Objective: To evaluate the characteristics of strabismus in infants who underwent cataract surgery with and without intraocular lens (IOL) implantation.
Design: Secondary outcome analysis in a prospective, randomized clinical trial. Participants: The Infant Aphakia Treatment Study is a randomized, multicenter (n = 12), clinical trial comparing treatment of aphakia with a primary IOL or contact lens in 114 infants with a unilateral congenital cataract.
Intervention: Infants underwent cataract surgery with or without placement of an IOL.
Main Outcome Measures: The proportion of patients in whom strabismus developed during the first 12 months of follow-up was calculated using the life-table method and was compared across treatment groups and age strata using a log-rank test.
Results: Strabismus developed within the first 12 months of follow-up in 38 pseudophakic infants (life-table estimate, 66.7%) and 42 infants (life-table estimate, 74.5%) treated with contact lenses (P = 0.59). The younger cohort (<49 days) at the time of surgery demonstrated less strabismus (29 of 50; life-table estimate, 58.0%) than the older cohort (≥49 days; 51 of 64; life-table estimate, 80.0%; P<0.01).
Conclusions: Intraocular lens placement does not prevent the early development of strabismus after congenital cataract surgery. However, strabismus was less likely to develop in infants whose cataract was removed at an earlier age. Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article.
Purpose
To study the structural features of human post-LASIK corneas.
Methods
A pair of post-mortem donor corneas, from a 55-year old patient who underwent uncomplicated LASIK surgery five years previously, were bisected and fixed in 4% paraformaldehyde. The right cornea and one half of the left cornea were processed for light microscopy and scanning electron microscopy. One half of the right cornea was also examined by transmission electron microscopy.
Results
The flap-bed interface could be easily detected several years after LASIK and, although the flap appeared to be in close association with the stromal bed, there was a noticeable absence of reconnection between adjacent severed lamellae. Tissue gaps were evident at the flap margin, which once free of cellular components revealed the presence of a few bridging fibres.
Conclusion
Examination of corneas five years after LASIK revealed evidence of primitive reparative scar development at the wound interface, but no reconnection of severed collagen lamellae. Such findings may explain the occurrence of flap dislocation following trauma in some patients months or years after surgery.
Patients with idiopathic intracranial hypertension (IIH) frequently have coexisting obstructive sleep apnea (OSA). We aimed to determine if the prevalence and severity of OSA is greater in patients with IIH than would be expected, given their other risk factors for OSA. We included 24 patients (20 women, four men) with newly-diagnosed IIH who had undergone overnight polysomnography. We calculated the expected apnea-hypopnea index (AHI) for each patient, based on their age, sex, race, body mass index (BMI), and menopausal status, using a model derived from 1,741 randomly-sampled members of the general population who had undergone overnight polysomnography. We compared the AHI values obtained from polysomnography with those predicted by the model using a paired t test. Our study had 80 % power to detect a 10-unit change in mean AHI at α = 0.05. Eight patients (33.3 %; six women, two men) had OSA by polysomnography. AHIs from polysomnography were not significantly different from those predicted by the model (mean difference 3.5, 95 % CI: -3.0-9.9, p = 0.28). We conclude that the prevalence and severity of OSA in IIH patients is no greater than would be expected for their age, sex, race, BMI, and menopausal status. It remains unclear whether the presence or treatment of OSA influences the clinical course of IIH.
Descemet's stripping automated endothelial keratoplasty (DSAEK) has rapidly become the standard of care for endothelial dysfunction of the cornea in adults. There are few reports of DSAEK in children and infants, mainly because most pediatric corneal opacities are full-thickness and therefore not amenable to lamellar procedures but also because of the unique difficulties of performing this procedure in the youngest patients. We report the case of an 8-month-old girl who underwent DSAEK for congenital hereditary endothelial dystrophy. At 24 months' follow-up, her visual acuity was 20/40 in the operated eye. To our knowledge, this is the first report of an objective visual outcome in a child with DSAEK performed in infancy.
In this case we introduce Sporothrix pallida, a non-pathogenic environmental Sporothrix species as a cause of infectious keratitis in a corneal transplant recipient. Human infections caused by S. schenckii are well-known but human infection with Sporothrix pallida has not been previously reported.
PURPOSE OF REVIEW: The purpose of this study is to review commonly encountered adverse ocular effects of illicit drug use. RECENT FINDINGS: Drug and alcohol abuse can produce a variety of ocular and neuro-ophthalmic side effects. Novel, so-called 'designer', drugs of abuse can lead to unusual ocular disorders. Legal substances, when used in manners for which they have not been prescribed, can also have devastating ophthalmic consequences. SUMMARY: In this review, we will systematically evaluate each part of the visual pathways and discuss how individual drugs may affect them.
An 80-year-old white woman with a history of hyperthyroidism treated with radioactive iodine ablation, gastroesophageal reflux disease complicated by Barrett esophagus, osteoarthritis, breast cancer status post-bilateral mastectomy, and diverticulosis presented with severe left-sided headache and diplopia. Three weeks prior to presentation, she developed a sharp pain located over the left temporal, parietal, and occipital regions. It was associated with exquisite scalp tenderness. Over the next few days, the pain progressed, involving the left side of the face, including the periorbital region. There was no radiation of the pain, and she had little relief with over-the-counter acetaminophen. She also experienced earache, sore throat, and left jaw pain with mastication.
Idiopathic intracranial hypertension (IIH) is increasingly recognized as a cause of spontaneous cerebrospinal fluid (CSF) leak in the otolarnygological and neurosurgical literature. The diagnosis of IIH in patients with spontaneous CSF leaks typically is made a few weeks after surgical repair of the leak when symptoms and signs of elevated intracranial pressure (ICP) appear. Case reports and literature review. Two young obese women developed spontaneous CSF rhinorrhea related to an empty sella in one and a cribriform plate encephalocele in the other. Both patients underwent surgical repair of the CSF leak. A few weeks later, they developed chronic headaches and bilateral papilledema. Lumbar punctures showed elevated CSF opening pressures with normal CSF contents, with temporary improvement of headaches. A man with a 3-year history of untreated IIH developed spontaneous CSF rhinorrhea. He experienced improvement of his headaches and papilledema after a CSF shunting procedure, and the rhinorrhea resolved after endoscopic repair of the leak. These cases and the literature review confirm a definite association between IIH and spontaneous CSF leak based on: 1) similar demographics; 2) increased ICP in some patients with spontaneous CSF leak after leak repair; 3) higher rate of leak recurrence in patients with raised ICP; 4) patients with intracranial hypertension secondary to tumors may develop CSF leak, confirming that raised ICP from other causes than IIH can cause CSF leak. CSF leak occasionally may keep IIH patients symptom-free; however, classic symptoms and signs of intracranial hypertension may develop after a CSF leak is repaired, exposing these patients to a high risk of recurrence of the leak unless an ICP-lowering intervention is performed.
by
Mark J. Mannis;
Edward J Holland;
Robin L. Gal;
Mariya Dontchev;
Craig Kollman;
Dan Raghinaru;
Steven P. Dunn;
Robert L. Schultze;
David D. Verdier;
Jonathan H. Lass;
Irving M. Raber;
Joel Sugar;
Mark S. Gorovoy;
Alan Sugar;
R Doyle Stulting Jr.;
Monty M. Montoya;
Jeffery G. Penta;
Beth Ann Benetz;
Roy W. Beck
Objective: To determine whether the 10-year success rate of penetrating keratoplasty for corneal endothelial disorders is associated with donor age.
Design: Multicenter, prospective, double-masked clinical trial. Participants A total of 1090 participants undergoing penetrating keratoplasty at 80 sites for Fuchs' dystrophy (62%), pseudophakic/aphakic corneal edema (34%), or another corneal endothelial disorder (4%) and followed for up to 12 years.
Methods: Forty-three eye banks provided corneas from donors aged 12 to 75 years, using a randomized approach to assign donor corneas to study participants without respect to recipient factors. Surgery and postoperative care were performed according to the surgeons' usual routines.
Main Outcome Measures:Graft failure defined as a regraft or, in the absence of a regraft, a cloudy cornea that was sufficiently opaque to compromise vision for 3 consecutive months.
Results: In the primary analysis, the 10-year success rate was 77% for 707 corneas from donors aged 12 to 65 years compared with 71% for 383 donors aged 66 to 75 years (difference, +6%; 95% confidence interval, -1 to +12; P = 0.11). When analyzed as a continuous variable, higher donor age was associated with lower graft success beyond the first 5 years (P < 0.001). Exploring this association further, we observed that the 10-year success rate was relatively constant for donors aged 34 to 71 years (75%). The success rate was higher for 80 donors aged 12 to 33 years (96%) and lower for 130 donors aged 72 to 75 years (62%). The relative decrease in the success rate with donor ages 72 to 75 years was not observed until after year 6.
Conclusions: Although the primary analysis did not show a significant difference in 10-year success rates comparing donor ages 12 to 65 years and 66 to 75 years, there was evidence of a donor age effect at the extremes of the age range. Because we observed a fairly constant 10-year success rate for donors aged 34 to 71 years, which account for approximately 75% of corneas in the United States available for transplant, the Cornea Donor Study results indicate that donor age is not an important factor in most penetrating keratoplasties for endothelial disease. Financial Disclosure(s) Proprietary or commercial disclosure may be found after the references.
Purpose.
A mouse mutation, tvrm148, was previously reported as resulting in retinal degeneration. Tvrm148 and Rpe65 map between markers D3Mit147 and D3Mit19 on a genetic map, but the physical map places RPE65 outside the markers. We asked if Rpe65 or perhaps another nearby gene is mutated and if the mutant reduced 11-cis-retinal levels. We studied the impact of the tvrm148 mutation on visual function, morphology, and retinoid levels.
Methods.
Normal phase HPLC was used to measure retinoid levels. Rpe65+/+, tvrm148/+ (T+/−), tvrm148/tvrm148 (T−/−), RPE65KO/KO (Rpe65−/−), and Rpe65T/− mice visual function was measured by optokinetic tracking (OKT) and electroretinography (ERG). Morphology was assessed by light microscopy and transmission electron microscopy (TEM). qRT-PCR was used to measure Rpe65 mRNA levels. Immunoblotting measured the size and amount of RPE65 protein.
Results.
The knockout and tvrm148 alleles did not complement. No 11-cis-retinal was detected in T−/− or Rpe65−/− mice. Visual acuity in Rpe65+/+ and T+/− mouse was ∼0.382 c/d, but 0.037 c/d in T−/− mice at postnatal day 210 (P210). ERG response in T−/− mice was undetectable except at bright flash intensities. Outer nuclear layer (ONL) thickness in T−/− mice was ∼70% of Rpe65+/+ by P210. Rpe65 mRNA levels in T−/− mice were unchanged, yet 14.5% of Rpe65+/+ protein levels was detected. Protein size was unchanged.
Conclusions.
A complementation test revealed the RPE65 knockout and tvrm148 alleles do not complement, proving that the tvrm148 mutation is in Rpe65. Behavioral, physiological, molecular, biochemical, and histological approaches indicate that tvrm148 is a null allele of Rpe65.