Diabetes in pregnancy
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Diabetes in pregnancy

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done by Al Yaqdhan Al Atbi

done by Al Yaqdhan Al Atbi

Sultan Qaboos university- Oman

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  • : maternal hyperglycemia leads to fetal hyperglycemia, which leads to fetal polyuria (a major source of amniotic fluid)
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Diabetes in pregnancy Presentation Transcript

  • 1.  Iman a 41 year leady G10P6A1E2 at 13 weeks of gestation, LMP: 27/10/2012  k/c/o DM on metformine in 2011  Presented to the OPD with FBG 9.9 admitted for glycemic and VPG control.  She complain of polydepsia, polyphagia, and labiality of mood  She diened any nausea, vomiting, dysurea, vaginal discharge or fever.
  • 2.  OBS Hx:  1st: uneventfull  2nd: spontaneous abortion, 23 y, at 14 weeks, D&C done, no       complication 3rd , 4th ,5th: uneventfull 6th: LSCS (big baby), 1998, 40+ weeks, GDM on diet, 4.39 Kg, girl 7th: ectopic pregnancy, 2003, at 8 weeks, Lt salpingoectomy done 8th: ectopic pregnancy, 2011, at 8 weeks, treated with methotraxate. After this ectpoics she diagnosed with DM on metformine 9th: LSCS (preeclempsia), 2012, at 37+ weeks, DM on insulin and HTN on tablet, 3.4 Kg,. Current: DM on insuline, at 13 weeks, antenatal scan and investigations were normal.
  • 3.  Menstrual Hx:  regular, 5/28days, small amount, mild pain, no intramenstrual bleeding, age of Menarche 14 y, LMP: 27/10/2012  PMH:  apart from OBS Hx, unremarkable  Allergy:  nil  Family Hx:  No consanguinity  strong Family Hx of DM and HTN in first degree relatives  Social HX:  Not smoker or alcohol consumer
  • 4. General examination: Looks well, comfortable, obese, afebrile, alert and cooperative not in distress. - BMI: 32 - There no pallor , jaundice, dehydration - BP: 139/90
  • 5.  Abdominal examinations:  Inspection:          The abdomen is distended symmetrically Umbilical is inverted scars No Striae gravidarum No Linea nigra No visible veins No obvious masses No change in skin colour Normal hair distribution  Palpation:  No tenderness on light or deep palpation  Uterus at 1cm above pubis symphysis  Other systems are normal
  • 6.  Investigations:  Hb: 11.9, platelet normal  LDH, LFT, coagulation, and electrolytes normal  VPG at the day of admission: Pre breakfast Post breakfast Post lunch Post dinner 4.9 7.4 8.6 8.7
  • 7. Gestational Diabetes Mellitus GDM
  • 8.  Diabetes mellitus refers to a chronic disorder of metabolism that due to an absolute or relative lack of insulin  It is characterized by hyperglycaemia in postprandial or fasting state or both.  GDM is defined as glucose intolerance of variable degree with onset or first recognition during the present pregnancy.  Gestational diabetes affects 3-10% of pregnancies
  • 9. TRADITIONAL Type 1 – IDDM – Juvenile diabetes Type 2 – NIDDM – Maturity onset diabetes Type 3 – Gestational diabetes
  • 10. Type 1. Immune mediated & idiopathic B cell dysfn Type 2. DM of adult onset due to insulin resistance & relative insulin deficiency, or from a secretory defect. Type 3. Specific types of diabetes 1.Genetic defect of B cell function 2.Genetic defect in insulin action 3. Diseases of exocrine pancreas. Type 4. Gestational diabetes
  • 11. A1 Gestational diabetes – FBS and Postprandial plasma glucose normal A2 Gestational diabetes- FBS > 105mg/dl or 2- hr PPBS >120mg/dl B Overt diabetes developing after 20yr & duration <10yr C Overt diabetes developing before 20 yr/ duration > 10yr D Overt diabetes developing between age 10 and 19yr or duration 10-19 yr and or background retinopathy F Overt diabetes at any age/ duration with nephropathy R Overt diabetes at any age/duration with prolif. retinopathy H Overt diabetes at any age/duration + arteriosclerotic HD
  • 12. The precise mechanisms causing GDM remain unknown  In the pathophysiology of GDM we have to consider one main point.  Role of feto-placental unit in GDM.
  • 13. pregnancy-associated hormones estrogen, progesterone, cortisol, and placental lactogen decrease insulin sensitivity Increase Insulin resistance
  • 14. HCG shows higher level
  • 15.  Screening is generally performed between 24-28 gestation.  Method: oral glucose screening test (OGST)  Need no preparation: not  weeks of or OGCT fasting 50 gm glucose is giving in glass of water  Venous plasma glucose taking before the test and after 1 hr  Results:  <7.8 mmol/L = no GDM  ≥7.8-10.3 mmol/L = further investigation with OGTT  ≥10.3 mmol/L= (185 mg/dL) = GDM
  • 16.  There are six different ways of performing OGTT.  NICE guidelines recommend WHO method  How to do?  Overnight fasting  75 gm glucose giving in 300 ml of water  Venous plasma glucose taking before the test and after 2hr
  • 17.  OGTT on 75 mg oral glucose load  Diabetes Mellitus  FBS ≥ 7.8 mmol/l  2 PPBS ≥ 11.1 mmol/l  GDM  FBS ≥ 5.5 mmol/L  2 PPBS ≥ 9 mmol/L WHO criteria for the 2-hour OGTT Whole blood venous (mmol/L) Whole blood capillary (mmol/L) Plasma venous (mmol/L) Plasma capillary (mmol/L) Fasting >=6.1 >=6.1 >=7.0 >=7.0 2 hours >=6.7 >=7.8 >=7.8 =>8.9
  • 18.  At booking (14 weeks) if at high risk:  Family history of DM  Previous GD  Obesity  Previous still birth  Macrosomia  Congenital malformation  multiparty
  • 19.  Done in day care unit or in the ward  Patient on diet or insulin  4 venous sampling are collected:  Fasting…5.5 mmol/ll  2 hr post breakfast…8 mmol/l  2 hr post break lunch…8 mmol/l  2 hr post break dinner…8 mmol/l
  • 20.  Diet providing 30 kcal/kg –normal pregnant,  24 kcal/kg – over wt pregnancy women .  Postprandial hyperglycemia - decreased by CHO restricted, low glycemic index diets & small frequent meals  Increase Exercise improve blood sugar control  30 minutes a day recommended by NICE guidelinies
  • 21.  If already on medication, generally switch to insulin therapy:  continuing glyburide or metformin controversial  teratogenicity unknown for other oral anti-hyperglycemics  Tight glycemic control  diet management first line therapy  post-prandial blood glucose values seem to be the most effective at determining thelikelihood of macrosomia or other adverse pregnancy outcomes  aim for Fasting Plasma Glucose (PG) ≤5.3 mmol/L  1-hour post prandial PG ≤7.8 mmol/L  2-hour post prandial PG ≤6.7 mmol/L
  • 22.  If blood glucose not well controlled, initiate insulin therapy  ƒInsulin dosage may need to be adjusted in T2 due to increased demand and increased insulin resistance  Insulin requirement- 0.6, 0.7 & 0.8 units / kg /day- 1st, 2nd & 3rd trimesters  Given as 2 injections/day (some require 3- 4 injections) 2/3rd am 2/3rd N 1/3rd pm 1/3rd R ½N ½R
  • 23. Type Onset Peak (hours) Duration (hours) Rapid Lispro* Aspart* Glulisine < 15 min < 15 min 1–2 1–2 3–4 3–4 0.5 – 0.7 hour 2–4 5–8 Intermediate NPH(neutral protamine hagedorn) 1 – 2 hours 6 – 12 18 – 24 Lente 1 – 2 hours 6 – 12 18 – 24 Long acting Ultralente Glargine* 4 – 6 hours 2 – 4 hours 16 – 18 peakless 20 – 36 18 – 24 Short regular insulin
  • 24. TARGETS OF GLYCEMIC CONTROL 8 7 6 5 4 MM/L 3 2 1 0 FASTING POST B.F. POST LUNCH Cut values Pre: 5.5 Post: 8.0 V.P.G PROFILE PRE DINNER POST DINNER
  • 25. Management of DM in pregnancy  Monitor as for normal pregnancy plus initial 24-hr urine protein and creatinine clearance  Retinal exam, HbA1C  HbA1C: >8.5% of pre-pregnancy value associated with increased risk of spontaneous abortion and congenital malformations  Increased fetal surveillance (BPP, NST)
  • 26. preterm labour Increase incidence of pre-eclampsia Polyhydramnios - AFI >240mm Macrosomia >4000gm Poorly controlled DM- subfertility, miscarriage, congenital anomalies, UTI Shoulder dystocia Perinatal mortality  Increase incidence of      
  • 27. •Obstetric: • Hypertension/preeclampsia (especially if pre-existing nephropathy/proteinuria) •Polyhydramnios Diabetic Emergencies • Hypoglycemia • Ketoacidosis • Diabetic coma •Other •Pyelonephritis/UTI •Increased incidence of spontaneous abortion (in DM1 and DM2, not in GDM) End-organ involvement or deterioration (occur in DM1 and DM2, not in GDM) • Retinopathy • Nephropathy
  • 28. Growth Abnormalities • Macrosomia: maternal hyperglycemia leads to fetal hyperinsulinism resulting in accelerated anabolism • (IUGR): due to placental vascular insufficiency Congenital Anomalies (occur in DM1 and DM2, not in GDM) • 2-7x increased risk of cardiac (VSD), NTD, GU (cystic kidneys), GI (anal atresia), and MSK (sacral agenesis) anomalies due to hyperglycemia Delayed Organ Maturity • Fetal lung immaturity
  • 29. •Labour and Delivery •Preterm labour/prematurity: •Preterm labour is associated with poor glycemic control •Increased incidence of stillbirth •Birth trauma: due to macrosomia, can lead to difficult vaginal delivery and shoulder dystocia •Neonatal •Hypoglycemia: due to pancreatic hyperplasia and excess insulin secretion in the neonate •Hyperbilirubinemia and jaundice: due to prematurity and polycythemia •Hypocalcemia: exact pathophysiology not understood, may be related to functional hypoparathyroidism •Polycythemia: hyperglycemia stimulates fetal erythropoietin production
  • 30.  Caused by a complete lack of insulin but usually precipitated by something else e.g. infection, infarction  associated with fetal loss rates in excess of 50% and maternal mortality rates are generally less than 1%.  Signs and Symptoms of DKA: Malaise Nausea/Vomiting Headache Polyuria/polydypsia Dry mouth Shortness of breath Weight loss Abdominal pain Dehydration Mental status changes
  • 31.  DIAGNOSIS (need all 3 features) 1- Raised blood glucose 2- Ketonuria 3- Acidosis  Goals of therapy  Re-hydration  Correction of acidemia  Normalization of serum glucose  Restoration of electrolyte homeostasis  Elimination of the underlying cause
  • 32.  Goals  Minimize/eliminate the risk of fetal death  Early detection of fetal compromise  Prevent unnecessary premature delivery
  • 33.  Frequent ANC  Confirm viability & Gestational Age by early scan  Detailed anomaly scan ( 18-20 wks)  Fetal echo cardiogram ( 24 weeks)  Growth scans ( after 30 wks)  BPP & Doppler ( after 34 wks)
  • 34.  Monthly VPG profile  HbA1c once every 3 monthes  FBS & PPBS every visit
  • 35.  Patient well controlled on diet only to be delivered by 40 weeks.  GDM well controlled to be delivered at 38 weeks.  NICE guidelines recommends that pregnant women with diabetes be offered elective birth after 38 completed weeks gestation
  • 36. o Spontaneous o Induced – PG/ARM/Syntocin o Caesarean section
  • 37.  Hourly reflos – keep Blood Sugar ( 5-8 mmols)  < 5 mmols – start 5% dextrose  > 8 mmol - I.V insulin pump –1unit/hr & titrate  Continous CTG  Watch for progress of labour  Anticipate & prepare for shoulder dystocia
  • 38.  Continue regular dose of insulin till the time of induction.  Reflo 4 hourly initially and 1-2 hourly in established labour.  Continue infusion of regular insulin in 5% dextrose at rate of .5 to 2 U of insulin/ hr and insulin dosage adjusted accordingly to maintain plasma glucose level (5-8 mmol)
  • 39.  NICU facility should be available  Neonatologist present for delivery  No need for routine admission to NICU  Check for hypoglycemia .  Watch out for other problems
  • 40.  Insulin requirements dramatically drop with expulsion of placenta (source of insulinantagonists)  No insulin is required for 48-72 hours postpartum in most Type 1 DM  Monitor glucose q6h, restart insulin at two-thirds of pre- pregnancy dosage when glucose >8 mmol/L     GDM on diet ( no reflows/diet required) GDM on insulin ( reflows on Normal Diet if high Diabetic Diet ) NIDDM ( Diabetic Diet - reflows – pre-pregnancy. Oral agent.) IDDM ( Diabetic Diet –reflows -pre-pregnancy dose.)
  • 41.  Evaluation of glycemic control       HbA1c – gives control 2-3 months If high – control diabetes before conception Evaluation of B.P Evaluation of retinal status Evaluation of renal function Change to Insulin prior to / when pregnancy is diagnosed.
  • 42. 1. 2. 3. 4. 5. 6. 7. Toronto Notes 2011; OB13 Pubmed Uptodate.com Hacker/Moore,2010 essentials of Obstetrics & Gynecology,saunders, fifth edition Obstetrics Guidelines, University of Illinois at Chicago, Sept 2008 Pathophysiology of Gestational Diabetes Mellitus: The Past, the Present and the Future,Mohammed Chyad Al Noaemi1 and Mohammed Helmy Faris Shalayel2 1Al-Yarmouk College, Khartoum,2National College for Medical and Technical Studies, Khartoum,Sudan Diabetic ketoacidosis in pregnancy,D Kamalakannan, V Baskar, D M Barton, T A M Abdu