White Phosphorus Exposure

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 high 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.[9] Pathologic changes have been documented in the liver and kidney.[9] These changes result in the development of progressive anuria, decreased creatinine clearance, and increased blood phosphorus levels. Depression of the 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.

In Turkey from 1997-2012, 16 deaths of children ages 2-15 years old were attributed to the ingestion of phosphorus firecrackers.[10]  White phosphorous is widely used illicitly in fireworks in South America. One study of Ecuadorian hospitals found a 5.9% death rate among patients who ingested these firecrackers.[11]

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 (eg, 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.

Since most exposures to white phosphorus occur in the military setting with the use of munitions, a history frequently is obtained easily. However, 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.

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.

Patients who have ingested white phosphorus present with nausea, vomiting, and diarrhea. Those who present with nausea, vomiting, and hypotension generally deteriorate rapidly and may enter a coma.[10] 11 Inhalation of white phosphorus fumes can result in chemical pneumonitis.[8]

There is no biomarker that can be used to identify acute poisoning from white phosphorus. However, a basic trauma panel that includes the following should be obtained:

• Complete blood cell count (CBC)

• Basic metabolic panel

• Prothrombin time (PT), activated partial thromboplastin time (aPTT), or both

• Blood type and crossmatch

In addition, the following should be obtained:

• Serum calcium, phosphorus, and magnesium levels

• Urine phosphate levels

Successful chemical identification of phosphorus on the remains of burned clothes using gas chromatograph mass spectrometer (GCMS) after headspace adsorption using solid phase microextraction (SPME) has been reported.[12]

Direct prehospital management toward the evaluation and management of trauma, as follows:

• Secure the scene, because live munitions may be in the area

• Assess and manage ABCs (airway, breathing, circulation)

• Perform decontamination

For decontamination, irrigate or place saline-soaked and/or water-soaked pads on areas of exposure, to terminate further oxidation of phosphorus. Do not use an oily or greasy dressing because the element is lipid soluble and can penetrate into the tissue. Remove contaminated clothing because the white phosphorus may re-ignite and set the clothing on fire, causing more extended and worse burns.

Continue a trauma-management approach to the patient, as follows:

• Avoid contact with ignited white phosphorus, as that may result in a chemical burn injury to the health care provider.

• Continue irrigation; do not allow areas of exposure to dry, as that 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.

• Ensure that tetanus immunization is current.

Copper sulfate has been found to be an effective in vitro neutralizer of white phosphorus and has been traditionally used to treat burns.[9] 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. Silver nitrate may provide safer and more reliable antagonism of white phosphorus dermal absorption.[9]

Irrigation with cool water is necessary. As white phosphorus become liquid at 44 °C,, it is critical that the use of warm water is avoided. However, aggressive irrigation with copious amounts of water may result in adverse effects with phosphorus particles transported to uninvolved areas of the skin and reignite when exposed to the air. Saline soaked gauze for wound coverage facilitates oxygen depletion to any remaining phosphorus particles.[4]

Recent in vitro research has shown that moist gauze was effective in extinguishing white phosphorous from a simulated wound, and could be used to absorb white phosphorus pieces, preventing deeper penetration of white phosphorus particles. This was more effective than a stream of water, which splashed and moved white phosphorus pieces around.[13]

Ingestion of white phosphorus can result in elevation of hepatic trigylceride levels, which can lead to fatty liver. Pretreatment with glutathione and propyl gallate, which are antioxidants and free radical scavengers, has been shown to antagonize the increase in triglycerides.[5]

Fatality is highly likely for patients who ingest white phosphorus and present with concomitant hepatorenal failure and cardiovascular collapse. However, when only hepatic failure develops, liver transplantation can be lifesaving.[14]

Direct inpatient care toward further trauma management and burn care. Consider scar revisions associated with burns later in the patient's hospitalization. Transfer the patient to a trauma center with burn care capabilities if such facilities are not available initially.

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.

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

Class Summary

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

Tetanus toxoid adsorbed or fluid

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.

Class Summary

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.

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.

Class Summary

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.

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.

Class Summary

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

Neomycin/polymyxin B/bacitracin topical (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.

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.