done by Al Yaqdhan Al Atbi Sultan Qaboos university- Oman

2.  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.

3.  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.

4.  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

5. General examination:
Looks well, comfortable, obese, afebrile, alert and
cooperative not in distress.
- BMI: 32
- There no pallor , jaundice, dehydration
- BP: 139/90

6.  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

7.  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

8. Gestational Diabetes Mellitus
GDM

9.  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

10. TRADITIONAL
Type 1 – IDDM – Juvenile diabetes
Type 2 – NIDDM – Maturity onset diabetes
Type 3 – Gestational diabetes

11. 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

12. 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

14. 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.

15. pregnancy-associated hormones
estrogen, progesterone, cortisol,
and placental lactogen
decrease insulin
sensitivity
Increase Insulin
resistance

16. HCG
shows higher level

18.  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

19.  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

20.  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

21.  At booking (14 weeks) if at high risk:
 Family history of DM
 Previous GD
 Obesity
 Previous still birth
 Macrosomia
 Congenital malformation
 multiparty

22.  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

25.  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

26.  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

27.  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

28. 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

29. 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

30. 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)

31. 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







32. •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

33. 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

34. •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

35.  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

36.  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

38.  Goals
 Minimize/eliminate the risk of fetal death
 Early detection of fetal compromise
 Prevent unnecessary premature delivery

39.  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)

40.  Monthly VPG profile
 HbA1c once every 3 monthes
 FBS & PPBS every visit

42.  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

43. o Spontaneous
o Induced – PG/ARM/Syntocin
o Caesarean section

44.  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

45.  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)

46.  NICU facility should be available
 Neonatologist present for delivery
 No need for routine admission to NICU
 Check for hypoglycemia .
 Watch out for other problems

47.  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.)

48.  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.

49. 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