DIABETES MELLITUS IN

PREGNANCY
MAFABI MATHIAS
SABAIDHU JIMMY
TUTOR:DR SEKIKUBO MUSA
CONTENTS

• Definition
• Types
• Classification
• Epidemiology
• Risk factors
• Pathophysiology
• Clinical presentation
• Fetal & maternal effects
• complications
• Management
Definition
• Diabetes Mellitus is a chronic metabolic disorder due to insulin
deficiency or peripheral tissue resistance to insulin characterized by
alteration in glucose, fat and protein metabolism.
Definition
 Diabetes mellitus is defined as a raised fasting blood glucose level of
equal to or >7.0mmol/L(126mg/dl) and/ or 2-hour blood glucose equal
to or >11.1mmol/L (200mg/dl) following a 75g glucose load (WHO)
HBA1c=>48mmol/mol(>6.5%).

 Gestational diabetes is carbohydrate intolerance of variable severity

with onset or first recognition during pregnancy

 Gestational DM is a fasting plasma glucose 5.1-6.9mmol/l and/ or 2

hourly plasma glucose 8.5-11.0 mmol/l following a 75g oral glucose
load. (WHO, 2013)

NB Pregnacy is a state of chronic low grade inflammation, with

increased circulating levels of crp, and IL6 which enhance insulin
resistance.
 TYPES

A. Type 1 (Insulin Dependent); IDDM

• Immune mediated disorder involving T cell dysfunction of beta cells
• Absolute insulinopenia due to autoantibodies against beta cells
• Onset often <40 years. (Juvenile)
• 10% of cases
• Duration of symptoms- weeks
B. Type 2 (Non-Insulin Dependent) ; NIDDM
o Defective insulin action(resistance) with normal/reduced insulin secretion
as disease progresses
o Onset often >50yrs
o 90% of cases.
o Duration of symptoms – months to years
C. Gestational DM
 WHO CLASSIFICATION
• Pre-gestational DM : Pre-existing Type 1 or Type 2 diabetes
• Gestational DM (GDM) : refer to above slides.
• If the abnormality in glucose tolerance persists after pregnancy, the
diagnosis is revised to type 1, type 2, or impaired glucose tolerance
(IGT).
Gestational Diabetes risk assessment.
• Begins at ANC booking visit.involves;
BMI>30Kg/m2
Previous macrosomic baby >4.5kg
Previous GD.
Family history of DM in first degree relative.
An ethnicity with high prevalence of DM.
Urinalysis for glycosuria of 2+ on 1 occasion or glycosuria of 1+ on 2 or more occasions.
(not so reliable :physiological glycosuria)

• NB. For women with risk factors,

• use 75g 2hour oral glucose tolerance test to test for GD, repeat at 24-28
weeks if first results were normal.
• However, this may also be as a result increased insulin resistance during
pregnancy stemming from anti insulin hormones ie prolactin, HPL and
cortisol.
EPIDEMIOLOGY

• Commonest pregnancy complication worldwide.1

• Prevalence is approx. 15% globally2
• Affects 1 in 7 births worldwide
• Prevalence rates higher in Black, Hispanic, Native Americans and
Asian women than in white women
• GDM accounts for 90% of the cases. However, the rising prevalence
of type 2 DM has resulted in an increase in the numbers of pregnant
women with pre-existing DM. In addition, almost 50% of women
with GDM will become overt T2DM in 5-20 years.
• According to 2017 study by Nakabuye et al, 31.9% of pregnant
Ugandan women were diagnosed with GDM.
Carbohydrate metabolism during
pregnancy
• During the first and early part of the mid trimester, there is
increased sensitivity to insulin and diabetic patients have a
tendency towards hypoglycemia. This is probably due to the
high levels of estrogen.

• In 3rd trimester, there is increased insulin resistance due to the

antagonistic effect of HPL,prolactin and cortisol.

• To ensure continuous glucose supply to the growing fetus.

• Also accelerated insulin catabolism by renal and placental
insulinases and the anti-insulin effects of other hormones
(cortisol, estriol, progesterone) produced in large amounts
during pregnancy also contribute to insulin resistance.

• As a result of the physiologic changes of pregnancy, the

normal fasting blood sugar is 65 ± 9 mg/dl. The mean non
fasting blood sugar level is 80 ± 10 mg/dl. Postprandial
elevations normally never exceed 140 mg/dl .

• During lactation,glucose level fall and insulin resistance

returns to normal as glucose homeostasis is reset.
Risk Factors

• A previous diagnosis of gestational diabetes

• A family history revealing a first degree relative with type 2
diabetes
• Maternal age; a woman’s risk factor increases as she gets
older(esp. above 35yrs)
• Ethnicity (more in blacks>whites)
• Obesity; BMI above 30kg/m2
• Previous delivery of a baby greater than 4kg
• Viral infections like CMV, Coxsackie virus etc.
 Risk Factors
History of abnormal glucose tolerance
Previous unexplained perinatal loss or birth of a malformed
child(anencephaly,spina bifida,microcephaly)
Glycosuria at the 1st prenatal visit(R)
Current use of glucocorticoids
Essential or pregnancy related hypertension
Previous still birth with pancreatic islet hyperplasia on autopsy.
Pathophysiology GDM

During pregnancy the placenta secretes substances that have an

anti-insulin action, including human placental lactogen (hPL),
progesterone, human chorionic gonadotrophin (hCG) and cortisol.

If the maternal beta islet cells are unable to produce the additional
insulin required to counteract this effect, the woman will develop
hyperglycemia.

As the maternal glucose (but not insulin) can readily cross the
placenta, the fetal pancreas will secrete additional insulin if there is
maternal hyperglycemia. (hyperplasia and hypertrophy)
CONT…

• Human Placental Lactogen (HPL)

Produced by syncytiotrophoblasts of placenta.
Acts to promote lipolysis  increased FFA which
increases hepatic insulin resistance by inhibiting insulin
mediated suppression of glycogenolysis. “Anti-insulin”
Progesterone
• Increases adipocyte insulin resistance >prevents uptake of
glucose into adipocytes.
• Insulinase
• Placental product that may play a minor role.
GDM EFFECTS TO THE FOETUS
Due to maternal hyperglycaemia, there’s:
• Hypertrophy and hyperplasia of foetal islets of Langerhans
• Increase in insulin-like growth factors involved in foetal growth
• Acceleration of triglyceride synthesis and increased transfer of FFA to
foetus
• Congenital malformation is associated with genetic susceptibility,
hyperglycaemia, ketone body excess, and free radical excess.
• GDM EFFECT TO THE MOTHER.
• Increased risk of miscarriage.
• Increased risk of pre eclampsia.
• Increased risk of infections.
• Increased operative delivery rates.
Clinical Presentation

Signs and symptoms.

• Classical triad: polyuria, polyphagia, polydipsia (not
universal in all patients)
• Obesity, Excessive weight gain in type 2/loss in type 1.
• Fatigue, Blurred vision.
• Parathesias.
• Recurrent Skin infections eg boils.
• Glycosuria, Nausea
• Frequent bladder infections
• Frequent episodes of Vulvo vaginal candidiasis
 Effects of diabetes on pregnancy
fetal complications
FETAL Neonatal complications

• Fetal macrosomia • Hypoglycemia

• Congenital malformation • Respiratory distress syndrome
• Birth injuries • Hyperbilirubinemia
• Growth restriction • Polycythemia
• Fetal death • Hypocalcemia
• Hypomagnesemia
Long term effects
• Childhood obesity • cardiomyopathy
• Neuropsychological effects
• diabetes
 Maternal complications
• Increased During pregnancy:
• Abortion
• Preterm labor(20%)
• Infection
• incidence of pre-eclampsia (25%)
• Polyhydramnios (25%)
• Maternal distress
• Diabetic retinopathy
• Diabetic nephropathy
• ketoacidosis
Maternal complications

• During labour; there’s increased incidence of

• Prolongation of labor due to big baby
• Shoulder dystocia
• Perineal injuries
• Postpartum hemorrhage.
• Operative interference
• Puerperium
• Puerperal sepsis
• Lactation failure
 DIAGNOSTIC CRITERIA FOR DM PRIOR TO
PREGNANCY
1. Symptoms of diabetes plus random plasma glucose
concentration equal to or greater than 200
mg/dL(11.1mmol/l)
2. . The classic symptoms of diabetes include polyuria,
polydipsia, and unexplained weight loss.
3. Fasting plasma glucose (FPG) equal to or greater than 126
mg/dL(7.0mmol/l). Fasting is defined as no caloric intake
for at least 8 hours.
4. 2hr post-load glucose level equal to or greater than 200
mg/dL (11.1mmol/l)during an oral glucose tolerance test
(OGTT). The test uses a glucose load containing the
equivalent of 75 g anhydrous glucose dissolved in water.
 DIAGNOSTIC CRITERIA FOR GESTATIONAL DM

• Risk assessment for GDM is performed at the first antenatal visit in all women
who do not already have diagnosed diabetes.
• Women with risk factors should be screened as soon as feasible and retested
between 24 to 28 weeks if results don’t demonstrate DM
• All women of ordinary or high risk should be screened between 24 and 28
weeks' gestation.
• During the antenatal period, clinical findings that suggest maternal
hyperglycemia, such as fetal weight 70% or greater for gestational age or
polyhydramnios (amniotic fluid index equal or more than 24 cm) should
prompt re-evaluation for GDM.
 PRECONCEPTION CARE
• Care of women with type 1 or type 2 diabetes ideally begins
before conception
• A pre-pregnancy assessment should be undertaken to
document a woman's overall fitness for pregnancy
Assess vascular status
Baseline creatinine clearance
Protein excretion levels should be evaluated
Electrocardiogram performed.
Ophthalmologic consultation
• Optimization of blood glucose control should be achieved
before the woman is advised to become pregnant
• Appropriate contraceptive therapy while they are
preparing for pregnancy
• Extensive period of education and the institution of
self blood glucose monitoring.
• Counselling for women with GDM immediately after
delivery:
Significant risk for developing GDM in subsequent
pregnancies
Increased risk for developing type 2 diabetes as they
age
• Measurement of glycosylated Hb gives a retrospective
picture of DM ctrl and should also be taken prior to
conception
MANAGEMENT

Goal: To achieve/maintain euglycemia throughout

pregnancy.
The treatment approach requires a combination of;
• Diet
• Exercise
• Intensive insulin regimens
• Oral medications (metformin)
• Daily multiple blood glucose determinations.
• Antepartum Surveillance
 DIET
Goal: to meet the additional nutritional requirements
while still maintaining good glycemic control.
• Recommended total caloric intake;
30 kcal/kg of body weight per day for normal weight
40 kcal/kg per day for underweight women
24 kcal/kg per day for overweight women
• a goal of nutrition therapy is to blunt postprandial
hyperglycemia
• The postprandial blood glucose level is most
influenced by the carbohydrate content of the meal
 EXERCISE
• Pregnancy is not a time to initiate a new exercise
program
• Women who have been exercising regularly should
continue
• Women with type 1 diabetes are vulnerable to
exercise-related hypoglycaemia
• Caution against becoming dehydrated, overheated,
tachycardic, or dyspneic.
• Exercise should not be prescribed for patients with
hypertension or autonomic dysfunction with a
diminished counter-regulatory response.
 PHARMACOLOGIC THERAPY
• Rapid-acting insulin analogs
• Continuous sub-cutaneous insulin infusion
pumps
• Pharmacologic therapy should be initiated in all
women with GDM who fail to maintain
euglycemia with diet and exercise.
SELF MONITORING OF BLOOD GLUCOSE
• Blood glucose measurements should be obtained at
least 4 times a day (fasting and 1 to 2 hours after
meals) in women with GDM and 5 to 7 times a day in
women with preexisting diabetes
• Test whenever they feel symptoms of either
hyperglycaemia or hypoglycaemia
• Detailed record keeping to help identify glucose
patterns
• Daily urine ketone testing
• Ketone testing any time the blood glucose level
exceeds 200 mg/dL, during illness, or when the
patient is unable to eat.
 GLYCOSYLATED HAEMOGLOBIN
• Glycosylation (non-enzymatic, post synthetic
attachment of glucose to various amino acids) occurs
slowly and is irreversible
• Glycosylated haemoglobin levels reflect glycaemic
control over the preceding 2 to 3 months
• High glycosylated haemoglobin levels increase risk of
having a severely affected infant.
• Risk of miscarriage is increased with marked
elevations in first-trimester glycosylated haemoglobin.
• Glycosylated hemoglobin levels should be measured
before conception
• Pregnancy should be delayed until normal levels are
reached
• Elevations in first-trimester indicate an increased risk
for congenital malformations
• Elevations in the second half of pregnancy identify
infants at risk for perinatal morbidity and mortality:
 neonatal hypoglycaemia
neonatal hyperbilirubinaemia
perinatal death
macrosomia.
 ANTEPARTUM SURVEILLANCE
Goal: Avoid intrauterine death by early detection of
foetal compromise.
• The non-stress test(NST): evaluates the presence of
accelerations from the baseline fetal heart rate
• Foetal biophysical profile(BPP): evaluates foetal status
using foetal heart rate monitoring and ultrasound
assessment of amniotic fluid volume, foetal
movement and foetal breathing motion
• Women with diabetes should count foetal movements
beginning at 28 weeks gestation.
 FETAL ASSESSMENT
• Additional foetal evaluation and assessment is
required
• Ultrasonography
A first-trimester scan to date the pregnancy and
establish viability.
4- to 6-week interval scans during the 2nd and 3rd
trimesters of pregnancy to assess foetal growth and
amniotic fluid volume
• Foetal echocardiography (20-22weeks)
• Maternal serum alpha-fetoprotein screening test(16-
18wks) for neural tube defects
 TIMING AND MODE OF DELIVERY
• If in good metabolic control and receiving good foetal
surveillance, delivery may be safely delayed until term
or the onset of spontaneous labour
• Women with poor metabolic control, worsening
hypertensive disorders, foetal macrosomia, growth
retardation, or polyhydramnios may be electively
delivered after foetal lung maturity has been
confirmed.
• During labour and delivery, good blood glucose control
should be maintained to prevent neonatal
hypoglycaemia(below 100mg/dL)
REFERENCES

• DC Dutta’s Textbook of Obstetrics 2014

• Clinical Obstetrics – The Fetus and Mother
• Obstetrics by Ten Teachers