Dataset Information

Anatomical dimensions of the lumbar dural sac predict the sensory block level of continuous epidural analgesia during labor

ABSTRACT:

Background

The anatomical dimensions of the lumbar dural sac determine the sensory block level of spinal anesthesia; however, whether they show the same predictive value during continuous epidural anesthesia (CEA) remains undetermined. We designed the present study to verify the efficacy of the anatomical dimensions of the lumbar dural sac in predicting the sensory block level during labor analgesia.

Methods

A total of 122 parturients with singleton pregnancies requesting labor analgesia were included in this study. The lumbar dural sac diameter (DSD), lumbar dural sac length (DSL), lumbar dural sac surface area (DSA), and lumbar dural sac volume (DSV) were measured with an ultrasound color Doppler diagnostic apparatus. CEA was performed at the L2-L3 interspace. After epidural cannulation, an electronic infusion pump containing 0.08% ropivacaine and sufentanil 0.4 μg/ml was connected. The sensory block level was determined with alcohol-soaked cotton, a cotton swab, and a pinprick. The analgesic efficacy of CEA was determined with a visual analog scale (VAS). The parturients were divided into two groups, “ideal analgesia” and “nonideal analgesia,” and the groups were compared by t test. Pearson’s correlation was performed to evaluate the association between the anatomical dimensions of the lumbar dural sac and sensory block level. Multiple linear regression analysis was used to create a model for predicting the sensory block level.

Results

In the ideal analgesia group, the height, DSL, DSA, DSV and DSD were significantly smaller, and the body mass index (BMI) was significantly larger (P < 0.05). In addition, the DSL demonstrated the strongest correlation with the peak level of pain block (r = − 0.816, P < 0.0001; Fig. 2A), temperature block (r = − 0.874, P < 0.0001; Fig. 3A) and tactile block (r = − 0.727, P < 0.0001; Fig. 4A). Finally, the multiple linear regression analysis revealed that DSL and BMI contributed to predicting the peak sensory block level.

Conclusion

In conclusion, our study shows that the sensory block level of CEA is higher when the DSL, DSA, DSV and DSD of puerperae are lower. DSL and BMI can be treated as predictors of the peak sensory block level in CEA during labor analgesia.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12871-021-01485-5.

SUBMITTER: Xu C

PROVIDER: S-EPMC8567596 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ImportanceA recent cohort study found that epidural analgesia during labor was associated with an increased risk of autism in offspring.ObjectiveTo investigate if labor epidural increases the risk of autism in offspring.Design, setting, and participantsThis nationwide retrospective cohort study identified all live-born children in Denmark between January 2006 and December 2013. Follow-up commenced at children's first birthday and ended in December 2017. Among 485 093 live-born children, 5915 were excluded because of occurrences during the first year of life including death, emigration, misregistration of birth, diagnosis of disease inherently linked to autism, or diagnosis of autism.ExposuresAdministration of epidural analgesia during labor, as identified by procedure code.Main outcomes and measuresThe main outcome of interest was incident diagnosis of autism spectrum disorder based on International Statistical Classification of Diseases and Related Health Problems, 10th Revision codes in the Danish Psychiatric Central Register or National Patient Register. Hazard ratios were estimated using Cox regression, adjusted for covariates describing maternal comorbidity, sociodemographic factors, lifestyle, pregnancy, psychiatric illness, psychotropic medication, medical-seeking behavior, and family history of autism. A secondary analysis used a within-mother design including only children of mothers with both exposure and nonexposure to labor epidural analgesia in different deliveries.ResultsThe cohort included 479 178 children (233 405 girls [48.7%]; median maternal age at delivery, 30.9 [IQR, 27.6-34.2] years); of these, 92 900 (19.4%) were exposed to epidural analgesia during labor. Median follow-up was 7.0 years (IQR, 4.9-9.0 years), and by the end of follow-up, 6428 children (1.3%) had been diagnosed with autism. Exposed children had an autism diagnosis incidence rate of 23.1 per 10 000 person-years compared with 18.5 per 10 000 person-years in the unexposed group (crude hazard ratio, 1.29 [95% CI, 1.21-1.37]; adjusted hazard ratio, 1.05 [95% CI, 0.98-1.11]). A secondary within-mother analysis including 59 154 children (12.3%) estimated an autism diagnosis incidence rate of 20.8 per 10 000 person-years in the exposed group and 17.1 per 10 000 person-years in the unexposed group (adjusted hazard ratio, 1.05 [95% CI, 0.90-1.21]).Conclusions and relevanceIn this nationwide cohort study of Danish children, maternal exposure to epidural analgesia during labor was not significantly associated with autism spectrum disorder in offspring.

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Project description:ImportanceEpidural labor analgesia (ELA) has been associated with an increased offspring risk of autism spectrum disorder (ASD). Whether this finding may be explained by residual confounding remains unclear.ObjectiveTo assess the association between ELA and offspring risk of ASD.Design, setting, and participantsLongitudinal cohort study of vaginal deliveries of singleton live infants born from 2005 to 2016 from a population-based data set linking information from health care databases in Manitoba, Canada; offspring were followed from birth until 2019 or censored by death or emigration. Data were analyzed from October 19, 2020, to January 22, 2021.ExposuresEpidural labor analgesia.Main outcomes and measuresAt least 1 inpatient or outpatient diagnosis of ASD in offspring aged at least 18 months. For the full population and a sibling cohort, inverse probability of treatment-weighted Cox proportional hazards regression analyses were used to control for potential confounders.ResultsOf the 123 175 offspring included in this study (62 647 boys [50.9%]; mean [SD] age of mothers, 28.2 [5.8] years), 47 011 (38.2%) were exposed to ELA; 2.1% (985 of 47 011) of exposed vs 1.7% (1272 of 76 164) of unexposed offspring were diagnosed with ASD in the follow-up period (hazard ratio [HR], 1.25; 95% CI, 1.15-1.36). After adjusting for maternal sociodemographic, prepregnancy, pregnancy, and perinatal covariates, ELA was not associated with an offspring risk of ASD (inverse probability of treatment-weighted HR, 1.08; 95% CI, 0.97-1.20). In the within-siblings design adjusting for baseline covariates, ELA was not associated with ASD (inverse probability of treatment-weighted HR, 0.97; 95% CI, 0.78-1.22). Results from sensitivity analyses restricted to women without missing data who delivered at or after 37 weeks of gestation, firstborn infants only, and offspring with ASD classified with at least 2 diagnostic codes were consistent with findings from the main analyses.Conclusions and relevanceIn a Canadian population-based birth cohort study, no association between ELA exposure and an increased offspring risk of ASD was found.