In spite of the fact that blebs and bullae are frequently found in patients with primary spontaneous pneumothorax, they seldom seem to be the actual cause of the pneumothorax. Inflammatory changes in the distal airways play an important role in the occurrence of the pneumothorax during transpulmonary pressure changes.The value of the routine use of additional expiratory chest radiographs in diagnosing pneumothoraces has been doubted in previous studies. In this review, the diagnostic yield from additional expiratory chest radiographs is analysed. The role of previous pneumothoraces at presentation and the presence of blebs and bullae are discussed in predicting future recurrences and choosing appropriate treatment for optimal cost-effectiveness. Recommendations are made regarding treatment of primary and secondary spontaneous pneumothorax. Eur Respir J 1997; 10: 1372-1379 Pneumothorax is defined as the presence of air in the pleural cavity [1]. As early as 1819, LAENNEC [2] described the symptoms and signs of a patient with a pneumothorax. Although most pneumothoraces were then caused by tuberculosis, he also found pneumothoraces during autopsies of patients with apparently healthy lungs; he named these "pneumothorax simple". Aetiology and pathogenesisToday, pneumothoraces are divided into spontaneous pneumothorax, occurring without a preceding event, and traumatic pneumothorax, due to direct or indirect trauma. Iatrogenic pneumothoraces, resulting from diagnostic or therapeutic medical procedures, are also categorized as traumatic pneumothoraces.Spontaneous pneumothoraces are divided into primary and secondary spontaneous pneumothoraces. Secondary spontaneous pneumothoraces are associated with underlying pulmonary pathology, usually chronic obstructive pulmonary disease (COPD). Acquired immune deficiency syndrome (AIDS) and Pneumocystis carinii infections appear to play an increasing role in the aetiology of secondary spontaneous pneumothoraces [3].No underlying pulmonary disease is present in patients with primary spontaneous pneumothorax. However, blebs and bullae seem to play a role in the pathogenesis, since they are frequently found during thoracoscopy, thoracotomy or sternotomy (table 1). Thoracoscopic studies have shown the presence of blebs and bullae in 48-79% of patients with unilateral primary spontaneous pneumo-thorax [4][5][6][7][8]. With the development of video-assisted techniques, the recognition of blebs and bullae during thoracoscopy has improved. In more than 76% of patients,
C Co os st t--e ef ff fe ec ct ti iv ve en ne es ss s o of f v vi id de eo o--a as ss si is st te ed d t th ho or ra ac co os sc co op pi ic c s su ur rg ge er ry y v ve er rs su us sc co on ns se er rv va at ti iv ve e t tr re ea at tm me en nt t f fo or r f fi ir rs st t t ti im me e o or r r re ec cu ur rr re en nt t s sp po on nt ta an ne eo ou us s p pn ne eu um mo ot th ho or ra ax x Patients in both periods had comparable clinical characteristics. Irrespective of first time or recurrent spontaneous pneumothorax at presentation, drainage and hospitalization times were longer, and complication and recurrence rates were higher in Period 1. When costs due to the waiting time before VATS were excluded, the total costs in Period 1 were higher than in Period 2.Video-assisted thoracoscopic surgery is more effective in treating patients with first time or recurrent spontaneous pneumothorax, with less morbidity and total costs compared to conservative therapy. In view of cost-effectiveness, we feel that a different management of first time or recurrent spontaneous pneumothorax is not justified.
A relationship between idiopathic spontaneous pneumothorax (ISP) and visible parenchymal bullae and blebs has been reported. The causal relationship between blebs and bullae and ISP is questionable. Consequently, resection of the involved area is only indicated if it predisposes to recurrence of the pneumothorax. CT studies on 101 cases of ISP were analysed. The presence of bullae and their distribution was then related to the first and recurrent pneumothorax. CT demonstrated bullae in 56% of first ISP and in 64% of recurrent ISP, mostly among older patients. Only eight patients had bullae larger than 2 cm on the side of the pneumothorax. The location of the bullae was not a factor in predicting recurrent pneumothorax.
Expiratory chest radiographs do not improve visibility of small apical pneumothoraces by enhanced contrast. F.M.N.H. Schramel, R.P. Golding, C.D.E. Haakman, T.G. Sutedja, K.A. de Jong, P.E. Postmus. ERS Journals Ltd 1996. ABSTRACT: Demonstration of small apical pneumothoraces is supposed to be facilitated by expiratory chest radiographs. This study aimed to analyse the assumed enhancement of visual contrast on expiratory chest radiographs in patients with small apical pneumothoraces.Optical densities (OD) were obtained with a densitometer (X-rite 3001) on 54 paired inspiratory and expiratory chest radiographs of 22 consecutive patients with small apical pneumothoraces. The ODs were measured: at the intervertebral space between the first and second thoracic vertebrae (Area 1); at the peripheral part of the affected lung parenchyma (Area 2); and at the adjacent intrapleural space (Area 3).Excellent correlations of OD of each area were obtained between paired inspiratory and expiratory chest radiographs. The ODs of all areas on expiratory chest radiographs were significantly higher than on inspiratory chest radiographs. Contrast between pulmonary parenchyma and intrapleural air in inspiratory and expiratory films did not differ significantly.Expiratory chest radiographs do not improve visibility of small apical pneumothoraces by enhanced contrast between pulmonary parenchyma and intrapleural air. Expiratory chest radiographs show equally increased OD in the area of lung tissue and intrapleural air, caused by increased extrapulmonary tissue density during expiration, resulting in increased radiation exposure monitored by the ionization chambers of standard radiological equipment. If expiratory chest radiographs are really improving the visibility of apical pneumothoraces, there must be other reasons than contrast enhancement to explain this.
Summanr Carboplatin. a cisplatinum analogue, has no reported nephrotoxicity in phase I'II studies, assessed by creatinine clearance. We prospectively deterniined renal function in 10 untreated lung cancer patients with normal baseline renal function, treated with carboplatin 400mgm 2 day 1 and vincristine 2mg day 1 al., 1985). An alternative approach was the synthesis of analogues of cisplatin with the aim to find Pt-complexes with less nephrotoxicity and more or comparable antitumour activity (Burchenal et al., 1979). About 2,000 second generation Pt-compounds have been synthesised and screened for cytotoxicity. Only a few have been selected for clinical evaluation, of which carboplatin (CBDCA, JM8) probably is the most promising. In human and animal studies carboplatin has demonstrated increased haematological toxicity compared to CDDP, but it is less emetogenic and has little or no oto-or neurotoxicity and no nephrotoxicity even in the absence of forced diuresis (Lelieveld et al.. 1984: Van Glabbeke et al., 1988. In these studies the renal function was measured by monitoring serum creatinine and creatinine clearances. However, the determination of creatinine as a reflection of the glomerular filtration rate has proved to be a relatively insensitive method to monitor CDDP-induced renal damage (Meijer et al., 1983;Daugaard et al., 1988). Moreover, using 52Cr EDTA clearances, Calvert et al. (1982) were also unable to identify CBDCA as a nephrotoxic drug.In this study we prospectively determined changes in glomerular filtration rate and effective renal plasma flow by the more sensitive method developed by Donker et al. (1977) in 10 patients treated with standard dose carboplatin. The possible tubular damage was monitored by measuring the excretion of tubular enzymes. Methods Patients and therapyTen patients, one female, nine male, were studied. All had histologically proved lung cancer (eight small cell lung cancer, one squamous cell carcinoma, one endobronchial carcinoid). One All patients were treated with carboplatin 400mgm 2 day 1 and vincristine 2mg day 1 and 8 every 4 weeks. Carboplatin was dissolved in 250 ml of glucose 5% and given as a 30 mn i.v. infusion on day 1. Vincristine was given as bolus injection. No pre-or post-hydration was given.Seven responding patients received the maximum of five courses. The treatment had to be stopped in two patients after three and in one patient after two courses. because of tumour progression.Renal function studies Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured simultaneously in supine position with radioisotopes. ERPF was determined by measuring the clearance of 1311-hippuran (I x V P) and GFR by the clearance of '251-iothalamate (Ux V P) (I= counts per minute of I ml sustaining solution, V= infusion volume or urine volume in ml per minute, P =counts per minute in 2 ml of plasma and U=counts per minute in 2ml urine). After a standard pnrmary dose and sustaining infusion for 2h, 1-h clearances were determined for acute ef...
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