Ophthalmic herpes zoster (HZO) is a viral condition affecting the eye and its surrounding structures. It results from the reactivation of the varicella-zoster virus (VZV), the same virus that causes chickenpox and shingles. After a chickenpox infection, VZV remains dormant in nerve cells. When reactivated, it can travel along nerve pathways, causing shingles, and in some cases, specifically target nerves supplying the eye, leading to HZO.
Understanding the Condition
After chickenpox, the varicella-zoster virus (VZV) remains dormant in sensory neurons, often in the trigeminal ganglion, which controls facial sensation. For unknown reasons, the dormant virus can reactivate, replicate, and travel along nerve pathways to the skin, causing the characteristic painful, unilateral rash of shingles. This rash follows a specific dermatomal distribution, meaning it affects the area supplied by a single nerve. The pain, including that of HZO, is often neuropathic and can be severe. Risk factors for VZV reactivation include advancing age (over 50), a weakened immune system (e.g., due to HIV or immunosuppressive therapies), and psychological stress.
Recognizing Eye Involvement
HZO causes specific signs and symptoms in and around the eye. A painful rash on the forehead, eyelids, or tip of the nose (known as Hutchinson’s sign) often accompanies eye involvement, indicating that the nasociliary branch of the trigeminal nerve is affected and increasing the likelihood of ocular complications. Common ocular symptoms include severe eye pain, redness, eyelid swelling, and photophobia (increased sensitivity to light).
The inflammation can affect various parts of the eye. Conjunctivitis, an inflammation of the conjunctiva (the membrane lining the inside of the eyelids and covering the white part of the eye), is often an initial manifestation. Keratitis, or inflammation of the cornea (the clear front part of the eye), is a common and potentially serious manifestation. This can present as punctate keratitis, with small lesions on the corneal surface, or pseudodendritic keratitis, which are branching lesions. Deeper inflammation, known as stromal keratitis, can also occur, sometimes months after the initial rash, and may lead to significant corneal edema.
Internal eye inflammation can include uveitis, affecting the middle layer of the eye, presenting as floating cells and protein in the eye’s fluid. Glaucoma, characterized by increased eye pressure, can also develop due to inflammation of the eye’s drainage system. In some cases, inflammation may extend to the retina or affect cranial nerves, potentially leading to vision changes like blurred vision or eye muscle weakness. Immediate medical attention from an ophthalmologist is important if eye symptoms are suspected, due to the potential for vision loss.
Diagnosis and Treatment Approaches
Diagnosis of HZO relies on a clinical examination, focusing on the characteristic skin rash and a detailed eye assessment by an ophthalmologist. A unilateral rash on the forehead, eyelid, or nose, often with pain or tingling, strongly suggests the diagnosis. While clinical findings are usually sufficient, laboratory tests like polymerase chain reaction (PCR) for VZV DNA from corneal samples can be used if the diagnosis is uncertain or if ocular symptoms appear without a typical rash.
Treatment aims to reduce viral replication, manage pain, and minimize ocular complications. Antiviral medications are the primary treatment and should start as soon as possible, ideally within 72 hours of rash onset, to improve outcomes. Common oral antivirals include acyclovir (800 mg five times daily), valacyclovir (1000 mg three times daily), or famciclovir (500 mg three times daily), typically for 7 to 10 days. Intravenous acyclovir may be necessary for severe or immunocompromised cases.
Pain management involves over-the-counter relievers or, for severe pain, medications like gabapentin or pregabalin. Specific eye treatments are tailored to complications. Topical corticosteroids (eye drops) reduce inflammation in conditions like stromal keratitis and uveitis, requiring careful ophthalmologist monitoring. Cycloplegic eye drops may also dilate the pupil and reduce pain from inflammation.
Potential Long-Term Effects and Prevention
HZO can lead to chronic complications impacting vision and quality of life, even after the acute infection resolves.
Long-Term Effects
One common long-term effect is post-herpetic neuralgia (PHN), persistent nerve pain lasting months or years after the rash heals. This neuropathic pain can be severe. Ocular complications can also persist or recur, including:
Chronic or recurrent keratitis: Corneal nerve damage (neurotrophic keratitis) can lead to persistent surface defects, permanent corneal scarring, and vision impairment. Severe scarring may require a corneal transplant.
Chronic glaucoma: Elevated eye pressure can develop as a long-term consequence of initial inflammation.
Persistent inflammation: Within the eye, optic nerve damage, or retinal involvement can also contribute to lasting vision problems.
Prevention
Vaccination against shingles is the primary prevention method for HZO. The recombinant herpes zoster vaccine (Shingrix) is recommended for adults aged 50 and older, and for immunocompromised adults aged 19 and older. It has shown high efficacy in preventing shingles and its complications, including HZO. While the vaccine significantly reduces the risk of shingles and PHN, some research suggests potential HZO recurrence in individuals with a prior history after vaccination, emphasizing the need for continued ophthalmic monitoring.