Sukhpal S. Sandhu

Comment on macular full-thickness and lamellar holes in association with type 2 idiopathic macular telangiectasia

PurposeTo describe patients with full-thickness macular holes (FTMHs) and lamellar macular holes (LMHs) in association with type 2 idiopathic macular telangiectasia (type 2 IMT).MethodsSix patients with either FTMH or LMH and type 2 IMT were evaluated by means of optical coherence tomography (OCT) imaging, funduscopy, and fluorescein angiography.ResultsThe age of the examined patients ranged from 57 to 70 years (mean 62.5±5.2), and best-corrected visual acuity of the affected eyes ranged from 20/50 to 20/200 (mean 20/100). All eyes showed macular abnormalities typical for nonproliferative type 2 IMT except for one eye with a proliferative disease stage. Three patients had an FTMH, one presenting with bilateral FTMH, and three had an LMH on OCT. In all cases of FTMH, the macular holes did not have elevated margins. Surgery was performed in two patients with a FTHM without subsequent functional improvement.ConclusionsThe altered foveal anatomy with progressive atrophic changes within the neurosensory retina in type 2 IMT may predispose to the development of FTMH and LMH. Type 2 IMT should be considered in the differential diagnosis in patients presenting with macular holes. The association between the two may reflect alternative pathogenetic mechanisms in the development of macular holes.

Displacement of submacular hemorrhage associated with age-related macular degeneration using vitrectomy and submacular tPA injection followed by intravitreal ranibizumab

Background/aims: To evaluate retrospectively the clinical outcomes of patients presenting with submacular hemorrhage (SMH) secondary to neovascular age-related macular degeneration (nAMD), treated by vitrectomy, submacular tissue plasminogen activator (tPA) injection and pneumatic displacement of SMH with air followed by postoperative intravitreal ranibizumab (RZB). Methods: Patients with SMH and nAMD had 25-guage vitrectomy and subretinal tPA (12.5 micrograms/0.1 mL) with fluid/air exchange. Intravitreal RZB was administered postoperatively to patients eligible for National Health Service (NHS) funded treatment. Results: Of the total of 16 patients, 11 (68.7%) had complete displacement of SMH. The remaining five had residual SMH, mainly subretinal pigment epithelium in location. Three of the four patients who previously had a failed expansile gas pneumatic displacement were successfully displaced with vitrectomy surgery. At presentation 5/16 (31.3%) patients were eligible for NHS funded intravitreal RZB. This increased to 12 patients after the vitrectomy procedure (75.0%). At 6 months postoperatively all improved by ≥1 line. Ten of the 16 patients (63%) improved by ≥2 lines, with 10 of the 12 patients (83%) treated with RZB improving by ≥2 lines. Conclusion: Vitrectomy/subretinal tPA/air to displace SMH followed by intravitreal RZB injection can stabilize/improve vision in patients with nAMD. This technique displaces hemorrhage not displaced by attempted expansile gas techniques.

Submacular haemorrhages associated with neovascular age-related macular degeneration

The exact incidence of submacular haemorrhage (SMH) in patients with neovascular age-related macular degeneration (nAMD) is unknown, and risk factors for its occurrence ill defined. It is known, however, to be a relatively common problem and important because the visual prognosis of these patients is poor. Unfortunately, patients with significant SMH were excluded from all the recent major randomised control trials for nAMD with antivascular endothelial growth factor (VEGF) agents and photodynamic therapy, and as such, the optimum management of patients is uncertain. SMH can present initially or during treatment of nAMD. The location, size, thickness and duration of SMH have an important bearing on treatment and outcomes. Thin or extrafoveal SMH are probably best treated with anti-VEGF agents alone. It has been proposed that patients with moderate-sized SMH, particularly thick haemorrhages, have an improved prognosis with surgical SMH displacement combined with treatment of CNVM if present. SMH drainage, macular translocation and RPE patch grafting are reserved for more severe extensive cases of SMH. Using these techniques, outcomes better than the natural history have been achieved. This review aims to summarise what is known about SMH in nAMD and will discuss a variety of therapeutic interventions.

Frequency of goldmann applanation tonometer calibration error checks.

Purpose:To investigate how quickly Goldmann applanation tonometers used in clinical practice develop calibration errors, and to determine the frequency of checks required to detect these errors. Materials and Methods:Prospective check of the calibration error of all Haag-Streit Goldmann applanation tonometers in the department at month zero, month one, and month four. The tonometers were checked according to the Haag-Streit method using a standard calibration check weight bar by two independent observers. Calibration errors were classed as ±0.5 to 2.5 mm Hg, ±3 to 4 mm Hg, or >±4 mm Hg. Tonometers with a calibration error greater than ±2.5 mm Hg were returned to the manufacturer for re-calibration. Results:At month zero 2 of 34 (5.9%), at month one 3 of 29 (10.3%), and at month four 0 of 33 (0.0%) tonometers fell within the manufacturers recommended calibration range of ±0.5 mm Hg. A total of 14 of 34 (41.2%) tonometers at month zero, 10 of 29 (34.5%) tonometers at month one, and 17 of 33 (51.5%) tonometers at month four were identified to have calibration errors greater than ±2.5 mm Hg. Conclusions:Goldmann applanation tonometers are not as accurate as the manufacturers recommended calibration error tolerance of ±0.5 mm Hg would suggest. Calibration error of less than ±2.5 mm Hg is clinically acceptable. Calibration error checks should be carried out once monthly and tonometers with calibration error greater than ±2.5 mm Hg returned to the manufacturer for re-calibration. Additional checks should be made if tonometers suffer specific damage. Ideally individual ophthalmologists should check calibration before each session.

Correlation of optical coherence tomography and fundus fluorescein angiography following photodynamic therapy for choroidal neovascular membranes

Aims: To assess the correlation between optical coherence tomography (OCT) and leakage on fundus fluorescein angiography (FFA) following photodynamic therapy (PDT) with verteporfin for choroidal neovascularisation (CNV). Methods: Retrospective comparative observational case series of patients who were treated with PDT for CNV from one centre. All patients had 3 monthly FFA and OCT following initial PDT to assess if further treatment was required. A pair of FFA and OCT images from the same visit at a random follow up date were taken from each patient’s series and assessed separately by different observers. The presence of pigment epithelial detachment, subretinal fluid, vitreomacular traction, intraretinal fluid, absence of foveal depression, and the retinal thickness on OCT were correlated with presence of leaks on FFA. Results: A total of 121 eyes of 121 patients were included. The presence of subretinal fluid, gross cystoid macular oedema, sponge-like retinal thickening and retinal thickness of more than 350 μm on OCT correlated well with leak on FFA (p value <0.01). The likelihood ratios were 3.0, 5.7, 2.7, and 3.6, respectively. The presence of a solitary foveal cyst did not correlate well with leaks on FFA. Conclusions: The presence of subretinal fluid, intraretinal fluid in the form of gross cystoid macular oedema, or sponge-like retinal thickening, or a retinal thickness more than 350 μm correlates with leaks on FFA and so suggests the need for repeat PDT.

Acute optic neuropathy in patients with Behçet's disease. Report of two cases.

Although acute optic neuropathy has been rarely reported in patients with Behçet’s disease, a detailed description of its clinical course is lacking. We report in detail the course of acute optic neuropathy in two patients with Behçet’s disease. Our experience suggests that it can be bilateral, can affect both eyes simultaneously, and can be recurrent. The severity of the visual loss and its recovery can be very variable even in the same patient. Early recognition of this entity and treatment with high-dose systemic corticosteroids may limit the degree of permanent visual loss. However, the optimal treatment has not been established.

The accuracy of continued clinical use of goldmann applanation tonometers with known calibration errors.

OBJECTIVESnWith normal clinical use, Goldmann applanation tonometers frequently develop calibration errors. Only the manufacturer can perform recalibration. This study aimed to assess whether intraocular pressure (IOP) measured by Goldmann applanation tonometers with known small calibration errors could be adjusted to reflect true IOP to allow continued clinical use.nnnDESIGNnEvaluation of diagnostic test.nnnPARTICIPANTSnPatients under regular review who had undergone previous applanation tonometry.nnnMETHODSnPatients with a range of IOPs underwent IOP measurement using a gold standard 0-error tonometer and tonometers with known calibration errors in a randomized blind fashion. The calibration errors of the tonometers ranged 0 to +5 mmHg.nnnMAIN OUTCOME MEASURESnIntraocular pressure.nnnRESULTSnFor the first part of the study, 125 eyes of 125 patients with a mean IOP of 18.5 mmHg (range, 8-43 mmHg) were tested. Mean IOP measured by the tonometer with an error of +1 mmHg was +1.0 (95% confidence interval [CI], 0.3-1.7 mmHg; P = 0.0076, compared with gold standard 0-error), with the +2 mmHg error was +1.2 (95% CI, 0.8-1.7 mmHg; P<0.0001), with the +3 mmHg error was +1.6 (95% CI, 1.2-1.9 mmHg; P<0.0001), with the +4 mmHg error was +3.6 (95% CI, 2.9-4.2 mmHg; P<0.0001), and with the +5 mmHg error was +3.3 (95% CI, 2.9-3.8 mmHg; P<0.0001). In the second part of the study, IOP measured by each of the tonometers with +2 mmHg error was +0.6 mmHg (95% CI, 0.1-1.1 mmHg; P = 0.0241), +1.5 mmHg (95% CI, 1.0-2.0 mmHg; P<0.0001), and +1.5 mmHg (95% CI, 1.9-2.1 mmHg; P<0.0001).nnnCONCLUSIONSnThere is a relationship between calibration error and clinical error in IOP measured, but it is not a one-to-one relationship. The error overestimates IOP and is consistent over a clinical range of IOPs. In certain circumstances where resources are limited, it may be clinically acceptable to use tonometers with calibration errors of less than +3 mmHg, because they do not overestimate IOP by more than 2 mmHg.nnnFINANCIAL DISCLOSURE(S)nThe author(s) have no proprietary or commercial interest in any materials discussed in this article.

Short-term effects of focal argon laser treatment in diabetic maculopathy as demonstrated by optical coherence tomography.

Purpose: To assess the short-term effects of argon laser on retinal thickening as demonstrated by optical coherence tomography (OCT). Methods: A prospectively collected consecutive series of patients undergoing routine focal argon laser treatment for sight-threatening diabetic maculopathy had bilateral OCT performed before laser treatment and 1 hour, 24 hours, and 2 weeks after treatment. The main outcome measure was change in retinal thickness in the region of laser treatment. Results: Forty-six eyes were analyzed. There was a small increase in retinal thickness in the treated area 1 hour after laser treatment, with a mean change from before laser treatment of +2.6 &mgr;m (95% confidence interval [CI], +0.2 to + 5.0). However, there was a larger change 24 hours after treatment of +39.0 &mgr;m (95% CI, +31.6 to + 46.4) and a significant decrease 2 weeks after treatment of −14.6 &mgr;m (95% CI, −21.6 to −7.7) from before laser treatment values. Conclusion: Focal argon laser treatment remains the first-line treatment for sight-threatening diabetic maculopathy. This study shows that in the short-term, areas of retinal thickening worsen before settling in response to argon laser treatment as demonstrated by OCT.

Original articleThe Prevalence and Causes of Vision Loss in Indigenous and Non-Indigenous Australians: The National Eye Health Survey

PURPOSEnTo conduct a nationwide survey on the prevalence and causes of vision loss in Indigenous and non-Indigenous Australians.nnnDESIGNnNationwide, cross-sectional, population-based survey.nnnPARTICIPANTSnIndigenous Australians aged 40 years or older and non-Indigenous Australians aged 50 years and older.nnnMETHODSnMultistage random-cluster sampling was used to select 3098 non-Indigenous Australians and 1738 Indigenous Australians from 30 sites across 5 remoteness strata (response rate of 71.5%). Sociodemographic and health data were collected using an interviewer-administered questionnaire. Trained examiners conducted standardized eye examinations, including visual acuity, perimetry, slit-lamp examination, intraocular pressure, and fundus photography. The prevalence and main causes of bilateral presenting vision loss (visual acuity <6/12 in the better eye) were determined, and risk factors were identified.nnnMAIN OUTCOME MEASURESnPrevalence and main causes of vision loss.nnnRESULTSnThe overall prevalence of vision loss in Australia was 6.6% (95% confidence interval [CI], 5.4-7.8). The prevalence of vision loss was 11.2% (95% CI, 9.5-13.1) in Indigenous Australians and 6.5% (95% CI, 5.3-7.9) in non-Indigenous Australians. Vision loss was 2.8 times more prevalent in Indigenous Australians than in non-Indigenous Australians after age and gender adjustment (17.7%, 95% CI, 14.5-21.0 vs. 6.4%, 95% CI, 5.2-7.6, P < 0.001). In non-Indigenous Australians, the leading causes of vision loss were uncorrected refractive error (61.3%), cataract (13.2%), and age-related macular degeneration (10.3%). In Indigenous Australians, the leading causes of vision loss were uncorrected refractive error (60.8%), cataract (20.1%), and diabetic retinopathy (5.2%). In non-Indigenous Australians, increasing age (odds ratio [OR], 1.72 per decade) and having not had an eye examination within the past year (OR, 1.61) were risk factors for vision loss. Risk factors in Indigenous Australians included older age (OR, 1.61 per decade), remoteness (OR, 2.02), gender (OR, 0.60 for men), and diabetes in combination with never having had an eye examination (OR, 14.47).nnnCONCLUSIONSnVision loss is more prevalent in Indigenous Australians than in non-Indigenous Australians, highlighting that improvements in eye healthcare in Indigenous communities are required. The leading causes of vision loss were uncorrected refractive error and cataract, which are readily treatable. Other countries with Indigenous communities may benefit from conducting similar surveys of Indigenous and non-Indigenous populations.

Do topical ophthalmic corticosteroids suppress the hypothalmic-pituitary-adrenal axis in post-penetrating keratoplasty patients?

PurposeTo establish whether hypothalmic-pituitary-adrenal axis suppression is possible secondary to long-term topical ophthalmic corticosteroid use in patients who have undergone penetrating keratoplasty (PKP).MethodsPatients who had undergone a PKP and had been using corticosteroid-based eye drops continuously for more than 6 months, with no history of concomitant steroid (oral, inhaled, or cutaneous) use, were included within the study. A low-dose short Synacthen (LDSST) test was performed in each patient followed later by a short Synacthen test (SST). The mean SST and LDSST after 30u2009min were calculated along with their corresponding 95% confidence intervals (CIs). Correlation between both baseline SST and baseline LDSST with duration of treatment was determined using Spearmans correlation.ResultsIn all, 20 patients were included within the study. The mean duration treatment was 28.2 months (range 11–96 months). All patients had normal baseline cortisol levels in both SST and LDSST tests. The mean 30u2009min SST was 753.8u2009nmol/l (95%CI: 696.6u2009nmol/l, 811.0u2009nmol/l) and no patients displayed inadequate adrenal response. The mean 30u2009min LDSST was 709.8u2009nmol/l (95%CI: 665.1u2009nmol/l, 754.5u2009nmol/l) and only one patient had an inadequate adrenal response. There was no correlation between baseline SST or LDSST and duration of treatment.ConclusionsThis study found no evidence that patients using continuous long-term corticosteroid eye drops after PKP experienced inadequate adrenal response. We did not find any evidence of a negative correlation between length of treatment and SST or LDSST measurements at baseline.