A patent ductus arteriosus (PDA) is an arterial shunt between the pulmonary artery and the aorta that is normally open in fetuses but should constrict and close within hours after birth. Incomplete closure (patency) yields a variable size channel whose minimum diameter primarily determines the amount and direction of blood flow through the shunt. PDA is the most common congenital cardiovascular abnormality in dogs and is caused by a structural defect in the ductus wall.^1,2

1. Normal anatomy and function
2. Angiography
3. Gross pathology
4. Histopathology
5. Diagnosis
6. Epidemiology
7. Etiology
8. Significance
9. Treatment
10. Complications
11. References

1. Normal Anatomy and Function

The ductus arteriosus is commonly called the arterial duct, arterial canal, or ductus Botalli in Europe. It extends from the bifurcation of the main pulmonary artery to the ventral aspect of the descending aorta between the left subclavian and intercostal arteries (Figs 1-3). It carries relatively oxygenated blood from the right heart into the descending aorta thus bypassing the nonfunctioning lungs. The ductus is functionally closed by constriction in the first few hours after birth and later by anatomic closure in 2-4 weeks (Fig 4).

Fig. 1 Necropsy photograph of thoracic viscera in a 45-day gestational age canine fetus after removal of the left thoracic wall. The open ductus arteriosus (D) is similar in size to the main pulmonary artery (P) and extends dorsally to the aorta (A).	Fig. 2 Photograph of the heart and great vessels in a normal newborn dog that breathed. The ductus (D) is partially constricted where it extends between the pulmonary artery (P) and the aorta (A).
Fig. 3A Sagital histologic section through the ductus (D), main pulmonary artery (P), and aorta (A), in a normal newborn dog in which the ductus has just begun to constrict. An elastic stain reveals muscular ductus tissue extending a variable distance into the adjacent vessels (arrows). The transition between muscle and elastic tissue is abrupt and without septae.	Fig. 3B Transverse histologic section through the middle of a normal ductus arteriosus before birth. The internal elastic lamina of the ductus in most dogs is minimal or not apparent. There are no intimal mounds before birth as in humans. The aorta is above and the main or left pulmonary artery is below the ductus in this and all subsequent images.
Fig. 4A Transverse histologic section through the middle of the ductus in a normal 3 day-old dog. The ductus is completely occluded by contraction. The central segment is totally separated from adjacent vessels and the entire wall is muscular except for an adventitial rim of elastic and collagen fibers. Anatomic closure with non-inflammatory cytolysis of ductus smooth muscle occurs in 2-4 weeks. Proliferative intimal fibrosis occurs only at the extreme ends of the ductus where it smoothes over the orifices of the ductus in the great vessels.	Fig. 4B Transverse section of a "ligamentous" ductus in a 2 month-old dog shows residual elastic and collagen figers that form the degenerate ligamentum arteriosum.

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2. Angiography

PDAs vary considerably in diameter, shape and length. The majority of PDAs are funnel shaped with maximal narrowing at the pulmonary artery orifice. They are categorized as long or short and tubular or tapering based on angiography for the purpose of selecting an occluding device or recommending surgery. These distinctions are arbitrary labels in a continuum of the histologic abnormality that causes PDA. Most of the ductus arteriosus lies within the wall of the aorta in dogs (not in humans) and the aortic wall segment may not be evident externally (Fig 5A). In other dogs, it may appear as a ventral and lateral bulge in the aorta (Fig 5B, C). The dilated portion is commonly called a ductus diverticulum or ampulla. It is in fact a ductal-aortic aneurysm caused by distal extension of the histologic abnormality and probably magnified by continued hemodynamic effects. The aneurysm remains after surgical or transcatheter closure of the orifice (Fig 5D).

Fig. 5A Aortic injection angiocardiogram showing left-to-right (L-R) shunting through a small tubular PDA in the wall of the aorta with a small opening into the main pulmonary artery.	Fig 5B Medium size tubular PDA with a significant L-R shunt indicated by pulmonary artery enlargement.
Fig. 5C Largefunnel shaped PDA with a medium sized orifice and typical enlargement of the pulmonary vessels, ascending and transverse aorta.	Fig. 5D Post operative angiocardiogram showing a ductal-aortic aneurysm one year after ligation of the PDA in a 2-month old dog. The aneurysm was minimal at surgery.

Large PDAs with pulmonary hypertension and right-to-left shunting usually do not appear to have an aneurysm (Fig 6). The pulmonary vasculature may appear almost normal or mildly dilated and tortuous (Fig 7).

Fig. 6

Right ventricular injection angiocardiogram in a dog with pulmonary hypertension and a right-to-left shunt through a large cylindrical PDA.

Fig. 7AB

Bidirectional (balanced) PDA in a one-year-old dog with pulmonary hypertension and polycythemia (pcv 75%). The right ventricular (RV) injection angiocardiogram shows right-to-left shunting through a large PDA (D), RV hypertrophy, tricuspid insufficiency, and enlarged and tortuous pulmonary arteries (P). B. The left ventricular (LV) injection angiocardiogram shows left-to-right shunting through the PDA into the pulmonary arteries.

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3. Gross Pathology

External examination of gross specimens does not reveal the true size of the defect since most of the ductus length lies within the wall of the aorta (Fig 8). Internal PDA diameter varies with location but the narrowest segment is almost always at the pulmonary artery orifice where an intimal ridge or short tunnel defines the minimum diameter. Vary rarely, the narrowest segment is found in the middle or towards the aortic end of the ductus and is probably due to a shift in the location of the hypoplastic ductus muscle mass.

Fig. 8A Gross photograph of the left atrial appendage (LA), left ventricle (LV), right ventricle (RV), main pulmonary artery (P), external ductus (D), and aorta (A) in a 4 month-old dog with PDA.

Fig. 8B In sagittal section, the distal portion of the PDA courses through the wall of the aorta forming a ductal-aortic aneurysm (a.k.a. diverticulum or ampulla). When large, this appears as a leftward bulge in the aorta in a DV or VD radiograph. An intraluminal flap of variable length (plica reunions) separates the ductus ampulla from the aorta (arrow head). The ductal-pulmonary orifice is usually restricted by an intimal ridge in the external ductus.

Surgery through the left 4^th intercostal space usually provides good exposure to the external portion of a PDA (Fig 9). Generally, the external PDA length varies inversely with the size of the aneurysm. When the PDA is very short and/or the aneurysm is large, the external segment resembles an aorta-pulmonary window although it is not the same defect embryologically.

Fig. 9A 8mm diameter PDA in an 8-month-old, 7 kg dog viewed through the left 4th intercostal space. The vagus nerve is retracted ventrally exposing the recurrent laryngeal nerve circling caudally around the PDA.	Fig. 9B A short 3mm diameter PDA in a 2-week-old, 220 gram dog is encircled with a silk ligature. Eyelid retractors and a one-inch needle are shown for size comparison.
Fig. 9C Pre- and postoperative photographs of 220 gram dogs with hereditary PDA.

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4. Histopathology

Fig. 10 Sagittal histologic section of the great vessels in a 13-day-old dog with a large, short PDA. A small amount of ductus muscle is present in the caudal wall of the ductus (arrow). The spectrum of abnormalities in dogs with PDA are best characterized in elastic stained transverse sections of the central zone of a PDA (Fig 11).	Fig. 11 Transverse histologic section through the PDA and adjacent vessels in an 11-day-old dog with hereditary PDA. The asymmetric ductus muscle (DM) is constricted and degenerating near the pulmonary artery (P). The aorta-like portion of the ductus wall adjacent to the aorta (A) is not constricted and contains thicker elastic fibers. Simultaneous contact with the aorta and pulmonary artery indicates that the PDA is short (2). Elastic stain.
Fig. 12 Transverse histologic section through the PDA and adjacent vessels in a 3-month-old Collie with PDA and not related to the hereditary PDA family. The elastic wall next to the aorta should be muscular. (See section 7- Etiology)

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5. Diagnosis

Physical examination is usually sufficient to diagnose PDA. However, additional studies are usually performed to assess secondary changes, determine the urgency of PDA closure and to rule out coexisting abnormalities. A continuous (machinery) murmur at the left heart base is the cardinal sign of a PDA (Fig 13). The intensity, frequency, duration and radiation of the murmur are determined by the diameter and length of the PDA and the degree of pulmonary hypertension. Dogs with a small PDA have a focal, relatively high pitched, continuous murmur heard only at the left heart base.

Fig. 13

A. Preoperative phonocardiogram illustrating a continuous (machinery) murmur over the left 3^rd intercostal space in a dog with patent ductus arteriosus. B. Postoperative phonocardiogram recorded in the same area shows normal 1^st and 2^nd heart sounds.

The continuous murmur in dogs with a medium or larger size PDA can usually be heard all over the thorax and is accompanied by a precordial thrill. When the heart is enlarged, a systolic murmur of mitral regurgitation due to annular dilation also may be heard. Dogs with a large PDA may have so much flow through the PDA that diastolic blood pressures equalize in the aorta and pulmonary artery (Fig 14) and the diastolic murmur is abbreviated or not present.

Fig. 14

Simultaneous pressure recordings in the aorta and pulmonary artery during surgery in a dog with a large PDA show pressure changes when the PDA was closed. This dog had no murmur during diastole because pressures were essentially equalized. When the PDA was open, the large pressure difference between systole and diastole in the aorta (wide pulse pressure) caused bounding pulses.

The pathognomic radiographic sign of a medium or large PDA is a leftward bulge of the aorta in a DV or VD radiograph at the one-o'clock position caused by a ductal-aortic aneurysm (Fig 15). Other radiographic signs of a medium or large PDA include left heart enlargement and increased pulmonary vascular markings (Fig 16). Pulmonary edema is seen when congestive heart failure develops. Electrocardiograms usually have high amplitude R waves indicative of left ventricular hypertrophy. Atrial fibrillation is the most common arrhythmia. Echocardiograms typically show an enlarged, hyperdynamic left ventricle. Doppler interrogation shows continuous, turbulent, retrograde flow into the main pulmonary artery from the aorta (Fig 17).

Fig. 15A Dorsoventral radiograph of a dog with PDA showing leftward bulge of the aorta caused by a ductal-aortic aneurysm.	Fig. 15B One-year postoperative DV angiogram showing persistence of a ductal-aortic aneurysm causing a bilateral bulge in the aorta.
Fig. 16 Two weeks preoperative lateral radiograph of the 8-month old dog with a large PDA shown in Figure 9A reveals marked cardiomegaly, pulmonary edema and increased pulmonary vascular markings. The diameters of the right apical pulmonary artery (A) and vein (V) exceed the minimum diameter of the 4th rib (arrowheads).
Fig. 17A Color Doppler echocardiogram from a dog with PDA oriented like an angiocardiogram. The mosaic pattern shows turbulent flow in the cranial half of the main pulmonary artery.	Fig. 17B Standard echocardiogram orientation.

The clinical signs of PDA can be grouped into four types of cases.

Type 1 (Small PDA)

Asymptomatic left-to-right shunt

High frequency continuous murmur only at the left heart base

Precordial thrill is faint or absent at the left heart base

Heart rate and pulse quality are normal

Radiographs and ECG normal even at 1-2 years of age

Focused, turbulent, continuous retrograde PA flow in color Doppler echo.

PDA closure is not urgent but is recommended for a normal life span

Type 2 (Medium size PDA)

Asymptomatic left-to-right shunt

Coarse continuous murmur and at the left heart base and also at the left apex

Precordial thrill easily palpable at the left heart base

Pulses normal or slightly bounding

Mild-moderate left heart enlargement before 1 year of age

Small-to-medium size ductal-aortic aneurysm

Borderline increase in pulmonary vascular markings

Electrocardiogram lead II R waves usually exceed 3 mV

Color Doppler shows turbulent continuous flow in dilated main pulmonary artery

PDA closure is recommended but it can still wait a few weeks

Type 3a. (Large PDA before congestive heart failure)

Usually reduced exercise capacity

Coarse continuous murmur and thrill over most of the left thorax

Systolic murmur of mitral regurgitation often present at left apex and usually persisting a few days after PDA closure

Pulses bounding due to wide pulse pressure

Marked left heart enlargement before 6 months of age

Medium-to-large ductal aortic aneurysm usually present

Definite increase in pulmonary vascular markings

ECG lead II R waves may exceed 5 mV

Color Doppler shows large turbulent flow continuous flow in dilated MPA

PDA closure recommended without delay

Type 3b. (Large PDA plus congestive herart failure)

All the 3a features plus dyspnea due to pulmonary edema

Usually poor body condition (cachexia)

Atrial fibrillation occasionally present

Pulmonary edema must be resolved as much as possible by cage rest, oxygen, digitalization and diuresis before anesthesia and PDA closure

Animals with atrial fibrillation should be digitalized before anesthesia.

Type 4. (Large PDA with right-to-left or balanced shunt)

Two weeks to 12 years old

Hind leg weakness or collapse with excercise

Cyanosis usually limited to caudal part of the body

Pulses normal or weak

Polycythemia (packed cell volume as high as 80%)

Usually no murmur or precordial thrill after one month old

Split or prominent 2^nd heart sound

Right side apex beat stronger than left

Right axis deviation in ECG

Large right heart and main pulmonary artery

Pulmonary vessels may appear normal or decreased with slight tortuosity

PDA closure is contraindicated

Treat polycythemia by periodic phlebotomy or chemotherapy

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6. Epidemiology

PDA was the most frequent cardiovascular abnormality in a tabulation of 1000 dogs with congenital heart disease (Table 1).¹ It was diagnosed most frequently in small breed dogs (Table 2).

Table 1

Table 2

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7. Etiology

This Information is based on serial section study of the ductus and adjacent vessels in 145 fetuses and neonates from a mixed poodle strain with hereditary PDA, 55 unrelated normal fetuses and neonatal dogs and 8 dogs of various breeds with sporadic PDA.^2,4 Sections were routinely stained for elastic tissue to differentiate muscular and elastic elements. Early observations revealed inconsistencies between segments so a standardized method was developed to allow different regions of the ductus to be selectively compared (Fig 18).⁴

Fig. 18

Sagittal histologic section of the pulmonary artery (P), ductus arteriosus (DA), and aorta (A) in a normal newborn dog. The dotted lines outline the ductus muscle. Horizontal lines indicate ductus levels that are identifiable in transverse sections and are used to divide the ductus into 5 zones. Level 1 is the most proximal extent of ductus muscle in the PA wall. Level 2 is the separation point of the left PA. Level 4 is the separation of the ductus and the left PA. Level 6 is the juncture of the ductus and the aorta. Level 8 is the opening of the ductus into the aorta. Level 9 is the distal extent of ductus muscle that sometimes extends into the aorta. Levels 3, 5, and 7 are mid points in their respective zones determined by counting and halving the number of sections in each zone.

Serial section histology revealed a consistent pattern of abnormality in dogs with hereditary as well as sporadic PDA.² The ductus is shorter than normal, the ductus smooth muscle is hypoplastic and eccentric, and aorta-like elastic tissue is present in segments that should be muscular (Figs 11, 19). These changes vary in degree and can be categorized into 6 histologic phenotypes (Fig 21).

Fig 19 Type 5 abnormality. Transverse histologic section through the ductus in an 11-day-old dog with hereditary PDA. The hypoplastic, asymmetric ductus muscle is constricted and degenerating near the pulmonary artery. The thin aorta-like portion of the ductus wall adjacent to the aorta is not constricted, has smaller cells and contains thicker elastic fibers. The ductus is shorter than normal indicated by contact with the aorta while still connected to the pulmonary artery.	Fig. 20 Photomicrograph of degenerating ductus muscle showing foamy macrophages in an area of muscle lysis.
Fig. 21 Grading system for 6 types of hereditary PDA abnormality based on the extent of aorta-like elastic tissue (shaded area) in the normally muscular ductus wall adjacent to the aorta at level 6. In type1, the elastic tissue is present in less than half of the DA wall; in type 2 it extends through more than half of the DA wall. In increasing grade abnormalities, the elastic tissue extends through progressively greater percentages of the DA circumference. The non-shaded muscular areas are progressively smaller.

The histologic abnormalities recognized in dogs with PDA were also detectable in fetuses predisposed to PDA (Fig 22, 23).

Fig. 22 Type 4 abnormality. Transverse histologic section through the center of the ductus in a full term fetus predisposed to PDA. The ductus muscle only extends partway round the circumference. The portion of the ductus wall adjacent to the aorta has mainly elastic fibers.	Fig. 23A Transverse histologic section through the center of the ductus arteriosus in 3 littermate fetuses from a family with hereditary PDA. A. Normal ductus architecture.
Fig. 23B Transverse histologic section through the center of the ductus arteriosus in 3 littermate fetuses from a family with hereditary PDA. B. Type 1 abnormality.	Fig 23C Fig. 23. Transverse histologic sections through the center of the ductus arteriosus in 3 littermate fetuses from a family with hereditary PDA. C. Type 2 abnormality.

Both normal and abnormal ductuses were found in most of the PDA families studied histologically (Fig 24A); however, the average litter abnormality correlated with the proportion of PDA genes in each litter (Fig 24B). The ductus lengths were inversely correlated with the grade of abnormality.

Fig. 24A Histologic ductus types in 37 fetuses from 8 litters in a family with hereditary PDA.

Fig. 24B Average ductus types in 8 litters of dogs with hereditary PDA.

Functional studies of the closure mechanism in isolated perfused ductuses from fetal pups genetically pre-disposed to PDA showed an absent or diminished constrictor response to oxygen, norepinephrine and actylcholine.⁵ There was an increasing degree of impaired physiologic closure when there was an increasing proportion of the genome derived from dogs with PDA. Diminished response to oxygen was evidenced by increased conductance which corresponded to increased degrees of histologic abnormality (Fig 25).

Fig. 25

Maximal ductal responses to increased oxygen tension in unrelated normal fetuses and fetuses with various proportions of the PDA genome. The horizontal line represents two standard deviations above the mean input conductance of the control fetuses. Higher levels of input conductance (decreased responsiveness) correlated with the proportion of the PDA genome. Numbers indicate the type of histologic abnormality found in each fetus without knowledge of functional results.

The initial morphologic abnormality recognized in dogs with hereditary PDA was inappropriate ductal elastic tissue. This formed the basis of the 6 grade classification system. Further studies revealed the co-importance of hypoplasia of ductal smooth muscle so special attention was given to the 3-dimensional distribution of the ductus muscle. Three-dimensional analysis was aided by wax reconstruction of an isolated ductus muscle mass. This was done by projecting histologic sections on wax sheets and carving out the muscular area of the ductus wall of a type 4 fetus that would have had a PDA (Fig 26). The carved out portions were then stacked and fused.⁶

Fig. 26AB A. Transverse histologic section through the center of a ductus with type 4 abnormality (Fig 22 rotated). B. Stacked wax sheets after removal of ductus muscle cutouts.	Fig. 26C Wax model of ductus muscle mass made by stacking and fusing the muscle cut outs. Focused light above the model yields a shadow depicting the distribution and thickest portion of the ductus muscle.
Fig. 27 Clay models of ductus muscle showing grades 2-6 muscle patterns from an aortic perspective. The open segments correspond to the location of elastic tissue. The muscle develops in a wrap around pattern with the thickest portion of muscle always at the lateral aspect of the ductus wall near the pulmonary artery (Fig 28).
Fig. 28 Grade 6 abnormality in a 15-day-old dog with right-to-left PDA. The contracted ductus muscle is only present in the lateral wall of the ductus near the pulmonary artery. More than half of the ductus circumference has an elastic wall.	Fig. 29 Post mortem pulmonary angiogram of a one-year-old dog with a right-to-left PDA. The lungs were inflated and contrast material was injected into the main pulmonary artery at systemic pressure. There is blunting and tortuosity of the small pulmonary arteries along with tortuosity and an increase in bronchial arteries which filled retrogradely. Small uniform nodules at the ends of the smallest pulmonary arteries are presumably plexiform lesions (Fig 30).
Fig. 30ABC A. Diagram of plexiform lesions typically located at branch points just beyond muscular pulmonary arteries. B. Developing plexiform lesion in a 19-day-old dog with a large PDA. (Trichrome stain). C. Plexiform lesion in a 4-month-old dog with a large right-to-left shunting PDA. Movat pentachrome stain demonstrates medial hypertrophy, increased elastic laminae increased mucopolysaccharide, and proliferation of myointimal cells.	Fig. 30D Uniform sized plexiform lesions in a 4-month-old dog with R-L PDA.

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8. Significance

The size of a PDA determines its significance. Very small PDAs may not affect life span as evidenced by a 2 mm diameter PDA orifice found at necropsy in a 15 year-old Cocker Spaniel who never developed signs of cardiac compromise.⁷ However, the majority of dogs with PDA develop cardiac signs before middle age and life span would be shortened without treatment. Therefore PDA closure is always recommended except when right-to-left shunting is present. The only other instance when PDA closure should not be done is the presence of a co-existing ductus dependent heart abnormality such as pulmonary atresia or right to left tetralogy of Fallot.

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9. Treatment

Medical treatment: PDA closure with a prostaglandin synthetase inhibitor such as Indomethacin or aspirin requires responsive ductus muscle and is only effective in children in the first week after birth. In dogs with PDA, the small amount of ductus muscle and its eccentric distribution preclude closure in response to drugs even in the neonatal period. The diagnosis of PDA in dogs usually is not made until they are several weeks or months old and degeneration has already occurred in the small amount of muscle they have.

Transcatheter occlusion: Transarterial or transvenous deployment of coils and other devices to occlude a PDA has gained favor in many hospitals in recent years. Coils usually work well in tapered PDAs (Fig 31) but are less reliable in tubular types. More recently, an occluding device designed for dogs has been developed but it is considerably more expensive than a coil. A table comparing surgery versus coils lists many of the issues involved (Table 3).

Fig. 31ABC

A. A funnel shaped PDA (arrow) often can be occluded by a single transcatheter coil (B). C. Occlusion is confirmed by a repeat ductal-aortogram.

Table 3

Surgical treatment: PDA closure by surgery was the main treatment option for 40 years before the advent of transcatheter devices. Currently, most PDAs are closed with coils but about 10% of dogs with PDA still go to surgery because they are too small to insert devices or very large and/or their PDA is tubular and coils will not stay in place. Ductus closure is done through the left 4^th intercostal space. Triple ligation is preferred with the middle ligature transfixing the PDA lumen (Fig 32, 33). Single ligation is not recommended because closure is incomplete in about 25% of cases.

Fig. 32

A left 4^th intercostal space thoracotomy provides good exposure of most PDAs. Elevation of the descending aorta with a gentle latex retractor (Penrose drain tube) makes dissection easier and gives more length to the PDA allowing pre-placement and separation of 3 ligatures.

Fig. 33A The 2-0 silk ligature next to the aorta is tied first to reduce pressure in the rest of the ductus. The 4-0 transfixing suture-ligature is tied next. Then the 2-0 ligature adjacent to the pulmonary artery is tied. Moistened umbilical tape is used in place of 2-0 silk in large dogs such as a German Shepherd.

Fig. 33B Necropsy photograph demonstrating ligation of the external segment of a PDA.

Closure of a PDA with hemoclips (Fig 34) is an alternative to ligation but it is not a preferred method because tip placement is less precise than a ligature and metal is left in contact with the surrounding vessels.

Fig. 34A Lateral radiograph of 4-week-old dog with PDA showing marked cardiomegaly and pulmonary edema.	Fig. 34B Immediate post-operative radiograph showing two hemoclips positioned across the PDA.
Fig. 34C One year post-operative radiograph of the same dog showing normal heart size, clear lung fields and hemoclips.

A division method is used when the PDA is very short or has a diameter greater than 10mm because of the danger of lacerating a short, large vessel when tightening a ligature (Fig 35). The division method was used in 26 of 48 dogs with PDA in the first reported series (Fig 36, 37).⁸ Although division takes longer, the success and complication rates for the division method were the same as the ligation method.⁸ PDA division is mandatory when a persistent right aortic arch is present.^8,9

Fig. 35 Large PDAs such as this 15mm diameter one should be divided using special PDA clamps with atraumatic jaws (Figs. 36, 37).	Fig. 36 Diagram of the PDA division method. (A) The recurrent laryngeal nerve passes caudally around the ductus and aorta; (B) PDA clamps are positioned as far apart as possible while avoiding the recurrent laryngeal nerve; (C) the ductus is cut midway between the clamps and the clamps are slightly rotated to facilitate suturing; (D) two rows of simple continuous sutures are placed independently before removing the clamp; (E) slight outward traction on the tied sutures permits reapplication of the clamp if necessary after the clamp is released; (F) appearance after the division is completed. A pad of Gelfoam is placed between the suture rows.
Fig. 37A-F. (below) Photographs showing division of 10 mm diameter PDAs. Gentle tension is applied to the uncut suture ends (E) to facilitate re-clamping if necessary.
Fig. 37A Photographs showing division of 10 mm diameter PDAs. Gentle tension is applied to the uncut suture ends (E) to facilitate re-clamping if necessary.	Fig. 37B
Fig. 37C	Fig. 37D
Fig. 37E	Fig. 37F

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10. Complications

Complications can occur at any stage in the management PDA. The two most common ones are congestive heart failure and uncontrollable hemorrhage during ductus dissection. Congestive heart failure manifested as pulmonary congestion or edema (Figs 16, 34) may occur early in dogs with large PDAs and is sometimes the first noted sign of heart disease. It is important to treat such cases medically for a few days before operating because necessary manipulation of the lungs during thoracotomy is not tolerated. Hemorrhage during dissection is often uncontrollable and occurs most frequently during the initial phase in the learning curve of a surgeon (Table 4).

Table 4

Other complications include arrhythmias, pulmonary hypertension (Fig 38), endarteritis (Fig 39), thrombosis (Fig 40), and aortic or ductal rupture (Fig 41). Patient size is not a complication for surgery (Fig 9). The surgical mortality rates in very small dogs was actually less than in larger dogs.⁸

Fig. 38 Simultaneous aortic (A) and right ventricular (RV) pressures in a 2-month old dog with PDA and pulmonary hypertension. The RV pressure began to fall and the aortic pressure rose after ligation (Lig) of the PDA. The dog died 6 hours later and had plexiform lesions, pulmonary arterial hemorrhage, and fibrinoid necrosis (Heath-Edwards grade 6 vascular lesions) in the lungs (Fig 30).	Fig. 39 Necropsy photograph of a recanalized PDA showing thrombus where the umbilical tape ligature eroded through the PDA. The still-tied ligature was found in the pericardial sac.
Fig. 40A Necropsy photograph of a thrombus in the ductal-aortic aneurysm in a 9 year-old dog one year after division of the PDA.	Fig. 40B Saddle thromboembolus at the bifurcation of the aorta in the same dog.
Fig. 41 Necropsy photograph of a ruptured ductal-aortic aneurysm. The dog exsanguinated one hour after completion of surgery during which the ductus was divided. For photography an incision was made in the dorsal wall of the aorta and a hemostat was passed through the ductal-aortic aneurysm. It protrudes through a 1.5 cm long rupture found 1 cm caudal to the ductus suture line.

Complications also occur with transcatheter occlusion of PDAs. The most frequent one is pulmonary artery embolism of one or more coils. Others include hematoma formation at vascular access sites and systemic coil embolism (Fig 42, 43) (Table 5).¹⁰

Fig. 42 Aortic injection angiocardiogram showing a coil embolism in the right pulmonary artery. These usually can be retrieved but seldom cause trouble if left in place.
Fig. 43A Necropsy photographs of a thrombosed coil displaced into the main and left pulmonary artery.	Fig. 43B Necropsy photographs of a thrombosed coil displaced into the main and left pulmonary artery.

Table 5

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11. References

1. Buchanan JW: Prevalence of cardiovascular disorders. In Canine and Feline Cardiology. 2^nd ed. Fox P, Sisson D, and Moise NS, eds, WB Saunders Co. 1999, p 457-470.

2. Buchanan JW and Patterson DF. Etiology of patent ductus arteriosus in dogs. J Vet Intern Med 17:167-171, 2003

3. Buchanan JW: Morphology of the ductus arteriosus in fetal and neonatal dogs genetically predisposed to patent ductus arteriosus. Birth Defects: Original article series 14:349-360, 1978.

4. Buchanan JW and Chmielewski S: Three-dimensional histology. A 35mm photographic method. Microscopy 99:353-356, 1973.

5. Knight DH, Patterson DF, and Melbin J: Constriction of the fetal ductus arteriosus induced by oxygen, acetylcholine, and norepinephrine in normal dogs and those genetically predisposed to persistent patency. Circulation 42:127-132,1973.

6. Buchanan JW. Patent ductus arteriosus: Morphology, pathogenesis, types and treatment. J Vet Cardiology 3:7-17, 2001

7. Pyle RL Patent ductus arteriosus in an aged dog. JAVMA 158:202-7,1971

8. Buchanan JW: Patent ductus arteriosus and persistent right aortic arch surgery in dogs. J Sm Anim Pract. 9;409-428,1968.

9. Holt D, Heldmann E, Michel K, and Buchanan JW. Esophageal obstruction caused by a left aortic arch and an anomalous right patent ductus arteriosus in two German Shepherd littermates. Veterinary Surgery. 29:264-70, 2000

10. Goodrich KR, Kyles AF, Kass PH, and Campbell F. Retrospective comparison of surgical ligation and transarterial catheter occlusion for treatment of patent ductus arteriosus in 204 dogs (1993-2003). Vet Surg 36:43-49,2007.

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