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Neonatal Hypoglycemia and Infant of a Diabetic Mother

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  • 1. Hypoglycemia, Infant of a Diabetic Mother Dr. Kalpana Malla MD Pediatrics Manipal Teaching HospitalDownload more documents and slide shows on The Medical Post [ www.themedicalpost.net ]
  • 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. HypoglycemiaDefinition: 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. ETIOLOGYIncreased 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. Causes1. Decreased production/store - Preterm , IUGR 67%, LGA 38% - Inadequate intake2. ↑utilization/↓production - Perinatal stress - Septicemia, birth asphyxia, Hypothermia - Defect in CHO metabolism- IEM - Endocrine defic - adrenal insufficiency - cong hypopituitarism - Polycythemia
  • 12. Causes3. 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 MalformationsSkeletal/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 componentsCaudal Regression with limbsintact but malformed Sirenomelia Absence of hind limbs, external genitalia, anus and rectum; Potter sequence secondary renal agenesis
  • 28. Congenital MalformationsCardiac• Transposition + VSD• Ventricular septal defect• Coarctation + VSD or PDA• Atrial septal defect• Hypertrophic Cardiomyopathy
  • 29. Congenital MalformationsRenal• Hydronephrosis• Renal agenesis• Ureteral duplication
  • 30. Congenital MalformationsGI• 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 birthB) 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 teratogenicity1. CNS- neural tube defects- Anencephaly, holoporencephaly, meningocele2. Vertebral –caudal regression syndrome – lumbo sacral agenesis3.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 anomalies4. Cardiac….. – VSD, ASD, Co.Aorta, TGA5.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. DIAGNOSISBabies 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/mingRBS 20-30 minstill low 10 % dextrose 2 ml/kg glucose infusion 8 mg/kg/mingRBS 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: baby1. Asymptomatic & normoglycemic: Early feeding Frequent BSL2.Asymptomatic & Hypoglycemic: Frequent feed IV glucose 10% 2ml/kg bolus
  • 56. Management: baby3.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 - DM1 Acute complications2. Intermediate complications2.Long-term complications3.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 - pathophysiologyInsulin deficiency→ Hyperglycemia ↓ Osmotic diuresis & electrolyte loss ↓ Decreased volume →dehydration ↓ Metabolic acidosis
  • 65. DKA - pathophysiologyInsulin 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 DKAVenous Mild Moderate SeverebloodCO2 16-20 10-15 <10mEq/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. ManagementCorrection 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 complicationsDiabetic 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 complicationsDiabetic neuropathy• Autonomic changes - 40% of IDDMMI and stroke - with IDDM have twice the riskAtherosclerosis - 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 youDownload more documents and slide shows on The Medical Post [ www.themedicalpost.net ]