Herpes Zoster Ophthalmicus (HZO) is a severe form of shingles caused by the reactivation of the varicella-zoster virus, the same virus that causes chickenpox. This reactivation targets the ophthalmic division of the trigeminal nerve, which supplies the forehead, upper eyelid, and nose. HZO is considered an ophthalmologic emergency due to the high risk of permanent vision loss if not treated quickly. Approximately 10% to 25% of all shingles cases involve this part of the face. Immediate medical intervention is necessary to prevent irreversible damage to the delicate structures of the eye.
Recognizing the Early Signs
HZO begins with non-specific symptoms a few days before the characteristic rash appears. Patients often experience a prodromal phase marked by malaise, low-grade fever, headache, and fatigue. This is quickly followed by a sensation of burning, tingling, or shooting pain strictly confined to one side of the face or head, corresponding to the affected nerve pathway.
The definitive sign of shingles is a unilateral rash that starts as red spots and quickly develops into fluid-filled blisters (vesicles). When this rash occurs in the area supplied by the ophthalmic nerve—the forehead, upper eyelid, and scalp—it signals HZO. A particularly important indicator is the presence of lesions on the tip or side of the nose, known as Hutchinson’s sign.
Hutchinson’s sign is a strong predictor of eye involvement because the skin at the nasal tip is supplied by the nasociliary nerve, which also innervates the internal structures of the eye. When this sign is present, the risk of ocular inflammation, such as keratitis or uveitis, can be as high as 85%. However, eye complications can still occur in up to one-third of HZO cases even without a rash on the nose.
Once the eye is involved, symptoms directly affecting vision and comfort manifest. These include significant eye pain, noticeable redness, excessive tearing, and a foreign body sensation. Light sensitivity (photophobia) is a common complaint, and blurred or decreased vision may also occur, indicating damage to the eye’s internal components.
Potential Vision-Threatening Complications
If the infection is not quickly controlled, the varicella-zoster virus can damage nearly every structure within the eye. About 50% of people diagnosed with HZO develop some form of ocular complication. The virus can lead to keratitis, which is inflammation of the cornea, the transparent outer layer of the eye.
Another serious internal complication is uveitis, inflammation of the uvea (the middle layer of the eye). Uveitis can lead to an increase in intraocular pressure, potentially causing secondary glaucoma, which damages the optic nerve and leads to permanent vision loss. Long-term effects include corneal scarring, which significantly impairs vision, or neurotrophic keratitis, where nerve damage causes the cornea to lose sensation.
Even after the initial infection clears, many patients experience postherpetic neuralgia (PHN), a form of chronic neuropathic pain that can persist for months or years in the affected nerve area. In rare but severe cases, the virus can affect the back of the eye, causing retinitis or optic neuritis, which threaten irreversible blindness.
Immediate Steps and Medical Diagnosis
Upon recognizing the early signs of HZO, especially the one-sided rash and accompanying eye symptoms, immediate medical attention is necessary. The most important factor for reducing disease severity and preventing long-term complications is the prompt initiation of antiviral therapy, which is most effective when started within 72 hours of the skin rash first appearing.
Patients should contact an eye specialist, such as an ophthalmologist, or visit an emergency room immediately for rapid diagnosis. Diagnosis is primarily based on the characteristic appearance of the rash and the patient’s symptoms. The doctor will perform a comprehensive eye examination, which includes a specialized slit-lamp examination.
The slit-lamp allows the ophthalmologist to view the internal structures of the eye under high magnification to check for signs of viral damage, such as corneal inflammation or uveitis. They will look for Hutchinson’s sign and test for corneal sensation, as loss of sensation indicates significant nerve involvement. If the rash is atypical, fluid collected from a blister may be analyzed to confirm the presence of the varicella-zoster virus DNA.
Treatment Protocol
The cornerstone of treating HZO is the immediate administration of systemic antiviral medication. These medications slow the virus’s replication, limiting nerve damage and reducing rash severity. Oral antiviral drugs, such as valacyclovir or famciclovir, are typically prescribed in high doses for a course lasting seven to ten days.
Valacyclovir is often preferred due to its higher bioavailability and simpler three-times-daily dosing schedule. Starting this treatment within the initial 72-hour window is crucial for reducing the risk of ocular complications. In severe cases, or for patients with a compromised immune system, intravenous acyclovir may be necessary.
Adjunctive therapies manage specific symptoms and inflammation within the eye. Topical steroid eye drops may be prescribed to control significant inflammation, such as uveitis, but require careful monitoring by an eye specialist to prevent side effects like elevated intraocular pressure. Other supportive treatments include pain relievers and lubricating eye drops to manage dryness or irritation. Extended follow-up care is important to monitor for potential recurrences and the development of chronic conditions like postherpetic neuralgia.