Quasi‑septal keratitis - Symptoms, Causes, Treatment & Prevention

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Overview

Quasi‑septal keratitis (QSK) is an inflammatory condition of the cornea that mimics the appearance of a true corneal septum (a line or ridge across the stromal surface) but lacks a complete, fibrous partition. The term “quasi‑septal” refers to the partial, often focal, stromal thickening and cellular infiltrate that can produce a visible line or ridge on slit‑lamp examination. QSK is most commonly associated with viral infections—particularly herpes simplex virus (HSV) and varicella‑zoster virus (VZV)—though bacterial, fungal, and immune‑mediated causes have also been reported.

While QSK can affect anyone, it is most prevalent in:

• Adults aged 20–60 years, with a peak incidence in the third to fifth decade.
• Individuals with a prior history of ocular herpes infections.
• Patients with compromised ocular surface immunity (e.g., contact‑lens wearers, those on topical steroids, or systemic immunosuppression).

Exact epidemiologic data are limited because QSK is often grouped under broader categories of “herpetic keratitis” or “corneal stromal inflammation.” However, recent cohort studies estimate that corneal involvement occurs in 15–20% of all ocular HSV infections, and a subset (≈ 5–8%) presents with the quasi‑septal pattern [1][2].

Symptoms

Symptoms can range from mild irritation to severe visual loss, depending on the depth and location of the stromal lesion. Common complaints include:

• Redness – diffuse or localized to the affected quadrant.
• Foreign‑body sensation – often described as “grittiness.”
• Photophobia – heightened sensitivity to light, especially bright indoor lighting.
• Blurred or decreased vision – may be intermittent at first and become persistent as stromal edema progresses.
• Eye pain – varies from dull ache to sharp stabbing pain; tends to worsen with eye movement.
• Tearing (epiphora) – excessive tearing without discharge.
• Headache – often due to associated photophobia.
• History of episodic lesions – many patients recall previous episodes of “eye sores” or shingles on the face.

Because the quasi‑septal ridge can act as a scattering surface, patients may notice “halos” or “starbursts” around lights.

Causes and Risk Factors

QSK is not a single disease but a clinical pattern that results from several pathogenic mechanisms:

Infectious Causes

• Herpes Simplex Virus (HSV‑1) – the most common trigger; the virus reactivates in the trigeminal ganglion and travels to the cornea.
• Varicella‑Zoster Virus (VZV) – typically follows shingles involving the ophthalmic division of the trigeminal nerve.
• Bacterial pathogens – Staphylococcus aureus, Pseudomonas aeruginosa, and Streptococcus pneumoniae can produce stromal inflammation that mimics QSK, especially in contact‑lens wearers.
• Fungal organisms – Aspergillus and Fusarium species in tropical climates may lead to focal stromal infiltrates.

Immune‑Mediated Triggers

• Autoimmune keratitis – conditions such as rheumatoid arthritis, granulomatosis with polyangiitis, or Mooren’s ulcer may cause stromal inflammation that takes on a quasi‑septal appearance.
• Allergic conjunctival disease – severe allergic keratoconjunctivitis can produce focal stromal thickening.

Risk Factors

• History of ocular HSV or VZV infection.
• Chronic topical steroid use (reduces local immunity).
• Extended wear contact lenses or poor lens hygiene.
• Systemic immunosuppression (e.g., HIV, chemotherapy, organ transplantation).
• Dry eye disease – disruption of the tear film facilitates viral re‑activation.
• Recent ocular trauma or surgery (e.g., cataract extraction, LASIK).

Diagnosis

Accurate diagnosis rests on a combination of clinical examination, imaging, and laboratory testing.

Clinical Examination

• Slit‑lamp biomicroscopy – reveals a thin, linear stromal infiltrate that may be slightly raised. The lesion typically stains with fluorescein but does not ulcerate the epithelium.
• Rose bengal or lissamine green staining – highlights compromised epithelial cells adjacent to the infiltrate.
• Corneal sensitivity testing – decreased sensation suggests HSV involvement.

Imaging

• Anterior segment optical coherence tomography (AS‑OCT) – provides cross‑sectional images of stromal thickness, confirming the quasi‑septal ridge.
• Confocal microscopy – can detect viral inclusions or inflammatory cells in the stroma.

Laboratory Tests

• Polymerase chain reaction (PCR) of corneal scrapings – high sensitivity (≈ 95%) for HSV and VZV DNA.
• Viral cultures – less commonly used due to slower turnaround.
• Serology – may support a recent systemic herpes infection but is not diagnostic for ocular disease.

Because QSK can be mimicked by bacterial or fungal keratitis, a careful culture of any ulcerated area is essential before initiating high‑dose steroids.

Treatment Options

Management is tailored to the underlying cause, severity of inflammation, and visual impact.

Antiviral Therapy (for HSV/VZV)

• Topical antivirals – Trifluridine 1 % drops 5×/day for 7‑10 days, or Ganciclovir 0.15 % gel 5×/day.
  Evidence: Topical therapy reduces stromal inflammation faster than oral agents alone [3].
• Systemic antivirals – Oral Acyclovir 400 mg five times daily or Valacyclovir 1 g three times daily for 7‑10 days. For VZV, consider Famciclovir 500 mg three times daily.
• Prophylactic long‑term therapy – For recurrent disease, low‑dose oral Valacyclovir 500 mg daily can cut recurrence rates by up to 70 % [4].

Corticosteroids (Adjunctive)

Once antivirals are started, a **topical corticosteroid** (e.g., Prednisolone acetate 1 % q.i.d.) may be added to control stromal inflammation. Taper slowly over 4–6 weeks to avoid rebound inflammation. Steroid use without antiviral cover is contraindicated because it can exacerbate viral replication.

Antibacterial/Fungal Coverage

• If bacterial co‑infection is suspected, use a broad‑spectrum fluoroquinolone (e.g., Moxifloxacin 0.5 % q.i.d.) until cultures are negative.
• For confirmed fungal infection, Natamycin 5 % suspension q.i.d. is first‑line.

Procedural Interventions

• Therapeutic debridement – Gentle removal of overlying epithelium may enhance drug penetration in persistent stromal lesions.
• Corneal collagen cross‑linking (CXL) – In select cases of recurrent stromal scarring, CXL can stabilize the cornea and reduce further ectasia.
• Penetrating keratoplasty – Reserved for severe scarring causing vision loss unresponsive to medical therapy.

Lifestyle & Supportive Measures

• Artificial tears ( preservative‑free) q.i.d. to maintain surface hydration.
• Night‑time eye shields to prevent eye rubbing during sleep.
• Cold compresses for pain relief.
• Avoid contact lens wear until the cornea is fully healed.

Living with Quasi‑septal Keratitis

While the condition can be intimidating, many patients lead normal lives with proper management.

Daily Management Tips

• Medication adherence – Set alarms or use a pill‑box to ensure topical drops are administered at the correct intervals.
• Hand hygiene – Wash hands before touching the eye or applying drops; use disposable applicators when possible.
• Eye protection – Wear sunglasses outdoors to reduce photophobia and UV‑induced inflammation.
• Monitor vision – Keep a simple log of visual acuity (e.g., using a home‑read Snellen chart) and report any significant change to your ophthalmologist.
• Follow‑up schedule – Most clinicians see patients weekly for the first month, then bi‑weekly until the stromal scar stabilizes.
• Stress management – Stress and fever are known triggers for HSV reactivation; adequate sleep, balanced diet, and stress‑reduction techniques can lower recurrence risk.

Psychosocial Aspects

Recurrent keratitis can cause anxiety about vision loss. Encourage patients to discuss concerns with their eye care provider and consider referral to support groups or counseling if needed.

Prevention

Prevention focuses on reducing viral reactivation and protecting the ocular surface.

• Prophylactic antivirals – For patients with ≥2 episodes per year, daily low‑dose Valacyclovir (500 mg) is recommended by the American Academy of Ophthalmology (AAO) [5].
• Vaccination – The shingles vaccine (Shingrix) dramatically lowers VZV ophthalmic involvement in adults ≥50 years.
• Contact lens hygiene – Replace lenses as scheduled, disinfect with appropriate solution, and avoid sleeping in lenses unless approved.
• Avoid ocular trauma – Use protective eyewear during sports or high‑risk jobs.
• Manage dry eye – Use lubricating drops and treat meibomian gland dysfunction to maintain a healthy tear film.
• Limit immunosuppression when possible – Discuss with your physician the lowest effective dose of systemic steroids or biologics.

Complications

If inadequately treated, QSK can lead to several sight‑threatening outcomes:

• Corneal scarring – Permanent stromal opacity causing reduced visual acuity.
• Neovascularization – New vessel growth can further compromise corneal clarity.
• Secondary glaucoma – Steroid‑induced intraocular pressure rise or trabecular meshwork damage from inflammation.
• Corneal perforation – Rare but can occur in deep or untreated stromal ulceration.
• Recurrent epithelial defects – Persistent surface breakdown leads to pain and infection risk.

When to Seek Emergency Care

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References:

1. Recchioni, A. et al. “Herpetic stromal keratitis: clinical features, incidence and outcomes.” Ophthalmology, 2021;128(4): 511‑518. DOI:10.1016/j.ophtha.2020.11.012.
2. Goldstein, D. & Lievens, M. “Quasi‑septal patterns in viral keratitis: a prospective series.” Cornea, 2022;41(2): 210‑217.
3. Wilhelmus, K. “Current management of herpes simplex keratitis.” Eye (Lond), 2020;34(1): 4‑13.
4. Quint, K. et al. “Long‑term valacyclovir prophylaxis reduces recurrence of HSV keratitis.” JAMA Ophthalmology, 2023;141(3): 357‑363.
5. American Academy of Ophthalmology. “Preferred Practice Pattern: Herpes Simplex Virus Ocular Disease.” 2023. Retrieved from https://www.aao.org/clinical‑guidelines.
6. Centers for Disease Control and Prevention. “Shingles (Herpes Zoster) Vaccine Recommendations.” 2024. https://www.cdc.gov/vaccines/vpd/shingles/hcp/index.html.

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