Introduction Characterized by hyperextension of PIP flexion of DIP Caused by lax volar plate imbalance of muscle forces on PIP (extension force > flexion force) Injuries include MCP joint volar subluxation (rheumatoid arthritis) mallet finger FDS laceration intrinsic contracture Seen in rheumatoid arthritis Pathoanatomy Primary lesion is lax volar plate that allows hyperextension of PIP. Causes include trauma generalized ligament laxity rheumatoid arthritis Secondary lesion is imbalance of forces on the PIP joint (PIP extension forces that is greater than the PIP flexion force). Causes of this include mallet injury leads to transfer of DIP extension force into PIP extension forces FDS rupture leads to unopposed PIP extension combined with loss of integrity of the volar plate intrinsic contracture tethering of the lateral (collateral) bands by the transverse retinacular ligament as a result of PIP hyperextension. if the lateral (collateral) bands are tethered, excursion is restricted and the extension force is not transmitted to the terminal tendon, and is instead transmitted to the PIP joint MCP joint volar subluxation caused by rheumatoid arthritis Presentation Symptoms snapping and locking of the fingers Physical exam hyperextension of PIP flexion of DIP Imaging Radiographs recommended views AP and lateral view of the affected hand Treatment Nonoperative double ring splint indications can prevent hyperextension of PIP Operative volar plate advancement and PIP balancing with central slip tenotomy indications progressive deformity technique address volar plate laxity with volar plate advancement correct PIP joint muscles imbalances with either FDS tenodesis indicated with FDS rupture spiral oblique retinacular ligament reconstruction central slip tenotomy (Fowler)
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