In recent years, there have been considerable improvements in the care and outcome for newborn infants, particularly those with complex health care needs. In addition to physicians and nurses, an increasing number of health care professionals, including respiratory therapists, physiotherapists, pharmacists, dietitians, occupational therapists and others, have become important members of the neonatal health care team.

That evolution of enhanced roles in neonatal care began with the development of increased interests, knowledge and skills among all health care professionals. Just as pediatricians sub-specialized in neonatology, neonatal nurses, respiratory therapists, dietitians, social workers and pharmacists developed a range of knowledge and skills specific to the performance of clinical service in the neonatal unit, and in neonatal research and education.

Subsequently, practitioners developed skills that previously had been limited to other groups of health care professionals, most often physicians. Nurses and respiratory therapists performed such delegated acts as arterial puncture or intubation following a process of certification. Dietitians and clinical pharmacists ordered parenteral nutrition; a counter signature by a physician was often required.

The third stage in the evolution of enhanced performance was the development of staff with a wider range of specialized knowledge and technical and nontechnical skills designed to meet specific needs in a limited practice environment. This is exemplified by the development of roles, such as a transport nurse or transport respiratory therapist, through a process of hospital-based certification that may follow university or college courses and/or educational programs developed in individual hospitals. While enhanced roles have developed somewhat differently among various nonmedical health professional groups, they share several common factors:

• the increasing complexity and range of technology provided in neonatal care;
• the availability of a different set of qualifications and skills provided by other professionals;
• increasing survival, particularly of very low birth weight infants, resulting in increasing patient numbers requiring specialized care;
• the need to supplement declining numbers and availability of residents working in the neonatal intensive care unit (NICU); and
• the need for all health care professionals to develop or establish a broader scope of practice and increased academic responsibility.

Because of their size and stage of development, the health needs of neonates are quite different from those of adults.

In this continuing education unit, you will explore some of those needs, review developmental stages and the various diseases that afflict newborn infants (including numerous congenital defects). You will also learn about the various scoring and diagnostic tests utilized in neonatal care.

Upon successful completion of this course you will be able to:

• Describe the stages of development in fetal circulation.
• Identify and discuss the stages of fetal lung development.
• Explain the role surfactant plays in the development of neonates.
• Identify and discuss the processes of labor and delivery, the complications that can occur, and preventive steps that can be taken.
• Explain how to interpret neonatal radiographs
• List the markers for a high-risk pregnancy, and high-risk infants.
• Identify the clinical signs and appropriate treatments for common neonatal pathology.

We will begin with a review of pre and postnatal anatomical and physiological development. As you will see below, Table 1 summarizes the various stages of development experienced by the embryo.

Fetal Circulation

In utero, the prenatal circulation depends heavily on the mother's circulatory system for survival and development. During development, fetal nutrition, oxygenated blood, excretion, respiration, and protection are provided by the placenta. Development begins when the blastocyst attaches itself somewhere near the upper portion of the uterine cavity. Diffusion of substances between maternal and fetal blood occurs in the intervillous space created there.

While the ductus venosus and foramen ovale rarely cause problems at birth, if the ductus arteriosus does remain patent or reopens in response to hypoxia, this can lead to problems. If fetal circulation is maintained it can lead to a massive shunt causing hypoxia and pulmonary hypertension. The normal newborn shunt of 20 to 25% is much higher in the presence of a patent ductus arteriosus.

Pulmonary Circulation and Lung Development

The difference between fetal circulatory and nonfetal circulatory systems is that, since the fetus does not use the lungs for gas exchange, very little blood actually perfuses the pulmonary circulation. In the fetus, the body has mechanisms to bypass the lungs.

By 16 to 20 weeks of gestation, the process of pulmonary arterial branching has been nearly completed. The central pulmonary trunk in the fetus has elastic laminae and its walls have become thick. Prior to birth, blood bypasses the lungs in utero, with only about 10% of the cardiac output carried by the pulmonary circulation. With the majority of cardiac output being shunted past the lungs via the ductus arteriosus, fetal pulmonary vascular resistance (PVR) is very high, making flow through the ductus the path of least resistance.

Branching away from the main pulmonary artery, arterial elastic laminae decrease. Arteries with diameters of 2 mm down to approximately 200 microns undergo a transition to a more muscular type of vessel where there are changes in PVR. These periacinar are located adjacent to the terminal bronchioles. As the vessels get smaller, the amount of muscle gradually decreases and eventually disappears entirely in vessels adjacent to the alveoli.

Stages of Lung Development

Fetal lung development occurs in five phases:

1. During the embryonic phase, which begins at about 4-6 weeks of gestational age, the lung begins as a bud from the foregut. That bud branches into right and left primary bronchi. The branching continues, forming the proximal airways. Common malformations originating in this phase are the laryngeal cleft and tracheoesophageal fistula. There are few structural pulmonary abnormalities that occur during the embryonic phase because an embryo damaged during this period does not usually survive.
2. During the pseudoglandular phase, which lasts from about week seven to week sixteen, the predominant feature involves the formation of conducting airways. At about week 8, the diaphragm is also formed. During the pseudoglandular phase, the mucous glands, cilia, goblet cells, and cartilage also begin to appear in the conducting airways. Respiratory epithelium begins to differentiate during this phase, so injuries then can result in abnormal bronchial positions, connections, or number of bronchi. If the diaphragm does not form sufficiently to separate the thoracic and abdominal cavities, diaphragmatic hernia may result.
3. During the canalicular phase, weeks seventeen to twenty-eight, the gas exchanging area of the lung develops. Multivesicular and lamellar bodies associated with surfactant production begin to appear at about 20 weeks, and differentiation of Type I and Type II pneumocytes begins during this phase. Pulmonary capillaries are near alveoli at this point, but not near enough for effective gas exchange. Alveolar wall thickness is approximately 45 microns at 20 weeks gestation, and it decreases to about 20 microns at 32 weeks, then eventually to fifteen microns at term. In comparison, adult thickness is about 1 micron.

Surfactant produced during the canalicular phase is immature and easily destroyed. Its chemical composition (thus its functional capability) changes dramatically in the latter stages of gestation. The alveolar surface area at the end of this phase is approximately 1 square meter, and it increases to about 4 square meters at birth. Injuries to the fetus during this time can cause damage to the gas-exchanging area of the lung, causing a deficiency in alveoli, which may be severe enough to produce pulmonary hypoplasia. The gas-exchanging portion of the lung matures during the final two phases:

4. During the saccular phase, which lasts from weeks twenty-nine to thirty-five, interstitial tissue space decreases and airspace walls narrow. They become more compact, and lateral projections extend from the walls to divide the airspaces into smaller units. At 32 to 36 weeks alveoli are present.
5. The alveolar phase, from week thirty-six on, is devoted to final development and maturation of the alveoli. The number of alveoli at birth has been estimated to be anywhere from 10 to 150 million, and increases after birth becoming complete by the time the infant is 2 to 3 years old. At this point, the structure of the lung is usually sufficient to survive injuries, but injuries in this phase may interfere with alveolarization and lung function

Fetal Breathing and Lung Fluid

The prenatal lungs do not function as gas exchange organs, but they do serve important purposes:

1. The lung is a primary source of amniotic fluids.
2. Lungs act as reservoirs of carbohydrates needed for fetal energy.
3. They produce surfactant beginning at about 24 weeks

Fetal breathing movements, which appear to be essential for normal development, begin at around 12 weeks gestation. Factors that can affect fetal breathing movements include:

• maternal cigarette smoke, which stops fetal breathing for many hours.
• maternal consumption of alcohol or drugs
• decreases in 02, C02, or glucose
• stress
• prostaglandins

Arousal of the fetus appears to be more related to fetal breathing movements than central nervous system or chemoreceptor stimulation. When fetal breathing movements are absent, the cause is related to chromosomal and other abnormalities, or death. The fetus has breathing movements approximately 30% of the time during the last 10 weeks of gestation.

In utero, the lungs are filled with fluid, and fetal breathing movements exchange this fluid with amniotic fluid. Diagnostic testing of lung maturation via amniocentesis is made possible as a result of this fluid exchange. When Type II pneumocytes mature, they secrete surfactant into the lung and amniotic fluid.

Normal fetal development requires the presence of adequate amounts of lung and amniotic fluid. A diminished amount of either can result in a hypoplastic lung. Hypoplasia is a decrease in either lung weight or volume at birth. A decrease in alveolar number or an increase in alveolar size also can occur. An absence of fetal breathing movements or a lack of adequate space for lung growth may also cause hypoplasia.

The presence and chemical composition of surfactant can be tested in the amniotic fluid samples. Caution needs to be taken while obtaining these samples via amniocentesis because at 14-17 weeks, amniocentesis may reduce birth weight and lung volume; while at 22-25 weeks, amniocentesis may cause a decrease in the size and number of alveoli

Lung fluid, which contains glucose and other carbohydrates, acts as a storage reservoir that can be utilized after delivery. When the lung fluid is absorbed at birth, the materials are made available for use by the newborn's entire body. After delivery, the flow of fluid from lungs into the interstitium and lymphatics is facilitated by increased alveolar pore size.

During lung development, collagen is the dominant connective tissue in airways, blood vessels, and nonrespiratory components of the lung. While collagen fibers appear disorderly in actively branching airways, they are orderly in formed airways. Elastin, not collagen, is the dominant connective tissue in lung parenchyma.

Elastin first appears at 20 to 25 weeks gestation. Neither collagen nor elastin is particularly prominent at birth; however, the amount of elastin increases rapidly within 6 months after birth, helping to explain the easy rupture and decreased elastic recoil of the newborn's lungs. As the amount of elastin increases, the lung becomes more elastic.

A hypoplastic lung, one that has defective or incomplete development, is generally smaller than normal. Lung size is assessed via lung weight, volume, or DNA; however, lung weight is considered a poor indicator of development because most problems increase lung weight. When a lung weight-body ratio is used for assessment, a ratio <0.015 in a fetus less than 28 weeks old or a ratio <0.012 in an older fetus, is considered hypoplastic.

A better indicator of lung size is a measurement of inflated lung volume, because lung volume is unaffected by most fetal lung diseases. The correlation between crown-rump length and lung volume over the last half of gestation is excellent. Lung volume can therefore be predicted from crown-rump length, with lungs less than 69% of predicted volume being considered hypoplastic. Using lung DNA to reveal the number of cells present is another technique for assessing lung size. If lung DNA is <100 mg/kg body weight, the lungs are considered hypoplastic.

Surfactant

Surfactant is the active agent in the alveoli that cuts surface tension and reduces the need for high pressures to open the alveoli on inspiration. Surfactant is also important for changing capillary and interstitial pressures, facilitating removal of fluids from the lungs, and lowering pulmonary vascular resistance at birth.

The production of surfactant, a mixture of phospholipids (70-80%) and protein in relatively consistent proportions, sharply decreases after 34 to 35 weeks gestation. Evaluation of the content of the surfactant provides valuable information regarding the surfactant-producing system's maturity. Just prior to term, the lungs' volume stabilizes, and the lipid composition of aspirates changes. After about 20 weeks gestation, phosphatidylcholine in surfactant is produced and saved.

By contrasting amount of lecithin with that of sphingomyelin in the amniotic sample, a ratio of lecithin/sphingomyelin (L/S) can be calculated. A ratio of greater than 2 indicates lung maturity, while ratios less than 1 can be suggestive of pulmonary immaturity and the potential for respiratory distress syndrome (RDS). However, the RCP should be aware of the potential for deceptively high L/S ratios in infants whose mothers are diabetic, or if there is blood or meconium in the amniotic fluid.

The so-called shake-test can provide an estimate of the presence of surfactant. Mix the amniotic fluid with ethanol and shake the mixture approximately 15 seconds. Because surfactant produces stable bubbles, a closed ring of bubbles seen at the container's edge after 15 minutes indicates the presence of adequate surfactant. When no bubbles are seen after 15 minutes, an L/S ratio test should be conducted.

Surfactant production can be accelerated in premature (<34 weeks gestation) neonates by administering corticosteroids, which can also reduce the incidence and severity of RDS in some infants. Since steroids can mask the presence of infections in infants, they should be used with caution.

Fetal lung maturation can also be accelerated by the release of catecholamines during birth. The secretion of surfactant can be accelerated by: beta-adrenergic drugs, methylxanthines, a decrease in PaC02, alveolar stretch, and cAMP (Cyclic Adenosine Monophosphate). Inhibition of surfactant secretion can be caused by: decreased pulmonary blood flow, cholinergic stimulation, hypoxia, hyperoxia, and decreased pH levels.

The High-Risk Infant

Infants at high-risk are those who are expected to need special medical procedures at delivery. Both maternal and infant conditions can put a newborn at risk, and some of the factors include but are not limited to those on the following list. At the end of the outline, you will find a more in-depth discussion of some risk factors.

Maternal issues that can put an infant at risk for a problem delivery include:

• Health: Obesity or overweight condition, diabetic, emotionally stressed, viral infection early in pregnancy, exposure to radiation
• Lifestyle issues: tobacco, drug or alcohol use
• Obstetrical issues and complications:
• Previous delivery problems (still borns, preemies)
• First pregnancy late in life
• Multiple birth (twins, etc.)
• Post or prematurity
• Breech positioning
• Cesarean section
• Toxemia of pregnancy
• Abnormal or insufficient placenta
• Prolapsed cord
• Premature rupture of amniotic sac
• Meconium in amniotic fluid

At the time of delivery, the infant can present with conditions that signal high-risk condition, including:

• Less than 36 weeks of gestation
• Acute Respiratory Distress Syndrome (ARDS)
• Infection, blood diseases, or other anomalies
• The need for medications or special surgeries at delivery

It is crucial to assess fetal risk factors prior to birth. Approximately 29% of all pregnancies are deemed to be at risk for at least one of the complications listed above. In addition, approximately 5-10% of those at-risk pregnancies require the administration of CPR.

Reviewing of maternal history is an obvious way to identify potentially high-risk neonates. Complications may occur if you find evidence of a history of heart or lung disease, use of controlled substances, cigarette smoking, or infections. Low socioeconomic status or lack of education can also be indicators of potential problems because they are often related to inadequate prenatal care.

Expectant mothers >17 years of age or <38 should be seen as potentially being at risk, and the history of both current and all previous pregnancies should be reviewed for risk factors no matter the age of the soon-to-be mother. When reviewing clinical records, remember that the term gravida refers to pregnancy. Para refers to a pregnancy that terminated with the delivery of a viable neonate. Primipara refers to the mother's first delivery. Multiparous refers to a woman who has had two or more pregnancies which resulted in viable fetuses.

A mother's prior pregnancies involving problems should be considered carefully because history has a strong tendency to repeat itself in matters relating to childbirth. A history of fetal asphyxia, prematurity, RDS, maternal toxemia, ruptured membranes, infections, or bleeding during the current pregnancy are all reasons to consider the current fetus as being at risk for complications.

Multiple gestations can lead to problems, including: a breech birth, placental and cord problems, intrauterine growth retardation, and increased chance for premature death. Mortality increases with twins, particularly identical twins. Twin transfusion syndrome, where the circulations are connected, is also possible. This causes one baby to be polycythemic and the other to be anemic. The polycythernic baby manifests congestive heart failure and increased bilirubin levels. The anemic baby manifests hypotensive symptoms.

The presence of maternal diabetes mellitus (DM) is another cause for concern because problems commonly associated with DM include:

• prematurity
• congenital anomalies
• a predisposition to toxemia
• birth injury due to large baby
• still birth

Less severe DM is associated with delayed maturation of the lung, while severe DM causes chronic intrauterine stress and can accelerate lung maturation. Infants of diabetic mothers are more susceptible to infection, and more likely to be hypoglycemic, hypocalcemic, or have hyperbilirubinemia.

Toxemia involves the spread of bacterial toxins by the bloodstream and is a condition resulting from metabolic disturbances, such as those that occur during pregnancy. The resultant maternal hypertension can have serious consequences and lead to eclampsia (convulsions and/or coma). The term pre-eclampsia, which is often used interchangeably with toxemia, means a toxemia of late pregnancy which is characterized by hypertension, edema and proteinuria.

Toxemia during pregnancy causes a decrease in placental blood flow leading to uteroplacental insufficiency (UPI). UPI may occur in post-maturity infants, cyanotic maternal heart disease, or chronic hypoxia from maternal pulmonary disease.

UPI is more likely in the older primigravida, and can result in: intrauterine growth retardation, fetal death, chronic asphyxia, or the passage of meconium. When UPI is suspected, it can be assessed by measuring maternal urinary estriol levels. Urinary estriol normally increases throughout pregnancy, but measurements showing low or falling levels are indicative of UPI.

The placenta normally implants in the upper wall of the uterine cavity, but when an implantation takes place in the lower portion of the uterus, it is called placenta previa, or if the placenta separates prematurely from the uteral wall (abruptio placentae), the fetus is placed at risk. There are three types of placenta previa:

• A low implantation occupies the lower portion of the uterus, but does not cover the cervical opening.
• A partial placenta previa,covers a portion of the cervical opening, but does not cover it completely.
• In total placenta previa, the placenta is implanted low and completely covers the cervical opening.

All types of placenta previa can be readily diagnosed by ultrasound, and all cause varying degrees of obstruction to fetal passage and increase the chance of premature labor, early separation of the placenta, and hemorrhage. The most serious of these complications involves the early separation of the placenta from the uterus, referred to as abruptio placentae.

Separation of the placenta frequently causes premature labor, complete with its attendant risks, to begin. Fetal mortality approaches 50% due to the acuteness of blood loss, and maternal mortality ranges from 2 to 10% in severe cases ending in fetal death. The most common cause of abruption is maternal hypertension of any origin, including preeclampsia. Treatment of abruptio placentae includes strict management of blood volume, maintaining a hematocrit of 30-vol%. This is accomplished by IV administration of blood or crystalloid solutions.

Premature rupture of membranes (ruptures occurring 24 or more hours prior to delivery) put premature neonates at risk because of the increased potential for infection. Infants are considered postmature after the 42nd week of gestation, at which time the placenta begins to deteriorate. These babies often appear small for their gestational age and show signs of dwindling away. Postmaturity also predisposes to increased morbidity, including intrauterine asphyxia, meconium passage, difficult labor, and even premature death.

The delivery circumstances can also be predictive of potential problems. Vaginal delivery literally squeezes much of the fluid out of the neonate's lungs, easing the transition to life outside the mother's womb. On the other hand, cesarean-section deliveries don't allow for the squeezing action, increasing the chances that neonate will need special treatment to clear fluid out of the lungs and airway.

The neonate's amniotic fluid should be examined at birth for odor, color, consistency, and the presence of meconium. Normal amniotic fluid is thin, pale, and watery. Thick or foul smelling fluid may be indicative of infection. Yellow fluid can be related to infection or hypoxia. If part of the placenta is not perfused, the amniotic fluid may have a red wine color.

Meconium, a dark greenish stool, passes into the amniotic fluid in about 3-5% of preterm births, 10% in term babies, and about 40% of the time in post-term fetuses of more than 42 weeks gestation. The presence of thick particulate meconium in the amniotic fluid requires that as soon the head is delivered, the mouth, oro- and laryngopharynx be thoroughly suctioned to remove any meconium present. Upon delivery of the distressed neonate, the trachea should immediately intubated, suction applied to the end of the endotracheal tube, and the tube withdrawn.

Suction pressure should be set at 100 mm Hg, and suction applied for no more than 3-5 seconds. If meconium is suctioned out of the trachea, the neonate should be re-intubated with a new endotracheal tube and the procedure repeated until no meconium is suctioned. Blowby oxygen can then be delivered to help alleviate hypoxia with positive pressure ventilation beginning after completion of suctioning.

Each hospital needs to have a protocol covering the problem created when a severely depressed newborn has also aspirated meconium. Which risk is greater: that of blowing meconium further into the lungs with PPV before the trachea is clear, or risking asphyxia by not providing PPV until the trachea is clear? The general consensus on the issue seems to be that in severely depressed newborns, it may not be possible to clear the trachea of all meconium before initiating PPV. Be sure you know your hospital's policy on this clinical dilemma.

The average fetal heart rate (FHR) in early gestation is 140 beats per minute, dropping to an average of 120/min near term. FHR should be monitored continuously during labor, with normal ranging from 120 to 160/min. Fetal cardiac status can be measured either by simple auscultation with a stethoscope, or with relatively easy-to-use sophisticated electronics. Either way, routine monitoring of fetal heart rates has so significantly diminished adverse results of delivery that nearly every labor room now has a fetal heart monitor.

There is a normal beat-to-beat variation in the FHR, and an intact neural system responds to stimuli by increasing or decreasing FHR. For example, in a normal fetus, a loud noise causes a transient increase in FHR. If there is no FHR response to stimuli, higher brain-functions may not exist, and a total lack of variation may indicate brain stem activity only.

FHR monitoring can identify fetal distress (see Table 2) that is difficult to diagnose otherwise, and because the FHR monitor shows heart responses to asphyxia, it is an excellent way to identify infants who are being asphyxiated in utero. Since FHR also should correlate with contractions (normally, there is an increase of 15-20 beats in FHR with each contraction), FHR is usually monitored along with uterine contractions so the correlation between the two can be observed.

If fetal distress is suspected following FHR monitoring, the assessment of fetal scalp pH is used as a secondary tool to determine fetal well-being. The acid-base balance of the fetus is determined by the viability of the placenta, and its ability to exchange oxygen and carbon dioxide between maternal and fetal blood. If that exchange is disrupted, either at the placenta or in the cord, the resultant drop in pH can be measured.

There are two reasons for the drop in pH:

1. as blood gas exchange decreases, fetal PaCO2 increases, decreasing the pH;
2. facing hypoxia, the fetus begins to metabolize glycogen without oxygen, resulting in a dramatic increase in lactic acid. This metabolic acid, combined with increased PaCO2, causes the pH to drop.

The fetal scalp blood sample is obtained through the cervix between contractions. Normal fetal blood pH is considered to be above 7.25. A pH of 7.2 to 7.24 shows slight asphyxia, and a pH of less than 7.2 signifies severe asphyxia. Since maternal pH can influence fetal pH, it may also be necessary to determine the acid-base status of the mother concurrently. Fetal scalp pH is useful only in the presence of abnormal FHR tracings, since normal tracing indicates a healthy infant in most instances.

Equipment Preparation for the High-Risk Infant

In the presence of any of the high-risk situations just discussed, practitioners should anticipate respiratory problems and be prepared with whatever equipment will be necessary to:

• create a patent airway
• deliver warm and moist oxygen
• ventilate the patient
• deliver emergency medications
• maintain infant warmth
• provide for any or all of the above

Thermoregulation

The neonate is at highest risk of heat loss shortly after delivery. Thermoregulation is of utmost importance in the care of a newborn. The goal in the delivery room is to maintain an environmental temperature such that the neonate's core temperature remains in the normal range of 36.5 to 37.5°C. For this goal to be achieved, all avenues of heat loss must be minimized or eliminated. The mechanisms of heat loss in the newborn include:

• Evaporation can occur shortly after birth, when the infant is wet. As the liquid dries and evaporates it takes valuable heat with it. Immediately after delivery, every newborn should immediately be completely dried with a warmed towel or blanket. The head and face are particularly important. This drying helps reduce the evaporative heat loss. Thereafter, the neonate should be kept dry.
• Radiant loss involves the loss of heat from merely being placed near a cold surface, causing the transfer of heat from the warm baby to the nearby cooler object. After being dried, the neonate should be wrapped in a warm blanket and immediately placed beneath a radiant heater for resuscitation or examinations. Since a tremendous amount of heat loss can occur from the infant's head, a cap or other covering should be used.
• Both convective and conductive losses pose threats to the neonate's thermoregulation. Conduction takes place when the infant is placed on a cold surface, which pulls heat away from the baby. Convective heat loss is caused by air turbulence in the room that cools the infant. The neonate should be placed on a warming mattress and kept covered as much as possible to avoid convective heat loss. As quickly as possible, the neonate should be placed in a pre-warmed incubator. The longer the baby is left out in the open, the greater the chance of hypothermia.

The goal regarding neonates' thermoregulation is to achieve and maintain a neutral thermal environment (NTE), an environment that allows the infant to maintain his/her internal temperature without increasing oxygen consumption. Too much or too little heat are both adverse situations that lead to increased 02 consumption and apnea. To maintain that proper temperature:

• a thermistor is placed on the neonate's skin to monitor skin temperature
• the thermistor is connected to a servo control on the heat source
• the servo control then adjusts the heat to maintain the NTE. used as a general guideline:

WEIGHT
(grams)

Having reviewed development of fetal anatomy and physiology, risk factors, monitoring, anticipation, and preparation for problems, it is time to discuss the actual delivery and the first few minutes of extrauterine life.

The labor and delivery processes go through three distinct stages, including:

• Stage 1: The mother's contractions begin to dilate cervix and continue until dilation measures approximately 10 cm.
• Stage 2: The fetus is forced through the mother's cervical canal as a result of the contractions and abdominal wall pushing forces. The newborn's head normally presents first, and then the fetus rotates about 90 so the shoulders can present, permitting it to pass through the canal. As the infant's delivery is completed, the umbilical cord is clamped.
• Stage 3: When the placenta is expelled, the delivery is complete.

The Infant

At birth, expansion of the lungs causes PVR to fall dramatically. Ventilation helps to overcome fetal pulmonary vasoconstriction through several mechanisms. The first is a rise in Pa02 associated with filling the alveoli with air. This has a direct vasodilator effect on the capillaries. As more blood passes through the lungs and is exposed to air, vasoconstricting prostaglandins are inactivated. In the fetus, these prostaglandins are necessary to help maintain a high PVR and keep blood flowing through the ductus arteriosus.

A rising Pa02 also increases circulating bradykinin levels. This helps constrict the ductus and force more blood through the pulmonary circulation. Mechanical expansion of the lungs stretches and straightens the capillaries which, in turn, decrease the resistance to flow. In utero, the capillaries are very kinked and the path is tortuous. This keeps the PVR high. Stretching the alveoli and surrounding tissue corrects this.

As the lungs expand with air, P02 rises, the pathway is straightened, and prostaglandins are metabolized. More blood is now able to flow through the pulmonary capillaries and less through the ductus. Catecholamine release, triggered by the delivery process and the cutting of the umbilical cord, causes active constriction of the ductus to begin. Flow through the ductus is furthered impeded by rising aortic pressure.

Following delivery, neonatal pulmonary artery pressure declines incrementally from an average mean pressure of 39mm Hg at ten hours, to about 29 mm Hg at 15 hours. During the same time frame, neonatal aortic pressure rises to between 80-100 mm Hg at 20 hours post delivery.

The normal newborn shunt (20-25%) is considerably different from that of normal adults (5-10%), possibly due to continued leakage through the neonate's ductus and foramen ovale.

Neonate's average blood pressure varies according to gestational age and weight. The average neonatal systemic blood pressure at one hour is:

Average blood pressure at 12 hours is:

Infant Scoring Systems

As soon as the delivery is complete, there are numerous assessments to be made in order to determine the infant's health status. These include checking the respiratory and cardiac status, and weight. The Apgar scoring system (see Figure 1), named after Dr. Virginia Apgar, was developed as an objective way to evaluate the general status of the newborn at one minute and five minutes after birth. APGAR is also an acronym for what the practitioner will assess: The practitioner evaluates newborn Appearance, Pulse, Grimace, Activity, Respiratory rate and effort.

The five areas examined are respiratory effort, heart rate, muscle tone, reflex irritability, and color (see Figure 1). Each area is given a score of 0, 1, or 2 depending on the response noted. A score of "0" indicates maximum distress/dysfunction for that parameter. A score of "2" means the opposite. The first score is assessed at 1 minute after delivery, with a second evaluation performed at 5 minutes. Since the Apgar is an objective assessment of the infant's status, a 5-minute score that is higher than the 1-minute score indicates the effectiveness of the resuscitation.

After assigning numerical scores for the categories, scores are totaled, with normal infants scoring 7 to 10, moderately depressed infants scoring 4 to 6, and severely depressed infants scoring less than 4. Realistically, in the clinical setting the latter infants are not scored immediately because they are obviously in severe distress, and resuscitation measures are instituted before there is time to total scores.

The Apgar evaluations can be done every 5 minutes as needed, up to 20 minutes or when the resuscitation ends. The 5-minute Apgar score is predictive of future impairment, with a low score being associated with a likelihood of long-term damage. For example, an Apgar score of two or less at one minute is associated with a high mortality rate. An Apgar score of 8-10 is considered normal.

Figure 1. The Apgar scoring system.

As you can see, the Apgar is an excellent method for assessing the effectiveness of resuscitation; however it should not be used as the sole basis for making resuscitative decisions. One limitation of the Apgar system is that it was designed to assess normal full term infants, not preemies, so it is less valuable in their assessment. For evaluating premature neonates, umbilical cord pH or the Silverman-Anderson scoring system may be more valuable than Apgar.

In order to assess the degree of respiratory distress in neonates, practitioners often use the Silverman-Anderson scoring system. Like the Apgar system it evaluates five parameters and assigns a numerical score for each parameter. However, unlike the Apgar score, the lower the total score the better the baby's condition in the Silverman-Anderson system. The best score possible in each category is a "0" the worst is a "2". Parameters assessed are: retractions of the upper chest, lower chest, and xiphoid, nasal flaring, and expiratory grunt.

Table 3. Silverman-Anderson Scoring System

As you can see from Table 3, neonates with no retractions, flaring or grunting with synchronized respiratory movements are scored with "0s". Infants with visible retractions of the lower chest and xiphoid, with the upper chest lagging compared to the lower on inspiration, receive a "1". Minimal nasal flaring and an expiratory grunt heard only with a stethoscope also receive a "1". Marked retractions with a "see-saw" movement of the upper and lower chests scores a "2". Marked nasal flaring and audible expiratory grunting also receive a "2". Normal babies have a cumulative score close to "0". Severely depressed babies score close to "10".

RCPs need to be alert to the clinical signs of cardiac and pulmonary diseases in infants, including:

• Tachypnea (respiratory rate above 60)
• Wheezing (can indicate edema in small airways)
• Retractions (can indicate increased work of breathing)
• Rales (indicate fluid in small airways)
• Grunting (can increase the functional residual capacity)
• Nasal flaring (sign of respiratory distress)

Meconium Aspiration

Meconium is present in the amniotic fluid of nearly 10% of all infants at birth, and of those, between 20-25% go on to suffer some form of significant pulmonary disorder. Pneumothorax is frequently a complication of meconium aspiration.  Clinical indications include: tachypnea, rasping or faint respirations, patchy infiltrates on x-rays, hyperinflation, and severe cyanosis.

Aggressive suctioning is called for to eliminate airway obstructions, and placement of a nasogastric tube is needed to evacuate swallowed meconium and stomach contents. Treatment for metabolic acidosis is required, and supplemental oxygen with mechanical ventilation may be needed in order to maintain the infant's ABGs. Oxygen consumption and carbon dioxide production can be kept to a minimum through thermoregulation.

Pneumothorax

Tension pneumothorax can present as a complication of meconium aspiration, ventilation with positive pressure, pneumonia, hyaline membrane disease, and diaphragmatic hernia. Any newborn in respiratory distress should be reviewed for the presence of pneumothorax. Since pneumothorax can be seen in nearly 1% of all normal deliveries, even asymptomatic infants require observation of vital signs.

Clinical signs include onset of respiratory agitation or distress, tachypnea, nasal flaring and grunting, cyanosis, an