INFANTS HYPOGLICEMIA

NEONATAL
HYPOGLYCEMIA

Bambang Mulyawan
FK-UMM
NEONATAL HYPOGLYCEMIA

http://www.who.int/child-
adolescent-
health/New_Publications/NUTR
ITION/
hypoclyc.htm
Bambang Mulyawan – FK UMM
Pendahuluan
 Hipoglikemia lebih sering terjadi pd bayi baru lahir ( masa
neonatatal) dibanding anak yang lebih besar
 Kadar glukose darah normal terjadi karena adanya
keseimbangan antara penyediaan glukose dalam darah
dengan pemakaiannya oleh tubuh
 Hipoglikemia merupakan keadaan yang berbahaya karena
glukose merupakan kebutuhan pokok otak
 Secara klinis hipoglikemia dibedakan menjadi simptomatik
( dengan gejala) dan asimptomatik (tanpa gejala). Risiko
kerusakan otak lebih tinggi pada hipoglikemia simptomatik
Incidence of Hypoglycemia
 Overall Incidence = 1- 5/1000 live births
 Normal newborns – 10% if feeding is
delayed for 3-6 hours after birth
 At-Risk Infants – 30%
• LGA – 8%
• Preterm – 15%
• SGA – 15%
• IDM – 20%

McGowan, 1999 as cited by Verklan

& Walden
Definisi
 Hipoglikemia : kadar glukose plasma < 45
mg/dl pada bayi atau anak-anak dengan atau
tanpa gejala.

 Tidak ada keraguan pemberian terapi dextrose

intravena jika ditemukan kadar glukose rendah
pada bayi kejang, untuk mengembalikan kadar
gula darah kembali normal
What is Normal?
 Defining a normal glucose level remains
controversial
 50 – 110 mg/dl (Karlsen, 2006)
 > 40 mg/dl (Verklan & Walden, 2004)
 > 30 term, > 20 preterm (Kenner & Lott, 2004)
 > 45 mg/dl (Cowett, R. as cited by Barnes-Powell, 2007)
Definition
 The S.T.A.B.L.E. Program defines
hypoglycemia as:
• “Glucose delivery or availability is inadequate to
meet glucose demand” (Karlsen, 2006)
 Who is at risk?

 Infants of diabetic mothers

 Maternal use of B-adrenergic agonist/ antagonist
 IUGR
 LGA
 Preterm
 Polycythemia
 Asphyxia
 Sick infant
Hipoglikemia pada neonatus
 Bersifat sementara dan biasanya terjadi pada bayi
baru lahir, misalnya karena masukan glukose yg
kurang ( starvasi, kelaparan), hipotermia, syok,
dan pada bayi dari ibu diabetes
 Besifat menetap atau berulang yg dapat terjadi
akibat defisiensi hormon, hiperinsulinisme,
kelainan metabolisme karbohidrat dan asam amino
 Hipoglikemia yg berkepanjangan dan berulang dpt
mengakibatkan dampak yg menetap pd SSP.
Infants at Highest Risk
 < 37 weeks gestation
 Infant of a diabetic mother
 Small for gestational age
 Large for gestational age
 Stressed/ill infants
 Exposure to certain medications
 Treatment of preterm labor
 Treatment of hypertension
 Treatment of type 2 diabetes
 Benzothiazide diuretics
 Tricyclic antidepressants in the 3rd trimester
Karlsen, 2006
Bayi risiko tinggi hipoglikemia
 Bayi Kecil utk masa kehamilan
 Bayi Besar utk masa kehamilan
 Bayi dari ibu dg Diabetes Melitus
 Hipoglikemia dapat menjadi penyebab
dasar kejang BBL dan gejala neurologis
lainnya seperti apnu, letargi dan jiternes
 Hypoglycemia
 Serum glucose is below 45 mg/dL
 Tx: feed infant formula or breast milk and retest
until glucose stable
 S & S: jitteriness, lethargy, poor feeding, high-
pitched cry, irregular respirations, cyanosis,
seizures
 Risk factors: DM, PIH, preterm, post term, LGA,
cold stress, maternal intake of ritodrine or
terbutaline
Neonatal hypoglycemia

September , 2012.
Why is hypoglycemia a problem?

 Glucose is the primary fuel for the brain.

 The brain needs a steady supply of
glucose to function normally.
 Glucose is the fetus’s only source of
carbohydrate.

Karlsen, 2006
Why is hypoglycemia a problem?

“Compared with adults, infants have a

higher brain to body weight ratio,
resulting in higher glucose demand in
relation to glucose production capacity”.
“Cerebral glucose utilization accounts for
90% of the neonate’s glucose
consumption”.

Verklan & Walden, 2004

Signs & Symptoms of Hypoglycemia

 Jitteriness  Poor suck

 Irritability  Tachypnea
 Hypotonia  Cyanosis
 Lethargy  Apnea
 High-pitched cry  Seizures
 Hypothermia  Cardiac arrest

Verklan & Walden, 2004

Signs and Symptoms of Hypoglycemia
Symptoms are NON-SPECIFIC

 Jitteriness
 Apnea
 Irritability
 Grunting
 Lethargy
 Seizures
GLUCOSE HOMEOSTASIS AND
METABOLIC ADAPTATION AT BIRTH
 Physiology

Fetal Glucose Metabolism

 Fetus does not produce glucose

 Maternal glucose is the only source of
fetal glucose
 Baseline fetal blood glucose is 60-70% of
maternal serum glucose
 Physiology
Glucose metabolism after birth

Cessation of maternal
glucose supply

Blood glucose Nadir

( ~1-2 hrs after birth)
Glucose Metabolism After Birth
Cessation of maternal
glucose supply

Surge in glucagon, catecholamine

Decrease insulin

Gluconeogenesis:
Hepatic glycogen, amino acid, fatty acid metabolism

Normal blood glucose

Factors that negatively affect glucose
availability after birth

 Inadequate Glycogen

 Increased Utilization of Glucose

 Excessive Insulin

Karlsen, 2006
Etiology of neonatal
hypoglycemia
1. Increased utilization (e.g.: hyperinsulinism)
2. Decreased production/stores
3. Increased utilization and/or decreased
production
Preparation for Birth
 Fetal plasma glucose is 60 – 80% of the
maternal glucose level.
 The fetus stores glucose in the form of
glycogen (liver, heart, lung, and skeletal
muscle).
 Most of the glycogen is made and stored
in the last month of the 3rd trimester.

Karlsen, 2006
Preparation for Birth
 The fetus has limited ability to convert
glycogen to glucose and must rely upon
placental transfer of glucose to meet
energy needs.
 When the infant is born, the cord is cut
and so is the major supply of glucose!

Haney, 2005
Preparation for Birth
 The transition from fetus to newborn
creates a significant energy drain on the
newborn.
 The newborn is now required to meet
increased metabolic demands while
changing the energy source from a
placenta-supplied source to an external
food source.
Haney, 2005
Inadequate Glycogen
 Glycogen stores increase rapidly in the
last month of the 3rd trimester
 Preterm infants are born before this
occurs. What little glycogen is available
is used up rapidly and their supply is
depleted.

Karlsen, 2006
Inadequate Glycogen
 SGA – birth weight < 10 percentile.
Chronically stressed infants have higher
metabolic demands and use up available
glucose for growth and survival.
 Markedly post-mature infants are at
increased risk due to increased metabolic
demand.
Increased Utilization of Glucose
 Sick/Stressed infants
 Causes increase in metabolic demand

 Uses up glucose quickly.

 These include all sick, premature and SGA infants.

Karlsen, 2006
Increased Utilization
 Diabetic mother
 Large for gestational age (LGA) infant
 Erythroblastosis
 Islet cells hyperplasia
 Beckwith-Wiedemann syndrome
 Insulin producing tumors
 Maternal tocolytic therapy with B-sympathomimetric
agents
 Malposition of umbilical artery catheter
Decreased Production/Stores
 Prematurity
 Intrauterine growth retardation(IUGR)
 Inadequate caloric intake
 Delayed onset of feeding
 Increased utilization AND
Decreased production

 Perinatal stress eg. shock, sepsis, asphyxia

 Enchange transfusion
 Defect in carbohydrate metabolism eg. glycogen storage
disease
 Endocrne deficiency eg. adrenal insufficiency,
hypopituitarism
 Defect in amino acid metabolism
 Polycythemia
 Maternal therapy with B-blocker
Excessive Insulin - IDM
 Infants of Diabetic Mothers
 Many consequences for the neonate
 Single most important factor in determining
the outcome for the infant is maternal
glucose control
IDM – Risks > general population

 Birth injury is doubled

 C/S is tripled
 NICU admission is quadrupled
 Stillbirth is x 5 greater
 Congenital anomalies are x 2 – 5 greater
IDM - Incidence
 106,000 in 1999
 Rate of Type II Diabetes has increased by
33% in past 20 years
 Women at highest risk
 African-American
 Hispanic
 American Indian
 Asian
 Obese
Pathophysiology : infants of diabetic mothers
Other Effects on the Neonate
 RDS
 CHD
 VSD
 Asymmetric septal hypertrophy
 Thickened myocardium
 Transposition of the greater vessels
 Polycythemia and vascular sludging
Nursing Management
 Complete evaluation and review of
systems
 Early breast or bottle feeding within 30
minutes
 Glucose monitoring within 1 hour
 Monitor pre-feeding levels thereafter
Recommendations for Prevention and
Management

 Early and exclusive breastfeeding is

safe to meet the nutritional needs of
healthy term newborns worldwide.
 Healthy term newborns who are
breastfeeding on demand need not
have their blood glucose routinely
checked and need no supplementary
foods or fluids.
Monitoring
 Serum glucose level  Monitor at least
is the gold standard hourly until glucose
 Bedside glucose level has stabilized
levels are for  Know your hospital
screening policy for monitoring
infants at risk for
hypoglycemia

Kenner, 1998
Tata laksana hipoglikemi simptomatik neonatus

 Berikan glukosa 10% iv sebanyak 2 ml/kg dg

pelahan selama 1 menit. Lanjutkan dg pemberian
infus glukosa 10% dan pertimbangkan juga
pemberian elektrolit. Kebutuhan glukosa
diperkirakan sekitar 1-10 mg/kg/menit. Untuk
pemberian glukose sebanyak 8 mg/kg/menit,
dibutuhkan dekstrose 10% dg kecepatan 110
ml/kg/hari iv
How do you treat this
patient?
 Feeding?
 IV therapy?
 Medication?
Treatment
 Oral feedings as tolerated
 If glucose is very low or the infant is not able to
feed orally:
 2ml/kg of D10W IV bolus
 Follow up screenings within 30 minutes
 Repeat bolus if glucose is < 50 mg/dl
 If unable to stabilize glucose consider increasing IV
rate or glucose concentration

Karlsen, 2006
Prevention
 Increase awareness of conditions that
predispose an infant to hypoglycemia
 Early screening of at-risk infants
 Early and frequent feedings
 Maintain temperature
 Hypoglycemia
Definition: A plasma glucose of less than 45 mg/dl

Plasma glucose is higher than whole blood glucose by

15%
 When do you screen?
1. Symptoms that could be due to
hypoglycemia.
2. At risk infants.
Screening
Blood glucose or point of care testing
(POC) should be done in high risk
infants within the first 1 to 2 hours after
birth
Management – Oral Feeds
 Can be used in asymptomatic infants
 Only formula (never administer glucose water!!)
 Follow up blood glucose within 1 hour of feeding.
 If the glucose level doesn’t rise, a more aggressive
therapy may be needed.
Management – IV therapy
Indications:
 Inability to tolerate oral feeding
 Symptomatic infant
 Lack of response with oral feeds
 Glucose < 25 mg/dL, regardless of patient’s
symptoms
Management – IV therapy
Urgent treatment
 Bolus 2 ml/kg of D10W
 Do not use 25% or 50% glucose !!
 Follow bolus with continuous dextrose fluid
 Management – IV therapy
Continuing IV fluid
 Start infusion of glucose at a rate of 6-8 mg/kg/min
 Glucose infusion rate formula (GIR):

GIR = %IV fluid x rate(ml/hr)

6 x BW(kg)
Management – IV therapy
 Re-check serum glucose 20-30 min after bolus and
hourly until stable
 If glucose is normal and stable, feeding may be continued
and glucose infusion tapered
 If glucose can’t be maintained > 50 mg/dL, increase GIR by
1-2 mg/kg/hr
 If glucose can’t be maintained > 50 mg/dL, with a GIR 12
mg/kg/min, medication should be added.
Management – Medication
Persistent hypoglycemia despite a GIR > 12
mg/kg/min.

 Work up – Critical Labs:

 Serum cortisol, insulin, growth hormone when glucose is low
and prior to treatment
 DO NOT wait >5 minutes for labs prior to treating
hypoglycemia

 Medication
 Hydrocortisone
 Glucagon
 Diazoxide
Selamat belajar

Terima kasih
 Identification of High Risk
Infants
 Assess for congenital anomalies

 Determine Gestational Age Assessment

 Priority Needs of Newborns
 Initiating and Maintaining Respirations
 Establishing Extrauterine Balance
 Fluid and Electrolyte Balance
 Temperature Regulation
 Adequate Nutritional Intake
 Parent-Infant Bonding
 HIGH RISK NEWBORN
 GESTATIONAL AGE ASSESSMENT
 MOST COMMON PROBLEMS-
hypoglycemia, hypocalcemia, resp. distress,
hypothermia
 SGA
 AGA
 LGA
 Small for Gestational Age
 <2500 g (5 1/2 lbs)
 Commonly due to placenta abnormality,
decreased blood flow, smoking, narcotics
 Appearance
 SGA INFANTS- COMMON
COMPLICATIONS
 PERINATAL ASPHYXIA
 ASPIRATION SYNDROME
 HEAT LOSS
 HYPOGLYCEMIA
 HYPOCALCEMIA
 POLYCEMIA
 MENTAL DEVELOPMENT
 LGA INFANTS
 Causes:
 a. Diabetic Mother
 b. Babies with Transposition of the Great
Vessels
 c. Multiparous Mothers
 Hypoglycemia
 Threat to Brain Cells
 Less than 30 mg/100 ml of blood = harmful
 After birth levels fall
 Infants prone to hypoglycemia
 Treatment
 Appropriate for Gestational Age
 Healthiest Babies

 Between 3000 - 4000 g

 Preterm Infant
 Less than 37 weeks
 Less than 3500 g = LBW
 1000 - 1500 g = VLBW
 500 - 1000 g = Extremely VLBW
 PRETERM INFANTS
 SMALL AND SCRAWNY
 LARGE HEAD
 TRANSLUCENT SKIN, VISABLE
BLOOD VESSELS
 ABUNDANT LUNAGO
 SOLES OF FEET- minimal creases
 MALES- few scrotal rugae, & testes
undescended
PRETERM INFANTS- Potential
Complications
 Anemia
 Kernicterus
 Persistent Patent Ductus Arteriosus
 Periventricular/Intraventricular Hemorrhage
 PRETERM INFANTS-Nursing
Diagnosis
 Impaired Gas Exchange
 Risk for Fluid Volume Deficit
 Risk for Altered Nutrition
 Risk for Infection
 Risk for Altered Parenting
 Diversional Activity Deficit
 Risk for Disorganized Infant Behavior
 POSTERM INFANTS

 ABSENT LANUGO
 LITTLE VERNIX CASEOSA
 ABUNDANT SCALP HAIR
 SKIN CRACKED & PARCHMENTLIKE
 WASTED APPEARANCE
 RESPIRATORY DISTRESS
SYNDROME
 CAUSE- Surfactant Production
 WORK HARDER- Use more O2 & expend
more energy, get hypoxic, hypercapnia,
metabolic acidosis, vasoconstriction
 RISK- <2500g, <28 weeks, male, IDM
 SIGNS
 DIAGNOSIS
 TREATMENT & PREVENTION
 ILLNESS IN THE NEWBORN
 TRANSIENT TACHYPNEA
 MECONIUM ASPIRATION SYNDROME
 SUDDEN INFANT DEATH SYNDROME
 PERIVENTRICULAR LEUKOMALACIA
 HEMOLYTIC DISEASE OF THE
NEWBORN
 MANAGEMENT OF HIGH
RISK INFANT
 PHYSICAL ASSESSMENT
 THERMOREGULATION- need neutral
thermal environment, use brown fat
 CONSEQUENCES OF COLD STRESS-
hypoxia, metabolic acidosis, hypoglycemia
 GLUCOSE & CALCIUM
 PROTECT FROM INFECTION
 MANAGEMENT OF HIGH
RISK INFANT
 HYDRATION- IVF for calories,
electrolytes & H2O
 NUTRITION- no coordination of sucking
until 32-34 weeks; not synchronized until
36-37 weeks; gag reflex not developed until
36 weeks
 EARLY FEEDING- within 3-6 hours
 BREAST FEEDING
 GAVAGE FEEDING- <32 wks. or <1500g
 MANAGEMENT OF HIGH
RISK INFANT

 SKIN CARE OF PREMATURE- increased

sensitivity & fragile
 MEDICATION - caution
 DECREASE STRESS
 DEVELOPMENTAL
INTERVENTION

 BEFORE 33 WEEKS- minimum

stimulation
 34-36 WEEKS- stimulate senses but don’t
tire out
 NURSING CARE

 PAIN CONTROL
 FACILITATE PARENT-CHILD
RELATIONSHIP
 NEONATAL LOSS- see, hold, photo;
support groups, baptize
 PRETERM INFANTS

 GIRLS- labia and clitoris prominent

 INACTIVE & LISTLESS- extremities
remain in any position placed
 IMMATURE LUNGS, SUCK, TEMP
 HYPERBILIRUBINEMIA
 INCREASED UNCONJUGATED FORM
(0.2-1.4mg/dl)
 JAUNDICE WITHIN 24 HOURS
 AFTER 1-2 WKS. TERM; 2 WKS
PRETERM
 TOTAL > 12-13 mg/dl
 INCREASE >5 mg/dl/day
 DIRECT >1.5-2 mg/dl
 HYPERBILIRUBINEMIA
 DIRECT COOMB’S TEST- ABO/Rh-
detect the infant’s antibodies coating the
RBS (circulating erythrocytes)
 TYPES OF
HYPERBILIRUBINEMIA
 PHYSIOLOGICAL JANUDICE
 BREAST-FEEDING ASSOCIATED
JAUNDICE
 BREAST MILK JAUNDICE
 HEMOLYTIC DISEASE- Blood antigen
incompatibility
 a. Treatment- phototherapy, exchange
transfusion, prevention (RhoGAM)
 b. Nursing Care
 EXCHANGE TRANSFUSION
 CRITERIA- + Direct Coombs, Hg<12g/dl,
Bilirubin > 20 mg/dl
 AMOUNT - 2X blood volume of infant
 UMBILICAL VEIN
 CHECK FOR HYPOCALCEMIA
 MONITOR VS, RADIENT WARMER
 HYPOGLYCEMIA
 SGA, LGA, IDM, STRESSED,
INTERUTERINE MALNUTRITION
 JITTERY, HIGH-PITCHED CRY,
LETHARGIC
 Dx- glucose <40 1st 24 hours or <50 after
24 hours, heel stick
 PREVENT- early feedings
 HYPOCALCEMIA
 RISK- preterm with hypoxia, IDM,
hypoglycemic
 Dx- serum calcium <7 mg/dl
 Tx- increase milk feedings, cal.
supplements, Vit D
 NEONATAL SEIZURES
 NOT ORGANIZED
 SIGN OF BRAIN DISTURBANCE
 MOST COMMON CAUSE- Asphyxia &
Hypoglycemia
 Dx- EEG, lab test, CAT scan
 Treatment and Nursing Care
 HYPOXIC-ISCHEMIC
ENCEPHALOPATHY
 COMPLICATION OF HYPOXEMIA

 RISK

 SIGNS
 SEPSIS
 SUSCEPTIBLE- Diminished nonspecific
and specific immunity
 ETIOLOGY- Infected amniotic fluid, +BGS
 DIAGNOSIS- Cultures
 TREATMENT- Ampicillin & Gentamycin
 NECROTIZING
ENTERCOLITIS
 SICK PRETERM & HIGH-RISK
 ISCHEMIA & NECROSIS OF GI TRACT
 RELATIONSHIP WITH FORMULA
 SIGNS- Abdominal Distention, etc.
 TREATMENT- D/C oral feedings,
Antibiotics, Observations
 BULLOUS IMPETIGO
 STAPHYLOCOCCUS AUREUS- red moist
denuded area with very little crusting

 WARM SALINE COMPRESSES,

 ANTIBIOTICS

 PREVENT SPREAD
 INFANTS OF DIABETIC
MOTHERS(IDM)
 BLOOD SUGAR- Hypoglycemic <40 in 1st
24 hours, 40-50 later
 TRANSIENT HYPERGLYCEMIA
 LGA- Fat deposits & excessive growth
 HYPOGLYCEMIA- Within 1/2-4 hours
 CHECK BLOOD SUGAR
 NARCOTIC-ADDICTED
INFANTS
 WITHDRAWAL
 AUTONOMIC NERVOUS SYSTEM-
Hyperirritability, suck vigorously but poor
suckers
 TREATMENT- Sedative/Hypnotic,
Antianxiety
 PROGNOSIS- Neuro and growth problems
 NURSING- Decrease stimuli, nutrition,
snuggle, protect skin
 COCAINE EXPOSURE
 CNS STIMULANT
 RISK SIDS
 NEURO DEPRESSION/EXCITABILITY
 SMALL HEAD CIRCUMFERENCE,
LBW, LOWER BIRTH LENGTH
 TREATMENT- Supportive, occ. sedative
 FETAL ALCOHOL
SYNDROME
 MOM CHRONIC ALCOHOLIC

 MENTAL RETARDATION

 CHARACTERISTICS- Growth retardation,

CNS manifestations, facial characteristics,
fail to thrive
 MATERNAL SMOKING
 GROWTH RETARDATION

 INCREASED ABORTION

 EMOTIONAL DEFICITS

 INCREASED SIDS
 MATERNAL INFECTION
 T- Toxoplasmosis
 O- Other ( hepatitis, measles, mumps, HIV)
 R- Rubella- pregnant no contact
 C- Cytomegalovirus infection-pregnant no
contact
 H- Herpes simplex- Stop transmission
 S- Syphilis (Gonococcal conjunctivitis &
chylamydial conjunctivitis)
 CONGENITAL
ABNORMALITIES
 DOWN’S SYNDROME- Extra chrosome
21
 a. GREATER RISK IN WOMEN >35
 b. CHARACTERISTICS- Mental
retardation, low set ears, head round, short
stubby fingers, bridge of nose flat, tongue
thick, heart defects
 CONGENITAL
ABNORMALITIES
 CHEMICAL AGENTS
 a. BETWEEN 15-90 DAYS OF
GESTATION

 b. PREVENTION
 CONGENITAL
HYPOTHYROIDISM
 INADEQUATE THYROXINE (T4)

 CLINICAL SIGNS- Hypotonia, wide-

spread fontanelles, large thyroid, prolonged
jaundice

 TREATMENT- Thyroid hormone

replacement
 PHENYLKETONURIA
 ABSENSE OF PHENYLALANINE
HYDROXYLASE
 AFFECTS DEVELOPMENT OF BRAIN
AND CNS
 SCREENING OF NEWBORNS, REPEAT
SCREENING
 TREATMENT- Diet restricts phenylalanine
(Lofenalac), meat and diary products
restricted
 GALACTOSEMIA
 DISORDER OF GALACTOSE
METABOLISM
 GLACTOSE ACCUMULATES IN
BLOOD ORGANS
 SIGNS- Lethargy, hypotonia, diarrhea
 TREATMENT- Eliminate galactose
(Prosobee)