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Diabetes In Pregnancy


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A comprehensive guide to the management of hyperglycaemia in pregnancy aimed at the primary care physician and based on latest evidenced based criteria. Includes information from latest studies such as HAPO study and ACHOIS, and involves guidelines from the IADPSG, ADA, WHO and Malaysia.

Published in: Health & Medicine
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Diabetes In Pregnancy

  1. 1. DIABETES IN PREGNANCY All You Need To Know About The Management Of Gestational Hyperglycaemia by " Associate Professor Dr Hanifullah Khan 1
  2. 2. Hyperglycemia in Pregnancy 2
  3. 3. What is DM? A metabolic condition characterized by chronic hyperglycemia as a result of defective insulin secretion, insulin action or both • • • • Type 1(IDDM) Type 2(NIDDM) Gestational diabetes Others -genetic defects in insulin processing or action -endocrinopathies -drugs -exocrine pancreatic defects -genetic syndromes associated with DM 3
  4. 4. Pregnancy predisposes to persistent hyperglycaemia • Glucose is made available to the fetus – ↑ placental hormones – ↑ plasma cortisol – A state of insulin resistance – Further aggravated by ↑ body weight and ↑ caloric intake during pregnancy • GDM develops when the pancreas cannot overcome the effect of these hormones 4 • Pregestational diabetes becomes worse during pregnancy
  5. 5. Diabetes & Pregnancy This prevalence is increasing nowadays, more and more women go into pregnancy with increased body weight and caloric intake the prevalence of women with preexisting T2DM getting pregnant (diabetic pregnancies) seems to be rising 5
  6. 6. • Glucose intolerance of variable severity with onset or first identification during the pregnancy – – • resolving after delivery 6 Generally occurs in the latter half of pregnancy Previously, found to constitute 90% of diabetes in pregnancy
  7. 7. Important facts To understand the effects of hyperglycaemia on the fetus, it should be remembered that glucose crosses the placenta freely but maternal insulin does not Thus, maternal hyperglycaemia leads to fetal hyperglycaemia with a consequent rise in fetal insulin secretion Pregnancy is a state of insulin resistance, especially towards term 7
  8. 8. What does chronic hyperglycaemia lead to? 8
  9. 9. Pathogenesis of tissue injury Hyperglycaemia leads to the production of reactive oxygen species (ROS)! ROS lead to tissue damage through various mechanisms! This ultimately leads to micro- and macrovascular complications Giacco F. Circulation Research, 2010 9
  10. 10. Maternal Complications antenatal • Pre-eclampsia$ • Recurrent infection-vaginal candidiasis,UTI$ • Polyhydramnios—PPROM, discomfort$ • Anomalies & abortions$ • Sudden IUD 10
  11. 11. Maternal Complications delivery • Increased instrumental rates$ • Birth trauma$ • Operative delivery • Polyhydramnios— premature membrane rupture, cord prolapse 11
  12. 12. Maternal Complications postpartum Increased risk of developing DM later in life Past history of GDM increases the risk of recurrence in subsequent pregnancies Retnakaran R. Diabetes Care, 31, 1275–1281 12
  13. 13. Maternal Complications Medical • Retinopathy$ • Nephropathy$ • Neuropathy $ • Micro/macroangiopathy 13
  14. 14. Fetal complications ! ! Congenital anomalies (4 fold) - sacral agenesis, NTD, cardiac and renal anomalies$ Macrosomia$ Malpresentation$ Shoulder dystocia$ Prematurity$ Respiratory distress syndrome$ Hypoglycemia$ Polycythemic -jaundice “strong continuous associations of several perinatal outcomes with maternal glucose levels below those diagnostic of diabetes”$ HAPO study 2008 14
  15. 15. Fetal macrosomia 15
  16. 16. The child - later on…. Obesity$ Diabetes mellitus$ Reproductive problems$ Metabolic syndrome 16
  17. 17. Why is it important to differentiate between gestational & pregestational DM? 17
  18. 18. This is important because each diagnosis imparts a different clinical significance 18
  19. 19. The significance of GDM mothers are at risk of future development of T2DM adverse obstetrical outcomes! - esp. fetal overgrowth 19
  20. 20. The significance of pregestational DM Most of the risk is to the fetus similar to GDM complications during organogenesis! growth restriction 20
  21. 21. Pregestational diabetic pregnancies • carry a graver consequence$ • should be managed immediately once identified$ • Ideally, evaluation for DM should occur before pregnancy$ • to prevent complications during organogenesis (1st trimester) 21
  22. 22. Hyperglycaemia in the st trimester 1 confers a significantly increased risk of major malformations Type of Diabetes in pregnancy Risk of Major congenital abnormality (%) T1DM$ T2DM$ GDM$ (n=221) (n=317) (n=1822) 5.9 4.4 1.4 Farrel T 2002 22
  23. 23. Fetal malformations & Glycaemic control • HAPO study $ • a continuum of increasing risk of perinatal outcomes as glucose levels increase$ • even within levels that were previously defined as normal HAPO study. NEJM 2008 23
  24. 24. Hyperglycaemia later in pregnancy • High blood glucose increases fetal growth$ • Postprandial normoglycemia can reduce the rate of macrosomia FBG>5mmol/L, HbA1c>5.3% MAC ROS OMI A! HAPO study. NEJM 2008 24
  25. 25. Issues of concern 1. The frequently undiagnosed nature of T2DM before pregnancy 2. Lack of preconception care 3. The increase in complications of pregnancy due to the coexistence of obesity and T2DM 25
  26. 26. Difference between GDM & DM • DM + Pregnancy$ • GDM$ – – – – – – early pregnancy BS normal Usually no effect on organogenesis less likely to have congenital defects diabetes disappears after delivery macrosomia more likely – – – elevated BS since before pregnancy effect during organogenesis more likely to have congenital fetal defects (up to 8x more than normal pregnancy) fetes may be growth restricted overall though, perinatal outcomes are worse whatever the cause of the hyperglycaemia 26
  27. 27. How do we detect those asymptomatic mothers with DM? 27
  28. 28. Pregnant women with DM are frequently asymptomatic They need to be identified before harm can come to the fetus 28
  29. 29. Screening • during antenatal check-ups, mothers with unknown elevations of blood glucose need to be identified eleva tions of mate rnal bloo d glu cose deem are ed ha rmfu to th l e fet us • this process of looking for asymptomatic diabetics is termed screening • The benefits and importance of screening for GDM have been proven (ACHOIS & HAPO study) Crowther NEJM 2005 29
  30. 30. In Malaysia we base our screening strategy on • screen selectively those considered high risk (1-step testing) 30
  31. 31. Who are those considered high risk? 31
  32. 32. Added criteria • In recent time, this list has been expanded$ • Include factors such as $ • physical inactivity$ • certain dietary patterns$ • polycystic ovarian syndrome (PCOS)$ • biochemical markers such as adiponectin & C-reactive protein Retnakaran R. Clin Endocrinol 2007 Lo JC. Diabetes Care, 2006 32
  33. 33. PCOS • Ex-GDM mothers investigated for PCOS$ • A majority of them displayed characteristic polycystic ovarian morphology Kousta E. Clin Endocrinol, 2000 33
  34. 34. What is done now • At booking - assess risk$ • if risk present, do OGTT Current'screening'protocol' First Obstetric Visit Risk Factors - check risk status ' Absent Consider'normal' Present Risk Factors OGTT performed after 24 weeks gestation Consider'GDM'if' diagnostic'criteria'met' 34 Note: •Age >=40 yrs •Unexplained SB •P/H recurrent miscarriages •P/H BW >=4.0 kg •Weight >100 kg •P/H oligomenorrhoea •Strong maternal/sibling F/H OGTT not performed in: Known preexisting DM cases & Cases with P/H of GDM
  35. 35. Schedule for screening Between 24-28 weeks of gestation or earlier if there are stronger indications If the original OGTT is negative, recommend periodic repeat testing (may be required until 34 weeks of gestation) If the glucose tolerance remains normal at 34 weeks, stop testing 35
  36. 36. Recent Recommendations • Based on HAPO study data - even the slightest hypoglycaemia increases pregnancy adversity$ • IADPSG formulated recommendations • In a bid to achieve international consensus$ • Try to catch as many patients with pregnancy hyperglycaemia as possible IADPSG. Diabetes Care 2010 36
  37. 37. IADPSG strategy IADPSG. Diabetes Care 2010 37
  38. 38. IADPSG screen 2 discrete phases • 1st phase - early pregnancy$ • aimed at detecting previously undiagnosed overt diabetes$ • HbA1c or plasma glucose (fasting or random) measurements$ • carried out on high-risk women (adult non-pregnant criteria) • 2nd phase - 24-28 weeks$ • if 1st phase normal$ • 2-hour 75 g OGTT IADPSG. Diabetes Care 2010 38
  39. 39. Adult non-pregnant risk factors ADA. Diabetes Care 2013 39
  40. 40. The OGTT 40
  41. 41. OGTT • The first-line diagnostic test$ • Initially developed to identify the diabetic in the general population because of the many controversies surrounding this topic, numerous iterations of the OGTT abound with different criteria for diagnosis O’Sullivan, Mahan. Diabetes 1964. 41
  42. 42. Procedure 42
  43. 43. Procedure for OGTT 75 grams of oral glucose given is 3 readings fasting gluc ose level, 1 hr a nd 2 hr post glucose IADPSG. Diabetes Care 2010 43
  44. 44. Table 1: Values for Diagnosis Fasting Random Diagnostic Values Venous Plasma Glucose ≥ 11.1 mmol/L ≥ Table 2: Diagnostic values for Type 2 Diabetes Mellitus/Glucose Intolerance – oral glucose tolerance test (OGTT) [IDF 2005] 5 (Level III) OGTT Plasma Glucose Values (mmol/L) Category 0-hour ≥ DM 2-hour ≥ 11.1 2 Recommendations: Screening and Diagnosis 44
  45. 45. More recent diagnostic criteria Commonly referred to diagnostic criteria for the 75 gram OGTT include the WHO and the ADA criteria More recently, the IADPSG have adopted stringent criteria based on the HAPO study IADPSG. Diabetes Care 2010 45
  46. 46. Postpartum considerations P/H GDM woman Postpartum oGTT Abnormal GT IGT/DM Normal GT Diet & exercise F/U Blood Glucose Stable glucose Raised glucose Manage as appropriate 75g oGTT Diet & exercise F/U Blood Glucose 12:20:10 Normal GT 46 Should be carried out after 2 months postpartum
  47. 47. Is there any other way to diagnose DM in pregnancy? 47
  48. 48. Yes, but… HbA1c limitations$ • costs! • unavailability! • inaccuracy in anaemia • Only in early pregnancy$ • Glycated haemoglobin (HbA1c) and plasma glucose (random or fasting)$ • HbA1c has been validated for the diagnosis of DM outside of pregnancy (≥6.5%) with many authorities favouring its use in pregnancy as well In te r n a t i o n a l E x p e r t C o m m i t te e . Diabetes Care 2009 48
  49. 49. Plasma glucose • Fasting or random$ • FPG level of ≥7.0 mmol/L is diagnostic of overt diabetes$ • RPG of ≥11.1 mmol/L has to be confirmed with either an FPG or A1c value ≥ the threshold 49
  50. 50. How do we manage hyperglycaemia in pregnancy? 50
  51. 51. Strategy • Rapid normalisation of blood glucose$ • Limited weight gain$ • Monitoring for anomalies and complications$ • Avoiding macrosomia$ • Planned delivery 51
  52. 52. Optimization of metabolic control • BS control dependant upon diet modification, exercise and hypoglycaemic medications • Lifestyle modification (dietary advice & appropriate exercise) should be the primary interventions considered • Resort to medications only when these fail to achieve the desired targets 52
  53. 53. What is the dietary advice for diabetes in pregnancy? 53
  54. 54. Less weight gain • In overweight or obese mothers$ • No specific guidelines for women with diabetes$ • Less weight gain is safe and has a beneficial effect on perinatal outcomes in obese women$ • Access to dietitian 54
  55. 55. Individualised counselling • From a registered dietician experienced with pregnancy and diabetes$ • Basic plan - based on dietary recommendations for all pregnant women, adjusted to the individual needs of the patient • Carbohydrate and caloric contents - modified based on the woman’s height, weight, and degree of glucose intolerance 55
  56. 56. Caloric restriction • A 33% reduction of calories results in clinically relevant improvement in glycemic parameters $ • 30-35 kcal/kg/day = 1200 Kcal/d is safe$ • 50% of these calories should be from complex carbs$ • Exact amount unknown - carbohydrates, like calories, should be determined based on individual needs$ • mother’s weight, activity, home & personal circumstances$ • Base calculations on home blood glucose levels 56
  57. 57. Specific targets • Avoid concentrated sweets and highly processed foods contribute to unwanted weight gain$ • soft drinks, ice cream, cakes and sweets$ • restrict CHO to those found in vegetables and dairy products like cheese and cottage cheese • Small frequent meals (4 hourly) instead of fewer larger meals $ • reduces the amount of insulin needed at any one time, resulting in lower glucose excursions$ • also reduce hunger and prevent overeating Hone J. J Clin Endocrinol Metab 2010 57
  58. 58. Some more targets • Breakfast should be especially small and low in carbs because insulin resistance is highest in the morning$ • High-fiber and low-GI foods should be substituted wherever possible for simple sugars $ • higher fiber/low GI may assist in delaying absorption of food, thus allowing the insulin peak to “catch up”$ • Foods rich in antioxidants have a role in reducing the incidence of fetal anomalies$ • fruits and vegetables are recommended 58
  59. 59. Folic acid • Supplemental $ • Proven to reduce the risk of neural tube defects$ • The prescription should begin at least 3 months preconceptionally and through the first trimester $ • Minimum dose of 4 mg daily 59
  60. 60. ical Med nal tritio Nu apy Ther T MN If MNT doesn't work? Medication is implemented if 2 or more glucose values are elevated after 1 wk of lifestyle management 60
  61. 61. What to do if dietary intervention does not work? 61
  62. 62. Oral medication? • Previously, next step would be insulin therapy $ • because oral medications were thought unsafe, ineffective & teratogenic$ • enough data to show the utility and safety of oral hypoglycaemic agents (OHAs) in pregnancy 62
  63. 63. When to start OHAs? • When fasting or premeal BS values constantly exceed 5.5 mmol/L$ • OHAs should be started without hesitation whilst encouraging dietary and exercise efforts 63
  64. 64. Glibenclamide • The first OHA to have proven efficacy and safety in pregnancy $ • At a dose of 2.5 mg daily to a maximum of 20 mg per day$ • Similar birth outcomes can be achieved when comparing glibenclamide use to insulin initiation in pregnancy Langer et al. N Eng J Med 2000 64
  65. 65. Metformin • The starting dose is 500 mg once daily & increasing to 500 mg tds$ • Similar outcomes between metformin and insulin initialisation$ • Although 46% of mothers on metformin required additional insulin supplementation for blood sugar optimisation$ • An early indicator that metformin therapy alone might be inadequate to achieve target values is a higher fasting glucose Rowan et al. N Eng J Med 2008 65
  66. 66. General considerations • OHA dosage should be increased every 4-5 days to achieve the desired blood sugar target values • Although both metformin and glibenclamide cross the placenta, there have been no reports of fetal adversity so far • The long term effects of these OHAs are still under study but there is optimism that their safety will be proven$ • decreased overall weight gain has been noted in pregnant mothers on metformin Rowan et al. N Eng J Med 2008 66
  67. 67. When do we use insulin? 67
  68. 68. When MNT & OHA fails to achieve glycemic goals after 1 wk 68
  69. 69. be encouraged to walk for about 30 minutes per day. An example of a therapy guide agents need to be introduced when lifestyle and dietary measures fail to control the glycaem ropriate to consider starting oral hypoglycaemic agents in the first instance whenever the fastin levels consistently exceed 5.5 mmol/l, definitely if the value exceeds 7.0 mmol/l. Recent research clinical efficacy of glibenclamide [gliburide] during pregnancy. Glibenclamide should be started a ncreased every 4-5 days to a maximum of 20 mg/day. If control is not achieved, then the sulpho insulin. An alternative oral hypoglycaemic agent if metformin, though the use of this is still unde started as a 500 mg daily dose, increasing the dose to 500 mg t.d.s. depending on gastrointestina Class A1 A2 Fasting/preprandial Blood glucose Always <5.1 mmol/l 5.1-7.0 mmol/l B1 >7.0 mmol/l 2-hour postpradial Blood glucose Always <6.7 mmol/l 6.7-7.0 mmol/l >7.0 mmol/l Management options Management option Diet alone Diet +/pharmacological Rx Diet + Insulin Savonna-Ventura. UMMS Malta 2011 69
  70. 70. How do we use insulin? 70
  71. 71. Insulins A basic understanding of the dynamics and actions • Each type of insulin has an onset time, a peak and duration of action$ • The onset time is delineates how soon the blood glucose lowering action comes into effect and is commonly used to classify this class of medications$ • either rapid-, short-, intermediate- or long-acting 71
  72. 72. Development of Insulins • Originally, from animals$ • Biosynthetic preparations in the 1970s - more effective and cheaper preparations$ • The first such insulins - regular insulin (or “human” insulins)$ • classed as short-acting, $ • mainstay of diabetes treatment in pregnancy in the 1980s $ • not fully satisfactory due to a late peak (2-3 h after injection) - not very effective for postprandial control$ • too long duration of action - tending to cause hypoglycaemia 72
  73. 73. Insulin analogues • They provide more optimal glucose control during pregnancy$ • technically not insulin, but something similar that retains the hormone’s glucose lowering function$ • They are considered safe for pregnancy use - no teratogenic or embryotoxic effects have ever been demonstrated$ ! • They act rapidly, peak in about 1 hour with a duration of action between 2-4 hours. $ • The first such insulin developed was insulin lispro followed soon after by insulin aspart 73
  74. 74. NPH insulin • An intermediate acting insulin originally developed in the 1930’s $ • now synthetically produced to give better absorption rates when injected subcutaneously$ • May be mixed with shorter acting ones in the same syringe to complement its longer duration of action and to allow for better dosing and blood sugar control$ • NPH remains in the market today specifically for the reason that it can be marketed in premixed formulations for ease of use 74
  75. 75. More recent insulin analogues • Insulin glargine and detemir$ • Absorbed more steadily after injection, providing a “peakless” mode of action, followed by a rapid decline and all the while producing a more constant glucose lowering effect$ • Duration of action is approximately 24 hours, thus needing only once-daily administration - long-acting insulins$ • also induce less hypoglycaemia and weight gain compared to conventional insulins$ • Despite these attractive features, they are currently unlicensed for pregnancy use due to lack of systematic data although several reports have not demonstrated any adverse effects or teratogenicity. 75
  76. 76. Summary of insulins Table&1&Commonly&used&insulins&and&their&properties& Type&of& insulin& ! Rapid'acting! ! ! ! Short'acting! ! Intermediate! acting! ! Long'acting! ! ! Generic& name& Insulin!lispro! Onset& Peak& Duration& 15!minutes! 30'90! minutes! 3'5!hours! Regular! insulin! 30'60! minutes! 2'4!hours! 5'8!hours! NPH!insulin! 1'3!hours! 8!hours! 12'16!hours! Insulin! glargine! Insulin! detemir! 1!hour! Peakless!! 20'26!hours! Insulin!aspart! 76
  77. 77. Modes of administration • The most frequent mode of parenteral administration is via subcutaneous injection $ • using repeat-use insulin pens with fine needles$ • Intravenous administration - in intensive care settings$ • Insulin pumps provide fine-tuned insulin delivery & consequent better blood glucose control$ • financial & technical considerations 77
  78. 78. How do we calculate the amount of insulin to use? 78
  79. 79. Philosophy behind insulin • Mimic physiologic secretion of insulin as close as possible$ • In pregnancy, this entails multiple injections of various combinations of rapid, short and intermediate-acting insulin A tried and tested insulin combination is a rapidacting and NPH one 79
  80. 80. Starting values • Slightly higher starting doses may be used for obese patients$ • These values are a safe guide to insulin initiation $ • Must be optimised rapidly to achieve the target blood glucose values by using (home blood glucose monitoring) HBGM 80
  81. 81. Starting dose calculation Time of pregnancy Dose Prepregnancy 0.6 U/kg/day First trimester 0.7 U/kg/day Second trimester 0.8 U/kg/day Third trimester$(29-34 wks) 0.9 U/kg/day Term (35-39 wks) 1.0 U/kg/day Jovanovic. Diab Care 1982$ Lapolla et al. Diab Med 2009 81
  82. 82. Starting doses • The regimens are based on predicted total daily insulin requirements - based on current weight and stage of pregnancy $ • 50% of the total dose is given as a basal dose using NPH insulin (intermediate-acting)$ • at bedtime or bedtime+breakfast time$ • the other 50% of the total dose - given as boluses before meals using insulin analogues (rapid-acting)$ • before meals (within 15 minutes) in divided doses (1/6 of the total dose per meal) 82
  83. 83. Adjustments • These doses are starting doses only$ • Necessary to rapidly adjust dose to achieve glucose goals using HBGM data & A1C testing$ • Serial blood sugars - carried out between 3-7 days after starting & the dosage of insulin adjusted commensurately 83
  84. 84. How do we know if the diabetes is under control? 84
  85. 85. Pillar of assessment • Glycaemic adequacy is assessed through regular blood glucose estimations$ • Tight glucose control achieved through dietary, physical and pharmaceutical interventions Adequate BS control is proven beneficial to the pregnancy. Despite this, no clearly established glucose targets exist. Crowther et al. N Eng J Med 2005 85
  86. 86. Techniques of assessment • 2 techniques of assessment - HBGM & HbA1c $ • Most data regarding target values in pregnancy - derived from pregnant T1DM & T2DM patients Kitzmiller et al. Diab Care 2008 86
  87. 87. Target Values - FPG • FPG of ≤5.0 mmol/L $ • Associated with a reduction in the risk of macrosomia, neonatal hypoglycemia, and maternal preeclampsia in GDM during the third trimester Prutsky et al. JCEM 2013 87
  88. 88. Target Values - FPG & postprandial • FPG of ≤4.9 mmol/L & and 2-hour postprandial glucose between 5.9–6.4 mmol/L$ • risk of birthweight greater than 4 kg, prematurity, neonatal hypoglycaemia & preeclampsia are all lowered Rowan et al. Diab Care 2010 88
  89. 89. Target Values - HbA1C Amongst pregnant Type 1 diabetic mothers, maintaining HbA1c levels to less than 6% before and during pregnancy predicated outcomes similar to non-diabetic pregnant mothers Wyatt et al. Diab Med 2005 89
  90. 90. Recommendations Timing Glucose Level Premeal, bedtime, overnight 3.3–5.4 mmol/L Postprandial 5.4-7.1 mmol/L HbA1c 6.0% ADA.Diabetes Care 2013 90
  91. 91. Monitoring • Regular blood glucose monitoring - mainstay of objective optimization of metabolic control$ • between 3-4 times a day$ • a prebreakfast and postprandial (2 hours post-lunch and dinner) and/or night test$ • Initially, clinic attendance - primarily for patient education purposes$ • Subsequently, self-monitoring of blood glucose is the optimum$ • Assessment of long-term control and further optimization - 4-6 weekly by measuring HbA1c levels$ 91
  92. 92. Postprandial blood glucose monitoring Do This • Glycaemic control has been shown to be improved by limiting postprandial glucose excursions$ • Postprandial glucose correlates well with HbA1C$ • By measuring and controlling the postprandial and fasting sugars, the occurrence of neonatal hypoglycaemia and macrosomia may be reduced de Veciana M. NEJM 2013 92
  93. 93. Assessment of the pregnancy The pregnancy must be treated as a whole$ Take precise history - maternal well-being, FM$ Examine for complications - remember; maternal, fetal & placental$ Investigations - in order of priority$ ultrasound scan, urine, blood tests, CTG 93
  94. 94. Pat ie nt c o mp lain nd scans! ltrasou U ts! Do not manage the blood sugar, manage the patient! ion! inat am al Ex ysic Ph 94
  95. 95. Are you able to manage a patient with diabetes in pregnancy? 95
  96. 96. You can if.. • You routinely manage antenatal patients$ • You know how to screen for & diagnose this condition$ • You know how to implement & monitor treatment$ • You know how to monitor for complications Do not hesitate to seek help! 96
  97. 97. Case Studies Test Yourself! 97
  98. 98. Case 1 • A 34-year-old Malay woman, known DM, who is in her second pregnancy and has had one live birth is seen for prenatal care at 8 weeks gestation • Her weight is 96 kg, and her blood pressure is 130/80 mmHg. Uterine size is appropriate for gestational age. Her family history reveals that her mother has type 2 diabetes mellitus. A urine dipstick shows 3+ glycosuria and negative ketones$ Q. . What tests should be done to evaluate the patient's glucose tolerance? Q. How is the diagnosis of GDM established? Q. What would be the best treatment and follow-up strategy? 98
  99. 99. Case 2 • 25 year old G1P0 at 10 weeks gestation. No significant past medical, surgical or reproductive history. No family history of DM. A regular patient of the GP, antenatal booking bloods includes a diabetic screen utilizing HbA1c. HbA1c was 6.2%. $ Q. Is this patient GDM?$ Q. Does she need to be started on insulin 99
  100. 100. Case 3 • 35 year old G2P1 at 8 weeks gestation. Her first pregnancy – delivered LSCS for obstructed labour 4 years prior – 3.6 kg baby girl. No contraception prior to this pregnancy. $ • Routine ANC by GP – incorporate HbA1c – 8%. Diagnosed as DM with pregnancy. Based on local knowledge and guidelines, this patient requires insulin but patient refuses. Q. What should the GP do next? Q. Should this patient be started on oral medication immediately? 100
  101. 101. Case 4 • 38 year old G4P3 at 35 weeks, known DM diagnosed since last pregnancy, on metformin 850 mg bd. Since the patient is already on treatment, the GP has continued the oral medication. Regular serial sugar estimations are carried out – pre-breakfast, post-lunch and dinner – 6.2/7.7/7.8$ • Maternal and fetal well-being established$ ! Q. Should she be started on insulin now? 101
  102. 102. Thank You 102