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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 30s or 40s
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 Diabetes
Non 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
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
+

Duration
+
+
+
+
+
+
+

Vascular Dis

Insulin Need

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)

Gestational Diabetes
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

Gestational Diabetes
Diagnosis

OGTT

3H

Fasting 5.3
1h
10.6
2h
9.2
3h
8.1

2H

Fasting 5.3
1h
10.6
2h
8.9

2 or more values greater than or equal to above


cutoffs diagnostic of GDM
single abnormal value indicates CHO intolerance

Gestational Diabetes
Maternal Risks
birth trauma
operative delivery
50% lifetime risk in developing Type II
DM
recurrence risk of GDM is 30-50%

Gestational Diabetes

Gestational Diabetes
Fetal Risks
no increase in congenital anomalies
increased risk of stillbirth if fasting + pc
hyperglycemia
macrosomia
birth trauma-shoulder dystocia and
related complications

Gestational Diabetes
Management
goal is to optimize BG levels to minimize
risk of adverse perinatal outcomes
diet
exercise
insulin therapy

Gestational Diabetes
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

Gestational Diabetes

Diet : general principles


55% CHO 25% Protein 20% fat
Normal weight gain 10-12 kg
avoid ketosis
liberal exercise program to optimize BG
control

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

6-14 weeks
14-26 weeks
26-36 weeks
36-40weeks

0.5u/kg/day
0.7u/kg/day
0.9u/kg/day
1 u /kg/day

Gestational Diabetes
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

Gestational Diabetes
Intrapartum management
check BG hourly
maintain BG 4-6 mmol/L

Gestational Diabetes
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

Gestational Diabetes
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

Preexisting Diabetes

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

Preexisting Diabetes
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

Preexisting Diabetes

Fetal Risks
congenital anomalies 3x increased risk
unexplained stillbirth
shoulder dystocia
macrosomia
IUGR

Preexisting Diabetes
Neonatal Risks

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

Preexisting 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

Preexisting Diabetes

Preexisting Diabetes
Congenital anomalies
CVS

GI
duodenal atresia,
anorectal atresia, situs
inversus

GU

ASD/VSD,coarctation,transp
osition,
cardiomegaly

CNS
anencephaly, NTD,
microcephaly

renal agenesis
Polycystic kidneys

MSK
caudal regression
siren

Preexisting Diabetes
Maternal Surveillance

Blood pressure
renal function *
urine culture **
thyroid function
BG control HB A1C*

* q trimester

** monthly

Preexisting Diabetes
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

Preexisting Diabetes
Multidose Insulin
breakfast 25% H
lunch
supper
hs
Gabbe Obstet Gynecol 2003

15% H
25% H
35% NPH

indicates insulin as a % of total


daily dose

Insulin Therapy

insulin analogs
rapid acting
intermediate

onset (h)

peak

.25
0.5

0.5-1.5
2-4

6-8
8-12

4-8

12-18

1-1.5

duration

Insulin Therapy
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

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)

Peripartum Management
insulin rate usually based on BG and predelivery insulin requirement
eg. For each 75-100 total units /24h of predelivery insulin, 1 unit per hour needed
measure capillary BG hourly VPG (Venous
Plasma Glucose) q2-3h
target: 4-6 mmol/L

Peripartum Management
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

Oral Hypoglycemic agents


Glyburide
Achieved N BG
LGA infants
Macrosomia
C Section
Hypoglycemia
Preeclampsia
Anomalies

Insulin

82%
12%
7
23

88%
13%
4
24
9
6

6
6
2

Langer NEJM 2000

Fetal Surveillance
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
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%

Diabetic Ketoacidosis
Management
ABCs 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

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

Replace Bicarb and phosphate as needed

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