Optimizing CCh Treatment
Understanding conjunctivochalasis (CCh) – and tips for achieving the best surgical outcomes for patients with the disorder
Brett P. Bielory | | 8 min read | Discussion
Conjunctivochalasis (CCh) is a chronic ocular surface disorder characterized by loose, redundant, nonedematous folds on the bulbar conjunctiva (1). CCh typically develops bilaterally and is most commonly found on the inferior bulbar conjunctiva (2). Generally considered a condition secondary to the normal aging process, the prevalence of CCh increases with age, affecting 44–98 percent of individuals in two large studies conducted in Asian populations aged 60 years and older (3, 4). Besides old age, other risk factors for CCh include female sex, dry eye disease (DED), contact lens usage, hyperopia, pinguecula, ultraviolet radiation, and eyelid disorders (1).
Despite being a common disease, CCh is often overlooked in the clinical setting and its pathogenesis is poorly understood. It is thought to be initiated primarily by a degeneration of the Tenon’s capsule, which is traversed by the subconjunctival connective tissue as part of the normal aging process.
Breakdown of the Tenon’s capsule reduces the attachment of the bulbar conjunctiva to the sclera, leading to conjunctival laxity, periorbital fat prolapse, and obliterated tear reservoir and tear meniscus (1, 5). These structural changes, in turn, lead to chronic mechanical friction between the eyelid and conjunctiva, activating inflammatory responses and matrix metalloproteinases (MMPs). MMPs are enzymes that degrade and remodel the extracellular matrix, resulting in further damage to the tissue and worsening the condition (6).
CCh is associated with a wide range of symptoms and signs, including tear film instability in mild cases, epiphora in moderate cases, and exposure difficulties in severe cases (7). Other symptoms include dry eye, foreign body sensation, pain, blurry vision, and subconjunctival hemorrhage (1). Symptoms of CCh overlap considerably with those of DED and meibomian gland dysfunction (MGD), such that CCh is also known as mechanical dry eye. In fact, DED and MGD are common comorbid conditions observed among patients with CCh, often resulting in more severe symptoms (8, 9).
Under the umbrella of DED, CCh and MGD are distinct in their pathology. MGD-associated dry eye is characterized by meibomian gland abnormalities that alter the composition of tear film and the rate of tear evaporation (10). In individuals with CCh, the development of conjunctival folds contributes to symptoms of dry eye via the impediment of tear flow, disruption of the tear meniscus, and obliteration of the fornix tear reservoir (1). Through different mechanisms, MGD-associated DED and CCh both disrupt the stability, distribution, and clearance of the tear film (8).
Common but neglected
Although a common condition in older adults, CCh often goes undiagnosed or misdiagnosed. The condition is asymptomatic in some mild cases, but in more severe cases it can be misattributed to other coexisting ocular surface disorders. Despite the diagnostic approach to CCh being relatively straightforward, the disorder is not typically considered as a potential cause of an individual’s reported symptoms.
The diagnosis of CCh typically involves a combination of clinical examination, diagnostic studies, and review of a patient’s history. Some of the diagnostic studies that can be performed include measurements of tear film break-up time (TBUT), to evaluate tear film stability; the Schirmer’s test, to determine the rate of tear production; and measurements of MMP-9 level at the ocular surface, to assess the amount of underlying inflammation caused by degenerated Tenon’s capsule.
Clinical suspicion of CCh can be confirmed by the slit lamp examination and ocular surface vital staining (1). Slit lamp biomicroscopy can reveal conjunctival folds, which are the characteristic sign of CCh. Staining with dyes, such as lissamine green, also helps reveal the presence of conjunctival folds and devitalized epithelial cells – both of which are indicative of an obliterated tear reservoir. Other related and nonexclusive conditions, such as blepharitis and MGD, also should be considered during the diagnostic assessment.
Since an official grading system has yet to be established for CCh (1), I typically grade the condition using a three-stage approach. In stage 1, conjunctival staining reveals irregular staining (resembling dashes and dots of tears and loose conjunctiva, which are similar to Morse code) in the lateral one-third of the lower lid. In stage 2, redundant conjunctival folds override the lower eyelid margin up to the halfway point of the lower limbus, covering 50 percent of the lower eyelid. In the most severe stage (stage 3), redundant conjunctiva cover more than two-thirds of the lower eyelid and may occlude the lower lid puncta.
As patients frequently experience multiple conditions that contribute simultaneously to their dry eye, I typically proceed to address the diseases individually. By managing the issues one at a time, a more optimized therapeutic approach may be taken to better address the underlying pathology.
In patients who present with both MGD and CCh, I typically elect to treat the MGD first. Management of MGD may involve a combination of warm compresses, topical ointments and drops, and eyelid hygiene. If the symptoms persist despite successful control of MGD, CCh surgery should be the next line of treatment.
Alternatively, for patients who present with CCh and no other ocular surface disorders, I usually begin with topical lubricants and immunomodulatory therapies (for example, low-dose prednisolone eye drops). Surgical intervention may be considered when conservative topical treatments fail to achieve symptom relief (2). Generally, surgery is an excellent option for the treatment of CCh that has progressed to late stage 2 or stage 3 in severity.
The main goals of CCh surgery are to reconstruct the conjunctival surface, restore the function of the tear meniscus, and reduce the effects of redundant conjunctiva (2). Although various surgical options are available, most surgeries involve conjunctival cauterization or conjunctival resection/excision procedures (11).
Although surgical management of CCh is relatively easy to perform and has a high success rate, some challenges remain; for example, under-cauterization and under-resection are common concerns that require repeat procedures to achieve satisfactory outcomes (1). Additionally, conjunctival excision may cause suture- and scarring-related complications, such as discomfort, foreign body sensation, shortening of the inferior fornix, ocular motility restriction, and prolonged healing.
Enhancing surgical success with CAM
The benefits of amniotic membrane (AM) transplantation in the surgical management of CCh have long been established (12, 13). AM has intrinsic healing properties that enhance epithelial cell regeneration; promote goblet cell differentiation; and suppress scar formation, inflammation, and vascularization (1, 14). Following CCh surgery, AM supports postoperative tissue healing and tear reservoir restoration.
AM is typically dehydrated or cryopreserved during the manufacturing process (14). Among the various treatment options, I exclusively use cryopreserved AM (CAM; AmnioGraft and Prokera, BioTissue, Miami, FL) in ocular surface restoration. Unlike dehydrated AM, the cryotechnology used to produce CAM preserves the structural integrity of the tissue and maintains important biological factors responsible for its therapeutic properties. Specifically, CAM retains a critical heavy-chain-hyaluronic-acid/pentraxin 3 (HC‑HA/PTX3) complex that has beneficial anti-inflammatory and anti-scarring properties (15). In contrast, the dehydration process used to create dehydrated AM breaks down the HC-HA/PTX3 complex into smaller components that include a low-molecular-weight hyaluronic acid – a pro-inflammatory molecule that may further exacerbate ocular surface inflammation (16).
CCh surgery with CAM generally leads to higher patient satisfaction, with most individuals impressed by the reduction in dryness, irritation, and inflammation. Patients also understand that they may experience bleeding beneath the graft as a normal sequela of surgery, which can take 6 to 8 weeks to resolve. Overall, the improvement in functional capacity and day-to-day activities that patients experience render such surgery worthwhile.
Tips for further improving outcomes
There are several best practices that I use to optimize surgical outcomes in patients with CCh. First, I aim to debulk as much orbital fat as possible with excision and cauterization, to help reconstruct the tear reservoir. During surgery, I like to use two layers of CAM, with the first layer placed over the inferior rectus and inferior muscle insertion sites, and a second layer placed over the sclera to reduce adhesion to the tissue below. Additionally, I tend to oversize the graft by 2 to 4 mm, so the tissue can be tucked beneath the conjunctiva on the fornix and bulbar edges.
Prior to any ocular surface surgery, it is essential to educate patients on the procedure and the anticipated outcomes. Appropriate consultation is particularly relevant to the surgical management of CCh; after all, it is an elective surgery and may involve grafts derived from amniotic origin. For the latter, I found that most patients are impressed when they learn that amniotic tissues that once supported fetal development can play new roles in medicine.
In my experience, CAM is one of the best treatment options for patients with moderate to severe dry eye and superficial punctate keratitis. CAM is also ideal for restoring the tear fornix, lower fornix, and tear reservoir. Overall, CAM is a versatile product that produces excellent anatomical and visual outcomes in many ocular surface disorders. I recommend that surgeons who have not yet incorporated CAM into their practice attempt to use the procedure because of its ease of use and superior results.
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