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CAPILLARIES IN THE FETAL SCALP
544 CAPILLARIES IN THE FETAL SCALP
SIR,-As admirers of the ingenious transcutaneous (Tc) P02 electrode developed by A. and R. Huch we aredismayed that they and their colleagues (Feb. 16, p. 369) seem to have misread our Nov. 3 paper. We did not "disclaim any merit in fetal scalp blood samplirig or in fetal transcutaneous TcP02 monitoring"; we simply raised doubts about its validity, particularly in the second stage of labour. We do not accept that the "important issue is whether it is possible to obtain reliable and reproducible results with the TcP02 technique". The veracity of the electrode is not in contention ; the real issue is whether the fetal scalp circulation is representative of the rest of the fetal circulation. We believe that often it is not, and we agree with our critics when they say that "too low fetal TcP02 levels may be obtained ... if there is stasis in the fetal scalp". In their 1977 paper’ they state that "... a fetal TcP02 level of below 15 mm Hg may suggest insufficient O2 supply to the fetus". Indeed it may, but on other occasions it clearly does not; how can we tell? If the head-to-cervix pressure is, as Lundgren2and we have frequently above 100 mm Hg in both the first and second stages if labour. No capillary squeezed between the cervix and an unyielding skull can remain patent at that pressure, whatever the intracapillary pressure is. How then can we tell when the capillary circulation is unimpeded? We look forward to the solution promised by Professor Rooth and his colleagues, but we can refute in advance any suggestion that the energy required to heat the electrode gives reliable indication of blood flow. We are not alone in that opinion-for example, SeveringhausJ as shown that even under ideal circumstances "only one third of the power was flow dependent". We are also unimpressed by the proposed effect of oedema under the electrode after 2 h; in our experience even after 12 h of recording where zero TcP02 values were obtained in the second stage of labour, the electrode responded immediately to the infant’s first breath. We have great respect for Professor Saling’s work and are saddened by his criticisms in your Feb. 16 issue. When we said that there were "surprisingly few comparisons between scalp values and those in other parts of the circulation" we referred, as the context made plain, to P02 of the human fetus in labour. The papers cited which refer to comparisons in the newborn, in the fetus at caesarean section, or in animals are not relevant. Of the relevant papers cited all but one refer to comparisons of pH, with correlations of around 0.7 between values in fetal scalp blood just before delivery and in umbilical cord blood. In the one study, by Kubli et al.,4 where P02 was also measured ten comparisons were made again with a corre7 lation coefficient of 0-7—0-8. Even a good correlation (and 0.7 is weak) over a large range of POz can conceal a poor correlation at the lower end of the range where accurate interpretation is crucial. A later paper from Kubli’s department5 shows between the last tissue pH "no significant correlation values one minute before’birth and the umbilical arterial or 6 venous blood pH values", much as we found for TcP02" ...
1. Huch
A, Huch R, Schneider H, Rooth G. Continuous transcutaneous moni-
toring of the fetal oxygen tension in labour. Br J Obstet Gynœcol 1977; 84: suppl 1, 30. 2. Lundgren L. The concept of pressure in biology and pressure transducers. Acta Obstet Gynecol Scand 1977; suppl 66: 87. 3. Parker D, Delpy D, Reynolds EOR, St. Andrew D. (discussion by Severinghaus). A transcutaneous PO2 electrode incorporating a thermal clearance: Local blood flow sensor. Acta Anœsth Scand 1978; suppl 68: 33. 4. Kubli F, Berg D, Köhnlein G, Hüter, J, Bretz D. Die mikroblutuntersuchung am fetus: I kritik dev methode. Geburtsh Frauenheilk 1966; 26: 1537. 5. Boos R,
Rüttgers H, Muliawan D, Heinrich D, Kubli F. Continuous of tissue pH in the human fetus. Arch Gynecol 1978; 226:
Professor Saling is also critical of our technique. We did indeed press on the electrode as a simple direct method of observing changes in POz as the underlying blood flow changed, having previously shown that pressure on the electrode itself did not influence its performance. But he is mistaken in his belief that the whole fetus is subject only to intrauterine pressure once the membranes are ruptured. The scalp is at atmospheric pressure and the ring of scalp in contact with the cervix at very high intermittent pressure, as LundgrenZ and we have shown. It is not surprising that the venous congestion associated with this ring of pressure, like a tourniquet on the arm, gives a good flow of blood from a cut.
Despite the attempts by Professor Rooth’s Nordic forbears, among others, to obtain scalp blood from the "ancient kings of Sligo", it is notable that they, of all the Irish royal families, have survived for over 1500 years.7 Division of Perinatal Medicine, Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ
MICHAEL C. O’CONNOR FRANK E. HYTTEN GUISEPPE D. ZANELLI
U.S. PERINATAL MORTALITY STATISTICS
SIR,-There is an error in Dr Hobel’s report on perinatal health in the U.S.A. (Jan. 5, p. 31). A table taken from a U.S. government publication’ is presented, showing changes in fetal and infant mortality over time. The first two rows of mortality data are labelled "fetal, 20 wk" and "fetal C20 wk" (i.e., spontaneous abortion). However, in the original publication these data are labelled "fetal, 20 weeks or more" and "fetal, 28 weeks or more", respectively. This is not a trivial point: Dr Hobel’s table suggests that the occurrence of spontaneous abortion has declined in the same manner as has other fetal and infant mortality, whereas there are no published data from the U.S. or anywhere else (to my knowledge) which address this question. -
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, U.S.A.
ALLEN
J. WILCOX
** Dr Wilcox is quite right, but no blame attaches to Dr Hobel. This was a transcription error for which we apologise to one and all.-ED.L.
CHEST PAIN WITH NORMAL CORONARY ARTERIES
SiR,-Nowhere in
your
Jan. 19 editorial do
you
even con-
sider the
possibility that chest pain, associated with normal cardiological investigations (including coronary angiography’ and not responding to drugs used to treat angina, might be oesophageal. The oesophagus remains a neglected organ sitting in the centre of the thoracic cavity with a retrosternal location. Oesophageal smooth muscle spasm may produce pain: this pain can radiate into the jaws and back, and while it does not have the distinctive association with effort that "effort angina" does, it
can;
because of its location, distribution, and seventy.
myopic cardiologist. Somewhere along the line of investigation of obscure angina-like pain ought to come oesophageal manometry. But even before that the discerlllng clinician will have elicited clinical clues-for example, the pa-
confuse the
measurement
183. 6 O’Connor MC,
Hytten FE. Measurement of fetal transcutaneous oxygen tension-problems and potential. Br J Obstet Gynœcol 1979; 36: 948.
7. McGarry JP. The House of O’Conor. Dublin: Dakota, 1971. 1. Improvement in infant and perinatal mortality in the United States 1965-1973, D-HEW publication (HSA) 78-5743, 1977.
SIR,-As admirers of the ingenious transcutaneous (Tc) P02 electrode developed by A. and R. Huch we aredismayed that they and their colleagues (Feb. 16, p. 369) seem to have misread our Nov. 3 paper. We did not "disclaim any merit in fetal scalp blood samplirig or in fetal transcutaneous TcP02 monitoring"; we simply raised doubts about its validity, particularly in the second stage of labour. We do not accept that the "important issue is whether it is possible to obtain reliable and reproducible results with the TcP02 technique". The veracity of the electrode is not in contention ; the real issue is whether the fetal scalp circulation is representative of the rest of the fetal circulation. We believe that often it is not, and we agree with our critics when they say that "too low fetal TcP02 levels may be obtained ... if there is stasis in the fetal scalp". In their 1977 paper’ they state that "... a fetal TcP02 level of below 15 mm Hg may suggest insufficient O2 supply to the fetus". Indeed it may, but on other occasions it clearly does not; how can we tell? If the head-to-cervix pressure is, as Lundgren2and we have frequently above 100 mm Hg in both the first and second stages if labour. No capillary squeezed between the cervix and an unyielding skull can remain patent at that pressure, whatever the intracapillary pressure is. How then can we tell when the capillary circulation is unimpeded? We look forward to the solution promised by Professor Rooth and his colleagues, but we can refute in advance any suggestion that the energy required to heat the electrode gives reliable indication of blood flow. We are not alone in that opinion-for example, SeveringhausJ as shown that even under ideal circumstances "only one third of the power was flow dependent". We are also unimpressed by the proposed effect of oedema under the electrode after 2 h; in our experience even after 12 h of recording where zero TcP02 values were obtained in the second stage of labour, the electrode responded immediately to the infant’s first breath. We have great respect for Professor Saling’s work and are saddened by his criticisms in your Feb. 16 issue. When we said that there were "surprisingly few comparisons between scalp values and those in other parts of the circulation" we referred, as the context made plain, to P02 of the human fetus in labour. The papers cited which refer to comparisons in the newborn, in the fetus at caesarean section, or in animals are not relevant. Of the relevant papers cited all but one refer to comparisons of pH, with correlations of around 0.7 between values in fetal scalp blood just before delivery and in umbilical cord blood. In the one study, by Kubli et al.,4 where P02 was also measured ten comparisons were made again with a corre7 lation coefficient of 0-7—0-8. Even a good correlation (and 0.7 is weak) over a large range of POz can conceal a poor correlation at the lower end of the range where accurate interpretation is crucial. A later paper from Kubli’s department5 shows between the last tissue pH "no significant correlation values one minute before’birth and the umbilical arterial or 6 venous blood pH values", much as we found for TcP02" ...
1. Huch
A, Huch R, Schneider H, Rooth G. Continuous transcutaneous moni-
toring of the fetal oxygen tension in labour. Br J Obstet Gynœcol 1977; 84: suppl 1, 30. 2. Lundgren L. The concept of pressure in biology and pressure transducers. Acta Obstet Gynecol Scand 1977; suppl 66: 87. 3. Parker D, Delpy D, Reynolds EOR, St. Andrew D. (discussion by Severinghaus). A transcutaneous PO2 electrode incorporating a thermal clearance: Local blood flow sensor. Acta Anœsth Scand 1978; suppl 68: 33. 4. Kubli F, Berg D, Köhnlein G, Hüter, J, Bretz D. Die mikroblutuntersuchung am fetus: I kritik dev methode. Geburtsh Frauenheilk 1966; 26: 1537. 5. Boos R,
Rüttgers H, Muliawan D, Heinrich D, Kubli F. Continuous of tissue pH in the human fetus. Arch Gynecol 1978; 226:
Professor Saling is also critical of our technique. We did indeed press on the electrode as a simple direct method of observing changes in POz as the underlying blood flow changed, having previously shown that pressure on the electrode itself did not influence its performance. But he is mistaken in his belief that the whole fetus is subject only to intrauterine pressure once the membranes are ruptured. The scalp is at atmospheric pressure and the ring of scalp in contact with the cervix at very high intermittent pressure, as LundgrenZ and we have shown. It is not surprising that the venous congestion associated with this ring of pressure, like a tourniquet on the arm, gives a good flow of blood from a cut.
Despite the attempts by Professor Rooth’s Nordic forbears, among others, to obtain scalp blood from the "ancient kings of Sligo", it is notable that they, of all the Irish royal families, have survived for over 1500 years.7 Division of Perinatal Medicine, Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ
MICHAEL C. O’CONNOR FRANK E. HYTTEN GUISEPPE D. ZANELLI
U.S. PERINATAL MORTALITY STATISTICS
SIR,-There is an error in Dr Hobel’s report on perinatal health in the U.S.A. (Jan. 5, p. 31). A table taken from a U.S. government publication’ is presented, showing changes in fetal and infant mortality over time. The first two rows of mortality data are labelled "fetal, 20 wk" and "fetal C20 wk" (i.e., spontaneous abortion). However, in the original publication these data are labelled "fetal, 20 weeks or more" and "fetal, 28 weeks or more", respectively. This is not a trivial point: Dr Hobel’s table suggests that the occurrence of spontaneous abortion has declined in the same manner as has other fetal and infant mortality, whereas there are no published data from the U.S. or anywhere else (to my knowledge) which address this question. -
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, U.S.A.
ALLEN
J. WILCOX
** Dr Wilcox is quite right, but no blame attaches to Dr Hobel. This was a transcription error for which we apologise to one and all.-ED.L.
CHEST PAIN WITH NORMAL CORONARY ARTERIES
SiR,-Nowhere in
your
Jan. 19 editorial do
you
even con-
sider the
possibility that chest pain, associated with normal cardiological investigations (including coronary angiography’ and not responding to drugs used to treat angina, might be oesophageal. The oesophagus remains a neglected organ sitting in the centre of the thoracic cavity with a retrosternal location. Oesophageal smooth muscle spasm may produce pain: this pain can radiate into the jaws and back, and while it does not have the distinctive association with effort that "effort angina" does, it
can;
because of its location, distribution, and seventy.
myopic cardiologist. Somewhere along the line of investigation of obscure angina-like pain ought to come oesophageal manometry. But even before that the discerlllng clinician will have elicited clinical clues-for example, the pa-
confuse the
measurement
183. 6 O’Connor MC,
Hytten FE. Measurement of fetal transcutaneous oxygen tension-problems and potential. Br J Obstet Gynœcol 1979; 36: 948.
7. McGarry JP. The House of O’Conor. Dublin: Dakota, 1971. 1. Improvement in infant and perinatal mortality in the United States 1965-1973, D-HEW publication (HSA) 78-5743, 1977.