Neonatal and Pediatric Respiratory Care

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Neonatal and Pediatric Respiratory Care

Daniel W. Chipman and Patricia English

Caring for infants and children is one of the most challenging and rewarding aspects of respiratory care. Competent clinical practice in this area requires knowledge of the many pathophysiologic differences among infants, children, and adults. Understanding the unique pathophysiology involved in neonatal and pediatric respiratory disorders (see Chapter 31) can assist the respiratory therapist (RT) in providing quality care to infants and children. A thorough understanding of how the respiratory system develops in the fetus is the first step toward acquiring the specialized knowledge needed to practice neonatal respiratory care (see Chapter 8). This chapter begins with an overview of neonatal and pediatric patient assessment and then describes respiratory care modalities used to treat these patients.

Assessment of the Newborn

Assessment of the newborn begins before birth with assessment of the maternal history, the maternal condition, and the status of the fetus.

Maternal Factors

Maternal risk factors include many medical, physical, and social conditions. Maternal health and individual physiology, pregnancy complications, and maternal behaviors affect the health of the fetus. Any condition that causes an interference with placental blood flow or the transfer of oxygen (O2) to the fetus can result in an adverse outcome. The clinician must be prepared for the possibility of resuscitation at delivery. This possibility is best anticipated by identifying risk factors that relate to neonatal compromise. Table 48-1 lists maternal risks and related outcomes of which the team preparing to receive the infant should be aware when the infant is delivered.

TABLE 48-1

Maternal Condition and Neonatal Outcomes

Maternal Condition Fetal or Neonatal Outcome
Previous pregnancy complication Same outcome as previous fetus
Diabetes mellitus LGA, congenital malformations, RDS, hypoglycemia
Pregnancy-induced hypertension Prematurity, SGA (preeclampsia)
Maternal age <17 years Low birth weight, prematurity
Maternal age >35 years Prematurity, chromosomal defects
Placenta previa Prematurity, bleeding, SGA
Abruptio placentae Fetal asphyxia, bleeding
Alcohol consumption SGA, CNS dysfunction, mental retardation, facial dysmorphology
Smoking SGA, prematurity, mental retardation, SIDS
Drug use Placental abruption, IUGR, prematurity, CNS abnormalities, withdrawal disorders

IUGR, Intrauterine growth restriction; RDS, respiratory distress syndrome; SIDS, sudden infant death syndrome.

Fetal Assessment

Fetal assessment is performed with ultrasonography, amniocentesis, fetal heart rate monitoring, and fetal blood gas analysis. Ultrasonography uses high-frequency sound waves to obtain an image of the infant in utero. This image allows the physician to view the position of the fetus and placenta, measure fetal growth, identify possible anatomic anomalies, and assess the amniotic fluid qualitatively.

Amniocentesis involves direct sampling and quantitative assessment of amniotic fluid. Amniotic fluid may be inspected for meconium (fetal bowel contents) or blood. In addition, sloughed fetal cells can be analyzed for genetic normality. Lung maturation can be assessed with amniocentesis. The lecithin-to-sphingomyelin ratio (L : S ratio) involves measurement of two phospholipids, lethicin and sphingomyelin, synthesized by the fetus in utero. As shown in Figure 48-1, the L : S ratio increases with increasing gestational age. At approximately 34 to 35 weeks’ gestation, this ratio abruptly increases to greater than 2 : 1. An L : S ratio greater than 2 : 1 indicates stable surfactant production and mature lungs. Phosphatidylglycerol is another lipid found in the amniotic fluid that is used to assess fetal lung maturity. Phosphatidylglycerol first appears at approximately 35 to 36 weeks’ gestation. If phosphatidylglycerol is more than 1% of the total phospholipids, the risk of respiratory distress syndrome is less than 1%.

Fetal heart rate monitoring is the measurement of fetal heart rate and uterine contractions during labor. Examination of fetal heart rate changes related to uterine contractions identifies a fetus in distress. Fetal well-being is obtained by examining the variability and reactivity of the fetal heart rate. A normal fetal heart rate ranges from 120 to 160 beats/min. Fetal tachycardia can be a sign of fetal hypoxemia or could be related to other factors, such as prematurity or maternal fever. Temporary declines in fetal heart rate are called decelerations and can be mild (<15 beats/min), moderate (15 to 45 beats/min), or severe (>45 beats/min). Decelerations are classified by their occurrence in the uterine contraction cycle.

Figure 48-2 illustrates the three common patterns of early decelerations, late decelerations, and variable decelerations. Early decelerations occur when the fetal heart rate decreases in the beginning of a contraction. This type of deceleration is benign and in most cases is caused by a vagal response related to compression of the fetal head in the birth canal. A late deceleration occurs when the heart rate decreases 10 to 30 seconds after the onset of contractions. A late deceleration pattern indicates impaired maternal-placental blood flow, or uteroplacental insufficiency. With variable decelerations, there is no clear relationship between contractions and heart rate. This pattern is the most common of the three and probably related to umbilical cord compression. Short periods of cord compression are generally benign, but prolonged periods of compression result in impaired umbilical blood flow and can lead to fetal distress. Fetal heart rate variability is the beat-to-beat variation in rate that occurs because of normal sympathetic or parasympathetic influences. A completely monotonous heart rate tracing may be indicative of fetal asphyxia. Fetal heart rate reactivity is the ability of the fetal heart rate to increase in response to movement or external stimuli. A healthy fetus has two accelerations within a 20-minute period.

In utero, the fetus receives its blood supply from the placenta. Only a small portion of the blood that enters the fetal right heart flows through the lungs. This is a result of fetal pulmonary blood vessels being constricted with a high resistance to blood flow. There are two openings in the fetal heart through which most fetal blood flows. These normal anatomic shunts in the fetus are called patent foramen ovale and patent ductus arteriosus (PDA). Blood flows through these openings and into the umbilical vessels before returning to the mother. Pressure in the umbilical vessels is low. During the transition from fetal life to newborn life, the umbilical cord is clamped, and the infant’s systemic blood pressure is increased. The infant begins to breathe, and O2 enters the infant’s blood. Oxygenated blood entering the pulmonary vessels causes the vessels to dilate and decreases pulmonary resistance. With higher systemic resistance and lower pulmonary resistance, less blood flows through the anatomic openings, and these openings begin to close. Evidence of normal transitional circulation is noted as the infant’s skin turns from a bluish hue to pink over the first several minutes of life.

Evaluation of the Newborn

All newborns should be assessed immediately on delivery. Most newborns (>90%) do not need intervention when transitioning from intrauterine to extrauterine life. The two categories of newborns most likely to need intervention are infants born with evidence of meconium in their airway and premature infants. The need for intervention is determined by assessing for the presence of meconium, breathing or crying, muscle tone, color, and gestational age.

Meconium is the medical term for the infant’s first stools. It is a sticky green-black substance that if inhaled by the infant can cause significant respiratory problems. It is most likely present in a term or postterm newborn. Term infants delivered without evidence of meconium who are crying or breathing and have good tone should not routinely be separated from the mother. They should be dried, covered, and given to the mother and observed for breathing, activity, and color. If meconium is present and the infant is vigorous, pharyngeal suctioning with a bulb suction is appropriate. Simultaneously the infant should be dried and placed under a warmer and assessed for signs of respiratory distress. See later section on Respiratory Assessment of the Infant. If meconium is present in a nonvigorous infant, stimulation should be avoided.

Immediate endotracheal intubation before positive pressure ventilation (PPV) is indicated as a means to clear meconium from the airway. The endotracheal tube should be attached to a meconium aspirator, and a suction device should be regulated for −70 to −100 mm Hg. As soon as the endotracheal tube is inserted, suction should be applied to the tube, and then the endotracheal tube is withdrawn. Reintubation and repeat suctioning may be necessary if meconium is still visible in the airway. Frequent assessment of the heart rate is indicated during this process, and if bradycardia is present, bag-mask ventilation should be considered. Intubation of the trachea is not recommended in a vigorous infant with meconium. Preterm infants frequently need intervention. The more preterm the infant, the more likely the infant will need some level of resuscitation. If an infant is preterm, is not breathing, is not vigorous, or does not have good tone, resuscitation efforts should be initiated. Efforts are directed at warming the infant because cold stress may increase O2 consumption and impair all subsequent resuscitation efforts.

After the infant is dried and warmed, the infant is positioned supine, with the head in a neutral position or slightly extended. A bulb syringe or 8F to 10F suction catheter may be used for secretion removal; however, in the absence of blood or meconium, catheter suctioning should be limited because aggressive pharyngeal suctioning may cause laryngospasm or bradycardia. Suction pressure should not exceed −100 mm Hg. Once the infant is suctioned, dried, and warmed, if apnea or inadequate respirations are present, tactile stimulation may be used to encourage spontaneous breathing. Many infants respond to stimulation and need no further resuscitative efforts. If after 30 seconds the infant has a heart rate of less than 100 beats/min or is apneic, bag-mask ventilation at a rate of 40 to 60 beats/min should be initiated.

The most important and effective action in neonatal resuscitation is effective ventilation. Recommendations from the American Academy of Pediatrics are to attach a pulse oximeter to the infant, begin resuscitation efforts using room air, and assess carefully the amount of O2 needed.1 Effective PPV usually results in rapid improvement of heart rate. Initial ventilating pressures of 30 to 40 cm H2O may be necessary to achieve noticeable chest movement, particularly in a preterm newborn with surfactant deficiency. Continuous assessment of the lowest pressure needed to observe the chest rise is essential throughout the resuscitation. After application of PPV for 30 seconds, the heart rate is reassessed. If the heart rate is less than 60 beats/min, chest compressions are begun, and PPV is maintained. If the heart rate remains less than 60 beats/min after adequate ventilation with 100% O2 and chest compressions for 30 seconds, appropriate medications are given. As soon as the heart rate is noted to be greater than 100 beats/min, compressions are discontinued. If spontaneous breathing is present, PPV may be gradually reduced and then discontinued. If spontaneous breathing remains inadequate or if heart rate remains less than 100 beats/min, assisted ventilation is continued via bag-mask or endotracheal tube. Figure 48-3 outlines a newborn resuscitation algorithm and includes the targeted saturation levels for the first 10 minutes of life.

Apgar Score

An Apgar score is assigned at 1 minute and 5 minutes of life. The Apgar score is an objective scoring system used to evaluate a newborn rapidly. As shown in Table 48-2, the score has five components: heart rate, respiratory effort, muscle tone, reflex irritability, and skin color. Each component is rated according to standard definitions, resulting in a composite assessment score. Generally, infants scoring 7 or higher at 1 minute are responding normally. An infant with a score of 7 may require supportive care, such as O2 or stimulation to breathe. Infants with a 1-minute Apgar score of 6 or lower may require more aggressive support.

TABLE 48-2

Apgar Scoring System for Newborn Assessment

  Score
Sign 0 1 2
Heart rate Absent <100/min >100/min
Respirations Absent Slow, irregular Good, crying
Muscle tone Limp Some flexion Active motion
Reflex irritability (catheter in nares, tactile stimulation) No response Grimace Cough, sneeze, cry
Color Blue or pale Pink body with completely blue extremities Pink

image

From Koff PB, Eitzman DV, Neu J: Neonatal and pediatric respiratory care, ed 2, St Louis, 1993, Mosby.

Assessment of Gestational Age

Gestational age assessment and assessment of relationship of weight to gestational age are performed shortly after delivery. Determination of gestational age involves assessment of multiple physical characteristics and neurologic signs. Two common systems are used to determine gestational age: the Dubowitz scales and the Ballard scales. The Dubowitz scales involve assessment of 11 physical and 10 neurologic signs.2 Physical criteria include assessment of skin texture, skin color, and genitalia. Neurologic criteria include posture and arm and leg recoil. The Ballard scales are a simplified version of the Dubowitz scales and include six physical and six neurologic signs as illustrated in Figure 48-4. Soon after delivery, the newborn is stabilized and weighed, followed by determination of gestational age. Infants born between 38 weeks and 42 weeks are considered term gestation. Infants born before 38 weeks are preterm. Infants born after 42 weeks are postterm.

All newborns weighing less than 2500 g are considered low birth weight. Newborns weighing less than 1500 g are considered very low birth weight (VLBW). Newborns weighing less than 1000 g are considered extremely low birth weight (ELBW). A newborn with a weight that is either too large or too small or who has been born preterm or postterm has a higher risk of morbidity and mortality. As shown in Figure 48-5, by plotting the infant’s gestational age against weight, the newborn’s relative developmental status can be classified. Infants whose weight falls between the 10th and 90th percentiles are appropriate for gestational age (AGA). Infants whose weight is above the 90th percentile are large for gestational age (LGA). Infants whose weight is below the 10th percentile are small for gestational age (SGA).

By classifying infants into one of the combined categories, such as “preterm, AGA,” the clinician can help identify infants at highest risk and predict the nature of the risks involved and the likely mortality rate. Small, preterm infants are at highest risk. Compared with term infants, the lungs of these infants are not yet fully prepared for gas exchange. In addition, their digestive tracts cannot normally absorb fat, and their immune systems are not yet capable of warding off infection. Small, preterm infants also have a very large surface area-to-body weight ratio; this increases heat loss and impairs thermoregulation. Finally, the vasculature of these small infants is less well developed, increasing the likelihood of hemorrhage (especially in the ventricles of the brain).

Respiratory Assessment of the Infant

Not all respiratory problems occur at birth; many respiratory disorders develop after birth and may develop slowly or suddenly. RTs are commonly called on to help assess and treat infants who develop respiratory distress after birth.

Physical Assessment

Physical assessment of the infant begins with measurement of vital signs. A normal newborn respiratory rate is 40 to 60 breaths/min. The lower the gestational age, the higher the normal respiratory rate will be. A 28-week gestational age infant may normally breathe 60 times a minute, whereas the rate more typical of a term newborn is 40 breaths/min. Tachypnea (>60 breaths/min) can occur because of hypoxemia, acidosis, anxiety, or pain. Respiratory rates less than 40 breaths/min should be interpreted with previous trends of the newborn’s respiratory rate. A baseline respiratory rate of 36 breaths/min in a term newborn is within normal limits; however, a respiratory rate of 36 breaths/min in a preterm newborn previously breathing at 70 breaths/min may indicate compromise. Causes of slow respiratory rates include medications, hypothermia, or neurologic impairment.

Normal infant heart rates range from 100 to 160 beats/min. Heart rate can be assessed by auscultation of the apical pulse, normally located at the fifth intercostal space, midclavicular line. Alternatively, the brachial and femoral pulses may be used. Weak pulses indicate hypotension, shock, or vasoconstriction. Bounding peripheral pulses occur with major left-to-right shunting through a patent ductus arteriosus (PDA).3A strong brachial pulse in the presence of a weak femoral pulse suggests either PDA or coarctation of the aorta. Table 48-3 lists normal ranges of blood pressure for neonates of different sizes.

TABLE 48-3

Normal Neonatal Blood Pressures

Weight (g) Systolic (mm Hg) Diastolic (mm Hg)
750 35-45 14-34
1000 39-59 16-36
1500 40-61 19-39
3000 51-72 27-46

image

From Whitaker K: Comprehensive perinatal and pediatric respiratory care, ed 3, Albany, NY, 2001, Delmar.

Chest examination in an infant is more difficult to perform and interpret than in an adult because of the small chest size and the ease of sound transmission through the infant chest. Thorough observation of the infant greatly enhances the assessment data obtained. Infants in respiratory distress typically exhibit one or more key physical signs: nasal flaring, cyanosis, expiratory grunting, tachypnea, retractions, and paradoxical breathing. Nasal flaring is seen as dilation of the ala nasi on inspiration. The extent of flaring varies according to facial structure of the infant. Nasal flaring coincides with an increase in work of breathing. In concept, nasal flaring decreases the resistance to airflow. It also may help stabilize the upper airway by minimizing negative pharyngeal pressure during inspiration.4 Cyanosis may be absent in infants with anemia, even when arterial partial pressure of oxygen (PaO2) levels are decreased. In addition, infants with elevated fetal hemoglobin levels may not become cyanotic until PaO2 decreases to less than 30 mm Hg. Hyperbilirubinemia, common among newborns, may mask cyanosis. Grunting occurs when infants exhale against a partially closed glottis. By increasing airway pressure during expiration, grunting helps prevent airway closure and alveolar collapse. Grunting is most common in infants with respiratory distress syndrome, but it is also seen in other respiratory disorders associated with alveolar collapse. Figure 48-6 illustrates the Silverman score, which is a system of grading severity of lung disease.

Retractions refer to the drawing in of chest wall skin between bony structures. Retractions can occur in the suprasternal, substernal, and intercostal regions. Retractions indicate an increase in work of breathing, especially because of decreased pulmonary compliance. Paradoxical breathing in infants differs from paradoxical breathing normally seen in adults. Instead of drawing the abdomen in during inspiration, an infant with paradoxical breathing tends to draw in the chest wall. This inward movement of the chest wall may range in severity. As with retractions, paradoxical breathing indicates an increase in ventilatory work. Applying continuous positive airway pressure (CPAP) to a newborn exhibiting signs of respiratory distress including grunting, flaring, and retracting may help to increase lung volume and improve gas exchange. The benefits of CPAP in children are discussed in more detail later.

Surfactant

Surfactant production begins around the 24th week of gestation and continues through gestation. Surfactant contributes to the stability of the alveolar sacs by reducing the surface tension of the fluids that coat the alveoli. Surfactant deficiency places an infant at increased risk for respiratory distress. By about 34 weeks’ gestation, most infants have produced enough surfactant to keep the alveoli from collapsing. There are two specific approaches to preventing and treating surfactant deficiency. Surfactant deficiency is due to lung immaturity. When a premature delivery is anticipated, steroids are given to the mother to help promote lung maturation. In addition, infants born before 35 weeks’ gestation, especially infants born very prematurely (<30 weeks), should be assessed for the need to receive exogenous surfactant. The need for surfactant is determined by assessing the infant’s lung volume on chest x-ray, evaluating the inspired O2 concentration to maintain O2 saturations greater than approximately 88%, and clinically assessing the infant’s work of breathing. Once surfactant deficiency is determined, administering exogenous surfactant as soon as possible has been found to be most beneficial.5

Surfactant administration has also been shown to be useful in conditions in which surfactant function has been altered. These conditions include meconium aspiration, neonatal pneumonia, and pulmonary hemorrhage. Administration of surfactant requires intubation. It is essential to ensure the endotracheal tube is properly positioned, approximately 0.5 to 1 cm above the carina, before delivering surfactant. The dose depends on the specific brand of surfactant being administered. Close monitoring of the infant’s vital signs, O2 saturation, and compliance is necessary during and after surfactant administration. Soon after surfactant is delivered, the infant’s compliance should begin to increase resulting in improved gas exchange. Ventilating pressures and fractional inspired oxygen (FiO2) need to be decreased to avoid lung injury and excessive partial pressure of O2. The ventilating pressure should be decreased to the level that maintains a tidal volume (VT) of 5 to 7 ml/kg. FiO2 should be decreased to maintain an oxygen saturation level (SpO2) of approximately 88% to 92% in preterm infants and to the lowest FiO2 possible to maintain SpO2 greater than 95% in term or postterm infants.

Blood Gas and Pulse Oximetry Analysis

Blood gas analysis is helpful in assessing respiratory distress in an infant. Many noninvasive techniques, such as transcutaneous partial pressure of oxygen (PtcO2), transcutaneous partial pressure of carbon dioxide (PtcCO2), end tidal carbon dioxide (CO2), and pulse oximetry (SpO2), are used to obtain comparable data, although blood gas analysis is more precise when results are critical. An infant blood gas sample can be obtained from an artery or capillary. Chapter 18 summarizes the advantages, disadvantages, and complications of these sampling methods. Care must be taken in assessing the results of capillary sampling. Capillary blood gases provide only information regarding ventilation and acid-base status, and accuracy is highly dependent on technique.6 Normal values for infant blood gases are listed in Table 48-4.

TABLE 48-4

Age-Related Values Commonly Reported for Normal Blood Gases

  Normal Preterm Infants (at 1-5 Hours) Normal Term Infants (at 5 Hours) Normal Preterm Infants (at 5 Days) Children, Adolescents, and Adults
pH (range) 7.33 (7.29-7.37) 7.34 (7.31-7.37) 7.38 (7.34-7.42) 7.40 (7.35-7.45)
PCO2 (range) 47 (39-56) 35 (32-39) 36 (32-41) 40 (35-45)
PO2 (range) 60 (52-68) 74 (62-86) 76 (62-92) 95 (85-100)
HCO3 range 25 (22-23) 19 (18-21) 21 (19-23) 24 (22-26)
BE range −4 (−5 to −2.2) −5 9 (−6 to −2) −3 (−5.8 to −1.2) 0 (−2 to +2)

image

BE, Base excess; HCO3, bicarbonate.

Modified from Orzalesi MM, Mendicini M, Bucci G, et al: Arterial oxygen studies in premature newborns with and without mild respiratory disorders. Arch Dis Child 42:174, 1967. From Koff PB, Eitzman DV, Neu J: Neonatal and pediatric respiratory care, ed 2, St Louis, 1993, Mosby.

Monitoring O2 saturation using a pulse oximeter is a standard of care for sick newborns. Saturation probes must be carefully placed on the newborn; the most common sites are the wrist, the medial surface of the palm, or the foot. Sufficient cardiac output and skin blood flow are essential to provide an accurate saturation value. The pulse rate indicated on the oximeter should correlate with the infant’s actual pulse before any conclusions regarding saturation can be drawn. Intracardiac shunting and intrapulmonary shunting are causes of decreased saturation in sick infants. When interpreting saturation levels in a newborn, it is important to consider where the saturation is being monitored. Saturation probes placed on the right hand assess preductal saturations. Probes placed on other extremities indicate postductal saturation levels. Infants at risk for pulmonary hypertension should have saturation probes placed to monitor preductal and postductal saturations. A large difference (>5%) between the two readings should prompt the clinician to consider pulmonary hypertension as a potential concern. Conditions that prevent the closing of the ductus arteriosus and foramen ovale result in decreased saturation. Many congenital heart defects result in significant intracardiac shunting. Interpreting adequate saturation for a newborn requires knowledge of any cardiac defect along with the infant’s pulmonary condition.

Mini Clini

Neonatal Ventilation

Solution

Because the patient was manually ventilated during transport, it is unclear what VT has been delivered. Initial PIP of 20 cm H2O and PEEP of 5 cm H2O are safe and common settings. Immediate observation of the chest would allow the RT to evaluate chest expansion and adjust PIP as required. Over the next several minutes if VT monitoring is available, targeting VT of 6 to 8 ml/kg would guide subsequent settings.

Set respiratory rate of 40 breaths/min is at the lower end of the normal range for this patient; however, use of the A/C mode with appropriately set trigger sensitivity would allow the patient to establish a more comfortable respiratory rate. Adjustment of the inspiratory time may also be necessary to increase patient comfort and improve patient ventilator synchrony. Further adjustments may be guided by PaCO2. Because this patient was born prematurely, rapid assessment of SpO2 is essential, and FiO2 should be adjusted to maintain SpO2 between 88% and 92%.

This patient should receive surfactant replacement therapy. The clinician may consider volume-targeted, pressure-limited ventilation (e.g., pressure-regulated volume control, volume guarantee) during and immediately after surfactant delivery. This modality may help prevent lung overdistention until compliance has stabilized.44,45

Respiratory Assessment of the Pediatric Patient

Normal breathing in children is evidenced by quiet inspiration and passive expiration at an age-appropriate rate. Respiratory rates are rapid in neonates and decrease in toddlers and older children. Table 48-5 lists normal respiratory rates. The initial assessment of a pediatric patient starts with evaluating airway patency. Normal heart rates are higher in younger children and decrease with age. In assessing a pediatric patient, establishing if the airway is patent or has any obstructive component is essential. Signs that suggest upper airway obstruction include increased inspiratory effort with retractions or inspiratory efforts with no airway or breath sounds.

TABLE 48-5

Normal Respiratory and Heart Rates by Age

Age Breaths/Minute Heart Rates
Infants (<1 yr) 30-60 90-120
Toddler (1-3 yr) 24-40 80-100
Preschooler (4-5 yr) 22-34 70-90
School age (6-12 yr) 18-30 70-90
Adolescent (13-18 yr) 16-22 60-80

The clinician observes for movement of the chest or abdomen. The clinician listens for breath sounds focusing on both inspiratory sounds and expiratory sounds. Chest or abdominal movement without breath sounds may indicate total airway obstruction, and basic life support maneuvers are indicated. High-pitched sounds heard on inspiration (stridor) are often indicative of upper airway conditions, whereas expiratory noises are more often associated with lower airway obstruction.

Causes of stridor in children can be infections, such as croup; foreign body aspiration, particularly in a small child; congenital or acquired airway abnormalities; allergic reactions; or edema after a procedure. Inhaled epinephrine via nebulizer and intravenous steroids are commonly used to treat stridor. Common causes of lower airway obstruction are bronchiolitis and asthma. When wheezing is noted, inhaled bronchodilators are indicated. If the patient is able to use a metered dose inhaler (MDI), repeated inhalations can act quickly to improve aeration. When the patient is unable to use the MDI appropriately or when severe symptoms are present, delivering a bronchodilator with a nebulizer can bring relief. More than one nebulizer treatment often is necessary to relieve airway inflammation. A common approach is to deliver three consecutive treatments. If the patient continues to be symptomatic, continuous bronchodilator therapy may be delivered with a nebulizer attached to an infusion pump set to administer a bronchodilator continuously. Tachycardia secondary to the beta-1 effect of inhaled bronchodilators can be seen. Frequent reassessment of any patient receiving continuous bronchodilator therapy is essential. Heliox, an inhaled mixture of helium and O2 (described in the section on specialty gases), has been shown to be beneficial in cases of some airways conditions in children.

As noted in the section describing newborn assessment, use of accessory muscles, grunting, flaring, and retracting all can be signs of respiratory distress. Head bobbing, noted by chin up and neck extended during inspiration with chin falling during expiration, and seesaw respirations, indicated by the chest retracting and the abdomen expanding during inspiration, are signs of impending respiratory failure. Assessing the child’s level of alertness is essential. Levels of alertness range from fully awake, agitated, minimally responsive, to unresponsive. A child’s ability to protect his or her airway should be questioned in a minimally responsive or unresponsive child.

Respiratory Care

Respiratory care of infants and children incorporates approaches taken from adult practice. Important physiologic and age-related differences between adults and children require variations in the provision of respiratory care. This section focuses on neonatal and pediatric O2 therapy, bronchial hygiene, humidity and aerosol therapy, airway management, and resuscitation.

Oxygen Therapy

Goals and Indications

O2 should be administered as any other drug, using the lowest dose necessary to achieve the intended goal. The goal of O2 therapy is to provide adequate tissue oxygenation. However, O2 therapy is most frequently adjusted according to O2 saturation levels. A clear understanding of the limitation of O2 saturation is needed to interpret the saturation reading and make appropriate decisions. Infants and children receiving O2 therapy have variable O2 saturation target ranges depending on age and underlying condition.

Lower saturation levels are targeted in infants less than 32 weeks’ gestation. There is evidence that exposure to supplemental O2 in a premature infant is a risk factor for the development of retinopathy of prematurity (ROP). ROP is caused by an abnormal vascularization of the retina, which in the most severe cases leads to retinal detachment. Preterm neonates weighing less than 1500 g are most susceptible. Hyperoxia is not the only factor associated with ROP, but close monitoring and adjusting of O2 therapy to avoid hyperoxia is crucial to decrease the risk of ROP. Specific saturation goals for this age group should be established, and O2 should be adjusted to maintain the intended target. Avoiding very high or very low saturation levels is critical. Adjusting the delivered O2 concentration by small increments avoids large swings in saturation levels.711

In a term infant with primary pulmonary hypertension of the newborn (PPHN), a higher targeted saturation level is desired to avoid further pulmonary constriction associated with hypoxemia. The position of the saturation probe needs to be considered when interpreting saturation. Intracardiac shunting can occur in the presence of PPHN. One saturation probe positioned on the upper right extremity represents preductal saturations and is indicative of the saturation of blood being delivered to the brain. O2 saturation measured on other extremities is considered postductal and represents saturation to other parts of the body.

Newborns with certain cardiac anomalies are dependent on their intracardiac shunt through the ductus arteriosus to survive. An increased saturation in newborns promotes constriction of the ductus arteriosus. Although this constriction is normally a positive response, it may cause premature closure of the ductus arteriosus in infants with ductal-dependent congenital heart defects. An infant born with hypoplastic left heart syndrome, a defect in which the left-sided heart structures are poorly developed, relies on the patency of the ductus arteriosus for systemic blood supply. In addition, hyperoxia can increase aortic pressures and systemic vascular resistance, decreasing the cardiac index and O2 transport in children with acyanotic congenital heart disease. The emphasis for O2 therapy for all newborns should be to provide only as much O2 as indicated by the infant’s condition. O2 therapy should be administered using a written care plan with specified clinical outcomes (e.g., titrate flow/FiO2 to maintain SpO2 88% to 92%, notify physician if FiO2 is >0.40).

Methods of Administration

The effectiveness of O2 devices depends on the performance characteristics of the device (delivered FiO2, flow rate, relative humidity), the interface of the device, and the tolerance of the patient for using the device. Children are often frightened and combative, making it impractical to use some O2 administration devices. Selection of an O2 device must be based on the degree of hypoxemia and the emotional and physical needs of the child and family. O2 can be administered to infants and children by mask, cannula, high-flow nasal cannulas, or oxyhood. Table 48-6 compares the advantages and disadvantages of standard O2 delivery methods.

TABLE 48-6

Oxygen Delivery Devices

Device Age FDO2 Advantages Disadvantages
Air entrainment mask ≥3 yr High flow; 0.24-1 Precise FiO2; good for transport; ease of application Low relative humidity; pressure necrosis to face; difficult to fit and maintain on active child, not recommended for infants; risk of aspiration
Nasal cannula Premature infants to adult Low flow; 25 ml/min–6.0 L/min Tolerated well by all ages Inaccurate FiO2; low relative humidity; excessive flows may cause inadvertent CPAP in infants; precise FiO2 may be achieved with O2 blender
Incubator Newborns ≤28 days <0.40 FiO2, combine use with cannula or hood for precise FiO2 Low FiO2 for stable infants; neutral thermal environment for premature infants Varying FiO2; long stabilization time; limits access to child for patient care
Oxyhood Premature infants to ≤6 mo 0.21-1 FiO2 with O2 blender maintained at 30° C to 34° C Warmed and humidified gas at stable FiO2 during routine patient care Overheating may cause apnea and dehydration; underheating may cause O2 consumption; inadequate flow causes CO2 buildup; noise produced by humidification device may cause hearing loss
Mist tent Infants to toddlers High flow; 0.21-0.40 FiO2 Allows child movement, high humidity, cool temperatures Isolation of child from family; wet bedding and clothes; difficult to maintain stable FiO2; risk of cross-contamination; limits patient care

image

FDO2, Delivered oxygen concentration.

Secretion Clearance Techniques

Secretion clearance techniques that can be applied to infants and children include chest physiotherapy, positive expiratory pressure therapy, autogenic drainage, flutter therapy, and mechanical insufflation-exsufflation.12,13 Secretion clearance techniques are considered when accumulated secretions impair pulmonary function and an infiltrate is visible on a chest radiograph. Secretion retention is common in children who have pneumonia, bronchopulmonary dysplasia, cystic fibrosis, bronchiectasis, and some neuromuscular diseases. Figure 48-7 shows postural drainage and percussion positions for infants and children.

Humidity and Aerosol Therapy

Key differences in humidity and aerosol therapy in infants and children include assessment of patient response to therapy, age-related physiologic changes, and equipment application.

Humidity Therapy

In children with an intact upper airway, O2 therapy devices, such as low-flow nasal cannulas, do not routinely need to be humidified When the upper airway is bypassed by intubation, supplemental humidification must be provided using a heated humidifier. Humidification of inspired gases for infants and children receiving mechanical ventilation is commonly provided by a servo-controlled humidifier. Ideal features for these systems include the following: (1) low internal volume and constant water level to minimize compressed volume loss; (2) closed, continuous feed water supply to avoid contamination; (3) distal airway temperature sensor and high/low alarms. Common problems with humidifier systems include condensation in the tubing, inadequate humidification, and hazards associated with the heating coil.15,16 Using heated wire circuits can also reduce condensation in the circuit. Frequent evaluation of the humidification system is necessary to increase the potential of adequate humidity delivered to the airway. Inadequate humidification occurs in nonheated circuits when the humidifier temperature probe is placed too far upstream from the airway connector. Variable humidification problems occur when ventilator circuits pass through an environment and then into a warmed enclosure, such as an incubator or radiant warmer.

Aerosol Drug Therapy

Drug action in infants and children differs significantly from drug action in adults because of differences in physiology, which may include immature enzyme systems, immature receptors, and variable gastrointestinal absorption. Dosing may be imprecise, and systemic effects may be hard to predict. Table 48-7 lists aerosolized medications commonly used in children.

TABLE 48-7

Commonly Used Aerosolized Medications

Medication Name Dosage Form Usual Child Dose Comments
Bronchodilators      
Beta-2 Agonists      
Albuterol (Proventil, Ventolin) MDI (90 mcg/puff) 1-2 puffs MDI q 15 min to q 6 hr ± PRN May be used 15 min before exercise to prevent exercise-induced bronchospasm; should be used as a rescue medication
Nebs (0.5%, 5 mg/ml) 0.01-0.05 ml/kg/dose (maximum 1 ml/dose) neb q 15 min to q 6 hr ± PRN
Rotohaler (200 mcg caps) 1-2 caps inhaled q 15 min to q 6 hr ± PRN
Levalbuterol (Xopenex) Nebs (0.63 mg/3 ml, 1.25 mg/3 ml) 0.32-1.25 mg neb q 6-8 hr ± PRN May still cause extrapulmonary side effects including tachycardia and hypokalemia
Salmeterol (Serevent) MDI (21 mcg/puff) 2 puffs inhalation q 12 hr Not to be used as a rescue medication; long-acting beta-2 agonist; QTC prolongation has occurred in overdose
  DPI-Diskus (50 mcg/inhalation) 1 inhalation q 12 hr
Nonselective Bronchodilator      
Racemic epinephrine (Vaponefrin) Nebs (2.25%) 0.25-0.5 ml neb q 1-4 hr ± PRN If shortage occurs, may use L-epinephrine (1 : 1000) 2.5-5 ml neb q 1-4 hr ± PRN
Anticholinergic      
Ipratropium (Atrovent) MDI (18 mcg/puff) 2 puffs inhalation q 4-6 hr ± PRN MDI is contraindicated in patients with peanut allergy; for neonates, use 25 mcg/kg/dose neb tid; may cause mydriasis if aerosolized drug gets into the eye
  Nebs (0.02%) 0.25-0.5 mg neb q 4-6 hr ± PRN
Antiinflammatory Agents      
Corticosteroids      
Beclomethasone (Beclovent, Vanceril) MDI (42 mcg/puff) 1-2 puffs inhalation qid or 2-4 puffs inhalation bid Start at lower end of dosing range if patient not previously on steroids; titrate to lowest dose that is effective; always rinse mouth after each treatment
  MDI double strength (84 mcg/puff) 2 puffs inhalation bid
Budesonide (Pulmicort) DPI-Turbuhaler (200 mcg/inhalation) 1-2 puffs inhalation bid May take several weeks to see benefit; not to be used as a rescue medication
  Nebs-Respules (0.25 mg/2 ml, 0.5 mg/2 ml) 0.25-0.5 mg neb bid or 0.5-1 mg neb qd
Flunisolide (Aerobid, Aerobid-M) MDI (250 mcg/puff) 2-3 puffs inhalation bid  
Fluticasone (Flovent) MDI (44 mcg/puff, 110 mcg/puff, 220 mcg/puff) 2 puffs inhalation bid (maximum 880 mcg/day)  
  Rotadisk (50 mcg/blister) 50-100 mcg inhalation bid  
Triamcinolone (Azmacort) MDI (100 mcg/puff) 1-2 puffs inhal qid  
Mast Cell Stabilizers      
Cromolyn (Intal) MDI (800 mcg/puff) 2 puffs inhalation qid May take several weeks to see benefit; not to be used as a rescue medication
  Nebs (20 mg/2 ml) 20 mg neb qid
Nedocromil (Tilade) MDI (1.75 mg/puff) 2 puffs inhalation qid  
Mucolytics      
N-acetylcysteine (Mucomyst) Nebs (20%, 200 mg/ml) 3-5 ml neb qid Consider pretreatment with albuterol 15 min before N-acetylcysteine secondary to bronchospasm
Dornase alfa (Pulmozyme) Nebs (2.5 mg/2.5 ml) 2.5 mg neb qid-bid May cause hemoptysis
Antiinfectives      
Pentamidine (Pentam) Nebs (300 mg) 8 mg/kg/dose (maximum 300 mg/dose) neb q month Used for PCP prophylaxis
Ribavirin (Virazole) Powder (6 g vial) 2 g over 2 hr neb q 8 hr × 3-7 days or 6 g over 12-18 hr neb q 24 hr × 3-7 days Used for RSV treatment; mutagenic, teratogenic
Tobramycin (TOBI) Nebs (300 mg/5 ml) 300 mg neb q 12 hr Used for pseudomonal infection of the lungs

image

Neb, Nebulizer.

PCP, Pneumocystis jiroveci pneumonia; RSV, respiratory syncytial virus.

Small volume nebulizers (SVNs), MDIs, and dry powder inhalers (DPIs) can be used to deliver aerosolized drugs via mouthpiece or face mask to infants and children.17 Continuous aerosol drug therapy is also used for patients unresponsive to intermittent SVN treatments. Aerosol drug administration to intubated infants and children is challenging because of the decreased deposition from baffling of small endotracheal tubes in these patients, which prevents approximately 90% of the drug from entering the lungs, regardless of delivery system. In addition, careful adjustments must be made to the ventilator so that nebulizer flows do not alter delivered VT and inspiratory pressure and interfere with triggering efforts.18

Airway Management

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