Shingles

Shingles is a painful, vesicular dermatomal eruption caused by reactivation of latent varicella zoster virus within sensory ganglia. It occurs in individuals with prior primary varicella (chickenpox) infection.

Reactivation risk increases substantially with age and with any form of impaired cell mediated immunity.

Significant complications are possible. They include postherpetic neuralgia, ophthalmic involvement with risk of visual loss, and disseminated disease in significantly immunocompromised patients.

Prompt recognition and, where indicated, early antiviral treatment are therefore clinically important.

Pathophysiology

• After primary varicella infection, the virus establishes lifelong latency within the dorsal root and cranial nerve sensory ganglia.
• Reactivation is typically triggered by age related or other causes of declining cell mediated immune surveillance. Viral replication then travels along the sensory nerve to the corresponding dermatome.
• This produces the characteristic localised vesicular eruption. Associated neuritis is responsible for the often severe accompanying pain.
• The thoracic dermatomes are most commonly affected. Any dermatome can be involved, including the ophthalmic division of the trigeminal nerve (herpes zoster ophthalmicus, given its specific complications) and the geniculate ganglion (Ramsay Hunt syndrome).

• A prodromal phase of localised pain, tingling or altered sensation within the affected dermatome is common. It sometimes precedes the visible rash by several days.
• Before the rash appears, it can occasionally cause diagnostic confusion with other causes of localised pain, such as cardiac or intra abdominal pathology depending on the dermatome involved.
• The characteristic rash comprises grouped vesicles on an erythematous base. It is strictly confined to a single dermatome (or occasionally two adjacent dermatomes) and notably does not cross the midline. It progresses over several days from vesicles to pustules and then crusting, with resolution typically over two to four weeks.
• Pain is frequently the most prominent and troublesome symptom. It is described as burning, stabbing or aching, and can be severe. The intensity of acute pain is a recognised risk factor for subsequent postherpetic neuralgia.
• Herpes zoster ophthalmicus affects the ophthalmic division of the trigeminal nerve. It carries specific risk of significant ocular complications, including keratitis, uveitis and, in severe cases, visual loss.
• Vesicles on the tip or side of the nose (Hutchinson sign) reflect involvement of the nasociliary branch, which also innervates the globe. The sign indicates a significantly increased risk of ocular involvement and warrants urgent ophthalmological assessment.
• Disseminated zoster presents with widespread vesicular lesions extending beyond the primary and adjacent dermatomes, with potential visceral involvement (pneumonitis, hepatitis, encephalitis). It occurs in significantly immunocompromised patients. It is a more severe, potentially life threatening presentation requiring intravenous antiviral therapy.

• Diagnosis is generally clinical, based on the characteristic dermatomal vesicular eruption and associated pain. Typical presentations do not routinely need laboratory confirmation.
• Polymerase chain reaction testing on vesicle fluid offers rapid and sensitive confirmation of varicella zoster virus. Use it where confirmation is required: atypical presentation, diagnostic uncertainty, or significant immunosuppression where confirming and characterising disseminated involvement may be clinically important.
• Ophthalmological assessment is essential for any suspected herpes zoster ophthalmicus, particularly with a positive Hutchinson sign or any visual symptoms. Ocular complications can be severe, and prompt specialist input is important.
• Assess for underlying immunosuppression in any patient with shingles at an unusually young age, with multidermatomal or disseminated involvement, or with recurrent episodes. Reactivation is associated with impaired cell mediated immunity.
• HIV testing is a relevant consideration in appropriate epidemiological or clinical contexts.

• Oral antiviral therapy is most effective when started within seventy two hours of rash onset. It is recommended for patients over fifty years (given increased risk of postherpetic neuralgia in this age group), those with moderate to severe pain or rash, involvement of the face or eye, and any degree of immunocompromise.
• Effective options are aciclovir 800 mg orally five times daily for seven to ten days, valaciclovir 1 g orally three times daily for seven days, or famciclovir 500 mg orally three times daily for seven days. Valaciclovir and famciclovir have the practical advantage of less frequent dosing, supporting better adherence.
• Treatment started beyond seventy two hours may still be considered, particularly where new vesicle formation is ongoing or in higher risk patients (older age, immunocompromise, ophthalmic involvement). Benefit may continue in these circumstances, although the evidence base beyond the classical treatment window is reduced.
• Herpes zoster ophthalmicus requires oral antiviral therapy at the doses above, with urgent ophthalmological assessment. Where significant ocular inflammation is present, add topical corticosteroid therapy under specialist ophthalmological guidance. Consider intravenous aciclovir for severe disease or evidence of significant ocular or orbital complications.
• Disseminated zoster in significantly immunocompromised patients requires intravenous aciclovir 10 mg per kg every eight hours (adjusted for renal function), given the potential severity and risk of visceral involvement. It is generally managed as an inpatient with close monitoring.
• Adequate analgesia is essential, given the frequently significant pain. Use a stepwise approach. Start with simple analgesics (paracetamol, nonsteroidal anti inflammatory drugs). For more severe pain, progress to opioid analgesia.
• Where neuropathic pain features are prominent, agents such as gabapentin or amitriptyline are used. Introduce them early, as adequate acute pain control may reduce the risk of subsequent postherpetic neuralgia.
• Postherpetic neuralgia is defined as pain persisting beyond three months from rash onset. It is managed according to the principles detailed under central neuropathic pain. Standard first line pharmacological options are gabapentin, pregabalin or tricyclic antidepressants (amitriptyline). Add topical lidocaine or capsaicin for more localised pain. Refer refractory cases to specialist pain management services.
• Prevention through vaccination is an important public health measure. The recombinant adjuvanted zoster vaccine (given as a two dose intramuscular course) is recommended for adults from age fifty and above, and from age eighteen in significantly immunocompromised individuals.
• It has substantially superior efficacy in preventing both shingles and postherpetic neuralgia compared with the older live attenuated vaccine. The live vaccine remains contraindicated in significantly immunocompromised patients given its live viral component.
• Patients with active shingles should avoid direct contact with individuals who have not had chickenpox or varicella vaccination, particularly pregnant women and immunocompromised individuals. Direct contact with vesicle fluid can transmit primary varicella infection. The transmission risk is generally lower than with primary varicella itself, given the more localised viral shedding in shingles.