Napalm Toxicity

Etiology

Napalm toxicity occurs almost exclusively as a result of military action. Military uses include dropping napalm-containing bombs from aircraft, using flamethrowers (handheld or vehicle-borne), and in-ground explosive devices. Non-military-related exposure may arise from improvised handheld firebombs or "Molotov cocktails." Homemade firebombs may employ fuel-thickening agents to create a weapon with an effect similar to military-grade napalm. Individuals or groups utilizing these weapons may not necessarily have affiliations with a uniformed military. "Prison napalm" refers to a boiling sugar mixture reported to be used in jails to cause significant burn injuries. The sugar component of the mix acts as a thickening agent, allowing for higher temperatures and increasing contact time due to its viscosity.[1]

Epidemiology

Chemists developed napalm in 1942, and its first documented military use was in 1944. Allied bombers used napalm in incendiary bombs throughout the European and Pacific theaters during World War II. Handheld or vehicle-borne flamethrowers deployed napalm primarily against dug-in positions, given its ability to kill or displace defenders where other weapon systems would fail. Militaries have deployed napalm in multiple other conflicts, including the Korean and Vietnam Wars and numerous smaller engagements. Civilian exposures to napalm are rare outside of military conflicts. Although the United Nations banned the use of napalm on civilian targets in 1980, numerous reports suggest it has been used in several modern conflicts. Homemade mixtures approximating napalm have exploded during manufacture or improvised use, causing injuries outside of armed conflicts.

Pathophysiology

Napalm burns at the same temperature as the flammable liquid used in its composition, typically gasoline, kerosene, diesel fuel, or benzene. Direct contact with flaming napalm results in full-thickness burns. Large surface area contact results in rapid loss of blood pressure, loss of consciousness, and death.[2] Napalm can also produce localized areas of high carbon dioxide concentration due to incomplete combustion. Carbon dioxide levels of 4% can cause death in approximately 1 hour while burning napalm creates concentrations near 20%.[3] Contained areas near burning napalm can rapidly de-oxygenate, resulting in loss of consciousness and death in minutes due to asphyxiation. Surface exposure to non-ignited napalm may cause mild skin irritation similar to gasoline exposure. No reports exist of ingestion of napalm, but treatment would be as ingestion of the individual components such as benzene and polystyrene.

Toxicokinetics

The duration of ignited napalm combustion is influenced by the underlying material fueling it, often extending for several hours. The hypoxia caused by burst ignition resolves relatively rapidly (seconds to minutes) in open areas but can take much longer in closed environments. Elevated carbon dioxide levels can persist for hours in enclosed environments, mainly due to its density, causing it to settle in the lowest terrain levels, where cross currents may not promptly disperse the gas. Carbon monoxide is roughly equivalent to ambient air density and will spread depending on the degree of cross-current ventilation.

History and Physical

The militarized deployment of napalm usually leaves a discernible exposure history, either reported by the victims or evident through general situational awareness. In contrast, recognizing combustion from homemade napalm may be less apparent. The physical examination of survivors exposed to ignited napalm will vary based on the type of exposure. If first responders arrive promptly, direct contact exposure can result in full-thickness burns, sometimes with ongoing active combustion. The intense heat from a napalm blast may burn off all clothing. Those with second-degree burns will have severe pain, while some with third-degree burns will appear potentially pain-free.

Napalm dropped by aircraft, as opposed to flamethrower-deployed, will include a blast component that may cause typical blast injuries. A thorough physical exam may find blunt and penetrating injuries due to blast effect that may cause life-threatening internal or external hemorrhage, cardiac tamponade, tension pneumothorax, or open pneumothorax requiring immediate treatment. The remarkable severity of the burns may divert clinicians’ attention from more urgently requiring traumatic injuries, necessitating a structured trauma approach for blast-burn injuries. 

Initial assessment of the airway consists of evaluation for mucosal burn injuries such as charred facial and nasal hair and soot or fire debris in the oropharynx or nasopharynx. Careful repeated assessment of the appearance of the uvula, tongue, lips, and palate for signs of edema that portends impending airway compromise is vital. Some patients not exposed to direct contact with flaming napalm may present with altered mental status from blast effect-induced head trauma or hypoxia, carbon monoxide, or carbon dioxide toxicity.

Evaluation

Initial evaluation of napalm-exposed patients includes immediate efforts to stop any ongoing burning, generally by smothering or chemical fire extinguishers. In patients exposed to napalm via a blast dispersal, typical trauma evaluation should be undertaken by looking systematically for blunt and penetrating injuries requiring immediate treatment. For exposures beyond minor incidents, clinicians should contemplate early intubation and airway control to avert delayed recognition of airway edema, which could lead to challenging or failed intubation. Many more severely injured patients will require high doses of opioids to control pain, which may impair their respiratory drive when already under physiologic distress. Patients not intubated early must be re-evaluated at short intervals to determine the airway status. Drooling, change in voice, and swelling of the uvula, palate, tongue, or lips are signs of a worsening airway and should prompt consideration of intubation before developing an airway crisis.

After decontamination and airway control, clinicians should assess breathing and oxygenation. Impaired ventilation and oxygenation may result from head injury, carbon dioxide exposure, carbon monoxide exposure, exposure to other toxins burning in the environment, or restricted chest movement due to burns. Victims of a blast may present with pneumothoraces or sucking chest wounds that necessitate decompression and the application of chest seals. Rapid evaluation by auscultation, visualization of chest rise, oxygen saturation, and evaluation of respiratory rate may prompt interventions unrelated to burns. Torso burns may require early chest escharotomy to allow ventilation. 

A circulatory evaluation includes the measurement of blood pressure, peripheral pulses, and the assessment of shock. Hypotensive patients may have internal injuries from the blast effect, and clinicians should evaluate the need for surgical intervention. Clinicians must evaluate for external bleeding, cardiac tamponade, tension pneumothorax, hemothorax, intraabdominal, and retroperitoneal bleeding apart from visible burns. Inhalation of cyanide from nearby combustibles may cause shock and elevate serum lactate.

Once initial stabilization of the airway, breathing, and circulation is complete, additional evaluation depends on the clinical situation. Some patients will require extensive trauma evaluation, including computerized tomography scans of the brain, cervical spine, chest, abdomen, and pelvis for internal injuries. Altered patients may require arterial blood gas and co-oximetry for carbon monoxide. In more severely ill patients, highly elevated serum lactate may suggest cyanide inhalation. Determination of the total body surface area burned aids in the determination of fluid resuscitation and the necessity for transfer to a burn center.

Treatment / Management

Individuals affected by blast-burn injuries from napalm undergo a standard trauma evaluation, with a crucial emphasis on avoiding an excessive focus on burns before addressing other life-threatening injuries during management. Early airway control and mechanical ventilation are often required. Unstable patients may require chest thoracostomy, chest wound seals, escharotomy, blood transfusion, and prompt exploratory laparotomy or thoracotomy. Unstable patients with high lactate levels and an enclosed space burn history may benefit from treatments aimed at cyanide toxicity. Carbon monoxide and carbon dioxide exposure are typical, requiring supplemental oxygen treatment. Clinicians can achieve pain control with opioids, though the doses required may result in a drop in blood pressure or respiratory drive. Alternatively, some military and civilian providers may use ketamine in either a low-dose or dissociative dose protocol to achieve initial pain control.[4]

While fluid resuscitation protocols for burns are well described, resuscitation in burn-blast victims may be complicated by blast injuries causing hemorrhage. Some hypotensive patients will require a blood transfusion in addition to crystalloids. The volume of crystalloids infused for burn patients typically follows an algorithm such as the Parkland formula, which predicts fluid requirements over the first 24 hours from the time of the burn. Four mL of crystalloid per percent body surface area burned per kg of patient weight estimates the total volume for 24 hours, with half given in the first 8 hours from the time of the burn and the second half given for the remaining 16 hours. Clinicians generally should transfer patients with napalm burns to a burn center, given the unusual nature of these burns and the tendency for complications such as keloids.[5]

Differential Diagnosis

The diagnosis of napalm burns is typically apparent by history. However, in situations where a history of exposure is unknown, patients exposed to napalm effects but not burned may present with altered mental status, hypoxia, respiratory collapse, or shock. The area surrounding the patient’s initial location would show clear signs of combustion. Clinicians should consider carbon monoxide toxicity, carbon dioxide toxicity, cyanide inhalation, and blunt head injury in such patients.

Prognosis

The prognosis of napalm exposure varies. Most patients who die from exposure do so immediately by immolation, blast effect, or respiratory failure. Those with a large surface area burn risk death by infection and multi-organ system failure in hours to days. Patients with less severe burns will likely survive with treatment from burn centers and specialists.

Complications

Napalm burns result in severe skin damage that can cause multi-organ system failure and death. Severe disfigurement and loss of function are common, requiring skin grafting and specialized care. Keloid formation may occur in some individuals. The psychological effect of exposure to napalm may be severe.