Pediatr Surg Int DOI 10.1007/s00383-014-3482-1
CASE REPORT
Surgical salvage of acquired lung lesions in extremely premature infants Greg D. Sacks • Katherine Chung • Kevin Jamil • Meena Garg • James C. Y. Dunn • Daniel A. DeUgarte
Accepted: 30 January 2014 Ó Springer-Verlag Berlin Heidelberg 2014
Abstract Acquired neonatal lung lesions including pneumatoceles, cystic bronchopulmonary dysplasia, and pulmonary interstitial emphysema can cause extrinsic mediastinal compression, which may impair pulmonary and cardiac function. Acquired lung lesions are typically managed medically. Here we report a case series of three extremely premature infants with acquired lung lesions. All three patients underwent aggressive medical management and ultimately required tube thoracostomies. These interventions were unsuccessful and emergency thoracotomies were performed in each case. Two infants with acquired pneumatoceles underwent unroofing of the cystic structure and primary repair of a bronchial defect. The third infant with pulmonary interstitial emphysema, arising from cystic bronchopulmonary dysplasia, required a middle lobectomy for severe and diffuse cystic disease. When medical management fails, tube thoracostomy can be attempted, leaving surgical intervention for refractory cases. Surgical options include oversewing a bronchial defect in the setting of a bronchopleural fistula or lung resection in cases of an isolated expanding lobe. Keywords Lung Pulmonary Lymphatic Bronchopleural fistula Thoracotomy Pulmonary interstitial emphysema Cystic bronchopulmonary dysplasia Persistent air leak G. D. Sacks K. Jamil J. C. Y. Dunn D. A. DeUgarte (&) Division of Pediatric Surgery, Department of Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, P. O. Box 709818, Los Angeles, CA 90095-7098, USA e-mail: [email protected] K. Chung M. Garg Division of Pediatric Neonatology, David Geffen School of Medicine at UCLA, Los Angeles, USA
Introduction Acquired lung lesions are a source of significant morbidity and mortality in neonates. In addition to the intrinsic effects on pulmonary function and gas exchange, these lesions may also cause extrinsic compression on mediastinal structures, causing further pulmonary and cardiac impairment. These lesions typically arise as a complication of mechanical ventilation but have become rare in the era of surfactant treatment of respiratory distress syndrome [1]. As opposed to symptomatic congenital lung lesions in the neonate, acquired lung lesions are typically managed nonoperatively [1, 2]. Medical therapy hinges on minimizing airway pressures in the affected lung. In the case of rapid expansion or tension physiology, urgent decompression is necessary, usually with tube thoracostomy. Here we describe three cases of acquired lung lesions in neonates that were successfully treated with surgical intervention at our academic medical center. Case 1: ruptured pneumatocele with tension pneumothorax A 695-g 24-week estimated gestational age (EGA) female born to a G4P0 mother was transferred to our institution at 10 days of life with worsening respiratory failure. Despite steroid and surfactant therapy, she developed a small right pneumothorax on her second day of life (DOL). The pneumothorax resolved with high frequency oscillator ventilation (HFOV). One week later, she developed a tension pneumothorax requiring two chest tubes and transfer to our institution for higher level of care (Fig. 1a). After transfer, the patient continued to have frequent episodes of desaturation, hypotension and bradycardia requiring frequent chest tube revisions (Fig. 1b). On DOL
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Pediatr Surg Int
Fig. 1 A 24-week EGA infant developed a tension pneumothorax (a), which failed decompression with tube thoracostomy (b), and required thoracotomy and surgical repair of bronchial defect within a ruptured pneumatocele (c)
22, due to persistent hemodynamic instability, she was taken to the operating room and was noted to have a cystic cavity on the undersurface of the middle lobe extending to the diaphragmatic surface. The pneumatocele was debrided, and a large hole with air leak was noted in the bronchus just distal to the takeoff of the right middle lobe. The defect was repaired primarily with interrupted 6-0 prolene sutures resulting in resolution of the air leak (Fig. 1c). The patient was extubated 30 days later and ultimately discharged at 4 months of age with home oxygen therapy. One year later, she is doing well on room air. Case 2: pneumatocele with mass-effect A 645-g, 24-week EGA male was born to a G1P0 mother with a history of cadaveric renal transplant on immunosuppression. The mother developed severe pre-eclampsia and oligohydramnios. Antenatal steroids were administered, and a Cesarean section was performed. Despite a spontaneous cry, the newborn had poor inspiratory effort and bradycardia and was immediately intubated. The first chest radiograph, obtained shortly after intubation, revealed a well-demarcated lucency at the right lung base. Shortly after intubation, the child experienced pulmonary hemorrhage evidenced by frank blood suctioned from the endotracheal tube, as well as an evolving parenchymal hemorrhage on chest radiograph. At 1 week of life, the child developed worsening respiratory acidosis and hypoxemia. A repeat chest radiograph demonstrated an enlarging right cystic mass (Fig. 2a). Pigtail thoracostomy tubes were placed in an attempt to decompress the pneumatocele (Fig. 2b). Overnight, a large pneumothorax and pneumomediastinum developed, and a right thoracotomy was performed at the bedside. A thin-walled cyst was identified and unroofed. Within the cyst, a large defect with massive air leak from an adjacent bronchus was identified.
123
The defect was approximated with a single figure-of-eight 7-0 prolene suture. The air leak resolved, and the patient was weaned of ventilator support without evidence of cyst recurrence (Fig. 2c).
Case 3: lobar pulmonary interstitial emphysema with mass-effect A 500-g, 23-week EGA male was born to a G4P2 mother after an uncomplicated prenatal course. Despite preterm premature rupture of membranes and breech positioning, the baby was delivered vaginally. The baby was immediately intubated due to extreme prematurity and concern for respiratory distress syndrome. The patient developed severe respiratory distress with chest radiographs demonstrating diffuse cystic changes concerning for cystic bronchopulmonary dysplasia. All attempts to improve the patient’s respiratory status, including high frequency oscillatory ventilation and intravenous corticosteroids, were unsuccessful. After 2 days of aggressive medical management, a repeat chest X-ray demonstrated the development of prominent pneumomediastinum, subcutaneous emphysema tracking up the neck, and mediastinal shift (Fig. 3a). The patient developed severe acidosis and hypotension requiring vasopressor support. In an attempt to relieve the mass-effect of the cystic lung, a right-sided tube thoracostomy was placed which resulted in a pneumothorax (Fig. 3b) and continuous air leak. The patient remained hemodynamically unstable, and a right thoracotomy was performed at the bedside. The right middle lobe contained diffuse thin-walled cystic changes, was massively hyperinflated, and herniating into the left chest. A vessel-sealant device (Ligasure; Covidien Surgical, Boulder, CO) was initially used to quickly collapse the lobe providing better exposure; it was then used to divide the lobar vessels and
Pediatr Surg Int
Fig. 2 A 24-week EGA infant developed an enlarging symptomatic cystic mass in the right lung (a), which failed decompression with pigtail catheters (b), and required thoracotomy and surgical repair of bronchial defect within a ruptured pneumatocele (c)
Fig. 3 A 23-week EGA infant developed diffuse cystic bronchopulmonary dysplasia with pneumomediastinum, midline shift and pulmonary interstitial emphysema (a). Tube thoracostomy reduced
the midline shift but resulted in a persistent air leak (b). The patient underwent thoracotomy and was found to have a hyperinflated right middle lobe, which was successfully resected (c)
pulmonary parenchyma. A followup chest X-ray demonstrated resolution of mediastinal shift and persistence of diffuse interstitial disease in the remaining lung parenchyma (Fig. 3c). Pathology demonstrated findings consistent with pulmonary interstitial emphysema.
Two of the cases we report were ruptured pneumatoceles resulting in high-flow continuous air leaks. In both cases, a focal bronchial defect was identified and successfully repaired with prolene suture. Pneumatoceles occur in 1.8 % of premature infants and represent thin-walled gas-filled cysts that develop within the lung parenchyma as a result of a contained air leak [1]. The pathophysiology of these lesions remains controversial but is thought to arise from an acute lung injury in the setting of surfactant deficiency, which results in alveolar collapse after PPV-induced barotrauma. In addition, oxygen and oxygen-free radicals damage the epithelial lining of the lung parenchyma causing a focal area of inflammation. The combination of these factors leads to a check-valve type airway obstruction, air trapping and pseudocyst formation [1]. The third case illustrates how cystic BPD can be complicated by lobar pulmonary interstitial emphysema resulting in mass-effect, pneumomediastinum and pneumothorax.
Discussion Acquired lung lesions in premature infants including pneumatoceles, cystic bronchopulmonary dysplasia (BPD), and pulmonary interstitial emphysema (PIE) are frequently a consequence of positive pressure ventilation (PPV) and are typically managed medically. In this case series, we report the role of surgical intervention in the management of acquired lung lesions in premature infants. All three reported cases failed the most aggressive medical management options necessitating surgical intervention.
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Pediatr Surg Int
We found the vessel-sealant device helpful in decompressing the lobe and providing exposure. In the premature infant, we also found the vessel-sealant device helpful in ‘sealing’ parenchyma and minimizing air leak when transecting the lung and lobar vessels [3]. Cystic BPD with hyperinflation and atelectasis can be seen in both ‘‘new BPD’’, characterized by alveolar and capillary hypoplasia leading to a reduction gas exchange, and ‘‘old BPD’’, which is characterized by airway injury, inflammation and parenchymal fibrosis [4]. PIE is a type of acquired air leak believed to arise from a disruption of the basement membrane of the alveolar wall allowing air entry into the interstitial space. Since the perivascular connective tissue is more abundant and less dissectible in preterm than in older infants, this predisposes to air trapping in the perivascular space, resulting in cystic changes [5]. These conditions are distinguished from congenital lobar emphysema (CLE), which is a congenital anomaly involving the lower respiratory tract. In contrast to CLE, which is classically a surgical disease managed with resection, acquired lung lesions are generally managed non-operatively. Primary medical management for acquired lung lesions involves minimizing airway pressures in the affected lung. Options include positioning the patient with the affected side down, the use of high frequency oscillator ventilation and selective intubation of the contralateral bronchus. Several case reports have demonstrated the successful use of tube thoracostomy to decompress an overinflated lung due to cystic lung disease or the resulting sequelae [6–8]. This intervention is typically considered only if more conservative measures fail. The rationale for chest tube placement is to improve pulmonary and hemodynamic physiology either by evacuating air from a tension pneumothorax or pneumomediastinum or decompressing a large pneumatocele, which is causing a mass-effect [7, 8]. We performed chest tube decompression in all three cases without noting any clinical improvement. The risk of injury to either lung cysts or healthy lung parenchyma during chest tube placement is high in small neonates with frail, cystic lung tissue. In at least two of the cases we report, chest tube placement converted a contained air leak into a pneumothorax with a continuous high-flow air leak that further impaired ventilation. Because of the potential need for surgical salvage, early surgical consultation and
123
involvement are advisable if thoracostomy tube placement is contemplated. Surgical intervention is reserved for cases unresponsive to medical management and in cases in which disease is isolated to a single lobe. Preoperative imaging with CT scans could theoretically aid in diagnosis and preoperative planning. However, preterm infants with acquired cystic lung lesions that are refractory to medical management are usually too unstable for transport. Therefore, clinicians usually depend on serial radiographs to aid their decisionmaking as was done in the cases described. If the pathology is isolated to a single lobe, two surgical techniques can be employed. In cases of a continuous air leak resulting from a focal defect in the bronchus, primary repair can be performed. In cases of isolated lobar pathology, lobectomy should be considered [9–11].
References 1. Hussain N et al (2010) Pneumatoceles in preterm infants-incidence and outcome in the post-surfactant era. J Perinatol 30(5):330–336 2. Staden U et al (2004) Asymmetric evolution of pulmonary interstitial emphysema in a preterm newborn infant. Pediatr Int 46(4):487–489 3. Rothenberg SS (2003) Experience with thoracoscopic lobectomy in infants and children. J Pediatr Surg 38(1):102–104 4. Jobe AH, Bancalari E (2001) Bronchopulmonary dysplasia. Am J Respir Crit Care Med 163:1723–1729 5. Matta R et al (2011) Diffuse persistent interstitial pulmonary emphysema treated by lobectomy. Ann Thorac Surg 92(4):e73– e75 6. Fox RB, Wright AM (1998) Case 30-1997: pulmonary interstitial emphysema in infancy. New Engl J Med 338(10):688–690 7. Chambers HM, van Velzen D (1989) Ventilator-related pathology in the extremely immature lung. Pathology 21(2):79–83 8. Do¨rdelmann M et al (2008) Therapeutic lung puncture for diffuse unilateral pulmonary interstitial emphysema in preterm infants. Eur J Pediatr Surg 18(4):233–236 9. Gessler P et al (2001) Lobar pulmonary interstitial emphysema in a premature infant on continuous positive airway pressure using nasal prongs. Eur J Pediatr 160(4):263–264 10. Kugelman A et al (1997) Acquired pulmonary cyst in the newborn infant. Pediatr Pulmonol 24(4):298–301 11. Rao J, Hochman MI, Miller GG (2006) Localized persistent pulmonary interstitial emphysema. J Pediatr Surg 41(6):1191– 1193
CASE REPORT
Surgical salvage of acquired lung lesions in extremely premature infants Greg D. Sacks • Katherine Chung • Kevin Jamil • Meena Garg • James C. Y. Dunn • Daniel A. DeUgarte
Accepted: 30 January 2014 Ó Springer-Verlag Berlin Heidelberg 2014
Abstract Acquired neonatal lung lesions including pneumatoceles, cystic bronchopulmonary dysplasia, and pulmonary interstitial emphysema can cause extrinsic mediastinal compression, which may impair pulmonary and cardiac function. Acquired lung lesions are typically managed medically. Here we report a case series of three extremely premature infants with acquired lung lesions. All three patients underwent aggressive medical management and ultimately required tube thoracostomies. These interventions were unsuccessful and emergency thoracotomies were performed in each case. Two infants with acquired pneumatoceles underwent unroofing of the cystic structure and primary repair of a bronchial defect. The third infant with pulmonary interstitial emphysema, arising from cystic bronchopulmonary dysplasia, required a middle lobectomy for severe and diffuse cystic disease. When medical management fails, tube thoracostomy can be attempted, leaving surgical intervention for refractory cases. Surgical options include oversewing a bronchial defect in the setting of a bronchopleural fistula or lung resection in cases of an isolated expanding lobe. Keywords Lung Pulmonary Lymphatic Bronchopleural fistula Thoracotomy Pulmonary interstitial emphysema Cystic bronchopulmonary dysplasia Persistent air leak G. D. Sacks K. Jamil J. C. Y. Dunn D. A. DeUgarte (&) Division of Pediatric Surgery, Department of Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, P. O. Box 709818, Los Angeles, CA 90095-7098, USA e-mail: [email protected] K. Chung M. Garg Division of Pediatric Neonatology, David Geffen School of Medicine at UCLA, Los Angeles, USA
Introduction Acquired lung lesions are a source of significant morbidity and mortality in neonates. In addition to the intrinsic effects on pulmonary function and gas exchange, these lesions may also cause extrinsic compression on mediastinal structures, causing further pulmonary and cardiac impairment. These lesions typically arise as a complication of mechanical ventilation but have become rare in the era of surfactant treatment of respiratory distress syndrome [1]. As opposed to symptomatic congenital lung lesions in the neonate, acquired lung lesions are typically managed nonoperatively [1, 2]. Medical therapy hinges on minimizing airway pressures in the affected lung. In the case of rapid expansion or tension physiology, urgent decompression is necessary, usually with tube thoracostomy. Here we describe three cases of acquired lung lesions in neonates that were successfully treated with surgical intervention at our academic medical center. Case 1: ruptured pneumatocele with tension pneumothorax A 695-g 24-week estimated gestational age (EGA) female born to a G4P0 mother was transferred to our institution at 10 days of life with worsening respiratory failure. Despite steroid and surfactant therapy, she developed a small right pneumothorax on her second day of life (DOL). The pneumothorax resolved with high frequency oscillator ventilation (HFOV). One week later, she developed a tension pneumothorax requiring two chest tubes and transfer to our institution for higher level of care (Fig. 1a). After transfer, the patient continued to have frequent episodes of desaturation, hypotension and bradycardia requiring frequent chest tube revisions (Fig. 1b). On DOL
123
Pediatr Surg Int
Fig. 1 A 24-week EGA infant developed a tension pneumothorax (a), which failed decompression with tube thoracostomy (b), and required thoracotomy and surgical repair of bronchial defect within a ruptured pneumatocele (c)
22, due to persistent hemodynamic instability, she was taken to the operating room and was noted to have a cystic cavity on the undersurface of the middle lobe extending to the diaphragmatic surface. The pneumatocele was debrided, and a large hole with air leak was noted in the bronchus just distal to the takeoff of the right middle lobe. The defect was repaired primarily with interrupted 6-0 prolene sutures resulting in resolution of the air leak (Fig. 1c). The patient was extubated 30 days later and ultimately discharged at 4 months of age with home oxygen therapy. One year later, she is doing well on room air. Case 2: pneumatocele with mass-effect A 645-g, 24-week EGA male was born to a G1P0 mother with a history of cadaveric renal transplant on immunosuppression. The mother developed severe pre-eclampsia and oligohydramnios. Antenatal steroids were administered, and a Cesarean section was performed. Despite a spontaneous cry, the newborn had poor inspiratory effort and bradycardia and was immediately intubated. The first chest radiograph, obtained shortly after intubation, revealed a well-demarcated lucency at the right lung base. Shortly after intubation, the child experienced pulmonary hemorrhage evidenced by frank blood suctioned from the endotracheal tube, as well as an evolving parenchymal hemorrhage on chest radiograph. At 1 week of life, the child developed worsening respiratory acidosis and hypoxemia. A repeat chest radiograph demonstrated an enlarging right cystic mass (Fig. 2a). Pigtail thoracostomy tubes were placed in an attempt to decompress the pneumatocele (Fig. 2b). Overnight, a large pneumothorax and pneumomediastinum developed, and a right thoracotomy was performed at the bedside. A thin-walled cyst was identified and unroofed. Within the cyst, a large defect with massive air leak from an adjacent bronchus was identified.
123
The defect was approximated with a single figure-of-eight 7-0 prolene suture. The air leak resolved, and the patient was weaned of ventilator support without evidence of cyst recurrence (Fig. 2c).
Case 3: lobar pulmonary interstitial emphysema with mass-effect A 500-g, 23-week EGA male was born to a G4P2 mother after an uncomplicated prenatal course. Despite preterm premature rupture of membranes and breech positioning, the baby was delivered vaginally. The baby was immediately intubated due to extreme prematurity and concern for respiratory distress syndrome. The patient developed severe respiratory distress with chest radiographs demonstrating diffuse cystic changes concerning for cystic bronchopulmonary dysplasia. All attempts to improve the patient’s respiratory status, including high frequency oscillatory ventilation and intravenous corticosteroids, were unsuccessful. After 2 days of aggressive medical management, a repeat chest X-ray demonstrated the development of prominent pneumomediastinum, subcutaneous emphysema tracking up the neck, and mediastinal shift (Fig. 3a). The patient developed severe acidosis and hypotension requiring vasopressor support. In an attempt to relieve the mass-effect of the cystic lung, a right-sided tube thoracostomy was placed which resulted in a pneumothorax (Fig. 3b) and continuous air leak. The patient remained hemodynamically unstable, and a right thoracotomy was performed at the bedside. The right middle lobe contained diffuse thin-walled cystic changes, was massively hyperinflated, and herniating into the left chest. A vessel-sealant device (Ligasure; Covidien Surgical, Boulder, CO) was initially used to quickly collapse the lobe providing better exposure; it was then used to divide the lobar vessels and
Pediatr Surg Int
Fig. 2 A 24-week EGA infant developed an enlarging symptomatic cystic mass in the right lung (a), which failed decompression with pigtail catheters (b), and required thoracotomy and surgical repair of bronchial defect within a ruptured pneumatocele (c)
Fig. 3 A 23-week EGA infant developed diffuse cystic bronchopulmonary dysplasia with pneumomediastinum, midline shift and pulmonary interstitial emphysema (a). Tube thoracostomy reduced
the midline shift but resulted in a persistent air leak (b). The patient underwent thoracotomy and was found to have a hyperinflated right middle lobe, which was successfully resected (c)
pulmonary parenchyma. A followup chest X-ray demonstrated resolution of mediastinal shift and persistence of diffuse interstitial disease in the remaining lung parenchyma (Fig. 3c). Pathology demonstrated findings consistent with pulmonary interstitial emphysema.
Two of the cases we report were ruptured pneumatoceles resulting in high-flow continuous air leaks. In both cases, a focal bronchial defect was identified and successfully repaired with prolene suture. Pneumatoceles occur in 1.8 % of premature infants and represent thin-walled gas-filled cysts that develop within the lung parenchyma as a result of a contained air leak [1]. The pathophysiology of these lesions remains controversial but is thought to arise from an acute lung injury in the setting of surfactant deficiency, which results in alveolar collapse after PPV-induced barotrauma. In addition, oxygen and oxygen-free radicals damage the epithelial lining of the lung parenchyma causing a focal area of inflammation. The combination of these factors leads to a check-valve type airway obstruction, air trapping and pseudocyst formation [1]. The third case illustrates how cystic BPD can be complicated by lobar pulmonary interstitial emphysema resulting in mass-effect, pneumomediastinum and pneumothorax.
Discussion Acquired lung lesions in premature infants including pneumatoceles, cystic bronchopulmonary dysplasia (BPD), and pulmonary interstitial emphysema (PIE) are frequently a consequence of positive pressure ventilation (PPV) and are typically managed medically. In this case series, we report the role of surgical intervention in the management of acquired lung lesions in premature infants. All three reported cases failed the most aggressive medical management options necessitating surgical intervention.
123
Pediatr Surg Int
We found the vessel-sealant device helpful in decompressing the lobe and providing exposure. In the premature infant, we also found the vessel-sealant device helpful in ‘sealing’ parenchyma and minimizing air leak when transecting the lung and lobar vessels [3]. Cystic BPD with hyperinflation and atelectasis can be seen in both ‘‘new BPD’’, characterized by alveolar and capillary hypoplasia leading to a reduction gas exchange, and ‘‘old BPD’’, which is characterized by airway injury, inflammation and parenchymal fibrosis [4]. PIE is a type of acquired air leak believed to arise from a disruption of the basement membrane of the alveolar wall allowing air entry into the interstitial space. Since the perivascular connective tissue is more abundant and less dissectible in preterm than in older infants, this predisposes to air trapping in the perivascular space, resulting in cystic changes [5]. These conditions are distinguished from congenital lobar emphysema (CLE), which is a congenital anomaly involving the lower respiratory tract. In contrast to CLE, which is classically a surgical disease managed with resection, acquired lung lesions are generally managed non-operatively. Primary medical management for acquired lung lesions involves minimizing airway pressures in the affected lung. Options include positioning the patient with the affected side down, the use of high frequency oscillator ventilation and selective intubation of the contralateral bronchus. Several case reports have demonstrated the successful use of tube thoracostomy to decompress an overinflated lung due to cystic lung disease or the resulting sequelae [6–8]. This intervention is typically considered only if more conservative measures fail. The rationale for chest tube placement is to improve pulmonary and hemodynamic physiology either by evacuating air from a tension pneumothorax or pneumomediastinum or decompressing a large pneumatocele, which is causing a mass-effect [7, 8]. We performed chest tube decompression in all three cases without noting any clinical improvement. The risk of injury to either lung cysts or healthy lung parenchyma during chest tube placement is high in small neonates with frail, cystic lung tissue. In at least two of the cases we report, chest tube placement converted a contained air leak into a pneumothorax with a continuous high-flow air leak that further impaired ventilation. Because of the potential need for surgical salvage, early surgical consultation and
123
involvement are advisable if thoracostomy tube placement is contemplated. Surgical intervention is reserved for cases unresponsive to medical management and in cases in which disease is isolated to a single lobe. Preoperative imaging with CT scans could theoretically aid in diagnosis and preoperative planning. However, preterm infants with acquired cystic lung lesions that are refractory to medical management are usually too unstable for transport. Therefore, clinicians usually depend on serial radiographs to aid their decisionmaking as was done in the cases described. If the pathology is isolated to a single lobe, two surgical techniques can be employed. In cases of a continuous air leak resulting from a focal defect in the bronchus, primary repair can be performed. In cases of isolated lobar pathology, lobectomy should be considered [9–11].
References 1. Hussain N et al (2010) Pneumatoceles in preterm infants-incidence and outcome in the post-surfactant era. J Perinatol 30(5):330–336 2. Staden U et al (2004) Asymmetric evolution of pulmonary interstitial emphysema in a preterm newborn infant. Pediatr Int 46(4):487–489 3. Rothenberg SS (2003) Experience with thoracoscopic lobectomy in infants and children. J Pediatr Surg 38(1):102–104 4. Jobe AH, Bancalari E (2001) Bronchopulmonary dysplasia. Am J Respir Crit Care Med 163:1723–1729 5. Matta R et al (2011) Diffuse persistent interstitial pulmonary emphysema treated by lobectomy. Ann Thorac Surg 92(4):e73– e75 6. Fox RB, Wright AM (1998) Case 30-1997: pulmonary interstitial emphysema in infancy. New Engl J Med 338(10):688–690 7. Chambers HM, van Velzen D (1989) Ventilator-related pathology in the extremely immature lung. Pathology 21(2):79–83 8. Do¨rdelmann M et al (2008) Therapeutic lung puncture for diffuse unilateral pulmonary interstitial emphysema in preterm infants. Eur J Pediatr Surg 18(4):233–236 9. Gessler P et al (2001) Lobar pulmonary interstitial emphysema in a premature infant on continuous positive airway pressure using nasal prongs. Eur J Pediatr 160(4):263–264 10. Kugelman A et al (1997) Acquired pulmonary cyst in the newborn infant. Pediatr Pulmonol 24(4):298–301 11. Rao J, Hochman MI, Miller GG (2006) Localized persistent pulmonary interstitial emphysema. J Pediatr Surg 41(6):1191– 1193
