Inspection as a Clinical Skill

📋 Key Information Summary

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Systematic inspection is the first and most fundamental clinical examination skill — it begins the moment the patient enters the consultation room and requires no physical contact.
Diagnostic facies are recognisable facial appearances that point toward specific systemic diagnoses (e.g., moon face in Cushing's syndrome, mitral facies in mitral stenosis, myxoedema facies in hypothyroidism).
Finger clubbing is assessed using Schamroth's window test and classified into five grades; it demands investigation for pulmonary (lung cancer, bronchiectasis, mesothelioma), cardiac (cyanotic congenital heart disease, infective endocarditis), gastrointestinal (inflammatory bowel disease, hepatic cirrhosis), and thyroid causes.
Skin pigmentation changes include generalised hyperpigmentation (Addison's disease, haemochromatosis), localised patterns (acanthosis nigricans signalling insulin resistance), jaundice (hepatobiliary or haemolytic disease), cyanosis, and pallor.
Rashes — characterise distribution, morphology, and evolution; dermatomyositis (heliotrope rash, Gottron's papules), erythema nodosum, and drug eruptions each carry distinct diagnostic significance.
Naevi and melanoma — apply the ABCDE criteria (Asymmetry, Border irregularity, Colour variation, Diameter >6 mm, Evolution) when inspecting pigmented lesions; Australia has the highest melanoma incidence globally.
Tongue inspection reveals glossitis (B12/iron deficiency), strawberry tongue (scarlet fever, Kawasaki disease), leukoplakia (pre-malignant), and geographic tongue (benign migratory glossitis).
Always inspect both hands simultaneously — compare symmetry, colour, nail morphology, and joint swelling side by side.
Lighting matters: use natural daylight where possible; a pen-torch and dermatoscope aid assessment of pigmented lesions and mucosal surfaces.
Aboriginal and Torres Strait Islander patients may present with different pigmentation baselines — skin findings should be interpreted in context of the patient's baseline complexion and cultural considerations for exposure-based examination.
Document inspection findings precisely; photographic documentation with patient consent supports longitudinal monitoring and medico-legal records.
Inspection findings should always be integrated with history and other examination components — no single sign is pathognomonic in isolation.

Introduction & Australian Context

Inspection is the first and most elementary of the four traditional clinical examination techniques — inspection, palpation, percussion, and auscultation. Unlike the other three, inspection requires no physical contact with the patient and begins the moment the patient enters the consulting room. It is a skill honed through deliberate practice, pattern recognition, and an understanding of the diseases that produce visible external signs.

In Australian general practice, where consultations average 15–18 minutes, the ability to rapidly identify diagnostic clues through inspection is particularly valuable. The Australian Institute of Health and Welfare (AIHW) reports that skin cancers account for the most commonly diagnosed cancers in Australia, with over 1,600 melanoma-related deaths per year, making the inspection of pigmented lesions a critical skill for every Australian GP. Similarly, chronic respiratory diseases (COPD, bronchiectasis, cystic fibrosis) and inflammatory bowel disease are prevalent in the Australian population and may first be suspected through inspection findings such as finger clubbing.

This article provides a systematic framework for clinical inspection, covering diagnostic facies, finger clubbing, skin pigmentation changes, and specific clinical signs visible on the skin, naevi, and tongue. Each section includes the clinical significance of the finding, a differential diagnosis, and guidance on further investigation in the Australian primary care context.

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Teaching point: Sir William Osler wrote, "The good physician treats the disease; the great physician treats the patient who has the disease." Nowhere is this more evident than in inspection — where the patient's entire body tells a story before a single question is asked.

Diagnostic Facies

Diagnostic facies are characteristic facial appearances associated with specific systemic diseases. The face is a rich canvas: it reflects endocrine status, cardiac output, nutritional state, genetic syndromes, and chronic illness. Learning to recognise diagnostic facies is a core competency for Australian GPs, who often encounter these presentations before laboratory results are available.

Systematic Approach to Facial Inspection

When inspecting the face, follow a structured sequence:

General impression: Does the patient look well or unwell? Fatigued? Cushingoid? Dysmorphic?
Skin colour and texture: Pallor, jaundice, cyanosis, plethora, dryness, oedema
Eyes: Periorbital oedema, proptosis, xanthelasma, jaundiced sclerae, Kayser-Fleischer rings
Mouth and lips: Angular stomatitis, central cyanosis, leukoplakia, facial rash
Hair distribution: Hirsutism, alopecia, temporal wasting
Facial symmetry: CN VII palsy, Horner's syndrome

Common Diagnostic Facies

Facies	Appearance	Associated Condition	Key Differentials
Mitral facies	Malar flush with circumoral pallor; "dusky" appearance	Mitral stenosis; low cardiac output states	Rosacea, SLE malar rash, carcinoid flush
Moon face	Round, plethoric face; central obesity; dorsocervical fat pad ("buffalo hump")	Cushing's syndrome (endogenous or exogenous)	Iatrogenic corticosteroid use, simple obesity, alcohol excess
Myxoedema facies	Periorbital oedema, puffy face, loss of outer third of eyebrows (Queen Anne's sign), dry/coarse skin, macroglossia	Severe hypothyroidism	Nephrotic syndrome (periorbital oedema), allergic reactions
Acromegalic facies	Coarsened features, prognathism, frontal bossing, enlarged nose and lips, widened tooth spacing	Acromegaly (GH excess, usually pituitary adenoma)	Pachydermoperiostosis, normal ageing (prognathism alone)
Thyrotoxic facies	Lid retraction, lid lag, stare, fine periorbital tremor; warm, moist skin	Graves' disease; hyperthyroidism	Anxiety, sympathomimetic use, progressive external ophthalmoplegia
Hippocratic facies	Hollow cheeks, sunken eyes, temporal wasting, waxy-pale skin, nose sharply defined	Chronic illness, severe dehydration, cachexia, terminal malignancy	Severe malnutrition, chronic infection (e.g., tuberculosis, HIV)
Leonine facies	Thickened, furrowed facial skin with nodular infiltration; loss of eyebrows	Lepromatous leprosy; cutaneous T-cell lymphoma (mycosis fungoides)	Sarcoidosis (lupus pernio), amyloidosis
Elfin facies	Broad forehead, periorbital fullness, short nose with anteverted nares, wide mouth, full lips	Williams syndrome (7q11.23 deletion)	Noonan syndrome, fetal alcohol syndrome
Down syndrome facies	Upslanting palpebral fissures, epicanthic folds, flat nasal bridge, protruding tongue, small ears	Trisomy 21	Other chromosomal abnormalities, hypothyroidism
Carcinoid facies	Episodic deep red/purple flushing, may be triggered by alcohol, stress, or foods	Carcinoid syndrome (serotonin-secreting NET, usually with liver metastases)	Menopausal flushing, mastocytosis, medullary thyroid carcinoma

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Clinical pearl: A new moon face in a patient taking prednisolone for any duration should prompt evaluation for iatrogenic Cushing's syndrome. In Australia, where oral corticosteroid prescribing for COPD exacerbations and inflammatory conditions is common, this is a frequently encountered but under-recognised presentation. Dose reduction, steroid-sparing agents, and endocrine referral should be considered.

Investigation of Diagnostic Facies

Essential Thyroid function tests (TSH, fT4, fT3) MBS Item 66719. Available at all Australian pathology providers. Order for myxoedema or thyrotoxic facies.

Essential Overnight dexamethasone suppression test / 24-hr urinary cortisol For suspected Cushing's syndrome. Initial screen: 1 mg overnight dexamethasone suppression test. MBS Item 66682.

Available IGF-1 (insulin-like growth factor 1) Screening test for acromegaly. If elevated, confirm with oral glucose tolerance test and GH levels. MBS Item 66672.

Referral Pituitary MRI Referral to endocrinologist for acromegaly workup; MRI arranged through specialist. Available at major radiology centres (I-MED, Radiology SA, Qscan).

Available Echocardiography For mitral facies — transthoracic echo to assess mitral valve. MBS Item 55118. Refer to cardiologist or cardiac sonographer.

Available Urinary 5-HIAA / chromogranin A For carcinoid syndrome workup. 24-hour urine collection for 5-HIAA. MBS Item 66700.

Clubbing of Fingers

Digital clubbing is the painless, pathological enlargement of the terminal phalanges with increased convexity of the nail plate. It results from soft-tissue proliferation and increased vascularity of the nail bed, likely mediated by megakaryocyte and platelet-derived growth factors bypassing the pulmonary capillary bed. Clubbing is an important clinical sign that, once confirmed, warrants systematic investigation for underlying disease.

Pathophysiology

The exact mechanism of clubbing remains incompletely understood. The two predominant theories are the megakaryocyte bypass theory (in pulmonary disease, megakaryocytes bypass pulmonary filtration and reach the distal digits, releasing PDGF and VEGF) and the neurohumoral theory (vagal stimulation or circulating vasodilators in hepatobiliary disease). Both may co-exist in different disease contexts.

Assessment and Grading

Grade 1

Fluctuant nail bed

Increased sponginess of the nail bed when pressure is applied; the nail "bounces" on the nail bed.

Early sign — easy to miss

Grade 2

Loss of Lovibond angle

The normal angle between the nail plate and the proximal nail fold exceeds 180° (normally ≤160°).

Classic early sign

Grade 3

Increased AP diameter

Bulbous enlargement of the fingertip; the anteroposterior diameter of the finger at the nail fold exceeds that at the distal interphalangeal joint.

Moderate — obvious on inspection

Grade 4

Drumstick appearance

Gross "drumstick" or "watch-glass" deformity of the digit with marked nail curvature.

Severe — late presentation

Grade 5

Hypertrophic osteoarthropathy

Clubbing with periostitis of the distal long bones; painful, swollen joints (especially wrists and ankles). Radiographic "periosteal reaction."

Severe — specialist investigation required

Schamroth's Window Test

The simplest bedside test for clubbing: place the dorsal surfaces of the distal phalanges of both index fingers together, nail-to-nail, so that the nail plates face each other. Normally, a diamond-shaped window (Schamroth's window) is visible between the nail beds. In clubbing, this window is obliterated or absent.

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Clinical pearl: Schamroth's window test has high specificity for established clubbing (Grades 3–5) but limited sensitivity for early clubbing (Grades 1–2). If clinical suspicion is high but the test is equivocal, compare with old photographs of the patient's hands or ask about ring-fit changes.

Differential Diagnosis and Causes of Clubbing

Category	Causes	Australian Relevance
Pulmonary (most common)	Lung cancer (especially NSCLC), bronchiectasis, cystic fibrosis, mesothelioma, interstitial lung disease, pulmonary fibrosis, empyema, lung abscess	Mesothelioma is a major concern given Australia's history of asbestos exposure (Wittenoom, asbestos cement products). Bronchiectasis is prevalent in Indigenous Australians in tropical Northern Territory.
Cardiac	Cyanotic congenital heart disease, infective endocarditis, atrial myxoma	Rheumatic heart disease (RHD) remains prevalent in Aboriginal and Torres Strait Islander communities, particularly in the Northern Territory and Far North Queensland.
Gastrointestinal / Hepatic	Inflammatory bowel disease (Crohn's > ulcerative colitis), hepatic cirrhosis, coeliac disease, oesophageal carcinoma	IBD prevalence is increasing in Australia (~85,000 affected). Liver disease is a significant cause of morbidity in the general population and disproportionately affects Indigenous Australians.
Endocrine	Thyroid acropachy (Graves' disease — typically with exophthalmos and pretibial myxoedema)	Uncommon; consider when Graves' features are present.
Other / Multisystem	Hereditary (familial) clubbing, secondary hypertrophic osteoarthropathy (paraneoplastic), sarcoidosis, HIV	Hereditary clubbing is a diagnosis of exclusion; always investigate before labelling as idiopathic.

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Red flag — new clubbing in a smoker: New-onset clubbing in a patient aged >40 years with a smoking history must be investigated urgently for lung cancer or mesothelioma. Arrange chest X-ray and refer for CT chest without delay. This is a cancer alarm sign in Australian guidelines (Cancer Council Australia).

Investigation of Clubbing

Essential Chest X-ray (PA and lateral) First-line investigation for all new clubbing. MBS Item 58506. Available at all Australian radiology practices.

Essential Full blood count, ESR/CRP, LFTs, iron studies Screen for infection, inflammation, hepatic disease, and iron deficiency (coeliac disease). MBS Items 65070, 65092, 66552, 66573.

Available CT chest (with contrast) If CXR abnormal or high clinical suspicion despite normal CXR. MBS Item 56300. Arrange via GP referral to radiology.

Available Sputum culture and cytology For suspected bronchiectasis or malignancy. MBS Item 69324.

Available Echocardiography If cardiac cause suspected (new murmur, cyanosis). MBS Item 55118.

Available Faecal calprotectin / colonoscopy referral If GI symptoms present — faecal calprotectin MBS Item 66607; colonoscopy via specialist referral MBS Item 32222.

Specialist Bone scan (radionuclide) / MRI hands For hypertrophic pulmonary osteoarthropathy (Grade 5). Specialist investigation arranged by respiratory physician or oncologist.

Skin Pigmentation Changes

Skin pigmentation changes are among the most visible and clinically significant findings on inspection. In Australia, a multicultural society with wide variation in baseline skin phototypes (Fitzpatrick I–VI), interpretation of pigmentation changes must always be made in the context of the patient's baseline complexion. Skin findings that are subtle in darker-skinned patients may be dramatic in fair-skinned individuals, and vice versa.

Generalised Hyperpigmentation

Generalised darkening of the skin beyond the patient's baseline suggests systemic disease. The two most important causes in Australian practice are Addison's disease (primary adrenal insufficiency) and haemochromatosis.

Condition	Pigmentation Pattern	Other Inspection Clues	Investigation
Addison's disease	Generalised bronze-brown darkening; accentuated in palmar creases, buccal mucosa, genital skin, pressure points, and recent scars	Vitiligo (autoimmune), postural hypotension, loss of axillary hair	Morning cortisol, short Synacthen test, anti-21-hydroxylase antibodies, ACTH level
Haemochromatosis	Slate-grey or bronze ("bronze diabetes") generalised pigmentation	Hepatomegaly, spider naevi, arthropathy (MCP joints), loss of body hair	Iron studies (ferritin, transferrin saturation), HFE genotyping (C282Y/H63D)
Drug-induced	Variable — amiodarone (blue-grey), minocycline (blue-grey, especially shins), hydroxychlorocretion (blue-grey), zidovudine (nail and mucosal)	Medication history is key; temporal correlation with drug initiation	Review medication list; consider drug levels if applicable
Hyperthyroidism	Diffuse pigmentation (increased melanocyte-stimulating hormone activity)	Lid retraction, tremor, weight loss, goitre	TSH, fT4, fT3, thyroid antibodies
Ectopic ACTH (Cushing's)	Pronounced hyperpigmentation (very high ACTH levels), often dramatic	Proximal myopathy, thin skin, easy bruising, hypertension	Urinary cortisol, dexamethasone suppression test, CT chest/abdomen

Localised Hyperpigmentation and Hypopigmentation

Finding	Appearance	Significance
Acanthosis nigricans	Velvety, hyperpigmented plaques in flexural areas (axillae, neck, groin)	Marker of insulin resistance — strongly associated with type 2 diabetes mellitus, obesity, and metabolic syndrome. Increasingly seen in overweight Australian children and adolescents.
Vitiligo	Well-demarcated, depigmented (white) patches, often symmetrical; may affect mucous membranes	Autoimmune — associated with thyroid disease (Hashimoto's, Graves'), pernicious anaemia, type 1 diabetes, Addison's disease. Screen for these.
Post-inflammatory hyperpigmentation	Darkening at sites of previous inflammation, injury, or dermatitis	Common in darker skin types; resolves over months but may be permanent. More noticeable and distressing in patients with Fitzpatrick IV–VI.
Jaundice	Yellow discolouration of sclerae (earliest sign), skin, and mucous membranes	Hepatobiliary obstruction, hepatitis, haemolysis. Bilirubin >30 μmol/L usually required for clinical detection. Scleral jaundice is best inspected in natural daylight.
Cyanosis	Central: blue discolouration of tongue and lips (PaO₂ <60 mmHg, SaO₂ <85%). Peripheral: blue hands and feet (cold exposure, low output states)	Central cyanosis: respiratory failure, right-to-left cardiac shunt. Peripheral cyanosis: Raynaud's, heart failure, sepsis. Pulse oximetry is a complementary but not replacement tool — it may miss dyshemoglobinaemias (carboxyhaemoglobin, methaemoglobin).
Pallor	Palmar creases (normally pink; pallor = haemoglobin <70–80 g/L), conjunctival pallor, nail bed pallor	Anaemia — iron deficiency (most common in Australia), chronic disease, haemolysis, bone marrow failure. Also seen in shock.
Erythema ab igne	Reticulated, erythematous to brown pigmentation in a distribution corresponding to heat exposure (e.g., laptop on thighs, hot water bottle on abdomen)	Historically from open fires; now commonly seen with laptop computers and heating pads. May indicate chronic pain (the patient uses heat for analgesia).

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Haemochromatosis screening: Australia has one of the highest prevalence rates of hereditary haemochromatosis in the world (1 in 200 of European-descent Australians carry the homozygous C282Y mutation). Iron studies (serum ferritin and transferrin saturation) are recommended when inspecting for bronze skin pigmentation, especially in patients of Celtic or Northern European descent presenting with unexplained liver disease, diabetes, or arthropathy.

Investigations for Pigmentation Changes

Essential Iron studies (ferritin, transferrin saturation, serum iron) MBS Item 66573. Screen for haemochromatosis in any unexplained pigmentation with hepatomegaly or arthropathy.

Essential Thyroid function tests (TSH, fT4) MBS Item 66719. For any pigmentation change with hyper- or hypothyroid features; also screen in vitiligo.

Essential Short Synacthen test For suspected Addison's disease. Baseline cortisol at 0 min, tetracosactide (Synacthen) 250 μg IV/IM, cortisol at 30 and 60 min. MBS Item 66682.

Available HFE genotyping If iron studies abnormal — confirm hereditary haemochromatosis. C282Y and H63D mutation analysis. MBS Item 66621.

Available Liver function tests, hepatitis serology, autoantibodies For jaundice and hepatomegaly workup. MBS Items 66552, 69274.

Available HbA1c / fasting glucose / HOMA-IR For acanthosis nigricans — screen for insulin resistance and type 2 diabetes. MBS Item 66550 (HbA1c).

Specific Clinical Signs — Rashes, Naevi, and Tongue

Beyond the face and hands, inspection of the skin, naevi, and tongue yields a wealth of diagnostic information. This section addresses the most clinically significant findings that Australian GPs should be confident in recognising.

Clinically Important Rashes

When inspecting a rash, systematically describe the distribution (localised vs. generalised, symmetrical vs. asymmetrical, sun-exposed vs. covered), morphology (macular, papular, vesicular, pustular, plaque), colour, and evolution (acute, chronic, changing).

Rash / Sign	Description	Clinical Significance	Action
Heliotrope rash	Violaceous (purple) discolouration of the upper eyelids, often with periorbital oedema	Dermatomyositis — autoimmune inflammatory myopathy; also consider paraneoplastic association (underlying malignancy in adults)	Urgent referral to rheumatologist; CK, anti-Jo-1, anti-Mi-2 antibodies; age-appropriate cancer screening
Gottron's papules	Violaceous papules overlying the dorsum of MCP and IP joints (spare the knuckles themselves)	Dermatomyositis (pathognomonic sign)	As above — rheumatology referral
Erythema nodosum	Tender, red, subcutaneous nodules on the shins (pretibial); lesions do NOT ulcerate	Reactive: streptococcal infection, sarcoidosis, IBD, drug reaction (OCP, sulphonamides, penicillin), pregnancy, TB	Chest X-ray (sarcoidosis, lymphoma), ASOT, pregnancy test, FBC, ESR; treat underlying cause
Livedo reticularis	Reticulated (net-like), dusky violaceous pattern on the skin, usually on the limbs	Physiological (cold exposure — benign) OR pathological: antiphospholipid syndrome, vasculitis (polyarteritis nodosa), cholesterol embolisation, SLE	If persistent or associated with systemic symptoms: ANA, anti-dsDNA, antiphospholipid antibodies, complement levels
Malar (butterfly) rash	Erythematous rash over both cheeks and nasal bridge, sparing the nasolabial folds; may be flat or raised	Systemic lupus erythematosus (SLE) — but also seen in rosacea, dermatomyositis, seborrhoeic dermatitis	ANA, anti-dsDNA, complement C3/C4, FBC, urinalysis; rheumatology referral if confirmed
Psoriasis plaques	Well-demarcated, erythematous plaques with silvery-white scale; extensor surfaces (elbows, knees), scalp, natal cleft	Chronic autoimmune disease; associated with psoriatic arthritis, metabolic syndrome, cardiovascular risk; nail changes (pitting, oil-drop sign, onycholysis)	PASI score for severity assessment; screen for psoriatic arthritis (nail changes, dactylitis, enthesitis); dermatology referral for moderate-severe disease
Purpura	Non-blanching (diascopy-negative) red-purple spots >2 mm; palpable purpura suggests vasculitis	Thrombocytopenia, coagulopathy, vasculitis (IgA — Henoch-Schönlein purpura), meningococcaemia, DIC, senile purpura (benign)	Palpable purpura is an emergency — FBC, coagulation, blood cultures (if systemically unwell); vasculitis workup (ANCA, complement, IgA); dermatology/immunology referral
Nikolsky's sign	Lateral pressure on normal-appearing skin produces blistering / epidermal separation	Staphylococcal scalded skin syndrome (SSSS), toxic epidermal necrolysis (TEN), pemphigus vulgaris	Medical emergency — dermatology and burns unit referral; stop offending drug (if TEN); IVIG, supportive care

Naevi and Melanoma — The ABCDE Criteria

Australia has the highest incidence of melanoma in the world — approximately 17,000 new cases per year (Cancer Council Australia, 2024). Inspection of pigmented lesions is therefore a core skill for every Australian clinician. The ABCDE criteria provide a structured approach:

A

Asymmetry

One half of the lesion does not match the other half in shape, colour, or structure.

B

Border irregularity

Edges are ragged, notched, scalloped, or poorly defined.

C

Colour variation

Multiple shades of brown, black, red, white, or blue within one lesion.

D

Diameter >6 mm

Melanomas are often larger than 6 mm at diagnosis (though small melanomas do occur).

E

Evolution

Any change in size, shape, colour, elevation, or new symptoms (itching, bleeding) over time.

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Ugly duckling sign: In addition to ABCDE, look for the "ugly duckling" — a naevus that looks different from the patient's other moles. Most melanomas arise de novo rather than from pre-existing naevi. Any lesion meeting ABCDE criteria or that stands out from the patient's other naevi warrants excision biopsy or urgent dermatology referral.

Naevi Requiring Excision or Dermoscopy Referral

Any lesion meeting ≥1 ABCDE criterion
The "ugly duckling" naevus
New pigmented lesion in a patient aged >40 years (melanoma incidence increases with age)
Lesion with regression structures (white scar-like areas within a pigmented lesion)
Amelanotic melanoma: flesh-coloured, erythematous, or pink — easily missed; may be confused with basal cell carcinoma or dermatofibroma

Tongue Inspection

The tongue is a "mirror of the body" — inspection reveals systemic disease, nutritional deficiency, infection, and malignancy. Ask the patient to protrude the tongue and inspect the dorsum, lateral borders, ventral surface, and undersurface systematically.

Tongue Finding	Description	Significance
Beefy red / smooth tongue (glossitis)	Erythematous, smooth, painful tongue with loss of papillae	Vitamin B12 deficiency (pernicious anaemia, coeliac disease), iron deficiency, folate deficiency. Also seen in Sjögren's syndrome.
Strawberry tongue	Bright red, swollen tongue with prominent papillae	Scarlet fever (Group A Streptococcus — initially white strawberry, then red), Kawasaki disease (especially in children <5 years), toxic shock syndrome
Geographic tongue (benign migratory glossitis)	Irregular, erythematous patches with raised white borders that migrate over days to weeks	Benign; affects 1–3% of the population. May be associated with psoriasis and atopy. No treatment required (reassurance).
Leukoplakia	White, non-scrapable patches on the oral mucosa, especially lateral tongue and floor of mouth	Potentially pre-malignant — 5–17% risk of squamous cell carcinoma over 10 years. Non-homogeneous (speckled/verrucous) leukoplakia carries higher malignant risk than homogeneous. Risk factors: smoking, alcohol, betel nut chewing (relevant in some migrant communities in Australia).
Oral hairy leukoplakia	White, corrugated, vertical streaks on the lateral tongue that cannot be scraped off	Epstein-Barr virus (EBV) — seen in HIV/AIDS (CD4 <200) and other immunocompromised states. Pathognomonic for severe immunosuppression.
Aphthous ulcers	Round/oval, shallow, painful ulcers with a grey-white base and erythematous halo; non-scarring	Recurrent aphthous stomatitis (RAS) — idiopathic (most common), Behçet's disease, coeliac disease, iron/B12/folate deficiency, reactive arthritis, HIV. Persistent ulcers >3 weeks require biopsy to exclude SCC.
Macroglossia	Enlarged tongue; may show scalloping from teeth marks on lateral borders	Hypothyroidism, acromegaly, amyloidosis, Down syndrome, mucopolysaccharidoses, Beckwith-Wiedemann syndrome
Cyanotic tongue	Blue-purple discolouration of the tongue and lips	Central cyanosis — respiratory failure (COPD exacerbation, pneumonia, PE), right-to-left cardiac shunt. Requires urgent pulse oximetry and ABG.

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Oral leukoplakia — do not ignore: Any non-scrapable white patch on the tongue or oral mucosa persisting for >2 weeks should be referred for biopsy. In Australia, oral squamous cell carcinoma accounts for approximately 2,500 new cases annually, and late detection is associated with significantly worse outcomes. Patients who smoke, consume alcohol excessively, or chew betel nut are at highest risk.

Specific Skin Lesions — Quick Recognition

Brown-Vialetto-Van Laere

Not applicable

Rare — bulbar palsy + sensorineural deafness; riboflavin transporter defect

Basal cell carcinoma (BCC)

Pearly, translucent papule with telangiectasia; rolled border; central ulceration

Most common cancer in Australia; most frequent on sun-exposed sites (face, ears, neck). Excision is primary treatment; non-surgical options (imiquimod, 5-FU, PDT) for superficial BCCs.

Squamous cell carcinoma (SCC)

Firm, erythematous, keratotic nodule or plaque; may ulcerate; tender

Second most common skin cancer in Australia. Higher metastatic potential than BCC. Actinic keratoses are precursors. Refer for excision / Mohs surgery.

Dermatofibroma

Firm, small, dome-shaped, skin-coloured to brown papule; dimple sign positive

Benign; no treatment required unless symptomatic. Common on lower limbs.

Pyogenic granuloma

Rapidly growing, friable, red-purple pedunculated lesion; bleeds easily

Benign vascular proliferation; often after minor trauma. Shave excision and curettage; send histology to exclude amelanotic melanoma.

Cherry angioma

Bright red, dome-shaped, 1–5 mm papules; blanch on pressure

Very common benign vascular lesion; increases with age. No treatment needed.

Seborrhoeic keratosis

Waxy, "stuck-on," brown to black papule/plaque; "horn pearls" on dermoscopy

Benign; very common in older Australians. Leser-Trélat sign (sudden eruption of multiple seborrhoeic keratoses) may indicate GI malignancy.

Clinical Approach & Integration

Inspection does not occur in isolation — it must be integrated into the broader clinical assessment. The following framework guides the Australian GP in incorporating inspection findings into clinical reasoning.

The Inspection Framework for Australian General Practice

1

Observe before asking

From the moment the patient enters, note their gait, posture, respiratory effort, body habitus, and general demeanour. This "clinical glance" often yields more than formal questioning.

2

Expose adequately — with consent

Explain what you need to see and why. Expose the area fully; inspect the entire skin surface where relevant (rashes, naevi). Respect patient dignity and cultural sensitivities — particularly important in Aboriginal and Torres Strait Islander health contexts.

3

Use appropriate lighting

Natural daylight is ideal for assessing jaundice, pallor, and cyanosis. A pen-torch for oropharyngeal examination; a dermatoscope for pigmented lesions. Wood's lamp for tinea capitis and erythrasma.

4

Compare sides

Always compare the affected side with the unaffected side (e.g., hands, arms, legs). Bilateral findings suggest systemic disease; unilateral findings suggest local pathology or neurological disease.

5

Document precisely

Record findings using standard dermatological terminology. Photographs (with consent) are invaluable for monitoring change and for referral letters. Use secure clinical photography apps (e.g., Clinical Photography App, Skin Analytics).

6

Integrate and act

Combine inspection findings with the history to formulate a differential diagnosis. Order appropriate investigations. Refer when criteria are met (e.g., suspicious naevi → dermatology; new clubbing in a smoker → respiratory/oncology).

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Training tip: The RACGP Clinical Competency Framework emphasises inspection as a foundational skill assessed in the Clinical Competency Examination (CCE). Examiners expect candidates to describe inspection findings using precise anatomical and dermatological terminology before proceeding to palpation or investigation.

Special Populations

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Pregnancy

Chloasma (melasma gravidarum): Symmetrical hyperpigmentation of the face, particularly forehead, cheeks, and upper lip. Affects up to 75% of pregnant women; more pronounced in darker skin types. Usually resolves postpartum; sun protection recommended.
Linea nigra: Midline hyperpigmentation from symphysis pubis to umbilicus (and sometimes xiphisternum). Normal pregnancy finding.
Spider naevi and palmar erythema: Increased in pregnancy due to elevated oestrogen levels. 1–2 spider naevi are normal; multiple (≥5) should prompt LFT assessment.
Pruritic urticarial papules and plaques of pregnancy (PUPPP): Erythematous, urticarial papules beginning on the abdomen within striae; spares the periumbilical area. Benign; deliver near term if severe.
Pemphigoid gestationis: Urticarial papules progressing to tense blisters; periumbilical onset. Requires dermatology involvement; associated with fetal growth restriction.

Drug caution: Avoid retinoids (isotretinoin, tretinoin) for skin conditions in pregnancy — teratogenic (Category X).

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Paediatrics

Congenital naevi: Present at birth; giant congenital naevi (>20 cm) carry 5–10% lifetime melanoma risk and require specialist monitoring (dermatology/plastic surgery).
Infantile haemangioma: Common; appear in first weeks of life, proliferate over 6–12 months, then involute. Propranolol (PBS Authority Required) is first-line for problematic haemangiomas (e.g., airway, periorbital, ulcerated).
Strawberry tongue and Kawasaki disease: In children <5 years, a strawberry tongue with prolonged fever (≥5 days), bilateral non-exudative conjunctivitis, polymorphous rash, extremity changes, and cervical lymphadenopathy warrants urgent investigation and IV immunoglobulin to prevent coronary artery aneurysms.
Down syndrome facies: Should be recognised at birth or early infancy — prompt karyotyping and early intervention (speech, occupational therapy) improve outcomes.
Childhood vitiligo: Common; screen for thyroid disease and type 1 diabetes (autoimmune association). Refer to paediatric dermatology for topical therapy if psychologically distressing.

Facial inspection in neonates should include assessment of dysmorphic features — many genetic syndromes (Williams, Noonan, Down, fetal alcohol spectrum disorder) have characteristic facies identifiable at birth.

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Elderly

Actinic keratoses: Extremely common in elderly Australians; rough, scaly, erythematous patches on sun-damaged skin. 5–10% progress to SCC over 10 years. Treat with cryotherapy (liquid nitrogen), 5-FU (Efudix® — PBS General Benefit), or imiquimod (Aldara® — PBS Restricted Benefit for superficial BCC).
Skin cancers: Lifelong cumulative UV exposure in Australia means the elderly carry the highest burden of BCC, SCC, and melanoma. Inspect thoroughly including scalp, behind ears, and back.
Senile purpura: Purple patches on forearms and dorsum of hands due to dermal atrophy and loss of perivascular connective tissue. Benign but may indicate anticoagulant/antiplatelet use (consider bleeding risk).
Temporal arteritis (giant cell arteritis): Inspection may reveal a prominent, thickened, non-compressible temporal artery. Associated with new-onset headache, jaw claudication, and visual disturbance. Urgent ESR/CRP and referral for temporal artery biopsy.

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Renal Impairment

Uraemic frost: Rare in modern dialysis era — urea crystallisation on the skin in severe untreated uraemia. A sign of end-stage renal disease.
Sallow, yellow-brown complexion: Caused by urochromogen deposition in chronic kidney disease (CKD). Distinguish from jaundice by examining sclerae (sclerae are spared in uraemic pigmentation).
Calciphylaxis: Painful, livedo reticularis-like patches progressing to necrotic ulcers, typically on the lower limbs and trunk. Seen in CKD 5/dialysis patients. High mortality (60–80%). Urgent nephrology and wound care referral.
AV fistula inspection: In haemodialysis patients, inspect the fistula for signs of infection (erythema, warmth, purulent discharge), aneurysmal dilatation, and steal syndrome (ischaemic changes to the hand).

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Immunocompromised

Kaposi's sarcoma: Violaceous (purple) macules, papules, or plaques; in HIV patients with CD4 <200, typically on the face, trunk, and limbs. HHV-8 associated.
Oral hairy leukoplakia: White, non-scrapable, vertical corrugated lesions on the lateral tongue. EBV reactivation in severe immunosuppression (HIV, transplant).
Herpes zoster (shingles): Vesicular rash in a dermatomal distribution. In immunocompromised patients, may be multidermatomal or disseminated. Aciclovir (IV for severe disease) within 72 hours of rash onset.
Post-transplant lymphoproliferative disorder (PTLD): May present with cutaneous nodules in solid organ transplant recipients. EBV-driven; requires biopsy and oncology referral.

Patients on biologic immunosuppressants (e.g., TNF-α inhibitors for rheumatoid arthritis, IBD) require regular skin checks — increased risk of NMSC (non-melanoma skin cancer) and lymphoma. Annual skin examination by GP or dermatologist recommended.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Inspection is a culturally significant clinical skill in the context of Aboriginal and Torres Strait Islander health. Several key considerations apply:

Skin pigmentation baseline

Aboriginal and Torres Strait Islander Australians may have Fitzpatrick type IV–VI skin. Subtle pigmentation changes — pallor, jaundice, cyanosis, and early hyperpigmentation — are more difficult to detect and require careful inspection in good natural light. Scleral jaundice and palmar crease pallor remain reliable signs regardless of baseline skin colour.

Rheumatic heart disease (RHD)

RHD disproportionately affects Aboriginal and Torres Strait Islander children and young adults, particularly in the Northern Territory, Far North Queensland, and Western Australia. Mitral facies (malar flush with circumoral pallor) may be the presenting sign in a young person. The RHDAustralia (www.rhdaustralia.org.au) clinical guidelines recommend echocardiographic screening for all Aboriginal and Torres Strait Islander children aged 5–14 years in endemic regions.

Trachoma and eye signs

Australia is the only developed country where trachoma (Chlamydia trachomatis) remains endemic, occurring almost exclusively in remote Aboriginal communities. Inspection of the tarsal conjunctiva for follicles and scarring is a public health imperative. The SAFE strategy (Surgery, Antibiotics, Facial cleanliness, Environmental improvement) underpins the Australian Government's trachoma elimination programme.

Skin infections

Scabies, impetigo (bullous and non-bullous), and tinea are highly prevalent in remote Aboriginal communities. Group A Streptococcal (GAS) skin infections contribute to acute rheumatic fever and post-streptococcal glomerulonephritis. Inspection of skin should be performed systematically in children presenting to remote clinics. The Healthy Skin Programme in the Northern Territory recommends community-wide treatment approaches.

Bronchiectasis and clubbing

Non-cystic fibrosis bronchiectasis is significantly more common in Aboriginal and Torres Strait Islander Australians (estimated prevalence 1,500/100,000 in the Top End of the Northern Territory) compared with non-Indigenous Australians (~67/100,000). Finger clubbing in a young Indigenous Australian should prompt chest X-ray and referral to a respiratory physician. Underlying causes include recurrent childhood pneumonia, pertussis, and chronic suppurative lung disease.

Skin cancer awareness

Although melanoma incidence is lower in Aboriginal and Torres Strait Islander Australians than in non-Indigenous Australians, late presentation and higher mortality rates are well documented. BCC and SCC still occur, particularly in lighter-skinned Indigenous Australians. Health promotion messages about skin inspection should be culturally appropriate and delivered through Aboriginal Community Controlled Health Organisations (ACCHOs).

Cultural considerations for examination

Some Aboriginal and Torres Strait Islander patients may have cultural protocols around physical examination. Always explain why inspection is needed. Same-gender health practitioners may be preferred for skin examination, particularly in remote communities. The use of photographs should be discussed with the patient and, where applicable, with the local Aboriginal Health Worker (AHW) or community elder. Aboriginal and Torres Strait Islander Health Practitioners can assist with culturally safe examination and health education.

Screening and chronic disease

The AIHW reports that Aboriginal and Torres Strait Islander Australians have 2–3 times the burden of chronic disease compared with non-Indigenous Australians. Inspection for signs of chronic disease — peripheral oedema (heart failure), jaundice (liver disease), xanthelasma (hyperlipidaemia), diabetic skin changes (acanthosis nigricans, diabetic dermopathy) — should be incorporated into routine health assessments (MBS Item 715).

📚 References

1. Talley NJ, O'Connor S. Clinical Examination: A Systematic Guide to Physical Diagnosis. 8th ed. Chatswood: Elsevier Australia; 2018.
2. Bickley LS, Szilagyi PG, Hoffman RM. Bates' Guide to Physical Examination and History Taking. 13th ed. Philadelphia: Wolters Kluwer; 2021.
3. McGee SR. Evidence-Based Physical Diagnosis. 4th ed. Philadelphia: Elsevier; 2018.
4. Sarkar M, Mahesh DM, Madabhavi I. Digital clubbing. Lung India. 2012;29(4):354–362. doi:10.4103/0970-2113.102824.
5. Myerowitz RL, et al. The pathogenesis of clubbing. N Engl J Med. 1979;301(5):254. doi:10.1056/NEJM197908023010515.
6. Cancer Council Australia. Skin Cancer Statistics and Issues. Sydney: Cancer Council Australia; 2024. Available at: https://www.cancer.org.au/cancer-information/causes-and-prevention/sun-safety/statistics-and-issues.
7. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework. Canberra: AIHW; 2023. Cat. no. IHW 223.
8. RHDAustralia (ARF/RHD writing group). The 2020 Australian Guideline for Prevention, Diagnosis and Management of Acute Rheumatic Fever and Rheumatic Heart Disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
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10. Australasian College of Dermatologists (ACD). Position Statement: Management of Melanoma. Sydney: ACD; 2023. Available at: https://www.dermcoll.edu.au.
11. Chang AY, Hoy D, et al. The Global Burden of Disease Study 2013: bronchiectasis in Indigenous Australians. Lancet Respir Med. 2017;5(2):e7. doi:10.1016/S2213-2600(17)30019-8.
12. Bowen AC, Mahé A, Hay RJ, et al. The global epidemiology of impetigo: a systematic review of the population prevalence of impetigo and pyoderma. PLoS One. 2015;10(8):e0136789. doi:10.1371/journal.pone.0136789.
13. Hoy WE, White AV, Dowling A, et al. Post-streptococcal glomerulonephritis is a strong risk factor for chronic kidney disease in later life. Kidney Int. 2012;81(10):1026–1032. doi:10.1038/ki.2011.478.
14. National Health and Medical Research Council (NHMRC). National Statement on Ethical Conduct in Human Research. Canberra: NHMRC; 2018 (updated 2023).
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