eMedicine Specialties > Emergency Medicine > Warfare - Chemical, Biological, Radiological, Nuclear and Explosives

CBRNE - Incendiary Agents, White Phosphorus

Lisandro Irizarry, MD, MPH, FAAEM, Chair, Department of Emergency Medicine, Brooklyn Hospital Center; Assistant Professor, Department of Emergency Medicine, Weill Cornell School of Medicine
Mollie V Williams, MD, Assistant Clinical Professor, Fellow in Disaster Preparedness, Department of Emergency Medicine, State University of New York Downstate Medical Center, Brooklyn; Geri M Williams, MD, Staff Physician, Department of Emergency Medicine, Brooklyn Hospital Center; José Eric Díaz-Alcalá, MD, FAAEM,, Consulting Staff in Medicine Service, Division of Emergency Medicine/Medical Toxicology, Veterans Affairs Caribbean Healthcare System; Medical Director, Puerto Rico Poison Control Center, San Juan, Puerto Rico

Updated: Oct 21, 2009

Introduction

Background

White (or yellow) phosphorus is the most common and most reactive of the 3 allotropic forms of phosphorus. Because of its reactivity, white phosphorus has been used as an incendiary agent by the military or as an igniter for munitions. An incendiary agent is one that is primarily designed to set fires. It commonly is found in hand grenades, mortar and artillery rounds, and smoke bombs.

Munitions-quality white phosphorus is generally found as a waxy, yellow transparent solid. When exposed to air, it spontaneously ignites and is oxidized rapidly to phosphorus pentoxide. Such heat is produced by this reaction that the element bursts into a yellow flame and produces a dense white smoke. Phosphorus also becomes luminous in the dark, and this property is conveyed to "tracer bullets." This chemical reaction continues until either all the material is consumed or the element is deprived of oxygen.

Most injuries associated with white phosphorus are the result of accidents due to either human or mechanical error.

Pathophysiology

White phosphorus can cause significant injury and death, and its use by the military has been highly criticized. Morbidity and mortality can occur by exposure to soft tissue, through inhalation, and by ingestion.

White phosphorus skin exposure results in painful chemical burn injuries. The resultant burn typically appears as a necrotic area with a yellowish color and characteristic garliclike odor. These burns carry a higher risk of morbidity and mortality. White phosphorus is highly lipid soluble and, as such, is believed to have rapid dermal penetration once particles are embedded under the skin. This deep absorption can result in heart, liver, and kidney damage. It has also been postulated that, because of its enhanced lipid solubility, these injuries result in delayed wound healing.

Few studies have investigated the degree of tissue destruction associated with white phosphorus injuries. In the experimental animal model, most tissue destruction appears to be secondary to the heat generated by oxidation.

Systemic toxicity has been described extensively in the animal model.¹ Pathologic changes have been documented in the liver and kidney.¹ These changes result in the development of progressive anuria, decreased creatinine clearance, and increased blood phosphorus levels. Depression of serum calcium level with an elevation in the serum phosphorus level (reversed calcium-phosphorus ratio) with electrocardiographic changes including prolongation of the QT segment, ST-segment depression, T-wave changes, and bradycardia also have been observed.

Oral ingestion of white phosphorus in humans has been demonstrated to result in pathologic changes to the liver and kidneys. The ingestion of a small quantity of white phosphorus can cause gastrointestinal complaints such as nausea, abdominal cramps, and vomiting. Individuals with a history of oral ingestion have been noted to pass phosphorus-laden stool ("smoking stool syndrome"). The accepted lethal dose is 1 mg/kg, although the ingestion of as little as 15 mg has resulted in death.

Inhalation of white phosphorus smoke is presumed to be the least severe form of exposure, as it has not been shown to cause casualties. It may result in irritation to the eyes and nose and may cause a violent cough. However, prolonged exposure to the gas does have the potential to cause death.

Mortality/Morbidity

Morbidity and mortality are related directly to trauma and burns sustained from exposure or to intentional or accidental ingestion.

Burns usually are limited to areas of exposed skin (upper extremities, face). Burns frequently are second and third degree because of the rapid ignition and highly lipophilic properties of white phosphorus.
Trauma usually is a combination of blunt and penetrating. Blunt trauma results from the percussion and force of the blast, and penetrating trauma results from projectiles produced from the explosion.

Clinical

History

Since most exposures occur in the military setting with the use of munitions, history frequently is obtained easily.
It may be necessary to solicit a history about suicidality or possible accidental ingestion in a patient with signs or symptoms of exposure.
Be aware of unconscious individuals with a history of percussion injuries from white phosphorus–containing munitions who may pose an exposure hazard to the health care provider.

Physical

Direct the physical examination toward the identification of traumatic and burn injuries. Pay particular attention to areas where phosphorus may be embedded as a result of explosion.
Fully expose the patient for the primary survey. Exercise care when handling potentially contaminated clothing to prevent secondary exposure and burns to the health care provider.

Causes

Most exposures to white phosphorus are accidental in etiology.

Differential Diagnoses

Acute Respiratory Distress Syndrome
Burns, Chemical
Burns, Ocular
Burns, Thermal
Dermatitis, Contact
Sunburn

Workup

Laboratory Studies

Obtain a basic trauma panel (CBC, basic metabolic panel, prothrombin time and/or activated partial thromboplastin time, type and crossmatch) with the addition of calcium, phosphorus, and magnesium levels.
Urine and serum phophate levels should be obtained with the addition of calcium and magnesium levels.
There has been no biomarker that could be of utility in identifying acute poisoning.

Treatment

Prehospital Care

Direct prehospital management toward the evaluation and management of trauma.

Secure the scene because live munitions may be in the area.
Perform ABCs of resuscitation.
Terminate further oxidation of phosphorus by irrigation or placement of saline-soaked and/or water-soaked pads on areas of exposure.
- Do not use an oily or greasy dressing because the element is lipid soluble and can penetrate into the tissue.
- Remove contaminated clothing because it may re-ignite and cause more extended and worsened burns than those sustained with white phosphorus alone.

Emergency Department Care

Continue a trauma management approach to the patient.

Avoid contact with ignited white phosphorus. Such contact may result in a chemical burn injury to the health care provider.
Continue irrigation; do not allow areas of exposure to dry, as this may result in re-ignition of white phosphorus.
Grossly debride as much white phosphorus as possible. The use of a Wood lamp (ultraviolet light) results in the fluorescing of the white phosphorus and may facilitate its removal.
Copper sulfate has been found to be an effective in vitro neutralizer of white phosphorus and has been traditionally used to treat burns.¹ Copper sulfate reacts with phosphorus to form cupric phosphate, which is black and assists in visualizing phosphorus. However, copper can be very toxic and can lead to death by causing massive intravascular hemolysis. This phenomenon is believed to be due to copper's activity as an inhibitor of several enzymes of the erythrocyte hexose monophosphate shunt.
Studies have shown that pretreatment with glutathione and propyl gallate antagonize the white phosphorus – induced increase in triglycerides.¹
Take care to ensure that tetanus immunization is up-to-date as a standard component of burn therapy.

Consultations

Consultation with a burn team is mandatory for most patients. In addition, obtain trauma consultation for all patients with a history of significant trauma, especially those who may require surgical debridement of injuries.

Medication

Direct medical therapy to the treatment of any underlying condition. As always, provide tetanus prophylaxis.

Toxoid

Toxoid is used for immunization; a booster injection in previously immunized individuals is recommended.

Tetanus toxoid

Used to induce active immunity against tetanus in selected patients. The immunizing agents of choice for most adults and children >7 y are tetanus and diphtheria toxoids. Necessary to administer booster doses to maintain tetanus immunity throughout life.
Pregnant patients should receive only tetanus toxoid not a not a diphtheria-antigen-containing product.
In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is mid thigh laterally.

Dosing

Adult

Primary immunization: 0.5 mL IM; administer 2 injections 4-8 wk apart; third dose 6-12 mo after second injection
Booster dose: 0.5 mL q10y

Pediatric

Administer as in adults

Interactions

Patients receiving immunosuppressants, including corticosteroids or radiation therapy, may remain susceptible despite immunization because of poor immune response; cimetidine may enhance or augment delayed-hypersensitivity responses to skin-test antigens; avoid concurrent use of medication with systemic chloramphenicol because it may impair amnestic response to tetanus toxoid; concurrent use of tetanus immune globulin may delay development of active immunity by several days (interaction nevertheless is clinically insignificant and does not preclude concurrent use)

Contraindications

Documented hypersensitivity; history of any type of neurologic symptoms or signs following administration; FDA recommends that elective tetanus immunization be deferred during any outbreak of poliomyelitis because tetanus toxoid injections are an important cause of provocative poliomyelitis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use to treat actual tetanus infections or for immediate prophylaxis of unimmunized individuals (use tetanus antitoxin instead, preferably human tetanus immune globulin); diminished antibody response to active immunization may be observed in patients receiving immunosuppressive therapy; better to defer primary diphtheria immunization until immunosuppressive therapy discontinued; routine immunization of symptomatic and asymptomatic HIV-infected persons is recommended

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma.

Morphine sulfate (Duramorph, Astramorph, MS Contin, MSIR, Oramorph)

DOC for analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Various IV doses are used; commonly titrated until desired effect obtained.

Dosing

Adult

Starting dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC; reassess hemodynamic effects of dose

Pediatric

Infants and children: 0.1-0.2 mg/kg dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose

Interactions

Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects of morphine

Contraindications

Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate

Meperidine (Demerol)

Analgesic with multiple actions similar to those of morphine; may produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine.

Dosing

Adult

50-150 mg PO/IV/IM/SC q3-4h prn

Pediatric

1-1.8 mg/kg (0.5-0.8 mg/lb) PO/IV/IM/SC q3-4h prn; not to exceed adult dose

Interactions

Monitor for increased respiratory and CNS depression with coadministration of cimetidine; hydantoins may decrease effects of meperidine; avoid with protease inhibitors

Contraindications

Documented hypersensitivity; MAOIs; upper airway obstruction or significant respiratory depression; during labor when delivery of premature infant is anticipated

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with head injuries since meperidine may increase respiratory depression and CSF pressure (use only if absolutely necessary); caution when using postoperatively and with history of pulmonary disease (suppresses cough reflex); substantially increased dose levels due to tolerance may aggravate or cause seizures even if no history of convulsive disorders; monitor closely for morphine-induced seizure activity if seizure history

Nonsteroidal anti-inflammatory agents (NSAIDs)

These agents have analgesic, anti-inflammatory, and antipyretic activities. Mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions, may exist as well.

Ibuprofen (Motrin, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Dosing

Adult

200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Naproxen (Aleve, Naprelan, Naprosyn, Anaprox)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis.

Dosing

Adult

500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Interactions

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Topical antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Neomycin and polymyxin B (Neosporin)

Used in treatment of minor infections. Inhibits bacterial protein synthesis and growth. Polymyxin B disrupts bacterial cytoplasmic membrane, permitting leak of intracellular constituents and causing inhibition of bacterial growth.

Dosing

Adult

Apply qd/qid to affected areas

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in treating extensive burns (>20% BSA) because absorption of neomycin is possible and may cause nephrotoxicity and ototoxicity; prolonged use may result in overgrowth of nonsusceptible organisms

Silver sulfadiazine (Silvadene, Thermazene, SSD, SSD-AF)

Useful in prevention of infections from second- or third-degree burns. Has bactericidal activity against many gram-positive and gram-negative bacteria, including yeast.

Dosing

Adult

Apply qd/bid to a thickness of 1/16 inch; burned area should be covered with medication continuously

Pediatric

Apply as in adults

Interactions

Effect of proteolytic enzymes is reduced when used concomitantly with this product

Contraindications

Documented hypersensitivity; neonates and infants <2 y

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in G-6-PD deficiency and renal insufficiency

Follow-up

Further Inpatient Care

Direct inpatient care toward further trauma management and burn care. Consider scar revisions associated with burns later in the patient's hospitalization.

Transfer

Transfer the patient to a trauma center with burn care capabilities if such facilities are not available initially.

Deterrence/Prevention

Care in handling and use of munitions should serve as the primary prevention of injuries and burns associated with white phosphorus.

Patient Education

For excellent patient education resources, visit eMedicine's Bioterrorism and Warfare Center. Also, see eMedicine's patient education articles Chemical Warfare and Personal Protective Equipment.

Miscellaneous

Medicolegal Pitfalls

Legal issues are associated with inadvertent exposure to the agent and to its inappropriate use in situations other than wartime deployment.

References

Agency for Toxic Substances and Disease Registry (ATSDR). U.S. Department of Health and Human Services, Public Health Service. Toxicological Profile for White Phosphorus. 1997. [Full Text].
Geehr EC, Salluzzo RF. Dermal injuries and burns from hazardous materials. In: Sullivan JB Jr,Krieger GR. Hazardous Materials Toxicology, Clinical Principles of Environmental Health. Williams and Wilkins; 1992:415-424.
Harbison RD. Phosphorus. In: Harbison RD. Hamilton and Hardy's Industrial Toxicology. 5^th ed. Mosby Yearbook; 1998:194-7.
Konjoyan TR. White phosphorus burns: case report and literature review. Mil Med. Nov 1983;148(11):881-4. [Medline].
Merrifield RB. The automatic synthesis of proteins. Sci Am. Mar 1968;218(3):56-62 passim. [Medline].
Mozingo DW, Smith AA, McManus WF, Pruitt BA Jr, Mason AD Jr. Chemical burns. J Trauma. May 1988;28(5):642-7. [Medline].
Obermer E. Phosphorus burns. Lancet. 1943;1:202.
Pande TK, Pandey S. White phosphorus poisoning--explosive encounter. J Assoc Physicians India. Mar 2004;52:249-50. [Medline].
Rabinowitch IM. Treatment of phosphorus burns. Can Med Assoc J. 1943;48:291-296.
Summerlin WT, Walder AI, Moncrief JA. White phosphorus burns and massive hemolysis. J Trauma. May 1967;7(3):476-84. [Medline].

Keywords

yellow phosphorus, Willy P, hand grenades, mortar rounds, artillery rounds, smoke bombs, munition igniter, chemical burn, munitions, white phosphorus exposure, white phosphorus burn, incendiary agent

Contributor Information and Disclosures

Author

Lisandro Irizarry, MD, MPH, FAAEM, Chair, Department of Emergency Medicine, Brooklyn Hospital Center; Assistant Professor, Department of Emergency Medicine, Weill Cornell School of Medicine
Lisandro Irizarry, MD, MPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Mollie V Williams, MD, Assistant Clinical Professor, Fellow in Disaster Preparedness, Department of Emergency Medicine, State University of New York Downstate Medical Center, Brooklyn
Mollie V Williams, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Geri M Williams, MD, Staff Physician, Department of Emergency Medicine, Brooklyn Hospital Center
Geri M Williams, MD is a member of the following medical societies: American College of Physicians, American Medical Association, Emergency Medicine Residents Association, Medical Society of the State of New York, and National Medical Association
Disclosure: Nothing to disclose.

José Eric Díaz-Alcalá, MD, FAAEM,, Consulting Staff in Medicine Service, Division of Emergency Medicine/Medical Toxicology, Veterans Affairs Caribbean Healthcare System; Medical Director, Puerto Rico Poison Control Center, San Juan, Puerto Rico
José Eric Díaz-Alcalá, MD, FAAEM, is a member of the following medical societies: American Academy of Emergency Medicine and American College of Medical Toxicology
Disclosure: Nothing to disclose.

Medical Editor

Mark Keim, MD, Senior Science Advisor, Office of the Director, National Center for Environmental Health, Centers for Disease Control and Prevention
Mark Keim, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Robert G Darling, MD, FACEP, Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine
Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.

Further Reading