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The Issue of Contact Lens Related Corneal Neovascularization

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Dr. Barry Weissman joined the Southern California College of Optometry at Marshall B. Ketchum University in 2012 as a Professor. Dr. Weissman has experience in private practice, and was a member of the Contact Lens Service of the Hadassah-Hebrew University Medical School Department of Ophthalmology in Jerusalem, Israel. He then went to UCLA as an Assistant Professor and retired as Professor of Ophthalmology and Chief of the Contact Lens Service of the Jules Stein Eye Institute in 2012 when he joined MBKU.

“On behalf of the entire university, I’d like to congratulate Dr. Weissman for this prestigious honor,” said University President Kevin Alexander, O.D., Ph.D. “Since 2012, Barry has dedicated himself to the Southern California College of Optometry. He has mentored optometric students ensuring that the doctors who graduate from our university are prepared for today’s competitive environment and shifting health care environment.”

Dr. Weissman is a Fellow of the American Academy of Optometry, and a Diplomate in its Cornea, Contact Lens and Refractive Technologies section. He has received numerous awards, including the William Feinbloom and Max Schapero Awards of the AAO, and the BCLA Medal from the British Contact Lens Association. He was honored with the Nathan Springer Lectureship at the University of Alabama School of Optometry.

He has served on the Examination Committee of the California State Board of Optometry and as both an Expert Examiner and an Item Writer for the National Board of Examiners in Optometry. He has also served as an advisor to the FDA Ophthalmic Devices Panel. Dr. Weissman has authored approximately 150 research papers and textbook chapters, as well as several texts.

“I’m thrilled to enter as president of COA at such an exciting time,” says Dr. Weissman. “We have immense opportunity ahead of us with an outstanding leadership to guide us to new opportunities in the profession of optometry.”

Among his goals, Dr. Weissman seeks to increase access to affordable eye health and vision care. Additionally, he will actively encourage the development of leadership at the student, staff and doctor level to ensure a continued promising future for optometry in California.

For more than a century, the COA has been dedicated to making optometry a stronger, better and more visible profession. Its mission is to support and advance the profession of optometry to assure quality health care for all Californians. Dr. Weissman will lead the COA’s Board of Trustees as their President for one year.


The Issue of Contact Lens Related Corneal Neovascularization 

There are a variety of complications of contact lens wear encountered by the clinician in both asymptomatic (Forister et al 2009) and symptomatic populations (Lee et al 2012).  Of these, only direct microbial corneal infection, usually associated with poor care and/or extended wear (Keay & Stapleton 2008), and corneal neovascularization, pose direct threats to vision.

Of this pair of, by definition, more severe contact lens complications, microbial keratitis is usually acute and symptomatic, while corneal neovascularization is usually asymptomatic initially and chronic; slow in progression and hence subject to clinical intervention at many opportunities before vision is affected; provided patients present for contact lens evaluations at reasonable intervals (e.g. 6-12 months). Of interest, reports of contact lens related vascularization of the normally avascular clear cornea have been documented since at least 1929 (Lauber 1929).

Early contact lens wear related corneal neovascularization usually presents as a superficial pannus, commonly at the superior limbus, under the upper lid. As this is likely related to hypoxia (Duffin et al 1982; Chan and Weissman 1996), it is principally associated with extended wear of soft contact lenses, and/or highly minus powered soft lenses and occurs but is not common. The location is likely dictated by the coverage of this area by the upper lid with the additional imposition of a CL edge, particularly if high in minus power (and therefore thick), leading to further decrease in the availability of oxygen at this site.

Physiologically, it is known that hypoxia causes cells to release inflammatory cytokines (e.g. VEGF) which can induce new vascular growth (Shweiki et al 1992). This is as true in the cornea as it is in the retina.

Occasionally toric hydrogel contact lenses can also elicit such a pannus -- but at the lower limbus, where these lenses are thickest by design (Westin et al 1989).

The wear of GP CLs has minimal risk of causing neovascularization but might, if of low oxygen permeability, similarly induce corneal vessels if these lenses chronically ride over the corneal limbus with minimal movement (Duffin et al 1982).

Many other corneal disease conditions, however, can lead to similar appearing pannus, for example phlytenulosis secondary to chronic bacterial blepharitis. More severe disease (e.g .herpetic keratitis, interstitial keratitis due to lues or TB, corneal transplantation, etc) can also lead to corneal neovascularization but these vessels are usually at the depth of the corneal insult (eg often deep in the stroma and not necessarily superficial). Shah et al (1998) found that keratoconic corneas could occasionally also show deep stromal neovascularization, suggesting to these authors that keratoconus might be a disease with low grade inflammation (consistent with other research (e.g. Lema and Duran 2005)).

But even though the “normal” soft lens pannus appears mild and only slowly progressive, do not be complacent in the diagnosis and management of contact lens related corneal neovascularization. Patients can eventually suffer vision loss (Wong et al 2003). Such loss may be due directly to the vessels’ presence if they reach the corneal apex, but even more so indirectly when/if the vessels leak lipids into the normally transparent corneal stromal apex. It is the nature of new blood vessels, whether in the corneal stroma or the retina to be “leaky”; we also know this from our understanding of the pathophysiology of diabetic retinopathy. It is likely that any systemic hyperlipidemia will accentuate this process, as was true in the case reported by Wong et al (2003). These vessels may also break easily leading to intracorneal hemhorrhage (Donnenfeld et al 1991); this is quite rare but the author has seen several patients with this condition.

Management of contact lens wear induced corneal neovascularization in the second decade of the 21st century, however, is much improved compared to previous years, with the availability of modern contact lens designs and highly oxygen permeable materials.

Many patients can be helped by just decreasing wear from extended to daily use, and perhaps increasing the oxygen permeability of the lenses they use (e.g. refitting from a hydrogel to a silicone hydrogel). Photo-documentation to monitor vessel length is helpful in these cases as the blood column often continues to be observable in the vessels.

Another usually successful technique is to refit to rigid GP CLs (Chan & Weissman 1996), provided as noted above that such GP lenses do not ride over the limbus. With GP lenses, and strictly daily wear, commonly the vessels become ghosts so that photo-documentation is not as helpful.

Both topical steroid treatment and laser closure of the vessels (and some other surgical procedures as well) have been clinically attempted but without much documented success and with risks of additional problems.

If vision dysfunction is severe, and especially if due to lipid deposition in the corneal apex, unfortunately, it is most likely that the patient will require a corneal transplant, perhaps lamellar or penetrating, to restore vision.

The final clinical maneuver would be to discontinue CL wear, if new corneal vessels continue to grow after the patient is restricting wear to daily use and the lenses are of the best mechanical fit and highest oxygen transmissibility available. This would be very unlikely, in the author’s clinical experience, unless the lenses used were sclerals, wherein oxygen availability may be limited not only by the transmissibility of the lens itself but also by the thickness of the tear layer between the lens and the cornea (Jaynes et al 2015).

In conclusion, while corneal neovascularization is one of the common complications of contact lens use, such new corneal vessels can also be observed as signs of other corneal diseases. The clinician must therefore consider other causes and work through an appropriate differential diagnosis process.

If contact lenses are the only likely cause, the clinician should consider treatment options and monitor at reasonable intervals to provide his or her patients with successful outcomes.



Forister JF, Forister EF, Yeung KK, Ye P, Chung MY, Tsui A, Weissman BA.Prevalence of contact lens-related complications: UCLA contact lens study. Eye Contact Lens. 2009;35(4):176-80

Lee SY, Kim YH, Johnson D, Mondino BJ, Weissman BA. Contact lens complications in an urgent-care population: the University of California, Los Angeles, contact lens study. Eye Contact Lens. 2012;38(1):49-52.

Keay L, Stapleton F.Development and evaluation of evidence-based guidelines on contact lens-related microbial keratitis. Cont Lens Anterior Eye. 2008;31(1):3-12.

Lauber H. Praktisch durchfurung von myopiekorrektion mit kontaktglassern. Klin Monatsbl Augenheilkd. 1929;82: 535-542.

Duffin RM, Weissman BA, Ueda J. Complications of extended wear hard contact lenses on rabbits. Int. Contact Lens Clin 1982; 9, 101-105.

Chan WK, Weissman BA.Corneal pannus associated with contact lens wear. Am J Ophthalmol. 1996;121(5):540-6.

Shweiki D, Itin A, Soffer D, Keshet E. Vascular endothelial growth factor induced by hypoxia may mediate hyoxia induced angiogenesis. Nature 1992;359:843-845.

Westin, E., McDaid, K. and Benjamin, W.J. Inferior corneal vascularization associated with extended wear of prism ballasted toric hydrogen contact lenses. Int. Contact Lens Clin 1989; 16, 20-22.

Shah SS, Yeung KK, Weissman BA. Contact lens related deep stromal neovascularization. Cont Lens Ant Eye. 1998;25:128-136.

Lema I, Durán JA. Inflammatory molecules in the tears of patients with keratoconus. Ophthalmology. 2005;112(4):654-9.

Wong AL, Weissman BA, Mondino BJ. Bilateral corneal neovascularization and opacification associated with unmonitored contact lens wear. Am J Ophthalmol. 2003;136(5):957-8.

Donnenfeld ED, Ingraham H, Perry HD et al. Contact lens related deep stromal intracorneal hemhorrhage. Ophthalmology 1991;98:1793-1796.

Jaynes JM, Edrington TB, Weissman BA. Predicting scleral GP lens entrapped tear layer oxygen tensions. Cont Lens Anterior Eye. 2015;38(1):44-7. 


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