The neonatal patient requiring surgery presents a unique challenge in the delivery of safe and effective airway management, ventilation, sedation, and anesthesia. The physiology of the neonate is unique and cannot simply be extrapolated from experiences with the older pediatric surgical patient. This chapter will begin with a review of fetal lung development, transitional physiology, and congenital anomalies as they pertain to the development of operative ventilation strategies. The remainder of the chapter will explore the procedural components that may improve patient safety and outcomes such as a risk and facilities assessment to determine if the patient is best served by undergoing the operation in the intensive care unit or the standard operating theater.
When considering operative intervention for the neonate, a multidisciplinary preoperative review of clinical status, with consideration given to anatomic complexities, current modality and degree of respiratory support, medications, and recent laboratory and radiographic data, should be performed. In preparation for the operation, a thoughtful approach to premedication for intubation and selection of the appropriate endotracheal tube is recommended. The use of a standardized checklist in the perioperative period may facilitate enhancing the situational awareness of the patient’s condition during these important transitions of care ( Table 37-1 ). During the operation, ventilation of the patient may be performed successfully using vigilant monitoring of the vital signs and blood gas parameters.
| Presurgical | Postsurgical |
|---|---|
| Gestational age Pertinent medical history Current mode of ventilation Review of recent labs and radiographs Medication list and dosing Airway status including type and depth of artificial airway Confirm consent has been obtained | Estimated blood loss Modifications to preoperative mode of ventilation Description of intraoperative patient stability Medications administered during operation Intraoperative blood gas review Challenges or complications that occurred intraoperatively Operation performed Status of parental postoperative update |
“Children are not simply small adults” is a tenet within pediatrics. An accurate reinterpretation of this maxim could be “Neonates are not simply small children.” The acutely ill newborn population is often cohorted in the neonatal intensive care unit (NICU) until the first discharge from the hospital. Despite the commonality of location, the physiology and developmental status of the pulmonary system for patients within the NICU are heterogeneous. A fetus delivered at a gestational age considered at the margin of viability will have lungs with marked developmental immaturities. The pulmonary system of this patient may be in the canalicular stage of development, reliant on newly formed acini as the basic structure for gas exchange with a paucity of both alveolar development and surfactant production by type II pneumocytes. Unique physiology is also encountered in the NICU. The transition from fetal to extrauterine circulation may occur without interruption after birth or may present ongoing management challenges for the patient who requires surgery during the first several days of life. Concerns for pulmonary hypertension may persist for some neonates as a sequela of ventilator dependence, birth depression, prematurity, or congenital anomalies. Finally, congenital anomalies requiring surgical intervention necessitate a disease- and patient-specific management plan to account for challenges that may be encountered during the operation.
Transitional Physiology and Pulmonary Hypertension
During pregnancy the fetus is dependent on gas exchange, which occurs at the level of the placenta. For centuries, the uterus had been referred to as the uterine lung. This description is appropriate, as development of the fetus requires oxygen delivery and elimination of carbon dioxide through the placenta. Both maternal and fetal blood flow to the placenta increases throughout gestation. Oxygenated blood is supplied to the fetus through the umbilical vein and returns to the placenta through the umbilical arteries. This unique circulation results in an oxygen saturation of approximately 60% in the term fetus prior to delivery.
Once the baby is delivered and the umbilical cord is clamped, the newborn is dependent on ventilation occurring at the level of the alveolar capillary interface. With spontaneous breathing, the lungs become inflated and stretch receptors are activated, which promote pulmonary vasodilation. Inspired oxygen and the newborn’s production of endogenous nitric oxide result in a decrease in pulmonary vascular resistance. Shunts at the level of the foramen ovale and ductus arteriosus, which had previously been very important in fetal development, close. The transition from fetal to extrauterine circulation is clinically apparent within the first 10 minutes of life. The immediate newborn oxygen saturation level will reflect the native fetal oxygen saturation of approximately 60%, but by 10 minutes of life the preductal oxygen saturation should increase to greater than 90%.
This transition to extrauterine circulation can be delayed in some newborns. The diagnosis of persistent pulmonary hypertension (historically referred to as persistent fetal circulation) should be suspected if the baby does not have primary lung disease (e.g., surfactant deficiency, aspiration syndrome) and is requiring additional oxygen to maintain ideal oxygen saturations and if there is a significant difference in oximetry measured in the preductal (right hand) and postductal location (left hand or either foot). The differential diagnosis for persistent pulmonary hypertension of the newborn (PPHN) is found in Table 37-2 (and further discussed in Chapter 14 , Chapter 32 ). Pulmonary vascular resistance will often decrease throughout the first several days of life. This can be assessed through serial echocardiography, the difference in pre- and postductal saturation levels, and a bedside evaluation of the fraction of inspired oxygen required to maintain ideal preductal saturations.
| Persistent fetal circulation (idiopathic) Meconium aspiration Blood aspiration Pulmonary hypoplasia Congenital diaphragmatic hernia Pneumonia/sepsis | Respiratory distress syndrome Hypothermia Chronic lung disease Maternal medications
|
This is clinically relevant for the anesthetist when surgery is considered in the first postnatal days for a baby diagnosed with primary pulmonary disease with or without PPHN. If the baby is improving from the perspective of pulmonary hypertension, waiting to perform a nonemergent procedure may allow a greater margin for safety and effective ventilation during the case. Preoperative identification of a patient with a history of PPHN or lung disease who may develop PPHN intraoperatively allows the anesthetist to predict risk for rebound pulmonary hypertension and be prepared to recognize and initiate appropriate therapies.
The diagnosis of pulmonary hypertension may also become clinically relevant in the former premature infant with bronchopulmonary dysplasia (BPD). Premature infants with BPD are at risk for concomitant pulmonary hypertension, though it remains unclear which of the two is the principal diagnosis. In most cases, infants with BPD and associated pulmonary hypertension will continue to require oxygen and sometimes diuretic supplementation for several months after birth. In severe cases, medications such as sildenafil may also be prescribed. These infants may present to the anesthetist just prior to discharge from the initial hospitalization for procedures including gastrostomy tube placement, inguinal herniorrhaphy, and intervention for progressive retinopathy of prematurity.
There are special considerations for the surgical patient with pulmonary hypertension. Ventilation strategies that were being utilized in the NICU prior to the operation may continue to be effective during the operation. These strategies typically include avoidance of hypoxemia and acidosis. Hypoxemia and acidosis increase pulmonary vascular resistance, placing strain on the right ventricle and worsening pulmonary hypertension. Pharmacologic and nonpharmacologic interventions to decrease pain and agitation are indicated. Inhaled nitric oxide, a selective pulmonary vasodilator, may be a component of the ventilation strategy utilized in the NICU and should be continued throughout the operation. Alternatively, it may be considered as an intraoperative rescue strategy through the mechanical ventilation circuit. Additional therapies considered in the treatment of pulmonary hypertension include milrinone or vasopressin as adjunctive intravenous infusions that may provide additional pulmonary vasodilatory effects. Milrinone may also affect systemic vascular resistance, necessitating vigilant blood pressure monitoring.
Key Points
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Common causes of pulmonary hypertension in the infant are delayed transition to extrauterine life, prematurity, and primary pulmonary disease.
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Suspect pulmonary hypertension if there is a significant difference in pre- and postductal oxygen saturation and an increased oxygen requirement.
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Intraoperative treatment strategies for patients with PPHN include avoidance of hypoxemia and acidosis, adequate sedation, and utilization of inhaled nitric oxide.
Pulmonary Development and Lung Injury
The diversity of size of patients within the NICU is remarkable. There may be a tenfold difference in weight of the smallest to largest patient. Beyond the marked variation in the birth weight of this population, the individual patients are at different stages of the lung development continuum. The smallest and often most premature babies are dependent on primordial gas exchange units within the lungs, whereas the largest patients may have progressed toward a fully developed alveolar capillary interface. Additionally, a patient who began life as a fragile extremely low birth-weight newborn may have developed BPD while hospitalized. Despite the appearance of a now robust infant approaching or past the estimated due date, the pulmonary system of the former premature patient may be markedly abnormal. Recognition of normal lung development stages and potential abnormal pathophysiology will allow the anesthetist to develop a ventilation strategy appropriate for the individual patient.
The respiratory system of many premature babies in the NICU may be at the canalicular stage, which typically occurs between 16 and 25 weeks of gestation. Characteristics of this stage of lung development include the formation of the earliest gas exchange units and early evidence of surfactant production by the type II pneumocytes. The lungs begin to develop both respiratory and nonrespiratory bronchioli. During this developmental stage, an extensive capillary network becomes progressively approximated to the epithelium of the developing airspaces.
Beyond 25 weeks the lung enters into the terminal sac stage of development. The appearance of mature alveoli may be seen as early as 28 weeks’ gestation. Lung volume and surface area increase throughout this stage to allow for sufficient gas exchange.
Premature infants are at risk for the development of BPD, a disease in which there is arrest of lung maturation (see Chapter 35 ). A multitude of factors may contribute to this pathology including the administration of exogenous corticosteroids, exposure to prolonged mechanical ventilation, and inadequate postnatal nutrition. Following the initial injury, further exposure to excessive oxygen delivered to the developing airway, mechanical ventilation, and barotrauma may activate release of cytokines, thus contributing to continued airway inflammation. BPD is characterized by reduced lung compliance and increased airway resistance. Radiographically, a heterogeneous appearance to the lung, with areas of atelectasis and hyperinflation, may be observed.
The patient may have a chronic supplemental oxygen requirement to achieve target oxygen saturations. Often the blood gas of infants with BPD will demonstrate a markedly compensated respiratory acidosis, with serum bicarbonate levels significantly above expected values. Blood gases in the operating room probably will continue to reflect a long-standing compensated hypercarbic baseline. Operative strategies to support adequate gas exchange while minimizing risks to the developing lung, such as utilizing lower tidal volumes and proper oxygen saturation limits, being used in the NICU may remain a viable option during the procedure.
Key Points
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Postnatally, premature infants continue to develop sufficient gas exchange by maturation of the alveolar capillary interface.
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Premature infants are at risk for BPD and require lung-protective ventilatory strategies such as lower tidal volumes and oxygen saturation limits to prevent exposure to barotraumas and excess oxygen exposure.
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Infants with BPD have reduced lung compliance and increased airway resistance; they may require supplemental oxygen and unique ventilator strategies intraoperatively.
Intraoperative homeostasis for a chronic BPD patient may be to replicate the compensated respiratory acidosis from the preoperative state rather than the achievement of “normal” blood gases.
Anatomic Considerations
A variety of congenital anomalies requiring operative intervention shortly after birth are commonly encountered in the NICU. In the case of a thoracic anomaly, the lungs may be smaller than those of an equivalently aged healthy infant. Alternately, infants born with abdominal wall defects may have healthy lungs equivalent to those of healthy newborns, but the operation to repair the defect may cause a temporary reduction in total lung capacity and loss of functional residual capacity due to displacement of the diaphragm cephalad after restoration of the contents to an intra-abdominal position ( Fig. 37-1 ).
Intrathoracic Masses
Infants with a prenatally diagnosed intrathoracic mass, such as a congenital diaphragmatic hernia (CDH) or a congenital pulmonary adenomatous malformation, are at high risk for pulmonary hypoplasia owing to abnormal fetal lung development. Pulmonary hypoplasia is most typically encountered in the lung ipsilateral to the mass, but in severe cases, both lungs may be significantly hypoplastic. In addition to pulmonary hypoplasia, a patient with CDH may have marked developmental abnormalities of the smooth muscle of the pulmonary vasculature leading to a severe form of PPHN. When viewed microscopically, the lungs of infants with CDH have fewer alveoli, increased interstitial tissue, thickened alveolar walls, and pulmonary arteries with increased medial and adventitial tissue present. These findings and altered autonomic regulation are likely to unite to create higher pulmonary pressures, which are often “fixed,” or not responsive to typical pulmonary vasodilators like inhaled nitric oxide. In fact, the largest study as of this writing investigating the role of inhaled nitric oxide in patients with CDH demonstrated immediate short-term improvements in oxygenation in some treated infants but no reduction in the need for ECMO or death.
Following delivery, infants with CDH are often ventilated over several days with a lung-protective strategy, minimizing exposure to barotrauma, until pulmonary vascular resistance has decreased prior to operative interventions. High-frequency ventilation with a high-frequency oscillator or jet ventilation may be considered. It is appropriate during the surgical repair of CDH to continue a lung-protective strategy while being mindful of recurrence of pulmonary hypertension. Although the entirety of the pulmonary hypertension in these patients may not be responsive to acute modulation, avoidance of hypoxemia and acidosis is recommended while monitoring for acute pulmonary vasculature hyperreactivity. Pulmonary hypertension in the setting of operative stress or alterations in pH and carbon dioxide levels may be recognized by continuous intraoperative monitoring of pre- and postductal saturations as well as continuous transcutaneous P co 2 levels. An increasing difference between pre- and postductal saturations during the case suggests a right-to-left shunting of deoxygenated blood through the patent ductus arteriosus. At the time of hernia reduction, it is also important to maintain awareness of thoracic anatomy and recognize that as the tracheobronchial tree shifts toward midline, tube displacement could potentially occur, resulting in the tip of the endotracheal tube becoming located within the right main stem bronchus. This scenario should be considered if the patient develops worsening respiratory stability after the bowel has been reduced and the hernia repaired. Following the reduction of intestine and repair of the hernia, a “potential” space within the thoracic cavity remains on the affected side. In concept, this can be considered a pneumothorax ex vacuo, and this space will fill with fluid postoperatively. The decision to leave a chest tube in place at the end of the operation is dependent more on the surgeon’s preference than evidence. Increasingly, pediatric surgeons are no longer leaving chest tubes in place following these types of repairs, which may prevent potential exposure of the hypoplastic lung to excess distention by allowing some fluid to accumulate in the intrapleural space.
Abdominal Wall Defects
Infants with omphalocele and gastroschisis often have normal fetal lung development. Infants with giant omphaloceles are at risk for pulmonary hypoplasia, most likely due to abnormal thoracic cage development related to liver displacement. However, most often infants with abdominal wall defects are born at term, require no significant respiratory intervention at the time of birth, and remain without respiratory support until the time of surgery.
Some lesions, depending on the amount of displaced bowel content, can be replaced intra-abdominally in the first few hours of life. However, larger lesions may require a staged approach. Over the first days to week of life, attempts are made to reduce the bowel slowly into the relatively hypoplastic abdominal cavity through a silastic silo created soon after birth. When the surgeon determines that bowel reduction from the silastic silo into the peritoneum is adequate, complete operative reduction and abdominal wall closure occur. Once the abdominal contents are reduced, intraperitoneal pressure increases, resulting in a reduction of total lung capacity and functional residual capacity (FRC). With a reduction in FRC, lung compliance decreases and the infant may require increased peak inspiratory pressures to maintain adequate minute ventilation. Positive end-expiratory pressure (PEEP) may need to be increased once the bowel has been reduced to preserve FRC. Maintaining appropriate minute ventilation may also be addressed by increasing the mandatory rate or through high-frequency ventilation. Postoperatively the use of pulmonary function studies may help guide ventilator management.
Key Points
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Intraoperative ventilation strategies for the patient with congenital anomalies should include consideration of how the anatomy may influence respiratory mechanics.
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Infants with thoracic anomalies are at high risk for pulmonary hypoplasia and require a lung-protective ventilatory strategy that minimizes barotrauma.
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Infants with abdominal wall defects can develop reduced total lung capacity following surgery and may require a ventilatory strategy that focuses on maintaining minute ventilation. This can be accomplished by an increased ventilation rate and lung recruitment through increased PEEP.
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An operative ventilatory strategy should include close monitoring for pulmonary vascular hyperreactivity for infants with pulmonary hypoplasia who are at high risk for pulmonary hypertension.
Location of Operation
Performing neonatal surgery in the intensive care unit is well described. One of the primary incentives for operating at the patient’s bedside is the inherent risk associated with transporting the unstable neonatal patient between the intensive care unit and the operating room. In addition to central line placement, the two most common neonatal surgeries that occur at the patient bedside are ligation of the patent ductus arteriosus and laparotomy or peritoneal drain placement for necrotizing enterocolitis. Other surgeries frequently performed at the bedside include reservoir placement for posthemorrhagic hydrocephalus and surgeries associated with extracorporeal membrane oxygenation including cannulation and decannulation. Though it may seem desirable to bring the surgeon to the baby’s bedside, there is concern for and increased risk for infection and, of most concern, inadequate lighting in the operative field. At centers with experience bringing the operating team and requisite equipment to the intensive care unit, these interventions have been performed safely and with outcomes at least equivalent to, if not better than, transporting the patient to the operating room. The provider who will direct the ventilation during the operation will need to become familiar with mechanical ventilators that may not be commonly used in the operating room. This can be achieved by performing a presurgical briefing between the anesthesia team that will be managing the case and the neonatology team that has been providing care for the patient preoperatively. The mode of ventilation and recent blood gases should be discussed collaboratively to determine if change is necessary and anticipated prior to surgery. Once the operation has finished, a similar postsurgical debriefing should occur between teams to ensure a safe transition of care.
Premedication for Intubation
Neonatal tracheal intubation and mechanical ventilation support will probably be necessary for the operative procedure. Recent position statements recognize that intubation may need to proceed without premedication during an emergent resuscitation or in certain neonates with airway anomalies. However, most presurgical neonatal intubations present an opportunity to provide premedication prior to insertion of the endotracheal tube. This painful procedure is known to induce apnea, hypoxemia, and bradycardia while causing increases in systemic and intracranial pressure. Along with the technical skill required to successfully intubate, an evidence-based approach to selection of analgesia, sedation, vagolytics, and muscle relaxants is essential to optimize the quality of this procedure.
Providing adequate analgesia for this invasive procedure is indicated to provide patient comfort, avoid hypertension, and optimize intubation conditions. The ideal analgesic would be fast acting, with a short half-life and minimal side effects.
The opioids most commonly considered for neonatal premedication include natural (morphine) as well as synthetic (fentanyl and remifentanil) opioids. Administration of intravenous morphine results in peak analgesia in 15 minutes. The clearance of morphine is gestational age dependent, with a longer half-life observed in premature infants compared to term. Fentanyl has a rapid onset of action within 2 to 3 minutes and a short duration of action of 60 minutes. Clearance of fentanyl is also positively correlated with gestational age and birth weight. Remifentanil has an immediate onset of action, has a half-life of less than 5 minutes, and has been used in the term and preterm populations. Benzodiazepines and barbiturates have been investigated as classes of medications that may be used for premedication because of their sedative effects. Midazolam is the most widely used benzodiazepine for premedication for endotracheal intubation. Pharmacokinetics varies among individual neonates, and clearance appears to be positively correlated with gestational age. Propofol is an amnestic sedative that appears to have several mechanisms of action including activation of γ-aminobutyric acid receptors, inhibition of N -methyl- d -aspartate receptors, modulation of calcium influx through slow calcium ion channel activity, and sodium channel blockade. Early reports of the use of propofol as an induction agent for endotracheal intubation in preterm infants with gestational ages of 25 to 30 weeks suggested a reassuring safety profile. However, more recent data suggest that propofol use for this indication in this population should be approached with caution owing to its significant cardiovascular side effects.
Vagolytic agents have been investigated as medications to be used for premedication because of the ability to reduce vagal-induced bradycardia and to decrease oral secretions. Both atropine and glycopyrrolate have been shown to be effective in preventing vagal bradycardia during endotracheal intubation in neonates.
Muscle relaxation is another component of optimizing intubation conditions. The intended effect is primarily to decrease patient movement, allowing the provider to have a more controlled field for visualization. The secondary effect of neuromuscular blockade is a decrease in intracranial pressure. These medications act at the end plate of the neuromuscular junction to block transmission between motor nerve endings, causing paralysis of the skeletal muscles to facilitate endotracheal intubation. Neuromuscular blockers can be classified as nondepolarizing (atracurium, mivacurium, vecuronium, rocuronium, and pancuronium) and depolarizing (succinylcholine). Succinylcholine should be approached with caution in patients with hyperkalemia or a family history of malignant hyperthermia.
It is recommended to use premedication for nonurgent neonatal intubations, including analgesic agents or an anesthetic dose of hypnotic drugs. Vagolytic agents and rapid-onset muscle relaxants should be considered. Use of sedatives alone such as benzodiazepines without analgesics should be avoided, and muscle relaxants should be given only after an analgesic agent has been used ( Table 37-3 ).
| Drug | Dose (IV) | Onset of Action | Common Adverse Effects |
|---|---|---|---|
| Analgesic | |||
| Fentanyl | 1-4 μg/kg | Almost immediate | Apnea, hypotension, CNS depression, chest wall rigidity—give slowly |
| Remifentanil | 1-3 μg/kg | Almost immediate | Apnea, hypotension, CNS depression, chest wall rigidity |
| Morphine | 0.05-0.1 mg/kg | 5-15 min | Apnea, hypotension, CNS depression |
| Hypnotic/Sedative | |||
| Midazolam | 0.05-0.1 mg/kg | 5-10 min | Apnea, hypotension, CNS depression |
| Propofol | 2.5 mg/kg | 30 s to 10 min | Histamine release |
| Apnea | |||
| Bronchospasm | |||
| Bradycardia | |||
| Muscle Relaxant | |||
| Pancuronium | 0.05-0.1 mg/kg | 1-3 min | Hypertension |
| Tachycardia | |||
| Bronchospasm | |||
| Salivation | |||
| Vecuronium | 0.1 mg/kg | 2-3 min | Hypertension/hypotension |
| Tachycardia | |||
| Bronchospasm | |||
| Arrhythmias | |||
| Rocuronium | 0.6-1.2 mg/kg | 1-2 min | Hypertension/hypotension |
| Tachycardia | |||
| Bronchospasm | |||
| Arrhythmias | |||
| Vagolytic | |||
| Atropine | 0.02 mg/kg | 1-2 min | Dry hot skin |
| Tachycardia | |||
| Glycopyrrolate | 4-10 μg/kg | 1-10 min | Dry hot skin |
| Tachycardia | |||
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