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During the normal transition to extrauterine life, blood glucose concentration in

the healthy term newborn falls during the first one to two hours after delivery,
reaching a nadir (median concentration of approximately 55 mg/dL). It is
important to differentiate this normal physiologic transitional response from
disorders that result in persistent or recurrent hypoglycemia, which may lead to
neurologic sequelae.

Clinically significant neonatal hypoglycemia requiring intervention cannot be


defined by a precise numerical blood glucose concentration because of the
following:

some newborns become symptomatic at the same or even higher blood


glucose concentrations than are observed in asymptomatic infants.

Lack of outcome data − Ideally, clinically significant neonatal hypoglycemia


would be defined as the blood glucose concentration at which intervention
should be initiated to avoid significant morbidity, especially neurologic
sequelae. However, this definition remains elusive because the blood
glucose concentration and duration of hypoglycemia associated with poor
neurodevelopmental outcome has not been established

Hyperinsulinism — Increased glucose utilization primarily results from


hyperinsulinism. Excess insulin also suppresses hepatic glucose production. The
infant of a diabetic mother is the most common neonatal clinical situation in
which hyperinsulinism causes hyperinsulinemic hypoglycemia. In this setting, it is
postulated that intermittent maternal hyperglycemia causes fetal hyperglycemia,
which leads to hypertrophied and hyperfunctioning beta cells resulting in fetal
and neonatal hyperinsulinemia. After termination of the maternal glucose supply
at delivery, hypoglycemia from persistent hyperinsulinism in the newborn usually
is transient and typically resolves two to four days after birth

Increased glucose consumption can occur with heart failure or perinatal asphyxia

Hypoglycemia associated with polycythemia may result from greater glucose


utilization by the increased mass of red blood cells.

Asymmetric neonates with FGR have relatively large (spared) head and brain size
compared with their birth weight.

Although the mechanism is not known, sepsis is sometimes associated with


hypoglycemia.
Hypothermic infants who have increased rates of glucose utilization in an attempt
to maintain normal temperaturas

Symptomatic infants — In the symptomatic infant, signs are nonspecific


and reflect responses of the nervous system to glucose deprivation. These
can be categorized as neurogenic or neuroglycopenic findings [9]:
●Neurogenic (autonomic) symptoms result from changes due to
neural sympathetic discharge triggered by hypoglycemia.
•Jitteriness/tremors
•Sweating
•Irritability
•Tachypnea
•Pallor
●Neuroglycopenic symptoms are caused by brain dysfunction from
impaired brain energy metabolism due to a deficient glucose supply.
•Pathologic poor feeding
•Weak or high-pitched cry
•Change in level of consciousness (lethargy, coma)
•Seizures
•Pathologic hypotonia for gestational age

In newborns, additional nonspecific signs of hypoglycemia include apnea,


bradycardia, cyanosis, and hypothermia.

Risk factors that warrant routine glucose testing

 Prematurity (gestational age <37 weeks)

 Large for gestational age

 Maternal diabetes

 Small for gestational age

Blood glucose concentrations should not be measured in healthy


asymptomatic term infants born after an uncomplicated pregnancy and delivery

How glucose testing is performed — Most nurseries perform capillary blood


glucose measurements using a point of care glucose meter as a rapid screening
method. However, glucose meters show large variations in values compared with
laboratory methods, especially at low glucose concentrations, and are of
unproven reliability to document hypoglycemia in newborns

For a symptomatic infant, treatment should be started as soon as


possible after the blood sample is obtained and before confirmatory results are
available, especially for infants experiencing neuroglycopenic symptoms (ie,
pathologic poor feeding, weak or high-pitched cry, change in level of
consciousness, seizures, pathologic hypotonia for gestational age).

We use the following parameters outlined by the 2011 American Academy


of Pediatrics (AAP) clinical report and guidelines from the Pediatric
Endocrine Society to make the diagnosis of neonatal hypoglycemia
requiring medical intervention [8,9] (see "Management and outcome of
neonatal hypoglycemia"):

●Symptomatic patients (eg, jitteriness/tremors, pathological


hypotonia, changes in level of consciousness, apnea/bradycardia,
cyanosis, tachypnea, pathological poor feeding, sustained
hypothermia, and/or seizures) (see 'Clinical presentation' above):

•Who are less than 48 hours of life with plasma glucose levels <50
mg/dL (2.8 mmol/L)
•Who are greater than 48 hours of life with plasma glucose levels
<60 mg/dL (3.3 mmol/L)

●Asymptomatic patients at risk for hypoglycemia (eg, preterm infant,


an infant of a diabetic mother, or an infant who is large or small for
gestational age) or patients in whom low glucose was identified as an
incidental laboratory finding (see 'Who should be screened?' above):

•Who are less than 4 hours of life with plasma glucose levels <25
mg/dL (1.4 mmol/L)
•Who are between 4 and 24 hours of life with plasma glucose <35
mg/dL (1.9 mmol/L)
•Who are between 24 and 48 hours of life with plasma glucose
levels <50 mg/dL (2.8 mmol/L)
•Who are greater than 48 hours of life with plasma glucose levels
<60 mg/dL (3.3 mmol/L)
FOLLOW-UP MONITORING AND EVALUATION

Asymptomatic patients — Asymptomatic patients are typically identified


because they are at risk for hypoglycemia. Management is focused on
normalizing their blood glucose levels and preventing them from
becoming symptomatic. The first intervention for these patients is usually
oral feeding. (See "Management and outcome of neonatal hypoglycemia",
section on 'Asymptomatic and mildly symptomatic infants'.)
●In neonates identified with low glucose concentrations, monitoring
should continue until concentrations can be maintained with regular
feedings in a normal range: >50 mg/dL (2.8 mmol/L) in newborns <48
hours old and >60 mg/dL (3.3 mmol/L) in newborns >48 hours old [8].
●If an infant is unable to maintain plasma glucose concentrations >60
mg/dL after 48 hours of age, a hypoglycemia disorder should be
considered and further evaluation is warranted [8].
(See "Management and outcome of neonatal hypoglycemia", section
on 'Evaluation of infants with persistent hypoglycemia'.)

Symptomatic patients — Patients who have severe neuroglycopenic signs


(eg, lethargy, coma, seizures) and are hypoglycemic should be treated
promptly with intravenous dextrose. Treatment should be initiated as soon
as the confirmatory blood sample is drawn, and without waiting for results.

We manage less severely symptomatic patients with dextrose gel followed


by feeds.

Management of neonatal hypoglycemia is discussed elsewhere.

Diagnostico diferencial:

 Sepsis
 Neonatal abstinence syndrome (NAS)
 Inborn errors of metabolism
 Hyponatremia
 Neonatal encephalopathy due to perinatal asphyxia
 Neuroglycopenia
IV dextrose infusion — Hypoglycemic neonates with severe symptoms
(lethargy, coma, seizures) require urgent intervention with IV dextrose.
●Initial treatment – Initial treatment is as follows:
•An initial bolus of IV dextrose (0.2 g/kg) given over 5 to 15
minutes (2 mL/kg of 10% dextrose in water [D10W])
•Followed by a continuous IV dextrose infusion at a rate of 5 to 8
mg/kg of dextrose per minute

●Subsequent monitoring and titration – Plasma glucose


concentration should be measured 30 to 45 minutes after the
initiation of IV therapy, and the infusion rate or dextrose
concentration adjusted as needed to maintain BG >50 mg/dL (2.8
mmol/L) during the first 48 hours after birth and >60 mg/dL (3.3
mmol/L) beyond 48 hours [2] with an upper limit of 90 to 100 mg/dL
(5 to 5.5 mmol/L). (See 'Treatment target' above.)

Repeat BG levels should be obtained 30 to 45 minutes after any


increase in the IV dextrose infusion rate.

●Weaning and transition to oral feeds – When the BG is stabilized


and maintained within the target range, the glucose infusion rate can
be tapered slowly, and the infant can be transitioned to oral feeds.
(OJITO, ESTO ES VARIABLE PARA CADA CENTRO)

• Weaning is typically started when the infant's BG levels have been in


the target range for at least six to nine hours.

Other therapeutic options

Glucagon — Administration of glucagon should be considered in the


rare patients with persistent BG <50 mg/dL (2.8 mmol/L) despite
continuous maximum IV dextrose infusion.

Diazoxide — Diazoxide therapy is commonly used to manage


neonatal hyperinsulinemic hypoglycemia, which is one cause of
persistent or severe hypoglycemia [14].

Asymptomatic and mildly symptomatic infants

Mild symptoms of hypoglycemia include jitteriness or tremors.


Oral feeds — Oral feeding is the initial intervention for newborns who are
at risk for hypoglycemia and those with documented hypoglycemia if they
have no associated symptoms or have only mild symptoms

Initial feeding – Infants who are at risk for hypoglycemia should be fed
within the first hour of life [1]. The BG should be measured within 30
minutes after the initial feeding

While breast milk is strongly preferred, formula feeding may be provided


for infants when breast milk is not available.

Our suggested approach is as follows:

•Initial BG within target range – Infants whose initial


postprandial BG is >25 mg/dL (1.4 mmol/L) should be offered
feedings at two- to three-hour intervals and should be monitored
for signs of hypoglycemia. Prefeeding BG levels should be checked
every three to six hours for the first 24 to 48 hours

Infants between 4 and 24 hours of age with BG below threshold:


For these infants, we suggest buccal dextrose gel followed by an oral
feed (preferably with breast milk). BG should be measured 30 to 45
minutes after completion of the feed. If the subsequent BG increases
within the target range (table 1), oral feedings should continue every two
to three hours with preprandial BG measurements. However, if the BG
remains below threshold after the additional oral feed, IV dextrose is
administered.

•Infants with persistent BG <45 mg/dL (2.5 mmol/L) after three oral
feedings – For these infants, we suggest IV dextrose.

●General criteria (*discharge*) – In our practice, for infants who have


been identified as having hypoglycemia, preprandial BG through three
feed-fast cycles should be >50 mg/dL (2.8 mmol/L) in infants <48 hours
of age, and >60 mg/dL (3.3 mmol/L) in those who are ≥48 hours of life
[2,7]. In general, if a neonate can maintain BG >60 mg/dL (3.3 mmol/L)
after a 6- to 8-hour fast, it is likely that the infant is safe for discharge

Buccal dextrose gel is given at a dose of 0.2 g/kg (0.5 mL/kg of 40%
dextrose gel) which does not impair subsequent feeding [24].
Prophylactic early use in at-risk infants – We suggest not using
dextrose gel to prevent hypoglycemia in at-risk newborns in the absence
of documented hypoglycemia.

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