- Email: [email protected]
APPEAL TO DOCTORS
196 6. The power of infecting exists firmed disease, and even for about death of the animal.
every period of twenty-four hours at
the conafter the
I find it dffhcult to believe that the virus does not get into the circulation every time someone is bitten by a rabid animal, and I believe that there is an inherent biological probability that this is the route of infection of the central nervous system as well as the heart, pancreas, salivary elands, &c. Department of Pathology, Joyce Green Hospital, J. C. BURNE. Dartford, Kent.
APPEAL TO DOCTORS
SIR,-II appreciated Sir George Thomson’s appeal (Dec. 20, p. 1353). It was timely and pertinent. He a modification of our accepted code of ethics is needed,and implies that religious considerations are " non-medical ", and not only irrelevant but also
suggests that
dangerous. Science (including medicine) cannot make value judgments, but only factual ones.l One of the great values of the Christian ethic is that it is an independent outside authority to guide and control the application of our scientific knowledge. This is an unfashionable view, but a valid and practical one.2 The Christian medical ethic has been summarised as two principles 3-to save life, and to relieve suffering. Our scientific enthusiasm is easily applied to the first, and leads to a harshness that may even increase suffering unless controlled by the second. This second principle is not easily defined in scientific (or legal) terms, but needs to be applied just as openly. To do so, the doctor must have the full confidence of patient and relatives; and it is this aspect of our professional behaviour that is most in danger and is in most need of modification or restoration. These two rules do not pretend to form an all-embracing code which provides easy answers to every problem, but they are guidelines on which we are to base our judgments. Again it needs to be emphasised that these are not factual, but value judgments, requiring wisdom as well as knowledge. As such they are hard to bring into the overcrowded curriculum of our medical schools, but it is at this level that there is a further need for our professional awareness to be awakened and fostered. Children’s Orthopedic Hospital and Medical Center, R. C. M. COOK. Seattle, Washington.
IDIOPATHIC THROMBOCYTOPENIC PURPURA AND LOW BLOOD-IODINE SIR,-A patient with well-authenticated thrombocytopenic purpura has been under hospital care for ten years; during this time she has had a splenectomy. Her thrombocyte-count has varied between 10,000 and 63,000 per c.mm. At intervals she has been subject to purpura, rectal and vaginal bleeding, and severe anaernia. These were not usually related to falls in the thrombocyte-count. For severe episodes of anxmia she has had a total of three blood-transfusions, usually with very temporary benefit. She is an obese, rather lethargic, person. Although she not clinically hypothyroid this diagnosis was considered possible; blood was taken for a protein-bound iodine (P.B.I.), and she was put on thyroid extract, which had no effect.
was
The P.B.I. was later reported as 0-7 g. per 100 ml. Either this was erroneous or the patient ought to have been in hypothyroid coma-which she was not. She still had purpura and anaemia, neither of which was improving. It was felt that the low blood-iodine had nothing to do with the thyroid gland, and that there was some disturbance of iodine metabolism of a different nature. Potassium iodide, 320 mg. twice daily, was given and-here is the of interest-very quickly the bleeding stopped and the purpura and ansemia cleared up. After 12 weeks a further P.B.I. was reported as 30 g. per 100 ml. So far there has been no recurrence of purpura or bleeding. I myself would like to check the P.B.I. in every patient with thrombocytopenic purpura and assess the value of potassium iodide in each case (the drug can have no adverse effects in the dosage used). This is not practicable since cases are only rarely seen; but it is suggested that this should be done throughout the country by physicians who have such patients. It may well be that the low P.B.I. and the clinical response to iodine were fortuitous, and that the patient was getting over a phase of purpura; but in such a puzzling disorder this simple line of investigation is surely worth
point
further consideration. St.
Mary’s Hospital, Colchester, Essex.
TREATMENT OF ACUTE PORPHYRIA VARIEGATA WITH PROPRANOLOL SIR,-Many of the symptoms of acute porphyria result from hyperactivity of the adrenergic system.1-3 It has been suggested that adrenergic-blocking agents may be beneficial in the acute attack,3 and this was strikingly confirmed in a
patient with porphyria variegata. The patient, a woman of 26, was admitted to the hospital because of severe, diffuse abdominal pain of several days duration, accompanied by nausea and vomiting. For the past 7 years she had had severe itching of the exposed parts of her skin during the summer months and also during pregnancy. The itching was at times associated with small blisters. During the same period she had noted that her urine was at times brownish-red in colour. On admission the patient looked sick and was emotionally labile. Her pulse-rate was 150 per minute, and her bloodpressure 150/90 mm. Hg. The abdomen was extremely tender, and there was rebound tenderness in the lower part of the abdomen with splashing sounds on auscultation. The exposed parts of her skin showed hyperpigmentation, small areas of hypopigmentation, and some blisters. Abnormal neurological signs, both central and peripheral, were noted. Her urine had an unusual reddish-brown colour and contained proteins and 20-30 red-cells, many white-cells, and many granular and hyaline casts per high power field. Her blood-urea was 90 mg. per 100 ml. A Watson-Schwartz test for porphobilinogen was strongly positive. Additional laboratory examinations confirmed the diagnosis of por-
phyria variegata. Her clinical course was marked by continuous severe abdominal pain, vomiting, paralytic ileus and periods of mental confusion and hallucinations. Very large amounts of pethidine and chlorpromazine were administered with little effect. On her 5th day in hospital, treatment with small doses of propranolol was started, and the clinical signs and symptoms abated. Since the 1.
2.
Bentley, G. B. Ethics in Medical Progress. London, 1966. Aldis, A. S. Science—Its Own Arbiter? Christian Medical Fellowship. London, 1967. 3. Jackson, D. MacG. The Sanctity of Life. London, 1962.
1. 2.
KENNETH HAZELL.
3.
propranolol, given by mouth,
Goldberg, A., Rimington, C. Diseases of Porphyrin Metabolism. Springfield, Illinois, 1962. Watson, C. J. in Cecil and Loeb’s Textbook of Medicine (edited by P. B. Beeson and W. McDermott). Philadelphia, 1963. Bock, K. D., Merguet, P., Schley, G., Schnemann, H. G., RauchStrooman, J. G., Hocevar, V., Schroeder, E., Murata, T. Dt. med. Wschr. 1968, 93, 2119.
every period of twenty-four hours at
the conafter the
I find it dffhcult to believe that the virus does not get into the circulation every time someone is bitten by a rabid animal, and I believe that there is an inherent biological probability that this is the route of infection of the central nervous system as well as the heart, pancreas, salivary elands, &c. Department of Pathology, Joyce Green Hospital, J. C. BURNE. Dartford, Kent.
APPEAL TO DOCTORS
SIR,-II appreciated Sir George Thomson’s appeal (Dec. 20, p. 1353). It was timely and pertinent. He a modification of our accepted code of ethics is needed,and implies that religious considerations are " non-medical ", and not only irrelevant but also
suggests that
dangerous. Science (including medicine) cannot make value judgments, but only factual ones.l One of the great values of the Christian ethic is that it is an independent outside authority to guide and control the application of our scientific knowledge. This is an unfashionable view, but a valid and practical one.2 The Christian medical ethic has been summarised as two principles 3-to save life, and to relieve suffering. Our scientific enthusiasm is easily applied to the first, and leads to a harshness that may even increase suffering unless controlled by the second. This second principle is not easily defined in scientific (or legal) terms, but needs to be applied just as openly. To do so, the doctor must have the full confidence of patient and relatives; and it is this aspect of our professional behaviour that is most in danger and is in most need of modification or restoration. These two rules do not pretend to form an all-embracing code which provides easy answers to every problem, but they are guidelines on which we are to base our judgments. Again it needs to be emphasised that these are not factual, but value judgments, requiring wisdom as well as knowledge. As such they are hard to bring into the overcrowded curriculum of our medical schools, but it is at this level that there is a further need for our professional awareness to be awakened and fostered. Children’s Orthopedic Hospital and Medical Center, R. C. M. COOK. Seattle, Washington.
IDIOPATHIC THROMBOCYTOPENIC PURPURA AND LOW BLOOD-IODINE SIR,-A patient with well-authenticated thrombocytopenic purpura has been under hospital care for ten years; during this time she has had a splenectomy. Her thrombocyte-count has varied between 10,000 and 63,000 per c.mm. At intervals she has been subject to purpura, rectal and vaginal bleeding, and severe anaernia. These were not usually related to falls in the thrombocyte-count. For severe episodes of anxmia she has had a total of three blood-transfusions, usually with very temporary benefit. She is an obese, rather lethargic, person. Although she not clinically hypothyroid this diagnosis was considered possible; blood was taken for a protein-bound iodine (P.B.I.), and she was put on thyroid extract, which had no effect.
was
The P.B.I. was later reported as 0-7 g. per 100 ml. Either this was erroneous or the patient ought to have been in hypothyroid coma-which she was not. She still had purpura and anaemia, neither of which was improving. It was felt that the low blood-iodine had nothing to do with the thyroid gland, and that there was some disturbance of iodine metabolism of a different nature. Potassium iodide, 320 mg. twice daily, was given and-here is the of interest-very quickly the bleeding stopped and the purpura and ansemia cleared up. After 12 weeks a further P.B.I. was reported as 30 g. per 100 ml. So far there has been no recurrence of purpura or bleeding. I myself would like to check the P.B.I. in every patient with thrombocytopenic purpura and assess the value of potassium iodide in each case (the drug can have no adverse effects in the dosage used). This is not practicable since cases are only rarely seen; but it is suggested that this should be done throughout the country by physicians who have such patients. It may well be that the low P.B.I. and the clinical response to iodine were fortuitous, and that the patient was getting over a phase of purpura; but in such a puzzling disorder this simple line of investigation is surely worth
point
further consideration. St.
Mary’s Hospital, Colchester, Essex.
TREATMENT OF ACUTE PORPHYRIA VARIEGATA WITH PROPRANOLOL SIR,-Many of the symptoms of acute porphyria result from hyperactivity of the adrenergic system.1-3 It has been suggested that adrenergic-blocking agents may be beneficial in the acute attack,3 and this was strikingly confirmed in a
patient with porphyria variegata. The patient, a woman of 26, was admitted to the hospital because of severe, diffuse abdominal pain of several days duration, accompanied by nausea and vomiting. For the past 7 years she had had severe itching of the exposed parts of her skin during the summer months and also during pregnancy. The itching was at times associated with small blisters. During the same period she had noted that her urine was at times brownish-red in colour. On admission the patient looked sick and was emotionally labile. Her pulse-rate was 150 per minute, and her bloodpressure 150/90 mm. Hg. The abdomen was extremely tender, and there was rebound tenderness in the lower part of the abdomen with splashing sounds on auscultation. The exposed parts of her skin showed hyperpigmentation, small areas of hypopigmentation, and some blisters. Abnormal neurological signs, both central and peripheral, were noted. Her urine had an unusual reddish-brown colour and contained proteins and 20-30 red-cells, many white-cells, and many granular and hyaline casts per high power field. Her blood-urea was 90 mg. per 100 ml. A Watson-Schwartz test for porphobilinogen was strongly positive. Additional laboratory examinations confirmed the diagnosis of por-
phyria variegata. Her clinical course was marked by continuous severe abdominal pain, vomiting, paralytic ileus and periods of mental confusion and hallucinations. Very large amounts of pethidine and chlorpromazine were administered with little effect. On her 5th day in hospital, treatment with small doses of propranolol was started, and the clinical signs and symptoms abated. Since the 1.
2.
Bentley, G. B. Ethics in Medical Progress. London, 1966. Aldis, A. S. Science—Its Own Arbiter? Christian Medical Fellowship. London, 1967. 3. Jackson, D. MacG. The Sanctity of Life. London, 1962.
1. 2.
KENNETH HAZELL.
3.
propranolol, given by mouth,
Goldberg, A., Rimington, C. Diseases of Porphyrin Metabolism. Springfield, Illinois, 1962. Watson, C. J. in Cecil and Loeb’s Textbook of Medicine (edited by P. B. Beeson and W. McDermott). Philadelphia, 1963. Bock, K. D., Merguet, P., Schley, G., Schnemann, H. G., RauchStrooman, J. G., Hocevar, V., Schroeder, E., Murata, T. Dt. med. Wschr. 1968, 93, 2119.