The beneficial effects of nocturnal oxygen therapy (NOT) in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate daytime hypoxaemia (arterial oxygen tension (Pa,O 2 ) in the range 7.4±9.2 kPa (56±69 mmHg)) and exhibiting sleep-related oxygen desaturation remains controversial. The effectiveness of NOT in that category of COPD patients was studied. The end points included pulmonary haemodynamic effects after 2 yrs of follow-up, survival and requirement for long-term oxygen therapy (LTOT).Seventy-six patients could be randomized, 41 were allocated to NOT and 35 to no NOT (control). The goal of NOT was to achieve an arterial oxygen saturation of >90% throughout the night. All these patients underwent polysomnography to exclude an associated obstructive sleep apnoea syndrome. The two groups exhibited an identical meanSD daytime Pa,O 2 of 8.40.4 kPa (633 mmHg) at baseline.Twenty-two patients (12 in the NOT group and 10 in the control group, p=0.98) required LTOT during the whole follow-up (3514 months). Sixteen patients died, nine in the NOT group and seven in the control group (p=0.84). Forty-six patients were able to undergo pulmonary haemodynamic re-evaluation after 2 yrs, 24 in the NOT and 22 in the control group. In the control group, mean resting pulmonary artery pressure increased from 19.85.6 to 20.56.5 mmHg, which was not different from the change in mean pulmonary artery pressure in the NOT group, from 18.34.7 to 19.55.3 mmHg (p= 0.79).Nocturnal oxygen therapy did not modify the evolution of pulmonary haemodynamics and did not allow delay in the prescription of long-term oxygen therapy. No effect of NOT on survival was observed, but the small number of deaths precluded any firm conclusion. These results suggest that the prescription of nocturnal oxygen therapy in isolation is probably not justified in chronic obstructive pulmonary disease patients. Eur Respir J 1999; 14: 1002±1008. The beneficial effects of long-term oxygen therapy (LTOT) have been demonstrated in chronic obstructive pulmonary disease (COPD) patients with marked daytime hypoxaemia, i.e. in patients with an arterial oxygen tension (Pa,O 2 ) measured in the stable state of the disease, of <7.3 kPa (<55 mmHg) or in the range 7.4±7.8 kPa (56±59 mmHg), and exhibiting "cor pulmonale" or polycythaemia [1, 2]. These beneficial effects include improved survival [1, 2], but also an amelioration of pulmonary haemodynamics [3,4]. The beneficial effects of LTOT on survival have not been observed in COPD patients with moderate hypoxaemia (Pa,O 2 in the range 7.4±8.6 kPa (56±65 mmHg)), as indicated by a very recent Polish study [5].The worsening of hypoxaemia during sleep, and particularly during rapid eye movement sleep, has been well established in patients with advanced COPD [6±10]. It must be underlined, however, that most of these studies have included patients with severe COPD, exhibiting marked daytime hypoxaemia. Conventional LTOT, given for >15±18 h . day -1 , compulsorily includes sleep time and, accordingly, sle...

It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia.We have investigated the relationships between pulmonary function data, sleeprelated desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O 2 therapy (daytime arterial oxygen tension (Pa,O 2 ) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending ≥30% of the recording time with a transcutaneous O 2 saturation <90%. An obstructive sleep apnoea syndrome was excluded by polysomnography.Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O 2 (8.4±0.6 vs 8.4±0.4 kPa (63±4 vs 63±3 mmHg)) but arterial carbon dioxide tension (Pa,CO 2 ) was higher in Group 1 (6.0±0.7 vs 5.3±0.5 kPa (45±5 vs 40±4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6±0.7 vs 2.5±0.6 kPa (19±5 vs 19±4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension.It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension. Eur Respir J 1997; 10: 1730-1735 The worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease (COPD) has been documented since the early 1960s [1], and has since been confirmed by polysomnographic studies [2,3], which have included continuous monitoring of oxygen saturation from the late 1970s [4][5][6][7][8][9][10]. It must be emphasized that most of these studies have included patients with severe COPD exhibiting marked daytime hypoxaemia. Is sleep-related hypoxaemia present in patients with less severe COPD with mild or absent daytime hypoxaemia? Several studies of the literature [11][12][13] have shown that a relatively high percentage of these COPD patients exhibit significant nocturnal hypoxaemia, which naturally raises the question: Does this hypoxaemia, limited to sleep, deserve treatment with nocturnal oxygen? Such a treatment could be justified if nocturnal hypoxaemia had deleterious effects on life expectancy, which is rather controversial [14,15], and on pulmonary haemodynamics. It has been hypothesized [16,17] that isolated nocturnal hypoxaemia, occurring in patients without significant daytime hypoxaemia, could lead to permanent (daytime) pulmonary hypertension, but this hypothesis has not, so...

Latex has been documented as causing immediate hypersensitivity reactions ranging from contact urticaria to severe anaphylaxis. Latex proteins may also act as airborne allergens causing rhinitis and asthma. The prevalence of occupational asthma due to latex gloves among health care workers is unknown. We surveyed the employees of a primary care hospital including nurses (n = 201), members of the cleaning staff (n = 50), and laboratory technologists (n = 38). In the initial part of the study, a questionnaire and skin-prick tests with latex and common inhalant allergens were administered to 273 of 289 (94%) members of the target population. Thirteen of the 273 subjects (4.7%; 95% CI: 2.6 to 8.1%) showed skin reactivity to latex. All latex-sensitive subjects reported glove-related urticaria, which was associated with rhinoconjunctivitis in 12 subjects and asthma in five subjects. No subject had a history suggestive of occupational asthma among those who had negative skin tests to latex. In the second part of the study, a histamine inhalation challenge was performed on 12 of 13 latex-sensitive subjects, including the five subjects with a history of occupational asthma. These 12 subjects demonstrated significant bronchial hyperresponsiveness. All underwent specific inhalation challenges with latex gloves in the laboratory. Seven subjects developed a significant bronchial response (four immediate and three dual reactions) to latex glove exposure. We conclude that occupational asthma due to latex occurred in 2.5% (95% CI: 1.0 to 5.2%) of hospital employees. Widespread use of latex gloves should therefore be considered a significant risk to the respiratory health of hospital employees.

Simple thoracoscopic talcage (TT) is a safe and effective treatment of primary spontaneous pneumothorax (PSP). However, its efficacy has not previously been estimated in comparison with standard conservative therapy (pleural drainage (PD)).In this prospective randomised comparison of two well-established procedures of treating PSP requiring at least a chest tube, cost-effectiveness, safety and pain control was evaluated in 108 patients with PSP (61 TT and 47 PD).Patients in both groups had comparable clinical characteristics. Drainage and hospitalisation duration were similar in TT and PD patients. There were no complications in either group. The immediate success rate was different: after prolonged drainage (w7 days), 10 out of 47 PD patients, but only 1 out of 61 TT patients required a TT as a second procedure. Total costs of hospitalisation including any treatment procedure were not significantly different between TT and PD patients. Pain, measured daily by visual analogue scales, was statistically higher during the first 3 days in TT patients but not in those patients receiving opiates. One month after leaving hospital, there was no significant difference in residual pain or full working ability: 20 out of 58 (34%) versus 10 out of 47 (21%) and 36 out of 61 (59%) versus 26 out of 39 (67%) in TT versus PD groups, respectively. After 5 yrs of follow-up, there had been only three out of 59 (5%) recurrences of pneumothorax after TT, but 16 out of 47 (34%) after conservative treatment by PD. Cost calculation favoured TT pleurodesis especially with regard to recurrences.In conclusion, thoracoscopic talc pleurodesis under local anaesthesia is superior to conservative treatment by chest tube drainage in cases of primary spontaneous pneumothorax that fail simple aspiration, provided there is efficient control of pain by opioids.

Planar pulmonary scintigraphy is still regularly performed for the evaluation of pulmonary embolism (PE). However, only about 50-80% of cases can be resolved by this approach. This study evaluates the ability of tomographic acquisition (single photon emission computed tomography, SPECT) of the perfusion scan to improve the radionuclide diagnosis of PE. One hundred and fourteen consecutive patients with a suspicion of PE underwent planar and SPECT lung perfusion scans as well as planar ventilation scans. The final diagnosis was obtained by using an algorithm, including D-dimer measurement, leg ultrasonography, a V/Q scan and chest spiral computed tomography, as well as the patient outcome. A planar perfusion scan was considered positive for PE in the presence of one or more wedge shaped defect, while SPECT was considered positive with one or more wedge shaped defect with sharp borders, three-plane visualization, whatever the photopenia. A definite diagnosis was achieved in 70 patients. After exclusion of four 'non-diagnostic' SPECT images, the prevalence of PE was 23% (n =15). Intraobserver and interobserver reproducibilities were 91%/94% and 79%/88% for planar/SPECT images, respectively. The sensitivities for PE diagnosis were similar for planar and SPECT perfusion scans (80%), whereas SPECT had a higher specificity (96% vs 78%; P =0.01). SPECT correctly classified 8/9 intermediate and 31/32 low probability V/Q scans as negative. It is concluded that lung perfusion SPECT is readily performed and reproducible. A negative study eliminates the need for a combined V/Q study and most of the 'non-diagnostic' V/Q probabilities can be solved with a perfusion image obtained by using tomography.