Diabetes Dalam Kehamilan

Diabetes dalam kehamilan

Epidemiologi

• Adalah komplikasi dalam kehamilan yang sering terjadi

• Kurang lebih 2-3% kehamilan– Gestational DM 90%– Preexisting DM 10%

Pankreas

Pengaruh kehamilan terhadap metabolisme karbohidrat

– mild fasting hypoglycemia; postprandial hyperglycemia

– due to increase plasma volume in early gestation and inc fetal glucose utilization as pregnancy advances

– progressive increase in tissue resistance to insulin– increase insulin secretion to maintain euglycemia– suppressed glucagon response– increase prolactin, cortisol– HPL has GH like effects

Metabolisme Glukosa

• Normal pregnancy : Diabetogenic state– increase in post-coenam BG– insulin resistance– Early Pregnancy

• Anabolic state– increase in maternal fat stores– decreased Free Fatty Acid concentration– decrease in insulin requirements

Type I Diabetes

• abrupt onset• usually young age• occasionally occurs in 30’s or 40’s• lifelong requirement for insulin replacement• may have genetic predisposition for islet cell

abnormalities• concordance in MZ twins for development of DM is

33%• suggests other factors also influencing

(environmental)

Type 2 Diabetes

• Abnormalities of insulin sensitive tissues– decreased skeletal muscle and hepatic sensitivity

to insulin – abnormal B cell response

• inadequate response for a given degree of glycemia

• usually older• increased BMI• insidious onset• strong genetic component

– MZ twin data lifetime risk 58-100%

Diagnosis of DiabetesNon Pregnant

• Fasting plasma BG >7.0mmol/l• Casual plasma BG >11.1mmol/l

Impaired Fasting Glucose• FPG 6.1-7.0 mmol/l

Impaired Glucose Tolerance • normal FPG• 2 h 75gOGTT test with BG 7.8-11.1 mmol/l

Canadian Diabetes Association 1998

Classification and Risk Assessment

Class DM onset Duration Vascular Dis Insulin Need

Gestational DM

A1 Any Any - -

A2 Any Any - +

Pregestational DM

B >20 <10 - +

C 10-19 10-19 - +

D <10 >20 + +

F Any Any + +

R Any Any + +

T Any Any + +

H Any Any + +

Diabetes Dalam Kehamilan

A. Gestational Diabetes

B. Preexisting Diabetes

A. Gestational Diabetes

• Definition• Carbohydrate intolerance of variable severity first

diagnosed in Pregnancy• Prevalence 2-4%• Risk Factors

• maternal age >25• Family history• glucosuria• prior macrosomia• previous unexplained stillbirth• ethnic group: Hispanic, Black, First Nations

Gestational Diabetes

• Screening

– PC 50/Trutol– 1 hr after 50g load of glucose – >7.8 mmol/l abnormal*– 15% of patients screen positive

* value >10.3 diagnostic of GDM (no OGTT needed)


• Screening

– 24-28 weeks routine– no need to fast– screen at 1st prenatal visit if hx of previous

GDM– screen earlier (12-24 weeks ) if risk factors

• Diagnosis OGTT

• 2 or more values greater than or equal to above cutoffs diagnostic of GDM

• single abnormal value indicates CHO intolerance


Fasting 5.31h 10.62h 9.23h 8.1

Fasting 5.31h 10.62h 8.9

3 H 2H

Maternal Risks

• birth trauma

• operative delivery

• 50% lifetime risk in developing Type II DM

• recurrence risk of GDM is 30-50%


Fetal Risks

• no increase in congenital anomalies• increased risk of stillbirth if fasting + pc

hyperglycemia• macrosomia• birth trauma-shoulder dystocia and

related complications


• Management

– goal is to optimize BG levels to minimize risk of adverse perinatal outcomes

– diet – exercise– insulin therapy


• Management : Diet

• patients without fasting hyperglycemia

• average 8000-9000 kj/day.• BMI>27 -- 25 kcal/kg/ideal body weight/d• BMI 20-26 -- 30 “• BMI<20 -- 38 “


• Diet : general principles

• 55% CHO 25% Protein 20% fat

• Normal weight gain 10-12 kg

• avoid ketosis

• liberal exercise program to optimize BG control


• If persistent hyperglycemia after one week of diet control proceed to insulin

• 6-14 weeks 0.5u/kg/day• 14-26 weeks 0.7u/kg/day• 26-36 weeks 0.9u/kg/day• 36-40weeks 1 u /kg/day


• If fasting hyperglycemia start with NPH hs • initial dose 6-8 U • if only pc hyperglycemia use humalog 2-4u ac

the specific meal • adjust 2u/time 1 formula /time

• BG target ac <5.3 2 h pc <6.7


Intrapartum management

• check BG hourly

• maintain BG 4-6 mmol/L


Postpartum• often will not require insulin• if fasting hyperglycemia - more likely to

develop persistent Diabetes• 6 weeks post partum 75g OGTT• yearly fasting BG• emphasize importance of maintaining Normal

weight, exercise


Neonatal Risks

• hypoglycemia 50% in macrosomic 5-15% if N BG control in Pgy

• Hyperbilirubinemia• polycythemia• hypocalcemia• hypomagnesiumia


B. Preexisting Diabetes

Preconception Counselling

• risk of NTD ~1-2%• Folic Acid 1-4 mg /day• BG 3.5-5.3 prior to meals• switch to MDI (multiple daily Insulin) regimen

(insulin a.c meals and h.s bed time)• keep track of cycles

• Normoglycemia prior to conception • ideally HBA1C 6% or less• Team approach• glucose monitoring qid• ACE contraindicated : should be D/C at

conception or use Diltiazem instead• baseline HBA1C, 24h urine for protein Cr Cl ,

opthalmology review• switch from OHA to insulin

Preexisting Diabetes

• Assess for end organ disease– assess for nephropathy - increase risk of PIH

(Pregnancy Induced Hypertension– Assess and treat retinopathy - may progress– assess for neuropathy

• generally remains stable during pregnancy

– assess and treat vasculopathy• CAD (Coronary Artery Disease) is a relative C/I

for pregnancy


• Maternal Risks– PIH /PET (preeclampsia-toxemia)– polyhydramnios– preterm labour– operative delivery ~50%– birth trauma– infection– increase in insulin requirements– DKA (Diabetic Keto Acidosis)


Prexisting Diabetes

• Fetal Risks

• congenital anomalies 3x increased risk

• unexplained stillbirth

• shoulder dystocia

• macrosomia

• IUGR


• Neonatal Risks • hypoglycemia• hypocalcemia• hyperbilirubinemia/polycythemia• idiopathic RDS• delayed lung maturity• prematurity• predisposition to diabetes


• Congenital anomalies

• 3x the general population risk • approaches the general population risk

(2-3%) if optimal control in periconception period

• related to glycemic control during embryogenesis


• CVS– ASD/

VSD,coarctation,transposition,

– cardiomegaly

• CNS– anencephaly, NTD,

microcephaly


• GI– duodenal atresia,

anorectal atresia, situs inversus

• GU• renal agenesis

• Polycystic kidneys

• MSK• caudal regression

• siren

Congenital anomalies

• Maternal Surveillance

• Blood pressure • renal function *• urine culture **• thyroid function

• BG control HB A1C*

• * q trimester

• ** monthly


• Fetal Surveillance

• U/S for dating/viability ~ 8 weeks• Fetal anomaly detection

– nuchal translucency 11-14w– maternal serum screen– anatomy survey 18-20 w– Fetal echo 22 w



Multidose Insulin

• breakfast 25% H

• lunch 15% H• supper 25% H• hs 35%

NPH

• indicates insulin as a % of total daily dose

Gabbe Obstet Gynecol 2003

Insulin Therapy

onset (h) peak duration

• insulin analogs .25 0.5-1.5 6-8

• rapid acting 0.5 2-4 8-12

• intermediate 1-1.5 4-8 12-18

• Insulin Pump– Allows insulin release close to physiologic – Use short acting insulin– 50-60% of total dose is basal rate– 40-50% given as boluses– Potential complications

• Pump failure• Infection• Increased risk of DKA if above happens

Insulin Therapy

Peripartum Management

• Withhold subcutaneous insulin from onset of labour or induction

• IV D10 @50cc/h• IV short acting insulin in NS usually

starting at 0.5-1u/h* *10cc insulin in 100 cc NS(1U=10cc)

• insulin rate usually based on BG and pre-delivery insulin requirement

• eg. For each 75-100 total units /24h of pre-delivery insulin, 1 unit per hour needed

• measure capillary BG hourly VPG (Venous Plasma Glucose) q2-3h

• target: 4-6 mmol/L


• Following delivery– stop insulin infusion – begin sub Q insulin– resume previous MDI schedule at 1/2 -2/3

the pre pregnancy dose– maintain IV D5W @50cc/h until oral feeds

tolerated


Oral Hypoglycemic agents

• Traditionally not recommended in pregnancy

• Recent RCT of oral glyburide vs insulin for GDM

• 440 patients• BG measured 7x daily• Treatment started after 11 weeks gestation

Langer NEJM 2000

Glyburide Insulin

Achieved N BG 82% 88%LGA infants 12% 13%Macrosomia 7 4C Section 23 24Hypoglycemia 9 6Preeclampsia 6 6Anomalies 2 2

Oral Hypoglycemic agents

Langer NEJM 2000

• Goals– Minimize/eliminate the risk of fetal death– Early detection of fetal compromise – Prevent unnecessary premature delivery

• Main benefit is the NPV of these tests– Provides reassurance that fetus with a N test

unlikely to die in utero– Allow prolongation of pregnancy – fetal maturation

Fetal Surveillance

Fetal Surveillance

• Gestational Diabetic Diet controlled

– Can start fetal surveillance at term (40 weeks)

• GDM on insulin/Type II DM/ Type I DM

– Start weekly BPP from 32 weeks– Consider earlier testing if

• suboptimal control• Hypertension• vasculopathy

Timing of Delivery

GDM Diet controlled– Same as non diabetic

– Offer induction at 41 weeks if undelivered

GDM on Insulin/Type II/Type I– If suboptimal control deliver following confirmation

of lung maturity if <39 weeks– Otherwise deliver by 40 weeks– Generally do not allow to go postterm

Mode of Delivery

• Macrosomic infants of diabetic mothers have higher rates of shoulder dystocia than non diabetic mothers

• Ultrasound estimates of fetal weight become significantly inaccurate after 4000g

• Reasonable to recommend C/S delivery if EFW is >4500g

Diabetic Ketoacidosis

• 5-10% of pregnant Type 1 pts

• Risk factors– New onset DM– Infection– Insulin pump failue– Steroids– B mimetics

• Fetal mortality 10%

• Management– ABC’s and ABG

• Assess BG, ketones electrolytes– Insulin

• .2-.4U/Kg loading and 2-10U/h maintenance– Begin 5% dextrose when BG is 14 mmol/l– When potassium is N range begin 20mEq/h– Rehydration isotonic NaCl

• 1L in 1st hour • .5-1l/h over 2-4h• 250cc/h until 80% replaced• Replace Bicarb and phosphate as needed


– Rehydration isotonic NaCl• 1L in 1st hour • .5-1l/h over 2-4h• 250cc/h until 80% replaced

– Replace Bicarb and phosphate as needed


Diabetes Dalam Kehamilan

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