Would you have it on your differential with unilateral alveolar pattern?

Unilateral pulmonary edema in a dog with a large, left-to-right shunting patent ductus arteriosus

M. McMullen, K.L. Maneval, C.S. Ferrel, M. Holland, R.L. Winter

Background
This case report describes a four-month-old, 5-kg male mixed-breed dog diagnosed with a large, left-to-right shunting patent ductus arteriosus (PDA). The PDA caused severe left heart volume overload and unilateral pulmonary edema (UPE), a condition not previously reported in dogs secondary to PDA. The dog presented with a history of lethargy, hyporexia, and mild respiratory distress, as well as a grade 6/6 heart murmur and crackles in the right lung field.

Methods
Diagnostic evaluation included transthoracic echocardiography, which confirmed severe left ventricular and atrial dilation with a large PDA, and thoracic radiography, which revealed cardiomegaly, pulmonary overcirculation, and severe alveolar disease localized to the right lung lobes. Medical management with oxygen, furosemide, pimobendan, and spironolactone was initiated. Transcatheter PDA occlusion was performed using an Amplatz Canine Ductal Occluder (ACDO). Postoperative management included tapering of cardiac medications over weeks.

Results
Medical and interventional management resolved the UPE and improved cardiac dimensions. Follow-up imaging showed complete resolution of the UPE and a persistent reduction in heart enlargement. The PDA occlusion was deemed successful despite mild residual ductal flow. The dog remained asymptomatic six months postoperatively.

Limitations
A computed tomography angiogram was not performed to rule out other congenital anomalies, such as systemic-to-pulmonary shunts, due to concerns over patient stability. This limits the ability to definitively attribute UPE to the PDA. Additionally, the exact mechanism for right-sided UPE remains speculative, as lymphatic drainage disparities and preferential blood flow into the right pulmonary artery were considered but not conclusively demonstrated.

Conclusions
This is the first report of UPE caused by PDA in a dog, highlighting the potential for unilateral manifestations of cardiogenic pulmonary edema. The case underscores the efficacy of combining medical and interventional strategies for resolving UPE and managing heart failure. Further studies are needed to elucidate the pathophysiology of UPE in similar cases.