Delayed fatal hyperkalemia in a patient with acute fluoride intoxication

Mclvor, Michael E

doi:10.1016/s0196-0644(87)80478-x

Cited by 31 publications

(16 citation statements)

References 11 publications

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“…In addition to direct binding and precipitation of free ionized calcium, potassium abnormalities have been described with sodium fluoride toxicity. These abnormalities are postulated to result from at least two other cellular actions of fluoride anion: 1) fluoride-mediated inactivation of the Na + /K + ATPase, contributing to the accumulation of intracellular sodium and extracellular potassium; and 2) activation of a Na + /Ca ++ ion exchanger that results in the intracellular accumulation of calcium, triggering a calciumdependent potassium channel which in turn mediates potassium efflux (4,26). The addition of sodium fluoride to in vitro suspensions of red blood cells induces a delayed efflux of potassium from the erythrocytes (18,23).…”

Section: Discussionmentioning

confidence: 99%

“…The concentration of HF in household products is usually less than 10%, while industrial products may have concentrations as high as 70% (3). Acute systemic toxicity from HF occurs through dermal exposure to highly concentrated solutions, and through ingestion (1,2,(4)(5)(6)(7)(8)(9)(10)(11). Ingestion of the sodium salt form of HF (NaF), which was historically used as a pesticide, resulted in many deaths (12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

“…Hyperkalemia, which may be delayed in onset, has also been proposed as an etiology of fluoride-associated ventricular dysrhythmias (4,18,(23)(24)(25)(26)(27). Hyperkalemia has been documented in a number of cases of human poisoning with fluoride (22,27) and in dog studies of fluoride poisoning (24,25).…”

Section: Introductionmentioning

confidence: 99%

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Recurrent life-threatening ventricular dysrhythmias associated with acute hydrofluoric acid ingestion: Observations in one case and implications for mechanism of toxicity

Vohra

Velez

Rivera

et al. 2008

Clinical Toxicology

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University of Texas, Southwestern Medical Center at Dallas, Dallas, Texas, USAIntroduction. Hydrofluoric acid (HF) is a weak inorganic acid used for etching and as rust remover. Systemic toxicity is manifested as ventricular dysrhythmias. The mechanisms for these dysrhythmias are not well elucidated. Case report. An 82-year-old woman ingested 8 ounces of 7% HF. Shortly after emergency department (ED) arrival, she became pulseless, developing recurrent ventricular dysrhythmias. She was defibrillated 17 times and received several doses of calcium, magnesium, and lidocaine. After three hours, she returned to sustained NSR. She was discharged home after four days. Discussion. The electrocardiographic findings in this patient demonstrate hypocalcemia, which has been implicated as the culprit in HF-induced arrhythmias. However, despite correction of the hypocalcemia, the ventricular arrhythmias persisted. The proposed mechanisms of systemic HF toxicity and the relevant literature are discussed. Conclusion. Ventricular dysrhythmias due to HF toxicity seem to be independent of either hypocalcemia or hyperkalemia. Systemic toxicity after ingestions may be delayed and precipitous.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Recurrent life-threatening ventricular dysrhythmias associated with acute hydrofluoric acid ingestion: Observations in one case and implications for mechanism of toxicity

Vohra

Velez

Rivera

et al. 2008

Clinical Toxicology

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“…The systemic effects are primarily related to electrolyte disturbances -mainly hypocalcemia -but also hypomagnesemia, acidosis, fluorosis and hyperkalemia, which can lead to disturbances of renal, hepatic and cardiac function (12,13). Fluoride ions bind calcium and magnesium, and this process may occur at a rate exceeding the body's ability to mobilize calcium and magnesium in the serum.…”

Section: Systemic Toxicitymentioning

confidence: 99%

A review of hydrofluoric acid burn management

McKee¹,

Thoma²,

Bailey³

et al. 2014

CAN J PLAST SURG

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“…HFA exposures have led to systemic complications owing to the potential of fluoride ions (F) to penetrate the skin 1) . There are many clinical reports on cardiac dysfunction a few hours after accidental HFA exposure [2][3][4][5] . Furthermore, there have also been many reports on the acute lethal effects of inhaled HFA in relation to occupational accidents 6,7) .…”

mentioning

confidence: 99%

Time‐dependent Changes of Blood Parameters and Fluoride Kinetics in Rats after Acute Exposure to Subtoxic Hydrofluoric Acid

Imanishi

Dote

Tsuji

et al. 2009

Journal of Occupational Health

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In our previous study, we reported that even a sublethal dose of hydrofluoric acid (HFA) could cause acute toxic effects 60 min after intravenous injection. This study was designed to investigate the time-and dosedependent changes associated with these disorders. The serum fluoride (F) kinetics are also considered in the discussion of the relationship between the concentrations of serum F and the disorders. Methods: Rats were injected with HFA (1.6 or 9.6 mg/kg body weight) for the dose-response relationship study. For each dose, the rats were assigned to one of seven groups. Blood samples of the 0-min group were obtained from the carotid artery prior to injection as a control. The other six groups were labeled according to sampling times (5, 10, 30, 60, 120 and 300-min) in the time-dependent study. Results: The 1.6 mg/kg dose decreased the ionized calcium (Ca 2+ ) level significantly after 30 min, and it also decreased the total calcium (Ca) level after 300 min. The 9.6 mg/kg dose rapidly worsened renal dysfunction after 60 min. It increased the serum potassium level after 60 and 120 min and it decreased Ca and Ca 2+ levels until 300 min. Although there was respiratory compensation, the base excess and HCO 3 -level and had not completely recovered by 300 min. Conclusions: Even low exposure to HFA caused renal dysfunction, and electrolyte abnormalities and metabolic acidosis lasted for several hours in rats. Therefore, persons involved in HFA accidental exposure should be closely monitored over time, even if the exposure is less than the sublethal dose. (J Occup Health 2009; 51: 287-293)

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Delayed fatal hyperkalemia in a patient with acute fluoride intoxication

Cited by 31 publications

References 11 publications

Recurrent life-threatening ventricular dysrhythmias associated with acute hydrofluoric acid ingestion: Observations in one case and implications for mechanism of toxicity

Recurrent life-threatening ventricular dysrhythmias associated with acute hydrofluoric acid ingestion: Observations in one case and implications for mechanism of toxicity

A review of hydrofluoric acid burn management

Time‐dependent Changes of Blood Parameters and Fluoride Kinetics in Rats after Acute Exposure to Subtoxic Hydrofluoric Acid

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