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Hepatitis and encephalopathy: case report A 44-year-old man developed hepatitis during treatment with isoniazid, rifampicin and pyrazinamide for pulmonary tuberculosis. He also developed encephalopathy during treatment with moxifloxacin for multi-drug resistant (MDR) tuberculosis [routes stated not stated, not all times to reactions onsets stated]. The man, who had been diagnosed with pulmonary tuberculosis presented with a six-month history of slight walking difficulty, along with a one-week history of productive cough and fever. Five days before the presentation, he started receiving category I antitubercular therapy (ATT) with isoniazid 300 mg/day, rifampicin 600 mg/day and pyrazinamide 1500 mg/day, along with ethambutol and pyridoxine. On admission (at the current presentation), he was oriented and conscious without any cranial nerve involvement. His deep tendon reflexes, power and tone were normal in the lower and upper limbs. No sphincter disturbance or sensory loss was observed. His respiratory system examination revealed bilateral micronodular pulmonary infiltrates, lytic areas of the first and second dorsal vertebrae and spondylodiscitis, indicative of Pott’s spine. His sputum and blood investigations were normal, except for elevated ESR. During hospitalisation, he developed hepatitis due to rifampicin, pyrazinamide and isoniazid. Hence, rifampicin, pyrazinamide and isoniazid were discontinued, and the man started receiving modified ATT therapy with streptomycin, levofloxacin and ethambutol. After 10 days of hospitalisation, he was discharged in an afebrile condition. Treatment with a modified ATT regimen was continued. One day after the discharge (16 days after onset of productive cough and fever), he was re-admitted because of high-grade fever and severe breathlessness. He needed ventilatory support. Hence, he was admitted to the ICU. His blood examination revealed mildly elevated transaminase levels, which were gradually decreased. Hence, he started receiving empiric treatment with ceftriaxone, while modified ATT was ongoing. After 7 days, he was extubated. Afterwards, his liver enzyme levels became stable. Therefore, treatment with isoniazid was re-started [dosage not stated]. He continued to have severe lethargies, poor appetite and recurrent spikes of fever. Based on his clinical presentation, MDR tuberculosis was suspected. Therefore, his ATT regimen was modified, and subsequently, he started receiving moxifloxacin 600 mg/day, along with isoniazid 300 mg/day, amikacin, ethionamide, ethambutol and pyridoxine. Three days after treatment modification, he became drowsy and was slept for most of the days. He also stopped talking to his relatives with no interaction with family members. A contrastenhanced brain MRI was normal, while the MRI spine findings indicated Pott’s spine. His CSF analysis revealed the following: white cell count: 2 /mL with 100% lymphocytes, protein: 109.7 mg/dL and glucose: 39 mg/dL. CSF analysis for autoimmune antibodies and pan neuro viruses were negative. Electroencephalog