Section I: Patent ductus arteriosus (excluding prematurity)
Definition
Patent ductus arteriosus (PDA) is abnormal persistence of a patent lumen in the fetal ductus arteriosus, which usually connects the upper descending thoracic aorta with the proximal portion of the left pulmonary artery (LPA). When the aortic arch is right-sided, the ductus usually connects to the proximal right pulmonary artery. The ductus may at times connect to the adjacent subclavian or brachiocephalic artery rather than to the upper descending thoracic aorta.
This is primarily concerned with isolated PDA. PDA associated with other anomalies is discussed briefly here and in more detail in other chapters (Ventricular Septal Defect, Chapter 33 ; Tetralogy of Fallot, Chapter 34 ; Coarctation of the Aorta and Interrupted Aortic Arch, Chapter 40 ).
Historical note
The ductus arteriosus apparently was first described by Galen (born ad 129). It was rediscovered by Botallo in the 16th century, although some attribute the description of its postnatal closure to Acierno , and Harvey. , In 1888, Munro demonstrated in an infant cadaver the feasibility of dissecting and ligating a PDA. In 1900, Gibson described the characteristic continuous murmur of this anomaly. However, it was not until 1937 that Strieder in Boston attempted to close a PDA surgically in a patient with fulminating infective endarteritis; the patient died on the fourth postoperative day with gastric distention and aspiration of vomitus.
Cardiac surgery received a great impetus on August 26, 1938, when Gross successfully ligated the PDA of a 7-year-old girl at Boston Children’s Hospital. Subsequently, he developed division rather than ligation as the surgical technique of choice. , The first successful repair of an infected PDA was reported in 1940 by Touroff and Vesell, who later reported successful division of an infected PDA. , Portsmann and colleagues reported catheter closure of this anomaly in 1971. The first successful catheter partial pressure of oxygen closure of a PDA in a neonate or infant was performed by Rashkind and Cuaso in 1977. , Thus, PDA is the anomaly that initiated not only the surgical treatment of congenital heart disease but also its transcatheter treatment.
Morphology and morphogenesis
Morphology of normal ductal closure
At birth, the fetal ductus arteriosus is patent, resembling, according to Gittenberger-de Groot and colleagues :
“…a muscular artery with an intact, wavy internal elastic lamina, interrupted only underneath the intimal cushions. At those sites the elastic lamina is fragmented and is sometimes split up into several layers. The media is composed mainly of circularly arranged smooth muscle cells, with only minimal elastin fibers in between. The medial components may be widely separated, predominantly along the line of junction with intimal cushions, thereby creating large pools filled with a mucoid, slightly eosinophilic substance, the so-called mucoid lakes. In more advanced stages of anatomic closure, necrosis of cellular components of the media and a diffuse fibrous proliferation of the intima begin to appear.”
Postnatal closure occurs in two stages. The first stage is complete within 10 to 15 hours after birth in full-term infants; smooth muscle in the media of the ductal wall contracts, producing shortening and an increase in wall thickness. This functional closure is assisted by approximation of the intimal cushions. The intimal cushions (or mounds or pillows) are swellings composed of longitudinally oriented smooth muscle cells that protrude into the lumen and lie between the endothelium and internal elastic lamina and thus within the intima. They thicken as the duct matures and are most prominent at the pulmonary end. Muscle contraction occurs both circumferentially from the circularly arranged smooth muscle cells that fill almost the entire media, and longitudinally from one or more bands of muscle in the inner media.
The second stage of closure is usually completed by 2 to 3 weeks. It is the result of diffuse fibrous proliferation of the intima, sometimes associated with necrosis of the inner layer of the media and hemorrhage into the wall. The latter may be due to intimal tears producing a limited dissection of the ductus wall; there may also be small thrombi within the lumen, but gross luminal thrombus is rare. These changes result in permanent sealing of the lumen and produce the fibrous ligamentum arteriosum.
Closure usually begins at the pulmonary end and may remain incomplete at the aortic end, leaving an aortic ampulla from which the ligamentum arteriosum arises. Less commonly, there may be a ductus diverticulum arising from the proximal LPA.
The ductus arteriosus normally closes in the first 3 days after birth in full-term neonates. It is completely closed by 8 weeks of age in 88% of infants with a normal cardiovascular system. Delayed closure occurs in 80% of neonates born between 25 to 28 weeks of gestation (see Section II ). When the process is delayed, the term prolonged patency of the ductus arteriosus is appropriate; when the process ultimately fails, persistent patency of the ductus arteriosus is the appropriate term. Numerous factors contribute to ductus closure. It is a complex interplay of molecular and mechanical mechanisms with underlying genetic factors. This includes stimulation by rising oxygen tension; withdrawal of vasodilatory mediators (prostaglandins, nitric oxide, adenosine); and the presence of vasoconstrictors (endothelin-1, catecholamines, contractile prostanoids). Oxygen tension and prostaglandins act in opposite directions, with an increasing partial pressure of oxygen (Po 2 ) constricting the ductus and prostaglandins relaxing it; the potency of each varies at different gestational ages. Thus, the ductus is considerably more sensitive to Po 2 in the mature fetus and to prostaglandins (specifically, Prostaglandin E1 (PGE 1 )) in the immature fetus. The complex interplay of these factors is the reason prolonged patency of the ductus is more common in premature than term infants, particularly when there is associated respiratory distress syndrome (see “ Special Situations and Controversies ” later in this chapter). Intermittent patency of the ductus arteriosus has been documented.
Position and absence
At birth, usually in subjects with other cardiac anomalies, the ductus may be unilateral, bilateral, or (rarely) completely absent. It is absent in 35% of autopsy specimens with tetralogy of Fallot with pulmonary stenosis, in 40% of those with tetralogy of Fallot with pulmonary atresia, in almost all patients with tetralogy of Fallot and absent pulmonary valve (see Chapter 34 ), and in truncus arteriosus (see Chapter 43 ). It is rarely absent in patients with pulmonary atresia and intact ventricular septum (4%) (see Chapter 36 ) or in those with pulmonary atresia and other complex anomalies (15%).
Anatomic details
Isolated patent ductus arteriosus
The usual isolated PDA connects to the upper descending thoracic aorta 2 to 10 mm beyond the aortic origin of the left subclavian artery ( Fig. 28.1 ). From the aorta, it passes centrally toward the origin of the LPA from the pulmonary trunk, either directly or angling superiorly and hugging the undersurface of the distal aortic arch. When, as in the normally developing heart, the ductus delivers approximately 55% of the combined ventricular output into the descending aorta, the ductus meets the aorta at a proximal acute angle (<40 degrees) and a distal obtuse angle (110 to 160 degrees, mean 134 degrees) ( Table 28.1 ; see also Fig. 28.1 ). , ,
TABLE 28.1
Morphologic Features of Ductus Arteriosus in Fixed Autopsy Specimens
Data from Calder AL, Kirker JA, Neutze JM, Starling MB. Pathology of the ductus arteriosus treated with prostaglandins: comparisons with untreated cases. Pediatr Cardiol . 1984;5:85.
| AGE | DUCTAL STATUS | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Cardiac Diagnosis | n | Range | Median | Open | Closed | Average Length (mm) | Average Width (mm) | Average Prox Angle (°) | Average Distal Angle (°) |
| Normal | 13 | SB-5 mo | 2 d | 10 | 3 | 8 | 5.9 | 29 | 134 |
| Pulmonary atresia | 32 | SB-11 mo | 8 d | 13 | 19 | 9.7 | 3.7 | 83 c | 90 |
| Aortic atresia | 13 | 2 d-11 wk | 4 d | 12 | 1 | 7.9 | 7.2 | 70 c | 127 |
| Coarctation | 14 | 3 d-6 mo | 14 d | 8 | 6 | 5.6 | 6.0 | 70 c | 139 |
| Miscellaneous CHD | 37 | 1 d-8 mo | 23 d | 18 | 19 | 7.1 | 4.6 | 52 | 124 |
CHD , Congenital heart disease; d , days; mo , months; prox , proximal; SB , stillborn; wk , weeks.
Specimen of isolated patent ductus arteriosus in an infant. Ductus passes from junction of pulmonary trunk (PT) and left pulmonary artery (LPA) in an inferior and lateral direction to join descending aorta. Angle between superior border of ductus and aorta is acute, and that between the lower border and aorta is obtuse.
The PDA is generally 5 to 10 mm in length (in autopsy specimens, 2.5-8 mm), with a wide aortic orifice (4-12 mm) and a considerably narrower pulmonary orifice, and it is restrictive to flow. The PDA may be longer or shorter than this and may have a wide pulmonary as well as aortic orifice.
Patent ductus arteriosus as a coexisting anomaly.
When other cardiac anomalies are present, orientation of the ductus to the aortic arch varies, as does the flow pattern in fetal life. When there is pulmonary atresia and the pulmonary circulation is ductus dependent, with ductal flow in utero occurring from the aorta to the pulmonary artery, the ductus becomes a downwardly directed branch of the distal aortic arch. The proximal angle is much less acute and often obtuse, and the distal angle is often acute ( Fig. 28.2 ; see also Table 28.1 ). , When this is not the case, pulmonary atresia likely developed late in pregnancy. The ductus is also usually narrower and longer (see Fig. 28.2 ). The lumen is usually narrower at the pulmonary end and wider at the aortic end, as in isolated PDA.
Specimen of patent ductus arteriosus (D) in an infant with pulmonary atresia. Compared with the ductus in Fig. 28.1 , it is long and relatively narrow and joins the aorta (Ao) at a completely different angle: Proximal angle is obtuse and distal angle acute. PT, Pulmonary trunk.
(From Calder AL, Kirker JA, Neutze JM, Starling MB. Pathology of the ductus arteriosus treated with prostaglandins: comparisons with untreated cases. Pediatr Cardiol . 1984;5:85.)
In aortic atresia and coarctation of the aorta, the distal angle is normal, but the proximal angle in these shorter, broader examples of PDA is much less acute, probably because ductal flow enters both the ascending and descending aorta.
Uncommonly, in the presence of a left aortic arch, the ductus may arise from an aortic diverticulum (thought to represent persistence of the most distal portion of the right fourth branchial arch) that projects from the medial aspect of the left arch just distal to the origin of the left subclavian artery. In rare cases in which the ductus is bilateral, the right-sided PDA connects the right pulmonary artery to the brachiocephalic artery.
In the presence of a right aortic arch, a left-sided ductus is still more common than a right-sided ductus. When there is mirror-image branching of the right arch, the left PDA arises from the distal brachiocephalic (or proximal left subclavian) artery (see Chapter 39 ). Much less commonly, the right PDA persists in mirror image to the normal, passing from the right arch beyond the right subclavian artery to the right pulmonary artery origin. A PDA (or ligamentum arteriosum) arising from an aortic diverticulum or from an aberrant left subclavian artery is one form of vascular ring (see Chapter 39 ).
Histology
Histology of a persistent PDA is different from that of simple prolonged patency of the ductus. It is also different from that of the adjoining great arteries. A persistent PDA has a relatively thick intima with an unfragmented elastic lamina separating it from the media, an additional and pronounced wavy unfragmented subendothelial elastic lamina, and variable mucoid material in the media where there is an intricate helicoid spiral muscular arrangement. The media contains variable amounts of elastic material that may form conspicuous lamellae, making the ductus wall resemble the wall of the aorta (aortification).
Aneurysms of ductus arteriosus
Aneurysms of the ductus arteriosus, which are rare lesions, appear to be of two types. One is the spontaneous infantile ductal aneurysm, which is present at birth or develops shortly thereafter. The other develops in childhood or adult life.
The aneurysm involves the entire length of the ductus arteriosus, often seen as a tortuous and dilated vascular structure, with a maximum diameter toward the aortic end. It may be associated with occlusion of the pulmonary artery end and a relatively narrow but patent aortic end. It generally contains thrombus and is occasionally a site of infection and embolism. Rarely, it may be a true dissecting aneurysm of the ductal wall. This rare lesion manifests most often in newborns with a history of respiratory difficulties due to compression of adjacent structures or erosion into airways. , It produces a tumorlike shadow of variable size that projects beyond the mediastinum adjacent to the aortic knob in the posteroanterior chest radiograph. The aneurysm usually regresses spontaneously within weeks or months, presumably as a result of complete thrombosis and organization, but progressive enlargement or onset of hoarseness from recurrent laryngeal nerve involvement is an indication for surgical exploration and excision. Less marked dilatation of the ductus can be seen on the plain chest radiograph as a fusiform shadow between 6 and 18 hours after birth, disappearing by 24 to 48 hours of age. It has been called the ductus bump.
The second type of ductal aneurysm is thought to be unrelated to the infantile form. There is a tendency for progressive enlargement, and death may occur from rupture. ,
Clinical features and diagnostic criteria
Symptoms and signs of a PDA are the consequence of left-to-right shunting, with the magnitude of the shunt dependent upon size of the communication and relationship between systemic and pulmonary vascular resistances. In this regard, it is similar to other types of high-pressure shunts, which include those across the ventricular septum and others from the aorta.
Large patent ductus arteriosus
Aortic and pulmonary artery pressures are essentially equal when the PDA is large, and the magnitude and direction of shunting are dependent on changes in pulmonary vascular resistance because systemic vascular resistance remains fairly constant after birth. As neonatal pulmonary vascular resistance decreases, left-to-right shunting increases and severe heart failure develops within a month or so of birth. There is tachypnea, tachycardia, sweating, irritability, poor feeding, and slow weight gain. Pulmonary edema and pneumonia or less severe recurrent respiratory infection may occur.
On examination, there is an overactive precordium, sometimes with a systolic thrill, and evidence of cardiac enlargement with a thrusting left ventricular apical impulse. The pulse is jerky or frankly collapsing, and the pulse pressure is correspondingly wide. These features become more obvious when heart failure is medically controlled. On auscultation, there is a systolic murmur maximal in the pulmonary area, with late systolic accentuation and minimal spillover into diastole. Occasionally the murmur is continuous, but sometimes with severe heart failure, no murmur is heard. The first and second heart sounds are accentuated, and there is a third sound at the apex or a prominent mid-diastolic mitral flow murmur. The liver enlarges and jugular venous pressure rises; frequently, rales are heard in the lung bases.
The electrocardiogram (ECG) shows left ventricular enlargement with deep Q and tall R waves in the left ventricular leads. There may be evidence of right ventricular hypertrophy with upright T waves in the right precordial leads and evidence of left atrial enlargement with widened P waves. The chest radiograph shows marked cardiomegaly and plethora with or without interstitial or alveolar pulmonary edema. The pulmonary trunk is enlarged, as is the ascending aorta. The echocardiogram shows left atrial enlargement. The ductus may be visualized with two-dimensional echocardiography.
In some infants with a large PDA, heart failure may be less marked, presumably because pulmonary vascular resistance does not fall to the usual level. Histologic changes of pulmonary vascular disease may develop within the first few months of life. These changes may occur in infants in whom heart failure is controlled medically and the ductus is not closed by intervention. These patients become asymptomatic, and the left-to-right shunt diminishes. The murmur becomes purely systolic, the pulmonary component of the second heart sound is markedly accentuated, the apical mid-diastolic murmur disappears, and the pulse loses its jerky quality. Right ventricular hypertrophy becomes dominant in the ECG, the heart becomes smaller on the chest radiograph, and pulmonary plethora disappears. Cyanosis develops as pulmonary vascular resistance increases above systemic vascular resistance (Eisenmenger syndrome), typically earlier than with ventricular septal defect (see Chapter 33 ). Differential cyanosis may be noted, with blueness of the feet and sometimes the left hand, but not of the face or right hand.
Moderate-sized patent ductus arteriosus
Left-to-right shunt in moderate-sized PDA is regulated by size of the ductus arteriosus. In this setting, pulmonary artery pressure is only moderately elevated. As neonatal pulmonary vascular resistance declines, the shunt increases and heart failure may occur. By the second or third month of life, however, compensatory left ventricular hypertrophy is usually associated with clinical improvement and stabilization of symptoms. Physical development may be somewhat retarded, and breathlessness and fatigue may occur, but many patients with moderate-sized PDA remain essentially asymptomatic until the second decade of life or later.
On examination, the pulse is jerky, the precordium is mildly overactive, and the left ventricle is palpable at the apex in association with some cardiac enlargement. The classic continuous murmur is usually heard by age 2 to 3 months, although it varies in intensity. The murmur is generally loud and often masks the heart sounds. It is maximal over the pulmonary artery and radiates upward beneath the mid-third of the clavicle. As described by Gibson in 1900, “it begins after the commencement of the first sound—it persists through the second sound and dies away gradually during the long pause. The murmur is rough and thrilling. It begins softly and increases in intensity so as to reach its acme at or immediately after the occurrence of the second sound, and from that point gradually wanes until its termination.” Subnormal physical growth is common; Krovetz and Warden found body weight below the third percentile in 26% of 515 surgically proven cases. The ECG may be relatively normal during infancy, but some degree of left ventricular hypertrophy develops in older children. The chest radiograph shows moderate cardiac enlargement and plethora and a prominent ascending aorta (in contrast to findings in patients with a large ventricular or atrial septal defect). In adults, the PDA may be calcified. It is rare for pulmonary vascular resistance to increase, and Eisenmenger syndrome does not develop.
Small patent ductus arteriosus
Left-to-right shunt is small in early life, and pulmonary vascular resistance decreases rapidly to normal after birth. Left ventricular failure does not occur, and symptoms are absent in infancy and childhood. They may appear later in life, but usually attention is drawn to the condition by a murmur detected on physical examination.
Physical development is normal unless there is maternal rubella. The pulse is normal and the precordium not overactive. By age 2 to 3 months, a short systolic murmur is usually replaced by one that spills over into diastole, or it may be continuous in the second left intercostal space but less intense, and with less radiation than when the ductus is moderate in size. The continuous murmur varies greatly in intensity between patients and sometimes is detectable only when the patient is sitting or standing upright. The ECG and chest radiograph are normal or nearly so.
Special investigations
Most children and young adults with a PDA and a continuous murmur that is maximal in the second left intercostal space do not need preoperative invasive studies unless other defects are suspected; such studies may be necessary for diagnosis in atypical cases. Instead, two-dimensional echocardiography is usually performed and will image the ductus arteriosus. It has identified so-called silent ductus (a PDA without auscultatory findings). Managing patients with isolated silent ductus remains controversial, although endarteritis has been reported , and may be an indication for closure. Cardiac catheterization and angiography are indicated if the echocardiogram suggests elevated pulmonary vascular resistance or associated cardiac anomalies.
Natural history
Isolated PDA in infants occurs in approximately 1 in 2000 live births and accounts for 5% to 10% of all types of congenital heart disease. It is twice as common in females and may occur in siblings, suggesting a genetic factor. It is particularly common when the mother contracts rubella during the first trimester of pregnancy and may then be associated with multiple peripheral pulmonary artery stenoses and renal artery stenosis.
Because of the early introduction of surgical treatment of PDA, which antedated methods for establishing the diagnosis, its natural history is not completely documented.
Spontaneous closure
Campbell’s study concluded that spontaneous closure of isolated PDA occurs in 0.6% of patients per year and that this rate is fairly constant through the first 4 decades of life. If this is accepted, it means that in approximately 20% of patients, the PDA will have closed by age 40. His study involved only patients diagnosed beyond age 12 months and was based entirely on clinical findings, closure being assumed to have occurred when a typical murmur was no longer audible, regardless of size of the ductus or initial right-to-left shunt. Other experience suggests that the closure rate is much lower, and it is generally agreed that spontaneous closure is uncommon beyond age 3 to 5 months in full-term infants. Delayed closure of the ductus arteriosus in preterm infants is, however, common (see “ Special Situations and Controversies ” later in this chapter).
Pulmonary vascular disease
Prevalence and type of pulmonary vascular disease in patients with large PDA are similar to those in patients with large ventricular septal defect (see “ Pulmonary Vascular Disease ” under “Morphology” in Section I of Chapter 33 ).
Rupture
Rupture of both nonaneurysmal and aneurysmal PDA has been reported.
Death
Mortality with untreated PDA in infancy is high, and it has been estimated that, particularly in earlier eras, 30% of patients born with an isolated PDA died within the first year. , Risk of death is highest in the first few months of life among preterm infants (see Section II ).
After infancy, the annual death rate of patients with untreated PDA decreases dramatically to approximately 0.5% per year. By the third decade, the death rate has increased to about 1% per year; by the fourth decade, 1.8% per year; and in subsequent decades, as high as 4% per year. As a result, approximately 60% of patients with PDA die by age 45. Most of the deaths in older patients are related to development of intractable left ventricular failure secondary to long-standing volume overload.
Modes of death
In infants with a large PDA, mode of death is usually heart failure. Recurrent respiratory infection terminating in pneumonia is a less common mode. In those with a large PDA who survive infancy, death is usually due to acute or chronic right-sided heart failure secondary to development of severe pulmonary vascular disease by the second or third decade of life.
In patients with a moderate-sized PDA, mode of death from the third and fourth decades onward is heart failure. Excluding infants and deaths from pulmonary vascular disease, Campbell estimated that heart failure was the cause of death in 30% of patients.
Infective endarteritis occurs mainly as a complication of small and moderate-sized PDA. It rarely occurs when the ductus is large. In the preantibiotic era, endarteritis was responsible for approximately 45% of deaths in patients with surgically untreated PDA. , , After the advent of antibiotics, few patients died from this cause, although they remained subject to recurrent infection. In the current era, risk of infective endarteritis is extremely low.
Technique of operation
Unless the patient is an infant in severe heart failure or elderly, an intra-arterial monitoring catheter is usually unnecessary. After the usual induction of anesthesia and preparations for operation (see Chapter 4 ), the patient is positioned on the right side ( Fig. 28.3 B ). A small roll or pillow is placed under the mid-chest. The patient is positioned near the surgeon’s side of the table but not so much so that the first assistant across the table from the surgeon cannot see into the field well and work comfortably.
Closure of patent ductus arteriosus (PDA) by division. (A) Posterolateral incision in a patient properly positioned for operation. (B) Rib retractor has been placed and opened slowly to its final width. Lung is gently retracted anteriorly. Vertical incision is made in mediastinal pleura, and traction sutures are placed on pleural flaps. Left vagus and left recurrent laryngeal nerves are identified and protected. (C) Areolar tissues and pericardial lappet anterior to ductus are elevated with forceps and sharply dissected free of it. Care is taken to leave the adventitial layer of ductus undisturbed. (D) After anterior surface of ductus has been freed far enough medially so that junction of PDA with left pulmonary artery is visible, superior and inferior surfaces are similarly dissected. Right-angled clamp is passed behind ductus. Clamp stretches areolar tissue behind ductus, which is then grasped with forceps and cut away. (E) This maneuver is repeated several times and creates a space behind ductus. (F) Clamps are placed at aortic and pulmonary ends of ductus (see text), and it is divided midway between them. (G) Aortic end of ductus is oversewn with two rows of 5-0 or 6-0 polypropylene suture. Clamp on aortic end of ductus is generally kept in place following closure and provides traction to expose pulmonary end, which is then oversewn in a similar fashion. Clamps are then released.
Posterolateral thoracotomy
A curving skin incision is made, centered about 1 to 2 cm below the tip of the scapula. In infants and young children, the incision is really a lateral one because only the latissimus dorsi and posterior part of the serratus anterior is divided. In older children, the incision is posterolateral, extending posterosuperiorly to overlie the lower 1 or 2 cm of the trapezius, which is also incised. In patients who are in the second decade of life or older, the incision extends from the anterior axillary line around the scapula and up midway between the spine and posterior scapular border over the lower 3 to 4 cm of the trapezius.
After incising the latissimus dorsi (and trapezius if indicated), the scapula is elevated with a retractor and the ribs are counted from the top down to the fifth rib. Identifying the appropriate rib or intercostal space requires an accurate point of reference. There are three possible points of reference (the second and third are often more reliable than the first):
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First rib: The surgeon passes his or her left hand under the serratus and identifies the first rib by palpation.
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Second rib: The serratus anterior attaches superiorly to the second rib. The surgeon identifies this attachment using upward traction on the scapular retractor, which makes the prominent posterior border of this muscle taut.
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Second intercostal space: This is usually appreciably wider than the third intercostal space.
Counting down from the reference point, the fifth rib is identified and scored. Only then are the posterior and midportions of the serratus anterior divided so that the muscle incision may be directly over the fifth rib. The fourth interspace may be opened with a scalpel or cautery or the chest may be entered through the superior part of the bed of the nonresected fifth rib.
After the incision in the rib cage is extended anteriorly and posteriorly, the rib retractor is placed with the ratcheted portion anteriorly ( Fig. 28.3 A ). The retractor is opened only partially at first, but as the operation proceeds, it is gradually opened farther to obtain adequate exposure.
A retractor is gently placed on the lung, and a vertical incision is made in the mediastinal pleura over the proximal descending thoracic aorta (see Fig. 28.3 A ). Traction sutures are placed on the anterior and posterior pleural flaps. The lung retractor is removed, moist gauze is placed over the lung, and the anterior pleural traction sutures are pulled taut and anchored to the retractor or drapes. The vein that traverses the aorta obliquely on its anterior surface is divided. The PDA is completely dissected from the surrounding tissue ( Fig. 28.3 C-E ). In small infants, particular care is taken to be certain that the structure identified as the PDA connects the aorta and pulmonary artery, and that it is not the LPA or distal aortic arch. As dissection proceeds, the left recurrent laryngeal nerve is not isolated, although it should be clearly visualized behind the areolar tissue over the LPA, just inferior and posterior to the PDA (see Fig. 28.3 C ).
When the PDA is an uncomplicated one, ligation may be performed. Division of a larger PDA may be necessary. Both techniques, when done properly, ensure complete closure with low risk.
Division.
When division is elected and the patient is an infant or young child, one straight and two angled fine-toothed Potts ductus clamps are selected. In teenagers and adults, longer-handled vascular clamps are used. At this time, and particularly in older children and adults, the anesthesiologist reduces arterial blood pressure (see Chapter 4 ) and maintains it below baseline level until the clamps are removed.
The straight clamp is placed completely across the aortic end of the PDA, making sure that its tip does not grasp the recurrent laryngeal nerve or other soft tissue posterior to the ductus. The clamp is placed in the surgeon’s left hand and is gently pulled anteriorly. One angled ductus clamp is placed on the aortic side of the straight clamp and usually on the aorta contiguous with the PDA rather than on the ductus itself. The straight clamp is removed. With the clamp on the aortic origin of the PDA, which is held in the surgeon’s right hand, the other angled clamp is placed with the left hand on the pulmonary end of the ductus. To avoid dislodgment from the clamp and retraction into the pericardial cavity, the clamp must grasp only the ductus and not any of the lappet of pericardium or other tissue. This clamp, like the one on the aortic end, is “squeezed” onto the pulmonary artery as much as possible when it is being placed to give added length to the ductus. The ductus is divided midway between these clamps by Potts scissors or a scalpel ( Fig. 28.3 F ).
The aortic end of the PDA is oversewn with two rows of 5-0 or 6-0 polypropylene suture placed as a whip stitch ( Fig. 28.3 G ). The pulmonary end is similarly closed. Although accurate suturing is of obvious importance, the key to a safe repair is separating the clamps widely enough so that a substantial cuff of ductus remains beyond them after the ductus is divided. This permits placing additional sutures for hemostasis.
The clamp on the pulmonary end of the divided ductus generally is removed first. The clamp on the aortic end is then removed, and a sponge is placed between the divided ends and held in place with pressure for several minutes. Unless the original placement of the clamps has been faulty or the suture closure is inadequate, the bleeding that occurs when the clamps are released usually stops within this period. If not, and if there is no major bleeding that would require replacing one or both clamps, a 5-0 polypropylene suture approximating the adventitia from both sides of the suture line usually controls the bleeding. A pledget of absorbable porcine gelatin sponge is left between the divided ends of the ductus to prevent the suture lines from rubbing against each other.
Ligation.
If the situation is uncomplicated and the PDA is pliable, it may be ligated rather than divided. The technique is basically that described by Blalock in 1946. The operation proceeds exactly as described for ductal division until the PDA is completely dissected. Using a double-armed 5-0 or 6-0 polypropylene suture, adventitial stitches are placed into the accessible superior, inferior, and anterior aspects of the aortic wall contiguous with the PDA ( Fig. 28.4 A ). One end of the suture is passed beneath the ductus, and the ends are held. A similar stitch is placed on the pulmonary end of the ductus ( Fig. 28.4 B ). The aortic stitch is pulled up and snugly tied, and then the suture at the pulmonary end is tied. This leaves a long length of ductus between the tied sutures. Finally, a transfixion ligature of 5-0 or 6-0 polypropylene is placed at the middle of the ductus, and the ends are passed in the opposite direction around the ductus and tied to complete the ligation ( Figs. 28.4 C-F ). Alternatively, in small to moderate-sized PDA in infants and children, two separate silk ligatures may be used for ligation.
Closure of PDA by ligation. (A) Dissection has been completed as shown in Fig. 28.3 . Adventitial purse-string suture of 5-0 or 6-0 polypropylene is placed around aortic end of ductus. (B) Similar purse-string suture is placed around pulmonary end of ductus. (C) The two purse-string sutures are snugly tied. Transfixion suture is placed through ductus. One end is passed beneath ductus. (D) Other end of suture is passed beneath ductus in opposite direction, and the two ends are tied on anterior surface. (E) Cross-sectional diagram showing scheme for passing ends of suture. (F) Transfixion suture has been tied, leaving a space between it and other sutures.
