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Understanding Overdose
This CE activity is approved by EMS World Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS) for 1 CEU. To take the CE test that accompanies this article, go to www.rapidce.com to take the test and immediately receive your CE credit. Questions? E-mail editor@EMSWorld.com.
Bob and Jerry, both EMTs, are dispatched to a reported unconscious person at a rural residential address about two miles from their station. They hear the ALS fly car, staffed by their paramedic friend Linda, also sent to the call and realize she is about 10 miles away, across town, and will have a longer response time.
They arrive on scene to find Mrs. Smith waiting for them at the front door. “Please hurry,” she says. “It’s my husband—he’s on the couch, and I don’t know what’s wrong with him.” Mr. Smith, a 52-year-old white male, presents supine and unconscious with obviously slow, shallow and snoring breathing and peripheral cyanosis. Bob and Jerry immediately move him to the floor, where Bob moves to the airway while Jerry checks for a pulse.
“His radial pulse is about 80 and weak,” Jerry reports as Bob suctions a bit of vomit from Mr. Smith’s airway. “I’m going to start BVM ventilations,” Bob responds. “Could you hook the bag up to some oxygen?” Bob measures and inserts an oropharyngeal airway. “No gag reflex,” he observes and begins ventilating Mr. Smith 12 times a minute with the BVM while Jerry sets the oxygen flow rate at 15 lpm.
Jerry gets a history of recent events and a past medical history from Mrs. Smith. She says she left about five hours ago to visit a friend. Her husband decided to stay home because he’d hurt his back the day before while doing yard work, was in pain and wanted to rest. Their son, who lives on the next block, came by to visit him as she left. She returned home to find Mr. Smith on the couch, unconscious.
Mr. Smith is very healthy without any significant medical history and does not presently take any medications. He has no known drug allergies.
A quick physical exam reveals no obvious trauma or any other reason for Mr. Smith’s presentation. His pupils are 5 mms, equal and reactive to light. There is no JVD or peripheral edema, and his lung sounds are equal bilaterally with slight rales. There is no response to painful stimuli.
“Any ideas?” Bob asks Jerry.
“Maybe stroke or hypoglycemia?” Jerry replies.
Overview
Death from poisoning kills many people in the United States every year, and unintentional poisoning is one of the leading causes of death by injury. In 2010, 42,837 persons died as the result of poisoning.1 Of these deaths, about 77% (33,041) were unintentional, 15.5% (6,599) were the result of suicide attempts, and 7.5% (3,197) were of undetermined intent. To put it into perspective, unintentional poisoning was second only to motor vehicle crashes (33,687) as the most frequent cause of unintentional death for all ages in 2010. Among persons 25–64, unintentional poisoning was responsible for more deaths than MVCs.1
EMS education puts a focus on trauma and injuries, but arguably less of a focus on poisoning. With poisoning being such a major contributor to unintentional deaths in the U.S., it is important that EMTs and paramedics are familiar with the most common causes of unintentional poisoning and their treatment. This month’s CE article will focus on the most common cause of unintentional death by poisoning, prescription painkiller drugs. Data collected from 1999–2010 show the incidence of death from prescription painkillers has grown linearly with the sales of these medications (Figure 1).
The Basics
A poison is any substance that is harmful to your body if ingested, inhaled, absorbed or injected. A poisoning occurs when exposure to a substance adversely affects the function of body systems. If a large enough quantity is administered, any substance has the potential to be a poison, including seemingly harmless and even essential substances such as vitamins.
Poisonings can be classified as intentional or unintentional. An intentional poisoning occurs when a person administers a substance with an intent to cause harm to themselves or another. An unintentional poisoning occurs when a person taking or administering a substance lacks intent to cause harm but still provides or consumes a dangerous quantity.
A painkiller is any medication that provides analgesia, or relief from pain. The analgesics most frequently involved in unintentional death by poisoning belong to the family of drugs known as opioids. An opioid is a chemical that binds to opioid receptors in the central and peripheral nervous systems as well as the gastrointestinal tract. When they bind with opioid receptors in the brain (central nervous system), opioids produce decreased perception of and reaction to pain, as well as increased pain tolerance. Opioids are used to treat acute pain (such as postoperative pain or pain from injury), as well as chronic pain associated with conditions such as back/spinal injury, arthritis and cancer. For examples of commonly prescribed opioid medications, see Table 1.
Standard oral preparations of opioids are readily absorbed by the gastrointestinal tract, achieving peak blood levels about 30–60 minutes after ingestion. Sustained-release formulas take longer to achieve peak blood levels. Most ingested opioids undergo first-pass metabolism by the liver, meaning they will be metabolized in the liver prior to entering the systemic circulation. As a result, the bioavailability of ingested opioids is reduced as much as 80% after ingestion, and at equal doses most opioids will be much more potent when administered intravenously (parenterally) than by ingestion or transdermal patches.
The Growing Problem
In 2009, 91% of unintentional poisoning deaths were caused by prescription medications. Opioid pain medications and benzodiazepines were most commonly involved. Prescription painkiller overdoses were responsible for more than 15,500 deaths in 2009, more than the total for cocaine and heroin combined.2 This number is almost four times greater than the 4,000 people killed by prescription painkiller medications in 1999. While all prescription painkillers have contributed to the increase in overdose deaths over the last decade, methadone has played a central role. More than 30% of prescription painkiller deaths involve it, even though only 2% of painkiller prescriptions are for it.2 More than 12 million Americans reported using prescription painkillers for nonmedical reasons in 2012.3
Where do these drugs come from? While about 17.3% of those who misuse prescription painkillers do so with their own medications prescribed to them, more than three-fourths of prescription painkillers involved in overdoses come from prescriptions diverted to persons without them.3 Diversion is a term used by the Drug Enforcement Administration to describe prescription medications that are used for other than their original purposes. The majority of misused prescription painkillers (55%) are obtained for free from friends or relatives. Fewer persons actually buy (11.4%) or steal (4.8%) prescription painkillers from friends or relatives or get them from drug dealers or strangers (4.4%).
The CDC has identified groups susceptible to death from unintentional overdose of prescription painkillers:4
• Men are twice as likely to die of prescription painkiller overdoses as women.
• Middle-aged adults have the highest overdose rates.
• Persons living in rural counties are nearly twice as likely to overdose as those living in urban areas.
• Whites, Native Americans and Alaska natives are more likely to overdose.
• About 1 in 10 Native American or Alaska natives 12 or older used prescription painkillers for nonmedical reasons in the past year, compared to 1 in 20 whites and 1 in 30 African-Americans.
Clinical Presentation
The diagnosis of opioid intoxication and overdose can be reached based on a history and physical examination. It is a clinical diagnosis, and toxicology screens are not always necessary. EMS providers should concentrate on obtaining clear histories and identifying specific components of opioid toxidromes.
A toxidrome is a group of signs and symptoms characteristic of an exposure to a specific substance or class of substances. The classic toxidrome associated opioid toxicity is CNS depression, respiratory depression and miosis (constricted pupils). Additional signs and symptoms include GI symptoms like nausea and vomiting, decreased motility, ileus, cardiac symptoms including bradycardia and hypotension, and respiratory symptoms including acute lung injury and pulmonary edema, plus respiratory arrest.
The respiratory depression associated with opioid intoxication is characterized by breathing that is both slow (bradypnea) and shallow (hypopnea). Opioids decrease respiratory drive by suppressing the sensitivity of the respiratory centers in the medulla oblongata. This depression occurs in a dose-dependent manner, with more severe depression occurring with higher doses of opioids. Inadequate ventilation can lead to development of hypoxia (and cyanosis) and hypercarbia, and profound hypoxia can lead to seizures. Acute lung injury and pulmonary edema can occur with therapeutic opioid use but are more common after overdose.5 The exact mechanisms are unclear, but theories include capillary leakage secondary to hypoxia6 or excessive negative pressure created when a comatose patient with an obstructed airway from a closed or collapsed glottis attempts to breathe.7
While miosis is considered a classic finding associated with opioid overdose, there are factors that can prevent it from occurring. Not all opioids will produce miosis, and it is not typically seen with meperidine (Demerol), pentazocine (Talwin) or propoxyphene (Darvon, Darvocet) overdose. In addition, the coingestion of another drug can alter the clinical presentation of the patient with an opioid overdose. About half of prescription painkiller deaths involve at least one other drug (benzodiazepines, cocaine, heroin), and alcohol is a component in many overdose deaths.8 Mydriasis (dilated pupils) can occur secondary to coingestants or signal cerebral hypoxia secondary to respiratory depression.9 If miosis is absent but other symptoms of the opioid toxidrome are present along with physical evidence on scene, it is safe to treat with opioid overdose as your working diagnosis.
The hypotension associated with opioid ingestion and overdose is typically orthostatic in nature and presents secondary to histamine release. Nausea and vomiting can occur secondary to delayed gastric emptying, indirect stimulation of the vomit center in the medulla, and vestibular stimulation. Decreased gastrointestinal motility is a common finding with both therapeutic use and overdose of opioids. Ileus, a severe decrease in motility leading to bowel obstruction, can occur in severe cases. For reasons that are unclear, hypoglycemia often occurs with opiate overdose. It is thought that coingestants such as alcohol may play a role.6
Obtain an accurate and thorough patient history from bystanders, family members, friends or the patient, if they are alert, oriented and reliable. Pertinent aspects of the history include:
• Does the patient have a history of opioid abuse, either via prescription medications or illicit drugs? Is there a history of substance abuse? Is there a history of suicide attempt?
• Does the patient have access to opioid painkillers? Does the patient have chronic pain/recent surgery/cancer that could predispose them to accidental overdose? Are they prescribed painkiller medication, or does anyone in the home have a prescription? Does a friend or family member outside the home have a prescription?
• Are prescription medication bottles present on scene? What are the medications? Do the bottles actually contain the medications listed on them? To whom are they prescribed? Are there pills missing?
• Does the patient have any pills on their person or in personal items such as their purse or backpack? Has an attempt been made to identify unknown pills or tablets? (Remember to bring all pill bottles to the ED.)
• What was the time of ingestion? How much was ingested? Were other medications or alcohol also ingested?
• Has the patient vomited? Were there pills in the vomit?
Treatment
Respiratory depression is the primary morbidity and cause of almost all the mortality associated with opioid toxicity and overdose.9 Therefore, opening the airway, keeping the airway open, correcting inadequate ventilation and reversing hypoxia is the most important treatment for the patient with opiate toxicity or overdose. Open the airway with a manual maneuver such as the head-tilt chin-lift. A modified jaw thrust or other manual maneuver that maintains inline cervical spine stabilization can be used for patients who require that; however, except in cases where overdose is complicated by major trauma, spine stabilization is rarely indicated. Inspect the airway for vomit and secretions and suction as needed. Snoring is indicative of the tongue acting as an airway obstruction and can be anticipated in the comatose patient who is lying supine. In such a case, an oropharyngeal or nasopharyngeal airway opens the airway adequately.
Patients with inadequate breathing require ventilations with a bag-valve mask and 100% oxygen. The goal is to correct the bradypnea and hypopnea associated with opioid toxicity. A ventilation rate of 10–12 per minute with enough tidal volume to result in normal chest rise and fall should be adequate. Use a pulse oximeter to monitor the SpO2, which will reflect the effectiveness of ventilation and correction of the hypoxia. If available, monitoring end-tidal carbon dioxide can help gauge the effectiveness of ventilation and correction of hypercarbia. For patients with acute lung injury and pulmonary edema, continuous positive airway pressure is an effective adjunct that improves lung ventilation, pushes pulmonary edema back into the bloodstream and helps keep alveoli inflated in diseased states.
If airway control and ventilation are successful with BLS measures, endotracheal intubation can be withheld until after administration of naloxone, as the patient’s altered level of consciousness and respiratory depression can be expected to resolve. Reserve endotracheal intubation for those with uncontrollable airways or who remain in prolonged comatose conditions.
Naloxone is the antidote of choice for opiate intoxication and overdose. It is a pure opioid antagonist that competes for and blocks opiate receptors, reversing the effects of circulating opioids in the blood. Because naloxone has a greater affinity for opioid receptors than the opioid drugs themselves, it is effective in reversing the effects opioids have on the body. Naloxone can be administered via the oral, intravenous, intramuscular, subcutaneous, endotracheal and intranasal routes. While the IV administration of naloxone has been the domain of paramedics for many years, the ease and efficacy of IN administration has been explored with favorable results, and it arguably is a safe and effective treatment that can be utilized in the EMS environment.10,11 In fact, IN naloxone is so easy to administer that nonmedical persons have been trained in its use in community-based opioid overdose prevention programs, with positive outcomes. In the February 17, 2012 issue of Morbidity and Mortality Weekly Report, the CDC reported that more than 53,000 laypersons from at least 15 states had been trained in administration of IN naloxone and reported the successful reversal of over 10,000 episodes of opioid overdose.12
The dose of naloxone is 0.4–2.0 mg for adults and children. Higher doses may be required for synthetic opioids such as fentanyl. Naloxone administration can result in acute withdrawal symptoms in patients who are physically dependent on their drug. Patients with suspected opioid dependency can receive a titrated dose of naloxone starting at 0.4 mg and administered in 0.4-mg increments until respiratory depression is corrected.
Naloxone can also be a valuable diagnostic tool, as in the case of a patient with an altered level of consciousness of unknown etiology. In many prehospital protocols, such a patient would receive a dose of naloxone. If the patient responds, it can be concluded that opioids at least contributed to the patient’s decreased level of consciousness.
Consider administration of activated charcoal in patients who are conscious, alert and oriented, can protect their airway, and have an oral opioid ingestion that occurred within the hour.6,9 Activated charcoal has fallen out of favor for oral overdoses in general, but it has a proven benefit in patients when given soon after drug ingestion. Given orally, the common dose in children and adults is 1.0 g/kg, or adults may receive a limited dose of 50–100 g.6 As the risk of vomiting is high in patients with opioid toxicity, consider carefully the risk of decreasing metal status and level of consciousness, loss of the ability to protect the airway, and the possibility of vomiting or regurgitation and subsequent aspiration.
Paramedics who routinely place oral and nasal gastric tubes can improve patient outcomes by placing a gastric tube and administering activated charcoal via the NG/OG tube when patients cannot be trusted to swallow. Involving medical control in a decision this important—and with a procedure that has such significant side effects—is always a good idea.
Scenario Conclusion
The paramedic, Linda, arrives on scene and takes a report from Bob and Jerry. She immediately asks Mrs. Smith, “Are there any pain medications in the house—maybe an old prescription for him or one for you?”
“No,” Mrs. Smith replies, “but my son takes pain medications. He’s had many back surgeries and is out of work on disability. Should I call him?”
“Please do,” Linda replies. She then administers 2.0 mgs of naloxone IN and prepares to place Mr. Smith on the cardiac monitor while Jerry sets up her equipment for an IV attempt.
“He’s waking up, and his breathing is picking up,” Bob says, pulling the BVM off Mr. Smith’s face but continuing to give oxygen via blow-by.
“Well, that answers that question!” Linda says with a smile.
“If this is an opioid overdose, why are his pupils not pinpoint?” Bob asks.
“I know some opioid overdoses won’t result in pinpoint pupils, but I’m not sure which ones,” Linda replies.
“My son is coming right over,” Mrs. Smith says as she comes back from the kitchen. “He says he gave my husband some of his Demerol because he was in so much pain.”
Linda initiates IV access with an 18-gauge catheter in Mr. Smith’s left arm. Mr. Smith is now conscious and alert to pain. His son arrives, visibly upset, and tells the EMS crew and his mother how he gave his father five 100-mg tablets of Demerol to use for his back pain. “I told him to be careful with it and not take more than one every six hours,” the son laments. “I didn’t mean for this to happen!”
Mr. Smith’s level of consciousness and mental status eventually improve to where he can describe taking all 500 mgs of the Demerol “because my back really hurt and I wanted some relief.” He is transferred to the ambulance and transported to the ED without incident, though he requires an additional 1.2 mgs of IV naloxone en route.
References
1. Centers for Disease Control and Prevention. Web-based Injury Statistics Query and Reporting System (WISQARS), www.cdc.gov/injury/wisqars/index.html.
2. Centers for Disease Control and Prevention. Vital Signs: Prescription Painkiller Overdoses in the U.S., www.cdc.gov/vitalsigns/painkilleroverdoses/.
3. Substance Abuse and Mental Health Services Administration. Results from the 2010 National Survey on Drug Use and Health: Summary of National Findings, https://www.samhsa.gov/data/nsduh/2k10nsduh/2k10results.htm.
4. Op cit., Centers for Disease Control and Prevention, Vital Signs.
5. Soto J, Sacristan JA, Alsar MJ. Pulmonary oedema due to fentanyl? Anaesthesia, 1992 Oct; 47: 913–4.
6. Bardsley CH. Chapter 160: Opioids. In: Marx J, Hockberger R, Walls R, Rosen’s Emergency Medicine, 7th ed. Mosby, 2010.
7. PulmCCM. Managing Opioid Overdose in the ICU (Review, NEJM), https://pulmccm.org/2012/critical-care-review/managing-opioid-overdose-in-the-icu-review-nejm/.
8. Warner M, Chen LH, Makuc DM. Increase in fatal poisonings involving opioid analgesics in the United States, 1999–2006. NCHS Data Brief, 2009 Sept, www.cdc.gov/nchs/data/databriefs/db22.pdf.
9. Doyon S. Chapter 180: Opioids. In: Tintinalli JE, et al., Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed. New York: McGraw-Hill, 2011.
10. Robertson TM, Hendey GW, Stroh G, Shalit M. Intranasal naloxone is a viable alternative to intravenous naloxone for prehospital narcotic overdose. Prehosp Emerg Care, 2009 Oct–Dec; 13(4): 512–5.
11. Barton ED, et al. Efficacy of intranasal naloxone as a needleless alternative for treatment of opioid overdose in the prehospital setting. J Emerg Med, 2005 Oct; 29(3): 265–71.
12. Morbidity and Mortality Weekly Report. Community-based opioid overdose prevention programs providing naloxone—United States, 2010. MMWR, 2012 Feb 17; 61(6): 101–5.
13. Olson KR. Activated charcoal for acute poisoning: one toxicologist’s journey. J Med Toxicol, 2010; 6: 190–8.
Scott R. Snyder, BS, NREMT-P, is a faculty member at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. E-mail scottrsnyder@me.com.
Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California, San Francisco. E-mail sean.kivlehan@gmail.com.
Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is performance improvement coordinator for Vitalink/Airlink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. E-mail kcollopy@colgatealumni.org.
