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Patient Care

Acute Alcohol Poisoning

alcohol poisoning
alcohol poisoning

EMS providers frequently encounter intoxicated patients. But how much do they really know about alcohol, how it works, and how to help those who have overindulged?

An alcohol is an organic compound in which a hydroxyl group (-OH) is bound to a central carbon atom that in turn is bound to three other atoms. As such, alcohols are also referred to as hydroxylated hydrocarbons. Common alcohols encountered in the prehospital environment are ethanol, methanol, ethylene glycol and isopropyl alcohol. While the term toxic alcohol has traditionally been used to refer to methanol, ethylene glycol and isopropyl alcohol, the ingestion of any alcohol, including ethanol, can be toxic in a large enough quantity.1 This month’s continuing education article focuses on acute ethanol intoxication in the nonalcoholic patient. Next month we’ll take an in-depth look at ethanol and the chronic alcoholic.

Epidemiology

Ethanol intoxication is common in patients who seek care in emergency departments, but it’s not always their primary reason. A late-’80s study found that depending on the location of the ED, 15%–40% of presenting patients had detectable levels of ethanol in their blood.2

A common cause of acute ethanol intoxication is binge drinking.3 The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines binge drinking as a pattern of drinking that increases a person’s blood alcohol concentration (BAC) to 0.08 g/dL. In women this usually occurs after about 4 drinks within about 2 hours. In men it occurs after about 5 drinks within about 2 hours. The CDC reports that according to national surveys:4

• One in six U.S. adults binge drinks about four times a month, consuming about eight drinks per binge.

• Although binge drinking is more common among young adults (18–34), binge drinkers 65 and older report binge drinking more often—an average of 5–6 times a month.

• Compared to those with lower incomes, binge drinking is more common among those with household incomes of $75,000 or more.

• More than half of the alcohol consumed by adults in the United States is in the form of binge drinks, as is about 90% consumed by youth under age 21.

• The CDC reports that in addition to acute alcohol poisoning, binge drinking is associated with unintentional injuries (auto crashes, falls, burns, drownings), intentional injuries (domestic violence, sexual assault, firearm injuries), poor control of diabetes, liver disease, hypertension, stroke and cardiovascular disease. In 2011, 9,878 people were killed in alcohol-impaired-driving crashes, accounting for 31% of the total motor vehicle traffic fatalities in the United States.5 All of these sequelae have direct impact on the prehospital emergency environment.

Ethanol is available in our communities in many different forms. The most familiar is probably alcoholic beverages, but ethanol is also found in many common household products. The amount of ethanol contained in an alcoholic beverage is typically measured in terms of alcohol by volume (ABV) and defined in units by the number of milliliters of pure ethanol present in 100 milliliters of solution at 20°C, expressed as a percentage of total volume. There are about 0.5 ounces (15 gm) of ethanol in a standard drink. The NIAAA identifies examples of standard drinks as 12 fluid ounces (355 mL) of beer (about 5% ABV), 5 fluid ounces (148 mL) of wine (about 12% ABV) and 1.5 fluid ounces (44 mL) of “hard” liquor, or 80-proof spirits (about 40% ABV).6 Common household products containing ethanol include over-the-counter medications, mouthwash and perfumes.

Pathophysiology

The ingestion of any of the alcohols can result in clinical inebriation, and the strength of any alcohol’s inebriating effects is directly proportional to its molecular weight. As such, at the same concentration, isopropyl alcohol is more intoxicating than ethanol, which is more intoxicating than methanol. Ethanol and isopropyl alcohol are the most common alcohols ingested, and their acute toxic effects are due to the effects of their parent compounds. Conversely, the toxic effects of methanol and ethylene glycol are a result of the toxic metabolites they produce.

Ethanol (CH3CH2OH), aka ethyl alcohol, is a volatile, flammable, colorless liquid that readily crosses cell membranes. Ethanol is absorbed in the gastrointestinal system, with the majority of absorption taking place in the stomach (70%) and duodenum (25%); a small amount (5%) is absorbed by the more distal intestinal tract.7 With an empty stomach, peak ethanol levels are reached about 30–60 minutes after ingestion. The absorption of ethanol is slowed by the presence of food in the stomach.

Ethanol is a central nervous system (CNS) depressant, and its mechanism of action is not completely understood. One important action of ethanol is its effect on GABA receptors in the brain. GABA receptors are a class of receptors that respond to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. Ethanol increases the effects of GABA, resulting in sedative effects similar to those of benzodiazepines, a class of drugs that bind to the same GABA receptor.

There are multiple pathways for ethanol metabolism, but the primary pathway occurs in the liver via the actions of alcohol dehydrogenase, an enzyme. In addition to the liver, alcohol dehydrogenase is also located in the lining of the stomach (gastric mucosa), and ethanol metabolism occurs there as well. Gastric metabolism of ethanol is decreased in women, which leads to a decreased “first-pass” metabolism that may contribute to the higher blood ethanol levels seen in women compared to men after ingesting an equivalent dose per kilogram of body weight. About 90% of ethanol elimination takes place in the liver, with small amounts also excreted in the urine, sweat and exhaled breath. It is this excreted ethanol in the breath that is detectable in a breath alcohol testing device such as a Breathalyzer. Ethanol intoxication occurs when ethanol enters the bloodstream faster than the liver can metabolize it into nonintoxicating byproducts.

Acute ethanol intoxication can lead to metabolic disturbances such as lactic acidosis, hypophosphatemia, hypokalemia and hypomagnesemia. These electrolyte abnormalities occur when the electrolytes are used during the metabolism of alcohol, and also as a result of the dehydration and malnutrition that can occur with alcohol use. Both acute and chronic alcohol consumption can decrease cardiac function, promote dysrhythmias and exacerbate coronary artery disease. Cardiac function is altered by the direct toxic effects of alcohol on the myocardium and also by the hypertension that can accompany acute ingestion. The loss of electrolytes such as phosphate, potassium and magnesium can result in cardiac dysrhythmia. Acute alcohol ingestion can result in a decreased cardiac output in nonalcoholic patients with preexisting cardiac disease. This may be clinically significant.

Clinical Exam Findings

Most EMS providers are familiar with the signs of ethanol toxicity. The most recognizable clinical sign is inebriation. Patients mildly inebriated may initially appear euphoric and exhibit diminished fine motor coordination and decreased social inhibition, which can deteriorate to impaired judgment and coordination, agitation, combativeness and altered mental status (Figure 1). Clinical signs such as slurred speech, ataxia and nystagmus are common in moderate to severe ethanol intoxication. The warm, flushed skin common to ethanol toxicity is the result of peripheral vasodilation and may also lead to symptoms such as a feeling of warmth described by the patient. This vasodilation, as well as fluid loss secondary to vomiting and urination, can result in hypotension and a compensatory tachycardia. In children, ethanol ingestion can lead to hypoglycemia and hypoglycemic seizures. This is less common in the adult patient.

As intoxication becomes more severe, patients will exhibit an unsteady gait and impaired balance. Progressing central nervous system depression will result in the patient becoming increasingly lethargic, and he may have difficulty sitting upright without assistance. As intoxication increases coma will develop, and respiratory depression can lead to respiratory failure. Figure 1 shows the clinical exam findings associated with ethanol intoxication, though it should be noted there is a poor correlation between BAC and clinical exam findings in patients with alcohol habituation.

For example, respiratory depression and subsequent death may occur in the nonhabituated patient at concentrations of 0.4–0.5 g/dL, but it is not uncommon for a chronic alcoholic to appear minimally intoxicated with a BAC as high as 0.4 g/dL.8 Another factor that may affect a patient’s clinical exam is whether the patient is presenting with an increasing or decreasing BAC. It is a known phenomenon, termed the Mellanby effect, that the clinical manifestations of ethanol intoxication are more prominent when BAC is rising.9

Consider ethanol intoxication as a source of altered mental status or altered level of consciousness only after all other possible causes have been assessed for and ruled out. Medical and traumatic causes such as hypoglycemia, stroke, hypothermia, hypoxia, drug overdose, head trauma and other causes have serious consequences if not identified, managed correctly in the field, and their sufferer transported to an appropriate receiving hospital.

An intoxicated patient and any bystanders on scene should be asked about the use of any additional drugs or medications. Of particular concern is the coingestion of drugs such as opiates, barbiturates, benzodiazpines and other CNS depressants. The combined effect of such drugs and ethanol increases the risk of respiratory depression and respiratory arrest. The use of sympathomimetic drugs should also be elicited. The use of alcohol mixed with energy drinks by adolescents and young adults has been increasing, and combining caffeine with alcohol can contribute to a complex clinical presentation where the caffeine in an energy drink antagonizes some of the effects of alcohol.9 Cocaine may be used in combination with ethanol, and the combined use of these drugs can result in the formation of the metabolite cocaethylene. Although cocaethylene is less toxic than cocaine, its half-life is 3–5 times longer. The risk of sudden death among persons coingesting ethanol and cocaine may be as high as 18 times that among cocaine users alone.8

Treatment

Treatment of the patient with ethanol toxicity is mostly supportive in nature, as there is no antidote currently available in the United States. Ethanol is rapidly absorbed via the gastrointestinal tract, so activated charcoal is not indicated unless there is coingestion of another toxic absorbable substance.

Due to the CNS-depressant properties of ethanol, respiratory depression is possible, and BVM ventilation should be provided if breathing is inadequate. Vomiting or regurgitation and subsequent aspiration is a concern in any patient with CNS depression, requiring frequent if not constant monitoring of the airway. An antiemetic such as ondansetron (Zofran) or prochlorperazine (Compazine) can be administered in intoxicated patients who are nauseous and/or vomiting. For those patients who are semi- or unconscious, keep a suction unit nearby and ready for immediate use should the patient vomit or regurgitate. In addition, a patient can be rolled onto their side and placed in the recovery position in order to clear the airway and keep it cleared. If a patient cannot protect their airway or if breathing is inadequate, perform endotracheal intubation and bag-mask ventilation as necessary.

That being said, every intoxicated patient with an altered level of consciousness and subsequent decreased GCS score does not necessarily require endotracheal intubation. A 2009 study looked at 73 patients who presented to the ED with decreased consciousness as a result of drug or alcohol intoxication. Their GCS scores ranged from 3–14, and 12 patients had scores of 8 or less. No patient with a GCS of 8 or less aspirated or required intubation. There was one patient who required intubation, and this patient had a GCS of 12 on admission to the ward. So, while the well-known adage from trauma may state that “a GCS less than 8 means intubate,” it may not necessarily hold true in drug or alcohol intoxication. Rather, a decreased level of consciousness (and subsequently a decreased GCS) is simply one data point to consider when determining an airway and ventilation management plan for your patient.

Patients with ethanol intoxication can be uncooperative, combative and even violent. Any behavior or actions that infringe on scene safety (on the scene or in the back of your ambulance) and place you, your crew or the patient in danger should not be tolerated. If verbal strategies are insufficient to correct inappropriate and dangerous behavior, the patient should be restrained via physical or chemical means. If you decide to use physical restraints, call for law enforcement backup to assist. IV benzodiazepines such as midazolam (Versed) or lorazepam (Ativan) and IV antipsychotics such as haloperidol (Haldol) are useful for sedation. Whether physical or chemical methods are used to restrain a patient, pay constant attention to their airway, breathing and circulation status. Administration of a benzodiazepine or antipsychotic may worsen the respiratory depression in a severely intoxicated patient.

All patients with altered mental status should have a blood glucose determined and dextrose administered if they are found to be hypoglycemic. In patients with altered and/or decreased mental status, establish IV access and give dextrose via that route. Intoxicated patients who are alert and oriented, have an intact gag reflex and can follow directions may be administered oral glucose. However, the risk of aspiration should be evaluated, and IV dextrose administered if any risk of aspiration or vomiting exists.

While patients with chronic alcoholism may suffer from vitamin and mineral deficiency, this is not usually the case with nonalcoholics suffering an episode of acute intoxication. Therefore, the administration of IV or intramuscular thiamine is not necessary in this population. If a patient presents in a coma secondary to acute alcohol toxicity and their history is unknown, 100 mg of thiamine can be administered IV to prevent or treat Wernicke’s encephalopathy.

IV fluid volume administration with fluids such as normal saline hould be performed only in patients with clinically significant hypotension that may accompany cases of severe intoxication. IV fluid administration is not necessary in cases of mild or severe intoxication, as it will not decrease the severity of intoxication or increase the elimination of ethanol.11

While there is no medication currently approved by the FDA for the treatment of acute ethanol intoxication, there is one that has been studied. Metadoxine has been shown to decrease the half-life and accelerate the elimination of ethanol from the blood, improve the symptoms of ethanol intoxication and decrease its recovery time.9,12–13

References

1. Jammalamadaka D, Raissi S. Ethylene glycol, methanol and isopropyl alcohol intoxication. Am J Med Sci, 2010 Mar; 339(3): 276–81.
2. Cherpitel CJ. Breath analysis and self-reports as measures of alcohol-related emergency room admissions. J Stud Alcohol, 1989 Mar; 50(2): 155–62.
3. Naimi TS, Brewer RD, Mokdad A, Denny C, Serdula MK, Marks JS. Binge drinking among US adults. JAMA, 2003 Jan 1; 289(1): 70–5.
4. Centers for Disease Control and Prevention. Fact Sheets—Binge Drinking, http://www.cdc.gov/alcohol/fact-sheets/binge-drinking.htm.
5. AlcoholAlert! 2007 Drunk Driving Statistics, http://www.alcoholalert.com/drunk-driving-statistics-2007.html.
6. National Institute on Alcohol Abuse and Alcoholism. What’s a “Standard” Drink? http://rethinkingdrinking.niaaa.nih.gov/whatcountsdrink/whatsastandarddrink.asp.
7. Marco CA, Kelen GD. Acute intoxication. Emerg Med Clin North Am, 1990 Nov; 8(4): 731–48.
8. Smith JC, Quan D. Chapter 179: Alcohols. In: Tintinalli JE, et al., Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed. New York: McGraw-Hill, 2011.
9. Cowan E, Su M. Ethanol intoxication in adults. UpToDate, http://www.uptodate.com/contents/ethanol-intoxication-in-adults.
10. Duncan R, Thakore S. Decreased Glasgow Coma Scale score does not mandate endotracheal intubation in the emergency department. J Emerg Med, 2009 Nov; 37(4): 451–5.
11. Li J, Mills T, Erato R. Intravenous saline has no effect on blood ethanol clearance. J Emerg Med, 1999 Jan–Feb; 17(1): 1–5.
12. Díaz Martínez MC, Díaz Martínez A, Villamil Salcedo V, Cruz Fuentes C. Efficacy of metadoxine in the management of acute alcohol intoxication. J Int Med Res, 2002 Jan–Feb; 30(1): 44–51.
13. Shpilenya LS, Muzychenko AP, Gasbarrini G, Addolorato G. Metadoxine in acute alcohol intoxication: a double-blind, randomized, placebo-controlled study. Alcohol Clin Exp Res, 2002 Mar; 26(3): 340–6.

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 AirLink/VitaLink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. E-mail kcollopy@colgatealumni.org.

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