16 | How to care for patients with ethylene glycol toxicity as a vet nurse

PodcastRenalEmergency and Critical Care
Written By Laura Jones

I’m sure when I say ‘antifreeze poisoning’ you’ll have a case you’ve seen that comes to mind.

 

They’re usually collapsed cats who present with severe renal failure, and they require a ton of nursing care. Though they do have a poor prognosis, there are a lot of nursing skills we can use to support these patients - and to do that, we first need to look at what happens when our patients ingest ethylene glycol.

What is ethylene glycol?

Ethylene glycol is a highly nephrotoxic compound found most commonly in vehicle radiator antifreeze, though it is also found in other solvents, household products and automotive products too.

Because antifreeze is readily available, often improperly stored, prone to spillage with improper use, and sometimes, disposed of improperly, exposure to EG is common. That, combined with the low minimum lethal concentration and the fact that the solution has a sweet taste, makes ingestion relatively common.

Though we can theoretically see ethylene glycol toxicity in any species, cats tend to present with it most commonly. In part, this is because the minimum lethal dose is lower - 1.4ml/kg of undiluted ethylene glycol is required in cats, compared with 4.4-4.6ml/kg in dogs. Cutaneous absorption of ethylene glycol is also reported in cats, so they do not need to ingest the solution orally to be susceptible to its effects.

Toxicity cases are usually seasonal, with a spike in cases over the winter to early-spring period, or in colder climates, since more antifreeze is used over the colder periods.

So your patient ingests ethylene glycol. What happens?

When a patient ingests ethylene glycol, the first thing to note is that the ethylene glycol itself is not actually toxic - it is the body’s reaction to the ethylene glycol, and the metabolites that it is broken into, that cause the marked renal damage we see in these patients.

Ethylene glycol is absorbed rapidly from the GI tract after ingestion - within the first 1-4 hours. About half of it actually gets excreted unchanged - but the rest is metabolised in the liver and kidneys, and after a series of oxidative reactions, the patient is left with ethylene glycol metabolites. These are highly toxic, and cause marked acidosis, as well as significant damage to the renal tubules within the nephrons.

So how is ethylene glycol metabolised?

Firstly, an enzyme called alcohol dehydrogenase turns the ethylene glycol into glycoaldehyde. This glycoaldehyde is quickly metabolised again, this time to glycolic acid. Glycolic acid accumulates, and is then metabolised to glyoxylic acid. And then, the glyoxylic acid is broken down into oxalic acid (aka oxalate), glycine, formic acid, and other metabolites.

So you’ve now got a patient who has lots of these additional acidic compounds circulating in the body. Not only do these cause severe metabolic acidosis, but they also have a direct effect on the renal tubules, causing acute tubular necrosis.

On top of that, the oxalate combines with calcium, causing calcium oxalate crystals to form inside the renal tubules, further damaging renal function.

What signs do we see in these patients?

Well, the clinical signs we see depend on 2 things - firstly, how much ethylene glycol the patient consumed, and secondly, when they consumed it.

Within the first 30 minutes to 12 hours of ingestion, most clinical signs mimic alcohol (ethanol) intoxication. These patients tend to have gastrointestinal signs, PUPD, and neurological signs including depression, ataxia, and proprioceptive deficits. These signs are associated with the unmetabolised ethylene glycol - not the toxic metabolites. Sometimes, around 12 hours after ingestion, the patient may briefly improve.

After this period, the signs we see begin to change, because they’re now associated with the toxic metabolites from the ethylene glycol, rather than the EG itself.

These signs include acute kidney injury, oliguria progressing to anuria, painful, enlarged kidneys on palpation, tachycardia or bradycardia, tachypnoea, anorexia, vomiting and diarrhoea, oral ulceration and hypersalivation. Central nervous system signs are also commonly seen - varying from lethargy to seizure activity, to even coma.

How do we diagnose ethylene glycol toxicity?

It’s very rare that ingestion will be witnessed - so, like most of our medical conditions, we instead diagnose based on a combination of history, physical examination, blood work, and urine analysis. 

Alongside this, you can perform ethylene glycol testing - however, it’s not widely available, and often doesn’t change the management of the condition significantly. Factoring in how quickly we need to stabilise and treat these patients, we’re also not in a position to wait for external results, or find a local centre that might have them.

In most cases, we’ll instead be documenting evidence of metabolic acidosis and acute kidney injury with calcium oxalate crystalluria.

And how are we going to treat these patients?

Treating ethylene glycol toxicity aims to:

  • Decrease absorption of any ingested ethylene glycol

  • Increase excretion of any unmetabolised ethylene glycol

  • Prevent metabolism of ethylene glycol, and 

  • Correct any metabolic derragements the patient has been left with as a result.

Decreasing absorption

Decreasing absorption of ethylene glycol is achieved by performing GI decontamination - this would be achieved through inducing emesis, or by performing gastric lavage. 

However, there are a few things to think about here. Firstly, ethylene glycol is so rapidly absorbed from the GI tract, it’s of limited use.

Secondly, we often don’t see these patients within the first 12 hours of absorption, let alone the first 1-4 - so by the time they present, there’s a good chance they will have absorbed the ethylene glycol already. 

We also shouldn’t be making any neurological patient vomit, due to the aspiration risk - and we know these patients are often neurological. On top of this, activated charcoal doesn’t work for ethylene glycol - so there’s no point reaching for that in these patients.

Increasing excretion

Since these patients have usually ingested and absorbed the ethylene glycol before presentation, we need to increase excretion instead. 

This is achieved by administering fluid therapy to correct dehydration, improve urine production (potentially) and compensate for ongoing fluid losses. So, perform a hydration and perfusion assessment in these patients, calculate their fluid deficit, and correct this over an appropriate period of time, depending on the individual patient.

Preventing metabolism

By preventing the metabolism of ethylene glycol, we prevent those toxic metabolites from forming, allowing the patient to pass unmetabolised ethylene glycol out of the system, and minimising the catastrophic effects to our patient. 

To prevent ethylene glycol metabolism, we need to give the body something for that enzyme - alcohol dehydrogenase - to bind to instead of the ethylene glycol, or to inactivate it. In dogs, a drug called fomepizole can be used to inactivate alcohol dehydrogenase. It can also be used in cats, but they require a higher dosage than dogs. A more common alternative to fomepizole is ethanol. This is usually given as a bolus initially, followed by a constant rate infusion.

Managing acid-base and electrolyte abnormalities

If your patient is severely acidotic, they require bicarbonate administration. However, this drug must be used carefully, slow IV to prevent overdose, with thorough patient monitoring, and regular pH/blood gas analysis.

Hypoglycaemia is also common in patients with ethylene glycol toxicity. This is corrected by administering boluses of glucose as needed, followed by a dextrose CRI at 2.5-5%, depending on the individual patient. Blood glucose levels should be regularly monitored throughout treatment.

Hypocalcaemia is another common electrolyte derangement in EG toxicity. Ideally, we would use ionised calcium measurement to assess calcium levels in these patients. Where they are low, a calcium gluconate bolus (+/- infusion) is administered. Since intravenous calcium therapy can cause cardiac arrhythmias, these patients require continuous ECG monitoring throughout treatment.

Another very common electrolyte abnormality in these patients is hyperkalaemia. If your patient is hyperkalaemic, we’ll need to take steps to reduce that potassium level, since it can cause life-threatening arrhythmias. We usually reduce it using a combination of fluid therapy, glucose, or neutral insulin and glucose solution, alongside giving calcium gluconate to protect the heart from the effects of the potassium itself.

On top of all of this, we need to think about supportive treatment for these patients - things like antiemetics, and analgesia.

What about nursing care?

In terms of nursing care, we’ll be managing these patients very similarly to patients with other causes of AKI - except their monitoring requirements are generally much higher.

So, this means:

  1. Keeping a really close eye on vital parameters, blood pressure, heart rate, temperature, respiratory pattern and rate, ECG trace… all the things, and tailoring our monitoring frequency to the individual patient

  2. Stabilising any cardiovascular, respiratory, or neurological changes - so administering a fluid bolus to a hypovolaemic patient, for example, or managing seizures, or performing things like glasgow coma scale monitoring in neurological patients

  3. Performing repeat fluid balance assessments, and working with our vet team to adjust the patient’s fluid rate as needed, based on their hydration status and their urine output

  4. Placing and managing urinary catheters, so that we can quantify urine output and quickly detect any oliguria (low urine output) or anuria (no urine output)

  5. Placing NO feeding tubes, performing nutritional assessments, and creating and implementing a nutritional plan

  6. And I also want to mention vascular access as one final nursing consideration for these patients. We’ll regularly be measuring pH, ionised calcium, electrolytes, creatinine, etc - and this means lots of needle sticks. A PICC line (or a central line, if your patient is stable enough for a GA/sedation) would be a really handy extra here - since we’ll be able to sample through it. And on top of that, it’s a great practical nursing skill!

So there you have it - an overview of all of the treatment and nursing considerations for ethylene glycol toxicity patients. 

Yes, these patients often present critically unwell - and the prognosis IS poor. But with rapid identification and treatment, alongside intensive nursing care, we can improve outcomes for these patients - and the intensive monitoring, hands-on nursing and things like placing PICC lines, urinary catheters, and feeding tubes make them fantastic cases to nurse.

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on instagram (@vetinternalmedicinenursing) so I can give you a shout out, and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
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