Background The WHO's Vision 2020 global initiative against blindness, launched in 2000, prioritises children. Progress has been hampered by the global paucity of epidemiological data about childhood visual disability. The British Childhood Visual Impairment and Blindness Study 2 (BCVIS2) was undertaken to address this evidence gap. Methods UK-wide prospective population-based observational study of all those aged under 18 years newly diagnosed with visual impairment or blindness between Oct 1, 2015 and Nov 1 2016. Eligible children were notified simultaneously but independently by their managing ophthalmologists and paediatricians via the two national active surveillance schemes, the British Ophthalmic and Paediatric Surveillance Units. Standardised detailed data were collected at diagnosis and one year later. Incidence estimates and relative rates by key sociodemographic factors were calculated. Descriptive analyses were undertaken of underlying ophthalmic disorders and nonophthalmic comorbidities. FindingsOf 784 cases, 72% had additional non-ophthalmic impairments/disorders and 4% died within the year. Annual incidence was highest in the first year of life, 5•2 per 10,000 (95% CI 4•7-5•7) with cumulative incidence by 18 years of 10•0 per 10,000 (95% CI 9•4 to 10•8). Rates were higher for those from any ethnic minority group, the lowest quintile of socio-economic status, born preterm or with low birthweight. Only 44% had a single ophthalmic condition: disorders of the brain/visual pathways affected 48% overall. Prenatal or perinatal aetiological factors accounted for 84% of all conditions. InterpretationBCVIS2 provides a contemporary snapshot of the heterogeneity, multi-morbidity and vulnerability associated with childhood visual disability in a high income country, and the arising complex needs. These findings will facilitate developing and delivering healthcare and planning interventional research. They highlight the importance of including childhood visual disability as a sentinel event and metric in global child health initiatives.

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Authors did not look at effects on all deliberate and accidental self poisoningEditor-Hawton et al provide some evidence of a decrease in the severity and incidence of paracetamol and salicylate poisonLetters 633 BMJ VOLUME 323 15 SEPTEMBER 2001 bmj.com ing after pack sizes of these drugs were restricted.1 They have not, however, considered the effect on deliberate self poisoning as a whole, or on self poisoning with other drugs.Limiting access to one type of drug may simply increase the incidence of overdose with other potentially more dangerous substances. It is important to determine if poisoning with other agents increases.2 Although the authors allude to this in their discussion, they mention only the small but significant increase in overdoses with paracetamol compounds and paracetamol with other drugs. Using self poisoning with paracetamol and salicylates alone as a measure of the effect of this legislation on self poisoning is erroneous and potentially dangerous.Hawton et al have not considered the effect of the legislation on accidental poisoning in children. This is a critical public health issue and needs to be evaluated alongside deliberate self poisoning to assess the impact of any change in legislation. Data from poison information centres would be useful to evaluate any changes in paediatric accidental poisoning.With only one year of data after the change of legislation available, it is of concern that the results are not significant for the larger liver transplant units alone. Furthermore, the biochemical data do not support the decrease in severity of cases, with no change in the mean highest blood paracetamol concentration. The slight decrease in mean highest prothrombin time is a poor measure of severity: about half of patients with paracetamol poisoning without hepatotoxicity will have a raised prothrombin time, 3 so it is a poor indicator of liver poisoning.We are concerned that the authors conclude that the legislation has been relatively successful without properly assessing its effects on all deliberate and accidental self poisoning. Geoff Isbister toxicology registrar Paracetamol should be packaged with its antidoteEditor-Paracetamol overdose is the most common cause of acute hepatic failure. Hepatocytes become sensitive to paracetamol metabolites and inflammatory mediators 1 when intracellular glutathione is depleted due to metabolism of paracetamol.2 For this reason, many clinical conditions associated with glutathione depletionfor example, chronic alcohol abuse, multiorgan system failure, chemotherapy, and certain metabolic diseases-place patients at risk of paracetamol toxicity, even at therapeutic doses of paracetamol. In addition, patients without predisposing disease are at risk because over the counter preparations often contain paracetamol and represent sources of potential overdose.Importantly, Hawton et al report that morbidity and mortality from paracetamol overdose decreased after legislation in the United Kingdom to restrict the package sizes of the drug.3 As the authors n...