Isopropanol Toxicity


Article Author:
John Ashurst


Article Editor:
Thomas Nappe


Editors In Chief:
Jon Parham
Jon Sivoravong


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
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Patrick Le
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Saad Nazir
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John Shell
Matthew Varacallo
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Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
3/15/2019 10:08:15 AM

Introduction

Isopropanol, or isopropyl alcohol, is a clear, colorless liquid that emits an odor that resembles acetone. It is a commercially available product mainly is found as a 70% solution in rubbing alcohol and hand sanitizers. Unlike the other toxic alcohols, isopropanol rarely causes death and is associated with ketosis without acidosis. Treatment of isopropanol ingestions are typically supportive therapy and ingestions are rarely lethal.[1][2][3]

Etiology

Typically caused by an accidental overdose of isopropyl alcohol.

Epidemiology

Isopropanol ingestion is the second most common alcohol ingestion following ethanol but is the most common toxic alcohol ingestion reported to the United States poison control centers each year. In 2009, more than 20,000 cases were reported to the American Association of Poison Control Centers, with more than 80% of these cases being unintentional. Isopropanol has also classically been used as an ethanol substitute for the user to garner inebriation given its relative availability and low cost.  Although typically used as an ethanol substitute, accidental exposures have been reported when large amounts of rubbing alcohol were used transdermally or children ingested it accidentally.

Toxicokinetics

Much like the other toxic alcohols, the absorption of isopropanol is rapid, with nearly 80% being absorbed within 30 minutes of ingestion. Approximately 80% of the absorbed isopropanol is metabolized by the liver through first-order kinetics and is broken down into acetone by the enzyme alcohol dehydrogenase. Typically, blood levels of isopropanol peak between 30 minutes and 3 hours of ingestion, and isopropanol has a half-life of 3 to 7 hours. When ethanol is co-ingested with isopropanol, the half-life of isopropanol is increased because ethanol has a higher affinity to alcohol dehydrogenase as compared to isopropanol. Acetone, however, has a half-life of 22 hours and is primarily excreted by the kidneys. A potentially lethal dose is 2 to 4 mL/kg, but case reports have noted survival in adults with higher reported levels.[4][5][6][7]

History and Physical

Classically, isopropyl alcohol toxicity is associated with rapid inebriation followed by hemorrhagic gastritis. History and physical exam findings are not specific for the type of toxic alcohol ingested by a patient. However, acetone is a potent central nervous system depressant, causing dizziness, headache, and inebriation. Given that isopropanol is a gastrointestinal irritant, patients also may complain of abdominal pain, nausea, vomiting, and hematemesis.

On physical examination, isopropanol intoxication mimics that ethanol intoxication. Due to having a higher molecular weight than ethanol, isopropanol, it is more intoxicating than ethanol and can produce an altered sensorium, hypotension, hypothermia, and even cardiopulmonary collapse. Hypotension is associated with a severe overdose and is related to a mortality rate of nearly 45%. On pupillary examination, miosis is the most common finding. Patients also may experience a loss of deep tendon and corneal reflexes and may experience an extensor reaction to plantar reflex testing.

Evaluation

Patients suspected of a toxic alcohol ingestion in which the toxic alcohol is unknown should undergo routine blood testing to include a complete blood count, basic metabolic profile, transaminases, pregnancy status, serum or urine ketones, lactate, ethanol, and acetaminophen and salicylate concentrations. An electrocardiogram should be obtained on all toxicological patients. Following an acute, unknown ingestion, toxic alcohol concentrations would be the best tests to perform but have limited availability in most hospitals because gas chromatography measures these concentrations with mass-spectroscopy confirmation.

Unlike the other toxic alcohols, isopropanol ingestion will reveal labs consistent with a ketosis without an apparent metabolic acidosis and a normal serum glucose level. The reason that a metabolic acidosis does not develop in an isopropanol ingestion is that the active metabolite, acetone, is a terminal ketone in the metabolic pathway and is an uncharged molecule, unlike the active metabolites in other toxic alcohol ingestions. However, the physician may note an elevated osmolar gap early in the presentation prior to significant metabolism, and reports have shown that an increase of 1 mg/dL in the serum of isopropanol will cause a 0.17 mOsm/kg rise in serum osmolality.

Pseudo-renal failure is a possible laboratory finding in isopropanol toxicity and is related to the Jaffe reaction, an analytical colorimetric method used to determine creatinine levels in both serum and urine. However, the presence of acetone in the serum can falsely elevate creatinine levels if this method is used without a corresponding elevation in blood urea nitrogen. Previous data has shown a creatinine level increase of 1 mg/dL for every 100 mg/dL of acetone in the serum. With this knowledge, a physician can calculate the serum acetone level in a patient by using this equation:

  • Acetone = (measured serum creatinine – baseline creatinine) X 100

Treatment / Management

Treatment for isopropanol ingestion is mainly supportive with intravenous hydration. Gastric emptying or activated charcoal administration is not recommended due to the known rapid absorption. Unlike the other toxic alcohols, alcohol dehydrogenase inhibitors should not be used because the metabolites are not associated with any acidosis or significant end-organ toxicity. Treatment with fomepizole would prolong the elimination of isopropanol and would result in extended periods of intoxication. When there is a concern for malnutrition secondary to chronic alcoholism, the physician should prescribe thiamine, folate, and a multi-vitamin.[8]

Hemodialysis is generally not indicated for the removal of the toxin but could be considered if a patient has persistent hypotension, lactic acidosis, or a serum concentration of more than 500 mg/dL. Due to the rapid absorption of isopropanol, those patients who do not develop coma within 6 hours of ingestion are unlikely to require extracorporeal removal of the toxin. Overall, the need for dialysis would be exceedingly rare. The patient should be monitored until clinical sobriety is achieved.

Differential Diagnosis

After an ingestion of isopropanol, patients will typically present with altered mental status. Although the differential diagnosis of a patient with an altered mental status is extensive, the mnemonic “AEIOU-TIPS” should be employed to aid the physician in narrowing down the cause of a patient’s altered sensorium:

  • A – Alcohol or acidosis
  • E – Electrolytes or encephalopathy
  • I – Infection
  • O – Overdose or oxygen disorder
  • U – Uremia
  • T – Trauma or toxin
  • I – Insulin
  • P – Psychogenic
  • S – Stroke or shock

Explore secondary causes of ketosis because ingestion of isopropanol will cause ketosis without acidosis. Include diabetic ketoacidosis, alcoholic ketoacidosis, starvation ketosis, and other toxic alcohol ingestions in the differential.

Pearls and Other Issues

  • Isopropanol ingestions are rarely lethal.
  • The hallmark of isopropanol intoxication is ketosis without acidosis.
  • The classic presentation is acute inebriation with hemorrhagic gastritis.
  • Psuedo-renal failure is a common laboratory value noted with isopropanol ingestion.
  • Treatment is typically supportive care, and patients usually recover without consequence.

Enhancing Healthcare Team Outcomes

The management of isopropanol toxicity is best done with a multidisciplinary team that includes a nephrologist, intensivist, emergency department physician, nurse practitioner, hematologist and poison control. The key is to hydrate the patient and promote diuresis. Lactic acidosis usually reverses with hydration. A few patients may require ICU admission for monitoring of neurovitals. The prognosis for most patients is excellent. (Level V)

 


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Isopropanol Toxicity - Questions

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A 35-year-old male presents to the emergency department secondary to an accidental ingestion of isopropanol. On examination, he appears inebriated and complains of abdominal pain. Which of the following is the best treatment for an isopropanol ingestion?



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A 22-year-old male presents after drinking isopropyl alcohol as an ethanol substitute. Which of the following is the active metabolite after an isopropyl alcohol ingestion?



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A 46-year-old female presents to the emergency department severely intoxicated after falling down the stairs. She has no specific toxidrome. During her stay, she reported persistent epigastric discomfort and had three episodes of blood-streaked emesis. She eventually improved and requested to be discharged. Her laboratory evaluation includes a normal bicarbonate value and detectable ketones in her urine. Which of the following toxic alcohols is most consistent with this presentation?



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A 17-year-old male with no past medical history presents to the emergency department severely intoxicated after reportedly ingesting a bottle of isopropyl alcohol. His labs are remarkable for a creatinine of 1.8 mg/dL and a BUN of 10 mg/dL. Ketones are detectable in urine. He vomited twice and urinated in his hospital bed. What is the most appropriate management?



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A 39-year-old male presents to the emergency department very intoxicated and encephalopathic. He was last seen 24 hours earlier and is suspected to have been unconscious with possibly 12 hours of downtime. His neighbor called emergency medical services after finding him unresponsive with blood-streaked emesis and two empty bottles of isopropyl alcohol nearby. His laboratory analysis revealed bicarbonate 14 mmol/l, ethanol 43 mg/dl, glucose 60 mg/dL, creatinine 2.1 mg/dL, BUN 10 mg/dL, creatine kinase 250 IU/L, and urinary ketones 15 mg/dL ketones in his urine. A CT scan revealed a subdural hematoma. He received two liters of D5 normal saline and his acid-base status markedly improved. What might account for his acidosis?



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Isopropanol Toxicity - References

References

Abo T,Yuki T,Xu R,Araki D,Takahashi Y,Sakaguchi H,Itagaki H, Expansion of the applicability domain for highly volatile substances on the Short Time Exposure test method and the predictive performance in assessing eye irritation potential. The Journal of toxicological sciences. 2018;     [PubMed]
Beauchamp GA,Valento M,Kim J, Toxic alcohol ingestion: prompt recognition and management in the emergency department [digest]. Emergency medicine practice. 2016 Sep 22;     [PubMed]
Beauchamp GA,Valento M, Toxic Alcohol Ingestion: Prompt Recognition And Management In The Emergency Department. Emergency medicine practice. 2016 Sep;     [PubMed]
Slaughter RJ,Mason RW,Beasley DM,Vale JA,Schep LJ, Isopropanol poisoning. Clinical toxicology (Philadelphia, Pa.). 2014 Jun;     [PubMed]
Désy O,Carignan D,de Campos-Lima PO, Short-term immunological effects of non-ethanolic short-chain alcohols. Toxicology letters. 2012 Apr 5;     [PubMed]
Cogliano VJ,Grosse Y,Baan RA,Straif K,Secretan MB,El Ghissassi F, Meeting report: summary of IARC monographs on formaldehyde, 2-butoxyethanol, and 1-tert-butoxy-2-propanol. Environmental health perspectives. 2005 Sep;     [PubMed]
Jammalamadaka D,Raissi S, Ethylene glycol, methanol and isopropyl alcohol intoxication. The American journal of the medical sciences. 2010 Mar;     [PubMed]
Kuroda Y,Fueta Y,Kohshi K,Nakao H,Imai H,Katoh T, [Toxicity of dichloropropanols]. Journal of UOEH. 2002 Sep 1;     [PubMed]

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