Early Active Motion After Zone II Flexor Tendon Repair: Stiffness or Rupture?

The concerning findings are the large active-passive flexion gap, the loss of active flexion since day 5, edema, and the patient's fear-driven inactivity. Rupture after a four-strand repair usually presents with a sudden event, a palpable gap, loss of active flexion, and often an abnormal tenodesis effect; passive motion may remain relatively preserved because the joint and capsule are not the limiting structures. In this case the passive range is also reduced (PIP 45°, DIP 35°), the loss appears gradual rather than sudden, the repair site is not tense, and edema is prominent. That pattern fits adhesion formation, edema-related stiffness, and pain guarding better than complete rupture. I would still check active composite flexion, the tenodesis effect, and whether the patient can demonstrate any active DIP flexion. A new extension lag, absent active DIP flexion with a normal passive range, or a sudden change in symptoms would prompt urgent surgeon contact and imaging. I would not use forceful passive flexion to test the repair.

I would keep the dorsal blocking splint within the prescribed parameters and check that it is not blocking IP extension or causing dorsal pressure. The patient needs education that early controlled active flexion is intended to glide the repair, not load it, and that pain should guide but not eliminate motion. I would use active place-and-hold flexion within the splint, isolated FDP and FDS gliding as allowed by the protocol, and light edema management with elevation, retrograde massage, and compressive wrapping if tolerated. I would avoid resisted gripping, passive stretching into extension, and combined full PIP/DIP flexion under load. Because the patient has stopped the program, I would shorten the home session, rehearse it in clinic, and give a written cue card. I would contact the surgeon to report the active-passive gap, the edema, and the patient's fear, and ask whether the protocol should be modified. The message should be factual, not alarmist: no sudden pop, no tense repair site, but reduced active flexion and poor adherence.

I would track active and passive PIP and DIP flexion, composite finger flexion, extension lag, and total active motion at each visit. I would also record pain at rest and with exercise, edema using a consistent circumferential measure, and pulp pinch. A rising passive range with a stable or improving active range suggests stiffness responding to edema control and gentle motion. A falling active range, new extension lag, or loss of the tenodesis effect suggests a mechanical problem and warrants surgeon contact. I would also document whether the patient can reproduce the home program and whether pain is settling. If active flexion plateaus despite good adherence and controlled edema, I would discuss scar management and possible tendon glide progression with the surgeon rather than independently advancing resistance. The decision rule is not one number but the direction of active motion, the active-passive gap, and any sudden change.