Hydrofluoric Acid Burns - Etiology, Pathophysiology, Clinical Manifestations, Evaluation, and Treatment

Introduction

Hydrofluoric acid, also known as HF, was discovered in 1771 by Carl Wilhelm Scheele during his investigation of the mineral fluorite. It is a powerful inorganic acid used in various industrial applications such as aluminum and stainless steel production, glass etching, chemical manufacturing, and more. Hydrofluoric acid is also found in consumer products like rust removers, detergents, and cleaners. It exists as a gas composed of hydrogen and fluorine atoms and forms a polymeric compound in its liquid state. It is colorless or slightly tinted, depending on the concentration. Hydrofluoric acid is highly corrosive, soluble in water, and has a pungent odor at certain concentrations.

What Is the Etiology of Hydrofluoric Acid Burns?

Hydrofluoric acid exposure requires immediate specialized medical treatment to prevent deep tissue penetration and minimize the toxic effects. It is classified as a weak acid but can cause severe burns and cardiac arrhythmias due to the rapid absorption of fluoride ions through the skin. Dermal exposure is the most common route of entry, and burns to the fingers are particularly concerning. The incidence of hydrofluoric acid exposure is relatively rare compared to other industrial injuries, with an estimated 1,000 cases annually. Most cases occur in adult males, primarily affecting the upper extremities.

What Is the Pathophysiology of Hydrofluoric Acid Burns?

There are three routes through which hydrofluoric acid can enter the human body: skin or eye exposure, inhalation, and ingestion. Cutaneous exposure, whether the skin is intact or damaged, is the most common pathway for entry when dealing with aqueous solutions. Inhalation can occur through exposure to hydrogen fluoride gas or vapors emitted by hydrogen fluoride liquid.

Hydrofluoric acid is a highly lipophilic acid that readily penetrates deep tissues through the skin. It causes injury through three distinct mechanisms:

• At high concentrations (> 50 percent), hydrofluoric acid acts as a potent acid, resulting in corrosive burns upon immediate contact with the skin, eyes, respiratory system, and gastrointestinal mucous membranes. This leads to visible tissue destruction, ulceration, and necrosis, accompanied by intense pain caused by the activation of underlying pain receptors.

• At lower concentrations, the small fluoride ion can penetrate the dermal layer. Unlike other acidic substances that release hydrogen cations and cause coagulative necrosis, the fluoride ion continues to dissolve through the skin, leading to further tissue destruction. It affects nerves, blood vessels, and underlying soft tissues through liquefaction necrosis and cellular death.

• Fluoride ions can be absorbed into the bloodstream when present alongside other cations, specifically calcium and magnesium. This results in the formation of insoluble chelate salts through hydrofluoric fixation. The binding of fluoride ions to calcium and magnesium leads to hypocalcemia (low serum calcium level), hypomagnesemia (low serum magnesium level), and the destruction of underlying tissue. Calcium depletion inhibits the sodium-potassium ATPase pump, increasing cellular membrane permeability to potassium and causing hyperkalemia (increased serum potassium level). Electrolyte imbalances can result in cardiac arrhythmias, including prolonged QTc (due to hypocalcemia), polymorphic ventricular tachycardia (due to hypomagnesemia), and T-wave elevation and QRS widening (due to hyperkalemia).

What Is the Clinical Manifestation of Hydrofluoric Acid Burns?

Depending on the location of hydrofluoric acid exposure and the acid concentration, patients may exhibit immediate severe caustic burns on the body, accompanied by severe pain that is disproportionate to the injury, serving as a hallmark finding. Solutions with concentrations greater than 14.5 percent produce immediate symptoms, while 12 percent of solutions may take up to an hour, and solutions less than seven percent can take several hours before symptoms manifest. When any chemical is splashed or sprayed on the face, there is a concern for ocular and respiratory injury.

Obtaining a detailed history is crucial and should include any recent workplace or domestic exposure to hydrofluoric acid, as well as potential products containing the acid, such as rust removers or cleaning agents, within the past 24 hours. Information should be gathered regarding the concentration of the solution, duration of exposure to hydrofluoric acid, use of protective agents, and any other chemicals present in the solution. Additionally, it is important to note any treatments that have been administered thus far.

During the physical assessment, immediate evaluation for life-threatening emergencies should be conducted, including assessing for airway compromise, respiratory distress, and cardiac arrhythmias. Furthermore, one should evaluate for pulmonary edema, ocular injuries, and signs of hypocalcemia, such as Chvostek and Trousseau signs and tetany.

Assessment of chemical burns should be based on the route of exposure and should include:

• Dermal Exposure: Evaluate the location of the burn, with common sites of injury being the head and neck, hands, legs, and arms. Assess the color of the skin surrounding the burn, the degree of ulceration and necrosis, and the involvement of underlying structures such as tendons or bones. Even a brief exposure of 20 seconds to 70 percent hydrofluoric acid can cause cellular alteration in four to five epidermal layers within one minute, penetrating the dermis completely within five minutes. After one hour of exposure, necrosis of all skin layers can occur, with complete necrosis of the epidermal layer and underlying structures observed after 24 hours.

• Ocular Exposure: Initial signs include irritation and pain, followed by conjunctivitis with edema (swelling) and congestion. Minor splashes with hydrofluoric acid can lead to subsequent corneal erosion, sloughing, and ulceration of the corneal epithelium, resulting in corneal opacification. Even low concentrations of hydrofluoric acid (2.5 percent) can fully penetrate the cornea and cause ocular burns within four minutes. Prolonged exposure can result in total eye destruction and vision loss.

• Inhalation Exposure: Toxic gasses or vapors can cause nasal irritation, inflammation of the mucosa, mucosal bleeding, ulceration, and perforation of the nasal septum. Additional respiratory symptoms, dependent on the hydrofluoric acid concentration and duration of exposure, may include coughing, dyspnea (shortness of breath), laryngitis (voice box inflammation) with upper airway symptoms like laryngospasms (vocal cord spasm), tracheobronchitis (windpipe inflammation) with stridor, or lower airway symptoms such as wheezing, bronchial obstruction, bleeding of the airway, pulmonary edema and congestion, or pneumothorax (collapsed lung). Chronic dyspnea has been reported in individuals with repeated exposure to hydrofluoric acid fumes or gasses.

• Ingestion Exposure: Ingesting solutions containing hydrofluoric acid can cause caustic burns on the mucosa of the oropharynx, esophagus, and stomach. Symptoms may include dysphagia, nausea, vomiting, diarrhea, and severe abdominal pain. Hydrofluoric acid ingestion can lead to erosive gastritis, resulting in hematemesis (blood in vomit) and melena (dark stools) due to hemorrhagic gastritis or, in severe cases, potential stomach perforation.

• Neuromuscular Symptoms: Individuals exposed through any route may develop neurologic and muscular disorders due to hypocalcemia and hyperkalemia, which interfere with the normal electrical signal transmission in neurons. These symptoms can include anxiety, confusion, headaches, paresthesia, seizures or paralysis, carpopedal and generalized tetany, and coma secondary to cerebral edema.

How Are Hydrofluoric Acid Burns Evaluated?

Electrolyte imbalance is a significant concern in cases of systemic poisoning resulting from hydrofluoric acid exposure through any route. It is essential to conduct immediate electrolyte assessment, including measuring calcium, potassium, and magnesium levels, to identify hypocalcemia, hypomagnesemia, and hyperkalemia. Even in cases of simple exposures, patients may develop these electrolyte imbalances.

Cardiac monitoring and electrocardiography (EKG or ECG) play a crucial role in evaluating clinically significant electrolyte imbalances. They can help identify QT prolongation caused by hypocalcemia, peaked T waves, and arrhythmias associated with hyperkalemia, as well as polymorphic ventricular tachycardia, specifically Torsades de Pointes, resulting from hypomagnesemia.

For patients with respiratory exposure, performing chest X-rays is recommended to assess for the presence of pulmonary edema or pneumonitis. Consideration may be given to including EtCO2 (end-tidal carbon dioxide) monitoring for individuals with inhalation-type exposures. Urinalysis should be conducted to evaluate for hematuria and proteinuria, which can indicate renal dysfunction, insufficiency, and renal cortical necrosis.

How Is Hydrofluoric Acid Burns Treated?

Preventing exposure to hydrofluoric acid should be the primary concern due to its high corrosiveness and toxicity. All individuals using HF should be knowledgeable about its toxic properties and follow procedures for safe handling, transportation, storage, waste management, decontamination, and medical treatment. Hydrofluoric acid should be limited to industrial settings and properly equipped laboratories with exposure control plans and on-site treatment capabilities. Household cleaning agents should be stored out of children's reach.

Personal and general protective equipment and measures must be implemented and adhered to at all times. This includes wearing personal protective equipment such as a laboratory coat, long pants, an acid-resistant apron, closed-toed shoes, a full-face shield with tightly sealed goggles, and rubber gloves made from nitrile, butyl, or neoprene. Additionally, respiratory filter devices should be used. General protective measures involve handling HF inside a fume hood, ensuring proper ventilation or exhaust systems, displaying warning signs, providing easy access to running water, having safety showers and eyewashes available, and following a Standard Operating Procedure (SOP) document. HF containers should be made of polyethylene or Teflon, clearly labeled, securely supported, tightly closed, and stored away from heat and direct sunlight. A first aid kit should be readily accessible, including 2.5 percent Calcium gluconate gel and 1 percent Calcium gluconate eyewash solution containing 0.13 percent Benzalkonium chloride (Zephiran Chloride).

In cases of dermal exposure, immediate actions should include quick assessment, removal of contaminated clothing and jewelry, and double-bagging to prevent secondary exposure. Decontamination should be performed using copious amounts of water, saline, or a soap and water solution. Neutralization agents such as Calcium gluconate, Benzalkonium chloride, Polyethylene glycol, Magnesium oxide, or Hexafluoride can be used. Assessment and management of life-threatening conditions like airway compromise or cardiac arrhythmias are crucial.

The decontamination and neutralization process primarily involves rinsing and diluting the acid with water, which lacks the ability to actively bind or chelate the chemical. Therefore, neutralizing agents like Calcium gluconate are vital as they can chelate the free fluoride ions, forming insoluble salts. Calcium gluconate should be applied multiple times to mitigate fluoride ion damage.

Treatment modalities vary based on the route of exposure. For dermal exposure, rinsing with water or saline for at least 30 minutes is commonly used, along with decontamination using dish soaps with a pH of 8 to 10.5. Calcium gluconate gel (2.5 percent) should be applied and reapplied every ten to 15 minutes, turning white as it binds to fluoride ions. Subcutaneous infiltration or injections of Calcium gluconate may be necessary, considering compartment syndrome. Topical therapy can also include Benzalkonium chloride solution (0.13 percent) or Hexafluoride.

For eye exposure, irrigation with cool water or saline for 15 to 30 minutes is recommended. Intermittent irrigation with a sterile one percent Calcium gluconate solution or Hexafluoride can be used. Inhalation exposure may require artificial respiration, 100 percent oxygen, and nebulized Calcium gluconate (2.5 to 3 percent). Severe cases may necessitate endotracheal intubation or surgical airway. Burns with concentrated HF require intensive care unit admission, careful monitoring, and blood sampling for fluoride, potassium, and calcium levels. Hemodialysis might be necessary for fluoride removal and correction of imbalances. Burns larger than four square inches or gaseous HF exposure with respiratory irritation warrant immediate ICU admission. Analgesic agents are not advisable, and pain relief indicates treatment effectiveness.

Conclusion

In conclusion, exposure to hydrofluoric acid can result in serious chemical burns called hydrofluoric acid burns. These burns can have serious effects on the victim, frequently needing urgent medical care and specialized therapy. In order to avoid severe burns, it is imperative to handle hydrofluoric acid with the utmost caution and to make sure the necessary safety precautions are in place. To reduce potential consequences and speed up the healing process for those who have suffered burns with hydrofluoric acid, prompt and adequate medical care is required.