Shingles
Exam Tips
- Classic sequence: dermatomal pain/allodynia first, then unilateral vesicles that do not cross the midline.
- If rash involves the nose (Hutchinson sign), treat as high-risk ophthalmic zoster and arrange same-day ophthalmology input.
- Antivirals are most effective early: learn the UK oral doses (aciclovir 800 mg five times daily, valaciclovir 1 g TDS, famciclovir 500 mg TDS for 7 days).
- In viva/OSCE, always mention transmission counselling: shingles can transmit VZV to non-immune contacts causing chickenpox, not shingles.
- See Figure: unilateral dermatomal vesicular eruption progression (macule -> papule -> vesicle -> crust) and cranial nerve warning patterns.
Definition
Shingles (herpes zoster) is a reactivation of latent varicella-zoster virus in a sensory ganglion, causing inflammation in a single nerve and the skin supplied by that dermatome. It classically presents with unilateral dermatomal neuropathic pain followed by a vesicular rash, usually many years after primary chickenpox infection.
Pathophysiology
After primary varicella infection, varicella-zoster virus remains dormant in dorsal root or cranial nerve ganglia. With reduced VZV-specific cell-mediated immunity (for example with ageing or immunosuppression), the virus reactivates, replicates in the ganglion, and spreads along sensory nerves to skin, producing neuritis (burning/stabbing pain) and a dermatomal vesicular eruption. Inflammation and neuronal injury can persist after rash healing, which explains post-herpetic neuralgia; viraemia in severe immunosuppression can cause multi-dermatomal or visceral dissemination.
Risk Factors
- Increasing age (incidence and severity rise markedly in older adults)
- Immunocompromise: HIV, lymphoproliferative malignancy, chemotherapy, organ transplantation, prolonged systemic corticosteroid use
- Comorbid disease: COPD/asthma, chronic kidney disease, cardiovascular disease, diabetes, autoimmune/inflammatory disease, malignancy
- Female sex
- Psychological stress and adverse psychosocial stressors
- Head/neck involvement, severe prodromal pain, extensive rash, or CNS/visceral features (risk factors for complications)
Clinical Features
Symptoms
- Prodrome over 2-3 days (sometimes longer): localized pruritus, paraesthesia, dysaesthesia, numbness
- Dermatomal neuropathic pain (burning, stabbing, shooting, throbbing; constant or intermittent)
- Acute pain with or before rash; may disturb sleep and daily function
- Systemic upset in a minority: headache, fever, malaise, fatigue
- Rarely pain without rash (zoster sine herpete)
Signs
- Unilateral erythematous maculopapular eruption in a dermatomal distribution (often thoracic T1-L2 in immunocompetent people; see Figure: thoracic dermatome map)
- Progression to grouped vesicles within 1-2 days, then pustules, ulceration, and crusting
- Healing over about 2-4 weeks with possible scarring or pigment change
- Disseminated or multi-dermatomal lesions in immunocompromised patients
- Hutchinson sign (lesions on tip/side/root of nose) suggesting nasociliary involvement and higher ocular risk
- Ear canal/pinna vesicles with ipsilateral facial weakness in herpes zoster oticus (Ramsay Hunt syndrome)
Investigations
Management
Lifestyle Modifications
- Start treatment promptly and advise early review if eye symptoms, ear symptoms, neurological deficits, or widespread rash develop
- Keep rash clean/dry, avoid scratching, and cover lesions to reduce secondary bacterial infection
- Infection control: avoid close contact with non-immune pregnant people, neonates, and severely immunocompromised contacts until lesions have crusted
- Optimize sleep, hydration, and pain-coping strategies; safety-net for worsening pain or fever
Pharmacological Treatment
Oral antivirals (start as early as possible, ideally within 72 hours of rash onset; consider later if new vesicles or high risk)
- Aciclovir 800 mg orally five times daily for 7 days
- Valaciclovir 1 g orally three times daily for 7 days
- Famciclovir 500 mg orally three times daily for 7 days
Reduce acute viral replication and may reduce acute pain/severity. Adjust dose in renal impairment (especially aciclovir/valaciclovir) and maintain hydration due to nephrotoxicity risk. Use urgent IV aciclovir in severe immunocompromise or disseminated/visceral disease under specialist care.
Analgesia
- Paracetamol 1 g every 4-6 hours (maximum 4 g/day)
- Ibuprofen 200-400 mg three times daily with food if suitable
- Codeine phosphate 30-60 mg every 4 hours as needed (maximum 240 mg/day)
Stepwise pain control based on severity. Avoid/limit NSAIDs in renal disease, peptic ulcer risk, heart failure, or anticoagulation; caution opioid adverse effects (constipation, sedation, dependence risk). Persistent neuropathic pain may need neuropathic agents per local protocol.
Antibacterial treatment (only if secondary bacterial infection)
- Flucloxacillin 500 mg to 1 g four times daily for 5-7 days (if non-severe cellulitis pattern)
- Clarithromycin 500 mg twice daily for 5-7 days if penicillin allergy (local guidance dependent)
Not routine for uncomplicated zoster. Use local antimicrobial guidance and assess for severe soft tissue infection/sepsis needing urgent admission.
Complications
- Post-herpetic neuralgia (pain persisting or appearing more than 90 days after rash onset)
- Herpes zoster ophthalmicus: keratitis, uveitis, corneal ulceration, optic involvement, glaucoma, vision loss
- Herpes zoster oticus (Ramsay Hunt syndrome): facial palsy, hearing loss, vestibular symptoms
- CNS complications: encephalitis, meningoencephalitis, myelitis, cerebellitis, radiculitis, Guillain-Barre syndrome
- Increased short-term vascular risk: stroke, TIA, myocardial infarction
- Peripheral motor neuropathy causing focal weakness
- Secondary bacterial infection (cellulitis, osteomyelitis, necrotizing fasciitis, sepsis)
- Visceral dissemination in severe immunosuppression (pneumonia, hepatitis, encephalitis, DIC)
Prognosis
Most episodes are self-limiting, with rash evolution to crusting and healing over about 2-4 weeks, but pain can be severe and recovery slower in older adults. Risk of complications and recurrence is higher in immunocompromised people; recurrence is uncommon in immunocompetent patients but does occur, and post-herpetic neuralgia is the main cause of long-term morbidity.
Sources & References
🏥BMJ Best Practice(1)
✅NICE Guidelines(1)
- Shingles[overview]
📖Textbook References(1)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1495, 1496)[context]