Rheumatology & Rehabilitation 2018-2019
Rheumatology & Rehabilitation 2018-2019
Rheumatology & Rehabilitation 2018-2019
Rheumatology and
Rehabilitation
STAFF OF
Rheumatology and Rehabilitation Department
Mansoura Faculty of Medicine
2018- 2019
1
Preface
This book is written by the staff members of Rheumatology,
Physical Medicine and Rehabilitation Department, Faculty of Medicine,
Mansoura University. It has been made to provide, in brief, the basic
knowledge of this specialty in a systemic, concisely written, well-
illustrated and comprehensive manner to be easily memorized by the
undergraduate students.
We hope that this book provides our students with adequate basic
rheumatological knowledge to make accurate clinical observations,
arrive at a diagnosis and be aware of relevant differential diagnosis. We
hope that this book can also provide our students with different
modalities of physical medicine and role of interdisciplinary rehabilitation
program in different medical conditions.
STAFF OF
Rheumatology and Rehabilitation Department
Mansoura Faculty of Medicine
2
STAFF MEMBERS
of Rheumatology, Physical Medicine and Rehabilitation
Department Faculty of Medicine
Mansoura University
3
APPROACH TO A PATIENT WITH
1 RHEUMATIC DISEASE
3 SIMPLE SCREENING QUESTIONS Rheumatism: is any painful disorder
1. Have you any pain or stiffness in your muscle, joints or back? affecting the musculoskeletal system
including: joints, muscles, connective
2. Can you dress yourself without any difficulty? tissues, soft tissues around the joints and
3. Can you walk up and down stairs easily? bones.
If any answer is positive to any question, then detailed history must Rheumatology: science dealing with the
diagnosis and management of painful
be obtained. conditions in musculoskeletal system from
conservative aspect.
ARTICULAR SYMPTOMS The diagnosis of many rheumatic diseases
is mainly clinical.
Pain
• Articular pain: localized to joint.
• Non-articular pain: originates from peri-articular structures e.g. tendon or bursae.
• Referred pain: e.g. cervical spondylosis presenting as shoulder pain.
• Inflammatory disease: joint pain tends to be worse at night.
• Mechanical disorder: pain is worse at the end of the day and after activity; relieved by rest.
Swelling
Fatigue
• Important feature of many rheumatic disorders (e.g. rheumatoid arthritis and SLE).
• Prominent feature in fibromyalgia.
Stiffness
• Early morning stiffness: inflammatory arthritis (may last for several hours).
• Joint stiffness after rest may indicate osteoarthritis (gelling).
• Fibromyalgia.
Weakness
Caused by: muscle weakness, pain, mechanical factors (e.g. tendon and joint impairment) and nerve damage.
Limitation of movement
Caused by pain, contracture, arthritis, capsular fibrosis (e.g. frozen shoulder).
Deformities
e.g. genu varus, genu valgum, Boutonnière deformity, Swan-neck deformity, Dupuytren's contracture.
ANALYZING SYMPTOMS
Precipitating Factor
4
Acute or Chronic
Table 1.1. Pain due to mechanical versus inflammatory
• Acute (<6 weeks duration): infectious
causes
arthritis, gout.
Feature Inflammatory Mechanical
• Chronic: OA, RA.
Morning stiffness >1 hour <30 minutes
Onset and Course of the Disease Fatigue Significant Minimal
Activity Improve Worsen
• Slow insidious pattern: degenerative arthritis.
symptoms symptoms
• Rapid onset, severe, self-limiting: Crystal-
Rest Worsen Improve
related inflammation.
symptoms symptoms
• Remission and exacerbation:
Systemic Yes No
Inflammatory arthritis.
involvement
Inflammatory or mechanical in nature Corticosteroid Yes No
requirements
See Table 1.1
Which Joints are Involved
Symmetry
EXTRA-ARTICULAR MANIFESTATIONS
• Constitutional symptoms (fever, weight loss, fatigue): connective tissue disease (CTD), vasculitis.
• Mucocutaneous: SLE (malar rash; discoid lesion; alopecia; oral ulcers), psoriasis, Behcet's disease (oral ulcer),
Reiter's disease (circinate balanitis), Sjogren (dry eye: sicca syndrome; dry mouth: xerostomia).
• Diarrhea: enteropathic arthritis (ulcerative colitis; Crohn’s disease); coeliac disease; Whipple’s disease; proceed
reactive arthritis.
5
• Eyes: conjunctivitis; iritis (Reiter’s syndrome), uveitis (seronegative spondylo-arthropathies), episcleritis (RA),
scleritis (RA), kerato-conjunctivitis sicca (RA and Sjogren's syndrome).
• Cardio-respiratory: Episodes of pericardial or pleuritic chest (connective tissue disease). Dyspnea due to
pulmonary fibrosis or cardiac affection e.g. aortic regurgitation (spondyloarthropathies).
• Neurological:
• Prodromal symptoms and events: Acute rheumatic disease may follow events e.g. upper respiratory tract
infections, diarrhoea, genitourinary infection, insect bites (e.g. Lyme disease) and vaccinations.
• Past history: previous attacks of the symptoms; psoriasis; diarrhea; risk of sexually transmitted infection.
EXAMINATION
General
• Check for associated features: skin or eye involvement; disorders of the respiratory, cardiovascular, abdominal or
neurological systems.
Joint examination
• Check joints for tenderness and swelling; asymmetry of colour; deformity; limitation of movement; muscle wasting.
A) Upper limbs
• Assess pronation, supination and grip, and dexterity by placing tip of each finger on tip of thumb.
B) Lower limbs
• Observe patient standing to check for deformity of upper leg, lower leg or foot.
• with patient on couch: check hip and knee ROM; knee crepitus.
• Examine each knee for joint effusion: patellar tap, cross fluctuation tests.
6
• Check for quadriceps bulk.
• Check feet for synovitis, for callosities, deformities and high or low arch.
C) Spine
• With the patient standing, check from behind to detect lateral spinal curvature, difference in level of the
iliac crests and asymmetry of the paraspinal muscles.
INVESTIGATIONS
Serologic
• Rheumatoid factor support diagnosis of RA.
• Anti-CCP: more specific than rheumatoid factor in RA.
• ANA (Table 2.2).
Genetic
HLA B27 – Increased positivity in ankylosing spondylitis and other spondyloarthropathies.
Synovial fluid
Table 2.2. Selected ANA with High Sensitivity or Specificity for Rheumatic Diseases
Anti- SLE Other conditions
dsDNA 60–80%, Highly Specific to SLE (>97%)
Serum Level correlate with lupus nephritis and SLE
flare
Sm 10–40%, Highly Specific to SLE
U1 RNP 30–40% MCTD: 100%
Ro (SS-A) 50%, associated with photosensitivity, subacute Sjögren syndrome: 75%
cutaneous lupus, interstitial lung disease. RA: 10–15%
Can cross the placenta causing neonatal cutaneous
lupus and congenital complete heart block.
La (SS-B) 10–15% Primary Sjögren syndrome: 40–50%
congenital complete heart block: 90%
neonatal cutaneous lupus: 70%
centromere CREST: 60% (Highly specific: >98%)
Scleroderma: 15%
Scl-70 Scleroderma: 40% (Specificity, 100%).
Histones SLE: 50–70% Drug induced lupus: >95%
7
• Gram stain (tuberculosis)
• Culture and sensitivities.
• Crystal identification – urate, calcium pyrophosphate.
Others
Imaging:
• X-rays: RA (juxta-articular osteoporosis; erosions); OA (osteophytes; asymmetric narrowing).
• Ultrasound.
• CT scan
• MRI – much greater information of bone, joint and soft tissue.
Arthroscopy
Direct view of joint and intra-articular structures.
8
2 CONNECTIVE TISSUE DISEASE
• A group of chronic inflammatory disorders predominantly affecting
females. CTD include
• They involve many different organs therefore exhibit a wide • Rheumatoid arthritis.
• Constitutional features.
• Overlapping clinical features.
• Overlapping pathologic features.
• Prominent immunologic abnormalities.
Rheumatoid
Arthritis
A chronic systemic inflammatory disease involving synovial joints and occasionally extra-articular manifestations
are present.
EPIDEMIOLOGY
ETIOLOGY
PATHOGENESIS
EXTRA-ARTICULAR MANIFESTATIONS
• Skin: palmar erythema, purpuric eruption, vasculitis, Raynaud's Figure 2.4. Common site for
phenomenon. rheumatoid nodules
• Chest: pleural effusion, pleurisy, pulmonary fibrosis, rheumatoid
nodules.
• Eye: keratoconjunctivitis sicca (Sjogren syndrome in 10%), episcleritis, scleritis, scleromalacia, scleromalacia
perforans.
• Heart: Pericarditis and pericardial effusion (usually asymptomatic).
• Vasculitis:
• May occur in severe and long-standing RA.
• Small vessel vasculitis: nailfold infarct, leg ulcers, purpura.
• Medium vessel vasculitis: large areas of skin necrosis, digital gangrene.
• Nervous system:
• Compression neuropathy e.g. carpal tunnel syndrome.
• Peripheral neuropathy: mild glove and stock sensory impairment.
• Mononeuritis multiplex: occurs as a result of vascultitis.
• Atlanto-axial subluxation, a common finding in x-ray (25%), usually asymptomatic (cervical cord
compression is rare).
• Renal: secondary amyloidosis with proteinuria and nephrotic syndrome.
• Felty syndrome: triad of RA + splenomegaly +
neutropenia. Table 2.1. conditions other than RA with positive
RF.
LABORATORY INVESTIGATIONS Normal Overall 4%
population Elderly 25%
Blood count Other Sjogren syndrome 90%
Rheumatic SLE 35%
• Anemia of chronic disease, iron deficiency diseases Scleroderma 30%
Dermatomyositis 5%
anemia. Other Sarcoidosis
• Leukocytosis. immunologic Cryoglobulinaemia
diseases Transplant recipients
• Neutropenia (Felty syndrome). Chronic HCV 60%
infections TB 15%
Rheumatoid Factor (usually low Bacterial endocarditis 25%
+ve in 85% of RA patients (70% in early RA). titer) Syphilis 10%
Leprosy 10%
• Value of RF: Parasitic: bilharziasis,
malaria
Miscellaneous Neoplasms especially after
radiation and chemotherapy.
11
• Help in diagnosis (one of the criteria for
diagnosis).
• +ve RF does not make diagnosis: as RF
can be found in other conditions (Table
Sites susceptible to
2.1). direct attack by
• -ve RF does not exclude possible RA. pannus
• +ve FR factor indicate bad prognosis.
Synovial Fluid
• Yellow, cloudy, low viscosity, cell count
2000-40000/mm3.
12
• Functional disability at 1 year after start of disease
• Radiographic erosions within the first 2 years from onset.
• HLA-DR4 genetic marker.
To be diagnosed as having RA, a patient must meet 4 or more of the following 7 criteria (Criteria 1,2,3,4 should
present for at least 6 weeks):
1. Morning stiffness in or around joints for at least l hour before maximal improvement.
4. Symmetric arthritis
5. Subcutaneous nodules
13
• Physical: heat therapy, paraffin wax bath, ultra-sound therapy, interferential current and TENS for muscles and
tender points.
• Medical:
• NSAIDs: relief pain and stiffness but have no disease modifying effect.
• Systemic steroids: 5-10 mg daily to achieve symptomatic control as a "bridge therapy" before the onset of
action of DMARDs.
• Local steroid injections: of inflamed tendons, bursae or intra-articular.
• Biologic agents
• Newly developed targeted therapies with rapid onset of action and highly effective for control of disease
activity and prevention of structural joint damage.
• Patients who fail to respond to DMARDs therapy within 6 months should receive a biologic agent (e.g.
tumor necrosis factor [TNF] inhibitors such as etanercept or adalimumab) usually in combination with
MTX or as monotherapy.
• RA patients who fail to respond to an initial biologic agent should be switched to another biologic agent
with a different mode of action.
• Rituximab (monoclonal antibody against the protein CD20, which is primarily found on the surface of
immune system B cells) is typically reserved for seropositive RA patients who have failed one or more
biologic agents including at least one TNF inhibitor.
• Limitations: very high cost and unknown long term consequences.
14
• Static exercise during pain and inflammation.
• Active graduated exercises when pain subsides.
• Passive stretching
• Hydrotherapy
• Ultrasound
• Electric muscle stimulation: faradic stimulation help strengthening weak muscles.
EPIDEMIOLOGY
• Female:male ratio is 9:1
Table 2.3. WHO classification of
• Age: mainly in age of 18-45 years (females in the child glomerulonephritis in SLE
bearing period). WHO Clinical features
classification
CLINICAL FEATURES I. Normal Asymptomatic
glomeruli
Constitutional manifestations
II. Mesangial Low grade hematuria
• Low grade fever. disease or proteinuria
• Anorexia. III. Focal Nephritic urinary
• Malaise. proliferative GN sediment (hematuria,
casts), proteinuria
• Chronic fatigue.
IV. Diffuse Hypertension, variable
Musculoskeletal manifestations proliferative GN renal insufficiency.
• Arthralgia (commonest > 90%). V. Membranous Nephrotic syndrome
nephropathy
• Arthritis (non-erosive).
VI. Sclerosing Inactive urinary
• Joint deformities due to tendon or ligament laxity (joint
nephropathy sediment, azotemia
erosion is uncommon).
• Inflammatory myopathy may cause muscle wasting.
15
• Vasculitis: lesions at finger tips and around nail fold.
• Photosensitivity: skin rash as a result of unusual reaction to sun light.
• Raynaud’s phenomenon.
Renal manifestations
• Common in SLE (> 50%).
• Patients with active lupus nephritis have proteinuria >0.5 gm/day (commonest, may be asymptomatic),
hematuria (microscopic).
• ↑ serum creatinine and BUN.
• Renal biopsy in patients with active urinary sediment to determine type and activity of renal pathology (Table
2.3).
Pulmonary manifestations
• Recurrent pleurisy and pleural effusion (common),
• Pulmonary hypertension (secondary to pulmonary vasculitis).
Cardiac
• Pericarditis with small pericardial effusion (common).
• Myocarditis.
• Coronary artery vasculitis (in severe cases).
• Premature atherosclerosis (especially in patients treated with steroids).
• Non-bacterial endocarditis (Libman sack’s endocartitis).
Gastrointestinal manifestations
• Non-specific symptoms: nausea, vomiting, abdominal pain are frequent.
• Vasculitis of mesenteric vessels bowel ischemia, infarction, perforation.
• Pancreatitis secondary to disease or steroid use.
• Gastritis secondary to NSAIDs or steroids.
Hematological manifestations
• Anemia (of chronic disease, hemolytic)
• Lymphopenia.
• Thrombocytopenia.
• Elevated ESR, normal CRP but raised if secondary infection occurs.
• Coagulation abnormalities:
• Phospholipid antibody (lupus anti co-agulant). Interference with coagulation profile causing prolongation
of the PTT.
16
• However, patients are not prone to bleeding but rather have higher incidence of thrombosis.
• Recurrent 2nd trimester abortion.
Immunological abnormalities
• Low C3 and C4 level reflect activation of immune complex cascade.
• Hyper gammaglobulinaemia due to hyperactivity of B cells.
• Autoantibodies are common:
o ANA are present almost in all SLE patients (patients with –ve ANA are unlikely to have SLE).
o +ve ANA are found in many other conditions (high sensitivity but low specificity).
• Anti-dsDNA: specific to SLE but present in 60% of patients, levels of these antibodies rise with active
disease.
• Anti-Sm: specific for SLE.
• Anti-histone antibodies specific for drug induced lupus.
• Anti-Ro and anti-La antibodies: seen in SLE and Sogren’s Syndrome.
• Antiphospholipid antibodies (40%), but only minority has thrombotic events.
DIAGNOSTIC CRITERIA (SLICC “Systemic Lupus International Collaborating Clinics” 2012 CRITERIA)
Patient must have ≥ 4 criteria (at least 1 clinical and 1 laboratory criteria) or biopsy-proven lupus nephritis with positive
ANA or Anti-DNA:
Clinical Criteria Immunologic Criteria
1- Acute cutaneous lupus 1- ANA
2- Chronic cutaneous lupus 2- Anti-DNA
3- Oral or nasal ulcers 3- Anti-Sm
4-Non-scarring alopecia 4- Antiphospholipid Ab
5- Arhritis 5- Low complement (C3, C4, CH50)
6- Serositis 6- Direct Coombs’ test (do not count in
7- Renal the presence of hemolytic anemia)
8- Neurologic
9- Hemolytic anemia
10- Leukopenia
11- Thrombocytopenia (˂100,000/mm3)
TREATMENT
Treatment should be tailored to the patients findings.
Preventive measures
• Patient education.
• Regular evaluation.
• Assess lupus activity
• Routine investigations
• Control of blood pressure
17
• Control of hyper-lipidemia
• Photoprotection
• Avoid exposure to sun.
• Sun screens
• Pregnancy
• Birth control with active lupus (especially nephritis) and with cytotoxic drugs.
• Infection control.
• Suspect infection whenever there is fever.
• Antibiotic prophylaxis for dental, gynecologic procedures.
• Influenza and pneumococcal immunizations
Mild disease
• NSIADs: for joint pain, fever and mild systemic features e.g. serositis.
• Hydroxyl-chloroquine: for arthritis not controlled by NSAIDS, skin lesions and fatigue.
• Steroids:
• Topical preparations: for skin lesions.
• Low dose steroids (5-10 mg/day).
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3 OSTEOARTHRITIS
Joint symptoms and signs of articular cartilage degeneration, in addition to the related changes in the underlying bone and at
the joint margin.
Classification of OA
• Primary: unknown cause, affect certain joints in old age.
• Secondary (can affect any joint at any age): to
• Local mechanical factors (trauma, menisectomy).
• Joint diseases (RA, septic arthritis).
• Systemic diseases (hyperparathyroidism).
• Congenital anatomical abnormalities (leg discrepancy, scoliosis)
Primary Osteoarthritis
RISK FACTORS
• Age: advancing age loss of glycosamino-glycan leaving unsupported cartilage collagen fibers.
• Genetic: may be present especially in generalized OA.
• Sex: both sexes are affected but generalized OA is
more common in females especially after menopause.
• Obesity: predisposes to knee OA.
• Repeated overload
PATHOLOGY
• Manifested first by fibrillation of the cartilage articular
surface.
• Clefts in the cartilage surface then develop and
eventually loss of the cartilage can be seen.
• Synovial membrane hypertrophy, fibrosis and Figure 3.1. Pathologic changes in OA.
contracture of the capsule.
• Bone changes include: subchondral sclerosis, marginal osteophytes (Figure 3.1)
19
SYMPTOMS
SIGNS
• Swelling due to synovial thickening, effusion or bony swelling.
• Wasting of muscles acting on the affected joints.
• Joint tenderness. Figure 3.2 joints commonly
• Joint crepitus (coarse). affected by OA.
• Deformity e.g. flexion deformity of the knee, genu varum, genu valgum.
INVESTIGATIONS
• Don’t load the joint when it is very painful. Figure 3.3. common radiologic features in OA
20
• Reduction of body weight in obese patients.
• Physiotherapy (heat, cold, electric stimulation, laser, massage and exercise). Benefits of physiotherapy include
• Decrease pain, stiffness, muscle spasm.
• Improve joint range of motion.
• Strengthen peri-articular structures improve joint support.
• Improve blood supply and metabolism.
21
4 GOUT
Disorders of purine metabolism, which are characterized by serum uric acid elevation (hyperuricaemia) and urate deposition
in the articular or extra-articluar tissue (Figure 4.1).
CLASSIFICATION
1. Primary gout (90%): hyperuricemia result from disorders of purine metabolism or abnormal excretion of uric acid.
2. Secondary gout (10%): due to either:
a) Impaired excretion: caused by:
• Chronic renal diseases.
• Drugs (thiazide diuretics, low dose aspirin, cyclosporine and INH).
• Hypertension.
• Lead toxicity.
• Hyperparathyroidism.
• Hypothyroidism.
• Increased lactic acid production (e.g. alcohol, starvation).
• Glucose 6 phosphatase deficiency.
CLINICAL PICTURE
Intercritical gout
• Asymptomatic intervals between acute attacks of gout.
• Some patients never experience 2nd attack.
• With repeated attacks of acute arthritis, the interval between attacks progressively shortens, and finally, joints become
permanently mildly swollen and deformed with mild to moderate persistent pain.
Chronic gout
• Recurrent acute attacks may lead to progressive joint damage, deformity and pain.
22
• Chronic tophaceous gout: large mono-sodium urate crystals
deposits produce firm nodules (tophi), usual sites around extensor
Gout involving
surfaces of fingers, hands, elbows, Achilles tendon and the ear. the 1st MTPj.
Peri-articular
INVESTIGATIONS swelling with
• Evaluation of pateint for causes of secondary gout. ‘punched out’
erosion located
• Fresh synovial fluid examination under polarized light microscope away from the
articular
for presence of urate crystals (diagnostic). Synovial fluid is surface with an
inflammatory in nature with predominance of neutrophils. over-hanging
lip appearance.
• Elevated serum uric acid (not diagnostic): may be normal in 30% of
patients at time of acute attack. A high level alone is not diagnostic
as asymptomatic hyperuricaemia is common
• Blood tests: leucocytosis, raised ESR and CRP (varies with gout
severity).
• Radiologic features (Figure 4.2): Large
tophaceous
• Soft tissue swelling around the affected joint. deposits
• In chronic gout: tophi, punched out erosions with sclerotic margin
and overhanging edge.
TREATMENT
Figure 4.2. Common radiologic features of
Asymptomatic hyperuricemia: no treatment except if
gout.
• Uric acid level > 11 mg/dl
Treatment of acute attack
• NSAIDs in maximum doses.
• Colchicine: 0.5 mg/3 hours for 12 hours.
• Systemic steroids and ACTH: cases with contraindications to NSAIDs and colchicine.
• Effusion in large joints should be aspirated and corticosteroid injected to reduce inflammation.
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− Side effects: rash, vasculitis, agranulocytosis.
− Contraindications: acute gout.
− Concurrent treatment: low dose NSIADs or colchicin for at least 4 months.
• Febuxostat :
− Action: inhibits xanthine oxidase enzyme.
24
5 LOW BACK PAIN
A very common condition affecting 80% of the individuals at some Table 5.1. Red flags for serious diagnosis
point in their life time. in LBP
Alarming (Red flag) Suggested
CAUSES OF LBP symptom/sign serious
diagnosis
• Congenital: e.g. spina bifida, scoliosis. Severe persistent pain Infection,
• Traumatic: e.g. lumbar disc prolapse, fracture of the spine, tears or not changes by position, malignancy
not improved by rest
sprain of spinal ligament and/ or muscle. Fever, chills, weight loss Infection,
• Degenerative: e.g. intervertebral disc (lumbar spondylosis), facet malignancy
Pain worse in walking, spinal stenosis
joint (osteoarthritis), spinal canal stenosis. radiating to lower limbs,
• Postural: e.g. bad posture (sitting, standing), inequality of limb exacerbated by spinal
extension and relieved
length, high heels, pendulous abdomen. by sitting in flexion
• Inflammatory: e.g. ankylosing spondylitis, Reiter's disease, Pain and stiffness > 30 Spondylo-
minutes, worse in the arthropathy
psoriatic arthritis, enteropathic arthritis. morning in young adult
• Infection: e.g. non-specific (osteomyelitis), specific (Pott's disease male
Bilateral radiation of Cauda equina
in TB). pain, Abnormal compression
• Metabolic: e.g. osteoporosis, osteomalacia, Paget's diseases. neurologic findings, (e.g. Central
sensory deficit, bowel/ disc prolapse,
• Neoplasm: benign, malignant (secondaries are more common than bladder dysfunction, rarely cancer)
primaries). saddle anesthesia, +ve
Babiniski, ankle clonus
• Referred (visceral): e.g. peptic ulcer, pancreatitis, pancreatic tumor, Acute severe pain with Fracture
pyelonephritis, aortic aneurysm, peritoneal tumor, pelvic disease. point tenderness, history
of Severe trauma (or
• Psychogenic LBP. even minor trauma in
osteoporosis).
N.B.
Although the most of LBP is mechanical in nature (e.g. disc prolapse, spondylosis, postural), however, the most serious
rare causes must be excluded (Table 5.1).
Mechanical LBP
• Over 95% of LBP.
• Due to anatomic or functional abnormality, without underlying inflammatory or neoplastic diseases.
• Pain increases with physical activity and is released by rest and recumbency.
• Causes:
− Postural (sprain or strain, lumbago, non-specific): 70%.
− Lumbar spondylosis: 10%.
− Disc herniation: 6%.
− Spinal stenosis.
− Spondylolisthesis.
− Diffuse idiopathic skeletal hyperostosis.
− Factures.
25
1. POSTURAL BACK PAIN (STRAIN AND SPRAIN, LUMBAGO)
• Bad posture is probably the most common cause of persistent back pain.
• Correcting bad postural habits may be difficult for a patient to accept and may need re-inforcement through
programs as back school.
2. LUMBAR SPONDYLOSIS
Degenerative joint disease affecting lumbar vertebrae and intervertebral disc causing pain and stiffness, sometimes with
sciatic radiation (L4-5, S1,2,3) due to nerve root pressure by associated osteophytes.
Clinical Features
• Pain: midline, radiating to the region of buttock, occasionally sciatica. Pain worse towards end of the day and often
not aggravated by coughing and sneezing.
• Lumbar morning stiffness, inactivity stiffness.
• Diminished spinal mobility.
• Midline tenderness.
• Sensory and motor neurological signs (if there is root compression by osteophytes).
Radiology
• Narrow disc space.
• Osteophytes.
• Evidence of apophyseal osteoarthritis.
Etiology
Trauma, is usually not a direct one, typically lifting a heavy weight while back unsupported (bending).
Pathology
Back signs
• Diminished or obliterated lumbar lordosis.
26
• Sciatic scoliosis (lateral bending to one side).
• Midline tenderness opposite prolapsed disc.
• Restriction of back movement.
Stretch signs
• +ve straight leg raising test (sciatic stretch):
o The leg is lifted with knee extended. Sciatic roots are tightened over
a herniated disc between 30o and 70o.
o Indicate sciatic compression i.e. lower lumbar disc prolapse (Figure
5.1).
• +ve femoral stretch test:
o The knee is flexed and lifted superiorly. Sharp pain that is generated
in the anterior thigh is considered a positive test.
Figure 5.1. Straight leg raising
o Indicate femoral nerve compression i.e. high lumbar disc prolapse test.
(Figure 5.2).
Neurologic signs
Investigations
Conservative treatment is the main line. Tailored to the specific needs of the individual patient.
• Days to few weeks.
Rest
• Kept to minimum and early mobilization should be encouraged.
• Early referral to physical therapy is essential.
• Positioning:
Instructions
• Sleep on firm matrix avoiding back sagging.
• Setting: increase disc pressure minimize in disc prolapse.
• Standing: avoid prolonged standing.
• Weight reduction.
• Analgesics and NSAIDs: during acute attack, infrequent courses.
Medication
• Muscle relaxants.
• Anticonvulsants.
• Anti-depressants
27
− Local anti-inflammatory effect.
− Decrease pain and muscle spasm.
− Decrease fibrosis and adhesions.
• Exercise program
− Cornerstone of conservative treatment and prevention.
− Benefits:
• Support vertebral column.
• Restore normal curves of the spine.
• Decrease intradiscal pressure.
• Decrease load on facet joints and open intervertebral foramina.
• Restore strength, flexibility, function.
• Reduce pain.
• Traction:
− Help suction of prolapsed disc.
− Stretch vertebral ligaments, support the disc.
Psychogenic LBP
• Psychogenic illness may be manifested as LBP.
• Diagnosis is usually based on:
• Detection of inadequate personality and psychological illness.
• An organic disease is excluded.
• Symptoms usually very diffuse and not follow anatomic distribution.
• The description of pain is exaggerated.
• Patient is usually highly demonstrative, hands used to point out various painful areas.
• No root signs could be detected and patient is hesitating about areas of paraesthesia.
Inflammatory Spondylo-
arthritis
(Inflammatory LBP)
• Spodylo-arthritis include: ankylosing spondylitis, enteropathic arthritis, psoriatic arthritis and reactive arthritis.
28
• The European Spondylo-arthropathy
Figure 5.3. The European Spondyloarthropathy Study Group
Study Group Criteria for Spondylo-
Criteria for Spondyloarthropathy
arthropathy are shown in Table 5.3.
• Characterized by:
N.B. Table 5.2 represent the differences between Inflammatory and mechanical LBP.
Table 5.2. Comparison between the mechanical versus inflammatory back pain.
Mechanical Inflammatory
Example Disc prolapse Ankylosing spondylitis
Onset Acute Insidious
Age Any age Usually < 35 years
Effect of exercise Worsen pain Improve pain
Morning/inactivity stiffness + +++
Pain radiation Anatomical (L4, L5, S1) Diffuse
Sensory/motor deficit + -
Other system is involved - +
Sleep disturbance + +++
Scoliosis + -
Decrease ROM Asymmetric Symmetric
Spinal tenderness Localized Diffuse
Sacroiliac/hip involvement - ±
EPIDEMIOLOGY
• AS occurs in:
29
o 20% of B27 +ve individuals with an affected family member.
• Onset of AS usually begin in late adolescence or early adulthood. Onset after age 45 years is
uncommon
MUSCULOSKELETAL MANIFESTATIONS
Back Pain
• Insidious onset of LBP and/or buttock pain that persists for > 3 months
• Pain awakens the patient from sleep, is accompanied by morning stiffness. Pain and stiffness
typically improve by exercise.
Enthesitis
• In AS, the initial inflammatory process involves the enthesis, followed by a process that results
in new bone formation or fibrosis
Peripheral arthritis
• Typically this is asymmetrical oligo-arthritis affecting leg joints, most commonly the knee.
PHYSICAL EXAMINATION
These tests produce pain in patients with sacroiliac joint disease (Figure 5.4).
30
• Pelvic compression. With the patient lying on one side, compression of the pelvis should elicit
sacroiliac joint pain.
• Gaenslen’s test. With the patient supine, a leg is allowed to drop over the side of the
examination table while the patient draws the other leg toward the chest. This test elicit SIJ pain
on the side of the dropped leg.
• Patrick’s test. With the patient’s heel placed on the opposite knee, downward pressure on the
flexed knee with the hip now in flexion, abduction, and external rotation elicit contralateral SIJ
tenderness.
• Modified Schober test –Detects limitation of forward flexion of the lumbar spine: Place a mark
at the level of the posterior superior iliac spine (dimples of Venus) and another 10 cm above in
the midline. With maximal forward spinal flexion with extended knees, the measured distance
should increase from 10 cm to at least 15 cm.
• Occiput-to-wall test. Assesses loss of cervical range of motion. Normally with the heels and
scapulae touching the wall, the occiput should also touch the wall. Any distance from the
occiput to the wall represents a forward stoop of the neck due to cervical spine involvement
with AS. The tragus to-wall test could also be used.
• Chest expansion. Detects limited chest mobility. Measured at the fourth intercostal space in
men and just below the breasts in women, normal chest expansion is approximately 5 cm. Chest
expansion less than 2.5 cm is abnormal.
EXTRA-MUSCULOSKELETAL MANIFESTATIONS
Ocular inflammation
31
o Typically causes pain, photophobia and, if untreated, impairment in visual acuity.
Cardiopulmonary manifestations
• Pulmonary fibrosis.
DIAGNOSIS
The diagnosis is based on the modified New York criteria (Table 5.3). Radiographic assessment is a
key element of these criteria.
INVESTIGATIONS
x-ray
• SIj - classical changes in the SIjs include erosions in the joint line, pseudo-widening,
subchondral sclerosis and finally ankylosis, reflected as obliteration of the SIJ.
• Spine - may reveal squaring and shiny corners of the vertebral bodies and, later,
syndesmophytes and facet - joint fusion.
MRI
As radiographic sacroiliitis often develops late. Patients without sacroiliitis on plain radiograph
usually have inflammation detected on MRI.
HLA-B27
HLA - B27 is rarely the definitive factor for diagnosis, but when the clinical suspicion is high, the
test has high sensitivity and specificity.
Table 5.3. The modified New York criteria for ankylosing spondylitis (1984)
A. Diagnosis B. Grading
1. Clinical criteria 1. Definite ankylosing spondylitis if the radiologic
a. Low back pain and stiffness >3months with criterion is associated with >1 clinical criterion
improvement on exercise, not relieved by 2. Probable ankylosing spondylitis if:
rest a. the three clinical criteria are present
b. Limitation of spinal motion in both sagittal b. the radiologic criterion is present without any
and frontal planes signs or symptoms satisfying the clinical criteria
c. Limitation of chest expansion
2. Radiologic criteria
Sacroiliitis: Grade >2 bilaterally or Grade 3–4
unilaterally
To diagnose AS: one radiologic criterion + at least one clinical criterion is required
32
Management
2. Physiotherapy.
4. Glucocorticoid:
• Patients with axial disease should not receive long-term treatment with systemic steroid.
6. Biological DMARDs:
7. Surgical treatment:
33
6 OSTEOPOROSIS
OP is a systemic skeletal disease characterized by low bone mass and micro - architectural deterioration of bone tissue
that results in a high risk of fracture.
PATHOPHYSIOLOGY
• The human skeleton is composed of 20% trabecular bone and 80% cortical bone.
• Bone undergoes a continual process of resorption and formation (10% of the adult skeleton is remodeled per year).
• Irreversible bone loss results from imbalance between the rates of resorption and formation.
• Trabecular bone is the more metabolically active type, and osteoporotic fractures are more common at sites that
contain >50% trabecular bone.
• Trabecular thinning and perforation occurs particularly in situations of increased bone turnover, e.g. after the
menopause.
• Post-menopausal estrogen deficiency leads to accelerated bone loss (predominantly loss of trabecular bone).
• This typically results in fractures of vertebral bodies, neck of the femur and distal forearm.
CLASSIFICATION OF OSTEOPOROSIS
• Secondary OP
ASSESSMENT OF OSTEOPOROSIS
- Age
- Sex
34
- Low body mass index (≤19kg/m2)
- Current smoking
- Alcohol intake
2. Plain Radiographs
o The assessment of bone mass on plain radiographs is unreliable. Suspected osteopaenia require confirmation by
bone densitometry prior to any therapeutic decisions.
TREATMENT
The ultimate goal of osteoporosis management is to reduce the future risk of fracture.
I. Lifestyle Modification
• Sun exposure
Vitamin D (800 units daily) and calcium (1000–1200 mg daily) to maintain normal level with all therapies for osteoporosis.
1. Bisphosphonates
35
• Due to poor absorption, these agents must be taken on an empty stomach 1 hour before breakfast or in the
middle of a 4 - hour fast.
2. Denosumab
It is a monoclonal antibody directed against RANK ligand (RANK-L). Activation of RANK by RANKL
promotes the maturation of pre-osteoclasts into osteoclasts. Denosumab inhibits this maturation of
osteoclasts by binding to and inhibiting RANKL and therefore inhibits bone resorption.
• HRT is suitable to control climacteric symptoms, or in women under 50 who have undergone an early
menopause.
• Raloxifene: a synthetic agents has an oestrogen like action on bone and lipids, but without effect on breast
and endometrial tissues (less risk of breast cancer).
4. Calcitonin
• This agent has analgesic properties that may be useful in the acute management of vertebral fracture.
- Expensive agents and their use is limited to patients with severe, progressive osteoporosis despite exposure to
antiresorptive therapy.
V. Pain Relief
o Analgesics
o Physical measures
36
o Eliminate predisposing factors e.g. postural hypotension or drowsiness due to drugs, visual disturbance.
o Provide patients with appropriate walking aids.
o Eliminate hazards e.g. loose rugs and cables from the path of the patients.
VII. Rehabilitation
o Physiotherapy: exercise.
o Occupational therapy.
VIII. Surgery
o Fixation of fracture
o Spinal decompression
37
7 APPROACH TO A PATIENT WITH ARTHRITIS
INFLAMMATORY VERSUS NON-INFLAMMATORY
Inflammatory disorders
Characterized by:
• Systemic symptoms (fever, stiffness, weight loss, fatigue).
• Joint stiffness after prolonged rest (morning stiffness), improves with activity, duration of >1 hour.
• Signs of joint inflammation on physical examination (erythema, warmth, swelling, pain).
• Lab evidence of inflammation (elevated ESR, elevated CRP, hypoalbuminemia, normochromic normocytic
anemia, thrombocytosis).
• Examples: systemic lupus erythematosus, rheumatoid arthritis, reactive arthritis, infectious (gonococcal
arthritis), or crystal induced (gout, pseudogout).
Non-Inflammatory Conditions
Characterized by:
• Absence of systemic symptoms, pain without erythema or warmth, normal lab tests.
• May cause stiffness usually lasting <1 hour
• Joint symptoms increase with use and weight bearing.
• Examples: OA, fibromyalgia, and traumatic conditions.
ARTICULAR VERSUS NON-ARTICULAR
Pain may originate from:
1. Articular structures (synovial membrane, cartilage, intra-articular ligaments, capsule, or juxta-articular bone):
• Cause deep or diffuse pain that worsens with active and passive movement.
• Physical examination may show:
o Deformity
o Warmth
o Swelling (bony swelling or soft tissue swelling)
o Effusion
o Crepitus.
• Synovitis (inflammation of the synovial membrane that covers the joint):
o The joint looks is a boggy, tender and swollen.
o The joint loses its sharp edges on examination.
2. Periarticular structures (bursae, tendons, muscle, bone, nerve, skin).
3. Non-articular structures (i.e., cardiac pain referred to the shoulder).
ARTHRALGIA VERSUS ARTHRITIS
Arthralgia
• Refers to joint pain without abnormalities on joint examination.
Arthritis
• Indicates the presence of abnormality in the joint (warmth, swelling, erythema, tenderness).
38
Approach to Monoarthritis
Acute pain or swelling of a single joint (acute monoarthritis) is an emergency condition and requires immediate
evaluation for septic arthritis that can rapidly destroy the joint if left untreated.
Common causes of mono-arthritis are:
• Infection
• Crystal-induced arthritis
• Trauma.
The history
• Exclude trauma
• Give clues to other diagnoses such as history of tick bite (Lyme disease), sexual risk factors (GC arthritis), Colitis,
uveitis, and urethritis (ReA).
Physical examination
Usually distinguishes between articular and non-articular disorders.
Investigations
• Perform arthrocentesis in patients with acute monoarthritis. Send synovial fluid for:
o Leukocyte count with differential (>2000/mm3 suggest an inflammatory process).
o Gram stain and culture.
o Crystal analysis. A wet mount of the fluid examined under polarizing microscopy may identify crystals, but the
presence of crystals does not exclude infection.
o Culture other potential sources of infection (throat, cervix, rectum, wounds, blood).
• Synovial biopsy and arthroscopy are sometimes used to diagnose chronic mono-arthritis.
• Radiographs are useful in cases of trauma and may show OA or chondrocalcinosis in calcium pyrophosphate
deposition disease.
• A patient with synovial fluid that is highly inflammatory requires empiric antibiotic therapy until the evaluation,
including cultures, is completed.
Approach to Polyarthritis
• Polyarthritis is one of the most common problems in rheumatology.
• The number and pattern of joint involvement suggest the diagnosis.
• History and examination:
o Differentiate polyarthritis from non-articular causes of generalized joint pain.
o Disorders of periarticular structures (tendons, bursae) cause joint pain but usually involve a single
joint.
o Myopathies occasionally cause widespread pain, but muscle weakness is the primary symptom.
o PMR causes shoulder and pelvic girdle pain with morning stiffness, but there is usually no arthritis on
examination; weakness is not a feature of this disease.
• Neuropathies, primary bone diseases (Paget’s disease), and fibromyalgia can also cause widespread pain but are
distinguished by history and physical examination.
39
8 DIFFERENTIAL DIAGNOSIS OF COMMON ARTHROPATHIES
40
Ankylosing • Mostly young males. • RF- ve
spondylitis Axial arthritis • HLA B27 +ve in 95%
• Stiffness and pain in spine and • of cases.
girdle joints (hips and shoulders). • Sacroiliac joint
Iritis in 30% involvement evident in
x- ray.
Enteropathic • Asymmetrical polyarthritis often • Ulcerative colitis or • RF – ve.
arthropathy • associated with relapse of colitis. • Crohn’s disease.
41
9 CAUSES OF POLYARTHRITIS
Cause Characteristics
Rheumatoid arthritis Symmetrical, small and large joints, upper and lower limbs.
Spondylo-arthropathies Asymmetrical, large > small joints, lower > upper limbs, spondylitis,
sacroiliitis.
Juvenile idiopathic Symmetrical, small and large joints, upper and lower limbs
arthritis
Generalized osteoarthritis Very common, Symmetrical, small and large joints, Heberden's nodes, only a
inflammatory
42
Anti-Rheumatic Drugs Mechanism of action
Celecoxib Etodolac
Rofecoxib Lumiracoxib
Meloxicam Valdecoxib
Nimesulide Deracoxib
Paracoxib Etoricoxib
43
Contraindications Physical therapy) which are effective in
treating local pain and inflammation without
• Absolute: Hypersensitivity to drug.
causing side effects of NSAIDs and decreases
• Relative contraindications
the need for them.
• Peptic ulcer.
• Bleeding tendency. Disease Modifying anti-rheumatic
• Bronchial asthma. Drugs (DMARDs)
• Hepatic impairment. Group of drugs used in systemic rheumatic
• Renal impairment. diseases to minimize disease activity and
• Pregnancy and lactation. progression (Table 8).
Precautions for the use of NSAIDs Synonyms
• Do not prescribe NSAIDs when they are not • Specific anti-rheumatic drugs
necessary: in degenerative joint diseases, (no • Slow Acting Anti-Rheumatic Drugs (SAARDs):
evidence of inflammation) simple analgesics their effect takes 4-8 weeks to appear
may do the same function with much less side • 2nd line anti-inflammatory drugs.
effects.
Mechanism of action
• Prescribe one NSAID: combination of two or
more NSAIDs increase side effects with no One or more of the following
better efficacy. • Inhibition of lysosomal enzymes.
• Use NSAIDs at the lowest possible effective • Inhibition of phagocytosis.
dose, never exceed therapeutic dose. • Inhibition of prostaglandins.
• Use NSAIDs for shortest time needed. • Inhibitory effect on immune system
• Select proper group for the patient: response • Reduction of immune complex formation.
to NSAIDs varies from patient to patient • Sulphasalazine has antimicrobial activity.
(individual variation). • Immunosuppressive drugs has anti RNA and
• Beware of high risk patients. anti DNA properties.
• Maintain close supervision.
Biological agents
• Consider the use of other modalities (e.g.
44
(Anticytokine therapy) Muscle Relaxants
Anti-TNF-α • Indicated in conditions associated with muscle
spasm.
• TNF is a major inflammatory mediator in RA
and a potent inducer of IL-1. Colchicine
• TNF-α and IL-1 are considered to be master • In gouty arthritis, sarcoidosis, and familial
cytokines in RA. Mediterranean fever.
• Anti-TNF therapy shows great efficacy in RA
patients. However, it is not effective in all Nerve tonics
patients, nor does it fully control the arthritic • e.g. drugs containing vit B1, B6 and B12 used
process in affected joints of good responders. in diseases associated with neuralgias e.g.
• Indications: RA, spondyloarthropathy, sciatica, brachialgia.
polyarticular JIA.
• Precautions: chest x-ray and tuberculin test Hypouricaemic drugs
(to avoid activation of TB), hepatitis b • Decrease serum uric acid level in chronic gout.
scereening.
Tricyclic antidepressants, gabapentin,
• Examples: etanercept, infliximab, adalimumab
pregabalin
(Table 9).
• Used in fibromyalgia, neuropathic pain.
Anti-IL-1
• E.g. Anakinra: IL-1 receptor antagonist, given
subcutaneously in a dose of 100 mg daily.
• Toxicities include injection-site reactions and
pneumonia.
Anti-IL-6
• Indications: systemic JIA.
• E.g. tocilizumab.
B cell depletion
• Indications: SLE, vasculitis.
• E.g. rituximab.
Miscellaneous Anti-rheumatic Drugs
Etanercept Subcutaneously TNF-α soluble receptor Injection site reaction, upper respiratory
(Enbrel) (TNF-α blocker) infection (URI), development of
25 mg twice weekly antibodies to drug
Adalimumab Subcutaneously TNF-α blocker URIs, injection site pain, headache, rash,
(Humira) sinusitis, autoantibodies
40 mg every 2 weeks
45
Physical Therapy and Rehabilitation • LMNL e.g. Bell's palsy, neuropathy.
• UMNL e.g. hemiplegia, paraplegia,
Rehabilitation monoplegia.
Rehabilitation means the restoration of the • Post-operative e.g. laminectomy, repair of
maximum possible function of an organ or part of nerve lesions.
the body. 3. Pediatric conditions
The rehabilitation program is individualized • Erb's palsy
according to patient needs. This requires proper • Torticollis
evaluation. • Cerebral palsy
• Spina bifida
Rehabilitation program include:
4. Orthopedic conditions
• Rest: during active stages and acute • Post-plaster stiffness of joints.
exacerbations. The amount and type of rest • Correction of deformities.
vary with joint involvement and severity of
the disease. 5. Sports injuries
• Medical treatment: according to the cause of • Sprains, tears etc.
the disease. 6. Gynecologic conditions
• Physical therapy. • Short wave diathermy in pelvic tubal
• Splints and walking aids. adhesions (in infertility).
• Surgical treatment when indicated. • Post-partum abdominal muscle weakness.
7. Others
Physical Therapy
• Cardiac rehabilitation.
It is the use of physical agents in treatment of the • Respiratory rehabilitation.
musculoskeletal disorders. • Rehabilitation of peripheral vascular diseases.
• Geriatric rehabilitation.
Various forms of physical agents play an
important role in the treatment of Forms of physical therapy
musculoskeletal disorders • Heat therapy.
Physiotherapy may be prescribed alone or in • Cold therapy.
conjunction with medical and other measures to • Electrotherapy.
get therapeutic benefits without the hazardous • Exercise therapy.
effect of the anti-inflammatory drugs. • Massage.
• Others e.g. traction, suspension, laser etc.
Therapeutic benefits
• Relief of pain and stiffness. Cold Therapy
• Relief of muscle spasm The external use of cooling for therapeutic
• Restoration of movement. purposes.
• Increase muscle strength.
• Prevent deformity. Forms
• Restoration of maximal functional capacity. • Various forms of ice
Indications • Frozen gel packs
Therapeutic effects
1. Rheumatic conditions
• Osteoarthritis. • Sedative effects on sensory nerves pain
• Rheumatoid arthritis. relief.
• Cervical spondylosis and disc prolapse. • Reduction of spasticity and spasm.
• Lumbar spondylosis and disc prolapse. • Vasoconstriction of blood vessels which
• Joint pain or stiffness e.g. frozen shoulder reduce swelling and bleeding (used in
syndrome. mechanical trauma).
• Soft tissue rheumatism e.g. tendinitis, bursitis. • Cryotherapy improves inflammation, more
• Sciatica. effectively in the acute phase than in the
chronic phase.
2. Neurologic and neurosurgical conditions
46
Heat Therapy • Training of new muscle action after tendon
transplantation.
Forms of heat therapy • Analgesic effect: low frequency current for
Superficial heat stimulating afferent sensory component of
• For heating of superficial tissues (at a depth of peripheral nerves for relief of pain (acute or
about 0.5 cm beneath the skin) e.g. superficial chronic) e.g. back pain, neck pain, OA, RA,
ligaments, small joints, tendons, muscles. neuralgia.
• e.g. infra-red rays
Exercise therapy
Deep heat
Passive exercise
• For heating superficial and deep structures at
a depth may reach 5 cm under the skin e.g. • Accomplished only by therapist or apparatus
large joints, bulky muscles. • Used to maintain body mobility and prevent
• e.g. short wave diathermy, ultrasonic waves, contracture when muscles are weak.
microwave.
Active exercise
Therapeutic effects
Active assistive:
1. Anti-inflammatory effects
• Accomplished by active contraction by the
Dilatation of arterioles and capillaries patient with the assistance of the therapist or
increase blood flow increase O2 supply, mechanical devices
food stuffs, antibiotics, WBCs removal of • Used as first step in the muscle re-education
waste products resolution of inflammation for weak muscles.
and healing.
Active exercise
2. Analgesic effect
• Accomplished by patient without assistance
Application of heat to peripheral nerves • Used to improve function and strength.
increase pain threshold in the area supplied
Active resisted
by the nerve without affecting the motor
function. • Accomplished by the patient with various
additional resistance either manual or
3. Effect on muscles
mechanical depending on the muscle power.
Muscle relaxation, decrease muscle spasm. • Used to develop muscle power
4. Mechanical effect Stretching
The to-and-fro movements of the ultrasound • Accomplished by forced motion to restore
waves through the tissue particles causing normal range of motion which is limited due
micro-massage which soften adhesions to loss of elasticity of soft tissues.
5. Biologic effect of US and laser Massage
Stimulate growth of tissue tissue repair and Therapeutic effects
healing (e.g. ulcers and bed sores).
• Assists blood and lymph drainage
Electrotherapy swelling.
Forms • Decrease adhesions between muscle fibers.
• Decrease pain sensation.
• Faradic current • Muscle relaxation.
• Galvanic current
• TENS Spinal Traction
47
Techniques • Widen the intervertebral foramina relief
• Manual: force applied by therapist hands. root compression
Used in cervical traction only (Figure 15). • Separate apophyseal joints relief of pain
• Mechanical: administered using pulley and following degenerative joint space narrowing.
free weight system (Figure 15).
Splints
• Motorized: mechanical traction applied by
Aim and types
motorized system, administered in continuous
• Rest splints
or intermittent periods.
Rest and relief from pain for active joints
• Gravity: hanging upside down. • Corrective splint.
• Auto-traction: uses specially designed device Prevention and correction of deformities.
b
Figure 15: Motorized Traction (a) cervical
motorized traction and (b) lumbar motorized
traction.
Therapeutic effects
• Prolonged pull on the muscle may lead to
paraspinal muscle fatigue which alleviates
muscle spasm.
• Enlarge the intervertebral space leading to
retraction of herniated disc material.
• Tighten the posterior longitudinal ligament to
exert a centripetal force on the annulus
fibrosis.
48
Clinical signs
Testing for swelling.
The bulge sign in the knee: The
back of the hand gently pushes
the fluid from one side of the
knee to the other, filling out the
“dimples” on either side of the
patella. This is most helpful in
detecting small knee effusions.
Rheumatoid nodules in a
patient with rheumatoid
arthritis
49
Boutonniere deformity.
PIP flexion and DIP
hyperextension.
50
Nailfold infarcts due to
vasculitis in a patient with
rheumatoid arthritis
51
Classic discoid lupus
erythematosus of the face.
Note central scarring and
erythematous hyperkeratotic
borders.
52
Large tophi involving the distal
interphalangeal joints are
commonly seen in gouty
patients. This is particularly
characteristic of late-onset
gout.
53
Hand orthoses may decrease
pain and correct deformities.
From top to bottom: a resting
splint that restricts motion and
maintains a functional position,
a functional wrist splint that
supports the wrist during hand
activities, and a silver ring splint
that corrects and/or prevents
deformities.
54
MCQ Which has the most specificity for the disease
matched?
Which of the following is most specific for SLE?
a) Anti-Ro (SS-A) – Sjögren’s
a) Anti-Sm
b) ANA – SLE
b) anti Jo 1
c) Anti-Sm – SLE
c) ANA
d) Rheumatoid factor – Rheumatoid arthritis
d) Anti-La
e) Anticentromere
Which of the following is the most sensitive to
differentiate RA from SLE?
Q2:A 25 year old woman in her first pregnancy is
concerned about her sister’s history of a child that
a) Rheumatoid factor
died in the neonatal period with complete heart
b) Keratoconjunctivis sicca
block. Best choice of investigations for this
c) Bilateral knee effusions
woman?
d) Nodules over the MCP joint
a) ANA
e) Erosion of the ulnar styloid
b) Anti La (SSB) antibodies
c) Anti-phospholipid antibodies
Female patient with rheumatoid arthritis and
d) Anti-cardiolipin antibodies
occipital headaches. Next Investigation should be
e) Anti DNA
a) CT of neck
b) Lateral flexion X-ray of cervical spine
Which of the following is not included in the
c) ESR
American College of Rheumatology (ACR)
d) Myelogram
diagnostic criteria for SLE?
e) Anti-CCP
a) Thrombocytopenia
b) Elevated ANA antibody titre
Uric acid excretion is
c) Psychosis
a) increased by low dose aspirin
d) Alopecia
b) decreased in leukemia
e) Photosensitivity
c) Increased in hypertension
d) increased by alcohol consumption
A disproportionate rise in CRP compared to the
e) largely unaffected by Indomethacin
ESR is typically found in which of the following
clinical situations?
A 26-year-old woman attended the early arthritis
a) RA
clinic with a 3-month history of an inflammatory
b) Sepsis in a patient with SLE
polyarthritis affecting her hands and feet.
c) Gout
Investigations: haemoglobin 125 g/L (115–165),
d) Cerebral lupus
white cell count 7.3 x 109/L (4.0–11.0), platelet
e) Felty's syndrome
count 350 x 109/L (150–400), ESR 40 mm/1st h
(<20), X-rays of hands and wrists periarticular
A patient has mild SLE with butterfly rash &
osteopenia. What investigation is most likely to
Arthralgia. ESR ↑, ANA +ve, renal function
distinguish between persistent and self-limiting
normal, platelets mildly ↓. What is the best
arthritis?
treatment?
a) Anti-citrullinated peptide antigen antibodies
a) Prednisone
b) Antinuclear antibodies
b) Hydroxychloroquine
c) IgA rheumatoid factor
c) NSAID
d) IgG rheumatoid factor
d) Cyclophosphamide
e) IgM rheumatoid factor
e) Observe
Which of the following is not a feature in
Which of the following has the least prognostic
rheumatoid hand
value in early RA?
a) Wasting of small muscles of the hand
a) C-reactive protein
b) Tenosynovitis
b) Extra-articular affection
c) Heberden's nodules.
c) Radiographic evidence of erosions
d) Swan neck deformity
d) Decreased peripheral lymphocyte count
e) Z shaped thumb
55
Which of the following articular regions are Regarding rheumatoid factor, which of the
unlikely to be involved in rheumatoid arthritis following is not true?
a) Distal interphalangeal joints a) May be present in the absence of rheumatoid
b) Proximal interphalangeal joints arthritis.
c) Metaocarpophalangeal joints b) High titer early in rheumatoid arthritis
d) Knee joints indicate bad prognosis.
e) Wrist joints c) Usually present in rheumatoid patients with
subcutaneous nodules
Which of the following radiologic appearance is d) Absent in normal population
not associated with in rheumatoid arthritis e) One of the criteria of diagnosis of rheumatoid
a) Marginal erosions. arthritis.
b) Juxtaarticular osteoporosis.
c) Increased joint space Which of the following is most specific for
d) Subluxation rheumatoid arthritis
e) Soft tissue swelling a) Rheumatoid factor
b) Anti CCP
Regarding systemic lupus erythematosus, which of c) Anti ds DNA
the following is true? d) Anti Sm
a) It is commoner in males. e) Anti Ro
b) Phtotsensitivity may occur
c) Complement level C3 and C4 are increased The following is associated with poor prognosis in
d) Erosion is common in plain x-ray rheumatoid arthritis except
e) Antinuclear antibodies are usually negative a) Acute onset
b) Bone erosion on x-ray
The following is not a clinical feature of SLE c) Subcutaneous nodules
a) Depression d) Low ESR
b) Alopecia e) Extraarticular manifestations
c) Pleural effusions
d) Extraarticular nodules. Chloroquine
e) Arthralgia a) Used in treatment of osteoarthriris
b) May cause retinopathy
Hyperuricaemia may result from low dose of c) May cause hyperuricaemia
a) Methotrexate d) Contraindicated in rheumatoid arthritis
b) Aspirin e) 2nd line treatment of osteoarthritis
c) Corticosteroids
d) Anti-TNF α agents The following is not a feature of Felty's syndrome
e) Indomethacin a) Associated with rheumatoid arthritis
b) Splenomegaly
The following drug is used in acute gout c) Dry eye and mouth
a) Aspirin d) Neutropenia
b) Probenecid e) Rheumatoid factor is usually positive
c) Allopurinol
d) Colchicine Which of the following is not a feature of
e) Methotrexate osteoarthritis
a) Heberden's nodes
Gout b) Osteophyte formation
a) Is associated with calcium pyrophosphate c) Bouchard's nodes
crystals deposited in the cartilage. d) Raised ESR.
b) May cause subcutaneous nodules. e) Morning stiffness < 1 hour.
c) Commonly affect 1st metacarpophalangeal
joint. Regarding rheumatoid arthritis, which of the
d) Typically has symmetric polyarthritis pattern following is not true?
e) Associated with HLA-DR a) Commoner in females
b) Associated with HLA-DR
56
c) Insidious onset indicate bad prognosis Regarding therapeutic cold, which of the following
d) Corticosteroids in high doses is a mainstay of is not true?
the treatment a) Has sedative effect on sensory nerves
e) Pregnancy usually associated with disease b) increase spasticity
remission c) Reduce swelling
d) Reduce bleeding
Which of the following is not a side effect of e) Used in mechanical trauma
NSAIDs
a) Long term use may enhance joint Forced motion used to restore normal range of
degeneration process. motion which is limited due to loss of elasticity of
b) Headache soft tissues
c) Peptic ulcer a) Passive exercise
d) Retinal damage b) Active assistive exercise
e) Transient elevation of liver enzymes c) Active resisted exercise
d) Stretch exercise
The following may exacerbate systemic lupus e) Traction
erythematosus
a) Low dose aspirin Patient with osteoarthritis is advised to
b) Exposure to the sun a) Sit too long in one position.
c) High purine diet b) Use low chairs.
d) Prednisolone c) Walk for long periods.
e) Alcohol d) Over exercise the affected joints.
e) Reduce his body weight.
Regarding sjogren's syndrome:
a) Associated with systemic lupus As regards physical therapy, which of the
erythematosus. following is not true?
b) Associated with dry eye and mouth a) It is the use of physical agents in treatment of
c) Associated with Anti-Sm in most patients the musculoskeletal disorders.
d) Associated with high serum uric acid b) Heat and cold are forms of physical therapy
e) Osteophyte is a common finding in x-ray agents
c) Has no rule in female infertility
Sulphasalazine d) Good alternative that reduce hazards of
a) Is ineffective in RA. NSAIDs
b) Is effective in osteoarthritis e) Have a role in sports injuries
c) May cause infertility in male
d) May cause neutrophilia Splints are not used to
e) Is the first drug of choice in chronic gout a) Relief pain for active joints
b) Prevent deformities
Regarding osteoarthritis c) Correct deformities.
a) Knee joint affection is rare d) Place of damaged joint in good functional
b) Tophi are common findings position.
c) There is articular cartilage destruction e) Produce separation of the vertebrae
d) Obesity is a risk factor
e) Methotrexate is effective Red flags for low back pain include the following
except
Therapeutic heat a) Bilateral radiation of pain
a) Produce capillary and arteriolar b) Bowel or bladder dysfunction
vasoconstriction c) Saddle anesthesia
b) Decrease pain threshold d) Positive stretch test
c) Increase muscle spasm e) Pain and stiffness > 30 minutes,
d) Used in muscle re education
e) Has analgesic effect
f) Stretch adhesions in among muscle fibers
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