Introduction

        Although seemingly insignificant, finger fractures present enormous potential for fine motor dysfunction and chronic problems (Prentice, 2006).  Injury may not only limit the function of a finger in sport, especially those requiring tremendous control, but also the finger’s usefulness in activities of daily living. Less than optimal intervention, either conservative by means of rest and rehabilitation or more aggressive operative methods, can lead to additional disability and complications, such as malunion, nonunion, and posttraumatic osteoarthritis (Ring, 2005).

        A fairly common occurrence in finger fractures is malunion. Malunion fractures are those that heal with a deformity, and are caused by bone regeneration with fragments in an imperfect, or malaligned position (Freeland, 2006; Delforge, 2002). Common causes of malunion are the inability to effect position of fracture reduction and inadequate maintenance of immobilization. Most malunions involve joint surface incongruency, angular deformity, or rotational deformity. Bony union does occur; however, an angular or rotary deformity is the common result (the individual finger appears turned downward in relation to the others or looks crooked/deviated from the center) (Ring, 2005; Delforge, 2002). These deformities may present individually or all together. Bony shortening is also a possible deformity (Freeland, 2006).

      Major complications of malunion finger fractures are the sticking together of flexor or extensor tendons. Malunion increases the likelihood of tendon adhesions, permanent shortening (contracture), and limitation of joint motion (Skinner, 2003). Extensor tendons inserting on the middle bone of the finger transmit extensor forces to the bone, leading to tendon imbalance and permanent bending of the second joint on the finger (Ring, 2005; Skinner, 2003). Flexor tendons inserting on the bottom side cause dorsal angulation, and the segment moves toward the back of the hand if the fracture is closer to the tendon insertion.  Fractures farther away from the insertion angulate with the apex toward the palm side of the hand. All finger fractures closer to the hand angulate with the apex facing the hand’s palm because of the sideways force from bands passing palmarly toward the axis of the second joint (Skinner, 2003). This angulation is further contributed by the greater distance the extensor tendons have from the axis of rotation of the fracture site compared to that of the flexor tendons (Freeland, 2006). Secondary correction may be required if these tendon forces begin to produce a serious deformity (Skinner, 2003).

      Malunion of a finger generates aesthetic and functional problems, such as trouble gripping and picking up due to associated pain or diminished motion. The functional impact depends on the location, type, and severity of the malunion. Time since injury, joint involvement, and joint adhesions also play a role in determining functional impact. Neither chronic finger flexion nor a substantial angular deformity is functional (Ring, 2005; Freeland, 2006).

            A less frequent complication of finger fractures is a prolonged amount of healing time. Normal healing time for bones is four to six weeks. Smaller bones may even heal in as little as three weeks. Delayed union occurs after the normal amount of time has passed and the fracture is not a single complete union. If longer time passes and still no union exists, the term nonunion is used, and a nonunion fracture has occurred. Delayed healing may or may not lead to nonunion (Scudder, 1915).
Nonunion is not to be confused with no union. Rather than complete separation, nonunion concerns only a particular area that is not fully healed. In many cases, fibrous union is present and the fracture is almost totally healed, except in a certain area. There are localized and general causes of nonunion. Local causes are the impedance or interference of surrounding soft tissue between fracture fragments, such as periosteum strips, fascia, or muscle. Distance between pieces or substandard immobilization also may cause nonunion. General systemic causes can be syphilis, pregnancy, prolonged lactation, and acute febrile diseases (Scudder, 1915).

      Although persistent hand pain is multifactorial, nonunion suspicion should increase if a fracture is involved. The majority of nonunions are post-surgical and result from either poor bone fixation or a combination of that and decreased blood supply. An overwhelming number of nonunions in the hand are atrophic, meaning the fractured bone decreases in size and wastes away. Like malunion fractures, nonunions in the hand are also associated with tendon adhesions or contracture, which will require operation (Ring, 2005). Delaying operation can cause degenerative bone and joint disease, such as osteoarthritis. Osteoarthritis is a progressing loss of joint cartilage accompanied by attempted repair and hardening of underlying bone (Buckwalter, 2003). Development of the posttraumatic form secondary to a fracture has several contributing factors. These include involvement of surfaces within the joint, joint incongruency, resulting angular deformity, quantity and quality of nearby blood vessels, and degree of immobilization. Upper extremity joints are less likely to develop arthritis due their reduced role in load carrying (Maeurer, 2004; Wright, 1990).
 
      The in vivo canine studies by Vener et al. have shown development of posttraumatic (occurring after an injury) osteoarthritis in response to a fracture within the joint. Damage is first seen as cracks in the zone of calcified cartilage and bone beneath the cartilage, which extends to surface cracks on the cartilage. Actual failure of cartilage begins in the zone of calcified cartilage and sub-cartilage bone, spreading deeper to this area and the overlying cartilage. Such damage is expected to respond the same in humans, leading to degeneration of cartilage. Geometry of certain joints may predispose one surface to damage (Vener, 1992).

     Similar to canine studies, human research has shown joint cartilage damage associated with fractures inside the joint, as well as abnormal loading (Court-Brown, 2006). As in the canine studies, human research has shown a link between substantial single, repetitive, or torsional loading forces, and damage in the calcified cartilage and bone regions beneath the cartilage without damaging the joint surface or surrounding soft tissue. Progression causes these surface irregularities to become clefts, penetrating the entire cartilage until reaching the bone (Buckwalter, 2003).

     Members of the medical community debate the adverse effects of malunion on surrounding joints. Scant evidence suggests that malunion in the upper extremity contributes to posttraumatic osteoarthritis.  A number of authors have shown posttraumatic osteoarthritis in the knee from a malunion of the tibia. In theory, these principles could be applied to other joints. Even with this debate put aside, posttraumatic osteoarthritis can be a complication of any fracture (Court-Brown, et al., 2006).

Case Report