Development of severe hypoxaemia in chronic obstructive pulmonary disease patients at 2,438m (8,000 ft) altitude. C.C. Christensen, M. Ryg, O.K. Refvem, O.H. Skjùnsberg. #ERS Journals Ltd 2000. ABSTRACT: The arterial oxygen tensions (Pa,O 2 ) in chronic obstructive pulmonary disease (COPD) patients travelling by air, should, according to two different guidelines, not be lower than 7.3 kPa (55 mmHg) and 6.7 kPa (50 mmHg), respectively, at a cabin pressure altitude of 2,438 m (8,000 ft). These minimum in-flight Pa,O 2 values are claimed to correspond to a minimum Pa,O 2 of 9.3 kPa (70 mmHg) at sea-level. The authors have tested whether this limit is a safe criterion for predicting severe in-flight hypoxaemia.The authors measured arterial blood gases at sea-level, at 2,438 m and at 3,048 m (10,000 ft) in an altitude chamber at rest and during light exercise in 15 COPD patients with forced expiratory volume in one second (FEV1) <50% of predicted, and with sea-level Pa,O 2 >9.3 kPa.Resting Pa,O 2 decreased below 7.3 kPa and 6.7 kPa in 53% and 33% of the patients, respectively, at 2,438 m, and in 86% and 66% of the patients at 3,048 m. During light exercise, Pa,O 2 dropped below 6.7 kPa in 86% of the patients at 2,438 m, and in 100% of the patients at 3,048 m. There was no correlation between Pa,O 2 at 2,438 m and preflight values of Pa,O 2 , FEV1 or transfer factor of the lung for carbon monoxide.In contrast to current medical guidelines, it has been found that resting arterial oxygen tension >9.3 kPa at sea-level does not exclude development of severe hypoxaemia in chronic obstructive pulmonary disease patients travelling by air. Light exercise, equivalent to slow walking along the aisle, may provoke a pronounced aggravation of the hypoxaemia. Eur Respir J 2000; 15: 635±639.

In a 2-yr prospective follow-up study of patients presenting clinically with possible reactive arthritis (ReA), 17 (9%) of the patients turned out to have acute sarcoid arthritis (SA). The number of new cases of SA per year was 2.9/100,000 persons in the city of Oslo between 18 and 60 yr of age. The onset of SA clustered in the spring. All the SA patients presented with bilateral ankle joint involvement and bilateral hilar lymphadenopathy, and ten (59%) presented with the triad of erythema nodosum, arthritis and lung involvement. A prospective follow-up after 104 weeks showed complete remission of arthritis in all 17 cases of SA. The total duration of arthritis [median (range)] was 11 (2-107) weeks. Erythema nodosum was mild and transient in all cases. At week 104, the lung and hilar manifestations had resolved. We conclude that the outcome of SA appeared favourable. Bilateral ankle joint involvement, erythema nodosum and bilateral hilar lymphadenopathy found at the routine chest X-ray examination are important clues for the diagnosis of SA.

Several publications have reported effects of hypobaric conditions in patients with chronic obstructive pulmonary disease. To the current authors' knowledge, similar studies concerning patients with restrictive lung disease have not been published.The effect of simulated air travel in a hypobaric chamber on arterial blood gases, blood pressure, and cardiac frequency during rest and 20 W exercise, and the response to supplementary oxygen in 17 patients with chronic restrictive ventilatory impairment has been investigated.Resting oxygen tension in arterial blood (Pa,O2) decreased from 10.4±1.6 kPa at sea level to 6.5±1.1 kPa at 2,438 m simulated altitude, and decreased further during light exercise in all patients (5.1±0.9 kPa).Pa,O2at this altitude correlated positively with sea-levelPa,O2and transfer factor of the lung for carbon monoxide (TL,CO), and negatively with carbon dioxide tension in arterial blood (Pa,CO2).Pa,O2increased to acceptable levels with an O2supply of 2 L·min−1at rest and 4 L·min−1during 20 W exercise.In conclusion, most of the patients with restrictive ventilatory impairment developed hypoxaemia below the recommended levels of in-flight oxygen tension in arterial blood during simulated air travel. Light exercise aggravated the hypoxaemia. Acceptable levels of oxygen tension in arterial blood, with only a minor increase in carbon dioxide tension in arterial blood, were obtained by supplementary oxygen.

The pharmacokinetics and protein binding of prednisolone were studied in 7 patients before and after 3 weeks of rifampicin therapy. The elimination half‐time for prednisolone decreased by 45±8.1% (p<0.01), and the total body clearance of prednisolone increased by 91±26% (p<0.01). The area under the time‐concentration curve (AUC) of total (free plus protein‐bound) prednisolone decreased by 48±7.3% (p<0.01) and of free, unbound prednisolone by 57±9.8% (p<0.01). The reduction in AUC was greater for free than for total prednisolone (p<0.05) mainly due to the non‐linear nature of prednisolone protein binding. There was no significant change in the volume of distribution. Because of the marked reduction in total and especially free prednisolone, the dosage should be adjusted accordingly if prednisolone and rifampicin are prescribed concomitantly.

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