Indian pediatrics最新文献

Context: Heel prick is one among the common painful procedures in neonates. We performed a systematic review and network meta-analysis (NMA) to compare the efficacy of different interventions for analgesia during heel prick in neonates.

Evidence acquisition: Medline, Cochrane, Embase and CINAHL databases were searched from inception until February 2023. Randomized and quasi-randomized trials that evaluated different pharmacological and non-pharmacological interventions for analgesia during heel prick for neonates were included. Data from the included trials were extracted in duplicate. A NMA with a frequentist random-effects model was used for data synthesis. Certainty of evidence (CoE) was assessed using GRADE. We adhered to the PRISMA-NMA guidelines.

Results: One-hundred-and-three trials comparing 51 different analgesic measures were included. Among the 38 interventions, for pain "during" heel prick, non-nutritive suckling (NNS) plus sucrose [SMD -3.15 (-2.62, -3.69)], followed by breastfeeding, glucose, expressed breast milk (EBM), sucrose, NNS and touch massage, had a high certainty of evidence (CoE) to reduce pain scores when compared to no intervention. Among the 23 interventions for pain at 30 seconds after heel-prick, moderate CoE was noted for facilitated tucking plus NNS plus music, glucose, NNS plus sucrose, sucrose plus swaddling, mother holding, EBM, sucrose and NNS.

Conclusions: Oral sucrose 2 minutes before combined with NNS during the procedure, was the best intervention for reducing pain during heel prick. It also effectively reduced pain scores 30 seconds and 1 minute after the procedure. Other interventions with moderate to high CoE for a significant reduction in pain during and at 30 seconds after heel prick are oral sucrose, oral glucose, EBM and NNS. All these are low-cost and feasible interventions for most of the settings.

Objective: To estimate the change in serum hepcidin levels and its correlation with change in hemoglobin (Hb) level during the initial two weeks of oral iron therapy in children with iron deficiency anemia (IDA).

Methods: A prospective observational study was carried out in children aged 2-12 years with IDA. Children with severe anemia (Hb < 7 g/dL), those with fever, infections, history of oral iron intake or blood transfusion within the preceding three months, or intolerant to oral iron were excluded. Serum hepcidin-25 was assessed using ELISA-based kits on day 0 (pre-therapy), after 24 hours and 14 days of starting oral iron therapy.

Results: Out of 78 children who were screened, we included 64 children with IDA with a mean (SD) hemoglobin of 8.81 (1.22) g/dL. The baseline mean (SD) serum hepcidin-25 levels [7.81 (4.88) ng/mL] increased significantly to 8.38 (4.96) ng/mL at 24 hours and 9.51 (5.2) ng/mL on day 14 of oral iron therapy (P < 0.001). 63 children showed a good response to oral iron therapy. No significant correlation was observed between baseline hepcidin levels with change in hemoglobin on day 1 (r = -0.10, P = 0.40) or day 14 (r = -0.10, P = 0.43) of therapy.

Conclusion: Serum hepcidin levels rise significantly as early as 24 hours after starting oral iron therapy and should be explored to assess response to oral iron therapy in children with anemia.

Objective: To determine the normative values of cerebral blood flow (CBF) velocities in very low birth weight (VLBW) neonates during the first 28 days of life.

Method: In this prospective observational study, doppler assessment of CBF velocities was performed from the anterior cerebral artery (ACA), middle cerebral artery (MCA) and basilar artery (BA) at 2-8 hours, 24 hours, day 3, 7, 14 and 28 of life. Neonates with gross congenital malformations, those requiring extensive resuscitation at birth, mechanical ventilation with mean airway pressure >12 mbar, requiring inotropes, or those who developed intraventricular hemorrhage (grade II or more) were excluded.

Results: A total of 103 VLBW neonates were enrolled, in whom 1178 doppler measurements were recorded. The mean (SD) peak systolic velocity, end diastolic velocity and mean velocity (cm/s) in ACA increased from 26.53 (8.56) to 51.35 (9.36), 9.22 (2.91) to 13.9 (3.24) and 17.75 (3.97) to 25.84 (3.27) respectively from 2 to 8 hours to day 28 of life. In MCA and BA also, CBF velocities increased with post-natal age.

Conclusion: We report normative data of CBF velocities in VLBW neonates in first 28 days of life.

Objective: To describe the clinical profile and determine the factors affecting mortality of children admitted with adenovirus infection in a tertiary care centre in South India.

Methods: In this observational study, respiratory specimens (nasopharyngeal swab / endotracheal aspirate) were collected from all hospitalized pediatric patients presenting with fever, cough, breathlessness, gastrointestinal symptoms, unexplained encephalopathy or multisystem involvement, between February 2023 and August 2023. Infection with adenovirus was determined by viral pathogen panel based on polymerase chain reaction (PCR) technique. Those referred from elsewhere with positive adenovirus report but non-availability of treatment details and children with coinfections were excluded. The clinical and laboratory profile of children with adenovirus infection were collected and predictors for in-hospital mortality were determined by logistic regression analysis.

Results: Out of 527 children who were screened, 130 children with a median (IQR) age of 18 (10, 48) months, had adenovirus infection. 84.5% were aged below 5 years. 62 (41.33%) children required intensive care admission. Abnormal chest radiograph, multisystem involvement and non-respiratory illness were present in 90 (69.2%), 97 (74.62%) and 26 (20%) children. Complications included acute respiratory distress syndrome (n = 8), hemophagocytic lymphohistiocytosis (n = 7), left ventricular dysfunction (n = 11), acute liver cell failure (n = 7), acute kidney injury (n = 13), and multiorgan dysfunction (n = 16). Overall mortality was 13%. Acute kidney injury, left ventricular dysfunction and pancytopenia were identified as factors that may be significantly associated with death.

Conclusion: Multisystem involvement was observed in majority of children presenting with adenovirus infection. Non respiratory presentation is seen in a fifth of children with adenovirus infection.

Objective: To assess the prevalence and predictors of splenic dysfunction in children with sickle cell disease (SCD).

Methods: A cross-sectional study was conducted between June 2019 and December 2020 where children aged 1 to 15 years of age with SCD were screened for splenic dysfunction. Children who were splenectomised, those with other diseases known to affect splenic function like congenital malformations, immunodeficiencies, and chronic diseases like tuberculosis, nephrotic syndrome, diabetes mellitus, chronic liver disease, celiac disease or malignancy were excluded. Splenic size was assessed by clinical examination and ultrasonography. Splenic dysfunction was assessed by Technetium-99m (99mTc) labeled autologous RBCs and by the presence of Howell Jolly bodies in the peripheral smear. Laboratory and clinical predictors of splenic dysfunction were assessed by multiple logistic regression.

Results: We evaluated 66 children with SCD with a mean (SD) age of 7.41 (3.3) years. Impaired and absent splenic function as assessed by 99mTc scintigraphy was found in 13 (19.7%), and 3 (4.6%) children, respectively. Howell Jolly bodies in peripheral smear were found in 5 (7.5%) children; 3 of them had abnormal uptake on scintigraphy; all five had splenomegaly. Age > 5 years, > 4 episodes of vaso-occlusive crisis (VOC), > 3 hospitalization events in the past, > 5 blood transfusions, children not receiving hydroxyurea, reticulocyte count > 4%, and HbS > 70% were independent predictors of splenic dysfunction.

Conclusion: The prevalence of splenic dysfunction in children with SCD in Central India is lower than that reported from the West. The decision to start antibiotic prophylaxis can be individualized in these children.