CHAPTER 42. Toxicologic Emergencies
Patty Sturt
An estimated 5 million poisonings or drug overdoses occur annually in the United States. 25 Children account for approximately two thirds of all human toxic exposures reported to the American Association of Poison Control Centers. 3 Toxic agents are manufactured or naturally occurring chemicals that have deleterious effects on humans. Toxins can enter the body through ingestion, inhalation, injection, mucosal absorption, ocular exposure, or dermal contact. The quantity of toxin required to produce symptoms varies widely among substances. Exposure may be accidental or intentional and related to recreation or occupation.
Management of the poisoned patient may involve continuous respiratory and hemodynamic support, careful evaluation of toxicosis potential, interventions to reduce toxin absorption and promote excretion, and substance-specific therapy, including use of antidotes. An overview of assessment and management of the patient with a toxicologic emergency is followed by discussion of specific, common poisonings.
PATIENT MANAGEMENT
Determining the precise agent or agents involved in a toxicologic emergency can be challenging due to the vast number of potentially toxic substances. Poison control centers are an excellent resource for information on various drugs, potential toxicity, and patient management. Poison control centers, available nationwide through the telephone number 1-800-222-1222 and staffed by nurses and or pharmacists, provide professionals and the public with 24-hour telephone access to evidence-based treatment regimens. Many emergency departments (EDs) have rapid access to computer programs such as Micromedex that provide information on care of patients exposed to specific agents.
Symptoms of toxic exposures range from minor to severe and vary widely with the causative agent, dose, and extent of exposure. Toxins are capable of affecting every body system, and certain toxins produce predictable clinical signs and symptoms. Assess the patient carefully by obtaining a detailed history from the patient, family, or prehospital care providers. Consider the possibility of ingestion of or exposure to a toxic agent if the patient presents with a decreased level of consciousness without an identifiable cause. Table 42-1 describes essential assessment information related to toxic exposure.
Item | Description |
---|---|
Substance | If possible, visually confirm substance(s) involved. Ask what medications the patient takes at home. |
Time of exposure | Time since exposure influences both symptoms and treatment. |
Acute or chronic | Acute exposures have different presenting symptoms and are managed differently than chronic exposures. |
Amount of toxin | Determine the maximum quantity possible. Count pills in the bottle; confirm when the prescription was filled. |
Signs and symptoms | Assess for symptoms in all systems. Toxins can affect every tissue in the body. |
Prior treatment | Clarify any interventions provided by lay and prehospital personnel. Some home remedies can be detrimental. |
Intentional or accidental | Poisoning is a popular form of suicide and suicidal gesture. Have there been previous suicide attempts? Does the patient have a history of depression or preexisting mental health problems? Was the poisoning recreational? Is this a possible homicide attempt? |
Provision of meticulous supportive care, identification of patients requiring treatment with an antidote, and appropriate use of methods limiting poison absorption or increasing elimination remain the cornerstones of management10 for patients with a toxicologic emergency.
General Interventions
Stabilization of airway, breathing, and circulation are the first priorities when caring for an individual with a toxicologic emergency. Protect the airway, ensure adequate oxygenation and ventilation, and support the cardiovascular system while attempting to identify specific toxins involved. Significant exposures may require endotracheal intubation, mechanical ventilation, and vasoactive medications.
Substance-to-substance variations in toxicologic management exist; however, the need to ensure patient safety and provide emotional support is common to all poisonings. Knowledge of common toxidromes and interventions associated with each will assist the emergency nurse in the management of the patient with a toxicologic emergency.
Limit Absorption
Decontamination is a mechanism to limit or decrease absorption of the poison or toxic agent. Decontamination can be divided into gastrointestinal (GI) decontamination for ingestions and external decontamination for dermal or ocular injuries from a toxic agent. Specific interventions are determined by patient condition and the precise toxin involved.
GASTROINTESTINAL DECONTAMINATION
GI decontamination refers to specific efforts used to inhibit absorption of drugs and poisons in the GI tract. There are five methods of GI decontamination: induced emesis, gastric lavage, activated charcoal, whole bowel irrigation, and binding agents.
Induced Emesis
Emesis may be induced with syrup of ipecac. It is prepared from the Cephaelis plant, which contains the alkaloids emetine and cephaeline. These emetics induce vomiting via gastric irritation and stimulation of the vomiting center in the brainstem. The use of syrup of ipecac in the management of poisoned patients has declined. Several studies have found that use of syrup of ipecac has been associated with aspiration pneumonia, dehydration, a longer ED course, and more complications. In addition, no studies demonstrate that the use of ipecac in the treatment of acute poisoning changes or improves clinical outcomes. 4 The American Academy of Pediatrics no longer recommends home stocking of ipecac.
This agent has an unpredictable onset of action and intensity of effect. Violent, protracted vomiting after administration of ipecac predisposes the patient to fluid loss, acid-base abnormalities, electrolyte disturbances, and Mallory-Weiss tears and delays administration of activated charcoal and oral antidotes. Use of syrup of ipecac for hydrocarbon or caustic ingestion increases the incidence of oral, upper airway, and pulmonary injury.
Overall, the majority of clinical experts do not recommend the use of syrup of ipecac to induce vomiting for gastric decontamination in adult or pediatric patients.
Gastric Lavage
The benefit of using gastric lavage to decrease absorption is limited. Generally, gastric lavage is considered only when a patient has ingested a potentially life-threatening amount of poison and the procedure can be initiated within 60 minutes of exposure. Gastric lavage may propel gastric contents past the pylorus, moving the poison into the small intestine, where most of the ingested agent may be absorbed. 22 Some clinical trials indicate that gastric lavage does not improve patient outcomes and increases the risk for complications, such as hypoxia and aspiration, when compared to those treated without gastric lavage. 2
Before initiating lavage, place the patient in a left lateral position to decrease risk for aspiration. Lavage should not be performed on patients who have ingested medications that may cause abrupt central nervous system (CNS) deterioration, such as tricyclic antidepressants (TCAs), unless the patient has been intubated. If the gag reflex is diminished, protect the airway with endotracheal intubation before lavage. Monitor for bradycardia secondary to vagal stimulation during tube placement. Lavage is not recommended for patients who have ingested a corrosive agent due to the increased risk for esophageal perforation. For adult patients with pill ingestion, insert a large-diameter (36 Fr to 40 Fr) orogastric tube with a bite block to prevent tube occlusion. Nasogastric tube aspiration may be effective in cases of liquid poisoning but is not adequate for ingestion of pills.
With mechanical suction or a catheter tip syringe, withdraw as much of the gastric contents as possible. To perform lavage, repeatedly instill and remove 200- to 300-mL aliquots of tepid tap water or normal saline until the return is clear; 2 to 5 L may be needed to achieve this goal. 11 For pediatric patients, administer 10 to 15 mL/kg in 50-mL boluses through a 24- to 28-Fr orogastric tube.
Activated Charcoal
Activated charcoal is the preferred means of GI decontamination for management of most toxic ingestions. Charcoal is “activated” by exposure to high temperatures that dramatically increase its surface area. This agent has an extensive network of interconnecting pores that are capable of binding and trapping chemicals within minutes of contact, thus preventing their absorption and toxicity. Binding prevents absorption into the bloodstream, allowing toxins to be eliminated in feces. Studies suggest that, used alone, activated charcoal administration is as effective as or even more effective than administration of activated charcoal after emesis or gastric lavage procedures.
Activated charcoal should be administered as soon as possible after the ingestion. Some clinical experts report it is most effective if administered within 60 minutes of the ingestion. 1. and 2. However, there is limited evidence to determine at what time frame activated charcoal is no longer beneficial. It may be effective for some agents beyond the 60-minute window, particularly for sustained-release preparations or anticholinergic medications.
Activated charcoal readily absorbs most poisons except heavy metals (e.g., lithium, iron) and alcohols (e.g., methanol, ethylene glycol). It is not recommended in patients who have ingested acidic or alkaline corrosives or who require endoscopy because charcoal will obstruct the view during the procedure. Substances poorly absorbed by charcoal include acids, alkali, cyanide, ethanol, fluoride, lead, mercury, mineral acids, organic solvents, and potassium. Contraindications to charcoal administration include bowel obstruction or bowel perforation. Adverse effects of activated charcoal include nausea, vomiting, GI obstruction, and pulmonary aspiration.
Activated charcoal is given orally or through a gastric tube in doses of 25 to 100 g (1 g/kg for children). The commercial product should be vigorously agitated before administration to resuspend all the activated charcoal. If the quantity of an ingested substance is known, give at least 10 times the ingested dose of toxin (by weight) to prevent desorption of the substance in the lower intestine. Administration of one or two follow-up doses at 1- to 2-hour intervals is common.
Activated charcoal is prepared as an aqueous solution with or without sorbitol. Sorbitol helps the toxins that are bound to the activated charcoal pass through the GI tract. Follow the recommendations of regional poison control centers for the type of activated charcoal to be used.
Binding Agents
Binding agents limit the bioavailability of certain poisons. Magnesium hydroxide has been found to be effective in reducing serum iron levels. Sodium polysterene sulfonate, often used to treat hyperkalemia, has been effective in limiting serum lithium levels. Other specific binding agents may not be as clinically applicable due to limited availability (e.g., cholestyramine, fuller’s earth) Activated charcoal is often considered a binding agent because it limits absorption of many agents.
Whole Bowel Irrigation
Whole bowel irrigation is a method of GI decontamination that entails administering polyethylene glycol orally or through a gastric tube until the resulting rectal effluent is clear. Polyethylene is not absorbed and is less likely to produce a fluid or electrolyte imbalance. Whole bowel irrigation is used to treat large ingestions of drugs not absorbed by activated charcoal (such as lithium and iron), large ingestions of enteric-coated or sustained-release tablets, and patients who have ingested packages of illicit drugs (body packers).
The dose is usually 2 L/hr for adults and 500 mL/hr for children until the rectal effluent is clear. Contraindications to its use include bowel obstruction, paralytic ileus, or GI hemorrhage.
EXTERNAL DECONTAMINATION
External decontamination is the removal of a toxic substance from the skin or eyes to reduce the risk for absorption.
Dermal Decontamination
Skin decontamination is indicated for dermal exposure to any toxic substance. Remove contaminated clothing and jewelry as soon as possible, and rinse areas of contact for 10 to 15 minutes with copious amounts of water or saline. It is important to rinse the toxic agent from the hair, ears, nose, and skin folds. Dry substances should be brushed from the body before washing. Neutralizing agents should not be applied because the resulting chemical reaction produces heat and can increase local tissue damage. Depending on the substance and amount, both clothing and irrigation fluids may be considered hazardous waste. Individuals with toxic dermal exposures also represent a risk to others. Health care personnel should wear appropriate personal protective equipment (e.g., gloves, gowns, and goggles) to avoid secondary contamination.
Ocular Decontamination
Ocular decontamination involves vigorous eye irrigation with copious amounts of water or normal saline. Prolonged flushing may be necessary after exposure to caustic substances, particularly alkalis. An ophthalmologist should be consulted if ocular complaints persist after irrigation. Refer to Chapter 45 for discussion of eye irrigation and ocular burns.
Enhance Elimination
After initial efforts to limit absorption, enhancing elimination of absorbed toxins is the next priority in managing the poisoned patient. Techniques to enhance toxin elimination include repeat-dose activated charcoal, cathartic administration, forced diuresis, hemodialysis, charcoal hemoperfusion, and continuous hemofiltration.
REPEAT-DOSE ACTIVATED CHARCOAL
Repeat-dose activated charcoal is used in cases of theophylline, phenobarbital, dapsone, digoxin, and carbamazepine toxicity. 8 Even when parenterally administered, these agents may be effectively removed with activated charcoal in a process that is distinctly different from the agent’s usual GI decontamination effect. Not only does charcoal bind toxins in the intestines and prevent absorption, it also facilitates elimination by decreasing serum concentrations of certain already absorbed poisons through a process of “gastrointestinal dialysis.” This occurs as a result of the concentration gradient between charcoal in the gut and the toxin in the blood. Because of the intestine’s tremendous blood supply, activated charcoal can draw select poisons from the circulation and bind them for elimination in feces, a process enhanced with repeated doses of charcoal.
CATHARTIC ADMINISTRATION
Cathartics, such as sorbitol and magnesium citrate, can be mixed with activated charcoal to increase elimination of ingested toxins by stimulating intestinal motility. Without concomitant use of a cathartic, charcoal may cause constipation, leaving both charcoal and toxins in the gut and creating the potential for toxin unbinding and systemic absorption. Cathartic use is contraindicated after corrosive ingestion and when vomiting, diarrhea, or ileus is present. Half the original cathartic dose may be repeated if there has been no charcoal stool within 6 to 8 hours. Multiple doses of cathartic agents should be avoided because the subsequent diarrhea has been associated with fatal electrolyte imbalances, particularly in children. Occasionally cathartics are used without activated charcoal to remove largely nontoxic materials or substances with poor affinity for charcoal, such as iron tablets or hydrocarbons. All cathartics should be used with caution in pediatric patients. Sorbitol is not recommended for infants because of the potential for fluid and electrolyte abnormalities.
HEMODIALYSIS, HEMOPERFUSION, AND HEMOFILTRATION
Hemodialysis, hemoperfusion, and hemofiltration not only remove toxins and their metabolites from the circulation, but also rapidly and effectively correct acid-base and electrolyte disturbances. Substances such as acetaminophen, alcohols, lithium, salicylates, and phenobarbital can be removed with dialysis. Because of requirements for vascular access, dialysis equipment, and skilled personnel, hemodialysis is generally reserved for poisonings associated with severe acidosis. Hemoperfusion is similar to hemodialysis, but it binds toxins as blood moves across a charcoal or resin filter rather than the traditional hemodialysis filter and dialysate. Hemoperfusion achieves greater clearance rates than hemodialysis and is particularly effective for severe cases of poisoning with paraquat, theophylline, phenytoin, and some sedative-hypnotic agents. 14 Continuous arteriovenous and venovenous hemofiltration have been suggested as alternatives to conventional hemodialysis when the need for rapid drug removal is less urgent. The role of these modalities in management of the acutely poisoned patient remains uncertain.
Substance-Specific Interventions
In addition to minimizing absorption and enhancing excretion, key interventions include antidote administration and urinary alkalinization.
Antidote Administration
Antidotes are available for specific drugs and poisons. If the ingested substance is unknown, determine if the signs and symptoms match with a specific classification of drugs. Table 42-2 lists antidotes and their indications.
Antidote | Indication |
---|---|
Amyl nitrite | Cyanide |
Atropine | Organophosphates |
BAL/dimercaprol | Heavy metals |
Calcium chloride/calcium gluconate | Calcium channel blockers |
Deferoxamine | Iron |
Ethylenediaminetetraacetic acid (EDTA) | Heavy metals |
Ethanol | Ethylene glycol, methanol |
Fab fragments | Digitalis |
Flumazenil | Benzodiazepines |
Fomepizole | Ethylene glycol, methanol |
Glucagon | β-Blockers, calcium channel blockers |
Insulin and glucose | Calcium channel blockers |
Methylene blue | Nitrites |
N-Acetylcysteine | Acetaminophen |
Naloxone | Opiates |
Octreotide | Sulfonylureas |
Oxygen | Carbon monoxide |
Penicillamine | Heavy metals |
Physostigmine | Anticholinergics |
Pralidoxime (2-PAM) | Organophosphates |
Pyridoxine | Isoniazid |
Sodium bicarbonate | Tricyclic antidepressants |
Sodium nitrite | Cyanide |
Sodium thiosulfate | Cyanide |
Vitamin K | Warfarin |
Urinary Alkalinization
Urinary alkalinization can increase renal elimination of salicylates, phenobarbital, and chlorpropamide by changing them to a less-absorbable ionized form. Continuous infusions of sodium bicarbonate achieve desired urinary alkalinization.
SPECIFIC TOXICOLOGIC EMERGENCIES
Patients may present with toxicity from a single agent or from ingestion of multiple agents. Caregivers should never assume the patient with a toxicologic emergency ingested only one pill or one type of pill. Specific toxicologic emergencies are reviewed in the following section.
Salicylates
Salicylates have analgesic, antiinflammatory, and antipyretic properties, making them frequent components of both prescription and nonprescription drugs. Aspirin (acetylsalicylic acid) is the most readily available salicylate. Oil of wintergreen (methyl salicylate) is a highly toxic, liquid form of salicylate used in products such as BenGay. Bismuth subsalicylate is an ingredient in Pepto-Bismol. The incidence of acute salicylate ingestion has dropped in the United States over the last two decades because of increased use of acetaminophen and ibuprofen. However, acute and chronic overdoses of salicylates continue to occur.
Clinical findings vary significantly with patient age, amount of salicylate consumed, and whether ingestion was chronic or acute. Acute salicylate ingestions can be divided into mild, moderate, and severe based on the dose ingested and the symptoms. Mild toxicity occurs with an ingested dose of greater than 150 mg/kg. Symptoms of mild toxicity include nausea, vomiting, dizziness, and tinnitus. Moderate toxicity occurs with an ingested dose of greater than 250 mg/kg, and symptoms include tachypnea, hyperpyrexia, sweating, dehydration, agitation, and ataxia. Severe toxicity is associated with an ingested dose of more than 500 mg/kg. Patients with severe toxicity (greater than 700 mg/dL) may exhibit hypotension, metabolic acidosis, renal failure, coma, and convulsion. Acidosis can lead to cardiac dysrhythmias and cardiac failure.
Chronic toxicity may occur with ingestion of more than 100 mg/kg/day for 2 or more days. Symptoms include lethargy, confusion, dehydration, hallucinations, pulmonary edema, elevated liver enzymes, and prolonged prothrombin time (PT). Direct GI irritation causes nausea, vomiting, and hematemesis. Patients may also exhibit hyperthermia, renal failure, tinnitus, and hypoglycemia.
Salicylates stimulate the respiratory center of the brainstem, resulting in hyperventilation and respiratory alkalosis. They also decrease adenosine triphosphate (ATP) production, which leads to metabolic acidosis. Metabolic acidosis decreases the renal elimination of salicylates and increases CNS toxicity. Children tend to present to the ED with metabolic acidosis whereas adults often present with respiratory alkalosis. Decreased platelet function can lead to petechiae. Hypoglycemia is more common in children.
Diagnostic studies include serial measurements of salicylate levels, arterial blood gases, electrolytes (particularly potassium), glucose, blood urea nitrogen (BUN), creatinine, platelets, PT, and urine pH. Obtain a serum salicylate level initially or at least within 4 hours after ingestion and then approximately every 4 hours until the concentration has peaked. Levels may not peak for 12 to 18 hours after ingestion of enteric-coated tablets.
Initial treatment consists of administration of activated charcoal. Repeat doses of activated charcoal should be administered at 2-hour intervals until serum levels start decreasing. Gastric lavage may be considered if patients present within 1 hour of ingestion of greater than 500 mg/kg. Urinary alkalinization is an effective method of increasing renal excretion of salicylates in patients who exhibit moderate toxicity. 21 This can be accomplished by adding 100 mEq of sodium bicarbonate to each liter of intravenous (IV) fluid and infusing at 200 to 300 mL/hr. Potassium may be added to the IV fluid to avoid potassium loss associated with alkaline diuresis. Hemodialysis is very effective for poisonings that do not respond to simpler measures and should be considered in patients with a salicylate level of more than 700 mg/dL who exhibit symptoms of severe toxicity that do not improve with treatment. Patients in significant metabolic acidosis may need 50 mL of 8.4% sodium bicarbonate IV push. Short-acting benzodiazepines should be used for emergency treatment of salicylate-induced seizures.
Acetaminophen
As with salicylates, acetaminophen is a common ingredient in many over-the-counter analgesics, antipyretics, and cold remedies. Acetaminophen overdoses are usually unintentional in the pediatric patient and intentional in adults. Although initial symptoms are mild, severe acetaminophen poisoning causes life-threatening hepatotoxicity.
Acetaminophen is rapidly absorbed from the gut and broken down by the liver, forming a toxic metabolite. In therapeutic doses, endogenous hepatic enzymes rapidly detoxify this intermediary product. However, toxic doses deplete these essential enzymes, damaging both the liver and kidneys as metabolites accumulate. An acute toxic dose of acetaminophen for children over the age of 6 years is 10 g or 200 mg/kg, and 7.5 g is considered an acute toxic dose in adults. 7 Higher levels are tolerated in pediatric patients without toxicity because of their ability to metabolize the drug better.
Serum acetaminophen levels of 200 mcg/mL or greater 4 hours post ingestion are considered toxic, and treatment should be initiated. Levels may continue to rise up to 4 hours after ingestion of a toxic amount. Individuals at risk for acetaminophen toxicity at lower doses include those with malnutrition, preexisting hepatic dysfunction, and those taking anticonvulsant medications such as phenytoin or carbamazepine.
Signs and symptoms of acetaminophen toxicity develop slowly and can be overlooked until significant damage has occurred. The clinical course of acetaminophen toxicity occurs in 4 phases. Table 42-3 describes the time frame and symptoms for each stage. Initial acetaminophen levels should be drawn 4 hours after ingestion. Plotting the 4-hour acetaminophen value on the Rumack-Matthew nomogram (Figure 42-1) determines whether the patient is at risk for potential hepatotoxicity. This nomogram is useful only for acute, single-dose poisonings not combined with other agents (such as opioids or anticholinergics) that delay absorption. Obtain liver function studies, PT, complete blood count, BUN, and creatinine levels on patients who present with clinical symptoms and those whose levels fall within the “possible hepatic toxicity” range on the nomogram.
PTT, Partial thromboplastin time. | ||
Stage | Time Frame | Symptoms |
---|---|---|
I | 0-24 hours | May be asymptomatic or experience lethargy, diaphoresis, mild gastric upset, including nausea, vomiting, and anorexia |
II | 24-48 hours | May have no complaints or develop liver failure, abnormal liver function tests, prolonged PTT, increasing bilirubin levels, right upper quadrant pain, hepatomegaly, oliguria |
III | 72-96 hours | Massive hepatic dysfunction, liver enzymes >100 times normal, hypoglycemia, jaundice, patient appears acutely ill, can progress to hepatic failure, encephalopathy, and death |
IV | 4 days to 2 weeks | If patient survives Stage III, enters recovery phase characterized by slow resolution of hepatic dysfunction |