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TABLE OF CONTENTS Chapter 1: Evidence-Based Management of Knee Osteoarthritis
[4 Contact Hours] The purpose of this course is to provide physical therapists and physical therapist assistants with up-to-date, evidence-based information pertaining to the diagnosis, treatment and prevention of knee OA. Although this course will be most applicable to physical therapists and physical therapist assistants who work with older individuals in outpatient settings, the increased incidence of OA makes the information in this course relevant to therapists in a variety of settings. Even therapists who specialize and treat patients in areas other than orthopedic settings will likely encounter individuals whose OA affects their participation, mobility, or function. Chapter 2: Introduction to Wheelchair Seating and Positioning [5 Contact Hours] This course, designed to provide the healthcare practitioner with a broad overview of the assessment and provision of wheelchair seating, is written at a basic to intermediate-level for the occupational and physical therapist who have little or no experience in this specialty practice area. Many people require the use of a wheelchair for dependent or independent mobility, and each wheelchair provides some form of seating. Wheelchair seating directly affects a client’s position, which in turn affects function for all of that person’s daily tasks. It is essential that occupational therapy practitioners be able to competently participate as members of the interprofessional team in determining the optimal seating and wheeled mobility interventions for a particular client. Common diagnoses for a client using a wheelchair include cerebral palsy, spinal cord injury, traumatic brain injury, multiple sclerosis, and muscular dystrophies. Chapter 3: Pain Assessment and Management: Role of the PT [1 Contact Hour] This course provides an overview of pain, the physiology of pain, its impact on economic and personal status, and pain assessment and treatment. Final Examination Answer Sheet
©2022: All Rights Reserved. Materials may not be reproduced without the expressed written permission or consent of Colibri Healthcare, LLC. The materials presented in this course are meant to provide the consumer with general information on the topics covered. The information provided was prepared by professionals with practical knowledge in the areas covered. It is not meant to provide medical, legal or professional services advice. Colibri Healthcare, LLC recommends that you consult a medical, legal or professional services expert licensed in your state. Colibri Healthcare, LLC has made all reasonable efforts to ensure that all content provided in this course is accurate and up to date at the time of printing, but does not represent or warrant that it will apply to your situation or circumstances and assumes no liability from reliance on these materials. PHYSICAL THERAPY CONTINUING EDUCATION Book Code: PTNC1023 i
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Chapter 1: Evidence-Based Management of Knee Osteoarthritis
Chapter 2: Introduction to Wheelchair Seating and Positioning
Chapter 3: Pain Assessment and Management: Role of the PT
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How do I complete this course and receive my certificate of completion? See the following page for step by step instructions to complete and receive your certificate. Are you a North Carolina board-approved provider? Our courses are accepted via reciprocity based on approval by another state’s physical therapy board. Are my credit hours reported to the North Carolina board? No. The North Carolina Board of Physical Therapy Examiners perform audits at which time proof of continuing education must be provided. What is my continuing competency reporting period? New PT licensees in NC are assigned to the continuing competence reporting period that begins on January 1 following the date of first licensure. Each PT licensee must accumulate 30 points and each PTA licensee must accumulate 20 points of continuing competence activities during the assigned reporting period to be eligible for license renewal. The points must include one mandatory point from a Jurisprudence exercise. There is a 25 month period to complete the continuing competence requirement. License renewal is EVERY year. Licensees renewing at the end of their reporting period must complete continuing competence activities no later than January 31 . Licensees renewing at the mid-point of the reporting period should report continuing competence activities completed during that year, then renew. Is my information secure? Yes! We use SSL encryption, and we never share your information with third-parties. We are also rated A+ by the National Better Business Bureau. Important information for licensees: Always check your state’s board website to determine the number of hours required for renewal, mandatory subjects (as these are subject to change), and the amount that may be completed through home-study. Also, make sure that you notify the board of any changes of address. It is important that your most current address is on file. What if I still have questions? What are your business hours? No problem, we have several options for you to choose from! Online at EliteLearning.com/Physical-Therapy you will see our robust FAQ section that answers many of your questions, simply click FAQs at the top of the page, e-mail us at firstname.lastname@example.org, or call us toll free at 1-888-857-6920, Monday - Friday 9:00 am - 6:00 pm, EST.
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North Carolina Board of Physical Therapy Examiners 8300 Health Park, Suite 233 Raleigh, NC 27615
Phone: (919) 490-6393 | Toll Free: (800) 800-8982 Fax: (919) 490-5106 Website: http://ncptboard.org
Book Code: PTNC1023
PHYSICAL THERAPY CONTINUING EDUCATION
How to complete continuing education
Please read these instructions before proceeding. Read and study the enclosed courses and answer the final examination questions. To receive credit for your courses, you must provide your customer information and complete the evaluation. We offer three ways for you to complete. Choose an option below to receive credit and your certificates of completion.
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Online • Go to EliteLearning.com/Book . Use the book code PTNC1023 and enter it in the example box that pops up then click GO . • If you already have an account created, sign in to your account with your username and password. If you do not have an account already created, you will need to create one now. • Follow the online instructions to complete your final exam. Complete the purchase process to receive course credit and your certificate of completion. Please remember to complete the online survey. By mail • Fill out the answer sheet and evaluation found in the back of this booklet. Please include a check or credit card information and e-mail address. Mail to Elite, PO Box 37, Ormond Beach, FL 32175. • Completions will be processed within 2 business days from the date it is received and certificates will be e-mailed to the address provided. • Submissions without a valid e-mail will be mailed to the address provided.
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PHYSICAL THERAPY CONTINUING EDUCATION
Book Code: PTNC1023
Chapter 1: Evidence-Based Management of Knee Osteoarthritis 4 Contact Hours
By: Joseph Zeni Jr., PT, PhD Learning objectives
After completing this course, the learner will be able to: Describe the anatomical structures of the lower extremity affected by knee osteoarthritis. Explain the disease process and epidemiology of knee osteoarthritis. Describe components of a physical therapy evaluation for patients with knee osteoarthritis. Course overview With aging of the general population and increase in body mass of the average individual, the incidence and prevalence of knee osteoarthritis (OA) has increased dramatically over the past 10 years. In the past several years, new evidence has emerged from several large epidemiological, interventional, and mechanistic studies that have expanded our understanding of OA initiation, progression, and treatment. Organizations such as the American College of Rheumatology and American Academy of Orthopaedic Surgeons have also synthesized recent evidence about how to manage this disease to provide updated recommendations for healthcare practitioners. Advancements in biomechanical technologies have revealed new details about how forces in our joints can contribute to both the incidence and progression of this OA. The information in this course will help to fill the expanding gap between research and clinical practice as this disease becomes more prevalent. People who complete
Discuss interventions commonly used by physical therapists to reduce symptoms and impairments associated with knee osteoarthritis. Identify factors that may make someone a candidate for surgical and conservative treatments of knee osteoarthritis.
this course will gain insight into risk factors that may lead to OA progression and develop a better understanding of the most effective treatment options. The purpose of this intermediate-level course is to provide physical therapists and physical therapist assistants with up-to- date, evidence-based information pertaining to the diagnosis, treatment, and prevention of knee OA. Although this course will be most applicable to physical therapists and physical therapist assistants who work with older individuals in outpatient settings, the increased incidence of OA makes the information in this course relevant to therapists in a variety of settings. Even therapists who specialize and treat patients in areas other than orthopaedic settings will likely encounter individuals whose OA affects their participation, mobility, or function.
WHAT IS OSTEOARTHRITIS?
Knee osteoarthritis (OA) is a common degenerative musculoskeletal condition. Although it is commonly thought of as a disorder of the hyaline cartilage at the ends of the tibia and femur, advances in imaging techniques have revealed that Relevant joint anatomy When discussing the pathogenesis, risk factors, and treatments for knee OA, it is necessary to have a solid understanding of the structures in and around the knee joint. Although OA is often considered a condition that solely affects the cartilage in the joint, there are direct and indirect changes to the ligaments, menisci, muscle, subchondral bone, and joint capsule as well. Damage to these structures can lead to the development of OA, and conversely, OA progression can lead to morphological changes within these supporting structures. The primary structures within this joint are shown in Figure 1 and will be discussed throughout this section. Bony articulations The knee consists of two primary articulations that are encased within a single joint capsule. The tibiofemoral articulation occurs between the tibial plateau and the femoral condyles. This is an important weight-bearing joint, and much of the force experienced by this portion of the knee joint during static and dynamic activities is a result of the body mass. Recent studies have shown that greater body mass index (BMI) is related to greater tibiofemoral joint contact forces in individuals with and without OA (Harding, Dunbar, Hubley-Kozey, Stanish, & Astephen Wilson, 2016). In the tibiofemoral compartment, the medial and lateral menisci help to distribute the load between the femur and tibia. Damage to the menisci can change the contact stress within the joint and ultimately increase the risk for cartilage breakdown and OA (Khan et al., 2016). The medial side of the tibiofemoral joint (the medial compartment) is the most common side for OA.
it also affects the bone, muscle, and ligaments in the knee. Pharmacological and physical therapy interventions should target all aspects of the joint that are affected by the disease.
Figure 1: Knee Joint Anatomy
Relevant structures within the knee joint include the bone, cartilage, ligaments, and menisci. Note . ©joshya/Adobe Stock. The patellofemoral joint is the articulation between the posterior side of the patella and the femoral condyles and femoral trochlea. Although this joint often is overlooked clinically in individuals with later stages of knee OA, cartilage deterioration is thought to occur first in the patellofemoral joint, with ultimate progression to other regions of the knee (Lankhorst et al., 2016). The patella is maintained in the center of the femoral trochlea by the strong contractions of the quadriceps muscle, as well the patella’s attachments to the medial and lateral retinaculum of
Book Code: PTNC1023
the joint capsule. Injuries to the patella and the surrounding soft tissue, including patellar dislocations, are a known risk factor for OA progression in this articulation (Carbone & Rodeo, 2016). Soft tissue structures Several soft tissue structures play a vital role in maintaining the stability of the knee joint during dynamic activities. In particular, the medial and lateral collateral ligaments prevent valgus and varus (abduction and adduction, respectively) motions of the knee joint in the frontal plane. In the sagittal plane, the anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) provide stability in conjunction with the quadriceps and hamstring muscles. In addition to restricting motion in the Diagnosis criteria Although knee OA is a fairly common, it is important to know that it can be diagnosed by different methods. It is most commonly diagnosed by either radiographic (X-ray) images or clinical features. As a physical therapist or physical therapist assistant, it is important to understand the distinction between these two methods of diagnosis as there can be a weak relationship between radiographic OA and the symptoms a person may experience. Individuals with similar grades of radiographic OA may have dramatically different levels of joint pain, and similarly, individuals with different radiographic grades of OA may have similar symptom presentation. This distinction between diagnostic criteria is also important when interpreting the results from research studies. The method of OA diagnosis may make the results more applicable to patients with either symptomatic or structural disease and may reduce the generalizability of the findings. Radiographic diagnosis Radiographic knee OA is commonly diagnosed using the methods described by Kellgren and Lawrence many decades ago (Kellgren & Lawrence, 1957). Using this method, subjects undergo weight-bearing X-rays in which the knee is slightly flexed. Because cartilage does not absorb X-rays as they pass through, the area occupied by cartilage appears as dark areas or blank space on an X-ray film. Conversely, bone is radiopaque, meaning that it blocks the X-ray beam and appears as white
sagittal plane, the ACL and PCL also prevent abnormal rotations in the transverse plane at the tibiofemoral joint. Damage to any or all of these ligaments can dramatically alter the location of joint forces throughout the knee. Even after reconstructive surgery for ligamentous injuries, motions within the knee do not return to normal. Demanding motions like cutting (Stearns & Pollard, 2013) and jumping (Pozzi, Di Stasi, Zeni, & Barrios, 2017) show dramatic alterations in joint biomechanics and loading patterns. Therefore, the integrity of these soft tissue structures not only a plays role in normal knee function, but also can result in OA progression when injured due to persistent abnormal motion, loads, or alignment. regions on an X-ray film. Therefore, the dark space between the bones can be measured and is correlated with cartilage thickness. This area of cartilage is known as joint space width on the X-ray. As cartilage starts to deteriorate with OA progression, the joint space width will appear smaller until ultimately, there is no cartilage left on the ends of the bones. This results in an X-ray image in which the bones appear to be touching and there is no joint space width. This is how the term bone-on-bone arthritis got its name, and it is indicative of end-stage knee OA, meaning there is no cartilage left between the two articular surfaces. In this condition there is a total loss of joint space. According to the Kellgren & Lawrence method of diagnosis, the X-ray image is graded on a scale of 0 to 4. A score of 0 indicates that there is no evidence of OA within the tibiofemoral knee joint. A grade of 4 means that there are substantial degenerative changes within the joint. The grades get progressively higher as the joint space gets smaller. The grades also factor in other changes associated with knee OA, including the presence of bone spurs, also known as osteophytes, which often occur as cartilage wears away in the joint and abnormal loads between the bones develop. Because this grading scale is somewhat subjective, a grade of 2 is often used as a cutoff for definitive OA, while a grade of 1 is indicative of possible OA-related changes. Examples of a normal knee X-ray and one with substantial OA are shown in Figure 2.
Figure 2: Radiographs of Knees With and Without OA
A posterior to anterior radiograph with no evidence of osteophytes or loss of joint space is seen in image (A).
Image (B) shows knees with a more severe OA, which is evidenced by small joint space in the medial tibiofemoral compartment and large osteophytes on the femur and tibial plateau.
Note. Left: © joeyphoto/Adobe Stock. Right: © stockdevil/Adobe Stock.
Clinical diagnosis Unlike the radiographic diagnosis, which relies solely on changes to the joint structure to confirm the presence of knee OA, other diagnostic methods rely on a phwysical examination combined with patient symptoms. A clinical definition proposed by the American College of Rheumatology is widely used in clinical settings and research studies (Altman et al., 1986). According to the clinical diagnosis criteria, a patient has clinical symptoms of OA if they have knee pain most days of the prior month and at least three of the following six criteria: 1. Age >50 years. 2. Morning stiffness that lasts less than 30 minutes. 3. Crepitus during active joint motion.
4. Tenderness of the bony margins of the joint. 5. Palpable bony enlargement of the knee upon physical examination. 6. No palpable warmth of the joint. While most of the established clinical diagnostic methods for knee OA target the tibiofemoral articulation, recent studies have evaluated whether clinical diagnostic criteria are able to detect patellofemoral knee OA (Stefanik, Duncan, Felson, & Peat, 2017). Unfortunately, there was no one clinical test that was indicative of patellofemoral OA on X-ray. The presence of pain while climbing stairs had very high sensitivity (96%), but poor specificity (15%). This means that patients without pain during stair climbing likely do not have patellofemoral OA, but
Book Code: PTNC1023
pain with stair climbing does not necessarily mean the patient has patellofemoral OA. Similar results were also found for whether anterior knee pain was predictive of patellofemoral OA, suggesting that the accuracy of asking patients about pain location may not be the best discriminator of actual joint Joint-level impairment OA is often considered as a loss of cartilage thickness within the joint; however, recent evidence has revealed that changes in and around the joint actually are part of the disease process. Advanced imaging techniques, such as magnetic resonance imaging (MRI), and new biochemical analyses have revealed that there are changes to many of the soft tissues, fluids, and bony structures in individuals with knee OA. Cartilage deterioration Cartilage loss remains the hallmark characteristic of knee OA progression. The presence and amount of cartilage loss is typically assessed using X-rays, which are relatively low-cost and quick to complete compared with more advanced imaging techniques. Recently, sophisticated MRI acquisition and analysis techniques have revealed that other morphological changes occur within cartilage during the OA process that are distinct from the deterioration seen on X-rays. Specifically, scientists have determined that cartilage in very early or “pre-OA” conditions undergoes a loss of proteoglycan content (Baum et al., 2013). This decreases the cartilage’s ability to hold water, which can reduce its ability to withstand compressive and shear forces and make it more likely to degrade from mechanical stress. Developing new methods to identify patients early in the disease process when cartilaginous changes may not appear on normal radiographs is a high-priority research area. If patients can be identified and treated before actual loss of cartilage tissue occurs, it may be possible to prevent the disability, pain, and functional deficits associated with end-stage disease. Change in muscle function It is often assumed that that changes in muscle function or progressive weakness happens as a result of decreased physical activity in the presence of knee pain and OA. Results from several large studies have shown that when there is a decrease in functional ability in individuals with knee OA there is also a decrease in muscle strength (Ruhdorfer, Wirth, & Eckstein, 2016). However, there is also evidence from large meta-analyses to suggest that muscle weakness may actually precede future OA (Øiestad, Juhl, Eitzen, & Thorlund, 2015). This means that individuals who are weaker are at a greater risk of developing OA in the future. Strengthening should be considered an important component of any preventive rehabilitation strategy for individuals at risk for OA. In the clinic setting and in research studies, muscle strength is often defined as the peak force from a maximal voluntary isometric contraction. While this is a reliable way to measure strength, individuals with knee OA may have muscle dysfunction beyond isometric weakness. Individuals with knee OA have greater activation deficits than individuals without knee OA (Lewek, Rudolph, & Snyder-Mackler, 2004). Activation deficits are defined as the difference between force output from the quadriceps when maximally stimulated using electrical stimulation and force output when the patient kicks as hard as they can without any augmentation from electrical stimulation, as in a maximal voluntary isometric contraction (Figure 3). When the patient is asked to kick as hard as possible, there is a rapid increase in the force output that plateaus for several seconds. However, when the burst of electrical stimulation is provided midway through the trial, there is a large increase in the force output, suggesting that the capability of the muscle exceeded what the patient was able to do on their own. The ratio of maximal force with and without electrical stimulation is defined as the activation ratio. In the example shown in Figure 3, the individual had an activation ratio of 75%, or an activation deficit of 25%. This is an important measure as greater activation deficits indicate a lack of full motor unit excitability and can
cartilage loss (Stefanik et al., 2014). Physical therapists evaluating patients with knee pain should rely on clinical presentation, but may consider obtaining X-rays if patellofemoral knee OA is suspected.
impair functional ability in persons with OA (Fitzgerald, Piva, Irrgang, Bouzubar, & Starz, 2004). Interventions that reduce activation deficits have the potential to improve not only strength, but also functional performance. Figure 3: Quadriceps Strength Testing With and Without Activation Deficit
Note. From Western Schools, 2018. In addition to lower peak force developed by the quadriceps, patients with knee OA also may have lower rates of force development. This means that they may not be able to generate muscle force and muscle power quickly, which is related to diminished gait function in patients with OA (Winters & Rudolph, 2014). The rate at which a person can generate muscle force is important for dynamic abilities, particularly when responding to unanticipated perturbations. Reduced rate of force development may make a person more susceptible to falls if they cannot generate muscle contraction quickly enough to overcome an unexpected loss of balance. When evaluating and treating muscle function in patients with knee OA, factors other than peak muscle strength should be addressed. Although researchers have identified several types of muscle dysfunction, it is not entirely clear what the underlying mechanisms of poor muscle function are in patients with OA. Some of the weakness may be attributed to disuse atrophy as the patient modifies his or her levels of activity. Artificially induced swelling and pain in the knee joint also have been shown to immediately reduce muscle force production in healthy patients, suggesting that afferent signals can attenuate muscle output. Other studies have shown that individuals with knee OA have greater intramuscular fat, which can reduce the physiological cross-sectional area (Kumar et al., 2014). Regardless of the underlying mechanism, increasing quadriceps strength, improving rate of force development, and decreasing muscle activation deficits are common targets in rehabilitation of Osteoarthritis should be considered a disease of the bone, as well as a disease of the cartilage and soft tissue. Emerging evidence has shown that subchondral bone marrow lesions are associated with knee OA (Teichtahl et al., 2017), which can lead to a rapid loss of cartilage and OA progression (Edwards et al., 2016). Bone marrow lesions are diagnosed using MRI, but our understanding of how and why these lesions lead to more pain and faster OA progression is not well understood. This is an emerging area of research in the field of OA that supports the theory that factors other than cartilage loss play a role in this disease. patients with knee OA. Subchondral edema
Book Code: PTNC1023
EPIDEMIOLOGY OF KNEE OA
Epidemiology is the branch of clinical research that focuses on how diseases occur or are spread. These studies often include hundreds or thousands of individuals. Much of the understanding pertaining to the incidence, prevalence, and risk factors of OA are derived from several large epidemiological studies that have taken place over the past 40 years. Some of Incidence and prevalence Arthritis is a catch-all term that describes many different conditions, including osteoarthritis, rheumatoid arthritis, gout, lupus, and many other diseases that affect the joints. Osteoarthritis is by far the most common type of arthritis, and it is associated with a substantial economic burden. The number of individuals with knee OA has been steadily increasing over the past several decades. Recent estimates suggest that 14 million individuals in the United States are afflicted with symptomatic knee OA (Deshpande et al., 2016). Although OA is often thought of as a disease that affects older people, individuals younger than age 45 years were found to comprise 2 million of the 14 million affected individuals, and more than half of those with symptomatic knee OA were younger than age 65. The trend towards younger patients is particularly concerning as these individuals may have a substantial increase in pain and decline in function due to OA over the remaining decades of their life. Risk factors Knowing which patient characteristics predict the future development or progression of OA is essential to reducing the burden of the disease. Treatment targets are needed before interventions can be developed and tested. Several large epidemiological studies have identified consistent and significant risk factors. The Framingham Heart Study, a prospective, health- based epidemiological study that was initiated several decades ago, has provided some of the first epidemiological information regarding who is at risk for knee OA. More recent and targeted epidemiological studies include the Johnston County Osteoarthritis Project, the Osteoarthritis Initiative (OAI), and the Multicenter Osteoarthritis Study (MOST). These studies have enrolled and tested thousands of people with or at risk for OA and have followed them for multiple years. Scientists evaluate the data to identify factors such as radiographic, symptomatic, biomechanical, and functional changes that are associated with OA development or progression. Results from these studies have provided the majority of information regarding characteristics that increase the risk of developing joint disease. Risk factors can be classified in many different ways, but most can be classified as either systemic or local. Systemic risk factors are things that occur in the body, outside of the joint, that may make the knee joint more susceptible to OA. For example, recent advances in genetic testing have revealed that there may be a genetic predilection to OA (Ramos et al., 2014), which would be considered a systemic risk factor. A local risk factor would be something that occurs within the joint itself, placing the cartilage at greater risk for deterioration. An example of this would be a previous joint injury. Several studies have shown that individuals who have had damage to the joint, be it a meniscal injury or ligament rupture, are more likely to develop OA in the future (Silverwood et al., 2015). Risk factors also can be classified as modifiable or nonmodifiable. Modifiable risk factors are characteristics that can be changed or altered through the course of an intervention. These risk factors can be targeted by physical therapy interventions in order to reduce the risk of future disability from OA. One common modifiable risk factor is body weight. There is a strong link between body mass and OA risk; heavier individuals are much more likely to develop OA in the future. A recent meta-analysis found that individuals age 50 years or older who were overweight or obese were more likely to have or develop knee OA (Silverwood et al., 2015). Body mass is something that can be changed through dietary and exercise interventions and
these studies only included individuals with OA, while other studies have included the general population. Because OA is a common condition, even the studies that have included the general population often have a large number of individuals with knee OA.
Younger individuals who have been diagnosed recently with OA have a considerable amount of psychological distress, work- related disability, and lower quality of life (Ackerman et al., 2015). Increased disability may lead to a greater societal impact of this condition, and physical therapists should be aware of this trend. Costs associated with OA include not only the healthcare-related expenses, but also the expenses due to loss of labor productivity due to work absences and costs of informal care provided by family and friends. Recent estimates put the national cost of this condition at 0.25% to 0.50% of the country’s gross domestic product (Puig-Junoy & Ruiz Zamora, 2015). In the United States, this could mean that the total economic cost of OA could reach close to 85 billion dollars. While this value includes osteoarthritis from all joints, the knee is the most common joint to be affected. should be considered a primary or secondary outcome when treating patients with knee pain or knee OA. Nonmodifiable risk factors are things that cannot be changed, such as biological sex. Women are more likely to develop knee OA compared to their male counterparts (Silverwood et al., 2015). While this is not something that can be changed through rehabilitation interventions, considering this risk when developing treatment plans can be important. For example, an older woman with several other risk factors for OA (such as higher BMI and previous joint injury) should be educated on her greater risk for OA and provided information or treatment to reduce this elevated risk. Body mass has been one of the most consistent risk factors that has emerged from various epidemiological studies and meta- analyses. A recent study used statistical techniques to determine how many new cases of OA could be attributed to different risk factors and the greatest indicator by far was body weight. Of all the new diagnoses of knee OA, it is estimated that nearly one-quarter of those cases (24.6%) could be attributed to having a BMI of greater than 25 (Silverwood et al., 2015). Previous knee joint injury was the next highest attributable condition, accounting for 5.1% of new cases of OA. Vocational and recreational participation may be another contributor to knee OA risk. As previously mentioned, participation in sports in which there is a knee injury increases the risk of OA. This is concerning not only because people with previous knee injury are 2.83 times more likely to develop OA (Silverwood et al., 2015), but also because the onset of OA can happen quickly and at a young age after knee injury. In a recent study, almost 50% of patients who sustained a noncontact rupture of the ACL had signs of knee OA on X-rays within 5 years (Wellsandt et al., 2016). Individuals who developed OA also walked with less force through the injured limb, suggesting that underloading of the knee may be a predictor of OA progression after injury. Rehabilitation strategies that normalize movement patterns and restore normal and symmetrical joint biomechanics may offer some protective effect against OA. Vocational activities that include squatting, kneeling, bending, and lifting also have been explored as potential risks for knee OA. There is fairly strong evidence that supports a causal link between squatting and lifting and future knee OA (Silverwood et al., 2015). Other vocations, such as farming and construction, also have potential links to OA development. Physical therapists should include vocational history when evaluating patients with
Book Code: PTNC1023
knee pain or knee OA. Physical therapists can offer education and strategies that may offset this risk for patients in these professions. Protective equipment like knee pads, proper lifting techniques, or assistive devices like mechanical lifts may offer protection against OA development, although these interventions have yet to be studied in this context. When treating patients with or without OA, it is important to keep risk factors for OA in mind. Being overweight or obese is one of the most common and modifiable risk factors for OA. Previous joint injury and female sex are two common Biomechanical pathogenesis Knee OA is somewhat unique in that there is a biomechanical pathway of disease initiation and progression in addition to the risk factors previously discussed. The magnitude, rate, and location of loading within the knee joint is thought to play an important role in whether or not a person develops knee OA. Understanding how biomechanics can influence OA risk is important because physical therapy interventions, such as gait retraining or bracing, may help to offset the pain and cartilage degeneration associated with OA progression. Knee adduction moment During weight-bearing activities, such as walking, a reaction force acts upwards from the ground and pushes back into our feet according to Newton’s Third Law of Motion. These reaction forces create joint moments, which can be conceptualized as the product of the distance between the reaction force and the center of the weight-bearing joint; this is commonly described as the force × 3 distance. A common application of this is the relationship between the ground reaction force and the knee when standing and squatting. When standing, the ground reaction force acts in an upward direction with a trajectory that passes close to the knee joint center when viewed from the sagittal plane. As a result, the distance between the knee joint and the ground reaction force is essentially zero, and thus the joint moment in the sagittal plane is zero. During a squat, the knee joint moves in an anterior direction, which increases the distance between the joint and the force. As a result, the force passes behind the knee and the joint moment that would act to flex the knee increases. Muscle force must be generated from the quadriceps to help overcome the moment caused by the ground reaction force to prevent collapsing into the ground. The adduction moment is similar but occurs in the frontal plane (Figure 4). The adduction moment has been shown to be related to OA severity and OA progression. Larger adduction moments at baseline predict more OA progression (Miyazaki et al., 2002) and more severe knee OA is associated with larger adduction moments (Zeni & Higginson, 2009). This is likely attributed to the fact that larger adduction moments are associated with greater contact forces in the medial side of the tibiofemoral joint and larger forces may degrade the cartilage more quickly. The adduction moment can increase as the ground reaction force becomes oriented in a medial direction, or it can be larger in patients who have a more genu varus alignment (see Figure 4). Because the adduction moment is related to OA progression and is a potentially modifiable biomechanical parameter, reducing this moment has been the target of many interventions. Interventions designed to reduce the adduction moment include gait retraining, unloader bracing, variable stiffness shoes, and contralateral cane use. The benefits and considerations of these interventions will be discussed in subsequent sections of this course.
nonmodifiable factors. Biomechanical factors also predict OA incidence and progression, and these will be discussed in the next section. In summary, the following is a list of factors that are generally accepted to increase the risk of OA development or progression: ● BMI >25. ● Previous joint injury, such as ligament tear or meniscus injury. ● Genetic predisposition. ● Female sex.
Figure 4: Ground Reaction Force During Gait
The external adduction moment can be conceptualized as the distance between the ground reaction force vector and the center of rotation of the knee joint in the frontal plane. When the ground reaction force vector is close to the knee joint, the adduction moment is relatively low, as shown in (A). A change in ground reaction force direction that moves the force vector medially will increase the external adduction moment by increasing the distance between the axis of rotation and the force, as shown in (B). This change in vector position can occur when the individual pushes laterally into the ground when walking. A greater distance between the vector and the knee joint also may occur when the patient presents with greater knee varus, which shifts the knee laterally in space relative to the foot-ground contact. This could increase the adduction moment even if the direction of the ground reaction vector does not change. Note. From Western Schools, 2018. Joint compression Although larger adduction moments may contribute to greater compression forces in the medial tibiofemoral compartment, other patient characteristics can change the overall magnitude of forces in the knee joint. Obesity, which has been discussed in this course as a strong predictor of knee OA, increases the compressive forces within the knee joint. Data from mathematical models of human walking have found that for every 1 pound of weight gained or lost, there is a fourfold change in joint compression forces (Messier, Gutekunst, Davis, & DeVita, 2005). Findings from recent experimental and simulated weight gain have also revealed that joint compression exceeds the amount of weight gained (Knarr, Higginson, & Zeni, 2016). Diet and exercise interventions that reduce body mass also reduce knee joint loads (Messier et al., 2013). In a landmark study by Felson et al., women who lost weight demonstrated a substantial reduction in the risk of developing knee OA in the future (Felson, Zhang, Anthony, Naimark, & Anderson, 1992). It appears that excessive body weight increases the risk of knee OA, at least in part, by increasing the forces experienced by the joint.
Book Code: PTNC1023
PHYSICAL THERAPY EVALUATION FOR PATIENTS WITH KNEE OA
Like most conditions treated with physical therapy, OA is a heterogeneous condition, and patients with the same diagnosis may present very differently. It is critical that each patient be assessed using a variety of clinical, self-reported, and performance-based measures to ensure that the impairments, Physical examination Patients with knee OA have musculoskeletal impairments that worsen as the disease progresses. Muscle weakness, joint contractures, and joint pain are common among individuals with knee OA. Measuring these impairments in a standardized fashion is essential to assessing the efficacy of treatment or when benchmarking a person’s condition compared to normative values. Muscle strength Muscle weakness in individuals with knee OA is most notable in the quadriceps muscles, but also can affect other muscles of the lower extremity. In particular, the knee flexors, ankle plantarflexors, and hip abductors may be weak from disuse atrophy, altered walking patterns that unload the affected side, or joint pain (Alnahdi, Zeni, & Snyder-Mackler, 2012). Muscle weakness in the lower extremity can have negative implications on overall function. Several studies have shown that lower extremity muscle weakness is the primary predictor of poor physical function. People with weakness have difficulty climbing stairs, walking long distances, and are at a greater risk of falling (de Zwart et al., 2015). There are several valid and reliable methods to assess muscle strength in individuals with knee OA. The most common method of measuring quadriceps strength is using maximal isometric contractions on an electrodynamometer (Figure 5). Figure 5: Isometric Knee Extension Strength Measurement
activity limitations, and participation restrictions of each individual are identified. These findings will inform the patient-specific treatment plan, whether it be strengthening to reduce instability, stretching to normalize range of motion, modalities to reduce pain, or a combination. Hip abductors are commonly weak in individuals with knee OA, which is related to worse functional ability (Tevald et al., 2016). Therefore, it is important to measure the hip muscles in addition to the quadriceps. Standardized measures of hip abductor strength can be taken using electrodynamometers, but recent studies have shown that using hand-held dynamometers also can provide meaningful and reliable results (Alnahdi, Zeni, & Snyder-Mackler, 2014). One method of standardizing hip abductor strength testing in patients with OA is to position the patient side lying with the extremity to be tested facing toward the ceiling. A nonelastic strap is placed around the leg just proximal to the femoral epicondyles. The strap is secured to the table so that it is taut when the leg is abducted to neutral. A hand-held dynamometer is placed between the strap and the thigh. The patient is instructed to provide a maximal abduction effort by saying “Push your leg as hard as you can toward the ceiling.” The peak force can then be determined from the dynamometer, or torque can be calculated by measuring the length of the femur. This method has been found to be reliable in patients with knee OA and is shown in Figure 6 (Tevald et al., 2016). Figure 6: Isometric Hip Abductor Strength Measurement Note. From Western Schools, 2018. Plantarflexor weakness is common among older adults and can negatively impact walking ability (Anderson & Madigan, 2014). Evaluating plantarflexor strength using hand-held dynamometry is not useful or valid in older adults with knee pathology (Marmon, Pozzi, Alnahdi, & Zeni, 2013). Strength values from hand-held dynamometry of the plantarflexors are different from values acquired using electrodynamometers, which are considered the gold standard. Because the plantarflexors are a very powerful muscle, the strength of the examiner is likely the limiting factor in hand-held measures of plantarflexor strength. Other clinical methods of measuring plantarflexor strength can be used when an electrodynamometer is not available. The heel rise test for endurance is quick to perform and reliable when the patients are given standardized instructions (Silbernagel, Nilsson-Helander, Thomeé, Eriksson, & Karlsson, 2010). Using one leg at a time, the patient stands on a box that has an incline of 10 degrees. A metronome can be used to provide audio feedback so the patient can perform a heel rise at a rate of one every 2 seconds. The patient is instructed to perform heel rises until the frequency can no longer be maintained, or until the patient’s form changes and they cannot do a heel rise to the full height. The strength measure for this test is the total number of heel rises performed. As with the other measures, a symmetry index can be created by dividing the number by the value from the unaffected side, but these strength deficits may be bilateral, even if the patient has symptoms on only one side.
Setup for measuring maximal isometric contraction of the quadriceps on an electrodynamometer. The axis of the dynamometer should be located at the center of the knee joint, the resistance pad should be located just proximal to the ankle joint, and the arms should be placed across the chest. Note. From Western Schools, 2018. When using this method, it is important to document the knee joint angle at which the test was performed, which is commonly 90 or 75 degrees of knee flexion. Changing the knee flexion angle between testing sessions can change the amount of force produced by the muscle. As a result, the patient may appear to be getting stronger or weaker, but the only thing that changed was the position at which they were tested. The strength of the muscles can be measured in Newtons for force or in Newton-meters (or foot-pounds) for torque. The strength of the affected side can be divided by the strength of the nonaffected side to obtain a symmetry index; however, it is important to remember that many individuals have bilateral disease, so the nonaffected limb may not be normal.
Book Code: PTNC1023
Joint range of motion Evaluating joint range of motion should be part of the standard evaluation for individuals with knee OA. Loss of full extension at the knee is an important indicator of symptomatic progression. In a sample of individuals with knee OA, knee flexion contractures of any amount were predictive of future need for total knee replacement (Zeni, Axe, & Snyder-Mackler, 2010). Therefore, making sure patients achieve and can maintain normal range of motion is important to prevent future disability. When testing range of motion, it is important to document the patient position. There are many multiarticular muscles in the lower extremity, and changing the position of the hip, knee, or ankle during testing may change the individual’s range of motion. It also should be documented whether the range of motion was active or passive. Because patients with knee OA often have substantial pain, they may have substantial active range of motion deficits, even if they have normal passive ranges. Frontal plane joint position Because the knee position in the frontal plane can change the magnitude of the adduction moment, a severe varus or valgus position may increase the risk of OA progression. Individuals with a varus knee are more likely to develop OA in the medial tibiofemoral compartment, whereas individuals with a valgus knee are more likely to develop lateral compartment OA. Measuring the joint position in the frontal plane will help make informed decisions about whether or not bracing may be appropriate for the patient. Alignment can be measured using a variety of methods. The gold standard for lower extremity structural alignment in the frontal plane is done using long leg X-rays, where the position of the femur can be compared to the position of the tibia. In a clinical setting, the therapist can use the quadriceps angle (Q-angle) to ascertain a relative lower extremity position. This measure estimates the line of force of the quadriceps muscle, which is driven by the underlying bony structure. To measure this angle, the clinician should place the patient in a supine position. The hip and knee should be extended, and the hip should not be rotated internally or externally. The center of the goniometer should be placed over the anterior patella, with the proximal arm aligning with the anterior superior iliac spine (ASIS) and the distal arm aligning with the tibial tuberosity (Figure 7). The angle is recorded, along with a descriptor of varus or valgus to differentiate the direction of the alignment. There are alternate positions for this test, including standing, which will account for the effect of weight bearing on lower extremity alignment. Figure 7: Q-Angle Measurement
the clinical diagnosis of knee OA that was discussed previously in this course. Pain frequency can be assessed by asking the patient whether the pain is intermittent or constant, although both are implicated in poor function in patients with knee OA (Davison, Ioannidis, Maly, Adachi, & Beattie, 2016). It also can be assessed by asking the number of days in the past week in which the patient had pain or by asking whether the patient had pain most days of the month. There are also knee-specific questionnaires that can be used to measure aspects of a patient’s pain. The Intermittent and Constant Osteoarthritis Pain (ICOAP) scale is a questionnaire that asks questions about constant pain, as well as pain that “comes and goes.” This questionnaire recently has been shown to be responsive and reliable for patients with knee OA, and it may offer a more comprehensive and objective evaluation of how different types of pain associated with knee OA impact function and quality of life (Turner, Moreton, Walsh, & Lincoln, 2017). Instability Joint instability is a common complaint among individuals with knee OA. Even without pain, patients may complain that functional activities such as descending stairs are difficult because of knee joint instability. Instability is a general term, but is often thought of as the result of laxity within the knee joint (a structural issue) or poor muscular control during dynamic activities (a neuromuscular issue). It is likely a combination of the two, as changes to the structure may affect the afferent feedback system to the central nervous system, which in turn cannot produce the required motor output. Instability may be described as “knee buckling” by patients, which can arise as a result of muscle weakness, particularly of the knee extensors. Reducing instability through bracing or neuromuscular retraining can have a positive impact on outcomes and may benefit the joint structure. Recent experimental studies in rat models of knee OA have revealed that controlling instability delays degeneration of the knee cartilage (Murata et al., 2017), although these results have not been shown in humans. The presence of instability can be ascertained through patient self-report by asking “Have you had any episodes of knee buckling?” Other measures of instability, such as joint laxity and thrust gait, can be assessed through physical examination and observational gait analysis. Laxity Laxity of the knee joint can be evaluated through manual assessment of the arthrokinematic motions in the frontal and sagittal planes. As the cartilage becomes thinner, the ligaments and joint capsule surrounding the knee joint become loose. This may allow excessive “play” within the joint, which may contribute to abnormal frontal plane knee motions during walking. To date, there is inconclusive evidence as to whether joint laxity is related to the incidence or progression of knee OA, and prospective studies in this area are needed (Freisinger, Schmitt, Wanamaker, Siston, & Chaudhari, 2016). Frontal plane thrust gait Thrust gait is a term given to individuals who present with a rapid motion into knee varus or valgus when walking. It typically occurs as the individual transitions to the single limb stance portion of the gait cycle and full body weight is placed on the affected limb. Varus thrust appears as an apparent increase in the varus angle, or worsening of leg-bowing, during single limb stance. Valgus thrust is the opposite. Thrust gait has traditionally been assessed through a visual assessment of the patient’s gait, although the presence of this thrust has been substantiated using three-dimensional motion analysis techniques (Sosdian et al., 2016). The presence or absence of thrust gait should be considered when evaluating individuals with knee OA, as stabilizing braces may offer more normal gait dynamics for individuals with a positive thrust. Effusion Joint swelling and irritation to the joint capsule can be one cause of joint pain, abnormal motor control, or muscle inhibition. Effusion, or swelling within the joint, is a consistent feature
Note. From Western Schools, 2018.
Pain Knee OA is a chronic condition that is characterized by mild to severe joint pain; therefore, assessing pain is a key component of any evaluation. The magnitude of pain can be evaluated using visual analog scales or numeric pain ratings that range from 0 to 10; however, there are other dimensions of pain that may provide valuable insight into the patient’s rehabilitation potential and appropriate interventions. One common additional domain of pain is pain frequency. Pain frequency is one component of
Book Code: PTNC1023
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