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PHOSPHORUS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Phosphorus is a nonmetallic chemical element of the nitrogen family. Its name is derived from Greek, meaning "light-bearing".
    B) This management deals only with YELLOW OR WHITE PHOSPHORUS and its evolved PHOSPHORUS OXIDES. "PHOSPHORUS" as used in this management indicates only yellow or white phosphorus unless otherwise stated.
    1) Toxic quantities of yellow or white phosphorus may be absorbed from the skin and by inhalation of phosphorus vapors.
    C) Confusion may exist between the identity of the involved agent (organophosphates, phosgene, phosphates, phosphine, or phosphorus) all of which have different toxicity and treatments.
    D) NOTE: This management does NOT deal with phosphates or salts of phosphorus as found in cleaning products.

Specific Substances

    A) PHOSPHORUS (YELLOW/WHITE)
    1) Phosphorus (white)
    2) Phosphorus (yellow)
    3) Yellow Phosphorus
    4) White Phosphorus
    5) Molecular Formula: P4
    6) CAS 7723-14-0
    RELATED COMPOUNDS - PHOSPHORUS OXIDES
    1) Phosphorus pentaoxide
    2) Phosphorus pentoxide
    3) Phosphorus (V) oxide
    4) Phosphoric anhydride
    5) Diphosphorus pentoxide
    6) Phosphorus sesquioxide

    1.2.1) MOLECULAR FORMULA
    1) P (red phosphorus)
    2) P4 (white phosphorus)

Available Forms Sources

    A) FORMS
    1) Yellow or white phosphorus is a colorless or yellow wax-like crystalline solid, with a garlic-like odor, and almost insoluble in water (Budavari, 1996; Felton, 1982). However, it diffuses through water as a vapor and forms a dilute colloidal solution. It spontaneously ignites on contact with air at or above 30 degrees Celsius and explodes when exposed to oxidizing materials, releasing primarily phosphorus sesquioxide (P2O5).
    a) The phosphorus then becomes luminous in the dark (phosphoresces). The oxidation occurs with the liberation of such heat that the element bursts into a yellow flame and produces a dense white smoke. The reaction progresses until all of the material is consumed, or until the material is deprived of oxygen, as by flooding. However, the phosphorus will reignite upon drying.
    b) To prevent spontaneous combustion, yellow phosphorus is stored under water. Phosphorus can cause full thickness burns, and is likely to do so if it reaches the ignition temperature (44 degrees Celsius or 111 degrees Fahrenheit).
    2) Yellow phosphorus is soluble in fats and in bile and is absorbed from the intestine and from subcutaneous injections, especially when administered in a finely divided form.
    B) USES
    1) SUMMARY
    a) Yellow or white phosphorus is used in the manufacture of rodenticides, incendiaries, phosphorus compounds, and pyrotechnics (fireworks), and as a semiconductor additive (ITI, 1995).
    b) Yellow or white phosphorus was used in the manufacture of matches in the past and was responsible for both chronic poisoning in workers and acute poisoning from ingestion of matches.
    2) SPECIFIC PRODUCTS
    a) MATCHES - Modern matches (including the "Strike Anywhere" variety) do NOT contain yellow or white phosphorus. Modern matches contain phosphorus sesquifluoride and potassium chlorate, and a one-year-old child could consume 20 matches before any toxicity would occur. Chronic phosphorus poisoning is now seldom encountered (Gosselin et al, 1984; Harbison, 1998).
    1) RED PHOSPHORUS is used in the manufacture of safety matches. It is nonvolatile, unabsorbable, insoluble substance that is nontoxic in oral ingestions.
    b) HOMEOPATHIC - Although no longer used in medicine, phosphorus is still used in some homeopathic medicines (S Sweetman , 2000).
    c) MILITARY - White or yellow phosphorus may be used as an igniter for other munitions such as in hand grenades, mortar and artillery rounds and other weapons. White phosphorus is mainly used for military purposes. In its acid form, phosphorus is used in the preparation of silicon wafers (Felton, 1982; Eldad et al, 1995).
    1) INADVERTENT EXPOSURE - White phosphorus was used during World War II in grenades, flares and tracer bullets. After the war was over, white phosphorus was dumped into the Baltic Sea, and over time residues of phosphorus have been found on the shore line. When exposed to air, phosphorus can spontaneously ignite and burn at temperatures of up to 1300 degrees C. There have been several cases of severe burns after mistaking phosphorus for amber along the Baltic Coast (Frank et al, 2008).
    d) FIREWORKS - In some Latin American countries, variable amounts of white phosphorus can be found in some firecrackers and fireworks. In this study, it was found that firecrackers in this region could contain between 4 mg to 9 mg of white phosphorus. Three cases of acute liver failure secondary to the ingestion of firecrackers containing white phosphorus were reported; two patients survived (with one requiring liver transplantation) and one patient died after ingesting 12 firecrackers (Santos et al, 2009).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: "Phosphorus" as used in this management indicates only yellow or white phosphorus unless otherwise stated. Phosphorus is a nonmetallic chemical element of the nitrogen family. It is essential for many biologic processes including synthesis of ATP. Yellow and white phosphorus are used in the manufacture of rodenticides, incendiaries, phosphorus compounds, as an igniter in munitions and flares, as an igniter and pigment in fireworks, and as a semiconductor additive. Although no longer used in medicine, phosphorus is still used in some homeopathic medicines. Yellow or white phosphorus was used in the manufacture of matches in the past and was responsible for both chronic poisoning in workers and acute poisoning from ingestion of matches. Modern matches (including the "Strike Anywhere" variety) do NOT contain yellow or white phosphorus, but contain phosphorus sesquifluoride and potassium chlorate. Chronic phosphorus poisoning is now rarely encountered. Red phosphorus is used in the manufacture of safety matches. It is nonvolatile, unabsorbable, and insoluble substance with limited toxicity in humans. However, it may contain traces of yellow phosphorus (up to 0.6%) and large ingestions may result in adverse effects. Black phosphorus is the inert, nontoxic allotropic form of elemental phosphorus.
    B) TOXICOLOGY: Systemic phosphorus poisoning may occur following oral, inhalational, and dermal exposure. Phosphorus poisoning may cause acute fatty degeneration of the liver, kidneys, brain, and other organs. Early sudden death due to cardiovascular collapse may be induced by hypocalcemia or a direct cardiotoxic effect. Induced hypoglycemia has been responsible for deaths in the past. Phosphorus-induced liver injury may be due to free radical injury and/or inhibition of protein synthesis.
    C) EPIDEMIOLOGY: Phosphorous poisoning is rare. "Phossy jaw", an occupational illness of matchmakers who developed mandibular necrosis, has been eliminated as matches are no longer manufactured by hand and no longer contain white or yellow phosphorus.
    D) WITH POISONING/EXPOSURE
    1) ORAL: Ingestion can produce throat irritation and burns, followed by nausea, vomiting, and abdominal pain. Diarrhea may or may not be an early symptom. Gastric contents and stools may be "smoking" and luminescent in the dark, and have a garlicky odor. Phosphorescent eructations from the nose and mouth have also been reported. The absence of early gastrointestinal symptoms should not lead to the conclusion that significant poisoning has not occurred. Neurological symptoms may occur soon after ingestion or late in the clinical course with fulminant hepatic encephalopathy. Lethargy, irritability, delirium, psychosis, stupor, generalized weakness, seizures, and coma may occur. Severe poisoning may manifest as severe electrolyte abnormalities (eg, hypokalemia, hyperchloremia, hypocalcemia and either hyperphosphatemia or hypophosphatemia), hypoglycemia, encephalopathy, cardiac dysrhythmias, liver necrosis, and hepatic and/or renal failure. Other effects following oral ingestion may include clotting abnormalities, hypoprothrombinemia, thrombocytopenia, leukopenia, anemia, pancytopenia, tachypnea, shallow respirations, hyperventilation, and laryngospasm causing dyspnea and/or apnea. Death usually occurs 4 to 8 days after ingestion, but may be delayed. Death in the first 12 hours is usually the result of peripheral vascular collapse. Death within 24 to 48 hours may ensue from peripheral vascular collapse and is frequently accompanied by acute renal failure. Deaths within 48 to 72 hours may result from peripheral vascular collapse or cardiac arrest with hepatic and/or renal failure.
    2) INHALATION: Acute inhalational exposure to phosphorus fumes would be expected to produce upper respiratory irritation and possibly delayed onset of acute lung injury. Inhalational exposure may also produce conjunctivitis, ocular irritation, and mucosal irritation of the nose and throat. Acute hepatic damage has also been reported. Chronic industrial inhalational exposure to phosphorus fumes has resulted in symptoms that include bronchitis, anemia, cachexia, and mandibular necrosis ("phossy" or "Lucifer's jaw").
    3) DERMAL: Dermal exposure may result in severely painful, necrotic, partial to full thickness yellowish color burns from chemical and thermal effects with a garlic-like odor. Second and third degree burns can occur within a few minutes to hours. Phosphorus absorbed from damaged skin may result in acute systemic phosphorus poisoning.
    4) OCULAR: Ocular injury includes foreign body sensation, excessive tearing, blepharospasm, and corneal defect evident by fluorescein staining, corneal perforation, endophthalmitis, and ectropion. Exposure to phosphorus oxides causes eye irritation, blepharospasm, photophobia, and lacrimation. Direct eye contact can cause severe eye damage.
    0.2.20) REPRODUCTIVE
    A) Phosphorus has been shown to cross the placental barrier, but cases of human fetal poisoning have not been reported.

Laboratory Monitoring

    A) Laboratory evaluation should include CBC and platelet count, serum electrolytes, liver enzymes, renal function, urinalysis, ECG, urine output, serum calcium and phosphorus concentrations, and prothrombin time.
    B) Following inhalational exposure to phosphorus fumes, evaluation should include pulse oximetry, chest radiograph, arterial blood gases, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Following dermal exposure, wash exposed areas with large volume of water. Phosphorus absorbed from damaged skin may result in acute systemic phosphorus poisoning. Cutaneous burns in which white or yellow phosphorus are embedded should be immersed in water or kept very wet to prevent an exothermic reaction in the presence of oxygen, debrided surgically, and then copiously irrigated with a large volume of water. Particles removed should be immediately immersed in cool water to avoid ignition. Avoid the application of any lipid or oil based ointments as these may increase the absorption of phosphorus through the skin. Following thorough decontamination, burn management may be needed. Irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If present, carefully remove contact lenses. Manage mild hypotension with IV fluids.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Following an inhalational exposure, move the patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists and systemic corticosteroids if bronchospasm develops. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Phosphorus may cause prolongation of the QT interval. Treat torsades de pointes with IV magnesium sulfate, and correct electrolyte abnormalities, overdrive pacing may be necessary. Treat ventricular dysrhythmias using ACLS protocols.
    C) DECONTAMINATION
    1) PREHOSPITAL: Emesis is not recommended because of the corrosive potential of phosphorus. Phosphorus absorption is enhanced when dissolved in solvents (eg, alcohol, digestible fats, oils). These agents are contraindicated in the management of oral or dermal phosphorus exposure. Activated charcoal is never indicated. Following dermal exposure, prompt removal of all clothing, including jewelry, and copious irrigation with cool water should occur as soon as possible. Following an inhalational exposure, move the patient to fresh air. Monitor for respiratory distress. Irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If present, carefully remove contact lenses.
    2) HOSPITAL: ORAL EXPOSURE: Emesis is not recommended because of the corrosive potential of phosphorus. Phosphorus absorption is enhanced when dissolved in solvents (eg, alcohol, digestible fats, oils). These agents are contraindicated in the management of oral or dermal phosphorus exposure. Consider the insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestions; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining phosphorus from the stomach. Caution should be used to prevent any healthcare providers from being injured by the lavage material. Gastric contents that are removed should be immersed in water. Activated charcoal may bind to white phosphorous but there is no evidence to support its use. DERMAL EXPOSURE: Prompt removal of all clothing, including jewelry, and copious irrigation with cool water should occur as soon as possible. Phosphorus becomes liquid at 44 degrees C (or 111 degrees F) which can make decontamination more difficult. Immerse exposed areas in water or cover with wet dressings at all times. Continuous cool water irrigation can prevent further oxidation and allow removal of phosphorus particles from the skin without ignition. Particles removed should be immediately immersed in cool water to avoid ignition. Avoid application of any lipid or oil based ointments as these may increase the absorption of phosphorus through the skin. Visualization of phosphorus particles may fluoresce under an ultraviolet light source (black light, Wood's lamp). With the exposed areas immersed in water, loose or imbedded phosphorus particles that are visualized under UV light can be mechanically but delicately removed safely under water. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If present, carefully remove contact lenses.
    D) AIRWAY MANAGEMENT
    1) Patients with phosphorus exposure can develop multiorgan failure and require early intubation for airway protection. In addition, due to the intense pain of these burns, adequate pain control may lead to respiratory depression and precipitate intubation.
    E) ANTIDOTE
    1) None.
    F) VENTRICULAR DYSRHYTHMIAS
    1) Institute continuous cardiac monitoring, obtain an ECG, and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders. Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Because phosphorus exposure can cause QTc prolongation and torsades de pointes, amiodarone should only be used with extreme caution. Unstable rhythms require immediate cardioversion.
    G) ENHANCED ELIMINATION
    1) There is no role for dialysis or extracorporeal elimination. Hemodialysis may be efficacious if oliguric or anuric renal failure occurs.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with white or yellow phosphorus exposure should be evaluated in a healthcare facility.
    2) OBSERVATION CRITERIA: In some cases of oral ingestion, early gastrointestinal symptoms may resolve after a few hours. A relatively asymptomatic period may follow before more severe toxicity becomes apparent. Early improvement should not be interpreted as meaning that serious exposure has not occurred. Patients with phosphorus exposure should be monitored during the first 48 hours after exposure with frequent laboratory checks. Patients that remain asymptomatic after this monitoring period can be discharged.
    3) ADMISSION CRITERIA: Patients with severe symptoms should be admitted to the hospital. Patients with persistent cardiac dysrhythmias, mental status changes, seizures, and respiratory failure should be admitted to an ICU setting. Patients with significant burns should be admitted to a burn center.
    4) CONSULT CRITERIA: Due to the unusual nature of this exposure, consult a medical toxicologist or a regional poison center for any patient with systemic symptoms, severe exposure, or in whom the diagnosis is unclear. Patients with severe burns will also need burn specialist consultation.
    I) PITFALLS
    1) Forgetting to keep phosphorus exposed skin areas irrigated with cool water or wrapped in cool water soaked gauze after gentle removal of visible phosphorus residue from skin.
    J) TOXICOKINETICS
    1) Absorbed phosphorus may be metabolized to hypophosphoric acid. Conversion to phosphates occurs in the body. Some phosphorus may be slowly oxidized to harmless acids and excreted via the kidneys.
    K) DIFFERENTIAL DIAGNOSIS
    1) Phosphorus burns may be confused with other forms of thermal, electrical, or chemical burns. Acute liver failure may be caused by viral infections, autoimmune conditions, biliary disorders, and many other toxicants. Multisystem organ failure may be caused by sepsis or other toxicants (eg, colchicine, antineoplastic medications, and radiation).
    0.4.3) INHALATION EXPOSURE
    A) Following an inhalational exposure, move the patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists and systemic corticosteroids if bronchospasm develops.
    0.4.4) EYE EXPOSURE
    A) Irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If present, carefully remove contact lenses.
    B) Keep exposed eyes covered with wet compresses.
    C) The patient should be referred for evaluation at a health care facility and formal ophthalmologic examination.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) SUMMARY
    a) Prompt removal of all clothing, including jewelry, and copious irrigation with cool water should occur as soon as possible. Phosphorus becomes liquid at 44 degrees C (or 111 degrees F) which can make decontamination more difficult. Immerse exposed areas in water or cover with wet dressings at all times. Continuous cool water irrigation can prevent further oxidation and allow removal of phosphorus particles from the skin without ignition. Particles removed should be immediately immersed in cool water to avoid ignition. Avoid application of any lipid or oil based ointments as these may increase the absorption of phosphorus through the skin. Visualization of phosphorus particles may fluoresce under an ultraviolet light source (black light, Wood's lamp). With the exposed areas immersed in water, loose or imbedded phosphorus particles that are visualized under UV light can be mechanically but delicately removed safely under water.
    2) DECONTAMINATION
    a) Prompt removal of all clothing, including jewelry, and copious irrigation with cool water should occur as soon as possible. Phosphorus becomes liquid at 44 degrees C (or 111 degrees F) which can make decontamination more difficult (Frank et al, 2008).
    b) Immerse exposed areas in water or cover with wet dressings at all times.
    c) Continuous cool water irrigation can prevent further oxidation and allow removal of phosphorous particles from the skin without ignition (Mozingo et al, 1988). Particles removed should be immediately immersed in cool water to avoid ignition.
    1) Controversy exists regarding the use of topical copper sulfate solution which can make debridement easier because it blackens any remaining phosphorus particles. However, it is not an antidote or neutralizing agent. It can also be easily absorbed through an open wound and potentially cause intravascular hemolysis, and acute renal and cardiovascular failure; it is NOT routinely recommended (Frank et al, 2008). Some authors recommend that contaminated wounds be washed several times with a solution of 5% sodium bicarbonate AND 3% copper sulfate AND 1% hydroxy-ethyl-cellulose AND 1% sodium lauryl sulfate; rinse thoroughly with saline between washings (Ben-Hur, 1978)
    d) Avoid application of any lipid or oil based ointments as these may increase the absorption of phosphorous through the skin.
    e) Visualization of phosphorus particles may be enhanced under an ultraviolet light source (black light, Wood's lamp). Phosphorus particles should fluoresce under UV light. With the exposed areas immersed in water, loose or imbedded phosphorus particles that are visualized under UV light can be mechanically but delicately removed safely under water.
    f) Monitor the patient for the development of systemic signs or symptoms of phosphorus poisoning.

Range Of Toxicity

    A) TOXICITY: The estimated acute lethal adult dose by ingestion is 1 mg/kg with survival reported following ingestion of 1,570 mg. Ingestion of 15 mg by an adult has produced severe symptoms. As little as 3 mg has been reported to cause death in a 2-year-old child.

Clinical Effects

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) PANCYTOPENIA
    1) WITH POISONING/EXPOSURE
    a) Severe cases of inorganic phosphorus ingestions have resulted in pancytopenia and monocytosis. Positive correlations between MCV and MCH, and MCV and MCHC have been demonstrated in grade I toxicities (Fahim et al, 1992).
    B) HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Both hypoprothrombinemia and thrombocytopenia may occur following ingestion (McCarron et al, 1981), and lead to a delayed onset of hematemesis, hematochezia, hematuria, and hemorrhages into the skin and mucous membranes (HSDB , 2000; S Sweetman , 2000; McCarron et al, 1981; Chretien, 1945; Rubitsky & Myerson, 1949).
    b) CASE SERIES: In a case series of 13 yellow phosphorus ingestions, all 13 had varying degrees of hypoprothrombinemia (Makalinao & Young, 1993).
    C) LEUKOPENIA
    1) WITH POISONING/EXPOSURE
    a) Leukopenia has been observed following oral ingestion (Chretien, 1945).
    b) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), leukopenia developed in 6 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    D) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), leukocytosis developed in 4 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    E) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), thrombocytopenia developed in 2 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    F) BLOOD COAGULATION DISORDER
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), increased coagulation times developed in 15 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    G) ANEMIA
    1) WITH POISONING/EXPOSURE
    a) Patients with chronic inhalation exposure may develop anemia (Gosselin et al, 1984).
    H) NEUTROPENIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 17-year-old woman was admitted to the ED 9 hours after ingesting 3/4 of a diablillo (approximately 5.5 mg of yellow phosphorus). Granulocyte count decreased during the first 24 hours and a bone marrow biopsy was performed. Intense interstitial edema, hemorrhages, and necrotic foci were reported. During the next 48 hours, the neutropenia spontaneously resolved and the patient was discharged(Tafur et al, 2004).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Dermal phosphorus exposure produces a yellow, necrotic, severely painful second or third degree chemical burn with a garlic-like odor, and occasionally systemic toxicity (Konjoyan, 1983). Saydjari et al (1986) reported gray skin discoloration from chemical burns of white phosphorus (Saydjari et al, 1986).
    b) Eldad et al (1992) report the case of a 51-year-old chemist with a phosphorus pentachloride dermal splash injury. He sustained partial skin thickness burns over 20% of his body surface area. The wounds were treated with 1% silver sulfadiazine cream twice daily. Healing was slow (8 weeks) and painful (Eldad et al, 1992).
    B) THERMAL BURN
    1) WITH POISONING/EXPOSURE
    a) WHITE PHOSPHORUS: Four separate cases of white phosphorus burn (thermal and chemical ) injuries were reported after each individual picked up a whitish material found along the Baltic Sea Coast thinking the item was amber. Each person placed the item in their pocket, which ignited spontaneously within as little as one hour to several hours causing partial and full thickness burns to lower extremities and commonly to the hands (while attempting to put out the fire). Treatment included decontamination, irrigation and debridement in all patients; two patients required skin grafting (Frank et al, 2008).
    C) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) DERMAL IRRITATION: Patients exposed to phosphorus oxides vapors have developed skin irritation (Wason et al, 1984).
    D) PALE COMPLEXION
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a case series of 13 yellow phosphorus ingestions, 36% presented with pallor (Makalinao & Young, 1993).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) DISORDER OF BONE
    1) WITH POISONING/EXPOSURE
    a) PHOSPHORUS BANDS: Radiographs of the long bones may demonstrate increased density of metaphyseal lines (phosphorschicht) after survival of acute oral poisoning (Blumenthal & Lesser, 1938).
    b) PHOSSY JAW: Chronic phosphorus poisoning may result in osteomyelitis of the jaw bones ("phossy jaw"), most frequently of the mandible, commonly beginning as a dental abnormality. Phossy jaw is often fatal (HSDB , 2000).
    B) INCREASED MUSCLE TONE
    1) WITH POISONING/EXPOSURE
    a) MUSCLE SPASMS: Acute systemic phosphorus toxicity may result in hypocalcemia or hyperventilation with resultant effects of muscle spasms or contractions.
    1) CASE REPORT: A low birth weight infant developed hypocalcemia with severe laryngospasm and generalized muscle spasms in both arms and legs following an accidental overdose of 10 times the prescribed amount of phosphorus in an enteral feeding (van den Anker et al, 1992).

Summary Of Exposure

    A) USES: "Phosphorus" as used in this management indicates only yellow or white phosphorus unless otherwise stated. Phosphorus is a nonmetallic chemical element of the nitrogen family. It is essential for many biologic processes including synthesis of ATP. Yellow and white phosphorus are used in the manufacture of rodenticides, incendiaries, phosphorus compounds, as an igniter in munitions and flares, as an igniter and pigment in fireworks, and as a semiconductor additive. Although no longer used in medicine, phosphorus is still used in some homeopathic medicines. Yellow or white phosphorus was used in the manufacture of matches in the past and was responsible for both chronic poisoning in workers and acute poisoning from ingestion of matches. Modern matches (including the "Strike Anywhere" variety) do NOT contain yellow or white phosphorus, but contain phosphorus sesquifluoride and potassium chlorate. Chronic phosphorus poisoning is now rarely encountered. Red phosphorus is used in the manufacture of safety matches. It is nonvolatile, unabsorbable, and insoluble substance with limited toxicity in humans. However, it may contain traces of yellow phosphorus (up to 0.6%) and large ingestions may result in adverse effects. Black phosphorus is the inert, nontoxic allotropic form of elemental phosphorus.
    B) TOXICOLOGY: Systemic phosphorus poisoning may occur following oral, inhalational, and dermal exposure. Phosphorus poisoning may cause acute fatty degeneration of the liver, kidneys, brain, and other organs. Early sudden death due to cardiovascular collapse may be induced by hypocalcemia or a direct cardiotoxic effect. Induced hypoglycemia has been responsible for deaths in the past. Phosphorus-induced liver injury may be due to free radical injury and/or inhibition of protein synthesis.
    C) EPIDEMIOLOGY: Phosphorous poisoning is rare. "Phossy jaw", an occupational illness of matchmakers who developed mandibular necrosis, has been eliminated as matches are no longer manufactured by hand and no longer contain white or yellow phosphorus.
    D) WITH POISONING/EXPOSURE
    1) ORAL: Ingestion can produce throat irritation and burns, followed by nausea, vomiting, and abdominal pain. Diarrhea may or may not be an early symptom. Gastric contents and stools may be "smoking" and luminescent in the dark, and have a garlicky odor. Phosphorescent eructations from the nose and mouth have also been reported. The absence of early gastrointestinal symptoms should not lead to the conclusion that significant poisoning has not occurred. Neurological symptoms may occur soon after ingestion or late in the clinical course with fulminant hepatic encephalopathy. Lethargy, irritability, delirium, psychosis, stupor, generalized weakness, seizures, and coma may occur. Severe poisoning may manifest as severe electrolyte abnormalities (eg, hypokalemia, hyperchloremia, hypocalcemia and either hyperphosphatemia or hypophosphatemia), hypoglycemia, encephalopathy, cardiac dysrhythmias, liver necrosis, and hepatic and/or renal failure. Other effects following oral ingestion may include clotting abnormalities, hypoprothrombinemia, thrombocytopenia, leukopenia, anemia, pancytopenia, tachypnea, shallow respirations, hyperventilation, and laryngospasm causing dyspnea and/or apnea. Death usually occurs 4 to 8 days after ingestion, but may be delayed. Death in the first 12 hours is usually the result of peripheral vascular collapse. Death within 24 to 48 hours may ensue from peripheral vascular collapse and is frequently accompanied by acute renal failure. Deaths within 48 to 72 hours may result from peripheral vascular collapse or cardiac arrest with hepatic and/or renal failure.
    2) INHALATION: Acute inhalational exposure to phosphorus fumes would be expected to produce upper respiratory irritation and possibly delayed onset of acute lung injury. Inhalational exposure may also produce conjunctivitis, ocular irritation, and mucosal irritation of the nose and throat. Acute hepatic damage has also been reported. Chronic industrial inhalational exposure to phosphorus fumes has resulted in symptoms that include bronchitis, anemia, cachexia, and mandibular necrosis ("phossy" or "Lucifer's jaw").
    3) DERMAL: Dermal exposure may result in severely painful, necrotic, partial to full thickness yellowish color burns from chemical and thermal effects with a garlic-like odor. Second and third degree burns can occur within a few minutes to hours. Phosphorus absorbed from damaged skin may result in acute systemic phosphorus poisoning.
    4) OCULAR: Ocular injury includes foreign body sensation, excessive tearing, blepharospasm, and corneal defect evident by fluorescein staining, corneal perforation, endophthalmitis, and ectropion. Exposure to phosphorus oxides causes eye irritation, blepharospasm, photophobia, and lacrimation. Direct eye contact can cause severe eye damage.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER: Temperature elevations in the absence of infectious complications may be seen (Rubitsky & Myerson, 1949; Blumenthal & Lesser, 1938).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTENSION: Hypotension or shock may occur early in the course of an oral ingestion or may be a delayed finding during the third stage of toxicity (McCarron et al, 1981).

Heent

    3.4.2) HEAD
    A) WITH POISONING/EXPOSURE
    1) ORAL EXPOSURE
    a) Ingestion can produce throat irritation and burns (HSDB , 2000; McCarron et al, 1981).
    b) Odor of garlic to the breath may be noted (HSDB , 2000; Rubitsky & Myerson, 1949; Simon & Pickering, 1976).
    c) Phosphorescent eructations from the mouth and nose have been reported (HSDB , 2000; Rubitsky & Myerson, 1949).
    2) INHALATION EXPOSURE
    a) Acute exposure may produce conjunctivitis, ocular irritation, and mucosal irritation of the nose and throat (HSDB , 2000; Wason et al, 1984).
    b) Chronic industrial exposure has resulted in mandibular necrosis ("phossy jaw" or "Lucifer's jaw"). Chronic inhalation of phosphorus vapors can produce mandibular necrosis (HSDB , 2000; Harbison, 1998; Felton, 1982). The mandibular necrosis was coined "phossy jaw" due to the mutilating and devastating effect it had on workers in the 1800's. The shortest recorded exposure (to unmeasured amounts) causing this effect was 10 months (Hughes, 1962).
    c) Phosphorus absorbed through inhalation can result in acute hepatic damage and systemic phosphorus poisoning.
    3) DERMAL EXPOSURE
    a) Ocular injury includes foreign body sensation, excessive tearing, blepharospasm, and corneal defect evident by fluorescein staining, corneal perforation, endophthalmitis, and ectropion. Exposure to phosphorus oxides vapors causes eye irritation (Wason et al, 1984), blepharospasm, photophobia, and lacrimation (HSDB , 2000; Scherling & Blondis, 1945). Direct eye contact can cause severe eye damage (Grant & Schuman, 1993).
    b) CASE REPORT: A 51-year-old chemist sustained superficial corneal erosions when phosphorus pentachloride solution splashed into his eyes. His corneal erosions healed within 72 hours (Eldad et al, 1992).
    c) Dermal exposure may cause severely painful, necrotic, partial to full thickness yellowish color burns from chemical and thermal effects with a garlic-like odor. This is likely to occur if it reaches the ignition temperature (44 degrees Celsius or 111 degrees Fahrenheit).
    d) Phosphorus absorbed from damaged skin may result in acute systemic phosphorus poisoning. There are isolated reports of retinal edema, retinal hemorrhages, neuritic and edematous changes in the optic nervehead, and destruction of the orbit and the globe from a necrotic and destructive process in the maxilla extending into the orbit in chronic systemic phosphorus poisoning in humans (Grant & Schuman, 1993).
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CHEMICAL OCULAR BURNS: Direct eye contact can cause severe eye damage (Grant & Schuman, 1993).
    a) CASE REPORT: A 51-year-old chemist sustained superficial corneal erosions when phosphorus pentachloride solution splashed into his eyes. His corneal erosions healed within 72 hours (Eldad et al, 1992).
    2) CONJUNCTIVITIS: Exposure to phosphorus oxides vapors causes eye irritation (Wason et al, 1984), blepharospasm, photophobia, and lacrimation (HSDB , 2000; Scherling & Blondis, 1945). White phosphorus particles are caustic, and may result in severe tissue damage when exposed to eyes (Grant & Schuman, 1993).
    3) CHRONIC POISONING: There are isolated reports of retinal edema, retinal hemorrhages, neuritic and edematous changes in the optic nerveheads, and destruction of the orbit and the globe from a necrotic and destructive process in the maxilla extending into the orbit in chronic systemic phosphorus poisoning in humans (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) MUCOSAL IRRITATION: Inhalation exposure can cause irritation of the nasal mucosa (HSDB , 2000; Wason et al, 1984).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) MUCOSAL IRRITATION: Inhalation exposure can cause irritation of the pharyngeal mucosa (Wason et al, 1984). Ingestion can produce throat irritation and burns (HSDB , 2000; McCarron et al, 1981).
    2) GARLIC ODOR: A garlic odor may be noted on the breath (HSDB , 2000; Rubitsky & Myerson, 1949; Simon & Pickering, 1976). Phosphorescent eructations from the nose and mouth have rarely been described (Rubitsky & Myerson, 1949).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CARDIOTOXICITY: Early cardiovascular collapse may occur after ingestion and may represent a direct phosphorus cardiotoxicity (Diaz-Rivera et al, 1961). Cardiovascular collapse may lead to death within 24 to 48 hours, in the first stage of poisoning (HSDB , 2000; Flomenbaum, 1998; Kelkar & Gandhi, 1995).
    b) CASE REPORT: An 18-year-old man was brought to the ICU unconscious and gasping after ingesting tea poisoned with white phosphorus. His blood pressure was not recordable, he was areflexic and he had an irregular heart rate of 40 beats/minute. A tube was inserted to obtain stomach contents and for gastric lavage. After insertion, a small cloud of whitish smoke and a yellow flame was seen coming out of the open end of the tube. Within seconds, there was an explosion and a huge ball of dense white smoke emerged from the tube. Moments later, the patient's hair and shirt were on fire. In spite of intense resuscitation and lavage with potassium permanganate, the patient died of peripheral circulatory failure within the next 2 minutes (Pande & Pandey, 2004).
    B) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) ECG changes include tachycardia, ST-T wave changes, prolonged QTc, low voltage QRS after ingestion (Diaz-Rivera et al, 1961). ECG changes may be due to a direct toxic action of phosphorus on the myocardium, or may be due to metabolic disturbances.
    C) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Various dysrhythmias, including nodal rhythms and ventricular fibrillation, have been noted after ingestion (Diaz-Rivera et al, 1961). Some patients with white phosphorus burns have had sudden death and documented ventricular dysrhythmias (Konjoyan, 1983).
    b) At least one of these patients with dermal burns and sudden death had a reversed calcium-phosphorus ratio (Konjoyan, 1983).
    c) Hypocalcemia and hypomagnesemia with associated QTc prolongation and ventricular dysrhythmias including bigeminy, ventricular tachycardia, refractory ventricular fibrillation, and cardiac arrest may occur following ingestion and dermal exposure (McCarron et al, 1981; Konjoyan, 1983).
    d) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), dysrhythmias developed in 2 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    D) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), bradycardia developed in 1 patient after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    E) TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), tachycardia developed in 3 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY FINDING
    1) WITH POISONING/EXPOSURE
    a) ORAL EXPOSURE
    1) Tachypnea, shallow respirations, hyperventilation.
    2) Laryngospasm causing dyspnea and or apnea may occur. Periods of apnea with cyanosis as a result of laryngospasm occurred in a low birth weight infant following an accidental overdose of 10 times the prescribed amount of phosphorus in an enteral feeding. Severe hypocalcemia was also present (van den Anker et al, 1992).
    b) INHALATION EXPOSURE
    1) Inhalation of phosphorus oxide vapors can produce respiratory tract irritation with wheezing, cough, dyspnea, and chest discomfort. Abnormalities of pulmonary function tests may be seen after inhalation exposure, but have a tendency to return toward normal with time. Mild systemic toxicity may occur with inhalation exposure (Wason et al, 1984).
    2) Dutton et al (1993) report a prospective occupational exposure study over a 3 to 7 year period involving 131 workers exposed to elevated inhalation levels of phosphoric acid, phosphorus pentoxide, fluorides and coal tar pitch volatiles. After adjusting for age and smoking, no residual significant effect of industrial exposure could be reported following annual pulmonary function testing.
    3) Potential for delayed non-cardiogenic pulmonary edema was also present (van den Anker et al, 1992).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) TOXIC ENCEPHALOPATHY
    1) WITH POISONING/EXPOSURE
    a) NEUROTOXICITY: Neurological symptoms may occur soon after ingestion or late in the clinical course with fulminant hepatic encephalopathy (McCarron et al, 1981; Rubitsky & Myerson, 1949).
    1) Lethargy, irritability, delirium, generalized weakness, seizures, and coma may be seen (HSDB , 2000; Kelkar & Gandhi, 1995; McCarron et al, 1981; Simon & Pickering, 1976).
    2) Patients in one series who had early neurological symptoms without gastrointestinal symptoms had nearly three times the incidence mortality (73%) as did those with only early gastrointestinal symptoms (23%) (McCarron et al, 1981).
    b) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), encephalopathy developed in 8 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been noted following ingestion or inhalation exposure (Chretien, 1945; Wason et al, 1984).
    b) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), headache developed in 5 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    C) LOSS OF CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), temporary loss of consciousness developed in 4 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting may be seen early after ingestion (HSDB , 2000; Simon & Pickering, 1976; Rubitsky & Myerson, 1949), or may not occur until late in the clinical course (McCarron et al, 1981). The vomitus has been described as "smoking", luminescent, and with a garlicky odor (HSDB , 2000; Flomenbaum, 1998; Kelkar & Gandhi, 1995; Harbison, 1998).
    1) The absence of early gastrointestinal symptoms should not lead to the conclusion that significant poisoning has not occurred (McCarron et al, 1981).
    b) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), nausea and vomiting developed in 21 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus). Hematemesis developed in 3 patients (Gonzalez-Andrade & Lopez-Pulles, 2011).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea may or may not be an early symptom (McCarron et al, 1981).
    b) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), diarrhea developed in 60 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    C) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), abdominal pain and cramps developed in 60 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    D) STOOL FINDING
    1) WITH POISONING/EXPOSURE
    a) SMOKING STOOLS: Gastric contents and stools may be smoking, luminescent in the dark, or fluorescent under an ultraviolet light (HSDB , 2000; Flomenbaum, 1998; Simon & Pickering, 1976; Chretien, 1945; Rubitsky & Myerson, 1949). These findings may be absent in the majority of patients ingesting phosphorus (McCarron et al, 1981).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) Perilobar hepatic necrosis and hepatic failure with fatty degeneration of the liver may occur. Delayed sequelae includes severe acute yellow atrophy of the liver, which may become fatal (HSDB , 2000).
    b) Fatty degeneration of the liver with severe hepatic failure and encephalopathy may occur following oral ingestion and usually is delayed in onset for at least 24 hours after exposure (HSDB , 2000; Kelkar & Gandhi, 1995; McCarron et al, 1981; Chretien, 1945).
    c) Hepatomegaly, jaundice, abnormal liver function tests, and hypoprothrombinemia may be seen (McCarron et al, 1981).
    d) CASE SERIES: Hepatic toxicity was reported in 15 cases of yellow phosphorus-containing fireworks ingestion. Four (27%) developed fulminant liver failure, while 5 (33%) had varying degrees of hepatocellular necrosis and cholestasis, 4 (27%) had subclinical hepatic injury, and 2 (13%) showed no evidence of hepatic damage (Fernandez & Canizares, 1995).
    e) CASE REPORTS: In Latin America, three cases of acute liver damage developed following the ingestion of firecrackers containing white phosphorus (Santos et al, 2009).
    1) A 4-year-old child inadvertently ingested 10 firecrackers and gradually developed jaundice, malaise and weakness, along with an elevated serum aminotransferase level (887 International Units) and coagulopathy. Her mentation declined and she became comatose. Following a protracted hospital course, the patient completely recovered after liver transplantation.
    2) A 32-year-old male who intentionally ingested 12 firecrackers developed a prolonged prothrombin and elevated liver enzymes. Shortly after admission, the patient developed multi-organ failure including renal and liver dysfunction, grade II encephalopathy, metabolic acidosis, and severe coagulopathy. The patient died 3 days after admission, despite aggressive care.
    3) A 15-year-old female who intentionally ingested 9 firecrackers developed a prolonged prothrombin with initially normal liver and renal function. By day 3, her prothrombin, aminotransferase and bilirubin levels were elevated with no new symptoms. Over the next 10 days, laboratory studies gradually improved and the patient recovered completely.
    f) CASE REPORT: A 30-year-old male developed hepatic encephalopathy with coma 5 days after an intentional ingestion of yellow phosphorus, 30 grams of Ratol(R), a rodenticide. The patient remained hospitalized for 4 weeks, until his hepatic laboratory values returned to normal (Kelkar & Gandhi, 1995).
    g) CASE REPORT: A 25-year-old woman presented with a history of ingestion of an unknown quantity of Ratol(R) (3% yellow phosphorus) 5 days prior to admission. On admission, liver enzymes were elevated and prothrombin time (PT) was over 2 minutes. She was hospitalized for 2 weeks and discharged when liver enzymes and PT were returning to normal(Karanth & Nayyar, 2003).
    h) Subclinical elevations of liver function tests have been seen in patients exposed to phosphorus oxide vapors by inhalation (Wason et al, 1984).
    B) JAUNDICE
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), jaundice developed in 31 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    C) HYPERBILIRUBINEMIA
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), hyperbilirubinemia developed in 31 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    D) CIRRHOSIS OF LIVER
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), cirrhosis developed in 2 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    E) CHOLESTATIC JAUNDICE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), cholestatic syndrome developed in 3 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    F) INFLAMMATORY DISEASE OF LIVER
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), hepatitis developed in 5 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    G) INCREASED LIVER ENZYMES
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), elevated liver enzymes developed in 27 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    H) SERUM ALKALINE PHOSPHATASE RAISED
    1) WITH POISONING/EXPOSURE
    a) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), elevated alkaline phosphatase developed in 20 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).
    I) HEPATIC FAILURE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 21-year-old woman was admitted to the ICU 6 days after consuming a phosphorous-based rodenticide. A diagnosis of acute fulminant hepatic failure secondary to toxic hepatitis due to poisoning was made. By day 3 of admission, her Glasgow Coma Scale was 4/15. She subsequently developed hemodynamic instability and bradycardia followed by ventricular fibrillation. She was resuscitated, but her condition worsened and she expired on 6th day of admission(Karanth & Nayyar, 2003).
    b) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), acute liver failure developed in 4 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Abnormal renal function tests, hematuria, albuminuria, and oliguric or anuric renal failure may develop following ingestion (HSDB , 2000; McCarron et al, 1981; Rubitsky & Myerson, 1949). A common pathological finding at autopsy is fatty degeneration of the liver and kidneys (HSDB , 2000).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FAILURE ACUTE
    a) Nephrotoxicity with decreased creatinine clearance, elevated blood urea nitrogen, and progressive anuric renal failure has been demonstrated in phosphorus dermal burn in animal models (Konjoyan, 1983).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) Hypoglycemia may occur after oral ingestion (McCarron et al, 1981).
    b) CASE SERIES: In a case series of 13 yellow phosphorus ingestions, all 13 had varying degrees of hypoglycemia (Makalinao & Young, 1993).
    c) In a cross-sectional study (n=85; age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years), hypoglycemia developed in 11 patients after the ingestion of up to 40 units of firecrackers (containing up to 12 g of white phosphorus) (Gonzalez-Andrade & Lopez-Pulles, 2011).

Reproductive

    3.20.1) SUMMARY
    A) Phosphorus has been shown to cross the placental barrier, but cases of human fetal poisoning have not been reported.
    3.20.3) EFFECTS IN PREGNANCY
    A) PLACENTAL BARRIER
    1) HUMANS
    a) Phosphorus has been shown to cross the placental barrier (Gosselin et al, 1984), but cases of human fetal poisoning have not been reported.
    2) ANIMAL STUDIES
    a) Phosphorus was found to cause post-implantation mortality and affect litter size when administered orally (RTECS , 2000).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7723-14-0 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Laboratory evaluation should include CBC and platelet count, serum electrolytes, liver enzymes, renal function, urinalysis, ECG, urine output, serum calcium and phosphorus concentrations, and prothrombin time.
    B) Following inhalational exposure to phosphorus fumes, evaluation should include pulse oximetry, chest radiograph, arterial blood gases, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Laboratory evaluation should include CBC and platelet count, serum electrolytes, liver enzymes, renal function, and serum calcium and phosphorus concentrations.
    B) COAGULATION STUDIES
    1) Monitor international normalized ratio (INR) or prothrombin time.
    C) HEMATOLOGIC
    1) Monitor CBC and platelet count carefully, especially in symptomatic patients.
    D) ACID/BASE
    1) Baseline arterial blood gases should be obtained in patients with significant inhalation exposure to phosphorus oxides vapors or respiratory tract irritation.
    4.1.3) URINE
    A) URINALYSIS
    1) Monitor urine output and urinalysis.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) Following inhalational exposure to phosphorus fumes, evaluation should include pulse oximetry, chest radiograph, arterial blood gases, and pulmonary function tests.
    2) ECG
    a) Obtain serial ECGs and institute continuous cardiac monitoring to detect possible QRS or QTc interval changes or ventricular dysrhythmias due to hypocalcemia or hypokalemia.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Baseline chest x-ray should be obtained in patients with significant inhalation exposure to phosphorus oxides vapors or respiratory tract irritation.
    B) RADIOGRAPHIC-OTHER
    1) PHOSSY JAW: Routine x-ray film of the mandible is a good dental practice in exposed workers. Necrosis may occur in the absence of any visible roentgenogram pathology (Hughes, 1962).

Methods

    A) OTHER
    1) While serum phosphorus levels can be measured in most hospital laboratories, they may be either normal, elevated, or decreased after acute oral ingestions (McCarron et al, 1981) and are not useful for diagnosis.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with severe symptoms should be admitted to the hospital. Patients with persistent cardiac dysrhythmias, mental status changes, seizures, and respiratory failure should be admitted to an ICU setting. Patients with significant burns should be admitted to a burn center.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with white or yellow phosphorus exposure should be evaluated in a healthcare facility.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Due to the unusual nature of this exposure, consult a medical toxicologist or a regional poison center for any patient with systemic symptoms, severe exposure, or in whom the diagnosis is unclear. Patients with severe burns will also need burn specialist consultation.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) In some cases of oral ingestion, early gastrointestinal symptoms may resolve after a few hours. A relatively asymptomatic period may follow before more severe toxicity becomes apparent. Early improvement should not be interpreted as meaning that serious exposure has not occurred. Patients with phosphorus exposure should be monitored during the first 48 hours after exposure with frequent laboratory checks. Patients that remain asymptomatic after this monitoring period can be discharged.

Monitoring

    A) Laboratory evaluation should include CBC and platelet count, serum electrolytes, liver enzymes, renal function, urinalysis, ECG, urine output, serum calcium and phosphorus concentrations, and prothrombin time.
    B) Following inhalational exposure to phosphorus fumes, evaluation should include pulse oximetry, chest radiograph, arterial blood gases, and pulmonary function tests.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Emesis is not recommended because of the corrosive potential of phosphorus. Phosphorus absorption is enhanced when dissolved in solvents (eg, alcohol, digestible fats, oils). These agents are contraindicated in the management of oral or dermal phosphorus exposure. Activated charcoal is never indicated. Following dermal exposure, prompt removal of all clothing, including jewelry, and copious irrigation with cool water should occur as soon as possible. Following an inhalational exposure, move the patient to fresh air. Monitor for respiratory distress. Irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If present, carefully remove contact lenses.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Emesis is not recommended because of the corrosive potential of phosphorus. Phosphorus absorption is enhanced when dissolved in solvents (eg, alcohol, digestible fats, oils). These agents are contraindicated in the management of oral or dermal phosphorus exposure. Consider the insertion of a small, flexible nasogastric or orogastric (preferred) tube to suction gastric contents after recent large ingestions; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining phosphorus from the stomach. Caution should be used to prevent any healthcare providers from being injured by the lavage material. Gastric contents that are removed should be immersed in water.
    2) Activated charcoal may bind to white phosphorous but there is no evidence to support its use (Beuhler, 2013).
    B) NASOGASTRIC ASPIRATION
    1) INDICATIONS: Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after large, recent ingestion of caustics. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
    b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:
    1) Complications of gastric aspiration may include: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach (Vale, 1997). Combative patients may be at greater risk for complications.
    3) Gastric lavage with potassium permanganate (1:5,000 solution) has been recommended to convert phosphorus to harmless oxidation products (Chretien, 1945). However, there are no controlled clinical data regarding its efficacy.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Following dermal exposure, wash exposed areas with large volume of water. Phosphorus absorbed from damaged skin may result in acute systemic phosphorus poisoning. Cutaneous burns in which white or yellow phosphorus are embedded should be immersed in water or kept very wet to prevent an exothermic reaction in the presence of oxygen, debrided surgically, and then copiously irrigated with a large volume of water. Particles removed should be immediately immersed in cool water to avoid ignition. Avoid the application of any lipid or oil based ointments as these may increase the absorption of phosphorus through the skin. Following thorough decontamination, burn management may be needed. Irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If present, carefully remove contact lenses. Manage mild hypotension with IV fluids.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Following an inhalational exposure, move the patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists and systemic corticosteroids if bronchospasm develops. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Phosphorus may cause prolongation of the QT interval. Treat torsades de pointes with IV magnesium sulfate, and correct electrolyte abnormalities, overdrive pacing may be necessary. Treat ventricular dysrhythmias using ACLS protocols.
    B) MONITORING OF PATIENT
    1) Laboratory evaluation should include CBC and platelet count, serum electrolytes, liver enzymes, renal function, urinalysis, ECG, urine output, serum calcium and phosphorus concentrations, and prothrombin time.
    2) Following inhalational exposure to phosphorus fumes, evaluation should include pulse oximetry, chest radiograph, arterial blood gases, and pulmonary function test.
    C) BLOOD AND FLUIDS PRECAUTIONS
    1) Protect patient and healthcare providers from secondary exposure to phosphorus, vomitus, gastric washings, and feces. Gastric contents and stools that are luminescent or smoking contain phosphorus.
    2) Medical personnel should wear gloves and other protective clothing as required to avoid dermal contact.
    3) FIRE PRECAUTIONS
    a) Fire fighters should wear flame retardant full protective clothing and positive pressure, self-contained breathing apparatus (SCUBA) when fighting fires.
    b) Deluge fire with water, taking care not to scatter, until fire is extinguished and phosphorus has solidified, then cover with wet sand.
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    E) TRANSFUSION
    1) If frank bleeding is apparent, blood product replacement may be necessary.
    F) BLOOD COAGULATION DISORDER
    1) Hypoprothrombinemia should be managed with fresh frozen plasma and vitamin K.
    G) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    H) HYPOCALCEMIA
    1) Hypocalcemia in the absence of clinical tetany may occur following oral ingestion or dermal exposure. Check patient for a positive Trousseau's or Chvostek's sign.
    2) Correct known or suspected hypocalcemia with intravenous CALCIUM GLUCONATE (10%) 0.1 to 0.2 mL/kg up to 10 mL/dose or intravenous CALCIUM CHLORIDE. Repeat dose if necessary.
    3) Monitor ECG continuously and serial calcium and potassium levels hourly during therapy. Suspect hypocalcemia and/or hypomagnesemia if QTc interval is prolonged.
    a) Treat aggressively with intravenous calcium in the presence of any ECG or clinical signs of hypocalcemia (ie, hypotension) while serum calcium levels are pending. Serum levels should be obtained as soon as possible to monitor calcium therapy.
    I) CONDUCTION DISORDER OF THE HEART
    1) Monitor ECG carefully for dysrhythmias or QTc interval prolongation.
    2) Institute calcium replacement in patients with ECG evidence of hypocalcemia (QTc interval prolongation).
    3) LIDOCAINE
    a) LIDOCAINE/DOSE
    1) ADULT: 1 to 1.5 milligrams/kilogram via intravenous push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given at 5 to 10 minute intervals to a maximum dose of 3 milligrams/kilogram (Neumar et al, 2010). Only bolus therapy is recommended during cardiac arrest.
    a) Once circulation has been restored begin a maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus and increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (Neumar et al, 2010).
    2) CHILD: 1 milligram/kilogram initial bolus IV/IO; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (de Caen et al, 2015).
    b) LIDOCAINE/MAJOR ADVERSE REACTIONS
    1) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010).
    c) LIDOCAINE/MONITORING PARAMETERS
    1) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
    4) TORSADE DE POINTES
    a) SUMMARY
    1) Withdraw the causative agent. Hemodynamically unstable patients with Torsades de pointes (TdP) require electrical cardioversion. Emergent treatment with magnesium (first-line agent) or atrial overdrive pacing is indicated. Detect and correct underlying electrolyte abnormalities (ie, hypomagnesemia, hypokalemia, hypocalcemia). Correct hypoxia, if present (Drew et al, 2010; Neumar et al, 2010; Keren et al, 1981; Smith & Gallagher, 1980).
    2) Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. Overdrive pacing or isoproterenol may be successful in terminating TdP, particularly when accompanied by bradycardia or if TdP appears to be precipitated by pauses in rhythm (Neumar et al, 2010). In patients with polymorphic VT with a normal QT interval, magnesium is unlikely to be effective (Link et al, 2015).
    b) MAGNESIUM SULFATE
    1) Magnesium is recommended (first-line agent) for the prevention and treatment of drug-induced torsades de pointes (TdP) even if the serum magnesium concentration is normal. QTc intervals greater than 500 milliseconds after a potential drug overdose may correlate with the development of TdP (Charlton et al, 2010; Drew et al, 2010). ADULT DOSE: No clearly established guidelines exist; an optimal dosing regimen has not been established. Administer 1 to 2 grams diluted in 10 milliliters D5W IV/IO over 15 minutes (Neumar et al, 2010). Followed if needed by a second 2 gram bolus and an infusion of 0.5 to 1 gram (4 to 8 mEq) per hour in patients not responding to the initial bolus or with recurrence of dysrhythmias (American Heart Association, 2005; Perticone et al, 1997). Rate of infusion may be increased if dysrhythmias recur. For persistent refractory dysrhythmias, a continuous infusion of up to 3 to 10 milligrams/minute in adults may be given (Charlton et al, 2010).
    2) PEDIATRIC DOSE: 25 to 50 milligrams/kilogram diluted to 10 milligrams/milliliter for intravenous infusion over 5 to 15 minutes up to 2 g (Charlton et al, 2010).
    3) PRECAUTIONS: Use with caution in patients with renal insufficiency.
    4) MAJOR ADVERSE EFFECTS: High doses may cause hypotension, respiratory depression, and CNS toxicity (Neumar et al, 2010). Toxicity may be observed at magnesium levels of 3.5 to 4.0 mEq/L or greater (Charlton et al, 2010).
    5) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respiratory rate, motor strength, deep tendon reflexes, serum magnesium, phosphorus, and calcium concentrations (Prod Info magnesium sulfate heptahydrate IV, IM injection, solution, 2009).
    c) OVERDRIVE PACING
    1) Institute electrical overdrive pacing at a rate of 130 to 150 beats per minute, and decrease as tolerated. Rates of 100 to 120 beats per minute may terminate torsades (American Heart Association, 2005). Pacing can be used to suppress self-limited runs of TdP that may progress to unstable or refractory TdP, or for override refractory, persistent TdP before the potential development of ventricular fibrillation (Charlton et al, 2010). In a case series overdrive pacing was successful in terminating TdP associated with bradycardia and drug-induced QT prolongation (Neumar et al, 2010).
    d) POTASSIUM REPLETION
    1) Potassium supplementation, even if serum potassium is normal, has been recommended by many experts (Charlton et al, 2010; American Heart Association, 2005). Supplementation to supratherapeutic potassium concentrations of 4.5 to 5 mmol/L has been suggested, although there is little evidence to determine the optimal range in dysrhythmia (Drew et al, 2010; Charlton et al, 2010).
    e) ISOPROTERENOL
    1) Isoproterenol has been successful in aborting torsades de pointes that was resistant to magnesium therapy in a patient in whom transvenous overdrive pacing was not an option (Charlton et al, 2010) and has been successfully used to treat torsades de pointes associated with bradycardia and drug induced QT prolongation (Keren et al, 1981; Neumar et al, 2010). Isoproterenol may have a limited role in pharmacologic overdrive pacing in select patients with drug-induced torsades de pointes and acquired long QT syndrome (Charlton et al, 2010; Neumar et al, 2010). Isoproterenol should be avoided in patients with polymorphic VT associated with familial long QT syndrome (Neumar et al, 2010).
    2) DOSE: ADULT: 2 to 10 micrograms/minute via a continuous monitored intravenous infusion; titrate to heart rate and rhythm response (Neumar et al, 2010).
    3) PRECAUTIONS: Correct hypovolemia before using; contraindicated in patients with acute cardiac ischemia (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    a) Contraindicated in patients with preexisting dysrhythmias; tachycardia or heart block due to digitalis toxicity; ventricular dysrhythmias that require inotropic therapy; and angina. Use with caution in patients with coronary insufficiency (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    4) MAJOR ADVERSE EFFECTS: Tachycardia, cardiac dysrhythmias, palpitations, hypotension or hypertension, nervousness, headache, dizziness, and dyspnea (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    5) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respirations and central venous pressure to guide volume replacement (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    f) OTHER DRUGS
    1) Mexiletine, verapamil, propranolol, and labetalol have also been used to treat TdP, but results have been inconsistent (Khan & Gowda, 2004).
    g) AVOID
    1) Avoid class Ia antidysrhythmics (eg, quinidine, disopyramide, procainamide, aprindine), class Ic (eg, flecainide, encainide, propafenone) and most class III antidysrhythmics (eg, N-acetylprocainamide, sotalol) since they may further prolong the QT interval and have been associated with TdP.
    J) INJURY OF LIVER
    1) N-ACETYLCYSTEINE
    a) Data indicate that phosphorus-induced liver injury may be a free radical mediated process. Administration of antioxidants may play a role in mitigating the resultant tissue injury (Di Lusio, 1966).
    1) Panganiban (1993) reports on the use of N-acetylcysteine (NAC) in patients with stage I or stage III phosphorus toxicity. A dose regimen of 150 mg/kg in 200 mL D5W for 15 min, then 50 mg/kg in 500 mL D5W for 4 hr, then 100 mg/kg in 1000 mL D5W for 16 hours was given. The author concluded that NAC may be effective in preventing progression of liver damage when given in stage I of illness (Panganiban, 1993).
    b) Additional studies are needed to determine the efficacy of antioxidant therapy in phosphorus-induced liver failure.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Follow treatment recommendations in the ORAL EXPOSURE section where appropriate.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) APPLICATION OF DRESSING
    1) Keep exposed eyes covered with wet dressings until definitive surgical removal of phosphorus can be accomplished.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) PHOSPHORUS REMOVAL
    1) Brush all nonadherent phosphorus from the skin. Avoid application of any lipid based ointments as these may increase the skin penetration of phosphorus.
    2) Remove clothing and promptly begin continuous water irrigation of the affected site (Mozingo et al, 1988).
    3) Continuous irrigation can prevent further oxidation and allow removal of white phosphorus particles from the skin surface without re-ignition (Frank et al, 2008; Mozingo et al, 1988).
    4) Cool water- or saline-soaked dressings applied to the affected area will allow the patient to be transported without re-ignition of the remaining particles. Keep dressing moist until debridement is accomplished (Frank et al, 2008; Mozingo et al, 1988).
    B) PHOSPHORUS VISUALIZATION/REMOVAL
    1) WOOD'S LAMP
    a) Visualization of phosphorus may be enhanced by employing the use of the Wood's lamp (Frank et al, 2008; Anon, 1975). Phosphorus will fluoresce under ultraviolet light. With the exposed areas immersed in water, loose or imbedded phosphorous particles that are visualized under UV light can be mechanically but delicately removed safely under water. This technique may be a safer alternative than either the use of copper sulfate or silver nitrate, and may be the method of choice (Mozingo et al, 1988).
    2) COPPER SULFATE
    a) Traditionally, copper sulfate solution has been topically applied to skin burns caused by yellow phosphorus(Zong-Yue et al, 1985), but it is NOT routinely recommended currently.
    b) The rationale for the use of copper sulfate is based on a chemical reaction that binds up the phosphorus thereby preventing further burning due to phosphorus oxidation. The granules of Cu3P2 are black and decompose easily (Zong-Yue et al, 1985). 
         3Cu(+2) + 2P + 6e --> Cu3P2
     Cu3P2 + 402 --> 3Cu(+2) + 2PO4(-3)

    c) CAUTION - Acute renal failure and massive hemolysis may occur if significant copper sulfate is absorbed from the burn site (Frank et al, 2008; Zong-Yue et al, 1985; Curreri et al, 1970; Mendelson, 1971; Summerlin et al, 1967; Konjoyan, 1983).
    d) ANIMAL STUDY - Copper sulfate as a solution or emulsion proved more harmful when applied to rats with white phosphorus skin burns. Water irrigation alone was a more efficacious treatment (Eldad & Simon, 1991; Eldad et al, 1995).
    3) SILVER NITRATE
    a) Silver nitrate application to a burn area caused by phosphorus can aid in visualization of the imbedded phosphorus although, it too can be absorbed and produce systemic silver poisoning (Zong-Yue et al, 1985). The silver coats the phosphorus and prevents further combustion. 
    5AgNO3 + P + 4H2O --> 5Ag + H3PO4 + 5HNO3
     6AgNO3 + P --> Ag3P + 3AgNO3 +3NO3(-)

    b) Additional studies are needed to determine the efficacy of silver nitrate in the treatment of phosphorus-induced skin burns.
    4) IMBEDDED PHOSPHORUS REMOVAL
    a) A Waterpik(R) appliance may facilitate mechanical elimination of phosphorus particles (Kaufman et al, 1988).
    b) Remove visualized particles delicately with metal forceps (Kaufman et al, 1988).
    c) Remaining particles may be detected by discontinuing the moist dressing long enough for oxidation to begin again, which can be visualized as smoke being released from the area of an imbedded particle remains (Kaufman et al, 1988).
    d) For deep and extensive injury, consult a burn specialist.
    6.9.2) TREATMENT
    A) SUPPORT
    1) Follow treatment recommendations in the ORAL EXPOSURE section where appropriate.
    B) DEBRIDEMENT
    1) Meticulous surgical debridement of all embedded phosphorus particles is required; consult a burn specialist.
    C) SILVER SULFADIAZINE
    1) Partial skin thickness burns from a phosphorus pentachloride splash were treated with 1% silver sulfadiazine cream twice daily. Healing was slow (8 weeks) and painful, and no signs of hypertrophic scarring were evident at follow-up. Retrospectively, the authors suggest this patient would have been better treated if his wounds had been excised and grafted early (Eldad et al, 1992).
    D) SKIN ABSORPTION
    1) Dermal exposure to phosphorus can produce hypocalcemia, hypokalemia, and cardiac dysrhythmias.
    2) HYPOCALCEMIA: Correct known or suspected hypocalcemia with intravenous calcium gluconate (10%) 0.1 to 0.2 mL/kg up to 10 mL/dose or intravenous calcium chloride. Repeat dose if necessary.
    a) Monitor ECG continuously and serial calcium, magnesium, and potassium levels hourly during therapy. Suspect hypocalcemia and/or hypomagnesemia if QT interval is prolonged.
    b) Treat aggressively with intravenous calcium in the presence of any ECG or clinical signs of hypocalcemia (ie, hypotension) while serum calcium levels are pending. Serum levels should be obtained as soon as possible to monitor calcium therapy.
    E) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    F) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis may be efficacious if oliguric or anuric renal failure occurs, but has not been used to remove circulating phosphorus.

Range Of Toxicity

Summary

    A) TOXICITY: The estimated acute lethal adult dose by ingestion is 1 mg/kg with survival reported following ingestion of 1,570 mg. Ingestion of 15 mg by an adult has produced severe symptoms. As little as 3 mg has been reported to cause death in a 2-year-old child.

Minimum Lethal Exposure

    A) SUMMARY
    1) The estimated lethal adult dose by oral ingestion is 1 milligram/kilogram (ACGIH, 1998).
    B) CASE REPORTS
    1) PEDIATRIC
    a) As little as 3 mg has been reported to cause death in a 2-year-old child (Simon & Pickering, 1976).
    b) In a cross-sectional study from 7 Ecuadorian hospitals, 5 (6%) of 85 patients (age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years) died after ingesting up to 40 units (about 12 g of white phosphorus) of firecrackers. Seven patients ingested pesticides, anxiolytic or recreational drugs concurrently. Twenty patients also ingested alcohol (Gonzalez-Andrade & Lopez-Pulles, 2011).
    2) ADULT
    a) An adult died of multi-organ failure, including hepatic and renal failure, encephalopathy, metabolic acidosis and severe coagulopathy after intentionally ingesting 12 firecrackers containing white phosphorus (the estimated dose ranged between 48 to 108 mg) (Santos et al, 2009).
    b) In a cross-sectional study from 7 Ecuadorian hospitals, 5 (6%) of 85 patients (age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years) died after ingesting up to 40 units (about 12 g of white phosphorus) of firecrackers. Seven patients ingested pesticides, anxiolytic or recreational drugs concurrently. Twenty patients also ingested alcohol (Gonzalez-Andrade & Lopez-Pulles, 2011).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) ADULT
    a) Serious systemic toxicity in an adult has been reported after ingestion of only 15 milligrams (Rubitsky & Myerson, 1949). Adults have, however, survived ingestions of up to 1,570 milligrams (McCarron et al, 1981).
    b) In a cross-sectional study from 7 Ecuadorian hospitals, 85 cases (age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years) of firecracker (containing white phosphorus [WP]) ingestions were identified. Forty-five (52.9%), 32 (37.6%), 9 (10.6%), and 5 (5.9%) patients ingested 1 to 5 units (0.3 to 1.5 g; 0.03 to 0.15 g WP), 6 to 10 units (1.8 to 3 g; 0.18 to 0.3 g WP), 11 to 20 units (3.3 to 6 g; 0.33 to 0.6 g WP), and more than 21 units (greater than 6.3 g; greater than 0.63 g WP) of firecrackers, respectively. The maximum amount of units ingested was 40 (about 12 g). Seven patients ingested pesticides, anxiolytic or recreational drugs concurrently. Twenty patients also ingested alcohol. Overall, 6% (n=5) of patients died. The following adverse effects were observed: abdominal pain and cramps, diarrhea, nausea and vomiting, hematemesis, jaundice, hyperbilirubinemia, elevated liver enzymes, elevated alkaline phosphatase, hepatitis, acute liver failure, cholestatic syndrome, cirrhosis, increased coagulation times, leukopenia, leukocytosis, thrombocytopenia, hypoglycemia, hyperproteinemia, hyperuricemia, encephalopathy, headache, temporary loss of consciousness, tachycardia, dysrhythmias, bradycardia (Gonzalez-Andrade & Lopez-Pulles, 2011).
    2) PEDIATRIC
    a) A 4-year-old child inadvertently ingested 10 firecrackers containing white phosphorus (the estimated dose ranged between 40 to 90 mg) and developed coagulopathy, coma and acute liver failure requiring liver transplantation. Following a protracted hospital course, the patient recovered completely (Santos et al, 2009).
    b) A 15-year-old female intentionally ingested 9 firecrackers containing white phosphorus (the estimated dose ranged between 36 to 81 mg) and developed initially mild symptoms and only a slightly elevated prothrombin. By day 3, her prothrombin, aminotransferase and bilirubin levels were elevated with no new symptoms. Over the next 10 days, laboratory studies gradually improved and the patient recovered completely (Santos et al, 2009).
    c) In a cross-sectional study from 7 Ecuadorian hospitals, 85 cases (age range, 12 to 50 years of age; mean age, 21.6 +/- 7.1 years) of firecracker (containing white phosphorus [WP]) ingestions were identified. Forty-five (45.9%), 32 (37.6%), 9 (10.6%), and 5 (5.9%) patients ingested 1 to 5 units (0.3 to 1.5 g; 0.03 to 0.15 g WP), 6 to 10 units (1.8 to 3 g; 0.18 to 0.3 g WP), 11 to 20 units (3.3 to 6 g; 0.33 to 0.6 g WP), and more than 21 units (greater than 6.3 g; greater than 0.63 g WP) of firecrackers, respectively. The maximum amount of units ingested was 40 (about 12 g). Seven patients ingested pesticides, anxiolytic or recreational drugs concurrently. Twenty patients also ingested alcohol. Overall, 6% (n=5) of patients died. The following adverse effects were observed: abdominal pain and cramps, diarrhea, nausea and vomiting, hematemesis, jaundice, hyperbilirubinemia, elevated liver enzymes, elevated alkaline phosphatase, hepatitis, acute liver failure, cholestatic syndrome, cirrhosis, increased coagulation times, leukopenia, leukocytosis, thrombocytopenia, hypoglycemia, hyperproteinemia, hyperuricemia, encephalopathy, headache, temporary loss of consciousness, tachycardia, dysrhythmias, bradycardia (Gonzalez-Andrade & Lopez-Pulles, 2011).

Workplace Standards

    A) ACGIH TLV Values for CAS7723-14-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7723-14-0 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Phosphorus (yellow)
    2) REL:
    a) TWA: 0.1 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 5 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7723-14-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: White phosphorus
    a) D : Not classifiable as to human carcinogenicity.
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Phosphorus (yellow)
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7723-14-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Phosphorus (yellow)
    2) Table Z-1 for Phosphorus (yellow):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.1
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)MOUSE:
    1) 4820 mcg/kg ((RTECS, 2000))
    B) LD50- (ORAL)RAT:
    1) 3030 mcg/kg ((RTECS, 2000))

Pharmacology Toxicology

Toxicologic Mechanism

    A) Phosphorus is a general protoplasmic poison (Gosselin et al, 1984). Extensive fatty degeneration of the liver, kidneys, brain, and other organs may occur (Rubitsky & Myerson, 1949). Early sudden death in cardiovascular collapse may be secondary to induced hypocalcemia or a direct cardiotoxic effect (Diaz-Rivera et al, 1961). Induced hypoglycemia has been responsible for deaths in the past (Blumenthal & Lesser, 1938).
    B) Data indicate that phosphorus-induced liver injury may be a free radical mediated process. Administration of antioxidants may play a role in mitigating the resultant tissue injury (Di Lusio, 1966).
    C) Inhibition of protein synthesis has also been postulated as a mechanism of phosphorus-induced liver injury (Pani et al, 1972).

Physicochemical

Physical Characteristics

    A) Yellow/white phosphorus is colorless or white to yellow, soft, waxy, crystalline solid with an odor of garlic which darkens on exposure to light (HSDB , 2000; Budavari, 1996; Ellenhorn et al, 1997).

Molecular Weight

    A) 123.90

Animal Toxicology

Clinical Effects

    11.1.3) CANINE/DOG
    A) EYE - Chronic poisoning of dogs for 2 to 3 weeks caused retinal hemorrhages, degenerative changes in all layers of the retina, papilledema, fatty and hyalin degeneration of the blood vessels, and leukocytic infiltration (Grant, 1986).
    11.1.6) FELINE/CAT
    A) EYE -
    1) Chronic ophthalmological poisoning of cats for 2 to 3 weeks caused retinal hemorrhages, degenerative changes in all layers of the retina, papilledema, fatty and hyalin degeneration of the blood vessels, and leukocytic infiltration (Grant, 1986).
    B) SYSTEMIC -
    1) CASE REPORT - A 4-year-old cat was given an overdose of a urinary acidifier containing phosphorus. A dehydration of 12% was noted due to tacky mucous membranes. Serum analysis revealed hyperphosphatemia, azotemia, high anion gap metabolic acidosis, hyperproteinemia attributed to hyperalbuminemia, and increased alanine transaminase activity. CBC was normal except for hemoconcentration.
    a) Treatment consisted of sodium bicarbonate, metoclopramide, and aluminum hydroxide. Intravenous fluid replacement with sodium bicarbonate reversed the metabolic acidosis. 60 hours after admission, the cat was discharged and slowly recovered at home over the following 10 weeks (Fulton & Fruechte, 1991).
    11.1.13) OTHER
    A) OTHER
    1) Violent gastroenteritis, bloody diarrhea, abdominal pain, polydipsia, muscular weakness. Vomitus may be luminous in the dark, with a garlic-like odor.

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) Begin treatment immediately.
    2) Keep animal warm.
    3) Sample vomitus, blood, urine, and feces for analysis.
    4) NATIONAL ANIMAL POISON INFORMATION CENTER -
    a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.2.4) DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) SMALL ANIMALS
    a) Gastric lavage with 0.2 to 0.4% copper sulfate (20 to 100 mL) orally or 1:10,000 solution potassium permanganate 2 to 4 mL/kg.
    b) Administer activated charcoal, 5 to 50 g, orally, as a slurry in water.

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) DOG
    1) Subcutaneous injection of 0.2 to 0.4 milligrams/kilogram/day in dogs resulted in death within a few days (Buchanan et al, 1954).

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) Begin treatment immediately.
    2) Keep animal warm.
    3) Sample vomitus, blood, urine, and feces for analysis.
    4) NATIONAL ANIMAL POISON INFORMATION CENTER -
    a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.4.2) DECONTAMINATION
    11.4.2.2) GASTRIC DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) SMALL ANIMALS
    a) Gastric lavage with 0.2 to 0.4% copper sulfate (20 to 100 mL) orally or 1:10,000 solution potassium permanganate 2 to 4 mL/kg.
    b) Administer activated charcoal, 5 to 50 g, orally, as a slurry in water.

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