Nail bed injuries are extremely common in children and young adults, with most occurring in males between the ages of 4 and 30 years. The middle finger is most commonly affected because of its increased length compared with the other digits. Most injuries involve the nail bed and soft tissue of the fingertip. Many (50%) also involve fractures of the distal phalanx. One of the core procedures first learned in plastic surgery is repair of the nail bed which typically involves removal of the nail plate (if not already removed) cleansing of the area, minimal debridement, and placement of absorbable sutures to tack the nail bed and/or pulp together. Most surgeons will then replace the nail plate as a splint, although there is no strong evidence to support this approach over leaving the nail off. A randomized control trial exists in the United Kingdom called the NINJA trial to evaluate the two options. The pilot study suggested that more complications and infections were seen when the nail plate was replaced.1,2
once only or not at all.) Options: For Fig. 79.2, the anatomic components of the nail bed complex are as follows: The fingertip includes the volar pulp and dorsal nail complex. The perionychium is a collective description of the nail bed, nail plate, hyponychium, and eponychium. The paronychial regions are the lateral borders adjacent to the nail plate; i.e., they run parallel to the nail edge. The hyponychium is the area between the distal nail and pulp and has a keratin plug that acts as a mechanical barrier. It represents the junction of the sterile matrix and fingertip skin. The eponychium is the distal portion of the nail fold where it is attached to the nail plate. Paronychia refers to an infection of the soft tissues surrounding the nail complex. Treatment normally involves removal of the nail plate to drain the abscess collection. The germinal and sterile matrices are both important in nail growth.1,2 v. iv. iii. ii. i. Germinal matrix Eponychium Paronychium Sterile matrix Hyponychium Fig. 79.2 Anatomy of the fingertip and nail bed.
Nail growth occurs at three key sites: the germinal matrix, the dorsal roof of the nail fold, and the sterile matrix. Of these, the germinal matrix is the most important area, as it is responsible for 90% of nail production. It lies immediately distal to the extensor tendon insertion. Nail production occurs through gradient parakeratosis with cells initially moving in a volar–dorsal direction before growing in a proximal–distal direction. The lunula is a white arc just distal to the eponychium that represents the distal part of the germinal matrix. It is white because of the presence of nail cell nuclei within it. The nail fold has a ventral floor and dorsal roof, both of which are involved in nail growth. The ventral floor is the site of the distal germinal matrix and the dorsal roof hosts cells that impart nail shine. The sterile matrix is important for contributing to nail strength and thickness by adding squamous cells to the nail plate. The hyponychium represents the junction of the sterile matrix and the fingertip skin beneath the nail and is not involved in the nail growth but does represent a high concentration of dermal lymphatics.1,2
Normal nail growth is variable but is typically 3 to 4 mm per month.1,2 It therefore takes about 4 months to regrow a nail fully. Factors that seem to increase growth include greater digital length (the nail of the middle finger grows faster than that of the little finger), time of year (growth is increased in the summer), younger age, and a nail-biting habit (onychophagia). There may be a slight sex difference, with growth in males being greater than in females, although this is not confirmed and may simply be a factor of differences in digit length.
The classification system described by Van Beek has five categories.1 Types I and II are both subungual hematomas and are differentiated by their size. Type I is less than 25% and type II is greater than 50%. The difference is arbitrary, since both are usually treated the same using a trephination technique under local anesthetic to drain the hematoma. Type III injuries involve a nail bed laceration and a distal phalangeal fracture. These are treated with repair of the laceration and splinting of the fracture. Types IV and V involve more significant damage to the nail bed that precludes simple repair. They do not necessarily involve a distal phalangeal fracture, although they may well do so. These are best managed using nail bed grafts from the same digit or the great toe, because leaving them to heal by secondary intention will lead to misshapen and nonadherent nail plates.
Nail bed tissue is highly specialized, and debridement must be minimal to optimize preserved tissue. Furthermore, crushed and bruised nail bed tissue often survives. Following debridement, careful repair of the nail bed should be performed with a fine absorbable suture (e.g., 6–0 or 7–0 rapidly absorbable suture) under loupe magnification. A finger tourniquet should be used to provide a blood-free field and the application and removal times must be noted by the surgeon and documented by the operating room staff. Strict adherence to this will reduce the chances of inadvertently leaving a tourniquet in situ. A general rule of thumb is to prescribe a short course of antibiotics for nail bed injuries that have a distal phalanx fracture, but not for those without. Tuft fractures do not require K-wire stabilization, as the nail plate and soft tissues provide adequate support. Unstable shaft fractures close to the distal interphalangeal (DIP) joint will, however, normally require K-wiring. Wound extension proximal to the nail fold is required only when access to the germinal matrix is required. Use of glue instead of sutures has shown comparable results for nail bed repair and may be considered.1
The main theoretical benefit of replacing the nail plate within the nail fold is to keep the fold open in the early stages of regrowth and prevent nail fold adhesions (synechiae). Nail fold adhesions are thought to lead to ridging of the nail. There is no effect on nail regrowth, postoperative pain, or rates of infection. Although cosmesis may be improved in the short term, the nail plate remains in situ only for a short period of time and will not remain in place until a new nail has completely regrown.1,2
phalanx? Originally described in 1966, a Seymour fracture is an open distal phalanx fracture involving the physis with an associated nail bed injury. Special consideration must be taken, as these injuries have interposed soft tissue, including germinal matrix, within the fracture site so a failure to recognize this may result in fracture nonunion, physeal arrest, nail plate deformity, and/or chronic osteomyelitis. These injuries can easily be overlooked as a minor injury to the nail bed but clinical suspicion should be raised where there appears to be a mallet deformity with a nail bed injury in children. The difference between a normal mallet deformity and a Seymour fracture is that the mallet deformity occurs through the distal phalanx growth plate rather than through the DIP joint. A good lateral radiograph should clearly allow differentiation between a typical mallet and a Seymour fracture. Treatment involves surgical removal of the soft-tissue interposition, reduction, and stabilization of the fracture, possibly with a K-wire. The DIP joint should not be directly affected and because the flexor tendon insertion remains in continuity, DIP joint flexion should be retained. Normal nail growth could be affected, but there should not be a complete failure. Sensation to the fingertip should be unaffected.1
The hook-nail deformity is caused by a lack of distal phalanx bone support beneath the nail bed which continues to grow distally over the top of the short bone end. It is best prevented by matching bone length and nail bed length so that underlying support is achieved for the full length of the nail bed. Therefore, preservation of distal phalanx length and primary shortening of the nail bed during a revision amputation may avoid subsequent development of this deformity. Neither germinal or sterile matrix damage is the cause of a hook-nail deformity as evidenced by continued growth of the nail, and splinting alone will not prevent it. Once established, the deformity may be corrected using the antennae procedure, which was described by Atasoy et al.1 This is a two-stage procedure that addresses the lack of support for the nail bed and the relative lack of volar soft tissue. In the first stage, the pulp and nail bed are elevated off the distal phalanx and the nail bed is then splinted in a straight position with two or three small K-wires (hence the term “antennae”). The residual soft-tissue pulp deficit is then reconstructed using a cross-finger flap from the adjacent index finger.