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GESTATIONAL DIABETES

MELLITUS

Dr. Yunus Tanggo SpPD.PhD


Definition

Gestational Diabetes mellitus is


defined carbohydrate intolerance of
varying degrees of severity with onset
or first recognition during pregnancy

GDM is associated with a variety of


maternal and fetal complications
Epidemiology of GDM

GDM affects 7% of all pregnancies


> 200,000 cases per year
prevalence may range from 1 to 14%
All pregnancies complicated by
diabetes, GDM accounts for ~ 90%.
ADA and WHO Criteria for
the Diagnosis of GDM
ADA ADA WHO
100-g OGTT 75-g OGTT 75-g OGTT
Fasting (mg/dl) 95 95 126
1-hour (mg/dl) 180 180
2-hour (mg/dl) 155 155 140
3-hour (mg/dl) 140

For the ADA criteria, two or more of the values from either the 100- or 75-g
OGTT must
be met or exceeded to make the diagnosis of GDM. For the WHO criteria,
one of the two
values from the 75-g OGTT must be met or exceeded to make the
diagnosis of GDM
Pathophysiology (1)

Pregnancy is a condition characterized


by progressive insulin resistance that
begins near midpregnancy and
progresses
through the third trimester
In late pregnancy, insulin sensitivity
falls by until 50%
Pathophysiology (2)
Two main contributors to insulin resistance
include increased maternal
adiposity and the insulin desensitizing
effects of hormones produced by the
placenta
The placenta produces human chorionic
somatomammotropin (HCS, formerly called
human placental lactogen), bound and free
cortisol, estrogen, and progesterone
Pathophysiology (3)
HCS stimulates pancreatic secretion of
insulin in the fetus and inhibits peripheral
uptake of glucose in the mother
In non diabetic pregnant women, the first-
and second phase insulin responses
compensate for
this reduction in insulin sensitivity, and
this is associated with b-cell hypertrophy
and hyperplasia
Pathophysiology (4)
However, women who have a deficit in this
additional insulin secretory capacity
develop GDM
b-Cell dysfunction in women diagnosed with
GDM may fall into one of three major
categories:
1) autoimmune,
2) monogenic,
3) occurring on a background of insulin
resistance (as is most common).
Pathophysiology (5)

The loss of the first-phase insulin


response leads to postprandial
hyperglycemia, whereas impaired
suppression of hepatic glucose
production is responsible for fasting
hyperglycemia when present.
Because insulin does not cross the
placenta, the fetus is exposed to the
maternal hyperglycemia
Pathophysiology (6)

The fetal pancreas is capable of


responding to this hyperglycemia
The fetus thus becomes
hyperinsulinemic, which in turn
promotes growth and subsequent
macrosomia.
Screening strategy for detecting
gestational diabetes mellitus (1)
Low risk Blood glucose testing not
routinely required if all of the
following characteristics are present
Member of an ethnic group with a low
prevalence of GDM
No known diabetes in first-degree relatives
Age <25 years
Weight normal at birth
Weight normal before pregnancy
No history of abnormal glucose metabolism
No history of poor obstetric outcome
Screening strategy for detecting
gestational diabetes mellitus (2)

Average risk Perform blood


glucose testing at 24
28 weeks in the
following
All subjects not classified as
low risk or high risk
Subjects initially designated
high risk that did not
have GDM at early testing
Screening strategy for detecting
gestational diabetes mellitus (3)

High risk Perform blood glucose testing as soon as


feasible after booking if one or more of the
following characteristics are present

Severe obesity according to local standards


Strong family history of Type 2 diabetes mellitus
Previous history of GDM or glucose intolerance
outside of pregnancy
Glucosuria

If GDM is not diagnosed, blood glucose testing should be


repeated at 2428 weeks, or at any time a patient has symptoms
or signs that are suggestive of hyperglycemia
Two approaches may be followed for
GDM screening at 2428 weeks (1)

1. Two-step approach:
A. Perform initial screening by measuring
plasma or serum glucose 1 h after a 50-g oral
glucose load. A glucose threshold after 50-g
load of 140 mg/dl identifies 80% of women
with GDM, while the sensitivity is further
increased to 90% by a threshold of 130 mg/dl.
B. Perform a diagnostic 100-g OGTT on a
separate day in women who exceed the
chosen threshold on 50-g screening
Two approaches may be followed
for GDM screening at 2428 weeks
(2)
2. One-step approach (may be preferred in
clinics with high prevalence of GDM):
Perform a diagnostic 100-g OGTT in all
women to be tested at 2428 weeks.The
100-g OGTT should be performed in the
morning after an overnight fast of at least 8
h.
A diagnosis of GDM requires at least two of
the following plasma glucose values:
Fasting: 95 mg/dl (5.3 mmol/l)
1 h: 180 mg/dl (10.0 mmol/l)
2 h: 155 mg/dl (8.6 mmol/l)
3 h: 140 mg/dl (7.8 mmol/
Complications
Maternal complications
Antepartum morbidity in women with GDM
mostly consists of higher risk for development
of hypertensive disorders and preeclampsia
GDM increases the risk of cardiovascular
disease (CVD)
increased risk of cesarean delivery
GDM have an increased risk of developing
diabetes after pregnancy compared to the
general population
Complications
Fetal complications
Macrosomia
Neonatal hypoglycemia
Perinatal mortality
Congenital malformation
Hyperbilirubinemia,
Polycythemia, hypocalcemia,
Respiratory distress syndrome.
Treatment(1)
Glucose Monitoring
The goal of monitoring is to detect glucose
concentrations elevated enough to increase
perinatal mortality
The Fourth International Workshop Conference
on Gestational Diabetes Mellitus recommends
maintaining the
following capillary blood glucose values:
preprandial glucose < 95 mg/dl, 1-
hour postprandial glucose < 140 mg/dl,
and 2-hour postprandial glucose < 120mg/dl
Treatment(2)

Medical Nutrition Therapy(MNT)


The goals of MNT are to provide
adequate nutrition for the mother and
fetus, provide sufficient calories for
appropriate maternal weight gain,
maintain normoglycemia,and avoid
ketosis
Treatment(3)
Insulin
Insulin therapy is the most commonly
used treatment when MNT fails to
maintain blood glucose levels at the
desired ranges or when there is
evidence of excessive fetal growth
insulin lispro was as effective as regular
insulin in controlling glucose levels with
fewer episodes of hypoglycemia.

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