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Ann Thorac Surg 1996;61:231-234
© 1996 The Society of Thoracic Surgeons
Services de Chirurgie Thoracique et Radiologie, Hôpital Laennec, Paris, France
Accepted for publication July 14, 1995.
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Abstract |
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Introduction |
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The patient was 59 years old and had had a panlobular emphysema since he was 18 years old. Emphysema increased with smoking (40 pack-years) until severe respiratory insufficiency developed. The forced expiratory volume in 1 second was 0.35 L (11% of the predictive value). The patient was confined to bed with continuous oxygen therapy (1.5 L/min). Blood gases without oxygen were as follows: arterial oxygen tension, 38 mm Hg; arterial carbon dioxide tension, 48 mm Hg. Single-lung transplantation was performed on the left lung. The postoperative period was uneventful. Two months after intervention, the clinical state was good without oxygen therapy, oxygen and carbon dioxide tension improved to 91 and 36 mm Hg before effort and 93 and 31 mm Hg after effort (25 W during 5 minutes). The forced expiratory volume in 1 second was 2 L, 62% of the predicted value.
Eighteen months after transplantation, the patient was dyspneic again. Transbronchial biopsy found a bronchiolar fibrosis of the left lower lobe. Oxygen and carbon dioxide tension were 86 and 38 mm Hg, decreasing to 77 and 40 mm Hg after effort (Fig 1
). The forced expiratory volume in 1 second was 1.2 L, 36% of the predicted value. Hyperexpansion of the remaining recipient's lung was found on chest roentgenogram (Fig 2). Twenty-five months later, the patient was not able to walk more than 500 m at a slow pace, and he needed two pauses to climb up one floor. Oxygen and carbon dioxide tensions were 84 and 40 mm Hg, changing to 73 and 40 mm Hg after effort, and the forced expiratory volume in 1 second was 0.92 L (29% of predicted). The thoracic computed tomographic scan showed hyperinflation of the remaining lung and a mediastinal shift compressing the graft (Fig 3). The compression was clearly demonstred on three-dimensional computed tomographic reconstruction (Fig 4). The echocardiography was normal. Right pulmonary reduction was planned to suppress the compressive effect of the NL. At 26 months after SLT, a right upper lobectomy was performed. The postoperative period was uneventful. Three months later, there was a clear clinical improvement: the patient was able to walk 2 km at a sustained pace and to climb up one floor without pausing. On the chest roentgenogram (Fig 5), the diaphragmatic dynamic was improved without mediastinal shift during expiration. On the computed tomographic scan (Fig 6), the mediastinum was back to its normal place, the NL no longer made contralateral parenchymatous hernia (Fig 7), and the compression of the graft had disappeared. The forced expiratory volume in 1 second had increased to 1.3 L (42% of predicted) and remained stable thereafter (Fig 8). The oxygen and carbon dioxide tensions were 76 and 37 mm Hg.
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Comment |
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Numerous SLTs have now been performed on emphysematous patients. Mild temporary hyperinflation of the native lung has often been reported, but specific decompression therapies were rarely required and were generally performed in the early postoperative period (Table 1). In a recent series studying 16 patients, Low and associates [3] did not report any case of pulmonary hyperexpansion.
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When compression of the graft by the native lung is observed postoperatively, a complete evaluation of the functional repercussion is required. The compression is usually moderate and transitory. In some patients with large mediastinal shift, the situation may be critical on cardiac and respiratory grounds. Separate ventilation followed by early extubation must at first be attempted [4, 5]. This therapy is often sufficient to diminish the hyperinflation of the NL and permits excellent clinical improvement. In exceptional cases, a bullous resection [6], a lobectomy (our observation), or even a pneumonectomy [7] can be required. No complementary examination other than chest roentgenogram and blood gas measurement is necessary in such cases.
On the contrary, progressive deterioration of pulmonary function tests requires a complete new evaluation. Signs of side setting on transbronchial biopsies may necessitate medical treatment or even a new transplantation. Testing for infection is necessary. Computed tomographic scan demonstrates signs of graft compression, with areas of crowded parenchyma. The mediastinal shift is evaluated on chest roentgenogram and computed tomographic scan. Echocardiography may show compression of the cardiac cavities. When clinical degradation is related to NL hyperexpension, surgical decompression may be proposed. The good clinical outcome in our case, indicates that screening for such an event late after the SLT is necessary.
In conclusion, hyperinflation of the native lung after SLT for emphysema is frequent in the postoperative period. Moderate forms are often spontaneously regressive. Some cases require treatment, ranging from separated ventilation to bullectomy or lobectomy. Late complication a few years after transplantation may also occur, and sometimes requires a decompression operation, as in our case.
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