Recognition, Stabilization, and Transport of the High-Risk Newborn

At delivery, the newborn infant makes a complicated transition from intrauterine to extrauterine life. Although most newborns adapt without difficulty, the first few hours of life can be a precarious time for the high-risk infant. Health care professionals who provide care to newborns must anticipate potential problems for the high-risk infant before delivery. Early recognition of high-risk factors in the maternal history and of significant findings in the newborn allows for timely and appropriate monitoring and treatment. The goal of this approach of active anticipation and intervention is to prevent the development or progression of more serious illness and to minimize the risk of morbidity and mortality in the high-risk newborn. A newborn infant should receive a level of care specific to his or her unique needs. If an infant is critically ill, it is essential to intervene rapidly and effectively to stabilize the infant. In contrast, some infants with perinatal risk factors may do quite well postnatally. After an initial assessment and careful observation, such an infant might be advanced to well newborn care. This chapter outlines an approach to the preparation for, and management of, the high-risk infant in the first hours of life, including initial stabilization and transport.

Maternal History

During fetal growth the infant is somewhat protected in the intrauterine environment. However, in the course of a pregnancy the health of the mother affects the well-being of the fetus. Both acute and chronic maternal illnesses can adversely affect embryogenesis and fetal growth and maturation. Maternal nutrition, medications, smoking, and drug use all affect the growth and development of the fetus. Such prenatal maternal factors may continue to have effects on the postnatal course of the newborn. Intrapartum factors, including obstetric complications, maternal therapy, and mode of delivery may also affect the condition of the newborn infant.

It is essential to obtain a complete maternal history to anticipate and prepare for a high-risk newborn. The physician should obtain this information before the delivery of the infant whenever possible. The maternal record should be reviewed, including the current hospital chart and, as available, the prenatal care record. Particular attention should be paid to the results of maternal prenatal laboratory studies, peripartum cultures, underlying maternal illnesses, and peripartum complications ( Box 4-1 ). Maternal illnesses and medical problems have an important impact on the well-being of the fetus and the newborn ( Table 4-1 ). Discussions with the obstetrician and nursing staff are essential to clarify the status of the mother and infant. When high-risk factors are identified, the physician and nursery staff are then prepared to deal with the anticipated problems of the newborn during delivery and subsequent hospital course.

Box 4-1

Review of Obstetric and Perinatal History

Routine prenatal care

Last menstrual period

Estimated date of conception (by dates and ultrasound)

Onset of prenatal care

Previous pregnancies


Outcome of each

Previous prenatal, intrapartum, neonatal complications

Maternal laboratory studies

Blood type and Rh

Antibody screen

Rapid plasma regain (syphilis)

Hepatitis B surface antigen

Rubella immunity

Human immunodeficiency virus antibody

Alpha-fetoprotein and other prenatal markers

Results of cultures or antibody titers

Maternal illnesses and infections



Thyroid disease

Seizure disorder

Infections (gonorrhea, syphilis, chlamydia, herpes simplex, HIV)

Pregnancy-related and perinatal conditions

Pregnancy-induced hypertension, eclampsia

Chorioamnionitis, maternal fever

Premature labor (use of tocolytics)

Maternal medications and drug use












Heroin or methadone

Phencyclidine (PCP)

Fetal laboratory studies

Amniotic fluid lung maturity studies

Fetal karyotype and other genetic tests

Amniotic fluid delta 450 to assess fetal bilirubin

Cordocentesis labs (complete blood count, platelet count)

Scalp pH

Fetal status

Singleton, twins, higher multiples

Ultrasound findings (weight, gestational age, anomalies, intrauterine growth restriction)

Amniotic fluid (polyhydramnios, oligohydramnios, meconium staining)

Time of rupture of membranes

Cord injuries or prolapse

Results of fetal heart rate monitoring

Maternal bleeding; placenta previa, abruptio placentae


Method of delivery: vaginal or cesarean section (indication)

Instrumentation at delivery: forceps, vacuum

Presentation and position

Prolonged second stage

Shoulder dystocia

Cord complications: nuchal cord, true knot, laceration, avulsion

Social factors

Maternal support system

History of family violence, neglect, or abuse

Previous childen in foster care

Stable living situation, homelessness

History of depression, psychosis

Table 4-1

Maternal Medical Conditions and the Newborn

Maternal Condition Potential Effects on the Fetus or Newborn
Diabetes mellitus Hypoglycemia, macrosomia, hyperbilirubinemia, polycythemia, increased risk for birth defects, birth trauma, small left colon syndrome, cardiomyopathy, and respiratory distress syndrome
Hypoparathyroidism Fetal hypocalcemia, neonatal hyperparathyroidism
Hyperparathyroidism Neonatal hypocalcemia and hypoparathyroidism
Graves’ disease Fetal and neonatal hyperthyroidism, intrauterine growth restriction, prematurity
Obesity Macrosomia, birth trauma, hypoglycemia
Phenylketonuria (poorly controlled) Mental restriction, microcephaly, congenital heart disease
Vitamin D deficiency Neonatal hypocalcemia, rickets
Asthma Increased rates of prematurity, toxemia, and perinatal loss
Congenital heart disease Effects of cardiovascular drugs; risk of maternal mortality
Pregnancy-induced hypertension Premature delivery due to uncontrolled hypertension or eclampsia.Uteroplacental insufficiency, abruptio placentae, fetal loss, growth restriction, thrombocytopenia, neutropenia
Severe anemia (hemoglobin <6 mg/dL) Impaired oxygen delivery, fetal loss
Iron deficiency anemia Reduced iron stores, lower mental and developmental scores in follow-up
Idiopathic thrombocytopenic purpura Thrombocytopenia, central nervous system (CNS) hemorrhage
Fetal platelet antigen sensitization Thrombocytopenia, CNS hemorrhage
Rh or ABO sensitization Jaundice, anemia, hydrops fetalis
Sickle cell anemia Increased prematurity and intrauterine growth restriction
Chorioamnionitis Increased risk for neonatal sepsis, prematurity
Gonorrhea Ophthalmia neonatorum
Hepatitis A Perinatal transmission
Hepatitis B and C Perinatal transmission, chronic hepatitis, hepatic carcinoma
Herpes simplex Encephalitis, disseminated herpes (risk of neonatal disease is much higher with primary versus recurrent maternal infection)
Human immunodeficiency virus Risk of transmission to the fetus or newborn
Syphilis Congenital syphilis, intrauterine growth restriction
Tuberculosis Perinatal and postnatal transmission
Systemic lupus erythematosus Fetal death, spontaneous abortions, heart block, neonatal lupus, thrombocytopenia, neutropenia, hemolytic anemia
Inflammatory bowel disease Increase in prematurity, fetal loss, and growth restriction
Urinary tract infection Prematurity, intrauterine growth restriction
Chronic renal failure Prematurity, intrauterine growth restriction
Transplant recipients Prematurity, intrauterine growth restriction, possible effects of maternal immunosuppressive therapy and mineral disorders

Maternal Diseases

Maternal diabetes mellitus affects the fetus before conception and throughout the entire pregnancy. Uncontrolled diabetes during the periconceptional period and during early embryogenesis increases the risk for fetal malformations, including congenital heart disease, limb abnormalities, and central nervous system anomalies. Small left colon syndrome, femoral hypoplasia–unusual facies syndrome, and caudal regression syndrome are particularly associated with maternal diabetes. Poor diabetic control with resulting chronic hyperglycemia during the third trimester leads to fetal macrosomia, which increases the risk for birth trauma and the need for cesarean delivery. Fetal lung maturation is also delayed by maternal diabetes, increasing the risk for respiratory distress syndrome even in near-term infants. The infant of the diabetic mother is at risk for hypoglycemia, hypocalcemia, hypomagnesemia, polycythemia, and hyperbilirubinemia.

Maternal thyroid disease can have a wide variety of effects on the newborn, depending on the combined effects of maternal transplacental antithyroid antibodies and thyroid medications. The neonate born to a mother with Graves disease can be hypothyroid, euthyroid, or hyperthyroid at birth. When the mother’s Graves disease is well controlled with medications (e.g., propylthiouracil) during the pregnancy, then the infant is usually euthyroid at birth. However, as the effects of maternal antithyroid medication wear off, persistent maternal antithyroid antibodies may stimulate the neonatal thyroid gland and cause thyrotoxicosis.

Maternal preeclampsia has a number of adverse effects on the fetus and the newborn. When preeclampsia occurs early in the pregnancy, it may have severe effects on fetal growth. Fetal distress caused by preeclampsia may necessitate premature delivery of the infant before maturation of the lungs. Preeclampsia also causes neonatal neutropenia and thrombocytopenia.

Particular attention must be paid to infectious illnesses during the pregnancy and in the perinatal period. The results of the prenatal RPR (rapid plasma reagin), as well as any maternal treatment for syphilis, should be recorded in the neonatal record. In communities with a high prevalence of syphilis or in high-risk patients, repeat testing (despite negative prenatal results) of the mother for syphilis at the time of delivery should be considered. All women should be tested for hepatitis B surface antigen during pregnancy, and all neonates born to positive mothers should receive both hepatitis B immunoglobulin and hepatitis B vaccine. Maternal testing for antibody to the human immunodeficiency virus (HIV) should be recommended for all women prenatally. Treatment of the HIV-positive mother during the pregnancy and through the intrapartum course, combined with postnatal treatment of the infant, greatly reduces the risk of transmission of HIV to the infant. Any infant born to a mother who tests positive for HIV antibody or other evidence of HIV infection should be referred, when possible, to an infectious disease specialist for appropriate evaluation and possible treatment.

Active maternal genital infection with herpes simplex virus (HSV) in a woman with ruptured membranes or who delivers vaginally puts the infant at risk for neonatal herpes disease. The risk for vertical transmission of HSV is particularly high when the mother has active primary infection at the time of delivery or the infant is born prematurely. In contrast, with recurrent maternal herpes, the risk for vertical transmission of HSV is about 2%.

Maternal chorioamnionitis increases the risk for bacterial sepsis in the newborn, particularly in the premature infant. It is strongly encouraged to follow the recommendations of the Centers for Disease Control and Prevention (CDC) regarding the use of intrapartum prophylactic antibiotics for mothers at risk to transmit group B STREPTOCOCCUS to their infants. When clinical chorioamnionitis is diagnosed in a mother, the risk for sepsis in the newborn is greatly increased. Such infants should have a sepsis screen—a blood culture obtained and the infant started on broad spectrum antibiotics (e.g., ampicillin and gentamicin) pending culture results.

Maternal Medications

Medications given to the mother may have adverse effects on the fetus ( Table 4-2 ). One area of great concern has been the risk for fetal malformations caused by maternal drug use. Because organogenesis occurs primarily in the first 12 weeks of gestation, the fetus can easily be exposed to a variety of potentially teratogenic toxins and drugs before a woman knows that she is pregnant or before the first prenatal visit. Appropriate counseling about the dangers of maternal drug use on the fetus is further complicated if prenatal care is delayed or lacking. Hence, the issue of medications and drugs during pregnancy is truly a public health issue. Women of childbearing age need to be educated about the potential risks associated with use of medications (both prescribed and over the counter) and illicit drugs before conception and embryogenesis. Besides their teratogenic potential, medication used by the mother can have a variety of other effects on the fetus and newborn. Fetal growth can be impaired by antineoplastic agents, heroin, cocaine, irradiation, and some anticonvulsants. Drugs used for tocolysis of labor can cause symptoms in the neonate. Beta-sympathomimetics are associated with neonatal hypoglycemia resulting from the mobilization of glycogen from the fetal liver. Magnesium sulfate, which is used for treatment of preterm labor and preeclampsia, depresses respiratory effort and can lead to respiratory failure in the newborn. In contrast, prenatal steroids for fetal lung maturation are generally safe and without adverse effects on the newborn.

Table 4-2

Maternal Medications and Toxins: Possible Effects on the Fetus and Newborn

Medication Effect on Fetus and Newborn
Acetaminophen Generally safe except with maternal overdose
Aspirin Hemorrhage, premature closure of ductus arteriosus, pulmonary artery hypertension (effects not seen at ≤100 mg/day)
Opiates Neonatal abstinence syndrome with chronic use
Ibuprofen Reduced amniotic fluid volume when used in tocolysis; risk for premature ductus arteriosus closure and pulmonary hypertension
Indomethacin Closure of fetal ductus arteriosus and pulmonary artery hypertension
Meperidine Respiratory depression peaks 2 to 3 hours after maternal dose
General anesthesia Respiratory depression of infant at delivery with prolonged anesthesia just before delivery
Lidocaine High serum levels cause central nervous system (CNS) depression; accidental direct injection into the fetal head causes seizures
Aminoglycosides Ototoxicity reported after use of kanamycin and streptomycin
Cephalosporins Some drugs in this group displace bilirubin from albumin
Isoniazid Risk for folate deficiency
Metronidazole Potential teratogen and carcinogen, but not proven in humans
Penicillins Generally no adverse effect
Tetracyclines Yellow-brown staining of infant’s teeth (when given at ≥5 months’ gestation); stillbirth and prematurity due to maternal hepatotoxicity
Sulfonamides Some drugs in this group displace bilirubin from albumin; can cause kernicterus
Trimethoprim Folate antagonism
Vancomycin Potential for ototoxicity
Carbamazepine Neural tube defects; midfacial hypoplasia
Phenobarbital Withdrawal symptoms, hemorrhagic disease; midfacial hypoplasia
Phenytoin Hemorrhagic disease; fetal hydantoin syndrome: growth and mental deficiency, midfacial hypoplasia, hypoplasia of distal phalanges
Trimethadione Fetal trimethadione syndrome: growth and mental deficiency, abnormal facies (including synophrys with upslanting eyebrows), cleft lip and palate, cardiac and genital anomalies
Valproic acid Neural tube defects, midfacial hypoplasia
Warfarin (Coumadin) Warfarin embryopathy: stippled epiphyses, growth and mental deficiencies, seizures, hypoplastic nose, eye defects, CNS anomalies including Dandy-Walker syndrome
Heparin No direct adverse effects on the fetus
Aminopterin Cleft palate, hydrocephalus, meningomyelocele, intrauterine growth restriction
Cyclophosphamide Intrauterine growth restriction, cardiovascular and digital anomalies
Methotrexate Absent digits, CNS malformation
Iodide-containing drugs Hypothyroidism
Methimazole Hypothyroidism, cutis aplasia
Potassium iodide Hypothyroidism and goiter, especially with chronic use
Propylthiouracil Hypothyroidism
Iodine 131 Hypothyroidism, partial to complete ablation of thyroid gland
Acyclovir No definite adverse effects
Ribavirin Teratogenic and embryolethal in animals
Zidovudine Potential for fetal bone marrow suppression; combined maternal and neonatal treatment reduces perinatal transmission of human immunodeficiency virus
Angiotensin-converting enzyme inhibitors Fetal hypocalvaria, oligohydramnios and fetal compression, oliguria, renal failure
β-Blockers (propranolol) Neonatal bradycardia, hypoglycemia
Calcium channel blockers If maternal hypotension occurs, this could affect placental blood flow
Diazoxide Hyperglycemia; decreased placental perfusion with maternal hypotension
Digoxin Fetal toxicity with maternal overdose
Hydralazine If maternal hypotension occurs, this could affect placental blood flow
Methyldopa Mild, clinically insignificant decrease in neonatal blood pressure
Furosemide Increases fetal urinary sodium and potassium levels
Thiazides Thrombocytopenia, hypoglycemia, hyponatremia, hypokalemia
Androgenics (danazol) Masculinization of female fetuses
Corticosteroids Cleft lip/palate
Diethylstilbestrol (DES) DES daughters: vaginal adenosis, genital tract anomalies, increased incidence of clear cell adenocarcinoma, increased rate of premature delivery in future pregnancy
DES sons: possible increase in genitourinary anomalies
Estrogens, progestins Risk for virilization of female fetuses reported with progestins; small, if any, risk for other anomalies
Insulin No apparent direct adverse effects, uncertain risk related to maternal hypoglycemia
Tamoxifen Animal studies suggest potential for DES-like effect
Barbiturates Risk for hemorrhage and drug withdrawal
Benzodiazepines Drug withdrawal; possible increase in cleft lip/palate
Selective serotonin reuptake inhibitors (SSRIs) Pulmonary artery hypertension, jitteriness, irritability
Lithium Ebstein anomaly, diabetes insipidus, thyroid depression, cardiovascular dysfunction
Thalidomide Limb deficiency, cardiac defects, ear malformations
Tricyclic antidepressants Jitteriness, irritability
Alcohol Fetal alcohol syndrome, renal and cardiac anomalies
Amphetamines Withdrawal, prematurity, decreased birth weight and head circumference, cerebral injury
Cocaine Decreased birth weight, microcephaly, prematurity, abruptio placentae, stillbirth, cerebral hemorrhage; possible teratogen: genitourinary, cardiac, facial, limb, intestinal atresia/infarction
Heroin Increased incidence of low birth weight and small for gestational age, drug withdrawal, postnatal growth and behavioral disturbances; decreased incidence of respiratory distress syndrome
Marijuana Elevated blood carboxyhemoglobin; possible cause of shorter gestation, dysfunctional labor, intrauterine growth restriction, and anomalies
Methadone Increased birth weight as compared to heroin, drug withdrawal (worse than with heroin alone)
Phencyclidine (PCP) Irritability, jitteriness, hypertonia, poor feeding
Tobacco smoking Elevated blood carboxyhemoglobin; decreased birth weight, increased prematurity rate, increased premature rupture of membranes, placental abruption and previa, increased fetal death, possible oral clefts
Magnesium sulfate Respiratory depression, hypotonia, bone demineralization with prolonged (weeks) use for tocolysis
Ritodrine Neonatal hypoglycemia
Terbutaline Neonatal hypoglycemia
A (preformed, not carotene) Excessive doses (≥50,000 IU/day) may be teratogenic
Acitretin Activated form of etretinate (see later)
D Megadoses may cause hypercalcemia, craniosynostosis
Etretinate Limb deficiency, neural tube defect; ear, cardiac, and CNS anomalies
Folate deficiency Neural tube defects
Isotretinoin (13- cis -retinoic acid) Ear, cardiac, CNS, and thymic anomalies
Menadione (vitamin K 3 ) Hyperbilirubinemia and kernicterus
Phytonadione (vitamin K 1 ) No adverse effect
Anticholinergics Neonatal meconium ileus
Antiemetics Doxylamine succinate and/or dicyclomine HCl with pyridoxine reported to be teratogens, but bulk of evidence is clearly negative
Aspartame Contains phenylalanine; potential risk to fetus of a mother with phenylketonuria
Chorionic villus sampling (CVS) Limb deficiency with early CVS
Irradiation Adverse effects primarily associated with therapeutic, not diagnostic doses, and is dose dependent: fetal death, microcephaly, intrauterine growth restriction
Lead Decreased IQ (dose related)
Methylene blue Hemolytic anemia, hyperbilirubinemia, methemoglobinemia; intraamniotic injection in early pregnancy associated with intestinal atresia
Methylmercury CNS injury, neurodevelopmental abnormalities, microcephaly
Misoprostol Möebius sequence
Oral hypoglycemics Neonatal hypoglycemia
Polychlorinated biphenyls Cola skin coloration, minor skeletal anomalies, neurodevelopmental deficits

Psychotropic drugs used during pregnancy have the potential for effects on the fetus and newborn. Fluoxetine, a selective serotonin reuptake inhibitor (SSRI), has been reported to increase the risk for neonatal problems and may have some neurobehavioral effects. SSRIs in general may put the neonate at risk for pulmonary artery hypertension. Benzodiazepines may increase the risk for oral clefts. Lithium is associated with a small increased risk for Ebstein anomaly.

Illicit and recreational drug use among pregnant women remains a major problem that affects both the fetus and the newborn. Maternal heroin and methadone use cause neonatal abstinence syndrome, which is characterized by irritability, hypertonia, jitteriness, seizures, sneezing, tachycardia, diarrhea, and difficulties with feedings. Withdrawal symptoms can be prolonged, particularly with methadone exposure. Intrauterine opiate exposure is also associated with intrauterine growth restriction, poor postnatal growth, and abnormal neurodevelopmental outcome. Maternal cocaine exposure has also been reported to be associated with neurobehavioral disturbances in the newborn, although true withdrawal symptoms are less pronounced than with heroin or methadone. In utero cocaine exposure affects fetal growth, and such infants tend to have a lower birth weight and smaller head circumference. Cocaine use in pregnancy is associated with neonatal cerebral hemorrhage, premature delivery, abruptio placentae, and stillbirth. There are conflicting data about the role of prenatal cocaine exposure and the risk for congenital malformations (including intestinal atresia, urogenital anomalies, and limb reduction anomalies), and necrotizing enterocolitis. Prenatal opiate and cocaine exposure is associated with an increased incidence of sudden infant death syndrome. Persistent illicit drug activity in the mother or other family members can continue to affect the care of the high-risk infant throughout hospitalization and at the time of discharge, especially if the infant requires any type of special treatment at home. The management of the dysfunctional drug-exposed family can complicate the care of the sick newborn.

Prenatal alcohol use has serious adverse effects on the fetus that can manifest as problems in the neonatal period and beyond. The greatest risk to the fetus seems to be associated with heavy chronic drinking during the pregnancy (four to six drinks per day). However, with even more modest alcohol consumption (e.g., two drinks per day), effects have been noted in some studies. The most extreme result of maternal alcohol use is fetal alcohol syndrome. Signs of this syndrome at birth may include symmetrical intrauterine growth restriction, central nervous system problems (microcephaly, irritability, tremulousness), facial dysmorphic features, congenital heart disease, and ear, eye, and limb (joint contractures, nail hypoplasia) anomalies. The facial dysmorphic features include short palpebral fissures, thin upper lip, smooth philtrum, maxillary hypoplasia, and a short nose. Later in life, these infants may have continued poor growth, neurobehavioral problems, and low IQ scores. Many infants exposed to alcohol in utero do not have sufficient physical features or anomalies required to make the diagnosis of fetal alcohol syndrome. However, these same infants may still demonstrate neurobehavioral and motor problems, which have been referred to as fetal alcohol effects .

Maternal smoking increases blood levels of carboxyhemoglobin and impairs oxygen delivery to the fetus. Smoking is associated with a decrease in birth weight of 175 to 250 grams. Several studies have suggested that nonsmoking mothers who are exposed to environmental tobacco smoke are more likely to have low-birth-weight infants than mothers with minimal tobacco exposure. Maternal smoking has also been implicated in placental abruption, preterm delivery, and postnatal respiratory illnesses. Whether prenatal exposure to tobacco causes an increased incidence of congenital malformations is unclear.

Preparations for Delivery

After the maternal record has been reviewed, the physician should meet with the parents before the delivery of a high-risk infant. Important information regarding the prenatal course is not always reflected in the hospital obstetric record, particularly if prenatal care was lacking or fragmented, and this information may be available from the mother. This is particularly relevant regarding familial and genetic disorders. If the delivery of a premature infant is expected, it is appropriate to explain the role of the pediatrician, neonatal nurse practitioner, neonatologist, or other health care professionals in the delivery room, as well as resuscitation and subsequent management procedures ( Box 4-2 ). Aspects of the anticipated hospital course for a sick premature infant should be discussed. Preparing parents for the prolonged hospitalization of a premature infant begins to build the foundations of trust and communication that will be needed between the family and the medical team. If time is limited because of the imminent delivery of the infant, the physician should, at the least, introduce himself or herself to the parents and briefly explain how the infant will initially be managed.

Box 4-2

Subjects to Discuss with Parents Before Delivery of a Premature Newborn

Anticipated birth weight and gestational age

Approximate risk of death and major morbidities

Anticipated length of hospitalization

Respiratory distress syndrome, oxygen, ventilation, surfactant

Procedures: intubation, intravenous catheters, umbilical catheterization, lumbar puncture

Blood transfusion: risks, benefits, alternatives, use of designated donor

Potential problems: patent ductus arteriosus, intraventricular hemorrhage, jaundice

Possible need for transport (if not delivered in a tertiary center)

Role of the parents in the intensive care nursery

Importance of providing breast milk

Depending on the type and severity of anticipated problems, specific equipment or extra personnel may be needed in the delivery room. For example, if an infant is known to have hydrops with pleural effusions and ascites, then the resuscitation team should have equipment fully prepared before the delivery for needle thoracentesis, chest tube drainage, intubation, ventilation, and umbilical catheterization. For such a high-risk delivery, the presence of two physicians to care for the infant may be indicated. Neonatal nursing personnel should be kept informed regarding the admission of high-risk mothers and possible pending deliveries. The pediatric surgeon should be notified of the anticipated delivery of any infants with abdominal wall defects, possible gastrointestinal anomalies or obstruction, diaphragmatic hernia, or tracheoesophageal fistula. The cardiology team, including cardiothoracic surgery, should be informed of impending deliveries of infants with known cardiac defects.

The pediatrician can also play an important role in the appropriate prepartum management of a high-risk mother. Aggressive tocolysis and use of prenatal steroids to induce fetal lung maturity should be strongly encouraged for the mother in preterm labor. Despite the multiple postnatal benefits for premature infants who were given prenatal steroids ( Box 4-3 ) , maternal steroids are sometimes withheld in the presence of ruptured membranes, extreme prematurity, or an anticipated interval of less than 24 hours before delivery. Assessing the gestational age of the fetus can be very important in extremely premature infants. The discussion with the parents regarding outcomes will be markedly different for a 23-week as opposed to a 26-week fetus or newborn. Unless there are clear contraindications to steroid treatment or proven fetal lung maturity, in the setting of anticipated premature delivery, the mother should be given steroids. The pediatrician should also advocate for delivery of high-risk mothers in the most appropriate setting. The needs of the mother, the fetus, and the newborn infant must all be recognized, and the personnel, equipment, and expertise must be available to meet these needs. Certain high-risk mothers, if stable for transport, should be transferred to a perinatal center. In particular, if premature delivery is anticipated before 32 weeks’ gestation or if there are known major fetal congenital anomalies that would affect the stabilization of the newborn, then maternal transfer to a perinatal center with an intensive care nursery is most appropriate.

Box 4-3

Effects of Prenatal Steroids on the Premature Newborn

Increased tissue and alveolar surfactant

Maturational effects on the lung: structural and biochemical

Possible maturational effects on brain, gastrointestinal tract, and other organs

Decreased mortality rate

Decreased incidence and severity of respiratory distress syndrome

Decreased incidence of necrotizing enterocolitis

Decreased incidence of intraventricular hemorrhage

Decreased incidence of significant patent ductus arteriosus

Decreased length of stay and costs of hospitalization

Labor and Delivery

Appropriate supplies and a well-trained staff are essential in the delivery room. Whether the birth occurs in a birthing room or in the operating room, the equipment and procedures need to be the same—an infant warming table with working lights, Apgar timer, air and oxygen supply, and an oxygen blender. A person needs to be delegated to ensure that the infant table is adequately prepared. There needs to be mechanical suction and a device to deliver positive pressure ventilation. Endotracheal tubes of different sizes, meconium aspirators, and a laryngoscope must be readily available. If a multiple delivery is anticipated, there must be a stocked infant table for each infant. An emergency crash cart designated specifically for neonates must be close by and well stocked in case of emergency.

The value of a staff that is well trained and prepared cannot be overstated. Health care workers who attend deliveries should have appropriate training in NRP (neonatal resuscitation program). Additionally, emergency procedures for alerting more subspecialized health care professionals (e.g., neonatologists or pediatricians) must be in place in the event of an acutely ill infant.

There are additional special considerations in the delivery room when anticipating the delivery of a preterm infant. Preterm infants are especially prone to cold stress and hypothermia. Infants less than 29 weeks should be placed in a polyurethane bag up to the neck to minimize heat loss. Most premature infants should have a pulse oximeter applied shortly after birth in the delivery room. A proportion of infants born at 32 weeks or less will develop respiratory distress syndrome from surfactant deficiency. Preparations to support such an infant should include the potential to provide nasal continuous positive airway pressure (CPAP), intubation, and surfactant administration as needed. If available, a neonatal respiratory therapist should be present to facilitate the stabilization of these infants. There has been increasing evidence that infants resuscitated in the delivery room with room air, rather than 100% oxygen, have lower levels of oxygen-free radicals, which may affect the incidence of retinopathy of prematurity. In addition, oxygen may have an adverse affect on cerebral circulation and breathing physiology. Most extremely low-birth-weight (ELBW) infants will need some supplemental oxygen in the delivery room, and it is suggested to begin with about 30% O 2 in such infants who require resuscitation and then adjust Fi o 2 as needed, guided by pulse oximetry.


Transition is a term used to describe a series of events that are centered around birth itself, beginning in utero and continuing into the postnatal period. The fetus is well adapted to the intrauterine environment. However, during this intricate symbiotic relationship with the mother, the fetus must also prepare for transition to extrauterine life. This transition requires striking adaptive changes in multiple organ systems of the newborn. Some of these dynamic changes are largely completed in the first minutes to hours after birth. Others are initiated at birth, but continue to evolve over the first weeks of life. The ability of the newborn to make this transition safely and expeditiously affects the health and survival of the infant. Recognition of the factors that may adversely affect the transitional period allows the health professional to act promptly and judiciously for the benefit of the infant.

The most dramatic changes during transition involve the cardiovascular and respiratory systems. During fetal life, gas exchange is accomplished by the placenta, whereas the fetal lungs are gasless and filled with fluid. In the several days before delivery, fetal lung water begins to decrease and is accelerated by labor. Various hormones, including epinephrine and vasopressin, decrease fluid secretion into the pulmonary intraluminal space. Plasma protein levels increase with labor, and this augmented oncotic pressure likely increases pulmonary intraluminal water reabsorption. Intraluminal fluid is transported to the interstitium and is removed primarily by augmented postnatal pulmonary blood flow as pulmonary artery pressure decreases. Some intraluminal fluid is transported by the lymphatics through the mediastinal tissues or across the pleural space. Previously, it has been suggested that thoracic compression during vaginal birth played a prominent role in the expulsion of lung fluid through the oropharynx, but such a mechanism does not seem to have a major role in the reduction of lung water in the newborn.

Fetal breathing is episodic and occurs primarily during periods of low-voltage electrocortical activity. It likely plays a role in the conditioning of respiratory muscles and may have other effects on chest wall, lung, and muscle growth. A variety of phenomena contribute to the onset of continuous breathing, which occurs shortly after birth in relatively healthy nonasphyxiated infants. Aspects of the physical environment may play a role, such as light, sound, cutaneous stimulation, and heat loss. Cord occlusion and an increase in blood oxygen appear to be potent stimulants of continuous breathing by the newborn. The fetus prepares for air breathing by the synthesis and release of surfactant into the alveolar space. The process can be accelerated by premature rupture of fetal membranes, β-mimetic tocolysis, and the administration of steroids to the mother. Delivery of a term infant by elective cesarean section without labor may prevent maturation of this late process of surfactant production and release, resulting in an infant with respiratory distress syndrome. If an infant is scheduled to be delivered via elective cesarean section before 39 weeks, fetal lung maturity should be checked to avoid the sequelae of surfactant deficiency.

The transitional changes in the cardiovascular system are primarily an adaptation to the elimination of the placental circulation and an adaptation to pulmonary gas exchange. As the lungs expand at birth, pulmonary artery pressure declines, and there is a dramatic increase in pulmonary blood flow. Systemic arterial resistance increases with cord occlusion and elimination of the low resistance placental circulation. These factors combine to favor an increase in pulmonary blood flow rather than the passage of blood via the ductus arteriosus into the distal aorta. Because of the increase in pulmonary blood flow, left atrial pressure increases and functionally closes the foramen ovale, thereby eliminating this source of previous right-to-left shunting. The right and left ventricles now function primarily in series versus pumping in parallel as in the fetal state. The ductus arteriosus remains open for a variable period, but it begins to close in response to exposure to highly oxygenated blood. It generally functionally closes by 1 to 2 days in a term infant, but frequently remains open in the premature or the seriously ill term newborn with pulmonary artery hypertension. The ductus venosus closes within 1 to 2 days (contributing to the technical difficulty of passing an umbilical venous catheter to the right atrium beyond the first day of life). Pulmonary artery pressure continues to decline through the first weeks of life. During these dramatic changes in the cardiovascular system, the sick newborn may demonstrate difficulties in making these transitions. Because of the parallel pumping systems of the fetal cardiovascular system, most infants with complex congenital heart disease are well adapted to the in utero state. However, these infants often do poorly in the transition to extrauterine life. In infants with ductal dependent cyanotic congenital heart disease, progressive cyanosis develops as the ductus arteriosus closes. In those infants with left-sided obstructive lesions (e.g., hypoplastic left heart), acidosis and shock develop as the ductus arteriosus closes and distal aortic blood flow is lost. Infants with pulmonary artery hypertension shunt right to left at the foramen ovale or patent ductus arteriosus. Recognition of infants at risk for pulmonary artery hypertension (e.g., meconium aspiration) may lead the physician to earlier interventions (e.g., endotracheal suctioning, oxygen, ventilation) to reverse or prevent this problem.

The uterine environment is relatively quiet, very dark, and rather unchanging until labor and passage through the birth canal. At birth, the newborn is bombarded with stimuli, including exposure to light, different sounds, and tactile stimuli. In addition, the newborn must begin to defend its core temperature against heat loss, despite being born both wet and into a much cooler environment. These multiple stresses result in a surge of sympathetic nervous system activity. Catecholamines increase dramatically at birth. Brown fat (nonshivering) thermogenesis causes the hydrolysis of stored triglycerides and the release of fatty acids. Box 4-4 summarizes these and other events during transition.

Box 4-4

Summary of Transitional Events in the Newborn


  • Reabsorption of intraluminal fluid

  • Onset of continuous breathing

  • Expansion of pulmonary air spaces

  • Pulmonary gas exchange replaces placental circulation

  • Surfactant synthesis and release


  • Removal of the placental circulation

  • Decline in pulmonary artery pressure and increase in pulmonary blood flow

  • Closure of ductus arteriosus, foramen ovale, and ductus venosus

Glucose homeostasis

  • Loss of transplacental glucose transport with decline in serum glucose

  • Increase in glucagon and decrease in insulin levels


  • Sympathetic nervous system activation caused by cold stress

  • Nonshivering thermogenesis (brown fat)

Hormonal and metabolic

  • Shift from primarily glucose metabolism (RQ = 1) to glucose and fat (RQ = 0.8-0.85)

  • Increase in oxygen consumption

  • Increase in levels of epinephrine and norepinephrine

  • Acute increase in TSH with subsequent decline

  • Peak increase in T 4 , free T 4 , and T 3 at 48 hours

  • Decrease in reverse T 3

  • Decline in serum calcium with nadir at 24 hours and subsequent elevation

  • Increase in parathyroid hormone, 1,25 OH vitamin D, and calcitonin

  • Increase in glycerol and free fatty acids

Nervous system

  • Adaptive interaction with parents and environment

  • Movement between states

  • Increase in motor activity


  • Increase in renin production

  • Increase in sodium reabsorption

  • Onset of long-term maturational changes with improving glomerular filtration rate

  • Reduction of extracellular fluid compartment (diuresis)


  • Marked reduction in erythropoietin and erythrogenesis

  • Postnatal increase in blood leukocyte and neutrophil count

  • Improved vitamin K-dependent carboxylation of coagulation factors


  • Evacuation of meconium

  • Induction of intestinal enzymes with feeding

Establishment of effective coordinated suck, swallow, breathing

Specific physical and behavioral changes, which occur in the healthy newborn in the hours after birth, have been described ( Fig. 4-1 ). The healthy newborn may have some initial bradycardia or tachycardia, and cutaneous perfusion may be mottled or pale. Respirations may be initially somewhat irregular but should improve steadily and become regular and vigorous. There may be some mild transient grunting and flaring, but true respiratory distress with retractions should not be present. If the infant has made a stable transition, these parameters stabilize within the first hour of life. After birth, the healthy newborn often undergoes a quiet alert phase, which has been referred to as the first phase of reactivity . When placed skin-to-skin on the mother’s chest shortly after birth, the infant often becomes quiet or exploring. Rhythmic, pushing movements of the lower extremities have been described as the infant searches for the mother’s breast. If left undisturbed, the infant crawls and searches for the areola in an attempt to attach and suckle ( Fig. 4-2 ). Suckling causes release of oxytocin in the mother, stimulating milk production and uterine contractions. Sucking movements in the infant stimulate the release of multiple gastrointestinal hormones, which prepare the infant to digest enteral nutrients. The warmth provided by the mother’s chest maintains a stable temperature in the infant, as long as a blanket is also placed over the infant and the room is not too cold. Early contact with the mother has been shown to increase the success of breast feeding, and it is an important first step in the bonding process. Most hospital staff in birthing centers recognize the importance of this early contact between the mother and infant. Sometimes mothers are encouraged to promptly attempt to nurse their infant immediately after birth. It may be more appropriate to quickly dry the infant and to rapidly determine that the infant is healthy and requires no immediate interventions. Then the infant can be placed on the mother’s chest, skin to skin, and allowed to have a private quiet time with the parents.

Sep 29, 2019 | Posted by in PEDIATRICS | Comments Off on Recognition, Stabilization, and Transport of the High-Risk Newborn
Premium Wordpress Themes by UFO Themes