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BACTERÆMIA WITH HYPOTENSION DUE TO GRAM-NEGATIVE BACILLI
609 On the basis of several experiments of this type, some of which were performed continuously over 48 hours, I concluded that carbohydrate inhibits the transfer of fats from the alimentary canal to the lymph. Indirectly it may be inferred that depression of lipasmia must also follow. 2nd Central Clinical Hospital,
A.
Szaserów, 2, Warsaw.
MICHAJLIK.
BACTERÆMIA WITH HYPOTENSION DUE TO GRAM-NEGATIVE BACILLI
SIR,-The report of the management of Dr. Cusack’s patient (Feb. 27) calls for comment. Dr. Cusack suggests " that the initial routine empirical antibiotic therapy"in the bacterasmic shock syndrome 12 should be penicillin, 60 mega-units, and streptomycin, 2 g., daily ". We strongly dispute this treatment from our own experience. We have treated many patients with gram-negative septicxmia and shock; our earlier experience was embodied in a report 3 to which Dr. Cusack makes no reference. We have no doubt that, in a patient with obvious gram-negative bactermmic shock syndrome, on clinical grounds the primary treatment should always be kanamycin sulphate, 0.25 g. six-hourly, intramuscularly. At the same time the blood-urea, and the blood-levels of the antibiotic, should be estimated daily, and the dose of kanamycin adjusted if the blood-urea is raised or rising. With such therapy we expect the mortality from this condition to approach nil. Further experience in the management of this condition has recently been reportedand if facilities are not immediately available for the daily monitoring of blood-levels we suggest that the next best treatment is now cephaloridine, 0.25 g. sixhourly, intramuscularly. We hope it is appreciated that massive penicillin and streptomycin therapy is not free from danger while cephaloridine, in this dosage, is non-toxic. The recognition of bacteraemic shock is becoming more "
common, and the mortality depends upon the type of therapy given. Surely it is correct to employ the best available non-toxic bactericidal drug in these circumstances, thus dramatically reducing the mortality. Department of Infectious Diseases, J. MCC. MURDOCH City Hospital,
Edinburgh,
SIR,-Whilst admiring the therapeutic vigour of Dr. Cusack (Feb. 27) one wonders how he dismissed a drugreaction as the cause of his patient’s fever and hypotension. The patient was " quite well " and had no pyrexia when nitrofurantoin was commenced. 10 days later, when she was also receiving sulphafurazole, she had a rigor and was apparently pyrexial for 9 days despite streptomycin, tetracycline, and chloramphenicol. No rash was reported, but this is not an essential accompaniment of drug-fever. The repeatedly sterile blood and urine cultures in this case may be particularly significant. Wales’s Hospital, London, N.15.
ROBERT S. WINWOOD.
SUBACUTE PULMONARY ŒDEMA
SIR,-It is well known that in pulmonary oedema after left ventricular failure the fluid accumulates in the interalveolar septum and later finds its way into the acute
alveolar spaces. With repeated pulmonary oedema, the condition may progress to organisation and fibrosis. But before this takes place there is a distinct phase which may be mistaken for chronic pneumonia.55 A 1. 2. 3. 4. 5
patient, aged 40,
had
This oedema
myocardial
infarction. On the 3rd
Weil, M. H., Spink, W. W. Arch. intern. Med. 1958, 101, 184. Aldridge, R. T. Lancet, 1960, ii, 76. Murdoch, J. McC., Geddes, A. M., Syme, J. ibid. 1962, i, 457. Murdoch, J. McC., Speirs, C. F., Geddes, A. M., Wallace, E. T. Brit. med. J. 1964, ii, 1238. McMichael, J. Brit. med. J. 1964, i, 362.
case
should be considered
as
subacute
pulmonary
simulating typical pneumonia. P. K. KRISHNANKUTTY.
Madras, 10, India.
21-TRISOMY AND XYY
SIR,-Except for the XYY pattern, the association of 21-trisomy and all known autosomal and gonosomal trisomies or equivalent numerical abnormalities has been reported. We have detected the expected association of 21-trisomy and XYY (see accompanying figure) in a
Karyotype (21-trisomy
and
XYY) of the patient.
9-year-old boy whose clinical appearance is purely mongoloid. It is too early to determine whether hypogonadism is present. The ages of the father and the the time he was born were 44 and 35 years. Karyotypes of the father, the mother, and two elder brothers of the proband were normal.
mother
at
Vesalius Institute, Department of Cytogenetics, University of Louvain, Belgium.
A. M. GEDDES.
10.
Prince of
day after admission he showed tachycardia, pulmonary oedema, cyanosis. On the llth day there were physical signs of right-lower-lobe consolidation with dullness and tubular breath sounds. A chest X-ray displayed a homogenous opacity at the right base. He had no significant pyrexia, and the leucocyte-count was normal. Later the consolidation spread to the opposite side. He died on the 45th day after myocardial infarction without any change in the physical findings. and
H. VERRESEN H. VAN DEN BERGHE.
MULTIPLE CHROMOSOMAL ABNORMALITIES IN AN ACUTE EXACERBATION OF MYELOID LEUKÆMIA SIR,-Numerous chromosomal abnormalities have been described in leukaemia,1 including: a PhI chromo-
(almost constant in chronic myeloid leukaemia),2 haplosomy-21 (in certain cases of acute myeloblastic leukaemia),3 and the supernumeration of a chromosome of the middle group first described, in a mongolian with acute leukaemia, by Lejeune et al. and later by Weinstein some
and Weinstein.5 These abnormalities appear systematic; they
are
totally
different from the anarchic abnormalities which are observed mainly in leukaemia patients already treated ... and which may be due to the therapy rather than to the disease. Numerous abnormalities may be seen in the same patient, as in case of haplosomy-21 with PhI chromosome. We have observed the association of 3 abnormalities in a patient with myeloid leukaemia who recently presented in an acute phase with a greatly enlarged spleen. Blood examinations on March 5 gave the following results: red blood-cells 2,200,000, platelets 700,000, white blood-cells 220,000 (all per c.mm.); differential count (percentages), polymorphonuclears
51,
1. 2. 3. 4. 5. 6.
Ruffie, J. Nouv. Rev. franç. Hémat. 1963, 3, 830. Nowell, P. C., Hungerford, D. A. Science, 1960, 132, 1497. Ruffie, J., Lejeune, J. Rev. franç. etud. clin. biol. 1962, 7, 644. Lejeune, J., Berger, R., Haines, M., Lafourcade, J., Vialate, J., Satge, P., Turpin, R. C.R. Acad. Sci., Paris, 1963, 256, 1195. Weinstein, A. S., Weinstein, E. D. New Engl. J. Med. 1963, 268, 253 Atkin, N. B., Taylor, M. C. Cytogenetics, 1962, 1, 97.
A.
Szaserów, 2, Warsaw.
MICHAJLIK.
BACTERÆMIA WITH HYPOTENSION DUE TO GRAM-NEGATIVE BACILLI
SIR,-The report of the management of Dr. Cusack’s patient (Feb. 27) calls for comment. Dr. Cusack suggests " that the initial routine empirical antibiotic therapy"in the bacterasmic shock syndrome 12 should be penicillin, 60 mega-units, and streptomycin, 2 g., daily ". We strongly dispute this treatment from our own experience. We have treated many patients with gram-negative septicxmia and shock; our earlier experience was embodied in a report 3 to which Dr. Cusack makes no reference. We have no doubt that, in a patient with obvious gram-negative bactermmic shock syndrome, on clinical grounds the primary treatment should always be kanamycin sulphate, 0.25 g. six-hourly, intramuscularly. At the same time the blood-urea, and the blood-levels of the antibiotic, should be estimated daily, and the dose of kanamycin adjusted if the blood-urea is raised or rising. With such therapy we expect the mortality from this condition to approach nil. Further experience in the management of this condition has recently been reportedand if facilities are not immediately available for the daily monitoring of blood-levels we suggest that the next best treatment is now cephaloridine, 0.25 g. sixhourly, intramuscularly. We hope it is appreciated that massive penicillin and streptomycin therapy is not free from danger while cephaloridine, in this dosage, is non-toxic. The recognition of bacteraemic shock is becoming more "
common, and the mortality depends upon the type of therapy given. Surely it is correct to employ the best available non-toxic bactericidal drug in these circumstances, thus dramatically reducing the mortality. Department of Infectious Diseases, J. MCC. MURDOCH City Hospital,
Edinburgh,
SIR,-Whilst admiring the therapeutic vigour of Dr. Cusack (Feb. 27) one wonders how he dismissed a drugreaction as the cause of his patient’s fever and hypotension. The patient was " quite well " and had no pyrexia when nitrofurantoin was commenced. 10 days later, when she was also receiving sulphafurazole, she had a rigor and was apparently pyrexial for 9 days despite streptomycin, tetracycline, and chloramphenicol. No rash was reported, but this is not an essential accompaniment of drug-fever. The repeatedly sterile blood and urine cultures in this case may be particularly significant. Wales’s Hospital, London, N.15.
ROBERT S. WINWOOD.
SUBACUTE PULMONARY ŒDEMA
SIR,-It is well known that in pulmonary oedema after left ventricular failure the fluid accumulates in the interalveolar septum and later finds its way into the acute
alveolar spaces. With repeated pulmonary oedema, the condition may progress to organisation and fibrosis. But before this takes place there is a distinct phase which may be mistaken for chronic pneumonia.55 A 1. 2. 3. 4. 5
patient, aged 40,
had
This oedema
myocardial
infarction. On the 3rd
Weil, M. H., Spink, W. W. Arch. intern. Med. 1958, 101, 184. Aldridge, R. T. Lancet, 1960, ii, 76. Murdoch, J. McC., Geddes, A. M., Syme, J. ibid. 1962, i, 457. Murdoch, J. McC., Speirs, C. F., Geddes, A. M., Wallace, E. T. Brit. med. J. 1964, ii, 1238. McMichael, J. Brit. med. J. 1964, i, 362.
case
should be considered
as
subacute
pulmonary
simulating typical pneumonia. P. K. KRISHNANKUTTY.
Madras, 10, India.
21-TRISOMY AND XYY
SIR,-Except for the XYY pattern, the association of 21-trisomy and all known autosomal and gonosomal trisomies or equivalent numerical abnormalities has been reported. We have detected the expected association of 21-trisomy and XYY (see accompanying figure) in a
Karyotype (21-trisomy
and
XYY) of the patient.
9-year-old boy whose clinical appearance is purely mongoloid. It is too early to determine whether hypogonadism is present. The ages of the father and the the time he was born were 44 and 35 years. Karyotypes of the father, the mother, and two elder brothers of the proband were normal.
mother
at
Vesalius Institute, Department of Cytogenetics, University of Louvain, Belgium.
A. M. GEDDES.
10.
Prince of
day after admission he showed tachycardia, pulmonary oedema, cyanosis. On the llth day there were physical signs of right-lower-lobe consolidation with dullness and tubular breath sounds. A chest X-ray displayed a homogenous opacity at the right base. He had no significant pyrexia, and the leucocyte-count was normal. Later the consolidation spread to the opposite side. He died on the 45th day after myocardial infarction without any change in the physical findings. and
H. VERRESEN H. VAN DEN BERGHE.
MULTIPLE CHROMOSOMAL ABNORMALITIES IN AN ACUTE EXACERBATION OF MYELOID LEUKÆMIA SIR,-Numerous chromosomal abnormalities have been described in leukaemia,1 including: a PhI chromo-
(almost constant in chronic myeloid leukaemia),2 haplosomy-21 (in certain cases of acute myeloblastic leukaemia),3 and the supernumeration of a chromosome of the middle group first described, in a mongolian with acute leukaemia, by Lejeune et al. and later by Weinstein some
and Weinstein.5 These abnormalities appear systematic; they
are
totally
different from the anarchic abnormalities which are observed mainly in leukaemia patients already treated ... and which may be due to the therapy rather than to the disease. Numerous abnormalities may be seen in the same patient, as in case of haplosomy-21 with PhI chromosome. We have observed the association of 3 abnormalities in a patient with myeloid leukaemia who recently presented in an acute phase with a greatly enlarged spleen. Blood examinations on March 5 gave the following results: red blood-cells 2,200,000, platelets 700,000, white blood-cells 220,000 (all per c.mm.); differential count (percentages), polymorphonuclears
51,
1. 2. 3. 4. 5. 6.
Ruffie, J. Nouv. Rev. franç. Hémat. 1963, 3, 830. Nowell, P. C., Hungerford, D. A. Science, 1960, 132, 1497. Ruffie, J., Lejeune, J. Rev. franç. etud. clin. biol. 1962, 7, 644. Lejeune, J., Berger, R., Haines, M., Lafourcade, J., Vialate, J., Satge, P., Turpin, R. C.R. Acad. Sci., Paris, 1963, 256, 1195. Weinstein, A. S., Weinstein, E. D. New Engl. J. Med. 1963, 268, 253 Atkin, N. B., Taylor, M. C. Cytogenetics, 1962, 1, 97.