A 44-year-old man with a previous history of depression and alcoholism was taken to a regional hospital three hours after voluntary ingestion of arsenic. The patient was found to be agitated, with nausea, vomiting and severe watery diarrhoea. His blood pressure was 75/45 mmHg, his heart rate was 130 beats/minute and his temperature was 37ºC. Blood tests showed acute metabolic acidosis (pH 7.21, PO2 91 mmHg, PCO2 21 mmHg and bicarbonate 11.8 mmol/l with FiO2 of 0.21), lactate 6 (normal level: < 2.2) mmol/l and hypokalaemia 3.3 mmol/l. Electrocardiogram (ECG) revealed sinus tachycardia at 135 beats/minute and QTc interval of 0.46 seconds. He was initially treated with sodium bicarbonate (220 mmol intravenously [i.v.]), fluid overload, gastric lavage and administration of activated charcoal and dimercaprol (300 mg intramuscularly [i.m.]). Due to a progressive deterioration of the level of consciousness, the patient was intubated and transferred to the intensive care unit.
On admission, the patient was sedated and mechanically ventilated. Physical examination revealed miosis and a temperature of 35.2°C, a blood pressure of 70/40 mmHg, a heart rate of 95 beats/minute and a central venous pressure of 8 cmH2O. The most salient analytical data were: glucose 64 mg/dl, sodium 148 mmol/l, potassium 1.8 mmol/l, calcium 7.8 mg/dl, magnesium 2.7 mg/dl, phosphorus 0.4 mg/dl, creatinine 2.3 mg/dl, urea 52 mmol/l, creatine kinase 273 U/l, troponin I 0.74 (normal level: 0.06) µg/l, leucocytes 17.6 x 109/l with 80% neutrophils and haemoglobin 12.5 g/dl. Arterial blood gases were (FiO2, 0.5): pH 7.27, PO2 105 mmHg, PCO2 38 mmHg and bicarbonate 18 mmol/l. Chest X-ray was within normal limits. ECG showed sinus rhythm at 95 beats/minute, prolonged QTc interval (0.70 seconds) and ST-segment depression in leads I, II, aVL and V2 to V6. Several minutes later, ECG recording revealed several episodes of polymorphic and self-limited ventricular tachycardias compatible with PAD, which were suppressed with magnesium and potassium supplementation. Due to the onset of acute renal failure, a haemodialysis session was performed. Eight hours after admission, a pulmonary arterial catheter revealed the following haemodynamic parameters: pulmonary arterial pressure, 28/20 mmHg; pulmonary wedge pressure, 12 mmHg; cardiac index, 4.7 beats/minute/m2 and systemic vascular resistances, 435 dynes.sec.cm-5. He was treated with aggressive volume expansion, dimercaprol administration (3.2 mg/kg/4 hours), phosphorus repletion and high-dose noradrenaline. Subsequently, blood pressure rose to 120/65 mmHg and systemic vascular resistances reached 1019 dynes.sec.cm-5. Serum arsenic levels obtained on admission were 319 (normal level: < 20) µg/l and urinary arsenic levels were 946 (normal level: < 35) µg/l. An ECG performed 24 hours after admission revealed a normal QTc interval (0.40 sec) and an absence of Q waves and ST segment shifts. At this time, serum troponin I levels were 25.6 µg/l and serum creatine kinase levels were 1523 (MB fraction 98.1) U/l. After 48 hours of admission, the patient developed a fever of 40°C and severe arterial hypotension due to pneumonia caused by Staphylococcus aureus, Klebsiella oxytoca and Serratia marcescens. The patient died 60 hours after admission. A partial autopsy revealed histological signs of massive renal necrosis, hepatic centrolobulillar necrosis and, at the cardiac level, absence of acute myocardial infarction, coronary thrombosis or typical signs of myocarditis (myocytolysis and lymphocyte infiltration).