Table 2.

The features of toxic alcohol poisonings.

Type of toxic alcohol	Core clinical features	Core laboratory features	General principles of treatment	Indications for RRT
Methanol	CNS depression AMS Seizures Visual changes/retinal toxicity Hemodynamic instability	HAGMA High osmolal gap Elevated lactic acid (formic acid mediated inhibition of mitochondrial electron transport chain)	Supportive care Fomepizole Ethanol (if fomepizole is unavailable) Folic acid or folinic acid	pH < 7.3 Methanol level > 50 mg/dL Visual changes AKI Severe electrolyte derangements Hemodynamic instability and progression despite appropriate care
Ethylene glycol	CNS depression AMS Seizures AKI Calcium oxaluria	HAGMA High osmolal gap Hypocalcemia Electrolyte abnormalities AKI Calcium oxalate crystals in the urine Falsely elevated lactic acid (glycolic acid can be mistaken for lactic acid)	Supportive care Fomepizole Ethanol (if fomepizole is unavailable) Thiamine Pyridoxine	pH < 7.3 Ethylene glycol level > 50 mg/dL Glycolic acid level > 8 mmol/L Refractory hyperosmolarity AKI Severe electrolyte derangements Hemodynamic instability and progression despite appropriate care
Diethylene glycol	CNS depression AMS Seizures AKI Gastrointestinal symptoms Peripheral neuropathy	HAGMA High osmolal gap Elevated liver enzymes	Supportive care Fomepizole Ethanol (if fomepizole is unavailable) Thiamine Pyridoxine	Hemodynamic instability and progression despite appropriate care Persistent HAGMA
Isopropyl alcohol	CNS depression AMS Hemodynamic instability in advanced cases	High osmolal gap Increased ketones in the blood and urine Absence of HAGMA Falsely elevated creatinine (due to acetone cross reactivity)	Supportive care Fomepizole Ethanol (if fomepizole is unavailable)	Hemodynamic instability and progression despite appropriate care Isopropyl alcohol level > 4000 mg/dL

CNS: central nervous system.

AMS: altered mental status.

HAGMA: high anion gap metabolic acidosis.

AKI: acute kidney injury.