: Muscle weakness and wasting is increasingly recognized as a problem in children admitted to the pediatric intensive care unit (PICU). Muscle weakness and wasting could potentially affect a child’s function and development, imposing a burden on the child and their families. We aimed to summarize the literature on muscle weakness and wasting in critically ill children, discuss methods to measure muscle changes as well as areas for future research. Intensive care unit weakness in children has been reported through numerous case reports and a cohort study. These papers demonstrated that muscle weakness can be persistent in critically ill children, with reduced strength reported even after hospital discharge. A prevalence of approximately 2% has been reported in critically ill children, lower than that reported in adults. This may be related to an under-detection of muscle weakness in critically ill children, as identification of muscle weakness and wasting in critically ill children can be challenging. Some methods that have been used to assess muscle changes in critically ill children include arm muscle circumference derived from triceps skinfold thickness and upper-arm circumference, ultrasound-derived limb and diaphragm muscle size, lean body mass from bioelectrical impedance analysis. Using these methods, various patterns have been reported including increase, decrease and no change in muscle. However, studies have not explored the relationship between muscle changes and function. Evidence suggests that there is heterogeneity in the muscle changes that critically ill children may experience. Future research may need to consider differences in age, illness severity and body composition in interpreting changes in muscle size and strength in critically ill children. Importantly, understanding the role of nutrition and physical rehabilitation in relation to muscle changes and function is an important direction in optimizing long-term outcomes in critically ill children.
{"title":"Muscle weakness and wasting in pediatric critical illness","authors":"C. Ong, J. Lee, Z. Puthucheary","doi":"10.21037/PM-20-83","DOIUrl":"https://doi.org/10.21037/PM-20-83","url":null,"abstract":": Muscle weakness and wasting is increasingly recognized as a problem in children admitted to the pediatric intensive care unit (PICU). Muscle weakness and wasting could potentially affect a child’s function and development, imposing a burden on the child and their families. We aimed to summarize the literature on muscle weakness and wasting in critically ill children, discuss methods to measure muscle changes as well as areas for future research. Intensive care unit weakness in children has been reported through numerous case reports and a cohort study. These papers demonstrated that muscle weakness can be persistent in critically ill children, with reduced strength reported even after hospital discharge. A prevalence of approximately 2% has been reported in critically ill children, lower than that reported in adults. This may be related to an under-detection of muscle weakness in critically ill children, as identification of muscle weakness and wasting in critically ill children can be challenging. Some methods that have been used to assess muscle changes in critically ill children include arm muscle circumference derived from triceps skinfold thickness and upper-arm circumference, ultrasound-derived limb and diaphragm muscle size, lean body mass from bioelectrical impedance analysis. Using these methods, various patterns have been reported including increase, decrease and no change in muscle. However, studies have not explored the relationship between muscle changes and function. Evidence suggests that there is heterogeneity in the muscle changes that critically ill children may experience. Future research may need to consider differences in age, illness severity and body composition in interpreting changes in muscle size and strength in critically ill children. Importantly, understanding the role of nutrition and physical rehabilitation in relation to muscle changes and function is an important direction in optimizing long-term outcomes in critically ill children.","PeriodicalId":74411,"journal":{"name":"Pediatric medicine (Hong Kong, China)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44430185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neonatal jaundice (NJ) is one of the most common causes for medical intervention in the newborn period. While transitory hyperbilirubinemia (HB) is present in almost all newborns, detection of jaundice requires a trained observer and good lighting. Thus, jaundice in the newborn has a reported incidence between 60% to more than 90%. Bilirubin, the molecule that causes the color of jaundice, is the end product of disassembly of heme-containing molecules, primarily hemoglobin. Therefore, conditions that increase hemolysis will increase bilirubin production and cause jaundice. Common conditions in the newborn are blood group incompatibilities and congenital hemolytic anemias. A family history of NJ increases the likelihood of jaundice in the present newborn, and is one of several examples of genetic conditions that contribute. Endocrine and metabolic conditions contribute, the most common being maternal diabetes. An increased incidence is seen in infants of Southeast Asian mothers, while African infants have a lower incidence unless they suffer from G-6-PD-deficiency. Drugs taken by the mother during pregnancy may impact on hepatic metabolism of bilirubin in the newborn, often by reducing the incidence of jaundice, and the same may happen with certain drugs given to the newborn. Birth trauma, through extravasation of blood, will increase bilirubin production and jaundice. Preterm infants have immature bilirubin metabolism and a higher incidence of jaundice. Breast-fed infants have an increased incidence of jaundice, which may also last longer. Extreme NJ, associated with risk of kernicterus spectrum syndrome, has an estimated worldwide incidence of 99/100,000 or more, thus affecting 130,000 or more infants each year and calling for increased vigilance and preparedness for rapid therapeutic intervention.
{"title":"The epidemiology of neonatal jaundice","authors":"T. Hansen","doi":"10.21037/PM-21-4","DOIUrl":"https://doi.org/10.21037/PM-21-4","url":null,"abstract":"Neonatal jaundice (NJ) is one of the most common causes for medical intervention in the newborn period. While transitory hyperbilirubinemia (HB) is present in almost all newborns, detection of jaundice requires a trained observer and good lighting. Thus, jaundice in the newborn has a reported incidence between 60% to more than 90%. Bilirubin, the molecule that causes the color of jaundice, is the end product of disassembly of heme-containing molecules, primarily hemoglobin. Therefore, conditions that increase hemolysis will increase bilirubin production and cause jaundice. Common conditions in the newborn are blood group incompatibilities and congenital hemolytic anemias. A family history of NJ increases the likelihood of jaundice in the present newborn, and is one of several examples of genetic conditions that contribute. Endocrine and metabolic conditions contribute, the most common being maternal diabetes. An increased incidence is seen in infants of Southeast Asian mothers, while African infants have a lower incidence unless they suffer from G-6-PD-deficiency. Drugs taken by the mother during pregnancy may impact on hepatic metabolism of bilirubin in the newborn, often by reducing the incidence of jaundice, and the same may happen with certain drugs given to the newborn. Birth trauma, through extravasation of blood, will increase bilirubin production and jaundice. Preterm infants have immature bilirubin metabolism and a higher incidence of jaundice. Breast-fed infants have an increased incidence of jaundice, which may also last longer. Extreme NJ, associated with risk of kernicterus spectrum syndrome, has an estimated worldwide incidence of 99/100,000 or more, thus affecting 130,000 or more infants each year and calling for increased vigilance and preparedness for rapid therapeutic intervention.","PeriodicalId":74411,"journal":{"name":"Pediatric medicine (Hong Kong, China)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42461855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Constipation is a common but understudied complication in the critically ill child. Its diagnosis is frequently delayed because it is not usually considered to be such a severe complication for these patients. However, constipation has been associated with worse outcomes in critically ill adults and children. There are only few studies in critically ill children focused on epidemiology and risk factors and there are no studies about diagnostic criteria, diagnostic tests or treatments in this population. The lack of studies in this field within critically ill children contrasts with the increasing number of studies in critically ill adults during these past two decades. Constipation clinical findings in children admitted to a pediatric intensive care unit are very similar to those observed in children with functional constipation. However, these critically ill children cannot meet the diagnostic criteria for functional constipation. As there is no a standard definition, carrying out studies about this topic is quite difficult. The treatment of constipation in critically ill children includes pharmacologic and non-pharmacologic therapies but there is also little evidence about this. Polyethylene glycol and lactulose are the preferred therapeutic options but there is a broad range of different possibilities. A new research area has emerged for treatments in opioid-induced constipation.
{"title":"Constipation in the critically ill child","authors":"Jorge López, M. J. Solana, J. López‐Herce","doi":"10.21037/PM-20-63","DOIUrl":"https://doi.org/10.21037/PM-20-63","url":null,"abstract":"Constipation is a common but understudied complication in the critically ill child. Its diagnosis is frequently delayed because it is not usually considered to be such a severe complication for these patients. However, constipation has been associated with worse outcomes in critically ill adults and children. There are only few studies in critically ill children focused on epidemiology and risk factors and there are no studies about diagnostic criteria, diagnostic tests or treatments in this population. The lack of studies in this field within critically ill children contrasts with the increasing number of studies in critically ill adults during these past two decades. Constipation clinical findings in children admitted to a pediatric intensive care unit are very similar to those observed in children with functional constipation. However, these critically ill children cannot meet the diagnostic criteria for functional constipation. As there is no a standard definition, carrying out studies about this topic is quite difficult. The treatment of constipation in critically ill children includes pharmacologic and non-pharmacologic therapies but there is also little evidence about this. Polyethylene glycol and lactulose are the preferred therapeutic options but there is a broad range of different possibilities. A new research area has emerged for treatments in opioid-induced constipation.","PeriodicalId":74411,"journal":{"name":"Pediatric medicine (Hong Kong, China)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43471088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The genesis of neonatal hyperbilirubinemia is characterized by etiologic heterogeneity, environmental modulation, and the interaction of multiple gene loci. In addition to inherited hemolytic conditions, common icterogenic gene variants may act as modifiers of hyperbilirubinemia and kernicterus risk. The current review targets the effect of biologic sex, uridine diphosphate glucuronosyltransferase isoenzyme UGT1A1 gene variants of Gilbert syndrome, including their role in breastmilk jaundice, and the co-expression of icterogenic alleles have on potentiating hyperbilirubinemia risk in neonates. Notably, evidence accrued during the past two decades, from around the globe, confirm that breastmilk jaundice is a prevalent Gilbert syndrome phenotype in neonates. Moreover, novel data from humanized murine models suggest an important repressive effect of breastmilk oligosaccharides on intestinal (as opposed to hepatic) UGT1A1 expression in driving breast milk jaundice risk. More specifically, human milk oligosaccharides block intestinal Toll-like receptor activation and downstream IĸB kinase phosphorylation. This in turn represses newborn intestinal UGT1A1 activity. Formula feeding, by contrast, activates IĸB and induces intestinal (but not hepatic) UGT1A1 activity thereby lowering the total serum bilirubin (TSB). Whether this phenomenon is operative in human neonates is unclear. Although UGT1A1 is expressed in adult intestine, there are no comparable developmental data on intestinal UGT1A1 expression in the human fetus or neonate, a knowledge gap that is ripe for clinical investigation.
{"title":"The contribution of genetic factors to hyperbilirubinemia and kernicterus risk in neonates: a targeted update","authors":"J. Watchko","doi":"10.21037/PM-21-7","DOIUrl":"https://doi.org/10.21037/PM-21-7","url":null,"abstract":"The genesis of neonatal hyperbilirubinemia is characterized by etiologic heterogeneity, environmental modulation, and the interaction of multiple gene loci. In addition to inherited hemolytic conditions, common icterogenic gene variants may act as modifiers of hyperbilirubinemia and kernicterus risk. The current review targets the effect of biologic sex, uridine diphosphate glucuronosyltransferase isoenzyme UGT1A1 gene variants of Gilbert syndrome, including their role in breastmilk jaundice, and the co-expression of icterogenic alleles have on potentiating hyperbilirubinemia risk in neonates. Notably, evidence accrued during the past two decades, from around the globe, confirm that breastmilk jaundice is a prevalent Gilbert syndrome phenotype in neonates. Moreover, novel data from humanized murine models suggest an important repressive effect of breastmilk oligosaccharides on intestinal (as opposed to hepatic) UGT1A1 expression in driving breast milk jaundice risk. More specifically, human milk oligosaccharides block intestinal Toll-like receptor activation and downstream IĸB kinase phosphorylation. This in turn represses newborn intestinal UGT1A1 activity. Formula feeding, by contrast, activates IĸB and induces intestinal (but not hepatic) UGT1A1 activity thereby lowering the total serum bilirubin (TSB). Whether this phenomenon is operative in human neonates is unclear. Although UGT1A1 is expressed in adult intestine, there are no comparable developmental data on intestinal UGT1A1 expression in the human fetus or neonate, a knowledge gap that is ripe for clinical investigation.","PeriodicalId":74411,"journal":{"name":"Pediatric medicine (Hong Kong, China)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46897892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Newborn jaundice is a benign condition commonly seen in the first postnatal week of life (or the transitional period). It is primarily due to an imbalance between the rate of production of the yellow-orange pigment bilirubin and its elimination by the liver. Infants with high bilirubin production rates (such as those who are undergoing hemolysis) or with insufficient hepatic bilirubin conjugating ability [such as those with uridine 5'-diphosho-glucuronosyltransferase (UGT1A1) deficiencies] can subsequently develop excessive circulating total serum/plasma bilirubin (TB) levels or hyperbilirubinemia. Bilirubin is formed during the degradation of heme, derived from the turnover of red blood cells (RBCs). In this reaction, which is catalyzed by the rate-limiting enzyme heme oxygenase (HO), carbon monoxide (CO), iron (Fe), and bilirubin are produced in equimolar quantities. As a result, measurements of total body CO production rates can be used as indices of bilirubin production. Standard treatment strategies for hyperbilirubinemia involves the use of phototherapy (specifically narrow-band blue wavelength light) and/or exchange transfusion. However, if infants with excessive hyperbilirubinemia are not identified or treated in a timely manner, they are at risk for developing bilirubin neurotoxicity, which can manifest as bilirubin-induced neurologic dysfunction (BIND) and result in neurologic sequelae (such as acute or chronic bilirubin encephalopathy. Here, we review the biology of bilirubin production and current technologies and approaches to identify and treat these high-risk
{"title":"The biology of bilirubin production: detection and inhibition","authors":"D. K. Stevenson, R. J. Wong","doi":"10.21037/PM-21-8","DOIUrl":"https://doi.org/10.21037/PM-21-8","url":null,"abstract":"Newborn jaundice is a benign condition commonly seen in the first postnatal week of life (or the transitional period). It is primarily due to an imbalance between the rate of production of the yellow-orange pigment bilirubin and its elimination by the liver. Infants with high bilirubin production rates (such as those who are undergoing hemolysis) or with insufficient hepatic bilirubin conjugating ability [such as those with uridine 5'-diphosho-glucuronosyltransferase (UGT1A1) deficiencies] can subsequently develop excessive circulating total serum/plasma bilirubin (TB) levels or hyperbilirubinemia. Bilirubin is formed during the degradation of heme, derived from the turnover of red blood cells (RBCs). In this reaction, which is catalyzed by the rate-limiting enzyme heme oxygenase (HO), carbon monoxide (CO), iron (Fe), and bilirubin are produced in equimolar quantities. As a result, measurements of total body CO production rates can be used as indices of bilirubin production. Standard treatment strategies for hyperbilirubinemia involves the use of phototherapy (specifically narrow-band blue wavelength light) and/or exchange transfusion. However, if infants with excessive hyperbilirubinemia are not identified or treated in a timely manner, they are at risk for developing bilirubin neurotoxicity, which can manifest as bilirubin-induced neurologic dysfunction (BIND) and result in neurologic sequelae (such as acute or chronic bilirubin encephalopathy. Here, we review the biology of bilirubin production and current technologies and approaches to identify and treat these high-risk","PeriodicalId":74411,"journal":{"name":"Pediatric medicine (Hong Kong, China)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43011557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Health care for children who move in the time of COVID: lack of 1 visibility as a determinant of health","authors":"Ayesha Kadir","doi":"10.21037/PM-21-1","DOIUrl":"https://doi.org/10.21037/PM-21-1","url":null,"abstract":"","PeriodicalId":74411,"journal":{"name":"Pediatric medicine (Hong Kong, China)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48949312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Preterm infants hospitalized in the neonatal intensive care unit (NICU) often display symptoms of gastroesophageal reflux (GER). Little is known about symptoms of GER in this population after neonatal discharge. The purpose of this study was to describe symptoms of GER across the first 6 months of life in infants based on gestational age at birth and to explore factors associated with GER symptoms. Methods: This was a descriptive, cross-sectional study. Parents of 582 infants less than 6 months old participated in an online survey about their child’s symptoms of GER. Gestational age at birth, corrected age at time of study, infant sex, mode of birth, and family history of allergy were explored for their relationships to symptoms of GER. Results: Infants born at <32 weeks gestation had more symptoms of GER than infants born at later gestational ages. While full-term infants showed a decrease in symptoms across the first 6 months of life, infants born at 32–36 6/7 weeks showed no improvement, and infants born at <32 weeks gestation showed worsening symptoms over time. Infant sex and mode of birth were not associated with GER symptoms. Infants with a family history of allergy had more symptoms of GER than infants without a family history of allergy. Conclusions: Infants born prior to 32 weeks gestation experience more symptoms of GER than infants born at later gestation, with worsening of symptoms over the first 6 months of life. Preterm infants (<37 weeks gestation at birth) do not show the same improvement in symptoms over the first 6 months as full-term infants. Infants born 32 0/7–36 6/7 weeks, who may otherwise may be considered lower risk for morbidity than infants born before 32 weeks, did not experience the same improvement in symptoms over the first 6 months as full-term infants. Family history of allergy is related to increased symptoms of GER. Additional research is needed on the underlying mechanisms and evolution of GER symptoms in preterm infants.
{"title":"Preterm infants born prior to 32 weeks gestation experience more symptoms of gastroesophageal reflux in the first 6 months of life than infants born at later gestational ages","authors":"B. Pados, Grace Briceno, V. Feaster, K. Gregory","doi":"10.21037/PM-20-100","DOIUrl":"https://doi.org/10.21037/PM-20-100","url":null,"abstract":"Background: Preterm infants hospitalized in the neonatal intensive care unit (NICU) often display symptoms of gastroesophageal reflux (GER). Little is known about symptoms of GER in this population after neonatal discharge. The purpose of this study was to describe symptoms of GER across the first 6 months of life in infants based on gestational age at birth and to explore factors associated with GER symptoms. Methods: This was a descriptive, cross-sectional study. Parents of 582 infants less than 6 months old participated in an online survey about their child’s symptoms of GER. Gestational age at birth, corrected age at time of study, infant sex, mode of birth, and family history of allergy were explored for their relationships to symptoms of GER. Results: Infants born at <32 weeks gestation had more symptoms of GER than infants born at later gestational ages. While full-term infants showed a decrease in symptoms across the first 6 months of life, infants born at 32–36 6/7 weeks showed no improvement, and infants born at <32 weeks gestation showed worsening symptoms over time. Infant sex and mode of birth were not associated with GER symptoms. Infants with a family history of allergy had more symptoms of GER than infants without a family history of allergy. Conclusions: Infants born prior to 32 weeks gestation experience more symptoms of GER than infants born at later gestation, with worsening of symptoms over the first 6 months of life. Preterm infants (<37 weeks gestation at birth) do not show the same improvement in symptoms over the first 6 months as full-term infants. Infants born 32 0/7–36 6/7 weeks, who may otherwise may be considered lower risk for morbidity than infants born before 32 weeks, did not experience the same improvement in symptoms over the first 6 months as full-term infants. Family history of allergy is related to increased symptoms of GER. Additional research is needed on the underlying mechanisms and evolution of GER symptoms in preterm infants.","PeriodicalId":74411,"journal":{"name":"Pediatric medicine (Hong Kong, China)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46780573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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