- Email: [email protected]
THE RESIDENT PATHOLOGIST
158 say how many beds are required the Ministry decide which of these patients are a psychiatric responsibility and which are not. Good management demands that they decide quickly, for planning and nnancins still take a loniz time. E. HOWARTH. Doncaster Royal Infirmary.
anyone
can
of Health
must
THE RESIDENT PATHOLOGIST
SIR,-We believe that Professor Landon and his colleagues (July 5, p. 41) have made the right recommendations on emergency services in chemical pathology. Their suggestions for grouping hospitals and sharing technical staff are, in fact, very similar to ideas put forward by one of us 21/2 years ago. For the past year we have been part of the St. Mary’s Hospital teaching group, but we were not, so far as we know, included in the survey by Professor Landon and his coileagues. It might, therefore, be of interest if we detailed our existing arrangements, which have not changed since we became a teaching hospital. Resident staff are on call for emergency work, and cover over a thousand beds. They do L
all the
tests
in Professor Landon’s table
I
except O2
satura-
tion/Po2. Quality-control samples are run for emergency electrolytes and calciums. Teaching is given in basic techniques ; training is given for the primary M.C.PATH.2; and residents are allowed time off to attend the primary M.c. PATH. course at the Middlesex Hospital. We thought the last points, especially, should be brought to your notice since Professor Landon’s paper gives the impression that few, if any, hospitals in London are trying to help junior pathologists with in-service training. I. J. L. GOLDBERG P. R. N. KIND.
London.
FAT-EMBOLISM
SIR,-We should like to comment on the criticism by (June 14, p. 1213) of some of the deductions in
Mr. Ross
paper on fat-embolism associated with the inhalation of aviation fuel and general anaesthesia (May 31, p. 1059). We are very much aware of the need to distinguish mere histological evidence of fat-embolism from the clinical syndrome of fat-embolism. Histological evidence of systemic embolism can be found unassociated with symptoms. Pulmonary fat-embolism is extremely common after trauma, and, in healthy individuals, is usually symptomless. Many patients who develop the fat-embolism syndrome recover. In the paper by Watts,3 quoted by Mr. Ross, there is no supporting evidence whatever for his statement that after long-bone fractures there is a 10%incidence of the fat-embolism syndrome. 6 of Watts’ small series of 7 cases recovered. Fatal systemic fat-embolism after long-bone fractures is rare. In the necropsy series reported from the Birmingham Accident Hospital4 it was believed to be the main cause of death in 4°o. Newman,5 in his series of 89 cases with longbone fractures, concluded that it was the cause of death in
our
3-4%. In both the airmen described in
our
paper, death
was
undoubtedly caused by systemic fat-embolism. There was histological evidence of gross embolism in the brain, kidneys, and spleen. In both men, the first clinical 1. 2. 3. 4. 5.
was seen
and Pathology, Department of Health, Queensland, Brisbane, Australia.
J. I. TONGE J. FERGUSON.
ORAL CONTRACEPTIVES AND DEPRESSION
Departments of Chemical Pathology, St. Mary’s Hospital (Harrow Road) and St. Charles’ Hospital,
evidence of embolism
The pilot, who was exposed to petrol for 25 minutes, died 45 hours after the accident. In the passenger, exposed to petrol for 5 minutes, death was delayed until 75 hours after the accident. Assuming the incidence of fatal fat-embolism after long-bone trauma to be in the vicinity of 4%, there would have been 1 chance in 1000 of both persons in the accident developing fatal systemic embolism from the fractured bones alone. It therefore seems reasonable to suppose that there was some additional factor; and such a factor was found in the gross hepatocellular damage with fatty accumulation in each case. We suggest that this liver damage was due to exposure to petrol vapour, possibly aggravated by the subsequent ansesthetic. Supporting evidence for this hypothesis is provided by the direct correlation between the length of exposure to petrol, the degree of liver damage, the extent of the pulmonary and systemic fat-embolism, and the survival period in both airmen. We stated clearly that the fat-embolism could have come from the fractured long bones, from the liver, or from both sources. Systemic fat-embolism arising from hepatocellular damage is admittedly rare, but, as we pointed out, it is well documented. Exposure to petrol, causing hepatocellular damage subsequently aggravated by an anaesthetic agent, is also rare, but this does not preclude the possibility that this is what happened. Laboratory of Microbiology
30 hours after the accident.
Goldberg, I. J. L. Lancet, 1966, ii, 586. Goldberg, I. J. L. ibid. 1967, ii, 992. Watts, J. McK. Aust. N.Z.J. Surg. 1962, 32, 31. Sevitt, S. Fat Embolism. London, 1962. Newman, P. H. J. Bone Jt Surg. 1945, 30B, 290.
interested in Dr. Winston’s suggestion1 that pyridoxine might protect women on oral contraceptives from depression. He bases this on the assumption that dysfunction of tryptophan metabolism is implicated in some forms of depression, and that by activating tryptophan pyrollase oral contraceptives may create a functional deficiency of pyridoxine along the tryptophan-niacin pathway. We should like to carry his argument a stage further. We now have evidence of disturbance of tryptophan metabolism in twenty women on oral contraceptives. This is based on the finding of increased urinary levels of 3hydroxyanthranilic acid without prior trytophan loading. We also believe that the levels can be restored to normal by administration of pyridoxine.23 further, there have been reports of abnormal urinary levels of various tryptophan metabolites in conditions such as rheumatoid arthritis, disseminated lupus erythematosus, scleroderma 4carcinoma of the bladder 6and carcinoma of the breast,8 as well as following the administration of oestrogens3 and during pregnancy.9 More recently there have also been reports of11 symptoms and signs mimicking rheumatoid arthritis,10 and exacerbations of disseminated lupus,12 13 in women on oral contraceptives. On the basis of this evidence, is there not a case for routine administration of pyridoxine to all women on contraceptive
SIR,-We
are
Winston, F. Lancet, 1969, i, 1209. Toseland, P. A., Price, S. A. Br. med. J. 1969, i, 777. Rose, D. P. Clin. Sci. 1966, 31, 265. McMillan, M. J. clin. Path. 1960, 13, 140. Bett, I. Ann. rheum. Dis. 1966, 25, 556. Brown, R. R., Price, J. M., Wear, J. B. Proc. Am. Ass. Cancer Res. 1955, 2, 7. 7. Boyland, E., Williams, D. C. Biochem. J. 1956, 64, 578. 8. Rose, D. P. Lancet, 1967, i, 239. 9. Brown, R. R., Thornton, M. J., Price, J. M. J. clin. Invest. 1961, 40, 617. 10. Bole, G. G., Friedlander, M. H., Smith, C. K. Lancet, 1969, i, 323. 11. Speira, H., Plotz, C. ibid. p. 571. 12. Pimstone, B. L. S. Afr. J. Obstet. Gynœc. 1966, 4, 62. 13. Pimstone, B. L. Lancet, 1968, i, 1153. 1. 2. 3. 4. 5. 6.
anyone
can
of Health
must
THE RESIDENT PATHOLOGIST
SIR,-We believe that Professor Landon and his colleagues (July 5, p. 41) have made the right recommendations on emergency services in chemical pathology. Their suggestions for grouping hospitals and sharing technical staff are, in fact, very similar to ideas put forward by one of us 21/2 years ago. For the past year we have been part of the St. Mary’s Hospital teaching group, but we were not, so far as we know, included in the survey by Professor Landon and his coileagues. It might, therefore, be of interest if we detailed our existing arrangements, which have not changed since we became a teaching hospital. Resident staff are on call for emergency work, and cover over a thousand beds. They do L
all the
tests
in Professor Landon’s table
I
except O2
satura-
tion/Po2. Quality-control samples are run for emergency electrolytes and calciums. Teaching is given in basic techniques ; training is given for the primary M.C.PATH.2; and residents are allowed time off to attend the primary M.c. PATH. course at the Middlesex Hospital. We thought the last points, especially, should be brought to your notice since Professor Landon’s paper gives the impression that few, if any, hospitals in London are trying to help junior pathologists with in-service training. I. J. L. GOLDBERG P. R. N. KIND.
London.
FAT-EMBOLISM
SIR,-We should like to comment on the criticism by (June 14, p. 1213) of some of the deductions in
Mr. Ross
paper on fat-embolism associated with the inhalation of aviation fuel and general anaesthesia (May 31, p. 1059). We are very much aware of the need to distinguish mere histological evidence of fat-embolism from the clinical syndrome of fat-embolism. Histological evidence of systemic embolism can be found unassociated with symptoms. Pulmonary fat-embolism is extremely common after trauma, and, in healthy individuals, is usually symptomless. Many patients who develop the fat-embolism syndrome recover. In the paper by Watts,3 quoted by Mr. Ross, there is no supporting evidence whatever for his statement that after long-bone fractures there is a 10%incidence of the fat-embolism syndrome. 6 of Watts’ small series of 7 cases recovered. Fatal systemic fat-embolism after long-bone fractures is rare. In the necropsy series reported from the Birmingham Accident Hospital4 it was believed to be the main cause of death in 4°o. Newman,5 in his series of 89 cases with longbone fractures, concluded that it was the cause of death in
our
3-4%. In both the airmen described in
our
paper, death
was
undoubtedly caused by systemic fat-embolism. There was histological evidence of gross embolism in the brain, kidneys, and spleen. In both men, the first clinical 1. 2. 3. 4. 5.
was seen
and Pathology, Department of Health, Queensland, Brisbane, Australia.
J. I. TONGE J. FERGUSON.
ORAL CONTRACEPTIVES AND DEPRESSION
Departments of Chemical Pathology, St. Mary’s Hospital (Harrow Road) and St. Charles’ Hospital,
evidence of embolism
The pilot, who was exposed to petrol for 25 minutes, died 45 hours after the accident. In the passenger, exposed to petrol for 5 minutes, death was delayed until 75 hours after the accident. Assuming the incidence of fatal fat-embolism after long-bone trauma to be in the vicinity of 4%, there would have been 1 chance in 1000 of both persons in the accident developing fatal systemic embolism from the fractured bones alone. It therefore seems reasonable to suppose that there was some additional factor; and such a factor was found in the gross hepatocellular damage with fatty accumulation in each case. We suggest that this liver damage was due to exposure to petrol vapour, possibly aggravated by the subsequent ansesthetic. Supporting evidence for this hypothesis is provided by the direct correlation between the length of exposure to petrol, the degree of liver damage, the extent of the pulmonary and systemic fat-embolism, and the survival period in both airmen. We stated clearly that the fat-embolism could have come from the fractured long bones, from the liver, or from both sources. Systemic fat-embolism arising from hepatocellular damage is admittedly rare, but, as we pointed out, it is well documented. Exposure to petrol, causing hepatocellular damage subsequently aggravated by an anaesthetic agent, is also rare, but this does not preclude the possibility that this is what happened. Laboratory of Microbiology
30 hours after the accident.
Goldberg, I. J. L. Lancet, 1966, ii, 586. Goldberg, I. J. L. ibid. 1967, ii, 992. Watts, J. McK. Aust. N.Z.J. Surg. 1962, 32, 31. Sevitt, S. Fat Embolism. London, 1962. Newman, P. H. J. Bone Jt Surg. 1945, 30B, 290.
interested in Dr. Winston’s suggestion1 that pyridoxine might protect women on oral contraceptives from depression. He bases this on the assumption that dysfunction of tryptophan metabolism is implicated in some forms of depression, and that by activating tryptophan pyrollase oral contraceptives may create a functional deficiency of pyridoxine along the tryptophan-niacin pathway. We should like to carry his argument a stage further. We now have evidence of disturbance of tryptophan metabolism in twenty women on oral contraceptives. This is based on the finding of increased urinary levels of 3hydroxyanthranilic acid without prior trytophan loading. We also believe that the levels can be restored to normal by administration of pyridoxine.23 further, there have been reports of abnormal urinary levels of various tryptophan metabolites in conditions such as rheumatoid arthritis, disseminated lupus erythematosus, scleroderma 4carcinoma of the bladder 6and carcinoma of the breast,8 as well as following the administration of oestrogens3 and during pregnancy.9 More recently there have also been reports of11 symptoms and signs mimicking rheumatoid arthritis,10 and exacerbations of disseminated lupus,12 13 in women on oral contraceptives. On the basis of this evidence, is there not a case for routine administration of pyridoxine to all women on contraceptive
SIR,-We
are
Winston, F. Lancet, 1969, i, 1209. Toseland, P. A., Price, S. A. Br. med. J. 1969, i, 777. Rose, D. P. Clin. Sci. 1966, 31, 265. McMillan, M. J. clin. Path. 1960, 13, 140. Bett, I. Ann. rheum. Dis. 1966, 25, 556. Brown, R. R., Price, J. M., Wear, J. B. Proc. Am. Ass. Cancer Res. 1955, 2, 7. 7. Boyland, E., Williams, D. C. Biochem. J. 1956, 64, 578. 8. Rose, D. P. Lancet, 1967, i, 239. 9. Brown, R. R., Thornton, M. J., Price, J. M. J. clin. Invest. 1961, 40, 617. 10. Bole, G. G., Friedlander, M. H., Smith, C. K. Lancet, 1969, i, 323. 11. Speira, H., Plotz, C. ibid. p. 571. 12. Pimstone, B. L. S. Afr. J. Obstet. Gynœc. 1966, 4, 62. 13. Pimstone, B. L. Lancet, 1968, i, 1153. 1. 2. 3. 4. 5. 6.