Kristiana D. Neff

Introduction

Conjunctivochalasis (CCh) is a characteristically bilateral condition where redundant, nonedematous conjunctiva causes a spectrum of clinical findings ranging from exacerbation of an unstable tear film to mechanical disruption of tear flow. The origination of the term conjunctivochalasis came from W. L. Hughes in 1942; however, descriptions of this same entity were noted as early as 1908 by Elschnig and by Braunschweig and Wollenberg in 1921 and 1922, respectively.¹ They described the more severe spectrum of findings in CCh of subconjunctival hemorrhage, pain, and exposure keratopathy. Later work described the more mild symptomatology of CCh, including dry eye to the more moderate symptoms of excess lacrimation by impeding tear clearance.²

Because CCh can be asymptomatic, it is often overlooked as a normal variant of aging. However, it is an important clinical diagnosis that must be considered in the evaluation of patients with ocular irritation and tearing. CCh typically presents as loose inferior conjunctiva, that disrupts the inferior tear meniscus; however, it is thought to also involve the superior conjunctiva in some cases.3,4 Aside from the most common symptoms of irritation and lacrimation, other associated complaints include blurred vision, discharge, dryness, ocular fatigue, subconjunctival hemorrhage, and eye stiffness on awakening.⁵ The severity of CCh symptoms tends to worsen with both downgaze and digital pressure.

Slit lamp biomicroscopy can show prolapse of the conjunctiva over the lower lid margin in the temporal, medial or nasal regions, or any combination of these regions (Fig. 20.1). This conjunctival prolapse can impede tear outflow through the inferior punctum, resulting in epiphora. Mechanical trauma can also cause recurrent subconjunctival hemorrhage in this sector (Fig. 20.2).

The diagnostic dilemma in managing CCh lies in the fact that other more common etiologies of tearing and ocular irritation must be ruled out as causative or contributory agents to the tear flow disruption or tear instability. The same symptom constellation can be seen in isolated dry eye syndrome, isolated CCh or a mixed presentation of these diseases. Lid pathology, as well as systemic entities, such as ocular allergy and thyroid eye disease can also present with similar symptoms. One must be able to determine how much the presence of redundant conjunctiva contributes to the patient’s irritation. This can be particularly challenging in cases of mild CCh.

Epidemiology

Conjunctivochalasis has been identified to be an age-dependent phenomenon by several studies.4,6–8 It has been seen in patients as early as the first decade of life and tends to increase in prevalence and severity with age. The Zhang study estimated the prevalence to be 44.08% in a senile Chinese population, while Mimura noted an even higher prevalence in a hospital-based Japanese population. There was no increase in grade of severity of CCh based on gender in Mimura’s study. The location of CCh is most frequently found in the nasal and temporal regions of inferior conjunctiva, versus middle zone of inferior conjunctiva or superior conjunctiva.^4,7,8 Conjunctivochalasis has also been noted to be more frequent in patients with thyroid disease and with contact lens wear.^6,9

Pathophysiology

Information regarding the pathogenesis of conjunctivochalasis is minimal and often conflicting. The earliest publications suggested senile changes involving the subcutaneous, elastic or supporting tissue, in the conjunctiva. Eye rubbing, mechanical irritation or trauma to conjunctiva, and abnormal eyelid position, were all implicated in development of CCh; however, no true etiology has been determined. More recent studies have offered a more mechanistic approach to evaluating the pathogenesis of CCh.

Francis et al., in a prospective clinical and histopathological study of 29 CCh patients, showed that 22 of 29 specimens displayed normal conjunctival histology, while only four specimens showed inflammatory changes and three specimens showed elastosis (Fig. 20.3).¹⁰ They hypothesized, based on these results, that the pathogenesis of CCh is therefore, multifactorial, including local trauma, ultraviolet radiation and delayed tear clearance as inciting factors. Watanabe et al. demonstrated microscopic lymphangiectasia of the subconjunctiva in 39 of 44 specimens taken from patients with severe CCh, with no evidence of inflammation.¹¹ They also noted loss of typical fiber patterns with fragmented elastic fibers and sparse assemblages of collagen fibers in all 44 specimens. Their conclusion was that mechanical forces between the lower eyelid and conjunctiva gradually impaired lymphatic flow, resulting in lymphatic dilation and clinical CCh. Immunostaining by Yokoi et al. supported the negligible role of inflammation in CCh, by comparing conjunctival samples in CCh patients to those of known normal and known inflammatory ocular surface disease.⁵

Although there is little histopathologic support of inflammation playing a role in CCh, mechanistic evidence suggests a shift in the normal balance of conjunctival matrix metalloproteinases (MMPs) and tissue inhibitors (TIMPs). These enzymes serve to degrade extracellular matrix, possibly contributing to the pathogenesis of CCh.¹² Specifically, Li, et al. showed overexpression of MMP-1 and MMP-3 mRNA in tissue cultured conjunctivochalasis fibroblasts, versus normal human conjunctival fibroblasts. No difference was noted in MMP-2, TIMP-1, TIMP-2, and urokinase plasminogen activator in the same study. Further studies then showed that inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) may increase expression of MMP-1 and MMP-3 in conjunctivochalasis fibroblasts.¹³ Other proinflammatory cytokines, tear IL-6 and IL-8, were shown to be increased in the tear film of CCh patients.¹⁴