Diabetes in Pregnancy Case File

Diabetes in Pregnancy Case File

Eugene C. Toy, MD, Patti Jayne Ross, MD, Benton Baker III, MD, John C. Jennings, MD

CASE 27

A 27-year-old G3P0020 who is at 32 weeks’ gestation presents to the Obstetrical Unit for fatigue and lethargy. The patient has a history of type 1 diabetes for 12 years. She denies hypertension, retinopathy, and renal disease. Her obstetric history is significant for two first trimester pregnancy losses occurring 1 and 3 years previously. Her medications include twice-daily subcutaneous insulin. On examination, her blood pressure (BP) is 84/44 mm Hg, heart rate (HR) is 120 bpm, and respiratory rate (RR) is 32 breaths per minute. She appears sleepy and confused. The mucous membranes are dry. The urine on dipstick shows a specific gravity of 1.030, 4+ glucose, and 3+ ketones. The fingerstick glucose is 280 mg/dL. The fetal heart tones’ rate tracing is noted below (Figure 27–1).

» What is the most likely diagnosis?

» What is the next step in therapy for this patient?

» What does the fetal heart rate (FHR) tracing indicate?

» What is the best management for the pregnancy?

Figure 27–1. (A) and (B) FHR tracing. (Reproduced with permission from Eugene C. Toy, MD.)

ANSWER TO CASE 27:

Diabetes in Pregnancy                                           

Summary: A 27-year-old G3P0020 type 1 insulin-requiring diabetic with multiple miscarriages is at 32 weeks’ gestation. She is presenting with fatigue and lethargy. She denies hypertension, retinopathy, and renal disease. Her blood pressure (BP) is 84/44 mm Hg, heart rate (HR) is 120 bpm, and respiratory rate (RR) is 32 breaths per minute. She appears sleepy and confused, and her mucous membranes are dry. The urinalysis shows a specific gravity of 1.030, 4+ glucose, and 3+ ketones. The fingerstick glucose is 280 mg/ dL. The fetal heart tones’ rate tracing demonstrates late decelerations and decreased variability.

• Most likely diagnosis: Diabetic ketoacidosis (DKA). This should be confirmed with a STAT arterial blood gas, blood sugar, electrolytes with anion gap (AG), and serum ketones.
• Next step in therapy for this patient: Aggressive isotonic fluid hydration begins intravenous (IV) insulin infusion to lower the glucose, remedy any electrolyte abnormalities, and treat the trigger of the DKA (such as infection).
• Fetal heart rate tracing: Baseline of 140 bpm with decreased variability and recurrent late decelerations, indicative of severe hypoxia or acidosis.
• Best management for the pregnancy: Treat the DKA and observe the FHR tracing carefully.

ANALYSIS

Objectives

1. Describe the maternal and fetal complications associated with pregestational diabetes.
2. Describe the maternal and fetal complications associated with gestational diabetes.
3. Be aware that DKA can occur with lower blood sugars and more rapidly in pregnancy.
4. List the differences in the pathophysiology and clinical manifestations of pregestational versus gestational diabetes.

Considerations

This pregnant woman at 32 weeks’ gestation presents with lethargy, hypotension, tachycardia, dry mucous membranes, hyperglycemia, and ketonuria. She has a 12-year history of type 1 diabetes. This is most likely diabetic ketoacidosis, which is a medical emergency. DKA can be difficult to diagnose during pregnancy. Note that this patient’s blood sugar is only 280 mg/ dL; pregnant diabetics can develop DKA with lower blood sugars and more rapidly than nonpregnant patients. The priority in this patient should be IV fluid infusion with two large bore IVs using an isotonic solution such as NS, since these individuals may have up to a 5-L deficit. This is the most important initial management. Arterial pH will confirm acidosis. Serum electrolytes should also be obtained especially to assess the potassium level and the anion gap. The management of DKA is similar to that of the nonpregnant patient: (a) IV fluid hydration, (b) correction of acidosis, (c) insulin to correct glucose (usually takes 6-10 hours), (d) correction of electrolyte and other metabolic abnormalities, and (e) treatment of the underlying etiology. The fetal pH is dependent on the maternal pH to clear excessive acids; the fetal pH is generally 0.1 units less than the maternal pH. Thus, maternal acidosis will cause fetal acidosis, which accounts for the late decelerations on the FHR tracing. The FHR pattern of late decelerations is a reflection of the maternal acidosis. Generally, correction of the maternal DKA will correct the FHR pattern as the fetal pH is normalized. Usually, it is an error to take the DKA patient for an emergency cesarean due to the late decelerations, since the acidosis is correctable, and these individuals are unstable. In this case, the baby is also preterm. The patient could suffer significant complications if rushed for an emergency surgery. Thus, as uncomfortable as it is, careful observation in the face of persistent late decelerations and quickly treating the maternal DKA is the best treatment course.

APPROACH TO:

Diabetes in Pregnancy                                          

DEFINITIONS

ANION GAP: Defined as Na–(Cl+HCO3). An abnormal AG > 12 mEq/ L. Possible causes include DKA, uremia, lactic acidosis, ethylene glycol or methanol ingestion, and salicylates.

DIABETIC KETOACIDOSIS: Life-threatening complication of diabetes in pregnancy associated with hyperglycemia and ketoacidosis that requires emergency treatment with insulin and intravenous fluids.

DKA IN PREGNANCY: Serious medical emergency with hyperglycemia, anion gap acidosis, and increased serum ketones. Lab values differ from a nonpregnant patient since the baseline acid base values are different (Table 27– 1).

GESTATIONAL DIABETES: Condition of hyperglycemia caused by insulin resistance that occurs during the pregnancy. There are two principal diagnostic criteria for this condition and no consensus about the best approach.

PREGESTATIONAL DIABETES: Condition of hyperglycemia which existed prior to pregnancy, and can be associated with type 1 or type 2 diabetes.

TYPE 1 DIABETES: Condition of absolute insulin deficiency leading to hyperglycemia, usually having its onset in the childhood or teen years.

TYPE 2 DIABETES: Condition of relative insulin deficiency due to insulin resistance leading to hyperglycemia. The absolute insulin levels are often normal or even increased.

 

WHITE CLASSIFICATION: System of characterizing diabetes in pregnancy using letters (A, B, C, D, F, H, etc) based on duration of disease and presence of end-organ dysfunction.

Table 27–1 • DIAGNOSTIC CRITERIA FOR DKA IN PREGNANCY

pH < 7.35 Blood sugar of 200 mg/dL or greater (rarely can be less) Serum ketones >5 mEq/L Often also serum bicarbonate level <18 mEq/L and ketonuria

CLINICAL APPROACH

Diabetes affects approximately eight million women annually and complicates approximately 1% of all pregnancies. Pregestational diabetes accounts for about 10% of cases, and gestational diabetes accounts for 90%. Because pregestational diabetes may cause high blood sugars at conception and during embryo organogenesis, pregestational diabetes is associated with miscarriage and congenital anomalies. In contrast, gestational diabetes is due to insulin resistance as a process of the pregnancy, and typically elevated glucose levels are not seen until the second trimester. Thus, gestational diabetics are not at risk for congenital anomalies or miscarriage. Additionally, pregestational diabetics are at risk for vascular and renal disease, whereas gestational diabetics do not have the same risk. Pregestational diabetics may be classified as type 1, which is an insulin deficiency (prone to DKA) and type 2 which is an insulin resistant.

Physiologic changes of pregnancy cause insulin resistance resulting in a need to adjust insulin dosing as the pregnancy progresses. (See Table 27– 2 for maternal and neonatal complications associated with diabetes in pregnancy.) Additionally, DKA is seen more often in the second and third trimesters. There are physiologic mechanisms to ensure the availability of glucose, the primary fuel source for the fetus; these mechanisms also decrease maternal utilization of glucose. The placenta produces diabetogenic hormones such as growth hormone, corticotrophin-releasing hormone, human placental lactogen (hPL), and progesterone which create an insulin-resistant state.

Table 27–2 • MATERNAL AND NEONATAL COMPLICATIONS OF DIABETES IN PREGNANCY
	Neonatal	Maternal
All diabetics (gestational and pregestational)	Birth injury NICU admission Hypoglycemia Hyperbilirubinemia Macrosomia Hydramnios Long-term: childhood obesity	Increased risk for cesarean Increased maternal lacerations and injury Preeclampsia Long-term: metabolic syndrome, overt diabetes
Pregestational diabetics	Congenital anomalies Growth restriction Miscarriage Prematurity	Worsening proliferative retinopathy Worsening nephropathy (if moderate/severe preexisting)

PREGESTATIONAL DIABETES

The White classification has been used in the past based on duration of disease and presence of end-organ dysfunction to predict maternal and fetal outcome. Today, this classification has proven to be less useful than categorizing the disease as type 1 (insulin deficiency) and type 2 (insulin resistance), and presence or absence of end-organ disease.

Fetal Risks

Diabetics with suboptimal glycemic control have higher rates of pregnancy loss, birth defects, preterm delivery, disturbances in fetal growth, and stillbirth. Longstanding diabetes, presence of vascular, hypertensive, or renal disease are particular risk factors for growth restriction. Fetal monitoring and intermittent ultrasound examinations for fetal growth are warranted. Fetal macrosomia can also be seen with maternal hyperglycemia. The incidence of fetal anomalies is a function of glucose control at conception and organogenesis (up to 8 weeks’ gestational age), correlating to the HbA1c level.

Maternal Risks

Women with pregestational diabetes often experience hyperglycemia during pregnancy. They are also at increased risk of chronic hypertension, preeclampsia, diabetic retinopathy, and cesarean delivery.

Diabetic retinopathy is the leading cause of blindness in reproductive age women. Diabetic retinopathy is often accelerated during pregnancy. Rapid changes in glucose control are associated with worsening retinopathy; for this reason, it is preferred that control be achieved prior to pregnancy in a gradual manner. Laser photocoagulation during pregnancy may be necessary.

Renal damage, with minimal preexisting disease, does not appear to be worsened by pregnancy. However, women with moderate-to-severe preexisting renal damage, such as creatinine levels exceeding 1.4 mg/ dL, microalbuminuria or proteinuria, often will experience a worsening of renal pathology and also develop hypertensive disorders.

Hypertensive disorders, both chronic hypertension and preeclampsia, are major complications of pregnant pregestational diabetics. Frequently, it is the severity of the hypertension that leads to morbidity and subsequent iatrogenic preterm delivery. In other words, the usual scenario necessitating preterm scheduled delivery involves markedly elevated blood pressures, or significant proteinuria. The incidence of preeclampsia increases with the number of risk factors of renal disease and/or retinopathy.

Management

Frequent physician visits are vital to monitor glycemic control. Fasting targets should be <105 mg/ dL and 1-hour postprandial targets <140 mg/ dL (or 2-hour postprandial sugars <120 mg/ dL). Those diabetics that are “brittle” and prone to dramatic swings from hyperglycemia to hypoglycemia may benefit from a less strict insulin regimen to avoid life-threatening hypoglycemia. Other monitoring usually includes:

Ophthalmologic evaluations every trimester and during the postpartum period.

• Detailed anatomy ultrasound and potentially a fetal echocardiogram during the second trimester.
• Fetal surveillance with antenatal testing and serial growth ultrasounds.
• If glycemic control is optimal, in the absence of comorbidities, delivery should occur between 38 and 39 weeks’ gestation.
• Women with suboptimal control should be delivered prior to 39 weeks after fetal lung maturity is confirmed.
• Route of delivery should be based on the estimated fetal weight (EFW) by ultrasound and most would agree that elective cesarean delivery should be considered in diabetics with EFW of >4500 g due to the potential for shoulder dystocia.

Glycemic control is critically important during labor and delivery. Maternal hyperglycemia can lead to neonatal hypoglycemia after birth. Infants born with neonatal hypoglycemia are more likely to have neurodevelopmental delay. Insulin therapy should be titrated to achieve and maintain glucose levels between 80 and 110 mg/ dL.

Preconception Counseling

Preconception counseling can optimize pregnancy outcome as well as maternal well-being. A detailed history and physical examination including baseline laboratory testing should be completed to assess the disease severity. Effective contraception should be offered to delay conception until diabetic control is optimized. A glycosylated hemoglobin level (HbA1c) <7% correlates to neonatal morbidity and mortality rates similar to the general population. In contrast, those with HbA1c levels >10% experience rates of congenital anomalies (typically cardiac, skeletal dysplasias, and neural tube defects) as high as 20% to 25%. Folate supplementation is extremely important to decrease the risk of NTDs. Other important tests include: thyroid and renal function, 24-hour urine for protein, and an ophthalmological examination for retinopathy. ACE inhibitors should be discontinued prior to conception, since they are associated with teratogenicity.

Diabetic Ketoacidosis (DKA)

DKA is a serious medical emergency associated with a fetal loss rate of up to 25% and maternal mortality rate of about 1%. The diagnostic criteria are different from that of nonpregnant patients (see Table 27– 1), and the diagnosis is more difficult to reach in pregnant women. Although its prevalence is higher in patients with type 1 diabetes, ketoacidosis may also occur in patients with type 2 diabetes or even with gestational diabetes. DKA occurs more in the second and third trimesters since serum hPL levels are higher. It can occur with blood glucose levels as low as 200 mg, and should be suspected with an arterial pH of <7.35.

DKA usually develops as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counterregulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesis, glycogenolysis, and lipolysis. In pregnancy, several physiological factors predispose to DKA:

• Increased counterregulatory hormones including hPL, progesterone, and cortisol which cause insulin resistance.
• Decreased serum bicarbonate levels to compensate for the primary respiratory alkalosis, which reduces the buffering capacity.
• Increased tendency for ketosis with increased lipolysis and free fatty acids and ketones.

Precipitating factors include emesis, infection, noncompliance or unrecognized new onset of diabetes, and maternal steroid use. Signs and symptoms are similar to those in the nonpregnancy state; however, they also may mimic normal symptoms of pregnancy (Table 27– 3). Because of the high risk of morbidity and mortality, and subtle findings, every diabetic pregnant woman who has vague complaints should be assessed for DKA by checking blood sugar and urine for ketones.

Aggressive and early resuscitation is the key to effective management of DKA. Fluid replacement should begin with 1 to 2 L of isotonic saline during the first hour followed by 300 to 500 mL/h of normal saline. As glucose levels approach 250 mg/dL, 5% dextrose may be added. Insulin therapy should also be initiated as soon as the diagnosis is made. An appropriate loading dose of regular insulin is 0.2 to 0.4 U/ kg regular insulin followed by continuous insulin infusion of 6 to 10 U/ h. When glucose levels approach 200 to 250 mg/dL, the insulin infusion rate may be decreased to 1 to 2 U/ h.

Electrolyte replacement should be provided as needed. Inevitably, the total body potassium is depleted, even though the serum potassium may be normal or even elevated due to the shifting of potassium extracellularly as the excess hydrogen ions move intracellularly. If serum potassium is elevated, potassium replacement should be provided at 20 mEq/h after urine output is established. If serum potassium is below normal, replacement should be initiated immediately at the above rate. Serum magnesium and phosphorus levels should be evaluated and provided as needed.

Table 27–3 • SYMPTOMS AND SIGNS OF DKA IN PREGNANCY

General: Malaise, weight loss CNS: Headache, confusion, or lethargy Volume: Dehydration, excessive thirst, dry mouth GI: Abdominal pain, nausea, and vomiting Renal: Polyuria/polydipsia, oliguria Metabolic: Shortness of breath

The fetal heart rate pattern will often exhibit loss of variability and late decelerations due to the maternal acidosis. This will almost always correct with resolution of the DKA. Delivery of the fetus for heart rate abnormalities should not be performed unless the abnormalities are persistent even after maternal stabilization.

GESTATIONAL DIABETES

Diagnosis

There has been much debate about whether diabetic screening should be selective or universal, and which screening test to use. Selective screening based on risk factors would reduce the number of women requiring screening by 10% to 15%, however, it would fail to identify one-third to one-half of affected individuals. For this reason, the American College of Obstetrics and Gynecology (ACOG) supports universal screening in all persons except those deemed to be at low risk. Many practitioners perform early screening at 16 weeks’ gestation for those at high risk for diabetes, and repeated at 26 weeks. Routine screening is usually performed at 26 to 28 weeks’ gestation.

Traditional diagnostic strategy (two steps): A two-step approach has been recommended in order to identify women with GDM. The first step involves a 50-g 1-hour screening test, and the second step utilizes a 100-g 3-hour diagnostic test for those women identified via the initial screening test. The threshold for an abnormal 1-hour test varies from 130 to 140 mg/ dL depending on the practice’s philosophy of false positive and false negatives. The diagnosis of gestational diabetes depends on noting two abnormal values on the 100-g 3-hour test with variations on the cutoffs. Common thresholds are as follows:

• Fasting: 95 to 105 mg/ dL
• 1 hour: 180 to 190 mg/ dL
• 2 hours: 155 to 165 mg/ dL
• 3 hours: 140 to 145 mg/ dL

IADPSG diagnostic strategy (one step): The new International Association of Diabetes in Pregnancy Study Group (IADPSG) supports the use of a 2-hour 75-g diagnostic test utilizing values concurrent with fasting, 1- and 2-hour values. A positive result requires at least two abnormal values (Table 27– 4). The American

Table 27–4 • DIAGNOSTIC CRITERIA FOR GESTATIONAL DIABETES
	Traditional 3-h 100-g GTT (mg/dL)	International Association of Diabetes in Pregnancy Study Groups (IADPSG) 2-h 75-g GTT (mg/dL)
Fasting	95-105	92
1 h	180-190	180
2 h	155-165	153
3 h	140-145

Diabetes Association recognizes this as an acceptable option although at this time, the 100-g test is generally used in the United States. In 2008, the hyperglycemia and adverse pregnancy outcome (HAPO) trial published its findings of maternal and fetal implications of maternal hyperglycemia less than that which is diagnostic for diabetes. The HAPO trial utilized a one-step diagnostic process with a 75-g 2-hour test. They found a linear relationship between maternal glucose levels and adverse outcomes, even at glucose concentrations below those that are usually diagnostic of GDM. The results of this study are likely to alter not only classification criteria for GDM but are also likely to modify treatment modalities.

Those who have not adopted the IADPSG diagnostic strategy claim that up to 13% to 15% of pregnant women would be diagnosed with diabetes using the 2-hour 75-g test, and that there are not yet prospective randomly controlled trials to show that using this new criterion leads to improved outcomes.

Risk factors for GDM for developing gestational diabetes including age >25 years, belonging to an ethnic group with an increased risk for the development of type 2 diabetes, obesity, and prior macrosomic infant.

Treatment options: Diet is the first line of therapy for GDM. For those patients who fail dietary treatment, insulin is the gold standard for diabetes therapy, although the use of glyburide, an oral hypoglycemic agent, has been found to be effective in select patients. Targets for glucose control include fasting glucose of 90 to 105 mg/ dL and 1-hour postprandial glucose of <140 mg/ dL. Potential maternal and fetal complications are summarized in Table 27– 2.

Postpartum management: All women diagnosed with GDM should be screened for overt diabetes mellitus using a 75-g oral glucose tolerance test at 6 weeks’ postpartum. Fasting glucose levels > 126 mg/ dL or 2-hour values > 200 mg/ dL are diagnostic for diabetes mellitus. Contraception options are very important to consider in this population as we know that recurrent pregnancies in a woman with GDM increases her risk for overt diabetes mellitus (see Case 44).

Breast-feeding should be encouraged for both infant and maternal benefits. Breast-feeding is associated with a greater decrease in maternal weight, which may reduce their risk of developing type 2 diabetes.It may also decrease the risk of childhood obesity and the development of diabetes mellitus compared to formulafed infants.

Controversies

• Oral hypoglycemic medications in pregnancy are being used with some success. More research needs to be performed to understand its exact role.
• Patients in whom the estimated fetal weight exceeds 4500 g should be offered cesarean delivery in order to decrease risk of traumatic delivery.
• Carpenter and Coustan diagnostic criteria for the 3-hour 100-g OGTT are recommended by the Fourth and Fifth International Workshop-Conference of GDM and endorsed by ACOG; however, these expert bodies recognize that the 2-hour 75-g diagnostic criteria tests are acceptable.
• Further data in pregnancy are needed before the use of metformin for the treatment of GDM can be recommended.

CASE CORRELATION See also Case 4 (Shoulder Dystocia) to review the two main risk factors for shoulder dystocia (macrosomia and diabetes), Case 19 (Parvovirus Infection in Pregnancy) since diabetes and parvovirus are two causes of hydramnios, and Case 22 (IUGR) (pregestational diabetes is a cause for IUGR).

COMPREHENSION QUESTIONS

27.1 A 36-year-old G2P1001 woman presents for her initial prenatal visit at 6 weeks’ gestation. She has a 9-year history of type 2 diabetes mellitus which is managed with oral hypoglycemic medications. Which of the following is the best indicator for fetal outcome of the pregnancy?

A. Blood sugar value in the office

B. Hemoglobin A1c value

C. Nuchal translucency on ultrasound

D. Umbilical artery Doppler studies at 18 weeks’ gestation

27.2 A 32-year-old G3P2002 female presents for her postpartum visit. Her obstetrical history is significant for GDM with her last pregnancy only ending in a term delivery of a 7 lb (3 kg) infant, 8 weeks ago. Her body mass index (BMI) is 24 kg/m2. Besides the routine examination and Pap smear, what is your next step regarding this patient?

A. Recommend fasting glucose and HbA1c every 3 years

B. Recommend 3-hour 100-g GTT if she has a first-degree relative with DM

C. Recommend 2-hour 75-g GTT at this time

D. No intervention due to her optimal BMI

27.3 A 21-year-old G1P0 woman at 11 weeks’ gestation is seen in the emergency center complaining of nausea, vomiting, abdominal pain, and fatigue. The patient is a known diabetic since age 12 years and has been in good control. On examination, her BP is 90/ 60 mm Hg, HR 120 beats per minute, and RR 28 per minute. The arterial blood gas reveals a pH of 7.28, pO2 of 100 mm H g, pCO2 of 22 mm H g, and bicarbonate level of 12 mEq/ L. Which of the following is the best management of this patient?

A. Administer 2 L of normal saline intravenously

B. Infuse two ampules of bicarbonate IV

C. Obtain a spiral computed tomography scan to assess for pulmonary embolism

D. Obtain an ultrasound for a possible concealed abruption

27.4 A 31-year-old woman is diagnosed with gestational diabetes based on two abnormal values on a 3-hour 100-g GTT. She is at 28 weeks’ gestation. The patient is concerned about the risks of congenital anomalies after she has read about the adverse effects of diabetes on the Internet. What is your response to this patient?

A. Your risk of fetal congenital anomalies is essentially the same as the general population since this is GDM.

B. We can draw an HbA1c test at this time, and your risk of fetal anomalies depends on the HbA1c result.

C. Tight glucose control from this point onward and during labor and delivery will determine the risk of congenital anomalies.

D. The majority of GDMs had normal glucose levels at conception and no increased risk of fetal anomalies.

ANSWERS

27.1 B. The hemoglobin A1c value correlates with the risk of fetal anomalies and fetal morbidity. An optimal HbA1c is <7% and the fetal risks approach the general population with this value. In contrast, an HbA1c of 11% corresponds to a risk of fetal anomalies as high as 25%. Nuchal translucency is one factor used to identify an increased risk of Down syndrome. Umbilical Dopplers are used in the evaluation of IUGR and fetal anemia.

27.2 C. All women with gestational DM should have a screening test at 6 weeks’ postpartum for overt diabetes. The 2-hour 75-g GTT test is probably the optimal test for these individuals.

27.3 A. This patient likely has diabetic ketoacidosis. Pregnancy will often cause diabetes to become more difficult to control. The pH is acidotic, whereas the normal pH in pregnancy is slightly alkalotic. Together with the low bicarbonate level, this is consistent with an anion gap metabolic acidosis. The patient’s oxygenation is good, and thus, a pulmonary embolus is not suspected. The pCO2 is lower than the normal 28 mm H g seen in pregnancy, which is indicative of partial respiratory compensation. The blood sugar is likely to be elevated. The cornerstones of management of DKA include IV fluid hydration, insulin intravenous drip to control the blood sugars and correct the acidosis, correction of metabolic abnormalities such as hypokalemia, hypophosphatemia, or hypomagnesemia, and addressing the etiological factor.

27.4 D. The vast majority of those patients with gestational diabetes are true gestational diabetics, and their glucose levels at conception and at organogenesis were normal; this means the risk of congenital anomalies were the same as the general population. However, a small fraction of the “so-called GDM” were type 2 pregestational diabetics who were not detected. In this setting, there could have been hyperglycemia at conception.

    CLINICAL PEARLS    

» Diabetic retinopathy or nephropathy may worsen during pregnancy and regular monitoring is warranted. » Preeclampsia rates may be as high as 50% in some diabetic gravidas. » HbA1c levels <7% prior to conception is associated with neonatal morbidity and congenital anomaly rates are comparable to the general population. » HbA1c levels >10% prior to conception are associated with neonatal morbidity rates as high as 25%. » The most common congenital anomalies associated with pregestational diabetes are cardiac and neural tube defects. » DKA occurs more rapidly and at lower serum glucose levels during pregnancy compared to outside of pregnancy. Different DKA diagnostic criteria are used for pregnant women. » Neonatal hypoglycemia can occur especially with maternal hyperglycemia during labor and delivery. Thus, tight control of maternal glucose during labor is crucial. » Risks factors for GDM include maternal obesity, family history, polycystic ovarian syndrome, previous gestational diabetes, fetal macrosomia or unexplained fetal or neonatal demise. » There is debate about the best diagnostic criteria for diagnosing GDM. » All women with GDM should be screened for overt diabetes at 6 weeks’ postpartum. » Glyburide is considered a safe alternative to insulin for treatment of GDM. » Most patients with GDM can be managed with diet alone, and when diet is inadequate, then insulin or oral therapy is used.

REFERENCES

ACOG Practice Bulletin. Gestational diabetes: clinical management guidelines for obstetriciangynecologists. Number 137; 2013 (level III). 

ACOG Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists. Number 60, March 2005. Pregestational diabetes mellitus. Obstet Gynecol. 2005;105:675-685. (Reaffirmed 2014.) 

Coustan DR. Pharmacological management of gestational diabetes: an overview. Diabetes Care. 2007;30(Suppl 2):S206-S208 (level III). 

Diagnosis and classification of diabetes mellitus. Diabetes Care. 2006;29(Suppl 1):S43-S48. 

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Metzger BE, Lowe LP, Dyer AR, et al. H yperglycemia and adverse pregnancy outcomes. N Engl J Med. 2008;358(19):1991-2002 (level I). 

Moore TRCP. Diabetes in pregnancy. In: Creasy RK RR, Iams JD, Lockwood CJ, Moore TR, eds. Creasy and Resnik’s Maternal-Fetal Medicine, Principles and Practice. Philadelphia, PA: Saunders Elsevier; 2009. 

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