283
link5-1O outnumber negative reports,l-3 even sceptics might acknowledge that GOR aggravates bronchospasm in some asthmatic patients. So the question is not so much whether the association exists, but how often, to what degree, and by what mechanism? Experimental data or clinical observations linking GOR and asthma come in several forms. Oesophageal pH
coughs. However, four of the nine patients were asthmatic, so it is unclear whether the GOR caused the cough directly or indirectly via aggravation of the asthma. Moreover, since the observations were uncontrolled there is no certainty that the antireflux regimen was related to the gradual improvement in the cough. Nonetheless, the concept is thought provoking and deserves further consideration
monitoring may show a temporal relation between wheezing and oesophageal acidity:l4 airways resistance increases in some asthmatics during oesophageal acid perfusion;6,8,15 and antireflux treatment sometimes improves the asthma.7,16-18 What is the underlying mechanism? Microaspiration of acid into the airways, and reflex bronchoconstriction as a result of oesophageal acidification are the most plausible suggestions; the second hypothesis has rather more appeal, but neither has been unequivocably substantiated.3,4,9,10 The possibility that asthma or its treatment predisposes to reflux has also been entertained but most of the evidence points in the opposite direction.4,9 The best experimental support for the microaspiration theory comes from a study in cats,l9 in which tracheal infusion of minute amounts of acid led to large increases in airways resistance, an effect abolished by prior vagotomy. Clinical observations in asthmatic patients are less impressive and a scintigraphic technique did not show induces acidification aspiration. 13 Oesophageal bronchospasm in some patients, possibly via a vagal reflex
because it may prove association.
mechanism.6
More recently, Ekstrom and Tibbling10 in Sweden examined nocturnal respiratory and oesophageal events in a large population of patients with asthma and GOR. Although nocturnal reflux significantly reduced the early morning peak expiratory flow it was neither a strong nor an immediate trigger for bronchospasm in most cases. These workers concluded that GOR may increase vagal bronchomotor tone without necessarily eliciting an asthma attack but may stimulate bronchial reactivity and lower the threshold for other bronchospastic factors. Does antireflux treatment alleviate asthma? Most of the supportive observations are anecdotal2 or, at best, open trials.16,17 Two controlled trials7,18 ofH2 receptor antagonists in patients with GOR and asthma have shown only very modest improvements in asthma control and little or no effect on lung function. The most recent addition of respiratory complaints to be attributed to GOR is chronic cough. Although several writers have alluded to this association, the main advocate is Irwin2O,21 from Worcester, Massachusetts. Some years ago he reported that while asthma, postnasal drip, and bronchitis were responsible for most chronic unexplained coughs, in about 10% GOR was the sole cause .20 He has lately conducted detailed investigations in nine patients in whom chronic cough was considered to be the presenting manifestation of GOR. These patients underwent oesophageal pH monitoring before and after the cough had settled on treatment (on average 6 months later). Although all nine had demonstrable GOR by standard definition, only three admitted to minor reflux symptoms. Four were also asthmatics, but standard asthma remedies had failed to relieve the cough. Reflux was treated medically-details of the regimen are sketchy but included diet, sleeping posture, and drugs-and oesophageal pH monitoring was repeated when patients no longer complained of cough. Compared with the initial figures, those after treatment showed a reduction in reflux events, coughs, and reflux-induced
to
be
a
real and remediable clinical
Kennedy JH. "Silent" gastroesophageal reflux: an important but little known cause of pulmonary complications. Dis Chest 1962; 12: 42-45. 2. Davis MV. Relationship between pulmonary disease, hiatal hernia, and gastroesophageal reflux. N Y J Med 1972; 72: 935-38. 3. Nelson HS. Gastroesophageal reflux and pulmonary disease. J Allergy Clin Immunol 1984; 73: 547-56. 4. Barish CF, Wallace CWu, Castell DO. Respiratory complications of gastroesophageal reflux. Arch Intern Med 1985; 145: 1882-88. 5. Mays EE. Intrinsic asthma in adults. JAMA 1976; 236: 2626-28. 6. Mansfield LE, Stein MR. Gastroesophageal reflux and asthma: a possible reflex mechanism. Ann Allergy 1978; 41: 224-26. 7. Goodall RJR, Earis JE, Cooper DN, Bernstein A, Temple JG. Relationship between asthma and gastro-oesophageal reflux. Thorax 1.
1981; 36: 116-20. 8.
Spaulding HS, Mansfield LE, Stein MR, Sellner JC, Gremillion DE. Further investigation of the association between gastroesophageal reflux and bronchoconstriction. J Allergy Clin Immunol 1982; 69:
9.
Boyle JT, Tuchman DN, Altschuler SM, Nixon TE, Pack AI, Cohen S.
516-21. Mechanisms for the association of gastroesophageal reflux and bronchospasm. Am Rev Respir Dis 1985; 131 (suppl): S16-20. 10. Ekstrom T, Tibbling L. Gastro-oesophageal reflux and nocturnal asthma. Eur Respir J 1988; 1: 636-38. 11. Ekstrom T, Tibbling L. Gastro-oesophageal reflux and triggering of bronchial asthma: a negative report. Eur Respir Dis 1987; 71: 177-80. 12. Hughes DM, Spier S, Rivlin I, Levison H. Gastroesophageal reflux during sleep in asthmatic patients. J Pediatr 1983; 102: 666-72. 13. Ghaed N, Stein MR. Assessment of a technique for scintigraphic monitoring of pulmonary aspiration of gastric contents in asthmatics with gastroesophageal reflux. Ann Allergy 1979; 42: 306-08. 14. Martin ME, Grunstein MM, Larsen GL. The relationship of gastroesophageal reflux to nocturnal wheezing of children with asthma. Ann Allergy 1982; 49: 318-22. 15. Herve P, Denjean A, Jian R, Simonneau G, Durous P. Intraesophageal perfusion of acid increases in the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects. Am Rev Respir Dis 1986; 134: 986-89. 16. Harper PC, Bergner A, Kaye MD. Antireflux treatment for asthma. Arch Intern Med 1987; 147: 56-60. 17. Kjellen G, Tibbling L, Wranne B. Effect of conservative treatment of oesophageal dysfunction on bronchial asthma. Eur J Respir Dis 1981; 62: 190-97. 18. Ekstrom T, Lindgren BR, Tibbling L. Effects of ranitidine treatment on patients with asthma and a history of gastro-oesophageal reflux. Thorax 1989; 44: 19-23. 19. Tuchman DN, Boyle JT, Pack IA, et al. Comparison of airways responses following tracheal or esophageal acidification in the cat. Gastroenterology 1984; 87: 872-81. 20. Irwin RS, Corrao WM, Pratter MR. Chronic persistent cough in the adult: the spectrum and frequency of causes and successful outcome of specific therapy. Am Rev Respir Dis 1981; 123: 413-17. 21. Irwin RS, Zawacki JK, Curley FJ, French CL, Hoffman PJ. Chronic cough as the sole presenting manifestation of gastroesophageal reflux. Am Rev Respir Dis 1989; 140: 1294-300.
CARDIAC BIOPSY IN MYOCARDITIS The diagnosis of myocarditis is often overlooked. In its mildest form the disorder may present as an abnormal electrocardiogram in a young person or, for example, at a routine medical examination in aircraft pilots. More obvious acute illness leads to earlier presentation, sometimes with chest pain due to myopericarditis; a fair proportion of such cases are diagnosed accurately, especially if serological changes are specific. Between the two extremes there is a
1990
284
wide range of illness and many patients slip through the diagnostic net. For many years the diagnostic evidence fell short of direct histological proof. Now that cardiac biopsy has been accepted as a routine procedure, we should focus more carefully on guidelines for clinical practice. Histological information, obtained by catheter-mounted endocardial biopsy methods, was first shown to be helpful in determining the optimum dose of immunosuppressant agents for patients with transplanted hearts. Subsequently biopsies were undertaken in patients with suspected acute myocarditis to establish the diagnosis before instituting treatment. Sometimes there is no difficulty in mounting a case for embarking on specialised therapy, but there are pitfalls. Whereas the histological features of myocarditis are readily identified by the microscopist,’ the patchy nature of the changes can lead to false-negative reports. The need to follow through, with a repeat biopsy, has lately been emphasised by Dec and colleagues,2who reviewed the results of repeat procedures undertaken in patients with dilated or failing hearts, with cardiac arrhythmias, or with dubious first biopsy results. In the cases reported, myocarditis was clinically suspected but the first right ventricular biopsy was negative. Twenty-eight such patients, with normal coronary arteriograms, were restudied by repeat biopsy. Of six patients with "borderline" myocarditis at first study, four had clear-cut histological features at a second biopsy. The second biopsy was done about thirty days after the first. Such information is helpful in therapeutic terms only if the data are available at the time when immunosuppressant treatment (eg, prednisolone and azathioprine) can influence the outcome. In the patients identified by the second biopsy, immunosuppressants led to an improvement in the clinical features of heart failure and the measured ejection fraction in three, all of whom had a lymphocytic myocarditis. The fourth patient did not respond and died of intractable cardiac failure; histology showed granulomatous myocarditis. Thus, a repeat study when the disease is well advanced may confirm a clinical diagnosis but treatment may be too late to help the patient. Perhaps the most important point is to repeat the biopsy early in the case of negative result. Before doing so it is very important to assess all the evidence that can be obtained by non-invasive methods. Biopsy studies should be limited to those patients in whom the additional information is likely to alter therapy and improve the outcome. Billingham ME, Edwards WD, et al. Myocarditis: a histopathologic definition and classification. Am J Cardiovasc Pathol
1. Aretz HT,
1987; 1: 3-14. 2. Dec GW, Fallon JT, Southern JF, Palacios I. "Borderline" myocarditis: an indication for repeat endomyocardial biopsy. JACC 1990; 15: 283-89. 3. Factor SM. Editorial comment. JACC 1990; 15: 290-91.
accomplished with the panache of a snooker player who has already won the game and is finishing off the colours from their spots-for the achievement and mastery of the thing. Were Schulz practising in Birmingham during the past lustrum or two, he is unlikely to have been so inspired. From Dudley Road Hospital, Constantine and Redrnan1 reported that during the 10 years from 1974 to 1983 only 06% of deliveries of the second twin after vaginal delivery of the first were by caesarean section. During the ensuing triennium, from 1984 to 1986, the frequency of combination delivery had increased ten-fold, so that 6.5% of births after vaginal delivery of the first twin were by caesarean section. Samra et al2 have now reported from the Birmingham Maternity Hospital rates for combination delivery of 0-2-4% from 1980 to 1983 and of 5-2%-8-6% from 1984 to 1988. In twelve of their twenty-two cases the indication for caesarean section was "transverse lie/high breech". Compound presentation accounted for four cases and contracted cervix for two, while brow presentation, shoulder presentation, fetal distress/placental abruption, and fetal distress/failed breech extraction made up the remainder. In only one case was the second twin more than 500 g heavier than the first. There were no perinatal deaths. Similar increases in the frequency of combination delivery have been reported from the USA3 and Sweden.4 Neither Birmingham publication mentions how often internal version and breech extraction were used in the delivery of second twins who did not come to caesarean section, but a declining use of these skills is assumed and lamented. Those who have never known the joy cannot feel the loss; and in the march of progress many skills are inevitably discarded as new ones are acquired. The young obstetrician of today may never deliver a second twin by internal podalic version and breech extraction, but the ease and speed of his section are comparable to the talents of squirrel eating nuts. He also has at his disposal epidural anaesthesia, electronic fetal heart rate monitoring, effective uterine stimulation and tocolysis, and, above all, intrapartum real-time ultrasound scanning. Olofsson and Rydhstrom’ responded to the increasing frequency of combination delivery in their unit by developing a protocol for intrapartum management of twins that incorporated all these things. Management of malpresentation of the second twin begins before the delivery of the leading baby and relies heavily on intrapartum scanning and on another endangered skill, external version. In writing for a predominantly North American readership, Olofsson and Rydhstrom acknowledged the hesitation and cautiousness of obstetricians who work in a more litiginous society than theirs, but many obstetricians devising labour ward protocols will find the Swedish paper worthy of consideration. Much depends, as Samra et al have hinted, on medical staffing. Seventeen of the twenty-two combination caesarean
THE SECOND TWIN
deliveries in their report occurred between 1700 and 0900 most experienced obstetricians may not have been immediately available.
Had Charles M. Schulz been an obstetrician, as well as the creator of the Peanuts gang, two decades ago his "Happiness is for obstetricians" must have included "... delivering the second twin by internal podalic version and breech extraction." The lie was longitudinal. The birth canal had been dilated by the first twin; the cervix was fully dilated. One passed a hand high into the uterus. Apprehension was followed by joy as a fetal foot was recognised by its heel and brought down. The following breech extraction was
1. Constantine G, Redman CWE. Caesarean section for the second twin—an increasing trend? Lancet 1987; i: 618-19. 2. Samra JS, Spillance H, Mukoyoko J, Tang L, Obhrai MS. Caesarean section for the birth of the second twin. Br J Obstet Gynaecol 1990; 97: 234-36. 3. Rattan PK, Knuppel RA, O’Brian WF, Scerbo JC. Cesarean delivery of the second twin after vaginal delivery of the first twin. Am J Obstet Gynecol 1986; 154: 936-39. 4. Olofsson P, Rydhstrom H. Twin delivery: how should the secondtwin be delivered? Am J Obstet Gynecol 1985; 153: 479-81.
hours, when the
...
link5-1O outnumber negative reports,l-3 even sceptics might acknowledge that GOR aggravates bronchospasm in some asthmatic patients. So the question is not so much whether the association exists, but how often, to what degree, and by what mechanism? Experimental data or clinical observations linking GOR and asthma come in several forms. Oesophageal pH
coughs. However, four of the nine patients were asthmatic, so it is unclear whether the GOR caused the cough directly or indirectly via aggravation of the asthma. Moreover, since the observations were uncontrolled there is no certainty that the antireflux regimen was related to the gradual improvement in the cough. Nonetheless, the concept is thought provoking and deserves further consideration
monitoring may show a temporal relation between wheezing and oesophageal acidity:l4 airways resistance increases in some asthmatics during oesophageal acid perfusion;6,8,15 and antireflux treatment sometimes improves the asthma.7,16-18 What is the underlying mechanism? Microaspiration of acid into the airways, and reflex bronchoconstriction as a result of oesophageal acidification are the most plausible suggestions; the second hypothesis has rather more appeal, but neither has been unequivocably substantiated.3,4,9,10 The possibility that asthma or its treatment predisposes to reflux has also been entertained but most of the evidence points in the opposite direction.4,9 The best experimental support for the microaspiration theory comes from a study in cats,l9 in which tracheal infusion of minute amounts of acid led to large increases in airways resistance, an effect abolished by prior vagotomy. Clinical observations in asthmatic patients are less impressive and a scintigraphic technique did not show induces acidification aspiration. 13 Oesophageal bronchospasm in some patients, possibly via a vagal reflex
because it may prove association.
mechanism.6
More recently, Ekstrom and Tibbling10 in Sweden examined nocturnal respiratory and oesophageal events in a large population of patients with asthma and GOR. Although nocturnal reflux significantly reduced the early morning peak expiratory flow it was neither a strong nor an immediate trigger for bronchospasm in most cases. These workers concluded that GOR may increase vagal bronchomotor tone without necessarily eliciting an asthma attack but may stimulate bronchial reactivity and lower the threshold for other bronchospastic factors. Does antireflux treatment alleviate asthma? Most of the supportive observations are anecdotal2 or, at best, open trials.16,17 Two controlled trials7,18 ofH2 receptor antagonists in patients with GOR and asthma have shown only very modest improvements in asthma control and little or no effect on lung function. The most recent addition of respiratory complaints to be attributed to GOR is chronic cough. Although several writers have alluded to this association, the main advocate is Irwin2O,21 from Worcester, Massachusetts. Some years ago he reported that while asthma, postnasal drip, and bronchitis were responsible for most chronic unexplained coughs, in about 10% GOR was the sole cause .20 He has lately conducted detailed investigations in nine patients in whom chronic cough was considered to be the presenting manifestation of GOR. These patients underwent oesophageal pH monitoring before and after the cough had settled on treatment (on average 6 months later). Although all nine had demonstrable GOR by standard definition, only three admitted to minor reflux symptoms. Four were also asthmatics, but standard asthma remedies had failed to relieve the cough. Reflux was treated medically-details of the regimen are sketchy but included diet, sleeping posture, and drugs-and oesophageal pH monitoring was repeated when patients no longer complained of cough. Compared with the initial figures, those after treatment showed a reduction in reflux events, coughs, and reflux-induced
to
be
a
real and remediable clinical
Kennedy JH. "Silent" gastroesophageal reflux: an important but little known cause of pulmonary complications. Dis Chest 1962; 12: 42-45. 2. Davis MV. Relationship between pulmonary disease, hiatal hernia, and gastroesophageal reflux. N Y J Med 1972; 72: 935-38. 3. Nelson HS. Gastroesophageal reflux and pulmonary disease. J Allergy Clin Immunol 1984; 73: 547-56. 4. Barish CF, Wallace CWu, Castell DO. Respiratory complications of gastroesophageal reflux. Arch Intern Med 1985; 145: 1882-88. 5. Mays EE. Intrinsic asthma in adults. JAMA 1976; 236: 2626-28. 6. Mansfield LE, Stein MR. Gastroesophageal reflux and asthma: a possible reflex mechanism. Ann Allergy 1978; 41: 224-26. 7. Goodall RJR, Earis JE, Cooper DN, Bernstein A, Temple JG. Relationship between asthma and gastro-oesophageal reflux. Thorax 1.
1981; 36: 116-20. 8.
Spaulding HS, Mansfield LE, Stein MR, Sellner JC, Gremillion DE. Further investigation of the association between gastroesophageal reflux and bronchoconstriction. J Allergy Clin Immunol 1982; 69:
9.
Boyle JT, Tuchman DN, Altschuler SM, Nixon TE, Pack AI, Cohen S.
516-21. Mechanisms for the association of gastroesophageal reflux and bronchospasm. Am Rev Respir Dis 1985; 131 (suppl): S16-20. 10. Ekstrom T, Tibbling L. Gastro-oesophageal reflux and nocturnal asthma. Eur Respir J 1988; 1: 636-38. 11. Ekstrom T, Tibbling L. Gastro-oesophageal reflux and triggering of bronchial asthma: a negative report. Eur Respir Dis 1987; 71: 177-80. 12. Hughes DM, Spier S, Rivlin I, Levison H. Gastroesophageal reflux during sleep in asthmatic patients. J Pediatr 1983; 102: 666-72. 13. Ghaed N, Stein MR. Assessment of a technique for scintigraphic monitoring of pulmonary aspiration of gastric contents in asthmatics with gastroesophageal reflux. Ann Allergy 1979; 42: 306-08. 14. Martin ME, Grunstein MM, Larsen GL. The relationship of gastroesophageal reflux to nocturnal wheezing of children with asthma. Ann Allergy 1982; 49: 318-22. 15. Herve P, Denjean A, Jian R, Simonneau G, Durous P. Intraesophageal perfusion of acid increases in the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects. Am Rev Respir Dis 1986; 134: 986-89. 16. Harper PC, Bergner A, Kaye MD. Antireflux treatment for asthma. Arch Intern Med 1987; 147: 56-60. 17. Kjellen G, Tibbling L, Wranne B. Effect of conservative treatment of oesophageal dysfunction on bronchial asthma. Eur J Respir Dis 1981; 62: 190-97. 18. Ekstrom T, Lindgren BR, Tibbling L. Effects of ranitidine treatment on patients with asthma and a history of gastro-oesophageal reflux. Thorax 1989; 44: 19-23. 19. Tuchman DN, Boyle JT, Pack IA, et al. Comparison of airways responses following tracheal or esophageal acidification in the cat. Gastroenterology 1984; 87: 872-81. 20. Irwin RS, Corrao WM, Pratter MR. Chronic persistent cough in the adult: the spectrum and frequency of causes and successful outcome of specific therapy. Am Rev Respir Dis 1981; 123: 413-17. 21. Irwin RS, Zawacki JK, Curley FJ, French CL, Hoffman PJ. Chronic cough as the sole presenting manifestation of gastroesophageal reflux. Am Rev Respir Dis 1989; 140: 1294-300.
CARDIAC BIOPSY IN MYOCARDITIS The diagnosis of myocarditis is often overlooked. In its mildest form the disorder may present as an abnormal electrocardiogram in a young person or, for example, at a routine medical examination in aircraft pilots. More obvious acute illness leads to earlier presentation, sometimes with chest pain due to myopericarditis; a fair proportion of such cases are diagnosed accurately, especially if serological changes are specific. Between the two extremes there is a
1990
284
wide range of illness and many patients slip through the diagnostic net. For many years the diagnostic evidence fell short of direct histological proof. Now that cardiac biopsy has been accepted as a routine procedure, we should focus more carefully on guidelines for clinical practice. Histological information, obtained by catheter-mounted endocardial biopsy methods, was first shown to be helpful in determining the optimum dose of immunosuppressant agents for patients with transplanted hearts. Subsequently biopsies were undertaken in patients with suspected acute myocarditis to establish the diagnosis before instituting treatment. Sometimes there is no difficulty in mounting a case for embarking on specialised therapy, but there are pitfalls. Whereas the histological features of myocarditis are readily identified by the microscopist,’ the patchy nature of the changes can lead to false-negative reports. The need to follow through, with a repeat biopsy, has lately been emphasised by Dec and colleagues,2who reviewed the results of repeat procedures undertaken in patients with dilated or failing hearts, with cardiac arrhythmias, or with dubious first biopsy results. In the cases reported, myocarditis was clinically suspected but the first right ventricular biopsy was negative. Twenty-eight such patients, with normal coronary arteriograms, were restudied by repeat biopsy. Of six patients with "borderline" myocarditis at first study, four had clear-cut histological features at a second biopsy. The second biopsy was done about thirty days after the first. Such information is helpful in therapeutic terms only if the data are available at the time when immunosuppressant treatment (eg, prednisolone and azathioprine) can influence the outcome. In the patients identified by the second biopsy, immunosuppressants led to an improvement in the clinical features of heart failure and the measured ejection fraction in three, all of whom had a lymphocytic myocarditis. The fourth patient did not respond and died of intractable cardiac failure; histology showed granulomatous myocarditis. Thus, a repeat study when the disease is well advanced may confirm a clinical diagnosis but treatment may be too late to help the patient. Perhaps the most important point is to repeat the biopsy early in the case of negative result. Before doing so it is very important to assess all the evidence that can be obtained by non-invasive methods. Biopsy studies should be limited to those patients in whom the additional information is likely to alter therapy and improve the outcome. Billingham ME, Edwards WD, et al. Myocarditis: a histopathologic definition and classification. Am J Cardiovasc Pathol
1. Aretz HT,
1987; 1: 3-14. 2. Dec GW, Fallon JT, Southern JF, Palacios I. "Borderline" myocarditis: an indication for repeat endomyocardial biopsy. JACC 1990; 15: 283-89. 3. Factor SM. Editorial comment. JACC 1990; 15: 290-91.
accomplished with the panache of a snooker player who has already won the game and is finishing off the colours from their spots-for the achievement and mastery of the thing. Were Schulz practising in Birmingham during the past lustrum or two, he is unlikely to have been so inspired. From Dudley Road Hospital, Constantine and Redrnan1 reported that during the 10 years from 1974 to 1983 only 06% of deliveries of the second twin after vaginal delivery of the first were by caesarean section. During the ensuing triennium, from 1984 to 1986, the frequency of combination delivery had increased ten-fold, so that 6.5% of births after vaginal delivery of the first twin were by caesarean section. Samra et al2 have now reported from the Birmingham Maternity Hospital rates for combination delivery of 0-2-4% from 1980 to 1983 and of 5-2%-8-6% from 1984 to 1988. In twelve of their twenty-two cases the indication for caesarean section was "transverse lie/high breech". Compound presentation accounted for four cases and contracted cervix for two, while brow presentation, shoulder presentation, fetal distress/placental abruption, and fetal distress/failed breech extraction made up the remainder. In only one case was the second twin more than 500 g heavier than the first. There were no perinatal deaths. Similar increases in the frequency of combination delivery have been reported from the USA3 and Sweden.4 Neither Birmingham publication mentions how often internal version and breech extraction were used in the delivery of second twins who did not come to caesarean section, but a declining use of these skills is assumed and lamented. Those who have never known the joy cannot feel the loss; and in the march of progress many skills are inevitably discarded as new ones are acquired. The young obstetrician of today may never deliver a second twin by internal podalic version and breech extraction, but the ease and speed of his section are comparable to the talents of squirrel eating nuts. He also has at his disposal epidural anaesthesia, electronic fetal heart rate monitoring, effective uterine stimulation and tocolysis, and, above all, intrapartum real-time ultrasound scanning. Olofsson and Rydhstrom’ responded to the increasing frequency of combination delivery in their unit by developing a protocol for intrapartum management of twins that incorporated all these things. Management of malpresentation of the second twin begins before the delivery of the leading baby and relies heavily on intrapartum scanning and on another endangered skill, external version. In writing for a predominantly North American readership, Olofsson and Rydhstrom acknowledged the hesitation and cautiousness of obstetricians who work in a more litiginous society than theirs, but many obstetricians devising labour ward protocols will find the Swedish paper worthy of consideration. Much depends, as Samra et al have hinted, on medical staffing. Seventeen of the twenty-two combination caesarean
THE SECOND TWIN
deliveries in their report occurred between 1700 and 0900 most experienced obstetricians may not have been immediately available.
Had Charles M. Schulz been an obstetrician, as well as the creator of the Peanuts gang, two decades ago his "Happiness is for obstetricians" must have included "... delivering the second twin by internal podalic version and breech extraction." The lie was longitudinal. The birth canal had been dilated by the first twin; the cervix was fully dilated. One passed a hand high into the uterus. Apprehension was followed by joy as a fetal foot was recognised by its heel and brought down. The following breech extraction was
1. Constantine G, Redman CWE. Caesarean section for the second twin—an increasing trend? Lancet 1987; i: 618-19. 2. Samra JS, Spillance H, Mukoyoko J, Tang L, Obhrai MS. Caesarean section for the birth of the second twin. Br J Obstet Gynaecol 1990; 97: 234-36. 3. Rattan PK, Knuppel RA, O’Brian WF, Scerbo JC. Cesarean delivery of the second twin after vaginal delivery of the first twin. Am J Obstet Gynecol 1986; 154: 936-39. 4. Olofsson P, Rydhstrom H. Twin delivery: how should the secondtwin be delivered? Am J Obstet Gynecol 1985; 153: 479-81.
hours, when the
...
