Upside-down lens syndrome: ocular complications secondary to inverted implantation of the Kelman Multiflex anterior chamber intraocular lens.

PURPOSE: To describe ocular complications resulting from inverted insertion of a Kelman Multiflex anterior chamber intraocular lens (ACIOL). DESIGN: Retrospective observational case series. METHODS: We describe the outcomes of 4 cases of complicated cataract surgery in which a flexible open-loop polymethylmethacrylate (PMMA) ACIOL (Kelman Multiflex type) was placed in an inverted configuration, all of which were referred to a single institution. RESULTS: In all 4 cases, the placement of an inverted ACIOL resulted in ocular complications including chronic iritis, cystoid macular edema, pupil capture, iris adhesions, and corneal decompensation. CONCLUSIONS: Inadvertent inverted placement of the Kelman Multiflex anterior chamber intraocular lenses can lead to a constellation of severe ocular complications. When inserting such lenses, the surgeon should ensure that the lens is correctly oriented such that the optic vaults anteriorly and not posteriorly.

Computerized binocular pupillography of the swinging flashlight test detects afferent pupillary defects.

PURPOSE: To investigate the ability of a portable pupillometer, capable of 20-second binocular recordings of the swinging flashlight test (SFT), to detect relative afferent pupillary defects (rAPDs). METHODS: Pupillary response curves were recorded from both eyes in healthy volunteers (n = 22) with and without simulated rAPDs (using neutral density filters (NDFs)) and in abnormal patients (n = 24) with clinically graded rAPDs. The light stimulus (0.2 sec on and 1 sec off, or 2 sec on and 0.4 sec off) alternated between both eyes, simulating the SFT. Constriction amplitude (CA), constriction velocity (CV), and pupillary release were calculated by computer algorithm. In abnormal patients, NDFs were used to neutralize inter-eye differences. RESULTS: Significant correlation (Spearman's rho 0.71, 0.73) between NDF strength and absolute inter-eye differences was seen for CA and CV in simulated rAPDs. All abnormal patients (15/15) having rAPDs greater than 0.5 log units were distinguished from normals using either the upper bound of the one-sided 95% confidence interval (95% CI) value of CA or CV as determined from 22 healthy volunteers. Inter-eye variability in some normals prevented confident distinction of six abnormal patients with 0.3 log unit rAPDs. Using NDFs, subtle rAPDs were predicted in three patients having questionable rAPDs on clinical examination. CA and CV were more sensitive than pupillary release for all comparisons. CONCLUSIONS: This binocular pupillometer identified all of our patients with > 0.5 log unit rAPDs. Using NDFs, all of our abnormal patients were accurately identified and their rAPDs quantified. Variability in some normals makes them indistinguishable from patients with subtle rAPDs.

Pupillary block glaucoma associated with a secondary piggyback intraocular lens.

A 53-year-old woman developed pupillary block glaucoma associated with iris capture of a piggyback intraocular lens (IOL) that was treated with laser peripheral iridotomy. The piggyback IOL was repositioned by dilating the iris pharmacologically and reclining the patient. The IOL maintained its proper position behind the iris with the use of low-concentration pilocarpine eyedrops. Pupillary block glaucoma can occur as a complication of secondary piggyback IOL implantation.

Contemporaneous retinal and optic nerve infarcts, choroidal non-perfusion, and Hollenhorst plaque: are these all embolic events?

A 76-year-old man developed a sudden painless superior field defect in the right eye, retinal whitening along the inferior temporal arcade, and fluorescein angiographic evidence of lobular choroidal non-perfusion. One week later, ophthalmoscopy revealed inferior optic nerve edema with splinter hemorrhages consistent with an anterior ischemic optic neuropathy (AION) and a new cholesterol plaque near the macula. There was no clinical, serologic, or pathologic evidence of giant cell arteritis. Carotid ultrasound revealed no evidence of significant stenosis but did show an echolucent soft plaque in the right carotid artery. Transthoracic echocardiography demonstrated normal left ventricular function with no source of emboli. The presumed cause of the clinical findings in this patient was embolism, a rarely reported cause of AION. An embolic origin may be considered in non-arteritic AION associated with choroidal non-perfusion.

Development of epithelial downgrowth several decades after intraocular surgery.

PURPOSE: To report the management of a patient with the longest reported interval between intraocular surgery and the development of epithelial downgrowth. METHODS: A 53-year-old man who underwent right eye penetrating keratoplasty in 1970 for keratoconus and removal of an iris cyst in 1977 developed epithelial downgrowth 25 years after cyst removal. RESULTS: The area of epithelial downgrowth was initially treated with cryotherapy. Two weeks postoperatively, the patient had no resolution of epithelial downgrowth and developed diffuse corneal edema. Penetrating keratoplasty was performed along with extracapsular cataract extraction. At 6 months of follow-up, the patient's graft was clear, without evidence of recurrence of epithelial downgrowth, and he had 20/50 visual acuity. CONCLUSION: Epithelial downgrowth is an uncommon yet serious complication of intraocular surgery, making early detection of this condition important. This case illustrates that epithelial downgrowth can occur several decades after intraocular surgery.