- Email: [email protected]
Shifts in mortality curves
colleagues1 note, analysis of data from other laboratories could support or counter these findings. Gabor Komaromy-Hiller, *Kern L Nuttall Department of Pathology, University of Utah, Salt Lake City, UT, USA; and *ARUP Laboratories, Salt Lake City, UT 84108 (e-mail: [email protected]) 1
Lawrence JM, Petitti DB, Watkins M, Umekubo MA. Trends in serum folate after food fortification. Lancet 1999; 354: 915–16. 2 Malinow MR, Duell PB, Hess DL, et al. Reduction of plasma homocyst(e)ine levels by breakfast cereal fortified with folic acid in patients with coronary heart disease. N Engl J Med 1998; 338: 1009–15. 3 Wu LL, Wu J, Hurt SC, et al. Plasma homocyst(e)ine as a risk factor for early coronary artery disease. Clin Chem 1994; 40: 552–61. 4 Abramsky L, Botting B, Chapple J, Stone D. Has advice on periconceptional folate supplementation reduced neural-tube defects? Lancet 1999; 354: 998–99.
Sir—Jean Lawrence and colleagues1 report that blood folate concentrations have increased in the USA after folic acid fortification of enriched grain products. Their findings are consistent with those recently reported by Jacques and colleagues.2 Both groups attribute these trends to folic acid fortification, which is believed to have been implemented by mid-1997. Although these findings are encouraging, to date we have seen no studies that examine the potential effects of fortification on the prevalence of NTDs. We present here an early assessment of the birth prevalence of NTDs after fortification. From the North Carolina Birth Defects Monitoring Program, a population-based surveillance programme that covers about 100 000 live births per year, we identified 361 liveborn and stillborn infants with NTDs who were delivered between Jan 1, 1995, and Dec 31, 1998. We matched case records with North Carolina vital statistics files and used the reported date of last menses to estimate the date of conception for each case. Rates of NTDs were calculated on the basis of the date of conception by dividing the number of cases conceived during a given period by the total number of liveborn infants whose conception occurred during that time. NTD rates for the 36 months immediately before fortification (July, 1994, to June, 1997) were used to predict the rates among conceptions occurring after fortification began (July, 1997, to March, 1998). A slight downward trend in the rate of total NTDs (from 10·2 to 7·5 per 10 000 live births) and spina bifida (from 6·0 to 4·4 per 10 000 live births) was seen for conceptions occurring during the 36-month prefortification
2168
period, whereas the rate for anencephaly remained constant (2·2 per 10 000 live births). Among fetuses conceived during the 9 months after fortification, we found very little difference between the observed and expected rates of total NTDs, anencephaly, and spina bifida. In fact, the rate for fetal NTDs increased to 7·9 per 10 000 live births after fortification. Folic acid fortification in the USA was predicted to increase the average woman’s consumption of folic acid by only 100 g per day, or a quarter the amount recommended for birth-defect prevention.3 Our early findings, which show no evidence of a change in NTD trends after fortification, support the assertion that the current fortification concentration in the USA is too low for full prevention of birth defects. We continue to monitor these trends and will reassess the situation in the future. However, on the basis of our data, we cannot assume that the increased postfortification blood folate concentrations reported in the studies by Lawrence et al,1 and Jacques et al,2 are any indication that fortification has led to a decline in NTD rates. Seldom do we have an opportunity to implement a cheap, simple, and safe public-health programme that can present severe, life-altering conditions such as spina bifida and anencephaly. To improve the health of children, governments should immediately implement fortification programmes that will increase consumption of folic acid by at least 400 g a day. Until such programmes are implemented, we should teach women of reproductive age to consume daily vitamin supplements containing 400 g of synthetic folic acid. The North Carolina Birth Defects Monitoring Program is funded by a grant from the North Carolina chapters of the March of Dimes Birth Defects Foundation and by a cooperative agreement (U50/CCU416075-01) with the Division of Birth Defects and Pediatric Genetics, Centers for Disease Control and Prevention.
*Robert E Meyer, Godfrey P Oakley Jr *Division of Public Health, North Carolina Department of Health and Human Services, Raleigh, NC 27699, USA; and Rollins School of Public Health, Emory University, Atlanta, GA (e-mail: [email protected]) 1
Lawrence JM, Petitti DB, Watkins M, Umekubo MA. Trends in serum folate after food fortification. Lancet 1999; 354: 915–16. 2 Jacques PF, Selhub J, Bostom AG, Wilson PWF, Rosenberg IH. The effect of folic acid fortification on plasma folate and total homocysteine concentrations. N Engl J Med 1999; 340: 1449–54. 3 Institute of Medicine, Food and Nutrition Board. Dietary reference intakes: thiamine, riboflavin, niacin, vitamin B6, folate vitamin B12, pantothenic acid, biotin, and choline. Washington, DC: National Academy Press, 1999.
Shifts in mortality curves Sir—L B Tan and R Murphy’s review (Oct 16, p 1378)1 on presentation of trial mortality data is both highly relevant and timely in the context of current medical practice. With the onslaught of evidence-based medicine derived from large randomised trials, the practice of medicine is becoming more dogmatic. As Tan and Murphy state, there is substantial public and peer pressure to prescribe drugs that are widely reported as being beneficial. For the practising clinician, it is difficult to distinguish between statistical benefit and clinical relevance of a specific therapeutic agent, as reported in trials. Thus, knowledge of the extra time gained with an improved quality of life will certainly help patients and clinicians to decide whether a drug should be taken daily for the rest of the patient’s life. Further, drugs carry costs and may have adverse effects, including death. Undertaking of a trial with wide entry criteria to show the benefits of a drug can only produce findings relevant to the specific trial population that are valid only for the duration of the trial. The “law of averages” is at work here. If a specific drug benefits more patients than it harms, then this drug would be of positive value, and its prescription is encouraged. The entry criteria for the trial then determine which patients get the new treatment, but these criteria may not identify whether a therapeutic agent would benefit a particular patient on an individual basis. In this traditional approach, a patient is told that if he or she takes a drug, and if there are x number of other patients doing the same for y length of time, then z number of lives would be saved within the timeframe. The drawback is that there is no way of telling whether this patient will be one of the z patients. This is a pressing issue when x and y are large, with a small z and the disease is chronic. We should be putting more effort into the classification of patients before drug initiation, and the development of more objective measures to assess and monitor both the beneficial and harmful effects of drugs. This difficulty is especially acute in chronic heart failure in which each new therapy (angiotensin-converting enzyme inhibitor, -blocker, angiotensin II antagonist, and so on) causes a further fall in the patient’s already low blood pressure. This difficulty may force us into more tailoring of therapy to the individual. For example, we reported that angiotensin-converting enzyme inhibitors only enhance
THE LANCET • Vol 354 • December 18/25, 1999
natriuresis in diuretic-treated heartfailure patients with neurohormonal activation.2–4 Others have shown that angiotensin-converting enzyme inhibition is not associated with any haemodynamic advantage in patients without neurohormonal activation. 5 Research should thus be directed to find out which individuals would benefit from a specific therapy. *Pitt O Lim, Allan D Struthers Cardiovascular Research Group, Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK (e-mail: [email protected]) 1
Tan LB, Murphy R. Shifts in mortality curves: saving or extending lives? Lancet 1999; 354: 1378–81. 2 Lim PO, MacFadyen RJ, Struthers AD. Is there a role for renin profiling in selecting chronic heart failure patients for ACE inhibitor therapy? Heart (in press). 3 Swedberg K, Eneroth P, Kjekshus J, Snapinn S. Effects of enalapril and neuroendocrine activation on prognosis in severe congestive heart failure (follow-up of the CONSENSUS trial). Am J Cardiol 1990; 66: 40D–44D. 4 Francis GS, Cohn JN, Johnson G, Rector TS, Goldman S, Simon A. Plasma norepinephrine, plasma renin activity, and congestive heart failure. Relations to survival and the effects of therapy in V-HeFT II. Circulation 1993; 87: V140–48. 5 Cody RJ, Laragh JH, Atlas SA, Case DB. Converting enzyme inhibition to identify and treat renin-mediated or sodium-volume related forms of increased peripheral resistance in hypertension and in congestive heart failure. J Hypertens 1983; 1 (suppl): 77–84.
Sir—L B Tan and R Murphy’s review of mortality curves 1 is a useful guide to the meaningful interpretation of large mortality trials. However, the example used to expose the difficulties in decision making, with respect to prescribing angiotensin-converting enzyme inhibitors to a group of wheelchair-bound patients with incontinence and heart failure, rather suggests that attempts at prolonging the life of these patients (often elderly) should not be made, even for an average of 6 months as Tan and Murphy suggest. The general practitioner in the example is more likely to be making use of the other known benefits of angiotensinconverting enzyme inhibitors in this group of patients, to improve the symptoms of heart failure2,3 and thereby reducing the frequency of admission for this condition.4,5 Sean P Brotheridge
of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987; 316: 1429–35. 3 The SOLVD Investigators. Effects of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991; 325: 293–302. 4 Riegger GAJ. ACE inhibitors in early stages of heart failure. Circulation 1993; 87: 117–19. 5 Hart W, Rhodes G, McMurray J. The cost effectiveness of enalapril in the treatment of chronic heart failure. Br J Health Econ 1993; 6: 91–98.
Episiotomy and faecal incontinence Sir—3 months after Marsden Wagner’s (June 5, p 1977)1 call for an international campaign against episiotomy and the assumption that episiotomy does more harm than good 2 as far as faecal incontinence is concerned, Michelle Fynes and colleagues (Sept 18, p 983) 3 in their observational study of obstetric injury to the anal sphincters do not even mention the potential risk of this procedure. Once such an important risk factor has been overlooked, recourse to caesarean delivery may seem hasty. At a time when the increased rate of caesarean sections is a matter of concern, 4 a clear identification of avoidable risk factors (such as episiotomy) for faecal incontinence should be the first step. If episiotomy is one of the main risk factors for anal injury, it is certainly not wise to recommend another surgical procedure that carries an even higher level of risk to overcome what most view as an iatrogenic hazard. There is a worrying damnation in gynaecology, a medical specialty in which the question of doing more harm than good could be raised f r e q u e n t l y . 5 I suggest that a moratorium of episiotomies would have a greater impact on women’s faecal continence and quality of life than any further increase in caesarean section rate. Marc Girard
*Michael Bowen, Hilary Ockendon
1, boulevard de la République, 78000 Versailles, France
*Department of Obstetrics and Gynaecology, Oxford Radcliffe Trust Hospitals, Horton Hospital, Banbury OX16 9AG, UK; and University of Oxford Centre for Industrial and Applied Mathematics, Mathematical Institute, Oxford
1 2
3
Department of Medicine for the Elderly, Harrogate District Hospital, Harrogate HG2 7SX, UK (e-mail: [email protected]) 1
2
Tan LB, Murphy R. Shifts in mortality curves: saving or extending lives? Lancet 1999; 354: 1378–81. The Consensus Trial Study Group. Effects
THE LANCET • Vol 354 • December 18/25, 1999
Sir—Michelle Fynes and colleagues 1 suggest that primiparous women who develop symptomatic and symptomless anal-sphincter injuries after their first vaginal delivery are more likely to sustain symptomatic injury after a second vaginal delivery. They go on to suggest the injury may be related to a lengthened pudendal-nerve terminal motor latency, which may be prevented by elective caesarean section. It is disappointing that at no point do they explore the effects of episiotomy or consider that increasing the vaginal aperture may reduce the tension in the surrounding tissues and in particular reduce the risk of anal-sphincter disruption. We are currently exploring various mathematical models that could be applied to what is essentially a biological engineering problem. In engineering, at most levels of stress all but the very shortest cracks have an energetic incentive to propagate. The Griffith energy balance (the possibility of a crack of more than a certain length to propagate) is common to all elastic materials. When cracks in tissues are shallow, propagation consumes more energy as surface energy than it releases as relaxed strain energy, and therefore conditions are unfavourable for the crack to propagate. As the crack becomes larger these conditions are reversed, and beyond the critical Griffith length the crack may run away in an explosive manner in brittle materials.2 These conditions are influenced by fault lines introduced into materials, and geometric changes in the outlet, such as occurs with a surgical cut to the perineal outlet. A modified median episiotomy 3 increases the diameter at the vaginal outlet 83% more than that provided by a median episiotomy and 10% greater than a mediolateral episiotomy. If episiotomy is indicated, the exclusive use of this procedure makes the occurrence of third-degree tears extremely rare.
4 5
Wagner M. Episiotomy: a form of genital mutilation. Lancet 1999; 353: 1977–78. Kelleher C, Braude P. Recent advances: gynaecology. BMJ 1999; 319: 689–92. Fynes M, Donnelly V, Behan M, O’Connell PR, O’Herlihy C. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet 1999; 354: 983–86. Editorial. What is the right number of caesarean sections? Lancet 1997; 349: 815. Pini P. Doctors should have left well alone. Lancet 1996; 347: 1174.
1
2
3
Fynes M, Donnelly V, Behan M, O’Connell PR, O’Herlihy C. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet 1999; 354: 983–86. Gordon JE. The new science of strong materials. London: Pelican, 1968: 99–120. May-James L. Modified median episiotomy minimizes the risk of third-degree tears. Obstet Gynaecol 1994; 83: 156–57.
2169
Lawrence JM, Petitti DB, Watkins M, Umekubo MA. Trends in serum folate after food fortification. Lancet 1999; 354: 915–16. 2 Malinow MR, Duell PB, Hess DL, et al. Reduction of plasma homocyst(e)ine levels by breakfast cereal fortified with folic acid in patients with coronary heart disease. N Engl J Med 1998; 338: 1009–15. 3 Wu LL, Wu J, Hurt SC, et al. Plasma homocyst(e)ine as a risk factor for early coronary artery disease. Clin Chem 1994; 40: 552–61. 4 Abramsky L, Botting B, Chapple J, Stone D. Has advice on periconceptional folate supplementation reduced neural-tube defects? Lancet 1999; 354: 998–99.
Sir—Jean Lawrence and colleagues1 report that blood folate concentrations have increased in the USA after folic acid fortification of enriched grain products. Their findings are consistent with those recently reported by Jacques and colleagues.2 Both groups attribute these trends to folic acid fortification, which is believed to have been implemented by mid-1997. Although these findings are encouraging, to date we have seen no studies that examine the potential effects of fortification on the prevalence of NTDs. We present here an early assessment of the birth prevalence of NTDs after fortification. From the North Carolina Birth Defects Monitoring Program, a population-based surveillance programme that covers about 100 000 live births per year, we identified 361 liveborn and stillborn infants with NTDs who were delivered between Jan 1, 1995, and Dec 31, 1998. We matched case records with North Carolina vital statistics files and used the reported date of last menses to estimate the date of conception for each case. Rates of NTDs were calculated on the basis of the date of conception by dividing the number of cases conceived during a given period by the total number of liveborn infants whose conception occurred during that time. NTD rates for the 36 months immediately before fortification (July, 1994, to June, 1997) were used to predict the rates among conceptions occurring after fortification began (July, 1997, to March, 1998). A slight downward trend in the rate of total NTDs (from 10·2 to 7·5 per 10 000 live births) and spina bifida (from 6·0 to 4·4 per 10 000 live births) was seen for conceptions occurring during the 36-month prefortification
2168
period, whereas the rate for anencephaly remained constant (2·2 per 10 000 live births). Among fetuses conceived during the 9 months after fortification, we found very little difference between the observed and expected rates of total NTDs, anencephaly, and spina bifida. In fact, the rate for fetal NTDs increased to 7·9 per 10 000 live births after fortification. Folic acid fortification in the USA was predicted to increase the average woman’s consumption of folic acid by only 100 g per day, or a quarter the amount recommended for birth-defect prevention.3 Our early findings, which show no evidence of a change in NTD trends after fortification, support the assertion that the current fortification concentration in the USA is too low for full prevention of birth defects. We continue to monitor these trends and will reassess the situation in the future. However, on the basis of our data, we cannot assume that the increased postfortification blood folate concentrations reported in the studies by Lawrence et al,1 and Jacques et al,2 are any indication that fortification has led to a decline in NTD rates. Seldom do we have an opportunity to implement a cheap, simple, and safe public-health programme that can present severe, life-altering conditions such as spina bifida and anencephaly. To improve the health of children, governments should immediately implement fortification programmes that will increase consumption of folic acid by at least 400 g a day. Until such programmes are implemented, we should teach women of reproductive age to consume daily vitamin supplements containing 400 g of synthetic folic acid. The North Carolina Birth Defects Monitoring Program is funded by a grant from the North Carolina chapters of the March of Dimes Birth Defects Foundation and by a cooperative agreement (U50/CCU416075-01) with the Division of Birth Defects and Pediatric Genetics, Centers for Disease Control and Prevention.
*Robert E Meyer, Godfrey P Oakley Jr *Division of Public Health, North Carolina Department of Health and Human Services, Raleigh, NC 27699, USA; and Rollins School of Public Health, Emory University, Atlanta, GA (e-mail: [email protected]) 1
Lawrence JM, Petitti DB, Watkins M, Umekubo MA. Trends in serum folate after food fortification. Lancet 1999; 354: 915–16. 2 Jacques PF, Selhub J, Bostom AG, Wilson PWF, Rosenberg IH. The effect of folic acid fortification on plasma folate and total homocysteine concentrations. N Engl J Med 1999; 340: 1449–54. 3 Institute of Medicine, Food and Nutrition Board. Dietary reference intakes: thiamine, riboflavin, niacin, vitamin B6, folate vitamin B12, pantothenic acid, biotin, and choline. Washington, DC: National Academy Press, 1999.
Shifts in mortality curves Sir—L B Tan and R Murphy’s review (Oct 16, p 1378)1 on presentation of trial mortality data is both highly relevant and timely in the context of current medical practice. With the onslaught of evidence-based medicine derived from large randomised trials, the practice of medicine is becoming more dogmatic. As Tan and Murphy state, there is substantial public and peer pressure to prescribe drugs that are widely reported as being beneficial. For the practising clinician, it is difficult to distinguish between statistical benefit and clinical relevance of a specific therapeutic agent, as reported in trials. Thus, knowledge of the extra time gained with an improved quality of life will certainly help patients and clinicians to decide whether a drug should be taken daily for the rest of the patient’s life. Further, drugs carry costs and may have adverse effects, including death. Undertaking of a trial with wide entry criteria to show the benefits of a drug can only produce findings relevant to the specific trial population that are valid only for the duration of the trial. The “law of averages” is at work here. If a specific drug benefits more patients than it harms, then this drug would be of positive value, and its prescription is encouraged. The entry criteria for the trial then determine which patients get the new treatment, but these criteria may not identify whether a therapeutic agent would benefit a particular patient on an individual basis. In this traditional approach, a patient is told that if he or she takes a drug, and if there are x number of other patients doing the same for y length of time, then z number of lives would be saved within the timeframe. The drawback is that there is no way of telling whether this patient will be one of the z patients. This is a pressing issue when x and y are large, with a small z and the disease is chronic. We should be putting more effort into the classification of patients before drug initiation, and the development of more objective measures to assess and monitor both the beneficial and harmful effects of drugs. This difficulty is especially acute in chronic heart failure in which each new therapy (angiotensin-converting enzyme inhibitor, -blocker, angiotensin II antagonist, and so on) causes a further fall in the patient’s already low blood pressure. This difficulty may force us into more tailoring of therapy to the individual. For example, we reported that angiotensin-converting enzyme inhibitors only enhance
THE LANCET • Vol 354 • December 18/25, 1999
natriuresis in diuretic-treated heartfailure patients with neurohormonal activation.2–4 Others have shown that angiotensin-converting enzyme inhibition is not associated with any haemodynamic advantage in patients without neurohormonal activation. 5 Research should thus be directed to find out which individuals would benefit from a specific therapy. *Pitt O Lim, Allan D Struthers Cardiovascular Research Group, Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK (e-mail: [email protected]) 1
Tan LB, Murphy R. Shifts in mortality curves: saving or extending lives? Lancet 1999; 354: 1378–81. 2 Lim PO, MacFadyen RJ, Struthers AD. Is there a role for renin profiling in selecting chronic heart failure patients for ACE inhibitor therapy? Heart (in press). 3 Swedberg K, Eneroth P, Kjekshus J, Snapinn S. Effects of enalapril and neuroendocrine activation on prognosis in severe congestive heart failure (follow-up of the CONSENSUS trial). Am J Cardiol 1990; 66: 40D–44D. 4 Francis GS, Cohn JN, Johnson G, Rector TS, Goldman S, Simon A. Plasma norepinephrine, plasma renin activity, and congestive heart failure. Relations to survival and the effects of therapy in V-HeFT II. Circulation 1993; 87: V140–48. 5 Cody RJ, Laragh JH, Atlas SA, Case DB. Converting enzyme inhibition to identify and treat renin-mediated or sodium-volume related forms of increased peripheral resistance in hypertension and in congestive heart failure. J Hypertens 1983; 1 (suppl): 77–84.
Sir—L B Tan and R Murphy’s review of mortality curves 1 is a useful guide to the meaningful interpretation of large mortality trials. However, the example used to expose the difficulties in decision making, with respect to prescribing angiotensin-converting enzyme inhibitors to a group of wheelchair-bound patients with incontinence and heart failure, rather suggests that attempts at prolonging the life of these patients (often elderly) should not be made, even for an average of 6 months as Tan and Murphy suggest. The general practitioner in the example is more likely to be making use of the other known benefits of angiotensinconverting enzyme inhibitors in this group of patients, to improve the symptoms of heart failure2,3 and thereby reducing the frequency of admission for this condition.4,5 Sean P Brotheridge
of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987; 316: 1429–35. 3 The SOLVD Investigators. Effects of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991; 325: 293–302. 4 Riegger GAJ. ACE inhibitors in early stages of heart failure. Circulation 1993; 87: 117–19. 5 Hart W, Rhodes G, McMurray J. The cost effectiveness of enalapril in the treatment of chronic heart failure. Br J Health Econ 1993; 6: 91–98.
Episiotomy and faecal incontinence Sir—3 months after Marsden Wagner’s (June 5, p 1977)1 call for an international campaign against episiotomy and the assumption that episiotomy does more harm than good 2 as far as faecal incontinence is concerned, Michelle Fynes and colleagues (Sept 18, p 983) 3 in their observational study of obstetric injury to the anal sphincters do not even mention the potential risk of this procedure. Once such an important risk factor has been overlooked, recourse to caesarean delivery may seem hasty. At a time when the increased rate of caesarean sections is a matter of concern, 4 a clear identification of avoidable risk factors (such as episiotomy) for faecal incontinence should be the first step. If episiotomy is one of the main risk factors for anal injury, it is certainly not wise to recommend another surgical procedure that carries an even higher level of risk to overcome what most view as an iatrogenic hazard. There is a worrying damnation in gynaecology, a medical specialty in which the question of doing more harm than good could be raised f r e q u e n t l y . 5 I suggest that a moratorium of episiotomies would have a greater impact on women’s faecal continence and quality of life than any further increase in caesarean section rate. Marc Girard
*Michael Bowen, Hilary Ockendon
1, boulevard de la République, 78000 Versailles, France
*Department of Obstetrics and Gynaecology, Oxford Radcliffe Trust Hospitals, Horton Hospital, Banbury OX16 9AG, UK; and University of Oxford Centre for Industrial and Applied Mathematics, Mathematical Institute, Oxford
1 2
3
Department of Medicine for the Elderly, Harrogate District Hospital, Harrogate HG2 7SX, UK (e-mail: [email protected]) 1
2
Tan LB, Murphy R. Shifts in mortality curves: saving or extending lives? Lancet 1999; 354: 1378–81. The Consensus Trial Study Group. Effects
THE LANCET • Vol 354 • December 18/25, 1999
Sir—Michelle Fynes and colleagues 1 suggest that primiparous women who develop symptomatic and symptomless anal-sphincter injuries after their first vaginal delivery are more likely to sustain symptomatic injury after a second vaginal delivery. They go on to suggest the injury may be related to a lengthened pudendal-nerve terminal motor latency, which may be prevented by elective caesarean section. It is disappointing that at no point do they explore the effects of episiotomy or consider that increasing the vaginal aperture may reduce the tension in the surrounding tissues and in particular reduce the risk of anal-sphincter disruption. We are currently exploring various mathematical models that could be applied to what is essentially a biological engineering problem. In engineering, at most levels of stress all but the very shortest cracks have an energetic incentive to propagate. The Griffith energy balance (the possibility of a crack of more than a certain length to propagate) is common to all elastic materials. When cracks in tissues are shallow, propagation consumes more energy as surface energy than it releases as relaxed strain energy, and therefore conditions are unfavourable for the crack to propagate. As the crack becomes larger these conditions are reversed, and beyond the critical Griffith length the crack may run away in an explosive manner in brittle materials.2 These conditions are influenced by fault lines introduced into materials, and geometric changes in the outlet, such as occurs with a surgical cut to the perineal outlet. A modified median episiotomy 3 increases the diameter at the vaginal outlet 83% more than that provided by a median episiotomy and 10% greater than a mediolateral episiotomy. If episiotomy is indicated, the exclusive use of this procedure makes the occurrence of third-degree tears extremely rare.
4 5
Wagner M. Episiotomy: a form of genital mutilation. Lancet 1999; 353: 1977–78. Kelleher C, Braude P. Recent advances: gynaecology. BMJ 1999; 319: 689–92. Fynes M, Donnelly V, Behan M, O’Connell PR, O’Herlihy C. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet 1999; 354: 983–86. Editorial. What is the right number of caesarean sections? Lancet 1997; 349: 815. Pini P. Doctors should have left well alone. Lancet 1996; 347: 1174.
1
2
3
Fynes M, Donnelly V, Behan M, O’Connell PR, O’Herlihy C. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet 1999; 354: 983–86. Gordon JE. The new science of strong materials. London: Pelican, 1968: 99–120. May-James L. Modified median episiotomy minimizes the risk of third-degree tears. Obstet Gynaecol 1994; 83: 156–57.
2169