To investigate whether children with autistic spectrum disorder (ASD) have bowel symptoms consistent with underlying enterocolitis.
Information on children’s stool patterns and gut symptoms collected by questionnaire at 4 weeks and at 6, 18, 30 and 42 months of age were available for 12 984 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Data on the 78 children identified by local health and/or education systems to have special educational provision for ASD were compared with the 12 906 remaining children in the cohort.
Comparison of the ASD and control group during the first 3.5 years of life showed no major differences in stool colour or consistency, or in frequency of diarrhoea, constipation, bloody stools or abdominal pain. The ASD children had similar stool frequency up to 18 months, but there was a trend for ASD children to pass more stools at 30 months (OR 3.73, 95% CI 1.11 to 12.6; p = 0.004) and at 42 months (OR 6.46, 95% CI 1.83 to 22.7; p<0.001), although only three children passed more than 4 stools/day. Repeating the analysis on only those cases diagnosed as having classical childhood autism resulted in very similar findings.
During the first 42 months of life, ASD children had a stool pattern that was very similar to that of other children, apart from a slight increase in stool frequency at 30 and 42 months. There were no symptoms to support the hypothesis that ASD children had enterocolitis.
To evaluate potential markers of serious bacterial infection (SBI) in infants under 3 months of age presenting with fever of unknown origin.
We retrospectively studied all infants under 3 months of age seen in the emergency department between January 2004 and December 2006 for a febrile syndrome with no identifiable focus. Clinical data, procalcitonin (PCT), C reactive protein (CRP) and leucocyte count were evaluated for their ability to discriminate between SBI and non-SBI; receiver operating characteristic (ROC) curves were constructed for the laboratory markers and analysis was performed by multivariate logistic regression.
The sample comprised 347 patients (23.63% with SBI). Mean PCT, CRP, leucocyte and neutrophil count were significantly higher in the group with SBI unlike the other criteria studied. The area under the ROC curve (AUC) for PCT was 0.77 (95% CI 0.72 to 0.81) and 0.79 for CRP (95% CI 0.75 to 0.84); both these variables were stronger predictors than leucocyte count (0.67, 95% CI 0.63 to 0.73). In the 15 infants with more invasive bacterial infections (sepsis, bacteraemia, bacterial meningitis), the diagnostic value of PCT (AUC 0.84, 95% CI 0.79 to 0.88) was higher than CRP (AUC 0.68, 95% CI 0.63 to 0.73). In infants who had been febrile for under 12 h, the differences between PCT, CRP and leucocyte count were statistically significant in both SBI and non-SBI groups, with increasing predictive value of PCT and decreasing value of CRP.
PCT, CRP, and leucocyte count have intrinsic predictive value for SBI in febrile infants under 3 months of age. The diagnostic value of PCT is greater than CRP for more invasive bacterial infections and for fever of short duration.
Pulmonary arterial hypertension (PAH) has been linked to mutations in genes encoding two members of the transforming growth factor-β family, BMPR2 and ALK1, the latter of which is also associated with hereditary haemorrhagic telangiectasia (HHT). Relatively little is known about the genetics of childhood PAH, or about the clinical features of PAH in young patients with an ALK1 mutation.
Three individuals diagnosed with PAH at 4, 16 and 17 years of age were found on subsequent genetic screening to have non-synonymous mutations of ALK1. All probands met criteria for HHT, although two presented with PAH before HHT was diagnosed. Extended family history revealed relatives with HHT in all three kindreds, a presumptive family history of PAH in two, one with multiple family members dying from PAH at young ages. All three patients in this series had systemic or suprasystemic right ventricular pressure and significantly elevated pulmonary vascular resistance, initially not responsive to oxygen and/or inhaled nitric oxide. All patients had pulmonary arteriovenous malformations and systemic arterial desaturation.
This report highlights ALK1 mutations associated with a variable PAH phenotype, including pulmonary arteriovenous malformations and severe PAH presenting early in life. Echocardiographic screening for elevated right ventricular pressure may be indicated in patients with HHT, particularly those with an identified ALK1 mutation. Clinical features or a family history of HHT should be elicited in children and adolescents with idiopathic PAH; ALK1 screening may be appropriate when such features are present.
Few studies have reported on nutritional recovery, survival and growth among severely malnourished children with HIV. This study explores nutritional recovery in HIV-infected and HIV-uninfected children during inpatient nutrition rehabilitation and 4 months of follow-up.
Prospective cohort study.
Lilongwe district, Malawi.
Weight gain, anthropometrics.
In our sample of 454 children with severe acute malnutrition (SAM), 17.4% (n = 79) of children were HIV infected. None of the children were on antiretroviral therapy upon admission. Among the HIV-infected children, 35.4% (28/79) died, compared with 10.4% (39/375) in HIV-uninfected children (p<0.001). All children who survived achieved nutritional recovery (>85% weight for height and no oedema), regardless of HIV status. HIV-infected children had similar weight gain to HIV-uninfected children (8.9 vs 8.0 g/kg/d, not significant (NS)). Mean increases in z-scores for both subscapular (2.72 vs 2.69, NS) and triceps (1.26 vs 1.48, NS) skinfolds were similar between HIV-infected and HIV-uninfected children, respectively, during nutrition rehabilitation. 362 children were followed for 4 months, at which time mean weight for height z-score was similar in HIV-infected and HIV-uninfected children (–0.85 vs –0.64, NS).
HIV-infected children with SAM have higher mortality rates than HIV-uninfected children. Among those who survive, however, nutritional recovery is similar in HIV-infected and HIV-uninfected children.
There is limited literature describing dental admissions in preschool children. This paper describes dental hospital admissions and associated factors in children aged under 5 years.
This study uses total population data for Western Australia, which link midwives’ information with birth defects, intellectual disability, hospital admissions and deaths. Children born 1980–1995 (n = 383 665) were followed until 5 years. Intellectual disability data were available for children born between 1983 and 1992. Admission data including length of stay were examined.
Admissions for each relevant 9th Revision of the International Classification of Diseases, Clinical Modification (ICD-9) principal diagnosis category and factors associated with having had a dental admission (all categories) and ICD-9 521 (mostly caries) in particular were investigated.
There were 11 523 dental admissions involving 10 493 children. Of all dental admissions, 76% were in ICD-9 category 521, which included admissions for dental caries. After adjusting for confounders, children with intellectual disability (odds ratio 1.92; 95% CI 1.63 to 2.27) and birth defect 1.85 (1.68 to 2.05) were more likely to have had a dental admission. Children living in a region without fluoridated water were also more likely to have had a dental admission 2.16 (1.94 to 2.40). Males were more likely to have had a dental admission 1.16 (1.08 to 1.25), as were children with an indigenous mother 1.17 (1.02 to 1.34). Investigation of ICD-9 521 admissions showed associations similar to those described above except for mother being indigenous, which was associated with reduced likelihood of admission.
Given the burden of dental admissions in young children, these findings highlight the need for improved oral care for children.
This article explores gender in relation to Scottish child injury mortality over time.
Injury mortality data for children aged 0–14 years in Scotland were obtained from the General Register Office for Scotland. The study period was 1982–2006 inclusive. Data were analysed in terms of age, gender, year of death and cause of death. Age-adjusted injury mortality rates, male:female (m:f) ratios and temporal trends were calculated.
Scotland, UK.
Children, aged 0–14 years, resident in Scotland, who died from injury during the study period.
There was an overall significant male excess (m:f ratio 1.70). Boys were significantly more likely to die from injuries in all age groups except infancy (m:f ratio 1.20, 1.32, 2.09, 2.09 in age groups <1, 1–4, 5–9 and 10–14 years). For childhood as a whole, the most gender-related fatal injury causes were poisoning (m:f ratio 3.21), falls (m:f ratio 2.75), suicide (m:f ratio 2.19), drowning and suffocation (m:f ratio 2.09), pedestrian (m:f ratio 1.72) and road traffic injuries (m:f ratio 1.65). The only cause that did not show a significant m:f ratio was fire. The male excess declined markedly over time.
The gender pattern of child injury mortality in Scotland is highly variable and changing over time to the point where the previous male excess has almost disappeared in some age and cause categories. The overall male excess in child injury mortality has, however, remained consistent over time although the trend is downwards and converging. These findings are largely unexplained.
Congenital valvular aortic stenosis is a common congenital heart malformation. The rate of progression in childhood, however, remains to be established. We assessed the progression of peak aortic velocity before intervention as well as the frequency of intervention in paediatric patients with isolated congenital valvular aortic stenosis.
A retrospective cohort study was performed in 245 consecutive patients with aortic stenosis. Both clinical and echocardiographic data were obtained.
Over a period of 9.0 (SD 5.2) years (range 0.1–19.4), the mean annual increase in peak systolic velocity was 0.04 m/s/year (95% CI 0.028 to 0.056 m/s/year; p<0.001) as shown by ANOVA. 40 patients underwent a cardiac intervention shortly after their first echocardiogram. Another 33 patients underwent intervention during follow-up. Interventions were performed significantly more often in patients diagnosed at a younger age and/or with a higher peak velocity at diagnosis (p<0.001). Mortality was considerable in those diagnosed in infancy (5-year survival rate of 73% (SD 9%), whereas it was nearly absent in patients diagnosed after infancy. Most patients who died during infancy had progressive left ventricular dysfunction despite adequate relief of left ventricular outflow obstruction.
Valvular aortic stenosis in the paediatric age group usually has a good prognosis beyond the neonatal period. Progression over time is usually limited, although a considerable proportion of patients need intervention shortly after initial diagnosis. Mortality, except for the neonatal age group, is nearly absent.
Inhaled corticosteroids (ICS) are commonly used to treat wheezing disorders in children, but few studies have investigated the effect of ICS on lung function in infants. We evaluated the efficacy of inhaled budesonide for decreased specific airway conductance (sGaw) as an indication of bronchial obstruction in very young children with recurrent cough and/or wheeze.
Functional residual capacity (FRC) and sGaw of steroid-naive children aged 3–26 months with respiratory symptoms were measured using an infant whole-body plethysmograph. Clinically indicated bronchoscopy was performed in 79% of the patients to exclude anatomical abnormalities before randomisation. Children with abnormal lung function and respiratory symptoms were randomised into two treatment groups, receiving either inhaled budesonide (400 µg/day) or placebo with NebuChamber for 6 weeks. Inhaled terbutaline 0.25 mg/dose was used as a rescue medication. Lung function measurements were repeated after 6 weeks.
Lung function.
44 children with a median age of 11.3 months (range 3.7–25.9) completed the study. Median sGaw improved from a z score of –3.6 to –1.2 (p<0.001) in the budesonide group and from –3.2 to –2.6 (p = 0.033) in the placebo group; between group difference p = 0.014. Improvement in sGaw was more pronounced in children with atopy (p = 0.017). Symptom-free days increased in both the budesonide and placebo groups with no difference between groups.
Treatment with inhaled budesonide for 6 weeks improved sGaw in young children with chronic cough or wheeze and bronchial obstruction.
At least 5% of paediatric admissions are complicated by medication error. Nurses can prevent some errors by correctly verifying prescriptions before administering drugs, which requires adequate drug calculation skills and familiarity with the BNFc. We wished to explore whether a newly devised chart would improve nurses’ dose calculation ability and thus potentially reduce doctors’ prescription errors.
To explore nurses’ ability to calculate doses of gentamicin for neonates and children using a new simple dosing chart compared with the BNFc.
Two gentamicin dosing charts (paediatric and neonatal) devised by a multidisciplinary group to simplify dose calculation and selection of frequency were compared with the BNFc using four questions (two neonatal, two paediatric) asking ward nurses to calculate gentamicin doses. Answers were scored for both the correct dosage and correct frequency.
51 nurses participated. 11 nurses (22%) answered all four questions correctly. A higher proportion correctly answered both the dosage and frequency questions simultaneously when using the chart compared with the BNFc: paediatric questions 100% (51/51 chart) versus 80% (41/51 BNFc) (OR 0.20) and neonatal questions 55% (28/51 chart) versus 35% (18/51 BNFc) (OR 0.2). Errors when using the BNFc were due to selection of the incorrect regimen (23%), wrong frequency (17%) and one 10-fold dosing error. When using the chart, there were no dosing errors, only frequency errors for the neonatal regimen.
The chart was more reliable, quicker and may be useful for patient safety. Revising the format of the BNFc may be beneficial for nurses.
To determine whether age is associated with serious spinal injury in paediatric motor vehicle occupants, after controlling for crash-related factors.
Retrospective record review.
All motor vehicle passengers aged 0–16 years treated at two major children’s hospitals from 1999 to 2004 with ICD-10 codes for spinal trauma. Injury outcomes were categorised as minor and serious. Minor injuries were analogous to AIS 1 injuries. Serious injuries were those that posed some risk to the integrity of the spinal column or cord.
72 cases were identified (58 <12 years of age, 14 >=12 years of age). Using logistic regression to adjust for confounders, including crash severity and crash type, age <12 years was found to be significantly associated with serious spinal injury. Compared to older children, children aged less than 12 years were more likely to sustain serious spinal injury (OR 7.1, 95% CI 1.2 to 42.9).
Children up to age 12 have an elevated risk of serious spinal injury in car crashes. This age breakpoint may reflect the adequacy of seat belt fit, and use of adult seatbelts alone before age 12 may increase a child’s risk of serious spinal injury. An association between age and serious spinal injury should also be considered in the triage of paediatric motor vehicle occupants.
To identify infants with early weight faltering at the 6–8-week check and examine their family circumstances, feeding and behavioural development.
Over a 2-year period, the weight gain of all infants born in an area of North East England was screened. z Scores for weights at birth and at 6–8 weeks were used to calculate a "thrive index" (z score for weight gain). In a nested case–control study within the larger cohort, infants below the fifth centile on the thrive index were identified. 74 cases and 86 controls were followed up. Their development was assessed at 4 and 9 months using the Bayley Scales and their mothers interviewed.
Of 1996 infants, weights at birth and at 6–8 weeks were available for 1880 (94%), and 6.1% of term-born infants were identified as weight faltering over the first 6–8 weeks. These infants had more feeding problems and showed some developmental delay as assessed using the Bayley Scales (at 4 months, mean difference and 95% CI –3.5, –0.6 to –6.4 for the Mental Developmental Index (MDI) and –3.6, –0.2 to – 6.9 for the Psychomotor Developmental Index (PDI); at 9 months –2.3, 1.3 to –5.8 for MDI and –2.2, 2.5 to –7.0 for PDI). Their families were not significantly different from those of controls on any economic or educational measure.
Infants whose early weight gain is slow show more feeding problems than controls, and some developmental delay. They can be identified using a thrive index at the 6–8-week check.
Bannayan–Riley–Ruvalcaba syndrome (BRRS) is an autosomal dominant condition characterised by macrocephaly, developmental delay and subtle cutaneous features. BRRS results from mutations in the PTEN gene. In adults, PTEN mutations cause Cowden syndrome where, in addition to the macrocephaly, there is a higher risk of tumour development. Diagnosis of BRRS is often delayed as presentation can be variable, even within families.
To identify characteristics of this condition which might facilitate early diagnosis. Prompt diagnosis not only avoids unnecessary investigations in the child but potentially identifies heterozygote parents who are at risk of tumour development.
Six children with a PTEN mutation were identified. All had extreme macrocephaly. Four parents and a male sibling were found to have a PTEN mutation on subsequent testing. Affected parents had extreme macrocephaly and a history of thyroid adenoma, or breast or skin lesions. All six children had presented to medical attention before the age of 2.5 years (3/6 were investigated as neonates), but the median age at diagnosis was 5 years. Four of the children had multiple investigations prior to identification of a PTEN mutation.
BRRS should be considered in children with extreme macrocephaly as it is the most consistent clinical feature seen, particularly where there is a family history of macrocephaly.