Toxic alcohol poisoning in Child
Methanol: Sources include windshield washer fluid, moonshine, cooking fuel, coolant, antifreeze, perfume, and other industrial products. Methanol is absorbed from the gastrointestinal tract within minutes. Lethal doses can begin in amounts as small as 1 g/kg. Methanol only becomes toxic as it is metabolized by the body into formate. Thus, there is a period of approximately 6-24 hours, directly after ingestion, in which patients are asymptomatic. Shortly after ingestion, an osmolar gap can be detected, but only once the methanol has started metabolizing can the anion gap metabolic acidosis be detected.
Symptoms may begin with central nervous system (CNS) depression, nausea, vomiting, and abdominal pain. They may progress to hyperventilation, pulmonary dysfunction, organ failure, coma, or death. Parkinsonism rarely occurs. Visual effects may include retinal edema, mydriasis, central scotomata, blurred vision, photophobia, optic neuritis, afferent pupillary defect, optic disc hyperemia, and blindness, which may be permanent. These visual effects are primarily seen with methanol among the different toxic alcohols and, if identified, support methanol as the etiology of toxic alcohol poisoning.
When absorbed through the skin, methanol can be toxic. In June 2020, the US Food and Drug Administration (FDA) identified methanol contamination in some commercially available hand sanitizers (see list at FDA website), which have been voluntarily recalled in the United States. Ingestion of contaminated hand sanitizer has resulted in blindness, hospitalizations, and death.
Ethylene glycol: Sources of exposure include antifreeze, coolant, and industrial solvents. It is sweet tasting and occasionally used as a highly dangerous substitute for ethanol. Dermal absorption is less likely than it is for the other toxic alcohols. Ethylene glycol is rapidly absorbed once ingested. Lethal doses may be in amounts as small as 1 g/kg. Like methanol, ethylene glycol only becomes toxic once it is metabolized by the body into glycolate, glyoxylate, and oxalate. Shortly after ingestion, an osmolar gap can be detected, but only once the ethylene glycol has begun metabolizing can the anion gap metabolic acidosis be detected.
A patient presenting soon after ingestion may appear inebriated with possible CNS depression. As metabolization of the ethylene glycol occurs over the next 4-12 hours, patients develop malaise, worsening CNS depression, hypertension, tachycardia, and fast, deep breathing. Between 12 and 24 hours after ingestion, acute kidney injury caused by oxalate accumulation can present with increased creatinine, flank pain, hematuria, and oliguria. The presence of flank pain, hematuria, and oliguria suggest ethylene glycol as the etiology of toxic alcohol poisoning if present. Hypocalcemia with resultant complications of cranial nerve palsies, seizures, tetany, and cardiac dysfunction can occur in this time frame. After 24 hours, patients may suffer from acute respiratory distress syndrome, stroke, heart failure, multisystem organ failure, coma, or death.
Isopropanol (isopropyl alcohol): Sources of exposure include rubbing alcohol, hand sanitizer, and antifreeze. Statistics show isopropanol is the most ingested alcohol after ethanol. It may be used as a dangerous substitute for ethanol. It is less dangerous than methanol and ethylene glycol. A lethal dose may start at 4 g/kg, although adults have been confirmed to survive much larger ingestions. After ingestion, it is absorbed within 30 minutes. The highest levels of isopropanol will be found in the blood 30 minutes to 3 hours after exposure. If performed soon after ingestion, laboratory tests will display an elevated osmolar gap. Later tests will reveal ketosis without metabolic acidosis.
Affected patients may appear inebriated, with altered mental status, difficulty thinking, stupor, dizziness, headache, and gastrointestinal (GI) complaints such as abdominal pain, nausea, and vomiting with or without blood. Other signs include fruity smelling breath, miosis, areflexia, hypotension, hypothermia, difficulty breathing, hemorrhagic gastritis, acute pancreatitis, pseudo-renal failure, coma, and cardiovascular collapse.
Diethylene glycol: Sources of exposure include brake fluid and industrial products. It has been the culprit in more than 12 epidemic poisonings when used in medicine. Diethylene glycol may taste sweet. When ingested, it is absorbed rapidly. Poisoning can occur via transcutaneous exposure.
Patients may appear inebriated with altered mental status and will have metabolic acidosis. They may present with GI complaints of abdominal pain, nausea, vomiting, and diarrhea. Reports of acute pancreatitis, liver dysfunction, central neuropathy, peripheral neuropathy, quadriplegia, and acute renal failure have been made. Neurological complications can continue to arise days after exposure.
Propylene glycol: Sources of exposure include antifreeze, electronic cigarettes, and medications, where it is used as a preservative. When toxicity occurs due to medication exposure, the patients have either received an overdose or will be on a chronic high dose. Propylene glycol toxicity can be seen with lorazepam or diazepam administration. Children and burn patients are at a higher risk. Lethal dose may be greater than 10 g/kg.
Affected patients may present with hyperosmolarity, anion gap metabolic acidosis, lactic acidosis, CNS depression, agitation, seizures, hypotension, cardiac dysrhythmia, acute kidney injury, or multiorgan failure.
T51.8X1A – Toxic effect of other alcohols, accidental (unintentional), initial encounter
67426006 – Toxic effect of alcohol