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Acute pancreatitis and Wernicke encephalopathy: case report A 55-year-old woman developed acute pancreatitis and Wernicke encephalopathy during treatment with arsenic-trioxide and tretinoin for acute promyelocytic leukaemia [routes not stated]. The obese woman, who had hypertriglyceridaemia, presented to the hospital August 2019 due to gingival bleeding, cough and fever. She was looking pale and had purpura all over the body. Upon further investigations, she was diagnosed with acute promyelocytic leukaemia. Therefore, treatment with tretinoin [all-trans-retinoic acid] 45 mg/m2, arsenic trioxide 0.15 mg/kg and idarubicin [Idamycin] was initiated. Additionally, she received fibrinogen and platelets. On day 12 of the arsenic-trioxide and tretinoin treatment, she reported epigastric pain, vomiting and nausea. Her peripheral blood test showed Hb 101 g/L, WBC 2.57 × 109/L, platelet count 23 × 109/L and C-reactive protein of 27.30 mg/L. Tenderness in her epigastric pancreas was noticed upon physical examination and an ultrasound of the abdomen showed cholecystitis. Hence, unspecified antibiotic therapy was given. However, her pain did not resolve. Additional tests showed an increase in the lipase and amylase levels. These findings were suggestive of acute pancreatitis and a CT scan demonstrated bulky oedematous pancreatitis with no evidence of necrosis. The woman was treated with analgesics and hydration was provided that led to normalisation of the lipase and amylase level. But, she still had intermittent abdominal pain and discomfort causing reduced appetite. She was receiving parenteral nutrition supplementation. During the supplementation therapy, she developed apathy and hypotension. Her blood pressure decreased to 95/60mm Hg and maintained at the same level afterwards. She also developed hyponatraemia that required sodium supplement therapy. Despite the continuous sodium administration for seven days, she had continued hyponatraemia and it was considered that the hyponatraemia was refractory to the sodium supplement therapy. Her confusion and apathy continued after 20 days of parenteral nutrition supplement. Thereafter, she developed a decreased range of motion, generalised muscle weakness, vertical nystagmus and dysarthria. Her neurological examination showed slow pupillary reaction to light and signs of nystagmus along with paralysis of the abduction nerves bilaterally. She underwent a lumbar puncture and normal intracranial pressure was noted. Her CT scan of the brain showed normal results. Subsequently, she was diagnosed with Wernicke encephalopathy and her MRI confirmed the diagnosis of Wernicke encephalopathy. An MRI demonstrated symmetric cortical abnormalities in her frontal and parietal lobes of the brain and the third ventricle and aqueduct surrounded by typical lesions, indicative of Wernicke encephalopathy. Hence, she was treated with thiamine that led to resolution of her symptoms. Eventually, she discontinued the treatment. Jiang Y, et al. Severe Wernicke encephalopathy and acute pancreatitis due