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Letters to the Editor Figure 1. Visante anterior segment optical coherence tomography (OCT) measurement of right eye (a) and left eye (b) cornea showing interface fluid pocket in the left eye.

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Difficulty in measuring IOP in the setting of IFS has been reported, particularly with the limitations of GAT in setting of IFS.3,4 In IFS, the IOP measured by GAT underestimates the true IOP because the tissue in direct contact with the applanation tip is the thin LASIK flap, which has lower tissue rigidity compared with normal full-thickness cornea. Furthermore, the fluid space under the LASIK flap will have a lower pressure gradient on the posterior surface of the flap, as compared with the pressure in the anterior chamber on the posterior surface of the corneal endothelium. Previous publications on IFS have suggested performing tonometry at the peripheral cornea outside the boundary of the LASIK flap (where there is no interface fluid) using the Tono-pen in order to obtain a better estimate of the IOP.4 However, it is likely that such measurements may overestimate IOP due to the higher corneal thickness in the peripheral cornea. Rebound tonometry (iCare) on the other hand measures the rebounding velocity of a fine probe to estimate IOP.5 In the setting of IFS although the probe first makes contact with the thin LASIK flap and interface fluid, the estimation of IOP does not begin until all forward movement of the probe has been completely stopped by the firmer underlying stromal bed and the actual pressure on the posterior corneal surface. Therefore, IOP estimation using the principle of rebound velocity through the central cornea is more likely to provide a better estimation of actual IOP and is less affected by the presence of the interface fluid. LASIK is a commonly performed procedure affecting corneal thickness and integrity. One should have a high index of suspicion of IFS in patients with a previous history of LASIK who present with signs of corneal thickening inconsistent with DLK. One should be aware of the limitation of GAT in this setting and employ multiple modalities of IOP measurements, including manual palpation and rebound tonometry, to exclude elevated IOP. Failure to detect elevated IOP in such a setting could lead to a delay in instituting appropriate management.

Yu Xiang G Kong MBBS PhD, Jennifer C-C Fan Gaskin FRANZCO MD and Ghee S Ang FRANZCO Glaucoma Investigation and Research Unit, The Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia Received 16 March 2015; accepted 23 March 2015.

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REFERENCES 1. Smith RJ, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998; 105: 1721–6. 2. Wirbelauer C, Pham DT. Imaging interface fluid after laser in situ keratomileusis with corneal optical coherence tomography. J Cataract Refract Surg 2005; 31: 853–6. 3. Galal A, Artola A, Belda J et al. Interface corneal edema secondary to steroid-induced elevation of intraocular pressure simulating diffuse lamellar keratitis. J Refract Surg 2006; 22: 441–7. 4. Senthil S, Rathi V, Garudadri C. Misleading Goldmann applanation tonometry in a post-LASIK eye with interface fluid syndrome. Indian J Ophthalmol 2010; 58: 333–5. 5. Kontiola AI. A new induction-based impact method for measuring intraocular pressure. Acta Ophthalmol Scand 2000; 78: 142–5.

Blepharoptosis onset after topical prostaglandin therapy for glaucoma A 46-year-old woman came to our neurological clinic because of the occurrence of unilateral ptosis in the left eye with onset a year before. Ptosis did not show a progressive course for several months nor fluctuations during the day or worsening after intense efforts. Patient reported no history of head trauma, ocular or periorbital pain, acute headache or previous infections. Neurological examination was normal except for left eye blepharoptosis at the upper margin of the pupil (Fig. 1), with very mild orbicularis oculi muscle deficit without fatigability. Patient did not show diplopia, and there were not ocular motility alterations nor deficit or fatigue in the muscles of the four limbs. Brain magnetic resonance imaging with orbital study and angiographic sequences excluded the presence of spaceoccupying lesions, encephalic parenchymal changes, only showing focal ectasia on the basilar artery. An extensive Competing/conflict of interest: None. Funding sources: None.

© 2015 Royal Australian and New Zealand College of Ophthalmologists

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Letters to the Editor Matteo Lucchini MD,1 Francesco A Losavio MD,1 Massimiliano Mirabella PhD1 and Viviana Nociti PhD1,2 1 Institute of Neurology, Department of Geriatrics, Neurosciences and Orthopedics, Catholic University, Rome; and 2Neurorehabilitation Department, Don Carlo Gnocchi Foundation, Milan, Italy Received 23 March 2015; accepted 1 April 2015.

Figure 1.

REFERENCES

Left eyelid ptosis at the upper level of pupil.

neurophysiological study was performed, including single-fibre electromyography and repetitive nerve stimulation: no abnormalities were found. Serological markers of inflammation and muscle necrosis, blood level of lactic acid and an extensive study of thyroid function were normal. Antibodies against acetylcholine receptor and muscle-specific kinase resulted negative. Serology for neurotropic viruses was negative. Patient had no familiar history of ptosis or autoimmune/neurological pathologies. She suffered from glaucoma secondary to uveal ectopia on left eye. Because of this, she followed topical therapy with travoprost on left eye. Ptosis began 4 weeks after initiation of topical travoprost therapy and were confined to the treated eye. We therefore attributed the onset of unilateral ptosis to travoprost therapy by excluding the main known causes of acquired ptosis. Ptosis onset in adulthood may be the first manifestation of a neuromuscular junction disease, such as myasthenia gravis. Also, several familiar or acquired myopathies can clinically present with ptosis, especially mitochondrial myopathy or orbital myositis; other common causes of ptosis are head injury in frontal or temporal region or third cranial nerve palsy related to endocrine or metabolic or vascular diseases. All of these diseases have been excluded in our patient.1 According to the ophthalmologist, we substituted travoprost with timolol. After 4 months, ptosis showed no modifications. Topical prostaglandin-analogues use is highly effective in the treatment of glaucoma. The most common side effects are ocular hyperaemia and abnormalities of iris and periorbital pigmentation. Prostaglandin-associated periorbitopathy includes all periorbital soft tissue alterations, particularly in adipose tissue, which are caused by topical prostaglandin-analogues use. These alterations include deepening of the eyelid sulcus, orbital fat atrophy, enophthalmos, dermatochalasis of involution and ptosis,2 and could be irreversible.3 There are only few reports of isolated ptosis related to prostaglandin-analogues therapy.4 Ptosis generally occurred from 5 months to several years after therapy initiation; in contrast, our patient reported ptosis after only 4 weeks of therapy. The hypothesized mechanism of ptosis is an alteration of periorbital adipose tissue metabolism with reduction of periorbital fat because of direct action of prostaglandin analogues.5 Therefore, it is necessary to rapidly recognize eventual periorbital modifications to discontinue prostaglandin-analogue therapy, avoiding a possible permanent tissue damage.

1. Castelluccia A, Nociti V, Frisullo G, Batocchi AP. A prospective study on 132 cases of ocular palsy. Eur Neurol 2013; 70: 10–5. 2. Kucukevcilioglu M, Bayer A, Uysal Y, Altinsoy HI. Prostaglandin associated periorbitopathy in patients using bimatoprost, latanoprost and travoprost. Clin Experiment Ophthalmol 2014; 42: 126–31. 3. Tan J, Berke S. Latanoprost-induced prostaglandinassociated periorbitopathy. Optom Vis Sci 2013; 90: e245–7. 4. Wang PX, Koh VT, Cheng JF. Periorbital muscle atrophy associated with topical bimatoprost therapy. Clin Ophthalmol 2014; 8: 311–4. 5. Taketani Y, Yamagishi R, Fujishiro T, Igarashi M, Sakata R, Aihara M. Activation of the prostanoid FP receptor inhibits adipogenesis leading to deepening of the upper eyelid sulcus in prostaglandin-associated periorbitopathy. Invest Ophthalmol Vis Sci 2014; 55: 1269–76.

Contact lens induced Baerveldt tube extrusion The patient was a 57-year-old man who presented with a left ruptured globe and scleral laceration following a football injury. His past medical history was significant for hypertension, asthma, left finger tendon release, fixated ankle, colonic polyps and anxiety. His past ocular history was significant for myopia, for which he wore contact lenses (−9.0 right eye, −7.0 left eye). On initial examination, he was found to have a flat anterior chamber (AC), hyphaema, vitreous in AC, vitreous haemorrhage, aniridia, aphakia, subconjunctival haemorrhage and an anterior scleral laceration. An urgent primary repair was performed. Two months later, he developed a secondary retinal detachment for which a posterior vitrectomy and scleral buckling were performed. Two months post-silicone oil removal, he developed a recalcitrantly elevated intraocular pressure despite multiple topical agents and oral acetazolamide. His best corrected left visual acuity (VA) remained stable during this period at 6/24. Ketorolac eye drops were commenced during this time and the patient was referred to the glaucoma service for further management. A left Competing/conflicts of interest: None. Funding sources: None.

© 2015 Royal Australian and New Zealand College of Ophthalmologists

Blepharoptosis onset after topical prostaglandin therapy for glaucoma.

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