Post on 01-Jul-2015
description
transcript
Aches and Pains: The Health Concerns of the
Aging Population
Allan D. Corpuz
Fellow, section of Rheumatology
All over the world, We have an aging population
h"p://rt.com/business/aging-‐popula6on-‐elderly-‐double-‐2050-‐904/
Better health care has resulted in better survival
At what cost?
AGE-RELATED health PROBLEMS ARE ON THE RISE
overview • Low Back Pain • Osteoarthritis • Soft Tissue Rheumatisms
LOW BACK PAIN
Epidemiology
• 65-80%: during entire lifetime • Most prevalent chronic pain
syndrome • Leading cause of limitation: <45 y/
o • 2nd most frequent reason for MD
visit • 3rd most common surgical
indication
Epidemiology
• Pain and function improve substantially within 1 month
• >90% are better at 8 weeks (but are susceptible to future brief relapses)
• 7-10% chronic LBP
• Risk Factors – Heredity – Psychosocial factors – Heavy lifting – Obesity – Pregnancy – Weaker trunk strength – Cigarette smoking
• Persistent disabling LBP – Maladaptive pain coping behavior – Non-organic signs – Functional impairment – Poor general health status – Psychiatric comorbidities
ANATOMY
ANATOMY
HISTORY AND PHYSICAL EXAMINATION
CLINICAL EVALUATION
HISTORY • Identify those with neural compression or
underlying systemic disease (<5%) • Look for “Red Flags” • Look for social or psychologic distress – Job dissatisfaction – Pursuit of disability compensation – Depression
RED FLAGS
HISTORY MECHANICAL LBP INFLAMMATORY LBP
>95% Less common
Usually seen in elderly people, postmenopausal women
Seen in men <40y/o (sPA)
Typically increases with physical ac6vity and upright posture
Marked morning s6ffness >30mins Worse during 2nd half of the night
Alterna6ng bu"ock pain
Relieved by rest and recumbency Improves with exercise but not rest
Most common cause is degenera6ve change in the LS
Spondyloarthri6des
PHYSICAL EXAMINATION
INSPECTION Scoliosis; Spina bifida occulta; muscle atrophy
PALPATION Paravertebral muscle spasm (loss of normal lumbar lordosis); Fibromyalgia (widespread tender points) Spondylolisthesis (palpable step-‐off b/n adjacent spinous processes) ROM: -‐Limited spinal mo6on (flexion, extension, lateral bending, rota6on): more useful for Tx monitoring -‐Chest expansion <2.5cm (AS) -‐Tenderness over greater trochanter of femur (trochanteric bursi6s) –Decreased ROM hip (hip OA)
PERRCUSSION Point tenderness over spine (Sensi6ve but not specific for Vertebral OM
AUSCULTATION Bruits (AAA)
PHYSICAL EXAMINATION
PHYSICAL EXAMINATION
• Litigation or with psychologic distress • Exaggerated symptoms • Nonorganic signs • Most reproducible tests*: – Superficial tenderness – Overreaction during examination – Discrepancy in the SLR test done in seated and supine
positions *Waddell G, McCullogh JA, Kummel E, Venner RM: Non-‐organic physical signs in low back pain, Spine 5:117–125, 1980.
IMAGING ELECTRODIAGNOSTICS LAB STUDIES
DIAGNOSTIC TESTS
IMAGING Imaging is NOT required UNLESS significant symptoms
PERSIST BEYOND 6-8 weeks Dixit RK: Approach to the patient with low back pain. In Imboden J, Hellmann D, Stone J, editors. Current diagnosis and
treatment in rheumatology, ed 2, New York, 2007, McGraw-Hill
NEITHER MRI NOR PLAIN RADIOGRAPHS taken EARLY
in the course of LBP evaluation improves clinical outcome, predicts recovery course, or reduces overall
cost of care Chou R, Fu R, Carrino JA, Deyo RA: Imaging strategies for low back pain: systematic review and meta-analysis, Lancet
373:463–472, 2009.
IMAGING • Weak association between imaging abnormalities
and symptoms • Up to 85%: cannot make precise pathoanatomic Dx
with identification of the pain generator
• Reinforce suspicion of serious disease, magnify the importance of non-specific findings, and label patients with spurious diagnosis
Deyo RA, Weinstein DO: Low back pain, N Engl J Med 344(5):363– 370, 2001.
IMAGING: Plain Xrays
IMAGING: MRI • Best initial test for LBP patients who require advanced
imaging • Preferred for detection of spinal infection, cancers,
herniated disks, and spinal stenosis • INDICATIONS: – Suspicion of systemic disease – Preop evaluation of surgical candidates on clinical grounds – Pxs with radiculopathy or spinal stenosis who are candidates
for epidural steroids
Jarvik JG, Deyo RA: Diagnos6c evalua6on of low back pain with emphasis on imaging, Ann Intern Med 137:586–597, 2002
Chou R, Qaseem A, Snow V, et al: Diagnosis and treatment of low back pain: a joint clinical prac6ce guideline from the American College of Physicians and the American Pain Society, Ann Intern Med 147(7):478–491, 2007
IMAGING: CT Scan • Superior to MRI in evaluation of bone anatomy • Safe in patients with ferromagnetic implants • CT myelography is preferred in patients with
surgically placed spinal hardware
IMAGING: CT Scan
IMAGING: Bone Scan • Infection, bony
metastases, Occult fractures
• Differentiation from degenerative changes
• Limited specificity: Poor spatial resolution
• Require confirmatory imaging by MRI
ELECTRODIAGNOSTIC STUDIES
• LS Radiculopathy • EMG-NCV • Confirm nerve root compression and define the distribution
and severity of involvement • INDICATIONS: – Pxs with persistent disabling symptoms of radiculopathy with
discordance b/n clinical presentation and findings on imaging – Evaluation of possible factitious weakness
• LIMITATIONS: – delayed detection – Persistent abnormalities
ELECTRODIAGNOSTIC STUDIES
LABORATORY STUDIES
• CBC • ESR, CRP • Alkaline phosphatase • Tumor markers
Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: a joint clinical prac6ce guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147:478-‐491.
DIFFERENTIAL DIAGNOSIS
CASE • 55M, fisherman, with low back pain • >5 years duration • Pain radiates to buttock and anterior thigh • Alleviated by forward flexion • Exacerbated by bending to the right side of the body
Plain APL Xray
Diagnosis • LUMBAR SPONDYLOSIS (Facet Syndrome) • Degenerative changes in facet joints • Imaging evidence is common in the general
population, increases with age and maybe unrelated to back symptoms
• Patients with severe mechanical LBP may have minimal radiographic changes, and conversely, patients with advanced changes may be asymptomatic
CASE • 35M, businessman • Low back pain that radiates to the medial aspect foot • Sudden onset • Duration: 6 weeks • Lancinating, sharp pain with numbness and tingling • Worsened by coughing, sneezing or when he defecates • +SLR Right • Weak dorsiflexion of foot and great toe
MRI
Diagnosis • SCIATICA secondary to INVERTERBRAL DISK
HERNIATION L4-L5 • Occurs when the NP in a degenerated disk prolapses
and pushes out the weakened annulus, usually posterolaterally
• Seen in 27% of asymptomatic individuals Jensen MC, Brandt-‐Zawadski MN, Obuchowski N, et al: Magne6c resonance imaging of the lumbar spine in people without back pain, N Engl J Med 331:69–73, 1994
Diagnosis • LS spine is susceptible to herniation because of its
mobility • 75% of flexion-extension occurs at the LS joint (L5-
S1) • 20% occurs at L4-5 • Therefore, 90-95% of clinically significant
compressive radiculopathies occur at these 2 levels
Diagnosis • Disk herniation is rare in young individuals • Frequency increases with age • Peak: 44-50y/o (progressive decline in frequency
thereafter)
Diagnosis • L1 radiculopathy: rare; pain, paresthesias and sensory
loss in inguinal areas • L2-4 radiculopathies: uncommon; seen in elderly with
spinal stenosis • Cauda equina syndrome: midline L4-5 herniation – LBP, bilateral radicular pain, bilateral motor deficit with leg
weakness – Urinary retention with Overflow incontinence – Asymmetric PE – Saddle anesthesia – Surgical emergency!
Diagnosis • Natural history is favorable (progressive
improvement in most patients) • Regression in sequential MRI • Partial or complete resolution in 2/3 of cases after 6
mos • Only 10% have sufficient pain after 6 weeks of
conservative care (consider decompressive surgery))
CASE • 70F, store owner • Chronic aching low back pain • Duration: 8 years • Occasionally relieved by Paracetamol, Mefenamic
Acid, rest • Normal PE
Plain APL Xray
Diagnosis • DEGENERATIVE SPONDYLOLISTHESIS • Anterior displacement of a vertebra on the one
beneath it • Two types
ISTHMIC DEGENERATIVE
Caused by bilateral spondylolyis
Caused by severe degenera6ve changes with subluxa6on at the facet joints
Acquired early in life; young boys
Older age group >60, women
Most commonly a defect in the pars ar6cularis at L5
MC L4-‐5
Nerve root impingement Spinal stenosis
CASE • 73M, carpenter • Chronic low back pain • >5 years • Pain and paresthesias in buttocks, thighs
and legs • Exacerbated by erect posture and walking
but has no problems cycling • Relieved by sitting or flexing forward • Unsteady gait, weakness lower
extremities • SLR (-) • DTRs: + on both LE
MRI
Diagnosis • SPINAL STENOSIS • Neurogenic claudication • Simian stance; shopping cart sign • Wide based gait (90% specific) • 20-30% asymptomatic adults have
abnormal imaging • Factors that favor neurogenic claudication
(vs vascular) – Preservation of pedal pulses – Provocation of Sxs by standing erect as
readily as walking – Relief of symptoms by spine flexion – Location of maximal discomfort to the
thighs rather than calves
Diagnosis • Indolent, benign • Symptoms unchanged
in 70%, improved in 15%, worsened in 15%
• Prophylactic surgical intervention not warranted
CASE • 55M, previously diagnosed with prostate cancer, s/p
cTURP • Persistent, progressive Low back pain for 2 months • Not alleviated by rest • Worse at night • Minimal relief with Paracetamol, NSAIDs • Weight-loss, anorexia • Recently, acute weakness of both lower extremities
(MMT 2/5) • Urinary retention with overflow incontinence
MRI
Diagnosis • CAUDA EQUINA Syndrome 2 to Vertebral
Metastases from Prostate Ca • Neoplasia accounts for <1% of patients with LBP • Prior history of Ca was the most important
predictor for likelihood of underlying Ca
Diagnosis • Leptomeningeal carcinomatosis: Breast, lung,
lymphoma, leukemia • Metastatic: kidney, prostate, breast, lung, thyroid • Multiple myeloma • Rare: SC tumors, primary vertebral tumors,
retroperitoneal tumors
Diagnosis • Plain radiographs less sensitive • Metastatic lesions may be lytic (radiolucent), blastic
(radiodense) or mixed. • Unlike infections, the disk space is usually spared • MRI: greatest sensitivity and specificity • Purely lytic lesion (MM) will not be detected by
bone scan
CASE • 30M, kargador, IV drug user • Fever, low back pain, weight loss • Pain is persistent, present at rest, exacerbated by
activity • +point tenderness: L4-L5 • Grade 3/6 systolic murmur over the 4th ICS RPSB • Leukocytosis • Elevated ESR, CRP • Blood CS: Moderate growth of S. aureus
MRI
Diagnosis • Vertebral OM • Hematogenous, direct inoculation, contiguous
spread • MC: lumbar spine • MC: #1 S. aureus #2 E.coli • Leukocytosis in 2/3 • CRP correlates with clinical response to Tx • Bone Bx if Blood CS (-)
Diagnosis • Plain Xray: initial imaging (late and non-specific) – Loss of disk height and loss of cortical definition – Bony lysis of adjacent vertebral bodies
• MRI: most sensitive and specific – Classic finding: involvement of 2 vertebral bodies with
their intervening disk
CASE • 40F, housewife • Low back pain after lifting bag of laundry • Duration: 3 days • SLR (-) • No LOM
Diagnosis • Nonspecific LBP • Lumbago, strain, sprain • Self-limited, acute, mechanical • Mild to severe • Trauma, lifting, twisting injury • Most patients are better within 1-4 weeks but
remain susceptible to similar future episodes • <10% develop chronic non-specific LBP
TREATMENT
ACUTE (Less than 3 mos)
• Excellent prognosis • Only 1/3 seek medical care • >90% recover within 8weeks or earlier
• Stay active; continue ordinary daily activities within limits permitted by pain
• Discourage bedrest >1-2days • Acetaminophen and NSAIDs: 1st line for symptom relief • Short term opioids: for severe disabling LBP or if with CI to NSAIDS • Muscle relaxants are moderately effective (but high prev of adverse
events
Coste J, Delecoeuillerie G, Cohen deLara A, et al: Clinical course and prognos6c factors in acute low back pain: an incep6on cohort study in primary care prac6ce, BMJ 308:577, 1994.
Chou R: Pharmacological management of low back pain, Drugs 70(4):384–402, 2010.
ACUTE (Less than 3 mos)
• Back exercises not helpful in the acute phase • PT referral not usually necessary in the first month • Individually tailored exercise program • Educational booklets strongly recommended
• Heating pads or blankets
Chou R, Qaseem A, Snow V, et al: Diagnosis and treatment of low back pain: a joint clinical prac6ce guideline from the American College of Physicians and the American Pain Society, Ann Intern Med 147(7):478–491, 2007.
ACUTE (Less than 3 mos)
• INSUFFICIENT EVIDENCE – Spinal manipulation – Cold packs, corsets or braces – Acupuncture, massage
– Traction
– TENS, PENS, interferential therapy, low-level laser therapy, shortwave diathermy, ultrasound
– Injection of trigger points, ligaments, SI joints, facet joints, intradiskal steroid injections
Clarke JA, van Tulder MW, Blomberg SE, et al: Trac6on for low back pain with or without scia6ca, Cochrane Database Syst Rev (23):CD003010, 2007.
Chou R, Qaseem A, Snow V, et al: Diagnosis and treatment of low back pain: a joint clinical prac6ce guideline from the American College of Physicians and the American Pain Society, Ann Intern Med 147(7):478–491, 2007
Chou R, Loeser JD, Owens DK, et al: Interven6onal therapies, surgery, and interdisciplinary rehabilita6on for low back pain. An evidence based clinical prac6ce guideline from the American Pain Society, Spine 34(10):1066–1077, 2009.
SUBACUTE (More than 6wks)
– Injection therapy – Epidural CCS: remarkable but unjustified popularity – Evidence of moderate benefit compared to placebo for
short term relief of leg pain from HNP – No significant functional benefit – No reduction in need for surgery
Care"e S, Leclaire R, Marcouxs S, et al: Epidural cor6costeroid injec6ons for scia6ca due to herniated nucleus pulposus, N Engl J Med 336(23):1634–1640, 1997.
ACUTE to SUBACUTE
– Vertebroplasty and Kyphoplasty
ACUTE to SUBACUTE
– Vertebroplasty vs Kyphoplasty
CHRONIC (More than 3 mos)
– Overall: results of treatment are unsatisfactory – Complete relief of pain is unrealistic for most – High costs – Acetaminophen and NSAIDs as first line – Opioid analgesics for severe disabling LBP – No evidence that long-acting RTC dose is superior to
short-acting PRN dosing – Continuous exposure leads to tolerance and dose
escalation Chou R: Pharmacological management of low back pain, Drugs 70(4):384–402, 2010.
CHRONIC (More than 3 mos)
– Muscle relaxants are not recommended for long-term use
– Antidepressants that inhibit NE uptake: pain modulating properties
– Low dose TCAs are an option – No evidence for SSRIs (except for concomitant Tx of
depression) – Duloxetine (SNRI) has marginal efficacy – Insufficient evidence for Gabapentin and topiramate
CHRONIC (More than 3 mos)
– PT modalities and injection techniques: not recommended – Lumbar supports and traction: ineffective – Medium firm mattress or back-conforming mattress (water-
bed or foam): superior to a firm mattress – Spinal manipulation is superior to sham manipulation but is
no more effective than conventional medical Tx – Less evidence for massage and acupuncture – Chemonucleolysis with chymopapain: potentially life-
threatening – Radiofrequency denervation: lacks evidence
CHRONIC (More than 3 mos)
– Lack of evidence: • Radiofrequency denervation • Intradiskal electrothermal therapy • Percutaneous intradiskal RF thermocoagulation • Prolotherapy • Spinal cord stimulation • Instraspinal drug infusion systems (?): morphine
CHRONIC (More than 3 mos)
– Supportive measures • Interdisciplinary rehabilitation • Functional restoration (work hardening)
– Surgery • As a general rule, the results of back surgery are disappointing when the
goal is relief of back pain rather than relief of radicular symptoms from resulting neurologic compression
• Role of surgical treatment for chronic disabling LBP w/o neurologic improvement in patients with degenerative disease remains controversial
• MC: spinal fusion • For non-radicular back pain with degenerative changes, fusion is no more
effective than intensive interdisciplinary rehab but is associated with small to moderate benefits compared with standard non-surgical care
CHRONIC (More than 3 mos)
NERVE ROOT COMPRESSION SYNDROMES Disk HerniaDon Spinal Stenosis Spondylolithesis Treat nonsurgically (as in Acute LBP) unless with serious or progressive neuro deficit
Conserva6ve non-‐opera6ve Tx Surgery if with serious or progressive neuro deficit
Treat conserva6vely
Only about 10% have sufficient pain aoer 6 weeks of conserva6ve Tx to warrant Surgery
Symptoms stable for yrs; may improve in some Drama6c improvement uncommon
Surgery: moderate short term benefits (thru 6-‐12wks) vs non-‐Sx but outcome differences diminish over 6me and no longer present in 1-‐2 yrs
PT: mainstay of mgt Core strengthening, stretching, aerobic, loss of wt, Px educa6on; Cycling Lumbar corsets
Open diskectomy or microdiskectomy
Laminectomy, par6al fascetectomy, excision of hypertrophied LF
Epidural CCS injec6ons: moderate benefit for short term relief but no func6onal benefit and don’t reduce need for Surgery
Lumbar epidural CCS injec6ons: small RCT showed reduc6on in pain and improvement in fxn at 6 mos but don’t influence fxnal status and need for surgeyr at 1yr
Decompression surgery with fusion be"er than non-‐surgical care for isthmic spondylolisthesis and disabling isolated LBP or scia6ca for at least a year
An6TNF being inves6gated Titanium interspinous spacer
OUTCOME • Natural history of acute LBP is favorable • Improvement in pain and fxn within 1 month in the
majority of patients; >90% are better at 8weeks • Only 1/3 of acute LBP patients seek medical care • Rest resolves
OUTCOME • Improvement is also the norm for Pxs with sciatica 2
to HNP • 1/3 better in 2 weeks, 75% improve after 3 mos,
10% ultimately undergo surgery • Spinal stenosis: stable in 70%, improved in 15%,
worsened in 15% • 7-10% with chronic LBP: responsible for high costs
Factors that predict
chronicity • Maladaptive coping behavior
• Presence of non-organic signs • Functional impairment • Poor general health status • Psychiatric comorbidities • Job dissatisfaction • Disputed compensation claims • High level of “fear avoidance”
SUMMARY • History and PE are more important than Imaging • Prognosis of acute LBP is excellent • Prognosis of chronic LBP is unsatisfactory • Surgery is reserved for neurologic deficits
Osteoarthritis
Prevalence
Diagnosis " Pathologically " Radiographically " Osteophyte " Joint space narrowing (JSN) on Plain Xray (or MRI)
" Clinically " Nodal changes in the hands " Limited and painful internal rotation of the hip " Crepitus with knee movement
SYMPTOMATIC OA = pain, aching or stiffness in a joint with radiographic OA
Diagnosis ACR Criteria
1986 (Knee), 1991 (Hip), 1990 (Hand)
SENSITIVITY SPECIFICITY
Hand 92% 98%
Hip 91% 89%
Knee 91% 86%
ACR Radiologic and Clinical Criteria
" HAND 1. Hand pain, aching, or stiffness on most days of prior months 2. Hard tissue enlargement of >=2 of 10 selected joints* 3. Fewer than 3 swollen MCP joints 4. Hard tissue enlargement of >=2 DIP joints 5. Deformity of >=2 of 10 selected joints* " DIAGNOSIS REQUIRES ITEMS 1-3 AND EITHER 4 OR 5 " 10 Selected Joints: DIP 2-3, PIP 2-3, and CMC 1
bilaterally
Hand OA
ACR Radiologic and Clinical Criteria
" KNEE: Clinical 1. Knee pain for most days of prior month 2. Crepitus with active joint motion 3. Morning stiffness lasting <=30 min 4. Bony enlargement of the knee on examination 5. Age >=38 yr
" Diagnosis REQUIRES 1+2 + 4, or 1+2+3+5, or 1+4+5
ACR Radiologic and Clinical Criteria
" KNEE: Clinical AND Radiographic 1. Knee pain for most days of prior month 2. Osteophytes at joint margins 3. Synovial fluid typical of OA 4. Age ≥ 40 y/o 5. Morning stiffness lasting ≤ 30min 6. Crepitus with active joint motion
" Diagnosis REQUIRES 1+2, or 1+3+5+6, or 1+4+5+6
ACR Radiologic and Clinical Criteria
" HIP: Clinical AND Radiographic 1. Hip pain for most days of the prior month 2. ESR ≤20mm/hr 3. Radiographic femoral and/or acetabular
osteophytes 4. Radiographic hip joint space narrowing
Diagnosis REQUIRES 1+2+3, or 1+2+4, or 1+3+4
Primary vs Secondary
• Primary: absence of an injury history or other joint disease
• Secondary: (+) of predisposing disorder • Division currently less clear • Genetics, Hx of injury/jt damage, mechanical
factors, psychosocial milieu à joint à end-stage or failed joint
Etiologies of Secondary OA 1637CHAPTER 99 | CLINICAL FEATURES OF OSTEOARTHRITIS
Table 99-1 American College of Rheumatology Radiologic and Clinical Criteria for Osteoarthritis
Hand8
1. Hand pain, aching, or stiffness on most days of prior mo2. Hard tissue enlargement of ≥2 of 10 selected joints*3. Fewer than 3 swollen MCP joints4. Hard tissue enlargement of ≥2 DIP joints5. Deformity of ≥2 of 10 selected joints*Diagnosis requires items 1-3 and either 4 or 5*10 selected joints: DIP 2-3, PIP 2-3, and CMC 1 bilaterally
Knee: Clinical6
1. Knee pain for most days of prior mo2. Crepitus with active joint motion3. Morning stiffness lasting ≤30 min4. Bony enlargement of the knee on examination5. Age ≥38 yrDiagnosis requires 1 + 2 + 4, or 1 + 2 + 3 + 5, or 1 + 4 + 5
Knee: Clinical and Radiographic
1. Knee pain for most days of prior mo2. Osteophytes at joint margins3. Synovial fluid typical of osteoarthritis4. Age ≥40 yr5. Morning stiffness lasting ≤30 min6. Crepitus with active joint motionDiagnosis requires: 1 + 2, or 1 + 3 + 5 + 6, or 1 + 4 + 5 + 6
Hip: Clinical and Radiographic7
1. Hip pain for most days of the prior mo2. ESR ≤20 mm/hr3. Radiographic femoral and/or acetabular osteophytes4. Radiographic hip joint space narrowingDiagnosis requires: 1 + 2 + 3, or 1 + 2 + 4, or 1 + 3 + 4
CMC, carpometacarpal; DIP, distal interphalangeal; ESR, erythrocyte sedi-mentation rate; MCP, metacarpophalangeal; PIP, proximal interphalangeal.
From Altman R, Asch E, Bloch D, et al: Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association, Arthritis Rheum 29(8):1039–1049, 1986; Altman R, Alarcon G, Appelrouth D, et al: The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip, Arthritis Rheum 34(5):505–514, 1991; and Altman R, Alarcon G, Appelrouth D, et al: The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand, Arthritis Rheum 33(11):1601–1610, 1990.
Table 99-2 Prevalence of Symptomatic Osteoarthritis (OA)
Site (Age in Yrs) Source
% with Symptomatic OA
Male Female Total
Hands (≥26) Framingham89 3.8 9.2 6.8Knees ≥26 Framingham13 4.6 4.9 4.9 ≥45 Framingham13 5.9 7.2 6.7 ≥45 Johnston County14 13.5 18.7 16.7 ≥60 NHANES III12 10.0 13.6 12.1Hips (≥45) Johnston County90 8.7 9.3 9.2
NHANES, National Health and Nutrition Examination Survey.From Lawrence RC, Felson DT, Helmick CG, et al:. Estimates of the preva-
lence of arthritis and other rheumatic conditions in the United States. Part II, Arthritis Rheum 58(1):26–35, 2008.
Primary and Secondary Osteoarthritis
Historically, osteoarthritis was considered to be “primary” in the absence of an injury history or other joint disease and “secondary” if a predisposing disorder was present (Table 99-3). However, as more and more local risk factors for OA
have been identified (such as femoroacetabular impinge-ment at the hip and malalignment at the knee) and a broader range of associated factors have been discovered (genetic, biomechanical, and environmental factors), the division between primary and secondary is less clear. Many individuals who develop secondary OA are likely predis-posed to the condition with or without the identified incit-ing event; other individuals who have a disorder that is linked to secondary OA may not develop clinical OA. It may be most useful to think of OA as a common pathway through which an individual’s genetics, history of injury or other joint damage, mechanical factors, and psychosocial milieu act on the joint, in some cases leading to an “end-stage” or “failed” joint.
CLINICAL FEATURESGeneral Symptoms and Signs
OA most commonly affects the knees, hands, feet, hips, and spine. These joints may be symptomatic or may be affected only on radiographs. Individuals with OA generally describe pain in the joint(s) that is worse with activity, with limited morning stiffness (<30 minutes), and pain and stiffness with rest. This stiffness after inactivity, or “gelling” phenomenon, is often a main complaint, although morning stiffness is generally less severe and of shorter duration than that seen
Table 99-3 Etiologies of Secondary OsteoarthritisMetabolic
Crystal-associated arthritisCalcium pyrophosphate or apatite deposition
AcromegalyOchronosisHemochromatosisWilson’s diseaseHyperparathyroidismEhlers-DanlosGaucher’s diseaseDiabetes
Mechanical/Local Factors
Slipped capital femoral epiphysisEpiphyseal dysplasiasLegg-Calvé-Perthes diseaseCongenital dislocationFemoroacetabular impingementCongenital hip dysplasiaLimb-length inequalityHypermobility syndromesAvascular necrosis/osteonecrosis
Traumatic
Joint trauma (e.g., ACL tear)Fracture through jointPrior joint surgery (i.e., meniscectomy, ACL)Charcot joint (neuropathic arthropathy)
Inflammatory
Rheumatoid arthritis or other inflammatory arthropathiesCrystalline arthropathy (gout)History of septic arthritis
ACL, anterior cruciate ligament.Modified from Altman R, Asch E, Bloch D, et al: Development of criteria
for the classification and reporting of osteoarthritis. Classification of osteo-arthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association, Arthritis Rheum 29(8):1039–1049, 1986.
Etiologies of Secondary OA
1637CHAPTER 99 | CLINICAL FEATURES OF OSTEOARTHRITIS
Table 99-1 American College of Rheumatology Radiologic and Clinical Criteria for Osteoarthritis
Hand8
1. Hand pain, aching, or stiffness on most days of prior mo2. Hard tissue enlargement of ≥2 of 10 selected joints*3. Fewer than 3 swollen MCP joints4. Hard tissue enlargement of ≥2 DIP joints5. Deformity of ≥2 of 10 selected joints*Diagnosis requires items 1-3 and either 4 or 5*10 selected joints: DIP 2-3, PIP 2-3, and CMC 1 bilaterally
Knee: Clinical6
1. Knee pain for most days of prior mo2. Crepitus with active joint motion3. Morning stiffness lasting ≤30 min4. Bony enlargement of the knee on examination5. Age ≥38 yrDiagnosis requires 1 + 2 + 4, or 1 + 2 + 3 + 5, or 1 + 4 + 5
Knee: Clinical and Radiographic
1. Knee pain for most days of prior mo2. Osteophytes at joint margins3. Synovial fluid typical of osteoarthritis4. Age ≥40 yr5. Morning stiffness lasting ≤30 min6. Crepitus with active joint motionDiagnosis requires: 1 + 2, or 1 + 3 + 5 + 6, or 1 + 4 + 5 + 6
Hip: Clinical and Radiographic7
1. Hip pain for most days of the prior mo2. ESR ≤20 mm/hr3. Radiographic femoral and/or acetabular osteophytes4. Radiographic hip joint space narrowingDiagnosis requires: 1 + 2 + 3, or 1 + 2 + 4, or 1 + 3 + 4
CMC, carpometacarpal; DIP, distal interphalangeal; ESR, erythrocyte sedi-mentation rate; MCP, metacarpophalangeal; PIP, proximal interphalangeal.
From Altman R, Asch E, Bloch D, et al: Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association, Arthritis Rheum 29(8):1039–1049, 1986; Altman R, Alarcon G, Appelrouth D, et al: The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip, Arthritis Rheum 34(5):505–514, 1991; and Altman R, Alarcon G, Appelrouth D, et al: The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand, Arthritis Rheum 33(11):1601–1610, 1990.
Table 99-2 Prevalence of Symptomatic Osteoarthritis (OA)
Site (Age in Yrs) Source
% with Symptomatic OA
Male Female Total
Hands (≥26) Framingham89 3.8 9.2 6.8Knees ≥26 Framingham13 4.6 4.9 4.9 ≥45 Framingham13 5.9 7.2 6.7 ≥45 Johnston County14 13.5 18.7 16.7 ≥60 NHANES III12 10.0 13.6 12.1Hips (≥45) Johnston County90 8.7 9.3 9.2
NHANES, National Health and Nutrition Examination Survey.From Lawrence RC, Felson DT, Helmick CG, et al:. Estimates of the preva-
lence of arthritis and other rheumatic conditions in the United States. Part II, Arthritis Rheum 58(1):26–35, 2008.
Primary and Secondary Osteoarthritis
Historically, osteoarthritis was considered to be “primary” in the absence of an injury history or other joint disease and “secondary” if a predisposing disorder was present (Table 99-3). However, as more and more local risk factors for OA
have been identified (such as femoroacetabular impinge-ment at the hip and malalignment at the knee) and a broader range of associated factors have been discovered (genetic, biomechanical, and environmental factors), the division between primary and secondary is less clear. Many individuals who develop secondary OA are likely predis-posed to the condition with or without the identified incit-ing event; other individuals who have a disorder that is linked to secondary OA may not develop clinical OA. It may be most useful to think of OA as a common pathway through which an individual’s genetics, history of injury or other joint damage, mechanical factors, and psychosocial milieu act on the joint, in some cases leading to an “end-stage” or “failed” joint.
CLINICAL FEATURESGeneral Symptoms and Signs
OA most commonly affects the knees, hands, feet, hips, and spine. These joints may be symptomatic or may be affected only on radiographs. Individuals with OA generally describe pain in the joint(s) that is worse with activity, with limited morning stiffness (<30 minutes), and pain and stiffness with rest. This stiffness after inactivity, or “gelling” phenomenon, is often a main complaint, although morning stiffness is generally less severe and of shorter duration than that seen
Table 99-3 Etiologies of Secondary OsteoarthritisMetabolic
Crystal-associated arthritisCalcium pyrophosphate or apatite deposition
AcromegalyOchronosisHemochromatosisWilson’s diseaseHyperparathyroidismEhlers-DanlosGaucher’s diseaseDiabetes
Mechanical/Local Factors
Slipped capital femoral epiphysisEpiphyseal dysplasiasLegg-Calvé-Perthes diseaseCongenital dislocationFemoroacetabular impingementCongenital hip dysplasiaLimb-length inequalityHypermobility syndromesAvascular necrosis/osteonecrosis
Traumatic
Joint trauma (e.g., ACL tear)Fracture through jointPrior joint surgery (i.e., meniscectomy, ACL)Charcot joint (neuropathic arthropathy)
Inflammatory
Rheumatoid arthritis or other inflammatory arthropathiesCrystalline arthropathy (gout)History of septic arthritis
ACL, anterior cruciate ligament.Modified from Altman R, Asch E, Bloch D, et al: Development of criteria
for the classification and reporting of osteoarthritis. Classification of osteo-arthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association, Arthritis Rheum 29(8):1039–1049, 1986.
Etiologies of Secondary OA
1637CHAPTER 99 | CLINICAL FEATURES OF OSTEOARTHRITIS
Table 99-1 American College of Rheumatology Radiologic and Clinical Criteria for Osteoarthritis
Hand8
1. Hand pain, aching, or stiffness on most days of prior mo2. Hard tissue enlargement of ≥2 of 10 selected joints*3. Fewer than 3 swollen MCP joints4. Hard tissue enlargement of ≥2 DIP joints5. Deformity of ≥2 of 10 selected joints*Diagnosis requires items 1-3 and either 4 or 5*10 selected joints: DIP 2-3, PIP 2-3, and CMC 1 bilaterally
Knee: Clinical6
1. Knee pain for most days of prior mo2. Crepitus with active joint motion3. Morning stiffness lasting ≤30 min4. Bony enlargement of the knee on examination5. Age ≥38 yrDiagnosis requires 1 + 2 + 4, or 1 + 2 + 3 + 5, or 1 + 4 + 5
Knee: Clinical and Radiographic
1. Knee pain for most days of prior mo2. Osteophytes at joint margins3. Synovial fluid typical of osteoarthritis4. Age ≥40 yr5. Morning stiffness lasting ≤30 min6. Crepitus with active joint motionDiagnosis requires: 1 + 2, or 1 + 3 + 5 + 6, or 1 + 4 + 5 + 6
Hip: Clinical and Radiographic7
1. Hip pain for most days of the prior mo2. ESR ≤20 mm/hr3. Radiographic femoral and/or acetabular osteophytes4. Radiographic hip joint space narrowingDiagnosis requires: 1 + 2 + 3, or 1 + 2 + 4, or 1 + 3 + 4
CMC, carpometacarpal; DIP, distal interphalangeal; ESR, erythrocyte sedi-mentation rate; MCP, metacarpophalangeal; PIP, proximal interphalangeal.
From Altman R, Asch E, Bloch D, et al: Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association, Arthritis Rheum 29(8):1039–1049, 1986; Altman R, Alarcon G, Appelrouth D, et al: The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip, Arthritis Rheum 34(5):505–514, 1991; and Altman R, Alarcon G, Appelrouth D, et al: The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand, Arthritis Rheum 33(11):1601–1610, 1990.
Table 99-2 Prevalence of Symptomatic Osteoarthritis (OA)
Site (Age in Yrs) Source
% with Symptomatic OA
Male Female Total
Hands (≥26) Framingham89 3.8 9.2 6.8Knees ≥26 Framingham13 4.6 4.9 4.9 ≥45 Framingham13 5.9 7.2 6.7 ≥45 Johnston County14 13.5 18.7 16.7 ≥60 NHANES III12 10.0 13.6 12.1Hips (≥45) Johnston County90 8.7 9.3 9.2
NHANES, National Health and Nutrition Examination Survey.From Lawrence RC, Felson DT, Helmick CG, et al:. Estimates of the preva-
lence of arthritis and other rheumatic conditions in the United States. Part II, Arthritis Rheum 58(1):26–35, 2008.
Primary and Secondary Osteoarthritis
Historically, osteoarthritis was considered to be “primary” in the absence of an injury history or other joint disease and “secondary” if a predisposing disorder was present (Table 99-3). However, as more and more local risk factors for OA
have been identified (such as femoroacetabular impinge-ment at the hip and malalignment at the knee) and a broader range of associated factors have been discovered (genetic, biomechanical, and environmental factors), the division between primary and secondary is less clear. Many individuals who develop secondary OA are likely predis-posed to the condition with or without the identified incit-ing event; other individuals who have a disorder that is linked to secondary OA may not develop clinical OA. It may be most useful to think of OA as a common pathway through which an individual’s genetics, history of injury or other joint damage, mechanical factors, and psychosocial milieu act on the joint, in some cases leading to an “end-stage” or “failed” joint.
CLINICAL FEATURESGeneral Symptoms and Signs
OA most commonly affects the knees, hands, feet, hips, and spine. These joints may be symptomatic or may be affected only on radiographs. Individuals with OA generally describe pain in the joint(s) that is worse with activity, with limited morning stiffness (<30 minutes), and pain and stiffness with rest. This stiffness after inactivity, or “gelling” phenomenon, is often a main complaint, although morning stiffness is generally less severe and of shorter duration than that seen
Table 99-3 Etiologies of Secondary OsteoarthritisMetabolic
Crystal-associated arthritisCalcium pyrophosphate or apatite deposition
AcromegalyOchronosisHemochromatosisWilson’s diseaseHyperparathyroidismEhlers-DanlosGaucher’s diseaseDiabetes
Mechanical/Local Factors
Slipped capital femoral epiphysisEpiphyseal dysplasiasLegg-Calvé-Perthes diseaseCongenital dislocationFemoroacetabular impingementCongenital hip dysplasiaLimb-length inequalityHypermobility syndromesAvascular necrosis/osteonecrosis
Traumatic
Joint trauma (e.g., ACL tear)Fracture through jointPrior joint surgery (i.e., meniscectomy, ACL)Charcot joint (neuropathic arthropathy)
Inflammatory
Rheumatoid arthritis or other inflammatory arthropathiesCrystalline arthropathy (gout)History of septic arthritis
ACL, anterior cruciate ligament.Modified from Altman R, Asch E, Bloch D, et al: Development of criteria
for the classification and reporting of osteoarthritis. Classification of osteo-arthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association, Arthritis Rheum 29(8):1039–1049, 1986.
CLINICAL FEATURES
General Symptoms & Signs – Knees, hands, feet, hips and spine – Symptomatic or radiographic – Pain in the joints that is:
• Worse with activity • Limited morning stiffness (≤30mins) • Pain and stiffness with rest (gelling phenomenon)
– Bony enlargements, crepitus, reduced ROM – Soft tissue swelling or effusion
Joint-Specific Symptoms and Signs
Knee • Insidious onset of pain • Gelling • Limitation of ROM – Walking, transferring, stair climbing – Sense of instability or “giving out” at the knee
• Locking sensation – Stiffness – Loose bodies in the joint space – Meniscal lesions
• Crepitus, bony enlargement
Knee • Pain: medial or lateral joint line • Effusions: cool, generally w/o redness – Association with Baker’s cyst
• Pain over anserine bursa or greater trochanter: altered biomechanics • Malalignment (mc: varus) – risk factor for progression • Severe disease: flexion deformities or joint stability • Risk factors: Quadriceps weakness (modifiable) à muscle atrophy
(late stage); loss of proprioception and vibratory sense • Patellofemoral OA: pain, disability; often overlooked
Hip • Groin pain (specific) • Vague: pain in the thigh, buttock, low back, or ipsilateral knee • Consider differential Dx – Femoral neck Fx, Avascular Necrosis
• Limitations in walking, bending, transferring, stair climbing – Internal rotation: limited and painful (even in early dse) – Putting on socks, tying shoes, trimming toe nails
• Visible deformity, hip flexion contracture, severe limitations of ROM à severe dse (superior migration of the femoral head)
• Consider: Femoroacetabular impingement – young, groin pain worsened by sitting, pain and limitation on F-IR-AD of the hip
Hip OA
Hand • Heberden’s nodes: DIP; Bouchard’s nodes: PIP • Erosive arthritis: episodic inflammation, pain and swelling (elderly women) • First CMC: significant pain, limitations in fucntionality, reduced grip strength
– CMC squaring: osteophyte formation and JSN • Bilateral involvement of multiple joints:
– Within (multiple PIPs) and across (both DIPs and PIPs) • MCP involvement: increasing; consider inflammatory arthropathies or secondary OA
(hemochromatosis) • DeQuervain’s tenosynovitis: mimic or aggravate symptoms
Spine
• Osteophytosis of the spine à older individuals; often asymptomatic • Lumbar disk degeneration (DSN, end plate sclerosis, herniation): often seen in
association with radiographic osteophytosis (relationship controversial) • Cervical spine:
– pain in the neck, radiation to the arms, weakness or paresthesia (osteophytic compression)
– Dysphagia (anterior cervical spine osteophytes) • Lumbar spine:
– Osteophytes and DSN à sciatic nerve impingement (pain, burning, numbness and/or weakness down one or both legs)
Shoulder • Symptoms are more often due to
osteophytosis and narrowing of the acromioclavicular and/or sternoclavicular jts rather than the glenohumeral jt itself
• DDx: Subacromial bursitis, Rotator Cuff pathology, Adhesive capsulitis, Cervical spine pathology
• Milwaukee shoulder syndrome – Destructive arthropathy: glenohumeral
joint – Large effusions • High RBC count • Basic Calcium crystals
Other Joints • 1st MTP: pain and hallux valgus (bunion)
deformity • Loss of function due to ankylosis
(hallux rigidus) à altered gait • Other joints: – TMJ – Ankles: talonavicular, subtalar – Elbow OA: rare • Trauma, vibration damage,
pseudogout
Polyarticular OA • Generalized OA: no universally understood or accepted
definition • Kellgren and Moore (1952): – Primarily: Heberden’s nodes and CMC – With: spine, knees, hips, feet (descending frequency)
• Later studies: – >3 or >5 joint sites affected – Affected joint counts – Multiple hand involvement – Nodal hand OA with other jt involvement – Summed scores of OA across multiple joints
DIAGNOSTIC TESTING
Diagnostic Approach • Clinical! • Labs RARELY required • If Hx and PE ok à RadioGrx OFTEN NOT required • Testing is for exclusion of DDx
Lab Testing • RF, ANA, Serologic studies à rarely indicated • CBC, Chem panel (Glucose, Crea), LFTs • MCP involvement: test for hypothyroidism,
hemochromatosis
Synovial Fluid Analysis • Normal or mildly inflammatory • Clear and colorless to slightly yellowish • WBC ct ≤ 2000 cells/mm3 (<2cells/hpf) • Concomitant CPPD +/-
Imaging: Conventional Radiography, General Considerations
• Confirm Dx • Exclude DDx • Typical findings: – Osteophytes – JSN – Sclerosis – Cysts of subchondral bone
Kellgren-Lawrence Grading System
Knee: sunrise view
Hip: Frog Leg View
Hand: Gull-wing deformities
Spine
Imaging: Advanced Modalities • MRI: – Exclude DDx – Define early changes (before Xray changes occur) – BM lesions (knee) = correlate with pain, bone
attrition, progressive cartilage damage • Arthroscopy – Often used as a response to MRI findings – Overused and generally ineffective – Cost not indicated in routine practice
• Ultrasound – Bedside procedure – Detect small effusions, early cartilage changes, diff infx vs non-inflx arthropathies – Therapeutic adjunct
Mortality in OA • Increased compared to gen pop • CV and GI causes • Inc mortality with inc jt involvement • Reduced survival: hand, B knees, cervical
(NOT: hip, foot, lumbar) • Contributors:
– Reduced physical activity – Comorbid conditions – Adverse SE of meds
SOFT TISSUE RHEUMATISMS
SHOULDER • Subacromial bursitis • Bicipital Tendinitis • Rotator Cuff Tendinitis
HAND • DeQuervain’s Tenosynovitis • Carpal Tunnel Syndrome • Trigger Finger
Knee • Anserine bursitis
Foot and ANKLE • Plantar fasciitis
SUMMARY • Aging has caused a lot of health-related disorders • It is important to get the correct diagnosis so
appropriate treatment can be given • Most cases of low-back pain are benign, do not need
imaging and respond to conservative therapy • Osteoarthritis is a degenerative disease that
responds to analgesics and physical therapy • Soft tissue rheumatisms are overuse diseases and
respond to rest and steroid injections
Thank you for your attention
www.allancorpuzmd.com