An Atlas Of Diseases Of The Nail

The medial and lateral borders of the great toe are most commonly affected.1,4 The affected nail fold becomes erythematous, edematous, tender, and hypertrophic as the nail grows into the neighboring soft tissue (Figure 1). The condition is exquisitely painful, especially if pressure is applied to the affected area.5 Secondary bacterial infection with seropurulent discharge, paronychia, and formation of granulation tissue typically ensue (Figure 2).

An Atlas of Diseases of the Nail

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Trauma that facilitates entry of the organism into the paronychial tissue may result from a splinter or thorn, overzealous manicuring and cuticle damage, finger sucking, nail biting, ingrown nail, artificial nail, nail biting, or picking at a hangnail.3 Other predisposing factors include immunosuppression (eg, diabetes mellitus, malignancy, HIV infection) and occupations in which the hands or feet are frequently immersed in water (eg, homemakers, hairdressers, dishwashers, bartenders).4,5 The female to male ratio is approximately 3 to 1.2,4

Clinically, the condition is characterized by acute onset of throbbing pain, erythema, edema, and tenderness in the proximal and lateral portions of the nail bed (Figure 1), usually within a few days after a local minor trauma.2,5 Usually, only one nail is involved, and the fingernail is affected more often than the toenail.2 Occasionally, the infection may spread along the proximal nail fold to the other side of the nail, resulting in the so called runaround infection.1 An area of fluctuance indicates the presence of an abscess. The digital pressure test, performed by asking the patient to oppose the thumb and the affected finger, thereby applying light pressure to the distal volar aspect of the affected finger, is useful in the early stage of infection to determine the presence and extent of an abscess.2 An increase in pressure within the paronychium causes blanching of the overlying skin and clear demarcation of the abscess.2

If acute paronychia is not properly treated, it can lead to formation of granulation tissue around the nail fold, cellulitis, felon, ischemic necrosis of the fingertip, osteomyelitis, Beau lines, onychomadesis, and nail dystrophy.1 Acute paronychia can be treated with warm soaks with antiseptics (eg, povidone-iodine, chlorhexidine) or water, and topical antibiotics (eg, fusidic acid, mupirocin) with or without topical corticosteroids.2,5 Acetaminophen or a nonsteroidal anti-inflammatory drug may be used for symptomatic relief of pain. The routine use of oral antibiotics is controversial.1 Severe cases or cases not responding to topical antibiotic treatment might require the use of oral antibiotic therapy (clindamycin, flucloxacillin, amoxicillin-clavulanate, doxycycline).3,5 Once an abscess has developed, incision and drainage is necessary.3 Infiltrative anesthesia or a wing block is preferred to a digital block to ensure comfort and complete drainage of the abscess.2,4 For prophylaxis, patients should be advised to avoid trauma to the paronychial folds and cuticle by trimming back hangnails with fine scissors.

Chronic paronychia usually involves multiple digits.2 Clinically, chronic paronychia presents with chronic mild erythema and edema of the proximal nail fold without fluctuance and disappearance of the cuticle (Figure 2).3 With time, the nail folds become hypertrophic, followed by marked retraction of the proximal nail fold. The nail plate may become thickened, discolored, or dystrophic.3,4 Pitting, Beau lines, longitudinal grooving, and onychomadesis may be present due to inflammation of the nail matrix.1,6 The diagnosis is mainly clinical, based on a history of chronic exposure to moisture and irritants and the characteristic physical findings.

The etiology of chronic paronychia is multifactorial.6 Chronic paronychia may be caused by Candida species, pseudomonas (suggested by a discolored green nail bed as is shown in Figure 3), and streptococci.4 Although Candida species are the most frequently cultured microorganism in patients with chronic paronychia, some authors suggest that hypersensitivity to Candida species is more likely to be the etiology, rather than the infection itself.7 Chronic paronychia may also be caused by frequent exposure of the digit to moisture (such as finger sucking) and irritants.6 The condition may follow the use of certain medications such as retinoids, protease inhibitors, chemotherapeutic agents, and antiretrovirals.2,6 Chronic paronychia is more common in individuals with inflammatory skin diseases (eg, atopic dermatitis, psoriasis) and individuals with immunosuppression (eg, diabetes mellitus, malignancy, HIV infection).2

Treatment is directed at the underlying cause, such as avoiding exposure of the digit to moisture and irritants and wearing gloves while performing work with probable exposure to moisture and irritants. Offending medication should be discontinued. The use of topical corticosteroids or calcineurin inhibitors is the first-line therapy.1,2,5,6 Topical or systemic antifungal agents (eg, terbinafine, itraconazole, fluconazole) may be considered if Candida infection is suspected. Chronic paronychia may recur in susceptible individuals.4 In recalcitrant cases, en bloc excision of the proximal nail fold or an eponychial marsupialization, with or without removal of the nail plate, should be considered.6

Onychomycosis is the most common fungal infection of the nail unit caused by dermatophytes (tinea unguium), nondermatophyte molds, and yeasts.1,2 Approximately 90% of toenail onychomycosis cases and 75% of fingernail onychomycosis cases are caused by dermatophytes, notably Trichophyton mentagrophytes and Trichophyton rubrum.3,4

In general, toenails are affected 7 to 10 times more frequently than fingernails, presumably because of repeated blunt pressure from footwear and wearing of occlusive and tight shoes.2,7,8 The big toenails are most often affected.4 Generally, several toenails are affected. Tinea pedis is also often present.9,10 Furthermore, it is unusual to have more than one fingernail involved without concomitant toenail involvement unless there is a history of trauma or the patient is immunocompromised.5

Based on the pattern of invasion and location of the nail bed involvement, onychomycosis can be divided into the following 5 clinical subtypes: distal lateral subungual onychomycosis, white superficial onychomycosis, proximal subungual onychomycosis, endonyx onychomycosis, and total dystrophic onychomycosis. Patients may have a combination of these subtypes.

In white superficial onychomycosis, the upper surface of the nail plate is invaded by the fungus, notably T mentagrophytes.6,11,12 Typically, white superficial onychomycosis presents as crumbly, soft, chalky white discoloration of the dorsal surface of the nail plate (Figure 4) that can be easily scraped off.3,5,6,11,12

Proximal subungual onychomycosis is usually caused by T rubrum and Fusarium spp.6 In proximal subungual onychomycosis, the fungus invades the undersurface of the proximal nail fold in the vicinity of the cuticle and then extends distally.5,11 Clinically, proximal subungual onychomycosis presents as an area of leukonychia in the proximal nail plate and moves distally with nail growth (Figure 5).12 Proximal subungual onychomycosis usually occurs in immunocompromised patients, especially those with AIDS.3,5,7

Endonyx onychomycosis is usually caused by Trichophyton soudanense and Trichophyton violaceum.5,10 In endonyx onychomycosis, the fungus infects the nail plate but not the nail bed.6,9,10 Clinically, endonyx onychomycosis is characterized by milky patches of the nail plate, indentations, and lamellar splitting.5,10 The nail plate is firmly attached to the nail bed, and subungual hyperkeratosis is absent.10,11

Total dystrophic onychomycosis is characterized by total destruction of the entire nail apparatus and is often the end stage of onychomycosis that may follow any of other subtypes.6,9,12 Clinically, total dystrophic onychomycosis presents as a severely dystrophic and crumbed nail plate that is yellowish, diffusely thickened, and friable (Figure 6).10,12

Oral antifungal therapy is considered the gold standard for onychomycosis because of shorter courses of treatment and higher cure rates compared with topical antifungal therapy.8,9 Oral antifungals, when used in combination with topical antifungals, increase the cure rate.3,6,10 Nd:YAG nonspecific laser heating of onychomycosis may offer some benefit, although more research is needed.2 Surgical or chemical (eg, high-concentration urea) avulsion of especially thick nails with onychomycosis is also an option where medical therapy has failed.6

Typically, trachyonychia presents with roughness of the nail plate associated with longitudinal ridging that may give the nail an opaque, sandpaper-like appearance (opaque trachyonychia).2 Less commonly, trachyonychia presents with diffuse, closely aggregated, small superficial pits that reflect light, which may give the nail a shiny appearance (shiny trachyonychia).1,2 Opaque trachyonychia and shiny trachyonychia represent the spectrum of disease severity, with opaque trachyonychia being the more severe type.3 The two varieties may coexist.4

Trachyonychia may involve the nail of one, several, or all digits. The degree of severity may, however, vary from nail to nail. Typically, the involvement is bilateral and symmetric. Multiple nails are usually affected at the time of presentation.3 The adjacent cuticles are usually ragged, hyperkeratotic, and thickened.1 Affected nails are often thin and brittle.5 Koilonychia is commonly seen.

Most cases occur sporadically and are idiopathic.1,6 However, trachyonychia has been reported in association with a number of dermatologic diseases (eg, alopecia areata, atopic dermatitis, vitiligo, psoriasis, lichen planus, lichen nitidus, ichthyosis vulgaris, pemphigus vulgaris, systemic sclerosis, incontinentia pigmenti, congenital cutaneous candidiasis, pachyonychia congenita), nondermatologic diseases (eg, immunoglobulin A deficiency, autoimmune hemolytic anemia, immune thrombocytopenia, juvenile dermatomyositis, graft-versus-host disease, sarcoidosis, amyloidosis, primary biliary cirrhosis, reflex sympathetic dystrophy), and syndromes (eg, nail-patella syndrome, Down syndrome, Clouston syndrome, Bart syndrome, Sézary syndrome, Hay-Wells syndrome, Brauer-Buschke-Fischer syndrome, and Zinsser-Engman-Cole syndrome).1,2,6,7 Familial cases have also been reported. An autosomal dominant mode of inheritance has been described.5 041b061a72