Many factors, including environmental and genetic factors, interact to result in myopia [25]. Genetic and embryonic developmental abnormalities mainly cause congenital myopia, manifesting as axial myopia and typical ocular tissue changes [26]. Pathological myopia (PM) refers to a series of degenerative changes in the eye’s fundus because of excessive elongation of the eye axis, with a refraction > -6.0 D or an eye axis > 26.5 mm [27]. In congenital myopia, the excessive growth of the eye axis can easily progress into pathological myopia, causing irreversible visual impairment. Posterior staphyloma (PS), a common fundus change in pathological myopia, is a morphological change in the fundus caused by axial elongation of the eye axis [28], which affects local blood circulation in the macula [29]. Histological studies have revealed a thin sclera, decreased choroidal thickness, and misalignment of scleral collagen fibers at the edge of the uveitic zone [30]. Reinforcing a graft (biological or synthetic material) in the weak sclera at the posterior pole of the eye increases scleral stress and promotes collagen reconstruction, thereby preventing further progression of the eye axis and pathological myopia [8]. In this case, the patient was diagnosed with congenital myopia and amblyopia in both eyes at the age of 3. The fundus examination revealed posterior scleral staphyloma, and the length of the eye axis had already exceeded the level of the adult eye axis (23–24 mm). Considering these factors, posterior scleral consolidation was performed in both eyes after excluding contraindications to surgery. It is hoped that PSR would improve the patient’s fundus health and further have a positive effect on myopia control.

The procedure used the modified Snyder-Thompson approach to transplant the allograft scleral tissue. The modified Snyder-Thompson approach is a widely used procedure that involves creating a U-shaped pocket wrapped around the macular and posterior scleral vitreous areas, allowing for individualized pressure, widening, and padding. It has been demonstrated that posterior scleral reinforcement effectively controls the lengthening of the eye axis, stabilizes the refractive state, and has a low postoperative complication rate [31, 32]. Li et al. [33] observed that the mean eye axis length in the PSR group 5 years after the procedure (29.79 ± 1.26 mm) was significantly shorter than that in the control group (30.78 ± 1.30 mm), effectively controlling the lengthening of the eye axis and myopic progression in pathological myopic eyes. Széll et al. [34] also observed an improvement in BCVA, averaging 0.15 ± 0.09 D in the PSR group 5 years after the procedure, compared to almost no change in refraction in the control group (0.01 ± 0.1 D). In addition, patients with amblyopia showed a more significant improvement in BCVA after undergoing posterior scleral consolidation (0.35 ± 0.12 D). In retrospect, the ocular refractive status of our patient remained stable 4 years postoperatively, with corrected refractions of -5.00/-0.75 × 180 diopters in the right eye and − 6.50DS/-0.50 × 60 diopters in the left. After 1 year postoperatively, both eyes archived a BCVA of 20/20, resulting in the resolution of amblyopia.

Although there was a tendency for the eye axis length to increase within the first 4 years after surgery, the increase was minimal. According to the Public Health Ophthalmology Branch of the Chinese Society of Preventive Medicine [35], the growth rate of the axis length occurs from birth to 3 years of age, with a total growth of approximately 5 mm over that period. From age 3–6 years, the average total growth length of the axis is no more than 1 mm (21.5-22.5 mm), and for Chinese school-age children between 6 and 15 years, the average total growth length of the axis length is 0.93 mm. The growth of the axis length from 6 to 11 years was incremental. The trend of large and rapid growth was 0.09 mm/year for school-age children after 6 years of age, 0.10 mm/year to 0.22 mm/year for 7–8 years of age, 0.13 mm/year to 0.18 mm/year for 9–11 years of age, and 0.01 mm/year to 0.06 mm/year for 12–15 years of age. This patient underwent posterior scleral consolidation in both eyes at the age of 3 years, and the average postoperative axial increase was 0.26 mm/year in the right eye and 0.16 mm/year in the left eye, with the average total length of growth controlled within 1 mm. Posterior scleral consolidation effectively controlled the axis growth in this patient with congenital myopia. It is believed that the improvement in the blood flow status of the retrobulbar vessels and the corresponding change in the axis length because of choroidal thickening contributed to this control. Although conjunctival edema was observed within a short postoperative period, no rejection of the graft material or any other serious and lasting complications, such as elevated intraocular pressure, optic nerve compression, retinal detachment, or retinal hemorrhage, were observed.

The choroid is rich in vascular tissue and essential for maintaining eye physiology. Evidence suggests that the choroid is crucial in controlling eye elongation and developing refractive errors [36, 37]. Animal studies have shown that the choroidal thickness is significantly thinner in models of myopia than in those of hyperopia during choroidal development [38, 39]. The choroidal thickness in the myopia model may be attributed to the short-term thickening of the choroid, which continues to reduce extracellular matrix molecule synthesis and slows eye development [39]. In addition, some clinical studies have suggested the role of choroidal thickness changes in myopia development. Zheng et al. [40] observed an increase in choroidal thickness 1 month after PSR, but there was no statistically significant difference from the control group. Peng et al. [41] found statistically significant differences in choroidal thickness changes between groups from 2 to 3 years after PSR, demonstrating that PSR significantly inhibited eye elongation and induced alterations in choroidal thickness beyond 2 years postoperatively [42]. In this case, the sub-foveal choroidal thickness (SFCT) was found to be thickened from 1 to 2.5 years postoperatively, and ocular ultrasound showed that the hemodynamic parameters of the ophthalmic, central retinal, and posterior ciliary arteries returned to normal 6 months postoperatively. The superficial and deep retinal perfusion in the area increased significantly from the preoperative levels ([33.82 ± 4.33% and 14.29 ± 3.89%] to [48.18 ± 4.56% and 31.47 ± 5.11%]).

Recently, the pathogenesis hypothesis of myopia has suggested that the sclera is the ultimate effector of myopia development, and scleral microenvironmental hypoxia triggers extracellular matrix remodeling and myopia [43, 44]. Conversely, increased choroidal perfusion effectively improves scleral hypoxia and inhibits axis length elongation and myopia development [45]. In this case, the choroidal thickness improved compared to the preoperative level, and amblyopia was cured at 1 year postoperatively. The recovery of visual acuity may be related to the improved blood flow status of the choroid, enhancing visual sensitivity.

In this case report, the patient was found to have a high refractive error with amblyopia during visual development. As children’s physical development progresses, myopia was likely to increase, which could lead to abnormal visual function and binocular gaze stability, fusion, and adjustment, even serious fundus complications. After 3 years of surgery, it was observed that the child exhibited fusion dysfunction. Consequently, the child underwent 1 year of visual function training to stabilize the perceptual eye position, enhance gaze stability and restore normal stereopsis function.

In the 1960s, orthokeratology lenses were first proposed for controlling development [46]. The lens material was upgraded from the early rigid polymethylmethacrylate material to a highly oxygen-permeable fluorosilicone acrylate polymer. A possible mechanism for controlling myopia progression is now attributed to the myopic eye’s relative peripheral refraction, which exhibits myopic defocus with orthokeratology lenses and slows the elongation of the axis length [44, 47, 48]. Recently, with optimized lens design and standardized fitting processes, many clinical trials have shown that orthokeratology lenses can effectively control myopia development with a certain degree of safety [49]. Charm et al. [14] found that high myopia patients wearing orthokeratology lenses could effectively control the axial length growth, with an average increase of 0.19 mm over 2 years, compared to an average increase of 0.51 mm in the control group. Atropine is a competitive muscarinic receptor inhibitor. It is believed that atropine prevents and controls myopia by regulating the ciliary muscles. Although the molecular mechanisms by which atropine controls myopia progression are not fully elucidated, most current studies suggest that atropine may achieve myopia control by acting on relevant receptors and signaling pathways in the retina and posterior sclera. These include M1/M4 receptors in the retina that perform biological functions [50], the cholinergic signaling pathway that mediates retinal M receptors [51], and the G protein signaling pathway that mediates M receptors in the retinal and scleral tissues [52, 53].

Furthermore, atropine has been shown to control the growth of the ocular axis by antagonizing muscarinic receptors and inhibiting fibroblast proliferation in the scleral collagen matrix [18]. In addition, atropine may affect γ-aminobutyric acid, dopamine receptors, and α2 adrenergic receptors to control myopia progression. However, further scientific studies and clinical observations are needed, as the involvement of the receptors and signaling pathways is currently at the animal study level. Notably, the effectiveness of atropine in controlling myopia progression shows concentration dependence [54], and 0.05% atropine is considered the most effective in controlling the equivalent spherical lens degree and axis length. However, the use of high concentrations of atropine is associated with side effects such as photophobia and blurred vision [55]. Therefore, several clinical trials have been conducted to observe the effect of 0.01% atropine on myopia control. It was found that low concentrations of atropine were effective in delaying myopia progression and slowing the growth rate of the axis length in children. Also, it reduces adverse reactions after administration and rebound reactions after discontinuation of the drug and improves compliance with atropine treatment [56, 57]. Clinical studies have also shown that orthokeratology combined with atropine is more effective than orthokeratology alone in controlling the elongation of the axis length and myopia development [58,59,60,61,62]. In this case, we initiated orthokeratology combined with atropine in the fourth year after surgery to better control myopia development. During the combined treatment period, low-prescription frames were worn during the day to maintain clear vision and achieve better myopia control. According to the Public Health Ophthalmology Branch of the Chinese Society of Preventive Medicine, the average total growth length of the axis length in Chinese school-age children between 6 and 15 years old is 0.93 mm [35]. The trend of the large and rapid growth of the axis length between 6 and 11 years old is reflected in the increase of the axis length in both eyes, which is 0.02 mm/year and 0.03 mm/year in the first year of treatment and 0.05 mm/year and 0.07 mm/year in the 2nd year.

In the 3th and 4th years, there was a decrease in the results of the axis length examination compared to those of the previous years. The reason for this was that the patient could not visit the hospital for a review because of the COVID-19. Additionally, the instrument used to measure the axis length was different at this time than from the previous one, which could have caused the discrepancy. Therefore, the increase in the axis length in the fourth year was 0.14 mm/year and 0.03 mm/year, indicating effective control. In this case study, in addition to keratomileusis, atropine was used to control myopic defocus and effectively improve choroidal thickness and retrobulbar perfusion, thereby controlling the rate of increase in axis length and development [45, 63, 64]. The vision was not fully corrected due to the high refractive error and flat keratometry (-5.00/-0.75 × 180 diopters in the right eye and − 6.50/-0.50 × 60 diopters in the left eye, flat keratometry/steep keratometry 41.00/43.00 in the right eye and 42.50/42.75 in the left eye). In order not to affect the patient’s quality of life and pursue better myopia control effect during the daytime, we recommended the patient to wear glasses to correct the remaining refractive error.

In conclusion, early intervention is crucial for preventing the development of congenital myopia. Particularly, the presence of posterior scleral staphyloma in this patient underscores the importance of preventing and treating myopia to avoid the progression of pathological myopia, which can lead to irreversible visual impairment. Several synthetic materials have recently been developed for posterior scleral reinforcement, such as artificial pericardial patches, polyester fiber mesh, and modified liquid silicone [9, 65]. Scleral collagen crosslinking [66] and scleral regeneration therapy [67] are potential treatments. This case involved early interventional treatment of a patient with congenital myopia using a combination of posterior scleral consolidation, optical correction with medication, and visual function training to intervene in myopia development, with a follow-up period of up to 8 years. The combined effect of posterior scleral consolidation, orthokeratology, and low concentration of atropine exhibited remarkable results in controlling myopia development, resulting in a slow increase in axial length, even below the physiological growth rate. The patient achieved stable myopic refractive error and could live and study normally, significantly improving self-confidence. This case provides a novel approach to managing congenital myopia in children and confirms that combined interventions can restore clear vision and normal visual function in patients with congenital myopia.