Diabetes in Pregnency
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Transcript of 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