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Summary: Socio‐economic deprivation is associated with adverse maternal and childhood outcomes. Epidural analgesia, the gold standard for labour analgesia, may improve maternal well‐being. We assessed the association of socio‐economic status with utilisation of epidural analgesia and whether this differed when epidural analgesia was advisable for maternal safety. This was a population‐based study of NHS data for all women in labour in Scotland between 1 January 2007 and 23 October 2020, excluding elective caesarean sections. Socio‐economic status deciles were defined using the Scottish Index of Multiple Deprivation. Medical conditions for which epidural analgesia is advisable for maternal safety (medical indications) and contraindications were defined according to national guidelines. Of 593,230 patients in labour, 131,521 (22.2%) received epidural analgesia. Those from the most deprived areas were 16% less likely to receive epidural analgesia than the most affluent (relative risk 0.84 [95%CI 0.82–0.85]), with the inter‐decile mean change in receiving epidural analgesia estimated at ‐2% ([95%CI ‐2.2% to ‐1.7%]). Among the 21,219 deliveries with a documented medical indication for epidural analgesia, the socio‐economic gradient persisted (relative risk 0.79 [95%CI 0.75–0.84], inter‐decile mean change in receiving epidural analgesia ‐2.5% [95%CI ‐3.1% to ‐2.0%]). Women in the most deprived areas with a medical indication for epidural analgesia were still less likely (absolute risk 0.23 [95%CI 0.22–0.24]) to receive epidural analgesia than women from the most advantaged decile without a medical indication (absolute risk 0.25 [95%CI 0.24–0.25]). Socio‐economic deprivation is associated with lower utilisation of epidural analgesia, even when epidural analgesia is advisable for maternal safety. Ensuring equitable access to an intervention that alleviates pain and potentially reduces adverse outcomes is crucial. [ABSTRACT FROM AUTHOR]

Background: Maternal depression and anxiety during pregnancy have been associated with offspring-attention deficit problems. Aim: We explored possible intrauterine effects by comparing maternal and paternal symptoms during pregnancy, by investigating cross-cohort consistency, and by investigating whether parental symptoms in early childhood may explain any observed intrauterine effect. Methods: This study was conducted in two cohorts (Generation R, "n" = 2,280 and ALSPAC, "n" = 3,442). Pregnant women and their partners completed questionnaires to assess symptoms of depression and anxiety. Child attention problems were measured in Generation R at age 3 with the Child Behavior Checklist, and in ALSPAC at age 4 with the Strengths and Difficulties Questionnaire. Results: In both cohorts, antenatal maternal symptoms of depression (Generation R: OR 1.23, 95% CI 1.05-1.43; ALSPAC: OR 1.33, 95% CI 1.19-1.48) and anxiety (Generation R: OR 1.24, 95% CI 1.06-1.46; ALSPAC: OR 1.32, 95% CI 1.19-1.47) were associated with a higher risk of child attention problems. In ALSPAC, paternal depression was also associated with a higher risk of child attention problems (OR 1.11, 95% CI 1.00-1.24). After adjusting for maternal symptoms after giving birth, antenatal maternal depression and anxiety were no longer associated with child attention problems in Generation R. Moreover, there was little statistical evidence that antenatal maternal and paternal depression and anxiety had a substantially different effect on attention problems of the child. Conclusions: The apparent intrauterine effect of maternal depression and anxiety on offspring-behavioural problems may be partly explained by residual confounding. There was little evidence of a difference between the strength of associations of maternal and paternal symptoms during pregnancy with offspring-attention problems. That maternal symptoms after childbirth were also associated with offspring-behavioural problems may indicate a contribution of genetic influences to the association. (Contains 2 tables.) [Additional Supporting Information is provided with the online version of this article.]

There is growing evidence that childhood IQ is inversely associated with mortality in later life. However, the specificity of this association in terms of causes of death, whether it is continuous over the whole range of IQ scores and whether it is the same according to age and sex is not clear. In a large cohort (N = 11,603) of a complete population of children born in one city in the UK in the early 1950s, IQ measured at age 7 years (using a routinely administered picture test) was found to be inversely associated with mortality between the ages of 15 and 57 years. For every 1 SD increase in IQ at 7, the all cause mortality hazard ratio was 0.79 (95% CI 0.73, 0.85). On adjustment for a range of perinatal factors, father's social class at birth, number of sibs in the household and childhood height and weight, this was attenuated slightly to 0.81 (0.74, 0.88). Almost identical associations of IQ with mortality were seen for men and women as well as at younger (15-39) and older (40+) ages. These associations were across the entire IQ range, although some of the high mortality in the lowest category of IQ (less than 70) was accounted for by causes associated with congenital disorders. Overall, external causes of death showed the strongest association, with weaker associations being seen for cancer. Further work is required to understand the mechanisms whereby childhood IQ has such a robust association with mortality in later life. (Contains 6 tables.)

Objective: To identify the clinical characteristics and patterns of ultrasound use amongst pregnancies with an antenatally unidentified small‐for‐gestational‐age (SGA) fetus, compared with those in which SGA is identified, to understand how to design interventions that improve antenatal SGA identification. Methods: This was a prospective cohort study of singleton, non‐anomalous SGA (birth weight < 10th centile) neonates born after 24 + 0 gestational weeks at 13 UK sites, recruited for the baseline period and control arm of the DESiGN trial. Pregnancy with antenatally unidentified SGA was defined if there was no scan or if the final scan showed estimated fetal weight (EFW) at the 10th centile or above. Identified SGA was defined if EFW was below the 10th centile at the last scan. Maternal and fetal sociodemographic and clinical characteristics were studied for associations with unidentified SGA using unadjusted and adjusted logistic regression models. Ultrasound parameters (gestational age at first growth scan, number and frequency of ultrasound scans) were described, stratified by presence of indication for serial ultrasound. Associations of unidentified SGA with absolute centile and percentage weight difference between the last scan and birth were also studied on unadjusted and adjusted logistic regression, according to time between the last scan and birth. Results: Of the 15 784 SGA babies included, SGA was not identified antenatally in 78.7% of cases. Of pregnancies with unidentified SGA, 47.1% had no recorded growth scan. Amongst 9410 pregnancies with complete data on key maternal comorbidities and antenatal complications, the risk of unidentified SGA was lower for women with any indication for serial scans (adjusted odds ratio (aOR), 0.56 (95% CI, 0.49–0.64)), for Asian compared with white women (aOR, 0.80 (95% CI, 0.69–0.93)) and for those with non‐cephalic presentation at birth (aOR, 0.58 (95% CI, 0.46–0.73)). The risk of unidentified SGA was highest among women with a body mass index (BMI) of 25.0–29.9 kg/m2 (aOR, 1.15 (95% CI, 1.01–1.32)) and lowest in those with underweight BMI (aOR, 0.61 (95% CI, 0.48–0.76)) compared to women with BMI of 18.5–24.9 kg/m2. Compared to women with identified SGA, those with unidentified SGA had fetuses of higher SGA birth‐weight centile (adjusted odds for unidentified SGA increased by 1.21 (95% CI, 1.18–1.23) per one‐centile increase between the 0th and 10th centiles). Duration between the last scan and birth increased with advancing gestation in pregnancies with unidentified SGA. SGA babies born within a week of the last growth scan had a mean difference between EFW and birth‐weight centiles of 19.5 (SD, 13.8) centiles for the unidentified‐SGA group and 0.2 (SD, 3.3) centiles for the identified‐SGA group (adjusted mean difference between groups, 19.0 (95% CI, 17.8–20.1) centiles). Conclusions: Unidentified SGA was more common amongst women without an indication for serial ultrasound, and in those with cephalic presentation at birth, BMI of 25.0–29.9 kg/m2 and less severe SGA. Ultrasound EFW was overestimated in women with unidentified SGA. This demonstrates the importance of improving the accuracy of SGA screening strategies in low‐risk populations and continuing performance of ultrasound scans for term pregnancies. © 2022 The Authors. Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology. [ABSTRACT FROM AUTHOR]

Background: Intermittent claudication can be neurogenic or vascular. Physicians use a profile based on symptom attributes to differentiate the 2 types of claudication, and this guides their investigations for diagnosis of the underlying pathology. We evaluated the validity of these symptom attributes in differentiating neurogenic from vascular claudication. Methods: Patients with a diagnosis of lumbar spinal stenosis (LSS) or peripheral vascular disease (PVD) who reported claudication answered 14 questions characterizing their symptoms. We determined the sensitivity, specificity and positive and negative likelihood ratios (PLR and NLR) for neurogenic and vascular claudication for each symptom attribute. Results: We studied 53 patients. The most sensitive symptom attribute to rule out LSS was the absence of 'triggering of pain with standing alone' (sensitivity 0.97, NLR 0.050). Pain alleviators and symptom location data showed a weak clinical significance for LSS and PVD. Constellation of symptoms yielded the strongest associations: patients with a positive shopping cart sign whose symptoms were located above the knees, triggered with standing alone and relieved with sitting had a strong likelihood of neurogenic claudication (PLR 13). Patients with symptoms in the calf that were relieved with standing alone had a strong likelihood of vascular claudication (PLR 20.0). Conclusion: The classic symptom attributes used to differentiate neurogenic from vascular claudication are at best weakly valid independently. However, certain constellation of symptoms are much more indicative of etiology. These results can guide general practitioners in their evaluation of and investigation for claudication. Contexte : La claudication intermittente peut avoir une etiologie neurogene ou vasculaire. Les medecins utilisent un profil fonde sur les particularites des symptomes pour distinguer l'une de l'autre et ceci oriente leur choix des methodes de diagnostic de la pathologie sous-jacente. Nous avons evalue la validite de ces particularites des symptomes utilisees pour distinguer la claudication d'origine neurogene de la claudication d'origine vasculaire. Methodes : Des patients atteints d'une stenose spinale lombaire (SSL) ou d'une maladie vasculaire peripherique (MVP) averees qui se plaignaient de claudication ont repondu a 14 questions afin de caracteriser leurs symptomes. Nous avons determine la sensibilite, la specificite et les rapports de probabilite positifs et negatifs (RPP et RPN) a l'egard de la claudication neurogene ou vasculaire pour chacune des particularites des symptomes. Resultats : Notre etude a regroupe 53 patients. La particularite des symptomes dotee de la sensibilite la plus elevee pour ce qui est d'ecarter le diagnostic de SSL a ete l'absence de <> (sensibilite 0,97; RPN 0,050). Les donnees sur ce qui soulageait la douleur et sur la localisation des symptomes ont eu une faible portee clinique en ce qui a trait a la SSL et a la MVP. La presence d'une constellation de symptomes a donne lieu aux associations les plus solides : les patients qui manifestaient un signe du <> positif et dont les symptomes etaient localises au-dessus du genou, declenches par la station debout seule et soulages en position assise presentaient une forte probabilite de claudication d'origine neurogene (RPP 13). Chez les patients dont les symptomes etaient localises au mollet et qui etaient soulages par la station debout, on notait une forte probabilite de claudication d'origine vasculaire (RPP 20,0). Conclusion : Consideres individuellement, les attributs classiques des symptomes utilises pour distinguer la claudication d'origine neurogene de la claudication d'origine vasculaire sont au mieux faiblement valides. Toutefois, certaines constellations de symptomes eclairent bien davantage l'etiologie. Ces resultats peuvent guider l'omnipraticien dans son examen et dans son diagnostic de la claudication., Intermittent claudication, recognized as pain in the legs associated with walking, is commonly reported among I elderly patients. (1-4) Two common pathologies produce intermittent claudication: lumbar spinal stenosis (LSS) resulting [...]