White Phosphorus BurnMANAGEMENT

ENVIRONMENTAL AND EXPOSURE PRESENTATIONS · 12 SECTIONS

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377 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Acute Mountain Sickness Arterial Gas Embolism Bee-Wasp Sting (Anaphylaxis)Chilblains Ciguatera Fish Poisoning Coral Cut Decompression Sickness Electrical Burn Injury Envenomation (snake, spider, insect)High Altitude Cerebral Edema (HACE)High Altitude Pulmonary Edema (HAPE)High-altitude illness Hypothermia Hypothermia (Mild)Hypothermia (Severe)Immersion Foot Lightning Strike Injury Scombroid Fish Poisoning Scorpion Envenomation Sea Urchin Injury Shark Bite Snake Envenomation Spider Bite (Black Widow)Spider Bite (Brown Recluse)Stingray Spine Injury Tick paralysis White Phosphorus Burn

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp28

Immediate Priorities

›Immediate stabilization priorities

›Airway assessment for inhalation injury (stridor, hoarseness, singed nasal hairs)

›Activate burn team and consider early intubation for evidence of airway edema

›Nasopharyngoscopy or direct laryngoscopy if upper airway injury suspected

›Secure airway before edema progresses if facial or oropharyngeal burns present

›Remove all clothing immediately — embedded WP re-ignites on air exposure

›Cover wounds with saline-soaked dressings — WP re-ignites when dry

Hemodynamic Goals

›Resuscitation targets

›Two large-bore IV access sites or central venous access

›Crystalloid resuscitation via Parkland formula: 4 mL/kg per percent TBSA over 24 hours

›Half in first 8 hours from time of burn

›Half in subsequent 16 hours

›Urine output target 0.5–1.0 mL/kg/hour in adults

›Urine output target 1.0 mL/kg/hour in pediatric patients

Critical Alerts

›Life-threatening complications requiring immediate action

›Cardiac arrhythmia (QTc prolongation, torsades de pointes) from hypocalcemia

›Continuous cardiac monitoring and 12-lead ECG

›IV calcium gluconate 1–2 g over 10–20 minutes for symptomatic hypocalcemia

›Hypocalcemia-induced seizures — IV benzodiazepine plus emergent calcium replacement

›Re-ignition of embedded WP particles if wounds allowed to dry

›Progressive multi-organ failure: hepatorenal syndrome, ARDS, hemolytic anemia, DIC

›Mortality disproportionate to TBSA — small burns can be fatal due to systemic toxicity

Consults

›Mandatory consultations

›Burn surgery for all WP burn patients

02History/hx38

Mechanism and Exposure

›Exposure context

›Military or combat exposure (most common historical context)

›Industrial accident — munitions manufacturing, fertilizer production

›Fireworks handling or manufacturing

›Civilian contact with unexploded WWII-era ordnance residues (Baltic Sea, North Sea beaches)

›Duration of WP contact and quantity involved

›Enclosed-space exposure increasing inhalation injury risk

Prehospital Course

›Prehospital decontamination and first aid

›Clothing removed immediately or delayed removal (delayed leads to deeper burns)

›Wounds kept moist during transport

›Type of dressing applied prehospital

›Any copper sulfate applied prehospital — must document given toxicity risk

›Time elapsed from exposure to presentation

Symptoms

›Presenting symptoms

›Severe, disproportionate pain relative to burn size (characteristic of WP burns)

›Garlic-like or acrid odor from wounds

›Luminescent or smoking wounds observed in the dark

›Respiratory: cough, dyspnea, stridor

›Cardiac: palpitations, chest pain, syncope (arrhythmia from hypocalcemia)

›GI: nausea, vomiting, abdominal pain, jaundice (hepatotoxicity)

›Renal: decreased urine output, dark or cola-colored urine

›Neurological: paresthesias, muscle cramps, tetany, seizures (hypocalcemia)

›Musculoskeletal: muscle spasms and weakness

Risk Factors

›Populations at elevated risk

03Physical Exam/exam29

Vital Signs

›Hemodynamic assessment

›Tachycardia (systemic toxicity, pain, fluid losses)

›Hypotension (distributive shock, significant fluid loss)

›Tachypnea (inhalation injury, ARDS, metabolic acidosis)

›Fever or hypothermia (infection, systemic inflammatory response)

›Oxygen saturation — may be falsely normal in inhalation injury

Wound Assessment

›WP burn wound characteristics

›Yellowish necrotic appearance typical of WP burns

›Wounds may be smoking or luminescent in a darkened room — examine in dim lighting

›Garlic-like or acrid odor from embedded WP particles

›Depth typically full-thickness extending into subcutaneous fat (WP has high lipid solubility)

›TBSA calculation using Lund-Browder chart (preferred over rule of nines for precision)

›Re-ignition upon wound drying — confirms WP presence

Airway and Respiratory

›Upper and lower airway evaluation

›Stridor, hoarseness, voice change (supraglottic edema)

›Singed nasal hairs or eyebrows

›Facial or oropharyngeal burns or erythema

›Carbonaceous sputum

›Wheeze or decreased air entry bilaterally (lower airway injury)

Hypocalcemia Signs

›Neuromuscular signs of hypocalcemia

›Chvostek sign: facial twitch with tapping of facial nerve

›Trousseau sign: carpal spasm with blood pressure cuff inflation for 3 minutes

›Tetany or carpopedal spasm

›Paresthesias of lips, fingertips

04Differential Diagnosis/ddx16

Other Chemical Burns

›Chemical burn differential

›Hydrofluoric acid burn — also causes severe hypocalcemia and disproportionate pain

›Distinguished by lack of luminescence and different odor

›Alkali burns — liquefactive necrosis, no luminescence

›Acid burns — coagulative necrosis, no luminescence

›Napalm burn — incendiary but does not continue burning in oxygen-depleted wounds

›Magnesium burns — also burns in contact with water, lacks garlic odor

Thermal Burns

›Standard thermal burn without chemical component

›Flame burns — do not re-ignite, no systemic phosphorus toxicity

›Scald burns — liquid mechanism, no luminescence

›Electrical burns — deep tissue injury disproportionate to surface, entry/exit wounds

Systemic Toxicological Mimics

›Conditions mimicking WP systemic toxicity

›Organophosphate poisoning — cholinergic toxidrome, no burn wound

›Severe hypocalcemia from other causes (hypoparathyroidism, pancreatitis)

›Acute phosphorus ingestion (rodenticides) — no burn wound, GI predominance

›Radiation burns — no garlic odor, no luminescence, insidious onset

05Laboratory Tests/lt22

Electrolytes

›Critical electrolyte monitoring

›Ionized calcium — hypocalcemia is common and potentially lethal in WP burns

›Serial monitoring every 4–6 hours in acute phase

›Target ionized calcium greater than 1.1 mmol/l

›Serum phosphorus — hyperphosphatemia expected from WP systemic absorption

›Serum magnesium — hypomagnesemia worsens hypocalcemia resistance to treatment

›Sodium, potassium, chloride, bicarbonate panel

Renal and Hepatic Function

›Organ function markers

›Creatinine and urea — acute kidney injury from hemolysis, direct WP nephrotoxicity

›AST, ALT, alkaline phosphatase, total bilirubin — hepatotoxicity from systemic WP absorption

›Direct and indirect bilirubin fractionation if jaundice present

›Urinalysis — hemoglobinuria or myoglobinuria (dark urine)

Hematologic

›Hematologic injury assessment

›Complete blood count — hemolytic anemia (WP has direct hemolytic effect on erythrocytes)

›Coagulation panel: PT, INR, PTT, fibrinogen — DIC risk in major WP burns

›Peripheral blood smear if hemolysis suspected

›Type and screen for anticipated surgical debridement or transfusion requirement

Muscle and Metabolic

›Systemic injury markers

›Creatine kinase — rhabdomyolysis assessment

›Lactate — metabolic acidosis and tissue hypoperfusion

›Arterial blood gas or venous blood gas — metabolic acidosis, hypoxemia in inhalation injury

›Carboxyhemoglobin if smoke inhalation in enclosed space

06Diagnostic Tests/dt41

Scoring Systems

›Burn severity scoring

›Revised Baux Score (age + TBSA + 17 if inhalation injury)

›Score over 140 associated with very high mortality

›Less accurate in WP burns due to systemic toxicity independent of TBSA

›Baux Score (age + TBSA) — original burn mortality prediction tool

›WP burns carry higher mortality than predicted by TBSA alone

›Lund-Browder chart for precise TBSA estimation

›Preferred over rule of nines especially in pediatric patients

MRI

›MRI utility in WP burns

›MRI generally not indicated in acute WP burn management

›Metallic WP fragments may retain ferromagnetic properties — contraindication until cleared

›Plain radiograph is preferred initial imaging for particle localization

›MRI of extremities may be considered for deep soft tissue injury delineation in subacute phase

›After all WP particles confirmed removed by surgical debridement

›CT imaging indications

›CT chest for suspected significant inhalation injury or ARDS progression

›Findings: ground-glass opacities, consolidation, bronchial wall thickening

›Plain radiograph of burn areas preferred for initial WP particle localization

›WP particles may be radiopaque and visible on plain X-ray aiding debridement planning

›CT of affected extremities if deep tissue necrosis extent unclear after clinical assessment

›Helps delineate surgical planning for excision and grafting

Ultrasound

›Point-of-care ultrasound applications

›Focused cardiac ultrasound for hypocalcemia-induced cardiomyopathy assessment

›Reversible cardiomyopathy documented with ionized calcium below 0.8 mmol/l

07Disposition/dispo19

ICU Admission

›Criteria for ICU-level care

›Burns greater than 10% TBSA

›Any evidence of inhalation injury

›Hemodynamic instability or arrhythmias

›Significant electrolyte derangements (hypocalcemia, hyperphosphatemia)

›Multi-organ dysfunction (hepatic, renal, hematologic)

›Altered mental status or seizure activity

›Concern for ongoing systemic WP absorption

Burn Center Transfer

›Transfer criteria to verified burn center

›All WP burns should be transferred to a verified burn center when available

›Mortality at one burn center decreased from 13.8% (1969-1985) to 0% (1986-2000) with protocol improvements (Barillo et al., Burns 2004)

›Transfer should not be delayed for definitive wound debridement if center accepts

›Keep wounds moist during transfer to prevent WP re-ignition

Discharge Criteria

›Criteria for outpatient management (extremely rare in WP burns)

›All WP particles confirmed removed by Wood's lamp and surgical inspection

›Serum calcium normalized and stable without IV replacement

›No evidence of systemic toxicity (hepatic, renal, hematologic)

›Very small, superficial burn with confirmed particle removal

›Reliable follow-up with burn surgery within 24–48 hours

08Treatment/t60

Decontamination

›Immediate wound decontamination

›Remove all clothing and jewelry immediately — may ignite or re-ignite

›Double bag all clothing as hazardous material

›Copious continuous irrigation with normal saline or water

›Avoid direct high-pressure water streams that may splash WP particles

›Continue irrigation until all particles identified and removed

›Moist saline-soaked gauze as first-line dressing (Witkowski et al., Med Sci Monitor 2015)

›Most effective method for extinguishing WP and facilitating particle removal

›Maintain moist environment at all times during wound management

Particle Removal

›WP particle identification and removal

›Wood's lamp examination in darkened room to locate fluorescing particles

›Mechanical debridement with forceps under direct visualization

›Remove all visible and UV-fluorescing particles before dressing

›Do NOT use copper sulfate for particle identification

›Cochrane 2014 review: no evidence of benefit

›Documented harm: renal failure, hemolytic anemia, death from systemic copper absorption

›Avoid silver sulfadiazine until all WP particles are removed — may obscure particles

›Sequential re-examination after initial debridement

Calcium Replacement

›Hypocalcemia management protocol

›IV calcium gluconate for symptomatic hypocalcemia or ionized calcium below 1.1 mmol/l

›Symptomatic: 1–2 g IV over 10–20 minutes (1 g calcium gluconate = 93 mg elemental calcium)

›Maintenance infusion: 0.5–2 g/hour titrated to ionized calcium level

›Monitor ECG during infusion

›Serial ionized calcium every 4–6 hours

›IV calcium chloride if central access available for faster elemental calcium delivery

›1 g calcium chloride = 273 mg elemental calcium

›Use central line only due to risk of tissue necrosis with extravasation

›Correct hypomagnesemia before expecting calcium replacement to be effective

›Magnesium sulfate 2 g IV over 10–15 minutes for magnesium below 0.7 mmol/l

Fluid Resuscitation

›IV fluid resuscitation protocol

›Parkland formula: lactated Ringer's 4 mL/kg per percent TBSA over 24 hours

›Half of calculated volume in first 8 hours from time of burn

›Half of calculated volume in subsequent 16 hours

›Titrate to urine output 0.5–1.0 mL/kg/hour in adults

›Avoid over-resuscitation — associated with abdominal compartment syndrome and ARDS

›Avoid colloids in first 12–24 hours in major burns per standard burn protocols

Analgesia

›Pain management

›IV opioid analgesia — WP burns are extremely painful

›Morphine 0.1 mg/kg IV titrated to pain control

›Hydromorphone 0.02 mg/kg IV as alternative

›Fentanyl 1–2 mcg/kg IV for procedural analgesia during debridement

›Ketamine for procedural sedation during wound debridement

›1–2 mg/kg IV over 1–2 minutes for procedural analgesia

›Provides analgesia and dissociation without respiratory depression

›Multimodal analgesia: acetaminophen, ibuprofen (if no renal compromise) as adjuncts

Wound Management

›Definitive wound care

›Serial debridement of necrotic tissue at planned intervals

›Early excision and skin autografting for wounds not healing by 14 days (Chou et al., Burns 2001)

›Porcine xenograft or cadaveric allograft as temporizing biological coverage

›Vacuum-assisted wound closure for large wounds pending definitive grafting

›Topical antimicrobial agents (mafenide acetate preferred — penetrates eschar)

›Apply only after WP particle removal is confirmed

Adjunct Treatment

›Supportive and adjunct therapies

›Tetanus prophylaxis per standard protocol

›Inhalation injury management: humidified oxygen, bronchodilators, mucolytics, nebulized heparin

›Mechanical ventilation with lung-protective strategy (tidal volume 6 mL/kg IBW) for ARDS

›PEEP titration to maintain SpO2 above 92% on minimal FiO2

›Nutritional support: high-protein high-calorie diet or enteral feeding

›Target protein 1.5–2 g/kg/day for wound healing

›Proton pump inhibitor for Curling ulcer prophylaxis

09Special Populations/sp32

Pregnancy

›WP burns in pregnancy

›Dual patient considerations: maternal stabilization takes priority

›Fetal monitoring with continuous electronic fetal monitoring if viable gestation

›Obstetrics consultation immediately for any burn in pregnancy

›Fluid resuscitation requirements may be higher due to increased plasma volume

›Pregnant patients have 40–50% increase in circulating blood volume

›Hypocalcemia management

›IV calcium gluconate preferred over calcium chloride in pregnancy

›Maternal hypocalcemia may cause fetal hypocalcemia and arrhythmia

›WP systemic toxicity poses significant risk of fetal hepatotoxicity and teratogenicity

›No safe threshold established; anticipate fetal distress with maternal systemic toxicity

Geriatric

›Considerations in elderly patients

›Higher mortality risk — reduced physiologic reserve and comorbidities

›Revised Baux Score even less predictive in elderly WP burns due to systemic toxicity

›Fluid resuscitation must balance resuscitation goals against heart failure and renal insufficiency

›Consider invasive hemodynamic monitoring earlier in elderly patients

›Polypharmacy — QT-prolonging medications compound hypocalcemia-induced arrhythmia risk

›Review all medications on presentation

›Reduced skin elasticity and healing capacity prolongs graft healing

›Higher baseline risk of acute kidney injury from systemic WP nephrotoxicity

Pediatrics

›Pediatric-specific management

›Weight-based fluid resuscitation using Parkland or Galveston formula

›Galveston formula: 5000 mL/m2 TBSA burned + 2000 mL/m2 total BSA over 24 hours

›Urine output target 1.0 mL/kg/hour in children

›Lund-Browder chart mandatory for TBSA calculation (rule of nines inaccurate in children)

10Background/b37

Epidemiology

›Epidemiological profile of WP burns

›WP burns are rare but historically significant in military medicine

›Historically most common in combat contexts; civilian cases increasingly reported

›Civilian exposures documented in munitions workers, fireworks handlers, beachgoers near WWII ordnance sites

›Mortality trends

›13.8% mortality rate (1969-1985) at one US burn center

›0% mortality (1986-2000) at same center with protocol-driven improvements (Barillo et al., Burns 2004)

›Disproportionate severity: small TBSA burns can be fatal due to systemic WP toxicity

›WP is used in military munitions, industrial manufacturing (fertilizers, pesticides), and fireworks

Pathophysiology

›Mechanisms of injury

›Dual injury mechanism: thermal and chemical

›Thermal: WP ignites spontaneously at approximately 30 degrees Celsius in air

›Burns at 800-1200 degrees Celsius continuing until oxygen-deprived or fully consumed

›Chemical: systemic absorption causes multi-organ toxicity

›WP properties driving injury

›High lipid solubility allows rapid penetration into subcutaneous fat and systemic absorption

›Spontaneous re-ignition when wounds dry — ongoing tissue destruction

›Systemic toxicity cascade

›Phosphorus directly binds calcium leading to hypocalcemia

›Hyperphosphatemia compounds cardiac and neuromuscular effects

›Hepatotoxicity from direct WP cytotoxicity and oxidative stress

›Hemolytic anemia from direct WP effect on erythrocyte membranes

›Acute kidney injury: direct nephrotoxicity plus pigment nephropathy from hemolysis

›ARDS from inhalation injury and systemic inflammatory response

Therapeutic Considerations

›Evidence base for WP burn treatment

11Patient Discharge Instructions/pdi28

copy discharge instructions

›Discharge instructions for White Phosphorus Burn

›Wound care at home

›Keep all wound dressings moist at all times — never allow wounds to dry

›Change dressings as instructed by your burn surgeon

›Do not remove any dressings without guidance from your medical team

›Medications

›Take all prescribed medications as directed

›Calcium supplements as prescribed — do not stop without physician guidance

›Pain medications as prescribed for wound pain

›Activity restrictions

›No smoking or open flames near wounds

›Protect healing skin from sun exposure

›Follow all wound care and rehabilitation instructions from your burn team

›Return to the Emergency Department immediately for

›Any wound that begins smoking, glowing, or re-igniting

›Worsening pain disproportionate to wound appearance

›Palpitations, chest pain, or fainting

›Dark, brown, or cola-colored urine

›Jaundice (yellowing of skin or eyes)

›Shortness of breath or worsening cough

›Muscle cramps, tetany, or spasms

›Numbness or tingling of lips or fingers

›Fever above 38.5 degrees Celsius

›Confusion or seizure activity

›Follow-up

›Burn surgery clinic within 24–48 hours if discharged from hospital

›Continued monitoring of calcium and phosphorus levels as directed

12References/r27

Guidelines and Key Sources

›Cochrane systematic review on phosphorus burn treatment

›Barqouni L, Abu Shaaban N, Elessi K. Interventions for Treating Phosphorus Burns. Cochrane Database of Systematic Reviews. 2014

›Found no evidence supporting copper sulfate use

›Documented harm from copper sulfate: renal failure, hemolytic anemia, death

›Supports Wood's lamp as preferred particle detection method

›Chou TD, Lee TW, Chen SL, et al. The Management of White Phosphorus Burns. Burns. 2001

›Clinical management series supporting early excision and grafting

›Barillo DJ, Cancio LC, Goodwin CW. Treatment of White Phosphorus and Other Chemical Burn Injuries at One Burn Center Over a 51-Year Period. Burns. 2004

›Demonstrated mortality reduction from 13.8% to 0% with protocol-driven burn center care

Clinical Studies and Case Reports

›Supporting literature

›Wang M, Bai Y, Zhang X, et al. White Phosphorus Munitions: Pathophysiology, Clinical Management, and Multidisciplinary Perspectives on Burn Injuries and Humanitarian Challenges. Frontiers in Public Health. 2025

›Comprehensive review of WP pathophysiology and current management approaches

›Frank M, Schmucker U, Nowotny T, et al. Not All That Glistens Is Gold: Civilian White Phosphorus Burn Injuries. American Journal of Emergency Medicine. 2008

›Documents civilian WP exposure cases including WWII-era ordnance beach exposures

›Berndtson AE, Fagin A, Sen S, et al. White Phosphorus Burns and Arsenic Inhalation: A Toxic Combination. Journal of Burn Care and Research. 2014

›Describes co-exposure with arsenic in industrial settings

›Witkowski W, Surowiecka-Pastewka A, Biesaga M, Gierczak T. Experimental Comparison of Efficiency of First Aid Dressings in Burning White Phosphorus. Medical Science Monitor. 2015

›Confirmed moist saline gauze as most effective first-aid dressing

Hypocalcemia and Cardiac References

›Cardiac and metabolic complication literature

›Newman DB, Fidahussein SS, Kashiwagi DT, et al. Reversible Cardiac Dysfunction Associated With Hypocalcemia: Systematic Review and Meta-Analysis. Heart Failure Reviews. 2014

›Confirms hypocalcemia-induced cardiomyopathy is reversible with calcium repletion

›Ilveskoski E, Sclarovsky S, Nikus K. Severe Hypocalcemia Simulating ST-elevation Myocardial Infarction. American Journal of Emergency Medicine. 2012

›Documents ECG findings of hypocalcemia mimicking STEMI

›Orloff LA, Wiseman SM, Bernet VJ, et al. American Thyroid Association Statement on Postoperative Hypoparathyroidism. Thyroid. 2018

›Provides guidance on hypocalcemia management applicable to WP burn patients

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Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

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