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65. Volatile Alcohol Ingestion: A Good Ole Boy Drinking Ethylene Gly, Singin This’ll Be How I Get AKI
Keywords
Medical emergenciesToxicologyToxic alcoholEthylene glycolMethanolIsopropyl alcoholCase
Pertinent History
The patient is a 45-year-old male with a history of alcohol abuse and depression who was brought in by Emergency Medical Services (EMS) after an intentional ingestion of an unknown substance.
Per EMS, the patient appeared significantly intoxicated at the scene. The patient had been consuming what they assumed was alcohol throughout the day per family and was mumbling that his drink tasted “so bitter.” He was combative for EMS causing him to be sedated and ultimately intubated en route to the hospital. Of note, the paramedics reported difficulty with the intubation secondary to a large amount of emesis.
Pertinent Physical Exam
Except as noted below, the findings of the complete physical exam are within normal limits.
Constitutional: He appears well-developed and well-nourished. Intubated with vomitus around the mouth.
HENT: Normocephalic and atraumatic.
Eyes: Conjunctivae are normal. Pupils are equal, round, and reactive to light. No scleral icterus.
Cardiovascular: Tachycardia, regular.
Pulmonary/chest: Intubated, clear bilaterally.
Abdomen: Soft. Bowel sounds are normal. He exhibits no distension.
Neuro: Intubated and paralyzed.
Pertinent Test Results
Test | Result | Units | Normal range |
|---|---|---|---|
WBC | 26 ↑ | K/μL | 3.8–11.0 103/mm3 |
Hgb | 15.1 ↑ | g/dL | Male: 14–18 g/dL Female: 11–16 g/dL |
Platelets | 379 | K/μL | 140–450 K/μL |
Sodium | 142 | mEq/L | 135–148 mEq/L |
Potassium | 5.6 ↑ | mEq/L | 3.5–5.5 mEq/L |
Chloride | 109 | mEq/L | 96–112 mEq/L |
Bicarbonate | 9 ↓ | mEq/L | 21–34 mEq/L |
BUN | 15 | mg/dL | 6–23 mg/dL |
Creatinine | 1.54 ↑ | mg/dL | 0.6–1.5 mg/dL |
Glucose | 208 ↑ | mg/dL | 65–99 mg/dL |
pH (venous) | 6.92 ↓ | – | 7.320–7.420 |
Lactate | 3.8 ↑ | mmol/L | <2.0 mmol/L |
Alcohol | 0 | mg/dL | <10 mg/dL |
Measured osmoles | 348 ↑ | mOsm/kg | 285–295 mOsm/kg |
UA – Other | Muddy brown casts, Ca-oxalate crystals | – | – |
Chest X-ray: Dense opacity at the left base may represent atelectasis and/or airspace disease. Small adjacent left pleural effusion noted.
ED Course and Medical Decision-Making
Based on the history of ingestion and the patient’s family’s concern for self-harm, the above lab-work, as well as a volatile alcohol panel, was sent on the patient. While awaiting results of the alcohol panel, the clinicians calculated an increased osmolar and anion gaps (see below), leading them to conclude that the patient was currently poisoned with a toxic alcohol. He was therefore started on fomepizole and bicarb. However, the patient continued to display a refractory acidosis, and nephrology was consulted for immediate dialysis. This was initiated in the ED and the patient was admitted to the ICU for further care.
Learning Points
Priming Questions
- 1.
When would you suspect toxic alcohol ingestion in someone with altered mental status if there is no clear history of ingestion?
- 2.
What are the various treatment options for toxic alcohol ingestion and what are their indications?
- 3.
How does ethylene glycol compare to methanol and isopropyl alcohol regarding presentation and management?
Introduction/Background
- 1.
The term toxic alcohol is a bit ambiguous and could technically refer to any alcohol, as even ethanol causes inebriation and has end-organ effects. For our purposes, we will be discussing the most commonly ingested, nonrecreational alcohols: ethylene glycol, methanol, and isopropyl alcohol [1].
- 2.
Ethylene glycol is found in antifreeze and engine coolant. It naturally has a very sweet odor and flavor which historically has thought to account at least in part for its accidental ingestion. Ethylene glycol’s metabolite, oxalic acid, bind with calcium to form calcium oxalate monohydrate crystals in the renal tubules, causing acute tubular necrosis and renal failure [1].
- 3.
Methanol (or wood alcohol) is found in cologne and windshield washer fluid. In addition to ingestion, methanol poisonings can also occur via inhalation and transdermal exposure [1, 2]. Methanol’s metabolite, formate, is a mitochrondrial toxin that for unclear reasons only has significant effects on retinal cells and cells of the basal ganglia [1].
- 4.
Isopropyl Alcohol is the most frequently ingested toxic alcohol, likely due to it being easily obtained, inexpensive, and confused with ethanol due to having the word “alcohol” in its name. It is found in rubbing alcohol and hand sanitizer. While ingestion causes intoxication, there is little in the way of significant end-organ damage [1].
- 5.
A high clinical suspicion is needed to identify a toxic alcohol exposure when the patient is unable to give a clear history as in the case above. An intoxicated patient without clear history of ethanol use or smell of ethanol should raise suspicion. Other “red flag” initial findings include vision changes (methanol), gastric irritation, acetone smell (isopropyl), calcium oxalate crystals in urine, and fluorescent urine (ethylene glycol) [1].
- 6.
All alcohols contribute to the oncotic pressure of a solution; therefore, all alcohols will cause an osmolar gap. Only methanol and ethylene glycol have metabolites which act as acids and cause an anion gap acidosis. Isopropyl alcohol is metabolized to acetone and therefore causes the classically described ketosis without acidosis [1].
- 7.
In treating ethylene glycol and methanol poisonings, the mainstay of treatment involves halting the production of toxic metabolites and/or facilitating the excretion of toxic metabolites. Treatment of ethanol and isopropyl alcohol ingestions on the other hand is largely composed of supportive care.
Physiology/Pathophysiology
- 1.
When thinking about alcohol metabolism, there are two main enzymes to keep in mind: alcohol dehydrogenase and aldehyde dehydrogenase. The alcohol component itself causes intoxication; however, it is toxic metabolites which cause the most significant pathology in toxic alcohol ingestions.
Under “normal” drinking circumstances, alcohol dehydrogenase converts ethanol to acetaldehyde. Acetaldehyde is then converted to acetate by aldehyde dehydrogenase. Acetate is a rather benign compound which is then further broken down and eventually repurposed and/or excreted.
Drunk as a Skunk and Red as a Beet! [4]
Some people of East Asian descent have a variant of the alcohol dehydrogenase enzyme which is significantly more efficient at converting alcohol to acetaldehyde leading to increased acetaldehyde concentrations. Also, aldehyde dehydrogenase has two isoenzymes. Caucasians have both isoenzymes. Up to 50% of East Asians lack one form of aldehyde dehydrogenase. This increased efficiency of alcohol dehydrogenase and decreased efficiency of aldehyde dehydrogenase results in increased acetaldehyde concentrations. Elevated acetaldehyde levels cause many downstream effects, but the most evident is histamine release. This leads to a condition called “Asian Flush” which is erythema of the face neck and shoulders and occasionally the whole body. Most interestingly, elevated acetaldehyde levels are linked to higher risk of esophageal cancer, and thought to be the main cause of increased rates of esophageal cancer seen in Japan.
Following the same sequence methanol is metabolized to formaldehyde and then formic acid [3].
Formic acid is then converted to formate, a mitochrondrial toxin that is believed to cause most of the end-organ damage in methanol toxicity. For unclear reasons, its significant effects appear to be localized to retinal cells and cells of the basal ganglia. These effects tend to be permanent [1].
Acute kidney injury (AKI) and pancreatitis have also been described in methanol toxicity, though this too is not fully understood [1].
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