Metabolic and endocrine disorders

Hawdon, Jane; Cheetham, Tim; Schenk, Daniel; Wraith, J. E.; Jones, Simon A.; Bishop, Nick

doi:10.1016/b978-0-7020-3479-4.00035-0

Cited by 5 publications

(12 citation statements)

References 550 publications

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“…27 The metabolism in the newborn depends greatly on the function of vital enzymes: hepatic glycogen phosphorylase for glycogenolysis, phosphoenolpyruvate carboxykinase for gluconeogenesis, and carnitine acyltransferase for ketogenesis. 8,30 Glucagon, as the major glucoregulatory hormone, induces glycogenolysis, gluconeogenesis, and ketogenesis in liver. Catecholamines, cortisol, and growth hormone do play a key role in glucose homeostasis as counter-regulatory hormones.…”

Section: Metabolic and Endocrine Adaptation At Birthmentioning

confidence: 99%

“…While on breast feeds, when blood glucose concentrations are low, these infants will have high ketone body levels and the ketone bodies function as alternative fuels, preventing neuronal injury. 8,33 Formula-fed infants generate low ketone body levels compared to breastfed infants. 34,35 Gastrointestinal adaptation at birth…”

Section: Metabolic and Endocrine Adaptation At Birthmentioning

confidence: 99%

“…The fetus has the ability to regulate its blood glucose concentration independently of maternal glucose levels and placental diffusion. 8 In placental insufficiency or maternal starvation, the fetus can activate gluconeogenesis at the expense of growth and storage. 8 On the contrary, suboptimal control of diabetes in the mother will lead to increased secretion of insulin resulting in greater than normal fetal growth.…”

mentioning

confidence: 99%

“…8 In placental insufficiency or maternal starvation, the fetus can activate gluconeogenesis at the expense of growth and storage. 8 On the contrary, suboptimal control of diabetes in the mother will lead to increased secretion of insulin resulting in greater than normal fetal growth. 6,8 A healthy fetus differs from adults in that there is a blunted insulin response to high glucose concentrations, and that insulin secretion is more sensitive to amino acids than to glucose.…”

mentioning

confidence: 99%

“…8 On the contrary, suboptimal control of diabetes in the mother will lead to increased secretion of insulin resulting in greater than normal fetal growth. 6,8 A healthy fetus differs from adults in that there is a blunted insulin response to high glucose concentrations, and that insulin secretion is more sensitive to amino acids than to glucose. 9 The fetus is less sensitive than the neonate to the glycogenolytic actions of glucagon but sensitivity increases with advancing gestational age.…”

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confidence: 99%

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Current perspectives on neonatal hypoglycemia, its management, and cerebral injury risk

Hussain¹,

Chandran²,

Rajadurai³

et al. 2015

RRN

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Glucose is an essential substrate for mammalian cells; in particular, the brain needs glucose continuously as a primary source of energy. Hypoglycemia is the most common biochemical finding in the neonatal period. However, despite the common occurrence, there is still controversy on the definition of hypoglycemia in the newborn period. This has led to the development of guidelines designed to identify infants "at-risk" and the implementation of an "operational threshold" for physicians to consider intervention. In healthy term infants, the optimal hormonal and metabolic adaptations during the immediate neonatal period ensure an adequate energy substrate for the vital organs, whereas the abnormal glucose homeostasis observed in preterm and growth-retarded infants is multifactorial in origin. For these high-risk infants, it is important to identify, screen, and prevent significant hypoglycemia. Detailed investigations are warranted in infants with severe and persistent hypoglycemia. Neonatal hypoglycemia is a major cause of brain injury. The speculated mechanisms of cellular injury include excitatory neurotoxins active at N-methyl-D-aspartate receptors, increased mitochondrial free radical generation with initiation of apoptosis and altered cerebral energetic characteristics. This hypoglycemic brain injury predominantly affects parieto-occipital regions causing cognitive, sensory, psychomotor, and behavioral deficits in children. This state of the art review article covers the fetal-neonatal metabolic adaptation, glucose homeostasis in normal and abnormal conditions, management strategies, and late neurological sequelae of hypoglycemia.

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Section: Metabolic and Endocrine Adaptation At Birthmentioning

confidence: 99%

Section: Metabolic and Endocrine Adaptation At Birthmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Current perspectives on neonatal hypoglycemia, its management, and cerebral injury risk

Hussain¹,

Chandran²,

Rajadurai³

et al. 2015

RRN

View full text Add to dashboard Cite

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Incidence of hypoglycemia in newborn infants identified as at risk

Stärk

Simma

Blassnig-Ezeh

2019

The Journal of Maternal-Fetal & Neonatal Medicine

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Severe bilateral adrenal hemorrhages in a newborn complicated by persistent adrenal insufficiency

Zessis

Nicholas

Stone

2018

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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SummaryBilateral adrenal hemorrhages rarely occur during the neonatal period and are often associated with traumatic vaginal deliveries. However, the adrenal gland has highly regenerative capabilities and adrenal insufficiency typically resolves over time. We evaluated a newborn female after experiencing fetal macrosomia and a traumatic vaginal delivery. She developed acidosis and acute renal injury. Large adrenal hemorrhages were noted bilaterally on ultrasound, and she was diagnosed with adrenal insufficiency based on characteristic electrolyte changes and a low cortisol (4.2 µg/dL). On follow-up testing, this patient was unable to be weaned off of hydrocortisone or fludrocortisone despite resolution of hemorrhages on ultrasound. Providers should consider bilateral adrenal hemorrhage when evaluating critically ill neonates after a traumatic delivery. In extreme cases, this may be a persistent process.Learning points:Risk factors for adrenal hemorrhage include fetal macrosomia, traumatic vaginal delivery and critical acidemia.Signs of adrenal hemorrhage include jaundice, flank mass, skin discoloration or scrotal hematoma.Adrenal insufficiency often is a transient process when related to adrenal hemorrhage.Severe adrenal hemorrhages can occur in the absence of symptoms.Though rare, persistent adrenal insufficiency may occur in extremely severe cases of bilateral adrenal hemorrhage.Consider adrenal hemorrhage when evaluating a neonate for shock in the absence of an infectious etiology.

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Metabolic and endocrine disorders

Cited by 5 publications

References 550 publications

Current perspectives on neonatal hypoglycemia, its management, and cerebral injury risk

Current perspectives on neonatal hypoglycemia, its management, and cerebral injury risk

Incidence of hypoglycemia in newborn infants identified as at risk

Severe bilateral adrenal hemorrhages in a newborn complicated by persistent adrenal insufficiency

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