Ernest Sliwinski, MD

Ernest Sliwinski, MD

Author, Resident

Dr. Sliwinksi is a Northwell Health Emergency Medicine resident physician

Adam Berman

Adam Berman

Toxicology Editor, theEMpulse.org

Dr. Berman is a Medical Toxicologist and Toxicology Editor at theEMpulse.org

Introduction

Case:

A 43-year-old woman with a past medical history of alcohol abuse presented with right 4th and 5th digit burns. She reported spilling brick cleaner on her right hand the night before. On presentation, the patient complained of pain and blistering to the affected area. She denied any other exposures or any other complaints at presentation. On physical exam, the patient was afebrile with a HR 88 bpm, BP 161/101 mmHg, RR 16/min and O2 sat 100% on room air. She was in no acute distress but had visible burns to her right 4th and 5th digits. Lab work and EKG were within normal limits.

 

Discussion

 

Introduction:

This patient was exposed to Hydrofluoric Acid (HF) in brick cleaner. Hydrofluoric acid is a corrosive inorganic acid used in glass etching, and as a rust remover and brick cleaner.  HF usually penetrates the epidermal and dermal layers quickly and it can cause severe local and systemic injuries. By rapidly binding up available calcium and magnesium cations the Fluoride anion leads to hypocalcemia and hypomagnesemia, which can in turn cause significant cardiac toxicity.

Management:

The mainstay of treatment for local toxicity is irrigation with calcium (preferably in gel form) in order to bind up free fluoride ions.  This also results in pain relief. The patient described above did not show any signs of systemic toxicity such as QTc prolongation, cardiac arrhythmia, or any electrolyte abnormalities. Calcium gluconate 2.5% gel was placed directly over the burns and covered by a surgical glove to hold the gel in place. The gel was massaged into the area over 30-60 minutes. In more severe cases, an intradermal injection of 5% calcium gluconate solution can be performed as well.

 

Ultimately, this patient’s pain did not improve with the local application of calcium gluconate and he required a Bier block for relief. A Bier block involves exanguinating the affected extremity and then, in this case, injecting 10% calcium gluconate IV distal to the affected skin (more info on the Bier Block can be found at NYSORA. An intrarterial infusion of calcium has also been described in the literature but was not performed in our patient. The patient felt improvement with the Bier block. The patient was eventually discharged with hand surgery follow up.

Conclusion

The key points for treating a hydrofluoric acid burn are recognizing the exposure and determining whether there are any signs of systemic toxicity requiring more aggressive treatment. In the absence of systemic toxicity, calcium is the primary antidote used for local burns, whether topically, intrarterially, or intravenously.

Tox Tidbits

  • Hydrofluoric acid (HF) is found in brick cleaners, metal and glass etching, and numerous industrial settings (pharmaceutical, refrigeration, petrochemical, and others)
  • HF can cause local burns, tissue damage, and severe pain. Cardiotoxicity is mediated primarily by sequestering calcium. 
  • Be sure to obtain an ECG and check electrolytes
  • Treatment:
    • Local: Apply topical Calcium Gluconate (gel if available) to bind Fluoride ions. Consider intradermal 5% Calcium Gluconate injection if not better in 30-40 min.
    • Cardiac/Systemic Toxicity: IV Calcium, and Magnesium for some
    • Inhalation injury: Nebulized Calcium Gluconate (4ml, 2.5%-5%). Avoid Succinylcholine if intubating.

References

  1. Kaushik, S. Bird, S. “Topical Chemical Burns.” Accessed on Up To Date. March 2017.
  2. Su M. Hydrofluoric Acid and Fluorides. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. eds. Goldfrank’s Toxicologic Emergencies, 10th ed. New York, NY: McGraw-Hill; 2015. Accessed online, May 01, 2017.
  3. Ryan JM, McCarthy  GM, Plunkett  PK: Regional intravenous calcium—an effective method of treating hydrofluoric acid burns to limb peripheries. J Accid Emerg Med. 1997;14:401–402
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