Chapter 86

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1438 PART 5 ■ Anesthetic, Surgical, and Interventional Procedures: Considerations national bodies, for example, the U.S. Food and Drug Administra - tion (FDA), and more information will most likely be available within the next 5 to 10 years. For more in-depth information re - garding these issues the reader is referred to the reviews by Mellon 13 and Anand. 14 This chapter aims at providing a comprehensive review of the theoretical aspects of neonatal anesthesia and at giving practical guidelines for the most frequently performed surgical interven - tions during the neonatal period. PHYSIOLOGIC PARTICULARITIES PRONE TO INFLUENCE ANESTHESIA MANAGEMENT Development of the Nociceptive System and Stress Response All structural components of the nociceptive system are already developed at the end of the second trimester, 15 as described in Chapter 4. In a pivotal study, Giannakoulopoulos and coworkers verified a competent stress reaction as well as behavioral signs indicative of a fully functional nociceptive system even in the fetus. 16 Two different groups of subjects were studied during fetal exchange transfusion due to fetomaternal blood group incom patibility. To achieve fetal venous access, the umbilical vein is usually punctured close to the insertion of the umbilical cord in the placenta under ultrasonographic guidance. Since the umbilical cord is uninnervated, such a procedure should not be associated with any pain or stress reaction. However, due to anatomic factors, this approach for fetal venous access is not always feasible, and in such cases the venous system of the fetus has to be accessed by puncture of the intrahepatic vein. This method, thus, involves perforation of the skin, muscle, and liver capsule, and if the fetus does have functionally intact stress and nociceptive systems, such a puncture would be associated with measurable signs of a neuro endocrine stress reaction as well as behavioral signs indicative of a pain reaction. As could be expected, puncture and exchange transfusion performed via the umbilical cord was not associated with any measurable stress reaction or behavioral signs of pain. However, in fetuses undergoing intrahepatic vein cannulation and transfusion, a distinct stress reaction could be observed (increase in cortisol and -endorphin). The stress response was also found to correlate with the duration of the needling and transfusion procedure in these fetuses. Moreover, during puncture of the abdominal wall and the liver capsule, the babies were found to start breathing rapidly (as well as starting to move the extremities vigorously). No such behavioral reactions were noted during puncture of the umbilical cord and the transfusion process itself did not induce any stress response. Neonatal pain is capable of producing a “pain memory,” either as a result of plasticity changes within the nervous system itself or due to a psychological process. A number of studies performed in neonatal rodents have investigated the maturational changes of the opioid system and the descending pain inhibitory control pathways. The main differences between the neonatal and adult rodent are summarized in Table 86–1. Although the current knowledge is almost exclusively based on the neonatal rodent studies, it is reasonable to assume the conditions may be similar in the human neonate. TABLE 86-1. Developmental Changes in the Nociceptive System of the Fetal and Newborn Rat 1. High density of -receptors both in superficial and deeper layers of the gray matter in the spinal cord. A more adult localization of -receptors to the superficial layers of the dorsal horn are not achieved until postnatal day 14–28 (P14–28) (approximately equal to a human toddler). 28 2. Nociceptive A-fiber input predominates over C-fiber input in the neonatal period. 29 3. Descending inhibitory control pathways from the brainstem to the spinal cord are not functional in neonates or during early infancy. 30 4. Predominance of enkephalin over endorphin in the initial perinatal period. 31 5. Enhanced intracellular calcium-release in response to NMDA (N-methyl-D-aspartate) stimulation compared to adults. 32 6. A 40-fold increase in efficacy of morphine from P3 (approx. human preterm baby) to P14 (approximately late infancy). 33 Very interesting new knowledge currently exists regarding the growth factor effects of endogenous opioids in relation to normal neuronal development during the neonatal period. In rat models, endogenous opioids have, through a receptor mediated process, been found to have an inhibitory influence on dendrite and spine elaboration in 10-day-old rodents. 17 Suppression of astrocyte growth has also been shown in vitro following met-enkephalin administration. 18 Furthermore, morphine administration has been found to cause inhibition of DNA synthesis in the neonatal rat brain but not in older animals. This effect could be blocked by pretreatment with naloxone once again indicating receptor me - diated mechanisms. 19 Despite the apparently normal development of most neonates following neonatal surgery, including significant postoperative administration of morphine or other opioids, further knowledge is required to delineate the potential problem of interference with normal neuronal development of the neonate if exposed to high doses of exogenous opioids. 20 A number of studies in preterm and term human babies reported the presence of a fully competent neuroendocrine stress reaction in response to surgical stimula - tion. 21,22 The neuroendocrine stress response has been found to be correlated with degree of surgical trauma 23 and can be beneficially modified by adequate anesthesia and analgesia. 24 The attenuation of the neuroendocrine stress response in both preterm and neonates by proper analgesia has been found to reduce morbidity. In the specific setting of neonatal cardiac surgery, high-dose sufentanil anesthesia and postoperative analgesia (n 30) have been shown to reduce the incidence of sepsis/necrotizing entero - colitis, disseminated intravascular coagulation, and metabolic acidosis by 20 to 25 percent 24 compared with a halothanemor phine based anesthetic technique (n 15). This study was also prematurely ended because of apparently lower mortality figures in the sufentanil group (0%) compared to the previous halothane-morphine based anesthetic technique (27%). 24 The reader should bear the small number of patients enrolled in this study in mind, but these results clearly point to a more favorable outcome for sick children if adequate intra- and postoperative analgesia is provided.
CHAPTER 86 ■ Management of the Neonate: Anesthetic Considerations 1439 Cardiovascular System The physiology and main developmental stages of the cardiovas - cular systems are discussed in Chapter 3. Transitional Circulatory Adaptation Following birth, the circulation changes from a fetal parallel pattern characterized by both ventricle pumping the majority of their output into the systemic circulation (pulmonary blood flow 10% of combined ventricular output 25 ) to an extrauterine series pattern with the right and left ventricles assuming responsibility for the pulmonary and the systemic circulations, respectively (see Chapter 3). The three embryological shunts close during the immediate postnatal period. The placenta circulation and the flow through the ductus venosus cease when the umbilical cord is clamped at birth. The foramen ovale will close within 1 to 2 hours after delivery, as the pressure in the left atrium will surpass that of the right atrium due to the rapid decrease in pulmonary pressures associated with initiation of breathing and the subsequent aeration of the lung. The foramen ovale will remain patent during the neonatal period and anatomic closure will often not take place until 1 year of age. Anatomic closure will not take place in all individuals and a patent foramen ovale can be present in up to 10 to 20% of the adult population. The ductus arteriosus will start to close approximately 10 to 15 hours following delivery and is usually physiologically closed by the 2nd day of life. However, permanent anatomic closure with formation of the ligamentum arteriosus is not completed until about 3 weeks postnatally. During this period the ductus arteriosus might reopen if exposed to unfavorable neuroendocrine mediators or increasing pulmonary pressures. The main factors that modulate pulmonary vascular resistance and neonatal pulmonary resistance at birth and during the first days of life are summarized in Table 86–2. During certain circumstances in the early neonatal period, a relapse into the fetal circulatory pattern most often occurs due to pulmonary vasospasm with resulting pulmonary hypertension but can also be a consequence of, e.g., severe hypoxia or hypercarbia. Pulmonary vasospasm resulting in persistent pulmonary hyper - tension of the newborn (PPHN) is characterized by profound hypoxia due to right-to-left shunting through the fetal extrapul - monary shunts combined with right ventricular strain and circulatory compromise. A number of different neonatal condi - tions predispose to the development of PPHN, for example, con - genital diaphragmatic hernia, meconium aspiration syndrome, asphyxia, hypoxia and sepsis, all of which can coincide with the need for neonatal surgical intervention (Table 86–3). Thus, the neonatal anesthesiologist needs to be familiar with the pathophy - siology of PPHN, its diagnosis, and treatment. Conventional treatment consists of tracheal intubation and mechanical ven - tilation, induction of alkalosis by attempted hyperventilation, and acidosis correction, analgosedation, muscle paralysis, volume replacement, and inotropic/pressor support (dopamine, norepine phrine). 26 More recent treatments include selective pulmonary vasodila tation by means of inhaled nitric oxide (iNO) or inhalation of nebulized prostacyclin and the use of high-frequency oscillatory ventilation. 27 Regarding iNO, the effective dose range appears to be within the 1 to 30 ppm dose range, although doses up to 80 ppm might be attempted in severe cases for brief periods of time. 28 Side effects of the treatment are few and mainly limited to the risk of methemoglobin formation and minor prolongation of bleeding time. The most dangerous complication of iNO treatment is severe rebound pulmonary hypertension in association with abrupt discontinuation of the iNO therapy either accidentally or during deliberate weaning. The risk of severe rebound necessitates the immediate option to reinstate therapy and to be able to handle an accidental delivery device malfunction situation; a back-up system needs to be available at the bedside. Since NO and especially concomitant and unavoidable nitrogen dioxide (NO 2 ) exposure at higher concentrations (100 ppm and 2 ppm, respectively) can be toxic it is imperative to use an approved delivery device and also to measure continuously the NO and NO 2 levels in the in - spired gases. The anesthesiologist must be prepared to conduct the anesthetic without interrupting these new and effective treat - ments. If the anesthesiologist is not comfortable in this situation, help should be sought from an experienced neonatologist. TABLE 86-2. Factors That Modulate Pulmonary Vascular Resistance in the Near-Term and Term Transitional and Neonatal Pulmonary Circulation Endogenous mediators and mechanisms Mechanical factors Lowers Pulmonary Vascular Resistance Oxygen, nitric oxide PGI2, E2, D2 Adenosine, ATP, magnesium Bradykinin, atrial natriuretic factor Alkalosis, K channel activation Histamine, acetylcholine Vagal nerve stimulation b-Adrenergic stimulation Lung inflation Vascular cell structural changes Interstitial fluid and pressure changes Shear stress PGI2, E2, D2 prostaglandins I2, E2, D2; ATP adenosine triphosphate; PGF2a prostaglandin F2a. Increases Pulmonary Vascular Resistance Hypoxia, acidosis Endothelin-1, leukotrienes, thromboxanes Platelet activating factor Ca channel activation a-Adrenergic stimulation PGF2a Overinflation or underinflation Excessive muscularization, vascular remodeling Altered mechanical properties of smooth muscle Pulmonary hypoplasia, pulmonary thromboemboli Alveolar capillary dysplasia Main pulmonary artery distention Ventricular dysfunction, venous hypertension
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