Update on Imaging for Identification of Choroidal Melanoma

During a recent retinal consultation, I encountered a case in which the end result was the diagnosis of a large choroidal melanoma.  The past ocular history was reviewed and was significant for a “suspicious choroidal nevus” identified approximately 1.5 years ago by a local optometrist. Unfortunately, the patient did not return for follow-up to his optometrist until he had a recent change in vision. Currently, the medical workup and treatment decisions have yet to be made for this patient and the final outcome is pending. Keeping in mind that the 5 year survival rate of small choroidal melanoma versus large melanoma is 84% vs 47%, respectively. In cases like this, I often wonder what could have been done to identify this lesion as an early malignancy and how the outcome could have been altered if caught sooner.

The evaluation of suspicious pigmented choroidal lesions are a daily requirement in the life of a retinal specialist. This assessment includes the use of multiple diagnostic tools (or multimodal imaging) in conjunction with the clinical exam to determine the diagnosis or in some cases, provide a relative degree of malignant suspicion. Twenty years ago, we relied heavily upon clinical characteristics, supplemented by the diagnostic tools of BScan imaging and fluorescein angiography to make decisions. However, over the past two decades there have been significant advancements in diagnostic technologies which fortunately can be employed in assisting with the identification of choroidal melanoma.  These technologies can allow us to determine malignancies earlier and hopefully have an impact in the long term outcomes for these patients.

To quote Carol Shields, MD at Wills Eye Hospital in Philadelphia, the goal is to, “Find small ocular melanoma.”  Her collaborative work is paramount in the diagnosis and treatment of these tumors and she recently provided an update to her approach to identification.  She has upgraded her classic pneumonic to TFSOM-DIM.  This translates, To Find Small Ocular Melanoma, Do IMaging. This is a reminder to identify the following significant characteristics: Thickness greater than 2mm (BScan or OCT), subretinal Fluid (OCT), Symptoms, Orange pigment (fundus autofluorescence), Melanoma acoustic hollowness (BScan) and Imaging (fundus photos showing lesions greater than 5 mm in diameter and absence of drusen.) The real world application of implementing imaging technologies can greatly assist the eyecare provider in making the correct diagnosis. This can be illustrated when evaluating the case mentioned above in the following actual examples:

Figure 1: OCT demonstrating SRF and “shaggy photoreceptors” finding

Figure 2: OCT demonstrating SRF and hyperreflective deposits correlating to orange pigment

Figure 3: Fundus photo demonstrating lesion greater than 5mm in diameter, no drusen

Figure 4: Fundus autofluorescence demonstrating spotty fluorescence of orange pigment 

Figure 5: BScan demonstrating  acoustic hollowness, thickness greater than 2mm and RPE excavation

      Figure 1 Figure 2

Figure 3 

Figure 4 Figure 5

As delineated by the world’s experts, the early identification of ocular melanoma can be greatly assisted by imaging. In many of our clinical practices, we have several of these technologies that can be utilized to image suspicious choroidal lesions to recognize their potential for malignancy. Implementing these diagnostics in the care of these patients will allow eyecare providers to raise the bar in their ability to identify small ocular melanomas at earlier stages which should lead to better long term patient outcomes. 

Richard Lee, OD

Richard Lee, OD, FAAO

Specialty: Medical Eye Care

Seattle – Northgate
Renton

My topic of identifying choroidal melanoma stems from a desire to inform community colleagues of the updated algorithms to improve patient care. Early identification is critical when caring for these patients.

As a provider at NW Eye Surgeons, I enjoy caring for all patients with vitreoretinal disorders and collaborating with community providers. It is my passion to provide the best care available in the state of Washington to all patients who entrust us with their medical needs.

References

Eye cancer – statistics. Cancer.Net. (2020, February 14). Retrieved November 13, 2022, from https://www.cancer.net/cancer-types/eye-cancer/statistics#:~:text=The%205%2Dyear%20relative%20survival%20rate%20for%20people%20with%20small,large%20choroidal%20melanoma%20is%2047%25. Shields, C. L., Lally, S. E., Dalvin, L. A., Sagoo, M. S., Pellegrini, M., Kaliki, S., Gündüz, A. K., Furuta, M., Mruthyunjaya, P., Fung, A. T., Duker, J. S., Selig, S. M., Yaghy, A., Ferenczy, S. R., Eydelman, M. B., & Blumenkranz, M. S. (2021). White Paper on ophthalmic imaging for Choroidal Nevus Identification and transformation into melanoma. Translational Vision Science & Technology, 10(2), 24. https://doi.org/10.1167/tvst.10.2.24

Pediatric Blepharokeratoconjunctivitis

Pediatric Blepharokeratoconjunctivitis

Pediatric blepharokeratoconjunctivitis (BKC) winds up in my chair way more than I would have predicted when I left optometry school. Our clinic sees this so much, we even have a drop-down phrase in our electronic record system for diagnosis and plan that we can adjust. This condition is a chronic inflammatory disease stemming from lid margin inflammation leading to ocular surface disease. BKC comes with a wide array of symptoms and clinical signs. Pediatric BKC can lead to vision threatening complications if not treated promptly and properly.

Symptoms of BKC are varying in type and intensity. I have had BKC patients referred by pediatricians for chronic red eyes or decreased vision and referred by comanaging optometrists for difficult exams due to extreme photophobia. Patients or parents may note recurrent chalazia/styes, ocular irritation, chronic redness and tearing, blurry vision, chronic eye rubbing and extreme light sensitivity.

Clinical signs of BKC are often bilateral, though potentially asymmetric. Signs include anterior and/or posterior blepharitis, phlyctenular conjunctivitis, conjunctival hyperemia or chemosis, corneal neovascularization, punctate keratitis, pannus, edema, peripheral corneal thinning/scarring. I also routinely see concurrent lagophthalmos in my pediatric BKC patients.

Studies have noted more frequent and more severe corneal involvement for pediatric patients as opposed to adult BKC patients. In addition, pediatric patients that are diagnosed at an older age are more at risk for corneal involvement. Often, corneal thinning and scarring will start peripheral, but can spread centrally in severe or untreated cases. This can lead to decreased visual potential and/or irregular astigmatism.

Pediatric Blepharokeratoconjunctivitis corneal neovascularization

Figure 1: Example of corneal neovascularization with visually significant corneal scarring.

Corneal Topography of Pediatric Blepharokeratoconjunctivitis

Figure 2: Corneal topography of same patient in Figure 1. Although not a high-quality scan, irregular astigmatism induced due to corneal scarring is noted.

I often describe BKC as a cascading series of events that is triggered by lid disease. It is important that both patients and guardians understand the importance of proper lid hygiene and maintenance therapy ongoing. Treatment must be a combined approach of mechanical, lubricating, antibiotic, and anti-inflammatory techniques. Providers must be sure to stress the importance of lid hygiene and discuss techniques in depth. I will often provide samples of lid scrubs or sprays. Warm compresses are also essential. I highly recommend microwavable or electronic eye masks. Devices such as iLux and Lipiflow are great options, though often cost prohibitive. Severe cases may require systemic immunosuppression or even steroidal injections.

My goal is to get patients on a maintenance therapy approach of daily lid hygiene, daily warm compresses, artificial tears at least twice per day (nighttime gel or ointment with lagophthalmos) and Cyclosporine twice per day. I try to limit the extended use of steroids as much as possible. Some patients do require ongoing lose dose or gentle steroids and must be monitored for any development of a steroid response or cataract formation.

BKC requires ongoing monitoring and treatment. Patients will often grow out of pediatric BKC before adulthood, but not in every case. BKC can be a frustrating condition to manage, but seeing a pediatric patient finally have comfortable eyes and be able to see is always rewarding.

Lee Gongaware, OD

Specialty: Medical Eye Care

Mount Vernon
WES Bellingham

I decided to write about BKC due to the number of pediatric BKC patients that I see and how drastically this condition can change a child’s future visual potential when managed properly or not. I enjoy continuing to see a wide variety of medical optometry patients of all ages. At Northwest Eye Surgeons, I value working on a team of providers with unique specialties that can come together to treat patients.

Sources

American Academy of Ophthalmology. Blepharokeratoconjunctivitis (BKC) of Childhood. EyeWiki. March 2022. https://eyewiki.aao.org/Blepharokeratoconjunctivitis_(BKC)_of_Childhood

American Academy of Pediatrics. Pediatric Care Online. Tetracycline (Systemic). https://publications.aap.org/pediatriccare/drug-monograph/18/5383/Tetracycline-Systemic

Daniel, Moritz Claudius, et al. Challenges in the Management of Pediatric Blephrokeratoconjunctivitis / Ocular Rosacea. Expert Review of Ophthalmology, 11:4, 299-309. https://www.tandfonline.com/doi/full/10.1080/17469899.2016.1209408

Rodriguez-Garcia, A., et al. Blepharokeratoconjunctivitis in childhood: corneal involvement and visual outcome. Eye 30, 438-446. March 2016. https://www.nature.com/articles/eye2015249

Sabeti, Saama, et al. Management of meibomian gland dysfunction: a review. Elsevier: ScienceDirect. January 2019. https://www.nueyecal.com/files/teaching-schedule/article%202-1619577119.pdf

Successful Surgery Starts on the Surface

The importance of managing dry eye prior to cataract surgery

We’ve all had the patient with uncorrected 20/20 acuity after cataract surgery, yet they are still expressing “20/unhappy” frustration with their day-to-day vision. Often one of the most  unrecognized causes of patient dissatisfaction postoperatively is dry eye disease.1

According to the Prospective Health Assessment of Cataract Patients’ Ocular Surface (PHACO) study, more than 75 percent of patients presenting for cataract surgery had evidence of at least stage 2 dry eye (figure 1) yet nearly 60 percent had never complained of a foreign body sensation.2

Flourescein Corneal Staining in a patient with dry eye disease

Figure 1

Dry eye disease is an extremely common pre-existing condition in patients planning for cataract surgery and can have significant consequences on various aspects of cataract surgery. An irregular ocular surface affects preoperative planning reducing the repeatability of keratometry readings and diminishing the accuracy of intraocular lens calculations. Research shows that treating dry eye preoperatively results in better visual outcomes, speed of recovery and postoperative satisfaction.3

Treating dry eye disease can be challenging due to its multifactorial etiology and no single dry eye management formula will suit all patients. Although dry eye disease is traditionally classified as either aqueous deficient or evaporative, the TFOS DEWS II report estimated that 30-70 percent of patients with symptoms of ocular surface disease had a variable combination of these two categories (figure 2).4 The ultimate goal in treating dry eye and ocular surface disease prior to cataract surgery is to reduce inflammation and restore the homeostasis of the surface of the eye and tear film as quickly as possible.

Classification of Dry Eye

 Figure 2: Classification of dry eye3

For patients with meibomian gland dysfunction and blepharitis, hot compresses, lid hygiene and oral nutritional supplements such as flaxseed oil or fish oils are initiated in combination with a cyclosporin. In more severe cases, Doxycycline can be considered and if there is significant SPK and inflammation, liftegrast and a short course of loteprednol may be prescribed to get the corneal epithelium in the best possible shape before proceeding with surgery. Improvement is often seen 2 weeks after initiation of treatment, but 4 weeks of therapy prior to surgery is preferred. This allows for stable, reproducible imaging and biometry, which is especially important for a patient hoping for Cataract Surgery with Vision Correction.5

Now more than ever, with premium IOLs, we have the ability to optimize patients’ vision after cataract surgery. This ability relies on the health of the ocular surface both pre- and postoperatively. Dr. Eric Donnenfeld says, “One cannot perform premium cataract surgery using premium lenses without ensuring a premium ocular surface.”6

We all want our patients to have a great experience when it is time for cataract surgery. To meet or exceed patient’s expectations of high quality vision, clinicians must pay special attention to ocular surface health and treat dry eye disease preoperatively.

  • Gibbons A, Ali T, Waren D, Donaldson K. Causes and correction of dissatisfaction after implantation of presbyopia-correcting intraocular lenses. Clin Ophthalmol. 2016;10:1965–70.
  • Trattler W, Majmudar P, Donnenfeld E, et al. The prospective health assessment of cataract patient (PHACO) study: the effect of dry eye. Clin Ophthalmol. 2017;11:1423-30.
  • Chuang J, Shih KC, Chan T, Wan KH, Jhanji V, Tong L. Preoperative optimization of ocular surface disease before cataract surgery. J Cataract Refract Surg. 2017;43(12):1596-1607
  • Craig JP, Nichols KK, Akpek EK, et al. TFOS DEWS II definition and classification report. Ocul Surf. 2017;15(3):276-83.
  • Epitropoulos AT, Matossian C, Berdy GJ, Malhotra RP, Potvin R. Effect of tear osmolarity on repeatability of keratometry for cataract surgery planning. J Cataract Refract Surg. 2015 Aug;41(8):1672-7.
  • Donnenfeld, E. Lessons From the PHACO Study. com. Jan/Feb 2018.

Dr. Kerri SvandaAuthor: Kerri Svanda, OD

Specialty: Medical Eye Care

Seattle –Northgate

Working on the cornea, cataract and refractive team allows me to combine my passion for refractive surgery with treating patient’s medical conditions. I chose this topic because premium IOLs have transformed cataract surgery into refractive surgery with outcomes often rivaling SMILE and LASIK. In order to help my patients achieve and maintain their best vision, I have to help them achieve and maintain a healthy, hydrated ocular surface.

The Latest in Cataract Surgery Technology: Light Adjustable Lenses

 

Northwest Eye Surgeons and Whatcom Eye Surgeons have recently begun offering the latest in cataract surgery technology, the Light Adjustable Lens (LAL) from RxSight. LALs are made of a special photosensitive material that allows the surgeon to shift the shape, and therefore power, of the lens after cataract surgery, using a UV Light Delivering Device (LDD). Patients receive their initial treatment around 2-3 weeks after their 1 day and 1 week evaluations. The non-invasive LDD treatments take anywhere from about 45 seconds to 2 minutes depending on the amount of refractive error to be corrected. At least 3 treatments will be necessary to lock in the final post-refractive desired outcome. Immediately after surgery, the patient will need to wear the provided UV glasses during all waking hours, to prevent outside sources of UV from self-adjusting the lens. The refraction will set in about 48 hours after the first treatment. The patient can then “test drive” their vision, returning for a re-refraction and follow-up to see how they feel about their vision a week later. Once the desired target is reached, 2 “lock-in” treatments are needed at least one week apart to officially set the lens. After the final lock-in, the patient wears their UV glasses for 48 hours, then can discontinue wear.

safety sunglassesClear safety glasses
 
In my clinical observations thus far, around 4-5 total treatments appears to be the standard. Patients generally seemed to be so pleased with their vision after surgery, and report that wearing the provided UV protecting glasses does not seem to bother them much at all. Patients also seem to appreciate making the minor tweaks in the prescription, having the ability to go out in the world, and then return with feedback. It puts some of the care in the patient’s hands, which I believe makes them more comfortable making decisions about their surgical outcomes. Studies have shown that patient’s uncorrected vision has a 1.3% chance of being less than 20/32, as compared to 10.9% risk or more with other lenses.
 
cataract implant
According to Rx Sight, “The ability to treat 0.50 D of postoperative cylinder makes the RxSight LAL the only IOL in the United States approved to correct this level of vision-altering astigmatism. Astigmatism of as little as 0.50 D can reduce visual acuity by one line, and the impact on dynamic, functional visual acuity and low-contrast acuity is even greater.” Another great option is offering Extended Depth of Focus, or anywhere from -0.50 to -1.25 in the non-dominant eye that allows patients to function well for computer or near distances. Patients that I have treated thus far with EDOF have been very happy with their vision. The initial EDOF treatment must be performed at treatment #1 in the non-dominant eye; for example, if a patient changes their mind later and wants EDOF after the initial treatment, this unfortunately is not possible to do. This is one of the reasons it is important to thoroughly discuss post-operative vision goals with the patient before starting any LDD treatments.
7884b695-9c31-49ee-ba24-c800427305a8.png
The technology behind LAL’s is absolutely fascinating, and I believe it will be the way of the future for cataract surgery. Seeing patients experience improved sight and discuss the way it has changed their lives for the better is so very rewarding. 
 

Author: Lauren E. Bobick, OD, FAAO

Specialty: Medical Eye Care

Mount Vernon
Bellingham

I joined NWES in January 2022 in order to continue my focus on ocular disease and post-operative care. Working in a team format with our ophthalmologists and other optometrists is a great example of how the professions can not only coexist for the betterment of our patients, but thrive.

 

 

The Case of the Christmas Tree… Cataract

2022 arrived on a wave of headlines, and I’m sure we all await a year where COVID isn’t the number one news story. In the midst of our dark winter days, I know some who continue to cope by extending the “happy holiday season” well into the new year. I would like to revisit an interesting case that captures the holiday theme — I call it: The Case of the Christmas Tree… Cataract.

Meet MM. A 72 year old Caucasian female who presented with complaints of deteriorating vision over the past few years. She has the classic cataract complaints of difficulty reading, increased glare when driving, and eye strain (especially when not wearing her glasses). She is currently using Refresh artificial tears to manage her dry eye symptoms. She has a history of LASIK, dry eye syndrome, mild Fuch’s dystrophy, combined cataracts, extramacular drusen, and PVD. You can see her vision statistics, exam findings, and health history below:

 Current glasses RxVision
OD+0.25+0.50×103; ADD +2.5020/40-2
OS-1.25+0.75×136; ADD +2.5020/40

 Anterior segmentPosterior Segment
ODInspissated glands, mild conjchalasis, LASIK scar, 2+ guttata, 2+ NS with 2+ cortical opacitiesWell perfused ONH with C/D 0.45, drusen throughout arcades, PVD
OSInspissated glands, mild conjchalasis, LASIK scar, 2+ guttata, ?salzmann nodule 9:30, 2+ NS with 2+ cortical opacities and refractile opacity superocentralWell perfused ONH with C/D 0.35, drusen throughout arcades, PVD

Medical historyMedications
Arthritis
Migraines
Liver disease (as a child)
Blood clots
ASD (hx surgery)
Granulomatous polyangitis
GERD
Depleted hormones
Vitamin D3, B12
Aspirin 325mg
Azathioprine
Colchicine (anti-inflammatory drug)
Omeprazole
HRT/premarin

A Christmas Tree Cataract (CTC) is a rare lens change often described as polychromatic needle shaped crystals crisscrossing the deep cortex and nucleus of the lens. Due to the refractive, colorful nature of the cataract when observed, it often gives the appearance of colored lights on the branches of a Christmas tree. Most of the time, a CTC is visually non-disturbing and is often monitored until other forms of cataract worsen and cause visually symptomatic effects.

Several postulations exist to describe the formation of a CTC. It has been postulated that the cataract is made of cholesterol crystals and is the result of lens metabolism, that the cataract forms from diffraction of light from parallel sided stacks of fused cell membranes, that the cataract is formed from cysteine crystals and an age-related aberrant breakdown of crystalline induced by elevated calcium levels, or that an accelerated breakdown of membrane associated proteins and excess cysteine concentration leads to crystal growth.1

It is interesting to look at the connection between calcium levels and cataract formation. Hypercalcemia and increased intracellular calcium levels can change the organization of proteins within the membrane gap junctions and affect the ease with which substances can pass from one lens cell to the next. It has been shown that lenses with extremely high calcium concentrations form dense precipitates of calcium salts whereas lenses with moderate calcium concentrations undergo protein aggregation. The ability of calcium to induce cellular uncoupling may explain why many lens opacities involving higher calcium levels are highly localized.2 With this information about calcium and cataract formation combined with the postulations of why a CTC forms, it is plausible to say that any medical disease causing hypercalcemia can increase the risk of developing a Christmas Tree Cataract (as in the case of our patient MM above). Since hypercalcemia can occur in various granulomatous diseases, our patient MM may have developed her unilateral CTC from hypercalcemia in response to her condition of granulomatosis with polyangiitis.

Finally, it would be rude of me to talk about Christmas Tree Cataracts without mentioning myotonic dystrophy. As most of us remember from school, this type of cataract is often related to myotonic dystrophy and one study notes that myotonic dystrophy is found in 16% of CTC cases. With regards to myotonic dystrophy, a retrospective review of medical records of 23 patients with myotonic dystrophy type 1 (DM1) revealed the presence of CTC in 56% of cases and CTC was found to be unilateral in most cases with a few cases being asymmetrically bilateral. The average age of CTC diagnosis was 35-52 years of age and CTC was found to be the first sign of the disease in nearly half the cases.3 With this knowledge, detection of a Christmas Tree Cataract on routine exam should necessitate a referral for neuromuscular assessment, since nearly half of the patients with DM1 are asymptomatic and a CTC is the first sign of the disease.

I hope this case served as a little refresher for you all while brightening up your winter days with the beautiful glow of a Christmas Tree Cataract.

References:

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866154/
  2. https://www.researchgate.net/profile/William-Garner/publication/16627284_Non-Invasive_Techniques_in_the_Study_of_Cataract_Development_at_the_Metabolic_and_Protein_Molecular_Level/links/5bb0f32b299bf13e605854af/Non-Invasive-Techniques-in-the-Study-of-Cataract-Development-at-the-Metabolic-and-Protein-Molecular-Level.pdf#page=142
  3. https://www.nature.com/articles/s41433-018-0161-9

Author: Alana N. Curatola, OD 

Specialty: Medical Eye Care

Renton

A large part of why I enjoy working at NWES is the opportunity to work directly with our wonderful and amazingly talented surgeons. I enjoy the connections made with our referring community of optometrists and the team work it takes to help care for the eyes of our patients. I enjoy challenging cases that make me think outside the box or delve me into more research. 

 

Sustained Release Intravitreal Implants

Any doctor who treats patients with ocular inflammation knows the usefulness of corticosteroids to calm an inflamed eye. Should inflammation extend to the macula, vision loss follows and if not promptly treated can lead to permanent visual disability. While mild, uncomplicated macular edema can be managed with topical steroids, macular edema caused by posterior disease processes such as vascular occlusion, diabetic retinopathy or non-infectious posterior uveitis is best treated with intravitreal steroid. Intravitreal triamcinolone 40mg/mL (Triesence) has a long-demonstrated ability to treat posterior inflammation although its therapeutic effect may only last 2-3 months. 

Increasingly more common are sustained-release steroid intravitreal implants. The following article reviews current implants being used in the USA, their indications and important considerations in patients being treated with these novel therapies.

Ozurdex (dexamethasone intravitreal implant) 0.7ug is approved for diabetic macular edema, macular edema from vascular occlusion as well as non-infectious posterior uveitis. The implant is a cylindrical rod that slowly exudes medication treating macular edema over 4-6 months. Iluvien (fluocinolone acetonide intravitreal implant) 0.19mg has a similar shape and is also inserted in office with an inserting device. It is FDA approved to treat diabetic macular edema up to 3 years with 1 treatment. Yutiq (fluocinolone acetonide intravitreal implant) 0.18mg is very similar in appearance and design however its approval is only for chronic, non-infectious posterior uveitis. 

The last implant, Retisert (fluocinolone aceonide intravitreal implant) 0.59mg is also approved to provide treatment of chronic, non-infectious posterior uveitis over 30 months. Unlike the other aforementioned implants that are inserted using an injecting device and float freely in the vitreous body, Retisert is surgically implanted through an incision in the eyewall and is sutured behind the lens.

Figure 1: An Iluvien implant measuring 3.5mm x 0.37mm on the surface of the fingertip (left) and suspended in the posterior vitreous body (right).

In the case of chronic macular edema from diabetes or vein occlusion, our clinic has found use of these implants after the clinical failure of an anti-VEGF drug like Eyelea. Patients are generally enthused about the idea of fewer injections using longer acting implants like Iluvien, however, the potential side effects must be conveyed to patients beforehand.

Risks for endophthalmitis, migration of the implant into the anterior chamber and possible reactivation of herpetic disease must be discussed. All of the implants are expected to cause cataract formation in phakic patients. Increases in intraocular pressure are very common. The MEAD study that assessed the risk of IOP increases from dexamethasone implants found that around 25% of patients had a rise in ocular pressure <10mmHg, most of which were treatable with a single topical hypotensive1. Comparisons to large trials with fluocinolone delivery systems showed even greater increases in IOP; 34% of Iluvien patients saw an increase in IOP <10mmHg over the treatment period and 77% of Retisert patients were treated with IOP lowering medications2,3.

These trials revealed that most ocular hypertension was treated medically, however, 0.6% of Iluvien patients required incisional surgery to correct pressure, 1.2% of cases with repeated intravitreal triamcinolone (4mg), 4.8% of patients treated with Iluvien and 34-37% of patients treated with Retisert4.

Table 1: Comparison of Intravitreal Steroid Treatments 

DrugDuration of Action (months)Risk of IOP Increase 10mmg† or Need for IOP Lowering Medication*Risk of Incisional Glaucoma Surgery
Triesence (triamcinolone 4mg)†2-320-60%0.6%
Ozurdex (dexamethasone 0.7ug)†4-625%1.2%
Iluvien (fluocinolone 0.19mg)†Up to 3634%4.8%
Retisert (fluocinoline 0.59mg)*Over 3077%34-37%

In our clinic, we have found a use for steroid implants in a select group of chronically inflamed patients who have failed anti-VEGF drugs. We generally trial Triescene first to assess the patient’s intraocular pressure response before consideration of longer acting agents such as Iluvien. Many patients feel that if cataracts are inevitable and pressure can be controlled, they are accepting of an implant. It is always stressed that even after treatment, close monitoring is required.

 

References:

(1) Maturi, Raj K. MD; Pollack, Ayala MD; Uy, Harvey S. MD; Varano, Monica MD; Gomes, Andre M. V. MD; Li, Xiao-Yan MD; Cui, Harry MS; Lou, Jean MD; Hashad, Yehia MD; Whitcup, Scott M. MD for the Ozurdex MEAD Study Group INTRAOCULAR PRESSURE IN PATIENTS WITH DIABETIC MACULAR EDEMA TREATED WITH DEXAMETHASONE INTRAVITREAL IMPLANT IN THE 3-YEAR MEAD STUDY, Retina: June 2016 – Volume 36 – Issue 6 – p 1143-1152

(2) ILULIEN [Package Insert]. Alpharetta, GA: Alimera Sciences, Inc.; November 2016.

(3) RETISERT [Package Insert]. Rochester, NY: Bausch & Lomb Incorporated.; May 2019.

(4) Yonekawa, Y. & Wolfe, J; Dexamethasone Intravitreal Implant: Pharmacology and Clinical Update. Retina Today: September 2015


Author: Daniel T. Nolan, OD, FAAO

Specialty: Medical Eye Care

Mount Vernon & Bellingham

When treating patients suffering from chronic disease, chairside conversions generally involve new treatments available to help them. Working alongside Dr. Kristi Bailey in our medical retina service, I always look forward to educating patients and colleagues on new developments in retina. I am also grateful for the opportunity to help patients see better through co-managing with the greater optometric community.”

PCR ANALYSIS — NOT JUST FOR COVID TESTING

 

 Figure 1: Peripheral Corneal Ulcer

Figure 1: Peripheral Corneal Ulcer

One of the joys of living in the Pacific Northwest is the easy access to fresh water lakes, mountains, hiking and biking trails, and world class rock climbing.  However, with the beauty, thrills, and jealousy inducing social media posts, come eye injuries filled with dirt, grime, and microbes.  As a member of the cornea and refractive surgery team, a common appointment line on my schedule reads, “new patient, corneal ulcer referral.”  We all know the patient.  Maybe they’re a 25 year old mountain biker who sleeps in his contacts for days at a time, and thinks maybe he got some dirt in his eye over the weekend.  Perhaps they’re a 65 year old woman, who was swimming in Lake Washington with her grandchildren on a coveted sunny day.  We look behind the slit lamp, and we see a large, central infiltrate.

What we might not all feel comfortable with where to go from here.  While most ulcers will respond well to empirical treatment with frequent, broad spectrum antibiotics (and a little steroid), there does come a time when more concrete information is necessary in guiding our treatment.  In cases of vision threatening ulcers, corneal culturing becomes an essential tool in providing the best outcome for our patients.

Traditional culturing methods, involving swabbing the cornea to collect a specimen and streaking the sample onto nutrient agar plates, may seem cumbersome or impractical.  Eye care providers often shy away from culturing due to a lack of confidence in technique and the logistics of storing the proper materials. “Quick cultures,” with use of a sterile swab and included culturing broth, certainly have a lower barrier to entry, but with this ease may come less frequent positive results.

The answer to our woes may be polymerase chain reaction.  PCR is a rapid, highly sensitive method of identifying microbes by extracting and amplifying small samples of DNA. Over the last year and a half (and counting), we’ve all become familiar with the term in reference to viral respiratory cultures, but PCR has utility in ophthalmology as well.  Collecting a sample is similar to “quick culturing,” with a sterile swab placed in a provided medium, which is then sent to the lab for analysis.  Culturing kits are stored at room temperature, making it reasonable to have a few on hand in clinic.  Results come quickly, typically within 24 hours of being received by the lab, and just one swab can include bacterial, viral, and fungal cultures, plus susceptibilities.  This turn around time is particularly useful in cases of suspected fungal keratitis, where traditional culturing methods may take several weeks to yield final results.  Downsides to consider include only testing for a limited number of pathogens and potentially cost; but hey, nothing’s perfect!

Figure 3: Organisms Tested by HealthTrackRx

Through a combination of thoughtful empirical treatment, traditional culturing, and PCR analysis, we can all feel confident handling these scary, all too common, sight threatening conditions.  That way, we can get our patients out of our chairs, and back on the trails where they belong!

 

References:

  1. Robinson, Jessica. Et al. “Collecting a Corneal Culture.” Review of Optometry. April 15, 2016. www.reviewofoptometry.com/article/collecting-a-corneal-culture. Oct 13, 2021.
  2. Fairbanks, Aaron. Et al. “Culturing the Cornea.” org. University of Iowa Healthcare. Sept 26, 2016. webeye.ophth.uiowa.edu/eyeforum/tutorials/cornea-culture/index.htm. Oct 13, 2021.
  3. Kim, Elma. Et al. “Prospective Comparison of Microbial Culture and Polymerase Chain Reaction in the Diagnosis of Corneal Culture.” American Journal of Ophthalmology. Nov 2008, 146(5):714-23.
  4. HealthTrackRx PCR Testing, 2021. www.healthtrackrx.com/our-menus/. Oct 13, 2021.

Author: Stacey M. Keppol, OD, FAAO 

Specialty: Medical Eye Care

Seattle Northgate Clinic

Working on the cornea and refractive surgery team at NWES has exposed me to a plethora of interesting cases of microbial keratitis.  I chose to write about a lesser utilized, but effective tool in managing these patients.  Like many of the individuals we care for, I enjoy spending my time participating in outdoor sports and recreation, and relate to the desire to get back to activities quickly.  My goal is to help patients do that with efficient diagnosis and treatment of their conditions.

Healthy Aging Eyes

While no ocular fountain of youth exists and not all eye conditions are preventable, one of our most important roles as eye clinicians is helping the public maintain their vision and ocular health as they age. 

Unfortunately, there is still the idea among the public that if one has good vision, then they don’t need to have an eye exam. Many of us have experienced a patient who hasn’t had an eye exam for 5 plus years and who now has advancing eye disease. Imagine the impact if we could convince everyone to have full eye exams more consistently as this can help to detect conditions which can occur with no ocular symptoms like glaucoma or diabetic eye disease. We encourage patients to have regular eye exams not simply because it is a good practice, but more importantly because it is our hope that we can help maintain one of their most precious senses. 

Another component of the comprehensive eye examination which has gained some traction and will likely accelerate in the coming years is to obtain baseline imaging of the fundus including the optic nerve at least by young adulthood. This can help improve our ability to appropriately monitor the eye for changes like glaucoma. Considering the prevalence of Primary Open Angle Glaucoma increases significantly from age 40 to 80, it is helpful to have a reference point available for future comparison when such early changes become evident. Even if there is no pathology evident to be able to medically bill for baseline images, acquiring them is still helpful for the future care of the patient. 

glaucoma

glaucoma

 

 

(Fundus photos of a 20 year old with congenital glaucoma)

Beyond regular exams, most additional methods to promote healthy eyes are the same to maintain good systemic and mental health. Good cardiovascular health, including regular physical activity as well as maintaining good blood pressure and cholesterol levels helps not just improve ocular health but impacts wellness as a whole.

The same can be said about the benefits of good nutrition. Consuming foods rich in antioxidants, vitamins and minerals has been notably shown to help prevent advancing stages of macular degeneration and even dry eye. 

Utilizing proper sunwear is also helpful in promoting ocular health both of the external and internal anatomy of the eye. Some encourage patients to wear sunglasses when outside for more than 5-10 minutes. 

Let’s not forget to mention promoting protective eyewear to avoid accidental ocular injuries. Blunt force trauma can lead to serious long term consequences. Therefore, we should promote extra care with high speed machinery, airsoft and paintball guns, as well as bungee chords and exercise bands (just to name a few of the culprits of injuries we’ve seen over the years).

 Smoking cessation, or what’s more, avoiding starting smoking is also a concept that we as eye providers should help to champion. 

As we promote regular ocular examination, healthy lifestyles, nutrition, and proper eye protection we can help improve the quality of our patient’s lifelong vision and in turn the quality of their lives. 

Citations:

1) Grzybowski A, Och M, Kanclerz P, Leffler C, Gustavo De Moraes C. Primary Open Angle Glaucoma and Vascular Risk Factors: A Review of Population Based Studies from 1990 to 2019. J Clin Med 2020 Mar 11; 9(3):761. doi: 10.3390/jcm9030761.

2) Domalpally A, Agrón E, Pak JW, Keenan TD, Ferris FL 3rd, Clemons TE, Chew EY. Prevalence, Risk, and Genetic Association of Reticular Pseudodrusen in Age-related Macular Degeneration: Age-Related Eye Disease Study 2 Report 21. Ophthalmology. 2019 Dec;126(12):1659-1666. doi: 10.1016/j.ophtha.2019.07.022. Epub 2019 Jul 29. PMID: 31558345


Wright

 

Author: Justin Wright, OD

Specialty: Medical Eye Care

Mount Vernon & Bellingham

 

 

“I consider it a privilege to help care for patients and their eyes. As we, as an eye care community, promote proper ocular health we can improve the quality of patients’ vision and in turn the quality of their lives.”

Pediatric Disc Edema Overview

Finding disc edema on one of your patients presents clinical challenges on its own, but this is exacerbated even further when you have a pediatric patient to manage. Although pediatric disc edema is less common than in adults, every provider should have a well-established plan of action to address any possible cases that are in their chair. Disc edema can be due to both life and sight threatening conditions and must be handled swiftly.

Optic neuritis is inflammation of the optic nerve. This can be anterior (papillitis) or this can be posterior to the globe (retrobulbar). Papillitis is more common in pediatric patients. Pediatric optic neuritis is quite rare at about 10% of the adult rate. Typically presenting symptoms aid in the diagnosis of neuritis, but getting reliable symptom reports from a pediatric patient can be challenging. Common symptoms include decreased vision, pain with eye movement, changes in color vision or decrease in brightness. A relative afferent pupillary defect is often present as well if the case is unilateral. Pediatric optic neuritis tends to be more often bilateral with more severe visual decrease than adults. Post-infectious optic neuritis is more common than demyelinating causes for pediatric patients. Vaccinations have been rarely found to cause optic neuritis, with the diseases themselves coming with a higher risk of optic neuritis than the vaccines. Upon a literature review, there are no cases of the COVID vaccine causing optic neuritis to date. There are rare reports of COVID infected patients developing neuritis. 

Figure 1: Pediatric patient with OS optic neuritis, initial evaluation.

Figure 2: Same pediatric patient as figure 1 after IV and oral steroid treatment.

Papilledema is optic disc swelling due to elevated intracranial pressure. Causative factors are diverse, but can include life-threatening conditions such as compressive lesions, meningitis or subdural or subarachnoid hemorrhaging. Papilledema can present with a wide variety of symptoms. The patient may be asymptomatic or complain of headaches, dizziness, vomiting and nausea. Another symptom is pulsatile tinnitus or a rhythmic whooshing sound experienced by patients. The patient may report vision loss, diplopia, color changes or transient visual obscurations, but these visual symptoms tend to present later than in other disc edema cases. For pediatric patients with vomiting, nausea and/or headaches, the additional finding of papilledema has been found to strongly correlate with hydrocephalus due to a primary brain tumor.

Idiopathic intracranial hypertension or pseudotumor cerebri can also cause papilledema. In pre-pubescent patients, body mass is much less of a causative factor than in post-pubescent patients as is female gender. Renal disease, anemia, hormone imbalance, steroid treatment, medications, dural sinus thrombosis and more can cause idiopathic intracranial hypertension.

Figure 3: Unilateral disc edema with hemorrhaging and vascular changes.

Figure 4: RNFL of figure 3 patient demonstrating disc edema OD.

Pseudopapilledema is when the optic nerves falsely appear swollen due to varying factors such as disc drusen, tilted nerves, crowded or hypoplastic nerves. One review paper mentions that 75% of pediatric patients referred for papilledema were found to have pseudopapilledema.  

Anterior ischemic optic neuropathy (AION) is an ischemic infarction of the anterior optic nerve. AION is exceptionally rare in patients younger than 50. There are rare case reports in pediatric patients undergoing continuous peritoneal dialysis or undergoing major surgical procedures that have experienced non-arteritic anterior ischemic optic neuropathy due to chronic hypotension. Autosomal recessive polycystic kidney disease, hypotension or the lack of a kidney creates higher risks for dialysis induced AION in pediatrics.

Variable other factors can create disc edema including hereditary conditions (Leber’s hereditary optic neuropathy, dominant optic atrophy, recessive optic atrophy, x-linked optic atrophy), infectious conditions (tuberculosis, toxoplasmosis, cytomegalovirus, toxocariasis, Lyme disease), non-infectious (sarcoid, lupus), nutritional (vitamin B or folic acid deficiencies), toxic (ethambutol, lead, arsenic and many others) or ocular (pars planitis).

The list of differential diagnosis for disc edema is vast. Finding the causative factor is imperative. Life-threatening and sight-threatening conditions must be identified and proper treatment initiated as swiftly as possible. Neuroimaging is an important step. MRI of the brain and orbits with and without contrast is often recommended. MRV may also be indicated to assess venous anatomy. For papilledema, a lumbar puncture, after MRI results have been obtained, may be indicated to determine opening pressure and cerebrospinal fluid composition. Keep in mind that when ordering neuroimaging and lumbar puncture for pediatrics, it is not the same as ordering for your adult patients. Many radiology centers do not perform imaging on pediatric patients. Often, pediatric patients must have anesthesia in order to undergo these evaluations. Be sure to call your local radiology departments. Some will attempt imaging without anesthesia, but many will not. In Northwest Washington, our pediatric patients are typically sent to Seattle Children’s Hospital for neuroimaging and/or lumbar punctures. 

Remember to take time to be empathetic and compassionate towards your pediatric patient and their guardians. Finding disc edema in a young patient can be scary, especially considering the numerous differential diagnoses of varying severity. Take time to explain your findings and your plan. If you are not personally comfortable ordering further testing, send them to a pediatric specialist. Be sure to call ahead to either set-up a stat appointment or to alert the ER department at a children’s hospital what patient is on the way and why.

 

References:

Al-Kaabi, Abdullah, et al. Bilateral Anterior Ischaemic Optic Neuropathy in a Child on Continuous Peritoneal Dialysis. Sultan Qaboos University Medical Journal. November 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5135466/

Allen, Evan, et al. The Clinical and Radiological Evaluation of Primary Brain Tumors in Children, Part I: Clinical Evaluation. Journal of the National Medical Association, Vol 85, No 6. 1993. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2571872/pdf/jnma00281-0043.pdf

Dufek, Stephanie, et al. Anterior Ischemic Optic Neuropathy in Pediatric Peritoneal Dialysis: Risk Factors and Therapy. Pediatric Nephrology. 2014. https://pubmed.ncbi.nlm.nih.gov/24488506/

Gupta, Divakar, et al. Traumatic Optic Neuropathy. American Academy of Ophthalmology, EyeWiki. May 2021. https://eyewiki.aao.org/Traumatic_Optic_Neuropathy

Hobbs, Brianne and Osmotherly, Kaila. Long-term Follow-up of Suspected Vaccine-Induced Papillitis: A Teaching Case Report. Association of Schools and Colleges of Optometry. Vol 41, num 2, 2016. https://journal.opted.org/article/long-term-follow-up-of-suspected-vaccine-induced-papillitis-a-teaching-case-report/

Kaiser, Peter and Friedman, Neil. The Massachusetts Eye and Ear Infirmary: Illustrated Manual of Ophthalmology. Fourth Edition.  2014 Elesevier.

Kanonidou, Evgenia, et al. Unilateral Optic Disc Edema in a Paediatric Patient: Diagnostic Dilemmas and Management. Hindawi. December 2010. https://www.hindawi.com/journals/crim/2010/529081/

Mancha, Saoul, et al. With Disc Edemas, Act Fast. Review of Optometry. March 2020. https://www.reviewofoptometry.com/article/with-disc-edemas-act-fast

McCafferty, Brandon, et al. The Diagnostic Challenge of Evaluating Papilledema in the Pediatric Patient. Taiwan Journal of Ophthalmology. March 2017. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5525598/

McDowell, Paula and Williamson, Alexandra. Vaccines and Vulnerable Eyes: What to Look For. Review of Optometry. 15 March 2021. https://www.reviewofoptometry.com/article/vaccines-and-vulnerable-eyes-what-to-look-for

Peragallo, Jason. How to Manage Pediatric Optic Neuritis. Review of Ophthalmology. April 2018. https://www.reviewofophthalmology.com/article/how-to-manage-pediatric-optic-neuritis

Rigi, Mohammed, et al. Papilledema: Epidemiology, Etiology and Clinical Management. Dovepress Eye and Brain. August 2017. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5398730/

Ubhi, Pavanjeet, et al. Discern Optic Nerve Head Drusen from True Papilledema. Review of Optometry. December 2015. https://www.reviewofoptometry.com/article/discern-optic-nerve-head-drusen-from-true-papilledema

Weiner, Gabrielle. Case Studies of Disc Edema. American Academy of Ophthalmology. October 2015. https://www.aao.org/eyenet/article/case-studies-of-optic-disc-edema#Quick


Author: Leigh M. Gongaware, OD, MS 

Specialties: Medical Eye Care

 Mount Vernon & Bellingham 

Working with Dr. Ingrid Carlson and pediatric patients continues to be rewarding and fulfilling.  I enjoy asking kids about their hobbies and vacations, you hear about all kinds of things this way. I also enjoy letting kids take a look at someone’s eye in the slit lamp, they think it’s either great or super gross!

Thyroid Eye Disease – No More NO SPECS

 

Thyroid eye disease is an autoimmune condition affecting the ocular tissues. It occurs in up to 25% of patients with Graves’ disease. It is most common in patients who have hyperthyroidism (Graves’ disease), however, it can also occur under eurthyroid (10%) or autoimmune mediated hypothyroid conditions. Thyroid eye disease is more common in women, typically around 30 years old, but with another peak near 60 years of age. Men, older individuals, and smokers tend to develop more severe disease.

The most common course is triggered by the immune system recognizing the thyroid stimulating hormone receptor (TSHR) as an antigen. This triggers an inflammatory cascade mediated by T-cells and B-cells that results in fibroblast and adipocyte proliferation through activation of TSHR and connected insulin like growth factor (IGF-1) receptors. These receptors may also be upregulated in retro-orbital tissues of patients with thyroid eye disease. Hydrophilic glycosaminoglycans such as hyaluronic acid are produced and lead to swelling of soft tissues.

At the time of diagnosis approximately 20% of patients will have normal thyroid levels without any history of abnormal test results, 40% will have hyperthyroidism, and 20% will develop hyperthyroidism within 6 months of developing the ocular signs and symptoms. The rest develop ocular complications following treatment of hyperthyroidism. Hypothyroidism following treatment with radioactive iodine for hyperthyroidism is a risk factor for development of thyroid eye disease. 

 

Diagnosis of thyroid orbitopathy is made based on the presence of swelling of eyelids (image 2)  or conjunctiva, eye pain, eye pain with eye movement, presence of conjunctival injection or eyelid erythema, and inflammation of the plica or caruncle. If more than 3 of these findings are present, then there is active thyroid eye disease (see table 1). Severity grading is based on the amount of lid retraction, exophthalmos, soft tissue involvement, corneal involvement, diplopia, and optic nerve involvement (see table 2). Lid retraction (image 1) and lid lag (upper lids remain elevated on downgaze) may be signs of hyperthyroidism and may improve with normalization of thyroid hormone levels.

Table 1: Clinical Activity Score (CAS)

Initial exam: add up positive findings on items 1-7
1) Spontaneous orbital pain or pressure
2) Gaze evoked orbital pain or pressure
3) Eyelid edema-if considered to be secondary to active Graves’ orbitopathy
4) Eyelid erythema
5) Conjunctival injection – if considered to be secondary to active Graves’ orbitopathy
6) Chemosis
7) Inflammation of caruncle or plica
Follow-up exam (1-3 months): add up positive findings on items 8-10
8) Increase of >2mm proptosis
9) Decrease in ocular excursion in any direction of >8 degrees
10) Decrease in acuity equivalent to 1 Snellen Line
Active orbitopathy exists if score is >3/7 on initial exam or >4/10 on follow-up

 

Table 2: Severity Chart for Graves Orbitopathy

CharacteristicMildModerate to SevereSight Threatening
Eyelid retraction<2mm>/=2mm 
Exophthalmos

Norms by race & gender
Asian (Thai) F/M: 16/17
(18.6 Chinese)
Black F/M: 23/24
White F/M: 19/21
Norm is </= 2mm between eyes
<3mm from norm>/=3mm from norm 
Soft-tissue involvementMildModerate to severe 
DiplopiaNone to transientInconstant to constant 
Corneal involvementAbsent to mildModerate to severeSevere
Optic nerve involvementNoneNoneCompression

Symptoms of hyperthyroidism include rapid heart rate, heat intolerance, anxiety, excessive sweating, difficulty sleeping, and tremors. Patients may also exhibit other manifestations of Graves’ disease such as enlarged thyroid gland, pretibial myxedema (red, swollen skin of lower leg), or acropachy (swollen skin on hands and clubbing of fingers). If diagnosis is uncertain, or in the setting of unilateral or severe orbitopathy, consider CT or MRI orbits without contrast to evaluate for swelling of extraocular muscles and proptosis. Never use iodinated contrast as it may exacerbate hyperthyroidism or interfere with radioactive iodine therapy.

Labs to consider are: TSH, total T3 (triiodothyronine), free T4 (thyroxine), TRAb (Thyroid stimulating receptor antibodies: thyroid stimulating immunoglobulin (TSI) & TSH receptor binding inhibitory antibodies (TBII)), Tg (thyroglobulin), and TgAb (thyroglobulin antibodies), and TPOAb (thyroid peroxidase antibodies). Thyroglobulin and thyroid peroxidase antibodies can be found in those without thyroid disorders and in those with Hashimoto’s thyroiditis as well. In hyperthyroidism, TSH will be low, T3 and T4 will usually be high. Graves orbitopathy is more likely to occur in those with TRAb and TgAb. The course of the disease is likely to be more severe if the TSI is above 400. Approximately 5% of patients develop a severe course of the disease. Thyroid stimulating immunoglobulin will often elevate following radioactive iodine therapy. The levels peak approximately 4 months following therapy and may remain elevated for years. The clinical activity score (Table 1) is used to measure response to therapy.

Therapy consists of treatment to normalize thyroid levels. Methimazole, radioactive iodine, and/or thyroid surgery are used to reduce hyperthyroidism and levothyroxine is used to treat hypothyroidism. Levothyroxine should be used promptly following radioactive iodine therapy. Glucocorticoids should be used concurrently with radioactive iodine if the patient is at increased risk for orbitopathy. Methimazole is typically used for 1-2 years. Therapy also consists of methods to control symptoms such as a beta blocker to reduce rapid heart rate, shaking, nervousness, and anxiety; and corticosteroids are used to reduce swelling and inflammation.

The course of the eye disease is somewhat independent of treatment of thyroid hormone levels and is typically active for 1 to 3 years. Untreated hyperthyroidism can exacerbate orbitopathy but treated hyperthyroidism does not reduce the risk of orbitopathy. Moderate to severe orbitopathy is a contraindication to radioactive iodine therapy. Orbitopathy treatment is based on severity and activity. Counsel patients on the importance of smoking cessation to lessen risk of more severe orbitopathy. Use lubricating drops and anti-inflammatory drops to control dry eye. Consider sleep goggles if exposure is a concern. Sleep with the head of the bed elevated to minimize edema. Use eye pressure lowering drops to control ocular hypertension or glaucoma. Consider patching or prism glasses to minimize symptoms from diplopia.

Mild disease may improve with 100mcg Selenium twice daily by mouth, however, long term Selenium has been associated with a higher risk of type 2 diabetes. Moderate to severe disease in the active phase typically will respond to immunomodulating therapy. Prednisone or methylprednisolone are primary treatment options. Prednisone is used at 30mg/d for 4 weeks, then tapered to the lowest daily dose for maintenance of symptoms. Methylprednisolone is used for more severe orbitopathy, or if not responding to oral prednisone. It is dosed through IV at 500mg per week for 6 weeks, followed by 250mg weekly for the next 6 weeks. If severe optic nerve compression is present, the patient should be admitted to the hospital for 4g IV methylprednisolone and possible orbital decompression surgery. Teprotumumab is a newer treatment option for patients not responding to steroid therapy. It is administered by IV. The first two doses are given over 90 minutes but if tolerated well, the next 6 doses can be administered over 1 hour. It is dosed every 3 weeks for 8 doses. The first dose is 10mg/kg, the rest are 20mg/kg. Mycophenolate mofetil or tocilizumab may be other steroid sparing immunomodulatory therapies effective at reducing orbitopathy symptoms. Surgical intervention via orbital decompression or external orbital radiation may be necessary for sight threatening orbitopathy. Orbital decompression surgery is sometimes used for cosmesis once a patient has reached an inactive phase. Other surgeries to consider in the inactive phase are strabismus surgery to reduce diplopia and eyelid surgery to reduce eyelid retraction. Strabismus surgery should be performed after orbital decompression. 

Thyroid eye disease can cause serious limitations on a patient’s quality of life. As primary eye care providers, we may be the first to diagnose a patient with this condition and help get them the treatment that they need. Prompt diagnosis and treatment will help maintain vision and improve their quality of life.  

References:

Davies, T.F. (2021) Pathogens of Graves’. In J.E. Mulder (Ed). UpToDate. Retrieved on 07/20/21 from https://www.uptodate.com/contents/pathogenesis-of-graves-disease?search=graves&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2

Davies, T.F., Burch, H.B. (2021) Treatment of Graves’ orbitopathy (ophthalmopathy). In J.E. Mulder (Ed). UpToDate. Retrieved on 07/20/21 from https://www.uptodate.com/contents/treatment-of-graves-orbitopathy-ophthalmopathy?search=thyroid%20eye%20disease&source=search_result&selectedTitle=2~62&usage_type=default&display_rank=2

Ross, D.S. (2021) Graves’ hyperthyroidism in nonpregnant adults: Overview of treatment. In J.E. Mulder (Ed). UpToDate. Retrieved on 07/20/2021 from

https://www.uptodate.com/contents/graves-hyperthyroidism-in-nonpregnant-adults-overview-of-treatment?search=graves&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

Sathyadeepak, R. Thyroid Eye Disease: Its Causes and Diagnosis. Review of Ophthalmology. 2018 Nov 9. Retrieved 07/20/21 from https://www.reviewofophthalmology.com/article/thyroid-eye-disease-its-causes-and-diagnosis

Gupta, L, Prendes M.A., Douglas, R. (2021) Teprotumumab. In J. Giacometti (Ed). UpToDate/EyeWiki. Retrieved on 07/20/21 from https://eyewiki.aao.org/Teprotumumab

Ponto KA, Kanitz M, Olivo PD, Pitz S, Pfeiffer N, Kahaly GJ. Clinical relevance of thyroid-stimulating immunoglobulins in graves’ ophthalmopathy. Ophthalmology. 2011 Nov;118(11):2279-85. doi: 10.1016/j.ophtha.2011.03.030. PMID: 21684605.

Lytton SD, Ponto KA, Kanitz M, Matheis N, Kohn LD, Kahaly GJ. A novel thyroid stimulating immunoglobulin bioassay is a functional indicator of activity and severity of Graves’ orbitopathy. J Clin Endocrinol Metab. 2010 May;95(5):2123-31. doi: 10.1210/jc.2009-2470. Epub 2010 Mar 17. PMID: 20237164.


Author: Davina S. Kuhnline, OD

Specialties: Medical Eye Care 

Sequim 

 

 

 

I chose thyroid eye disease because it is a topic that I am interested in and wanted to find more information on and I thought it may be useful for others as well. I learned the NO SPECS classification in school and found the CAS table more useful. I enjoy working with you to help manage challenging and unusual cases. 

 

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