CHAPTER 17 1 Identify the risk factors and maternal and fetal history for complications related to gestational age and birthweight issues in the neonate such as prematurity, postmaturity, and small for gestational age (SGA) and large for gestational age (LGA) infants. 2 Describe physical characteristics of preterm, late preterm, postterm, SGA, and LGA infants. 3 Recognize potential problems related to preterm, late preterm, postterm, SGA, and LGA infants. 4 Describe the immediate assessment parameters and management of the premature infant. 5 Identify risk factors and the maternal and fetal history that are predictive of respiratory distress syndrome (RDS). 6 Describe the specific pathophysiology, assessment parameters, and mangement of RDS. 7 Identify risk factors and the maternal and fetal history that are predictive of transient tachypnea of the newborn (TTN). 8 Describe the specific pathophysiology, assessment parameters, and mangement of TTN. 9 Identify risk factors and the maternal and fetal history that are predictive of meconium aspiration syndrome (MAS). 10 Describe the specific pathophysiology, assessment parameters, and mangement of MAS. 11 Identify risk factors and the maternal and fetal history that are predictive of persistent pulmonary hypertension of the newborn (PPHN). 12 Describe the specific pathophysiology, assessment parameters, and mangement of PPHN. 13 Describe the maternal and neonatal factors that contribute to jaundice in the neonate, and distinguish among the various causal factors and related outcomes of jaundice in the neonate. 14 Describe the physiologic process of the production, conjugation, and elimination of bilirubin in the neonate; the differences between conjugated and unconjugated bilirubin; and assessment parameters and mangement of hyperbilirubinemia. 15 Describe the maternal and neonatal factors that contribute to congenital anomalies in the neonate, and distinguish the differences among the various causal factors and related outcomes. 16 Describe the specific pathophysiology, assessment parameters, and mangement of common congenital anomalies in the neonatal period. Most newborns will transition to extrauterine life without a problem. However, even when transition is uneventful, the first 48 hours of life is when vigilant observation and anticipatory caregiving are essential. Most infants with serious illness present at birth or within the first 48 hours during the transition to extrauterine life. The challenge for the caregiver is to be able to discriminate the subtle signs of disease from the dynamically changing characteristics of normal transition and adaptation to the environment. Without excellent nursing care and good family education, early discharge might lead to some of these infants not being identified and thus being susceptible to poorer outcomes. Some of the most common disease processes that can appear in the newborn period include gestational age and birthweight-related issues, hypothermia, hypoglycemia, RDS, TTN, MAS, PPHN, sepsis, congenital anomalies, hyperbilirubinemia, and drug exposure of the infant. Newborn sepsis is discussed in Chapter 20, and the drug-exposed infant is covered in Chapter 25. For ease of discussion, gestational age and birthweight-related issues are addressed first followed by prematurity, respiratory and cardiac conditions, hyperbilirubinemia, and the most common congenital anomalies. However, it is important to note that these processes can occur concurrently, and in reality often infants diagnosed with any one of the previously noted newborn disease processes are more susceptible to the others. A An infant is defined as SGA when the weight is below the 10th percentile (Anderson & Hay, 2005; Townsend, 2005). B The SGA infant may also be known as having intrauterine growth restriction (IUGR). C Not all IUGR infants are SGA; IUGR from placental insufficiency usually reduces birthweight more than length and to a greater degree than head circumference; the greater the severity of IUGR, the greater is the deviation of weight, length, and (less so) head circumference as compared with population norms (Anderson & Hay, 2005; Rosenberg, 2008). D The SGA infant can be preterm, term, or postterm. E Conditions (alone or in combination) associated with SGA babies are as follows (Hendrix & Berghella, 2008): a. Chronic hypertension (associated with a four- to eightfold increase in the incidence of abruptio placentae) d. Drug exposure (diethylstilbestrol, antineoplastics, narcotics, and illicit drugs) e. Smoking (frequently associated with abruptio placentae, placenta previa, prematurity, and respiratory distress) and alcohol consumption f. Young adolescent (10 to 14 years of age) or advanced maternal age (older than 35 years) b. Heart disease and hemolytic disease c. Intrauterine infection: toxoplasmosis, rubella, cytomegalovirus, and herpes simplex (TORCH) 3. Factors affecting the intrauterine environment F Conditions altering fetal growth produce insults that affect all organ systems and are known to produce two patterns of growth that depend on the timing of the insult to the developing embryo or fetus (Rosenberg, 2008). 1. Conditions affecting early gestation (generally less than 28 weeks) occur at a time when rapid cell proliferation (hyperplasia) occurs. a. An insult at this stage results in organs with cells of normal size but fewer numbers of cells than if the insult had not occurred. b. Infants are symmetrically grown (weight, length, and head circumference plot similarly on a growth curve) and all organ systems are small. c. Generally these infants have the poorest long-term prognosis and commonly have chromosomal abnormalities; postnatal nutrition is unable to correct for growth deficits; symmetrically grown SGA babies may never catch up in size when compared with unaffected children. 2. Later in gestation (greater than 28 weeks), growth occurs as a combination of rapid cell proliferation (hyperplasia) but also as a result of increases in cell size (hypertrophy). a. An insult at this stage typically results in intrauterine malnutrition; organ systems have normal numbers of cells that are smaller. b. The brain and heart are larger in proportion to body size as a whole, whereas the liver, spleen, adrenals, thymus, and placenta are small. c. This type of infant is asymmetrically grown in that head size and length are spared, but overall weight and organ sizes are diminished. d. Generally, the asymmetrically IUGR infant has a better prognosis than one who is symmetrically IUGR; in utero malnutrition, however, is associated with increased risk of intrauterine death (Rosenberg, 2008; Townsend, 2005). e. Optimal postnatal nutrition generally restores normal growth potential because the number of body cells is normal. G The SGA infant may present with problems from the moment of birth (Rosenberg, 2008; Townsend, 2005). 1. Fewer reserves are available to help the fetus tolerate the rigors of labor and delivery, leading to the development of fetal asphyxia or meconium passage in utero and the need for resuscitation at delivery. a. Uteroplacental circulation is often impaired. A small placenta may have diminished capability for gas exchange, nutrient delivery, and removal of waste products from the fetal circulation. b. Cardiac glycogen stores may already be reduced, leading to the development of fetal bradycardia. c. Uterine contractions may add an additional hypoxic stress on the chronically hypoxic fetus with a marginally functioning placenta. 2. The combination of intrapartum and neonatal asphyxia places the infant at increased risk for a continuum of central nervous system insults that are the sequelae of perinatal asphyxia. 3. Decreased glycogen stores increase the potential for early development of hypoglycemia and temperature instability in the transition period (see later discussion of preterminfants). 4. Polycythemia frequently occurs as a result of chronic subacute hypoxia and dehydration. H Congenital anomalies are more frequently associated with intrauterine insult early in gestation during organogenesis; mortality rates for term SGA infants are five times that of term, appropriately grown infants resulting from the occurrence of major congenital anomalies (Mandruzzato et al, 2008). I The SGA infant is more frequently exposed to intrauterine infections such as rubella, cytomegalovirus (CMV), and toxoplasmosis; risk for impaired fetal gas exchange related to inadequate umbilical cord perfusion, hypoxia, and hypercarbia (Rosenberg, 2008). J Immune function in the SGA infant may be depressed as in older children with postnatal onset of malnutrition (Anderson & Hay, 2005; Mandruzzato et al, 2008). K The prognosis for SGA infants must consider adverse perinatal consequences in addition to being SGA; when perinatal problems are minimal or avoided because of early optimal obstetric intervention, the SGA neonate may still demonstrate developmental handicaps, especially in head growth restriction (Rosenberg, 2008). L Socioeconomic status and environment are the major determinant of developmental outcome at 2 years of age and older; SGA infants born to families of higher socioeconomic status demonstrate fewer developmental differences on follow-up, whereas those born to poorer families have significant developmental handicaps (Mandruzzato et al, 2008). 1. History (Rosenberg, 2008; Townsend, 2005) (2) Age and socioeconomic status (3) Maternal illnesses or conditions (4) Substance use or abuse such as alcohol, illicit drugs, or tobacco 2. Physical findings (Rosenberg, 2008; Townsend, 2005) a. Soft-tissue wasting and dysmaturity (1) Decreased amount of breast tissue (2) Diminished subcutaneous fat tissue (3) Loose, dry, and cracked skin, with decreased turgor (4) Diminished muscle mass especially noticeable in the buttocks and extremities (5) Scaphoid abdomen resulting from shrinkage of the abdominal contents b. Smaller-than-average weight, length, and head circumference 3. Presenting behavioral findings seen at or soon after delivery depend on the occurrence of asphyxia (postasphyxial encephalopathy) (Rosenberg, 2008; Towsend, 2005). a. Mild degree (duration less than 24 hours) exhibited by hyperalertness and sympathetic overactivity b. Moderate degree exhibited by lethargy, stupor, hypotonia, suppressed primitive reflexes, and seizures c. Severe degree manifested by coma, flaccid tone, suppressed brainstem function, seizures, and increased intracranial pressure 4. Placental examination (Hendrix & Berghella, 2008) 5. Diagnostic procedures (Townsend, 2005) a. Weight, length, and head circumference b. Gestational age assessment and plotting of growth parameters on curve c. Serial bedside glucose assessment d. Assessment for infection (see Chapter 20 for a complete discussion of sepsis) B Interventions/Outcomes (Rosenberg, 2008; Townsend, 2005) 1. Interventions are described for the most common problems: birth asphyxia; respiratory distress; temperature instability; blood glucose instability; nutritional support; polycythemia; infection related to possible exposure to intrauterine infection (see Chapter 20 for complete discussion of newborn sepsis). a. Anticipate the need for and provide neonatal resuscitation according to Neonatal Resuscitation Program (NRP) guidelines as indicated by condition at the time of delivery. b. Monitor and record trends in transition vital signs, blood pressure, and clinical parameters; anticipate clinical manifestations such as tachypnea, respiratory distress, acidosis, cardiovascular instability, cyanosis, and hypoxemia. c. Provide oxygen as indicated based on pulse oximeter saturation monitoring, blood gas values, and close observation. d. Provide stabilization care in a neutral thermal environment (NTE), and allow the infant to stabilize and self-correct mild acidosis, clear lung fluid, stabilize blood glucose, and stabilize blood pressure. e. Monitor infant’s body temperature: axillary should be in the range of 36.4˚ to 37˚C (97.6˚ to 98.6˚ F). f. Examine the environment for potential sources of heat loss to prevent cold stress; for example, prewarm equipment, and avoid exposure to drafts. g. Monitor incubator or warmer bed temperature and heater output; the nurse should be concerned if heater output is constant. h. Monitor blood glucose levels if temperature instability occurs (to determine if hypoglycemia is causing temperature instability); anticipate blood glucose instability and hypothermia if the infant is fasting or as the infant transitions to bolus feedings; administer intravenous glucose (see discussion of hypoglycemia under care of preterm infant). i. Initiate early and frequent oral feedings (every 2 to 3 hours) if not contraindicated by respiratory status; provide a high-calorie formula (>20 calories/ounce [30 mL]) as ordered to provide additional nutrients. j. Obtain serum hemoglobin (normal 15 to 21.5 g/dL) and hematocrit (normal 45% to 65%) levels. k. Observe for signs and symptoms of polycythemia. l. Consider partial exchange transfusion for polycythemia when an infant is symptomatic to relieve capillary congestion and hyperviscosity. a. Infant’s 5-minute Apgar score is 7 to 10. b. Vital signs, blood pressure, blood glucose, and clinical parameters are stable. c. Oxygen saturation is maintained within normal limits. d. Normal body temperature is maintained. e. Neutral thermal environment is maintained. f. Infant shows no signs of cold stress, for example, increased oxygen consumption, hypoglycemia, and/or respiratory distress. g. Blood glucose levels are maintained at greater than 40 mg/dL. h. Oral feedings are tolerated well. i. Intravenous (IV) dextrose infusion, if indicated, maintains blood sugar within normal limits. j. Infant’s initial weight loss stabilizes within 3 to 5 days of life, and weight increases thereafter at an average of at least 15 to 30 g (0.5 to 1 ounce) per day. k. Serum hematocrit is less than 65%. l. Signs and symptoms of hypoglycemia and polycythemia are absent. m. Neonate’s intake is sufficient to achieve a urine output greater than 1.5 mL/kg/hr. A The LGA infant is one whose weight is above the 90th percentile for gestational age (Townsend, 2005). B LGA babies may be preterm, term, or postterm. C Birthweight more than 4000 grams (8 pounds, 14.5 ounces) often reflects a genetic predisposition, except for the infant of a diabetic mother (IDM). 1. Large parents tend to have large babies. 2. Some Native Americans are more likely to have LGA infants. D Large size of the fetus may predispose the mother to an operative delivery. E If an LGA infant is born vaginally, the incidence of operative vaginal delivery (forceps or vacuum-assisted delivery) is higher than in the non-LGA infant; birth trauma is higher when compared with non-LGA babies and may include: F The LGA fetus may show evidence of nonreassuring fetal heart rate patterns during a prolonged and difficult second stage of labor; neonatal respiratory depression may occur at the time of the delivery. 1. Shoulder or body dystocia may occur. 2. Particulate meconium-stained amniotic fluid may occur with risk of aspiration. G LGA infants are at risk for hypoglycemia related to early depletion of glycogen stores (see Chapter 22 for a complete discussion regarding the IDM). (1) Previous delivery of an LGA neonate (2) Large weight gain during pregnancy (3) Diabetes (classes A through C) during the pregnancy (4) Prolonged or difficult labor and birth, particularly a long second stage 2. Physical findings (Townsend, 2005) a. Weight greater than 90th percentile for gestational age b. Presence of caput succedaneum on the head (1) Localized soft tissue swelling over the presenting scalp area (2) Is present at birth and does not increase in size c. Presence of a cephalohematoma (1) Increased incidence with vacuum extraction (2) Soft, fluctuant swelling in which the margins are limited to a cranial bone; does not cross suture lines (3) Increases in size for 2 to 3 days after birth (4) Disappears 6 to 8 weeks after birth (5) May be associated with complications d. Evidence of facial nerve damage, resulting from intrapartum pressure on facial nerves related to abnormal fetal position or forceps trauma (1) The eye on the affected side does not completely close as it normally does while the infant is crying. (2) The forehead does not wrinkle. (3) The side of the face is smooth.
The Infant at Risk
INTRODUCTION
SMALL FOR GESTATIONAL AGE INFANTS
CLINICAL PRACTICE
HEALTH EDUCATION
LARGE FOR GESTATIONAL AGE INFANTS
CLINICAL PRACTICE
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