657
tinguishes it clearly from the biliary ducts and from the roots of the hepatic veins.2 We agree about the difficulty in visualising the splenic vein; this is because of the gas content of the stomach and the narrowness of the vessel. The splenic vein can be better studied with "real time" apparatus.3 Visualisation of the other large vessel that contribute to the portal trunk seems easier: the superior mesenteric vein is easily visualised in longitudinal scans and the junction with the portal trunk can often be seen
(fig. 2). The increased calibre of the portal vein in intrahepatic portal hypertension found on the ultrasonograms by Webb et al. is very interesting, suggesting that ultrasound can be used as a first approach in the diagnosis of portal hypertension. Is portal dilatation detectable by ultrasound when no other signs of
portal hypertension (e.g., oesophageal varices) are present? Diagnosis by non-invasive techniques is still not possible. Other applications of ultrasound in this area may be the demonstration of portacaval surgical anastomosis, more precise morphological evaluation of the vascular architecture, and, by Doppler methods, determination of the direction and velocity of blood-flow in the portal vein/ Clinica Medica I, Università di Bologna, Policlinico S. Orsola,
L. BOLONDI
Bologna, Italy Servizio di Endoscopia Digestiva, Ospedale M. Malpighi, Bologna
L. GANDOLFI
:" This letter has been shown lows.-ED. L.
to
Dr
Berger,
whose
reply
in atherosclerotic plaques of the cervical arteries, is of great interest, and we will try to confirm these findings with fibrinogen labelled with technetium-99m. The Stockholm group will learn, when they investigate their first case with complete obliteration of one carotid artery, that it is still visualised with 121 1-fibrinogen. Indeed, the vessels shown in fig. 2 in the region between the chin and the supraclavicular zone are not the arteries but the jugular veins. Studies with 1231-fibrinogen’ and with 99m-Tc-fibrinogen2 have shown that the arteries are visualised only during the first passage of the radioactive bolus; thereafter, because the venous blood pool is five times greater than the arterial one and because of the greater calibre of the veins, it is the venous network that is visualised and not the arterial one at the peri-
uptake
phery. a hot spot, such as the one presented in fig. is (right), only very indirect evidence of deposition of fibrinogen. We make the same mistake early in our experience with 99m-Tc-fibrinogen: enhanced activity at venous junctions is a common finding and only represents a greater blood volume. Nevertheless, the quantitative data presented are convincing, and there will be great interest in the method if these findings can be confirmed on a large scale.
Furthermore,
2
Department of Radiological and Physical Sciences, Academisch Ziekenhuis, Vrije Universiteit Brussel, 1090 Brussels, Belguim
M. H. JONCKHEER
fol-
structures in front of the vena cava in fig. 1 of the paper portal vein. It is not uncommon, when scanning a structure that follows a curved or tortuous course, to show two parts of it and not the intervening portion. On longitudinal scans in particular one frequently sees the portal vein in the porta hepatis and, separate from it, the extrahepatic portal vein superior to the pancreas. The differentiation of the portal vein from the gallbladder is not difficult, and we have never encountered this problem in several thousand scans: one is a discrete pear-shaped structure, and the other is tubular, receives tributaries, and branches. I agree with Dr Bolondi and Dr Gandolfi that one can scan obliquely to show the portal vein, though we have rarely found this necessary. In difficult cases we now routinely use the left lateral decubitus position which not only permits excellent visualisation but also shows the vessels close to their maximum size. I do not think that real-time ultrasound will significantly increase the rate of visualisation of the splenic vein. The problem is not in recognising the vessel, but in getting penetration through gas, and real time has as much difficulty here as conventional ultrasound. I agree that the superior mesenteric vein is easier to see than the splenic vein. We concentrated on the splenic and portal veins in our article because these veins are more commonly thrombosed than the superior mesenteric vein. I also agree about the ease of demonstrating portacaval shunts. We have shown nine out of the last ten that we have scanned.
SIRs,-Both
our
are
Main
X-ray Department, Royal Free Hospital, London
NW3
2QG
L. A. BERGER
GAMMA SCANNING FOR CAROTID-ARTERY
PLAQUES SiR,—The preliminary report by Dr Mettinger and his colleagues (Feb. 4, p. 242), who demonstrated 1231-fibrinogen 2. Carlsen, E. N., Filly, R.A.J. clin.Ultrasound, 1976, 4, 85. 3.Weill, F., Eisencher, A.J. Radiol.Electrol. 1976, 57, 311. 4.Goldberg, B. B., Patel, J.J. clin. Ultrasound, 1977, 5, 304.
CRITICAL EVALUATION OF ADENOIDECTOMY
S!R,—Much as I commend the use of prospective controlled studies in otorhinolaryngology, I wonder whether the paper by Mr Hibbert and Mr Stell (March 4, p. 489) really answers the main questions about the role and place of adenoidectomy. The patients studied were children whose main symptoms were attributable to tonsillar disease severe enough to merit tonsillectomy rather than children whose main symptoms were attributable to adenoid hypertrophy. Though there is controversy over what symptoms can be caused by adenoid hypertrophy, snoring, speech problems, and nasal obstruction were not the primary complaints in the children studied. Indeed the positive decision was made in one group not to perform adenoidectomy, presumably because the above symptoms were unimportant or because they were not thought to be due to adenoid hypertrophy. In the other group, where adenoidectomy was done with tonsillectomy, this may have been because the surgeon routinely did an adenoidectomy when performing a tonsillectomy rather than because the symptoms themselves indicated removal of the adenoids. If the aim of the study was to evaluate adenoidectomy it would have been better to study children with symptoms which indicated adenoidectomy without tonsillectomy, an operation not infrequently
performed. What Hibbert and Stell really assessed was whether was of value when performed with tonsillectomy for tonsillar disease. Even this question would have been better answered by taking a group of children on the waitinglist for tonsillectomy and adenoidectomy and then randomly allocating them either to have or not have adenoidectomy. Furthermore the follow-up of six weeks was surely too short for Hibbert and Stell to discount the value of adenoidectomy when performed with tonsillectomy, especially since the symptoms recorded are so subjective and episodic. The most important question remains unanswered. IS"
adenoidectomy
1. De Nardo, S. J., De Nardo, G. L. Sem. nucl. Med. 1977, 7, 245. 2. Jeghers, O., Abramovici, J., Jonckheer, M., Ermans, A. M. Eur. Med. (in the press).
J.
nucl.
658
adenoidectomy of value for the two main indications for adenoidectomy-nasal blockage and serous otitis media? In both of these conditions there are measurements and such studies would prove of inestimable value. Department of Otolaryngology, Royal Infirmary, Glasgow G4 0SF
CHECK-LIST OF DIURNAL SYMPTOMS
monitor,
to
G. G. BROWNING
IS BED WETTING PSYCHOLOGICAL?
SiR,—Your editorial response’ to Berg’s paperand others perpetuates many of the incomplete observations, unwarranted assumptions, and oversights which cloud the issue of enuresis. You uncritically accept or make the following assumptions: that the spontaneous-cure rate is 20% per annum; that most bedwetting children have normal radiographs and smallerthan-normal bladder capacities; and that physical factors, easily detected, seldom cause enuresis. And you ask "is the incontinence one symptom of a wider emotional disorder?" and is urgency, which night wetters are likely to have "a conditioned response which can be modified by behaviour therapy for the child--or its parents?" Since many enuretics achieve a dry bed by becoming nocturic and carry symptoms of frequency, urgency, and stress incontinence and prostatic problems3 and impotence4into adult life, a dry bed is an incomplete criterion of cure. Most wetters, particularly those with diurnal symptoms, have abnormal cystourethrograms, including reflux in about 10%.5-9 The enuretic’s bladder size is normal. 10 Premature detrusor contractions, irritation, produces a funcgenerally secondary to peripheral tional reduction in capacity. 11I The misconception that physical disease seldom causes enuresis-a misconception which underlies and largely explains untenable sociological and psychiatric hypotheses---derives from the belief, entirely erroneous,’ that negative physical and urinary examination ensures the absence of disease and from neglect of the weighty case for organic enuresis. 5-8, 11-14, 16 Physicians fail to appreciate the more subtle aspects of the spectrum of urethral disorders.’,12,14 and flow dynamics. 15 Exclusion of cases with gross disease, about which there is no controversy, leaves some 90% of wetters with associated diurnal symptoms (see table) while 10% have none that we can detect. Persistent daytime voiding invariably reflects organic disease-usually lower urinary tract, sometimes anorectal.11 Urological treatment relieves diurnal problems within weeks in about 85%,7 and, after a longer period, night wetting is improved in 50-75%7,8,12,14,16 of the patients. Sleep depth and factors we cannot detect or do not understand probably account for most of the 10% minority who have no symptoms during the day. Deep sleep, ignored in your editorial, is a central factor in both groups. 7,17 1. Lancet, 1977, ii, 1214. 2. Berg, I., Fielding, D., Meadow, R. Archs Dis. Childh. 1977, 52, 651. 3. Medical News J. Am. med.Ass. 1969, 209, 354. 4. Huhner, M., Disorders of the Sexual Function in Male and Female;
p. 210.
Philadelphia, 1928. 5. Brodny, M. L., Robins, S. A.J.Am. med.Ass. 1944, 126, 1000. 5. Fisher, O. D., Forsythe, W. I. Archs Dis. Childh. 1954, 29, 460. 7. Arnold, S. J. Postgrad med. 1968, 43, 191. 8. Arnold, S. J., Ginsburg, A. Urology, 1974, 4, 145. 9. Arnold, S. J., Ginsburg, A., Berg, R. ibid. 1973, 1, 397. 10. Troup, C. W., Hodgson, N. B.J. Urol. 1971, 105, 129. 11. Winsbury-White, H. P. in Textbook of Genito-urinary Surgery 12. 13. 14. 15. 16. 17.
H. P. Winsbury-White); p. 275. Edinburgh, 1948. Mahoney, D.T.J. Urol. 1971, 106, 1971. Arnold, S. J., Ginsburg, A. Postgrad med. 1975, 58, 73. Hendren, W. H.J. Urol. 1971, 106, 298. Ritter, R. C., Zinner, N. R., Paquin, A. J.J. Urol. 1964, Arnold, S. J., Ginsburg, A. Urology, 1973, 2, 1973. Pierce, C. M. Can. spychiat. Ass-J. 1963, 8, 415.
(edited by
That bute to
widely
a
factors
must
somehow
cause or
contri-
held but
unsupported belief. IS Urgency,
an
irritative
phenomenon not a conditioned reflex (to what?), does not warrant suggesting that child or parent requires behaviour modification therapy. Correction of voiding difficulties produces psychological benefits.’ One would expect parental and peer response to daytime wetting to create more behaviour disturbances than night wetting alone which is easier to hide. We agree that most children’s doctors can be confident diagnosis and management of enuresis-provided are aware of the limitations of your editorial. they S. J. ARNOLD 11 Pine Street, A. GINSBURG Morristown, New Jersey 079 60, U.S.A.
about the
DECUBITUS ULCERS AND AMYOTROPHIC LATERAL SCLEROSIS were intrigued by the Lancet correspondence on suggestion that pressure sores spare patients with amyotrophic lateral sclerosis (A.L.s.). At the Inglis House of Philadelphia, a chronic disease institution with nearly three hundred long-term residents having debilitating diseases such as paraplegia, quadriplegia, multiple sclerosis, Parkinson’s disease, and cerebral palsy, the prevalence of decubitus ulcers is 10% and this seldom varies, despite the annual turnover of fifty patients. A review of our records for the past decade, encompassing nearly eight hundred patients, revealed five residents with
SIR,-We
the
of whom had decubitus ulcers. The three who remained free of ulcers were a 44-year-old White woman whose disease ran a rapid downhill course and who died 3 years later; a 47-year-old woman who died 8 years after diagnosis of A.L.S.; and a 58-year-old man with A.L.S. for 10 years. A 41-year-old woman who had had A.L.s. for 17 years had decubitus ulcers over the sacrum 7 months before her death. A 41-year-old woman with A.L.S. for 21 years acquired a large decubitus ulcer over the sacrum 9 months ago. Examination confirms the neurological diagnosis, and histopathological examination of the ulcer and adjoining skin fits the appearances of specimens taken from other patients with decubitus ulcers. A.L.S. two
18.
91, 161.
psychological
persistent bedwetting and voiding difficulties remains
Shaffer, D.
in Bladder Control and Enuresis
(edited by I. Kolvin, R. C. Mac-
Keith, and S. R. Meadow); p. 133. London, 1973. 1. Forrester, J. M. Lancet, 1976, i, 970. 2. Furukawa, T. ibid. p. 862. 3. Furukawa, T., Toyokura, Y. ibid. Jan. 21, 1978, p. 159.
tinguishes it clearly from the biliary ducts and from the roots of the hepatic veins.2 We agree about the difficulty in visualising the splenic vein; this is because of the gas content of the stomach and the narrowness of the vessel. The splenic vein can be better studied with "real time" apparatus.3 Visualisation of the other large vessel that contribute to the portal trunk seems easier: the superior mesenteric vein is easily visualised in longitudinal scans and the junction with the portal trunk can often be seen
(fig. 2). The increased calibre of the portal vein in intrahepatic portal hypertension found on the ultrasonograms by Webb et al. is very interesting, suggesting that ultrasound can be used as a first approach in the diagnosis of portal hypertension. Is portal dilatation detectable by ultrasound when no other signs of
portal hypertension (e.g., oesophageal varices) are present? Diagnosis by non-invasive techniques is still not possible. Other applications of ultrasound in this area may be the demonstration of portacaval surgical anastomosis, more precise morphological evaluation of the vascular architecture, and, by Doppler methods, determination of the direction and velocity of blood-flow in the portal vein/ Clinica Medica I, Università di Bologna, Policlinico S. Orsola,
L. BOLONDI
Bologna, Italy Servizio di Endoscopia Digestiva, Ospedale M. Malpighi, Bologna
L. GANDOLFI
:" This letter has been shown lows.-ED. L.
to
Dr
Berger,
whose
reply
in atherosclerotic plaques of the cervical arteries, is of great interest, and we will try to confirm these findings with fibrinogen labelled with technetium-99m. The Stockholm group will learn, when they investigate their first case with complete obliteration of one carotid artery, that it is still visualised with 121 1-fibrinogen. Indeed, the vessels shown in fig. 2 in the region between the chin and the supraclavicular zone are not the arteries but the jugular veins. Studies with 1231-fibrinogen’ and with 99m-Tc-fibrinogen2 have shown that the arteries are visualised only during the first passage of the radioactive bolus; thereafter, because the venous blood pool is five times greater than the arterial one and because of the greater calibre of the veins, it is the venous network that is visualised and not the arterial one at the peri-
uptake
phery. a hot spot, such as the one presented in fig. is (right), only very indirect evidence of deposition of fibrinogen. We make the same mistake early in our experience with 99m-Tc-fibrinogen: enhanced activity at venous junctions is a common finding and only represents a greater blood volume. Nevertheless, the quantitative data presented are convincing, and there will be great interest in the method if these findings can be confirmed on a large scale.
Furthermore,
2
Department of Radiological and Physical Sciences, Academisch Ziekenhuis, Vrije Universiteit Brussel, 1090 Brussels, Belguim
M. H. JONCKHEER
fol-
structures in front of the vena cava in fig. 1 of the paper portal vein. It is not uncommon, when scanning a structure that follows a curved or tortuous course, to show two parts of it and not the intervening portion. On longitudinal scans in particular one frequently sees the portal vein in the porta hepatis and, separate from it, the extrahepatic portal vein superior to the pancreas. The differentiation of the portal vein from the gallbladder is not difficult, and we have never encountered this problem in several thousand scans: one is a discrete pear-shaped structure, and the other is tubular, receives tributaries, and branches. I agree with Dr Bolondi and Dr Gandolfi that one can scan obliquely to show the portal vein, though we have rarely found this necessary. In difficult cases we now routinely use the left lateral decubitus position which not only permits excellent visualisation but also shows the vessels close to their maximum size. I do not think that real-time ultrasound will significantly increase the rate of visualisation of the splenic vein. The problem is not in recognising the vessel, but in getting penetration through gas, and real time has as much difficulty here as conventional ultrasound. I agree that the superior mesenteric vein is easier to see than the splenic vein. We concentrated on the splenic and portal veins in our article because these veins are more commonly thrombosed than the superior mesenteric vein. I also agree about the ease of demonstrating portacaval shunts. We have shown nine out of the last ten that we have scanned.
SIRs,-Both
our
are
Main
X-ray Department, Royal Free Hospital, London
NW3
2QG
L. A. BERGER
GAMMA SCANNING FOR CAROTID-ARTERY
PLAQUES SiR,—The preliminary report by Dr Mettinger and his colleagues (Feb. 4, p. 242), who demonstrated 1231-fibrinogen 2. Carlsen, E. N., Filly, R.A.J. clin.Ultrasound, 1976, 4, 85. 3.Weill, F., Eisencher, A.J. Radiol.Electrol. 1976, 57, 311. 4.Goldberg, B. B., Patel, J.J. clin. Ultrasound, 1977, 5, 304.
CRITICAL EVALUATION OF ADENOIDECTOMY
S!R,—Much as I commend the use of prospective controlled studies in otorhinolaryngology, I wonder whether the paper by Mr Hibbert and Mr Stell (March 4, p. 489) really answers the main questions about the role and place of adenoidectomy. The patients studied were children whose main symptoms were attributable to tonsillar disease severe enough to merit tonsillectomy rather than children whose main symptoms were attributable to adenoid hypertrophy. Though there is controversy over what symptoms can be caused by adenoid hypertrophy, snoring, speech problems, and nasal obstruction were not the primary complaints in the children studied. Indeed the positive decision was made in one group not to perform adenoidectomy, presumably because the above symptoms were unimportant or because they were not thought to be due to adenoid hypertrophy. In the other group, where adenoidectomy was done with tonsillectomy, this may have been because the surgeon routinely did an adenoidectomy when performing a tonsillectomy rather than because the symptoms themselves indicated removal of the adenoids. If the aim of the study was to evaluate adenoidectomy it would have been better to study children with symptoms which indicated adenoidectomy without tonsillectomy, an operation not infrequently
performed. What Hibbert and Stell really assessed was whether was of value when performed with tonsillectomy for tonsillar disease. Even this question would have been better answered by taking a group of children on the waitinglist for tonsillectomy and adenoidectomy and then randomly allocating them either to have or not have adenoidectomy. Furthermore the follow-up of six weeks was surely too short for Hibbert and Stell to discount the value of adenoidectomy when performed with tonsillectomy, especially since the symptoms recorded are so subjective and episodic. The most important question remains unanswered. IS"
adenoidectomy
1. De Nardo, S. J., De Nardo, G. L. Sem. nucl. Med. 1977, 7, 245. 2. Jeghers, O., Abramovici, J., Jonckheer, M., Ermans, A. M. Eur. Med. (in the press).
J.
nucl.
658
adenoidectomy of value for the two main indications for adenoidectomy-nasal blockage and serous otitis media? In both of these conditions there are measurements and such studies would prove of inestimable value. Department of Otolaryngology, Royal Infirmary, Glasgow G4 0SF
CHECK-LIST OF DIURNAL SYMPTOMS
monitor,
to
G. G. BROWNING
IS BED WETTING PSYCHOLOGICAL?
SiR,—Your editorial response’ to Berg’s paperand others perpetuates many of the incomplete observations, unwarranted assumptions, and oversights which cloud the issue of enuresis. You uncritically accept or make the following assumptions: that the spontaneous-cure rate is 20% per annum; that most bedwetting children have normal radiographs and smallerthan-normal bladder capacities; and that physical factors, easily detected, seldom cause enuresis. And you ask "is the incontinence one symptom of a wider emotional disorder?" and is urgency, which night wetters are likely to have "a conditioned response which can be modified by behaviour therapy for the child--or its parents?" Since many enuretics achieve a dry bed by becoming nocturic and carry symptoms of frequency, urgency, and stress incontinence and prostatic problems3 and impotence4into adult life, a dry bed is an incomplete criterion of cure. Most wetters, particularly those with diurnal symptoms, have abnormal cystourethrograms, including reflux in about 10%.5-9 The enuretic’s bladder size is normal. 10 Premature detrusor contractions, irritation, produces a funcgenerally secondary to peripheral tional reduction in capacity. 11I The misconception that physical disease seldom causes enuresis-a misconception which underlies and largely explains untenable sociological and psychiatric hypotheses---derives from the belief, entirely erroneous,’ that negative physical and urinary examination ensures the absence of disease and from neglect of the weighty case for organic enuresis. 5-8, 11-14, 16 Physicians fail to appreciate the more subtle aspects of the spectrum of urethral disorders.’,12,14 and flow dynamics. 15 Exclusion of cases with gross disease, about which there is no controversy, leaves some 90% of wetters with associated diurnal symptoms (see table) while 10% have none that we can detect. Persistent daytime voiding invariably reflects organic disease-usually lower urinary tract, sometimes anorectal.11 Urological treatment relieves diurnal problems within weeks in about 85%,7 and, after a longer period, night wetting is improved in 50-75%7,8,12,14,16 of the patients. Sleep depth and factors we cannot detect or do not understand probably account for most of the 10% minority who have no symptoms during the day. Deep sleep, ignored in your editorial, is a central factor in both groups. 7,17 1. Lancet, 1977, ii, 1214. 2. Berg, I., Fielding, D., Meadow, R. Archs Dis. Childh. 1977, 52, 651. 3. Medical News J. Am. med.Ass. 1969, 209, 354. 4. Huhner, M., Disorders of the Sexual Function in Male and Female;
p. 210.
Philadelphia, 1928. 5. Brodny, M. L., Robins, S. A.J.Am. med.Ass. 1944, 126, 1000. 5. Fisher, O. D., Forsythe, W. I. Archs Dis. Childh. 1954, 29, 460. 7. Arnold, S. J. Postgrad med. 1968, 43, 191. 8. Arnold, S. J., Ginsburg, A. Urology, 1974, 4, 145. 9. Arnold, S. J., Ginsburg, A., Berg, R. ibid. 1973, 1, 397. 10. Troup, C. W., Hodgson, N. B.J. Urol. 1971, 105, 129. 11. Winsbury-White, H. P. in Textbook of Genito-urinary Surgery 12. 13. 14. 15. 16. 17.
H. P. Winsbury-White); p. 275. Edinburgh, 1948. Mahoney, D.T.J. Urol. 1971, 106, 1971. Arnold, S. J., Ginsburg, A. Postgrad med. 1975, 58, 73. Hendren, W. H.J. Urol. 1971, 106, 298. Ritter, R. C., Zinner, N. R., Paquin, A. J.J. Urol. 1964, Arnold, S. J., Ginsburg, A. Urology, 1973, 2, 1973. Pierce, C. M. Can. spychiat. Ass-J. 1963, 8, 415.
(edited by
That bute to
widely
a
factors
must
somehow
cause or
contri-
held but
unsupported belief. IS Urgency,
an
irritative
phenomenon not a conditioned reflex (to what?), does not warrant suggesting that child or parent requires behaviour modification therapy. Correction of voiding difficulties produces psychological benefits.’ One would expect parental and peer response to daytime wetting to create more behaviour disturbances than night wetting alone which is easier to hide. We agree that most children’s doctors can be confident diagnosis and management of enuresis-provided are aware of the limitations of your editorial. they S. J. ARNOLD 11 Pine Street, A. GINSBURG Morristown, New Jersey 079 60, U.S.A.
about the
DECUBITUS ULCERS AND AMYOTROPHIC LATERAL SCLEROSIS were intrigued by the Lancet correspondence on suggestion that pressure sores spare patients with amyotrophic lateral sclerosis (A.L.s.). At the Inglis House of Philadelphia, a chronic disease institution with nearly three hundred long-term residents having debilitating diseases such as paraplegia, quadriplegia, multiple sclerosis, Parkinson’s disease, and cerebral palsy, the prevalence of decubitus ulcers is 10% and this seldom varies, despite the annual turnover of fifty patients. A review of our records for the past decade, encompassing nearly eight hundred patients, revealed five residents with
SIR,-We
the
of whom had decubitus ulcers. The three who remained free of ulcers were a 44-year-old White woman whose disease ran a rapid downhill course and who died 3 years later; a 47-year-old woman who died 8 years after diagnosis of A.L.S.; and a 58-year-old man with A.L.S. for 10 years. A 41-year-old woman who had had A.L.s. for 17 years had decubitus ulcers over the sacrum 7 months before her death. A 41-year-old woman with A.L.S. for 21 years acquired a large decubitus ulcer over the sacrum 9 months ago. Examination confirms the neurological diagnosis, and histopathological examination of the ulcer and adjoining skin fits the appearances of specimens taken from other patients with decubitus ulcers. A.L.S. two
18.
91, 161.
psychological
persistent bedwetting and voiding difficulties remains
Shaffer, D.
in Bladder Control and Enuresis
(edited by I. Kolvin, R. C. Mac-
Keith, and S. R. Meadow); p. 133. London, 1973. 1. Forrester, J. M. Lancet, 1976, i, 970. 2. Furukawa, T. ibid. p. 862. 3. Furukawa, T., Toyokura, Y. ibid. Jan. 21, 1978, p. 159.
