PAINFUL CONDTIONS
From the annual Family Practice Review, sponsored by the Temple University School of Medicine, Philadelphia, PA
| INFLAMMATORY MYOPATHIES —Steven N. Berney, MD, Professor of Medicine, and Chief, Section of Rheumatology,
Temple University School of Medicine, Philadelphia, PA
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| Inflammatory myopathies: cause unknown; clinical expression result of muscle injury; muscle weakness confined
primarily to proximal areas; patients have difficulty rising from chair and reaching, but have strong grip; inflammation
major pathologic feature; subtypes—polymyositis; dermatomyositis; diagnosis of inclusion body myositis depends
on pathologic findings; childhood myositis; muscle weakness and inflammation with malignancy; overlap syndromes
(eg, inflammatory myositis in patients with lupus)
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| Patient history: assess joint symptoms; Raynaud’s phenomenon—skin color changes of extremities exposed to cold;
eg, with exposure to cold, hands turn white, then blue (cyanotic), become red upon rewarming, and return to normal;
check rash and skin texture changes to identify dermatomyositis and to rule out scleroderma (leathery thick skin); difficulty
swallowing; sensation of food stuck in throat; coughing while eating; aspiration (consider pulmonary involvement);
other visceral abnormalities uncommon; alcohol and drug use; vigorous physical activity; arthritis and
arthralgias accompanying feature in 25% to 50% of patients; nondeforming arthropathy; typical rheumatoid distribution
(ie, affects small joints symmetrically); no abnormalities on imaging studies
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| Skin abnormalities in dermatomyositis: rashes; Gottron’s papules and heliotrope rash (violaceous discoloration
of upper eyelids) pathognomonic for dermatomyositis; photosensitivity; V-shaped rash along upper thorax; shawl
sign; mechanic’s hands (cracked roughened hands); panniculitis—vague pain syndrome; superficial tenderness along
skin with inflamed adipose tissue; patients complain of abdominal pain; calcinosis (calcium deposition in skin); amyopathic
dermatomyositis—typical skin findings without evidence of muscle inflammation
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| Gastrointestinal (GI) involvement: 50% to 60% of patients complain of difficulty swallowing; nasal regurgitation;
coughing with swallowing; aspiration (some patients have aspiration pneumonia); lower two thirds of esophagus
involved in patients with scleroderma and dysphagia, upper third in patients with dermatomyositis or polymyositis;
verify with videofluoroscopy (remind radiographer to use water-soluble radiocontrast in patients with suspected inflammatory
myositis with dysphagia)
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| Pulmonary involvement: acute alveolitis; diaphragm weakness; aspiration; infection (eg, pneumonitis); interstitial
fibrosis end stage of dermatomyositis; methotrexate-induced pulmonary toxicity rare; high-resolution computed tomography
(CT) of chest most useful imaging study for diagnosis
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| Cardiac involvement: electrocardiographic abnormalities; diastolic dysfunction; myocarditis; heart block
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| Polymyositis: autoimmune systemic disorder; inflammation, injury, and weakness of proximal muscles; muscle enzymes
elevated; extramyopathic features
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| Diagnosis of myositis: creatinine kinase (CK) or creatinine phosphokinase (CPK) and aldolase; transaminases and
lactic dehydrogenase (LDH) may be elevated; antinuclear antibody (ANA; sensitive, but specificity low) usually positive;
myositis-specific autoantibodies (eg, antisynthetase antibody [Anti-Jo1]); magnetic resonance imaging (MRI) useful
for identifying muscle edema; unilateral electromyography (EMG) shows evidence of myopathic process; muscle
biopsy
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| Differential diagnosis of myositis: use of cholesterol-lowering agents; alcohol or cocaine abuse; endocrinopathies;
infections (eg, hepatitis C with associated cryoglobulinemia); trauma; neurologic abnormalities
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| Treatment: corticosteroids mainstay of treatment; dosage variable (40-100 mg daily); patient should respond quickly;
if patient fails to respond, add methotrexate or azathioprine; when lowering corticosteroids, go slow and consider potential
for side effects; immunosuppressants; intravenous (IV) immunoglobulin; biologic agents
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| GOUT —Marlin E. Wenger, MD, Clinical Assistant Professor of Medicine, Temple University School of Medicine,
Philadelphia, PA, and Staff Rheumatologist, Lancaster General Hospital, Lancaster, PA
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| Gout: incidence increasing; more common in men; clinical syndrome resulting from deposition of urate crystals in tissues
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| Hyperuricemia: 90% of problem due to underexcretion of urate, 10% due to overproduction of uric acid; contributing
factors—alcohol use; rare inherited disorders (eg, uric acid renal stones) in patients 20 to 30 yr of age with gout;
psoriasis; sickle cell anemia and hemolytic anemia; genetic idiopathic problem; renal insufficiency; thiazide diuretics;
cyclosporine; low-dose aspirin; premenopausal women have ≈1 mg/dL less urate than men; physiologic point at which
urate crystal becomes insoluble ≈6.8 mg/dL; hyperuricemia defined by 2 SDs beyond mean (eg, 7.8-8.5 mg/dL); more
common in postmenopausal women; higher uric acid indicates higher likelihood of developing gout
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| Development of gout: acute hyperuricemic silent phase—may last 4 to 20 yr before presentation of acute flare; hyperuricemia
can result in deposition of urates in medulla of kidney and papillary tissues, resulting in nephropathy or
gouty stones; ischemic heart disease, hypertension, and metabolic syndrome may be associated with prolonged hyperuricemia;
acute phase—acute attack of gout with remission within several days; returns in 2 to 3 yr; attacks become
stronger and closer together with time; advanced gout—tophaceous gout phase; persistent joint disease with acute
flares; involvement of upper extremities
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| Acute gouty arthritis: onset sudden, often at night; ≥50% of initial attacks occur in first metatarsophalangeal (MTP)
joint (podagra); can occur in midfoot, knee, wrist, and fingers; usually initially monoarticular, but can become polyarticular;
subsides spontaneously; look for uric acid crystals in synovial fluid; hyperuricemia may not be present; infection
main differential diagnosis; palindromic rheumatism—episodes of painful rheumatoid arthritis in major joint
lasting few days and returning in few weeks; bursa in elbow common site for gout (could be rheumatoid joint; check
for rheumatoid factor positivity); diagnosis of gouty arthritis based on urate crystals in synovial fluid
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| Treatment of gout: nonsteroidal anti-inflammatory drugs (NSAIDs); indomethacin (Indocin), naproxen (Naprosyn),
and sulindac approved by Food and Drug Administration (FDA); cyclooxygenase (COX)-II inhibitors (contraindicated
in elderly due to renal insufficiency; use corticosteroids); 5 to 15 mg daily of oral steroids (increase to 40-60 mg
daily in patients treated with cyclosporine); do not use allopurinol or probenecid before controlling acute attack;
colchicine—3 to 4 doses 1 to 2 hr apart and taper over week; maintain with 0.6 mg daily and introduce urate-lowering
drug; can lead to nausea, vomiting, diarrhea, bone marrow suppression, and myeloneuropathy; use small doses
(eg, 0.6 mg daily every second or third day) in patients with renal insufficiency; avoid IV colchicine; probenecid—
ineffective when creatinine clearance <50 mL/min; start low and gradually increase over 1 to 2 wk; target urate level
6.0 mg/dL; risk for urolithiasis; allopurinol—can be used to treat overproduction and renal urate underproduction;
adjust dose based on creatinine clearance; safe medication
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| COMMON KNEE INJURIES —William R. Vollmar, MD, Chief of Sports Medicine, Family Practice Residency Program,
Lancaster General Hospital, Lancaster, PA
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| Acute knee injuries: positive hemarthrosis—swelling of knee with blood; caused by fracture, ligament tear, or meniscal
tear; negative hemarthrosis—intra-articular swelling occurs over longer time; caused by sprains, traumatic
synovitis, contusions, muscle tears or pulls, and flares of degenerative joint disease (DJD)
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| Patient history: acute injury—look for immediate swelling; patient often unable to bear weight or walk; knee locks
or gives way (common in cartilage or meniscal tears); pop heard or felt during injury; limited range of motion most
sensitive test for cartilage tears; chronic injury—knee stiff during morning, improves with activity, and hurts with
excessive activity; jumping or plyometric forces more bothersome than low-level continuous forces (suggests tendonitis
or biomechanic issue); knee develops true effusion (ie, intra-articular effusion) or periarticular effusion (eg, peripatellar
swelling); intra-articular swelling suggest synovitis and DJD; extra-articular swelling suggests patellofemoral
pain and tendonitis; pain with ascending stairs (consider tendonitis or DJD); pain with descending stairs (consider patellofemoral
pain or biomechanic problem); lateral motion more bothersome than forward motion (suggests iliotibial
[IT] band pain or pes anserine bursitis); pain wakes patient up during night (requires immediate x-ray); patient grew
>4 in in last year or gained 2 shoe sizes in last 6 mo
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| Training issues in overuse injuries: recent change in duration or intensity of exercise; change in shoes or surface
for physical activity; replace shoes at least every 6 mo; warming up (eg, stretching) decreases risk for injury; nutritional
habits
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| Imaging studies: not all knee injuries require radiography; observe knee; examination for overuse injuries nonspecific,
unless testing for IT band or patellofemoral pain; if needed, anteroposterior (AP) and lateral films first step; for
patellofemoral pain, sunrise and notch views may be needed; perform image studies of overuse injuries only after 4 to
6 wk of treatment failure; not all knee pain originates from knee (arthritic pain can originate from hip or femur); obtain
plain films before performing MRI; bone scanning usually not useful (stress fractures around knee uncommon); ultrasonography
of posterior fossa can find Baker’s cyst, popliteal aneurysm, and deep vein thrombosis (DVT)
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| Patellofemoral pain: result of poor patellar tracking in femoral groove; more common in women because of wider
female pelvis; often seen with femoral anteversion; strengthen vastus medialis obliquus (VMO) with terminal extension
exercises; biomechanic evaluation (femoral anteversion may be corrected with custom orthotics in patients with
pronated foot)
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| Apophysitis: traction injury; tenderness over tibial tuberosity (Osgood-Schlatter disease) or inferior patellar pole
(Sinding-Larsen-Johansson disease); patient history of >4 in of growth in 1 yr or increase in >2 shoe sizes in 6 mo
common; common in younger girls (10-13 yr of age) and adolescent boys (12-16 yr of age); treatment conservative
(ie, relative rest, ice, anti-inflammatory drugs, patellar strap [strap around leg and over patellar tendon used to decrease
tension to tuberosity; no supportive data])
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| Tendonitis: diagnosed by patient history and physical examination; stiffness during morning improves with activity
and becomes bothersome with overuse; conservative treatment; corticosteroid injection around large tendons discouraged;
evaluate biomechanics and ask about training habits
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| Bursitis: stiffness during morning improves with activity and becomes bothersome with overuse; prepatellar
bursitis—may require aspiration or injection; infected 50% of time (pretreat with cephalexin [Keflex])
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| Synovitis: more common in older athletes; usually responds to conservative treatment; aspiration often helpful for diagnosis;
if not infected, steroid injection helpful
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| IT band syndrome: usually presents in athletes during side-to-side motion; running on same side of road can create
artificial leg length discrepancy and cause irritation to knee; differentiating from lateral collateral ligament (LCL)
pain—1) while patient on side abducting leg in extension at knee, hold lower leg and ask patient to push with resistance;
ask patient to flex knee 15º to 20º and repeat; IT band pain occurs when patient resists abduction with slight
flexion of knee; 2) Ober’s test; while patient on side, bend knee 90º and gently pull backwards behind other leg; see
whether knee can touch table; stretching tight IT bands helpful
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| Baker’s cyst: forms on weakened posterior side of joint capsule; usually associated with degenerative changes; filling
of popliteal fossa greatest problem; treat conservatively; aspiration and injection reasonable, but “remember popliteal
nerve, artery, and vein are sitting right there where you’re placing your needle”; surgical intervention only when lower
leg shows neurovascular compromise
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| Conservative measures: ice; NSAIDs; relative rest (“50/50 rule” [perform 50% of activity at 50% intensity]); cross
training; when conservative measures fail, consider biomechanic issues
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| Basic biomechanics: observe patient walk and run while barefoot and in running shoes; look for smooth motion in
heel strike to toe-off and in lines of legs and hips; identify abrupt motions or unilateral changes; watch feet from heel
strike, midstance, and toe-off; observe ankle and midfoot for increased or abnormal pronation (ie, middle of foot heads
towards ground with standing or walking); measure leg length from anterior superior iliac spine (ASIS) to medial malleolus
and from umbilicus to medial malleolus
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| General treatment: “if it ain’t broke, don’t fix it”; never use bracing or orthotics when problem can be improved
with strengthening or proprioception; only correct half of difference of any deficit found on initial evaluation (eg, if
one leg shorter by 1.0 cm, correct by 0.5 cm); allow adequate time for results
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Educational Objectives
| The goal of this program is to educate the listener about inflammatory myopathies, gout, and common knee injuries. After
hearing and assimilating this program, the participant will be better able to:
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 | 1. Identify signs of dermatomyositis and polymyositis.
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| 2. List contributing factors to hyperuricemia.
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| 3. Describe development of acute gouty arthritis.
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| 4. Identify causes of acute or chronic knee pain based on patient history and physical examination.
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| 5. Consider conservative treatment and biomechanics for management of knee pain.
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Discussed on This Program
Allopurinol [Aloprim, Zyloprim]
Colchicine
Indomethacin [Indocin, Indocin SR, Indomethacin SR, Indomethacin Extended-Release]
Naproxen [Aleve, Anaprox, Anaprox DS, EC-Naprosyn, Naprosyn, Naprelan]
Probenecid
Sulindac [Clinoril]
Suggested Reading
Baer AN: Differential diagnosis of idiopathic inflammatory myopathies. Curr Rheumatol Rep 8:178, 2006; Drabicki
RR et al: Stress fractures around the knee. Clin Sports Med 25:105, 2006; Ebell MH: A tool for evaluating patients
with knee injury. Fam Pract Manag 12:67, 2005; Khanna D et al: An unusual presentation of polyarticular tophaceous
gout. Rheumatology (Oxford) 45:1095, 2006; MacLean C et al: Influence of a custom foot orthotic intervention
on lower extremity dynamics in healthy runners. Clin Biomech (Bristol, Avon) 21:623, 2006; Peers KH et al:
Patellar tendinopathy in athletes: current diagnostic and therapeutic recommendations. Sports Med 35:71, 2005; Rao S
et al: Fine needle aspiration of tophi in asymptomatic gout--a case report. Indian J Pathol Microbiol 49:244, 2006;
Rennie WJ et al: Pes anserine bursitis: incidence in symptomatic knees and clinical presentation. Skeletal Radiol
34:395, 2005; Rothenberg MH et al: Evaluation of acute knee injuries. Postgrad Med 93:75, 1993; Targoff IN:
Myositis specific autoantibodies. Curr Rheumatol Rep 8:196, 2006; Thompson TL et al: Massive prepatellar bursa.
J Natl Med Assoc 98:90, 2006; Watura R et al: Magnetic resonance imaging of the knee: direct access for general
practitioners. BMJ 311:1614, 1995; Ytterberg SR: Treatment of refractory polymyositis and dermatomyositis. Curr
Rheumatol Rep 8:167, 2006; Zhang Y et al: Alcohol consumption as a trigger of recurrent gout attacks. Am J Med
119:800, 2006.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the
faculty reported nothing to disclose.
Drs. Berney, Wenger, and Vollmar spoke in Lancaster, PA, at the 30th Annual Spring Family Practice Review, presented
March 26-31, 2006, by the Temple University School of Medicine and Lancaster General Hospital. The Audio-
Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.
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