- Email: [email protected]
POSTOPERATIVE DEEP-VEIN THROMBOSIS, PULMONARY EMBOLISM, AND HIGH-FIBRE DIET
1197 is there any need for more elaborate computer matching, a procedure which has to be planned and executed with the greatest care and the most open documentation if it is going to be either more precise or faster than a visual match. After three years it is perhaps in order to divulge this much of the actions, or rather inactions, of the past. No doubt matters are better now, but unless the pathology of the past is studied by responsible journalism the health of the future will continue to be threatened by producer-directed funding in the consumer-starvation society of the National Health Service. I possess, from the Birmingham Regional Hospital Board, also from 1973, an even more remarkable letter which came to me by an indirect route although I had, at that time, responsibilities in chromosome diagnosis. The letter includes the paragraph : "The Department is currently reviewing its priorities D funding and, in particular, had been for equipment R & looking at the field of automatic chromosome analysis. More specifically it appears that with recent advances in pattern recognition techniques it may now be possible to manufacture devices for :a. the automatic location of metaphases (for subsequent manual analysis); b. a. plus user interactive karyotyping." A belief in the realistic and economic possibility of regular cytogenetic studies being delegated to the computer within this decade seems to be yet another mirage at the Department: such investments may be socially useful if they lead to byproducts which would do some simpler tasks, such as cervical smears or counts of broken chromosomes. Unfortunately it seems possible that the failure to fund adequate numbers of training posts from which the consultant-grade cytogeneticists so urgently needed may anticipate promotion is a residual effect of the circumstances giving rise to this extraordinary document. Fortunately computers have universal properties, and some of the less fortunate projects are near vigorous and underequipped university departments which could make use of much of the equipment now somewhat vaguely employed, to the advantage of the taxpayer without detriment either to the N.H.S. or to the careers of those whose future would otherwise depend on the continued existence, and even expansion, of what appear to be either lost causes, or schemes rendered inappropriate as a result of changes in computer design, in clinical or laboratory practice, or in the financial environment. in use
in
commerce
schemes, such
as
Infant
Develop Unit, Queen Elizabeth Medical Centre, Birmingham B15 2TG
J. H. EDWARDS
POSTOPERATIVE DEEP-VEIN THROMBOSIS, PULMONARY EMBOLISM, AND HIGH-FIBRE DIET
especially in relation to his statement regarding the absence of deep-vein thrombosis and pulmonary emboli in patients on a high-fibre diet. This low incidence has its correspondence in the underdeveloped countries whose peoples traditionally live diet rich in fibre. At the Royal Berkshire Hospital we have had a similar experience to Mr Frohn. For four years all patients in a ward, mamly dealing with urological conditions, have been given bran before and after surgery. There have been no pulmonary emboli and only one case of clinical deep-vein thrombosis, and this in a man who was very reluctant to take his bran. It has been suggested that the simple mechanism described by Surgeon Captain T. L. Cleave and illustrated by Mr Frohn may not be the correct one. An alternative explanation may be that bran produces changes in the fibrinolytic activity of the
on a
thrombosis and pulmonary emboli, 35-40% of the patients have positive I125-fibrinogen tests after retropubic prostatectomy. Estimations of possible changes in fibrinolysis have not yet been completed. If, as Mr Frohn suggests, we can, by such a simple measure as giving patients bran and the like, eliminate a large number of our cases of deep-vein thrombosis and pulmonary emboli, then this requires most serious consideration and much fuller scientific verification. Royal Berkshire Hospital, Reading RG1 5AN
SIR,-Mr Frohn (Nov. 6, p. 1019) suggests that varicose veins, hypostatic ulceration, deep-vein thrombosis, and even atherosclerotic gangrene more often affect the left leg. Many clinicians have the impression that varicose veins are more common in the left leg, but I could find no published statistics on the distribution of primary varicose veins. On reviewing the first 200 cases in my series of more than 5000 patients no statistical difference was found for primary varicose veins, the figures being right 36, left 39, and bilateral 118. The distribution for secondary cases (post-thrombotic syndrome) were: right 1, left 5, bilateral 1. Only patients with gross proximal incompetence are treated by limited surgery, and the analysis of patients treated during the past two years was: 48 right leg only, 43 left leg only, and 80 bilateral. Thus I find that primary varicose veins are more commonly a bilateral disorder, with no preponderance for the left side. In studies of deep-venous thrombosis in the calf using the radioactive fibrinogen test there was no statistical difference between the right and left legs. 1however, when the ilio- femoral segment is affected there is a striking preponderance of left-side’ lesions. Negus3 reviewed the incidence of iliofemoral thrombosis reported during the past six decades and found the ratio of left side only to right side only to be more than 2/1. Antero-posterior compression of the left common iliac vein is common, and sufficient to cause a radiological filling defect in about 50% of patients with an otherwise normal iliac venogram.4 However, the compression is compensated by an increase in lateral diameter so that the cross-sectional area is not reduced. In a smaller number of otherwise normal people the degree of compression is more striking and is accompanied by adhesion or band formation at the mouth of the left common iliac vein. A review of the literature showed that these bands were found in 22% of 1000 dissections, and in Negus’s own series band formation was always associated with notable compression of the vein and a decrease in cross-sectional area.’ Thus Negus has demonstrated that compression and band formation at the mouth of the left common iliac vein is a normal anatomical anomaly which usually causes no symptoms or physical signs in healthy ambulant subjects. However, in the presence of a restricted venous flow and hypercoagulability, as happens during severe illness, operation, or trauma, acute thrombosis of the left common iliac vein may be precipitated. This careful study by Negus and his colleagues has demonstrated the reason for the fact that iliac-vein thrombosis or "white leg" affects the left side more commonly than the right. Most vascular surgeons now support this view, so well demonstrated by the St. Thomas’s group. There is no evidence to support that the left iliac vessels are affected by the sigmoid mesocolon and by the nature of the stools contained in this part of the colon. I cannot believe that starting patients on a wholemeal and bran diet when admitted
1.
are in
and, despite
the middle of a trial using the 121-fibrinogen test, the virtual complete absence of clinical deep-vein
Diener, L.
m
Thromboembolism
(edited by
A. N. Nicolaides). Lancaster,
1975. 2. 3.
blood. We
CONRAD LATTO
4. 5.
Nicolaides, A. N., O’Connell, J. D ibid.
Negus, D. in Pathology and Surgery of the Veins of the Lower Limb (edited by H. Dodd and F. B Cockett). Edinburgh, 1976. Negus, D., Edwards, J. M., Kinmonth, J. B Br. J. Surg 1969, 56, 481. Negus, D., Fletcher, E. W. L., Cockett, F. B., Lea Thomas, M. ibid. 1968, 55, 368.
1198 to hospital immediately before surgery will prevent postoperative deep-vein thrombosis but Mr Frohn is to be congratulated for carrying out 1400 operations during three years without a case of postoperative clinical deep-vein thrombosis or pulmonary embolism. There is no evidence that atherosclerosis affects the left leg more than the right side, and again I would suggest that this
is
a
generalised disease which is most often bilateral.
Vein Clinic, St. Mary’s Hospital, London W2 1NY
J. T. HOBBS
different from the rates he derived fp=0 26 shown are also within the time and space variations noted in the Collmann and Stoller report.’ Professor Ferguson-Smith (July 31, p. 252) suggests that retrospective studies such as that done by Dr Hook grossly underestimate the agespecific risks of Down syndrome. Since our intense prospective study supports Dr Hook’s retrospective study, this criticism is not
The
significantly rates
justified. Although our data are not large enough to present bv single years of age, they are given in table n by 2-year maternal-age intervals to demonstrate how rapidly the risk increases in not
35. We agree with Dr Hook that maternal ageas given by single years of age in Dr Hook’s article, should be used for genetic counselling. women over
specific prevalence-rates, DOWN SYNDROME AND MATERNAL AGE
SiR,—Dr Hook (July 3, p. 33) estimates the
rates of Down in to be intervals syndrome 5-year maternal-age higher than those observed by Collmann and Stoller, which are generally accepted as the most reliable age-specific rates available. Our data from the Child Health and Development Studies, a longitudinal study of pregnancy and the development of the offspring, supports the higher estimates derived by Dr Hook. Among the 18 639 single live births in our population (1959-67) there were 37 cases of Down syndrome. Our study population is of diverse ethnicity and generally represents an employed urban population which encompasses a broad range of economic, social, and educational characteristics. The mothers, members of the Kaiser Foundation Health Plan, were interviewed early in their pregnancies, and the families were intensively followed up until the youngest child was 5 years old. At 1 year of age the health status of all but 48 of the live-born children was known; these 48 children, on average, had been followed up for 3tmonths before contact with them was lost. Among the 37 children with Down syndrome 35 were suspected of having the condition at birth. The other 2 cases were first suspected in the second month of life. However, a definite diagnosis was delayed in 11 cases and never made in 1 child who died shortly after birth (the cause of death listed for this child was prematurity and probable Down syndrome). Delays in confirming the diagnosis, which in this study ranged from 1 week to 13 months, are no doubt responsible for many cases not being officially recorded. Since all cases were suspected at very young ages and no such suspicion existed among those lost to follow-up in the first year of life, we believe that ascertainment of Down syndrome in our cohort of live births was
complete. The distribution of the children with Down syndrome by 5-year maternal age intervals is given in table i. The rates shown for this cohort studied prospectively are slightly higher than those presented by Dr Hook, but they are
of California, School of Public Health, Child Health and Development Studies, Oakland, California 94611, U.S.A.
University
COMPUTATIONS FOR PRENATAL PREDICTION OF MYOTONIC DYSTROPHY
SIR,-Insley et al.’ report the risk calculations for a fetus in a family with myotonic dystrophy illustrating how gene-linkage information can be used to predict phenotypes prenatally. Myotonic dystrophy is an autosomal dominant, late-onset disease closely linked to the secretor locus (Se). Secretor phenotypes can be detected in utero.2
To illustrate some additional points of concern for prenatal prediction, we present the following family (see figure). Initial testing indicates that the proband (III-1) is a non-secretor and his mother (11-2) must be doubly heterozygous. 1. 2.
1.
Collmann, R.
D.
Stoller,
A.
Am. J. publ. Hlth, 1962, 52,
813.
ROBERTA E. CHRISTIANSON
Insley, J., Bird, G. W G., Harper, P. S., Pearce, G. W. Lancet, 1976, i, 806. Harper, P. S., Bias, W. B., Hutchmson, J. R., McKusick, V.A. J. med. Genet. 1971, 8, 438.
TABLE I-PREVALENCE OF DOWN SYNDROME BY MATERNAL AGE AMONG SINGLE LIVE BIRTHS
TABLE II-PREVALENCE OF DOWN SYNDROME BY MATERNAL-AGE INTERVALS OF TWO YEARS AMONG SINGLE LIVE BIRTH
in
commerce
schemes, such
as
Infant
Develop Unit, Queen Elizabeth Medical Centre, Birmingham B15 2TG
J. H. EDWARDS
POSTOPERATIVE DEEP-VEIN THROMBOSIS, PULMONARY EMBOLISM, AND HIGH-FIBRE DIET
especially in relation to his statement regarding the absence of deep-vein thrombosis and pulmonary emboli in patients on a high-fibre diet. This low incidence has its correspondence in the underdeveloped countries whose peoples traditionally live diet rich in fibre. At the Royal Berkshire Hospital we have had a similar experience to Mr Frohn. For four years all patients in a ward, mamly dealing with urological conditions, have been given bran before and after surgery. There have been no pulmonary emboli and only one case of clinical deep-vein thrombosis, and this in a man who was very reluctant to take his bran. It has been suggested that the simple mechanism described by Surgeon Captain T. L. Cleave and illustrated by Mr Frohn may not be the correct one. An alternative explanation may be that bran produces changes in the fibrinolytic activity of the
on a
thrombosis and pulmonary emboli, 35-40% of the patients have positive I125-fibrinogen tests after retropubic prostatectomy. Estimations of possible changes in fibrinolysis have not yet been completed. If, as Mr Frohn suggests, we can, by such a simple measure as giving patients bran and the like, eliminate a large number of our cases of deep-vein thrombosis and pulmonary emboli, then this requires most serious consideration and much fuller scientific verification. Royal Berkshire Hospital, Reading RG1 5AN
SIR,-Mr Frohn (Nov. 6, p. 1019) suggests that varicose veins, hypostatic ulceration, deep-vein thrombosis, and even atherosclerotic gangrene more often affect the left leg. Many clinicians have the impression that varicose veins are more common in the left leg, but I could find no published statistics on the distribution of primary varicose veins. On reviewing the first 200 cases in my series of more than 5000 patients no statistical difference was found for primary varicose veins, the figures being right 36, left 39, and bilateral 118. The distribution for secondary cases (post-thrombotic syndrome) were: right 1, left 5, bilateral 1. Only patients with gross proximal incompetence are treated by limited surgery, and the analysis of patients treated during the past two years was: 48 right leg only, 43 left leg only, and 80 bilateral. Thus I find that primary varicose veins are more commonly a bilateral disorder, with no preponderance for the left side. In studies of deep-venous thrombosis in the calf using the radioactive fibrinogen test there was no statistical difference between the right and left legs. 1however, when the ilio- femoral segment is affected there is a striking preponderance of left-side’ lesions. Negus3 reviewed the incidence of iliofemoral thrombosis reported during the past six decades and found the ratio of left side only to right side only to be more than 2/1. Antero-posterior compression of the left common iliac vein is common, and sufficient to cause a radiological filling defect in about 50% of patients with an otherwise normal iliac venogram.4 However, the compression is compensated by an increase in lateral diameter so that the cross-sectional area is not reduced. In a smaller number of otherwise normal people the degree of compression is more striking and is accompanied by adhesion or band formation at the mouth of the left common iliac vein. A review of the literature showed that these bands were found in 22% of 1000 dissections, and in Negus’s own series band formation was always associated with notable compression of the vein and a decrease in cross-sectional area.’ Thus Negus has demonstrated that compression and band formation at the mouth of the left common iliac vein is a normal anatomical anomaly which usually causes no symptoms or physical signs in healthy ambulant subjects. However, in the presence of a restricted venous flow and hypercoagulability, as happens during severe illness, operation, or trauma, acute thrombosis of the left common iliac vein may be precipitated. This careful study by Negus and his colleagues has demonstrated the reason for the fact that iliac-vein thrombosis or "white leg" affects the left side more commonly than the right. Most vascular surgeons now support this view, so well demonstrated by the St. Thomas’s group. There is no evidence to support that the left iliac vessels are affected by the sigmoid mesocolon and by the nature of the stools contained in this part of the colon. I cannot believe that starting patients on a wholemeal and bran diet when admitted
1.
are in
and, despite
the middle of a trial using the 121-fibrinogen test, the virtual complete absence of clinical deep-vein
Diener, L.
m
Thromboembolism
(edited by
A. N. Nicolaides). Lancaster,
1975. 2. 3.
blood. We
CONRAD LATTO
4. 5.
Nicolaides, A. N., O’Connell, J. D ibid.
Negus, D. in Pathology and Surgery of the Veins of the Lower Limb (edited by H. Dodd and F. B Cockett). Edinburgh, 1976. Negus, D., Edwards, J. M., Kinmonth, J. B Br. J. Surg 1969, 56, 481. Negus, D., Fletcher, E. W. L., Cockett, F. B., Lea Thomas, M. ibid. 1968, 55, 368.
1198 to hospital immediately before surgery will prevent postoperative deep-vein thrombosis but Mr Frohn is to be congratulated for carrying out 1400 operations during three years without a case of postoperative clinical deep-vein thrombosis or pulmonary embolism. There is no evidence that atherosclerosis affects the left leg more than the right side, and again I would suggest that this
is
a
generalised disease which is most often bilateral.
Vein Clinic, St. Mary’s Hospital, London W2 1NY
J. T. HOBBS
different from the rates he derived fp=0 26 shown are also within the time and space variations noted in the Collmann and Stoller report.’ Professor Ferguson-Smith (July 31, p. 252) suggests that retrospective studies such as that done by Dr Hook grossly underestimate the agespecific risks of Down syndrome. Since our intense prospective study supports Dr Hook’s retrospective study, this criticism is not
The
significantly rates
justified. Although our data are not large enough to present bv single years of age, they are given in table n by 2-year maternal-age intervals to demonstrate how rapidly the risk increases in not
35. We agree with Dr Hook that maternal ageas given by single years of age in Dr Hook’s article, should be used for genetic counselling. women over
specific prevalence-rates, DOWN SYNDROME AND MATERNAL AGE
SiR,—Dr Hook (July 3, p. 33) estimates the
rates of Down in to be intervals syndrome 5-year maternal-age higher than those observed by Collmann and Stoller, which are generally accepted as the most reliable age-specific rates available. Our data from the Child Health and Development Studies, a longitudinal study of pregnancy and the development of the offspring, supports the higher estimates derived by Dr Hook. Among the 18 639 single live births in our population (1959-67) there were 37 cases of Down syndrome. Our study population is of diverse ethnicity and generally represents an employed urban population which encompasses a broad range of economic, social, and educational characteristics. The mothers, members of the Kaiser Foundation Health Plan, were interviewed early in their pregnancies, and the families were intensively followed up until the youngest child was 5 years old. At 1 year of age the health status of all but 48 of the live-born children was known; these 48 children, on average, had been followed up for 3tmonths before contact with them was lost. Among the 37 children with Down syndrome 35 were suspected of having the condition at birth. The other 2 cases were first suspected in the second month of life. However, a definite diagnosis was delayed in 11 cases and never made in 1 child who died shortly after birth (the cause of death listed for this child was prematurity and probable Down syndrome). Delays in confirming the diagnosis, which in this study ranged from 1 week to 13 months, are no doubt responsible for many cases not being officially recorded. Since all cases were suspected at very young ages and no such suspicion existed among those lost to follow-up in the first year of life, we believe that ascertainment of Down syndrome in our cohort of live births was
complete. The distribution of the children with Down syndrome by 5-year maternal age intervals is given in table i. The rates shown for this cohort studied prospectively are slightly higher than those presented by Dr Hook, but they are
of California, School of Public Health, Child Health and Development Studies, Oakland, California 94611, U.S.A.
University
COMPUTATIONS FOR PRENATAL PREDICTION OF MYOTONIC DYSTROPHY
SIR,-Insley et al.’ report the risk calculations for a fetus in a family with myotonic dystrophy illustrating how gene-linkage information can be used to predict phenotypes prenatally. Myotonic dystrophy is an autosomal dominant, late-onset disease closely linked to the secretor locus (Se). Secretor phenotypes can be detected in utero.2
To illustrate some additional points of concern for prenatal prediction, we present the following family (see figure). Initial testing indicates that the proband (III-1) is a non-secretor and his mother (11-2) must be doubly heterozygous. 1. 2.
1.
Collmann, R.
D.
Stoller,
A.
Am. J. publ. Hlth, 1962, 52,
813.
ROBERTA E. CHRISTIANSON
Insley, J., Bird, G. W G., Harper, P. S., Pearce, G. W. Lancet, 1976, i, 806. Harper, P. S., Bias, W. B., Hutchmson, J. R., McKusick, V.A. J. med. Genet. 1971, 8, 438.
TABLE I-PREVALENCE OF DOWN SYNDROME BY MATERNAL AGE AMONG SINGLE LIVE BIRTHS
TABLE II-PREVALENCE OF DOWN SYNDROME BY MATERNAL-AGE INTERVALS OF TWO YEARS AMONG SINGLE LIVE BIRTH