Ethylene Glycol and Propylene Glycol Toxicity
What Are the Stages of Ethylene Glycol Intoxication?
Course: WB 1103
CE Original Date: October 3, 2007
CE Renewal Date: October 3, 2010
CE Expiration Date: October 3, 2012
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Learning Objectives |
Upon completion of this section, you should be able to
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Introduction |
Ethylene glycol itself is toxic, but its harmful effects mainly result from the accumulation of its more toxic metabolites. Ethylene glycol is a central nervous system (CNS) depressant that can produce acute effects similar to those of ethanol. These CNS effects predominate during the first hours after exposure. |
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Mechanism of Toxicity |
The main toxicity results from hepatic metabolism of ethylene glycol to glycoaldehyde, glycolate, glyoxylate, and oxalate. These metabolites inhibit
The accumulation of organic acid metabolites, especially glycolic acid, results in anion gap metabolic acidosis which affects many cellular functions. |
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Stages of Ethylene Glycol Intoxication |
Severe ethylene glycol poisoning may go through three stages: CNS depression, cardiopulmonary toxicity, and renal toxicity (Table 1) (Friedman, Greenberg et al. 1962). However, signs and symptoms in an individual patient might not be separated so cleanly and could have much overlap. Stage 1 (CNS depression phase)CNS depression begins soon after exposure, lasting for up to 12 hours after ingestion. This depression appears similar to ethanol intoxication, but without the characteristic odor of alcohol. Initially, the inebriation, euphoria, slurred speech, sleepiness, and so forth are due to the unmetabolized ethylene glycol. After the glycoaldehyde forms (at 4-12 hours) and metabolic acidosis begins, CNS depression—if it is a serious intoxication—can lead to the following effects:
An osmolal gap, without metabolic acidosis, or an anion gap may be seen before significant metabolism of ethylene glycol occurs. As ethylene glycol is metabolized, the osmolal gap, if present, will decrease and an anion gap metabolic acidosis evolves. Patients who present late may have renal failure with normal osmolal and anion gaps and no acidosis or measurable ethylene glycol levels (Ford M 1991). Signs of metabolic acidosis due to the metabolites may become apparent late in stage 1. Stage 2 (Cardiopulmonary toxicity phase)The following cardiorespiratory symptoms may appear 12-24 hours after ingestion
The following conditions may develop in this stage
Formation of oxalic acid may lead to deposition of calcium oxalate crystals in
These deposits can cause tissue injury. They also may lead to hypocalcemia secondary to calcium oxalate precipitation. Most deaths from ethylene glycol poisoning occur during stage 2. Stage 3 (Renal toxicity phase)Kidney damage usually develops 24-72 hours after exposure. Acidosis and acute renal failure may result from deposition of calcium oxalate crystals in the kidneys. The following conditions characterize the third phase
Prolonged, rarely permanent, kidney failure is distinguished by
Calcium oxalate crystals may appear in the urine as early as stage 1, but absence of these crystals does not rule out the diagnosis of ethylene glycol poisoning.
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Key Points |
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