Clinical Definition
Herpes Zoster, commonly referred to as Shingles, is a localized, blistering, painful rash caused by the reactivation of the Varicella-Zoster Virus (VZV). Following primary infection (Varicella/Chickenpox), the virus establishes permanent latency in the dorsal root or cranial nerve ganglia. Reactivation typically occurs decades later due to a decline in cell-mediated immunity, resulting in viral replication and anterograde migration along the sensory nerve axon to the corresponding dermatome.
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 (involvement of the eye) |
| CPT (Preventive) | 90750 | Zoster (shingles) vaccine, recombinant, subunit, adjuvanted (RZV), IM use |
| Affected System | Neurological; Integumentary | Dermatomal distribution |
Epidemiology & Statistics
The incidence of Herpes Zoster rises sharply with age, correlating with the natural senescence of the immune system. Approximately one in three individuals will develop zoster during their lifetime. The incidence rate is roughly 4-5 cases per 1,000 person-years in the general population, increasing to 11 per 1,000 in individuals aged 80 and older. Immunocompromised states (e.g., HIV, malignancy, organ transplantation) significantly elevate risk.
Pathophysiology (Mechanism)
The pathophysiology involves a specific sequence of viral activity:
1. Latency: Following primary varicella infection, VZV genome persists as an episome in the nucleus of neurons in the sensory ganglia.
2. Reactivation: Triggered by stress, immunosuppression, or aging, VZV resumes replication.
3. Neuronal Inflammation: The virus causes inflammation and necrosis within the ganglion and peripheral nerve, leading to prodromal neuropathic pain.
4. Dermatomal Eruption: The virus travels down the sensory nerve to the skin, causing a vesicular eruption strictly limited to the dermatome supplied by that nerve.
Standard Management Protocols
Treatment goals include accelerating healing, reducing pain, and preventing complications such as Postherpetic Neuralgia (PHN).
- Pharmacological Classes:
- Nucleoside Analogues (Antivirals): (e.g., Acyclovir, Valacyclovir, Famciclovir) Inhibit viral DNA polymerase. Most effective when initiated within 72 hours of rash onset.
- Analgesics / Neuropathic Agents: (e.g., Gabapentin, Pregabalin, TCAs) Used to manage acute neuritic pain and PHN.
- Corticosteroids: Occasionally used adjunctively to reduce acute neuritis, though efficacy in preventing PHN is debated.
- Preventive Intervention:
- Recombinant Zoster Vaccine (RZV): Recommended for adults aged 50 years and older to boost T-cell immunity against VZV.
Healthcare Resource Utilization
Herpes Zoster presents a substantial economic burden, primarily driven by the management of complications.
- Postherpetic Neuralgia (PHN): Up to 20% of patients develop PHN, a chronic pain syndrome requiring long-term pharmacological management and pain specialist consultations.
- Ophthalmic Complications: Herpes Zoster Ophthalmicus (HZO) requires urgent ophthalmological intervention to prevent keratitis and vision loss.
- Hospitalization: While rare in immunocompetent hosts, disseminated zoster in immunocompromised patients often necessitates inpatient IV antiviral therapy.
