Orthopaedic Handbook

PREPARED BY: STANISH ORTHOPAEDIC INCORPORATED Dr. William D. Stanish Professor of Orthopaedic Surgery, Dalhousie University, and Director, Orthopaedic and Sport Medicine Clinic of Nova Scotia Halifax, Nova Scotia, Canada March 2011

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Table of Contents

OSTEOARTHRITIS ...................................................... 2

LEG LENGTH INEQUALITY (Discrepancy) ........ 11

INJURIES TO THE MENISCUS OF THE KNEE .. 16

PLANTAR FASCIITIS ............................................... 21

HALLUX RIGIDUS ..................................................... 26

DEGENERATIVE DISC DISEASE .......................... 33

DISORDERS OF THE ROTATOR CUFF ............... 43

PAIN ............................................................................... 50

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OSTEOARTHRITIS Introduction Osteoarthritis (OA) is the most common joint disorder in adults. It occurs secondary to the deterioration of the joint (articular) cartilage. The cartilage is the material that provides cushioning and shock absorption at the end of the bones. It also allows the joint surfaces to glide smoothly over one another.1, 3 Osteoarthritis of the degenerative type affects the lower joints that are involved in weight- bearing such as knees, hips, spine and feet. The joints of the hand that are used to grip objects may also be affected, primarily the thumb and the index finger.2 There are basically two types of arthritis. The first type, as stated, is a degenerative type of arthritis, usually secondary to injury, aging or mechanical disturbance. The second type is inflammatory osteoarthritis. With inflammatory arthritis, the joint cartilage usually deteriorates because of invasion of inflammatory by-products that damage the cartilage. Examples are gout, psoriasis, inflammatory bowel disease and rheumatoid arthritis.

Figure 1. Severe osteoarthritis of the knee. Retrieved January 7, 2011 from httpme.queensu.capeopledeluz ioimagesOsteoarthritisKnee1.jpg

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Osteoarthritis Incidence and Prevalence Estimating the prevalence of osteoarthritis is difficult because structural changes of the disease may be detected by x-rays, but are not accompanied by symptoms.4 Furthermore, estimates can vary, depending on whether or not mild arthritic change within the joint is included with moderate and severe alterations.4 The prevalence of symptomatic OA (persons with both x-ray evidence and pain) in any joint does affect 14% of adults aged 25 and older, and 34% of those 65 years of age and older.5 From 1990 to 2005, the number of North American adults with osteoarthritis has risen by 28%.4 The prevalence of symptomatic OA in each joint is presented below. Key Points:

Hand = 8% of adults 60 years of age or older6 Knee = 12% of adults 60 years of age or older7 Hip = 5% of adults 55 years of age or older4 Feet = 2% of adults over 15 years of age4

It is important to note that when considering x-ray evidence of osteoarthritis alone, estimates have been as high as 80% of the population greater than 65 years of age.8 Symptomatic OA is generally more prevalent in females than males, with the exception of hip OA4, 6, 7. Age is an important factor in the incidence of OA. Arthritis is uncommon in patients under the age of 40, with incidence rates increasing with age and leveling off around 80 years of age.4, 9 It is important to note that age itself is not the sole cause of osteoarthritis. Osteoarthritis appears more in the elderly because their load bearing joints, such as hips, knees and feet, have been subjected to a lifetime of stress.3 A higher incidence of osteoarthritis in most joints has been linked to obesity, especially in the knee.10, 11

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Osteoarthritis Excess body weight puts more stress on the weight bearing joints, increasing the wear of the cartilage.3, 12, 13 Interestingly, non-weight bearing joints such as those in the hand have been linked with obesity, suggesting obesity also leads to OA through other pathways.14, 15 The incidence of osteoarthritis also increases following major joint injuries and mechanical malalignment, such as bow-legs. Repetitive joint movements, and work requiring excessive knee bending and/or lifting, has been incriminated as provoking cartilage degeneration.16, 17 Key Points:

34% of patients, 65 years or older, have evidence of osteoarthritis. From 1990 to 2005, the number of North American adults with osteoarthritis

has risen by 28%. When considering x-ray evidence of osteoarthritis alone, 80% of the

population greater than 65 years of age suffers with osteoarthritis. A high incidence of osteoarthritis has been linked to obesity, particularly in

the knee joint. Natural History The natural history of osteoarthritis is not well documented and not easily generalized. This is due to the fact that the development of osteoarthritis is insidious, taking years to evolve, and the natural history differs at the varying joint sites. The disease tends to progress most rapidly in the finger joints and rather slowly about the knee.18 The process of osteoarthritis is characterized by progressive loss of joint cartilage, with the secondary development of bone spurs called osteophytes.8, 19

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Osteoarthritis

The loss of cartilage leads to a compromised joint surface, and thus the joint is unable to effectively transfer the forces applied during daily activities. Once the joint space becomes narrower, bone spurs will begin to form, thus increasing the surface area of the joint. This allows the joint force to be distributed over a greater surface area.19 The pain associated with osteoarthritis is not caused by these initial changes.

The pain is a consequence of the secondary changes of the joint capsule (with distension) and inflammation.8 These changes only start to appear after the disease has moderately progressed. Initially the symptoms of discomfort; i.e., pain, usually come and go, and the patient will experience exacerbations that last a few days or months.20 It has been noted that some patients have periods of months, or even years, in which they experience little discomfort.20 The studies of the natural history of osteoarthritis demonstrate that the symptoms tend to recur; i.e., complete remission is uncommon. In a 15 year follow-up study, about 50% of patients with knee osteoarthritis experienced joint deterioration, while the other 50% showed no change.21 Key Points:

The natural history of osteoarthritis is not well documented. Osteoarthritis is characterized by progressive loss of joint cartilage. Symptoms usually come and go, but can be subject to flare-ups that last days

or months. Studies of the natural history of osteoarthritis show that improvement of

symptoms in the long term is extremely uncommon. Implications Osteoarthritis often causes functional disability and has been shown to decrease quality of life.22 Osteoarthritis causes more disability in the elderly, compared to any other disease. The pain and psychological factors involved with OA may influence joint function, as much as the degree of the OA present.2, 23 Patients suffering with osteoarthritis tend to avoid activities that trigger their symptoms.23

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Osteoarthritis

Symptoms can be alleviated through medication, exercise, muscle strengthening, weight reduction, footwear modification and the judicious use of a brace and/or walking aids.24, 25 Advanced OA may be treated through surgical means.3 It is important to note that the degree of joint pain does not always coincide with the degree of x- ray evidence of osteoarthritis.26

Even in very advanced cases of OA, there may be very few symptoms; i.e., of pain. Osteoarthritis is a manageable condition. When proper interventions are taken, the resulting limitations can be reduced, allowing the afflicted person to carry on with their daily activities.

Fig 3. X-ray images displaying front view of a normal knee (left) and an osteoarthritic knee (right) with joint space narrowing and bony deformation. Retrieved from http://www.mendmyknee12481.com/knee_osteoarthritis_diagnosis.php on Jan 7, 2011. Key Points:

Osteoarthritis is the most common form of joint disorder in adults. It primarily affects the load bearing joints, such as the hips and knees. Obesity is an important risk factor for OA, especially for the knee. Disease onset is not well understood and is insidious. Some patients have periods of months where they experience few symptoms. Even in the most advanced cases of OA, there may be few symptoms present. Treatments, both conservative and surgical, are available.

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Osteoarthritis Summary:

Osteoarthritis is the most common form of joint disorders in adults.

This very common disorder usually afflicts joints that have underlying mechanical difficulties, predisposing them to early wear of the cartilage.

Advanced osteoarthritis may be treated through surgical means, but symptoms can be alleviated by a number of non-surgical techniques; i.e., muscle strengthening, weight reduction and walking aids.

Even in the most advanced cases of osteoarthritis, there may be but a few symptoms.

Profile - Patient #1 Forty-nine year old female presents with painful swelling about both knees and her wrists. X-rays demonstrate advanced tricompartmental arthritis. It is noted that she has psoriatic plaques on both her elbows and both knees. She has been treated for psoriasis since the age of twenty-three. There is also a family history of the same skin disorder. This patient suffers with psoriatic arthritis, which is an inflammatory condition, frequently inherited. Profile - Patient #2 A forty-nine year old male patient presents with pain about the medial side of the knee. The patient’s history is that he had knee surgery at the age of eighteen. The surgery was removal of the medial meniscus. Clinical examination and x-ray review reveal degenerative osteoarthritis of the medial side of the knee with a varus (bow-legged) deformity. Knee bracing is recommended. This is the story of a person who suffers with osteoarthritis, secondary to surgical removal of the medial meniscus, which is a common byproduct of that type of procedure.

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Osteoarthritis References 1. Peyron J. 1984. The Epidemiology of Osteoarthritis. In R. Moskowitz, D. Howell, V.

Goldberg , H. Mankin. (eds) Osteoarthritis: Diagnosis and Management. Toronto, Ontario, Canada; W.B. Saunders Company, p 9-27.

2. Felson D. 1993. Epidemiology of Rheumatic Diseases. In D. McCarty, W. Koopman.

(Eds). Arthritis and Allied Conditions; 12th ed. London: Lea & Febiger; p 37-39. 3. Apley G, Solomon L, Mankin H. 1993. Apley’s System of Orthopaedics and Fractures;

7th ed. London: Butterworth Heinemann. 4. Lawrence RC, Felson DT, Helmick CG, et al. 2008. Estimates of the prevalence of

arthritis and other rheumatic conditions in the United States. Part II. Arthritis and Rheumatism; 58: 26-35.

5. Centres for Disease Control and Prevention. 2007-2008; National Health and Nutrition

Examination Survey. 2011. 6. Dillon CF, Hirsch R, Rasch EK, Gu Q. 2007. Symptomatic Hand Osteoarthritis in the

United States: Prevalence and functional impairment estimates from the third U.S. National Health and Nutrition Examination Survey; 1991-1994. American Journal of Physical Medicine & Rehabilitation/Association of Academic Physiatrists; 86: 12-21.

7. Dillon CF, Rasch EK, Gu Q, Hirsch R. 2006. Prevalence of Knee Osteoarthritis in the

United States: Arthritis data from the third National Health and Nutrition Examination Survey, 1991-1994. The Journal of Rheumatology; 33: 2271-2279.

8. Oddis CV. 1996. New Perspectives on Osteoarthritis. The American Journal of

Medicine; 100: 10S-15S. 9. Buckwater JA, Saltzman C, Brown T. 2004. The Impact of Osteoarthritis: Implications

for research. Clinical Orthopaedics and Related Research; (427 Suppl): S6-15. 10. Grotle M, Hagen KB, Natvig B, Dahl FA, Kvien TK. 2008. Obesity and Osteoarthritis

in Knee, Hip and/or Hand: An epidemiological study in the general population with 10 years follow-up. BMC Musculoskeletal Disorders; 9: 132.

11. Reijman M, Pols HA, Bergink AP, et al. 2007. Body mass index associated with onset

and progression of osteoarthritis of the knee, but not of the hip: The Rotterdam Study. Annals of the Rheumatic Diseases; 66: 158-162.

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Osteoarthritis 12. Segal NA, Yack HJ, Khole P. 2009. Weight, rather than obesity distribution, explains

peak external knee adduction moment during level gait. American Journal of Physical Medicine & Rehabilitation/Association of Academic Physiatrists; 88: 180-188; quiz 189-191, 246.

13. Wearing SC, Hennig EM, Byrne NM, Steele JR, Hills AP. 2006. Musculoskeletal

Disorders Associated with Obesity: A biomechanical perspective. Obesity Reviews: An Official Journal of the International Association for the Study of Obesity; 7: 239-250.

14. Haara MM, Heliovaara M, Kroger H, et al. 2004. Osteoarthritis in the carpometacarpal

joint of the thumb. Prevalence and associations with disability and mortality. The Journal of Bone and Joint Surgery. American. Vol. 86-A: 1452-1457.

15. Brandt KD, Radin EL, Dieppe PA, van de Putte L. 2006. Yet more evidence that

osteoarthritis is not a cartilage disease. Annals of the Rheumatic Diseases; 65: 1261-1264.

16. Toivanen AT, Heliovaara M, Impivaara O, et al. 2010. Obesity, physically demanding

work and traumatic knee injury are major risk factors for knee osteoarthritis - A population-based study with a follow-up of 22 years. Rheumatology (Oxford, England); 49: 308-314.

17. Maetzel A, Makela M, Hawker G, Bombardier C. 1997. Osteoarthritis of the hip and

knee and mechanical occupational exposure - A systematic overview of the evidence. The Journal of Rheumatology; 24: 1599-1607.

18. Dieppe P. 1994. Osteoarthritis: Clinical features and diagnostic problems. In J Klippel

& P Dieppe (eds). Rheumatology, Toronto, Ontario, Canada: Mosby; p 7.4.1 - 7.4.16. 19. Klug S, Weseion G. 2000. Clinical Picture of Osteoarthritis. In J Grifka & DJ Ogilvie-

Harris (eds). Osteoarthritis: Fundamentals and strategies for joint preserving treatment. New York: Springer; p. 9-22.

20. Gooberman-Hill R, Woolhead G, Mackichan F, et al. 2007. Assessing Chronic Joint

Pain: Lessons from a focus group study. Arthritis and Rheumatism; 57: 666-671. 21. Felson DT, Zhang Y, Hannan MT, et al. 1995. The incidence and natural history of knee

osteoarthritis in the elderly. The Framingham Osteoarthritis Study. Arthritis and Rheumatism; 38: 1500-1505.

22. Moskowitz RW. 2009. The Burden of Osteoarthritis: Clinical and quality-of-life issues.

The American Journal of Managed Care; 15: S223-9.

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Osteoarthritis 23. Creamer P, Lethbridge-Cejku M, Hochberg MC. 2000. Factors associated with

functional impairment in symptomatic knee osteoarthritis. Rheumatology (Oxford, England); 39: 490-496.

24. Altman RD. 2010. Early Management of Osteoarthritis. The American Journal of

Managed Care; 16 Suppl Management: S41-7. 25. Zhang W, Moskowitz RW, Nuki G, et al. 2008. OARSI recommendations for the

management of hip and knee osteoarthritis, Part II: OARSI Evidence-Based, Expert Consensus Guidelines. Osteoarthritis and Cartilage / OARS, Osteoarthritis Research Society; 16: 137-162.

26. Hannan MT, Felson DT, Pincus T. 2000. Analysis of the discordance between

radiographic changes and knee pain in osteoarthritis of the knee. The Journal of Rheumatology; 27: 1513-1517.

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LEG LENGTH INEQUALITY (Discrepancy) Leg length inequality (LLI), as the name implies, is a disorder characterized by different leg lengths. The discrepancy between legs can vary from less than a centimeter to over 20 cm. - which has been published. Leg length inequality can cause asymmetry of forces on the spine, hips and knees.1

Incidence and Prevalence Leg length inequalities are quite common in the population. Up to 93% of children have LLI.2 These discrepancies generally correct themselves during growth or by surgical options.1 In adults, prevalence of leg length inequality has been estimated as high as 40 to 70% of the general population. 2, 3 Most leg length discrepancies are 2 cm or less and thus are not considered clinically significant in an adult.1

Figure 1. Rear view of pelvic tilt and spinal curvature caused by severe leg-length discrepancy. Retrieved from www.cbppatient.com on Feb 18, 2011.

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Leg Length Inequality Only 1 out of every 1000 people has a leg length inequality of over 2 cm.4

Total hip replacement surgery, which is a common procedure, can cause LLI.4, 5 In fact, over 25% of patients undergoing this surgery have resulting leg-length discrepancy.4 Key Points:

Most leg-length discrepancies are 2 cm or less and are not considered clinically significant in an adult.

Only 1 out of every 1000 patients has been estimated to have a leg length

discrepancy of over 2 cm. Natural History Leg length inequalities typically result during childhood growth. Disruptions of the growth plate can result from trauma and/or from disorders affecting the growth plates. Most large discrepancies can be corrected or diminished before adulthood.1 The kinetic chain is composed of the lower limbs and spine. If there is a disruption in the chain, as with leg length inequality, joints and muscles are placed under abnormal stresses during stance and movement.6 Leg length inequalities have been implicated in a variety of disorders, including low back pain, scoliosis and hip and knee osteoarthritis.6, 7 Research has shown individuals who acquire leg length inequality at a younger age are able to better compensate for the discrepancies than those who acquire leg length inequalities later in life. More demanding adults, such as athletes, are more sensitive to leg length inequalities compared to less active individuals, due to the greater amount of force placed on their musculoskeletal systems.6 Key Points:

Leg length inequalities typically result during childhood growth. Leg length discrepancies have been implicated in a variety of disorders,

including low back pain. Implications As mentioned previously, most leg length inequalities are resolved or diminished during childhood growth.

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Leg Length Inequality Small leg length discrepancies are quite common in adults, but the effects are reduced by the compensatory abilities of the kinetic chain. Leg length inequalities under 2 cm are believed to have limited significance, as individuals tend to compensate with other joints and muscles.1 Studies have shown that walking patterns are essentially unchanged with small leg length inequalities.8 Therefore, no treatment is usually needed for discrepancies that are 2 cm or less.1 Athletes and active individuals may have increased sensitivity to small leg length inequalities and may require treatment.6 For leg length inequalities that cause symptoms, foot lifts are a simple and excellent treatment. Such lifts have been shown to restore normal function and effectively reduce symptoms, such as hip and low back pain.1, 6, 9 In leg length inequalities over 5 cm, foot lifts are poorly tolerated. If the length discrepancy is very severe, surgery may be necessary. Key Points:

Leg length inequalities under 2 cm are believed to have limited significance. Athletes and active individuals may have increased sensitivity to small leg

length inequalities. Foot lifts are a simple and excellent treatment.

Summary

Leg length inequalities can cause asymmetry and pain in the joints of the lower limbs and in the spine.

In the adult population, the prevalence of leg length inequalities have been estimated as high as 70%.

Most leg length inequalities are 2 cm or less and thus the body can readily compensate.

Most athletes and active individuals are typically more sensitive to leg length inequalities than inactive individuals.

Foot lifts are a simple and effective treatment for reducing pain and improving function.

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Leg Length Inequalities Profile - Patient #1 A sixty-five year old female patient underwent a total hip replacement for severe arthritis in her right hip. Post-operatively she did well, except for developing considerable low back discomfort. It was noted that her corrected extremity was now 3 cm longer than her non-operated side. A shoe lift balanced her hips and her spine, alleviating the discomfort. Profile - Patient #2 A fifty-eight year old male had previous surgery to his right knee, resulting in considerable osteoarthritis and marked varus deformity (bow-legged). The absolute leg length discrepancy was 3 cm. Following total knee replacement, the patient was given a straight leg and thus balanced the surgical knee, bringing the leg lengths back to a normal compensated position; i.e., both leg lengths were equalized. References 1. Moseley CF. 2006. Leg Length Discrepancy. In: Morressy RT, Weinstein SL, editors.

Lovell and Winter’s Pediatric Orthopaedics; 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins.

2. Subotnick SI. 1981. Limb Length Discrepancies of the Lower Extremity (the short leg

syndrome). The Journal of Orthopaedic and Sports Physical Therapy; 3: 11-16. 3. Woerman AL, Binder-MacLeod SA. 1984. Leg Length Discrepancy Assessment:

Accuracy and precision in five clinical methods of evaluation. The Journal of Orthopaedic and Sports Physical Therapy; 5: 230-239.

4. Gurney B, Mermier C, Robergs R, Gibson A, Rivero D. 2001. Effects of limb-length

discrepancy on gait economy and lower extremity muscle activity in older adults. The Journal of Bone and Joint Surgery. American Volume; 83-A: 907-915.

5. Canadian Institute for Health Information. 2009. Hip and Knee Replacements in Canada

- Canadian Joint Replacement Registry (CJRR) 2008-2009 Annual Report. 6. Gurney B. 2002. Leg Length Discrepancy. Gait & Posture; 15: 195-206.

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Leg Length Inequalities 7. Golightly YM, Allen KD, Renner JB, et al. 2007. Relationship of Limb Length

Inequality with Radiographic Knee and Hip Osteoarthritis. Osteoarthritis and Cartilage/OARS, Osteoarthritis Research Society; 15: 824-829.

8. Gofton JP, Trueman GE. 1971. Studies in Osteoarthritis of the Hip. II. Osteoarthritis of

the Hip and Leg Length Disparity. Canadian Medical Association Journal; 104: 791-799. 9. Golightly JP, Tate JJ, Burns CB, Gross MT. 2007. Changes in pain and disability

secondary to shoe lift intervention in subjects with limb length inequality and chronic low back pain: A preliminary report. The Journal of Orthopaedic and Sports Physical Therapy; 37: 380-388.

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INJURIES TO THE MENISCUS OF THE KNEE Introduction The knee menisci are two cartilage wedges that work in conjunction within the joint to perform vital function. Basically, the knee menisci work as shock absorbers, providing cushions between the thigh bone (femur) and the shin bone (tibia). Further, the menisci provide an element of stability within the knee joint 1, 2, as the knee moves front to back and side to side. Also, they provide an element of stability when the knee rotates or pivots.

Therefore, the knee menisci are under stress in all everyday activities. The meniscus can tear under several situations, most commonly when the knee is bent and then rotated.

Incidence and Prevalence There are two distinct types of injuries to the meniscus.

Type #1 - A Traumatic Tear This normally occurs in a younger population and is a result of excessive force placed on the meniscus. Maneuvers that place load on the meniscus, when the knee is bent and then rotated, lead to the most common mechanism of injury.5 Pivoting maneuvers in soccer, basketball, wrestling and skiing are most common.3

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Injuries to the Meniscus of the Knee

Type #2 - Degenerative Tears This type of tear is most prevalent in the older population and results from cumulative stress on the meniscus.3 Such degenerative tears are not uncommon in those individuals who have associated degenerative arthritis of the joint cartilage. Tears of the meniscus are more common in males than in females, with the ratio ranging from 2.5:1 to 4:1. The incidence of traumatic tears of the meniscus is about 60 to 70 cases per 100,000 people, peaking in men between 20-30 years of age. For both sexes, degenerative tears become more common after the age of 303. Degenerative tears are most prevalent amongst the elderly. One study found that 76% of people with an average age of 65 years, and without knee pain, had x-ray evidence of a tear of the meniscus.4

Key Points:

Meniscal tears may be traumatic or degenerative. Degenerative tears are more prevalent in older people. Most degenerative tears are accompanied by osteoarthritis on the adjacent

joint surfaces. 76% of patients, with an average age of 65 years, have evidence of a meniscal

tear radiographically. Natural History The natural history of meniscal tears is variable, depending on the location, size and type of tear. As previously mentioned, injuries of the meniscus can result from either a single traumatic event, which most commonly occurs in the younger population, or degeneration within the meniscus. Meniscus tears can be asymptomatic or they can be accompanied by varying degrees of pain, swelling and catching within the knee 5. Degenerative tears occur in the meniscus that lose their elasticity with age and as mentioned, are often accompanied with knee osteoarthritis 6, 7. These degenerative tears can occur from routine activities and may very well remain asymptomatic throughout life 3.

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Injuries to the Meniscus of the Knee Tears can vary in size, shape and orientation, resulting in a variety of symptoms and treatment strategies 8. Minor tears of the meniscus are usually left alone, whereas larger tears, which are usually post traumatic, are treated with surgical repair or a partial excision. Both of these techniques are done arthroscopically in a minimally invasive fashion. Key Point:

Small tears of the meniscus can be left alone, without treatment, and do not lead to progressive osteoarthritis.

Implications Both traumatic and degenerative meniscal tears can be asymptomatic or they can cause symptoms of pain, swelling and/or locking. The treatment of meniscal tears depends on several factors: the location, size, age, symptoms and quality of tissue 10. If the tear causes symptoms, there are minimally invasive surgical techniques to preserve as much of the meniscus as possible and relieve the symptoms 7, 11, 12, 13. Degenerative meniscal tears with associated osteoarthritis rarely require surgery. Key Point:

If the patient requires surgery, the goal is to preserve as much meniscus as possible, thus reducing the risk of developing post surgical osteoarthritis.

Summary

There are two types of meniscal tears: traumatic and degenerative.

Meniscal tears are often asymptomatic and may never require treatment.

Traumatic tears are more prevalent in young people, whereas degenerative tears are more common in people over 30 years of age.

Meniscal tears are more common in men.

Minor/small tears are stable and can be left untreated.

Treatment depends on size, shape, location, symptoms and quality of the tissue.

Surgical treatments usually result in returning to an active lifestyle, particularly if the

meniscal tear is post traumatic.

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Injuries to the Meniscus of the Knee Profile - Patient #1 Twenty-eight year old male twists his knee while stepping down from a ladder. The patient feels immediate pain on the inside of the knee and has difficulty extending the knee. This patient complains that the knee feels locked, and also complains of slight swelling. This is a typical story of a vertical traumatic tear of the meniscus, with a piece of the cartilage locked in the joint - a so-called Bucket Handle tear of the meniscus. This situation is rectified with arthroscopic surgery, which is designed to repair the meniscus tear or remove the unstable fragment. Patient #2 A fifty-eight year old male patient complains of pain on the inside of the knee. The pain is aggravated by jogging and deep squatting. The patient has mild bow-legness and the MRI reveals a medial meniscus tear with early osteoarthritis. This is a typical story of a degenerative medial meniscus tear, with associated early degenerative arthritis of the medial compartment. Initially this patient is treated with mild pain medication, physiotherapy and a knee brace. References 1. Messner K, Gao J. 1998. The Menisci of the Knee Joint. Anatomical and functional

characteristics, and a rationale for clinical treatment. Journal of Anatomy. 193 (Pt 2): 161-178.

2. Wojtys EM, Chan DB. 2005. Meniscus Structure and Function. Instructional course

lectures. 54: 323-330. 3. Brockmeier S, Rodeo S. 2009. Meniscal Injuries. In: DeLee J, Drez D, Miller M,

editors. DeLee and Drez’s Orthopaedic Sports Medicine; 3rd ed. Electronic: Saunders. 4. Bhattacharyya T, Gale D, Dewire P, et al. 2003. The clinical importance of meniscal

tears demonstrated by magnetic resonance imaging in osteoarthritis of the knee. The Journal of Bone and Joint Surgery. American Volume. 85A: 4-9.

5. Arendt L. 2009. Acute Knee Injuries. In: Brukner P, Khan K, editors. Clinical Sports

Medicine; 3rd ed. London: McGraw-Hill. 6. Brady OH, Hurson BJ. 2000. Acute Injuries of the Meniscus. In: Harries M, Williams

C, Stanish WD, Micheli LJ; editors. Oxford Textbook of Sports Medicine; 2nd ed. New York: Oxford University Press Inc., p 441.

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Injuries to the Meniscus of the Knee

7. Englund M, Guermazi A, Lohmander LS. 2009 The Meniscus in Knee Arthritis. Rheumatic Diseases, Clinics of North America; 35: 579-590.

8. Starke C, Kopf S, Petersen W, Becker R. 2009. Meniscal Repair. Arthroscopy: The

Journal of Arthroscopic & Related Surgery. Official Publication of the Arthroscopy Association of North America and the International Arthroscopy Association. 25: 1033-1044.

9. Arnoczky SP, Warren RF. 1982. Microvasculature of the Human Meniscus. The

American Journal of Sports Medicine. 10: 90-95. 10. Jarit GJ, Bosco JA. III. 2010. Meniscal Repair and Reconstruction. Bulletin of the NYU

Hospital for Joint Diseases. 68: 84-90. 11. Sgaglione NA, Steadman JR, Shaffer B, Miller MD, Fu FH. 2003. Current Concepts in

Meniscal Surgery: Resection to Replacement. Arthroscopy: The Journal of North America and the International Arthroscopy Association. 19 Suppl 1:161-188.

12. Fairbank TJ. 1948. Knee Joint Changes after Meniscectomy. The Journal of Bone and

Joint Surgery. British Volume. 30B: 664-670. 13. Salata MJ, Gibbs AE, Sekiya JK. 2010. A systematic review of clinical outcomes in

patients undergoing meniscectomy. The American Journal of Sports Medicine; 38: 1907-1916.

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PLANTAR FASCIITIS Plantar fasciitis is a common source of heel pain. It is generally caused by overuse, which can occur under many circumstances - including modified footwear, excessive walking, standing or walking on a different terrain. The plantar fascia is a bridge of tissue that extends from the heel to the front of the foot, on the underside. It is generally under significant resting tension in order to provide shock absorption and maintain proper arches in the foot. Excessive stress on the plantar fascia can lead to inflammation and pain on the underside of the heel.

Incidence and Prevalence It has been noted that as many as 1 in 10 people will develop plantar fascia in their lifetime 1. It can occur at any age, but is more prevalent among those 40-60 years of age. Common risk factors for plantar fasciitis include increased body weight and abrupt change in challenges to the plantar fascia with standing or walking. Certain foot types are commonly observed with individuals suffering with plantar fasciitis. Most typically the patient has a high-arched foot, pes cavus deformity or a mobile flat foot pes planus.

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Plantar Fasciitis

Key Points Common risk factors include:

Increased body weight. Abrupt excessive challenge and/or change in terrain. Pes cavus and pes planus are commonly seen in patients who suffer with

plantar fasciitis. Natural History Plantar fasciitis is generally a self-limiting disease, whereby 80% of cases can be expected to resolve on their own within a year. Non-surgical treatments, such as physiotherapy, the use of orthotics and the intermittent use of anti-inflammatory medications lead to resolution in 90% of cases. Usually time alone will resolve the problem. Surgical intervention is rarely necessary. Key Point:

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80% of cases can be expected to resolve on their own within a year. Implications Plantar fasciitis is a bothersome disorder that can be resolved, in most cases, with non-surgical treatment. Generally the challenge in resolving plantar fasciitis lies in the willingness of the patient to allow the tissue to heal, understanding that the natural history of the problem is that it is usually self-limiting. Healing involves resting the affected area and limiting the challenges that have provoked the problem initially. To reiterate, the problem is usually self-resolving and very rarely requires surgical intervention.

Plantar Fasciitis

Key Points

Most cases resolve with a conservative program. Summary

Plantar fasciitis is a very common source of foot pain. It is usually caused by overuse of the foot with a rapid change in challenges such as

standing, walking or running. Symptoms can usually be resolved with conservative treatment alone.

Profile - Patient #1 A thirty-eight year old nurse, who is overweight, develops heel pain when she prompts herself to adopt a weight reduction program. This weight reduction program includes walking 10 km a day. Further, she was using a new pair of rather rigid walking shoes.

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She experienced pain on the front part of her heel. The remainder of her physical examination and x-ray review was normal. This is a typical story of a person who develops acute plantar fasciitis, which is a reflection of an exercise program that was too strenuous for the deconditioned plantar fascia. The patient was placed on a program of physiotherapy, with a heel sponge, coupled with weight reduction and the problem resolved after six months. Profile - Patient #2 A twenty-four year old male developed heel pain when ramping up his exercise program. Physical examination revealed a very high-arched foot with distinct tenderness over the heel. The problem resolved with a custom-made orthotic, combined with physiotherapy and an anti-inflammatory medication. This is a typical story of a person who has an underlying anatomical problem related to their longitudinal arch of the foot, and makes them quite prone to developing plantar fasciitis and/or Achilles tendinitis.

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Plantar Fasciitis References 1. Riddle DL , Schappert SM. Volume of ambulatory care visits and patterns of care for

patients diagnosed with plantar fasciitis: A national study of medical doctors. Foot and

Ankle Int. 2004; 25(5): 303-310. 2. Buchbinder R. Clinical Practice: Plantar Fasciitis. N Engl J Med 2004. 20;350(21):

2159-2166. 3. Davis PF, Severud E, Baxter DE. Painful Heel Syndrome: Results of non-operative

treatment. Foot and Ankle Int. 1994; 15(10): 531-535.

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HALLUX RIGIDUS Hallux rigidus, which means “stiff big toe,” is an arthritic condition that affects the first joint of the big toe. This joint is called the metatarsophalangeal joint. Essentially the condition is osteoarthritis of the joint which results from deterioration of the joint cartilage. Secondarily, bone spurs around the joint then form. The degeneration of the joint can range from mild to severe and likewise the symptoms associated with hallux rigidus can range from mild to disabling. On examination, the joint becomes enlarged (secondary to bone spur formation). There is usually associated inflammation and joint stiffness. Upon movement by the practitioner, there is reduced range of motion and pain, if the toe is moved aggressively. Hallux rigidus is seen in two distinct populations. Persons may present in adolescence and invariably have a family history of this condition. The second population is those who present in adulthood.1, 2

Figure #1: x-ray showing osteoarthritis of the joint - hallux rigidus

27

Hallux Rigidus

Key Points

Hallux rigidus is an arthritic condition of the first metatarsophalangeal joint. Stiffness of the joint is the paramount finding. The degree of degeneration and restricted range of motion may be mild,

moderate or severe. Hallux rigidus may appear in adolescence and in the more aged population.

Incidence and Prevalence Hallux rigidus is the most common arthritic condition affecting the feet and the second most common condition of the big toe, second only to Hallux valgus (bunions).2, 3 There is contradicting information regarding the gender distribution of hallux rigidus, with multiple studies suggesting an increased prevalence existing with females 4, 6 while others cite a greater prevalence amongst males 7, 8. As with most arthritic conditions, the prevalence of hallux rigidus appears to increase with age. It has been estimated that 10% of people aged 20-34 have evidence on x-ray of the condition. Upwards of 44% of people over the age of 80 years of age have radiographic features of hallux rigidus. It has been reported that for younger people the incidence of hallux rigidus increases with a history of hyperextension injuries or by repeated stubbing of the big toe.9, 10 In a recent major literature review, it was estimated that between 6.3 and 39% of the population have hallux rigidus; however, the majority of the studies were making this diagnosis by x-ray alone.11 It has been previously estimated that between 2 and 3% of the population have symptomatic hallux rigidus.12 In upwards of 80% of cases of hallux rigidus, the problem is in both feet.13 Key Points

44% of patients over the age of 80 years have x-ray evidence of hallux rigidus.

It remains unclear as to whether trauma can produce hallux rigidus, particularly when there has been no evidence of fracture.

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In upwards of 80% of cases, the problem is bilateral; i.e., involves both feet.

Hallux Rigidus Natural History Hallux rigidus is a chronic, degenerative disorder. It can develop due to a traumatic injury to the joint (specifically when there has been evidence of a fracture of the joint) or as a result of progressive degeneration of the joint cartilage. Unfortunately, due to the nature of articular cartilage (poor innervation, poor vascular supply), once degradation begins, the process continues as cartilage has no ability to heal.14 Damage and degeneration of the cartilage weakens its structure, resulting in the inefficient transmission of force within the joint. With the loss of cartilage, the space within the joint becomes narrower and the surface of the bone can become exposed, devoid of cartilage. Secondarily, bone spurs commence to form and the joint becomes more rigid.2, 14 Pain is usually noticed most with extremes of movement of the joint. By the time the threshold of pain has been reached and the patient begins to present with symptoms of hallux rigidus, there is usually significant degeneration and wear of the joint surface, but such is not always the case. 2, 14

The degree of wear of the joint does not always coincide with the degree of degeneration. The pain produced by movement of the joint is typically made worse with loading of the joint (weight bearing activities). This may lead to the patient walking with a limp in an effort to reduce the pain. The natural progression usually results in complete fusion of the joint, but the pain can be reduced through bracing and/or surgery.2, 14 Key Points

Hallux rigidus is a chronic degenerative disorder. It may be painful with activity. The degree of pain does not always coincide with degree of degeneration.

Implications The natural course of this disorder is loss of the articular cartilage of the joint, joint space narrowing, and bone spur formation on the first metatarsophalangeal joint. This may cause pain with activities sufficient to impair quality of life and activities of daily living. During the early stages, the symptoms can be adequately controlled by activity modification. For example, refraining from high heeled shoes and avoiding high impact activities such as running on ones toes. Additionally, patients in the early phase may benefit from the use of stiff soled shoes.2

29

Hallux Rigidus

Hallux rigidus has been shown to be manageable through non-surgical procedures. A study by Smith et al (2000) found that although there was radiographic evidence of further degeneration of joint space, 90% of patients surveyed stated that their pain had not changed 15 years after their diagnosis.15 The indication for surgical intervention with hallux rigidus is an unacceptable level of pain with associated disturbance of daily activities. Surgical options include debridement of the spurs of the joint. More aggressive surgery options include arthrodesis (fusion of the joint) or synthetic joint replacements. The results from such surgical interventions are highly successful and are tailored for the individual patient. Summary

Hallux rigidus is a common arthritic condition affecting the first metatarsophalangeal joint of the big toe.

Hallux rigidus is a chronic, degenerative condition that results in pain and reduction of

mobility of the big toe.

It has been estimated that 2 to 3% of the population are afflicted with hallux rigidus.

Hallux rigidus is effectively managed through conservative measures; in severe cases, surgical interventions have been shown to improve symptoms and restore motion.

Figure #2: Hallux Rigidus at Surgery- Complete loss of cartilage

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Hallux Rigidus Patient Profile #1 A twenty year old male presents with pain and limitation of motion of the great toe. Physical examination reveals enlargement of the toe and reduced range of motion. The patient claims discomfort when the great toe is forcibly moved. X-rays reveal degeneration of the first metatarsophalangeal joint, compatible with osteoarthritis; i.e., hallux rigidus. The patient is markedly improved with the use of a rigid walking shoe. Patient Profile #2 A sixty year old female presents with pain and limitation of motion of the first metatarsophalangeal joint. It is first noticed when she walks in a shoe with an elevated heel. X-rays reveal evidence of early osteoarthritis of the first metatarsophalangeal joint; i.e., hallux rigidus. Attempts at modification of her footwear do not improve her circumstance, but she does become asymptomatic after a minor surgical debridement of the joint.

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Hallux Rigidus References 1. Gould J. (1993). Painful Feet. In D. McCarty & W. Koopman (Eds), Arthritis and Allied

Conditions; 12th edition (pp 1553-1561). London: Lea & Febiger 2. Michelson J. (2007) Lower Extremity Considerations: Foot and Ankle. In RW

Moskowitz, RD Altman, MC Hochberg, JA Buckwater & VM Goldberg (Eds), Osteoarthritis: Diagnosis and medical/surgical management; 4th edition (pp 415-425). Philadelphia: Lippincot Williams & Wilkins.

3. Gilheany MF, Landorf KB, & Robinson P. (2008) Hallux valgus and hallux rigidus: a

comparison of impact on health-related quality of life in patients presenting to foot surgeons in Australia. Journal of Foot and Ankle, 1:14-19

4. Bremner JM, Lawrence JS, Miall WE. (1968) Degenerative Joint Disease in a Jamaican

Rural Population. Ann Rheum Dis., 27(4): 326-332 5. Solomon L, Beighton P, Lawrence JS. (1976) Osteoarthritis in a Rural South African

Negro Population. Ann Rheum Dis., 35(3): 274-278

6. Van Saase JL, van Romunde LK, Cats A, Vandenbroucke JP, Valkenburg HA. (1989) Epidemiology of Osteoarthritis: Zoetermeer Survey. Comparison of radiological osteoarthritis in a Dutch population with that in 10 other populations. Ann Rheum Dis.

48(4) 271-280. 7. Brighton SW, de la Harpe AL, van Staden DA. (1985) The prevalence of osteoarthritis in

a rural African Community. Br J Rheumatol, 24(4): 321-325 …/6

8. Wilder FV, Barrett JP, Farina EJ. (2005) The association of radiographic foot osteoarthritis radiographic osteoarthritis at other sites. Osteoarthritis Cartilage, 13(3): 211-215

9. Gilmore MFX. (1987) The overuse syndromes. In S Hughes, M Benson, C Colton (Eds),

Orthopaedics: The principles and practice of musculoskeletal surgery and fractures (pp 232-243). New York: Churchill Livingstone.

10. Bentley G. (1987) Surgical management of osteoarthritis. In S. Hughes, M Benson, C

Colton (Eds), Orthopaedics: The principles and practice of musculoskeletal surgery and fractures (pp 120-151). New York: Churchill Livingstone.

11. Triveldi B, Marshall M, Belcher J, Roddy E. (2010) A systematic review of radiographic

definitions of foot osteoarthritis in population based studies. Osteoarthritis & Cartilage, 18: 1027-1035.

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Hallux Rigidus 12. Gould N, Schnider W, Ashikaga T. (1980) Epidemiological survey of foot problems in

the continental United States, 1978-1979. Foot and Ankle, 1: 9-10. 13. Coughlin MJ, Shurnas PS. (2003) Hallux rigidus: demographics, etiology, and

radiographic assessment. Foot and Ankle Int, 24(10): 731-743. 14. Poole AR, Guilak F, Abramson SB. (2007) Etiopathogenesis of osteoarthritis. In RW

Moskowitz, RD Altman, MC Hochberg, JA Buckwater & VM Goldberg (Eds), Osteoarthritis: Diagnosis and medical/surgical management, 4th edition (27-49). Philadelphia: Lippincott Williams & Wilkins.

15. Smith RW, Katchis SD, Ayson LC (2000) Outcomes in hallux rigidus patients treated

nonoperatively: A long-term follow-up study. Foot and Ankle Int, 21(11): 906-913.

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DEGENERATIVE DISC DISEASE There is no standard definition for degenerative disc disease (DDD). It has been suggested that DDD be defined as “an aberrant, cell-mediated response to progressive structural failure”.1 Although an exact definition is unclear, the term degenerative disc disease is widely used to describe changes in spine anatomy that are part of the normal aging process. The vertebrae form a motion segment connected by intervertebral discs, joints, ligaments and muscles

The discs act like spacers and flexible connectors. The muscles produce movement and the ligaments prevent excessive movement. The intervertebral discs change with age. We do not know what starts the process or exactly what influences its progression. In the earliest stage of degeneration, small tears appear in the outer part of the disc and the inner part of the disc begins to dry out. These changes start fairly early in life.

Figure 1 – The different sections of the spine (available from: http://boneandspine.com/spine/thoracic-lumbar-spine/lumbar-spinemorphologic-functional-anatomy/

34

Degenerative Disc Disease

The disc starts to lose some of its shock absorbing ability. This process lets the vertebrae slide, resulting in segmental instability and putting more pressure on the joints. Over time, arthritis will occur in those joints, thus eventually stiffening the spine and rendering it less mobile.

Figure 3 – Degenerative changes in the spine (available at: http://www.oispine.com/subject.php?pn=lumbar-degenerative-disc-002)

Figure 2 – The motion segment includes two vertebrae, the disc and joints between them, and the ligaments and muscles that connect them (available at: msd.com.mx)

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Degenerative Disc Disease The process is similar to degenerative arthritis in other joints, such as the hip and knee. Tears in the outer part of the disc usually result from wear and tear over a period of time - the accumulation of many small injuries. Most injuries result from compressing the disc with a combination of a twisting motion, especially while bending forward. Tears can also weaken the outer ring and thus allow the inner nucleus pulposus of the disc to bulge outward through the weakened ring and sometimes herniate completely. The large bulges can cause pain that is felt in the buttock and leg. Herniations can sometimes press on the nerve roots exiting from the spine, causing weakness and numbness.

Key Points

There is no standard definition for degenerative disc disease. The intervertebral discs change with age. With aging of the disc, the joints of the spine become overloaded and can

develop a secondary osteoarthritis. The casing of the disc may tear, resulting in a protrusion of the central nucleus

pulposus.

Incidence and Prevalence Degenerative changes occur in the disc by late adolescence, increase linearly with age and occur in nearly 100% of people by old age. Degenerative changes are extremely common in the neck, as well as the lower back, and so increase with aging.

Figure 4 – Tears in the outer part of the disc can let the inner nucleus pulposus bulge outward against, or even through, the outer rings. Theses bulges can press on nerve roots, but also can cause pain just by stretching the annulus fibrosus.

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Degenerative Disc Disease Over 60% of people have degenerative changes in their cervical spine by age forty, and even 25% of those younger than age forty also show degenerative changes. In the lumbar spine the numbers are even higher, whereby tears in the discs start when people are in their twenties. By age seventy, 75% to 98% of people have degenerative disc disease. Low back pain affects 20% of the population on any given day, and upwards of 80% of people experience low back pain. Low back pain is the most common musculoskeletal complaint and the second most common complaint of pain to headache, which ranks number 1. Many people with degenerative disc disease do not experience pain. We cannot predict who will have back pain based on the presence of degenerative changes of the disc that are visible on x-rays and/or MRI.

Figure 5 – X – rays do not show the intervertebral discs, but changes can be inferred from the altered spatial relationships between adjacent vertebral bodies. (available at: http://bookmasters.com/markplc/rr00941.htm

Figure 6 – Degenerative changes of the lumbar spine, including disc bulging at the L-3/4, L-4/5 and L-5/S-1 discs. Degeneration of the nucleus pulposus results in the discs appearing darker than those above, with no central lighter area. These changes are common, and are not accompanied by low back pain in most people.13

Available at: http://emedicine.medscape.com/article/95294-overview

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Degenerative Disc Disease

Key Point

Degenerative disc disease is common and does not necessarily cause back or neck pain. 20% of the population suffers with low back pain on any given day, and upwards of 80% of people experience low back pain during their lifetime.

Risk Factors for Low Back Pain Since degenerative disc disease alone does not cause pain, it is unclear why some people develop low back pain and others do not. Age, smoking and genetic factors (as yet unknown) seem to be the strongest risk factors for developing low back pain.2 Getting older increases the chances of developing low back pain, as well as degenerative disc disease. Heavy lifting, vibration, driving, prolonged postures - all of these have been described as risk factors for low back pain, but the evidence linking these factors to causing degenerative disc problems is tenuous. In fact, both increased and decreased loading can contribute to DDD.20 Risk factors, then, may increase the symptoms of low back pain, but do not appear to cause an increase in degenerative changes in the spine. Low back pain probably comes from a combination of changes in the spine, genetic factors, and loading patterns.1, 2 Implications and Natural History Degenerative disc disease is not really a disease at all, but a normal part of the aging process. Changes begin in adolescence or early adulthood in men, about a decade later in women, then progress linearly until old age. There is an interesting phenomenon in as much as low back pain becomes less frequent and less severe with age. 90% of the people who experience low back pain for the first time, get better in two to six weeks. Only about 5% of people with low back pain develop chronic low back problems; e.g., pain lasting longer than six months. Since degenerative disc disease is a normal aging process, no treatment is required if there is no pain present or it is mild. Treatments should be divided into non-surgical and surgical options, although the latter is required for only a few people. Non-surgical treatments can involve medications, exercise, weight loss, physiotherapy and low back education.

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Degenerative Disc Disease Certainly, all treatment for low back pain should include education about the process and the lack of association between degenerative disc disease and the low back pain. Healthcare professionals should encourage the patient to stay as active as possible because rest does not change the overall course of recovery for low back pain. Key Points

Treatment for back and neck pain should always include education that degeneration is normal and does not necessarily cause pain.

Advised to exercise and stay as active as possible. Reassurance is necessary that pain is not equal to harm.

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Reassurance that most people get better in a few weeks. Addendum Types of Back Pain Annular Tears & Internal Disc Disruption This type of problem is usually caused primarily by multiple small tears in the annulus, prompting mechanical back pain and secondary inflammation. The treatment is postural retraining, exercises and anti-inflammatory medications. Disc Protrusions and Herniations Even normal discs can be injured. Heavy repetitive bending, twisting or lifting can place too much pressure on the disc, tearing some fibers and making it weaker.5, 15, 20 A large disc herniation, that is resistant to non-surgical measures, may require surgical treatment. Facet Joint Arthritis With degeneration of the disc, the facet joints become arthritic. In such patients, manipulation or joint mobilizations 9 can be helpful, coupled with reduction in body weight.

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Degenerative Disc Disease Summary

Degenerative disc disease is a natural part of the aging process and affects everyone eventually.

Treatment for low back pain can be quite successful if it is tailored to the patient’s condition.

Surgery is seldom necessary, except in cases of large disc herniations.

Patient Profile #1 Twenty year old male complains of acute low back pain while lifting. He presents with significant paravertebral spasm, but no evidence of any sciatic nerve root irritation; however, there is limitation of motion about the lumbar spine. This gentleman presents with a classic story of a small tear of the annulus surrounding the central part of the disc. The inflammatory process has triggered paravertebral spasm, but without any evidence of nerve root pressure. This patient is treated non-surgically with anti-inflammatory medication, reduction in activities and physiotherapy program using passive modalities. He is back to work in three weeks. Patient Profile #2 A sixty-two year old female presents with recurrent episodes of low back pain. On physical examination the patient is overweight, with a pendulous abdomen and x-ray evidence of degenerative disc disease at L4-L5. There is no evidence of any neurological deficit. This patient suffers with mechanical back pain as a consequence of degenerative disc disease and facet joint osteoarthritis. This situation is treated without surgery but with enhanced fitness, weight reduction, postural retraining and education regarding low back care.

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Degenerative Disc Disease References 1. Adams MA, Roughley PJ. What is intervertebral disc degeneration, and what causes it?

Spine, 2006; 31(18): 2151-2161 2. Battie MC, Videman T, Parent E. Lumbar disc degeneration. Epidemiology and genetic

influences. Spine, 2004; 29(23): 2679-2690 3. Binder AI. Cervical spondylosis and neck pain. BNJ; 2007; 334: 527-531 4. Boden SD, et al. Abnormal magnetic-resonance scans of the crevical spine in

asymptomatic subjects. A prospective investigation. JBJS, 1990; 72-A(8): 1178-1184 5. Bogduk N. Clinical anatomy of the lumbar spine and sacrum, Third Edition. Churchill

Livingstone, 1997 6. Burton K et al. The Back Book: the Best Way to Deal with Back Pain; Get Back Active.

TSO (The Stationary Office) publishers, 2002, available at: http://www.tsoshop.co.uk/bookstore.asp 7. Friedendberg ZB, Miller WT. Degenerative disc disease of the cervical spine: a

comparative study of asymptomatic and symptomatic patients. JBJS, 1963; 45-A(6): 1171-1178

8. Gross DP, et al. A population-based survey of back pain beliefs in Canada. Spine, 2006;

31(18): 2142-2145 9. Hebert J, Koppenhaver S, Fritz J, Parent E. Clinical prediction for success of

interventions for managing low back pain. Clin Sports Med, 2008; 27(3): 463-479 10. Hicks GE, Morone N, Weiner DK. Degenerative disc and facet disease in oder adults:

prevalence and clinical correlates, Spine; 34(12): 1301-1316 11. Long A, Donelson R, Fung T. Does it matter which exercise? A randomized controlled

trial of exercise for low back pain. Spine 2004; 29:2593-602 12. Maetzel A, Li L. The economic burden of low back pain: a review of studies published

between 1996 and 2001. Best Practice & Research Clinical Rheumatology, 2002; 16(1), 23-30

13. Malanga GA, Eisenberg ME. Degenerative lumbar disc disease in the mature athlete.

Downloaded Jan. 20, 2011 from: http://emedicine.medscape.com/article/95294-overview. 14. Martin MD, Boxell CM, Malone DG. Pathophysiology of lumbar disc degeneration: a

review of the literature. Neurosurg Focus, 2002; 13(2): 1-6

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Degenerative Disc Disease 15. McGill S. Low back disorders: evidence-based prevention and rehabilitation, 2nd edition.

Human Kinetics, 2007 16. McKenzie R, May S. The lumbar spine. Mechanical Diagnosis and Therapy, Spinal

Publications, 2003 17. Okada E, et al. Aging of the cervical spine in healthy volunteers. Spine, 2009; 34(7):

706-712 18. Perez C. Chronic back problems among workers. Health Reports, 2000; 12(1): 41-55,

Statistics Canada, Catalogue 82-003 19. Richardson CA, Jull G, Hodges PW, et al. Therapeutic exercise for spinal segmental

stabilization in low back pain. London: Churchill Livingstone, 1999 20. Stokes IA, Iatridis JC. Mechanical conditions that accelerate intervertebral disc

degeneration: overload vs immobilization. Spine, 2004; 29(23): 2724-2732 21. Wilkins K. Incident arthritis in relation to excess weight. Health Reports, 2004; 15(1):

39-49. Statistics Canada, Catalogue 82-003

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DISORDERS OF THE ROTATOR CUFF The shoulder is the most mobile and unstable joint in the body. The four rotator cuff muscle/tendon units aid in shoulder movements and also stabilize the joint. Due to the large complex movements of the shoulder joint, injuries of the rotator cuff are quite common.1

Incidence and Prevalence The prevalence of rotator cuff injuries has been well documented. It is reported that more than 50% of individuals older than 60 years of age have at least a partial thickness rotator cuff tear.2 Rotator cuff tears typically develop from natural degeneration of tendons and as a result, prevalence does increase with age.3-6 The incidence of rotator cuff tears rises sharply after the age of 50.7 Athletes and labourers, especially those that use overhead arm motion, have higher incidence of rotator cuff disruptions.1 Tears of the rotator cuff in younger individuals generally result from traumatic shoulder injuries, but are quite uncommon. Sher et al reported only 4% of individuals 19-39 years of age had a tear of the rotator cuff.5

Fig1. Front and back views of the four muscles that compose the rotator cuff. Retrieved on January 24, 2010 from http://www.physicaltherapystretchingexercises.com/wp-content/uploads/2010/05/b3.jpg

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Disorders of the Rotator Cuff It is important to note that many rotator cuff tears are asymptomatic, even when the tears are full thickness.5, 8 One study has shown that 26% of people, with an average age of 44 years, had radiographic evidence of at least partial rotator cuff tear despite having no symptoms.8 Another study reports 7.6% of individuals, between the ages of 50-79 years, had full-thickness tears which were asymptomatic. Key Points:

50% of people over the age of 60 years have rotator cuff pathology. Full tears of the cuff may be asymptomatic.

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Overhead workers are at increased risk. Natural History Degeneration is the most common cause of rotator cuff tears. In degenerative rotator cuff disruptions, the tendons weaken with age and even routine activities can cause injury in the elderly. Other factors can accelerate the degenerative process, such as impingement of the tendons between the bones of the shoulder joint or from repetitive overhead shoulder movements in the athletes or labourers. Traumatic rotator cuff tears are far less common and typically result from an acute shoulder injury, such as shoulder dislocations or acromioclavicular joint separations.1

Fig 2. Computer-generated image of a rotator cuff tear in the right shoulder. Retrieved on January 24, 2011 from http://www.sportsmd.com/SportsMD_Articles/id/262/n/torn_rotator_cuff.aspx

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Disorders of the Rotator Cuff Disease progression has not been well studied. One study found that 50% of asymptomatic tears had developed into symptomatic tears over 5 years. They also found that 36% of the tears increased in size.9 Another study demonstrated that pain development in asymptomatic tears is associated with an increase in the size of the tear.10 Another important finding is that very few rotator cuff tears actually heal or decrease in size over time.9, 11, 12 The aforementioned studies on progression provide some evidence that untreated rotator cuff tears have a good chance of progressing in symptoms and size. Larger tears are associated with decreased strength 4 and increased pain.4, 6 Chronic tears can progress and become very large in size, being referred to as “massive” rotator cuff disruptions. In such a case, the humeral head migrates up, causes further impingement and leading to joint arthritis.13 Key Points:

Degeneration is the most common cause of cuff tears. Acute trauma is far less common in triggering rotator cuff tears. Untreated tears may progress in size and symptoms.

Implications It is important to note that up to 75% of rotator cuff tears are asymptomatic and the presence of tearing should not be the sole guide to treatment.1, 14 Many individuals with full thickness tears can have normal functioning with no pain.6 In most cases, symptomatic rotator cuff tears should be treated conservatively.15 Physiotherapy, flexibility and strengthening exercises have been found to improve shoulder function, allowing individuals to perform daily activities.14, 15 Conservative treatment has proven especially effective in the elderly where there is a reduced need for a strong shoulder.16 It is important to note that conservative treatment does not heal the tear. The goal is to improve the function of the healthy tissue around the tear.15 When conservative treatment is ineffective, surgical options can be considered.1 Surgical decisions are based on level of symptoms, level of physical activity, size of tear, quality of tissue, and response to conservative treatment.15 For example, surgery is generally recommended for younger individuals with a traumatic tear, because they will likely have healthy tissue, a good chance of healing, and typically require higher shoulder function than older patients.1, 16

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Disorders of the Rotator Cuff Summary

Degenerative rotator cuff tears are very common in the elderly; more than 50% of 60 year olds.

The incidence of rotator cuff tears increases with age, rising sharply after 50 years.

Many tears are asymptomatic - 26% of 44 year olds have tears with no symptoms.

Individuals with full-thickness tears can still have full function of the shoulder.

Conservative treatment is highly effective, especially in the elderly.

Surgical options exist when conservative treatment is ineffective.

Profile - Patient #1 A thirty-eight year old truck driver slips on the threshold of his truck, grabs on to the rearview mirror and has a severe pain in his shoulder. Upon presentation, he is unable to move the shoulder away from his side beyond 25 degrees. The MRI of the shoulder reveals a complete tear of the rotator cuff. Within three weeks of injury, the patient undergoes surgery to repair the rotator cuff disruption. Six months after the repair he is back to full and unrestricted duties. This is a typical story of an acute rotator cuff tear in a relatively young person, that responds best to a surgical program. Profile - Patient #2 A seventy-three year old gentleman suffers with pain about his right shoulder, when he fell in his garden on his outstretched arm. He had a history of intermittent shoulder pain, dating back for fifteen years. On examination, his range of motion is 90 degrees of forward elevation. An MRI of the shoulder reveals a tear of the rotator cuff, with retraction and evidence chronic impingement. This patient responded well to a physiotherapy and exercise program, designed to strengthen his complimentary muscles.

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Disorders of the Rotator Cuff Five months after the injury the patient is functioning fine, with a range of motion of 140 degrees and he has returned to all his daily activities, including gardening and golf. This is a typical story of a chronic rotator cuff problem, with an acute injury in a more geriatric patient. Most patients in this age group respond best to a conservative, non-surgical program. References 1. Lin KC, Krishnan SG, Burkhead WZ. 2009. Impingement Lesions in Adult and

Adolescent Athletes. In: DeLee J, Drez D, Miller M, editors. DeLee and Drez’s Orthopaedic Sports Medicine; 3rd Ed., Saunders.

2. Wolf BR, Warme BA, Kibler WB, Sciascia A, Kuhn JE. 2009. Non Acute Shoulder

Injuries. Knowledge Update: Sports Medicine, American Academy of Orthopaedic Surgeons; p 19-39.

3. Milgrom C, Schaffler M, Gilbert S, vanHolsbeeck M. 1995. Rotator cuff changes in

asymptomatic adults. The effect of age, hand dominance and gender. The Journal of Bone and Joint Surgery; British Volume; 77: 296-298.

4. Moosmayer S, Smit HJ, Tariq R, Larmo A. 2009. Prevalence and characteristics of

asymptomatic tears of the rotator cuff: An ultrasonographic and clinical study. The Journal of Bone and Joint Surgery. British Volume; 91: 196-200.

5. Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin MB. 1995. Abnormal findings on

magnetic resonance images of asymptomatic shoulders. The Journal of Bone and Joint Surgery; American Volume; 77: 10-15.

6. Yamaguchi K, Ditsios K, Middleton WD, et al. 2006. The demographic and

morphological features of rotator cuff disease. A comparison of asymptomatic and symptomatic shoulders. The Journal of Bone and Joint Surgery. American Volume; 88: 1699-1704.

7. Christian C. 1998. Shoulder and Elbow Injuries. Campbell’s Operative Orthopaedics,

9th Ed. Toronto, Ontario, Canada: Mosby 8. Reilly P, MacLeod I, MacFarlane R, Windley J, Emery RJ. 2006. Dead Men and

Radiologists Don’t Lie: A review of cadaveric and radiological studies of rotator cuff tear prevalence. Annals of the Royal College of Surgeons of England; 88: 116-121.

9. Yamaguchii K, Tetro AM, Blam O, et al. 2001. Natural history of asymptomatic rotator

cuff tears: A longitudinal analysis of asymptomatic tears detected sonographically. Journal of Shoulder and Elbow Surgery / American Shoulder and Elbow Surgeons...[et al] 10: 199-203.

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Disorders of the Rotator Cuff 10. Mall NA, Kim HM, Keener JD, et al. 2010. Symptomatic progression of asymptomatic

rotator cuff tears: A prospective study of clinical and sonographic variables. The Journal of Bone and Joint Surgery. American Volume; 92: 2623-2633.

11. Yamanaka K, Matsumoto T. 1994. The joint side tear of the rotator cuff. A follow-up

study by arthrography. Clinical Orthopaedics and Related Research. (304): 68-73. 12. Maman E, Harris C, White L, et al. 2009. Outcome of non-operative treatment of

symptomatic rotator cuff tears monitored by magnetic resonance imaging. The Journal of Bone and Joint Surgery. American Volume; 91: 1898-1906.

13. Goldstein J, Zuckerman JD. 2000. Selected orthopaedic problems in the elderly.

Rheumatic Diseases Clinics of North America; 26: 593-616. 14. Mantone JK, Burkhead WZ, Jr., Noonan J, Jr. 2000. Non-operative treatment of rotator

cuff tears. The Orthopaedic Clinics of North America; 31: 295-311. 15. Smith MA, Smith WT. 2010. Rotator cuff tears: An overview. Orthopaedic Nursing /

National Association of Orthopaedic Nurses; 29: 319-322; quiz 323-324. 16. Williams GR, Jr., Rockwood CA, Jr., Bigliani LU, Iannotti JP, Stanwood W. 2004.

Rotator Cuff Tears: Why do we repair them? The Journal of Bone and Joint Surgery. American Volume; 86-A: 2764-2776.

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PAIN Introduction on Pain The official definition of pain, as described by the International Association for the Study of Pain is “an unpleasant sensory and emotional experience associated with actual or potential tissue damage”.1 Pain is highly variable, having symptoms depend on the degree, type, duration, and location of the stimulus. Interpretation of pain depends on the person’s subjective experience and consequently, there are no objective measures of pain.1, 2 It is important to note that pain is an important protective biological function that acts as a warning signal of tissue damage or potential damage.2

In order to properly understand the concept of pain, one must understand the physiological components of the nervous system associated with pain. A painful stimulus (mechanical, thermal, or chemical) acts on specialized pain receptors called nociceptors. Nociceptors then transmit the signal to the central nervous system, where the pain signal is interpreted.2 For example (Fig. 1), when someone steps on a sharp object, the nociceptors in the damaged skin transmit signals to the central nervous system, causing a reflex which lifts the foot off the sharp object. Finally, the brain interprets the type and degree of pain. This is an example of acute pain, which is a relatively simplistic model and the pain generally subsides. However, chronic pain is typically more complicated and often involves other confounding variables which may include psychological distress, obesity, social support and smoking.

Source of Pain Fig 1. Diagram of simple pain reflex. Pain signal

is sent to central nervous system (Spinal Cord and brain) where pain is interpreted and reflex signal is sent to leg muscles

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Pain Key Points:

Interpretation of pain depends on the person’s subjective experience. There are no objective measures of pain.

Chronic Pain Syndrome Chronic pain is defined as pain lasting longer than 3 months. It develops from an acute injury, degenerative tissue, or a systemic illness and is most commonly located in the back, head, and joints.2, 3 Chronic pain causes substantial direct and indirect economic costs, primarily by work absence.2 After an acute injury, it is unknown why some individuals develop chronic pain while other get better. Studies have identified several risk factors that increase the likelihood of developing chronic pain including: depression, stress, anxiety, smoking, obesity, sleep disturbance, and poor social support.2 There is evidence that the nervous system gets rewired after the injury causing the pain receptors to become more sensitive.4 When pain lasts longer than 3 months, it is likely to persist for at least 12 months.2 In patients seeking chronic pain management, approximately 50% had psychological distress such as depression and/or anxiety. Psychological distress increases both the development and the persistence of chronic pain. Psychological treatment should be addressed when managing persistent pain.2 The prevalence of chronic pain in the general population has been estimated at 46-48%.5, 6 Clearly, a corresponding percentage of the population is not disabled, indicating pain and function can be effectively managed.3 Three important categories of chronic pain are summarized below including: chronic low back pain, central nervous system pain, and peripheral nervous system pain.

Fig 2. The above diagram highlights the complexity chronic pain. Psychological distress increases the likelihood of developing chronic pain, and in turn, can cause the symptoms to persist.

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Pain

Key Points:

In patients seeking chronic pain management, approximately 50% have psychological distress, such as depression and/or anxiety.

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The prevalence of chronic pain in the general population has been estimated at 48%

1) Chronic Low Back Pain Low Back Pain (LBP) is the most common type of chronic pain.2 Approximately 80% of the world’s population will develop low back pain at some point in their adult life.7 Most chronic LBP is mechanical and develops after acute low back pain injuries.8 The majority of acute low back pain incidents improve within a few weeks 9 but approximately 20% develop into persistent symptoms, resulting in work absence. This group is responsible for a disproportionate (80%) of low back pain related costs.10

Similar to most chronic pain problems, there is limited knowledge to identify which acute low back injuries progress to chronic episodes. There are several pre-existing factors that have been shown to increase the likelihood of developing persistent pain including: psychological conditions, poor coping strategies, poor general health, smoking, obesity, age, and persons that catastrophize or exaggerate pain.11 Chronic low back pain treatment should incorporate medication, physiotherapy, exercise, psychological, and social strategies.12, 13 Patients should not expect complete pain resolution but proper treatment can effectively control pain and improve function.13

Pain

2) Central Nervous System Pain The central nervous system (CNS) is composed of the brain and spinal cord. One of the primary functions of the CNS is integrating and processing sensory information from the

Fig 3. Low back pain is the most common type of chronic pain. Retrieved on Feb 14, 2011 from www.severelowerbackpain.net/

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body, including pain. Central nervous system pain develops from lesions caused by traumatic injury or disease. CNS lesions result from a variety of disorders which may include traumatic brain and spinal cord injuries, strokes, tumors, multiple sclerosis, and Parkinson’s disease. CNS pain is caused by heightened pain sensitivity and is often described as burning, aching, or pricking.14, 15 It is important to note that not all lesions produce CNS pain.14 At least 8% of stroke patients are affected by CNS pain.16 35-40% of traumatic spinal cord injury patients and 30% of Multiple Sclerosis patients suffer from CNS pain.15, 17 Treatment of central and peripheral nervous system pain depends on the ability to treat the underlying condition. Pharmaceutical options do not typically provide sufficient relief.14

3) Peripheral Nervous System Pain (Peripheral Neuropathy) The peripheral nervous system (PNS) is composed of all other parts of the nervous system lying outside the brain and spinal cord. The role of the PNS is relaying messages to and from the central nervous system, including pain. As mentioned above, “nociceptors” are pain receptors that detect harmful or potentially harmful stimuli, which are then transferred along the spinal nerves to the central nervous system for processing.2

Fig 4. Fig 4. Central and peripheral nervous systems. CNS is composed of the brain and spinal cord. PNS is composed of the peripheral nerves. Retrieved on Feb 14, 2011 from http://reasonablywell-julia.blogspot.com/

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Pain Peripheral neuropathy typically results from damage to the nociceptors or spinal nerves by toxic, metabolic, traumatic, or autoimmune pathways. Symptoms typically begin at the feet and gradually move up the body. Common symptoms include numbness, loss of temperature detection, “burning” sensations, tightness, and tingling. Peripheral neuropathy can also affect the motor pathways, affecting muscle weakness, loss of proprioception, painful muscle cramping, sweating, and even major organ function.18 There are too many different causes of peripheral neuropathy to describe in detail but the most common types will be described below. i) Diabetic peripheral neuropathy affects 47% of individuals with diabetes.19 Prevalence increases with age, duration of diabetes and being male.20 Symptoms can be controlled by tight regulation of blood-sugar levels, reducing weight, physical activity, and ceasing smoking.2 ii) Alcoholic neuropathy results from a lifetime of excessive alcohol consumption. Neuropathic symptoms are observed in 25-66% of alcoholics.21 Recovery is possible if alcohol consumption is discontinued.22 iii) Carpal tunnel syndrome (CPS) - Bones and ligaments of the wrist form the carpal tunnel. Muscle tendons and the median nerve pass through the carpal tunnel. Swelling of muscle tendons can compress the median nerve, causing carpal tunnel syndrome. Symptoms include burning, tingling, numbness, and muscle weakness in areas of the hand and wrist. The prevalence rate of CPS in the general population is higher in women (5.9%) than in men (0.6%). Conservative treatment can improve symptoms but when ineffective, surgical options are effective.23 Chronic Pain Summary

Chronic pain can be caused by acute injuries, degenerative tissue, or systemic illnesses.

After an acute injury, it is unknown why some develop chronic pain and others do not.

Psychological distress and other health factors increase the likelihood of developing chronic pain.

The prevalence of chronic pain in the general population has been estimated at

46-48%. Clearly, a corresponding percentage of the population is not disabled, indicating pain and function can often be effectively managed.

Chronic low back pain is the most common type of chronic pain.

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Pain

Central and peripheral nervous system disorders are important causes of chronic pain.

Treatment of central and peripheral nervous system pain primarily depends on

the ability to treat the underlying condition. Profile – Patient #1 A thirty-eight year old female has a minor injury to her left elbow when she bumps her arm against a filing cabinet. She reports immediate severe pain to her employer. Initial x-rays and physical examination are normal. After two years, she continues to complain bitterly of pain about her left elbow. She has been unable to return to the workplace. On physical examination the arm is held in a protected position. The skin is glossy. The range of motion of the finger joints are reduced and the hair, as well as her fingernails have overgrown. This is a classic story of an individual suffering with a chronic pain syndrome, secondary to a regional dystrophy after an episode of minor trauma. Profile – Patient #2 A forty-eight year old sanitary engineer injures his neck and upper back in a low energy motor vehicle collision. He complains of pain in his neck and his shoulders, which fails to respond to physiotherapy, medications and time away from the workplace. Eighteen months later he remains unemployed. All investigations are normal. He is seen by his neighbors playing baseball with his children, shopping for groceries and gardening. This is a classic story of a person with chronic low back pain. There is no objective evidence of disease. The patient complains of chronic difficulties.

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