2020/2/29 ‫أطﻔﺎل‬ (8) ‫ﻋﺪد اﻻوراق‬

Lec: 1 ‫ ﻧﺰار‬.‫د‬
Neonatology
Hypothermia, Hypoglycemia, Infant of diabetic mother,
Hypocalcemia, Neonatal seizures
Objectives:
• To recognize the ways of heat loss in newborn baby, and
etiology, clinical features and management of hypothermia in
newborn baby
• To list the risk factors, clinical features, differential diagnosis,
and management of hypoglycemia in neonate
• To understand the pathophysiology ,clinical manifestations,
complications, and management of infant of diabetic mothers
• To recognize the definition, etiology, clinical manifestations of
hypocalcemia in neonate
• To understand the etiology, types, and management of neonatal
seizures
HYPOTHERMIA:
Heat balance: heat production= heat loss
Heat is produced as product of cell metabolism by non-shivering
thermo genesis from chemical reactions of [ATP] hydrolysis in
specialized areas of tissue containing brown adipose tissue.

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Four ways a new
born may lose
heat to the
environment

Heat loss in newborn infant is by:

1-Convection: heat is lost from skin surface to the surrounding air by
convection[ loss is high if the air is cold]
2-Radiation: heat is lost from skin surface to the nearest surface which
faces the skin by means of radiation.
3-Evaporation: heat is lost as water evaporates from the surface of the
skin[ loss is high in preterm infant who have high transepidermal
water loss due to passive diffusion of water vapor through the thin
poorly keratinzed immature epidermis.
4-Conduction: heat loss from skin surface to the cold structure in
direct contact with it.
Three levels are defined:
1. “Cold stress” or mild hypothermia: temperature 36.0°C–36.4°C
2. Moderate hypothermia: temperature 32.0°C–35.9°C
3. Severe hypothermia: temperature below 32°C
Etiology:
1. 1-Accidental hypothermia: due to cold exposure in hospital or at
home specially in low birth weight baby due to inadequate
clothing or cold thermal environment.
2. Other causes:
- sepsis
- severe heart failure or with marked cyanosis
- malnutrition
- hypothyroidism

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Clinical features:
Symptoms develop when temp. falls below 34°c.
Early features: baby lethargic,feed poorly,week cry,&reduced
movement.
Late features: peripheral edema, sclerema, marked facial erythema
with striking cold skin.
In severe hypothermia: profound bradycardia, slow shallow
respiration, apnea, hypoglycemia, acidosis,& infant appear to be dead.
Diagnosis: is by recording temp. by low reading rectal temp. to 30° c.
Treatment:
Is by rewarming and if there is underlying cause should be treated.
In mild hypothermia rewarming takes place rapidly.
In moderate or severe cases rewarming takes place slowly.
Rewarming is by using radiant warmer or incubator or heated cot. Use
plasma expander during rewarming has been advocated.
Hypoglycemia may occur during rewarming. It should be treated or
prevented by slow I.V infusion of 10% dextrose water.
Skin-to-Skin Care:
“Kangaroo mother care” was originally used as an effective way
for mothers to keep their full-term babies warm while breastfeeding
and subsequently as an alternative method of caring for low birth
weight (LBW) babies in resource-limited countries. In these original
versions, the infant is placed skin-to-skin in a vertical position
between the mother’s breasts and under her clothes and is exclusively
(or almost exclusively) breastfed.
More recently, intermittent SSC, provided by the mother or father,
has been introduced in resource rich countries for babies requiring
neonatal intensive care—even extremely premature infants and those
on ventilators.

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Enhanced parental bonding, facilitation of breastfeeding, better sleep
patterns, and procedural pain relief are some of its purported benefits.

Complications:
1. Abdominal distension & ileus
2. NEC &hemorrhagic pulmonary edema.
3. In severe hypothermia mortality 25-50%.
Hypoglycemia:
Is common during the neonatal period.
Definition: Blood glucose level below 40 mg/dl.
Risk factors for neonatal hypoglycemia:
Common
1-Prematurity.
2-Infant of diabetic mother.
3-IUGR.
4-Asphyxia-perinatal stress.
5-Hypothermia.
6-Large for gestational age.
7-Maternal medication.
[tocolytics, propranolol, chlorpropamide, high glucose infusion in
labor]

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Uncommon causes
1-Erythyroblastosis fetalis.
2-Islet cell adenoma.
3-Familial and non-familial hyperinsulinism.
4-Inborn error of metabolism.
5-Growth hormone deficiency.
6-Adrenal insufficiency.

Clinical manifestations:
Hypoglycemia usually noted on first or second day of life, could be
asymptomatic, to central nervous system, and cardiopulmonary
disturbances.
Hypotonia, lethargy, apathy, poor feeding, jitteriness ,and seizure are
common.
Tachycardia, cyanosis, pallor, diaphoresis, apnea, and hypothermia.

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Differential diagnosis:
1-Congenital heart disease.
2-Sepsis.
3-IVH.
4-Hypocalcemia.
5-Hypomagnesemia.
6-Inborn error of metabolism.
7-Narcotic withdrawal.
Prevention:
All newborn infant at risk for hypoglycemia should be monitored with
serial capillary blood glucose levels measured during first day of life.
Newborn at risk for hypoglycemia should be breast feed or given
formula within the first few hours of birth.
If oral feeding not possible because of cardiopulmonary disease 10%
dextrose water should be given intravenously.

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Treatment:
Requires initial intravenous bolus infusion of 200mg/kg [2ml/kg]
10%glucose, this should be followed immediately by continuous
infusion of 6-8mg/kg/min of glucose.
In resistant cases can use hydrocortisone intravenously.
Other drugs can be used diazoxide, nifidipine, or somatostatin.
Surgery:
Indicated in adenoma of pancreas, or diffuse hyperplasia of pancreas.

Prognosis:
In symptomatic neonatal hypoglycemia with seizure is poor, and is
associated with abnormal neurointellectual development.
Infant of Diabetic Mother
DM present before pregnancy or develop during pregnancy
[gestational diabetes is noted in about 5% of women] adversely
influences fetal and neonatal well being.
Pathophysiology:
Poorly controlled maternal diabetes leads to maternal hyperglycemia,
this produce fetal hyperglycemia that stimulate fetal pancreas results
in hyperplasia of islets of Langerhans leads to hyperinsulinism.

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1. 1-Fetal hyperinsulinism acts as a fetal growth hormone, in last
trimester results in increased fat& protein synthesis& fetal
macrosomia with organomegaly [all organs enlarge except the
brain], fetus large for gestational age.
2. Fetal acidosis which may result in increased rate of still birth.
3. Increased extramedullary erythropoiesis results in polycythemia.
4. The separation of placenta suddenly interrupts glucose infusion
in to the neonate without proportional effect on hyperinsulinism,
resulting in hypoglycemia in the first hours after birth.

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Clinical manifestations:
Baby tend to be large and plump, puffy plethoric facies.
The baby tend to be jumpy, tremulous, and hyperexcitable.

Complications:
Maternal:
1. Ketoacidosis.
2. Hypoglycemia.
3. Preeclampsia.
4. Polyhydromnias.
5. Retinopathy.
Neonatal:
1. Prematurity.
2. Macrosomia.
3. Birth trauma & birth asphyxia.
4. RDS, TTN
5. Hypoglycemia, nadir of blood glucose level at 1-3 hours.
6. Hypocalcemia, polycythemia, unconjugated hyperbilirubinemia.
7. Cardiomegaly & asymmetric septal hypertrophy.
8. Renal vein thrombosis.
9. Intrauterine fetal death.
10. Neurodevelopmental delays.
Congenital anomalies:
Central nervous system anomalies including failure of neural tube
closure (encephalocele, meningomyelocele, and anencephaly
cardiovascular system anomalies including transposition of great
vessels, ventricular septal defect (VSD), atrial septal defect (ASD),
hypoplastic left heart, aortic stenosis, and coarctation of the aorta.
Other, less common anomalies include
caudal regression syndrome, intestinal atresia, renal agenesis,
hydronephrosis, and cystic kidneys.

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 Small left colon syndrome is a rare anomaly that develops in the
second and third trimester because of rapid fluctuations in maternal
and therefore fetal glucose, leading to impaired intestinal motility and
subsequent intestinal growth.
Infant of a diabetic mother
showing macrosomia and
plethora.
Born vaginally at 36 weeks'
gestation,
she weighed 5.5 kg and
suffered a right-sided
brachial plexus injury .

Treatment:
Management of these infants should be initiated before birth [during
pregnancy].
After birth infant should receive intensive observation and care.
Asymptomatic infant should have a blood sugar determination hourly
for first 6hours.
Infants should initiate feedings within 1 hr after birth. A screening
glucose test should be performed within 30 min of the first feed.
Transient hypoglycemia is common during the 1st 1-3 hr after birth
and may be part of normal adaptation to extrauterine life.
The target plasma glucose concentration is ≥40 mg/dL before feeds in
the 1st 48 hr of life.
Feeding is the initial treatment for asymptomatic hypoglycemia. Oral
or gavage feeding with breast milk or formula can be given. An
alternative is prophylactic use of dextrose gel, although early
feedings may be equally effective. If baby can not take orally give I.V
fluid 10%glucose.
Symptomatic hypoglycemic treated by 2ml/kg 10% glucose water
I.V.

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HYPOCALCEMIA:
Definition: Total serum calcium of less than7mg/dl, and ionized
calcium levels of less than3-3.5mg/dl .
Etiology:
1-Early neonatal hypocalcemia: occurs in first 3days of life and is
often asymptomatic.
A-Transient hypoparathyroidism.

Prematurity.
Respiratory distress syndrome (RDS).
Birth asphyxia.
IDM.
Neonatal sepsis.
B-Congenital absence of parathyroid gland and DiGeorge syndrome.
C-Hypomagnesemia[<1.5mg/dl] may be associated with
hypocalcemia.
2-Late neonatal hypocalcemia or neonatal tetany:
A-Ingestion of high-phosphate containing milk and is associated with
hyperphosphatemia[>8mg/dl].
B-Vit D deficiency and malabsorption
Clinical Manifestations:
Apnea, muscle twitching, seizures, laryngospasm, [chvostek sign &
Trosseau sign are rare in newborn period].
Treatment:
Symptomatic hypocalcemia treated by 2-4ml/kg of 10%calcium
gluconate given I.V slowly over10-15min then continous infusion of
75mg/kg/24hr of calcium.
If hypomagnesemia is associated with hypocalcemia magnesium
sulfate 0.1ml/kg I.M& repeated every 8-12hr.
Late hypocalcemia: include immediate management as early
hypocalcemia, and giving formula of low phosphate level.

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Neonatal Seizures
Etiology:
1. 1-Hypoxic-ischemic encephalopathy: usually occur 12-24hours
after birth. There is history of birth asphyxia, also may be
associated with metabolic disorder such as hypoglycemia &
hypocalcemia.
2. IVH: is common cause of seizure in premature infants and occur
between 1-3 days of age. Usually there is bulging fontanel,
hemorrhagic spinal fluid, anemia, lethargy, coma.
3. Hypoglycemia: occur in at risk patients.
4. Hypocalcemia& hypomagnesemia.
5. Seizure in delivery room may be due to:
A- Injection of local anesthetic agents in fetal scalp.
B- Severe anoxia.
C- Congenital brain malformation.
6. Infection: bacterial or viral infection of brain usually occur after
5days.

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 7. Drug withdrawal: like methadone or heroin usually occur after
5days.
8. Inborn error of metabolism: usually there is lethargy, acidosis,
and family history of infant death.
9. Other causes.
-subarachnoid hemorrhage.
-benign familial seizure.
-vit B6 deficiency or dependency.
Types of Neonatal Seizures:
1. 1-Subtle: most common type occur in more than 75% of cases
-Eye signs: eyelid fluttering, eye deviation, fixed open stare,
blinking.
-Apnea, cycling, boxing, stepping, swimming movement of
limbs.
-Mouthing, chewing, lip smacking, smiling.
2. Tonic: stiffening, decerebrate posture.
3. Clonic: repetitive jerking.
4. Myoclonic: arrhythmic contraction of muscle groups of the
limb, face, or trunk.

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Differential diagnosis:
Jitteriness & tremor: fine and rapid movement are sensory
dependent elicited by stimuli, and interrupted by holding the
extremity and not associated with abnormal eye movements.
Investigations:
1- immediate determination of capillary blood glucose with
chemstrip.
2-blood glucose, calcium, sodium, & bilirubin determination.
3-when infection suspected cerebrospinal fluid and blood culture.
Other investigations done in selected cases:
1. MRI, C.T scan, or ultrasound of brain.
2. Test for inborn error of metabolism.
3. EEG: often demonstrates seizure activity when clinical
diagnosis is uncertain especially in subtle seizure.
Treatment:
1-Specific: such as treatment of meningitis, hypoglycemia,
hypocalcemia, hypomagnesemia, hyponatremia, or vit B6 deficiency
or dependency.
2-Treatment of seizure:
A-Phenobarbital 20-40mg/kg I.V
B-Phenytoin 10-20mg/kg I.V infusion
C-Diazepam 0.1-0.3mg/kg I.V.

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