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Isopropyl alcohol poisoning

Isopropyl alcohol poisoning
Literature review current through: Jan 2024.
This topic last updated: May 25, 2023.

INTRODUCTION — Isopropyl alcohol (isopropanol, 2-propanol, propan-2-ol) is commonly used as a disinfectant, hand sanitizer, antifreeze, and solvent, and typically comprises 70 percent of "rubbing alcohol." People ingest isopropyl alcohol either unintentionally or with the intent to become intoxicated (ie, ethanol substitute) or to harm themselves. Isopropyl alcohol functions primarily as a central nervous system (CNS) inebriant and depressant, and its toxicity and treatment resemble those of ethanol.

Fatality from isolated isopropyl alcohol toxicity is rare but can result from subsequent injury while inebriated, from untreated coma with airway compromise, or, rarely, from cardiovascular depression and shock following massive ingestion. Supportive care can avert most morbidity and mortality. It is important to differentiate isopropyl alcohol from methanol and ethylene glycol, which are more dangerous when ingested. Isopropyl alcohol does not cause an elevated anion gap acidosis, retinal toxicity (as does methanol), or renal failure (as does ethylene glycol), although it does increase the osmol gap. (See 'Differential diagnosis' below.)

This topic review will discuss the diagnosis and management of isopropyl alcohol intoxication. A summary table to facilitate emergency management is provided (table 1). Discussions of other toxic alcohols and a general approach to the poisoned patient are found elsewhere.

(See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

(See "Ethanol intoxication in adults".)

(See "General approach to drug poisoning in adults".)

(See "Approach to the child with occult toxic exposure".)

PHARMACOLOGY AND TOXICOLOGY — Isopropyl alcohol is a sedative-hypnotic agent whose toxicity closely resembles that of ethanol, with which it shares strong structural similarity. Like ethanol, isopropyl alcohol's precise mechanism of action in the central nervous system (CNS) remains uncertain. Changes in membrane fluidity and/or function, and interactions with neurotransmitter receptors, are believed to account for the CNS effects of alcohols and other simple hydrocarbons. There is a linear relationship between the molecular weight of alcohols and their sedative effects: as size increases, so does sedation. Thus, isopropyl alcohol is marginally more potent than ethanol at comparable concentrations.

In untreated animals, the median lethal dose lies between 4 and 8 g/kg. Many sources mistakenly estimate the lethal dose to be 250 mL in humans (eg, less than 400 mL of a 70 percent solution) [1]. It is important to recognize that, with supportive treatment alone, adults and children have survived much larger ingestions [2,3].

Isopropyl alcohol is metabolized by the alcohol dehydrogenase family of enzymes to acetone (figure 1). Following ingestion of at least several grams, the elimination of acetone is slower than its formation, and this metabolic end-product accumulates. Acetone itself is a mild CNS depressant and may exacerbate the CNS depression caused by isopropyl alcohol (see 'Clinical features of overdose' below). Acetone is also responsible for the marked ketosis that is present in most isopropyl alcohol ingestions. (See 'Laboratory evaluation' below.)

Isopropyl alcohol does NOT cause an elevated anion gap acidosis, unlike the toxic alcohols methanol and ethylene glycol. Methanol and ethylene glycol are both primary alcohols, which are oxidized (via alcohol dehydrogenase and then aldehyde dehydrogenase) to carboxylic acids (formic acid in the case of methanol and glycolic, glyoxylic, and oxalic acids in the case of ethylene glycol). These acid metabolites cause the severe toxicity (ie, blindness, renal failure, and death) characteristic of methanol and ethylene glycol poisoning. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

Isopropyl alcohol is a secondary alcohol; as such, it is metabolized to a ketone (via alcohol dehydrogenase), rather than an aldehyde. Ketones cannot be oxidized to carboxylic acids. As a result, only very limited acidemia can occur; isopropyl alcohol is considerably less toxic than methanol or ethylene glycol.

KINETICS — Like ethanol, isopropyl alcohol is rapidly and completely absorbed following oral ingestion [4,5]. Peak serum concentration and clinical effects occur approximately one hour after ingestion [1]. Substantial absorption and even toxicity are possible following dermal exposure, especially in infants [6-9].

Isopropyl alcohol is primarily metabolized to acetone via alcohol dehydrogenase, but the affinity of this enzyme family for isopropyl alcohol is approximately an order of magnitude less than for ethanol. Accordingly, small quantities of coingested ethanol effectively block metabolism of isopropyl alcohol and slow its serum elimination. In the absence of alcohol dehydrogenase (ADH) inhibition, the serum elimination half-life is approximately 2.5 to 8 hours [10-13]. Acetone elimination is slower, with a variable half-life of over 10 hours [14,15]. When ADH inhibitors (eg, ethanol or fomepizole) are present, isopropyl alcohol clearance is markedly reduced, with a serum elimination half-life of 28 hours in one case report [16]. Both isopropyl alcohol and acetone are rapidly cleared by hemodialysis, with clearance rates in excess of 200 mL/min [17,18].

CLINICAL FEATURES OF OVERDOSE

Major effect and clinical course — Isopropyl alcohol can cause varying degrees of central nervous system (CNS) depression, ranging from inebriation with disinhibition, to sedation, to stupor and coma. These effects, due primarily to the parent alcohol (isopropyl alcohol), develop shortly after exposure, and peak within the first hour after ingestion [1]. The absence of early symptoms excludes a significant isolated ingestion.

Isopropyl alcohol's primary metabolite, acetone, causes less sedation. As a result, steady improvement in the patient's level of consciousness is the expected clinical course. Of note, cross-tolerance in chronic alcoholics reduces the degree and duration of these effects.

History — It is important to attempt to establish the product ingested, ideally by retrieving the original container and consulting product databases. In addition to ascertaining the timing and quantity of isopropyl alcohol ingested, clinicians should attempt to quantify any ethanol coingestion, to learn whether the ingestion was intentional, and, if intentional, to learn whether it was for recreational use or self-harm.

Individuals with alcohol use disorder and limited access to beverage-grade ethanol may ingest hand sanitizer solution, given its typical composition of around 70 percent alcohol. However, a given sanitizer product may at times contain mostly ethanol, isopropyl alcohol, or even methanol; labels can be misleading given limited regulatory oversight. Patients who have ingested large amounts of concentrated isopropyl alcohol may complain of nausea, vomiting, and abdominal pain. A discussion of how to approach the patient poisoned with unknown agents is found elsewhere. (See "General approach to drug poisoning in adults", section on 'Diagnosis of poisoning' and "Approach to the child with occult toxic exposure" and "Initial management of the critically ill adult with an unknown overdose".)

Physical examination — Isopropyl alcohol poisoning causes an alteration in mental status similar to that seen in ethanol intoxication. Level of responsiveness, presence of disconjugate gaze, and ciliary reflex should be assessed in any patient with an alteration of mental status. A fruity breath odor is often perceptible, suggesting acetone accumulation. Following massive ingestion, signs of shock may be present, as may hematemesis, pulmonary edema, and hemorrhagic tracheobronchitis.

DIFFERENTIAL DIAGNOSIS — It is important to exclude the possibility of methanol or ethylene glycol ingestion in any patient suspected of isopropyl alcohol poisoning. The early clinical course of all the toxic alcohols is quite similar, but important treatment differences exist. The absence of a high anion gap metabolic acidosis four to six hours post-ingestion enables the clinician to distinguish isopropyl alcohol from methanol or ethylene glycol intoxication in most cases. However, the presence of ethanol or the administration of fomepizole delays the appearance of such an acidosis in methanol and ethylene glycol poisoning, obscuring the diagnosis. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

Starvation, alcoholic, and diabetic forms of ketoacidosis can also present with depressed mental status and ketosis. The presence of a metabolic acidosis helps to differentiate these entities from isopropyl alcohol overdose. Ketone bodies other than acetone are produced by these metabolic states; in particular, the presence of beta-hydroxybutyrate demonstrates the ketosis is not due to isopropyl alcohol. (See "Fasting ketosis and alcoholic ketoacidosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis in children: Clinical features and diagnosis".)

Less common causes of ketosis include inborn errors of metabolism such as branched-chain ketonuria and propionic acidemia, salicylism, and ingestion of acetone itself. (See "Metabolic emergencies in suspected inborn errors of metabolism: Presentation, evaluation, and management" and "Organic acidemias: An overview and specific defects" and "Salicylate (aspirin) poisoning: Clinical manifestations and evaluation".)

LABORATORY EVALUATION

Tests to obtain — The following tests should be obtained in all poisoned patients following intentional ingestion for self-harm:

Basic electrolytes with calculation of anion gap

Blood urea nitrogen (BUN) and creatinine

Fingerstick glucose, to rule out hypoglycemia as the cause of any alteration in mental status

Acetaminophen and salicylate levels, to rule out these common coingestions

Electrocardiogram (ECG), to rule out conduction system poisoning by drugs that affect the QRS or QTc intervals

Pregnancy test in women of childbearing age

The following tests and calculations should also be performed in symptomatic patients suspected of ingesting isopropyl alcohol:

Serum isopropyl alcohol and acetone levels (or serum osmolality, if direct serum drug levels are unavailable) (see 'Osmolal gap' below)

Serum and urine ketones

Arterial or venous blood gas

Serum isopropyl alcohol and acetone levels — Serum concentrations of isopropyl alcohol and acetone can be quantified directly using gas chromatography. The main use of such testing is to confirm the diagnosis, as treatment is largely supportive. However, many hospitals do not have rapid access to such testing.

Confirmation of the diagnosis is important when uncertainty exists regarding the cause of a given patient's altered mental status and is essential when another toxic alcohol may be present. Definitive serum levels may also quantify the amount of unmetabolized isopropyl alcohol and provide an estimate of the patient's tolerance. Serum concentrations of at least 100 mg/dL (17 mmol/L) are necessary to cause a decreased level of consciousness, although tolerance will increase this threshold. Isopropyl alcohol may be detected at low concentrations in the serum of patients with severe diabetic or alcoholic ketoacidosis, due to endogenous reduction of acetone to isopropyl alcohol [19-21], and fatalities have been misattributed to isopropyl alcohol exposure [22].

Osmolal gap — The osmolal gap provides important diagnostic information when quantitative serum testing for the toxic alcohols is not readily available (see "Serum osmolal gap"). By comparing the measured plasma osmolality (determined by freezing point depression) with the calculated osmolarity, the clinician can infer the presence of an osmotically active, electrically neutral substance present at serum concentrations above 10 mmol/L (ie, at least 60 mg/dL of isopropyl alcohol and acetone combined). Both isopropyl alcohol and acetone will raise the osmolal gap [10]. The plasma osmolal gap cannot distinguish isopropyl alcohol from methanol or ethylene glycol, and so cannot be used to exclude ingestion of these more toxic alcohols. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

Unlike methanol and ethylene glycol poisoning, neither a metabolic acidosis nor an elevated anion gap are expected after isopropyl alcohol ingestion. These findings should prompt the clinician to investigate alternative diagnoses. (See 'Differential diagnosis' above and "Approach to the adult with metabolic acidosis" and "Approach to the child with metabolic acidosis".)

Serum and urine ketones — Testing for serum and urine ketones using the nitroprusside reaction will be strongly positive in the presence of acetone. These tests are calibrated for ketonemia due to endogenous metabolism, and are thus very sensitive to the high acetonemia that follows a substantial ingestion of isopropyl alcohol. Low concentrations of serum ketones exclude any significant isopropyl alcohol exposure, provided at least two hours have transpired since ingestion, and alcohol dehydrogenase has not been blocked by coingested ethanol or fomepizole [12]. Many laboratories now measure beta-hydroxybutyrate concentrations when "serum ketones" are requested. Acetone (with three carbon atoms, like isopropyl alcohol) is the predominant ketone generated by metabolism of isopropyl alcohol, and serum beta-hydroxybutyrate (with four carbon atoms) concentrations remain low even following large ingestions.

Additional tests — Acetone concentrations of 100 mg/dL or greater can falsely elevate the serum creatinine [23]. Thus, a high serum creatinine with a normal BUN and pH suggests the possibility of acetonemia due to isopropyl alcohol ingestion [24,25].

A clinician caring for a patient with altered mental status attributed to isopropyl alcohol must pursue alternative diagnoses if the patient fails to improve steadily over a few hours of observation. In such circumstances, additional testing, such as computed tomography (CT) of the head or lumbar puncture, may be indicated. (See "Diagnosis of delirium and confusional states".)

MANAGEMENT — Management begins with assessment and stabilization of the airway, breathing, and circulation. Clinicians should consider endotracheal intubation if there is doubt about the patient's ability to protect the airway and avoid aspiration. A summary table to facilitate emergency management is provided (table 1). Advanced cardiac life support measures must be provided as required. (See "Advanced cardiac life support (ACLS) in adults".)

Patients with manifestations of significant intoxication (eg, stupor, hypotension) and those presenting immediately after ingestion should be closely observed and placed on cardiac and pulse oximetry monitors. Intravenous access should be obtained. Intravenous crystalloids are usually sufficient to correct any hypotension due to vasodilatation, but vasopressors may occasionally be required. Hypoglycemia should be corrected. As with ethanol overdose, most symptomatic patients recover within several hours of their ingestion.

Decontamination — There is no role for gastrointestinal (GI) decontamination in most cases of isolated isopropyl alcohol intoxication. Its rapid absorption after oral ingestion and its low toxicity make such interventions unnecessary. Gastric aspiration via a flexible nasogastric tube may be considered if it can be performed within one hour of a massive ingestion, as it may shorten the duration of coma, but this is not a critical intervention. Activated charcoal may be useful for coingestants [26].

Alcohol dehydrogenase (ADH) inhibition — Since acetone (the primary metabolite) is less toxic than isopropyl alcohol (the parent alcohol), there is no indication for ADH inhibition with fomepizole or ethanol following isopropyl alcohol exposure [16,27,28]. Suspected methanol or ethylene glycol exposures should be managed accordingly. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

Massive ingestion — Rare patients with massive intentional ingestions may be hemodynamically unstable despite intravenous fluids and vasopressors. Serum isopropyl alcohol concentrations in such patients are generally over 500 mg/dL (80 mmol/L), and the plasma osmolal gap is generally over 100 mosmol/L [1].

Clinicians caring for such a patient with hemodynamic instability despite aggressive fluid resuscitation should consider hemodialysis, if it is readily available [3,17]. It should be emphasized that hemodialysis is almost never required [1]. In most patients, the risks of hemodialysis outweigh the benefits [2].

Disposition — Symptoms from isopropyl alcohol manifest quickly. Therefore, patients with unintentional ingestions can be discharged after two hours if they remain asymptomatic and isopropyl alcohol is known to be the only substance involved [5]. Patients ingesting isopropyl alcohol recreationally or as an ethanol substitute should be evaluated for alcohol and substance misuse and managed accordingly. Patients who have deliberately ingested isopropyl alcohol for self-harm should undergo assessment for concealed coingestions, suicidality, and psychiatric evaluation as necessary. (See "General approach to drug poisoning in adults" and "Screening for unhealthy use of alcohol and other drugs in primary care".)

PEDIATRIC CONSIDERATIONS — Most exposures in children under the age of six years consist of accidental spills and sips. The irritant effects of high concentrations of isopropyl alcohol deter younger children from ingesting large amounts. Asymptomatic patients can be managed with home observation alone, assuming the product composition is known with certainty and the ingestion is estimated to be a mouthful or less [5]. Clinicians should counsel caretakers about measures to prevent poisoning, with particular emphasis paid to proper storage of hazardous products and to avoiding the transfer of such materials from their original child-resistant containers. (See "Prevention of poisoning in children", section on 'Anticipatory guidance'.)

Intentional recreational ingestions occur in adolescents with limited access to ethanol. Such exposures often happen in group settings, and product identification may be difficult. It is essential to rule out methanol or ethylene glycol ingestion, to locate all exposed patients, and to counsel such patients about substance abuse.

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Toxic alcohol poisoning".)

SUMMARY AND RECOMMENDATIONS

Toxicology and kinetics – The hallmark of isopropyl alcohol metabolism is a marked ketonemia and ketonuria in the absence of metabolic acidosis. Isopropyl alcohol is rapidly and completely absorbed following oral ingestion. (See 'Pharmacology and toxicology' above and 'Kinetics' above.)

Clinical presentation – Isopropyl alcohol is commonly ingested intentionally (either as an ethanol substitute or for self-harm) or in accidental exposures. It is used as a disinfectant, antifreeze, and solvent, and typically comprises 70 percent of "rubbing alcohol." (See 'History' above.)

It is important to establish with accuracy the product ingested. Clinicians must rule out ingestion of more toxic alcohols (methanol and ethylene glycol), which are associated with a high anion gap metabolic acidosis. (See 'Differential diagnosis' above and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

When ingested, isopropyl alcohol functions primarily as a central nervous system (CNS) inebriant and depressant, and its toxicity and treatment resemble that of ethanol. (See 'Clinical features of overdose' above.)

Laboratory studies – In addition to the basic studies obtained in all poisoned patients, the following laboratory tests and calculations should be obtained in the symptomatic patient suspected of ingesting isopropyl alcohol (see 'Laboratory evaluation' above):

Serum isopropyl alcohol and acetone levels

Or serum osmolality (by freezing point depression), with calculation of osmolal gap, if serum isopropyl alcohol level not readily available (see 'Osmolal gap' above)

Basic electrolytes, with calculation of osmolal gap (elevated in the setting of any toxic alcohol ingestion)

Blood urea nitrogen (BUN) and creatinine (high serum creatinine with a normal BUN and pH suggest the possibility of acetonemia due to isopropyl alcohol ingestion)

Serum and urine ketones (low concentrations of serum ketones by nitroprusside test exclude any significant isopropyl alcohol exposure, provided at least two hours have transpired since ingestion and alcohol dehydrogenase has not been blocked by ethanol or fomepizole)

Arterial or venous blood gas (the presence of a metabolic acidosis or an anion gap is not expected with isopropyl alcohol intoxication and should prompt investigation of alternative diagnoses)

General management – A summary table to assist emergency management is provided (table 1). Clinicians can manage an isopropyl alcohol overdose in similar fashion to an ethanol overdose. Clinicians should consider tracheal intubation if there is doubt about the patient's ability to protect their airway and avoid aspiration. Hypotension is treated with intravenous crystalloid, and vasopressors if necessary. Rapid recovery with supportive care alone is the expected course. (See 'Management' above.)

For isolated ingestions of isopropyl alcohol, there is no role for antidotal therapy with either fomepizole or ethanol. Gastrointestinal (GI) decontamination and hemodialysis are rarely necessary.

Massive ingestion – Rare patients with massive intentional ingestions are hemodynamically unstable despite supportive treatment. Serum isopropyl alcohol concentrations in such patients are generally over 500 mg/dL (80 mmol/L), and the osmolal gap generally over 100. Clinicians caring for these patients should obtain immediate nephrology consultation. In a patient with persistent hemodynamic instability despite aggressive treatment with intravenous fluid and pressors, we suggest treatment with hemodialysis (Grade 2C). It should be emphasized that treatment with hemodialysis is almost never required. (See 'Massive ingestion' above.)

Pediatric considerations – Asymptomatic children with accidental ingestions can be managed with home observation alone, assuming the product composition is known with certainty and the ingestion is estimated to be a mouthful or less. (See 'Pediatric considerations' above.)

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