OBJECTIVE: This investigation evaluated the effectiveness of calcium and magnesium in treating oral hydrofluoric acid (HF) poisoning. METHODS: The controlled laboratory investigation used anesthetized pigs. Subjects received HF via NG tube, titrated to abolish electrocardiographic abnormalities. The untreated group received saline infusion. The treatment group received serial injections of calcium chloride (CaCl2) and magnesium chloride (MgCl2). A third group received oral infusions of Calcium fluoride (CaF2). We measured heart rate, QRS interval, pH, bicarbonate, calcium, magnesium, and potassium. The Wilcoxon Rank Sum test was used to compare intra- and inter-subject differences. RESULTS: Fatality occurred in all pigs receiving HF. Compared to the untreated group, trends for the treatment group were toward a larger amount of HF to produce fatality (83.1 +/- 17.5 grams vs. 37.7 +/- 16.1 grams, p = 0.08), to cause QRS prolongation (72.5 +/- 25.8vs. 33.8 +/- 14.9 grams, p = 0.08), and to lower potassium at mortality (4.9 +/- 0.7 vs. 8.7 +/- 2.7 mEq/L, p = 0.08). No major changes in calcium (-1.0 +/- 0.7 mEq/L) or magnesium (0.4 +/- 0.6 mEq/L) occurred in the untreated group. Tachycardia developed in all pigs and ventricular arrhythmias occurred in 2 of 3 pigs of both groups [CaF2 administration caused no QRS prolongation or ventricular arrhythmias and had no effect on laboratory parameters]. CONCLUSION: CaCl2 and MgCl2 replacement delayed but did not prevent fatality and QRS prolongation. Although this result suggests Ca++ and Mg++ may be beneficial in the treatment of systemic HF toxicity, factors other than hypocalcemia and hypomagnesemia play a role in toxicity.
OBJECTIVE: This investigation evaluated the effectiveness of calcium and magnesium in treating oral hydrofluoric acid (HF) poisoning. METHODS: The controlled laboratory investigation used anesthetized pigs. Subjects received HF via NG tube, titrated to abolish electrocardiographic abnormalities. The untreated group received saline infusion. The treatment group received serial injections of calcium chloride (CaCl2) and magnesium chloride (MgCl2). A third group received oral infusions of Calcium fluoride (CaF2). We measured heart rate, QRS interval, pH, bicarbonate, calcium, magnesium, and potassium. The Wilcoxon Rank Sum test was used to compare intra- and inter-subject differences. RESULTS: Fatality occurred in all pigs receiving HF. Compared to the untreated group, trends for the treatment group were toward a larger amount of HF to produce fatality (83.1 +/- 17.5 grams vs. 37.7 +/- 16.1 grams, p = 0.08), to cause QRS prolongation (72.5 +/- 25.8vs. 33.8 +/- 14.9 grams, p = 0.08), and to lower potassium at mortality (4.9 +/- 0.7 vs. 8.7 +/- 2.7 mEq/L, p = 0.08). No major changes in calcium (-1.0 +/- 0.7 mEq/L) or magnesium (0.4 +/- 0.6 mEq/L) occurred in the untreated group. Tachycardia developed in all pigs and ventricular arrhythmias occurred in 2 of 3 pigs of both groups [CaF2 administration caused no QRS prolongation or ventricular arrhythmias and had no effect on laboratory parameters]. CONCLUSION:CaCl2 and MgCl2 replacement delayed but did not prevent fatality and QRS prolongation. Although this result suggests Ca++ and Mg++ may be beneficial in the treatment of systemic HF toxicity, factors other than hypocalcemia and hypomagnesemia play a role in toxicity.