AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab 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

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Drug Category: Toxoid

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

Drug Category: 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.

Drug Category: 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.

Drug Category: Topical antibiotics

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

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

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

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. 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].
2. 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.
3. Harbison RD. Phosphorus. In: Harbison RD. Hamilton and Hardy's Industrial Toxicology. 5^th ed. Mosby Yearbook; 1998:194-7.
4. Konjoyan TR. White phosphorus burns: case report and literature review. Mil Med. Nov 1983;148(11):881-4. [Medline].
5. Merrifield RB. The automatic synthesis of proteins. Sci Am. Mar 1968;218(3):56-62 passim. [Medline].
6. Mozingo DW, Smith AA, McManus WF, Pruitt BA Jr, Mason AD Jr. Chemical burns. J Trauma. May 1988;28(5):642-7. [Medline].
7. Obermer E. Phosphorus burns. Lancet. 1943;1:202.
8. Pande TK, Pandey S. White phosphorus poisoning--explosive encounter. J Assoc Physicians India. Mar 2004;52:249-50. [Medline].
9. Rabinowitch IM. Treatment of phosphorus burns. Can Med Assoc J. 1943;48:291-296.
10. Summerlin WT, Walder AI, Moncrief JA. White phosphorus burns and massive hemolysis. J Trauma. May 1967;7(3):476-84. [Medline].

Article Last Updated: Aug 22, 2007