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Surgeons explore ways to manage recurrent pterygium
Sealing the gap between the conjunctiva and the Tenon may be beneficial.
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The ocular surface has recently gained increasing attention among cataract and anterior segment surgeons due to its direct impact on quality of vision, especially after surgery. This ocular domain encompasses pterygium, which can be cosmetically disturbing to the patient. Additionally, with its induced corneal astigmatism and blurred vision, surgical intervention may be the only route that the patient may have to improve cosmesis, become symptom-free, and augment visual outcome.
Surgical intervention, however, is not always an easy solution because a subset of these patients (range: 24% to 89%) may have recurrence of the pterygium that often can be worse than the primary pterygium. Globally, pterygium prevalence is about 2% to 7%. It is more common in areas with more ultraviolet radiation, and hence, not surprisingly, the pterygium belt spans the latitudes between 35° north and 35° south of the equator. In addition to ultraviolet radiation, inflammation also contributes to ocular surface compromise. Every ophthalmologist at some time in his or her clinical practice is faced with pterygium management.
Ophthalmic surgeons have continued over the years to explore various techniques in an attempt to prevent pterygium recurrence after excision. To date, there is no single procedure that is foolproof with regard to preventing such recurrences. Limbal stem cells are thought to be the barrier for preventing conjunctival invasion of the cornea. As such, a focal deficiency in the limbal stem cells is thought to open the doors to conjunctival and fibrovascular tissue invasion of the cornea in pterygium. Currently, there is some general consensus regarding pterygium surgery, namely, the need for a graft after excision of a pterygium, either a conjunctival autograft or an amniotic membrane transplant. Additionally, various techniques have been utilized to attach the graft, including sutures, fibrin glue and more recently autologous blood. Introduction of mitomycin in 1963 for pterygium surgery was associated with potential complications so its use has become very selective. Although there are no easy answers to pterygium surgery, we need to continue exploring better methods to decrease recurrences with pterygium excision.
In this column, Drs. Sheha and Tseng describe their principles in pterygium surgery, with a focus on recurrent pterygium.
Thomas “TJ” John, MD
OSN Surgical Maneuvers Editor
Hosam Sheha
Scheffer C.G. Tseng
Pterygium is a common ocular surface disease characterized by inflammation and fibrovascular tissue proliferation and invasion resulting in focal conjunctivalization of the cornea presumably due to localized ultraviolet-induced damage to the limbal stem cells. Aggressive fibroblasts in the head of the pterygium that overexpress metalloproteinases are responsible for corneal invasiveness. The indications for surgery include reduced vision due to encroachment on the visual axis, irregular astigmatism, chronic irritation, recurrent inflammation, restrictive ocular motility and cosmetic reasons. Numerous surgical techniques, including bare sclera excision with or without the use of beta irradiation, thiotepa or mitomycin C, and/or transplantation of amniotic membrane or conjunctival autograft, have been described. The main complication of pterygium treatment is the unpredictable rate and timing of recurrences.
Inflammation a risk factor
Ocular surface inflammation plays an important role in pterygium growth and recurrence. It may activate the transformation of the remaining pterygial body fibroblasts into an invasive phenotype, identical to that of the pterygium head fibroblasts, thus increasing the risk of pterygium recurrence. The surgical technique could probably be the single most important factor influencing recurrence. Due to the inflammatory nature of pterygium tissue, the surgically induced inflammation is usually more intense after pterygium excision. Therefore, minimal surgical manipulation during dissection of pterygium is crucial in reducing the recurrence. The use of fibrin glue in lieu of sutures in pterygium surgery has significantly reduced postoperative conjunctival inflammation by reducing the surgical trauma.
Surgical manipulations can elicit various extents of host conjunctival inflammation (Figure 1) adjacent to the transplanted cryopreserved amniotic membrane after pterygium excision despite intraoperative application of MMC. Nevertheless, its incidence might be higher if pterygium excision is not accompanied by transplantation of cryopreserved amniotic membrane, which is known to exert anti-inflammatory, anti-scarring and anti-angiogenic actions. Postoperative injections of long-acting steroid or 5-fluorouracil have been advocated to halt the progression of recurrence by aborting host tissue inflammation. Recently, we have identified that ocular Demodex mite infestation (demodicosis) is an overlooked risk factor for pterygium recurrence, presumably by perpetuating chronic inflammation mediated by Th17 lymphocytes. Therefore, control of inflammation mediated by ocular demodicosis before and after surgery is important for reducing recurrence and should be considered as a strategy in managing pterygium growth and recurrence.
Figure 1. Grading of postoperative host conjunctival inflammation. According to the degree of blood vessel injection, inflammation is graded as grade 0 (no inflammation, a), grade I (mild, b), grade II (moderate, c) and grade III (severe, d).
Images: Sheha H, Tseng SCG
MMC application
For primary pterygium, intraoperative application of MMC significantly reduces pterygium recurrence by inhibiting fibroblast proliferation and migration. Postoperative but not intraoperative application of MMC on the exposed sclera has the potential risk of sight-threatening complications such as necrotizing scleritis, scleral melt, corneal edema and uveitis. To further reduce such a complication, it is advised that intraoperative application of MMC be performed over the truncated fibrovascular tissue, in the gap between the conjunctival edge and the underlying Tenon (Figure 2). This approach reduces MMC dosage and avoids overspill to the entire ocular surface.
Figure 2. After bare scleral excision of pterygium, a gap is invariably created between the conjunctiva and the Tenon (white arrow). This gap allows herniation of the fibrovascular tissue (gray arrow) sandwiched in between to cause recurrence.
Surgical pearls
For recurrent pterygium, it is advised to wait for at least 6 months before re-operation to avoid stirring up more inflammation. The surgery for recurrent pterygium is different from that for primary pterygium (Figure 3). The first key step is to dissect and recess, but not resect, the conjunctiva back to the fornix to avoid conjunctival shortening or symblepharon. This is also based on the recent publication that has identified the importance of saving the residual conjunctiva. The second key step is to seal the gap between the conjunctiva and the Tenon using running sutures so as to restore caruncle morphology and ocular motility, to prevent granuloma pyogenicum, and to create a stronger barrier against further recurrence.
Figure 3. Different approach for primary and recurrent pterygia. For primary pterygium, incision starts anterior to the semilunar fold (a) to resect the fibrovascular tissue including the Tenon from the cornea (b, arrow). For recurrent pterygium, incision starts from the head by lifting the remaining conjunctiva from the cornea (c) and being recessed to the fornix without resection (d, arrow).
This new surgical approach is based on the universal observation of a large unsealed gap present between the conjunctiva edge and the excised Tenon during surgical correction of a number of patients with recurrent pterygium with or without motility restriction. It is advised that the gap be sealed by a continuous running 9-0 nylon suture. Hence, it is likely that the same technique can also be added for primary pterygium to improve the outcome and reduce recurrence. Furthermore, intraoperative application of MMC is not needed. Because the medial rectus muscle is invariably exposed after conjunctival recession and release of conjunctival cicatrix, it is advised to cover the muscle with one layer of cryopreserved amniotic membrane to recreate the muscle sheath and an anti-adhesion biological barrier. For eyes with sufficient conjunctiva in the caruncle area, the remaining bare sclera can be covered by another larger layer of cryopreserved amniotic membrane. However, for eyes with insufficient residual conjunctiva in the caruncle, a small conjunctival autograft or oral mucosal graft is needed. As focal and partial limbal stem cell deficiency is invariably present in all pterygia, including recurrent ones, restoration of limbal integrity is also important. In this regard, it is important to point out that transplantation of cryopreserved amniotic membrane is effective to correct partial limbal stem cell deficiency in many other diseases by promoting expansion of the remaining limbal epithelial stem cells.
In conclusion, several preoperative and postoperative measures to control ocular surface inflammation have been identified to prevent pterygium recurrence. For recurrent pterygium, several key surgical techniques are proposed, including sealing of the gap between the conjunctiva and the Tenon.