The patient was a 22-year-old Asian woman who presented with headache, nausea, and vomiting, which had started one day before admission. Fever, dyspnea, chest pain, and cough were absent. She denied the use of oral contraceptives, corticosteroids, hormonal replacement therapy, erythropoietin, or antipsychotic drugs. She also had no history of thromboembolism, immobilization, smoking, pregnancy, abortion, or any significant family history, including thromboembolism.
On physical examination, her body mass index was 18.4 kg/m2, and vital signs were within normal limits. Her lung sounds were clear and cardiovascular and abdominal examinations were unremarkable. Her legs were unswollen and Homan's sign was negative. She was alert and oriented, and no muscle weakness or sensory disturbances were found. Photophobia, neck stiffness, and Kernig's sign were absent.
Laboratory findings on admission are shown in Table 1. Briefly, the blood test revealed normal white blood cell and platelet count, elevated C-reactive protein, D-dimer, and fibrin degradation product. Activation of antithrombin III (AT-III) and proteins S and C were within normal limits. Lupus anticoagulant, anti-nuclear and anti-cardiolipin antibodies were also negative. The interferon-gamma releasing assay (IGRA) was positive, however, initial acid-fast staining of sputum and gastric aspirate, and polymerase chain reaction for Mycobacterium tuberculosis were negative.
Chest radiography revealed a protruding shadow in the left hilum (Fig. 1A). Chest computed tomography (CT) revealed thick-walled cavitating lesions in the upper left lung (Fig. 1B). Contrast-enhanced CT revealed thromboses in the bilateral pulmonary arteries and lymphadenopathy in the left hilum (Fig. 1C-D). No mass suspicious of cancer was found in a whole-body contrast-enhanced CT. DVT in the lower limbs was not detectable on contrast-enhanced CT or Doppler ultrasonography. CT of the head revealed high-density lesions in the superior sagittal, straight, and sigmoid sinuses (Fig. 1E). Magnetic resonance venography (MRV) showed loss of signals in the superior sagittal, transverse, and sigmoid sinuses (Fig. 1F).
Thus, a diagnosis of acute PTE and CVST was confirmed and intravenous heparin (15000 U/day) was administered. We also initiated glycerol and levetiracetam (200 mg/day) because she developed right-sided hemiplegia and mildly impaired consciousness caused by brain edema and non-convulsive epilepsy after admission. Although TB was not confirmed on admission, active pulmonary TB was strongly suspected based on the radiological findings and the positive result of the IGRA test. Accordingly, isoniazid (220 mg/day), rifampin (450 mg/day), ethambutol (750 mg/day), and pyrazinamide (1100 mg/day) were initiated. After two weeks of heparin administration, we switched to warfarin (3 mg/day). However, the prothrombin time-international normalized ratio (PT-INR) did not reach the therapeutic range even with an increased dose of warfarin (5 mg/day) because of the inhibitory effect of interaction with rifampicin. Therefore, treatment with edoxaban (30 mg/day) was initiated. After three weeks of admission, a followed-up CT scan revealed the amelioration of the cerebral sinus thrombosis (not shown) and bilateral pulmonary thromboembolism (Fig. 2A-B). Her symptoms completely resolved and she was discharged from our hospital. M. tuberculosis was confirmed in both sputum and gastric aspirates after eight weeks of culture. She continued standard anti-TB therapy and anticoagulation therapy for six months. After the completion of the treatment, a follow-up chest radiography showed shrinkage of the left hilar lymphadenopathy, and MRV of the brain indicated recovery of the venous blood flow in the cerebral sinuses (Fig. 2C-D).