913
individual needs, it shows a wide range of compatibility with added drugs-e.g., antibacterial agentsto meet
and
can
be
produced cheaply
Selly Oak Hospital, Birmingham, 29.
in bulk. A. P. LAUNCHBURY Deputy chief pharmacist.
TOXIC EFFECTS OF STEROIDS SIR,-A few weeks agoII asked Dr. Treadwell and his colleagues (reporting2 on 128 steroid patients reduced to 99) what has happened to 113 of the 212 reported by Savage et a1.3 in 1961. Dr. Treadwell, a temporary member of the team now living in New Zealand, has written to the Medical Journal of Australia 4" I agree... that we should have stated the number who had died." But he did not state the number who died; nor has Dr. Copeman, the chief of the clinic. Instead, Dr. Treadwell5 has obligingly changed the subject by attacking my letter of Aug. 29 about indomethacin. Institute of Rheumatology, 410, Albert Street, East
Melbourne,
MICHAEL KELLY.
Victoria, Australia.
Postscript.-I have just seen Professor Elliott’s ingenious proposals, launched simultaneously in Americaand Britainfor treatment of the self-limited virus disease herpes zoster with large doses of prednisone. And I approve of them no more than does Dr. G. V. Irons,s who says that such risks
cannot
be
justified.
NEONATAL RESPIRATORY DISTRESS ASSOCIATED WITH A HIGH HÆMATOCRIT READING
SIR, The article by Dr. Danks and Dr. Stevens (Sept. 5) prompts us to draw attention to a very similar condition, caused by a different mechanism. Stephan and Otto 9 reported bilateral hydrothorax as "aa previous unrecognised cause of neonatal asphyxia ", in which severe respiratory distress began immediately after the birth of an apparently normal baby, with pronounced retraction of the ribs and sternum. Spontaneous breathing ceased after a few minutes. Artificial intratracheal respiration was successful, but met with unusual resistance during the inspiratory phase. Bilateral puncture of the chest with removal of a total of 75 ml. clear fluid led to permanent cure. We have had a similar case. Pregnancy, as in the case reported by Dr. Danks and Dr. Stevens, was complicated by hydramnion. Both lung-fields were completely opaque, except for a central area of a few bubbles on both sides of the spine. The ribs were in maximal inspiratory position. The diagnosis was missed, however, and the baby died after 6 hours of artificial respiration, partly on the Engstrom-respirator. At necropsy, only some 40 ml. of clear yellow fluid was found in each pleural cavity. The lungs were atelectatic, but otherwise normal. An infant presenting in the same way in Vienna was saved by bilateral punctùre.1o Not impressed by the relatively small amount of pleural fluid, the pathologist did not recognise it as the principal cause of respiratory distress. This has been proved, however, by the two surviving cases. The condition may be quite common, but cannot be diagnosed in the living except
by radiography. Kelly, M. Lancet, Aug. 22, 1964, p. 415. Treadwell, B. L. J., Sever, E. D., Savage, O. A., Copeman, W. S. C. ibid. 1964, i, 1121. 3. Savage, O. A., Copeman, W. S. C., Davis, P. S., Wells, M. V. Atti X. Congr. Lega int. Rheum. (Rome) 1961, 1, 374. 4. Treadwell, B. L. J. Med. J. Aust. Sept. 5, 1964, p. 391. 5. Treadwell, B. L. J. Lancet, Oct. 3, 1964, p. 754. 6. Elliott, F. A. J. Amer. med. Ass. Aug. 24, 1964, p. 649. 7. Elliott, F. A. Lancet, Sept. 19, 1964, p. 610. 8. Irons, G. V. J. Amer. med. Ass. Aug. 24, 1964, p. 649. 9. Stephan, W. K., Otto, M. L. ibid. 1961, 176, 615. 10. Wolf, H. G. Personal communication. 1. 2.
The negative intrathoracic pressure needed for the initial expansion of the lung of a newborn reaches up to 70 ml. water." A reduction of this pressure, even by a moderate amount of fluid which would be tolerated later in life without symptoms, can lead to disaster in the newborn. Without artificial respiration, these babies die shortly after birth and will be filed as primary atelectasis of the lung". "
-
University Pædiatric Department, Zürich, Switzerland.
A. GIEDION.
PULMONARY HYPERTENSION FOLLOWING ANGIOCARDIOGRAPHY WITH SODIUM METRIZOATE
SIR,-Dr. Watson’s preliminary communication (Oct. 3) reinforces our unpublished experience that sodium metrizoate (75%), while providing cineangiocardiograms of excellent definition, is not without toxic effects. Nevertheless, in the course of 121 examinations of 76 children weighing from 2-8 kg. to 39 kg., we have not encountered a rising pressure in the pulmonary artery or right ventricle; pressure recording was continued for not less than fifteen minutes in 45 instances, although for not more than five minutes in the remainder. during right ventricular injection and 3 times during main-pulmonary-artery injections a localised pulmonary opacity appeared suddenly, but this was not accompanied by symptoms or abnormal physical signs; complete radiological resolution occurred within twenty-four hours in 3, but only gradually over four days in the 4th. Intramural extravasation of contrast medium from the right ventricle, persisting for not more than a few hours, occurred five times unaccompanied by symptoms or clinical signs. Both features might be causally related to the low viscosity of the agent and to the pressure of injection; but we do not know whether the pulmonary lesions, whose appearance coincided with the injection, were due to extravasated contrast medium or to localised pulmonary Once
oedema. Transient arrhythmias occurred but not with undue frequency. One death was, however, preceded by a progressive arrhythmia. This patient at 15 months had severe pulmonary hypertension and a ventricular septal defect; 75% sodium metrizoate (1-5 ml. per kg.) was injected into the ascending aorta 1-5 cm. above the aortic valve. The coronary circulation seemed particularly well delineated, and about a minute after the injection first-degree atrioventricular block appeared and proceeded to complete atrioventricular dissociation while the QRS complexes widened and the ST segments became elevated; ventricular tachycardia was quickly followed by fibrillation, which was only briefly influenced by electrical defibrillation. Perhaps there is a connection between this onset of arrhythmia after coronary-artery filling and the postulated increase in pulmonary vascular resistance in Dr. Watson’s patients, on the assumption that the contrast medium may in some subjects exert a toxic (perhaps vasoconstrictor) effect on small arteries, whether pulmonary or coronary. The other death in this series was of an infant, aged 8 weeks, who had a ventricular septal defect and a persistent ductus arteriosus, and who almost immediately after the injection of contrast medium into the right ventricle developed pulmonary and systemic hypotension with peripheral circulatory failure, relieved only temporarily by resuscitative measures.
Nowadays in this laboratory we seldom employ general anxsthesia for cineangiocardiography; and, because violent coughing may be caused by sodium metrizoate injected into the main pulmonary artery or the right ventricle of a conscious child, we no longer use this contrast medium. Experience of contrast agents of different viscosities leads us to suspect that the untoward effects described 11.
Karlberg, P. J. Pediat. 1960, 56,
585.