Mallet Finger (Extensor Tendon Rupture at DIP)

Mallet finger (also baseball finger, drop finger, hammer finger) is a common closed extensor tendon injury occurring at the distal interphalangeal (DIP) joint, characterized by disruption of the terminal extensor tendon at its insertion into the dorsal aspect of the distal phalanx, causing inability to actively extend the fingertip and a characteristic flexion deformity. It is one of the most common closed tendon injuries of the hand, often in athletes and middle-aged adults. The injury typically occurs from forced flexion of the DIP joint while the extensor tendon is actively contracting (against resistance) — classic mechanism is axial blow to the extended fingertip when catching a ball that strikes the tip rather than being caught in the palm (baseball, basketball, volleyball, dodgeball, softball). Other mechanisms: hyperflexion of fingertip (e.g., catching finger on bedsheet), direct laceration to dorsal DIP, forceful extension against fixed object. Anatomy: the extensor digitorum communis tendon contributes the central slip (inserting into middle phalanx base) and lateral slips (combining with intrinsic muscles to form the lateral bands), with the lateral bands joining over the middle phalanx to form the terminal slip (terminal tendon) that inserts into the dorsal aspect of the distal phalanx, providing DIP extension. Disruption of this terminal tendon at its insertion (through tendon rupture or bony avulsion) causes loss of active DIP extension, while passive extension and flexion are preserved (passive extension by tenodesis effect, flexion by intact flexor digitorum profundus). Two pathophysiologic types: (1) Closed tendon disruption (60-70%): extensor tendon ruptures at its osseous insertion or just proximal — purely soft tissue injury. (2) Bony avulsion (30-40%): tendon avulses a fragment of distal phalanx dorsal lip with attached bone — bony injury, often visible on lateral radiograph as small triangular fragment dorsal to distal phalanx base.

Doyle classification (most commonly used): Type I — closed injury with or without small dorsal avulsion fragment (less than 1/3 of joint surface), no subluxation. Most common type, treated conservatively. Type II — open injury (laceration) with tendon disruption (clean cut). Treated with primary tendon repair or open splinting. Type III — open injury with skin and soft tissue loss in addition to tendon injury. Treated with debridement, soft tissue coverage (skin grafting, flap), and tendon reconstruction. Type IV — subluxation of distal phalanx with bony avulsion: IVa (transepiphyseal injury in children, Salter-Harris II or III pattern of distal phalanx growth plate), IVb (hyperflexion injury with bony avulsion fragment greater than 20% of articular surface), IVc (hyperextension injury with bony avulsion fragment greater than 50% of articular surface plus volar subluxation of distal phalanx). Demographics: typical age 30-50 years (range adolescent to elderly), male predominance (2:1 in athletic injuries), middle finger most commonly involved (28%), then ring finger (24%), little finger (22%), index (16%), thumb (10%), bilateral injury rare. Clinical presentation: classic — flexion deformity at DIP joint (15-45 degrees flexion drop), inability to actively extend the fingertip (patient holds finger in characteristic 'mallet' position with DIP flexed), pain and swelling at DIP joint, palpable depression or defect over dorsal DIP. Other findings: bruising over dorsal DIP, sometimes visible bony fragment, intact passive range of motion (passive extension fully possible by examiner — important to distinguish from intra-articular fracture or dislocation that would limit passive motion). Often history of recent ball sport injury or jammed finger.

Workup: clinical diagnosis is straightforward. Imaging: (1) Lateral radiograph of injured finger (ESSENTIAL): assesses for bony avulsion fracture (small triangular fragment dorsal to distal phalanx base), volar subluxation of distal phalanx (suggests significant injury requiring surgical intervention), size of fragment relative to joint surface (small, more than 1/3, more than 50%). (2) Posteroanterior and oblique radiographs: complete fracture evaluation. (3) MRI rarely needed (clinical diagnosis sufficient in most cases). Treatment: depends on injury type and timing from injury. (1) Closed mallet finger (Doyle Type I): GOLD STANDARD treatment is continuous DIP extension splinting (Stack splint, custom thermoplastic splint, or simple aluminum splint with foam padding). Critical principles: (a) DIP joint must be maintained in full extension or slight hyperextension (5-10 degrees) at ALL TIMES, even during dressing changes and bathing. (b) Splint is worn 24 hours a day for 6-8 weeks without removal. (c) Even momentary flexion during the splinting period restarts the healing process and the 6-8 weeks must restart from that point. (d) Patient education on proper technique to switch splints (one finger holds DIP extended while removing/applying splint) is essential. (e) After 6-8 weeks of full-time splinting, gradually wean to nighttime splinting only for additional 2-4 weeks. (f) Splint must allow proximal interphalangeal (PIP) joint to flex (do not include PIP in splint). Outcomes with conservative management: 70-90% good to excellent results, with mild residual extensor lag (5-15 degrees) common but functional. Patient compliance is critical — non-compliance is the most common reason for failure. (2) Bony mallet (Doyle Type IV) without subluxation: typically conservative management with same splinting protocol, with good outcomes. (3) Doyle Type IVb/IVc with subluxation: surgical management indicated. Options: (a) Closed reduction and percutaneous extension block pinning (Ishiguro technique): K-wire placed in extension block position dorsally to prevent fragment displacement, with second K-wire across DIP joint. Most commonly used technique. (b) Open reduction and internal fixation (ORIF): direct visualization with screw, K-wire, or pull-out wire fixation of the bony fragment, with consideration of hook plate (Ishimasa hook plate or modifications) for unstable fragments. (c) Volar pull-out wire technique (Pratt-Burnett or similar). (4) Open mallet (Doyle Types II, III): irrigation and debridement, primary tendon repair (figure-of-eight suture or modified Bunnell), skin closure with or without flap coverage, postoperative splinting. (5) Chronic mallet (more than 3-4 months) or failed splinting: tendon imbrication, central slip tenotomy (Fowler), oblique retinacular ligament reconstruction (Thompson), DIP arthrodesis for refractory cases or post-traumatic arthritis. Complications: (a) Residual extensor lag (5-15 degrees common, more than 20 degrees considered failure). (b) Swan-neck deformity (PIP hyperextension secondary to disruption of extensor tendon balance). (c) Skin maceration or breakdown under splint (proper splint fit and air exposure during careful changes important). (d) Poor splint compliance leading to failure. (e) Chronic mallet (untreated for months) with stiffness, arthritis. (f) Surgical complications: infection, nail deformity (matrix injury), pin tract infection, chronic regional pain, arthritis, loss of motion. Long-term outcomes: even with appropriate treatment, residual extensor lag of 5-15 degrees is common and considered acceptable. Functional outcomes generally good with well-treated mallet finger. Patient education and counseling about expected outcomes important. Prevention: protective gloves with finger reinforcement in athletic activities (although limited evidence for prevention).