Reply re: "Panophthalmitis and Visual Loss as a Complication of Acute Dacryocystitis".

seen in hypotony secondary to ocular surgery and the authors’ suggestion that scleral microscopic perforation could have been responsible for the “intraocular” spread is not unreasonable; a degree of vitritis, even if low, would have been likely though in this situation. Besides, even if the authors want to indicate this was very early “intraocular” spread involving only the choroid, in the absence of appropriate management for endophthalmitis, rapid progress to other intraocular structures would have probably ensued. Providing the intraocular pressure measurement would be useful to differentiate between possible etiologies of choroidal folds in this case—intraocular pressure elevation would have pointed toward scleritis or external compression, and hypotony toward microscopic perforation. Finally, it is important to highlight the sudden deterioration of vision and development of relative afferent pupillary defect after deroofing of the scleral abscess. As hypothesized by the authors, a vascular occlusion or optic neuritis—either infectious or compressive—are the likely causes for the observed visual loss. In summary, the authors describe a unique case of loss of vision secondary to orbital and scleral spread of infection originating in the nasolacrimal system. Both scleritis and orbital cellulitis are medical emergencies and prompt initiation of treatment is essential to prevent sight-threatening complications. However, in this case, the vision loss does not appear to be a consequence of panophthalmitis and the diagnosis of panophthalmitis is not supported and should be reconsidered.