Pediatrics

Chapter 31 Pediatrics




Developmental physiology




1. How does the oxygen consumption of a neonate compare with that of an adult?


2. How does the cardiac output of a neonate compare with that of an adult?


3. Are changes in the cardiac output of a neonate more dependent on changes in the heart rate or stroke volume?


4. How does the position of the oxyhemoglobin dissociation curve in a neonate compare with that of an adult? Describe how this affects the affinity of oxygen for hemoglobin. At what age does the curve approximate that of an adult?


5. How does the hemoglobin level of a neonate compare with that of an adult? How does the hemoglobin level change as the infant progresses to 2 years old?


6. What hemoglobin level is worrisome in the newborn? What hemoglobin level is worrisome in infants older than 6 months of age?


7. At what age does the foramen ovale close? What percent of adults have a probe patent foramen ovale?


8. How well do neonates reflexively respond to hemorrhage as compared with adults?


9. How does alveolar ventilation in neonates compare with that of adults?


10. How does the tidal volume per weight in neonates compare with that of adults?


11. How does the respiratory rate in neonates compare with that of adults?


12. How does carbon dioxide production in neonates compare with that of adults? How does the PaCO2 in neonates compare with that of adults?


13. How does the PaO2 change in the first few days of life?


14. How predictable is the neonate’s response to hypoxia?


15. What percent body weight in neonates is contributed by the extracellular fluid volume? How does this compare with an adult?


16. What are some ways in which infants and children maintain normal body temperature? Why is maintenance of normal body temperature more difficult in neonates and children than in an adult?


17. How effective is kidney function at birth? When does kidney function become approximately equivalent to that of an adult?


18. After fluid restriction, what is the maximum urine osmolarity possible for term neonates at birth? At what age are adult levels of urine concentrating abilities achieved?








Induction and maintenance of anesthesia




48. How can the induction of anesthesia be achieved in pediatric patients without an intravenous catheter in place?


49. What are some risks of an inhaled induction of anesthesia?


50. What is the indication for the placement of an intravenous catheter in the pediatric patient undergoing a surgical procedure?


51. How can the anesthesiologist regulate the intravenous fluids to be administered in the pediatric patient?


52. How can the induction of anesthesia be achieved in pediatric patients with an intravenous catheter in place?


53. How can the induction of anesthesia be achieved in pediatric patients without an intravenous catheter in place and in whom an inhalation induction is not possible?


54. What is the concern regarding the use of succinylcholine in pediatric patients? What are some alternatives that may be used?


55. Under what circumstances is succinylcholine accepted for use for neuromuscular blockade in the pediatric population?


56. What are some physiologic characteristics of the pediatric airway that differ from the adult airway?


57. Why has the classic teaching that uncuffed endotracheal tubes should be used for intubating the trachea of pediatric patients under the age of 8 years changed?


58. What is the benefit of the administration of heated and humidified gases or using a condenser humidifier in children undergoing prolonged operations?


59. What are some signs the clinician may use to determine the adequacy of the depth of anesthesia for surgery in the pediatric population?


60. When hypotension accompanies the administration of volatile anesthetics to neonates, what is it likely to be indicative of?


61. How does intraoperative monitoring in the pediatric population differ from intraoperative monitoring in the adult population?


62. What problem may be encountered with the monitoring of end-tidal carbon dioxide concentrations in pediatric patients?


63. How should the size of a blood pressure cuff be selected? What errors in blood pressure measurement may be encountered with an erroneously sized cuff?


64. What veins may be used to monitor the central venous pressure in the neonate? In infants? In children?


65. What are some regional anesthetic blocks that can be administered in the pediatric population?


66. What local anesthetic and what dose is commonly used in a caudal anesthetic? What is the approximate duration of the postoperative pain relief obtained from this caudal anesthetic? How is the length of the dural sac different in children and adults?




Medical and surgical diseases that affect pediatric patients




71. What is respiratory distress syndrome?


72. What are some physiologic complications that result from respiratory distress syndrome?


73. How should neonates with respiratory distress syndrome be managed intraoperatively?


74. What is bronchopulmonary dysplasia? What are some characteristic findings in these patients?


75. What is retinopathy of prematurity? What is another name for this pathologic finding?


76. What is a risk factor for retinopathy of prematurity? At what age does the risk of retinopathy of prematurity become negligible?


77. What PaO2 should be maintained during anesthesia in the premature neonate to minimize the risk of retinopathy of prematurity?


78. Patients of what age are at risk of apnea spells in the postoperative period? What is the recommendation for these patients in the postoperative period?


79. Which pediatric patients are at risk of hypoglycemia?


80. What are some manifestations of hypoglycemia in this population? How do these manifestations change with general anesthesia? What is the immediate treatment of hypoglycemia in these patients?


81. Which pediatric patients are at risk of hypocalcemia?


82. When might hypocalcemia occur intraoperatively? How might intraoperative hypocalcemia manifest?


83. What is the incidence of malignant hyperthermia in the pediatric population? What is the incidence in the adult population?


84. What is the association between malignant hyperthermia and the calcium ion channel?


85. What are some anesthetic triggering drugs for malignant hyperthermia?


86. What are some clinical signs of malignant hyperthermia?


87. What is the treatment of malignant hyperthermia?


88. How can the patient at risk for malignant hyperthermia be identified preoperatively?


89. Which anesthetic regimen is reliably safe for patients susceptible to malignant hyperthermia? Name some drugs used in anesthesia that have not been shown to trigger malignant hyperthermia.


90. What preparations must take place before the administration of anesthesia to patients susceptible to malignant hyperthermia?


91. Is regional anesthesia considered safe for patients at risk for malignant hyperthermia?


92. What is a congenital diaphragmatic hernia? How is a congenital diaphragmatic hernia manifest in the neonate at birth?


93. What are some comorbid conditions associated with congenital diaphragmatic hernias?


94. How is the diagnosis of a congenital diaphragmatic hernia made?


95. What is the immediate treatment for the neonate with a congenital diaphragmatic hernia? What is the risk of hand ventilation with bag and mask in these neonates?


96. What is the risk of positive pressure ventilation of the lungs of the neonate with a congenital diaphragmatic hernia?


97. What inhaled anesthetics should be avoided in neonates with a congenital diaphragmatic hernia?


98. What clinical circumstance leads to suspicion of a tracheoesophageal fistula in a neonate?


99. What are some other congenital anomalies associated with a tracheoesophageal fistula?


100. How should neonates with a tracheoesophageal fistula be managed?


101. What is pyloric stenosis? What is the incidence of pyloric stenosis per live birth?


102. How does the neonate with pyloric stenosis typically present?


103. What electrolyte imbalances are seen in infants with pyloric stenosis?


104. Is the surgical correction of pyloric stenosis in infants an elective or emergent procedure?


105. How should the induction of anesthesia in infants with pyloric stenosis proceed?


106. What is necrotizing enterocolitis, and which patients are at risk?


107. How is necrotizing enterocolitis treated, and what are some of the anesthetic considerations for this disease?


108. What are gastroschisis and omphalocele? What are the similarities and differences between these conditions?


109. How are gastroschisis and omphalocele treated surgically in the modern era? What are some of the anesthetic considerations for these conditions?


110. What is the significance of a patent ductus arteriosus (PDA) in the premature infant? What are the medical and surgical approaches to treatment?


111. What are some anesthetic considerations and pitfalls for PDA closure in the premature neonate?


112. What is myelomeningocele, and how is it managed surgically? What are some of the anesthetic considerations?




Answers*



Developmental physiology




1. The oxygen consumption of a neonate is about twice that of an adult. In neonates the oxygen consumption increases from 5 mL/kg per minute at birth to about 7 mL/kg per minute at 10 days of life and 8 mL/kg per minute at 4 weeks of life. Oxygen consumption gradually declines over the subsequent months. (548, Table 34-1)


2. The cardiac output of a neonate is 30% to 60% higher than that of adults. This helps to meet the increase in oxygen demand neonates have as compared with adults. (549)


3. Changes in the cardiac output of a neonate or infant are dependent on changes in the heart rate, because stroke volume is relatively fixed by the lack of distensibility of the left ventricle in this age group. The neonate’s myocardium depends heavily on the concentration of ionized calcium, such that hypocalcemia can significantly depress myocardial function. (549)


4. In neonates, the oxyhemoglobin dissociation curve is shifted to the left. This reflects a P50 lower than 26 mm Hg, meaning that less of a PaO2 is required for a 50% saturation of hemoglobin. Conversely, the oxygen is more tightly bound to hemoglobin in neonates, necessitating a lower PaO2 for release of oxygen to the tissues. This occurs as a result of fetal hemoglobin. The position of the oxyhemoglobin dissociation curve becomes equal to that of adults by 4 to 6 months of age. (550)


5. The hemoglobin level of a neonate is approximately 17 g/dL. This, along with the increase in cardiac output, helps to offset the increase in oxygen requirements characteristic of neonates. At 2 to 3 months of age the hemoglobin of infants decreases to about 11 g/dL during the time period when fetal hemoglobin is being replaced by adult hemoglobin. This is termed the physiologic anemia of infancy, which may persist for a few months. During the remainder of the first year of life the hemoglobin level gradually increases and continues to do so until puberty, when hemoglobin levels approach adult hemoglobin levels. (550)


6. A hemoglobin level of 13 g/dL or less is worrisome in the newborn. In infants older than 6 months of age, a hemoglobin level less than 10 g/dL is worrisome. (550)


7. The foramen ovale closes between 3 and 12 months of age. Twenty to thirty percent of adults have a probe patent foramen ovale. (549)


8. Because of the decreased ability of neonates to vasoconstrict in response to hypovolemia, neonates are less able to tolerate hemorrhage with vasoconstrictive responses. (549)


9. Alveolar ventilation in neonates is 4 to 5 times higher than that of adults. (547, Table 34-1)


10. Tidal volume per weight in neonates is similar to that of adults. (547, Table 34-1)


11. The respiratory rate in neonates is three to four times higher than that of adults. (547, Table 34-1)


12. Carbon dioxide production in neonates is higher than that of adults. The PaCO2 in neonates is similar to that of adults, despite the increase in production. This is due to the increase in alveolar ventilation in neonates when compared with adults. (547, Table 34-1)


13. The PaO2 in the first few days after birth increases rapidly. The initially low PaO2 is due to a decrease in the functional residual capacity and to the perfusion of alveoli filled with fluid. The functional residual capacity of neonates increases over the first few days of life until it reaches adult levels at about 4 days of age. (547, Table 34-1)


14. The neonate’s response to hypoxia is somewhat unpredictable, owing to the immaturity of the central nervous system’s regulatory centers for ventilation in this age group. Neonates have decreased ventilatory responses to hypoxemia and hypercarbia. (547)


15. Extracellular fluid volume accounts for approximately 40% of the body weight of the neonate at birth. This compares with approximately 20% of body weight in adults being accounted for by extracellular fluid volume. The proportion of extracellular fluid volume to body weight in neonates approaches the adult proportion by 18 to 24 months of age. (552)


16. Some ways in which infants and children maintain normal body temperature include the metabolism of brown fat, crying, and vigorous movements. The metabolism of brown fat is stimulated by circulating norepinephrine. Children and infants, unlike adults, do not shiver to maintain their body temperature. Maintenance of normal body temperature is more difficult in neonates and infants than in adults because of their larger body surface area-to-volume ratio, as well as the relative lack of fat for insulation. (556)


17. Kidney function at birth is immature. There is a decreased glomerular filtration rate, decreased sodium excretion, and decreased concentrating ability relative to that of an adult. Kidney function progressively matures over the first 2 years of life. Initially, in the first 3 months of life, kidney function increases rapidly to double or triple the glomerular filtration rate possible at birth. Kidney function then matures more slowly from 3 months to 24 months, when adult levels of kidney function are reached. (550)


18. After fluid restriction, the term neonate at birth can only concentrate urine to a maximum osmolarity of about 525 mOsm/kg. After 15 to 30 days of age, neonates are able to concentrate their urine to a maximum osmolarity of about 950 mOsm/kg. Adult levels of urine concentrating ability are achieved by 6 to 12 months of age. (550)



Pharmacologic differences




19. Some physiologic characteristics of neonates that explain the pharmacologic differences between pediatric and adult responses to drugs include an increased extracellular fluid volume, increased metabolic rate, decreased renal function, and decreased receptor maturity. (550, 551)


20. The uptake and distribution of inhaled anesthetics is more rapid in neonates than in adults. This is most likely due to a smaller functional residual capacity per body weight in neonates, as well as to greater tissue blood flow to the vessel-rich group. The vessel-rich group of tissues includes the brain, heart, kidneys, and liver. This group comprises approximately 22% of total body volume in neonates, as compared with the 10% of total body volume in adults. (551)


21. The minimum alveolar concentration (MAC) of inhaled anesthetics changes from birth to puberty. Preterm neonates have a lower MAC than term neonates, whose MAC is approximately 0.87% that of adults. The MAC of inhaled anesthetic agents is highest in infants 1 to 6 months old. The MAC is 30% less in full-term neonates for isoflurane and desflurane. Sevoflurane MAC at term is the same as at age 1 month. (551)

May 31, 2016 | Posted by in ANESTHESIA | Comments Off on Pediatrics

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