Shingles (Herpes Zoster) is caused by the reactivation of the Varicella-Zoster Virus (VZV), the same virus that causes chickenpox. After recovery, VZV remains dormant in nerve tissue. Shingles occurs when the virus reactivates and travels along nerve fibers to the skin, causing a painful rash. While the rash usually appears on the torso, if the virus affects nerves extending to the face and eye area, it can cause vision complications. Shingles can cause blindness, though this is a relatively rare outcome resulting from the virus affecting nerves near the eye.
The Specific Risk Ophthalmic Shingles
The shingles virus threatens vision when it reactivates along the ophthalmic division of the trigeminal nerve, which is the fifth cranial nerve. This condition is called Herpes Zoster Ophthalmicus (HZO), involving 10% to 20% of all shingles cases.
This nerve branch supplies the forehead, upper eyelid, and the side and tip of the nose. When the rash appears in these locations, it indicates the virus is traveling along a pathway connected to the eye structures. A rash that includes the tip of the nose is known as Hutchinson’s sign, which is a strong indicator of potential eye involvement.
The presence of this sign suggests the virus has infected the nasociliary nerve, which directly innervates the eye. Initial HZO symptoms often include a painful, tingling sensation on the forehead, followed by the characteristic vesicular rash that respects the midline of the face. These early skin signs require prompt medical attention to protect vision.
Progression to Permanent Vision Loss
Vision loss from HZO is caused by inflammation and damage to the internal structures of the eye, not the skin rash itself. The virus can inflame almost any part of the eye, impairing vision. The most common complications are keratitis (inflammation of the cornea) and uveitis (inflammation inside the eye).
Keratitis often leads to corneal scarring, which is the leading cause of permanent moderate or severe vision loss following HZO, accounting for over 90% of cases. The scarring creates an opaque area on the eye’s surface, blocking light from reaching the retina. Uveitis, inflammation of the middle layer of the eye, can trigger a rise in intraocular pressure.
This increased pressure can damage the optic nerve, causing secondary glaucoma and irreversible vision loss. These complications can develop weeks or months after the skin rash clears, meaning the threat to vision persists. Severe vision loss is more likely in older or immunosuppressed patients, or those who develop uveitis.
Prevention and Treatment
Prevention offers the most effective way to avoid the risk of HZO and its complications. The recombinant zoster vaccine, Shingrix, is highly effective, demonstrating over 89% effectiveness against HZO in adults aged 50 and older. Vaccination significantly reduces the incidence of shingles, preventing the viral reactivation that leads to eye involvement.
If shingles is suspected in the eye area, immediate treatment with antiviral medication is necessary to limit viral replication and reduce complication severity. Antiviral drugs such as acyclovir or valacyclovir should be started within 72 hours of the rash first appearing. Starting treatment within this narrow window reduces the risk of developing eye disorders.
Anyone with suspected HZO should consult a healthcare professional immediately to begin antiviral therapy and be referred to an ophthalmologist. An eye specialist monitors for signs of internal ocular inflammation and damage, such as keratitis or uveitis, and manages long-term complications. Extended use of antiviral medication for up to a year has shown promise in reducing the risk of new or worsening eye disease in patients who have already developed HZO.