“…The importance of infection cannot be over-emphasized (Harley, 1971), and has been stressed in the context of tracheo-oesophageal fistula by a number of workers (Atherstone and Ryder, 1967;Toty, Hertzog, Diane, and Aboudi, 1967;Nicolas et al, 1967;St0ren and Vasli, 1968). Other factors such as chemical irritation, hypotension, and antiinflammatory agents, such as steroids or phenylbutazone (Nicolas et al, 1967;Hedden, Ersoz, and Safar, 1969), may further add to the damage caused by pressure-infective necrosis. If ulceration extends through the whole thickness of the membraneous wall of the trachea before a fibrotic reaction, leading to stenosis, has had time to occur then a tracheo-oesophageal fistula may result (Harley, 1971).…”