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Neonatal Hypoglycemia and Infant of a Diabetic Mother

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Neonatal Hypoglycemia and Infant of a Diabetic Mother

  1. 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. 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. 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. 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. 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. 6. • Incidence - 8.1% of term LGA 14.7 % of SGA
  7. 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. 8. Decreased stores or decreased production• Prematurity• IUGR• Decreased calorie intake• Delayed onset of feeding
  9. 9. Increased utilization/decreased production• Perinatal stress • Defects in CHO- Sepsis metabolism- Shock - glycogen storage disease- Asphyxia - galactosemia- Hypothermia- RDS
  10. 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. 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. 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. 13. SYMPTOMS• Asymptomatic• Lethargy, apathy and limpness• Apnea• Cyanosis• Weak or high pitched cry• Seizures, coma• Poor feeding, vomiting• Tremors, jitteriness or irritability
  14. 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. 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. 16. Infant of diabetic mother
  17. 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. 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. 19. Hypoglycemia• Pedersen Hypothesis – Maternal hyperglycemia – Fetal hyperglycemia – Fetal -cell hyperplasia – Neonatal hyperinsulinemia
  20. 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. 21. Fetal Hyperglycemia• 1-2 hours of fetal hyperglycemia can have detrimental effects• insulin secretion – Storage of excess nutrients macrosomia – Post natal hypoglycemia
  22. 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. 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. 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. 25. Congenital Malformations• No increase in major congenital malformations among offspring of – Diabetic fathers – Prediabetic women – GDM after first trimester
  26. 26. Congenital MalformationsSkeletal/CNS• Caudal regression syndrome not considered pathognomonic occurs 600 x more frequently among IDDM• Neural tube defects• Microcephaly
  27. 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. 28. Congenital MalformationsCardiac• Transposition + VSD• Ventricular septal defect• Coarctation + VSD or PDA• Atrial septal defect• Hypertrophic Cardiomyopathy
  29. 29. Congenital MalformationsRenal• Hydronephrosis• Renal agenesis• Ureteral duplication
  30. 30. Congenital MalformationsGI• Duodenal atresia• Anorectal atresia• Small left colon syndrome
  31. 31. Perinatal and Neonatal Complications• Disorders of fetal growth• Intrauterine and perinatal asphyxia• Hypoglycemia• Respiratory distress syndrome
  32. 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. 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. 34. • Myocardial hypertrophy• Extramedullary hemopoesis• Hyperinsulinism---acidosis----still birthB) Post natal:• Hypoglycemia 1-3hrs (lack of maternal glucose supply + Persistent hyperinsulinemia
  35. 35. Problems• Antenatal :• Polyhydramnios• Pre-eclampsia• Pyelonephritis• Previous H/O still birth, premature delivery, abortion
  36. 36. www.drsarma.in 39
  37. 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. 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. 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. 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. 41. 4.Cardiac• 5 times more common—• Transient hypertrophic subaortic stenosis• Septal hypertrophy,• Hypertrophic cardiomyopathy• CCF
  42. 42. Associated Cong anomalies4. Cardiac….. – VSD, ASD, Co.Aorta, TGA5.Gastrointestinal - Small left colon syndrome-abdominal distension, Duodenal or anorectal atresia
  43. 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. 44. On examination• Large , plump, Plethoric, features of preterm• Hypotonic, hypothermia• Hypertrichiosis- hairy pinna
  45. 45. On examination• Hypoglycemia-jitteriness, lethargy, cyanosis, poor feeding, vomiting, tremor, seizures Apnoeic spells• Tachypnia-HMD,CCF• Asociated cong anomalies +
  46. 46. On examination• Polycythemia— if PCV>65%• signs of hyperviscosity —jitteriness, tachypnoea, cyanosis ,seizures, poor feeding. At times RV thrombosis, hyperbilirubinemia
  47. 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. 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. 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. 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. 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. 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. 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. 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. 55. Management: baby1. Asymptomatic & normoglycemic: Early feeding Frequent BSL2.Asymptomatic & Hypoglycemic: Frequent feed IV glucose 10% 2ml/kg bolus
  56. 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. 57. If recurs• Hypertonic glucose 12-20% IV hydrocortisone oral prednisolone IM GH• If hyperinsulinemic hypoglycemia oral diazoxide oral octretide
  58. 58. Management: baby• Treat complications• Treat infections• If severe polycythaemia—partial ET with plasma/saline
  59. 59. Complications - DM1 Acute complications2. Intermediate complications2.Long-term complications3.Complications by associated autoimmune diseases.
  60. 60. Complications - DM• Acute complications - - Hypoglycemia - Hyperglycemia (DKA)
  61. 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. 62. Intermediate complications• Delayed sexual maturity –• Intellectual development – insult to developing brain by hypo or hypryglycemia
  63. 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. 64. DKA - pathophysiologyInsulin deficiency→ Hyperglycemia ↓ Osmotic diuresis & electrolyte loss ↓ Decreased volume →dehydration ↓ Metabolic acidosis
  65. 65. DKA - pathophysiologyInsulin deficiency→ lipolysis in peripheral tissue ↓ ↓  Glucagon, cortisol, GH →→  FFA ↓ liver/kidney ↓  ketone bodies
  66. 66. Risk Factors - DKA• ↓insulin therapy• Infections• Trauma/burns• Surgical procedures• Steroid therapy• Any other stress
  67. 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. 68. Diagnosis• C/F• Assess for – State of consciousness - Severity of dehydration - Severity of acidosis -Precipitating factors
  69. 69. Lab• Ketonuria• Ketonemia• Blood glucose->250mgldl• pH < 7.3• HCO3 < 20 mEq/L
  70. 70. ManagementCorrection of - Dehydration - Dyselectrolytemia - Start insulin
  71. 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. 72. Treatment protocol• Repeat ECG – 6-8 hrly• Electrolytes , pH 2-4 hrly- Monitor I/O, monitor blood glucose hrly
  73. 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. 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. 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. 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. 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. 78. Follow up– Growth assessment– Injection site examination– Retinoscopy or other retinal screening– Blood pressure
  79. 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. 80. Tips &Terminologies
  81. 81. Phases of diabetes• Development of clinical symptoms• Honeymoon phase• Relapse• Total diabetes - irreversible
  82. 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. 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. 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. 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. 86. Brittle diabetes• Control of blood glucose fluctuates widely & rapidly despite frequent adjustment of dose of insulin• Somogyi & dawn phenomenon – most common causes
  87. 87. Thank youDownload more documents and slide shows on The Medical Post [ www.themedicalpost.net ]

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