Pregnancy at Risk: / Preexisting Conditions

ENDOCRINE AND METHABOLIC DISORDERS

Prepared by Ass. Prof. N. Petrenko, MD, PhD

 

LEARNING OBJECTIVES

•  Differentiate the types of diabetes mellitus and their respective risk factors in pregnancy.

•  Compare insulin requirements during pregnancy, postpartum, and lactation.

•  Identify maternal and fetal risks or complications associated with diabetes in pregnancy.

•  Develop a plan of care for the pregnant woman with pregestational or gestational diabetes.

•  Explain the effects of thyroid disorders on pregnancy.

 

KEY TERMS AND DEFINITIONS

Euglycemia Pertaining to a normal blood glucose level; also called normoglycemia

Gestational diabetes mellitus (GDM) Glucose intolerance first recognized during pregnancy

Glycosylated hemoglobin A1c Glycohemoglobin, a minor hemoglobin with glucose attached; the glycosylated hemoglobin concentration represents the average blood glucose level over the previous several weeks and is a measurement of glycemic control in diabetic therapy

Hyperglycemia Excess glucose in the blood

Hyperthyroidism Excessive functional activity of the thyroid gland hypoglycemia Less than normal amount of glu­cose in the blood; usually caused by administration of too much insulin, excessive secretion of insulin by the islet cells of the pancreas, or dietary deficiency

hypothyroidism Deficiency of thyroid gland activity with underproduction of thyroxine

ketoacidosis The accumulation of ketone bodies in the blood as a consequence of hyperglycemia; leads to metabolic acidosis

macrosomia Large body size as seen in neonates of mothers with pregestational or gestational diabetes

pregestational diabetes mellitus Diabetes melli­tus type 1 or type 2 that exists before pregnancy

 

 

For most women, pregnancy represents a normal part of life. This chapter discusses the care of women for whom pregnancy represents a significant risk because it is superimposed on a preexisting condition.

However, with the active participation of well-motivated women in the treatment plan and careful management from a multidisciplinary health care team, positive pregnancy outcomes are often possible.

Providing safe and effective care for women experiencing high risk pregnancy and their fetuses is a challenge. Although there are unique needs related to the preexisting conditions, these high risk women also experience the same feelings, needs, and concerns associated with a nor­mal pregnancy. The primary objective of nursing care is to achieve optimal outcomes for both the pregnant woman and the fetus.

This chapter focuses on diabetes mellitus and other metabolic disorders and cardiovascular disorders. Select disorders of the respiratory, gastrointestinal, integumentary, and central nervous systems; substance abuse; and human immunodeficiency virus are also discussed.

METABOLIC DISORDERS

Diabetes Mellitus

The perinatal mortality rate for well-managed diabetic pregnancies, excluding major congenital malformations, is approximately the same as for any other pregnancy. The key to an optimal preg­nancy outcome is strict maternal glucose control before conception, as well as throughout the gestational period. Consequently, much emphasis is placed on preconception counseling for women with diabetes.

Pregnancy complicated by diabetes is still considered high risk. It is most successfully managed by a multidisciplinary approach involving the obstetrician, internist or diabetologist, neonatologist, nurse, nutritionist or dietitian, and social worker. A favorable outcome requires commitment and active participation by the woman and her family.

 

Pathogenesis

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in in­sulin secretion, insulin action, or both (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997). Insulin, produced by the beta cells in the islets of Langerhans in the pancreas, regulates blood glucose levels by enabling glucose to enter adipose and muscle cells, where it is used for energy. When insulin is insufficient or ineffective in promoting glucose uptake by the muscle and adipose cells, glucose accumulates in the bloodstream, and hyperglycemia results. Hyperglycemia causes hyperosmolarity of the blood, which attracts intracellular fluid into the vascular system, resulting in cellular dehydration and expanded blood volume. Consequently, the kidneys function to excrete large volumes of urine (polyuria) in an attempt to regulate excess vascular volume and to excrete the unusable glucose (glycosuria). Polyuria, along with cellular dehydration, causes excessive thirst (polydipsia).

The body compensates for its inability to convert carbohydrate (glucose) into energy by burning proteins (muscle) and fats. However, the end products of this metabolism are ketones and fatty acids, which, in excess quantities, produce ketoacidosis and acetonuria. Weight loss occurs as a result of the breakdown of fat and muscle tissue. This tissue breakdown causes a state of starvation that compels the individual to eat excessive amounts of food (polyphagia).

Over time, diabetes causes significant changes in both the microvascular and macrovascular circulations. These structural changes affect a variety of organ systems, particularly the heart, eyes, kidneys, and nerves. Complications resulting from diabetes include premature atherosclerosis, retinopathy, nephropathy, and neuropathy.

Diabetes may be caused by either impaired insulin secretion, when the beta cells of the pancreas are destroyed by an autoimmune process, or by inadequate insulin action in target tissues at one or more points along the metabolic pathway. Both of these conditions are commonly present in the same person, and it is unclear which, if either, abnormality is the primary cause of the disease (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997).

 

Classification

The current classification system for diabetes includes four groups: type 1 diabetes, type 2 diabetes, other specific types (e.g., diabetes caused by infection or drug induced), and gestational diabetes mellitus (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997).

Type 1 diabetes includes those cases that are primarily due to pancreatic islet beta cell destruction and that are prone to ketoacidosis. People with type 1 diabetes usually have an absolute insulin deficiency. Type 1 diabetes includes cases currently thought to be caused by an autoimmune process, as well as those for which the cause is unknown (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997).

Type 2 diabetes is the most prevalent form of the disease and includes individuals who have insulin resistance and usually relative (rather than absolute) insulin deficiency. Specific etiologies for type 2 diabetes are unknown at this time. Type 2 diabetes often goes undiagnosed for years because hyperglycemia develops gradually and often is not severe enough for the patient to recognize the classic signs of polyuria, polydipsia, and polyphagia. Many people who develop type 2 diabetes are obese or have an increased amount of body fat distributed primarily in the abdominal area. Other risk factors for the development of type 2 diabetes include aging, a sedentary lifestyle, hypertension, and prior gestational diabetes. Type 2 diabetes often has a strong genetic predisposition (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997).

Pregestational diabetes mellitus is the label sometimes given to type 1 or type 2 diabetes that existed before pregnancy. Gestational diabetes mellitus (GDM) is any degree of glucose intolerance with the onset or first recognition occurring during pregnancy. This definition is appropriate whether or not insulin is used for treatment or the diabetes persists after pregnancy. It does not exclude the possibility that the glucose intolerance preceded the pregnancy. Women experiencing gestational diabetes should be reclassified 6 weeks or more after the pregnancy ends (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997).

 

Metabolic changes associated with pregnancy

Normal pregnancy is characterized by complex alterations in maternal glucose metabolism, insulin production, and metabolic homeostasis. During normal pregnancy, adjustments in maternal metabolism allow for adequate nutrition for both the mother and the developing fetus. Glucose, the primary fuel used by the fetus, is transported across the placenta through the process of carrier-mediated facilitated diffusion. This means that the glucose levels in the fetus are directly proportional to maternal levels. Although glucose crosses the placenta, insulin does not. Around the tenth week of gestation the fetus begins to secrete its own insulin at levels adequate to use the glucose obtained from the mother. Thus, as maternal glucose levels rise, fetal glucose levels are increased, resulting in increased fetal insulin secretion.

During the first trimester of pregnancy the pregnant woman's metabolic status is significantly influenced by the rising levels of estrogen and progesterone. These hormones stimulate the beta cells in the pancreas to increase insulin production, which promotes increased peripheral use of glucose and decreased blood glucose, with fasting levels being reduced by approximately 10% (Fig. 1, A).

There is a concomitant increase in tissue glycogen stores and a decrease in hepatic glucose production, which further encourage lower fasting glucose levels. As a result of these normal metabolic changes of pregnancy, women with insulin-dependent diabetes are prone to hypo-glycemia during the first trimester.

During the second and third trimesters, pregnancy exerts a "diabetogenic" effect on the maternal metabolic status. Because of the major hormonal changes, there is decreased tolerance to glucose, increased insulin resistance, decreased hepatic glycogen stores, and increased hepatic production of glucose. Rising levels of human chorionic somatomammotropin, estrogen, progesterone, prolactin, cortisol, and insulinase increase insulin resistance through their actions as insulin antagonists. Insulin resistance is a glucose-sparing mechanism that ensures an abundant supply of glucose for the fetus. Maternal insulin requirements may double or quadruple by the end of the pregnancy, usually leveling off or declining slightly after 36 weeks (Fig. 1, B and C).

At birth, expulsion of the placenta prompts an abrupt drop in levels of circulating placental hormones, cortisol, and insulinase (Fig. 1, D). Maternal tissues quickly regain their prepregnancy sensitivity to insulin. For the nonbreastfeeding mother the prepregnancy insulin-carbohydrate balance usually returns in approximately 7 to 10 days (Fig. 1, E). Lactation uses maternal glucose; thus the breastfeeding mother's insulin requirements will remain low during lactation. On completion of weaning, the prepregnancy insulin requirement is reestablished (Fig. 1, F).

 

 

Fig. -1 Changing insulin needs during pregnancy.

A, First trimester: insulin need is reduced because of increased production by pancreas and increased peripheral sensitivity to insulin; nausea, vomiting, and decreased food intake by mother and glucose transfer to embryo or fetus contribute to hypoglycemia.

B, Second trimester: insulin needs begin to increase as placental hormones, cortisol, and insulinase act as insulin antagonists, decreasing insulin's effectiveness.

C, Third trimester: insulin needs may double or even quadruple but usually level off after 36 weeks of gestation.

D, Day of birth: maternal insulin requirements drop drastically to approach prepregnancy levels.

E, Breastfeeding mother maintains lower insulin requirements, as much as 25% less than prepregnancy; insulin needs of nonbreastfeeding mother return to prepregnancy levels in 7 to 10 days.

F, Weaning of breastfeeding infant causes mother's insulin needs to return to prepregnancy levels.

 

Pregestational Diabetes Mellitus

Women who have pregestational diabetes may have either type 1 or type 2 diabetes, which may or may not be complicated by vascular disease, retinopathy, nephropathy, or other diabetic sequelae. Almost all women with pregestational diabetes are insulin dependent during pregnancy.

The diabetogenic state of pregnancy imposed on the compromised metabolic system of the woman with pregestational diabetes has significant implications. The normal hormonal adaptations of pregnancy affect glycemic control, and pregnancy may accelerate the progress of vascular complications.

During the first trimester, when maternal blood glucose levels are normally reduced and the insulin response to glucose is enhanced, glycemic control is improved. The insulin dosage for the woman with well-controlled diabetes may need to be reduced to avoid hypoglycemia. Nausea, vomiting, and cravings typical of early pregnancy result in dietary fluctuations that influence maternal glucose levels and may also necessitate a reduction in insulin dosage.

Because insulin requirements steadily increase after the first trimester, insulin dosage must be adjusted accordingly to prevent hyperglycemia. Insulin resistance begins as early as 14 to 16 weeks and continues to rise until it stabilizes during the last few weeks of pregnancy.

Diabetic nephropathy has more impact on perinatal outcome than any other vascular complication. Increased risks of preeclampsia, preterm labor, intrauterine growth restriction (IUGR), fetal distress, stillbirth, and neonatal death are associated with this condition (Moore, 1999).

 

Preconception counseling

Preconception counseling is recommended for all women of reproductive age who have diabetes because it is associated with an improved pregnancy outcome (Landon, Catalano, & Gabbe, 2002; Moore, 1999). Under ideal circumstances, women with pregestational diabetes are counseled before the time of conception to plan the optimal time for pregnancy, establish glycemic control before conception, and diagnose any vascular complications of diabetes. However, it has been estimated that fewer than 20% of women with diabetes in the United States participate in preconception counseling (Landon, Catalano, & Gabbe, 2002).

The woman's partner should be included in the counseling to assess the couple's level of understanding related to the effects of pregnancy on the diabetic condition and of the potential complications of pregnancy as a result of diabetes. The couple should also be informed of the anticipated alterations in management of diabetes during pregnancy and the need for a multidisciplinary team approach to health care. Financial implications of diabetic pregnancy and other demands related to frequent maternal and fetal surveillance should be discussed. Contraception is another important aspect of preconception counseling to assist the couple in planning effectively for pregnancy.

Some types of oral hypoglycemic agents (e.g., sulfonylureas such as tolbutamide) may have teratogenic effects on the fetus; they should be discontinued in the preconception period in women with type 2 diabetes. When the pregnancy is planned, these women are started on insulin before pregnancy, or as soon as the pregnancy is diagnosed when it is unplanned.

 

Maternal risks and complications

Although maternal morbidity and mortality rates have improved significantly, the pregnant woman with diabetes remains at risk for the development of complications during pregnancy. Poor glycemic control around the time of conception and in the early weeks of pregnancy is associated with an increased incidence of miscarriage. Women with good glycemic control before conception and in the first trimester are no more likely to miscarry than women who do not have diabetes (Moore, 1999).

Poor glycemic control later in pregnancy, particularly in women without vascular disease, increases the rate of fetal macrosomia. Macrosomia occurs in 20% to 25% of diabetic pregnancies. These large infants tend to have a disproportionate increase in shoulder and trunk size. Because of this, the risk of shoulder dystocia is greater in these babies than in other macrosomic infants. Thus women with diabetes face an increased likelihood of cesarean birth because of failure to progress or descend, or of operative vaginal birth (birth involving the use of episiotomy, forceps, or vacuum extractor) (Landon, Catalano, & Gabbe, 2002; Moore, 1999).

Pregnancy-induced hypertension, or preeclampsia, occurs more frequently during diabetic pregnancy. The highest incidence occurs in women with preexisting vascular changes related to diabetes (Cunningham et al., 2001).

Hydramnios (polyhydramnios) occurs approximately 10 times more often in diabetic than in nondiabetic pregnancies. Hydramnios (amniotic fluid in excess of 1500 ml) is associated with premature rupture of membranes (PROM), onset of preterm labor, and postpartum hemorrhage.

Infections are more common and more serious in pregnant women with diabetes. Disorders of carbohydrate metabolism alter the body's normal resistance to infection. The inflammatory response, leukocyte function, and vagi­nal pH are all affected. Vaginal infections, particularly monilial vaginitis, are more common. Urinary tract infections (UTIs) are also more prevalent. Infection is serious because it causes increased insulin resistance and may result in ketoacidosis. Postpartum infection is more common among women who are insulin dependent.

Ketoacidosis occurs most often during the second and third trimesters, when the diabetogenic effect of pregnancy is the greatest. When the maternal metabolism is stressed by illness or infection, the woman is at increased risk for diabetic ketoacidosis (DKA). The use of tocolytic drugs such as terbutaline to arrest preterm labor may also contribute to the risk for hyperglycemia and subsequent DKA (Hagay & Reece, 1999). DKA may also occur because of the woman's failure to take insulin appropriately. The onset of previously undiagnosed diabetes during pregnancy is another cause of DKA. DKA may occur with blood glucose levels barely exceeding 200 mg/dl, compared with 300 to 350 mg/dl in the nonpregnant state. In response to stress factors such as infection or illness, hyperglycemia occurs as a result of increased hepatic glucose production and decreased peripheral glucose use. Stress hormones, which act to impair insulin action and further contribute to insulin deficiency, are released. Fatty acids are mobilized from fat stores to enter into the circulation, and as they are oxidized, ketone bodies are released into the peripheral circulation. The woman's buffering system is unable to compensate, and metabolic acidosis develops. The excessive blood glucose and ketone bodies result in osmotic diuresis with subse­quent loss of fluid and electrolytes, volume depletion, and cellular dehydration. Prompt treatment of DKA is necessary to avoid maternal coma or death. Ketoacidosis occurring at any time during pregnancy can lead to intrauterine fetal death and is also a cause of preterm labor. The perinatal mortality rate is approximately 20% with maternal ketoacidosis (Cunningham et al, 2001) (Table 22-1).

The risk of hypogiycemia is also increased. Early in pregnancy, when hepatic production of glucose is diminished and peripheral use of glucose is enhanced, hypogiycemia occurs frequently, often during sleep. Later in pregnancy hypogiycemia may also result as insulin doses are adjusted to maintain normoglycemia. Women with a prepregnancy history of severe hypogiycemia are at increased risk for severe hypogiycemia during gesta­tion. Mild to moderate hypoglycemic episodes do not appear to have significant deleterious effects on fetal well-being. The long-term fetal effects of severe maternal hypogiycemia are as yet uncertain (Hagay & Reece, 1999) (see Table 1).

 

Table 1. Differentiation of Hypogiycemia (Insulin Shock) and Hyperglycemia (Diabetic Ketoacidosis)

 

Fetal and neonatal risks and complications

From the moment of conception, the infant of a woman with diabetes faces an increased risk of complications that may occur during the antepartum, intrapartum, or neonatal periods. Infant morbidity and mortality rates associated with diabetic pregnancy are significantly reduced with strict control of maternal glucose levels before and during pregnancy.

Despite the improvements in care of pregnant women with diabetes, sudden and unexplained stillbirth is still a major concern. Typically, this is observed in pregnancies after 36 weeks in women with vascular disease or poor glycemic control. It may also be associated with DKA, preeclampsia, hydramnios, or macrosomia. Although the exact cause of stillbirth is unknown, it may be related to chronic intrauterine hypoxia.

The most important cause of perinatal loss in diabetic pregnancy is congenital malformations, accounting for up to 40% of all perinatal deaths. The incidence of congenital malformations is related to the severity and duration of the diabetes. Anomalies commonly seen in infants pri­marily affect the cardiovascular system, central nervous system (CNS), and skeletal system (Hagay & Reece, 1999).

The fetal pancreas begins to secrete insulin at 10 to 14 weeks of gestation. The fetus responds to maternal hyperglycemia by secreting large amounts of insulin (hyperinsulinism). Insulin acts as a growth hormone, causing the fetus to produce excess stores of glycogen, protein, and adipose tissue, leading to increased fetal size, or macrosomia. Macrosomia is often defined as a weight of 4000 to 4500 g or greater. During birth, the macrosomic infant is at risk for a fractured clavicle, liver or spleen laceration, brachial plexus injury, facial palsy, phrenic nerve injury, or subdural hemorrhage (Hagay & Reece, 1999; Moore, 1999) (for further discussion, see Chapter 27).

IUGR is often seen in infants of mothers with diabetes complicated by vascular disease. It is related to compromised uteroplacental circulation and may be worsened in the presence of ketoacidosis and preeclampsia. The amount of oxy­gen available to the fetus is decreased as a result of maternal vascular changes (Bernstein, Gabbe, & Reed, 2002).

Infants of mothers with diabetes are also at increased risk for respiratory distress syndrome. Hyperglycemia and hyperinsulinemia may be instrumental in delaying pulmonary maturation in the fetus (Hagay & Reece, 1999).

For infants of a diabetic pregnancy the transition to extrauterine life is often associated with metabolic abnormalities. Within the first 30 to 60 minutes after birth, neonatal hypoglycemia often occurs. This is caused by the interruption of the glucose supply with the cutting of the umbilical cord, effects of fetal hyperinsulinism, and the rapid use of glucose after birth. Hypocalcemia, hypomagnesemia, hy-perbilirubinemia, and polycythemia also occur more frequently (Landon, Catalona, & Gabbe, 2002).

 

CARE MANAGEMENT

 

Assessment and Nursing Diagnoses

Interview

When a pregnant woman with diabetes initiates prenatal care, a thorough evaluation of her health status is completed. In addition to the routine prenatal assessment, a detailed history regarding the onset and course of the diabetes and its management and the degree of glycemic control before pregnancy is obtained. Effective management of the diabetic pregnancy depends on the woman's adherence to a plan of care. The woman's knowledge regarding diabetes and pregnancy, potential maternal and fetal complications, and the plan of care are also assessed. With subsequent visits, follow-up assessments are completed. Data from these assessments are used to identify the woman's specific learning needs.

The woman's emotional status is assessed to determine how she is coping with pregnancy superimposed on preexisting diabetes. Although normal pregnancy typically evokes some degree of stress and anxiety, pregnancy designated as "high risk" serves to compound anxiety and stress levels. Fear of maternal and fetal complications is a major concern. Strict adherence to the plan of care may necessitate alterations in patterns of daily living and may be an additional source of stress.

The woman's support system is assessed to identify those people significant to her and their roles in her life. It is important to assess reactions of the family or significant other to the pregnancy and to the strict management plan, and their involvement in the treatment regimen.

 

Physical examination

At the initial visit a thorough physical examination is performed to assess the woman's current health status. In addition to the routine prenatal examination, specific efforts are made to assess the effects of the diabetes. A baseline electrocardiogram may be done to assess cardiovascular status. Evaluation for retinopathy is done, with follow-up by an ophthalmologist each trimester and more frequently if retinopathy is diagnosed. Blood pressure is monitored carefully throughout pregnancy because of the increased risk for preeclampsia. The woman's weight gain is also monitored at each visit. Fundal height is measured, noting any abnormal increase in size for dates, which may indicate hydramnios or fetal macrosomia. Leopold's maneuvers may be performed to check for fetal size and possible hydramnios.

 

Laboratory tests

Routine prenatal laboratory examinations are performed. In addition, baseline renal function may be assessed with a 24-hour urine collection for total protein excretion and creatinine clearance. Urinalysis and culture are performed on the initial prenatal visit and as needed throughout the pregnancy to assess for the presence of UTI, which is common in diabetic pregnancy. At each visit urine is tested for the presence of glucose and ketones. Because of the risk of coexisting thyroid disease, thyroid function tests may also be performed (see later discussion of thyroid disorders).

For the woman with pregestational type 1 or type 2 diabetes, laboratory tests may be done to assess past glycemic control. At the initial prenatal visit, the glycosylated hemoglobin A_lc level may be measured. With prolonged hyperglycemia some of the hemoglobin remains saturated with glucose for the life of the red blood cell. Therefore a test for glycosylated hemoglobin provides a measure of glycemic control over time, specifically over the previous 4 to 6 weeks. Regular measurements of glycosylated hemoglobin provide data for altering the treatment plan and lead to improvement of glycemic control. Values for the measurement of hemoglobin A_lc, the most commonly used index of glycosylated hemoglobin, are as follows (Pagana & Pagana, 2001):

•  Adult/elderly without diabetes: 2.2% to 4.8%

•  Good diabetic control: 2.5% to 5.9%

•  Fair diabetic control: 6% to 8%

•  Poor diabetic control: greater than 8%

Fasting blood glucose or random (1 to 2 hours after eating) glucose levels may be assessed during antepartum visits (Fig. 2). Self-blood glucose monitoring records may also be reviewed.

 

Fig. 2 A, Clinic nurse collects blood to determine glucose level.

B, Nurse interprets glucose value displayed by monitor.

 

Nursing diagnoses for the woman with pregestational diabetes include the following:

·   Deficient knowledge related to

- diabetic pregnancy, management, and potential effects on pregnant woman and fetus

- insulin administration and its effects

- hypoglycemia and hyperglycemia

- diabetic diet

·        Anxiety, fear, dysfunctional grieving, powerlessness, disturbed body image, situational low self-esteem, spiritual distress, ineffective role performance, disrupted family processes related to

- stigma of being labeled "diabetic"

-effects of diabetes and its potential sequelae on the pregnant woman and the fetus

·        Risk for noncompliance related to

-lack of understanding of diabetes and pregnancy and requirements of treatment plan

-lack of financial resources to purchase blood glucose monitoring supplies or insulin and necessary supplies

-insufficient funds or lack of transportation to grocery store to follow dietary regimen

·        Risk for injury to fetus related to

- uteroplacental insufficiency

- birth trauma

·        Risk for injury to mother related to

- improper insulin administration

- hypoglycemia and hyperglycemia

- cesarean or operative vaginal birth

- postpartum infection

 

Expected Outcomes of Care

Expected outcomes of management for the pregnant woman with pregestational diabetes include that she will do the following:

•  Demonstrate/verbalize understanding of diabetic pregnancy, the plan of care, and the importance of glycemic control

•  Achieve and maintain glycemic control

•  Demonstrate effective coping

•  Give birth to a healthy infant at term

 

Plan of Care and Interventions

Antepartum

Because of her high risk status, a woman with diabetes is monitored much more frequently and thoroughly than low risk pregnant women. During the first and second trimesters of pregnancy her routine prenatal care visits will be scheduled every 1 to 2 weeks. Throughout the last trimester she will likely be seen one to two times each week. In the past, routine hospitalization for management of the diabetes, such as insulin dose changes, was common. With the availability of better home glucose monitoring and the growing reluctance of third-party payers to reimburse for hospitalization, these women are now generally managed as outpatients. Some patient and family education and maternal and fetal assessment may be done in the home, depending on the woman's insurance coverage and care provider preference (Lowdermilk & Grohar, 1998).

Achieving and maintaining constant euglycemia, with blood glucose levels in the range of 65 to 130 mg/dl (Table 2), is the primary goal of medical therapy. Euglycemia is achieved through a combination of diet, in­sulin, exercise, and blood glucose determinations. Providing the woman with the knowledge, skill, and motivation she needs to achieve and maintain excellent blood glucose control is the primary nursing goal.

 

Table 2

Target Blood Glucose Levels During Pregnancy

TIME OF DAY	TARGET GLUCOSE LEVEL (mg/dl)
Premeal	>65 but <95
Postmeal (1 hour)	<130
Postmeal (2 hours)	<120
During hours of sleep	No less than 70

Source: Moore, I (1999). Diabetes in pregnancy. In R. Creasy & R. Resnik (Eds.), Maternal-fetalmedicine(4th ed.). Philadelphia: WB Saunders.

 

Achieving euglycemia requires commitment on the part  of the woman and her family to make the necessary lifestyle changes, which can sometimes seem overwhelming. Maintaining tight blood glucose control necessitates that the woman follow a consistent daily schedule. She must get up and go to bed, eat, exercise, and take insulin at the same time each day. Blood glucose measurements are done frequently to determine how well the major components of therapy—diet, insulin, and exercise—are working together to control blood glucose levels.

Because the woman is at risk for infections, eye problems, and neurologic changes, foot care and general skin care are important. Daily bathing that includes good perineal care and foot care is important. For dry skin, lotions, creams, or oils can be applied. Tight clothing should be avoided. Shoes or slippers should be worn at all times, should fit properly, and are best worn with socks or stockings. Feet should be inspected regularly; toenails should be cut straight across, and professional help should be sought for any foot problems. Extremes of temperature should be avoided.

Diet. The woman with pregestational diabetes has likely been previously exposed to nutritional counseling regarding management of the diabetes. However, pregnancy precipitates special nutritional concerns and needs; the woman must be educated to incorporate these changes into dietary planning. Nutritional counseling is usually provided by a registered dietitian.

Dietary management during diabetic pregnancy must be based on blood (not urine) glucose levels. The diet is individualized to allow for increased fetal and metabolic requirements, with consideration of such factors as prepregnancy weight and dietary habits, overall health, ethnic background, lifestyle, stage of pregnancy, knowledge of nutrition, and insulin therapy. The dietary goal is to provide weight gain consistent with a normal pregnancy, to prevent ketoacidosis, and to minimize widely fluctuating blood glucose levels.

Energy needs are usually calculated on the basis of 30 to 35 calories per kilogram of ideal body weight, with the average diet including 2200 calories (first trimester) to 2500 calories (second and third trimesters). Total calories may be distributed among three meals and one evening snack or, more commonly, three meals and at least two snacks. Meals should be eaten on time and never skipped. Snacks must be carefully planned in accordance with in­sulin therapy to avoid fluctuations in blood glucose levels. A large bedtime snack of at least 25 g of carbohydrate with some protein is recommended to help prevent hypoglycemia and starvation ketosis during the night.

The ratio of carbohydrate, protein, and fat is important to meet the metabolic needs of the woman and the fetus. Approximately 50% to 60% of the total calories should be carbohydrate, with a minimum of 250 g per day. Simple carbohydrates are limited; complex carbohydrates that are high in fiber content are recommended because the starch and protein in such foods help regulate the blood glucose level as a result of more sustained glucose release. Protein intake should constitute 12% to 20% of the total kilocalories. From 20% to 30% of the daily caloric intake should come from fat, with no more than 10% saturated fats (see Self-Care box). Weight gain for most women should be approximately 12 kg during the pregnancy (Gilbert & Harmon, 1998).

Exercise. Although it has been shown that exercise enhances the use of glucose and decreases insulin need in women without diabetes, data are limited regarding exercise in women with pregestational diabetes. Any prescrip­tion of exercise during diabetic pregnancy should be done by the primary health care provider and should be closely monitored to prevent complications, especially for women with vasculopathy. Women with vasculopathy typically depend completely on exogenous insulin and are at greater risk for wide fluctuations in blood glucose levels and ketoacidosis, which can be made worse by exercise.

Careful instructions are given to the woman. Exercise need not be vigorous to be beneficial: 15 to 30 minutes of walking four to six times a week is satisfactory for most pregnant women. Other exercises that may be recommended are non-weight-bearing activities such as arm ex­ercises or use of a recumbent bicycle. The best time for exercise is after meals, when the blood glucose level is rising. To monitor the effect of insulin on blood glucose levels, the woman can measure blood glucose before, during, and after exercise.

 

NURSE ALERT Uterine contractions may occur during exercise; the woman should stop exercising immedi­ately if they are detected.

 

Insulin therapy. Adequate insulin is the primary factor in the maintenance of euglycemia during pregnancy, thus ensuring proper glucose metabolism of the woman and fetus. Insulin requirements during pregnancy change dramatically as the pregnancy progresses, necessitating frequent adjustments in insulin dosage. In the first trimester there is little or no change in prepregnancy insulin requirements; however, insulin dosage may need to be decreased because of hypoglycemia. During the second and third trimester, because of insulin resistance, dosage must be increased to maintain target glucose levels.

For the woman with type 1 pregestational diabetes who has typically been accustomed to one injection per day of intermediate-acting insulin, multiple daily injections of mixed insulin are a new experience. The woman with type 2 diabetes previously treated with oral hypoglycemics is faced with the task of learning to self-administer injections of insulin. The nurse is instrumental in education and support of pregestational diabetic women with regard to insulin administration and adjustment of insulin dosage to maintain euglycemia (see Self-Care box).

Many types of biosynthetic human insulin preparations (Humulin or Novolin) are available, including regular, NPH, Lente, Semi-lente, and mixed. Lispro (Humalog), a rapid-acting insulin with a shorter duration than regular insulin, is also available. Advantages of lispro include convenience, because it is injected immediately before mealtime; less hyperglycemia following meals; and fewer hypoglycemic episodes in some patients. Because its effects last 5 hours, most patients require a longer-acting insulin along with lispro to maintain optimal blood glucose levels (Moore, 1999) (Table 3). Lispro can be used safely in pregnancy, but, unlike other insulins, it is available only with a prescription.

        

Table 3 Insulin Administration During Pregnancy:

Expected Time of Action

 

Type of insulin	Onset	Peak	Duration
Lispro (rapid acting)	Within 15 min	30-90 min	3 hr
Regular (rapid acting)	30 min-1 hr	2-4 hr	5-8 hr
Intermediate acting	2-4 hr	5-10 hr	12-24 hr
Long acting	3-4 hr	14-24 hr	24-36 hr

 

Most women with insulin-dependent diabetes are managed with two to three injections per day. Usually, two thirds of the daily insulin dose, with longer-acting (NPH) and short-acting (regular or lispro) insulin combined in a 2:1 ratio, is given before breakfast. Sometimes, the remaining one third, again a combination of longer- and short-acting insulin, is administered in the evening before dinner. To reduce the risk of hypoglycemia during the night, separate injections often are administered, with short-acting insulin given before dinner, followed by longer-acting insulin at bedtime. Another alternative insulin regimen that works well for some women is to administer short-acting insulin before each meal and longer- acting insulin at bedtime (Hagay & Reece, 1999).

Although subcutaneous insulin injections are most commonly used, continuous insulin infusion systems may be used during pregnancy. The insulin pump is designed to mimic more closely the function of the pancreas in secreting insulin (Fig. 3). This portable, battery-powered device infuses regular insulin at a set basal rate and has the capacity to deliver up to four different basal rates in 24 hours. The pump also delivers bolus doses of insulin before meals to control postmeal blood glucose levels. The infusion tubing from the insulin pump can be left in place for several weeks without local complications. Although the insulin pump is convenient and generally provides good glycemic control, complications such as DKA, infection, or hypoglycemic coma can still develop. Use of the insulin pump requires a knowledgeable, motivated pa­tient; skilled health care providers; and 24-hour availability of emergency assistance (Hagay & Reece, 1999; Moore, 1999).

 

Fig 3. Insulin pump shows basal rate for pregnant women with diabetes.

 

Monitoring blood glucose levels. Blood glucose testing at home with a glucose reflectance meter or biosensor monitor is the commonly accepted method for monitoring blood glucose levels. Some third-party payers will cover the cost of a meter and necessary supplies.

To perform blood glucose monitoring, an individual obtains a drop of blood by means of a finger stick and places it on a test strip. After a specified amount of time the glucose level can be read by the meter. Blood glucose levels are routinely measured at various times throughout the day, such as before breakfast, lunch, and dinner; 2 hours after each meal; at bedtime and in the middle of the night. Hyperglycemia will most likely be identified in 2-hour postprandial values, because blood glucose levels peak approximately 2 hours after a meal. The health care provider will determine for each in­dividual woman the number and timing of routine blood glucose determinations. More frequent testing is needed when there is any readjustment in insulin dosage or diet; if nausea, vomiting, or diarrhea occur; or if any infection is present.

Target levels of blood glucose during pregnancy are lower than nonpregnant values. Acceptable fasting levels are generally between 65 and 95 mg/dl, and 2-hour postprandial levels should be less than 120 mg/dl (Moore, 1999). The woman should be told to immediately report episodes of hypoglycemia (less than 60 mg/dl) and hyperglycemia (more than 200 mg/dl) to her health care provider so that adjustments in diet or insulin therapy can be made.

Pregnant women with diabetes are much more likely to develop hypoglycemia than hyperglycemia. Most episodes of mild or moderate hypoglycemia can be treated with oral intake of 10 to 15 g of simple carbohydrate (see Self-Care box). If severe hypoglycemia occurs, in which the woman experiences a decrease in or loss of consciousness or an inability to swallow, she will require a parenteral injection of glucagon or intravenous (IV) glucose (American Diabetic Association [ADA], 1994; Becton Dickinson & Co., 1997). Because hypoglycemia can develop rapidly and because impaired judgment can be associated with even moderate episodes, it is vital that family members, friends, and work colleagues be able to quickly recognize signs and symptoms and initiate proper treatment if necessary.

Hyperglycemia is less likely to occur, but it can rapidly progress to diabetic ketoacidosis. Women and family members should be particularly alert for signs and symptoms of hyperglycemia, especially when infections or other illnesses occur (see Self-Care box)

Urine testing. Urine testing for ketones continues to have a place in diabetic management because it may pro­vide vital information for the pregnant woman, such as the onset of DKA. Women may be taught to perform urine testing daily with the first morning urine. Testing may also be done if a meal is missed or delayed, when illness occurs, or when the blood glucose level is greater than 200 mg/dl.

Spilling a trace or a small amount of ketones requires no treatment. However, if ketones appear repeatedly at the same time each day, some adjustment in diet may be needed. If testing shows a large amount of ketones, the health care provider should be contacted immediately (ADA, 1995).

Complications requiring hospitalization. Occasionally, hospitalization is needed to regulate insulin therapy and stabilize glucose levels. Infection, which can lead to hyperglycemia and diabetic ketoacidosis, is an indication for hospitalization, regardless of gestational age. Hospitalization during the third trimester for closer maternal and fetal observation may be indicated for women with vasculopathy because of the increased risk for renal impairment, hypertensive disorders, and fetal compromise (ADA, 1994).

Fetal surveillance. Diagnostic techniques for fetal surveillance are often performed to assess fetal growth and well-being. The goals of fetal surveillance are to detect fetal compromise as early as possible and to prevent intrauterine fetal death or unnecessary preterm birth.

Early in pregnancy, efforts are made to determine the estimated date of birth. A baseline sonogram is done during the first trimester to assess gestational age. Follow-up ultrasound examinations are usually performed during the pregnancy (as often as every 4 to 6 weeks) to monitor fetal growth; estimate fetal weight; and detect hydramnios, macrosomia, and congenital anomalies.

Because diabetic pregnancies are at greater risk for neural tube defects (e.g., spina bifida, anencephaly, microcephaly), measurement of maternal serum alpha-fetoprotein is performed between 16 and 18 weeks of gestation. This is often done in conjunction with a detailed ultrasound study to examine the fetus for neural tube defects.

Fetal echocardiography may be performed between 18 and 22 weeks of gestation to detect cardiac anomalies. Some practitioners repeat this fetal surveillance test at 34 weeks. Doppler studies of the umbilical artery may be performed in women with vascular disease to detect pla-cental compromise.

The majority of fetal surveillance measures are concen­trated in the third trimester, when the risk of fetal com­promise is greatest. Pregnant women should be taught how to do daily fetal movement counts.

The nonstress test used to evaluate fetal well-being may be used weekly or more often, typically beginning around 28 to 30 weeks of gestation. After 32 weeks, testing may be done twice weekly. For the woman with vascular disease, testing may begin earlier and continue more fre­quently. In the presence of a nonreactive nonstress test, a contraction stress test or fetal biophysical profile may be used to evaluate fetal well-being (Hagay & Reece, 1999; Landon, Catalano, & Gabbe, 2002).

Determination of birth date and mode of birth. Today, most diabetic pregnancies are allowed to progress to term (38 to 40 weeks of gestation), as long as good metabolic control is maintained and all parameters of antepartum fetal surveillance remain within normal limits. Reasons to proceed with birth before term include poor metabolic control, worsening hypertensive disorders, fetal macrosomia, or fetal growth restriction (Hagay & Reece, 1999; Moore, 1999).

Many practitioners plan for elective labor induction between 38 and 40 weeks. To confirm fetal lung maturity before birth, an amniocentesis may be performed in pregnancies earlier than 39 weeks. For the pregnancy compli­cated by diabetes, fetal lung maturation is better predicted by the amniotic fluid phosphatidylglycerol than by the lecithin/sphingomyelin ratio. If the fetal lungs are still immature, birth should be postponed as long as the results of fetal assessment remain reassuring. Amniocentesis may be repeated to monitor lung maturity (Landon, Catalano, & Gabbe, 2002).

Although vaginal birth is expected for most women with pregestational diabetes, the cesarean rate for these women is approximately 45%. Cesarean birth is often performed when antepartum testing suggests fetal distress or the estimated fetal weight is 4000 to 4500 g. Also, cesarean birth is necessary when the cervix fails to dilate completely during induction of labor (Hagay & Reece, 1999; Moore, 1999).

 

Intrapartum

During the intrapartum period the woman with pregestational diabetes must be monitored closely to prevent complications related to dehydration, hypoglycemia, and hyperglycemia. Most women use large amounts of energy (calories) to accomplish the work and manage the stress of labor and birth; however, this calorie expenditure varies with the individual. Blood glucose levels and hydration must be carefully controlled during labor. An IV line is inserted for infusion of a maintenance fluid, such as lactated Ringer's solution or 5% dextrose in lactated Ringer's solution. Insulin may be administered by continuous infusion or intermittent subcutaneous injection. Determinations of blood glucose levels are made every hour, and fluids and insulin are adjusted to maintain blood glucose levels between 60 and 100 mg/dl. It is essential that these target glucose levels be maintained because hyperglycemia during labor can precipitate metabolic problems in the neonate, particularly hypoglycemia.

During labor, continuous fetal heart monitoring is necessary. The woman should assume a side-lying position during bed rest in labor to prevent supine hypotension because of a large fetus or polyhydramnios. Labor is allowed to progress provided normal rates of cervical dilation, fetal descent, and fetal well-being are maintained. Failure to progress may indicate a macrosomic infant and cephalopelvic disproportion, necessitating a cesarean birth. The woman is observed and treated during labor for diabetic complications such as hyperglycemia, ketosis, ketoacidosis, and glycosuria. During second-stage labor, shoulder dystocia may occur if delivery of a macrosomic infant is attempted (see Chapter 24). A neonatologist, pediatrician, or neonatal nurse practitioner may be present at the birth to initiate assessment and neonatal care.

If a cesarean birth is planned, it should be scheduled in the early morning to facilitate glycemic control. The morning dose of insulin should be withheld and the woman given nothing by mouth. Epidural anesthesia is recommended because hypoglycemia can be detected earlier if the woman is awake. After surgery, glucose levels should be closely monitored, at least every 2 hours, and an IV solution containing 5% dextrose is infused (Landon & Gabbe, 1995).

 

Postpartum

In the immediate postpartum period, insulin require­ments decrease substantially because the major source of insulin resistance, the placenta, has been removed. Women with type 1 diabetes may require only one half to two thirds of the prenatal insulin dose on the first postpartum day, provided that they are eating a full diet. It takes several days after birth to reestablish carbohydrate homeostasis (see Fig. 1, D and E). Blood glucose levels are monitored in the postpartum period, and insulin dosage is adjusted ac­cordingly. Usually insulin is not given until the blood glucose level is greater than 200 mg/dl (Hagay & Reece, 1999). The woman with insulin-dependent diabetes must realize the importance of eating on time even if the baby needs feeding or other pressing demands exist. Women with type 2 diabetes often require no insulin in the postpartum period and are able to maintain euglycemia through diet alone or with oral hypoglycemics.

Possible postpartum complications include preeclampsia-eclampsia, hemorrhage, and infection. Hemorrhage is a possibility if the mother's uterus was overdistended (hy-dramnios, macrosomic fetus) or overstimulated (oxytocin induction). Postpartum infections such as endometritis are more likely to occur in a woman with diabetes.

Mothers are encouraged to breastfeed. In addition to the advantages of maternal satisfaction and pleasure, breastfeeding has an antidiabetogenic effect. Insulin requirements may be half the prepregnancy levels because of the carbohydrate used in human milk production. Because glucose levels are lower, breastfeeding women are at increased risk for hypoglycemia, especially in the early postpartum period and after breastfeeding sessions (Hagay & Reece, 1999; Moore, 1999). Breastfeeding mothers with diabetes may be at increased risk for mastitis and yeast infections of the breast. Insulin dosage, which is decreased during lactation, must be recalculated at weaning (Landon, Catalano, & Gabbe, 2002; Lawrence, 1999) (see Fig. 1, F).

The mother may have early breastfeeding difficulties. Poor metabolic control may delay lactogenesis and contribute to decreased milk production (Moore, 1999). Initial contact and opportunity to breastfeed the infant may be delayed if infants are placed in neonatal intensive care units or special care nurseries for observation during the first few hours after birth. Support and assistance from nursing staff and lactation specialists can facilitate the mother's early experience with breastfeeding and encourage her to continue.

The new mother needs information about family planning and contraception. Although family planning is important for all women, it is essential for the woman with diabetes to safeguard her own health and to promote optimal outcomes in future pregnancies. The woman and her partner should be informed that the risks associated with pregnancy increase with the duration and severity of the diabetic condition and that pregnancy may contribute to vascular changes associated with diabetes.

The risks and benefits of contraceptive methods should be discussed with the mother and her partner before discharge from the hospital. The barrier method is the preferred method of contraception for women who are insulin dependent. Barrier methods such as the diaphragm or condom and spermicide pose the least risk; however, inconsistency of use often leads to unplanned pregnancy (Landon, Catalano, & Gabbe, 2002).

Use of oral contraceptives by diabetic women is controversial because of the risk of thromboembolic and vascular complications and the effect on carbohydrate metabolism. In women without vascular disease or other risk factors, low-dose oral contraceptives and Norplant may be prescribed. Close monitoring of blood pressure and glucose levels is necessary to detect complications (Kjos, 1996).

Intrauterine contraceptive devices increase the risk of infection, especially during the first 4 months after insertion. However, they may be used for women who are older or who have hypertension or other vascular disease. These women must be able to recognize the signs of pelvic infection and sexually transmitted infections (STIs) and notify their health care providers promptly if these signs occur (Kjos, 1996).

Sterilization should be discussed with the woman who has completed her family or who has significant vascu-lopathy (ADA, 1994).

 

Evaluation

Evaluation of the care of the pregnant woman with pregestational diabetes is based on the previously stated expected outcomes of care and is closely associated with the degree of maternal metabolic control during pregnancy (see Plan of Care).

Gestational Diabetes Mellitus

Gestational diabetes mellitus (GDM) complicates approximately 4% of all pregnancies in the United States and accounts for 90% of all cases of diabetic pregnancy. Prevalence varies by racial and ethnic groups. GDM is more likely to occur among Hispanic, Native American, Asian, and African-American populations than in Caucasians (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997). GDM is likely to recur in future pregnancies, and there is an increased risk in development of overt diabetes in later life (Jones & Stone, 1998). This is especially true of women whose GDM is diagnosed early in pregnancy or who manifest fasting hyperglycemia (Landon, Catalano, & Gabbe, 2002). Classic risk factors for GDM include maternal age over 30 years; obesity; family history of type 2 diabetes; and an obstetric history of an infant weighing more than 4000 g, hydramnios, unexplained stillbirth, miscarriage, or an infant with congenital anomalies. Women at high risk for GDM are often screened at their initial prenatal visit and then rescreened later in pregnancy if the initial screen is negative.

The diagnosis of gestational diabetes is usually made during the second half of pregnancy. As fetal nutrient demands rise during the late second and the third trimester, maternal nutrient ingestion induces greater and more sustained levels of blood glucose. At the same time, maternal insulin resistance is also increasing because of the insulin-antagonistic effects of the placental hormones, cortisol, and insuhnase. Consequently, maternal insulin demands rise as much as threefold. Most pregnant women are capable of increasing insulin production to compensate for insulin resistance and to maintain eug-lycemia. When the pancreas is unable to produce suffi­cient insulin or the insulin is not used effectively, gestational diabetes can result.

 

Maternal-fetal risks

Women with GDM have twice the risk of developing hypertensive disorders compared with normal pregnant women (Metzger & Coustan, 1998). They also have increased risk for fetal macrosomia, which can lead to in­creased rates of perineal lacerations, episiotomy, and cesarean birth (Jones & Stone, 1998). Infants born to women with GDM are at risk for macrosomia with associated shoulder dystocia and birth trauma. GDM also places the neonate at increased risk for hypoglycemia, hypocalcemia, hyperbilirubinemia, thrombocytopenia, polycythemia, and respiratory distress syndrome (Jones & Stone, 1998; Metzger & Coustan, 1998).

The overall incidence of congenital anomalies among in­fants of women with gestational diabetes approaches that of the general population because gestational diabetes usually develops after the twentieth week of pregnancy—after the critical period of organogenesis (first trimester) has passed.

 

PLAN OF CARE. The Pregnant Woman with Pregestational Diabetes

Nursing Diagnosis Deficient knowledge related to lack of recall of information as evidenced by patient questions and concerns

Expected Outcomes Patient will be able to verbalize important information regarding diabetes, its management, and potential effects on the pregnant woman and fetus.

Nursing lnterventions/Rationales

Assess patient's current knowledge base regarding disease process, management, effects on pregnancy and fetus, and potential complications to provide database for further teaching.

Review the pathophysiology of diabetes, effects on preg­nancy and fetus, and potential complications to promote patient recall of information and compliance with treatment plan.

Review procedure for insulin administration, demonstrate procedure for blood glucose monitoring and insulin measurement and administration, and obtain return demonstration to establish patient comfort and competence with procedures.

Discuss diet and exercise as prescribed to promote self-care.

Review signs and symptoms of complications of hypoglycemia and hyperglycemia and appropriate interventions to promote prompt recognition of complications and self-care.

Provide contact numbers for health care team for prompt in­terventions and answers to questions on an ongoing basis to promote patient comfort.

Review information on diagnostic tests, schedule of visits to primary health care provider, and expected plan of care to allay anxiety and enlist cooperation of woman in her care.

Nursing Diagnosis Risk for fetal injury related to elevated maternal glucose levels

Expected Outcome Fetus will remain free of injury and be delivered at term in a healthy state.

Nursing Interventions/Rationales

Assess patient's current diabetic control to identify risk for fetal mortality and congenital anomalies.

Monitor fundal height during each prenatal visit to identify appropriate fetal growth.

Monitor for signs and symptoms of pregnancy-induced hy­pertension to identify early manifestations because preg­nant women with diabetes are more at risk.

Assess fetal movement and heart rate during each prenatal visit and perform weekly nonstress tests during the last 4 weeks of pregnancy to assess for fetal well-being.

Review procedure for blood glucose testing and insulin ad­ministration to promote self-care.

Nursing Diagnosis Anxiety related to threat to maternal and fetal well-being as evidenced by patient verbal expressions of concern

Expected Outcomes Patient will identify sources of anxiety and report feeling less anxious.

Nursing Interventions/Rationales

Through therapeutic communication, promote an open rela­tionship with patient to promote patient trust.

Listen to patient's feelings and concerns to assess for any misconception or misinformation that may be contributing to anxiety.

Review potential dangers by providing factual information to correct any misconceptions or misinformation.

Encourage patient to share concerns with her health care team to promote patient and team collaboration in her care.

 

Screening for gestational diabetes mellitus

There is lack of agreement about universal screening. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus stated in its 1997 report that it is neither cost-effective nor necessary to screen certain  women who are at low risk for GDM. This low risk group includes normal-weight women younger than 25 years of age who have no family history of diabetes and are not members of an ethnic or racial group known to have a high prevalence of the disease. The American College of Obstetricians and Gynecologists (ACOG) (1994) stated that selective screening may be appropriate in some low risk settings (e.g., teen clinics) but that universal screening might be more appropriate for high risk populations. ACOG also states that screening is unnecessary in certain populations with a high prevalence of GDM; these women should proceed directly to diagnostic testing.

The screening test (Glucola screening) most often used consists of a 50 g oral glucose load, followed by a plasma glucose determination 1 hour later. Screening is performed at 24 to 28 weeks of gestation. It is not necessary that the woman be fasting. A glucose value of 140 mg/dl is considered a positive screen and should be followed by a 3-hour oral glucose tolerance test (OGTT). The 3-hour OGTT is administered after an overnight fast and at least 3 days of unrestricted diet (at least 150 g of carbohydrate) and physical activity. The woman is instructed to avoid caffeine because it tends to increase glucose levels and to abstain from smoking for 12 hours before the test. A fasting blood glucose level is drawn before giving a 100 g glucose load. Blood glucose levels are then drawn 1, 2, and 3 hours later. The woman is diagnosed with gestational diabetes if two or more values are met or exceeded (Fig. 4).

Nursing diagnoses are similar to those identified for women with pregestational diabetes. Expected outcomes of care for the woman with GDM are basically the same as those for women with pregestational diabetes except that the time frame for planning may be shortened with GDM because the diagnosis is usually made later in pregnancy.

 

 

1 -hr (50 g) oral glucose tolerance test (OGTT)
Negative (<14O mg/dl)	Positive (≥ 140 mg/dl)
Routine prenatal care	3-hr (100 g)OGTT
	Negative	Positive for GDM Two or more levels are met or exceeded: Fasting      105 mg/dl 1                 Hr 190 mg/dl 2                 hr165 mg/dl 3                 Hr 145 mg/dl

 

Fig. 4 Screening and diagnosis for gestational diabetes. (From American Diabetes Association. [1997]. Position statement: Gestational diabetes mellitus. Diabetes Care, 20[suppl 1], S44.)

 

 

Antepartum care

When the diagnosis of gestational diabetes is made, treatment begins immediately, allowing little or no time for the woman and her family to adjust to the diagnosis before they are expected to participate in the treatment plan. The nurse and other health care providers should educate the woman and her family, providing detailed and comprehensive explanations to ensure understanding, participation, and adherence to the necessary interventions. Potential complications should be discussed, and the need for maintenance of euglycemia throughout the remainder of the pregnancy is reinforced. It may be reassuring for the woman and her family to know that gestational diabetes typically disappears when the pregnancy is over.

As with pregestational diabetes, the aim of therapy in women with GDM is strict blood glucose control. Fasting blood glucose levels should be less than 105 mg/dl, and 2-hour postprandial blood levels should be less than 120 mg/dl (Landon, Catalano, & Gabbe, 2002).

Diet. Dietary modification is the mainstay of treatment for GDM. The woman with GDM is placed on a standard diabetic diet. The usual prescription is for 30 to 35 kcal/kg of present pregnancy weight, which translates into 2000 to 2500 calories per day for most women. Dietary counseling by a nutritionist is recommended. Most women with GDM do not require hospitalization for dietary instruction and management.

Exercise. Exercise in women with GDM appears to be safe. It helps lower blood glucose levels and may be instrumental in eliminating the need for insulin. Women with GDM who already have an active lifestyle should be encouraged to continue an exercise program. Brisk walking, use of a recumbent bicycle, and swimming are often recommended; exercises that use the upper body are ideal for most women because they are not associated with increased uterine contractions. Sedentary women may also be encouraged to increase their physical activity. Of course, any exercise program should always be initiated or continued with the knowledge and consent of the primary health care provider.

Monitoring blood glucose levels. Blood glucose monitoring is necessary to determine whether euglycemia can be maintained by diet and exercise. Fasting and postprandial glucose levels should be monitored at least weekly (ACOG, 1994). Women with GDM may perform self-monitoring at home, or monitoring may be done only at the clinic or office visit.

Insulin therapy. Many women with GDM will require insulin during the pregnancy to maintain adequate blood glucose levels, despite compliance with the prescribed diet. This occurs because as pregnancy progresses, placental hormones increase blood glucose levels and cause insulin to work less effectively. ACOG (1994) recommends that women who repetitively exceed the glucose thresholds of 105 mg/dl fasting and 120 mg/dl 2 hours postprandial be started on insulin therapy. In practice, however, either lower or higher thresholds for initiating insulin may be used (Landon, Catalano, & Gabbe, 2002).

Fetal surveillance. There is no standard recommendation if for fetal surveillance in pregnancies complicated by GDM. Women whose blood glucose levels are well controlled by diet are at low risk for fetal death. These women usually progress to term and spontaneous labor with only routine fetal assessments (ACOG, 1994; Metzger & Coustan, 1998).

Women with GDM whose blood glucose levels are not well controlled or who require insulin therapy, have hy­pertension, or have a history of previous stillbirth generally receive more intensive fetal biophysical monitoring. Nonstress tests and biophysical profiles are often performed weekly, beginning anywhere from 32 to 36 weeks of gestation (ACOG, 1994; Landon, Catalano, & Gabbe, 2002).

 

Intrapartum care

During the labor and birth process, blood glucose lev­els are monitored at least every 2 hours to maintain levels at 100 mg/dl or less. Glucose levels within this range will decrease the severity of neonatal hypoglycemia. IV fluids containing glucose are not given as a bolus, although they may be necessary as maintenance fluids. Although gesta-tional diabetes is not an indication for cesarean birth, it may be necessary in the presence of problems, such as preeclampsia or macrosomia.

 

Postpartum care

More than 90% of women with GDM will return to normal glucose levels after childbirth (Metzger & Coustan, 1998). Assessment for carbohydrate intolerance can be initiated 4 to 6 weeks postpartum or after breastfeeding has stopped. Obesity is a major risk factor for the later development of diabetes. Thus women with a history of GDM, particularly those who are overweight, should be encouraged to make lifestyle changes that include weight loss and exercise to reduce this risk (Hagay & Reece, 1999; Metzger & Coustan, 1998). The risk of developing GDM in subse­quent pregnancies is 50% or higher (Kendrick, 1997). Because infants born to women with GDM are at risk for de­veloping obesity and diabetes in childhood or adolescence, regular health care for these children is essential (Metzger & Coustan, 1998).

Thyroid Disorders

Hyperthyroidism

Hyperthyroidism occurs in approximately 1 or 2 of every 1000 pregnancies (Seely & Burrow, 1999). It is most often caused by Graves' disease, although other possible but rare causes include acute thyroiditis, toxic solitary nodules, toxic multinodular goiter, and trophoblastic disease. Clinical manifestations of hyperthyroidism are associated with an increased basal metabolism rate and increased sympathetic nervous system activity. Typical symptoms include nervousness, hyperactivity, weakness, fatigue, weight loss (or poor weight gain), diarrhea, tachycardia, shortness of breath, excessive perspiration, heat intolerance, and muscle tremors. Exophthalmos and enlargement of the thyroid gland (goiter) may also occur. Diagnosis may be difficult because many of the signs and symptoms of hyperthyroidism are typical of pregnancy. Laboratory findings include an elevated free thyroxine index and a suppressed thyroid-stimulating hormone (TSH) level (Diehl, 1998; Seely & Burrow, 1999). Hyperthyroidism should be treated during pregnancy; untreated or inadequately treated women give birth to infants with low birth weight and more minor fetal anomalies. Women with hyperthyroidism are also at increased risk to develop severe preeclampsia (Diehl, 1998; Seely & Burrow, 1999). Hyperemesis gravidarum is often associated with elevated thyroid hormone levels (Mestman, 2002; Seely & Burrow, 1999).

The primary treatment of hyperthyroidism during pregnancy is drug therapy; the medication of choice is propylthiouracil (PTU). The usual starting dose is 100 to 150 mg every 8 hours. Women generally show clinical improvement within 2 weeks of beginning therapy, but the medication requires 6 to 8 weeks to reach full effectiveness. During therapy the woman's free T₄ levels are measured monthly and the results used to taper the drug to the smallest effective dosage to prevent unnecessary fetal hypothyroidism (Diehl, 1998; Seely & Burrow, 1999). PTU is well tolerated by most women. Rare side effects include pruritus, skin rash, fever, a metallic taste, nausea, bronchospasm, oral ulcerations, hepatitis, and a lupus-like syn­drome (Seely & Burrow, 1999). The most severe side effect is agranulocytosis, which is more common in women over 40 years of age and in those taking high doses of PTU (Seely & Burrow, 1999). Symptoms of agranulocytosis are fever and sore throat; these symptoms should be reported immediately to the health care provider, and the woman should stop taking the PTU. Transient, benign leukopenia may occur as a result of PTU therapy. PTU readily crosses the placenta and may induce fetal hypothyroidism and goiter, although these complications rarely occur (Mestman, 2002; Seely & Burrow, 1999).

Beta-adrenergic blockers such as propranolol may be used in severe hyperthyroidism. Long-term use is not rec­ommended because of the potential for IUGR and altered response to anoxic stress, postnatal bradycardia, and hypoglycemia (Seely & Burrow, 1999).

Radioactive iodine must not be used in diagnosis or treatment of hyperthyroidism in pregnancy because it may compromise the fetal thyroid. If a mother taking hyper-thyroid medication chooses to breastfeed, she should be aware that physiologically significant doses of the drug are passed to the infant through the breast milk. The infant's thyroid status should be monitored periodically so that hypothyroidism can be prevented (Cunningham et al., 2001; Seely & Burrow, 1999).

In severe cases surgical treatment of hyperthyroidism, subtotal thyroidectomy, may be performed during the second or third trimester. Because of the increased risk of mis­carriage and preterm labor associated with major surgery, this treatment is usually reserved for women with severe disease, those for whom drug therapy proves toxic, and those who are unable to adhere to the prescribed medical regimen. Postoperative hypothyroidism is common, oc­curring in at least 20% of previously hyperthyroid women.

 

NURSE ALERT! A serious but uncommon complication of undiagnosed or partially treated hyperthyroidism is thyroid storm, which may occur in response to stress such as infection, birth, or surgery. A woman with this emergency disorder may have fever, restlessness, tachycardia, vomiting, hypotension, or stu­por. Prompt treatment is essential; IV fluids and oxy­gen are administered along with high doses of PTU. Potassium iodide, antipyretics, dexamethasone, and beta-adrenergic blockers may also be given; sedation may be necessary for extreme restlessness (Inzucchi & Burrow, 1999; Mestman, 2002).

Hypothyroidism

Hypothyroidism during pregnancy is a rare phenome­non because women with this disorder are often infertile. Hypothyroidism is usually caused by Hashimoto disease, thyroid gland ablation by radiation, previous surgery, or antithyroid medications. Reduced thyroid function resulting from hypothalamic or pituitary failure is rare. Iodine deficiency in the United States is also rare (Diehl, 1998).

Characteristic symptoms of hypothyroidism include weight gain; fatigue; cold intolerance; constipation; cool, dry skin; coarsened hair; and muscle weakness. Laboratory values in pregnancy include low or low-normal T₃ and T₄ levels and elevated levels of TSH (Diehl, 1998; Inzucchi & Burrow, 1999).

Pregnant women with untreated hypothyroidism are at risk for preeclampsia, placental abruption, and stillbirth. Infants born to mothers with hypothyroidism may be of low birth weight, but for the most part they are healthy and without evidence of thyroid dysfunction (Diehl, 1998; Inzucchi & Burrow, 1999).

Thyroid hormone supplements are used to treat hypothyroidism. Levothyroxine (e.g., L-thyroxine [Synthroid]) is most often prescribed during pregnancy. The usual beginning dosage is 0.10 to 0.15 mg per day, in a single daily dose. The aim of drug therapy is to maintain the woman's TSH level within the normal range for pregnant women.

 

NURSE ALERT! If taking iron supplementation, pregnant women should be told to take L-thyroxine 2 hours before or after iron tablets, because ferrous sulfate lowers the effectiveness of the medication (Diehl, 1998).

 

The fetus depends on maternal thyroid hormones until 12 weeks of gestation, when fetal production begins. Thus maternal hypothyroidism does not cause fetal hypothyroidism. However, maternal treatment of hypothyroidism may result in increased fetal levels of thyroid hormones. Careful monitoring of the neonate's thyroid status is im­portant to detect any abnormalities.

Maternal Phenylketonuria

Phenylketonuria (PKU), a recognized cause of mental retardation, is an inborn error of metabolism caused by an autosomal recessive trait that creates a deficiency in the enzyme phenylalanine hydrolase. Absence of this enzyme impairs the body's ability to metabolize the amino acid phenylalanine, found in all protein foods. Consequently, there is toxic accumulation of phenylalanine in the blood, which interferes with brain development and function. PKU affects 1 in every 10,000 live births in the United States. All newborns are tested soon after birth for this disorder. Prompt diagnosis and therapy with a phenylalanine-restricted diet significantly decreases the incidence of mental retardation. Dietary therapy for PKU has been recommended for continuation throughout adulthood, although some people discontinue it because of the difficulty in adhering to the specially prepared diet (Acosta, 1995; Kirby, 1999).

The key to prevention of fetal anomalies caused by PKU is the identification of women in their reproductive years who have the disorder. Screening programs in the preconception period and even earlier, such as during school physical examinations, may help identify those in­dividuals with PKU so that dietary therapy can be instituted before conception occurs. Screening for undiag­nosed maternal PKU at the first prenatal visit may be warranted, especially in individuals with a family history of the disorder, with low intelligence of uncertain etiology, or who have given birth to microcephalic infants. Women with PKU should continue the low-protein diet during pregnancy. Nutritional intake and phenylalanine levels must be monitored twice weekly during pregnancy. Ultrasound examinations are used for fetal surveillance beginning in the first trimester (Kirby, 1999). A spontaneous vaginal birth is anticipated.

Infants diagnosed with PKU can be breastfed safely if the amount of breast milk ingested is monitored so that phenylalanine levels do not get too high. Mothers who choose to breastfeed must still supplement the infant's diet with a special milk preparation that contains little or no phenylalanine. Monitoring amounts of phenylalanine can be tedious and frustrating. Health care providers can help parents in their decision making about how to feed their infant (Kirby, 1999). Referral to community support groups for parents of children with PKU may be useful.

PATIENT INSTRUCTIONS FOR SELF-CARE

Dietary Management of Diabetic Pregnancy

•  Follow the prescribed diet plan.

•  Eat a well-balanced diet, including daily food requirements for a normal pregnancy.

•  Divide daily food intake between three meals and two to four snacks, depending on individual needs.

•  Eat a substantial bedtime snack to prevent a severe drop in blood glucose level during the night.

•  Limit the intake of fats if weight gain occurs too rapidly.

•  Take daily vitamins and iron as prescribed by the health care provider.

•  Avoid foods high in refined sugar.

•  Eat consistently each day; never skip meals or snacks.

•  Reduce the intake of saturated fat and cholesterol.

•  Eat foods high in dietary fiber.

•  Avoid alcohol and caffeine.

 

Self-Administration of Insulin

Procedure for mixing NPH (intermediate-acting) and regular (short-acting) insulin

•  Wash hands thoroughly and gather supplies. Be sure the insulin syringe corresponds to the concentration of insulin you are using.

•  Check insulin bottle to be certain it is the appropriate type and check the expiration date.

•  Gently rotate (do not shake) the insulin vial to mix the insulin.

•  Wipe off rubber stopper of each vial with alcohol.

•  Draw into syringe the amount of air equal to total dose.

•  Inject air equal to NPH (intermediate-acting) dose into NPH vial. Remove syringe from vial.

•  Inject air equal to regular insulin dose into regular insulin vial.

•  Invert regular insulin bottle and withdraw regular insulin dose.

•  Without adding more air to NPH vial, carefully withdraw NPH dose.

Procedure for self-injection of insulin

•  Select proper injection site (remember to rotate sites).

•  Injection site should be clean. No need to use alcohol. If alcohol is used, let it dry before injecting.

•  Pinch the skin up to form a subcutaneous pocket and, holding the syringe like a pencil, puncture the skin at a 45-to 90-degree angle. If there is a great deal of fatty tissue at the site, spread the skin taut and inject the syringe at a 90-degree angle.

•  Slowly inject the insulin.

•  As you withdraw the needle, cover the injection site with sterile gauze and apply gentle pressure to prevent bleeding.

•  Record insulin dosage and time of injection

 

Self-Testing of Blood Glucose Level

•  Gather supplies, check expiration date, and read instructions on testing materials. Prepare glucose reflectance meter for use according to manufacturer's directions.

•  Wash hands in warm water (warmth increases circulation).

•  Select site on side of any finger (all fingers should be used in rotation).

•  Pierce site with lancet (may use automatic, springloaded, puncturing device). Cleaning the site with alcohol is not necessary.

•  Drop hand down to side; with other hand gently squeeze finger from hand to fingertip.

•  Allow blood to drop onto testing strip. Be sure to cover entire reagent area.

•  Determine blood glucose value using the glucose reflectance meter, following manufacturer's instructions.

•  Record results.

•  Repeat as instructed by health care provider and as needed for signs of hypoglycemia or hyperglycemia.

 

Treatment for Hypoglycemia

•  Be familiar with signs and symptoms of hypoglycemia (nervousness, headache, shaking, irritability, personality change, hunger, blurred vision, sweaty skin, tingling of mouth or extremities).

•  Check blood glucose level immediately when hypoglycemic symptoms occur.

•  If blood glucose is <60 mg/dl, immediately eat or drink something that contains 10 to 15 g of simple carbohydrate. Examples are:

-Y₂ cup (4 ounces) unsweetened fruit juice

-V₂ cup (4 ounces) regular (not diet) soda

-5 to 6 LifeSavers candies

-1 tablespoon honey or corn (Karo) syrup

-1 cup (8 ounces) milk

-2 to 3 glucose tablets

•  Rest for 15 minutes, then recheck blood glucose.

•  If glucose level is still <60 mg/dl, eat or drink another serving of one of the "glucose boosters" listed above.

•  Wait 15 minutes, then recheck blood glucose. If it is still <60 mg/dl, notify health care provider immediately.

 

What to Do When Illness Occurs

•  Be sure to take insulin even though appetite and food intake may be less than normal. (Insulin needs are increased with illness or infection.)

•  Call the health care provider and relay the following information:

-Symptoms of illness (e.g., nausea, vomiting, diarrhea)

-Fever

-Most recent blood glucose level

-Urine ketones

-Time and amount of last insulin dose

•  Increase oral intake of fluids to prevent dehydration.

•  Rest as much as possible.

•  If unable to reach health care provider and blood glucose exceeds 200 mg/dl with urine ketones present, seek emergency treatment at the nearest health care facility. Do not attempt to self-treat for this.

INFANTS OF MOTHERS WITH DIABETES

A better understanding of maternal and fetal metabolism, resulting in stricter control of maternal diabetes and improved obstetric and neonatal intensive care, has led to a decrease in the perinatal mortality rate in diabetic pregnancy. However, all infants born to mothers with diabetes are at some risk for complications. The degree of risk is af­fected by the severity and duration of maternal disease. Problems seen in the infants include congenital anomalies, macrosomia, birth trauma and perinatal asphyxia, respira­tory distress syndrome (RDS), hypoglycemia, hypocal-cemia and hypomagnesemia, cardiomyopathy, and hyper-bilirubinemia and polycythemia.

 

Pathophysioiogy

The mechanisms responsible for the problems seen in the infants are not fully understood. Congenital anomalies are believed to be caused by fluctuations in blood glucose levels and episodes of ketoacidosis in early pregnancy. Later in pregnancy, when the mother's pancreas cannot release sufficient insulin to meet increased demands, ma­ternal hyperglycemia results. The high levels of glucose cross the placenta and stimulate the fetal pancreas to re­lease insulin. The combination of the increased supply of maternal glucose and other nutrients, the inability of maternal insulin to cross the placenta, and increased fetal insulin results in excessive fetal growth termed macrosomia (see later discussion).

Hyperinsulinemia accounts for many of the problems the fetus or infant develops. In addition to fluctuating glucose levels, maternal vascular involvement or superimposed maternal infection adversely affects the fetus. Normally, maternal blood has a more alkaline pH than carbon dioxide-rich fetal blood does. This phenomenon encourages the exchange of oxygen and carbon dioxide across the placental membrane. When the maternal blood is more acidotic than the fetal blood, such as during ketoacidosis, little carbon dioxide or oxygen exchange occurs at the level of the placenta. The mortality rate for unborn babies resulting from an episode of maternal ketoacidosis may be as high as 50% or more (Fanaroff & Martin, 1997).

There are indications that some neonatal conditions—macrosomia, hypoglycemia, polyhydramnios, preterm birth, and perhaps fetal lung immaturity—may be eliminated or the incidence decreased by maintaining control over maternal glucose levels within narrow limits (Reece et al., 1998).

 

Congenital Anomalies

Congenital anomalies occur in approximately 7% to 10% of infants. Their incidence is two to four times that for infants born to mothers without diabetes. The incidence is greatest among newborns who are small for gestational age (SGA). Intrauterine growth restriction (IUGR) leading to SGA infants is seen when the mother has severe vascular disease. The most frequently occurring anomalies involve the cardiac, musculoskeletal, and central nervous systems. In most defects associated with diabetic pregnancies, the structural abnormality occurs before the eighth week after conception. This reinforces the importance of control of blood glucose both before conception and in the early stages of pregnancy.

The incidence of congenital heart lesions in these in­fants is five times higher than that in the general population. Coarctation of the aorta, transposition of the great vessels, and atrial or ventricular septal defects are the most common lesions encountered. Maternal diabetic control is related to the incidence of lesions; that is, the better the control, the fewer the lesions.

Central nervous system (CNS) anomalies include anencephaly, encephalocele, meningomyelocele, and hydrocephalus. The musculoskeletal system may be affected by caudal regression syndrome (sacral agenesis, with weakness or deformities of the lower extremities, malformation and fixation of the hip joints, and shortening or deformity of the femurs). Hypertrichosis on the pinnae (excessive hair growth on the external ear) has been added to the list of characteristic clinical features (Fanaroff & Martin, 1997). Other defects noted in this population include gastrointestinal (GI) atresia and urinary tract malformations.

 

Macrosomia

Despite improvements in the control of maternal blood sugar levels, the incidence of macrosomia in the woman with insulin-dependent diabetes is higher than in infants born of mothers who do not have diabetes. At birth the typical LGA infant has a round, cherubic ("tomato" or cushingoid) face, a chubby body, and a plethoric or flushed complexion (Fig. 4). The infant has enlarged internal organs (hepatosplenomegaly, splanchnomegaly, car-diomegaly) and increased body fat, especially around the shoulders. The placenta and umbilical cord are larger than average. The brain is the only organ that is not enlarged. Infants may be LGA but physiologically immature.

 

Fig. 27-4 Macrosomia. (From O'Doherty, N. [1986]. Neona-tology: Micro atlas of the newborn. Nutley, NJ: Hoffmann-La Roche.)

 

The macrosomic infant is at risk for hypoglycemia, hypocalcemia, hyperviscosity, and hyperbilirubinemia. The excessive shoulder size in these infants often leads to dystocia, particularly because the head may be smaller in proportion to the shoulders than in a nonmacrosomic in­fant. Macrosomic infants, born vaginally or by cesarean birth after a trial of labor, may incur birth trauma.

Birth Trauma and Perinatal Asphyxia

Birth injury (resulting from macrosomia or method of birth) and perinatal asphyxia occur in 20% of infants of mothers with gestational diabetes and 35% of infants of mothers with diabetes. Examples of birth trauma include cephalhe-matoma; paralysis of the facial nerve (seventh cranial nerve); fracture of the clavicle or humerus; brachial plexus paralysis, usually Duchenne-Erb (right upper arm) palsy; and phrenic nerve paralysis, invariably associated with diaphragmatic paralysis.

 

Respiratory Distress Syndrome

Infants of mothers with diabetes are four to six times more likely than normal infants to develop RDS. With improved maternal glucose control, this risk has been substantially reduced. In the fetus exposed to high levels of maternal glucose, synthesis of surfactant may be delayed because of the high fetal serum level of insulin. Fetal lung maturity, as evidenced by a lecithin/sphingomyelin (L/S) ratio of 2:1, is not reassuring if the mother has diabetes mellitus or gestation-induced diabetes mellitus. For the infants of such mothers, an L/S ratio of 3:1 or more or the presence of phosphatidylglycerol in the amniotic fluid is more indicative of adequate lung maturity.

 

Hypoglycemia

Hypoglycemia affects many infants. After constant exposure to high circulating levels of glucose, hyperplasia of the fetal pancreas occurs, resulting in hyperinsulinemia. Disruption of the fetal glucose supply occurs with the clamping of the umbilical cord, and the neonate's blood glucose level falls rapidly in the presence of fetal hyperinsulinism. Hypoglycemia is most common in the macrosomic or preterm infant, but blood glucose levels should be monitored in all infants of mothers with known or suspected diabetes.

Asymptomatic or symptomatic hypoglycemia most commonly manifests within the first 1 to 3 hours after birth. Signs of hypoglycemia include jitteriness, apnea, tachypnea, and cyanosis. Significant hypoglycemia may result in seizures. Hypoglycemia is worsened by the presence of hypothermia or respiratory distress.

 

Hypocalcemia and Hypomagnesemia

Hypocalcemia occurs in as many as 50% of these infants. A number of these cases are related to hypoxia or prematurity; however, the overall incidence of hypocalcemia is higher than in nondiabetic pregnancies. Hypomagnesemia is be­lieved to develop because of maternal renal losses that occur in diabetes. Hypocalcemia is associated with preterm birth, birth trauma, and perinatal asphyxia. Signs of hypocalcemia are similar to those of hypoglycemia, but they occur between 24 and 36 hours of age. Hypocalcemia must be considered if therapy for hypoglycemia is ineffective.

 

Cardiomyopathy

All infants of mothers with diabetes need careful observa­tion for cardiomyopathy because an increased heart size is often found among these infants. Two types of cardiomyopathy can occur. Clinicians must correctly identify the type of lesion so that appropriate therapy is instituted. Both types of lesions are associated with respiratory symptoms and congestive heart failure.

 

Hyperbilirubinemia and Polycythemia

These infants are at increased risk of developing hyperbilirubinemia. Many are also polycythemic. Polycythemia increases blood viscosity, thereby impairing circulation. In addition, this increased number of RBCs to be hemolyzed increases the potential bilirubin load that the neonate must clear. The excessive RBCs are produced in extramedullary foci (liver and spleen) in addition to the usual sites in bone marrow. Therefore both liver function and bilirubin clearance may be adversely affected. Bruising associated with birth of a macrosomic infant will con­tribute further to high bilirubin levels.

Ideally, planning for the care of the infant begins during the antenatal period. Pediatric staff members are pre­sent at the birth. Nursing care depends on the neonate's particular problems. If the maternal blood glucose level was well controlled throughout the pregnancy, the infant may require only monitoring. Because euglycemia is not always possible, the nurse must promptly recognize and treat any consequences of maternal diabetes that arise.