Nail Disorders

Nail disorders are a common reason for presentation in Australian primary care, accounting for an estimated 10% of all dermatological consultations. The nails are highly visible structures that serve as both protective organs and diagnostic windows into local and systemic pathology. Changes in nail colour, shape, texture, or attachment may reflect dermatological conditions (psoriasis, lichen planus, eczema), infectious aetiologies (dermatophytes, yeasts, bacteria), systemic diseases (anaemia, thyroid dysfunction, cardiopulmonary disease), trauma, or iatrogenic effects from medications.

In Australia, onychomycosis is the most prevalent nail disorder, affecting approximately 5–10% of the adult population, with prevalence rising sharply after age 60 to an estimated 20–30%. Dermatophytes — principally Trichophyton rubrum and T. interdigitale — are responsible for the majority of cases. Candida species are more common in fingernail infections, particularly in individuals with chronic paronychia or immunosuppression. Non-dermatophyte moulds (e.g. Scopulariopsis brevicaulis, Aspergillus species) account for a small but clinically significant proportion.

Nail psoriasis affects an estimated 1–2% of the general Australian population. Among patients with established cutaneous psoriasis, nail involvement is present in up to 50%, and among those with psoriatic arthritis, the figure approaches 80–90%. Nail psoriasis is a significant predictor of future development of psoriatic arthritis and therefore warrants active surveillance in primary care.

Ingrowing toenails (onychocryptosis) are particularly common in adolescents and young adults, with a male-to-female ratio of approximately 2:1. The hallux nail is affected in >95% of cases. Risk factors include improper nail trimming, tight footwear, hyperhidrosis, and obesity. In the Australian paediatric population, ingrowing toenails are among the most frequent reasons for referral to paediatric surgery or podiatry.

Koilonychia is encountered less frequently but has important diagnostic implications. In Australian practice, iron-deficiency anaemia remains the most common cause in women of reproductive age and in Indigenous Australians, where dietary iron insufficiency and chronic disease-related anaemia are more prevalent. Splinter haemorrhages, while often traumatic in origin, must be distinguished from those caused by infective endocarditis, systemic vasculitis, or antiphospholipid syndrome.

This article provides a structured approach to the diagnosis and management of common nail disorders encountered in Australian primary care, with reference to current evidence-based guidelines and the Australian healthcare context.

A thorough understanding of nail anatomy is essential for accurate clinical assessment and localisation of pathology. Each nail unit is a complex integumentary structure with distinct components that produce, support, and anchor the nail plate.

Components of the Nail Unit

Normal Nail Variants

• Longitudinal ridges: Increase with age (senile nail); rarely indicate lichen planus or peripheral vascular disease.
• Leukonychia (white spots): Most commonly due to minor matrix trauma; usually a normal finding in children.
• Mees lines: Transverse white bands following systemic insult (arsenic, chemotherapy, severe illness); grow out with the nail.
• Beau lines: Transverse depressions from temporary arrest of nail matrix mitosis (fever, illness, trauma); useful for timing systemic events.

Functions of the Nail

• Protection of the distal digit from mechanical injury.
• Fine manipulation — the counterforce of the nail plate enhances fingertip precision and grip.
• Sensory function — the nail plate transmits pressure to the nail bed, enhancing two-point discrimination at the fingertip.
• Scratching — an important pruritus-relief mechanism and, in pathologic states, a vector for secondary infection.

Alterations in nail plate thickness and surface texture are among the most common presenting complaints in nail disorders. The pattern, distribution, and associated features are crucial for narrowing the differential diagnosis.

Nail Thickening (Onychauxis)

Nail plate thickening may be generalised or focal, and arises from increased keratin production or accumulation of subungual debris. The major causes are summarised below.

Nail Thinning (Onychoschizia / Onychorrhexis)

• Onychoschizia (lamellar splitting): Horizontal splitting at the distal free edge; very common in women; caused by repeated wetting and drying, exposure to detergents, nail polish removers (acetone). Management: minimise water exposure, use cotton-lined gloves, apply nail hardeners containing formaldehyde, moisturise with urea-based emollients.
• Onychorrhexis (longitudinal splitting): Longitudinal fissures along the nail plate; seen in lichen planus, peripheral vascular disease, Darier disease, and hypothyroidism. Investigate underlying cause.
• Lichen planus: Affects nails in ~10% of cases; can cause thinning, longitudinal ridging, pterygium (scarring fusion of proximal nail fold to nail plate), and ultimately permanent nail loss. Requires early dermatology referral for intralesional or systemic corticosteroids to prevent irreversible matrix destruction.
• Brittle nails: Affects up to 20% of the population; more common in women and with ageing. Biotin supplementation (2.5 mg daily) may improve nail strength, though evidence is limited.

Nail Pitting

Pitting results from defective superficial keratinisation of the proximal nail matrix. The pattern, depth, and distribution of pits are diagnostically useful.

Onychomycosis

Onychomycosis is fungal infection of the nail plate, nail bed, or both. It is the most common nail disease worldwide and accounts for approximately 50% of all nail consultations in Australian general practice.

Classification

Diagnosis

• Mycological confirmation is mandatory before initiating systemic antifungal therapy. Send nail clippings and subungual scrapings for potassium hydroxide (KOH) mount, fungal culture, and/or polymerase chain reaction (PCR) testing.
• Sample from the most proximal affected area of the nail bed (not the free edge) to maximise yield.
• Dermatophyte PCR (available through most Australian pathology providers including Douglass Hanly Moir, Sullivan Nicolaides, and QML) offers higher sensitivity (~80–95%) and faster turnaround (2–5 days) compared with culture (2–6 weeks).
• Clippings for histopathology with Periodic acid-Schiff (PAS) staining are useful when mycological tests are negative but clinical suspicion remains high.
• Consider differential diagnoses: psoriasis, lichen planus, trauma, subungual melanoma, yellow nail syndrome.

Treatment

Nail Colour Changes

Discolouration of the nail plate or nail bed is a frequent finding and has a broad differential. The colour, distribution, and pattern of change guide the diagnosis.

Ingrowing Toenail (Onychocryptosis)

An ingrowing toenail occurs when the lateral edge of the nail plate penetrates the adjacent lateral nail fold, causing inflammation, pain, and often secondary infection. The medial aspect of the hallux nail is most commonly affected. The condition is classified into three stages:

Management by Stage

• Stage 1 (Conservative): Warm saline soaks (10–15 minutes, 2–3 times daily); cotton-wick insertion beneath the lateral nail edge to elevate it away from the fold; proper nail trimming (cut straight across, do not round corners); well-fitting shoes; topical antiseptic (povidone-iodine or chlorhexidine).
• Stage 2 (Procedural): Gutter splinting (a plastic tube or vinyl strip sutured along the lateral nail edge to act as a shield); consider partial nail avulsion with chemical matrixectomy (see below); if infection is present, oral flucloxacillin 500 mg QDS for 5–7 days (or cephalexin 500 mg QDS if penicillin allergy); topical mupirocin 2% TDS for localised cellulitis.
• Stage 3 (Surgical): Wedge excision or partial nail avulsion with chemical matrixectomy using phenol (88% aqueous phenol applied to the matrix for 60–90 seconds) or sodium hydroxide (10% NaOH for 30–60 seconds). Phenol matrixectomy has a recurrence rate of approximately 5–10%. The procedure can be performed under local anaesthesia (digital nerve block with lignocaine 1–2% without adrenaline) in a GP procedural room, podiatry clinic, or day surgery setting.

Koilonychia (Spoon Nails)

Koilonychia describes concavity of the nail plate, such that the nail is thin and brittle and curves upward at the edges, resembling a spoon. It most commonly affects the fingernails, particularly the index and middle fingers.

Aetiology

Investigation of Koilonychia

• First-line: FBC, serum ferritin, serum iron, transferrin, transferrin saturation, TFTs.
• If iron studies abnormal: Consider coeliac serology (anti-tTG IgA), faecal occult blood test, and GI investigation (colonoscopy and/or gastroscopy) in patients over 50 or with red-flag symptoms to exclude GI blood loss.
• If haemochromatosis suspected: HFE gene testing (C282Y, H63D mutations); if confirmed, screen first-degree relatives.

Splinter Haemorrhages

Splinter haemorrhages are thin, longitudinal, red-brown to black linear streaks in the nail bed, representing microthrombi or emboli in the longitudinally oriented nail-bed capillaries. They typically appear in the distal two-thirds of the nail and grow out distally.

Aetiology

The investigation of nail disorders depends on the clinical differential. The following summarises commonly used investigations in the Australian primary care context.

Onychomycosis Treatment Algorithm

Nail Psoriasis Management

Paronychia

• Acute paronychia: Usually Staphylococcus aureus. Warm soaks; if abscess present, incision and drainage under local anaesthetic. Oral flucloxacillin 500 mg QDS for 5–7 days (or cephalexin 500 mg QDS if penicillin allergy). MRSA risk in healthcare workers or recent hospitalisation — consider trimethoprim+sulfamethoxazole (160/800 mg BD) or doxycycline 100 mg BD.
• Chronic paronychia: Usually Candida species; associated with frequent wet work, loss of cuticle barrier. Eliminate moisture exposure; topical miconazole 2% cream or ketoconazole 2% cream BD for 4–6 weeks; resistant cases: itraconazole 200 mg daily for 2–4 weeks. Topical corticosteroid (mometasone furoate 0.1%) may reduce inflammation.

Quick Reference — Common Nail Presentations

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