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0.01% atropine for myopia control


Elspeth Wrigley
BVisSc MOptom

Dr Ann Webber
PhD MS BAppSc(Optom)(Hons)


Childhood myopia

Brothers A and B have a strong family history of myopia. While their mother’s myopia is moderate (-3.50 DS), their father’s myopia is very high (-17.00 D). Both boys had onset of myopia initially identified at approximately seven years of age and were prescribed dual focus soft contact lenses as myopic progression treatment.

In 2014, the older brother’s myopia showed a marked progression over a six-month period, prompting the prescribing of 0.01% atropine, one drop, both eyes, at night. Before commencing 0.01% atropine, brother A’s myopic refractive error had increased from -0.50 DS to -4.75 DS over four years, with rate of progression approximately -1.00 D/year. Progression rate slowed to -0.38 D/year following commencement of 0.01% atropine treatment (-4.75 DS to -5.50 DS over two-year interval).

Younger brother B was showing a comparable myopia progression profile, with onset at a similar age to that of his brother who preceded him by three years. Prior to commencing 0.01% atropine, brother B was becoming more myopic at a rate of -1.25 D/year in the right eye and -0.25 D/year in the left eye. Following commencement of atropine 0.01% treatment, progression rate reduced to -0.25 D/year in both eyes, with current myopic refractive error R -2.25/-0.50x90 L -1.50 DS.

The prevalence of myopia globally has rapidly increased to disturbing levels in recent decades, a finding that is concerning due to the increased risk of associated ocular pathology such as cataracts, glaucoma and retinal detachment.1,2 The prevalence of myopia is alarmingly high in various Asian countries, where 70-80 per cent of young adults are significantly myopic.4 This trend is also apparent in Australia with a recent report that 31 per cent of 17-year-olds are myopic.3

Risk factors for the development of myopia have been identified, which are useful tools in clinical practice for identifying at-risk patients. While the most significant predictor of myopia is a lower hyperopic refraction at baseline, less time spent outdoors, increased near work, family history and East-Asian ethnicity are all identified as risk factors for incident myopia.2,3

In recent years, there has been a shift in clinical management, especially of young progressing myopes with a strong family history of myopia. Previously, mainstay treatment for myopia was aimed at correcting myopic refractive error to maximise distance visual acuity without controlling progression. Now, treatment has shifted to other forms of correction or management protocols that are designed to not only correct visual acuity but also control or minimise myopic progression.2

Treatment options that have been shown to slow continued myopia development include progressive addition lenses, dual focus contact lenses, orthokeratology and low dose atropine.5,6 Topical antimuscarinic medication such as atropine and pirenzepine appears to be the most effective treatment for controlling myopia.5,6

Eyes treated with atropine have statistically significant reduced myopia progression and less axial elongation compared to controls.7 Initial studies reported the mean myopic progression after one year in the 1% atropine treatment group was significantly less than in controls (+0.3 D ± 0.50 D compared to -0.76 D ± 0.44 D [p < 0.0001]);7 after two years the mean myopic progression in the 1% atropine treatment group was -0.25 D ± 0.92 D compared to -1.20 D ± 0.69 D in controls.

Further studies to investigate the minimum dose required to effectively minimise myopic progression over five years demonstrated that 0.01% atropine was the most effective concentration in slowing myopia progression with fewer side-effects and less rebound progression compared to higher doses.8 Over five years the mean myopic progression was -1.38 ± 0.98 D in the 0.01% atropine group compared to -1.83 ± 1.16 D in the 0.1% group and -1.98 ± 1.10 D in the 0.5% group. Over five years, the mean change in axial length was least in the 0.01% group (+0.19 ± 0.18 mm) compared to other concentrations.8

Overall, it appears that 0.01% atropine slowed myopia progression by at least 50 per cent.


Atropine is a belladonna alkaloid that blocks the action of acetylcholine. As a non-selective muscarinic antagonist, atropine blocks the M1-M5 receptors found in the eye.9 Low dose 0.01% atropine appears to have minimal effect on the M3 receptor, which is related to pupil size and accommodation.10 Animal studies suggest that the M1 and M4 receptors are involved with myopic progression.11

In a study that involved deprivation-induced myopia in tree shrews, it was shown that eyes that were injected with M1 and M4 blocking compounds displayed a marked reduction in myopic progression compared to controls.11 The site of action within the eye for myopic progression inhibition is still unknown but studies have postulated that it could be within the retina or sclera.9,11

Currently, 0.01% atropine solution is not commercially available in Australia so it must be compounded by a pharmacy that has access to a sterile room. The compounded 0.01% atropine is diluted from a higher concentrated stock solution of atropine sulphate and then combined with BZA 0.1mg/mL. Non-active ingredients include disodium edetate, benzalkonium chloride and hypromellose, boric acid and distilled water.

To ensure you have a comprehensive understanding of the solution that you are prescribing, it is important to talk to the compounding pharmacy about any other non-active ingredients that are added to the compound. Compounded 0.01% atropine solution has a 30-day life after opening. A non-preserved solution is available, depending on the pharmacy, but it has a very short shelf-life of seven days.

Use of 0.01% atropine for myopia control treatment

0.01% atropine is intended to be used in conjunction with spectacle or contact lens correction. One drop of atropine 0.01% should be instilled in the specified eye(s) at night before bed. While shown to be effective in slowing myopia progression in the short term, the long-term use of 0.01% atropine is still not completely understood. After ceasing atropine following 24 months of use, some patients demonstrated rebound myopia, with the rebound effect more pronounced in patients who had been treated with higher initial concentrations of atropine (0.5% and 0.1%).8 However, the rebound effect was linked to the dose of atropine with minimal rebound in the 0.01% group.8

Clinical implications

  • 0.01% atropine is an effective way to control myopia and is a good alternative to dual focus contact lenses or orthokeratology lenses, especially in young patients.5
  • Daily administration of 0.01% atropine is required for myopia control. One drop of 0.01% atropine should be instilled at night before bed in the specified eye(s).
  • If atropine treatment is ceased, some patients will demonstrate a rebound effect so they must be monitored for signs of progression.8
  • Atropine can be used in conjunction with other myopia control techniques such as dual focus contact lenses. The combined effect is unknown.
  • 0.01% atropine is a compounded solution. For a patient to obtain the medication, a valid prescription must be sent to the compounding pharmacy. The compounding process is initiated after the parent or carer contacts the pharmacy to verify the order, and confirm payment and delivery.
  • 0.01% atropine has a use-by date of 90 days as an unopened product or 30 days after opening the bottle. Different compounding pharmacies may have different recommendations: verify this with the compounding pharmacist.
  • Approximate cost is $130-$150 for three bottles, plus courier fee. The cost of the product will vary depending on the compounding pharmacy and the collection/delivery options.
  • To increase compliance, discuss and provide a written instruction sheet that includes ordering, administration, storage and potential adverse effects.

Ocular and systemic side-effects

0.01% atropine appears to be very well tolerated with no known serious adverse effects.10 Ocular side-effects of increase in pupil size and responsiveness have been reported.10 While glare was reported during trials, there was no impact on overall quality of life with the use of the medication.10

At slightly higher doses of atropine, some patients have developed associated ocular allergies.9 Systemic side-effects of atropine include mucous membrane dryness, flushing of skin, confusion, unusual behaviour and irritability. These side-effects are rare and related to higher doses of the medication than the dose prescribed for myopia control.

Current legislation

The current legislation in Queensland, the Health (Drugs and Poisons) Regulations 1996 (QLD), stipulates that therapeutically endorsed optometrists can prescribe only preparations listed on the Australian Register of Therapeutic Goods. The Department of Health in Queensland has indicated that optometrists cannot prescribe compounded medications. This legislation is in the process of being reviewed.


Given the increasing prevalence of myopia and the associated ocular complications, strategies must be implemented to reduce myopic progression. 0.01% atropine is an effective way to control myopia and is a good alternative to other treatment options. Low dose atropine appears to be very well tolerated without serious adverse effects.10

1.            Saw S, Gazzard G, Shih-Yen EC, et al. Myopia and associated pathological complications. Ophthal Physiolog Optics 2005; 25: 381-391.

2.            McMonnies C. Clinical Prediction of the need for interventions for the control of myopia. Clin Exp Optom 2015; 98: 518-526.

3.            French A, Morgan I, Mitchell P, et al. Risk factors for incident myopia in Australian schoolchildren: the Sydney adolescent vascular and eye study. Ophthalmology 2013; 120: 2100-2114.

4.            Morgan I, Ohno-Matsui K, Saw S. Myopia. Lancet 2012; 379: 1739-1748.

5.            Walline JJ, Lindsley K, Vedula SS, et al. Interventions to slow progression of myopia in children. Cochrane Database of Systematic Review 2011; 12: CD004916. doi: 10.1002/14651858.CD004916.pub3.

6.            Huang J, Wen D, Wang Q, et al. Efficacy comparison of 16 interventions for myopia control in children. Ophthalmology 2016; 123: 697-708.

7.            Chua V, Balakrishnan V, Tan D, et al. Efficacy Results from the Atropine in the Treatment of Myopia (ATOM) Study. Invest Ophthal Vis Sci 2003; 44: 3119.

8.            Chia A, Lu Q, Tan D. Five-year clinical trial on atropine for the treatment of myopia 2. Am Acad Ophthalmol 2016; 123: 391-399.

9.            Ganesan P, Wildsoet C. Pharmaceutical Intervention for myopia control. Expert Rev Ophthalmol 2010; 5: 759-787.

10.          Loughman J, Flitcroft D. The acceptability and visual impact of 0.01% atropine in a Caucasian population. Br J Ophthalmol 2016; pii: bjophthalmol-2015-307861. doi: 10.1136/bjophthalmol-2015-307861. [Epub ahead of print]

11.          Arumugam B, McBrien N. Muscarinic antagonist control of myopia: evidence for M4 and M1 receptor-based pathways in the inhibition of experimentally-induced axial myopia in the tree shrew. Invest Ophthal Vis Sci 2012; 53: 5827-5837.

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