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Cavalier King Charles Spaniel with PDA
- 2. • 4 week old male entire Cavalier King Charles Spaniel • Presented for investigation of heart murmur
- 4. Left ventricular dilatation Turbulent flow in pulmonary artery Visualisation of PDA
- 5. • Important part of foetal circulation • Shunt between pulmonary trunk and aorta (RL) • Allows deoxygenated blood to bypass the lungs and enter the aorta • When first breath is taken: Aortic pressure increases Blood flows back into ductus arteriosus Ductus arteriosus pressure increases Walls of ductus arteriosus collapse Ductus arteriosus closes
- 6. • Left sided heart failure • LV dilatation and mitral regurgitation • LV myocardial failure • LA enlargement • Atrial fibrillation
- 7. • Maltese • Pomeranian • Shetland Sheepdog • English Springer Spaniel • Bichon frise • Poodle • YorkshireTerrier • German Shepherd
- 9. • “triple knuckle” • Cardiomegaly • Distended pulmonary vessels • +/- pulmonary oedema
- 10. • Vascular occlusion coils • Amplatz Canine Duct Occluder (ACDO) • Furosemide • Pimobendan • (ACE inhibitors) • (Spironolactone)
- 12. • Catheter passed via femoral artery aorta ductus arteriosus • Suitable size of occluder chosen • Occluder released in DA • Encourage embolus formation ductus occlusion • Referral procedure
- 14. • Left ventricular systolic dysfunction • Cardiomegaly/enlarged chamber size • Mitral regurgitation o Confirmed CHF o Age: > 2 years old? o Weight: >23kg ?
- 15. • Methadone • Meloxicam • Synulox • Frusemide • Pimobendan
Editor's Notes
- Patent ductus arteriosus is one of the most common congenital cardiac abnormalities seen in dogs and it is the only potentially curable congenital cardiac defect and so I thought it would be a good condition to discuss today.
- Leo had presented to his own vets because one of the other puppies in his litter was ill so the breeder decided to take them all to the vets to get checked (she had not actually had any concerns about Leo’s health). His vet discovered that he had a grade 6/6 murmur. Since the murmur was of a much higher grade than would be expected with the normal “innocent” murmurs occasionally found in puppies the vet recommended referral for investigation.
- On questioning we found out that Leo was the smallest of his littermates though the owners didn’t feel that he was struggling to keep up with them when it came to energy levels. Leo was a very bright and lively puppy. His heart rate was high end of normal with a continuous grade 6 (murmur can be heard when stethoscope is lifted off the chest). His respiratory rate was increased but the lungs sounded normal. It was decided that echocardiography would be carried out in order to find the cause of the heart murmur.
- The first thing that was noted on echo was that the left ventricle was dilated (diameter of LV should be no bigger than 1.5x diameter of aorta and based on other images the LV measured bigger than that). There was also turbulent flow in the pulmonary artery found on the colour doppler setting (i.e. not all blood in the pulmonary artery was flowing as normal, there was a jet of blood entering the pulmonary artery from somewhere abnormal causing turbulence in the vessel) and so the next step was to try and find where the turbulent blood was coming from. A patent ductus arteriosus was then visualised (and was found to be the source of the turbulence). And so based on these echo findings we came to the diagnosis of PDA with left right shunting and mild cardiac remodelling.
- The ductus arteriosus makes up part of the normal foetal circulation. In the foetus, the lungs are not functional. The ductus arteriosus connects the pulmonary artery to the aorta so that deoxygenated blood flows through the pulmonary artery into the aorta rather than into the lungs (essentially the ductus arteriosus enables blood to shunt from the right to the left side of the heart in the foetus). This deoxygenated blood then enters umbilical arteries and can be oxygenated by the placenta. At birth the lungs inflate and the umbilical arteries are occluded, increasing systemic vascular resistance and reducing pulmonary vascular resistance. Increased pressure in the aorta causes blood to flow back into the ductus arteriosus (left right) which in turn causes ductus arteriosus pressure to increase. This pressure increase puts stress on the walls of the ductus causing them to collapse thus closing the ductus. The ductus arteriosus should close within 48-72 hours of birth leaving the ligamentum arteriosum, a remnant of the foetal vessel.
- If the ductus arteriosus remains patent postnatally then it acts as a vascular channel between the pulmonary artery and the descending aorta. As the pressure is higher in the aorta than the pulmonary artery, blood shunts from the aorta into the pulmonary artery (LR shunting). The pulmonary artery then carries increased volumes of blood to the lungs causing over-circulation of the pulmonary vasculature and lung fields. The increased volume of blood is then carried in the pulmonary vein from the lungs to the left side of the heart resulting in volume overload in the LA & LV. This LHS cardiac overload may progress to left sided heart failure. Mitral regurgitation can then develop secondary to the left ventricular dilatation. In some cases of untreated long-standing PDA, LV myocardial failure can develop secondary to the chronic volume overload. The LA may become very enlarged, predisposing to atrial fibrillation. It should also be noted that in rare cases the PDA can shift and shunt from right left rather than left to right. This happens if pulmonary hypertension develops in response to the overcirculation of the pulmonary vasculature and causes pressure in the pulmonary artery to exceed pressure in the aorta. In this situation deoxygenated blood will enter the aorta and pass to caudal parts of the body (cranial body protected because brachiocephalic trunk and L subclavian artery arise from the aorta prior to the DA). This can result in differential cyanosis (caudal mucous membranes – vulva and prepuce). However actual change from left right to right left is not well documented in dogs and it is thought that right left shunting PDA is more likely a different form associated with pulmonary hypertension (which could be secondary to prematurity or neonatal hypoxia). R L shunting PDAs are very rare. (Cats are more likely to develop pulmonary hypertension over time than dogs and will sometimes present with biventricular shunting).
- It has been proven that PDA in miniature poodles is hereditary. It is caused by a gene defect in the structure of the ductus which results in hypoplasia of the smooth muscle in the vessel and presence of aorta-like elasticity. This lack of normal smooth muscle and increased elasticity of the DA results in it remaining patent rather than closing normally at birth. (In healthy dogs the walls of the ductus are comprised mainly of smooth muscles cells and very little elastic tissue). This means that medications used in human children to cause ductal contraction are ineffective because the muscle tissue is missing from the DA wall. It has been suggested that this is also the problems in other breeds – 8 dogs of different breeds with PDA, 7 of 8 showed these histopathological changes, however one did not and sample size is small. It is believed to be polygenic. For this reason dogs with PDA should not be used for breeding. PDA is the only congenital cardiac defect where there’s a distinct sex predisposition for females (3:1). This is thought to be due to an autosomal dominant mode of inheritance. There are a number of predisposed breeds. It can also occur in cats but it is less common.
- Some puppies with PDA may have a history of poor growth and even weight loss plus possible exercise intolerance. Coughing may also be reported but this is only seen when the condition has progressed to left sided heart failure and pulmonary oedema. However in most cases PDA is an incidental finding when the puppy comes in to the vets for its first check. On clinical exam you will find a loud grade 5 or 6 heart murmur which continues throughout both systole and diastole with a point of maximum intensity just under the triceps muscle at the dorsal left heart base. The femoral pulses will be hyperdynamic or “tapping” You may find signs of left sided heart failure such as coughing and crackles in the lungs due to pulmonary oedema but only if the dog has progressed to that stage.
- The continuous high grade “machinery” murmur is almost pathognomonic for PDA however you must confirm the diagnosis and exclude other differentials before moving on to treatment (Continuous murmurs can also be present with aorticopulmonary windows and aberrant broncho-oesophageal arteries). Thoracic radiographs: “triple knuckle” appearance due to enlargement of the aortic arch, pulmonary artery and left atrium, however this is not always present with PDAs Normal vertebral heart score for dogs is 9.7+/- 0.5. Dogs with PDA often have an enlarged heart based on their VHS. You may also see congestion of the pulmonary vessels There may be evidence of pulmonary oedema if the dog is in L sided heart failure. This usually appears as a perihilar alveolar pattern (fluffy infiltrate at the caudal aspect of the trachea). These changes may not always be present so you can’t necessarily diagnose PDA based on radiography. ECG: You cannot diagnose a PDA based on ECG but you can have changes reflecting changes in chamber size that may be suggestive of PDA With LV enlargement the R wave is taller than normal With LA enlargement the P wave may be wider but this is not common However these changes are not sensitive or specific Echocardiography: Echo is the mainstay for diagnosis of PDA Can measure chamber sizes and assess for left sided enlargement Can detect turbulent flow in the pulmonary artery With experience can visualise the PDA connecting the pulmonary artery and aorta – thus echo enables you to make a definitive diagnosis and is the diagnostic tool of choice for PDAs
- If a PDA is left uncorrected then it often results in left-sided congestive heart failure and the mortality rate is over 60% within the first year. For this reason it should be corrected as early as possible. The most common methods of PDA correction are surgical ligation of the vessel or occlusion of the vessel using a transarterial coil or plug occluder. Each method has advantages and disadvantages and there are situations where one method will be more suitable than the other. If the animal has signs of congestive heart failure then you must treat this before attempting to correct the PDA. In many animals the PDA is detected before any congestive heart failure has developed so this is not always necessary.
- Surgical ligation used to be the mainstay of PDA correction. It involves performing a thoracotomy, carefully dissecting the ductus then placing two non-absorbable ligatures around the ductus in order to occlude it. Surgeon may choose to place a chest drain in order to remove any fluid or air left in the thorax from the surgery and to monitor further production of fluid/air in the chest post-operatively. There are a number of variations of this surgical procedure. The animal must be manually ventilated throughout the procedure since you are entering the thorax. This is a referral procedure.
- The most common things used for transarterial closure of PDAs are occlusion coils or Amplatz canine duct occluders. Both work by the same method: a catheter is passed via the femoral artery, up through the aorta and into the ductus. The ductus diameter is measured (using angiogram) and an appropriate sized coil or ACDO is then chosen and passed via the catheter into the ductus where it is released. These devices encourage embolus formation and in doing so they occlude the ductus arteriosus. Placement of such devices is also a referral procedure as it requires specialist equipment and should be performed by experienced cardiologists.
- It has been reported that surgical ligation has a shorter procedure time than transarterial occlusion, however a paper comparing the two techniques that I read found there was no significant difference in procedure times between the two (surgery: 105 minutes, TO: 115 minutes). The same paper reported that surgical ligation had higher initial success rates (i.e. ability to fully occlude DA immediately) than coil occlusion. The main disadvantages of surgical ligation are that is a very invasive surgery and also it has a higher risk of major complications such as severe haemorrhage from the ductus or one of the other major vessels (reportedly seen in 0-12% of dogs) and also inadvertent damage to the left cranial lung lobe (1.7% in one large study). Both surgical ligation and transarterial techniques have low mortality and morbidity rates and the same paper found no significant difference between the two. Both the transarterial techniques have the advantage of being minimally invasive with a lower risk of major complications in comparison with surgery. However with the coil occluders there is a risk of the coil dislodging from the ductus and embolising in the lungs, or, more rarely the systemic circulation. Also more than one coil may have to be placed in order to achieve full occlusion of the vessel. Due to its shape the ACDO is more likely to stay in place (as it is placed in such a way that it lodges in the area where the ductus opens into the pulmonary artery). Transarterial methods generally cannot be used in animals under 4kg due to their small vessel size and the inability to get catheters small enough. I read one report where coils were used in 10 dogs under 3kg, and it was unsuccessful in two of the dogs. Due to the small sample size and 20% failure rate I don’t feel that this is sufficient to prove that this method can be safely and successfully carried out in patients under 4kg. In the SAH the ACDO is the number one choice for correction of PDA, except in dogs under 4kg where surgical ligation is the treatment of choice.
- In uncomplicated PDA cases (i.e. with no concurrent issues and no congestive heart failure) the prognosis is excellent and these dogs tend to go on to live normal lives with no problems associated with the PDA. Reported maximum survival with PDA closure is 168months/14years, compared to a maximum survival of 114months/9.5years without PDA closure (and 60% die within one year). The cardiac changes that may be present due to the PDA such as cardiomegaly, mitral regurgitation and LV dysfunction may fully reverse, partially reverse or never reverse. One article reported that left ventricular dysfunction (which is a relatively common finding in PDA) was reversible in 50% of cases. This article also stated that mitral valve murmurs caused by LV dilatation due to the PDA normally disappear within two weeks of PDA occlusion when the heart returns to normal size. The protocol in the SAH is to repeat echocardiography 4 weeks after PDA correction has been carried out to assess if the cardiac changes have reversed at all. If the animal still has significant mitral regurgitation at this point then it is advised to come back after 6months for another heart scan. Many articles report that there is an increased rate of intra-operative death and failure of procedure in dogs over 2 years old and over 23kg. However one article I read (204 dogs from 1993-2003) reported that these factors had no prognostic influence on mortality or success. Dogs with confirmed congestive heart failure are significantly more likely to have un unsuccessful procedure than dogs without CHF.
- Once the PDA was diagnosed the owners were given the option of waiting until Leo was over 4kg then having an Amplatz Canine Duct Occluder placed or booking him in for surgical ligation of the PDA when he was 12 weeks old (a bit safer to anaesthetise). The owners opted for surgery as it could be carried out at a younger age. Leo was sent home on frusemide in order treating any existing CHF. When he turned 12 weeks old the surgery was carried out successfully and a chest drain was placed to monitor for blood or air production in the surgical site. Post-op radiographs were taken to assess drain position and echo was repeated to assess heart size and contractility. As you can see on the xrays the heart was enlarged but contractility was good. He was on methadone, meloxicam, synulox and frusemide post-operatively. Leo’s recovery was quite rocky to begin with and he remained recumbent, non-responsive and oxygen dependent for the first 24hours. However he then improved greatly, was eating and drinking and walking about his kennel so he was sent home 3 days after his operation on all the meds he was on except methadone. Leo is coming back 4 weeks after his surgery for a repeat echocardiogram. Hopefully the repeat scan will show that the heart size has reduced and Leo will go on to live a long and healthy life!