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Although the nail no longer has a defensive role in humans, it nevertheless retains an important function. It is the only rigid element stabilizing the distal pulp of the fingers beyond the distal phalanx tuft. It limits pulp deformation and thus participates in allowing precise pinch. Certain actions such as picking up very small objects become difficult or impossible in the absence of the nail. In response to any pulp pinch, the nail plate exerts a counterpressure that improves the sensory function of the pulp. In the absence of a nail, two-point discrimination regresses. Finally, the aesthetic role of the nail cannot be minimized. Nail deformity from these injuries often motivate requests for corrective surgery, especially in women.
The nail itself or nail plate is a conglomerate of stratum corneum cells arranged in successive layers. Its surface is smooth and shiny. Its deep surface is streaked with longitudinal grooves that contribute to fastening it to the underlying nail bed. The distal limit of this adhesion is the hyponychium, which marks the transition between the adhering nail and the free edge of the nail ( Fig. 13.1 ).
The hyponychium is a histologically specialized area marking the transition between the nail bed and pulp tissue. This level marks the end of the adhesion of the nail plate to the underlying nail bed. This zone acts as a mechanical barrier that prevents accumulation of foreign bodies between the nail and nail bed. Added to this mechanical role is an immunologic function, as evidenced by the local concentration of neutrophils.
The paronychium includes all of the soft tissue lateral to the nail, specifically the junction between skin and nail in the lateral nail grooves. This border area is again histologically specialized. Through its adherence, it protects adjacent nail structures from contamination. When even a minor injury threatens the integrity and tightness of this junction, it creates favorable conditions for bacterial infection (paronychia).
The eponychium is the dorsum or superficial aspect of the proximal nail groove. It ends with a thin epithelial layer tightly adherent to the superficial aspect of the nail plate. The eponychium plays a role in the “finishing” of the surface of the nail, giving it a shiny appearance.
The nail bed is the tissue that the nail plate rests on and adheres to. It has characteristic longitudinal serrations corresponding exactly to those present on the deep surface of the nail plate. The close correspondence between the nail plate and its bed is responsible for the adhesion between these two structures. The nail bed can be divided into two areas of different histologic specificity. The sterile matrix is the portion of the nail bed between the hyponychium and the distal limit of the lunula. This sterile matrix contributes to the formation of the nail by adding new layers of cells to the already formed nail, thereby thickening it. It is also at this level that this specialized surface is developed, with its longitudinal striations anchoring the nail to its bed.
The germinal matrix forms the palmar segment of the proximal nail groove and extends to the distal edge of the lunula. Most of the nail synthesis processes are carried out by this tissue. Histologically this area has a multilayered epithelium. The deep layer is composed of germ cells whose duplication is the basis of nail plate formation.
The lunula is a whitish arcuate area situated immediately distal to the dorsal aspect of the proximal nail fold.
The nail complex is supplied by the terminal branches of the palmar digital arteries. These are connected by dorsal anastomotic arches in contact with the bone. Flint distinguishes three dorsal anastomotic arches. The distal arch is projected at the level of the nail lunula. The proximal arch is located in the most proximal part of the nail in the proximal nail fold. These two arches are powered by a single branch on either side from the palmar digital artery at the neck of the distal phalanx. The palmar digital artery travels along the lateral border of the distal phalanx before dividing into two branches forming the distal and proximal arches.
The third “superficial” arch is situated at the base of the distal phalanx and for its part receives a dual vascular supply. The first branch that feeds it comes from the palmar digital artery at the proximal phalanx and crosses the distal interphalangeal joint dorsally. The second branch arises from the palmar digital artery in the distal interphalangeal joint. These two branches anastomose to give rise to the superficial arch.
Because these different arches are all joined together by anastomotic branches, it is clear that the nail unit is not reliant on the distal phalanx for adequate circulation. In other words a pulp loss exposing the entire palmar surface of the distal phalanx does not necessarily threaten the vitality of the nail.
Restoring a nail's length, morphology, and normal appearance is possible only if certain conditions are met.
The length of the nail bed should be restored. This requires not only repairing or reconstructing the nail bed but also providing it with adequate skeletal support. Absence of this support in cases of skeletal shortening results in the growth of a curved nail. If the shortening is minimal, this curve will be aesthetically and functionally acceptable. If the shortening is major, the nail claw that results is difficult to tolerate.
Besides the length, the morphology of the nail bed is also of crucial importance because it contributes to giving the nail its final form. With the nail bed resting directly on the periosteum of the underlying phalanx, any defect or abnormally protruding bone spike is likely to result in deformation of the nail bed and of the nail itself.
The goal of surgery is determined by the clinical situation. Therefore in distal amputations when a replantation cannot be carried out, nail preservation only makes sense if there is sufficient residual skeletal support. After a proximal amputation (area 4), this support is no longer available and it is permissible to immediately offer nail matrix ablation.
Nail adhesion is also a major objective of reconstruction. It is only possible if the nail matrix is repaired or reconstructed adequately. We shall see that there is no substitute for this specialized tissue and that all techniques using dermal or epidermal grafts or flaps are doomed to failure.
Crush injuries are by far the most common. Inadvertent trauma from a hammer or the unexpected closing of a door are the usual causes. At a minimum, the injury causes hematoma formation under the nail. The latter can be limited in scale, with an area of detachment not affecting the entire surface of the nail bed. More severely, this hematoma completely detaches the nail from its bed. When the crushing is violent, it can cause a simple or comminuted fracture, most often affecting the distal phalangeal tuft. This fracture is usually stabilized by the nail itself and does not require osteosynthesis.
A predictable pattern of injury results from crushing the nail with a flexion force. The base of the nail plate dislocates out of its proximal cul-de-sac, whereas most of the distal nail plate remains adherent to the nail bed.
When the trauma has been sufficient, a distal phalanx fracture often occurs in the distal neck. The distal fragment becomes angulated palmarly. This type of injury is particularly common in the classic fingertip slammed by the door. In young children, the fracture may be more proximal involving the growth plate of the distal phalanx, causing a Salter-Harris type I physeal fracture.
Simple wounds by knife, cutter or other sharp instruments are rare because the nail itself is an effective barrier. In contrast, industrial machine tools (circular saws, milling machines) easily breach this barrier and cause injuries that are difficult to treat because they often involve tissue loss.
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