DESCRIPTION

Phosphorus is a nonmetallic element that is highly flammable.

FORMS AND USES

• "Red" phosphorus is used in safety matches and is nontoxic in single oral doses (see SECTION I, Nontoxic Ingestion chapter), although, rarely, repeated doses may result in systemic poisoning.
• "Black" phosphorus is the inert nontoxic form of elemental phosphorus.
• "Yellow" or "white" phosphorus is a translucent solid with a garliclike odor that is practically insoluble in water but soluble in most oils; spontaneous combustion occurs on exposure to air. It is highly toxic.

TOXIC DOSE

• An acute dose of about 1 mg/kg of yellow or white phosphorus may be fatal for an adult.
• A total dose of 3 mg was reported to be fatal for a 2-year-old.

EPIDEMIOLOGY

Poisoning is uncommon.

CAUSES

Child neglect or abuse should be considered if the patient is less than 1 year of age, suicide attempt if the patient is over 6 years of age.

PATHOPHYSIOLOGY

Phosphorus ions are taken into the kidneys and later into the liver and other organs, resulting in acute systemic phosphorus poisoning.

WORKPLACE STANDARDS

• OSHA. PEL TWA for yellow phosphorus is 0.1 mg/m³. PEL TWA for phosphorus pentachloride is 1 mg/m³.
• ACGIH. TLV TWA for yellow phosphorus is 0.02 ppm. TLV TWA for phosphorus pentachloride is 0.10 ppm.

Section Outline:

• DESCRIPTION
• FORMS AND USES
• TOXIC DOSE
• EPIDEMIOLOGY
• CAUSES
• PATHOPHYSIOLOGY
• WORKPLACE STANDARDS

SIGNS AND SYMPTOMS

Skin Exposure

Skin exposure may cause severely painful necrotic partial- and full-thickness yellowish burns from chemical and thermal effects.

Inhalation of Phosphorus Fumes

Vital Signs

Chronic inhalation may result in cachexia.

HEENT

Inhalation may have marked irritant effects on the eyes.

Pulmonary

Inhalation may cause upper airway irritation, dyspnea, and delayed noncardiogenic pulmonary edema; bronchitis may be seen in cases of chronic inhalation.

Gastrointestinal

Inhalation may cause nausea and vomiting.

Hepatic

Inhalation may cause acute hepatic damage and systemic phosphorus poisoning.

Hematologic

Chronic inhalation may produce anemia.

Musculoskeletal

Mandibular necrosis, such as "phossy" or "Lucifer's" jaw, may be seen with chronic inhalation.

Phosporus Ingestion

Toxicity is enhanced when it is dissolved in solvents (e.g., alcohol, oils). Phosphorus poisoning is classically divided into an initial gastrointestinal stage, followed by a relatively asymptomatic period, and terminating in acute liver failure with metabolic derangements.

Cardiovascular

Phosphorus ingestion may produce hypotension, tachycardia, and ECG with ST- and T-wave changes, QTc prolongation, low voltage QRS, and dysrhythmia.

Pulmonary

Ingestion may cause dyspnea, tachypnea, and pulmonary edema.

Gastrointestinal

Ingestion results in acute onset of nausea, vomiting, abdominal pain, diarrhea, and hematemesis.

Renal

Renal failure may develop within 24 hours.

Hepatic

Ingestion may, after delay of a day or more, produce liver injury and fulminant hepatic failure.

Hematologic

Ingestion may result in clotting abnormalities in severe cases.

Endocrine

• Early hypoglycemia has a grave prognosis.
• Normal or hypocalcemia, and hyper- or hypophosphatemia may occur.

Neurologic

Restlessness, irritability, lethargy, weakness, delirium, stupor, coma, or seizures may develop.

PROCEDURES AND LABORATORY TESTS

Essential Tests

• Serum electrolytes, BUN, creatinine, calcium, phosphorus, and urinalysis should be ordered to assess renal injury and electrolyte abnormalities.
• Serum liver function tests should be performed to assess liver injury.

Recommended Tests

• Complete blood count, international normalized ratio, and prothrombin time should be obtained to assess blood loss and coagulopathy.
• Arterial blood gas should be studied if respiratory symptoms are present.
• A chest radiograph should be obtained to assess pulmonary injury.

Section Outline:

• SIGNS AND SYMPTOMS
  • Skin Exposure
  • Inhalation of Phosphorus Fumes
  • Phosporus Ingestion
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• Supportive care with appropriate airway management is vital.
• The dose and time of exposure for all substances involved should be determined.

DIRECTING PATIENT COURSE

The health-care professional should call the poison control center when:

• Severe or persistent effects develop.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

The patient should be referred to a health-care facility when:

• Suicide or homicide attempt is possible.
• Toxic effects develop.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

Admission Considerations

Symptomatic patients should be admitted.

DECONTAMINATION

During decontamination, the patient and health-care provider should be protected from vomitus, gastric washings, and feces.

Skin or Eye Exposure

• The patient should be admitted to a burn unit.
• Exposed areas should be covered with wet dressings at all times.
• Exposed areas should be washed several times with a solution of 5% sodium bicarbonate-3% copper sulfate-1% hydroxy-ethyl-cellulose or 1% sodium lauryl sulphate, and rinsed thoroughly with saline between washings.
• Meticulous surgical debridement may be necessary.
• Exposed eyes should be continuously flushed with copious amounts of water; formal ophthalmologic examination should be performed.

Inhalation

• The patient should be moved to fresh air, and 100% oxygen with assisted ventilation should be administered as required.
• Careful observation for development of systemic effects or delayed pulmonary edema.

Ingestion

• The use of gastric lavage is controversial because of the corrosive effects of phosphorus poisoning.
• Gastric lavage with potassium permanganate (1:5,000 solution) is recommended to convert phosphorus to harmless oxidation products; however, there are no controlled clinical data regarding its efficacy.

ANTIDOTES

There is no specific antidote for phosphorus poisoning.

ADJUNCTIVE TREATMENT

Burns

Burned area should be thoroughly cleaned and debrided, followed by typical burn supportive care.

Hypotension

• The patient should receive normal saline 10 to 20 ml/kg and be placed in the Trendelenburg position.
• Further fluid therapy should be guided by central pressure monitoring.
• A vasopressor may be added.
  • The dose of dopamine is 2 to 5 µg/kg/min titrated upward to effect; rates greater than 20 µg/kg/min are unlikely to provide further benefit.
  • The dose of norepinephrine is 0.1 to 0.2 µg/kg/min, titrated upward to effect.
  • High rates of infusion may cause tissue ischemia.

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
  • Skin or Eye Exposure
  • Inhalation
  • Ingestion
• ANTIDOTES
• ADJUNCTIVE TREATMENT
  • Burns
  • Hypotension

PATIENT MONITORING

• Continuous respiratory and cardiac monitoring should be performed in symptomatic patients.
• In cases of inhalation, careful observation for development of systemic effects or delayed pulmonary edema is needed.

EXPECTED COURSE AND PROGNOSIS

Phosphorus poisoning is classically divided into an initial gastrointestinal stage, followed by a relatively asymptomatic period, and terminating in acute liver failure with metabolic derangements. The fatality rate after ingestion is approximately 50%.

DISCHARGE CRITERIA/INSTRUCTIONS

Patients may be discharged from the emergency department or hospital when toxic effects resolve or stabilize and after psychiatric evaluation, if needed.

Section Outline:

• PATIENT MONITORING
• EXPECTED COURSE AND PROGNOSIS
• DISCHARGE CRITERIA/INSTRUCTIONS

Pulmonary injury may be delayed after inhalation.

Toxic effect of other substances, chiefly nonmedicinal as to source.

See Also: SECTION I, Nontoxic Ingestion chapter.

RECOMMENDED READING

Ben-Hur N. Phosphorus burns. Prog Surg 1978;16:180-181.

Blumenthal S. Lesser A. Acute phosphorus poisoning. Am J Dis Child 1938;55:1280-1287.

McCarnon MM, Gaddis GP. Acute yellow phosphorus poisoning from pesticide paste. Clin Toxicol 1981;18:693-711.

Author: Luke Yip

Reviewer: Richard C. Dart