1. Arthritides
A report by: Kenneth Pierre
M. Lopez

2. Rheumatoid Arthritis

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. 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. 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. Deformities
Swan-neck Boutonniere

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. 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. Deformities
Baker’s Cyst Calluses

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. Keratoconjunctivitis
Sicca

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

14. Criteria for classification of RA
1. Morning stiffness lasting at least (1) hour before
maximum improvement
2. Arthritis of 3 or more joints simultaneously involved with
soft tissue swelling
3. Arthritis of hand joints involving a joint in the wrist, MCP
or PIP
4. Symmetric arthritis of the same joints simultaneously
5. Rheumatoid nodules over bony prominences, extensor
surfaces or juxtaarticular regions
6. Abnormal titer of serum rheumatoid factor
7. 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

15. 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)

16. 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

17. 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

18. Systemic Lupus
Erythematosus

19. 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

20. 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 symmetrical
1. Serositis which can manifest as pleuritis or pericarditis
2. Hematologic as hemolytic form of anemia, leukopenia
and/or thrombocytopenia
3. Immunologic disorder with positive SLE cell preparation of
AntiDNA titers
4. Neurologic disorder present as either seizures or psychosis
5. Renal disorder
6. Oral ulcers which are typically painless
7. Arthritis
8. Discoid rash
9. Malar rash
10. Antinuclear antibody titer
11. Photosensitivity

22. Treatment
1. NSAID’s
2. Corticosteroids
3. Plasma Exchange
4. Dialysis and transplantation
5. Relaxation and energy conservation
* Procainamide is the most common agent
implicated in producing lupus like syndrome
associated with drug related SLE

23. Osteoarthritis

24. 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

25. 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.

26. 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

27. Heberden’s/Bouchard’s

28. 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

29. 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

30. 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

31. Ankylosing Spondylitis

32. 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

34. 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

35. 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

36. 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 in
patients with AS but as a rule does not contribute to
significant pulmonary problems because
diaphragmatic breathing contributes to maintaining
pulmonary competence

37. 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

38. Bacterial Arthritis (Septic
Arthritis)

39. 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

40. 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

41. 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

43. Gouty Arthritis

44. 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 the
catabolism of purines. It represents the major end
product in the breakdown of amino acid and purine
nitrogen

45. 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 an
excessive rate of uric acid production and a
decrease in the renal excretion of uric acid
 Podagra – gout of first MTP
 Gonagra – gout of the knee
 Cheiragra – gout of the wrist

47. 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

48. 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

49. 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

50. 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

51. 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

52. 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

53. 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

54. Fibromyalgia

55. 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

56. 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

58. 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

59. Reflex Sympathetic
Dystrophy

60. 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, posture
and emotional stress
*pain does not follow dermatomal pattern; weakness,
spasms contractures (MC palmar fascia and tendon
sheaths of the hand)

62. 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

63. 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

64. Treatment
 Medical Treatment
 Sympathetic blockade
 Surgical sympathectomy
 Oral medications such as steroids
 PT Management
 Gentle ROM’s to the extremity
 US
 Hand desentization
 TENS

65. Juvenile Rheumatoid
Arthritis

66. 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

67. 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

68. 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

69. 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

70. 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

71. Polymyositis -
Dermatomyositis

72. 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

73. 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

74. 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

75. 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)

76. 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

78. 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

79. Progressive Systematic
Sclerosis/ Scleroderma

80. 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

81. 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

83. 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

85. Reiter’s Syndrome

86. 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

87. 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

89. 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

90. Psoriatric Arthritis

91. 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

93. 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”

94. Sjorgen’s Syndrome

95. 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

97. Rehabilitation of Patients
with Rheumatic Disease

98. Key Elements
 Maintenance of critical ROMs
 Maintenance of posture
 Improve or maintain strength
 Maximize pain relief
 Provision of appropriate orthosis

99. 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

100. 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

101. 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

102. 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

103. 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

104. Thanks for your
Attention 