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Printed in China. Library of Congress Cataloging-in-Publication Data. Manual of neonatal care / editors, John P. Cloherty [et al.]. — 7th ed. Cloherty Of Neonatal Care 7th Edition Free cloherty and starks manual of neonatal care pdf - manual of neonatal care pdf epub mobi ebook. Cloherty and Stark's Manual of Neonatal Care - Wolters Kluwer. Cloherty and stark's manual of neonatal care 8th Edition PDF free download For measurements.
Insulin causes increased erythropoietin. All classes below A require insulin. Cloherty, John P. These infants may be at increased risk for neonatal infection. Free T4 levels rise much less than total T4 in early pregnancy see I. Intrapartum management of preeclampsia 1. Reduced matemal25 0H vitamin D levels have recently been associated with an increased risk of preeclampsia.
The White classification is a risk stratification profile based on length of disease and presence of vascular complications see Table 2.
Risk factors for GDM include advanced maternal age, multifetal gestation, increased body mass index, and strong family history of diabetes. Pathophysiology for diabetoi antedating pregnancy. In the first half of pregnancy, as a result of nausea and vomiting, hypoglyamia can be as much of a problem as hyperglycemia. Hypoglycemia, followed by hyperglycemia from counter-regulatory hormones, may complicate glucose control.
Maternal hyperglycemia leads to fetal hyperglycemia and fetal hyperinsulinemia, which results in fetal overgrowth. Gastroparesis from long-standing diabetes may be a factor as well. There does not appear to be a direct relation between hypoglycemia alone and Diabetes not known to be present before pregnancy Abnormal glucose tolerance test in pregnancy. Onset before 10 years of age 0 2: Duration 20 years 0 3: Calcification of vessels of the leg Cmacrovascular disease 0 4: Benign retinopathy microvascular disease Hypertension not preeclampsia.
All classes below A require insulin. Classes R, F, RF, H, and T have no criteria for age of onset or duration of disease but usually occur in long-term diabetes. Modified from Hare JW. Gestational diabetes. Diabetes complicating pregnancy: The Joslin Clinic Method. New York: Alan R. Liss; Throughout pregnancy, insulin requirements increase because of the increasing production of placental hormones that antagonize the action of insulin. Tills is most prominent in the mid-third trimester and requires intensive blood glucose monitoring and frequent adjustment of insulin dosage.
Differential diagnosis a. Ketoacidosis is an uncommon complication during pregnancy. Ketoacidosis can be present in the setting of even mild hyperglycemia mgldL and should be excluded in every patient with type 1 diabetes who presents with hyperglycemia and symptoms such as nausea, vomiting, or abdominal pain.
Stillbirth remains an uncommon complication of diabetes in pregnancy. It is most often associated with poor glycemic control, fetal anomalies, severe vasculopathy, and intrauterine growth restriction IUGR , as well as severe preeclampsia.
Shoulder dystocia that cannot be resolved can also result in fetal death. Polyhydramnios is not an uncommon finding in pregnancies complicated by diabetes. It may be secondary to osmotic diuresis from fetal hyperglycemia. Careful ultrasonographic examination is required to rule out structural anomalies, such as esophageal atresia, as an etiology, when polyhydramnios is present. Severe maternal vasculopathy, especially nephropathy and hypertension, is associated with uteroplacental insufficiency, which can result in IUGR, fetal intolerance oflabor, and neonatal complications.
General principles for type 1 or type 2 diabetes. Management of type 1 or type 2 diabetes during pregnancy begins before conception. Tight glucose control is paramount during the periconceptional period and throughout pregnancy. Optimal glucose control requires coordinated care between endocrinologists, maternal-fetal medicine specialists, diabetes nurse educators, and nutritionists. Preconception glycemic control has been shown to decrease the risk of congenital anomalies to close to that of the general population.
Physicians should discuss pregnancy planning or recommend contraception for all diabetic women of childbearing age until glycemic control is optimized. General principles for gestational diabetes. In the United States, most women are screened for GDM between 24 and 28 weeks' gestation by a g, 1-hour glucose challenge. A positive test is defined as two or more elevated values on the GTT.
There is a current movement to move to a single diagnostic test, consisting of a g, 2-hour GTT, a method that is used uniformly outside of the United States. Uncontrolled GDM can lead to fetal macrosomia and concomitant risk of fetal injury at delivery.
GDM shares many features with type 2 diabetes. Testing first trimester for type 1 and type 2 diabetes a. Measurement of glycosylated hemoglobin in the first trimester can give a risk assessment for congenital anomalies by reflecting ambient glucose concentrations during the period of organogenesis.
Accurate dating of the pregnancy is obtained by ultrasonography. Ophthalmologic examination is mandatory, because retinopathy may progress because of the rapid normalization of glucose concentration in the first trimester. Women with retinopathy need periodic examinations throughout pregnancy, and they are candidates for laser photocoagulation as indicated.
Renal function is assessed by hour urine collection for protein excretion and creatinine clearance. Patients with recent diagnosis of diabetes can have screening of renal function with urine microalbumin, followed by a hour collection if abnormal. Thyroid function should be evaluated. Nuchal translucency and first-trimester serum screening.
This is part of routine pregnancy care. It is especially important, as an abnormal nuchal translucency is also associated with structural abnormities, the risk of which is increased in this group of patients. Testing second trimester for type 1 and type 2 diabetes a. Maternal serum screening for neural tube defects is performed between 15 and 19 weeks' gestation. Women with diabetes have a fold increased risk of neural tube defects compared to the general population.
All patients undergo a thorough ultrasonographic S11I'lq", including fetal echocardiography for structural anomalies. Women older than 35 years of age or with other risk factors for fetal aneuploidy are offered chorionic villus sampling or amniocentesis for karyotyping.
Testing third trimester for type 1 and type 2 diabetes, GDM a. Treatment for all types of glucose intolerance. Insulin therapy has the longest record of accomplishment of perinatal safety. It has been demonstrated that human insulin analogs do not cross the placenta. More recently, the oral hypoglycemic agent glyburide has been shown to be effective in the management of GDM.
Data are emerging that metformin may also be an alternative to achieve glycemic goals during pregnancy. General principles. The risk of spontaneous preterm labor is not increased in patients with diabetes, although the risk of iatrogenic preterm delivery is increased for patients with microvascular disease as a result ofiUGR, nonreassuring fetal testing, and maternal hypertension. Antenatal corticosteroids for induction of FLM should be employed for the usual obstetric indications.
Corticosteroids can cause temporary hyperglycemia; therefore, patients may need to be managed. Elective delivery after 39 weeks does not require FLM testing.
Nonemergent delivery before 39 weeks requires documentation ofFLM testing using the lecithin-sphingomyelin LIS ratio greater than 3. Emergent delivery should be carried out without FLM testing.
Route of delivery is determined by ultrasonography-estimated fetal weight, maternal and fetal conditions, and previous obstetric history. The ultrasonography-estimated weight at which an elective cesarean delivery is recommended is a controversial issue, with the American College of Obstetricians and Gynecologists recommending discussion of cesarean delivery at an estimated fetal weight of greater than 4, g due to the increased risk of shoulder dystocia.
Blood glucose concentration is tightly controlled during labor and delivery. If an induction of labor is planned, patients are instructed to take onehalf of their usual basal insulin on the morning of induction.
During spontaneous or induced labor, blood glucose concentration is measured every 1 to 2 hours. N insulin is very short acting, allowing for quick response to changes in glucose concentration. Active labor may also be associated with hypoglycemia, because the contracting uterus uses circulating metabolic fuels.
Continuous fetal monitoring is mandatory during labor. Cesarean delivery is performed for obstetric indications. Patients with advanced microvascular disease are at increased risk for cesarean delivery because of the increased incidence of IUGR, preeclampsia, and nonreassuring fetal status. A history of retinopathy that has been treated in the past is not necessarily an indication for. Figure 2. Rate of respiratory distress syndrome RDS versus gestational age in nondiabetic and diabetic pregnancies at the Boston Hospital for Women from to Association between maternal diabetes and the respiratorydistress syndrome in the newborn.
N Engl] Med ; Patients with active proliferative retinopathy that is unstable or active hemorrhage may benefit from elective cesarean delivery. Postpartum patients are at increased risk for hypoglycemia, especially in the postoperative setting with minimal oral intake. Patients with pregestational diabetes may also experience a "honeymoon'' period immediately after delivery, with greatly reduced insulin requirements that can last up to several days.
Lactation is also associated with significant glucose utilization and potential hypoglycemia, especially in the immediate postpartum period. For women with type 2 diabetes, the use of metformin and glyburide is compatible with breastfeeding. The evaluation of the infant begins before actual deli-very.
If pulmonary maturity is not certain, amniotic fluid can be obtained before delivery through amniocentesis. Treatment 1. After the infant is hom, assessment is made on the basis of Apgar scores to determine the need for any resuscitative efforts see Chap. The infant should be dried and placed under a warmer. The airway is bulb suctioned for mucus, but the stomach is not aspirated because of the risk of reflex: A screening physical examination for the presence of major congenital anomalies should be performed, and the placenta should be examined.
Glucose level and pH may be determined. In the nursery, supportive care should be given while a continuous evaluation of the infant is made. This includes providing wannth, suction, and oxygen as needed while checking vital signs e. Cyanosis should make one consider cardiac disease, respiratory distress syndrome RDS , transient tachypnea of the newborn, or polycythemia.
An examination should be repeated for possible anomalies because of the increased incidence of major congenital anomalies in IDMs. Special attention should be paid to the brain, heart, kidneys, and skeletal system. The infant is fed orally or given IV glucose by 1 hour of age see VI. Hematocrit levd. Calcium levels are checked if the infant appears jittery or is sick for any reason see VIII. Bilirubin levels are checked if the infant appears jaundiced see Chap.
Every effort is made to involve the parents in infant care as early as possible. The onset is frequently within 1 to 2 hours of age and is most common in macrosomic infants. The pathogenetic basis of neonatal hypoglycemia in IDMs is explained by the Pederson maternal hyperglycemia-fetal hyperinsulinism hypothesis.
The correlation among fetal macrosomia, elevated HbA1 in maternal and cord blood, and neonatal hypoglycemia, as well as between elevated cord blood C-peptide or immunoreactive insulin levels and hypoglycemia, suggests that control of maternal blood sugar in the last trimester may decrease the incidence of neonatal hypoglycemia in IDMs.
Mothers should not receive large doses of glucose before or at delivery, because this may stimulate an insulin response in the hyperinsulinemic offspring. We attempt to keep maternal glucose level at delivery at approximately mgldL.
Other factors that may cause hypoglycemia in IDMs are decreased catecholamine and glucagon secretion, as well as inadequate substrate mobilization diminished hepatic glucose production and decreased oxygenation of fatty acids. Diagnosis 1. Oinical praentation. Symptomatic, hypoglycemic IDMs are usually quiet and lethargic rather than jittery.
Symptoms such as apnea, tachypnea, respiratory distress, hypotonia, shock, cyanosis, and seizures may occur. If symptoms are present, the infant is probably at greater risk for sequelae.
L appears to be indicated. Laboratory studies. Our neonatal protocol is explained in V. The blood glucose level is measured more often if the infant is symptomatic or has had a low level previously.
The blood glucose level is also measured to see the response to therapy. Asymptomatic infants with normal blood glucose levels. Larger infants can be fed hourly for three or four feedings until the blood sugar determinations are stable. This schedule prevents some of the insulin release associated with oral feeding of pure glucose. The feedings can then be given every 2 hours and later every 3 hours, and as the interval between feedings increases, the volume is increased.
The basic treatment element is IV glucose administration through reliable access. Administration is usually by peripheral IV catheter. Peripheral lines may be difficult to place in obese IDMs, and sudden interruption of the infusion may cause a reactive hypoglycemia in such hyperinsulinemic infants. Rarely, in emergency situations, we have used umbilical venous catheters in the inferior vena cava until a stable peripheral line is placed. Specific treatment is determined by the infant's condition.
If the infant is in severe distress e. This is followed by a continuous infusion at a rate of 4 to 8 mg of glucose per kg of body weight per minute. The concentration of dextrose in the N fluid depends on the total daily fluid requirement. However, the concentration of dextrose and the infusion rates are increased as necessary to maintain the blood glucose level in the normal range Fig.
Blood glucose levds must be carefully monitored at frequent intervals after beginning N glucose infusions, both to be certain of adequate treatment of the hypoglycemia and to avoid hyperglycemia and the risk of osmotic diuresis and dehydration. Parenteral sugar should never be abruptly discontinued because of the risk of a reacti-vt: It is vital to measure blood glucose levels during tapering of the N infusion.
In difficult cases, hydrocortisone 5 mglkglday intramuscularly in two divided doses has occasionally been helpful. In our experience, other drugs epinephrine, diazoxide, or growth hormone have not been necessary in the treatment of the hypoglycemia ofiDMs. In a hypoglycemic infant, if difficulty is experienced in achieving vascular access, we may administer crystalline glucagon intramuscularly or subcutaneously JJ.
The rise in blood glucose may last 2 to 3 hours and is useful until parenteral glucose can be started. This method is rarely used. The hypoglycemia of most IDMs usually responds to the treatment mentioned earlier and resolves by 24 hours. Persistent hypoglyt: Efforts should be made to decrease islet cell stimulation e.
Pneumonia, pneumothorax, and diaphragmatic hernia should also be considered. Delayed lung maturity may occur in IDMs because hyperinsulinemia blocks cortisol induction oflung maturation.
Laboratory studies See Chap. Blood gas analysis should be performed to evaluate gas exchange and the presence of right-to-left shunts.
Blood cultures, with spinal-ftuid examination and culture, should be taken if the infant's condition permits and infection is a possibility. Imaging a.
A chest x-ray should be viewed to evaluate aeration, presence of infiltrates, cardiac size and position, and the presence of pneumothorax or anomalies.
An electrocardiogram and an echocardiogram should be taken if hypertrophic cardiomyopathy or a cardiac anomaly is thought to be present.
Congenital anomalies. Congenital anomalies occur more frequently in IDMs than in infants of nondiabetic mothers. As mortality from other causes such as prematurity, stillbirth, asphyxia, and RDS falls, malformations become the major cause of perinatal mortality in IDMs. Infants of diabetic fathers show the same incidence of anomalies as the normal population; therefore, the maternal environment may be the important factor.
The most common fetal structural defects associated with maternal diabetes are cardiac malformations, neural tube defects, renal agenesis, and skeletal malformations. Situs inversus also occurs. The central nervous system anencephaly, meningocele syndrome, holoprosencephaly and cardiac anomalies make up two-thirds of the malformations seen in IDMs. Although there is a general increase in the anomaly rate in IDMs, no anomaly is specific for IDMs, although half of all cases of caudal regression syndrome sacral agenesis are seen in IDMs.
There have been several studies correlating metabolic control of diabetes in early pregnancy with malformations in the IDMs. Among the more recent studies, that performed by the Joslin Clinic showed a relation between elevated HbA1 in the first trimester and major anomalies in IDMs.
The data are consistent with the hypothesis that poor metabolic control of maternal diabetes in the first trimester is associated with an increased risk of major congenital malformations. Hypocalcemia see Chap. Hypocalcemia in IDMs may be caused by a delay in the usual postnatal rise of parathyroid hormone or vitamin D antagonism at the intestinal level from elevated cortisol and hyperphosphatemia that is due to tissue catabolism.
There is no evidence of elevated serum calcitonin concentrations in these infants in the absence of prematurity or asphyxia. Other causes of hypocalcemia, such as asphyxia and prematurity, may be seen in IDMs. Hypocalcemia in "well" IDMs usually resolves without treatment, and we do not routinely measure serum calcium levels in asymptomatic IDMs. Infants who are sick for any reason-prematurity, asphyxia, infection, respiratory distress--or IDMs with symptoms of lethargy, jitteriness, or seizures that do not respond to glucose should have their serum calcium levels measured.
If an infant has symptoms that coexist with a low calcium level, has an illness that delays onset of calcium regulation, or is unable to feed, treatment with calcium may be necessary see Chap. Hypomagnesemia should be considered in hypocalcemia in IDMs because the hypocalcemia may not respond until the hypomagnesemia is treated. Polycythemia see Chap. This condition is common in IDMs.
It may be due to reduced oxygen delivery secondary to elevated HbA1 in both maternal and fetal blood. In SGA infants, polycythemia may be related to placental insufficiency, causing fetal hypoxia and increased erythropoietin. If fetal distress has occurred, there may be a shift of blood from the placenta to the fetus.
Bilirubin production is increased in IDMs as compared with infants of nondiabetic mothers. Mild hemolysis is compensated for but may cause increased bilirubin production.
Insulin causes increased erythropoietin. When measurement of carboxyhemoglobin production is used as an indicator of increased heme turnover, IDMs are found to have increased production as compared with controls. There may be decreased erythrocyte life span because of less deformable cell membranes, possibly related to glycosylation of the erythrocyte cell membrane.
Other factors that may account for jaundice are prematurity, impairment of the hepatic conjugation of bilirubin, and an increased enterohepatic circulation of bilirubin as a result of poor feeding. Infants born to well-controlled diabetic mothers have fewer problems with hyperbilirubinemia.
The increasing gestational age of IDMs at delivery has contributed to the decreased incidence of hyperbilirubinemia. Hyperbilirubinemia in IDMs is diagnosed and treated as in any other infant see Chap. Poor feeding. Infants born to women with class F diabetes are often preterm.
There was no difference in the incidence of poor feeding in large-for-gestational-age infants versus appropriate-for-gestational-age infants, and there was no relation to polyhydramnios. Sometimes, poor feeding is related to prematurity, respiratory distress, or other problems; however, it is often present in the absence of other problems. Poor feeding is a major reason for prolonged hospital stays and parent-infant separation.
Macrosomia is not usually seen in infants born to women with class F diabetes. Macrosomia may be linked with an increased incidence of primary cesarean section or obstetric trauma, such as fractured clavicle, Erb palsy, or phrenic nerve palsy as a result of shoulder dystocia.
Associations have been found between macrosomia and the following: Third-trimester elevated maternal blood sugar 2. Fetal and neonatal hyperinsulinemia 3. Neonatal hypoglycemia. Myocardial dysfunction. In IDMs, transient hypertrophic subaortic stenosis resulting from ventricular septal hypertrophy has been reported.
Infants may present with heart failure, poor cardiac output, and cardiomegaly. The cardiomyopathy may complicate the management of other illnesses such as RDS. Cardiac output decreases with increasing septal thickness. Most symptoms resolve by 2 weeks of age, and septal hypertrophy resolves by 4 months.
Most infants respond to supportive care. Oxygen and furosemide Lasix are often needed. Inotropic drugs are contraindicated unless myocardial dysfunction is seen on echocardiography. Propranolol is the most useful agent. The differential diagnosis of myocardial dysfunction that is due to diabetic cardiomyopathy of the newborn includes the following: Postasphyxial cardiomyopathy Myocarditis Endocardial fibroelastosis Glycogen storage disease of the heart Aberrant left coronary artery coming off the pulmonary artery.
There is some evidence that good diabetic control during pregnancy may reduce the incidence and severity of hypertrophic cardiomyopathy see Chap.
Renal vein thrombosis. Renal vein thrombosis may occur in utero or postpartum.
Intrauterine and postnatal diagnosis may be made by ultrasonographic examination. Postnatal presentation may include hematuria, Bank mass, hypertension, or embolic phenomena. Most renal vein thrombosis can be managed conservatively, allowing preservation of renal tissue see Chaps. Small left colon syndrome.
Small left colon syndrome presents as generalized abdominal distension because of inability to pass meconium. Meconium is obtained by passage of a rectal catheter. An enema performed with meglumine diatrizoate Gastrograffin makes the diagnosis and often results in evacuation of the colon. The infant should be well hydrated before Gastrograffin is used. The parents ofiDMs are often concerned about the eventual development of diabetes in their children. There are conflicting data on the incidence of insulin-dependent diabetes in IDMs.
Perinatal survival. Oinical management guidelines for obstetrician-gynecologists. Number 30, September Number 60, March Pregestational diabetes mellitus. American Diabetes Association. Gestational diabetes mellitus. Buchanan TA. Metzger BE, Freinkel N, et al. Insulin sensitivity and B-cdl responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes. Cloherty JP. Neonatal management.
Brown F, ed. Wiley-Liss; Hyperglycemia and adverse pregnancy outcomes. Preconception care of diabetes: Landon MB. Diabetes in pregnancy. Fetal surveillance in pregnancies complicated by insulin-dependent diabetes mellitus.
Shoulder dystocia: A comparison of glyburide and insulin in women with gestational diabetes mellitus. Elevated maternal hemoglobin A1 c in early pregnancy and major congenital anomalies in infants of diabetic mothers. Metformin compared with glyburide in gestational diabetes: Cesarean delivery in relation to birth weight and gestational glucose tolerance: Toronto Trihospital Gestational Diabetes lnvestigators.
Third-trimester maternal glucose levels from diurnal profiles in nondiabetic pregnancies: Reece EA. Homko CJ. Infant of the diabetic mother. Multiple changes occur in maternal thyroid physiology during normal pregnancy.
Increased iodine clearance. Starting early in pregnancy, increased renal blood flow and glomerular filtration lead to increased clearance of iodine from maternal plasma. Iodine is also transported across the placenta for iodothyronine synthesis by the fetal thyroid gland after the first trimester.
These processes increase the maternal dietary requirement for iodine but have little impact on the maternal plasma iodine level or maternal or fetal thyroid function in iodine-sufficient regions such as the United States.
To ensure adequate intake, supplementation with meg per day of iodine is recommended for pregnant and lactating women; of note, many prenatal vitamins lack iodine. In contrast, in regions with borderline or deficient iodine intake, increased iodine clearance and transplacental transfer may lead to decreased thyroxine T4 and increased thyroid-stimulating hormone TSH levels, as well as increased thyroid gland volume in both the mother and fetus.
The high circulating level of hCG in the first trimester leads to a small, transient increase in free T 4 accompanied by partial suppression of TSH that resolves by approximately the 14th week of gestation. Increased thyroxine-binding globulin TBG levels occur early in pregnancy. TBG doubles by mid-gestation then plateaus at a high level.
Estrogen also stimulates TBG synthesis in the liver. Free T4 levels rise much less than total T4 in early pregnancy see I. Direct free T 4 assays may be affected by TBG and should not be used to monitor maternal thyroid function during pregnancy. After the first trimester, TSH levels return to the normal, nonpregnant range. R The negative feedback control mechanisms of the hypothalamic-pituitarythyroid HPT axis remain intact.
Placental metabolism and transplacental passage. The placenta is also permeable to In the setting of fetal hypothyroxinemia, maternal-fetal transfer ofT4 is increased, particularly in the second and third trimesters, protecting the developing fetus from the effects of fetal hypothyroidism.
Hyperemesis gravidarum is associated with transient subclinical or mild hyperthyroidism that may be due to the thyroid stimulatory effects of hCG and typically resolves without treatment.
Signs and symptoms of hyperthyroidism may be nonspecific and include tachycardia, increased appetite, tremor, anxiety, and fatigue. Poorly controlled maternal hyperthyroidism is associated with serious pregnancy complications, including spontaneous abortion, preterm delivery, intrauterine growth restriction IUGR , fetal demise, preeclampsia, placental abruption, thyroid storm, and congestive heart failure CHF.
Treatment of maternal hyperthyroidism substantially reduces the risk of associated maternal and fetal complications. Antithyroid drugs are indicated for the treatment of moderate-to-severe hyperthyroidism. In the first trimester, propylthiouracil PTU , rather than methimazole MMI , is recommended due to possible teratogenic effects of MMI, which has been associated with aplasia cutis congenita, tracheoesophageal fistula, and choana! The fetus is more sensitive than the mother to the effects of antithyroid drugs, so fetal hypothyroidism and goiter can occur even with doses in the therapeutic range for the mother.
Clinicians should use the lowest possible dose and monitor closely, aiming to maintain T 4 levels in the high-normal range and TSH levels in the low-normal or suppressed range. Mild hyperthyroidism can be monitored without treatment. Surgical thyroidectomy may be necessary to control hyperthyroidism in women who cannot take antithyroid drugs due to allergy or agranulocytosis or in cases of maternal nonadherence to medical therapy.
Iodine given at a pharmacologic dose is generally contraindicated because with prolonged use, it can cause fetal hypothyroidism and goiter. However, a short course of iodine in preparation for thyroidectomy appears to be safe, and clinicians may also use iodine in selected cases in which antithyroid drugs cannot be used. Radioactive iodine is contraindicated after the first trimester. High levels of these antibodies in maternal serum are predictive of fetal and neonatal hyperthyroidism.
All pregnant women with Graves' disease should be monitored for fetal hyperthyroidism through serial assessment of fetal heart rate and prenatal ultrasound to detect the presence of fetal goiter and monitor fetal growth. Maternal treatment with antithyroid drugs is effective in treating fetal hyperthyroidism, but if excessive, it can also suppress the fetal thyroid gland and cause hypothyroidism.
Fetal and neonatal hypothyroidism and maternal Gravei disease. In the setting of a history of prior maternal Graves' disease, transplacental passage ofTSH receptor-blocking antibodies may cause fetal hypothyroidism. A rare neonatal outcome of maternal Graves' disease is transient pituitary suppression and central hypothyroidism, which may be due to prolonged intrauterine hyperthyroidism.
Usually, the serum concentration of TSH receptor-stimulating antibodies is only modestly elevated. Infants of mothers with Graves' disease can present with thyrotoxicosis or hypothyroidism in the newborn period and require close monitoring after birth see VII.
The most common cause of matemal hypothyroidism in iodine-sufficient regions is chronic autoimmune thyroiditis. Other causes include previous treatment of Graves' disease or thyroid cancer with surgical thyroidectomy or radioablation, drug- and external radiation-induced hypothyroidism, congenital hypothyroidism in the mother, and pituitary dysfunction. Chronic autoimmune thyroiditis is more common in patients with type 1 diabetes mellitus.
Rarely, mothers with a prior history of Graves' disease become hypothyroid due to the development ofTSH receptor-blocking antibodies. Signs and symptoms of hypothyroidism in pregnancy include weight gain, cold intolerance, dry skin, weakness, fatigue, and constipation and may go unnoticed in the setting of pregnancy, particularly in subclinical hypothyroidism.
Unrecognized or untreated hypothyroidism is associated with spontaneous abortion and maternal complications of pregnancy, including anemia, preeclampsia, postpartum hemorrhage, placental abruption, and need for cesarean delivery. Associated adverse fetal and neonatal outcomes include preterm birth, IUGR, congenital anomalies, fetal distress in labor, and fetal and perinatal death. However, these complications are avoided with adequate treatment of hypothyroidism, ideally from early in pregnancy.
Affected fetuses may experience neurodevelopmental impairments, particularly if both the fetus and the mother are hypothyroid during gestation e. Women with preexisting hypothyroidism who are treated appropriately typically deliver healthy infants.
Thyroid function tests should be measured as soon as pregnancy is confirmed, 4 weeks later, at least once in the second. Routine thyroid function testing in pregnancy is currently recommended only for symptomatic women and women with a family history of thyroid disease. Because this strategy detects only two-thirds of women with hypothyroidism, many authors advocate universal screening in early pregnancy; however, this topic remains controversial.
TSH receptor-blocking antibodies cross the placenta and may cause fetal and transient neonatal hypothyroidism see VI. Maternal Graves' disease is the most common cause of fetal and neonatal goiter, which results most often from fetal hypothyroidism due to PTU or MMI. Fetal and neonatal goiter can also result from fetal hyperthyroidism due to TSH receptor-stimulating antibodies. Antibody-mediated fetal effects can occur in women with active Graves' disease or women previously treated with surgical thyroidectomy or radioablation.
Maternal history and serum antibody testing is usually diagnostic. Rarely, cord blood sampling is necessary to distinguish between PTU- or MMI -induced fetal hypothyroidism and TSH receptorstimulating antibody-induced fetal hyperthyroidism.
Thyroid function tests usually normalize by 1 week of age, and treatment is not required. Other causes of fetal and neonatal goiter include fetal disorders of thyroid hocmonogenesis usually inherited , excessive maternal iodine ingestion, and iodine deficiency.
Goiter resolves with suppression of the serum TSH concentration by L-thyroxine treatment on iodine replacement. Fetal goiter due to hypothyroidism is usually treated with maternal L-tbyroxine administration. Rarely, treatment with intra-amniotic injections of Lthyroxine in the third trimester is used to reduce the size of fetal goiter and minimize complications of tracheoesophageal compression, including polyhydramnios, lung hypoplasia, and airway compromise at birth. A The fetal HPT axis develops relatively independent of the mother due to the high placental concentration of D3, which inactivates most of the T4 presented from the maternal circulation see I.
Thyroid embryogenesis is complete by 10 to 12 weeks' gestation, by which time the fetal thyroid gland starts to concentrate iodine and synthesize and secrete T 3 and T 4.
T 4 and TBG levels increase gradually throughout gestation. Circulating T 3 levels remain low, although brain and pituitary T 3 levels are considerably higher as a result of a local intracellular type 2 deiodinase D2 enzyme, which converts T4 to the active isomer T 3 In the setting of fetal hypothyroidism, D2.
TSH from the fetal pituitary gland increases from mid-gestation. The negative feedback mechanism of the HPT axis statts to mature by 26 weeks of gestation. Circulating levels ofTRH are high in the fetus relative to the mother, although the physiologic significance is unclear.
The ability of the thyroid gland to adapt to exogenous iodine does not mature until 36 to 40 weeks' gestation. Thus, premature infants are more sensitive than are full-term infants to the thyroid suppressing effects of exogenous iodine. Neonatal physiology.
The TSH surge causes marked stimulation of the neonatal thyroid gland. Serum T 3 and T 4levels increase sharply and peak within 24 hours oflife, followed by a slow decline. In the preterm infant, the pattern of postnatal thyroid hormone change is simi-. Umbilical cord blood thyroid hormone levels are directly related to gestational age and birth weight Table 3.
CH is one of the most common preventable causes of mental retardation. The incidence of CH varies globally. In the United States, the incidence is approximately 1: CH is more common among Hispanic 1: The female-to-male ratio is 2: CHis also more common in infants with trisomy 21, congenital heart disease, and other congenital malformations, including renal, skeletal, gastrointestinal anomalies, and cleft palate.
CH may be permanent or transient. Hypothyroxinemia with delayed TSH rise can be caused by permanent or transient conditions.
Causes of permanent CH Table 3. Thyroid dysgenesis. Thyroid dysgenesis includes aplasia, hypoplasia, and dysplasia; the latter often accompanied by failure to descend into the neck ectopy.
It is almost always sporadic with no increased risk to subsequent siblings. Thyroglobulin TG reflects the amount of thyroid tissue present and is low in aplasia and hypoplasia. The most common synthetic defect is abnormal thyroid peroxidase activity, which.
Developmental trends in cord and postpartum serum thyroid hormones in preterm infants. J Clin Endocrinol Metab ;89 Additional reported defects affect other key steps in thyroid hormone synthesis, such as thyroglobulin synthesis, iodine trapping, hydrogen peroxide generation, and tyrosine deiodination. Pendred syndrome is characterized by a goiter due to an underlying mild organification defect.
It is an important cause of sensorineural deafness, but hypothyroidism rardy occurs in the newborn period. In thyroid dyshormonogenesis, goiter may be present. Defects in TG synthesis can be distinguished from other abnormalities in thyroid hormone formation by measurement of serum TG, which is low in TG synthetic defects and high in other thyroid hormone synthetic defects. Unlike in thyroid dysgenesis, thyroid imaging typically reveals a normally placed thyroid gland, which may be of normal size or enlarged.
Rardy, it is due to a loss-of-function mutation in the G-stimulatory subunit that links TSH binding to action Albright hereditary osteodystrophy. Characteristically, the thyroid gland is small. T 4 is normal or low and TSH is devated.
The severity of the hypothyroidism depends on the degree of resistance. Central hypothalamic-pituitary hypothyroidism is less common than primary hypothyroidism. Affected infants may have other signs of pituitary dysfunction, such as hypoglycemia, microphallus, and midline facial abnormalities. Septo-optic dysplasia is an important cause of central hypothyroidism.
Goiter is not present. If central hypothyroidism is suspected, cortisol and growth hormone levels should be measured and a magnetic resonance imaging MRI scan done to visualize the hypothalamus and pituitary gland. Causes of transient CH see Table 3. Antithyroid drugs.
As discussed in section IV. The elimination half-life of PTU is 1. Iodine excess. Preterm infants are particularly susceptible to the thyroid suppressing effects of excess iodine see V.. Iodine is also passed through breast milk and can be excessive in mothers who ingest large amounts of seaweed e. Goiter may be present. T 4 is low and TSH is elevated. RAJ or 99mTc uptake is blocked by excess iodine, and ultrasound shows a normally positioned thyroid gland, which may be enlarged.
Worldwide, iodine deficiency is the most common cause of transient hypothyroidism, particularly in preterm infants but is less common in the United States, a generally iodine-sufficient region. Unlike in primary hypothyroidism, the TSH is inappropriately "normal.
Measurement of reverse T 3, which is high in sick euthyroid syndrome but low in hypothyroidism, may be helpful but, frequendy, results are not immediately available.
Observational studies in premature infants have demonstrated an association of transient hypothyroxinemia with adverse short- and long-term outcomes, including neonatal death, intraventricular hemorrhage, periventricular leukomalacia, cerebral palsy, intellectual impairment, and school failure.
However, several randomized trials of routine L-thyroxine supplementation have failed to show a beneficial effect, thus the extent to which low T 4 levels cause these adverse outcomes is unclear. These antibodies freely cross the placenta and persist in the neonatal circulation with a half-life of approximately 2 weeks. Both stimulating and blocking antibodies may be present simultaneously and their relative proportions may change over time. Hypothyroidism typically persists for 2 to 3 months and depends on the potency of the blocking activity.
High concentrations ofTSH receptor-blocking antibodies are present in maternal and neonatal serum. On thyroid scintiscanning, uptake may be absent, but a normally placed thyroid gland is seen on ultrasound. Large liver hemangiomas can be associated with severe, refractory hypothyroidism due to expression of D3 activity by the hemangioma. Infants typically present after the newborn period as the hemangioma enlarges.
Large doses of L-thyroxine are required for treatment. The hypothyroidism resolves as the hemangioma regresses.
Hypothyroxinemia with delayed TSH devation atypical CH is often due to recovery from sick euthyroid syndrome but needs to be distinguished from. Rare, usually present after newborn period Requires high L-thyroxine doses ""lJ. Monozygotic twins can also present with delayed TSH rise due to fetal blood mixing before birth. Some screening programs require repeat testing at 2 to 6 weeks of age for infants at high risk for delayed TSH elevation and a few require repeat testing for all infants.
In the United States, 1, cases of mental retardation per year are prevented through newborn screening for CH. Newborn screening for CHis routine in most developed countries but currently is not performed in many developing countries. It is mandated by law in the United States, where specific screening protocols and cutoff values vary by state. There are advantages and disadvantages to each approach. A few states measure both T 4 and TSH in the initial screen for all newborns, or for a subset of high-risk newborns, which is an ideal but expensive strategy.
L or in the lowest lOth percentile for the set of samples run together. Infants with abnormal screening test results should be evaluated urgently in consultation with a pediatric endocrinologist see VI. A filter paper blood spot specimen should be sent from all newborns, optimally at 48 to 72 hours of age but, often, this is not possible due to the practice of early discharge. For infants discharged prior to 48 hours of age, a specimen should be sent prior to discharge.
Infants discharged before 24 hours of age should be retested at 48 to72 hours to minimize risk of false negative results. For infants transferred to another hospital, the receiving hospital should send a specimen if it cannot be confirmed that the hospital of birth sent one. If clinical signs of hypothyroidism are present prolonged jaundice, constipation, hypothermia, poor tone, mottled skin, poor feeding, large tongue, open posterior fontanel , thyroid function tests should be sent immediately, even if the initial screen was normal.
Rarely, screening programs miss cases of CH as a result of early discharge, improper or no specimen collection e. Human error in reporting abnormal results can also occur. Primary TSH screening programs may miss infants. Acquired hypothyroidism will also be missed on newborn screening. Follow-up of newbom screening for CH in hospitalized preterm infants is outlined in Figure 3.
Any infant with abnormal screening results should be evaluated without delay. Consultation with a pediatric endocrinologist is recommended.
Maternal and family history should be reviewed and a physical examination performed. Thyroid function tests should be repeated in serum within 24 hours.
If it is not possible to see the patient promptly, therapy should be initiated as soon as the diagnosis is confirmed. Figure 3. Suggested approach to follow-up of newborn screening for hypothyroidism in the hospitalized preterm infant. Primary Care ofthe Premature Infant. Elsevier Saunders; These tests are not necessary if transient hypothyroxinemia of prematurity is suspected.
Treatment should not be ddayed to perform thyroid scanning. Unlike thyroid scintiscan, ultrasound can be performed irrespective of the TSH concentration. Bone age may be helpful in assessing the severity and duration of intrauterine hypothyroidism but currently is performed less frequently than in the past.
Treatment and monitoring. An optimal neurodevelopmental outcome depends on early, adequate treatment of CH. For infants with suspected transient or permanent CH, L-thyroxine should be initiated at 10 to 15 mcglkglday, with a higher dose used for infants with the lowest T. Ideally, the T4 level will normalize within 1 week, and the TSH level within 2 weeks, of starting therapy.
A recent pilot study suggests that more rapid correction of thyroid hormone levels may be even better. Repeat T4 and TSH measurements should be performed 1 week after starting therapy, 2 weeks after any dose change, and every 1 to 2 months in the first year of life. Noncompliance can have serious, permanent neurodevelopmental consequences for the infant and should always be considered by caregivers when thyroid function tests fail to normalize with treatment.
L-thyroxine tablets should be crushed and fed directly to the infant or mixed in a small amount of juice, water, or breast milk.
Soy-based formulas, ferrous sulfate, and fiber interfere significandy with absorption and should be administered at least 2 hours apart from the L-thyroxine dose; there are no commercially available liquid preparations in the United States.
For preterm infants suspected of having transient bypothyroxinemia of prematurity, treatment decisions are complicated by incomplete knowledge regarding the risks and benefits of treatment.
While observational studies have found an association of a low serum T 4 concentration with increased morbidity and mortality, randomized trials have failed to demonstrate a short- or longterm benefit of routine L-thyroxine supplementation for all preterm infants.
For infants with suspected transient CH, a brief trial off medication can be attempted at 3 years of age, after thyroid hormone-dependent brain development is complete. Usually in infants with transient hypothyroidism, the dose required to maintain normal thyroid function does not change with age. With prompt diagnosis and treatment, the neurodevelopmental outcome is excellent for infants with CH.
Subtle visuospatial processing, memory, and sensorimotor defects have been reported, particularly in those infants with. In contrast, infants who are diagnosed late may have substantial cognitive and behavioral defects ranging from mild to severe, depending on the severity of the CH and the length of delay in starting treatment. Most newborns with hyperthyroidism are born to mothers with Graves' disease. Rarely, permanent hyperthyroidism can be caused by an activating mutation of the TSH receptor with autosomal dominant inheritance, a condition that may require thyroid gland ablation.
The overall incidence of neonatal hyperthyroidism is , Clinical hyperthyroidism in the neonate results from transplacentally acquired maternal TSH receptor-stimulating antibodies. Rarely, both potent stimulating and blocking antibodies are present simultaneously. Due to differential clearance from the neonatal circulation, infants may present with hypothyroidism and develop thyrotoxicosis later with the disappearance of the more potent thyroid-blocking antibodies that initially masked the thyroid-stimulating antibody effects.
Initial hypothyroidism may also be present as a result of the transplacental passage of PTU or MMI and typically resolves within the first week of life. Neonatal hyperthyroidism usually occurs with active maternal disease, but may also occur in infants of mothers who have undergone surgical thyroidectomy or radioablation. These mothers are no longer hyperthyroid but continue to produce thyroid autoantibodies.
High maternal serum levels of stimulating antibodies predict the presence of hyperthyroidism in the newborn, but precise values differ depending on the sensitivity of the assay used. Thyrotoxicosis usually presents toward the end of the first week of life as maternal antithyroid medication is cleared from the neonatal circulation but can occur earlier. Clinical manifestations in the newborn infant include prematurity, IUGR, tachycardia, irritability, poor weight gain, goiter, prominent eyes, hypertension, and craniosynostosis.
Arrhythmias and CHF can be life threatening. Rarely, neonatal thyrotoxicosis can present with signs and symptoms suggestive of congenital viral infection, including hepatosplenomegaly, petechiae, fulminant hepatic failure, and coagulopathy.
Maternal history, high titers of thyroid-stimulating antibodies, elevation of the total and free T 4 levels, and suppression ofTSH are diagnostic. If CHF develops, propranolol should be discontinued, and treatment with digoxin considered. Supportive care maintains adequate oxygenation, fluid balance, calorie and nutrient intake for growth, and temperature regulation.
Treatment course. Thyroid function tests free T 4, total T 3, and TSH are repeated every few days initially, and the dose of antithyroid drug is adjusted to maintain levels within the normal range.
Treatment is usually required for 2 to 3 months but may be longer. Once control is gained, the infant can be discharged with close follow-up. Iodine solutions are given until the thyroid function tests normalize. Infants are weaned off propranolol as indicated by the heart rate, and then the dose of PTU or MMI is tapered as allowed by the T4level and clinical symptoms.
With early diagnosis and proper treatment, most newborns improve rapidly, and therapy can be withdrawn within 2 to 3 months. Rarely, persistent central hypothyroidism may occur as a result of fetal pituitary exposure to high serum thyroid hormone levels at a critical period in development. There is limited transfer of propranolol into breast milk. It is considered safe to breast feed while taking propranolol. Only minimal amounts of L-thyroxine are transferred to the breast milk.
Thus, breastfeeding is safe for women taking L-thyroxine replacement. Iodine is excreted into the breast milk, and the iodine status of the exclusively breast fed infant is dependent on adequate iodine nutrition in the mother.
Even in regions considered iodine sufficient such as the United States, pregnant and lactating women should take meg per day of supplemental iodine. Of note, many prenatal vitamins do not contain iodine. Preterm infants are particularly susceptible to the thyroid-suppressive effects of excess iodine, which can lead to subclinical hypothyroidism. Excess iodine in the mother can come from the diet e. Update of newborn screening and therapy for congenital hypothyroidism. Pediatrics ; 6: Brown RS. Disorders of the thyroid gland in infancy, childhood, and adolescence.
Available at: Updated November Glinoer D. Thyroid regulation and dysfunction in the pregnant patient. Updated August Chronic hypertension. Hypertension preceding pregnancy or first diagnosed before 20 weeks' gestation. Chronic hypertension with superimposed preeclampsia. Worsening hypertension and new-onset proteinuria, in addition to possible concurrent hyperuricemia, thrombocytopenia, or transaminase derangements after the 20th week of pregnancy in a woman with known chronic hypertension.
Pregnancy-induced hypertension. Hypertension without proteinuria after 20 weeks' gestation. Hypertension with proteinuria after 20 weeks' gestation.
Generalized tonic-donie seizure activity in a woman with no prior history of a seizure disorder. In the United States, hypertensive disorders are the second leading cause of maternal mortality after thrombotidhemorrhagic complications. Eclampsia itself is much less frequent, occurring in 0. Several risk factors have been identified, as outlined in Table 4.
Preeclampsia has been called the "disease of theories," and many etiologies have been proposed. What is dear, however, is that it is a condition of dysfunction within the maternal endothelium. Increased levels of the soluble receptors sFLTJ and endoglin within the maternal circulation for vascular endothelial growth factor VEGF and transforming growth factor-beta TGF-,8 , respectively, may be associated with preeclamptic pathology.
Higher circulating levels of these soluble receptors reduce the bioavailable levels ofVEGF, placental growth factor PlGF , and TGF-,8, resulting in endothelial dysfunction within the maternal circulatory system. Neonatal Care Cloherty.
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