A case of bismuth intoxication with irreversible renal damage
A 21-year-old woman was admitted to the emergency department 4 hours after taking 20 tablets of CBS in a suicide attempt. Each tablet included 300 mg of CBS, which is equivalent to 120 mg of Bi2O3. There was no alcohol or another intravenous drug usage. In the emergency service, the patient underwent gastric lavage and received intravenous fluid therapy, after which she was admitted to the internal medicine intensive care unit.\nPhysical examination upon admission was unremarkable: blood pressure, 100/60 mm Hg; pulse, 76 beats/minute; respiration rate, 12 breaths/minute; and body temperature, 36.5°C. Laboratory tests were as follows: white blood cell count, 7860/mm3; hemoglobin, 10.8 g/dL; platelet count, 445,000/mm3; serum sodium, 141 mEq/L; potassium, 4.3 mEq/L; chloride, 104 mEq/L; glucose, 108 mg/dL; amylase, 85 U/L; aspartate aminotransferase (AST), 35 U/L; alanine aminotransferase (ALT), 14 U/L; lactate dehydrogenase (LDH), 150 U/L; hepatitis B surface antigen, nonreactive; and anti-hepatitis C virus, nonreactive. Her INR was reported to be normal at 1.1. Thyroid function tests were normal. Chest radiography also showed no abnormalities. Abdominal ultrasonography demonstrated slightly increased echogenicity in the renal parenchyma. Electrocardiography and echocardiography findings were normal. The patient rapidly became oliguric (<500 mL/day) and thereafter was anuric (0 mL/day). Blood creatinine increased to 2.6 mg/dL (blood urine nitrogen [BUN], 8 mg/dL) during the first 24 hours and to 3.1 mg/dL (BUN, 11 mg/dL) the next day. The baseline creatinine value was normal. Nevertheless, levels of LDH, ALT, and AST were elevated at 1,129 U/L, 62 U/L, and 139 U/L, respectively. Her scleraes were anicteric. The abdomen was soft, flat, and without palpable organomegaly. There was no edema. Arterial blood gases showed metabolic acidosis with a pH of 7.28, PaCO2 of 30 mmHg, PaO2 of 80 mmHg, BE of −11 mmol/L, and HCO3 of 14 mmol/L. Blood chemistry and urine sediment showed signs of proximal tubular dysfunction (Fanconi’s syndrome) with hypophosphatemia, hypouricemia, metabolic acidosis, and renal glycosuria despite normal plasma glucose concentration.\nAfter consultation with personnel at Turkey’s National Poison Information Center, we started oral treatment with the chelating agent sodium-2,3-dimercapto-1-propanesulfonate (DMPS), which is related structurally to 2,3-dimercapto-1-propanol (dimercaprol, also known as British anti-Lewisite), using the following regimen: DMPS, 600 mg orally every 8 hours for 14 days. Hemodialysis was performed because of anuria and severe metabolic acidosis. Hemodialysis was conducted daily for the first 4 days and then three times weekly. Arterial blood gases returned to normal. Afterwards, the patient’s urine output progressively increased. Levels of LDH, ALT, and AST also returned to normal. The patient recovered clinically and was discharged after 15 days in hospital. Her serum creatinine and BUN levels upon discharge were 5.2 mg/dL and 20.0 mg/dL, respectively. Eight weeks after discharge, the patient’s renal function (serum creatinine and BUN) test results remained high. The patient is still on hemodialysis approximately 1 year later.