This document provides an overview of disorders of carbohydrate metabolism during pregnancy, including gestational diabetes and pre-existing diabetes. It discusses the physiological changes in carbohydrate metabolism during pregnancy, pathogenesis and clinical features of type 1 and type 2 diabetes, effects of diabetes on pregnancy outcomes, management through medical treatment, diet, and obstetric care, and considerations for pre-pregnancy counseling and care during labor and delivery. The goal of management is to achieve near normal blood glucose levels in order to reduce risks of complications for both mother and baby.

1. Dr BHASKAR J .PAUL
MBBS , MD , MRCOG 1
Associate Professor
Obstetrics and Gynecology

2. Learning objectives
Knowledge criteria :
Understand the epidemiology , etiology, pathophysiology,
clinical characteristics, prognostic features, and mx of
disorders of carbohydrate metabolism
 Type 1 and type 2 diabetes
 Maternal, fetal and neonatal complication
 Diabetic ketoacidosis
 Diet
 Drugs
Clinical competency : diagnosis, investigate, manage under
supervision Impaired glucose tolerance and IDDM

3. Outliners
 Physiological changes
 Pregnancy with pre existing diabetes
 Gestational diabetes
 Pregnancy effect on diabetes
 Diabetes effect on baby and mother
 Management
 Fetal and maternal complications

4. Physiological changes in
carbohydrate metabolism
 Pregnancy , last trimester  physiological insulin
resistance and relative glucose intolerance
 Fasting glucose are decreased
 serum levels following a meal or glucose load are
increased compared to non pregnant state
 Glucose tolerance decreases progressively with
increasing gestation
 anti insulin hormone secreted by the placenta
human placental lactogen , glucagon and cortisol

5. Physiological changes
 Normal woman doubles the production of insulin
during pregnancy and insulin requirements of
diabetics also increases
 The renal threshold for glucose falls during pregnancy
if all urine samples are tested, most pregnant women
will have glycosuria at some time
 The diagnosis of gestational diabetes is arbitrary
depending on where the cutoff is placed on the
spectrum of glucose tolerance .

6. Diabetes in pregnancy
Pre existing gestational diabetes
 IDDM True GDM
 NIDDM Pre Existing

7. Pathogenesis : IDDM
 IDDM : this is an organ specific auto immune disease
with islet cell antibody
 There is a genetic component and has strong
association with the human leucocytic antigen HLA –
DR3 and DR 4
 A possible viral etiology is thought to explain the
seasonal incidence ( spring and autumn )

8. NIDDM
 There is no evidence of immune pathogenesis in
contrast to IDDM
 There is a strong genetic component and the incidence
increases with age and degree of obesity

9. Clinical features
 IDDM : patient usually present as children, young
adults
 Most commonly affects the Europeans , who are not
usually overweight
 C/F relates to insulin deficiency ..thirst , polyuria,
weight loss , ketoacidosis

10. Clinical features
 Usually older and some times over weight
 All racial groups are affected , but asians and affro-
caribbean are mosre affected.
 Clinical features relates to partial insulin deficiency
and insulin resistance.
 Insulin is required to treat this condition , but they do
not become ketotic if with drawn.

11. Classical features
 Candida infection (pruritus vulvae)
 Staphylococcal skin infection
 Blurred vision
 Macrovascular arterial disease ( CAD, CVD, PVD)
 Microvascular disease ( diabetic retinopathy,
nephropathy, neuropathy )
 Reduced life expectancy due to accelerated arterial
disease ( 2 fold risk of stroke, 4 fold risk of MI) ,
microangiopathy.

12. Diagnosis
 If patients are symptomatic , a single elevated blood
glucose level is sufficient
 Fasting : 140 mg /l ( 7.8 mmnol)
 Random : 200 mg/l ( 11.1 mmol)
 Asymptomatic patients are diagnosd on the basis of 2
fasting venous plasma glucose levels (> 7.8 mmol/dl)
or 2 random venous plasma glucose ( 11.1 mmol/l)
 Border line cases should undergo oral glucose
tolerance test ( 75 g) after which diabetes may be
diagnosed if 2 hour value is > 11.1 mmol

13. Effect of pregnancy on diabetes
 Patient with IDDM and with NIDDM (with insulin
)require increasing dose of insulin as pregnancy
advances.
 Maximun requirement at term usually reach at least 2
fold pre-pregnancy dose.
 Rapid increase occurs between 28 to 32 weeks when
fetus is growing rapidly

14. Effect of pregnancy
 Renal function and degree of proteinuria detoriates
 Creatinine clearance decreases
 Usually reversed following delivery
 2 fold risk of progression of diabetic retinopathy.
 Rapid improvement of glycemic control causes
increase in flow in retinal artery
 Hypoglycemia is more common in pregnancy ( tighter
diabetic control )
 Diabetic ketoacidosis is rare in pregnancy.

15. Effect of pre existing diabetes on
pregnancy
 Increased risk of congenital abnormality
 Woman with Hb1c < 8 % risk is 5 %
 Woman with Hb1c >25% risk is 25 %
 The specific congenital abnormality of diabetes is
sacral agenesis
 Common are Congenital heart defects and skeletal and
neural tube defects .

16. Effect of diabetes on pregnancy
 Poorly controlled diabetes have increased risk of
miscarriage.
 Preecclampsia, risk compounded if there is preexisting
hypertension, or renal disease.
 Protenuria , hypoalbuminaemia , normochromic
normocytic anemia
 Risk of infection ( UTI, respiratory , endometrial and
wound infection )
 Vaginal candidiasis

17. Effect of diabetes on pregnancy
 Perinatal and neonatal mortality can be increased up
to 2 to 4 fold
 Mortality figure have been fallen over last 2 decades
largely due to improved diabetic control
 Sudden unexplained intrauterine death.
 Risk is related to degree of diabetic control and is
higher after 36 weeks

18. Effect of diabetes on pregnancy
 Maternal hyperglycemia , particularly ketoacidosis is
detrimental
 Maternal hypoglycemia is well tolerated by fetus
 Neonatal morbidity is increased in infants of diabetic
mothers
 Chronic hypoxia ( macrosomic babies), presence of
hyperglycemia , lactic acidosis
 It is not possible to predict IUD from either
cardiotocograph (CTG, Doppler velocimetry, or
biophysical profiles )

19. Pederson’s hypothesis
 Maternal hyperglycemia
 Fetal hyperglycemia
 Fetal pancreatic Beta cell hyperplasia
 Fetal hyperinsulinaemia
 Macrosomia- organomegaly-hypogly-RDS
 Polycythemia – Jaundice

20. Macrosomia
 Definition : birth weight > 4.5 kg
 Or > 90 th percentile for gestational age
 Insulin is an anabolic growth promoting hormone
 This macrosomic baby are fat, plethoric , with liver
enlarged ,
 Incidence increases significantly when mean maternal
blood glucose concentration > 7.2 mmol/L

21. Management
 Managed jointly with diabetic clinic by obstetricians
and physicians
 Specialist dieticians, nurses, midwives who are trained
to look after pregnant women with diabetes

22. Medical management
 To achieve maternal near normo glycemia
 Adverse perinatal outcomes are related to the degree
of maternal diabetic control .
 Ideal plasma glucose concentrations are < 5.0 mmol/l
fasting and 7.5 mmol/l post prandial
 Woman with IDDM require increasing doses of insulin
throughout the pregnancy
 Those with NIDDM usually require treatment with
insulin during pregnancy

23. Medical management
 Oral hypoglycemics are (sulphonyl ureas and
biguanides ) should be avoided in pregnancy because
they cross placenta and there is risk of fetal hypo
glycemia
 Strict adherance to low sugar, low fat , high fibre diet
is important in pregnancy
 Starvation should be avoided because of risk of ketosis

24. Medications
 Twice daily mixed short and intermediate acting
insulins may be adequate early in pregnancy ,
 A short acting insulin before each meal and
intermediate acting before bed time , sometime in the
morning is usually required .
 Insulin should not be stopped during period of
intercurrent illness, may need to be increased in the
presence of infection ,

25. Medications
 The degree of diabetes control may need to be
assessed with HbA1c measurements
 Detailed ophthalmic examination
 Diabetic nephropathy needs regular regular renal
screen
 Hypertension is found in 30 % of women with diabetic
nephropathy and three quarter will develop
hypertension by the end of pregnancy .

26. Diet
 A pregnant diabetics will need to increase the
frequency of home blood glucose monitoring , using
glucose oxidase strip and glucometer
 Inevitable result of tighter control is an increased risk
of hypoglycemic attacks
 A pregnant diabetic would require a snack mid
morning, mid after noon and before retiring at night .
 Glucagon and oral intake of food has to be kept ready
in case of hypoglycemia

27. Obstetric management
 As there is increased risk of congenital abnormalities
diabetic women should be offered serum screening for
neural tube defect and detailed ultrasound at 18 to 20
weeks of gestation
 Full hospital care is appropriate with regular blood
pressure and urineanalysis check up to detect
preecclampsia

28. Obstetrics management
 Regular ultrasound assessment of fetal growth and
liquor volume in the third trimester is advisable to
detect macro somia and poly hydramnios
 Particular care to use , beta sympathomimetics,
corticosteroids
 Timing of delivery between 36 – 38 weeks is no more
because the risk of ARDS is more than intrauterine
fetal death

29. Obstetrics management
 Most unit prefer a well controlled diabetics to continue
until 38 to 40 wks in absence of macrosomia
 Over all risk of CS ( both elective and emergency ) is
increased in diabetics to avoid the devastating
complication of shoulder dystocia

30. Intra partum Mx
 Follows the same principle as management of surgery
in the diabetic woman throughout active labor and
delivery and until the woman is eating
 Insulin administered via intravenous sliding scale
determined by her individual daily insulin
requirements and adjusted according to the capillary
blood – glucose level .

31. Intrapartum management
 The usual dose range is 2-6 unit per hour
 The target glucose during labor and delivery is about
4- 7 mmol /l
 A 5 0r 10 % dextrose is administered simultenously via
a separate IV giving set
 Following delivery of the placenta the rate of infusion
of insulin is decreased by 50 %

32. Post partum Mx
 Post partum insulin requirements return rapidly to
prepregnancy levels
 Adjustment is needed depending on whether the
mother breast feeding and howmuch weight she has
gained during pregnancy

33. Pre pregnancy counseling
 One of the most important features in the mangement
of diabetes
 Better the control of the diabets and lower the HbA1c ,
lower the risk of congenital abnormality
 A woman can be given a more accurate estimation of
the level of risk of developing pre ecclampsia
 Proliferative retinopathy can be treated with photo
coagulation

34. Prepregnancy councelling
 It allows optimisation of diabetic control prior to
conception plus assessment of the presence and
severity of complications such as hypertension,
nephropathy and retino pathy

35. 
TAKE A BREAK

36. .
Gestational
Diabetes
Part II

37. Gestational diabetes
 Definition :
 Carbohydrate intolerance of variable severity with
onset or first recognition during the present pregnancy
.
 It includes women with pre existing but previously
unrecognised diabetes

38. Incidence
 This is hugely variable
 It depends on the level of glucose intolerence used to
define the condition and the ethnicity of the
population under study
 In the Uk , the prevalence is increased about 11 fold in
women from the indian subcontinent ,

39. Incidence
 8 fold from SE asian women ,
 6 fold in arab / mediterrian
 3 fold in afro caribbean women
 In european population it is lowest ( 0.2 -0.5 )

40. Clinical features
 Usually asympomatic and develops in the second
trimester , induced by maternal changes in
carbohydrate metabolism and insulin sensitivity
 May be diagnosed by routine biochemical screening,
 Suspected by macrosomic fetus, poly hydramnios ,
persistent heavy glycosuria or recurrent infection

41. Clinical features
 More commonly associated with previous GDM,
 women with a family history of diabetes ,
 women with previouly large for gestational age infants
,
 obese and older women
 Unlike preexisting diabetes there is no increase in the
congenital abnormality rate

42. Clinical features
 Associated with increased perinatal morbidity and
mortality in the same way but to a
 lesser degree than preexisting diabetes
 Associated with increased risk of pre ecclampsia

43. Importance of GDM
 Women indentified as having GDM have a greatly
increased risk ( 40 -60 )% of developing NIDDM
within 10 to 15 years
 It may be delayed with life style modification and diet
 A small percentage of women identified as having
GDM will infact have diabetes predating the
pregnancy

44. Importance of GDM
 They are therefore at risk from all features associated
with preexisting diabetes
 Women with GDM have a higher incidence of
macrosomia and adverse pregnancy outcome than
controlled population without GDM

45. Screening and diagnosis
 Who ?
 Some advocate universal biochemical screening
 Some advocate screening those > 25 years age
 Many unit use clinical risk factors testing women only
with
 Preivious GDM
 Family history of having diabetes

46. Screening and Diagnosis
 Previous macrosomic baby
 Previous unexplained stillbirth
 Obesity
 Glycosuria
 Polyhydramnios
 Large for fetal age in current pregnancy

47. When ?
 The later in pregnancy , the screen is performed the
higher the detection rate of GDM
 The earlier in pregnancy the GDM is diagnosed , the
greater the potential to treat hyper glycemia and
possibly improved out come

48. HOW ?
 In the US , a 50 g short glucose tolerance test is used to
screen all women at 26 to 28 weeks gestation
 Followed by screen positive ( I hour level > 7.8
mmol/l)
 A full 100g oral glucose tolerance test for which there
are specific criteria for the diagnosis of GDM

49. Diagnostic criteria
 The WHO have proposed criteria equivalent to those
for diagnosis of impaired glucose tolerance in the non
pregnant.
 Following a 75 g oral glucose tolerance test , a women
is diagnosed as having GDM if either fasting or 2hour
level is > 7.8 mmol /l

50. Diagnostic criteria
 It is now widely believed that mild degree of impaired
glucose tolerance in pregnancy probably do not have a
significantly worse perinatal outcome
 Others favour screening and diagnosis using random
or PP blood glucose measurement .

51. Management
 Close collaboration between obstetricians and
physicians
 Diet with reduced fat , increased fibre and carb intake
 Obese women are given reduced calorie diet , to
maintain weight for the remainder of the pregnancy
 Induction of insulin therapy : fasting hyperglycemia 
: 5.5- 6.0 mmol

52. Management
 post prandial hyperglycemia  : 7.5 – 8.0 mmol/l
 Short acting insulin is given before meals
 Regular assessment by ultrasound for fetal growth
 Increased risk for pre ecclampsia , should receive full
hospital care
 A formal 75 g oral glucose tolerance test following 6
weeks after delivery is advisable .
 Advised for increased physical activity and reduced
energy intake

53. Recurrence
 GDM ususally recurs in subsequent pregnancies
 Some time if a women has lot of weight between
pregnancies and modified her diet substantially , she
may not develop GDM
 Risk of future diabetes and GDM and ideally have their
blood glucose checked prior to conception incase they
have developed D since last pregnancy
 In any case they should have a blood glucose checked
in early pregnancy

54. Glycemic control : recommended
level
 Pre conception : < 7 %
 First trimester :
 HbA1c < 7 %
 Pre prandial BS : 3.5- 5.9mmol/L
 Post prandial BS : <7.8 mmol/L
 Second / third trimester
 Use of HbA1c not recommended
 Pre prandial : 3.5- 5.9mmol/L
 Post prandial : < 7.8 mmol/l

55. Monitoring
 Fasting level and 1 hour after every meal
 Test before bed time who take insulin
 With type 1 diabetes should be offered ketone testing
strips
 Medical review on regular basis (1-2 weekly)

56. Complications of pregnancy
associated diabetes
 Fetal risks
 Miscarriage
 Congenital anomalies
 Still birth
 Prematurity
 Risk of diabetes
 Macrosomia
 Shoulder dystocia and birth traumma
 RDS
 Neonatal hypoglycemia

57. Complications
 Maternal risks
 Hypoglycemia
 Diabetic ketoacidosis
 Operative delivery
 Worsening of retinal disease
 Worsening of preexisting renal impairment
 Pre eclampsia

58. Effect of pregnancy on gestational
diabetes
 Pregnancy is associated with increase in insulin
requirement ,
 Women with IDDM and those with NIDDM require
increasing doses of insulin as pregnancy progresses
 Maximum requirement at term reaches at least 2 fold
increase of pre pregnancy doses
 Rapid increase in insulin requirement occur
particularly between 28 to 32 weeks when fetus is
growing rapidly

59. Effect of pregnancy on gestational
diabetes .
 Women with diabetic nephropathy may exoerience
deterioration during pregnancy in both renal function
and degree of proteinuria
 Any deterioration is usually reversed following delivery
and there is no longer term detrimental effect of the
pregnancy on renal function
 2 fold risk of progression of diabetic retinopathy
during pregnancy .

60. Effect of pregnancy on gestaional
diabetes
 Worsening retinopathy is often related to rapid
improvement in glycemic control , which is feature in
pregnancy
 Hypoglycemia is commoner because of tighter control
 Ketoacidosis is less common because of close super
vision ,
 Is a risk in presence of hyperemesis , infection ,
tocolytic therapy or cortico steroid therapy

61. Effect of gestational diabetes on
pregnancy
 maternal hyperglycemia 
 Fetal hyperglycemia 
 Fetal pancreatic beta cell hyperplasia 
 Fetal hyperinsulinaemia 
 Macrosomia / organomegaly /hypoglycemia RDS
 Poly cythaemia  jaundice

62.  Macrosomia : has different definition
 Most commonly taken as birth weight > 4.5 Kg or > 90
percentile for gestational age
 Insulin is an anabolic growth promoting hormone
 Macrosomic babies are fat , plethoric with all organs but
particularly the liver being is enlarged
 Incidence increased when mean maternal blood glucose
concentrations are > 7.2 mmol/l
 Macro somia is related to poly hydramnios related to fetal
polyuria , leading to PROM
 Macro somia , traummatic delivery and shoulder dystocia

63.  Fetal hyperinsulinemia
 When the cord is clamped the neonate is cutoff from
maternal supply and ia at risk for neonatal
hypoglycemia
 Fetal HI lead to chronic fetal hypoxia , stimulating
extra medullary hemopoiesis , fetal poly cythemia and
neonatal jaundice

64. Take home message
 Increased risk of congenital abnormalities is related to the
degree of periconceptual diabetic control
 Insulin requirement increases during pregnancy
 Retinopathy may deteriorate during pregancy
 Patients with nephropathy and hypertension have
increased risk of preecclampsia
 Neonatal and perinatal morbidity and mortality are
increased
 Pregnant women with diabetes should be managed with
obstetricians and diabetologist
 Goal is to achieve maternal near normoglycemia

65. Take home message
 Increased risk of congenital abnormality and this
correlated with HbA1c
 Increased risk of misscarriage
 Preecclampsia
 Diabetes with nephro pathy are complicated with
severe odema, related to proteinuria , and hypo
albuminemia

66. Take home message
 Increased infection in pregnancy , UTI , vag
candidiasis
 Perinatal and neonatal mortality increases up to 2- 4
fold
 fetus of diabetic mother are at risk of sudden
unexplained intra uterine fetal death
 Maternal hyperglycemia and ketosis is detrimental to
fetus and associated with 20 -50 % fetal mortality
 Neonatal risk are explained by modified pederson
hypothesis

67. THANK YOU