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Patent Ductus Arteriosus
NOTES
Patent Ductus Arteriosus Some Historical Highlights Norman H. Boyer, M.D.
S
ince the ductus arteriosus was a structure known to Galen in A.D. 131, it is remarkable that it became known as the ductus Botalli (Botallo, 1530). This is all the more extraordinary because Botallo apparently had no claim on the ductus whatever! In 1660 Van Horne published a compilation of the works of Botallo and, deceived by a mistranslation, introduced a sketch (presumably his own) purporting to show the anatomy of the ductus [l]. T h e error was perpetuated for the next three centuries." Harvey in 1628 recognized the purpose of the arterial interconnection and indicated the direction of blood flow. T h e architecture of the ductus differs from both that of the aorta and the pulmonary artery. T h e muscle layer of its wall is well developed and, in addition, there is a subintimal layer of muscle which is continuous with the elastica of the aorta. It has been supposed that this architecture favors contraction and obliteration of the lumen. T h e suggestion has also been made that the development, after birth, of an increase in aortic and a fall in pulmonic pressure favors closure through traction and torsion on the ductus. A fold of the aortic wall near the mouth of the ductus (Strassmann's fold) may also facilitate closure. Normally, closure of the ductus is accomplished in two phases. A slow anatomical phase begins in the last trimester of pregnancy and consists of thickening of the intima, composed of laminated collagen and elastic tissue, producing ridges and folds (Shaeffer, 1914 [lo]; From the Division of Medicine, Boston University Medical Center, Boston, Mass. *Having disposed of Botallo, it might be well, as suggested to me by Dr. Eugene G. Laforet, friend, colleague, and purist, to correct the term patent ductus to persistent ductus (the strucLure has to be patent in order to be a duct) before another three centuries have elapsed.
570
THE ANNALS OF THORACIC SIJRGERY
NOTE:
Historical Highlights of Patent Ductus
Scammon and Norris, 1918 [9]; Melka, 1926 [7]). In persistency of the ductus the wall and the intima are thin, but it is not at all clear whether this is a consequence, or the cause, of patency. Rapid closure, due to contraction of the muscularis, begins with the onset of respiration at birth. The physiological triggering of this mechanism depends on an increase in oxygen in the blood. Kennedy and Clark in 1942 [6] observed that in newborn guinea pigs (delivered under water) contraction of the ductus could be turned on and off at will. Inflation of the lungs with air or oxygen caused constriction, but inflation with nitrogen did not. Intravenous oxygen, without inflation of the lungs, also caused constriction, and these effects were not altered by complete denervation of the area. Local mechanical stimulation also caused contraction. Since the ductus which remains patent (as an isolated defect) is exposed to the level of oxygenation which normally closes the ductus, the defect must be in the ductus itself, but the nature of this defect remains obscure. The size of the ductus per se does not seem to be a compelling factor, though it may well play a subsidiary role. It is of interest that in 85 cases of asphyxia neonatorum, persistency of the ductus occurred in none [5].Furthermore, the ductus may close when, due to associated defects, life depends upon its remaining open. Closure is completed in the first few weeks of life, but it may not occur for several years, as judged by disappearance of typical signs, although I am not aware that late closure has been established by modern methods of study. Familial occurrence suggests a genetic defect, while teratogenic agents indicate other causes. It is possible that the latter attack only the genetically susceptible. Recapitulation of eons of philogeny, from aquatic creature to air-breathing mammal, during the few months of fetal development, is a wondrous thing. T h e marvel is that it goes off so smoothly most of the time. Certainly deserving of historical acclaim is the description, made by Gibson in 1898, of the typical “machinery” murmur: I t begins softly and increases in intensity so as to reach its acme just about or immediately after the second sound and from that point gradually wanes till its termination. The second sound can be heard to be loud and clanging.
What is especially noteworthy about this description is the accurate timing of the murmur as encompassing the second sound, amply demonstrated by phonocardiography. Despite this, the murmur for many years was described as continuous, with systolic accentuation. While this defect was occasionally encountered in patients in later life, it soon became clear that most who had it died young. On May 6, 1907, John C. Munro suggested in a paper delivered before the Philadelphia Academy of Surgery that closure of a patent ductus by ligation VOL.
4,
NO.
6,
DEC.,
1967
571
BOYER
or crushing was feasible, and he outlined the procedure in some detail [81. There is no record, however, that either he or anyone else attempted this for the ensuing thirty years. Dr. John W. Strieder made such an attempt on March 16, 1937 [3]. The patient was a 22-year-old girl with Streptococcus uiridans endarteritis of at least three months’ duration. Her general condition being fair, but deteriorating rapidly, and her prognosis hopeless, the decision to attempt obliteration of the ductus was made. Nothing in the literature encouraged the idea that such a procedure, if successful, would lead to cure of the infection. Indeed, the postoperative possibilities were quite the opposite, as one of Dr. Maude Abbott’s cases had developed bacterial endarteritis on a dimple in the pulmonary artery at the end of a ligamentum arteriosum. Circumstances proved inauspicious for pioneering. The ductus was relatively short and wide. In the published case report [3] it was described (inaccurately) as 1.0 cm. long and 0.5 cm. in diameter, but the actual wording in the operative note was that it “seemed to be less than 1.0 cm. long and about 0.5 cm. in diameter.” Moreover, it was described as too short to permit double ligation and division. At autopsy it was “0.1 cm. long and 0.3 cm. in diameter,” but it is known that the ductus shrinks remarkably after death. It seems probable that at operation it was perhaps 0.5 cm. long. Furthermore, the ductus was firmly bound down by fibrous tissue posteriorly. Neither the shortness nor the fibrous tissue would daunt the modern cardiac surgeon, but thirty years ago the conditions seemed hazardous in the extreme. Obliteration was attempted, therefore, by plicating sutures. This resulted in a striking decrease in the intensity of the thrill, and it was hoped that the reduction in flow might be sufficient to lead to eventual obliteration. This was not to be known, however, as death occurred on the fourth postoperative day. As is now so well known, on August 26, 1938, a patent ductus was successfully ligated by Gross [4] to save a young girl from intractable heart failure. Soon thereafter (1940), Touroff and Vesell [ 111 reported successful control of bacterial endarteritis by ligation, and in the ensuing years of the preantibiotic era this was to be verified repeatedly. Although refinement in techniques and improvemlent in our understanding has gradually increased, historical interest necessarily ends here. It is beyond the scope of this essay to documenit every contribution. Finally, it seems proper to observe that, although it is preferable to clear infection before ligation of the ductus, this may not always hold true. Infection with resistant organisms, negative blood cultures, intractable heart failure, or other considerations, such as fulminating course, may dictate early operation. Since ligation has proved curative 572
THE ANNALS OF THORACIC SURGERY
NOTE:
Historical Highlights of Patent Ductus
in both infection and heart failure, the surgeon’s hand should not be stayed unduly. If surgical correction is to be effective, it must be done while infection is limited to the ductus and its immediate environs. REFERENCES 1. Franklin, K. J. Ductus venosus (Arantii) and ductus arteriosus (Botalli). Bull. Hist. M e d . 9:580, 1941. 2 . Gibson, G. A. Disease o f the Heart and Aorta. London: Pentland, 1898. 3. Graybiel, A., Strieder, J. W., and Boyer, N. H. An attempt to obliterate the patent ductus arteriosus in a patient with bacterial endarteritis. A m e r . Heart J . 15:621, 1938. 4. Gross, R. E., and Hubbard, J. P. Surgical ligation of a patent ductus arteriosus. J.A.M.A. 112:729, 1939. 5. Hellstrom, B., and Jonsson, €3. Late prognosis in asphyxia neonatorum. Acta Paediat. Scand. 42:398, 1953. 6. Kennedy, J. A., and Clark, S. L. Observations on the physiological reactions of the ductus arteriosus. A m e r . J. Physiol. 136:140, 1942. 7. Melka, J. Beitrag zur Kenntnis der Morphologie und Obliteration des Ductus arteriosus Botalli. A n a t . Anz. 61:348, 1926. 8. Munro, J. C. Ligation of the ductus arteriosus. Ann. Surg. 46:335, 1907. 9. Scammon, R. E., and Norris, E. H. A statistical summary of the data on the time of obliteration of the foramen ovale, ductus arteriosus and ductus venosus in man. A n a t . Rec. 15:165, 1918. 10. Shaeffer, J. P. T h e behavior of elastic tissue of the post-foetal occlusion and obliteration of the ductus arteriosus (Botalli) in Sus scrofa. J . E x p . M e d . 19:129, 1914. 11. Touroff, A. S. W., and Vesell, H. Subacute Streptococcus uiridans endarteritis complicating patent ductus arteriosus. J.A.M.A. 115:1270, 1940.
VOL.
4,
NO.
6,
DEC.,
1967
573
Patent Ductus Arteriosus Some Historical Highlights Norman H. Boyer, M.D.
S
ince the ductus arteriosus was a structure known to Galen in A.D. 131, it is remarkable that it became known as the ductus Botalli (Botallo, 1530). This is all the more extraordinary because Botallo apparently had no claim on the ductus whatever! In 1660 Van Horne published a compilation of the works of Botallo and, deceived by a mistranslation, introduced a sketch (presumably his own) purporting to show the anatomy of the ductus [l]. T h e error was perpetuated for the next three centuries." Harvey in 1628 recognized the purpose of the arterial interconnection and indicated the direction of blood flow. T h e architecture of the ductus differs from both that of the aorta and the pulmonary artery. T h e muscle layer of its wall is well developed and, in addition, there is a subintimal layer of muscle which is continuous with the elastica of the aorta. It has been supposed that this architecture favors contraction and obliteration of the lumen. T h e suggestion has also been made that the development, after birth, of an increase in aortic and a fall in pulmonic pressure favors closure through traction and torsion on the ductus. A fold of the aortic wall near the mouth of the ductus (Strassmann's fold) may also facilitate closure. Normally, closure of the ductus is accomplished in two phases. A slow anatomical phase begins in the last trimester of pregnancy and consists of thickening of the intima, composed of laminated collagen and elastic tissue, producing ridges and folds (Shaeffer, 1914 [lo]; From the Division of Medicine, Boston University Medical Center, Boston, Mass. *Having disposed of Botallo, it might be well, as suggested to me by Dr. Eugene G. Laforet, friend, colleague, and purist, to correct the term patent ductus to persistent ductus (the strucLure has to be patent in order to be a duct) before another three centuries have elapsed.
570
THE ANNALS OF THORACIC SIJRGERY
NOTE:
Historical Highlights of Patent Ductus
Scammon and Norris, 1918 [9]; Melka, 1926 [7]). In persistency of the ductus the wall and the intima are thin, but it is not at all clear whether this is a consequence, or the cause, of patency. Rapid closure, due to contraction of the muscularis, begins with the onset of respiration at birth. The physiological triggering of this mechanism depends on an increase in oxygen in the blood. Kennedy and Clark in 1942 [6] observed that in newborn guinea pigs (delivered under water) contraction of the ductus could be turned on and off at will. Inflation of the lungs with air or oxygen caused constriction, but inflation with nitrogen did not. Intravenous oxygen, without inflation of the lungs, also caused constriction, and these effects were not altered by complete denervation of the area. Local mechanical stimulation also caused contraction. Since the ductus which remains patent (as an isolated defect) is exposed to the level of oxygenation which normally closes the ductus, the defect must be in the ductus itself, but the nature of this defect remains obscure. The size of the ductus per se does not seem to be a compelling factor, though it may well play a subsidiary role. It is of interest that in 85 cases of asphyxia neonatorum, persistency of the ductus occurred in none [5].Furthermore, the ductus may close when, due to associated defects, life depends upon its remaining open. Closure is completed in the first few weeks of life, but it may not occur for several years, as judged by disappearance of typical signs, although I am not aware that late closure has been established by modern methods of study. Familial occurrence suggests a genetic defect, while teratogenic agents indicate other causes. It is possible that the latter attack only the genetically susceptible. Recapitulation of eons of philogeny, from aquatic creature to air-breathing mammal, during the few months of fetal development, is a wondrous thing. T h e marvel is that it goes off so smoothly most of the time. Certainly deserving of historical acclaim is the description, made by Gibson in 1898, of the typical “machinery” murmur: I t begins softly and increases in intensity so as to reach its acme just about or immediately after the second sound and from that point gradually wanes till its termination. The second sound can be heard to be loud and clanging.
What is especially noteworthy about this description is the accurate timing of the murmur as encompassing the second sound, amply demonstrated by phonocardiography. Despite this, the murmur for many years was described as continuous, with systolic accentuation. While this defect was occasionally encountered in patients in later life, it soon became clear that most who had it died young. On May 6, 1907, John C. Munro suggested in a paper delivered before the Philadelphia Academy of Surgery that closure of a patent ductus by ligation VOL.
4,
NO.
6,
DEC.,
1967
571
BOYER
or crushing was feasible, and he outlined the procedure in some detail [81. There is no record, however, that either he or anyone else attempted this for the ensuing thirty years. Dr. John W. Strieder made such an attempt on March 16, 1937 [3]. The patient was a 22-year-old girl with Streptococcus uiridans endarteritis of at least three months’ duration. Her general condition being fair, but deteriorating rapidly, and her prognosis hopeless, the decision to attempt obliteration of the ductus was made. Nothing in the literature encouraged the idea that such a procedure, if successful, would lead to cure of the infection. Indeed, the postoperative possibilities were quite the opposite, as one of Dr. Maude Abbott’s cases had developed bacterial endarteritis on a dimple in the pulmonary artery at the end of a ligamentum arteriosum. Circumstances proved inauspicious for pioneering. The ductus was relatively short and wide. In the published case report [3] it was described (inaccurately) as 1.0 cm. long and 0.5 cm. in diameter, but the actual wording in the operative note was that it “seemed to be less than 1.0 cm. long and about 0.5 cm. in diameter.” Moreover, it was described as too short to permit double ligation and division. At autopsy it was “0.1 cm. long and 0.3 cm. in diameter,” but it is known that the ductus shrinks remarkably after death. It seems probable that at operation it was perhaps 0.5 cm. long. Furthermore, the ductus was firmly bound down by fibrous tissue posteriorly. Neither the shortness nor the fibrous tissue would daunt the modern cardiac surgeon, but thirty years ago the conditions seemed hazardous in the extreme. Obliteration was attempted, therefore, by plicating sutures. This resulted in a striking decrease in the intensity of the thrill, and it was hoped that the reduction in flow might be sufficient to lead to eventual obliteration. This was not to be known, however, as death occurred on the fourth postoperative day. As is now so well known, on August 26, 1938, a patent ductus was successfully ligated by Gross [4] to save a young girl from intractable heart failure. Soon thereafter (1940), Touroff and Vesell [ 111 reported successful control of bacterial endarteritis by ligation, and in the ensuing years of the preantibiotic era this was to be verified repeatedly. Although refinement in techniques and improvemlent in our understanding has gradually increased, historical interest necessarily ends here. It is beyond the scope of this essay to documenit every contribution. Finally, it seems proper to observe that, although it is preferable to clear infection before ligation of the ductus, this may not always hold true. Infection with resistant organisms, negative blood cultures, intractable heart failure, or other considerations, such as fulminating course, may dictate early operation. Since ligation has proved curative 572
THE ANNALS OF THORACIC SURGERY
NOTE:
Historical Highlights of Patent Ductus
in both infection and heart failure, the surgeon’s hand should not be stayed unduly. If surgical correction is to be effective, it must be done while infection is limited to the ductus and its immediate environs. REFERENCES 1. Franklin, K. J. Ductus venosus (Arantii) and ductus arteriosus (Botalli). Bull. Hist. M e d . 9:580, 1941. 2 . Gibson, G. A. Disease o f the Heart and Aorta. London: Pentland, 1898. 3. Graybiel, A., Strieder, J. W., and Boyer, N. H. An attempt to obliterate the patent ductus arteriosus in a patient with bacterial endarteritis. A m e r . Heart J . 15:621, 1938. 4. Gross, R. E., and Hubbard, J. P. Surgical ligation of a patent ductus arteriosus. J.A.M.A. 112:729, 1939. 5. Hellstrom, B., and Jonsson, €3. Late prognosis in asphyxia neonatorum. Acta Paediat. Scand. 42:398, 1953. 6. Kennedy, J. A., and Clark, S. L. Observations on the physiological reactions of the ductus arteriosus. A m e r . J. Physiol. 136:140, 1942. 7. Melka, J. Beitrag zur Kenntnis der Morphologie und Obliteration des Ductus arteriosus Botalli. A n a t . Anz. 61:348, 1926. 8. Munro, J. C. Ligation of the ductus arteriosus. Ann. Surg. 46:335, 1907. 9. Scammon, R. E., and Norris, E. H. A statistical summary of the data on the time of obliteration of the foramen ovale, ductus arteriosus and ductus venosus in man. A n a t . Rec. 15:165, 1918. 10. Shaeffer, J. P. T h e behavior of elastic tissue of the post-foetal occlusion and obliteration of the ductus arteriosus (Botalli) in Sus scrofa. J . E x p . M e d . 19:129, 1914. 11. Touroff, A. S. W., and Vesell, H. Subacute Streptococcus uiridans endarteritis complicating patent ductus arteriosus. J.A.M.A. 115:1270, 1940.
VOL.
4,
NO.
6,
DEC.,
1967
573