Secondary Logo

Journal Logo

Pediatric Thoracic Anesthesia

Hammer, Gregory B., MD

doi: 10.1097/00000539-200106000-00021
PEDIATRIC ANESTHESIA: Review Article
Free

Department of Anesthesia, Stanford University Medical Center, Stanford, California

January 26, 2001.

Address correspondence to Gregory B. Hammer, MD, Associate Professor, Department of Anesthesia, Room H3580, Stanford University Medical Center, 300 Pasteur Drive, Stanford, CA 94305-5115. Address e-mail to ham@leland.stanford.edu.

Providing perioperative care to infants and children undergoing thoracic surgery presents many challenges to the pediatric surgeon, anesthesiologist, pulmonologist, and intensivist. This review will focus on the intraoperative anesthetic care of infants and children undergoing noncardiac thoracic surgery. Surgical disorders of infants and children are reviewed, with an emphasis on features affecting anesthetic management. Techniques for performing single-lung ventilation (SLV) in pediatric patients are summarized. Anesthetic management, including regional anesthetic techniques, is described.

Back to Top | Article Outline

Surgical Lesions of the Chest

Neonates and Infants

A variety of congenital intrathoracic lesions for which surgery is required may present in the newborn period or within the first year of life. These include lesions of the trachea and bronchi, lung parenchyma, and diaphragm.

Tracheal stenosis may be acquired or congenital. Tracheal stenosis occurs most often because of prolonged tracheal intubation, often in neonates with infant respiratory distress syndrome associated with prematurity. Ischemic injury of the tracheal mucosa may occur because of a tight-fitting endotracheal tube (ETT) at the level of the cricoid cartilage, which becomes scarred and constricted. Subglottic stenosis may develop, resulting in stridor after tracheal extubation. Reintubation may be required because of oxygen desaturation and hypercarbia.

Fiberoptic bronchoscopy is used to evaluate the severity of the stenosis and exclude other causes of stridor (e.g., vocal cord paralysis or laryngomalacia). When general anesthesia is required, inhaled anesthesia may be administered via a face mask, with the fiberoptic bronchoscope inserted through an adaptor in the mask and into the nasopharynx. This is usually performed with the patient breathing spontaneously (1). Alternatively, a laryngeal mask may be used as a conduit (2). Local anesthesia is applied to the vocal cords and trachea through the bronchoscope. Attention must be directed to the dose of local anesthetic used, as systemic absorption may lead to local anesthetic toxicity (3).

A cricoid split procedure may be performed for infants with acquired subglottic stenosis. After diagnostic bronchoscopy, either the patient is intubated with an ETT or a rigid bronchoscope is left in place during the operation. During rigid bronchoscopy, positive pressure ventilation is performed by connecting the anesthesia breathing circuit to the side arm of the bronchoscope. Anesthesia may be maintained with inhaled anesthetics or an IV anesthetic technique, such as propofol and remifentanil (4). A horizontal incision is made over the cricoid cartilage, after which a vertical incision is made through the inferior portion of the thyroid cartilage, the cricoid cartilage, and the first tracheal ring. Typically, an ETT a half size larger than the original tube is placed after the repair.

Congenital tracheal stenosis may be segmental, occurring in the region of the cricoid cartilage, the midtrachea, or just above the carina. In some cases, the stenotic segment is long, including multiple small tracheal cartilages. Infants present with suprasternal, intercostal, and subcostal retractions, which worsen during agitation and with intercurrent respiratory infections.

For patients with severe tracheal stenosis, a laryngotracheoplasty may be performed. This procedure involves the placement of a costal, auricular, or laryngeal cartilage graft into the anterior trachea, the posterior trachea, or both (5). In some cases, a stent may be positioned within the trachea. A previously indwelling tracheostomy tube may be exchanged for an anode tube during the procedure, and this may be either removed or replaced at the end of the operation, depending on whether or not additional staged operations are planned. Rarely, repair of distal tracheal and bronchial stenosis may require cardiopulmonary bypass. Patients may remain intubated and ventilated for a variable period of time after surgery. In these cases, sedation, analgesia, and neuromuscular blockade are maintained after surgery.

Pulmonary sequestrations result from disordered embryogenesis producing a nonfunctional mass of lung tissue supplied by anomalous systemic arteries. Intralobar sequestrations are usually found in the left posterior segments. Arterial supply arises from the aorta, above or below the diaphragm, whereas venous drainage is usually through the pulmonary veins. They are usually isolated anomalies and may not present until late in childhood or adulthood. Extralobar sequestrations occur just above or below the diaphragm and are also usually left-sided. Their arterial supply is from small, anomalous pulmonary or systemic arterial branches, and venous drainage is systemic (e.g., portal or azygous vein). Communication with the foregut and associated anomalies are common, including bronchial agenesis, duplication of the colon, vertebral anomalies, and diaphragmatic defects. Presenting signs include cough, pneumonia, and failure to thrive and often present during the neonatal period, usually before the age of 2 yr. Diagnostic studies include arteriography and computerized tomography (CT) scans of the chest and abdomen. Magnetic resonance imaging may provide high-resolution images, including definition of vascular supply. This may obviate the need for angiography (6). Surgical resection is performed after diagnosis.

Pulmonary sequestrations do not generally become hyperinflated during positive-pressure ventilation. Nitrous oxide administration may result in expansion of these masses, however, and should be avoided.

Pulmonary hypoplasia may be caused by a variety of intrauterine problems, including those that compress the developing lungs (congenital diaphragmatic hernia, tumor, pleural effusion), oligohydramnios (fetal renal failure with oliguria), and absent or poor fetal breathing movements (Werdnig-Hoffman disease, congenital myotonic dystrophy, anencephaly, agenesis of phrenic nerves). Space occupying intrathoracic lesions may cause unilateral lung hypoplasia, whereas the latter conditions usually result in bilateral hypoplasia that is not often amenable to surgery. The scimitar syndrome presents with hypoplasia of the right lung and anomalous pulmonary venous drainage to the inferior vena cava. Chest radiography may reveal a crescent-shaped shadow along the right heart border that resembles a Turkish sword or scimitar. Unilateral lung hypoplasia may be associated with recurrent pneumonia, hypoxemia, or both caused by ventilation/perfusion (V/Q) mismatching and may therefore require surgical resection. Excessive positive-pressure ventilation may result in barotrauma and pneumothorax, pneumomediastinum, or interstitial emphysema on the affected or contralateral side (see discussion below).

Congenital cystic lesions in the thorax may be classified into three categories (7). Bronchogenic cysts result from abnormal budding or branching of the tracheobronchial tree. They may cause respiratory distress, recurrent pneumonia, or atelectasis caused by lung compression. Bronchogenic cysts may be paratracheal, hilar, carinal, or paraesophageal and usually do not communicate with the airways. These cysts are most often unilocular and are filled with mucoid material. Bronchogenic cysts associated with clinical signs are generally treated with surgical excision (8). Rarely, these lesions do communicate with the airway; rupture with spillage of fluid into the tracheobronchial tree during anesthesia has been reported (9). Dermoid cysts are clinically similar to bronchogenic cysts but differ histologically, because they are lined with keratinized, squamous epithelium rather than respiratory (ciliated columnar) epithelium. They usually present later in childhood or adulthood. Cystic adenomatoid malformations (CAM) are structurally similar to bronchioles but lack associated alveoli, bronchial glands, and cartilage (10). Because these lesions communicate with the airway, they may become overdistended because of gas trapping, leading to respiratory distress in the first few days of life. When they are multiple and air filled, CAM may resemble congenital diaphragmatic hernia (CDH) radiographically. Treatment is surgical resection of the affected lobe. As with CDH, prognosis depends on the amount of remaining lung tissue, which may be hypoplastic because of compression in utero(11).

Congenital lobar emphysema often presents with respiratory distress shortly after birth (12). This lesion may be caused by ball-valve bronchial obstruction in utero, causing progressive distal overdistension with fetal lung fluid. The resultant emphysematous lobe may compress the lung bilaterally, resulting in a variable degree of hypoplasia. Congenital cardiac deformities are present in about 15% of patients (13). Radiographic signs of hyperinflation may be misinterpreted as tension pneumothorax or atelectasis on the contralateral side (Fig. 1). Surgical resection is usually performed when the Pao2 is <50 mm Hg despite supplemental oxygen administration (14). Positive-pressure ventilation may exacerbate lung hyperinflation. Nitrous oxide is contraindicated, and isolation of the lungs during anesthesia is desirable.

Figure 1

Figure 1

CDH is a life-threatening condition occurring in approximately 1 in 2000 live births. Failure of a portion of the fetal diaphragm to develop allows abdominal contents to enter the thorax, interfering with normal lung growth. Most often (70%–80% of diaphragmatic defects), a portion of the left posterior diaphragm fails to close, forming a triangular defect known as the foramen of Bochdalek. Hernias through the foramen of Bochdalek occurring early in fetal life usually cause respiratory failure immediately after birth because of pulmonary hypoplasia. Distension of the gut postnatally, as with bag-and-mask ventilation, exacerbates the ventilatory compromise by further compressing the lungs. The diagnosis is often made before birth, and fetal surgical repair has been described (15). Neonates present with tachypnea, a scaphoid abdomen, and absent breath sounds over the affected side. Chest radiography (CXR) typically shows bowel in the left hemithorax, with deviation of the heart and mediastinum to the right and compression of the right lung (Fig. 2A). Right-sided hernias (Fig. 2B) may occur late and present with milder signs. In the presence of significant respiratory distress, bag-and-mask ventilation should be avoided and immediate tracheal intubation performed.

Figure 2

Figure 2

Because pulmonary hypertension with right-to-left shunting contributes to severe hypoxemia in neonates with CDH, a variety of vasodilators have been used. These include tolazoline, prostacyclin, dipyridamole, and nitric oxide (16–20). High-frequency oscillatory ventilation has been used in conjunction with pulmonary vasodilator therapy to improve oxygenation before surgery (21). In cases of severe lung hypoplasia and pulmonary hypertension refractory to these therapies (e.g., Pao2 <50 mm Hg with a fraction of inspired oxygen of 1.0), extracorporeal membrane oxygenation (ECMO) should be initiated early to avoid progressive lung injury. Improved outcomes have been associated with early use of ECMO followed by delayed surgical repair (22).

A particularly poor prognosis is predicted if CDH is associated with cardiac deformities, a preoperative alveolar-to-arterial oxygen gradient >500 mm Hg, or severe hypercarbia despite vigorous ventilation (23,24). Prognosis has also been correlated with pulmonary compliance and radiographic findings (25–27).

Surgical correction via a subcostal incision with ipsilateral chest tube placement may be performed before or during ECMO (28,29). In patients undergoing surgical repair off ECMO, pulmonary hypertension is the major cause of morbidity and mortality. Hyperventilation to induce a respiratory alkalosis and 100% oxygen should be administered to decrease pulmonary vascular resistance. The anesthetic should be designed to minimize sympathetic discharge that may exacerbate pulmonary hypertension (e.g., a large-dose opioid technique). Infants should be ventilated with small tidal volumes and low inflating pressures to avoid pneumothorax on the contralateral (usually right) side. Both nitric oxide and high-frequency oscillatory ventilation have been used during surgical repair (30,31). A high index of suspicion of right-sided pneumothorax should be maintained, and a thoracostomy tube should be placed in the event of acute deterioration of respiratory or circulatory function. It is also imperative that normal body temperature, intravascular volume, and acid-base status be maintained. Mechanical ventilation is continued after surgery in nearly all cases.

Failure of the central and lateral portions of the diaphragm to fuse results in a retrosternal defect, the foramen of Morgagni. This usually presents with signs of bowel obstruction rather than respiratory distress. Repair is usually performed via an abdominal incision.

Tracheoesophageal fistula (TEF), esophageal atresia, or both occur in approximately 1 in 4000 live births. In 80%–85% of infants, this lesion includes esophageal atresia with a distal esophageal pouch and a tracheal fistulous connection (32,33). The fistula is usually located 1 or 2 tracheal rings above the carina. Afflicted neonates present with spillover of pooled oral secretions from the pouch and may develop progressive gastric distension and tracheal aspiration of acidic gastric contents via the fistula. A common association is the VACTERL complex, consisting of vertebral, anorectal, cardiac, tracheoesophageal, renal, or limb defects (34). Esophageal atresia is confirmed when an orogastric tube passed through the mouth cannot be advanced more than about 7 cm (Fig. 3). The tube should be secured and placed on continuous suction, after which a chest radiograph is diagnostic.

Figure 3

Figure 3

Mask ventilation and tracheal intubation are avoided before surgery if possible, because they may exacerbate gastric distension and respiratory compromise. When the trachea is intubated, an attempt is made to occlude the tracheal orifice of the fistula with the tracheal tube. The tip of the tracheal tube is positioned just above the carina by auscultation of diminished breath sounds over the left axilla as the tube is advanced into the right mainstem bronchus, after which the tube is retracted until breath sounds are increased (Fig. 4A). A small fiberoptic bronchoscope may be passed through the tracheal tube to confirm appropriate placement. Occasionally, emergency gastrostomy is performed because of massive gastric distension. Placement of a balloon-tipped catheter in the fistula via the gastrostomy may be performed under guidance with a fiberoptic bronchoscope to prevent further gastric distension and enable effective positive-pressure ventilation in cases of significant lung disease (Fig. 4B) (35). Antegrade occlusion of a TEF has also been reported with a balloon-tipped catheter advanced through the trachea into the fistula (Fig. 4C) (36). Preoperative evaluation should be performed to diagnose associated anomalies, particularly cardiac, musculoskeletal, and gastrointestinal defects, which occur in 30%–50% of patients (37). A poorer prognosis in infants with TEF and esophageal atresia is correlated with prematurity and underlying lung disease, as well as the coexistence of other congenital anomalies (33).

Figure 4

Figure 4

Surgical repair usually involves a right thoracotomy and extrapleural dissection of the posterior mediastinum. In most cases, the fistula is ligated, and primary esophageal anastomosis is performed (short gap atresia). In cases in which the esophageal gap is long, the proximal segment is preserved for subsequent staged anastomosis with or without intestinal interposition (33).The trachea may be intubated with the patient breathing spontaneously or during gentle positive-pressure ventilation with small tidal volumes to avoid gastric distension. If a gastrostomy tube is in place, occlusion of the fistula may be confirmed by cessation of bubbling via an underwater tubing connected to the gastrostomy or appearance of CO2 by gas analysis (38). Alternatively, the tracheal tube may be positioned in the mainstem bronchus opposite the side of the thoracotomy incision until the fistula is ligated.

Esophageal atresia without connection to the trachea occurs much less often. These lesions are generally diagnosed by radiography after inability to pass an orogastric tube, at which time an absence of gas in the abdomen may be noted (Fig. 5). So-called H-type TEF without esophageal atresia is relatively rare. Patients with H-type lesions may present later in childhood or adulthood with recurrent pneumonias or gastric distension during positive-pressure ventilation (39).

Figure 5

Figure 5

Patent ductus arteriosus (PDA) and coarctation of the thoracic aorta (COTA) are relatively common vascular lesions with a wide range of presentations. PDA occurs in approximately 1 in 2500 live full-term births and accounts for approximately 10% of congenital heart defects (40). Forty percent of premature infants weighing <1750 g and 80% of those <1200 g have a PDA (41). The PDA in these infants is typically quite large and often results in congestive heart failure because of left-to-right shunting of blood, with pulmonary edema and decreased systemic perfusion. Small PDAs may close spontaneously or in response to the administration of indomethacin. Alternatively, small lesions may present with a heart murmur in asymptomatic children.

Surgical repair via a left thoracotomy (or right thoracotomy in infants with a right-sided aortic arch) may be performed in the neonatal intensive care unit in premature infants. In this setting, an IV anesthetic with fentanyl for analgesia, a benzodiazepine for amnesia and hypnosis, and a neuromuscular blocking drug may be most pragmatic. Many of these patients have congestive heart failure and are mechanically ventilated both before and after surgery. Larger infants may be well suited for regional anesthesia plus inhaled or short-acting IV anesthesia and planned tracheal extubation in the operating room.

COTA is a localized narrowing of the aorta occurring close to the insertion of the ductus arteriosus into the aorta. COTA occurs in 1 in 1200–2000 live births (42,43). COTA may present in the newborn as a critical aortic obstruction in which the PDA supplies most of the perfusion to the lower body. These patients are frequently critically ill, with a metabolic acidosis and cyanosis of the lower body. Prostaglandin E1 is infused before surgery to maintain ductal patency until surgical correction can be performed.

COTA more typically presents later in childhood with arterial hypertension in the upper extremities and low blood pressure in the lower extremities, with poor or absent femoral pulses. Turner’s syndrome and bicuspid aortic valve or other congenital cardiac defects may be associated with COTA. Cardiomegaly, systemic hypertension, and congestive heart failure may be present.

The surgical treatment of COTA is usually accomplished via a left thoracotomy and may consist of resection of the coarcted segment of aorta with end-to-end anastomosis, subclavian flap repair, or the use of synthetic graft material. Arterial blood pressure should be monitored above and below the coarctation, e.g., with a radial arterial catheter and a blood pressure cuff on a lower extremity. The distal arterial pressure should generally be maintained >45 mm Hg to maintain renal perfusion (44). The patient’s body temperature is often cooled to 35°C to minimize ischemic spinal cord injury during aortic occlusion. Despite this, the incidence of paraplegia after COTA repair is approximately 1 in 250 (44). Proposed mechanisms for paraplegia include inadequate distal perfusion pressure during aortic occlusion, interruption of the blood supply via the anterior spinal artery, and increased cerebrospinal fluid pressure.

Hypertension after surgery may be treated with β-blockers (e.g., esmolol) or a variety of other drugs (45). Untreated systemic hypertension may be accompanied by abdominal pain and even bowel perforation secondary to mesenteric insufficiency, thought to be caused by arteritis associated with an acute increase in arterial perfusion. These findings may be accompanied by fever, leukocytosis, melena, and abdominal distension and are referred to as postcoarctectomy syndrome. As an alternative to coarctectomy, balloon angioplasty may be performed for both native and recurrent coarctations (46).

Vascular rings are anomalies of the aortic arch, right subclavian artery, or pulmonary arteries that compress the trachea and esophagus. These abnormalities are generally produced by the failure of portions of the fourth or sixth embryonic aortic arches to regress or develop normally. The most common varieties of vascular rings are composed of a double aortic arch, a right-sided arch with a left ductus (or ligamentum) arteriosus, anomalous right subclavian or innominate artery, or a pulmonary artery sling. Most children with vascular rings are asymptomatic or mildly symptomatic during infancy and outgrow their respiratory signs (e.g., stridor) as the trachea becomes more cartilaginous. In cases of severely compromised airways caused by vascular rings, infants present during the first month of life with stridor, recurrent respiratory infections, or dysphagia (47). CXR and barium esophagrams are diagnostic. Surgical repair is generally performed through a left lateral thoracotomy.

Patients with tracheomalacia caused by extrinsic compression may have airway obstruction because of tracheal collapse during the induction of anesthesia and after tracheal extubation. Vascular rings may cause tracheal compression similar to anterior mediastinal masses. Inhaled induction has been recommended, followed by administration of assisted or controlled ventilation before the administration of muscle relaxants (48). A rigid bronchoscope should be at hand, because it may be lifesaving in the event of tracheal collapse. Airway compression may be exacerbated during lateral decubitus positioning, in which case immediate repositioning should be performed. Because of the risk of hemorrhage during surgery, appropriate vascular access should be secured before skin incision, and blood must be available for transfusion.

Back to Top | Article Outline

Childhood

Many of the lesions described above may not be diagnosed until childhood. These include pulmonary sequestration, arteriovenous abnormalities, cystic lesions, lobar emphysema, PDA, COTA, and vascular rings. Other disorders for which thoracic surgery is performed in children, either for definitive treatment or diagnostic purposes, include tumors, infectious diseases, and musculoskeletal deformities.

Tumors of the lung, mediastinum, and pleura may be primary or metastatic (49). Primary tumors of the chest are uncommon in children. Perhaps the most common are lymphoblastic lymphoma, a form of non-Hodgkin’s lymphoma, and Hodgkin’s disease. These neoplasms usually present as an anterior mediastinal (thymic) mass with pleural effusion, dyspnea caused by airways obstruction, pain, or superior vena cava syndrome (swelling of the upper arms, face, and neck) (Fig. 6) (50,51). The induction of anesthesia in patients with anterior mediastinal masses may be associated with severe airway and circulatory collapse (52,53). Accordingly, institutions should have an algorithm in place for the evaluation of these patients, including preoperative CT scanning, echocardiography, and flow-volume studies, as well as their treatment (Fig. 7). Careful consideration should be given to performing a biopsy under local anesthesia or initiating chemotherapy or limited radiation therapy before subjecting the child to general anesthesia to effect a decrease in tumor mass and life-threatening airway or vascular occlusion.

Figure 6

Figure 6

Figure 7

Figure 7

Neuroblastoma, the most common solid extracranial solid tumor of childhood, often arises in the posterior thoracic sympathetic chain. Signs and symptoms of intrathoracic neuroblastoma include Horner’s syndrome (lesions of the cervical and upper thoracic sympathetic chain), spinal cord compression, and bone pain. Uncommonly, hypertension, tachycardia, and flushing may occur spontaneously or during surgical manipulation because of tumor catecholamine secretion. Ganglioneuroblastomas and ganglioneuromas are variants of neuroblastoma that are also derived from neural crest cells and are histologically benign. Osteogenic sarcoma (osteosarcoma) and Ewing’s sarcoma arise in long bones but often metastasize to the lung. Other tumors of childhood, including rhabdomyosarcoma and germ cell tumors, may also metastasize to the lung.

Empyema is a complication of bacterial pneumonia most often caused by Staphylococcus aureus and Streptococcus pneumoniae. Haemophilus influenzae type b is much less common because of the use of the Haemophilus influenzae type b vaccine in young children (54). Empyema is diagnosed by CXR or CT scan, or both, and is associated with prolonged fever and leukocytosis. Despite therapy with antibiotics and chest tube drainage, with or without pleural streptokinase or urokinase instillation, surgical treatment is often necessary (55). Rarely, lung abscesses that persist despite antibiotics and percutaneous drainage may also require surgical treatment. Surgical lung biopsy may be performed for diagnostic purposes in cases of interstitial lung disease, which may be infectious (Pneumocystis, respiratory syncytial virus, cytomegalovirus) or noninfectious (e.g., nonspecific or allergic).

Pulmonary arteriovenous fistulas and malformations occur most often along with widespread vascular abnormalities, as in patients with Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasis) (56). These lesions may present during infancy or childhood with hypoxemia because of right-to-left shunting of blood, or with congestive heart failure. Acquired arteriovenous fistulas may develop in children with liver disease, increased pulmonary artery pressure (e.g., pulmonary hypoplasia, mitral stenosis, cystic fibrosis), after cavopulmonary shunting, or after chest trauma (57,58). Surgical intervention is warranted when these lesions are focal and severe. Many of these fistulas can be completely or partially coil occluded in the catheterization laboratory. Persistent lesions may require surgical resection.

Pectus excavatum results from excessive growth of the costochondral cartilages, with resultant inward depression of the sternum. Pectus excavatum may be associated with Marfan’s syndrome or chronic airway obstruction with large negative intrathoracic pressure during inspiration. Children with severe deformities may have circulatory impairment caused by distortion of the heart and great vessels, or respiratory compromise caused by lung compression. If possible, surgical repair is deferred until late childhood or adolescence, when the ribs and sternum are more fully calcified. A variety of surgical repairs have been described, ranging from complete resection of the sternum to minimally invasive surgery with placement of a retrosternal strut through small incisions in the lateral chest. Of note, complications of the latter technique include perforation of the lungs and heart (59). Preoperative pulmonary function abnormalities may not be significantly improved after surgery (60,61).

Kyphoscoliosis is a curvature of the spine measuring 10° or more in the frontal plane. This disorder may present as infantile (<3 yr old), juvenile (3–10 yr old), or adolescent (>10 yr old) forms. Kyphoscoliosis may be associated with congenital malformations of the vertebra, neuromuscular disease (e.g., muscular dystrophy), or neoplastic diseases (e.g., neurofibromatosis), or it may be idiopathic. Surgical correction is delayed until the teenage years unless the deformity is severe, and it consists of posterior spinal fusion with instrumentation with or without anterior spinal fusion. The latter may be performed thoracoscopically (62,63).

Back to Top | Article Outline

Ventilation/Perfusion During Thoracic Surgery

Ventilation is normally distributed preferentially to dependent regions of the lung, so that there is a gradient of increasing ventilation from the most nondependent to the most dependent lung segments. Because of gravitational effects, perfusion normally follows a similar distribution, with increased blood flow to dependent lung segments. Therefore, ventilation and perfusion are normally well matched. During thoracic surgery, several factors act to increase V/Q mismatch. General anesthesia, neuromuscular blockade, and mechanical ventilation cause a decrease in functional residual capacity of both lungs. Compression of the dependent lung in the lateral decubitus position may cause atelectasis. Surgical retraction or SLV results in collapse of the operative lung. Hypoxic pulmonary vasoconstriction (HPV), which acts to divert blood flow away from the underventilated lung, thereby minimizing V/Q mismatch, may be diminished by inhaled anesthetics and other vasodilating drugs. These factors apply equally to infants, children, and adults. The overall effect of the lateral decubitus position on V/Q mismatch, however, is different in infants compared with older children and adults.

In adults with unilateral lung disease, oxygenation is optimal when the patient is placed in the lateral decubitus position with the healthy lung dependent (down) and the diseased lung nondependent (up) (64). Presumably, this is related to an increase in blood flow to the dependent, healthy lung and a decrease in blood flow to the nondependent, diseased lung caused by the hydrostatic pressure (or gravitational) gradient between the two lungs. This phenomenon promotes V/Q matching in the adult patient undergoing thoracic surgery in the lateral decubitus position.

In infants with unilateral lung disease, however, oxygenation is improved with the healthy lung up (65). Several factors account for this discrepancy between adults and infants. Infants have a soft, easily compressible rib cage that cannot fully support the underlying lung. Therefore, functional residual capacity is closer to residual volume, making airway closure likely to occur in the dependent lung even during tidal breathing (66). When the adult is placed in the lateral decubitus position, the dependent diaphragm has a mechanical advantage because it is “loaded” by the abdominal hydrostatic pressure gradient. This pressure gradient is reduced in infants, thereby reducing the functional advantage of the dependent diaphragm. The infant’s small size also results in a reduced hydrostatic pressure gradient between the nondependent and dependent lungs. Consequently, the favorable increase in perfusion to the dependent, ventilated lung is reduced in infants.

Finally, the infant’s increased oxygen requirement, coupled with a small functional residual capacity, predisposes the infant to hypoxemia. Infants normally consume 6–8 mL · kg−1 · min−1 of oxygen compared with a normal oxygen consumption in adults of 2–3 mL · kg−1 · min−1(67). For these reasons, infants are at an increased risk of significant oxygen desaturation during surgery in the lateral decubitus position.

Back to Top | Article Outline

Indications and Techniques for SLV in Infants and Children

Before 1995, nearly all thoracic surgery in children was performed by thoracotomy. In most cases, anesthesiologists ventilated both lungs with a conventional tracheal tube, and the surgeons retracted the operative lung to gain exposure to the surgical field. During the past decade, the use of video-assisted thoracoscopic surgery (VATS) has dramatically increased in both adults and children. Reported advantages of thoracoscopy include smaller chest incisions, reduced postoperative pain, and more rapid postoperative recovery compared with thoracotomy (68–70). Recent advances in surgical technique, as well as technology, including high-resolution microchip cameras and smaller endoscopic instruments, have facilitated the application of VATS in smaller patients.

VATS is being used extensively for pleural debridement in patients with empyema, lung biopsy and wedge resections for interstitial lung disease, mediastinal masses, and metastatic lesions. More extensive pulmonary resections, including segmentectomy and lobectomy, have been performed for lung abscess, bullous disease, sequestrations, lobar emphysema, CAM, and neoplasms. In selected centers, more advanced procedures have been reported, including closure of PDA, repair of hiatal hernias, and anterior spinal fusion.

VATS can be performed while both lungs are being ventilated by using CO2 insufflation and placement of a retractor to displace lung tissue in the operative field. However, SLV is extremely desirable during VATS because lung deflation improves visualization of thoracic contents and may reduce lung injury caused by the use of retractors (71). There are several different techniques that can be used for SLV in children.

Back to Top | Article Outline

Single-Lumen Endotracheal Tube.

The simplest means of providing SLV is to intentionally intubate the ipsilateral mainstem bronchus with a conventional single-lumen ETT (72). When the left bronchus is to be intubated, the bevel of the ETT is rotated 180° and the head turned to the right (73). The ETT is advanced into the bronchus until breath sounds on the operative side disappear. A fiberoptic bronchoscope may be passed through or alongside the ETT to confirm or guide placement. When a cuffed ETT is used, the distance from the tip of the tube to the distal cuff must be shorter than the length of the bronchus so that the upper lobe bronchus is not occluded (74).

This technique is simple and requires no special equipment other than a fiberoptic bronchoscope. This may be the preferred technique of SLV in emergency situations such as airway hemorrhage or contralateral tension pneumothorax.

Problems can occur when using a single-lumen ETT for SLV. If a smaller, uncuffed ETT is used, it may be difficult to provide an adequate seal of the intended bronchus. This may prevent the operated lung from adequately collapsing or fail to protect the healthy, ventilated lung from contamination by purulent material from the contralateral lung. The operated lung cannot be suctioned with this technique. Hypoxemia may occur because of obstruction of the upper lobe bronchus, especially when the short right mainstem bronchus is intubated.

Variations of this technique have been described, including intubation of both bronchi independently with small ETTs (75–78). One mainstem bronchus is initially intubated with an ETT, after which another ETT is advanced over a fiberoptic bronchoscope into the opposite bronchus.

Back to Top | Article Outline

Balloon-Tipped Bronchial Blockers.

A Fogarty embolectomy catheter or an end-hole, balloon-wedge catheter may be used for bronchial blockade to provide SLV (Fig. 8) (79–82). Placement of a Fogarty catheter is facilitated by bending the tip of its stylette toward the bronchus on the operative side. A fiberoptic bronchoscope may be used to reposition the catheter and confirm appropriate placement. When an end-hole catheter is used, the bronchus on the operative side is initially intubated with an ETT. A guidewire is then advanced into that bronchus through the ETT. The ETT is removed, and the blocker is advanced over the guidewire into the bronchus. An ETT is then reinserted into the trachea alongside the blocker catheter. The catheter balloon is positioned in the proximal mainstem bronchus under fiberoptic visual guidance. With an inflated blocker balloon, the airway is completely sealed, providing more predictable lung collapse and better operating conditions than with an ETT in the bronchus.

Figure 8

Figure 8

A potential problem with this technique is dislodgement of the blocker balloon into the trachea. The inflated balloon will then block ventilation to both lungs, prevent collapse of the operated lung, or both. The balloons of most catheters currently used for bronchial blockade have low-volume, high-pressure properties, and overdistension can damage or even rupture the airway (83). One study, however, reported that bronchial blocker cuffs produced lower cuff-to-tracheal pressures than double-lumen tubes (DLTs) (84). When closed-tip bronchial blockers are used, the operated lung cannot be suctioned, and continuous positive airway pressure cannot be provided to the operated lung if it is needed.

Recently, adapters have been used that facilitate ventilation during placement of a bronchial blocker through an indwelling ETT (85,86). The risk of hypoxemia during blocker placement is diminished, and repositioning of the blocker may be performed with fiberoptic guidance during surgery. The ETT must be at least 5.0 mm internal diameter, however, generally limiting the use of this technique to children over the age of 2 yr.

Back to Top | Article Outline

Univent Tube.

The Univent tube (Fuji Systems Corporation, Tokyo, Japan) is a conventional ETT with a second lumen containing a small tube that can be advanced into a bronchus (87–89). A balloon located at the distal end of this small tube serves as a blocker. Univent tubes require a fiberoptic bronchoscope for successful placement. Univent tubes are now available in sizes as small as a 3.5- and 4.5-mm internal diameter for use in children >6 yr old (90).

Because the blocker tube is firmly attached to the main ETT, displacement of the Univent blocker balloon is less likely than when other blocker techniques are used. The blocker tube has a small lumen that allows egress of gas and can be used to insufflate oxygen or suction the operated lung.

A disadvantage of the Univent tube is the large amount of cross-sectional area occupied by the blocker channel, especially in the smaller-sized tubes. Smaller Univent tubes have a disproportionately high resistance to gas flow (91). The Univent tube’s blocker balloon has low-volume, high-pressure characteristics, so mucosal injury can occur during normal inflation (92,93).

Back to Top | Article Outline

Double-Lumen Tubes.

All DLTs are essentially two tubes of unequal length molded together. The shorter tube ends in the trachea and the longer tube in the bronchus. Marraro (94) described a bilumen tube for infants. This tube consists of two separate uncuffed tracheal tubes of different lengths attached longitudinally. This tube is not available in the United States. DLTs for older children and adults have cuffs located on the tracheal and bronchial lumens. The tracheal cuff, when inflated, allows positive-pressure ventilation. The inflated bronchial cuff allows ventilation to be diverted to either or both lungs and protects each lung from contamination from the contralateral side.

Conventional plastic DLTs, once available only in adult sizes (35F, 37F, 39F, and 41F), are now available in smaller sizes. The smallest cuffed DLT is a 26F (Rusch, Duluth, GA), which may be used in children as young as 8 yr old. DLTs are also available in sizes 28F and 32F (Mallinckrodt Medical, Inc., St. Louis, MO), suitable for children 10 yr and older.

DLTs are inserted in children by using the same technique as in adults (95). The tip of the tube is inserted just past the vocal cords, and the stylette is withdrawn. The DLT is rotated 90° to the appropriate side and then advanced into the bronchus. In the adult population, the depth of insertion is directly related to the height of the patient (96). No equivalent measurements are yet available in children. If fiberoptic bronchoscopy is to be used to confirm tube placement, a bronchoscope with a small diameter and sufficient length must be available (97).

A DLT offers the advantage of ease of insertion as well as the ability to suction and oxygenate the operative lung with continuous positive airway pressure. Left DLTs are preferred to right DLTs because of the shorter length of the right main bronchus (98). Right DLTs are more difficult to accurately position because of the increased risk of right upper lobe obstruction.

DLTs are safe and easy to use. There are very few reports of airway damage from DLTs in adults, and none in children. Their high-volume, low-pressure cuffs should not damage the airway if they are not overinflated with air or distended with nitrous oxide while in place.

Guidelines for selecting appropriate tubes (or catheters) for SLV in children are shown in Table 1. There is significant variability in overall size and airway dimensions in children, particularly in teenagers. The recommendation shown in Table 1 are based on average values for airway dimensions. Larger DLTs may be safely used in large teenagers.

Table 1

Table 1

Back to Top | Article Outline

Monitoring and Anesthetic Techniques

A thorough preoperative evaluation is essential in caring for the pediatric patient scheduled for thoracic surgery. As discussed above, appropriate imaging and laboratory studies should be performed before surgery according to the lesion involved. Guidelines for fasting, choice of premedication, and preparation of the operating room are used as for other infants and children scheduled for major surgery. After the induction of anesthesia, placement of an IV catheter, and tracheal intubation, arterial catheterization should be performed for most patients undergoing thoracotomy, as well as those with severe lung disease who are having VATS. This facilitates monitoring of arterial blood pressure during manipulation of the lungs and mediastinum, as well as of arterial blood gas tensions during SLV. For thoracoscopic procedures of relatively short duration in patients without severe lung disease, insertion of an arterial catheter is not required. Placement of a central venous catheter is generally not indicated if peripheral IV access is adequate for projected fluid and blood administration.

Inhaled anesthetics are often administered in 100% oxygen during maintenance of anesthesia. Isoflurane may be preferred because of less attenuation of HPV compared with other inhaled anesthetics, although this has not been studied in children (99). Nitrous oxide is avoided. Use of IV opioids may facilitate a decrease in the concentration of inhaled anesthetics used and therefore limit impairment of HPV. Alternatively, total IV anesthesia may be used with a variety of drugs. The combination of general anesthesia with regional anesthesia and postoperative analgesia is particularly desirable for thoracotomy but may also be beneficial for VATS, especially when thoracostomy tube drainage, a source of significant postoperative pain, is used after surgery. A variety of regional anesthetic techniques have been described for intraoperative anesthesia and postoperative analgesia, including intercostal and paravertebral blocks, intrapleural infusions, and epidural anesthesia.

Intercostal nerve blocks may be performed before skin incision or under direst vision by the surgeon before chest closure. Because of overlap of sensory dermatomes, nerves above and below the level of surgery must be blocked. This may require large doses and therefore large plasma concentrations of local anesthetics, especially in infants (100). Intraoperative placement of an intercostal catheter for postthoracotomy pain relief has also been described (101,102). Paravertebral blocks provide analgesia comparable to intercostal blockade. Although not reported for postthoracotomy pain in children, the use of continuous paravertebral blockade has been described in children undergoing renal surgery (103). Complications associated with paravertebral blockade include spinal, epidural, and intravascular injection.

The use of intrapleural anesthesia in children was first described in 1988 (104). Although continuous infusions of bupivacaine of 1.25 mg · kg1 · h1 were not associated with clinical signs of toxicity in this report, plasma concentrations were as large as 7 μg/mL. Because a relatively large volume of local anesthetic solution is required to achieve satisfactory analgesia with this technique, the use of a more dilute bupivacaine solution has been described (105). In this study of eight children undergoing thoracotomy, bupivacaine 0.1% was infused up to 1.0 mL · kg1 · h1 after surgery. The maximum plasma bupivacaine concentration measured was 2.16 μg/mL, and no signs of toxicity were observed. Satisfactory analgesia was achieved in all children. Several studies in adult patients, however, have shown that intrapleural bupivacaine does not produce reliable postthoracotomy analgesia (106–109). In a randomized, prospective, double-blinded study, epidural hydromorphone provided superior analgesia compared with intrapleural bupivacaine after thoracotomy (110).

Of the regional anesthesia techniques described above, only epidural anesthesia facilitates excellent intraoperative anesthesia, a small risk of local anesthetic toxicity, and titratable postoperative analgesia.

Back to Top | Article Outline

Epidural Anesthesia.

To attenuate the stress response associated with thoracic surgery and to provide optimal postoperative analgesia, a combination of epidural opioids and local anesthetics may be used. Although local anesthetics may spread to thoracic dermatomes when administered via the caudal or lumbar epidural space, potentially toxic doses of local anesthetics are required to achieve thoracic analgesia (111,112). When the epidural catheter tip is placed in proximity to the spinal segment associated with surgical incision (i.e., a thoracic epidural catheter is placed for thoracic surgery), segmental anesthesia may be achieved with smaller doses of local anesthetic than those needed when the catheter tip is distant from the surgical site.

In infants, a catheter can usually be advanced from the caudal to the thoracic epidural space (113,114). With the infant in the lateral decubitus position after the induction of general anesthesia, a 20-gauge epidural catheter may be inserted via an epidural needle or an 18-gauge IV catheter placed through the sacrococcygeal membrane. The epidural catheter is then advanced 16–18 cm to the midthoracic epidural space. Minor resistance to passage of the catheter may be overcome by simple flexion or extension of the spine. If continued resistance is encountered, no attempt should be made to advance the catheter further, because the catheter may become coiled within or exit the epidural space.

In older children, a thoracic epidural catheter may be inserted under general anesthesia directly between T4 and T8 to provide intraoperative neuraxial blockade and postoperative analgesia. Although the safety of placing epidural catheters in anesthetized patients has been questioned (115), this technique is widely used by pediatric anesthesia practitioners (116). The incidence of neurologic sequelae related to epidural catheterization in pediatric patients is unknown. Flandin-Blety and Barrier (117) reported five cases of serious neurologic injury in a retrospective review of 24,005 regional anesthetics performed in France and Belgium over a 10-yr period. All of these patients were infants <3 mo old, and the etiology of neurologic injury and association with epidural anesthesia were unknown. In a separate retrospective survey of 119 pediatric hospitals, including more than 150,000 epidural blocks, there were no reports of permanent neurologic injury, epidural hematoma, infection, or death (118). The authors concluded that the risk of a major complication was less than approximately 1:10,000. This complication rate is consistent with that observed in adult patients (119,120), who are usually awake and able to report pain or paresthesias during needle and catheter placement.

A variety of local anesthetics have been used to provide epidural anesthesia and analgesia in infants and children, including chloroprocaine (121), lidocaine (122,123), bupivacaine (124,125), and ropivacaine (125,126). Advantages of lidocaine are that it has less cardiotoxicity than bupivacaine and blood concentrations can be readily measured in most hospital laboratories. Nevertheless, most reports of the use of thoracic epidural anesthesia and analgesia in children include the use of bupivacaine (123,127–130). A new drug, levobupivacaine (Chirocaine®; Purdue Pharma, Norwalk, CT), causes less cardiovascular toxicity than racemic bupivacaine in adults, but no studies have been published in children (131,132).

Clearance and protein binding for local anesthetics are reduced in neonates and young infants, causing the potential for drug accumulation during continuous infusion and increased central nervous system and cardiovascular toxicity (133–135). Maximum infusion rates for lidocaine of 1 mg · kg1 · h1 (e.g., 1 mL · kg1 · h1 of a 0.1% solution) have been recommended for young infants (123). Plasma concentrations of lidocaine and its principal active metabolite, monoethylglycinexylidide, should be measured twice daily in infants if possible, because both compounds are epileptogenic (135). Maximal bupivacaine infusion rates of 0.2–0.3 mg · kg1 · h1 should be used when prolonged epidural infusion is planned in infants <3 mo old.

Epidural opioids are often combined with local anesthetics to provide maximal pain relief and to minimize tachyphylaxis. The concomitant use of opioids allows the use of smaller concentrations of local anesthetics and decreases the risk of local anesthetic toxicity. Epidural morphine (136,137), hydromorphone (138), fentanyl (139), and sufentanil (140) have been used in infants and children. Of these, morphine has the lowest lipid solubility, followed by hydromorphone, fentanyl, and sufentanil (141). Morphine has been associated with delayed respiratory depression and a relatively frequent incidence of pruritus, nausea, and vomiting (142,143). By comparison, hydromorphone has been associated with rapid onset of analgesia, a small incidence of side effects, and a low risk of delayed respiratory depression (127,144–146). More highly lipophilic drugs, such as fentanyl, achieve minimal spread in the epidural space, and optimal postoperative analgesia is achieved only when the epidural catheter is placed at or near the level of surgery (147). In a study comparing side effects with epidural morphine, hydromorphone, and fentanyl, hydromorphone was associated with the least incidence of pruritus, nausea, and vomiting (138). Regimens used for continuous thoracic epidural analgesia in children in published reports are shown in Table 2. Suggested treatment for side effects related to spinal and epidural opioids is shown in Table 3.

Table 2

Table 2

Table 3

Table 3

Recent reports have described epidural administration of a number of other drugs to provide analgesia or decrease the side effects of epidural opioids. These include ketamine (148,149), clonidine (150,151), and butorphanol (152,153). The role of these drugs inproviding epidural anesthesia and analgesia for pediatric patients undergoing thoracic surgery remains to be defined.

For patients who are not receiving a regional anesthetic technique to provide postoperative analgesia, systemic opioids are used after thoracotomy. Although intermittent IM and subcutaneous injections have been used widely in the past, these routes of administration are painful and are associated with unpredictable and erratic uptake and distribution. Intermittent IV injections with opioids of short or moderate duration are also associated with periods of excessive sedation and inadequate analgesia. The use of methadone, which has a half-life of approximately 19 h in children over the age of 1 yr, 1 may provide more continuous analgesia than shorter-acting drugs (154). For moderate to severe pain, intermittent IV doses of methadone between 0.05 and 0.08 mg/kg as needed may be given (155).

Continuous analgesia may be achieved when opioids are administered by continuous IV infusion, with or without patient-controlled analgesia (PCA) dosing. Morphine is the drug used most often for postoperative analgesia. In neonates <1 mo old, clearance is reduced and elimination half-life is prolonged, about three times that in adults (156). For continuous infusions of morphine, an initial dose of 0.025–0.075 mg/kg followed by infusion rates of 0.005–0.015 mg · kg1 · h1 result in therapeutic plasma concentrations in neonates (157). Older infants and children require an initial dose of 0.05–0.10 mg/kg followed by an initial infusion rate of 0.01–0.03 mg · kg1 · h1. In children receiving PCA, dosing in the range of 0.01–0.03 mg/kg with a lockout interval of 6–10 min, with or without a continuous infusion, has been recommended (158). In children at risk for morphine-induced histamine release, fentanyl (0.0005–0.001 mg · kg1 · h1 ± 0.0005–0.001 mg/kg PCA dose) or hydromorphone (0.003–0.005 mg · kg1 · h1 ± 0.003–0.005 mg/kg PCA dose) may be used (158).

The side effects that may occur with IV opioid administration are similar to those described with epidural opioids and may be treated similarly (Table 3). With epidural or IV techniques, improved analgesia and a decrease in opioid dosing (and side effects) may be achieved with the concomitant administration of nonopioid analgesics. The use of these adjuvant drugs, including acetaminophen and a variety of nonsteroidal antiinflammatory drugs, has been reviewed elsewhere (159).

Back to Top | Article Outline

Conclusions

The anesthesiologist caring for infants and children undergoing thoracic surgery faces many challenges. An understanding of the primary underlying lesion, as well as associated anomalies that may affect perioperative management, is paramount. A working knowledge of respiratory physiology and anatomy in infants and children is required for the planning and execution of appropriate intraoperative care. Familiarity with a variety of techniques for SLV suited to the patient’s size will allow maximal surgical exposure while minimizing trauma to the lungs and airways. Finally, the use of regional anesthetic techniques, including epidural anesthesia and analgesia, facilitates optimal postoperative pain control and pulmonary function.

Back to Top | Article Outline

FOOTNOTES

1 Berde CB, Sethna NF, Holtzman RS, et al. Pharmacokinetics of methadone in children and adolescents in the perioperative period [abstract]. Anesthesiology 1987;67:A519.
Cited Here...

Back to Top | Article Outline

References

1. Khoo ST. Anaesthesia for fiberoptic bronchoscopy in children. Anaesthesia 1990; 45: 248–9.
2. Baraka A, Choueiry P, Medawar A. The laryngeal mask airway for fiberoptic bronchoscopy in children. Paediatr Anaesth 1995; 5: 197–8.
3. Amitai Y, Zylber-Katz E, Avital A, et al. Serum lidocaine concentrations in children during bronchoscopy with topical anaesthesia. Chest 1990; 98: 1370–3.
4. Hammer GB, Lammers CR. Pediatric otolaryngology. In: Jaffe RA, Samuels SI, eds. Anesthesiologist’s manual of surgical procedures. Philadelphia: Lippincott Williams & Wilkins, 1999: 872–5.
5. Vinograd I, Klim B, Efrati Y. Airway obstruction in neonates and children: surgical treatment. J Cardiovasc Surg 1994; 35: 7–12.
6. Vegunta RK, Teich S. Preoperative diagnosis of extralobar pulmonary sequestration with unusual vasculature: a case report. J Pediatr Surg 1999; 34: 1307–8.
7. Kravitz RM. Congenital malformations of the lung. Pediatr Clin North Am 1994; 41: 453–72.
8. Suen HC, Mathisen DJ, Grillo HC, et al. Surgical management and radiologic characteristics of bronchogenic cysts. Ann Thorac Surg 1993; 55: 476–81.
9. Politis GD, Baumann R, Hubbard AM. Spillage of cystic pulmonary masses into the airway during anesthesia. Anesthesiology 1997; 87: 693–6.
10. Ryckman FC, Rosenkrantz JG. Thoracic surgical problems in infancy and childhood. Surg Clin North Am 1985; 65: 1423–54.
11. Schwartz MZ, Ramachandran P. Congenital malformations of the lung and mediastinum: a quarter century of experience from a single institution. J Pediatr Surg 1997; 32: 44–7.
12. Raynor AC, Capp MP, Sealy WC. Lobar emphysema of infancy: diagnosis, treatment, and etiologic aspects. Ann Thorac Surg 1967; 4: 374–85.
13. Lincoln JC, Stark J, Subramanian S, et al. Congenital lobar emphysema. Ann Surg 1971; 173: 55–62.
14. Karnak I, Senocak ME, Ciftci AO, Buyukpamukcu N. Congenital lobar emphysema: diagnostic and therapeutic considerations. J Pediatr Surg 1999; 34: 1347–51.
15. Mychaliska GB, Bullard KM, Harrison MR. In utero management of congenital diaphragmatic hernia. Clin Perinatol 1996; 23: 823–41.
16. Sumner E, Frank JD. Tolazoline in the treatment of congenital diaphragmatic hernias. Arch Dis Child 1981; 56: 350–3.
17. Kaapa P, Koivisto M, Ylikorlaka O, Kouvalainen K. Prostacyclin in the treatment of neonatal pulmonary hypertension. J Pediatr 1985; 107: 951–3.
18. Roberts JD, Polaner DM, Lang P, Zapol WM. Inhaled nitric oxide in persistent pulmonary hypertension of the newborn. Lancet 1992; 340: 818–9.
19. Ivy DD, Ziegler JW, Kinsella JP, et al. Dipyridamole attenuates rebound pulmonary hypertension after inhaled nitric oxide withdrawal in postoperative congenital heart disease. J Thorac Cardiovasc Surg 1998; 115: 875–82.
20. Mariani G, Barefield ES, Carlo WA. The role of nitric oxide in the treatment of neonatal pulmonary hypertension. Curr Opin Pediatr 1996; 8: 118–25.
21. Miguet D, Claris O, Lapillonne A, et al. Preoperative stabilization using high-frequency oscillatory ventilation in the management of congenital diaphragmatic hernia. Crit Care Med 1994; 22: S77–82.
22. Frenckner B, Ehren H, Granholm T. Improved results in patients who have congenital diaphragmatic hernia using preoperative stabilization, extracorporeal membrane oxygenation, and delayed surgery. J Pediatr Surg 1997; 32: 1185–9.
23. Harrison MR, Bjordal RI, Langmark F, et al. Congenital diaphragmatic hernia: the hidden mortality. J Pediatr Surg 1978; 13: 227–30.
24. Adelman S, Benson CD. Bochdalek hernias in infants: factors determining mortality. J Pediatr Surg 1976; 11: 569–73.
25. Kavvadia V, Greenough A, Laubscher B. Perioperative assessment of respiratory compliance and lung volume in infants with congenital diaphragmatic hernia: prediction of outcome. J Pediatr Surg 1997; 32: 1665–9.
26. Donnelly LF, Sakurai M, Klosterman LA. Correlation between findings on chest radiography and survival in neonates with congenital diaphragmatic hernia. Am J Roentgenol 1999; 173: 1589–93.
27. Geary MP, Chitty LS, Morrison JJ. Perinatal outcome and prognostic factors in prenatally diagnosed congenital diaphragmatic hernia. Ultrasound Obstet Gynecol 1998; 12: 107–11.
28. Truog RD, Schena JA, Hershenson MB, et al. Repair of congenital diaphragmatic hernia during extracorporeal membrane oxygenation. Anesthesiology 1990; 72: 750–3.
29. Clark RH, Hardin WD Jr, Hirschl RB. Current surgical management of congenital diaphragmatic hernia: a report from the Congenital Diaphragmatic Hernia Study Group. J Pediatr Surg 1998; 33: 1004–9.
30. Leveque C, Hamza J, Berg AE, et al. Successful repair of a severe left congenital diaphragmatic hernia during continuous inhalation of nitric oxide. Anesthesiology 1994; 80: 1171–5.
31. Bouchut JC, Dubois R, Moussa M, et al. High frequency oscillatory ventilation during repair of neonatal congenital diaphragmatic hernia. Paediatr Anaesth 2000; 10: 377–9.
32. Cumming WA. Esophageal atresia and tracheoesophageal fistula. Radiol Clin North Am 1975; 13: 277–95.
33. Holder TM, Ashcraft KW, Sharp RJ, et al. Care of infants with esophageal atresia, tracheoesophageal fistula, and associated anomalies. J Thorac Cardiovasc Surg 1987; 94: 828–35.
34. Barry JE, Auldist AW. The VATER association: one end of a spectrum of anomalies. Am J Dis Child 1974; 128: 769–71.
35. Bloch EC, Filston HC. A thin fiberoptic bronchoscope as an aid to occlusion of the fistula in infants with tracheoesophageal fistula. Anesth Analg 1988; 67: 791–3.
36. Filston HC, Chitwood WR Jr, Schkolne B, et al. The Fogarty balloon catheter as an aid to management of the infant with esophageal atresia and tracheoesophageal fistula complicated by severe RDS or pneumonia. J Pediatr Surg 1982; 17: 149–51.
37. Humphreys GH, Hogg BM, Ferrer J. Congenital atresia of the esophagus. J Thorac Surg 1956; 32: 332–48.
38. Schwartz N, Eisencraft JB. Positioning of the endotracheal tube in an infants with tracheoesophageal fistula. Anesthesiology 1988; 69: 289–90.
39. Grant DM, Thompson GE. Diagnosis of congenital tracheoesophageal fistula in the adolescent and adult. Anesthesiology 1978; 49: 139–40.
40. Mitchell SC, Korones SB, Berendes HW. Congenital heart disease in 56,109 births: incidence and natural history. Circulation 1971; 43: 323–32.
41. Hallman GL, Cooley DA. Surgical treatment of congenital heart disease. Philadelphia: Lea and Febiger, 1975.
42. Keith JD, Rowe RD, Vlad P. Coarctation of the aorta. In: Heart disease in infancy and childhood. 38th ed. New York: Macmillan, 1978: 226.
43. McNamara DG. Coarctation of the aorta: difficulties in clinical recognition. Heart Dis Stroke 1992; 1: 202–6.
44. Watterston KG, Dhasmana JP, O’Higgins JW, et al. Distal aortic pressure during coarctation operation. Ann Thorac Surg 1990; 49: 978–90.
45. Leandro J, Williamson Balfe J, Smallhorn JF, et al. Coarctation of the aorta and hypertension. Child Nephrol Urol 1992; 12: 124–7.
46. Rao PS, Galal O, Smith PA, et al. Five- to nine-year follow-up results of balloon angioplasty of native aortic coarctation in infants and children. J Am Coll Cardiol 1996; 27: 462–70.
47. Roesler M, deLeval M, Chrispin A, Stark J. Surgical management of vascular ring. Ann Surg 1983; 197: 139–46.
48. Rosen DA, Rosen KR. Anomalies of the aortic arch and valve. In: Lake CL, ed. Pediatric cardiac anesthesia. 3rd ed. Stamford, CT: Appleton and Lange, 1998: 460.
49. Franken EA Jr, Smith JA, Smith WL. Tumors of the chest wall in infants and children. Pediatr Radiol 1977; 6: 13–8.
50. Azizkhan RG, Dudgeon DL, Colombani PM, et al. Life-threatening airway obstruction as a complication to the management of mediastinal masses in children. J Pediatr Surg 1985; 20: 816–22.
51. Azarow KS, Pearl RH, Zurcher R, et al. Primary mediastinal masses: a comparison of adult and pediatric populations. J Thorac Cardiovasc Surg 1993; 106: 67–72.
52. Keon TP. Death on induction of anesthesia for cervical node biopsy. Anesthesiology 1981; 55: 471–2.
53. Piro AH, Weiss DR, Hellman S. Mediastinal Hodgkin’s disease: a possible danger for intubation anesthesia. Int J Radiat Oncol Biol Phys 1976; 1: 415–9.
54. Alkrinawi S, Chernick V. Pleural infection in children. Semin Respir Infect 1996; 11: 148–54.
55. Klena JW, Cameron BH, Langer JC, et al. Timing of video-assisted thoracoscopic debridement for pediatric empyema. J Am Coll Surg 1998; 187: 404–8.
56. Swanson KL, Prakash UB, Stanson AW. Pulmonary arteriovenous fistulas: Mayo Clinic experience, 1982–1997. Mayo Clin Proc 1999; 74: 671–80.
57. Bernstein HS, Ursell PC, Brook MM, et al. Fulminant development of pulmonary arteriovenous fistulas is an infant after cavopulmonary shunting. Pediatr Cardiol 1996; 17: 46–50.
58. Barbe T, Losay J, Grimon G, et al. Pulmonary arteriovenous shunting in children with liver disease. J Pediatr 1995; 126: 571–9.
59. Onursal E, Toker A, Bostanci K. A complication of pectus excavatum operation: endomyocardial steel strut. Ann Thorac Surg 1999; 68: 1082–3.
60. Kowalewski J, Barcikowski S, Brocki M. Cardiorespiratory function before and after operation for pectus excavatum: medium-term results. Eur J Cardiothorac Surg 1998; 13: 275–9.
61. Nuss D, Kelly RE Jr, Croitoru DP. A 10-year review of a minimally invasive technique for the correction of pectus excavatum. J Pediatr Surg 1998; 33: 545–52.
62. Newton PO, Wenger DR, Mubarak SJ. Anterior release and fusion in pediatric spinal deformity: a comparison of early outcome and cost of thoracoscopic and open thoracotomy approaches. Spine 1997; 22: 1398–406.
63. Rothenberg S, Erickson M, Eilert R. Thoracoscopic anterior spinal procedures in children. J Pediatr Surg 1998; 33: 1168–70.
64. Remolina C, Khan AU, Santiago TV, Edelman NH. Positional hypoxemia in unilateral lung disease. N Engl J Med 1981; 304: 523–5.
65. Heaf DP, Helms P, Gordon MB, Turner HM. Postural effects on gas exchange in infants. N Engl J Med 1983; 28: 1505–8.
66. Mansell A, Bryan C, Levison H. Airway closure in children. J Appl Physiol 1972; 33: 711–4.
67. Dawes GS. Fetal and neonatal physiology. Chicago: Yearbook Medical, 1973.
68. Weatherford DA, Stephenson JE, Taylor SM, et al. Thoracoscopy versus thoracotomy: indications and advantages. Ann Surg 1995; 61: 83–6.
69. Mouroux J, Clary-Meinesz C, Padovani B, et al. Efficacy and safety of videothoracoscopic lung biopsy in the diagnosis of interstitial lung disease. Eur J Cardiothorac Surg 1997; 11: 22–6.
70. Angelillo Mackinlay TA, Lyons GA, Chimondeguy DJ, et al. VATS debridement versus thoracotomy in the treatment of loculated postpneumonia empyema. Ann Thorac Surg 1996; 61: 1626–30.
71. Benumof JL. Anesthesia for thoracic surgery. 2nd ed. Philadelphia: WB Saunders, 1995.
72. Rowe R, Andropoulos D, Heard M, et al. Anesthetic management of pediatric patients undergoing thoracoscopy. J Cardiothorac Vasc Anesth 1994; 8: 563–6.
73. Kubota H, Kubota Y, Toshiro T, et al. Selective blind endobronchial intubation in children and adults. Anesthesiology 1987; 67: 587–9.
74. Lammers CR, Hammer GB, Brodsky JB, Cannon WB. Failure to isolate the lungs with an endotracheal tube positioned in the bronchus. Anesth Analg 1997; 85: 946–7.
75. Cullum AR, English CW, Branthwaite MA. Endobronchial intubation in infancy. Anaesthesia 1973; 28: 66–70.
76. McLellan I. Endobronchial intubation in children. Anaesthesia 1974; 29: 757–8.
77. Yeh TF, Pildes RS, Salem MR. Treatment of persistent tension pneumothorax in a neonate by selective bronchial intubation. Anesthesiology 1978; 49: 37–8.
78. Watson CB, Bowe EA, Burk W. One-lung anesthesia for pediatric thoracic surgery: a new use for the fiberoptic bronchoscope. Anesthesiology 1982; 56: 314–5.
79. Hammer GB, Manos SJ, Smith BM, et al. Single lung ventilation in pediatric patients. Anesthesiology 1996; 84: 1503–6.
80. Ginsberg RJ. New technique for one-lung anesthesia using a bronchial blocker. J Thorac Cardiovasc Surg 1981; 82: 542–6.
81. Lin YC, Hackel A. Paediatric selective bronchial blocker. Paediatr Anaesth 1994; 4: 391–2.
82. Turner MWH, Buchanon CCR, Brown SW. Paediatric one lung ventilation in the prone position. Paediatric Anaesthesia 1997; 7: 427–9.
83. Borchardt RA, LaQuaglia MP, McDowall, Wilson RS. Bronchial injury during lung isolation in a pediatric patient. Anesth Analg 1998; 87: 324–5.
84. Guyton DC, Besselievre TR, Devidas M, et al. A comparison of two different bronchial cuff designs and four different bronchial cuff inflation methods. J Cardiothorac Vasc Anesth 1997; 11: 599–603.
85. Takahashi M, Horinouchi T, Kato M, et al. Double-access-port endotracheal tube for selective lung ventilation in pediatric patients. Anesthesiology 2000; 93: 308–9.
86. Arndt GA, De Lessio ST, Kranner PW, et al. One-lung ventilation when intubation is difficult: presentation of a new endobronchial blocker. Acta Anaesthesiol Scand 1999; 43: 356–8.
87. Kamaya H, Krishna PR. New endotracheal tube (Univent tube) for selective blockade of one lung. Anesthesiology 1985; 63: 342–3.
88. Karwande SV. A new tube for single lung ventilation. Chest 1987; 92: 761–3.
89. Gayes JM. The Univent tube is the best technique for providing one-lung ventilation: pro—one-lung ventilation is best accomplished with the Univent endotracheal tube. J Cardiothorac Vasc Anesth 1993; 7: 103–5.
90. Hammer GB, Brodsky JB, Redpath J, Cannon WB. The Univent tube for single lung ventilation in children. Paediatr Anaesth 1998; 8: 55–7.
91. Slinger PD, Lesiuk L. Flow resistances of disposable double-lumen, single-lumen, and Univent tubes. J Cardiothorac Vasc Anesth 1998; 12: 142–4.
92. Kelley JG, Gaba DM, Brodsky JB. Bronchial cuff pressures of two tubes used in thoracic surgery. J Cardiothorac Vasc Anesth 1992; 6: 190–4.
93. Benumof JL, Gaughan SD, Ozaki GT. The relationship among bronchial blocker cuff inflation volume, proximal airway pressure, and seal of the bronchial blocker cuff. J Cardiothorac Vasc Anesth 1992; 6: 404–8.
94. Marraro G. Selective bronchial intubation in paediatrics: the Marraro paediatric bilumen tube. Paediatr Anaesth 1994; 4: 255–8.
95. Brodsky JB, Mark JBD. A simple technique for accurate placement of double-lumen endobronchial tubes. Anesth Rev 1983; 10: 26–30.
96. Brodsky JB, Macario A, Mark JBD. Tracheal diameter predicts double-lumen tube size: a method for selecting left double-lumen tubes. Anesth Analg 1996; 82: 861–4.
97. Slinger PD. Fiberoptic bronchoscopic positioning of double-lumen tubes. J Cardiothorac Anesth 1989; 3: 486–96.
98. Benumof JL, Partridge BL, Salvatierra C, Keating J. Margin of safety in positioning modern double-lumen endotracheal tubes. Anesthesiology 1987; 67: 729–38.
99. Benumof JF, Augustine SD, Gibbons JA. Halothane and isoflurane only slightly impair arterial oxygenation during one-lung ventilation in patients undergoing thoracotomy. Anesthesiology 1987; 67: 910–4.
100. Bricker SRW, Telford RJ, Booker PD. Pharmacokinetics of bupivacaine following intraoperative nerve block in neonates and infants less than 6 months. Anesthesiology 1987; 66: 832–4.
101. Cooper MG, Seaton HL. Intraoperative placement of intercostal catheter for post-thoracotomy pain relief in a child. Paediatr Anaesth 1992; 2: 165–7.
102. Richardson J, Sabanathan S, Mearns AJ, et al. Efficacy of preemptive analgesia and continuous extra-pleural intercostal nerve block on post-operative pain and pulmonary mechanics. J Cardiovasc Surg 1994; 35: 219–28.
103. Lonnqvist PA, Olsson GL. Paravertebral vs. epidural block in children: effects on postoperative morphine requirement after renal surgery. Acta Anaesthesiol Scand 1994; 38: 346–9.
104. McIlvaine WB, Knox RF, Fennessey PV, Goldstein M. Continuous infusion of bupivacaine via intrapleural catheter for analgesia after thoracotomy in children. Anesthesiology 1988; 69: 261–4.
105. Giaufre E, Bruguerolle B, Rastello C, et al. New regimen for interpleural block in children. Paediatr Anaesth 1995; 5: 125–8.
106. Scneider RF, Villamena PC, Harvery J, et al. Lack of efficacy of intrapleural bupivacaine for postoperative analgesia following thoracotomy. Chest 1993; 103: 414–6.
107. Miguel R, Hubbell D. Pain management and spirometry following thoracotomy: a prospective, randomized study of four techniques. J Cardiothorac Vasc Anesth 1993; 7: 529–34.
108. Ferrante FM, Chan VW, Arthur GR, et al. Interpleural analgesia after thoracotomy. Anesth Analg 1001;72:105–9.
109. Rosenberg PH, Scheinin M, Lepantalo M, et al. Continuous infusion of intrapleural of bupivacaine for analgesia after thoracotomy. Anesthesiology 1987; 67: 811–3.
110. Gaeta RR, Macario A, Brodsky JB, et al. Pain outcomes after thoracotomy: lumbar epidural hydromorphone versus intrapleural bupivacaine. J Cardiothorac Vasc Anesth 1995; 9: 534–7.
111. Schulte-Steinberg O, Rahlfs VW. Spread of extradural analgesia following caudal injection in children. Br J Anaesth 1982; 49: 1027–34.
112. Satoyoshi M, Kaniyama Y. Caudal anaesthesia for upper abdominal surgery in infants and children: a simple calculation of the volume of local anaesthesia. Acta Anaesthesiol Scand 1984; 28: 57–60.
113. Bosenberg AT, Bland BA, Schulte-Steinberg O, et al. Thoracic epidural anesthesia via the caudal route in infants. Anesthesiology 1988; 69: 265–9.
114. Gunter JB, Engl C. Thoracic epidural anesthesia via the caudal approach in children. Anesthesiology 1992; 76: 935–8.
115. Bromage PR, Benumof JL. Paraplegia following intracord injection during attempted epidural anesthesia under general anesthesia. Reg Anesth Pain Med 1998; 23: 104–7.
116. Krane EJ, Dalens BJ, Murat I, Murrell D. The safety of epidurals placed during general anesthesia. Reg Anesth Pain Med 1998; 23: 433–8.
117. Flandin-Blety C, Barrier G. Accidents following extradural analgesia in children: the results of a retrospective study. Paediatr Anaesth 1995; 5: 41–6.
118. Goldman LJ. Complications in regional anesthesia. Paediatr Anaesth 1995; 5: 3–9.
119. Kane RE. Neurologic deficits following epidural or spinal anesthesia. Anesth Analg 1981; 60: 150–61.
120. Bridenbaugh PO. Complications of local anesthetic neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. Philadelphia: JB Lippincott, 1988: 705–9.
121. Tobias JD, Rasmussen GE, Holcomb GW, et al. Continuous caudal anaesthesia with chloroprocaine as an adjunct to general anaesthesia in neonates. Can J Anaesth 1996; 43: 69–72.
122. McBride WJ, Dicker R, Abajian JC, Vane DW. Continuous thoracic epidural infusions for postoperative analgesia after pectus deformity repair. J Pediatr Surg 1996; 31: 105–7.
123. Yaster M, Andresini J, Krane EJ. Epidural analgesia. In: Yaster M, Krane EJ, Kaplan RF, et al., eds. Pediatric pain management and sedation handbook. St. Louis: Mosby, 1997: 113–47.
124. Scott DA, Beilby DS, McClymont C. Postoperative analgesia using epidural infusions of fentanyl with bupivacaine: a prospective analysis of 1,014 patients. Anesthesiology 1995; 83: 727–37.
125. Moriarty A. Postoperative extradural infusions in children: preliminary data from a comparison of bupivacaine/diamorphine with plain ropivacaine. Paediatr Anaesth 1999; 9: 423–7.
126. Ivani G, Mereto N, Lampugnani E. Ropivacaine in paediatric surgery: preliminary results. Paediatr Anaesth 1998; 8: 127–9.
127. Hammer GB, Ngo K, Macario A. A retrospective examination of regional plus general anesthesia in children undergoing open heart surgery. Anesth Analg 2000; 90: 1020–4.
128. Cassidy JF, Lederhaas G, Cancel DD, et al. A randomized comparison of the effects of continuous thoracic epidural analgesia and intravenous patient-controlled analgesia after posterior spinal fusion in adolescents. Reg Anesth Pain Med 2000; 25: 246–53.
129. Gunter JB. Thoracic epidural anaesthesia via the caudal approach in children. Anesthesiology 1992; 76: 935–8.
130. Tobias JD, Lowe S, O’Dell N, Holcomb GW. Thoracic epidural anaesthesia in infants and children. Can J Anaesth 1993; 40: 879–82.
131. Huang YF, Pryor ME, Mather LE, Veering BT. Cardiovascular and central nervous system effects of intravenous levobupivacaine and bupivacaine. Anesth Analg 1998; 86: 797–804.
132. Bardsley H, Gristwood R, Baker H, et al. A comparison of the cardiovascular effects of levobupivacaine and rac-bupivacaine following intravenous administration to healthy volunteers. Br J Clin Pharmacol 1998; 46: 245–9.
133. Luz G, Wieser C, Innerhofer P, et al. Free and total bupivacaine plasma concentrations after continuous epidural anesthesia in infants and children. Paediatr Anaesth 1998; 8: 473–8.
134. Larsson BA, Lonnqvist PA, Olsson GL. Plasma concentrations of bupivacaine in neonates after continuous epidural infusion. Anesth Analg 1997; 84: 501–5.
135. Miyabe M, Kakiuchi Y, Kihara S, et al. The plasma concentration of lidocaine’s principle metabolite increases during continuous epidural anesthesia in infants and children. Anesth Analg 1998; 87: 1056–7.
136. Shayevitz JR, Merkel S, O’Kelly SW. Lumbar epidural morphine infusions for children undergoing cardiac surgery. J Cardiothorac Vasc Anesth 1996; 10: 217–24.
137. Malviya S, Pandit UA, Merkel S, et al. A comparison of continuous epidural infusion and intermittent intravenous bolus doses of morphine in children undergoing selective dorsal rhizotomy. Reg Anesth Pain Med 1999; 24: 438–43.
138. Goodarzi M. Comparison of epidural morphine, hydromorphone and fentanyl for postoperative pain control in children undergoing orthopaedic surgery. Paediatr Anaesth 1999; 9: 419–22.
139. Lovstad RZ, Halvorsen P, Raeder JC, Steen PA. Post-operative epidural analgesia with low dose fentanyl, adrenaline and bupivacaine in children after major orthopaedic surgery: a prospective evaluation of efficacy and side effects. Eur J Anaesthesiol 1997; 14: 583–9.
140. Kokki H, Tuovinen K, Hendolin H. The effect of intravenous ketoprofen on postoperative epidural sufentanil analgesia in children. Anesth Analg 1999; 88: 1036–41.
141. Roy SD, Flynn GL. Solubility and related physicochemical properties of narcotic analgesics. Pharm Res 1988; 5: 580–6.
142. Attia J, Ecoffy C, Sandouk P, et al. Epidural morphine in children: pharmacokinetics and CO2 sensitivity. Anesthesiology 1986; 65: 590–4.
143. White MJ, Berghaus EJ, Dumont SW, et al. Side effects during continuous infusion of morphine and fentanyl. Can J Anaesth 1992; 39: 576–82.
144. Parker RK, White PF. Epidural patient-controlled analgesia: an alternative to intravenous patient-controlled analgesia for pain relief after cesarian delivery. Anesth Analg 1992; 75: 245–51.
145. Chaplan R, Duncan SR, Brodsky JB, Brose WG. Morphine and hydromorphone epidural analgesia. Anesthesiology 1992; 77: 1090–4.
146. Moon RE, Clements FM. Accidental epidural overdose of hydromorphone. Anesthesiology 1985; 63: 238–9.
147. Lejus C, Roussiere G, Testa S, et al. Postoperative extradural analgesia in children: comparison of morphine with fentanyl. Br J Anaesth 1994; 72: 156–9.
148. Semple D, Findlow D, Aldridge LM, Doyle E. The optimal dose of ketamine for caudal epidural blockade in children. Anaesthesia 1996; 51: 1170–2.
149. Johnston P, Findlow D, Aldridge LM, Doyle E. The effect of ketamine on 0.25% and 0.125% bupivacaine for caudal epidural blockade in children. Paediatr Anaesth 1999; 9: 31–4.
150. Ivani G, Bergendahl HT, Lampugnani E, et al. Plasma levels of clonidine following epidural bolus injection in children. Acta Anaesthesiol Scand 1998; 42: 306–11.
151. Luz G, Innerhofer P, Oswald E, et al. Comparison of clonidine 1 microgram kg1 with morphine 30 micrograms kg1 for post-operative caudal analgesia in children. Eur J Anaesthesiol 1999; 16: 42–6.
152. Gunter JB, McAuliffe J, Gregg T, et al. Continuous epidural butorphanol relieves pruritus associated with epidural morphine infusions in children. Paediatr Anaesth 2000; 10: 167–72.
153. Lawhorn CD, Stoner JM, Schmitz ML, et al. Caudal epidural butorphanol plus bupivacaine versus bupivacaine in pediatric outpatient genitourinary procedures. J Clin Anesth 1997; 9: 103–8.
154. Berde CB, Beyer JE, Bournaki MC, et al. A comparison of morphine and methadone for prevention of postoperative pain in 3 to 7 year old children. J Pediatr 1991; 119: 136–41.
155. Berde CB. Pediatric postoperative pain management. Pediatr Clin North Am 1989; 36: 921–40.
156. Lynn AM, Slattery JT. Morphine pharmacokinetics in early infancy. Anesthesiology 1987; 66: 136–9.
157. Lynn AM, Opheim KE, Tyler DC. Morphine infusion after pediatric cardiac surgery. Crit Care Med 1984; 12: 863–6.
158. Yaster M, Billett C, Monitto C. Intravenous patient controlled analgesia. In: Pediatric pain management and sedation handbook. St. Louis: Mosby, 1997: 89–111.
159. Yaster M. Nonsteroidal antiinflammatory drugs. In: Pediatric pain management and sedation handbook. St. Louis: Mosby, 1997: 19–28.
© 2001 International Anesthesia Research Society