A 61-year-old Chinese woman presented with weakness and loss of appetite for the previous 20 days. She had a medical history of cholecystitis and underwent a cholecystectomy several years ago. Physical examination showed that the patient had a temperature of 36.7 C, blood pressure of 128/76 mmHg, and a heart rate of 77 beats/min. There were coarse breath sounds in both lungs and diminished breath sounds in both lower lungs; a small number of wet rales could be heard, and diminished heart sounds with enlarged heart borders due to pericardial effusion.
The electrocardiogram (Figure 1) suggested a sinus heart rate with low voltage in the limb leads. The patient's laboratory data at admission are shown in Table 1. Echocardiography indicated moderate to severe pericardial effusion (Figure 2), and echo-free areas were seen in the pericardial cavity. The diastolic fluid width was measured as 14 mm in the anterior wall of the right ventricle, 16 mm in the posterior wall of the left ventricle, 19 mm in the lateral wall of the left ventricle, and 20 mm in the apical part of the left ventricle. A bedside color doppler ultrasound showed bilateral pleural effusions. After admission, the patient had a fever intermittently, with a temperature of up to 38.3 C without chills and shivering. The patient's temperature was elevated within 24 h of admission, meaning that the possibility of community-acquired pneumonia could not be excluded. After blood cultures were retained, the patient was also given empirical anti-infective treatment with moxifloxacin. However, as the patient's improvement in relevant tests was considered not to exclude tuberculosis, the use of fluoroquinolones alone should be avoided, and the patient's moxifloxacin was discontinued and changed to ampicillin. The patient's blood culture later indicated no bacterial growth. A computed tomography (CT) scan of the lungs revealed sporadic inflammation in both lungs, inflammatory nodules in the upper left and lower right lung lobes, calcification in the upper left lobe (Figure 3), and bilateral pleural effusions. Furthermore, the mediastinal lymph nodes were enlarged and partially calcified. Pericardiocentesis and drainage were used to relieve the patient's symptoms, such as chest tightness and shortness of breath. The patient's pericardial effusion was hematogenous, with routine results as follows: protein 53.96 g/L; Reye's test positive; total erythrocyte count 214300.00 x 106/L; total leukocyte count 3762.00 x 106/L; percentage of single nucleated cells 84%; adenosine deaminase (ADA) 32.0 U/L; lactate dehydrogenase (LDH) 326 U/L; and carcinoembryonic antigen (CEA) 0.47 ng/ml.
The above results indicated that the patient's pericardial effusion was exudate. The pericardial effusion smear did not find acid-fast bacilli, and Xpert MTB/RIF (Xpert Mycobacterium TB/RIF test is a new test, which is helpful for rapid diagnosis of TB and drug resistance, thus bringing revolutionary changes to TB control.) and T-SPOT tests (The T-SPOT test is a unique TB blood test designed to reduce variability and maximize sensitivity, even in people with low immune function.) were negative. The exfoliated cells of the pericardial effusion showed lymphocytes and lobulated nuclei, and no cancer cells were found. Female tumor markers such as CEA, cancer antigen (CA) 125, CA 199, and neuron-specific enolase were below the reference values to exclude tumor-derived pericardial effusion. Further positron emission tomography/computed tomography (PET/CT) was performed, which showed inhomogeneous thickening of the pericardium, enhanced metabolism, mediastinal lymph nodes, and uterine metabolism fibroids. Therefore, we could almost exclude the possibility that pericardial effusion was caused by a tumor. The patient's thyroid function test suggested that her free triiodothyronine (FT3) of 2.31 pmol/L was only mildly depressed, and it was unlikely that the pericardial effusion was caused by hypothyroidism. To rule out the possibility that the patient's pericardial effusion was caused by autoimmune disease, we further performed autoimmune marker screening, and the patient's antinuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA), and antiphospholipid. The antiphospholipid syndrome antibodies were all negative, which essentially excluded autoimmune diseases.
Three days after admission, the patient had no fluid flow from the pericardial drainage tube, so the pericardial drainage tube was removed. Seven days after admission, the patient's bedside color doppler ultrasound showed that the right pleural effusion was less than at the time of admission. However, there was still a considerable amount of pleural effusion on the left side. We gave the patient left-sided thoracic puncture drainage, and the drainage fluid was light-red. Routine examination of the pleural fluid showed protein 42.83 g/L; a positive Reye's test; total red blood cell count of 67,500.00 x 106/L; total white blood cell count of 1359.00 x 106/L; and percentage of single nucleated cells 97%. Its property was approximately the same as that of pericardial effusion, which was an exudate and the possibility of extravasation of a large amount of pericardial effusion could not be excluded. After receiving symptomatic supportive treatment, the patient's symptoms showed improvement, and the family refused to undertake further specific investigations to determine the cause.
However, 2 months later, the patient was readmitted with malaise, chest pain, and low-grade fever. She had been treated with cephalosporin at a local hospital before admission, but the outcome was poor. A small amount of pericardial effusion was again detected by echocardiography at the time of admission. To determine the cause of the pericardial effusion, the patient was referred to the department of thoracic surgery for a biopsy of the pericardial mass. Pathological findings showed granulomatous lesions and fibrous hyperplasia of the mediastinal lymph nodes (Figure 4) and granulomatous lesions of the pericardial fibrofatty tissue (Figure 5). Furthermore, the patient's pulmonary CT indicated a nodular calcified shadow in the left upper lung and enlarged and partially calcified lymph nodes in the mediastinum and part of the bilateral hilum. The patient was considered to have stable tuberculosis in the upper lobe of the left lung, and the pericardial puncture fluid was exudate with increased leukocytes, mainly monocytes, and mildly elevated ADA. TBP can be suspected according to the diagnostic criteria, and the patient was advised to go to an infectious disease hospital for further treatment. The dosing regimen was: isoniazid 300 mg orally one time a day (QD), rifampicin 600 mg orally QD, ethambutol 100 mg orally QD, and pyrazinamide 100 mg orally QD. The four drugs were administered for 8 weeks and then reduced to isoniazid and rifampicin to continue the treatment for 6 months. According to the PET-CT results, the patient's pericardium had become unevenly thickened. To avoid progression to constrictive pericarditis, the patient was given prednisolone 50 mg, and the dose was gradually reduced. After 8 months, we followed up with the patient by telephone; her symptoms, such as weakness and chest pain, were improved following the anti-tuberculosis treatment.