GDM Gestational diabetes mallitus

1. GESTATIONAL DIABETES
MELLITUS

2. DEFINITION AND CLASSIFICATION OF
DIABETES MELLITUS
o Diabetes mellitus is a metabolic disorder caused by
defects in insulin secretion or action, which lead to
abnormalities in the metabolism of carbohydrates,
lipids and protein (ADA, 2008a).
o Chronic hyperglycemia associated with diabetes
causes tissue damage in all organ systems.

3. TYPE 1 DIABETES
o An immune-mediated disorder characterized by
destruction of the beta cells of the pancreas, which leads
to an absolute insulin deficiency.
o Accounts for 5 percent to 10 percent of all diabetes and 1
percent of diabetes in pregnancy (ADA, 2008 a;
Lethbridge-Cejku et al., 2004).

4. TYPE 2 DIABETES
o Is the most prevalent form of diabetes, accounting
for 90 percent to 95 percent of cases (CDC, 2008)
o Is a disease of insulin resistance and relative insulin
deficiency.
o Can be controlled with lifestyle modification and
oral medications.

5. DIABETES IN PREGNANCY: TYPES
 Gestational Diabetes Mellitus (GDM)
Type A1: abnormal oral glucose tolerance test (OGTT) but
normal blood glucose levels during fasting and 1-2 hours
after meals; diet modification is sufficient to control
glucose levels
Type A2: abnormal OGTT compounded by abnormal
glucose levels during fasting and/or after meals; additional
therapy with insulin or other medications is required

6. DIABETES IN PREGNANCY: CLASSIFICATION

7. DIABETES IN PREGNANCY: CLASSIFICATION…
 White’s Group A: Diabetes existing prior to or detected
during pregnancy, needing only diet, no insulin treatment
being necessary.
 White’s Group A/B: Diabetes appearing before or during
pregnancy, insulin treatment becoming necessary during
pregnancy.
 White’s Group B: Diabetes pre-existing and necessitating
insulin treatment before conception, onset of diabetes after
maternal age of 20 years, and/or duration of diabetes
shorter than 10 years.

8.  White’s Group C: Duration of 10-19 years and/or onset of
diabetes between 10-19 years of maternal age, insulin
dependent diabetes. (These four groups are characterized by
the absence of diabetic angiopathy.)
 White’s Group D: Onset insulin dependent Diabetes before
the age of 10 years and/or duration exceeding 20 years. All
pregnant mothers with discernible but not proliferative diabeti
retinopathy are classified as group D.
c
 White’s Group F: Severe proliferative diabetic retinopathy
and/or diabetic nephropathy before or during pregnancy.
DIABETES IN PREGNANCY: CLASSIFICATION…

9. GESTATIONAL DIABETES MELLITUS (GDM)
 Gestational Diabetes Mellitus (GDM) is defined as
‘carbohydrate intolerance with recognition or onset during
pregnancy’, irrespective of the treatment with diet or insulin.
 Many are denovo pregnancy induced
 Some are type 2 ( 35-40%)
 10% have antibodies
 The importance of GDM is that two generations are at risk of
developing diabetes in the future.
 Women with a history of GDM are at increased risk of future
diabetes, predominately type 2 diabetes, as are their children.

10. EPIDEMIOLOGY
 GDM happens in about 7 of every 100 pregnancies.
 The recent data on the prevalence of GDM in India was
16.55% by WHO criteria of 2 hr PG ≥ 140 mg/dl
 Significant disturbances in carbohydrate metabolism occur in
about 1 % pregnancies
 The incidence of GDM increases by approximately 8 times for
pregnant women aged 35 years and over compared with
women aged 25 years or under

11. MAGNITUDE OF PROBLEM: GLOBAL
 Prevalence of GDM varies worldwide and
among different racial and ethnic groups within a
country.
 America – white women (3.9%)
 Asian (8.7%)
 Europe – 0.6% to 3.6%
 Australia – 3.6% to 4.7%
 China – 2.3%; Japan – 2.9%
 Variability is partly because of the different
criteria and screening regimens

12. PATHOPHYSIOLOGY
 The maternal metabolic adaptation is to maintain the mean
fasting plasma glucose of 74.5 ± 11 mg/dl and the post prandial
peak of 108.7 ± 16.9mg/dl.
 This fine tuning of glycemic level during pregnancy is possible
as the normal
due to the compensatory hyperinsulinaemia,
pregnancy is characterized by
 Increased insulin resistance and
 Decreased insulin sensitivity.
 A pregnant woman who is not able to increase her insulin
secretion to overcome the insulin resistance that occurs even
during normal pregnancy develops gestational diabetes.

13. PATHOPHYSIOLOGY…
INCREASED INSULIN RESISTANCE
o Due to hormones secreted by the placenta that are
“diabetogenic”:
 Growth hormone
 Human placental lactogen
 Progesterone
 Corticotropin releasing hormone
o Transient maternal hyperglycemia occurs after
meals because of increased insulin resistance.

14. PATHOPHYSIOLOGY…
Relative baseline hypoglycemia
o Proliferation of pancreatic beta cells (insulin-secreting
cells) leads to increased insulin secretion.
 Insulin levels are higher than in pregnant than nonpregnant
women in fasting and postprandial states.
o Hypoglycemia between meals and at night because of
continuous fetal draw
 Blood glucose levels are 10-20% lower.

15. PATHOPHYSIOLOGY…
 24-hour insulin requirement before conception is approximately 0.6
units / kg.
 In the first trimester, the insulin requirement rises to 0.7units / kg of
the pregnant weight – more unstable glycemia with a tendency to
low fasting plasma glucose and high postprandial excursions and
the occurrence of nocturnal hypoglycemia.
 By the second trimester, the insulin requirement is 0.8 units per
kilogram. From 24th month onwards steady increase in insulin
requirement and glycemia stabilizes.
 By third trimester the insulin requirement is 0.9 - 1.0 unit /kg
pregnant weight per day.
 Last month – may be a decrease in insulin and hypoglycemias
esp. nocturnal.

16. PATHOPHYSIOLOGY…

17. RISK FACTORS
a) Positive family history of diabetes (parents or sibling). Family
history should include uncles, aunts and grand parents
b) Having previous birth of an overweight baby of 4 kg or more
c) Previous stillbirth with pancreatic islet hyperplasia revealed on
autopsy
d) Unexplained perinatal loss
e) Presence of polyhydroamnios or recurrent vaginal candidiasis in
present pregnancy
f) Persistent glycosuria
g) Age over 30 years
h) Obesity
i) Polycystic ovary syndrome
j) Current use of glucocorticoids
k) Essential hypertension or pregnancy-related hypertension

18. SCREENING
 American Diabetes Association (ADA) recommends two step
procedures for screening and diagnosis of diabetes and that
too in selective (high risk) population.
 Compared with selective screening, universal screening for
GDM detects more cases and improves maternal and
neonatal prognosis.
 In the Indian context, screening is essential in all pregnant
women as the Indian women have 11 fold increased risk of
developing glucose intolerance during pregnancy compared to
Caucasian women.

19. SCREENING…
 Practically all the pregnant women should undergo screening
for glucose intolerance.
 The usual recommendation for screening is between 24 and
28 weeks of gestation.
 The recent concept is to screen for glucose intolerance in the
first trimester itself as the fetal beta cell recognizes and
responds to maternal glycemic level as early as 16th week of
gestation.
 If found negative at this time, the screening test is to be
performed again around 24th – 28th week and finally around
32nd – 34th week

20. SCREENING…
 American Diabetes Association (2003) recommends 3 hour
100 gm OGTT and Gestational Diabetes Mellitus is diagnosed
if any 2 values meet or exceed FPG > 95 mg/dl, 1 hr PG >
180 mg/dl, 2 hr PG > 155 mg/dl and 3 hr PG > 140 mg/dl.
 This criteria was originally validated against the future risk of
these women developing diabetes and not on the fetal
outcome.
 Now according to recent ADA guidelines 2012, it is
recommended that a 2 hour OGTT with 75 gm glucose should
be used for screening.

21. SCREENING…
The reason for this change is that-
 When a glucose tolerance test is administered to non-
pregnant individuals, it is standard to use the 75-g, 2-hour
OGTT.
 Using a different glucose challenge in pregnant versus non-
pregnant patients leads to confusion in the laboratory and
may result in errors in applying the proper diagnostic criteria.
 Further, the 75g, 2-hour OGTT is in use during pregnancy in
many countries around the world, typically using the same
thresholds as in non-pregnant individuals.

22. ADA GUIDELINES 2012 FOR GDM
SCREENING…
 Screen for undiagnosed type 2
diabetes at the first prenatal visit
in those with risk factors, using
standard diagnostic criteria.
previously known to
 In pregnant women not
have
diabetes, screen for GDM at 24–
28 weeks’ gestation, using a 75-
g 2-h OGTT and the diagnostic
cut points.

23. ADA GUIDELINES 2012 FOR GDM
SCREENING…
 Screen women with GDM for persistent diabetes at 6–12
weeks’ postpartum, using a test other thanA1C.
 Women with a history of GDM should have lifelong screening
for the development of diabetes or prediabetes at least every
3 years.
 Women with a history of GDM found to have prediabetes
should receive lifestyle interventions or metformin to prevent
diabetes.

24. ADA GUIDELINES 2012 FOR GDM
SCREENING…
 These new criteria will significantly increase the prevalence of
GDM, primarily because only one abnormal value, not two, is
sufficient to make the diagnosis.
 ADA recognizes the anticipated significant increase in the
incidence of GDM diagnosed by these criteria and is sensitive
to concerns about the “medicalization” of pregnancies
previously categorized as normal.
 These diagnostic criteria changes are being made in the
context of worrisome worldwide increases in obesity and
diabetes rates, with the intent of optimizing gestational
outcomes for women and their babies.

25. ADA GUIDELINES 2012 FOR GDM
SCREENING…
 Admittedly, there are few data from randomized clinical trials
regarding therapeutic interventions in women who will now be
diagnosed with GDM based on only one blood glucose value
above the specified cut points (in contrast to the older criteria
that stipulated at least two abnormal values).
 However, there is emerging observational and retrospective
evidence that women diagnosed with the new criteria (even if
they would not have been diagnosed with older criteria) have
increased rates of poor pregnancy outcomes similar to those
of women with GDM by prior criteria

26. DIAGNOSTIC CRITERIA

27. DIAGNOSTIC CRITERIA

28. COMPLICATIONS
• Maternal
• Fetal

29. MATERNAL COMPLICATIONS
 Diabetes complications during pregnancy:
1. Diabetic ketoacidosis
2. Deterioration of diabetic retinopathy
3. Deterioration of diabetic nephropathy
4. Hypoglycemia (when using insulin)
 Obstetric complications during pregnancy:
1. Spontaneous abortion.
2. Premature birth
3. Pregnancy-induced hypertension
4. Polyhydramnios

30. MATERNAL COMPLICATIONS…
Obstetric complications
during labour:
1. Prolonged labour
2. Shoulder dystocia
3. Perineal injuries
4. Postpartum haemorrhage
5. Operative interference
Obstetric complications in
puerperium:
1. Puerperal sepsis
2. Failing lactation

31. FETAL COMPLICATIONS
 Antenatal complications:
1. Fetal distress/fetal death
2. Congenital malformations- Cardiac abnormalities
(ventricular atrial septal defects), Neural tube defects,
(anencephaly, spina bifida, microcephaly) and Caudal
regression syndrome (sacral agenesis)
3. Macrosomia
4. Delayed fetal development
 Complication during birth:
1. Birth injury due to shoulder dystocia

32. FETAL PROBLEMS ASSOCIATED WITH MATERNAL
HYPERGLYCEMIA ACCORDING TO TRIMESTERS OF
GESTATION
FIRST TRIMESTER SECOND
TRIMESTER
THIRD TRIMESTER
 Malformations
 Growth Retardation
 Fetal Wastage
 Hypertrohic
Cardiomyopathy
 Polyhydramnios
 Erythremia
 Placental
Insufficiency
 Preeclampsia
 Fetal loss
 Low IQ
 Hypoglycemia
 Hypocalcemia
 Hyperbilirubinemia
 Respiratory Distress
Syndrome
 Macrosomia
 Hypomagnesemia
 Intrauterine death

33. MANAGEMENT
• Examination
• Investigations
• Non-pharmacological
• Pharmacological

34. EXAMINATION
 Physical findings: blood pressure, heart rate,
(measured every day while the patient is hospitalized)
weight
 Height of uterine fundus measured once per week
 Pelvic examination: check for indications of premature birth;
vaginal culture

35. INVESTIGATIONS
 Blood and urine testing
a. Self-monitoring of blood glucose
b. HbA1c, KFT, peripheral blood in general: measured once per month.
c. Anti-insulin antibody, anti-GAD antibody, islet cell antibody (ICA): carried out
once as early in the pregnancy as possible.
d. Urine protein, quantitative measurement of urinary glucose: twice per month
e. Urine ketone bodies, protein, qualitative measurement of urinary glucose:
twice per week
f. Blood ketone bodies: once per month
g. Trace urinary albumin: early pregnancy

36. INVESTIGATIONS…
 Self-monitoring of blood glucose (SMBG)
As a rule, blood glucose is measured 7 times per day. Blood glucose
testing times: before each meal, 2 hours after each meal (2 hours after
the start of the meal), and before going to sleep at night.
Depending on the patient’s symptoms, blood glucose may also be
measured at 2 a.m. or 3 a.m.; in the case of mild glucose intolerance
symptoms, blood glucose may be measured 4 times per day.
In the case of patients with type 1 diabetes, blood glucose is measured
6–7 times per day throughout the pregnancy.
While hospitalized, the values obtained with self-monitoring of blood
glucose are checked against laboratory blood glucose values once to
check consistency

37. HbA1C
 Provides valuable supplementary information for glycemic control
 To safely achieve target glucose levels, combine A1C with frequent
self-monitoring of blood glucose (SMBG)1,2
 Recent research suggests weekly A1Cs duringpregnancy:1
SMBG alone can miss certain high glucose values
SMBG + A1C = more complete data for glucose control
Clinicians can further optimize treatment decisions with weekly A1C
INVESTIGATIONS…

38.  Continuous Glucose Monitoring Systems (CGMS)
• A temporary sensor implanted subcutaneously makesit
possible to measure glucose in the interstitial fluid.
• CGMS cannot replace SMBG; they can, however, provide more
information on the diurnal variation in blood glucose than
SMBG.
• Indications for use of CGMS in pregnancy:
 Frequent episodes of hypo- or hyperglycemia
 Diabetic ketoacidosis
 Lack of correlation between reported blood glucose and A1C
 Improved glycemic control during third trimester
 Reduced infant birth weight
 Decreased risk of infant macrosomia1,2,3
INVESTIGATIONS…

39.  Urine-ketone Testing
• To ensure adequate intake ruling out starvation ketosis, pregnant
women should test urine for ketones daily from the first void.
• Hyperglycemic levels >200 mg/dl warrant ketone testing.
• Hyperglycemia and ketosis may indicate an infection and should be
evaluated thoroughly.
 Examination of the ocular fundus
• Once per month if blood glucose control is poor.
INVESTIGATIONS…

40. INVESTIGATIONS…
Fetal ultrasound
 Measurement of fetal development
 Fetal congenital malformations
 Check for presence of hydramnios.
 Evaluation of fetal well-being- Non-stress Test (NST), Biophysical
profile scoring (BPS)
 Assessment of fetal maturity- Amniocentesis for assessing the lecithin
to Sphingomyelin (L:S) ratio.

41. GOALS FOR GLYCEMIC CONTROL
 As regards goals for glycemic control for women with GDM,
recommendations from the Fifth International Workshop- Conference on
Gestational Diabetes are to target maternal capillary glucose
concentrations of:
Preprandial: ≤95mg/dL (5.3mmol/L), and either:
1-h postmeal: ≤ 140mg/dL (7.8mmol/L) or
2-h postmeal: ≤ 120mg/dL (6.7mmol/L)

42. GOALS FOR GLYCEMIC CONTROL…
 For women with preexisting type 1 or type 2 diabetes who become
pregnant, a recent consensus statement recommended the following
as optimal glycemic goals, if they can be achieved without excessive
hypoglycemia:
Premeal, bedtime, and overnight glucose 60–99 mg/dL (3.3–5.4
mmol/L)
Peak postprandial glucose 100–129 mg/dL (5.4–7.1 mmol/L)
A1C ,6.0%

43. NON-PHARMACOLOGICAL TREATMENT
Diet therapy:
 During pregnancy, as pregnant women patients
adequate energy, protein, and minerals
need to consume
 Either low-carbohydrate, low-fat calorie-restricted, or Mediterranean
diets may be effective in the short-term
 For patients on low-carbohydrate diets, monitor lipid profiles, renal
function, and protein intake (in those with nephropathy), and adjust
hypoglycemic therapy as needed.
 Recommendation for dietary fiber (14 g fiber/1,000 kcal) and foods
containing whole grains (one-half of grain intake).

44. Diet therapy:
 The diet schedule must be planned in such a way as to prevent
postprandial hyperglycemia.
 Diabetic fetopathy which is the result of maternal postprandial
hyperglycemia can be minimized when the peak postprandial response
is blunted.
 The peak postprandial response is minimized in a woman with
gestational diabetes if her meal plan is carbohydrate restricted.
 Saturated fat intake should be ,7% of total calories.
 Reducing intake of trans fat lowers LDL cholesterol and increases HDL
cholesterol, therefore intake of trans fat should be minimized.
NON-PHARMACOLOGICAL TREATMENT

45. Medical Nutrition Therapy (MNT)
• MNT by a registered dietitian is the cornerstone for diabetes
management in women with pregestational and gestational
diabetes.
• The nutritional management of women with preexisting and
gestational diabetes does not differ and has the same
therapeutic goals: adequate nutrition and weight gain, plus
prevention of ketosis and postprandial hyperglycemia.
• The diet for a pregnant woman with diabetes includes at least
175 g/day of carbohydrate, 28 g/day of fiber and 1.1 g of
protein per kg/day (Reader & Thomas, 2008).
NON-PHARMACOLOGICAL TREATMENT

46. Medical Nutrition Therapy (MNT)
• All pregnant women should take a prenatal vitamin with 600
mcg of folic acid daily (IOM, 1998).
• All pregnant women should limit caffeine to 200 mg/day.
• After a thorough assessment, the dietitian and the woman
develop an individualized meal plan to achieve desired
treatment goals.
• The dietitian and the woman examine and discuss lifestyle
influences that have a bearing on MNT.
NON-PHARMACOLOGICAL TREATMENT

47. NON-PHARMACOLOGICAL TREATMENT
Exercise:
 Patients GDM should be referred to an effective ongoing
support program targeting weight loss of 7% of body weight
and increasing physical activity to at least 150 min per week of
moderate activity such as walking.

48. PHARMACOLOGICAL TREATMENT
 When MNT alone fails, pharmacologic therapy is indicated
AACE guidelines recommend insulin as the optimal approach1
Insulin therapy is required for the treatment of T1DM during pregnancy2
 Metformin and the sulfonylurea glyburide are the 2 most commonly
prescribed oral antihyperglycemic agents during pregnancy.
 Due to efficacy and safety concerns, the ADA does not recommend
oral antihyperglycemic agents for gestational diabetes mellitus (GDM)
or preexisting T2DM
Medication Crosses
Placenta
Classification Notes
Metformin Yes Category B1 Metformin and glyburide may
be insufficient to maintain
normoglycemia at all times,
particularly during
postprandial periods2
Glyburide Minimal
transfer
Some formulations category B,
others category C1,5,6

49. PHARMACOLOGICAL TREATMENT
Metformin therapy for prevention:
 Metformin therapy for prevention of type 2 diabetes may be
considered in those women with prior GDM.
 It was as effective as lifestyle in women with a history of GDM,
metformin and intensive lifestyle led to an equivalent
50%reduction in the risk of diabetes
 Metformin therefore might reasonably be recommended for
very-high-risk individuals (those with a history of GDM, the
very obese, and/or those with more severe or progressive
hyperglycemia).

50. PATIENT EDUCATION
• Insulin administration, dietary modifications in response to self-monitoring of blood
glucose (SMBG), hypoglycemia awareness and management.
BASAL INSULIN
• Intermediate- or long-acting insulin administered by injection, or
• Rapid-acting insulin administered by insulin pump2,3
POSTPRANDIAL HYPERGLYCEMIA
• Recommended approach: rapid-acting insulin analogues2
• Alternative approach: regular insulin to control postprandial glucose spikes; must be
administered 60-90 minutes prior to meals (considered less effective than rapid-acting
insulin and may increase hypoglycemia risk)3
INSULIN OPTIONS
• Insulin NPH: safe intermediate alternative (category B)2
• Insulin detemir: safe long-acting alternative (category B)2,3
• Lispro and aspart: safe rapid-acting insulin analogues (category B)2,3
• Insulin glargine: frequently prescribed in pregnancy; however, safety in pregnancy
has not been definitively established (category C)2,3
PHARMACOLOGICAL TREATMENT- INSULIN USE DURING
PREGNANCY

51. PHARMACOLOGICAL TREATMENT-INITIATION OF
INSULIN
GLUCOSE LEVELS FOR INSULIN INITIATION
IN GDM1
Fasting plasma glucose ≤105 mg/dL
(5.8 mmol/L)
1-hour postprandial plasma glucose ≤155 mg/dL
(8.6 mmol/L)
2-hour postprandial plasma glucose ≤130 mg/dL
(7.2 mmol/L)

52. PHARMACOLOGICAL TREATMENT-INSULIN
 Following a positive pregnancy test, patients with preexisting diabetes
being treated with insulin or oral antihyperglycemic medications should be
transitioned to one of the above options2
.

53. PHARMACOLOGICAL TREATMENT-INSULIN

54. PHARMACOLOGICAL TREATMENT-INSULIN DOSING

55.  CSII: Administration of rapid-acting insulin via insulin pump
Safe and reliable method for satisfying basal insulin needs in pregnant
patients with gestational diabetes mellitus (GDM), T2DM, or T1DM1,2
 CSII may need to be combined with CGM for optimal glycemic control in T1DM1
Can be used to effectively mimic physiologic insulin secretion2
No significant difference in glycemic control for pregnancy outcomes with
CSII versus multiple-dose insulin (MDI) therapy3
Can help address daytime or nocturnal hypoglycemia or a prominent dawn
phenomenon4
 Insulin aspart and lispro are the standard of care for CSII5
 Disadvantages of CSII:
Complexity–requires counseling and training
Cost
Potential for insulin pump failure/user error or infusion site problems2,4
INSULIN PUMP THERAPY/CONTINUOUS
SUBCUTANEOUS INSULIN INFUSION (CSII)

56. TREATMENT
56
Diagnosis of and management procedures for pregnant women
complicated with carbohydrate intolerance

57. MANAGEMENT DURING LABOR & DELIVERY
Timing and mode of delivery
 In the case of a GDM patient undergoing insulin therapy
where fetal development is thought to be within the normal
range, there is no difference in the caesarean section rate
between women for whom labor is induced at 38 weeks and
those for whom labor is not induced.
 Moreover, it has also been reported that there is no difference
in the incidence of macrosomia or caesarean section between
insulin-treated GDM patients for whom labor is induced at 38–
39 weeks and insulin-treated GDM patients who electively
waited for labor and childbirth to take their natural course.

58. MANAGEMENT DURING LABOR & DELIVERY
Timing and mode of delivery…
 In the case that the GDM patient has good blood glucose
control and fetal development is thought to be within the
normal range, as a general rule it is considered that the
pregnancies of GDM patients may be managed in the same
manner as those of normal glucose-tolerant women.
 In the case that birth weight is estimated at 4,000g or higher,
an elective caesarean section is considered.
 However, in the case that the patient has poor blood glucose
control, induced delivery at 38 weeks onward is considered.

59. MANAGEMENT DURING LABOR & DELIVERY
Insulin therapy during labor & delivery:
 When carrying out insulin therapy, special care is needed as
the amount of insulin required during pregnancy, during
delivery, and after birth differs tremendously.
 Thus, insulin requirements at the end of pregnancy increase
by approximately two-fold.
 During first-stage labor the required amount decreases, while
in second-stage labor it increases slightly and after birth
decreases rapidly.

60. MANAGEMENT DURING LABOR & DELIVERY
Insulin therapy during labor & delivery…
 Accordingly, attention needs to be paid to such changes in
required insulin amounts during pregnancy and the amount of
insulin administered reduces by half following delivery.
 In particular, since it becomes difficult for the patient to eat
during first- and second-stage labor, especially careful
management of blood glucose levels is necessary in the case
that labor and delivery are prolonged

61. MANAGEMENT DURING LABOR & DELIVERY
Insulin therapy during labor & delivery…
 At the onset of labor the patient is administered an electrolyte
fluid containing 5% glucose at a rate of 100–120ml/hr, then
administered insulin intravenously via an infusion pump.
 Depending on the individual case, blood glucose is measured
at intervals of 1–2 hours.
 Insulin administration begins with a dosage of 0.5 units/hr and
the insulin dosing rate is determined based on fluctuations in
blood glucose levels.

62. TAKE HOME MESSAGE
 Diagnosis of GDM with 75-g oral glucose load
Fasting ≥ 92mg/dl; 1hr ≥180mg/dl; 2hr ≥153mg/dl.
 Metformin and Glyburide can be used but ADA does not
recommend it, ADA recommends Insulin.
 Glucose levels for insulin initiation in GDM when
non-pharmacological measures fails.
Fasting <105mg/dl; 1hr ≤155mg/dl; 2hr ≤130mg/dl.

63. THANK YOU…