DIABETES MELLITUS IN PREGNANCY

Group 2 2011/2012

DIABETES MELLITUS

A metabolic disorder characterized by chronic hyperglycaemia with impairment in carbohydrates, fat and protein metabolism. can be due to: i) relative or absolute insulin deficiency ii) insulin resistance iii) combination of both

Diabetes Mellitus in Pregnancy

Established diabetes mellitus a) type 1 DM (insulin-dependent DM) b) type 2 DM (non-insulin-dependent DM) Gestational Diabetes Mellitus - DM that develop for the first time during pregnancy and will disappear after delivery

GESTATIONAL DIABETES MELLITUS

Raised blood glucose level (MOGTT):

Fasting blood glucose - >7.0mmol/L or 2 hours Post-glucose - >11.1 mmol/L

1-2% of women will develop GDM Women with GDM has risk to develop DM type 2 in future

RISK FACTORS FOR GDM

Maternal age >35 years old Obesity (BMI >30kg/m) Previous macrosomic baby (4kg or above) Previous gestational diabetes Family history of DM among 1st degree relatives History of unexplained perinatal death History of congenital anomaly in previous pregnancy Ethnic background (South Asian, black Caribbean and Middle Eastern)

Mechanism of GDM

Pregnancy is diabetogenic state: Placenta secretes anti insulin hormone

Estrogen,

progesterone, Human placental lactogen,

cortisol

These hormones antagonizes the peripheral effects of insulin. Thus, develop insulin resistance in mother To counter this effect, the pancreas produces and secretes more insulin

Then, the level of plasma insulin is raised by the action of the placental hormones, placing a burden on the insulin-secreting cells of the pancreatic islets.
The pancreas may be unable to meet these demands in women genetically predisposed to develop both types of diabetes.

Pregnancy placental anti-insulin hormones (hPL, cortisol, estrogen,progesterone) anti-insulin effect Develop insulin resistance in mother insulin production to maintain CHOs metabolism burden on pancreatic islets develop diabetes in those genetically

Clinical Features

Usually asymptomatic Sometimes may develop: - polyuria -sweet smelling breath - polyphagia - nausea and vomitting - fatigue - unusual weight loss - polyphagia - frequent infection

DIAGNOSIS

1.

Risk assesment (1st antenatal visit) High Risk

-undergo OGTT as soon as feasible. -retested at 24-28 weeks of gestation if not found to hv GDM

2. Average Risk
-OGTT done at 24-28 weeks of gestation.

OGTT
Timing of taking blood glucose Normal (mmol/L) Impaired oral glucose tolerance (mmol/L) 6.1-7.8 GDM (mmol/L)

Fasting

4-6.1

> 7.8

2 hours 6.1-7.8 7.8-11.1 > 11.1 postprandial Unrestricted carbohydrate diet for 3 days before test. Fasted overnight (at least 8 hours) Rest before test(30min), no smoking, seated for duration of test. Plasma glucose measured before and 2hrs after, 75g of glucose load.

MANAGEMENT & INVESTIGATION S

Pre-conception Counseling

Should be informed that establishing good glycemic control before conception and continuing this throughout pregnancy will reduce risk of miscarriage, congenital malformation, stillbirth and neonatal death. It is important to explain that risk can be reduced but not eliminated. Importance of avoiding unplanned pregnancy. When to stop contraception. Retinal and renal assesment. Diet, body weight and exercise including weight loss for women with BMI> 27

Antenatal Management
The aim of treatment is to maintain the blood glucose level as near normal as possible, with a combination of diet and insulin. For all patients with impaired glucose tolerance and diabetes 1.Determine accuracy of gestational age by ultrasound. 2.Perform BSP -pre breakfast, pre lunch, pre dinner, pre bed

-asses present glucose control

-every 2 weeks -aim to achieve 4-6mmol/L

3.Perform HbA1C
-reflects glucose control for previous 2-3 months.
-once in each trimester -reflects adequacy of BSP testing schedule - target is HbA1C < 6%

4. Advice on diet control

-sufficient calories for pregnancy (2000-2500kcal) -Low glycemic index diet -breakfast carbohydrate needs to be restricted more. -ingest more fiber in food with whole grains, fruits and vegetables.

5.Patient should be instructed in self-monitoring with their own glucose meters. 6.Subcutaneous Insulin
-if BSP is more than 7mmol/L -three premeal injections of short acting insulin (Actrapid) -Desirable pre-prandial blood sugar is 4-6mmol/L

7.Ophthalmology assesment

8.Serial ultrasound (fortnightly) 9.Antenatal visit done every 2weeks until 32-34weeks and then weeks after that because frequent change in insulin dosage required esp in 3rd trimester. 10.Ward admission is indicated :
-fortnighly cannot be done as outpatient

-if diabetic control not good

-complications occur such as PE or foetal compromise -when delivery is indicated

11. Amniocentesis for lecithine:syringomyline ratio

-to asses foetal lung maturity

12.if Diabetes is optimally controlled, pregnancy should be allowed to progress to at least 38-39weeks but not go beyond EDD. 13.Vaginal delivery is allowed if no other complication such as dysfunctional labour.

14. Elective caesarean section:

-bad obstetric hx
-hx of subfertility -poor diabetic control -vascular complications

-baby estimated more than 4.0kg

Intrapartum Management

During induced or spontaneous labour, normoglycemia should be maintained using a sliding scale of insulin. Blood glucose levels should be tested at hourly intervals. Fetal scalp blood sampling taken in the presence of abnormal CTG.

Postpartum Management

Following delivery, the insulin requirement will rapidly fall and return to pre-pregnancy levels. Women with GDM should stop their insulin at delivey. For patients with pre-existing DM, restart prepregnancy treatment. A full glucose tolerance test is performed 6 weeks following delivery to ensure that the diabetes has resolved.

COMPLICATIONS

Complications of GDM
Maternal
Long-term DM Future GDM Gestational Hypertension /Pre-eclampsia Microangiopathy Large vessel disease Infection Abortion Preterm labour

Fetus/Neonate
Fetus Congenital anomalies Macrosomia Polyhydroamnios Polycythemia and hyperbilirubinemia Unexplained stillbirths Neonate Jaundice Respiratory distress Hypoglycemia

Maternal Complications

Gestational Hypertension/Pre-eclampsia (PE)

Hyaline

arteriolosclerosis in DM causes hypertension of PE increased 2-4 folds in women with diabetes

particularly

Risk

in those with co-existing microalbuminuria and frank nephropathy

Maternal Complications
Hyperglycemia
Non-enzymatic glycosylation Formation of advanced glycosylated end-products (AGE) AGE accumulates on vessel wall and traps LDL Cholesterol deposition on intima of blood vessels Large vessel disease Coronary artery disease Thromboembolic disease De novo synthesis of diacylglycerol Signal transduction Increased deposition of basement membrane Diffuse thickening of basement membrane Diabetic microangiopathy Retinopathy Nephropathy Neuropathy

Maternal Complications

Infection (eg UTI and candidiasis)

Organisms

more likely to grow in urine with high levels of glucose

Miscarriage
Placental

insufficiency (microangiopathy at

placenta) Increased lactate and decreased pH in fetal blood

Fetal Complications
Chronic hyperglycaemia Placental insufficiency (Microangiopathy at placenta) Decreased uterine blood flow and decreased oxygen tension Increased anaerobic metabolism Increased lactate and decreased pH Abortion

Impaired organogenesis

Congenital abnormalities

Fetal Complications

Common congenital anomalies

Cardiac:

ASD, VSD Neural tube: Sacral agenesis, spina bifida Skeletal: Orofacial clefts, varus foot deformity Renal: Polycystic kidney disease, renal agenesis GIT: duodenal atresia, tracheo-esophageal fistula

Fetal Complications
Maternal hyperglycaemia Glucose cross placenta via facilitated diffusion Fetal hyperinsulinaemia

Fetal hypoglycaemia
Increase insulin-like growth factor

Fetal hyperglycaemia
Fetal osmotic diuresis

Stimulates nutrient storage and accelerated growth

Fetal macrosomia
Obstructed labour Birth asphyxia Shoulder dystocia
Brachial plexus injuryErbs palsy Facial nerve palsy Cephalohematoma

Polyhydroamnios

Fetal and Neonatal Complications

Fetal hyperglycemia

Decreased fetal oxygen tension

Stimulation of fetal erythropoietin production Increased erythropoiesis Polycythemia

Hyperviscosity of fetal blood Ischemia and infarction of vital organs eg kidneys and CNS

Increased RBC breakdown

Hyperbilirubinemia Jaundice

Neonatal Complications
Maternal hyperglycaemia Glucose cross placenta via facilitated diffusion Fetal hyperglycaemia Neonatal hyperinsulinaemia Neonatal hypoglycaemia Decreased surfactant synthesis in lungs Respiratory distress

Decreased cortisol production