Boutonnière Deformity in RA MCQ — NEET PG Practice Question | NEETPGAI
Boutonnière Deformity in RA
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bone Orthopedics
A 52-year-old woman with a 10-year history of rheumatoid arthritis presents with progressive deformity of her right index finger. On examination, the proximal interphalangeal (PIP) joint is held in flexion, and the distal interphalangeal (DIP) joint is hyperextended, as shown in the diagram. The structure marked **A** represents the PIP flexion deformity. Which of the following best explains the pathophysiological mechanism underlying this characteristic deformity?
A. Rupture of the central slip of the extensor digitorum tendon causing volar subluxation of the lateral bands, which now act as PIP flexors rather than extensors
B. Attenuation of the collateral ligaments of the PIP joint with compensatory flexor digitorum profundus hyperactivity
C. Contracture of the intrinsic hand muscles with secondary tightening of the flexor digitorum superficialis tendon
D. Direct synovial erosion of the PIP joint cartilage leading to mechanical joint instability and flexion contracture
Explanation
Why option 1 is right
Boutonnière deformity is pathognomonic for rupture or attenuation of the central slip of the extensor digitorum tendon. When the central slip is damaged (commonly by rheumatoid synovitis eroding the tendon over the PIP joint), the lateral bands—which normally assist in PIP extension—subluxate volarly (below the axis of rotation of the PIP joint). Once volar to the PIP axis, these lateral bands become flexors of the PIP joint while paradoxically continuing to extend the DIP joint through their insertion on the terminal extensor tendon. This biomechanical reversal produces the characteristic PIP flexion (marked A) with compensatory DIP hyperextension (marked B). This mechanism is the cornerstone of boutonnière deformity pathophysiology and is confirmed by Elson's test: when the PIP is flexed 90° and the patient attempts to extend the middle phalanx, a ruptured central slip results in rigid DIP extension due to lateral band recruitment. [Harrison's 21e Ch 351; Greene's Hand Surgery]
Why each distractor is wrong
Option 2 (intrinsic muscle contracture): While intrinsic tightness can contribute to hand deformities in RA, it does not explain the specific mechanism of boutonnière deformity. Intrinsic contracture typically produces MCP flexion and PIP extension (swan-neck pattern), not PIP flexion. The defining lesion in boutonnière is central slip rupture, not intrinsic muscle pathology.
Option 3 (direct cartilage erosion): Although RA does cause synovial proliferation and marginal erosions visible on radiographs (marked C and D in the diagram), cartilage erosion alone does not produce the characteristic deformity. The deformity results from the specific biomechanical consequence of central slip rupture and lateral band subluxation, not from joint destruction per se. Many RA patients have erosions without boutonnière deformity.
Option 4 (collateral ligament attenuation with flexor profundus hyperactivity): Collateral ligament laxity does occur in RA and can contribute to joint instability, but it is not the primary mechanism of boutonnière deformity. The defining feature is central slip rupture causing lateral band volar subluxation. Flexor profundus hyperactivity is not a recognized pathophysiological driver of this deformity.
High-YieldNEET PG
Boutonnière = central slip rupture → lateral bands subluxate volar → become PIP flexors (not extensors) → PIP flexion + DIP hyperextension. Swan-neck is the opposite (PIP hyperextension + DIP flexion).
Harrison's 21e Ch 351; Greene's Hand Surgery; ASSH Guidelines
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