Diabetes in Pregnency

8/18/2019 Diabetes in Pregnency

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DIABETES IN PREGNANCY

BYDR ROEDA SHAMS

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DEFINITION

NORMAL GLUCOSE METTABOLISM

METABOLIC CHANGES DURING

PREGNANCY

CLASSIFICATION

EPIDEMIOLOGY

PATHOPHYSIOLOGY

Gestational Diabetes

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DEFINITION:-

Clinical

syndrome characterized bydeficiency or insensitivity to insulin.

NORMAL GLUCOSE METABOLISM:-• Glucose enters blood stream from

food source insulin aids in storage ofglucose as fuel for cells.

• Insulin resistance results in increasedlevels of glucose in bloodstream.HPL,CORTISOL

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METABOLIC CHANGES DURING PREGNACY

Caloric Requirements for a pregnant

women is 300 kcal than a non pregnant

lady

PLACENTAL HORMONES( Growth

hormone, human placental lactogen,

progesterone and corticotrophin releasing

hormone) affect glucose and lipidmetabolism.

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Transient maternal hyperglycemia occurs

after meals because of insulin resistance.

Hypoglycemia occurs because of

proliferation of pancreatic beta cells leads to

increased insulin secretion

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CLASSIFICATION:-

Diabetes inpregnancy

Pre-existingdiabetes

IDDM(Type1)

NIDDM(Type2)

Gestationaldiabetes

Pre-existingdiabetes

True GDM

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TYPE 1 DIABETES MELLITUS IDDM)

Autoimmune process that destroys

pancreatic beta cells.

The disease is typically diagnosed during

an episode of hypoglycemia , ketosis and

dehydration .

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TYPE II DIABETES MELLITUS (NIDDM)

Acquired insulin resistance to obesity.

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DIABETES IN PREGNANCY EPIDEMIOLOGY

Preexisting diabetes complicates 1% of

pregnancies.

4% of all pregnancies are affected by

diabetes

88% due to gestational diabetes mellitus

8% due to Type 2 diabetes mellitus

4% due to Type 1 diabetes mellitus

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PATHOPHYSIOLOGY

Lack of Insulin

Hyperglycemia

Glycosuria

Osmotic Diuresis

Salt and Water

depletion

Increased secretion:

Glucagon

Cortisol

CatecholaminesGrowth Hormone

Increased Catabolism

Glycogenolysis

gluconeogenesis

lipolysis

Hyperketonemia

Acidosis(DKA)

Fatigue

Vulvitis

Polyuria

Polydypsia

Tachycardia

Hypertension

Wasting

Weightloss

Peripheral

vasodilatation

Hyperventillatio

Glycosuria

HPL, PROLACTIN,ESTROGEN & PROGESTERONE- DIABETOGENIC 11


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GESATIONAL DIABETES

DEFINITION:-

Carbohydrate intolerance of variableseverity first recognized during the present

pregnancy.

RISK FACTORS:-

Age>25yrs

BMI >25

Previous GDM

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Family history of DM in first degree relative

Previous macrsomic baby

Polyhydromias Large for date baby in current pregnancy

Previous unexplained stillbirth.

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SCREENING AND DIAGNOSIS:-

The test is performed b/w 24-28wks because

at this point in gestation the diabetogeniceffect of pregnancy is manifest and there is

sufficient time remaining in pregnancy for

therapy to exert its effect.

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DIAGNOSTC AND SCREENING CRITERIA

DIAGNOSTIC CRITEIA:-

1- Symptoms of Diabetes

Polyuria Polydipsia

Unexpected weight loss

2-Fasting plasma glucose>126mg/dl orrandomized blood glucose >200mg/dl

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SCREENING TESTS:- 50gm 1 hour glucose challenge test(GCT)

SCREENING THRESHOLDS:- 130mg/dl :90% sensitivity (23% screening

positive)

140mg/dl:80% sensitivity (14% screenpositive)

IF PATIENT SCREENS POSITIVE SHEGOES ON TO TAKE A 3-HOUR GLUCOSETOLERANCE TEST(GTT)

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ORAL GLUCOSE TOLERANCE TEST

Patients undergoing oral glucose tolerance

testing for gestational diabetes should

undertake carbohydrate loading for 3 days

preceeding the test (>150g carbohydrates)and over night fast of 8-14 hours the night

before Time 100 g Glucose Load,

mg/dL (mmol/L)

Fasting 95 (5.3)

1 hour 180 (10.0)

2 hours 155 (8.6)

3 hours 140 (7.8) 17


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EFFECT OF PREGNANCY ON DIABETES

FIRST TRIMESTER:- Hyperemesis -- Hypoglycemia &

ketosis

SECOND TRIMESTER:-

Inc in counter regulatory hormone-

progressive peripheral resistance to

insulin Decreased renal threshold--glycosuria

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THIRD TRIMESTER---Inc level of

placental hormones-inc need of insulin.

DURING LABOUR--Inc consumption of

carbohydrates by uterine activity reduces the

insulin need

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EFFECTS OF DIABETES ON PREGNANCY

MATERNAL RISKS:_

1—DIABETIC RETINOPATHY:-

Diabetic retinopathy is the leading cause ofblindness in women aged 24-64yrs.

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Half of patients with preexisting retinopathy

experienced deterioration during pregnancy

all the patients had partial regression

following delivery and returned to their

prepregnant state by 6 months postpartum.

Consider an ophthalmologic evaluation in the

first trimester.

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2-RENAL DISEASE:- Patients with underlying nephropathy can

expect varying degrees of deterioration of

renal function during a pregnancy.

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Perinatal complications are greatly

increased in patients with diabetic

nephropathy .

Preterm births, growth restriction and

preeclampsia are more common

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3-ELAVATED BLOOD PRESSURE:-

Chronic hypertension complicates 1 in 10

diabetic pregnancies overall.

Patients with chronic hypertension and

diabetes are at increased risk of intrauterine

growth restriction, superimposed

preeclampsia, abrutio placentae

and maternal stroke.

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FOETAL EFFECTS

1—MISCARRIAGES:- Frequency directly related to degree of

maternal glycemic control.

Up to 44% with poorly controlled Diabetesmellitus.

2---PRETERM DELIVERY:-

Increases birth defects (1-2%)

Two thirds of birth anomalies involve thecardiovascular and central nervous system

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Neural tube defects occur 13-20 times morefrequently in diabetic pregnancies andgenitourinary, gestrointestinal and skeletalanomalies are also more common.

3---GROWTH RESTRICTION:-

Growth restriction is fairly common amongType 1 diabetic mothers

Best predictor is presence of maternalvascular disease.

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4---OBESITY:-

Maternal obesity common in diabetes

appears to significantly accelerate the risk of

LGA

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5---MACROSOMIA:-

Defined as birth weight >4000grams

occurs in 15-45% of diabetic pregnancies, a4 fold increase over normal

Carries many morbidities including birth

trauma, RDS, neonatal jaundice and severe jaundice

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6-POLYCYTHEMIA :-

Hypoglycemia stimulates fetal erythropoetin

production

Can lead to tissue ischemia and infection.

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7---HYPOGLYCEMIA:- Baby is used to having lots of maternal

glucose so it makes lots of insulin. when born

maternal glucose is no longer available butinsulin remains high--.hypoglycemia

Can lead to seizures, coma and braindamage.

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8---POSTNAL HYPERBILLRUBINEMIA:-

Occurs in approx 25%, double that of normal

Thought to be due to polycythemia.

9----RESPIRATORY DISTRESS SYNDROME:-

5-6 fold increased frequency

May be due to delay in lung maturation or

simply due to increased frequecy of pretermdeliveries.

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10---TRAUMATIC DELIVERY e.g shoulder dystocia

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11----OPERATIVE VAGINAL DELIVERY:-

Vaccum assisted

Forceps assisted

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12—POLYHYDROMIAS:-

Amniotic fluid volume >2000ml

Increased risk of placental abruption and

preterm

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MANAGEMENT

KNOWN DIABETES

A---PREPREGNANCY CARE :In patients with preexisting diabetes

nutritional and metabolic intervention must be

initiated well before pregnancy .

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Prepregnancy HbA1C level should be 6.1 toreduce structural malformation

Commence Follic acid suppliments

Switch to short acting insulin analogueContinue contraception if HbA1C >10 %

Continue oral hypoglcemic like

sulphonylureas and metformin

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B—PRENATAL

Screen for gestational diabetes and do oralglucose tolerance test

Do antenatal visit and commence foetal

growth monitoring

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DIETARY THERAPY:-

Low carbohydrate diet ,high fibre with caloric

restriction

Frequent small snacks may be needed

between 3 major meals

Avoid starvation

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INSULIN THERAPY:-Gold standard, does not cross placenta

GDM on diet control will require insulin if

fasting glucose >95mg% or post parendial>130mg%.

Insulin lispro ,aspart ,regular and

neutral potamine hagedor (NPH) are safe and effective .

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Advise about management of hypoglycemia.

Advice women how to suspect early DKA and

how to self monitor for ketonemia or ketonuria.

Admit the pregnant lady with DKA in multidisciplinary unit.

Follow up retinal scans based on initial findings.

Refer to nephrology if serum creatinine>120micro mol/L

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Arrange anomaly scan at 18-21 wks

Include cardiac outflow tracts in anatomy

scan.

Refer for fetal echocardiography selectively

Scan for fetal growth scan and amniotic fluid

index at 4 wk interval from 26 wks gestation

Review and intensify hypoglycemic regime if

inpatient macrosomia

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Initiate tests of fetal wellbeing if IUGR is

diagnosed

Offer induction of labour/elective c sectionMonitor fetal wellbeing weekly in women who

wish to continue their pregnancy beyond 38

wks

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Avoid beta –sympathomimetics in preterm

labour

Elective preterm birth in maternal diabetes

should be in a unit with neonatal ICU

facilities

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LABOUR AND DELIVERY

Standeredized i/v Protocol & Insulin & DextroseTherapy

Nil by mouth until after the birth of baby.

Start i/v Dextrose in 500ml .100ml/hr byelectronic pump.

Hourly blood glucose estimation.

If initial blood glucose is 4-7mmol/L commenceinsulin infusion at 1 unit/hr.

If blood glucose is more then 7mmol/L startinsulin infusion at 2 unit/hr.

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If glucose is less then 4mmol/L decrease insulinrate by 1 Unit/hr & increase by 0.5Unit/hr whenglucose increases > 7mmol/Litre.

After delivery of placenta half the insulin to aminimum of 0.5Unit/hr to maintain blood glucoseat 4-7mmol/Litre.

POSTNATAL

Return to prepregnancy insulin/hypoglycemiatherapy

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Discontinue hypoglycemic therapy in women

with GDM and monitor blood glucose levels

for evidence of type 2 diabetes

Offer contraceptive advice

Check fasting plasma glucose at 6 wk post

delivery and annually to exclude a new

diagnosis of type 2 diabetes

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RCOG GUIDE LINES

Pre-conception Care

Education: risks / diet / exercise / weight

loss if BMI>27 folic acid supplements (5 mg/day)

blood glucose meter for self-monitoring

monthly HbA1c

retinal assessment by fundoscopy

renal assessment

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SAFETY OF MEDICATIONS BEFORE AND

DURING PREGNANCY

Metformin (and Glibenclamide ) and insulinmay be used before and during pregnancy.

Isophane insulin is the first-choice long-acting insulin during pregnancy.

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BEFORE OR AS SOON AS PREGNANCY IS

CONFIRMED

Stop oral hypoglycaemic agents, apart from

metformin, and commence insulin if required

Stop angiotensin-converting enzyme

inhibitors and angiotensin-II receptor

antagonists and consider alternative

antihypertensives

Stop statins.

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POST NATAL CARE

Advise women with gestationaldiabetes:

•

To stop taking hypoglycaemic medicationimmediately after birth

• On weight control, diet and exercise

• On the risks of gestational diabetes insubsequent pregnancies and screening fordiabetes when planning pregnancy.

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THANK YOU

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