Spontaneous pneumothorax

Withers, John N.; Fishback, Malcolm E.; Kiehl, Paul V.; Hannon, Joseph L.

doi:10.1016/0002-9610(64)90030-3

Cited by 95 publications

(10 citation statements)

References 4 publications

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“…The average length of hospital stay in several large series treated by intercostal catheter varied from 5 to 30 days, with a mean of 13 days (Klassen and Meckstroth, 1962;Smith and Rothwell, 1962;Killen and Jackson, 1963;Ransdell and McPherson, 1963;Withers et al, 1964;Lynn, 1965;Timmis et al, 1965;Thompson and Bailey, 1966). There was an average failure rate of 19%.…”

Section: Discussionmentioning

confidence: 99%

Oxygen Therapy for Spontaneous Pneumothorax

Northfield¹

1971

BMJ

149

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obtained is similar to those of other investigators as noted in the review of Doolan et al. (1962).In analysing the data of Kim et al. two possibilities are suggested for the discrepancy. Firstly the normal values they report for inulin clearance-that is, 95±17 ml/min for men and 94±16 for women-are considerably below the 124±26 for men and 109±13 for women published by Homer Smith (1956). Secondly, it is possible that their patients were not in a steady state after preclearance water loading. It has been shown by Porter et al. (1966) that sudden augmentation of urine flow may "wash out" a reservoir of creatinine, presumably from renal tubular cells. The increased rate of tubular transit tends to make the U/P ratio for creatinine less at any one time, creating a more favourable gradient for creatinine excretion. The net effect during the period of "wash out" would be for creatinine clearance to overestimate simultaneously measured inulin filtration rate.It has been well established that creatinine can be secreted by the renal tubules particularly if the glomerular filtration rate is decreased-that is, Ccr >Cin (Brod and Sirota, 1948;Miller et al., 1952). This is usually true only if the serum creatinine is measured as true creatinine and not as total chromogen. When the latter is used (most clinical laboratories and autoanalyzer techniques) the addition of non-creatinine chromogens increase the measured serum creatinine and cancels out the urinary creatinine contributed by tubular secretion. The absolute amount of non-creatinine chromogen stays relatively constant as the filtration rate falls and true creatinine rises with renal disease. Thus the creatinine clearance tends to increase in relation to inulin when tubular secretion is maximal (low filtration rate) and non-creatinine chromogen is a small fraction of serum creatinine. Skov (1970) showed that with severe renal disease Ccr may overestimate Cin. Twenty-two of his patients had Cin less than 5 ml/min while our series had only four patients below 20 ml/min. The low filtration rates of his series no doubt account for the higher Ccr/Cin observed.What was variable in our study were successive inulin or creatinine clearances while in a steady state, and this was true of the normals, the post catheter patients, and those with renal disease. Table II and III summarize these data both in absolute ml/min and in per entage. The change in successive creatinine clearance reached as high as 27°h in the 13 patients with inulin clearances < 50 ml/min. It is noteworthy that this is the range of filtration rate found in many patients with various renal diseases and after renal transplantation. If the spontaneous variability of filtration rate is not recognized erroneous conclusions as regards progression of disease or results of therapy may be drawn. Though with a 24-hour clearance of creatinine the variability of successive clearances might be minimized, the urinary excretion of creatinine is also inconstant as Edwards et al. (1969) emphasized. Further, it is obvious th...

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Section: Discussionmentioning

confidence: 99%

Oxygen Therapy for Spontaneous Pneumothorax

Northfield¹

1971

BMJ

149

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“…Patients with PSP tend to be taller than control patients 10 11. The gradient of negative pleural pressure increases from the lung base to the apex, so that alveoli at the lung apex in tall individuals are subject to significantly greater distending pressure than those at the base of the lung, and the vectors in theory predispose to the development of apical subpleural blebs 12…”

Section: Introductionmentioning

confidence: 99%

Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010

MacDuff

Arnold

Harvey

2010

Thorax

1,190

1,394

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“…The latter phenomenon may explain the high recurrence rates of up to 20% of bullectomy alone (without associated pleurodesis) as therapy [22,23,24,25]. The development of blebs, bullae and areas of pleural porosity may be linked to a variety of factors, including distal airway inflammation [21,22,23,24,25,26], hereditary predisposition [27], anatomical abnormalities of the bronchial tree [28], ectomorphic physiognomy with more negative intrapleural pressures [29] and apical ischemia [30] at the apices [31], low body mass index and caloric restriction [15, 32], and abnormal connective tissue [33, 34]. The role of increased plasma aluminium concentrations in the pathogenesis of PSP remains unresolved [35, 36].…”

Section: Primary Spontaneous Pneumothoraxmentioning

confidence: 99%