Background
Full-thickness idiopathic macular hole (IMH) usually causes serious visual deformities and visual acuity loss. Pseudophakic cystic macular edema, also known as Irvine-Gass syndrome, is another entity that causes visual disturbances, and occurs mainly after cataract extraction. We present a case report of a patient that was diagnosed with a full-thickness macular hole that spontaneously closed after the resolution of an Irvine-Gass syndrome, which occurred after an uneventful cataract extraction.
Case presentation
A 75 years-old female presented with the complaints of decreased visual acuity and color contrast sensitivity on both eyes (OU) and central visual field deformations on her left eye (LE). She was diagnosed with a full-thickness IMH on her LE, and cataract on OU. After an uneventful cataract extraction via phacoemulsification, she developed an Irvine-Gass syndrome at her LE, which was treated topically. The IMH closed spontaneously after the resolution of the Irvine-Gass syndrome, and the patient is being followed with no further complaints.
Conclusion
The exact mechanism for spontaneous closure of full-thickness idiopathic macular holes is still not completely understood. In this case, we hypothesize that the coalesced intraretinal cysts caused by the Irvine-Gass syndrome formed a bridge-like structure connecting the inner walls of the macular hole, thus connecting the remnants of the Muller cells which enabled the full recovery of the normal foveal structure.
Background
Papilledema is the main ocular finding in patients with idiopathic intracranial hypertension (IIH) although several chorioretinal abnormalities may also occur and contribute to visual loss. The purpose of this paper is to describe two cases of chorioretinal abnormalities associated with idiopathic intracranial hypertension: one with choroidal folds and another with polypoidal choroidal vasculopathy, an extremely unusual ocular complication in the disease.
Case presentation
Case 1: A 47-year-old woman previous diagnosed with idiopathic intracranial hypertension treated with weight loss and acetazolamide that over the following 6 months had optic disc edema gradually resolved. The patient was follow-up for a period of 10 years and the papilledema disappeared, but choroidal folds remained unchanged. Case 2: A 61-year-old female patient was seen as a follow-up examination of a 5-year history of IIH that presented with papilledema. The patient was asymptomatic but fundoscopy evaluation revealed a yellowish white peripapillary subretinal nodular lesion temporally in OD. Multimodal imaging studies were made, and the patient was diagnosed with a rare and just recent described association of IIH and polypoidal choroidal vasculopathy.
Conclusion
Papilledema, RNFL and retinal ganglion cell loss are the most common structural complications of IIH, but chorioretinal complications are important findings and should be carefully evaluated in such patients. Awareness of such occurrence and the use of appropriated clinical and multimodal imaging studies are of great importance for its early detection, leading to proper treatment and prevention of further visual loss.
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