A Cure for Foaming and Spill-out in the Melrose Oxygenator.

Foaming and spill-out from the drive end of the rotating stainless steel cylinder oxygenator has been a serious problem, but sure remedies for both defects have been discovered. Oxygenation has always been 85 to 100% even with flow rates over 6 litres/minute. The machine was passed as safe for clinical use after test runs had been made on dogs in 1959, at which time the cause of oxygenator failure was found to be non-filming discs. At the beginning of 1960, clinical perfusions were started, and the two problems of spill-out and foaming were encountered. The minor fault of spill-out is due to incorrect assembly of the first (drive) section of the oxygenator when the next sections are fitted with the large area, oval-holed discs. Blood entering the machine surges to and fro on hitting the plate instead of going through the plate hole. The waves thus formed spill out of the drive end orifice, causing drive failure of the oxygenator. The simple cure is always to assemble the oxygenator with the disc location groove in the first (drive) segment advanced rotationally by one bolt hole from the same groove in the second segment. This advance must be related to the actual rotation direction of the oxygenator. Foaming, the major fault, which came on within the first 30 minutes of perfusion, was much more difficult to eliminate. Foaming of the blood caused froth to escape out of the drive end orifice in considerable quantities, resulting in loss of blood and failure of the adjacent oxygenator friction drive. More alarming was the collection of much fine froth in the arterial filter, which had to be blown out periodically to prevent the filter becoming completely filled with air bubbles, which would then be forced through the filter screen. Such an air embolism will produce atypical, bizarre, and ill-defined cerebral or other symptoms. There may even be a failure to regain consciousness followed by death. Details are given of three patients in whom trouble developed during perfusion. Case 2 was admitted in April 1960 with aortic stenosis. The body surface area was 1 57m.2 Gross foaming and frothing out developed at 3,500 ml./ min., and the modified arterial filter (Atherstone, 1961) had to be blown out repeatedly to prevent it becoming overwhelmed with froth. The oxygenator had to be hand-turned because of drive slip; much blood was lost out of the drive end orifice, and it was very difficult to see the blood level in the oxygenator bell housing because of all the froth. Unfortunately this patient died on the table due to a failure of the left venting system. There was no discernible evidence of air having got through the filter. The cause of this apparently unpredictable foaming was investigated, especially as it was found that foaming could not be reproduced by running the machine identically on the residual blood therein after the patient had been disconnected. At that time, detailed examination of the dismantled oxygenator and trombone assemblies yielded no clues. Case 3 was admitted in May 1960 with pulmonary stenosis. The body surface area was 1 48 M.2 Frothing out, with all its sequelae, recurred at 3,400 ml./min., and again the modified arterial filter filled with froth. The blood level was difficult to discern, and the oxygenator had to be handturned. Much blood was lost from the machine. This patient awoke rapidly on the table at the end of the operation and showed no embolic phenomena. He left hospital fit and improved. Another attempt to reproduce foaming, using the residual blood in the machine, was unsuccessful. Again detailed scrutiny of the oxygenator and trombone assemblies yielded no clue as to the cause of the foaming. After this case, various changes in the application of M.S. Silicone/Antifoam to parts of the oxygenator and the trombone were made, and foaming vanished completely in the subsequent 29 patients, most of whom were adults requiring flow