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SPECIALISTS IN FAMILY MEDICINE
MORE and more people agree that the practice of medicine outside the hospital-which it comprises threequarters of this country’s total medical care and occupies half its doctors-requires special preparation. In the United States the proposal is now made that " family practice " (an occupation not confined to general practitioners 18should be made a board-accredited specialty. This movement has its strongest roots in the State of Ohio,29 and is particularly associated with the name of Dr. Thomas Rardin. The plan is that an American Board of Family Practice, comparable to the other specialty boards, should be created to establish minimum standards of training, to conduct examinations, and (a bold step) to make rules about continuing certification. The recommended period of special graduate training is " at least five years, three in a hospital centred programme, two in approved active private practice ". A written examination would be taken after three years, with a further oral one at the end of the five years; and doctors holding the board’s diploma would be " subject to re-certification every six years. Whether this scheme would work depends on whether universities and hospitals were willing to mount the necessary residency programmes, whether these programmes were fully used by young graduates of high calibre, and whether the family specialists produced fulfilled everybody’s hopes-including their own. For this country, we should doubt the advantage of creating yet more examinations-which already have too large a place in medical education. What really matters is that a high standard of training should be set and maintained; and this will require the active help of those already experienced in teaching-the universities and colleges. Moreover, the quality of medical care will not be permanently enhanced until it is recognised that a certain amount of teaching and research is as necessary for the health of family practice as it is for the health of a hospital. CADAVER BLOOD FOR TRANSFUSION
FOR many years Russian surgeons have collected blood from those who have died a violent death, and infused it into those who need urgent transfusion; and we are now indebted to Swan and Schecter30 and Moore et al. 31 for a critical review of this subject, from the first observations by John Hunter in 1786, the first experimental work in dogs by Shamov and Kostriukov in Kharkov in 1928, and the first clinical application by Yudin in Moscow in 1930. By 1938 Yudin had performed a series of 2500 transfusions of cadaver blood, and Farmer of Chicago some 35. Nowadays some 2000-4000 transfusions with cadaver blood are given each year at the Sklifassovski Institute of Traumatic Diseases in Moscow. Donors must have died suddenly, and blood should be collected within six hours of death to avoid bactereemia. Some 2-3 litres can usually be obtained; and this needs no anticoagulant, though a glucose-phosphate stabiliser is 27.
Lancet, 1959, ii, 1075.
28. See Lancet, Feb. 23, p. 429. 29. Why an American Board of Family Practice for Family Physicians ? Ohio Academy of General Practice. (4075, North High Street, Columbus 14, Ohio, U.S.A.) 30. Swan, H., Schecter, D. C. Surgery, 1962, 52, 545. 31. Moore, C. L., Pruitt, J. C., Meredith, J. H. Arch. Surg. 1962, 85, 364.
none of this blood comes from the portal The blood remains liquid owing to the rapid system. onset of complete fibrinolysis; but the products of fibrinolysis do not seem to harm the recipients-and indeed, after the first 1000 cases, Yudin encountered no significant reactions. Clearly cadaver blood can be obtained only in a large city, and then only if the city has a central institute of traumatology, to which, in addition to accidents, all cases of sudden death are referred. Our present system of decentralised accident services helps to ensure that survivors obtain slirgical care as soon as possible, but renders it difficult to use cadaver blood since no one hospital or hospital group would receive enough cases to justify the special equipment and staff which are necessary. The coroners’ areas, now relatively small, might have to be replaced by much larger units based on a population of several millions, with an Institute of Forensic Medicine and Traumatology serving this large population. But if, when a cadaver was brought to it, necropsy were to be automatic, and the surgeon were to procure tissues without delay, legislation far beyond that of the Human Tissue Act of 1961 would be needed; and this the public may-
usually added;
perhaps understandably-be unready
to countenance.
PAPILLŒDEMA IN CHRONIC RESPIRATORY DISEASE
THIRTY years ago Cameron1 described papilloedema in the course of serious respiratory disease, and subsequent experience has shown that this is by no means rare: it has been noted in about 10% of patients with grave exacerbations of chronic respiratory insufficiency.23 Exactly how the papillcedema is produced is unknown; but factors are right heart-failure, hypercapnia, hypoxia, and a rise in pressure of the cerebrospinal fluid.4-7 Of 20 reported cases of papilloedema associated with chronic respiratory disease,256 8-15 information about subsequent progress is available in 11:in 5 of these the patients were dead within five months, and in 4 within two years; of the remaining 2 patients, 1 survived for at least one year and the other for at least three years. Not surprisingly, papilloedema is generally regarded as an ominous prognostic sign. But Stevens et al.16 now point out that a subsequent rapid downhill course is by no means invariable. They report that 3 patients who during an exacerbation of chronic respiratory disease had papilloedema, heartfailure, hypercapnia, hypoxia, and impaired consciousness were still alive six years afterwards. Moreover, the results of lung-function tests at the end of the follow-up period were not significantly poorer than the results of tests at its beginning, even though in the interval 2 of the patients had a recurrence of cardiorespiratory failure and papilloedema. The onset of congestive cardiac failure has itself a gloomy prognostic significance, but here again Cameron, A. J. Brit. J. Ophthal. 1933, 17, 167. Simpson, T. Brit. med. J. 1954, i, 297. Flint, F. J. Lancet, 1954, ii, 51. Simpson, T. Brit. med. J. 1948, ii, 639. Kaye, N., Westlake, E. K. ibid. 1954, i, 302. Mithoefer, J. C. J. Amer. med. Ass. 1952, 149, 1116. Friedfeld, L., Fishberg, A. M. J. clin. Invest. 1934, 13, 495. Loman, J., Dameshek, W. New Engl. J. Med. 1945, 232, 394. Meadows, S. P. Proc. R. Soc. Mea. 1947, 40, 555. Beaumont, G. E., Jearn, J. B. Brit. med. J. 1948, i, 50. McCann, W. Postgrad. med. J. 1951, 9, 225. Carter, C. C., Fuller, T. J. Neurology, 1957, 7, 169. Westlake, E. K., Simpson, T., Kaye, M. Quart. J. Med. 1955, 24, 155 Conn, H. O., Dunn, J. P., Newman, H. A., Belkin, G. A. Amer. J. Med. 1957, 22, 524. 15. Miller, W. F. Arch. intern. Med. 1961, 107, 589. 16. Stevens, P. M., Austen, K. F., Knowles, J. H. J. Amer. med. Ass. 1963, 183, 161. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.