Clinician's Corner

Mark Schaeffer, OD

Clinical Excellence Captain at MyEyeDr, Birmingham, AL

Patients who have keratoconus have an increased risk for ocular surface disease (OSD). In a recent study, patients with severe and mild keratoconus had statistically significant lower tear break-up times and Schirmer’s test scores. Patients also self-reported higher Ocular Surface Disease Index (OSDI) scores, which pointed to more symptoms. Impression cytology showed goblet cell loss, which translated to worsening ocular surface disease.¹ This group tends to get overlooked regarding ocular surface issues because their keratoconus typically requires more visually impactful concerns to take precedence in treatment.

While contact lens wear improves vision and is a viable treatment for keratoconus, it can still lead to OSD symptoms. For example, one study showed that 90% of participants had OSDI scores over 33 and “reported symptoms indicative of dry eye disease.”² The good news is that scleral contact lenses can improve these symptoms in patients.³ The same study noted that OSDI scores and symptoms decreased after only one month of wear.

Using heat to treat patients with meibomian gland dysfunction (MGD) and keratoconus can create a possible conundrum: will the heat worsen or even induce the disease? One such case report described a young patient who treated MGD with hot compresses and inadvertently induced keratoconus. However, the heat itself was not the culprit of the keratoconus. Rather, the heat caused the patient to rub their eyes excessively, which led to the keratoconus.⁴

It is important to manage the signs and symptoms of ocular surface disease with keratoconus patients because they need a comprehensive solution to their visual and ocular needs. Utilizing all available therapies to address the increased inflammation, decreased tear break-up time and goblet cell loss is paramount. If you choose heat and expression treatment for MGD, be sure to monitor carefully and screen for mechanical rubbing to reduce the risk for disease worsening.

Research Update,
Commentary on Abstract of the Week

Blair Lonsberry, MS, OD, MEd, FAAO

Diplomate, American Board of Optometry

Keratoconus (KC) is a corneal disease characterized by alterations in the structure and organization of the cornea, leading to progressive thinning and ectasia of the central and paracentral cornea. These alterations in corneal structure result in significant changes in myopia and astigmatism. Genetic and environmental factors are involved in the development and progression of KC.^1-2 Traditionally, KC has been thought of as a non-inflammatory condition.³ However, recent evidence has shown that patients with KC have increased pro-inflammatory mediators linked to increased dry eye disease (DED) and rigid contact lens wear. These pro-inflammatory mediators are thought to increase the progression of KC by stimulating eye rubbing.⁴ Blepharitis has also been found to be more prevalent in patients with KC.⁵

Evaluating dry eye parameters in KC patients reveals low tear break-up time (TBUT) and marked corneal staining, increased Ocular Surface Disease Index (OSDI) scores and dropout/ distortion in meibomian glands (MG).^4,6 Early diagnosis is important so that patients can be treated with corneal cross-linking (CXL), which aims to create new covalent bonds between collagen fibers to strengthen the cornea’s stability and stiffness.

The goal of this study was to evaluate the potential influence of CXL on corneal structure and several objective parameters of DED in patients with KC. The study was a prospective, non-randomized, single-center, observational study designed to compare the preoperative and postoperative changes in anterior segment parameters, endothelial structure and MG morphology in patients with progressive KC who underwent CXL treatment. Corneal topography, specular microscopy, OSDI, non-invasive tear break-up time (NITBUT) and meibography indices were evaluated preoperatively and at one, three and six months after CXL in 39 eyes of 39 patients with KC. The NITBUT was performed with the Phoenix-tear film imaging module on the Sirius topography device. Corneal topography and meibography were performed with the Sirius corneal topography device and the Phoenix-meibography imaging software module. Specular microscopy was used to examine the corneal endothelium. CXL was performed with an epithelial off technique.

Previous studies evaluating keratometry changes after CXL have shown a significant decrease in Kmax and averaged K readings or stabilization of keratometry values at the end of one year.7 In the current study, no significant difference was found in the Kmax value during the six-month follow-up, whereas a significant flattening was found in K1 and K2 readings after CXL. Significant thinning was detected in central (CCT), apical (ACT) and thinnest (TCT) corneal thickness until the sixth month. This reduction in corneal thickness is thought to be secondary to decreases in the treatment area after CXL, as well as changes in compactness of the stroma.

The investigators concluded that the dextran-free riboflavin used during the CXL treatment is protective of corneal endothelial cells, which remained unchanged. The NITBUT values decreased after CXL, possibly due to the regeneration of the completely removed epithelium and the decrease in sub-basal and anterior stromal nerve density. These elements affect the amount, quality and long-term stability of tears on the corneal surface. However, there was no significant change in OSDI index, so even with the decreased NITBUT, there was no significant increase in CXL ocular symptoms. This result may be because of hypoesthesia that develops with the reduction in nerve density in the corneas of CXL patients. There were no significant alterations in meiboscore, MG loss or morphology of the MG after CXL, but the results indicate the quality of meibum may deteriorate without an architectural change in meibography after CXL.

References:
1. Meek KM, Tuft SJ, Huang Y, et al. Changes in collagen orientation and distribution in keratoconus corneas. Invest Ophthalmol Vis Sci. 2005 Jun;46(6):1948–1956. doi:10.1167/iovs.04-1253
2. Sherwin T, Brookes NH. Morphological changes in keratoconus: pathology or pathogenesis. Clin Exp Ophthalmol. 2004 Apr;32(2):211–217. doi:10.1111/j.1442-9071.2004.00805.x
3. Spoerl E, Huhle M, Seiler T. Induction of cross-links in corneal tissue. Exp Eye Res. 1998 Jan;66(1):97–103. doi:10.1006/exer.1997.0410
4. Carracedo G, Recchioni A, Alejandre-Alba N, et al. Signs and symptoms of dry eye in keratoconus patients: a pilot study. Curr Eye Res. 2015;40(11):1088–1094. doi:10.3109/02713683.2014.987871
5. Mostovoy D, Vinker S, Mimouni M, Goldich Y, Levartovsky S, Kaiserman I. The association of keratoconus with blepharitis. Clin Exp Optom. 2018 May;101(3):339–344. doi:10.1111/cxo.12643
6. Dogru M, Karakaya H, Ozçetin H, et al. Tear function and ocular surface changes in keratoconus. Ophthalmology. 2003 Jun;110(6):1110–1118. doi:10.1016/S0161-6420(03)00261-6
7. Vinciguerra P, Albé E, Frueh BE, Trazza S, Epstein D. Two-year corneal cross-linking results in patients younger than 18 years with documented progressive keratoconus. Am J Ophthalmol. 2012 Sep;154(3):520–526. doi:10.1016/j.ajo.2012.03.020

Coding

Ryan Ames, OD, MBA

Owner of InSight Eye Care, Oshkosh, WI

99000 or 92000…Does It Matter?

The underlying theme of this article is that 92000 codes are medical office visit codes and can be used like the 99000 E/M codes. As long as the exam that was performed was appropriate for the reason for visit and the documentation is complete, providers can use either code set.

 

 

Every 99000 and 92000 code has documentation requirements that must be met before they can be used to code the office visit. Let’s review the requirements for both intermediate and comprehensive ophthalmological codes as stated in AMA’s Current Procedural Terminology (CPT). Alternatively, the coding requirements for the 99000 office visit codes can be found here.

Many doctors have adopted the idea of using 99000 codes exclusively for billing medical office visits (i.e., visits for keratoconus, AMD, glaucoma, red eyes and other conditions we encounter frequently), and they bill 920x4 for “routine” eye exams. In doing so, however, they have completely ignored the 92000s for the purpose of medical care, or they assume anything that is NOT a comprehensive exam earns 920x2. Every payor’s reimbursement schedule is different, but 92012 will typically reimburse higher than 99212, according to a sampling of several payors that I’ve performed personally. Keep in mind that you cannot simply use 920x2 as a substitute for 99212. There are occasions when an office visit will not meet the requirements listed above for either 92000 code, and it must be billed with the appropriate 99000 code.

Let’s say a stable keratoconic patient presents for their yearly exam and you plan to bill the care to their medical insurance. Assuming the exam contains all the elements we traditionally think of for a “yearly” exam, the visit would earn either 92014 or 99213. So, which do you choose? The choice becomes obvious when you look at the fee schedule for most payors. Using the national average fee schedule for Medicare, 92014 reimburses $34.06 more than 99213.

But if the exam is simply a follow-up visit, should you still use the 92000 code set? Maybe not. Using the Documentation Guidelines, a stable keratoconus follow-up visit would likely earn 99213 or 92012. The difference in reimbursement is not as dramatic—just $1.96. However, if you’re a higher-volume keratoconus clinic seeing a handful of these visits a day, those couple of dollars would add up to a couple thousand dollars a year in net revenue.

How do we use this information practically in our day-to-day practice? It’s as simple as being aware that either code set can be used for medical care and being aware of how the codes reimburse in relation to each other. Both code sets are medical; treat them as such.