Call Us: 703.273.2398

Tag Archives: Blood vessel

Retinal Ischemia: Supply vs. Demand

Retinal ischemia causes VEGF to be liberated inside the eye.  In cases of diabetes this can lead to diabetic retinal detachment or neovascular glaucoma.  Treatments included pan-retinal photocoagulation (laser) or anit-VEGF medication such as Lucentis or Avastin.

Ischemia results when oxygen supply does not meet oxygen demand to any tissue.  Other examples  are the heart and legs.  With strenuous activity, O2 demand increases.  If the body can’t compensate, chest pain or leg pain develops.

In cases of proliferative diabetic retinopathy, the retina becomes ischemic due to the loss of the microcirculation of the eye.  The small capillary beds that help feed the retina often get blocked and close off.  Blood flow is reduced, and therefore, so are oxygen levels.

In response to this lack of blood, or oxygen, supply, the ischemic retina produces Vascular Endothelial Growth Factor (VEGF).  VEGF causes abnormal blood vessels to grow on the surface of the retina and other structures inside the eye.  This can lead to blindness by causing a diabetic retinal detachment or glaucoma.

Stop the Ischemia

If we were to stop the ischemia, the VEGF production would cease. If we can change conditions so that supply is equal to demand, the imbalance is gone.

But we don’t know how to improve oxygen supply to the retina.  Presently, laser treatment and anti-VEGF medications are employed.

Laser Treatment Reduces Demand

As we are unable to increase oxygen supply, laser photocoagulation (specifically, pan-retinal photocoagulatoin, aka PRP) is used to decrease demand.  By ablating, a fancy term for killing, retinal tissue, we are in effect, reducing the demand.

If enough laser is performed, the overall O2 requirements will decrease.  Ischemia is stopped and VEGF is no longer produced.

The eye becomes stable.  A diabetic retinal detachment and glaucoma are prevented.

anti-VEGF Medications Block VEGF

Anti-VEGF medications such as Lucentis and Avastin block VEGF from doing its job.  In doing so, neovascularization can not be initiated and diabetic retinal detachment and glaucoma are avoided.

Is the eye stable?

What Does This Mean? Actually I am not sure.  The end result of laser (PRP) and anti-VEGF treatments are the same; preventing retinal detachment and glaucoma.

The use of laser for proliferative diabetic retinopathy is old hat.  It has been saving the sight of diabetics for about 40 years.  It is a good treatment because it fixes the problem.  PRP, when properly performed, stabilizes the eye by eliminating the ischemia.  It secondarily stops VEGF by halting the initial O2 imbalance.

I am not sure; however, if intraocular injections of Lucentis/Avastin actually fix the problem.  There is no mechanism to fix the ischemia.  VEGF is still liberated as the ischemia still exists.  Therefore, careful monitoring and repeated injections are needed.

Reblog this post [with Zemanta]

You Look All Bent Out of Shape

Distortion, also known as metamorphopsia, is a symptom of many macular diseases.   Anything that affects the macula can cause distortion; epiretinal membranes, macular holes, macular edema, diabetic retinopathy and macular degeneration.  The macula is a place in the retina, the functional center.  Thus, the term “macular” becomes an adjective when describing retinal disease located in the center of the retina.

OCT scan of a retina at 800nm with an axial re...
Image via Wikipedia

The macula is a small area of the retina measuring about 1.5 x 1.5 mm.  It is very sensitive and allows us our best color vision and the ability to see 20/20.  A normal macula (fovea) is smooth and slightly concave (see OCT).  Light falls on the normal macula giving us vision.  This is very similar to a projector focusing images onto a movie screen.  If there is a physical change to the macula or disease, central vision is usually affected.

Macular Pucker or Epiretinal Membranes

Epiretinal membranes are, as the name implies, membranes that develop on the surface of the retina and cause the underlying retina to wrinkle, or “pucker.”  This physical wrinkling of the macula causes decreased vision and distortion.

Surgically removing the membrane usually improves the distortion and can improve the vision, too.

Macular Holes

If you were to poke a pin through a piece of ballon and then stretch out the rubber, you’d create a nice round hole.  A macular hole is actually a stretch hole in the center of the macula.  Images that fall within this hole are not seen as there literally is no retina in the center of the macula.

Symptoms include decreased vision, distortion and sometimes, scotomas, which are the fancy name for blindspots.

Macular Edema

Swelling of the macula can occur from a variety of causes.  The two most common causes germaine to this web site are diabetic retinopathy (more specificially, diabetic macular edema) and swelling secondary to choroidal neovascularization in cases of wet macular degeneration.

Other causes, however, include central serous retinopathy, central and branch vein occlusions, cystoid macular edema from cataract surgery (uncommon these days) and from cases of intraocular inflammation (aka uveitis).

Macular Degeneration Causes Distortion 3 Different Ways

As above, choroidal neovascularization can physically distort the retina and cause distortion.  These abnormal blood vessels can develop in between the layers of the retina causing physical disruption of the retina.  The analogy here is exactly like the “Princess and the Pea.”

Wet macular degeneration can also cause macular edema as we discussed above.

Dry macular degeneration can also cause symptoms of distortion.  One of the layers of the retina, called the RPE, becomes diseased and degenerates.  This loss of one of the principle layers of the retina can cause distortion.

What Does This Mean? Distortion, or metamorphopsia, can be a symptom of a variety of retinal or macular disorders, not just macular degeneration.  The key for saving your sight is early detection and diagnosis.  Usually this may require consultation with a retina specialist to discuss the various treatments.

A fluorescein angiogram and/or an OCT (Optical Coherence Tomography) may be very helpful to your doctor, but this can vary.

Other causes of metamorphopsia, not related to the retina, could include large amounts of astigmatism or a decentered lens.

While most causes are indeed retina related, it is also important to note that most have a treatment with the exception of dry macular degeneration.  There is some rumbling; however, that there may be some promising treatments for dry macular degeneration in the near future.

Reblog this post [with Zemanta]

Neovascularization Causes Blindness

Both macular degeneration and diabetic retinopathy can cause “blindness” from neovascularization.  Both are diseases of the retina, both can lead to “blindness,” both increase with age/time and both can be associated with abnormal blood vessel formation known as neovascularization.”

The two diseases differ in the location of the neovascularization.

Diabetic Retinopathy – In cases of diabetic retinopathy, the presence of neovascularization defines a particular stage of eye disease; proliferative diabetic retinopathy.  The neovascularization may “proliferate” along the surface of the retina and other structures inside the eye.  As long as the VEGF is circulating, the vessels will continue to grow.

Diabetic retinal detachments may occur if the the neovascular tissue proliferates out of control.  Neovascular glaucoma may develop if the abnormal blood vessels “clog” the internal drain of the eye.  In this case, intraocular fluid that normally filters out of the eye can no longer escape as the drain is closed.  The pressure escalates out of control and severe pain (and redness) develop.

In short, proliferative diabetic retinopathy, as defined by the presence of neovascularization, can causes retinal detachments and neovascular glaucoma (not the usual form of glaucoma).  Both are mechanisms by which diabetes can cause blindness.

Macular Degeneration – “Wet” macular degeneration, by definition, exists when neovascularization develops underneath the retina.  This neovascular tissue causes physical separation of the layers of the retina and destruction of the normal tissue.  Almost all neovascularization leaks, and, at times, bleeds.  Loss of central vision occurs due to this rather rapid growth of abnormal blood vessels.

VEGF – In either case, neovascular tissue is a complex of “abnormal blood vessels.”  As best we can tell, neovascular tissue develops in response to Vascular Endothelial Growth Factor, or VEGF.  This growth factor causes both proliferation of the neovascular tissue and sustains existing neovascularization.  Without circulating VEGF, the neovascular tissue shrinks up and goes away.

Anti-VEGF treatments are simply directed at blocking the effects of VEGF.

Anti-VEGF medications (e.g. Avastin, Lucentis and Macugen) are antibody like molecules that find circulating VEGF and prevent VEGF from “doing its duty.”   The treatment of choice for proliferative diabetic retinopathy remains pan-retinal photocoagulation (PRP).  The end result of PRP is decreased … VEGF.

With timely diagnosis, both diseases can usually be controlled.  Neovascularization in diabetes can be reversed before a retinal detachment is formed, neovascular glaucoma may be reversed and “wet” macular degeneration can be halted.

What Does This Mean? A few years ago, I would not have been able to write this article.  We have learned a lot about the mechanisms by which both diabetic retinopathy and macular degeneration cause blindness.  It amazes me how the pathogenesis (i.e. the disease process) of both diseases are so similar.  Both diseases can cause blindness via VEGF.

This is why it is so confusing.  Two separate diseases that respond to the same treatment.

Reblog this post [with Zemanta]

Macular Degeneration Treatment and the Blood Brain Barrier

The retina is part of the central nervous system.  Delivering medicine into the central nervous system, or to the retina, by traditional means has historically been very difficult; hence the popularity of intraocular injections.  By bypassing the blood-brain-barrier (or blood-retina-barrier), drugs are now effectively delivered to the “target” tissue.

The usual methods for treating a disease, be it an infection, hypertension, or even diabetes, is to take a pill.  The pill is dissolved in our stomach and the medicine is absorbed into the bloodstream.  The bloodstream delivers the pharmaceutical to the target tissue… and bingo! the drug does its thing.

More direct methods require intravenous (IV) delivery for the medicines.  A drug is delivered directly into the bloodstream via a vein.  This delivery method bypasses the digestive system and does not require absorption.  This method is great for delivering higher doses of medication into the body and for delivering drugs that get altered when swallowed.

In the eye, and in the brain, drugs that have been either absorbed, or administered via an IV, get trapped within the blood vessels and are not able to diffuse into the eye or brain.  This is called the “blood-brain-barrier.”  Essentially, drugs do not get to the brain/retina by normal methods due to the uniqueness of the blood vessels in the central nervous system and the eye.

To beat a dead horse – This is why we are using intraocular injections to deliver steroids and anti-VEGF medications to treat macular degeneration and diabetic retinopathy.  These drugs do not get into the eye via the bloodstream.  By injecting directly into the eye, we bypass the blood-retina-barrier and put the medicine right where we want it.

What Does This Mean? This is one large reason why there are no pills or medicines to treat macular degeneration or diabetic retinopathy.  We can’t get the medicine to the retina.  The idea of intraocular injections is relatively new, but has gained wide acceptance as it is highly effective (works better than anything else), is convenient (done in the office), is safe…and is painless.

By directly injecting agents into the eye, we are able to treat the retina with “old” drugs.  Steroids are certainly not new, but we have discovered many “new” uses for treating retinal disease simply because we can get the drug to the tissue.

The next generation of injections will be the sustained release drug delivery systems that I talk about once in a while.  It shares the same theme as the introacular injections; it bypasses the blood-retina-barrier.

Avastin: An Adjunctive Therapy for Proliferative Diabetic Retinopathy

Avastin® is useful for a variety of eye conditions;  it is principally used to treat wet macular degeneration and is becoming a popular option to treat diabetic macular edema.  On occasion, Avastin has also been useful, in my practice, to treat patients with proliferative diabetic retinopathy.

VEGF (Vascular Endothelial Growth Factor) also causes abnormal blood vessels to grow in cases of “wet” macular degeneration and … proliferative diabetic retinopathy.

Proliferative Diabetic Retinopathy (PDR) is defined by the presence of abnormal “neovascularization.”  These are abnormal proliferations of blood vessels that grow inside the eye.  In patients with diabetic retinopathy, the VEGF is produced in response retinal ischemia; retinal demand for oxygen exceeds the supply due to poor blood supply.  VEGF then causes neovascularization to develop.  This neovascularization can cause blindness by causing retinal detachments or neovascular glaucoma.

The  traditional treatment for proliferative diabetic retinopathy has been laser photocoagulation.  The laser treatment, called pan-retinal photocoagulation (PRP), has been the treatment of choice for years.  The PRP destroys enough tissue so that the available blood supply is adequate to meet the oxygen requirements of the tissue.  When this occurs the “ischemia” is cured, VEGF is no longer produced and the proliferative retinopathy becomes stable.

Occasionally, I have  patients that do not respond well, or completely, to pan-retinal photocoagulation.  Lately, on select cases, I have used Avastin as an alternative to pan-retinal photocoagulation for the treatment of proliferative diabetic retinopathy.

So far the treatment works well.  The neovascular tissue regresses quickly and I recheck patients every 4-6 weeks.  The injections do need to be repeated.

What Does This Mean? Pan-retinal Photocoagulation has been the gold-standard for the treatment of proliferative diabetic retinopathy.  The PRP can decrease light to dark adapatation, that is, it takes awhile to get used to light when coming out of a movie theater.  It is a difficult procedure to perform, but has been very effective over the years.  I consider it a good “fix.”

An alternative therapy is welcomed for two reasons.  Avastin injections are certainly easier to perform and seem not too affect the vision.  Avastin also treats the disease by a different mechanism and may increase the chances of achieving stability.  On the other hand, Avastin does NOT change the relative ischemia in the retina, that is, the oxygen demand is still greater than oxygen supply.  It may be less of a permanent “fix.”


Randall V. Wong, M.D.
Retina Specialist, Ophthalmologist
Fairfax, Virginia

Reblog this post [with Zemanta]

Blood in the Eye: You Make the Call

Last week another long time patient of mine (as most are with diabetic retinopathy and macular degeneration) returned with complaints of the sudden onset of floaters in the left eye.   The floaters had been present for about one month, they hadn’t cleared and he made an appointment.

I’ve added this illustration that resembles what I saw after dilating his pupils.  What do you see?

Vitreous Hemorrhage

My patient has had diabetes mellitus for about 18 years.  He is 64 years old.  Several years ago, he had a similar problem in the other eye.  He developed a vitreous hemorrhage from proliferative diabetic retinopathy.  In the illustration above, note the abnormal blood vessels, so-called “neovascularization,” that has formed on the surface of the retina.

Neovascularization develops when the oxygen supply to the retina is poor, causing retinal ischemia.  The ischemic retina then produces VEGF (vascular endothelial growth factor) in response to this lack of oxygen – sounding familiar?  The VEGF causes neovascularization to proliferate.

Neovascular blood vessels are also very fragile.  They can break open and bleed at any time and without apparent cause.  The blood physically blocks light.  A little bit of blood may cause “floaters,” while substantial bleeding seems to fill the eye, severely affecting vision.

What is next?  My first job is to make sure that nothing else is causing the vitreous hemorrhage.  A tear in the retina can cause a similar picture.  If there is no hemorrhage, then I am more confident that the hemorrhage might be due to diabetic retinopathy.  Our choices at this point are; observation (aka do nothing) or perform a vitrectomy eye surgery.  Ultimately, any patient with proliferative diabetic retinopathy needs pan-retinal photocoagulation (laser treatment).  At the present state, blood physically blocks light, therefore, laser treatment is not possible.  We can either wait for the blood to absorb, and then perform laser surgery, or go ahead an perform a vitrectomy, remove the blood and perform laser all at once.  We operated.

What Does This Mean? In cases of vitreous hemorrhage due to diabetic retinopathy, the single most important therapeutic option is to perform PRP (pan-retinal photocoagulation).  This will indirectly stop the VEGF from being produced and the neovascular tissue will regress; that is, shrink up and go away.  Vision is stable, chance of blindness is halted.

VEGF is also implicated macular degeneration.  It is the same VEGF.  Avastin and other anti-VEGF drugs (Lucentis/Macugen) are also used to control proliferative diabetic retinopathy…at times.  I use it when the laser doesn’t seem to be working, but I expect more and more docs will use it the future.


Randall V. Wong, M.D.
Ophthalmologist, Retina Specialist
Fairfax,  Virginia

Reblog this post [with Zemanta]

VEGF Causes Blindness in Diabetes and Macular Degeneration

Vascular Endothelial Growth Factor is implicated in both diabetic retinopathy and wet macular degeneration.  Anti-VEGF medications, such as Macugen®, Lucentis® and Avastin® have changed the way we handle both diseases.

This week we’ll review VEGF and the three key anti-VEGF medications.

What is VEGF? Vascular Endothelial Growth Factor (VEGF) is a substance that is produced in the eye.  There are several forms of VEGF.  VEGF has three significant properties;

  1. Causes Inflammation
  2. Causes angiogenesis (creates new blood vessels)
  3. Causes vascular permeability (blood vessels leak)

VEGF in Diabetic Retinopathy causes diabetic macular edema and proliferative diabetic retinopathy (see illustration).  Proliferative diabetic retinopathy, by definition, is the proliferation of abnormal blood vessels on the surface of the retina and other internal structures of the eye, such as the iris. It can cause a vitreous hemorrhage.

Proliferative Diabetic Retinopathy
VEGF Causes Retinal Neovascularization

VEGF in Macular Degeneration causes the “wet” form of macular degeneration.  The “wet” form derives from the presence of “choroidal” neovascularization, or, abnormal blood vessels growing within the layers of the retina.

Wet Macular Degeneration
VEGF Causes Choroidal Neovascularization

VEGF Binds to Receptors to cause its effects on the blood vessels in the eye.  At the molecular level, the VEGF protein binds to a receptor the same way an electrical cord plugs into the wall.  You could say that the VEGF protein “plugs in” to the receptor.  Once activated, the receptor is then causes inflammation, angiogenesis and vascular leakage.

Blocking VEGF is possible using anti-VEGF agents such as Macugen, Lucentis and Avastin.  Once blocked, the receptor can no longer be activated and the effects on the blood vessels are reversed.  More specifically, once the VEGF pathway becomes blocked, macular edema may reverse, neovascularization of the retina may stop and, in macular degeneration, the choroidal/abnormal blood vessels may shrink, too.

Later this week, we’ll review each of the current anti-VEGF medications.


Randall V. Wong, M.D.

Ophthalmologist, Retina Specialist
Fairfax Virginia

Reblog this post [with Zemanta]

Tree Bark May Be Beneficial To Diabetics: Supplement or Drug?

“Ever Eat A Pine Tree?  Many Parts are Edible.”

That famous line by Euell Gibbons lives on.  Now, “researchers” have described that Pycnogenol®, an extract from the bark  of the French maritime pine tree, has the potential to improve vision in patients with diabetic retinopathy.  The tree is found  along the coast of southwest France.

In a small study involving 46 patients with early diabetic retinopathy, 24 patients were given Pycnogenol tablets daily and the remainder were given placebo (sugar pill).

After 2 months, patients taking Pycnogenol had statistically significant improvement in vision and decreased macular edema.  An increase in retinal blood flow was also noted.  (The standard treatment for diabetic macular edema is laser photocoagulation.)

The researchers think that Pycnogenol (Horphag Research) works by increasing blood flow to the retina that secondarily decreases the diabetic macular edema.  Pycnogenol is said to be an antioxidant, anti-inflammatory and aids in vascular dilation.

CAUTION: What Does This Really Mean?

Pycnogenol is not a drug.  It is a supplement.  There are big differences in the requirements needed to bring a supplement to market vs. a drug.

Pycnogenol is marketed in the United States as a dietary supplement.  As such, the manufacturers of dietary supplements do not have to provide safety and health information regarding their products as long as they do not claim the supplements can prevent, treat, or cure any specific disease.

On the other hand, drug manufacturers must submit health and safety data from carefully designed clinical trials to the FDA before marketing their products.

Lastly, supplements are not necessarily tested to find out if they interact with medicines, foods, or other herbs and supplements. Even so, such data is not necessarily available or provided.

Be careful out there!  There’s a lot of masquerading of supplements.  Be cautious.


Randall V. Wong, M.D.
Ophthalmologist, Retina Specialist
Fairfax, Virginia

Reblog this post [with Zemanta]

Retina Laser Treatment Saves Vision

There are two conditions where laser treatment is needed in patients with diabetic retinopathy:  macular edema and evidence of proliferative retinopathy.  In cases where macular edema, swelling of the retina in the macular area, is present, “focal” photocoagulation is needed.  In cases of proliferative diabetic retinopathy, “pan-retinal photocoagulation,” or PRP, is needed.

  • Focal Laser —> Diabetic Macular Edema
  • PRP  —> Proliferative Diabetic Retinopathy

Focal Laser and Diabetic Macular Edema

If you remember, this is the most common stage of diabetic retinopathy.  Almost every patient with diabetic retinopathy develops some leakage in the macula, potentially causing decreased vision.  The normal retinal blood vessels develop tiny little blebs along the blood vessel walls.  Theses outpouchings are called “microaneurysms.”  We know, and can prove, using fluorescein angiography, that these microaneurysms leak both blood and the clear, fluid part of blood.  “Focal” laser is presently the treatment of choice for diabetic macular edema.

"Focal" Laser Treatment to Treat Microaneurysms
"Focal" Laser Treatment to Treat Microaneurysms

A small lens is placed on the surface of the eye.  The laser does not hurt, is performed in the office and takes less than 10-15 minutes.  The idea is to treat the microaneurysms near the macula, but not the actual macula.  Treating the actual macula will cause permanent blind spots in your vision (not good).

It may take several months to determine if the laser was successful.  There is no care needed after the laser is performed.  It will most likely need to be repeated some day.

Treating the leaky microaneurysms is like weeding a garden, new areas will crop up.

Pan-Retinal Photocoagulation (PRP) is Used to Treat Proliferative Diabetic Retinopathy

Proliferative diabetic retinopathy, or PDR, affects about 10%  of patients with diabetic retinopathy and can lead to blindness.  Proliferative diabetic retinopathy develops when the retina becomes ischemic.  When a tissue is “ischemic,” it is not getting enough oxygen, usually from poor, or insufficient, blood flow.

Ischemia = Oxygen Demand Exceeds Supply

When the retina becomes ischemic, it releases a protein called Vascular Endothelial Growth Factor (VEGF).  The vascular endothelial growth factor (VEGF) causes abnormal blood vessels (neovascularization) to develop on the surface of the retina and on other parts of the inside of the eye such as the optic nerve and iris.

Blindness may develop from massive proliferation of the neovascularization (aka abnormal blood vessels) causing either retinal detachment or, a rare type of painful glaucoma (neovascular glaucoma – NOT the regular glaucoma).

Neovascularization, aka "Abnormal Blood Vessels"
Neovascularization, aka "Abnormal Blood Vessels"

In the illustration above, neovascularization has developed on the surface of the retina.  These abnormal blood vessels have also broken and bled causing a very small vitreous hemorrhage.  This blood may be seen as sudden floaters, or if large enough, may block most of the light from hitting the retina, causing significant loss of vision.

Remember the word ischemia? (Oxygen demand exceeds oxygen supply).

So far, ischemia has caused vascular endothelial growth factor (VEGF) to be liberated.  The VEGF has caused neovascularization to develop.

Stop the ischemia, Stop VEGF,  Stop the Proliferation

If we laser the peripheral retina, the portion of the retina away from the macula, we can stop the production of VEGF in most cases and arrest the proliferative phase of the diabetic retinopathy.

In effect, we are killing small portions of the peripheral retina with each laser pulse. Since we (scientists and other smart guys) are unable to increase oxygen supply, we must decrease demand.  The “ischemia” is over, VEGF production stops and the neovascularization goes away.  Disease process halted!

Pan Retinal Photocoagulation (PRP) Used to Treat Proliferative Diabetic Retinopathy
Pan Retinal Photocoagulation (PRP) Used to Treat Proliferative Diabetic Retinopathy

This procedure is also performed in the office.  It can be uncomfortable (actually it can hurt!) and I prefer to numb up the entire eye.  The procedure can take 30-45 minutes.  It make take several weeks to determine if enough laser is performed.  It is not uncommon for 1000 pulses or more to be required.

If performed timely, this potentially blinding phase of the disease can be halted!

Thanks for reading.


Enhanced by Zemanta

Laser Treatment Still The Best

Laser treatment for diabetic macular edema is still the preferred treatment for most patients with diabetic retinopathy.  Despite all the recent news about intraocular injections of anti-VEGF and steroid medications, the laser remains the mainstay.

The most common manifestation of diabetic retinopathy is the development of macular edema (also known as diabetic macular edema (DME) or clinically significant macular edema (CSME)).  Almost all patients who develop diabetic retinopathy develop some degree of swelling in the macula.  The normal retinal blood vessels begin to leak into the surrounding tissue.  It is not unlike a “soaker” hose for your lawn.  Of all the stages of diabetic retinopathy, this is the most common and does NOT lead to blindness.

The development of swelling, or edema, can decrease the central vision.  This is the most common way vision is lost.  The surgical goal is to arrest further swelling by treating the retina with laser photocoagulation.  The laser treatment is focused on areas of leakage called “microaneurysms” which are the actual incompetent areas in the normal retinal vessels.

Once treated, the macular swelling usually stays the same.  About 80% of the time, the macular edema, and vision stabilize!  My job is achieve status quo.  At times, especially when caught early, the vision improves as the swelling decreases.  Rarely, the laser doesn’t work.

Intraocular injections of Avastin® for macular edema or intraocular Kenalog® can be used for cases in which laser doesn’t work.  In the future, Ozurdex® or other intraocular sustained release delivery systems may be useful.

The laser used is usually a “hot” laser, that is, it works by transferring heat to the tissue.  The procedure is performed in the office setting, takes no longer than a regular office visit and is painless.  There is no post-operative care needed.

The result of the laser can take months to assess.  I usually will not see a patient back for another 4 monthas or so.


Randall V. Wong, M.D.

Ophthalmologist, Retina Specialist
Fairfax, Virginia

Reblog this post [with Zemanta]


Currently, I see patients with retinal diseases; macular degeneration, retinal detachment, macular holes, macular pucker within several different's a different arrangement, but it allows more continuous care with many eye specialists. In addition, I am very accessible via the web. To schedule your own appointment, call any of the numbers below.

Virginia Lasik | Office of Anh Nguyen, M.D.
Randall V. Wong, M.D.
Contact: Layla

A: 431 Park Avenue, Suite 103 • Falls Church, Virginia 22046
Ph: 703.534. 4393
View Map

Dressler Ophthalmology Associates, PLC
Randall V. Wong, M.D.
Contact: Ashley (Surgery/Web)
Chrissy Megargee (Web)

A: 3930 Pender Drive, Suite 10 • Fairfax, Virginia 22030
Ph: 703.273.2398
F: 703.273.0239
View Map