Contribution of intrapulmonary shunt to the pathogenesis of profound hypoxaemia in viral infection: a mechanistic discussion with an illustrative case.

Abstract

Background: The formation of anastomoses between the pulmonary arteries and pulmonary veins, or the pulmonary and the bronchial circulation, is part of normal foetal lung development. They persist in approximately 30% of adults at rest, and open in almost all adults during exertion. Blood flowing through these anastomoses bypasses the alveolar surface and increases in such shunting can thus cause hypoxaemia. This is now known to contribute to the pathogenesis of hypoxaemia in COVID-19 disease. We here provide evidence to support a similar role in influenza A infection.

Illustrative case presentation: We describe a case of influenza A infection associated with severe hypoxaemia, poorly responsive to supplemental oxygen and which worsened following the application of continuous positive airway pressure (CPAP), despite the presence of a normal physical examination, chest radiograph and echocardiogram. This combination suggests a significant intrapulmonary (extra-alveolar) shunt as a cause of the severe hypoxaemia. The shunt fraction was estimated to be approximately 57%.

Discussion and conclusion: Intrapulmonary vascular shunts can contribute substantially to hypoxaemia in viral infection. Seeking to understand the pathogenesis of observed hypoxaemia can help guide respiratory therapy. Mechanistic research may suggest novel therapeutic targets which could assist in avoiding intubation and mechanical ventilatory support.