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MORTALITY FROM PNEUMOCOCCAL MENINGITIS
255 The symptoms in their full severity lasted for 8 h, and she was left with headache continuing for 36 h. Any doctor prescribing or patient receiving this potent drug should consider carefully the effect of withdrawal which has not, to my knowledge, been researched. Harewood, Gt. Oakley, Harwich,
BENEDICT L. HOSKYNS
Essex CO12 5AD
MAXIMAL ACID OUTPUT AND RISK OF ULCER
SIR,-I was disappointed in the
two papers by Mr Fiddianyour Dec. 25 issue, because I felt that some useful information that might have come out of such an inquiry was not sought. For example, what was the relationship between maximal acid output and total (24 h) or mean fasting acid output? I was also disappointed because their data were, on the whole, poorly presented and tended to imply a firmness of conclusion which their results did not justify. The most glaring example of this, and one where their deduction is clearly incorrect, is in fig. 1 of the first paper in which they seek to prove that, in their initially normal medical students, peak acid output correlates with the likelihood of developing an ulcer. Since each "group", as defined by peak acid output, contains only one ulcer sufferer, the claim for a correlation is unwarranted.
Green and his
colleagues in
East Birmingham Hospital, Birmingham B9
R. A. FISKEN
POSTOPERATIVE HYPOPHOSPHATÆMIA
SIR,-Mr Spurr (Jan. 15,
p.
146) does
well
to
draw your
readers’ attention to the role of red cell 2, 3-diphosphoglycerate (2, 3-D.P.G.) in the control of the oxygen affinity of hmmoglobin. Hypophosphataemia causes a decrease in 2, 3-D.P.G. with a subsequent shift to the left of the oxyhaemogiobin dissociation curve and tissue hypoxia.In one patient the symptoms of hypoxia disappeared with restoration of the plasma-phos-
SIR,-In their interesting discussion of factors which might explain the continuing high mortality from pneumococcal meningitis in Africa, Baird et a1.l do not mention the location of the initial lesions of pneumococcal meningitis. At least in Uganda it was not unusual in pneumococcal meningitis, in contrast to other pyogenic meningitides, to see at necropsy individuals, often pregnant women, who died of this disease without exhibiting the usual signs and symptoms of meningitis. They had a cap of thick green pneumococcal pus covering the vertex of the brain without the involvement of the basal meninges which produces the usual signs and symptoms of pyogenic meningitis. Such individuals had complained of fever and headaches and died with occasional convulsions. This meant that when, in pneumococcal meningitis, the typical signs of meningeal involvement developed the disease process was far more advanced than was the case with other forms of pyogenic meningitis, and diagnosis was much delayed. Any discussion of the influence of duration of symptoms before admission should take account of this feature and it may
explain why a short history often carries a worse prognosis than a long history. A further feature is that, in my experience, initial lumbar puncture may disclose crystal-clear cerebrofluid without evidence of a cell increase or pneumococci whereas a repeat some 20 min later may show a turbid highly cellular fluid swarming with organisms. Surely no consideration of the high mortality of pneumococcal meningitis, especially that of hxmatogenous origin, should neglect the frequency with which initial involvement is of the vertical meninges rather than the basal. an
spinal
Department of Pathology, Albany Medical College, Albany, N.Y. 12208, U.S.A.
J.
N. P. DAVIES
RESISTANT STAPHYLOCOCCI IN HOSPITALS
all described a hospital outbreak of staresistant to gentamicin, methicillin, and other antibiotics. We recently reported an outbreak of hospital-acquired infection due to a similar strain of staphylococcus.3 Despite the fact that these strains of staphylococci have not yet established themselves as major pathogens in North American hospitals, sporadic outbreaks are increasingly common. The epidemic strain in our 1000-bed community hospital was not phage typable as was the London strain; and the antibiotic-susceptibility pattern was dissimilar in that our isolates were all resistant to erythromycin and trimethoprim in addition to the antibiotics listed by Shanson et al. Although initial isolates were sensitive to gentamicin, this antibiotic was not successful in eradicating the organism once it became a coloniser or a pathogen. Most of our patients who acquired the organism had not been previously given an aminoglycoside antibiotic, either parenterally or topically. Since gentamicin was not an effective antimicrobial agent in our patients despite in-vitro susceptibility, the sense of alarm expressed by Shanson et al. over the appearance of "new" strain may not be justified. This situation is reminiscent of the problems arising from the differences in in-vitro susceptibility and in-vivo ineffectiveness of the cephalosporins when dealing with these methicillin-resis4 tant strains. The finding by the London group of transient carriers among staff supports our contention that hospital staff can play an important role in patient-to-patient spread of these organisms. Indeed, we detected transfer of the organism to two SiR-Shanson
et
phylococcal infection
phate.’ Postoperative hypophosphataemia
in association with intrainfusions of dextrose or saline, as described by Guillou et a1.2 occurs at a time when the patient may be hypoxic from the changes which take place in ventilation of the lungs after anaesthesia, especially in upper-abdominal surgery.3 Hypoxsmia usually leads to an increased concentration of 2, 3-D.P.G. which decreases the oxygen affinity of haemoglobin thus improving tissue oxygenation. This adaptive increase in 2, 3-D.P.G. will be prevented by hypophosphatasmia. The situation may be aggravated should blood-transfusion be required during surgery since blood stored in acid-citrate dextrose has a very low concentration of 2, 3-D.p.G. Synthesis of 2, 3-D.P.G. after transfusion requires availability of phosphates and a normal acid-base status.6 Raised plasma-inorganic-phosphate levels and a systemic alkalosis will encourage rapid resynthesis of 2, 3-D.P.G. and also a more optimal revenous
sponse to hypoxia.
Theoretically, therefore, it would appear that patients having upper-abdominal surgery, especially accompanied by bloodtransfusion, would benefit from intravenous infusions containing phosphate. Department of Anæsthesia, Leeds (St James’s) University Hospital, Leeds LS9 7TF
MORTALITY FROM PNEUMOCOCCAL MENINGITIS
ROSEMARY MACDONALD
1. Travis, S. F., Sugerman, H. J., Ruberg, R. L., Dudrick, S. J., Delivoria Papadopoulos, M., Miller, L. D., Oski, F. A. New Engl. J. Med. 1971, 285, 763. 2. Guillou, P.M., Morgan, D. B., Hill, G.L.Lancet, 1976, ii, 710. 3. Alexander, J. I., Spence, A. A., Parikh, R. K., Stuart, B. Br. J.Anœsth. 1973, 45, 34. 4.Miller, L.D., Oski, F.A., and Diaco, J.F.Surgery, 1970, 68, 187. 5.Torrance, J.D. J.Lab. clin. Med. 1973, 82, 489. 6.Valen, C. R.Clins Hœmat. 1974, 3, 661.
1. Baird, D.R.,Whittle,H.C.,Greenwood,B. M. Lancet, 1976,n, 1344. 2. Shanson, D. C., Kensit,J. G., Duke, R. ibid. p. 1347. 3. Klimek, J. J., Marsik, F. J., Bartlett, R. C., Weir, B., Shea, P., Quintiliani, R. Am. J. Med. 1976, 61, 340. 4. Acar,
J. F., Chabbert, X. A. Antimicrob. Ag. Chemother.1971, p. 280.
BENEDICT L. HOSKYNS
Essex CO12 5AD
MAXIMAL ACID OUTPUT AND RISK OF ULCER
SIR,-I was disappointed in the
two papers by Mr Fiddianyour Dec. 25 issue, because I felt that some useful information that might have come out of such an inquiry was not sought. For example, what was the relationship between maximal acid output and total (24 h) or mean fasting acid output? I was also disappointed because their data were, on the whole, poorly presented and tended to imply a firmness of conclusion which their results did not justify. The most glaring example of this, and one where their deduction is clearly incorrect, is in fig. 1 of the first paper in which they seek to prove that, in their initially normal medical students, peak acid output correlates with the likelihood of developing an ulcer. Since each "group", as defined by peak acid output, contains only one ulcer sufferer, the claim for a correlation is unwarranted.
Green and his
colleagues in
East Birmingham Hospital, Birmingham B9
R. A. FISKEN
POSTOPERATIVE HYPOPHOSPHATÆMIA
SIR,-Mr Spurr (Jan. 15,
p.
146) does
well
to
draw your
readers’ attention to the role of red cell 2, 3-diphosphoglycerate (2, 3-D.P.G.) in the control of the oxygen affinity of hmmoglobin. Hypophosphataemia causes a decrease in 2, 3-D.P.G. with a subsequent shift to the left of the oxyhaemogiobin dissociation curve and tissue hypoxia.In one patient the symptoms of hypoxia disappeared with restoration of the plasma-phos-
SIR,-In their interesting discussion of factors which might explain the continuing high mortality from pneumococcal meningitis in Africa, Baird et a1.l do not mention the location of the initial lesions of pneumococcal meningitis. At least in Uganda it was not unusual in pneumococcal meningitis, in contrast to other pyogenic meningitides, to see at necropsy individuals, often pregnant women, who died of this disease without exhibiting the usual signs and symptoms of meningitis. They had a cap of thick green pneumococcal pus covering the vertex of the brain without the involvement of the basal meninges which produces the usual signs and symptoms of pyogenic meningitis. Such individuals had complained of fever and headaches and died with occasional convulsions. This meant that when, in pneumococcal meningitis, the typical signs of meningeal involvement developed the disease process was far more advanced than was the case with other forms of pyogenic meningitis, and diagnosis was much delayed. Any discussion of the influence of duration of symptoms before admission should take account of this feature and it may
explain why a short history often carries a worse prognosis than a long history. A further feature is that, in my experience, initial lumbar puncture may disclose crystal-clear cerebrofluid without evidence of a cell increase or pneumococci whereas a repeat some 20 min later may show a turbid highly cellular fluid swarming with organisms. Surely no consideration of the high mortality of pneumococcal meningitis, especially that of hxmatogenous origin, should neglect the frequency with which initial involvement is of the vertical meninges rather than the basal. an
spinal
Department of Pathology, Albany Medical College, Albany, N.Y. 12208, U.S.A.
J.
N. P. DAVIES
RESISTANT STAPHYLOCOCCI IN HOSPITALS
all described a hospital outbreak of staresistant to gentamicin, methicillin, and other antibiotics. We recently reported an outbreak of hospital-acquired infection due to a similar strain of staphylococcus.3 Despite the fact that these strains of staphylococci have not yet established themselves as major pathogens in North American hospitals, sporadic outbreaks are increasingly common. The epidemic strain in our 1000-bed community hospital was not phage typable as was the London strain; and the antibiotic-susceptibility pattern was dissimilar in that our isolates were all resistant to erythromycin and trimethoprim in addition to the antibiotics listed by Shanson et al. Although initial isolates were sensitive to gentamicin, this antibiotic was not successful in eradicating the organism once it became a coloniser or a pathogen. Most of our patients who acquired the organism had not been previously given an aminoglycoside antibiotic, either parenterally or topically. Since gentamicin was not an effective antimicrobial agent in our patients despite in-vitro susceptibility, the sense of alarm expressed by Shanson et al. over the appearance of "new" strain may not be justified. This situation is reminiscent of the problems arising from the differences in in-vitro susceptibility and in-vivo ineffectiveness of the cephalosporins when dealing with these methicillin-resis4 tant strains. The finding by the London group of transient carriers among staff supports our contention that hospital staff can play an important role in patient-to-patient spread of these organisms. Indeed, we detected transfer of the organism to two SiR-Shanson
et
phylococcal infection
phate.’ Postoperative hypophosphataemia
in association with intrainfusions of dextrose or saline, as described by Guillou et a1.2 occurs at a time when the patient may be hypoxic from the changes which take place in ventilation of the lungs after anaesthesia, especially in upper-abdominal surgery.3 Hypoxsmia usually leads to an increased concentration of 2, 3-D.P.G. which decreases the oxygen affinity of haemoglobin thus improving tissue oxygenation. This adaptive increase in 2, 3-D.P.G. will be prevented by hypophosphatasmia. The situation may be aggravated should blood-transfusion be required during surgery since blood stored in acid-citrate dextrose has a very low concentration of 2, 3-D.p.G. Synthesis of 2, 3-D.P.G. after transfusion requires availability of phosphates and a normal acid-base status.6 Raised plasma-inorganic-phosphate levels and a systemic alkalosis will encourage rapid resynthesis of 2, 3-D.P.G. and also a more optimal revenous
sponse to hypoxia.
Theoretically, therefore, it would appear that patients having upper-abdominal surgery, especially accompanied by bloodtransfusion, would benefit from intravenous infusions containing phosphate. Department of Anæsthesia, Leeds (St James’s) University Hospital, Leeds LS9 7TF
MORTALITY FROM PNEUMOCOCCAL MENINGITIS
ROSEMARY MACDONALD
1. Travis, S. F., Sugerman, H. J., Ruberg, R. L., Dudrick, S. J., Delivoria Papadopoulos, M., Miller, L. D., Oski, F. A. New Engl. J. Med. 1971, 285, 763. 2. Guillou, P.M., Morgan, D. B., Hill, G.L.Lancet, 1976, ii, 710. 3. Alexander, J. I., Spence, A. A., Parikh, R. K., Stuart, B. Br. J.Anœsth. 1973, 45, 34. 4.Miller, L.D., Oski, F.A., and Diaco, J.F.Surgery, 1970, 68, 187. 5.Torrance, J.D. J.Lab. clin. Med. 1973, 82, 489. 6.Valen, C. R.Clins Hœmat. 1974, 3, 661.
1. Baird, D.R.,Whittle,H.C.,Greenwood,B. M. Lancet, 1976,n, 1344. 2. Shanson, D. C., Kensit,J. G., Duke, R. ibid. p. 1347. 3. Klimek, J. J., Marsik, F. J., Bartlett, R. C., Weir, B., Shea, P., Quintiliani, R. Am. J. Med. 1976, 61, 340. 4. Acar,
J. F., Chabbert, X. A. Antimicrob. Ag. Chemother.1971, p. 280.