Best way to treat Filamentary Keratitis

Filamentary Keratitis & Best Way to Treat Filamentary Keratitis

Filamentary Keratitis is due to a damaged epithelial or Bowman’s layer of the cornea. A combination of factors (ie, aqueous tear deficiency, mucin deficiency, meibomian gland/oil irregularities, as well as viruses in some cases) combined with the shearing of the eyelids can lead to a vicious cycle of epithelial damage, inflammation, and filament formation which can be very painful. 

Causes of Filamentary Keratitis:

1. #1 is Dryness or Irregularity of the tear film, such as from
a. Meibomian Gland Dysfunction: oil glands at base of eyelashes are clogged
b. Sjögren’s syndrome: immune system dysfunction that can cause dry mouth & arthritis & dry eyes 
2. Too Tight Contact Lenses
3. Graft Versus Host Disease
4. Viruses: FK can occur in EKC-Epidemic Keratoconjunctivitis
5. Any ocular procedure: Surgical procedures, such as corneal transplants (penetrating keratoplasty), cataract surgery, and keratorefractive surgery like LASIK or PRK, can have adverse effects on corneal innervation, tear secretion, and ocular surface health. These procedures have the potential to produce filament formation in patients with tear film and/or ocular surface problems.

We use a tiered approach and recommended the following first steps. If no improvement seen with first treatments, we proceed to higher tiered treatments. 

1. Frequent debridement: we will see a patient every 3-6months and as needed if pain continues to recur from the filament formation.
2. Nonpreserved Artificial Tears 4-8x/day and nonpreserved gels at night at least: best are ones with Sodium hyaluronate and/or polyacrylic acid (carbomer); Preservatives in artificial tears and other drops can make FK worse. Thus avoid ophthalmic preservatives, such as benzalkonium chloride, chlorobutanol, and thimerosal.
3. Meibomian Gland Lid Hygiene: see “Lid Hygiene”
4. Diclofenac sodium 0.1% drops and/or gel (Voltaren) 4x/day often helps FK.
5. Hypertonic Saline like Muro 128 drops 4x/day and ointment at night which promotes adherence of the epithelial cells on the surface to the underlying corneal tissue and, hence, prevents formation of new receptor sites for filament formation.
6. Mucolytic Agents: 10% acetylcysteine N-acetylcysteine (Mucomyst 20% is diluted to a 10% solution with artificial tears. Use of this medication dissolves mucous plaqueskept refrigerated; stable for only 60 days. This is ordered from a compounding pharmacy: 
Foer’s pharmacy locations on website:

7. Punctal Plugs: can be temporary or permanent
8. Therapeutic bandage contact lens
9. Autologous serum: 4x/day or more if nonpreserved
10. Topical steroids if none of the above are helping: start with lease strong & move to stronger steroids if needed (Lotemax/Alrex<FML mild<FML,Predforte<Durezol)
11. In GVHD patients or severe Sjögren’s syndrome we recommend oral tacrolimus and prednisolone therapy.
12. Continue to look out for any signs of Herpes Zoster: treat with anti-virals if dendrites noted.
13. Excimer Laser Phototherapeutic Keratectomy (PTK) helps in some patients unresponsive to above.

Corneal filaments or plaques generally only last a few days to a few weeks; however, they can reoccur but usually not in the same location.

Sandra Lora Cremers, MD, FACS

More information below:

Filamentary Keratitis

Original article contributed by: Tova Mannis, MD
All contributors: Tova Mannis, MD
Assigned editor:
Review: Not reviewed

Disease Entity[edit source]

Filamentary Keratitis ICD-9 370.23

Disease[edit source]

Filamentary keratitis is a condition in which strands (“filaments”) composed of degenerated epithelial cells and mucus develop on and adhere to the corneal surface causing pain and foreign body sensation.

Etiology[edit source]

The etiology of filamentary keratitis is related to an alteration in the components of the tear film and/or abnormalities of the corneal surface. It is associated with a number of ocular surface diseases and conditions.

Risk Factors[edit source]

Any alteration of the tear film or corneal surface can increase the risk for filamentary keratitis. Common risk factors include: aqueous tear deficiency as in keratoconjunctivitis sicca, corneal exposure (e.g. seventh nerve palsy), occlusion abnormalities such as blepharoptosis, ocular surgery (e.g. keratoplasty), systemic diseases with effects on the ocular surface (e.g. Sjogren’s syndrome), extended use of anticholinergic medications, and other ocular surface abnormalities.

General Pathology[edit source]

In filamentary keratitis, there is often an increase in the tear film mucus to aqueous ratio. This is commonly due to a decrease in aqueous tear production, but may also be due to increased production or accumulation of the mucinous component. This alteration in tear film makeup sets the stage for formation of mucoid filaments. Small defects in the corneal epithelium provide an anchoring surface for the filaments. Mucin attaches to the epithelial defect and loose epithelial strands are incorporated into the mucin strand attached to the surface. Filaments may be small sessile adhesions or longer strings that cause irritation and discomfort.

Pathophysiology[edit source]

It is hypothesized that the initial step in the development of filamentary keratitis is damage to basal epithelial cells, epithelial basement membrane, or Bowman’s layer leading to focal detachments of the epithelial basement membrane. Blinking causes these areas of detachment to become elevated leading to irritation, inflammation, and increased mucus production. The sites of epithelial damage provide the scaffold for filaments to develop. A postmortem analysis of a cornea in a patient with this condition revealed inflammatory cells and fibroblasts just beneath the basal epithelium.

Primary prevention[edit source]

Filamentary keratitis generally occurs in association with an underlying condition. The primary preventative measure is lubrication in the setting of dry eye.

Diagnosis[edit source]

History[edit source]

Patients with filamentary keratitis complain of foreign body sensation. They may also have redness, epiphora, blepharospasm, and photophobia.

Physical examination[edit source]

Slit lamp examination reveals filaments (‘mucoepithelioid” strands) adherent to the corneal surface. The filaments can vary from 0.5mm to 10mm in length. A gray colored subepithelial opacity can sometimes be seen at the base of the filament. Blinking causes painful traction on the filaments and may detach them, leaving behind an epithelial defect. Filaments stain best with rose Bengal, but can be seen with fluorescein as well. The location of the filaments can help determine the underlying cause. Filaments due to dry eye syndromes tend to be found in the interpalpebral space, those due to ptosis superiorly, and those due to surgery at the site of the wound or surgical trauma

Signs[edit source]

Signs include multiple filamentary attachments firmly adherent to the corneal surface, decreased aqueous tears, increased mucin in the precorneal tear film, subepithelial opacities at the base of filaments, or frank corneal epithelial defects.

Symptoms[edit source]

Symptoms can vary from mild to severe foreign body sensation that is exacerbated by blinking and is associated with photophobia, blepharospasm, and epiphora. The patient may also complain of a red eye.

Clinical diagnosis[edit source]

The diagnosis of filamentary keratitis is made clinically with history and slit lamp biomicroscopy.

Diagnostic procedures[edit source]

Slit lamp biomicroscopy demonstrates firmly adherent filaments on the corneal surface. A Schirmer test may be helpful in establishing the diagnosis of a dry eye syndrome.

Laboratory test[edit source]

There is no specific laboratory testing indicated for filamentary keratitis. However, if suspicion is high for underlying systemic disease that has not yet been diagnosed such as Sjogren’s syndrome, a systemic work-up may be indicated.

Differential diagnosis[edit source]

Corneal filaments are pathognomonic for this condition, but there is a broad differential for the underlying cause of filamentary keratitis. The differential for underlying disease includes tear film abnormalities, lid malpositions, previous ocular surgery, and toxic keratopathies.

Management[edit source]

General treatment[edit source]

The treatment of filamentary keratitis can be challenging and is often chronic. Paramount in the overall treatment of filamentary keratitis is management of underlying conditions such as the dry eye syndromes, medication toxicity, contact lens overuse, and blepharoptosis.

Medical therapy[edit source]

First line treatment includes topical therapy with lubricant drops and ointment. Low water-content bandage contact lenses may be helpful temporarily in cases that do not respond to lubrication alone. The bandage contact lens should be used in combination with artificial tears and prophylactic topical antibiotic. A mucolytic agent such as 10% N-Acetylcysteine can be used topically to decrease the viscosity of the mucinous component of the tear film. Topical sodium chloride drops may also help by deturgescing and compacting the corneal epithelium.

Medical follow up[edit source]

Patients should be re-examined 3-4 weeks after the initiation of medical therapy. Bandage contact lenses should be left in place for no more than one month.

Surgery[edit source]

Filaments can be removed at the slit lamp using jeweler’s forceps. Care should be taken to avoid disrupting the epithelium at the base of the filament if possible. Manual removal of the filaments may help in alleviating symptoms temporarily but is only a temporizing measure and is not successful without concurrent medical treatment. Punctal occlusion may also be helpful in cases of underlying aqueous tear deficiency.

Complications[edit source]

Infectious keratitis is a potential complication, especially when a bandage contact lens is used for therapy.

Prognosis[edit source]

Prognosis depends upon effectiveness in managing the predisposing condition, but is generally good. Patience is often required in the chronic management of this condition.

References[edit source]

Davidson RS, Mannis MJ. Filamentary Keratitis. In: Krachmer JH, Mannis MJ, Holland EJ, editors. Cornea. Vol 1. 3rd ed. Philadelphia: Elsevier/Mosby; 2011. P. 1093-96.
Van Meter WS, Katz D, Cook BG. Filamentary Keratitis. In: Holland EJ, Mannis MJ, Lee WB, editors. Ocular Surface Disease: Cornea, Conjunctiva, and Tear Film. Philadelphia: Elsevier Saunders; 2013. P. 213-16.
Zaidman GW, Geeraets R, Paylor RR, et al. The histopathology of filamentary keratitis. Arch Ophthalmology 1985; 103: 1178-81.
Tanioka H, Yokoi N, Komuro A, et al. Investigation of the corneal filament in filamentary keratitis. Invest Ophthalmol Vis Sci 2009; 50:3696-702.

Fighting Filamentary Keratitis

Don’t mistake this complex condition for a more typical ocular surface disorder.

By Alan G. Kabat, OD, and Joseph W. Sowka, OD


 One of the most common complaints we encounter in the clinical setting is ocular discomfort, typically in the form of dryness, irritation and foreign body sensation. These annoying symptoms are among the most pervasive and vague. While dry eye syndrome is an exceedingly prevalent diagnosis in our adult population, we must differentiate aqueous deficiency or evaporative dry eye from more complex and, potentially, refractory conditions. Filamentary keratitis is one such condition. 
In this column, we’ll discuss the key diagnosing filamentary keratitis, as well as the various treatment modalities for controlling it.
At-Risk Patients While the exact prevalence of filamentary keratitis is unknown, experience suggests it’s more common in elderly patients, females and those with connective tissue disorders or immune deficiency.1,2 The exact nature and severity of symptoms ranges from mild ocular discomfort to pronounced pain. Tearing, photophobia and even blepharospasm may accompany these symptoms in severe cases.3  
Associated Signs Signs associated with filamentary keratitis include ocular hyperemia, particularly in the limbal area, as well as a pseudoptosis in some individuals. Corneo-mucus filaments are the hallmark finding. These usually consist of a focal “head,” which may

Corneal filaments stained with lissamine green are evident in this red, inflamed eye.
firmly adhere to compromised areas of the corneal epithelium, and a strand-like “tail” of varying length that extends across the ocular surface. Applying vital dyes, such as lissamine green, rose bengal and sodium fluorescein, can aid biomicroscopic filament visualization.3 A rapid tear break-up time and punctate epithelial keratopathy may also be present.
Not only does filamentary keratitis accompany dry eye, it also appears alongside a variety of other ocular surface disorders, including superior limbic keratoconjunctivitis, prolonged patching following ocular surgery, epitheliopathy due to aerosol or radiation keratitis, herpetic keratitis, recurrent corneal erosion, neurotrophic keratitis and bullous keratopathy.1-5
Mechanism Research suggests that individual filaments consist of desquamated corneal epithelial cells (at their cores), surrounded primarily by degenerating conjunctival epithelial cells and entwined in a thick layer of membrane-associated mucins.4,5 Patients with filamentary keratitis appear to suffer progressive dysfunction within the basal epithelial and Bowman’s layers of the cornea, leading to focal detachments at the level of the basement membrane. Under constant shear pressure from the eyelids, these corneal foci become inflamed, and sloughing of epithelial cells may ensue.6 At the same time, frictional stress from blinking and eye movement combined with diminished tear volume and ocular surface inflammation results in abnormal tear mucin production and degeneration of conjunctival epithelial cells.5  
These combined elements form filaments, which may appear clinically as long strands, large clumps or irregular dendriform deposits, depending upon whether they are stretched, twisted or tightly coiled.4,7 The filaments are motile in the tear film, but have an affinity for compromised areas of the corneal surface, where they form strong adhesions. Lid movement across these bound filaments induces vertical traction and further shearing of the corneal epithelium with each blink, resulting in microtrauma and stimulation of the pain-sensitive corneal nerves. Thus, a vicious cycle of epithelial damage, inflammation and filament formation ensues.
Management The management of filamentary keratitis is aimed at alleviating the stressors that cause ocular surface inflammation and epithelial degradation. Elimination of the filaments is the initial step, but identifying and treating the underlying pathology is vital to breaking the cycle of this disease. You can remove large filaments mechanically using fine-tipped forceps at the slit lamp under topical anesthesia. Recognize, however, that this process can further contribute to epithelial damage and should be undertaken only by skilled and experienced clinicians. Ocular lubricants are helpful in addressing discomfort and also stabilizing the tear film in mild to moderate cases. 
In recalcitrant cases, topical N-acetylcysteine can help to dissolve cornea-bound mucus plaques.1 This mucolytic agent is employed primarily as an oral inhalant for patients with bronchial disease (e.g. emphysema, cystic fibrosis), and hence it must be prepared by a compounding pharmacist for topical ophthalmic use. In those with filamentary keratitis secondary to chronic dry eye disease, we have seen excellent results with 10% acetylcysteine eye drops used four times daily for several weeks. Other treatments for refractory cases of filamentary keratitis may include the use of bandage soft contact lenses, amniotic membrane therapy or Botox (onabotulinumtoxinA, Allergan) injection to the pretarsal orbicularis muscle.2,8
Long-term Treatment Addressing the underlying ocular surface disease may ultimately prove more challenging than temporary elimination of corneal filaments. Because an inflammatory etiology is often assumed, the use of anti-inflammatory drugs such as corticosteroids and non-steroidal agents has been widely advocated, often with clinical success.9,10 In those cases where dry eye disease is identified as the primary etiology of filamentary keratitis, short-term use of corticosteroids such asLotemax (loteprednol etabonate 0.5%, Bausch + Lomb) QID combined with long-term use of Restasis (cyclosporine, Allergan) BID can help.11  
Severe cases may require treatment with autologous serum eye drops, which—as the name implies—are derived from the patient’s own blood serum.12,13 
Therapy for filamentary keratitis may take weeks or even months before adequate resolution is realized, depending on the etiology, severity of presentation and aggressiveness of care. Patients should understand that the underlying condition is often chronic and filaments may recur after therapy is discontinued. Proper long-term care includes ongoing treatment for ocular surface disease with close monitoring, i.e., three to four times annually. In addition, patients with chronic or severe dry eye disease may benefit from a rheumatologic investigation to determine the presence of Sjögren’s syndrome.14
Dr. Kabat is a consultant to Alcon Laboratories, Bio-Tissue and BlephEx. Neither he nor Dr. Sowka has any direct financial interest in the products mentioned in this article.

1. Albietz J, Sanfilippo P, Troutbeck R, Lenton LM. Management of filamentary keratitis associated with aqueous-deficient dry eye. Optom Vis Sci. 2003 Jun;80(6):420-30. 2. Gumus K, Lee S, Yen MT, Pflugfelder SC. Botulinum toxin injection for the management of refractory filamentary keratitis. Arch Ophthalmol. 2012 Apr;130(4):446-50.  3. Diller R, Sant S. A case report and review of filamentary keratitis. Optometry. 2005 Jan;76(1):30-6. 4. Tabery HM. Filamentary keratopathy: a non-contact photomicrographic in vivo study in the human cornea. Eur J Ophthalmol. 2003 Aug-Sep;13(7):599-605. 5. Tanioka H, Yokoi N, Komuro A, et al. Investigation of the corneal filament in filamentary keratitis. Invest Ophthalmol Vis Sci. 2009 Aug;50(8):3696-702. 6. Zaidman GW, Geeraets R, Paylor RR, Ferry AP. The histopathology of filamentary keratitis. Arch Ophthalmol. 1985 Aug;103(8):1178-81. 7. Pandit RT. Dendriform filamentary keratopathy. Cornea. 2009 Jan;28(1):123-5.  8. Suri K, Kosker M, Raber IM, et al. Sutureless amniotic membrane ProKera for ocular surface disorders: short-term results. Eye Contact Lens. 2013 Sep;39(5):341-7. 9. Perry HD, Doshi-Carnevale S, Donnenfeld ED, Kornstein HS. Topical cyclosporine A 0.5% as a possible new treatment for superior limbic keratoconjunctivitis. Ophthalmology. 2003 Aug;110(8):1578-81. 10. Terry G Coursey, Cintia S de Paiva. Managing Sjögren’s Syndrome and non-Sjögren Syndrome dry eye with anti-inflammatory therapy. Clin Ophthalmol. 2014; 8: 1447–1458. 11. Sheppard JD, Donnenfeld ED, Holland EJ, et al. Effect of loteprednol etabonate 0.5% on initiation of dry eye treatment with topical cyclosporine 0.05%. Eye Contact Lens. 2014 Sep;40(5):289-96. 12. Jirsova K, Brejchova K, Krabcova I, et al. The application of autologous serum eye drops in severe dry eye patients; subjective and objective parameters before and after treatment. Curr Eye Res. 2014 Jan;39(1):21-30.  13. Hussain M, Shtein RM, Sugar A, et al. Long-term use of autologous serum 50% eye drops for the treatment of dry eye disease. Cornea. 2014 Dec;33(12):1245-51.  14. Shen L, Kapsogeorgou EK, Yu M, et al. Evaluation of salivary gland protein 1 antibodies in patients with primary and secondary Sjogren’s syndrome. Clin Immunol. 2014 Nov;155(1):42-6.

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