You are in: eMedicine Specialties > Dermatology > SURGICAL Nail SurgeryArticle Last Updated: Sep 18, 2006AUTHOR AND EDITOR INFORMATIONAuthor: Neh Onumah, MD, Fellow, Department of Dermatology, Presbyterian Medical Center, Columbia University Coauthor(s): Richard K Scher, MD, Professor of Dermatology, University of North Carolina Editors: Désirée Ratner, MD, Director of Dermatologic Surgery, George Henry Fox Assistant Clinical Professor, Department of Dermatology, Columbia Presbyterian Medical Center, New York Presbyterian Hospital; David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic; John G Albertini, MD, Consulting Staff, Dermatologic Surgery, The Skin Surgery Center; Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital; William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System Author and Editor Disclosure Synonyms and related keywords: paronychia, onychocryptosis, ingrown nail, subungual hematoma, splinter hemorrhage, nail unit tumor, myxoid cysts, warts, pyogenic granuloma, nail laceration, fibroadenoma, glomus tumor, subungual exostoses, basal cell carcinoma, squamous cell carcinoma, melanoma, nail biopsy, nail avulsion, matricectomy, chemical matricectomy, ablative matricectomy, radical matricectomy, electrosurgery, laser treatment INTRODUCTIONThe nail complex is the structural and functional unit of the nail. The nail consists of the plate; bed; matrix; proximal, lateral, and distal grooves; proximal and lateral folds; and hyponychium (Zaias, 1990; Scher, 1996; Fleckman, 1997). Aside from being aesthetically appealing, the healthy nail unit has the important function of protecting the distal phalanges, fingertips, and surrounding soft tissues from external injury, as well as enhancing precise delicate movements of the distal digits through the mechanistic action of counterpressure exerted over the volar skin and pulp (Dawber, 1984; Dawber, 1994:1-34). Performing successful nail surgery requires a comprehensive understanding of nail anatomy and physiology (Haneke, 2006). An understanding of both the vascular and neural pathways supplying the nail complex and the functions and relationship of each component of the nail unit is also essential. Thus, the nail surgeon should be equipped with knowledge of nail pathology, surgical techniques and instrumentation, anesthesia, preoperative evaluation, management of complications, and wound care and healing after surgery. This knowledge ensures minimal patient discomfort, maximal patient satisfaction, and optimal surgical success. With these goals in mind, this article reviews the nail anatomy and focuses on common nail pathologies with the corresponding surgical techniques used for their diagnosis and treatment. INDICATIONSMultiple indications for surgical exploration of the nail unit exist; most of the indications range from infectious and inflammatory to neoplastic and traumatic causes. Some commonly encountered disease processes affecting the nail complex include onychomycosis (ie, fungal infection), onychocryptosis (ie, recalcitrant ingrown nails), onychogryphosis (ie, hornlike hypertrophy of the nail plate), and onychauxis (ie, thickened nails), as well as psoriasis, lichen planus, congenital nail dystrophies, and tumors. In addition, nail surgery is frequently performed to aid in a suspected diagnosis, to relieve pain, and to correct or prevent anatomical deformities of the nail. ParonychiaAcute paronychia is an acute inflammation of the nail fold and frequently results from minor trauma, such as an accidental break in the skin, a splinter in the distal edge of the nail, a thorn in the lateral groove, a hang nail, or excessive nail biting leading to infection of the surrounding soft tissues (Zaias, 1990; Dawber, Diseases of the Nail, 1994; Ceilley, 1992). The infectious process initiates in the lateral perionychium and is followed by the development of erythema, intense inflammation, swelling, pain, and local tenderness. Vesicles and blisters may also form. Chronic paronychia is characterized by acute exacerbations of self-limiting inflammation and infection followed by remissions. Chronic paronychia commonly occurs in hands that are repeatedly exposed to water (Pardo-Castello, 1960). The proximal nail fold (PNF), the lateral nail fold (LNF), and the cuticle are destroyed. The potential barrier formed by the PNF is impaired, and the cuticle eventually detaches from the nail plate. The warm moistened environment is ideal for bacterial proliferation. Secondary Candida and bacterial infections (eg, Pseudomonas aeruginosa, Staphylococcus aureus) are implicated in acute exacerbations (Salasche, 1997). Exacerbations may be initiated through contact with irritants and allergens. Chemical and irritant contact dermatitis is common. Exacerbations usually resolve several days after abscesses spontaneously drain, but they lead to prolonged edema and fibrosis of the nail folds (Salasche, 1997). OnychocryptosisIn onychocryptosis (ingrown nail), the toenails are most commonly affected; the fingernails are rarely afflicted. Predisposing factors involved in the pathogenesis of an ingrown nail include congenital malalignment of the digit; hyperhidrosis (commonly occurs in athletic adolescents); increased pressure from external sources (eg, trauma); poorly fitted shoes; poor posture and gait; excess internal pressure, which results in overcurvature of the nail plate; incorrectly trimmed nails or naturally short nails; underlying systemic disease (eg, obesity, diabetes mellitus); arthritis; skeletal disease; onychomycosis and other diseases that result in abnormal changes in the nail plate; and senile nail diseases (eg, onychauxis, subungual hyperkeratosis) (Scher, 1996; Dawber, Diseases of the Nail, 1994; Siegle, 1982). In onychocryptosis, the primary direction of nail growth is lateral instead of the normal, forward orientation of nail growth in the longitudinal plane. The laterally curved edge of the nail plate, or the nail spicule, penetrates the adjacent LNF, perforating the fold skin and the surrounding dermal components. Perforation of the lateral fold skin results in painful inflammation that manifests clinically as mild edema, erythema, and pain (Salasche, 1997). In advanced stages, drainage, infection, ulceration, and hyperhidrosis may be present. Hypertrophy of the lateral nail wall occurs, and granulation tissue forms over the nail plate and the nail fold during healing of the ulcerated skin. The resulting edema further exacerbates the problem by compressing the lateral dermal tissue between the sharp nail plate and the bony phalanx. Myxoid cystsMyxoid cysts are dome-shaped, translucent, solitary nodules occurring on the dorsal aspect of the finger (Salasche, 1997; Miller, 1992; Norton, 1997). Occasionally, the toes may develop these cysts in a similar location. Typically, the cysts are lateral to the midline between the PNF and the distal interphalangeal (DIP) joint (Miller, 1992). Their pathogenesis and etiology have not been clearly established. Myxoid cysts occurring on the DIP joint have been associated with the formation of a tract or communication with the joint. The cysts are believed to occur secondary to degenerative disease of the DIP joint and in association with marginal osteophytes, thus explaining their presence in patients with osteoarthritis (Salasche, 1997; Baran, 1981). As a result, myxoid cysts are frequently mistaken for synovial cysts. Myxoid cysts of the PNF may result from increased synthesis of hyaluronic acid by local fibroblasts (Salasche, 1997; Johnson, 1965). Whether or not these mechanisms of cyst formation occur is controversial. WartsPeriungual and subungual warts are benign, fibroepithelial tumors that commonly affect the paronychial region of the nail unit. Also referred to as common warts, these hypertrophic growths have a rough, keratotic surface and tend to occupy the nail grooves, the retroungual nail folds, and the subungual area under the nail plate. Periungual and subungual warts are the single most common benign tumors of the perionychium and are caused by the human papillomavirus (HPV). Certain subtypes of HPV associated with periungual and subungual warts may cause squamous atypia. Usually, these warts are mildly infective tumors and present as multiple lesions. However, they appear to be more aggressive and destructive than other types of common warts in this location (Salasche, 1997). In the absence of fissuring, periungual warts are usually asymptomatic. Subungual warts initially infect the hyponychium, gradually move toward the nail bed, and lastly involve the nail plate. They commonly cause pain. Typically, the nail plate is spared, except for ridging that occurs on the surface of the nail plate. The differential diagnosis in clinical presentations of periungual and subungual warts should include epidermoid carcinoma and keratoacanthoma (Zaias, 1990; Dawber, Diseases of the Nail, 1994). The warts may be mistaken for a glomus tumor. The spread of periungual warts is assisted by biting and picking the nail and surrounding soft tissue. Picking infected lesions can lead to autoinoculation of noninfected fingers (Dawber, Diseases of the Nail, 1994; Pardo-Castello, 1960; Samman, 1994). Common warts in the posterior nail fold may exert pressure on the matrix, resulting in a deformed nail plate. If left alone, periungual and subungual warts tend to linger and persist as they continue to grow and invade the skin of the other neighboring digits. Nail traumaTraumatic injuries of the nail unit include simple or complex lacerations, crush injuries, avulsions, terminal phalanx fractures, and partial or complete hematomas. Preservation of nail structure and function is the most important consideration when managing injuries to the nail complex. To ensure optimal management in cases of nail unit trauma, early treatment of the patient should be initiated. The goal is to explore and repair the wound within hours or days of the injury. Sometimes, the wound is still capable of repair 1-2 weeks following the injury. Subungual hematoma Acute subungual hematoma frequently results from blunt trauma to the underlying vascular nail bed. Subungual hematoma may result from chronic repeated injury to the nail caused by minor trauma, such as trauma of the toenail from poorly fitted shoes. They may also occur in older patients with atrophy of the skin and nails (Pardo-Castello, 1960). Bleeding ensues, and the accumulated blood is limited to the subungual compartment of the nail unit. A hematoma develops and is accompanied by inflammation and severe pain due to increased pressure of the entrapped blood on the subungual tissue and underlying periosteum. When acute subungual hematomas are directly under the transparent nail, they have an immediate onset and are conspicuous. In acute subungual hematoma, the nail color is initially red and changes to black after coagulation (Pardo-Castello, 1960). The hematoma is uniform in color with sharply demarcated margins, and it usually grows distally with the nail plate until reaching the free distal edge of the plate where it is no longer seen. Occasionally, the hematoma may persist under the nail and does not move distally with nail growth. Hemorrhages resulting from trauma to the dorsal nail fold may not appear with forward nail growth for several days. The differential diagnosis of subungual hematoma should include melanoma, glomus tumor, Kaposi sarcoma, basal cell carcinoma, squamous cell carcinoma (SCC), exostosis, melanonychia striata, fungal melanonychia, and keratoacanthomas, all of which must be excluded (Clark, 1998). To exclude a diagnosis of melanoma, biopsy must be performed in all pigmented lesions of unknown etiology. Lacerations Simple superficial lacerations of the nail are usually confined to the nail plate, nail bed, and LNFs. Complex lacerations involve the nail matrix and PNF and result in partial or total nail avulsion or fragmentation of the nail plate; in complex avulsive lacerations, the finger pulp, nail bed, and distal phalanx are destroyed (Clark, 1998). Complex lacerations may lead to serious complications after injury and should be promptly treated to prevent abnormal nail morphology and function. Fractures A major function of the distal phalanx is to support the distal soft tissues of the finger (Coyle, 1980). Fracture of the distal phalanx occurs in approximately one half of nail bed injuries. The type of fracture (open vs closed) (Clark, 1998), the position of the fracture, and the extent of comminution determine treatment. Healing of the fracture is mostly related to the degree of initial displacement and soft tissue injury. Splinter hemorrhageMost commonly, trauma or certain disease processes easily injure the small, fine capillaries that line the epidermal-dermal ridges on the nail bed (Zaias, 1990; Dawber, Diseases of the Nail, 1994). Splinter hemorrhages result from the extravasation of blood into the potential space between the nail plate and the nail bed after capillaries are disrupted. They develop in the long axis of the nail bed, which conforms to the orientation of the dermal ridges and the subungual vessels. Other etiologic factors are associated with the formation of splinter hemorrhages in the nail bed; the hemorrhages may clinically occur in such conditions as psoriasis, vasculitis, bacterial endocarditis, arterial embolism, lupus, Darier disease, cirrhosis, hemochromatosis, thyrotoxicosis, and trichinosis (Zaias, 1990; Dawber, Diseases of the Nail, 1994; Daniel, 1997:219-250). Certain drugs (eg, tetracycline) and drug reactions may also induce their formation. The hemorrhages may be single or multiple, and they appear as brown, red, or black linear streaks, usually in the distal one third of the nail (Dawber, Diseases of the Nail, 1994). As the nail grows, the hemorrhages move distally and superficially. They do not tend to blanch on palpation of the nail plate. Splinter hemorrhages that occur proximally near the lunula are frequently associated with systemic disease (Daniel, 1997:219-250). Involvement of multiple nails by these hemorrhages may indicate the presence of an underlying systemic disease. Overall, splinter hemorrhages occur most often in males and in blacks. They commonly involve the thumb and index finger of the dominant hand. However, in studies with single and multiple hemorrhages, the left thumb was found to be the most frequently involved digit. Nail unit tumorsHigh-resolution MRI gained prominence in the noninvasive diagnosis of nonmelanoma nail tumors and is capable of detecting lesions that are smaller than or equal to 1 mm in diameter (Alam, 1999). This modality is helpful in identifying lesions in the following presentations of benign and malignant tumors of the nail: glomus tumors, periungual fibromas or fibrokeratomas, mucous cysts, and exostoses. Pyogenic granuloma Pyogenic granuloma is a benign granulomatous lesion commonly seen after a minor trauma penetrates the skin. It usually starts as a small, red papule on the PNF and rapidly grows to the size of a pea (Dawber, Diseases of the Nail, 1994; Pardo-Castello, 1960). Pyogenic granuloma may also localize to the nail bed after a trauma penetrates the overlying nail plate. Erosion of its surface by pressure necrosis of the overlying epidermis may occur. Fibroadenoma Various types of fibroadenoma may occur in the periungual or subungual region. They are usually distinctive in their etiology and presentation. Glomus tumor A glomus tumor is a small, well-differentiated, hamartomatous growth of the soft tissues encapsulated in a fibrous covering. A glomus tumor appears as a small, blue or reddish blue spot that is visible through the nail plate (Dawber, Diseases of the Nail, 1994; Pardo-Castello, 1960; Norton, 1997). Most commonly, the tumors are localized to the hand with involvement of the fingertips and the subungual region. Ultrasonography can be used to identify and locate the tumors. The onset of intense pulsating pain with the slightest pressure or with exposure to cold temperatures is pathognomonic for subungual glomus tumors. Microscopically, all the components in a glomus body are present in this tumor; the components are an afferent arteriole, an efferent venule, glomus cells, smooth muscle cells, and myelinated and nonmyelinated nerves (Dawber, Diseases of the Nail, 1994; Herndon, 1997). Subungual exostosis Subungual exostoses are painful outgrowths of healthy bone or remnants of calcified cartilage that frequently occur on the great toe in young persons (Dawber, Diseases of the Nail, 1994; Pardo-Castello, 1960). Subungual exostosis is not a true tumor (Dawber, Diseases of the Nail, 1994). Trauma has been implicated as the inciting cause. The exostosis begins as a small elevation on the dorsal surface of the terminal phalanx. Over time, it may appear as an outgrowth under the distal nail edge, or it may completely destroy the nail plate, creating an environment for tissue erosion and infection. Clinically, patients present with pain that may be accompanied by an abnormal gait because of difficulty walking and a deformed nail. The differential diagnosis includes osteochondroma, which has a similar presentation. Basal cell carcinoma, squamous cell carcinoma, and melanoma Although cutaneous malignancy is the most common form of cancer, malignancy involving the nail unit is a relatively uncommon phenomenon. When the nail unit is affected by cancer, it is usually a SCC that rarely metastasizes. Although curable in most cases, SCC of the nail complex is potentially fatal if not aggressively treated. Subungual melanoma is another rare malignancy of the nail unit that is commonly mistaken for other benign and malignant tumors, thus prolonging accurate diagnosis and early treatment. RELEVANT ANATOMYThe nail plate, the largest segment of the nail unit, is a dense, keratinous horny structure derived from the germinal matrix, or nail root (Zaias, 1990; Scher, 1996; Fleckman, 1997; Dawber, 1984; Dawber, 1994:1-34). Destruction of the nail root, despite an intact nail bed, results in permanent loss of the nail plate. Nail growth occurs in a forward distal direction, and growth of the nail plate is directly proportional to the turnover rate of cells in the matrix. Complete growth of the fingernail plate, measured from the matrix to the distal free edge of the plate, is estimated to occur every 4-6 months, corresponding to a rate of 0.1 mm daily (Zaias, 1990; Scher, 1996; Fleckman, 1997; Ditre, 1992). The turnover time for the toenail plate is longer, averaging around 12-18 months (Zaias, 1990; Scher, 1996). Grossly, the nail plate is composed of 3 distinct layers: a dorsal thin layer, a thick intermediate layer, and a ventral layer (Dawber, 1984; Dawber, 1994:1-34). The nail plate originates beneath the PNF and can be seen passing over the lunula (Miller, 1991) and the richly vascularized nail bed where it firmly attaches. The nail plate is bordered by the PNF and LNFs, and it is distally adjoined by the hyponychium, although its free distal border generally extends beyond the distal phalanx. The healthy nail plate appears as a smooth, convex, nearly rectangular, translucent structure that has a pink color when light is reflected from its surface; the color is due to the underlying vascular-enriched nail bed (Zaias, 1990; Dawber, 1984; Dawber, 1994:1-34). The shape of the nail plate largely conforms to the convexity of the distal margin of the lunula, the visible crescent-shaped distal segment of the matrix. The nail plate exhibits a thickness gradient with the nail thickness, increasing proximally to distally and with age. Thus, the nail plate tends to be thinner at the lunula (Zaias, 1990; Dawber, 1984; Dawber, 1994:1-34; Gonzalez-Serva, 1997). Nail thickness is directly related to the length of the matrix (Zaias, 1990; Ditre, 1992). In darkly pigmented persons, a hyperplasia of melanocytes is commonly seen throughout the matrix epithelium, resulting in longitudinal linear bands of light brown to black pigment visible through the nail plate (Zaias, 1990; Fleegler, 1992; Ditre, 1992). Although the linear bands of pigment may represent pathological states, they may be a normal finding in people of color, secondary to hyperproduction and accumulation of melanin. The onychodermal band is the narrow, transverse delineation at the distal end of the nail plate. This band appears yellowish white in whites or reddish brown in darkly pigmented persons. The onychodermal band marks the point of separation of the nail bed from the nail plate (Siegle, 1982), and it appears to be important in preventing onycholysis after trauma. This band may be prominent in cirrhosis, acrocyanosis, and other chronic diseases (Fleckman, 1997; Dawber, Diseases of the Nail, 1994). The onychodermal band has been postulated to have a separate vascular supply from the rest of the nail bed (Dawber, 1984; Dawber, 1994:1-34; Pardo-Castello, 1960). Hyponychium The hyponychium is the anatomical area that begins at the onychodermal band, where the nail bed ends, and terminates at the distal groove. The distal groove is a transverse demarcation extending across the distal digit that divides the hyponychium from the volar epidermis of the digit. This groove is the first component of the nail unit to be recognized during the embryologic period, and it is the origin point of the volar epidermis (Zaias, 1990). In persons who bite their nails, the distal groove is easily identified (Zaias, 1990). The solehorn is the ventral cuticle layered between the ventral nail plate and the distal nail bed; it functions as a potential waterproof barrier (Ditre, 1992) in the space created by its firm attachment to the nail plate and the distal bed epithelium. In this capacity, the solehorn prevents the entrance and invasion of offending organisms and, therefore, protects the nail plate from infection (eg, distal subungual onychomycosis). Frequent aggressive manicuring of the hyponychial area results in disruption of this barrier and allows microbes to enter it. Proximal nail fold The PNF is a continuation of the dorsal skin of the digit that folds back on itself at the nail root to create 2 epithelial surfaces: a superficial dorsal layer and a deep ventral layer (Fleckman, 1997; Dawber, 1984; Dawber, 1994:1-34; Siegle, 1982). The ventral layer travels to the base of the nail plate to create the nail matrix. Thus, the PNF obscures most of the nail root (germinal matrix) and the area where the proximal nail plate embeds itself into the proximal groove. The PNF is contiguous with the LNFs that border the nail plate. Where the 2 epithelial surfaces meet, the cuticle converges onto the distal nail plate (Fleckman, 1997; Dawber, 1984; Dawber, 1994:1-34). The cuticle is the horny end product of the PNF, adhering to the dorsal wall of the nail plate. It is the true nail vest that appears as a fine white band (Ditre, 1992). The role of the cuticle is similar to that of the solehorn; it functions as an impermeable barrier, sealing off the potential area that exists between the PNF and the nail plate. Eventually, the cuticle is shed like the cornified horny layer of epidermal skin. When the cuticle is disrupted, usually due to overzealous manicuring (Ditre, 1992), the individual becomes susceptible to paronychia and other infectious and inflammatory diseases. Damage to the cuticle can also result in increased chemical insults, such as irritant contact dermatitis (Dawber, Diseases of the Nail, 1994). Loops of blood capillaries are sometimes found in and around the PNF, and they may be pathognomonic for certain diseases, such as dermatomyositis and lupus erythematosus. However, the loops may be a normal finding in certain individuals (Zaias, 1990; Dawber, 1984; Dawber, 1994:1-34; Pardo-Castello, 1960). Nail matrix The nail matrix is the germinative portion of the nail complex, giving rise to the nail plate (Zaias, 1990; Dawber, 1984; Dawber, 1994:1-34; Ditre, 1992). The matrix is at the most proximal point of the nail bed and is seated deep beneath the PNF; it is separated from the distal phalanx by only a few millimeters. According to Zaias, "the top half of the nail plate (the dorsal aspect) is derived from the proximal matrix, while the derivation of the lower half (the ventral aspect) is from the distal matrix." The proximal matrix continues proximally and laterally to form the lateral matrix horn. The nail surgeon should be cognizant that the lateral matrix horn may be extensive. The lunula is an opaque, grayish white, half-moon–shaped structure that extends beyond the distal limit of the PNF. The lunula is usually seen through the transparent nail plate, especially on the thumbs and great toes, as the visible distal component of the nail matrix (Zaias, 1990; Dawber, 1984; Dawber, 1994:1-34; Pardo-Castello, 1960). The distal margin of the lunula must always be preserved during nail surgery if the normal shape of the nail is to be maintained (Zaias, 1990; Ditre, 1992; Salasche, 1997). An active granular layer typically found in the PNF is missing from the nail matrix; therefore, keratohyaline granules cannot be found in the matrix. The basal cells of the matrix actively participate in the process of differentiation and keratinization to eventually produce the dead horny product, the nail plate. Several reasons exist why the nail surgeon must attempt to leave the structural and functional boundaries of the nail matrix intact when performing nail surgery; some of the reasons include the following:
Disruption of any of these components of the nail matrix can result in scarring and onychodystrophy of the evolving nail plate. The most common indication for partial or complete destruction of the matrix is a recurring problem of ingrown nails recalcitrant to conventional therapies. The healthy matrix synthesizes a complete fingernail plate on an average of every 6 months (Zaias, 1990; Scher, 1996; Samman, 1994). Nail bed and dermis The nail bed is the sterile component of the nail unit and the primary site of nail keratinization (Dawber, 1984; Dawber, 1994:1-34). The nail bed extends from the distal lunula to the point of origin of the hyponychium. It shares similar boundaries with the nail plate, with the lunula marking the proximal border of the nail bed, with the lateral folds marking the lateral border, and with the hyponychium marking the distal border. The epidermis of the nail bed is relatively thin, with a dimensional thickness of only 1-2 cells (Dawber, 1984; Dawber, 1994:1-34). The epidermal surface of the bed has parallel longitudinal ridges that interlock with similar folds on the ventral surface of the nail plate (Zaias, 1990; Fleckman, 1997; Dawber, 1984; Dawber, 1994:1-34; Ditre, 1992). The ridges securely bind the nail plate to the nail bed, allowing a firm adhesion between the 2 structures. The area marking the point at which living cells become keratinized and continue to become dead horny cells of the nail plate is abrupt (Dawber, 1984; Dawber, 1994:1-34). The nail bed is a highly vascular structure that lacks an underlying subcutaneous layer of adipose tissue. As a result, nothing separates the dermis from the periosteum of the distal phalanx. The lack of this layer becomes apparent when one is confronted with aggressive tumors of the nail because such tumors may easily extend to involve the underlying bone. The connective tissue of the dermis, the dermal collagen, contains a balanced mixture of lymphatics, blood vessels, and elastic fibers. The dermis also has a wealth of glomus bodies and a rich capillary network longitudinally oriented with the parallel ridges. Splinter hemorrhages of the nail plate form when a small amount of blood leaks from the capillary bed into one of these folds and becomes trapped by the nail plate (Scher, 1996). Melanocytes are not found in the nail bed, although they are present in significant numbers in the matrix. Blood supply An abundantly rich arterial and capillary vascular network supplies the nail unit. The ulnar and posterior tibial arteries divide into the proper palmar and plantar digital arteries, respectively. The 2 digital arteries, which occupy the lateral and medial aspects of the digit, form a cruciate anastomosis at the level of the deep dermis in the ventral pulp space. Upon anastomosing on the volar aspect of the terminal phalanx, the 2 arteries contribute branches to a superficial arcade and the underlying phalangeal periosteum (Ditre, 1992). The superficial arterial arcade, which also receives a contribution from a vessel coursing dorsally over the DIP joint, supplies the PNF, including the capillary loops of the nail fold and the nail matrix. The digital arteries continue around the waist of the terminal phalanx and onto the dorsal surface where they divide near the DIP joint to form the dorsal and ventral arches supplying the nail bed and the nail matrix. The dorsal arch courses dorsally over the DIP joint where it terminates in an anastomosis with the proximal arch to supply the matrix and the PNF. The capillary loop system in the PNF is derived from the anastomosis between the 2 arches (Zaias, 1990; Dawber, Diseases of the Nail, 1994; Ditre, 1992). Therefore, perfusion of the nail matrix comes from 2 arterial systems: the superficial arcade and the proximal arcade. Anatomically, the superficial arcade sits at the base of the PNF, while the proximal arcade lies deep to the matrix (Ditre, 1992). The ventral or distal branch supplies the remainder of the nail unit, specifically its most distal aspect, including the fingertips. An accessory blood supply that is separate from the main blood supply in the pulp space also exists. This accessory system is important in providing adequate perfusion of the nail unit for normal nail growth when the primary vasculature is compromised by disease, which sometimes occurs in scleroderma or infection (Fleckman, 1997). Specialized neurovascular structures called glomus bodies are widely distributed throughout the arterial and deep venous circulation. These oval bodies are encapsulated, consisting of tortuous blood vessels and a neural supply of mostly cholinergic nerves (Fleckman, 1997; Dawber, Diseases of the Nail, 1994). The glomus bodies form an extensive arteriovenous (AV) anastomotic network, which functions in modulating the thermoregulatory response of the nail unit. Under circumstances where the nail is exposed to cold temperatures, the glomus bodies enhance blood flow to the nail complex by dilating and shunting blood through their complex AV anastomotic systems to prevent ischemia (Fleckman, 1997; Dawber, 1984; Dawber, 1994:1-34; Pardo-Castello, 1960; Hale, 1960). The nail apparatus is also richly innervated by a complex neural system allowing tactile sensitivity and sensory discrimination. Anatomically, the laterally positioned digital nerves and their divisions nearly parallel the vascular supply to the nail unit. CONTRAINDICATIONSRelative contraindications to performing surgery in the nail unit include the presence of established peripheral vascular disease, collagen vascular disease, diabetes mellitus, and disorders of hemostasis. Patients presenting with acute infection or inflammation of the nail unit, including the surrounding paronychial tissues, are considered to have relative contraindications to nail surgery. When possible, surgery in these patients should be postponed until the acute event has resolved. When administering anesthetic for nail surgery, the use of epinephrine should be avoided, especially in patients with a history of extensive vascular disease. Therefore, patients with a history of thrombotic or vasospastic disease should not receive epinephrine (Denkler, 2001). Epinephrine has vasoconstricting properties, and it has been associated with necrosis and poor wound healing of tissues. However, these complications appear to be mostly theoretical and have rarely been noted to occur in practice. Wilhelmi et al performed an extensive review of the medical literature and found no reports of epinephrine as a primary cause of ischemic necrosis or finger gangrene when appropriately mixed with lidocaine for digital block. The authors confirmed this finding when they performed 23 digital blocks with 1% lidocaine with 1:100,000 and 1:200,000 epinephrine. They recommend the use of epinephrine as an adjunctive component to help augment the effect of the local anesthetic, decreasing the total amount of anesthetic required and lowering the risk of toxicity. Recently, several studies have proposed that epinephrine can be used safely in the digits (Krunic, 2004). Epinephrine is also beneficial in reducing blood loss at the surgical site because of its hemostatic properties. However, Wilhelmi et al caution that the maximum dose of epinephrine used in healthy individuals should not exceed 1 mg. Also, epinephrine should be cautiously administered in patients presenting with pheochromocytoma, severe hypertension, hyperthyroidism, and heart disease (Wilhelmi, 1998). Sylaidis and Logan determined that digital blocks of 2% lidocaine with 1:80,000 epinephrine were safe, although intense local vasoconstriction was noted at the injection site. In their prospective study involving 100 patients, they observed the effect of 2% lidocaine mixed with 1:80,000 epinephrine on several variables of digital arterial perfusion. No ischemic necrosis of the digit was reported after the application of a digital block. The fingers remained well perfused despite the apparent vasoconstriction at the injection site (Sylaidis, 1998). Therefore, epinephrine can be a safe and valuable adjunct when appropriately mixed with lidocaine to perform a digital block. In the event that ischemia does occur, it can be reversed with phentolamine injection or nitroglycerin ointment (Denkler, 2001). A thorough medical history is important to rule out underlying diseases (eg, vascular disease). In patients with severe diseases, epinephrine might be excluded or cautiously used. During nail surgery, the application of a tourniquet at the base of the digit allows the surgeon to operate in a bloodless surgical field (Richert, 2006). However, to avoid complications such as vascular compromise of the extremity, the use of a tourniquet for more than 15 minutes should be avoided. Optimal hemostasis is achieved when the tourniquet is applied for a maximum period of 15 minutes during the most critical part of the surgery. WORKUPDiagnostic Procedures
TREATMENTSurgical therapyNail avulsionNail avulsion is the most common surgical procedure performed on the nail unit. It is the excision of the body of the nail plate from its primary attachments, the nail bed ventrally and the PNF dorsally. Avulsion of the nail plate may be initially performed to allow full exposure of the nail matrix before chemical or surgical matricectomy (Salasche, 1997). Other indications for performing nail avulsion are to treat recalcitrant onychocryptosis; to excise tumors of the nail unit; to allow full examination and exploration of the nail bed, the nail matrix, the PNF and the LNF, and the nail grooves for the presence of pathology; or to use as a preliminary step before performing biopsy on the nail bed and the nail matrix. Avulsion of the nail plate is frequently used as a therapeutic adjunct in long-standing fungal infections of the nail, such as chronic onychomycosis, and in acute bacterial infections (Salasche, 1997; Bureau, 1994). In traumatic nail injuries, avulsion may be used to evaluate the stability of the nail bed or to release a subungual hematoma after failed puncture aspiration. Paring the nail plate is the process of taking off pieces of the nail in a transverse or longitudinal fashion to fully observe an involved area on the nail bed (Salasche, 1997). In the case of verrucae, nail paring may be performed to determine the extent of disease involvement of the nail plate and the underlying nail bed. The 2 primary methods for performing nail avulsion are distal avulsion (Scher, 1996; Siegle, 1982; Scher, 1981; Dawber, The Nails in Disease, 1994) and proximal avulsion (Zaias, 1990; Dawber, Diseases of the Nail, 1994; Scher, 1970; Siegle, 1982). A third method, chemical avulsion with urea paste, is a nonsurgical avulsion technique that may be performed. A partial or complete nail avulsion can be performed, depending on location and extent of disease. Surgical nail avulsion is not a definitive cure in cases of nail dystrophy caused by onychocryptosis, nail matrix disease (Clark, 1998), or extensive nail bed pathology (eg, SCC). Before avulsion, anesthesia of the digit is achieved through a digital block performed with 1% lidocaine. A Penrose drain secured with a hemostat clamp is used for hemostasis. Any of the following 3 blunted instruments may be used to separate the nail plate from its attachments: the mosquito hemostat, the Freer septum elevator, or the dental spatula. In distal nail avulsion, the instrument is introduced under the distal free edge of the nail plate to separate the nail plate from the underlying nail bed hyponychium on its ventral surface. All attempts at separation are directed proximally toward the matrix, with significant resistance occurring until the matrix is reached. When the matrix is contacted, the surgeon usually experiences less resistance and might feel a laxity because of a weaker attachment. After reaching the matrix, the elevator is reinserted with several longitudinal forward and backward strokes performed side by side until the nail bed is completely freed from the overlying nail plate. To free the nail plate from its association with the PNF and the cuticle, the Freer elevator is inserted under the PNF in the proximal nail groove between the eponychium and the nail plate. Aggressively inserting the instrument into the proximal nail groove causes unnecessary injury and postoperative morbidity, and it should be avoided. Next, the hemostat clamp is used to gently secure and remove the nail plate. If the hemostat blade is used, the serrated, toothed portion of the blade must be oriented to lie directly against the undersurface of the plate and the PNF. Proximal nail avulsion is attempted when creating a cleavage plane between the nail plate and the nail bed distally is impossible because of the presence of distal nail dystrophy, which prevents access to the distal free edge of the nail plate. This presentation may be seen in distal subungual onychomycosis (Dawber, Diseases of the Nail, 1994; Scher, 1981; Baran, 1984). First, the Freer elevator is inserted beneath the cuticle in the proximal groove to separate the PNF from the nail plate. Then, it is repositioned to allow its concave surface to match the curved contour of the ventral surface of the nail plate (Clark, 1998). The instrument is advanced until it finally reaches the distal edge of the nail plate. A hemostat is used to gently remove the nail plate. The use of urea ointment to debride and avulse dystrophic nails has been applied in the treatment of onychomycosis, onychogryphosis, psoriasis, and candidal and bacterial infections (South, 1980; White, 1982; Averill, 1986). Nail plates that are significantly dystrophic appear to respond better to avulsion with urea paste. The benefits of performing nonsurgical nail avulsion with urea ointment include pain relief; a low risk of infection, hemorrhage (ie, bloodless procedure), and other morbidity; a quick improvement after avulsion; and the absence of pain during and after treatment (South, 1980). Nail avulsion with urea is ideal for the treatment of symptomatic dystrophic nails in patients with diabetic neuropathy, vascular disease, or immunosuppression (South, 1980). A disadvantage of urea avulsion is the required length of application and the potential irritation that may result from the acidity of urea. Urea acts by dissolving the bond between the nail bed and the nail plate, and it also softens the nail plate. Urea ointment paste is formulated to include 40% urea, 5% white beeswax or paraffin, 20% anhydrous lanolin, and 35% white petrolatum (South, 1980; White, 1982). Alternatively, Ureacin-40 ointment is an over-the-counter commercial product that is ready made and can be used as a substitute. Prior to the application of urea, the paronychial area is protected with adhesive tape to prevent chemical irritation of the soft tissues. Urea ointment is liberally applied to the nail plate, and an adhesive felt (eg, moleskin) or a waterproof, stretchable, hypoallergenic tape (eg, Blenderm) is used to create a well around the treated thickened nail to hold the paste (Averill, 1986). The patient is instructed to keep the nail occluded and to avoid wetting the treated area. After 1 week of occlusion, a blunt dissection is performed to facilitate removal of the dystrophic nail by using a nail elevator and a nail clipper, while leaving the underlying normal nail intact. The avulsion procedure is painless, thus negating the need for anesthesia. The avulsed area is treated with a topical antifungal agent. When necessary, this treatment is complemented with oral antifungals until the new nail is well formed. Gross thickening of the nail without significant nail dystrophy may be the etiology of a poor response to urea treatment (Dawber, Diseases of the Nail, 1994; South, 1980). In this case, gentle abrasion of the nail surface may be tried to help improve penetration of the chemical agent. Contact of the urea-treated nail with water and poor occlusion by the dressing are other causes of treatment failure. When minimally dystrophic nails are being avulsed, a combination of 20% urea and 10% salicylic acid ointment under a 2-week occlusion may be tried (Dawber, Diseases of the Nail, 1994). Onychogryphosis commonly leads to nonreversible nail dystrophy. Urea avulsion is indicated in the treatment of this condition to provide pain relief, and it may be performed twice a year for this purpose. MatricectomyThe nail matrix is the germinative epithelium that forms the nail plate by means of the continuous differentiation of its basal cells. Matricectomy is the process of surgically, chemically, or electrically ablating or destroying the nail matrix. Complete excision of the viable nail matrix results in loss of the nail plate. Therefore, a new nail plate cannot be regenerated. Multiple indications for performing matricectomy exist, the most common being a diagnosis of recalcitrant recurrent onychocryptosis or ingrown nails (Siegle, 1992; Siegle, 1982; Ceilley, 1992). In this and other debilitating nail conditions, matricectomy should only be considered after all conventional therapies, including temporary partial or complete nail avulsion, have been unsuccessful and the condition remains refractory to treatment. Other indications for performing matricectomy include chronic nail dystrophies, such as onychauxis, onychogryphosis, onycholysis, psoriatic nail, symptomatic onychomycosis that is unresponsive to aggressive antifungal therapy, and painful nail conditions, including pincer nail deformity (Salasche, 1997; Clark, 1994; Siegle, 1982; Leshin, 1988). For most of these conditions, matricectomy is the definitive cure. When a decision is made to perform matricectomy, a complete or partial procedure can be completed. Most commonly, a partial matricectomy (the removal of the diseased portion of the nail matrix with an attempt to preserve the central portion of the nail plate) is preferred because preservation of the normal structure and function of the nail plate is possible. Total matricectomy permanently destroys the ability of the nail complex to produce a nail plate (Clark, 1998). Complete matricectomy is reserved for cases of chronic or severe nail dystrophy, especially when the condition has become refractory to multiple attempted treatments. Some examples of chronic nail dystrophies that may require total matricectomy include, but are not limited to, onychauxis, onychogryphosis, onychomycosis, psoriasis, and pincer nail deformity (Ceilley, 1992; Leshin, 1988). Partial matricectomies are especially useful in the management of persistent onycholysis and onychocryptosis. Some surgeons prefer bilateral partial matricectomy, even when the contralateral side may not yet be affected by onychocryptosis. This procedure allows the nail plate to maintain its function and aesthetics (Siegle, 1982; Ceilley, 1992). Onycholysis (Zaias, 1990; Dawber, Diseases of the Nail, 1994; Pardo-Castello, 1960) is the separation of the nail plate from the nail bed distally and laterally. When onycholysis extends to the matrix, the detachment is considered complete (Dawber, Diseases of the Nail, 1994). In onycholysis, the nail color may become grayish white from air trapped under the nail. In onycholysis associated with psoriasis, a yellow border may be present between the healthy pink nail and the separated white portion of the nail plate (Dawber, Diseases of the Nail, 1994). Onychomycosis and trauma are the 2 major causes of onycholysis of the toenail. Other causes of onycholysis include local trauma; fungal, viral (wart), or bacterial infection; inflammatory disease (eg, lichen planus); alopecia areata; psoralen plus ultraviolet A (PUVA); certain antibiotics (eg, tetracycline); some chemotherapeutic agents (ie, 5-fluorouracil, doxorubicin, bleomycin); and congenital disease as in congenital paronychial infection and partial hereditary onycholysis (Dawber, Diseases of the Nail, 1994; Daniel, 1997:251-61). Onycholysis is usually painless, but the patient might complain of mild pain during the early inflammatory period (Dawber, Diseases of the Nail, 1994). Before matricectomy, the preoperative evaluation should include a medical history and physical examination to exclude patients with documented small and large vessel occlusive disease (eg, atherosclerosis, diabetes mellitus, collagen vascular disease) in whom, because of delayed healing, this type of surgery is considered to be relatively contraindicated. Patients presenting with claudication, absent distal pulses on palpation and Doppler examination, poor capillary refill, poor wound healing, or low oxygen saturation should be excluded (Ceilley, 1992). Matricectomy should be deferred until all acute infection of the digit and paronychial tissues has resolved. Matricectomy can be performed by using surgical, chemical, or electrical modalities. Ablative matricectomy involves the use of chemocautery, electrocautery, or laser (Ceilley, 1992) to destroy the nail matrix. Excisional matricectomy uses cold steel surgery, cutting electrosurgery, or cutting laser (Ceilley, 1992) to remove the matrix. Conservative treatment to correct an ingrown nail includes removing the nail spicule (the inciting cause), trimming the nail transversely to promote forward growth, and daily packing of nonabsorbent cotton under the involved area of the nail plate to allow the nail to grow out straight. A partial or complete nail avulsion may be curative, but, in some cases, it only serves as a temporary measure. Surgical intervention is indicated when conservative measures fail. In preparation for surgical extirpation of the matrix, all nail spicules are removed by curettage. Hypertrophied granulation tissue can be reduced with an intralesional corticosteroid injection of triamcinolone acetonide, high-potency steroid preparations, cauterization, or excision. Removal of granulation tissue frees the previously fixed nail plate, allowing the plate to be elevated out of the LNF groove. Surgical resection of the LNF, lateral nail plate, hyponychium, nail bed, and nail matrix is scheduled at 4 weeks after curettage and excision of the granulation tissue. Essentially, the entire lateral nail-forming unit is removed. Two important issues must be considered before performing matricectomy: (1) All excisions must extend to the periosteum with caution to avoid the insertion of the extensor tendon on the distal phalanx. (2) No remnant of the lateral matrix horn must be left behind to prevent recurrence of nail spicules (Salasche, 1997; Ceilley, 1992). In the surgical management of onychocryptosis, several procedures and techniques are available to the nail surgeon, with each technique having benefits and disadvantages. When performing a partial matricectomy, the digit is first prepared in a sterile environment (iodine or chlorhexidine scrub may be used), and anesthetic is administered through a digital block. A 3/8-inch Penrose drain is used as a tourniquet to provide hemostasis. Some surgeons may prefer an exsanguinating tourniquet to maintain a bloodless field (Siegle, 1992; Ceilley, 1992). The area to be excised is outlined with a surgical pen, and a partial nail avulsion is performed. A nail splitter is used to cut the nail plate longitudinally, consisting of approximately one fourth of the distance from the lateral nail wall. After cutting the nail plate, a nail elevator or a straight hemostat is applied to separate the nail from its attachments at the PNF, the nail bed, and the matrix. The laterally avulsed nail is grasped and rotated out toward the disease-free nail to prevent embedding of nail spicules into the LNF. The PNF is reflected back to allow full visualization of the matrix. After avulsion, a scalpel blade is used to make 2 longitudinal incisions, measuring 4 mm in width, beginning at the distal edge of the nail to include the hyponychium and advancing proximally. The nail bed, the nail matrix, and the lateral aspect of the PNF are excised. The incision also extends to include the LNF and the lateral matrix horn in the lateral nail groove. The surgical sample is a wedge of tissue containing the nail-producing components of the nail unit. Fine scissors are used to remove the tissue sample. After obtaining the sample, the PNF is repositioned to its original anatomical site. Hemostasis is achieved with electrocoagulation, Monsel solution, or aluminum chloride solution. The wound may be allowed to heal by secondary intention. Alternatively, the wound may be closed by passing sutures through the nail plate and the LNF. When dressing the wound, the lateral nail groove is packed with iodoform or petroleum jelly gauze. A nonadherent dressing (eg, Telfa) is applied, followed by the placement of a bulky dressing or cling that is secured with elastic tape. Elastoplast may be used. At 24-48 hours after the initial dressing is applied, the wound is soaked in warm water, and the dressing is removed and changed. After surgery, the nail plate remains functional and is cosmetically acceptable. As a result of partial excision of the nail matrix, the newly formed nail plate is narrower because of a decreased width. In total matricectomy, the entire nail plate is avulsed. A scalpel is used to make 2 incisions oriented proximally and laterally; these incisions extend to the PNF and the LNF. The PNF is dorsally reflected to allow full exposure of the nail matrix, including the lateral matrix horn area. During matricectomy, the first incision is made about 1 mm distally to the distal border of the lunula and is carried 4-5 mm proximally under the PNF in the proximal nail groove to include all matrix tissue. The excised matrix is removed with fine scissors. Sutures or Steri-Strips are used to place the PNF into its normal position. Hemostasis is controlled by direct pressure and electrocoagulation. Postoperatively, patients experience significant pain, morbidity, and prolonged healing (Siegle, 1982; Leshin, 1988). A possible complication of cold steel surgery with scalpel excision may be a higher rate of nail regrowth in the area of the lateral matrix horn; this regrowth is caused by inadequate removal of the matrix from this recessed area (Clark, 1998; Siegle, 1992). Dorsally reflecting the PNF to fully expose the nail matrix helps to reduce the likelihood of this complication. After surgery, the extremity should be elevated to reduce subsequent pain and swelling. Local bupivacaine can be administered immediately after surgery to provide extended pain relief for at least 8-12 hours. Pain control is usually managed with acetaminophen with codeine. Chemical matricectomy Chemical cauterization of the nail matrix with the application of phenol is used to partially or permanently destroy the matrix. Phenol matricectomy is the most widely practiced matricectomy procedure (Salasche, 1997; Ceilley, 1992; Leshin, 1988). Phenol denatures protein and retains antibacterial and anesthetic properties. If the goal of surgery is to narrow the nail plate to correct the disparity of a nail too wide for its bed, a partial phenolization is performed. After unilateral, partial bilateral, or total nail avulsion is performed under digital block, a number-1 curette is used for curettement of the hyponychium, the lateral nail groove, the lateral matrix horn, and the proximal matrix. Curettage appears to lower the rate of recurring nail spicules in the lateral nail horn area, resulting in higher cure rates and a better treatment outcome (Ceilley, 1992). An exsanguinating tourniquet is used to maintain a bloodless surgical field for 2 reasons: (1) Blood is known to inactivate phenol (Ceilley, 1992). (2) A dry surgical field helps to facilitate contact between the matrix and the chemocauterant (Clark, 1998). Before applying phenol, the surrounding soft tissues are covered with petroleum jelly to protect them against chemical damage and resulting chemonecrosis. A supersaturated solution of 88% phenol is used. A total of three 30-second applications of phenol are required in partial matricectomy and five 30-second applications are used in complete matricectomy (Salasche, 1997; Siegle, 1982). A sterile cotton-tipped applicator dipped in the concentrated phenol solution is directed laterally into the recessed area of the lateral matrix horn and dorsally to contact the matrix tissue on the ventral surface of the PNF. During the procedure, the cotton applicator is used to vigorously massage the matrix with a twisting motion (Siegle, 1982; Ceilley, 1992). After phenol application, lavage of the treated area is performed by using 70% isopropyl alcohol to neutralize the concentrated phenol. Sodium chloride solution, boric acid, or 3-5% acetic acid may also be used to neutralize phenol (Clark, 1998). At this point, the tourniquet is removed. Bleeding is usually minimal and is controlled with aluminum chloride and direct pressure. An antibiotic ointment, petroleum jelly gauze, and number-2 tube gauze are used to dress the wound. Elastoplast or Hypafix tape is placed to secure the dressing. The dressing is removed in 24 hours after a warm-water soak, and the wound is cleansed in diluted hydrogen peroxide solution. This procedure is the standard wound care used in all types of matricectomy procedures. The patient is instructed to perform dressing changes twice daily for 2-3 weeks. Soaking the wound in a warm, diluted Betadine solution may help to accelerate healing. Phenol matricectomy has a success rate of 95% and higher (Salasche, 1997; Ceilley, 1992; Leshin, 1988), and postoperative morbidity is minimal. However, the associated risks of performing this procedure include pain, frequent recurrence, periostitis, unpredictable persistent wound drainage, and extended healing times (Ceilley, 1992; Leshin, 1988). The wound usually heals completely within 2-4 weeks by secondary intention. Chemocauterization of the nail matrix is contraindicated in patients with vascular disease. A newer approach to chemocauterization of the nail matrix involves the use of 10% sodium hydroxide (Ceilley, 1992). Chemocauterization of the nail matrix with sodium hydroxide is similar to the phenol alcohol method. One difference between the 2 procedures is the required use of a tourniquet for hemostasis in phenol matricectomy. During the procedure, a cotton-tipped applicator is dipped in a solution of 10% sodium hydroxide and is carefully applied to all areas, including the proximal and lateral nail grooves, where matrix tissue is found. The endpoint of this procedure is the visible white blanching of the capillaries (Ceilley, 1992). Once blanching is apparent, the sodium hydroxide is neutralized with 5% acetic acid. The success rate of this procedure reportedly parallels that of the phenol method. However, some nail surgeons prefer 10% sodium hydroxide because of decreased postoperative morbidity with lower recurrence rates, minimal drainage, and faster healing time. A surgeon experienced in sodium hydroxide matricectomy should perform the procedure to avoid excessive chemical-induced tissue destruction with resultant pain and prolonged healing. Chemonecrosis of the surrounding tissues is a potential problem with phenol matricectomy and sodium hydroxide matricectomy. Ablative matricectomy In the electrodesiccation and curettage method, the diseased portion of the nail plate is avulsed. A tourniquet is used only during the avulsion procedure. This procedure is followed by vigorous curettage of the exposed matrix and its lateral horn. Electrodesiccation of the area curetted is performed. To ensure complete destruction of all matrix tissue, electric current is applied twice to the treatment site for an estimated 5 seconds (Clark, 1998). A cooling period of 10-20 seconds should occur between treatments. Excellent hemostasis is provided by means of electrocoagulation. A potential complication of this method is thermal destruction of the nail folds, the surrounding periungual tissues, and the underlying bony phalanx. This complication may be circumvented by using Teflon-coated probes to direct energy primarily to the matrix (Clark, 1998). Electrosurgical ablation of the nail matrix involves the use of an electrode that is directly applied to the matrix tissue, leading to its destruction. Matrix destruction is carried out independent of incisions and electrodesiccation. A dry surgical field must be maintained (Ceilley, 1992), which is accomplished by applying a tourniquet before performing nail avulsion. The electrode has an insulated surface and an exposed surface (Ceilley, 1992). The insulated surface protects the adjacent healthy tissues from electrical destruction. Bleeding is usually absent because of adequate electrocoagulation. This method is associated with a rapid healing time, a low recurrence rate, and little postoperative pain. However, scarring may be significantly greater than that seen with the laser technique (Siegle, 1982). Anesthesia must be adequate throughout the procedure. Ablative matricectomy with carbon dioxide laser vaporization provides selective destruction of the matrix tissue. Carbon dioxide matricectomy is associated with minimal postoperative morbidity, protracted healing time, decreased edema and inflammation, and absence of extensive necrosis of the adjacent dermal tissue (Ceilley, 1992). The carbon dioxide laser was first used in the treatment of onychogryphosis (Ceilley, 1992). Before laser treatment, 1% lidocaine is used to perform a digital block. The matrix may be curetted, and the PNF is reflected back with skin hooks to fully expose the matrix. Wet towels are placed around the surgical site to limit injury to the adjacent soft tissues. The laser beam is directed into the deep recessed areas of the lateral matrix horn and the ventral surface of the posterior nail fold (Leshin, 1988), completely obliterating all the matrix tissue and preventing recurrent nail growth. Hemostasis is well controlled. After laser treatment, a bacitracin pressure dressing is placed over the digit. In 24 hours, the dressing is removed, the surgical site is cleansed, and bacitracin is reapplied. Dressing changes are performed 2-3 times daily over a period of several weeks. The surgical site heals by secondary intention, and healing is rapid with minimal patient discomfort. The advantage of carbon dioxide laser vaporization of the matrix is the use of a defocused laser beam that is limited in its depth of penetration (Ceilley, 1992; Miller, 1991; Borovoy, 1996). Thus, laser energy is directed at only matrix tissues. Therefore, carbon dioxide laser vaporization of the matrix is as effective as the other methods in destroying the nail matrix. Radical matricectomy Radical matricectomy (the Syme procedure) is the radical en bloc excision of the entire nail complex. This procedure, which is less commonly performed today, is reserved for patients with symptomatic, recurrent onychocryptosis that is refractory to repeated treatments of total nail matricectomy. The plantar flap formed from amputation of the distal half of the terminal phalanx is sutured dorsally over the defect created from the excision of the nail bed and the nail matrix for primary wound closure (Ceilley, 1992). Radical matricectomy has a success rate of almost 100%, with low postoperative morbidity, despite the poor cosmetic and functional outcome (Siegle, 1982). Soft tissue resection for ingrown nails is performed in cases of lateral nail wall hypertrophy. This procedure spares the nail matrix and the nail plate, which most likely have a normal shape, and it removes the surrounding paronychial tissues. Soft tissue resection for ingrown nails can be performed in 3 ways: simple nail avulsion, peridigital resection, or elliptical wedge excision. Simple (partial or complete) nail avulsion may be performed with a 1% lidocaine digital block, especially if significant pain and infection are present. Typically, removing a narrow strip of nail from the embedded side is adequate. Simple avulsion alone has low postoperative morbidity and an estimated cure rate of 30% (Siegle, 1982; Dawber, The Nails in Disease, 1994), relieving pain and resolving infection in this presentation. In cases where granulation tissue has formed, electrodesiccation (Siegle, 1992), cauterization (Siegle, 1992), or excision is used to remove the excess tissue. If the hypertrophied granulation tissues epithelialize, scalpel excision or electrodesiccation with curettage is performed (Siegle, 1992). The patient is instructed to place cotton wool at the previously embedded site to keep the nail plate elevated. Repeated attempts at avulsion are associated with failed treatment outcomes and a greater risk of recurrence. Peridigital resection may be used to treat the soft tissue hypertrophy. When this approach is used, 2 incisions are made: the first incision is a curved line, hugging the lateral surface of the digit, and the second incision is made parallel to the first and is extended to the underlying subcutaneous fat to remove a wedge-shaped sample of tissue. At closure, the nail folds in the nail groove are oriented away from the nail plate, limiting contact between the 2 structures. Elliptical wedge excision of the lateral nail wall and the nail fold is a third option. At closure, Steri-Strips are placed to secure the nail plate to the newly created lateral nail wall (Siegle, 1982). Alternatively, interrupted 4-0 nylon sutures first passed through the skin and then the nail plate may be used to close the defect. The success rate of the last 2 approaches is 50-70% (Siegle, 1982). In presentations where recurrence is extensive or where multiple sites are involved, cold steel excision followed by a single treatment of phenol on the wound is recommended (Siegle, 1982). Paronychial surgeryThe paronychial region is primarily defined by the PNF, the LNF, and the nail walls; the distal cuticle attached to the nail plate; and the ventrally situated eponychium (Zaias, 1990; Dawber, 1984; Dawber, Diseases of the Nails and their Management, 1994; Pardo-Castello, 1960). These components of the nail unit function collectively to prevent infection and inflammation from reaching the proximal nail matrix. A physical or chemical insult most often precedes the introduction of inflammation or infection into the paronychial area. Examples of pathologic conditions that commonly involve the perionychium include acute and chronic paronychial infections, periungual and subungual verrucae, deep fungi, atypical mycobacteria, myxoid cysts, foreign body and pyogenic granulomas after trauma, and tumors (ie, periungual fibroma associated with tuberous sclerosis and acquired digital fibrokeratoma) (Salasche, 1997). Emergent antibiotic treatment is paramount in preventing permanent nail dystrophy. Before initiating treatment, culture and sensitivity studies for bacteria are performed. Staphylococcus aureus is the most common organism cultured in acute paronychial infection (Zaias, 1990; Dawber, Diseases of the Nail, 1994; Pardo-Castello, 1960). Other organisms less commonly identified in acute paronychia are Streptococci pyogenes and gram-negative enteric bacteria. Early empiric antimicrobial therapy with a broad-spectrum penicillinase-resistant antibiotic and a topical antimicrobial agent is recommended. Based on culture results, antibiotic treatment is later streamlined to cover the specific organism identified on culture. Wet compresses with Burrow solution, warm soaks, or alcoholic baths and elevation are also used to help control early infection (Dawber, Diseases of the Nail, 1994). If the acute infection fails to respond to antibiotic treatment within 48 hours, surgical management is indicated. When present, pockets of collected pus can extend around the base of the nail under the PNF and inflame the nail matrix. The pus may dissect the nail away from its weaker underlying proximal attachment. A pressure necrosis can develop within 48 hours with resultant nail dystrophy that may be transient or permanent if surgery is delayed. Before evacuating the pus, a proximal block is administered. A small incision is made parallel to the nail fold and directly over the collection of pus to drain the abscess. Baran and Bureau recommend incising the site of maximum pain rather than the site of maximum soft tissue induration. Formed septa in the abscess base are destroyed by using the tip of a curved hemostat (Salasche, 1997). If infection spreads under the distal nail bed (subungual extension), excision of the entire nail base along with distal avulsion is performed to expose the nail bed. Then, the nail bed is carefully debrided. Postoperative care involves changing the dressing daily and moistening it with sodium chloride solution or an antiseptic solution. This process is performed daily and is continued until all purulent drainage has resolved. In recalcitrant disease, a crescentic excision of the diseased nail fold along with the proximal nail plate is performed (Dawber, Diseases of the Nail, 1994; Salasche, 1997; Baran, 1981). Healing occurs by secondary intention, restoring the normal anatomical barrier function of this area. Wound toilet includes the application of an antibiotic dressing. The patient should be instructed to avoid contact with water when possible and to protect the hands by wearing rubber gloves. Another surgical approach is to excise the involved tissue and to create an eponychial pouch (Herndon, 1997). The Bunnell technique involves the avulsion of the proximal one third of the nail by cutting across with scissors followed by the placement of nonstick gauze under the PNF (Dawber, Diseases of the Nail, 1994). If the infection is confined to one side and has tracked beneath the nail plate, avulsion of the lateral nail adjacent to the infection is performed. Surgery of myxoid cystsMyxoid cysts are usually asymptomatic. However, surgical removal of the cysts is indicated when they become too large and cause pressure on the underlying matrix, resulting in longitudinal nail deformities, such as splitting of and ridging on the nail plate. Other indications for surgery include pain, persistent drainage, and development of secondary infection. Conservative treatment may initially be attempted with intralesional corticosteroid injections or by freezing with cryotherapy (Salasche, 1997). When conservative measures prove unsuccessful, elective en bloc excision of the PNF is performed (Clark, 1998). The goal during surgery is to perform a full-thickness excision of the PNF that includes symmetric small portions of the LNF. Standard preparation of the digit is performed under sterile conditions. Effective anesthetic is administered, and a wide Penrose drain is applied for tourniquet action. A surgical pen is used to outline the area of planned excision. A Freer elevator is placed in the proximal nail groove to help define the proximal extent of the cyst and to direct movement of the scalpel. The Freer elevator should be positioned to move synchronously with and below the advancing scalpel to avoid cutting deeply into the matrix or cutting the proximal extensor tendon (Salasche, 1997). Hemostasis of the wound may be achieved by means of spot electrodesiccation. Gelfoam or Instat pads are used to control capillary bleeding. A bulky, loose dressing is applied over the wound. The wound is cleansed twice daily with dilute hydrogen peroxide followed by the application of an antibiotic ointment and a replacement of the dressing. If the wound is allowed to heal by secondary intention, the new position of the PNF will be 3-5 mm more proximal to the original position (Salasche, 1997). This outcome is cosmetically appealing with a slender appearance to the digit. If the nai |