According to the Centers for Disease Control and Prevention (CBC) in 2016, there are 29 million Americans living with diabetes and another 86 million with insulin resistance or prediabetes.¹ The rapid increase in patients with this disease spectrum is especially relevant in our patient population, given pregnancy’s inherent insulin resistance and the role that this can play in maternal and fetal morbidity and mortality. More than 6% to 7% of deliveries are now occurring in patients with either pregestational diabetes or gestational diabetes mellitus (GDM).² To care for these patients safely, the OB/GYN providers must be familiar with the common complications of diabetes during pregnancy as well as the antepartum, intrapartum, and postpartum management of patients with all classifications of diabetes (Fig. 24-1).

Apart from the associated complications surrounding delivery, as elaborated upon in the section entitled “Intrapartum Considerations,” later in this chapter, pregnant patients with diabetes are at higher risk of developing multiple pregnancy-related complications, including infection (e.g. pyelonephritis, influenza), preeclampsia, venous thromboembolism (VTE), cardiovascular disease (CVD), and diabetic ketoacidosis (DKA). They are also at higher risk of exacerbating diabetes-related complications like retinopathy and nephropathy.

Ideally, gravid diabetic patients will have been started on low-dose aspirin after 12 weeks of gestation to decrease the risk of developing preeclampsia;^4–6 however, they will still have up to a fourfold higher risk of developing this morbid disease.⁷ Furthermore, this risk is closely correlated to their level of glycemic control.⁸ Thus practitioners should have a high level of suspicion for preeclampsia if patients present with headache, visual changes, right-upper-quadrant pain, epigastric pain, or worsening peripheral edema. Complicating the diagnosis of preeclampsia is the fact that diabetics have varying levels of baseline proteinuria prior to pregnancy. Evaluating for an acute elevation in proteinuria in comparison to baseline levels obtained early in pregnancy may be beneficial.⁹ The risk of preeclampsia is even higher in the setting of concomitant diabetes and chronic hypertension. Optimization of chronic hypertension using modalities other than angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers is imperative.¹⁰

Pregnancy and diabetes are both independent risk factors for deep venous thrombosis (DVT) and pulmonary embolism.^11,12 Thus for patients presenting with concerning symptoms for VTE such as asymmetric lower-extremity edema, new-onset dyspnea, or pleuritic chest pain, practitioners should have a lower threshold for initiating a diagnostic workup.

Diabetes is a strong risk factor for CVD, and this is especially relevant given that that is now the leading cause of pregnancy-related mortality.¹³ Physiologic changes during pregnancy lead to volume overload, increased cardiac output, and increased heart rate, all of which may reveal or overwhelm a previously well compensated defect caused by diabetes-related vascular disease.¹⁴ Practitioners should have a higher level of suspicion for peripartum cardiomyopathy and myocardial infarction if diabetic pregnant patients present with concerning cardiac symptoms. Further, if patients were taking a statin prior to pregnancy, this should have been discontinued as soon as pregnancy is confirmed.

Maternal hyperglycemia is associated with up to a threefold increase in the rate of spontaneous abortion,^15,16 a fivefold increase in preterm delivery, and a fourfold increase in intrauterine fetal demise.^17,18 The overall fetal death rate is further increased when fetal birth weight is >4250 g.¹⁹ Diabetes during pregnancy is also associated with a threefold-to-eightfold increase in fetal malformations, with neural tube defects and congenital heart diseases being the most common.^17,20 Importantly, the severity of hyperglycemia—especially during the first trimester—is correlated with an increased incidence of these complications, and therefore expedited normalization of sugars may reduce morbidity (Fig. 24-2).

Furthermore, as excess glucose in the maternal bloodstream crosses the placenta, fetal hyperinsulinemia acts as a growth hormone and can lead to macrosomia through increased fetal adipose deposition, which is associated with an increased risk for shoulder dystocia and birth trauma.²¹ This may include fractures of the clavicle and humerus as well as nerve palsies.^15,22

Polyhydramnios is 30 times more common in patients with diabetes and can occur in 3% to 32% of pregnancies. It is thought to occur secondary to fetal polyuria from an increased fetal glycemic load, decreased fetal swallowing, or fetal gastrointestinal obstructions. In gestational diabetics, polyhydramnios has been correlated with a fivefold higher risk of stillbirth, in addition to higher proportions of large-for-gestational age infants, macrosomia, neonatal respiratory distress, and neonatal jaundice.²³ In pregestational diabetics, polyhydramnios has been associated with increased risks of preterm delivery and cesarean section (C-section).²⁴

While fetal macrosomia is more common, intrauterine growth restriction (IUGR) also occurs with significant frequency. It is more common in type 1 and long-standing type 2 diabetic mothers, and is thought to arise from placental insufficiency in the setting of maternal vasculopathy. Antepartum fetal monitoring, as well as umbilical and uterine artery Doppler studies, can guide the surveillance and timing of delivery in these pregnancies.²⁵

Following delivery, neonates born to diabetic mothers have increased risk of hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia, respiratory distress syndrome, and need for neonatal intensive care.^26,27 However, the complications do not end in the neonatal period. Children born to diabetic mothers are also predisposed to metabolic syndrome and glucose intolerance later in life,^28,29 and 15-year follow-up studies have found a negative influence on intellectual and psychomotor development.³⁰

Treatment of GDM has been associated with a significant reduction in the rate of composite perinatal outcomes (perinatal death, shoulder dystocia, and birth trauma). It has also been associated with a decreased frequency of large-for-gestational age infants from 22% to 13%, and decreased risk of preeclampsia from 18% to 12%.³¹

Classics signs and symptoms of pregestational diabetes include polydipsia, polyuria, and unexplained weight loss. Patients that present with any of these symptoms and a random plasma glucose level of >200 mg/dL meet the diagnosis of diabetes.³ However, frequently the clinician’s suspicion may be elevated in the circumstance of an incidental finding of glucosuria or an elevated serum glucose level. These diagnostic criteria are based on criteria from the American Diabetes Association (ADA)³, shown in Figure 24-3.

For the diagnosis of GDM, all pregnant women should be routinely screened between 24 and 28 weeks of gestation, and possibly sooner in the first trimester if they have risk factors (see Fig. 24-4). While historically, a 2-hour oral glucose tolerance test (OGTT) was performed, it is now recommended that testing first begin with a 1-hour OGTT. During a 1-hour OGTT, a 50-g load of glucose is given to a nonfasting patient. If the patient screens positive, a diagnostic 3-hour OGTT will be performed. Choosing a screening threshold serum glucose level ≥140 mg/dL will identify 80% of patients with GDM, while a threshold of ≥130 mg/dL will be more sensitive and identify 90% of patients with GDM, but that also will have a higher false positive rate.³² Notably, if the glucose level is ≥200, a diagnosis of GDM can be made without having to proceed with a 3-hour OGTT. Criteria for the diagnosis of GDM via 3-hour OGTT can be found in Figure 24-5. Classically, two out of the four values had to be abnormal for diagnosis; however, given the risks for adverse perinatal outcomes, diagnosis may be considered if even one level is abnormal.³³ Finally, if an OGTT is performed while someone is an inpatient, be sure that it is delayed at least 7 days following betamethasone (BMZ) administration.

Admission to the hospital for glycemic control during pregnancy often occurs in order to expedite the normalization of plasma glucose levels and establish an appropriate insulin regimen. Not only is this important for reducing long-term fetal and maternal morbidity but it may be critical in preventing mortality.

DIABETIC KETOACIDOSIS

Diabetic ketoacidosis (DKA) is one of the most dangerous complications of diabetes during pregnancy, and it warrants immediate hospital admission to avoid maternal and fetal mortality. With improved treatment strategies and patient education, maternal mortality has continued to decrease to approximately 1%; however, fetal mortality over the last decade has ranged from 9% to 35%.^2,34–37 While DKA is well known to occur in type I diabetics, it can still occur in type 2 diabetics and gestational diabetics. An important consideration in patients who present in DKA is latent autoimmune diabetes in adults (LADA), a slow-progressing form of autoimmune diabetes which may include about 25% of women under 35 years old who were presumed to have type II diabetes.³⁸ Finally, practitioners should have a high level of suspicion for DKA in pregnancy, given that up to 30% of cases occurred in patients not previously known to have any diagnosis of diabetes.³⁵ Notably, DKA is more likely to occur during the second and third trimesters.^39,40

DKA is caused by relative or absolute insulin deficiency that leads to severe hyperglycemia and glucosuria, which causes osmotic diuresis. This diuresis leads to dehydration and urinary electrolyte loss. The insulin deficiency also leads to lipolysis and hepatic oxidation of fatty acids, which leads to ketosis and metabolic acidosis. Interestingly, while DKA is typically characterized by grossly abnormal glucose levels (>300 mg/dL), during pregnancy, DKA can occur with only mildly elevated glucose levels, or even normal glucose levels.^41,42

Thus if one cannot rely on glucose levels to raise suspicion, the clinician should be on alert for the following signs and symptoms: nausea, vomiting, poor oral intake or dehydration, weakness, polyuria, fever, hyperventilation (often accompanied by a fruity odor on the patient’s breath), blurry vision, altered mental status, or maternal tachycardia.⁴³ In fact, one of the most common precipitating events for DKA is emesis itself. Other precipitating factors for DKA include infection, diabetic gastroparesis, poor compliance with therapy or insulin pump failure, use of β-sympathomimetic agents (for tocolysis) or corticosteroids, or physician management error.⁴⁴

Laboratory findings of hyperglycemia, acidosis, and ketonemia are typically present. Acidosis is confirmed when the pH on an arterial blood gas (ABG) is <7.3. In addition, the ABG will often reveal an elevated base deficit and anion gap >12 mEq/L secondary to an abnormal elevation of the unmeasured anions, such as ketoacids and lactic acid. Ketonemia is confirmed by evaluating for urine and/or serum ketones (3-β-hydroxybutyrate). Finally, serum bicarbonate levels are often decreased to <15 mEq/L; sodium, potassium, and phosphate levels may be abnormal; and the blood urea nitrogen and creatinine may be elevated in the setting of dehydration or renal failure.⁴³ Laboratory assessment should be repeated every 1 to 2 hours as needed in severe cases.⁴⁵

Initial management is hallmarked by volume replacement as well as correction of hyperglyclemia and electrolyte abnormalities. The primary insult leading to DKA should be established and treated if necessary (e.g. sepsis), and a multidisciplinary team including a maternal fetal medicine (MFM) specialist, anesthesiologist, general internist or endocrinologist, and often intensive care team members should be mobilized. Importantly, recommendations for early management are almost identical to that of nonpregnant patients.

Immediate resuscitation with intravenous (IV) 0.9% sodium chloride is started at a rate of 1000 mL/hour for the first 1 to 2 hours, and a Foley catheter should be placed to strictly monitor urine output (goal > 0.5 mL/kg/hour).⁴³ A simple way of estimating a patient’s fluid deficit is by calculating 100 mL/kg of body weight. This is often between 4 and 10 L.⁴⁶ After the first 1 to 2 hours, the rate can be decreased to 250 to 500 mL/hour with the goal of correcting 75% of the fluid deficit over a 24-hour period. If hypernatremia occurs, 0.45% normal saline can be used instead of isotonic saline. Once the serum glucose levels are <250 mg/dL (14 mmol/L), isotonic saline should be switched to 5% dextrose. Once the glucose levels normalize, continue fluid repletion until the fluid deficit is met as calculated previously. Note that in patients whom DKA was provoked by sepsis (especially pyelonephritis), the risk of acute respiratory distress syndrome is elevated.⁴⁷ Thus practitioners should maintain a high level of suspicion for the development of pulmonary edema or acute respiratory distress syndrome (ARDS), and fluid status should be managed vigilantly.

During repletion, if the patient is becoming hyperchloremic, switching to a more physiologic fluid like PlasmaLyte can help to prevent hyperchloremic acidosis.⁴⁸ Note that even with normal serum potassium levels, often the total body potassium is low, and upon administration of insulin, potassium will be driven intracellularly. Thus in this acute setting, consider evaluation and repletion of electrolytes frequently, with the goal of maintaining a potassium level between 4 and 5 mEq/L, and a phosphate level >1 mg/dL (although normal is 2.8–4.6 mg/dL). Repletion of calcium and magnesium is debatable, and repletion with bicarbonate to correct acidosis is also controversial. One may consider adding one ampule (44 mEq) of bicarbonate to 1 L of 0.45% normal saline in settings when the pH is <7.1 or in patients complicated by cardiac dysfunction, sepsis, or shock.^43,45

A regular insulin drip can be initiated starting with a 0.1-U/kg bolus, and followed by a 0.1-U/kg/hour rate. If glucose levels do not fall by 50 to 75 mg/dL over the first hour, consider doubling the hourly infusion rate. Even upon normalizing the serum glucose levels, continue the insulin drip at a rate of 1 to 2 U/hour until the ketosis and acidosis resolves, because it is the intracellular hypoglycemia that drives the counterregulatory hormone activity, and thus the ketoacidosis.

Euglycemia is defined as consistent fasting blood sugar levels of 60 to 90 mg/dL (3.3–5.0 mmol/L), preprandial levels of 60 to 105 mg/dL (3.3–5.8 mmol/L), 1-hour postprandial levels less than 140 mg/dL (7.8 mmol/L), 2-hour postprandial levels less than 120 mg/dL (6.7 mmol/L), and levels between 2 and 4 am glucose <60 mg/dL (3.3 mmol/L).^49,50 Thus after the hyperglycemia acidosis resolve, a subcutaneous insulin regimen will need to be either titrated or established. Deciding upon a proper insulin regimen should be individualized and factors including body weight, body fat, physical activity, insulin sensitivity, blood glucose levels, and target blood glucose should be taken into account.⁵¹ Insulin dosage is usually determined based on body weight (insulin U/kg), and is discussed in more detail later in this chapter. Once the appropriate regimen has been established and the first subcutaneous dose of insulin is administered, the insulin drip can be discontinued.⁴²

During DKA, continuous fetal heart rate (FHR) monitoring should be initiated for gestational ages >24 weeks gestation. However, FHR abnormalities are common while both the mother and fetus are in an acidotic state. When considering delivery for a nonreassuring FHR tracing, the risks and benefits must be carefully weighed, in that the patient may be unstable and operative intervention can result in increased risk of maternal death. Furthermore, neonatal morbidity is higher when delivering a preterm infant and when the infant is in a severely acidotic state. If the metabolic abnormalities are corrected, both the maternal and fetal status will likely improve over the next 4 to 8 hours.^2,52 However, if the fetal status is not improving or maternal condition continues to deteriorate, delivery is warranted.

HYPEROSMOLAR HYPERGLYCEMIC STATE

Hyperosmolar hyperglycemic state (HHS) can have a similar presentation; however, it is characterized by extreme hyperglycemia (≥1000 mg/dL) and hyperosmolality (≥320 mOsm/kg) without development of ketoacidosis. A total of 25% to 50% of patients also have neurologic findings, and other common laboratory findings include an elevated blood urea nitrogen (BUN)–to-creatinine ratio and bicarbonate >15 mEq/L. There can be low-level ketonemia/ketonuria. Infection is the leading precipitating factor of HHS (about 60% of cases). Inadequate fluid intake during the acute illness combined with the ensuing stress response can decrease the effectiveness of circulating insulin and lead to significant hypertonic osmotic diuresis and dehydration. The management is very similar to DKA and the mainstays should include treating the underlying cause, providing aggressive IV hydration, insulin therapy, and electrolyte replacement.^53,54

Similar to the euglycemic levels discussed previously, actual glycemic targets for pregestational diabetics include fasting, premeal, and bedtime levels between 60 and 99 mg/dL (3.3–5.4 mmol/L), peak postprandial levels of 100 to 129 mg/dL (5.4–7.2 mmol/L), and hemoglobin A1c levels <6.0. For gestational diabetics, targets include preprandial levels <95 mg/dL (5.3 mmol/L), 1-hour postprandial levels <140 mg/dL (7.8 mmol/L), and 2-hour postprandial levels <120 mg/dL (6.7 mmol/L).^30,55 ACOG’s recommendations for pregestational diabetic targets are less stringent and reflect those of the gestational diabetic targets given previously.⁴⁵

ADMISSION FOR GLYCEMIC CONTROL

For less severe levels of hyperglycemia, there is no expert consensus or clear evidence to support recommendations regarding what glucose levels warrant admission to the hospital for glycemic control. The decision must be individualized and take into account the severity of abnormal glucose levels, the gestational age, comorbidities, access to care, and predicted compliance. However, OB providers face this scenario often, and so they must understand how to initiate and titrate insulin therapy in the hope of decreasing maternal and fetal morbidity and mortality.

While occasionally an insulin drip is started and titrated to calculate the insulin requirements during a 24-hour period, it is common to start a weight-based, subcutaneous insulin regimen. While basal-bolus regimens are the most commonly used, many types of insulin regimens can be employed.^51,56 However, before these regimens can be understood, one must have a thorough understanding of the types of insulin.^50,51,57

Figures 24-6 and 24-7

The initial dosing decision and the titration of insulin are primarily based on gestational age and current weight. However, individualized considerations also should take into account the patient’s response to interventions such as diet or exercise. During pregnancy, progressive insulin resistance, increased weight gain, and decreasing physical activity will cause insulin requirements to grow progressively. In fact, insulin requirements may double or triple during the course of pregnancy.³⁰ It is also notable that obese women may require higher insulin dosages to start, that no more than 50 units of insulin should be administered in one site because it has decreased or delayed absorption, and that the preferred site for injection is the subcutaneous layer of the abdomen to maximize absorption.⁵⁸

Figure 24-8 features the steps recommended by the American Diabetes Association (ADA) in calculating insulin dosing for women with GDM if more than one-third of her fasting values are >90 and <120 mg/dL or more than one-third of postmeal values are >130 and <180 mg/dL.⁵⁹ If a patient’s GDM is poorly controlled, or the patient has type 1 or 2 diabetes, proper steps in calculating insulin dosing can be found in Figure 24-9.³⁰ Notably, these recommendations by Jovanovic, Kitzmiller, and Coustan are held by the ADA and the California Diabetes and Pregnancy Program (CDAPP) Sweet Success Program (Fig. 24-9);^60,61 however, many institutions are familiar with Gabbe’s more simplified recommendations (Fig. 24-10).⁶² Ultimately, regardless of the initial regimen that is chosen, insulin levels will often need to be adjusted and individualized. Once a starting total insulin dose has been determined, the total daily doses should not be adjusted by more than 10% at a time. Postmeal insulin sliding scales are never recommended because they lead to overtreatment without avoiding fetal exposure to hyperglycemia.⁶³

While discussing every consideration for choosing an insulin regimen is beyond the scope of this chapter, a few other notes are important to make here. Normal pressure hydrocephalus (NPH) is still the recommended standard for basal insulin.^30,56 In comparison to NPH, some practitioners are starting to favor glargine, given it has been associated with less pregnancy hypertension, microalbuminuria and macroalbuminuria, hypoglycemic episodes, neonatal intensive care unit (NICU) admissions, fetal death, jaundice, and fetal malformations in one study.^64,65 However, in a meta-analysis, there were no differences in outcomes between long-acting insulin and intermediate-acting insulin.⁶⁶ In the most recent research, Negrato and colleagues again reviewed 17 studies in 2012, looking at more than 1000 pregnant patients that had been treated with the long-acting analogs, and did not find any increase in maternal or neonatal morbidity. Ultimately, they encourage the use of long-acting agents but desire more conclusive safety profiling before recommending them over the gold standard treatment during pregnancy.⁵⁰ Finally, the use of nonimmunogenic insulins is preferred.^50,67,68

ORAL HYPOGLYCEMICS

Often, oral hypoglycemic agents (OHAs) will not be initiated by an OB hospitalist, given the circumstances in which their use is typically recommended. However, an understanding of these medications and their adverse effects is imperative. The appeal of these agents stem from their pharmacology, route, cost, and decreased risk of hypoglycemia; however, these benefits must be balanced with their risk of maternal hyperglycemia, maternal side effects, transplacental passage with potential for teratogenicity, and postpartum implications, including breastfeeding.^69–71

The two most common classes of oral agents used in pregnancy include insulin secretagogues (e.g. glyburide), and insulin sensitizers (e.g. metformin). There are some smaller studies where α-glucosidase inhibitors have been evaluated; however, all other classes of OHAs either have no evidence to support their use, or else evidence recommending against their use. Figure 24-11 highlights the pharmacology, effectiveness, safety, and dosing of such medications.^{69,70,72–75} Notably, insulin remains the preferred agent for treating diabetes in pregnancy, and patients with type 1 or long-standing type 2 diabetes are not candidates for oral therapies, given residual pancreatic β-cell function is required.

INSULIN PUMPS

In reliable and motivated patients, insulin pumps are more convenient and may improve glycemic control. This is especially true in patients with recurrent hypoglycemia or a prominent dawn phenomenon, given that they can be programmed to infuse varying levels of both basal and bolus insulin and can be titrated based off carbohydrate counting.³⁰ However, in comparison to basal-bolus regimens as described previously, the evidence has found no difference in macrosomia, operative births, C-section rates, DKA, or perinatal outcomes.^76,77 Usually, 50% to 60% of the total daily dose is administered at a continuous basal rate, with 40% to 50% administered as boluses before meals and snacks.⁷⁸ Importantly, patients and practitioners should be vigilant for pump-tubing occlusion or infusion set leakage, especially as their body changes to accommodate the growing fetus.

Unfortunately, insulin pumps can become a conundrum when patients are admitted to the hospital. To rely on the glucose readings from patients’ monitors and allow patients to administer their own insulin creates liability and quality assurance issues; thus the use of insulin pumps may be either discouraged or not allowed. If a patient using continuous subcutaneous insulin infusion (CSII) is admitted, check with your hospital’s policy regarding its use. If CSII is allowed, as with all basal-bolus regimens, the patient and staff must be educated in carbohydrate counting with hospital meals to decrease hypoglycemia or hyperglycemia. If there is a need to convert to a basal-bolus regimen in the hospital, interrogate the patient’s pump to find the average doses that have been given recently, and individualize the treatment based on the patient’s condition and hospital diet. Further information regarding their use during labor is discussed later in this chapter.

SELF-MONITORING BLOOD GLUCOSE

It is recommended that finger-stick capillary glucose levels are evaluated frequently, depending upon whether our patients are using insulin and what the route is. Postprandial levels have been found to be superior to preprandial levels in predicting macrosomia and morbidity during pregnancy.⁷⁹ For diet-controlled gestational diabetic patients, fasting blood glucose (FBG) and 1-hour postprandial glucose levels should be tested. For gestational or pregestational diabetic patients using OHAs or insulin, the monitoring should remain the same unless 2 to 3 a.m. glucose levels are needed to evaluate for the Somogyi effect (also known as the dawn phenomenon). For patients using an insulin pump, preprandial and postprandial glucose levels are typically monitored. Patients should also understand how to perform ketone measurements (using blood ketone testing strips) at times of illness, or when the blood glucose levels are >200 mg/dL. Home tests for β-hydroxybutyric acid are commercially available, but they have not been evaluated in pregnancy.^30,56

Multiple conditions can increase glucose levels, including preterm labor, preeclampsia, surgery, infections, and medications like beta-mimetics or steroids. Corticosteroid therapy is often administered during pregnancy when concern for preterm delivery arises, in the hope of increasing pulmonary lung maturity and decreasing the risk of intraventricular hemorrhage. Corticosteroids should not be withheld from women who have diabetes out of fear of DKA or exacerbating uncontrolled diabetes in patients <34 weeks gestational age. The use of corticosteroids in the late preterm setting (34–36 5/7 weeks gestation) in diabetics is more controversial. Instead, one must plan accordingly. Corticosteroids will result in acute elevations in serum glucose values within 6 hours after the initial dose and can last up to 3 days after the last dose.⁸⁰ Pregnant diabetic patients receiving steroids should be hospitalized for frequent serum glucose checks, titration of insulin dosing, or even consideration of an insulin drip to control blood glucose levels.^2,43 Treatment must be individualized to patient response; however, Figure 24-12 presents one recommended algorithm.

As a patient’s insulin requirements and clinical status changes during pregnancy, another concerning complication may be hypoglycemia. Hypoglycemia is defined as <60 mg/dL (3.3 mmol/L) during pregnancy,³⁰ and this most commonly occurs at 8 to 9 weeks and 15 to 16 weeks gestation.^81,82 While this most often occurs after inappropriate dosing of insulin or glyburide, it also may occur with inadequate nutritional intake or in patients with an infection. Common neurogenic signs and symptoms of hypoglycemia include sweating, shaking, tachycardia, or tingling in the hands, feet, lips, or tongue. In this setting, the patient should ingest 15 g of fast-acting carbohydrates (4 glucose tabs with water, 8 ounces of nonfat milk, or 4 ounces of juice) and then recheck her blood sugar with a standard capillary blood glucose meter. If her blood glucose has not risen above 70 mg/dL after 15 minutes following treatment, or if she still feels low, then she should treat again. This is known as the “Rule of 15.”⁸³ When levels have returned to normal, the patient should consume a snack or meal to prevent recurrence.

More severe neuroglycopenic signs include mood changes, confusion, irritability, seizure, or coma. If the patient is unable to swallow or is found unconscious, the patient’s partner, family member, or close companion should inject 1 mg of glucagon subcutaneously and call an emergency service for help.³⁰

Another special consideration is while patients are nil per os (NPO). While the OB hospitalist will frequently experience this scenario while patients are in labor (discussed later in this chapter), there are a variety of other situations when a patient may be NPO. For example, patients are typically made NPO at midnight the day of their scheduled C-section. They should be encouraged to take their bedtime basal insulin dose the night before and hold their morning doses of insulin. Upon arrival, their blood glucose should be checked. If the patient’s blood glucose is between 50 and 70 mg/dL, infuse IV D5 solution at 200 mL/hour, and check blood glucose every 15 minutes until it is >70 mg/dL twice. When the blood glucose is >70 mg/dL, reduce D5 to 100 mL/hour. If the NPO patient was previously on an insulin drip, the drip can be restarted at a lower rate once the glucose level is stable over 70 mg/dL. If the blood glucose is ever <50 mg/dL, it is recommended to infuse D10 instead of D5 at 200 mL/hour, and consider giving 10 mL of D50 IV push if the blood glucose is continuing to fall, or does not rise above 70 mg/dL within 30 minutes.^84,85 As an inpatient, avoid glucagon unless the patient is losing consciousness or IV access is lost given it can cause nausea and vomiting and will block insulin for hours.⁸⁶

For pregestational diabetics, a first-trimester ultrasound should be performed not only for proper dating but also to perform a nuchal translucency to evaluate for neural tube defects. For both pregestational and newly diagnosed gestational diabetics, at approximately 18 to 20 weeks, a specialized (Level 2) anatomy scan and fetal echocardiogram should be performed. These evaluations can be considered while your patient is admitted to the hospital if there is concern for delaying these tests.

In the second trimester, the patient should be taught how to perform fetal kick counts. Low-risk, diet-controlled gestational diabetic patients do not require nonstress testing unless indicated for other reasons; however, ACOG PB 190 recommends considering testing according to local practice. For medication-controlled gestational and pregestational diabetics without vasculopathy, begin twice weekly antepartum FHR testing at 32 to 34 weeks. For diabetic women with vasculopathy, hypertension, uncontrolled diabetes, or history of ketoacidosis during the current pregnancy, initiate testing twice weekly at 28 weeks.^45,87,88 These recommendations remain unchanged while an inpatient unless there is another reason to perform FHR testing more frequently. Serial growth ultrasounds and umbilical artery Doppler studies are indicated for fetal growth restriction.⁸⁷

SPECIAL ANTEPARTUM CONSIDERATIONS

If a diabetic patient has preexisting retinopathy, it is even more imperative that she or he has follow-up with ophthalmology, given it is the leading cause of blindness in individuals 24 to 64 years of age.⁴⁵ Retinopathy is known to progress during pregnancy, and rapid improvement in glycemic control is associated with worsening preexisting retinopathy.^89,90 Pregnancy is also known to worsen any underlying nephropathy in diabetic patients. Outpatient monitoring of glomerular filtration rate (GFR), creatinine, and random urine protein and urine creatinine should be obtained. Consideration of nephrology referral is recommended if any of these exams are abnormal.^56,91 Given the increased likelihood of preeclampsia during pregnancy, baseline preeclampsia labs should be considered and 81 mg of aspirin should be initiated. Thyroid disease is a common comorbidity, and thyroid function tests should also be considered. Women with diabetic gastroparesis are at a higher risk for maternal and fetal morbidity, and standard medications for hyperemesis and nutritional support should be provided. For all patients with poorly controlled diabetes, a fasting triglyceride level can be considered during the antepartum period, given their increased risk of hypertriglyceridemia-induced pancreatitis. Finally, all patients should be educated about foot care and should be screened for symmetric distal polyneuropathy and autonomic neuropathy at least annually.³⁰