01Approach to the Critical Patient/attcp52

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

02History/hx70

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

03Physical Exam/exam57

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

04Differential Diagnosis/ddx43

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

05Laboratory Tests/lt40

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

06Diagnostic Tests/dt64

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

07Disposition/dispo38

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

›Safe discharge requirements

08Treatment/t103

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

09Special Populations/sp63

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

10Background/b73

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

11Patient Discharge Instructions/pdi32

copy discharge instructions

›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

12References/r19

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

Evidence & Review

Evidence & Review