Abstract
Patent foramen ovale (PFO) is the most common congenital heart anomaly of fetal origin and is present in approximately 25 per cent of general adult population, a common finding in adult life. The majority of PFO’s are asymptomatic. PFO is implicated in cryptogenic stroke; the pathogenesis is from the paradoxical emboli that migrate from right sided cardiac chambers to the left, and thence the systemic circulation with catastrophic results.
Case Report
A 60-year-old male presented to an Accident and Emergency department (A&E) with a left quadriceps tendon tear after a fall. He underwent routine surgical repair and was discharged two days later with a knee brace and analgesia.
10 days post-discharge he collapsed at home with shortness of breath, chest tightness and an obviously swollen, erythematous left leg. Electrocardiogram (ECG) showed sinus tachycardia, with evidence of right heart strain; transthoracic echocardiography (TTE) demonstrated an acutely dilated right ventricle with tricuspid regurgitation. No other structural heart lesions were noted.
Due to a high suspicion of pulmonary emboli (PE) he was thrombolysed with 50mg alteplase and a continuous heparin infusion. Post-thrombolysis, the patient developed ventricular tachycardia (VT) with loss of cardiac output. He underwent one cycle of cardiopulmonary resuscitation, and was intubated and ventilated before a spontaneous circulation returned. He was kept sedated and ventilated and an urgent computerised tomography pulmonary angiogram (CTPA) was performed, which demonstrated bilateral massive PE. He was then transferred to our cardiothoracic centre for consideration of open pulmonary embolectomy.
The patient was deemed unsuitable for pulmonary embolectomy and was admitted to the intensive care unit (ICU) for medical management, centred on sedation, invasive ventilation, anticoagulation and inotrope therapy. His ventilation-perfusion mismatch improved over 48 hours and his sedation was stopped. He was noted to be neurologically inappropriate with agitation and inability to obey commands, with accompanying weakness of right upper and lower limbs. An urgent CT scan of the brain (Fig.1) showed bilateral, massive sub-acute infarcts across multiple vascular territories, with mass effect. We considered it likely that he had an undiagnosed cardiac septal defect which had given rise to paradoxical (systemic) emboli when, as a result of his PE’s, the right-sided cardiac pressures exceeded the left; this pushed thrombus into the left heart and, thence, the systemic circulation. There were no other peripheral embolic phenomena to see, and our neurosurgery team recommend medical management alone.
Fig. 1 CT head showing bilateral PCA territory infarcts involving both occipital lobes as well as acute infarct in left MCA territory involving left frontoparietal lobe.
A transoesophageal echocardiography (TOE) was performed which confirmed a dilated right ventricle with a large (0.5-1.0cm) PFO (Fig.2). Ultrasound examination of the veins in both lower limbs excluded persistent venous thrombus and an inferior vena cava (IVC) filter was not inserted, but the need for anti-coagulation raised the risk of secondary cerebral haemorrhage in an already injured brain. Repeat CT of the brain 10 days later showed interval haemorrhagic transformation had indeed occurred with evidence of further mass effect and brain parenchymal herniation. A ‘do not resuscitate’ order was signed after discussion with patient’s family and 5 days later the patient died from a fatal arrhythmia having shown no signs of neurological recovery.
Figure 2: TOE Showing PFO (right – red arrow) and reverse blood flow through PFO (left – red arrow)
Discussion:
Deep venous thrombosis (DVT) and PE are known complications of quadriceps tendon repair affecting 2.5% of all patients (1). Patients with reduced mobility post-repair should be started on thromboprophylaxis (2). PFO remains the most common congenital cardiac anomaly affecting 25% of the adult population (3). Whilst mostly asymptomatic in adult life they have been associated with paradoxical embolism via a right-to-left shunt, resulting in systemic emboli and increased risk of cryptogenic stroke (3 & 4). The gold standard method for diagnosis of PFO is TOE, which represents a highly sensitive and specific method for both diagnosis and estimation of the PFO size (5). We hypothesise that in this case the patient developed a DVT in the postoperative period that resulted in massive bilateral PE’s. The resulting right heart strain created a right-to-left shunt through the PFO, resulting in multiple bilateral cerebral infarcts, via multiple arterial paths.
Conclusion:
TOE should be considered in patients with a diagnosis of PE and evidence of right heart strain on TTE or ECG to rule out a PFO. In those in whom PFO is diagnosed with evidence of residual DVT, consideration should be given to the early insertion of an IVC filter to prevent further emboli from migrating via a right-to-left shunt into the systemic circulation. The hope that this is may reduce the risk of paradoxical (systemic) embolism and stroke.
Acknowledgements: None
Conflict of interest: There is no conflict of interest
Funding: This work received no specific funding
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Authors
Amer Harky*, Megan Garner, Avinder Gobindpuri, Phil Jones, Department of Radiology, St Bartholomew’s Hospital, Barts Heart Centre, West Smithfield, EC1A 7BE
* Corresponding Author:
Amer Harky – M.B.Ch.B, MRCS, Department of Peri-operative Medicine, St. Bartholomew’s Hospital, 1st Floor KGV Building, Barts Heart Centre, West Smithfield, London, EC1A 7BE. Tel: +44 (0)78 4259 9657
Email: amer.harky@doctors.org.uk
