Hyperopia is a refractive state of the eye in which parallel light rays entering the eye without accommodation focus behind the retina. In other words, it is a condition where the far point is at a finite distance behind the eye, meaning that light converging toward the back of the eye comes to a focus on the retina.
This condition is mainly caused by the combined refractive power of the cornea and lens being too weak relative to the axial length of the eye. Generally, hyperopia of +6D or more is called high hyperopia, and extreme hyperopia of +10D or more may fall into the category of microphthalmos.
Hyperopia is classified into the following three types based on the measurement method.
Total hyperopia = Manifest hyperopia + Latent hyperopia holds true.
| Type | Definition |
|---|---|
| Total hyperopia | Hyperopic refractive error measured under complete cycloplegia with cycloplegic agents such as atropine. |
| Manifest hyperopia | Hyperopic refractive error detectable by routine refraction testing without cycloplegia. |
| Latent hyperopia | Hyperopic refractive error that is latent and not detected by routine testing, but becomes apparent only under cycloplegic examination. It is large in children. |
Latent hyperopia is a hyperopic component that is compensated by accommodation during routine refraction testing and therefore not detectable, but becomes apparent only when examined with cycloplegic agents (such as cyclopentolate or atropine). Children have very strong accommodative ability, so the proportion of latent hyperopia is high. Missing latent hyperopia can lead to inadequate diagnosis and treatment of amblyopia or accommodative esotropia, so cycloplegic examination is always performed in pediatric hyperopia evaluation.
| Type | Definition |
|---|---|
| Facultative hyperopia | The part of manifest hyperopia that can be compensated by accommodation. The hyperopic degree that can be clearly seen with the naked eye through accommodation. |
| Absolute hyperopia | The part of manifest hyperopia that is not compensated by accommodation. Clear vision is not possible without corrective lenses. |
| Relative hyperopia | Related to eye position: hyperopia that can be clearly seen by accommodation, but which causes esotropia. |
As the elasticity of the lens decreases with age, accommodative power declines, so the component that was hidden as facultative hyperopia in youth becomes apparent as eye strain and decreased vision in middle age and beyond.
| Classification | Definition | Main causes |
|---|---|---|
| Refractive hyperopia | Weak combined refractive power of the cornea and lens | Flat cornea, posterior dislocation of the lens, refractive changes due to diabetes, aphakia |
| Axial hyperopia | Short axial length of the eye | Congenital (neonatal), acquired (compression by orbital tumor, retinal elevation in retinal detachment, etc.) |
Generally, newborns are hyperopic, with a distribution centered around +2D. By around 1 year of age, they become nearly emmetropic. Hyperopia tends to increase until around 7–8 years of age and then decreases. This is called emmetropization. In a study by Herrnheiser in 1892, the frequency of hyperopia decreased by around age 20, while the frequencies of emmetropia and myopia increased.
The prevalence of amblyopia is reported to be about 2–4% in children, with hyperopic anisometropic amblyopia and hyperopic binocular amblyopia accounting for a large proportion 1). The risk of amblyopia and accommodative esotropia particularly increases with hyperopia of +2D or more, and the risk of developing amblyopia becomes significantly higher at +6D or more (see table) 1).
The mean hyperopia in pure accommodative esotropia is +5.43D ± 2.25 D (in amblyopic eyes without esotropia, +6.11D ± 1.84 D), indicating that high hyperopia is a major risk factor for amblyopia and esotropia 1). Even in special cases with high anisometropia (e.g., -17.50D) such as unilateral megalophthalmos associated with neurofibromatosis type 1 (NF1), severe amblyopia can result if early ophthalmology referral is not made 11).
Symptoms of hyperopia vary greatly depending on the degree.
Mild Hyperopia (less than +3D)
Symptoms: Usually asymptomatic.
Mechanism: Compensated by accommodation as facultative hyperopia.
Need for correction: If asymptomatic, observation may be sufficient. However, be aware of the risk of amblyopia and strabismus.
Moderate Hyperopia (+3 to +6D)
Symptoms: Accommodative asthenopia (easy fatigability, headache, eye pain, tearing). Fatigue during near work often precedes.
Mechanism: Constant accommodation to see clearly leads to overcontraction of the ciliary muscle.
Need for correction: Correction with convex lenses reduces accommodative load.
High Hyperopia (+6D or more)
Symptoms: Hyperopic amblyopia and accommodative esotropia. Distance vision also decreases. Risk of acute angle-closure glaucoma due to shallow anterior chamber and narrow angle.
Mechanism: Accommodation cannot fully compensate, resulting in persistently poor retinal focus.
Need for correction: Early spectacle correction is essential. It should be combined with amblyopia and strabismus treatment.
High hyperopia presents characteristic fundus findings.
High hyperopia (especially +2D or more) is prone to the following complications.
It occurs when the refractive power of the cornea or lens is relatively weak.
It occurs when the axial length of the eye is shorter than normal.
The following examinations are necessary for diagnosing hyperopia.
| Examination | Purpose |
|---|---|
| Objective refraction test (autorefractor) | Quantification of refractive error (reference value) |
| Retinoscopy (retinoscope) | Objective refraction measurement in children. Excellent accommodation control. |
| Subjective refraction test (corrected visual acuity) | Determination of final prescription power |
| Refraction under cycloplegia | Detection of true hyperopia (total hyperopia). Essential in children. |
| Corneal topography analysis and biometry | Evaluation of axial length and anterior chamber depth. Anatomical assessment of high hyperopia. |
In young children, due to lack of concentration to maintain proper focus on distant objects, instillation of cycloplegic eye drops is essential for objective refraction testing.
First choice: 1% cyclopentolate (Cyplegin®) eye drops
One to two instillations per day provide sufficient cycloplegia. Onset of effect is 30–60 minutes after instillation, lasting about half a day. Be aware of side effects (facial flushing, tachycardia, excitement).
Atropine eye drops (when stronger cycloplegia is needed)
Regardless of age, 1% atropine eye drops are used, instilled twice daily for 7 days. This provides the most complete cycloplegia and can detect the full amount of latent hyperopia. Since the effect lasts 1–2 weeks and mydriasis and photophobia persist, it is important to explain this to the patient.
Objective refraction under cycloplegia is essential for detecting latent hyperopia; without cycloplegia, there is a risk of significantly underestimating the degree of hyperopia.
| Age | Normal refractive value | Refractive value requiring glasses |
|---|---|---|
| 3 months | S+4D | S+6D or more |
| 1 year | S+2D | S+4D or more |
| 2 years | S+1D | S+3D or more |
| 3 years old | S+1D | S+3D or more |
If the refractive error is 2D or more stronger than the normal value, consider prescribing glasses.
Also, as diagnostic criteria for amblyopia, use interocular difference ≥2 lines or binocular ≤20/50 for ages 3-4, and interocular difference ≥2 lines or binocular ≤20/40 for ages 5 and older1).
It is important to differentiate pseudoneuritis from papilledema. In high hyperopia, the optic disc margins may appear blurred, but there is no leakage on fluorescein angiography, and visual fields and acuity are usually within normal limits.
Children have much greater accommodative power than adults, and even with hyperopia, they unconsciously accommodate to see clearly. Therefore, a standard refraction test without cycloplegic drugs significantly underestimates the degree of hyperopia. In particular, latent hyperopia is not detected without cycloplegia. By measuring with complete cycloplegia using cyclopentolate or atropine eye drops, the true hyperopic refractive error becomes apparent. Prescribing appropriate corrective glasses based on this value leads to prevention and treatment of amblyopia and accommodative esotropia.
Based on the refractive error under cycloplegia induced by cycloplegic eye drops, prescribe glasses or contact lenses.
The selection of prescription power is based on the following:
In a prospective study by the Pediatric Eye Disease Investigator Group (PEDI), 27% of children aged 3–6 years with anisometropic amblyopia achieved resolution of amblyopia with spectacle correction alone, with an average improvement of 0.29 logMAR 2). The current standard approach is to observe with refractive correction alone until visual acuity stabilizes after prescribing glasses 2).
First step: Full-time wear of full correction glasses
Prescribe full correction glasses based on cycloplegic refraction and have the child wear them full-time. Often, visual acuity improves to some extent with glasses alone. The current standard approach is to observe with refractive correction alone until visual acuity stabilizes after prescribing glasses 2).
Second step: Occlusion therapy (patching)
If visual acuity does not improve sufficiently with glasses alone, apply an adhesive patch to the sound eye.
Third step: Atropine eye drops (penalization)
Instill 1% atropine in the sound eye to blur near vision via cycloplegia, encouraging use of the amblyopic eye. It is nearly as effective as patching for moderate amblyopia 7). Useful as an alternative when patching compliance is poor.
Bangerter filters
A method of attaching a translucent filter to the spectacle lens of the sound eye. In a PEDI study, the difference in visual acuity improvement compared to patching was within 0.5 lines after 24 weeks 1).
For pure accommodative esotropia, instill 0.5% atropine three times daily for 3–5 days, and have the patient wear fully corrective glasses or glasses with a power reduced by 0.5 D. It is important to ensure that the glasses are worn continuously and that the frame does not slip down.
For partially accommodative esotropia, hyperopic glasses are similarly prescribed, but residual esotropia is treated with surgery or prism therapy.
Classification and management of accommodative esotropia
| Type | Features | Treatment |
|---|---|---|
| Pure accommodative esotropia | Esotropia completely resolves with hyperopic correction | Full hyperopic correction glasses (no Fresnel prism needed) |
| Partially accommodative esotropia | Residual esotropia after correction (>10∆) | Glasses + surgery (for residual deviation) |
| High AC/A type | Normal hyperopia but esotropia increases at near | Hyperopic correction + bifocal glasses (near addition +2.5 to +3.0 D) |
| Non-refractive accommodative esotropia | Abnormally high AC/A ratio | Miotic agents (echothiophate) or bifocal glasses |
In accommodative esotropia complicated by hyperopic amblyopia, it is necessary to concurrently perform spectacle prescription, amblyopia treatment, and strabismus correction. If strabismus surgery is performed while amblyopia remains untreated, there is a risk of binocular suppression being released postoperatively, leading to diplopia. Therefore, the principle is to prioritize or concurrently conduct amblyopia treatment 1).
In adults with accommodative esotropia (esotropia without glasses), removing glasses may cause social and occupational limitations. In such cases, refractive surgery (e.g., LASIK) may be performed to improve strabismus. However, the primary purpose of refractive surgery is refractive correction, and the surgical effect on strabismus is secondary. This must be fully explained preoperatively 15).
High hyperopia (+6D or more) in children can cause amblyopia and accommodative esotropia. It is necessary to detect the full hyperopic power early and correct it with glasses or other means. After childhood, contact lenses are also an option. Since findings such as short axial length and shallow anterior chamber persist, continuous attention to the risk of complications in adulthood (e.g., angle-closure glaucoma) is required. In cases of nanophthalmos complicated by uveal effusion syndrome, scleral window surgery is effective 3). Regular follow-up is recommended for nanophthalmos cases 3).
In adults (aged 20 or older, with stable refractive error), hyperopia can be corrected by excimer laser procedures such as LASIK (laser in situ keratomileusis) or PRK (photorefractive keratectomy). The guidelines for refractive surgery (8th edition) recommend an upper limit of approximately +6D (spherical equivalent) for hyperopic correction; for higher degrees of hyperopia, the indication should be carefully considered 4).
Hyperopic LASIK is more prone to regression compared to myopic correction, especially for high hyperopia of +4D or more, where long-term refractive stability tends to decrease 4). This is related to the specific corneal ablation pattern (peripheral ablation, central sparing), and the interaction with age-related corneal shape changes accelerates regression.
PRK does not create a corneal flap, so it may be chosen for patients with thin corneas or those with high activity levels (sports, occupation). However, postoperative subepithelial haze is more common in hyperopic correction than in myopic correction, which may affect long-term correction accuracy 4).
Hyperopia correction with phakic intraocular lenses (ICL, IPCL, etc.) is positioned as an option for cases with high hyperopia (over +6 D) that are not candidates for LASIK. Since no corneal ablation is performed, the risk of regression is low, but there are separate risks of complications such as cataract, increased intraocular pressure, and corneal endothelial cell loss 4).
Many children have physiological hyperopia (around +2 D) in infancy, and as they grow, the axial length elongates and emmetropization occurs. However, the process of emmetropization follows a course where hyperopia temporarily increases until around 7–8 years of age and then decreases. Mild hyperopia often improves naturally with growth, but in cases of high hyperopia (over +6 D) or when complicated by amblyopia or accommodative esotropia, correction may still be needed after growth. Additionally, in high hyperopia, a shallow anterior chamber persists even in adulthood, so ongoing risk management for angle-closure glaucoma is necessary.
Hyperopia occurs when the combined refractive power of the cornea and lens is relatively weak relative to the axial length. In a normal eye, the combined refractive power of about 58–60 D and an axial length of about 24 mm are balanced, so that parallel light rays focus precisely on the retina. In a hyperopic eye, this balance is disrupted, and the focal point is formed behind the retina.
The lens can increase its refractive power by thickening through contraction of the ciliary muscle (accommodation), compensating for hyperopia. As long as the hyperopia is within the range of accommodation, no visual impairment occurs (facultative hyperopia). However, because accommodation must be maintained constantly, fatigue of the accommodative muscles (asthenopia) is likely to occur.
With aging, the elasticity of the lens decreases and accommodative power declines, so hyperopia that was asymptomatic in youth may manifest as asthenopia and decreased vision in middle age and beyond. The proportion of absolute hyperopia increases, and corrective glasses become necessary.
The axial length of a newborn is short (about 17–18 mm), and there is physiological hyperopia (around +2 D). With growth, the axial length elongates (to about 24 mm in adults), and the balance between refractive power and axial length is achieved, leading to emmetropization. This emmetropization process is regulated by a feedback mechanism that depends on visual input.
Around the age of 7 to 8 years, there is a temporary slight increase in hyperopic power. If refractive error evaluation is neglected during this period, amblyopia and esotropia may be missed.
Children have stronger ciliary muscle tension and greater accommodative power compared to adults. Therefore, much of hyperopia is hidden as latent hyperopia, and accurate hyperopic power cannot be measured without cycloplegia. Glasses prescribed without detecting latent hyperopia result in inadequate correction, reducing the effectiveness of amblyopia and strabismus treatment.
In high hyperopia due to axial hyperopia, the axial length is short, leading to a shallow anterior chamber. Eyes with a shallow anterior chamber tend to have narrow angles, increasing the risk of acute angle-closure glaucoma attacks. Additionally, relative crowding of the posterior pole due to short axial length can cause blurred optic disc margins (pseudoneuritis) and posterior pole retinal folds.
In nanophthalmos with high hyperopia, pathological abnormalities of the sclera may constrict the vortex veins (draining vessels of the choroidal system) at the scleral penetration site, potentially causing uveal effusion syndrome. In type I (true nanophthalmos with scleral thickening), which presents with short axial length and high hyperopia, scleral window surgery is effective when exudative retinal detachment occurs 3). Regular follow-up is recommended in nanophthalmos cases.
Eyes with high hyperopia (especially +6D or more, axial hyperopia) tend to have shallow anterior chambers and narrow angles. With aging, the lens thickens, further narrowing the angle and increasing the risk of acute angle-closure glaucoma (AACG).
The following are recommended for AACG risk management 1):
Cataract surgery replaces the lens with a thinner intraocular lens, thus eliminating the angle-closure risk in high hyperopia. In very short axial length high hyperopia (+8D or more, axial length <21 mm), prophylactic lens extraction (clear lens extraction) before cataract development may be considered for angle-closure glaucoma prevention.
Excimer laser correction for hyperopia (LASIK/PRK) has been considered less stable than for myopia, with a tendency for regression (myopic shift). In recent years, improvements in corneal ablation patterns have enhanced accuracy, and good outcomes have been reported for moderate hyperopia (around +3 D).
Expansion of SMILE (small incision lenticule extraction) for hyperopia is also under research. For high hyperopia exceeding +6 D, there are still limitations, and surgical options including phakic intraocular lenses (ICL) for hyperopia may be considered 13). The KLEx (SMILE) guidelines have clarified the indications for myopia and myopic astigmatism, with LASIK remaining the mainstream for hyperopia correction 13). Attention to hyperopic eyes in IOL power calculation during cataract surgery (effects of anterior chamber depth and lens thickness) is also important, and newer formulas (e.g., Barrett Universal II) have improved accuracy for hyperopic eyes 14).
Photo screening devices have been shown to be effective for early detection of pediatric hyperopia and amblyopia, which are difficult to detect with traditional visual acuity tests 8). The introduction of photo screeners in 3-year-old health checkups is becoming more widespread, and improvements in early detection rates of amblyopia are expected. The Spot Vision Screener can measure refractive error, strabismus angle, pupil size difference, and interpupillary distance, and displays an abnormality when amblyopia risk factor thresholds are exceeded 8).
Treatment of hyperopic amblyopia (isoametropic/anisometropic) follows these steps 1).
Step 1 (0–18 weeks): Full correction glasses only
Prescribe full correction glasses based on cycloplegic refraction and observe with glasses alone until vision stabilizes. In PEDIG studies, spectacle correction alone improved amblyopic eye visual acuity by an average of 0.29 logMAR, and 27% no longer met amblyopia criteria 7). Skipping this step and proceeding directly to occlusion may lead to overtreatment in cases that would improve with glasses alone.
Step 2 (after 18 weeks): Add occlusion or atropine
If visual acuity plateaus at 18 weeks after glasses prescription, add occlusion or atropine. In bilateral amblyopia (isoametropic), occlusion is not possible because the amblyopic eye cannot be identified, so continuous wear of full correction glasses is the mainstay.
Stage 3 (After visual improvement): Tapering, discontinuation, and monitoring for recurrence
When visual acuity has normalized (or after confirming a plateau for 4 months), occlusion is gradually tapered. The recurrence rate of amblyopia is reported to be about 24% within one year after treatment discontinuation, making regular follow-up essential 2). In cases of recurrence, a good response to retreatment is often observed.
A study using Luminopia’s headset (72 hours of use in children) reported a visual acuity improvement of 0.15 logMAR 2). In adults with anisometropic amblyopia, an improvement of 0.15 logMAR (one line improvement per 27 hours) has been reported 2), and comparative studies with traditional occlusion therapy are ongoing. In dichoptic training under VR, 44 hours of training resulted in visual acuity improvement from 0.05 to 0.5 and acquisition of stereopsis 10). The adult strabismus PPP (2023) also emphasizes the importance of refractive correction for esotropia with hyperopia, and presents a systematic management flow for surgical indications when residual strabismus persists after correction 15). Research on the appropriate timing for discontinuing occlusion therapy in preschool vision screening shows high predictability of visual acuity at age 4 (r=0.83, p<0.01), indicating that continued occlusion after age 4 may not always be effective 9). Furthermore, in untreated amblyopic children aged 7–17, spectacle correction alone improved visual acuity in 25% after 24 weeks, and additional occlusion improved it in 53% (ages 7–12), demonstrating that treatment is possible even after the sensitive period 12).
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