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A CLASSIFICATION OF TETANUS
261
high dietary insulinism
though high
consumption. The fact that the hyperaccompanied by normoglycasmia suggests that
sucrose
was
sucrose
intake is associated with increased insulin
production, the action of insulin is at the same time impaired. Department of Nutrition, Queen Elizabeth College, University of London.
STEPHEN SZANTO.
ŒSOPHAGEAL MOTILITY IN DIABETES years ago, when seeing a 42-year-old man with diabetic visceroneuropathy, it occurred to me that his gastric atony and symptoms such as nocturnal diarrhoea might be a result of vagal neuropathy. If this were so, I reasoned that resophageal function might also be deranged. I managed to secure the patient’s cooperation in the performance of oesophageal manometrics, which showed that lower cesophageal
SIR,ŇTwo
sphincter tone was strikingly diminished, and there was complete lack of peristalsis. This man did not have systemic sclerosis or any other disease known to simulate this cecophageal pattern. To date I have performed oesophageal motility tests on 20 diabetic patients (many have had cine studies as well (including those with visceroneuropathies, age-matched with patients with peripheral neuropathies and those without neuropathy. I have found a spectrum of abnormalities, the incidence and characteristics of which overlap somewhat from the visceral to the peripheral neuropathic category and to a lesser extent into the group without clinical neuropathy. The salient features are decreased lower oesophageal sphincter tone, aperistalsis, altered amplitude contractions, and tertiary activity. A prominent contractile component of the lower oesophageal sphincter was a feature in 3 patients-one of whom was given methacholine (’ Mecholyl ’) and responded positively with pain and increased resophageal pressure. The oesophagus is a fairly accessible organ and, with wellstandardised manometric techniques, merits further attention in diabetic neuropathy. This may be an avenue toward better pathophysiological understanding of the disease. Department of Medicine, Johns Hopkins Hospital, 601 North
Broadway,
Baltimore, Maryland
21205.
WILLIAM M. COBURN, Jr.
A CLASSIFICATION OF TETANUS SIR,-It was interesting to read Dr. Phillip’s notational system for classification of tetanus and recording the progress of the disease.l Dr. Phillips divides various factors which he feels affect the prognosis into two groups--one determining the severity and the other determining the course. In fact the only difference between the factors of the two groups is that those of the first group do not change, while those of the second group change from time to time during the course of the disease. However, the factors in both groups determine severity and affect prognosis, and to that extent the separation of factors into two groups is artificial. We should have liked Dr. Phillips to have included period of onset-a very important factor, which determines the severity, 2-5 have course, and prognosis of the disease. Many workers that the shorter the reported period of onset the worse is the Phillips, L. A. Lancet, 1967, i, 1216. Cole, L. ibid. 1940, i, 164; Br. med. J. 1953, i, 150. Diaz Rivera, R. S., Deliz, L. R., Berio Suarez, J. J. Am. med. Ass. 1948, 138, 191. Khosla, H. L., Bhatt, A. H. J. Indian med. Ass. 1953, 22, 52. 3. Patel, J. C., Mehta, B. C., Modi, K. N. Proceedings of the First International Conference on Tetanus; p. 181. The Study Group of Tetanus, Bombay, 1965. 4. Ramsay, A. M., France, E. M., Dempsey, B. M. Lancet, 1956, ii, 548. Spaeth, R. Am. J. Dis. Child. 1940, 60, 130. Srivastava, S. P., Chatterji, G. C. J. Indian med. Ass. 1961, 36, 289. 5. Veronesi, R. Am. J. med. Sci. 1956, 232, 629. Yodh, B. B. Br. med. J. 1937, i, 855. Yodh, B. B., Shah, S. N. J. Ass. Physns India, 1956, 4, 337.
1. 2.
prognosis. Those patients who do not develop spasms almost always recover irrespective of other factors.3 We fail to understand the reasons for omission of this important factor from both the groups of indices proposed by Dr. Phillips. Complicating factors mentioned by Dr. Phillips contribute to the morbidity and mortality directly and not by altering the severity of the disease. His system suggests that trismus, generalised stiffness, opisthotonus, and limited spasms determine the course of the disease. In our experience these factors do not affect the prognosis, though they may increase the morbidity. Dr. Phillips claims that his proposed severity index " cannot change after admission as can Patel and Joag’s classification ".6e However, a patient with tetanus having the minimum score of 4 by Dr. Phillips’ severity index may have a course index of 2 on one day which may increase to 30 next day. In such a patient the ultimate outcome is determined by course index (variable from hour to hour) rather than by severity index. Each of the factors affecting the severity and the course have complex relations with one another. Presence of various combinations are worse than each factor in isolation. Dr. Phillips’ notational system, like that of Vaishnava et al.,7 is too simple to take care of this possibility. Tetanus Ward, J. C. PATEL King Edward Memorial Hospital, Bombay,
India.
B. C. MEHTA.
COMPULSIVE SALT INTAKE AND ŒDEMA SIR,-More attention has been paid to the study of salt excretion than to salt intake in order to find an explanation of idiopathic oedema. There is good evidence that sodium intake is regulated by the sensitivity of the receptor area8 by harmodynamic and osmotic impulses from the internal environment,9 and by central cortical and subcortical regulation.1o Among 26 patients with idiopathic oedema’1 we had 2 patients (a woman of 30 and a man of 42) who were strikingly different from the others. While all the other patients had very low sodium excretion and urinary sodium/potassium ratio with striking postural hyperaugmentation of aldosterone excretion in comparison with the control group,12 these 2 patients had pronounced oedema in the presence of a high urinary sodium excretion without saluretics (between 90 and 310 mEq. sodium a day) on an assumed restricted sodium intake equivalent to 30 mEq. a day; they had a low aldosterone excretion (1-4 and 3-0 (1.g. per day). In 1 of these 2 patients we found histologically a degranulation of the juxtaglomerular cells and a very striking hyperreactivity to the pressor effect of angiotensin-findings consistent with suppression of the renin/ angiotensin system. Excessive uncontrolled salt intake not admitted by the patients in their histories was discovered in a balance study. Both patients considered a diet of 100 mEq. sodium a day as very low in salt content and admitted that they consumed very much more salt in their food. Both patients had developed oedema and started using saluretics years before admission to hospital. But the effect of saluretics (as much as 250 mg. hydrochlorothiazide) soon tailed off. 1 of the 2 patients could be maintained in relatively good, but not oedema-free, condition by an injection of a mercurial diuretic every second day, and had a sodium excretion of 100-200 mEq. on the day without and 940 mEq. on the day with this diuretic; average daily sodium excretion over 3 weeks was 529 mEq. per day. Both patients were evidently psychopathic. The 1st patient described her need for salt as compulsive, " feeling bad " if salt was restricted. She had an electroencephalogram suspicious of a subcortical lesion and the disease later progressed to a Patel, J. C., Joag, G. C. Indian J. med. Sci. 1959, 13, 834. Vaishnava, H., Goyal, R. K., Neogy, C. N., Mathur, G. P. Lancet, 1966, ii, 1371. 8. Henkin, R. I., Gill, J. R., Jr., Bartter, F. C. J. clin. Invest. 1963, 42, 727. 9. Nováková, A., Cort, J. H. Am. J. Physiol. 1966, 211, 919. 10. Cort, J. H. Electrolytes Fluid Dynamics and the Nervous System. Prague, 1965. 11. Küchel, O., Horky, K. Sbo. lék. 1966, 68, 353. 12. Küchel, O., Horky, K., Gregorová, I., Havlová, A. ibid. (in the press). 6. 7.
high dietary insulinism
though high
consumption. The fact that the hyperaccompanied by normoglycasmia suggests that
sucrose
was
sucrose
intake is associated with increased insulin
production, the action of insulin is at the same time impaired. Department of Nutrition, Queen Elizabeth College, University of London.
STEPHEN SZANTO.
ŒSOPHAGEAL MOTILITY IN DIABETES years ago, when seeing a 42-year-old man with diabetic visceroneuropathy, it occurred to me that his gastric atony and symptoms such as nocturnal diarrhoea might be a result of vagal neuropathy. If this were so, I reasoned that resophageal function might also be deranged. I managed to secure the patient’s cooperation in the performance of oesophageal manometrics, which showed that lower cesophageal
SIR,ŇTwo
sphincter tone was strikingly diminished, and there was complete lack of peristalsis. This man did not have systemic sclerosis or any other disease known to simulate this cecophageal pattern. To date I have performed oesophageal motility tests on 20 diabetic patients (many have had cine studies as well (including those with visceroneuropathies, age-matched with patients with peripheral neuropathies and those without neuropathy. I have found a spectrum of abnormalities, the incidence and characteristics of which overlap somewhat from the visceral to the peripheral neuropathic category and to a lesser extent into the group without clinical neuropathy. The salient features are decreased lower oesophageal sphincter tone, aperistalsis, altered amplitude contractions, and tertiary activity. A prominent contractile component of the lower oesophageal sphincter was a feature in 3 patients-one of whom was given methacholine (’ Mecholyl ’) and responded positively with pain and increased resophageal pressure. The oesophagus is a fairly accessible organ and, with wellstandardised manometric techniques, merits further attention in diabetic neuropathy. This may be an avenue toward better pathophysiological understanding of the disease. Department of Medicine, Johns Hopkins Hospital, 601 North
Broadway,
Baltimore, Maryland
21205.
WILLIAM M. COBURN, Jr.
A CLASSIFICATION OF TETANUS SIR,-It was interesting to read Dr. Phillip’s notational system for classification of tetanus and recording the progress of the disease.l Dr. Phillips divides various factors which he feels affect the prognosis into two groups--one determining the severity and the other determining the course. In fact the only difference between the factors of the two groups is that those of the first group do not change, while those of the second group change from time to time during the course of the disease. However, the factors in both groups determine severity and affect prognosis, and to that extent the separation of factors into two groups is artificial. We should have liked Dr. Phillips to have included period of onset-a very important factor, which determines the severity, 2-5 have course, and prognosis of the disease. Many workers that the shorter the reported period of onset the worse is the Phillips, L. A. Lancet, 1967, i, 1216. Cole, L. ibid. 1940, i, 164; Br. med. J. 1953, i, 150. Diaz Rivera, R. S., Deliz, L. R., Berio Suarez, J. J. Am. med. Ass. 1948, 138, 191. Khosla, H. L., Bhatt, A. H. J. Indian med. Ass. 1953, 22, 52. 3. Patel, J. C., Mehta, B. C., Modi, K. N. Proceedings of the First International Conference on Tetanus; p. 181. The Study Group of Tetanus, Bombay, 1965. 4. Ramsay, A. M., France, E. M., Dempsey, B. M. Lancet, 1956, ii, 548. Spaeth, R. Am. J. Dis. Child. 1940, 60, 130. Srivastava, S. P., Chatterji, G. C. J. Indian med. Ass. 1961, 36, 289. 5. Veronesi, R. Am. J. med. Sci. 1956, 232, 629. Yodh, B. B. Br. med. J. 1937, i, 855. Yodh, B. B., Shah, S. N. J. Ass. Physns India, 1956, 4, 337.
1. 2.
prognosis. Those patients who do not develop spasms almost always recover irrespective of other factors.3 We fail to understand the reasons for omission of this important factor from both the groups of indices proposed by Dr. Phillips. Complicating factors mentioned by Dr. Phillips contribute to the morbidity and mortality directly and not by altering the severity of the disease. His system suggests that trismus, generalised stiffness, opisthotonus, and limited spasms determine the course of the disease. In our experience these factors do not affect the prognosis, though they may increase the morbidity. Dr. Phillips claims that his proposed severity index " cannot change after admission as can Patel and Joag’s classification ".6e However, a patient with tetanus having the minimum score of 4 by Dr. Phillips’ severity index may have a course index of 2 on one day which may increase to 30 next day. In such a patient the ultimate outcome is determined by course index (variable from hour to hour) rather than by severity index. Each of the factors affecting the severity and the course have complex relations with one another. Presence of various combinations are worse than each factor in isolation. Dr. Phillips’ notational system, like that of Vaishnava et al.,7 is too simple to take care of this possibility. Tetanus Ward, J. C. PATEL King Edward Memorial Hospital, Bombay,
India.
B. C. MEHTA.
COMPULSIVE SALT INTAKE AND ŒDEMA SIR,-More attention has been paid to the study of salt excretion than to salt intake in order to find an explanation of idiopathic oedema. There is good evidence that sodium intake is regulated by the sensitivity of the receptor area8 by harmodynamic and osmotic impulses from the internal environment,9 and by central cortical and subcortical regulation.1o Among 26 patients with idiopathic oedema’1 we had 2 patients (a woman of 30 and a man of 42) who were strikingly different from the others. While all the other patients had very low sodium excretion and urinary sodium/potassium ratio with striking postural hyperaugmentation of aldosterone excretion in comparison with the control group,12 these 2 patients had pronounced oedema in the presence of a high urinary sodium excretion without saluretics (between 90 and 310 mEq. sodium a day) on an assumed restricted sodium intake equivalent to 30 mEq. a day; they had a low aldosterone excretion (1-4 and 3-0 (1.g. per day). In 1 of these 2 patients we found histologically a degranulation of the juxtaglomerular cells and a very striking hyperreactivity to the pressor effect of angiotensin-findings consistent with suppression of the renin/ angiotensin system. Excessive uncontrolled salt intake not admitted by the patients in their histories was discovered in a balance study. Both patients considered a diet of 100 mEq. sodium a day as very low in salt content and admitted that they consumed very much more salt in their food. Both patients had developed oedema and started using saluretics years before admission to hospital. But the effect of saluretics (as much as 250 mg. hydrochlorothiazide) soon tailed off. 1 of the 2 patients could be maintained in relatively good, but not oedema-free, condition by an injection of a mercurial diuretic every second day, and had a sodium excretion of 100-200 mEq. on the day without and 940 mEq. on the day with this diuretic; average daily sodium excretion over 3 weeks was 529 mEq. per day. Both patients were evidently psychopathic. The 1st patient described her need for salt as compulsive, " feeling bad " if salt was restricted. She had an electroencephalogram suspicious of a subcortical lesion and the disease later progressed to a Patel, J. C., Joag, G. C. Indian J. med. Sci. 1959, 13, 834. Vaishnava, H., Goyal, R. K., Neogy, C. N., Mathur, G. P. Lancet, 1966, ii, 1371. 8. Henkin, R. I., Gill, J. R., Jr., Bartter, F. C. J. clin. Invest. 1963, 42, 727. 9. Nováková, A., Cort, J. H. Am. J. Physiol. 1966, 211, 919. 10. Cort, J. H. Electrolytes Fluid Dynamics and the Nervous System. Prague, 1965. 11. Küchel, O., Horky, K. Sbo. lék. 1966, 68, 353. 12. Küchel, O., Horky, K., Gregorová, I., Havlová, A. ibid. (in the press). 6. 7.