- Email: [email protected]
TETANUS: A DILEMMA PROLONGED
435
dramatic fall in gastric secretion to subnormal levels following bilateral vagotomy and pyloroplasty only. The patient became symptom-free and stayed so for twelve months, but thereafter
multiple
peptic ulceration recurred,
sites of
and secretion
climbed back to its previous level. Had the tumour tissue in the pancreas been too small to detect (which it was not) at the
intervening period one could have assuming that the effect of vagotomy on a benign situation. Finally, Mr. Lawrie and his colleagues might have explained what they mean by oxyntic-cell hyperplasia in the and distal parts of the stomach of their " proximal, middle, original operation,
"
"
Were, in fact, absolute cell-counts made, and if what method ?
case.
Clinical Research Office, Gastro-intestinal Unit, Western General Hospital,
so
by
W. SIRCUS.
4.
of tetanus." The position is not quite as gloomy as you suggest. In 1964 the Ministry of Health gave official recognition to the recommendations of an Advisory Group on Protection against Tetanus.’ The group stated that the use of antitoxin should be considered in certain types of wound, and suggested that it was not reasonable to require that every person who had received trivial injuries should be given either antitoxin or antibiotics. We have thus been finally delivered from the ridiculous position of having to overtreat large numbers of patients for fear of litigation should they develop tetanus. Admittedly this now places the onus of decision on the doctor, who has to decide which patients should receive antibiotic prophylaxis, and which, if any, should receive antitetanus serum (A.T.S.). These decisions are not always easy, and in fairness to junior medical staff every casualty department should have a policy, albeit a tentative one, for dealing with various types of injuries. An example of such a policy was outlined recently by Laurence et al.,2but there is clearly scope for individual variation. Any satisfactory scheme of prophylaxis against tetanus depends on a knowledge of the immune state of the patient. The routine injection of toxoid for all injuries irrespective of the immune state will probably eventually lead to trouble from reactions to toxoid. The lack of knowledge of the immune state of most patients does, as you suggest, constitute a major difficulty, and personal cards have a habit of going astray. This underlines the advisability of a National Health card on the lines of the identity cards used during the 1939-45 war. Such cards should be made compulsory for all patients receiving treatment under the National Health Service, and could forge a useful link between the three branches of the N.H.S. There is one comforting aspect to this problem which you do not mention: the success of treatment of established tetanus in specialist centres. In Leeds, for example, there have been over 40 consecutive cases of tetanus without a death. This high success-rate must remove much of the fear of this disease, provided that a policy for prompt transfer of tetanus cases is adopted. In this hospital group the medical staff committee has agreed that all cases of tetanus shall be admitted under one consultant, and this consultant has arranged that when the diagnosis is confirmed and the patient’s condition is stabilised the case will be transferred to a tetanus
delay.
The knowledge that with adequate
treatment
this disease has
a very low mortality must, I suggest, be part of the background against which a policy of prevention is formulated. But it is essential to have a prearranged treatment programme, because 1. See Lancet, 1964, ii, 196. 2. Laurence, D. R., Evans, D.
G., Smith, J.
W G. Br. med.
J. 1966, i,
DISACCHARIDES AND CŒLIAC DISEASE
SIR,-We have read with great interest the article by Mr. Arthur and his colleagues (Jan. 22) on the advantage of excluding not only gluten but also lactose and sucrose from the diet of children with coeliac disease. Our experience is very similar. As we have shown jointlyit takes several months of glutenfree diet before the decreased activity of the intestinal disaccharidases returns towards normal values. Since lactase is more depressed and recovers less rapidly than the other disaccharidase activities, we feel that the exclusion of lactose from the diet during the first few weeks of the dietary treatment is really important, and explains the old experience of good results with the lactose-poor Eiweiss-Milch (protein-
SIR,-In your leading article (Jan. 29) you write: "Thus there is little comfort for the doctor faced with the possibility
without
Glamorgan, South Wales.
activity
TETANUS: A DILEMMA PROLONGED
unit
’
in the
been misled into secretion indicated
Edinburgh,
of tetanus tend to be admitted into different departments of a hospital, and serious delay in transfer may occur because of the lack of an agreed policy. Bridgend General Hospital, A. W. FOWLER.
cases
33.
milk).2 We doubt, however, whether deficiency of intestinal disaccharidases is the main cause of the increased disacchariduria found in these children. The small fraction of the disaccharides which passes unhydrolysed through the intestinal mucosa is completely excreted in the urine. It may be abnormally large because of increased disaccharide concentration in the intestinal lumen,3 or because of a structurally damaged mucosa. The disaccharide concentration in the intestinal lumen is certainly higher if the disaccharidase activity in the mucosal cells is reduced. But we feel that this mechanism plays a minor role compared to the effect of the mucosal atrophy found in children with cceliac disease. This assumption is based on our experience with patients who have a congenital deficiency of sucrase and isomaltase with normal mucosal anatomy-3 The disacchariduria found in these patients before as well as during sucrose-tolerance tests is within normal limits.’ The same is true in patients with selective lactase deficiency as long as the mucosa is structurally intact. We suggest therefore that increased disacchariduria reflects more the mucosal atrophy than the disaccharidase
deficiencv. University Pædiatric Department, Kinderspital, Zurich, Switzerland
A. PRADER D. H. SHMERLING B. HADORN.
SiR,ňIwas very interested to read in the article by Dr. Arthur and his colleagues that vomiting and weight loss were the outstanding symptoms in their patients with coeliac disease and associated disaccharide intolerance. This presentation is not limited, of course, to cases with this complication. My own child, who also presented with these symptoms and initially without overt steatorrhcea, never showed any intolerance to lactose or sucrose, and made the usual dramatic response to a gluten-free diet. He has, however, shown intolerance in addition to that to wheat and rye gluten, in that he relapsed on the introduction into his diet of oat porridge and pearl barley. Oats caused only a mild steatorrhoea, while barley produced a recurrence of vomiting, and mood change as well. He remitted on withdrawal of these cereals, and relapsed again on reintroduction of oat porridge. I was therefore surprised to find that gluten-free diets from three hospitals and five food manufacturers, and in the book by Dixon,6 include oat products and barley as freely permitted foods. The only gluten-free diet that excludes oat and barley D. H., Auricchio, S., Rubino, A., Hadorn, B., Prader, A. Helv. pœdiat. Acta, 1964, 19, 507. 2. Fanconi, G. Schweiz. med. Wschr. 1928, 58, 789. 3. Sterk, V. V., Kretchmer, N. Pediatrics, Springfield, 1964, 34, 609. 4. Auricchio, S., Prader, A., Murset, G., Witt, G. Helv. pœdiat. Acta, 1.
Shmerling,
1961, 16, 483. 5. Auricchio, S., Rubino, A., Prader, A., Rey, J., Jos, J., Frézal, J., Davidson, M. J. Pediat. 1965, 66, 555. 6. Dixon, D J W Diets for Sick Children. Oxford, 1965.
dramatic fall in gastric secretion to subnormal levels following bilateral vagotomy and pyloroplasty only. The patient became symptom-free and stayed so for twelve months, but thereafter
multiple
peptic ulceration recurred,
sites of
and secretion
climbed back to its previous level. Had the tumour tissue in the pancreas been too small to detect (which it was not) at the
intervening period one could have assuming that the effect of vagotomy on a benign situation. Finally, Mr. Lawrie and his colleagues might have explained what they mean by oxyntic-cell hyperplasia in the and distal parts of the stomach of their " proximal, middle, original operation,
"
"
Were, in fact, absolute cell-counts made, and if what method ?
case.
Clinical Research Office, Gastro-intestinal Unit, Western General Hospital,
so
by
W. SIRCUS.
4.
of tetanus." The position is not quite as gloomy as you suggest. In 1964 the Ministry of Health gave official recognition to the recommendations of an Advisory Group on Protection against Tetanus.’ The group stated that the use of antitoxin should be considered in certain types of wound, and suggested that it was not reasonable to require that every person who had received trivial injuries should be given either antitoxin or antibiotics. We have thus been finally delivered from the ridiculous position of having to overtreat large numbers of patients for fear of litigation should they develop tetanus. Admittedly this now places the onus of decision on the doctor, who has to decide which patients should receive antibiotic prophylaxis, and which, if any, should receive antitetanus serum (A.T.S.). These decisions are not always easy, and in fairness to junior medical staff every casualty department should have a policy, albeit a tentative one, for dealing with various types of injuries. An example of such a policy was outlined recently by Laurence et al.,2but there is clearly scope for individual variation. Any satisfactory scheme of prophylaxis against tetanus depends on a knowledge of the immune state of the patient. The routine injection of toxoid for all injuries irrespective of the immune state will probably eventually lead to trouble from reactions to toxoid. The lack of knowledge of the immune state of most patients does, as you suggest, constitute a major difficulty, and personal cards have a habit of going astray. This underlines the advisability of a National Health card on the lines of the identity cards used during the 1939-45 war. Such cards should be made compulsory for all patients receiving treatment under the National Health Service, and could forge a useful link between the three branches of the N.H.S. There is one comforting aspect to this problem which you do not mention: the success of treatment of established tetanus in specialist centres. In Leeds, for example, there have been over 40 consecutive cases of tetanus without a death. This high success-rate must remove much of the fear of this disease, provided that a policy for prompt transfer of tetanus cases is adopted. In this hospital group the medical staff committee has agreed that all cases of tetanus shall be admitted under one consultant, and this consultant has arranged that when the diagnosis is confirmed and the patient’s condition is stabilised the case will be transferred to a tetanus
delay.
The knowledge that with adequate
treatment
this disease has
a very low mortality must, I suggest, be part of the background against which a policy of prevention is formulated. But it is essential to have a prearranged treatment programme, because 1. See Lancet, 1964, ii, 196. 2. Laurence, D. R., Evans, D.
G., Smith, J.
W G. Br. med.
J. 1966, i,
DISACCHARIDES AND CŒLIAC DISEASE
SIR,-We have read with great interest the article by Mr. Arthur and his colleagues (Jan. 22) on the advantage of excluding not only gluten but also lactose and sucrose from the diet of children with coeliac disease. Our experience is very similar. As we have shown jointlyit takes several months of glutenfree diet before the decreased activity of the intestinal disaccharidases returns towards normal values. Since lactase is more depressed and recovers less rapidly than the other disaccharidase activities, we feel that the exclusion of lactose from the diet during the first few weeks of the dietary treatment is really important, and explains the old experience of good results with the lactose-poor Eiweiss-Milch (protein-
SIR,-In your leading article (Jan. 29) you write: "Thus there is little comfort for the doctor faced with the possibility
without
Glamorgan, South Wales.
activity
TETANUS: A DILEMMA PROLONGED
unit
’
in the
been misled into secretion indicated
Edinburgh,
of tetanus tend to be admitted into different departments of a hospital, and serious delay in transfer may occur because of the lack of an agreed policy. Bridgend General Hospital, A. W. FOWLER.
cases
33.
milk).2 We doubt, however, whether deficiency of intestinal disaccharidases is the main cause of the increased disacchariduria found in these children. The small fraction of the disaccharides which passes unhydrolysed through the intestinal mucosa is completely excreted in the urine. It may be abnormally large because of increased disaccharide concentration in the intestinal lumen,3 or because of a structurally damaged mucosa. The disaccharide concentration in the intestinal lumen is certainly higher if the disaccharidase activity in the mucosal cells is reduced. But we feel that this mechanism plays a minor role compared to the effect of the mucosal atrophy found in children with cceliac disease. This assumption is based on our experience with patients who have a congenital deficiency of sucrase and isomaltase with normal mucosal anatomy-3 The disacchariduria found in these patients before as well as during sucrose-tolerance tests is within normal limits.’ The same is true in patients with selective lactase deficiency as long as the mucosa is structurally intact. We suggest therefore that increased disacchariduria reflects more the mucosal atrophy than the disaccharidase
deficiencv. University Pædiatric Department, Kinderspital, Zurich, Switzerland
A. PRADER D. H. SHMERLING B. HADORN.
SiR,ňIwas very interested to read in the article by Dr. Arthur and his colleagues that vomiting and weight loss were the outstanding symptoms in their patients with coeliac disease and associated disaccharide intolerance. This presentation is not limited, of course, to cases with this complication. My own child, who also presented with these symptoms and initially without overt steatorrhcea, never showed any intolerance to lactose or sucrose, and made the usual dramatic response to a gluten-free diet. He has, however, shown intolerance in addition to that to wheat and rye gluten, in that he relapsed on the introduction into his diet of oat porridge and pearl barley. Oats caused only a mild steatorrhoea, while barley produced a recurrence of vomiting, and mood change as well. He remitted on withdrawal of these cereals, and relapsed again on reintroduction of oat porridge. I was therefore surprised to find that gluten-free diets from three hospitals and five food manufacturers, and in the book by Dixon,6 include oat products and barley as freely permitted foods. The only gluten-free diet that excludes oat and barley D. H., Auricchio, S., Rubino, A., Hadorn, B., Prader, A. Helv. pœdiat. Acta, 1964, 19, 507. 2. Fanconi, G. Schweiz. med. Wschr. 1928, 58, 789. 3. Sterk, V. V., Kretchmer, N. Pediatrics, Springfield, 1964, 34, 609. 4. Auricchio, S., Prader, A., Murset, G., Witt, G. Helv. pœdiat. Acta, 1.
Shmerling,
1961, 16, 483. 5. Auricchio, S., Rubino, A., Prader, A., Rey, J., Jos, J., Frézal, J., Davidson, M. J. Pediat. 1965, 66, 555. 6. Dixon, D J W Diets for Sick Children. Oxford, 1965.