Manual of neonatal care pdf

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 re- sponse 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 sta- ble. 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 ele- ment 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.

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 IV fluid de- pends 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.

If the infant. Blood glu- cose levels must be carefully monitored at frequent intervals after beginning IV 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 reactive hypoglycemia. It is vital to measure blood glucose levels during tapering of the IV infusion.

In our experience, other drugs epinephrine, diazoxide, or growth hormone have not been neces- sary in the treatment of the hypoglycemia of IDMs. 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 treat- ment mentioned earlier and resolves by 24 hours.

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 of lung maturation. Laboratory studies See Chap. Blood gas analysis should be performed to evaluate gas exchange and the presence of right-to-left shunts. 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 hyper- trophic 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 environ- ment 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 anoma- lies 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. Infants who are sick for any reason—pre- maturity, 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 in- fants of nondiabetic mothers. Mild hemolysis is compen- sated 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 pro- duction 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 de- creased incidence of hyperbilirubinemia. Hyperbilirubinemia in IDMs is diag- nosed 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 poly- hydramnios. Sometimes, poor feeding is related to prematurity, respiratory distress, or other problems; however, it is often present in the absence of other problems.

Poor feed- ing 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 dys- tocia.

Associations have been found between macrosomia and the following: 1. Third-trimester elevated maternal blood sugar 2. Fetal and neonatal hyperinsulinemia 3. Neonatal hypoglycemia H. 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 cardio- myopathy 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. Oxy- gen 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: 1.

Postasphyxial cardiomyopathy 2. Myocarditis 3. Endocardial fibroelastosis 4. Glycogen storage disease of the heart 5. 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 examina- tion.

Postnatal presentation may include hematuria, flank mass, hypertension, or embolic phenomena. Most renal vein thrombosis can be managed conservatively, allowing preservation of renal tissue see Chaps. Other thromboses see Chap. Small left colon syndrome. Small left colon syndrome presents as generalized ab- dominal 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. Other causes of intestinal obstruction should be considered see Chap.

The parents of IDMs are often concerned about the eventual develop- ment of diabetes in their children. There are conflicting data on the incidence of insulin-dependent diabetes in IDMs. Perinatal survival. Clinical management guidelines for obstetrician—gynecologists. Number 30, September Obstet Gynecol ;— Number 60, March Pregestational diabetes mellitus. Obstet Gynecol ; 3 — American Diabetes Association. Gestational diabetes mellitus.

Diabetes Care Suppl ;25 suppl 1 :S94—S Insulin sensitivity and B-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes.

Am J Obstet Gynecol ;— Cloherty JP. Neonatal management. In: Brown F, ed. New York: Wiley-Liss; — Hyperglycemia and adverse pregnancy outcomes. Preconception care of diabetes: glycemic control prevents congenital anomalies. JAMA ;— Landon MB. Diabetes in pregnancy. Clin Perinatol ; Fetal surveillance in pregnancies complicated by insulin-dependent diabetes mellitus.

Shoulder dystocia: should the fetus weighing greater than or equal to grams be delivered by cesarean section? A comparison of glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med ; 16 — Elevated maternal hemoglobin A1c in early pregnancy and major congenital anomalies in infants of diabetic mothers. Metformin compared with glyburide in gestational diabetes: a randomized controlled trial.

Cesarean delivery in relation to birth weight and gestational glucose tolerance: pathophysiology or practice style? Toronto Trihospital Gestational Diabetes Investigators. JAMA ; 15 — Third-trimester maternal glucose levels from diurnal profiles in nondiabetic pregnancies: correlation with sonographic parameters of fetal growth. Diabetes Care ;24 8 — Infant of the diabetic mother. Semin Perinatol ;— Multiple changes occur in mater- nal 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 ma- ternal 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 mcg 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 T4 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. Increased total triiodothyronine T3 and T4 levels occur from early in ges- tation as a result of rapidly increasing TBG levels see I. Free T4 levels rise much less than total T4 in early pregnancy see I.

Direct free T4 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. The negative feedback control mechanisms of the hypothalamic-pituitary- thyroid HPT axis remain intact. Placental metabolism and transplacental passage.

The placenta is also permeable to. T4 crosses the placenta in limited amounts due to inactivation by the type 3 deiodinase D3 enzyme, which converts T4 to inac- tive reverse T3, rather than to T3.

T3 is similarly inactivated. In the setting of fetal hypothyroxinemia, maternal—fetal transfer of T4 is increased, particularly in the second and third trimesters, protecting the developing fetus from the effects of fetal hypothyroidism.

Hyperthyroidism complicates 0. Hy- peremesis gravidarum is associated with transient subclinical or mild hyperthy- roidism 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 tachy- cardia, 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 associ- ated 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, tracheoesopha- geal fistula, and choanal atresia.

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 T4 levels in the high-normal range and TSH levels in the low-normal or sup- pressed 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. 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.

Usually, the serum concentration of TSH receptor—stimulating antibodies is only modestly elevated. Maternal hypothyroidism in pregnancy can be either overt 0. The most common cause of maternal hypothyroidism in iodine-sufficient regions is chronic autoimmune thyroiditis.

Chronic autoimmune thyroiditis is more common in patients with type 1 diabetes mellitus. Signs and symptoms of hypothyroidism in pregnancy include weight gain, cold intolerance, dry skin, weakness, fatigue, and constipation and may go un- noticed 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, pre- eclampsia, 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 experi- ence 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.

Be- cause this strategy detects only two-thirds of women with hypothyroidism, many authors advocate universal screening in early pregnancy; however, this topic re- mains controversial. TSH receptor—blocking antibodies cross the placenta and may cause fetal and transient neonatal hypothyroidism see VI. Fetal ultrasound by an experienced ultrasonographer is an excellent tool for in- trauterine diagnosis and monitoring of fetal goiter.

Fetal and neonatal goiter can also result from fetal hyperthyroidism due to TSH receptor-stimulating antibodies. Maternal history and serum antibody testing is usually diagnostic. Rarely, cord blood sampling is necessary to distin- guish between PTU- or MMI-induced fetal hypothyroidism and TSH receptor- stimulating 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 hor- monogenesis 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-thy- roxine administration. Rarely, treatment with intra-amniotic injections of L- thyroxine in the third trimester is used to reduce the size of fetal goiter and minimize complications of tracheoesophageal compression, including poly- hydramnios, lung hypoplasia, and airway compromise at birth.

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. T4 and TBG levels increase gradually throughout gestation.

Circulating T3 levels remain low, although brain and pituitary T3 levels are considerably higher as a result of a local intracellular type 2 deiodinase D2 enzyme, which converts T4 to the active isomer T3.

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 starts to mature by 26 weeks of gestation. Circulating levels of TRH are high in the fetus relative to the mother, although the physiologic significance is unclear. 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 T3 and T4 levels increase sharply and peak within 24 hours of life, followed by a slow decline. In the preterm infant, the pattern of postnatal thyroid hormone change is simi- lar to the pattern seen in the full-term infant, but the TSH surge is less marked, and the T4 and T3 responses are blunted.

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 approxi- mately , and appears to be rising. CH is more common among Hispanic , and Asian Indian , infants but less common among non-His- panic black infants , The female-to-male ratio is CH is also more common in infants with trisomy 21, congenital heart disease, and other congenital malformations, including renal, skeletal, gastrointestinal anomalies, and cleft pal- ate.

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, hy- poplasia, 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. Table 3. Age Gestational age wks Birth 7 days 14 days 28 days. Developmental trends in cord and postpartum serum thyroid hormones in preterm infants. J Clin Endocrinol Metab ;89 11 — Additional reported defects affect other key steps in thyroid hormone synthesis, such as thyroglobu- lin synthesis, iodine trapping, hydrogen peroxide generation, and tyrosine deio- dination.

Pendred syndrome is characterized by a goiter due to an underlying mild organification defect. It is an important cause of sensorineural deafness, but hypothyroidism rarely occurs in the newborn period. In thyroid dyshor- monogenesis, 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. Rarely, it is due to a loss-of-function mutation in the G-stimulatory subunit that links TSH binding to action Albright hereditary osteodystrophy. Char- acteristically, the thyroid gland is small.

T4 is normal or low and TSH is ele- vated. 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 pres- ent. 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 thy- roid suppressing effects of excess iodine see V. Iodine is also passed through breast milk and can be exces- sive in mothers who ingest large amounts of seaweed e.

Goiter may be present. T4 is low and TSH is elevated. RAI 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 hy- pothyroidism, particularly in preterm infants but is less common in the United States, a generally iodine-sufficient region.

Measurement of reverse T3, which is high in sick euthyroid syndrome but low in hypothyroidism, may be helpful but, frequently, results are not im- mediately available. Observational studies in premature infants have demon- strated 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 supplementa- tion have failed to show a beneficial effect, thus the extent to which low T4 levels cause these adverse outcomes is unclear. These antibodies freely cross the pla- centa and persist in the neonatal circulation with a half-life of approximately 2 weeks. Both stimulating and blocking antibodies may be present simultane- ously 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.

Goiter is not present. High concentrations of TSH receptor-blocking antibodies are present in ma- ternal 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 hy- pothyroidism 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 elevation atypical CH is often due to recovery from sick euthyroid syndrome but needs to be distinguished from. 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 CH is routine in most developed countries but cur- rently 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 mea- sure both T4 and TSH in the initial screen for all newborns, or for a subset of high-risk newborns, which is an ideal but expensive strategy. Infants with abnormal screen- ing 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, opti- mally 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, con- stipation, 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 newborn 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. Ma- ternal and family history should be reviewed and a physical examination per- formed. 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.

Send newborn NB screen at 48—72 hours of life. Suspect TBG Physiologic immaturity deficiency vs. Figure 3. Suggested approach to follow-up of newborn screening for hypothyroidism in the hospitalized preterm infant. Primary Care of the Premature Infant. Philadelphia: Elsevier Saunders; These tests are not necessary if transient hypothyroxinemia of prematurity is suspected. Treatment should not be delayed 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.

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 lev- els 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 significantly 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 hypothyroxinemia 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 T4 concentration with increased morbidity and mortality, randomized trials have failed to demonstrate a short- or long- term 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 develop- ment 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 out- come 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 be- havioral defects ranging from mild to severe, depending on the severity of the CH and the length of delay in starting treatment.

Rarely, perma- nent hyperthyroidism can be caused by an activating mutation of the TSH receptor with autosomal dominant inheritance, a condition that may require thyroid gland ablation. Clinical hyperthyroidism in the neonate results from transpla- centally 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 thy- roid-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 pre- dict the presence of hyperthyroidism in the newborn, but precise values differ de- pending on the sensitivity of the assay used.

Clinical findings. 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, hyperten- sion, 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, el- evation of the total and free T4 levels, and suppression of TSH are diagnostic. If CHF develops, propranolol should be discontinued, and treatment with digoxin considered. Cloherty, Eric C. Eichenwald, Anne R. This portable text covers current and practical approaches to evaluation and management of conditions encountered in the fetus.

Cloherty, Ann R. Stark, Eric C. This manual provides a practical approach to the diagnosis and management of problems of neonates. An outline format provides quick access to a large amount of information. The Fifth Edition has been fully updated. Manual Neonatal Care Int Ed. Written by expert authors from major neonatology programs across the U. Now with the print edition, enjoy the bundled interactive eBook edition, which can be downloaded to your tablet and smartphone or accessed online and includes features like: Complete content with enhanced navigation Powerful search tools and smart navigation cross-links that pull results from content in the book, your notes, and even the web Cross-linked pages, references, and more for easy navigation Highlighting tool for easier reference of key content throughout the text Ability to take and share notes with friends and colleagues.

Download PDF. Download 1 , Download 2.