Normal pregnancy is characterized by complex alterations in maternal glucose metabolism, insulin production, and metabolic homeostasis. Glucose levels in the fetus are directly proportional to maternal levels. Glucose crosses the placenta, insulin does not. Women with insulin-dependent diabetes are prone to hypoglycemia during the first trimester. During the second and third trimesters, pregnancy exerts a “diabetogenic” effect on the maternal metabolic status. Major hormonal changes cause the following:
Decreased tolerance to glucose
Increased insulin resistance
Decreased hepatic glycogen stores
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
Smith, D. (2020). Insulin requirements in pregnancy - Diabetogenic State of Pregnancy.
Maternal insulin requirements gradually increase from approximately 18 to 24 weeks of gestation to approximately 36 weeks of gestation. Birth, expulsion of the placenta prompts an abrupt drop in levels of circulating placental hormones, cortisol, and insulinase. Maternal tissues quickly regain their pre-pregnancy sensitivity to insulin. For the non-breastfeeding mother, the pre-pregnancy insulin-carbohydrate balance usually returns in approximately seven to ten days. Lactation uses maternal glucose; the breastfeeding mother’s insulin requirements remain lower during lactation.
Prevalence of diabetes among women of childbearing age is increasing in the United States. Perinatal mortality rate for well-managed pregnancies complicated by diabetes, 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 and throughout the gestational period.
Diabetes mellitus refers to a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
Current classification system includes four groups: type 1 diabetes, type 2 diabetes, other specific types (e.g., diabetes caused by genetic defects in β cell function or insulin action, disease or injury of the pancreas, or drug-induced diabetes), and gestational diabetes mellitus (GDM). Pre-gestational diabetes mellitus is the label sometimes given to type 1 or type 2 diabetes that existed before pregnancy. Gestational diabetes mellitus is defined as carbohydrate intolerance with the onset or first recognition occurring during pregnancy. ADA has adopted a new definition for gestational diabetes that excludes women with preexisting diabetes (type 1 or type 2) that is diagnosed during pregnancy. This definition for GDM is simply diabetes diagnosed during pregnancy that is clearly not overt (preexisting) diabetes.
White's System of Diabetes Classification estimates risk associated with gestational diabetes. White’s system was based on age at diagnosis, duration of illness, and presence of end-organ, especially eye and kidney, involvement. A new system has since been developed by the ADA that further classifies type 1 and type 2 diabetes as: without vascular complications or with vascular complications that are specified.
"Diabete Type I & II" by Jessie MNG Lopez, used under CCBY SA 3.0/Cropped from original
Women who have pregestational diabetes mellitus can have either Type 1 or 2 diabetes, which may be complicated by vascular disease, retinopathy, nephropathy, or other diabetic complications. Type 2 is a more common diagnosis than Type 1. Almost all women with pregestational diabetes are insulin dependent:
During the first trimester, when maternal blood glucose levels are normally reduced and the insulin response to glucose is enhanced
Glycemic control may be improved because insulin requirements steadily increase after the first trimester, the insulin dose must be adjusted accordingly to prevent hyperglycemia
Insulin resistance begins as early as 14 to 16 weeks of gestation and continues to rise until it stabilizes during the last few weeks of pregnancy
Ideally a woman with diabetes who is planning to become pregnant will consult with their provider before they become pregnant and be in good glycemic control. For those who have pregestational diabetes, it must be controlled well before pregnancy as a high glucose level can be teratogenic and cause fetal demise late in pregnancy. They would also be at risk for hyperglycemia, hypoglycemia, and diabetic ketoacidosis (DKA). Women with diabetes should follow an 1800 to 2400 kcal diet made up of 20% protein, 60% carbohydrates, and 10% fat; goals for glucose levels should be between 60–90 fasting, <140 mg/dL 1-hour postprandial, and <120 mg/dL for 2-hour postprandial or at bedtime.
Euglycemia is a normal blood glucose level, which is the goal. Poor glycemic control around the time of conception and in the early weeks of pregnancy is associated with an increased incidence of miscarriage. Poor glycemic control later in pregnancy, particularly in women without vascular disease, increases the rate of fetal macrosomia. Macrosomia has been defined as a birthweight more than 4000 to 4500 g or greater than the 90th percentile. Infants born to women with diabetes tend to have a disproportionate increase in shoulder, trunk, and chest size. Women with diabetes face an increased likelihood of cesarean birth because of failure of fetal descent or labor progress or of operative vaginal birth (birth involving the use of episiotomy, forceps, or vacuum extractor). Women with preexisting diabetes are at risk for several obstetric and medical complications:
Hypertension
Preeclampsia
Cesarean birth
Preterm birth
Maternal mortality
Risk of developing these complications increases with the duration and severity of the woman’s diabetes.
Hydramnios (polyhydramnios) frequently develops during the third trimester of pregnancy in women with diabetes. Complications most frequently associated with hydramnios (defined as an amniotic fluid index [AFI] > 24 cm) are placental abruption, uterine dysfunction, and postpartum hemorrhage.
Infections are more common, including vaginal infections such as urinary tract infections (UTIs).
Ketoacidosis (accumulation of ketones in the blood resulting from hyperglycemia and leading to metabolic acidosis) occurs most often during the second and third trimesters, when the diabetogenic effect of pregnancy is greatest. DKA may occur with blood glucose levels barely exceeding 200 mg/dL, compared with 300 to 350 mg/dL in the nonpregnant state. During times of stress, such as infection or illness, stress hormones cause an increase in hepatic glucose production and decreased peripheral uptake of glucose, leading to hyperglycemia (a greater than normal amount of glucose in the blood). Ketoacidosis occurring at any time during pregnancy can lead to intrauterine fetal death.
Risk for hypoglycemia (a less than normal amount of glucose in the blood) is increased during pregnancy. Early in pregnancy, when hepatic production of glucose is diminished and peripheral use of glucose is enhanced, hypoglycemia occurs frequently.
Hyperglycemia creates an increased risk of:
Miscarriage
Congenital malformations
Respiratory distress syndrome
Extreme prematurity
Hyperglycemia during the first trimester of pregnancy, when organs and organ systems are forming, is the main cause of diabetes-associated birth defects. Anomalies commonly seen in infants born to women with diabetes are the cardiovascular system and central nervous system (CNS).
Fetal Risks and Complications
Fetal pancreas begins to secrete insulin at 10 to 14 weeks of gestation. 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 and leading to increased fetal size, or macrosomia. Birth injuries are more common in infants born to mothers with diabetes compared with mothers who do not have diabetes, and macrosomic fetuses have the highest risk for this complication. Common birth injuries associated with diabetic pregnancies include:
Brachial plexus palsy
Facial nerve injury
Humerus or clavicle fracture
Cephalhematoma
Hypoglycemia for the infant at birth due to the hyperinsulinism
Intrauterine Fetal Demise (IUFD - sometimes called stillbirth) remains a major concern. Poor glycemic control is the most consistent finding in women who had a stillbirth. In addition to hyperglycemia, other causes of stillbirth include:
Congenital abnormalities
Placental insufficiency
Fetal growth restriction
Macrosomia
Polyhydramnios
Obstructed labor (intrapartum stillbirth)
Routine prenatal laboratory tests are performed, and baseline renal function may be assessed with a 24-hour urine collection for total protein excretion and creatinine clearance. Urinalysis and culture are performed to assess for the presence of a UTI. Because of the risk for coexisting thyroid disease, thyroid function tests may also be performed (see later discussion of thyroid disorders). Glycosylated hemoglobin A1c level may be measured to assess recent glycemic control (“diabetic report card” or evaluation of past glycemic control). Hemoglobin A1c levels less than 6 to 6.5 in early pregnancy have been associated with the lowest rates of adverse fetal outcomes.
Problems often experienced by the woman with pregestational diabetes include the following:
Need for health teaching related to...
Diabetic pregnancy, management, and potential effects on pregnant woman and fetus
Insulin administration and its effects
Hypoglycemia and hyperglycemia
Diabetic diet
Anxiety, grieving, decreased ability to cope, decreased adherence, decreased self-esteem related to...
Stigma of being labeled “diabetic”
Effects of diabetes and its potential sequelae on the pregnant woman and the fetus
Potential for injury to fetus related to...
Disruption of oxygen transfer from environment to fetus
Birth trauma
Potential for injury to mother related to...
Improper insulin administration
Hypoglycemia and hyperglycemia
Cesarean or operative vaginal birth
Postpartum infection
During the first and second trimesters of pregnancy, routine prenatal care visits are scheduled every one to two weeks. In the last trimester women will likely be seen one or two times each week. Achieving and maintaining constant euglycemia is the primary goal of medical therapy. Blood glucose levels should be in the range of 60 to 105 mg/dL before meals and 140 mg/dL or less when measured one hour after a meal. Postmeal glucose levels at 2 hours should be no higher than 120 mg/dL. Euglycemia is achieved through a combination of diet, insulin, and exercise.
Dietary management during diabetic pregnancy must be based on blood (not urine) glucose levels. Diet is individualized to allow for increased fetal and metabolic requirements, with consideration of such factors as:
Prepregnancy weight
Dietary habits
Overall health
Ethnic background
Lifestyle
Stage of pregnancy
Knowledge of nutrition
Insulin therapy
Being active for 30 to 60 min/day is encouraged. Daily activity has been shown to:
Increase insulin sensitivity, thus lowering blood glucose levels
Increase utilization of glucose, especially after a meal
Improve glucose control, perhaps eliminating the need for insulin therapy
Reduce the risk for excessive weight gain
Reduce the weight of the newborn by approximately 150
Physical activity can be divided into 10- to 20-minute periods after each meal
Adequate insulin is the primary factor in the maintenance of euglycemia during pregnancy. Insulin requirements during pregnancy change dramatically as the pregnancy progresses.
Blood glucose testing at home using a glucose meter is considered the standard of care for monitoring blood glucose levels during pregnancy.
Urine testing for glucose is not beneficial during pregnancy.
Occasionally, hospitalization is necessary to regulate insulin therapy and stabilize glucose levels. Infection, which can lead to hyperglycemia and DKA, may be an indication for hospitalization. Hospitalization during the third trimester for close maternal and fetal observation may be indicated for women whose diabetes is poorly controlled. Women with diabetes are more likely than women who do not have diabetes to also have preexisting hypertension or develop preeclampsia, which may necessitate hospitalization.
Diagnostic techniques for fetal surveillance are often performed to assess fetal growth and well-being. Goals of fetal surveillance are to detect fetal compromise as early as possible and prevent IUFD or unnecessary preterm birth. Early in pregnancy the estimated date of birth is determined. Baseline ultrasound is obtained during the first trimester to assess gestational age. Follow-up ultrasound examinations are usually performed during the pregnancy (as often as every three to four weeks) to monitor:
Fetal growth
Estimate fetal weight
Detect hydramnios
Macrosomia
Congenital anomalies
Maternal serum α-fetoprotein is performed between 15 and 20 weeks of gestation
Detailed ultrasound study to examine the fetus for neural tube defects and other anomalies should be performed between 18 and 20 weeks of gestation
Women with pregestational diabetes are also more likely to give birth to infants with congenital cardiac anomalies. Fetal echocardiography may be performed between 20 and 22 weeks of gestation to detect cardiac anomalies. Most fetal surveillance measures are concentrated in the third trimester, when the risk of fetal compromise is greatest. Goals of antepartum testing during the third trimester are to monitor fetal growth and ensure fetal well-being. Pregnant women should be taught how to make daily fetal movement counts, beginning at 28 weeks of gestation. A nonstress test (NST) is the preferred primary method to evaluate fetal well-being. It usually begins by 32 weeks of gestation and performed at least twice weekly. If the NST is nonreactive, a biophysical profile or contraction stress test will be performed. Testing often begins earlier, between 28 and 32 weeks of gestation, in women who have vascular disease, poor glucose control, or suspected fetal growth restriction.
Optimal time for birth is between 39 and 40 weeks of gestation, as long as good metabolic control is maintained and parameters of antepartum fetal surveillance remain within normal limits. Induction of labor at 39 weeks of gestation is often planned for women with well-controlled diabetes who do not have vascular disease. Reasons to proceed with birth before term are poor metabolic control, coexisting hypertension, and nonreassuring responses to fetal testing. To confirm fetal lung maturity, amniocentesis should be performed when birth will occur before 38 weeks of gestation. The cesarean rate for these women is high.
Intrapartum care monitors dehydration, hypoglycemia, and hyperglycemia. IV line is inserted. Insulin is administered by continuous infusion, piggybacked into the main IV line. Only rapid- or short-acting insulin can be administered intravenously. Insulin may also be given intermittently by subcutaneous injection as needed to maintain glucose levels within the target range. Determinations of blood glucose levels are made every hour, and fluids and insulin are adjusted to maintain the blood glucose level between 90 and 110 mg/dL. Continuous fetal heart monitoring also occurs in this type of care.
During the first 24 hours postpartum, insulin requirements decrease substantially because the major source of insulin resistance, the placenta, has been removed. Possible postpartum complications include: preeclampsia or eclampsia, hemorrhage, or infections.
Global Health Media Project (2023, February 15). Dibetes in Pregnancy: https://globalhealthmedia.org/videos/diabetes-in-pregnancy-english/
Pathophysiology
As stated above, there are several factors that contribute to GDM. There are metabolic changes that promote the accumulation of adipose tissue early in gestation, followed by insulin resistance in the last half of pregnancy. Also, the growing placenta will produce hormones that have a blocking effect on insulin. These changes are known as the diabetogenic state of pregnancy. Normally, the pancreas can handle the increased need for insulin, but for those that cannot, a diagnosis of GDM is made. The image to the right displays the association of insulin needs as pregnancy progresses.
Gestational diabetes mellitus is diagnosed during the second half of pregnancy. Fetal nutrient demands rise during the late second and the third trimesters. Maternal nutrient ingestion induces greater and more sustained levels of blood glucose. Maternal insulin resistance is also increasing because of the insulin-antagonistic effects of the placental hormones, cortisol, and insulinase. Consequently, maternal insulin demands rise as much as threefold. Most pregnant women are capable of increasing insulin production to compensate for insulin resistance and maintain euglycemia. When the pancreas is unable to produce sufficient insulin or the insulin is not used effectively, GDM can result.
All pregnant women not known to have pregestational diabetes should be screened for GDM by history, clinical risk factors, and laboratory screening of blood glucose levels. Most women are screened for GDM between 24 and 28 weeks of gestation, those with strong risk factors should be screened earlier in pregnancy.
Two different blood glucose screening methods for GDM are used in the United States: the two-step method and the one-step method.
Smith, D. (2023). GDM Testing
No increase in the incidence of birth defects has been found among infants of women who develop GDM after the first trimester because the critical period of organ formation has already passed by the time that blood glucose levels increase. Important to note that obesity (BMI >30) also contributes to congenital defects even in the absence of GDM. As with pregestational diabetes, infants born to women with GDM are at risk for macrosomia and associated risks for birth trauma and electrolyte imbalances including neonatal hypoglycemia and hyperinsulinemia.
Complications Due to GDM
The delivery of higher glucose to the baby can cause macrosomia (large baby) potentially leading to:
Delivery complications such as cephalopelvic disproportion (CPD) where the passenger does not fit well in the passageway
Shoulder dystocia where the infant’s shoulder is stuck behind the pubic bone
Injury to the mother’s bony pelvis or soft tissue
Injury to the baby
Increased chance of assisted delivery with vacuum or forceps
Increased chance of cesarean section delivery
Hyperinsulinemia in the infant to accommodate for the mother’s higher blood sugar continues after the cord is cut, leading to hypoglycemia. Early feedings and glucose testing are done to intervene before it is too low (<40 mg/dL).
Treatment of GDM: Initially, women who are diagnosed with GDM will use dietary changes (20% protein, 40% carbohydrates, and 40% fat) and moderate exercise to control their blood glucose. Target blood levels are the same for people with pregestational diabetes. Insulin is the preferred first-line therapy for GDM; both rapid-acting and long-acting insulin are used, and neither pass through the placenta. Oral treatment such as metformin and glyburide can be used; however, both can cross the placenta affecting the fetus.
Fetal surveillance includes NSTs, BPPs, AFI, and Doppler flow studies and will occur every week or twice weekly through the third trimester. Women who have uncomplicated, well-controlled pregestational diabetes or GDM will be delivered by their due date. If they have poor glycemic control, vascular complications, or fetal compromise, delivery will occur between 36-0/7 weeks to 38-6/7 weeks.
Aim of therapy in women with GDM is strict blood glucose control. Fasting blood glucose levels less than 95 mg/dL, 1-hour postmeal blood glucose levels less than 140 mg/dL, and 2-hour postmeal glucose levels less than 120 mg/dL are optimum.
Dietary modification is the mainstay of treatment for GDM. Woman with GDM is placed on a standard diabetic diet. Usual prescription is 2000 to 2500 kcal/day, which represents approximately 35 kcal/kg/day of present pregnancy weight. For overweight or obese women, a reduction to 25 kcal/kg/day and 15 kcal/kg/day.
Few published studies on the benefits of exercise in women with GDM. Adults who are not pregnant, exercise increases lean muscle mass and improves sensitivity to insulin. Moderate exercise program is recommended for overweight or obese women with GDM to improve blood sugar control and facilitate weight loss.
Blood glucose monitoring is necessary to determine whether euglycemia can be maintained by diet and exercise.
If fasting plasma glucose levels are persistently greater than 95 mg/dL, 1-hour postmeal levels are persistently greater than 140 mg/dL, or 2-hour postmeal levels are persistently greater than 120 mg/dL, pharmacologic therapy is begun. Insulin is the preferred medication to treat Gestational Diabetes because it does not cross the placenta to the fetus. Metformin and glyburide are both used for blood glucose control in women with GDM, but they can cross the placenta and affect the fetal glycemic control.
Metformin works by decreasing hepatic glucose production and increasing peripheral sensitivity to insulin.
Glyburide works by causing the maternal pancreas to produce more insulin.
Women with GDM whose blood glucose levels are well controlled by diet are at low risk for IUFD. Antepartum fetal testing is not performed routinely in these women unless they also have:
Hypertension
History of a prior stillbirth
Suspected macrosomia
Women with these complications or those who require insulin or oral hypoglycemic agents for blood glucose control may have twice-weekly NSTs beginning at 32 weeks of gestation.
During the labor and birth process, blood glucose levels are monitored hourly to maintain levels at 80 to 110 mg/dL.
Most women with GDM return to normal glucose levels after birth, up to one-third will be found to have diabetes or impaired glucose metabolism when they are screened postpartum. Children born to women with GDM are at risk for future health-related complications because they may develop obesity and type 2 diabetes later in life. All women who had GDM should be assessed for carbohydrate intolerance with a 75-g, 2-hr OGTT or a fasting plasma glucose level at six to twelve weeks postpartum. Recommended lifelong repeat screening at least every three years for women with a history of GDM and normal postpartum glucose testing results. Low-dose combined oral contraceptives may be safely used by women with a history of GDM. The rate of subsequent diabetes in these women is no different from that in women without a history of GDM who use low-dose oral contraceptives.
Causes of nausea and vomiting in pregnancy (NVP) :
increasing levels of estrogen, progesterone, and human chorionic gonadotropin (hCG)
gastric changes
thyroid changes
When vomiting during pregnancy becomes excessive enough to cause weight loss, electrolyte imbalance, nutritional deficiencies, and ketonuria, the disorder is termed hyperemesis gravidarum. Hyperemesis gravidarum usually begins during the first trimester and is classified as NVP that persists beyond the first trimester.
Med Vids Made Simple (2018, May 12). Vomiting in Pregnancy/ Hyperemesis Gravidarum: https://www.youtube.com/watch?v=wgfQMhBY3CM
Risk Factors
Maternal characteristics:
younger maternal age
nulliparity
BMI less than 18.5 or greater than 25
low socioeconomic status
women with:
asthma
migraines
preexisting diabetes
psychiatric illness
hyperthyroid disorders
gastrointestinal disorders
previous pregnancy complicated by hyperemesis gravidarum
female fetus
multifetal gestation
gestational trophoblastic disease
maternal family history of hyperemesis
Complications
Although rare, maternal complications of hyperemesis gravidarum:
esophageal rupture
pneumomediastinum
deficiencies of vitamin K and thiamine
Infants born to women who had poor pregnancy weight gain because of hyperemesis may be small for gestational age, have a low birthweight, or be born prematurely.
Clinical Manifestations
A woman with hyperemesis gravidarum usually has:
significant weight loss and dehydration
dry mucous membranes
decreased BP
increased pulse rate
poor skin turgor
unable to keep down even clear liquids taken by mouth
laboratory tests that reveal electrolyte imbalances
Assessment
Physical assessment should include:
Frequency, severity, and duration of episodes of nausea and vomiting, including approximate amount and color of the vomitus
Presence of diarrhea, indigestion, and abdominal pain or distention
Precipitating and alleviating factors
Any pharmacologic or nonpharmacologic treatment measures used
Complete physical examination with special attention to measures of fluid and electrolyte balance, nutritional status, and gastric, liver, thyroid, heart, and lung function
Prepregnancy weight and gain or loss during pregnancy
Care Management
It is very important for initial laboratory testing to be obtained for the determination of dehydration and ketonuria
Other laboratory tests that may be ordered:
urinalysis
complete blood cell count
electrolytes
liver enzymes
bilirubin levels
thyroid levels
lab tests help to rule out underlying diseases:
gastroenteritis
pyelonephritis
pancreatitis
cholecystitis
peptic ulcer
hepatitis
hyperthyroidism
psychosocial assessment includes asking the woman about anxiety, fears, and concerns related to her own health and the effects on pregnancy outcome
Client Problems
Problems identified in women experiencing hyperemesis gravidarum include:
Dehydration related to excessive vomiting as evidenced by fluid and electrolyte imbalance
Inadequate weight gain, related to nausea and persistent vomiting as evidenced by weight decrease as compared with prepregnant weight
Anxiety related to effects of hyperemesis on fetal well-being as evidenced by woman’s statements of concern
Interventions
Initially the woman who is unable to retain clear liquids by mouth requires IV therapy for correction of fluid and electrolyte imbalances. Medications may be used if nausea and vomiting are uncontrolled including:
pyridoxine (vitamin B6), either alone or in combination with doxylamine (Unisom)
dopamine antagonists such as promethazine (Phenergan)
chlorpromazine (Thorazine)
prochlorperazine (Compazine)
metoclopramide (Reglan) accelerates gastric emptying and corrects gastric dysrhythmias
ondansetron (Zofran)
droperidol (Inapsine)
corticosteroids (methylprednisolone [Medrol] or hydrocortisone) may be prescribed for women who do not respond well to the medications previously discussed,
antiemetic drugs, medications to control heartburn or reflux may also be prescribed
antacids, histamine blockers, and proton pump inhibitors
In extreme cases of Hyperemesis, enteral or parenteral nutrition may be used
Nursing care of the woman with hyperemesis gravidarum:
Implementing the medical plan of care
initiating and monitoring IV therapy
administering drugs and nutritional supplements
monitoring the woman’s response to interventions
Observe for any signs of complications such as:
metabolic acidosis (secondary to starvation)
Jaundice
hemorrhage and alerts the health care provider should these occur
monitoring includes:
assessing nausea, retching without vomiting (sometimes called dry heaves), and vomiting
intake and output
oral hygiene
positioning and providing a quiet, restful environment that is free from odors may increase the woman’s comfort
Thyroid hormones are important in developing the brain and nervous system of the fetus. Initially the hormones are supplied through the placenta, but by about 18-20 weeks gestation, the fetus' thyroid begins to work and it will develop its own.
In early pregnancy, normal values are a little lower in early pregnancy; later in pregnancy, the values are more normal. Treatment is based on trimester-specific levels. Thyroid levels should be checked monthly.
Hypothyroidism: Treat with Synthroid
Hyperthyroidism: If prior to pregnancy, treat with radioactive iodine, delay pregnancy six months; if during pregnancy, can treat with propylthiouracil (PTU) (safe in the first trimester), then may transition to Tapazole later
Signs and Symptoms
The signs and symptoms of thyroid disease mimic the common discomforts of pregnancy, so they can be hard to diagnose. They include:
Hypothyroidism
Fatigue
Unexplained weight gain (more than expected in pregnancy and not due to edema)
Feeling frigid
Severe constipaton
Muscle cramping
Problems with memory
Hyperthyroidism
Fast or irregular heartbeat
Feeling shaky
Unexplained weight loss
Medmastery (2018, February 27). Examining Abnormal Thyroid Function During Pregnancy: https://www.youtube.com/watch?v=3srhQfWbe-0
Postpartum Thyroiditis can occur after delivery. Symptoms may be mild, but may last several months and could be confused with normal postpartum symptoms. They include:
Irritability
Heat itolerance
Fatigue, insomnia
Tachycardia
Mood disturbances
Effects on the Fetus
Hypothyroidism
Miscarriage, preterm birth
Low birth weight
Preeclampsia
Stillbirth
Anemia
Congestive heart failure
Hyperthyroidism
Miscarriage or preterm birth
Low birth weight
Preeclampsia
Thyroid Storm (sudden, severe increase in symptoms)
Congestive heart failure
Effects on the Newborn
Hypothyroidism
Decreased brain and nervous system development (because it is so important in the development); lower IQ as grows
Hyperthyroidism
Tachycardia
Early closing of the fontanels
Poor weight gain
Irritability
American College of Obstetricians and Gynecologis (2018). ACOG Practice Bulletin Number 201: Pregestational Diabetes Mellitus: National Library of Medicine: https://pubmed.ncbi.nlm.nih.gov/30461693/
American College of Obstetricians and Gynecologists (2022, May). FAQs: Pregnancy with Type 1 or Type 2 Diabetes: https://www.acog.org/womens-health/faqs/pregnancy-with-type-1-or-type-2-diabetes
American College of Obstetricians and Gynecologists (2022 July). FAQs: Gestational Diabetes. https://www.acog.org/womens-health/faqs/gestational-diabetes
Berghella, V., Caissutti, C., Saccone, G., & Khalife, A. (2019). American Journal of Obstetrics and Gynecology, 220(6): p P562-564. https://www.ajog.org/article/S0002-9378(19)30285-6/fulltext#:~:text=The%20One%20Step%20approach%20consists,153%20mg%2FdL%2C%20respectively.
HER Foundation (2022). Healthcare Provider information: https://www.hyperemesis.org/who-we-help/healthcare-providers/
Jennings, L.K. & Mahdy, H. (2023, July 31). Hyperemesis Gravidarum. National Institute of Health Stat Pearls: https://www.ncbi.nlm.nih.gov/books/NBK532917/#:~:text=Hyperemesis%20gravidarum%20refers%20to%20intractable,nausea%20and%20vomiting%20in%20pregnancy.
National Institute of Diabetes and Digestive and Kidney Diseases (2017). Thyroid Disease and Pregnancy: https://www.niddk.nih.gov/health-information/endocrine-diseases/pregnancy-thyroid-disease
OBGproject (n.d.). Updated ACOG Guidance on Gestational Diabetes: https://www.obgproject.com/2023/01/02/acog-releases-updated-guidance-gestational-diabetes/
Ramprasad, M, Bhattacharyya, S.S, & Bhattacharyya, A. ( 2012). Thyroid Disorders in Pregnancy. Indian Journal of Endocrinology and Metabolism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3603018/#:~:text=Maternal%20hypothyroidism%20is%20an%20easily,as%20conception%20is%20a%20problem.