RESUMO
Pulmonary oedema of uncertain aetiology is a diagnostic challenge to clinicians worldwide. Many indicators are proposed to differentiate between cardiogenic and non-cardiogenic pulmonary oedema. Mixed pulmonary oedema is an overlap between high hydrostatic pressure and increased permeability at the microvascular level. In our case, a 77-year-old patient presented with a nine-day history of shortness of breath. He was hypoxemic in the emergency department, had a pan-systolic murmur on auscultation, and blood results showed raised inflammatory markers without any fever. His chest X-ray and computed tomography pulmonary angiogram showed asymmetric pulmonary oedema in bilateral superior lobes and bilateral pleural effusions. Point-of-care echocardiography revealed severe mitral regurgitation. Trans-oesophageal echocardiography confirmed mitral valve prolapse with the chordae rupture and systolic vein reversal flow seen in the right superior pulmonary vein. He was treated with antibiotics and diuretics. After starting intravenous diuretics, there was a rapid symptomatic improvement, and a repeat chest X-ray showed significant improvements. We concluded that it was a case of mixed pulmonary oedema with predominant cardiac aetiology, and he was referred to cardiothoracic surgery for mitral valve replacement. The case showed that mixed pulmonary oedema with atypical chest radiography appearances would be a diagnostic challenge for clinicians. In such presentations, both cardiogenic and non-cariogenic causes of pulmonary oedema should be considered.
RESUMO
Subacute cardiac tamponade is a diagnostic challenge for clinicians because the symptoms would be non-specific upon presentation. The onset of cardiac tamponade may vary depending on the rate of accumulation and compensatory mechanism of the fibroelastic pericardial sac. In the case of subacute tamponade with effusion without cardiac arrest, it is usually challenging for the clinician to make the decision for urgent drainage. Usually, cardiac tamponade is treated as a medical emergency, and it occurs when fluid accumulated in the pericardial sac compresses the heart causing haemodynamic compromise and cardiac arrest. In our case, a 40-year-old man presented with a seven-day history of significant shortness of breath. He presented to the emergency department and the chest X-ray showed a large cardiac silhouette, which suggested a large pericardial effusion. ECG revealed minor changes in the heights of QRS complexes. Point-of-care echocardiography showed a large pericardial effusion, and he was immediately admitted to the cardiac unit. Urgent departmental echocardiography confirmed massive pericardial effusion with features of subacute tamponade. The patient was sent to the cardiac catheterisation lab and a total of approximately 4.2 litres of pericardial effusion was drained, while he was closely monitored for the risk of rapid physiologic decompensation after drainage. Pericardial fluid culture did not show any evidence of microorganism growth. The connective tissue disease screen was negative. CT scan did not show any stigmata of occult malignancy or features of infection. The coronavirus disease 2019 (COVID-19) polymerase chain reaction test was negative. He had rapid symptomatic improvement after the effusion was drained and recovery was uneventful. He was discharged from the hospital with a follow-up plan. We concluded that it was a case of subacute cardiac tamponade due to a massive pericardial effusion of idiopathic or subclinical viral causes. Clinical presentation of subacute cardiac tamponade could be easily missed, and a detailed assessment of the effusion with echocardiography was very helpful in making decisions for the management.