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Calcium-deficient tetany, hyperglycemia, glycosuria, twitching, hyperreflexia, and EEG abnormalities have also been reported. Most of these adverse effects are secondary to ammonia toxicity resulting from inability of the liver to convert the ammonium ion to urea. Because rapid IV injection may increase the likelihood of ammonia toxicity, IV infusions of ammonium chloride should be administered slowly to permit metabolism of ammonium ions by the liver. Patients receiving ammonium chloride should be closely monitored for signs and symptoms of ammonia toxicity such as pallor, sweating, irregular breathing, vomiting, bradycardia, cardiac arrhythmias, local or generalized twitching, asterixis, tonic seizures, and coma. ANIMAL STUDIES: Acute exposure in mice by intravenous administration resulted in hyperventilation and clonic movements which were followed sometimes by tonic extensor convulsions, but usually by profound coma; death was preceded by convulsions, but survivors made complete and rapid recovery. This syndrome was potentiated by short periods of hypoxia. In rabbits, replacement of aq. humor with 1% solution of ammonium chloride has caused considerable hyperemia of iris, but by next day eyes were almost normal, and in another day were completely recovered. The ingestion of ammonium chloride in doses of around 500-1000 mg/kg bw/day, for periods ranging from 1 to 8 days, has induced metabolic acidosis in mice, guinea-pigs, rats, rabbits, and dog. Pulmonary edema, central nervous system dysfunction, and renal changes are reported to have occurred after ingestion of ammonium chloride. Ammonium chloride is reported to cause alterations in calcium and bone metabolism in various species. Specific toxic effects on the kidneys as renal hypertrophy were found in rats receiving ammonium chloride in the diet. Other salts (ammonium citrate or sodium chloride) did not induce such effects. Rabbits showed cellular swelling and karyolysis of kidney tubulus cells after two daily oral administrations of 16.2 g/animal ammonium chloride. One-sixth molar ammonium chloride was given to mice orally in the drinking water after day 7 during pregnancy and although the offspring were small sized no congenital defects were found. In other study mice were given 600 mg/kg orally at 8 and 10 am and 12 and 1 pm on day 10 of gestation and produced 7% ectrodactyly in the offspring. Negative in the Ames test using Salmonella typhimurium TA 98, TA 100, TA 1535, TA 1537, TA 1538 at doses with and without metabolic activation. Negative in the Ames test using Escherichia coli WP2uvrA with and without metabolic activation.