Understanding the conundrum of conjunctivochalasis
Conjunctival chalasis, or conjunctivochalasis (Cch), is a commonly observed condition in our everyday patient care experiences. Because it is so common, and because a majority of patients are asymptomatic, optometrists seldom feel the need treat.
Conjunctival chalasis, or conjunctivochalasis (Cch), is a commonly observed condition in our everyday patient care experiences. Because it is so common, and because a majority of patients are asymptomatic, optometrists seldom feel the need treat.
However, some patients may break from the typical mold and present with a myriad of complicated complaints, which could not only merit further investigation but also discussion and treatment.
Conjunctivochalasis, an age-dependent, bilateral condition of redundant conjunctiva, is seen in over 98 percent of individuals over the age of 60.1 Within that age range, we may see it more often in patients who have concurrent dry eye or meibomian gland disease, though those often go hand in hand with the aging population and can all cause similar symptoms.
Related: Sagging lids and conjunctiva are an OD’s responsibility
As our median population and patient base increases in age, we may be seeing it with increasing frequency. It now becomes more important to keep this condition and its various presentations and treatments nearer the forefront of our differential diagnosis list.
Structural changes
Slit-lamp examination of the bulbar conjunctiva reveals loose, redundant, nonedematous tissue most often located between the globe and the lower eyelid margin.2 Conjunctivochalasis typically begins at the limbus and though mostly observed inferiorly and temporally on the bulbar conjunctiva, it can be found superiorly and 360 degrees around the globe.3
There are in fact a few diagnostic classification systems available to grade the severity of the conjunctivochalasis. An older one, the Meller system, has five levels of severity and allows for a wider berth of diagnosis. The more recent and more commonly used is the four-tier Zhang system.4
This classification ranges from G1, meaning no persistent conjunctival folds, to G2, with a single, small fold, to G3, which signifies more than two folds and not standing higher than the tear meniscus, to G4, with multiple folds and reaching higher than the tear meniscus.5
Generally, examination with a slit lamp under both diffuse light and slit beam is adequate to visualize and potentially grade the severity of the chalasis, with the patient in primary gaze (Figure 1). Fluorescein dye instillation could be helpful in further visualizing tear movement and finer conjunctival folds. Advanced examination with anterior segment optical coherence tomography (OCT) is possible, which could aid in assessing tear meniscus height over the conjunctivochalasis.
Symptoms
Conjunctivochalasis is an extraordinarily common, normal variant of the aging process until the patient becomes symptomatic. An amalgamation of complaints tend to be heard:
• Chronic dryness
• Redness
• Foreign body sensation
• Epiphora
• Burning
• Irritation
• Tired eyes
Up to 50 percent of individuals may report some or many of those symptoms.6 Some may report that the dryness is worsened by downgaze and frequent blinking.2
From a visual standpoint, patients may also describe intermittent bouts of blurry vision, which may or may not be worsened by contact lens wear or while reading.1
Irritation and visual complaints that worsens with soft contact lens wear may be a frequent complaint because it has been found that contact lenses can cause chronic conjunctival inflammation via hypoxia and mechanical trauma, which may exacerbate existing chalasis or in itself may result in stimulating conjunctivochalasis.7
The chalasis itself can impinge on the contact lens and fold over its edges to create friction and induce a tighter fit to the lens (Figure 2). Patients may complain of fluctuating vision with contact lenses and difficulty removing them at the end of the day.
Related: The role of lid hygiene in ocular surface disease
Pathophysiology
Conjunctivochalasis’s true underlying causative mechanism is unknown, though with recent advances in molecular biology, there is a growing literature that indicates that conjunctivochalasis may result from either age-related connective tissue degeneration or from chronic inflammation.8
Age-related connective tissue degradation of elastic fibers secondary to cumulative mechanical force from the eyelids onto the conjunctiva has been the predominating theory used to explain conjunctivochalasis’ pathophysiology.9 This theory indicates that repeated mechanical insult from the eyelids cause conjunctival elastic fibers to degrade over time, which result in the bulbar conjunctiva releasing from the sclera and causing the characteristic folds we see with conjunctivochalasis.10
The aging/mechanical insult theory is supported by work from Mimura and colleagues who found that contact lens wearers were more likely to have conjunctivochalasis than noncontact lens wearers. They also found that conjunctivochalasis was accentuated by more years of contact lens use and by wearing gas permeable contact lenses as compared to soft contact lenses.7
Alternatively, repeated mechanical insult may be activating inflammatory breakdown of conjunctival connective tissue, which could result in conjunctivochalasis.11 Meller and Tseng originally championed inflammation’s involvement in conjunctivochalasis.8
Their theory proposed that conjunctivochalasis likely resulted from underlying chronic inflammation that stemmed from decreased tear clearance, which allowed allow degradation enzymes to build up on the ocular surface and subsequently causing the enzymic break down of conjunctival connective tissue over time.12
Meller and Tseng’s theory has been supported by recent research.1Specifically, there is evidence that stress on the ocular surface caused by ultraviolet radiations, oxidative stress, dry eye, or mechanical trauma causes increased production of inflammatory molecules.9
This initial inflammatory stress could produce lid-parallel conjunctival folds (LIPCOF), lateral conjunctival folds located near the eyelid margin, which are likely a very early version of conjunctivochalasis.14 The presence of LIPCOF then displaces the tears, subsequently decreasing tear turnover/drainage.14
Simultaneously, the above insults are continuing to produce inflammatory molecules, which activate matrix metalloproteinases (MMPs).9,13 Decreased tear drainage would allow MMPs to stay on the ocular surface longer, allowing for compounding ocular surface damage, hence the additional irritation with dry eye and blepharitis.8
MMPs are proteins that degrade and remodel connective tissue.9 Their physiological inhibitors (TIMPs) inhibit MMPs, and a balance of MMPs and TIMPs is needed to maintain homeostatis.9 Evidence exists that conjunctivochalasis tissue overexpresses certain MMPs.9 Therefore, over time MMPs likely degrade conjunctival connective tissue, resulting in the looser and more pronounced conjunctival folds associated with conjunctivochalasis.8
The increasing severity of conjunctivochalasis likely creates a vicious cycle of more redundant tissue, worse tear flow, and even punctum blockages, which would keep more toxic tears on the ocular surface for longer.7
Furthermore, reduced tear turnover likely also cause increased tear osmolarity, additional inflammatory molecule production, and the characteristic dry eye symptoms associated with advanced conjunctivochalasis.14
Thankfully, evidence indicates that both topical and surgical intervention not only mitigates conjunctivochalasis’ disruptive folds, but surgery also reduces the inflammatory component of the condition.15
Related: Diagnosing and managing ocular allergy
Treatment
A good method to ease patient concerns is discussing the condition’s prevalence, etiology, and lack of dangerous nature while presenting multiple treatment options. Medically managing conjunctivochalasis can be frustrating and may require multiple approaches.
Topical pharmaceutical intervention can address chemosis and inflammation, allergies, and bacterial load as it relates to concurrent blepharitis and dry eye strategies. Corticosteroids such as loteprednol (Alrex, Lotemax; Bausch + Lomb) can target the chemosis and inflammation and may require extended periods of use.16-17 Topical antihistamines can assist in managing concurrent allergic conjunctivitis, whose inflammatory component can worsen chalasis symptoms.
A bacteriostatic approach meant to curtail existing blepharitis via antibiotic vehicles or lid hygiene may lessen irritation. Lubricants, including artificial tears and gels, can assist in both managing the foreign body sensation via stabilizing the tear film.
Success rates to these approaches are variable. If symptoms concur most often with contact lens use, the patient may be refit into a different modality or design. If unsuccessful, the next step would be surgical intervention.
Opportunities abound in this arena-from superficial conjunctival cauterization for mild to medium cases, to tightening the conjunctiva via excision or resection for moderate to severe cases.18 A more recently added procedure is an amniotic membrane transplantation in which an area of the conjunctiva is excised and an amniotic graft is attached to the globe via dissolvable sutures or fibrin tissue glue in place of the defect.19 Success rates of the various procedures are similar with moderate to high rates of improvement.19
Conjunctivochalasis is a complicated condition that not only can present with a variety of complaints but can also often coexists with other anterior segment disorders like dry eye. As we are seeing an increasing number of aging patients, we must keep in mind how significantly chalasis can impact a patient’s comfort and may warrant a unique treatment plan.
Related: Connecting allergy and osmolarity
References
1. Mimura T, Yamagami S, Usui T, Funatsu H, Mimura Y, Noma H, Honda N, Amano S. Changes of conjunctivochalasis with age in a hospital-based study. Am J Ophthalmol. 2009 Jan;147(1):171-177.e1.
2. Balci O. Clinical characteristics of patients with conjunctivochalasis. Clinical Ophthalmology. 2014 Aug 28;8:1655-60.
3. Elder D. The ocular adnexa. In: Conjunctival hyperplasia. System of OphthalmologyVol XIII: London; Kimpton, 1974.
4. Zhang XR, Zou HD, Li QS, Zhou HM, Liu B, Han ZM, Xiang MH, Zhang ZY, Wang HM. Comparison study of two diagnostic and grading systems for conjunctivochalasis. Chin Med J(Engl).2013 Aug:126(16): 3118-23.
5. Meller D, Tseng SC. Conjunctivochalasis: literature review and possible pathophysiology. Surv Ophthalmol. 1998 Nov-Dec; 43(3):225-32.
6. Qui W, Zhang M, Xu T, Liu Z, Lv H, Wang W, Li X. Evaluation of the effects of conjunctivochalasis excision on tear stability and contrast sensitivity. Sci Rep. 2016 Nov 28;6:37570.
7. Mimura T, Usui T, Yamamoto H, Yamagami S, Funatsu H, Noma H, Honda N, Fukuoka S, Amano S. Conjunctivochalasis and contact lenses. Am J Ophthalmol. 2009 Jul;148(1):20-5.e1.
8. Meller D, Tseng SC. Conjunctivochalasis: literature review and possible pathophysiology. Surv Ophthalmol. 1998 Nov-Dec;43(3):225-32.
9. Meller D, Li DQ, Tseng SC. Regulation of collagenase, stromelysin, and gelatinase B in human conjunctival and conjunctivochalasis fibroblasts by interleukin-1beta and tumor necrosis factor-alpha. Invest Ophthalmol Vis Sci. 2000 Sep;41(10):2922-9.
10. Acera A, Suarez T, Rodriguez-Agirretxe I, Vecino E, Durán JA. Changes in tear protein profile in patients with conjunctivochalasis. Cornea. 2011 Jan;30(1):42-9.
11. Huang Y, Sheha H, Tseng SC. Conjunctivochalasis interferes with tear flow from fornix to tear meniscus. Ophthalmology. 2013 Aug;120(8):1681-7.
12. Ward SK1, Wakamatsu TH, Dogru M, Ibrahim OM, Kaido M, Ogawa Y, Matsumoto Y, Igarashi A, Ishida R, Shimazaki J, Schnider C, Negishi K, Katakami C, Tsubota K. The role of oxidative stress and inflammation in conjunctivochalasis. Invest Ophthalmol Vis Sci. 2010 Apr;51(4):1994-2002.
13. Erdogan-Poyraz C, Mocan MC, Bozkurt B, Gariboglu S, Irkec M, Orhan M. Elevated tear interleukin-6 and interleukin-8 levels in patients with conjunctivochalasis. Cornea. 2009 Feb;28(2):189-93.
14. Pult H, Riede-Pult BH. Impact of conjunctival folds on central tear meniscus height. Invest Ophthalmol Vis Sci. 2015 Feb 3;56(3):1459-66.
15. Fodor E, Kosina-Hagyo K, Bausz M, Nemeth J. Increased tear osmolarity in patients with severe cases of conjunctivochalasis. Curr Eye Res. 2012 Jan;37(1):80-4.
16. Acera A, Vecino E, Duran JA. Tear MMP-9 levels as a marker of ocular surface inflammation in conjunctivochalasis. Invest Ophthalmol Vis Sci. 2013 Dec 23;54(13):8285-91.
17. Latkany R. Dry Eyes: etiology and management. Curr Opin Ophthalmol. 2008 Jul;19(4):287-91.
18. Haefliger IO, Vysniauskiene I, Figueiredo AR, et al. Superficial conjunctiva cauterization to reduce moderate conjunctivochalasis. Klin Monbl Augenheilkd. 2007 Apr;224(4):237-9.
19. Meller D1, Maskin SL, Pires RT, Tseng SC. Amniotic membrane transplantation for symptomatic conjunctivochalasis refractory to medical treatments. Cornea. 2000. Nov;19(6):796-803.
