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  1. 1. ArthritidesA report by: Kenneth PierreM. Lopez
  2. 2. Rheumatoid Arthritis
  3. 3. Etiology Vague, but is believed to be due to an autoimmune component, the end result of which is the formation of pannus, the destructive element of RA responsible for most of the deformities tat one sees in patients with RA.
  4. 4. Epidemiology/Incidence Women are affected 2-3 times more often than men Increases in incidence with advancing age Peak incidence in women is between 4th and 6th decades
  5. 5. Clinical Manifestations Articular signs and symptoms  Almost always bilateral  The articular manifestations of RA can affect any diarthrodial joint In the hands  Typically early sign is fusiform swelling of the finger (PIP)  Bilateral and symmetrical swelling of the MCP joints particularly the 2nd and 3rd is very common  Ulnar deviation at the MCP can coexist with radial deviation at the wrist  Swan neck deformity can occur which is characterized as extension of the PIPI and flexion of the DIP  Boutonniere or button hole deformity described as flexion of PIP and extension at the DIP caused by rupture of the sublimis tendon and associated disruption of the volar plates of the PIP joints
  6. 6. Deformities Swan-neck Boutonniere
  7. 7. Clinical Manifestations In the cervical spine  Commonly involves C1-C2  Early sign is neck stiffness with resulting limitation in ROM’s In the wrists  May be initially manifested as a painless ulnar swelling on the styloid area  One of the earliest ROM’s to be affected is wrist dorsiflexion  Synovial proliferation on the volar aspect may compress the median nerve and cause CTS  Pronation and supination are severely limited due to involvement of the inferior radioulnar joint
  8. 8. Clinical Manifestations In the knees  Intra-articular knee effusions result to a ballotable patella  Among the most frequently affected joints and is responsible for much disability  Quadriceps atrophy is often of great severity  May be accompanied by Baker’s cyst or pathologic enlargement of the gastrocnemius = semimembranosus bursa In the feet and ankles  Subluxation of the MTP heads with cocking up the toes  Fibular deviation of the first through fourth toe is common  Calluses in the plantar area can result from abnormal weight bearing forces
  9. 9. Deformities Baker’s Cyst Calluses
  10. 10. Clinical Manifestations Extra Articular Manifestations  Skin: presence of rheumatoid nodules usually on extensor surface  Ocular: can present as keratoconjunctivitis sicca (dry eye syndrome)  Cardiopulmonary: may be in the form of acute pericarditis and pneumonitis  Neurological 3 patterns of involvement  Cervical spine involvement  Peripheral nerve entrapment  Vasculitis  Hematologic: Patients with RA usually have a form of anemia that doesn’t respond to iron therapy
  11. 11. KeratoconjunctivitisSicca
  12. 12. Important facts Most commonly involves the small joints of the hands, wrists, knees and feet Often bilateral, symmetrical and polyarticular Most destructive element is the rheumatoid pannus, a vascular granulation tissue composed of proliferating fibroblasts, numerous small blood vessels and various numbers of inflammatory cells
  13. 13. Criteria for classification of RA1. Morning stiffness lasting at least (1) hour before maximum improvement2. Arthritis of 3 or more joints simultaneously involved with soft tissue swelling3. Arthritis of hand joints involving a joint in the wrist, MCP or PIP4. Symmetric arthritis of the same joints simultaneously5. Rheumatoid nodules over bony prominences, extensor surfaces or juxtaarticular regions6. Abnormal titer of serum rheumatoid factor7. Radiographic changes including erosions or bony decalcification localized or most marked adjacent to the involved joints 1. *4 out of 7 indicative of RA; for criteria 1-4 must be present for at least 6 weeks
  14. 14. Management Main objectives of management  Relief of pain  Reduction or suppression of inflammation  Minimizing undesirable side effects  Preservation of muscle and joint function  Maintain muscle strength  Return to a desirable and productive life, if possible Management  Patient education  PT and OT  NSAID’s/ antirheumatic drugs  Steroids (severe cases)
  15. 15. PT Management Joint protection strategies Maintain/improve joint mechanics and connective tissue functions Implementation of aerobic capacity/ endurance conditioning or reconditioning such as aquatic programs
  16. 16. Steinbrocker’s functional classification of RA Class I- remission or ability to perform normal activities Class II- moderate restriction but adequate for normal activities Class III- marked restriction, inability to perform most duties of usual occupation or self-care Class IV- incapacitation or confinement to bed or a wheelchair
  17. 17. Systemic LupusErythematosus
  18. 18. Epidemiology & Pathogenesis Primarily a disease of young females with a peak incidence occurring between the ages 15-40 with female; male ration of 5:1 Prevalence rate for black females is nearly 3 times that for white females Results from a disturbance of immune regulation, which may be initiated by an interplay of genetic environmental and hormonal factors Constitutional Symptoms include  Fever  Weakness  Fatigability  Weight loss
  19. 19. Clinical Signs and Symptoms *joint involvement is the most common manifestation of SLE *joints most commonly involved are the PIPs, knees, wrists and MCP’s. Joint involvement is remarkably symmetrical1. Serositis which can manifest as pleuritis or pericarditis2. Hematologic as hemolytic form of anemia, leukopenia and/or thrombocytopenia3. Immunologic disorder with positive SLE cell preparation of AntiDNA titers4. Neurologic disorder present as either seizures or psychosis5. Renal disorder6. Oral ulcers which are typically painless7. Arthritis8. Discoid rash9. Malar rash10. Antinuclear antibody titer11. Photosensitivity
  20. 20. Treatment1. NSAID’s2. Corticosteroids3. Plasma Exchange4. Dialysis and transplantation5. Relaxation and energy conservation* Procainamide is the most common agentimplicated in producing lupus like syndromeassociated with drug related SLE
  21. 21. Osteoarthritis
  22. 22. Etiology & Epidemiology DJD is a disease involving a progressive deterioration and loss of articular cartilage by reactive changes at the margins of the joints nad in the subchondral bone Most common disease of both axial and peipheral diarthrodial joints Found to be universally present in persons Common in females more than 45 y/o Common in males less than 45 y/o Almost universal in persons 65 years or older
  23. 23. Pathogenesis Current data suggest biomechanical, inflammatory and immunology factors in the development of DJD. A primary insult leads to the release of proteolytic and collagenolytic enzymes from chondrocytes which degrade matrix proteoglycans and collagen. Biomechanical factors such as fatigue and cartilage fracture therefore occurs even with minor loads as the cartilage ages. Normally blue translucent cartilage takes on an opaque yellowish appearance. Surface irregularities due to fissuring and pitting are followed by erosions. These erosions initially focal become confluent and lead to large areas of denuded surface. Initial involvement of superficial and middle layers is followed by full-thickness loss of cartilage down to bone.
  24. 24. Clinical Signs and Symptoms Usually involves weight bearing joints Hand involvement will present as formation of spurs at the dorsolateral and medial aspects of the DIP joint known as Heberden’s nodes Nodal osteoharthritis at the PIP joint is called Bouchard’s nodes Common subjective and objective findings are:  Limitation of motion  Locking of a joint during Rom  Crepitus  Pain in RO’s  Non-inflammatory swelling  Joint pain relieved by rest
  25. 25. Heberden’s/Bouchard’s
  26. 26. Clinical Signs and Symptoms Stiffness Enlargement with limitation of motion Associated secondary synovitis may be present which may be due to release of crystals from cartilage *osteophyte spur formation; a proliferative lesion is seen most prominently at joint margins *osteoarthritic changes in the hip lead to insidious onset of pain, often followed by a limp. Hip involvement is the most disabling form of osteoarthritis *DJD of the spine results from involvement of the IVD, vertebral bodies or posterior apophyseal articulations. Involvement of the lumbar spine is seen most commonly at the L3-4 area
  27. 27. Variant Forms Primary Generalized Osteoarthritis  Revelas involvement of the DIPs and PIPs of the hands, the 1st CMC jt., knees, hips and MTP joints Erosive Inflammatory Osteoarthritis  Involves primarily the DIPs of PIPs of the hands  There is eventual development of deformity and ankylosis Ankylosing Hyperostosis  Aka diffuse idiopathic skeletal hyperostosis (DISH)  Characterized by flowing ossification along the anterolateral aspect of the vertebral bodies Secondary Osteoarthritis  Produces clinical findings similar to those seen in the primary form of the disease  A relationship between generalized joint hypermobility, osteoarthritis and chondrocalcinosis has been noted
  28. 28. Treatment Principles of Treatment  Symptom relief  Maintaining or improving function  Limiting physical disability  Avoiding drug toxicity  Joint replacement (severe forms) Pharmacologic  NSAID’s  Intra-articular steroids PT Management  PT modalities  Weight reduction program  Assistive devices
  29. 29. Ankylosing Spondylitis
  30. 30. Epidemiology One of the most common among the seronegative spondyloarthrpathies Aka Von Bechterew’s dse or Marie-Strumpell’s dse or Rheumatoid Spondylitis Involves primarily the axial skeleton Majoirty of cases are males but can also occur among females but is usually less progressive among them More frequent in Pima and Hida Indians
  31. 31. Pathology Pathologic changes are concentrated around the enthesis, the site of the ligamentous insertion into the bone which undergoes inflammatory changes There is a high incidence among individuals who have inherited the HLA-B27 gene There is a tendency for the inflammatory reaction to involve the sacroiliac joints and the spine; to a lesser extent the peripheral joints can also be involved The typical “bamboo spine” deformity is a late sequalae
  32. 32. Variant Forms Primary  If no other rheumatologic disorder is present  Develops during the 2nd or 3rd decade Secondary  If the sacroiliitis is related to one of the other spondyloarthropathies  May occur at any age
  33. 33. Extra-Articular Manifestations Blurringof vision with resolution in 2-3 months Cardiovascular involvement, specifically aortitis of the ascending aorta with occasional aortic valve incompetence Neurotic involvement in the form of spinal fractures with resulting SCI (rare)*chest wall rigidity is a frequent problem noted inpatients with AS but as a rule does not contribute tosignificant pulmonary problems becausediaphragmatic breathing contributes to maintainingpulmonary competence
  34. 34. Treatment NSAID’s Ophthalmic steroids for eye affectation Exercise aimed at preventing or minimizing deformity  Spinal extension exercises  Deep breathing exercises Patient education  Keeping spine as straight as possible  Avoid stopping  Sleep on a firm mattress with a thin pillow as possible
  35. 35. Bacterial Arthritis (SepticArthritis)
  36. 36. Epidemiology Typically rapid in onset, pain is moderate to severe, with warmth, tenderness or restricted motion Majority are monoarticular, 15% polyarticular Frequently invovles the knee, hip shoulder and wrist in order of frequency Synovial fluid analysis will show elevated WBC count and positive culture
  37. 37. Routes of Infection Direct inoculation into a joint cavity from trauma or surgery From a contiguous source such as osteomyelitis, soft tissue abscess, or infected wound Via subsynovial blood vessel from a remote focus
  38. 38. In the Elderly & Among Kids Elderly  Almost half are over 60 years of age  Usually affects joints with prior arthritis  ESR is markedly elevated  Permanent joint damage can result with a majority of patients having poor functional outcome Kids  Almost always monoarticular  Can originate from distant source such as otitis media, infected umbilical catheters, meningitis  Common causative organisims are Staph and Haemophilus Influenzae
  39. 39. Gouty Arthritis
  40. 40. Epidemiology/Etiology Characterized by recurrent paroxysms of violent articular inflammation provoked by the release of microcrystals or monosodium urate monohydrate in the joint cavity Development of gross deposits of sodium urate (tophi) in and around the joints and in the kidneys*uric acid constitutes the major end product of thecatabolism of purines. It represents the major endproduct in the breakdown of amino acid and purinenitrogen
  41. 41. Epidemiology/Etiology Among adult men, peak incidence is the 5th decade Among women, usually post menopause because of the actions of estrogen with promotes renal excretion of uric acid*development of hyperuricemia may be due to anexcessive rate of uric acid production and adecrease in the renal excretion of uric acid Podagra – gout of first MTP Gonagra – gout of the knee Cheiragra – gout of the wrist
  42. 42. Pathogenesis Withgout, there are three general mechanisms responsible for the hyperuricemia  Urate over-production  Excessivepurine in diet  Severe muscle exertion  Increase nucleotide turnover as in some myeloproliferative states  Uric acid under-secretion  Intake of certain drugs such as cyclosporine  Starvation  Alcohol ingestion  Combined over-production and under-secretion
  43. 43. Stages of Gout Asymptomatic Hyperuricemia: defined as BUA >8.1 mg/dl in men & >7.2 mg/dl in women Acute intermittent gout: usually occurs decades after initial diagnosis of asymptomatic hyperuricemia; onset heralded by warmth, erythema, swelling and exquisite pain in the affected joint; 90% occurs in the first MTP; may be accompanied by fever and chills Intercritical Stage: patient is completely free of symptoms although monosodium urate crystalscan still be seen in the joint
  44. 44. Stages of Gout ChronicTophaceous gout: usually develops 10 or more years after acute intermittent attack  Involved joints are persistently swollen and uncomfortable but pain is less intense  Tendency to develop tophi usually increased with uric acid levels  Greater than 11.0 mg/dl  Tophi can usually be found in the fingers, wrist, ears knees and ulnar aspect of the forearm and achilles tendon
  45. 45. Unusual Forms of Gout Lesch Nyhan Syndrome  Results from a complete deficiency of HGPRTase which results in gout, spasticity, choreoathetosis, mental retardation and compulsive self-mutilationas well as profound overproduction of uric acid, which leads hyperuricemia and uric acid stone formation Kelley Seegmiller Syndrome  Partial HGRPTase deficiency without the neurological problems see in the complete deficient state
  46. 46. Treatment of Gout The management of a patient with gout requires that 2 aspects be considered independently  The immediate control of the acute attack of gouty arthritis  The long term treatment of hyperuricemia to prevent complications such as tophaceous deposits, joint destruction, renal calculi or renal insufficiency
  47. 47. Pharmacologic Management Colchicine- has significant GI side effects  Given for acute attacks  Associated with the “cholchicine toxicity” syndrome  Bone marrow suppression  Renal failure  Disseminated intravascular coagulation  Hypocalcemia  Cardiopulmonary failure  Seizures  Death secondary to toxicity causing agranulocytopenia
  48. 48. Pharmacologic Management NSAID’s Steroids Aspiration and intra-articular corticosteroid injection Allopurinol- drug of choice for patients with renal disease, tophi and renal stone formers
  49. 49. Fibromyalgia
  50. 50. Important Facts The most common cause of chronic diffuse pain The most important clinical feature of FMS are symptoms of diffuse aching, stiffness and fatigue coupled with a PE that demonstrates multiple tender points in specific areas
  51. 51. Clinical Features Soft tissue pain usually in axial locations such as knee and lower back Stiffness which is worse in the morning Fatigue which is attributed to poor sleep Tender points Association with other stress related conditions such as irritable bowel syndrome, tension, headaches and dysmenorrhea
  52. 52. Treatment Educate the patient and give reassurance: FMS is not a psychiatric disorder and is not life threatening Medications that improve sleep NSAID’s to treat pain from other conditions such as underlying DJD Intralesional injection of the tender points with anesthetic/steroids PT Management  Ultrasound  Massage  Superficial Heat with TENS
  53. 53. Reflex SympatheticDystrophy
  54. 54. Definition and Criteria Characterized by severe limb pain with autonomic dysfunction in the upper or lower extremities and typically preceded by and event such as MI, CVD, trauma in an extremity Definite: pain and edema in extremity; vasomotor instability and dystrophic skin changes Probable: pain and edema in extremity; vasomotor instability Possible: edematous extremity; vasomotor instability*pain is the most disabling feature of RSD: intense, deep,chronic and burning; aggravated by movement, postureand emotional stress*pain does not follow dermatomal pattern; weakness,spasms contractures (MC palmar fascia and tendonsheaths of the hand)
  55. 55. 3 Stages of RSD (Steinbrocker) Stage I (Acute)  Lasts a few weeks to 6 months  Pain presents as allodynia and hyperpathia  Local edema increased hair growth  Vasomotor changes  Dependent rubor and decreased ROM Stage II (Dystrophic)  3-5months post inciting event  (+) nail change  Spotty osteoporosis  Pain more diffuse  Decreased swelling, but stiffness & decreased ROM more pronounced  Atrophy of subcutaneous tissue and msucle  Early signs of contracture is seen  Brawny edema
  56. 56. 3 Stages of RSD (Steinbrocker) Stage III (Atrophic)  Lasts for months and goes on to irreversible alterations  Progressive atrophy of skin, muslce, bone and joints  Decreased pain but there is a severe reduction in the ROM  Skin is pale and glassy in appearance  Bood flow is decreased  (+) joint contractures  (+) diffuse osteoporosis Stage IV (Psychological Stage)  Response to medication causing depression and suicidal ideations
  57. 57. Treatment Medical Treatment  Sympathetic blockade  Surgical sympathectomy  Oral medications such as steroids PT Management  Gentle ROM’s to the extremity  US  Hand desentization  TENS
  58. 58. Juvenile RheumatoidArthritis
  59. 59. Clinical Aspects The diagnostic criteria for JRA are onset before age of 16, persistent arthritis in one or more joints for at least 6 months and exclusion of other types of childhood arthritis Characterized by chronic synovial inflammation of unknown cause Girls are more affected than boys
  60. 60. 3 Types Systemic onset JRA (Still’s Disease)  (+) of systemic manifestations such as fever, transient maculopapular, pale pink rash usually in the trunk and joint pains  Associated manifestations include growth delay, hepatosplenomegaly, pleuritis, anemia and lymphadenopathy  Peak onset: 1-6 years of age  Musculoskeletal manifestations early in the disease often consist only of recurrent arthralgia, myalgia and transient arthritis
  61. 61. Pauciarticular JRA Arthritisin 4 or less joints 2 distinct groups  Early onset- girls more than boys 4:1, have greater risk of developing iridocyclitis  Late onset- more common in boys, usually noted after 5 years of age Jointsmost frequently affected are some combination of the knees, ankles and elbows hips are generally spared and sacroiliitis is not seen
  62. 62. Polyarticular JRA Occurs in 40% of children with JRA Arthritis in 4 or less joints Pt presents with malaise, low grade fever, modest organomegaly, adenopathy, anemia and growth retardation or weight loss 2 distinct groups  Seropositive: almost always girls >8 years of age; have a greater risk for developing erosions and rheumatoid nodules with poor functional outcome  Seronegative: more benign than seropositive Cervical spine disease most often at the C2-3 apophyseal joints in most common
  63. 63. Treatment Asprin/NSAIDS Gold compounds Hydroxichloroquine Oral methotroxate Sulfazaline Intravenous gamma globulin Glucocorticoids for life threatening states that fail to respond to more conservative measures
  64. 64. Polymyositis -Dermatomyositis
  65. 65. Epidemiology/Etiology Diffuse inflammatory disorders of striated muscle which cause symmetrical weakness and to a lesser degree, atrophy of muscles principally of the limb girdles neck and pharynx Cause is unknown Females are affected twice as commonly as males
  66. 66. Clinical Features Weakness develops slowly and first affects the LE closely resembling muscular dystrophy Involvement of the posterior pharyngeal muscles account for dysphagia and dysphonia (nasal voice) Dusky-red patches slightly elevated and smooth or slightly scaly are found on the elbows, over the dorsum of the PIP and MCP jts, over the knees and on the medial malleoli at the ankles Erythematous eruption on the face, especially in the “butterfly” and periorbital areas Heliotrope rash, a peculiar dusky like diffusion is sometimes seen on the upper eyelids Calcinosis universalis, a widespread calcification of the skin, subcutaneous and periarticular tissues may develop particularly in children and young adults
  67. 67. Pathology Focal or extensive primary degeneration of muscle fibers Basophilia of some fibers with prominent central positioning of nuclei Necrosis of parts or entire groups of muscle fibers Focal or diffuse infiltrates or chronic inflammatory cells; when focal, these infiltrates are usually located around or near blood vessels or between individual muscle fibers Interstitial fibrosis which varies in severity especially with the duration of the disease A variation in cross-sectional diameter of the fibers
  68. 68. Characteristic Triad Spontaneous fibrillation and positive saw toothed (spike) potentials Complex polyphasic or short duration potentials which appear on voluntary contraction Salvos or repetitive high frequency action potentials (pseudomyotonia)
  69. 69. Classification Group I – Primary Idiopathic Polymyositis  Insidious onset  Weakness beginning in pelvic girdle, moderate arthritis, raynaud’s phenomenon, dysphagia, dysphonia  Remissions and exacerbations is common  Recover completely or left with residual muscle weakness and fatigue Group II – Primary Idiopathic Dermatomyositis  Acute onset  Proximal shoulder and pelvic girdle weakness  Erythematous heliotropic rash, skin of the eyelids and dorsum of the hands  Muscle tightness  Subacute joint findings
  70. 70. Classification Group III – Dermatomyositis (or Polymyositis) associated with Neoplasia  Associated with malignancy  M>F 40%  Muscle weakness may be pre-malignancy by 1-2 years  Death often due to respiratory complications Group IV – Childhood Dermatomyositis associated with Vasculitis  Characterized by rapid and progressive muscle weakness  Dysphagia, dysphonia and respiratory weakness  Severe joint contractures  Exacerbation with 7-10 years of remission
  71. 71. Progressive SystematicSclerosis/ Scleroderma
  72. 72. Etiology/Epidemiology Generalized disorder of connective tissue characterized by fibrosis and degenerative changes in the skin, synovium, digital arteries or certain internal organs, notably the esophagus, intestine, lungs, heart, kidney and thyroid Women are approximately 3-4 times as often as men Initial symptoms appear in 3rd to 5th decade of life High frequency in coalminers Silicosis is a predisposing factor
  73. 73. Pathogenesis Fibrosis of the skin and internal organs in PSS is the result of the overproduction of collagen Scleroderma en coup de sabre is a linear streak of band of sclerosis appears in the upper or lower extremities or in the frontoparietal area of the forehead and scalp
  74. 74. Classification PSS with diffuse Scleroderma  Symmetric diffuse involvement of the skin affecting trunk, face, proximal and distal portions of the extremities; relatively early appearance of disease of the esophagus, intestine, heart, lung and kidney CREST Syndrome  C- calcinosis  R- Raynaud’s Phenomenon  E- Esophageal Dysmotility  S- Sclerodactyly  T- Telangiectasia
  75. 75. Reiter’s Syndrome
  76. 76. Etiology/Epidemiology In the UK and North America, most of the cases appear to follow venereal exposure In Europe, Africa, Middle East and Far East, the postdysenteric form appears to be common Common in young males Rare in women, children and elderly persons
  77. 77. Clinical Features Illnessbegins most often with symptoms of urethritis, followed by conjunctivitis and arthritis Arthritis most commonly affects weight-bearing joints especially the knees and ankles Periostitis involving the inferior and posterior aspects of the os calcis (calcaneus) may be associated with painful heels or “lover’s heel” Keratoderma blennorhagicum is the characteristic manifestation (palmoplantar lesions composed of erythemas, erosions, crusting and hyperkeratosis
  78. 78. Treatment NSAID’s are useful in reducing joint pain Corticosteroids may relieve pain and swelling of the joints but do not shorten the course of the disease and are often quite ineffective
  79. 79. Psoriatric Arthritis
  80. 80. Clinical Features Affectsthe DIPs Three major clinical groups with peripheral arthritis  Pts with arthritis mutilans, often complicated by telescoping of the digits  Pts with asymmetric arthritis often involving only 2-3 joints at a time  Pts with a pattern of symmetric polyarthritis clinically indistinguishable from RA TheMTPs and the IPs of the fingers and toes are frequently affected
  81. 81. Clinical Features Tends to cause less pain and less disability than RA Subcutaneous nodules are not seen Fibrosis may be more prominent The severe resorptive arthropathy in which the loss of bone stock and joint surface is so extensive that the skin overlying the fingers or wrists may fold upon itself, “la main en-Lorgnette Syndrome”
  82. 82. Sjorgen’s Syndrome
  83. 83. Pathophysiology An immunologic disease characterized by deficient moisture production of the lacrimal salivary and other glands Dryness of the mouth eyes and other mucous membranes Affect primarily women over the age of 40 Frequently associated with Raynaud’s Phenomenon RA and lymphoma
  84. 84. Rehabilitation of Patientswith Rheumatic Disease
  85. 85. Key Elements Maintenance of critical ROMs Maintenance of posture Improve or maintain strength Maximize pain relief Provision of appropriate orthosis
  86. 86. Things to keep in mind Make goals realistic, measurable, precisely defined and discuss these with your patient Set a realistic time frame Educate the patient on preventive measures in anticipation of complications and deformities
  87. 87. Specific Approach per joint C1C2 involvement  Avoidance of prolonged positions  Exercise to stretch the cervical paraspinal muscles during the workday such as shoulder rolls, cervical isoms, ROMs with gentle stretching, shrugging  Do not use cervical traction  Soft collar may be given to stabilize Shoulder  Goals of managing shoulder pain and maintain ROMs  Codman’s exercise stretches the capsule and avoids active abductions, which can produce pain  Other shoulder mobility exercise can be avoided as ROM improves  Pts should be able to clasp their hands behind the head with the elbows back
  88. 88. Specific Approach per joint Elbow  Elbow requires at least 90degrees to allow midline activities to take place  Loss of extension and forearm supination and pronation can result in loss of UE extension  AROMs should be geared towards the preservation of elbow flexion and forearm supination Wrist and Hand  As a general rule all hand movements that result in force and exerted against the radial side of each finger should be avoided  Strongly grasping objects plus twisting motion should not be encouraged  Orthoses that immobilize and support the wrist can be given  Exercise of the wrist should involve stretching in extension flexion pronation and supination
  89. 89. Specific Approach per joint Hip  A cane on the opposite side of the involved hip can decrease loading on the hip by as much as 60%  Active ROMs should be done on the supine position to loosen tight muscles reduce spasm and increase ROMs  In the presence of pain, isometrics can be done by pressing the leg onto the bed in the supine, prone and side lying positions Knee  Flexion contracture greater than 5-10 degrees cause a limp  Quad setting should begin with isometric contractions  Resistive extension exercises will strengthen quads and improve walk time and endurance
  90. 90. Specific Approach per joint Foot and Ankle  Tibiofibular and subtalar arthritis could be decreased with weight-bearing AFO with cushioned shoe heel  Instability of the hind foot leads to collapse of the medial longitudinal arch and outward rotation of the calcaneus (valgus) Other modalities include: Heating modalities Cryotherapy (acute) TENS
  91. 91. Thanks for yourAttention 