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FINDING THE EPIDURAL SPACE
424 the tissues and disappearance of lymphoblasts in peripheral blood and bone-marrow. This aminoacid becomes " essential " for some proliferating cells-e.g., lymphoblasts. Low-protein diet might act similarly, though less selectively. Because of the probable scarcity and expense of L-asparaginase in the near future, it seems worth while trying to increase its action by a simultaneous low-protein diet. The evoked aminoacid imbalance, which can be the factor increasing the biological requirement for some aminoacids, seems to be more easily achieved when on a low-protein supply. This imbalance has been claimed also occasionally effective in patients with acute
leukaemia.7 Institute of Pædiatrics, Medical Academy, Cracow, Poland.
BOGUSLAW HALIKOWSKI STANISLAW GARWICZ JERZY ARMATA.
FINDING THE EPIDURAL SPACE SIR,- It is a custom of many anxsthetists who encounter some difficulty in inserting a needle into the epidural space to leave their first needle in position as a useful guide while making a fresh attempt in an adjacent intervertebral interval. A few years ago, when I had inserted two needles thus and was still a little uncertain whether the point of either was in the right layer, it occurred to me to wonder whether injection into one needle might run through to the other. This would demonstrate an easily permeable layer and might be extra evidence of proper insertion. Injection, in fact, ran very freely out of the second needle; on three later occasions circumstances have offered a similar opportunity to check the free run between two needles, and on all four occasions the epidural injection has been clinically effective. London E.11. JOHN BARNARD.
TREATMENT OF PATHOLOGICAL FRACTURES OF THE FEMUR SIR,-Last year I briefly described11 my method of treating fractures of the femur secondary to malignant deposits. Since then, I have had several requests for a more detailed description of the technique, which now follows. (1) All accessible neoplastic tissue in the operative field is removed. If the junction of the neck and shaft of the femur is heavily infiltrated, it is usually best to resect 1-2 in. (2-5-5 cm.) of bone. Alternatively, a window can be made in the lateral cortex with an oscillating Stryker saw (often a suitable hole has already been supplied by bone erosion) and the malignant tissue curetted away. At this stage, it is important to ensure that (a) what remains of the interior of the greater trochanter, the inner surface of the neck, and the upper 3 in. (7-5 cm.) of the shaft of the femur are almost normal bone; (b) that the bone surfaces, after curetting, are as rough as possible, so as to allow the bone cement to key into them; and (c) that opposing surfaces are as wide as possible. (2) If a segment has been excised, the proximal part of the bone is abducted, and the distal part displaced medially, as in McMurray’s osteotomy. (This is not always possible, but the manoeuvre increases mechanical stability, and reduces shearing stresses at the cement/bone union.) (3) The bone fragments are filled with bone cement. For the deeper and less accessible parts a bladder syringe is often useful for inserting the material, which is then pressed in firmly with the fingers. A large lump is used to bridge the gap, or to replace the excised segment. (4) Before the cement hardens, further fixation is recommended, using a metal spline, or a pin and plate. (5) An outer shroud of cement is applied around the bridging cement and the metallic fixation, and is made to flow down the 7. 8.
Allan, J. D. Ireland, J. T., Milner, J., Moss, A. D. Lancet, 1965, i, 302. Nargolwala, V. S. ibid. 1968, ii, 912.
lateral surface of the greater trochanter-this helps to distribute the stresses. (6) ’Redivac ’ drainage and postoperative antibiotics are recommended. The wound is allowed to heal, and then the patient is given deep-X-ray treatment. Weight-bearing is allowed after ten days. This operation may cause considerable shock and blood loss, but of the patients who were reported alive in October, 1968, all still survive, and none shows evidence of recurrence of the disease in the femur. Royal Victoria Infirmary, V. S. NARGOLWALA. Newcastle upon Tyne NE1 4LP.
LIFESPAN OF CULTURED CELLS IN PROGERIA SIR,-An excellent model for the study of ageing is available in human diploid fibroblasts cultured in vitro. These cells have a finite lifespan, so that, on repeated subculture, after an interval of vigorous growth, they become senescent and eventually die. Furthermore their potential to grow in vitro is inversely proportional to the age of their donor.2 Epstein et al. have reported that fibroblasts from a 48-year-old woman with Werner’s syndrome of premature ageing, lived for only 1 or 2 subcultures beyond the stage of primary explantation, while age-matched controls were passaged 9-14 times.34 We now report similar results in a 9-year-old boy with typical progeria. After 4 weeks’ explantation, characterised only in its early stages by heavy epithelial outgrowth, fibroblasts overran the dish to form a confluent monolayer. Later, cells could not be subcultured more than twice, on 2 separate occasions. Age-matched controls, under identical growth conditions, were capable of 20-30 subcultures. These results support the idea that an ageing phenotype can be demonstrated, both in vivo and in vitro, by a continuous decrease in viability. This study was supported by Children’s Bureau project and U.S. Public Health Service grant no. CA-04670. Genetics Unit, Children’s Service, Massachusetts General Hospital, Department of Pediatrics, Harvard Medical School, and Walter E. Fernald State School, Boston, Massachusetts.
no.
906
SAMUEL GOLDSTEIN.
CEREBRAL METABOLISM AFTER PORTACAVAL SHUNT SiR,—Ihave read with interest the letter by Professor Polli and his colleagues (Jan. 18, p. 153). I am a bit concerned, however, by some of the figures in their tables. For instance, " they say, referring to table i, In most cases, moreover, the cerebral metabolic rate of oxygen was slightly higher than normal, with an even greater increase in cerebral metabolic rate of glucose ". The figures in table I do show an increase for all these parameters, but the figure given for c.G./O Q. of 2-49 is not that which is calculated from the figures given in the table. The correct figure here is 2-42. In table 11 some of the mathematical discrepancies are even more striking. In the column c.G./O Q., for patients in hepatic coma (less than 24 hours) the figure given is 2-77 whereas that calculated from the figures given in the table is 2-32. For acute encephalopathy the figure given is 2-17, that calculated is 1-97; for hepatic coma (greater than 24 hours) the figure given is 1-93, that calculated from the figures in the table is 163; and for chronic encephalopathy that calculated is 2-08 compared with the quoted figure of 2-03. Department of Investigative Medicine, University of Cambridge, J. M. WALSHE. Cambridge CB2 1QN. 1. Hayflick, L. Expl Cell Res. 1965, 37, 614. 2. Green, H., Todaro, G. J. Ann. Rev. Microbiol. 1967, 21, 573. 3. Epstein, C. J., Martin, G. M., Motulsky, A. G. Trans. Ass. Am. Physns, 1965, 68, 73. 4. Martin, G. M., Gartler, S. M., Epstein, C. J., Motulsky, A. G. Fedn Proc. 1965, 24, 678.
leukaemia.7 Institute of Pædiatrics, Medical Academy, Cracow, Poland.
BOGUSLAW HALIKOWSKI STANISLAW GARWICZ JERZY ARMATA.
FINDING THE EPIDURAL SPACE SIR,- It is a custom of many anxsthetists who encounter some difficulty in inserting a needle into the epidural space to leave their first needle in position as a useful guide while making a fresh attempt in an adjacent intervertebral interval. A few years ago, when I had inserted two needles thus and was still a little uncertain whether the point of either was in the right layer, it occurred to me to wonder whether injection into one needle might run through to the other. This would demonstrate an easily permeable layer and might be extra evidence of proper insertion. Injection, in fact, ran very freely out of the second needle; on three later occasions circumstances have offered a similar opportunity to check the free run between two needles, and on all four occasions the epidural injection has been clinically effective. London E.11. JOHN BARNARD.
TREATMENT OF PATHOLOGICAL FRACTURES OF THE FEMUR SIR,-Last year I briefly described11 my method of treating fractures of the femur secondary to malignant deposits. Since then, I have had several requests for a more detailed description of the technique, which now follows. (1) All accessible neoplastic tissue in the operative field is removed. If the junction of the neck and shaft of the femur is heavily infiltrated, it is usually best to resect 1-2 in. (2-5-5 cm.) of bone. Alternatively, a window can be made in the lateral cortex with an oscillating Stryker saw (often a suitable hole has already been supplied by bone erosion) and the malignant tissue curetted away. At this stage, it is important to ensure that (a) what remains of the interior of the greater trochanter, the inner surface of the neck, and the upper 3 in. (7-5 cm.) of the shaft of the femur are almost normal bone; (b) that the bone surfaces, after curetting, are as rough as possible, so as to allow the bone cement to key into them; and (c) that opposing surfaces are as wide as possible. (2) If a segment has been excised, the proximal part of the bone is abducted, and the distal part displaced medially, as in McMurray’s osteotomy. (This is not always possible, but the manoeuvre increases mechanical stability, and reduces shearing stresses at the cement/bone union.) (3) The bone fragments are filled with bone cement. For the deeper and less accessible parts a bladder syringe is often useful for inserting the material, which is then pressed in firmly with the fingers. A large lump is used to bridge the gap, or to replace the excised segment. (4) Before the cement hardens, further fixation is recommended, using a metal spline, or a pin and plate. (5) An outer shroud of cement is applied around the bridging cement and the metallic fixation, and is made to flow down the 7. 8.
Allan, J. D. Ireland, J. T., Milner, J., Moss, A. D. Lancet, 1965, i, 302. Nargolwala, V. S. ibid. 1968, ii, 912.
lateral surface of the greater trochanter-this helps to distribute the stresses. (6) ’Redivac ’ drainage and postoperative antibiotics are recommended. The wound is allowed to heal, and then the patient is given deep-X-ray treatment. Weight-bearing is allowed after ten days. This operation may cause considerable shock and blood loss, but of the patients who were reported alive in October, 1968, all still survive, and none shows evidence of recurrence of the disease in the femur. Royal Victoria Infirmary, V. S. NARGOLWALA. Newcastle upon Tyne NE1 4LP.
LIFESPAN OF CULTURED CELLS IN PROGERIA SIR,-An excellent model for the study of ageing is available in human diploid fibroblasts cultured in vitro. These cells have a finite lifespan, so that, on repeated subculture, after an interval of vigorous growth, they become senescent and eventually die. Furthermore their potential to grow in vitro is inversely proportional to the age of their donor.2 Epstein et al. have reported that fibroblasts from a 48-year-old woman with Werner’s syndrome of premature ageing, lived for only 1 or 2 subcultures beyond the stage of primary explantation, while age-matched controls were passaged 9-14 times.34 We now report similar results in a 9-year-old boy with typical progeria. After 4 weeks’ explantation, characterised only in its early stages by heavy epithelial outgrowth, fibroblasts overran the dish to form a confluent monolayer. Later, cells could not be subcultured more than twice, on 2 separate occasions. Age-matched controls, under identical growth conditions, were capable of 20-30 subcultures. These results support the idea that an ageing phenotype can be demonstrated, both in vivo and in vitro, by a continuous decrease in viability. This study was supported by Children’s Bureau project and U.S. Public Health Service grant no. CA-04670. Genetics Unit, Children’s Service, Massachusetts General Hospital, Department of Pediatrics, Harvard Medical School, and Walter E. Fernald State School, Boston, Massachusetts.
no.
906
SAMUEL GOLDSTEIN.
CEREBRAL METABOLISM AFTER PORTACAVAL SHUNT SiR,—Ihave read with interest the letter by Professor Polli and his colleagues (Jan. 18, p. 153). I am a bit concerned, however, by some of the figures in their tables. For instance, " they say, referring to table i, In most cases, moreover, the cerebral metabolic rate of oxygen was slightly higher than normal, with an even greater increase in cerebral metabolic rate of glucose ". The figures in table I do show an increase for all these parameters, but the figure given for c.G./O Q. of 2-49 is not that which is calculated from the figures given in the table. The correct figure here is 2-42. In table 11 some of the mathematical discrepancies are even more striking. In the column c.G./O Q., for patients in hepatic coma (less than 24 hours) the figure given is 2-77 whereas that calculated from the figures given in the table is 2-32. For acute encephalopathy the figure given is 2-17, that calculated is 1-97; for hepatic coma (greater than 24 hours) the figure given is 1-93, that calculated from the figures in the table is 163; and for chronic encephalopathy that calculated is 2-08 compared with the quoted figure of 2-03. Department of Investigative Medicine, University of Cambridge, J. M. WALSHE. Cambridge CB2 1QN. 1. Hayflick, L. Expl Cell Res. 1965, 37, 614. 2. Green, H., Todaro, G. J. Ann. Rev. Microbiol. 1967, 21, 573. 3. Epstein, C. J., Martin, G. M., Motulsky, A. G. Trans. Ass. Am. Physns, 1965, 68, 73. 4. Martin, G. M., Gartler, S. M., Epstein, C. J., Motulsky, A. G. Fedn Proc. 1965, 24, 678.