Prehospital Care of the Intoxicated Individual
It’s 3 a.m. and you’re tired from a long night. You are about to take a brief nap after four hours of back-to-back calls and three hours of paperwork, when another call comes in: “Medic 79, report to 33rd & Main for an intoxicated male.” Intoxication—an irksome, loathsome call for EMS providers. The patients are combative, smelly and can supposedly sleep it off, but what happens if a patient who consumed too much alcohol aspirates and dies? As part of the job, EMS providers must be able to judge, assess and treat the inebriated individual.
Severity of the Problem
Alcohol kills approximately 100,000 Americans each year.1 Most of these deaths are not from drinking alone, but how it contributes to traffic accidents, homicide, suicide, domestic violence and unintentional injury deaths (e.g., drowning, death by fire). This is why it is important for EMS providers to develop an inquisitive nature that will allow critical evaluation of the patient’s condition and injuries.2
A 32-year-old male motor vehicle accident victim, who appears to be sober, presents with minor trauma to the head and a dark contusion to the abdomen. Pathophysiologically, the beers he drank an hour or two ago are being rapidly absorbed in his body. This is because ethanol (ETOH or alcohol) is a small molecule, soluble in water and lipids, which readily crosses biologic membranes and permeates all cells and tissues within the body.1
The gastrointestinal tract becomes eroded by alcohol over time and this ultimately results in the formation of ulcers and other deformities of the stomach and intestinal tract. Vitamins and minerals can no longer be adequately absorbed into the body, resulting in malnutrition of frequently intoxicated individuals.
Blood cells can easily become saturated with an excess of ethanol, permeating the blood vessels, and, in high concentrations, become poisoned by the alcohol, a potentially fatal condition. Cardiac function is thus impaired by this hematological effect of alcohol upon the cardiovascular system.
The brain is also damaged by alcohol, as the central nervous system is overcome by ethanol and sedates the patient. Microscopically, this occurs when the main inhibitory neurotransmitter in the brain, GABA, bonds with ethanol. This leads to an overall decrease in the firing of neurons (nerve cells) within the brain, which explains the sedation, lack of coordination and slurred speech many associate with an inebriated person.3 When GABA neurotransmitters become paralyzed by ethanol, nerve cells begin to shut down, breathing ceases and the patient dies.
Most of the ethanol is broken down by the liver, thus slowing down energy production. Ethanol is also excreted by the kidneys, lungs and skin. Excessive use of ethanol ultimately takes its toll upon these organs, resulting in liver cirrhosis, kidney failure, cancer of the liver and kidney, as well as possible sexual dysfunction.
The breaking down of ethanol presents new problems for EMS providers. As the stranglehold of ethanol begins to break down, a flood of binding sites appear on GABA neurotransmitters, resulting in an increased susceptibility to seizures, more commonly known in the medical community as “rum fits.” It is hypothesized that the neuronal changes that occur during repeated ethanol withdrawals are permanent, predisposing alcoholic patients to more frequent and severe seizures—a process known as kindling.4
- Those predisposed to alcoholic tendencies due to genetics.
- Those involved in high-stress activities and who have a high level of anxiety and/or low self-esteem.
- Those with poor social skills and/or conflicts within relationships.
Note: Do not assume that every high school/college student and/or homeless individual has a predisposition to alcoholic intoxication. Everyone has the potential for being “at risk” for alcoholic intoxication.
Assessing Intoxicated Individuals
An appropriate SAMPLE history and OPQRST medical assessment should reveal many of the following characteristics:
- Smell of alcohol on breath/clothing
- Confused and/or dazed presentation (blackouts)
- Lack of coordination and/or stupor
- Seizures and/or gross tremors (shaking)
- Redness and/or enlarged capillaries in the face
- Pale or jaundiced skin
- Secretive nature and noticeable agitation
- Evidence of frequent and unexplainable accidents
- Evidence of poor nutrition and/or hygiene
- History of alcoholism and/or predisposition to drinking
- Elevated body temperature/pulse/blood pressure.
- Nausea and/or bloating
- Vomiting and/or diarrhea
- Abdominal pain/cramping
- Loss of appetite
- Numbness and tingling throughout the body
Because chronic drinkers may be able to mask and/or dismiss many of these symptoms, you will need a critical eye to assess the patient accordingly. It is good policy to transport all patients who present with even mild intoxication, because the chemical effects of ethanol might have a delayed reaction upon the body. (Let the ED handle combative patients!)
For EMT-Basics, treating the intoxicated patient consists of constant mental status checks, ensuring stable ABCs, monitoring vitals and rapid transport to the nearest medical facility. In most cases, activated charcoal is not indicated for acute blood alcohol poisoning, because alcohol is rapidly absorbed into the bloodstream through the lining of the gastrointestinal tract.5 Always err on the side of caution with the intoxicated patient. It is important to be prepared for violent behavior at any time.
Paramedics should consider intravenous glucose to care for any nutritional deficiencies caused by the ethanol and an approved benzodiazepine (i.e., diazepam) to treat alcohol withdrawal, prevent convulsions from occurring and effectively sedate the patient.6
Note: An intoxicated patient who is experiencing grand mal seizures and/or gross tremors should be transported to a hospital as soon as possible.
Once diagnosis is confirmed by laboratory tests, the ED will follow up prehospital care by checking the effectiveness of previously administered activated charcoal, continue administration of anticonvulsant/sedative medications, and administer thiamine to care for nutritional insufficiency. After the patient is detoxified, psychological therapy and addiction rehabilitation, if recommended, can begin to treat the recovering alcoholic.
The addition of alcohol into a body can result in a condition known as alcoholic ketoacidosis. Pathophysiologically, this occurs when insulin is deficient and glucose is no longer able to get into the cells, so an alternative form of energy is needed. To produce this energy, the body must break down fat, which it does by producing ketones. Ketone acid made from the breakdown eventually overcomes body systems, resulting in dehydration and labored breathing. Key diagnostic signs are sweet, fruity-smelling breath, profuse vomiting and altered mental status. Intravenous fluids (dextrose, sodium bicarbonate and thiamine) are needed to treat a patient in alcoholic ketoacidosis.7
Those taking prescription and/or over-the-counter drugs should be especially careful because:
1. Certain drugs (Tylenol, Advil and aspirin) prolong the effects of alcohol for four to six hours.
2. Prescription drugs like-warfarin (Coumadin) prevent blood clotting, which may cause an uncoordinated drunk who falls to hemorrhage throughout the body. Other medications also affect intoxicated individuals in numerous ways, which is why taking a proper SAMPLE history is so vital for proper treatment and care.
Fetal Alcohol Syndrome
A pregnant woman who has more than five drinks a day puts her child at risk for physical, mental and emotional disabilities. Alcohol has also been found to induce birth prematurely.
Intoxication can be a serious medical emergency. Understanding how to judge, assess and treat the intoxicated patient can keep an EMT doing what he does best—helping others.
1. Andreoli TE, et al. Substance Abuse. Cecil Essentials of Medicine, 4th Ed., p. 942. Philadelphia, PA: W. B. Saunders Co., 1997.
2. Werfel P. When trauma masks a medical emergency.” JEMS 27(3):24, 2002.
3. Olmedo R, Hoffman RS. Withdrawal syndrome. Emerg Med Clin North Am 18(2):274, May 2000.
4. Ibid, p. 275.
5. Position Statements: Single-Dose Activated Charcoal. The American Academy of Clinical Toxicology. 2003. www.clintox.org/Pos_Statements/Charcoal.html. 14 June 2003.
6. Ibid, 278–282.
7. Alson R, Jobe D. Alcoholic Ketoacidosis. EMedicine. 16 May 2003. www.emedicine.com/EMERG/topic21.htm. 14 June 2003.