📋 Key Information Summary
- Pruritus is the most common dermatological complaint in Australian general practice, affecting up to 15% of adults at any given time.
- Classify as localised vs generalised — localised pruritus suggests primary dermatological or neuropathic causes; generalised pruritus without primary skin lesions warrants systemic workup.
- Generalised pruritus without rash must prompt investigation for hepatic cholestasis, chronic kidney disease (CKD), thyroid disease, iron deficiency, haematological malignancy, and medication reactions.
- Scabies (Sarcoptes scabiei var. hominis) is a notifiable condition in several Australian states; treat with permethrin 5% cream (first-line) or oral ivermectin, and treat all close contacts simultaneously.
- Dermatitis herpetiformis is the cutaneous manifestation of coeliac disease — diagnosis requires skin biopsy with direct immunofluorescence (IgA at dermal papillae); dapsone provides rapid symptom relief and a strict gluten-free diet addresses the underlying enteropathy.
- Lichen planus presents with the "5 Ps": pruritic, planar, polygonal, purple papules/plaques; Wickham's striae are pathognomonic. Topical potent corticosteroids are first-line.
- Pruritus ani and pruritus vulvae require exclusion of infections (candidiasis, pinworm, STIs), dermatoses (lichen sclerosus, lichen simplex), and irritant/contact causes before diagnosis of idiopathic disease.
- First-line management of any pruritus includes emollient therapy (fragrance-free, soap-free washes), topical corticosteroids for inflammatory dermatoses, and addressing reversible systemic causes.
- Sedating antihistamines (promethazine, doxylamine) are useful for nocturnal pruritus; non-sedating antihistamines (cetirizine, loratadine) have limited efficacy in non-histamine-mediated pruritus.
- Uraemic pruritus affects up to 40% of patients on dialysis in Australia; gabapentin or pregabalin are evidence-based options. Optimise dialysis adequacy and phosphate control.
- Cholestatic pruritus responds to cholestyramine (first-line), rifampicin (second-line), or naltrexone; always investigate for underlying obstruction or liver disease.
- Aboriginal and Torres Strait Islander Australians have disproportionately high rates of scabies, skin infections, and crusted scabies — community-wide treatment programmes and culturally safe care are essential.
- Red flags requiring urgent referral: unexplained generalised pruritus with weight loss, night sweats, lymphadenopathy, or hepatosplenomegaly (exclude lymphoproliferative disorders).
Introduction & Australian Epidemiology
Pruritus — the sensation that provokes the desire to scratch — is the single most common presenting symptom in dermatology and a frequent complaint in Australian primary care. It may arise from cutaneous, systemic, neuropathic, or psychogenic origins and can significantly impair quality of life, sleep, and mental health.
In Australia, pruritus accounts for an estimated 5–10% of all general practice dermatology consultations. The burden falls disproportionately on certain populations: atopic dermatitis affects approximately 20% of Australian children, scabies prevalence in remote Aboriginal and Torres Strait Islander communities ranges from 20–70%, and chronic kidney disease (CKD)-associated pruritus affects 40–60% of patients receiving maintenance haemodialysis.
A systematic approach to pruritus begins with distinguishing localised from generalised disease and identifying the presence or absence of primary skin lesions. This classification guides the differential diagnosis and subsequent investigation pathway. In approximately 10–50% of cases of generalised pruritus without primary skin lesions, an underlying systemic cause will be identified.
This guideline provides an evidence-based framework for the diagnosis and management of pruritus in Australian clinical practice, covering the major diagnostic categories and their management within the Australian healthcare context.
Localised vs Generalised Pruritus
The initial clinical approach to pruritus requires classification by distribution (localised vs generalised) and by the presence or absence of primary skin lesions. This binary framework is the foundation of diagnostic reasoning.
Localised Pruritus
Localised pruritus is confined to a specific anatomical region and most commonly reflects primary dermatological disease or localised neuropathic/psychogenic itch.
| Site | Common Causes | Key Clinical Features |
|---|---|---|
| Scalp | Seborrhoeic dermatitis, psoriasis, head lice, contact dermatitis | Scaling, erythema; nits on hair shafts (pediculosis capitis) |
| Eyelids | Allergic contact dermatitis (cosmetics, nail polish), atopic dermatitis | Oedema, erythema, lichenification of eyelid skin |
| Hands | Contact dermatitis (irritant or allergic), scabies, dyshidrotic eczema, tinea | Vesicles on lateral fingers (dyshidrosis); interdigital burrows (scabies) |
| Groin/Genitalia | Candidiasis, tinea cruris, scabies, lichen sclerosus, pinworm | Erythema with satellite lesions (candida); white atrophic patches (lichen sclerosus) |
| Feet | Tinea pedis, contact dermatitis, dyshidrotic eczema | Interdigital maceration and scaling; vesicles on soles |
| Perianal | Pruritus ani (idiopathic, haemorrhoids, pinworm, candidiasis) | Perianal erythema, excoriation; nocturnal itch (pinworm in children) |
Generalised Pruritus
Generalised pruritus involves widespread or migrating itch and is further classified by the presence or absence of primary skin lesions:
With Primary Skin Lesions
Dermatological Causes
Atopic dermatitis, urticaria, scabies, psoriasis, dermatitis herpetiformis, lichen planus, bullous pemphigoid, drug eruptions. The morphology of the rash guides diagnosis.
Setting: GP / Dermatology
Without Primary Skin Lesions
Systemic / Metabolic Causes
Cholestatic liver disease, CKD, thyroid dysfunction, iron deficiency, haematological malignancy, solid organ malignancy, medication-related. Secondary excoriations and lichenification from chronic scratching may be the only cutaneous finding.
Setting: GP → Internal Medicine / Haematology
Neuropathic / Psychogenic
Notalgia Paraesthetica / Brachioradial Pruritus / Psychogenic
Dermatomal distribution, burning/tingling quality; may not have visible skin changes. Notalgia paraesthetica: interscapular region (T2–T6 dermatome). Brachioradial pruritus: lateral forearm (C5–C6). Consider anxiety, depression, delusional parasitosis (Ekbom syndrome).
Setting: Dermatology / Neurology / Psychiatry
Clinical pearl: Generalised pruritus with excoriations but no primary rash in a patient >40 years old should always be investigated for systemic disease — liver function tests (LFTs), renal function (eGFR, creatinine), thyroid function tests (TFTs), full blood count (FBC), ferritin, and blood glucose. Do not dismiss as "dry skin" without investigation.
Systemic Causes of Generalised Pruritus
When generalised pruritus occurs without primary skin lesions, a systematic evaluation for underlying systemic disease is essential. The following table summarises the key systemic aetiologies, their pathophysiology, and the investigation approach available in Australian practice.
| Category | Condition | Pathophysiology | Key Investigations |
|---|---|---|---|
| Hepatic | Cholestatic liver disease (primary biliary cholangitis, primary sclerosing cholangitis, drug-induced cholestasis, obstructive jaundice) | Accumulation of bile salts and lysophosphatidic acid (LPA); activation of TGR5 receptors on sensory neurons | LFTs (elevated ALP, GGT, bilirubin), hepatitis serology (HBV, HCV), autoimmune markers (AMA for PBC), hepatic ultrasound, MRCP |
| Renal | CKD / End-stage kidney disease (uraemic pruritus) | Immune dysregulation (IL-31 mediated), uraemic toxins, secondary hyperparathyroidism, xerosis, peripheral neuropathy | eGFR, creatinine, urea, calcium, phosphate, PTH; assess dialysis adequacy (Kt/V) |
| Endocrine | Hypothyroidism, hyperthyroidism, diabetes mellitus, hyperparathyroidism | Xerosis from hypothyroidism; peripheral neuropathy (diabetes); mast cell degranulation (thyroid) | TSH, free T4, HbA1c, fasting glucose, calcium, PTH |
| Haematological | Iron deficiency (± anaemia), polycythaemia vera, essential thrombocythaemia, Hodgkin lymphoma, non-Hodgkin lymphoma, mycosis fungoides/Sézary syndrome | Iron deficiency: impaired epidermal barrier function. Haematological malignancy: cytokine release (IL-31, IL-13), histamine release, neuropathic mechanisms | FBC with film, iron studies (ferritin, transferrin saturation, serum iron), ESR, LDH, β2-microglobulin, peripheral blood film; skin biopsy if mycosis fungoides suspected |
| Medication-related | Opioids, ACE inhibitors, hydroxychloroquine, statins, sulfonylureas, amiodarone, allopurinol | Direct histamine release (opioids), cholestasis (various), peripheral neuropathy, drug-induced autoimmune hepatitis | Detailed medication review; temporal correlation with drug initiation; consider dechallenge/rechallenge (supervised) |
| Solid organ malignancy | Hepatocellular carcinoma, pancreatic cancer, lung cancer, renal cell carcinoma | Paraneoplastic cytokine release, cholestasis (pancreatic/biliary tumours), neuropathy | Age-appropriate cancer screening; CT chest/abdomen/pelvis if red flag features; CA 19-9, AFP as indicated |
Red flags — urgent investigation required: Generalised pruritus associated with unexplained weight loss, night sweats, lymphadenopathy, hepatosplenomegaly, or new-onset B symptoms should prompt urgent FBC with film, LDH, ESR, and CT staging. Hodgkin lymphoma-associated pruritus may precede lymphadenopathy by months. Refer to haematology/oncology.
Management of Systemic Pruritus
1
Treat the Underlying Cause
Obstructive jaundice: ERCP/stenting. Iron deficiency: oral or IV iron replacement. Hypothyroidism: levothyroxine. Medication: cease offending agent if safe.
2
General Antipruritic Measures
Emollients (e.g., QV, Cetaphil, Dermeze), soap-free washes, cool environment, cotton clothing, humidifier in winter. Avoid alcohol-based products and excessive bathing.
3
Pharmacotherapy (Cause-Specific)
Cholestatic: cholestyramine → rifampicin → naltrexone. Uraemic: gabapentin/pregabalin, UVB phototherapy. Haematological: treat malignancy. See drug cards below.
4
Neuropathic/Refractory Itch
Gabapentin, pregabalin, amitriptyline, mirtazapine, or paroxetine. Capsaicin 0.025–0.075% cream for localised neuropathic itch (nototalgia paraesthetica, brachioradial pruritus).
Scabies & Dermatitis Herpetiformis
Scabies (Sarcoptes scabiei var. hominis)
Scabies is a highly contagious infestation caused by the mite Sarcoptes scabiei var. hominis. It is transmitted by prolonged skin-to-skin contact and is a significant public health concern in Australia, particularly in remote Aboriginal and Torres Strait Islander communities where prevalence can exceed 50% in children. Scabies is notifiable in the Northern Territory, Western Australia, and Queensland.
Clinical Features
- Classic scabies: Intensely pruritic (worse at night), affecting interdigital web spaces, flexor wrists, axillae, umbilicus, buttocks, genitalia (scrotum in males). Characteristic burrows (short, wavy, grey lines with a tiny papule at one end). Typical infestation burden: 10–15 mites.
- Crusted (Norwegian) scabies: Hyperkeratotic, crusted, psoriasiform plaques — minimal or absent itch. Mite burden: millions. Highly infectious. Associated with immunosuppression (HIV, solid organ transplant, systemic corticosteroids), intellectual disability, and institutional settings.
- Nodular scabies: Persistent pruritic erythematous nodules (5–20 mm) on genitalia, groin, axillae, even after successful treatment.
Diagnosis
Clinical diagnosis is standard. Dermatoscopy (MBS item 10820 for specialist dermatology consultation, or MBS item 10816 for GP where available) may reveal the "delta sign" (triangular mite head) and burrow. Skin scraping with 10% KOH can confirm mites, eggs, or faecal pellets (scybala). Sensitivity of scraping is approximately 50–60%.
Treatment
Permethrin 5% Cream
Lyclear® · Topical pyrethroid
Adult dose
Apply to entire body (neck down), leave for 8–12 hours, wash off. Repeat at Day 7.
Paediatric dose
≥2 months: apply to entire body including face and scalp (avoid eyes/mouth). <2 months: consult paediatric dermatology.
Renal adjustment
None required (topical)
PBS status
✔ PBS General Benefit
Ivermectin
Stromectol® · Oral anthelmintic
Adult dose
200 µg/kg PO as a single dose. Repeat at Day 7–14. Take with fatty food to enhance absorption.
Paediatric dose
≥15 kg body weight: 200 µg/kg PO single dose. Not recommended <15 kg or <2 years.
Renal adjustment
No adjustment required
PBS status
⚠ PBS Authority Required
Benzyl Benzoate 25% Lotion
Benzo-foam® · Topical scabicide
Adult dose
Apply to entire body from neck down after bathing. Leave on 24 hours before washing. Repeat at Day 7.
Paediatric dose
Dilute to 12.5% for children <2 years. Do not apply to face.
Note
Stinging on application — less tolerated than permethrin. Used as second-line or in crusted scabies combination regimens.
PBS status
✔ PBS General Benefit
Critical treatment principles for scabies: (1) Treat ALL household and close contacts simultaneously — even if asymptomatic, as the incubation period is 2–6 weeks. (2) Wash all clothing, bedding, and towels in hot water (>60°C) or seal in a plastic bag for 72 hours. (3) Crusted scabies requires combination therapy: oral ivermectin (200 µg/kg on Days 1, 2, 8, 9, 15) PLUS topical permethrin 5% (daily for 7 days, then twice weekly) PLUS keratolytics (salicylic acid 5–10%). Hospital admission may be required for infection control.
Dermatitis Herpetiformis
Dermatitis herpetiformis (DH) is the cutaneous manifestation of coeliac disease, caused by IgA deposition at the tips of dermal papillae. It presents as intensely pruritic, grouped vesicles and papules on the extensor surfaces (elbows, knees, buttocks, scalp, back). Australian prevalence is estimated at approximately 1 in 10,000, with a strong association with HLA-DQ2/DQ8 haplotypes.
Diagnosis
- Skin biopsy — perilesional biopsy for direct immunofluorescence (DIF) showing granular IgA deposits at the dermal papillae. This is the gold standard and is essential — histopathology of the lesion alone shows a neutrophilic microabscess pattern (non-specific).
- Serology — anti-tissue transglutaminase (anti-tTG IgA), anti-endomysial antibodies (EMA), and total serum IgA (to exclude IgA deficiency). Anti-tTG IgA has sensitivity >95% for coeliac disease.
- Small bowel biopsy — not always required if DIF is diagnostic and serology is positive, but should be considered to confirm villous atrophy. Refer to gastroenterology (MBS item 30473 for endoscopy).
Treatment
Dapsone
Generic · Sulfone antibiotic
Adult dose
50–100 mg PO once daily. Rapid symptom relief within 24–48 hours. Maintenance: lowest effective dose (often 50 mg alternate days).
Monitoring
FBC and reticulocyte count at baseline, then weekly for 4 weeks, then monthly for 6 months. G6PD must be checked before commencing — haemolytic anaemia risk. Methaemoglobin levels if symptomatic.
Renal adjustment
Use with caution if eGFR <30 mL/min; dose reduction may be required
PBS status
✔ PBS General Benefit
Strict gluten-free diet is the cornerstone of long-term management of dermatitis herpetiformis and coeliac disease. It eliminates the underlying enteropathy, reduces the risk of small bowel lymphoma, and may eventually allow dapsone withdrawal. Refer to a dietitian with expertise in coeliac disease (Medicare-funded chronic disease management plan — MBS items 721/723 available through GP).
Lichen Planus & Pruritus Ani/Vulvae
Lichen Planus
Lichen planus (LP) is a T-cell-mediated inflammatory disorder affecting skin, mucous membranes, hair, and nails. It classically presents with the "5 Ps": pruritic, planar, polygonal, purple papules/plaques. Wickham's striae — fine, white, lace-like lines on the surface — are pathognomonic and best seen with dermatoscopy or application of mineral oil.
Clinical Variants
| Variant | Distribution & Features | Key Considerations |
|---|---|---|
| Classic cutaneous | Flexor wrists, forearms, shins, ankles, genitalia. Pruritic violaceous papules/plaques. Koebner phenomenon (isomorphic response to trauma). | Self-limiting in most cases (1–2 years); post-inflammatory hyperpigmentation common in darker skin types. |
| Oral LP | Buccal mucosa, tongue, gingiva. Reticular (white striae, often asymptomatic) vs erosive (painful, red, ulcerated). Wickham's striae on buccal mucosa. | Erosive form carries a small (1–2%) malignant transformation risk to squamous cell carcinoma — regular monitoring required. Lichenoid drug reactions (NSAIDs, ACE inhibitors, beta-blockers) must be excluded. |
| Lichen planopilaris | Scalp. Perifollicular erythema, scaling, and permanent scarring alopecia (frontal fibrosing alopecia is a variant). | Urgent referral to dermatology — irreversible hair loss if untreated. |
| Nail LP | Longitudinal ridging, nail plate thinning, pterygium formation, nail bed hyperpigmentation. | May cause permanent nail dystrophy. Refer to dermatology. |
| Genital LP | Glans penis (men): annular white plaques. Vulva (women): erosive LP can cause scarring, labial resorption, introital stenosis (vulvovaginal-gingival syndrome). | Erosive vulvar LP requires long-term follow-up — scarring complications and possible squamous cell carcinoma risk (reported but lower than oral erosive LP). |
Management of Lichen Planus
Clobetasol Propionate 0.05% Ointment
Dermovate® · Super-potent topical corticosteroid
Dose
Apply thin layer to affected areas once daily for 2–4 weeks, then taper to alternate-day use or step down to mometasone 0.1%. For genital/oral LP: use in a thin layer with review at 4 weeks.
Note
Limit continuous super-potent topical corticosteroid use to 2–4 weeks. Avoid thin skin areas (face, genital skin) long-term — use with caution and close monitoring for skin atrophy.
PBS status
✔ PBS General Benefit
Triamcinolone Acetonide Injection
Kenacort-A® · Intralesional corticosteroid
Dose
10 mg/mL (diluted) injected intralesionally into hypertrophic plaques every 4–6 weeks. Max 40 mg per session.
Indication
Hypertrophic lichen planus resistant to topical therapy. Also used for lichen planopilaris (to affected scalp areas).
PBS status
✔ PBS General Benefit
For extensive or refractory cutaneous LP, refer to dermatology for consideration of phototherapy (narrowband UVB), acitretin, methotrexate, or mycophenolate mofetil. Oral erosive LP may require topical tacrolimus 0.1% ointment (unlicensed indication; authority prescription).
Pruritus Ani
Pruritus ani is a common condition characterised by perianal itching and affects up to 5% of the population. It is more common in men (4:1 ratio) and in adults aged 30–60 years.
Classification & Causes
| Category | Causes | Management Approach |
|---|---|---|
| Primary (idiopathic) | Faecal soiling, mucosal prolapse, excessive perianal moisture; no identifiable cause in ~50–75% | Hygiene education, barrier cream (zinc oxide, Cavilon™), avoid soap |
| Infective | Pinworm (Enterobius vermicularis — children), candidiasis, dermatophytes, condylomata, STIs | Mebendazole/albendazole (pinworm); topical antifungal; STI screening |
| Dermatoses | Psoriasis, lichen sclerosus, contact dermatitis (wipes, topical preparations), lichen simplex chronicus | Biopsy if diagnostic uncertainty; potent topical corticosteroids (short course) |
| Proctological | Haemorrhoids, anal fissure, fistula-in-ano, rectal prolapse | Proctological assessment and management of underlying cause |
| Systemic | Diabetes mellitus, CKD, hepatic disease, thyroid disease | Screening FBC, LFTs, eGFR, glucose, TFTs |
Pruritus Vulvae
Pruritus vulvae is a common gynaecological complaint requiring careful assessment to distinguish dermatological, infective, neoplastic, and functional causes. It affects women of all ages and significantly impacts quality of life.
Key Causes & Approach
- Candidiasis — most common infective cause; thick white "cottage cheese" discharge, erythema, satellite lesions. First-line: topical clotrimazole 1% cream (3–7 days) or oral fluconazole 150 mg single dose (PBS general benefit).
- Lichen sclerosus — white atrophic "cigarette paper" skin, figure-of-eight distribution (vulva and perianal), dyspareunia. Treat with clobetasol propionate 0.05% ointment — long-term maintenance under dermatology/gynaecology supervision. 2–5% malignant transformation risk to vulval SCC — lifelong surveillance required.
- Lichen planus — erosive vulvar form with pain, bleeding, vaginal discharge, scarring.
- Contact dermatitis — fragranced washes, pads, underwear dyes, topical treatments. Remove all potential irritants.
- Vulvodynia — chronic vulval pain without identifiable cause; may coexist with itch. Multidisciplinary approach (pain medicine, pelvic floor physiotherapy, psychology).
- Paget's disease — persistent, well-demarcated erythematous plaque with superficial scaling. Vulval biopsy essential. Refer to gynaecology oncology.
When to biopsy: Vulval or perianal lesions that fail to respond to standard treatment within 4–6 weeks, or have atypical features (unilateral, eroded, indurated, pigmented), should be biopsied to exclude lichen sclerosus, lichen planus, intraepithelial neoplasia, or vulval Paget's disease.
Investigations
The investigation approach is guided by the classification of pruritus. Localised pruritus with primary skin lesions rarely requires extensive systemic workup. Generalised pruritus without primary skin lesions mandates systematic investigation.
Essential
Full Blood Count (FBC) with Film
MBS item 65060. Assess for eosinophilia (scabies, atopy, parasites), lymphocytosis/abnormal cells (lymphoproliferative disease), anaemia (iron deficiency, chronic disease).
Essential
Liver Function Tests (LFTs)
MBS item 66500. Bilirubin, ALP, GGT, ALT, AST, albumin. Elevated ALP/GGT suggests cholestatic pattern — further workup with hepatic ultrasound and hepatitis serology.
Essential
Renal Function (eGFR, Creatinine, Urea)
MBS item 66500. CKD is the most common systemic cause of pruritus in Australia due to high CKD prevalence.
Essential
Thyroid Function Tests (TSH, free T4)
MBS item 66716. Both hypo- and hyperthyroidism may cause pruritus.
Essential
Iron Studies (Ferritin, Transferrin Saturation, Serum Iron)
MBS item 66573. Iron deficiency without anaemia may cause pruritus. Ferritin <30 µg/L is diagnostic even if Hb is normal.
Available
Blood Glucose / HbA1c
MBS item 66555 (HbA1c). Screen for diabetes mellitus, which may cause pruritus via neuropathy and xerosis.
Available
Calcium, Phosphate, PTH
MBS item 66500. Secondary hyperparathyroidism in CKD; hypercalcaemia in malignancy/sarcoidosis.
Available
Chest X-ray
MBS item 58500. If lymphoproliferative disease suspected (mediastinal lymphadenopathy in Hodgkin lymphoma).
Referral
Hepatic Ultrasound / MRCP
MBS item 55039 (ultrasound). If cholestatic LFTs or obstructive picture. MRCP (MBS item 63001) if biliary obstruction suspected.
Referral
CT Chest / Abdomen / Pelvis
MBS item 56001/56007/56012. If red flag features (weight loss, lymphadenopathy, B symptoms) — exclude lymphoproliferative and solid organ malignancy.
Specialist
Skin Biopsy (with Direct Immunofluorescence)
MBS item 30071 (GP biopsy) or MBS item 30073 (specialist). Essential for dermatitis herpetiformis (perilesional biopsy for DIF), suspected cutaneous T-cell lymphoma, lichen planus, bullous pemphigoid.
Specialist
Bone Marrow Biopsy
MBS item 13700. If FBC film suggests haematological malignancy — perform under haematology supervision.
Available
Scabies Skin Scrape / Dermatoscopy
Skin scraping with 10% KOH; dermatoscopy (MBS item 10820 specialist). Mite, eggs, or scybala confirm diagnosis. Sensitivity ~50–60%.
Empirical & First-Line Therapy
While investigating the underlying cause, symptomatic management of pruritus should commence immediately. The following treatments are applicable to most forms of pruritus and are available in Australia.
General Measures
- Emollients: Apply liberally and frequently (at least twice daily). Fragrance-free, soap-free washes (e.g., QV Wash, Cetaphil Gentle Skin Cleanser, Hamilton Skin Therapy Wash). Bathing should be brief (<10 minutes), lukewarm water. Pat dry, don't rub. Apply emollient immediately after bathing.
- Cool compresses: Wet-wrapping with cool water provides immediate antipruritic effect.
- Environmental: Cotton clothing, cool room temperature, humidifier in winter, avoid wool and synthetic fabrics.
- Nail care: Keep nails short to minimise excoriation and secondary infection risk.
Pharmacological Therapy
Cetirizine
Zyrtec® · Non-sedating antihistamine
Adult dose
10 mg PO once daily
Paediatric dose
6 months–2 years: 2.5 mg PO once daily. 2–6 years: 5 mg PO once daily. >6 years: 10 mg once daily.
Renal adjustment
eGFR 30–50: 5 mg once daily. eGFR <30: 5 mg alternate days.
Indication
Urticaria, atopic dermatitis (adjunctive). Limited evidence for non-histamine-mediated pruritus.
PBS status
✔ PBS General Benefit
Promethazine
Phenergan® · Sedating antihistamine
Adult dose
10–25 mg PO at night (nocturnal pruritus). Max 50 mg/day.
Paediatric dose
2–5 years: 5–15 mg nocte (in divided doses). 5–10 years: 10–25 mg nocte. Use only for short-term symptom relief; avoid long-term use in children.
Cautions
Anticholinergic effects — use with caution in elderly (increased fall risk, confusion, urinary retention). Avoid in glaucoma, prostatic hypertrophy.
PBS status
✔ PBS General Benefit
Hydrocortisone 1% Cream
Sigmacort® · Mild topical corticosteroid
Dose
Apply thin layer to affected area once or twice daily for up to 2 weeks. Safe for face, genital skin, and skin folds.
Note
Use for mild inflammatory dermatoses. Escalate to moderate (mometasone) or potent (betamethasone valerate) for more severe disease.
PBS status
✔ PBS General Benefit
Gabapentin
Neurontin® · Anticonvulsant / Neuromodulator
Adult dose
Start 100 mg PO at night, titrate by 100–300 mg every 3–7 days to 300–900 mg TDS (max 3,600 mg/day). Target dose for uraemic pruritus: 200–300 mg after dialysis (on dialysis days).
Renal adjustment
Essential — dose depends on eGFR. eGFR 30–59: 200–700 mg BID. eGFR 15–29: 200–300 mg daily. eGFR <15: 100–300 mg daily. Supplemental dose after haemodialysis.
Indication
Uraemic pruritus (first-line for CKD-associated itch), neuropathic itch (notalgia paraesthetica, brachioradial pruritus), refractory generalised pruritus.
PBS status
⚠ PBS Authority Required (for neuropathic pain indication; uraemic pruritus is off-label)
Cholestyramine
Questran Light® · Bile acid sequestrant
Adult dose
4 g PO once or twice daily (before meals). Mix with water or juice. Onset: 1–3 weeks.
Cautions
May impair absorption of other medications (give other drugs 1 hour before or 4–6 hours after). Constipation, bloating. Fat-soluble vitamin malabsorption with long-term use.
Indication
Cholestatic pruritus — first-line pharmacotherapy. Effective in primary biliary cholangitis and obstructive jaundice.
PBS status
✔ PBS General Benefit
Refractory Cholestatic Pruritus — Stepwise Approach
Step 1
Cholestyramine 4 g PO BD (before meals)
Ongoing
First-line bile acid sequestrant
Step 2
Rifampicin 150–300 mg PO BD
Monitor LFTs monthly × 3, then quarterly
Hepatotoxicity risk — requires monitoring. PBS Authority Required.
Step 3
Naltrexone 25–50 mg PO once daily
Start at 25 mg, titrate to 50 mg
Opioid antagonist. Initial dose may precipitate opioid-like withdrawal in cholestasis. Start low, go slow.
Step 4
Sertraline 75–100 mg PO once daily
Ongoing
SSRI — adjunctive. Evidence limited but used in refractory cases.
Special Populations
Pregnancy
- Obstetric cholestasis (intrahepatic cholestasis of pregnancy — ICP): Presents with pruritus (typically palms and soles) in the second or third trimester, with elevated serum bile acids (>40 µmol/L is associated with increased fetal risk). Referral to obstetric medicine. Ursodeoxycholic acid (UDCA) 10–15 mg/kg/day is first-line for maternal symptom relief and may improve fetal outcomes.
- Pruritic urticarial papules and plaques of pregnancy (PUPPP): Polymorphic eruption of pregnancy — urticarial papules beginning in striae, spreading centrifugally. Exclude pemphigoid gestationis. Topical corticosteroids and oral antihistamines (cetirizine, loratadine Category A).
- Pemphigoid gestationis: Autoimmune blistering disease — urticarial plaques → tense bullae. Referral to dermatology and obstetric medicine. Requires systemic corticosteroids.
- Avoid in pregnancy: Permethrin (Category B1 — considered safe if required), dapsone (use with caution, monitor for neonatal haemolysis), ivermectin (contraindicated — Category B3), gabapentin (congenital malformations reported).
- Safe options: Emollients (first-line), hydrocortisone 1% cream, cetirizine/loratadine (Category A), calamine lotion, cool compresses.
Paediatrics
- Atopic dermatitis is the most common cause of pruritus in Australian children (~20% prevalence). First-line: liberal emollient use, short courses of low-potency topical corticosteroids (hydrocortisone 1% for face, mometasone for body). Wet-wrap therapy for flares.
- Scabies in children: permethrin 5% cream (≥2 months of age). For infants <2 months, consult paediatric dermatology; may use precipitated sulphur 6–10% in petrolatum (compounded). Ivermectin only if ≥15 kg body weight.
- Pinworm (Enterobius vermicularis): Common cause of perianal pruritus in children. Nocturnal perianal itch, restlessness. Scotch tape test for diagnosis. Mebendazole 100 mg PO single dose, repeated at 2 weeks. Treat whole household.
- Antihistamine caution: Sedating antihistamines (promethazine) should be used with extreme caution in children <2 years (risk of respiratory depression). Non-sedating antihistamines (cetirizine) are preferred for long-term use.
Elderly
- Xerosis (dry skin) is the most common cause of pruritus in the elderly. Ageing skin has reduced sebum production, decreased epidermal lipids, and impaired barrier function. Aggressive emollient therapy is essential.
- Higher prevalence of systemic causes: CKD, hepatic disease, haematological malignancy (especially polycythaemia vera, lymphoma), thyroid disease, and medication-related pruritus. Lower threshold for investigation.
- Antihistamine caution: Sedating antihistamines (promethazine, doxylamine) are on the Beers Criteria list — avoid in elderly due to anticholinergic effects (falls, confusion, urinary retention, constipation). Consider cetirizine or loratadine instead.
- Polypharmacy review: Comprehensive medication review essential — multiple medications may contribute to pruritus (opioids, ACE inhibitors, statins, diuretics). Involve pharmacist (Home Medicines Review — MBS item 900).
Renal Impairment
- Uraemic pruritus affects 40–60% of dialysis patients and is associated with increased mortality, depression, and impaired quality of life. Multifactorial: immune dysregulation (IL-31), peripheral neuropathy, xerosis, secondary hyperparathyroidism.
- First-line: Optimise dialysis adequacy (Kt/V ≥1.4 for haemodialysis), phosphate control (phosphate binders — calcium carbonate, sevelamer), and aggressive emollient therapy.
- Pharmacotherapy: Gabapentin (100–300 mg post-dialysis) or pregabalin (25–75 mg post-dialysis) — evidence-based first-line agents. Both require dose adjustment for eGFR. Narrowband UVB phototherapy (available in Australian dermatology departments) is second-line.
- Naltrexone (25–50 mg/day) has demonstrated benefit in uraemic pruritus in some RCTs — use as a third-line option.
Hepatic Impairment
- Cholestatic pruritus may be the presenting symptom of primary biliary cholangitis, primary sclerosing cholangitis, drug-induced cholestasis, or biliary obstruction. The itch is often generalised but may be worse on palms and soles.
- Treatment pathway: Cholestyramine → rifampicin (monitor LFTs closely for hepatotoxicity) → naltrexone (start at 12.5–25 mg to avoid opioid-withdrawal-like reaction) → sertraline. UDCA for PBC.
- Obstructive jaundice: ERCP and stenting may be required for mechanical biliary obstruction. The pruritus may be severe and refractory until obstruction is relieved.
Immunocompromised
- Crusted scabies: Immunocompromised patients (HIV, transplant recipients, systemic corticosteroids) may develop crusted (Norwegian) scabies — highly infectious, with minimal itch. Combination treatment: oral ivermectin + topical permethrin + keratolytics. Hospital isolation required.
- Disseminated herpes simplex/varicella-zoster: May present as pruritic or painful vesicles. Antiviral therapy (IV aciclovir if severe).
- Haematological malignancy: Pruritus in Hodgkin lymphoma may precede lymphadenopathy by months. Mycosis fungoides (cutaneous T-cell lymphoma) presents with pruritic patches/plaques — skin biopsy essential.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Skin health is a significant and often under-resourced area of Aboriginal and Torres Strait Islander health. Scabies and secondary bacterial skin infections are endemic in many remote and very remote communities, with scabies prevalence rates of 20–70% in children reported in the Northern Territory, Western Australia, and Far North Queensland. These infections contribute to the cascade of post-streptococcal glomerulonephritis, rheumatic heart disease, and chronic kidney disease — conditions that disproportionately affect Aboriginal and Torres Strait Islander Australians.
📚 References
- 1. Yosipovitch G, Berger T, Lebwohl MG, et al. International Forum for the Study of Itch (IFSI): guidelines for the clinical assessment of pruritus. Acta Derm Venereol. 2023;103:adv00881.
- 2. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Skin infections. Canberra: AIHW; 2023.
- 3. Romani L, Engelman D, Engelman J, et al. Scabies and impetigo prevalence and risk factors in Fiji: a national survey. PLoS Negl Trop Dis. 2023;9(3):e0003452.
- 4. Currie BJ, McCarthy JS. Permethrin and ivermectin for scabies. N Engl J Med. 2010;362(8):717–725.
- 5. Caproni M, Antiga E, Melani L, Fabbri P. Guidelines for the diagnosis and treatment of dermatitis herpetiformis. J Eur Acad Dermatol Venereol. 2009;23(6):633–638.
- 6. Gorris Z, Sherif H, Wessman L. Lichen planus: a comprehensive review. Aust J Gen Pract. 2022;51(10):736–741.
- 7. Metz M, Ständer S. Chronic pruritus — pathogenesis, clinical aspects and treatment. J Eur Acad Dermatol Venereol. 2010;24(11):1249–1260.
- 8. Royal Australian College of General Practitioners (RACGP). Guidelines for Preventive Activities in General Practice (Red Book). 9th ed. Melbourne: RACGP; 2018.
- 9. Weisshaar E, Szepietowski JC, Darsow U, et al. European guideline on chronic pruritus. Acta Derm Venereol. 2012;92(5):563–581.
- 10. Australian and New Zealand Vulvovaginal Society (ANZVS). Vulval Dermatology Guidelines. Melbourne: ANZVS; 2023.
- 11. Engelman D, Yoshizumi J, Hay RJ, et al. The 2020 International Alliance for the Control of Scabies (IACS) criteria for the diagnosis of scabies. Lancet Infect Dis. 2020;20(8):e192–e197.
- 12. Simonsen EN, Del Pozo LJ, Engelman D, et al. Crusted scabies: a systematic review of clinical trials and case reports. Br J Dermatol. 2023;188(3):346–355.
- 13. Kremer AE, Martens JJ, Kulik W, et al. Lysophosphatidic acid is a potential mediator of cholestatic pruritus. Gastroenterology. 2010;139(3):1008–1018.
- 14. Dalle S, Balme B, Sebban C, et al. Pruritus in Hodgkin lymphoma: clinical features and pathophysiology. Br J Dermatol. 2015;172(6):1557–1562.
- 15. Marks R, Ponniah T. Pruritus ani: a structured approach. Aust J Gen Pract. 2021;50(6):380–385.
- 16. National Aboriginal Community Controlled Health Organisation (NACCHO). Skin Health Programme: Guidelines for Remote Communities. Canberra: NACCHO; 2022.