Limited efficacy of calcium and magnesium in a porcine model of hydrofluoric acid ingestion

Coffey, J. A.; Brewer, Kori L.; Carroll, Robert G.; Bradfield, John F.; Meggs, William J.

doi:10.1007/bf03160907

Cited by 13 publications

(21 citation statements)

References 23 publications

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“…No statistically significant benefit was seen by giving either of these salts along with HF [33]. In a pig model, calcium fluoride administered orally did not lead to QRS prolongation or ventricular dysrhythmias [34]. The mechanism and efficacy of orally administered calcium and magnesium are presently unclear.…”

Section: What Is the Role For Decontamination In Hydrofluoric Acidmentioning

confidence: 97%

Case Files of the Toxikon Consortium in Chicago: Survival after Intentional Ingestion of Hydrofluoric Acid

Whiteley

Aks

2010

J. Med. Toxicol.

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A 19-year-old man with a history of past suicide attempts presented to the emergency department (ED) with severe abdominal pain. The patient's sister stated that, 30 min prior to presentation, the patient had tried to kill himself by drinking "poison." Per the patient, he drank about 120 mL of a cleaning agent immediately prior to informing his sister. The patient then had one bout of blood-tinged vomiting, so the sister activated emergency medical services (EMS). EMS arrived and transported the patient uneventfully to the ED while establishing an IV en route. Upon arrival to the ED, the patient had a pulse rate of 80/min, blood pressure of 150/90 mmHg, respiratory rate of 18/min, and oxygen saturation of 99% on room air.Soon after arrival to ED, the poison control center was contacted by the emergency medicine physician. By history, it was determined that the ingested cleaning agent was likely a brick-cleaning solution, although the ED staff were unable to definitively identify the composition at this time. The patient developed profound hematemesis within 15 min of arrival to the ED. He was endotracheally intubated for airway protection using 20 mg of etomidate and 5 mg of midazolam. Famotidine 40 mg IV was given and a propofol infusion was started for sedation. Due to the rapid progression of symptoms and recognition that many brickcleaning solutions contain hydrofluoric acid (HFA), the poison center specialist immediately forwarded the case to the medical toxicology consult service. Per telephone recommendation by the toxicology consultants, a nasogastric (NG) tube was placed and suction was started with minimal liquid return. This was followed by 30 mL of milk of magnesia given via the NG tube. An EKG was ordered, and a complete set of labs were sent including arterial blood gases. Ampules of 10% calcium gluconate were placed at bedside per toxicologist recommendation. One hour after presentation, initial lab results included pH 7.24, PaCO 2 46 mmHg, base excess −8 mEq/L, K + 7.4 mEq/L, and ionized Ca ++ 0.33 mEq/L (normal=1.15-1.29 mEq/L); the EKG showed sinus tachycardia at 106 with a QRS of 76 ms and a QTc of 406 ms. The combination of hypocalcemia, gastrointestinal distress, and a history of drinking "brick cleaner" heightened suspicion by the medical toxicology service for HFA ingestion. Two ampules (20 mL) of 10% calcium gluconate were then given IV over the next 30 min. The patient was then given one ampule (50 mL) of 8.4% sodium bicarbonate and an ampule (50 mL) of 50% dextrose along with 10

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Section: What Is the Role For Decontamination In Hydrofluoric Acidmentioning

confidence: 97%

Case Files of the Toxikon Consortium in Chicago: Survival after Intentional Ingestion of Hydrofluoric Acid

Whiteley

Aks

2010

J. Med. Toxicol.

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“…Therefore, we consider that the changes in PO 2 and PCO 2 at 30 to 120 min are attributable to respiratory compensation for metabolic acidosis. On the other hand, the BE and HCO 3 -levels did not recover from 30 to 300 min in the case of the 9.6 mg/ kg dose. As a mechanism of metabolic acidosis caused by F, it was reported that the HCO 3 -level and BE decreased owing to renal tubular acidosis 60 min after HFA administration (9.6 mg/kg) 9) .…”

Section: Discussionmentioning

confidence: 72%

“…On the other hand, the BE and HCO 3 -levels did not recover from 30 to 300 min in the case of the 9.6 mg/ kg dose. As a mechanism of metabolic acidosis caused by F, it was reported that the HCO 3 -level and BE decreased owing to renal tubular acidosis 60 min after HFA administration (9.6 mg/kg) 9) . It was also postulated that formation of fluorapatite requires dissociation of HPO 4 2-, which releases protons causing metabolic acidosis 18) .…”

Section: Discussionmentioning

confidence: 72%

“…The PCO 2 decreased in the 30-, 60-and 120-min groups. The changes in the HCO 3 -concentration are shown in Fig. 6.…”

Section: Resultsmentioning

confidence: 99%

“…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) .…”

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confidence: 99%

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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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Hydrofluoric acid ingestions: Retrospective evaluations from cases reported to the National Poison Data System 2007–2017

Illg,

Carpenter,

Moran

et al. 2023

JACEP Open

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BackgroundHydrofluoric acid (HF) is associated with systemic toxicity, particularly with high‐concentration formulations. However, most existing data describe dermal exposures; there is a paucity of data related to outcomes after ingestions.ObjectiveTo determine the morbidity and mortality associated with HF ingestions as reported to the National Poison Data System (NPDS). A secondary objective is to assess for clinical criteria that are associated with serious outcomes after HF ingestion.MethodsWe performed a retrospective review of HF ingestions reported to the NPDS from 2007 to 2017. Data including patient demographics, exposure and caller sites, electrolyte abnormalities, treatments, and serious (moderate or major effect or death as documented in NPDS) and non‐serious outcomes were abstracted from case narratives. Cases meeting the criteria for a qualifiable HF ingestion were included in the study.ResultsDuring the study period, there were 653 HF ingestions reported to NPDS, of which 142 were included in the final data analysis. Most HF exposures occurred in men (68.3%), and the most common exposure site was at the exposed individual's own residence (78.2%). Nearly half of all exposures (46.5%) were due to transfer into a non‐labeled secondary storage container. Total of 45.8% of the cases resulted in a serious outcome. Electrolyte disturbances were associated with an increased risk of a serious outcome. Hypocalcemia was the most frequently reported electrolyte abnormality, occurring in 24.6% of cases. Nine (6.3%) individuals died.ConclusionsMortality after HF ingestion is low. However, a large cohort of exposures occurred after the transfer of HF to secondary containers. Targeted interventions to reduce this practice are necessary to decrease hazardous chemical exposures.

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Limited efficacy of calcium and magnesium in a porcine model of hydrofluoric acid ingestion

Cited by 13 publications

References 23 publications

Case Files of the Toxikon Consortium in Chicago: Survival after Intentional Ingestion of Hydrofluoric Acid

Case Files of the Toxikon Consortium in Chicago: Survival after Intentional Ingestion of Hydrofluoric Acid

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

Hydrofluoric acid ingestions: Retrospective evaluations from cases reported to the National Poison Data System 2007–2017

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