A proper focus of any visual object in the macula cannot be obtained without an optically smooth ocular surface, which can only be produced through the interplay within the tear film, the ocular surface (cornea and conjunctiva), and the dynamic tear flow pumping mechanism by blinking of eyelids. The eyelids play a crucial role in the secretion, distribution, and drainage processes of the tear fluid. Moreover, since the delicate mixture of the tear fluid is not secreted from a single source, the blinking serves to combine the various components of the tear film.

During blinking, the normal healthy eyelids push the tear film evenly across the ocular surface. Blinking also assists pumping of the tear lake into the proximal part of lacrimal drainage system. However, the time between each blinking is the critical period to have a stable and optimal tear film in order to obtain a smooth optical ocular surface. An optimal tear film quality and quantity could maintain its stability for a certain period before discontinuity (dry spots) of the tear film form. The tear film also has a buffering capacity to overcome any corneal or conjunctival surface irregularities.

In reverse, any abnormalities of either the lid function or ocular surface may in turn jeopardize the tear film quality, changing the volume of the tear lake, and its buffering capabilities. These conditions may subsequently decrease the “tear breakup time,” which clinically contributes to the so-called dry eye syndrome [3, 5, 8].

If the blinking mechanism is affected severely and reduced by lagophthalmos either due to proptosis as well as lid retraction as in thyroid eye disease, severe exposure keratopathy may occur (Fig. 29.1).

Although Graves’ orbitopathy can present with a number of clinical signs, it is very unusual for patient to present with all of them.

The most frequent sign is upper eyelid retraction (Fig. 29.2a, b), which affects 90–98 % of patients at some stage [2].

The contour of the retracted upper eyelid often shows lateral flare, an appearance that is almost pathognomonic for Graves’ ophthalmopathy (GO) [2]. Proptosis is a very frequent sign, and if associated with significant upper or lower lid retraction, then these patients are more likely to demonstrate incomplete eyelid closure or lagophthalmos.

Many such patients, especially those with eyelid retraction, will show punctate inferior corneal staining with fluorescein, sometimes with thinning and very occationally corneal perforation. Corneal ulceration can develop when normal corneal protection is lost. This occurs in those patients who not only cannot close their eyes but also whose cornea remains visible when the eyelids are closed due to poor Bell’s phenomenon, the normal protective upward movement of the eyeball (Fig. 29.3a). Although this reflex is absent in 10 % of individuals, it is more likely to be affected in GO due to a very tight and thickened inferior rectus limiting the upward excursion of the eyeball (Fig. 29.3b).