Conjunctivochalasis (CCh) is often overlooked as a normal variation associated with aging. CCh tends to be associated with aqueous tear deficiency dry eye (ATD) and has been mistakenly believed to be nonspecifically caused by ATD. CCh tends to be bilateral and can be localized in the nasal, central or temporal part of the lower and upper eyelid margins.
Mild CCh may cause dry eye symptoms by contributing to or aggravating a pre-existing unstable tear film due to ATD; moderate CCh may cause episodic tearing by impeding tear clearance; and severe CCh may induce subconjunctival hemorrhage.1 Even though ATD is frequently associated with CCh, both conditions can independently cause dry eye- like symptoms and can be distinguished from one another according to symptomatology, past medical history and clinical signs.2 Differentiation of CCh from ATD is the first step toward effective treatments for dry eye.
Time of day. Patients with either ATD or CCh complain of dryness, but the dryness in ATD tends to be worse as the day progresses due to progressive exposure and desiccation. In contrast, patients with CCh tend to be worse in the morning just after awakening.
Close work. Patients with CCh complain of blurry vision and pain in addition to dryness. This is because CCh folds are increased in down-gaze during reading. In contrast, in ATD patients the dryness tends to be worsened in up-gaze—such as while working with a computer screen—because the interpalpebral exposure zone increases during up-gaze.
Vigorous and frequent blinking. Because vigorous and frequent blinking results in spreading of the redundant conjunctiva and worsening of CCh at the 6 o’clock position, both dryness and blurry vision are aggravated. In contrast, increasing blinking shortens the interblink interval, stabilizing the tear film and improving symptoms in ATD dry eye.3
Because of poor attachment of redundant conjunctiva onto the sclera in patients with CCh, subconjunctival vessels are prone to rupture during blinking or rubbing. Therefore, patients with CCh tend to have a past history of subconjunctival hemorrhage. Occurrence of this sign should prompt the clinician to look into CCh as a potential etiology. Although subconjunctival hemorrhage tends to occur in the inferior bulbar conjunctiva, where CCh is worse, it can also occur in the upper bulbar conjunctiva, supporting the notion that CCh is not confined to the lower bulbar area.
Although both ATD and CCh destabilize the tear film with a short tear breakup time, the following signs can differentiate them:
Dye staining. Fluorescein can be used to highlight the path (tear meniscus) and distribution of aqueous tears. Such a fluorescein-stained pattern is interrupted or obliterated by CCh but not by ATD. This is especially helpful if a Kodak Wratten yellow filter #12 is used. Using this technique, CCh folds can be easily demonstrated in both lower and upper tear meniscus. Furthermore, fluorescein staining also helps reveal anterior migration of the mucocutaneous junction of the lid in contact with CCh, which is presumably caused by overspill of aqueous tears due to obliteration of the tear meniscus by CCh. As a result, regional lid margin inflammation ensues and is frequently mistaken for blepharitis. Importantly, the lid margin adjacent to CCh frequently manifests meibomian gland dysfunction and lipid tear deficiency, which may also facilitate aqueous overspill to the skin.
By interrupting or obliterating tear meniscuses, CCh destabilizes the tear film immediately above the CCh area, resulting in dye staining that preferentially decorates the area above the redundant conjunctival fold in a linear pattern. Conversely, in pure ATD, an unstable tear film tends to develop at the interpalpebral exposure zone, which is characteristically stained by rose bengal.
Delayed tear clearance. Although patients with ATD and CCh complain of similar dry eye symptoms, the aqueous tear secretion of the former is low, while that of the latter may be normal. Our data suggest that ocular surface inflammation aggravates CCh.4 In CCh, inflammation might arise from the lid margin or meibomian gland dysfunction. We have noted that patients with CCh frequently exhibit delayed tear clearance (turnover). Therefore, inflammation, if pre-existing, could conceivably be worsened by delayed tear clearance.
It is not clear at the moment whether delayed tear clearance is pre-existing or whether CCh causes delayed tear clearance by obliterating the tear meniscus. In any event, once it sets in, delayed tear clearance will cause episodic tearing (epiphora) in patients with ATD plus CCh. Furthermore, delayed tear clearance aggravates ocular surface inflammation,5 leading to inflammatory symptoms that are particularly severe first thing in the morning and frequently are associated with swollen puncta. Patients with delayed tear clearance also tend to develop medicamentosa and sensitivities to preservatives.
|Dryness||Blinking||Hemorrhage History||Dye Staining||Tear Clearance|
|ATD||Worse in p.m.|
Worse in up-gaze.
|Vigorous blinking improves symptoms.||Less-frequent history of subjunctival hemorrhage.||Low tear meniscus without interruption.|
Staining of interpalpebral (exposure) zone.
|Can be normal.|
|CCh||Worse in a.m. and while reading.|
Worse in down-gaze.
|Vigorous blinking without symptoms.||More-frequent history of subconunctival hemorrhage.|
Tear meniscus interruption or obliteration.
Staining of CCh and nonexposure zone.
Staining of anterior migration of mucoutaneous junction.
|Frequently delayed with swollen puncta.|
|Note: Tear clearance can be masured by the fluorscein clearance test.5|
As CCh is associated with inflammation and delayed tear clearance, preservative- free corticosteroids effectively treat approximately 70 to 80 percent of CCh patients on a temporary basis. Pure ATD will also respond favorably to nonpreserved steroids, which suppress ocular surface inflammation. Nevertheless, it should be noted that if delayed tear clearance is also reversed (corrected) by this treatment, dryness might worsen. In this case, punctal occlusion by plug or cautery will help.
In patients with severe CCh and those patients with CCh who do not respond to medical treatment, surgery is the only option to recover a smooth ocular surface, which guarantees stable distribution of the tear film.
1 Meller, D. and S. C. G. Tseng. Surv Ophthalmol
2 Di Pascuale, M. A. et al. Br. J Ophthalmol
2004. In press.
3 Nakamori, K. et al. Am J Ophthalmol
4 Meller, D. et al. Invest Ophthalmol Vis Sci
5 Prabhasawat, P. and S. C. G. Tseng. Br. J Ophthalmol
_____________________________Drs. Di Pascuale and Espana are fellows in ophthalmology and Dr. Tseng is medical director of both the Ocular Surface Center and the Ocular Surface Research & Education Foundation, Miami. This research is supported in part by an unrestricted grant from the foundation.