Focus on Glaucoma

Glaucoma isn’t to blame for high IOP

Too much energy, too many pulses from a Nd:YAG laser, used to remove floaters, are to blame.

By Doreen Fazio, MD

At the Valley Eye Center in the San Fernando Valley, seven ophthalmologists and three optometrists see thousands of patients each year. But one patient, a 50-year-old financial executive, presented with a problem that was a first for us all: secondary open angle glaucoma caused by excessive, cumulative Nd:YAG laser energy used in the treatment of vitreous floaters.

Heavy on the pedal

The patient had a history of LASEK in the right eye for -5.75 D of myopia; that surgery was performed in November 2006. An enhancement LASEK procedure was performed OD the following April for an overcorrection that resulted in 1.75 D of hyperopia. Pre-LASEK central corneal thickness (CCT) OD was 499, and was 395 post-LASEK. YAG laser for vitreous floaters OD was performed Sept. 7, 2009 with 876 pulses of 7.0 mJ average energy, and on Sept. 14 with 241 pulses of 5.6 mJ average energy. On Oct. 2, 2009 the surgeon administered another 244 YAG pulses of 2.0 mJ average energy.

The patient was referred to Valley Eye Center in June 2010 by his optometrist for management of elevated intraocular pressure (IOP) in the right eye, which was 35 mm Hg on timolol/brimonidine (Combigan, Allergan). Vision in the right eye was 20/25-20/30 and improved with wear of a rigid gas permeable contact lens. The optic nerve was healthy with a C/D ratio of 0.5 with intact rims without notch or hemorrhage. The VF and OCT of the optic nerve were normal.

Treatment change in order

An IOP of 35 mm Hg on timolol/brimonidine indicated that a change in treatment was needed. His prior LASEK surgery made his cornea thinner, which likely meant that the IOP in the right eye was higher than measured. I started him on bimatoprost (Lumigan, Allergan), believing that its mechanism of action, increasing aqueous outflow through both the uveoscleral and trabecular meshwork, would be more effective. The likely pathophysiology of the increased intraocular meshwork after YAG-laser vitreolysis is obstruction of the trabecular meshwork by liquid vitreous or vitreous fibrils, and shock wave damage to the trabecular meshwork. A drug that enhances aqueous outflow might be more effective in this situation.

While this was the first time we had seen secondary open angle glaucoma caused by excessive Nd:YAG laser energy used for the treatment of vitreous floaters, we had seen patients who had elevated IOP after a Nd:YAG capsulotomy was created with many pulses and high total energy.

A literature review revealed several articles regarding elevated IOP after YAG laser treatment. The consensus was that too much YAG laser energy could cause elevated eye pressure. In 1985, Richter et al. specified that if a surgeon uses above 200 mJ of total YAG laser energy, there is a risk of an IOP spike up to 40 mm Hg.¹ Steinert stated that shock wave damage to the trabecular meshwork from YAG laser energy as the cause of elevated IOP is supported clinically by the association between increased IOP and higher total laser energy. The decreased facility of outflow associated with the elevated IOP is due to capsular debris, acute inflammatory cells, liquid vitreous and shock wave damage to the trabecular meshwork from the YAG laser.²

A poll and a referral

Because this was a novel situation, I polled members of the American Glaucoma Society’s list serve. The consensus from the AGS respondents was to wait before performing any surgery, hoping that the IOP problem could be temporary and might resolve over time. I also referred the patient for a second opinion regarding management to Dr. Brian Francis of the Doheny Eye Institute in October 2010. IOP OD was 19 mm Hg. Dr. Francis felt that consideration could be given to SLT, and to Trabectome electrosurgical ablation of the trabecular meshwork, if needed.

Initially the patient responded well to the bimatoprost OD, with an IOP of 18 recorded on June 24, 2010; by July 14, the IOP had increased to 41 mm Hg. Timolol/brimonidine b.i.d. was added OD; the patient’s IOP dropped to 19 mm Hg on July 21. His IOP OD fluctuated on this medication regimen. I treated the temporal 180 degrees of the trabecular meshwork with selective laser trabeculoplasty (SLT) in November 2010, and the nasal 180 degrees in January 2011. His IOP OD was 16 mm Hg in April 2011, and 15 mm Hg on December 2011. On his last visit with Dr. Francis in April 2012, IOP was 11 mm Hg OD. When I last examined the patient in November 2013, the IOP was 15 mm Hg, with a full visual field, and a stable optic nerve with a cup of 0.55.

Start low

To prevent the complication of elevated IOP, it is imperative to minimize the number of YAG laser pulses and the total energy used, both for YAG laser treatment of vitreous floaters as well as for YAG posterior capsulotomy.

For YAG laser posterior capsulotomy, I start with low YAG energy of 1.0 mJ and gradually increase the power until there is successful opening of the capsule. I try to minimize the total energy as well as the number of spots, by opening the capsule from 12-6 o’clock and then adding a few pulses at 9 and 3 o’clock. This creates a well-centered capsulotomy of appropriate size, without causing elevated IOP in either the short or long term post-laser. OM

REFERENCES

About the Author
	Doreen Fazio, MD, is a board-certified comprehensive ophthalmologist who specializes in medical and surgical management of glaucoma. Dr. Fazio has worked at Valley Eye Center for 17 years, and is also an assistant clinical professor of ophthalmology at Harbor-UCLA Medical Center. Contact her at 818-787-2020. Disclosure: Dr. Fazio has no relevent financial disclosures.