Orthopedic Rehabilitation: Principles and Practice 3031320255, 9783031320255

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Orthopedic Rehabilitation Principles and Practice

Tony K. George · S. Ali Mostoufi · Alfred J. Tria Jr.   Editors

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Orthopedic Rehabilitation

Tony K. George  •  S. Ali Mostoufi Alfred J. Tria Jr. Editors

Orthopedic Rehabilitation Principles and Practice

Editors Tony K. George University Orthopaedic Associates Somerset, NJ, USA Alfred J. Tria Jr. Department of Orthopedics Rutgers-Robert Wood Johnson Medical School New Brunswick, NJ, USA

S. Ali Mostoufi Tufts Orthopedics and Rehabilitation & New England Spine Care Associates Cambridge, MA, USA

ISBN 978-3-031-32025-5    ISBN 978-3-031-32026-2 (eBook) https://doi.org/10.1007/978-3-031-32026-2 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 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 Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

I dedicate this book to my wife Eva and my children Cameron, Yasmine, and Ariana Sky. Your endless love and support inspire me to work hard and actively contribute to medical science. To my business partner Bob Rosenberg, MD, and my dedicated Staff at New England Spine Care, thank you for giving me a platform to help patients over the past 20 years. You are an amazing team, and I am lucky to have you on my side. Ali Mostoufi, MD To George, Carlos, Jude, and Romie for their many years of service for the patients and me. Alfred J. Tria, Jr., MD

First and foremost, I thank my Lord and Savior for His amazing grace. I thank my dearest Mridula for her patience and love through these years. My children Aden and Arielle who are growing up faster than I would like. To my patients who lean on me, challenge me, and delight me every day at work. Tony K. George, DO

Foreword

As an endurance athlete, I am unfortunately very familiar with the concept of Orthopedic Rehabilitation. As both a physician and as a patient with significant trauma I have learned the need to return to function is very difficult to achieve and critical for the happiness and productivity of any individual. In this comprehensive textbook, Orthopedic Rehabilitation: Principles and Practice, George, Mostoufi, and Tria work with their colleagues to give a road map to successfully getting a person back to a successful recovery. In the past, this was an area focused on pain relief but in modern medicine, we are changing this goal to holistic outcomes. This includes functional outcomes such as ODI, sleep improvement, global satisfaction, and a reduction in catastrophizing. This book lays out the anatomical principles of the musculoskeletal system and correlates that to strategies of recovery through many methods including conservative care such as physical medicine, interventional care, and the use of surgery to improve function. In addition, this book serves as a great guide to treatments of both the axial spine and the extremities. Adding this great text to your library will both enhance your patients and your healthcare team as they are armed with new tools to change the patient and your local community. This book covers orthobiologics, tissue healing, complex surgery, injections, and other methods, but does so in a way that serves a “what do I need to know” function. The reader can get essential details and use the book as a one-time read, or more likely keep it on your desk as a reference to be used in clinical practice. This book is clinically relevant and offers great refervii

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ences for many complicated situations. This book will become a critical part of any library for those treating those with musculoskeletal disease or injury. Timothy Deer The Spine and Nerve Center of the Virginias Charleston, WV, USA

Preface

An integral part of the human body is recovery after an insult. Bones, muscles, and soft tissues have unique physiologic properties helping adapt, adjust, and recover from injury. An understanding of its physiologic properties helps the clinician plan recovery and optimize function. Orthopedic Rehabilitation: Principles and Practice concisely applies principles from insult to recovery, laying out anatomy and correlating it to function, highlighting common injuries affecting the musculoskeletal system and strategies to rehabilitate through conservative, interventional, and surgical treatments. Its book chapters explore injury and recovery in the axial spine and the appendicular extremities. The book begins with recovery after regenerative injections where physiologic cellular properties help tissue healing. Through its course, the reader becomes familiar with concepts of tissue injury and how to facilitate its recovery. For example, in Chap. 1 the reader will encounter Phases of rehabilitation after orthobiologic treatment and in Chap. 6 Heuristics to guide elbow rehabilitation. Each subsequent chapter looks at anatomy, physical examination, and common musculoskeletal conditions seen in sports, spine, and primary offices. The emphasis is on recovery in a quick, concise yet thorough fashion. Conservative care is addressed first including bracing, modalities, and physical therapy. This is followed by interventional treatments and, then, surgical management when it becomes necessary. As trauma or repetitive injury exceed conservative management, surgery becomes necessary. Each chapter includes common surgical treat-

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ments and rehabilitation before and after surgery. Goals and expectations with timelines help clinicians to care for patients and relieve their anxieties. All in all, this book’s objective is to aide clinicians in restoring optimal function for their injured patients. The editors, all busy clinicians and academicians, familiar with the demands of private practice and academic rigor, have distilled information to bitesized nuggets for quick reference and application. The editors hope that the book will serve as a concise, quick reference for the busy clinician in daily practice. We thank our authors who have concisely written each chapter to enable the reader to act on information in a timely, clinically appropriate fashion. I thank my fellow editors who have been gracious with their time, wisdom, and experience, helping me steer this book towards completion. Your purpose and striving for excellence and truth have been invigorating and I hope to emulate them in the years to come. We most of all hope that the book will benefit our patients who kindly seek our help to improve their lives. Somerset, NJ, USA

Tony K. George

Contents

1 Rehabilitation  Principles for Interventional Orthopedics and Orthobiologics����������������������������������  1 Walter I. Sussman, Marc P. Gruner, David R. Bakal, and Kenneth R. Mautner 2 Rehabilitation  of Cervical Spine Disorders ���������������� 41 Laurent Delaveaux, Matthew Thomas, Brielle Hansen, and Tony K. George 3 Rehabilitation  of Thoracic Spine Disorders���������������� 67 Tony K. George, Sneha Varghese, Mindy Chu, Brittney Tout, and Hemant Kalia 4 Rehabilitation  of Lumbar Spine Disorders ����������������119 Tony K. George, Matthew Thomas, Sruthi Nanduri, Liya Thomas, Wayne Bonkowski, and Bobby Oommen 5 Rehabilitation  of Shoulder Disorders��������������������������151 William Micheo, Anthony Lombardi, and Claudia Jimenez 6 Rehabilitation  of Elbow Disorders ������������������������������195 Robert Bowers, Joshua M. Romero, Robert Pagan-Rosado, and Dennis A. Colón 7 Rehabilitation  of Hand Disorders��������������������������������243 Remy V. Rabinovich, Robert M. Zbeda, Steven Beldner, and Daniel B. Polatsch

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8 R  ehabilitation of Wrist Disorders��������������������������������287 Robert M. Zbeda, Remy V. Rabinovich, Steven Beldner, and Daniel B. Polatsch 9 Rehabilitation  of Hip Disorders������������������������������������315 David A. Harwood, Anna H. Green, John P. Stelmach, and Alfred J. Tria Jr. 10 Rehabilitation  of Knee Disorders ��������������������������������341 Giles R. Scuderi, Matt H. Nasra, Jeremy Silver, Kara L. Sarrel, and Alfred J. Tria Jr. 11 Rehabilitation  of Foot and Ankle Disorders����������������379 Seyed Behrooz Mostofi and Naveen Joseph Mathai Index����������������������������������������������������������������������������������������407

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Rehabilitation Principles for Interventional Orthopedics and Orthobiologics Walter I. Sussman, Marc P. Gruner, David R. Bakal, and Kenneth R. Mautner

1.1 Background Key Points • The effects of prehabilitation in preparation for and rehabilitation after interventional orthopedic and orthobiologic procedures have received little attention in the literature.

W. I. Sussman Department of Orthopedics and Rehabilitation, Tufts Medical Center, Boston, MA, USA Boston Sports and Biologics, Wellesley, MA, USA e-mail: [email protected] M. P. Gruner Washington Sports Medicine Institute, An affiliate of Aligned Orthopedic Partners, McLean, VA, USA Department of Orthopedics and Rehabilitation, John Hopkins Sibley Hospital, Washington, DC, USA D. R. Bakal · K. R. Mautner (*) Department of Sports Medicine, Emory University School of Medicine, Atlanta, GA, USA e-mail: [email protected] © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. K. George et al. (eds.), Orthopedic Rehabilitation, https://doi.org/10.1007/978-3-031-32026-2_1

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• Exercise is the cornerstone of management, prior to and following interventional orthopedic and orthobiologic procedures.

1.2 Pre-procedure Considerations Prehabilitation is the practice of training and enhancing the patient’s functional capacity to prepare for a major procedure. Post-procedural inactivity can lead to a decline in function, and the objective of prehabilitation is to help the patient withstand the stress of this inactivity [1]. Prehabilitation has received little attention in the interventional orthopedic and orthobiologic literature. In total hip and knee arthroplasty, pre-operative functional status is a significant predictor of postoperative function [2–5]. In fact, one study found that baseline pain and function was the single best predictor of pain and function at 6 months after a total hip or knee replacement [3]. Patients may not report a perceived benefit from prehabilitation programs [2, 4], but studies have shown functional benefit [2]. Even a 3-week pre-operative strengthening program can increase lower extremity muscle strength prior to surgery and improve the immediate postoperative course [2]. The significant strength gains achieved in the 3–6 week pre-operative period suggests that the benefit of these short prehabilitation strength training programs is in increased neuromuscular coordination and not necessarily strength [6, 7]. While there may be short-term benefits to prehabilitation after arthroplasty, the longer-­ term benefits are unclear [8]. The literature on prehabilitation is more limited in other areas of orthopedics, but prehabilitation has been studied in anterior cruciate ligament (ACL) tears. Pre-operative quadriceps strength is a significant predictor of knee function 2 years after ACL reconstruction [9], and enhancing quadriceps strength and function pre-­ operatively has been shown to improve surgical outcomes [10–13]. In spinal surgery, prehabilitation showed no statistically significant difference in pain or disability, but patients reported feeling more prepared for surgery [14]. These principles have not been studied in orthobiologics or interventional orthopedic procedures,

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but it is reasonable to believe that preconditioning could also have a beneficial effect after the varied procedures outlined in this text. In addition to rehabilitation, nutrition and the metabolic response to injury have been important to recovery. In the trauma literature [15–17], poor nutrition can contribute to poor wound healing [18]. Proper nutrition is an essential parameter in musculoskeletal health including the prevention and treatment of diseases [19]. This is likely underrecognized in elderly patients, and older adults may not have the same physiologic reserves of younger adults [20]. Given the prolonged wound healing process, nutrition should be considered as part of the presurgical or pre-­ procedure assessment. Diagnostic markers of malnutrition remain elusive [21]. Attention should be focused on basic nutrition and a healthy diet, including adequate caloric and protein intake to support the increased energy demands of collagen synthesis, angiogenesis, fibroblast proliferation, tissue remodeling and wound contraction during the healing process [22]. Protein deficiency has been associated with impaired fibroblast proliferation, and collagen synthesis [21]. Adequate hydration can assist in promoting tissue perfusion, oxygenation, waste removal [23], and macroand micronutrients may assist in enhancing the healing process [21]. In the wound literature, there is evidence for supplementing vitamins A and C, and—if there is a deficiency—supplementing arginine, glutamine, and zinc [21]. However, literature is limited in orthobiologics. Malnutrition can take different forms. In addition to specific nutrient deficits, malnutrition can include inadequate intake and overconsumption [24]. There is evidence that obesity and associated disorders can affect stem cell function. Obesity and diabetes have been associated with abnormal cytokine signaling, impaired tissue repair, and delayed wound closure [25]. In rodent models of type 2 diabetes, endogenous mesenchymal stem cells (MSCs) were less effective at mobilizing to a site of injury than those in the nondiabetic controls [26], and high levels of glucose showed reduced mesenchymal progenitor cell growth [27]. High-glucose concentrations have been shown to reduce the osteogenic and chondrogenic potential of adipose-derived mesenchymal stem cells (ADSC) [28], and ADSC had a reduced differentiation

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potential and had a lower capacity for spontaneous or therapeutic repair in patients who were obese and had metabolic syndrome [29]. In contrast, caloric restriction is known to reduce inflammation and has been shown to increase proliferation of MSCs in mouse models [30, 31]; moreover, the restriction of glucose improved the self-renewal and ant-isenescence abilities of the MSCs [32]. Although the role of obesity or calorie restriction on clinical outcomes in orthobiologics is unclear, the literature suggests that there is a fine line between the beneficial effects of caloric restriction and the consequences of malnourishment. Education has also been shown to positively impact outcomes of total knee and hip arthroplasty [33, 34]. Being able to counsel patients regarding the expected post-procedural course can help them prepare for the procedure and post-procedure course, which in theory could impact the outcome after an orthobiologic procedure as well. The following section outlines the expected post-­ procedure course for many orthobiologic procedures.

1.3 Rehabilitation Phases After Orthobiologic Treatments The healing potential following orthobiologic injections will vary depending on the tissue type (e.g. tendon, ligament, muscle, bone), underlying pathology (e.g. tendinopathy vs. tear), and anatomic location (e.g. Achilles vs. rotator cuff). In general, healing of tendon, ligament, muscle, and bone injuries follow the normal wound healing cascade. The wound healing cascade is a complex series of events and is typically divided into three phases: (1) inflammatory phase; (2) proliferative phase; and (3) maturation or remodeling phase. Some authors may describe a fourth phase, the hemostasis phase, characterized by vasoconstriction and formation of a blood clot immediately following an injury (Fig. 1.1). There is limited evidence-based literature on the role of rehabilitation following orthobiologic or regenerative procedures [35– 37]. While rehabilitation is often encouraged for the management of many orthopedic conditions to improve range of motion, strength, and functional activities, rehabilitation may offer a more

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1  Rehabilitation Principles for Interventional Orthopedics… Proliferative phase

Inflammatory phase

Maturation phase

• Collagen accumulation • Remodeling Inflammation 0.1

0.3

Granulation tissue 1

3 Time (days)

Wound contraction 10

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Fig. 1.1  Phases of wound healing. (Kumar V, Abbas A, Fausto N.  Tissue renewal and repair: regeneration, healing, and fibrosis. In: Robbins and Cotran Pathologic Basis of Disease (7th Edition). Elsevier Saunders, PA, USA, 87–118 (2005))

specific role after orthobiologic procedures. The objective of many regenerative procedures is to trigger a healing response and stimulate the body’s own repair mechanism. Animal models of injury and repair are the primary means of understanding the fundamental process of healing in tendon, ligament, and muscle tissue. In one study by Virchenko and Aspenberg, rats with iatrogenically injured Achilles tendons were injected with platelet rich plasma (PRP). Half of the rats had an intramuscular injection of Botulinum toxin A (Botox) into the calf muscles to unload the tendon. The rats who received the Botox injection had no effect from the PRP injection; in comparison, the rats that were not treated with Botox showed neotendon development indicating a positive response to the PRP injection combined with activity [38]. The failure of the rats treated with Botox to develop neotendon suggests that mechanical stimulation is vital in the early phases of tendon regeneration. Ambrosio et al., in a mouse model,

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demonstrated that stem cell transplantation into injured skeletal muscle proliferated and terminally differentiated toward a ­myogenic lineage with daily treadmill running, while the transplanted stem cells failed to rapidly divide in the absence of loading [39]. Clinical studies have also supported the role of rehabilitation. In a pilot study of PRP for chronic patellar tendinopathy, Kon et  al. found that subjects who did not follow the post-procedure stretching and strengthening program had poorer outcomes [40]. Further insight is needed into the molecular and cellular response to therapeutic exercises and stress after regenerative therapies. Based on basic science studies showing that the effects of PRP are lost when tendons are unloaded mechanically, one conclusion is that tendon healing may require a combination of biologic and mechanical factors [37]. Mechanotransduction is often used to describe the physiologic responses by which cells convert mechanical stimuli into structural adaptation [41–43]. Mechanical stimuli or loads on a tendon are sensed by various cell surface receptors, integrins, stretch-activated ion channels, and other mechanisms. This triggers cell–cell communication and changes cellular biology within the cell nucleus [44]. Eccentric exercises, with slow lengthening of the muscle-­ tendon unit while under load, have been shown to stimulate a cellular response, including activation and proliferation of satellite stem cells [45]. Heavy-slow resistance (HSR) training in which each repetition is performed slowly for >6 s for both the eccentric and concentric phases has shown similar results to eccentric strengthening in long-term pain reduction. HSR training demonstrated normalization of tendon fibril morphology [46]. There is also interest in low-load resistance training with blood flow restriction (BFR), and recent studies have shown increased muscle protein synthesis and proliferation of myogenic stem cells after BFR training [47, 48]. Many translational questions exist about how to apply these principles to orthobiologic procedures. The topic of tissue repair and rehabilitation is vast, and this chapter is by no means exhaustive. The goal is to understand the basic tenants of the healing process to help clinicians design a rehabilitation program, which

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takes into consideration the patient and pathology (e.g. mechanism of injury, tissue injured, severity, age of patient), the ­treatment (e.g. intra-articular vs. intra-osseous or intra-tendinous vs. para-tendinous), and the different phase of healing. Rehabilitation recommendations can vary depending on the tissue treated. For example, tendons require loading in an earlier phase of rehabilitation to help support the development of tensile strength. Overall, the literature suggests that mechanical stress on the tendon is needed to optimize outcomes [35, 37]. The severity of pathology should also be considered. For example, strengthening exercises after platelet rich plasma injection (PRP) may be started later in high-grade partial tendon tears compared to tendinopathy. Guidance following a procedure must also be tailored to the injectate or treatment. For example, rehabilitation following an injection around a tendon (e.g. a high-volume injection between the Achilles tendon-Kager’s fat pad) will have a different expected post-procedural course than an intra-tendinous procedure (e.g. platelet rich plasma injection into the Achilles tendon). Likewise, an intra-articular knee injection of cortisone or ketorolac will have a different course than an orthobiologic injection.

1.4 The Healing Cascade 1.4.1 Phase I of Healing: The Inflammatory Phase (0–5 Days) The inflammatory phase is the initial response to tissue damage and generally occurs in the first 1–5 days after an injury [49–52]. This phase is initially characterized by hemostasis and “walling off” of the injured site, increased vascular permeability, and an influx of inflammatory cells. Platelets are among the first cells to respond to an injury and form the hemostatic plug and secrete chemokines [e.g. epidermal growth factor (EGF), fibronectin, fibrinogen, histamine, platelet-derived growth factor (PDGF), serotonin, and von Willebrand factor]. These factors recruit macrophages to the healing site, resulting in scavenging of debris and

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phagocytosis to debride the wound bed. Fibroblasts also migrate to the wound in this phase, initiating the formation of granulation tissue and the transition into the proliferative phase [49]. The specific cellular events will differ depending on the anatomy and physiology of the given tissue [53]. During this phase, patients may experience varying degrees of pain, swelling, redness, and limited range of motion.

1.4.2 Phase II of Healing: The Repair Phase (5–21 Days) The proliferative (granulation) phase is characterized by “rebuilding” the local tissue and generally lasts a few weeks after an injury [50–52]. Granulation tissue formation, collagen deposition, and angiogenesis create an extracellular matrix and network of blood vessels to supply the area. Neovascularization helps supply the wound bed with nutrients [49]. Macrophages continue to supply growth factors and fibroblasts differentiate and produce collagen, depositing and remodeling the extracellular matrix [49]. Initially, migrating fibroblasts will begin to synthesize collagen around day 5, but by the fourth week, there is a noticeable increase in the intrinsic proliferation of fibroblasts from the endotenon. Initially the collagen fibers are randomly oriented, but as the tissue starts to mature, the collagen fibers are increasingly oriented along the direction of force through the tendon, increasing the tensile strength of the tendon. By week 5, tenocytes become the main cell type [54]. During this phase, patients should feel a decrease in the initial post-injury/procedural pain. Pre-procedural symptoms may persist, slowly improve, or wax and wane.

1.4.3 Phase III of Healing: The Maturation Phase (21 Days–12 Months) The maturation or remodeling phase starts 3 weeks after an injury and lasts up to 12 months or longer with collagen deposition by

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fibroblasts continuing for this entire period [51]. Increased stability is acquired during the remodeling phase and is stimulated by continued use of the tendon. Mechanical stress influences cell signaling and contributes to collagen matrix remodeling and increases the tensile strength of the tissue [55]. As the maturation process continues, the collagen fibers continue to be reabsorbed and synthesized along the direction of force and cross linking of the collagen fibrils occurs, increasing the tendon’s tensile strength. Moreover, there is increased deposition of type I collagen in preference to type III collagen [54, 56]. The tensile strength is estimated to reach its maximum strength at 3 months [57, 58], but never completely regains its preinjury strength [59]. During this period, patients usually feel consistent improvement in symptoms, though their condition will still often wax and wane as tissue transitions from granulation tissue to scar formation.

1.5 Tissue Specific Considerations 1.5.1 Tendons and Ligaments Healing of tendons and ligaments follow the three phases of wound healing detailed above. In the initial phase, blood clot and granulation tissue fill the gap between the tendon and ligament fibers. In tendons, fibroblasts and tenocytes in the epitenon and paratenon are recruited and proliferate, bridging the injured gap and forming a stable scar. In the early stages, the matrix is composed of increased amounts of type III collagen [60]. After 10 weeks, a higher proportion of type I collagen is synthesized and type III collagen decreases, forming scar-like tendon tissue, a process that will continue for years [61, 62].

1.5.2 Muscles Muscle strains that result in a rupture of the myofibers go through three phases of healing. Satellite cells begin to proliferate and

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form new myoblasts, which fuse into myotubes within a couple of days [63]. Similar to tendons and ligaments, fibroblasts produce collagen and form scar tissue to bridge the gap between muscle fibers [64].

1.5.3 Cartilage Articular cartilage has poor intrinsic healing capacity and generally does not heal or only partial heals under certain conditions [65]. In most cases, surgical or biologic interventions may induce a repair response, and treatments include debridement, microfracture, and autologous tissue transplantation (e.g. autologous chondrocytes or mesenchymal stem cells). Little is known about the histologic effects of cartilage healing after these procedures. In vitro studies have demonstrated that mechanical stress can stimulate differentiation of MSCs into chondrocytes, extracellular matrix synthesis, and cytokine secretion [66], while excessive stress may cause cell death and matrix degeneration [67].

1.5.4 Bone Injured bone (e.g. fracture or necrotic bone) is resorbed and replaced by new bone following the three phases of healing. Macrophages and osteoclasts remove injured calcified bone, and osteoblasts fill the fracture gap forming granulation tissue. Delayed bone formation and nonunion have been attributed to variations in the local inflammatory environment, as well as the recruitment of muscle-derived stromal cells and osteogenesis early in the healing process [68]. Bone repair follows two phases of healing: (1) the initial cartilaginous soft callus followed by (2) remodeling and formation of a bony hard callus. Initially, the soft callus is formed when adjacent soft tissue and periosteum bridge the fracture site stabilizing the fracture [69]. Osteons travel along the cortical bone (by the Haversian system); they bridge the fracture gap [70, 71], and osteoblasts synthesize woven bone resulting in a hard callus [68, 72, 73]. This irregular woven bone callus

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remodels over months to years through continuous osteoclast resorption, while osteoblasts replace the matrix with lamellar bone to bring the bone back to its original shape, size, and strength/ stability [74].

1.6 Overview of Rehabilitation Guidelines in Each Phase of Healing The objective of many traditional orthopedic injections, such as corticosteroids or ketorolac injections, is to address inflammation. The objective of orthobiologic procedures in interventional orthopedics is different, and the aim is to heal the tissue. This is often achieved by stimulating a healing response, through delivery of growth factors to the target tissue (e.g. PRP, MSCs, etc.) or controlled microtrauma to convert a chronic injury into an acute injury with healing potential (e.g. percutaneous tenotomy or vacuum debridement). The literature on rehabilitation after orthobiologic or interventional orthopedic procedures is limited, and many of the rehabilitation protocols proposed in the literature are an attempt at translating these would-be wound healing principles into clinical practice [44, 75–78]. There is some variability in the duration and overlap of the phases of wound healing in the literature [49–52], and progression through the rehabilitation process should be individualized and informed by clinical progress through the program. The rehabilitation process should reflect the type of tissue undergoing recovery (e.g. tendon, bone, ligament, muscle), the severity of the underlying pathology, the patient’s pre-procedure fitness level, the patient’s physical abilities, and any existing comorbidities.

1.6.1 Rehabilitation in the Inflammatory Phase of Healing (0–5 Days) The goal of rehabilitation in the inflammatory phase is typically one of protection, and care usually focuses on pain management

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and managing post-procedural swelling. Management may vary depending on the procedure, but is typically achieved with ­immobilization or bracing, ice, elevation, medications, and gentle range of motion exercises to activate the vasomotor pump [75].

1.6.1.1 Immobilization/Bracing In most cases, protected weight bearing is recommended for pain control in the first 1–3 days. Most randomized controlled or prospective studies on orthobiologic procedures have prescribe a period of absolute or relative rest during the acute inflammatory phase, although no prospective studies have specifically studied these rehabilitation protocols [35]. Immobilization is sometimes recommended due to the concern that the orthobiologic may disperse to other locations with movement. However, in a cadaveric model, Achilles tendons that were injected with blue dye to simulate a PRP injection were manipulated through 100 cycles of ankle dorsiflexion and plantar flexion, and there was no significant difference in the spread of the dye compared to control specimens that were kept in a prone resting position for 15 min after the injection [79]. This suggests that early motion does not increase the spread or clearance of PRP from the target site and thus we recommend early mobilization of tendons following these procedures. Limiting joint motion can help reduce pain in the associated area, and weight-bearing restriction or bracing can be used for this objective. Avoiding any pain-provoking activities is a common recommendation, but recommendations have varied across the literature from avoiding all physical activity to limiting only repetitive movements. Crutches, a controlled ankle motion (CAM) walking boot, or unloader braces can be used to limit motion or decrease stress on a joint, bone or tendon/ligament after treatment. Any period of immobilization should be limited. In most randomized controlled or prospective studies that detailed post-­ procedure protocols, most patients were instructed to restrict weight bearing or immobilize the joint for 3 days to 2 weeks [35]. Prolonged immobilization has been associated with joint contractures and functional impairment in the surgical literature, and early gentle active range of motion is considered safe [75].

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1.6.1.2 Pain Management Post-procedure pain can vary among patients and procedures. For example, intra-articular injections are often less painful than intra-tendinous or intra-osseous injections. Periprocedural nerve blocks can help with acute post-procedural pain management when possible. Longer acting anesthetics, such as ropivacaine, can extend the efficacy of these blocks. Alternative approaches to pain management include cryotherapy and analgesic medications other than nonsteroidal anti-inflammatory drugs (NSAIDs). Cryotherapy: There are different methods of cryotherapy, including crushed ice, ice bags, chemical or gel packs, and circulating commercially available cryotherapy devices that provide continuous circulation of ice water. However, there is evidence that some of the methods are more effective than others [80–82]. There is some debate in the literature on limiting cryotherapy in the acute phase after an orthobiologic procedure [35, 83]. Cryotherapy has been shown to be effective for managing pain in certain situations [84] and is often accepted as an integral part of the treatment of acute soft tissue injuries despite a lack of robust evidence [85]. In one review of regenerative procedures for tendinopathy, 20% of prospective and randomized controlled studies prescribed cryotherapy for pain management [35]. The theoretical concern is that cryotherapy may reduce blood flow important for healing. However, the literature is limited and the effect of cryotherapy depends on a number of factors, including the temperature of the cooling device, the depth of the subcutaneous tissue, and the frequency and duration of treatment [81, 86–88]. Studies have shown that cryotherapy can temporarily decrease microcirculatory perfusion when measured at a depth of 2–8 mm [89, 90], but vary in whether this decrease in blood flow persists following active cooling [90, 91]. There is limited literature that the superficial effects of cooling impact the perfusion of deeper structures, and skin temperature has been shown to be a poor predictor of perfusion to deeper structures [92]. In one study evaluating the effect of cryotherapy on the microcirculation of the midportion Achilles tendon, the authors showed reduced blood flow within the first minute of cryotherapy and return of capillary blood flow during recovery [91]. Another theoretical concern is that cryo-

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therapy may decrease platelet activation, but in vitro studies have shown temperature did not affect platelet adhesion when tested at 0 and 37 °C [93]. NSAIDs: Limiting nonsteroidal anti-inflammatory drugs before and after an orthobiologic procedure is widely accepted across the literature. NSAIDs have been shown to inhibit platelet function and reduce the release of growth factors [94–96]. In a study using a rat animal model of a surgically repaired rotator cuff tendon, even initiating NSAIDs in the proliferative stage of healing decreased the biomechanical strength of the repaired tendon [97]. When comparing different classes of oral NSAIDs and their influence on clinical outcomes post-PRP for knee osteoarthritis, patients taking a nonselective cyclooxygenase (COX) inhibitor had lower functional scores and higher pain scores at 4- and 8-week post-PRP compared to patients taking a selective COX inhibitor [98]. Non-NSAID Medications: Pain medication without anti-­ inflammatory effect and prescription narcotics are often prescribed for the first 72 h post-procedure. Over the counter acetaminophen is often acceptable for pain control after most procedures and does not demonstrate any anti-inflammatory activity [96]. However, acetaminophen has been shown to inhibit platelet aggregation [99]. Although the impact of impaired platelet aggregation on clinical outcomes post-PRP is unclear, some have recommended that clinicians consider suspending acetaminophen prior to a PRP injection [99]. Narcotics can be used for breakthrough pain following opioid risk mitigation strategies, including patient education about opioids, clear instructions about when to use opioids (e.g. for moderate or severe pain only), and prescribing short-acting opioids at the lowest dose necessary. In geriatric patients, doses should be decreased by at least 50% if there is concern for cognitive impairment, risk of falls, respiratory dysfunction, or renal insufficiency [100].

1.6.2 Rehabilitation in the Proliferative Phase of Healing (5 Days–6 Weeks) The objective of rehabilitation in the proliferative phase is to gradually increase activity. There is no consensus on the optimal

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timing of a stretching or strengthening program, and most published study protocols do not specify the type of strengthening recommended [35]. Rehabilitation in this phase is progressive, and is typically governed by the patient’s tolerance. A good guideline is to limit any activity that increases the patient’s pain to greater than a 3/10 during or after that activity. Intra-osseous, intra-articular, intra-tendinous, intraligamentous, and axial injections may all require different periods of rest and activity modification [101, 102]. The literature on tendon healing clearly suggests early controlled loading influences the early phases of tendon healing after orthobiologic injection or microtrauma (i.e. needle tenotomy) [38, 103], and that the appropriate mechanical loading induces differentiation of tendon stem cells (TSCs) into tenocytes [104]. However, excessive loading can induce differentiation of TSCs into adipocytes, chondrocytes, and osteocytes [104]. It is possible in theory that the concerns about heterotopic ossification after PRP [105] may stem from the failure of rehabilitation rather than the orthobiologic injection.

1.6.2.1 Stretching In the literature, the timing of a stretching program has ranged from 24 h to 1 week post-procedure [35]. Studies have been performed to determine if dynamic stretching (DS), static stretching (SS), or proprioceptive neuromuscular facilitation (PNF) were superior in aiding recovery; however, there is no consensus on the best form of stretching in the early phases of healing. The literature on DS, SS, or PNF in sport shows a small to moderate effect on performance and a similar improvement in range of motion (ROM) with all the stretching approaches. There is no overall effect on injuries with SS and PNF, but no data is available for DS on injury prevention [106]. For tendinopathies, specifically, it is inferred that static stretching is the “safest” form of stretching due to its slow and steady nature [75, 106]. 1.6.2.2 Strengthening Strengthening during the proliferative phase has also been evaluated after regenerative procedures in tendinopathy [40]. This is typically started at 2 weeks in most published post-procedure pro-

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tocols [44, 75–78], but timing varies across the literature [35]. For joint injections, the strengthening program likely can be started sooner than with tendons or ligaments. Most recommendations are to have a progressive strengthening program. This is based on the progression of healing in tendons, where initially newly synthesized collagen fibers are oriented randomly, but as the proliferative phase progresses, the collagen fibers are increasingly oriented along the direction of force, thus increasing the tensile strength of the tendon [54]. The safest type of contraction in this phase of healing may be isometric since joint motion is limited. Isometric contractions can decrease blood flow to the active tissues, but the effect is likely temporal [75]. Isometric exercises have also been shown to be effective for short-term pain relief, and the authors will typically start with isometric strengthening exercises after a regenerative procedure [107–109]. Eccentric contraction or heavy-slow resistance training may be the most beneficial type of exercise for long-term pain reduction and functional improvement in tendinopathy, but it has not specifically been studied after regenerative injections [110]. Limited literature guides the ideal timing to initiate eccentric strengthening [111–113]. There is some concern that if eccentric strengthening is started too soon, it may have a hypovascular effect attenuating the healing cascade [83], and it has been suggested that eccentric exercises should be reserved for the late proliferative or remodeling phase [75]. There is also limited literature on open-­chain versus closed-chain exercises after regenerative procedures [35, 75].

1.6.3 Rehabilitation in the Remodeling Phase of Healing (6 Weeks–12 Months) The goal of rehabilitation in the remodeling, or maturation, phase is the safe return to higher level activities and sport. At this stage, patients should have completed the early rehabilitation protocols

1  Rehabilitation Principles for Interventional Orthopedics…

17

and have full range of motion across the joint. Eccentric strengthening should be started in this phase, if not initiated earlier during the late proliferative stage, and proprioceptive exercises should be added to the rehabilitation program [75]. The literature is limited to guide return to play decisions, and timing should be individualized to the athlete. Initially, there should be a focus on the reintroduction of functional activities specific to the athlete’s sport. Patients with lower extremity procedures can start jogging and progress activity as tolerated. Sport-­ specific movements and activities should be included in a controlled setting before progressing to a practice or game/competition setting.

1.7 Conclusion Post-procedure recommendations are based on the underlying physiology of the healing cascade and the relative time frames at each stage of healing. Suggested rehabilitation protocols are general guidelines (Table  1.1). Ultimately, rehabilitation protocols will have to be individualized to best benefit each particular patient in terms of their specific injury. Tables 1.2, 1.3, 1.4, 1.5, 1.6, 1.7, 1.8, 1.9, and 1.10 provide examples of post-procedure rehabilitation protocols for ten of the most common conditions that are treated with tenotomy or orthobiologic injections (Achilles tendinopathy, plantar fasciitis, patellar tendinopathy, quadriceps tendinopathy, hamstring tendinopathy, gluteal tendinopathy, knee osteoarthritis, elbow tendinopathy, shoulder tendinopathy, and shoulder osteoarthritis).

W. I. Sussman et al.

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Table 1.1  General post-procedural recommendations per phase of healing Phase of healing Phase I: Inflammatory phase

Phase II: Proliferative phase

Phase III: Remodeling phase

Timeframe Days 0–5

Restrictions/rehabilitation • Relative rest • Avoid excessive loading, consider NWB or PWB • Consider bracing to minimize ROM and provide protection • Avoid NSAIDs; use alternative pain management Day 5–week Early proliferative phase (day 5–week 2) 6  • Full WB with or without protection  • Active ROM  • Initiate gentle stretching program  • Avoid NSAIDs; use alternative pain management Late proliferative phase (weeks 2–6)  • Full WB without protective device  • Stretching program: adding “dynamic” stretching and passive ROM  • Progressive strengthening program starting with high-repetition isometric exercises and progressing to eccentric exercises closer to the end of this phase  • Avoid NSAIDs; use alternative pain management Week 6 and • Proprioceptive training and sportbeyond specific exercises • Return to sport/activity

NWB non-weight bearing, PWB partial weight bearing, WB weight bearing, ROM range of motion, NSAID nonsteroidal anti-inflammatory drug

Days 0–5

Phase I: Inflammatory phase

Weeks 4–6

Weeks 2–4

Phase II: Day 5–week 2 Proliferative phase

Timeframe

Phase of healing • Begin gentle active ankle ROM

• Continue gentle active ankle ROM

• PWB with crutches in CAM boot (pain limited)

• Initiate gentle ankle dorsiflexion stretching • Begin isometric ankle strengthening

• Week 2: WBAT, CAM boot for community ambulation

• Avoid painful exercises with pain >3/10

• Avoid extreme dorsiflexion (for insertional tendinopathy)

(continued)

• Aerobic training: stationary bike, walking program when gait mechanics have returned to normal

• Continue core strengthening

• Double and single limb balance/proprioception exercises

• Global lower limb strengthening: bridges, mini-squat, step-ups

• Gait training progressing to independent

• Avoid abrupt increases in tendon stress with exercise, lifting, or high- • Progressive ankle strengthening with resistance bands impact activity, such as running, jumping, and heavy weightlifting

• Begin non-impact aerobic exercise (stationary bike, anti-gravity treadmill or pool for walking once incision is healed and cleared by physician)

• Continue core strengthening

• PWB → WBAT, gait training for WBAT in CAM boot without crutches

• Continue active ankle ROM and joint mobilization as needed

• No use of NSAIDs or ice for 4 weeks

• Upper body aerobic and strength exercises

• Gait training for PWB with crutches

• Initiate lower limb strengthening in NWB

• Begin core strengthening

• Rest

• No use of NSAIDs or ice for 4 weeks

• Avoid stretching into ankle dorsiflexion (for insertional tendinopathy) • Gait training with crutches

• NWB with crutches in CAM boot

Rehabilitation • Rest

• No use of NSAIDs or ice for 4 weeks

Restrictions

Table 1.2  Achilles tendinopathy (insertional or mid-substance): rehabilitation protocol post-procedure (tenotomy or orthobiologics)

1  Rehabilitation Principles for Interventional Orthopedics… 19

Timeframe

• Gradual return to work/sport progression

• Plyometric, agility, and work/sport-specific training

• Begin double and single limb strengthening on leg press

• Continue balance/proprioceptive training

• Avoid extreme dorsiflexion (for insertional tendinopathy)

Rehabilitation • Increase loading capacity for lower limb strengthening exercises and core exercises

Restrictions

• Avoid painful activities/exercises of pain >3/10

NSAID nonsteroidal anti-inflammatory drug, NWB non-weight bearing, CAM controlled ankle movement, PWB partial weight bearing, WBAT weight bearing as tolerated, ROM range of motion

Phase III: Weeks 6 and Remodeling phase beyond

Phase of healing

Table 1.2 (continued)

20 W. I. Sussman et al.

Day 5–week 2

Phase II: Proliferative phase

Weeks 4–6

Weeks 2–4

Timeframe

Days 0–5

Phase of healing

Phase I: Inflammatory phase

• Begin core strengthening

• Avoid pain >3/10 during exercise or prolonged walking

• Initiate gentle ankle dorsiflexion stretching

• Week 3: WBAT in CAM boot, use crutches as needed

• Continue core strengthening

• Begin balance and proprioception exercises

• Begin functional strengthening

• Continue aerobic training

• Gait training progressing to independent

• Progressive strengthening

• Continue core strengthening

(continued)

• Begin non-impact aerobic exercise (stationary bike, anti-gravity treadmill or pool for walking once incision is healed and cleared by physician)

• Lower limb strengthening, PWB → WBAT

• Begin isometric ankle strengthening

• Continue active ankle ROM and joint mobilization as needed

• No use of NSAIDs or ice for 4 weeks

• Can begin upper body aerobic and strengthening exercises

• Initiate lower limb NWB strengthening

• Continue gentle active ankle ROM

• PWB with crutches in CAM boot (pain limited)

• Day 4: may begin isometric exercises (toe crunches)

• Avoid stretching into dorsiflexion

• No use of NSAIDs or ice for 4 weeks

• Begin gentle active ankle ROM

• NWB with crutches in CAM boot

Rehabilitation • Rest, elevate foot above heart

• No use of NSAIDs or ice for 4 weeks

Restrictions

Table 1.3  Plantar fasciitis: rehabilitation protocol post-procedure (tenotomy or orthobiologics)

1  Rehabilitation Principles for Interventional Orthopedics… 21

Restrictions

• Avoid pain >3/10 during exercise or prolonged walking

Rehabilitation

• Gradual return to work/sport progression

• Plyometric, agility, and work/sport-specific training

• Begin double and single limb strengthening on leg press

• Continue balance/proprioceptive training

• Increase loading capacity for lower limb strengthening exercises and core exercises

NSAID nonsteroidal anti-inflammatory drug, NWB non-weight bearing, CAM controlled ankle movement, PWB partial weight bearing, WBAT weight bearing as tolerated, ROM range of motion

Timeframe

Weeks 6 and beyond

Phase of healing

Phase III: Remodeling phase

Table 1.3 (continued)

22 W. I. Sussman et al.

• No use of NSAIDs or ice for 4 weeks

• Avoid exercises where pain >3/10

Weeks 2–4

Weeks 4–6

(continued)

• Aerobic training: stationary bike, walking program when gait mechanics have returned to normal

• Core strengthening

• Double and single limb balance/proprioception training

• Global lower limb strengthening: bridges, mini-squat, step-ups

• Gait training progressing to independent

• Progressive knee strengthening with resistance bands

• Begin non-impact aerobic exercise: stationary bike, anti-gravity treadmill, pool once incision is healed and cleared by physician

• Continue core strengthening

• Begin isometric knee strengthening and lower limb strengthening

• Continue active knee ROM and joint mobilization as needed

• Initiate upper body aerobic and strength exercises

• Initiate lower limb strengthening

• Begin core strengthening

• Continue active knee ROM

• Rest

• Gait training with crutches

• Knee immobilizer for 1 week

Day 5–week • No use of NSAIDs or ice for 4 weeks 2

• Begin gentle active knee ROM

• NWB with crutches for 4 days

Rehabilitation • Rest

Phase II: Proliferative phase

Restrictions

• No use of NSAIDs or ice for 4 weeks

Days 0–5

Timeframe

Phase I: Inflammatory phase

Phase of healing

Table 1.4  Quadriceps or patellar tendon: rehabilitation protocol post-­procedure (tenotomy or orthobiologics)

1  Rehabilitation Principles for Interventional Orthopedics… 23

Rehabilitation

• Continue core strengthening

• Begin double and single limb strengthening on leg press

• Begin low level plyometric exercises

• Continue balance/proprioceptive training

• Increase loading capacity for lower limb strengthening exercises, with goal of loading knee tendons

• Progress to high impact/intensity exercises such as running, jumping, and weightlifting

NSAID nonsteroidal anti-inflammatory drug, NWB non-weight bearing, ROM range of motion

Weeks 6 and • Avoid exercises that cause pain beyond >3/10, or post-activity soreness lasting >24 h

Phase III: Remodeling phase

Restrictions

Timeframe

Phase of healing

Table 1.4 (continued)

24 W. I. Sussman et al.

Weeks 6+

Weeks 2–6

• Activities as tolerated • Avoid painful activities/exercises of pain >3/10

• Avoid painful activities/exercises of pain >3/10

• No use of NSAIDs or ice for 4 weeks • No eccentric strengthening

Day 5–week 2 • No use of NSAIDs or ice for 4 weeks • Wean off crutches after day 7 • No eccentric strengthening • Avoid painful activities/exercises of pain >3/10

Restrictions • No use of NSAIDs or ice for 4 weeks • NWB for 4 days, TTWB using crutches until day 7

Rehabilitation • Rest • Begin gentle hip flexion ROM on day 4, perform four times per day • Use a seat cushion for comfort • Continue AROM and PROM • Begin isometric exercises • Begin straight leg raises and heel slides • Begin core stability exercises • May use pool once wound has healed and cleared by physician • Continue AROM as needed • Progressive strengthening: begin active knee flexion and hip extension strengthening • Begin gentle hamstring stretching • Begin balance exercises • Continue strengthening exercises • Begin sport-specific exercises • May begin soft tissue work with and without tools

NSAID nonsteroidal anti-inflammatory drug, NWB non-weight bearing, TTWB toe touch weight bearing, ROM range of motion, AROM active range of motion, PROM passive range of motion

Phase III: Remodeling phase

Phase II: Proliferative phase

Phase of healing Timeframe Phase I: Days 0–5 Inflammatory phase

Table 1.5  Hamstring tendinopathy: rehabilitation protocol post-procedure (tenotomy or orthobiologics)

1  Rehabilitation Principles for Interventional Orthopedics… 25

Weeks 6 and beyond

• No use of NSAIDs or ice for 4 weeks • Use crutches as needed • Avoid painful activities/exercises of pain >3/10 • Activities as tolerated • Avoid painful activities/exercises of pain >3/10

• No use of NSAIDs or ice for 4 weeks • NWB for 4 days, progress to TTWB with crutches starting day 4 • No use of NSAIDs or ice for 4 weeks • Progress to WBAT using crutches • Avoid painful activities/exercises of pain >3/10

Restrictions

• Continue strengthening exercises • Begin sport-specific exercises • May begin soft tissue work with and without tools (no foam rolling until week 6)

• Continue AROM and PROM • Begin isometric exercises • Begin straight leg raises and clam shells • Begin core stability exercises • May use pool once wound has healed and cleared by physician • Continue AROM as needed • Progressive hip abductor strengthening • May begin stationary bike

• Rest • Begin gentle hip flexion ROM on day 4, perform four times per day

Rehabilitation

NSAID nonsteroidal anti-inflammatory drug, NWB non-weight bearing, TTWB toe-touch weight bearing, WBAT weight bearing as tolerated, ROM range of motion, AROM active range of motion, PROM passive range of motion

Phase III: Remodeling phase

Day 5–week 2

Phase II: Proliferative phase

Weeks 2–6

Days 0–5

Timeframe

Phase I: Inflammatory phase

Phase of healing

Table 1.6  Gluteal tendinopathy: rehabilitation protocol post-procedure (tenotomy or orthobiologics)

26 W. I. Sussman et al.

Day 5–week 2

Phase II: Proliferative phase

Weeks 6 and beyond

Weeks 4–6

• Day 3: Can begin low-grade closed chain program including light squats and lunges (body weight only) • Continue squats/lunges, can add resistance as tolerated starting week 1

• Avoid excessing loading of the joint and impact activities including heavy weightlifting

• Weightlifting and strength training as tolerated

• Avoid impact activities

• Correct biomechanical issues that contributed to the original joint pain/injury

• Establish long-term HEP focusing on injury prevention and long-term functional goals

• Correct biomechanical issues that contributed to the original joint pain/injury

• Avoid painful activities/exercises of pain >3/10

• Activities as tolerated

• Establish long-term HEP focusing on injury prevention and long-term functional goals

• No use of NSAIDs or ice for 4 weeks

• Proprioceptive exercises

• Light agility training

• Can increase light aerobic activities such as biking, swimming, and walking

• No NSAIDs and ice for 4 weeks

• May begin swimming and biking (low resistance) starting week 1

• May begin light open kinetic chain exercises including leg curls and leg extensions with light weight starting week 1

• Continue ROM

• No NSAIDs and ice for 4 weeks

• No submerging under water for 72 h post-procedure

• Gentle ROM as tolerated during days 1–2

• WBAT, use crutches as needed for days 1–2

Rehabilitation

• No NSAIDs and ice for 4 weeks

Restrictions

NSAID nonsteroidal anti-inflammatory drug, WBAT weight bearing as tolerated, ROM range of motion, HEP home exercise program

Phase III: Remodeling phase

Days 0–5

Phase I: Inflammatory phase

Weeks 2–4

Timeframe

Phase of healing

Table 1.7  Knee joint: rehabilitation protocol post-orthobiologics

1  Rehabilitation Principles for Interventional Orthopedics… 27

Weeks 6 and beyond

Weeks 4–6

Weeks 2–4

Day 5–week 2

• Activities as tolerated

• Activities as tolerated

Restrictions • No use of NSAIDs or ice for 4 weeks • Use sling for 3 days, no driving in sling • May lift up to 5 pounds • No use of NSAIDs or ice for 4 weeks • May lift up to 10 pounds • Avoid repetitive elbow and hand activities • No sustained gripping (such as opening a jar) • No use of NSAIDs or ice for 4 weeks • May lift up to 20 pounds

NSAID nonsteroidal anti-inflammatory drug, ROM range of motion

Phase III: Remodeling phase

Phase II: Proliferative phase

Phase of healing Timeframe Phase I: Days 0–5 Inflammatory phase

• Continue active ROM as needed • May begin isometric wrist and elbow strengthening • Week 3: Can add light weight to wrist flexion and extension (starting with 2 pounds) • Progressive isotonic strengthening • May begin integrated strengthening (chest press, rows, and hammer curls) • Begin eccentric training • Continue strengthening • Begin sport-specific activities • Begin progressive loading exercises

• Continue rest and elevation • Regain full range of motion: perform ROM 3–5 times per day

Rehabilitation • Rest and elevation • Day 3: Begin gentle active ROM four times per day

Table 1.8  Elbow tendinopathy: rehabilitation protocol post-procedure (tenotomy or orthobiologics)

28 W. I. Sussman et al.

Timeframe

Weeks 6 and beyond

Weeks 2–6

Day 5–week 2

• No use of NSAIDs or ice for 4 weeks • Safe use of sling for first 3 days, including when sleeping, then wean out as tolerated • No sleeping on procedure side • No lifting >5 pounds • Avoid overhead activity for 2 weeks • No sustained gripping (such as opening a jar) • Discontinue exercise if pain becomes >3/10 • No use of NSAIDs or ice for 4 weeks • No sleeping on procedure side • No lifting >10 pounds • Avoid overhead activity for 2 weeks • Discontinue exercise if pain becomes >3/10 • No use of NSAIDs or ice for 4 weeks • May lift up to 10–20 pounds • Avoid eccentric exercises • Discontinue exercise if pain becomes >3/10 • Activities as tolerated • Discontinue exercise if pain becomes >3/10

Restrictions

• Begin eccentric training/loading • Continue strengthening exercises • Begin sport-specific exercises

• Continue active ROM as needed, goal of full active ROM • Progressive strengthening

• Continue AROM and PROM • Begin isometric exercises • Begin thoracic mobility exercises

• Begin strengthening with scapular pinch

• Rest • Begin gentle active ROM (pendulum exercises)

Rehabilitation

NSAID nonsteroidal anti-inflammatory drug, ROM range of motion, AROM active range of motion, PROM passive range of motion

Phase III: Remodeling phase

Phase II: Proliferative phase

Phase I: Days 0–5 Inflammatory phase

Phase of healing

Table 1.9  Shoulder tendon: rehabilitation protocol post-procedure (tenotomy or orthobiologics)

1  Rehabilitation Principles for Interventional Orthopedics… 29

Days 0–5

Phase I: Inflammatory phase

• May lift up to 10–20 pounds • Avoid eccentric exercises • Discontinue exercise if pain becomes >3/10 • Activities as tolerated • Discontinue exercise if pain becomes >3/10

• No use of NSAIDs or ice for 4 weeks • Safe use of sling for first 3 days, including when sleeping, then wean out as tolerated • No sleeping on procedure side • No lifting >5 pounds • Avoid overhead activity for 2 weeks • May return to work the following day as tolerated • Discontinue exercises if pain becomes >3/10 • No use of NSAIDs or ice for 4 weeks • No sleeping on procedure side • No lifting >10 pounds • Avoid overhead activity for 2 weeks • Discontinue exercise if pain becomes >3/10 • No use of NSAIDs or ice for 4 weeks

Restrictions

• Begin eccentric training/loading • Continue strengthening exercises • Begin sport-specific exercises

• Continue active ROM as needed, goal of full active ROM • Progressive strengthening

• Continue AROM and PROM • Begin isometric exercises • Begin thoracic mobility exercises

• Rest • Begin gentle active ROM (pendulum exercises)

Rehabilitation

NSAID nonsteroidal anti-inflammatory drug, ROM range of motion, AROM active range of motion, PROM passive range of motion

Phase III: Weeks 6 and Remodeling phase beyond

Weeks 2–6

Phase II: Day 5–week 2 Proliferative phase

Timeframe

Phase of healing

Table 1.10  Shoulder joint: rehabilitation protocol post-orthobiologics

30 W. I. Sussman et al.

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26. Shin L, Peterson DA. Impaired therapeutic capacity of autologous stem cells in a model of type 2 diabetes. Stem Cells Transl Med. 2012;1(2):125–35. https://doi.org/10.5966/sctm.2012-­0031. 27. Keats E, Khan ZA.  Unique responses of stem cell-derived vascular endothelial and mesenchymal cells to high levels of glucose. PLoS One. 2012;7(6):e38752. https://doi.org/10.1371/journal.pone.0038752. 28. Cramer C, Freisinger E, Jones RK, et al. Persistent high glucose concentrations alter the regenerative potential of mesenchymal stem cells. Stem Cells Dev. 2010;19(12):1875–84. https://doi.org/10.1089/ scd.2010.0009. 29. Oñate B, Vilahur G, Ferrer-Lorente R, et al. The subcutaneous adipose tissue reservoir of functionally active stem cells is reduced in obese patients. FASEB J. 2012;26(10):4327–36. https://doi.org/10.1096/fj.12­207217. 30. Cerletti M, Jang YC, Finley LW, Haigis MC, Wagers AJ.  Short-term calorie restriction enhances skeletal muscle stem cell function. Cell Stem Cell. 2012;10(5):515–9. https://doi.org/10.1016/j. stem.2012.04.002. 31. Kim HJ, Ji BR, Kim JS, Lee HN, Ha DH, Kim CW. Proteomic analysis of proteins associated with cellular senescence by calorie restriction in mesenchymal stem cells. In Vitro Cell Dev Biol Anim. 2012;48(3):186– 95. https://doi.org/10.1007/s11626-­012-­9485-­0. 32. Lo T, Ho JH, Yang MH, Lee OK. Glucose reduction prevents replicative senescence and increases mitochondrial respiration in human mesenchymal stem cells. Cell Transplant. 2011;20(6):813–25. https://doi.org/ 10.3727/096368910x539100. 33. Daltroy LH, Morlino CI, Eaton HM, Poss R, Liang MH. Preoperative education for total hip and knee replacement patients. Arthritis Care Res. 1998;11(6):469–78. https://doi.org/10.1002/art.1790110607. 34. Lin PC, Lin LC, Lin JJ. Comparing the effectiveness of different educational programs for patients with total knee arthroplasty. Orthop Nurs. 1997;16(5):43–9. 35. Sussman WI, Mautner K, Malanga G.  The role of rehabilitation after regenerative and orthobiologic procedures for the treatment of tendinopathy: a systematic review. Regen Med. 2018;13(2):249–63. https:// doi.org/10.2217/rme-­2017-­0110. 36. Townsend C, Von Rickenbach KJ, Bailowitz Z, Gellhorn AC.  Post-­ procedure protocols following platelet-rich plasma injections for tendinopathy: a systematic review. PM R. 2020;12:904. https://doi. org/10.1002/pmrj.12347. 37. Neph A, Schroeder A, Enseki KR, Everts PA, Wang JH, Onishi K. Role of mechanical loading for platelet-rich plasma-treated achilles tendinopathy. Curr Sports Med Rep. 2020;19(6):209–16. https://doi. org/10.1249/JSR.0000000000000719.

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Rehabilitation of Cervical Spine Disorders Laurent Delaveaux, Matthew Thomas, Brielle Hansen, and Tony K. George

2.1 Anatomy The cervical spine is a fulcrum for rotating the head, multidirectional bending the neck, and protecting the delicate spinal cord. It has a lordotic curve with seven bony segments. The first two segments are the anatomically unique atlas (C1) and the axis (C2). The occipitoatlantal (OA) or C0–C1 joint primarily  functions in flexion-extension, while the atlantoaxial (AA) or C1–C2 joint functions for head and neck rotation. The atlas does not have a spinous process, or vertebral body, but rather two lateral masses. These lateral masses con-

L. Delaveaux Hackensack Meridian JFK Johnson Rehabilitation Institute, Edison, NJ, USA e-mail: [email protected] M. Thomas Lake Erie College of Osteopathic Medicine, Bradenton, FL, USA e-mail: [email protected] B. Hansen St. Peters University Hospital, Somerset, NJ, USA e-mail: [email protected] T. K. George (*) University Orthopaedic Associates, Somerset, NJ, USA

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 T. K. George et al. (eds.), Orthopedic Rehabilitation, https://doi.org/10.1007/978-3-031-32026-2_2

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tain the facets which articulate with the occiput above and the axis below. The axis extends superiorly into the odontoid process and is secured to the atlas via the transverse ligament, allowing rotation of the head. The cervical spine has a unique bifid spinous process, with the exception of C1 and C7, where the C7 spinous process is typically longer than the rest. It also contains the nuchal ligament, an extension of the supraspinous ligament connecting the spinous processes to the occiput. Another feature, the transverse foramina is unique to the cervical spine and contains the vertebral artery (Fig. 2.1). The cervical spine and musculature are innervated by an extensive network of nerves. Each level has four nerve roots, with two on each side—a ventral root and a dorsal root. Ventral roots carry efferent motor signals to a corresponding myotome (muscle group). Dorsal roots carry afferent sensory signals to the brain from a corresponding dermatome (skin region). Each ventral and dorsal root originate as separate branches off the spinal cord and merge in the intervertebral foramen to form a spinal nerve. Outside the spine, the spinal nerves subdivide into dorsal and ventral rami.

Fig. 2.1  Cervical vertebral body. (Images courtesy of Naomi Oommen)

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Eight pairs of cervical spinal nerves innervate and provide sensation to the neck, shoulder, arm, and hand. The C1–C7 nerves exit above their corresponding vertebrae, while C8, similar to thoracic and lumbar  spinal nerves, exit below their corresponding vertebrae. In addition to nerves, a complex network of vasculature supplies the cervical spine. The vertebral arteries travel superiorly through the C1–6 transverse foramina and pass through the foramen magnum to supply the brain. At each cervical level, the anterior and posterior radicular arteries branch from these vertebral arteries entering the intervertebral foramina as spinal arteries and run along the nerve roots to supply the corresponding nerves. There are several key muscles that facilitate movement of the cervical spine. The trapezius is the largest muscle attaching to the posterior cervical spine originating proximally on the external occipital protuberance, ligamentum nuchae, and the spinous processes of C7–T12. It inserts bilaterally on the lateral 1/3 of the clavicle, the acromion, and the scapular spine. It primarily functions to facilitate scapular movement. It is innervated by the spinal accessory nerve (CN XI). Deep to the trapezius is the levator scapulae muscle. It originates at the transverse processes of C1– C4 and attaches distally at the medial border of the scapula, superior to the scapular spine. It is innervated by the dorsal scapular nerve, (C4–5) and branches of the C3–C4 anterior cervical rami. It primarily functions to elevate the scapula. In conjunction with other muscles, it assists in depressing and medially rotating the scapula and for extension, ipsilateral rotation, and lateral flexion of the neck. The erector spinae muscles are utilized in several functions of neck stability. It is the intermediate layer of the intrinsic (deep) back muscle group consisting of three muscles, from lateral to medial: iliocostalis (colli, thoracis, lumborum), longissimus (capitis, colli, thoracis), and spinalis (capitis, colli, thoracis). These muscles traverse the spine bilaterally extending from the base of the occiput to the sacrum and iliac crest. They extend the spine with bilateral contraction and laterally flex the spine (ipsilaterally) with unilateral contraction. Like other intrinsic back

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muscles, the erector spinae are innervated by the dorsal rami of spinal nerves C1–L1. Deep to the erector spinae is the suboccipital muscle group consisting of four muscles situated inferior to the occipital bone. These muscles include: rectus capitis posterior minor, rectus capitis posterior major, obliquus capitis superior, obliquus capitis inferior. The latter three muscles form the boundaries of the suboccipital triangle, a small triangular region on either side of the neck. The roof of the triangle is formed by the semispinalis capitis (a deep back muscle), the floor is formed by the posterior-atlanto-­occipital membrane and posterior arch of the atlas (C1). They are innervated by the suboccipital nerve. These muscles serve as postural support, as well as in extension and rotation of the neck (Fig. 2.2). Anteriorly, the sternocleidomastoid (SCM) muscle has a variety of functions and key protective roles. It consists of two heads, the sternal and clavicular head. The sternal head originates at the

lesser occipital nerve great occipital nerve ear

superior nuchal line

inferior nuchal line rectus capitis posterior minor rectus capitis posterior major

vertebral artery

Obliquus capitis superior posterior ramus of C1 obliquus capitis inferior

cervical plexus

semispinalis cervicis semispinalis capitis

brachial plexus

Cervical longissimus trapezius

Fig. 2.2  Superficial muscles of the cervical spine. (Jian-gang Shi, Wen Yuan, Jing-chuan Sun. Anatomy Atlas and Interpretation of Spine Surgery. Springer Singapore. Springer Nature Singapore Pte Ltd. and Shanghai Scientific and Technical Publishers 2018)

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anterior superior surface of the sternum, and the clavicular head originates at the superior medial 1/3 of the clavicle. Both heads merge and insert on the mastoid process. Unilateral contraction assists with rotation of the head to the opposite side, as well as obliquely. Bilateral contraction assists in flexion and extension of the neck. A large muscle, it additionally protects key structures deep to it, such as the carotid artery. It is primarily innervated by the spinal accessory nerve (CN XI) and branches of the cervical plexus (C2–C3). This highly vascularized muscle receives blood flow from branches of the occipital, superior thyroid, external carotid, and suprascapular arteries (Fig. 2.3). Deep to the SCM lie the loosely termed deep cervical flexors. This group includes: rectus capitis anterior, rectus capitis lateralis, longus capitis, longus colli, longus cervicis. These paired muscles function in neck flexion and spine stabilization. The longus colli and longus capitis play an important role in cervical stability and antagonizing the deep muscles of the upper back. The longus colli is innervated by the C2–C6 anterior rami. The longus capitis is innervated by the C1–C3 anterior rami.

Superior laryngeal nerve

cephalad

anterior belly of digastric muscle

facial artery

geniohyoid

facial vein

submandibular gland (distract)

hypoglossal nerve

hyoid superior belly of omohyoid (cut off)

carotid sheath

superior laryngeal artery Superior thyroid artery

great auricular nerve

sternohyoid transverse cervical nerve trachea

accessory nerve

sternocleidomastoid

Supraclavicular nerve

Fig. 2.3  Deep muscles of the cervical spine. (Jian-gang Shi, Wen Yuan, Jing-­ chuan Sun. Anatomy Atlas and Interpretation of Spine Surgery. Springer Singapore. Springer Nature Singapore Pte Ltd. and Shanghai Scientific and Technical Publishers 2018)

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2.2 Physical Examination 2.2.1 Cervical Spine Exam 2.2.1.1 Inspection Observe cervical spine alignment in the sagittal and coronal plane along with its natural cervical lordosis. Scapular positioning (e.g. elevation or medial/lateral winging) is noted and posture for a forward set, protracted head, and rounded shoulders positioning. 2.2.1.2 Palpation Typically, palpation is performed in supine position to promote muscle relaxation and to allow passive head control. Tissue texture changes, asymmetry, and tenderness are noted. Bony landmarks are palpated to determine skeletal integrity. Palpating the spinous processes of C3 through C6 would suggest a decreased lordotic curve. Joint stability is assessed for potential hypomobility or hypermobility. Normal range of motion of the cervical spine  (best tested in seated position) is flexion at 80–90°, extension at 20–45°, rotation up to 90°, and lateral bending at 45°. Cervical joint motion depends on laxity and tautness of supporting ligaments and connecting musculature. 2.2.1.3 Strength Testing Strength testing of the upper extremity, best tested in seated position, includes muscle testing of the scapula and the upper extremity joints, the shoulder, elbow, wrist, and digits.

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2.2.2 Manual Muscle Motor Strength Testing (Table 2.1) Table 2.1  Nerve root, innervation, muscle involved and its function Nerve root C5

Muscle Biceps brachii

Nerve Musculocutaneous

C6

Brachialis Brachioradialis Ext carpi rad longus Ext carpi rad brevis Ext carpi ulnaris

C7

Triceps brachii

Musculocutaneous Radial Radial Radial Posterior interosseous Radial

C8

Lumbricals Dorsal and palmar interossei (MCP) Flexor digitorum superficialis and profundus (PIP) Flexor digitorum profundus (DIP) Dorsal interossei Abductor digiti minimi

T1

Action Elbow and forearm flexion Shoulder abduction Wrist extension

Elbow and forearm extension Median, ulnar, ulnar Finger flexors

Median and median/ ulnar Median/ulnar Ulnar Ulnar

Finger abductors

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2.2.3 Upper Extremity Reflexes (Table 2.2) 2.2.3.1 Special Tests Spurling Test: With the patient seated, the physician extends and rotates with axial pressure on the head toward the side being tested. Pain radiating along the ipsilateral arm denotes a positive test. This test has low sensitivity (40–60%) and high specificity (92–100%). Contraindications to this test include fractures, cervical instability, infection, metastatic malignancy, and acute trauma (Fig. 2.4). Hoffman’s Sign: The provider passively snaps the distal phalanx of the middle finger. A positive test reveals passive flexion-­ adduction of the ipsilateral thumb and second digit. This test evaluates upper motor neuron involvement. Lhermitte’s Sign: The provider passively forward flexes the cervical spine in a seated position. A positive test is a sharp or electric sensation in the axial spine with passive forward flexion. This test assesses cervical spinal cord dysfunction. Adson’s Test: A positive test is a decrease or absence of the ipsilateral radial pulse with the patients’ head extended and rotated to the ipsilateral site with inspiration. This is indicated for thoracic outlet syndrome. Patient is instructed to flex his/her arms and elbows to 90° and open and close fists. If pain is reproduced within 3 min, a positive test is indicated for thoracic outlet syndrome. Table 2.2  Reflexes with muscle involved, its innervation and root supply Deep tendon reflex Biceps Triceps Brachioradialis

Muscle involved Biceps brachii Triceps Brachioradialis

Innervation Musculocutaneous n. Radial n. Radial n.

Root supply C5, C6 C7, C8 C5, C6

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Fig. 2.4  Spurling’s maneuver

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2.3 Pre-operative Management 2.3.1 Cervical Stenosis and Myelopathy Stenosis is narrowing of the central canal to 13  mm or less on sagittal MRI with “absolute” stenosis occurring at 10 mm. In this range stenosis may  lead to sensory/pain symptoms similar to radiculopathy. True cervical myelopathy occurs when spinal cord compression leads to neurologic compromise and focal neurologic deficits. A thorough physical and functional evaluation is crucial in guiding rehabilitation and appropriate specialist referral. The modified Japanese Orthopedic Association (mJOA) score helps stratify into mild (mJOA of 15–17), moderate (mJOA of 12–14), or severe myelopathy (mJOA of 0–11), to guide treatment [1] (Table 2.3). Conservative treatment measures can be used cautiously in mild scores, while moderate or severe scores should be referred to a surgical specialist [3]. Table 2.3  Modified Japanese Orthopedic Association (mJOA) score for cervical myelopathy [1, 2] A. Motor dysfunction score of the upper extremities  0: inability to move hands  1: inability to eat with a spoon but able to move hands  2: inability to button shirt but able to eat with a spoon  3: able to button shirt with great difficulty  4: able to button shirt with slight difficulty  5: no dysfunction B. Motor dysfunction score of the lower extremities  0: complete loss of motor and sensory function  1: sensory preservation without ability to move legs  2: able to move legs but unable to walk  3: able to walk on flat floor with a walking aid  4: able to walk up and/or down stairs with hand rail  5: moderate to significant lack of stability but able to walk up and/or down stairs without had rail  6: mild lack of stability but walk unaided with smooth reciprocation  7: no dysfunction

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Table 2.3 (continued) C. Sensation  0: complete loss of sensation  1: severe sensory loss or pain  2: mild sensory loss  3: no sensory loss D. Sphincter dysfunction score  0: inability to micturate voluntarily  1: marked difficulty with micturition  2: mild to moderate difficulty with micturition  3: normal micturition

2.3.1.1 Modalities • Although no definitive guidelines exist, heat or cold can be applied for pain relief [3]. • TENS assists some patients for short term relief. • Cervical traction did not show improvement, with some reports of worsening end points and is best to avoid in myelopathy [4]. • Similarly, manipulation has been linked to complications and should be considered with caution [4]. 2.3.1.2 Bracing • Short term soft cervical collar can be used to avoid end range flexion of the cervical spine [3, 4]. • Orthoses should be avoided beyond 1–2 weeks to prevent further deconditioning [3, 4]. • Cervical pillow may be beneficial for sleep and the patient’s comfort. 2.3.1.3 Pre-operative Rehabilitation • Therapy is trialed to restore strength, improve pain, and prevent further injury for mild mJOA without progressive symptoms [3–5] • Postural reeducation [3], passive range of motion with massage, and avoidance of painful end range flexion are included [3–5] • Cervical strengthening beginning with isometric exercises,

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progressing to limited isotonic exercises with pain-free range of motion [5]. • Attention is focused on scapulothoracic musculature (trapezius, serratus anterior, levator scapulae, rhomboid major, and pectoralis minor).

2.3.1.4 Interventional Procedures • Cervical interlaminar epidural injection for short term pain relief in the setting of symptomatic spinal stenosis and  mild chronic nonprogressive myelopathy [6, 7]. • Guidelines in general recommend an interlaminar C7-T1 injection; however, preprocedural imaging review is essential to avoid the myelopathic level. • Conservative care is facilitated with interventional treatments and close monitoring for functional/neurologic deficits.

2.3.2 Cervical Radiculopathy Cervical radiculopathy is a combination of pain, sensory, or motor disturbance resulting from a cervical spinal nerve root irritation or impingement. It encompasses nerve roots from C1 to C8, innervating the posterior occiput, upper back, arm, forearm, proximal and distal upper extremity. Most common cervical nerve root involved in radiculopathy is C7 followed by C6 and C5. Trauma and herniated discs are major etiology of cervical radiculopathy in younger adults as opposed to degenerative causes in later decades of life such as disc degeneration with bone spurring.

2.3.2.1 Modalities • Restoring strength, improving pain, and preventing injury are prioritized, where 85% of acute radiculopathies resolve within 8–12 weeks of conservative care [3, 6]. • No definitive guidelines exist between hot or cold therapy and can be applied for 20–30 min to relieve discomfort [3]. • Consider TENS for short term relief, but evidence is inconclusive [3]. • Intermittent mechanical cervical traction, with a required force of >20  lbs (or lowest weight inciting an effective response)

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applied for 10–15  min 2–3 times a day. Contraindications include C1–2 instability, RA, vertebro-basilar artery insufficiency, ligamentous instability, aortic arch aneurysm, cervical myelopathy, spinal cord tumor [3]. • Of available RCT trials, however, none shows superiority over sham in reducing pain or improving function [8]

2.3.2.2 Bracing • Acutely, a soft cervical collar could serve a proprioceptive role to improve posture and avoid painful end range of motion [3]. • Orthoses beyond 1–2 weeks should be avoided as it could cause further deconditioning [3]. • Cervical pillow may be beneficial for sleep and patient comfort. Neck position on the pillow should remain parallel to the mattress when side sleeping. Working desk ergonomics should be evaluated and neccessary correction should be made. 2.3.2.3 Pre-operative Rehabilitation • Restoration of cervical spinal flexibility with passive range of motion, massage, and mobilization, avoiding painful positions, followed by gradual static and progressive active range of motion activities [3] • Cervical strengthening with attention to scapulothoracic musculature, beginning with isometric exercises, progressing to isotonic exercises with pain-free range of motion [3] • Stretching of cervical spine muscles (upper trapezius, levator scapulae, scalene muscles) • Endurance and aerobic conditioning 2.3.2.4 Interventional Procedures • Cervical epidural injection for radicular symptoms • The C7-T1 level is the safest level for a cervical interlaminar epidural injection  and when possible, paramedian approach should be taken. Inadequate fusion of the ligamentum flavum could increase spinal cord injury at other cervical levels. Similarly, cervical transforaminal injections carry inherent risk of inadvertent vascular infiltration/injury  and care should be exercised when attempting transforaminal approaches.

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2.3.3 Cervical Facet Arthropathy Facet arthropathy is degenerative arthritis of the axial facet joints. The facet joint is formed by fusion of the inferior articular process of the superior vertebra to the superior articular process of the inferior vertebra. A synovial joint, it can be the source of axial pain in 35–42% of adults with cervical spine pain (variable age-­ related prevalence). Its capsular innervation is the target for interventional nerve blocks to relieve facet generated pain. Cervicogenic headache, as the name implies, describes head pain originating from the neck. This can be characterized as chronic, recurrent, or restricting range of motion. The C1–C3 nerve roots are typically implicated and responsible for innervating the cervical musculature.

2.3.3.1 Modalities • Cryotherapy is preferable due to anti-inflammatory effects. Heat may worsen pain from joint inflammation. • Cryotherapy regimen is as follows: 20 min, 3–4× a day. • Soft tissue massage and myofascial release is important as an adjunct but insufficient on its own. • Transcutaneous electric nerve stimulation (TENS). • Intermittent mechanical or manual cervical  traction may be beneficial. 2.3.3.2 Bracing • Bracing is rarely used for facet mediated neck pain. 2.3.3.3 Pre-operative Rehabilitation • Cervical range of motion (ROM) exercises. • Cervical and thoracic manipulation with mixed exercise for cervico-scapulothoracic and bilateral upper extremity with strength training, endurance exercises, stretching and stabilization of surrounding soft tissue, both static and dynamic [9]. –– Stretching of the larger neck movers (i.e., upper trapezius, levator scapulae, and scalene muscles) –– Strengthening of deep neck stabilizers (i.e., longus capitis and Longus colli muscles)

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• Coordination, proprioception, and postural reeducation. • Endurance and aerobic conditioning. • In a Cochrane review, manipulation was favored over medication in improving function, pain, and patient satisfaction for acute and subacute neck pain [10].

2.3.3.4 Interventional Procedures For Facet Arthropathy • Therapeutic zygapophyseal joint steroid injection may have short term pain relief benefits. • Successful medial branch diagnostic block ×2 followed by radiofrequency ablation treatment may provide 9–12 months of pain relief from facetogenic neck pain. Interestingly, relief from repeat RFA does not wane with subsequent intervention [9].  For Cervicogenic Headache • Management begins with physical therapy, eliminating pain severity by half in two-thirds of the population [11]. • Interventions are targeted toward sources of pain including lateral atlantoaxial (C1–C2) intra-articular steroid injection, C2– C3 facet steroid injection, C2+ C3 medial branch, and third occipital nerve RF ablation treatment. Surgical management serves as a final recourse [11].

2.3.4 Cervical Whiplash Cervical whiplash is a traumatic flexion extension injury. A common antecedent event is a motor vehicle accident and falls. It presents as a constellation of symptoms grouped into whiplash associated disorders (WAD). Whiplash injury is a clinical diagnosis where imaging is often negative or inconclusive. Minor injuries to the cervical paraspinal muscles, facet joint capsule, or ligaments may not appear on imaging but have symptomatic ­presentation.

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2.3.4.1 Modalities • Moist heat • Soft tissue massage • Transcutaneous electric nerve stimulation (TENS) for patients’ refractory to early improvement 2.3.4.2 Bracing • Most patients are transferred to the ER with a hard collar to immobilize the spine. Collar is discontinued once anatomical and neurologic stability is determined by examination and imaging. Patients can be transitioned to a soft collar for a short duration (~3 days). • Soft collars may provide pain relief, but long-term benefit is not supported in literature. Studies suggest physical therapy and mobilization to be superior to bracing in reducing disability and pain [12, 13]. • Hard collars do not have any documented role in the management of pain and are best utilized as a stopgap prior to surgical intervention for unstable, traumatic injury. Moreover, downstream complications such as stiffness, breathing discomfort, and skin breakdown are additional concerns with chronic use [14]. • Cervical pillow may be beneficial in the acute and chronic phases. 2.3.4.3 Pre-operative Rehabilitation • An active treatment program with quick return to normal activity is emphasized. Specific rehabilitation targets vary and can encompass annulus fibrosus tears, anterior longitudinal ligament tears, articular pillar fractures, end plate avulsion ­fractures, vertebral body fractures, and rupturing of the joint capsule. • For acute symptoms, reassure patients that the expected course of recovery is between 2 and 3 months. For chronic symptoms, cognitive behavior therapy (CBT) is considered. • Early mobilization is key, as prolonged immobilization can worsen symptoms [14, 15].

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• A regimen emphasizing postural and mobility exercises to reduce pain and improve ROM, shoulder girdle stabilization, cervical strength training. and bilateral upper extremity exercises [16]. • If symptoms remain, a progressive submaximal exercise regimen is encouraged for chronic symptoms. • Combination therapy may be more effective than unimodal therapy for functional restoration.

2.3.4.4 Interventional Procedures • Trigger point injections with intramuscular lidocaine, when combined with conservative management, are effective and well tolerated [16]. Most common muscles injected are the upper trapezius and cervical paraspinal muscles. • Intra-articular cervical facet injection (short term benefit) vs. cervical medial branch block and RF ablation treatment (9–12 months benefit) can be considered for whiplash associated neck pain due to cervical facet sprain. Levels treated will depend on clinical presentation of neck pain and referral pattern. • Occipital nerve blocks can be considered if the headache has lancinating characteristics in the distribution of lesser or greater occipital nerves.

2.3.5 Cervical Spine Trauma Cervical spine injuries can be classified as upper cervical (C1 and C2), or subaxial injuries (C3–C7). Injuries include vertebral fracture, spinous process fracture, facet fracture-dislocation, and ligamentous injuries.

2.3.5.1 Bracing Simple strains may require no bracing or a few days of soft color. Stable upper cervical injuries are treated with rigid orthosis, while unstable cervical injuries are treated with a halo vest or may require internal surgical fixation.

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2.3.5.2 Pre-operative Rehabilitation Odontoid Fracture Goals of Rehab: 1. Initial therapy is focused on limiting cervical ROM through use of a hard collar to allow for healing of fracture in partial and hairline (type 1) fractures. 2. After fracture has healed,  restoration of cervical ROM and strength is prioritized. Rehabilitation steps should be coordinated between spine surgeons and the rehabilitation team.  Length, dosage, and treatment of therapy: • Varies based on extent of injury and type of stabilization (when applicable) • Hairline or partial fractures—8–12 weeks to allow for bone healing. • Includes: –– Manual therapy to decrease tension in cervical paraspinals, upper trapezius, levator scapulae, and suboccipital muscles. [17] –– Strengthening on the deep neck flexors and extensors (longus capitis/colli, multifidi muscles). [17] –– Education on head and neck positioning and posture. [17]

2.3.5.3 Interventional Procedures • In selected cases, vertebral augmentation may be an option for isolated vertebral body fractures without other instabilities and ligamentous injuries. • Surgery is indicated with an odontoid screw fixation for type II and III fractures, odontoidectomy, or posterior fixation. • Surgery is indicated with anterior or posterior fusion for instability at other subaxial levels. 

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2.4 Post-operative Rehabilitation 2.4.1 Anterior Cervical Discectomy and Fusion (ACDF) Initial Treatment (Weeks 0–4/6): Immobilization via cervical collar is dependent on surgeon preference. Avoid lifting >5 lbs from floor to chest and to avoid all overhead lifting. No sudden movements of C/S. No high impact activity. Education on the following: maintaining a neutral spine with proper body mechanics, increasing positional tolerance to sitting/standing, transfer training (i.e. log rolling, sit to stand), and gradual increase in aerobic walking program. ROM: Gentle AROM of the C/S in pain-free range beginning at weeks 4–6. Avoid passive cervical stretching for the first 12 weeks or before full healing has occurred. Full, pain-free ROM is permitted after week 12. Strengthening: Begin submaximal cervical isometrics at weeks 4–6 into flexion, extension, side-bending, and rotation. Focus should be on regaining strength/endurance of the local deep neck flexor (DNF) musculature (rectus and longus capitis, longus cervicis) via DNF training with examples of progressions as shown (Fig. 2.5). Core stabilization training and scapulothoracic strengthening also appropriate beginning at week 4 to include focus on: transverse abdominis, upper, middle, and lower trapezius, latissimus dorsi, serratus anterior, etc. Expected Course of Physical Therapy: PT to begin at weeks 4–6, 2–3×/week. To initiate manual therapy including soft tissue mobilization of affected structures, cervical and thoracic joint mobilizations (>2 segments from site of fusion), peripheral nerve mobilization (without reproduction of symptoms), scapulothoracic and upper body strengthening, education on diaphragmatic breathing, balance training and continuation of cervical isometric/deep neck flexor training.

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a

b

c

Fig. 2.5 (a) Chin tuck in supine. (b) Progression to chin tuck in prone prop. (c) Further progression to chin tuck in quadruped

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Activities: Return to low-level ADLs between weeks 6 and 12. Begin high-level ADLs including plyometric programs and sports at weeks 12–18. Continued long-term avoidance of heavy overhead lifting advised, unless the surgeon specifies otherwise.

2.4.2 Posterior Cervical Laminectomy and Fusion Initial Treatment: (Weeks 0–4/6): Immobilization via cervical collar  is  dependent on surgeon preference. Gradual return to ADLs. No lifting >5 lbs from floor to chest and avoid all overhead lifting. No AROM until week 4. No sudden movements, or high impact activity. Education on the following: maintaining a neutral spine with proper body mechanics, increasing positional tolerance to sitting/standing, transfer training (i.e. log rolling, sit to stand), and gradual increase in aerobic walking program. ROM: Begin pain-free AROM at the earliest, week 4. Gentle PROM to begin at week 6 with care to avoid end-ranges. Avoid excessive cervical extension through week 8. Strengthening: Light upper extremity and prone scapulothoracic strengthening beginning at weeks 6–8. Begin training of transverse abdominis in hook lying at weeks 6–8 with progression to sitting/standing at weeks 8–12 and multiplanar training at week 6+. Begin cervical isometrics and training of deep neck flexors at weeks 8–12 along with progression of scapulothoracic and UE strengthening through end of treatment. Expected Course of Physical Therapy: PT to begin at week 6, 2–3×/week. Treatment to include: pain-management via appropriate modalities, soft tissue mobilization of affected structures, stretching per ROM guidelines, balance training, neural glides/mobilizations, joint mobilization (>2 segments from fusion), and therapeutic exercise education.

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Activities: Gradual return to ADLs without C-collar after clearance. To begin a plyometric program at week 16+ if appropriate. Gradual return to sports at week 32+ pending clearance by surgeon. Continued long-term avoidance of heavy overhead lifting advised.

2.4.3 Cervical Foraminotomy Initial Treatment (Weeks 0–2): Avoid bending and twisting of the spine, pushing and lifting >25 lbs for up to 6 weeks. Limit sitting to 30 min at a time for the first 2 weeks with gradual increase in sitting and standing tolerance after week 2. May begin an aerobic walking program and gentle scapulothoracic muscle activation to include: shoulder rolls and scapular squeezes. Patient education on the following: maintaining upright sitting posture, focus on neutral spine with functional movements and avoiding prolonged cervical flexion (i.e. reading, using phone, tablet, etc.). May begin light stretching of the pectorals only. Immobilization via cervical collar is dependent on surgeon preference myofacial. ROM: To begin gentle AROM within pain-free ROM at week 2 with emphasis on cervical retractions. No passive ROM until 6 weeks post-op. Strengthening: May begin light upper extremity exercise (25 lbs for up to 6 weeks. May begin an aerobic walking program to tolerance and scapular retractions. Patient education on the following: maintaining upright sitting posture, focus on neutral spine with functional movements and avoiding positions of prolonged cervical flexion. ROM: Gentle AROM of the cervical spine permitted at week 2. Avoid AROM into cervical extension until week 4. Gentle stretching permitted after week 6. Strengthening: May begin light upper extremity exercise (