Acid-Base Physiology

8.6 Metabolic Acidosis due to Drugs and Toxins

8.6.2 Ethylene Glycol Poisoning

Ethylene glycol is a colorless sweet tasting solvent which is used in antifreeze solutions. It is nontoxic itself but is converted to toxic metabolites in the liver:

Glycolic acid (->glycolate anion) is the major contributor to the often severe high anion gap acidosis that develops
Oxalic acid (->oxalate anion) is one of the final metabolic products which is excreted in the urine. Precipitation of calcium oxalate crystals in the kidney causes renal failure if a sufficient dose has been ingested.

Fig: Metabolism of Ethylene Glycol

If untreated, ingestion of only 30 to 60 mls may be sufficient to cause permanent organ damage or death. The osmolar gap may be raised (to > 10) early in the course but this is variable.

The detection of calcium oxalate crystals in the urine is often stated to be a useful guide but this is wrong. Certainly. these crystals have a characteristic appearance (lsee figure below) and a urinanalysis will easily detect them. The problem is that oxalate crystals in urine are generally very common (80% of specimens) and their presence alone means nothing for a diagnosis of ethylene glycol ingestion. Oddly, cases of ethylene glycol ingestion have also been reported without oxalate crystals in the urine. There is also no point in differentiating between the monohydrate and the dihydrate crystals.

Fig: Calcium dihydrate crystals in urine - the ones with the 'folded envelope' appearance

Toxicity is usually considered as occurring in 3 stages: intoxication, cardiorespiratory changes and renal toxicity (see below)

Stages of Ethylene Glycol Toxicity

Stage 1: Intoxication

Up to 12 hours post-ingestion

An ethanol-like intoxicated state (without an appropriate odour on the breath) progressing to CNS depression
Fits and coma may occur
A high anion gap metabolic acidosis develops
Nausea, vomiting, arrhythmias and tetany (due to hypocalcaemia) may occur

Stage 2: Cardiorespiratory Changes

From 12 to 24 hours post-ingestion.

Tachycardia, tachypnoea. Shock may occur in major ingestions

Stage 3: Renal Toxicity

At 24-72 hrs post-ingestion

Acute anuric renal failure may occur due to precipitation of calcium oxalate crystals in the renal tubules.

Principles of Treatment of Ethylene Glycol Poisoning

1. Emergency Management

R esuscitation: Airway, Breathing, Circulation. Obtunded patients require intubation for airway protection and ventilation.

2. Ethylene Glycol Removal from body

Haemodialysis is the most effective technique; it also removes ethanol so ethanol infusion rate must be increased during periods of dialysis
Avoid lavage - Lavage is effective only if used within the first hour after ingestion and patients do not present within this interval.
Avoid activated charcoal - This is NOT effective

3. Blocking of Metabolism

Ethanol: "Ethanol blocking" treatment is the traditional treatment but has the disadvantage of causing intoxication (CNS depression). It is also irritant and should be given via a central line.
Fomepizole ('Antizol'): This is currently approved for this use in some countries (eg USA and Canada). Its advantages are effectiveness, ease of administration and absence of intoxication. Its use may obviate the need for haemodialysis in patients without severe acidosis.

4. Intensive supportive care & monitoring

Management in Intensive Care Unit is recommended; Intubation & mechanical ventilation may be indicated if there is inadequate airway protection (eg CNS depression) or inadequate ventilation.

If intubated, hyperventilation must be maintained to mimic the body's compensatory response

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