Diabetes Mellitus in pregnancy " Gestational diabetes mellitus''

1. Diabetes in Pregnancy
Presented by :
Nassr Saif ALBarhi
SULTANTE OF
OMAN

2. OUTLINE:
 Case scenario.
 Definition of GDM.
 Classification.
 Diagnosis.
 Management.
 Antepartum care

3.  A 24 years old Omani lady, G4P1A2 at 23+2 wks of
gestation. LMP: 27/10/2013. EDD by date:3/8/2014 , by
scan: 29/7/2014.
 k/c/o Type I DM on insulin in 2012.
 Hypothyroidism on thyroxin 50mcg OD.
 Presented to the OPD with Reflow 15.8 mmol admitted for
glycemic and VPG control.

4.  Also, she admitted for abnormal scan finding as fetus found
to have ascites for further investigations.
 She complain of polyphagia, morning nausea and burning
sensation during voiding but she denied any polydepsia,
vomiting, fever, vaginal discharge or labiality of mood.

5. Past ObsH
 1st pregnancy>> abortion at 12weeks GA, no D&C.
 2nd pregnancy>> Abortion at 3 months GA, D&C done.
 3rd pregnancy>> FT LSCS for fetal distress , Diagnosed
as DM and IOL.
-----
 This is Spontaneous pregnancy:
During this pregnancy had admissions for Blood sugar control
and insulin adjustment last was 2/4/2014.
Was offered Insulin pump but patient not keen for that.

6.  Menstrual Hx:
 regular, 5/21days, small amount, mild pain, no intramenstrual
bleeding, LMP : 27/10/2013. EDD by date: 382014
 PMH:
 apart from OBS Hx, unremarkable
 Allergy:
 nil
 Family Hx:
 Her husband is 1st cousin of her father.
 Strong Family Hx of DM and HTN in first degree relatives
 Social HX:
 Not smoker or alcohol consumer

7.  General examination:
 Looks well, comfortable, obese, afebrile, alert and
cooperative not in distress.
 There no pallor , jaundice, dehydration
 BP: 110/69.
Physical examination:

8.  Abdominal examinations:
 Inspection:
 The abdomen is distended.
 Umbilical is inverted
 scars
 Striae gravidarum.
 Linea nigra
 No visible veins
 No obvious masses.
 No change in skin colour.
 Normal hair distribution.
 Palpation:
 Abdomen is soft, not tender, uterus is relax and no contraction.
 FSH=29 cm.
 Fundal occuping by breach, supin: right side, cephalic presentation.
 FHR= 130.
 Other systems are normal

9.  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
5 .5 6 .5 7 .10 7

10. Gestational diabetes

11. Introduction
 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.
 Reports show a rate of 3% to 8% of gestational diabetes mellitus
(GDM).

12. Traditional classification :
Type 1 – IDDM – Juvenile diabetes
Type 2 – NIDDM – Maturity onset diabetes
Type 3 – Gestational diabetes.
Classification of diabetes

13. Type 1. Immune mediated & idiopathic B cell dysfunction.
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
New classification

14. Classification of diabetes

15. why glucose Intolerance in
pregnancy??

17. Risk factors:
 Maternal age > 25 years
 Obesity.
 Family history of diabetes in a first-degree
relative.
 Previous large baby.
 Previous still birth, or a child with a birth defect
 Polyhydramnios.
 Previous pregnancy with GDM.

18. Diagnosis
 All women should be screened for GDM
between 24-28 weeks of gestation.
 Women with multiple risk factors!?

19. OGCT
 Method: oral glucose screening test (OGST)
or OGCT
 Need no preparation: not fasting
 A 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


20. How to do?
 150 to 200gm CHO diet to be given for 3 days before
doing OGTT.
 Overnight fasting
 75 gm glucose giving in 300 ml of water
 Venous plasma glucose taking before the test and
after 2hr.
OGTT

21.  OGTT on 75 mg oral glucose load
 GDM
 FBS ≥ 5.5 mmol/L
 2 PPBS ≥ 7.8mmol/L
ORAL GLUCOSE
TOLERANCE TEST
WHOcriteria forthe 2-hourOGTT
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
2hours =<.6 7 =<.7 8 =<.7 8 <=.8 9

22.  At booking (14 weeks) if at high risk:
 Family history of DM
 Previous GD
 Obesity
 Previous still birth
 Macrosomia
 Congenital malformation
 multiparty
When to do OGTT?

23.  Done in day care unit or in the ward
 Patient on diet or insulin
 4 venous sampling are collected:
 Fasting…
 2 hr post breakfast
 2 hr post break lunch.
 2 hr post break dinner.
Venous plasma glucose
profile

25. Management

26.  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
Diet and Exercise

27.  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
 AimforFasting Plasma Glucose (PG) 3.5-5.9 mmol/L
 1-hour post prandial PG ≤7.8 mmol/L
 2-hour post prandial PG ≤7 mmol/L
Management of DM in
pregnancy

29.  If blood glucose not well controlled, initiate insulin
therapy.
 ƒ Insulin 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)
Insulin therapy
2/3rd
am 1/3rd
pm
2/3rd
N 1/3rd
R
½N ½R

30. Available insulin preparations
Type Onset Peak (hours) Duration (hours)
Rapid
Lispro*
Aspart*
Glulisine
< 15 min
< 15 min
1 – 2
1 – 2
3 – 4
3 – 4
Short
regular insulin 0.5 – 0.7 hour 2 – 4 5 – 8
Intermediate
NPH(neutral protamine
hagedorn)
Lente
1 – 2 hours
1 – 2 hours
6 – 12
6 – 12
18 – 24
18 – 24
Long acting
Ultralente
Glargine*
4 – 6 hours
2 – 4 hours
16 – 18
peakless
20 – 36
18 – 24

31. TARGETS OF GLYCEMIC CONTROL
FASTING POST B.F. POST
LUNCH
PRE
DINNER
POST
DINNER
8
7
6
5
4
3
2
1
0
MM/
L
V.P.G PROFILE
Cut values
Pre: 5.5

32.  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)
Management of DM in
pregnancy

33. Why DM in pregnancy is a concern??
1. Maternal complications.
2. Fetal complications.

34.  Preterm labour.
 Increase incidence of pre-eclampsia.
 Polyhydramnios - AFI >240mm .
 Macrosomia >4000gm .
 Poorly controlled DM- subfertility,
miscarriage, congenital anomalies, UTI.
Shoulder dystocia
Perinatal mortalityPerinatal mortality
Complications of Diabetes

35. Maternal Complications
•Obstetric:
•
Hypertension/preeclampsia
(especially if pre-existing
nephropathy/proteinuria)
•Polyhydramnios
Diabetic Emergencies
•Hypoglycemia
•Ketoacidosis
•Diabetic coma
Diabetic Emergencies
•Hypoglycemia
•Ketoacidosis
•Diabetic coma
End-organinvolvement ordeterioration
)occur in DM1 and DM2, not in GDM(
•Retinopathy
•Nephropathy
End-organinvolvement ordeterioration
)occur in DM1 and DM2, not in GDM(
•Retinopathy
•Nephropathy
•Other
•Pyelonephritis/UTI
•Increased incidence of
spontaneous abortion (in
DM1 and DM2, not in
GDM)
•Other
•Pyelonephritis/UTI
•Increased incidence of
spontaneous abortion (in
DM1 and DM2, not in
GDM)

36. Fetal Complications
Growth Abnormalities
•Macrosomia: maternal hyperglycemia leads to fetal
hyperinsulinism resulting in accelerated anabolism
)•IUGR): due to placental vascular insufficiency
Growth Abnormalities
•Macrosomia: maternal hyperglycemia leads to fetal
hyperinsulinism resulting in accelerated anabolism
)•IUGR): due to placental vascular insufficiency
Delayed Organ Maturity
•Fetal lung immaturity
Delayed Organ Maturity
•Fetal lung immaturity
Congenital Anomalies (occurin 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

37. Fetal Complications
•Labourand 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
•Labourand 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
•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

38. Antepartum Care

39.  Goals
 Minimize/eliminate the risk of fetal death
 Early detection of fetal compromise
 Prevent unnecessary premature delivery
Fetal Surveillance

40.  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)
FETAL SURVEILLANCE

41.  Monthly VPG profile
 HbA1c once every 3 monthes
 FBS & PPBS every visit
ASSESSMENT OF GLYCEMIC
CONTROL

42. Timing and mode of
delivery

43.  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
Timing of Delivery

44. o Spontaneous
o Induced – PG/ARM/Syntocin
o Caesarean section
Mode of
delivery

45.  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
Spontaneous
labour

46.  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)
Induction of labour

47. For Elective Cesarean
 Omit the morning dose of insulin.
 Check Fasting Reflo
If Reflo <=4 mmol start 5% Dextrose at
125mlhours
If Reflo >=8 mmol start insulin infustion as per
sliding scale.

48. Postpartum period
 Patient with GDM: stop the insulin and FBS
and PPBS post-delivery.
 Pre existing diabetics: start pre-pregnancy
dose of insulinoral hypoglycemic agents.
 Patient with GDM are advised to do OGTT at
6 WEEKS POSTPARTUM.

49.  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.
Planning next pregnancy

50. 1. Pubmed
2. Uptodate.com
3. Hacker/Moore,2010 essentials of Obstetrics &
Gynecology,saunders, fifth edition.
4. Obstetrics Guidelines,.SQUH, 2012014.
5. Obstetrics Guidelines, University of Illinois at Chicago,
Sept 2008
6. Pathophysiology of Gestational Diabetes Mellitus: The
Past, the Present and the Future,Mohammed Chyad Al
Noaemi1 and Mohammed Helmy Faris Shalayel2 1 Al-
Yarm o uk Co lle g e , Kharto um , 2Natio nalCo lle g e fo r
Me dicaland Te chnicalStudie s, Kharto um , Sudan
References:

51. THANK YOU