Week 4 Joints Flashcards
Terms to know:
General Joint Pain Classifications
Inflammatory vs. non-inflammatory
Monoarticular vs. oligoarticular vs. polyarticular
Symmetrical vs. asymmetrical polyarthritis
Types of joints involved
Vertebral joints, sacroiliac joint
Wrists, carpometacarpals, MCP, PIP, DIP
Ankle, MTP
Shoulders, elbows, hips, knees
Inflammatory vs. non-inflammatory joint pain CHART
Mono/Oligoarticular vs polyarticular
Taking history for joint pain
Evaluate number and types of joints affected and symmetry if polyarthritis is present
Onset (sudden vs. gradual) and duration of pain/restriction (constant vs. intermittent)
History of overuse, repetitive stress, trauma
Pain/stiffness in the morning (with rest) vs. after activity
Previous medical history
Previous gastrointestinal or sexually transmitted disease
Obesity, hypertension, diabetes, kidney stones
Immunocompromised
Prior joint surgery, prosthetic joints
Medications
Thiazide diuretics, cyclosporine, procainamide, hydralazine
Family history
Social history
Drug and alcohol use, travel, tick bites, risky sexual behaviour
Physical Examination and Workup
Joint examination with evaluation of range-of-motion and function
Verify the pain is intraarticular and not periarticular
Signs of true intraarticular disorder:
Effusion, redness, swelling
Restricted AROM and PROM
Maximum pain at end range
Pain with motion in multiple directions
Periarticular problems may restrict only AROM
Pain on RROM suggest tendonitis or bursitis
Assess for extraarticular manifestations
Examine skin, eyes, oral cavity, lungs, heart
Tests to consider:
Synovial fluid analysis, blood tests (WBC count, ESR, CRP, serum uric acid, blood cultures, serology, rheumatoid factor, anticitrullinated peptide antibodies, ANA), X-ray, ultrasonography, CT, MRI
Approach to knee pain in adults
Septic Arthritis
aka infectious arthritis
Infection in a joint
Can involve bacteria, viruses, fungi, mycobacterium
Caused by nongonococcal bacteria in more than 80% of cases
Staphylocccocus aureus is the most common causative pathogen, followed by Streptococcus species
Children; persons > 55 years old
Increased risk with age, immunosuppression, lower socioeconomic status
Onset: sudden
Duration: until ~6 weeks after effective antimicrobial treatment
Usually no morning pain or stiffness
Fever (may or may not be present)
LR+ 0.67 (95% [CI] 0.43-1.0); LR- 1.7 (95% [CI] 1.0-3.0)
Joint pain and effusion, typically in large joint
Skin infection, cutaneous ulcers, osteomyelitis, septic bursitis, abscess
Due to contiguous spread from local infections
Previous intraarticular injection, arthrocentesis, arthroscopy, prosthetic joint, recent joint surgery, trauma
Due to direct inoculation
Diabetes mellitus, HIV infection, immunosuppressive medications, IV drug abuse, other cause of sepsis, sexual activity (specifically for gonococcal arthritis)
Due to hematogenous spread during bacteremia – most common route of entry into joint
Acute joint swelling, pain, erythema, warmth, and joint immobility
Usually monoarticular
Knee most commonly affected, followed by hip, shoulder, ankle, elbow, wrist
Sternoclavicular or sacroiliac joint infection more common in patients with history of IV drug abuse
Constitutional symptoms such as fever, chills, rigors may be present
Septic Arthritis – Evaluation and management
Complete blood count – elevated WBC count
Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)
Can be normal
When elevated, these markers used to monitor therapeutic response
Serum uric acid – should not be elevated; used to rule out gout
Other: blood cultures (positive in 25-50% cases)
Arthrocentesis for synovial fluid analysis
WBC count: > 50,000 WBC/mm3
Synovial fluid WBC differential: >90% polymorphonuclear cells
Gram stain, aerobic and anaerobic bacterial culture
Borrelia burgdorferi cannot be cultured from synovial fluid – PCR testing if suspecting Lyme arthritis (positive in 85% of patients)
Imaging may be considered: X-ray, ultrasonography, MRI
Medical emergency - Needs immediate diagnosis and urgent referral for treatment!
Failure to initiate appropriate antibiotic therapy within 24-48 hours of onset subchondral bone loss and permanent joint dysfunction
Algorithm
Gout
Middle-aged men (prevalence increases with advancing age); Post-menopausal women
Increasing prevalence in Western countries; analogous to obesity epidemic
Prevalence 2.7-6.7% in countries with a Western lifestyle
Onset: sudden
Duration: acute attacks lasting 3-14 days
Morning pain or stiffness usually present
Demographic factors
Indigenous Taiwanese, Pacific Islander, New Zealand Maori
Living in high-income countries (North America and western Europe)
Male sex (incidence 2-6x higher than in females)
Dietary factors
High alcohol intake
Diet rich in meat and seafood
High fructose consumption
Acute, rapidly developing, self-limiting monoarthritis
Commonly involving first metatarsophalangeal joint (The term podagra refers to a gout flare at the first MTP joint)
Other affected joints of lower limb: midfoot, knee
Flares usually self-resolve within 14 days and are interspersed between asymptomatic intercritical periods
Over time, flares can become more frequent and severe, and can also affect upper limbs and multiple joints (polyarticular flares)
Tophi located at the first MTP joint, other joints and tendons of foot and ankle (e.g. Achilles tendon), prepatella bursae, olecranon bursae, helix of ear
Gout – Comorbid Conditions
Hyperuricemia
Metabolic syndrome
Type 2 diabetes mellitus
Cardiovascular disease
Hypertension
Hyperlipidemia (elevated triglyceride and cholesterol levels)
Obesity
Chronic kidney disease
Diuretic use (loop and thiazide)
Obstructive sleep apnea
Menopause
Conditions that have rapid cell turnover (such as psoriasis, hemolytic anemia, or certain cancers)
Lesch-Nyhan syndrome
Rare hereditary condition of purine metabolism; X-lined recessive pattern – males affected; mutation in HPRT1 gene leading to deficiency or complete absence of hypoxanthine-guanine phosphoribosyltransferase (enzyme responsible for recycling purines)
Kelley-Seegmiller syndrome
Rare hereditary condition of purine metabolism; mild form of hypoxanthine-guanine phosphoriboxyltransferase (HPRT) deficiency
Gout progression
Gout Evaluation
Based on clinical diagnosis, classification criteria and microscopy-based diagnosis of synovial fluid
2015 ACR-EULAR Gout Classification Criteria
Not meant for diagnosis of gout, but can help inform the clinician; intended for research purposes to identify subjects who may be eligible for entry into clinical studies
Online calculator available here: https://goutclassificationcalculator.auckland.ac.nz/
Serum uric acid levels to identify hyperuricaemia
Gold standard for diagnosis: joint aspiration and microscopy analysis showing presence of monosodium urate crystals (identified by needle-like appearance and strong negative birefringence)
Other tests: ultrasonography, dual-energy CT
Calcium Pyrophosphate Dihydrate Crystal Deposition
aka pseudogout
Persons > 65 years old
Onset: sudden
Duration: flares lasting days to weeks
Morning pain or stiffness usually present
Calcium pyrophosphate dihydrate crystals are polymorphic, weakly positive under birefringent microscopy
Other types of crystal-induced arthritis: calcium oxalate, hydroxyapatite
Rheumatoid Arthritis (RA)
0.5-1% worldwide prevalence
Higher risk in women (2-3x higher than men), smokers, patients with family history of RA
Genetic predisposition: HLA-DR1 and HLA-DR4
Systemic autoimmune inflammatory disease
May have multisystem involvement
Chronic/relapsing destructive synovitis (local inflammation, cartilage destruction, bone erosion)
Cytokines (TNF-α, IL-1, IL-6) drive chronic synovial inflammation
RA- Clinical features, risk factors, evaluation
Symmetrical, polyarticular pain and stiffness – most often affecting wrists, PIP, MCP, MTP joints
Morning stiffness > 1 hour
Systemic symptoms: fatigue, weight loss, anemia
Visible boggy swelling caused by synovitis
Palpable synovial thickening
Affected joint painful if pressure applied on palpation or with movement
Advanced disease: ulnar deviation, MCP joint subluxation, swan neck deformity, Boutonniere deformity
Extra-articular manifestations: accelerated atherosclerosis, pericarditis, keratoconjunctivits sicca, episcleritis/scleritis, interstitial lung disease, pulmonary nodules, rheumatoid nodules, pleural effusion, vasculitis
Classification criteria
ACR/EULAR 2010 criteria (see next slide) replaced the 1987 ARA criteria
Lab findings:
Radiography: periarticular erosions, osteopenia, joint space narrowing
Inflammatory markers: ESR, CRP
Serology markers:
75-85% will test positive for RF, ACPA or both – these patients are designated as seropositive RA
Rheumatoid factor
sensitivity 65-73%; specificity 82-88%
LR+ 3.95-5.97; LR- 0.33-0.44
https://doi.org/10.7326/0003-4819-146-11-200706050-00008
Anti-citrullinated protein antibodies (ACPA, or anti-CCP antibodies)
sensitivity 53-71%; specificity 95-96%
LR+ 12.5-15.9; LR- 0.36-0.42
American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) 2010 Diagnostic Criteria for RA
At least 1 joint with definite clinical synovitis (swelling) not explained by another disease plus 1 of the following:
Presence of long-standing disease previously satisfying classification criteria
Presence of ≥ 2 typical periarticular erosions
Score ≥ 6 on following criteria:
Joint involvement (0-5)
1 large joint - 0
2-10 large joints - 1
1-3 small joints (with or without involvement of large joints) - 2
4-10 small joints (with or without involvement of large joints) - 3
> 10 joints (at least 1 small joint) - 5
Serology (0-3)
negative rheumatoid factor (RF) and antibodies to anti-citrullinated protein antibodies (ACPA) - 0
low positive RF or low positive ACPA - 2
high positive RF or high positive ACPA - 3
acute phase reactants (0-2)
normal C-reactive protein and normal erythrocyte sedimentation rate (ESR) - 0
abnormal C-reactive protein or abnormal ESR - 1
duration of symptoms (0-1)
< 6 weeks - 0
≥ 6 weeks - 1
RA - Management,
Low threshold for referral to rheumatologist
> 12-week delay in treatment associated with reduced chance of drug-free remission and increased risk for progressive joint damage
https://doi.org/10.1136/bmj.c6942
Goals of treatment:
Early diagnosis and early initiation of treatment to prevent irreversible joint damage
Achieve long-term clinical remission
Optimize quality of life
Monitor for extra-articular complications
Complications of RA
Osteopenia and osteoporosis fracture
Lung manifestations – pleuritis, bronchiolitis, interstitial fibrosis
Accelerated atherosclerosis coronary artery disease, peripheral vascular disease
Increased insulin resistance, diabetes mellitus
Vasculitis, thromboembolic disease
Depression
Anemia of chronic disease
Felty syndrome (RA, splenomegaly, neutropenia)
Osteoarthritis
Prevalence increases with age
7.3% in ages 18-44; 30% in ages 45-64; 50% in ages 65 and older
Women > men
Other risk factors: overweight/obese, previous joint injury, family history, frequent bending/squatting, repetitive impact
Degenerative disorder of articular cartilage associated with hypertrophic bone changes
Onset: gradual
Duration: lifelong with flares
Usually no morning pain or stiffness (or short-lived)
Asymmetric joint pain and stiffness – commonly affecting hands, knees, hips, feet, spine
May also have joint locking or joint instability
Joint pain worsened by movement/activity, especially following a period of rest
Joint swelling and tenderness
Bony enlargement in prolonged or severe OA
Pain on range of motion and limitation of range of motion
Crepitus (typically knee) may be felt and heard
Bouchard nodes on proximal interphalangeal joint
Heberden nodes on distal interphalangeal joints
Osteoarthritis – Evaluation
Primarily a clinical diagnosis based on history and PE
Imaging not required in patients with risk factors and typical symptoms
X-ray – can confirm diagnosis and rule out other conditions; helpful before referral for joint replacement
May see joint space narrowing (due to loss of articular cartilage), osteophyte formation, subchondral sclerosis, joint destruction
CT or MRI when diagnosis is in doubt or strong suspicion for other etiology (e.g., meniscal injury); growing use of ultrasonography
Laboratory testing not usually required
