With the advent of antenatal steroids, surfactant therapy, and the overall improvement in care of extremely premature infants, mortality from medical problems of prematurity has decreased. However, as survival rates of premature infants increase, the incidence of chronic medical conditions related to prematurity has also increased. As a consequence, anesthesia providers are exposed to a growing number of infants and children who were born prematurely and have a variety of chronic medical conditions that may influence their response to anesthesia. These patients have a higher risk for complications while sedated or anesthetized, and this risk persists into young adulthood.
Bronchopulmonary Dysplasia
The impact of prematurity on lung development and function will influence the preoperative evaluation of the formerly premature child. The terminology used to describe neonatal respiratory disorders can be confusing so to clarify: any pulmonary disease resulting from a neonatal respiratory disorder is termed chronic lung disease of infancy (CLDI). Causes of CLDI vary based on age. Bronchopulmonary dysplasia (BPD) is the most common form of chronic lung disease, and it is defined as the need for supplemental oxygen for at least 28 days after birth. It is categorized as mild, moderate, or severe, which is determined by the required amount of oxygen or respiratory support at 36 weeks postmenstrual age for infants born before 32 weeks and at 56 days for infants born greater than 32 weeks gestation.
A distinction has been made between “old” and “new” BPD. Old BPD occurred in near-term infants during the saccular and late alveolar stages of lung development (see Chapter 1 ), some of whom had direct lung injury in the form of pneumonia, sepsis, aspiration, or congenital heart or lung malformations. They were treated with prolonged, aggressive mechanical ventilation with high oxygen concentrations and developed a severe form of CLDI with histopathology consistent with diffuse alveolar hyperplasia, wide-spread inflammation, peribronchial smooth muscle hypertrophy and parenchymal fibrosis. In contrast, the histopathology in new BPD does not reveal diffuse inflammatory changes or alveolar hyperplasia. Instead, the histopathology is consistent with an arrest of alveolar development with large simplified alveoli leading to a reduced surface area for gas exchange and fewer alveolar-airway attachments that predispose to small airway collapse. Because the alveoli and pulmonary arterioles grow in parallel, patients with BPD may also have pulmonary hypertension. BPD-related pulmonary hypertension typically has a fixed component related to decreased vascular surface area and a dynamic component because of increased vascular reactivity.
The clinical manifestations of the classic, more severe form of BPD include tachypnea, rales, bronchospasm, and a persistent requirement for supplemental oxygen. Carbon dioxide retention is a prominent finding and is presumably because of increased dead space ventilation. Radiographic abnormalities include hyperinflation, bleb formation, and interstitial densities ( Fig. 12.1 ). Infants with severe BPD may also demonstrate episodes of sudden, severe bronchospasm, and cyanosis after agitation or physical stimulation (“BPD spells”). These are thought to be caused by nearly complete tracheal collapse as a result of underlying tracheomalacia, a complication of prolonged mechanical ventilation. These episodes are treated with sedation or calming of the infant combined with application of continuous positive airway pressure (CPAP) or positive pressure ventilation in the event of unremitting hypoxemia.
The clinical manifestations of the new milder form of BPD are characterized by a more benign clinical course with respect to respiratory support, but the pulmonary pathology in these children should not be underestimated ( Fig. 12.2 ). Formerly premature children still have a higher incidence of wheezing secondary to small airway collapse related to impaired alveolar development and the rate of readmission for respiratory tract infection in the first year of life is higher compared with children born at term. Thus, a concerted effort should be made to reduce exposure to passive smoke inhalation and viral infection in formerly premature infants with BPD. The wheezing exhibited by children with BPD is often mistaken for asthma and as a result these children may receive unnecessary steroid or beta-agonist therapy. As noted above, this new form of BPD is not an inflammatory process like asthma and is unlikely to have a significant clinical response to steroid treatment. Additionally, airway obstruction in BPD is only partially reversed with beta-agonist therapy. As the infant with mild BPD grows, there is a comparatively less bronchospastic component than with the more severe form. However, studies of school age children show that pulmonary function tests continue to show obstructive disease despite apparent resolution of symptoms, and one study demonstrated that adults who were born premature had an increased incidence of respiratory symptoms compared with those born full term.
With all forms of BPD, ventilatory management is focused on the minimization of barotrauma or volutrauma and the prevention of atelectasis. Attempts to limit inspired fractional concentration of oxygen will help prevent oxygen toxicity. Debate continues about the ideal ventilatory setting (volume limited or pressure limited) or the use of positive end expiratory pressure (PEEP) in patients with BPD to optimize oxygenation and ventilation while limiting damage to the lung. For ventilatory management in the NICU, it appears that volume targeted ventilation may have lower morbidity and mortality compared with pressure limited ventilation. Although PEEP maintains functional reserve capacity functional reserve capacity (FRC) and reduces atelectasis, the optimal PEEP level for neonates and formerly premature children is unknown. Ideal tidal volumes with mechanical ventilation remain controversial: some authors argue for 5 to 7 mL/kg while others suggest that lower volumes of 4 to 6 mL/kg might be best.
Anesthetic Management of Infants With BPD
Preoperative assessment of infants with BPD is focused on optimization of their respiratory status, with particular regard for treating underlying bronchoconstriction. Infants with BPD that present for surgery with a concomitant upper respiratory tract infection have a higher risk for an adverse respiratory event during the perioperative period (e.g., laryngospasm, bronchospasm, hypoxia, etc.) and may require prolonged oxygen support postoperatively. Therefore, postponement of elective procedures may be warranted.
Infants with severe BPD who are likely to develop bronchospasm and cyanosis during physical stimulation should receive an anxiolytic premedication. Tracheal intubation should be avoided if possible. Whenever feasible, a laryngeal mask airway (LMA) is preferred. If tracheal intubation is performed, a “deep extubation” may be warranted to avoid bronchospasm. In abdominal procedures, a regional analgesic technique is indicated for adequate postoperative pain control and to avoid chest wall splinting and to preserve the ability to cough without pain. There are insufficient data in infants with BPD with which to predict the incidence of intraoperative or postoperative pulmonary complications.
Laryngeal and Tracheal Injury
Premature infants who required prolonged endotracheal intubation and mechanical ventilation are prone to develop injury to the laryngeal and tracheal tissues, which results in scarring and upper-airway narrowing. Fibrotic narrowing of the airway typically occurs at the level of the cricoid cartilage and is termed subglottic stenosis (SGS) ( Fig. 12.3 ). Historically, the incidence of clinically significant SGS ranged from 0.9% to 8.3% in infants who survived prolonged mechanical ventilation in the neonatal period. However, there is speculation that with improved ventilatory management of the premature neonate the incidence may be declining. An Australian study found that the incidence of severe SGS requiring airway reconstruction approached 0.005%. Regardless of these changes, the anesthesia provider should prepare smaller diameter endotracheal tubes when planning to anesthetize a formerly premature infant, and attention should be paid to any resistance encountered when attempting to pass the tube through the vocal cords or subglottic area. After extubation, these children may develop stridor as a result of further tracheal narrowing from acute subglottic edema. Therefore, the endotracheal tube should permit an air leak below 30 cmH 2 O to help prevent excessive swelling of the subglottic mucosa.
