Key Points
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Children are physiologically different from adults. Familiarity with these differences is required for safe management of the medical and surgical problems of children.
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Providing optimal pediatric care requires attention to the child as a patient and to the adults as guardians.
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Involving the child in play may alleviate anxiety regarding procedures in the physical examination.
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With practice, physical examination can be conducted in an expedient fashion and will be relatively painless for the child yet complete for the surgeon.
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Management of the pediatric otolaryngology patient often requires a multidisciplinary team approach.
Pediatric otolaryngology has developed over the years into a formal subspecialty of otolaryngology head and neck surgery, led by surgeons who had specific interests in the care of children. What makes pediatric otolaryngology distinct from its parent discipline of otolaryngology head and neck surgery are the special problems that present in children with an often unique approach to their management.
The specific problems that a pediatric otolaryngologist may encounter include airway disorders that present congenitally or iatrogenically, swallowing disorders that may change with growth and development, head and neck tumors in children and infants, hearing loss that may be congenital or acquired, and other congenital anomalies that may present in the head and neck ( Figs. 1-1 through 1-6 ). As a subspecialty of otolaryngology head and neck surgery, the surgical techniques are not necessarily different, but the differential diagnosis, the approach to the child and parent, and the overall surgical management may diverge significantly. Not all enjoy treating both child and parent, but for those who do, pediatric otolaryngology is exceedingly rewarding. The specific problems that children may present with in the head and neck are often readily correctable, such that children may achieve their full potential as they grow and develop.
For many practitioners, there is no greater reward than helping children afflicted with illness. Pediatric otolaryngology has developed as a subspecialty as a bridge between pediatric medicine and the surgical discipline of otolaryngology. Nearly every otolaryngologist will treat children during his or her professional career, and an estimated 25% to 50% of a general otolaryngologist’s practice may be related to pediatric problems. Pediatric otolaryngology has therefore become an important part of all training programs in this field.
As the saying goes, children are not simply little adults. Often unique approaches are required for their evaluation, diagnosis, and management. Although the child is of prime concern, the parents—as the child’s guardians, who must make decisions regarding the ultimate treatment options—also must be kept informed and must be approached with compassion. This is obvious to nearly everyone who has had to make medical decisions for a loved one, but it may not be as obvious to those who have not. The love for and emotional bond with a child may make even the most calm and rational person unable to comprehend events and medical explanations. It is up to the surgeon to monitor and modify his or her approach and explanations to both the child and the parent. This is not always an easy task, but it is one that is highly rewarding.
Smaller and more premature neonates are surviving, and sicker children are recovering from significant illnesses, as neonatal and pediatric intensive care units and the skills of the physicians who care for children continue to advance. This development has led to a demand for practitioners well versed in the management of disorders encountered in this population—namely, intubation trauma, bronchoesophageal processes, infectious disease, tumors, and congenital malformations. A multidisciplinary approach is often required. Agreement among the pediatric specialists and with the general pediatrician is important and represents a third layer of communication that is required for successful treatment of the child and family.
Physiologic differences among infants, children, and adults have occupied major research efforts and constitute the subject of complete textbooks. This chapter outlines basic differences relevant to the practice of otolaryngology along with some related considerations. In the following discussion, the material presented for each of the major body systems is intended as a general introduction to be used as a starting point for further investigation.
Respiratory System
Control of Ventilation
Emergence from an underwater world, in which the child relied on placental exchange of gases and nutrition, induces tremendous changes in the neonate’s physiology and anatomy. Some of these changes occur rapidly at birth, whereas others proceed more slowly. These significant changes can complicate interpretation of the neonate’s problems. In particular, the assessment of the neonate’s ventilation may be difficult. Interventions used to obtain measurements, such as placement of a facemask or insertion of a laryngotracheal tube, may induce significant changes in ventilation. Measurements of ventilation to assess respiratory drive also depend on the assumption that the respiratory muscles are capable of converting this drive into work—which is not always the case in infants and neonates.
Muscle fibers may be classified as type I fibers, which are slow twitch, highly oxidative, and fatigue resistant, or type II fibers, which are fast twitch and easily fatigable. Newborns have a paucity of type I muscle fibers but develop them shortly after birth. The muscle fibers in the diaphragm of a preterm infant are composed of less than 10% of type I fibers, whereas the muscle fibers of a full-term infant may be 30% type I fibers; the percentage of type I fibers increases to 55%, the expected adult level, during the first year of life. Preterm infants are more prone to respiratory fatigue, although this predilection disappears as they reach maturity.
Other subtle differences in sleep patterns also affect control of ventilation. Preterm infants spend as much as 50% to 60% of their sleep state in the rapid eye movement (REM) state. During REM sleep, the intercostal muscles are inhibited, as are most of the other skeletal muscles. This places a greater burden on the diaphragmatic activity. Much of this activity may be wasted because the chest wall can move paradoxically in the very young. This purposeless movement readily leads to hypoventilation, increased respiratory drive, and diaphragmatic fatigue.
Biochemical and reflex controls of ventilation are similar but incompletely developed in full-term neonates when compared with adults. Neonates have a higher basal metabolic rate than that in adults, reflected in higher ventilatory rates relative to body mass at any given partial pressure of carbon dioxide (PaCO 2 ). In term infants and adults, an increased PaCO 2 results in a proportionately similar increase in ventilation; however, this concordance in response is not seen in preterm infants. Compared with full-term infants and adults, preterm infants have a blunted response to increases in PaCO 2 and an altered response to changes in partial pressure of oxygen. The administration of 100% oxygen decreases ventilation in the very young, suggesting the existence of chemoreceptor activity not generally seen in adults.
Gestational age, postnatal age, body temperature, and sleep state modify the ventilatory response of newborns to hypoxia. Preterm and full-term infants less than a week old who are awake and euthermic usually demonstrate biphasic breathing patterns. They often experience tachypnea followed by hypoventilation. Hypothermic infants demonstrate a blunted response to hypoxia with respiratory depression without initial hyperpnea. The central effects of hypoxia on the respiratory center may cause depression of ventilation. Active peripheral chemoreceptors are unable to maintain a significant influence over this response. REM sleep also may decrease the response to hypoxia in these infants, whereas sleep states other than REM sleep are associated with an increase in the ventilatory response to hypoxia. Arousal from sleep during hypoxia is not seen in newborns but develops during the first few weeks of life with further maturation of the chemoreceptors that increases their ventilatory drive to hypoxia. Of interest, a decreased response to hypercarbia associated with hypoxia also occurs in newborns but not in older infants and adults.
Reflexes that arise from the lung and chest wall probably are more important in maintaining ventilation in newborns and in determining the respiratory tidal volume. Periodic breathing is characterized by periods of alternating rapid ventilation followed by apnea and is common in preterm and full-term infants. It is thought to result from dyscoordination of the feedback loops that control ventilation. During the apneic part of periodic breathing, the PaCO 2 may increase but changes in heart rate do not. Generally, no serious physiologic consequences are seen, and periodic breathing is considered normal and typically resolves by 6 years of age. Some preterm infants, however, may demonstrate serious and potentially life-threatening episodes of apnea. These episodes may last longer than 20 seconds and are accompanied by bradycardia. Apneic episodes may represent a failed response to hypoxia. Because these episodes are more commonly seen during REM sleep, ventilatory fatigue, as well as impaired chemoreceptor response to hypoxia, may be the cause. Usually, stimulation is all that is required to terminate the apneic event. Aminophylline treatment generally decreases the apneic episodes through central stimulation. Continuous positive airway pressure may also be helpful to decrease apneic episodes by modifying the lung and chest wall reflexes.
Laryngospasm
The primary function of the larynx is to protect the lungs from aspiration. Hence, the laryngeal adductor response is a very strong reflex, such that it may be lethal in some instances. The robustness of the reflex has been shown to change with age and maturity in animal models. When laryngeal adduction is coupled with tachycardia, hypertension, and apnea, it is termed the laryngeal chemoreflex (LCR). The LCR can be induced by laryngeal exposure to acid, base, and pressure, but it is most sensitive to water and is ablated by saline. These properties of the LCR may have implications for sudden infant death syndrome (SIDS) because responses evolve with age to hypoxia, hypercarbia, and the laryngeal stimulation that causes the LCR, which may explain the age pattern seen with SIDS. Deaths attributed to SIDS have dramatically decreased as a result of a change in the recommended sleep position of children—from prone to supine. Elimination of hypercarbia from rebreathing may be the mechanism behind the decrease in SIDS deaths. Hypercarbia is a known potentiator of the LCR. An increased awareness of and more aggressive stance toward the treatment of infant reflux also may have decreased a potential stimulus for the LCR. Decreased bolus size, increased feeding frequency, frequent burping, and positioning to reduce regurgitation have been helpful to decrease the incidence of reflux in infants and perhaps the incidence of apneic spells and infant breathing issues.
Lung Volumes
In proportion to body size, the total lung capacity, functional residual capacity, and tidal volume are roughly equivalent in adults and in infants. In the full-term infant, the total lung volume is approximately 160 mL with functional residual capacity at one half this volume. Tidal volume is approximately 16 mL, and dead space is approximately 5 mL. Because of small lung volumes in infants, any increase in dead space is much more significant compared with adults. In contrast with static lung volumes, however, alveolar ventilation is proportionately much greater in newborns (100 to 150 mL/kg of body weight) than in adults (60 mL/kg of body weight). This higher alveolar ventilation in infants results in a higher alveolar–functional residual capacity ratio, 5:1, compared with 1.5:1 in adults. Consequently, the functional residual capacity is unable to provide the same buffer in infants, such that changes in the concentration of inspired gases are much more rapidly reflected in alveolar and arterial levels. This explains why induction of anesthesia using inhalational techniques is easier in infants than in adults. Along with the higher metabolic rate for body weight seen in infants, this difference also explains why infants have a smaller ventilatory reserve. The time from apnea to oxygen desaturation is much shorter in infants than in adults. Accordingly, surgical maneuvers that require short apneic periods may pose more of a challenge in infants than in adults.
The total surface area of the air-tissue interface of the alveoli in infants is small (2.8 m 2 ). When this relatively small gas exchange area is combined with the higher relative metabolic rate, infants have a reduced reserve capacity for gas exchange. This difference is of increased importance when congenital defects interfere with lung growth and development or if the lung parenchyma becomes damaged. The remaining healthy lung may not be adequate to sustain life.
Respiratory Rate
The most efficient respiratory rate for newborns has been calculated to be around 37 breaths per minute. This rate is close to that observed for average newborns. Full-term infants are similar to adults in requiring approximately 1% of their metabolic energy to maintain ventilation. The cost of breathing is then 0.5 mL/0.5 L of ventilation. In preterm infants, this nearly doubles to 0.9 mL/0.5 L of ventilation. The cost of respiration also dramatically increases if the lung parenchyma is diseased or damaged by processes other than prematurity. In either case, the result is higher caloric and nutritional demands. Respiratory rate can directly affect the infant’s ability to complete the suck-swallow-breathe cycle as well. If gas exchange is poor, ventilation rates may increase. This increase in respiratory rate may not allow adequate time for the suck-swallow portion of feeding. Caloric intake decreases precipitously as the infant expends energy toward breathing over feeding, which may lead to a vicious circle that results in failure to thrive.
Ventilation-Perfusion Relationships
Ventilation and perfusion are imperfectly matched in the neonatal lungs. Some persistent anatomic shunts in the newborn circulatory system, as well as a relatively high closing volume in the lungs, cause this mismatch. The normal arterial oxygen tension in a newborn breathing room air is 50 mm Hg. This increases dramatically during the first 24 hours of life with changes in fetal circulation and maturation of lung parenchyma, and it continues to change slowly during the ensuing months and years ( Table 1-1 ).
| Age | Pa o 2 in Room Air (mm Hg) |
|---|---|
| 0 to 1 week | 70 |
| 1 to 10 months | 85 |
| 4 to 8 years | 90 |
| 12 to 16 years | 96 |
Cardiovascular System
Newborn Heart and Cardiac Output
The heart of a healthy neonate is much different from that of an adult. The thickness of the right ventricle exceeds that of the left, as seen by the normal right axis deviation on the neonatal electrocardiogram. Shortly after birth, with closure of the fetal circulation, the left ventricle enlarges disproportionately. By the age of 6 months, the adult right/left ventricular size ratio is established.
The newborn myocardium is also significantly different from the adult myocardium. The myocardium of a newborn contains fewer contractile fibers and more connective tissue. Consequently, neonatal ventricles are less compliant at rest and generate less tension during contraction. The usual Starling curves of contractility for adult cardiovascular physiology do not hold true for the neonatal heart. Cardiac output is rate dependent in the neonatal heart, which has reduced compliance and contractility; the low compliance of the relaxed ventricle limits the size of the stroke volume, and therefore increases in preload are not as important in neonatal physiology as is heart rate. Bradycardia invariably equates with reduced cardiac output because the infant heart cannot achieve the increased contractility needed to maintain cardiac output. This distinction is extremely important to recognize during surgical and anesthetic procedures, which may induce bradycardia. Autonomic innervation also is incomplete in the neonatal heart, with its relative lack of sympathetic elements; this relative underdevelopment may further compromise the ability of the less contractile neonatal myocardium to respond to stress.
Heart rate is crucially important in the very young. The normal range for the newborn is 100 to 170 beats per minute, and the rhythm is regular. As the child grows, the heart rate decreases ( Table 1-2 ). Sinus arrhythmia is common in children, but all other irregular rhythms should be considered abnormal. The average newborn systolic blood pressure is 60 mm Hg; the diastolic pressure is 35 mm Hg.
