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Drug Overdose and Antidotes

2.00 Contact Hours
A score of 80% correct answers on a test is required to successfully complete any course and attain a certificate of completion.
Author:    Berthina Coleman (MD, BSN,RN)

Outcomes

The purpose of this activity is to provide nurses with a thorough understanding of drug poisoning and how to appropriately manage cases of acute poisoning.

Objectives

After completing this course, the learner will be able to meet the following objectives:

  1. List the factors that affect an individual’s reaction to a drug or a toxin
  2. State whether most poisoning events are intentional or unintentional
  3. Identify which substance is most commonly identified as the cause of death from poisoning
  4. Identify the most common cause of intentional poisoning
  5. Define the ABCDs of poisoning management

Definition and epidemiology

Drug poisoning refers to the adverse effects experienced following exposure to chemicals, drugs, or otherwise innocuous substances. It is important to note that the adverse side effects experienced are usually related to the dose. Even oxygen or water can cause toxicity in high enough doses. On the other hand, if the dose is low enough known toxic substances such as arsenic or botulinum may have no adverse effects.

The reaction to a given toxin depends on the toxin dose, but even with the same dose, there are variations in the way each individual responds to the toxin. The factors which affect an individual’s reaction to a drug include; acquired tolerance, genetic predisposition, the presence of other drugs in the system which may affect enzymatic activation and/or inhibition. Depending on the route of exposure, poisoning may be local or systemic.

Approximately 5 million exposures occur every year in the United States. Most poisoning events are; unintentional, occur in a home setting, involve one agent, involve children who are under the age of 6 and result in minor or mild toxic reactions.

The annual incidence of acute poisoning cases is over 1 million in the United States. However, only a few of these cases are fatal. The vast majority of deaths occur because of intentional suicidal overdose. Over the past 40 years, the increased use of safety packaging has markedly decreased the incidence of fatalities in children after the ingestion of toxic household products or drugs. Effective poisoning prevention education has also played a great role in reducing the incidence of acute poisoning in the United States.

Poisoning is rarely fatal if the patient receives immediate medical attention and appropriate ongoing supportive medical care. Improved survival in poisoning patients has been shown with improved management of hypotension, respiratory failure, seizures and temperature regulation.

Drugs are implicated in 47% of all poisonous exposures and 84% of all fatal poisonings. Unintentional exposure to toxins occurs at home, at work or while playing. Other reasons for exposures include; mislabeling in the workplace, misreading of labels, mistaken identification of unlabeled products either at home or work, uninformed self-medication and dosing errors committed by patients, nurses, physicians, and pharmacists.

Attempted suicide is the second most commonly reported cause of intentional poisoning with the first being alcohol poisoning. Unintentional self-poisoning can also result from the use of over the counter or prescription drugs either for euphoric or psychotropic effects.

Up to 25% of exposures necessitate evaluation by a healthcare professional, and 5% of those exposures are serious enough to require hospitalization. Poisonings account for up to 10% of ambulance trips. An astounding 30% of all admissions to a psychiatric unit are associated with a suicide attempt by overdose. The mortality rate from all drug exposures is approximately < 1%. The mortality rate among hospitalized patients admitted for intentional overdose is higher at approximately 2%.

The most frequently implicated drug in poisonings is acetaminophen. Carbon monoxide is the drug which is most commonly implicated as the cause of death from poisoning. Often, patients with carbon monoxide poisoning are dead prior to the arrival of emergency personnel.

Poisoning can be identified with careful history taking, detailed physical examination and thorough laboratory and toxicology evaluation. Clinicians also rely on the characteristic clinical course of poisoning by specific toxins to make the correct diagnosis.

Clinical History

When obtaining a patient’s history, clinicians should focus on the time, route and duration of the exposure. Circumstances surrounding the exposure such as the location and the intent must be clarified. The name and amount of each substance or drug the patient was exposed to should be recorded. Documentation of the severity of the symptoms and the response to the first aid measures administered is also necessary. Any underlying psychiatric illness should be clarified and documented.

In most cases, the patient may be confused, unconscious or unwilling to cooperate. Any suspicious findings in the history should be further investigated. Suspicious findings include sudden unexplained illness in previously healthy patients, history of psychiatric illness, the onset of symptoms after the ingestion of foods or drinks including alcohol or medications. Clinicians should remain vigilant for “body stuffing” or “body packing.” The onset of illness that occurs while at work is also characterized as suspicious activity.

Any relevant information should be documented along with the source providing the information including; family members, friends, police officers, paramedics, nursing staff, physicians, pharmacists, etc.

A search of the patient’s belongings may provide useful clues such as the drug ingested or the container containing the drug. The imprint on a pill or the label on a container can be used to identify the suspected toxins. Resources used to identify a suspected poison include a regional poison information center, a reference textbook, a computer database, or the pill or poison manufacturer. A review of the material safety data sheet (MSDS) from a job work site can help identify a suspected poison.

The ABCDs of poisoning management

The initial focus should be to assess the cardiopulmonary and neurologic systems. Frequent assessment of the patient’s vital signs is recommended. The neurologic exam includes neuromuscular abnormalities such as dyskinesia, dystonia, myoclonus, rigidity, and tremors. Mental status should be carefully monitored. Examine the patient for any evidence of trauma or underlying illness. Focal neurologic symptoms rarely occur with poisoning. If the patient presents with focal neurologic symptoms, they need to be promptly imaged to evaluate for any structural central nervous system abnormalities.

When evaluating patients with suspected poisoning such as patients who present with an altered mental status or even in a coma, the initial focus is on supportive care. The commonly used approach in the initial management of a patient with suspected poisoning is the ABCD approach: Airway, Breathing, Circulation and the Dextrose challenge.

Securing the airway is a priority. The airway should be cleared of any foreign bodies or vomitus. Next, it should be secured using either an oral airway device, a laryngeal mask airway, or an endotracheal tube. In case there are no airway devices readily available, positioning the patient in the lateral decubitus position is adequate because it moves the flaccid tongue away from the airway.

Breathing is usually assessed by observing the chest for adequate rise in the setting of immediate resuscitation. Subsequently, it is assessed by evaluating the pulse oximetry and if in doubt, by measuring arterial blood gases. Patients with respiratory failure should be immediately intubated and ventilated.

Circulation should be assessed by continuous evaluation of the blood pressure, pulse, and urinary output. An intravenous line should be placed as soon as possible, and routine labs should be sent off.

At this point, every patient should undergo the dextrose challenge which is done by administering concentrated dextrose unless a bedside blood glucose test shows a normal blood glucose level. The dose of dextrose for adults is usually 25 g intravenously, in children the dose is 0.5 mg/kg. The reason why the dextrose step is so critical is that patients who are intoxicated cannot be rapidly and accurately distinguished from poisoned patients.

Patients who are alcoholic or malnourished should also receive 100 mg of Thiamine (Vitamin B1) either intravenously or intramuscularly to prevent them from getting Wernicke’s syndrome. Wernicke’s syndrome is defined as an acute neurologic condition which is characterized by a classic triad of ophthalmoplegia, ataxia and altered mental status. It is caused by a Thiamine deficiency, and it is associated with chronic alcohol use. Other names used to describe Wernicke’s syndrome include cerebral beriberi and Wernicke’s encephalopathy.

Next, the opioid antagonist naloxone is administered. Usually, a dose of 0.4 mg is administered intravenously up to a maximum dose of 2 mg in 0.4 mg increments. Naloxone (Narcan) reverses respiratory depression and central nervous system (CNS) depression. Given that most CNS depressants cause death by respiratory depression, naloxone administration is a critical step.

Physical examination

The chart below includes vital signs that provide a clue as to the substances that were possibly ingested.

Chart 1

Vital SignsSubstances
Hypertension
Tachycardia
Amphetamines
Cocaine
Antimuscarinic drugs
Hypotension
Bradycardia
Beta blockers
Calcium channel blockers
Alpha agonists
Sedative hypontics
Hypotension
Tachycardia
Antidepressants
Trazodone
Beta agonists
HyperthermiaAnticholinergics
Sympathomimetics
Salicylates
Drugs that cause muscle rigidity
HypothermiaCNS depressants (especially if patient is exposed to a cold environment)
MydriasisAmphetamines
Cocaine
Atropine
Anticholinergic drugs
MiosisOpioids
Clonidine
Phenothiazine
Horizontal nystagmusIntoxication from alcohol
Phenytoin
Barbituates
Other sedative hypnotics
Vertical nystagmus and horizontal nystagmusPhencyclidine poisoning

Examining the patient’s mouth can sometimes provide a clue to the poisoning agent. For example, with cyanide poisoning, the patient may have an odor of bitter almonds. Physical examination of the skin can also be useful in identifying the toxin. Excessive sweating is seen with organophosphate, sympathomimetic and nicotine poisoning. Jaundice is seen with amanita phalloides, mushroom poisoning, as well as with acetaminophen poisoning. Cyanosis can be seen with hypoxemia and or methemoglobinemia.

Hyperactive bowels, diarrhea, and abdominal cramping can be seen with arsenic or organophosphate poisoning. Seizures can be seen with overdose from antidepressants, cocaine, amphetamines, and diphenhydramine.

Decontamination techniques

Decontamination procedures can be started simultaneously with the ABCD’s of initial stabilization. Decontamination can involve removing toxins from either the gastrointestinal tract and/or the skin. The patient’s clothes should be removed and double bagged to prevent the care provider contamination. Wash contaminated skin with soap and water. 

Decontamination of the gastrointestinal tract can be done by inducing emesis or gastric lavage. However, the benefits of gastric emptying by either emesis or gastric lavage remains controversial. Activated charcoal can be used to bind ingested poisons in the gastrointestinal tract before they can be absorbed. Ideally, gastric emptying techniques should be started within an hour of ingestion. Emesis is usually induced with ipecac syrup unless the toxin is a corrosive agent or a rapid-acting convulsant. Other methods of inducing emeses, such as fingertip stimulation of the pharynx and salt water, are dangerous and should be avoided. 

Activated charcoal is usually administered in a ratio of at least a 10:1 based on the weight of the toxin. Charcoal does not bind iron, lithium or potassium. Gastric lavage solutions should be kept at body temperature to avoid hypothermia. 
 

Toxins and their antidotes

The antidote for acetaminophen is acetylcysteine. Acetylcysteine is administered intravenously and is usually more effective if given within 8 - 10 hours from the time of ingestion. Mucomyst is the oral preparation of acetylcysteine that is administered orally. Incidentally, Mucomyst can be used as a mucolytic expectorant to help with the clearance of thick mucus secretions.

Atropine is used as the antidote for anticholinesterase or organophosphate poisoning. It is usually administered intravenously with an initial dose of 1-2 mg in adults with subsequent doubling of the dose every 15 minutes if there is no response. Atropine can also be used for rapid onset mushroom poisoning especially when there is a predominance of muscarinic excess symptoms such as bradycardia, hypotension, rhinorrhea, bronchospasm, respiratory distress, hypersalivation, abdominal cramping, and diarrhea.

In the case of tricyclic antidepressants and other membrane depressant cardiotoxic drugs, bicarbonate sodium is the antidote of choice. The dose is usually 1-2 mEq/kg administered intravenously. Cautious use is advised for patients with heart failure. In addition, clinicians should closely monitor these patients for signs of sodium overload.

The antidote for calcium channel blockers is calcium administered in large doses. The initial dose is usually 15 mg/kg intravenously.

The antidote for digoxin is digoxin specific antibodies. Each vial of digoxin antibodies binds approximately 0.5 mg of digoxin. Digoxin antibodies are usually indicated in patients with arrhythmias and hyperkalemia.

Deferoxamine is used in cases of intoxication with iron salts. 100 mg of deferoxamine administered intravenously binds 8.5 mg of iron.

An overdose of caffeine and theophylline is usually treated with Esmolol. Esmolol is a short acting beta blocker, and the dose for administration is 25 - 50 mcg/kg/min intravenously.

Methanol and ethylene glycol intoxication are usually treated with ethanol administration. Fomepizole is also an antidote to methanol and ethylene glycol intoxication and is much more convenient to use than ethanol. The dose for Fomepizole is 15 mg/kg and can be repeated every 12 hours.

Benzodiazepine overdose can be reversed with Flumazenil. In adults, the dose is 0.2 mg intravenously which can be repeated up to a maximum of 3 mg. Flumazenil should not be administered in patients with seizures, benzodiazepine dependence, or in cases of tricyclic overdose.

Cyanide poisoning is treated with hydroxocobalamin which converts cyanide to cyanocobalamin which is Vitamin B12. The dose of hydroxocobalamin is 5 g over 15 minutes intravenously.

Beta blocker overdose is managed by administering glucagon which reverses the beta blocker effects. 5 - 10 mg iv of glucagon is initial dose used to reverse the bradycardia and hypotension associated with beta blocker overdose.

Naloxone (Narcan) is used as the antagonists of opioid and other narcotics. Usually, 0.4 mg of naloxone is given initially and can be repeated up to a maximum of 2 mg. Naloxone can be administered intramuscularly, subcutaneously or intravenously. Larger doses may be necessary to reverse the effects of overdose from codeine, propoxyphene or fentanyl derivatives. It is also important to note that the duration of action for naloxone is usually 2 -3 hours while that of the intoxicant narcotic may be significantly longer.

Carbon monoxide poisoning can be either accidental or intentional. It is usually treated with 100% oxygen administered via a non-rebreather mask. Hyperbaric chambers can be used in cases of severe poisoning.

Physostigmine is used to treat the delirium associated with the anticholinergic drugs. Physostigmine can cause bradycardia and can increase bronchial secretions and even cause seizures. Do not use physostigmine in the case of tricyclic antidepressant overdose. In the case of physostigmine overdose, atropine can be used as an antidote.

Pralidoxime is also used to treat organophosphate and cholinesterase inhibitor overdose; although, the benefits in organophosphate overdose are not well established.

Case Study

A 21-year-old male is transported to the emergency department by emergency medical services after being found in his garage while his car was running by a neighbor. He is unresponsive at the time of admission. He has no identifying information on him, and there are no family or friends present to provide a medical history. Initial vital signs are BP 110/64, HR 95, respirations 8 per minute, pulse oximetry of 98%. You are the nurse assigned to take care of him. What should you do first?

Discussion

The primary survey includes the ABCDs; the patient’s airway should be secured. Breathing should be assessed, and the pulse oximetry should be obtained. Next, circulation should be assessed including an evaluation of the peripheral circulation. This patient’s nail beds and perioral regions are cyanotic. His respirations are depressed and slowed, but the pulse oximetry remains stable at 98%.

He should be immediately put on a non-rebreather oxygen mask on 100%. It is important to note that although the pulse oximetry in patients with carbon monoxide poisoning may appear normal, the patient may be in severe respiratory distress. Carbon monoxide (CO) binds to hemoglobin (Hb) with an affinity that is 200 times greater than that of oxygen. It reduces the oxygen capacity of blood and induces further hypoxia by shifting the oxygen dissociation curve to the left. Paradoxically patients with bound carboxyhemoglobin (COHb) in their blood will have a normal pulse oximetry rate, and clinical providers should not rely on pulse oximetry for adequate evaluation of tissue oxygenation. Instead, arterial blood gases should be drawn since they are much more reliable.

Conclusion

Nurses play a critical role in the primary evaluation of patients who are brought in with suspected poisoning. As such, nurses should have a good grasp of toxins and their antidotes and understand the principles of initial triage in patients with suspected poisoning.

References

Dart, R. D. Medical Toxicology. 3rd ed. N.p.: Lippincott Williams & Wilkins, 2004. Print.

Ferri, Fred F. "Wernicke Syndrome." FERRI'S CLINICAL ADVISOR 2018. 3rd ed. S.l.: MOSBY, 2017. 1376. Print.

Hoffman, Robert S., Mary Ann Howland, Neal A. Lewin, Lewis Nelson, Lewis R. Goldfrank, and Neal Flomenbaum. Goldfrank's Toxicologic Emergencies. New York: McGraw-Hill Education, 2015. Print.

Mycyk, Mark B.. "Poisoning and Drug Overdose." Harrison's Principles of Internal Medicine, 19e Eds. Dennis Kasper, et al. New York, NY: McGraw-Hill, 2014

Olson, K. R. "Management of the Poisoned Patient." Basic & Clinical Pharmacology. By Bertram G. Katzung and Anthony J. Trevor. Singapore: McGraw-Hill Education, 2016. N. pag. Print.


This course is applicable for the following professions:

Advanced Registered Nurse Practitioner (ARNP), Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Registered Nurse (RN)

Topics:

Advance Practice Nurse Pharmacology Credit, CPD: Practice Effectively


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