diabetes in pregnancy - idaho perinatal · 2016-02-04 · gestational same as type 2 diabetes onset...
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2/4/2016
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Diabetes in
PregnancyMark Alanis, MD, MSCRAssistant Clinical ProfessorMaternal-Fetal MedicineUniversity of Colorado Health
Memorial Hospital, Colorado Springs, CO
disclosuresI have no relevant financial conflicts of interest with any
commercial entity to disclose.
I will discuss the off-label use of insulin and insulin pumps
for use in pregnancy.
I will not discuss the off label use of any other
pharmaceutical agent or medical device during this
lecture.
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objectivesAt the end of this lecture, you will be better prepared to:
Counsel patients on the risks of gestationald and
pregestational diabetes
Sort through the confusion about gestational diabetes
testing paradigms
Reduce diabetes-related adverse outcomes through
achieving maternal euglycemia
Frederick BantingBorn 1891, died 1941
Canadian physician scientist
Discovery of insulin, 1922
Nobel prize, 1923
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Pricilla WhiteBorn 1900, died 1989
Mentored by Elliot P. Joslin
Among first to show importance of strict glucose control in pregnancy
White’s Classification in 1949
Banting Medal recipient
White’s ClassificationDescription Class Fetal Growth
Gestational Diabetes, no insulin A1 No vascular disease
High Risk for MacrosomiaGestational Diabetes, insulin A2
Age of onset, ≥ 20 y B1
Duration < 10 y, no vascular lesions B2
Age of onset, 10-19 y C1
Duration 10-19 y, no vascular lesions C2
Age of onset, < 10 y D1
Duration, ≥ 20 y D2
Benign (non-proliferative) retinopathy D3 Vascular disease
High Risk for IUGRCalcified arteries of the legs D4
Calcified arteries of the pelvis E
Nephropathy F
Many failures G
Cardiac disease H
Proliferating retinopathy R
Renal transplant T
Pridjian G. Obstet Gynecol Clin N Am 2010;37:143, adapted from: White P. Am J Obstet Gynecol 1978;130:228
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ADA Classification
Diabetes Type Findings Phenotype
Type 1 Autoimmune destruction of β-cells;
33% concordance among mono-
zygotic twins; Absolute insulinopenia
Onset in childhood or
adolescence; Thin;
Ketoacidosis
Type 2 Progressive insulin secretory defect;
insulin resistance; 58-100%
concordance among mono-zygotic
twins
Adult-onset, obese,
metabolic syndrome,
hyperosmolar coma
Gestational Same as type 2 diabetes Onset during
pregnancy, resolves in
postpartum;
Rare, other Pancreatic damage or insufficiency,
genetic defects in insulin action
Cystic fibrosis
American Diabetes Association, Standards of Medical Care in Diabetes – 2013. Diabetes Care 2013;36, Suppl 1: S11
85%
15%
Gestational DM
Pregestational DM
Epidemiology
Albrecht SS, et al. Diabetes Care 2010;33:768
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Prevalence increasing rapidly
Percent of Deliveries (%)
Type N 1994 1999 2004 % change
All diabetes 1,863,746 3.49 4.04 5.47 56.3
GDM 1,578,703 2.95 3.42 4.61 56.2
Type 1 130,300 0.24 0.31 0.33 33.2
Type 2 87,477 0.09 0.16 0.42 366.7
Hospital Discharge Data 1994-2004 of 43+ million delivery discharges
Albrecht SS, et al. Diabetes Care 2010;33:768
U.S. Adults Aged 18 Years or older
1994
1994
2000
2000
No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9% >26.0%
No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9% >9.0%
CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at http://www.cdc.gov/diabetes/statistics
2010
2010
DIABETES
OBESITY
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New diagnoses 2002-2005
Ra
te (
pe
r 100,0
00 p
er
ye
ar)
Youths 10-19 years of age
Type 2
Type 1
0
40
CDC, 2011 National Diabetes Fact Sheet, data from SEARCH for Diabetes in Youth Study:
Type 1 DiabetesAcute onset
Childhood or adolescence
Islet cell autoimmune antibodies
β-cell destruction
Absolute insulinopenia
Lifelong requirement for insulin
Threat of diabetic ketoacidosis
High rate of vascular disease
High rate of pregnancy complications
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Type 2 DiabetesInsidious onset
Asymptomatic
Relative insulin deficiency
Decreased insulin sensitivity in skeletal muscle
Decreased insulin response on hepatic glucose production
Inadequate β-cell response for given glucose level
Typically older, overweight or obese, family history
Most pregnant patients are White’s Class B
High rate of pregnancy complications
Gestational DiabetesOnset in late second trimester
Asymptomatic
Relative insulin deficiency
Decreased insulin sensitivity in skeletal muscle
Decreased insulin response on hepatic glucose production
Inadequate β-cell response for given glucose level
Typically older, overweight or obese, family history
Lower rate of pregnancy complications
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lots of risks…
how do you communicate it all?
Counseling the pregestational diabetic patient
Which diabetic patient has
the highest risk for
pregnancy
complications?a) Type 1 diabetes
b) Type 2 diabetes
c) Gestational diabetes
d) No difference between the 3
types
ARS
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Pregnancy affects retinopathy
in what way?a) It occurs de novo due to pregnancy
b) If already present at conception, it worsens during
pregnancy, then returns to baseline
c) If already present at conception, it worsens during
pregnancy, permanently
d) It is not affected by pregnancy
ARS
The most common cause of
perinatal mortality in diabetic
pregnancies is:a) Stillbirth
b) Congenital anomaly
c) Respiratory distress
d) Preterm birth
ARS
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What is the incidence of
brachial plexus injury with
shoulder dystocia?a) 5%
b) 15%
c) 25%
d) 35%
ARS
Which is true in normal pregnancy?a) Fasting glucose increases
over gestation
b) Insulin sensitivity increases in
first trimester
c) Postprandial glucose
increases over gestation
d) All of the above
ARS
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Diagnosing DiabetesType 1
Pregestation
Autoantibodies
Clinical characteristics
1-2% of persistent DM after diagnosis of GDM
Type 2
Pregestation
Clinical characteristics
98% of persistent DM after diagnosis of GDM
Gestational
Two-Step versus One Step
Overly confusing set of parameters
Philosophical argument of individual versus public health benefit
GDM Screening Dilemmas
Two
Step
1-hour 50 g
glucose load
3-hour 100 g
glucose load
GDM
Yes or No
When should
you do it?
What cutoff
to use?
Should you
fast?
High false negative
and positive rates
Very
inconvenient
What cutoffs
to use?
Arbitrary
diagnosis
Risk versus harm
with diagnosis
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GDM Screening Dilemmas
One
Step
2-hour 75 g
glucose load
GDM
Yes or No
Moderately
inconvenient3-fold increase in
prevalence
Arbitrary
diagnosis
1979 - 2009 20102008 2011 2012 2013 2014
Timeline of Recent
GDM Diagnostic
Crisis
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HAPOHyperglycemia and Adverse Pregnancy Outcomes
HAPO Study Group N Engl J Med 2008;358:1991
HAPO and IADPSG
Study Features
>25,000 patients
International, multicenter
2-hour, 75 g glucola
Providers blinded to test
results
Intent was to redefine
GDM diagnostic testing
cutoffs based on
outcomes ...but this
wasn’t the case
IADPSG had two goals:
1. Use HAPO to develop
cutoffs discretely linked
to GDM-related
morbidities
2. Develop international
standard diagnostic
guidelines
Cutoffs later arbitrarily
defined based Odds Ratios
of 1.75 for morbidities
International Association of Diabetes in Pregnancy Study Group
HAPO Study Group N Engl J Med 2008;358:1991IADPSG Diabetes Care 2010;33:676
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More GDM Diagnostic DilemmasShould you try to differeniate type 1 from
type 2 diabetes in unclear situations?
What do you call a patient whom you
diagnose early in pregnancy:
pregestational or gestational?
Should the hemoglobin A1c be used to
diagnose diabetes mellitus in pregnancy?
It’s not
important
ADA/IADPSG:
overt diabetes
ACOG:
undiagnosed type
2 DM
It can, but it
shouldn’t be
the only test
you order
EVEN More Diagnostic DilemmasShould early screening be performed?
Should you use NDDG or Carpenter-
Coustan criteria for the diagnosis in Two-
Step screening?
Should the One-Step paradigm be used
for the diagnosis of GDM?
ACOG: either
No! (ACOG and NIH)
Yes! (ADA, IADSPG, WHO)
Yes!(ADA and ACOG)
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GDM Screening Test Features
USPSTF Systematic Review Ann Intern Med 2013;159:115
A 1-hour, 50 g glucose cutoff of 140 mg has 15% false negative rate (CC criteria)
2-Step versus 1-StepCriteria Year Fasting
mg/dL
1-hour
mg/dl
2-hour
mg/dL
3-hour
mg/dL
Two
-Ste
p
(100 g
lo
ad
)
C-C 1982 95 180 155 140
NDDG 1979 105 190 165 145
CDA 2008 95 191 160
On
e-S
tep
(75 g
loa
d) WHO 1985 126 140
IADPSG 2010 92 180 153
NIH Consensus Development Conference Statement Vol. 29, Number 1. March 4-6, 2013
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GDM Screening and ACOG
Still allows for no lab screening for low-risk patients
Use either 135 mg/dL or 140 mg/dL for 1-hour cutoff
Use either Carpenter-Coustan or National Diabetes
Data Group for 3-hour cutoffs
Screen at-risk patients early in pregnancy GDM in previous pregnancy
Known impaired glucose metabolism
Obesity
Does NOT say WHEN or HOW to perform early screening
2013 Practice Bulletin No. 137
Maternal and Obstetric Fetal and Neonatal
Complications
Kidney dysfunction
Retinopathy
Myocardial infarction
Preeclampsia
Cesarean section
Preterm birth
Miscarriage and stillbirth
Structural malformations
Fetal overgrowth
Fetal growth restriction
Birth injury
Prematurity
Hypoglycemia
Infant death
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Retinopathy in pregnancy #1 cause of blindness
Asymptomatic until very
late stages
Macular edema
Retinal hemorrhage
Neovascularization
Retinal detachment
Neovascular glaucoma
Laser therapy to correct
Retinopathy progression
0
10
20
30
40
50
60
None Mild Mod-Severe
%
Progression by
baseline statusAssociated with
Pregnancy (2-fold)
Intensive insulin therapy
Initial A1c
Duration of disease
Chronic hypertension
Baseline retinal status
2-5 years after pregnancy
pregnancy effects
resolve
Chew EY, et al. Diabetes Care 1995;18:631Diabetes Control and Complications Trial Group. Diabetes Care 2000;23:1084
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Diabetic NephropathyDefinition
≥ 300 mg albuminuria in 24 hours
≥ 500 mg proteinuria in 24 hours
≥ 300 albumin-to-creatinine ratio (μg/mg) on spot urine
Microalbuminuria
30-299 mg albuminuria in 24 hours
30-299 μg/mg albumin-to-creatinine ratio on spot urine
Number 1 cause of end stage renal disease
Renal dialysis
Kidney transplantation
1 in 10-20 pregestational diabetic patients
Abnormal renal arteriolar dilation
Cannot handle hyperfiltration
Alteration in renin-angiotensin
Transient, mild worsening in pregnancy for mild disease
Possibly permanent worsening if severe disease
Preeclampsia, preterm birth, IUGR, stillbirth
Worst outcomes in: Baseline proteinuria > 3 g in 24
hours (heavy proteinuria) or baseline serum creatinine
≥ 1.5 g/dL (severe renal disease)
Peripheral dilation 5 weeks’
50% increase in renal blood flow 12 weeks’
50% increase in GRF 8 weeks’Physiology
Diabetes
Outcomes
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Microalbuminuria NephropathyRenal
InsufficiencyEnd Stage Renal
Disease
Diabetic Nephropathy
87%
3%
5%3% 2%
Normal (< 30mg/24h)
DM1 micro UA
DM2 micro UA
DM1 nephropathy
DM2 nephropathy
Damm JA, et al. Diabetes Care, in press
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Microalbuminuria
0
5
10
15
20
25
30
35
40
45
Preeclampsia PTB < 34 wk PTB < 37 wk
% Normal UA
Micro UA
Jensen DM, et al. Diabetes Care 2010;33:90
Diabetic NephropathyKitzmiller Grenfel Reece Gordon Rosenn
Year 1991 1986 1988 1996 1997
Subjects 26 20 31 45 61
Preeclampsia (%) 15 55 35 53 51
IUGR (%) 21 - 19 11 11
Delivery < 34 wk (%) 31 27 23 16 25
Perinatal mortality (%) 11 0 7 0 6
Gabbe Obstetrics: Normal and Problem Pregnancies, 6th Ed., 2012. Chapter 39: Diabetes Mellitus Complicating Pregnancy pp. 887-921
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Kidney Disease: Take Home1. Diabetic kidney disease is a progression from
microalbuminuria to overt nephropathy to impaired creatinine clearance to end stage renal disease
2. Microalbuminuria and nephropathy both strongly increase risk of preeclampsia
3. Good glucose control in pregnancy strongly reduces risk of preterm birth < 34 weeks in setting of microalbuminuria
4. Overt nephropathy strongly increases risk of IUGR and preterm birth < 34 weeks of gestation
Heart diseaseRare (24 case reports in literature between 1953-2007)
Mortality:
Before 1980 = 50% survived
After 1980 = 95% survived
Relative contraindication to pregnancy if untreated
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Diabetic ketoacidosis Kussmaul respirations
Maternal acidosis yields fetal acidemia
Severely hypovolemic, insulinopenic, hypokalemic
First: massive volume replacement with normal saline
Second: IV regular insulin 0.2 U/kg push
Third: Hang potassium 40-80 mEq in IV fluids
Fourth: continuous IV regular insulin infusion 0.1 U/kg/h
Fifth: BMP every 1-2 hours until anion gap closes
Sixth: reduce IV insulin infusion to 0.05 U/kg/h when serum glucose < 200 mg/dL
Medical ManagementFor prevention of maternal complications
Preconception consultation
Health maintenance screening:
Comprehensive eye exam, annually
Diabetic foot exam, annually
Evaluation of heart and kidneys
Laser photocoagulation if retinopathy
24-hour urine albumin, total protein, creatinine clearance
Aggressive management of blood pressure, <135/85
Strict diet, exercise, and tight glucose control
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Fetal Complications
In Utero Consequences Spontaneous Abortion
Congenital anomaly
Fetal overgrowth
Stillbirth
Hypertrophic cardiomyopathy
Respiratory distress syndrome
Polycythemia, jaundice
Neonatal mortality
Infant mortality
Lifelong risks of obesity, cardiovascular disease
MOST can be
negated by
early and
aggressive
glucose control
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What’s so bad about a big baby?
“big babies are so cute!”
1. Hypertrophic cardiomyopathy
2. Increased perinatal mortality
3. Shoulder dystocia
4. Brachial plexus injury
5. Respiratory distress syndrome
6. Hypoglycemia
7. Hyperbilirubinemia
8. Polycythemia
9. Epigenetic alterations to vascular tree
10. Childhood obesity, hypertension, and diabetes
11. Heart disease, Alzheimer’s disease
Fetal Overgrowth Large for gestational age = ≥ 90th percentile
Macrosomia = birth weight ≥ 4000 or 4500 g
Abnormal anthropometry
Increased fat mass
Broad chest
Increased shoulder diameter
Is birth weight best indicator for fetal overgrowth?1. In utero metabolism affects fat mass, not lean mass.
2. Normal body fat percentage is about 12-15% at birth.
3. Body fat percentage may be best measure of fetal growth.
Catalano PM and Hauguel-De Mouzon S. Am J Obstet Gynecol 2011;204:479
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Pedersen Hypothesis
Maternal
hyperglycemia
Fetal
hyperglycemia
Fetal
hyperinsulinemia
Increased
accretion of fat
MacrosomiaAltered
anthropometry
Structural AnomaliesStrong Association
Cardiac Defects most (septal and outflow defects)
Neural tube defects anencephaly
Moderate Association
Renal bilateral agenesis
Anogenital hypospadias
Almost pathognomonic
Caudal regression Sirenomelia, sacral agenesis
Correa A, et al (National Birth Defects Prevention Study) Am J Obstet Gynecol 2008;199:237Garne E, et al. Birth Defects Res A Clin Mol Teratol 2012;94:134
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Folic Acid and Spina Bifida
0
1
2
3
4
5
No Folic Acid Folic Acid
No diabetes
Diabetes
Parker SE, et al. Am J Obstet Gynecol 2013:209:239
Perinatal Mortality
Gabbe Obstetrics: Normal and Problem Pregnancies, 6th Ed., 2012. Chapter 39: Diabetes Mellitus Complicating Pregnancy pp. 887-921
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Offspring MortalityDeath Rates per 1000 deliveries
Type Diabete
s
No
Diabetes
Odds
Ratio
95% CI
Stillbirth 9.7 4.0 2.5 1.02-5.9
Perinatal
Mortality
17.4 5.9 3.0 1.6-5.9
Infant
Mortality
15.5 2.8 8.9 5.2-15.3
Yang J, et al. Obstet Gynecol 2006;108:644
Perinatal MortalityType 1 vs. Type 2 Diabetes Mellitus
Balsells M, et al. J Clin Endocrinol Metab 2009;94:4284
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Pregestational Diabetes
0
10
20
30
40
50
60
%
Type 2
Type 1
Clausen TD, et al. Diabetes Care 2005;28:323
Shoulder Dystocia
0
5
10
15
20
25
4000-4250 4250-4500 4500-4750 4750-5000
% U
na
ssis
ted
SV
D
Birth Weight
Non-Diabetic
Diabetic
Nesbitt TS, et al. Am J Obstet Gynecol 1998;179:476
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Principles of
ManagementBe aggressive! Time is of the essence!
Chief Principle #1
Oral agents have no place in the management
of pregestational diabetes during pregnancy
Preconception is the best opportunity to switch
from oral agents to insulin in order to achieve
glucose control
No matter what type of diabtes, the goal is
normal blood glucose levels
Corner stone of management is diet and hypoglycemic therapy
to achieve euglycemia
Managing Preexisting Diabetes in Pregnancy: American Diabetes Association Consensus Recommendations. Diabetes Care 2008;31-1060
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Normal glucose values Pooled analysis of
12 studies
Non-obese, non-
diabetic women
Period Plasma Glucose
Fasting 71 ± 8
1-hour post-
prandial
109 ± 13
2-hour post-
prandial
99 ± 10
24-hour average 88 ± 10
Hernandez et al. Diabetes Care 2011;34:1660Fifth International Workshop-Conference on Gestational Diabetes. Diabetes Care 2007;30:S251
ACOG/ADA
95*
140
120
110*
* Not included in 2013
Practice Bulletin
Insulin needs in early
pregnancy in type 1 diabetes
Gabbe Obstetrics: Normal and Problem Pregnancies, 6th Ed., 2012. Chapter 39: Diabetes Mellitus Complicating Pregnancy pp. 887-921
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Fasting glucose over gestation
Riskin-Mashiah S, et al. J Perinat Med 2011;39:209
Chief Principle #2
Time Glucose
(mg/dL)
Early AM, fast ≤ 95
Pre-prandial ≤ 100
1h post-prandial ≤ 140
2h post-prandial ≤ 120
2-6 AM > 60
Finger Sticks of Capillary Glucose
4 per day for GDM (fasting and
1- or 2-hour postprandial)
Variable (7 or more) per day
for pregestational DM
Hypoglycemia increases during
pregnancy, and further increases
with tighter monitoring than these
targets without known benefit
Frequent self monitoring of blood glucose and tight adherence
to recommended targets (ACOG)
ACOG Practice Bulletin No. 60. 2005ACOG Practice Bulletin No. 137. 2013
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Diet
SM blood
glucose
Intensive therapy
SQ insulin
Home Glucose Monitors Quality and storage are two most important issues
FDA Standards
Monitor should automatically convey glucose after
conversion to plasma standard
Readings need to be ± 20% within actual blood glucose
value 95% of the time when > 75 mg/dL
Readings need to be ± 15% within actual blood glucose
95% of the time when < 75 mg/dL
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Continuous glucose monitoringSmall RCT (n = 71) showed benefits
Intermittent use of CGM (5-7 d continuous every 4-6 weeks)
Decreased mean birth weight
Decreased macrosomia (OR = 0.38)
Improved A1c (5.8% vs. 6.4%)
Follow-up RCT (n = 154) showed no benefit
No difference in A1c
No difference in hypoglycemia episodes
No difference in macrosomia
Compliance was very poor (49% per protocol)
Secher AL, et al. Diabetes Care 2013;36:1877Murphy HR, et al. BMJ 2008;337:a1680
DietEarly referral to nutritionist
Caloric intake extremely important
Normal BMI: 35 kcal/d
Overweight: 25 kcal/d
Obese: 15 kcal/day
Excessive calories causes excessive gestational weight
gain, increasing further risks for preeclampsia, preterm birth,
and macrosomia
Total gestational weight gain per IOM guidelines
Balanced: 50% carbohydrate, 20% protein, 30% fat
Gabbe Obstetrics: Normal and Problem Pregnancies, 6th Ed., 2012. Chapter 39: Diabetes Mellitus Complicating Pregnancy pp. 887-921IOM. Weight Gain During Pregnancy: Reexamining the Guidelines, 2009 (www.iom.edu/reports)
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Oral Agents- GDM
Increases insulin secretion
Do not prescribe in women with sulfa allergy
Crosses placenta
Comparable to insulin in intention-to-treat studies*
Pharmacokinetics unpredictable in pregnancy
duration ~4.5 hours
Bad job of controlling fasting
glucose
Increased risk of hypoglycemia
Increases glucose uptake in skeletal muscle
Inhibits gluconeogenesis in liver
Crosses placenta
Very low risk of hypoglycemia
Comparable to insulin in intention-to-treat trial**
* Very high rates of switching back to insulin during trials: 20-40% for glyburide, 50%
for metformin
Glyburide Metformin
Subcutaneous insulinBrand Onset (h) Peak (h) Duration (h)
Short-acting
Regular (Lilly) Humulin-R 0.5 2-4 5-7
Regular (Novo Nordisk) Novolin-R 0.5 2.5-5 6-8
Lispro Humalog 0.25 0.5-1.5 4-5
Aspart NovoLog 0.25 1-3 3-5
Intermediate-acting
Lente insulin (Lilly) Humulin L 1-3 6-12 18-24
Lente insulin (Novo
Nordisk)
Novolin L 2.5 7-15 22
NPH (Lilly) Humulin-N 1-2 6-12 18-24
NPH (Novo Nordisk) Novolin N 1.5 4-20 24
Long-acting insulin
Ultralente (Lilly) Humulin Ultralente 4-6 8-20 >36
Glargine Lantus 1 none 24
Detemir Levemir 1-2 none 24
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Subcutaneous insulinAnalogues (lispro or aspart) preferred over regular insulin
faster onset and peak action to coincide with meals
decreased duration of action to prevent hypoglycemia between meals
Multiple-shot regimen vs. continuous infusion necessary
Glargine and detemir cannot be combined with other insulins in single shot like NPH can
Pregnant women often have differing basal insulin needs depending on time of day, making NPH easier to tailor to individual needs
Do not combine with oral hypoglycemic agents
Subcutaneous insulinMeta-analysis of lispro vs. regular insulin: numerous retrospective & prospective studies, improved postprandial glucose, lower insulin requirements, possibly increased rates of LGA, trend for lower hypoglycemia with lispro
One RCT of aspart vs. regular insulin (n = 322): no differences in outcomes), trend for lower hypoglycemia with aspart
One RCT of detemir vs. NPH (n = 310)
Tiny improvement in A1c (0.3%) with detemir
More women able to achieve target A1c with detemir
Slightly improved fasting glucose (12-16 mg/dL) with detemir
Mathiesen ER, et al. Diabetes Care 2012;35:2012Murphy HR, et al. BMJ 2008;337:a1680
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Subcutaneous InsulinNew Start
First trimester 0.7 U/kg/d
Second trimester 0.8
U/kg/d
Third trimester 1.0 U/kg/d
Divided Doses- usually 50-
60% as basal insulin and
40-50% as rapid acting
insulin
For example: New start at 24 weeks’ Patient weight 100 kg
Fasting glucose 115 mg/dL Postprandial glucose 155
mg/dL
Total insulin = 0.8 U x 100 kg = 80 units/day
Basal insulin 60% of total = 48 units
Rapid insulin 40% of total = 32 units (e.g. 12/8/12)
Insulin Adjustments Total daily insulin
demands increase, on average, 3-fold over gestation
Basal insulin increases 30-50% overall
Bolus insulin needs increase 400% overall
Many patients have lower first trimester demands
Roeder HA, et al. Am J Obstet Gynecol 2012;207:324
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Chief Principle #3
Antepartum Assessment
Daily fetal kick counts at
28 weeks’
Twice weekly testing with
NST or BPP at 32 weeks of
gestation
Delivery at term if no
complications
Follow a standard management plan in third trimester, delivery
at 39 weeks’
ACOG Practice Bulletin No. 60. 2005
Ultrasound
Level II ultrasoud exam at
mid-gestation
Fetal echocardiogram
Repeat scan every 4-6
weeks for fetal growth
and fluid
Blood PressureFor patients with
preexisting
Hypertension
Microalbuminuria
Nephropathy
American Diabetes
Association guidelines
SBP of 110-129 mmHg
DBP of 65-79 mmHg
For preexisting HTN:
Recommendations based on maternal longterm health and decreased heart and renal disease and incidence of stroke
For diabetic kidney disease:
Numerous small studies
Decreased proteinuria, preeclampsia, and preterm birth
ADA. Standards of Medical Care in Diabetes - 2013. Diabetes Care 2013;S1:11
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DeliveryACOG GDM Recommendations
Well-controlled with Diet: scheduled delivery not recommended
Well-controlled on hypoglycemia agent: 39+ wk
Poorly-controlled: Does not discuss
NIH Recommendations Well-controlled: 39 wk
Vascular disease: 37-39 wk
Poorly-controlled: 34-39 wk (individualize)
Very high rate of cesarean (75% in several studies for pregestational diabetic patients) and glucose control does not appear to affect
A1c ≥ 6.4% associated with abnormal fetal testing at term and prompt cesarean delivery
Use delayed cord clamping with caution
Miailhe G, et al. Obstet Gynecol 2013;121:983Lepercq J, et al. Obstet Gynecol 2010;115:1014Spong CY, et al. Obstet Gynecol 2011;118:323
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