Systemic Immunosuppression for Prevention of Recurrent Tendon Adhesions

The recovery for patients after tendon repair is frequently limited by development of tendon adhesions. This scar tissue formation is dependent on immune system activation. Tacrolimus has unique properties that may contribute to the prevention of overactive scarring by inhibition of inflammatory cytokines.

Herein, we present a case using systemic immunosuppression to prevent recurrent adhesion accumulation in a patient with a prior spaghetti wrist injury. Tacrolimus began 1 week before repeat-secondary tenolysis surgery, and it continued for 3 months postoperative. Dosing was tapered to a serum level between 5 and 8 µg/L.

The 27-year-old male patient suffered a volar wrist laceration transecting all flexor tendons and volar wrist nerves. He underwent immediate repair but had a poor outcome despite early range of motion therapy. A primary tenolysis only improved his average arc of finger motion from 72 to 95 degrees. Secondary tenolysis augmented with systemic tacrolimus improved his arc of finger motion from 95 to 202 degrees. Mechanistically, tacrolimus prevents proper function of activated T and B cells. This results in decreased proliferation, angiogenesis, and cytoskeletal organization of fibroblasts on inflammation and integrin adhesions, and it potentially explains the reduced tendon molecule adhesions seen in this patient.

Tacrolimus may be effective in reducing motion, limiting tendon adhesions. The novel use of this medication resulted in the return of near-normal hand function in a patient placed on low-dose tacrolimus after primary tenolysis had failed.