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INTRODUCTION

There are two naturally occurring types of elemental phosphorus: red and white. Red phosphorus is not well absorbed and has limited toxicity. In contrast, white phosphorus (also called yellow phosphorus) is a highly toxic cellular poison. White phosphorus is a colorless or yellow wax-like crystalline solid with a garlic-like odor and is almost insoluble in water but glows with exposure to air.

White phosphorous is used in the manufacture of fertilizers, food additives, cleaning compounds, and incendiaries in military ammunition. Historically, it has been used as a rodenticide and in the manufacture of fireworks. Red phosphorous is used in the manufacture of methamphetamine.

MECHANISM OF TOXICITY

  1. White phosphorous ignites spontaneously in air to form phosphorous pentoxide, which reacts with water to form phosphoric acid. White phosphorus is also a cellular poison.

  2. Toxicity resulting from red phosphorous is largely associated with methamphetamine production. This process may involve the inadvertent conversion of red phosphorous to white phosphorous and the generation of phosphine gas.

TOXIC DOSE

  1. Ingestion. The fatal oral dose of yellow/white phosphorus is approximately 1 mg/kg.

  2. Inhalation. The ACGIH-recommended workplace limit (TLV-TWA) for white phosphorus is 0.1 mg/m3 (0.02 ppm) as an 8-hour time-weighted average. The air level considered immediately dangerous to life or health (IDLH) is 5 mg/m3. Occupational exposure limits are not well established for red phosphorous.

CLINICAL PRESENTATION

(white phosphorous)

  1. Acute inhalation may cause mucous membrane irritation, cough, wheezing, chemical pneumonitis, and noncardiogenic pulmonary edema.

  2. Skin or eye contact with phosphorous may cause conjunctivitis or severe dermal or ocular burns. Large burns can result in systemic absorption and toxicity.

  3. Acute ingestion may cause GI burns, inflammation and hemorrhage, severe vomiting and abdominal pain, and diarrhea with "smoking" stools (due to spontaneous combustion on exposure to air).

  4. Systemic effects include headache, delirium, shock, seizures, coma, and arrhythmias (atrial fibrillation, QRS and QT prolongation, ventricular tachycardia and fibrillation). Acute renal injury and electrolyte derangements including hypocalcemia, hyperkalemia, and hyperphosphatemia may occur. Phosphorous is a hepatotoxin, and fulminant hepatic failure may occur after 2–3 days after exposure.

  5. Chronic exposure to phosphorous is associated with "phossy jaw" or mandibular osteonecrosis.

DIAGNOSIS

Is based on a history of exposure and the clinical presentation. Cutaneous burns, a garlic odor of the vomitus, and "smoking" or luminescent stools and vomitus caused by spontaneous combustion of elemental phosphorus suggest ingestion. Wood lamp examination of the skin will cause embedded phosphorus particles to fluoresce.

  1. Specific levels. Serum phosphorous concentrations are not useful in diagnosing phosphorous poisoning.

  2. Other useful laboratory studies include BUN, creatinine, potassium, calcium, liver aminotransferases, urinalysis, blood gases or oximetry, ECG, and chest radiography (after acute inhalation).

TREATMENT

  1. Emergency and supportive measures

    1. Observe ...

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