Ontario Cataract Quality Outcome Initiative: appropriateness and prioritization of cataract surgery.

OBJECTIVE: To explore the utility of the Catquest 9SF visual function (VF) questionnaire along with visual acuity (VA) for determining appropriateness and priority for cataract surgery. To evaluate the feasibility of administering the Catquest-9SF in a clinical setting using web-based electronic data capture and interpretation. DESIGN: Prospective multicentred interventional observational study. PARTICIPANTS: Subjects undergoing sequential cataract surgery in both eyes at 4 sites in Ontario. METHODS: We recorded best-corrected VA (BCVA) and VA with current correction (CCVA) in each eye and both eyes (OU) and Catquest-9SF responses on a tablet before and after cataract surgery. Linear regression models were employed to test for associations between VA and visual function (VF). RESULTS: Preoperative BCVA and CCVA in the worse eye were significant predictors of change in VF (p = 0.006 and p = 0.008, respectively); subjects with worse VA had a greater improvement in VF after surgery. There was a significant association between improvement in VF and improvement in CCVA OU (p = 0.001). Fourteen of 151 subjects (9%) had no improvement or worse VF scores after surgery. Within this group, 10 of 14 subjects had a preoperative score ≤-3, which is suggestive of minimal visual disability. Within this subset, 4 of 14 subjects (2.6%) had a preoperative BCVA of 20/30 or better in their worse eye. CONCLUSIONS: For patient groups with equal VA, the Catquest-9SF score can help determine priority for surgery. Web-based data capture and interpretation allow for efficient virtual assessments of VF. A BCVA in the worse eye of 20/30 or better combined with a Catquest-9SF score <-3 can be used as a guideline for lowest priority.

The incidence of giant cell arteritis in Ontario, Canada.

OBJECTIVE: The incidence of giant cell arteritis (GCA) is insufficiently documented for Canada, but important to ascertain for public health planning. We estimate the incidence of biopsy-proven GCA (BPGCA) in Kingston, Ontario, and for the province of Ontario. METHOD: The number of cases of BPGCA was tabulated from retrospective chart review of all temporal artery biopsies (TABx) in Kingston, Ontario from 2011-15. The relevant population denominator was determined from the Canada census federal electoral district and the patient's postal code. The province-wide estimate for the incidence of BPGCA was calculated from provincial billing data of TABx from 2015-17, the Canada census for Ontario, and the expected positive yield of TABx. RESULTS: There were 35 subjects with BPGCA in the Kingston area over the 4-year period, from a population of 179 503 individuals 50 years of age or older (≥50 years). Ontario billing data identified 2404 patients who underwent TABx for suspected GCA over a 2-year period, from a population of 5 143 610 persons ≥50 years. Meta-analysis of 5 provincial TABx series suggested a 21% positive yield from TABx procedures (95% CI 0.18-0.24). The minimum cumulative incidence of BPGCA was 4.9 per 100 000 persons ≥50 years in Kingston, and 4.9 (95% CI 4.2-5.6) per 100 000 persons ≥50 years for Ontario as a whole. CONCLUSION: The estimated incidence of BPGCA in Ontario using 2 different estimation techniques was comparable, but low compared with other countries. The actual incidence of GCA in Ontario may be higher.

Diabetic retinopathy screening in a Canadian community pediatric diabetes clinic.

OBJECTIVE: To evaluate the screening rates for diabetic pediatric patients in a regional center according to the Canadian Diabetes Association guidelines. DESIGN: Retrospective study. PARTICIPANTS: The study consisted of 82 patients seen in the pediatric diabetes clinic at Peterborough Regional Health Center. METHODS: Medical records for all pediatric patients with diabetes were reviewed between July 2016 and February 2017. Parents and children were surveyed on details of their ocular examination history. Logistic regression analysis was conducted to evaluate if any characteristics were associated with noncompliance to Canadian Diabetes Association guidelines. RESULTS: The average age of the patients in our study was 12 years old with a mean duration of diabetes of 4 years. The majority of patients had type 1 diabetes (n = 79/82, 96.3%) and the mean HbA1c level was 9.1. Only 16 patients (19.5%) adhered to the Canadian Diabetes Association guidelines for diabetic retinopathy screening. Of the 66 patients who did not comply with the guidelines, 65 (98.5%) had received more exams than recommended under their respective screening guidelines. All dilated eye examinations were normal, and no diabetic retinopathy was found. Statistical analysis revealed that the duration of diabetes may be a predicting factor of noncompliance to the guidelines (-0.2488, 95% CI -0.505, -0.042). CONCLUSIONS: This study shows a low compliance rate with screening guidelines in our diabetic pediatric population. Of interest, the low compliance in this cohort was related to excessive eye exams. This study also found a low incidence rate of diabetic retinopathy despite poor management of diabetes, similar to previous studies of pediatric diabetic eye disease.

Retinopathy and RAAS Activation: Results From the Canadian Study of Longevity in Type 1 Diabetes.

OBJECTIVE: The importance of renin-angiotensin-aldosterone system (RAAS) activation in retinopathy for long-standing diabetes is not well understood. We determined retinopathy stage and evaluated associations with other vascular complications before and after physiological RAAS activation in adults with long-standing (≥50 years duration) type 1 diabetes. RESEARCH DESIGN AND METHODS: Participants underwent retinal examination by digital funduscopic photography and optical coherence tomography and were classified as having nonproliferative diabetic retinopathy (NPDR), proliferative diabetic retinopathy (PDR), or no diabetic retinopathy (NDR) with or without diabetic macular edema (DME). Neuropathy was measured by clinical neuropathy examination scores, electrophysiologically, and by corneal confocal microscopy. Renal function was measured by inulin and para-aminohippurate clearance methods. Arterial stiffness was measured by applanation tonometry. Renal function, blood pressure, and arterial stiffness were measured before and after RAAS activation with angiotensin II (ANGII). Associations were determined using linear regression. RESULTS: Twelve (16%) of the 75 participants had NDR, 24 (32%) had NPDR, and 39 (52%) had PDR. A low overall prevalence of DME (4%) was observed. Those with PDR had worse nerve function and reduced corneal nerve density, were more likely to have macrovascular disease, and had increased arterial stiffness in response to ANGII compared with those with NPDR or NDR. Prevalence of kidney disease or renal hemodynamic function did not differ by retinopathy status. CONCLUSIONS: PDR was associated with neuropathy severity and cardiovascular and peripheral vascular disease. In those with PDR, RAAS activation may be linked to vascular stiffening, an effect that persists in long-standing type 1 diabetes.

Saccade dynamics in peripheral vs central sixth nerve palsies.

OBJECTIVE: To investigate differences between peripheral idiopathic and central sixth nerve palsies from brainstem damage by comparing peak velocities and durations of horizontal saccades. METHODS: Fourteen patients with unilateral incomplete sixth nerve palsies caused by idiopathic, presumed ischemic, peripheral damage, 5 with incomplete central (fascicular) palsy caused by brainstem lesions, and 10 controls were studied. Palsies under 1 month in duration were designated as acute and those of longer duration were chronic. Among peripheral palsies, five were acute, nine were chronic. Among central palsies, two were acute, three were chronic. Subjects made +/- 10 deg horizontal saccades while wearing search coils. Serial recordings were made in seven patients with acute palsy (five peripheral, two central). RESULTS: Centrifugal abducting saccadic velocities in the paretic eye were subnormal in both central and peripheral acute palsies, as anticipated from lateral rectus weakness. In chronic central palsies, abducting velocities in the paretic eye remained reduced. However, in chronic peripheral palsies, velocities became normal in the tested range of excursion, within 2 months of onset, despite persisting abduction deficit. CONCLUSIONS: Saccade peak velocities are reduced and their durations are prolonged in the field of action of acutely palsied peripheral and central nerves. Speeds remain reduced in chronic central (fascicular) palsies, consistent with limited regeneration within the brain. Saccade speeds are repaired in chronic peripheral palsies, probably by remyelination and axonal regeneration, and perhaps also by central monocular adaptation of innervation selectively to the paretic eye, in order to drive both eyes rapidly and simultaneously into the paretic field of motion.

Recovery of peripheral versus central nerves identified by saccadic velocity after abducens neuropathy.

The abducens is the motor nerve with the most substantial course, both within and outside the brain and it innervates only one muscle. Sixth nerve palsy affords an opportunity to compare recovery after central versus peripheral nerve damage by assessing the dynamics of abduction. Horizontal saccade peak velocities and durations in 14 patients with unilateral peripheral sixth nerve palsies (5 acute, 9 chronic) are compared with those in 5 patients with central sixth nerve palsies (2 acute, 3 chronic) and with those in 10 normal subjects. Acutely, abducting saccades in the paretic eye were slow in both central and peripheral palsies, as anticipated from weakness of the lateral rectus muscle. In chronic central palsies, abducting saccadic velocities remained reduced, but in chronic peripheral palsies, they increased to normal within the limited range of excursion. The chronically damaged peripheral nerve behaves like a high-pass filter in transmitting phasic velocity commands, whereas tonic position commands remain defective, accounting for limited abduction but normal velocities within the range of duction. In chronic central (fascicular) palsies, saccade velocities remain reduced. Impaired conduction from damage to central myelin or axons is more persistent in central palsies, consistent with limited regeneration within the brain. Recording of saccade velocities may aid the distinction of fascicular from peripheral palsies. Saccade speed is repaired in peripheral palsies, probably by remyelination, and perhaps also by central monocular adaptation of innervation selectively to the paretic eye in order to drive both eyes rapidly and simultaneously to a target in the paretic field of motion.