Her previous medical history revealed that she was diagnosed with RA at the age of 58 years old and was receiving orally 20 mg of leflunomide per day. She had been treated with methotrexate and hydroxychloroquine in the past, under which she had experienced many relapses that required oral corticosteroids. It was only when her antirheumatic therapy was switched to leflunomide that she had a long-term remission. The last time she had received oral corticosteroids was 3 years ago for a period of 6 months.
Initial laboratory studies were normal, apart from a slightly elevated C-reactive protein (CRP) (CRP: 4.7 mg/dl, normal range: <0.5 mg/dl) with a normal white blood cell count (WBC: 6,9 x 103/mul) and no history of fever.
In the next 48 h a single fever wave of 39 C was documented, followed by subfebrile body temperatures, and a slight deterioration of her speech and orientation. A brain MRI demonstrated a left parietal, rim-enhancing collection of fluid with diffusion restriction and dimensions of 48 mm x 25 mm x 19 mm that resembled a BA [Figure 2a-d]. Blood cultures were obtained and a CT scan of the thorax, abdomen and pelvis as well as a transesophageal echocardiogram were performed, to rule out a possible primary location. The initial antibiotic regimen included ceftriaxone, metronidazole, and vancomycin. Due to the suspected BA, dexamethasone was discontinued and a prophylactic therapy with levetiracetam 1000 mgIVq 12H was initiated, given the high risk of seizure. In the next 48 h her hemiparesis improved, as well as her laboratory infection parameters. However, her aphasia deteriorated further and she additionally developed dyscalculia. This deterioration of the neurological status was attributed to the space-occupying effect of the BA during the stage of the early capsule formation, as well as the expansion of the surrounding edema, due to the discontinuation of dexamethasone. Neurosurgery consultation led to patient's immediate surgical treatment. A left craniotomy was performed and an intraparechymal abscess was detected and evacuated. Cultures for common microbes as well as Mycobacterium tuberculosis and Nocardia were obtained intraoperatively from both the liquid and the solid part of the BA. The patient was extubated successfully and at her postoperative clinical evaluation she had a significant improvement of her neurological status. The intraoperatively obtained cultures came up negative, probably because of the early start of empirical antibiotic therapy. Histopathology revealed an aggregation of lymphocytes, macrophages, and neutrophils in a loose extracellular matrix, consistent with an abscess. No malignant cells were present.
Seven days postoperatively only a slight paresis of patient's right upper extremity remained. The patient was discharged 6 weeks after her surgery and she continued receiving an oral antibiotic therapy (amoxicillin/clavulanic acid in combination with levofloxacin) for another 4 weeks. At her follow-up examination (1 month postoperative) she did not have any focal neurological deficits and she was able to resume her daily activities. The postoperative brain MRI demonstrated only the usual postoperative changes of the brain without any sign of fluid collection or gadolinium enhancement [Figure 2e].
Despite this incident, leflunomide was resumed after the termination of the antibiotic therapy, since her RA was refractory to the other antirheumatic therapies.