DIABETES IN
PREGNANCY
Dr. Mtumweni,MD
Obstetrics and Gynaecology I (CMT 05104)
Department of Clinical Medicine
Mtwara College of Health and Allied Sciences
2.
LEARNING OBJECTIVES
• Definediabetes in pregnancy
• Explain epidemiology of diabetes in pregnancy
• Describe pathogenesis of diabetes in pregnancy
• Describe risk factors of diabetes in pregnancy
• Explain clinical features of diabetes in pregnancy
• Explain complications of diabetes in pregnancy
• Establish diagnosis of diabetes in pregnancy
• Manage diabetes in pregnancy
• Refer as appropriate
• Conduct follow up services
3.
The concept ofDiabetes
Mellitus (DM)
• Diabetes mellitus is a chronic
metabolic disorder due to either
insulin deficiency (relative or
absolute) or due to peripheral
tissue resistance (decreased
sensitivity) to the action of insulin
4.
How a persondevelops DM?
• The pathophysiology involved are:
(i) decreased sensitivity of skeletal
muscles and liver to insulin (insulin
resistance) and
(ii) Inadequate secretion of insulin (β cell
dysfunction).
• The defect lies both in insulin secretion
and action. The ultimate effect is the
hyperglycemia.
5.
• Human PlacentalLactogen (HPL)
• Produced by syncytiotrophoblasts of placenta.
• Acts to promote lipolysis increased FFA and to
decrease maternal glucose uptake and
gluconeogenesis. “Anti-insulin”
• Estrogen and Progesterone
• Interfere with insulin-glucose relationship.
• Insulinase
• Placental product that may play a minor role.
6.
Types of DiabetesMellitus
• Two types are generally described
i. Type–1 (IDDM) is characterized by young age onset
(Juvenile) and absolute insulinopenia. They have
genetic predisposition with presence of
autoantibodies.
ii. Type–2 (NIDDM) is characterized by late age onset,
overweight woman and peripheral tissue (skeletal
muscle, liver) insulin resistance (hyper
insulinemia). Genetic predisposition is also observed.
7.
How many Pregnantwomen are
affected by Diabetes mellitus?
• About 1–14 percent of all pregnancies
are complicated by diabetes mellitus
and 90 percent of them are
gestational diabetes mellitus (GDM).
• Nearly 50 percent of women with
GDM will become overt diabetes
(type-2) over a period of 5 to 20 years.
8.
NB: GLYCOSURIA IN
PREGNANCY
•About 5-50% of pregnant women have glucose in urine
(Glycosuria).
• This maybe normal but the woman has to be investigated
if she has DM or not.
• During pregnancy, renal threshold is diminished due to
the combined effect of increased glomerular filtration and
impaired tubular reabsorption of glucose.
• It is present most commonly in mid pregnancy.
• No treatment is required and the condition disappears
after delivery.
9.
SIGNIFICANCE OF GLYCOSURIAIN
PREGNANCY
• Glycosuria is specifically detected by testing a
second fasting morning specimen of urine,
collected a little later, after discarding the
overnight urine.
• Fasting glycosuria if present, is ominous.
• Glycosuria on one occasion before 20th
week
and on two or more occasions, thereafter, is an
indication for glucose tolerance test.
10.
INDICATIONS OF GLUCOSE
TOLERANCETEST
i. Glycosuria occurring any time during
pregnancy with a positive family history of
diabetes
ii. Past history of having a baby weighing 4 kg or
more.
iii. Fasting glycosuria on one occasion before 20th
week and on two or more occasions thereafter
iv. Following a positive ‘screening test’
11.
Note; The besttime to screen for diabetes
during pregnancy is at the end of the second
trimester between 24 and 28 weeks‘
gestation in women with low risk for GDM.
• . Pregnancy is a state of insulin resistance &
relative glucose intolerance
• This is due to placental production of anti-
insulin hormones : hPL, cotisol, and
glucagon
12.
GESTATIONAL DIABETES
MELLITUS (GDM)
•GDM is defined as carbohydrate
intolerance of variable severity with
onset or first recognition during the
present pregnancy.
• The entity usually presents late in the
second or during the third trimester.
• Previously, it was known as “Pregnancy
induced glucose intolerance”.
13.
Women who areat risk to get
GDM
(a) Positive family history of diabetes (parents or siblings, uncles, aunts and grand
parents)
(b) Having a 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 polyhydramnios or recurrent vaginal candidiasis in present
pregnancy.
(f) Persistent glycosuria.
(g) Age over 30 years
(h) Obesity
(i) Ethnic group (East Asian, Pacific island ancestry).
14.
OVERT DIABETES
• Apatient with symptoms of diabetes mellitus (polyuria,
polydipsia, weight loss) and random plasma glucose
concentration of 200 mg/dL or more is considered overt
diabetic.
• The condition may be pre-existing or detected for the first
time during present pregnancy.
• According to American Diabetic Association diagnosis is
positive if
(a) The fasting plasma glucose exceeds 126 mg/dL
(b) The 2 hours post glucose (75 gm) value exceeds 200
mg/dL
15.
EFFECTS OF PREGNANCY
ONDIABETES
• It is difficult to stabilize the blood glucose during pregnancy.
• This is due to altered carbohydrate metabolism and an impaired insulin
action.
• The insulin antagonism is due to the combined effect of human
placental lactogen, estrogen, progesterone, free cortisol and degradation
of the insulin by the placenta.
• The insulin requirement during pregnancy increases as pregnancy
advances.
• With the “accelerated starvation” concept, there is rapid activation of
lipolysis with short period of fasting.
• Ketoacidosis can be precipitated during hyperemesis in early pregnancy,
infection and fasting of labor.
• Insulin requirement falls significantly in puerperium.
16.
EFFECTS OF DIABETES
ONPREGNANCY
• MATERNAL
• During pregnancy:
• Abortion
• Preterm labor (20%)
• Infection: Urinary tract infection and vulvo vaginitis.
• Increased incidence of pre-eclampsia (25%).
• Polyhydramnios (25–50%)
• Maternal distress may be due to the combined effects
of an oversized fetus and polyhydramnios.
17.
• Diabetic retinopathy,microaneurysms,
hemorrhages and proliferative retinopathy
• Diabetic nephropathy—may lead to renal
failure.
• Ketoacidosis
18.
Maternal effects con’t…
•During labor:
• There is increased incidence of:
(1) Prolongation of labor due to big baby.
(2) Shoulder dystocia.
(3) Perineal injuries.
(4) Postpartum hemorrhage
(5) Operative interference.
• Puerperium: (1) Puerperal sepsis. (2) Lactation
failure.
• PERINATAL MORTALITY:
•The overall perinatal mortality is increased 2–
3 times.
• The neonatal deaths are principally due to
hypoglycemia, respiratory distress syndrome,
polycythemia and jaundice.
23.
Diagnosis of Diabetesin
Pregnancy
• Diagnosis of diabetes in pregnancy is based
on the history and laboratory findings.
• Typical features of polyuria, polydypsia and
polyphagia may be found in diabetic patients.
• World Health Organisation (WHO) defines
diabetes as raised fasting blood glucose
level (FBG) of 126mg/dl (7.0 mmol/l) or
more, random blood glucose level (RBG) of
200mg/dl (11.1 mmol/l)or more.
Investigations at Health
Center
•Fasting/Random blood glucose
• FBP or Hemoglobin level
• Urinalysis
• Serum creatinine
• Blood urea nitrogen
• Obstetric ultrasound
26.
Investigations at Hospitallevel
• Fasting/Random blood glucose
• FBP or Hemoglobin level
• Urinalysis
• Serum creatinine
• Blood urea nitrogen
• Obstetric ultrasound
• Estimation of glycosylated hemoglobin A (HbA1c) (Normal <
or = 6%)
• Maternal serum α fetoprotein level
27.
Management of Diabetesin
Pregnancy
• Management of diabetes in pregnancy
requires a team approach consisting of
obstetricians, neonatologists, physicians
and dieticians.
• Management of diabetes in pregnancy
involves both non-pharmacological
strategies (i.e. education, counselling,
diet, exercise) and pharmacological
strategies
28.
Pre-conceptional
counseling
• Goal isto achieve tight control of diabetes before the
onset of pregnancy. Ideally a diabetic woman should be
seen jointly by the diabetologist, obstetrician and dietician.
• Fetal congenital malformations are significantly low (0.8-
2%) in women who receive pre-conceptional counseling.
• Women are taught for self glucose monitoring.
Appropriate advice about diet and insulin is given.
• Chance of having a diabetic child is about 1-3% when the
mother is only diabetic, 6% when father is only diabetic,
rising to 20% if both the parents are diabetic.
29.
Management
Diet
• To providethe necessary nutrients for
the mother and foetus
• To control glucose levels
• To prevent starvation ketosis
Insulin Therapy
• Isusually recommended when dietary
management does not consistently maintain the
fasting blood glucose at less than 105mg/dl or
the two hour postprandial plasma glucose at less
than 120mg/dl
• A common initial dose is 0.7units/kg/day
• Two thirds (2/3) of total dose in the morning and
one third (1/3) in the evening
32.
• The doseshould be expected to
increase as pregnancy progresses and
insulin resistance increases. Up to 40%
of women with gestation diabetes
require insulin therapy.
33.
Oral Hypoglycaemic Drugs
•They are not recommended during
pregnancy (except glyburide) because
of their effects in pregnancy such as:
1. Foetal hyperinsulinaemia
2. Teratogenic effect
34.
Timing and Methodof Delivery
• Delivery should be after the gestation age of 37
weeks
• In well controlled gestational diabetes there is no
need to terminate at 38 weeks, wait for spontaneous
labour.
• If gestation age is uncertain then lecin: sphingomyelin
should be measured to ascertain foetal lung maturity.
• Caesarean section should be done with the estimated
foetal size is >4000g to avoid traumatic delivery and
shoulder dystocia.
35.
Intrapartum
• It isimportant to maintain euglycaemia to avoid
neonatal hypoglycaemia.
• Plasma glucose levels should be done every one
to two hours
• If initial glucose is between 80-120mg/dl, add 10IU
of insulin in 1L 5% dextrose at a rate of 125ml/hr
• If initial glucose levels are below 70mg/dl give 5%
dext without insulin at a rate of 100-120ml/hr
throughout labour
36.
Postpartum
• Breastfeeding shouldbe encouraged
• In patients who required insulin during pregnancy, it is
reasonable to check fasting and two hour postprandial
glucose levels before discharge
• Follow-up 100g oral glucose tolerance test at 6-12weeks
can determine the woman’s risk of developing diabetes
• Approximately 50% of gestation diabetes patients
develop type 2 in five to ten years if body mass index
(BMI) is >20kg/m2
37.
Contraceptives
• There’s nosingle contraceptive method
appropriate for all women with diabetes
• Oral contraceptives increase the risk of
thromboembolism (The risk of thromboembolism
is increased in those women who are using
contraception).
• Intra uterine contraceptives device (IUCD)
increase risk of pelvic infection
#19 Fetal macrosomia (30–40%) probably results from: (a) Maternal hyperglycemia → hypertrophy and hyperplasia of the fetal islets of Langerhans → increased secretion of fetal insulin → stimulates carbohydrate utilization and accumulation of fat. Insulin like growth factors (IGF-I and II) are also involved in fetal growth and adiposity. With good diabetic control, incidence of macrosomia is markedly reduced. (b) Elevation of maternal free fatty acid (FFA) in diabetes leads to its increased transfer to the fetus → acceleration of triglyceride synthesis → adiposity.
Congenital malformation (6–10%) is related to the severity of diabetes affecting organogenesis, in the first trimester (both in type 1 and type 2 diabetes). The factors associated with teratogenesis are multifactorial: (a) Genetic susceptibility (b) Hyperglycemia (c) Arachidonic acid deficiency (d) Ketone body excess (e) Somatomedin inhibition (f) Free oxygen radical excess (superoxide dismutase, an oxygen radical scavenging enzyme can protect excess malformation). Risks of fetal chromosomal abnormalities are not increased.