Exposure to hazardous chemical and related poisonings result from inadvertent residential, industrial, occupational, or transportation mishaps, natural disasters and hazardous-substance releases that are intended to cause harm.
Poisonings may result in mass casualties, challenging community and hospital preparedness and response efforts.
Chemicals include respiratory irritants, vesicants, asphyxiants, including cyanide, and cholinergic agents, organophosphate insecticides and military nerve agents.
Cyanide and organophosphate poisonings are encountered in inadvertent or suicidal exposures and are treated with specific antidotal therapy provided on an emergency basis after toxidrome recognition.
Up to 100,000 industrial chemicals are used each day in the United States.
It is estimated that more than 10,000 potentially consequential releases of hazardous substances occur annually.
Both toxic industrial chemicals and military chemical weapons are capable of causing mass casualties and may be deployed intentionally in the context of chemical terrorism.
Toxidromes refers to clinical signs, particularly vital signs, mental status, and ocular, respiratory, neurologic, and skin findings, that are characteristic of general classes of poisoning.
Chemicals react with specific target cellular macromolecules or create critical alterations in the cellular microenvironment and lead to altered cellular function, structural injury, or damaged genetic material.
After contact injury decontamination of skin, eyes, and wounds reduces the dose that patients absorb, and improves their health outcomes, while reducing the risk of secondary contamination.
Following exposure contaminated clothing is immediately removed and safely disposed of.
Following exposure high-volume, low-pressure flushing of hair and skin with water and washing with liquid soap, water, and nonabrasive sponges is perfomed.
Ocular decontamination begins by removal of contact lenses, if present, and immediate, copious irrigation with balanced salt solution, lactated Ringer’s solution, saline, or water.
Decontamination teams don personal protective equipment, consisting of a hooded, chemical-resistant body suit with a face shield, air-purifying respirator, and double layers of chemical-resistant gloves and boots
Critically ill patients may require immediate resuscitation before or concurrently with decontamination.
Resuscitation, performed by emergency personnel wearing personal protective equipment, includes airway, breathing, and circulatory support.
Anticonvulsant or other medications needed to maintain physiological homeostasis, is provided as soon as possible.
Routine laboratory tests, including measurements of blood glucose, electrolytes, and lactate, as well as blood gas analysis and hemoglobin speciation.
Cllinical or environmental laboratory results may confirm the responsible chemicals and allow for more targeted treatment.
Clinical manifestations of hazardous exposure depends on its intrinsic toxicity, physical state, exposure route, and dose, as well as factors affecting host susceptibility, such as genetic factors, age, and coexisting conditions.
Primary respiratory irritants injure mucous membranes by various mechanisms, including liberation of acids such as chlorine, phosgene, sulfur dioxide, and nitrogen, and alkali like ammonia, oxidant formation, and inflammatory-cascade initiation.
Respiratory irritation by hazardous chemicals are based on the agent’s water solubility, as highly water-soluble chemicals cause immediate irritant symptoms of burning, tearing, sneezing, rhinorrhea, and cough.
Massive exposure may involve the lower airway and gas-exchange surfaces.
Severe respiratory affected patients may present with airway obstruction, dyspnea, wheezing, and progressive acute lung injury.
Possible interventions for respiratory involvement include: inhaled or systemic glucocorticoids and nebulized sodium bicarbonate for chlorine inhalation.
Water-insoluble respiratory irritants cause few symptoms or upper-airway signs before delayed-onset acute lung injury is manifested. Inciting agents include oxides of nitrogen. and phosgene.
Treatment includes early administration of glucocorticoids, although the benefit of this treatment has not been proved.
Additional therapy of potential benefit include inhaled beta-agonists and N-acetylcysteine, as well as ibuprofen.
Vesicants, or blistering agents, may progress to more clinically significant injuries, with serious systemic effects.
Vesicants include nitrogen mustard, lewisite, and phosgene oxime, and sulfur mustard.
Mustards are alkylating agent, attacking cellular macromolecules and DNA and irreversibly damaging target tissues on contact, particularly skin, lung, and eye tissues.
Mustard exposure results in formation of a highly reactive sulfonium ion, which forms cross-links with guanine in DNA, arresting the cell cycle, initiating apoptosis, promoting oxidative stress, depleting glutathione antioxidants, and increasing inflammatory mediators.
Mustard injures skin basal keratinocytes, degrades adhesive proteins, and creates inflammation, causing dermal–epidermal separation.
Skin injury to mustard is manifested 2 to 24 hours after exposure.
Skin injury manifests initially as erythema, burning pain, with subsequent formation of vesicles, which coalesce into large bullae.
Mustard vapors penetrate clothes and concentrate in moist areas, with inguinal and axillary burns.
Mustard vapors may penetrate the dermis and result in systemic absorption and distant organ injury, such as lung and bone marrow injury.
Mustard vapors can cause cytotoxic injury and oxidative stress to the lungs, as can systemically absorbed adducts after skin exposure.
Respiratory mucosal sloughing, lung inflammation, and activation of the coagulation pathway may result in the acute respiratory distress syndrome, with high mortality.
Symptoms of mustard exposure include: pain in the nose, throat, epistaxes, hoarseness, cough, and dyspnea.
Most deaths from mustard exposure or related to respiratory failure.
After exposure to mustard fumes the eyes become red, irritated, with lid edema, corneal ulcerations, blepharospasm, and in extreme cases corneal rupture.
The systemic toxic effects of mustard exposure are similar to those of chemotherapeutic agents: bone marrow suppression,subsequent sepsis, mutagenesis, and carcinogenesis.
Management of mustard exposure: rapid skin and ocular decontamination to limit the dose and prevent the spread of contamination, as well as to the provision of supportive respiratory, eye, and burn care.
The use of copious soap and water to wash skin and hair, and copious eye irrigation.
Skin bullae contain no active mustard and may be débrided.
Instillation of combined antibiotic and glucocorticoid ophthalmic agents, is recommended.
Asphyxiant hazardous exposures cause tissue hypoxia, with profound neurologic and cardiovascular effects.
Asphyxiant exposures include: nitrogen, methane, carbon monoxide, methemoglobin, hydrogen sulfide, cyanide, phosphine, and azides can displace oxygen from inspired air, interfere with oxygen transport, or interfere with oxidative metabolism.
All of the above asphyxiant exposures result in hypoxemia.
The asphyxiant toxic reactions include: seizures, coma, hypotension, bradycardia, and apnea, headache, dizziness, fatigue, tachycardia, dyspnea, nausea, and vomiting.
Carbon monoxide exposure accounts for more than 50,000 ED visits in the United States each year.
Carbon monoxide occurs commonly from faulty heating systems, household combustion appliances, vehicle engine exhaust, and smoke from house fires, resulting in frequent unintentional and suicidal poisoning deaths.
Carbon monoxide interferes with the binding of oxygen to hemoglobin.
Carbon monoxide also inhibits mitochondrial cytochrome oxidase.
Hydrogen sulfide associated with catastrophic occupational exposures involving workers in sewers or other enclosed spaces.
Hydrogen sulfide lethality of this gas is associated with extremely high risk of injury to first responders.
Hydrogen sulfide causes serious irritant effects on the mucous membranes of the eye nose, and respiratory tract.
Cyanide exposure is associated with inhalation of smoke from house fires.
Other sources of exposure of cyanide include industrial and laboratory accidents, sodium nitroprusside hypertension therapy, cyanogenic chemical and plant ingestion, suicide attempts, and criminal or t2242orist activity.
Cyanide toxicity results in inhibiting mitochondrial cytochrome oxidase and thus oxidative phosphorylation.
Cyanide toxicity has asphyxiant clinical effects, metabolic acidosis, and hyperlactatemia.
Lactate levels above 10 mmol per liter in patients with smoke inhalation.are strongly associated with cyanide toxicity.
Asphyxiant poisoning management includes begins with fresh air, dermal decontamination for liquid exposures, 100% oxygen as the respired gas, and correction of metabolic acidosis.
Gastrointestinal decontamination is attempted for cyanide and azide ingestion.
Oxygen is beneficial in managing the toxic effects of cyanide and hydrogen sulfide.
Carbon monoxide toxicity may be mitigated by hyperbaric oxygen therapy.
The toxic effects of cyanide Is associated with altered sensorium, cardiovascular collapse, and severe metabolic acidosis.
Three are antidotes for the toxic effects of cyanide:
The sequential administration of nitrite forming methemoglobin, which dissociates cyanide from cytochrome oxidase, and induces nitric oxide synthesis, and thiosulfate which enhances conversion of cyanide to thiocyanate, which is less toxic.
Hydroxocobalamin, exchanges a hydroxyl group for cyanide, forming cyanocobalamin, which is nontoxic.
Cholinergic compounds include organophosphate and carbamate pesticides, military nerve agents, and several commonly used medications, including neostigmine and physostigmine.
Organophosphate pesticides, are widely used in agriculture, are highly toxic.
Organophosphates act primarily by inhibiting acetylcholinesterase at neural junctions.
When in excess, synaptic acetylcholine results in the cholinergic toxidrome involving the central nervous system (CNS), neuromuscular junction, and autonomic nervous systems.
Severe organophosphates poisonings probably also involve γ-aminobutyric acid and N-methyl-d-aspartate glutamate receptors, exacerbating toxic effects on the CNS.
Organophosphates result in muscarinic, nicotinic, and CNS effects ensue.
Muscarinic effects result from parasympathetic overstimulation result in miosis and blurred vision; excessive secretions, especially salivation, lacrimation, urination, defecation, gastric cramping, emesis, and bronchorrhea, bronchospasm, and bradycardia.
Nicotinic signs result from overstimulation of sympathetic ganglia with diaphoresis and tachycardia,and neuromuscular junctions with muscle fasciculation, profound muscle weakness, and paralysis.
Organophosphates toxicity results in CNS dysfunction occurs, including confusion, coma, apnea, and seizures.
Lethality from organophosphates is due primarily to respiratory compromise from central apnea, severe airway narrowing, excessive pulmonary secretions, and respiratory muscle paralysis.
The inhalation of nerve-agent vapor causes ocular, respiratory, and systemic effects, with an abrupt onset of seizures, paralysis, and respiratory arrest in severe cases.
Skin exposure to liquid organophosphate agents leads to dermal absorption, with potential early localized effects such as diaphoresis and fasciculation, followed by systemic toxic effects.
Organophosphate toxicity results in depression of serum and erythrocyte cholinesterase levels.
Management includes decontamination with consideration of gastrointestinal decontamination in the case of pesticide ingestion.
Supportive care, clearing of airway secretions, supplemental oxygen, and early endotracheal intubation in severe cases; and rapid antidote administration are required.
Atropine is administered for its antimuscarinic effects, to dry pulmonary secretions, relieve bronchoconstriction, correct hypotension, bradycardia, and potential mitigation of seizures.
Organophosphate poisoning confers a relative tolerance to atropine.
Large doses of atropine may be required in organophosphate poisoning.
Pralidoxime, an oxime acetylcholinesterase reactivator is widely recommended for the toxic effects of nerve agents.