Conjunctivochalasis (CCh) is defined as the presence of redundant non-oedematous conjunctiva that may be asymptomatic, or it may be symptomatic due to unstable tear film or mechanical disruption of tear flow. Conjunctivochalasis is usually found in older people and is often overlooked, and is classified as a normal variant of eye due to ageing. However, it has been seen in patients as early as first decade of life with an increase in prevalence and severity with age. It is usually bilateral condition and consists of an elevation of the bulbar conjunctiva over the lower lid margin, most commonly in the infero-temporal region. However, in addition to temporal region, it may involve bulbar conjunctiva along nasal, central lid-margin or any combination of these areas. The presence of loose redundant tissue causes disruption of inferior tear meniscus. This conjunctival prolapse may impede tear outflow through the inferior punctum, resulting in epiphora (watering from eyes). It may also involve upper bulbar area with loose conjunctiva, but it is less common.
Descriptions of conjunctivochalasis were noted as early as 1908 by Elschnig. Braunschweig in 1921 and Wollenberg (1922) also described this condition. The term conjunctivochalasis was coined by W L Hughes in 1942. (Hughes WL. Conjunctivochalasis. Am J Ophthalmol 1942; 25: 48-51).They described more severe findings of CCh such as pain, subconjuntival haemorrhage and exposure keratopathy. Later works described mild/ moderate symptoms of CCh like dry eye and excessive lacrimation.
Other conditions causing tearing and ocular irritation must be ruled out as causative or contributory agents. Similar symptoms may be present in:
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Höh H, Schirra F, Kienecker C, et al. Lid-parallel conjunctival folds are a sure diagnostic sign of dry eye. Ophthalmologe 1995; 92: 802-808.
Meller D, Tseng SCG. Conjunctivochalasis: literature review and possible pathophysiology. Surv Ophthalmol 1998; 43: 225-232.
Li DQ, Meller D, Liu Y, Tseng SC. Overexpression of MMP-1 and MMP-3 by cultured conjunctivochalasis fibroblasts. Invest Ophthalmol Vis Sci. 2000; 41: 404- 410.
Zhang X, Li Q, Zou H, et al. Assessing the severity of conjunctivochalasis in a senile population: a community-based epidemiology study in Shanghai, china. BMC Pub Health 2011; 11:198.
Francis IC, Chan DG, Kim P, et al. Case- controlled clinical and histopathological study of conjunctivochalasis. Br J Ophthalmol 2005; 89:302-305.
Watanabe A, Yokoi N, Kinoshita S, et al. Clinicopathologic study of conjunctivochalasis. Cornea 2004; 23:294-298.
Yokoi N, Komuro A, Nishii M, et al. Clinical impact of conjunctivochalasis on the ocular surface. Cornea [Clinical Trial] 2005; 24(Suppl.8):S24-3.
Hughes WL. Conjunctivochalasis. Am J Ophthalmol 1942; 25: 48- 51.
Elschnig A. Beitrag zur Aethiologie und Therapie der cronischen Konjunctivitis. Dtsch Med Wochenschr 1908; 26: 1133-1155. German.
Braunschweig P. Ueber faltenbildung der conjunctiva bulbi. Klin Monatsbl Augenheilkd 1921; 66: 123-124. German.
Wollenberg A. Pseudopterygium mit Faltenbildung der Conjunctiva bulbi. Klin Monatsbl Augenheilkd 1922; 68: 221-224. German.
Conjunctivochalasis may be asymptomatic.
Symptoms are non-specific and the onset is insidious.
Ocular (eye) symptoms of conjunctivochalasis may be:
Symptoms of CCh tend to worsen with both down gaze and digital pressure.
No true aetiology is known for conjunctivochalasis. Senile changes involving the subcutaneous, elastic or supporting tissue in the conjunctiva was suggested as the cause. Eye rubbing, mechanical irritation or trauma to conjunctiva, and abnormal eyelid position were all implicated.
Francis et al. based on clinical and histopathological study suggested that the development of CCh is multi-factorial, which includes local trauma, ultra-violet radiation and delayed tear clearance as inciting factors (Francis IC, Chan DG, Kim P, et al. Case- controlled clinical and histopathological study of conjunctivochalasis. Br J Ophthalmol 2005; 89:302-305).
Watanabe et al. showed microscopic lymphangiectasia of the subconjunctiva without any inflammation. There was loss of typical fiber patterns with fragmented elastic fibers and sparse collagen fibers. They suggested that mechanical forces between the lower eyelid and conjunctiva gradually impaired lymphatic flow, resulting in lymphatic dilatation and clinical CCh (Watanabe A, Yokoi N, Kinoshita S, et al. Clinicopathologic study of conjunctivochalasis. Cornea 2004; 23:294-298).
Yokoi et al. by immunestaining, compared conjunctival samples of CCh patients with those of known normal and known inflammatory ocular surface disease and showed negligible role of inflammation in CCh (Yokoi N, Komuro A, Nishii M, et al. Clinical impact of conjunctivochalasis on the ocular surface. Cornea [Clinical Trial] 2005; 24(Suppl.8):S24-31).
More recent studies have suggested a mechanistic approach to the development of CCh. Mechanistic evidence suggests a shift in the normal balance of conjunctival matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). MMPs are enzymes that modify or degrade extracellular matrix, possibly contributing to the pathogenesis of CCh. MMP-1 and MMP-3 enzymes have been noted to be over-expressed in conjunctivochalasis fibroblasts in tissue culture, while enzyme levels of TIMPs are unchanged (Li DQ, Meller D, Liu Y, Tseng SC. Over-expression of MMP-1 and MMP-3 by cultured conjunctivochalasis fibroblasts. Invest Ophthalmol Vis Sci. 2000; 41: 404- 410). This interaction or change in balance of MMPs and their inhibitors, which normally participate in connective tissue degradation and remodelling, leads to clinically evident redundant conjunctiva observed in conjunctivochalasis.
CCh is one of the most common under diagnosed and misdiagnosed ocular surface disease. Non-specific symptoms along with intermittent findings of conjunctival oedema often lead to misdiagnosis. Due to fluctuation in findings of disease process, several clinical exams may be required to confirm the diagnosis. Diagnosis of CCh is mainly clinical.
Slit lamp biomicroscopy (by an eye specialist) shows prolapsed or folds of conjunctiva in temporal, nasal or central part of lower lid-margin. Presence of redundant conjunctiva over lower lid margin suggests CCh. Prolapsed conjunctiva causes a disruption of tear movement and outflow through inferior lacrimal punctum resulting in epiphora.
Signs on slit lamp examination are:
Prior to correct diagnosis, patients with CCh are often diagnosed with more common ocular surface diseases, such as
Often CCh is not considered a significant clinical entity, or significance of the conjunctival finding is not recognised.
Many patients are first diagnosed when epiphora develops due to blocked puncta caused by redundant conjunctiva.
Höh et al., looked at the number of lid-parallel conjunctival folds (LIPCOF) (Höh H, Schirra F, Kienecker C, et al. Lid-parallel conjunctival folds are a sure diagnostic sign of dry eye. Ophthalmologe 1995; 92: 802-808). They noted the number of LIPCOF had a high predictive value for diagnosis of keratoconjunctivitis sicca.
At present, the most widely used grading system was proposed by Meller and Tseng in 1998 who adapted the scale by Höh and associates, and included the extent of CCh, changes with down-gaze and digital pressure, and presence of punctal occlusion (Meller D, Tseng SCG. Conjunctivochalasis: literature review and possible pathophysiology. Surv Ophthalmol 1998; 43: 225-232).
Accordingly, the grades of severity of conjunctivochalasis, based on the number of folds and their relationship to the tear meniscus height are:
The newest grading system proposed by Zhang et al. in 2011 further modified Meller and Tseng’s approach by including three symptoms (epiphora, feeling of dryness, and foreign body sensation) and unstable tear film break-up time (BUT) (Zhang X, Li Q, Zou H, et al. Assessing the severity of conjunctivochalasis in a senile population: a community-based epidemiology study in Shanghai, china. BMC Pub Health 2011; 11:198). These modifications rule out asymptomatic, normal older people from the noted very high prevalence rates of CCh. The validity of this requires further studies.
Most common histopathologic findings are elastosis or chronic non-granulomatous inflammation (Yanoff Myron, Sassani Joseph W. Ocular Pathology. Seventh Edition. Elsevier Saunders. 2015. P. 216.).
Microscopic lymphangiectasia is typically present.
Conjunctivochalasis should be differentiated from:
In dry eye, symptoms are worse in the evening, aggravates in up-gaze, Fluorescein sodium/ rose bengal dye stains inter-palpebral exposure zone, increased blinking and punctal occlusion improves it.
In conjunctivochalasis, symptoms are same throughout the day, aggravates in down-gaze, Fluorescein sodium/rose bengal dye stains non-exposure zone, increased blinking and punctal occlusion worsens it, unlike dry eye disease.
Management should be carried out under medical supervision.
Asymptomatic conjunctivochalasis requires no treatment.
Treat associated ocular diseases such as:
Therapeutic modalities for symptomatic patients:
Surgical therapy is indicated when conservative medical therapy fails and other associated ocular disease has been ruled out.
Surgical methods are directed against the redundant conjunctival folds.
Extensive conjunctival resections should be avoided in order to minimise complications, such as contraction of fornices, cicatricial entropion, and restriction of extra-ocular movement.
Prognosis is generally good when the correct treatment is adopted according to the symptom complex in each individual patient.