A New Theory on 3 and 9 O'clock Staining

BY GARY R. BELL, O.D., M.S.Ed.

Examining the dynamics of fluids in motion helped this practitioner develop a new explanation for 3 and 9 o'clock staining.

Peripheral corneal desiccation (PCD), more commonly called 3 and 9 o'clock staining, has long been an aggravating problem related to the wear of hard and RGP contact lenses. The condition can often be detected via slit lamp examination using the cobalt blue filter and fluorescein stain, with areas of confluent erosion evident on either side of the contact lens. A study by Henry et al. (1987) found that 53 percent of recently fitted RGP patients demonstrated this characteristic desiccation.

PATHOLOGICAL SEQUELAE FROM 3 AND 9 O'CLOCK STAINING

There is evidence that chronic, substantial 3 and 9 o'clock staining can lead to permanent corneal opacification, neovascularization and pterygium formation. Grohe and Lebow (1989) termed these long-term complications vascularized limbal keratitis. Tripathi et al. (1994) took a histological approach, finding reduced numbers of microvilli in the desiccated areas. They also noted basal cell edema of the affected epithelium with a loosening of the hemidesmosome attachments at the basement membrane. With advancement, Bowman's membrane became obliterated, which the authors believed was a precursor to neovascularization.

Collings, a physicist, noted that the microfilaments in tumor cells "...seem to be less ordered than in normal cells". This suggests an association between the regional microfilament disruption of chronic PCD and the benign tumor-like development seen in cases of RGP wear-related pterygium.

EXISTING THEORIES

A number of theories about the etiology of 3 and 9 o'clock staining have been suggested.

Barabas (1967) proposed that the cause was tear deficiency combined with lid gaping at the lens edge that inhibits the spread of mucus.

Graham (1968) proposed that dry spots were the cause, resulting from a three part mechanism of lens edge bridging, friction of the lens edge against the peripheral cornea and patient blink irregularities. He considered altered and incomplete blinks to be the most important of the three factors.

Sarver et al. (1969) performed clinical research that seemed to confirm the importance of contact lens blink alteration. They found that staining often persisted in the non-contact lens wearing eye of a monovision PMMA contact lens patient, although the pattern of stain in the non-wearing eye was diffused over a large area of the lower cornea, not just the 3 and 9 o'clock positions. Korb and Korb (1970) found a similar result.

Tripathi et al. (1994) considered 3 and 9 o'clock staining to be dry eye related, specifically that increased tear osmolarity destabilizes tear film properties and starts the cascade of events.

McDonald and Brubaker (1971) proposed that the peripheral curve meniscus of hard lenses increases the tear volume demands for marginally dry eyes. According to their theory, the meniscus draws nearby fluid to the lens edge, drying adjacent corneal areas, especially in cases of with-the-rule astigmatism.

Stein et al. (1990) attributed 3 and 9 o'clock staining to tear dehydration, bridging at the lens edge and an expression effect. The expression effect refers to compression of fluid under the lens with the blink in with-the- rule astigmats, forcing the fluid away from the center and toward the horizontal edges.

Holden et al. (1988) demonstrated the ability to reduce PCD by reducing peripheral curve clearance and to increase it by increasing edge lift. A recent study by Schnider et al. (1997) found that moderate edge lift was most efficacious, with very low edge lift increasing desiccation. That study also correlated larger sized lenses and lid attachment fitting with decreased PCD among a group predisposed to staining.

Only one author found a difference in RGP material performance in terms of degree of peripheral corneal desiccation.

THE LAWS OF PHYSICS APPLY TO THE EYE

The genesis of a new theory grew out of thoughts on friction, which seems to be a ubiquitous source of discomfort in contact lens wear. Since the on-eye environment of the contact lens is fluid, I investigated the field of fluid dynamics.

In the fluid state, friction becomes viscous drag. A number of formulas exist to compute fluid forces -- Stokes Law, Couette flow equations and the Bernoulli effect, for example -- but these are not applicable to contact lens situations, where interruptions in tear flow caused by blinking makes the environment a turbulent flow. Turbulence is characterized by chaos, and is considered a classic example of the mathematics of chaos. While predictive computations are nearly impossible, general tendencies from fluid dynamics seem to be applicable. Greater turbulence, for instance, is known to greatly increase viscous drag. One could say that the more turbulence in the tear flow that a contact lens produces, the more discomfort and tissue abrasion the wearer is likely to experience. Tear film turbulence is the basis for my theory.

LESSONS FROM AERODYNAMICS

It might seem irrelevant to examine the science of aerodynamics, but remember that air shares with the tear film the property of being a fluid. In aerodynamics, the following factors are associated with increased viscous drag: increased viscosity of the fluid, skin or surface drag factors, shape drag factors, increased mass, increased velocity, increased lift and boundary layer separation. Table 1 displays how these fluid dynamics factors manifest in contact lens wear. The new theory contends that all of these factors can contribute to 3 and 9 o' clock staining. One additional factor is tear film thickness, which relates to dry eye problems. According to Couette flow formulas, the thicker the fluid is, the more drag forces can dissipate before reaching the cornea.

THE NEW THEORY

My theory posits that 3 and 9 o'clock staining is caused by viscous drag secondary to fluid turbulence produced by the blink and lens movement. As the lens moves down on the cornea with the blink, a circumferential wake is generated (Fig. 1). Within this wake are swirling vortices of fluid particles that bombard the cornea. They collide with the semiorganized mucus gel of the tear film first, disrupting its delicate structure and obliterating the microvilli. Then the turbulent forces begin eroding the denuded corneal epithelium. Another circumferential wake occurs with the up-blink (Fig. 2). The whole process repeats with the commencement of the next blink. In both directions, the areas that are repeatedly impacted with elevated levels of viscous drag are the 3 and 9 o'clock areas (Fig. 3).

Knowing how surface waves move reveals how the swirling actions of fluid particles could produce the abrasive forces of PCD. The source of fluid displacement, whether it's the wind or a moving contact lens, causes circular cylinders of fluid particles to spin. These spinning particles then interact with the adhesive properties of other fluid molecules, propagating the process (Fig. 4). The wave is a phased phenomenon, with the crest located where the inertia of the swirls are at their uppermost peak and the trough located where the phased forces are pointed down. The process continues downward below the surface of the tear film and cornea but is dissipated by the fluid's cohesive properties and distance. In a shallow, unsteady environment, the regularity of the process breaks down into chaotic interactions.

Lens size modification seems to confirm the wake theory. If we increase the size of a lens for a patient suffering from 3 and 9 o'clock staining, the newly covered areas of the cornea will heal rapidly because we have removed these areas from the wake of edge drag. Areas still beyond the edge will continue to exhibit desiccation.

FIG.3: SUPERIMPOSED WAKES REVEALING ZONES OF CHRONIC TURBULENCE.

CORRELATING THE NEW THEORY TO PREVIOUS THEORIES

The new theory has some compatibility with existing theories. The compression/expression aspects of Stein, Slatt and Stein's theory form a fluid dynamics theory with a different mechanism -- a Bernoulli effect mechanism. They imply that flow compression occurs under the lens, so we'd expect staining to occur under the lens. Such a compression/expression approach may have some application in understanding the central staining typical of a flat-fitted lens, but it seems inconsistent with the characteristic 3 and 9 o'clock staining pattern.

The correlation of blink anomalies to PCD, as found by Sarver et al. and Korb and Korb, can be explained by thinning and increasing viscosity of the tear film. The staining of eyes not wearing lenses in monovision cases is diffused over a larger area of the inferior cornea. I believe the staining in both wearing and non-wearing eyes is due to increased viscous drag. In the non-wearing eye, the activator of desiccation is tear film thinning from incomplete blinking and reduced blink frequency. In the wearing eye, the added shear forces of the contact lens intensify tear film turbulence, forces which are at their maximum at the 3 and 9 o'clock positions.

McDonald and Brubaker's peripheral curve meniscus theory has some merit in that the meniscus created by the peripheral curve can contribute to tear film thinning. Since the total tear film volume in a normal eye is less than three drops of fluid, even the small increase of a peripheral curve meniscus could contribute to tear film thinning. However, the hypothesis that a localized thinning of the tear film occurs at the site of 3 and 9 o' clock staining seems implausible because fluids have little or no resistance to shear stress, and any localized thinning of the tear film would be immediately filled in by the flow of adjacent fluid.

FIG. 4: FLUID AGGREGATES MOVE IN PHASED, CIRCULAR EDDIES WHEN WAVE IMPULSES ACT ON THE BODY OF FLUID.

SUMMARY

I have presented a new theory for the cause of 3 and 9 o'clock staining in PMMA and RGP lens wear. Essentially, I postulate that lens movement causes a circumferential wake propagated in both the up- and down-blink and that these wakes throw off swirling particles of fluid which slowly abrade the 3 and 9 o'clock areas of the cornea. The theory is based on the physics of fluid dynamics and viscous drag applied to the contact lens environment for the first time.

Assuming that fluid dynamics principles are valid and applicable to the clinical fitting of contact lenses, I suggest corrective measures to re-
duce 3 and 9 o'clock staining (Table 2). Note that the suggestions presented here are not significantly different than measures that have evolved through clinical trial and error.

I hope this paper will help systematize the RGP fitting situation and increase the scientific basis of clinical trouble-shooting. Due to the chaotic nature of turbulent flow, detailed laboratory measurements will be required to quantify the shear forces involved in contact lens wear. CLS

References are available upon request from the editors. To receive references via fax, call (800) 239-4684 and request document #31.