Boutonnière deformity results from disruption of the central slip of the extensor tendon at its insertion onto the middle phalanx, with subsequent volar migration of the lateral bands. This causes loss of PIP extension, lateral bands becoming flexors of the PIP, and hyperextension of the distal interphalangeal joint. Etiologies include closed avulsion injury (jammed finger), open laceration over the dorsum of the PIP, burns, rheumatoid arthritis, and post-surgical complications. Acute injuries (within 6 weeks) are often missed initially and present as chronic deformity.
Examination shows PIP held in flexion with inability to actively extend, weakness of DIP flexion (Elson test: PIP held flexed at 90 degrees on table edge; if patient extends DIP forcefully, central slip is intact), tenderness over the dorsal PIP, and characteristic boutonnière posture in chronic cases. Imaging includes plain radiographs to identify avulsion fractures and ultrasound or MRI for soft-tissue assessment. Stages: stage I (mobile, supple deformity), stage II (fixed PIP flexion contracture but DIP correctable), stage III (rigid deformity with both joints fixed and articular changes).
Acute closed central slip injury is treated with continuous PIP extension splinting (full-time for 6 weeks, then night-only for 6 weeks) while allowing DIP flexion to mobilize the lateral bands. Surgical repair is indicated for displaced avulsion fractures, open injuries, and rheumatoid disease with subluxation. Chronic supple deformity may respond to staged splinting and hand therapy; fixed deformity requires surgical reconstruction including central slip repair, terminal tendon tenotomy (Fowler), lateral band relocation, or PIP arthrodesis for end-stage rigid disease.