High Risk Meibomian Glands!


Billing and Coding Update: This week I came across a few issues in practice and a few questions on ODs on Facebook where researching the answers was helpful for me and my practice.

Billing for the office visit and special testing for a patient taking a high risk medication (like plaquenil). First of all it is important to understand which ICD codes will need to be linked to the office visit and which ICD code should be linked to the special testing.

Link the diagnosis code for the systemic disease (e.g. rheumatoid arthritis - M06.09) to the office visit code (e.g. 92014). Link the diagnosis code for other long term drug therapy (z79.899) to the special tests (e.g. 92134, 92083)

Remember that if a patient does not have a definitive diagnosis, use the systemic disease that is the working diagnosis. If the patient does not know, contact the rheumatologist. This situation is similar to what occurs when we diagnose acute conjunctivitis but are unsure of the exact etiology, we may choose bacterial conjunctivitis even if we think there may also be an allergic component.

Smoking Cessation Education can be be billed to Medicare (and possibly other private insurers) with a -25 modifier appended to the below codes when 3 or more minutes are spent educating a patient on smoking cessation. Be sure to document the specific time spent for providing this additional service, preferably time started and time ended.

99407 ($28.65*) – Smoking and tobacco-use cessation counseling visit; intensive, greater than 10 minutes 99406 ($14.29*) – Smoking and tobacco-use cessation counseling visit; intermediate, greater than 3 minutes up to 10 minutes ICD codes: F17.200, F17.201, F17.210, F17.211, F17.220, F17.221, F17.290, F17.291, T65.211A, T65.212A, T65.213A, T65.214A, T65.221A, T65.222A, T65.223A, T65.224A, T65.291A, T65.292A, T65.293A, T65.294A, and Z87.891 *based on NV 2017 Medicare fee schedule See more here.

Clinical Update: Along with many others, I have developed a passion for taking care of patients with ocular surface dysfunction (OSD). I feel really fortunate to practice at at time where our diagnosis and treatment options (billing pun intended) allow us to drastically improve the symptoms of the vast majority of our OSD patients. With new literature being released so frequently in this area, I love to learn about something that transforms my understanding of the complex set of diseases and disorders we call OSD. My understanding of the ocular surface grew this week after reading this article. To summarize, my previous understanding of evaporative ocular surface dysfunction would be like this: obstructions occur in the meibomian glands (MG) from keratin plaques that collect in the central duct of the gland. My clinical intuition was that this was largely due to an increase in epithelial cells covering the MG oriface combined with biofilms that prevent meibum outflow. Clinical evidence of this can be seen with lissamine green staining of Marx line, and it is also why when we debride these epethelial cells some patients feel (temporary) relief from their symptoms. However, this article discusses that an increased evaporative state (i.e. arid evironment) of the ocular surface leads to actual changes in the meibomian glands that causes a proliferation of basal acinar cells which produce meibum, leading to ductal dilation which may contribute to eventual atrophy of the glands. This mechanism is thought to potentially be secondary to the innervation of the meibomian glands by parasympathetic, sympathetic, and sensory nerve fibers. To put it simply: the meibomian glands may FEEL when the eye is at an increased evaporative state and attempt to compensate by up regulating the flow of meibum which may contribute to structural changes that we see in MGD!