Ураження фтористоводневою кислотою

Pain is typically the first symptom to manifest after dermal exposure and precedes signs of chemical burns, such as erythema (1st degree), edema and bullae formation (2nd degree), or gray-white discoloration (3rd degree). Pain is often more severe than expected based on apparent dermal involvement. If the fingers and nail beds are burned, the nails may remain intact, and pain may be severe despite apparent absent or minimal involvement of the nails and skin.

Oral occupational exposure to HF is less common but may occur when aqueous solution containing HF is stored in unmarked containers (eg, water bottles). Nonoccupational oral HF exposure may result from attempts at self-harm or exploratory ingestion by young children.

Ingestion of dilute HF solution may result in oropharyngeal erythema and edema and gastrointestinal irritation; ingestion of a small volume may be asymptomatic. Ingestion of concentrated HF solution results in hemorrhagic gastritis and pulmonary toxicity similar to inhalational exposure.

Inhalational exposure to HF most commonly results in upper airway and chest pain (described as burning), cough, and shortness of breath. Patients may also report nausea, vomiting, and headache and a burning sensation in skin exposed to HF vapor. Time to symptom-onset is inversely proportional to the airborne concentration of HF. Pharyngeal erythema and edema may be present, as may wheezing, rales, and respiratory distress. With more severe inhalational exposure, patients may develop hemorrhagic alveolitis with hemoptysis or acute hypoxemic respiratory failure (adult respiratory distress syndrome [ARDS]), which may be fatal.

Dermal, oral, or inhalational HF exposure may result in systemic fluoride toxicity (ocular exposure has not been implicated in systemic toxicity). Onset of systemic toxicity is more rapid after oral HF exposure because systemic absorption is more rapid after oral exposure than dermal exposure. Dermal exposure to concentrated HF solution may result in systemic fluoride toxicity even when the body surface area involved is small.

Systemic fluoride toxicity is marked by hypocalcemia, hypomagnesemia, and impaired cardiac contractility. Hyperkalemia may also occur. Cardiac arrhythmias including polymorphic ventricular tachycardia (torsades de pointes), ventricular fibrillation, and asystole may occur. Coagulopathy may result from hypocalcemia.

Ocular exposure to HF may result from a splash injury involving an aqueous solution or from gaseous HF. Mild (more dilute) exposure may cause eye pain, conjunctival injection, and chemosis and may not manifest for hours after the exposure. If the exposure is more concentrated, onset of symptoms is more rapid; corneal coagulative necrosis may occur, and the globe may rupture.

Prognosis after mild dermal HF exposure is good if the patient is promptly evaluated and treated. As with other chemical burns, symptoms typically resolve over a period of days to weeks, depending on the severity of the burn.

Patients who have ingested a dilute HF solution may develop reversible oropharyngeal or gastrointestinal (GI) irritation or may remain asymptomatic and have a benign prognosis. Ingestion of concentrated HF solution may result in fatal GI hemorrhage or systemic fluoride toxicity, which may be fatal. If patients with severe GI burns survive, long-term sequelae including strictures may develop.

Patients with systemic fluoride toxicity are at high risk of cardiac arrhythmia and hypotension.

Prognosis after inhalational exposure depends on the intensity and chronicity of exposure. If inhalational exposure is mild to moderate, symptoms may resolve spontaneously over a period of hours to days. More intense exposures may result in persistent upper airway irritation (reactive upper airways dysfunction syndrome [RUDS]) or pulmonary irritation (reactive airways dysfunction syndrome [RADS]) that persists for months to years. Chronic occupational HF exposure may result in a bronchial hyperreactivity syndrome called "potroom worker’s asthma". Serial pulmonary function tests may be used to monitor RADS and bronchial hyperreactivity in workers exposed to HF.

If ocular exposure is mild, conjunctival irritation and chemosis (which typically occurs) resolves over a period of several days, and no long-term sequelae are anticipated. If exposure is more severe, corneal injury or sloughing may result in chronic conjunctivitis, corneal opacification or vascularization, glaucoma, or keratitis sicca.

Immediate decontamination should be done, including removing contaminated clothing or work gear and flushing the affected areas with water for 15 minutes. After decontamination, 2.5% calcium gluconate or calcium carbonate gel should be applied to the affected area and covered with an occlusive nonadherent dressing (for finger injuries, gel can be placed in a surgical glove put on the patient's hand). Application of the soluble calcium salt to areas exposed to HF results in complexation of calcium with fluoride, which forms soluble calcium fluoride. This reaction results in a fluoride concentration gradient that favors the diffusion of HF out of the body and into the gel.

Topical calcium is applied until pain is relieved.

If pain persists despite application of topical calcium or if the patient was exposed to concentrated HF solutions, calcium gluconate may be given by subcutaneous or intra-arterial injection. Calcium chloride should not be given by these routes because tissue necrosis is a risk.

For subcutaneous injection, 0.5 mL of 5% calcium gluconate per square centimeter can be infiltrated. Iatrogenic compartment syndrome is a risk in small tissue compartments (eg, the hand). If those areas are affected, risks and benefits of calcium infiltration should be weighed. No more than 0.5 mL of solution should be injected per digit.

For intra-arterial administration, 50 mL of 2% calcium gluconate can be infused into the artery perfusing the affected area over a 4-hour period. Risks of arterial cannulation should be considered when deciding whether to do this procedure.

All but the most minor or superficial exposures require transfer to a burn center for possible surgical intervention, including skin grafting, debridement of necrotic tissue, fasciotomy, and amputation.

Gastric emptying with an orogastric (OG) or nasogastric (NG) tube should be done as soon as possible after an oral HF exposure. Gastric emptying is unlikely to be beneficial if >1 hour has elapsed since the ingestion. The same OG or NG tube may be used to deliver calcium or magnesium salt to the GI tract, although evidence of its benefit is limited. As with other caustic ingestions, activated charcoal is contraindicated.

A GI specialist should be consulted about possible endoscopy.

Patients with systemic fluoride toxicity should be admitted to an intensive care unit for cardiac monitoring, serial electrocardiography and, if depressed cardiac contractility is suspected, echocardiography. Serial measurement of calcium, magnesium, potassium, and phosphate levels is done and treated as required.

Treatment of systemic fluoride toxicity includes calcium and magnesium salts, given IV, to replenish calcium and magnesium lost from complexation with fluoride. IV fluids, and vasopressor and/or inotropic support are given for depressed cardiac contractility. Magnesium sulfate may be given as a loading dose of 4 to 6 g IV over 60 minutes, followed by 2 to 4 g/hour infusion. Patients should be monitored for hypotension and respiratory depression. Calcium gluconate may be given as a loading dose of 6 g IV over 60 minutes, followed by infusion of 0.5 mEq/kg/hour. If a central venous catheter is available, calcium chloride may be used instead of calcium gluconate at a loading dose of 2 g, followed by infusion of 0.5 mEq/kg/hour. If hypocalcemia or hypomagnesemia persist or recur, loading doses of both magnesium and calcium may be repeated. Amount of supplementary electrolytes to administer should be guided by real time blood testing.

Sodium bicarbonate may be given IV for acidemia, although few studies address its efficacy.

Fluoride ions are eliminated by hemodialysis. Hemodialysis should be considered for patients with systemic toxicity, although such patients may be too clinically unstable to have the procedure.

Inhalational exposure may be treated with nebulized calcium gluconate; 2.5% and 5% calcium gluconate can be given as intermittent or continuous treatments. Patients with wheezing and bronchospasm can also be treated with a nebulized beta agonist (eg, albuterol), nebulized ipratropium, and oral or IV corticosteroids. Patients with ARDS-like symptoms may be treated with standard interventions for ARDS, including positive pressure ventilation, use of high positive end-expiratory pressure, and proning.

Prompt decontamination is most important. Irrigation at a workplace eyewash station should be followed by continued irrigation en route to the hospital. Continued irrigation in an emergency department may be done using normal saline or sterile water applied to the affected eye or eyes using a Morgan lens. Irrigation with at least 2 to 3 liters of fluid is recommended. Ocular irrigation with calcium-containing solutions, which are irritating and may create corneal injury, should not be used. Consultation with an ophthalmologist should be obtained in the acute care setting, and ophthalmology follow-up should be arranged.