2 Growth and Development
Normal and Abnormal Growth and Maturation
Growth is the quantitative development of the body and maturation is the acquisition of new functionalities; both phenomena occur during pregnancy and after birth. Prenatal growth is the most important phase in development, comprising organogenesis in the first 8 weeks (embryonic growth), followed by the functional development of organ systems and maturation of the fetus to full term (fetal growth). Rapid growth occurs particularly in the second trimester; a major increase in weight from subcutaneous tissue and muscle mass occurs in the third trimester. Environmental agents may affect the human embryo in a negative way. The duration of gestation and the weight of an infant have an important relationship (Table 2-1).
Gestation (weeks) | Mean Weight (grams) |
---|---|
28 | 1165 ± 109 |
32 | 1760 ± 128 |
36 | 2621 ± 274 |
40 (full term) | 3351 ± 448 |
Data from Naeye RL, Dixon JB. Distortions in fetal growth. Pediatr Res 1978;12:987-91.
Preterm infants are further classified according to their actual birth weight. A low–birth-weight (LBW) infant is one weighing less than 2500 g regardless of the duration of the pregnancy. A very low–birth-weight (VLBW) infant weighs less than 1500 g, and an extremely low–birth-weight infant weighs less than 1000 g. In addition, infants weighing less than 750 g are now being called “micropremies”; there is very little published information regarding the anesthetic management of this vulnerable subpopulation of neonates (see Chapter 35). Common neonatal problems as they relate to age and birth weight are presented in Table 2-2.
Gestation | Relative Weight | Neonatal Problems at Increased Incidence |
---|---|---|
Preterm (<37 weeks) | SGA | Respiratory distress syndrome |
Apnea | ||
Perinatal depression | ||
Hypoglycemia | ||
Polycythemia | ||
Hypocalcemia | ||
Hypomagnesemia | ||
Hyperbilirubinemia | ||
Viral infection | ||
Thrombocytopenia | ||
Congenital anomalies | ||
Maternal drug addiction | ||
Fetal alcohol syndrome | ||
AGA | Respiratory distress syndrome | |
Apnea | ||
Hypoglycemia | ||
Hypocalcemia | ||
Hypomagnesemia | ||
Hyperbilirubinemia | ||
LGA | Respiratory distress syndrome | |
Hypoglycemia: infant of a diabetic mother | ||
Apnea | ||
Hypocalcemia | ||
Hypomagnesemia | ||
Hyperbilirubinemia | ||
Normal (37-42 weeks) | SGA | Congenital anomalies |
Viral infection | ||
Thrombocytopenia | ||
Maternal drug addiction | ||
Perinatal depression | ||
Hypoglycemia | ||
AGA | — | |
LGA | Birth trauma | |
Hyperbilirubinemia | ||
Hypoglycemia: infant of a diabetic mother | ||
Postmature (>42 weeks) | SGA | Meconium aspiration syndrome |
Congenital anomalies | ||
Viral infection | ||
Thrombocytopenia | ||
Maternal drug addiction | ||
Perinatal depression | ||
Aspiration pneumonia | ||
Hypoglycemia | ||
AGA | — | |
LGA | Birth trauma | |
Hyperbilirubinemia | ||
Hypoglycemia: infant of a diabetic mother |
AGA, Appropriate for gestational age; LGA, large for gestational age; SGA, small for gestational age.
Gestational Age Assessment
The gestational age of an infant may be assessed in one of three ways. The most accurate means of assessing gestational age is by measuring the crown-rump length of the fetus during a first-trimester ultrasonographic examination. Another method involves calculating gestational age from the first day of the mother’s last menstrual period, but this is commonly inaccurate, leading to errors in estimation. Finally, the Dubowitz scoring system is a well-accepted method combining neurologic and physical criteria of the infant to provide an accurate assessment of gestational age.1,2 A summary of the more significant neurologic and physical signs of maturity is presented in Table 2-3.
Physical Examination | Preterm (<37 weeks) | Term (≥37 weeks) |
---|---|---|
Ear | Shapeless, pliable | Firm, well formed |
Skin | Edematous, thin skin | Thick skin |
Sole of foot | Creases on anterior third | Whole foot creased |
Breast tissue | Less than 1 mm diameter | More than 5 mm diameter |
Genitalia | ||
Male | Scrotum poorly developed Testes undescended |
Scrotum rugated Testes descended |
Female | Large clitoris, gaping labia majora | Labia majora developed |
Limbs | Hypotonic | Tonic (flexed) |
Grasp reflex | Weak grasp | Can be lifted by reflex grasp |
Moro reflex | Complete but exhaustible (>32 weeks) | Complete |
Sucking reflex | Weak | Strong, synchronous with swallowing |
Weight and Length
Assessment of growth is measured by changes in weight, length, and head circumference. Percentile charts are valuable for monitoring the child’s growth and development. Deviation from growth within the same percentile for a child of any age is of greater significance than any single measurement (Figs. 2-1 and 2-2). Weight is a more sensitive index of well-being, illness, or poor nutrition than length or head circumference and is the most commonly used measurement of growth. Change in weight reflects changes in muscle mass, adipose tissue, skeleton, and body water and thus is a nonspecific measure of growth. Measurement of length provides the best indicator of skeletal growth because it is not affected by changes in adipose tissue or water content.
Term infants may lose 5% to 10% of their body weight during the first 24 to 72 hours of life from loss of body water. Birth weight is usually regained in 7 to 10 days. A daily increase of 30 g (210 g/week) is satisfactory for the first 3 months. Thereafter, weight gain slows so that at 10 to 12 months of age it is 70 g each week (Table 2-4).
Age (years) | Weight (kg) |
---|---|
1 | 10 |
3 | 15 |
5 | 19 |
7 | 23 |
Weight and length are important but changes affect the composition of the body itself, especially total body water, which decreases at the expense of the extracellular compartment, with adult levels attained at 1 year of age.3,4 This finding has implications for drug dosing and distribution in the infant. Males have a greater percentage of water, whereas females have a slightly greater percentage of fat. The percentage decrease in extracellular water is greater than the decrease in total body water because of the simultaneous increase in intracellular water (Table 2-5).5
Another, more precise way to assess development is to calculate the body surface area (BSA).6
BSA can also be described using an allometric equation with an exponent of (see Chapter 6):
Head Circumference
The anterior fontanel should be palpated to assess whether it is sunken (dehydration) or bulging abnormally (suggesting increased intracranial pressure as in hydrocephalus, infection, hemorrhage, or increased partial pressure of carbon dioxide in the arterial blood [PaCO2]). If it is bulging, the sutures should be palpated for abnormal separation as a result of increased intracranial pressure. The anterior fontanel closes between 9 and 18 months of age; the posterior fontanel closes by 2 to 4 months of age (Fig. 2-3). Cranial molding occurs particularly in LBW infants and is usually of no clinical importance.
Teeth
The first tooth, usually a lower incisor, erupts at approximately 6 months after birth (deciduous dentition). Eruption of all deciduous teeth is usually complete by 28 months of age. Permanent teeth appear at 6 years, with the shedding of the deciduous teeth; this process takes place during the next 6 to 8 years. Abnormally developed teeth occur with hereditary disorders, Down syndrome, cerebral palsy, medications (eg., tetracycline) and nutritional defects. Preterm infants may show severe enamel hypoplasia in their primary dentition.7,8
Airway and Respiratory System
Upper Airway Development
The larynx is developed embryologically from ectodermal, endodermal, and mesodermal tissues that are derived from the third, fourth, and sixth branchial arch and pouch apparatus. The development of the larynx and airway in the neonate is outlined in detail in Chapter 12. The laryngeal opening (epiglottis and vocal cords) in a neonate and 2-year-old boy are shown in Figure 2-4. Note the omega-shaped long epiglottis and the pearly white vocal cords in the neonate.
The depth of the nasopharynx increases due to remodeling of the palate as well as changes in the angulation of the skull base. During childhood, the soft tissues of the pharyngeal structures surrounding the upper airway grow proportionally to the skeletal structures. After birth, the dimensions of the nasal cavity increase very rapidly. During the first year of life, the total minimal cross-sectional area is increased by 67%, and the volume of the anterior 4 cm of the nasal airways by 36%.9
Compared with the adult, the tongue in the neonate contains considerably less fat and soft tissue, but overall is large in size relative to the dimensions of the mouth, with relatively larger extrinsic musculature and a less developed superior longitudinal muscle resulting in a flat dorsal surface with poor lateral mobility (see also Chapter 12).
Respiratory System Development
Airways: The bronchial tree down to and including the terminal bronchioles forms by week 16 of gestation. The acinus, consisting of all the airway structures distal to the terminal bronchiole and the entire gas-exchanging apparatus, develops throughout the remainder of gestation.
Alveoli: Alveoli develop mainly after birth, increasing in number until approximately 8 years of life and in size until growth of the chest wall ceases.
Pulmonary vessels: Arteries and veins accompanying the bronchial tree form by week 16 of gestation. Those vessels lying within the acinus follow the development of the alveoli. The appearance and growth of arterial smooth muscle lags behind the sprouting of new vessels and is not completed until late adolescence.
Transition to Air Breathing
Fetal breathing movements have been detected as early as 11 weeks of gestational age; they are interspersed with long periods of apnea and produce little tidal movement of lung fluid.10,11 The critical event in the change from placental to pulmonary gas exchange is the first inspiration, which initiates pulmonary ventilation, promotes the clearance of lung fluid, and triggers the change from the fetal to the neonatal pattern of circulation.
The first breath is a gasp that generates a transpulmonary distending pressure of 40 to 80 cm H2O.12 This moves the tracheal fluid (100 times more viscous than air), overcomes surface forces that develop as the air−fluid interface reaches the small airways, and overcomes tissue resistance. In some children, the removal of lung fluid may be delayed, producing the syndrome called transient tachypnea of the newborn.13 Tachypnea lasts for 24 to 72 hours and is associated with a characteristic chest radiographic appearance consisting of increased perihilar markings, fluid in the interlobar fissures, and streaky linear opacities in the parenchyma.
In the first few minutes of life, a state of “normal” asphyxia exists as a result of impairment of placental blood flow during labor. The partial pressure of oxygen in arterial blood (PaO2) and pH are low, whereas the PaCO2 is increased immediately after birth, but these parameters change rapidly in the first hour of life. Extrapulmonary shunting through fetal channels and intrapulmonary shunting, probably through unexpanded regions of the lung, persist for some time after birth, so that in neonates the physiologic right-to-left shunt is about three times that in adults.14
Mechanics of Breathing
Chest Wall and Respiratory Muscles
The accessory muscles of inspiration are relatively ineffective in infants because of an unfavorable anatomic rib configuration. In infancy, the ribs extend horizontally from the vertebral column, moving little with inspiration.15 These factors increase the workload on the diaphragm. Consequently, and in contrast to an adult, thoracic cross-sectional area is fairly constant throughout the breathing cycle, and inspiration occurs almost entirely as a result of diaphragmatic descent.
The chest wall of a neonate is floppy because it comprises noncalcified cartilage, its musculature is poorly developed, and the ribs are incompletely calcified.16,17 As the work of breathing increases, diaphragmatic displacement must also increase to maintain the tidal volume. The increased workload may lead to diaphragmatic fatigue and respiratory failure or apnea, especially in preterm infants.18,19
The tendency to respiratory muscle fatigue is the result of the metabolic characteristics of the diaphragm, which has very little type I (slow twitch, high oxidative capacity) muscle fibers (see Fig. 12-11).
Elastic Properties of the Lung
Changes in the static pressure−volume relationship of the lungs during growth are caused by increases in volume and changes in the elastic properties of lung tissue. Volume is the principal factor that determines lung compliance, which increases throughout childhood. Specific lung compliance remains relatively constant throughout childhood.20 In contrast, specific compliance of the chest wall declines throughout childhood and adolescence, reflecting the progressive calcification of the ribs and the increasing bulk of the thoracic muscles.
Static Lung Volumes
Detailed information expressing static lung volumes on the basis of body weight are detailed in Table 2-6.
Total Lung Capacity
Adults have a markedly greater total lung capacity (TLC) than infants (Fig. 2-5). This difference reflects the fact that TLC is an effort-dependent parameter, depending on the strength and efficiency of the inspiratory muscles, which can be estimated by the maximum inspiratory pressure at functional residual capacity (FRC). An adult can generate negative pressures in excess of 100 cm H2O; negative inspiratory pressures as high as 70 cm H2O have been recorded for neonates, a surprisingly high value in view of their underdeveloped musculature and highly compliant chest wall. This may be a consequence of the small radius of curvature of an infant’s rib cage, which by the Laplace relationship converts a small tension into a large pressure difference.21
Functional Residual Capacity
FRC is similar on a per-kilogram basis at all ages, but the mechanical factors on which it is based are different in infants and adults.22 In adults, FRC is the same as the volume at which the elastic forces generated by the passive recoil of the chest wall are balanced by the recoil of the lung (Fig. 2-6); this is the volume attained at end-expiration with an open glottis.