A 58-year-old man was brought to the local hospital with chief complaints of lower extremity fatigue, severe bilateral lower extremity pitting oedema, particularly of the right leg, and intermittent, mild chest tightness. He first visited the neuropathy clinic. The CT, diffusion-weighted imaging, and angiography were unremarkable. Haemoglobin was 108 g/L (normal range within 130–175 g/L), urine protein was 0.43 g/24 h (normal range within 0.00–0.15 g/24 h), and albumin was 34.7 g/L (normal range within 40.0–55.0 g/L). Thyroid function was unremarkable. The initial transthoracic echocardiogram indicated the internal diameter of the ascending aorta 32 mm, right ventricular outflow 30 mm, the left atrium 30 mm, left ventricular (LV) end − diastolic/systolic dimension 50 mm/29 mm, LV dimension 18 mm, and LV function was normal with an ejection fraction (LVEF) of 72%, fractional shortening (FS) of 42%, stroke volume (SV) of 88 mL, and cardiac output (CO) of 10.9 L/min. A moderate pericardial effusion was detected, and the depth of liquid at the left ventricular apex was 5 mm. The diaphragmatic surface of the right ventricle was 12 mm. After the treatment with diuretic, there was little improvement in lower extremity fatigue, oedema of the lower extremities, or chest tightness. Therefore, the patient visited the outpatient clinic of cardiology for further treatment after new facial and ankle oedema appeared and his shortness of breath persisted. On admission to the cardiology department, a chest X-ray revealed bilateral pleural effusions. Echocardiogram showed normal left ventricular function with an LVEF of 65%, FS of 35%, SV of 76 mL, CO of 9.2 L/min, a small-medium pericardial effusion (left ventricular posterior wall 6.4 mm, right ventricular anterior wall 7.7 mm, apex of the heart 6 mm, right ventricular free wall 17 mm, left ventricular free wall 6 mm), increased size of the right heart (right atrial diameter 36 mm × 46 mm, right ventricle internal dimension 40 mm × 70 mm), dilation of the inferior vena cava (24 mm) and respiratory variation of the mitral peak E velocity of >25%. Electrocardiography showed sinus tachycardia, and T wave inversion. The coronary CTA and computed tomography pulmonary angiogram (CTPA) showed severe narrowing of the diagonal branch of left anterior descending artery, as well as the presence of pleural effusion and peritoneal effusion. Thoracentesis of the left thoracic cavity using imaging guidance was performed to determine the cause of the excess pleural effusions and to relieve his shortness of breath. A total of an estimated 1180 mL of fluid was drained from the pleural effusion during hospitalization. Laboratory tests of the pleural effusion indicated leakage fluid with the following results: light yellow turbid liquid, Rivalta test (+), total cells count 152 × 106, monocytes accounting for 90% of total white blood cells, white blood cells count 140 × 106, protein 27.7 g/L, glucose 11.87 mmol/L, lactate dehydrogenase (LDH) 106 U/L, and adenosine deaminase (ADA) 4 U/L. Thoracentesis of the right thoracic cavity was also performed later. A total of 3050 mL of fluid was drained from the pleural effusion during hospitalization. Laboratory tests of the pleural effusion indicated leakage fluid with the following results: light yellow turbid liquid, Rivalta test (+), total cells count 352 × 106, monocytes accounting for 72% of total white blood cells, white blood cell count 287 × 106, protein 31.6 g/L, glucose 12.55 mmol/L, LDH 111 U/L, and ADA 4 U/L. Hyperplastic mesothelial cells and lymphocytes were found in the pleural effusion. The oedema and shortness of breath was significantly improved after thoracentesis. After removing the drainage tube due to the concerns of iatrogenic infection and discomfort, however, the bilateral pleural effusions quickly reappeared. Based on the CTA result indicating the severe stenosis of the diagonal branch of left anterior descending artery, antiplatelet and lipid-lowering medications, and a beta-blocker were prescribed because the symptoms of fatigue, chest tightness, and dyspnoea were partially thought to be due to ischaemic heart disease. However, these symptoms were unsuccessfully treated as ischaemic heart disease. After being discharged from the department of cardiology without a clear aetiology, the patient complained of cough, expectoration, progressive dyspnoea, and bilateral lower extremity pitting oedema. He then visited the department of pulmonary medicine. After reviewing the initial CT results, a thickened pericardium was observed. Though there was no evident Kussmaul sign, CP was considered and this urged the physicians to get informed consent to perform a pericardectomy. The gross view of the heart in situ originally observed during pericardectomy indicated fibrinous pericarditis, a massive haemorrhagic pericardial effusion, and thickened pericardium. The maximum thickness of the pericardium was more than 6 mm. Haematoxylin and eosin (H&E) staining of the pericardial tissue biopsy obtained from five different regions of the thickened pericardium showed massive chronic inflammatory cell infiltration (phlogocytes and leucomonocytes) and fibroid necrosis (hyaline degeneration). There were no pathological characteristics of TB or malignancy (). The patient was diagnosed as idiopathic pericarditis. Chronic, non-specific vascular inflammation was proposed to be responsible for the haemorrhagic pericardial effusion. All of the symptoms gradually disappeared 1 week after pericardectomy. Prior to discharge, the repeated X-ray () indicated disappearance of the cavity effusion. At the first scheduled follow-up visit 1 month after pericardectomy, the echocardiogram indicated normal left ventricular function with an EF of 76%, FS of 44%, SV of 75 mL, and CO of 7.8 L/min. At the 2-, 5-, 7-, and 12-month follow-ups, the patient had no complaints of discomfort.