Chronic Dry Eye Disease: Treatments

Laura Periman, MD

#AlwaysDrinkUpstreamFromTheHerd – Part V

Originally Published on Ophthalmology Management

Part V: Pharmaceuticals, interventions and procedures for Ocular Surface Disease, as seen through lessons learned on the Montana ranch.

Back to installment 1 in this cliff notes series: #PutYourBootsOn…The Dry Eye definition by TFOS DEWS II talks about hyperosmolarity, inflammation, loss of homeostasis and neuro-sensory abnormalities. And this is how I organize my interventions. Speaking of loss of homeostasis, my ultimate goal is #PhysiologicRestoration. This is the Golden Ring on the bull’s nose. Mighty tough to anchor it in to a moving, angry target but totally worth it if you can achieve it.


Photo 1 – The Periman Family Ranch summer mountain pastures.

Inflammatory cytokines run amok and only one of the rowdy multitude are easily measurable by your clinical point of care tests. So, if MMP9 (InflammaDry, Quidel®) is negative, you still can’t say there is no inflammation present, and I sure wouldn’t drink that water. You have plenty of tools to clean up the water: oral omegas (eg HydroEye® and PRN®) and topical immunomodulators (eg Restasis® and Xiidra®) are my top two choices for a solid foundation. Shorter term options include loteprednol, doxycycline, amniotic membranes (ProKera®). For your MGD patient, Intense Pulsed Light (IPL) therapy and LipiFlow® studies have demonstrated some interesting anti-inflammatory benefits also. No matter which lasso you use, be confident you’ve roped in tears that are clean enough, because you can’t tell how clean the tears are just by looking. Even on the summer mountain ranch land (photo 1), we sure don’t drink the water from the clear-looking mountain stream before treating it for Giardia. Clean up the microbial component with Avenova®, Cliradex®, BlephEx®, etc.


Hyperosmolarity can trigger adaptive immunity by aberrantly activating TLRs (Toll Like Receptors) as discussed in Distilled #4. It can also corrode the ocular surface (photo 3) like salty winter roads can corrode the finish on a car (photo 2). It sure is satisfying to watch osmolarity (TearLab®) return to physiologic levels with treatment.

Photo 2

Photo 3. Used with permission from

Loss of Homeostasis and Neurosensory Abnormalities

Let’s say you’ve diligently cleaned up the inflammation and returned osmolarity to physiologic levels. You’ve buffed up the meibomian gland function, the goblet cell density and the lacrimal gland function. You’ve tuned up the Lacrimal Functional Unit (LFU) instruments, now come along and conduct the song. That’s where neural stimulation (TrueTear®) comes in handy. I’ve been impressed at how neural stimulation appears especially useful in patients who have compromised corneal nerves (disease, surgery, injury, inflammation-induced and hyperosmolarity-induced sub basal plexus damage, etc).

Neural stimulation to the nasociliary nerve is a back-gate approach to triggering the neural reflex arc from environmental sampling and sensation to the brainstem and command impulses to the LFU tear producing apparatus. When all is well, the neurosensory part of homeostatic tears is like a two-lane country highway on a sunny day. When the road is damaged by inflammation, osmolarity or injury, you’re as stuck as if driving on pothole-riddled, rush hour-congested big city streets. So, grab your lasso, jump in the truck and ease on down the road.

The entire TFOS DEWS II report is available to all for free at

Laura M. Periman, MD is Director of Dry Eye Services and Clinical Research at Evergreen Eye Center in Seattle, WA. Relevant to this series, she discloses relationships with Allergan, Bio-Tissue, Eyedetec, Lumenis, Science Based Health, Sun Pharmaceuticals, TearLab, Topcon and Visant.