First we would like to congratulate Shim and associates for the interesting and well-written article approaching the association between platelet dysfunction and disc hemorrhages (DHs) in patients with normal-tension glaucoma (NTG). We believe this is an interesting topic, as much still has to be elucidated regarding the role of DHs, their relationship with intraocular pressure (IOP) values, and underlying causative mechanisms. In fact, the fact that DHs are frequently observed at relatively lower IOPs suggests the contribution of IOP-independent mechanisms.

We also have poor knowledge about the clinical implications of a DH to a specific individual. Although DH is known to increase the risk of glaucoma development and disease progression, studies suggest that DH consequences can be highly variable for each patient. The Ocular Hypertension Treatment Study, for example, demonstrated that DH occurrence was associated with a 4-fold increased risk of developing glaucoma. However, nearly 90% of these patients did not experience a glaucoma endpoint until the end of follow-up. When we think about disease progression, our group has previously shown that visual field (VF) progression rates following a DH also differ significantly between patients. While some did not progress, others deteriorated by more than 5 dB/year during a 4-year follow-up period. With this information in mind, it is reasonable to ask: do all DHs represent the same clinical situation?

Shim and associates showed that platelet dysfunction increases the risk of DH in eyes with NTG, which is a subgroup of patients that presents a complex profile of disease progression; while some progress even after significant IOP reduction, others remain stable for years despite no treatment. Aspirin administration itself has also been previously associated with an increased risk of DH. Unfortunately, none of these studies evaluated glaucoma progression rates in these DH eyes. In this subgroup of patients, another important question must be raised: do these DHs represent uncontrolled glaucoma or are they solely a form of spontaneous bleeding (like a subconjunctival hemorrhage), thus not being associated with disease progression?

We believe the answers to these questions are important in daily practice. As aforementioned, even though the way a DH affects an individual patient varies significantly, we are always prone to promptly change our treatment regimen every time a DH is documented. Now that we know about this association between platelet dysfunction (and likely anticoagulant intake) and increased frequency and longer duration of DHs, the next step is to investigate whether these specific DHs would lead to glaucoma progression just like an “ordinary” DH would. With that in mind, we encourage the authors to longitudinally follow these patients in order to evaluate whether there is any difference in VF progression rates between those with and without platelet dysfunction. These results may add significantly to the management of patients presenting with DH, as they could guide us not only about how aggressively we should modify the treatment regimen of a specific patient, but also about whether we should consider including platelet function tests in their evaluation.