Thursday, August 31, 2017


Corneal topography of someone with regular astigmatism.
The cooler tones indicate the flatter parts of the cornea while the warmer tones indicate the steeper parts.
As you can see, this cornea is more curved along the vertical plane. 

Uh-stig-muh-tizum. It sounds like a terrible disease, but it's not. It is a type of refractive error- it affects how light bends, or refracts, when it enters your eye. Nearsightedness (myopia) and farsightedness (hyperopia) are also refractive errors. Astigmatism is an irregular curvature of the front part of the eye (the cornea and/or the lens). Most people have at least a small amount of astigmatism, but not everyone's vision is affected by it. To explain astigmatism in more detail, let's take a quick step back and review refractive errors.
Image: NEI
A quick review of refractive errors: 
We refer to the curvature of the cornea and lens as either spherical or astigmatic. When you have a spherical cornea or lens, it has the same roundness all over, like a basketball. Because of this uniform curvature, light entering the eye focuses at one point.
  • If that one point is in front of the back of the eye (the retina), you are nearsighted. You need minus power in your glasses/contacts to make the light focus ON the retina so you can see clearly. 
  • If that one point is behind the retina, you are farsighted. You need plus power in your glasses/contacts to make the light focus ON your retina so you can see clearly. 
With an astigmatic cornea or lens, the curvature is NOT the same all the way around (more like a football than a basketball), and light entering the eye focuses at two different points. This distorts and blurs things up close and far away, and it's especially noticeable when looking at street signs or electronic displays. As someone who has a fair amount of astigmatism, reading signs at the airport is a nightmare without my astigmatism correction!

There are different types of astigmatism. If the irregular curvature is found in the clear part of the front of your eye (the cornea), it's called corneal astigmatism. If it is found in the part of the eye that sits behind the iris (the lens), it's called lenticular astigmatism. You can have either or both. Corneal astigmatism is more common.

Astigmatism can also be classified as either regular or irregular. Be warned: this part will bore you.
  • Regular astigmatism occurs when the primary meridians/curvatures are 90 degrees apart, producing a bow-tie or figure-eight pattern on corneal topography (see below). This is much more common than irregular astigmatism. Regular astigmatism can be further classified based on which plane is steepest: 
    • With-the-rule astigmatism is when the vertical plane is the steepest. This would be similar to a football laying on its side.
    • Against-the-rule astigmatism is when the horizontal plane is the steepest. This would be similar to an upright football on a kick-off tee.
    • Oblique astigmatism is when the principal planes are not at or close to (within 30 degrees) the vertical or horizontal. 
Types of regular astigmatism, as seen on corneal topography
Image: Optometric Management
  • Irregular astigmatism is present when the curvature is not regular, and is generally a result of surgery, scarring, or disease. An example would be keratoconus

How do I know if I have astigmatism?
Astigmatism is diagnosed by your optometrist or ophthalmologist during a comprehensive eye exam. There are three instruments that may be used to detect astigmatism:
  • Keratometer- this instrument measures the average curvature of the central part of the cornea. In most offices, an automated keratometer is combined with an autorefractor (AKA the thing that has a picture of a hot air balloon or barn in it). 
  • Corneal topographer- this instrument maps the front surface of the eye, indicating where the cornea is steepest and flattest. The image at the top of this post is a corneal topogram.
  • Phoropter- AKA the "better one or two" instrument. By using the dials below, your eye doctor can figure out how much astigmatic correction you need and where it needs to be.

How do you treat astigmatism?
  • Glasses- Spectacle lenses can correct astigmatism. Unlike a spherical prescription, an astigmatic prescription has 3 numbers:
    • The first number is the spherical component- the amount of nearsightedness (-) or farsightedness (+).
    • The second number is the cylinder- the amount of the astigmatism. This can be written in either plus or minus form.
    • The third number is the axis- a number between 1 and 180 that indicates the position of the astigmatism.
  • Contact lenses- Contact lenses that correct astigmatism may be referred to as toric lenses. Soft contact lenses have come a long way in recent years, and are now available in a wide range of astigmatic prescriptions. However, they are not available in every axis and every cylinder, so they are not for everyone. With larger amounts of astigmatism, gas permeable contacts may give sharper, more consistent vision. Gas permeable contacts are an especially great option in patients with irregular astigmatism.
  • Surgery- Refractive surgeries, such as LASIK, are also an option.

CliffsNotes: Astigmatism isn't a disease; it's a refractive error. It means the cornea and/or lens is not completely round, so light doesn't focus at one point. That distorts and blurs things, but it can be corrected with glasses, contact lenses, or refractive surgery. 

Additional recommended resources:

Monday, June 19, 2017

prosthetic eyes

Who makes prosthetic eyes?
An ocularist is someone who fits and makes artificial, or prosthetic, eyes.

Why would one need a prosthetic eye?
There are cases in which the eye cannot be saved. Some of those include cancer and trauma/injury. A blind eye that becomes painful may also need to be removed. Prosthetic eyes are also utilized in cases of congenital abnormalities like anophthalmia, when a child is born without one or both eyes, or microphthalmia, when a child is born with one or both eyes being abnormally small. Beyond that, there are situations where the eye remains, but it is blind and misaligned. In those cases, a scleral shell can be made to be worn over the natural eye to improve cosmesis.

When the eye needs to be removed, it can be done via enucleation or evisceration. An enucleation involves removing the entire eye, while an evisceration involves removing the contents of the eye but keeping the outer shell of the eye (the sclera) and leaving the optic nerve and ocular muscles intact (1).

An orbital implant is then placed in the eye socket to maintain the volume of the eye. There are different types of orbital implants, mainly solid acrylic implants and porous implants. Porous implants allow tissue growth within them, leading to better mobility and stability. After an enucleation or evisceration, a temporary plastic conformer is placed in the socket in front of the implant to hold the shape until the wounds heal and a prosthetic can be placed. The prosthesis fits over the orbital implant and under the eyelids.
Examples of porous orbital implants via Marie Allen Ocularist

How is a prosthetic eye made?

I'm so glad you asked! I had the pleasure of spending a day at Carolina Eye Prosthetics to see how they make prosthetic eyes, and it was fascinating! I got to watch the process from start to finish, and here's my overview of the process. *I watched a couple of eyes get made that day, so the images below are of two different prosthetic eyes.*

1.  First, an impression is made. Vinyl polysiloxane impression material (the same stuff used to get dental impressions) is used to get an impression of the eye socket. The ocularist puts an impression tray into the eye, and uses a gun to push the impression "goo" into the eye socket. After a few minutes, the impression is removed from the eye socket. 

The impression tray (A) goes into the orbit, the nozzle of the gun enter the stem of the impression tray,
and the vinyl polysiloxane material is injected into the orbit (B). After a few minutes, the impression is made (C)!

2.  A cast is made to create a wax version of the eye. A flat, black iris disk is also put in the mold, with a clear, round acrylic button over top, simulating the cornea. There is a peg sticking out of the button that helps the ocularist determine the eye's gaze. 
The impression is used to make a mold (A,B), and the mold is then filled with wax (C). The wax eye is made (D) and the iris button is added (E).

The wax eye is put into the patient's eye socket, and modifications are made as needed. The ocularist alters and sculpts the wax eye many times to get the ideal fit and positioning. 
Sculpting the wax eyes

3. Dental stone is used to make a cast, and the mold is filled with polymethyl methacrylate, aka PMMA (the same substance contact lenses were made out of back in the day). This makes up the white part of the prosthetic eye. The eye then "cooks" in a hot water bath. When it's ready, the eye is then modified with hand tools as needed and polished using pumice stone.
The mold is prepared (A) and the PMMA is put into the mold (B). Photo (C) is what the eye looks like after cooking in the hot water bath. The mold is then modified using hand tools (D), and buffed with pumice stone(E). The eye is ready to paint (F)! 

4.  The eye is then hand-painted, layer by layer, using dry pigment. This is a critical step that adds depth and realism to the eye. The colored part of the eye (iris) is painted to match the color and size of the fellow eye, which is no easy task. The iris has texture and variations in color, making it complex and detailed. If you want to see how crazy-complex the iris is, check out these awesome close-up photos. Anna painted the prosthetic with the patient sitting across from her, so she could have the patient try the eye on every so often to see how well it matched the other eye. The white part of the eye (the sclera) is also painted to match the other eye. Then the blood vessels are added- those can be painted on, or fine embroidery thread can be used instead.
Painting the eye

5.  A final cap of clear acrylic is applied to seal the paint and create a smooth surface.

6. Finally, the eye is buffed and polished. TADA!
My souvenir from the day!

How are the prosthetic eyes inserted and removed?
To insert the prosthetic eye, hold the upper lid and gently push the prosthesis under the upper lid. If needed, a tug at the bottom lid helps get the bottom portion of the prosthesis under the lid. Removal is done with a DMV suction cup, which basically acts as a tiny plunger.

Special thanks to the lovely and talented ladies at Carolina Eye Prosthetics for allowing me to shadow them all day!

CliffsNotes: Ocularists are wizards, and prosthetic eyes are amazing. 

Additional Recommended Resources:

Thursday, June 1, 2017

recurrent corneal erosion

Brief anatomy review before beginning: The cornea is the clear part of the front of your eye. It is made up of 5 layers (or maybe 6 given recent research that suggests another layer- "Dua's layer"-exists between the stroma and Descemet's membrane). The outer layer is the epithelium, the second layer is Bowman's membrane, the third and largest layer is the stroma, beneath that is Descemet's membrane, and last is the endothelium. 
The layers of the cornea
Image: All About Vision

What is Recurrent Corneal Erosion?
Recurrent corneal erosion syndrome, or RCE, is a condition in which the outer layer of the cornea (the epithelium) repeatedly sloughs off due to poor adhesion to the tissue beneath it. This poor adhesion is most often due to either past superficial trauma or an inherited condition that affects the outer layers of the cornea (ie: EBMD/map-dot-fingerprint corneal dystrophy, lattice corneal dystrophy, Reis-B├╝cklers corneal dystrophy, granular corneal dystrophy).  Microerosions are smaller erosions with symptoms that last for a few minutes or hours, and they are more associated with corneal dystrophies. Macroerosions, on the other hand, are larger erosions with symptoms that last for many hours or even days, and tend to occur more in cases of past corneal trauma (1).

Why does it happen?
The basal layer of the epithelium is the innermost layer of the epithelium. It adheres to the underlying basement membrane via something called an adhesion complex. This complex is made up of hemidesmosomes and collagen fibrils- fancy words to say that it basically anchors the outer layers of the cornea. Due to trauma and/or dystrophy, the basement membrane is deposited abnormally, causing irregularities in the layers and disrupting the adhesion complexes. This weak adhesion leaves the epithelial cells more prone to sloughing off, or eroding.

A history of trauma is present in roughly half of RCE cases (2), especially when the trauma involved a fingernail or tree branch. Trauma disrupts the adhesions that exist in the epithelium. The subsequent inflammation from the injury also causes a breakdown in the adhesion complex. Matrix metalloproteinases (MMPs) are inflammatory mediators that are thought to play a role in degrading the protein and collagen matrix of the corneal tissue, leading to erosion. I picture MMPs as little ninjas that sneak in with swords to break apart the scaffolding proteins in the adhesion complex. People with RCE have been found to have increased MMP 2 and 9 levels in the tear film and epithelial cells (3,4)

Patients with EBMD, or other dystrophies affecting the outer layers of the cornea, experience similarly poor adhesion of the epithelium cells to the underlying basement membrane, due to changes in the cells of the epithelium and/or basement membrane.

A cell slide showing an irregular epithelial basement membrane
Image: Ophthalmology Management

What are the symptoms?

RCE presents with a painful, irritated, watery, red eye. Light sensitivity and blurry vision can result as well.

These symptoms are usually experienced during sleep or upon wakening. It tends to happen during sleep when your body enters REM sleep, because the eyes actually make small, quick movements from side to side (hence the name Rapid Eye Movement, aka REM). While you sleep, superficial corneal swelling and surface dryness occur, which can weaken the adhesion within the cornea and/or foster lid sticking. So when you open your eyes, the lids have a shearing effect, dislodging the epithelial cells and causing an erosion.

How is RCE treated? 
The initial goal of treatment is to heal the cornea and relieve symptoms. The next goal is to prevent or minimize recurrence by creating new, stronger junctions within the cornea.

To keep things organized, we will break the treatment options up into two categories: medical and surgical treatments. Let's begin by discussing some of the medical treatments for RCE:
  • Lubrication. This is the first-line treatment for RCE. The goal here is to help heal the cornea and prevent the inside of the eyelid from sticking to the outside of the cornea while it's healing. 
    • Artificial tear eyedrops. Preservative free artificial tears are best, and they are to be applied several times a day (every 1-2 hours) during acute episodes. 
    • Ointments. Hypertonic ointments (sodium chloride 5%) are good because they reduce swelling in the cornea while also lubricating the eye. Artificial tear ointments are also good options. For my RCE patients, I recommend applying artificial tear ointment before bedtime every night preventatively. Using an eye mask while sleeping has also helped some of my RCE patients avoid recurrences. Or you could wear a helmet to sleep, like this guy (that's a joke- don't do that).
    • Punctal occlusion. This is an option if lubrication with drops and ointments doesn't do the job. A punctal plug is essentially a cork that we place in the drainage system of the eye, to keep tears on the surface of the eye longer. Short term plugs are made of collagen and dissolve over time, and long term plugs are made of silicon. 
  • Bandage soft contact lenses (BSCL). Wearing a contact lens helps prevent lid/epithelial adhesion and the shearing effect we discussed earlier. The protection offered by the BSCL allows the adhesion complex to mature without disruption. The epithelium regenerates and symptoms subside within a few days (roughly 3-7 days), but the adhesion complex takes a few months to stabilize. Thus, treatment should be ongoing for at least 2-3 months (5). A study showed that after 3 months of treatment with a BSCL, 75% of the RCE patients were without recurrence after 1 year (6). It is important to note that a patient wearing a BSCL must visit their optometrist or ophthalmologist at regular intervals to replace the contact lens and to make sure there are no complications.
  • Anti-MMP therapy. As discussed earlier, MMPs play a role in degrading the adhesion complex. A category of antibiotics called tetracylines have anti-MMP properties, as do steroids. Doxycycline is the tetracycline used most often in this case. A combination of both oral doxycycline and topical steroids has been shown to be effective in treating RCE and preventing recurrences. One study found that eight weeks after starting the combination treatment, 71% of patients were symptom free. At 6 months, 83% denied any symptoms suggestive of relapse and at 12 months, 73% were free and clear (7). A second study followed a similar method and found no recurrences amongst the test subjects over an average followup period of 21.9 months. When the researchers cultured the corneal epithelium in the test subjects, they found that this combination treatment produced a statistically significant decrease in the amount and activity of MMP-9 (8).
  • Autologous serum. This is essentially an eyedrop made from a patient's own blood serum. Sounds weird, I know. The patient has blood drawn, the blood is spun around to separate out all the different components (centrifuged), and the serum is removed, diluted, and bottled. The properties of blood serum are similar to those of tears, so this method is used to treat various ocular surface diseases. While this sounds great, it is not the cheapest or easiest treatment option out there. But it does appear to be effective. Over a followup range of 1-2 years, 85% of RCE patients treated with autologous serum for 6 months had complete healing with no recurrences (9).
For chronic cases and/or frequent recurrences, bigger guns may be needed. Here are a few surgical options available:
  • Anterior stromal puncture (ASP). This is a procedure in which a tiny needle, or a Nd:YAG laser, is used to poke through the outer cornea to the beginning of the third layer of the cornea. The idea is that the puncture cause inflammation and creates pinpoint scars that strengthen the adherence of the epithelium to the underlying tissue. Since corneal scarring can affect vision, it is best to use this procedure if the area of erosion is NOT in the center of the cornea
  • Epithelial debridement and diamond bur polishing. This involves purposefully removing the weakly adhered epithelial cells and basically wiping the slate (basement membrane) clean. With the eye numbed, the loose epithelial cells are removed, leaving the outer edge of the cornea intact. Diamond bur polishing can be done after debridement and has been shown to reduce recurrence rate when compared to debridement alone (10). The bur basically buffs Bowman's membrane to create a smoother surface. A bandage soft contact lens is used, as well as drops for lubrication, protection against infection, and pain relief as needed.
    • Amniotic tissue membrane can be used here instead of a BSCL. Their role in RCE treatment would be similar to a BSCL, except that the amniotic membrane tissue has therapeutic qualities that help heal the cornea. Amniotic tissue is actually made up of some of the same collagens and proteins that the cornea is, and has anti-microbial and anti-inflammatory properties. Sutureless amniotic membranes can be cryopreserved (ProKera) or dehydrated (AmbioDisk or BioD Optyx). A study was done using ProKera following epithelial debridement; of the 11 eyes that were treated, only one eye had a recurrence over a followup span of 10-16 months (11).
  • Phototherapeutic keratectomy (PTK). The first layer of the cornea is removed (similar to the method described above), and an excimer laser is used to remove a small amount of the second layer of the cornea (Bowman's membrane), smoothing away irregularities. This allows formation of a new basement membrane and adhesion complex. Animal studies have shown an increase in anchoring proteins following excimer laser treatment (12). A BSCL or amniotic membrane is placed on the cornea while it heals. Like debridement, it takes a few days to recover; however it is more expensive since a laser is used and it is performed in an operating room. In a study of 76 eyes with RCE treated with PTK, only 11% had recurrences. Of those that had recurrences, only 25% continued to have recurrences after retreatment with PTK (13). Recurrence rates tend to be lower if corneal dystrophy is NOT the cause of RCE.

CliffsNotes: RCE is a condition in which the cells of the outer cornea repeatedly slough off. It is usually a result of past trauma or an inherited corneal condition. It hurts. A lot. But there are medical and surgical options that you and your optometrist or ophthalmologist can discuss to heal the erosion when it happens and to help prevent it from happening again. 

Additional Recommended Resources:

Monday, April 10, 2017

myopia control

What is myopia?
Myopia is the fancy name for near-sightedness. Myopia causes vision to be blurry in the distance. It is the result of light rays focusing in front of the light-sensitive tissue that lines the back of the eye (the retina) rather than on the retina. This can happen when the power of the front of the eye is too strong (refractive myopia) or when the eyeball is too long (axial myopia). Below is an illustration. A minus (concave) lens is used to focus the light rays on the retina so that images are clear. The most common type of myopia begins between the ages of 6 and 12.

A myopic eye focuses the image IN FRONT of the retina, producing a blurry image. Minus lenses are used to correct myopic eyes, putting the image ON the retina so you can see clearly. 

The prevalence of myopia has been increasing over the past decades. In 2000, 23% of the world's population was myopic, and researchers are predicting that 50% of the world's population will be myopic by 2050 (1). THAT'S HALF OF THE WORLD!! Higher rates of myopia, nearing 90%, occur in some Asian populations. The increase in myopia prevalence suggests that environmental factors play a role in its development, though there is certainly a genetic component as well. People with higher amounts of myopia are also at greater risk for eye health issues such as retinal detachment and myopic maculopathy (2), so the myopia "epidemic" is a public health concern.

How does myopia progress? 
The exact mechanism of myopia development is still unclear. The thought is that myopia progression is caused in large part by the elongation of the eye. Research suggests that peripheral hyperopic defocus causes elongation of the eye. The periphery can be blurred even if the center is clear, and this peripheral blur is not really something we notice. At near, the periphery is more out of focus than it is when looking in the distance, so near work may be implicated in the progression of myopia (3). Some more recent studies have shown a greater association between myopia development and the time spent outdoors than the time spent doing near work. Translation: increasing myopia is more closely related to how little time people spend outdoors than how much time people spend reading. So minimal time spent outdoors could be a risk factor for myopia development. Very recent research has identified a cell in the retina that may cause myopia when it dysfunctions. The dysfunction may be linked to the amount of time spent indoors/away from natural light (4).
image: Review of Optometry

Options that have been shown to slow the progression of myopia:
  1. Orthokeratology (aka ortho-K, corneal reshaping technology, CRT). These are customized contact lens worn only at night, temporarily changing the shape and power of the front part of your eye (the cornea).  When you wake up, you take the contacts out and you can see! Ortho-K lenses involve reverse geometry, meaning the curves of the lens are structured so that the tear film beneath the lens essentially flattens the center of the cornea while steepening the midperipheral cornea. This creates peripheral myopic defocus that negates the peripheral hyperopic defocus that is linked to eyeball growth (5). Orthokeratology is FDA approved for myopia up to -6.00D and mild amounts of astigmatism (up to 1.75D). There is no minimum age; the child just has to be able to put the contacts in, take them out, and maintain them on their own. It all depends on the child's maturity level. As with any contact lens wear, there is a small risk for infection. Studies have found that ortho-K treatment produced an average of 30-50% reduction in the progression of myopia.(6). Ortho-K appears to be more effective for those with higher amounts of myopia and larger pupils. Both the LORIC and later the CRAYON study showed that ortho-K slowed the axial growth of the eye, thus reducing myopia progression (7). The SMART study is yet another recent study that supports the theory that ortho-K reduces myopia progression. At the conclusion of this 3-year study, the ortho-K group saw an average increase in myopia of 0.12D while the soft lens control group increased by an average of 1.01D (8).
  2. Soft multifocal contact lenses. Multifocal contact lenses are those that correct your distance while also giving you plus power to help see up close when needed. The specific design of multifocal lenses that are used for myopia control are center distance design (see image below). Center distance means more plus power in the periphery of the lens, which decreases peripheral hyperopic defocus and induces peripheral myopic defocus, reducing axial elongation. Several study results have supported the use of distance-center soft multifocal contact lenses for myopia progression, averaging a 40% reduction in myopia progression (91011)The CONTROL study found a whopping 72% reduction in progression of myopia over a one year period when compared to wearing single vision soft contact lenses (12), though this study involved myopic children with a specific focusing/postural issue (eso-fixation at near).

  3. A multifocal lens with a center-distance design
    image: Review of Optometry

  4. Atropine. This method is different from the above two because it is not about changing the stimulus that contributes to eye elongation, but rather interfering with a biochemical pathway.  How does it work? We don't really know for sure. But it is thought to act on the white part of the eye (the sclera) or the tissue that lines the back of the eye (the retina) to prevent the sclera from thinning or stretching (13). If you have had your eyes dilated during an eye exam, the doctor likely used tropicamide.  This drop made your pupils big and your vision up close was blurry for 3 or 4 hours. Atropine is a similar drop from the same family of drugs, but the effects last for much longer. Atropine 1% has been shown to produce a 90% average reduction in myopic progression, from 0.5 D/yr to 0.05 D/yr (14). The downside: blurry near vision, light sensitivity, and large pupils. Other studies have shown comparable results using lower concentrations of atropine, which produce less side effects. Atropine 0.01% has been shown to slow myopia progression by 50%(1516) Pirenzepine has also been tested, showing slightly less efficacy (44%), but with fewer side effects. Unfortunately, it's not commercially available as an eyedrop or gel in the US. More research is being done on the long-term effects of atropine therapy, and whether or not its effects are permanent.

Options that are NOT GREAT for slowing the progression of myopia:
  1. Undercorrection of myopia. I've had some parents specifically ask me to give their child less powerful glasses in hopes that that would make the child need glasses less. There is no validity to this claim; actually, the undercorrection of myopia has been shown to INCREASE its progression (171819).
  2. Progressive addition lenses (PALs). Commonly called "no-line bifocals," PALs are lenses that have your distance prescription at the top and gradually become more plus-powered as you go vertically down the lens. Many people over the age of 40-ish wear these to help them see clearly at all distances. For the purposes of myopia control, they're not a top option. The COMET study found a small, statistically significant decrease in myopia progression in children wearing PALs vs children wearing regular, single-vision lenses, but only in the first year. So the conclusion was yes, it produces a little decrease in progression, but not enough to warrant a change in how we prescribe for myopic children (20). Also, other aspects of the child's binocular vision should be taken into consideration. 
  3. Spherical soft contact lenses or rigid gas-permeable (RGP) contact lenses (aka regular distance vision contacts). These two choices are excellent forms of vision correction, but they have shown little value in terms of controlling myopia progression. The CLAMP study showed some reduction in myopia with RGPs in year 1 in comparison to soft contact lenses; however, it was not clinically significant because it didn't change axial length and was likely due to the flattening of the cornea, which is not permanent (21).

CliffsNotes: Glasses and regular contact lenses don't help slow myopia progression. Undercorrection of myopia doesn't help either; it actually makes it worse. Atropine therapy, orthokeratology, and soft multifocal contact lenses have been shown to be effective in controlling myopia progression. Ask your optometrist for more information!

Additional recommended resources:

Tuesday, January 31, 2017

meibomian gland dysfunction

image: All About Vision
What are meibomian glands?
Meibomian glands are sebacous (oil) glands located in the upper and lower eyelids. There are more in the upper lid than the lower lid, and they are also larger in the upper lid (1). The glands sit vertically in the eyelids, and their openings are right behind the lash line. The job of the meibomian glands is to make and secrete oil. These secretions make up one of the 3 layers of the tear film, the lipid layer. Blinking helps spread the secretions on the surface of the eye, keeping the tear film stable and preventing it from evaporating too quickly. The function of the glands is regulated by hormones such as androgens, estrogens, and progestins. 

A visibly capped meibomian gland
What is MGD?
Meibomian gland dysfunction, or MGD, is not the most clearly defined condition.  Here's the technical definition:

"Meibomian gland dysfunction (MGDis a chronicdiffuse abnormality of the meibomian glands,commonly characterized by terminal duct obstruction and/or qualitative/quantitative changes in the glandular secretion. It may result in alteration of the tear filmsymptoms of eye irritation, clinically apparent inflammationand ocular surface disease." (2)  

Translation? MGD is when the meibomian glands don't work right. The dysfunction is typically either a result of a blockage in the gland or an abnormality in the oil being secretedA blockage may present as a clear or opaque dome at the opening of the glands (see photo above). MGD can also involve changes in the quality and quantity of secretions. When pressure is applied to normal glands, they should secret a small amount of clear oil. In the case of MGD, the secretion is thicker and more yellow-white in color. I liken it to when you leave a tube of toothpaste open for a while, and you get some crusty, solidified gunk at the opening that you have to squeeze out to get to the usable toothpaste. 

What are the signs and symptoms of MGD?
Some common symptoms include dryness, a sandy/gritty feeling, a burning sensation, eye and lid irritation, contact lens intolerance, eyelids sticking together in the morning, and even blurry vision. These symptoms are also symptoms of similar but distinct conditions, so a thorough examination of the eyelids, tear film, and front surface of the eye by an eye doctor is warranted to help identify what the source of the issue is. 

Common associated signs of MGD are thickened eyelid margins, frothy tears, and a low tear break-up time (the time it takes for the tear film to break up due to evaporation). In fact, dysfunction of the meibomian glands is one of the main causes of evaporative dry eye disease. Not only does it cause dryness, but insufficient lipids may cause increased bacterial growth on the lid margins, which can cause a number of secondary lid issues (2).

What is MGD associated with?
  • Age: MGD increases in prevalence with age (3).
  • Contact lens wear: Studies suggest a decrease in functional meibomian glands with contact lens wear (4, 5).
  • Ethnicity: MGD appears to have a much higher prevalence among Asian populations (2). 
  • Systemic factors: menopause, rosacea, Sjogren's syndrome, etc. 

How is it treated?
There are various treatment options available, depending on the severity and associated symptoms/signs.  Here is a list of treatments I typically recommend for MGD, going from least complex (for milder cases) to most complex. 

1) BLINK! Blinking stimulates the secretion of meibum, and helps spread it across the surface of the eye. Studies show you blink less when reading, and you blink 60% less when at the computer (6).  So take frequent breaks, and make a conscious effort to blink completely during those breaks.
2) Warm compresses with lid massage. Taking a page out of a colleague's book, it's the flossing of the eye world- it's something you SHOULD do daily to prevent disease, but not a lot of people do it religiously. 
  • Use a warm washcloth (or a boiled egg or warmed dry rice wrapped in a cloth- somethng that stays warms for a few minutes) and rest it over your eyelids with your eyes closed. Do so for at least 5-10 minutes. Gently massage your eyelids, rolling your fingers vertically down your upper lid and up your lower lid (towards your lashes). This helps get the oils flowing normally, and also helps remove any solidified gunk at the opening of the glands.
  • I recommend doing this twice daily when symptoms are present, or when MGD is first diagnosed. Beyond that, once daily is great for maintenance.
  • Follow up with a lid cleanser, gently scrubbing along the lash line to remove debris, makeup, and bacteria that may clog or infect the oil glands. A cleanser containing diluted tea tree oil is particularly beneficial if Demodex is present. 
Lipiflow is an in-office procedure that accomplishes the same thing, though more effectively.  The device heats the internal surface of the lids and simultaneously applies pressure to the external lid to express the glands, all in about 12 minutes. 

3) Omega-3 fatty acids. Omega-3s help improve the quality of the oil produced by the meibomian glands, and they have anti-inflammatory effects. A great source of omega-3s is fatty fish, like salmon and tuna. Another option is fish or flax seed oil supplements. It's always a good idea to consult with your doctor before starting any supplement.

4) Artificial tears can also help beef up the contents of the tear film.  Lipid-based artificial tears are best in the case of MGD because they help replenish the lipid layer of the tear film, and not just the aqueous layer. Some lipid-based drops: Systane Balance, Soothe XP, Retaine MGD, and Refresh Optive Advanced. 

5) Prescription medications.  Depending on the other presenting conditions, some patients with MGD may require the use of antibiotics. Topical azithromycin or low-dose, long-term use of oral doxycycline are thought to alter the eyelid bacteria and also provide anti-inflammatory effects (7, 8). Still others with severe MGD may need to have the inflammation controlled through the short-term use of a topical steroid drop or the long-term use of a dry-eye drop. 

CliffsNotes: MGD can alter the makeup of the tear film, leading to eye irritation, inflammation, and dry eye. So see your eye doctor STAT to nip it in the bud!

Additional Resources:

Thursday, December 8, 2016

central retinal vein occlusion

What is a CRVO?
A central retinal vein occlusion (CRVO) occurs when there is an obstruction of the central retinal vein, which is the main vein of the retina (the tissue that lines the back of the eye). A blood clot, or thrombus, may occur in the vein as a result of abnormalities in blood vessel size, blood composition and/or blood flow.

Veins carry blood back to the heart. When the main vein that drains the retina is blocked and blood cannot flow out, the blood builds up and leaks out of the walls of the vessels.  This leakage causes the retina to swell (retinal edema).  When fluid leakage occurs in the area of the retina called the macula (macular edema), central vision is impaired.  

We'll be talking specifically about central retinal vein occlusions in this post, but you can also have a branch retinal vein occlusion (BRVO), which affects a smaller vein, or a hemi-retinal vein occlusion (HRVO), which affects either the upper or lower half of the retina. It all just depends on the location of the blood clot. 

A CRVO can be classified as non-ischemic or ischemic.  Ischemic means there is a shortage of oxygen due to a reduced or restricted blood supply.  When ischemia exists in the retina, vascular endothelial growth factors (VEGF) are released. VEGF stimulates the growth of new, abnormal blood vessels (neovascular membranes) to help supply the retina with the necessary oxygen and nutrients.  This is bad, because those blood vessels are weak and leak. In the case of ischemic CRVOs, the abnormal vessels can cause a serious type of glaucoma, called neovascular glaucoma. This results in dangerously high eye pressure that is very difficult to treat. Fortunately, most cases (about 75%) of CRVOs are non-ischemic, which is the less serious form and involves less severe vision loss.  
Photos of a non-ischemic CRVO of the right eye
What are the symptoms and signs?
The most common presentation is sudden, painless loss of vision in one eyeWhen the eye doctor looks in the affected eye, he/she will see lots of hemorrhages (see photos) in all 4 quadrants of the retina and possibly cotton wool spots, which are fluffy white spots in the retina. The veins of the retina are widened and curly. There may also be swelling of the optic disc. CRVOs are sometimes described to have a "blood and thunder" appearance, because it pretty much looks like something exploded in the back of the eye. 
CRVO photo via Wills Eye
What are the risk factors?
CRVOs usually occur in persons over the age of 50, and hypertension is the most common systemic association. Other vascular diseases like atherosclerosis, high cholesterol, and diabetes are risk factors as well.  Hardening and/or narrowing of the arteries can compress the vein and cause clot formation.  Open angle glaucoma is also a risk factor.  If a CRVO occurs in someone under 40 years of age with no known risk factors, he/she may need to be tested for blood clotting or thickness abnormalities

How is it treated?

The blockage cannot be undone, so the goal is to treat/prevent the secondary complications. Namely, macular edema and neovascularization. Several clinical trials have shown there are treatment options that help reduce macular edema and improve vision to a certain degree. Early detection of complications and timely treatment are key.  

The most common treatment for macular edema as a result of a CRVO is intravitreal injections of anti-VEGF drugs. The drugs are injected into the gel part of the inner eye (the vitreous), and are usually administered every 4-6 weeks.  Two such drugs that are FDA-approved for treating macular edema due to CRVOs are Lucentis (ranibizumab) and Eylea (aflibercept). Avastin (bevacizumab), a cancer drug, is an anti-VEGF drug used extensively as well, though used off-label. Steroid injections/implants may be used instead of or in addition to anti-VEGF injections. An intravitreal steroid implant, Ozurdex, is an FDA-approved treatment for macular edema secondary to vein occlusion. Currently in FDA trials: a combo of Eyelea (intravitreal anti-VEGF injection) and Zuprata (suprachoroidal steroid injection) that has the potential to decrease the number of Eyelea injections a patient needs (read more about it here). Laser is not a common treatment with CRVOs, unless there is neovascularization present.

Macula OCT of the above-photographed CRVO patient
Aside from taking photos to help monitor the condition, your eye doctor may utilize other tools in the treatment process. 

  • Optical coherence tomography (OCT) is a scanning laser used to get a cross-sectional image of the retina (see scan above).  This helps assess the level of swelling in the macula and track the response to treatment.  
  • Fluorescein angiography (FA) is used to identify areas of the retina with poor/absent blood flow and helps guide treatment. A dye is injected into a vein in the arm and photos of the retina are taken as the dye reaches the retinal vessels.

CliffsNotes:  A CRVO occurs when a blood clot blocks the outflow of blood from the tissue that lines the back of the eye (the retina). If you notice a sudden, painless loss of vision, contact your eye doctor STAT!

Wednesday, October 19, 2016


What is Demodex?
Demodex is an 8-legged, microscopic mite. Two species live on humans: Demodex folliculorum, which are found in the eyelash follicles, and Demodex brevis, which are found in the sebaceous (sweat) and meibomian (oil) glands. These mites live primarily on the face and feed on skin cells and oil in the follicles and glands. They avoid sunlight and live for about 2 to 3 weeks. How common are they? Fairly common in adults (studies report they are found on the skin of 20-80% of adults- that's a pretty wide range and not a super helpful stat...), and nearly 100% of elderly people have the mites on their skin (1). Studies have shown that the prevalence of Demodex increases with age, and Demodex mites are present in higher numbers in those with rosacea, compromised immune systems, and possibly contact lens wearers (23).

Two D. folliculorum on a plucked eyelash (A) and one hanging solo (B)
image: JKMS

Fun (or disgusting) fact: Demodex mites have no anus. Their waste is stored in the gut and expelled when they die, which may cause additional inflammatory response. Shout-out to one of my patients who shared that fact with me. #mypatientsaresmarterthanme

Demodex being teased out of the follicle (arrow) via lash rotation
image: Optometry and Vision Science

What problems can Demodex cause?
Many people have Demodex mites on their skin and have no symptoms or complications. However, Demodex overpopulation (demodicidosis) has been linked to (not necessarily causative of) skin conditions such as blepharitis, rosacea and perioral dermatitis, as well as meibomian gland dysfunction, dry eye, recurrent chalazion, and ocular surface inflammation (45).

Demodex mites can cause problems by clogging hair follicles and sweat ducts, causing abnormal thickening and growth of the epithelial cells at the lid margin. Further, the exoskeleton and waste of the mites can cause an inflammatory response (67). Overpopulation of Demodex mites has been linked to an increase in the presence of certain cell-signaling proteins (cytokines, specifically interleukins) in the tears, which can cause an inflammatory or immunological response (8).

The presence of cylindrical dandruff or "waxy sleeves" around the base of the eyelashes is a very good indicator of demodicidosis. Symptoms may include itching and redness of the lid margin, loss of lashes or misdirected lashes, as well as burning or irritation.

Cylindrical flakes that are highly suggestive of demodex
image: Review of Optometry

How do you get rid of the little buggers?
Frequent scrubbing of the lids with diluted tea tree oil (TTO) was found to be the most effective way to eradicate Demodex and improve patient symptoms (9). The TTO has ingredients (namely, terpinen-4-ol) that kill mites and ticks while also luring the mites out of the hair follicle before they mate (10).  There are also lid wipes, scrubs and shampoos containing various concentrations of TTO that can be used for at-home treatment and long-term maintenance. It is best to keep the concentration of TTO at or below 50%; any higher than that may be too irritating (11). Your eye doctor may choose to add an antibiotic and/or steroid ointment or drop to the treatment as indicated, depending on what other symptoms and signs are present. 

CliffsNotes: If you suffer from dry, itchy, irritated, red, and/or crusty eyelids, have your optometrist take a look. You MITE (see what I did there?) have a Demodex party going on in your eyelashes. 

Additional Recommended Resources: