Signalment & History
A 5 month old MI German Shepherd dog presents with a 3 month history of abnormal behavior, weight loss, exercise intolerance and infrequent cough at night. On physical examination, he has pink mucous membranes, CRT <2 sec, RR 32 bpm, HR 120 bpm, 101.3 °F, synchronous hyperkinetic femoral pulses and continuous crescendo-decrescendo 5/6 murmur.
Findings
There is severe, generalized enlargement of the cardiac silhouette, with rounding of the cranial and caudal margins of the cardiac silhouette. In addition, there is a soft tissue bulge within the area of the left atrium and the cardiac silhouette is tall with an increased apical to basilar length, which causes dorsal displacement of the trachea. On the ventrodorsal projection, there are three distinct soft tissue bulges at the proximal aspect of the descending aorta, the 1-2 o’clock position (main pulmonary artery), and the 2-3 o’clock position (left auricle). The pulmonary arteries and veins are moderately enlarged, with pulmonary veins being relatively bigger than arteries. Throughout the perihilar and caudodorsal aspects of the left and right caudal lobes, there is an increased soft tissue opacity which causes the pulmonary vessels to be ill-defined. Within the stomach and gastrointestinal tract, there are multiple, well-defined, circular to angular metal opacities, measuring up to 4.5 mm. Within the cervical soft tissues, caudoventrally, approximately at the level of the thoracic inlet, there is a ill-defined linear band of multifocal mineral opacities. Multiple open physes are seen, and are consistent with the patient’s age.
Diagnosis
You have found a severely, generalized enlargement of the cardiac silhouette with an increased apical to basilar length and associated rounded cranial and caudal margins and soft tissue bulge within the area of the left atrium with resulting dorsal displacement of the trachea. You identified three distinct soft tissue bulges corresponding to enlarged proximal aspect of the descending aorta (diverticulum or “ductus bump”), main pulmonary artery and left auricle on the ventrodorsal projection. In addition, you have seen moderately enlarged pulmonary arteries and veins. Also, you found increased soft tissue opacity throughout the perihilar and caudodorsal aspects of the left and right caudal lung lobes. You recognize gastrointestinal metal foreign bodies. Mineral opacities over the caudal cervical tissues most likely represent an artifact or cutaneous debris. Your findings are consistent with severe pulmonary overcirculation, left-sided cardiomegaly, pulmonary venous congestion, ductus diverticulum and left sided congestive heart failure. These radiographic abnormalities are consistent with a left to right patent ductus arteriosus. Specific radiographic changes of PDA include progressive enlargement of the left atrium, left ventricle, aortic arch, and pulmonary arteries. The cardiac silhouette may appear elongated due to aortic arch enlargement cranially and left ventricular enlargement that extends the silhouette caudally. Extreme cardiomegaly may shift the heart into the right hemitorax. The most characteristic sign of PDA is an aneurysmal bulge in the aorta at the level of the ductus. This “ductus bump” can be seen radiographically as a lateral deviation of the left lateral wall of the descending aorta at the level of the main pulmonary artery; however this change is not always present. Overperfusion of the lungs can be appreciated, as well as left-sided heart enlargement indicated by dorsal elevation of the trachea and increased sternal contact. Electrocardiography should be performed to evaluate heart chamber enlargement. Echocardiography may confirm the diagnosis and help to identify any other cardiac defects. It can also demonstrate changes in the cardiac wall thickness and chamber size. Nuclear scintigraphy can also be used to quantify left-to-right and right-to-left shunts.
Conclusions
- PDA, also referred as arterial duct, arterial canal, and ductus Botalli, forms the sixth aortic arch. It extends from the bifurcation of the main pulmonary artery to the ventral aspect of the descending aorta between the left subclavian artery and the intercostal arteries.
- In the fetus, the DA shunts blood away from the nonfunctional lungs back to the systemic circulation. Physiologic closure of the DA occurs immediately after birth; anatomic closure of the DA follows within a 48 hours to a month. By one month the DA becomes a nonpatent elastic structure referred to as the ligamentum arteriosum.
- PDA is recognized as one of the most common congenital heart defects in dogs (incidence 25-30%). Female toy-breed dogs are overrepresented in this condition.
- A characteristic history and clinical sign, along with a classic “machinery” murmur, typically lead to thoracic radiography and echocardiography for confirmation. The larger the PDA and the older the patient at the time of evaluation, the more prominent the radiographic changes will be.
- Depending on the size and duration of the defect, diagnostic may reveal left ventricular enlargement, mitral regurgitation, and overcirculation of the pulmonary vasculature. Most dog with a PDA develop CHF by one year of age if ligation or occlusion is not performed.
- Some dogs are born with or may develop suprasystemic pulmonary hypertension that can result in reversal of flow through the PDA (right-to-left PDA). In these cases occlusion is contraindicated (symptomatic medical therapy is recommended).
- 70% of dogs with PDA develop clinical signs of CHF before 12 months of age. Thoracic auscultation is the primary diagnostic tool for detecting PDA.
- When the most appropriate option is selected and treatment is instituted early and skillfully patient can have an excellent long term prognosis.
References
Patent Ductus Arteriosus in Dogs. Broaddus KD, Tillson DM . Compend Contin Educ Vet 2010; Sep 32(9):E3
