Gestational diabetes

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Gestational diabetes

Classification and external resources

Universal blue circle symbol for diabetes.[1]

ICD-10 O24.

ICD-9 648.8

MedlinePlus 000896

MeSH D016640

Gestational diabetes (or gestational diabetes mellitus, GDM) is a condition in which

women without previously diagnosed diabetes exhibit high blood glucose levels during
pregnancy (especially during third trimester of pregnancy).

Gestational diabetes generally has few symptoms and it is most commonly diagnosed by
screening during pregnancy. Diagnostic tests detect inappropriately high levels of glucose
in blood samples. Gestational diabetes affects 3-10% of pregnancies, depending on the
population studied.[2]
Babies born to mothers with gestational diabetes are typically at increased risk of
problems such as being large for gestational age (which may lead to delivery
complications), low blood sugar, and jaundice. Gestational diabetes is a treatable
condition and women who have adequate control of glucose levels can effectively
decrease these risks.

Women with gestational diabetes are at increased risk of developing type 2 diabetes
mellitus (or, very rarely, latent autoimmune diabetes or Type 1) after pregnancy, as well
as having a higher incidence of pre-eclampsia and Caesarean section;[3] their offspring are
prone to developing childhood obesity, with type 2 diabetes later in life. Most patients are
treated only with diet modification and moderate exercise but some take anti-diabetic
drugs, including insulin.[3]

Contents
[hide]

• 1 Classification
• 2 Risk Factors
• 3 Pathophysiology
• 4 Screening
o 4.1 Pathways
o 4.2 Non-challenge blood glucose tests
o 4.3 Screening glucose challenge test
o 4.4 Oral glucose tolerance test
o 4.5 Urinary glucose testing
• 5 Management
o 5.1 Lifestyle
o 5.2 Medication
• 6 Prognosis
o 6.1 Complications
• 7 Epidemiology
• 8 References

• 9 External links

[edit] Classification
Gestational diabetes is formally defined as "any degree of glucose intolerance with onset
or first recognition during pregnancy".[4] This definition acknowledges the possibility that
patients may have previously undiagnosed diabetes mellitus, or may have developed
diabetes coincidentally with pregnancy. Whether symptoms subside after pregnancy is
also irrelevant to the diagnosis.[5]
The White classification, named after Priscilla White[6] who pioneered in research on the
effect of diabetes types on perinatal outcome, is widely used to assess maternal and fetal
risk. It distinguishes between gestational diabetes (type A) and diabetes that existed prior
to pregnancy (pregestational diabetes). These two groups are further subdivided
according to their associated risks and management.[7]

There are 2 subtypes of gestational diabetes (diabetes which began during pregnancy):

• Type A1: abnormal oral glucose tolerance test (OGTT) but normal blood glucose
levels during fasting and 2 hours after meals; diet modification is sufficient to
control glucose levels
• Type A2: abnormal OGTT compounded by abnormal glucose levels during
fasting and/or after meals; additional therapy with insulin or other medications is
required

The second group of diabetes which existed prior to pregnancy is also split up into
several subtypes.

[edit] Risk Factors

Classical risk factors for developing gestational diabetes are the following:[8]

• a previous diagnosis of gestational diabetes or prediabetes, impaired glucose

tolerance, or impaired fasting glycaemia
• a family history revealing a first degree relative with type 2 diabetes
• maternal age - a woman's risk factor increases as she gets older (especially for
women over 35 years of age)
• ethnic background (those with higher risk factors include African-Americans,
Afro-Caribbeans, Native Americans, Hispanics, Pacific Islanders, and people
originating from South Asia)
• being overweight, obese or severely obese increases the risk by a factor 2.1, 3.6
and 8.6, respectively.[9]
• a previous pregnancy which resulted in a child with a high birth weight (>90th
centile, or >4000 g (8 lbs 12.8 oz))
• previous poor obstetric history

In addition to this, statistics show a double risk of GDM in smokers.[10] Polycystic ovarian
syndrome is also a risk factor,[8] although relevant evidence remains controversial.[11]
Some studies have looked at more controversial potential risk factors, such as short
stature.[12]

About 40-60% of women with GDM have no demonstrable risk factor; for this reason
many advocate to screen all women.[13] Typically women with gestational diabetes exhibit
no symptoms (another reason for universal screening), but some women may demonstrate
increased thirst, increased urination, fatigue, nausea and vomiting, bladder infection,
yeast infections and blurred vision.
[edit] Pathophysiology

Effect of insulin on glucose uptake and metabolism. Insulin binds to its receptor (1) on
the cell membrane which in turn starts many protein activation cascades (2). These
include: translocation of Glut-4 transporter to the plasma membrane and influx of glucose
(3), glycogen synthesis (4), glycolysis (5) and fatty acid synthesis (6).

The precise mechanisms underlying gestational diabetes remain unknown. The hallmark
of GDM is increased insulin resistance. Pregnancy hormones and other factors are
thought to interfere with the action of insulin as it binds to the insulin receptor. The
interference probably occurs at the level of the cell signaling pathway behind the insulin
receptor.[14] Since insulin promotes the entry of glucose into most cells, insulin resistance
prevents glucose from entering the cells properly. As a result, glucose remains in the
bloodstream, where glucose levels rise. More insulin is needed to overcome this
resistance; about 1.5-2.5 times more insulin is produced than in a normal pregnancy.[14]

Insulin resistance is a normal phenomenon emerging in the second trimester of

pregnancy, which progresses thereafter to levels seen in non-pregnant patients with type
2 diabetes. It is thought to secure glucose supply to the growing fetus. Women with GDM
have an insulin resistance they cannot compensate with increased production in the β-
cells of the pancreas. Placental hormones, and to a lesser extent increased fat deposits
during pregnancy, seem to mediate insulin resistance during pregnancy. Cortisol and
progesterone are the main culprits, but human placental lactogen, prolactin and estradiol
contribute too.[14]

It is unclear why some patients are unable to balance insulin needs and develop GDM,
however a number of explanations have been given, similar to those in type 2 diabetes:
autoimmunity, single gene mutations, obesity, and other mechanisms.[15]

Because glucose travels across the placenta (through diffusion facilitated by GLUT3
carriers), the fetus is exposed to higher glucose levels. This leads to increased fetal levels
of insulin (insulin itself cannot cross the placenta). The growth-stimulating effects of
insulin can lead to excessive growth and a large body (macrosomia). After birth, the high
glucose environment disappears, leaving these newborns with ongoing high insulin
production and susceptibility to low blood glucose levels (hypoglycemia).[16]

[edit] Screening
 2006 WHO Diabetes criteria[17] edit
Condition 2 hour glucose Fasting glucose
mmol/l(mg/dl) mmol/l(mg/dl)
Normal <7.8 (<140) <6.1 (<110)
Impaired fasting glycaemia <7.8 (<140) ≥ 6.1(≥110) & <7.0(<126)
Impaired glucose tolerance ≥7.8 (≥140) <7.0 (<126)
Diabetes mellitus ≥11.1 (≥200) ≥7.0 (≥126)

A number of screening and diagnostic tests have been used to look for high levels of
glucose in plasma or serum in defined circumstances. One method is a stepwise approach
where a suspicious result on a screening test is followed by diagnostic test. Alternatively,
a more involved diagnostic test can be used directly at the first antenatal visit in high-risk
patients (for example in those with polycystic ovarian syndrome or acanthosis nigricans).
[16]

Tests for gestational diabetes

Non-challenge blood glucose tests

• Fasting glucose test

• 2-hour postprandial (after a meal) glucose test

Random glucose test

•
Screening glucose challenge test
Oral glucose tolerance test (OGTT)

Non-challenge blood glucose tests involve measuring glucose levels in blood samples
without challenging the subject with glucose solutions. A blood glucose level is
determined when fasting, 2 hours after a meal, or simply at any random time. In contrast,
challenge tests involve drinking a glucose solution and measuring glucose concentration
thereafter in the blood; in diabetes, they tend to remain high. The glucose solution has a
very sweet taste which some women find unpleasant; sometimes, therefore, artificial
flavours are added. Some women may experience nausea during the test, and more so
with higher glucose levels.[18][19]

[edit] Pathways

There are different opinions about optimal screening and diagnostic measures, in part due
to differences in population risks, cost-effectiveness considerations, and lack of an
evidence base to support large national screening programs.[20] The most elaborate regime
entails a random blood glucose test during a booking visit, a screening glucose challenge
test around 24–28 weeks' gestation, followed by an OGTT if the tests are outside normal
limits. If there is a high suspicion, women may be tested earlier.[5]
In the United States, most obstetricians prefer universal screening with a screening
glucose challenge test.[21] In the United Kingdom, obstetric units often rely on risk factors
and a random blood glucose test.[16][22] The American Diabetes Association and the
Society of Obstetricians and Gynaecologists of Canada recommend routine screening
unless the patient is low risk (this means the woman must be younger than 25 years and
have a body mass index less than 27, with no personal, ethnic or family risk factors)[5][20]
The Canadian Diabetes Association and the American College of Obstetricians and
Gynecologists recommend universal screening.[23][24] The U.S. Preventive Services Task
Force found that there is insufficient evidence to recommend for or against routine
screening.[25]

[edit] Non-challenge blood glucose tests

When a plasma glucose level is found to be higher than 126 mg/dl (7.0 mmol/l) after
fasting, or over 200 mg/dl (11.1 mmol/l) on any occasion, and if this is confirmed on a
subsequent day, the diagnosis of GDM is made, and no further testing is required.[5]
These tests are typically performed at the first antenatal visit. They are patient-friendly
and inexpensive, but have a lower test performance compared to the other tests, with
moderate sensitivity, low specificity and high false positive rates.[26][27][28]

[edit] Screening glucose challenge test

The screening glucose challenge test (sometimes called the O'Sullivan test) is performed
between 24–28 weeks, and can be seen as a simplified version of the oral glucose
tolerance test (OGTT). It involves drinking a solution containing 50 grams of glucose,
and measuring blood levels 1 hour later.[29]

If the cut-off point is set at 140 mg/dl (7.8 mmol/l), 80% of women with GDM will be
detected.[5] If this threshold for further testing is lowered to 130 mg/dl, 90% of GDM
cases will be detected, but there will also be more women who will be subjected to a
consequent OGTT unnecessarily.

[edit] Oral glucose tolerance test

Main article: Oral glucose tolerance test

The OGTT[30] should be done in the morning after an overnight fast of between 8 and 14
hours. During the three previous days the subject must have an unrestricted diet
(containing at least 150 g carbohydrate per day) and unlimited physical activity. The
subject should remain seated during the test and should not smoke throughout the test.

The test involves drinking a solution containing a certain amount of glucose, and drawing
blood to measure glucose levels at the start and on set time intervals thereafter.

The diagnostic criteria from the National Diabetes Data Group (NDDG) have been used
most often, but some centers rely on the Carpenter and Coustan criteria, which set the
cutoff for normal at lower values. Compared with the NDDG criteria, the Carpenter and
Coustan criteria lead to a diagnosis of gestational diabetes in 54 percent more pregnant
women, with an increased cost and no compelling evidence of improved perinatal
outcomes.[31]

The following are the values which the American Diabetes Association considers to be
abnormal during the 100 g of glucose OGTT:

• Fasting blood glucose level ≥95 mg/dl (5.33 mmol/L)

• 1 hour blood glucose level ≥180 mg/dl (10 mmol/L)
• 2 hour blood glucose level ≥155 mg/dl (8.6 mmol/L)
• 3 hour blood glucose level ≥140 mg/dl (7.8 mmol/L)

An alternative test uses a 75 g glucose load and measures the blood glucose levels before
and after 1 and 2 hours, using the same reference values. This test will identify less
women who are at risk, and there is only a weak concordance (agreement rate) between
this test and a 3 hour 100 g test.[32]

The glucose values used to detect gestational diabetes were first determined by
O'Sullivan and Mahan (1964) in a retrospective cohort study (using a 100 grams of
glucose OGTT) designed to detect risk of developing type 2 diabetes in the future. The
values were set using whole blood and required two values reaching or exceeding the
value to be positive.[33] Subsequent information led to alterations in O'Sullivan's criteria.
When methods for blood glucose determination changed from the use of whole blood to
venous plasma samples, the criteria for GDM were also changed.

[edit] Urinary glucose testing

Women with GDM may have high glucose levels in their urine (glucosuria). Although
dipstick testing is widely practiced, it performs poorly, and discontinuing routine dipstick
testing has not been shown to cause underdiagnosis where universal screening is
performed.[34] Increased glomerular filtration rates during pregnancy contribute to some
50% of women having glucose in their urine on dipstick tests at some point during their
pregnancy. The sensitivity of glucosuria for GDM in the first 2 trimesters is only around
10% and the positive predictive value is around 20%.[35][36]

[edit] Management
Main article: Diabetes management
A kit with a glucose meter and diary used by a woman with gestational diabetes.

The goal of treatment is to reduce the risks of GDM for mother and child. Scientific
evidence is beginning to show that controlling glucose levels can result in less serious
fetal complications (such as macrosomia) and increased maternal quality of life.
Unfortunately, treatment of GDM is also accompanied by more infants admitted to
neonatal wards and more inductions of labour, with no proven decrease in cesarean
section rates or perinatal mortality.[37][38] These findings are still recent and controversial.
[39]

A repeat OGTT should be carried out 2–4 months after delivery, to confirm the diabetes
has disappeared. Afterwards, regular screening for type 2 diabetes is advised.[8]

If a diabetic diet or G.I. Diet, exercise, and oral medication are inadequate to control
glucose levels, insulin therapy may become necessary.

The development of macrosomia can be evaluated during pregnancy by using

sonography. Women who use insulin, with a history of stillbirth, or with hypertension are
managed like women with overt diabetes.[13]

[edit] Lifestyle

Counselling before pregnancy (for example, about preventive folic acid supplements) and
multidisciplinary management are important for good pregnancy outcomes.[40] Most
women can manage their GDM with dietary changes and exercise. Self monitoring of
blood glucose levels can guide therapy. Some women will need antidiabetic drugs, most
commonly insulin therapy.

Any diet needs to provide sufficient calories for pregnancy, typically 2,000 - 2,500 kcal
with the exclusion of simple carbohydrates.[13] The main goal of dietary modifications is
to avoid peaks in blood sugar levels. This can be done by spreading carbohydrate intake
over meals and snacks throughout the day, and using slow-release carbohydrate sources
—known as the G.I. Diet. Since insulin resistance is highest in mornings, breakfast
carbohydrates need to be restricted more.[8]

Regular moderately intense physical exercise is advised, although there is no consensus

on the specific structure of exercise programs for GDM.[8][41]
Self monitoring can be accomplished using a handheld capillary glucose dosage system.
Compliance with these glucometer systems can be low.[42] Target ranges advised by the
Australasian Diabetes in Pregnancy Society are as follows:[8]

• fasting capillary blood glucose levels <5.5 mmol/L

• 1 hour postprandial capillary blood glucose levels <8.0 mmol/L
• 2 hour postprandial blood glucose levels <6.7 mmol/L

Regular blood samples can be used to determine HbA1c levels, which give an idea of
glucose control over a longer time period.[8]

Research suggests a possible benefit of breastfeeding to reduce the risk of diabetes and
related risks for both mother and child.[43]

[edit] Medication

If monitoring reveals failing control of glucose levels with these measures, or if there is
evidence of complications like excessive fetal growth, treatment with insulin might
become necessary. The most common therapeutic regime involves premeal fast-acting
insulin to blunt sharp glucose rises after meals.[8] Care needs to be taken to avoid low
blood sugar levels (hypoglycemia) due to excessive insulin injections. Insulin therapy can
be normal or very tight; more injections can result in better control but requires more
effort, and there is no consensus that it has large benefits.[16][44][45]

There is some evidence that certain oral glycemic agents might be safe in pregnancy, or
at least, are significantly less dangerous to the developing fetus than poorly controlled
diabetes. Glyburide, a second generation sulfonylurea, has been shown to be an effective
alternative to insulin therapy.[46][47] In one study, 4% of women needed supplemental
insulin to reach blood sugar targets.[47] Metformin has shown promising results, with its
oral format being much more popular than insulin injections.[3] Treatment of polycystic
ovarian syndrome with metformin during pregnancy has been noted to decrease GDM
levels.[48] A recent randomized controlled trial of metformin versus insulin showed that
women preferred metformin tablets to insulin injections, and that metformin is safe and
equally effective as insulin.[49] Severe neonatal hypoglycemia was less common in
insulin-treated women, but preterm delivery was more common. Almost half of patients
did not reach sufficient control with metformin alone and needed supplemental therapy
with insulin; compared to those treated with insulin alone, they required less insulin, and
they gained less weight.[49] With no long-term studies into children of women treated with
the drug, here remains a possibility of long-term complications from metformin therapy,
[3]
although follow-up at the age of 18 months of children born to women with polycystic
ovarian syndrome and treated with metformin revealed no developmental abnormalities.
[50]

[edit] Prognosis
Gestational diabetes generally resolves once the baby is born. Based on different studies,
the chances of developing GDM in a second pregnancy are between 30 and 84%,
depending on ethnic background. A second pregnancy within 1 year of the previous
pregnancy has a high rate of recurrence.[51]

Women diagnosed with gestational diabetes have an increased risk of developing

diabetes mellitus in the future. The risk is highest in women who needed insulin
treatment, had antibodies associated with diabetes (such as antibodies against glutamate
decarboxylase, islet cell antibodies and/or insulinoma antigen-2), women with more than
two previous pregnancies, and women who were obese (in order of importance).[52][53]
Women requiring insulin to manage gestational diabetes have a 50% risk of developing
diabetes within the next five years.[33] Depending on the population studied, the
diagnostic criteria and the length of follow-up, the risk can vary enormously.[54] The risk
appears to be highest in the first 5 years, reaching a plateau thereafter.[54] One of the
longest studies followed a group of women from Boston, Massachusetts; half of them
developed diabetes after 6 years, and more than 70% had diabetes after 28 years.[54] In a
retrospective study in Navajo women, the risk of diabetes after GDM was estimated to be
50 to 70% after 11 years.[55] Another study found a risk of diabetes after GDM of more
than 25% after 15 years.[56] In populations with a low risk for type 2 diabetes, in lean
subjects and in patients with auto-antibodies, there is a higher rate of women developing
type 1 diabetes.[53]

Children of women with GDM have an increased risk for childhood and adult obesity and
an increased risk of glucose intolerance and type 2 diabetes later in life.[57] This risk
relates to increased maternal glucose values.[58] It is currently unclear how much genetic
susceptibility and environmental factors each contribute to this risk, and if treatment of
GDM can influence this outcome.[59]

There are scarce statistical data on the risk of other conditions in women with GDM; in
the Jerusalem Perinatal study, 410 out of 37962 patients were reported to have GDM, and
there was a tendency towards more breast and pancreatic cancer, but more research is
needed to confirm this finding.[60][61]

[edit] Complications

GDM poses a risk to mother and child. This risk is largely related to high blood glucose
levels and its consequences. The risk increases with higher blood glucose levels.[62]
Treatment resulting in better control of these levels can reduce some of the risks of GDM
considerably.[42]

The two main risks GDM imposes on the baby are growth abnormalities and chemical
imbalances after birth, which may require admission to a neonatal intensive care unit.
Infants born to mothers with GDM are at risk of being both large for gestational age
(macrosomic)[62] and small for gestational age. Macrosomia in turn increases the risk of
instrumental deliveries (e.g. forceps, ventouse and caesarean section) or problems during
vaginal delivery (such as shoulder dystocia). Macrosomia may affect 12% of normal
women compared to 20% of patients with GDM.[16] However, the evidence for each of
these complications is not equally strong; in the Hyperglycemia and Adverse Pregnancy
Outcome (HAPO) study for example, there was an increased risk for babies to be large
but not small for gestational age.[62] Research into complications for GDM is difficult
because of the many confounding factors (such as obesity). Labelling a woman as having
GDM may in itself increase the risk of having a caesarean section.[63][64]

Neonates are also at an increased risk of low blood glucose (hypoglycemia), jaundice,
high red blood cell mass (polycythemia) and low blood calcium (hypocalcemia) and
magnesium (hypomagnesemia).[65] GDM also interferes with maturation, causing
dysmature babies prone to respiratory distress syndrome due to incomplete lung
maturation and impaired surfactant synthesis.[65]

Unlike pre-gestational diabetes, gestational diabetes has not been clearly shown to be an
independent risk factor for birth defects. Birth defects usually originate sometime during
the first trimester (before the 13th week) of pregnancy, whereas GDM gradually develops
and is least pronounced during the first trimester. Studies have shown that the offspring
of women with GDM are at a higher risk for congenital malformations.[66][67][68] A large
case-control study found that gestational diabetes was linked with a limited group of birth
defects, and that this association was generally limited to women with a higher body
mass index (≥ 25 kg/m²).[69] It is difficult to make sure that this is not partially due to the
inclusion of women with pre-existent type 2 diabetes who were not diagnosed before
pregnancy.

Because of conflicting studies, it is unclear at the moment whether women with GDM
have a higher risk of preeclampsia.[70] In the HAPO study, the risk of preeclampsia was
between 13% and 37% higher, although not all possible confounding factors were
corrected.[62]

[edit] Epidemiology
Gestational diabetes affects 3-10% of pregnancies, depending on the population studied.[2]

[edit] References
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41. ^ Mottola MF. The role of exercise in the prevention and treatment of gestational
diabetes mellitus. Curr Sports Med Rep 2007; 6(6): 381-6. PMID 18001611
42. ^ a b Langer O, Rodriguez DA, Xenakis EM, McFarland MB, Berkus MD, Arrendondo F.
Intensified versus conventional management of gestational diabetes. Am J Obstet
Gynecol 1994; 170(4): 1036-46. PMID 8166187
43. ^ Taylor JS, Kacmar JE, Nothnagle M, Lawrence RA. A systematic review of the
literature associating breastfeeding with type 2 diabetes and gestational diabetes. J Am
Coll Nutr 2005; 24(5): 320-6. PMID 16192255
44. ^ Nachum Z, Ben-Shlomo I, Weiner E, Shalev E. Twice daily versus four times daily
insulin dose regimens for diabetes in pregnancy: randomised controlled trial. BMJ 1999;
319(7219): 1223-7.
45. ^ Walkinshaw SA. Very tight versus tight control for diabetes in pregnancy
(WITHDRAWN). Cochrane Database Syst Rev 2007; (2): CD000226. PMID 17636623
46. ^ Kremer CJ, Duff P. Glyburide for the treatment of gestational diabetes. Am J Obstet
Gynecol 2004; 190(5): 1438-9. PMID 15167862
47. ^ a b Langer O, Conway DL, Berkus MD, Xenakis EM, Gonzales O. A comparison of
glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med.
2000;343(16):1134-8. PMID 11036118
48. ^ Simmons D, Walters BN, Rowan JA, McIntyre HD. Metformin therapy and diabetes in
pregnancy. Med J Aust 2004; 180(9): 462-4. PMID 15115425
49. ^ a b Rowan JA, Hague WM, Gao W, Battin MR, Moore MP; MiG Trial Investigators.
Metformin versus insulin for the treatment of gestational diabetes. N Engl J Med.
2008;358(19):2003-15. PMID 18463376
50. ^ Glueck CJ, Goldenberg N, Pranikoff J, Loftspring M, Sieve L, Wang P. Height, weight,
and motor-social development during the first 18 months of life in 126 infants born to
109 mothers with polycystic ovary syndrome who conceived on and continued metformin
through pregnancy. Hum Reprod. 2004;19(6):1323-30. PMID 15117896
51. ^ Kim C, Berger DK, Chamany S. Recurrence of gestational diabetes mellitus: a
systematic review. Diabetes Care 2007; 30(5): 1314-9. PMID 17290037
52. ^ Löbner K, Knopff A, Baumgarten A, et al. Predictors of postpartum diabetes in women
with gestational diabetes mellitus. Diabetes 2006; 55(3): 792-7. PMID 16505245
53. ^ a b Järvelä IY, Juutinen J, Koskela P et al. Gestational diabetes identifies women at risk
for permanent type 1 and type 2 diabetes in fertile age: predictive role of autoantibodies.
Diabetes Care 2006; 29(3): 607-12. PMID 16505514
54. ^ a b c Kim C, Newton KM, Knopp RH. Gestational diabetes and the incidence of type 2
diabetes: a systematic review. Diabetes Care. 2002;25(10):1862-8. PMID 12351492
55. ^ Steinhart JR, Sugarman JR, Connell FA. Gestational diabetes is a herald of NIDDM in
Navajo women. High rate of abnormal glucose tolerance after GDM. Diabetes Care.
1997;20(6):943-7. PMID 9167104
56. ^ Lee AJ, Hiscock RJ, Wein P, Walker SP, Permezel M. Gestational diabetes mellitus:
clinical predictors and long-term risk of developing type 2 diabetes: a retrospective
cohort study using survival analysis. Diabetes Care. 2007;30(4):878-83. PMID 17392549
57. ^ Boney CM, Verma A, Tucker R, Vohr BR. Metabolic syndrome in childhood:
association with birth weight, maternal obesity, and gestational diabetes mellitus.
Pediatrics 2005; 115(3): e290-6. PMID 15741354
58. ^ Hillier TA, Pedula KL, Schmidt MM, Mullen JA, Charles MA, Pettitt DJ. Childhood
obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia.
Diabetes Care 2007; 30(9): 2287-92. PMID 17519427
59. ^ Metzger BE. Long-term Outcomes in Mothers Diagnosed With Gestational Diabetes
Mellitus and Their Offspring. Clin Obstet Gynecol 2007; 50(4): 972-9. PMID 17982340
 60. ^ Perrin MC, Terry MB, Kleinhaus K, et al. Gestational diabetes and the risk of breast
cancer among women in the Jerusalem Perinatal Study. Breast Cancer Res Treat 2007
[Epub]. PMID 17476589
61. ^ Perrin MC, Terry MB, Kleinhaus K, et al. Gestational diabetes as a risk factor for
pancreatic cancer: a prospective cohort study. BMC Med 2007; 5: 25. Full text at PMC:
17705823
62. ^ a b c d HAPO Study Cooperative Research Group. Hyperglycemia and adverse
pregnancy outcomes. N Engl J Med. 2008;358(19):1991-2002. PMID 18463375
63. ^ Naylor CD, Sermer M, Chen E, Farine D. Selective screening for gestational diabetes
mellitus. Toronto Trihospital Gestational Diabetes Project Investigators. N Engl J Med
1997; 337(22): 1591–1596. PMID 9371855
64. ^ Jovanovic-Peterson L, Bevier W, Peterson CM. The Santa Barbara County Health Care
Services program: birth weight change concomitant with screening for and treatment of
glucose-intolerance of pregnancy: a potential cost-effective intervention? Am J Perinatol
1997; 14(4): 221-8. PMID 9259932
65. ^ a b Jones CW. Gestational diabetes and its impact on the neonate. Neonatal Netw.
2001;20(6):17-23. PMID 12144115
66. ^ Allen VM, Armson BA, Wilson RD, et al. Teratogenicity associated with pre-existing
and gestational diabetes. J Obstet Gynaecol Can 2007; 29(11): 927-34. PMID 17977497
67. ^ Martínez-Frías ML, Frías JP, Bermejo E, Rodríguez-Pinilla E, Prieto L, Frías JL. Pre-
gestational maternal body mass index predicts an increased risk of congenital
malformations in infants of mothers with gestational diabetes. Diabet Med 2005; 22(6):
775-81. PMID 15910631
68. ^ Savona-Ventura C, Gatt M. Embryonal risks in gestational diabetes mellitus. Early
Hum Dev 2004; 79(1): 59-63. PMID 15449398
69. ^ Correa A, Gilboa SM, Besser LM, et al. (September 2008). "Diabetes mellitus and
birth defects". American journal of obstetrics and gynecology 199 (3): 237.e1–9.
doi:10.1016/j.ajog.2008.06.028. PMID 18674752.
http://linkinghub.elsevier.com/retrieve/pii/S0002-9378(08)00639-X.
70. ^ Leguizamón GF, Zeff NP, Fernández A. Hypertension and the pregnancy complicated
by diabetes. Curr Diab Rep 2006; 6(4): 297-304. PMID 16879782

[edit] External links

• IDF Diabetes Atlas
• International Diabetes Federation
• National Institute of Child Health and Human Development - Am I at Risk for
Gestational Diabetes?
• National Institute of Child Health and Human Development - Managing
Gestational Diabetes: A Patient's Guide to a Healthy Pregnancy
• Gestational Diabetes Resource Guide - American Diabetes Association
• World Diabetes Day
• Diabetes.co.uk: Gestational Diabetes
• eGestationalDiabetes.com Gestational Diabetes Diet

[show]v · d · ePathology of pregnancy, childbirth and the puerperium (O,

630–679)
 Ectopic pregnancy (Abdominal pregnancy, Cervical
Pregnancy with
pregnancy, Ovarian pregnancy, Interstitial
abortive outcome
pregnancy) · Hydatidiform mole · Miscarriage

Oedema, proteinuria andGestational hypertension (Pre-eclampsia, Eclampsia,

hypertensive disordersHELLP syndrome) · Gestational diabetes

Hyperemesis gravidarum ·
Intrahepatic cholestasis of
Digestive systempregnancy · Acute fatty
liver of pregnancy ·
Hepatitis E

PUPPP · Gestational
pemphigoid
Impetigo herpetiformis ·
Intrahepatic cholestasis of
Integumentary system/
Other, predominantly pregnancy · Linea nigra ·
dermatoses of pregnancy
related to pregnancy Prurigo gestationis ·
Pruritic folliculitis of
pregnancy · Striae
gravidarum

Nervous systemChorea gravidarum

Gestational
thrombocytopenia ·
Blood
Pregnancy-induced
hypercoagulability

amniotic fluid (Polyhydramnios, Oligohydramnios) ·

chorion/amnion (Chorioamnionitis, Chorionic
hematoma, Premature rupture of membranes,
Maternal care related to theAmniotic band syndrome, Monoamniotic twins) ·
fetus and amniotic cavityplacenta (Placenta praevia, Placental abruption,
Monochorionic twins, Twin-to-twin transfusion
syndrome, Circumvallate placenta) · Braxton Hicks
contractions · Hemorrhage (Antepartum)

M: OBS phys/devp mthr/fetu/infc, epon proc, drug(2A/G2C)

[show]v · d · eDiabetes (E10–E14, 250)
 M: END anat/phys/devp/horm/cel noco(d)/cong/tumr, proc, drug
l sysi/epon (A10/H1/H2/H3/H5)
Retrieved from "http://en.wikipedia.org/wiki/Gestational_diabetes"
Categories: Obstetrics | Diabetes | Health issues in pregnancy

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What is this blue circle?
The universal symbol for diabetes.

The purpose of the diabetes symbol is to give diabetes a common identity.

Until 2006, there was no global symbol for diabetes. It aims to:

• support all existing efforts to raise awareness about diabetes

• inspire new activities, bring diabetes to the attention of the general public
• brand diabetes
• provide a means to show support for the fight against diabetes

Who owns the symbol? The International Diabetes

Federation.
The International Diabetes Federation (IDF) holds all rights to the blue circle symbol for
diabetes.

How can I promote the symbol? By using it.

We encourage everyone to use the symbol for diabetes as a reference to diabetes and the
millions of people affected by the disease.

We welcome the use of the logo in publications: magazines, video, online information,
etc.

The symbol cannot be used without prior permission by IDF. It cannot be used:

• to promote or refer to anything other than diabetes

• as a quality label
• for merchandizing or any other form of commercial aim

While IDF holds all rights to the diabetes symbol, IDF can provide permission for
merchandising carrying the diabetes symbol on a case-by-case basis. You can submit
your proposal to diabetessymbol@idf.org. Grounds for permission are (amongst others):

• type of organization
• distribution of the material

Where can I find the symbol?

Download the logo in different file formats and sizes.

Can I incorporate the symbol in logos? Yes, as a

reference to diabetes and only for non-commercial
use.
For any other types of logos, please contact diabetessymbol@idf.org.

Is this a quality label? No.

While this label can be used on any material as a reference to diabetes according to the
guidelines mentioned on this page or after approval by IDF, it can not be used as a quality
label. Any direct or indirect indication that the diabetes symbol provides a proof of
quality is prohibited. IDF cannot be liable to any misuse of the symbol.

I think someone is violating the policies as described

above. What should I do?
Please report any violation to diabetessymbol@idf.org. Anonymity is guaranteed.

Can you give examples of how the blue circle has been
used or can be used?
Some examples include:

• posters
• t-shirts
• flags
• pins (available at http://www.idf.org/bookshop)
• travel bugs (for more information, http://unite.geocaching.com)
• drawings & paintings

Who can I contact for specific questions?

Please direct any questions related to the usage of the blue circle to
diabetessymbol@idf.org.

What is the history of the blue circle?

The icon was developed originally for the campaign for a UN Resolution on diabetes.
The campaign for a United Nations Resolution on diabetes was a response to the diabetes
pandemic that is set to overwhelm healthcare resources everywhere. The campaign
mobilised diabetes stakeholders behind the common cause of securing a United Nations
Resolution on diabetes. The United Nations passed Resolution 61/255 ‘World Diabetes
Day’ on December 20th 2006.

Why a circle?
The circle occurs frequently in nature and has thus been widely employed since the dawn
of humankind. The significance is overwhelmingly positive. Across cultures, the circle
can symbolize life and health. Most significantly for the campaign, the circle symbolizes
unity. Our combined strength is the key element that made this campaign so special. The
global diabetes community came together to support a United Nations Resolution on
diabetes and needs to remain united to make a difference. As we all know: to do nothing
is no longer an option.

Why blue?
The blue border of the circle reflects the colour of the sky and the flag of the United
Nations. The United Nations is in itself a symbol of unity amongst nations and is the only
organization that can signal to governments everywhere that it is time to fight diabetes
and reverse the global trends that will impede economic development and cause so much
suffering and premature death.

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eMedicine Specialties > Endocrinology > Diabetes Mellitus

Diabetes Mellitus and Pregnancy

Author: Thomas R Moore, MD, Chairman, Professor, Department of Reproductive Medicine, University of
California at San Diego School of Medicine
Contributor Information and Disclosures

Updated: Jun 1, 2010

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Introduction

Background
Abnormal maternal glucose regulation occurs in 3-10% of pregnancies. Studies suggest that the
prevalence of diabetes mellitus (DM) among women of childbearing age is increasing in the United
States. This increase is believed to be attributable to more sedentary lifestyles, changes in diet,
continued immigration from high-risk populations, and the virtual epidemic of childhood and adolescent
obesity that is presently evolving in United States. Gestational diabetes mellitus (GDM) is defined as
glucose intolerance of variable degree with onset or first recognition during pregnancy. Gestational
diabetes mellitus accounts for 90% of cases of diabetes mellitus in pregnancy. Type II diabetes
mellitus accounts for 8% of cases of diabetes mellitus in pregnancy, and given its increasing incidence,
preexisting diabetes mellitus now affects 1% of pregnancies.

Infants of mothers with preexisting diabetes experience double the risk of serious injury at birth, triple
the likelihood of cesarean delivery, and quadruple the incidence of newborn intensive care unit
admission. Studies indicate that the risk of these morbidities is directly proportional to the degree of
maternal hyperglycemia. For this reason, the excessive fetal and neonatal morbidity attributable to
diabetes in pregnancy should be considered preventable with early diagnosis and effective treatment
therapies.

Pathophysiology
Maternal-fetal metabolism in normal pregnancy

With each feeding, the pregnant woman undergoes a complex series of maternal hormonal actions (ie,
a rise in blood glucose; the secondary secretion of pancreatic insulin, glucagon, somatomedins, and
adrenal catecholamines). These adjustments ensure that an ample, but not excessive, supply of
glucose is available to the mother and fetus. The key features of this complex interaction include the
following:

• Compared to nonpregnant subjects, pregnant women tend to develop hypoglycemia (plasma

glucose mean = 65-75 mg/dL) between meals and during sleep. This occurs because the
fetus continues to draw glucose across the placenta from the maternal bloodstream, even
during periods of fasting. Interprandial hypoglycemia becomes increasingly marked as
pregnancy progresses and the glucose demand of the fetus increases.
• Levels of placental steroid and peptide hormones (eg, estrogens, progesterone, and chorionic
somatomammotropin) rise linearly throughout the second and third trimesters. Because these
hormones confer increasing tissue insulin resistance as their levels rise, the demand for
increased insulin secretion with feeding escalates progressively during pregnancy. Twenty-
four–hour mean insulin levels are 50% higher in the third trimester compared to the
nonpregnant state.
• If the maternal pancreatic insulin response is inadequate, maternal and, then, fetal
hyperglycemia results. This typically manifests as recurrent postprandial hyperglycemic
episodes. These postprandial episodes are most significantly accountable for the accelerated
growth exhibited by the fetus.
 • Surging maternal and fetal glucose levels are accompanied by episodic fetal
hyperinsulinemia. Fetal hyperinsulinemia promotes excess nutrient storage, resulting in
macrosomia. The energy expenditure associated with the conversion of excess glucose into
fat causes depletion in fetal oxygen levels.
• These episodes of fetal hypoxia are accompanied by surges in adrenal catecholamines,
which, in turn, cause hypertension, cardiac remodeling and hypertrophy, stimulation of
erythropoietin, red cell hyperplasia, and increased hematocrit. Polycythemia (hematocrit
>65%) occurs in 5-10% of newborns of diabetic mothers. This finding appears to be related to
the level of glycemic control and is mediated by decreased fetal oxygen tension. High
hematocrit values in the neonate lead to vascular sludging, poor circulation, and postnatal
hyperbilirubinemia.

During a healthy pregnancy, mean fasting blood sugar levels decline progressively to a remarkably low
value of 74 ± 2.7 (SD) mg/dL. On the other hand, peak postprandial blood sugar values rarely exceed
120 mg/dL. Meticulous replication of the normal glycemic profile during pregnancy has been
demonstrated to reduce the macrosomia rate. Specifically, when 2 hour postprandial glucose levels
are maintained less than 120 mg/dL, approximately 20% of fetuses demonstrate macrosomia.
Conversely, if postprandial levels range up to 160 mg/dL, macrosomia rates rise to 35%.

Frequency
United States

In the United States today, 21 million people (7% of the population) have some form of diagnosed
diabetes.1 Another 6 million people may be undiagnosed.2 Approximately 3-10% of pregnancies in the
United States are complicated by diabetes, of which 90% is gestational diabetes and 8% is
preexisting, insulin-resistant (ie, adult-onset) diabetes. The incidence of insulin-resistant diabetes is
increasing markedly in the United States, probably related to rising population obesity and shifts in
ethnicity.

In addition to these factors contributing to a rise in the prevalence of diabetes among reproductive
aged women, medical interventions during pregnancy may increase the likelihood of developing
gestational diabetes. A study reported in 2007 has demonstrated and increased incidence of
gestational diabetes mellitus in women receiving prophylactic 17 alpha-hydroxyprogesterone caproate
for the prevention of recurrent preterm delivery (from 4.9% in control to 12.9% in treated patients).3

Race
The prevalence of gestational diabetes is strongly related to the patient's race and culture.

• Prevalence rates are higher in African, Hispanic, Native American and Asian women than in
white women.
• Typically, only 1.5-2% of Caucasian women develop gestational diabetes mellitus, while
Native Americans from the southwestern United States may have rates as high as 15%.
• In Hispanic, African American, and Asian populations, the incidence is 5-8%.
• In these high-risk populations, the recurrence risk with future pregnancies has been reported
to be as high as 68%.4 In addition, approximately one-third will develop overt diabetes mellitus
within 5 years of delivery, with higher risk ethnicities having risks nearing 50%.5
 • Race also influences many complications of diabetes mellitus in pregnancy. For instance,
African Americans have been shown to have lower rates of macrosomia, despite similar levels
of glycemic control. Conversely, Hispanic women have higher rates of macrosomia and birth
injury than women of other ethnicities, even with aggressive management.6,7

Clinical

History
Fetal morbidity with diabetes during pregnancy

Miscarriages

• In all women with preexisting diabetes mellitus, there is a 9-14% rate of miscarriage.
• Current data suggest a strong association between degree of glycemic control prior to
pregnancy and miscarriage rate. Suboptimal glycemic control has been shown to double the
miscarriage rate in women with diabetes. A correlation also exists between more advanced
diabetes and miscarriage rates. Patients with long-standing (>10 y) and poorly controlled
(glycohemoglobin exceeding 11%) diabetes have been shown to have a miscarriage rate of
up to 44%. Conversely, reports demonstrate a normalization of miscarriage rate with excellent
glycemic control.

Birth defects

• Among the general population, major birth defects occur in 1-2% of the population. In women
with overt diabetes and suboptimal glycemic control prior to conception, the likelihood of a
structural anomaly is increased 4- to 8-fold.
• Although initial reports demonstrated anomaly rates as high as 18% in women with
preexisting diabetes mellitus,8 more recent reports with more aggressive preconception and
first trimester management report anomaly rates between 5.1 and 9.8%.9,10
• Two-thirds of anomalies involve the cardiovascular and central nervous systems. Neural tube
defects occur 13-20 times more frequently in diabetic pregnancy. Genitourinary,
gastrointestinal, and skeletal anomalies are also more common.
• The fact that no increase in birth defects occurs among the offspring of fathers who are
diabetic and women who develop gestational diabetes after the first trimester is notable. This
suggests that periconceptional glycemic control is the main determinant of abnormal fetal
development in diabetic women.
• When the frequency of congenital anomalies in patients with normal or high first-trimester
maternal glycohemoglobin values was compared to the frequency in healthy patients, the rate
of anomalies was only 3.4% with glycosylated hemoglobin values (HbA1C) of less than 8.5%,
whereas patients with poorer glycemic control in the periconceptional period (HbA1C >8.5%)
had a 22.4% rate of malformations. An overall malformation rate of 13.3% was reported in 105
patients with diabetes, but the risk of delivering a malformed infant was comparable to a
normal population when the glycosylated hemoglobin (HbA1c ) was less than 7%.11 More
recently, in a review of 7 cohort studies, researchers found that patients with a normal
glycohemoglobin (0 SD above normal), the absolute risk of an anomaly was 2%. At 2 SD
above normal, this risk was 3%, with an odds ratio of 1.2 (1.1- 1.4). As the glycohemoglobin
increased so did the risk for malformation in a direct relationship.12
 • Because birth defects occur during the critical 3-6 weeks after conception, nutritional and
metabolic intervention must be initiated well before pregnancy begins. Clinical trials of
intensive metabolic care have demonstrated that malformation rates similar to those in the
nondiabetic population can be achieved with meticulous preconceptional glycemic control.13
Subsequent trials comparing a preconceptional intensive metabolic program to standard
treatment over 15 years duration have demonstrated lowered perinatal mortality (0% vs 7%)
and reduced congenital anomaly rate (14% to 2%). In addition, when the preconceptional
counseling program was discontinued, the congenital anomaly rate increased by over 50%.14

Growth restriction

• Although most fetuses of diabetic mothers exhibit growth acceleration, growth restriction
occurs with significant frequency in pregnancies in women with preexisting type 1 diabetes.
• The most important predictor of fetal growth restriction is underlying maternal vascular
disease. Specifically, pregnant patients with diabetes-associated retinal or renal
vasculopathies and/or chronic hypertension are most at risk for growth restriction.

Growth acceleration

• Excessive body fat stores, stimulated by excessive glucose delivery during diabetic
pregnancy, often extends into childhood and adult life.
• Approximately 30% of fetuses of women with diabetes mellitus in pregnancy are large for
gestational age (LGA). In preexisting diabetes mellitus this incidence appears slightly higher,
38%.6
• Maternal obesity, common in type 2 diabetes, appears to significantly accelerate the risk of
infants being LGA.
• A study of the effects of weight gain in women with gestational diabetes found that women
with the condition whose gestational weight gain was greater than that in the Institute of
Medicine’s (IOM’s) weight-gain guidelines had an increased risk of preterm delivery, of having
a newborn who was LGA, and of requiring a cesarean delivery.15 The chance that a newborn
would be small for gestational age was greater among women with gestational diabetes
whose weight gain was below the IOM guidelines.

Fetal obesity

• Macrosomia is typically defined as a birthweight above the 90th percentile for gestational age
or greater than 4000 grams. In pregnant diabetic women, macrosomia occurs in 15-45% of
cases, a 3-fold increase from normoglycemic controls.
• Newborns with macrosomia experience excessive rates of neonatal morbidity, as illustrated
by a study by Hunter et al in 1993, which compared the neonatal morbidity among infants of
230 women with insulin-dependent diabetes and infants of 460 women without diabetes. The
infants of diabetic mothers (IDMs) had 5-fold higher rates of severe hypoglycemia, a 4-fold
increase in macrosomia, and a doubled increase in neonatal jaundice.16
• Birth injury, including shoulder dystocia and brachial plexus trauma, are more common among
infants of diabetic mothers, and macrosomic fetuses are at the highest risk.
• The macrosomic fetus in diabetic pregnancy develops a unique pattern of overgrowth,
involving central deposition of subcutaneous fat in the abdominal and interscapular areas.
 Skeletal growth is largely unaffected. Neonates of diabetic mothers have a larger shoulder
and extremity circumference, a decreased head-to-shoulder ratio, significantly higher body fat,
and thicker upper extremity skin folds compared to nondiabetic control infants of similar
weights. Since fetal head size is not increased during poorly controlled diabetic pregnancy but
shoulder and abdominal girth can be markedly augmented, the risk of injury to the fetus after
delivery of the head (eg Erb palsy) is significantly increased.
• When serial ultrasonographic examination findings from diabetic fetuses are plotted, the
growth velocity of the abdominal circumference is often well above the growth centiles seen in
nondiabetic fetuses and is higher than the fetal head and femur centiles. The accelerated
growth of the abdominal circumference begins to rise significantly above normal after 24
weeks.

Metabolic syndrome

• The adverse downstream effects of abnormal maternal metabolism on the offspring have
been documented well into puberty. Glucose intolerance and higher serum insulin levels are
more frequent in children of diabetic mothers as compared to normal controls. By age 10-16
years, offspring of diabetic pregnancy have a 19.3% rate of impaired glucose intolerance.17
• The childhood metabolic syndrome includes childhood obesity, hypertension, dyslipidemia,
and glucose intolerance. A growing body of literature supports a relationship between
intrauterine exposure to maternal diabetes and risk of a metabolic syndrome later in life.18,19
• Fetuses of diabetic women that are born large for gestational age appear to be at the greatest
risk.19

Role of glucose levels

• Excess nutrient delivery to the fetus causes macrosomia and truncal fat deposition, but
whether fasting or peak glucose values are more correlated with fetal overgrowth is less clear.
• Data from the Diabetes in Early Pregnancy project indicate that fetal birthweight correlates
best with second- and third-trimester postprandial blood sugar levels and not with fasting or
mean glucose levels.20
• More recent data from the ACHOIS trial demonstrated a positive relationship between severity
of maternal fasting hyperglycemia and risk of shoulder dystocia, with a 1 mmol increase in
fasting glucose leading to a relative risk for shoulder dystocia of 2.09 (1.03- 4.25).21
• When postprandial glucose values average 120 mg/dL or less, approximately 20% of infants
can be expected to be macrosomic. When postprandial levels range as high as 160 mg/dL,
macrosomia rates can reach 35%.
• In addition, there appears to be a role for excessive fetal insulin levels in mediating
accelerated fetal growth. In the study by Simmons et al which compared umbilical cord sera in
infants of diabetic mothers newborns and controls, the heavier, fatter babies from diabetic
pregnancies were also hyperinsulinemic.22

Role of maternal obesity

• Maternal obesity has a strong and independent effect on fetal macrosomia. Birthweight is
largely determined by maternal factors other than hyperglycemia, with the most significant
 influences being gestational age at delivery, prepregnancy maternal body mass index (BMI),
maternal height, pregnancy weight gain, the presence of hypertension, and cigarette smoking.
• When women who are very obese (weight >300 lb) were compared to women of normal
weight, the obese women had more than double the risk of macrosomia compared to the
women who were of normal weight. This may explain the failure of glycemic control to
completely prevent fetal macrosomia in several series.

Perinatal morbidity and birth injury

Perinatal mortality

• In diabetic pregnancy, perinatal mortality has decreased 30-fold since the discovery of insulin
in 1922 and intensive obstetrical and infant care in the 1970s. Nevertheless, the current
perinatal mortality rates among women who are diabetic remain approximately twice those
observed in the nondiabetic population.
• Congenital malformations, respiratory distress syndrome (RDS), and extreme prematurity
account for most perinatal deaths in contemporary diabetic pregnancies.

Table 1. Perinatal Morbidity in Diabetic Pregnancy

Open table in new window

Morbidity Gestational Diabetes Type 1 Diabetes Type 2 Diabetes

Hyperbilirubinemia 29% 55% 44%

Hypoglycemia 9% 29% 24%

Respiratory distress 3% 8% 4%

Transient tachypnea 2% 3% 4%

Hypocalcemia 1% 4% 1%

Cardiomyopathy 1% 2% 1%

Polycythemia 1% 3% 3%

Morbidity Gestational Diabetes Type 1 Diabetes Type 2 Diabetes

Hyperbilirubinemia 29% 55% 44%

Hypoglycemia 9% 29% 24%

Respiratory distress 3% 8% 4%

Transient tachypnea 2% 3% 4%

Hypocalcemia 1% 4% 1%

Cardiomyopathy 1% 2% 1%

Polycythemia 1% 3% 3%

Adapted from California Department of Health Services, 1991

Birth injury

• Injuries of birth, including shoulder dystocia and brachial plexus trauma, are more common
among infants of diabetic mothers, and macrosomic fetuses are at the highest risk.
• Most of the birth injuries occurring to infants of diabetic mothers are associated with difficult
vaginal delivery and shoulder dystocia. While shoulder dystocia occurs in 0.3-0.5% of vaginal
deliveries among healthy pregnant women, the incidence is 2- to 4-fold higher in women with
diabetes. With strict glycemic control, the birth injury rate has been shown to be only slightly
higher than controls (3.2 vs 2.5%).
• Currently, clinical ability to predict shoulder dystocia is poor. Warning signs during labor (labor
protraction, suspected fetal macrosomia, need for operative vaginal delivery) successfully
predict only 30% of these events.
• Common birth injuries associated with diabetes are brachial plexus, facial nerve injury, and
cephalohematoma.

Polycythemia

• A central venous hemoglobin concentration greater than 20 g/dL or a hematocrit value greater
than 65% (polycythemia) is not uncommon in infants of diabetic mothers and is related to
glycemic control.
• Hyperglycemia is a powerful stimulus to fetal erythropoietin production mediated by
decreased fetal oxygen tension.
• Untreated neonatal polycythemia may promote vascular sludging, ischemia, and infarction of
vital tissues, including the kidneys and central nervous system.

Hypoglycemia

• Aproximately 15-25% of neonates delivered from women with diabetes during gestation
develop hypoglycemia during the immediate newborn period.23 Neonatal hypoglycemia is less
frequent when tight glycemic control is maintained during pregnancy24 and in labor.
 • Unrecognized postnatal hypoglycemia may lead to neonatal seizures, coma, and brain
damage.

Neonatal hypocalcemia

• Up to 50% of infants of diabetic mothers have low levels of serum calcium (<7 mg/100 mL).
With improved management of diabetes in pregnancy, this occurrence has been reduced to
5% or less.
• These changes in calcium appear to be attributable to a functional hypoparathyroidism,
though the exact pathophysiology is not well understood.

Postnatal hyperbilirubinemia

• Hyperbilirubinemia occurs in approximately 25% of infants of diabetic mothers, a rate

approximately double that in a healthy population. The causes of hyperbilirubinemia in infants
of diabetic mothers are multiple, but prematurity and polycythemia are the primary contributing
factors. Increased destruction of red blood cells contributes to the risk of jaundice and
kernicterus.
• Treatment of this complication is usually by phototherapy, but exchange transfusions may be
necessary if bilirubin levels are markedly elevated.

Respiratory problems

• Until recently, neonatal respiratory distress syndrome (RDS) was the most common and
serious morbidity in infants of diabetic mothers. In the 1970s, improved prenatal maternal
management for diabetes and new techniques in obstetrics for timing and mode of delivery
resulted in a dramatic decline in its incidence from 31% to 3%.25 Nevertheless, respiratory
distress syndrome continues to be a relatively preventable complication.
• The majority of the literature indicates a significant biochemical and physiological delay in
infants of diabetic mothers. Tyden26 and Landon27 and colleagues reported that fetal lung
maturity occurred later in pregnancies with poor glycemic control regardless of class of
diabetes when infants were stratified by maternal plasma glucose levels.
• The nondiabetic fetus achieves pulmonary maturity at a mean gestational age of 34-35
weeks. By 37 weeks' gestation, more than 99% of healthy newborn infants have mature lung
profiles as assessed by phospholipid assays. However, in a diabetic pregnancy, presuming
that the risk of respiratory distress has passed is unwise until after 38.5 gestational weeks
have been completed.
• Prior to contemplating any delivery before 38.5 weeks for other than the most urgent fetal and
maternal indications, perform an amniocentesis to document pulmonary maturity.

Maternal morbidity

Diabetic retinopathy

• This is the leading cause of blindness in women aged 24-64 years. Some form of retinopathy
is present in virtually 100% of women who have had type 1 diabetes for 25 years or more; of
these women, approximately 1 in 5 is legally blind.
 • A prospective study showed that while half the 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.
• Other studies have suggested that rapid induction of glycemic control in early pregnancy
stimulates retinal vascular proliferation.28 However, when the total effect of pregnancy on
ophthalmologic status was considered, women with pregnancies had a slower progression of
retinopathy than nonpregnant women, probably because the modest deterioration in retinal
status during rapid improvement in control is offset by the excellent control during the
remainder of the pregnancy.
• Current management recommendations include baseline ophthalmology referral for pregnant
patients with diabetes, with follow-up according to degree of retinopathy.

Renal function

• In general, patients with underlying nephropathy can expect varying degrees of deterioration
of renal function during a pregnancy. As renal blood flow and glomerular filtration rate
increase 30-50% during pregnancy, the degree of proteinuria will also increase.
• The most recent studies indicate that pregnancy does not measurably alter the time course of
diabetic renal disease, nor does it increase the likelihood of progression to end stage renal
disease. The progression to renal disease in diabetic patients appears to be related to
duration of diabetes and degree of glycemic control.
• Patients using the subcutaneous insulin pump have lower mean glucose levels than those
using intermittent injections. The effect on progression of nephropathy of 2 years of strict
metabolic control showed that none of the patients managed on the insulin pump progressed
to clinical nephropathy, while 5 patients with conventional treatment did.
• Perinatal complications are greatly increased in patients with diabetic nephropathy. Preterm
birth, intrauterine growth restriction, and preeclampsia are all significantly more common in
women with diabetic nephropathy during pregnancy.

Chronic hypertension

• This complicates approximately 1 in 10 diabetic pregnancies overall. Patients with underlying

renal or retinal vascular disease are at a substantially higher risk, with 40% having chronic
hypertension.
• Patients with chronic hypertension and diabetes are at increased risk of intrauterine growth
restriction, superimposed preeclampsia, abruptio placentae, and maternal stroke.
• Baseline renal function determination is recommended in all patients with preexisting
diabetes. Renal function assessments in each trimester should be performed in those with
overt vascular disease or who have had diabetes for more than 10 years.

Preeclampsia

• Consists of abrupt elevation in blood pressure, significant proteinuria, plasma uric acid levels
greater than 6 mg/dL or evidence of hemolysis, elevated liver enzymes, and low platelet count
(HELLP) syndrome.
• Preeclampsia is more frequent among women with diabetes, occurring in approximately 12%
as compared to 8% of the nondiabetic population. The risk of preeclampsia is also related to
 maternal age and the duration of preexisting diabetes. In patients who have chronic
hypertension coexisting with diabetes, preeclampsia may be difficult to distinguish from near-
term blood pressure elevations.
• The rate of preeclampsia has been found to be related to the level of glycemic control, with
fasting plasma glucose (FPG) less than 105, the rate of preeclampsia was 7.8%, if FPG was
greater than 105, the rate of preeclampsia was 13.8%.29
• In this same study, pregravid body mass index was also significantly related to the
development of preeclampsia.

Physical
Diagnosing diabetes

Patients with type 1 diabetes are typically diagnosed during an episode of hyperglycemia, ketosis, and
dehydration; this occurs most commonly in childhood or adolescence, before pregnancy. Type 1
diabetes is diagnosed only rarely during pregnancy and is most often accompanied by unexpected
coma because early pregnancy may provoke diet and glycemic control instability in patients with occult
diabetes. A pregnancy test should be ordered in all reproductive-aged women admitted to the hospital
for blood sugar management.

Diagnosing type 2 insulin-resistant diabetes is difficult during pregnancy because severe forms of
gestational diabetes mellitus have similar clinical characteristics. On the other hand, it is not unusual
for women tentatively diagnosed with gestational diabetes mellitus in early pregnancy to be found to
have overt diabetes after delivery. Although a first-trimester HbA1C value of 8% is highly suggestive of
preexisting type 2 diabetes, definitive diagnosis of type 2 diabetes must be made after pregnancy
using the 75-gram, 2-hour glucose tolerance test.2

According to the American Diabetes Association "Standards of Medical Care in Diabetes--2007,"30

diagnostic criteria for diabetes mellitus are as follows, and one of the following must be met:

• Symptoms of diabetes and a casual plasma glucose greater than 200 mg/dL (11.1 mmol/L).
Casual is defined as any time of day without regard to time since last meal. The classic
symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss.
• Fasting plasma glucose greater than 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric
intake for at least 8 h.
• Two-hour plasma glucose greater than 200 mg/dL (11.1 mmol/L) during a 75 g, 2-hour oral
glucose tolerance test (OGTT).

In the absence of unequivocal hyperglycemia with acute metabolic decompensation, the diagnosis
should be confirmed by repeat testing on a different day.

Prediabetes is a term used to distinguish people who are at increased risk of developing diabetes.
People with prediabetes have impaired fasting glucose (IFG) or impaired glucose tolerance (IGT).
Some people may have both impaired fasting glucose and impaired glucose tolerance.

• Impaired fasting glucose is a condition in which the fasting blood sugar level is elevated (100-
125 mg/dL) after an overnight fast but is not high enough to be classified as diabetes.
 • Impaired glucose tolerance is a condition in which the blood sugar level is elevated (140-199
mg/dL after a 2-h oral glucose tolerance test) but is not high enough to be classified as
diabetes.
• Patients with prediabetes identified prior to pregnancy should be considered at extremely high
risk of developing gestational diabetes mellitus during pregnancy. As such, they should
receive early (first trimester) diabetic screening. Prediabetes, impaired fasting glucose, and
impaired glucose tolerance are not meaningful terms in managing patients during pregnancy
unless they exceed the plasma glucose limits for diagnosing gestational diabetes mellitus.

Screening for gestational diabetes mellitus (GDM)

Gestational diabetes mellitus only occurs during pregnancy. The diagnosis is established by glucose
tolerance testing.

Risk factors for gestational diabetes include advanced maternal age, ethnicity, obesity, obstetrical
history of diabetes or macrosomia, and strong family history of diabetes.

The best method for diagnosing gestational diabetes mellitus continues to be controversial. The 2-step
system is currently recommended in the United States. A 50-gram 1-hour glucose challenge test
(GCT) is administered to all pregnant women at 26-28 weeks, followed by a 100-gram, 3-hour oral
glucose tolerance test (OGTT) for those with an abnormal screening result. Alternatively, for high risk
women, a one-step approach can be used by proceeding directly to the 100-g, 3-hour OGTT.

The sensitivity of gestational diabetes mellitus testing depends on the threshold value used for the 50-
g glucose challenge. Current recommendations from the American Diabetes Association "Standards of
Medical Care in Diabetes--2007"30 and the American College of Obstetricians and Gynecologists31 note
that a threshold value of 140 mg/dL results in approximately 80% detection of gestational diabetes,
while using a threshold of 130 mg/dL results in 90% detection. A potential disadvantage of using the
lower value of 130 mg/dL is an approximate doubling in the number of OGTTs performed.

Other tests (eg, maternal HbA1C, random postprandial or fasting blood sugar level, or fructosamine
level) are not recommended because of low sensitivity.

Oral Glucose Tolerance Test For Gestational Diabetes can be summarized as follows:

• One-hour 50-g glucose challenge result greater than 130 mg/dL

• Overnight fast of 8–14 hours
• Carbohydrate loading 3 days including more than 150 g carbohydrate
• Seated, not smoking during the test
• Two or more values must be met or exceeded for the diagnosis of gestational diabetes.

Table 2. Plasma Glucose Criteria for Gestational Diabetes

Open table in new window

Time 100 g Glucose Load, mg/dL (mmol/L)

Fasting 95 (5.3)
1-h 180 (10.0)

2-h 155 (8.6)

3-h 140 (7.8)

Time 100 g Glucose Load, mg/dL (mmol/L)

Fasting 95 (5.3)

1-h 180 (10.0)

2-h 155 (8.6)

3-h 140 (7.8)

Screening for gestational diabetes mellitus during pregnancy is recommended because fewer than
20% of women with significant glucose intolerance during pregnancy exhibit glucosuria or other
symptoms during pregnancy. However, whether universal screening of all pregnant women or targeted
screening of patients with risk factors is most efficacious continues to be controversial. At present, both
methods (universal and selective screening) are employed in reputable centers. In areas in which the
prevalence of insulin resistance is 5% or higher (eg, the southwestern and southeastern United
States), universal screening is recommended.

First-trimester screening should be performed on patients with risk factors during the first trimester in
order to identify those with occult type 2 diabetes. In 1995, when Moses et al assessed the prevalence
of gestational diabetes mellitus in patients with various risk factors, gestational diabetes mellitus was
diagnosed in 6.7% of the women overall, in 8.5% of the women aged 30 years, in 12.3% of the women
with a preconception BMI of 30, and in 11.6% of women with a family history of diabetes in a first-
degree relative. A combination of one or all of these risk factors predicted gestational diabetes mellitus
in 61% cases. Gestational diabetes mellitus was present in 4.8% of the women without risk factors.32
Screen patients with any of the following risk factors for gestational diabetes mellitus at the first
prenatal visit:

• Maternal age older than 35 years

• Previous infant weighing less than 4000 grams
• Previous unexplained fetal demise
• Previous pregnancy with gestational diabetes mellitus
• Strong immediate family history of NIDDM or gestational diabetes mellitus
• Obesity (>90 kg)
 • Fasting glucose value greater than 140 mg/dL (7.8 mmol/L) or random glucose value greater
than 200 mg/dL (11.1 mmol/L)

Patients with risk factors who have negative test results in the first trimester should be retested at 26-
28 weeks. Because the insulin resistance that causes hyperglycemia becomes increasingly prevalent
as the third trimester progresses, the condition may be missed during early testing on patients who will
become glucose intolerant later. However, performing the test too late in the third trimester abbreviates
the time in which metabolic intervention can take place. For this reason, glucose tolerance testing in all
patients is typically performed at 26-28 weeks’ gestation.

Patients with a single abnormal value on a 3 hour glucose tolerance test are likely to exhibit some
degree of glucose intolerance. When left untreated, these patients are at higher risk for macrosomia
and neonatal morbidity. Consequently, patients with a single abnormal value should receive dietary
and physical activity counseling. If the abnormal value on the OGTT was obtained prior to 26 weeks,
repeat OGTT should be performed approximately 4 weeks later.

Whether administered at 12 or 26 weeks’ gestation, the glucose challenge test can be performed
without regard to recent food intake (ie, nonfasting state). Indeed, results from tests performed in
fasting subjects are more likely to be falsely elevated than results from tests conducted between
meals.33

A nested case-control study indicated that another risk factor for the development of gestational
diabetes is the presence of hypertension before pregnancy or during early pregnancy.34 The report,
which looked at 381 women with hypertension or prehypertension (the latter being defined in the study
as 120-139/80-89 mmHg), as well as at 942 control subjects, found that women in whom
prehypertension existed prior to or during early pregnancy had a slightly increased risk of developing
gestational diabetes. Women with hypertension before or during early pregnancy, however,
demonstrated a two-fold increase in their risk of developing the gestational condition.

Causes
See Frequency.

More on Diabetes Mellitus and Pregnancy

Overview: Diabetes Mellitus and Pregnancy

Differential Diagnoses & Workup: Diabetes Mellitus and Pregnancy
Treatment & Medication: Diabetes Mellitus and Pregnancy
Follow-up: Diabetes Mellitus and Pregnancy
References
Further Reading
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