Hypocalcemia is a laboratory and clinical abnormality that is observed with relative frequency, especially in neonatal pediatric

patients. Laboratory hypocalcemia is often asymptomatic, and its treatment in neonates is controversial. However, children
with hypocalcemia in pediatric intensive care units (PICUs) have mortality rates higher than those of children with normal calcium
levels. (See Prognosis, Clinical, Workup, and Treatment.)
Hypocalcemia is defined as a total serum calcium concentration of less than 2.1 mmol/L (8.5 mg/dL) in children, less than 2 mmol/L
(8 mg/dL) in term neonates, and less than 1.75 mmol/L (7 mg/dL) in preterm neonates.
Calcium metabolism and function
Calcium is the most abundant mineral in the body. Of the body's total calcium, 99% is in bone, and serum levels constitute less than
[1]
1%. Various factors regulate the homeostasis of calcium and maintain serum calcium within a narrow range. These include
parathormone (PTH), vitamin D, hepatic and renal function (for conversion of vitamin D to active metabolites), and serum phosphate
and magnesium levels. (See Etiology and Workup.)
Although total serum calcium levels are often measured and reported, ionized calcium is the active and physiologically important
component. Total calcium level includes the ionized fraction and the bound fraction. The ionized calcium level is affected by the
albumin level, blood pH, serum phosphate, serum magnesium, and serum bicarbonate and may be reduced by exogenous factors
that may bind calcium, such as citrate from transfused blood or free fatty acids from total parenteral nutrition. At a physiologic pH of
7.4, 40% of total calcium is bound to albumin; 10% is complexed with bicarbonate, phosphate, or citrate; and the remaining 50%
exists as free ionized calcium. The normal range for ionized calcium is 1-1.25 mmol/L (4-5 mg/dL).
The concentration of calcium in the serum is critical to many important biologic functions, including the following:

Calcium messenger system by which extracellular messengers regulate cell function

Activation of several cellular enzyme cascades
Smooth muscle and myocardial contraction
Nerve impulse conduction
Secretory activity of exocrine glands
Hypoglycemia is the most common metabolic problem in neonates. In children, a blood glucose value of less than 40 mg/dL (2.2
mmol/L) represents hypoglycemia. A plasma glucose level of less than 30 mg/dL (1.65 mmol/L) in the first 24 hours of life and less
than 45 mg/dL (2.5 mmol/L) thereafter constitutes hypoglycemia in the newborn.
Patients with hypoglycemia may be asymptomatic or may present with severe central nervous system (CNS) and cardiopulmonary
disturbances. The most common clinical manifestations can include altered level of consciousness, seizure, vomiting,
unresponsiveness, and lethargy. Any acutely ill child should be evaluated for hypoglycemia, especially when history reveals
diminished oral intake. (See History and Physical Examination.)
Sustained or repetitive hypoglycemia in infants and children has a major impact on normal brain development and function.
Evidence suggests that hypoxemia and ischemia potentiate hypoglycemia, causing brain damage that may permanently impair
neurologic development. (See Prognosis.)
Causes of hypoglycemia in neonates differ slightly from those in older infants and children. The causes in neonates include the
following (see Etiology):

Inappropriate changes in hormone secretion

Inadequate substrate reserve in the form of hepatic glycogen
Inadequate muscle stores as a source of amino acids for gluconeogenesis
Inadequate lipid stores for the release of fatty acids
Hyperinsulinism, or persistent hyperinsulinemic hypoglycemia of infancy (PHHI), is the most common cause of hypoglycemia in the
first 3 months of life. It is well recognized in infants of mothers with diabetes. (See Etiology.)
Causes of hypoglycemia found in all ages include gram-negative sepsis, endotoxin shock, and ingestions, including of salicylates,
alcohol, hypoglycemic agents, or beta-adrenergic blocking agents.
Excluding insulin therapy, almost all hypoglycemia in childhood occurs during fasting. Postprandial hypoglycemia is rare in children in
the absence of prior gastrointestinal (GI) surgery. Management efforts are directed toward the immediate normalization of glucose
levels and the identification and treatment of the various causes. (See Treatment and Medications.)
Patient education
Provide genetic counseling for families with affected children, including information about a possible 25% risk of recurrence. Educate
pregnant women with diabetes.

Glucose metabolism
Normal blood glucose is very narrowly regulated, usually from 80-90 mg/dL (4.4-5 mmol/L). Glucose levels increase transiently after
meals to 120-140 mg/dL (6.6-7.7 mmol/L). Feedback systems return the glucose concentration rapidly back to the preprandial level,
usually within 2 hours after the last absorption of carbohydrates.
Insulin and glucagon are the important hormones in the immediate feedback control system of glucose. When blood glucose
increases after a meal, the rate of insulin secretion increases and stimulates the liver to store glucose as glycogen. When cells
(primarily liver and muscle) are saturated with glycogen, additional glucose is stored as fat.
When blood glucose levels fall, glucagon secretion functions to increase blood glucose levels by stimulating the liver to undergo
glycogenolysis and release glucose back into the blood. (See the diagram below.)
In starvation, the liver maintains the glucose level via gluconeogenesis. Gluconeogenesis is the formation of glucose from amino
acids and the glycerol portion of fat. Muscle provides a store of glycogen and muscle protein breaks down to amino acids, which are
substrates utilized in gluconeogenesis in the liver. Circulating fatty acids are catabolized to ketones, acetoacetate, and Bhydroxybutyrate and can be used as auxiliary fuel by most tissues, including the brain.
The hypothalamus stimulates the sympathetic nervous system, and epinephrine is secreted by the adrenals, causing the further
release of glucose from the liver. Over a period of hours to days of prolonged hypoglycemia, growth hormone and cortisol are
secreted and decrease the rate of glucose utilization by most cells of the body.
In the newborn, serum glucose levels decline after birth until age 1-3 hours, then they spontaneously increase. Liver glycogen stores
become rapidly depleted within hours of birth, and gluconeogenesis, primarily from alanine, can account for 10% of glucose
turnover in the newborn infant by several hours of age.
A new way to detect gestational diabetes mellitus
At first glance, screening pregnant women for gestational diabetes mellitus (GDM) seems like it should be straightforward. After all,
the tests are designed to identify pregnant woman with high concentrations of glucose (sugar) in their blood and laboratory tests
that measure glucose are accurate and precise. So whats the problem?
For one, experts dont agree on how best to screen pregnant women for GDM. While nearly everyone agrees that both mom and
baby can have adverse outcomes if GDM goes undetected and untreated, there is lack of consensus on the best way of identifying
GDM.
Consider how it has been done for several years here in the United States using either a 1 or 2 step process. In the 2-step approach,
a screening test is done first followed by a diagnostic test if the screening test is abnormal. To do the screening test, blood glucose is
measured 1 hour after the non-fasting patient drinks a 50-gram dose of glucose. A glucose result that is greater than 140 mg/dL is
usually used as the cutoff although a lower cutoff of 130 mg/dL is also used (again, no consensus). A woman that has an abnormal
screening test (i.e. glucose concentration greater than the cutoff) will go on to have the diagnostic test. In the 1-step approach the
screening test is skipped completely and only the diagnostic test is performed.
The test used to diagnose GDM is the oral glucose tolerance test (OGTT). The OGTT requires women to be fasting and then drink
either a 75- or a 100-gram dose of glucose. Blood samples are collected every hour for 2 or 3 hours if using the 75- or 100-gram
dose, respectively. The test is considered positive, and GDM confirmed, if 2 or more of the glucose results are above designated
cutoffs (which differ depending upon the glucose dose given).
Now, new criteria have recently been advocated.
The International Association of Diabetes in Pregnancy Study Groups (IADPSG) has maderecommendations for glucose tolerance
testing in pregnancy based on the results of theHyperglycemia and Adverse Outcomes (HAPO) study. That study clearly
demonstrated that the risks of adverse maternal and fetal outcomes continually increase as maternal glucose concentrations
increased. Importantly, the relationship between glucose concentration and risks were continuous. That is, there were no obvious
glucose cutoffs above which risks increased. The new recommendations from the IADPSG address this issue.
The IADPSG advocates for the use of the 75-gram OGTT in pregnant women between 24 and 28 weeks gestation. The test is
performed following an overnight fast of at least 8 hours and blood is collected at 1 and 2 hours after the glucose load. A diagnosis
of GDM is made when any of the following glucose results are met:

Fasting: greater or equal to 92 mg/dL

1 hour: greater or equal to 180 mg/dL

2 hour: greater or equal to 153 mg/dL

A couple of questions are called for here:

1.

Why were those cutoff selected? These are the glucose concentrations above which the adverse risks of hyperglycemia were
1.75-fold higher than for women whose glucose results were lower. Other thresholds were considered but higher cutoffs missed
lots of women with adverse pregnancy outcomes and lower cutoffs identified 25% of women as having GDM.

2.

What is the impact will this test have on the prevalence of GDM? It will definitely increase. Currently, about 7% of pregnant
women are diagnosed with GDM in the US each year. Using the IADPSG approach that will more than double to about 18% of
pregnant women.
Although the American Diabetes Association adopted the IAPDSG criteria and recommends that approach to identifying women with
GDM, it does recognize that there is the potential for harm. For example, more interventions such as earlier delivery and increased
C-section rates are likely to occur due to the increase in the prevalence of GDM. Also, an increased number of women being
diagnosed with GDM will be accompanied by a rise in health care costs. Despite those considerations, the ADA supports the new
criteria in light of the increased rates of obesity and diabetes throughout the US and the world.
Birth weight is the body weight of a baby at its birth.

[1]

There have been numerous studies that have attempted, with varying degrees of success, to show links between birth weight and
later-life conditions, including diabetes, obesity, tobacco smoking and intelligence.
Determinants[edit]
There are basically two distinct determinants for birth weight:

The duration of gestation prior to birth, that is, the gestational age at which the child is born

The prenatal growth rate, generally measured in relation to what weight is expected for any gestational age.
The incidence of birth weight being outside what is normal is influenced by the parents in numerous ways, including:

Genetics
The health of the mother, particularly during the pregnancy
[2]
Environmental factors, including exposure of the mother to secondhand smoke
Economic status of the parents gives inconsistent study findings according to a review on 2010, and remains speculative as a
[3]
determinant.
Other factors, like multiple births, where each baby is likely to be outside the AGA, one more so than the other
Abnormalities[edit]
A low birth weight can be caused either by a preterm birth (low gestational age at birth) or of the infant being small for gestational
age (slow prenatal growth rate), or a combination of both.
A very large birth weight is usually caused by the infant having been large for gestational age
Influence on adult life[edit]
Studies have been conducted to investigate how a person's birth weight can influence aspects of their future life. This includes
theorised links with obesity, diabetes and intelligence.
Obesity[edit]
A baby born small or large for gestational age (either of the two extremes) is thought to have an increased risk of obesity in later
[4][5]
[6]
life,
but it was also shown that this relationship is fully explained by maternal weight.
GH therapy at a certain dose induced catch-up of lean body mass (LBM). However percentage body fat decreased in the GH-treated
subjects. Bone mineral density SDS measured by DEXA increased significantly in the GH-treated group compared to the untreated
subjects, though there is much debate over whether or not SGA (small for gestational age) is significantly adverse to children to
[7]
warrant inducing catch-up.
Diabetes[edit]
Babies that have a low birth weight are thought to have an increased risk of developing type 2 diabetes in later life.

[8][9][10]

Intelligence[edit]
Some studies have shown a direct link between an increased birth weight and an increased intelligence quotient.
birth weight is also linked to greater risk of developing autism.

[11][12][13]

Increased