A 35 year-old male with a past medical history of severe mental retardation and a seizure disorder was observed eating 16 “snake” fireworks by nursing home staff. He presented to the ED uncooperative and was tachycardic. Initial laboratory data recorded a WBC count of 27K and serum potassium of 2.1. A wide-complex tachycardia was noted on ECG. An abdominal radiograph performed approximately 12 hours post-ingestion demonstrated multiple radio-opaque foreign bodies in the stomach. The patient became obtunded and subsequently required oral intubation. A post-intubation arterial blood gas revealed a metabolic acidosis with a pH of 7.03. Repeat serum potassium was 1.5. The regional poison control center recommended potassium replacement, whole bowel irrigation, and chelation therapy with dimercaprol (BAL). On day 4, the patient was extubated. On day 7, heavy metal analysis from the patient’s initial blood work revealed a serum barium level of 20,200 μ/L (normal less than 200). Lead, arsenic and mercury levels were negative.
While traumatic injuries involving the hands, face, and, eyes during Independence Day celebrations are well-documented, systemic toxicity due to fireworks is less common but can also result in morbidity and mortality.
Chemically, fireworks consist of an oxidizer (potassium nitrate or perchlorate), reducer (sulfur or chlorine), fuel (carbon), a binder (starch), and selected color (metals).
Toxic Components of Fireworks
Barium blocks efflux of intracellular potassium out of the cell, increases cell membrane permeability to sodium, and increases the activity of the Na+-K+ pump, driving more potassium into the cell. Profound progressive hypokalemia causes severe ventricular dysrhythmias, hypertension, flaccid muscle weakness, respiratory failure, rhabdomyolysis and seizures.
Toxic Barium Salts
Acetate= textile dyes
Chloride= rodenticide, welding rods
Oxide= glass, ceramics
Nitrate= ceramics and fireworks
Polysulfide= fluorescent tubes
Management includes aggressive repletion of potassium (watch for rebound hyperkalemia) and respiratory support. Intravenous magnesium is not recommended as it may cause precipitation of insoluble barium in the renal tubules. However, oral magnesium salts should be given to convert the soluble barium salts into their insoluble (non-toxic) form. Decontamination with activated charcoal is not effective and gastric lavage can be considered with larger acute ingestions. Hemodialysis should be considered in patients not responding to aggressive repletion of potassium.
A 3 year-old male ingested several Python brand “snake” fireworks. The child presented to ED one hour later with obtundation and profuse vomiting and diarrhea. A pulse of 150 beats/minute was recorded and an ECG revealed ventricular bigeminy. WBC count was 20K and an abdominal radiograph was negative for radiopaque foreign bodies. The child’s mental status and symptoms improved with supportive care over 24 hours. A spot urinary arsenic level measured 35μg/L and each “snake” was found to contain 15mg of arsenic.
There are several forms of arsenic. Inorganic trivalent arsenic (arsenite) is the most toxic. Acute ingestion of 100-300mg of trivalent arsenic can be fatal. Pentavalent (arsenate) is also toxic, but less so than the trivalent form. The organic form, found environmentally in some seafood (bivalve mollusks) and algae, is essentially non-toxic.
Ingestion of arsenic causes nausea, vomiting, profound diarrhea (often described as “rice water” stools) progressing to hemorrhagic gastroenteritis. Cardiovascular effects include prolonged QT intervals and may lead to torsades de pointes. Hypovolemic shock and rhabdomyolysis can occur. Neurologically, delirium, obtundation and axonal neuropathy have been described. Dermatologically, the patient may suffer delayed desquamation and classic Aldrich-Mees lines on the fingernails.
Gastric decontamination of arsenic is difficult since this element does not bind well to activated charcoal. With large oral ingestions, gastric lavage and whole bowel irrigation may be considered. Arsenic is poorly dialyzed. Chelating antidotes include intramuscular dimercaprol (BAL) and oral or intravenous unithiol (DMPS).
In a case report from Spain, a 32 year-old male ingested 12 firecrackers containing white phosphorus in a suicide attempt and developed abdominal pain, nausea and vomiting after approximately 12 hours. Two days later he presented to the ED with worsening abdominal pain and continuous vomiting and was subsequently transferred to a tertiary care hospital for further evaluation. On admission, he had jaundice, altered mental status, and asterixis.
Laboratory tests revealed direct hyperbilirubinemia (total bilirubin 6.9 mg/dL), and increased AST and ALT > 20 times upper limit of normal, and PT of 146. The patient was transferred to the ICU due to fulminant hepatic failure. The following day, he had worsening of renal function, oliguria and severe metabolic acidosis. He was placed on continuous venovenous dialysis. His liver function continued to worsen and he developed encephalopathy and severe coagulopathy with upper gastrointestinal bleeding requiring mechanical ventilation and vasopressor therapy. Despite supportive measures, the patient died three days after admission.
Greek for “light” (phos) and “bringing” (phorus), white phosphorus was initially used in “lucifers” or strike-anywhere matches. Chronically exposed factory workers often developed loss of teeth and mandibular osteonecrosis commonly referred to as “phossy jaw” in the 19th century. The Match Act of 1912 in US taxed these matches out of existence. As a result, red phosphorus, which is much less toxic, was used as a substitute in the match industry. In WWII, white phosphorous was used in bombs and other incendiary devices.
Consumer- grade fireworks in the U.S. do not contain white phosphorus. However, firecrackers used in Europe, Central American, and South America can contain up to 4-9mg of elemental phosphorus. Phosphorous is considered a general protoplasmic poison. It is rapidly absorbed from the GI tract within 2-3 hours with 75% of dose found in liver. Phosphorous induces hepatic toxicity by uncoupling oxidative phosphorylation causing massive hepatic steatosis with necrosis. The lethal dose is 1mg/kg. It is highly lipid-soluble and significant dermal absorption is possible. In terms of electrolyte homeostasis, rapid absorption causes hyperphosphatemia, profound hypocalcemia, and hyperkalemia. In large doses, it can cause seizures and cardiac dysrhythmias. Diagnostically, phosphorous fluoresces brightly under a Wood’s lamp.
Stage I (day 1): GI tract injury, dysrhythmias, and seizures
Stage II (days 2-3): Fulminant hepatic failure
Stage III (days 4-8): Death from hepatic failure or delayed cardiac toxicity
Stage IV (day 8): Recovery
For skin decontamination, keep phosphorus wet at all times, because it can react with ambient air resulting in an explosion. GI decontamination includes consideration of gastric lavage (with water), administration of activated charcoal, and with larger ingestions, whole bowel irrigation. One case report described an explosion when phosphorus was suctioned out into a vacuum container. There exists a theoretical advantage to gastric lavage with potassium permanganate (1:5000), copper sulfate, or mineral oil, but no clinical studies have demonstrated a benefit. The acetaminophen antidote, NAC (N-acetylcysteine), can be administered if evidence of phosphorous-induced hepatotoxicity.
Despite a few case reports in the literature, the vast majority of fireworks exposures are non-toxic. However, consider exposure to barium, arsenic, or white phosphorus in symptomatic patients and treat aggressively as clinically indicated.
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