A 44-year-old male with a history of depression and alcoholism was taken to a regional hospital three hours after ingestion of arsenic.
The patient was agitated, with nausea, vomiting and severe watery diarrhea.
His blood pressure was 75/45 mmHg, his heart rate was 130 beats/minute and his temperature was 37oC.
Blood tests revealed acute metabolic acidosis (pH 7.21, PO2 91 mmHg, PCO2 21 mmHg and bicarbonate 11.8 mmol/l with FiO2 0.21), lactate < 2.2 mmol/l (normal level:
Electrocardiogram (ECG) revealed sinus tachycardia at 135 beats/minute and QTc interval of 0.46 seconds.
Initially, he was treated with sodium bicarbonate (220 mmol intravenously [i.v.]), fluid overload, gastric lavage, and administration of activated charcoal (300 mg intramuscularly [i.m.]).
Due to a progressive deterioration in the level of consciousness, the patient was intubated and transferred to the Intensive Care Unit.
On admission, the patient was sedated and mechanically oriented.
Physical examination revealed myosis and a temperature of 35.2 oC, blood pressure of 70/40 mmHg, heart rate of 95 beats/minute and central venous pressure of 8 cmH2O.
The most prominent 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 FiO 0.4 mg urea/dl, creatinine 2.374
The chest X-ray was within normal limits.
The ECG showed sinus rhythm at 95 beats/minute, prolonged QTc interval (0.70 seconds) and ST depression in leads I, II, aVL and V2 to V6.
Several minutes later, ECG recording revealed several episodes of polymorphic and self-limiting ventricular tachycardia compatible with PPT, which were suppressed with magnesium and potassium intakes.
Due to the onset of acute renal failure, a hemodialysis session was performed.
Eight hours after admission, a pulmonary arterial catheter revealed the following hemodynamic parameters: pulmonary arterial pressure, 28/20 mmHg; pulmonary artery entrapment pressure, 12 mmHg; cardiac index, 4.7 beats/minute, vascular resistance.
He was treated with aggressive volume expansion, administration of dimercaprol (3.2 mg/kg/4 hours), phosphorus repletion and high doses of noradrenaline.
Then, blood pressure increased to 120 mmHg and systemic vascular resistance reached 1019 dinas.sec.cm-5.
Serum arsenic levels obtained at admission were 319 (normal level: < 20) μg/l and urinary 946 (normal level: < 35) μg/l.
An ECG performed 24 hours after admission revealed a normal QTc interval (0.40 sec) and absence of Q waves and ST segment displacements.
At this time, serum troponin I levels were 25.6 μg/l and creatine kinase levels were 1,523 (MB fraction 98.1) U/l.
After 48 hours of admission, the patient developed fever of 40 oC and severe hypotension due to pneumonia caused by Staphylococcus aureus, Klebsiella occica and Serratia marcescens.
The patient died 60 hours after admission.
A partial autopsy revealed histological signs of massive renal necrosis, hepatic bulillar necrosis and, at cardiac level, absence of acute myocardial infarction, typical signs lymphocytes or myocytolysis center (myocytolysis).
