Pterygium surgery has changed in the last ten years, giving an ophthalmologist several methods to select from. Conjunctival autograft (CA) and CA combined with adjunctive mitomycin C (MMC) are the most frequent methods used in the treatment of primary and recurrent pterygium [1-3]. Scleral necrosis/melting is a rare complication that may develop after pterygium surgery. The possible pathological mechanisms behind scleral necrosis after pterygium surgery may include infection, hypersensitivity reaction, and ischemia; the latter may be more important, and adjunctive MMC usage may predispose to its development [4-6]. Treatment modalities include antibiotics, systemic immunosuppressive agents, and surgical repair of the scleral defect with a variety of graft materials. In some reports, high doses of systemic immunosuppressive treatment have been needed to arrest the further progression of melting [7], whereas side effects have occurred. Symptoms include foreign body sensation, eye redness, and tearing. Advanced cases of pterygium may produce visual disturbances, both via astigmatism and by physically blocking the optical axis with pterygium tissue [8-11]. Gold standard surgery for clinically significant pterygium today is excision with conjunctival autograft, offering low recurrence rates [12-15]. Although quite effective, the procedure carries some risks. We detail a severe case of bacterial keratitis subsequent to pterygium excision with conjunctival autograft that progressed to sclerokeratitis and required large-diameter penetrating keratoplasty (PK). A variety of pharmacological agents used postoperatively have been implicated in the etiology of scleral melting. Potent topical corticosteroids such as prednisolone acetate 1%, while good at controlling inflammation, can cause impair wound healing by inhibiting fibroblast proliferation and collagen synthesis [16-19]. Similarly, NSAIDs, including ibuprofen, diclofenac, or ketorolac, have been linked to corneal and scleral melting, possibly because they inhibit prostaglandin-mediated epithelial repair and also constricting episcleral microcirculation. Conversely, milder corticosteroids such as fluorometholone would be safer and have enough anti-inflammatory effects without tending to delay healing [20,21]. The etiology of scleral necrosis after ocular surgery is multifactorial, i.e., surgical trauma, excessive cautery, ischemia, infection, and drug toxicity [8]. Eliminating infectious and autoimmune pursuits is vital for the proper assessment of drug risk. In this study, cases with elevated inflammatory markers (ESR, CRP) and positive conjunctival culture were excluded to study pharmacologic effects of anti-inflammatory regimens [22]. The rationale behind this study arose from observing that cases of scleral melt have been increasingly reported after pterygium excision, mainly when potent anti-inflammatory drops are prescribed empirically following surgery [11,23]. Data from Iraqi tertiary centers are scarce, and most of the literature numbers from either single-case reports or small case series abroad. Hence, this study was intended as a prospective cross-sectional one conducted at Al-Kindy Teaching Hospital and Imam Ali Hospital to systematically compare the incidence of scleral melt after the administration of three widely used post-pterygium surgery anti-inflammatory treatment modalities (fluorometholone, prednisolone acetate 1%, and ibuprofen) after standardized pterygium surgery with direct suturing technique. Knowing the drug-specific risk for scleral melting is of utmost necessity for the clinician in making valid decisions. Making an identifiable, safe yet effective anti-inflammatory regimen may help avoid catastrophic complications alongside maintaining a functional postoperative outcome. This investigation aims to provide regional evidence to inform post-pterygium-surgery guidelines in Iraq and similar climates.

Prospective cross-sectional study at Al-Kindy Teaching Hospital and Imam Ali Hospital, Baghdad (1 March–31 December 2024). Adults with primary nasal pterygium underwent excision with direct scleral suturing by a single surgeon. A total of 45 consecutive patients diagnosed with primary nasal pterygium were included. All patients presented with symptomatic lesions either threatening the visual axis, inducing astigmatism, or causing cosmetic concern.

Inclusion Criteria

• Age ≥ 18 years

• Primary (non-recurrent) nasal pterygium extending onto the cornea

• Normal preoperative erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)

Exclusion Criteria

• Autoimmune or collagen-vascular disorders (e.g., rheumatoid arthritis, lupus)

• Infectious conjunctivitis or positive bacterial culture on pre-operative swab

• Previous ocular surgery, trauma, or chemical injury

• Recurrent pterygium or double-headed lesions

Preoperative Evaluation

All participants underwent a full ophthalmologic assessment, including visual acuity, slit-lamp examination, intraocular pressure measurement, and documentation of lesion size and vascularity. Environmental and systemic data, such as occupation (outdoor/indoor work), residence (urban/rural), UV exposure, dry-eye symptoms, and diabetic status, were recorded to assess potential risk factors associated with scleral melt (as later analyzed in Table 5).

Surgical Technique

Each patient underwent pterygium excision using the direct scleral-suturing technique under facial block anesthesia with additional topical and subconjunctival lidocaine. The fibrovascular tissue was carefully dissected from the corneal surface, and the residual scleral bed was cleaned of Tenon’s tissue. Hemostasis was achieved by minimal bipolar cautery. The bare scleral defect was then closed with interrupted 8-0 vicryl sutures without using mitomycin-C, fibrin glue, or graft material to standardize outcomes.

All surgeries were performed in the same operating theater under aseptic conditions, and patients were discharged on the same day with standardized postoperative instructions.

Postoperative Medication Protocol and Grouping

To assess the influence of anti-inflammatory type on scleral healing, patients were randomly assigned into three equal treatment groups (n = 15 each) using simple randomization:

• Group I: Fluorometholone 0.1% + Ofloxacin 0.3% eye drops (1 drop × 5 daily)

• Group II: Prednisolone acetate 1% + Ofloxacin 0.3% (1 drop × 5 daily)

• Group III: Ibuprofen ophthalmic drops + Ofloxacin 0.3% (1 drop × 5 daily)

The antibiotic regimen was identical in all groups to control for antimicrobial influence. Patients were advised to avoid sun exposure and to use UV-protective eyewear postoperatively.

Follow-Up and Clinical Evaluation

Patients were examined at 1 week, 1 month, and 3 months after surgery. During each visit, detailed slit-lamp bio-microscopy was performed to evaluate wound healing, inflammation, and any evidence of scleral thinning, whitening, necrosis, or uveal exposure.

Cases presenting with melting underwent immediate microbiological swab for culture and sensitivity testing. Those with positive bacterial growth were excluded from analysis of drug-related necrosis to eliminate confounding infectious etiology.

Scleral melts were graded as:

• Mild: superficial thinning without uveal exposure,

• Moderate: focal uveal show or tissue loss <3 mm,

• Severe: progressive necrosis or impending perforation

Time to onset was calculated from the day of surgery to the first clinical detection of melt.

Management of Scleral Melt

Upon diagnosis, the offending anti-inflammatory drug was immediately discontinued. Management was stratified according to severity:

• Mild cases received copious preservative-free lubricants and close follow-up

• Moderate cases underwent amniotic membrane grafting to restore the ocular surface

• Severe cases required conjunctival autografting for tectonic support

• Healing duration and final visual outcome were recorded for all patients

Outcome Measures

The primary outcome was the incidence of scleral melt in each treatment group. Secondary outcomes included the severity, time to onset, environmental or systemic associations, and healing response after treatment.

Statistical Analysis

All collected data were tabulated and analyzed using SPSS version 26.0 (IBM Corp., Chicago, IL, USA). Categorical variables were presented as frequencies and percentages [n (%)], and continuous variables as mean ± standard deviation (SD). Comparative analyses between groups were performed using the Chi-square test or Fisher’s exact test for categorical data, and independent-sample t-tests for continuous variables where appropriate. A p-value<0.05 was considered statistically significant.

Table 1 demonstrates the demographic characteristics of the 45 patients who underwent pterygium excision at Al-Kindy Teaching Hospital and Imam Ali Hospital, Baghdad. The mean age of participants was 53.7 ± 12.8 years, indicating that pterygium predominantly affected middle-aged and older adults, consistent with chronic ultraviolet (UV) exposure and cumulative ocular surface irritation as contributing factors. The gender distribution showed a slight male predominance (53.33% males vs. 46.67% females), reflecting a higher likelihood of outdoor occupational exposure among men in this population. Regarding laterality, the right eye was slightly more frequently involved (55.56%) than the left (44.44%), possibly related to asymmetric sun exposure patterns during driving or work activities. Occupational analysis revealed that outdoor workers constituted two-thirds (66.67%) of the sample, supporting the strong etiologic link between UV radiation, wind, and dust exposure in pterygium development. Furthermore, urban residents (62.22%) were more represented than rural ones (37.78%), possibly due to easier access to surgical services or higher air pollution levels in urban areas.

Table 1: Demographic Profile of Patients

Table 2 highlights a clear relationship between the type of postoperative anti-inflammatory medication and the incidence and severity of scleral melt following pterygium surgery. No cases of scleral necrosis were reported among patients treated with fluorometholone (0.00%), confirming its safety and favorable healing profile. In contrast, the prednisolone acetate 1% group exhibited scleral melt in 4 patients (26.67%), distributed across mild (13.33%), moderate (6.67%), and severe (6.67%) forms, reflecting the deleterious impact of high-potency corticosteroids on scleral collagen integrity and wound repair. The ibuprofen group demonstrated the highest incidence (40.00%), with equal distribution among mild, moderate, and severe categories, supporting the well-documented association between topical NSAIDs and ischemic necrotizing complications due to inhibition of prostaglandin-mediated epithelial healing. Overall, scleral melt occurred in 10 of 45 patients (22.22%), underscoring that the postoperative regimen plays a pivotal role in postoperative tissue viability.

Table 2: Incidence and Severity of Scleral Melt by Treatment Group

Table 3 illustrates the average duration between pterygium surgery and the clinical appearance of scleral melt among patients receiving different postoperative anti-inflammatory regimens. No cases of scleral necrosis were observed in the fluorometholone group, reaffirming its safety and balanced anti-inflammatory efficacy. In contrast, patients using prednisolone acetate 1% developed scleral melt after an average of 18.6 ± 4.2 days (range 12–25 days), while those treated with ibuprofen eye drops experienced a significantly earlier onset at 14.2 ± 3.9 days (range 9–21 days). The differences between both treatment groups and the fluorometholone group were statistically significant (p = 0.04 and p = 0.02, respectively).

Table 3: Mean Time to Onset of Scleral Melt after Surgery

(*Significant vs Fluorometholone group)

Table 4 analyzes the association between patients’ demographic variables and the occurrence of scleral melt following pterygium surgery. The incidence of scleral melt was slightly higher among individuals aged 50 years and above (70.00%) compared to younger patients (30.00%), though this difference did not reach statistical significance (p = 0.71). This mild trend may reflect the cumulative effect of aging on ocular surface integrity and collagen remodeling, making older eyes more susceptible to postoperative ischemic or inflammatory injury. Similarly, scleral melt was more common in males (60.00%) than in females (40.00%), but again, the difference was not statistically significant (p = 0.64).

Table 4: Relationship between Age, Gender and Scleral Melt

Table 5 explores the influence of environmental and systemic risk factors on the development of scleral melt after pterygium surgery. A statistically significant relationship was found between chronic ultraviolet (UV) exposure and scleral melt occurrence (p = 0.03), as 9 of 30 patients (30.00%) with prolonged outdoor exposure developed postoperative necrosis. This finding underscores the critical role of cumulative solar radiation in weakening scleral collagen and promoting oxidative stress, which compromises tissue healing following surgery. Similarly, dry-eye symptoms were significantly associated with scleral melt (p = 0.04), with 4 of 12 affected patients (33.33%) developing scleral thinning. Reduced tear film stability and ocular surface desiccation likely contribute to local ischemia and delayed epithelial repair, exacerbating the risk of necrosis. Conversely, diabetes mellitus was not significantly correlated with scleral melt (p = 0.19), despite 2 of 6 diabetic patients (33.33%) being affected, suggesting that while systemic metabolic factors may influence healing, local environmental stresses exert a stronger effect.

Table 5: Association of Environmental and Systemic Factors with Scleral Melt

Table 6 presents the management approaches and healing outcomes for the ten patients who developed scleral melt following pterygium surgery. The majority of cases, 6 patients (60.00%), were successfully managed by immediate discontinuation of the causative anti-inflammatory drops combined with the intensive use of preservative-free lubricants, leading to complete recovery within an average of 18 ± 5 days. This conservative approach proved effective in mild-to-moderate cases where necrosis was limited to superficial scleral tissue. Amniotic membrane grafting, performed in 3 patients (30.00%), was indicated for deeper or progressive melts and achieved full recovery within 27 ± 6 days, demonstrating its regenerative and anti-inflammatory benefits in promoting ocular surface healing. One severe case (10.00%) required a conjunctival autograft, achieving stabilization though mild residual scarring persisted after approximately 35 ± 7 days. Collectively, these results indicate that early identification and prompt withdrawal of harmful topical agents can prevent disease progression in most cases, while surgical interventions such as amniotic membrane or conjunctival grafts remain essential for restoring ocular integrity in advanced necrosis.

Table 6: Management and Healing Outcome of Scleral Melt Cases (n = 10)

This prospective study at Al-Kindy Teaching Hospital and Imam Ali Hospital, Baghdad aimed to determine if the choice of anti-inflammatory drug in the postoperative period affects the occurrence of scleral melt after pterygium surgery. The cohort profile (mean age 53.7 ± 12.8 years; males 24 (53.33%); outdoor workers 30 (66.67%)) broadly represents the accepted epidemiology of pterygium: predominantly a disease of middle-to-older individuals with accumulated environmental insults. Given this predominantly outdoor working class and the predominance of the right eye involved, these affect asymmetric ultraviolet (UV) irradiation and ocular surface desiccation with respect to daily-life activities and driving. Thus, these findings concur with long-term outcomes on pterygium and its environmental factors, from larger series, and reviews, e.g., regarding recurrence and surface morbidity post-surgery [3,24], and with evidence that aging and ocular surface disease (mainly evaporative dry eye) adversely impact homeostasis and wound healing [25,26]. The main finding here was the very strong relationship between scleral melt and the postoperative regimen. Scleral melt was never associated with Fluorometholone 0.1% (0/15; 0.00%); however, it occurred in 26.67% (4/15) and 40% (6/15) of patients treated with prednisolone acetate 1% and ibuprofen respectively. In addition, the time-to-onset was significantly different between ibuprofen (mean 14.2 ± 3.9 days) and prednisolone acetate (mean 18.6 ± 4.2 days) compared with the fluorometholone regime, with ibuprofen being earlier than prednisolone acetate. Even though mitomycin C (MMC) was not used in our regimen, which is another risk for ischemic complications and scleral thinning [13,14], our complication records in the strong-steroid/NSAID groups stand consistent with previous reports on surgically induced necrotizing scleritis (SINS) and sclero-corneal compromise following ocular surface surgery. Those reports hold that tissue breakdown results from a confluence of factors, including surgical trauma, vascular compromise, and pharmacologic effects that block fibroplasia or delay epithelial and stromal repair distantly [4,8,18]. The signal for safety apparently seen for fluorometholone correlates with its pharmacologic profile as a weaker corticosteroid that reduces inflammation with less inhibition of collagen synthesis than prednisolone acetate 1%. The significance of steroid potency has been discussed broadly in the scleritis and ocular surface literature because early reparative over-suppression predisposes to structural weakening of the tissue [6,11]. Conversely, our ibuprofen data matches those clinical concerns (case-based and mechanistic) within corneoscleral literature that topical NSAIDs inhibit epithelial migration, reduce prostaglandin-mediated perfusion, and cause ischemic melts within susceptible beds in post-surgical cases (deduced from scleral/corneal melt case series and reviews) [4,8,11,18]. Although randomized head-to-head data for fluorometholone vs. prednisolone vs. NSAIDs during post-pterygium healing is lacking, the directionality of risk in our cohort indeed agrees with complication patterns described in contemporary complication audits [24] and SINS-focused reports [4,8,18]. Our analysis of risk factors strengthens the biological plausibility. A significantly large proportion of melts presented with chronic UV exposure (30/45; 66.67%) and dry-eye symptoms (12/45; 26.67%) (p = 0.03 and p=0.04 respectively). UV radiation has a cumulative effect on disturbing extracellular matrix turnover and raising oxidative stress, which thins scleral collagen and decreases potential for repair once surgery is done [3,24]. Aging carries with it a certain degree of immune senescence and a proinflammatory milieu that further diminishes epithelial barrier resilience and lacrimal function-yielding desiccating stress [25,26]. Although the trend of melts was more common in patients aged ≥50 years and in males, post-operative drug class remained the foremost and modifiable determinant of melt. Infectious confounders, significant contributors to post-pterygium keratitis/scleritis and late SINS [23,27,28,20] were excluded by culture, and culture-positive cases were left out of the drug effect analysis, confirming recommended pathophysiological evaluation avenues for post-surgical scleritis [22]. Our series shows concordance of management outcomes with previously reported scleral compromise treatment strategies. Withdrawal of the drug and adequate intensive lubrication without preservatives brought about a restoration of 60.00% (6 out of 10) within 18 ± 5 days, confirming that early superficial ischemia is reversible if the agent is promptly discontinued [11]. Amniotic membrane grafting restored the surface in the remaining 30.00% (3 out of 10) cases, consistent with the literature which reports its anti-inflammatory and pro-epithelial properties in scleral and conjunctival reconstruction [9,10,16]. One case, severe in nature, required conjunctival autografting with final residual scarring-an outcome pattern that has been previously documented when a deeper loss of stroma requires tectonic reinforcement [9,10,12,15,16]. These paths are the same for managing any scleritis: beginning with identifying trigger sources and lubrication, then moving on to surgical coverage; in immune-mediated SINS, systemic immunomodulation (i.e., tacrolimus, rituximab) has been described but never needed in our population [7,6,29]. Our results require interpretation concerning operative technique employed. We standardized surgical interventions to directly suture the sclera without MMC or any grafts, in view of isolating medication effects. MMC, which is the best on recurrence-preventive adjuvant, has been reported for scleral thinning and infrequent, if any, perforations by some authors [13,14]. So, by having excluded MMC, we aimed at avoiding confounding and provide pragmatic recommendations to centers favoring non-MMC primary excision procedures. Those employing MMC or bare sclera should be extra cautious, given the historical associations of these techniques with SINS and infectious keratitis [13,14,23,27,28].

Strengths

Strengths of this study included: (i) equal-sized randomized groups receiving a shared antibiotic backbone; (ii) prospective risk-factor capture (UV exposure, dry eye); and (iii) microbiologic exclusion of infectious etiologies in the melt analysis. 

Limitations

Limitations include the modest sample size and short (3-month) follow-up that could miss very late SINS (18,21). Moreover, there was no masking. 

Clinical Implications

One, fluorometholone provides a fine balance between inflammation control and safety when the eyes lack high-risk features and are undergoing routine care post-pterygium. Two, topical NSAIDs are best avoided during the immediate postoperative period, especially in UV-exposed or dry-eye subjects. Three, if stronger corticosteroids are considered necessary (exuberant inflammation), they should be given short-term under close review with patients being advised along the way about early warning signs. Four, environmental modification must be practiced with UV-blocking eyewear and aggressive lubrication, given the significant associations observed, and the pathophysiology of aging ocular surfaces [25,26]. Future studies should test these signals in a larger randomized trial comparing low- and high-potency steroids as well as various NSAIDs, incorporate objective surface metrics (Schirmer, tear breakup time, corneal sensitivity), and stratify by surgical approach (autograft vs. amniotic membrane vs. bare sclera) in order to quantify the interaction with pharmacologic risk [1-3,9,10,16]. Given the case-based literature on immune-mediated SINS and rare infections years post-surgery [18,20,21,27,28], longer follow-up registries would be useful in capturing late events and refining surveillance intervals. 

To conclude, our data show postoperative regimens to be a key modifiable determinant of scleral integrity following pterygium excision. The absence of melt in fluorometholone (0.00%) as opposed to very high and early melt under prednisolone acetate 1% and ibuprofen with the additive effect of significant UV and dry eye effects leads us to advocate for the practice paradigm of fluorometholone-lubrication-UV protection as first-line postoperative care, while potent steroids should be reserved on a case-by-case basis and closely monitored.

1. Kheirkhah, A. et al. “Randomized trial of pterygium surgery with mitomycin C application using conjunctival autograft versus conjunctival-limbal autograft.” Ophthalmology, vol. 119, 2012, pp. 227-232.

2. Díaz, L. et al. “Efficacy and safety of intraoperative mitomycin C as adjunct therapy for pterygium surgery.” Cornea, vol. 27, 2008, pp. 1119-1121.

3. Fernandes, M. et al. “Outcome of pterygium surgery: Analysis over 14 years.” Eye (London), vol. 19, 2005, pp. 1182-1190.

4. Jain, V. et al. “Surgically induced necrotizing scleritis after pterygium surgery with conjunctival autograft.” Cornea, vol. 27, 2008, pp. 720-721.

5. Morley, A.M. et al. “Surgically induced necrotising scleritis following three-port pars plana vitrectomy without scleral buckling: A series of three cases.” Eye (London), vol. 22, 2008, pp. 162-164.

6. de la Maza, M.S. et al. “Scleritis therapy.” Ophthalmology, vol. 119, 2012, pp. 51-58.

7. Young, A.L. et al. “Successful treatment of surgically induced necrotizing scleritis with tacrolimus.” Clinical and Experimental Ophthalmology, vol. 33, 2005, pp. 98-99.

8. Yamazoe, K. et al. “Surgically induced necrotizing scleritis after primary pterygium surgery with conjunctival autograft.” Clinical Ophthalmology, vol. 5, 2011, pp. 1609-1611.

9. Sangwan, V.S. et al. “Structural and functional outcome of scleral patch graft.” Eye (London), vol. 21, 2007, pp. 930-935.

10. Gregory, M.E. et al. “Excision of granulation tissue and free conjunctival autograft in the management of necrotizing scleritis.” Cornea, vol. 29, 2010, pp. 577-579.

11. Rachitskaya, A. et al. “An update on the cause and treatment of scleritis.” Current Opinion in Ophthalmology, vol. 21, 2010, pp. 463-467.

12. Davidson, R.S. et al. “Tarsoconjunctival pedicle flap for the management of a severe scleral melt.” Cornea, vol. 26, 2007, pp. 235-237.

13. Dadeya, S. et al. “Corneoscleral perforation after pterygium excision and intraoperative mitomycin C.” Ophthalmic Surgery, Lasers and Imaging, vol. 34, 2003, pp. 146-148.

14. Solomon, A. et al. “Long-term effects of mitomycin C in pterygium surgery on scleral thickness and the conjunctival epithelium.” Ophthalmology, vol. 111, 2004, pp. 1522-1527.

15. Yazici, B. “Use of conjunctiva-Müller muscle pedicle flap in surgical treatment of necrotizing scleritis.” Ophthalmic Plastic and Reconstructive Surgery, vol. 24, 2008, pp. 19-23.

16. Kim, B.H. “Surgical treatment of necrotic scleral calcification using combined conjunctival autografting and an amniotic membrane inlay filling technique.” Eye (London), vol. 25, 2011, pp. 1484-1490.

17. Díaz-Valle, D. et al. “Immunologic and clinical evaluation of postsurgical necrotizing sclerocorneal ulceration.” Cornea, vol. 17, 1998, pp. 371-375.

18. O'Donoghue, E. et al. “Surgically induced necrotising sclerokeratitis (SINS): Precipitating factors and response to treatment.” British Journal of Ophthalmology, vol. 76, 1992, pp. 17-21.

19. Fong, L.P. et al. “Immunopathology of scleritis.” Ophthalmology, vol. 98, 1991, pp. 472-479.

20. Singh, R.P. et al. “Scedosporium prolificans sclerokeratitis 10 years after pterygium excision with adjunctive mitomycin C.” Clinical and Experimental Ophthalmology, vol. 33, 2005, pp. 433-434.

21. Lai, T. et al. “Surgically induced necrotizing scleritis occurring 48 years after strabismus surgery.” Journal of Pediatric Ophthalmology and Strabismus, vol. 42, 2005, pp. 180-182.

22. Akpek, E.K. et al. “Evaluation of patients with scleritis for systemic disease.” Ophthalmology, vol. 111, 2004, pp. 501-506.

23. Soleimani, M. et al. “Infectious keratitis after pterygium surgery.” Eye (London), vol. 34, no. 5, 2020, pp. 986-988.

24. Kodavoor, S.K. et al. “Profile of complications in pterygium surgery - A retrospective analysis.” Indian Journal of Ophthalmology, vol. 69, no. 7, 2021, pp. 1697-1701.

25. Kitazawa, K. et al. “Impact of aging on the pathophysiology of dry eye disease: A systematic review and meta-analysis.” Ocular Surface, vol. 25, 2022, pp. 108-118.

26. Lewis, E.D. et al. “Age-associated alterations in immune function and inflammation.” Progress in Neuro-Psychopharmacology and Biological Psychiatry, vol. 118, 2022, p. 110576.

27. Teoh, R.J. et al. “Infectious surgically induced necrotising scleritis presenting 10 years post-pterygium excision: A case report.” Malaysian Journal of Ophthalmology, vol. 5, no. 1, 2023, pp. 1-8.

28. Lee, J.E. et al. “Methicillin-resistant Staphylococcus aureus sclerokeratitis after pterygium excision.” Cornea, vol. 26, no. 6, 2007, pp. 744-746.

29. Fidelix, T.S. et al. “Management of necrotizing scleritis after pterygium surgery with rituximab.” Arquivos Brasileiros de Oftalmologia, vol. 79, 2016, pp. 339-341.