Isopropyl alcohol poisoning - part 1

Isopropanol (isodiol) is commonly used as a disinfectant, antifreeze and solvent. Isopropyl alcohol poisoning is often caused by ethanol substitutes or self-injury. The ingestion of isopropyl alcohol mainly presents with CNS inhibition, and its toxicity and treatment are similar to that of ethanol. Isopropanol toxicity alone is rarely fatal, but can have a serious effect by exacerbating shock with cardiovascular inhibition after ingestion, and supportive treatment can prevent the vast majority of patient deaths. It is important to distinguish isopropyl alcohol poisoning from methanol and ethylene glycol. Isopropyl alcohol does not cause elevated anionic gap acidosis, retinal toxicity (methanol), or renal failure (ethylene glycol).

Isopropanol pharmacology and animal toxicology

Isopropyl alcohol is a sedative hypnotic whose toxicity is very similar to that of ethanol. The exact mechanism of action of isopropanol in the CNS is still uncertain. Currently, changes in membrane fluidity or function and interactions with neurotransmitter receptors are considered. There is a linear relationship between the molecular weight of alcohol and its sedative effect: the sedative effect increases with increasing size. The median lethal dose in animals is between 4 and 8g/kg. Many literature incorrectly estimated the lethal dose for humans to be 250 mL (< 400 mL 70% solution).
Isopropanol is metabolized to acetone by the alcohol dehydrogenase family of enzymes. Acetone begins to be produced after a few grams of ingestion and is eliminated more slowly than formed, leading to the accumulation of acetone. Acetone is a mild CNS inhibitor by itself, but may exacerbate CNS inhibition induced by isopropyl alcohol. That's why isopropyl alcohol produces ketosis.
Isopropanol is metabolized into ketones (alcohol dehydrogenases) rather than aldehydes. Ketones cannot be oxidized to carboxylic acids. As a result, isopropyl alcohol is rarely acidosis and is significantly less toxic than methanol or glycol

Isopropanol dynamics

Like ethanol, isopropyl alcohol is absorbed quickly and completely after oral administration. Peak serum concentration and clinical effect appear about 1 -- 2 hours after ingestion. After dermal exposure, especially in infants, there may be substantial absorption.

Isopropanol is metabolized to acetone primarily by alcohol dehydrogenases, but the affinity of this enzyme family for isopropanol is about an order of magnitude lower than that for ethanol. Therefore, a small amount of ethanol effectively blocks isopropyl alcohol metabolism and slows its clearance. In the absence of alcohol dehydrogenase (ADH) inhibition, the serum elimination half-life is about 2.5-8h. Acetone elimination rate is slow, variable half-life is more than 10h. In the presence of ADH inhibitors such as ethanol or mepyrazole, isopropanol clearance was significantly reduced, with a serum elimination half-life of 28h in one case. Isopropanol and acetone were quickly removed by hemodialysis with a clearance rate of more than 200 mL/min.

Isopropanol clinical picture

Isopropyl alcohol shows varying degrees of CNS inhibition, ranging from drunkenness, sedation, lethargy, and coma. This occurred mainly in isopropyl alcohol shortly after exposure and peaked within the first hour after ingestion. A steady increase in the level of consciousness is expected in the clinical course. Notably, cross-tolerance in chronic alcohol reduces the magnitude and duration of these effects.
Specific intake is important in taking the history. In addition to determining when and how much isopropyl alcohol should be ingested, clinicians should try to quantify any ethanol mixture and try to understand whether it is recreational or self-harming. Patients who ingest large amounts of concentrated isopropyl alcohol may complain of nausea, vomiting and abdominal pain.

Physical check

You can see altered mental state, similar to alcoholism. Any patient with altered mental state should be assessed for response. Alcohol breath is usually perceptible, and fruity breath often indicates acetone accumulation. After large intake, shock may occur, such as vomiting blood, pulmonary edema and hemorrhagic tracheal bronchitis.

The differential diagnosis

In patients with suspected isopropyl alcohol poisoning, it is important to rule out the possibility of methanol or glycol ingestion. The early clinical course of all toxic alcohols is very similar, but there are therapeutic differences. The lack of high anionic gap metabolic acidosis 4-6 hours after ingestion enables clinicians to distinguish isopropyl alcohol from methanol or glycol poisoning in most cases. However, the presence of ethanol or the use of mesylate can delay the onset of methanol and glycol acidosis, making the diagnosis unclear.

Ketoacidosis in the form of starvation, alcohol, and diabetes may also be accompanied by psychotic states and ketosis. The presence of metabolic acidosis helps to separate these entities from the isopropyl alcohol overdose. The presence of ketone bodies other than acetone produced through these metabolic states, especially the β -hydroxybutyrate, proves that ketosis is not caused by isopropyl alcohol. Less common causes of ketosis include congenital metabolic defects such as branched-chain ketouria and propionic acidemia, salicylic acid peroxidation, and acetone ingestion itself.