Acute kidney injury following ingestion of plate developer (sodium metasilicate): a case report.

BACKGROUND: Plate developer is a chemical used in the printing industry and is a corrosive alkaline agent containing sodium metasilicate as the main substance. Plate developer poisoning is rare. Literature search revealed only a single case report of fatal sodium metasilicate poisoning (Z Rechtsmed 94(3):245-250, 1985). There are no reports of acute kidney injury related to ingestion of sodium metasilicate containing substances. CASE REPORT: A 52-year-old Sri Lankan male with a history of hypertension and affective disorder presented following ingestion of about 150 ml of plate developer solution. He developed severe upper airway obstruction due to laryngeal edema and underwent tracheostomy. While in the ward he developed features of acute kidney injury with high serum creatinine levels and persistent hyperkalemia which necessitated temporary haemodialysis. Because of the corrosive effect, he developed severe inflammation of the upper gastro intestinal tract with narrowing of esophagus and pyloric region, requiring feeding jejunostomy. He died while waiting for the surgery for pyloric stenosis. CONCLUSIONS: Acute kidney injury is a potential treatable complication of plate developer poisoning other than its complications related to corrosive effects. Regular monitoring of renal functions in such a patient would be useful for early recognition of acute kidney injury.

Reactive airways dysfunction syndrome from acute inhalation of a dishwasher detergent powder.

Reactive airway dysfunction syndrome, a type of occupational asthma without a latency period, is induced by irritating vapour, fumes or smoke. The present report is the first to describe a case of reactive airway dysfunction syndrome caused by acute exposure to dishwater detergent containing sodium metasilicate and sodium dichloroisocyanurate. The diagnosis was based on exposure data, clinical symptoms and signs, as well as respiratory function tests. A 43-year-old nonatopic male apprentice cook developed respiratory symptoms immediately after exposure to a cloud of detergent powder that was made airborne by vigorous shaking of the package. In spirometry, combined obstructive and restrictive ventilatory impairment developed, and the histamine challenge test revealed bronchial hyper-responsiveness. Even routine handling of a strongly caustic detergent, such as filling a dishwasher container, is not entirely risk free and should be performed with caution.

[Case of concrete hardener poisoning complicated with acute renal failure treated by hemodialysis].

A 54-year-old man took approximately 180 mL of rapid-hardening cement (75% sodium silicate) with suicidal intent and was transferred to our department after at least 2 hours had elapsed from the time he took the poison. Milk, sodium alginate, and a proton pump inhibitor were administered to the patient, and intravenous fluid infusion in a large dose with antibiotics was started. Upper gastrointestinal endoscopy revealed lesions in the oral cavity, pharynx, esophagus, and stomach. The most severe lesions observed were in the greater curvature of the stomach body. Hemodialysis was performed because of persistent oliguria and worsening of the renal function parameters. The patient underwent 8 sessions of hemodialysis over a period of 11 days, after which the dialysis was stopped. The serum level of silicon was 25.1 microg/mL on admission and 9.2 microg/mL at the time of withdrawal from hemodialysis. The gastrointestinal mucosal lesions resolved completely in response to the treatment. There were no residual lesions except for some scarring in the greater curvature of the stomach. Although the serum levels of silicon decreased transiently following each hemodialysis session, they increased again on the following day. Based on the observations in this case, it was proposed that a serum silicon level of less than 10 microg/mL is unlikely to cause renal dysfunction.

Fibrosis of the lung and pleura and long-term exposure to wollastonite.

OBJECTIVES: The purpose of this study was to determine whether long-term exposure to wollastonite causes fibrosis of the lung and pleura in humans. METHODS: Forty-nine workers (mean exposure 25 years) in a Finnish limestone-wollastonite mine and mill were examined. Their work histories and symptoms of chronic bronchitis were recorded. The chest radiographs were classified according to the classification of the International Labour Office (1980); a radiographic follow-up from 1981 to 1990 was included. Spirometry and diffusion capacity were measured. Four workers underwent high-resolution computed tomography (HRCT) and bronchoalveolar lavage (BAL). Lung tissue specimens were available for 2 workers. Mineral fibers and asbestos bodies were analyzed from the BAL fluid and lung tissue specimens, which were also analyzed for lung fibrosis. RESULTS: Two workers (4%) had small irregular lung opacities (ILO 1/0), 1 worker (2%) ILO 0/1 of the s/t type. HRCT revealed no parenchymal fibrosis in the 2 workers with the ILO 1/0 classification. Of the 9 workers (18%) with pleural plaques, 5 had been exposed to asbestos. Multivariate logistic regression analyses revealed no association of plaques with the duration of wollastonite or asbestos exposure. Wollastonite fibers or bodies were not found in any of the 4 workers who underwent BAL, nor in either of the workers whose lung tissue specimens were available. CONCLUSIONS: No evidence was found that long-term exposure to wollastonite causes parenchymal fibrosis of the lung and pleura. Furthermore, the findings indicate that wollastonite fibers are poorly retained in human lungs.

The antioxidant enzymes activity in the conditions of systemic hypersilicemia.

The effect of an excessive inorganic silicon oral intake on the activity of basic antioxidant enzymes was studied in rats. Activities of superoxide dismutase, catalase, and glutathione peroxidase were measured in liver and kidney tissues of animals receiving per os sodium metasilicate nonahydrate (Na2SiO3.9H2O) (Sigma, [St. Louis, MO]) dissolved in their drinking water. A decrease of the activity of all the studied enzymes was found in the samples derived from the experimental group. The results obtained indicate the free oxygen radicals participation in the potential pathologic events in the conditions of systemic hypersilicemia.