CHP 24 MATERNITY

ADMINSTER O2

Administer oxygen therapy as ordered via nasal cannula or with positive-pressure ventilation. Monitor oxygen saturation levels via pulse oximetry to evaluate the newborn's response to treatment and to detect changes. Increased pulmonary pressures associated with meconium aspiration may cause blood to be shunted away from the lungs. The newborn may exhibit uneven pulmonary ventilation, with hyperinflation in some areas and atelectasis in others. This leads to poor perfusion and subsequent hypoxemia, which in turn may increase pulmonary vasoconstriction, resulting in a worsening of hypoxemia and acido -Expect to administer hyperoxygenation to dilate the pulmonary vasculature and close the ductus arteriosus or nitric oxide inhalation to decrease pulmonary vascular resistance, or to use high-frequency oscillatory ventilation to increase the chance of air trapping (Fanaroff & Fanaroff, 2020). In addition, administer vasopressors and pulmonary vasodilators as prescribed and administer surfactant as ordered to counteract inactivation by meconium. Monitor ABG results for changes and assist with measures to correct acid-base imbalances to facilitate perfusion of tissues and prevent pulmonary hypertension

INTERVENTIONS

Continuously monitor the infant's cardiopulmonary status via invasive or noninvasive means (e.g., arterial lines or auscultation, respectively). Monitor oxygen saturation levels continuously; assess pulse oximeter values to determine oxygen saturation levels. Closely monitor vital signs, acid-base status, and arterial blood gases. Administer broad-spectrum antibiotics if blood cultures are positive. Administer sodium bicarbonate or acetate as ordered to correct metabolic acidosis. Provide fluids and vasopressor agents as needed to prevent or treat hypotension. Test blood glucose levels and administer dextrose as ordered for prevention or treatment of hypoglycemia. Cluster caretaking activities to avoid overtaxing and compromising the newborn. Place the newborn in the prone position to optimize respiratory status and reduce stress. Perform gentle suctioning to remove secretions and maintain a patent airway. Assess level of consciousness to identify intraventricular hemorrhage. Monitor x-ray studies to detect atelectasis or air leak. Maintain a neutral thermal environment to reduce metabolic and oxygen needs. Provide sufficient calories via gavage and IV feedings. Maintain adequate hydration and assess for signs of fluid overload. Provide information to the parents about treatment modalities; give thorough but simple explanations about the rationales for interventions. Encourage the parents to participate in care (

Respiratory distress syndrome (RDS)

Cortisol-induced stimulation of lecithin/sphingomyelin (phospholipids) necessary for lung maturation is antagonized due to the high insulin environment within the fetus due to mother's hyperglycemia Less mature lung development than expected for gestational age. Decrease in the phospholipid phosphatidylglycerol (PG), which stabilizes surfactant, compounding risk -Most commonly, breathing normally at birth but developing labored, grunting respiration with cough and a hoarse complaining cry within a few hours with chest retractions and varying degrees of cyanosis • IDMs with vascular disease seldom develop RDS because the chronic stress of poor intrauterine perfusion leads to increased production of steroids, which accelerates lung maturation.

nas syndrome

Neonatal abstinence syndrome (NAS) compromises a constellation of drug-withdrawal symptoms that result from chronic intrauterine exposure to a variety of substances, including opioids, barbiturates, SSRIs, alcohol, benzodiazepines, caffeine, and nicotine. Newborns of women who abuse tobacco, illicit substances, caffeine, and alcohol can exhibit withdrawal behavior. Withdrawal symptoms start within 72 hours after birth and may last from 1 week to as long as 6 month CNS hypersensitivity, autonomic dysfunction, respiratory distress, temperature instability, hypoglycemia, tremors, seizures, hyperactive reflexes, abnormal excessive cry patterns, tight muscle tone, feeding difficulties, yawning, stuffy nose, and sneezing, and gastrointestinal disturbances (King et al., 2019). NAS has both medical and developmental consequences for the newborn. - Frequently, the first inkling of drug use appears in the newborn when symptoms of withdrawal begin within 48 to 72 hours after birth

preventing hypoglycemia

Prevent hypoglycemia by providing early oral feedings (within 1 hour after birth) with breast milk or formula at frequent intervals (every 2 to 3 hours). Feedings help to control glucose levels, reduce hematocrit, and promote bilirubin excretion. Maintain a neutral thermal environment to avoid cold stress, which may stimulate the metabolic rate, thereby increasing the demand for glucose. Provide rest periods to decrease energy demand and expenditure. Monitor blood glucose levels via heel stick every hour for the first 4 hours of life and then every 3 to 4 hours until stable. Document the results. Report unstable glucose values if oral feedings do not maintain and stabilize the newborn's blood glucose levels. If glucose levels are not stabilized, initiate IV glucose infusions as ordered and monitor that the infusions are flowing at the prescribed rate. MAINTAINING FLUID AND ELECTROLYTE BALANCE Monitor serum calcium levels for changes indicating the need for supplementation, such as with oral or IV calcium gluconate. Assess the newborn for signs of hypocalcemia, such as tremors, jitteriness, twitching, seizures, and high-pitched cry. Also administer fluid therapy as ordered to maintain adequate hydration. Monitor serum bilirubin levels and institute phototherapy if the newborn is over 24 hours old.

Brachial plexus injury

Primarily in large babies, babies with shoulder dystocia, or breech delivery Results from stretching, hemorrhage within a nerve, or tearing of the nerve or the roots associated with cervical cord injury Associated traumatic injuries include fracture of the clavicle or humerus or subluxations of the shoulder or cervical spine Erb palsy is an upper brachial plexus injury. Klumpke palsy is an injury to the lower brachial plexus (lower brachial injuries are less common) In Erb palsy, the involved extremity usually presents adducted, prone, and internally rotated; shoulder movement is absent; Moro, bicep, and radial reflexes are absent, but the grasp reflex is usually present. Klumpke palsy is manifested by weakness in the hand and wrist; grasp reflex is absent. Erb palsy usually involves immobilization of the upper arm across the upper abdomen/chest to protect the shoulder from excessive motion for the first week; then gentle passive range-of-motion exercises are performed daily to prevent contractures. There is usually no associated sensory loss, and this condition usually improves rapidly. Treatment for Klumpke palsy involves placing the hand in a neutral position and using passive range-of-motion exercises. In some cases deficits may persist, requiring continuing observation.

teachings

• Position your newborn with the head elevated to prevent choking. • To aid your newborn's sucking and swallowing during feeding, position the chin downward and support it with your hand. • Place your newborn on his or her back to sleep or nap, never on the stomach. • Keep a bulb syringe close by to suction your newborn's mouth in case of choking. • Cluster newborn care (bathing, feeding, dressing) to prevent overstimulation. • If your newborn is fussy or crying, try these measures to help calm him or her: • Wrap your newborn snugly in a blanket and gently rock in rocking chair. • Take the baby for a ride in the car (using a newborn car seat). • Play soothing music and "dance" with the newborn. • Use a wind-up swing with music. To help your newborn get to sleep, try these measures: Schedule a bath with a gentle massage prior to bedtime. • Change diaper and clothes to make the baby comfortable. • Feed the baby just prior to bedtime. • If the newborn cries when put in crib and all needs are met, allow him or her to cry. • Use a rocking chair to feed and sing a soft lullaby. • Call your primary care provider if you observe withdrawal behaviors such as: • Slight tremors (shaking) of hands and legs • Stiff posture when held in your arms • Irritability and frequent fussiness • High-pitched cry, excessive sucking motions • Erratic sleep pattern • Frequent yawning, nasal stuffiness, sweating • Prolonged time needed to feed • Frequent vomiting after feeding

NURSING ASSESSMENT

Abdominal distention develops as air builds up in the stomach. In esophageal atresia, a gastric tube cannot be inserted beyond a certain point because the esophagus ends in a blind pouch. The newborn may have rattling respirations, excessive salivation, and drooling, and "the three Cs" (coughing, choking, and cyanosis) if feeding is attempted. The presence of a fistula increases the risk of respiratory complications such as pneumonitis and atelectasis due to aspiration of food and secretions -Prepare the newborn and parents for radiographic evaluation. Diagnosis is made by x-ray or an ultrasound or MRI, which will demonstrate a gastric tube coiled in the upper esophageal pouch, and air in the gastrointestinal tract indicates the presence of a fistula (Kenner et al., 2020). Once a diagnosis of esophageal atresia is established, begin preparations for surgery if the newborn is stable.

S/S

Also observe the newborn for common signs and symptoms, which may include: Cardiorespiratory baseline changes Feeding intolerance Abdominal distention and tenderness Bloody or hemoccult-positive stools Diarrhea and vomiting Delayed gastric emptying Respiratory distress Metabolic acidosis Temperature instability Decreased or absent bowel sounds Signs of sepsis Occult/gross blood in stool Lethargy Apnea Shock

NURSING ASSESSMENT

Predisposing factors for MAS include post-term pregnancy; breech presentation, forceps, or vacuum extraction births; nulliparity; ethnicity (Pacific Islander, Indigenous Australian, African American); intrapartum fever; low Apgar score; prolonged or difficult labor associated with fetal distress in a term or post-term newborn; maternal drug abuse, especially of tobacco and cocaine; maternal infection/chorioamnionitis; maternal hypertension or diabetes; oligohydramnios; fetal growth restriction; prolapsed cord; or acute or chronic placental insufficiency -Observe the newborn for a barrel-shaped chest with an increased anterior-posterior (AP) chest diameter (similar to that found in a client with chronic obstructive pulmonary disease), prolonged tachypnea, progression from mild to severe respiratory distress, intercostal retractions, end-expiratory grunting, and cyanosis (Ahlfeld, 2020). Auscultate the lungs, noting coarse crackles and rhonchi.

Hypocalcemia and hypomagnesemia

Hypocalcemia (drop in calcium levels) is manifested by tremors, hypotonia, apnea, high-pitched cry, and seizures due to abrupt cessation of maternal transfer of calcium to the fetus, primarily in the third trimester and experiencing birth asphyxia. Associated hypomagnesemia is directly related to the maternal level before birth. About half of IDMs affected. - Newborn is at risk for a prolonged delay in parathyroid hormone production and cardiac dysrhythmias.

COMPLETE BLOOD COUNT

-Evaluate the complete blood count with a differential to identify anemia, leukocytosis, or leukopenia. Elevated C-reactive protein levels may indicate inflammation. As ordered, obtain x-rays of the chest and abdomen, which may reveal infectious processes located there. Blood, cerebrospinal fluid, and urine cultures are indicated to identify the location and type of infection present. Positive cultures confirm that the newborn has an infection. Initially, treatment is with ampicillin plus either gentamicin or cefotaxime, then narrowed down to organism-specific drugs as soon as the cultures identify the specific organism. This practice of empirically treating at-risk neonates leads to potentially harmful exposure for many uninfected infants, but in the absence of accurate rapid diagnostic tests, it is prudent to be safe MANGEMNT Formulate a sepsis prevention plan that includes education of all members of the health care team on identification and treatment of sepsis. Maintain medical and surgical asepsis for all providing care. Screen all newborns daily for signs of sepsis. Monitor sepsis cases and outcomes to reinforce continued quality-improvement measures or to modify current practices. Outline and carry out measures to prevent hospital-acquired infections, such as: Thorough handwashing hygiene for all staff Monitor and support nutritional status Frequent oral care and inspections of mucous membranes Proper positioning and turning to prevent skin breakdown Use of strict aseptic technique for all wound care Frequent monitoring of invasive catheter sites for signs of infection Identify newborns at risk for sepsis by reviewing risk factors. Monitor vital sign changes and observe for subtle signs of infection. Monitor for signs of organ system dysfunction: Cardiovascular compromise—tachycardia and hypotension Respira

PATHIO

Elevated pulmonary vascular pressures normally occur during fetal life and decrease partially in response to an increase in oxygen tension at birth when the newborn takes the first breath. However, interference with this ability to breathe allows pulmonary pressures to remain increased. Hypoxemia and acidosis also occur, leading to vasoconstriction of the pulmonary artery. These events cause an elevation in pulmonary vascular resistance. Normally, the decrease in pulmonary artery pressure and pulmonary vascular resistance with breathing leads to the closure of the ductus arteriosus and foramen ovale. However, with PPHN pulmonary vascular resistance is elevated to the point that venous blood is diverted to some degree through fetal shunts (i.e., the ductus arteriosus and foramen ovale) into the systemic circulation, bypasses the lungs, and results in systemic arterial hypoxemia.

pathiologic jaundice

Although neonatal jaundice is quite common, severe hyperbilirubinemia (>20 mg/dL) that could potentially lead to kernicterus and neurodevelopmental complications is much rarer. Pathologic jaundice is manifested within the first 24 hours of life when total bilirubin levels increase by more than 5 mg/dL/day and the total serum bilirubin level is higher than 20 mg/dL in a full-term infant. This condition requires intervention to prevent acute bilirubin encephalopathy or kernicterus (Ansong-Assoku & Ankola, 2019). Conditions that alter the production, transport, uptake, metabolism, excretion, or reabsorption of bilirubin can cause pathologic jaundice in the newborn. A few conditions that contribute to red blood cell breakdown and thus higher bilirubin levels include polycythemia, blood incompatibilities, and systemic acidosis. These altered conditions can lead to high levels of unconjugated bilirubin,possibly reaching toxic levels and resulting in a severe condition called kernicterus or bilirubin encephalopathy. It can be acute or chronic. Hyperbilirubinemia is a great concern because of the potential for brain injury. The spectrum of bilirubin-induced neurologic dysfunction ranges from acute bilirubin encephalopathy to the devastating and irreversible chronic bilirubin encephalopathy or kernicterus. Acute bilirubin encephalopathy describes the effects of hyperbilirubinemia in the first weeks of life. It is a devastating condition that can lead to death or life long neurodevelopmental handicaps. It is particularly tragic because it is completely preventable. Clinical signs include lethargy, poor feeding, high-pitched cry, poor tone, a poor Moro reflex with incomplete flexion of the extremities, and a high-pitched cry. As symptoms of acute bilirubin encephalopathy worsen, the newborn progresses to apnea, seizures, coma, a

Pathophysiology

Asphyxia occurs when oxygen delivery is insufficient to meet metabolic demands, resulting in hypoxia, hypercarbia, and metabolic acidosis. Any condition that reduces oxygen delivery to the fetus can result in asphyxia. These conditions may include maternal hypoxia, such as from cardiac or respiratory disease, anemia, or postural hypotension; maternal vascular disease that leads to placental insufficiency, such as diabetes or hypertension; cord problems such as compression or prolapse; and post-term pregnancies, which may trigger meconium release into the amniotic fluid. Initially, the newborn uses compensatory mechanisms including tachycardia and vasoconstriction to help bring oxygen to the vital organs for a time. However, without intervention, these mechanisms fail, leading to hypotension, bradycardia, and eventually cardiopulmonary arrest. With failure to breathe well after birth, the newborn will develop hypoxia (too little oxygen in the cells of the body). As a result, the heart rate falls, cyanosis develops, and the newborn becomes hypotonic and unresponsive. Newborn resuscitation is needed to help initiate breathing in newborns that fail to breathe spontaneously at birth.

ASSESSMENT N MANGMENT

Assess the newborn's status closely. A newborn with persistent pulmonary hypertension demonstrates tachypnea within 12 hours after birth. Observe for marked cyanosis, grunting, respiratory distress with tachypnea, and retractions. Auscultate the heart, noting a systolic ejection harsh sound (tricuspid insufficiency murmur), and measure blood pressure for hypotension resulting from both heart failure and persistent hypoxemia (Kenner et al., 2020). Measure oxygen saturation via pulse oximetry and report low values. Prepare the newborn for an echocardiogram, which will reveal right-to-left shunting of blood that confirms the diagnosis. MANGEMENT Nursing management focuses on ensuring adequate tissue profusion and minimizing oxygen demand and energy expenditure. When caring for the newborn with persistent pulmonary hypertension, pay meticulous attention to detail, with continuous monitoring of the newborn's oxygenation and perfusion status and blood pressure. The goals of therapy include improving alveolar oxygenation, inducing metabolic alkalosis by administering sodium bicarbonate, correcting hypovolemia and hypotension with the administration of volume replacement and vasopressors, and anticipating use of ECMO when support has failed to maintain acceptable oxygenation (Stark & Eichenwald, 2019). Provide immediate resuscitation after birth and administer oxygen therapy as ordered. Early and effective resuscitation and correction of acidosis and hypoxia are helpful in preventing persistent pulmonary hypertension. Monitor arterial blood gases frequently to evaluate the effectiveness of oxygen therapy. Provide respiratory support, which frequently necessitates the use of mechanical ventilation. Administer prescribed medications, monitor cardiopulmonary status, cluster care to reduce stimulation, and provide ongoing sup

physical exam

At birth, inspect the newborn for the following characteristic features. See also Figure 24.5. Puffy, rosy cheeks with a ruddy skin color Short neck (some describe "no-neck" appearance) Buffalo hump over the nape of the neck Massive shoulders with a full intrascapular area Distended upper abdomen due to organ overgrowth Excessive subcutaneous fat tissue, producing fat extremities Be alert for hypoglycemia, which may occur immediately after birth or within an hour. Assess blood glucose levels, which should remain above 40 mg/dL. Closely assess the newborn for signs of hypoglycemia, including listlessness, hypotonia, apathy, poor feeding, apneic episodes with a drop in oxygen saturation, cyanosis, temperature instability, pallor and sweating, tremors, irritability, and seizures.

Hypoxic-Ischemic Encephalopathy

At birth, the newborn's lungs are filled with fluid. This fluid must be cleared and replaced with air for successful respiration to begin after birth. As the newborn makes the transition to life outside the fluid-filled intrauterine environment, dramatic changes must occur to facilitate newborn respirations. Newborns normally start to breathe with routine warming, drying, airway suctioning, and mild stimulation. Most newborns make this transition such that by 1 minute of age, they are breathing well on their own. A newborn who fails to establish adequate, sustained respiration after birth is said to have asphyxia. Physiologically, asphyxia can be defined as impairment in gas exchange resulting in a decrease in blood oxygen levels (hypoxemia) and an excess of carbon dioxide or hypercapnia that leads to acidosis. It occurs when pulmonary oxygenation is delayed or interrupted. The newborn who experiences asphyxia is at risk for the development of HIE -is characterized by clinical and laboratory evidence of acute or subacute brain injury due to systemic hypoxemia or reduced cerebral blood flow

Bladder exstrophy

Bladder exstrophy is a rare developmental abnormality that is present at birth in which the bladder and related structures are turned inside out through an opening in the abdominal wall. In classic bladder exstrophy, a midline closure defect occurs during the embryonic period of gestation, leaving the bladder open and exposed outside of the abdomen. The incidence is between one in 10,000 to one in 50,000 live births, and happens in males slightly more than females (NORD, 2020a). The bony pelvis may also be malformed, resulting in an opening in the pelvic arch. Bladder exstrophy may be diagnosed by prenatal ultrasound. Complications include UTI from ascending organisms. Treatment of bladder exstrophy involves surgical repai Nursing Assessment On physical examination of the infant or child, note the red appearance to the bladder seen on the abdominal wall. Draining urine will be visible. Note excoriation of abdominal skin around the bladder resulting from contact with urine. A malformed urethra may be present in females, whereas males may have an unformed or malformed penis or a normal penis with an epispadias. Nursing Management Nursing management consists of identifying the genitourinary defect at birth so immediate treatment can be initiated, preventing infection and skin breakdown, providing postoperative care, and catheterizing the stoma PREVENTING INFECTION AND SKIN BREAKDOWN Bladder exstrophy requires surgical repair. In the preoperative period, care is focused on protecting the exstrophied bladder and preventing infection. Keep the infant in a supine position; keep the bladder moist and cover it with a sterile plastic bag. Change soiled diapers immediately to prevent contamination of the bladder with feces. Sponge-bathe the infant rather than immersing him or her in water to prevent pathogens in the bath water

manesfestations

CNS Dysfunction • Tremors and irritability • Generalized seizures • Hyperactive reflexes • Restlessness • Exaggerated Moro reflex • Hypertonic muscle tone, constant movement • Shrill, high-pitched excessive cry • Disturbed sleep patterns Metabolic, Vasomotor, and Respiratory Disturbances • Fever • Frequent yawning • Mottling of the skin • Sweating • Frequent sneezing • Nasal flaring • Tachypnea >60 bpm • Apnea • Poor feeding and failure to thrive • Frantic sucking or rooting • Loose or watery stools with perianal excoriation • Regurgitation or projectile vomiting

MANGEMTN

Care of the newborn with PIVH is primarily supportive. Correct anemia, acidosis, and hypotension with fluids and medications. Administer fluids slowly to prevent fluctuations in blood pressure. Avoid rapid volume expansion to minimize changes in cerebral blood flow. Keep the newborn in a flexed, contained position with the head elevated to prevent or minimize fluctuations in intracranial pressure. Continuously monitor the newborn for signs of hemorrhage, such as changes in the level of consciousness, bulging fontanel, seizures, apnea, and reduced activity level. Also, measuring head circumference daily to assess for expansion in size is essential in identifying complications early. Minimize handling of the newborn by clustering nursing care, and limit stimulation in the newborn's environment to reduce stress. Also reduce the newborn's exposure to noxious stimuli to avoid a fluctuation in blood pressure and energy expenditure. Provide adequate oxygenation to --Developmental care principles include avoiding lifting the lower extremities above the midline with diaper changes, giving rapid fluid boluses, and high oxygen and ventilation, as these can increase the chance of more cranial hemorrhage (Kenner et al., 2020). Support for the parents to cope with the diagnosis and potential long-term sequelae is essential. The long-term neurodevelopmental outcome is determined by the severity of the bleed. Provide education and emotional support for the parents throughout the newborn's stay. Discuss expectations for short- and long-term care needs with the parents and assist them in obtaining the necessary support from appropriate community resources

CHEST X-RAY

Chest x-rays show patchy, fluffy infiltrates unevenly distributed throughout the lungs and marked hyperaeration mixed with areas of atelectasis. ABG analysis will indicate metabolic acidosis with a low blood pH, decreased PaO2, and increased PaCO2 (Martin et al., 2020). Direct visualization of the vocal cords for meconium staining using an appropriate size laryngoscope is needed to confirm the presence of meconium below the larynx. -Upon delivery of the newborn's head, before the newborn takes the first breath, the nasal cavity and then the posterior pharynx are gently wiped to decrease the potential for aspiration. If the newborn is significantly depressed at birth, secondary clearing of the lower airways by direct tracheal suctioning may be necessary. Repeated suctioning and stimulation are limited to prevent overstimulation and further depression. In pregnancies complicated by meconium-stained amniotic fluid, suctioning of the hypopharynx before the birth of the infant's shoulders and postnatal suction of vigorous infants have been used in an effort to clear the airway and decrease the incidence and the severity of MAS -Maintain a neutral thermal environment, including placing the newborn under a radiant warmer or in a warmed isolette, to prevent hypothermia. In addition, minimize handling to reduce energy expenditure and oxygen consumption that could lead to further hypoxemia and acidosis

CHRONIC BILIRUBIN

Chronic bilirubin encephalopathy or kernicterus is a preventable neurologic syndrome resulting from the deposition of unconjugated (indirect) bilirubin in the basal ganglia and brainstem nuclei. It is characterized by four clinical manifestations: movement disorder (athetosis, dystonia, spasticity, hypotonia), auditory dysfunction (deafness), oculomotor impairment, and dental enamel hypoplasia of deciduous teeth (Shaughnessy & Goyal, 2020). Unconjugated bilirubin enters the brain and acts as a neurotoxin causing long-term neurologic sequelae. Cases of kernicterus should not be occurring today, but delays in diagnosing pathologic causes of prolonged jaundice are still being missed or overlooked ( -he most common condition associated with pathologic jaundice is hemolytic disease of the newborn secondary to incompatibility of blood groups of the mother and the newborn. The most frequent conditions are Rh factor and ABO incompatibilities.

INTERVENTIONS

Cluster newborn care to minimize oxygen demand. Maintain an optimal thermal environment to minimize oxygen consumption. Prevent and treat any complications such as hypotension, metabolic acidosis, or anemia. Incorporate developmental care practices when applicable. Pay special attention to systemic blood volume and blood pressure to reduce right-to-left shunting through the patent ductus. Administer broad-spectrum antibiotics to treat chemical pneumonitis. Continuously monitor the newborn's condition (cardiac and respiratory status, oximetry). Provide continuous reassurance and support to the parents throughout the experience

NEONATAL SEPSIS

Despite recent improvements in outcomes, neonatal sepsis remains a significant contributor to morbidity and mortality. Neonatal sepsis is defined as a clinical syndrome of bacteremia with systemic signs and symptoms of infection in the first month of life. Presenting clinical symptoms are unspecific (Singh & Gray, 2019). Newborns have increased susceptibility to infections because their immune systems are immature and slow to react, and they have a poorly developed skin barrier. The antibodies that newborns received from their mother during pregnancy and from breast milk help protect them from invading organisms. However, these need time to reach optimal levels. Bacterial infections of the newborn remain a major cause of illness and death in the neonatal period. The mortality rate from newborn sepsis may be as high as 50% if untreated ( Pathophysiology When a pathologic organism overcomes the newborn's defenses, infection and sepsis result. Neonatal sepsis is the presence of bacterial, fungal, or viral microorganisms or their toxins in blood or other tissues. Infections that have an onset within the first month of life are termed newborn infections. Exposure to a pathogenic organism, whether a virus, fungus, or bacteria, occurs, and it enters the newborn's body and begins to multiply. Newborn infections are usually grouped into three classes according to their time of onset: congenital infection, acquired in utero (intrauterine infections) by vertical transmission with onset before birth; early-onset infections, acquired by vertical transmission in the perinatal period, either shortly before or during birth; and late-onset infections, acquired by horizontal transmission in the nursery. About 85% of neonatal infections have their onset in the first 2 days of life and usually are pneumonia and meningitis Early-onse

Necrotizing Enterocolitis

NEC is an inflammatory disease of the bowel which can cause ischemic and necrotic injury in the gastrointestinal tract. It is the most common and most serious acquired gastrointestinal disorder among hospitalized preterm neonates and is associated with significant acute and chronic morbidity and mortality. NEC occurs in approximately 10% of infants who weigh less than 1,500 g, with mortality rates up to 50% (Brown, 2020). Attempts to improve gastrointestinal function and reduce the risk of NEC include enteral antibiotics, judicious administration of parenteral fluids, human milk feedings, antenatal corticosteroids, enteral probiotics (Lactobacillus acidophilus), and slow continuous drip feedings (

EARLY ONSET

Early-onset neonatal infections (<72 hours) are associated with acquisition of microorganisms perinatally from the mother's genitourinary system. Transplacental infection or an ascending infection from the cervix may be caused by organisms that colonize in the mother's genitourinary tract, with acquisition of the microbe by passage through a colonized birth canal at delivery. The microorganisms most commonly associated with early-onset infection include group B Streptococcus (GBS), Escherichia coli, coagulase-negative Staphylococcus, Haemophilus influenzae, and Listeria monocytogenes. -Late-onset infections (>72 hours), acquired in the postpartum period, are primarily through health care workers, horizontal transmission from family members or caregivers or through environmental exposures. Infections such as human immunodeficiency virus (HIV) and CMV can be acquired through breastfeeding (discussed in more detail in Chapter 20) or by direct contact with family members or health care providers. These types of contacts and exposures are especially important in infants, primarily preterm, with prolonged hospital stays, where they are more likely to be exposed to multidrug-resistant hospital-associated organisms potentially from contact with caregivers or contaminated equipment. Organisms that cause late-onset sepsis include Staphylococcus aureus, E. coli, Klebsiella, Pseudomonas, Enterobacter, Candida, and Anaerobes

Esophageal Atresia and Tracheoesophageal Fistula

Esophageal atresia and tracheoesophageal fistula are gastrointestinal anomalies in which the esophagus and trachea do not separate normally during embryonic development. Esophageal atresia refers to a congenitally interrupted esophagus where the proximal and distal ends do not communicate; the upper esophageal segment ends in a blind pouch and the lower segment ends a variable distance above the diaphragm. In short, the upper esophagus doesn't connect to the lower esophagus and stomach -Tracheoesophageal fistula is an abnormal communication between the trachea and esophagus. When associated with esophageal atresia, the fistula most commonly occurs between the distal esophageal segment and the trachea. The incidence of esophageal atresia is one per 4,100 live births (CDC, 2019a). The etiology has been attributed to genetic factors, infections, and teratogens, but in most cases, no cause is identifiable. PATHIO Several types of esophageal atresia exist, but the most common anomaly is a fistula between the distal esophagus and the trachea, which occurs in 90% of newborns with an esophageal defect. Esophageal atresia and tracheoesophageal fistula are thought to be the result of incomplete separation of the lung bed from the foregut during early fetal development. A large percentage of these newborns have other congenital anomalies involving the vertebra, kidneys, heart, and musculoskeletal and gastrointestinal systems (Khan & Matta, 2020); most have several anomalies. NURSING ASSESMR Review the maternal history for polyhydramnios. Often this is the first sign of esophageal atresia because the fetus cannot swallow and absorb amniotic fluid in utero, leading to accumulation. Soon after birth, the newborn may exhibit copious, frothy bubbles of mucus in the mouth and nose, accompanied by drooling. Abdominal distention deve

ASSESSMENT

Evaluate the newborn for an unexplained drop in hematocrit, pallor, apnea, and poor perfusion as evidenced by respiratory distress and oxygen desaturation. Note seizures, lethargy or other changes in level of consciousness, bulging fontanel, weak sucking, metabolic acidosis, high-pitched cry, or hypotonia. Palpate the anterior fontanel for tenseness. Assess vital signs, noting bradycardia and hypotension. Evaluate laboratory data for changes indicating metabolic acidosis or glucose instability. Frequently a bleed can progress rapidly and result in shock and death. Prepare the newborn for cranial ultrasonography, the diagnostic tool of choice to detect hemorrhage

PHOTOTHERAPY

For the newborn with jaundice, regardless of its etiology, phototherapy is used to convert unconjugated bilirubin to the less toxic water-soluble form that can be excreted. Phototherapy, via special lights placed above the newborn or a fiberoptic blanket placed under the newborn and wrapped around him or her, involves blue wavelengths of light to alter unconjugated bilirubin in the skin. For the newborn receiving phototherapy, place the newborn under the lights or on the fiberoptic blanket, exposing as much skin as possible. Cover the newborn's genitals and shield the eyes to protect these areas from becoming irritated or burned when using direct lights. Assess the intensity of the light source to prevent burns and excoriation -Turn the newborn every 2 hours to maximize the area of exposure, removing the newborn from the lights only for feedings. Maintain a neutral thermal environment to decrease energy expenditure, and assess the newborn's neurologic status frequently. Research is finding that intermittent versus continuous phototherapy is as efficacious to lower bilirubin levels -Assess the newborn's temperature every 3 to 4 hours as indicated. Monitor fluid intake and output closely and assess daily weights for gains or losses. Check skin turgor for evidence of dehydration. -With feedings, remove the newborn from the lights and remove the eye shields to allow interaction with the newborn. Encourage breast- or bottle-feedings every 2 to 3 hours. Follow agency policy about removing the eye shields periodically to assess the eyes for discharge or corneal irritation secondary to eye shield pressure. Typically, the eyes are assessed and eye shields removed once a shift. -Monitor stool for consistency and frequency. Unconjugated bilirubin excreted in the feces will produce a greenish appearance, and typically stoolLOOSE

hypoglycemia

Glucose is the major source of energy for organ function. Typical characteristics: • Poor feedings • Jitteriness • Lethargy • High-pitched or weak cry • Apnea • Cyanosis and seizures Some newborns are asymptomatic. -Low blood glucose levels are problematic during early post birth period due to abrupt cessation of high-glucose maternal blood supply and the continuation of insulin production by the newborn. Limited ability to release glucagon and catecholamines, which normally stimulate glucagon breakdown and glucose release Prolonged and untreated hypoglycemia leads to serious, long-term adverse neurologic sequelae such as learning disabilities and mental retardation.

Hyperbillirubinemia (jaundice)

Hyperbilirubinemia results from the overproduction bilirubin which is the end product of hemoglobin breakdown. It is clinically apparent when a total serum bilirubin level is above 5 mg/dL resulting from unconjugated bilirubin being deposited in the skin and mucous membranes (Martin & Rosenfeld, 2019). Hyperbilirubinemia is exhibited as jaundice (yellowing of the body tissues and fluids). Newborn jaundice is one of the most common reasons for hospital readmission. It occurs in 60% of term newborns and 80% of preterm infants in the first week of lif pathio Bilirubin has two forms—unconjugated or indirect, which is fat-soluble and toxic to body tissues, and conjugated or direct, which is water-soluble and nontoxic. Elevated serum bilirubin levels are manifested as jaundice in the newborn. Typically the total serum bilirubin level rises over the first 3 to 5 days and then declines. Newborn jaundice results from an imbalance in the rate of bilirubin production and bilirubin elimination. This imbalance determines the pattern and degree of newborn hyperbilirubinemia -During the newborn period, a rapid transition from the intrauterine to the extrauterine pattern of bilirubin physiology occurs. Fetal unconjugated bilirubin is normally cleared by the placenta and the mother's liver in utero, so total bilirubin at birth is low. After the umbilical cord is cut, the newborn must conjugate bilirubin (convert a lipid-soluble pigment into a water-soluble pigment) in the liver on his or her own. The rate and amount of bilirubin conjugation depend on the rate of red blood cell breakdown, the bilirubin load, the maturity of the liver, and the number of albumin-binding sites. Bilirubin levels rise in newborns by three main mechanisms: increased production (accelerated RBC breakdown), decreased removal (transient liver enzyme insuffi

LAB n diagnostic

Hypocalcemia is typically manifested in the first 2 to 3 days of life as a result of birth injury or a prolonged delay in parathyroid hormone production. Hypomagnesemia parallels calcium levels and is suspected only when hypocalcemia does not respond to calcium replacement therapy. Red blood cell breakdown leads to increased hematocrit and polycythemia. In addition, hyperbilirubinemia may be caused by slightly decreased extracellular fluid volume, hepatic immaturity, and birth trauma forming enclosed hemorrhages. It can appear within the first 24 hours of life (pathologic) or after 24 hours of life (physiologic).

ECHANGE TRANSUION

If the total serum bilirubin level remains elevated after intensive phototherapy, an exchange transfusion with albumin administered before the transfusion, the quickest method for lowering serum bilirubin levels, may be necessary. Exchange transfusions are a high-risk procedure and should be performed only when the benefit of the procedure offsets the risks (Chacham et al., 2019). In the presence of hemolytic disease, severe anemia, or a rapid rise in the total serum bilirubin level, an exchange transfusion is recommended. An exchange transfusion removes the newborn's blood and replaces it with nonhemolyzed red blood cells from a donor. During the transfusion, monitor the newborn's cardiovascular status continuously because serious complications can arise, such as acid-base imbalances, infection, hypovolemia, and fluid and electrolyte imbalances. Exchange transfusion is used only as a second-line therapy after phototherapy has failed to yield results. Intensive nursing care is needed. --Assist the physician or health care practitioner with an exchange transfusion if necessary. Monitor the newborn's status closely for changes, especially in vital signs and heart rate and rhythm, before, during, and after the procedure.

Nursing Management

If untreated, RDS will worsen. In many infants respiratory symptoms decline after 72 hours, paralleling the production of surfactant in the alveoli (Fanaroff & Fanaroff, 2020). The newborn needs supportive care until surfactant is produced. Effective therapies for established RDS include conventional mechanical ventilation, continuous positive airway pressure (CPAP), or positive end-expiratory pressure (PEEP) to prevent volume loss during expiration, and surfactant therapy. The use of exogenous surfactant replacement therapy to stabilize the newborn's lungs until postnatal surfactant synthesis matures has become a standard of care, but not necessarily evidence based. Knowledge of the surfactant proteins and lipids produced by the epithelial II cells were critical in the development of surfactant-replacement preparations used to treat RDS. This preparation has dramatically improved morbidity and mortality in preterm infants -A main breakthrough in treating RDS came was the development of surfactant replacement. Surfactant replacement therapy is crucial in the management of RDS, but the best preparation, optimal dose and timing of administration at different gestations has not been scientifically established. Respiratory support in the form of mechanical ventilation may also be lifesaving, but can cause bronchopulmonary dysplasia, and protocols should be directed at avoiding mechanical ventilation where possible by using nasal CPAP or nasal ventilation. Another mainstay of treatment for RDS is inhaled nitric oxide which improves oxygenation, reduces pulmonary inflammation and helps reduce the risk of chronic lung disease. For newborns with RDS to have best outcomes, it is essential that they have optimal supportive care, including maintenance of a normal body temperature, proper fluid management, good nutritional suppo

ASSESSMENT

In the newborn, observe for an appropriate anal opening. If the anal opening exists, observe for passage of meconium stool within the first 24 hours of life. Assess urine output to identify genitourinary problems. For the newborn with an imperforate anus, inspection of the perineal area would reveal absence of the usual opening. In addition, meconium generally is not passed or present within 24 hours of birth. In the infant with suspected imperforate anus, assess for common signs of intestinal obstruction, which may occur as a result of the malformation. These include abdominal distention and bilious vomiting. Prepare the newborn and family for a perineal ultrasound and an abdominal x-ray that will be ordered to identify the level of defect in the absence of a perineal fistula and also to assess for complications associated with imperforate anus. MANAGE Nursing management focuses on preparing the newborn and parent for surgery and providing postoperative care. Preoperatively, maintain the newborn's NPO status and provide gastric decompression. Administer IV therapy and antibiotic therapy as ordered and monitor the newborn's hydration status. Provide a full explanation of the defect, surgical options, potential complications, typical postoperative course, and long-term care needed to the parents. Make sure they are aware of the available treatment modalities. Prepare them for the possibility that the newborn may require an ostomy. Provide support to the parents and family. Postoperative care includes ensuring adequate pain relief, maintaining NPO status and gastric decompression until normal bowel function is restored, and providing colostomy care if applicable. Refer to Chapter 42 for additional information related to ostomy care and postoperative care for children undergoing an intestinal pull-through procedure.

MECONIUM ASPIRATION

It is expelled as the newborn's first stool after birth. Meconium is sterile and does not contain bacteria, the primary factor that differentiates it from stool. Intrauterine distress can cause passage of meconium into the amniotic fluid before birth. Factors that promote the passage in utero include placental insufficiency, maternal hypertension, preeclampsia, fetal hypoxia, transient umbilical compression, oligohydramnios, and maternal drug abuse, especially of tobacco and cocaine. Meconium can be aspirated before or during labor and after birth. Because meconium is rarely found in the amniotic fluid prior to 36 weeks' gestation, it mainly impacts infants born at term and post-term (Blackburn, 2018). It is usually expelled as the newborn's first stool after birth. -Meconium aspiration syndrome occurs when the newborn inhales particulate meconium mixed with amniotic fluid into the lungs while still in utero or on taking the first breath after birth. Meconium staining of the amniotic fluid, with the possibility of aspiration, occurs in approximately 10% to 15% of births after 36 weeks' gestation (Resnik et al., 2019). Aspiration induces airway obstruction, surfactant dysfunction, hypoxia, and chemical pneumonitis with inflammation of pulmonary tissues. Severe MAS can lead to persistent pulmonary hypertension and death. The use of surfactant and inhaled nitric oxide has led to the decreased mortality and the need for extracorporeal membrane oxygenatioN

LAB TESTING

Kidney, ureter, and bladder (KUB) of the abdomen x-ray: confirms the presence of pneumatosis intestinalis (air in the bowel wall) and persistently dilated loops of bowel An abdominal x-ray to demonstrate dilated bowel loops, abnormal gas patterns, air bubbles that occur from bacteria, and thickened bowel walls Blood values: may demonstrate metabolic acidosis, increased white blood cells, thrombocytopenia, neutropenia, electrolyte imbalance, or disseminated intravascular coagulation (DIC) ( ---- MAINTAINING FLUID AND NUTRITIONAL STATUS If NEC is suspected, immediately stop enteral feedings until a diagnosis is made. Administer IV fluids initially to restore proper fluid balance. If ordered, administer total parenteral nutrition (TPN) to keep the newborn supported nutritionally. Give prescribed IV antibiotics to prevent sepsis from the necrotic bowel (if surgery is required, antibiotics may be needed for an extended period of time). Institute gastric decompression as ordered with an orogastric tube attached to low intermittent suction. Carefully monitor intake and output. Restart enteral feedings once the disease has resolved (normal abdominal examination and KUB negative for pneumatosis) or as determined postoperatively by the surgeon PROVIDING SUPPORTIVE CARE Check stools for evidence of blood and report any positive findings. Measure the abdominal girth. Monitor blood pressure for hypotension. Palpate the abdomen for tenderness and rigidity. Auscultate for normal bowel sounds in all four quadrants. Monitor blood gases and oxygen saturation. Observe the abdomen for redness or shininess, which indicates peritonitis. Offer emotional support for parents/partners/significant others

congenital anomalies

Occur in up to 10% of infants of diabetic mothers, accounting for 30-50% of perinatal deaths. Incidence is greatest among small-for gestational-age newborns. Overall, infants of diabetic mothers have three times the usual incidence of congenital anomalies compared to newborns from the nondiabetic general population. Most common anomalies: • Coarctation of the aorta • Atrial and ventricular septal defects • Transposition of the great vessels • Sacral agenesis • Hip and joint malformations • Anencephaly • Spina bifida • Caudal dysplasia • Hydrocephalus

NURSING MANAGEMENT

Management of the newborn experiencing asphyxia includes immediate resuscitation. Ensure that the equipment needed for resuscitation is readily available and in working order. Essential equipment includes a wall suction apparatus, an oxygen source, a newborn ventilation bag, endotracheal tubes (2 to 3 mm), infant warmer, surgical blue towels, a laryngoscope, and ampules of naloxone (Narcan) with syringes and needles for administration. Effective ventilation is essential to successful newborn resuscitation. Ventilation is frequently initiated with a manual resuscitation bag and face-mask followed by endotracheal intubation if respiratory depression continues -Dry the newborn quickly with a warm towel and then place him or her under a radiant heater to prevent rapid heat loss through evaporation. Handling and rubbing the newborn with a dry towel may be all that is needed to stimulate the onset of breathing. If the newborn fails to respond to stimulation, then active resuscitation is needed. The procedure for newborn resuscitation is easily remembered by the "C-A-B" s"—Compressions-Airway-Breathing -Continue resuscitation until the newborn has a pulse above 100 bpm, a good healthy cry, or good breathing efforts and a pink tongue. This last sign indicates a good oxygen supply to the brain Maintain a neutral thermal environment to prevent hypothermia, which would increase the newborn's metabolic and oxygen demands. Check the blood glucose level and observe for signs of hypoglycemia; if this develops, it can further stress the newborn. The need for resuscitative measures can be extremely upsetting for the parents/partners/significant others. Explain to them the initial resuscitation activities being performed and offer ongoing explanations about any procedures being done, equipment being used, or medications given

assessment

Maternal history to identify risk behaviors for substance abuse: Previous unexplained fetal demise Lack of prenatal care Incarceration Prostitution Cigarette smoking Fetal growth restriction Preterm birth History of STIs and/or HIV and/or HCV Mental health disorders History of intimate partner violence History of missed prenatal appointments Severe mood swings Withdrawal Acronym W = Wakefulness: sleep duration less than 3 hours after feeding I = Irritability T = Temperature variation, tachycardia, tremors H = Hyperactivity, high-pitched persistent cry, hyperreflexia, hypertonus D = Diarrhea, diaphoresis, disorganized suck R = Respiratory distress, rub marks, rhinorrhea A = Apneic attacks, autonomic dysfunction W = Weight loss or failure to gain weight A = Alkalosis (respiratory) L = Lacrimation

head trauma

Mild trauma can cause soft tissue injuries such as cephalohematoma and caput succedaneum; greater trauma can cause depressed skull fractures. Cephalohematoma (subperiosteal collection of blood secondary to the rupture of blood vessels between the skull and periosteum) occurs in 2.5% of all births and typically appears within hours after birth. Caput succedaneum (soft tissue swelling) is caused by edema of the head against the dilating cervix during the birth process. Subarachnoid hemorrhage (one of the most common types of intracranial trauma) may be due to hypoxia/ischemia, variations in blood pressure, and the pressure exerted on the head during labor. Bleeding is of venous origin, and underlying contusions also may occur Subdural hemorrhage (hematomas) occurs less often today because of improved obstetric techniques. Typically, tears of the major veins or venous sinuses overlying the cerebral hemispheres or cerebellum (most common in newborns of a primipara and large newborns, or after an instrumented birth) are the cause. Increased pressure on the blood vessels inside the skull leads to tears. Depressed skull fractures (rare) may result from the pressure of a forceps delivery; can also occur during spontaneous or cesarean births and may be associated with other head trauma causing subdural bleeding, subarachnoid hemorrhage, or brain trauma. In cephalohematoma, suture lines delineate its extent; usually located on one side, over the parietal bone. In caput succedaneum, swelling is not limited by suture lines: it extends across the midline and is associated with head molding. It does not usually cause complications other than a misshapen head. Swelling is maximal at birth and then rapidly decreases in size In subarachnoid hemorrhage, some RBCs may appear in the CSF of full-term newborns. Newborns may present wi

cranial nerve trauma

Most common is facial nerve palsy Frequently attributed to pressure resulting from forceps May also result from pressure on the nerve in utero, related to fetal positioning such as the head lying against the shoulder Physical findings include asymmetry of the face when crying; mouth may be drawn toward the unaffected side; wrinkles are deeper on the unaffected side. The paralyzed side may be smooth, with a swollen appearance. Eye is persistently open on the affected side. Most infants begin to recover in the first week, but full resolution may take up to several months; parents need reassurance about this. In most cases, treatment is not necessary, only observation. If the eye is affected and unable to close, protection with patches and synthetic tears may be necessary. Parents need instruction about how to feed the newborn, since he or she cannot close the lips around the nipple without having milk seep ou

fractures

Most often occur during breech births or shoulder dystocia in newborns with macrosomia Midclavicular fractures are the most common type of fracture, secondary to shoulder dystocia. Long bone fractures of the humerus or femur, usually midshaft, also can occur. Midclavicular fractures: The newborn is irritable and does not move the arm on the affected side either spontaneously or when the Moro reflex is elicited. Femoral or humeral long bone fractures: The newborn shows loss of spontaneous leg or arm motion, respectively; usually swelling and pain accompany the limited movement. X-rays confirm the fracture. Midclavicular fractures typically heal rapidly and uneventfully; arm motion may be limited by pinning the newborn's sleeve to the shirt. Femoral and humeral shaft fractures are treated with splinting. Healing and complete recovery are expected within 2-4 weeks without incident. Explanation to the parents and reassurance are needed.

early and late

Neonatal hyperbilirubinemia has a higher frequency in breastfed infants compared to formula-fed ones. Early-onset breastfeeding jaundice is probably associated with ineffective breastfeeding practices because of relative caloric deprivation in the first few days of life. Decreased volume and frequency of feedings may result in mild dehydration and the delayed passage of meconium. This delayed defecation allows enterohepatic circulation reuptake of bilirubin and an increase in the serum level of unconjugated bilirubin. To prevent this, strategies to promote early effective breastfeeding are important. The AAP guidelines and the National Association of Pediatric Nurse Practitioners (NAPNAP) recommend early and frequent breastfeeding (NAPNAP, 2019). Early frequent feedings can provide the newborn with adequate calories and fluid volume (via colostrum) to stimulate peristalsis and passage of meconium to eliminate bilirubin. Successful breastfeeding decreases the risk of hyperbilirubinemia. Infants need to be fed at least eight to 12 times in the first few days after birth to help improve the mother's milk supply. The best way to judge successful breastfeeding is to monitor infant urine output, stool output, and weight. Newborns should have four to six wet diapers and three to four yellow, seedy stools per day by the fourth day after birth. Breastfeeding-associated jaundice is usually preventable through appropriate breastfeeding practices. late onset Late-onset breastfeeding jaundice occurs later in the newborn period, with the bilirubin level usually peaking in the first 6 to 14 days of life. It typically occurs between the fourth and seventh days of life, when mature milk begins to replace colostrum (Pan & Rivas, 2017). The specific cause of late-onset breast milk jaundice is not entirely understood, but it may be r

macrosomia problems

Newborn with an excessive birth weight; arbitrarily defined as a birth weight >4,000 g (8 lb 8 oz) to 4,500 g (9 lb 9 oz) or >90% for gestational age Complication in 10% of all pregnancies in the United States - Increased risk for shoulder dystocia, traumatic birth injury, birth asphyxia • Risks for newborn hypoglycemia and hypomagnesemia, polycythemia, and electrolyte disturbances • Increased maternal risk for surgical birth, postpartum hemorrhage and infection, and birth canal lacerations • Increased risk of developing type 2 diabetes later in life for both • Higher weight and accumulation of fat in childhood and a higher rate of obesity in adults

TEACHING AND USPPORT

Nurses can help the parents to understand the diagnostic tests and treatment modalities by offering individualized teaching. Nurses are the ones who give discharge instructions to the family. Explore with the family their understanding of jaundice and treatment modalities to reduce anxiety and gain their cooperation in monitoring the infant. Teach the parents about jaundice and its potential risk using written and verbal material. Also show the parents how to identify newborn behaviors that might indicate rising bilirubin levels. Emphasize the need to seek treatment from their pediatrician should any of the following occur: Lethargy, sleepiness, poor muscle tone, floppiness Poor sucking, lack of interest in feeding High-pitched cry, irritability Caring for Your Newborn Receiving Home Phototherapy • Inspect your newborn's skin, eyes, and mucous membranes for a yellow color. • Remember that a home health nurse will come to visit and help set up the light system. • Keep the lights about 12 to 30 in above your newborn. • Cover your newborn's eyes with patches or cotton balls and gauze to protect them. • Keep the newborn undressed except for the diaper area; fold the diaper down below the newborn's navel in the front and as far as possible in the back to expose as much skin area as possible. • Turn your newborn every 2 hours so that all areas of the body are exposed. • Remove the newborn from the lights only for feeding. • Remove the eye patches during feedings so that you can interact with your newborn. • Record your newborn's temperature, weight, and fluid intake daily. • Document the frequency, color, and consistency of all stools; the stools should be loose and green as the bilirubin is broken down Keep the skin clean and dry to prevent irritation. • NOTIFY PROVIDER IS LESS THAN 3 TO 5 DIAPERS LES

mangement

Nursing management is primarily supportive and focuses on assessing for resolution of the trauma or any associated complications along with providing support and education to the parents. Provide the parents with explanations and reassurance that these injuries usually resolve with minimal or no treatment. Parents are alarmed when their newborn is unable to move an extremity or demonstrates asymmetric facial movements. Provide parents with a realistic picture of the situation to gain their understanding and trust. Be readily available to answer questions and teach them how to care for the newborn, including any modifications that might be necessary. Allow parents adequate time to understand the implications of the birth trauma or injury and what treatment modalities are needed, if -ny. Provide them with information about the length of time until the injury will resolve and when and if they need to seek further medical attention for the condition. Spending time with the parents and providing them with support, information, and teaching are important to allow them to make decisions and care for their newborn. Anticipate the need for community referral for ongoing follow-up and care, if necessary.

Omphalocele and Gastroschisis

Omphalocele and gastroschisis are congenital anomalies of the anterior abdominal wall at or near the umbilicus. Fetal abdominal wall defects result from disturbances in organogenesis during the early embryonic period. Gastroschisis occurs in two to five babies per 10,000 live births (Genetics Home Reference [GHR], 2020), while omphalocele occurs in one in 4,200 live births (CDC, 2019b). An omphalocele is a defect of the umbilical ring that allows evisceration of the abdominal contents into an external peritoneal sac. Defects vary in size; they may be limited to bowel loops or may include the entire gastrointestinal tract and liver (Fig. 24.9). Bowel malrotation is common, but the displaced organs are usually normal. --Gastroschisis is a herniation of the abdominal contents through the ventral abdominal wall defect, at the umbilicus. Gastroschisis differs from omphalocele in that there is no peritoneal sac protecting the herniated organs, and thus exposure to amniotic fluid makes them thickened, edematous, and inflamed (GHR, 2020). Gastroschisis is associated with significant newborn mortality and morbidity rates. Despite surgical correction, feeding intolerance, failure to thrive, and prolonged hospital stays may occur newborns with this anomaly, though the long-term outcome is generally satisfactory Nursing Management Nursing management of newborns with omphalocele or gastroschisis focuses on preventing hypothermia, maintaining perfusion to the eviscerated abdominal contents by minimizing fluid loss, and protecting the exposed abdominal contents from trauma and infection. These objectives can be accomplished by placing the infant in a sterile drawstring bowel bag that maintains a sterile environment for the exposed contents, allows visualization, reduces heat and moisture loss, and allows heat from radiant warmers t

Persistent Pulmonary Hypertension of the Newborn

PPHN, previously referred to as persistent fetal circulation, is a cardiopulmonary disorder characterized by marked pulmonary hypertension that causes right-to-left extrapulmonary shunting of blood and hypoxemia. It occurs when the newborn's circulatory system does not have normal transition after birth due to the failure of pulmonary vascular relaxation PPHN can occur idiopathically or as a complication of perinatal asphyxia, MAS, maternal smoking, maternal obesity, hypocalcemia, maternal asthma, pneumonia, congenital heart defects, metabolic disorders such as hypoglycemia, hypothermia, hypovolemia, hyperviscosity, acute hypoxia with delayed resuscitation, sepsis, and RDS

PATHIO

Pathophysiology Lung immaturity and surfactant deficiency contribute to the development of RDS. Surfactant is a complex mixture of phospholipids and proteins that adheres to the alveolar surface of the lungs. Anatomically, the immature lung cannot support oxygenation and ventilation, because the alveolar sacs are insufficiently developed, causing a deficient surface area for gas exchange. Physiologically, the amount of surfactant is insufficient to prevent collapse of unstable alveoli. Surfactant forms a coating over the inner surface of the alveoli, reducing the surface tension and preventing alveolar collapse at the end of expiration. In the affected newborn, surfactant is deficient or lacking, and this deficit results in stiff lungs and alveoli that tend to collapse, leading to diffuse atelectasis. The work of breathing is increased because increased pressure similar to that required to initiate the first breath is needed to inflate the lungs with each successive breath. Hypoxemia and acidemia result, leading to vasoconstriction of the pulmonary vasculature. Right-to-left shunting occurs and alveolar capillary circulation is limited, further inhibiting surfactant production. As the disease progresses, fluid and fibrin leak from the pulmonary capillaries, causing hyaline membranes to form in the bronchioles, alveolar ducts, and alveoli. -Hyaline membranes produce a ground-glass appearance in the lung membranes that can be seen on x-rays. These membranes further decrease gas exchange. These factors decrease the total surface area of the gas exchange membrane. The end result is hypoxemia, academia, and a worsening respiratory distress. A vicious cycle is created, compounding the problem Observe the infant for expiratory grunting, shallow breathing, nasal flaring, chest wall retractions (Fig. 24.2), seesaw respirations

pathio

Pathophysiology The large size of the IDM arises secondary to exposure to high levels of maternal glucose crossing the placenta into the fetal circulation. Maternal hyperglycemia acts as a fuel to stimulate increased production of fetal insulin, which in turn promotes somatic growth within the fetus. The fetus responds to these high levels by producing more insulin, which acts as a growth factor in the fetus (Brown, 2020). How the fetus will be affected and the problems that the newborn experiences depend on the severity, duration, and control of the diabetes in the mother during the pregnancy. Table 24.1 summarizes the common problems that may occur in infants of diabetic mothers.

BIRTH INJURIES

Pathophysiology The process of birth is a blend of compression, contractions, torques, and traction. When fetal size, presentation, or neurologic immunity complicates this process, the forces of labor and birth may lead to tissue damage, edema, hemorrhages, or fractures in the newborn. For example, birth trauma may result from the pressure of birth, especially in a prolonged or abrupt labor, abnormal or difficult presentation, cephalopelvic disproportion, or mechanical forces, such as forceps or vacuum used during delivery assessment Recognition of trauma and birth injuries is imperative so that early treatment can be initiated. Review the labor and birth history for risk factors, such as a prolonged or abrupt labor, abnormal or difficult presentation, cephalopelvic disproportion, or mechanical forces, such as forceps or vacuum used during delivery. Also review the history for multiple fetus deliveries, large-for-date infants, extreme prematurity, large fetal head, or newborns with congenital anomalies. Complete a careful physical and neurologic assessment of every newborn admitted to the nursery to establish whether injuries exist. Inspect the head for lumps, bumps, or bruises. Note if swelling or bruising crosses the suture line. Assess the eyes and face for facial paralysis, observing for asymmetry of the face with crying or appearance of the mouth being drawn to the unaffected side. Ensure that the newborn spontaneously moves all extremities. Note any absence of or decrease in deep tendon reflexes or abnormal positioning of extremities. Assess and document symmetry of structure and function. Be prepared to assist with scheduling diagnostic studies to confirm trauma or injuries, which will be important in determining treatment modalities.

prevtning complications

Pharmacologic treatment is warranted if conservative measures, such as swaddling and decreased environmental stimulation, are not adequate. The AAP recommends that for newborns with confirmed drug exposure, drug therapy is indicated if the newborn has seizures, diarrhea, and vomiting resulting in excessive weight loss and dehydration, poor feeding, inability to sleep, and fever unrelated to infection (Benitz et al., 2019). Common medications used in the management of newborn withdrawal include an opioid (morphine or methadone) and sublingual buprenorphine or phenobarbital or clonidine as secondary drugs if the opiate does not adequately control symptoms (Wexelblatt, 2020). Administer the prescribed medications and document the newborn's behavioral responses. -The newborn is at risk for skin breakdown. Weight loss, diarrhea, dehydration, and irritability can contribute to this risk. Provide meticulous skin care and protect the newborn's elbows and knees against friction and abrasions. PROMOTING PARENT-NEWBORN INTERACTION For a mother who abuses substances, the birth of a drug-exposed newborn is both a crisis and an opportunity. The mother may feel guilty about the newborn's condition. Many of these newborns are unresponsive and have disorganized sleeping and feeding patterns. When awake, they can be easily overstimulated and irritated. Such characteristics make parent-newborn interactions difficult and frustrating, leading to possible detachment and avoidance. Nursing support, which includes a description of symptoms and their management, is vital if maternal-infant attachment is to occur and potential neglect or abuse is avoided (Kondili & Duryea, 2019). Instruct the mother or caretaker how to care for the newborn, including what to do after the newborn goes home

physiologic jaundice

Physiologic jaundice is an unconjugated hyperbilirubinemia that occurs after the first postnatal day and can last up to 1 week. Total serum bilirubin concentrations peak in the first 3 to 5 postnatal days and decline to adult values over the next several weeks. It occurs in 60% of term infants and up to 80% of preterm infants (Blackburn, 2018). Serum bilirubin levels reach up to 10 mg/dL and then decline rapidly over the first week after birth (Cunningham et al., 2018). Most newborns have been discharged by the time this jaundice peaks (at about 72 hours). Physiologic jaundice may result from an increased bilirubin load because of relative polycythemia, a shortened red blood cell lifespan, immature hepatic uptake and conjugation process, and increased enterohepatic circulation (Resnik et al., 2019). Newborns with delayed passage of meconium are more likely to develop physiologic jaundice because meconium contains high levels of bilirubin Physiologic jaundice differs between breast- and bottle-fed newborns in relation to the onset of symptoms. Breastfed newborns typically have peak bilirubin levels on the fourth day of life; levels for bottle-fed newborns usually peak on the third day of life. The rate of bilirubin decline is less rapid in breastfed newborns compared to bottle-fed newborns because bottle-fed newborns tend to have more frequent bowel movements. Jaundice associated with breastfeeding presents in two distinct patterns: early-onset breastfeeding jaundice and late-onset breast milk jaundice.

health history

Polycythemia Significant bruising or cephalhematoma, which increases bilirubin production Infections such as toxoplasmosis, hepatitis B, rubella, cytomegalovirus (CMV), herpes simplex virus Use of drugs during labor and birth such as diazepam (Valium) or oxytocin (Pitocin) Prematurity Gestational age of 34 to 36 weeks Hemolysis due to ABO incompatibility or Rh isoimmunization Macrosomic IDM Delayed cord clamping, which increases the erythrocyte volume Decreased albumin-binding sites to transport unconjugated bilirubin to the liver because of acidosis Hypoxemia and respiratory distress experienced at birth Delayed meconium passage, which increases the amount of bilirubin that returns to the unconjugated state and can be absorbed by the intestinal mucosa Siblings who had significant jaundice Inadequate breastfeeding leading to dehydration, decreased caloric intake, weight loss, and delayed passage of meconium Ethnicity, such as Asian American, Mediterranean, or Native American Male gender ASSESSMENT Assess the skin, mucous membranes, sclerae, and bodily fluids (tears, urine) for a yellow color. Detect jaundice by observing the infant in a well-lit room and blanching the skin with digital pressure over a bony prominence. Typically, jaundice begins on the head and gradually progresses to the abdomen and extremities. Also inspect for pallor (anemia), excessive bruising (bleeding), and dehydration (sluggish circulation), which may contribute to the development of jaundice and the risk for kernicterus. Assess the newborn for Rh incompatibility. Be alert for clinical manifestations such as ascites, anemia, congestive heart failure, edema, pallor, jaundice, hepatosplenomegaly, polyhydramnios, thick placenta, and dilation of the umbilical vein (Niss & Ware, 2020). Hydropic newborns appear pale, edematous, and limp at birth and

PREOPERTIVE CARE PROVIDING PREOPERATIVE CARE

Preoperative nursing interventions include the following measures: Initiate nothing by mouth (NPO) status. Elevate the head of the bed 30 to 45 degrees to prevent reflux and aspiration. Monitor hydration status and fluid and electrolyte balance; administer and monitor parenteral IV fluid infusions. Assess and maintain the patency of the orogastric tube; monitor the functioning of the tube, which is attached to low continuous suction; and avoid irrigation of the tube to prevent aspiration. Have oxygen and suctioning equipment readily available should the newborn experience respiratory distress. Assist with diagnostic studies to rule out other anomalies. Use comfort measures to minimize crying and prevent respiratory distress; provide nonnutritive sucking. Inform the parents about the rationales for the aspiration prevention measures. Document frequent observations of the newborn's condition POSTOPERATIVE CARE Immediate surgical management involves creating a gastrostomy opening for a tube for feeding and continuous suctioning of the blind esophageal pouch to prevent aspiration of fluids into the lungs. Surgery consists of closing the fistula and joining the two esophageal segments. Postoperative care involves closely observing all of the newborn's body systems to identify any complications. Expect to administer TPN and antibiotics until the esophageal anastomosis is proven intact and patent. Then begin oral feedings, usually within a week after surgery (Salik & Paul, 2019). Keep the parents informed of their newborn's condition and progress. Closely assess the newborn during feeding and report any difficulty with swallowing. Provide parent teaching. Demonstrate and reinforce all teaching prior to discharge.

MANGEMENT\

Promote and support successful breastfeeding or bottle-feeding. Assess infant for skin abnormalities noting yellowing of skin or sclera. Assess for risk factors that may increase bilirubin levels. Establish nursery protocols for identifying jaundice, including when a serum bilirubin can be ordered by a nurse. Monitor for increased temperature/fever. Measure total serum bilirubin on jaundiced infants in the first 24 hours. Interpret all bilirubin levels according to the infant's age in hours. Visual estimation of jaundice is inaccurate and shouldn't be used instead of labs. Infants <38 weeks, particularly if breastfed, should be considered high risk. Perform risk assessment on all newborns prior to discharge. Jaundiced newborns should be treated, if indicated, with phototherapy. Provide parents with written and oral information about jaundice at discharge. Follow-up care and referrals should be based on time of discharge and risk. Empower parents to make appropriate decisions once hom REDUCING BILIRUBIN LEVELS Encourage early initiation of feedings to prevent hypoglycemia and provide protein to maintain the albumin levels to transport bilirubin to the liver. Ensure newborn feedings (breast milk or formula) every 2 to 3 hours to promote prompt emptying of bilirubin from the bowel. Encourage the mother to breastfeed (eight to 12 feedings per day) to prevent inadequate intake and thus dehydration. Supplement breast milk with formula to supply protein if bilirubin levels continue to increase with breastfeeding only. Monitor serum bilirubin levels frequently to reduce the risk of severe hyperbilirubinemia.

HEALTH HISTORY AND PHYSICAL EXAMINATION

Review the perinatal history for risk factors related to TTN such as absence of labor, cesarean birth, precipitous delivery, prolonged labor, fetal macrosomia, infants born early, male gender, or maternal asthma and maternal smoking. Those factors are associated with a higher risk of TTN (Martin et al., 2020). Closely assess the newborn for signs of TTN. Within the first few hours of birth, observe for tachypnea, expiratory grunting, retractions, labored breathing, nasal flaring, and mild cyanosis. Mild to moderate respiratory distress is present by 6 hours of age; with respiratory rates as high as 100 to 140 breaths per minute. Also inspect the newborn's chest for hyperextension or a barrel shape. Auscultate breath sounds, which may be slightly diminished secondary to reduced air entry LABORATORY AND DIAGNOSTIC TESTING To aid in the diagnosis, a chest x-ray may be done. It usually reveals mild symmetric lung overaeration and prominent perihilar interstitial markings and streaking. These findings correlate with lymphatic engorgement of retained fetal fluid. In addition, an arterial blood gas (ABG) assessment is important to ascertain the degree of gas exchange and acid-base balance. It typically demonstrates mild hypoxemia, mildly elevated CO2, and a normal pH -As the retained lung fluid is absorbed by the infant's lymphatic system, the pulmonary status improves. Nursing management focuses on providing adequate oxygenation and determining whether the newborn's respiratory manifestations appear to be resolving or persisting. Provide supportive care while the retained lung fluid is reabsorbed. Administer intravenous (IV) fluids and/or gavage feedings until the respiratory rate decreases enough to allow safe oral feeding. Provide supplemental oxygen via a nasal cannula N MAINTAIN THERMOREGU

promoting comofrt

Supportive interventions to promote comfort include swaddling, low lighting, gentle handling, quiet environment with minimal stimulation, use of soft voices, pacifiers to promote "self-soothing," frequent small feedings, Kangaroo care, vertical rocking during infant disorganization periods, and rooming-in and positioning (Kondili & Duryea, 2019). Keep environmental stimuli to a minimum. For example, decrease stimuli by dimming the lights in the nursery, and swaddle the newborn tightly to decrease irritability behaviors. Other techniques such as gentle rocking, using a flexed position, and offering a pacifier can help manage CNS irritability. A pacifier also helps satisfy the newborn's need for nonnutritive sucking. Swaddling, pacifiers, low lighting, oscillating cribs, and avoidance of abrupt changes in the infant's environment can be helpful. Use a calm, gentle approach when handling the newborn and plan activities to avoid overstimulating the newborn, allowing time for rest periods MEETING NUTRITIONAL NEEDS Newborns suffering from NAS have impaired feeding behaviors, such as excessive sucking, poor feeding, regurgitation, and diarrhea, which may cause weight loss. To improve weight gain, they are supplemented with high-calorie formula. When feeding the newborn, use small amounts and position the newborn upright to prevent aspiration and to facilitate rhythmic sucking and swallowing. Frequent small feedings are preferable and should provide 150 to 250 kcal/kg per 24 hours for proper growth of the infant undergoing significant withdrawal (McQueen et al., 2019). Breastfeeding is encouraged unless the mother is still using drugs. Monitor the newborn's weight daily to evaluate the success of food intake. Assess hydration; check skin turgor and fontanels. Assess the frequency and characteristics of bowel movemen

Surgery to Repair Omphalocele and Gastroschisis

Surgical repair of gastroschisis is an emergency due to the high risk of intestinal atresia, resulting in obstruction. Primary repair of gastroschisis is usually performed without incident, unless the contents are unable to fit into the abdominal cavity. This occurs more often with a large omphalocele, requiring the surgeon to do a staged closure. This involves covering the defect with a synthetic material that is sequentially squeezed like toothpaste to reduce the defect into the abdominal cavity. After enough of the defect is in the abdominal cavity, a surgical repair is then performed (Brown, 2020). If damage to the exposed organs occurs, such as necrosis, then the necrotic sections are removed during the repair. If a significant amount of small intestine is lost, then the complication of short bowel syndrome may occur. Anorectal Malformations An imperforate anus is a rare birth defect that includes the absence or abnormal location of a normal anal opening (anus) and is identified in the newborn period. The rectum may end in a blind pouch that does not connect to the colon, or it may have fistulas (openings) between the rectum and the perineum (the vagina in girls or the urethra in boys) (Fig. 24.10). The malformations occur during early fetal development and may be associated with numerous other congenital anomalies. Elimination of feces may not be possible until surgery is performed (NORD, 2020c) in other body systems. Refer to Box 24.6 for anomalies associated with anorectal malformations. Imperforate anus occurs in about one of every 4,000 to 5,000 live births (NORD, 2020c). The defect can be further classified as a high or low type, depending on its level. The level significantly influences the outcome in terms of fecal continence as well as management Surgical intervention is needed for both high and low typ

ASSESSMENT

Temperature instability Hypotension Tachycardia Pallor or duskiness Hypotonia Cyanosis Poor weight gain Irritability Seizures Rash Petechiae Jaundice Grunting Nasal flaring Apnea Lethargy Hypoglycemia Poor feeding (lack of interest in feeding) Abdominal distention

Periventricular-Intraventricular Hemorrhage (PIVH)

The immaturity of the preterm infant's brain makes it vulnerable to injury. The area most vulnerable is the periventricular area. The periventricular area is the rim of brain tissue that lines the outside of the lateral ventricles. Each ventricular area contains a rich network of capillaries which are extremely fragile and can rupture easily. The tremendous physiologic stress during the birth process can cause these vessels to rupture and bleed into the periventricular area (PVH). If the bleeding persists, the expanding volume of blood dissects into the adjacent lateral ventricles leading to an intraventricular hemorrhage (IVH). PIVH occurs in up to 45% of infants with birth weight less than 1,500 g and/or born at less than 35 weeks' gestation. PATHIO The pathogenesis of PIVH is attributed to the intrinsic weakness of germinal vasculature and to the fluctuation in the cerebral blood flow. Genetics appear to play a role in this condition (Blackburn, 2018). The preterm newborn is at greatest risk for IVH because cerebral vascular development is immature, making it more vulnerable to injury. The earlier the newborn is, the greater the likelihood for brain damage. While all areas of the brain can be injured, the periventricular area is the most vulnerable Each ventricular area contains a rich network of capillaries that are very thin, fragile, and easily ruptured. The causes of rupture vary and include fluctuations in systemic and cerebral blood flow, increases in cerebral blood flow from hypertension, IV infusions, seizure activity, increases in cerebral venous pressure due to vaginal delivery, hypoxia, and respiratory distress. With a preterm birth, the fetus is suddenly transported from a well-controlled uterine environment into a highly stimulating one. This tremendous physiologic shock can cause hemorrhage within 72h

PATHIO

The pathophysiology of MAS is complex, and the timing of the insult resulting in aspiration remains controversial. Meconium may be passed in utero secondary to hypoxic stress. Hypoxia induces the fetus to gasp or attempt to breathe. The fetus may bear down and pass meconium into the amniotic fluid or he or she may experience a vagal reflex that causes relaxation of the anal sphincter, allowing meconium to be passed into the amniotic fluid. The fetus then sucks or swallows this amniotic fluid in utero, or the infant may aspirate meconium with the first breath after birth as air rushes into the lungs. -When aspirated into the lungs, meconium blocks the bronchioles, causing an inflammatory reaction as well as a decrease in surfactant production. Gas exchange is impaired and atelectasis occurs. A ball-valve effect occurs when air is inspired into the alveoli but cannot be fully expired secondary to reduced airway diameter. Significant respiratory distress is followed by persistent pulmonary hypertension, right-to-left shunting of blood, and patent ductus arteriosus. Management focuses on appropriate oxygenation, ventilation, improvement of persistent pulmonary hypertension, and maintenance of systemic circulation, which is largely symptomatic and supportive

PATHIO

The pathophysiology of NEC is not clearly understood and is thought to be multifactorial in nature. Current research points to three major pathologic mechanisms that lead to NEC: bowel hypoxic-ischemia events, perinatal stressors, an immature intestinal barrier, abnormal bacterial colonization, and formula feeding. The intestine of a preterm infant is characterized underdeveloped immune defenses and compromised mucosal barrier function. As a result, the immune intestine is susceptible to bacterial colonization by opportunistic pathogens, which follows oral feeding, which in turn incites an inflammatory response -During perinatal or postnatal stress, oxygen is shunted away from the gut to more important organs such as the heart and brain. Ischemia and intestinal wall damage occur, allowing bacteria to invade. High-solute feedings allow bacteria to flourish. Mucosal or transmucosal necrosis of part of the intestine occurs. Although any region of the bowel can be affected, the distal ileum and proximal colon are the region's most commonly involved. NEC usually occurs between 3 and 12 days of life, but it can occur weeks later in some newborns (Blackburn, 2018). The most effective prevention strategy for NEC is the use of human milk. It is well documented that newborns exclusively breastfed have a reduced risk of NEC.

BILLRUNIN

The rate and amount of bilirubin conjugation depend on the rate of red blood cell breakdown, the bilirubin load, the maturity of the liver, and the number of albumin-binding sites. Bilirubin levels rise in newborns by three main mechanisms: increased production (accelerated RBC breakdown), decreased removal (transient liver enzyme insufficiency), and increased reabsorption (delay in bowel excretion) (Wong & Bhutani, 2020). Bilirubin production increases after birth mainly -because of a shortened red blood cell lifespan (70 days in the newborn versus 90 days in the adult) combined with an increased red blood cell mass. Therefore, the amount of bilirubin the newborn must deal with is large compared to that of an adult.

Transient Tachypnea of the Newborn

Transient tachypnea of the newborn (TTN) is a self-limiting condition characterized by inadequate or delayed clearance of lung fluid leading to transient pulmonary edema. The newborn experiences a mild degree of respiratory distress that requires minimal intervention. It usually occurs within a few hours of birth and resolves by 72 hours of age. TTN occurs in approximately 1% to 2% of all live births and incidence is higher in males than females (Jha & Makker, 2020). Lower gestational age, cesarean birth, a perinatal hypoxic stress event, and male sex are independent risk factors for TTN. Performing elective cesarean sections no earlier than 39 weeks' gestation may decrease the risk of TTN. Labor before a cesarean section is not sufficient to decrease the frequency of TTN, even after 37 weeks' gestation, whereas vaginal birth appears to be protective against it Pathophysiology Most newborns make the transition from fetal to newborn life without incident. During fetal life, the lungs are filled with a serous fluid because the placenta, not the lungs, is used for nutrient and gas exchange. During and after birth, this fluid must be removed and replaced with air. An infant born by cesarean birth is at risk of having excessive pulmonary fluid as a result of not having experienced all the stages of labor. Passage through the birth canal during a vaginal birth compresses the thorax, which helps remove the majority of this fluid. Pulmonary circulation and the lymphatic drainage remove the remaining fluid shortly after birth. TTN occurs when the liquid in the lung is removed slowly or incompletely. - However, the symptoms of transient tachypnea rarely last more than 72 hours and if they d

NURSING ASSESSMENT

Trauma: injury to the central or peripheral nervous system secondary to a long or difficult labor, a precipitous birth, multiple gestation, abnormal presentation, cephalopelvic disproportion, shoulder dystocia, or extraction by forceps or vacuum Intrauterine asphyxia: for example, fetal hypoxia secondary to maternal hypoxia, diabetes, hypertension, anemia, cord compression, or meconium aspiration Sepsis: acquired bacterial or viral organisms from infected amniotic fluid, maternal infection, or direct contact while passing through the birth canal Malformation: congenital anomalies including facial or upper airway deformities, renal anomalies, pulmonary hypoplasia, neuromuscular disorders, esophageal atresia, or neural tube defects Hypovolemic shock: secondary to placental abruption, placenta previa, or cord rupture resulting in blood loss to the fetus -Medication: drugs given to mother during labor that can affect the fetus by causing placental hypoperfusion and hypotension; use of hypnotics, excessive maternal oxytocin administered, analgesics, anesthetics, narcotics, oxytocin, and street drugs during pregnancy ---------------------- Observe the infant's color, noting any pallor or cyanosis. Assess the work of breathing. Be alert for apnea, tachypnea, gasping respirations, grunting, nasal flaring, or retractions. Evaluate heart rate and note bradycardia. Assess the newborn's temperature, noting hypothermia. Determine the Apgar score at 1 and 5 minutes; if less than 7 at 5 minutes, repeat the assessment at 10 minutes of age. If the initial assessment is poor, begin resuscitation measures until the Apgar score is above 7. ------------ Laboratory or diagnostic testing may be used to identify etiologies for the newborn's asphyxia. For example, a chest x-ray may identify structural abnormalities that might interfere

hyperbillubemenia

Usually seen within the first few days after birth, manifested by a yellow appearance of the sclera and skin Excessive red cell hemolysis necessary to break down increased RBCs in circulation due to polycythemia Resultant elevated bilirubin levels Excessive bruising secondary to birth trauma of macrosomic infants, further adding to high bilirubin levels - If untreated, high levels of unconjugated bilirubin may lead to kernicterus (neurologic syndrome that results in irreversible damage) with long-term sequelae that include cerebral palsy, sensorineural hearing loss, and mental retardation.

polycethemia

Venous hematocrit of >65% in the newborn Increased oxygen consumption by IDM secondary to fetal hyperglycemia and hyperinsulinemia Increased fetal erythropoiesis secondary to intrauterine hypoxia due to placental insufficiency from maternal diabetes Hypoxic stimulation of increased red blood cell (RBC) production as compensatory mechanism - Increased viscosity, resulting in poor blood flow predisposing newborn to decreased tissue oxygenation and development of microthrombi

INFANTS OF DABIETES

preterm birth, macrosomia, asphyxia, respiratory distress, hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia and hyperviscosity, hypertrophic cardiomyopathy, and congenital anomalies, particularly of the central nervous system. Overt type 1 diabetes around conception produces marked risk of neural tube defects, cardiac defects, and caudal regression syndrome; later in gestation, severe and unstable type 1 maternal diabetes carries a higher risk of intrauterine growth restriction, asphyxia, and fetal death. IDMs born to mothers with type 2 diabetes are more commonly obese (macrosomic) with milder conditions of the common problems found in IDMs. IDMs from all causes of GDM also are predisposed to later-life risk of obesity, diabetes, and cardiovascular disease

RESPIRATORY DITRESS SYNDROME

respiratory distress syndrome, a breathing disorder resulting from lung immaturity and lack of alveolar surfactant, which keeps the air sacs in the lungs from collapsing and allows them to inflate easily. Without surfactant, the alveoli collapse at the end of expiration. Since the link between RDS and surfactant deficiency was discovered more than 30 years ago, tremendous strides have been made in understanding the pathophysiology and treatment of this disorder. The introduction of prenatal steroids to accelerate lung maturity and the development of synthetic surfactant can be credited with the dramatic improvements in the outcome of newborns with RDS

fetal alcohol syndrome

• Microcephaly (head circumference <10th percentile)a • Small palpebral (eyelid) fissuresa • Abnormally small eyes • Fetal growth restriction • Maxillary hypoplasia (flattened or absent) • Epicanthal folds (folds of skin of the upper eyelid over the eye) • Thin upper lipa • Missing vertical groove in median portion of upper lipa • Short upturned nose • Short birth length and low birth weight • Joint and limb defects • Small-for-gestational age • Altered palmar crease pattern Prenatal or postnatal growth ≤10th percentilea • Congenital cardiac defects (septal defects) • Delayed fine and gross motor development • Poor eye-hand coordination • Clinically significant brain abnormalitiesa • Mentally challenged • Narrow forehead • Performance substantially below expected level in cognitive or developmental functioning, executive or motor functioning, and attention or hyperactivity; social or language skillsa • Inadequate sucking reflex and poor appetite