Diabetes in pregnancy -Enam Medical College and Hospital
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Hormonal &Metabolic Changes during Pregnancy Patho-physiology of hyperglycemia in pregnancy Risk factors, Clinical Features & Investigations Complications of hyperglycemia in pregnancy Medical management of hyperglycemia in pregnancy Obstetric Management of hyperglycemia in pregnancy A seminar was arranged as a part of integrated teaching at Enam Medical College, Savar, Dhaka, Bangladesh which was presented by the students.
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Diabetes in pregnancy -Enam Medical College and Hospital
- 1. Hyperglycaemia in pregnancy Integrated Teaching Presenter: Rohan farabi (3rd year) Nahian rabbi (4th year) Nazia shammee Hussain (5th year) Sithi saha (5th year) Sankalpa karki (5th year) Gazi mazharul islam palash (5th year) Students of Enam Medical College and Hospital Savar, Dhaka, Bangladesh
- 2. Hormonal &Metabolic Changes during Pregnancy Rohan Farabi Roll no: 10 EM-14
- 3. 0.00% 10.00% 20.00% 30.00% 40.00% 50.00% 60.00% 70.00% 80.00% 90.00% 4th Qtr , 85.10% , 7.40% , 7.50% gestational diabetes Pregestational DM diagnosed for the first time Diagnosed pregestational DM International Diabetic Federation (IDF) estimated that 20.9 million or 16.2% of live births to women in 2015 had some form of hyperglycemia in pregnancy.
- 4. Prevalence •South-East Asia Region 24.2% •Africa Region 10.5% •Bangladesh: 27.9%
- 5. •Approximately half of women with a history of GDM go on to develop type 2 diabetes within five to ten years after delivery.
- 6. Metabolic & Hormonal Changes During Pregnancy
- 7. Major adaptations in maternal anatomy, physiology, and metabolism are required for successful pregnancy.
- 8. Total metabolism is increased due to needs of growing fetus and uterus. Metabolic rate is increased to the extent of 30% than that of the average of the non pregnant women.
- 9. The metabolic changes are due to hypertrophy of almost all the endocrine glands namely pituitary, thyroid, adrenal and islets of langerhans of pancreas.
- 13. Glucose is much needed from mother to fetus throughout pregnancy. Growth hormone, Thyroid hormone, Cortisol, Glucagon, Human placental lactogen (placental hormone) increases the blood glucose concentration through maternal insulin resistance.
- 14. Carbohydratemetabolismduring pregnancy Serum glucose level is increased Insulin secretion is increased (hyperplasia and hypertrophy of beta cells of pancreas) Plasma insulin increased, thus ensures continuous supply of glucose to fetus Sensitivity to insulin is decreased Plasma insulin increased, thus ensures continuous supply of glucose to fetus
- 15. Fat Metabolism
- 17. Average 3-4 kg of fat is stored during pregnancy mostly in the abdominal wall, breasts, hips and thighs. HDL level increases by 15%. LDL is utilized for placental steroid synthesis.
- 18. Lipolysis takes action and generates fatty acids for gluconeogenesis and fuel supply. During maternal fasting, there is hypoglycemia, hypoinsulinemia and hyperlipidemia .
- 22. At term, fetus and placenta contain 500 grams of protein and maternal gain is also about 500 gram. Amino acids are actively transported across the placenta to the fetus. Total concentration of serum proteins decreases by about 0.1g/dl during pregnancy. It is related to increased excretion and utilization.
- 24. Pathophysiology of hyperglycemia in pregnancy Nahian Rabby Roll: 46 EM 13
- 25. Classification of hyperglycaemia in pregnancy Hyperglycaemiainpregnancy Diabetes in pregnancy (DIP) Type I and type II DM Diagnosed pre-gestational DM Undiagnosed pre-gestational DM Gestational Diabetes Mellitus (GDM)
- 26. Pathophysiology of type I Diabetes mellites
- 27. So, Why T cell mediated autoimmune destruction occurs?
- 28. Pathophysiology of type I Diabetes mellites
- 29. Marcophage T cell T cell Beta cells T cells attacking beta cells of pancreas IFN-γ Infiltration of islets by mononuclear cell such as • activated macrophage • helper T cell • Cytotoxic T cell and suppressor T cell • NK cell • B lymphocyte
- 30. Destroyed beta cells Increase glucose in blood Diabetes
- 31. 1. 2. Genetic predisposition of Type I DM
- 32. HLA class ii genes on chromone 6 Code for Protein on the cell surface of β- cell These proteins are presented as foreign antigen to T- cell T-cell mediated destruction of β-cell Diabetes Genetic predisposition of Type I DM
- 33. Environmental factors of Type I DM First degree relatives with type I DM
- 34. Environmental factors of Type I DM Geographical and seasonal variation
- 35. Environmental factors of Type I DM Some viruses (mumps, retrovirus, rubella, CMV, EBV)
- 36. Environmental factors of Type I DM Coffee
- 37. Environmental factors of Type I DM Bovine serum albumin
- 38. Pathogenesis of Type II DM
- 40. Pathophysiology of GDM Fetoplacental hormones Increased insulin resistance Compensatory increase in insulin secretion Normal pregnancy Unable to produce enough insulin to counteract placental hormones Increased glucose level GDM Estrogen, progesterone, Prolactin, HPL, GH, Cortisol
- 41. Risk factors, Clinical Features & Investigations Nazia Shammee Hussain Roll: 95 EM 12
- 43. Risk factors Positive family history of diabetes
- 44. Risk factors Ethnic group (east Asian, pacific island ancestry)
- 46. Risk factors Age over 30 years
- 47. Risk factors IFG or, IGT on previous testing
- 48. Risk factors Persistent glycosuria glucose Normal Diabetic
- 49. Risk factors H/O previous baby of ≥4 kg birth weight
- 51. Risk factors H/O unexplained perinatal loss
- 52. Risk factors Presence of polyhydramnios
- 53. Risk factors recurrent vaginal candidiasis
- 54. Risk factors Polycystic ovarian syndrome
- 56. Clinical features of DIP Polyuria
- 57. Clinical features of DIP Polydypsia
- 58. Clinical features of DIP Polyphagia
- 59. Clinical features of DIP Alteration of weight
- 60. Clinical features of DIP Weakness
- 61. Clinical features of DIP Frequent infection
- 62. Clinical features of DIP Mood changes
- 63. Clinical features of DIP Irritability
- 64. Clinical features of DIP Apathy
- 65. Clinical features of DIP Difficulty in concentration
- 66. Clinical features of GDM May be asymptomatic
- 67. Investigation
- 68. Investigation in 1st Antenatal visit Blood grouping
- 69. Investigation in 1st Antenatal visit Complete blood count
- 70. Investigation in 1st Antenatal visit HBsAg
- 71. Investigation in 1st Antenatal visit VDRL test
- 72. Investigation in 1st Antenatal visit Urine R/M/E
- 73. Investigation in 1st Antenatal visit Ultrasonography
- 74. Investigation in 1st Antenatal visit Thyroid screening
- 75. Approach to diagnose a case of hyperglycemia in pregnancy
- 76. 1st trimester Diagnosed Pre-gestational DM No OGTT Only monitoring is required Undiagnosed Pre- gestational DM OGTT, HbA1c Increased DM Normal Screening at 24-28 weeks for GDM Increased GDM Normal Screen again at 32-34 weeks
- 77. Screening and diagnosis of GDM Universal screening for GDM done in between 24-28 weeks of pregnancy
- 78. Oral Glucose Tolerance Test
- 79. OGTT in GDM 1 step 2 step
- 80. One step strategy GDM Fasting ≥ 5.1 mmol/L 75gm glucose intake After 1hr ≥ 10.0 mmol/L After 2hr ≥ 8.5 mmol/L
- 81. 100gm GTT is indicated ≥7.8 mmol/L After 1 hour 50gm glucose intake • irrespective of food intake and time Two step strategy: Step #1
- 82. Two step strategy: Step #2 100 gm OGTT should be performed when the patient is fasting.
- 83. The diagnosis of GDM is made if at least two of the following four plasma glucose levels are met or exceeded: National Diabetes Data group Fasting 1 hr 2 hr 3 hr 5.8 mmol/L 10.6 mmol/L 9.2 mmol/L 8.0 mmol/L
- 84. Investigations for monitoring of blood sugar SMBG (Self Monitoring Blood Glucose) • Pre prandial plasma glucose level • Peak post-prandial plasma glucose level HbA1c
- 85. Anomaly scanning Congenital abnormality is very common in case of Diabetes in pregnancy. Scanning is done at 20- 22nd weeks of pregnancy
- 86. Investigations for anomaly scanning • Ultrasound • α- fetoprotein • Fetal echocardiography • MRI • PAPP-A • Amniocentesis • Chorionic villus sampling • Detection of chromosomal aberrations
- 87. Investigation of infant of diabetic mother Blood glucose Hct Serum calcium Serum Magnesium Serum Bilirubin X-ray Echocardiography ECG
- 88. Complications of hyperglycemia in pregnancy Shithi Saha Roll: 77 Batch: EM 12
- 89. Maternal complications Fetal and Neonatal complications
- 92. Maternal Complications: During pregnancy Increase risk of miscarriage
- 95. Maternal Complications: During pregnancy Increase risk of pre-eclampsia
- 96. Increased risk of infections. Eg. vaginal candidiasis, UTI Maternal Complications: During pregnancy
- 97. Maternal distress Maternal Complications: During pregnancy (Cont.)
- 98. Progression of Retinopathy Maternal Complications: During pregnancy (Cont.)
- 99. Progression of Nephropathy Maternal Complications: During pregnancy (Cont.)
- 100. Coronary artery diseases Maternal Complications: During pregnancy (Cont.)
- 102. Prolong labour Maternal Complications: During labour
- 103. Shoulder dystocia Maternal Complications: During labour
- 104. Perineal injury Maternal Complications: During labour
- 105. postpartum haemorrhage Maternal Complications: During labour
- 106. Operative interference Maternal Complications: During labour
- 107. Increased risk of puerperal sepsis Maternal Complications: During puerperium
- 108. Wound infection Maternal Complications: During puerperium
- 109. Lactation failure Maternal Complications: During puerperium
- 112. Neural tube defect Fetal Complications: CNS & skeletal system
- 113. Anencephaly Fetal complication: CNS & skeletal system
- 114. Microcephaly Fetal complication: CNS & skeletal system
- 115. Caudal regression syndrome Fetal Complications: CNS & skeletal system
- 116. Idiopathic hypertrophic aortic stenosis Fetal Complications: CVS
- 117. Atrial septal defect Fetal Complications: CVS
- 118. Ventricular septal defect Fetal Complications: CVS
- 119. Coarctation of the aorta Fetal Complications: CVS
- 120. Renal agenesis Fetal Complications: Renal system
- 121. Polycystic kidney Fetal Complications: Renal system
- 128. Hypoglycemia Respiratory distress syndrome Hyperbilirubinemia Polycythemia Hypocalcemia ≤7mg/dl Hypomagnesemia <7mg/dl Cardiomyopathy
- 130. Long term effects: Fetal Childhood obesity Metabolic syndrome Neuropsychological effects Diabetes Cardiovascular diseases
- 131. Long term effects: maternal Increased risk of Type II DM
- 132. Perinatal mortality: • Hypoglycemia • Respiratory Distress Syndrome • Polycythemia • Jaundice Increase two to three times.
- 133. Medical management of hyperglycemia in pregnancy Sankalpa Karki Roll: 124 EM 12
- 134. Aim of management •To attain maternal blood glucose level near to normal
- 135. Target glycaemic control Fasting 1hr 2hr < 5.3 mmol/L <7.8 mmol/L <6.7 mmol/L
- 136. HYPERGLYCAEMIA
- 137. Medical nutritional therapy (MNT) • Medical nutrition therapy and lifestyle modifications can effectively manage 70- 85% of cases.
- 139. Low carbohydrates diet MNT nutritional goals and recommendations
- 140. High fiber intake MNT nutritional goals and recommendations
- 141. Protein rich food MNT nutritional goals and recommendations
- 142. STOP
- 144. Frequent small meals MNT nutritional goals and recommendations
- 145. Exercise • Improves glucose homeostasis • Improves insulin sensitivity • When moderate variety of exercise is done, muscles use more glucose and as a result it lowers the blood glucose level.
- 148. Oral anti-hyperglycaemic drugs Medication Crosses placenta Metformin Yes Glyburide Minimal transfer
- 149. Biguanide – Metformin: M/A Decrease hepatic glucose production Increase peripheral utilization of glucose Decrease intestinal absorption of glucose
- 150. DOSE Starting dose: 500mg once daily for 7 days Gradually increase up to 1 gm then 2.5 gm
- 151. Glyburide: (Sulfonylurea): M/A Stimulation of release of insulin from beta cells Decrease insulin resistance
- 152. Dose Dose: 1.25-2.5mg twice daily, Starting dose
- 153. But it’s use is controversial
- 154. First line agent
- 155. Types A. Rapid acting: -Lispro -Aspart B. Short acting: -Regular insulin
- 156. Types C. Intermediate acting: -NPH (neutra protamine hagedron) D. Long acting: -Detemir
- 157. Regimen of insulin in pregnancy Multiple regular doses of insulin
- 158. Regimen of insulin in pregnancy Continuous Subcutaneous Infusion Pump
- 159. Requirement of insulin 0.3 U/kg/ day – 0.5 U/kg/day as starting dose Rapidly adjust dose based on SMBG
- 163. Aspirin is also given to prevent eclampsia and pre eclampsia
- 165. Timing and Mode of Delivery Individualized
- 166. Time of delivery Pattern of diabetes Nature of control Past obstetric outcome Test of fetal wellbeing Superimposed risk factor like pre-eclapmsia
- 167. •Low risk group and stable insulin dependent patient- at term •High risk and unstable insulin dependent patient - at 37-39th week •Small risk of late intra-uterine death even with good glycemic control – delivery usually at 38th week Time of delivery
- 168. Mode of Delivery Depends on- Parity Cervical score Pelvic adequacy Macrosomia Malpresentation Previous obstetrical history Associated complicating factors
- 169. Normal vaginal delivery preferred
- 170. Cesarean section preferred only for obstetric indication
- 171. GDM alone is not indication for cesarean section
- 173. No morning dose of insulin Management During Labor
- 174. Use of combined insulin & glucose infusion Management During Labor
- 175. Hourly monitoring of glucose level Management During Labor
- 176. Continuous fetal monitoring and monitoring of progress of labor by partograph Management During Labor
- 177. Presence of expert Obstetrician, Anesthetist, Neonatologist Management During Labor
- 178. Postpartum Management Prophylactic antibiotic Breast feeding Blood sugar estimation and readjust insulin dose
- 179. Postpartum management of DIP Following delivery sudden loss of insulin resistance majority of patient do not require insulin for 24-48 hours Glucose level starts to rise? Restart insulin therapy @ 1/2 - 2/3 of previous dose and adjust
- 180. Blood glucose level should be checked within 2 hours of delivery Strict monitoring of blood glucose level at least for first 24 hours Early breast feeding is given if the baby is feasible Close supervision to prevent complication Inj. Vit-k should be given Neonatal care
- 181. 50% has chance to develop GDM in next pregnancy. 50-70% has chance of developing type II DM within 3- 15 years
- 182. Post Partum Follow Up OGTT at 6th week Lifestyle Modification • Exercise • Weight reduction Contraceptive Advice • Barrier method • Low dose OCP • Permanent sterilization
- 183. Take home messages • Hyperglycaemia is teratogenic • Universal screening is mandatory • Maternal risk of type-II DM • Post partum follow-up is must • Above all awareness from “within” requires first
- 184. Thank you
Notes de l'éditeur
- There are some regional differences in the prevalence of hyperglycaemia in pregnancy, with the South-East Asia Region having the highest prevalence at 24.2% compared to 10.5% in the Africa Region.(IDF) Recent study done by Endocrine Dept. of BSMMU reported alarmingly high prevalence of hyperglycaemia in pregnancy in BD. It is 27.9%
- Previously diagnosed Previously unndiagnosed
- T cell mediated autoimmune disease where tcell mediated distruction of insulin secretory beta cell occur in pancreas
- Defective clonal dilatation of self reactive T cell Or Resistance of the effector t cell to be supressed by regulatory t cell
- Infiltration of islets by mononuclear cell such as activated macrophage helper T cell Cytotoxic T cell and suppressor T cell NK cell B lymphocyte
- রিসার্চে দেখা গেছে, majority of the mother age over 30 years এর GDM হয় Type 2 DM বেশি বয়সের দিকেই হয় ৩০ বছরের বেশি মা –রা এমনিতেই high risk group of preg
- Normal glucose threshold 160-180 mg/dl
- Death during delivery
- During pregnancy period
- In present pregnancy AFI amniotic fluid index- 8-18 5-6 oligo >20/24 poly
- More insulin> insulin goes to ovary> increase secretion of androgenic hormone> PCOS Why eccess insulin? কারণ সেল গুলো ইনসুলিন রেজিস্টেন্স হয়ে গেছে। এইজন্য বিটা সেল বেশি বেশি করে ইনসুলিন সিক্রেট করে ব্যাপারটা কম্পেন্সেট করতে চাচ্ছে। কিন্তু সে তো বেশিক্ষন বেশি বেশি ইনসুলিন সিক্রেশান ধরে রাখতে পারবে না। Fatigue হয়ে যাবে। আর এই ইনসুলিন কমে যাওয়ার ফলেই ডায়বেটিস হবে।
- More than 2.5 Liters
- Due to increase hunger
- As there are less glucose inside the cell to produce energy
- Its an immune deficiency state
- Polyhydramnions – নরমাল প্রেগ্নেন্সিতে পেট যতটুকু বড় হয় মা খেয়াল করবেন তার পেট তার চেয়ে বেশি বড় হয়ে যাচ্ছে এবং দ্রুতই বড় হচ্ছে। পেট বেশ ভারী ভারী লাগছে। এছাড়া ডায়বেটিসের যেসব সিম্পটমের কথা বললাম সেগুলোও থাকতে পারে। Increased fundal Hight
- Anaemia is common in preg
- UTI Glycosuria RBC Protin
- Because, diabetogenic hormone গুলো এই সময়ে সবচেয়ে peak এ থাকে। ফলে এই সময়ে insulin resistance হওয়ার সম্ভাবনা সবচেয়ে বেশি থাকে। তাই, এই সময় যদি আমরা স্ক্রিনিং করি তাহলে insulin resistance বা GDM নিয়ে সবচেয়ে ভালো রেজাল্ট পাওয়া যায়।
- After fasting
- Perform at GLT (non-fasting), with plasma glucose measurement at 1 hour, at 24-28 weeks of gestation in women not previously diagnosed with overt diabetes. 1 hour after the load is ≤ 7.2 mmol/L, 7.5 mmol/L or 7.8 mmol/L, proceed to a 100gm OGTT
- Anomaly scanning কেন ২০-২২ সপ্তাহে করা হয়? এর আগে কেন না? কারণ, এই সময় organogenesis already হয়ে যায়। ফলে কোন Anomaly থাকলে সেটা scanning এ ধরা পড়বে
- Blood glucose 2.6- 7.8 mmol/L- irrespective of Gestational age and birth weight After birth 2 hr int- 3 6 hr -3 12hr- 3 72hr - 3 HCT to detect Polycythemia
- birth weight >4kg High blood glucose level in mother, brings extra glucose to fetus Fetus makes more insulin to handle this extra glucose Extra glucose gets stored as fat & fetus becomes larger than normal Elevation of maternal free fatty acid in diabetes lead to it’s increase transfer to the fetus Acceleration of triglyceride synthesis Adiposity
- More common when diabetes is poorly controlled
- High dose Aspirin is contra-indicated But low dose aspirin(75mg) can be given in case of such cases
- Once their fasting or postprandial capillary glucose starts to rise , insulin therapy should be restarted using one-half to two-thirds of the dosage that the patient was receiving before delivery. This initial dose is adjusted according to the patient’s response.
- So in post partum follow up we will do OGTT at 6yh week after delivery to screen if GDM persists as type 2 DM or not as 50-70% has chance of developing type 2 DM within 3-15 years Patient is encouraged to modify her lifestyle by exercise and weight controle
- Hyperglycaemia is teratogenic Universal screening is mandatory GDM goes away that doesn’t mean Maternal risk of type-II DM will also go away. Post partum follow-up is must for early detection of type ii DM Above all awareness from “within” requires first