Fatal cases of acute suicidal sodium and accidental zinc fluorosilicate poisoning. Review of acute intoxications due to fluoride compounds.

Fluoride, of all inorganic substances, is among the least likely to be identified by a routine toxicological analysis. Acute poisonings with salts of hydrofluoric or fluorosilicic acid, however, although relatively uncommon, may occur. Some fluorosilicates, salts of fluorosilicic acid (e.g. Al, Zn, Pb, Mg) are used as stone consolidants, others (e.g. sodium fluorosilicate)--in the production of enamel and milk glass, or as insecticide. In this paper, two fatal cases of poisonings are presented: a suicide involving sodium fluorosilicate of a 39-year-old male who died in his flat, without hospitalization, and an accidental ingestion of zinc fluorosilicate solution (probably due to mistaking it for mineral water) by a 38-year-old male at his workplace (building), who died about 3h after ingestion of the liquid, in spite of intensive care at hospitals. Post-mortem samples were examined by the use of the spectrophotometric method with lanthanum nitrate and alizarin complexone for fluorine (after isolation of fluoride compounds by the microdiffusion method) and using a flame atomic absorption spectrometry method for zinc (after mineralization of biological material by sulfuric and nitric acids). In the first case, the results were: blood--130 µg F/ml, stomach--1150 µg F/g, small intestine content --19.6 µg F/g, kidney--56.0 µg F/g, and urine--1940 µg F/ml. In the second case, the contents of fluorine and zinc in blood and internal organs were the following: blood--6.03 µg F/ml, 23.8 µg Zn/ml; brain--1.39 µg F/g, 7.54 µg Zn/g; stomach--152 µg Zn/g; stomach content--293 µg F/g, 84.4 µg Zn/g; small intestine--37.5 µg Zn/g; small intestine content--63.4 µg F/g, 19.6 µg Zn/g; liver--9.49 µg F/g, 81.0 µg Zn/g; kidney--29.6 µg F/g, 39.2 µg Zn/g; and exceeded the normal levels of these elements in biological material many times. In addition, in stomach and liver large amounts of silica were detected. In the paper, a review of acute intoxications with various fluoride compounds (17 cases) is also presented.

Severe hypokalaemic metabolic alkalosis following ingestion of gaviscon.

INTRODUCTION: Uncommon metabolic abnormalities in the emergency department could be a result of drug overdose due to uncommon agents. CASE REPORT: A 35-year-old male presented to the emergency department with a Glasgow Coma Scale (GCS) of 3/15 and a normal pulse rate and blood pressure. Subsequent questioning after recovery revealed he had ingested 2 L of Gaviscon over the preceding 48 hours. He had normal haematology, liver, and renal function during admission. The electrocardiogram showed T wave inversion in the inferior leads on admission. Arterial blood gas on air was: pH 7.54, HCO3 50 mmol/L (50 meq/L), Chloride 66 mmol/L, anion gap was 19, pO2 11 kPa (82.5 mmHg), and pCO2 8 kPa (60 mmHg). Serum sodium was 127 mmol/L and serum potassium was 1.6 mmol/L. His GCS improved within one hour of admission with supportive care, and his serum potassium and bicarbonate improved within 24 hours. He subsequently made a full recovery. Discussion. Bicarbonate ingestion in the form of Gaviscon(R) and vomiting made this patient alkalotic, and simple supportive care provided effective management with a complete recovery. CONCLUSION: This case illustrates how a severe metabolic alkalosis can result from a significant ingestion of Gaviscon, and that such presentations can give rise to diagnostic dilemma.

[Death from fluoro-silicate in floor polish].

A fatal case of poisoning due to ingestion of an apparently innocuous household product is described. A healthy 28-year-old man accidentally drank floor polish (Cristalizador, a Spanish import). On arrival at the emergency room a few hours later he passed large amounts of bloody stool and lost consciousness. A call to the Spanish Poison Center revealed that although not indicated on the label, the polish contained a highly poisonous salt, fluoro-silicate. Blood gas analysis revealed severe metabolic acidosis. Serum calcium was 3.8 mg/dL. The post-resuscitation ECG showed subendocardial ischemia and ST-elevation in the anteroseptal wall and prolonged QT-interval. In the intensive care unit he received large amounts of fluids, dopamine, sodium bicarbonate and calcium. Despite the treatment, his condition continued to deteriorate: VPB's appeared, there was a short run of ventricular tachycardia and then atrial fibrillation developed. Further treatment included lidocaine, verapamil, amiodarone, and electrical cardioversion. Blood pressure remained low and 11 hours after admission he died of myocardial infarction, severe arrhythmia and multi-organ failure.

[The alkaline phosphatase and aminotransferase activity of the blood serum and liver in rats with chronic poisoning by the dust from a mineral wool made of ferronickel slag]. / Aktivnost' shchelochnoi fosfatazy, aminotransferaz syvorotki krovi i pecheny krys pri khronicheskoi intoksikatsii pyl'iu mineral'noi vaty iz ferronikelevogo shlaka.

The authors investigated the activity of alkaline phosphatase, alanine- and aspartate-aminotransferases of the blood serum, mitochondria and postmitochondrial fraction of the liver in conditions of administration of mineral cotton from ferronickel slag. It was shown that 1 and 3 months after introduction of mineral cotton dust changes occurred in the activity of these enzymes. Restoration of these enzymes occurred 6 months after introduction of mineral cotton dust.

[Death by peroral ingestion of soluble glass (sodium silicate)]. / Tod durch perorale Aufnahme von Wasserglas (Natriumsilikat).

The intake of 0.51 of water glass (sodium metasilicate; colloid pH 12.5) led to death within 1-1.5 h. Autopsy revealed alkali burns of the stomach mucosa. The stomach contained a small amount of liquid with a pH of 11.5. Histologically, numerous bronchioles and alveoles were filled with amorphous material. This material was chemically proved to be condensed water glass. The obstruction of large parts of the lungs by water glass led to an inhibition of alveolar gas diffusion, which may have been the cause of death. The transformation of the water glass from liquid to solid occurred in the lungs by means of the carbonic acid of expiration air. This was made possible because the pH of water glass had been changed by gastric secretions from 12.5 to 11.5. Water glass starts to solidify around pH 11.4-11.3.

Dissolution of silicic acid from dusts of kaolin, mica and talc and its relation to their hemolytic activity. -- an in vitro study.

Hemolysis induced by native kaolin dust was found to run parallel to the amount of silicic acid dissolved from it. Native mica and talc dusts were hemolytic only to a small extent and the silicic acid dissolution from these dusts was also smaller in comparison to that of native kaolin. The proportionality between hemolysis and the amount of dissolved silicic acid was not consistently observed in the case of acid, alkali and water treated kaolin, mica and talc dusts.