Conjunctivochalasis (CCh) is usually characterized by bilateral, loose and redundant conjunctival folds interspersed between the globe and eyelids, most notably in the inferior bulbar conjunctiva. Common risk factors of CCh include older age, female gender, contact lens use and dry eye disease.¹ While the etiology remains unclear, several pathological studies have observed changes in the extracellular matrix components of CCh tissue, such as degeneration of elastic fibers and increased collagenolytic activity,² which is likely a result of the increased expression of collagen degrading enzymes MMP-1 and MMP-3 found in CCh tissue and fibroblasts.^3,4 Meller and Tseng⁵ have suggested that inflammation may incite this process, as proteins related to the inflammatory response have been isolated from tears.⁶

Patients with CCh may present with a variety of symptoms including ocular discomfort, dry eye, irritation, foreign body sensation, epiphora and blurred or fluctuating vision. These symptoms may commonly arise due to the disturbance of the ocular tear film brought about by the mechanical factor, due to surface irregularities. The conjunctival folds can disrupt the continuity of the tear meniscus and block the punctum, triggering reflex tearing that presents as epiphora when tear clearance is delayed.^7-10 Furthermore, conjunctival folds extending from the lid margin to the fornix, coupled with fat prolapse, can obliterate the fornix tear reservoir and impede tear flow from the fornix reservoir to the tear meniscus.^11,12 Mechanical friction between the lid margin and the lax conjunctiva during blinking can further perpetuate the inflammatory response and exacerbate symptomatic dry eye.

In summary, CCh can lead to tear film instability (the hallmark of dry eye) by impeding tear flow to the tear meniscus and altering mechanical (hydrodynamic) factors — a key example of how structural alterations significantly affect function. Herein, we discuss in detail a surgical technique for the treatment of symptomatic CCh, as well as the beneficial outcomes of this procedure.

SURGICAL MANAGEMENT

As a result of tear film instability and obliteration of the tear reservoir, topical lubricants and immunomodulatory therapies alone may be ineffective in treating symptomatic CCh as tear volume retention is limited and contact time reduced. Thus, surgical treatment should be considered when patients do not respond to conservative treatment in order to address the source of pathophysiology, restore the normal anatomy of the ocular surface and tear reservoir, reduce inflammation and ensure a stable pre-ocular tear film.

While a variety of surgical approaches have been described,¹³ most methods, including conjunctival cauterization or conjunctival resection/excision, involve eliminating conjunctival folds close to the tear meniscus with little focus on restoring the fornix tear reservoir. Furthermore, conjunctival resection carries the risk of foreshortening the inferior fornix, motility restriction, scarring and prolonged healing if the surgeon is overzealous in the amount of conjunctiva resected.¹⁴ Alternatively, under-resection¹⁵ or under-cauterization¹⁶ can result in residual postoperative CCh, requiring repeat procedures.

Based on the notion that loose and redundant conjunctiva in CCh extends from the lid margin/meniscus to the fornix, we have devised a surgical strategy that aims to deepen the fornix through recession rather than resection. This ensures a continuous supply of tears from the reservoir to the tear meniscus and the preocular tear film.¹¹

TECHNIQUE

After monitored anesthesia care or surgeon’s preferred anesthesia, including local anesthesia, the loose conjunctiva is separated from the sclera with forceps. A 7-0 Vicryl traction suture is placed 2 mm posterior to the limbus at the 3 and 9 o’clock position and it is used to rotate the globe upward. An arc-like conjunctival peritomy is created 1-2 mm posterior to the limbus in the area of CCh and extended to remove pingueculae, if present. Conjunctiva is rearranged by recessing it from the limbus to the fornix. The abnormal Tenon’s capsule, under the overlying recessed conjunctival epithelial tissue and that adherent over the bare sclera, is grabbed and thoroughly removed by blunt and sharp dissection. The prolapsed fat from the fornix is identified and cauterized to create a strong seal of the gap to prevent fat herniation in the fornix, which obliterates the tear reservoir capacity.

The recessed conjunctival in the fornix is then anchored to the sclera with 8-0 Vicryl mattress sutures in each of the inferior quadrants. Two separate layers of cryopreserved amniotic membrane (cAM) (Amniograft, Bio-Tissue) are placed to replace Tenon (to cover the inferior rectus muscle) and the conjunctival tissue, respectively. cAM is well known to promote re-epithelialization and healing, while simultaneously reducing inflammation and scarring via the suppression of pro-inflammatory mediators such as TNF-α, TGF-β and IL-6.^17.18 The cAM is peeled from the nitrocellulose backing and slid over the bed of fibrin glue on the sclera to coat the stromal underside of the cAM graft. Use of fibrin glue in lieu of sutures reduces operating time, minimizes suture-induced inflammation and complications and helps minimize postoperative discomfort.

The tissue is carefully tucked under the conjunctival rim, and excess glue is squeegeed anteriorly toward the cornea to prevent sequestration of excess glue in the newly reconstructed fornix. In some cases, a few Vicryl sutures may be added as needed.

Immediately following the surgical procedure, the surgeon should be able to note a significant improvement in anatomical definition and deepening of the inferior fornix.

POSTOPERATIVE OUTCOMES

A number of studies have demonstrated significant improvement in ocular signs and symptoms of CCh following reconstruction of the fornix tear reservoir via conjunctival recession and amniotic membrane transplantation (AMT). Kheirkhah et al¹⁹ reported significant (>50%) resolution of symptoms in all 25 eyes, with complete resolution of symptoms observed in 44% of eyes. Conjunctival redundancy disappeared entirely without recurrence in all cases, resulting in a smooth conjunctival surface with reduced inflammation and restoration of a continuous tear meniscus. While four cases presented with focal inflammation and one case developed pyogenic granuloma, these complications were completely resolved after subconjunctival injection of triamcinolone acetonide.

Huang et al¹² found that eyes with CCh (n=15) had significantly slower recovery of the tear meniscus height after maximal depletion with and without blinking, compared to eyes without CCh (n=13). Deepening of the inferior fornix and reconstruction with cAM resulted in symptomatic relief and improved recovery rate in symptomatic CCh patients to the same extent as normal subjects as early as the first postoperative day. Cheng et al¹¹ later demonstrated that recession of the conjunctiva from the limbus to the fornix in 36 eyes resulted in a significant increase in basal tear volume, resolution of symptoms and a decrease in corneal staining, conjunctival inflammation and use of topical medications. Interestingly, this study also found that aqueous tear deficiency (ATD) was no longer existent in 10 of 18 eyes (56%) following surgery, suggesting ATD could be secondary to obliteration of the fornix tear reservoir.¹¹ In a case report by Fernández-Hortelano et al,²⁰ a 63-year-old male with bilateral conjunctivochalasis who failed to improve with topical treatment demonstrated biomicroscopic and symptomatic improvement immediately after surgery that remained stable at the 2-month follow-up.

CONCLUSION

Collectively, these findings support fornix deepening reconstruction with AMT to restore ocular surface integrity, improve tear film dynamics and alleviate symptomatic CCh. OM

REFERENCES

1. Marmalidou A, Kheirkhah A, Dana R. Conjunctivochalasis: a systematic review. Surv Ophthalmol. 2018;63:554-564.
2. Li YJ, Zhang XR, Xiang M, Yu Z, Li QS. Ultrastructure change of conjunctiva and fascia tissue of conjunctivochalasis. Zhonghua Shiyan Yanke Zazhi/Chinese Journal of Experimental Ophthalmology. 2012;30:638-640.
3. 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.
4. Meller D, Li DQ and 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;41:2922-2929.
5. Meller D, Tseng SC. Conjunctivochalasis: literature review and possible pathophysiology. Surv Ophthalmol. 1998;43:225-232.
6. Zhang XR, Xiang MH, Wu QQ, et al. [The tear proteomics analysis of conjunctivochalasis]. Zhonghua Yan Ke Za Zhi. 2009;45:135-140.
7. Liu D. Conjunctivochalasis. A cause of tearing and its management. Ophthalmic Plast Reconstr Surg. 1986;2:25-28.
8. Erdogan-Poyraz C, Mocan MC, Irkec M, Orhan M. Delayed tear clearance in patients with conjunctivochalasis is associated with punctal occlusion. Cornea. 2007;26:290-293.
9. Di Pascuale MA, Espana EM, Kawakita T, Tseng SCG. Clinical characteristics of conjunctivochalasis with or without aqueous tear deficiency. Br J Ophthalmol. 2004;88:388-392.
10. Gumus K, Crockett CH, Pflugfelder SC. Anterior segment optical coherence tomography: a diagnostic instrument for conjunctivochalasis. Am J Ophthalmol. 2010;150:798-806.
11. Cheng AM, Yin HY, Chen R, et al. Restoration of fornix tear reservoir in conjunctivochalasis with fornix reconstruction. Cornea. 2016;35:736-740.
12. Huang Y, Sheha H, Tseng SCG. Conjunctivochalasis interferes with tear flow from fornix to tear meniscus. Ophthalmology. 2013; 120:1681-1687.
13. Marmalidou A, Palioura S, Dana R, Kheirkhah A. Medical and surgical management of conjunctivochalasis. Ocul Surf. 2019;17:393-399.
14. Yokoi N, Komuro A, Sugita J, Nakamura Y, Kinoshita S. Surgical reconstruction of the tear meniscus at the lower lid margin for treatment of conjunctivochalasis. Adv Exp Med Biol. 2002;506(Pt B):1263-1268.
15. Wang H, Gao F, Pan YZ. The treatment outcomes of crescent-shaped conjunctiva resection combined with conjunctiva sclera fixation for severe conjunctivochalasis. Eur Rev Med Pharmacol Sci. 2016;20:3519-3522.
16. Haefliger IO, Vysniauskiene I, Figueiredo AR, Piffaretti JM. Superficial conjunctiva cauterization to reduce moderate conjunctivochalasis. Klin Monbl Augenheilkd. 2007;224:237-239.
17. Tseng SC, Espana EM, Kawakita T, et al. How does amniotic membrane work? Ocul Surf. 2004;2:177-187.
18. Tseng SC, Li DQ, Ma X. Suppression of transforming growth factor-beta isoforms, TGF-beta receptor type II, and myofibroblast differentiation in cultured human corneal and limbal fibroblasts by amniotic membrane matrix. J Cell Physiol. 1999;179:325-335.
19. Kheirkhah A, Casas V, Blanco G, et al. Amniotic membrane transplantation with fibrin glue for conjunctivochalasis. Am J Ophthalmol. 2007;144:311-313.
20. Fernández-Hortelano A, Moreno-Montañés J, Heras-Mulero H, Sadaba-Echarri LM. [Amniotic membrane transplantation with fibrin glue as treatment of refractory conjunctivochalasis]. Arch Soc Esp Oftalmol. 2007;82:571-574.

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