compared with the sham surgery group.

63.2.5 Adhesive Capsulitis The rat model has also served as an experimental model for induction of adhesive capsulitis/shoulder contracture [1, 42, 43]. To induce shoulder contraction, rats had their shoulders immobilized with either a molder plaster or with surgical internal fixation of the scapula to the humerus. The experimental groups demonstrated a significant decrease in the range of motion mostly at the cost of the capsule, together with synovitis, fibrosis, and collagen type III formation in the synovium tissue.

63.3 Mouse Model A mouse model for rotator cuff tears was also developed [44]. In addition to all the advantages of using a small, rodent model, the mouse model can take advantage of the vast array of transgenic technology and knock-out strains (Fig.  63.2). While surgery to repair a mouse rotator cuff tear

b

tion, characterized by fatty changes and atrophy. [From ref 35. Copyright: Journal of Shoulder and Elbow Surgery; published by Elsevier 2012. Reproduced with permission]

L. Cavinatto and L. M. Galatz

832

is vastly more difficult as compared to the rat or other larger animal models, recent studies showed a consistent and reproducible microsurgical repair technique of the mouse supraspinatus tendon in the acute and chronic settings [45–47]. These studies using the mouse model for rotator cuff repair open new avenues for basic science and translational research into signaling pathways and gene expression approaches. The mouse also served as a reproducible model for rotator cuff tear arthropathy [7]. Mice underwent operative ligation of their rotator cuff and were followed for 45 weeks after surgery. Histopathologic and microtomographic analysis revealed a progressive, time-dependent changes in the shoulder similar to human cuff tear arthropathy, including acetabularization of the coracoacromial arch and femoralization of the humeral head. Recently, a mouse model of shoulder implant infection was developed [6]. A surgical press-fit implant was introduced to the proximal humeral of a group of mice combined with inoculation of Staphylococcus aureus. Bacterial activity using bioluminescence and targeting probe and radiographs were used to monitor infection and radiographic changes. Osteolysis and catastrophic bone destruction could be observed in the chronic infectious joints after 10 and 42 days from the operation.

a

Fig. 63.3  Shoulder radiograph of a sheep (a), and of a dog (b), showing on both shoulders an elongated humeral head, a deep glenoid, and a prominent greater tuberosity.

63.4 Large Animal Models Large animals have shoulder joints and rotator cuff tendons that are similar in size to the human (Fig. 63.3). This allows more accurate and reproducible studies of repair techniques of the rotator cuff tendons to the proximal humerus insertion footprint. The smaller the animal, the more accelerated the healing process. Therefore, studies evaluating the strength and mechanical properties of a repair over a given time course potentially provide more applicable translational data. Novel shoulder prosthesis designs and techniques have been tested in large animal models [2, 48]. The use of large animal models for the study of prosthesis design and wear characteristics is potentially useful, but its use has not been validated or maximized at this time point. Nevertheless, large animals have several disadvantages for studying shoulder pathology. All the large non-primate animals used for shoulder research, including the sheep, the goat, the dog, the rabbit, and the calf, have very different bone and soft tissue anatomy compared to the human shoulder [15, 49]. In these quadruped animals, the acromion, the clavicle and the coracoid process are generally non-existent and do not cover the rotator cuff. In the rabbit, specifically, the acromion directs inferiorly and partially covers the infraspinatus and the teres minor tendons.

b

[From ref 66. Copyright: Journal of Shoulder and Elbow Surgery; published by Elsevier 2007. Reproduced with permission]

63  Animal Models in Shoulder Research

833

The rabbit subscapularis tendon passes through a bone tunnel in the anterior aspect of the joint. The soft tissues in the shoulder are also significantly different from humans, as the animal rotator cuff tendon fibers are very aligned, analogous to the Achilles tendon in humans. The tendons do not have fibers crossing in different directions and are not blended with the underlying capsule. In large animals, the rotator cuff tendons are mainly extra-capsular, preventing contact with the synovial fluid. In large animal models, among the rotator cuff tendons, the most utilized is the infraspinatus. This tendon has a size very similar to the human supraspinatus, and is easily accessible after the shoulder approach, and when injured, gait is significantly affected. One of the biggest disadvantages of the use of large animals for the study of rotator cuff disease is the ubiquitous rate of early tendon repair failure, often in the first few days. Because re-tears is frequently observed, what it is most commonly being studied is the scar tissue that forms between the stump of the tendon and the greater tuberosity, and not the newly formed enthesis itself [50–53]. One may argue that it embodies the character of rotator cuff tendon healing; however, the universal retraction presents a limitation. This phenomenon is seen even when the postoperative limb is protected by immobilization or by a softball affixed to the operated paw postoperatively [54, 55].

a

b

Fig. 63.4 (a) Tantalum bead markers were placed on the injured infraspinatus tendon (IFT-T, white arrows) and on the greater tuberosity of the humerus (HUM, black arrows) of adult mongrel dogs after full thickness supra-

63.4.1 Canine Model The canine shoulder has been used as a model for rotator cuff injury and repair, as well as other shoulder pathologies in a broad range of experiments. In one study, tantalum bead markers were placed on the injured tendons of adult mongrel dogs after full-thickness supraspinatus injury and repair. The repairs showed a 100% failure rate, as evaluated by bead displacement (Fig. 63.4). These failures occurred early in the postoperative period, regardless of the suture type, suture configuration or postoperative protocol [52]. To reduce the incidence of re-tears in the canine model, another experiment performed by the same group tried a partial-width lesion and subsequent repair, detaching only the upper two thirds of the infraspinatus tendon [56]. Although the retraction distance was reduced compared to the full-thickness injury model, a 100% repair failure rate was still observed. The authors concluded that the canine model represents a rigorous test for new sutures and repair techniques in rotator cuff repair, but is not suitable for studying the newly formed enthesis. The dog shoulder has some peculiar differences compared to the human shoulder. Canines have a flattened humeral head, a prominent greater tuberosity and a deep glenoid [57]. There are also important differences in the biomechanics of the dog shoulder compared with the

c

spinatus injury and repair. Fluoroscopy was done intraoperatively (b) and 5 days after repair (c). [From ref 12. Copyright: Journal of Shoulder and Elbow Surgery; published by Elsevier 2007. Reproduced with permission]

834

human, as the dog uses the forelimbs for weight bearing and has very limited overhead activity [13, 15, 49]. On the other hand, the canine model accurately reproduces the degenerative changes observed in the chronically ruptured human rotator cuff tendons. In fact, the canine model simulates muscle stiffness, atrophy, and fatty degeneration in the chronic and massive rotator cuff tears observed in the human clinical scenario [52, 58]. Additionally, dogs have been used to test scaffolds for augmenting tendon-to-bone repair [56]. The canine shoulder also has served as a model to test other clinically relevant experiments, such as shoulder reconstruction and arthroplasty. Wirth et  al. tested a new glenoid implant in the canine [48], and Matsen et  al. experimented with a novel technique for shoulder arthroplasty, where a prosthetic humeral component articulated in a reamed, non-implanted glenoid [2]. The authors from this last experiment subsequently applied the technique to clinical practice [59].

63.4.2 Sheep Model The sheep model has become a convenient large animal for the study of orthopedic diseases, including shoulder pathologies. The sheep has a well-developed and easy accessible infraspinatus tendon with a size comparable to the human supraspinatus tendon. These features make the sheep infraspinatus tendon a reasonable option for investigations involving rotator cuff repair (Fig. 63.5). Sheep are also easily handled animals and well accepted by society as a research animal [53, 60]. The sheep has been used to test different suture techniques and configurations [51], novel suture anchors [61], bioengineered scaffolds [62], and biological aids to try to enhance tendon-­to-­bone healing [63] in the setting of rotator cuff repair. It has also been used to study the degenerative consequences after tendon unloading, and to investigate the findings after tendon reloading [64].

L. Cavinatto and L. M. Galatz

The sheep model has two major shortcomings. Similar to other large animal models, a huge scar forms between the stump of the tendon and the bone after detachment. This is in direct opposition to the lack of healing evidenced in the clinical scenario, especially in chronic, degenerated, and massive tears. Additionally, in this model, it is not possible to keep the repaired tendon attached to the bone, regardless of the type of immobilization used in the postoperative period. The high loads imposed by muscle activity and weight bearing result in the formation of a gap between the distal end of the tendon and the proximal humeral attachment. Another distinct disadvantage of this model, especially when compared to the murine model, is the lack of probes and reagents for the sheep, limiting the variety of biological assays, like PCR, immunohistochemistry, and in situ hybridization [60]. Although limited, some research was conducted in the ovine model regarding glenohumeral instability. Because of the major anatomic differences, these studies have limited clinical applicability [65].

63.4.3 Rabbit Model The rabbit is another animal commonly used for shoulder research. Because of the larger size of the tendons compared to the rat, the repair is ultimately more manageable for surgical manipulation and for biomechanical testing. The rabbit model has been primarily used for the study of rotator cuff disease. The rabbit model has been extensively used to study muscle response after tendon injury and unloading. Muscular fatty degeneration and atrophy were observed after supraspinatus detachment, and the changes were shown to arise within the first 3 months after unloading [66]. In an attempt to reverse the muscle pathology after unloading, Uhthoff et  al. repaired rabbit supraspinatus tendon after 6 and 12 weeks after detachment [67]. The investigators showed that early supraspinatus repair did prevent an increase in the muscle fat. Interestingly, reloading via repair

63  Animal Models in Shoulder Research

a

835

d

b

e

c

Fig. 63.5 (a) Intraoperative view of the surgical approach to the sheep shoulder, showing the infraspinatus tendon insertion on the greater tuberosity of the right humerus (b, c, d) Anatomic dissection shows the anatomic location of the Teres Minor muscle, Infraspinatus tendon and foot-

print insertion, humeral head and joint capsule. (e) Bony anatomic landmarks. [From ref 69. Copyright: Sports Med Arthrosc; published by Lippincott Williams & Wilkins 2011. Reproduced with permission]

L. Cavinatto and L. M. Galatz

836

did not reverse the muscular degeneration, even when repaired as early as 6 weeks after detachment. The rabbit model has also provided new information about tendon-to-bone re-formation after cuff repair. Chondrocytes, non-chondrocytic cells, extracellular matrix, and collagen organization at the healing enthesis were quantified longitudinally from 2 to 24 weeks after the repair [68]. Although both cell lines were restored by 24 weeks, extracellular matrix formation and collagen organization did not reach normal levels. These results suggest that, at 24 weeks, the re-­ formed enthesis is still mechanically weaker than an original age-matched enthesis. Comparison of the anatomical site to perform biceps tenodesis (bone tunnel versus cortical surface fixation in the humerus) was performed using the rabbit model [69]. Tendon-to-bone healing, assessed by biomechanical testing, microcomputed tomography and histomorphometric analysis, showed similar healing profiles between the two sites. There was minimal intratunnel healing compared with the healing outside the tunnel on the cortical surface, suggesting that bone tunnels for biceps tenodesis might be unnecessary. Longitudinal investigations analyzing the temporal expression of metalloproteinases and tissue inhibitions of metalloproteinases, as well of growth factors and pro-inflammatory markers were also performed using the rabbit model. These experiments help determine the temporal expression of the biological factors involved in tendon-to-bone healing and provide preliminary data for future experimentation using biological adjuvants to enhance healing [50, 70]. A histological investigation comparing acute and delayed supraspinatus repair was also conducted in the rabbit model [68]. Interestingly, the authors found no difference between the tendons repaired immediately after detachment and after 6 or 12 weeks. The enthesis histology depended only on the time lapsed from repair to ultimate sacrifice or follow-up, and not on the period between detachment and repair. The rabbit supraspinatus tendon was used in several other rotator cuff pathology experiments,

including tendon-to-bone healing after the delivery of growth factors, and augmentation with scaffolds [71]. Recently, the rabbit subscapularis tendon, because of its particular anatomy passing through a bone tunnel in the anterior region of the shoulder, has been used in rotator cuff experiments [72] in order to attempt to replicate the potential effect of a coracoacromial arch.

63.4.4 Primate Model One study to date has used the primate model to investigate rotator cuff healing [73].The authors performed histology analysis to show that the new enthesis was not completely matured even after 15 weeks after repair—the furthest time-­ point analyzed. These results support the notion that the rotator cuff healing process is a reparative process, rather than a regenerative process. Another study with non-human primates investigated the naturally-occurring age-related degenerative changes of the shoulder joint in known-aged adult and elderly vervet monkeys [74]. According to the authors, the anatomical changes and retroversion of the glenoid and physical mobility could establish the vervet monkey as an animal model for shoulder degenerative disease. While the primate model is desirable in terms of its human applicability, the challenges with regards to cost and animal handling present major limitations. Use of primates also raises ethical issues surrounding care and use of experimental animals.

63.5 Summary No single animal model perfectly represents the clinical condition of a given clinical condition in the shoulder. However, each model has strengths and weaknesses that should be considered in determining appropriate applicability for answering a given scientific question. Smaller animals offer the advantage of low cost, anatomic similarity, and availability of biologic reagents. They are better for evaluating gene expression and protein

63  Animal Models in Shoulder Research

production. The larger models lend themselves to reproducible surgery but have high retraction rates. They are better utilized for evaluating surgical techniques. Both can be utilized for evaluating the utility of biologic augmentation strategies. As always, ethical, and appropriate use of animals should be carefully considered.

References 1. Kanno A, Sano H, Itoi E.  Development of a shoulder contracture model in rats. J Shoulder Elb Surg [Internet]. 2010;19(5):700–8. https://doi. org/10.1016/j.jse.2010.02.004. 2. Matsen FA 3rd, Clark JM, Titelman RM, Gibbs KM, Boorman RS, Deffenbaugh D, et  al. Healing of reamed glenoid bone articulating with a metal humeral ­hemiarthroplasty: a canine model. J Orthop Res Off Publ Orthop Res Soc. 2005;23(1):18–26. 3. Wirth MA, Tapscott RS, Southworth C, Rockwood CAJ.  Treatment of glenohumeral arthritis with a hemiarthroplasty. Surgical technique. J Bone Joint Surg Am. 2007;89(Suppl 2):10–25. 4. Packer JD, Varthi AG, Zhu DS, Javier FG, Young JD, Garver JV, et al. Ibuprofen impairs capsulolabral healing in a rat model of anterior glenohumeral instability. J Shoulder Elb Surg [Internet]. 2018;27(2):315–24. https://doi.org/10.1016/j.jse.2017.09.027. 5. Kovacevic D, Baker AR, Staugaitis SM, Kim MS, Ricchetti ET, Derwin KA.  Development of an arthroscopic joint capsule injury model in the canine shoulder. PLoS One. 2016;11(1):1–15. 6. Sheppard WL, Mosich GM, Smith RA, Hamad CD, Park HY, Zoller SD, et  al. Novel in  vivo mouse model of shoulder implant infection. J Shoulder Elb Surg [Internet]. 2020;29(7):1412–24. https://doi. org/10.1016/j.jse.2019.10.032. 7. Zingman A, Li H, Sundem L, DeHority B, Geary M, Fussel T, et  al. Shoulder arthritis secondary to rotator cuff tear: a reproducible murine model and histopathologic scoring system. J Orthop Res. 2017;35(3):506–14. 8. Kim HM, Galatz LM, Das R, Patel N, Thomopoulos S.  Musculoskeletal deformities secondary to neurotomy of the superior trunk of the brachial plexus in neonatal mice. J Orthop Res Off Publ Orthop Res Soc. 2010;28(10):1391–8. 9. Crouch DL, Hutchinson ID, Plate JF, Antoniono J, Gong H, Cao G, et al. Biomechanical basis of shoulder osseous deformity and contracture in a rat model of brachial plexus birth palsy. J Bone Jt Surg  - Am. 2014;97(15):1264–71. 10. Soslowsky LJ, Carpenter JE, DeBano CM, Banerji I, Moalli MR. Development and use of an animal model for investigations on rotator cuff disease. J Shoulder Elb Surg. 1996;5(5):383–92.

837 11. Carpenter JE, Thomopoulos S, Flanagan CL, DeBano CM, Soslowsky LJ.  Rotator cuff defect healing: a biomechanical and histologic analysis in an animal model. J Shoulder Elb Surg. 1998;7(6):599–605. 12. Soslowsky LJ, Thomopoulos S, Tun S, Flanagan CL, Keefer CC, Mastaw J, et  al. Neer Award 1999. Overuse activity injures the supraspinatus tendon in an animal model: a histologic and biomechanical study. J Shoulder Elb Surg. 2000;9(2):79–84. 13. Longo UG, Forriol F, Campi S, Maffulli N, Denaro V. Animal models for translational research on shoulder pathologies: from bench to bedside. Sports Med Arthrosc. 2011;19(3):184–93. 14. Warden SJ. Animal models for the study of tendinopathy. Br J Sports Med. 2007;41(4):232–40. 15. Edelstein L, Thomas SJ, Soslowsky LJ. Rotator cuff tears: what have we learned from animal models? J Musculoskelet Neuronal Interact. 2011;11(2):150–62. 16. Galatz LM, Sandell LJ, Rothermich SY, Das R, Mastny A, Havlioglu N, et  al. Characteristics of the rat supraspinatus tendon during tendon-to-bone healing after acute injury. J Orthop Res Off Publ Orthop Res Soc. 2006;24(3):541–50. 17. Cavinatto L, Malavolta EA, Pereira CAM, Miranda-­ Rodrigues M, Silva LCM, Gouveia CH, et  al. Early versus late repair of rotator cuff tears in rats. J Shoulder Elb Surg. 2018;27(4) 18. Galatz LM, Charlton N, Das R, Kim HM, Havlioglu N, Thomopoulos S. Complete removal of load is detrimental to rotator cuff healing. J Shoulder Elb Surg. 2009;18(5):669–75. 19. Galatz LM, Rothermich SY, Zaegel M, Silva MJ, Havlioglu N, Thomopoulos S. Delayed repair of tendon to bone injuries leads to decreased biomechanical properties and bone loss. J Orthop Res Off Publ Orthop Res Soc. 2005;23(6):1441–7. 20. Killian ML, Cavinatto LM, Ward SR, Havlioglu N, Thomopoulos S, Galatz LM.  Chronic degeneration leads to poor healing of repaired massive rotator cuff tears in rats. Am J Sports Med. 2015;43(10) 21. Thomopoulos S, Kim H-M, Rothermich SY, Biederstadt C, Das R, Galatz LM. Decreased muscle loading delays maturation of the tendon enthesis during postnatal development. J Orthop Res Off Publ Orthop Res Soc. 2007;25(9):1154–63. 22. Thomopoulos S, Williams GR, Soslowsky LJ. Tendon to bone healing: differences in biomechanical, structural, and compositional properties due to a range of activity levels. J Biomech Eng. 2003;125(1):106–13. 23. Gimbel JA, Van Kleunen JP, Williams GR, Thomopoulos S, Soslowsky LJ.  Long durations of immobilization in the rat result in enhanced mechanical properties of the healing supraspinatus tendon insertion site. J Biomech Eng. 2007;129(3):400–4. 24. Peltz CD, Sarver JJ, Dourte LM, Würgler-Hauri CC, Williams GR, Soslowsky LJ.  Exercise following a short immobilization period is detrimental to tendon properties and joint mechanics in a rat rotator cuff injury model. J Orthop Res Off Publ Orthop Res Soc. 2010;28(7):841–5.

838 25. Peltz CD, Dourte LM, Kuntz AF, Sarver JJ, Kim S-Y, Williams GR, et  al. The effect of postoperative passive motion on rotator cuff healing in a rat model. J Bone Joint Surg Am. 2009;91(10):2421–9. 26. De Aguiar G, Chait LA, Schultz D, Bleloch S, Theron A, Snijman CN, et al. Chemoprotection of flexor tendon repairs using botulinum toxin. Plast Reconstr Surg. 2009;124(1):201–9. 27. Ma J, Shen J, Smith BP, Ritting A, Smith TL, Koman LA. Bioprotection of tendon repair: adjunctive use of botulinum toxin A in Achilles tendon repair in the rat. J Bone Joint Surg Am. 2007;89(10):2241–9. 28. Hettrich CM, Rodeo SA, Hannafin JA, Ehteshami J, Shubin Stein BE. The effect of muscle paralysis using Botox on the healing of tendon to bone in a rat model. J Shoulder Elb Surg. 2011;20(5):688–97. 29. Killian ML, Cavinatto L, Galatz LM, Thomopoulos S.  The role of mechanobiology in tendon healing. J Shoulder Elb Surg [Internet]. 2012;21(2):228–37. https://doi.org/10.1016/j.jse.2011.11.002. 30. Manning CN, Kim HM, Sakiyama-Elbert S, Galatz LM, Havlioglu N, Thomopoulos S.  Sustained delivery of transforming growth factor beta three enhances tendon-to-bone healing in a rat model. J Orthop Res Off Publ Orthop Res Soc. 2011;29(7):1099–105. 31. Gulotta LV, Kovacevic D, Montgomery S, Ehteshami JR, Packer JD, Rodeo SA. Stem cells genetically modified with the developmental gene MT1-MMP improve regeneration of the supraspinatus tendon-to-bone insertion site. Am J Sports Med. 2010;38(7):1429–37. 32. Gulotta LV, Kovacevic D, Packer JD, Ehteshami JR, Rodeo SA.  Adenoviral-mediated gene transfer of human bone morphogenetic protein-13 does not improve rotator cuff healing in a rat model. Am J Sports Med. 2011;39(1):180–7. 33. Beason DP, Connizzo BK, Dourte LM, Mauck RL, Soslowsky LJ, Steinberg DR, et  al. Fiber-aligned polymer scaffolds for rotator cuff repair in a rat model. J Shoulder Elb Surg. 2012;21(2):245–50. 34. Leigh DR, Mesiha M, Baker AR, Walker E, Derwin KA. Host response to xenograft ECM implantation is not different between the shoulder and body wall sites in the rat model. J Orthop Res Off Publ Orthop Res Soc. 2012;30(11):1725–31. 35. Lipner J, Shen H, Cavinatto L, Liu W, Havlioglu N, Xia Y, et  al. In vivo evaluation of adipose-derived stromal cells delivered with a nanofiber scaffold for tendon-to-bone repair. Tissue Eng  - Part A. 2015;21(21–22) 36. Gulotta LV, Kovacevic D, Ehteshami JR, Dagher E, Packer JD, Rodeo SA. Application of bone marrow-­ derived mesenchymal stem cells in a rotator cuff repair model. Am J Sports Med. 2009;37(11):2126–33. 37. Gulotta LV, Kovacevic D, Packer JD, Deng XH, Rodeo SA.  Bone marrow-derived mesenchymal stem cells transduced with scleraxis improve rotator cuff healing in a rat model. Am J Sports Med. 2011;39(6):1282–9. 38. Zhu C, Qiu J, Thomopoulos S, Xia Y.  Augmenting tendon-to-bone repair with functionally graded scaffolds. Adv Healthc Mater. 2021;10(9):e2002269.

L. Cavinatto and L. M. Galatz 39. Liu X, Manzano G, Kim HT, Feeley BT. A rat model of massive rotator cuff tears. J Orthop Res Off Publ Orthop Res Soc. 2011;29(4):588–95. 40. Kim HM, Galatz LM, Lim C, Havlioglu N, Thomopoulos S.  The effect of tear size and nerve injury on rotator cuff muscle fatty degeneration in a rodent animal model. J Shoulder Elb Surg. 2012;21(7):847–58. 41. Chen M, Shetye SS, Huegel J, Riggin CN, Gittings DJ, Nuss CA, et  al. Biceps detachment preserves joint function in a chronic massive rotator cuff tear rat model. Am J Sports Med. 2018;46(14):3486–94. 42. Okajima SM, Cubria MB, Mortensen SJ, Villa-­ Camacho JC, Hanna P, Lechtig A, et  al. Rat model of adhesive capsulitis of the shoulder. J Vis Exp. 2018;2018(139):1–7. 43. Kim DH, Lee KH, Lho YM, Ha E, Hwang I, Song KS, et al. Characterization of a frozen shoulder model using immobilization in rats. J Orthop Surg Res [Internet]. 2016;11(1):1–6. https://doi.org/10.1186/ s13018-­016-­0493-­8. 44. Liu X, Laron D, Natsuhara K, Manzano G, Kim HT, Feeley BT.  A mouse model of massive rotator cuff tears. J Bone Joint Surg Am. 2012;94(7):e41. 45. Bell R, Taub P, Cagle P, Flatow EL, Andarawis-Puri N. Development of a mouse model of supraspinatus tendon insertion site healing. J Orthop Res Off Publ Orthop Res Soc. 2015;33(1):25–32. 46. Lebaschi AH, Deng XH, Camp CL, Zong J, Cong GT, Carballo CB, et  al. Biomechanical, histologic, and molecular evaluation of tendon healing in a new murine model of rotator cuff repair. Arthrosc  - J Arthrosc Relat Surg [Internet]. 2018;34(4):1173–83. https://doi.org/10.1016/j. arthro.2017.10.045. 47. Wang Z, Liu X, Davies MR, Horne D, Kim H, Feeley BT.  A mouse model of delayed rotator cuff repair results in persistent muscle atrophy and fatty infiltration. Am J Sports Med. 2018;46(12):2981–9. 48. Wirth MA, Korvick DL, Basamania CJ, Toro F, Aufdemorte TB, Rockwood CAJ.  Radiologic, mechanical, and histologic evaluation of 2 glenoid prosthesis designs in a canine model. J Shoulder Elb Surg. 2001;10(2):140–8. 49. Derwin KA, Baker AR, Iannotti JP, McCarron JA.  Preclinical models for translating regenerative medicine therapies for rotator cuff repair. Tissue Eng Part B Rev. 2010;16(1):21–30. 50. Rodeo SA, Potter HG, Kawamura S, Turner AS, Kim HJ, Atkinson BL.  Biologic augmentation of rotator cuff tendon-healing with use of a mixture of osteoinductive growth factors. J Bone Joint Surg Am. 2007;89(11):2485–97. 51. Gerber C, Schneeberger AG, Perren SM, Nyffeler RW.  Experimental rotator cuff repair. A preliminary study. J Bone Joint Surg Am. 1999;81(9):1281–90. 52. Derwin KA, Baker AR, Codsi MJ, Iannotti JP.  Assessment of the canine model of rotator cuff injury and repair. J Shoulder Elb Surg [Internet]. 2007;16(5):S140–8. Available from: https://www.

63  Animal Models in Shoulder Research ncbi.nlm.nih.gov/pmc/articles/PMC3624763/pdf/ nihms412728.pdf 53. Ahmad Z, Al-Wattar Z, Rushton N.  Tissue engineering for the ovine rotator cuff: surgical anatomy, approach, implantation and histology technique, along with review of literature. J Investig Surg [Internet]. 2020;33(2):147–58. https://doi.org/10.1080/0894193 9.2018.1483446. 54. Lewis CW, Schlegel TF, Hawkins RJ, James SP, Turner AS.  Comparison of tunnel suture and suture anchor methods as a function of time in a sheep model. Biomed Sci Instrum. 1999;35:403–8. 55. Lewis CW, Schlegel TF, Hawkins RJ, James SP, Turner AS.  The effect of immobilization on rotator cuff healing using modified Mason-Allen stitches: a biomechanical study in sheep. Biomed Sci Instrum. 2001;37:263–8. 56. Derwin KA, Codsi MJ, Milks RA, Baker AR, McCarron JA, Iannotti JP.  Rotator cuff repair augmentation in a canine model with use of a woven poly-L-lactide device. J Bone Joint Surg Am. 2009;91(5):1159–71. 57. Sager M, Herten M, Ruchay S, Assheuer J, Kramer M, Jäger M.  The anatomy of the glenoid labrum: a comparison between human and dog. Comp Med. 2009;59(5):465–75. 58. Safran O, Derwin KA, Powell K, Iannotti JP. Changes in rotator cuff muscle volume, fat content, and passive mechanics after chronic detachment in a canine model. J Bone Jt Surg - Ser A. 2005;87(12 I):2662–70. 59. Clinton J, Franta AK, Lenters TR, Mounce D, Matsen FA 3rd. Nonprosthetic glenoid arthroplasty with humeral hemiarthroplasty and total shoulder arthroplasty yield similar self-assessed outcomes in the management of comparable patients with glenohumeral arthritis. J Shoulder Elb Surg. 2007;16(5):534–8. 60. Turner AS.  Experiences with sheep as an animal model for shoulder surgery: strengths and shortcomings. J Shoulder Elb Surg. 2007;16(5 Suppl):S158–63. 61. Harrison JA, Wallace D, Van Sickle D, Martin T, Sonnabend DH, Walsh WR.  A novel suture anchor of high-density collagen compared with a metallic anchor. Results of a 12-week study in sheep. Am J Sports Med. 2000;28(6):883–7. 62. Easley J, Puttlitz C, Hackett E, Broomfield C, Nakamura L, Hawes M, et  al. A prospective study comparing tendon-to-bone interface healing using an interposition bioresorbable scaffold with a vented anchor for primary rotator cuff repair in sheep. J Shoulder Elb Surg [Internet]. 2020;29(1):157–66. https://doi.org/10.1016/j.jse.2019.05.024. 63. MacGillivray JD, Fealy S, Terry MA, Koh JL, Nixon AJ, Warren RF.  Biomechanical evaluation of

839 a rotator cuff defect model augmented with a bioresorbable scaffold in goats. J Shoulder Elb Surg. 2006;15(5):639–44. 64. Gerber C, Meyer DC, Frey E, von Rechenberg B, Hoppeler H, Frigg R, et al. Neer Award 2007: reversion of structural muscle changes caused by chronic rotator cuff tears using continuous musculotendinous traction. An experimental study in sheep. J Shoulder Elb Surg. 2009;18(2):163–71. 65. Obrzut SL, Hecht P, Hayashi K, Fanton GS, Thabit G 3rd, Markel MD. The effect of radiofrequency energy on the length and temperature properties of the glenohumeral joint capsule. Arthrosc J Arthrosc Relat Surg Off Publ Arthrosc Assoc North Am Int Arthrosc Assoc. 1998;14(4):395–400. 66. Björkenheim JM, Paavolainen P, Ahovuo J, Slätis P. Resistance of a defect of the supraspinatus tendon to intraarticular hydrodynamic pressure: an experimental study on rabbits. J Orthop Res Off Publ Orthop Res Soc. 1990;8(2):175–9. 67. Uhthoff HK, Matsumoto F, Trudel G, Himori K. Early reattachment does not reverse atrophy and fat accumulation of the supraspinatus--an experimental study in rabbits. J Orthop Res Off Publ Orthop Res Soc. 2003;21(3):386–92. 68. Koike Y, Trudel G, Curran D, Uhthoff HK.  Delay of supraspinatus repair by up to 12 weeks does not impair enthesis formation: a quantitative histologic study in rabbits. J Orthop Res Off Publ Orthop Res Soc. 2006;24(2):202–10. 69. Tan H, Wang D, Lebaschi AH, Hutchinson ID, Ying L, Deng XH, et  al. Comparison of bone tunnel and cortical surface tendon-to-bone healing in a rabbit model of biceps tenodesis. J Bone Jt Surg - Am. 2018;100(6):479–86. 70. Gulotta LV, Rodeo SA. Growth factors for rotator cuff repair. Clin Sports Med. 2009;28(1):13–23. 71. Yokoya S, Mochizuki Y, Nagata Y, Deie M, Ochi M.  Tendon-bone insertion repair and regeneration using polyglycolic acid sheet in the rabbit rotator cuff injury model. Am J Sports Med. 2008;36(7):1298–309. 72. Grumet RC, Hadley S, Diltz MV, Lee TQ, Gupta R.  Development of a new model for rotator cuff pathology: the rabbit subscapularis muscle. Acta Orthop. 2009;80(1):97–103. 73. Sonnabend DH, Howlett CR, Young AA. Histological evaluation of repair of the rotator cuff in a primate model. J Bone Joint Surg Br. 2010;92(4):586–94. 74. Plate JF, Bates CM, Mannava S, Smith TL, Jorgensen MJ, Register TC, et  al. Histological changes of the shoulder in non-human primates. J Shoulder Elb Surg. 2014;22(8):1019–29.