Common Lumps and Bumps

Cutaneous and subcutaneous lumps are among the most frequent presentations in Australian general practice, accounting for an estimated 5–10% of all consultations. The vast majority are benign, yet they generate significant patient anxiety and a substantial burden of specialist referrals. A structured, evidence-based approach to diagnosis and management allows general practitioners (GPs) to safely manage most lesions in primary care while identifying the minority that require surgical excision, specialist input, or histopathological assessment.

In Australia, the most commonly encountered lumps include epidermoid and pilar cysts, lipomas, viral warts, molluscum contagiosum, dermatofibromas, and keloid or hypertrophic scars. Their prevalence varies by age, sex, ethnicity, and geographic location. Viral warts affect approximately 7–12% of the Australian population, with peak incidence in school-aged children (5–15 years). Molluscum contagiosum is similarly paediatric-predominant. Lipomas are found in approximately 1% of adults and increase in prevalence with age. Keloid scarring shows marked ethnic variation, with higher rates in Aboriginal and Torres Strait Islander Australians and those of African, Asian, or Polynesian descent.

This article provides a practical, tissue-of-origin-based framework for classifying common lumps and bumps, followed by detailed guidance on the diagnosis and management of the most frequently encountered entities: epidermoid and pilar cysts, lipomas, warts, molluscum contagiosum, and keloid and hypertrophic scarring.

A tissue-of-origin approach is the most practical framework for the differential diagnosis of cutaneous and subcutaneous lumps. The table below summarises the major categories, common examples, and typical clinical features.

The following sections address the most commonly encountered lumps in Australian primary care in detail.

Epidermoid (Sebaceous) Cysts

Epidermoid cysts are the most common cutaneous cysts, arising from the infundibular (follicular) portion of the hair follicle. The term "sebaceous cyst" is a misnomer — these cysts do not originate from sebaceous glands, although they may contain sebaceous material. They are lined by stratified squamous epithelium and filled with laminated keratin.

Clinical features: Firm, round, mobile, subcutaneous nodules, typically 0.5–5 cm in diameter. A central punctum (a dark dot representing the occluded follicular ostium) is pathognomonic. They most commonly occur on the face, neck, trunk, and scrotum (where they may be multiple — scrotal cysts). They are usually asymptomatic but may become inflamed or infected, presenting as a painful, erythematous, fluctuant mass.

Diagnosis: Clinical diagnosis is usually sufficient. Dermoscopy may reveal the punctum. Ultrasound is rarely required but shows a well-defined, hypoechoic, avascular lesion with posterior acoustic enhancement. If diagnosis is uncertain or the lesion is atypical, excisional biopsy with histopathology is recommended.

Management:

• Asymptomatic cysts — observation and reassurance. No treatment is required unless the patient desires removal for cosmetic reasons or recurrent symptoms.
• Inflamed (non-infected) cysts — intralesional triamcinolone acetonide (5–10 mg/mL, 0.1–0.5 mL depending on size) can reduce inflammation. Warm compresses.
• Infected cysts (abscess) — incision and drainage (I&D) under local anaesthesia. A cruciate incision with curettage of the cyst wall is preferred. Complete excision of the cyst wall should be deferred until inflammation resolves (typically 6–8 weeks) to reduce recurrence.
• Definitive excision — elliptical excision with removal of the entire cyst wall and punctum under local anaesthesia (lidocaine 1% with adrenaline). The "squeeze technique" with a small incision over the punctum may be used for non-inflamed cysts, but recurrence rates are higher if the wall is not completely excised.

Pilar (Trichilemmal) Cysts

Pilar cysts arise from the outer root sheath of the hair follicle (trichilemmal keratinisation). They are less common than epidermoid cysts overall but account for approximately 90% of scalp cysts. They have a predilection for the scalp and are often multiple. Unlike epidermoid cysts, they typically lack a visible punctum.

Clinical features: Firm, smooth, mobile, subcutaneous nodules on the scalp, usually 1–4 cm. They are often multiple and may run in families (autosomal dominant). They are generally asymptomatic but may become inflamed or, rarely, undergo malignant transformation (proliferating trichilemmal tumour/cyst).

Management: As for epidermoid cysts. Definitive treatment is surgical excision with complete wall removal. Referral to a GP with surgical skills or general/plastic surgeon may be required for large or recurrent scalp cysts.

Lipoma

Lipomas are benign tumours of mature adipose tissue and represent the most common soft-tissue neoplasm. They are found in approximately 1% of the adult population, with peak incidence between 40 and 60 years of age. They may be solitary or multiple (lipomatosis), the latter sometimes associated with familial conditions (familial multiple lipomatosis) or syndromes (Dercum disease, adiposis dolorosa).

Clinical features: Soft, compressible, lobulated, mobile, subcutaneous masses that are typically painless. They are usually 2–10 cm but may grow much larger. Common sites include the trunk, shoulders, posterior neck, and proximal extremities. They have a characteristic "doughy" feel and may demonstrate a pseudo-fluctuant quality (slipping sign / "watermelon seed" sign — the lipoma slips from between the examiner's fingers on palpation).

Investigation: Clinical diagnosis is often sufficient for typical, superficial, small lipomas. Ultrasound demonstrates a well-defined, hyperechoic, avascular lesion. If any atypical features are present (see red flags above), MRI of the affected region is indicated.

Management:

• Observation — most lipomas require no treatment. Reassurance and monitoring for change in size or symptoms.
• Surgical excision — indicated for symptomatic lipomas (pain, restriction of movement, compression of adjacent structures), diagnostic uncertainty, or patient preference (cosmesis). Performed under local anaesthesia for small lesions; larger lesions may require general anaesthesia. Blunt dissection to enucleate the lipoma from the surrounding capsule is the standard technique.
• Liposuction — an alternative for large lipomas in cosmetically sensitive areas; higher recurrence rates than open excision.
• Injectable phosphatidylcholine / deoxycholate (Belkyra®) — not routinely recommended for lipomas in Australian practice; PBS not listed for this indication.

Histopathology: All excised lipomas should be sent for histopathological examination to exclude atypical lipomatous tumour (well-differentiated liposarcoma).

Viral Warts (Verrucae)

Viral warts are benign epithelial proliferations caused by the human papillomavirus (HPV). Over 200 HPV types have been identified; cutaneous warts are most commonly associated with HPV types 1, 2, 3, 4, 27, and 57. Prevalence in Australian children is estimated at 7–12%, with peak incidence between ages 12 and 16 years. Transmission occurs via direct skin-to-skin contact or fomites, with incubation periods of 1–6 months. Risk factors include skin barrier disruption, immunosuppression, and communal environments (swimming pools, change rooms).

Types of Cutaneous Warts

Treatment of Cutaneous Warts

Approximately 65% of cutaneous warts in immunocompetent individuals resolve spontaneously within 2 years. Treatment is indicated for painful, functionally limiting, cosmetically bothersome, or persistent warts. No single therapy has proven superiority; choice depends on wart type, location, patient age, and adherence capacity.

Molluscum Contagiosum

Molluscum contagiosum is a common, self-limiting viral infection of the skin caused by the molluscum contagiosum virus (MCV), a member of the Poxviridae family. It predominantly affects children aged 1–10 years (prevalence 5–8% in Australian children) and sexually transmitted cases in adults. In immunocompromised patients (particularly HIV/AIDS), lesions may be extensive, large, and atypical.

Clinical features: Small (2–5 mm), flesh-coloured, dome-shaped papules with a central umbilication (dell). They are typically asymptomatic but may be pruritic or inflamed. Commonly found on the trunk, axillae, antecubital and popliteal fossae (in children), and genitalia (in adults). Lesions may spread by autoinoculation. An eczematous ("id") reaction may develop around lesions.

Management:

• Watchful waiting (preferred in most paediatric cases) — molluscum is self-limiting in immunocompetent individuals; spontaneous resolution occurs within 6–18 months (occasionally up to 3 years). Scarring and pain from active treatment may be worse than the disease itself in children. Reassurance and education are key.
• Cryotherapy — liquid nitrogen applied to each lesion every 2–3 weeks. Effective but painful; better tolerated in older children and adults.
• Curettage / expression — central core expressed with a comedone extractor or curette under local anaesthesia (EMLA® cream applied 60 minutes prior in children). Quick and effective for limited numbers of lesions.
• Topical cantharidin (0.7%) — "blister beetle extract" applied in the clinic; not currently TGA-approved in Australia but available through compounding pharmacies. Applied sparingly, covered with tape; blistering occurs in 24–48 hours. Popular in paediatric dermatology.
• Topical potassium hydroxide (KOH) 5–10% solution — applied by the patient twice daily to lesions until mild inflammation occurs. Growing evidence base; useful in children as a home-based alternative. Off-label but increasingly used in Australian practice.
• Immunocompromised patients — consider combined antiretroviral therapy (cART) optimisation for HIV-positive individuals; referral to dermatology for extensive or refractory disease. Topical cidofovir 1–3% cream has been used in case series.

Keloid and hypertrophic scars result from abnormal wound healing characterised by excessive collagen deposition. Although they share pathophysiological features, they differ significantly in clinical behaviour, prognosis, and management.

Distinction Between Keloid and Hypertrophic Scars

Pathophysiology

Both conditions involve an imbalance in the wound healing cascade, with excessive deposition of types I and III collagen, fibronectin, and glycosaminoglycans. In keloids, there is overexpression of transforming growth factor-beta (TGF-β), connective tissue growth factor (CTGF), and plasminogen activator inhibitor-1 (PAI-1), leading to sustained fibroblast proliferation and resistance to apoptosis. The keloid fibroblast behaves in a tumour-like fashion, invading surrounding normal dermis.

Prevention

• Silicone gel sheeting or silicone gel (e.g. Strataderm®, Dermatix®) — first-line prevention and treatment. Applied for 12–24 hours daily for 2–6 months. Mechanism: occlusion, hydration, and reduction of TGF-β. Evidence supports efficacy in both prevention and treatment.
• Minimise tension on wounds — careful incision planning along relaxed skin tension lines (Langer's lines), meticulous wound closure, use of deep absorbable sutures to distribute tension.
• Pressure garments / earrings — continuous pressure (≥ 15–25 mmHg) for 6–12 months post-surgery, particularly for earlobe keloids after piercing.
• Patients at high risk (prior keloid, family history, Fitzpatrick III–VI) should be counselled before elective procedures, ear piercing, or cosmetic surgery.

Treatment of Established Keloids

Multimodal therapy combining two or more modalities yields the best outcomes. Monotherapy has high recurrence rates.

Additional Treatment Modalities

• Surgical excision with adjuvant therapy — excision alone has recurrence rates of 45–100%. Must be combined with adjuvant intralesional corticosteroids (immediately post-excision and serially), ± post-operative radiotherapy, ± silicone sheeting.
• Post-operative radiotherapy — superficial radiotherapy (e.g. orthovoltage or electron beam, 2–3 fractions of 4–6 Gy starting within 24–48 hours of excision) reduces recurrence to 10–20%. Referral to radiation oncology required. Generally reserved for recurrent or refractory keloids.
• Cryotherapy (intralesional) — liquid nitrogen injected directly into the keloid (cryoneedle technique). Effective for smaller lesions. May cause hypopigmentation — caution in Fitzpatrick IV–VI.
• Laser therapy — pulsed-dye laser (PDL, 585/595 nm) can reduce erythema, pruritus, and height. Often used as adjuvant. Fractional CO₂ laser may improve texture. Available in specialist dermatology settings.
• Botulinum toxin A (intralesional) — emerging evidence suggests benefit in reducing keloid size and symptoms by reducing mechanical tension on fibroblasts. Dose: 2.5–5 U/cm² of keloid, every 3 months. Not yet standard of care.
• Verapamil (intralesional) — 2.5 mg/mL, inhibits collagen synthesis. May be used as adjuvant or in combination. Limited evidence base.

Treatment of Hypertrophic Scars

• First-line: Silicone gel sheeting or silicone gel applied daily for 2–6 months.
• Intralesional triamcinolone — 10–20 mg/mL for thicker, symptomatic hypertrophic scars.
• Pressure therapy — particularly for burns-related hypertrophic scars.
• Observation — many hypertrophic scars improve spontaneously within 12–18 months.

Most common lumps and bumps can be diagnosed clinically. Investigations are reserved for uncertain diagnoses, suspected malignancy, or pre-operative planning.

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