Synopsis
Recognise mucocutaneous and invasive herpes simplex, start time-critical encephalitis and neonatal therapy, protect the eye, and tailor antiviral dose to site and host.
- HSV-1 commonly causes orolabial, ocular and encephalitic disease; HSV-2 commonly causes genital, neonatal and meningitic disease, but either type can occur at either site.
- Painful grouped vesicles become shallow erosions, while prodromal tingling and recurrent lesions in the same region reflect ganglionic latency and reactivation.
- Confirm atypical mucocutaneous disease with PCR from a freshly unroofed lesion base; serology cannot prove that a current lesion is herpetic.
Key red flags
Fever with new confusion, personality change, focal seizure, dysphasia or reduced consciousness requires immediate encephalitis assessment and empirical intravenous aciclovir.
Monomorphic punched-out erosions spread rapidly across eczematous skin with pain, fever and possible ocular or systemic involvement.
Investigation priorities
Confirm HSV and type an active mucocutaneous lesion.
Management branches
Fever and encephalopathy, focal seizure, dysphasia or compatible temporal features raise suspicion of viral encephalitis.
- Stabilise airway, breathing and circulation, treat seizures and hypoglycaemia, obtain blood cultures and cover bacterial meningitis when clinically indicated.
- Perform lumbar puncture promptly unless a specific contraindication requires imaging first; send cell count, protein, glucose and HSV or VZV PCR.
Key medicines
Intravenous aciclovir for HSV encephalitisGive 10 mg/kg intravenously every eight hours by one-hour infusion, usually for 14 to 21 days under the encephalitis protocol, with renal and obesity-adjusted dosing.
Oral aciclovir for mucocutaneous HSVGive 200 mg orally five times daily at roughly four-hour intervals while awake for five days; extend or use 400 mg per dose in defined severe immune impairment under specialist advice.