Anesthesia in the Neonate

41


Anesthesia in the Neonate


John E. Stork


Surgery in neonates is accompanied by a humoral stress response that leads to increased complications and mortality, as shown in landmark studies by Anand and colleagues in 1987.3,4 This response is diminished by adequate anesthesia (Figure 41-1; Table 41-1), resulting in improved surgical outcomes. Consequently over the subsequent decades, anesthesia for all surgical procedures in neonates has been accepted as both a clinical and an ethical imperative.



image
Figure 41-1 Change (Δ) from baseline of epinephrine and norepinephrine in nanomoles per liter (nmol/L) before surgery to the end of the operation and for the first 24 hours thereafter. The two groups reflect nitrous oxide-fentanyl anesthesia (red circles) and nitrous oxide anesthesia (blue circles). In the patients given fentanyl, there was no increase in epinephrine or norepinephrine, not only during surgery, but also for the first 24 hours after surgery, indicating a significantly blunted stress response.

It is also now generally accepted that neonates are capable of sensing pain and discomfort. We have no recallable memories before 3 to 4 years of age (termed infantile amnesia), but neonates do possess consciousness and a sense of self, and can form implicit memories, that is, changes in behavior based on prior experience that do not require intentional recall.16 Plasticity is an inherent characteristic of the developing nervous system, and early pain experiences can lead to exaggerated responses to later painful stimuli or stress, as well as impaired neurodevelopmental outcome.78,79 Changes in pain sensitivity in children exposed to nociceptive stimulation as neonates have been demonstrated using parental rating surveys,33 measurements of the child’s own perception,32 and psychologic testing.11,31,39 Activation of brain regions in response to graded moderate pain stimuli is significantly different in school-age children and adolescents with neonatal intensive care (NICU) experience compared with controls, as measured by functional magnetic resonance imaging (MRI).40 Based on such evidence, the goals of anesthesia in neonates are not restricted to prevention of the stress response to surgery, but also effective management of pain and discomfort.1,2,16


Coincident with a new understanding of the importance of anesthesia and pain management in neonates, since 1999 numerous animal studies, including some in nonhuman primates, have demonstrated abnormal neuroapoptosis and, in some, long-term cognitive defects after early exposure to virtually all commonly used anesthetic and analgesic agents.10,30,42,44,76 Development of the nervous system is complex, involving neuronal proliferation, migration, differentiation, and “pruning” accomplished by apoptosis. This development is in part dependent on the balance of excitatory and inhibitory stimuli and neurotransmitters. Given the complexity of the process, as well as the obvious physiologic and developmental differences inherent in application of animal studies to humans, the overall impact of these studies remains uncertain. Concerns have been raised with respect to the animal data regarding dosing and the time course of exposure. A clinically appropriate dose is the minimum necessary to induce anesthesia in the species. In some species, and with some agents, this dose also results in significant mortality, increasing the difficulty of interpreting the significance. Synaptogenesis in rats occurs postnatally over the first 2 weeks of life. An analogous period in humans would range from the third trimester of pregnancy through the first 3 years of life. Whether the child might be susceptible to anesthetic toxicity during this entire period is unknown. Other studies looking specifically at neurodevelopment suggest that a postnatal 7-day-old rat more closely corresponds to the human fetus between 17 and 22 weeks of gestation. Elucidation of the critical period is of prime importance in anesthetic management.55 Finally, most of the animal studies of apoptosis involve anesthesia without surgery. Because neurodevelopment is related to the balance of stimulatory and inhibitory neurotransmitters, there is some indication that the absence of surgical stress may alter the neurodevelopmental response to anesthetics.


At this point, studies in humans are predominantly retrospective cohort studies, some of which suggest a possible association between neonatal anesthetics and longer term neurocognitive defects. There is an ongoing initiative by the US Food and Drug Administration (FDA) to study these risks.60 Confirmation of such long-term and relatively subtle effects in humans is of course a daunting task. At this time, there have been approximately 14 studies of anesthetic effects in humans.5,9,20,21,25,26,34,36,43,46,74,75,84,89 These studies have recently been reviewed by Gleich et al., along with a summary of available animal data.30 Of the human studies, eight demonstrated a potential effect of anesthetic exposure,9,20,43,84 although in four of these studies, it was only after multiple exposures.21,25,74,89 Only one uses prospective data in a limited 1-year follow-up of infants undergoing pyloromyotomy.84 The studies all use varied sources of data, either from a single facility, a single payer system, or a defined geographic area. In many of the studies, there is little information with respect to the specific anesthetic agents and/or techniques used. The outcome measures utilized also vary, including group-administered achievement tests, individually administered achievement tests, parent and teacher ratings, and diagnostic codes of neurodevelopmental disabilities. The fact that significant adverse outcomes were seen only with multiple anesthetic exposures raises the question of the effect of comorbidities on the apparent anesthetic effect. The adverse outcome owing to multiple exposures did persist in one study in which an attempt was made to rigorously control for comorbidity.25


Should these data cause any change in current clinical practice? No one can question the overwhelming benefit of anesthesia in the setting in which a surgical procedure, or any noxious procedure with significant stress, is required. The detrimental effects of surgical stress have been well shown. Similarly the benefits of early repair of some surgical problems, such as tetralogy of Fallot or neonatal hernia with risk of incarceration, have been shown, although such repair may lead to anesthesia at a younger, and potentially more susceptible, age. The human studies of anesthetic outcomes suggest minimal effect with single brief exposures. In addition, as discussed by Gleich et al.,30 a cautious and balanced approach to interpretation of the human epidemiologic studies is warranted given the overwhelming known benefits of anesthesia. As they also point out, this does not mean a lack of concern, as a modest increase in the risk for cognitive problems given the millions of exposures each year would have major implications. There is a clear need for large, prospective studies, with a defined end point, but this is a daunting task, and it will take years to complete.


A reasonable compromise can be suggested. First, the benefit versus the risk of delay in surgical procedures, particularly if performed in premature infants, should be carefully considered. Similar concerns could be raised in older children if the procedure is elective. Second, it seems reasonable to perform a “simple” anesthetic. There is virtually no extensive experience with many anesthetic agents in neonates. This lack of extensive experience is not unusual in neonates or pediatrics in general, but may be of increased importance given the small therapeutic margin of most anesthetics. There would seem to be little utility in the combination of agents, such as midazolam, propofol, and isoflurane, when a single agent could be used as easily. Whether the use of multiple agents could decrease the required dose of each and whether this would be beneficial are questions impossible to answer.


One preference is to use a predominant narcotic technique in premature infants who may be most at risk, when appropriate. Fentanyl has little, if any, activity as either an N-methyl-d-aspartate (NMDA) antagonist or gamma-aminobutyric acid (GABA) agonist. It is well tolerated hemodynamically and effective at preventing the surgical stress reaction. This particular technique may prevent extubation, but in this generally ill population, this is not usually a consideration. The possibility of recall with a pure narcotic technique can be raised, but with a dose adequate to prevent the stress response, this may not be important.


The goals of neonatal anesthesia are the same as in adults, but require different skills, knowledge, and care. The differences between adults and children are most profound in neonates, particularly premature infants. Advances in neonatology and the almost routine survival of infants weighing greater than 1000 g have led to new challenges for pediatric anesthesiology. Successful anesthetic management in a neonate requires meticulous attention to detail and a thorough understanding of neonatal physiology and development, pharmacology, and pathophysiology. The neonatal period is characterized by immaturity of organ systems, homeostasis, and metabolic pathways. It is a time of major developmental changes, and the effects of anesthesia on that development are not well characterized.


Personnel, equipment, and the operating room environment need to be specifically adapted for neonates. Anesthesia-related morbidity is decreased in children anesthetized by pediatric anesthesiologists compared with children cared for by non–pediatric anesthesiologists.41 Monitors, anesthesia delivery systems, mechanical ventilators, and environmental controls all need to be appropriate for use with neonates.


It is important to emphasize the perioperative nature of anesthetic management. Anesthesia care does not start and end at the door to the operative suite, and this is as critical in neonates as in older children and adults. Preoperative condition and management affect intraoperative care. Transport to the operating room can be one of the most critical aspects of an operation in a premature neonate. The postoperative period requires close monitoring and management of ventilation, fluid balance, and an environment tailored to the special needs of neonates. Assessment and control of postoperative pain require methods and tools specific to neonates.


Knowledge of the anatomic and physiologic differences among neonates, children, and adults is critical to careful anesthetic administration and management. Maturity of organ systems and metabolic processes varies significantly not only between adults and neonates, but also between preterm and term neonates.



Anesthesia, Neonatal Physiology, and Specific Concerns


Transition Phase and Persistent Pulmonary Hypertension of the Neonate


In utero, the pulmonary circulation is a high resistance circuit so that the lungs receive little blood flow, and oxygenation is a placental function. At birth, approximately 35 mL of amniotic fluid is expelled from the lungs, the lungs re-expand, and respiration begins. The lungs are initially very stiff (compliance very low), and the first breath may require negative forces of 70 cm H2O or more. Pulmonary vascular resistance (PVR) decreases rapidly with lung distention, and oxygenation and pulmonary blood flow and cardiac output increase. The increase in pulmonary blood flow coupled with decreased venous return from the inferior vena cava with clamping of the placenta causes left atrial pressure to exceed right arterial pressure, resulting in closure of the foramen ovale. The ductus arteriosus closes between 1 and 15 hours after birth.


Although PVR decreases, the pulmonary arterioles possess abundant smooth muscle, and the pulmonary vascular bed remains very reactive. In this setting, hypoxia, hypercarbia, or acidosis can cause a sudden increase in PVR and a return to a fetal circulatory pattern, a condition known as persistent fetal circulation or persistent pulmonary hypertension of the neonate (PPHN). Persistent pulmonary hypertension of the neonate is an acute, life-threatening condition, as shunt fraction increases to 70% to 80%, and profound cyanosis results. Many factors during anesthesia can affect this transitional state. Anesthetic agents can markedly diminish systemic vascular resistance (SVR), resulting in right-to-left shunt. Hypoxia or hypercarbia and acidosis from inadequate ventilation can increase PVR, with similar effects on shunt.



Respiratory Physiology: Apnea, Central Control of Ventilation, and Respiratory Distress Syndrome


Anesthetic agents are respiratory depressants. Central regulation of breathing is obtunded under anesthesia, with a significant decrease in the ventilatory response to increased carbon dioxide (CO2). Compared with older children and adults, in neonates, lung volume and functional residual capacity (FRC) as a percentage of body size are much less. Alveolar ventilation per unit lung volume is very high because the neonate’s metabolic rate is about twice that of an adult. Most of this alveolar ventilation is provided by a rapid respiratory rate of 35 to 40 breaths/min because tidal volume is limited, owing to the structure of the chest wall.


One consequence of the reduced FRC and high metabolic rate in a neonate is a diminished reserve. Changes in the fraction of inspired oxygen (Fio2) are rapidly seen as changes in Po2, and the neonate quickly desaturates if ventilation is interrupted. This situation limits time for intubation, and airway management can be difficult. The high alveolar ventilation also accounts for a very rapid uptake of inhalational anesthetic agents, especially in premature infants, making it easy to overdose with these agents. Closing volume, which is the lung volume at which smaller airways tend to collapse, is very close to FRC in neonates. It is well known that anesthesia causes decreases in FRC.38 In a neonate, this low closing volume can result in airway closure at end expiration, with resultant atelectasis, ventilation/perfusion mismatch, and increased intrapulmonary shunting.


An awake infant uses laryngeal braking resulting in an auto-positive end-expiratory pressure (auto-PEEP) to maintain FRC, but laryngeal braking is diminished by anesthesia. In a premature neonate, alveoli are immature and thick-walled and saccular. Surfactant production begins at 23 to 24 weeks’ gestation, but it may remain inadequate until 36 weeks’ gestational age; because of this, lung volumes and compliance are decreased further in very premature infants. Although the lung is less compliant in an infant than in an older child, the chest wall in an infant is very compliant. This combination results in increased work of breathing. Because resistance to airflow is inversely proportional to the fourth power of the radius of the airway, the work of breathing is increased further in neonates, particularly small premature infants.


Changes in airway resistance are also common during anesthesia, often resulting from small endotracheal tubes and equipment factors such as inspiratory and expiratory valves in the breathing circuit. Kinking of the endotracheal tube or the presence of secretions also can adversely affect resistance. Respiratory failure from fatigue can occur easily. Most neonates require controlled positive pressure ventilation during operative procedures because of the low FRC, increased closing volume, and increased work, along with changes induced by anesthetics. Infants already being ventilated require some increase in their ventilator settings after induction of anesthesia, and most infants require increased postoperative ventilatory support.


Tracheomalacia is common in premature infants, and if low in the airway, it may not be obviated by intubation. Bronchomalacia may result in airway collapse on expiration. Continuous positive airway pressure (CPAP) or PEEP increases FRC and decreases closing volume and helps to stent open the airway during anesthesia. Slower respiratory rates should be used with positive pressure ventilation to allow time for passive exhalation and prevent air trapping. The premature lung is very susceptible to barotrauma and oxygen toxicity. Pneumothorax and interstitial emphysema may develop if high peak inspiratory pressures are used.


Periodic breathing with intermittent apneic spells is common in neonates up to 3 months of age. Small premature infants have a biphasic ventilatory response to hypoxia, with an initial increase in ventilation, followed by a progressive decrease and apnea. The ventilatory response to CO2 is decreased in premature infants and, as noted, is decreased further by anesthesia. Postoperative apneic spells are common in premature infants, although incidence decreases with advancing postconceptional age. These episodes can be secondary to the immature respiratory control system (central), a floppy airway (obstructive), or both (mixed or combined).



Airway Anatomy


Airway anatomy in infants differs from anatomy in older children. The infant’s head is much larger compared with body size than that of older children, although the infant’s neck is short. The infant’s tongue is large, but the larynx is higher and anterior, with the cords located at C4 in the infant compared with C5 or C6 in an adult. The epiglottis of the infant is soft and folded. The neonate’s larynx has commonly been described as conical, with the narrowest point in the subglottic area at the cricoid ring, based on an often-quoted article by Eckenhoff. Eckenhoff’s description was apparently based on earlier measurements from plaster castings of a few cadaveric larynxes, and by his own admission, may not apply to living infants.6,63


Two more articles revisit this anatomy using magnetic resonance imaging (MRI)52 and video-bronchoscopic imaging.15 Based on these studies, the larynx is cylindrical, although not round in cross-section, but rather elliptical, with the anteroposterior dimension slightly greater. A tight-fitting, round endotracheal tube might compress the lateral laryngeal mucosa; subglottic stenosis remains a common complication, especially with longer-term intubation. Although uncuffed endotracheal tubes previously were used in neonates and children, use of newer cuffed tubes, composed of very thin, low pressure cuffs and thin walls, is feasible in many infants, although an uncuffed tube is still required in the smallest neonates. New tubes are available with very thin cuffs, and without the Murphy eye, which decreases the length of the tube below the cuff. This ensures that the entirety of the cuff is below the cords, avoiding pressure on the cords. A cuffed tube can be sized smaller because the cuff prevents leakage and could decrease the incidence of subglottic stenosis, rather than increase it, as previously believed. Laryngeal and tracheal trauma is important because even modest airway edema can be serious. At the cricoid ring, 1 mm of edema results in a 60% reduction in the cross-sectional area of the airway, causing increased airway resistance and increased work of breathing. Laryngomalacia is also common in premature infants and can result in obstruction.



Cardiac Physiology and Patent Ductus Arteriosus


Transitional cardiac changes were discussed earlier. Immediately after birth, with an open ductus arteriosus, most of the cardiac output is from the left ventricle, and left ventricular end-diastolic volume is very high. Consequently, the neonatal heart functions at the high end of the Starling curve. As PVR decreases, output from the two ventricles becomes balanced at 150 to 200 mL/kg per minute. Heart rate is rapid at 130 to 160 beats/min. Because end-diastolic volumes are already high, the infant heart is unable to increase stroke volume to a significant degree, and increases in cardiac output depend entirely on increases in heart rate. Baseline blood pressure is lower in infants than in older children, particularly in preterm infants; because cardiac output is increased, this is owing to a low SVR.


Almost all anesthetic agents have significant effects on the cardiovascular system. Inhalational agents tend to be cardiovascular depressants, and they can result in decreased myocardial contractility with bradycardia and subsequent decreased cardiac output. Most anesthetic agents cause decreased autonomic tone and peripheral vasodilation, decreasing afterload and preload. Because baroreceptor reflexes also are blunted by anesthesia, these decreases may make it impossible for the infant to compensate for pre-existing volume contraction or volume losses during anesthesia. Inotropic support may be necessary in a sick neonate, and almost all infants require some degree of volume loading during anesthesia. This belief may be at odds with contemporary thoughts on respiratory management, which emphasize diuresis; volume therapy needs to be carefully balanced to support tissue perfusion, urine output, and metabolic needs.


Patent ductus arteriosus is common in preterm neonates, especially if the neonate is hypoxic, and can result in pulmonary overcirculation and congestive heart failure. The patent ductus arteriosus may close spontaneously. Medical therapy with nonsteroidal anti-inflammatory drugs is sometimes successful. A patent ductus arteriosus rarely requires surgical ligation.



Fetal Hemoglobin


The infant has approximately 80% fetal hemoglobin (hemoglobin F) at birth. Hemoglobin F has a P50 (partial pressure of oxygen at which hemoglobin is 50% saturated) of 20 mm Hg compared with a P50 of 27 mm Hg for hemoglobin A, which means that hemoglobin F has a higher affinity for oxygen and that the hemoglobin dissociation curve is shifted to the left. In utero, this hemoglobin dissociation curve favors transport of oxygen from the maternal to the fetal circulation. Put another way, for any given oxygen saturation, the infant has a lower Po2. Unloading of oxygen at the tissue level also is diminished, although this is compensated for by an increased hemoglobin level of approximately 17.5 g/dL at birth. The decreased unloading can result in tissue hypoxia, however, if Po2, hemoglobin, or cardiac output decreases during surgery, with secondary development of metabolic acidosis. The hemoglobin increases slightly just after birth, then decreases progressively to a level of 9.5 to 11 g/dL by 7 to 9 weeks of life, owing to decreased red blood cell life span, increasing blood volume, and immature hematopoiesis. Hemoglobin F synthesis begins to decrease after 35 weeks’ gestation, and hemoglobin F is completely replaced by hemoglobin A by 8 to 12 weeks of life, paralleling the decrease in hemoglobin and helping to maintain tissue oxygenation.



Renal Physiology


Nephrogenesis is complete at 34 weeks’ gestation, and the term neonate has as many nephrons as an adult, although they are immature, with a glomerular filtration rate (GFR) approximately 30% of the adult’s GFR. With increasing cardiac output and decreasing renal vascular resistance, renal blood flow and GFR increase rapidly over the first few weeks of life and reach adult levels by about 1 year of life. The diminished function over the first year is well balanced to the infant’s needs because much of the neonate’s solute load is incorporated into body growth, and excretory load is smaller.


Several aspects of renal physiology are pertinent to anesthesia care. First, the neonatal kidney has only limited concentrating ability, apparently owing to a diminished osmotic gradient in the renal interstitium, whereas antidiuretic hormone secretion and activity are normal. Coupled with an increased insensible loss owing to a “thin” skin and increased ratio of surface area to volume, the limited concentrating ability of the kidney implies a tendency to become water depleted if intake or administration is inadequate. The neonatal kidney also is unable to excrete dilute urine efficiently and cannot handle a large free water load. In addition, primarily owing to a short, immature proximal tubule, infants are obligate sodium wasters. There is a tendency toward hyponatremia, especially if too much free water is administered during surgery, which can easily happen with continuous infusions from invasive pressure transducers, especially if adult transducers are used. Because of the lower GFR, the neonate also cannot handle a large sodium load and can easily develop volume overload and congestive heart failure. One final aspect concerns acid-base status: The neonatal kidney wastes small amounts of bicarbonate, owing to an immature proximal tubule; infants are born with a mild proximal renal tubular acidosis, with serum bicarbonate of approximately 20 mmol/L. All these changes are greater in preterm infants, particularly before nephrogenesis is complete at 34 weeks.



Temperature Regulation


Given a large surface area, small body volume, and minimal insulation, neonates are extremely prone to heat loss. Any degree of cold stress is detrimental and increases metabolic demands in the neonate. Infants are unable to shiver effectively, and cold stress causes catecholamine release, which stimulates nonshivering thermogenesis by brown fat. The increased catechols can be detrimental, causing increased peripheral vascular resistance and SVR, increased cardiac stress, and increased oxygen consumption. Anesthesia blunts thermoregulatory sensitivity8 and interferes with nonshivering thermogenesis and brown fat metabolism.19 Anesthesia also increases heat loss by inducing cutaneous vasodilation. At all times, including during transport and in the operating room, the infant must be subjected to a neutral thermal environment. An environment that is too warm can be equally detrimental. Core temperature must be carefully monitored at all times in the operating room.



Carbohydrate Metabolism


Whole-body glucose demand corrected for body mass in neonates can be twice that in adults. Carbohydrate reserves, primarily hepatic glycogen, in a normal newborn are relatively low, and even lower in an infant with low birth weight. Hypoglycemia can readily occur if the infant is deprived of a glucose source. Even transient hypoglycemia has been associated with neurologic injury in neonates.49 In contrast with adults, in whom hyperglycemia seems to potentiate brain damage during global and focal ischemia,71 hyperglycemia in neonates may provide some protection from ischemic damage.18,56 Generally, intravenous glucose (10% dextrose) or intravenous hyperalimentation should be continued intraoperatively, especially in infants with low birth weight without adequate glycogen or fat stores. Nonetheless, hyperglycemia can also be a problem in the perioperative period. Insulin response is deficient in preterm infants, and high catecholamines owing to illness or intraoperative stress can result in hyperglycemia. Careful monitoring of serum glucose is indicated.



Oxygen Therapy and Retinopathy of Prematurity and Chronic Lung Disease


Hypoxia is a common pathologic condition in neonates because of the incidence of lung disease; congenital heart disease and disordered transition are other frequent causes. Tissue hypoxia, or oxygen delivery to the tissues inadequate to sustain oxidative metabolism, is harmful, with well-known pathologic sequelae. There is at present no good method for reliably detecting tissue hypoxia, particularly in a real-time manner. Oxygen therapy is widely used, particularly during anesthesia, to avoid hypoxia. Until more recently, oxygen has generally been given in excess in the operating room, almost universally resulting in hyperoxemia. Hyperoxemia is always an iatrogenic condition, and there is increasing evidence that it is causally associated with multiple pathologic conditions in neonates, and should be strenuously avoided.58,73


Oxygen is a highly reactive molecule, and free radical formation by oxygen is well known. Reperfusion injury, which refers to damage resulting from free radical formation on reoxygenation after a period of hypoxia, is well established. Retinopathy of prematurity is the most widely known complication of hyperoxia, but there is increasing evidence that oxygen may play a role in chronic lung disease, neurologic impairment, and other pathologic conditions. For retinopathy of prematurity, even a brief hyperoxic period, such as during an anesthetic procedure, may be detrimental.7 There is also evidence that wide fluctuations in oxygenation, as often experienced during anesthesia, may be damaging.


Monitoring of oxygenation during operative procedures is problematic. Continuous pulse oximetry is the standard of care and has contributed to the safety of anesthesia by avoidance of hypoxia. The pulse oximeter is not as helpful for detection of hyperoxia. At hemoglobin saturations greater than 95%, most infants are hyperoxic; this is altered further by varying amounts of fetal hemoglobin. Maintenance of saturations greater than 95% is almost universal in most operating rooms, but is probably not the best course for neonates. It has been suggested that for ongoing management of neonates in the NICU, oxygen saturation targets of 90% to 95% should be used.24,76a Similarly, it has become common practice to use blended oxygen levels of 30% to 40% during initial resuscitation. It seems reasonable that Fio2 during operative procedures should be kept as low as possible, as long as oxygen saturation is 90% or greater, at least as an initial target. Many neonates can be managed intraoperatively on room air. Further consideration probably should be given to the universal practice of using 100% oxygen during induction and emergence from anesthesia, although this is more problematic because hypoxia also should be avoided, and oxygen desaturation during induction and intubation is frequent. This possibility further underscores the need for experienced personnel during induction and intubation of neonates.



Conduct of an Anesthetic


Preoperative Evaluation and Preparation


The preoperative evaluation should encompass the infant’s physical condition, including significant illness, the degree of transition from fetal to newborn physiology, maturity, and the presence of any congenital anomalies. Particular attention should be paid to cardiorespiratory status, required ventilatory or hemodynamic support, blood chemistries, and nutritional support. The course of pregnancy, labor, and delivery and a full maternal history are important details. As is the case with older children, a family history of anesthetic difficulties may be important. Maternal diseases such as diabetes, systemic lupus erythematosus, and preeclampsia have implications for the neonate. Congenital infections, oligohydramnios, intrauterine growth restriction, and maternal drug and alcohol use are also important considerations.


Gestational age, birth weight, and postnatal age affect anesthetic care. Birth weight does not accurately reflect maturity unless the infant is appropriate for gestational age, which is defined as being within 2 standard deviations of the mean for gestational age. Infants who are small for gestational age are more mature than their birth weight would indicate. Infants who are large for gestational age are often children of diabetic mothers, and they are at increased risk of hypoglycemia in the first 48 hours after birth. Newborns are characterized by birth weight as low birth weight (≤2.5 kg), very low birth weight (≤1.5 kg), and extremely low birth weight (<1000 g). Term is gestational age of 37 to 42 weeks, preterm is younger than 37 weeks, and post-term is older than 42 weeks.


A history of birth asphyxia or neonatal resuscitation and Apgar scores are important. History should include complete details of the present illness and treatment. Medications and administration times, details of vascular access, and respiratory parameters including ventilator type and settings all are crucial details, especially in sicker infants. Infants on high-frequency oscillatory ventilation may need to be switched to conventional ventilation and observed for several hours to facilitate movement to an operating room. If the infant is on some other modality, such as inhaled nitric oxide or extracorporeal membrane oxygenation, arrangements also may need to be made, and transport to the operating room would require more resources and assistance.


The time of the last oral feed should be ascertained, especially in elective surgery in healthier infants. Attenuation of airway reflexes with induction of anesthesia places the infant at risk of aspiration of acidic gastric contents, which can lead to serious inflammatory pneumonitis. Nil per os (NPO; nothing by mouth) guidelines are summarized in Table 41-223,69; these guidelines are more liberal for newborns than adults. Studies suggest that a safe NPO time after a formula feed might be 4 hours.13 This shorter length of time partially reflects more rapid gastric emptying, although in an infant, dehydration occurs much more quickly than in an adult, and this is a concern in an infant without an intravenous line. As in adults, gastric emptying is delayed with stress, anxiety, and illness. Infants with diseases such as pyloric stenosis, duodenal atresia, malrotation, or other obstructive lesions are NPO before surgery, and they need an intravenous line to maintain appropriate hydration. Despite the NPO status, there usually are significant gastric contents, and rapid-sequence or awake intubation is required. Emptying the stomach via nasogastric drainage is undependable and usually inadequate. Nasogastric feeds in intubated infants also should be discontinued at an appropriate time because the infant may need to be reintubated during surgery, and a full stomach would increase the risk for aspiration.



Physical examination includes vital signs, including temperature. Volume status needs to be carefully assessed because major shifts can occur easily during surgery. Many infants requiring surgery are ill. Infants with congenital anomalies often have multiple defects, which may have an impact on anesthetic care. Often, a group of defects suggests a well-recognized and characterized syndrome. Common syndromes with their anesthetic implications are listed in Table 41-3. (This list is incomplete.)



TABLE 41-3


Anesthetic Implications of Neonatal Syndromes
















































Syndrome Clinical Manifestations Anesthetic Implications
Adrenogenital syndrome

Analbuminemia

Andersen syndrome

Apert syndrome

Chiari malformation

Arthrogryposis multiplex congenita

Beckwith-Wiedemann syndrome

CHARGE association

Cherubism

Cornelia de Lange syndrome

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  2. Normal Mother-Infant Attachment
  3. Neonatal Apnea and the Foundation of Respiratory Control
  4. White Matter Damage and Encephalopathy of Prematurity

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Jun 6, 2017 | Posted by in PEDIATRICS | Comments Off on Anesthesia in the Neonate

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