Influenza A Pneumonia Unmasking Platypnoea–Orthodeoxia Syndrome​ Secondary to Patent Foramen Ovale

Influenza A Pneumonia Unmasking Platypnoea–Orthodeoxia Syndrome Secondary to Patent Foramen Ovale

Background:

Platypnoea–orthodeoxia syndrome (POS) is a rare condition characterised by dyspnoea and arterial desaturation in the upright position with improvement when supine. It results from right-to-left shunting and may arise from intracardiac causes, most commonly patent foramen ovale (PFO), or extracardiac mechanisms including pulmonary arteriovenous malformations, hepatopulmonary syndrome, parenchymal lung disease, and thoracic structural abnormalities. A precipitating factor is often required to unmask a previously silent shunt.

Case Presentation:

A 76-year-old male presented with a six-week history of worsening dyspnoea, productive cough, and intermittent fever. His background included liver cirrhosis, oesophageal stricture, prior pulmonary embolism, and moderate aortic stenosis. Investigations confirmed Influenza A infection with left lower zone consolidation and type 1 respiratory failure requiring intensive care admission and mechanical ventilation.

Following clinical improvement, repeated attempts to wean the patient off supplemental oxygen were unsuccessful. Although oxygen could initially be discontinued with acceptable saturations, subsequent reassessment revealed recurrent desaturation to approximately 70%, necessitating reinstatement of high-flow oxygen. Notably, the patient remained relatively asymptomatic during these episodes and was predominantly managed in a supine position while recovering from influenza infection and recent intensive care admission.

Further assessment revealed marked positional hypoxaemia, with saturations improving to 95–98% when supine but consistently dropping when seated. CT pulmonary angiography excluded pulmonary embolism. Bubble contrast echocardiography demonstrated early left heart opacification within one cardiac cycle, consistent with a significant intracardiac right-to-left shunt. Further evaluation, including cardiac MRI and right and left heart catheterisation, supported this finding. Transoesophageal echocardiography was avoided due to oesophageal stricture. The patient was accepted for transfer for percutaneous PFO closure using intracardiac echocardiographic guidance.

Conclusion:

This case highlights diagnostic delay in POS due to atypical presentation, multiple comorbidities, and relative lack of symptoms despite severe hypoxaemia. Recognition of positional oxygen changes is crucial, as timely diagnosis allows definitive management.