The following was part of a listserve dialog on asymptomatic patent ductus arteriosus. It was published as a VIN page to facilitate rapid access to images.

Hi Dan, (and many others)

It looks like you opened a can of worms with your query about managing an asymptomatic PDA. I have been away and haven't checked my email for a few days but you have gotten good feedback from several folks and I have little to add except some unpublished data and a few pertinent cases I recall. I will preface my remarks by reminding everyone that we did not have echocardiography and Doppler to guide us in the "old" days so our clinical and pathophysiologic thinking was based on less sophisticated technology.

I operated on 7 dogs with R-L PDA in the 60's and 70's hoping to get to them before they were irreversible. The oldest was 1.5 years old and the youngest two were 2 months old. All died in 24-36 hours with dyspnea except for the oldest one which had hypotension and cardiac arrest following an unrecognized bleed from a femoral artery leak under the drapes. He was transfused and resuscitated but did not recover from anesthesia. The 1-2 day survivors all had severe pulmonary vascular disease with grade 6 Heath-Edwards changes including medial hemorrhage (Fig 1), acute fibrinoid necrosis (Fig 2) and plexiform lesions (Fig 3).

Figure 1

Figure 2

Figure 3

I never saw plexiform lesions or fibrinoid degeneration like this in the lungs of over 100 fetal and newborn dogs in our PDA colony including many with abnormal ductuses that would have stayed patent (Buchanan JW, and Patterson DF. Etiology of patent ductus arteriosus in dogs. JVIM 17:167-171, 2003.).

I attribute the hemorrhage and fibrinoid necrosis to altered hemodynamics associated with anesthesia/thoracotomy/ductus ligation/etc (take your pick). In the two 2-month old dogs, I left pressure catheters in the carotid arteries and RV until they were standing and walking around post op. Pressures were equal pre-ligation and began to diverge in seconds after PDA ligation ('Lig' in figure 4). Systemic pressure increased and RV pressures decreased so I mistakenly thought we were winning.

Figure 4

Plexiform lesions are similar sized, non-inflammatory, mushroom like proliferations of endothelial cells at branch points just beyond muscular pulmonary arteries throughout the lungs (Fig 5). They may look like renal glomeruli (Fig 6) but with serial sectioning of the same glomoid body, you can find their association with the parent artery (Fig 7) They were regularly seen in R-L dogs at 4 months of age ( Buchanan JW, Patterson DF, and Pyle RL: Plexiform lesions in dogs with hereditary patent ductus arteriosus and pulmonary hypertension. Circ. 49:III-50, 1974.).

Figure 5

Figure 6

Figure 7

I did not see hemorrhage and fibrinoid necrosis in dogs with R-L PDA that had not undergone surgery so I blame the necrosis (but not the plexiform lesions) on surgery. The youngest dog (non-operated) in which I found developing plexiform lesions (Fig 8) was 19 days old and had gross and grade 6 histologic PDA. Since none were seen in over 100 other fetuses and newborn dogs from the colony, many of which would have had PDA, I am convinced that the lesions develop after birth.

Figure 8

Some cases pertinent to the dialog you started:

Case 1. A 6y-old Poodle with PDA, exercise intolerance and VHS 13.4 was exercising normally 4 months after surgery and had VHS 10.8 (Fig 9) (Buchanan JW: Radiographic aspects of patent ductus arteriosus in dogs before and after surgery. Acta Radiologica, Suppl. 319, pp. 271-278, 1972.)

Figure 9a. Preoperative lateral radiograph showing marked generalized cardiac enlargement (VHS 13.4). The diameters of the right apical artery (a) and vein (v) just proximal to their branching at the border of the cardiac silhouette exceed the smallest diameter of the 4th rib indicating increased pulmonary blood flow.

Figure 9b Lateral radiograph 4 months after operation. The pulmonary vessels are normal but slight cardiac enlargement is still present (VHS 10.8). (Buchanan, JW, and Bucheler, J: Vertebral scale system to measure canine heart size in radiographs. JAVMA 206:194-199, 1995.)

Figure 9c and 9d

Corresponding DV radiographs presented with the dog's left to the viewers right. The dotted lines mark the 2nd and 13th vertebra indicating comparable magnification. The heart size is obviously reduced but the cardiothoracic ratios at the midpoint of the cardiac silhouette are essentially the same because the thoracic expansion with severe cardiomegaly is reduced and also the ratio is determined in a narrower part of the thorax.

Case 2. A 9y-old female Cocker spaniel with R-L PDA and rearleg collapsing after 50 yard trotting had symptoms relieved with periodic phlebotomy for 2 yrs. (n.b: 5 of 16 R-L PDA's were female Cockers: pg 460, 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)

Case 3. 15yr male Cocker spaniel with a 2mm orifice PDA was euthanized because of vomiting and a head tilt. It was asymptomatic for heart failure but had a grade 4/5 machinery murmur and precordial thrill, 2.9 mv lead II R waves and VHS 12.0. (Pyle RL: Patent ductus arteriosus in an aged dog. JAVMA 158:202-7, 1971).

Case 4. I did not examine the dog but received the heart of a 12 year-old male Cavalier KCS. It had mild pulmonic stenosis and a 1.5 mm PDA orifice. The PDA was previously known but he never showed signs of heart failure and it was not corrected. He also had significant mitral valve disease with one ruptured chorda tendina and a heart weight of 170 grams. Normal cavalier hearts weigh 60-90 grams.

On a sad note, your white Dodge developed terminal signs and didn't pass mandatory vehicle inspection so I am donating it to Purple Heart.

Best regards to you (and other friends who read this far)

James W. Buchanan, DVM, M Med Sci
Emeritus Professor of Cardiology
Sch Vet Med, Univ of Penn,
Philadelphia, PA 19104