From pen-and-paper questionnaire to a computer-assisted instrument for self-triage in the ophthalmic emergency department: Process and validation.

BACKGROUND/AIMS: The ISET (Instrument for SElf-Triage) is a validated pen-and-paper instrument for patient self-triage in ophthalmic emergency departments. The aim of the present study is to develop a validated computer-assisted ISET (ca-ISET) with a touch screen. METHODS: In the emergency department of the Eye Hospital Rotterdam, the Netherlands, successive computer-assisted versions of the ISET were tested by patients visiting the emergency department. The versions were developed by iteratively prototyping, testing, analysing and refining the computer-assisted ISET. In three test cycles, 16, 53 and 75 patients ≥ 18 years old, visiting the emergency department for the first time with their ophthalmic complaint, were monitored while using the ca-ISET. They were debriefed, and their input was used to adapt the computer-assisted ISET. To validate the ca-ISET, a sensitivity outcome of .80 and a specificity of .70 was required (CI=95%). The ca-ISET sensitivity and specificity were tested by comparing ca-ISET triage outcome to triage outcome as decided by the regular triage assistant. RESULTS: ISET accuracy increased from 0.69 in the first test to 0.79 in the third test. Sensitivity increased from 0.66 (CI 0.13-0.98) to 0.80 (0.51-0.95). Specificity increased from 0.69 (0.39-0.90) to 0.78 (0.65-0.88). To improve validity and usability, several adjustments were made in the text and the flow chart of the computer-assisted ISET. CONCLUSIONS: A ca-ISET prototype was developed, with minor textual modification of the pen-and-paper version. The new ca-ISET was validated by comparing against triage decided by the regular triage assistant.

Towards patient self-triage in the ophthalmic emergency department: sensitivity and specificity of a self-triage instrument.

PURPOSE: Trained ophthalmic triage staff may not constantly be available in the emergency department of a specialized ophthalmic hospital, particularly at night. To support the current triage process, the aim of this study was to develop an ophthalmic instrument of patient self-triage (ISET). METHODS: A preliminary ISET, in the form of a pen-and-paper questionnaire, was refined and validated in a two-step procedure. In a first explorative step, we compared the results of the ISET with the results of the regular triage process during the day, that is, triage by a trained triage assistant in a specialized ophthalmic hospital. As several patients needed guidance completing the questionnaire, the ISET was subsequently refined. The second step was to test the validity of the refined ISET by again comparing the outcome of this triage with that of the triage assistant in the emergency department. RESULTS: The first explorative step involved 279 patients and the final validation step 298. During the validation step, sensitivity of the ISET was 94.3% and specificity 76.4%. CONCLUSION: The results show that the ISET is a sensitive and specific instrument for ophthalmic triage compared with a trained ophthalmic triage assistant.

Retinal nerve fiber layer thickness in subgroups of multiple sclerosis, measured by optical coherence tomography and scanning laser polarimetry.

UNLABELLED: Optical coherence tomography (OCT) and scanning laser polarimetry (GDx ECC) are non-invasive methods used to assess retinal nerve fiber layer (RNFL) thickness, which may be a reliable tool used to monitor axonal loss in multiple sclerosis (MS). The objectives of this study are (1) to compare OCT with the GDx ECC; (2) to assess and compare the RNFL thickness in subgroups of MS. Ophthalmologic examination and RNFL assessment by OCT and GDx were performed in 65 MS patients (26 relapsing-remitting (RRMS), ten secondary-progressive (SPMS), 29 primary-progressive (PPMS)). Twenty-eight patients (43%) had a history of optic neuritis (ON). Adjustments were made for age and disease duration. RNFL thickness was reduced in eyes with previous ON (p < 0.01). No differences were found between PPMS and relapse-onset MS. OCT and GDx ECC measurements were moderately correlated (rho = 0.73, p < 0.01). Visual field-mean deviation (MD) values correlated with OCT means (r = 0.44, p < 0.01) and GDx ECC TSNIT average (r = 0.41, p < 0.01). In patients without previous ON, EDSS correlated with MD (r = -0.36, p < 0.01), visual field-pattern standard deviation (PSD) (r = 0.30, p < 0.05), OCT means (r = -0.31-0.30, p < 0.05) and macular volume (r = -0.37, p < 0.01). For MSIS-29 physical impact score, significant correlations were found with MD (r = -0.48, p < 0.01) and PSD (r = 0.48, p < 0.01). CONCLUSIONS: No differences between PPMS and relapse-onset MS subgroups were found. RNFL thickness was reduced in eyes with previous ON. Although OCT and GDx ECC findings were moderately correlated and showed significant correlations with measures of visual function in patients without previous ON, EDSS correlated significantly with visual and OCT measures, but not with GDx ECC.

A MELAS-associated ND1 mutation causing leber hereditary optic neuropathy and spastic dystonia.

OBJECTIVE: To report a novel mutation that is associated with Leber hereditary optic neuropathy (LHON) within the same family affected by spastic dystonia. DESIGN: Leber hereditary optic neuropathy is a mitochondrial disorder characterized by isolated central visual loss. Of patients with LHON, 95% carry a mutation in 1 of 3 mitochondrial DNA-encoded complex I genes. The complete mitochondrial DNA was screened for mutations in a patient with LHON without 1 of these 3 primary mutations. The heteroplasmy level and biochemical consequence of the mutation were determined. RESULTS: A pathogenic 3697G>A/ND1 mutation was detected and seemed associated with an isolated complex I deficiency. This family has similar clinical characteristics as the previously described families with LHON and dystonia with an ND6 mutation. CONCLUSIONS: The 3697G>A/ND1 mitochondrial DNA mutation causes the LHON and spastic dystonia phenotype in the same family. This mutation can also cause MELAS syndrome (which encompasses mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke), and other genetic factors may contribute to the clinical expression.

Symptoms and findings predictive for the development of new retinal breaks.

OBJECTIVE: To validate the conclusion of our previous prospective study of 250 patients with isolated posterior vitreous detachment: follow-up visits are only necessary if patients mention symptoms of flashes in combination with multiple floaters or a curtain or cloud at the initial examination, or an increase in number of floaters after the initial examination. METHODS: Prospective study of 270 consecutive patients with symptomatic isolated posterior vitreous detachment. All patients completed a questionnaire detailing their symptoms and had a full eye examination at the initial examination and at follow-up visits. Logistic regression with backward elimination was used for statistical analysis. We also performed pooled analysis of our previous and present study data. RESULTS: New retinal breaks developed in 10 patients (3.7%). Multiple floaters, a curtain or cloud, hemorrhages (retinal or vitreous) at the initial examination, and an increase in the number of floaters after the initial examination were found to be predictive factors for the development of new retinal breaks. These factors were also the only significant predictors after pooled analysis of both studies (520 patients, 23 breaks). CONCLUSIONS: We assume we can formulate a safe policy for scheduling patients with isolated posterior vitreous detachment: only patients with multiple floaters, a curtain or cloud, or hemorrhages (retinal or vitreous) at the initial examination should be scheduled for reexamination. All other patients should return only if the number of floaters increases.