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There is evidence that the provision of analgesia for children in emergency departments is often inadequate. Prompt assessment and treatment by nurses could improve matters. In South Australia (
) children with minor or moderate musculoskeletal injuries were studied. Initially, when there was no pain scoring and analgesia provision depended on doctors, the mean time from attendance to receiving analgesia for was 138 minutes and 21% of children received analgesia. After the introduction of pain scoring at triage by nurses the time to provision of oral analgesia fell to 93 minutes (not significant) and 23% of children received analgesia. When nurses both scored pain and provided analgesia, however, the time to analgesia provision fell significantly to 46 minutes and 43% of children were provided with analgesia. The researchers intend to extend their study by measuring whether, or to what extent, the changes actually reduce the pain experienced by these children.
Once the emergency phase is over, refugees in poor countries may have better health provision than the host population. In northern Uganda (
) during 1999–2002 maternal mortality was 2.5 times higher in the host population than in the refugee population in postemergency settlements. The refugees had greater access to health care. The authors of this report call upon humanitarian organisations to provide for both refugee and surrounding host populations.
Mutations in one gene, MSX1, have been associated with isolated cleft lip and palate, and account for about 2% of cases. Now another gene—the interferon regulatory factor 6 (IRF6) gene—has been implicated (
). The study included 1968 families with at least one affected member from ten populations with ancestry in East Asia, South America, Europe, or India, and 949 control families. A polymorphism in IRF6 (V274I) was responsible for 12% of the genetic contribution to isolated cleft lip and palate, and was particularly significant in some populations from South America and Asia. Among families with an affected child this polymorphism tripled the risk of recurrence. (The IRF6 gene was studied because it has been implicated in Van der Woude’s syndrome—an autosomal dominant condition in which isolated cleft lip and palate is associated with pits in the lower lip in 85% of cases).
In Philadelphia 60 children with recurrent steroid-responsive nephrotic syndrome and 195 healthy control children had whole body and spinal bone mineral content measured by dual-energy x ray absorptiometry (
). The children with nephrotic syndrome had a mean age of 9 years and had received a mean dose of 23 000 mg of prednisone (or equivalent) over a mean duration of 54 months. After adjustment for bone area, age, sex, Tanner stage, and race, whole body bone mineral content was significantly higher in patients than in controls, but there was no significant difference between the groups in spinal bone mineral content. On further adjustment for body mass index (BMI) z score, however, the two groups no longer differed significantly in whole body bone mineral content and the spinal bone mineral content was significantly lower in the patients than in controls. Long term intermittent steroid treatment was associated with slowed growth, increased weight gain, and increased BMI z score. This in turn was associated with an increase in whole body bone mineral content and preservation of spinal bone mineral content.
Virologists appear to be pessimistic about the prospects of avoiding a pandemic of avian influenza virus infection. Vaccination might be ineffective against the causative virus and treatment with viral neuraminidase inhibitors would play an important part in combating the pandemic. Now research in Japan (
) has shown that viral resistance to oseltamivir in treated children could be a problem. Nine of 50 children with influenza A (H3N2) virus infection treated with oseltamivir shed virus resistant to the drug beginning at day 4 of treatment. Three different viral neuraminidase mutations were identified that increased oseltamivir resistance 300-fold, 500-fold, and 10 000–100 000-fold, compared with pretreatment virus. The resistant virus was shed in appreciable quantities but transmission of such virus from person to person has not yet been reported. The transmissibility and pathogenicity of oseltamivir resistant virus are not known although animal work suggests that both may be reduced.
Air pollution stunts the growth of lung function in children. In southern California (
) 1759 10 year old children were recruited from 12 communities in 1993 and followed up with annual spirometric testing to 2001. Air pollution monitoring stations in each community provided continuous or regular measurements of atmospheric pollution. Growth in lung function between the ages of 10 and 18 years was related to the degree of air pollution and was slowed especially by exposure to greater concentrations of nitrogen dioxide, acid vapour, particulate matter of <2.5 μm diameter (PM2.5), and elemental carbon. For example, the proportion of children with an FEV1 at age 18 years less than 80% of the expected value was 7.9% at the highest level of exposure to PM2.5 and 1.6% at the lowest level. The findings remained significant after excluding children with a history of asthma or smoking.
The incidence of the sudden infant death syndrome (SIDS) fell rapidly after the “back to sleep” campaign of the early 1990s but it still remains an important mode of infant death. Some of the obstetric risk factors for unexplained stillbirth are also risk factors for SIDS and second trimester maternal serum alpha-fetoprotein (AFP) concentrations are linked to stillbirth risk. Now a large Scottish database has been used to show a direct relationship between maternal AFP level and SIDS risk (
). Among 214 532 singleton births there were 114 cases of SIDS. The incidence of SIDS among the infants of women with a high serum AFP level (fifth quintile) was 2.8 times that among the infants of women with a low level (first quintile) (7.5 vs 2.7 per 10 000 births). The odds ratios for SIDS in successive AFP quintiles were 1.0, 1.7, 1.8, 2.5, and 2.8, and after adjustment for birthweight and gestational age at birth, 1.0, 1.7, 1.7, 2.2, and 2.2. Both of these trends were significant. There is therefore a direct relationship between second trimester maternal AFP levels and risk of SIDS that is partly, but not completely, explained by poor intrauterine growth and early delivery. It is suggested that high maternal AFP is a marker of placental insufficiency and that placental insufficiency might affect infant cardiorespiratory control. The details remain to be elucidated.
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