Doc, my eyes still hurt, now what?

Recently a patient complained to me: ‘Doc, my eyes still hurt.’

I asked: ‘have you tried the artificial tears I recommended to you?

‘Yes, it doesn’t do any good.’

‘How many times did you put in a day?’

‘I just did that once and it did not work.’

‘I see. How about the warm compress?’

‘Not working either.’

‘How long did you do it and how many times a day?

‘Once or twice, I forgot.’

‘Are you taking the fish oil supplement?’

‘Yes. Did not feel any different.’

Here I have a patient who two months ago came to me for dry eye. He reported trying restasis from his previous eye doctor for months but no relief at all. Eye exam showed typical meibomian gland dysfunction (MGD) and poor tear film quality, without blepharitis or corneal staining. So this is a case of MGD-induced dry eye, that’s why I started him on eyelid warm compress 5 min x 2, and fish oil 1000 mg x 2 daily, with artificial tears as needed, up to 4 times daily. I asked him to follow up in 1 month. At which time he was not doing any of the things I asked, and of course his dry eye symptoms continued. After re-education, I asked him to do these consistently and follow up again in 1 month. He has probably done some of this now, but not consistently, and given up very quickly.

Rather than drilling him again for being more compliant with the treatment regimen, I offered him an alternative, which he clearly came looking for. I would like to refer him for a lipiflow treatment. I explained what it is, how it is done, and why it works. Then I told him that it’s not covered by insurance and may cost $1-2,000 for one session.

After a short moment of silence, he told me that he would like to give warm compress another try. And that he just started taking fish oil last week and would like to see if doing this for longer may help. I agreed, and asked him to return in 6 weeks to evaluate on progress.

No one likes having the dryness, foreign body sensation, redness, burning and tearing caused by dry eye. Fortunately there are effective treatments such as warm compress and artificial tears, and often these are enough to control dry eye symptoms. Unfortunately these treatments require consistent and long-term use. There is no cure for dry eye, which is a chronic condition and may require life-long management. When it comes to dry eye treatment, compliance is key. There are certainly those unlucky people who despite doing everything right still suffers from dry eye. But fortunately those are the minority.

For more information on dry eye and treatment, you can visit my previous posts and video.

https://bostoneyeblink.com/2020/05/25/dr-ding-dry-eye-disease-and-treatment/

https://bostoneyeblink.com/2017/08/06/when-artificial-tears-just-dont-cut-it-other-treatments-of-dry-eye/

https://bostoneyeblink.com/2016/06/28/why-are-your-eyes-dry/

孩子近视除了戴眼镜,还有这个矫正方法

中国学龄孩子从小学开始长期近距离用眼、或用眼不当,导致小学生近视率居高不下。生活中新冠时期,网课主宰学习方式,近视率进一步上升。为了不影响孩子日常生活和学习,多数家长会让孩子配戴相应度数的眼镜。

其实除了配戴眼镜,孩子解决近视的方法还有另外一个镜——OK镜。大量研究发现,OK镜和低浓度阿托品的使用可以控制近视的发展。今天我们单独来谈谈OK镜的优点和缺点。

OK镜是什么?

OK镜,是一个硬的透气的隐形镜片,用于晚上睡觉时佩戴。镜片暂时性改变角膜的曲率(角膜是眼睛最前面那层薄薄的透明膜), 这样当第二天早上将镜片取出以后,会有十几小时内看东西清楚的状态,从而矫正视力,无需戴眼镜。

这是OK镜的美妙之处,晚上戴镜,白天摘镜,佩戴第一晚,第二天就有明显的效果,不影响美观,也不影响运动。长期佩戴,可一定程度延缓近视的发展。

OK镜真的能够延缓近视发展吗?

大量研究证明,OK镜确实能延缓近视发展。这里附上两篇综述,总结相关研究[1] [2],供学霸家长阅读。

OK镜要一直佩戴吗?

OK镜是临时的,可逆的,可调整的,因此可以随时停,随时再开始。但延缓近视发展的效果,只有在佩戴期间才有作用,一旦停用,就会恢复为佩戴前的视力水平,也没有了延缓近视发展的效果。

如果眼睛发生过敏、感染等不适,比如发红、痒、疼痛、出现分泌物,那么需要暂停使用任何形式的隐形眼镜,找眼科医生进行治疗。直到症状完全消失才可以重新戴镜。这种暂时性停止佩戴,对于近视的加深可以忽略不计,因为近视是一个以年为单位发展的过程,不是一周两周就会加深度数的。

OK镜安全吗?会不会感染?

OK镜是安全,不过由于OK镜是晚上戴的,有研究发现,OK镜的感染风险和普通晚上戴的隐形眼镜相同,都是0.077% [3],也就是说每一万戴OK镜的人里面有不到8个人可能发生感染。在验配者经过认证培训的前提下,使用经过FDA验证的镜片材料,只要使用者保持良好的护理习惯可以大大减少感染风险。同时父母的监督也很重要。另外佩戴者需定期就诊,根据医生建议更换镜片。

OK镜对角膜有伤害吗?

戴OK镜的确容易发生角膜染色 [4],但这些是角膜表面微小的缺陷,在干眼等常见眼表疾病中也会发生,这是戴OK镜需要定期检查的原因。长期佩戴OK镜,一切都正常的情况下,每年至少也要检查一次,观察眼表健康情况,检查视力。如果有严重的角膜染色,需要停止戴镜,治疗恢复后在医生的指导下重新佩戴[J2] 。

OK镜适合什么样的人群?

OK镜适合近视不超过600度,散光不超过175度的人。并不是说度数超过这个范围的人就不能使用,只是可能不能完全脱镜。

至于年龄,有进展性近视的儿童可以佩戴,50多岁的成年人也可以佩戴。只是成年人佩戴不是起到延缓近视发展的作用,而是白天能够脱离眼镜的生活。对于佩戴的青少年,重点要培养其遵守镜片护理、清洁、消毒说明以及正确佩戴的方法。

日常生活怎么维护OK镜?

  • 注意卫生,接触镜片和眼睛之前一定要肥皂和清水洗干净手,擦手最好用不留纸屑的纸巾或不留纤维的毛巾,因为纸屑或者小的纤维可能会通过手传递到镜片上,然后进到眼睛里。
  • 晚上戴好镜片以后,需要清水彻底洗净眼镜盒,并风干。
  • 早上摘镜的时候,先用护理液在手心揉搓几下,然后放在新鲜护理液中,直到晚上使用。
  • 浸泡镜片的盒子每2-3个月更换一次。
  • 每3个月可以进行一次蛋白清洗,因为镜片上会不可避免沾上眼泪中的蛋白质等。推荐使用Menicon Progent(除蛋白护理液)。
  • 有条件可以每年更换一次新的镜片,即使镜片度数完全不变。

OK镜的优点

  • 有效控制近视发展
  • 只需晚上佩戴,白天完全无镜

OK镜的缺点

  • 贵!国产的一只镜片大概3000-5000,美国进口的就要4000-8000了。不过,在美国一对镜片大概也在1000美元以上。
  • 麻烦!和普通软的隐形眼镜一样,必须每天戴、摘、护理; 如果不注意卫生清洁,感染的风险增大。
  • 疼!初戴起来疼、不舒服,但适应期过后,大部分人不再出现不适感。

参考文献

1. Campbell E (2013) Orthokeratology: an update. Optometry & Visual Performance 1: 11-18.

2. Lipson MJ, Brooks MM, Koffler BH (2018) The Role of Orthokeratology in Myopia Control: A Review. Eye Contact Lens 44: 224-230.

3. Bullimore MA, Sinnott LT, Jones-Jordan LA (2013) The risk of microbial keratitis with overnight corneal reshaping lenses. Optometry and Vision Science 90: 937-944.4. Liu YM, Xie P (2016) The Safety of Orthokeratology—A Systematic Review. Eye & Contact Lens 42: 35-42.


近视怎么纠正和预防 (2/2)

近视有什么办法治疗?

最常见的当然就是戴镜框眼镜或者隐形眼镜了。请注意小孩子一定要通过散瞳之后得到的度数才准确。而且也不要完全亲信自动验光仪的数字,必须结合手动检影、主观验光或者试戴镜的检查手段多方面验证确定最终度数。

18岁以后(或者度数稳定之后)可以进行角膜激光手术矫正手术,见角膜手术一文。

这些方法都能矫正视力,但是并不能改变眼轴长度。目前认为,眼轴一旦增长似乎是不可逆的。幸运的是,现代的视光医学研究发现有几个方法可以延缓甚至停止眼轴继续增长。角膜塑形镜(orthokeratology, 俗称OK镜)是最有效的物理手段,而低浓度阿托品眼药水是最有效的药物方法。

OK镜我会单独开一篇文章讲讲。这是一种硬的可透气的隐形眼镜,夜间佩戴至少8小时,早上起床以后摘下。角膜在晚上被压平,因此暂时改变眼睛的屈光度,在整个白天这种屈光度能够维持,因此近视患者在白天无需戴眼镜也可以清楚的看到远处。这有点类似可逆LASIK,没有实际切削角膜组织,只是用隐形镜片将角膜临时压扁。如果停止使用,一周后角膜就会完全恢复常态。

OK镜于1994年FDA批准。临床研究效果显著,儿童使用两年眼轴增长能够减少45% [1];而且实验结果经得起重复 [2, 3]。目前临床应用广泛,不仅在研究中有着显著的效果,身边的例子也有着很高的成功率。我的一些视光医生朋友非常推崇。最让我印象深刻的是一个国内朋友自己的例子。他900度近视,他妻子接近2000度近视,所以他们很担心小孩的眼睛。当他们的女儿9岁时近视达到200度,经过研究他们带她去配了OK镜,戴了5年,度数没有变化!我知道OK镜每年可以减缓近视25-50度,但是这样的家族史,5年没有加深还是很惊人的。要注意的是,人与人之间的差别很大,的确也有少部分人效果一般或者没有效果。造成这种差异的原因以及我们怎么能够个性化的治疗近视也是现在研究的一个热点。

低浓度阿托品也眼药水也可以有效的减缓近视的发展,效果和OK镜类似甚至更加好一点点。阿托品虽然是一个用了很多年的药,它的控制近视这一目的目前还没有通过FDA批准。当前的研究表明低浓度阿托品眼药水在几年内持续使用是安全的 [4],但是远期副作用还没有数据。在美国,低浓度阿托品眼药水需要处方,并且只有特定的药房可以配制。

怎么发现孩子是不是开始近视?

有的孩子会抱怨说看黑板或者看电视模糊。但是小孩往往不知道自己看东西模糊,他们以为大家都是这样的。家长应该注意这些现象:看电视眯着眼,斜着眼看东西,或者不愿意在外边玩(因为在户外玩耍主要需要好的远处视力)。

美国视光协会推荐儿童应该在3岁的时候进行全面眼睛检查,在上小学以前全面检查一次眼睛,然后如果没有任何问题包括眼睛疾病、屈光不正和弱视的风险则可以每两年检查眼睛一次。如果儿童开始发展近视,则应该每年检查眼睛,更新眼镜度数。

孩子近视了,怎么办?

尽早发现近视,早进行治疗和干涉,可以避免近视发展过深。

  1. 带孩子去眼科医生或者视光医生去做全面眼睛检查包括散瞳和眼底检查,确定度数,佩戴镜框眼镜。
  2. 不要以为不戴近视眼镜或者戴故意矫正不足的眼镜可以减缓近视发展,研究表明恰恰相反,近视矫正不足会加快近视发展[5]。
  3. 18岁以下的儿童应该使用抗碰撞的聚碳酸酯材料制作的镜片以保护眼睛。
  4. 当孩子达到一定年龄,可以尝试隐形眼镜。但是一定要注意正确的佩戴、摘取和清洗护理,否则有角膜感染的风险。
  5. 如果对减缓近视的发展感兴趣,可以在视光医生的指导下使用OK镜。低浓度阿托品眼药水也是一个选择,但是目前没有通过FDA批准,远期安全性未知,需要承担风险。
  6. 等孩子18岁以后,又多一个选择,可以做LASIK。

有没有不花钱的办法可以控制近视?

不管是OK镜还是LASIK,价格都不菲。其实不花一分钱就可以预防或者减少近视的发展

  • 实行用眼卫生(visual hygiene)。这本来是一个视觉训练的概念,但是用在防止近视照样有用。1)看书的距离不应该小于手指第二个关节和胳膊肘间的距离。2)记住20-20-20的规则。每看书或者近距离用眼工作20分钟,就看20英尺(大约6米)以外20秒。
  • 改进室内照明。昏暗的光线会造成视网膜上成像的模糊,加快眼轴生长。
  • 夜晚睡觉时不要开灯。规律的昼夜节律不仅有益身心健康,而且对眼睛的正常发育和正视化也是必要的。这一点,从刚出生的婴儿做起
  • 多花时间呆在户外。如前所述,最新的研究发现每天两小时的户外活动会显著降低近视的发生。

需要指出的是,眼轴一旦增长,不能缩短,现有的方法都是防止眼轴进一步增长。以上的各种方法是有独立的研究和证据表明有效的。市面上可能有着各种各样的理疗器宣称治疗近视,我没有一个一个调查过,但是没有看到有独立研究(非商家赞助的研究)和证据表明它们有效。如果你看到有的广告宣传说能够缩短眼轴,那么这本身就是个伪命题。现在的研究者在积极寻求能够让眼轴逆生长的方法,可惜还没有找到。

近视是一个多因素的眼睛屈光不正问题。行为的改变可以有效的防止和减缓近视发展。最直接的例子是那些亚马逊流域部落的居民,以及我们的父辈那一代人(50年代出生的中国人),大部分人都是轻度远视。和肥胖一样,预防近视更应该是一个公众健康的问题,家庭、学校和社会推行用眼卫生和推广户外活动,能够减少大量的近视青少年,从而减少大量的近视中年人和老年人,能够给健康医疗系统减少很多花销和负担。遗憾的是,现代人的教育和生活方式,改变不是一朝一夕那么容易。和肥胖不同的是,近视从儿童期开始发展,一旦开始就不可逆,最多可以减缓发展。如果说减肥在受到充足教育的成年人里面可以成功,近视一旦形成,当我们变成懂事的成年人,都只有后悔年少的自己当年滥用了眼睛。时间不能倒流,也没有后悔药,因此防止近视要家长、学校和社会出大力气,抓住0-13岁这个窗口。

参考文献

1.            Li, X., et al., Update on Orthokeratology in Managing Progressive Myopia in Children: Efficacy, Mechanisms, and Concerns. Journal of Pediatric Ophthalmology and Strabismus, 2017. 54(3): p. 142-148.

2.            Walline, J.J., L.A. Jones, and L.T. Sinnott, Corneal reshaping and myopia progression. British Journal of Ophthalmology, 2009. 93(9): p. 1181-5.

3.            Chassine, T., et al., How can we prevent myopia progression? European Journal of Ophthalmology, 2015. 25(4): p. 280-5.

4.            Wu, P.C., Y.H. Yang, and P.C. Fang, The long-term results of using low-concentration atropine eye drops for controlling myopia progression in schoolchildren. Journal of Ocular Pharmacology and Therapeutics, 2011. 27(5): p. 461-6.

5.            Smith, E.L., 3rd, Optical treatment strategies to slow myopia progression: effects of the visual extent of the optical treatment zone. Experimental Eye Research, 2013. 114: p. 77-88.

Where is the pit?

Juan Ding, OD, PhD

Our central vision is seen by a structure called macula in the retina, and the center of the macula is called a fovea. Normally there is a pit dipping down at fovea as shown in Figure 1 below, and this is important for normal central vision.

Figure 1. Normal foveal pit indicated by the arrow.

Yesterday I saw a kid that had abnormal, or under-developed fovea.

This 6 year old boy came with his foster mother. He had fair skin, blond hair and was very light-sensitive. Mom never noticed anything abnormal, but he failed the vision test at his pediatrician’s office and that’s why they came here. 

His vision was 20/50 and 20/40, normal eye alignment, minimum refractive error, but after cycloplegia about +4.00 of hyperopia. At any rate, this hyperopia should not cause reduced vision at his age. So what can it be?

Interestingly when I looked at his retina I could not see a foveal reflex. And the retina was really light in terms of pigment. I attempted OCT and with some luck, managed to get photos from this well-behaved 6 year-old. It is apparent that his macula is lacking a normal foveal pit (Figure 2, right and left eye, respectively). 

Figure 2. Lack of a foveal pit in right and left retinas in our patient.

I gave this a tentative diagnosis of ‘fovea hypoplasia’. This condition can be seen in ocular albinism (lack of melanin) or aniridia (lack of iris), or it can happen as an isolated condition. He has normal eye structures everywhere else. Combined with a blonde fundus and extremely fair skin, I do suspect albinism. But he has no nystagmus, and vision is very good if he does have albinism. Since he was adopted, we do not know much about his family history. Mom adopted him while he was 18 months, and noted good health and normal developmental milestones up to now.

Given moderate to high hyperopia, I gave him a prescription of reading glasses. I referred him to his pediatrician to consider genetic testing.

近视怎么纠正和预防 (1/2)

在中国,据统计2014年7 到 18岁的人群中近视发病率高达 57.1% [1]。 今年新冠导致大量儿童蜗居在家,网课成为学习的主要手段。恐怕接下来会迎来一波新的近视高峰。为什么近视这么普遍?有什么办法可以纠正或者控制近视的发展?

什么是近视?

眼睛像个照相机,眼睛的整个透明介质包括角膜、晶体、玻璃体加在一起相当于镜头,视网膜相当于底片。光线被眼睛的透明介质汇聚后落在视网膜上我们就看到了清晰的图像(图一A)。近视的眼睛眼轴过长,导致远处来的光线不能到达视网膜(图一B),因此模糊。矫正近视可以在眼睛前面放个凹透镜,这样使得光线重新聚集在视网膜上。无论是镜框镜片,还是隐形眼镜片,或者之前讲过的角膜激光屈光手术,都是用这个原理矫正近视。这些方法,严格的来讲,只是治疗(treat),但不是治愈(cure)近视,因为眼轴的长度并没有变短。高度近视(大于等于600度近视)的一个后患就是由于眼轴增长导致视网膜脱离的风险增加。因此做了激光近视手术以后,虽然不戴眼镜看得也很清楚,但是视网膜脱离的风险并没有丝毫减少。顺便说一下,低度近视指300度以下,中度近视为300到600度之间。低度和中度近视的人视网膜脱离的风险大于正视(既不近视也不远视)的人,但是低于高度近视患者。

图一:近视的原理

假性近视vs真性近视

经常会看到各种文章提到假性近视,还有什么假性近视会发展成真性近视的说法。真性近视当然就是眼轴变长造成的近视。那什么是假性近视(pseudomyopia)?在这种情况,眼轴长度正常,但是眼睛汇聚光线的能力过强,因此光线还是聚在视网膜前方。眼睛里面有一块小小的环状肌肉叫做睫状肌(图一A),它的功能是调节晶体(图一A)的曲率。正常人的眼睛看远处时,睫状肌放松,晶体扁平;当看近处的时候,睫状肌收缩,晶体变凸,眼睛汇聚光线的能力变强。这样不论看远还是看近光线都可以汇聚在视网膜上。看近处时睫状肌收缩导致晶体汇聚力加强这一过程叫做调节。和身体别处的肌肉一样,睫状肌也会疲劳,有时也会痉挛。如果一直处于收缩状态,眼睛的汇聚光线力过大,远处的光线就会聚在视网膜之前,造成和近视一样的看远处模糊。

这种假性近视本质上说是眼睛调节能力的失调的一种。青少年学习时间长,加上眼睛还处于发育过程,调节能力失调时有发生。因此儿童和年轻人配眼镜,标准的方法是要用散瞳眼药水将睫状肌麻痹,迫使它放松,然后再验光,否则不能准确。我在临床上看过太多例子,自然状态下有低度近视(100度左右),散瞳后是平光甚至远视。甚至有一个已经33岁的西裔女子,多年来验光度数起起伏伏,大约近视100到200度,我给她散瞳后发现她其实有100度的远视,解释了她没法容忍近视眼镜,而且平时看书会累的症状。我还见过一个极端例子,13岁男孩从未戴过眼镜,自动验光仪测出900度近视,自述看东西模糊,视力表只能看清最上边0.05的字母。后来在验光的过程中,他的调节痉挛逐渐缓解,最终裸眼看到了1.0。显然这个小朋友没有近视,他需要的是视觉训练来帮助他恢复眼睛正确的调节功能。

以前人们以为真性近视是由假性近视发展来的。现在知道,这两者没有什么必然的关系。近视是眼轴过长,而假性近视作为眼睛功能失调的一种,不能算是严格意义上的近视。

那么为什么眼轴会增长?

眼睛的生长是由视网膜局部的信号来调节的。当眼睛清楚得看到一个物体时(也就是光线聚焦在视网膜上的时候),眼睛得到的信号是:一切正常,不需要生长。当长期注视近距离的物体时,光线会稍微聚焦在视网膜后边一点的位置上,视网膜得到的信号是:现在清晰度不是最优,我要稍微往后靠一点才能逮住这些光线。这样眼睛就稍微长长一点,长此以往近视就会不断加深。而且眼睛收到信号之后要么不变,要么生长,没有逆生长,换句话说,眼轴要么不变,要么变长。

人类的眼睛本来就不是设计来看近处的。远古的人类需要好的远处视力以便能够找到哪棵树上有果子,哪里有只兔子可以去捉住,或者那地平线上是不是有只狮子跑过来了。远古人类的平均寿命假如按照40岁算的话,还没来得及老花眼就死了,所以看近处从来不是问题。更何况,基因早在生育年龄就流传下去了,所以老花眼在进化中没办法被淘汰。总之,人的眼睛生来就是用来看远的。需要看近处的时候,动用一下眼睛的调节力,也就是睫状肌发力让晶体变凸从而让光线继续聚在视网膜上。不过,人的眼睛倾向于不过分工作,也就是有个轻微的小折扣,实际上光线没有正好在视网膜上,而是在视网膜后边一点点。问题就在于偶尔这么干还行,一天10小时看着书或者手机,这种信号就是让眼轴长长长。

近视有什么危害?

  1. 不能当飞行员
  2. 找不到男/女朋友

抛开玩笑,很多人觉得近视没什么大不了的,无非就是戴眼镜不太方便,况且现在还有各种隐形眼镜和激光手术。但是近视,尤其是高度近视(大于600度),由于眼轴的增长,会增加各种眼睛疾病的风险,包括视网膜脱离,巩膜新生血管,白内障,青光眼和黄斑萎缩 [2],这些疾病可以造成永久性失明。由于近视的发病率非常高,而1/5的近视是高度近视,算下来非常可观的人数有着这些永久失明的风险。而戴眼镜和激光手术并不能降低这些风险,原因是眼轴长度并未得到改变。

哪些因素会影响近视的发展?

近视是由基因和环境相互作用造成的。近视发展的风险因子包括:

  1. 家族历史。父母双方都近视的孩子的近视风险是父母双方都不近视的孩子的2倍还多。这个很好理解,基因的作用不容忽视。另外还有一些环境因素,比如近视的父母一般看书时间长,孩子也容易更喜欢看书。
  2. 近距离用眼的时间。工作性质、教育程度等等,这些不言而喻。
  3. 6-9岁时的眼睛屈光度。乍一看这点很奇怪。事实是,婴儿刚刚出生时的眼睛平均屈光度为200度远视(有很广的范围,从600度近视到1100度远视,但是大部分新生儿集中在200度远视左右),注意是远视而不是近视。然后在18个月的时候这种人与人之间巨大的区别就基本消失了,大家都差不多稳定在125度远视,这一过程叫做正视化(Emmetropization)。正视化是指眼睛生长发育达到正视,眼睛的聚光能力和眼轴的长度吻合的状态。可以想象,如果按照古代狩猎和畜牧的生活方式,人眼睛的这个度数就定了,直到病死饿死或者被老虎吃了。我们无从考查古代人的眼睛度数,但是一个非常有趣的例子是巴西亚马逊热带雨林的一个部落,至今没有太多的被现代文明侵入。我的一位老师,在近视研究领域内的一位先驱,曾经去那个村子考察当地居民的眼睛屈光度。在这个几百人的村子里,平均屈光度为75度远视,只有4个人有大于100度的近视。这四个人中,两个是村子里唯二的大学生,职业为老师,经常阅读;一个从儿童时代起就做裁缝;还有一个是个出生就高度近视的先天盲人。

由此可见,我们绝大多数人生来都不是近视眼,不幸的是,文字出现,书籍出现,ipad出现。现代人类的近视大概从7-9岁开始,每年增长100度;或者如果从10-13岁开始,则每年增长较慢,大约50度。近视的增长一般在17-23岁停止,但是像我之前在近视激光手术文章里讲的,成年人也可能会有缓慢的近视发展 — 多谢现代人的生活方式。

统计发现,6岁时候的眼睛屈光度如果是75度远视,那么将来近视的风险大为降低;相反,如果低于75度远视的话,则近视风险升高 [3]。

  • 种族: 近视青睐系数亚裔大于白人大于黑人 [4]。具体和基因还是文化、环境的差异有关,不得而知,可能都有关系。
  • 户外活动时间。最新的研究表明,户外活动,不管是运动还是静坐,不管是远眺还是读书,都会减少近视发展的几率和程度[5 , 6]。具体的机制是什么?加强了昼夜节律,更多的眺望了远处,在户外阳光下通过小瞳孔视力更加清晰,紫外线的照射,强烈的户外自然光促使视网膜合成多巴胺?还是由于维生素D的合成?现在还不清楚,也许是多种原因吧。
  • 规律的昼夜节律对眼睛的正常发育和正视化是必要的。婴儿期和儿童期晚上睡觉开夜灯会增大日后近视的风险。研究表明两岁前在黑暗中睡觉的婴儿后来只有10%的近视;那些开着夜灯睡觉的孩子后来有34%的近视;而那些开着正常灯睡觉的小孩后来的近视率有55% [7, 8]。

参考文献

1.            Dong, Y.H., et al., [Prevalence of myopia and increase trend in children and adolescents aged 7-18 years in Han ethnic group in China, 2005-2014]. Zhonghua Liu Xing Bing Xue Za Zhi, 2017. 38(5): p. 583-587.

2.            Wu, P.C., et al., Epidemiology of Myopia. Asia Pac J Ophthalmol (Phila), 2016. 5(6): p. 386-393.

3.            Zadnik, K., et al., Ocular predictors of the onset of juvenile myopia. Investigative Ophthalmology and Visual Science, 1999. 40(9): p. 1936-43.

4.            Hyman, L., et al., Relationship of age, sex, and ethnicity with myopia progression and axial elongation in the correction of myopia evaluation trial. Archives of Ophthalmology, 2005. 123(7): p. 977-87.

5.            Guo, Y., et al., Outdoor activity and myopia progression in 4-year follow-up of Chinese primary school children: The Beijing Children Eye Study. PLoS One, 2017. 12(4): p. e0175921.

6.            Suhr Thykjaer, A., K. Lundberg, and J. Grauslund, Physical activity in relation to development and progression of myopia – a systematic review. Acta Ophthalmol, 2016.

7.            Quinn, G.E., et al., Myopia and ambient lighting at night. Nature, 1999. 399(6732): p. 113-4.

8.            Czepita, D., et al., Role of light emitted by incandescent or fluorescent lamps in the development of myopia and astigmatism. Med Sci Monit, 2004. 10(4): p. CR168-71.

Keratoconus

Juan Ding, OD, PhD

This case is from one of my favorite patients. He first came to me as a referral from his ENT (ear, nose and throat) doctor, because he complained about dry eyes since his facial nerve palsy on the right side. His ENT doctor was not the one to diagnose facial nerve palsy of course, but since he was undergoing several sinus surgeries he happened to mention this during one of the visits. 

In his initial eye visit, I noticed that his vision was not able to be corrected to 20/20 by glasses, and he had a large amount of astigmatism. Retinoscopy showed scissor shaped light reflex, and slit lamp exam showed steepening cornea with prominent nerves and the right cornea actually had a mild scar. Corneal topography later confirmed keratoconus in both eyes, more so in the right eye.

Keratoconus literally means a corneal cone. Cornea is the front transparent layer of our eyes, and it is usually a regularly shaped dome like in the image on the left (Figure 1). But in keratoconus, the cornea gradually becomes thinner and thinner, and bulging more and more like in the image on the right. Because now the cornea is irregular, vision is blurry, even with glasses often still not good, since glasses do not correct this irregular surface of the cornea. Even regular soft contact lenses will not do much in this case because the soft lens material will just drape over the irregular cornea and still showing the irregular optics.

Figure 1. Normal cornea and cornea with keratoconus. Image from www.allaboutvision.com

Fortunately certain rigid contact lenses called rigid gas permeable (RGP) lenses can correct vision. These are stiff and can mask the irregularity of a keratoconus cornea. These are typically small, and often very uncomfortable especially in the beginning while the hard lens rubs against the surface of the eye and the eyelid.

Another type of lens to correct vision for keratoconus is a scleral lens (Figure 2). This is a large lens that sits on the white part of the eye called sclera, therefore causing minimum discomfort to the eye, and it corrects vision because the lens vaults over the irregular cornea to mask its imperfection.

Figure 2. How scleral lens corrects vision in keratoconus. Image from https://visualeyesboca.com/scleral-lenses/

Back to my patient, I initially fitted him with special RGP lenses designed for keratoconus, but due to advanced bulging, these lenses were unstable on the eyes and often popped out when he moved his eyes around or blinked. I then fitted him with Jupiter scleral lenses. These are very simple and easy on the patients as they are a relatively small scleral lens and easier to insert for beginners. However, in his case, the fitting was not ideal because the edge of the cornea kept being pressed close to the back surface of the lens. This is not good in scleral lens fitting, as it may not leave enough space for the cornea to breathe. I then switched to BostonSight scleral lens design, which is larger and more easily vaults over the entire cornea. He was very happy about his vision, with the right eye seeing 20/25 and left eye seeing 20/20. He told me that he ‘hasn’t seen this well since 16’- that was probably when he started developing keratoconus. He’s now in his early 40s, and this was the first time he heard of keratoconus. 

Keratoconus is a condition that affects about 1 in 2,000 individuals. It usually starts in teenage years or early 20s, but can happen as early as 8 or 9 years of age. It tends to get progressively worse until stabilization in the mid 30s. There is often a family history, but not always. Both eyes tend to be affected, though one eye may be much worse than the other. We do not know the cause of the disease, but one modifiable risk factor is rubbing of eyes. So I always ask patients not to rub eyes. While it is progressing, an effective treatment called corneal cross linking can stabilize the cornea and halt the worsening of the condition. This procedure is typically done by a corneal specialist. Once cornea is stable, these special contact lenses such as RGPs or scleral lenses can often help patients to see what they used to be able to. Any keratoconus patient should have at least two types of eye doctors, one a corneal specialist, and one an optometrist who fits specialty contact lenses for keratoconus.

I feel like there are rocks in my eyes

by Juan Ding, OD, PhD

Today I had an urgent visit from an established patient. She’s in her early 50s, and has a medical history of high blood pressure, anxiety and depression. Regarding her eye history, she had narrow angles, which means she is at risk of developing a type of glaucoma (angle closure glaucoma), and for that she had laser peripheral iridotomy (LPI) before. This procedure allows fluid to communicate in the front chamber of the eye, preventing closure of the drainage system of the eye (the angle) thereby preventing high eye pressure from happening which can cause glaucoma. 

She was very anxious because since she started a new antidepressant, desvenlafaxine (Pristiq), 3 months ago, she started feeling like there were rocks in her eyes, blurry vision, more migraine and her blood pressure went up. Desvenlafaxine is a serotonin-norepinephrine reuptake inhibitor (SNRI), and it may cause blurry vision and angle closure glaucoma. She was very much aware of her narrow angles and worried that it’s causing glaucoma in her eyes. On her psychiatrist and pharmacist’s recommendation, she stopped the medication 2 days ago, but was now suffering from serotonin withdrawal syndrome. Her psychiatrist prescribed prozac as a transition drug, but wanted to make sure her eye pressure was not elevated. She had the medication in her car, and if the test was normal she would go and have her first dose. If not, she would not be able to start this new medication.

Fortunately, eye exam showed that she had normal eye pressure, and that her LPI was still working and her angles were open. So she was cleared to go on with another antidepressant.

But her eyes were dry, and this explained her sensation of ‘rocks’ in her eyes. She did try refresh artificial tears and felt it immediately helped her symptoms. I advised her that she could actually use these artificial tears regularly, up to 4 times daily, as long as she’s feeling the dry eye symptoms.

All too often, antidepressants and other medications cause dry eye. It’s not only uncomfortable, in some cases, causing extreme eye irritation in patients, who are anxious and depressed to begin with; but it can also cause blurry vision because of disrupted tear film. Anyone taking antidepressant is at risk of developing dry eye, and may try some OTC remedies first, like artificial tears, before visiting their eye doctors. Glaucoma is a much more rare side effect, but anyone with a history of narrow angles or glaucoma suspicion should be very careful- it’s best if they visit eye doctors routinely while on certain antidepressants. In severe cases of recalcitrant dry eye and/or glaucoma, an alternative medication may need to be considered.