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INTRAVENOUS CEPHRADINE IN SERIOUS PÆDIATRIC INFECTIONS
38 to epileptics in high doses for more than a decade. He is right in saying, however, that we did not claim to have disproved that phenobarbitone is oncogenic, since we did not extrapolate to mice, guineapigs, rats, rabbits, and monkeys.
oncogenic when given
Cancer Registry, Danish Cancer Society, Finsen Institute,
Strandboulevard 49, Denmark.
Copenhagen 2100,
resistant. coaln1lase-DOsitive. Stabh.
JOHANNES CLEMMESEN.
VENTRICULAR FIBRILLATION IN HYPOTHERMIA SiR,—Dr Lloyd and Mr Mitchell (Nov. 30, p. 1294) may well be right in their hypothesis that ventricular fibrillation in hypothermia is due to a relatively greater degree of cooling of the conducting tissue which lies just under the endocardium.
However, they use the terms " nervous tissue " or neuromuscular " to describe the conducting tissue. The conducting system in mammalian myocardium consists of modified heart-muscle cells: nerve cells are not directly involved. "
Wellcome Medical Research Institute, Department of Medicine, University of Otago Medical School, Dunedin, New Zealand.
F. O. SIMPSON.
INTRAVENOUS CEPHRADINE IN SERIOUS PÆDIATRIC INFECTIONS SIR,—This is a follow-up letter to our reporton intravenous cephradine. To date, in an open clinical trial, we have treated 11 children with intravenous cephradine, doses ranging from 85 to 300 mg. per kg. body-weight per day. In 5, coagulase-positive Staphylococcus aureus In 2 was obtained from a variety of clinical specimens. patients, pneumococcal bacteraemia occurred simultaneously with lobar pneumonia (see accompanying table). 1 child had group-A oc-streptococcus bactersemia, in the presence of extensive cellulitis of the right lower extremity 1.
Macias,
E. G.
(case 8). No phlebitis or pain arose at the site of intravenous administration in any patients and Coombs-positive ansEmia or nephrotoxicity were not observed. The time of clinical improvement was closely parallel to the return to. negative culture-on average, 5-6 days after starting of intravenous cephradine. We believe that cephradine is an effective antibiotic in the treatment of serious peediatrit infections, particularly those produced by penicillin-
Lancet, 1973, ii, 683.
Department of Pediatrics, Section of Infectious Diseases, University of Texas Health Science Center at San Antonio, Texas 78284, U.S.A.
ENRIQUE G. MACIAS JERRY J. ELLER.
BODY NITROGEN AFTER TRAUMA
SIR,—The article by Dr O’Keefe and others (Nov. 2, p. 1035) on catabolic nitrogen loss will, we hope, be the first in a seriesexploring by isotopic techniques the flux of body nitrogen after trauma. They show that urinary urea nitrogen was little altered by operation in their 4 subjects but that protein breakdown was enhanced less than was the inhibition of protein synthesis. Thirty years ago we postulated an approximately linear
relationship between the extent of injury (measured by totality of tissue damage, blood loss, supervening infection, &c.) and the totality of metabolic response (e.g., catabolic nitrogen loss, water-salt conservation). In the past decade it has become clear that such linear relationships do not obtain for all the response parameters. Although minor degrees of injury (e.g., loss of 500 ml. of blood) are strong stimuli to salt and water conservation, they are but minor stimuli to the other components of the endocrine and metabolic responses. By contrast, severe injury with a maintained low-flow state and maximal catecholamine discharge (particularly if accompanied by infection) appears to constitute a near maximum stimulus to muscle catabolism. It is therefore our concern that the 4 patients studied by O’Keefe et al. were not representative of severe injury, and that conclusions from these findings should not be extended to the truly major injuries of military or civilian life. Evidence that protein nitrogen is lost from muscle after
TREATMENT OF INFECTIONS WITH INTRAVENOUS CEPHRADINE I
I
aureus.
I
* Incision and drainage performed. + Resistant to penicillin.
oncogenic when given
Cancer Registry, Danish Cancer Society, Finsen Institute,
Strandboulevard 49, Denmark.
Copenhagen 2100,
resistant. coaln1lase-DOsitive. Stabh.
JOHANNES CLEMMESEN.
VENTRICULAR FIBRILLATION IN HYPOTHERMIA SiR,—Dr Lloyd and Mr Mitchell (Nov. 30, p. 1294) may well be right in their hypothesis that ventricular fibrillation in hypothermia is due to a relatively greater degree of cooling of the conducting tissue which lies just under the endocardium.
However, they use the terms " nervous tissue " or neuromuscular " to describe the conducting tissue. The conducting system in mammalian myocardium consists of modified heart-muscle cells: nerve cells are not directly involved. "
Wellcome Medical Research Institute, Department of Medicine, University of Otago Medical School, Dunedin, New Zealand.
F. O. SIMPSON.
INTRAVENOUS CEPHRADINE IN SERIOUS PÆDIATRIC INFECTIONS SIR,—This is a follow-up letter to our reporton intravenous cephradine. To date, in an open clinical trial, we have treated 11 children with intravenous cephradine, doses ranging from 85 to 300 mg. per kg. body-weight per day. In 5, coagulase-positive Staphylococcus aureus In 2 was obtained from a variety of clinical specimens. patients, pneumococcal bacteraemia occurred simultaneously with lobar pneumonia (see accompanying table). 1 child had group-A oc-streptococcus bactersemia, in the presence of extensive cellulitis of the right lower extremity 1.
Macias,
E. G.
(case 8). No phlebitis or pain arose at the site of intravenous administration in any patients and Coombs-positive ansEmia or nephrotoxicity were not observed. The time of clinical improvement was closely parallel to the return to. negative culture-on average, 5-6 days after starting of intravenous cephradine. We believe that cephradine is an effective antibiotic in the treatment of serious peediatrit infections, particularly those produced by penicillin-
Lancet, 1973, ii, 683.
Department of Pediatrics, Section of Infectious Diseases, University of Texas Health Science Center at San Antonio, Texas 78284, U.S.A.
ENRIQUE G. MACIAS JERRY J. ELLER.
BODY NITROGEN AFTER TRAUMA
SIR,—The article by Dr O’Keefe and others (Nov. 2, p. 1035) on catabolic nitrogen loss will, we hope, be the first in a seriesexploring by isotopic techniques the flux of body nitrogen after trauma. They show that urinary urea nitrogen was little altered by operation in their 4 subjects but that protein breakdown was enhanced less than was the inhibition of protein synthesis. Thirty years ago we postulated an approximately linear
relationship between the extent of injury (measured by totality of tissue damage, blood loss, supervening infection, &c.) and the totality of metabolic response (e.g., catabolic nitrogen loss, water-salt conservation). In the past decade it has become clear that such linear relationships do not obtain for all the response parameters. Although minor degrees of injury (e.g., loss of 500 ml. of blood) are strong stimuli to salt and water conservation, they are but minor stimuli to the other components of the endocrine and metabolic responses. By contrast, severe injury with a maintained low-flow state and maximal catecholamine discharge (particularly if accompanied by infection) appears to constitute a near maximum stimulus to muscle catabolism. It is therefore our concern that the 4 patients studied by O’Keefe et al. were not representative of severe injury, and that conclusions from these findings should not be extended to the truly major injuries of military or civilian life. Evidence that protein nitrogen is lost from muscle after
TREATMENT OF INFECTIONS WITH INTRAVENOUS CEPHRADINE I
I
aureus.
I
* Incision and drainage performed. + Resistant to penicillin.