Clinical Definition
Herpes Zoster (HZ), colloquially known as Shingles, is a localized, painful cutaneous eruption resulting from the reactivation of latent Varicella-Zoster Virus (VZV) within the dorsal root ganglia or cranial nerve ganglia. The hallmark presentation is a unilateral, vesicular rash distributed strictly along a single sensory dermatome. It is distinct from Herpes Simplex, though both share the mechanism of viral latency and reactivation due to declining cell-mediated immunity (immunosenescence).
Clinical Coding & Classification
| System / Category | Code(s) | Description |
|---|---|---|
| ICD-10-CM | B02.9 | Zoster without complications |
| ICD-10-CM | B02.22 | Postherpetic neuralgia (PHN) |
| ICD-10-CM | B02.3 | Zoster ophthalmicus (Ophthalmic Nerve involvement) |
| CPT (Vaccine) | 90750 | Zoster (shingles) vaccine, recombinant, subunit, adjuvanted (RZV), IM use |
| Affected System | Neurological; Integumentary | Sensory Ganglia; Dermatomes |
Epidemiology & Statistics
Approximately one in three individuals will develop Herpes Zoster in their lifetime. The incidence rises sharply after age 50, correlating with the natural decline in VZV-specific T-cell immunity. The lifetime risk of recurrence is estimated at 1-6%. Postherpetic Neuralgia (PHN), the most common chronic complication, affects 10-18% of HZ patients, with risk increasing significantly with age.
Pathophysiology (Mechanism)
The disease process involves a distinct reactivation pathway:
1. Latency: Following primary varicella infection (Chickenpox), VZV DNA persists in the nucleus of neurons in the dorsal root ganglia (DRG) or trigeminal ganglia.
2. Reactivation: Triggers such as stress, immunosuppression, or aging cause viral replication. The virus travels anterograde along the sensory axon to the skin.
3. Neuronal Damage: Viral replication induces inflammation and necrosis within the ganglion and nerve, causing the characteristic prodromal neuropathic pain (burning, lancinating) prior to rash onset.
Standard Management Protocols
Treatment aims to reduce viral shedding, accelerate healing, and prevent PHN.
- Pharmacological Classes:
- Antivirals: (e.g., Valacyclovir, Famciclovir) Nucleoside analogues that inhibit viral DNA polymerase. Most effective if initiated within 72 hours of rash onset.
- Neuropathic Analgesics: (e.g., Gabapentin, Pregabalin, TCAs) Used to manage acute neuritis and PHN.
- Corticosteroids: Adjunctive therapy to reduce acute pain (controversial for PHN prevention).
- Prevention (Vaccination):
- Recombinant Zoster Vaccine (RZV): (e.g., Shingrix) A non-live, adjuvanted vaccine recommended for adults ≥50 years, showing >90% efficacy in preventing HZ and PHN.
Healthcare Resource Utilization
Herpes Zoster imposes a substantial burden due to long-term pain management:
- Pain Management: PHN often requires referral to pain specialists for nerve blocks or complex pharmacological management.
- Ophthalmology Referral: Zoster Ophthalmicus requires urgent assessment to prevent keratitis and vision loss.
