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DIGITALIS INTOXICATION IN ELDERLY PATIENTS
489
(3) We are dealing here with a systemic disease that primarily affects the lung but may also involve the haemopoietic and central
nervous
systems.
of the
published case-reports do not support the first explanation; Wolman’s article favours the second; but the experience with my own case makes me wonder Many
about the third. The Mairnonides Hospital, Coney Island Division, Brooklyn, N.Y., U.S.A.
bleeding. AVIR KAGAN.
DIGITALIS INTOXICATION IN ELDERLY PATIENTS SIR,-In the context of Dr. Dall’s valuable article (Jan. 23) and the subsequent letters (Feb. 6), it may be of interest to note that, in a recent analysis of 2000 consecutive electrocardiograms (E.c.G.s)j 597 tracings referred to 348 patients who had had digitalis within the fortnight preceding at least one E.c.G. Digitalis overdosage was suspected from the EC.G. in 42 (12%). Of these 42, 33 (78-5%) were over 61 and 22 (52%) over 71. These findings underline the importance of age in the susceptibility to digitalis. In addition, this analysis revealed several other factors, particularly important in the elderly but relevant also in patients of all age-groups, which proved to be largely responsible for the disturbingly high incidence of digitalis intoxication. These were: exhibition of digitalis without indication; premature start of digitalisation in hospital; mistaken methods for determining digitalis dosage clinically; unawareness that digitalis toxicity may manifest itself as refractory heartfailure or as increase in its severity; and inadequate action by the physician in the presence of signs of intoxication.
A. SCHOTT. EPSOM SALTS FOR HYALINE-MEMBRANE DISEASE comments on the unsurvival-rate in hyaline-membrane disease since the introduction of glucose-bicarbonate infusions. Increased concentration on biochemical alterations may have made the physician less alert to significant clinical change in the course of the disorder. This can best be illustrated by a brief review of three infants recently treated in our premature unit.
SIR,-Dr. Stowens (Jan. 16)
changed
CASE l.-A 41/2 lb. (2050 g.) female infant with respiratory distress had an initial pH of 7-20 which could be corrected to 7-36 by bicarbonate. At 2 days of age there was a sudden increase in distress, and her chest X-ray showed a tension pneumothorax. Needle aspiration and catheter drainage of the chest were carried out without success. Postmortem examination demonstrated hyaline-membrane formation, interstitial emphysema, and bilateral pneumothorax. CASE 2.-A 21/2 lb. (1170 g.) infant with respiratory distress was treated with TRIS buffer because of a pH of 7-13 and a Pco2 of 70 mm. The pH rose to 7.32 and the PC02 fell to 44 mm., but respiratory distress persisted. Clinical icterus was evident by the 2nd day of life, with a bilirubin level of 10.2 mg. per 100 ml. The infant died at 3 days of age, and postmortem examination demonstrated diffuse atelectasis, pulmonary intraalveolar haemorrhage, and bilirubin pigmentation of the basal ganglia and pons. CASE 3.-A 31/2 lb. (1600 g.) male infant developed progressive respiratory distress, but the pH could be raised from 7-20 to 7.32 with bicarbonate. 2 hours after pH determination the infant became apnaeic with a fall in pH to 6 78. Positive-pressure assisted ventilation and bicarbonate administration were only temporarily helpful. Postmortem examination demonstrated hyaline-membrane formation and intraventricular haemorrhage. In all these infants improvement in pH was achieved, 1.
Schott,
A. Post Grad.
but the onset of secondary difficulties was not averted. In case 1, serial chest X-rays might have proved more useful than acid-base determinations. In case 2, the development ofkemicterus despite a safe bilirubin level raised the question of possible competitive binding of TRIs buffer to albumin. In case 3, crying during repeated capillary punctures might have contributed to the onset of intracranial
med J. 1964, 40, 628.
Acidosis in infants with hyaline-membrane disease accompanies anoxia, which is due not only to the membrane formation per
but also
respiratory-centre and haemorrhagic shock. Attention should be directed to the possibility of any of these causes of anoxia, and pH, PC02, HCOs, and P02 determinations, and correction of acidosis should accompany careful clinical and radiological evaluation. se
to
depression, pneumonia, pneumothorax,
Departments of Pediatrics and Clinical Chemistry, Genesee Hospital, Rochester, New York.
BERNARD A. YABLIN MARTIN H. MURRAY RICHARD S. MELTZER.
DANGERS OF ANGIOTENSIN SIR,-Your leaderrightly emphasised the risks of
giving angiotensin by intravenous infusion. with this warning, but should like to add restricting its validity.
We fully agree some remarks
We find that the most important factor determining the risk of angiotensin infusion is the subject’s blood-pressure. If this and the cardiovascular system are normal, hyperreactivity to angiotensin is possible. In clinical conditions with pressor hyporeactivity-e.g., cirrhosis of the liver,2Addison’s disease,3 and hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalxmic alkalosis (Bartter’s syndrome) 4 -the risk is small provided the patient is under close observation. In some of these cases angiotensin is more of therapeutic than of diagnostic importance. We were able to demonstrate the diuretic action of intravenous angiotensin in ascitic cirrhosis of the liver5 in 8 patients when all diuretics, including spironolactone and triamterene, had failed.In a further 4 patients who did not respond to angiotensin or spironolactone separately we observed a profound diuretic response on giving both together.’ There was no similar diuretic effect in nephrotic oedema. Pressor hyperreactivity to angiotensin occurred in only 1 out of 45 patients-when we attempted to treat idiopathic oedema without pre-existing hypertension.8 In 56 infusions of angiotensin all our patients tolerated the drug well; the blood-pressure and cardiovascular reaction were closely controlled. We never infuse with angiotensin in patients with hypertension. We have never exceeded a dose of 2-89 jjt.g. of angiotensin per minute, except in a patient with all the signs and symptoms of Bartter’s syndrome,4 a 37-yearold man with primary hyperaldosteronism (Conn’s syndrome), but without hypertension; in him we did not obtain a pressor response to angiotensin in spite of increasing the dose to 7.4
g.s
The intravenous infusion of angiotensin is thus not merely an experimental procedure. It has its place in the diuretic treatment of ascitic cirrhosis resistant to other drugs, apart from its main use in shock. We are convinced of the diagnostic value of this drug since pressor and tubular reactivity may be an important diagnostic criterion, and its aldosterone-mobilising action can com1. 2. 3.
Lancet, 1964, ii, 1328. Johnston, C. J., Jose, A. D. J. clin. Invest. 1963, 42, 1411. Kuchel, O., Horky, K., Pazourek, M., Gregorová, I. Lancet, 1964, ii,
1316. 4. Bartter, F.
C., Pronove, P., Gill, J. R., MacCardle, R. C., Diller, E. Amer. J. Med. 1962, 33, 811. 5. Laragh, L. H., Cannon, P. J., Bentzel, C. J., Sicinski, A. M., Meltzer, J. I. J. clin. Invest. 1963, 42, 1179. 6. Pazourek, M., Küchel, O., HorkÝ, K. Arch. bohèm. méd. (Sbornik lékarskÝ), 1964, 66, 289. 7. HorkÝ, K., Kuchel, O., Pazourek, M. ibid. p. 345. 8. Küchel, O., HorkÝ, K., Kapitola, J., Motlík, K. Lancet, 1964, ii, 1341. 9. Küchel, O., HorkÝ, K. Čas. Lék. ces. 1964, 103, 778.
(3) We are dealing here with a systemic disease that primarily affects the lung but may also involve the haemopoietic and central
nervous
systems.
of the
published case-reports do not support the first explanation; Wolman’s article favours the second; but the experience with my own case makes me wonder Many
about the third. The Mairnonides Hospital, Coney Island Division, Brooklyn, N.Y., U.S.A.
bleeding. AVIR KAGAN.
DIGITALIS INTOXICATION IN ELDERLY PATIENTS SIR,-In the context of Dr. Dall’s valuable article (Jan. 23) and the subsequent letters (Feb. 6), it may be of interest to note that, in a recent analysis of 2000 consecutive electrocardiograms (E.c.G.s)j 597 tracings referred to 348 patients who had had digitalis within the fortnight preceding at least one E.c.G. Digitalis overdosage was suspected from the EC.G. in 42 (12%). Of these 42, 33 (78-5%) were over 61 and 22 (52%) over 71. These findings underline the importance of age in the susceptibility to digitalis. In addition, this analysis revealed several other factors, particularly important in the elderly but relevant also in patients of all age-groups, which proved to be largely responsible for the disturbingly high incidence of digitalis intoxication. These were: exhibition of digitalis without indication; premature start of digitalisation in hospital; mistaken methods for determining digitalis dosage clinically; unawareness that digitalis toxicity may manifest itself as refractory heartfailure or as increase in its severity; and inadequate action by the physician in the presence of signs of intoxication.
A. SCHOTT. EPSOM SALTS FOR HYALINE-MEMBRANE DISEASE comments on the unsurvival-rate in hyaline-membrane disease since the introduction of glucose-bicarbonate infusions. Increased concentration on biochemical alterations may have made the physician less alert to significant clinical change in the course of the disorder. This can best be illustrated by a brief review of three infants recently treated in our premature unit.
SIR,-Dr. Stowens (Jan. 16)
changed
CASE l.-A 41/2 lb. (2050 g.) female infant with respiratory distress had an initial pH of 7-20 which could be corrected to 7-36 by bicarbonate. At 2 days of age there was a sudden increase in distress, and her chest X-ray showed a tension pneumothorax. Needle aspiration and catheter drainage of the chest were carried out without success. Postmortem examination demonstrated hyaline-membrane formation, interstitial emphysema, and bilateral pneumothorax. CASE 2.-A 21/2 lb. (1170 g.) infant with respiratory distress was treated with TRIS buffer because of a pH of 7-13 and a Pco2 of 70 mm. The pH rose to 7.32 and the PC02 fell to 44 mm., but respiratory distress persisted. Clinical icterus was evident by the 2nd day of life, with a bilirubin level of 10.2 mg. per 100 ml. The infant died at 3 days of age, and postmortem examination demonstrated diffuse atelectasis, pulmonary intraalveolar haemorrhage, and bilirubin pigmentation of the basal ganglia and pons. CASE 3.-A 31/2 lb. (1600 g.) male infant developed progressive respiratory distress, but the pH could be raised from 7-20 to 7.32 with bicarbonate. 2 hours after pH determination the infant became apnaeic with a fall in pH to 6 78. Positive-pressure assisted ventilation and bicarbonate administration were only temporarily helpful. Postmortem examination demonstrated hyaline-membrane formation and intraventricular haemorrhage. In all these infants improvement in pH was achieved, 1.
Schott,
A. Post Grad.
but the onset of secondary difficulties was not averted. In case 1, serial chest X-rays might have proved more useful than acid-base determinations. In case 2, the development ofkemicterus despite a safe bilirubin level raised the question of possible competitive binding of TRIs buffer to albumin. In case 3, crying during repeated capillary punctures might have contributed to the onset of intracranial
med J. 1964, 40, 628.
Acidosis in infants with hyaline-membrane disease accompanies anoxia, which is due not only to the membrane formation per
but also
respiratory-centre and haemorrhagic shock. Attention should be directed to the possibility of any of these causes of anoxia, and pH, PC02, HCOs, and P02 determinations, and correction of acidosis should accompany careful clinical and radiological evaluation. se
to
depression, pneumonia, pneumothorax,
Departments of Pediatrics and Clinical Chemistry, Genesee Hospital, Rochester, New York.
BERNARD A. YABLIN MARTIN H. MURRAY RICHARD S. MELTZER.
DANGERS OF ANGIOTENSIN SIR,-Your leaderrightly emphasised the risks of
giving angiotensin by intravenous infusion. with this warning, but should like to add restricting its validity.
We fully agree some remarks
We find that the most important factor determining the risk of angiotensin infusion is the subject’s blood-pressure. If this and the cardiovascular system are normal, hyperreactivity to angiotensin is possible. In clinical conditions with pressor hyporeactivity-e.g., cirrhosis of the liver,2Addison’s disease,3 and hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalxmic alkalosis (Bartter’s syndrome) 4 -the risk is small provided the patient is under close observation. In some of these cases angiotensin is more of therapeutic than of diagnostic importance. We were able to demonstrate the diuretic action of intravenous angiotensin in ascitic cirrhosis of the liver5 in 8 patients when all diuretics, including spironolactone and triamterene, had failed.In a further 4 patients who did not respond to angiotensin or spironolactone separately we observed a profound diuretic response on giving both together.’ There was no similar diuretic effect in nephrotic oedema. Pressor hyperreactivity to angiotensin occurred in only 1 out of 45 patients-when we attempted to treat idiopathic oedema without pre-existing hypertension.8 In 56 infusions of angiotensin all our patients tolerated the drug well; the blood-pressure and cardiovascular reaction were closely controlled. We never infuse with angiotensin in patients with hypertension. We have never exceeded a dose of 2-89 jjt.g. of angiotensin per minute, except in a patient with all the signs and symptoms of Bartter’s syndrome,4 a 37-yearold man with primary hyperaldosteronism (Conn’s syndrome), but without hypertension; in him we did not obtain a pressor response to angiotensin in spite of increasing the dose to 7.4
g.s
The intravenous infusion of angiotensin is thus not merely an experimental procedure. It has its place in the diuretic treatment of ascitic cirrhosis resistant to other drugs, apart from its main use in shock. We are convinced of the diagnostic value of this drug since pressor and tubular reactivity may be an important diagnostic criterion, and its aldosterone-mobilising action can com1. 2. 3.
Lancet, 1964, ii, 1328. Johnston, C. J., Jose, A. D. J. clin. Invest. 1963, 42, 1411. Kuchel, O., Horky, K., Pazourek, M., Gregorová, I. Lancet, 1964, ii,
1316. 4. Bartter, F.
C., Pronove, P., Gill, J. R., MacCardle, R. C., Diller, E. Amer. J. Med. 1962, 33, 811. 5. Laragh, L. H., Cannon, P. J., Bentzel, C. J., Sicinski, A. M., Meltzer, J. I. J. clin. Invest. 1963, 42, 1179. 6. Pazourek, M., Küchel, O., HorkÝ, K. Arch. bohèm. méd. (Sbornik lékarskÝ), 1964, 66, 289. 7. HorkÝ, K., Kuchel, O., Pazourek, M. ibid. p. 345. 8. Küchel, O., HorkÝ, K., Kapitola, J., Motlík, K. Lancet, 1964, ii, 1341. 9. Küchel, O., HorkÝ, K. Čas. Lék. ces. 1964, 103, 778.