Most gast-forming infections occur in patients with diabetes. Carbon dioxide formation, resulting from fermentation of the high concentration of sugar in the urine and tissue by infecting organisms, was regarded as the key factor of gas formation in previous reports. Gas from an emphysematous infection of a polycystic kidney was analyzed to understand better the mechanisms involved in gas-forming infections of the urinary tract. The term emphysematous renal polycystic infection is proposed for this particular condition. Gas from the cysts contained 4.1% carbon dioxide, 10.5% oxygen, 67.3% nitrogen and 18.1% unknown gas. This finding is astonishingly similar to that of Wheeler in 1954 and cannot be fully explained by the sugar fermentation theory. Therefore, we propose a new hypothesis. Impaired transportation of gas produced by rapid catabolism leads to gas accumulation in the tissue, which will gradually expand and create chambers to form gas bubbles. Gas of adjacent tissues will attempt to come into equilibrium with the gas bubbles. Positive equilibrium will lead to continuous expansion of the lesion bubble. However, if the chamber is unable to withstand the increasing pressure then rupture or spontaneous drainage of the gas bubble may occur. During negative equilibrium gas in the bubble gradually simulates tissue gas with eventual shrinkage of the bubble. If the chamber is unable to sustain the pressure it collapses and the bubble disappears. However, if the chamber is capable of sustaining the pressure the bubble still may persist even when the gas content is equivalent to tissue gas. This hypothesis may lead to better understanding of emphysematous infections of the urinary tract and also may cast light on emphysematous infections of other organ systems.
All Science Journal Classification (ASJC) codes