Phosphorus toxicity
Background
- Two naturally occurring forms: red and white phosphorus
- Red is not absorbed well, limited toxicity[1]
- Used in manufacture of methamphetamines and also found in the illicit opioid "Krokodil"[2]
- Toxicity largely due to inadvertent production of white phosphorus or phosphine gas during manufacture
- White phosphorus is VERY toxic
- White-yellow waxy substance
- Exposure predominantly from use as incendiary munition by armed forces (though occasionally used in manufacture of fertilizers, food additives, and cleaning compounds)
- Caustic and cellular poison; ignites spontaneously in air, forms phosphorus pentoxide, which then reacts with water to form phosphoric acid
- Damage due to both thermal and chemical burns
Clinical Features
- Vomit and other secretions may have garlic-like odor
- Phosphorus particles may fluoresce under Wood's lamp
- Skin/eye contact causes severe, partial to full-thickness dermal/ocular chemical and thermal burns
- Inhalation: cough, wheeze, pneumonitis, pulmonary edema
- Ingestion: mucus membrane irritation/burns, abdominal pain, nausea/vomiting, GI bleeding, diarrhea (with smoking stools due to spontaneous combustion on exposure to air!!)[3]
- Systemic effects
- Headache, delirium, seizures, coma
- Dysrhythmias; prolonged QT and QRS, both atrial and ventricular arrhythmias
- AKI, electrolyte abnormalities
- Hepatotoxicity- may be delayed 2-3 days after exposure
- Chronic exposure associated with mandibular osteonecrosis ("phossy jaw")
- Phosphorus in Krokodil likely contributes to the significant skin, vascular, and muscle damage that earned it the nick name "the flesh-eating drug"[4]
Differential Diagnosis
Background
Heavy metal toxicity results from exposure to metals like lead, mercury, arsenic, or cadmium, which interfere with cellular function. Exposure may occur occupationally, environmentally, through ingestion, or from alternative medicines. Chronic toxicity can present insidiously, while acute toxicity may mimic sepsis or encephalopathy. Diagnosis is often delayed due to nonspecific symptoms.
Clinical Features
Symptoms depend on the metal and exposure duration but may include:
Neurologic: Peripheral neuropathy, confusion, tremor, encephalopathy
GI: Abdominal pain, nausea, vomiting, diarrhea, anorexia
Heme: Anemia (especially microcytic or hemolytic), basophilic stippling (lead)
Renal: Tubular dysfunction, proteinuria, Fanconi syndrome
Dermatologic: Mees’ lines (arsenic), hyperpigmentation, hair loss
Others: Fatigue, weight loss, hypertension (cadmium), immunosuppression
Differential Diagnosis
Sepsis or systemic inflammatory response
Drug toxicity or overdose
Metabolic disorders (e.g., porphyria, uremia)
Psychiatric illness (if symptoms are vague or bizarre)
Neurologic diseases (e.g., Guillain-Barré, MS, Parkinson’s)
Vitamin deficiencies (e.g., B12, thiamine)
Evaluation
Workup
History: Occupational exposures, home remedies, hobbies (e.g., jewelry making, battery recycling), diet, water source, imported goods
Labs:
- CBC, CMP, urinalysis
- Blood lead level, serum/urine arsenic, mercury, or cadmium (based on suspicion)
- Urine heavy metal screen (note: spot testing may require creatinine correction)
Imaging: Abdominal X-ray (radiopaque material in GI tract, especially with lead)
EKG: Evaluate for QT prolongation or arrhythmias in severe cases
Diagnosis
Confirmed by elevated blood or urine levels of the specific metal in the context of clinical findings. Hair and nail testing are unreliable for acute toxicity. Interpret results with toxicologist input if possible.
Management
Remove the source of exposure (e.g., occupational control, GI decontamination if recent ingestion)
Supportive care: IV fluids, seizure control, electrolyte repletion
Chelation therapy (in consultation with toxicology or Poison Control):
Lead: EDTA, dimercaprol (BAL), succimer
Mercury/arsenic: Dimercaprol or DMSA
Cadmium: No effective chelation—focus on supportive care
Notify local public health authorities if exposure source is environmental or occupational
Disposition
Admit if symptomatic, unstable, or requiring chelation
Discharge may be appropriate for asymptomatic patients with low-level exposure and outpatient follow-up
Arrange toxicology or environmental medicine follow-up for source control and serial testing
See Also
- Aluminum toxicity
- Antimony toxicity
- Arsenic toxicity
- Barium toxicity
- Bismuth toxicity
- Cadmium toxicity
- Chromium toxicity
- Cobalt toxicity
- Copper toxicity
- Gold toxicity
- Iron toxicity
- Lead toxicity
- Lithium toxicity
- Manganese toxicity
- Mercury toxicity
- Nickel toxicity
- Phosphorus toxicity
- Platinum toxicity
- Selenium toxicity
- Silver toxicity
- Thallium toxicity
- Tin toxicity
- Zinc toxicity
Burns
- Smoke inhalation injury (airway compromise)
- Chemical injury
- Acrolein
- Hydrochloric acid
- Tuolene diisocyanate
- Nitrogen dioxide
- Systemic chemical injury
- Specific types of burns
- Associated toxicities
Caustic Burns
- Caustic ingestion
- Caustic eye exposure (Caustic keratoconjunctivitis)
- Caustic dermal burn
- Airbag-related burns
- Hydrofluoric acid
- Tar burn
- Cement burn
Evaluation
- CMP, UA, EKG, CXR (if inhalational)
- Serum phosphorus level NOT helpful in diagnosing (though may want to monitor if concern for other electrolyte abnormalities)
- Consider EGD if concern for GI burns
Management
- Wear PPE to prevent exposure!
- Decontamination
- Remove contaminated clothing, wash exposed areas with soap and water
- Submersion in water/wet dressings can prevent spontaneous ignition of phosphorus particles
- Manually debride/remove remaining phosphorus particles- may need wood's lamp to find
- Unclear role of charcoal/whole bowel irrigation in ingestion
- Supportive/symptomatic management
- Inhalation: manage airway (may have significant irritation/edema), give oxygen therapy, bronchodilators, treat pulmonary edema
- Rehydrate if significant GI losses, correct electrolyte abnormalities
- Consider EGD if concern for GI burns