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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.


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Recent Posts See All. BIN To. ISO Converter Download. CUE files for. You're in preview mode. To share posts, head to your live site. This site was designed with the. Some are used antepartum, whereas others are used to monitor the fetus during labor. Antepartum tests generally rely on biophysical studies, which require a certain degree of fetal neurophysiologic maturity.

The following tests are not used until the third trimester; fetuses may not respond appropriately earlier in gestation. Fetal movement monitoring is the simplest method of fetal assessment. The mother lies quietly for an hour and records each perceived fetal movement.

Although she may not perceive all fetal movements that might be noted by ultrasonic observation, she will record enough to provide meaningful data. Fetuses normally have a sleep-wake cycle, and mothers generally perceive a diurnal variation in fetal activity.

Active periods average 30 to 40 minutes. The non. It is simple to perform, relatively quick, and noninvasive, with neither discomfort nor risk to mother or fetus. The NST is based on the principle that fetal activity results in a reflex acceleration in heart rate. The required fetal maturity is typically reached by approximately 32 weeks of gestation. Absence of these accelerations in a fetus who previously demonstrated them may indicate that hypoxia has sufficiently depressed the central nervous system to inactivate the cardiac reflex.

The test is performed by monitoring fetal heart rate FHR either through a Doppler ultrasonographic device or through skin-surface electrodes on the maternal abdomen. Uterine activity is simultaneously recorded through a tocodynamometer, palpation by trained test personnel, or the patient's report. The test result may be reactive, nonreactive, or inadequate. The criteria for a reactive test are as follows: A nonreactive test fails to meet the three criteria.

If an adequate fetal heart tracing cannot be obtained for any reason, the test is considered inadequate. Statistics show that a reactive result is reassuring, with the risk of fetal demise within the week following the test at approximately 3 in 1, A nonreactive test is generally repeated later the same day or is followed by another test of fetal well-being.

The contraction stress test CST may be used as a backup or confirmatory test when the NST is nonreactive or inadequate. The CST is based on the idea that uterine contractions can compromise an unhealthy fetus. The pressure generated during contractions can briefly reduce or eliminate perfusion of the intervillous space. A healthy fetoplacental unit has sufficient reserve to tolerate this short reduction in oxygen supply.

Under pathologic conditions, however, respiratory reserve may be so compromised that the reduction in oxygen results in fetal hypoxia. Under hypoxic conditions, the FHR slows in a characteristic way relative to the contraction. FHR begins to decelerate 15 to 30 seconds after onset of the contraction, reaches its nadir after the peak of the contraction, and does not return to baseline until after the contraction ends.

This heart rate pattern is known as a late deceleration because of its relationship to the uterine contraction. Synonyms are type II deceleration or deceleration of uteroplacental insufficiency. A CST is considered completed if uterine contractions have spontaneously occurred within 30 minutes, lasted 40 to 60 seconds each, and occurred at a frequency of three within a minute interval. If no spontaneous contractions occur, they can be induced with intravenous oxytocin, in which case the test is called an oxytocin challenge test.

A CST is positive if late decelerations are consistently seen in association with contractions. A CST is negative if at least three contractions of at least 40 seconds each occur within a minute period without associated late decelerations. A CST is suspicious if there are occasional or inconsistent late decelerations. If contractions occur more frequently than every 2 minutes or last longer than 90 seconds, the study is considered a hyperstimulated test and cannot be interpreted.

An unsatisfactory test is one in which contractions cannot be stimulated, or a satisfactory FHR tracing cannot be obtained. Statistically, about one-third of patients with a positive CST will require cesarean section for persistent late decelerations in labor. The biophysical pro6le combines an NST with other parameters determined by real-time ultrasonic examination. A score of 0 or 2 is assigned for the absence or presence of each of the following: The total score determines the course of action.

Reassuring tests are repeated at weekly intervals, whereas less-reassuring results are repeated later the same day.

Very low scores generally prompt delivery. The likelihood that a fetus will die in utero within 1 week of areassuring test is approximately the same as that for a negative CST, which is approximately 0. Doppler ultrasonography of fetal umbilical artery blood flow is a noninvasive technique to assess downstream placental resistance. Poorly functioning placentas with extensive vasospasm or infarction have an increased resistance to flow that is particularly noticeable in fetal diastole.

Umbilical artery Doppler flow velocimetry may be used as part of fetal surveillance based on characteristics of the peak systolic frequency shift S and the end-diastolic frequency shift D. The two commonly used indices of How are the systolic: Umbilical artery Doppler velocimetry measurements have been shown to improve perinatal outcome only in pregnancies with a presumptive diagnosis ofiUGR and should not be used as a screening test in the general obstetric population.

Absent or reversed enddiastolic flow is seen in the most extreme cases of IUGR and is associated with a high mortality rate. Doppler measurements of the middle cerebral artery can also be used in the assessment of the fetus that is at risk for either IUGR or anemia. Intrapartum assessment of fetal well-being is important in the management of labor.

Continuous dectronic fetal monitoring is widely used despite the fact that it has not been shown to reduce perinatal mortality or asphyxia relative to auscultation by trained personnel but has increased the incidence of operative delivery.

The fetal heart rate FHR can be monitored in one of three ways. The noninvasive methods are ultrasonic monitoring and surface-electrode monitoring from the maternal abdomen. The most accurate but invasive method is to place a small electrode into the skin of the fetal presenting part to record the fetal electrocardiogram directly. Placement requires rupture of the fetal membranes.

Uterine activity can also be recorded either indirectly or directly. A tocodynamometer can be strapped to the maternal abdomen to record the timing and duration of contractions as well as crude relative intensity. Invasive monitoring is associated with an increased incidence of chorioamnionitis and postpartum maternal infection.

Parameters of the fetal monitoring record that are evaluated include the following: Baseline heart rate is normally between and bpm. The baseline must be apparent for a minimum of 2 minutes in any minute segment and does not include episodic changes, periods of marked FHR variability, or segments of baseline that differ by more than 25 bpm.

In isolation, tachycardia is poorly predictive of fetal hypoxemia or acidosis unless accompanied by reduced beat-to-beat variability or recurrent decelerations. Beat-to-beat variability is recorded from a calculation of each RR interval. The autonomic nervous system of a healthy, awake term fetus constantly varies the heart rate from beat to beat by approximately 5 to 25 bpm. Decelerations of the FHR may be benign or indicative of fetal compromise, depending on their characteristic shape and timing in relation to uterine contractions.

They are benign and usually accompany good beat-to-beat variability. These decelerations are more commonly seen in active labor when the fetal head is compressed in the pelvis, resulting in a parasympathetic effect. The onset, nadir, and recovery of the deceleration occur after the beginning, peak, and end of the contraction, respectively.

A fall in the heart rate of only 10 to 20 bpm below baseline even if still within the range of is significant. Late decelerations are the result of uteroplacental insufficiency and possible fetal hypoxia. Repetitive late decelerations demand action. Usually, they result from fetal umbilical cord compression.

Variable decelerations are a cause for concern if they. Umbilical cord compression secondary to a low amniotic fluid volume oligohydramnios may be alleviated by amnioinfusion of saline into the uterine cavity during labor. A fetal scalp blood sample for blood gas analysis may be obtained to confirm or dismiss suspicion of fetal hypoxia. An intrapartum scalp pH above 7.

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Many obstetric Wlits have replaced fetal scalp blood sampling with noninvasive techniques to assess fetal status. FHR accelerations in response to mechanical stimulation of the fetal scalp or to vibroacoustic stimulation are reassuring. Role of second-trimester genetic sonography after Down syndrome screening.

Chorion villus sampling versus amniocentesis for prenatal diagnosis. Washington, DC: American College of Obstetricians and Gynecologists; Intrapartum Fetal Heart Rate Monitoring. Genetic amniocentesis in women years old: Prenat Diagn ;20 3: First- and second-trimester evaluation of risk for Down syndrome. First-trimester or second-trimester screening, or both for Down's syndrome. Fetal nuchal translucency: Br j Obstet Gynaecol ; 9: First-trimester fetal nuchal translucency thickness and risk for trisomies.

Sequential pathways of testing after first-trimester screening for trisomy Improved management of diabetes mellitus and advances in obstetrics, such as ultrasonography and measurement offetal lung maturity FLM , have reduced the incidence ofadverse perinatal outcome in infants ofdiabetic mothers IDMs.

With appropriate management, women with good glycemic control and minimal microvascular disease can expect pregnancy outcomes comparable to the general population. Pregnancy does not have a significant impact on the progression ofdiabetes. In women who begin pregnancy with microvascular disease, diabetes often worsens, but in most, the disease return to baseline.

Preconception glucose control may reduce the rate of complications to as low as that seen in the general population. General principles 1. Diabetes that antedates the pregnancy can be associated with adverse fetal and maternal outcomes. The most important complication is diabetic embryopathy resulting in congenital anomalies.

The risk of congenital anomalies is rdated to the glycemic profile at the time of conception. Women with type 1 and type 2 diabetes are at significantly increased risk for hypertensive disorders, such as preeclampsia, which is potentially deleterious to both maternal and fetal wellbeing.

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.

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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.

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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.

Effect of Birth Asphyxia on Serum Calcium and Glucose Level: A Prospective Study

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.Pregnancy-related hypertension.

If time permits, the problems should be discussed with the parent s. Corticosteroids can cause temporary hyperglycemia; therefore, patients may need to be managed. There does not appear to be a direct relation between hypoglycemia alone and Iodine is also passed through breast milk and can be excessive in mothers who ingest large amounts of seaweed e.

James R. Hypertension preceding pregnancy or first diagnosed before 20 weeks' gestation. Neonatal hypoglycemia. This site is like a library, Use search box in the widget to get ebook that you want.

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