This document discusses hypoglycemia in infants of diabetic mothers. It begins by outlining the risks of hypoglycemia in these infants, including transient drops in blood glucose levels after birth due to high insulin levels. It then discusses the causes, symptoms, diagnosis and management of hypoglycemia. Key points include the importance of monitoring blood glucose levels, treating low levels aggressively with IV dextrose boluses and infusions, and addressing any other issues such as hypocalcemia.

1. Hypoglycemia, Infant of a
Diabetic Mother
Dr. Kalpana Malla
MD Pediatrics
Manipal Teaching Hospital
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2. Preparation for Birth
• Newborn’s blood glucose 60-70 % of
maternal level falls during first 24 hrs
(lowest at 3 hrs)transient rise during next
24 hrs  falls again at 3-4 days stable
Karlsen, 2006

3. 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)

4. Incidence of Hypoglycemia
• 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

5. Hypoglycemia
Definition:
Blood glucose < 40mg/dl (< 2.2 mmol / L)
at any time regardless of gestational age
**Normal glucose level 30-60mg/dl (1.7-
3.3mmol/L)
** Target 1st D >40 mg/dl
> 40-50 mg/dl thereafter

6. • Incidence - 8.1% of term LGA
14.7 % of SGA

7. ETIOLOGY
Increased utilisation of glucose-
- Infant of diabetic mothers
- LGA babies
- Erythroblastosis fetalis
- Beckwith-Weidemann syndrome
- Insulin producing tumors
- UA catheter- used to infuse glucose
- After exchange transfusion

8. Decreased stores or decreased
production
• Prematurity
• IUGR
• Decreased calorie intake
• Delayed onset of feeding

9. Increased utilization/decreased
production
• Perinatal stress • Defects in CHO
- Sepsis metabolism
- Shock - glycogen storage disease
- Asphyxia - galactosemia
- Hypothermia
- RDS

10. • Endocrine causes • Defects in amino acid
- Adrenal insufficiency metabolism
- Glucagon deficiency - MSUD
- Epinephrine ” ” - Tyrosinemia, etc
- Congenital • Others:
hypopituitarism - Polycythemia
- Hypothalamic - Maternal use of drugs
deficiency - After exchange
transfusion

11. Causes
1. Decreased production/store
- Preterm , IUGR 67%, LGA 38%
- Inadequate intake
2. ↑utilization/↓production
- Perinatal stress - Septicemia,
birth asphyxia, Hypothermia
- Defect in CHO metabolism- IEM
- Endocrine defic - adrenal insufficiency
- cong hypopituitarism
- Polycythemia

12. Causes
3. Increased utilization of glucose -
hyperinsulinism
- I/O diabetic mother
- Erythroblastosis
- Beckwith –Weidmann syndrome
- Abruptly stopping high –glucose
infusions
- Insulin producing tumors- islet
cell adenoma

13. SYMPTOMS
• Asymptomatic
• Lethargy, apathy and limpness
• Apnea
• Cyanosis
• Weak or high pitched cry
• Seizures, coma
• Poor feeding, vomiting
• Tremors, jitteriness or irritability

14. DIAGNOSIS
• Reagent strips – Glucostix
- Confirmatory lab test is required
- Serial measurements for those having
symptoms
• Hypoglycemia lasting > a week
require endocrine work up -insulin,
GH, cortisol, ACTH, T4, glucagon,
amino acids and urine for ketones,
reducing substance, amino acids and
organic acids

15. MANAGEMENT
• Well neonates who are at risk –
Monitor/ feed
• Symptomatic- IV 10% dextose 2-
5ml/kg. Follow this by infusion
8mg/kg/min recheck after 30 min and
hourly until stable. Increase infusion as
required.
• Other therapy- Hydrocortisone,
glucagon, Epinephrine, diazoxide and
growth hormone

16. Infant of diabetic mother

17. Infants of Diabetic Mothers
**Babies born to diabetic or gestational
diabetic mothers
• 1st trimester------diabetic embryopathy
• Last trimester---------macrosomia
• Birth weight > 4000 g - 90th percentile GA

18. Introduction:
• Gestational diabetes (GDM): defined as
carbohydrate intolerance of variable severity first
diagnosed during pregnancy
• Affects 3 % of all pregnancies
• Risk factors for GDM:
- advanced maternal age
- multifetal gestation
- increased BMI
- family h/o DM

19. Hypoglycemia
• Pedersen Hypothesis
– Maternal hyperglycemia
– Fetal hyperglycemia
– Fetal -cell hyperplasia
– Neonatal hyperinsulinemia

20. Maternal Hyperglycemia
• Dose and time dependent
• Post implantation rat embryo 100% teratogenic
dose 950 mg/dl D-glucose
Day 10 primary neural tube defect
Day 11 cardiac defects
Day 12 no defects

21. Fetal Hyperglycemia
• 1-2 hours of fetal hyperglycemia can have
detrimental effects
• insulin secretion
– Storage of excess nutrients macrosomia
– Post natal hypoglycemia

22. IDM – Effects on Fetus
• Glucose crosses the placenta
• Insulin does not cross the placenta
• Results – fetus produces own insulin in the presence
of elevated glucose from the mother

23. 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

24. Congenital Malformations
• Overall incidence---5 to 9%
– 2-3 fold higher than general population
– Predominantly with IDDM
• Malformations of CNS seen most often
• Diversity-No malformation considered
pathognomonic

25. Congenital Malformations
• No increase in major congenital
malformations among offspring of
– Diabetic fathers
– Prediabetic women
– GDM after first trimester

26. Congenital Malformations
Skeletal/CNS
• Caudal regression syndrome
not considered pathognomonic
occurs 600 x more frequently among IDDM
• Neural tube defects
• Microcephaly

27. Caudal Regression Syndrome
• Spectrum of malformation
– cessation of growth of rostral
portion of spinal cord
– abnormal neural, muscular, skeletal
and vascular components
Caudal Regression with limbs
intact but malformed
Sirenomelia
Absence of hind limbs, external
genitalia, anus and rectum; Potter
sequence secondary renal agenesis

28. Congenital Malformations
Cardiac
• Transposition + VSD
• Ventricular septal defect
• Coarctation + VSD or PDA
• Atrial septal defect
• Hypertrophic Cardiomyopathy

29. Congenital Malformations
Renal
• Hydronephrosis
• Renal agenesis
• Ureteral
duplication

30. Congenital Malformations
GI
• Duodenal atresia
• Anorectal atresia
• Small left colon
syndrome

31. Perinatal and Neonatal Complications
• Disorders of fetal growth
• Intrauterine and perinatal asphyxia
• Hypoglycemia
• Respiratory distress syndrome

32. Macrosomia
• Birth Weight > 4000 g or > 90th %-ile
• Incidence 15 to 45% among IDM
• Increased rate of C-section
• Birth Trauma
shoulder and body dystocia
brachial plexus injury
facial nerve injury
asphyxia
abdominal trauma

33. Pathogenesis
• Maternal hyperglycemia → Fetal
hyperglycemia → Leads to islet cell
hyperplasia → Fetal hyperinsulinemia
↓↓
A) Prenatal: ↑wt of placenta
• Insulin acts as an anabolic hormone for
fetal growth. Organomegaly -not
brain/kidney

34. • Myocardial hypertrophy
• Extramedullary hemopoesis
• Hyperinsulinism---acidosis----still birth
B) Post natal:
• Hypoglycemia 1-3hrs (lack of maternal
glucose supply + Persistent
hyperinsulinemia

35. Problems
• Antenatal :
• Polyhydramnios
• Pre-eclampsia
• Pyelonephritis
• Previous H/O still birth, premature
delivery, abortion

36. www.drsarma.in 39

37. Problems
• Natal :
• Fetal macrosomia-difficult delivery,
birth injury - Erb’s palsy, Clavicle
fracture, Phrenic N palsy
• Sudden unexpected fetal death –
ketoacidosis
• Usually LSCS
• Large placenta
• Premature delivery
• TTN

38. Problems (post natal)
• Hypoglycemia- within 1-3 hrs of birth
IDM -75% get in 1st 24 hr
GDM -25% get in 1st 24 hr
• Hypocalcemia 24-72 hrs of birth(50%)
• Polycythemia
• Hyperbilirubinemia

39. Problems (post natal)
• Respiratory distress – HMD Large
baby( LFD)
• Delayed passage of meconium delayed
devl of left colon
• Hypomagnesemia –related with
maternal hypomagnesemia with DM

40. Associated Cong anomalies
• 3-4 times more common
• Hyperglycemia induced teratogenicity
1. CNS- neural tube defects-
Anencephaly, holoporencephaly,
meningocele
2. Vertebral –caudal regression syndrome –
lumbo sacral agenesis
3.Renal – R. vein thrombosis, renal
agenesis hydronephrosis

41. 4.Cardiac
• 5 times more
common—
• Transient
hypertrophic
subaortic stenosis
• Septal hypertrophy,
• Hypertrophic
cardiomyopathy
• CCF

42. Associated Cong anomalies
4. Cardiac….. – VSD, ASD, Co.Aorta,
TGA
5.Gastrointestinal - Small left colon
syndrome-abdominal distension,
Duodenal or anorectal atresia

43. Signs & Symptoms of Hypoglycemia
• Jitteriness • Poor suck
• Irritability • Tachypnea
• Hypotonia • Cyanosis
• Lethargy • Apnea
• High-pitched cry • Seizures
• Hypothermia • Cardiac arrest
Verklan & Walden, 2004

44. On examination
• Large , plump,
Plethoric, features
of preterm
• Hypotonic,
hypothermia
• Hypertrichiosis-
hairy pinna

45. On examination
• Hypoglycemia-jitteriness,
lethargy, cyanosis, poor feeding,
vomiting, tremor, seizures
Apnoeic spells
• Tachypnia-HMD,CCF
• Asociated cong anomalies +

46. On examination
• Polycythemia— if PCV>65%
• signs of hyperviscosity —jitteriness,
tachypnoea, cyanosis ,seizures, poor
feeding. At times RV thrombosis,
hyperbilirubinemia

47. DIAGNOSIS
Babies at high risk should be screened within the first
1-2 hours
- reagent strips-measure whole blood glucose-15% lower
than plasma levels
- Confirmatory blood sugar determination is required-
and the blood should taken to the lab immediately
since glucose levels can fall 18 mg/dl/hour in the
blood sample that awaits analysis
- Septic screen

48. Monitoring in IDM:
• Check blood glucose level at 1,2,3,6,12,24,26
and 48 hrs
• Hematocrit at 1 and 24 hrs
• Calcium levels if baby appears jittery or sick
• Bilirubin if clinically jaundiced

49. Investigations
• C BC-hct
• Blood sugar-1st hr of birth ,then
2,3,6,8,12,24,48th hrs of birth
• S.calcium, S. magnesium
• CXR – Cardiomegaly 30% HF-
10% Features of HMD
• USG-renal, gut anomalies
• ECHO

50. Management: mother
• 1. Proper control of maternal DM-
- No Oral Hypoglycemics- due to
teratogencity/intractable hypoglyce
- Insulin to keep BSL<120mg
• Assessment of fetal maturity—signs of
lung maturity—L:S ratio >3.5
(normally>2)
• Elective LSCS

51. Treatment
• Asymptomatic- breast feeds/formula- repeat
blood test in one hour- if glucose does not
come up-aggressive therapy is required
• IV therapy-indications
- Symptomatic
- Inability to tolerate oral feeds
- Glucose level < 25 mg%
- oral feedings do not maintain glucose levels

52. IV Dextrose:
• 2 ml/kg of 10%dextrose
• For symptomatic hypoglycemia- 10 %
dextrose 4 ml/kg
• Continuing treatment- 6-8mg/kg/min
• Recheck 20-30 min and hourly until stable
• Additional bolus infusion-2 ml/kg of 10%
dextrose
• If glucose is stable-feeding reintroduced
and glucose infusion tapered

53. continued
• Increase glucose infusion upto 12-15 mg/kg/min
• In these cases-hydrocortisone 10 mg/kg/day may be
used
• Glucagon (25-300 micrograms) -may be used in
neonates with good glycogen stores- temporary
measure-until IV access is available
• Other drugs- diazoxide/verapamil-refer to a tertiary
centre

54. hypoglycemia
10 % dextrose 2 ml/kg
glucose infusion 6 mg/kg/min
gRBS 20-30 min
still low
10 % dextrose 2 ml/kg
glucose infusion 8 mg/kg/min
gRBS still low
hydrocortisone 10 mg/kg/d
gRBS still low
glucagon IM (0.025-0.3 mg/kg)
diazoxide 2-5 mg/kg q8hr PO
epinephrine/ GH subtotal pancreatectomy

55. Management: baby
1. Asymptomatic & normoglycemic:
Early feeding
Frequent BSL
2.Asymptomatic & Hypoglycemic:
Frequent feed
IV glucose 10%
2ml/kg bolus

56. Management: baby
3.Symptomatic & hypoglycemia
If symptoms – 4ml /kg 10% glucose IV
followed by 10% glucose drip 8mg (.08ml
/kg / m for 2 days - monitor BSL 2 hrly
until >40mg/dl ,then monitor 4-6 hrly
– Then gradually decrease rate if stable
for 24-48 hrs

57. If recurs
• Hypertonic glucose 12-20%
IV hydrocortisone
oral prednisolone
IM GH
• If hyperinsulinemic hypoglycemia
oral diazoxide
oral octretide

58. Management: baby
• Treat complications
• Treat infections
• If severe polycythaemia—partial ET
with plasma/saline

59. Complications - DM
1 Acute complications
2. Intermediate complications
2.Long-term complications
3.Complications by associated autoimmune
diseases.

60. Complications - DM
• Acute complications -
- Hypoglycemia
- Hyperglycemia (DKA)

61. Intermediate complications
• Lipoatrophy – insulin use
• Limited joint mobility – flexion
contractures of Metacarpophalangeal &
proximal interp jt – inability to
approximate palmer surface of hands –
prayer sign
• Growth failure - poor metabolic control
Mauriac syndrome - extreme growth
failure

62. Intermediate complications
• Delayed sexual maturity –
• Intellectual development – insult to
developing brain by hypo or
hypryglycemia

63. Long-term complications
• Rare in childhood
– Eye - Retinopathy , Cataracts
– Nephropathy - Progressive renal failure
– Neuropathy, both peripheral and autonomic
– Early coronary artery disease
– Peripheral vascular disease, Hypertension
– Increased risk of infection

64. DKA - pathophysiology
Insulin deficiency→ Hyperglycemia
↓
Osmotic diuresis & electrolyte loss
↓
Decreased volume →dehydration
↓
Metabolic acidosis

65. DKA - pathophysiology
Insulin deficiency→ lipolysis in peripheral tissue
↓ ↓
 Glucagon, cortisol, GH →→  FFA
↓ liver/kidney
↓
 ketone bodies

66. Risk Factors - DKA
• ↓insulin therapy
• Infections
• Trauma/burns
• Surgical procedures
• Steroid therapy
• Any other stress

67. Classification of DKA
Venous Mild Moderate Severe
blood
CO2 16-20 10-15 <10
mEq/L
(20-28)
pH 7.25-7.35 7.15-7.25 <7.15
(7.35-7.45) -Oriented - Kuss .resp -Resp –Kussmal
-Alert but - Oriented / Depressed
-Fatigued - Sleepy but - Sensorium -
- Arousable Depressed to
coma

68. Diagnosis
• C/F
• Assess for – State of consciousness
- Severity of dehydration
- Severity of acidosis
-Precipitating factors

69. Lab
• Ketonuria
• Ketonemia
• Blood glucose->250mgldl
• pH < 7.3
• HCO3 < 20 mEq/L

70. Management
Correction of
- Dehydration
- Dyselectrolytemia
- Start insulin

71. Treatment protocol
• 1st Hr- 10-20 ml/kg 0.9 % NaCl or R/L
• Insulin drip @ 0.05 - 0.1u / kg /hr ( regular)
- NPO
- Repeat bolus till dehydration corrected
- Check Neurologic status
- Have Mannitol at bedside (C. Edema)

72. Treatment protocol
• Repeat ECG – 6-8 hrly
• Electrolytes , pH 2-4 hrly
- Monitor I/O, monitor blood glucose
hrly

73. Treatment protocol
• 2nd hr till DKA resolution –maintenance
fluids
• 0.45% NaCl + cont insulin drip + 20 mEq/L
potassium
• Blood sugar < 250mg/dl (14mmol/L) - add
5% dextrose to infusate

74. Treatment protocol
• Correction of acidosis by bicarbonate
is required only if pH < 7
• When blood glucose –normal give S/c
insulin and stop insulin drip 30 min
after this

75. Treatment protocol
• 0.5-0.7units/kg (IA) insulin + 0.1 units/kg
regular insulin SC at 4-6hrly
• Adjust dose daily until satisfactory
glycemic control is achieved
• Injection site – rotated to avoid
lipohypertrophy
• Posterior .upper extremity, anterior
thigh, buttocks, anterior abdominal wall

76. Long-term complications
Diabetic retinopathy
– Within 5 years of onset of diabetes.
– 80% with IDDM develop retinopathy.
Diabetic nephropathy
– Peak incidence is in post adolescents, 10-15
years after diagnosis
– 30% with IDDM.

77. Long-term complications
Diabetic neuropathy
• Autonomic changes - 40% of IDDM
MI and stroke - with IDDM have twice the
risk
Atherosclerosis - with IDDM have 4 times
risk

78. Follow up
– Growth assessment
– Injection site examination
– Retinoscopy or other retinal screening
– Blood pressure

79. Follow up
– Examination of hands, feet, and peripheral
pulses, signs of limited joint mobility,
peripheral neuropathy, and vascular disease
– Evaluation for signs of associated
autoimmune disease
– Urine examination for microalbuminuria

80. Tips
&
Terminologies

81. Phases of diabetes
• Development of clinical symptoms
• Honeymoon phase
• Relapse
• Total diabetes - irreversible

82. Honeymoon period
• Phase of remission after initial
stabilization
• Due to residual β-cell function –residual
insulin secretion
• 75% go into this phase
• 5% go into complete remission
• Phase – variable ( wks/months /1-2 yrs)

83. Somogyi phenomenon
• Hypoglycemic episode followed by rapid
onset of hyperglecemia
• Due to counter regulatory hormones in
response to insulin induced
hypoglycemia
• Also described as hypoglycemia
begetting hyperglycemia

84. Dawn phenomenon
• Hyperglycemia at 5-9 am without
preceeding hypoglycemia
• Due to Waning effects of biologically
available insulin & nocturnal surges of GH
• Normal event

85. Distinguish ( Somogyi& Dawm P)
• Blood glucose at 3,4,7 am
• Dawn P - >80mg/dl in 1st sample (3am)
and markedly higher in last sample &
am-↑ evening dose or delay evening
dose by 2-3 hrs
• Somogyi P – ≤ 60mg/dl in 1st
sample(3am) –rebound hyperglycemia at
7 am -↓ evening dose or delay insulin at
9 pm

86. Brittle diabetes
• Control of blood glucose fluctuates
widely & rapidly despite frequent
adjustment of dose of insulin
• Somogyi & dawn phenomenon – most
common causes

87. Thank you
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Medical Post [ www.themedicalpost.net ]