An 87-year-old female with R-R long intervals due to atrial fibrillation admitted to our hospital. On Day +15, she underwent leadless pacemaker implantation ("on Day +X" means that "on Day X after admission"). She received regular infection prevention treatment both preoperatively and postoperatively. On Day +16, she developed an unexplained low-grade fever without cough or sputum. She also had night sweats. Blood counts indicated slightly elevated neutrophil, C-reactive protein (CRP), and interleukin-6 (IL-6) levels. The T-SPOT test repeatedly suggested elevated levels of antigen A and antigen B. Additionally, her blood sedimentation level was significantly elevated, fluctuating between 60 mm/h and 70 mm/h.
On Day +23, she received regular anti-infective therapy with a specific regimen of cefoperazone-sulbactam 3 g/8 h. On Day +42, she underwent chest ultrasonography, which suggested that the amount of pleural fluid had increased compared to the previous amount. At this point, we considered regular anti-infection treatment ineffective. On Day +46, she underwent thoracentesis and drainage. We sent her pleural fluid for testing, and the results suggested that her pleural fluid/serum protein was >0.5. Therefore, we considered the pleural effusion to be exudate. Considering that the patient was an elderly woman, the patient's family refused to undergo pleural biopsy.
On Day +57, she received diagnostic anti-tuberculosis treatment. The specific regimen was isoniazid 0.3 g/d, rifapentine 0.9 g/week, pyrazinamide 0.25 g/8 h, levofloxacin 0.5 g/d, and methylprednisolone 40 mg/d. Additionally, she underwent a computer tomography (CT) scan of the chest, as shown in Figure 1A. We observed a moderate amount of liquid density shadow in the chest cavity bilaterally, mainly on the right side, with a CT value of 5 HU. Chest CT also suggested that adjacent lung tissue was compressed. After diagnostic anti-tuberculosis treatment, her low-grade fever resolved, and pleural fluid decreased. Besides, she has a 20-year history of exposure to tuberculosis (TB) patients. Therefore, we made a clinical diagnosis of tuberculous pleurisy for this patient.
On Day +72, she underwent ultrasonography of the chest, which showed no fluid in the chest cavity bilaterally. On Day +74, her platelet dropped from 189*109/L to 43*109/L. We considered thrombocytopenia in relation to the use of isoniazid. Therefore, we temporarily stopped the anti-tuberculosis treatment. Her platelet levels returned to normal after stopping anti-tuberculosis treatment.
On Day +92, we added linezolid 600 mg/12 h and moxifloxacin 0.4g/d. After using linezolid and moxifloxacin, her symptoms were better than before. On Day +110, she reappeared with thrombocytopenia, and she received platelet transfusion therapy. We believed that the cause of this thrombocytopenia was related to the use of linezolid. Therefore, we adjusted the anti-tuberculosis regimen to cycloserine 0.25 g/d and contezolid 400 mg/d. During the follow-up treatment, her platelet count increased from 68*109/L to 324*109/L. She did not have any further adverse reactions. Therefore, we increased the drug doses of cycloserine and contezolid. On Day +121, we modified the drug dose to cycloserine 0.25 g/12 h and contezolid 400 mg/12 h. On Day +131, she underwent another chest CT examination, as shown in Figure 1B. This result indicated a significant reduction in bilateral pleural effusion compared with the image in Figure 1A. Her body temperature fluctuated within the normal range. Therefore, we considered the anti-tuberculosis treatment effective.
For the treatment of heart diseases, rivaroxaban 10 mg/d was used for the treatment of atrial fibrillation. She was bedridden for a long time. Her pacemaker function was normal prior to death. Therefore, heart diseases have little relationship with the death of this patient. We considered that she died of a pulmonary embolism on Day +136. Besides, Figure 2 shows the treatment of this patient.