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What is the differential

diagnosis of joint pain?
CONSTRUCTING A DIFFERENTIAL DIAGNOSIS
• causes of joint pain range from common to rare
• from not particularly dangerous to joint and lifethreatening
• evaluation of a patient with joint pain calls for a
detailed history and physical exam (often
focusing on extra-articular findings) and
occasionally the sampling of joint fluid and
possibly analyzing radiologic and serologic tests

How would you frame the
differential?
• the use of 3 pivotal questions
1.is a single joint or are multiple joints
involved (is the joint pain articular or
polyarticular) ?
2.is the pain articular or extra-articular?
3.are the involved joints inflamed or not?
• the acuity of the pain may also be
important







































































































Leading Hypothesis: OA
Textbook Presentation
OA most commonly presents in older patients as chronic joint pain and stiffness. Pain is usually
worse with activity and improves w ith rest. Knees, hips, and hands are most commonly affected. On
examination of the joints, there is bony enlargement w ithout significant effusions. Mild tenderness
may be present along the joint lines. There is limited range of motion. Radiographs are diagnostic.
Disease Highlights
A. OA is a disease of aging, with peak prevalence in the eighth decade. However, as obesity is a risk
factor, it may be seen in much younger people w ith severe obesity.
B. More comm on in wom en than men
C. Although often referred to as “wear and tear” arthritis, the pathophysiology is actually quite
complicated.
D. Joint destruction m anifests as a loss of cartilage with change to the underlying bone seen as bony
sclerosis and osteophyte formation.
E. Joint distribution
1. OA is most common in the knees, hips, hands, and spine.
2. Nearly any joint can be affected.
3. Non–weight-bearing joints other than the hand, such as the elbow, wrist, and shoulder, are less
commonly affected by OA. The ankle is also not a common location.
F. Classic sym ptoms include
1. Pain with activity
2. Relief with rest
3. Periarticular tenderness
4. Occasional mildly inflam matory flares
5. Gelling: Joint stiffness brought on by rest and rapidly resolving with activity.
6. Late in the disease, constant pain with joint deform ation and severe disability is common.
G. Physical exam findings
1. Generally there is bony enlargement, crepitus, and decreased range of motion without signs of
inflammation or synovial thickening.
2. Knee
a. Crepitus
b. Tenderness on joint line
c. Varus or valgus displacem ent of the lower leg related to asymm etric loss of the articular
cartilage.
3. Hip
a. Marked decrease first in internal and then external rotation
b. Groin pain with rotation of the hip
4. Hand
a. Tenderness and bony enlargement of the first carpometacarpal joint
b. Joint involvem ent in decreasing order of prevalence is DIP, PIP, MCP.
c. Heberden nodes (prominent osteophytes of the DIP joints)
Figure 27-3 Osteoarthritis of the hand.
d. Bouchard nodes (prom inent osteophytes of the PIP joints)
e. Figure 27-3 shows a hand with som e of the classic findings of OA.
5. Spine
a. Signs of spinal OA vary depending on location.
b. Pain and limited range of m otion are com mon.
c. Radicular sym ptoms resulting from osteophyte impingement on nerve roots is seen.
d. Spinal stenosis with associated symptoms (radiculopathy and pseudoclaudication) can result
from bony hypertrophy (see Chapter 7, Back Pain).
Evidence-Based Diagnosis
A. The diagnosis of OA is clinical, based on a com patible history, physical exam, and radiologic
findings.
B. Because of the high prevalence of OA, the diagnosis should lead the differential in any patient with
suspicious symptoms.
C. Diagnostic criteria have been established.
1. Hand
a. Pain, aching, or stiffness
b. 3 of the following
(1) Hard tissue enlargement of at least 2 of the following joints:
(a) Second and third DIP joints
(b) Second and third PIP joints
(c) First MCP joint
(2) Hard tissue enlargement of 2 or m ore DIP joints
(3) Fewer than 3 swollen MCP joints
(4) Deformity of at least 1 of the joints listed in above entries a through c.
2. Hip
a. Hip pain
b. 2 of the following:
(1) ESR < 20 mm /h
(2) Osteophytes on radiograph
(3) Joint-space narrowing on radiograph
3. Knee: There are multiple criteria, the easiest to remember is
a. Knee pain
b. Osteophytes on radiograph, and
c. 1 of the following
(1) Age older than 50 years
(2) Stiffness < 30 minutes
(3) Crepitus
D. The test characteristics for these criteria are shown in Table 27-15.
Table 27-15. Test characteristics for the diagnostic criteria of OA.
Treatment
A. Nonpharmacologic
1. Patient education and improved social support have been shown to improve pain and improve
the efficacy of pharmacologic interventions.
2. Weight loss decreases the symptom s of lower extremity OA.
3. Physical and occupational therapy can help patients with functional impairm ent due to OA.
B. Pharmacologic
1. Acetaminophen
a. Standard initial therapy given its effectiveness and low side-effect profile.
b. Equally effective to NSAIDs for mild to moderate OA.
2. NSAIDs are probably more effective than acetaminophen for severe OA.
3. Oral com binations of glucosam ine and chondroitan sulfate probably are m odestly effective in
some patients and have a very favorable side-effect profile.
4. Intra-articular medications
a. Intra-articular corticosteroids are very effective for acute flares of OA.
b. Hyaluronic acid given by intra-articular injection may provide a small benefit to some
patients.
5. Tramadol and opioid analgesics are reasonable choices for patients with severe symptoms.
C. Surgical
1. Arthroscopic surgery for OA is probably ineffective.
2. Hip and knee replacem ent can have remarkable effects on decreasing pain and im proving
function in patients in w hom conservative therapy has failed

it is important to recognize that all of the
monoarticular
arthritides
can
present
in
a
polyarticular
distribution,
and
classically
polyarticular
diseases
may
occasionally only affect a single
joint. Thus, this organization is useful to
organize your thinking but should never
be used to exclude diagnoses from
consideration.

gout
penyakit heterogen yang diakibatkan
tingginya kadar asam urat dalam darah
karena adanya gangguan metabolisme asam
urat , sehingga kristal monosodium urat
terdeposisi dalam jaringan tubuh.
Manifestasi klinis :
1.Hiperurisemia asimtomatik
2.Artritis gout akut
3.Gout intertitial
4.Gout kronik bertofi

• Gouty attacks often occur after abrupt
changes in uric acid levels. Common
causes are:
• 1. Large protein meals
• 2. Alcohol binges
• 3. Initiation of thiazide or loop
diuretics
• 4. Initiation of urate-lowering therapy
• 5. Worsening kidney disease

• Forms of gout
• 1. Acute gouty arthritis is by far the most
common type of gout.
• 2. Chronic arthritis can develop in patients who
have untreated hyperuricemia.
• 3. Tophaceous gout occurs when there is
macroscopic deposition of sodium urate crystals
in and
• around joints.
• 4. The kidney can also be affected by gout.
Sodium urate stones or a urate nephropathy can
• develop in patients.

• Acute, inflammatory, monoarticular
arthritis is an absolute indication for
arthrocentesis.

• Kriteria diagnosis (ACR)
1.terdapat kristal asam urat pada cairan sendi
2.Terdapat kristal asam urat dari tofus
3.Terdapat 6 dari 12 parameter ( bila 2 di atas tidak ada)
a.Artritis akut
b.Puncak peradangan pada hari ke 1
c.Serangan monoartritis
d.Bengkok & nyeri MTP 1
e.Artritis unilateral meliputi MTP 1
f. 7. artritis unilateral termasuk sendi tarsal
g.Diduga ada tofus
h.Radiografi sendi : pembengkakan pada 1 sendi
i. Radiografi : kista subkortikal tanpa erosi sendi
j. Biakan cairan sendi (-) saat serangan radang

penatalaksanaan
• Non – farmakologi : modifikasi gaya
hidup, istirahatkan sendi dan
kompres air dingin untuk serangan
akut
• Farmakologi : allopurinol (fisrt line),
uricosuric







































Treatment
A. Therapy for gout is classified as either abortive (to treat an acute flare) or prophylactic (to prevent
flares and the destructive effects on the joints and kidneys).
B. Abortive therapy is outlined in Table 27-3.
Table 27-3. Immediate therapies for gout and their potential adverse effects.
1. All of the therapies are effective, and the choice is usually made by the potential adverse
effects.
2. Most frequently, patients are treated with a combination of a potent nonsteroidal
antiinflammatory drug (NSAID) and colchicine.
C. Prophylactic therapy
1. There are 5 basic indications for prophylactic therapy:
a. Frequent attacks
b. Disabling attacks
c. Urate nephrolithiasis
d. Urate nephropathy
e. Tophaceous gout
2. Prophylactic therapy should begin with nonpharmacologic interventions to decrease uric acid
levels and decrease the risk of gouty flares.
a. Abstinence from alcohol use
b. Weight loss
c. Discontinuation of medications that impair urate excretion (eg, aspirin, thiazide diuretics).
3. Potential prophylactic treatments are listed below.
a. NSAIDs
b. Colchicine
c. Allopurinol
d. Probenecid
e. Sulfinpyrazone
f. Febuxostat
g. Uricase agents (eg, pegloticase) are in the early stage for testing as prophylactic therapies.
4. Colchicine should be used during the initiation of urate-lowering therapy to prevent recurrent
gouty flares.
a. NSAIDs may be added if necessary.
b. Colchicine is usually continued for at least the first 6 months (longer in the case of patients
with tophi) of urate-lowering therapy.
5. Allopurinol is usually the first antihyperuricemic drug used, although it is relatively
contraindicated in patients with chronic kidney disease or liver disease.
6. If allopurinol is ineffective, uric acid excretion should be measured. Patients with low uric acid
excretion (present in 80% of patients with gout) should be given a uricosuric agent, such as
probenecid.





















Calcium Pyrophosphate
Deposition Disease
(CPPD)

A. CPPD is a crystal-induced arthropathy that can present in multiple different ways.
1. CPPD is often asymptomatic, being diagnosed as an incidental radiographic finding of
chondocalcinosis, the linear calcifications of articular cartilage.
2. Pseudogout is an acute, inflammatory, usually monoarticular arthritis that can be clinically
indistinguishable from gout, except for the presence of calcium pyrophosphate dihydrate
crystals in the joint fluid.
3. Pyrophosphate arthropathy is a chronic arthritis that is clinically similar to OA (sometimes
referred to pseudo OA); distinguishing between the 2 conditions may be difficult. However,
pyrophosphate arthropathy may affect joints less commonly affected by OA like the wrists,
MCPs, and shoulders.
4. A small percentage of patients with CPPD (≈5%) can have a chronic, inflammatory
polyarthritis resembling RA (sometimes referred to as pseudo RA).
5. Rarely, CPPD can present as pseudoneuropathic arthropathy, resembling a Charcot joint. In this
presentation there is a destructive monoarthropathy,
B. There are many other similarities between pseudogout and gout.
1. Both are caused by the inflammatory response to crystals in the synovial space.
2. Both cause acute painful monoarticular attacks.
3. Both can cause polyarticular flares.
4. Flares can be induced by trauma or illness.
5. Both can potentially cause destructive arthropathy.
6. Incidence increases with age.

• Pseudogout has been associated with
a number of diseases, the most
common of which are:
• 1. Hyperparathyroidism
• 2. Hemochromatosis
• 3. Hypomagnesemia
• 4. Hypophosphatasia

• The following characteristics should make a
clinician consider the diagnosis of CPPD:
• 1. Acute arthritis of a large joint, especially
the knees, in the absence of hyperuricemia.
• 2. Chronic arthritis with acute flares.
• 3. Chronic arthritis involving joints that
would be atypical for OA such as the wrists,
• metacarpophalangeal (MCP) joints, and
shoulders.

• A. Treat an associated underlying
disease, when present.
• B. Acute attacks can be managed with
• 1. NSAIDs
• 2. Joint aspiration with corticosteroid
injection
• 3. Colchicine
• C. Chronic degenerative arthritis is
difficult to treat. NSAIDs are usually
used.

4. Ankle
5. Cervical spine
a. Usually presents as
neck pain and stiffness.
b. C1–C2 instability can
occur secondary to
associated tenosynovitis.
(1) This can produce
cervical myelopathy.
(2) Advisable to

RA
• Penyakit autoimun yang
menyebabkan inflamasi sistemik
kronis yang manifestasi utamanya
adalah poliartritis yang progresif,
namun juga melibatkan seluruh
organ tubuh.
• Onset usia 20-60
• Sex perempuan > laki2

diagnosis
• Menurut ACR / EULAR

Acr/ elar 2010

SLE
• A. SLE is a truly systemic autoimmune disease primarily affecting women of childbearing
age.
• B. Various groups are more prone to disease.
• 1. Female:male ratio is about 9:1.
• 2. About 5% of patients reporting a first-degree relative with the disease.
• 3. Women of color are most commonly affected.
• C. Almost every organ can be involved, although the joints, skin, serosa, and kidneys are
most
• commonly affected.
• D. The pathogenesis of the disease is related to the formation of autoantibodies to a
number of nuclear
• antigens. The ANA is the most common.
• E. The most common features of SLE, both at presentation and later in follow-up, are listed
in Table
• 27-7.
• Table 27-7. Clinical manifestations of SLE at onset and during disease.
• Evidence-Based Diagnosis
• A. The diagnosis of SLE, especially in people with mild disease, can be difficult.
• B. The ACR has developed criteria to standardize the diagnosis for research purposes.
• 1. The criteria are:
• a. Malar






















A. The diagnosis of SLE, especially in people with mild disease, can be difficult.
B. The ACR has developed criteria to standardize the diagnosis for research purposes.
1. The criteria are:
a. Malar rash
b. Discoid rash
c. Photosensitivity
d. Oral ulcers
e. Arthritis (nonerosive arthritis)
f. Serositis (pleuritis or pericarditis)
g. Renal disorder (proteinuria or cellular casts)
h. Neurologic disorder (headache, seizures, or psychosis without other cause)
i. Hematologic disorder (hemolytic anemia or any cytopenia)
j. Immunologic disorder (anti-DNA, anti-SM, or antiphospholipid antibodies)
k. Positive ANA
2. The diagnosis of SLE requires the presence of 4 or more of these criteria.
3. Although the same reservations about using diagnostic criteria (that were developed for
research purposes) clinically that were discussed above in the section of RA apply here, the
SLE criteria are frequently used.
4. The test characteristics of these criteria are given in Table 27-8. Also included in this table are
the test characteristics for the various individual criteria.
Table 27-8. Test characteristics for the ACR criteria (4 or more positive criteria) and individual
criteria in the diagnosis of SLE.



























5. The presence of a malar rash, or satisfaction of the ACR criteria, is highly supportive of the
diagnosis of SLE.
C. Autoantibodies
1. Measuring autoantibodies in SLE provides important diagnostic information.
2. ANA and anti-DsDNA
a. ANA is the most sensitive test for SLE. It is very nonspecific.
b. Anti-DsDNA is highly specific. It is also associated with the presence of lupus nephritis.
c. ANA does not vary with disease activity while anti-DsDNA does.
d. The predictive values of ANA and Anti-DsDNA are
(1) ANA: sensitivity, 99%; specificity, 80%, LR+, 4.95; LR–, 0.0.1
(2) DsDNA: sensitivity, 73%; specificity, 98%; LR+. 36.5; LR–, 0.28
A negative ANA essentially rules out SLE. A positive anti-DsDNA essentially rules in SLE.
e. Staining patterns are often reported with the ANA.
(1) These patterns correlate, to some extent, with the other specific antibodies discussed
below and their use has, to a great extent, been supplanted by these tests.
(2) In general, the meanings of the staining patterns are as follows:
(a) Homogeneous: Seen in SLE, RA, and drug-induced lupus
(b) Peripheral: Most specific pattern for SLE
(c) Speckled: Least specific pattern. Commonly seen with low titer ANAs in people
without rheumatic disease
(d) Nucleolar: Common in patients with scleroderma and Raynaud phenomenon.
3. Other serologies are helpful because they tend to be associated with various subsets of disease.
a. Anti-RNP: Associated with Raynaud phenomenon and myositis
b. Anti-SSA/Ro and anti-SSB/La: Associated with Sjögren syndrome and photosensitivity
c. Anti-ribosomal P: Associated with CNS manifestations of SLE
4. Table 27-9 outlines a variety of serologies that may be obtained in persons in whom
rheumatologic disease is suspected

• D. Complement
• 1. Complement levels are helpful in tracking the activity of SLE but are
nonspecific.
• 2. C3, C4, and CH50 levels tend to decline during episodes of lupus activity.
• Treatment
• A. Similar to RA, the treatment of SLE is complicated and to a great extent the
purview of the
• rheumatologist.
• B. In general, NSAIDs, corticosteroids, and immunosuppressants are the mainstay
of therapy.
• C. NSAIDs are generally used for symptomatic relief of inflammatory symptoms
with careful
• monitoring because of their potential nephrotoxic effects.
• D. Corticosteroids and hydroxychloroquine are commonly used in long-term
therapy and high-dose
• corticosteroids are used for disease exacerbations.
• E. Cyclophosphamide, mycophenolate mofetil, and azathioprine are the most
commonly used
• immunosuppressants in SLE. They are used most widely for the treatment of lupus nephritis.