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Hydrofluoric Acid Burn
Cardiovascular Presentations
Abdominal aortic aneurysm
Acute coronary syndrome (NSTEMI)
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Bell's palsy
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Acute appendicitis
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Incarcerated or strangulated hernia
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Genitourinary and Reproductive Presentations
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Vaginal bleeding (non-pregnant)
Infectious Disease Presentations
Acute sinusitis
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Animal bite
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Febrile neutropenia
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Tick-borne illness (Lyme disease)
Tinea infection
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Viral exanthem
Wound infection
Trauma Presentations
Achilles tendon rupture
ACL and mceniscus tear
Ankle fracture
Ankle sprain
Burn
Calcaneus fracture
Cervical spine fracture
Clavicle fracture
Dental avulsion
Distal radius fracture
Drowning
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Electrical injury
Facial bone fracture
Facial laceration
Femur fracture
Fingertip amputation
Forearm fracture (radius and ulna)
Frostbite
Hand:finger laceration
Heat exhaustion
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Hip fracture
Humeral shaft fracture
Knee dislocation
Knee sprain
Lightning injury
Mandible fracture
Metacarpal fracture
Metatarsal fracture
Muscle strain
Nasal fracture
Non-accidental trauma
Orbital fracture
Patella fracture
Phalanx fracture (finger)
Proximal humerus fracture
Pulmonary contusion
Rib fracture
Rotator cuff tear (acute traumatic)
Scalp laceration
Scaphoid fracture
Shoulder dislocation
Skull fracture
Splenic laceration
Sternal fracture
Supracondylar pediatric fracture
Tendon laceration (hand:wrist)
Thoracic and lumbar spine fracture
Tibia:fibula fracture
Tibial plateau fracture
Toe fracture
Traumatic epistaxis
Traumatic hyphema
Toxicologic Presentations
Acetaminophen toxicity
Alcohol intoxication
Alcohol withdrawal
Anticholinergic toxicity
Anticoagulant overdose
Benzodiazepine overdose
Benzodiazepine:sedative overdose
Beta-blocker and calcium channel blocker toxicity
Carbon monoxide poisoning
Caustic ingestion
Digoxin toxicity
Drug eruption
Foreign body ingestion
Opioid intoxication
Opioid overdose
Opioid withdrawal
Organophosphate
Salicylate toxicity
Serotonin syndrome
Stimulant intoxication (cocaine, methamphetamine)
Tricyclic antidepressant overdose
Psychiatric Presentations
Acute anxiety
Acute psychosis
Agitation:behavioral emergency
Bipolar disorder
Conversion disorder
Major depressive episode
Neuroleptic malignant syndrome
Suicidal ideation and attempt
Musculoskeletal and Rheumatologic Presentations
Acute low back pain (mechanical)
Bursitis
Cervical radiculopathy
Costochondritis
Gout (acute)
Lumbar radiculopathy
Pseudogout
Tendinitis
Dermatology Presentations
Acute eczema (Eczema acute flare)
Allergic contact dermatitis
Erythema multiforme
Henoch-Schönlein purpura
Pressure injury
Psoriasis (acute flare)
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Urticaria (acute)
Environmental and Exposure Presentations
Envenomation (snake, spider, insect)
High-altitude illness
Hypothermia
Hematologic and Oncologic Presentations
Acute chest syndrome
Coagulopathy
Hyperviscosity syndrome
Sickle cell crisis (vaso-occlusive)
Symptomatic anemia
Thrombocytopenia (severe)
Tumor lysis syndrome
Pediatric-Specific Presentations
Bronchiolitis
Croup
Emergency delivery
Febrile seizure
Kawasaki disease
Neonatal jaundice
Neonatal sepsis
Nursemaid's elbow
Pediatric fever 0 to 28 days
Pediatric fever 29 to 60 days
Pediatric fever 61 to 90 days
Pyloric stenosis
Slipped capital femoral epiphysis
Intussusception
Endocrine and Metabolic Presentations
Adrenal crisis
Diabetic ketoacidosis
Hypercalcemia
Hyperosmolar hyperglycemic state
Hypertensive emergency
Hypertensive urgency
Hypoglycemia
Myasthenia gravis crisis
Myxedema coma
Severe hyperkalemia
Severe hyponatremia
Thyroid storm
ENT and Maxillofacial Presentations
Acute laryngitis
Acute otitis media
Acute pharyngitis
Cerumen impaction
Epistaxis (anterior)
Nasal foreign body
Otitis externa
Tympanic membrane perforation
Ophthalmologic Presentations
Acute angle-closure glaucoma
Central retinal artery occlusion
Chemical eye injury
Corneal abrasion
Corneal ulcer
Globe rupture
Ocular foreign body
Orbital cellulitis
Retinal detachment
Obstetric Presentations
Hyperemesis gravidarum
Painful vaginal bleeding in pregnancy
Placenta previa
Placental abruption
Preeclampsia:eclampsia
Preterm labor
Threatened:inevitable:incomplete abortion
Systemic and Miscellaneous Presentations
Anaphylaxis
Angioedema
Cannabis-induced hyperemesis
Hydrofluoric Acid Burn
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ECG Guide
Back
Clinical Assessment Checklist
Browse categories and answer follow-up questions to refine your symptom profile.
Approach to the Critical Patient
Immediate decontamination and stabilization
Primary decontamination priorities
▶
Remove all contaminated clothing and jewelry immediately
▶
Double-bag contaminated materials
Full PPE for treating staff (gloves, gown, face shield)
Copious water irrigation for minimum 15–30 minutes
▶
Begin within minutes of exposure — most critical factor in limiting injury
Diphoterine solution if available — superior fluoride chelation in ex vivo models
Topical calcium gluconate gel application after irrigation
▶
2.5% calcium gluconate gel applied liberally and continuously
Gently massage gel into affected area
Systemic toxicity recognition
High-risk exposure triggers for escalation
▶
TBSA >2.38% — evidence-based cutoff for systemic toxicity (sensitivity 87.5%, specificity 95.9%)
▶
TBSA >5% any concentration or >1% TBSA with >50% HF: ICU mandatory
Death reported with as little as 2.5% BSA burn from concentrated HF
Any electrolyte abnormality on initial labs
▶
Hypocalcemia: ionized Ca <1.12 mmol/l
Hypomagnesemia or hyperkalemia
ECG abnormalities
▶
Prolonged QTc, peaked T waves, widened QRS
Torsades de pointes or ventricular fibrillation: cardiac arrest protocol
Pain refractory to topical calcium gluconate
▶
Escalate to subcutaneous then intra-arterial calcium
Inhalation exposure with respiratory symptoms
▶
Dyspnea, stridor, wheezing: airway assessment and nebulized calcium
Ingestion of any amount of HF: immediate ICU
Resuscitation and monitoring
Mandatory monitoring for all significant exposures
▶
Continuous cardiac monitoring and 12-lead ECG immediately
▶
Repeat ECG hourly or with any symptom change
Telemetry for minimum 6–8 hours observation
Point-of-care ionized calcium every 1–2 hours
▶
Serial magnesium and potassium every 1–2 hours
Target ionized calcium >=1.12 mmol/l
IV access: two large-bore IVs
▶
Arterial line for intra-arterial calcium infusion when indicated
Cardiac arrest from fluoride toxicity
▶
Aggressive IV calcium gluconate (not chloride subcutaneously)
▶
Calcium chloride 1 g IV bolus acceptable in cardiac arrest only
IV magnesium sulfate 2–4 g bolus
Standard ACLS defibrillation
Hemodialysis or CRRT for refractory dysrhythmias
ECMO for refractory cardiac or respiratory failure
Consult triggers
Mandatory consultations
▶
Poison Control Center for all HF exposures (1-800-222-1222)
▶
Real-time guidance on calcium dosing route and concentration
Burn surgery or burn center
▶
TBSA >2.5%, high-concentration exposure, or systemic toxicity
Burns requiring surgical debridement or grafting
Interventional radiology or vascular surgery
▶
Intra-arterial calcium infusion for digital or hand burns
Medical toxicology if available
▶
Refractory electrolyte derangements
Novel exposure routes (ingestion, massive inhalation)
History
Exposure characterization
HF concentration and product type
▶
High concentration (>50%): immediate pain and visible necrosis
▶
Industrial HF, semiconductor etching solutions
Most dangerous — systemic toxicity within minutes to hours
Intermediate concentration (20–50%): pain within minutes
▶
Rust removers, metal cleaners, aluminum brighteners
Low concentration (<20%): delayed pain onset 1–24 hours
▶
Household rust removers, wheel cleaners, bathroom cleaners (5–12%)
Most dangerous diagnostic pitfall — delayed presentation
Exposure details
▶
Route of exposure
▶
Dermal (most common)
Inhalation, ingestion, or ocular splash
Duration of contact before decontamination
▶
Prolonged contact dramatically worsens prognosis
Prompt irrigation within minutes is most critical intervention
TBSA involved
▶
>2.38% TBSA — optimal evidence-based cutoff for systemic toxicity risk
Time elapsed since exposure
▶
Delayed presentations up to 16+ hours reported with dilute HF
Was calcium gluconate gel available and applied at scene
Symptom profile
Pain characterization
▶
Intense, deep, burning pain out of proportion to exam findings
▶
Classic hallmark of HF burns
High-concentration: immediate severe pain
Numbness or paresthesias
▶
May indicate deep fluoride penetration
Subungual burns may present with throbbing pain under nails
Absent pain in early low-concentration burns
▶
High-risk pitfall — may present as painless erythema only
Systemic alarm symptoms
▶
Palpitations, chest pain, syncope
▶
Suggest life-threatening cardiac dysrhythmia
Muscle cramps, tetany, weakness
▶
Hypocalcemia indicator
Nausea, vomiting, abdominal pain
▶
Systemic fluoride toxicity or ingestion
Dyspnea, wheezing, stridor
▶
Inhalation injury — risk of ARDS and pulmonary edema
Visual changes, eye pain, tearing
▶
Ocular HF splash — ophthalmology emergency
Occupational and exposure context
Occupational sources (approximately 80% of cases)
▶
Semiconductor and electronics manufacturing (61% in series)
▶
High-concentration HF used in chip etching
Vehicle washing and detailing
▶
Aluminum brighteners and wheel cleaners
MMWR 2015: significant occupational burden in car washing industry
Glass etching, metal cleaning, electroplating
Chemical and petroleum refining industry
Household exposures
▶
Rust removers, bathroom tile cleaners (5–12% HF)
▶
Often underestimated by patients and providers
Decontamination history
▶
Workplace first aid — availability of calcium gluconate kit
Duration and method of irrigation at scene
Product SDS obtained — confirm exact HF concentration
Past medical history and medications
Conditions increasing systemic toxicity risk
▶
Pre-existing hypocalcemia or hypoparathyroidism
▶
Lower threshold for life-threatening hypocalcemia
Renal disease
▶
Impaired fluoride excretion prolongs systemic exposure
Cardiac disease
▶
Lower threshold for dysrhythmia from electrolyte derangements
High-risk medications
▶
Calcium channel blockers
▶
Compound cardiac risk from hypocalcemia
Digoxin
▶
Electrolyte derangements increase toxicity risk
QT-prolonging drugs
▶
Synergistic with fluoride-induced QTc prolongation
Physical Exam
Vital signs and hemodynamic assessment
Vital sign patterns
▶
Heart rate
▶
Tachycardia: pain, systemic toxicity, or dysrhythmia
Bradycardia: severe hypocalcemia or cardiac arrest precursor
Blood pressure
▶
Hypotension: systemic fluoride toxicity, shock
SBP <90 mmHg: immediate resuscitation
Respiratory rate
▶
Tachypnea: inhalation injury, ARDS, pain response
Temperature
▶
Generally normal acutely unless secondary infection
Skin and wound assessment
Burn appearance by severity
▶
Early or low-concentration burns: deceptively benign appearance
▶
Erythema only — may appear as simple contact dermatitis
Pain out of proportion to visible findings is classic
Moderate burns: progressing gray-white discoloration
▶
Blistering developing over hours
Skin blanching and hardening
Severe or high-concentration burns: liquefactive necrosis
▶
Deep tissue destruction
Tissue may appear tan-gray or black
Anatomical distribution
▶
Hands and digits: most commonly affected site (74% upper limb)
▶
Assess all digit surfaces and subungual spaces
Subungual involvement may require nail removal
TBSA estimation
▶
Rule of nines or Lund-Browder for accurate TBSA
TBSA >2.38% = systemic toxicity risk threshold
Neuromuscular and systemic examination
Hypocalcemia signs
▶
Chvostek sign
▶
Facial muscle twitch on tapping anterior to ear
Trousseau sign
▶
Carpal spasm with BP cuff inflated 3 minutes above systolic
Muscle fasciculations or tetany
▶
Severe hypocalcemia manifestation
Respiratory assessment
▶
Wheezing or stridor: inhalation injury
▶
Rhinorrhea and oropharyngeal burns: ingestion or severe inhalation
Crackles: chemical pneumonitis or pulmonary edema
Vascular assessment
▶
Distal perfusion of digits
▶
HF-induced vasospasm can compromise digit perfusion
Compartment syndrome screen
▶
Tense swelling and pain with passive stretch
Compartment pressure measurement if suspected
PITFALLS
Diagnostic pitfalls
▶
Underestimating injury severity
▶
Visual appearance dramatically underestimates injury depth
Pain severity is more reliable than visual appearance
Missed delayed presentation with dilute HF
▶
Symptoms absent for 1–24 hours with <20% concentration
Reassure and discharge too early — systemic toxicity may follow
Assuming normal electrolytes on one check is sufficient
▶
Serial electrolytes every 1–2 hours mandatory in significant exposure
Ignoring subungual burns
▶
Fluoride concentrates under fingernails
Nail removal may be necessary for adequate calcium access
Differential Diagnosis
Chemical burns and related injuries
Other chemical burns
▶
Alkali burns (sodium hydroxide, lime)
▶
Liquefaction necrosis pattern
ICD-10 T54.3 — corrosive effect of alkalis
Lacks systemic fluoride toxicity
Other acid burns (sulfuric, nitric, hydrochloric)
▶
ICD-10 T54.2 — corrosive effect of other acids
Coagulation necrosis limits depth of penetration
No systemic calcium/magnesium/potassium derangement
HF burn
▶
ICD-10 T54.2 — corrosive effect of acids
SNOMED CT: chemical burn caused by hydrofluoric acid
Unique: deep penetration, systemic fluoride toxicity
Thermal burns
▶
Thermal burn ICD-10 T20–T32 range
▶
Immediate pain with visible injury proportional to depth
No systemic electrolyte derangement
History differentiates
Skin conditions mimicking HF burn
Contact dermatitis
▶
ICD-10 L23–L25 range
▶
Lacks deep pain and progressive necrosis
No systemic toxicity
Frostbite
▶
ICD-10 T33–T34 range
▶
Can mimic gray-white appearance
Cold exposure history
Necrotizing fasciitis
▶
ICD-10 M72.6
▶
Progressive tissue destruction but infectious etiology
Systemic sepsis signs, not electrolyte abnormalities
Phytophotodermatitis
▶
Milder course, sun exposure history
▶
No systemic toxicity
Systemic toxicity differentials
Hypocalcemia from other causes
▶
Hypoparathyroidism ICD-10 E20
▶
No burn injury
Chronic presentation typically
Vitamin D deficiency ICD-10 E55
▶
Insidious onset
Compartment syndrome
▶
ICD-10 T79.A — may coexist with HF digital burns
▶
Tense swelling, pain with passive stretch
Requires compartment pressure measurement
Laboratory Tests
Electrolyte and metabolic panel
Ionized calcium
▶
Most critical lab in HF exposure
▶
Normal ionized Ca: 1.12–1.32 mmol/l
Repeat every 1–2 hours in significant exposure
Hypocalcemia drives cardiac dysrhythmia and tetany
▶
Threshold for treatment: ionized Ca <1.12 mmol/l
Severe hypocalcemia: ionized Ca <0.8 mmol/l
Magnesium
▶
Hypomagnesemia: commonly co-occurs with hypocalcemia
▶
Normal serum Mg: 0.7–1.0 mmol/l
Repeat every 1–2 hours
Potassium
▶
Hyperkalemia: life-threatening in fluoride toxicity
▶
Fluoride inhibits Na/K-ATPase → cellular K efflux
Caution: standard glucose/insulin/bicarbonate may be less effective
Hypokalemia also reported in severe cases
Hematologic and coagulation studies
Complete blood count
▶
Baseline hematologic assessment
▶
Leukocytosis may indicate secondary infection in delayed presentation
Coagulation studies
▶
Fluoride inhibits coagulation enzymes
▶
PT/INR and aPTT as baseline
Fibrinogen if disseminated coagulopathy concern
Organ function and toxicology
Renal function panel
▶
BMP/CMP for baseline creatinine and BUN
▶
Renal impairment reduces fluoride excretion
Guides hydration and calcium dosing
Arterial or venous blood gas
▶
Metabolic acidosis: severe fluoride toxicity marker
▶
pH <7.35 with elevated anion gap
Lactate for tissue perfusion assessment
CK and myoglobin
▶
Rhabdomyolysis in significant exposures
▶
Especially with muscle cramping or tetany
Urinary fluoride
▶
Confirms exposure and guides duration of monitoring
▶
Not universally available
Serum fluoride level
▶
If available; takes time to result
▶
Not required for clinical management decisions
Diagnostic Tests
Scoring Systems
TBSA-based risk stratification
▶
TBSA >2.38%: evidence-based threshold for systemic toxicity
▶
Sensitivity 87.5%, specificity 95.9% for predicting systemic toxicity
Kim et al., Journal of Burn Care and Research 2023 (meta-analysis of 125 cases)
TBSA >5% (any concentration): mandatory ICU admission
▶
TBSA >1% with >50% HF concentration: mandatory ICU
TBSA <1% with dilute HF and normal electrolytes: low-risk, observe
HF burn severity classification
▶
Mild: <1% TBSA, dilute HF, pain responsive to topical calcium
▶
Observe 6–8 hours, serial electrolytes and ECG
Moderate: 1–5% TBSA or intermediate concentration
▶
Admission, IV calcium, subcutaneous or intra-arterial consideration
Severe: >5% TBSA, high concentration, systemic toxicity, ingestion
▶
ICU, aggressive calcium replacement, consider dialysis
MRI
MRI role in HF burns
▶
Limited acute utility for HF burn assessment
▶
CT and plain films preferred acutely
Motion artifact and availability limitations
Problem-solving indications
▶
Deep tissue involvement delineation when surgical planning complex
Suspected osteomyelitis in chronic or undertreated HF burns
Contraindications
▶
Unstable patient — not appropriate in acute phase
Ferromagnetic implants
CT
CT chest for inhalation injury
▶
Indications
▶
Significant inhalation exposure with respiratory symptoms
Hypoxemia not explained by clinical exam
Failure to improve or worsening after initial treatment
Findings in HF inhalation injury
▶
Diffuse ground-glass opacities (chemical pneumonitis)
Consolidation — "white lung" pattern in severe ARDS
Bilateral distribution in massive exposure
Contrast considerations
▶
Renal function assessment before contrast
Allergy history
CT hand and digits
▶
Bony erosion: hallmark of deep HF penetration into bone
▶
Distal phalanx most commonly affected
Indicates severe injury requiring surgical consultation
Soft tissue gas: compartment concern or necrotizing infection
CT not required for superficial burns
Ultrasound
POCUS applications in HF burns
▶
Cardiac assessment for systemic toxicity
▶
LV function impairment from hypocalcemia-induced cardiomyopathy
Pericardial effusion screen
IVC assessment for volume status
▶
Fluid responsiveness estimation
Integrate with clinical hemodynamic exam
Vascular ultrasound
▶
Digital and hand perfusion assessment
▶
Vasospasm from HF can compromise distal flow
Doppler assessment before intra-arterial catheter placement
Compartment syndrome adjunct
▶
Tissue edema depth assessment
Not definitive — compartment pressures remain standard
ECG as mandatory diagnostic tool
▶
Obtain immediately on all HF burn patients
▶
Hypocalcemia: prolonged QTc (specifically prolonged ST segment)
Risk of torsades de pointes
Hyperkalemia findings
▶
Peaked T waves, widened QRS, sine wave pattern
May herald refractory ventricular fibrillation
Continuous telemetry mandatory for minimum 6–8 hours
Disposition
ICU admission criteria
Mandatory ICU indications
▶
TBSA >5% any concentration
▶
Or TBSA >1% with HF concentration >50%
TBSA >2.38% with systemic toxicity concern
▶
Evidence-based risk threshold
Any electrolyte abnormality on initial or serial labs
▶
Hypocalcemia, hypomagnesemia, or hyperkalemia
ECG abnormalities or dysrhythmia
▶
Prolonged QTc, ventricular ectopy, or arrest
Ingestion of HF any amount
▶
Extremely high mortality — ICU regardless of TBSA
Significant inhalation exposure with respiratory symptoms
▶
Wheezing, hypoxemia, stridor
Pain refractory to topical and subcutaneous calcium
▶
Requires intra-arterial calcium consideration
Hemodynamic instability
Burn center transfer criteria
Transfer indications
▶
Large TBSA burns or high-concentration exposure
▶
Systemic toxicity requiring specialized management
Burns requiring intra-arterial calcium infusion
▶
Interventional radiology or vascular expertise needed
Surgical debridement or skin grafting requirement
▶
Deep tissue loss or bony involvement
Failure to achieve electrolyte stability despite aggressive treatment
Discharge criteria
Copy
Safe discharge requirements
▶
Small, isolated burn: <1% TBSA with dilute HF concentration
▶
Low-concentration product confirmed
Pain completely resolved with topical calcium gluconate
▶
No rebound pain during observation
Serial electrolytes normal on minimum two checks 2 hours apart
▶
Ionized calcium, magnesium, and potassium all normal
Normal ECG and no dysrhythmia over minimum 6–8 hours
▶
Continuous monitoring completed without event
Reliable patient with clear written return precautions
▶
Calcium gluconate gel dispensed for home use if applicable
Minimum observation period
▶
6–8 hours for any HF exposure regardless of initial appearance
▶
Delayed toxicity documented up to 16+ hours post-exposure
Treatment
Decontamination (first priority)
Immediate decontamination protocol
▶
Remove all clothing and jewelry
▶
Jewelry removal critical — fluoride concentrates under rings
Water irrigation: minimum 15–30 minutes
▶
Prompt irrigation within minutes most critical factor
Longer duration preferred for concentrated HF
Diphoterine amphoteric rinse if available
▶
Superior fluoride chelation vs water alone in ex vivo models
Not universally stocked — do not delay water irrigation
Topical 2.5% calcium gluconate gel post-irrigation
▶
Apply liberally and massage continuously into affected area
Reapply every 15–20 minutes while pain persists
Available commercially or compounded from 10% calcium gluconate + water-soluble gel
Calcium gluconate therapy by route
Topical calcium gluconate gel
▶
2.5% gel applied continuously to affected skin
▶
First-line for all dermal exposures
Continue until pain completely resolves
Use gloves — avoid applying with bare hands
Subcutaneous calcium gluconate injection
▶
10% calcium gluconate, 0.5 mL per cm2 of burn area
▶
Maximum 0.5 mL per digit to avoid compartment syndrome
Use 27-gauge or 30-gauge needle for precise infiltration
Indication: persistent pain despite topical therapy
▶
Class IIa recommendation for digital burns refractory to topical
Avoid calcium chloride subcutaneously
▶
Causes tissue necrosis — contraindicated by this route
Intra-arterial calcium gluconate infusion
▶
10 mL of 10% calcium gluconate in 40 mL normal saline
▶
Infuse over 4 hours via radial or brachial artery catheter
Indication: digital or hand burns refractory to topical and subcutaneous
▶
Vance et al. Annals of Emergency Medicine 1986 — landmark report
Thomas et al. Cardiovascular and Interventional Radiology 2009
Repeat as needed guided by pain response
▶
Monitor distal pulses and perfusion continuously
Regional IV (Bier block) calcium gluconate
▶
10 mL of 10% calcium gluconate plus 30–40 mL normal saline
▶
Tourniquet inflated above systolic pressure
Maintain tourniquet for 20–25 minutes
Indication: hand or forearm burns as alternative to intra-arterial
▶
Graudins et al. Annals of Emergency Medicine 1997
Systemic IV calcium gluconate
▶
20 mL of 10% calcium gluconate bolus IV
▶
Followed by continuous infusion titrated to ionized calcium
Target ionized calcium >=1.12 mmol/l
Indication: systemic hypocalcemia, ECG changes, or systemic toxicity
▶
Monitor ionized calcium every 1–2 hours
Calcium chloride IV in cardiac arrest only
▶
1 g (10 mL of 10% solution) IV push
More bioavailable than gluconate but caustic to tissues
Magnesium and electrolyte management
IV magnesium sulfate
▶
Loading dose: 2–4 g IV bolus over 20 minutes
▶
Followed by continuous infusion 1–2 g/hour as needed
Indication: hypomagnesemia concurrent with hypocalcemia
▶
Correct magnesium concurrently — hypomagnesemia worsens hypocalcemia correction
Monitor for hypermagnesemia with renal impairment
▶
Patellar reflex monitoring
Potassium management
▶
Standard hyperkalemia treatment may be less effective
▶
Fluoride inhibits Na/K-ATPase — insulin/glucose/bicarb less reliable
Calcium gluconate IV for membrane stabilization
Hemodialysis as definitive treatment for refractory hyperkalemia
Replace potassium if hypokalemia present
▶
KCl IV titrated to serum levels and renal function
Inhalation injury treatment
Nebulized calcium gluconate
▶
2.5–5% calcium gluconate solution via nebulizer
▶
Neutralizes inhaled fluoride in airways
Choe et al. Burns 2020 — mass exposure calcium nebulization
Continue until respiratory symptoms resolve
Supplemental oxygen and airway management
▶
High-flow oxygen for hypoxemia
▶
Intubation if airway compromise or severe ARDS
Bronchodilators for bronchospasm
▶
Salbutamol 2.5 mg nebulized PRN
Monitor for delayed pulmonary edema 12–24 hours post-exposure
▶
Serial chest radiographs
ECMO consideration
▶
Refractory respiratory failure from HF inhalation ARDS
▶
Pu et al. Medicine 2017 — ECMO combined with CRRT in HF burn
Advanced and refractory measures
Hemodialysis or CRRT
▶
Indications
▶
Refractory electrolyte derangements despite aggressive replacement
Massive HF exposure for fluoride ion removal
Renal failure complicating fluoride excretion
Highly effective for fluoride elimination
▶
Farkas et al. Pediatrics 2018 — VF from bifluoride treated with hemodialysis
Surgical interventions
▶
Fasciotomy for digital compartment syndrome
▶
Perform when compartment pressures elevated
Nail removal for subungual burns
▶
Required for adequate calcium gluconate access to nail bed
Wound excision for hypocalcemia unresponsive to medical therapy
▶
Removing fluoride depot source
Debridement of necrotic tissue
▶
Wait at least 7 days for wound demarcation before aggressive debridement
Skin grafting or flap reconstruction for deep tissue loss
▶
Han et al. Burns 2017 — surgical treatment after digital HF burns
Ocular HF exposure treatment
▶
Immediate copious irrigation: minimum 30 minutes
▶
Normal saline or LR preferred
1% calcium gluconate eyedrops if available
▶
Ophthalmology emergency consultation
Slit-lamp examination for corneal injury
▶
Morgan lens irrigation for sustained delivery
Special Populations
Pregnancy
Pregnancy-specific considerations
▶
Maternal systemic toxicity risk unchanged by pregnancy
▶
Aggressive calcium and magnesium replacement indicated
Fluoride crosses placenta — fetal hypocalcemia theoretically possible
Decontamination: copious water irrigation immediately
▶
Calcium gluconate gel safe in pregnancy
Subcutaneous and IV calcium gluconate acceptable
Calcium supplementation: fetal skeletal demands increase maternal requirements
▶
Monitor ionized calcium more frequently
Imaging in pregnancy
▶
Chest radiograph with abdominal shielding when indicated
▶
Inhalation injury: CXR benefit outweighs radiation risk
CT chest: radiation risk lower than risk of unrecognized ARDS
▶
Discuss with obstetrics and inform patient
Monitoring and disposition
▶
Fetal monitoring when gestational age viability reached
▶
Maternal hemodynamic stability prioritized first
Obstetrics consultation for all HF exposures in pregnancy
▶
ICU admission threshold lower given dual patient risk
Geriatric
Age-related vulnerability
▶
Reduced renal fluoride clearance
▶
Elevated creatinine common — monitor carefully
Extended monitoring period required
Reduced cardiac reserve
▶
Lower threshold for ECG changes to become hemodynamically significant
Calcium channel blocker and digoxin interactions common
Pre-existing electrolyte disorders common
▶
Baseline hypocalcemia or hypomagnesemia possible
Baseline ECG for comparison critical
Clinical presentation differences
▶
Reduced pain sensitivity may mask injury severity
▶
Do not rely on pain assessment alone in cognitively impaired patients
Thinner skin: faster dermal penetration of HF
▶
Lower concentration thresholds for toxicity
Management adjustments
▶
Lower admission threshold for systemic monitoring
▶
Even small burns warrant longer observation in older adults
Calcium gluconate dosing unchanged but monitor for hypercalcemia
▶
Serial ionized calcium every hour
Pediatrics
Pediatric exposure characteristics
▶
Household products most common source
▶
Rust removers and bathroom cleaners accessible in home
Higher body surface area to weight ratio
▶
Smaller TBSA burns produce greater systemic fluoride burden per kg
Lower absolute TBSA thresholds for systemic toxicity
Death from small area burns more likely than in adults
▶
Aggressive systemic monitoring mandatory even for small burns
Weight-based calcium gluconate dosing
▶
IV calcium gluconate: 0.6 mL/kg of 10% solution (60 mg/kg)
▶
Maximum 20 mL (2 g) per bolus
Repeat as needed guided by ionized calcium
Subcutaneous calcium gluconate: 0.5 mL per cm2 burn area
▶
Maximum dose per digit: 0.5 mL to avoid compartment syndrome
Ionized calcium target: >=1.12 mmol/l regardless of age
Hemodialysis for refractory cases
▶
Farkas et al. Pediatrics 2018: VF from ammonium bifluoride in child treated with hemodialysis
▶
Pediatric CRRT or hemodialysis effective for fluoride removal
Pediatric intensivist and nephrology consultation early
Child protection consideration
▶
Accidental vs intentional exposure assessment
▶
Document circumstances carefully
Occupational child labor context in some cases
▶
Mandatory reporting obligations if applicable
Background
Epidemiology
Incidence and burden
▶
HF burns account for approximately 1,000 emergency presentations annually in the US
▶
Exact epidemiology underreported — cases managed at primary sites
Occupational exposure: approximately 80% of cases
▶
Semiconductor/electronics manufacturing: 61% in one series
Vehicle washing and detailing: significant proportion
MMWR 2015: Washington State 2001–2013 car/truck washing burden documented
Household exposure: 20% of cases
▶
Rust removers and tile cleaners with 5–12% HF
Mortality and morbidity
▶
Death reported from as little as 2.5% TBSA with concentrated HF
▶
Cardiac arrest is primary cause of death
Delayed systemic toxicity up to 16+ hours after exposure
Permanent disability from deep digit and hand burns
▶
Bony erosion, compartment syndrome, digit loss possible
Taiwan Poison Control Center series 1991–2010: systemic toxicity in significant proportion of moderate-large burns
Pathophysiology
Dual injury mechanism
▶
Hydrogen ion burn component (acid injury)
▶
Causes immediate superficial tissue damage
Coagulative necrosis similar to other acid burns
Fluoride ion penetration component (unique to HF)
▶
HF is a weak acid (pKa 3.17) — dissociates poorly at physiologic pH
Unionized HF penetrates lipid membranes deeply and rapidly
Fluoride ions released in deep tissue and blood
Systemic fluoride toxicity mechanism
▶
Hypocalcemia
▶
Fluoride chelates ionized calcium forming insoluble calcium fluoride
Depletes intracellular and extracellular calcium stores
Hypomagnesemia
▶
Fluoride chelates magnesium — same binding mechanism
Hypomagnesemia worsens hypocalcemia by impairing PTH release
Hyperkalemia
▶
Fluoride inhibits Na/K-ATPase
Potassium efflux from cells
Glucose/insulin/bicarbonate less effective — enzyme target inhibited
Cardiac toxicity
▶
Hypocalcemia prolongs QTc → torsades de pointes risk
Hyperkalemia: peaked T waves, VF risk
Holstege et al. American Journal of Emergency Medicine 2005 — ECG toxidrome
Tissue destruction progression
▶
Liquefactive necrosis with ongoing fluoride penetration
▶
Unlike other acids, injury continues after initial contact
Bony erosion: fluoride dissolves calcium from bone (calcium fluoride formation)
Vasospasm
▶
Local fluoride effect on vascular smooth muscle
Impairs digit perfusion independently of systemic effects
Therapeutic Considerations
Calcium as fluoride antidote
▶
Mechanism: calcium ion chelates fluoride forming insoluble CaF2
▶
Neutralizes fluoride locally and systemically
Route selection principle
▶
Topical first for all burns
Escalate to subcutaneous if topical fails within 30–60 minutes
Escalate to intra-arterial for digit/hand burns refractory to subcutaneous
Systemic IV for electrolyte abnormalities or systemic toxicity
Calcium gluconate preferred over calcium chloride for subcutaneous routes
▶
Chloride salt: tissue necrosis risk
Gluconate salt: safe for subcutaneous and IM injection
Magnesium replacement
▶
Concurrent hypomagnesemia must be corrected
▶
Hypomagnesemia impairs PTH response and worsens hypocalcemia correction
Concurrent replacement: magnesium sulfate IV and calcium gluconate IV
Fluoride elimination
▶
Renal excretion: primary elimination route
▶
Adequate hydration to maintain urine output
Renal failure prolongs fluoride exposure
Hemodialysis: highly effective fluoride removal
▶
Reserve for refractory cases or renal failure
Wound source control
▶
Excision of burn depot source in refractory hypocalcemia
ECG monitoring as therapeutic guide
▶
QTc normalization confirms adequate calcium replacement
▶
Hyperkalemia resolution confirms fluoride burden decreasing
Continuous telemetry until ECG normal and electrolytes stable
Patient Discharge Instructions
copy discharge instructions
Copy
HF burn home care instructions
▶
Your skin injury may look mild but can worsen over the next 24–48 hours
▶
Continue topical calcium gluconate gel as instructed
Apply gel gently 3–4 times daily to the burn area or as directed
Keep the burn area clean and dry between gel applications
▶
Use a clean dressing as directed
Do not pop blisters
▶
Blisters protect healing tissue
Medications and follow-up
▶
Take all prescribed medications exactly as directed
▶
Do not stop calcium supplements without physician advice
Wound check within 24–48 hours with your treating physician or burn clinic
▶
Tissue damage may progress and appear worse before improving
Serial wound evaluation weekly for several weeks
▶
Full demarcation of injury may take 7 or more days
Return to the emergency department immediately if
▶
Increasing pain in the burn area despite gel application
▶
This may mean fluoride is penetrating more deeply
Spreading redness, swelling, or grey-white discoloration
Numbness or tingling in fingers or hands
Palpitations, chest pain, or feeling your heart racing or skipping
Muscle cramps, spasms, or weakness
Difficulty breathing or shortness of breath
Nausea, vomiting, or abdominal pain
Confusion, lightheadedness, or fainting
Prevention and workplace safety
▶
Do not return to the same work task without proper personal protective equipment
▶
Appropriate gloves rated for HF exposure (neoprene or thick rubber)
Report the incident to your workplace supervisor and occupational health
Ensure an HF first-aid kit including calcium gluconate gel is available at your workplace
Contact Poison Control at 1-800-222-1222 if any new symptoms develop
Household HF products: store out of reach of children and dispose safely
References
Guidelines and key sources
Primary evidence sources used
▶
Kim MS et al. Journal of Burn Care and Research 2023 — meta-analysis of 125 cases, TBSA cutoffs for systemic toxicity
Vance MV et al. Annals of Emergency Medicine 1986 — intra-arterial calcium gluconate for digital burns
Graudins A et al. Annals of Emergency Medicine 1997 — regional IV Bier block calcium for upper extremity burns
Thomas D et al. Cardiovascular and Interventional Radiology 2009 — intra-arterial calcium gluconate technique
Holstege C et al. American Journal of Emergency Medicine 2005 — ECG toxidrome of HF ingestion
Reeb-Whitaker CK et al. MMWR 2015 — occupational HF burns in car washing
Pu Q et al. Medicine 2017 — ECMO and CRRT in combined HF cutaneous and inhalation injury
Farkas AN et al. Pediatrics 2018 — hemodialysis for VF from bifluoride in child
Wu ML et al. Human and Experimental Toxicology 2014 — Taiwan Poison Control Center series 1991–2010
Ramesh S et al. Journal of Emergency Medicine 2025 — HF fatality from dermal exposure
Choe MSP et al. Burns 2020 — nebulized calcium for mass HF spill
Han HH et al. Burns 2017 — surgical management of digital HF burns
Hewett Brumberg EK et al. Circulation 2024 — AHA/ARC First Aid Guidelines
Coding reference
▶
ICD-10 T54.2 — corrosive effect of acids, includes HF burns
ICD-10 T54.3 — corrosive effect of alkalis (for differential)
ICD-10 T79.A — compartment syndrome (complication)
SNOMED CT: chemical burn caused by hydrofluoric acid
SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.
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Management Protocols
Hydrofluoric Acid Burn