Thoracoscopic treatment of spontaneous pneumothorax in children

WOS: 000186138000006PubMed ID: 14577068Background/Purpose: This study describes the authors experience and results with thoracoscopic treatment of spontaneous pneumotrorax (SP) in 22 children. Methods: A total of 32 thoracoscopic procedures were performed in 22 children. The patients ranged in age from 9 to 21 years at the time of their first thoracoscopy. SP was primary in 9 and secondary in 13 patients. Pleurodesis was performed in all thoracoscopies using talc in 28 and pleural abrasion in 4 procedures. In 2 of these, apical pleurectomy was added to abrasion. Blebectomy was the additional surgical procedure associated with pleurodesis in 4 patients. Results: Thoracoscopy usually was performed with the patient under general anesthesia. In children with severe respiratory insufficiency, regional anesthesia was used. The mean operative time was 42.6 minutes (range, 8 to 114 minutes). The mean time of postoperative chest tube drainage was 4.6 days (range, 2 to 12 days). Three patients with cystic fibrosis had prolonged air leak lasting longer than 7 days after thoracoscopy. None of them required an additional surgical intervention, and the air leak ceased in 8, 8, and 12 days with continuous suction. One patient required a repeat thoracoscopy for bleeding from an intercostal artery on postoperative day one. The mean follow-up was 4 years (range, 2.5 months to 14 years). There have been 2 partial recurrences (6.25%), both in patients with secondary SP, which were treated by a repeat thoracoscopy and talc pleurodesis. Conclusions: Thoracoscopic treatment of SP is safe and effective in children. It can be performed under regional anesthesia also in children with severe respiratory insufficiency. Because the complications and recurrences are encountered more frequently in children with an underlying lung disease, special care in surgical manipulation is required in this subgroup of patients with SP

Congenital diaphragmatic hernia: current status and review of the literature.

Treatment of congenital diaphragmatic hernia (CDH) challenges obstetricians, pediatric surgeons, and neonatologists. Persistent pulmonary hypertension (PPHT) associated with lung hypoplasia in CDH leads to a high mortality rate at birth. PPHT is principally due to an increased muscularization of the arterioles. Management of CDH has been greatly improved by the introduction of prenatal surgical intervention with tracheal obstruction (TO) and by more appropriate postnatal care. TO appears to accelerate fetal lung growth and to increase the number of capillary vessels and alveoli. Improvement of postnatal care over the last years is mainly due to the avoidance of lung injury by applying low peak inflation pressure during ventilation. The benefits of other drugs or technical improvements such as the use of inhaled nitric oxide or extracorporeal membrane oxygenation (ECMO) are still being debated and no single strategy is accepted worldwide. Despite intensive clinical and experimental research, the treatment of newborn with CDH remains difficult

The long-term follow-up of patients with a congenital diaphragmatic hernia: a broad spectrum of morbidity

Congenital diaphragmatic hernia (CDH) is a life-threatening anomaly with a mortality rate of approximately 40-50%, depending on case selection. It has been suggested that new therapeutic modalities such as nitric oxide (NO), high frequency oxygenation (HFO) and extracorporal membrane oxygenation (ECMO) might decrease mortality associated with pulmonary hypertension and the sequelae of artificial ventilation. When these new therapies indeed prove to be beneficial, a larger number of children with severe forms of CDH might survive, resulting in an increase of CDH-associated complications and/or consequences. In follow-up studies of infants born with CDH, many complications including pulmonary damage, cardiovascular disease, gastro-intestinal disease, failure to thrive, neurocognitive defects and musculoskeletal abnormalities have been described. Long-term pulmonary morbidity in CDH consists of obstructive and restrictive lung function impairments due to altered lung structure and prolonged ventilatory support. CDH has also been associated with persistent pulmonary vascular abnormalities, resulting in pulmonary hypertension in the neonatal period. Long-term consequences of pulmonary hypertension are unknown. Gastro-esophageal reflux disease (GERD) is also an important contributor to overall morbidity, although the underlying mechanism has not been fully understood yet. In adult CDH survivors incidence of esophagitis is high and even Barrett's esophagus may ensue. Yet, in many CDH patients a clinical history compatible with GERD seems to be lacking, which may result in missing patients with pathologic reflux disease. Prolonged unrecognized GERD may eventually result in failure to thrive. This has been found in many young CDH patients, which may also be caused by insufficient intake due to oral aversion and increased caloric requirements due to pulmonary morbidity. Neurological outcome is determined by an increased risk of perinatal and neonatal hypoxemia in the first days of life of CDH patients. In patients treated with ECMO, the incidence of neurological deficits is even higher, probably reflecting more severe hypoxemia and the risk of ECMO associated complications. Many studies have addressed the substantial impact of the health problems described above, on the overall well-being of CDH patients, but most of them concentrate on the first years after repair and only a few studies focus on the health-related quality of life in CDH patients. Considering the scattered data indicating substantial morbidity in long-term survivors of CDH, follow-up studies that systematically assess long-term sequelae are mandatory. Based on such studies a more focused approach for routine follow-up programs may be establishe