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LACTATE DEHYDROGENASE IN URÆMIA
906
hssmatological findings in 34 patients with other chronic infections, such as pulmonary tuberculosis and pyogenic lung abscess, with those in 41 subjects in apparent good health. Our results will be reported more fully elsewhere. Mean values in the patients with chronic infection were: Hb 9-6 g. per 100 ml. (range 4-8-13-5 g. per 100 ml.), M.C.H.C. 29.4% (range 25,0-32,5%). In the controls the means were: Hb 14-9 g. per 100 ml. (range 12-0-16-8 g. per 100 ml.), M.C.H.C. 33-3% (range 31-0-35-0%). Our belief that the hypochromic anaemia which is commonly associated with chronic infection is not due to irondeficiency is borne out by our finding 24 patients out of 34 in this series (and 15 among the 31 with amoebic liver abscess) with Hb under 12-0 g. per 100 ml., and M.C.H.C. values of 30% or less. Similar findings have been reported in Seattle,4although the proportion of patients with hypochromic anaemia was lower. the
Department of Medicine, University of Natal, and
E. B. ADAMS F. G. H. MAYET.
King Edward VIII Hospital, Durban, South Africa.
UROCANIC-ACID AND FOLIC-ACID ESTIMATION SIR,-The normal metabolic degradation of histidine to glutamic acid takes place via urocanic acid (imidazoleacrylic acid), an unstable intermediary, and formininoglutamic acid (FIGLU). Bennett and Chanarinfound that in states of folicacid deficiency, after a histidine load, FIGLU is often excreted in urine, together with its precursor, urocanic acid. Later, in describing their spectrophotometric method 6 for the combined estimation of FIGLU and urocanic acid, these workers stressed that urocanic acid may comprise more than 80% of the histidine derivatives appearing in the urine of patients with folic-acid deficiency. Thus the customary estimation of FIGLU, after a histidine load, which does not include urocanic acid, may be completely misleading in trying to prove folicacid deficiency, since FIGLU may comprise as little as 3% of the total histidine derivatives excreted; particularly in longstanding folic acid deficiency, mainly urocanic acid is excreted.’We present here a simple method for the estimation of urocanic acid, based on " two-solutions electrophoresis ". A comprehensive result may be obtained within a few hours. No additional equipment is required when FIGLU is examined
by electrophoresis. Procedure Untreated urine is separated by low-voltage " two-solutions paper-electrophoresis ". Reagents and apparatus are the same as described by us for estimation of vanilmandelic acid8 3,4-dihydroxyphenyl alanine (DOPA), and dopamine.99 An aliquot of urine corresponding to 0-075 mg. creatinine is on an electrophoretic paper-strip (30x4 cm.) 7 cm. from the anode-end of the strip, and run for two hours. Urocanic acid migrates about 8 cm. towards the cathode in this time. After air-drying and heating of the strip, it is dyed with diazotised p-nitroaniline. Urocanic acid gives a purple colour. A standard of urocanic acid can be run simultaneously on a second strip, to facilitate its identification, in addition to the urine. We also use another dye procedure, which is our modification of Pauly’s sulphanilic acid reagent. One part of 0-1% sulphanilic acid in 1% HCI v/v and, one part of 0-2% sodium nitrite are mixed under cooling; after 3 minutes one part of 0-025% ammonium sulphamate, and then two parts of 10% sodium carbonate, are added. The paper strips are immediately dipped through this mixture. Urocanic acid gives a roseyellow colour, next to histidine which migrates a little further and is dyed an intense orange. When viewed, after being airdried, under ultraviolet light (Wood’s light), urocanic acid gives a bright red fluorescence.
applied
4. 5. 6. 7. 8. 9.
Bainton, D. F., Finch, C. A. Bennett, M. C., Chanarin, I. Chanarin, I., Bennett, M. C. Bennett, M. C., Chanarin, I. Eichhorn, F., Rutenberg, A. Eichhorn, F., Rutenberg, A.
Am. J. Med. 1964, 37, 62. Lancet, 1961, ii, 1095. J. 1962, i, 27. Nature, Lond. 1962, 196, 171. Clin. Chem. 1963, 9, 615. ibid. 1965, 11, 563. Br. med.
Interpretation As urocanic acid may not be increased in some cases of folicacid deficiency, a negative result should be followed by an estimation of FIGLU. In the same way, a FIGLU estimation alone would not indicate a folic-acid deficiency in those cases where only urocanic acid is increased." Part of this project was supported by a grant from Lady Edith Wolfson’s Research Fund, through the Israel Cancer Association. Rappaport Laboratories, Biochemical Section, F. EICHHORN Beilinson Hospital, A. RUTENBERG. Petah Tiqva, Israel.
INHIBITION BY SERA OF URÆMIC PATIENTS SiR,ňThe preliminary communication by Dr. Emerson and her colleagues (Sept. 18) deals with the interesting problem of the interaction between ursemic serum and enzyme activities. We 11 have investigated the glutathione-reductase (G.R.) activity of erythrocytes in 53 patients with renal insufficiency, most of them with hyperazotsemia, and we found, in contrast with reports by other workers," considerably raised enzyme activity. Mean values of G.R. activity, in units per g. of Hb, for two groups of patients with chronic and acute renal insufficiency, were respectively 86-4 units (range 43-9-140-0) and 75-1 units (range 49-3-97-0), while in a group of control subjects the mean value was 37-9 units (range 21-0-49-3). G.R. activity increases with urea concentration, but it never reaches values higher than 100-150 units. In acute renal insufficiency, the increase in G.R. activity generally follows the rise of azotaemia, but high G.R. values may be found long after the resolution of the acute episode. Moreover, plasma from ursmic patients with high erythrocytic G.R. values has the remarkable property of inducing in normal erythrocytes a sharp elevation of G.R. activity, far above the normal range, in an incubation system at 37’C constituted by washed erythrocytes from normal blood-compatible donors and urxmic plasma, with the addition of glucose as follows:
Thus, plasma from urxmic patients seems to contain a factor of stimulating erythrocyte G.R.-activity, in agreement with the report 13 of high reduced-glutathione concentrations in red blood-cells of hyperazotxmic patients. Activation seems to be due to a stable and perhaps irreversible modification of the structure of the enzyme, since it is shown after haemolysis and successive dialysis of the haemolysate. Uraemic plasma completely loses its activating power after dialysis against saline, and, almost completely, after heat denaturation at 70-100°C. Further studies are needed to clarify the kinetics of the activation, and to establish the nature of the activating factor. PAOLO BRUNETTI GIUSEPPE G. NENCI Medical Clinic of the ALBERTO PARMA. of University Perugia, Italy.
capable
LACTATE DEHYDROGENASE IN URÆMIA SIR,-We are able to confirm the preliminary communication of Dr. Emerson and her colleagues (Sept. 18) concerning the increase of serum lactate dehydrogenase (L.D.H.) which is often found immediately after haemodialysis in urxmic patients. The possible removal of an easily diffusible inhibitor, as they stress, needs due consideration. We wish to draw attention, however, to other factors which might also play a part. Slight haemolysis, undetected to the naked eye, easily induces an increase of the order of 10% in a normal total serum L.D.H.; one then expects a shift towards the two fastest L.D.H.S (L.D.H. 1 10. 11.
Knowles, J. P. Lancet, 1961, ii, 1149. Brunetti, P., Parma, A., Nenci, G. G. Hœmatologica, 1965, 50, 415. Loehr, G. W., Waller, H. D. Schweiz. med. Wschr. 1962, 92, 1. Wernze, H., Koch, W. Klin. Wschr. 1965, 43, 451.
12. Bock, H. E., 13.
907 and L.D.H. 2) and, accordingly, a selective increase of the so-called 2-hydroxybutyrate dehydrogenase activity. But from our investigations 1-3 one most often encounters an increase of the slowest L.D.H. (L.D.H. 5), which may become quite pronounced in cases of renal tubular disease. Release of L.D.H. from renal tissue seems to us to constitute the most probable explanation for this shift. Indeed, from our observations,1-3 and also from the published reports,4-8 L.D.H. 5 is present in rather high amounts in outer and inner medulla of the kidney. If observations on the striking increase of renal blood-flow which should accompany hxmodialysis 9 are confirmed, one could accept that flushing of the kidney rapidly washes the L.D.H. out of the diseased cells. A detailed account of these thesis by one of us (S. R.).
investigations is being prepared
Medical Clinic of the University of Ghent, Academic
Hospital, Ghent, Belgium.
as a
S. RINGOIR R. J. WIEME.
BLOOD-SAMPLES FROM EAR-LOBE PUNCTURE SIR,-I should like to make some comments on the article by Dr. Langlands and Dr. Wallace (Aug. 14). Some time ago I considered the question whether, in heart and lung disease, the oxygen tension in the capillary blood obtained by ear-lobe puncture corresponds to the arterial oxygen tension. Simultaneous measurements of the oxygen tension of the arterial and capillary blood showed that the differences in these values in 23 patients with heart-disease were within +10% and -20% and those in 25 miners with various degrees of silicosis were within +10%. In heartfailure, the oxygen tension in the capillary blood was clearly lower than that in the arterial blood. With variable conditions of the blood-circulation, the difference between the arterial and capillary oxygen tension was found to be dependent on the degree of peripheral blood congestion. Thus, though the oxygen tension in the capillary blood in healthy subjects may be taken as corresponding to the oxygen tension in the arterial blood, this is not always true in patients with heart and lung disease. Bethanien Hospital, Moers on Rhine, 413, West Germany.
G. WORTH.
NEONATAL ENDOTRACHEAL CONNECTION SIR,-The accompanying figure shows a neonatal endotracheal connection which is made in three sizes intended for use with 2’5, 3’0, and 3’5 mm. Magill endotracheal tubes. The
tube should be bound on to the connection by a few turns of adhesive strapping: this prevents splitting of the tube and consequent separation from’the connection. 1. Ringoir, S., Wieme, R., Regniers, P. J. Urol. med. chir. 1964, 70, 126. 2. Ringoir, S. Proceedings of the 1st Conference of the European Dialysis
and Transplant Association; p. 141. Amsterdam, 1964. Ringoir, S., Wieme, R., Regniers, P. Excerpta med. Int. Cong. Ser. (in the press). 4. Conklin, J. L., Dewey, M. M., May, B. Proc. Soc. exp. Biol. Med. 1960, 105, 492. 5. Fine, I. H., Kaplan, N. O., Kuftinec, D. Biochemistry, 1963, 2, 116. 6. Guttler, F., Clausen, J. Enzymol. biol. clin. 1965, 5, 55. 7. Nisselbaum, J. S., Bodansky, O. J. biol. Chem. 1961, 236, 401. 8. Richterich, R., Schafroth, P., Franz, H. E. Enzymol. biol. clin. 1961, 1, 3.
114.
9.
Pedersen, F., Baunee, B. O., Berthelsen, H. C., Christiansen, P., Kemp, B., Ladefoged, J., Winkler, K. Excerpta med. Int. Cong. Ser. (in the press).
This connection allows stable anchorage of the endotracheal tube at the mouth, and easy introduction of a suction catheter. It is particularly suitable for chest operations in the newborn.’1 I wish to thank Mr. B. Reay Young, of Chas. F. Thackray, Ltd., for his cooperation. Newcastle Region Thoracic Surgical Unit, Seaham Hall Hospital, Seaham, Co. Durham.
H. E. BELL.
OPERATING-ROOM CONDITIONS SIR,-You have recently published a series of important articles dealing with the dissemination of bacteria from the bodies of members of surgical operating-teams, and I would like to comment on the articles by Mr. Bernard and his colleagues (Sept. 4) and by Dr. Blowers and Sister McCluskey which describe experiments seeking to improve the in operating-theatres. I doubt whether any of the innovations to surgical clothing so far suggested will make more than a marginal improvement in the bacterial content of the air in conventional theatres. I believe that surgeons will have to make the decision to classify types of operation as those fit for good conventional theatres, and those demanding conditions of almost perfect air-sterility, necessitating specially designed installations. My own experiments have reached a point where I can claim that it is possible to operate in air with a bacterial content as low as 0-01 colonies per c.ft. as a normal routine, without irksome encumbrance to the surgeon, and without reduction in the number of major operations performed in a given time. The meaning of this degree of air-cleanliness can be judged2 by regarding 10 colonies per c.ft. as good for a normal theatre, and 2-0-1colonies per c.ft as good for a special theatre. Blowers has emphasised that to reach a level of 2-0-1 colonies per c.ft in a well-ventilated conventional theatre it is necessary to prohibit the opening and closing of doors and the walking about of theatre personnel, and to delay the start of the operation until the general commotion of bringing in the patient has had time to settle down; all this impedes normal surgical routine, and will reduce the turnover of cases. In this centre we have been operating for the past four years in an enclosure3 which encourages conditions approximating to laminar air-flow, in a vertically downward direction, at a linear air-speed of about 20 ft. per minute. This speed of flow is still not sufficient to prevent movements of the surgeon’s arms producing local reversals of the direction of flow, and therefore bacteria-laden particles will not invariaby be swept downwards to the floor at their moment of emergence from the operating-gown, which was the original purpose of the system. To get a linear air-speed of 20 ft. per minute necessitates about 100 air-changes per hour, even in our small enclosure; so that the relative stagnation of air in a good modern theatre can be judged from the fact that it is not usual to have more than 15-20 air-changes per hour. To achieve a palpable draught in a vertically downward direction would need an air-flow of about 100 ft. per minute, and in our enclosure this would correspond to 500 air-changes per hour, which is clearly out of the question in a large operating-suite. Since we are still getting a certain amount of mixing of the air inside our enclosure, despite its 100 changes of air per hour, we have had the opportunity under actual operating conditions of making a large number of slit-sampler observations of the effects of different types of surgical clothing in protecting the incoming clean air from contamination by three surgeons and the lower half of the body of the patient. The surgeon and assistants wear a simple type of respirator " through which all expired air is sucked out of the mask so that it is not permitted to enter the enclosure. With the surgical team wearing all-enveloping sterile cotton helmets over the conventional cap and mask, and ordinary surgical gowns with wrap-over backs, the slit-sampler will show an average of 0-2 colonies per c.ft. in air taken through a long tube from the operating-table,
(Oct. 2) clothing
worn
"
1. 2. 3.
Bell, H. E. Thorax, 1965, 20, 1. Bourdillon, R. B., McFarlan, A. M., Thomas, J. C. Spec. Rep. Ser. med. Res. Coun. 1948, no. 262, p. 241. Charnley, J. Br. J. Surg. 1964, 51, 195.
hssmatological findings in 34 patients with other chronic infections, such as pulmonary tuberculosis and pyogenic lung abscess, with those in 41 subjects in apparent good health. Our results will be reported more fully elsewhere. Mean values in the patients with chronic infection were: Hb 9-6 g. per 100 ml. (range 4-8-13-5 g. per 100 ml.), M.C.H.C. 29.4% (range 25,0-32,5%). In the controls the means were: Hb 14-9 g. per 100 ml. (range 12-0-16-8 g. per 100 ml.), M.C.H.C. 33-3% (range 31-0-35-0%). Our belief that the hypochromic anaemia which is commonly associated with chronic infection is not due to irondeficiency is borne out by our finding 24 patients out of 34 in this series (and 15 among the 31 with amoebic liver abscess) with Hb under 12-0 g. per 100 ml., and M.C.H.C. values of 30% or less. Similar findings have been reported in Seattle,4although the proportion of patients with hypochromic anaemia was lower. the
Department of Medicine, University of Natal, and
E. B. ADAMS F. G. H. MAYET.
King Edward VIII Hospital, Durban, South Africa.
UROCANIC-ACID AND FOLIC-ACID ESTIMATION SIR,-The normal metabolic degradation of histidine to glutamic acid takes place via urocanic acid (imidazoleacrylic acid), an unstable intermediary, and formininoglutamic acid (FIGLU). Bennett and Chanarinfound that in states of folicacid deficiency, after a histidine load, FIGLU is often excreted in urine, together with its precursor, urocanic acid. Later, in describing their spectrophotometric method 6 for the combined estimation of FIGLU and urocanic acid, these workers stressed that urocanic acid may comprise more than 80% of the histidine derivatives appearing in the urine of patients with folic-acid deficiency. Thus the customary estimation of FIGLU, after a histidine load, which does not include urocanic acid, may be completely misleading in trying to prove folicacid deficiency, since FIGLU may comprise as little as 3% of the total histidine derivatives excreted; particularly in longstanding folic acid deficiency, mainly urocanic acid is excreted.’We present here a simple method for the estimation of urocanic acid, based on " two-solutions electrophoresis ". A comprehensive result may be obtained within a few hours. No additional equipment is required when FIGLU is examined
by electrophoresis. Procedure Untreated urine is separated by low-voltage " two-solutions paper-electrophoresis ". Reagents and apparatus are the same as described by us for estimation of vanilmandelic acid8 3,4-dihydroxyphenyl alanine (DOPA), and dopamine.99 An aliquot of urine corresponding to 0-075 mg. creatinine is on an electrophoretic paper-strip (30x4 cm.) 7 cm. from the anode-end of the strip, and run for two hours. Urocanic acid migrates about 8 cm. towards the cathode in this time. After air-drying and heating of the strip, it is dyed with diazotised p-nitroaniline. Urocanic acid gives a purple colour. A standard of urocanic acid can be run simultaneously on a second strip, to facilitate its identification, in addition to the urine. We also use another dye procedure, which is our modification of Pauly’s sulphanilic acid reagent. One part of 0-1% sulphanilic acid in 1% HCI v/v and, one part of 0-2% sodium nitrite are mixed under cooling; after 3 minutes one part of 0-025% ammonium sulphamate, and then two parts of 10% sodium carbonate, are added. The paper strips are immediately dipped through this mixture. Urocanic acid gives a roseyellow colour, next to histidine which migrates a little further and is dyed an intense orange. When viewed, after being airdried, under ultraviolet light (Wood’s light), urocanic acid gives a bright red fluorescence.
applied
4. 5. 6. 7. 8. 9.
Bainton, D. F., Finch, C. A. Bennett, M. C., Chanarin, I. Chanarin, I., Bennett, M. C. Bennett, M. C., Chanarin, I. Eichhorn, F., Rutenberg, A. Eichhorn, F., Rutenberg, A.
Am. J. Med. 1964, 37, 62. Lancet, 1961, ii, 1095. J. 1962, i, 27. Nature, Lond. 1962, 196, 171. Clin. Chem. 1963, 9, 615. ibid. 1965, 11, 563. Br. med.
Interpretation As urocanic acid may not be increased in some cases of folicacid deficiency, a negative result should be followed by an estimation of FIGLU. In the same way, a FIGLU estimation alone would not indicate a folic-acid deficiency in those cases where only urocanic acid is increased." Part of this project was supported by a grant from Lady Edith Wolfson’s Research Fund, through the Israel Cancer Association. Rappaport Laboratories, Biochemical Section, F. EICHHORN Beilinson Hospital, A. RUTENBERG. Petah Tiqva, Israel.
INHIBITION BY SERA OF URÆMIC PATIENTS SiR,ňThe preliminary communication by Dr. Emerson and her colleagues (Sept. 18) deals with the interesting problem of the interaction between ursemic serum and enzyme activities. We 11 have investigated the glutathione-reductase (G.R.) activity of erythrocytes in 53 patients with renal insufficiency, most of them with hyperazotsemia, and we found, in contrast with reports by other workers," considerably raised enzyme activity. Mean values of G.R. activity, in units per g. of Hb, for two groups of patients with chronic and acute renal insufficiency, were respectively 86-4 units (range 43-9-140-0) and 75-1 units (range 49-3-97-0), while in a group of control subjects the mean value was 37-9 units (range 21-0-49-3). G.R. activity increases with urea concentration, but it never reaches values higher than 100-150 units. In acute renal insufficiency, the increase in G.R. activity generally follows the rise of azotaemia, but high G.R. values may be found long after the resolution of the acute episode. Moreover, plasma from ursmic patients with high erythrocytic G.R. values has the remarkable property of inducing in normal erythrocytes a sharp elevation of G.R. activity, far above the normal range, in an incubation system at 37’C constituted by washed erythrocytes from normal blood-compatible donors and urxmic plasma, with the addition of glucose as follows:
Thus, plasma from urxmic patients seems to contain a factor of stimulating erythrocyte G.R.-activity, in agreement with the report 13 of high reduced-glutathione concentrations in red blood-cells of hyperazotxmic patients. Activation seems to be due to a stable and perhaps irreversible modification of the structure of the enzyme, since it is shown after haemolysis and successive dialysis of the haemolysate. Uraemic plasma completely loses its activating power after dialysis against saline, and, almost completely, after heat denaturation at 70-100°C. Further studies are needed to clarify the kinetics of the activation, and to establish the nature of the activating factor. PAOLO BRUNETTI GIUSEPPE G. NENCI Medical Clinic of the ALBERTO PARMA. of University Perugia, Italy.
capable
LACTATE DEHYDROGENASE IN URÆMIA SIR,-We are able to confirm the preliminary communication of Dr. Emerson and her colleagues (Sept. 18) concerning the increase of serum lactate dehydrogenase (L.D.H.) which is often found immediately after haemodialysis in urxmic patients. The possible removal of an easily diffusible inhibitor, as they stress, needs due consideration. We wish to draw attention, however, to other factors which might also play a part. Slight haemolysis, undetected to the naked eye, easily induces an increase of the order of 10% in a normal total serum L.D.H.; one then expects a shift towards the two fastest L.D.H.S (L.D.H. 1 10. 11.
Knowles, J. P. Lancet, 1961, ii, 1149. Brunetti, P., Parma, A., Nenci, G. G. Hœmatologica, 1965, 50, 415. Loehr, G. W., Waller, H. D. Schweiz. med. Wschr. 1962, 92, 1. Wernze, H., Koch, W. Klin. Wschr. 1965, 43, 451.
12. Bock, H. E., 13.
907 and L.D.H. 2) and, accordingly, a selective increase of the so-called 2-hydroxybutyrate dehydrogenase activity. But from our investigations 1-3 one most often encounters an increase of the slowest L.D.H. (L.D.H. 5), which may become quite pronounced in cases of renal tubular disease. Release of L.D.H. from renal tissue seems to us to constitute the most probable explanation for this shift. Indeed, from our observations,1-3 and also from the published reports,4-8 L.D.H. 5 is present in rather high amounts in outer and inner medulla of the kidney. If observations on the striking increase of renal blood-flow which should accompany hxmodialysis 9 are confirmed, one could accept that flushing of the kidney rapidly washes the L.D.H. out of the diseased cells. A detailed account of these thesis by one of us (S. R.).
investigations is being prepared
Medical Clinic of the University of Ghent, Academic
Hospital, Ghent, Belgium.
as a
S. RINGOIR R. J. WIEME.
BLOOD-SAMPLES FROM EAR-LOBE PUNCTURE SIR,-I should like to make some comments on the article by Dr. Langlands and Dr. Wallace (Aug. 14). Some time ago I considered the question whether, in heart and lung disease, the oxygen tension in the capillary blood obtained by ear-lobe puncture corresponds to the arterial oxygen tension. Simultaneous measurements of the oxygen tension of the arterial and capillary blood showed that the differences in these values in 23 patients with heart-disease were within +10% and -20% and those in 25 miners with various degrees of silicosis were within +10%. In heartfailure, the oxygen tension in the capillary blood was clearly lower than that in the arterial blood. With variable conditions of the blood-circulation, the difference between the arterial and capillary oxygen tension was found to be dependent on the degree of peripheral blood congestion. Thus, though the oxygen tension in the capillary blood in healthy subjects may be taken as corresponding to the oxygen tension in the arterial blood, this is not always true in patients with heart and lung disease. Bethanien Hospital, Moers on Rhine, 413, West Germany.
G. WORTH.
NEONATAL ENDOTRACHEAL CONNECTION SIR,-The accompanying figure shows a neonatal endotracheal connection which is made in three sizes intended for use with 2’5, 3’0, and 3’5 mm. Magill endotracheal tubes. The
tube should be bound on to the connection by a few turns of adhesive strapping: this prevents splitting of the tube and consequent separation from’the connection. 1. Ringoir, S., Wieme, R., Regniers, P. J. Urol. med. chir. 1964, 70, 126. 2. Ringoir, S. Proceedings of the 1st Conference of the European Dialysis
and Transplant Association; p. 141. Amsterdam, 1964. Ringoir, S., Wieme, R., Regniers, P. Excerpta med. Int. Cong. Ser. (in the press). 4. Conklin, J. L., Dewey, M. M., May, B. Proc. Soc. exp. Biol. Med. 1960, 105, 492. 5. Fine, I. H., Kaplan, N. O., Kuftinec, D. Biochemistry, 1963, 2, 116. 6. Guttler, F., Clausen, J. Enzymol. biol. clin. 1965, 5, 55. 7. Nisselbaum, J. S., Bodansky, O. J. biol. Chem. 1961, 236, 401. 8. Richterich, R., Schafroth, P., Franz, H. E. Enzymol. biol. clin. 1961, 1, 3.
114.
9.
Pedersen, F., Baunee, B. O., Berthelsen, H. C., Christiansen, P., Kemp, B., Ladefoged, J., Winkler, K. Excerpta med. Int. Cong. Ser. (in the press).
This connection allows stable anchorage of the endotracheal tube at the mouth, and easy introduction of a suction catheter. It is particularly suitable for chest operations in the newborn.’1 I wish to thank Mr. B. Reay Young, of Chas. F. Thackray, Ltd., for his cooperation. Newcastle Region Thoracic Surgical Unit, Seaham Hall Hospital, Seaham, Co. Durham.
H. E. BELL.
OPERATING-ROOM CONDITIONS SIR,-You have recently published a series of important articles dealing with the dissemination of bacteria from the bodies of members of surgical operating-teams, and I would like to comment on the articles by Mr. Bernard and his colleagues (Sept. 4) and by Dr. Blowers and Sister McCluskey which describe experiments seeking to improve the in operating-theatres. I doubt whether any of the innovations to surgical clothing so far suggested will make more than a marginal improvement in the bacterial content of the air in conventional theatres. I believe that surgeons will have to make the decision to classify types of operation as those fit for good conventional theatres, and those demanding conditions of almost perfect air-sterility, necessitating specially designed installations. My own experiments have reached a point where I can claim that it is possible to operate in air with a bacterial content as low as 0-01 colonies per c.ft. as a normal routine, without irksome encumbrance to the surgeon, and without reduction in the number of major operations performed in a given time. The meaning of this degree of air-cleanliness can be judged2 by regarding 10 colonies per c.ft. as good for a normal theatre, and 2-0-1colonies per c.ft as good for a special theatre. Blowers has emphasised that to reach a level of 2-0-1 colonies per c.ft in a well-ventilated conventional theatre it is necessary to prohibit the opening and closing of doors and the walking about of theatre personnel, and to delay the start of the operation until the general commotion of bringing in the patient has had time to settle down; all this impedes normal surgical routine, and will reduce the turnover of cases. In this centre we have been operating for the past four years in an enclosure3 which encourages conditions approximating to laminar air-flow, in a vertically downward direction, at a linear air-speed of about 20 ft. per minute. This speed of flow is still not sufficient to prevent movements of the surgeon’s arms producing local reversals of the direction of flow, and therefore bacteria-laden particles will not invariaby be swept downwards to the floor at their moment of emergence from the operating-gown, which was the original purpose of the system. To get a linear air-speed of 20 ft. per minute necessitates about 100 air-changes per hour, even in our small enclosure; so that the relative stagnation of air in a good modern theatre can be judged from the fact that it is not usual to have more than 15-20 air-changes per hour. To achieve a palpable draught in a vertically downward direction would need an air-flow of about 100 ft. per minute, and in our enclosure this would correspond to 500 air-changes per hour, which is clearly out of the question in a large operating-suite. Since we are still getting a certain amount of mixing of the air inside our enclosure, despite its 100 changes of air per hour, we have had the opportunity under actual operating conditions of making a large number of slit-sampler observations of the effects of different types of surgical clothing in protecting the incoming clean air from contamination by three surgeons and the lower half of the body of the patient. The surgeon and assistants wear a simple type of respirator " through which all expired air is sucked out of the mask so that it is not permitted to enter the enclosure. With the surgical team wearing all-enveloping sterile cotton helmets over the conventional cap and mask, and ordinary surgical gowns with wrap-over backs, the slit-sampler will show an average of 0-2 colonies per c.ft. in air taken through a long tube from the operating-table,
(Oct. 2) clothing
worn
"
1. 2. 3.
Bell, H. E. Thorax, 1965, 20, 1. Bourdillon, R. B., McFarlan, A. M., Thomas, J. C. Spec. Rep. Ser. med. Res. Coun. 1948, no. 262, p. 241. Charnley, J. Br. J. Surg. 1964, 51, 195.