• PDF / 171,459 Bytes
• 1 Pages / 595.245 x 841.846 pts (A4) Page_size
• 53 Downloads / 150 Views

DOWNLOAD

REPORT

---

1 S

Ciliochoroidal effusion syndrome and secondary angle closure: case report A 67-year-old man developed ciliochoroidal effusion syndrome and secondary angle closure during treatment with zonisamide and latanoprost [not all dosages and routes stated]. The man presented with bilateral blurry vision from the last week. His medical history was significant for acute myelogenous leukaemia (AML), laryngeal squamous cell carcinoma (in remission), hypertension, coronary artery disease and essential tremor. He reported that the ocular symptoms began while he was receiving a blood transfusion for anaemia secondary to his AML. On anamnesis, it was revealed that after onset of the blurry vision, the left eye became red and painful. By the next morning, both the eyes became painful and injected [sic]. Over the next week, he became increasingly photophobic and also experienced photopsia and a blurry shadow at the temporal side in both the eyes and was presented to the emergency department (the current presentation). His ocular history was significant for mild angle-recession glaucoma (left eye), for which he had been receiving latanoprost in the left eye at bedtime for the past 3 years. He further reported that, he stopped latanoprost 5 days prior to this presentation, as he thought that latanoprost might be contributing to his ocular symptoms. His other concomitant medications included decitabine chemotherapy for the AML. Upon further review of his medicinal history, it was revealed that he had started receiving zonisamide 100 mg/day for the essential tremor, from two weeks before the onset of his symptoms. At the current presentation, visual acuity was 20/50 in the right eye and 20/60 in the left eye, with pinhole to 20/25 and 20/30, respectively. An auto-refraction revealed roughly 2 dioptres of myopic shift (in both the eyes). The intraocular pressure (IOP) was found to be increased bilaterally (the right eye IOP was 33mm Hg, and IOP of the left eye was 36mm Hg). The Pupils (4mm) showed minimal reactivity. Relative afferent pupillary defect was absent. An anterior segment examination revealed bilateral chemosis and conjunctival injection. A slit-lamp examination revealed diffusely shallow anterior chambers, without presence of iris bombe and without iris or lens approximation to the corneal endothelium bilaterally. A gonioscopy revealed narrow angles with peripheral iristo-cornea touch and no visible angle structures. An ultrasonography demonstrated hypoechoic and choroidal effusions in both the eyes. The man was therefore treated with atropine, timolol, brimonidine and brinzolamide (eye instillations). Thirty minutes after instillation, the anterior chambers were found to be deepened and the IOP also found to be decreased to 17mm Hg in the right eye and 22mm Hg in the left eye. A dilated eye examination revealed bilateral choroidal effusions. However, the macula appeared to be attached and the optic nerve was seen with sharp margins with cup-to-disc ratio-0.3 in both the eyes. Eventually, he was diagnosed with bilateral c