Balancing Treatment Challenges

The management of chronic, vision-threatening ocular diseases can be quite challenging and frustrating to both patient and physician, as their relentless nature demands a continuous re-evaluation of the clinical picture and available treatment options. This is especially true when one patient has multiple chronic medical conditions, such as the patient discussed in this article.

PERTINENT HISTORY AND TREATMENT PLAN

On February 21, 2022, an 85-year-old male presented to my practice due to variable vision with glasses and symptoms of irritation (ie, grittiness, dryness, redness, and burning, especially with drop installation). He had primary open-angle glaucoma (his father had a history of glaucoma), Fuchs endothelial corneal dystrophy, age-related macular degeneration (AMD), chronic cystoid macular edema in the right eye, and severe ocular surface disease, and had undergone several surgical procedures (MicroPulse laser therapy [Iridex] OD, penetrating corneal transplant for Fuchs endothelial corneal dystrophy OU, photorefractive keratectomy x 2 OS, cataract surgery OU, and YAG capsulotomy OU). The central challenge in this case was achieving a reasonable target pressure with tolerable topical medications in the setting of macular, corneal, and ocular surface disease.

After Kelman phacoemulsification with insertion of a posterior chamber lens OU, the patient had Nd:YAG laser capsulotomy OU, irregular astigmatism (I/A) after penetrating keratoplasty OU for Fuchs endothelial corneal dystrophy (Figure 1), and two photorefractive keratectomy (PRK) procedures OS and MicroPulse laser therapy OD. The measurements of the patient’s central corneal thickness were 587 µm OD and 396 µm OS. He had a noted intolerance to brimonidine, netarsudil, and latanoprost ophthalmic solution 0.02%/0.005% (Rocklatan, Alcon), and significant periorbitopathy on latanoprostene bunod ophthalmic solution 0.024% (Vyzulta, Bausch + Lomb), although the cosmesis did not bother him.

On clinical examination, I noted chronic corneal endothelial failure and corneal edema, mild entropion, aqueous deficiency and evaporative dry eye, eyelid laxity with entropion, floppy eyelid syndrome, and meibomian gland dysfunction. The patient also had blepharitis and ocular surface inflammation (hyperosmolarity, strong (+) InflammaDry [Quidel]) He also has a history of macular edema OD and dry AMD OU, although his retina specialist reported no indication for treatment by injections. Additionally, this patient has a history of macular microaneurysm OD and a history of IOP of 53 mm Hg OD after Nd:YAG laser capsulotomy.

MARCH 30 FOLLOW-UP VISIT

At the patient’s follow-up visit 5 weeks later, his VA was 20/100 and his IOP was 23 mm Hg OD. At this point, he had been following his prescribed treatment regimen (timolol every morning, latanoprost bunod ophthalmic solution 0.024% every night at bedtime, dorzolamide HCl ophthalmic solution 2% [Trusopt, Merck] twice daily, and prednisolone acetate ophthalmic suspension USP 1% [Pred Forte, Allergan/AbbVie] once daily, ongoing every day) at the last visit.

As far as his glaucoma was concerned, his right eye visual field was stable, yet with marginal pressure (Figures 2-4), but there was a split fixation visual defect in his left eye. Our goal, therefore, was to improve his vision with a possible repeat transplant, but we needed to avoid use of carbonic anhydrase inhibitors (CAIs), especially because he was a high-risk patient with previous graft failure. IOP of 23 mm Hg was still too high, despite having MicroPulse laser therapy and maximum tolerable drop use. CAIs can negatively affect transplant success (in some clinical studies they have caused corneal decompensation); this is something we should be thinking about in our more at-risk patient population with glaucoma requiring tube shunt and previous history of failed corneal transplant. At current pressure, if discontinued, the patient’s right eye would be outside the target range of upper teens or lower.

At this point, several questions occurred to me regarding how to approach disease management: Should we recommend repeat corneal transplant at this time to improve his vision and treat the edema, or does the patient need another glaucoma procedure to control his pressure? Or does he need both? Should he undergo repeat MicroPulse laser therapy, trabeculectomy, or a tube shunt?

The patient agreed with my recommendation to wait on performing a repeat corneal transplant until his IOP was controlled off CAIs, if possible. A glaucoma surgical procedure would likely be needed, with the aim of targeting range IOP in the teens off CAIs, as well as ongoing use of a daily steroid eye drop to prevent transplant rejection. However, the patient’s IOP was unlikely to drop to that range with repeat MicroPulse laser therapy, given the response to initial MicroPulse therapy.

After considering corneal surgical options with our corneal specialist, a tentative plan of repeat Descemet stripping endothelial keratoplasty (DSEK), inferior peripheral iridotomy, superficial keratectomy (SK), superior cautery punctal occlusion, Quickert entropion repair, and temporary tarsorrhaphy OD once IOP was well controlled was identified as the likely best surgical approach. In addition, I would want to have the patient use tacrolimus ointment 1 week postoperatively once the bandage contact lens that was placed after the SK is removed. I would also start this patient on tacrolimus 0.03% ointment once daily OD, beginning 1 week after surgery. I discussed indications and techniques with him, including off-label ophthalmic use, and advised him to use 0.03% tacrolimus in the eye, as it helps minimize the amount of steroid needed without raising IOP and helps prevent rejection of the transplant.

APRIL 12 FOLLOW-UP VISIT

At this visit, the patient’s VA was 20/150 OD, and his IOP was 25 mm Hg OD. His medications were timolol once daily in the morning, latanoprostene bunod ophthalmic solution 0.024% every night at bedtime, dorzolamide twice daily, and prednisolone every day.

At this time, the patient’s IOP was not optimized for DSEK. His corneal edema did not appear as significant as it was at his last visit, although he remained frustrated with his level of vision and wanted surgical intervention. We considered a tube shunt or trabeculectomy before DSEK for better reduction of his IOP. Of note, the patient was taking blood thinners because of a pacemaker/aortic valve replacement.

After considering surgical options with our glaucoma specialist, the patient agreed to proceed with implantation of the Ahmed Glaucoma Valve Model FP7 (AGV-FP7, New World Medical) with a scleral patch graft OD to address his significant ocular surface inflammation. He also acknowledged the possibility of requiring use of ongoing drops after surgery.

JUNE 16 FOLLOW-UP VISIT

At day 1 after implantation with the drainage device, the patient’s postoperative appearance and IOPs were good (VA was hand motion and IOP was 9 mm Hg OD). His medications at this visit included prednisolone every 2 hours OD and gatifloxacin ophthalmic solution 0.5% (Zymaxid, Allergan/AbbVie) four times daily OD. Given the patient’s much improved early response, repeat DSEK approximately 3 months post tube would be the plan, as long as the pressure remained stable.

SEPTEMBER 13 FOLLOW-UP VISIT

At day 1 after the patient’s DSEK procedure, he underwent repeat DSEK, inferior laser peripheral iridotomy, superficial keratectomy, superior cautery punctal occlusion, entropion repair with Quickert sutures, and temporary tarsorrhaphy. His vision was hand motion with the tarsorrhaphy in place and pressure was soft with palpation of the eye.

FEBRUARY 2023 FOLLOW-UP VISIT

The patient returned 5 months later and his VA was 20/200 OD. His IOP was 20 mm Hg OD, and he was taking only brimonidine and timolol at this time.

As expected, after the need for multiple surgical procedures and ongoing topical pressure lowering, this patient’s surface punctate epithelial keratitis was more diffuse with filaments. He was also noticing “fleeting moments” of improved vision, as the variability of his vision and immediate tear break-up was more pronounced (Figures 5-8).

I thought we could consider more comprehensive ocular surface treatment, and that he would benefit from autologous serum, platelet rich plasma, amniotic membrane extract drops, and in-office OSD treatment (microblepharoexfoliation, intense pulsed light therapy with meibomian gland expression, and meibomian gland probing to further improve the surface of his corneal surface and the quality and production of his tear film). We would need to balance this with the patient’s ability to keep up with such an onerous ocular regimen. An additional recommendation would be for the patient to consider a scleral lens, assuming the ocular surface inflammation was improved, to help treat the evaporative component. The scleral lens would complement the in-office OSD treatments mentioned above and would be in addition to improving his overall irregular astigmatism and rough surface and plan for corneal sensitivity testing on follow-up before putting in any drops during the workup that day.

CONSIDER THE COMPLETE PICTURE

There are many important lessons to be learned from this case. One key habit to keep front and center is to ensure comprehensive communication between all specialists involved. We have a thorough understanding of how polypharmacy and the need for multiple surgeries can affect the ocular surface; thus, it’s important to keep this in mind any time a patient with vision compromise from multiple diseases is frustrated with variable vision, so that appropriate treatments can help these patients.

An important factor highlighted in this case is the effect that pressure-lowering treatment can have on a corneal transplant in a patient who is high-risk and the need for ongoing use of a steroid eye drop on variable IOPs. So, the next time you are near the end of the line with your glaucoma treatments for a patient with a previous failed transplant and comorbid glaucoma requiring a tube shunt, keep in mind the added risk of corneal decompensation with CAIs.^1-3 Alternatives may be more appropriate as you continue to balance multiple comorbid diseases, and ongoing ocular surface treatment can help improve the quality of remaining vision.