Rare Toxin Exposures: Recognition and Treatment in the Emergency Department

Introduction:

Toxic substance exposure casualties are encountered daily. Not everyone exposed will present to the emergency department, but when encountered, it may have a huge impact on the patient’s health and quality of life. One such exposure occurs through heavy metal poisoning. Heavy metals like zinc, copper, chromium, iron, and manganese play a vital role in the various metabolic processes of the human body. However, if excess accumulation reaches toxic levels, it can cause serious damage. One can get exposed to such toxins from industrial exposure, air and water pollution, food products, medications, improperly coated food containers, and even through ingestion of lead-based paints.

What Is Heavy Metal Poisoning?

Heavy metal poisoning refers to the excess accumulation of heavy metals in the soft tissues, reaching toxic levels to cause life-threatening effects. The clinical symptoms correlate with the heavy metal accumulated in the body.

What Are the Heavy Metal Poisoning Exposures Encountered, and How Are They Managed?

The human encountered heavy metal poisoning include,

1. Lead Poisoning:

• Exposure to high levels of lead leads to lead poisoning, affecting multiple organ systems.

• Lead accumulates in the brain, teeth, liver, kidney, and bones.

• Children are more commonly affected. Lead poisoning affects the fetus in a pregnant woman, as the lead is released into the bloodstream during pregnancy.

Causes:

• Occurs due to inhaling the lead particles during smelting, recycling, in brass foundries, from gasoline, glass, bridge, tunnel, and elevated highway constructions.

• Ingestion of lead-contaminated dust.

• Consuming water from lead pipes.

• Consuming from lead-coated containers.

• Calcium products, hair dyes, kajal, surma.

Symptoms: It takes around a three-week time period for the symptoms to develop. Symptoms in children include:

• Irritability, lethargy, slurred speech, less playful.

• Headache, vomiting, abdominal pain.

• Lack of appetite.

• Constipation.

• Slurred speech.

• Hyperproteinemia (high protein levels in the blood).

• Anemia.

Neurological symptoms include,

• Ataxia, convulsions, seizures.

• Encephalopathy, impaired consciousness.

Symptoms in adults include:

• High blood pressure.

• Loss of appetite.

• Joint pain.

• Insomnia.

• Altered mental status.

• Anemia.

• Peripheral neuropathy.

• Depression.

• Wrist drop.

• Muscular weakness.

Diagnosis:

• Elevated free erythrocyte protoporphyrins.

• Inhibited ALA-D (aminolevulinic acid - dehydratase) activity.

• Elevated lead levels in the hair.

• Increased lead content in deciduous teeth.

• Elevated urinary coproporphyrin and zinc protoporphyrin levels aid in diagnosis.

Treatment:

• First and foremost, steps should be taken to eliminate the toxic substance from the body by various means of laxatives, cathartics (to pass the objects out), and bowel irrigation.

• Surgery is indicated if the lead bullets are retained.

• Enhancing dietary supplementation of adequate iron, calcium, and zinc intake to counteract the effects of lead poisoning.

• Chelation therapy is indicated in children with a blood lead concentration higher than 45 mcg/dL (micrograms per deciliter), adults with a blood lead concentration of over 70 to 100 mcg/dL, and patients with lead encephalopathy.

• Calcium disodium ethylenediaminetetraacetic acid (EDTA), succimer, and British anti-Lewisite (BAL, also known as Dimercaprol) are commonly used chelating agents, which bind to lead to form a complex and thus gets excreted from the body.

2. Mercury Poisoning:

• Most commonly encountered human exposure occurs due to fish consumption and dental amalgam.

• Human toxicity depends on the form, dosage, and rate of encounter.

• Mercury induces a wide range of clinical presentations. The brain remains the target organ in case of inhaled mercury vapors.

Causes:

• Manufacturing of thermometers, mirrors, incandescent lights, X-ray machines, and vacuum pumps leads to occupational exposure to large amounts of mercury.

• Ingestion of contaminated water and fish.

• Dental amalgams.

• Batteries.

Symptoms:

• Coughing, breathlessness, tightness, or burning pain in the chest.

• Pulmonary edema, fibrosis.

• Ataxia (impaired balance or coordination caused due to brain or nerve damage).

• Choreoathetosis (involuntary twitching movements of the limbs).

• Polyneuropathy (disease affecting the peripheral nerves).

• Dysarthria (weakness of the muscle aiding in speech).

• Mad Hatter syndrome involves insomnia, excitability, excessive shyness, and memory loss.

• Visual disturbances.

• Acrodynia (mercury poisoning).

• Hyperesthesia (abnormally increased sensitivity to normal stimuli like touch, taste, and sound).

• Dehydration.

• Gingivitis (inflammation of the gums).

• Acute renal failure.

• Abdominal cramps.

• Bloody diarrhea.

Diagnosis:

• Chest X-ray.

• Urinalysis.

• Complete blood count.

• Electrocardiograms are of diagnostic importance in detecting mercury poisoning.

Treatment:

• Decontamination is done by eliminating the toxic substance from the clothing/skin to prevent further exposure.

• Chelation therapy using Dimercaprol is the drug of choice indicated in acute inorganic mercury toxicity. Dimercaprol preferably chelates with mercury salts.

• Dimercaprol is administered intramuscularly every four hours.

• Oxygen therapy is initiated through a face mask in severe cases.

• Medications for symptomatic treatment.

• Dialysis.

• Surgical interventions.

3. Arsenic Poisoning:

• Arsenic poisoning, or arsenicosis, occurs when a person gets exposed to toxic levels of arsenic through swallowing, absorbing, or inhaling the chemical.

• Arsenic is a natural semi-metallic chemical that is mostly found in groundwater.

• Arsenic poisoning can lead to life-threatening complications if left untreated or under-treated. Timely diagnosis and management play a major role.

Causes:

• Medications like Fowler’s solution (potassium arsenite).

• Certain topical creams are used in the treatment of some skin conditions.

• Ingestion of herbicides, insecticides, pesticides, fungicides, or rodenticides containing arsenic.

• Occupational encounters during the manufacture of paints, enamels, glass, and metals.

• Galvanizing, soldering, etching, lead plating, smelting, and wood preserving lead to arsenic exposure.

• Ingestion of contaminated water, seafood, and algae.

Symptoms:

• Headaches, drowsiness, confusion, seizures.

• Encephalopathy (damage to the brain causing impaired brain function).

• Peripheral neuropathy (the damage caused to the nerves supplying the peripheral organs leads to pain and numbness in the peripheral organs).

• Demyelination (the protective covering of the nerve called myelin is damaged).

• Transverse white bands on the fingernails and edema.

• Vomiting, abdominal pain, and bloody diarrhea.

• Anemia.

• Hypotension.

• Exfoliative dermatitis.

• Polyneuritis (disorder causing inflammation of many nerves).

• Burning mouth.

• Cardiomyopathy.

• Renal tubular acidosis (Impaired function of the kidneys leading to increased content of acid in the blood).

• Ventricular arrhythmias (irregular heartbeat due to impaired function of the ventricles).

• Coma.

• Intestinal hemorrhage.

• Jaundice.

• Muscle spasms.

Diagnosis:

• Arsenic exposure is best detected by a 24-hour urine test.

• Arsenic levels of 50 micrograms/L or 100 micrograms/L in urine confirm the diagnosis. Samples need to be collected in a metal-free polyethylene container.

• Urine samples are repeated every 24 hours to detect the arsenic levels during and after treatment until arsenic levels reach below 50 micrograms/L.

• An abdominal radiograph provides intestinal radiopaque metallic flecks in case of ingestion.

• CBC (complete blood count) is advised to detect anemia, thrombocytopenia, and relative eosinophilia.

• Elevated creatinine, aminotransferase, bilirubin levels, proteinuria, pyuria, hematuria, decreased haptoglobin level, and basophilic stippling in the peripheral smear gives a clue.

• Electrocardiograms demonstrate nonspecific ST-segment changes, ST depression, T wave flattening, prolonged QT, and QTC intervals. Arrhythmias, including torsades de pointe, are also considered.

• Nerve conduction studies are indicated if the patient presents with peripheral neurologic symptoms.

Treatment:

• Arsenic toxicity is a life-threatening condition that demands fluid resuscitation, blood pressure support, and cardiac monitoring.

• Casualties are treated by shifting the patients to the ICU (intensive care unit).

• Chelation therapy should be instituted as soon as possible and should not wait for laboratory confirmation.

• British Anti-Lewisite (BAL) is given as 3 to 5 mg/kg (milligram per kilogram) every four hours and then gradually tapered to every 12 hours.

• Dimercaptopropane Sulfonic acid (DMPS) of 3 to 5 milligrams/kg is given IM every four hours and administered as a 5 percent solution for two days, followed by Succimer, 3 to 5 mg/kg IM (intramuscular) every six to 12 hours.

• The endpoint for chelation therapy will be the 24-hour urinary arsenic of less than 50 ug/L.

• Ventricular tachycardia or torsades de point is treated with Magnesium sulfate, Lidocaine, Amiodarone, and defibrillation therapy.

• Potassium, calcium, and magnesium levels should be assessed and maintained within normal limits to avoid worsening QT prolongation.

• Seizures are treated by giving Benzodiazepines and general anesthesia as required.

Conclusion:

Early detection of toxin exposure enhances survival rates. A caregiver needs to be well-versed in clinical presentations, diagnosis, and treatment planning to manage the casualties effectively. Suspicion of acute exposure requires immediate chelation therapy and should be initiated as soon as possible. Dealing with arsenic and other toxicities requires an interprofessional collaboration that includes physicians, toxicologists, and the nursing fraternity to enhance patient outcomes.