Polyarthritis: How to reach a diagnosis

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Polyarthritis How to reach a diagnosis?

• By
• Kamel Heshmat Gado
• Professor of Internal Medicine
• Rheumatology Immunology Unit
• Cairo University

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• Differential diagnosis of chronic polyarthritis
  is a challenge. Patients do not appear in
  textbook form especially early in the course of
  their illness.
• Many diseases evolve from less specific to more
  specific forms.
• To add to the confusion, more than one disease
  can exist in the same patient as gout developing
  in the fingers of a patient with OA as in
  overlap syndromes.

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• The purpose of this presentation is to give some
  clinical hints to help treating physicians to
  differentiate between the most common clinical
  disorders causing chronic polyarthritis

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• Diseases to be recognized and differentiated from
  one another are
• Rheumatoid arthritis
• The spondyloarthropathies
• Ankylosing spondylitis
• Reactive arthritis
• Arthritis associated with inflammatory bowel
  disease
• Psoriatic arthritis
• Crystal deposition disease
• Gout
• Pseudogout (CPPD deposition disease)
• Osteoarthritis
• Connective tissue diseases
• SLE
• Scleroderma
• Polymyositis
• Mixed connective tissue disease

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• Five rules are applied to understand how physical
  findings predict the differential diagnosis of
  patients with chronic polyarthritis.
• 1. Pathogenetic aspects predict physical
  findings.
• The distribution of joint involvement around the
  body provides important clues to the differential
  diagnosis.
• The unique involvement of the hand foot refines
  the differential diagnosis.
• Extra-articular manifestations supply insight to
  diagnosis.
• Certain conditions produce symptoms out of
  proportion to physical findings.

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Rule 1

• Pathogenetic Aspects Predict Physical Findings.

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• R A The inflammatory process synovitis takes
  place within the confines of the joint itself
  (inside the boundaries of the joint capsule).

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• OA The primary process probably begins either in
  cartilage or subchondral bone. The degeneration
  causes the joint to make attempts at repair.
  Repair takes the form of osteophyte formation at
  the margins of the joint.
• Physical findings of OA are osteophyte formation,
  crepitus from rub of damaged surfaces against
  each other, deformities caused by joint
  incongruities small amount of non inflammatory
  fluid.

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• Spondyloarthropathies
• More typically involve the supporting structures
  around the joint (capsule, periosteum
  entheses).
• Inflammation occurs separatly at these sites
  producing pain swelling at a distance from
  beyond the confines of the joint.
• Sometimes inflammation is so extensive that it
  extends from one joint to another in a toe or a
  finger causing a sausage digit.

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• Crystal deposition diseases
• 2 conditions caused by deposition of a
  crystalline material in the joint each has a
  recurrent acute form chronic form.
• Acute form gout pseudo gout
• Chronic form Tophaceous gout CPPD deposition
  disease.

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• In acute gout, inflammation may be so intense to
  often extend well beyond the joint into the
  surrounding soft tissues. Physical findings are
  very dramatic may be mistaken for bacterial
  cellulitis. Pseudo gout is similar but less
  intense.
• If gout passes to chronic form, crystals coalesce
  to form hard yellow masses while CPPD takes the
  form of an aggressive type of OA in unusual
  locations like MCPs, wrist, shoulder or ankle.

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Rule 2

• Distribution of Joint Involvement Around the Body
  Provides Clues to the Diagnosis.

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• RA bilateral, symmetric, upper lower limbs,
  are equally affected, affects large small
  joints (usually spares DIPs).
• Spondyloarthropathies often unilateral,
  asymmetric, involves mostly large joints on lower
  extremities gt upper extremities, Axial
  involvement, enthesitis.
• OA Several forms, involves spine, hips knees
  unique distribution in hands (DIP, P1P, first
  CMC, never MCP).
• Crystal deposition connective tissue diseases
  no unique pattern.

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Rule 3

• Distribution in the Hand and Foot Refines the
  Specificity of the Diagnosis.

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• R A almost always involves MCPs in addition to
  IP.
• O A almost never (with few exceptions) affects
  the MCPs. It commonly involves PIPs, DIPs,
  first CMC.
• Spondyloarthropathies tend to involve IPs out of
  preportion to MCPs, usually asymmetric,
  frequently associated with sausage digits.
• Crystal deposition connective tissue diseases
  may affect any joint.

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RULE 4

• Extra-articular Features Supply Additional
  Insight into the Diagnosis.

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• The presence of extra-articular manifestations
  are important clues for diagnosis
• Skin SLE, psoriasis, scleroderma,
  dermatomyositis, sarcoidosis, reactive
  arthritis, Behcet, vasculitis, enthropathic.
• Eye Reactive arthritis, RA,
  spondyloarthropathies, Behcet, sarcoidosis.
• CNS SLE, Behcet, vasculitis.
• Kidney SLE, vasculitis.
• Bowel Inflammatory bowel disease.

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Rule 5

• Symptoms Out of Proportion to Physical Findings
  Facilitate Differential Diagnosis.

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• Joint involvement in connective tissue diseases
  (SLE, scleroderma, dermatomyositis and mixed
  connective tissue disease) has one common feature
  distinguishing this group from other groups.
  Symptoms are out of proportion to the physical
  findings.
• Patients experience pain in a joint clearly
  beyond what might be expected from the visible
  signs of inflammation. This could be due to
  periarticular soft tissue inflammation.

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• T H A N K Y O U