- Email: [email protected]
Use of reagent strips to diagnose bacterial meningitis
THE LANCET
surveillance system can neither be used as a source of information on the health status of children known to be at high risk of later problems, nor to track children born at very low gestational age. In addition to the known determinants of later problems, such as haemorrhagic and hypoxic-ischaemic cerebral damage, extremely preterm babies are exposed to several less well understood, potentially potent, influences at a stage of very rapid development, both antenatally and postnatally. These include prolonged endogenous and exogenous glucocorticoid exposure, chronic pain, chronic nutritional impairment, and a disordered environmental milieu. The lack of information on the later health of extremely preterm babies has been highlighted repeatedly.2–5 The results of our study have been conveyed to the Department of Health but we have had no response. The failure to ensure adequate follow-up of vulnerable infants and collection and collation of information nationally, represents failure of the duty of care towards a high-risk group and a lost opportunity to follow an interesting group into adulthood. *Neena Modi, Toni Carpenter Department of Paediatrics and Neonatal Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 0NN, UK
1
2
3
4
5
Kramer MS, Joseph KS. Enigma of fetal/infant-origins hypothesis. Lancet 1996; 348: 1254–55. Hall DMB, ed. Health for all children: a programme for child health surveillance. Report of the joint working party on child health surveillance, 2nd ed. Oxford: Oxford University Press, 1991. Expert Maternity Group. Changing childbirth. London: HM Stationery Office, 1993. Neonatal Intensive Care Clinical Standards Advisory Group. London: HM Stationery Office, 1993. Audit Commission. Children first: a study of hospital services. Audit Commission NHS services report no 7. London: HM Stationery Office, 1993.
SIR—Kramer and Joseph1 cast doubt on the association of deficiencies of fetal and infant growth with adult chronic illness without considering the mechanisms likely to contribute to the fascinating epidemiological observations which have been made by Barker, his colleagues, and other groups around the world. Poor intrauterine growth can result from protein/calorie malnutrition, toxic influences such as smoking or alcohol, deficiencies of several different micronutrients, or a combination of toxicity and deficiency, as well as from complications in the pregnancy. Both magnesium and zinc deficiency, for instance, correlated closely with poor intrauterine growth,2 women receiving zinc supplements had bigger babies,3 and small babies gained weight more quickly with a zinc supplement.4 Barker has distinguished different
Vol 349 • January 25, 1997
patterns of restriction of fetal and infant growth that correlate with different patterns of adult chronic disease, according to which tissue was most vulnerable at the time of restriction. Kramer and Joseph1 see difficulties in this work. First, they say, “studies of associations between fetal growth and subsequent chronic disease must control for socioeconomic status at birth and during early childhood if they are to avoid confounding those associations”. Second, different studies do not all show similar associations. To correct data for socioeconomic status would be a logical absurdity. How would the parents’ socioeconomic status affect the health of the child in later life? Surely low socioeconomic status is a marker for deprivation, characterised by a greater risk of various toxic influences and poor nutrition, all of which contribute to poor intrauterine growth. It is for those studying the effects of socioeconomic factors to ask whether these are equally effective throughout childhood, or whether the perinatal period is critical: animals and man are most susceptible to toxins and to deficiencies during early life, and deficiencies accentuate the effects of toxins. Even in developed countries several relevant nutritional deficiencies are common, particularly among the less well-off. Poor intrauterine and infant growth in these epidemiological studies will have had various causes in different areas and at different times. Iron is needed for haemoglobin, zinc for DNA and RNA synthesis and for healthy development of brain and immune system, iodine for the thyroid, &c. The effect on tissues will depend on their sensitivity to any toxin and/or their need for the particular nutrient that is deficient at the time. Deficiencies vary from place to place. No-one who asks questions about the mechanisms leading to the effects that Barker and colleagues have studied would expect them to be identical worldwide. The surprising thing is that such effects have been found in so many studies. The use of synthetic chemicals was starting to rise when the people in these epidemiological studies were born, but not identically everywhere; there has been an explosion since. What effect is this having on the future incidence of chronic disease? Is the increase in allergies a warning sign? We cannot afford to be complacent about these data. Over 7% of babies are less than 2500 g at birth in the less affluent areas of the UK, and the UK Ministry of Agriculture, Fisheries and Food5 reports that the average intake of iron, magnesium, and zinc are 93%, 84%, and 98% of the dietary reference values, with the intake of zinc steadily falling. We should be doing everything possible to reduce the number of
pregnancies in which there is poor intrauterine growth: nutritional supplementation before conception and during pregnancy has been claimed to work and should at least be tried. *H M Anthony, D J Maberly Airedale Allergy Centre, Keighley BD20 6SB, UK
1
2
3
4
5
Kramer MS, Joseph KS. Enigma of fetal/infant-origins hypothesis. Lancet 1996; 348: 1254–55. Doyle W, Crawford MA, Wynn AHA, et al. Maternal nutrient intake and birthweight. J Hum Nutr Diet 1989; 2: 415–22. Goldenberg RL, Tamura T, Neggers Y, et al. The effect of zinc supplementation on pregnancy outcome. JAMA 1995; 274: 463–68. Castillo-Duran C, Rodriguez A, Venegas G, et al. Zinc supplementation and growth of infants born small for gestational age. J Pediatr 1995; 127: 206–11. Ministry of Agriculture, Fisheries and Food. National food survey 1994. London: HM Stationery Office, 1995.
Use of reagent strips to diagnose bacterial meningitis SIR—Further study on the use of reagent strips to diagnose bacterial meningitis1 by Molyneux and Walsh (Oct 26, p 1170)2 prompts us to highlight an important aspect of the test area which indicates the presence of leucocytes. Specifically, these patches detect activity of esterase, which occurs in granulocytes.3 Moreover, the lowest absolute number of neutrophils detected (by the patch) in cerebrospinal fluid has been shown experimentally to be 40 per L. Only a trace reaction was found with 88 per L, and frankly positive results were apparent with concentrations equal to or greater than 175 per L. Finally, false-negative results may also occur when the cerebrospinal fluid total protein is substantially raised (eg, 3 g/L).3 These circumstances might explain the insensitivity of the strip to diagnose bacterial meningitis found by Molyneux and Walsh, insofar as white cells (ie, granulocytes) need to be concentrated at more than 200 per L for production of a cloudy fluid.4 They also preclude use of the strip in accurately diagnosing (presumptive) viral meningitis, a condition characterised by an excess in white cells, predominantly of mononuclear type.4 Or, indeed, its use for distinguishing normal from infected cerebrospinal fluid. We agree with Molyneux and Walsh that caution is needed in the use of reagent strips for the diagnosis of meningitis. V Bonev, *R F Gledhill Department of Neurology, MEDUNSA/Ga-Rankuwa Hospital, Medunsa 0204, South Africa
287
THE LANCET 1
2
3
4
Moosa AA, Quortum HA, Ibrahim MD. Rapid diagnosis of bacterial meningitis with reagent stips. Lancet 1995; 345; 1290–91. Molyneux E, Walsh A. Caution in the use of reagent strips to diagnose acute bacterial meningitis. Lancet 1996; 348: 1170–71. Smalley DL, Doyle VR, Duckworth JK. Correlation of leucocyte esterase detection and the presence of leucocytes in body fluids. Am J Med Technol 1982; 48: 135–37. Fishman RA. Cerebrospinal fluid in diseases of the nervous system. 2nd ed. Philadelphia: WB Saunders, 1992: 184 & 278.
Patent foramen ovale and decompression illness in divers SIR—Johnson and co-workers (Nov 30, p 1515)1 comment on Wilmshurst and colleagues’ report.2 Both groups discuss the potential role of right-to-left cardiac shunts in decompression illness. Atrial right-to-left shunts offer a route for a venous bubble to become arterialised. Wilmshurst offers a solution to the potential risk factor by way of closing the atrial communication with a button device. He describes the technique used in two divers with a large patent foramen ovale (PFO), one of whom had three episodes of decompression illness with a neurological component. Johnson claims the relation between PFO and acute decompression illness needs further investigation, before button devices are more widely used. His suggestion is to conduct a prospective study of PFO in divers. The forthcoming changes in the Diving at Work Regulations as published by the Health and Safety Executive (HSE) are cited as an opportunity to introduce such a study. Such a study would be both scientifically and ethically questionable for the following reasons. The professional diving community can be divided into two distinct groups: those that work offshore and those that work onshore. Decompression illness from offshore air-diving operations on the UK continental shelf has been well documented.3 Furthermore, the HSE, acting on recommendations in a followup report,4 have placed restrictions on offshore air diving operations that have reduced the frequency of decompression illness to a level acceptable to both the HSE and the industry. In offshore diving, between 1982 and 1990, a total of 115 446 air dives gave rise to an average decompression rate of 0·04%. Episodes of decompression illness with a neurological component for the years 1987, 1988, 1989, and 1990 were 1, 3, 3, and 5, respectively. On the other hand, the frequency of decompression illness in onshore divers is unknown. Both the HSE and the industry believe that there are no grounds for concern. In any event, if onshore divers were to adopt the same diving practices as the offshore
288
community, their decompression illness rates would probably be similar. And since the decompression illness rate in offshore divers is acceptably low (0·04%) what would be gained from the proposed study? Furthermore, who would ethically approve such a study, and would the population being studied have a choice in participation? Most professional divers pay for their own fitness-to-dive medical examination. If PFO screening is introduced as an HSE requirement, would professional divers be asked to pay for it as part of a research project? G D Laden 34 Lascelles Avenue, Withernsea, E Yorks HU19 2EB, UK
1
2
3
4
Johnston RP, Broome JR, Hunt PD, Benton PJ. Patent foramen ovale and decompression illness in divers. Lancet 1996; 348: 1515. Wilmshurst P, Walsh K, Morrison L. Transcatheter occlusion of foramen ovale with a button device after neurological decompression illness in professional divers. Lancet 1996; 348: 752–53. Shields TG, Lee WB. Report to the Department of Energy: decompression sickness from offshore air-diving operations on the UK continental shelf during 1982/83. Shields TG, Duff P, Wilcox SE. Report to the Health and Safety Executive: decompression sickness from commercial offshore air-diving operations on the UK continental shelf during 1990.
SIR—Turner (Nov 30, p 1515)1 states that it is not the patency of a foramen ovale but size of the shunt that is important in aetiology of decompression illness. Less than 5% of the population have a shunt large enough to put them at greatest risk.2 Most but not all shunts are across a patent foramen ovale (PFO). We have used two Amplatzer devices to close a fenestrated atrial septal defect in a diver who had spinal decompression illness after an unprovocative 32 m dive. We have occasionally seen cases in whom shunting was through pulmonary arteriovenous malformations. We have consistently referred to “right-to-left interatrial shunts” unless the anatomical natures of defects were confirmed.2,3 Larger PFOs will usually be associated with bigger shunts, but the pressure gradient is important. The gradient varies between individuals and across time, which may, in part, explain the observations of Johnston and colleagues.4 The report of a diver with an atrial septal defect but no history of decompression illness does not disprove the association between shunts and decompression illness. Many cases we described had uneventful deep dives but had decompression illness after shallower dives. There are factors besides variability in shunt size. Doppler studies show that for a given dive profile the amount of venous bubble nucleation varies considerably between divers and in the same individual on different
occasions. To get paradoxical gas embolism one needs coincidence of clinically significant shunting when there is appreciable venous bubbling. Contrast echocardiography proves that paradoxical gas embolism alone does not produce decompression illness. Our unpublished research on dive profiles of air, nitrox, and technical (trimix) divers who have shunt-related decompression illness supports the view that the partial pressure of nitrogen in target tissues that amplify emboli is critical. Shunt-related neurological decompression illness typically follows a single maximum nostop air dive to about 30 m of seawater. After such a dive the spinal white matter (nitrogen uptake half-time of 8–10 min) is virtually saturated with nitrogen at a partial pressure of 3·2 bar. For deeper no-stop dives the bottom time is reduced so that the nitrogen content of the cord is lower. For longer deep dives, the compulsory stops allow off-gassing of nitrogen from the cord before bubble embolism occurs. The proposed prospective study4 would be unethical. Could one conceal the result of contrast echocardiography from participants? If the study was open dive practices might be affected by knowledge of the results. Some prospective data have been obtained. Cross and colleagues described 26 divers who had a shunt but no history of decompression illness.5 Our observations2 suggest that less than five had shunts large enough to be at great risk of decompression illness. One such diver in whom Cross found “a patent foramen ovale which was evident on the first injection of contrast . . . during spontaneous respiration” had neurological decompression illness characteristic of a shunt-related bend after being told that his shunt did not necessitate any changes in dive practices. *Peter Wilmshurst, Kevin Walsh, Lindsay Morrison *Royal Shrewsbury Hospital, Shrewsbury SY3 8XQ, UK; Alder Hey Children’s Hospital, Liverpool; and Cardiothoracic Centre, Liverpool
1
2
3
4
5
Turner M. Patent foramen ovale and decompression illness in divers. Lancet 1996; 348: 1515. Wilmshurst P, Davidson C, O’Connell G, Byrne C. Role of cardiorespiratory abnormalities, smoking and dive charactistics in the manifestations of neurological decompression illness. Clin Sci 1994; 86: 297–303. Wilmshurst PT, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers. Lancet 1989; ii: 1302–06. Johnston RP, Broome JR, Hunt PD, Benton PJ. Patent foramen ovale and decompression illness in divers. Lancet 1996; 348: 1515. Cross SJ, Evans SA, Thomson LF, Lee HS, Jennings KP, Shields TG. Safety of subaqua diving with a patent foramen ovale. BMJ 1992; 304: 481–82.
Vol 349 • January 25, 1997
surveillance system can neither be used as a source of information on the health status of children known to be at high risk of later problems, nor to track children born at very low gestational age. In addition to the known determinants of later problems, such as haemorrhagic and hypoxic-ischaemic cerebral damage, extremely preterm babies are exposed to several less well understood, potentially potent, influences at a stage of very rapid development, both antenatally and postnatally. These include prolonged endogenous and exogenous glucocorticoid exposure, chronic pain, chronic nutritional impairment, and a disordered environmental milieu. The lack of information on the later health of extremely preterm babies has been highlighted repeatedly.2–5 The results of our study have been conveyed to the Department of Health but we have had no response. The failure to ensure adequate follow-up of vulnerable infants and collection and collation of information nationally, represents failure of the duty of care towards a high-risk group and a lost opportunity to follow an interesting group into adulthood. *Neena Modi, Toni Carpenter Department of Paediatrics and Neonatal Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 0NN, UK
1
2
3
4
5
Kramer MS, Joseph KS. Enigma of fetal/infant-origins hypothesis. Lancet 1996; 348: 1254–55. Hall DMB, ed. Health for all children: a programme for child health surveillance. Report of the joint working party on child health surveillance, 2nd ed. Oxford: Oxford University Press, 1991. Expert Maternity Group. Changing childbirth. London: HM Stationery Office, 1993. Neonatal Intensive Care Clinical Standards Advisory Group. London: HM Stationery Office, 1993. Audit Commission. Children first: a study of hospital services. Audit Commission NHS services report no 7. London: HM Stationery Office, 1993.
SIR—Kramer and Joseph1 cast doubt on the association of deficiencies of fetal and infant growth with adult chronic illness without considering the mechanisms likely to contribute to the fascinating epidemiological observations which have been made by Barker, his colleagues, and other groups around the world. Poor intrauterine growth can result from protein/calorie malnutrition, toxic influences such as smoking or alcohol, deficiencies of several different micronutrients, or a combination of toxicity and deficiency, as well as from complications in the pregnancy. Both magnesium and zinc deficiency, for instance, correlated closely with poor intrauterine growth,2 women receiving zinc supplements had bigger babies,3 and small babies gained weight more quickly with a zinc supplement.4 Barker has distinguished different
Vol 349 • January 25, 1997
patterns of restriction of fetal and infant growth that correlate with different patterns of adult chronic disease, according to which tissue was most vulnerable at the time of restriction. Kramer and Joseph1 see difficulties in this work. First, they say, “studies of associations between fetal growth and subsequent chronic disease must control for socioeconomic status at birth and during early childhood if they are to avoid confounding those associations”. Second, different studies do not all show similar associations. To correct data for socioeconomic status would be a logical absurdity. How would the parents’ socioeconomic status affect the health of the child in later life? Surely low socioeconomic status is a marker for deprivation, characterised by a greater risk of various toxic influences and poor nutrition, all of which contribute to poor intrauterine growth. It is for those studying the effects of socioeconomic factors to ask whether these are equally effective throughout childhood, or whether the perinatal period is critical: animals and man are most susceptible to toxins and to deficiencies during early life, and deficiencies accentuate the effects of toxins. Even in developed countries several relevant nutritional deficiencies are common, particularly among the less well-off. Poor intrauterine and infant growth in these epidemiological studies will have had various causes in different areas and at different times. Iron is needed for haemoglobin, zinc for DNA and RNA synthesis and for healthy development of brain and immune system, iodine for the thyroid, &c. The effect on tissues will depend on their sensitivity to any toxin and/or their need for the particular nutrient that is deficient at the time. Deficiencies vary from place to place. No-one who asks questions about the mechanisms leading to the effects that Barker and colleagues have studied would expect them to be identical worldwide. The surprising thing is that such effects have been found in so many studies. The use of synthetic chemicals was starting to rise when the people in these epidemiological studies were born, but not identically everywhere; there has been an explosion since. What effect is this having on the future incidence of chronic disease? Is the increase in allergies a warning sign? We cannot afford to be complacent about these data. Over 7% of babies are less than 2500 g at birth in the less affluent areas of the UK, and the UK Ministry of Agriculture, Fisheries and Food5 reports that the average intake of iron, magnesium, and zinc are 93%, 84%, and 98% of the dietary reference values, with the intake of zinc steadily falling. We should be doing everything possible to reduce the number of
pregnancies in which there is poor intrauterine growth: nutritional supplementation before conception and during pregnancy has been claimed to work and should at least be tried. *H M Anthony, D J Maberly Airedale Allergy Centre, Keighley BD20 6SB, UK
1
2
3
4
5
Kramer MS, Joseph KS. Enigma of fetal/infant-origins hypothesis. Lancet 1996; 348: 1254–55. Doyle W, Crawford MA, Wynn AHA, et al. Maternal nutrient intake and birthweight. J Hum Nutr Diet 1989; 2: 415–22. Goldenberg RL, Tamura T, Neggers Y, et al. The effect of zinc supplementation on pregnancy outcome. JAMA 1995; 274: 463–68. Castillo-Duran C, Rodriguez A, Venegas G, et al. Zinc supplementation and growth of infants born small for gestational age. J Pediatr 1995; 127: 206–11. Ministry of Agriculture, Fisheries and Food. National food survey 1994. London: HM Stationery Office, 1995.
Use of reagent strips to diagnose bacterial meningitis SIR—Further study on the use of reagent strips to diagnose bacterial meningitis1 by Molyneux and Walsh (Oct 26, p 1170)2 prompts us to highlight an important aspect of the test area which indicates the presence of leucocytes. Specifically, these patches detect activity of esterase, which occurs in granulocytes.3 Moreover, the lowest absolute number of neutrophils detected (by the patch) in cerebrospinal fluid has been shown experimentally to be 40 per L. Only a trace reaction was found with 88 per L, and frankly positive results were apparent with concentrations equal to or greater than 175 per L. Finally, false-negative results may also occur when the cerebrospinal fluid total protein is substantially raised (eg, 3 g/L).3 These circumstances might explain the insensitivity of the strip to diagnose bacterial meningitis found by Molyneux and Walsh, insofar as white cells (ie, granulocytes) need to be concentrated at more than 200 per L for production of a cloudy fluid.4 They also preclude use of the strip in accurately diagnosing (presumptive) viral meningitis, a condition characterised by an excess in white cells, predominantly of mononuclear type.4 Or, indeed, its use for distinguishing normal from infected cerebrospinal fluid. We agree with Molyneux and Walsh that caution is needed in the use of reagent strips for the diagnosis of meningitis. V Bonev, *R F Gledhill Department of Neurology, MEDUNSA/Ga-Rankuwa Hospital, Medunsa 0204, South Africa
287
THE LANCET 1
2
3
4
Moosa AA, Quortum HA, Ibrahim MD. Rapid diagnosis of bacterial meningitis with reagent stips. Lancet 1995; 345; 1290–91. Molyneux E, Walsh A. Caution in the use of reagent strips to diagnose acute bacterial meningitis. Lancet 1996; 348: 1170–71. Smalley DL, Doyle VR, Duckworth JK. Correlation of leucocyte esterase detection and the presence of leucocytes in body fluids. Am J Med Technol 1982; 48: 135–37. Fishman RA. Cerebrospinal fluid in diseases of the nervous system. 2nd ed. Philadelphia: WB Saunders, 1992: 184 & 278.
Patent foramen ovale and decompression illness in divers SIR—Johnson and co-workers (Nov 30, p 1515)1 comment on Wilmshurst and colleagues’ report.2 Both groups discuss the potential role of right-to-left cardiac shunts in decompression illness. Atrial right-to-left shunts offer a route for a venous bubble to become arterialised. Wilmshurst offers a solution to the potential risk factor by way of closing the atrial communication with a button device. He describes the technique used in two divers with a large patent foramen ovale (PFO), one of whom had three episodes of decompression illness with a neurological component. Johnson claims the relation between PFO and acute decompression illness needs further investigation, before button devices are more widely used. His suggestion is to conduct a prospective study of PFO in divers. The forthcoming changes in the Diving at Work Regulations as published by the Health and Safety Executive (HSE) are cited as an opportunity to introduce such a study. Such a study would be both scientifically and ethically questionable for the following reasons. The professional diving community can be divided into two distinct groups: those that work offshore and those that work onshore. Decompression illness from offshore air-diving operations on the UK continental shelf has been well documented.3 Furthermore, the HSE, acting on recommendations in a followup report,4 have placed restrictions on offshore air diving operations that have reduced the frequency of decompression illness to a level acceptable to both the HSE and the industry. In offshore diving, between 1982 and 1990, a total of 115 446 air dives gave rise to an average decompression rate of 0·04%. Episodes of decompression illness with a neurological component for the years 1987, 1988, 1989, and 1990 were 1, 3, 3, and 5, respectively. On the other hand, the frequency of decompression illness in onshore divers is unknown. Both the HSE and the industry believe that there are no grounds for concern. In any event, if onshore divers were to adopt the same diving practices as the offshore
288
community, their decompression illness rates would probably be similar. And since the decompression illness rate in offshore divers is acceptably low (0·04%) what would be gained from the proposed study? Furthermore, who would ethically approve such a study, and would the population being studied have a choice in participation? Most professional divers pay for their own fitness-to-dive medical examination. If PFO screening is introduced as an HSE requirement, would professional divers be asked to pay for it as part of a research project? G D Laden 34 Lascelles Avenue, Withernsea, E Yorks HU19 2EB, UK
1
2
3
4
Johnston RP, Broome JR, Hunt PD, Benton PJ. Patent foramen ovale and decompression illness in divers. Lancet 1996; 348: 1515. Wilmshurst P, Walsh K, Morrison L. Transcatheter occlusion of foramen ovale with a button device after neurological decompression illness in professional divers. Lancet 1996; 348: 752–53. Shields TG, Lee WB. Report to the Department of Energy: decompression sickness from offshore air-diving operations on the UK continental shelf during 1982/83. Shields TG, Duff P, Wilcox SE. Report to the Health and Safety Executive: decompression sickness from commercial offshore air-diving operations on the UK continental shelf during 1990.
SIR—Turner (Nov 30, p 1515)1 states that it is not the patency of a foramen ovale but size of the shunt that is important in aetiology of decompression illness. Less than 5% of the population have a shunt large enough to put them at greatest risk.2 Most but not all shunts are across a patent foramen ovale (PFO). We have used two Amplatzer devices to close a fenestrated atrial septal defect in a diver who had spinal decompression illness after an unprovocative 32 m dive. We have occasionally seen cases in whom shunting was through pulmonary arteriovenous malformations. We have consistently referred to “right-to-left interatrial shunts” unless the anatomical natures of defects were confirmed.2,3 Larger PFOs will usually be associated with bigger shunts, but the pressure gradient is important. The gradient varies between individuals and across time, which may, in part, explain the observations of Johnston and colleagues.4 The report of a diver with an atrial septal defect but no history of decompression illness does not disprove the association between shunts and decompression illness. Many cases we described had uneventful deep dives but had decompression illness after shallower dives. There are factors besides variability in shunt size. Doppler studies show that for a given dive profile the amount of venous bubble nucleation varies considerably between divers and in the same individual on different
occasions. To get paradoxical gas embolism one needs coincidence of clinically significant shunting when there is appreciable venous bubbling. Contrast echocardiography proves that paradoxical gas embolism alone does not produce decompression illness. Our unpublished research on dive profiles of air, nitrox, and technical (trimix) divers who have shunt-related decompression illness supports the view that the partial pressure of nitrogen in target tissues that amplify emboli is critical. Shunt-related neurological decompression illness typically follows a single maximum nostop air dive to about 30 m of seawater. After such a dive the spinal white matter (nitrogen uptake half-time of 8–10 min) is virtually saturated with nitrogen at a partial pressure of 3·2 bar. For deeper no-stop dives the bottom time is reduced so that the nitrogen content of the cord is lower. For longer deep dives, the compulsory stops allow off-gassing of nitrogen from the cord before bubble embolism occurs. The proposed prospective study4 would be unethical. Could one conceal the result of contrast echocardiography from participants? If the study was open dive practices might be affected by knowledge of the results. Some prospective data have been obtained. Cross and colleagues described 26 divers who had a shunt but no history of decompression illness.5 Our observations2 suggest that less than five had shunts large enough to be at great risk of decompression illness. One such diver in whom Cross found “a patent foramen ovale which was evident on the first injection of contrast . . . during spontaneous respiration” had neurological decompression illness characteristic of a shunt-related bend after being told that his shunt did not necessitate any changes in dive practices. *Peter Wilmshurst, Kevin Walsh, Lindsay Morrison *Royal Shrewsbury Hospital, Shrewsbury SY3 8XQ, UK; Alder Hey Children’s Hospital, Liverpool; and Cardiothoracic Centre, Liverpool
1
2
3
4
5
Turner M. Patent foramen ovale and decompression illness in divers. Lancet 1996; 348: 1515. Wilmshurst P, Davidson C, O’Connell G, Byrne C. Role of cardiorespiratory abnormalities, smoking and dive charactistics in the manifestations of neurological decompression illness. Clin Sci 1994; 86: 297–303. Wilmshurst PT, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers. Lancet 1989; ii: 1302–06. Johnston RP, Broome JR, Hunt PD, Benton PJ. Patent foramen ovale and decompression illness in divers. Lancet 1996; 348: 1515. Cross SJ, Evans SA, Thomson LF, Lee HS, Jennings KP, Shields TG. Safety of subaqua diving with a patent foramen ovale. BMJ 1992; 304: 481–82.
Vol 349 • January 25, 1997