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Alcohol Toxicity Clinical Presentation

  • Author: Michael D Levine, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Jul 06, 2016
 

History

A history of inebriation with associated slurred speech, ataxia, and impaired judgment is common in the initial stages of intoxication of each of these alcohols. Depending on the dose ingested, this may be followed by progressive levels of CNS depression, coma, and premorbid multiorgan failure. The history that can be obtained varies with the timing of presentation. The onset of the later stages of toxic alcohol intoxication can also be delayed if ethanol is coingested, prolonging the time it takes to develop metabolic acidosis and other symptoms. The following focuses on symptoms that may be unique to each alcohol.

Ethanol ingestion

The history itself can often point to a diagnosis of ethanol intoxication. An associated history of chronic alcoholism alters metabolism, associated comorbidities, and the expected course of recovery. A detailed discussion of this topic is beyond the scope of this article (see Ethanol Toxicity).

Attempting to elicit what has changed recently may reveal the immediate reason for presentation. A history of coingestants may also alter the patient's course.

Isopropanol ingestion

Following an isopropanol ingestion, the patient may not complain of anything specific. Rather, the patient may simply appear intoxicated, as with ethanol intoxication.

A history of abdominal pain, nausea, and sometimes hematemesis may be obtained.

Methanol ingestion

Following methanol ingestion, a patient is initially inebriated as with the other alcohols. Other symptoms can be delayed for up to 12-24 hours.

The patient may complain of headache, nausea, or anorexia. Occasionally, the patient may complain of shortness of breath related to hyperventilation.

Because one of the primary end-organs involved in methanol is the eye, the patient may complain of difficulty seeing. Specifically, vision is often described as a "snow field," though a variety of visual complaints may be verbalized.

Ethylene glycol ingestion

Ethylene glycol toxicity occurs in three stages, as follows:

  • The first stage, called the neurologic phase, can occur in less than 1 hour after ingestion and lasts up to 12 hours. During this stage, the patient appears inebriated. The patient may not have any other significant findings during this stage. Occasionally, hypocalcemia can occur at this point and induce muscle spasms and abnormal reflexes.
  • The second stage, which occurs between 12 and 24 hours after ingestion, is referred to as the cardiopulmonary stage. During this stage, the patient frequently develops mild tachycardia and hypertension. Acute respiratory distress syndrome (ARDS) can also occur. These findings are believed to result from calcium oxalate crystal deposition in the lung parenchyma and myocardium. Significant hypocalcemia can occur at this stage, with QT prolongation and associated arrhythmias. Expect hyperventilation as metabolic acidosis progresses.
  • The third stage, also called the renal stage, typically starts after 24 hours. During this stage, flank pain and acute renal failure can occur. A premorbid patient with ethylene glycol toxicity typically presents comatose, hyperventilating, and in multiorgan failure.
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Physical

Ethanol ingestion

The symptoms of ethanol intoxication depend on both the serum concentration as well as the frequency at which an individual ingests ethanol. Thus, a person who consumes large amounts of ethanol on a daily basis may appear sober at the same serum ethanol level at which a novice drinker exhibits cerebellar dysfunction.

As a general rule, levels less than 25 mg/dL are associated with a sense of warmth and well-being. Euphoria and decreased judgment occur at levels between 25-50 mg/dL. Incoordination, decreased reaction time/reflexes, and ataxia occur at levels of 50-100 mg/dL. Cerebellar dysfunction (ie, ataxia, slurred speech, nystagmus) are common at levels of 100-250 mg/dL. Coma can occur at levels of greater than 250 mg/dL, whereas respiratory depression, loss of protective reflexes, and death occur at levels greater than 400 mg/dL.

Isopropanol ingestion

As previously stated, the patient who consumes isopropanol may appear inebriated, as with ethanol. Isopropanol concentrations of 50-100 mg/dL typically result in intoxication, which can progress to include symptoms such as dysarthria and ataxia, while lethargy or coma can be seen with levels exceeding 150 mg/dL. Cardiovascular depression can occur with levels exceeding 450 mg/dL.

The presence of acetone may induce a fruity odor on the patient's breath.

Methanol ingestion

Unlike ethanol or isopropanol, methanol does not cause nearly as much of an inebriated state. If a patient has coingested ethanol, signs or symptoms specific to methanol intoxication are delayed.

The patient may be hyperventilating.

If vision is impaired, ocular examination may reveal dilated pupils that are minimally or unreactive to light with hyperemia of the optic disc. Over several days, the red disc becomes pale, and the patient may become blind. Typically, subjective complaints precede physical findings in the eye.

Ethylene glycol ingestion

The physical findings depend on the stage of the presentation. Thus, the patient may present simply inebriated or progressively more acidotic as renal failure, cardiovascular dysfunction, and coma develop.

Examination findings correlate with the symptoms, as previously described.

In patients who survive severe intoxication, calcium oxalate crystal deposition may occur in the brain parenchyma and can induce cranial neuropathies. These findings typically occur as the patient is recovering from the initial intoxication. Cranial nerves II, V, VII, VIII, IX, X, and XII are most commonly involved.

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Contributor Information and Disclosures
Author

Michael D Levine, MD Assistant Professor, Department of Emergency Medicine, Section of Medical Toxicology, Keck School of Medicine of the University of Southern California

Michael D Levine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Phi Beta Kappa, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Coauthor(s)

Tobias D Barker, MD Attending Physician, Department of Emergency Medicine; Director, Harvard Medical School Dubai Center Simulation Center

Tobias D Barker, MD is a member of the following medical societies: American College of Emergency Physicians, Phi Beta Kappa, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Jeffrey Glenn Bowman, MD, MS Consulting Staff, Highfield MRI

Disclosure: Nothing to disclose.

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