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A Different Animal: Post-LASIK Dry Eye
Research is shedding light on the cause of this phenomenon and the best way to treat it.
Mark B. Abelson, MD,
Ryan Fillipon and George Ousler III
North Andover, Mass.
There has been much interest in dry-eye symptoms experienced by patients who have undergone LASIK. Though these side effects are generally transient and differ from chronic dry eye in several ways, they can be treated with many of the same methods. In this article, we’ll explain how this post-LASIK condition differs from true dry eye, and explore the best treatments for it.
A study of LASIK’s effects on tear film stability from the Chinese University of Hong Kong, patient reports of dry-eye symptoms were the initial focus.1 Researchers asked patients if they regularly felt burning, irritation, dryness or foreign body sensations. These questions were asked the day before the surgery as well as one day, one week and one month after surgery.
Prior to surgery, 15.6 percent of patients reported dry-eye symptoms. That number rose to 94.8 percent one day postop, dropping to 85.4 percent and 59.4 percent at one week and one month, respectively. In this same study of the first 30 postop days, researchers demonstrated a sharp decrease in average tear film break-up time that did not return to baseline by month’s end. A sharp, continuous decrease in basal tear secretion value, that also showed no signs of returning to baseline, was present for the first month. There was also a compensatory increase in Schirmer test values, followed by a dramatic and continual decrease.
Other studies have questioned different post-LASIK signs.
For example, a study from Madrid focused on decreased tear secretion after LASIK and attempted to find a correlation to a decrease in corneal sensitivity.2 After the controls were set, 24 bilateral LASIK patients were tested preoperatively, then at one week and one, three, six and nine months with a Cochet-Bonnet esthesiometer. This instrument allows the clinician to apply pressure to the cornea with minimal risk of damage. The device can alter the pressure within a wide range. A positive patient response occurred when the subject felt pressure. Researchers averaged the results.
There was nearly an 80-percent drop in sensitivity between the immediate postoperative values and those at one month. A decrease in corneal sensitivity is subsequently responsible for a decreased blink rate, allowing for greater periods of unprotected time for the surface of the eye after the tear film breaks. Exacerbated signs and symptoms follow. In the study, these values rose to 50 percent of baseline sensitivity at three months, 90 percent at six months, and slowly returned to baseline by the nine-month mark. The researchers considered a disruption of the fifth cranial nerve as a possible reason behind the decreased sensitivity.
What It All Means
Several studies have examined this trend. For example, the Chinese study focused on the signs of dry eye1 and made a case that the post-LASIK condition is actually chronic dry eye. However, since the follow-up period of the study ends after 30 days, there’s a lot of room to interpret the long-term effects of LASIK.
A research group from Australia extended the tested values out to a year, and used dry-eye therapy as well as patient reports of chronic dry eye as preoperative controls.3 Its findings showed a return to—or at least a trend toward—baseline values for the tests in patients who did not suffer from dry eye. Patients who had chronic dry eye before LASIK took a much longer time to return to their baseline values.
It’s important to note for this study that these symptoms don’t match the severity of chronic dry eye for long periods. If these symptoms can be expected
A proposed mechanism for LASIK-induced dry eye. A decreased blink rate exacerbates the signs and symptoms.
to return to baseline if the time frames of the studies are extended indicates that a different set of factors from those of chronic dry eye causes this phenomenon.
One study from the University of Minnesota demonstrates an unstable lipid
layer after LASIK; a normal layer should be present to prevent evaporation of the tear film. Another study from Spain confirms a decreased lipid layer volume after LASIK.4 This only tells part of the story, as the primary secretion agents of this layer, the meibomian glands and the glands of Zeiss and Moll, have some problems with reception and secretion. Secretion, however, is just part of what controls TFBUT and ocular sensitivity.
The evidence on reflex tearing is where the primary difference between LASIK and chronic dry-eye symptoms arises. In 2000, William Mathers, MD, of Oregon Health and Science University, described a feedback model between the cornea and lacrimal gland that helps to explain dry-eye symptoms.5 The symptoms and possible denervation found in Sjögren’s syndrome and the resultant lacrimal gland malfunctions provide an excellent example of Dr. Mathers’ explanation. The necessity of a strong blink reflex in healthy patients shows that a weakened reflex is most likely responsible for post-LASIK side effects, and that decreased corneal sensitivity is both an effect and an exacerbating cause of these symptoms.
Researchers have developed the Ocular Protection Index (OPI), a scale that illustrates the damage to which sufferers are subjected. If a blink occurs before TFBUT, then the eye has total protection. If blinks occur after TFBUT, though, then for that time period the eye is subject to dryness and irritation, exacerbating the symptoms that caused the decreased TFBUT. This cycle of damage can permanently affect the eye if the condition is left untreated.6
LASIK v. Other Conditions
• PRK and grafts. As stated before, the corneal sensitivity of patients drops severely after LASIK,2 but then slowly rebuilds. This process represents the regeneration of the trigeminal nerve, whose fibers end in the cornea. This fifth cranial nerve is responsible for corneal sensitivity and supplies branches to the ciliary body, iris, conjunctiva and lacrimal gland, part of the mucous membrane of the nasal cavity, and the skin of the eyelids, eyebrow, forehead and nose.
The structure of the corneal nerves themselves is at the root of the debate among supporters of different methods of surgery. The sub-epithelial nerve fibers follow a similar, though slower, centripetal regeneration pattern after LASIK to that which occurs after PRK. A 1996 study of PRK and LASIK from Marburg, Germany, shows patients experiencing similar postoperative symptoms.7 This is because the incision of LASIK creates a broad area of dissected nerve fibers when compared to other surgeries. Although the incision with corneal grafting is a full-thicknes cut, there is apparently less damage to the trigeminal fibers leading to a decreased incidence of dry-eye symptoms.
• Neurotrophic keratitis. This condition causes dry-eye signs and symptoms as a result of surgical or viral manipulation of the trigeminal ganglion or c-fibers that affects the blink rate. Given an existing viral condition, manipulation of the trigeminal ganglion will elicit an inflammatory response of the herpes simplex virus,8 which also results in ocular surface symptoms. Neurotrophic keratitis can be a useful model for understanding LASIK dry eye.
• Surgical manipulation of the trigeminal nerve and ganglion. Trigeminal neuralgia is a disorder characterized by severe facial pain within the distribution of the various divisions of the trigeminal nerve. The treatment for this, Trigeminal Nerve
The three major divisions of the trigeminal nerve and the trigeminal ganglion (with V1 ending in the cornea), which, when damaged, can have a severe impact on corneal sensitivity, blink rate, and subsequently the OPI (ocular protection index).
thermocoagulation, may cause corneal numbness, which leads to severe dry-eye symptoms in the same way that LASIK damages nerve endings and induces dry eye until regeneration.
Neurotrophic keratitis and corneal anesthesia have long been documented as side effects of surgical treatment of trigeminal neuralgia. The first division of the trigeminal nerve innervates the epithelium of the cornea, and a loss of this innervation leads to decreased corneal sensitivity.9 Poorly regulated ocular tissue results, with epithelial cell loss and a destabilized cornea.
In a 1985 study of rabbit corneal epithelial cultures, researchers analyzed the specificity and responsiveness of the epithelial cell release of neuronotrophic factor, concluding that neuronotrophic factor was released in abundance only from corneal and conjunctival epithelia.10 Nerve regeneration thus stems from healthy epithelial cells, and a successful blink reflex system maintains a healthy epithelium. Because of the importance of blinking, ablation of the trigeminal ganglion creates a vicious cycle that deprives the cornea of sensation and nutrients essential for an absence of irritation and dry-eye symptoms.
Denervation will eventually result in a decrease in acetylcholine, an important
chemical in the corneal epithelium. Weaker epithelial cells have fewer microvilli that can accept and process acetylcholine. Treatment with acetylcholine increases epithelial cell proliferation in vitro because a greater concentration of the chemical allows for even compromised cells to accept it.
• Stromal herpetic keratitis. Another notion that compares to post-LASIK symptoms is visible in patients with latent stromal herpetic keratitis in a Leiden University Study from 2001.11
Ocular problems are often symptoms of an actively infected herpes simplex virus, and this study concluded that patients with stromal herpetic keratitis do indeed have dry eyes. Researchers found that the main and accessory lacrimal glands aren’t affected, and so the “reflex arc” still maintains its components but doesn’t function well enough to keep eyes lubricated.
One possible cause may be a demylenation of the trigeminal nerve in the eye, which lends credibility to the corneal sensitivity theory for post-LASIK symptoms. Additionally, a patient who had Herpes Zoster Ophthalmicus in an Ochsner Clinic Ophthalmology Department case study demonstrated an induced neurotrophic keratitis with the virus.12 The weakened signal reflex and resultant keratitis caused by HZO is more evidence for this theory of post-LASIK dry eye.
Sensitivity and Structural Changes
In the studies that focused on corneal sensitivity after LASIK, sensitivity returned with the appearance of small nerve fiber bundles, followed by a more rapid regeneration process. The Madrid study found that corneal hypesthesia directly compromises the blink reflex, decreases tear secretion and delays healing.2 A weakened blink reflex associated with aging can be correlated to the results of studies in which dry-eye symptoms show prominence in elderly populations. Proper blinking is necessary for avoiding these symptoms.
Long-term ocular damage can be attributed to a rapid TFBUT, which, while failing to protect the eye from infection, coincides with decreased tear production depriving the surface of the eye of epidermal growth factor, vitamin A and other substances necessary for good ocular health. Decreased corneal sensitivity continues the cycle, depriving the eye of more blinks, which could have helped reestablish the tear film and wash away infectious agents.
Current treatments for chronic dry eye don’t show the potential to return sensitivity to baseline values. Presently, the chronic condition continues to deprive the eyes of a strong and effective blink reflex and tear film.
Additionally, goblet cell densities drop severely after LASIK, as shown in another study from Queensland University of Technology in Australia. With this decrease in goblet cell densities comes a decrease in the mucin layer, an essential protective feature of the tear film.
The Queensland study3 also showed that patients with chronic dry eye showed a greater deviation in goblet cell densities from baseline (which is already lower than normals) after LASIK than normals. This indicates a definite change in the ocular structure and the blink reflex postop that causes dry-eye symptoms in normals and worsens them in dry-eye sufferers. Patients in this study experienced a steeper drop in goblet cell density in both inferior and temporal sites and produced a weaker mucin layer. Goblet cells in the cornea also have a role in mucin production, and, when damaged, take time to regenerate. In normals, goblet cell density climbs faster after LASIK.
Suggested Treatments
Use of artificial tears can lengthen TFBUT and alleviate symptoms of discomfort and is the most prescribed treatment after LASIK.
Physicians should consider the best tear treatment for the patient’s lifestyle. Common suggestions include a regimen of four to six uses of tear substitutes daily, with additional doses for extreme discomfort. Patients should test any products in the safety of their homes before driving or undertaking visually taxing projects.
Currently, research from Moscow suggests that patients undergoing antioxidant therapy for two weeks after LASIK may protect their corneas from free radicals.13 because antioxidants are believed to increase tear stability,14 they may decrease post-LASIK dry-eye symptoms.
Potential Therapies
For patients with dry eye and post-LASIK complications, the limitation of visual tasks is a common treatment. Patients should limit prolonged computer use and avoid dry environments.
In the future, improved polymers may lead to tear substitutes that last longer without common side effects such as blurred vision and caking. Increased duration of action would extend TFBUT and make for more protective and stable OPI.
Further study is under way about the roles of synthesizing glycoproteins that are responsible for the retention of tear fluid on the ocular surface and mucus layer (MUC1 to MUC8). Goblet cells are destroyed in LASIK, and, subsequently, the mucin layer is destabilized after the procedure. With the ability to stimulate the production of new mucin, researchers are hopeful that fewer LASIK and dry-eye patients alike will have noticeable symptoms.
Other chemicals, such as secretagogues that assist in the production of the aqueous and mucin layers, as well as anti-evaporatives that increase the duration of action for tear substances, are being studied for use in potential therapies for dry eye.
Currently, researchers are devising therapies to stimulate tear production using naturally occurring chemicals such as lactoferrin. These chemicals better protect epithelial cells that can also undergo damage during LASIK. Enhancement of tear volume would greatly aid in reducing the symptoms of dry eye after LASIK and limit the amount of time the ocular surface is unprotected, especially in the immediate period after LASIK. Such studies may lead to agents with prolonged effects and greater concentrations of enzymes and proteins.
Although the Queensland study didn’t find a value in conventional preop treatment for LASIK patients to alleviate dry-eye symptoms,3 the preop use of flaxseed oil may help. Since two to four months of flaxseed oil can help with dry eye, it’s possible that intense preoperative (three months before surgery) and postoperative (for about a year, according to what we know about the course of post-LASIK dry eye) flaxseed therapy may reduce symptoms and alleviate pain.
With this greater understanding of postop LASIK dry-eye symptoms we may be able to more appropriately select and institute therapy.
Dr. Abelson, an associate clinical professor of ophthalmology at Harvard Medical School and senior clinical scientist at Schepens Eye Research Institute, consults in ophthalmic pharmaceuticals. Mr. Fillipon is a research associate and Mr. Ousler is senior manager of dry eye at Ophthalmic Research Associates in North Andover.
1. Yu E, et al. Effect of laser in situ keratomileusis on tear stability. Ophthalmology. 2000;107:12:2131.
2. Benitez-del-Castillo J, et al. Decrease in tear secretion and corneal sensitivity after laser in situ keratomileusis. Cornea 2001;20:1:30-2.
3. Albietz J, et al. Effect of laser in situ keratomileusis for hyperopia on tear film and ocular surface. Journal of Refractive Surgery 2002 Mar-Apr;18:2:113-23.
4. Patel S, et al. Corneal sensitivity and some properties of the tear film after laser in situ keratomileusis. Journal of Refractive Surgery 2002 Mar-Apr;18:2:113-23.
5. Mathers, W. Why the eye becomes dry: a cornea and lacrimal gland feedback model. CLAO Journal 2000 Jul;26:3:159-65.
6. Ousler GW, Emory TB, Welch DW, Abelson MB. Factors that influence the Inter-blink Interval (IBI) as measured by the Ocular Protection Index (OPI) (abstract) ARVO 2002.
7. Kauffmann T, et al. Corneal reinnervation after photorefractive keratectomy and laser in situ keratomileusis: an in vivo study with a confocal videomicroscope. German Journal Ophthalmology 1996;5:6:508-12.
8. Kriesel J, et al. Neuronal reactivation of herpes simplex virus may involve interleukin-6. Journal Neurovirology 1997;3:6:441-8.
9. Umlauf P. Neuroparalytic keratitis. Journal of the American Optometric Association 1990;61:
3:196-9.
10. Chan K, et al. Specificity of a neuronotrophic factor from rabbit corneal epithelial cultures. Experimental Eye Research 1985;41:6:687-99.
11. Keijser S, et al. Reflex and steady state tears in patients with latent stromal herpetic keratitis. Investigative Ophthalmology & Visual Science 2002 Jan;43(1):87-91.
12. Costello D, et al. Herpes zoster ophthalmicus: two presentations of the same disease. www.optcom3.com/sjp/cpstello.htm.
13. Smirennaia E, et al. Antioxidant activity of tear fluid and antioxidant therapy in myopic patients after laser in situ keratomileusis. Journal of Refractive Surgery 2002;18:3:S364-5.
14. Blades KJ, et al. Oral antioxidant therapy for marginal dry eye. European Journal of Clinical Nutrition 2001 Jul;55(7):589-97.
Vol. No: 9:08Issue: 8/15/02
This Month's Issue
Product Guide
Subscribe to Review of Ophthalmology
OUR AFFILIATES
Copyright© 2000 - 2008 Jobson Publishing L.L.C. unless otherwise noted.
All rights reserved. Reproduction in whole or in part without permission is prohibited.
A Different Animal: Post-LASIK Dry Eye
Research is shedding light on the cause of this phenomenon and the best way to treat it.
Mark B. Abelson, MD,
Ryan Fillipon and George Ousler III
North Andover, Mass.
There has been much interest in dry-eye symptoms experienced by patients who have undergone LASIK. Though these side effects are generally transient and differ from chronic dry eye in several ways, they can be treated with many of the same methods. In this article, we’ll explain how this post-LASIK condition differs from true dry eye, and explore the best treatments for it.
A study of LASIK’s effects on tear film stability from the Chinese University of Hong Kong, patient reports of dry-eye symptoms were the initial focus.1 Researchers asked patients if they regularly felt burning, irritation, dryness or foreign body sensations. These questions were asked the day before the surgery as well as one day, one week and one month after surgery.
Prior to surgery, 15.6 percent of patients reported dry-eye symptoms. That number rose to 94.8 percent one day postop, dropping to 85.4 percent and 59.4 percent at one week and one month, respectively. In this same study of the first 30 postop days, researchers demonstrated a sharp decrease in average tear film break-up time that did not return to baseline by month’s end. A sharp, continuous decrease in basal tear secretion value, that also showed no signs of returning to baseline, was present for the first month. There was also a compensatory increase in Schirmer test values, followed by a dramatic and continual decrease.
Other studies have questioned different post-LASIK signs.
For example, a study from Madrid focused on decreased tear secretion after LASIK and attempted to find a correlation to a decrease in corneal sensitivity.2 After the controls were set, 24 bilateral LASIK patients were tested preoperatively, then at one week and one, three, six and nine months with a Cochet-Bonnet esthesiometer. This instrument allows the clinician to apply pressure to the cornea with minimal risk of damage. The device can alter the pressure within a wide range. A positive patient response occurred when the subject felt pressure. Researchers averaged the results.
There was nearly an 80-percent drop in sensitivity between the immediate postoperative values and those at one month. A decrease in corneal sensitivity is subsequently responsible for a decreased blink rate, allowing for greater periods of unprotected time for the surface of the eye after the tear film breaks. Exacerbated signs and symptoms follow. In the study, these values rose to 50 percent of baseline sensitivity at three months, 90 percent at six months, and slowly returned to baseline by the nine-month mark. The researchers considered a disruption of the fifth cranial nerve as a possible reason behind the decreased sensitivity.
What It All Means
Several studies have examined this trend. For example, the Chinese study focused on the signs of dry eye1 and made a case that the post-LASIK condition is actually chronic dry eye. However, since the follow-up period of the study ends after 30 days, there’s a lot of room to interpret the long-term effects of LASIK.
A research group from Australia extended the tested values out to a year, and used dry-eye therapy as well as patient reports of chronic dry eye as preoperative controls.3 Its findings showed a return to—or at least a trend toward—baseline values for the tests in patients who did not suffer from dry eye. Patients who had chronic dry eye before LASIK took a much longer time to return to their baseline values.
It’s important to note for this study that these symptoms don’t match the severity of chronic dry eye for long periods. If these symptoms can be expected
A proposed mechanism for LASIK-induced dry eye. A decreased blink rate exacerbates the signs and symptoms.
to return to baseline if the time frames of the studies are extended indicates that a different set of factors from those of chronic dry eye causes this phenomenon.
One study from the University of Minnesota demonstrates an unstable lipid
layer after LASIK; a normal layer should be present to prevent evaporation of the tear film. Another study from Spain confirms a decreased lipid layer volume after LASIK.4 This only tells part of the story, as the primary secretion agents of this layer, the meibomian glands and the glands of Zeiss and Moll, have some problems with reception and secretion. Secretion, however, is just part of what controls TFBUT and ocular sensitivity.
The evidence on reflex tearing is where the primary difference between LASIK and chronic dry-eye symptoms arises. In 2000, William Mathers, MD, of Oregon Health and Science University, described a feedback model between the cornea and lacrimal gland that helps to explain dry-eye symptoms.5 The symptoms and possible denervation found in Sjögren’s syndrome and the resultant lacrimal gland malfunctions provide an excellent example of Dr. Mathers’ explanation. The necessity of a strong blink reflex in healthy patients shows that a weakened reflex is most likely responsible for post-LASIK side effects, and that decreased corneal sensitivity is both an effect and an exacerbating cause of these symptoms.
Researchers have developed the Ocular Protection Index (OPI), a scale that illustrates the damage to which sufferers are subjected. If a blink occurs before TFBUT, then the eye has total protection. If blinks occur after TFBUT, though, then for that time period the eye is subject to dryness and irritation, exacerbating the symptoms that caused the decreased TFBUT. This cycle of damage can permanently affect the eye if the condition is left untreated.6
LASIK v. Other Conditions
• PRK and grafts. As stated before, the corneal sensitivity of patients drops severely after LASIK,2 but then slowly rebuilds. This process represents the regeneration of the trigeminal nerve, whose fibers end in the cornea. This fifth cranial nerve is responsible for corneal sensitivity and supplies branches to the ciliary body, iris, conjunctiva and lacrimal gland, part of the mucous membrane of the nasal cavity, and the skin of the eyelids, eyebrow, forehead and nose.
The structure of the corneal nerves themselves is at the root of the debate among supporters of different methods of surgery. The sub-epithelial nerve fibers follow a similar, though slower, centripetal regeneration pattern after LASIK to that which occurs after PRK. A 1996 study of PRK and LASIK from Marburg, Germany, shows patients experiencing similar postoperative symptoms.7 This is because the incision of LASIK creates a broad area of dissected nerve fibers when compared to other surgeries. Although the incision with corneal grafting is a full-thicknes cut, there is apparently less damage to the trigeminal fibers leading to a decreased incidence of dry-eye symptoms.
• Neurotrophic keratitis. This condition causes dry-eye signs and symptoms as a result of surgical or viral manipulation of the trigeminal ganglion or c-fibers that affects the blink rate. Given an existing viral condition, manipulation of the trigeminal ganglion will elicit an inflammatory response of the herpes simplex virus,8 which also results in ocular surface symptoms. Neurotrophic keratitis can be a useful model for understanding LASIK dry eye.
• Surgical manipulation of the trigeminal nerve and ganglion. Trigeminal neuralgia is a disorder characterized by severe facial pain within the distribution of the various divisions of the trigeminal nerve. The treatment for this, Trigeminal Nerve
The three major divisions of the trigeminal nerve and the trigeminal ganglion (with V1 ending in the cornea), which, when damaged, can have a severe impact on corneal sensitivity, blink rate, and subsequently the OPI (ocular protection index).
thermocoagulation, may cause corneal numbness, which leads to severe dry-eye symptoms in the same way that LASIK damages nerve endings and induces dry eye until regeneration.
Neurotrophic keratitis and corneal anesthesia have long been documented as side effects of surgical treatment of trigeminal neuralgia. The first division of the trigeminal nerve innervates the epithelium of the cornea, and a loss of this innervation leads to decreased corneal sensitivity.9 Poorly regulated ocular tissue results, with epithelial cell loss and a destabilized cornea.
In a 1985 study of rabbit corneal epithelial cultures, researchers analyzed the specificity and responsiveness of the epithelial cell release of neuronotrophic factor, concluding that neuronotrophic factor was released in abundance only from corneal and conjunctival epithelia.10 Nerve regeneration thus stems from healthy epithelial cells, and a successful blink reflex system maintains a healthy epithelium. Because of the importance of blinking, ablation of the trigeminal ganglion creates a vicious cycle that deprives the cornea of sensation and nutrients essential for an absence of irritation and dry-eye symptoms.
Denervation will eventually result in a decrease in acetylcholine, an important
chemical in the corneal epithelium. Weaker epithelial cells have fewer microvilli that can accept and process acetylcholine. Treatment with acetylcholine increases epithelial cell proliferation in vitro because a greater concentration of the chemical allows for even compromised cells to accept it.
• Stromal herpetic keratitis. Another notion that compares to post-LASIK symptoms is visible in patients with latent stromal herpetic keratitis in a Leiden University Study from 2001.11
Ocular problems are often symptoms of an actively infected herpes simplex virus, and this study concluded that patients with stromal herpetic keratitis do indeed have dry eyes. Researchers found that the main and accessory lacrimal glands aren’t affected, and so the “reflex arc” still maintains its components but doesn’t function well enough to keep eyes lubricated.
One possible cause may be a demylenation of the trigeminal nerve in the eye, which lends credibility to the corneal sensitivity theory for post-LASIK symptoms. Additionally, a patient who had Herpes Zoster Ophthalmicus in an Ochsner Clinic Ophthalmology Department case study demonstrated an induced neurotrophic keratitis with the virus.12 The weakened signal reflex and resultant keratitis caused by HZO is more evidence for this theory of post-LASIK dry eye.
Sensitivity and Structural Changes
In the studies that focused on corneal sensitivity after LASIK, sensitivity returned with the appearance of small nerve fiber bundles, followed by a more rapid regeneration process. The Madrid study found that corneal hypesthesia directly compromises the blink reflex, decreases tear secretion and delays healing.2 A weakened blink reflex associated with aging can be correlated to the results of studies in which dry-eye symptoms show prominence in elderly populations. Proper blinking is necessary for avoiding these symptoms.
Long-term ocular damage can be attributed to a rapid TFBUT, which, while failing to protect the eye from infection, coincides with decreased tear production depriving the surface of the eye of epidermal growth factor, vitamin A and other substances necessary for good ocular health. Decreased corneal sensitivity continues the cycle, depriving the eye of more blinks, which could have helped reestablish the tear film and wash away infectious agents.
Current treatments for chronic dry eye don’t show the potential to return sensitivity to baseline values. Presently, the chronic condition continues to deprive the eyes of a strong and effective blink reflex and tear film.
Additionally, goblet cell densities drop severely after LASIK, as shown in another study from Queensland University of Technology in Australia. With this decrease in goblet cell densities comes a decrease in the mucin layer, an essential protective feature of the tear film.
The Queensland study3 also showed that patients with chronic dry eye showed a greater deviation in goblet cell densities from baseline (which is already lower than normals) after LASIK than normals. This indicates a definite change in the ocular structure and the blink reflex postop that causes dry-eye symptoms in normals and worsens them in dry-eye sufferers. Patients in this study experienced a steeper drop in goblet cell density in both inferior and temporal sites and produced a weaker mucin layer. Goblet cells in the cornea also have a role in mucin production, and, when damaged, take time to regenerate. In normals, goblet cell density climbs faster after LASIK.
Suggested Treatments
Use of artificial tears can lengthen TFBUT and alleviate symptoms of discomfort and is the most prescribed treatment after LASIK.
Physicians should consider the best tear treatment for the patient’s lifestyle. Common suggestions include a regimen of four to six uses of tear substitutes daily, with additional doses for extreme discomfort. Patients should test any products in the safety of their homes before driving or undertaking visually taxing projects.
Currently, research from Moscow suggests that patients undergoing antioxidant therapy for two weeks after LASIK may protect their corneas from free radicals.13 because antioxidants are believed to increase tear stability,14 they may decrease post-LASIK dry-eye symptoms.
Potential Therapies
For patients with dry eye and post-LASIK complications, the limitation of visual tasks is a common treatment. Patients should limit prolonged computer use and avoid dry environments.
In the future, improved polymers may lead to tear substitutes that last longer without common side effects such as blurred vision and caking. Increased duration of action would extend TFBUT and make for more protective and stable OPI.
Further study is under way about the roles of synthesizing glycoproteins that are responsible for the retention of tear fluid on the ocular surface and mucus layer (MUC1 to MUC8). Goblet cells are destroyed in LASIK, and, subsequently, the mucin layer is destabilized after the procedure. With the ability to stimulate the production of new mucin, researchers are hopeful that fewer LASIK and dry-eye patients alike will have noticeable symptoms.
Other chemicals, such as secretagogues that assist in the production of the aqueous and mucin layers, as well as anti-evaporatives that increase the duration of action for tear substances, are being studied for use in potential therapies for dry eye.
Currently, researchers are devising therapies to stimulate tear production using naturally occurring chemicals such as lactoferrin. These chemicals better protect epithelial cells that can also undergo damage during LASIK. Enhancement of tear volume would greatly aid in reducing the symptoms of dry eye after LASIK and limit the amount of time the ocular surface is unprotected, especially in the immediate period after LASIK. Such studies may lead to agents with prolonged effects and greater concentrations of enzymes and proteins.
Although the Queensland study didn’t find a value in conventional preop treatment for LASIK patients to alleviate dry-eye symptoms,3 the preop use of flaxseed oil may help. Since two to four months of flaxseed oil can help with dry eye, it’s possible that intense preoperative (three months before surgery) and postoperative (for about a year, according to what we know about the course of post-LASIK dry eye) flaxseed therapy may reduce symptoms and alleviate pain.
With this greater understanding of postop LASIK dry-eye symptoms we may be able to more appropriately select and institute therapy.
Dr. Abelson, an associate clinical professor of ophthalmology at Harvard Medical School and senior clinical scientist at Schepens Eye Research Institute, consults in ophthalmic pharmaceuticals. Mr. Fillipon is a research associate and Mr. Ousler is senior manager of dry eye at Ophthalmic Research Associates in North Andover.
1. Yu E, et al. Effect of laser in situ keratomileusis on tear stability. Ophthalmology. 2000;107:12:2131.
2. Benitez-del-Castillo J, et al. Decrease in tear secretion and corneal sensitivity after laser in situ keratomileusis. Cornea 2001;20:1:30-2.
3. Albietz J, et al. Effect of laser in situ keratomileusis for hyperopia on tear film and ocular surface. Journal of Refractive Surgery 2002 Mar-Apr;18:2:113-23.
4. Patel S, et al. Corneal sensitivity and some properties of the tear film after laser in situ keratomileusis. Journal of Refractive Surgery 2002 Mar-Apr;18:2:113-23.
5. Mathers, W. Why the eye becomes dry: a cornea and lacrimal gland feedback model. CLAO Journal 2000 Jul;26:3:159-65.
6. Ousler GW, Emory TB, Welch DW, Abelson MB. Factors that influence the Inter-blink Interval (IBI) as measured by the Ocular Protection Index (OPI) (abstract) ARVO 2002.
7. Kauffmann T, et al. Corneal reinnervation after photorefractive keratectomy and laser in situ keratomileusis: an in vivo study with a confocal videomicroscope. German Journal Ophthalmology 1996;5:6:508-12.
8. Kriesel J, et al. Neuronal reactivation of herpes simplex virus may involve interleukin-6. Journal Neurovirology 1997;3:6:441-8.
9. Umlauf P. Neuroparalytic keratitis. Journal of the American Optometric Association 1990;61:
3:196-9.
10. Chan K, et al. Specificity of a neuronotrophic factor from rabbit corneal epithelial cultures. Experimental Eye Research 1985;41:6:687-99.
11. Keijser S, et al. Reflex and steady state tears in patients with latent stromal herpetic keratitis. Investigative Ophthalmology & Visual Science 2002 Jan;43(1):87-91.
12. Costello D, et al. Herpes zoster ophthalmicus: two presentations of the same disease. www.optcom3.com/sjp/cpstello.htm.
13. Smirennaia E, et al. Antioxidant activity of tear fluid and antioxidant therapy in myopic patients after laser in situ keratomileusis. Journal of Refractive Surgery 2002;18:3:S364-5.
14. Blades KJ, et al. Oral antioxidant therapy for marginal dry eye. European Journal of Clinical Nutrition 2001 Jul;55(7):589-97.
Vol. No: 9:08Issue: 8/15/02
This Month's Issue
Product Guide
Subscribe to Review of Ophthalmology
OUR AFFILIATES
Copyright© 2000 - 2008 Jobson Publishing L.L.C. unless otherwise noted.
All rights reserved. Reproduction in whole or in part without permission is prohibited.
ok so no miracle here --- I asked for just 1 day without pain and just 1 day is what I got. Wow, I should've known better than to get my hopes up. My 6 month follow up is tomorrow. I'm ready, I don't think my doctor is though.
Lucy
Comment