Hydrofluoric Acid Injury 

Hydrofluoric Acid Injury 

Summary

Key Points

  • HF (hydrofluoric acid) easily penetrates skin, soft tissues, and lipid membranes
  • Exposure causes both direct tissue damage and systemic toxicity
  • Identification and timely treatment are critical actions for HF burns to prevent further absorption and block progressive destruction by fluoride ions
  • Diagnosis is made based on exposure history and clinical findings; pain out of proportion to observed injuries in the setting of white-gray cutaneous chemical burns is pathognomonic
  • Clinical evaluation should include appropriate laboratory tests (most importantly electrolytes), imaging, and ECG to evaluate for complications of HF exposure
  • After decontamination, calcium gluconate should be administered to neutralize the acid
  • Consult with the Poison Control Center or a toxicologist for guidance with management and disposition; establish contact with nearest burn center for possible referral
  • Medical personnel must consider risk of contact and inhalation of HF before performing cardiopulmonary resuscitation in an unstable patient with HF exposure and all attempts should be made to use appropriate personal protective equipment
  • A variety of complications may arise dependent on the method and significance of exposure
  • Most exposures are more painful that dangerous; however, high mortality is seen in exposures with high concentrations of HF

Alarm Signs and Symptoms

  • Respiratory distress
  • Cardiac arrhythmia
  • Significant percentage of body surface involvement

Basic Information

Background Information

  • HF (hydrofluoric acid) is an inorganic acid used in various industrial fields and domestic products
  • Concentrations1
    • HF is available in concentrations less than 12% as a rust removal agent, domestic cleanser, and automobile wheel cleaner
    • Industrial HF solutions range from 20% to 70% concentration and are used in glass, semiconductor, and automobile industries1
  • Routes of exposure include skin/eye contact, inhalation, and ingestion
  • Exposure leads to both focal tissue destruction/burns and systemic toxicity

Epidemiology

  • Chemical burns account for up to 10.7% of all skin burns but are responsible for up to 30% of all burn-related deaths2
  • Upper extremity is the most often reported site of injury2
  • Young males are most commonly affected2
  • Most chemical burns are work-related incidents2

Etiology and Risk Factors

  • HF easily penetrates skin, soft tissues, and lipid membranes
  • Exposure causes both direct tissue damage and systemic fluoride toxicity, which leads to an array of dangerous sequelae
  • Tissue destruction occurs via 2 primary mechanisms
    • Hydrogen ion causes corrosive damage similar to other chemical burns3
      • Causes cutaneous, ocular, and mucus membrane burn lesions
      • Immediate effects create visible tissue destruction, discoloration, and ulceration or necrosis accompanied by intense pain
    • Fluoride anion causes direct tissue destruction through liquefactive necrosis
      • Fluoride ion is easily absorbed in the bloodstream and carried to all body organs (in proportion to their vascularity) where it induces liquefactive necrosis and cell death
      • Destroys nerves, blood vessels, and tissues2
  • Systemic fluoride toxicity
    • Toxicity may be out of proportion to total body surface area exposure1
      • Do not delay treatment due to lack of apparent symptoms, because this may allow for more severe systemic damage to occur1
    • Fluoride ion causes massive electrolyte imbalances through the process of chelating with cellular magnesium and calcium
      • Causes local calcium and magnesium depletion and inhibition of the Na-K-ATPase pump (adenosine triphosphatase) leading to local hyperkalemia4
      • Electrolyte imbalance and enzyme inhibition lead to cardiovascular, pulmonary, renal, and neuromuscular symptoms which can ultimately precipitate cardiac arrhythmias and death5

Diagnosis

Approach to Diagnosis

  • Decontamination of the patient should be completed before any patient contact
  • Diagnosis is made based on history of exposure and physical examination findings
  • Essential aspects of exposure history include type of exposure, chemical formulation, and concentration of HF (hydrofluoric acid)
    • Report of pain at the site of the exposure, which is out of proportion to the visible injury, is pathognomonic6
      • Due to shifts in potassium on cellular level, leading to continued nerve depolarization6
  • Physical examination should then proceed in a rapid, systemic manner to identify and treat any life-threatening findings followed by a thorough head to toe evaluation
  • No testing is readily available to aid in determination of substance; however, laboratory studies including an electrolyte panel are of utmost importance to assess for systemic toxicity
    • Possibility of delayed systemic toxicity poses diagnostic and therapeutic challenges
    • Electrolytes should be repeated during treatment to monitor for development of abnormalities or worsening of previously found imbalances2
  • Studies such as chest radiography, CT, endoscopy, and bronchoscopy are useful in specific clinical scenarios to assess for severity of injury
  • ECG is vitally important as cardiac arrhythmias are a significant complication of systemic HF toxicity
  • Poison Control Center (1-800-222-1222) is an invaluable resource that is available 24/7
    • Early consultation with a toxicologist via the Poison Control Center or an on-call toxicologist is recommended when presented with a patient reporting chemical exposure

Workup

History

  • Review any available EMS data (emergency medical services) such as vital signs enroute and any decontamination interventions before arrival
  • Clarify the circumstances of the exposure, including mechanism of exposure and any observations regarding environment where incident occurred
  • Key details regarding the incident should be elicited which are as follows:
    • Method of exposure (inhalation, skin/eye contact, ingestion)
    • Name or description of chemical solution (including concentration if available)
    • Timeline of exposure (time of initial exposure, duration)
    • Setting in which the injury occurred (ie, work, home, motor vehicle collision, gardening, assault)
  • Obtain a description of focal areas of pain and any other symptoms
    • Ocular exposures may cause irritation, pain, and tearing
    • Ingestion may cause the patient to report abdominal pain, dysphagia, nausea, vomiting, and diarrhea
    • Inhalation may cause nasal irritation, mucosal bleeding, coughing, dyspnea, laryngitis, laryngospasm, and/or retrosternal pain
    • Systemic absorption may cause confusion, seizures, and spasms/tetany
  • Past medical history should be obtained in a targeted manner; the mnemonic “AMPLE” may be useful
    • Allergies
    • Medications
    • Past medical/surgical history (including tetanus immunization status)
    • Last oral intake
    • Events/environment leading to injury
  • Review of systems should be obtained to minimize chance of missing pertinent associated symptom(s)

Physical Examination

  • Figure 1. Silver-gray necrosis due to extremity exposure to HF.HF, hydrofluoric acid. From Dinis-Oliveira RJ et al. Clinical and forensic signs related to chemical burns: a mechanistic approach. Burns. 2015;41(4):658-679.
  • All medical staff caring for patients with chemical exposure should take extreme precaution and use appropriate personal protective equipment before initiating contact or close proximity
  • Decontamination should be performed by EMS before transport or on arrival if patient arrives via private vehicle
    • All clothing and jewelry should be removed and double bagged
    • Exposed skin and hair should be rinsed with cold or warm water or saline for at least 30 minutes2 (may be done concurrently while providing evaluation and treatment)
    • A soft brush applied in a head to toe motion may be used to neutralize acid with soap and water solution with a pH less than 84
    • An ice pack may be used to induce vasoconstriction in an affected area
  • Obtain initial vital signs in addition to patient weight and point of care glucose measurement
    • Cardiac monitoring, IV access, continuous pulse oximetry, and blood pressure monitoring should be initiated on presentation with complaint of chemical injury
    • End-tidal CO2 monitoring should be used for patients with inhalation exposures
  • A primary survey should be conducted promptly to evaluate for life-threatening emergencies
    • Rapidly assess airway, breathing, and circulatory/neurologic functioning
    • Significant abnormalities should be addressed on identification
    • Spinal precautions, including spine immobilization and use of a cervical collar, may be indicated based on patient’s specific circumstances
  • Secondary survey should be performed as soon as possible once the primary survey has been completed, but it should not delay initiation of resuscitation measures
    • Secondary survey should progress from head to toe in a systematic fashion to minimize potential for missed injuries
    • Particular areas of focus related to type of exposure are as follows:
      • Dermatologic exposure
        • HF burns (hydrofluoric acid) classically present as white/gray tissue (Figure 1) with surrounding erythema and edema7
        • Ulcers and necrosis are rapidly observable with higher concentrations7
        • Low concentrations may not produce pain or erythema until as late as 24 hours after exposure1
        • Note surface area and thickness of cutaneous burns as well as any joint involvement
        • HF easily penetrates nailbeds; these should be examined thoroughly
      • Ocular exposure
        • Initially presents with conjunctival injection followed by edema and congestion
        • Corneal findings may include corneal erosion and ulceration, with eventual corneal opacification
        • Visual acuity testing should be completed
        • Modified Roper-Hall classification system may be used for grading of ocular chemical burns (Table 1)8
      • Ingestion
        • May cause oral mucosal erythema, bleeding, and/or ulcerations
        • Abdominal tenderness/peritonitis due to perforation may be present
      • Inhalation
        • Initial upper airway findings may include nasal irritation and inflammation, dryness, and mucosal bleeding
          • Later findings include eventual ulceration, bleeding, and possible perforation of the nasal septum
        • Laryngeal exposure may result in stridor, laryngitis, and/or laryngospasm
        • Pulmonary findings may include tachypnea and adventitious breath sounds triggered by pulmonary edema, pleural effusion, and possible lung collapse
    • Evidence of systemic sequelae may occur secondary to any route of exposure
      • Cardiac
        • Irregular cardiac rate, rhythm, or sounds
        • Poor extremity perfusion and/or cyanosis
      • Neurologic
        • Altered mental status or coma
        • Seizure activity
      • Musculoskeletal
        • Paresthesias, paresis, and/or paralysis
        • Carpopedal spasms and/or generalized tetany (possible findings in high concentration exposures or later in clinical course)
    • Laboratory Tests
    • No readily available test exists to evaluate for the presence of HF
    • Evaluating electrolyte imbalance is of utmost importance for patient management, because this may lead to cardiovascular collapse and death
      • Electrolyte testing should include:
        • Basic metabolic panel
        • Ionized serum calcium
          • Hypocalcemia may develop with as little as 1% total body surface area exposure to concentrated HF6
        • Serum magnesium
        • Serum fluoride
    • Other studies of import include:
      • Lactic acid
        • Indicative of metabolic acidosis and tissue ischemia
      • CK/CPK (creatine kinase/creatine phosphokinase)
        • Reflects extent of muscle breakdown and necrosis
      • Arterial (or venous) blood gas
        • Provides insight into gas exchange in the setting of inhalation injury as well as information on acid-base status
      • Troponin
        • Elevated troponin levels may indicate direct cardiac toxicity or demand ischemia due to systemic sequelae
      • Urinalysis
        • New hematuria or proteinuria may indicate renal dysfunction and/or cortical necrosis
    • Imaging Studies
    • Chest radiograph should be obtained in all patients with respiratory exposure to evaluate for pneumonitis or pulmonary edema2
      • Respiratory exposure should be considered even with dermatologic burns as close contact with solution can lead to inhalation
    • CT imaging to evaluate extent of soft tissue damage or organ involvement beneath burn site may be warranted2
      • Chemical burns are difficult to assess and commonly underestimated2
      • Deep tissue injury may be present beneath seemingly superficial burns1
    • Diagnostic Procedures
    • Endoscopy should be considered to determine extent of gastrointestinal mucosal injury after ingestion2
    • Bronchoscopy may aid in evaluation of pulmonary endothelium damage following inhalation/aspiration2
    • Diagnostic Tools
    • ECG is imperative for the evaluation of a patient with HF exposure
      • Electrolyte imbalances caused by the formation of the fluoride salts may precipitate a number of ECG abnormalities
        • Prolonged QT from hypocalcemia
        • Peaked T waves and progression to bradyarrhythmias and eventual arrest from hyperkalemia
        • Polymorphic ventricular tachycardia, specifically torsades de pointes, from hypomagnesemia9
      • Free fluoride ions may also stimulate the myocardium through direct activation of myocardial adenylyl cyclase which increases cyclic adenosine monophosphate, thus inducing refractory ventricular fibrillation
    • Echocardiogram may be useful to evaluate for cardiac sequelae such as decreased ejection fraction, wall motion abnormalities, or pericardial effusion due to systemic fluoride toxicity
    • Differential Diagnosis
    • View full sizeTable 2. Differential Diagnosis: Chemical burns.Chemical exposureDescriptionSigns and symptomsSulfuric acid
      • Clear, colorless, odorless, oily liquid
      • Easily accessible
      • Used to restore exhausted car batteries and in leather industry
      • Used in drain cleaner
      • Burns are dark brown colored
      • Dyspnea, mouth and throat pain
      • Chest pain, cardiovascular collapse, hypotension
      • Hematemesis, gastric perforation
      Hydrochloric (muriatic) acid
      • Colorless with distinctive pungent smell
      • Used as bleaching agent in food, textile, metal, and rubber industries
      • Used in production of batteries and fireworks
      • Gray or white discoloration of skin and mucosa
      • Bulla does not form
      • Vomiting, hematemesis
      • Tachypnea, cough, pneumonia, laryngospasm, respiratory failure
      Paraquat
      • Solution with pungent smell
      • Form marketed in the United States has blue dye to limit accidental ingestions
      • Widely used in herbicides
      • Usually deliberate ingestion but also accidental exposure when spraying
      • Skin burns/blisters
      • White nail discoloration
      • Ulcers in oral mucosa, esophagus, stomach
      • Pulmonary edema and fibrosis
      • Multiorgan failure, seizures
      White phosphorus
      • Smoke-producing, waxy, yellow transparent combustible solid
      • Used in fireworks, fertilizers, and hand grenades
      • Highly flammable
      • Partial to full thickness burns that are yellow, waxy, and necrotic
      • Eye irritation with foreign body sensation, lacrimation, photophobia, corneal perforation
      • Endophthalmitis, blindness
      • Respiratory tract irritation, cough
      Sodium hydroxide
      • White crystals without odor or taste, making it easy to swallow
      • Flakes, tablets, or solutions (most hazardous)
      • Used in manufacturing of soap, paper, explosives, paint, cotton, bleach, and beauty products
      • Skin burns ranging from white to sloughy gray to black
      • Oropharyngeal pain, dysphagia, drooling, vomiting, excessive salivation
      • Ulcerative mucosal burns
      • Dyspnea, stridor
      Caption: Data from Dinis-Oliveira RJ et al. Clinical and forensic signs related to chemical burns: a mechanistic approach. Burns. 2015;41(4):658-679.
    • Treatment
    • Approach to Treatment
    • Rapid decontamination to reduce ongoing absorption and progressive tissue damage is of utmost importance
      • All staff must wear appropriate personal protective equipment before initiating contact
      • Sterile water is currently the best decontaminating solution under most circumstances10
        • Both Diphoterine and Hexafluorine are safe for topical use and likely efficacious, but studies have yet to prove their superiority11
          • Hexafluorine is an amphoteric hypertonic compound with absorbing and chelating properties marketed as a decontamination fluid for HF skin exposures11
          • Diphoterine is an irrigating agent for chemical burns which rapidly neutralizes acids and alkalis, potentially faster than water alone, but larger trials are needed to prove its efficacy12
        • In addition, these are not readily available in most hospitals and EMS (emergency medical services) transport vehicles12
    • Life- or limb-threatening abnormalities identified on the initial examination should be addressed using escalating supportive measures and appropriate interventions
    • Calcium gluconate is the most appropriate antidote
      • Calcium gluconate chelates the free fluoride ions, thus neutralizing their toxic effects
      • Should be administered/applied immediately after decontamination is complete9
      • Available in a variety of formulations for different methods of application depending on route of exposure and characteristics of burn
    • Dermatologic Exposure
    • Calcium gluconate
      • Topical
        • Cover burn areas with sterile gauze moistened with 10% calcium gluconate solution4
        • When used as gel, rub 2.5% calcium gluconate into affected area using chemical-resistant gloves for 15 to 30 minutes with reapplication every 10 to 15 minutes, then 4 to 6 times daily for 3 to 4 days4
          • If 2.5% calcium gluconate gel is not available, combine 3.5 g of calcium gluconate to 5 ounce tube of any water-soluble lubricant and apply in same manner1
          • If burn is on hand, may apply surgical glove to patient’s hand after gel application to ensure sustained therapeutic effect1
        • Note: calcium gluconate gel cannot penetrate nails; thus, they must be drilled/split/removed to allow treatment to the subungual tissue3
      • Subcutaneous
        • Injection of sterile aqueous calcium gluconate solution underneath burned area and into adjacent skin improves the neutralizing efficacy13
          • Useful in cases of large burn areas, deep penetration of burns, exposure to high HF concentrations (more than 50%), treatment delay, or significant pain despite topical treatment
          • Recommended dose limited to a 0.5 mL/cm2 surface area with a 5% to 10% solution3
          • Maximum of 0.5 mL per digit for finger burns3
          • Use a small gauge needle (ie, 30G)3
          • Risks include compartment syndrome and pressure necrosis3
      • IV
        • Local IV infusion via Bier block technique2
          • Place IV catheter distal to burn
          • Place (but do not inflate) double-cuffed pneumatic tourniquet proximally on the limb
          • Elevate limb 1 to 2 minutes to aid in passive venous drainage
          • While still elevated, apply elastic bandage from the IV catheter to the pneumatic tourniquet to further encourage venous drainage
          • While maintaining elevation, inflate the cuff to a pressure at least 75 to 100 mm Hg above patient’s systolic blood pressure
          • Ensure brachial and radial pulses are absent
          • Over 2 minutes, inject 15 mL of 10% calcium gluconate diluted with 35 mL of 0.9% saline solution
          • After 20 minutes, slowly release cuff
          • Consider in burns of forearm, hand, or digits if topical therapy fails14
      • Intra-arterial
        • Used for digital burns and severe burns with intractable pain despite traditional gel therapy3
        • Most effective for HF burns in regions with clear arterial distributions such as extremities or digits2
        • Initial dose: 50 mL of 4% calcium gluconate infused over 4 hours2
          • May repeat at 12-hour intervals or use continuous infusion of 2% calcium gluconate2
        • Complications are frequent including arterial spasms and bleeding, ulnar and median nerve palsies, carpal tunnel syndrome, and hypercalcemia3
        • Consideration and utilization of this therapy is institution dependent
    • DMSO (dimethyl sulfoxide)
      • Topical DMSO may be considered as an adjunct medication
        • Apply topically using DMSO 50% with calcium gluconate 10% mixed together into a surgical jelly2
      • Functions as a solvent to increase penetrability of calcium and magnesium ions2
        • Reduces inflammatory response
        • Provides potential analgesic effect
    • Avoid using local anesthetic injections (eg, lidocaine)
      • This does not treat the source of the injury
      • Perception of pain is relied on as an indicator of treatment efficacy2
    • Gastrointestinal Exposure
    • Do not induce vomiting2
    • Calcium gluconate
      • Oral rinse
        • If patient is conscious and protecting their airway, rinse mouth with water or 5% to 10% solution of calcium gluconate16
      • Gastric lavage
        • Perform gastric suction and lavage with neutralizing solution (water, milk and/or 10% calcium gluconate mixture) using a small nasogastric tube within the first 60 minutes after ingestion17
          • Indicated if large-dose HF has been ingested, oral lesions are present, or patient exhibits persistent esophageal discomfort17
    • Endoscopy may be performed to evaluate extent of the injury after patient is stabilized and acid content is neutralized
    • Respiratory Exposure
    • Patient should be moved to fresh air immediately after event
    • 100% FiO2 should be administered at 10 to 12 L/minute flow rate as soon as possible with escalation in respiratory support as indicated based on patient’s respiratory status and response17
    • Calcium gluconate
      • Nebulized calcium gluconate solution 2.5% to 3% should be administered via positive pressure ventilation2
    • Bronchoscopy provides therapeutic (aspiration and lavage of affected bronchi) and prognostic benefit2
    • Ocular Exposure
    • Anesthetic eye drops may be administered for rapid onset anesthesia4
    • Early initiation of irrigation results in lower grade of ocular burn severity and improved outcomes18
      • There is current debate about which agent is optimal: 1% calcium gluconate eye drops, sterile saline solutions, or Hexafluorine19
      • Evidence most strongly supports immediate irrigation with copious water or 0.9% normal saline for 30 minutes (if available, devices such as Morgan Lens should be used)19
        • Hexafluorine shows potential to be a frontline agent in ocular exposures based on limited data available, but it has not yet been found to be any more effective than rinsing with water due to lack of high-quality independent research10
    • After irrigation, 1% calcium gluconate eye drops should be administered every 4 hours until ophthalmologic evaluation is possible for further recommendations16
    • Treat any corneal ulcers with antibiotic eye drops, typically a fluoroquinolone16
    • Management of Systemic Toxicity
    • Replace electrolytes (primarily magnesium, calcium, potassium) as quickly as possible, using institutional protocols where available
    • Consider administration of diuretics and alkalinization of urine with sodium bicarbonate to increase renal excretion and decrease systemic effects17
      • Half-life of fluoride is 12 to 24 hours and is eliminated primarily through renal excretion
    • Hemodialysis may be used in patients with severe systemic toxicity20
      • Significant fluoride level reduction (70%) after 3 hours of hemodialysis has been shown, indicating potentially vital role of hemodialysis21
    • Treat arrhythmias, such as ventricular fibrillation, per ACLS protocol (Advanced Cardiovascular Life Support)22
    • Extracorporeal membrane oxygenation may be used if other measures of respiratory support do not result in sufficient oxygenation4
    • Drug Therapy
    • View full sizeTable 3. Drug Therapy: Calcium gluconate.MedicationRouteAdministrationCalcium gluconateTopicalSolution: cover burn areas with sterile gauze moistened with 10% calcium gluconate solution4Gel: rub 2.5% calcium gluconate into area using chemical-resistant gloves for 15 to 30 minutes with reapplication every 10 to 15 minutes until evaluation by physician and then 4 to 6 times daily for 3 to 4 days4SubcutaneousInject a 5% to 10% solution (max of 0.5 mL per digit for finger burns) using a small gauge needle such as 30G6Recommended dose limited to a 0.5 mL/cm2 surface area due to risk of compartment syndrome and pressure necrosis7IVInfuse 15 mL of 10% calcium gluconate diluted with 35 mL of 0.9% saline solution over 2 minutes using Bier Block technique14Oral rinseRinse mouth with 5% to 10% solution of calcium gluconate16Gastrointestinal lavageAdminister 10% calcium gluconate mixture using a small nasogastric tube within 60 minutes after ingestionNebulizedNebulize calcium gluconate solution, 2.5% to 3%2Intra-arterialInitial dose: 50 mL of 4% calcium gluconate infused over 4 hours2OcularInstill 1% calcium gluconate eye drops every 4 hours until ophthalmologic evaluation is possible for further recommendations16
    • Treatment Procedures
    • Debridement
      • Immediate extensive surgical debridement is reserved for high-concentration burns or those that have systemic toxicity symptoms despite medical management3
      • Focal skin blisters should be opened with removal of necrotic tissue as soon as possible after initial stabilization as this decreases healing time4
    • Escharotomy
      • Edema in extremities may lead to compartment syndrome requiring emergent escharotomy2
    • Admission Criteria
    • Admission is typically recommended for any patient with HF burns
      • Use clinical acumen to determine appropriate level of admission
      • Err on the side of caution
        • Chemical burns are difficult to assess and are frequently underestimated
        • Potential systemic toxicity due to HF exposure is significant and may be delayed
        • Use specialist resources whenever possible for determination of disposition (eg, toxicologists, burn specialists)
      • ICU should be used for any life-threatening condition
        • Substantial skin burns (covering an area greater than the size of the palm of a hand and producing pain within 1 hour of exposure or with skin changes), seizures, coma, respiratory distress, hemodynamic instability, recurrent cardiac arrhythmias, and consideration of intra-arterial infusions23
    • American Burn Association’s burn center referral criteria recommend consultation with a burn specialist and consideration of transfer to the nearest burn center for any chemical burn24
      • These guidelines are designed to aid in clinical decision-making; local and regional infrastructure, resources, and relationships may determine the necessity and timeliness of burn center referral
    • Discharge after emergency department management may be considered in the following circumstances:23
      • Patients with isolated eye exposure without signs of irritation after treatment may be discharged with primary care and ophthalmological follow-up and return precautions
      • Per CDC guidelines, discharge with close follow-up and strict return precautions may be considered in patients with burn area less than the size of the palm of the hand who have normal calcium levels and have remained asymptomatic for 6 hours after treatment in the emergency department
    • Consultation with a toxicologist and/or the Poison Control Center may help determine most appropriate discharge in specific patient scenarios
    • Special Considerations
    • Contact Precautions
    • Recommended personal protective equipment includes tightly sealed goggles, full face shield, rubber gloves (nitrile, butyl, or neoprene), respiratory filter device, chemical-resistant jumpsuit (or at least long pants and long-sleeved shirt), and close-toed shoes23
    • Medical personnel must consider risk of contact and inhalation of HF before performing cardiopulmonary resuscitation in an unstable patient with HF exposure25
    • HF contaminated waste should be neutralized using sodium carbonate (Na2CO3) and/or calcium carbonate (Ca2CO3) powder; the subsequent neutralized solution can then be disposed of under running water4
    • Containers for HF contaminated waste should be chemically resistant and clearly labeled with a “hazardous waste” tag
    • Pediatric Patients
    • Children are more vulnerable to HF absorption
      • Relatively larger surface area to body weight ratio increases vulnerability to dermatologic absorption4
      • Greater lung surface area to body weight ratio and increased minute ventilation per weight lead to increased amount of inhalational absorption in children than in adults4
      • May consider nebulized racemic epinephrine for children who develop stridor26
        • Must monitor closely for arrhythmias during treatment due to cardiac-sensitizing nature of epinephrine
    • Follow-up
    • Complications
    • Reports of long-term visual defects and blindness have occurred in ocular exposures23
    • Chronic lung disease after HF inhalation is common25
    • Esophageal exposure may subsequently lead to esophageal scarring and stenosis25
    • Cutaneous burns and associated nerve damage may cause persistent pain and extensive scarring25
    • Congestive heart failure provoked by toxic myocarditis has been detected as a long-term complication, 4 months after HF ingestion4
    • Prognosis
    • Given the importance of timely treatment, prognosis is more favorable in patients who are exposed to high enough HF concentrations to exhibit early symptom onset (thus prompting immediate treatment)2
    • Most HF burns are more painful than dangerous, but mortality is a well-documented outcome; therefore, all exposures should be taken very seriously
      • Mortality approaches 100% with 20% total body surface area burn from high-concentration HF6
      • Death has been reported in a case of low body surface area involvement (less than 2.5%) with highly concentrated HF (70%)5
    • Referral
    • Follow-up referrals should be tailored to exposure
      • Ocular involvement requires ophthalmological follow-up
        • Corneal injuries require reexamination within 24 hours23
      • Ingestion requires gastroenterology follow-up
      • Inhalation exposure necessitates pulmonology follow-up
      • Cutaneous exposure may benefit from follow-up with a plastic surgeon or a burn specialist pending patient’s preference and burn location/characteristics
    • References
    • 1.Alper N et al. Management of hydrofluoric Acid burns. Eplasty. 2014;14:ic42.
    • View In Article|Cross Reference
    • 2.Wang X et al. A review of treatment strategies for hydrofluoric acid burns: current status and future prospects. Burns. 2014;40(8):1447-1457.
    • View In Article|Cross Reference
    • 3.McKee D et al. A review of hydrofluoric acid burn management. Plast Surg (Oakv). 2014;22(2):95-98.
    • View In Article|Cross Reference
    • 4.Bajraktarova-Valjakova E et al. Hydrofluoric acid: burns and systemic toxicity, protective measures, immediate and hospital medical treatment. Open Access Maced J Med Sci. 2018;6(11):2257-2269.
    • View In Article|Cross Reference
    • 5.Ozcan M et al. Possible hazardous effects of hydrofluoric acid and recommendations for treatment approach: a review. Clin Oral Investig. 2012;16(1):15-23.
    • View In Article|Cross Reference
    • 6.Robinson EP et al. Hand chemical burns. J Hand Surg Am. 2015;40(3):605-613.
    • View In Article|Cross Reference
    • 7.Dinis-Oliveira RJ et al. Clinical and forensic signs related to chemical burns: a mechanistic approach. Burns. 2015;41(4):658-679.
    • View In Article|Cross Reference
    • 8.Harun S et al. Modification of classification of ocular chemical injuries. Br J Ophthalmol. 2004;88(10):1353-1355.
    • View In Article|Cross Reference
    • 9.Lippert J et al. Management of hydrofluoric acid burns in the emergency department. Cureus. 2020;12(3):e7152.
    • View In Article|Cross Reference
    • 10.Brent J. Water-based solutions are the best decontaminating fluids for dermal corrosive exposures: a mini review. Clin Toxicol (Phila). 2013;51(8):731-736.
    • View In Article|Cross Reference
    • 11.Hultén P et al. Hexafluorine vs. standard decontamination to reduce systemic toxicity after dermal exposure to hydrofluoric acid. J Toxicol Clin Toxicol. 2004;42(4):355-361.
    • View In Article|Cross Reference
    • 12.Zack-Williams SD et al. The clinical efficacy of Diphoterine in the management of cutaneous chemical burns: a 2-year evaluation study. Ann Burns Fire Disasters. 2015;28(1):9-12.
    • View In Article|Cross Reference
    • 13.Stuke LE et al. Hydrofluoric acid burns: a 15-year experience. J Burn Care Res. 2008;29(6):893-896.
    • View In Article|Cross Reference
    • 14.Zhang Y et al. The clinical effectiveness of the intravenous infusion of calcium gluconate for treatment of hydrofluoric acid burn of distal limbs. Burns. 2014;40(4):e26-e30.
    • View In Article|Cross Reference
    • 15.Hatzifotis M et al. Hydrofluoric acid burns. Burns. 2004;30(2):156-159.
    • View In Article|Cross Reference
    • 16.Pu Q et al. Extracorporeal membrane oxygenation combined with continuous renal replacement therapy in cutaneous burn and inhalation injury caused by hydrofluoric acid and nitric acid. Medicine (Baltimore). 2017;96(48):e8972.
    • View In Article|Cross Reference
    • 17.Dünser MW et al. Critical care management of major hydrofluoric acid burns: a case report, review of the literature, and recommendations for therapy. Burns. 2004;30(4):391-398.
    • View In Article|Cross Reference
    • 18.Wiesner N et al. First aid therapy for corrosive chemical eye burns: results of a 30-year longitudinal study with two different decontamination concepts. Graefes Arch Clin Exp Ophthalmol. 2019;257(8):1795-1803.
    • View In Article|Cross Reference
    • 19.Atley K et al. Treatment of hydrofluoric acid exposure to the eye. Int J Ophthalmol. 2015;8(1):157-161.
    • View In Article|Cross Reference
    • 20.Zhang Y et al. Management of a rare case with severe hydrofluoric acid burns: important roles of neutralizers and continuous renal replacement therapy. Int J Low Extrem Wounds. 2017;16(4):289-295.
    • View In Article|Cross Reference
    • 21.Antar-Shultz M et al. Use of hemodialysis after ingestion of a mixture of acids containing hydrofluoric acid. Int J Clin Pharmacol Ther. 2011;49(11):695-699.
    • View In Article|Cross Reference
    • 22.Panchal AR; Adult Basic and Advanced Life Support Writing Group. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2020;142(16 suppl 2):S366-S468.
    • View In Article|Cross Reference
    • 23.Agency for Toxic Substances and Disease Registry. Medical management guidelines for hydrogen fluoride. Centers for Disease Control and Prevention. Reviewed October 21, 2014. Accessed June 15, 2023.
    • View In Article|Cross Reference
    • 24.American Burn Association/American College of Surgeons. Guidelines for the operation of burn centers. J Burn Care Res. 2007;28(1):134-141.
    • View In Article|Cross Reference
    • 25.Facts about hydrogen fluoride (hydrofluoric acid). Centers for Disease Control and Prevention. Reviewed April 4, 2018. Accessed June 15, 2023.
    • View In Article|Cross Reference
    • 26.Hydrogen fluoride (HF). Agency for Toxic Substances and Disease Registry. Accessed June 15, 2023.
    • View In Article|Cross Reference
    • 27.Gradinger R et al. Toxic myocarditis due to oral ingestion of hydrofluoric acid. Heart Lung Circ. 2008;17(3):248-250.
    • View In Article|Cross Reference
    • 28.Tepperman PB. Fatality due to acute systemic fluoride poisoning following a hydrofluoric acid skin burn. J Occup Med. 1980;22(10):691-692.
    • View In Article|Cross Reference
15585

Sign up to receive the trending updates and tons of Health Tips

Join SeekhealthZ and never miss the latest health information

15856