No abstract

Children who were abnormally hypermetropic at the age of6 months were randomly allocated treatment with spectacles or no treatment. The eventual incidence of squint was the same in both groups (approximately 24%). The last known visual acuity of the two groups was not significantly different either. Therefore there is no indication to screen infants with a view to preventing squint/amblyopia by optical correction of hypermetropia. If, however, the children allocated treatment are divided into two subgroups -those who wore glasses consistently and those who probably or certainly did not do so -the incidence of squint was the same, but the last known acuities of those who consistently wore glasses may be better than those who did not do so. This suggests that it may yet prove possible to prevent severe amblyopia.

Paraquat poisoning is very severe. When it is ingested, this herbicide may be responsible for causative lesions of the digestive tract, cytolytic hepatitis, renal tubular necrosis, circulatory failure, and/or pulmonary fibrosis. Since a very low dose (as little as one mouthful) is potentially lethal, it is important to understand why 11 of our 28 patients who entered our department for paraquat poisoning survived. The main prognostic factors appear to be the following: Route of administration. Of four patients who had inhaled paraquat aerosols and/or contaminated their skin with the herbicide, all survived. Ingested amount. Above 50 mg/kg, patients died of circulatory failure within 72 h; between 35 and 50 mg/kg, a progressive pulmonary fibrosis occurred. Delay between ingestion and the last meal. Paraquat is adsorbed and neutralized by foodstuffs. Caustic gastric lesions revealed by early endoscopic examination. The occurrence of an organic renal failure. The plasma paraquat concentrations within the first 24 h. Patients whose plasma concentrations do not exceed 2.0, 0.6, 0.3, 0.16, and 0.1 mg/L at 4, 6, 10, 16, and 24 h, respectively, are likely to survive. The different treatments that have been tested (fuller's earth, forced diarrhea, furosemide, hemodialysis, hemoperfusion, artificial ventilation with hypoxic breathing mixtures) did not modify the initial prognosis. The 11 survivals are only linked to the circumstances of the poisonings (route of administration, ingested amount, delay between ingestion and the last meal, etc.). The treatments did not modify the outcome.

SUMMARY In this series amblyopia, uncorrectable by spectacles and occlusion, was highly likely (48%) if a child had +3-50 or more dioptres of meridional hypermetropia at age 1 year. 45% of children with this refraction also had a squint. All those who remained with severely defective acuity in spite of treatment had either +3-50 or more dioptres of meridional hypermetropia or 4 or more dioptres of meridional myopia at age 1 year. These children were identifiable in the 3-7% of the population at age 1 year who showed high refractive errors. Squint as such was not so accurately predictable. Of those children with squint 71% had less than +3-50 dioptres of meridional hypermetropia at age 1 year-an incidence of 4-4% of the population. Apart from two 'congenital myopes' only 16% of these had residual amblyopia after treatment, and their last known acuity was never less than 6/12. Astigmatism in infancy or later is not significantly associated with squint or amblyopia.

14 patients with heavy metal poisoning received 2,3-dimercaptosuccinic acid (DMSA). 12 subjects were given 30 mg/kg/day for 5 days; 1 subject was started on a lower dose because of a history of atopy; another subject was treated for 15 days because of very high initial blood lead concentrations. In the 9 subjects who had lead poisoning, DMSA decreased blood lead concentrations by 35 to 81%, and induced a 4.5- to 16.9-fold increase in mean daily urinary excretion of the metal. In the acutely arsenic-poisoned case, the plasma arsenic concentration on day 7 was half the pretreatment value, while no clear decrease was observed in a chronically exposed subject. In 3 mercury cases, DMSA increased daily mercury urinary excretion 1.5-, 2.8- and 8.4-fold, respectively, while blood mercury concentrations remained below detection limits. No serious side effects were observed and 3 weeks after administration of the drug the clinical condition of all subjects was either stable or improved. These results indicate the efficacy of DMSA for lead poisoning in humans and provide a rationale for further investigating its usefulness in mercury and arsenic poisoning cases.