Filamentary Keratitis

Published on 08/03/2015 by admin

Filed under Opthalmology

Last modified 22/04/2025

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Filamentary Keratitis

Woodford S. Van Meter, Douglas Katz and Byron G. Cook

Introduction

Filamentary keratitis is a condition in which mucoid filaments are attached to the anterior corneal surface and cause a foreign body sensation in the patient (Fig. 28.1). Filamentary keratitis is associated with dry eyes, superficial punctate keratopathy, ptosis, and tear film stasis. Patients affected with filamentary keratitis are often highly symptomatic; the filaments may cause a persistent foreign body sensation, photophobia, and redness, that can range from moderate to severe in intensity. Filamentary keratitis is associated with a wide range of conditions in which the ocular surface is abnormal. Treatment can be acute or chronic, and severe cases may require multiple therapeutic modalities.

Figure 28.1 Filaments are composed of chains of epithelial cells and mucus attached to the corneal epithelial surface and can cause a foreign body sensation on blinking. (Courtesy Mark J. Mannis.)

Etiology

The filaments adherent to the corneal epithelium in filamentary keratitis are gelatinous and refractile in appearance and can vary from 0.5 mm sessile adhesions, to 10 mm strings;¹ filaments are generally attached to the basement membrane of the corneal epithelium at one end, with the other end freely moveable. Movement of the lids causes the filament to elongate and coil, which is thought to produce patient discomfort. Filamentary keratitis is associated with underlying basement membrane abnormalities, most of which are related to hypertonic tear film states. A list of conditions that are associated with filamentary keratitis can be seen in Box 28.1.^2–18

Box 28.1 Conditions Associated with Filamentary Keratitis

Aqueous tear deficiency and exposure syndromes

Keratoconjunctivitis sicca 1,28

Meibomian gland dysfunction ¹⁵

Seventh-nerve palsy ¹

Neurotrophic keratopathy ¹

Radiation keratopathy

Atopic/vernal keratoconjunctivitis ¹

Acute viral keratoconjunctivitis ¹

Lacrimal gland agenesis ⁵

Occlusion syndromes

Blepharoptosis 1,2,8

Chronic patching ²

Large-angle strabismus ⁷

Floppy-eyelid syndrome ¹⁵

Contact lens overwear ³

Profound CNS damage ⁴

Reactive ptosis ²

Post-surgical syndromes

Status post penetrating keratoplasty 9,12

Status post extracapsular cataract extraction ⁶

Status post limbal stem cell transplantation ¹⁰

Status post strabismus surgery ¹¹

Manifestations of systemic disease

Sjögren’s syndrome 1,28

Superior limbic keratoconjunctivitis ¹⁸

Diabetes mellitus ¹⁶

Sarcoidosis

Psoriasis ¹

Stevens-Johnson syndrome

Graft-versus-host disease

Systemic lupus erythematosus

Hereditary hemorrhagic telangiectasis ¹⁴

Medication-related

Topical medications

Anticholinergic medications ¹³

Cetuximab (EGFR antibody)¹⁷

Ocular surface abnormalities

Ocular cicatricial pemphigoid

Aniridia ¹

Trachoma

A relative deficiency in the aqueous component of the tear film is usually present in filamentary keratitis, which produces a relative increase in the mucinous component. The ratio of mucus to aqueous is usually increased because of a decrease in aqueous tear production, but can also occur from mucus production ¹⁹ or abnormal mucus accumulation. Abnormalities of the ocular surface result in defects in the corneal epithelium that allow for anchoring of filaments. Ptosis may lead to a reduction in oxygenation of the corneal epithelium, as well as poor tear distribution underneath the lid, which can predispose to or exacerbate filament formation.² Reactive ptosis from discomfort only serves to worsen the problem.

The disorder most frequently associated with filamentary keratitis is dry eye disease. The increase in the mucus-to-aqueous ratio in the tear film may be brought about by either reduced aqueous tear secretion or increased tear film stasis, both of which effectively increase tear film osmolarity. Mucus serves as a disposal system for exfoliated epithelial cells.²⁰ For example, changes in the composition of the mucinous layer, in which mucus becomes more viscous, enhance the adherence of mucus to irregularities in the corneal epithelium. One example of this change occurs when the normally predominant sialomucin is replaced by more viscous sulfomucin in certain disease states.¹⁹ Adherence of mucus to the epithelium is more likely with the latter. The combination of epithelial damage, such as that seen in dry eyes or stasis conditions, combined with an increase in mucus viscosity, can increase the potential for filaments to form on the cornea. Aqueous tear insufficiency decreases lubrication and increases the viscosity of the mucin layer, thereby leading to increased sloughing of epithelial cells, epithelial defects, and viscous mucus – the basic constituents of the corneal filament.

Diagnosis

Subjective

Patients with filamentary keratitis usually complain of a foreign body sensation. This irritation is exacerbated by blinking and usually present throughout the day. Patients may not be symptomatic with their eyes closed. Patients with severe filamentary keratitis may also complain of photophobia, blepharospasm, and tearing.

Objective

Filaments can vary in size from 0.5 mm to 10 mm in length. On biomicroscopy they appear as small, gray, mucoid threads that firmly adhere to the cornea (Fig. 28.2). Occasionally, blinking may dislodge large filaments. Small filaments can cause discomfort commenserate with larger filaments because of the underlying foreign body sensation, caused by the lids tugging on the filaments during blinking. Filaments stain with rose bengal, lissamine green and fluorescein; however, care should be taken during examination not to confuse frank epithelial defects, where a filament may have been dislodged, from sessile filaments that pool with fluorescein and may mimic small corneal abrasions.

Figure 28.2 Filaments which are attached to the epithelial surface of the cornea are associated with dry eyes and stasis conditions of the precorneal tear film. (Courtesy Mike Hanson.)

The location of the filaments may provide a clue as to the cause of the filamentary keratitis.¹ Filaments associated with dry eye or exposure keratopathy are frequently found in the interpalpebral space. Filaments associated with ptosis, prolonged lid closure, or superior limbic keratoconjunctivitis are frequently found superiorly. Filaments related to ocular surgery are often found in the vicinity of the surgical trauma. For example, following corneal transplantation, filaments can be seen near sutures at the graft–host junction (Fig. 28.3). After cataract surgery, they may be overlying or alongside the corneal incision. Surgery-specific factors, such as the disruption of proper tear flow, pooling, toxicity from medications, and local trauma, may predispose to filament formation.

Figure 28.3 Filamentary keratitis can occur on the graft following penetrating keratoplasty in patients with dry eyes or tear film stasis. (Courtesy Mark J. Manni.s)

Histopathology

Traditional teaching has centered on the premise that the filament is composed of mucus and degenerated epithelial cells, and is adherent to the corneal epithelium at the base. However, debate still exists over the exact structure of the filament because observations of the filament on a microscopic level have been heterogeneous in approach and conclusion. Wright used standard histochemical stains to suggest that filaments form when mucus in the tear film attaches to receptors on the corneal surface.²¹ Subsequent proliferation of a filament occurs as mucus accumulates cellular and other degenerative material. In contrast, Zaidman et al. used electron microscopy to report that scattered groups of inflammatory cells and fibroblasts are present below the basement membrane of the corneal epithelium where filaments are attached.²² The authors hypothesized that an underlying pathological process damages the basement epithelium, which leads to focal areas of basement membrane detachment from the underlying Bowman’s layer. This raised epithelium subsequently becomes a nidus for mucus and degenerated cells.²² Tabery confirmed these findings with in vivo photographs, showing aggregations of mucus and cell debris adherent to the corneal surface, adjacent to focal excrescences of the basement membrane.²³ Recently, based on observations made with light microscope and immunohistochemical analysis of 13 cases of filamentary keratitis, Tanioka et al. proposed an alternate theory. They observed that corneal epithelial cells form the core of the filament and an admixture of multiple surface mucins, DNA material, and degenerated conjunctival epithelial cells become wound around the core to produce a braided shape.²⁴ They theorize that blinking then transmits stress to the base of the filament, which in turn incites an inflammatory response below the corneal epithelial basement membrane.

Treatment

Filamentary keratitis can be an acute or chronic condition. Some acute conditions resolve spontaneously, but more often than not, treatment is chronic. Because of the multifactorial cause of filamentary keratitis and variability in patient discomfort, treatment of filamentary keratitis can be frustrating for both the patient and the treating physician.

Initially, improving the ocular surface by treating any underlying dry eye and blepharitis is undertaken. The underlying causes of filament formation, such as keratoconjunctivitis sicca, contact lens over wear, medication toxicity, or ptosis, should initially be identified and treated. For example, resolution of filamentary keratitis in a patient with blepharoptosis has been reported following blepharoptosis surgery.⁸ Because surgical correction of ptosis may lead to increased corneal exposure and subsequent exacerbation of filamentary keratitis, the exact etiology of the condition should be clearly identified prior to electing for surgical intervention.

Medical

The first line of treatment is administration of topical tear film substitutes throughout the day and ointments or higher viscosity tears at bedtime. Ideally, non-preserved tears are used. Lower viscosity tears may be helpful, improving the tear film osmolarity, but more viscous tear substitutes can also provide substantial relief from microscopic corneal abrasions, and so different tear substitutes should be tried and individualized to the patient. There are many different tear formulations available and any of them may be beneficial in a given patient. Chronic treatment of dry eye with topical cyclosporine can be considered. Oral tetracycline derivatives, omega-3 fatty acid supplementation, topical azithromycin, and lid hygiene, may be beneficial to help control meibomian gland dysfunction.

Hamilton and Wood reported a 95% success rate using 5% sodium chloride ophthalmic solution administered four times daily.²⁵ This regimen reportedly works directly at the level of the corneal epithelium by reducing edema of the epithelium and obviating the focal detachments. While our experience with this modality is not quite as dramatic, it certainly can be useful in some patients.

N-acetylcysteine has similarly been used topically for treatment.²⁶ N-acetylcysteine is a mucolytic agent that decreases the viscosity of mucus in the precorneal tear film. The ocular solution is not commercially available and must be compounded without preservatives from the commercially available respiratory preparation (20% solution) to create a 5% to 20% solution. However, the discomfort of the drops and the expense and difficulty of obtaining N-acetylcysteine in a preservative-free status, minimizes the usefulness of this treatment.

A bandage contact lens is frequently successful in treating cases of filamentary keratitis that do not respond to ocular lubrication.²⁷ The contact lens protects the corneal epithelium from the shearing forces of the lids and may help to eliminate or reduce reactive ptosis that often occurs and exacerbates the condition in these patients. High Dk soft contact lenses should be used and are well tolerated with frequent topical artificial tears and a prophylactic topical antibiotic. Patients should be closely monitored because of the inherent risks of contact lens wear in dry eye patients with a suboptimal ocular surface.

Treatment may also target inflammation. Marsh and Pflugfelder demonstrated in a retrospective case series 100% efficacy of topical methylprednisolone for resolution of filamentary keratitis, in the setting of Sjögrens’s syndrome and symptomatic keratoconjunctivitis sicca.²⁸ In their study, satisfactory control of symptoms and filaments was achieved with only short bursts of therapy in most cases.²⁸ Administration of topical nonsteroidal anti-inflammatory drugs (NSAIDs) has also been shown to reduce patient discomfort and accelerate resolution of severe cases.^29,30 The toxicity of NSAIDs on the damaged epithelium in a dry eye patient should be carefully weighed along with their beneficial effect in evaluating the pros and cons of this therapy.