Sildenafil-induced bilateral ciliochoroidal effusion syndrome: Case report.

PURPOSE: To report a case of bilateral ciliochoroidal effusion syndrome associated with sildenafil use. CASE REPORT: A 41-year-old male presented with a five-day history of bilateral blurred vision, elevated intraocular pressure, and myopic shift. Ultrasound biomicroscopy radial scans showed closed angles and 360 degrees of ciliochoroidal effusion in both eyes. Anterior segment coherence tomography angiography showed bilateral shallow anterior chamber. Further questioning revealed that the patient had taken sildenafil several times just a few days before symptoms appeared. Since then, the patient stopped dosing sildenafil. After treatment of anti-inflammation and shifting the lens-iris diaphragm posteriorly, the patient's visual acuity improved and intraocular pressure decreased. Follow-up ultrasound biomicroscopy and anterior segment coherence tomography angiography revealed resolution of ciliochoroidal effusion and increase of anterior chamber depth in both eyes. CONCLUSIONS: The patient demonstrated a rare case of sildenafil-induced bilateral ciliochoroidal effusion syndrome. This case report shows that sildenafil should be added to the possible causative agents of ciliochoroidal effusion syndrome.

BISPHOSPHONATE-INDUCED BILATERAL ANTERIOR UVEITIS AND CHOROIDAL EFFUSIONS WITH SECONDARY ANGLE CLOSURE.

PURPOSE: To report a case of bisphosphonate-induced bilateral anterior uveitis and choroidal effusions with secondary angle closure in a 64-year-old female patient. METHODS: Observational case report. RESULTS: A 64-year-old woman with history of scleroderma and antiphospholipid syndrome, presented with bilateral painless blurring of vision after commencement of alendronate. Clinical examination revealed bilateral anterior uveitis and choroidal effusions with resultant secondary angle closure in the left eye. Ultrasound biomicroscopy showed bilateral anteriorly rotated ciliary bodies. There was also a -2D myopic shift in the left eye. On drug cessation, complete resolution was seen within 2 weeks. CONCLUSION: In the absence of other plausible etiologies and with recent commencement of a new drug, we postulate that the anterior uveitis and choroidal effusions are likely due to alendronate. This is further supported by complete resolution of the inflammation and effusions once alendronate was withheld.

Unilateral Idiopathic Choroidal Effusion in a Patient Who Takes Sulfonamides.

Purpose: To report a challenging case of unilateral choroidal effusion.Methods: A case report about patient who presented with unilateral choroidal effusion and who was taking sulfonamides. Patient has been under care of a multidisciplinary team of uveitis consultant, ocular oncology consultant, and systemic oncology consultant. A comprehensive workup was done (blood tests, Spectralis OCT, FFA, chest X-rays, MRI, PETCT).Results: Baseline visual acuity on the affected (right) eye was 6/12. Patient is amblyopic and hypermetropic on that eye. Blood test results were negative on syphilis, tuberculosis, or sarcoidosis. MRI showed no mass lesions. PETCT scan showed no signs of malignant process out of the eye. Suprachoroidal drainage was done and analysis of the drainaged fluid showed no presence of malignant cells. Overall workup period patient's vision was stable.Conclusion: Definite diagnosis of unilateral choroidal effusion was done. A comprehensive workup is needed to exclude potential malignant process.

Zonisamide-induced Choroidal Effusion: A Case Report.

PURPOSE: To describe a case of zonisamide-induced bilateral choroidal effusion. CASE REPORT: A 72-year-old woman presented with a 4-day history of bilateral blurred vision 9 days after initiating oral zonisamide for essential tremor. Clinical examination revealed an asymmetric choroidal detachment with open anterior chamber angle and intraocular pressure within the normal range. Posterior segment ultrasonography and ultrasound biomicroscopy both confirmed the presence of bilateral ciliochoroidal effusion. Zonisamide treatment was discontinued. One month after treatment discontinuation, the ophthalmological examination was normal and no further treatment was needed. CONCLUSION: Zonisamide can cause an idiosyncratic reaction leading to choroidal effusion with or without acute angle closure. Early withdrawal of the causative agent is the key to reversing this condition. These findings indicate that zonisamide and other sulfa-derived drugs must be ruled out in the differential diagnosis of choroidal effusion of unknown cause.

Angiographic features of drug-induced bilateral angle closure and transient myopia with Ciliochoroidal effusion.

BACKGROUND: To report five cases of acute drug-induced angle closure and transient myopia with ciliochoroidal effusion and to analyze angiographic findings of these cases. METHODS: This study is an observational case series. Five patients with acute drug-induced angle closure and transient myopia with ciliochoroidal effusion were examined by fluorescein angiography, indocyanine green angiography (ICGA) and ultrasound biomicroscopy (UBM). RESULTS: Five patients presented with bilateral visual loss and ocular pain after intake of topiramate, methazolamide, phendimetrazine tartrate or mefenamic acid. All patients showed elevated intraocular pressure (IOP) with shallow anterior chamber and myopic shift from - 0.5 to - 17.0 diopters (D). UBM showed ciliochoroidal effusions with diffuse thickening of the ciliary body in all cases. Rapid normalization of IOP and decrease of myopic shift occurred in all patients after discontinuing the suspected drugs. We classified the ICGA findings into 2 major signs (hypofluorescent dark spots, hyperfluorescent pinpoints) and 3 minor signs (diffuse choroidal hyperfluorescence, early hyperfluorescence of choroidal stromal vessel, and leakage and dilated retinal vessels). CONCLUSIONS: The pathogenesis of acute drug-induced angle closure and transient myopia with ciliochoroidal effusion may be idiosyncratic reaction of uveal tissue to systemic drugs. Accumulation of extravascular fluid in the ciliochoroidal layer had a major role in the pathogenesis. ICGA could be a useful method to examine the pathophysiology of this condition by imaging of the choroidal layer.