94 | The essential guide to toxicology part five: how to manage ingestion of household hazards as a veterinary nurse

NursingPodcastToxicologyEmergency + Critical Care
Written By Laura Jones

In this episode, we’re nearing the end of our toxicology series with a look at the common household hazards our patients ingest, and how to care for those patients confidently.

Household hazards are something we see often - especially in my line of work, where things like caustic chemical ingestion or battery ingestion cause severe GI signs (or worse) needing intensive management. From fluid therapy, to nutrition, to analgesia, GI support and more, our role in caring for these patients cannot be overlooked.

Today, we’ll take a closer look at toxicosis from things like household cleaners, corrosive agents, alcohols and essential oils. We’ll discuss the impact they have on our patients, and the nursing support these patients need.

Let’s start by looking at corrosive agent ingestion.

There are tons of corrosive agents in our homes - from cleaning agents, to laundry detergents and even batteries. Corrosives can be either acidic or alkaline, and when they are ingested (or there is other exposure), they cause severe irritation and injury.

Regardless of the route of exposure, the result is the same - severe localised tissue injury and even full-thickness burns of the exposed area, be that the skin, cornea, mucous membranes, oral mucosa, oesophagus or stomach.

What happens when a patient ingests a corrosive chemical?

The severity of the patient’s injury (and therefore clinical signs) depends on a few things: the corrosive material, the area of exposure, and the duration of contact.

Acids produce immediate tissue necrosis and marked pain, which often limits exposure and results in more superficial contact with the agent. The extent of the burns/tissue damage is usually apparent shortly after contact.

However, with alkaline agents, they do not tend to produce marked pain on contact. This means that the duration of exposure is usually much longer, resulting in larger, deeper and more extensive tissue damage when compared with acid exposure. It can take up to 12 hours for an alkaline injury to become fully apparent. In addition, oesophageal burns are more likely with alkaline agents - even if there is no or minor evidence of oral injury.

In severe cases, full thickness burns can affect the gastrointestinal tract. Where extensive oesophageal injury occurs, oesophageal perforation can also be seen. This may cause leakage of corrosive content into the thoracic cavity, resulting in pleuritis and bacterial contamination of the thoracic cavity.

Gastric ulceration and perforation is thankfully less common, as the acidic pH within the stomach helps to neutralise the alkaline ingesta. However, with prolonged or extensive exposure it is possible - causing gastrointestinal haemorrhage, pain, and even peritonitis if perforation occurs.

Alkaline agents with a pH > 11 pose a significant risk of corrosive injury, though we can of course see injury with less alkaline agents, too.

What about other routes of exposure?

Respiratory, dermal and ocular exposure to corrosive agents are also common.

Where patients inhale corrosive agents (particularly acids), tracheobronchitis, penumonitis, tachypnoea, dyspnoea and other signs of respiratory distress are common. Tissue injury leads to localised swelling and oedema, as well as marked airway pain, impacting both ventilation and oxygenation. This is particularly challenging to manage given that we cannot decontaminate the lungs in the same way we can lavage the stomach, wash the skin, or flush the eyes.

Dermal, oral mucous membrane or ocular exposure results in severe ulceration and damage - of the dermis in the case of the skin, mucous membranes within the mouth/tongue, and of the cornea. In cases of severe corneal ulceration, corneal perforation may also occur.

What clinical signs do we see when a patient has caustic injury?

Initial clinical signs include:

  • Vocalisation

  • Hypersalivation

  • Lethargy

  • Polydipsia

  • Vomiting

  • Haematemesis

  • Dysphagia

  • Pharyngeal oedema

  • Dyspnoea

  • Abdominal pain

  • Oral and gastrointestinal ulceration

Patients can rapidly progress into signs of hypovolaemic shock, with bounding or poor pulses, tachycardia or bradycardia, pale mucous membranes, lethargy and hypothermia apparent. Where these signs are seen, immediate stabilisation is indicated - and as nurses and technicians, this is an area we’ll be heavily involved in.

Skin lesions are initially pale to grey, but will gradually turn black and form eschars, eventually sloughing days after exposure. Significant skin burns are usually seen with dermal exposure, with localised redness and pain, as well as marked tissue sloughing.

If ocular exposure is suspected, patients will present with (or develop) blepharospasm, epiphora, eyelid oedema and burns, conjunctivitis and/or corneal ulceration. This is significantly painful, though most patients do not show as obvious signs of ocular pain compared with other regions - so if there’s any doubt get analgesia on board ASAP.

Where corrosive agents are inhaled, respiratory lesions are common. These can affect the trachea, bronchi and pulmonary parenchyma, and on top of this, inhalation can cause aspiration pneumonia. Respiratory distress is common, with dyspnoea, tachypnoea and orthopnoea commonly seen..

So those are the signs we’ll see - but how do we treat and nurse these patients?

Like our other toxins, stabilisation and decontamination are the first and most important steps in managing these patients.

Dyspnoeic patients and those presenting with signs of shock need immediate stabilisation - with analgesia, anxiolytics and oxygen therapy for respiratory distress patients, and resuscitation of hypovolaemia with crystalloid boluses.

After this, we need to think about decontamination.

Recent oral exposure should be immediately diluted with water or milk, but aside from this, our decontamination options are very limited.

Under no circumstances should we attempt emesis in these patients. Since they’ve ingested corrosive material, there’s a risk of further corrosive damage to the oesophageal/oral mucosa if that comes into contact with the area again.

Gastric lavage is also contraindicated, because the oeaophgeal and gastric walls are weakened from tissue damage and ulceration. Inserting a stomach tube through these weakened structures could easily cause perforation. 

Trying to neutralise the exposure is also not recommended, since mixed chemical exposures can cause thermal burns. Activated charcoal is also not effective in corrosive agent ingestion; additionally, the charcoal sits over the damaged mucosa and can impair wound healing.

So if decontamination is (mostly) out, what other options do we have?

Supportive care is the mainstay of management for these patients, and this means that our role in their care as nurses and technicians is vital.

This includes:

  • Administering oxygen and monitoring respiration, oxygenation and ventilation

  • Administering analgesia and assessing pain at regular intervals

  • Performing careful wound assessment, care and management in the case of dermal exposure

  • Administering fluid therapy to support hydration and monitoring fluid balance

  • Performing special sense care, including oral and ocular care/lubrication as needed

  • Providing nutritional support as well as general nursing care

Patients with ingestion should have an endoscopic assessment of their mouth, oesophagus and stomach 12+ hours after exposure, when the extent of the damage should be evident. Depending on the severity and location of the ulceration, a feeding tube should be considered at the same time - either an oesophagostomy tube if there is oral ulceration (but not oesophgeal ulceration), or a PEG tube if oesophageal ulceration is present.

Patients should be treated with ongoing gastroprotectants such as sucralfate and omeprazole, to minimise further inflammation and ulceration, and promote healing. Strictures may occur in the future as the ulcerated oesophagus heals, needing further treatment.

Dermal or ocular exposures should be flushed copiously with sterile saline or sterile water - for at least 20 minutes in the case of ocular exposure. After this, the eyes should be fluoroscein stained and examined for corneal injury. Where this is present, it should be managed topically alongside providing analgesia and preventing patient interference.

What about managing battery ingestion?

Alkaline battery ingestion poses a risk not just of corrosive injury, but also of foreign body obstruction within the GI tract.

The alkaline gel in batteries causes tissue necrosis on contact, causing deep penetrative burns. Disc batteries (the ones found in watches) can also lodge themselves in the oesophagus easily; where this happens, they will generate a current against the oesophageal wall, causing deep circular oesophageal ulcers that are likely to perforate.

On top of the alkaline gel, many batteries are cased in metals such as mercury or zinc. As well as the battery and the metal housing posing an obstruction risk after ingestion, heavy metal toxicosis can also occur.

It’s also important to note that it isn’t just battery ingestion we can see - small disc batteries can also be inhaled in rare cases, causing airway obstruction as well as airway inflammation and burns.

What signs do we see with battery toxicity, and how do we manage it?

As well as the caustic injury caused by these corrosive materials, patients may present with signs of foreign body obstruction, including:

  • Vomiting

  • Anorexia

  • Abdominal pain

  • Tenesmus

Patients with suspected inhalation commonly present with acute onset dyspnoea, hypoventilation, hypercapnia and cyanosis.

Ingestion and toxicosis is diagnosed via a combination of the patient’s clinical signs, examination findings, and diagnostic imaging confirming the presence of a battery.

Treatment involves removal of the battery, followed by decontamination (if appropriate) and supportive care.

If there is any chance the battery casing has been punctured, emesis should not be attempted. If the battery was swallowed whole (for example, if ingestion was witnessed) recently enough for emesis to be effective, then this should be attempted.

If a disc/watch battery was ingested, administering regular tap water boluses is recommended to delay and minimise the development of oesophageal ulceration.

Batteries that have been punctured (or where this is suspected) must be removed surgically. If the battery has not been punctured, endoscopic removal from the stomach may be attempted. In some cases, batteries may pass on their own - but close monitoring of progression with serial x-ray is recommended, alongside use of bulk-forming fibre agents to aid passage.

Where gastrointestinal ulceration or burns are suspected, they are managed in exactly the same way we’ve already discussed - with careful supportive care, close monitoring, nutrition and hydration support and analgesia.

Bleach and household cleaning product toxicity in animals

A wide variety of household and personal care products pose a significant risk to our patients. Many of these products are corrosive/caustic, causing burns and GI damage as we’ve already discussed. However, there are a few specific - and common - agents to mention: bleach, and laundry detergent pods.

Laundry detergent pod ingestion is increasingly common, particularly in dogs.

One bite into one of these accidently left out by the washing machine can cause catastrophic damage.

Laundry pods are made up of surfactant chemicals, ethanol and propylene glycol and they have a pH ranging from 7-9. The fluid is usually a thick liquid-gel and contained within a dissolvable gel membrane, easily punctured by a dog or cat mistaking it for a toy.

When an animal bites into a pod, the fluid coats the back of the mouth and causes significant irritation - not just to the oral mucosa, but to the oesophagus in the case of ingestion, and the airways in the case of aspiration.

Patients usually present with profuse vomiting and regurgitation due to tissue irritation, further increasing the risk of aspiration and subsequent respiratory ulceration.

In these patients, preventing further vomiting is essential, since ongoing vomiting increases caustic exposure to the oesophagus and risks further aspiration. Antiemetics are vital. Alongside this, diluting the ingesta with water or dilute milk is recommended - this both minimises the potential for gastric ulceration, and prevents further vomiting triggered by that ulceration/inflammation.

And then there’s bleach exposure.

Exposure to undiluted bleach can result in significant respiratory irritation as well as gastrointestinal, dermal and ocular ulceration.

Bleach contains sodium hypochlorite and depending on the concentration, solutions have a pH of 9-11 - aka mildly irritating to corrosive. 

When patients ingest undiluted bleach, marked alkaline corrosive injury occurs. In addition, inhalation of chlorine bleach fumes can lead to marked respiratory injury and pulmonary oedema.

In rare cases, ingestion of larger volumes of bleach can cause hypernatraemia and hyperchloraemia, due to the large volumes of both sodium and chloride in the solution. Since chloride acts as an acid in the body, this can contribute to metabolic acidosis.

Patients are managed in the same way as previously described, due to the often significant corrosive injury bleach solutions cause. However, if a patient ingests or comes into contact with diluted bleach solution, the effects are typically milder (such as mild gastrointestinal signs).

What about alcohol toxicity in veterinary patients?

Alcohol exposure doesn’t just come from patients stealing beer from a slug trap or sneaking from a glass on the table - there are lots of alcohol-containing products in our homes.

When our patient comes into contact with them - either from GI exposure or absorption across the skin - rapid and significant clinical signs are seen. In severe cases, it can cause coma, seizures or even death, and these patients need intensive supportive care to make it through their toxicity successfully.

The most frequent alcohols seen in toxicosis cases are ethanol, methanol and isopropranolol.

These are found in beverages, rubbing alcohols, hand sanitisers and even in fermenting bread dough - as well as antifreeze (which we discussed in detail back in episode 16).

Alcohols are irritant to the GI tract and result in vomiting and hypersalivation. In addition, their metabolites cause marked CNS depression and impact things like catecholamine release, causing significant cardiovascular changes. Cardiac arrhythmias, vasodilation and bradycardia are commonly seen as a result.

Vasodilation contributes to hypothermia, and the combination of alcohol’s gastrointestinal, inebriative and CNS effects cause things like:

  • Vomiting

  • Diarrhoea

  • Ataxia

  • Disorientation

  • Lethargy

  • Tremors

  • Hypothermia

  • Seizures

  • Bradycardia

  • Respiratory depression

Hypoglycaemia is also common; in addition, any metabolites are acidic, contributing to metabolic acidosis.

How is alcohol toxcicity diagnosed and treated?

Like many other toxin ingestion cases, diagnosis is made based on a combination of clinical history, examination findings and supportive clinical signs. Measurement of blood alcohol levels can be used in some cases to confirm the diagnosis if needed.

Unfortunately, there is no specific treatment for these patients past supportive care. This means that, as nurses and technicians, our role is essential. Intensive monitoring, cardiovascular and respiratory support and seizure mangement is indicated, alongside neurological monitoring, reducing stimulation, active warming, and providing general nursing care.

The last toxin we’re chatting about today is essential oil toxicity in animals.

Essential oils are volatile plant compounds that give the plant their unique fragrance or taste. They are often distilled or extracted from plants directly, and used in varying concentrations commonly.

With both the rise of essential oils in home fragrance, cleaning and wellness products at home, and their improper use as a “natural” flea and tick repellent by well-meaning caregivers, toxicity is seen more and more often - meaning we need to recognise the signs, and know how to treat these patients confidently.

What happens when a patient is exposed, and which patients are at greatest risk?

Though both cats and dogs can be affected by essential oils, cats are much more sensitive to their effects. 

Like with paracetamol toxicity (as we chatted about in episode 92), cats lack the glucuronyl transferase enzyme needed to metabolise many agents in the body. This makes them very sensitive to phenol compounds, which many essential oils contain. 

In addition, given cats natural grooming behaviour, they are at a higher risk of both oral and dermal exposure. And whilst the risk is lower in dogs, it isn’t absent.

Exposure usually occurs either through passive diffusion (from reed diffusers, where exposure is limited unless the contents are spilled) or active diffusion (from a nebuliser which emit oil droplets into the air).

After exposure, the oil is either absorbed directly across the skin, or ingested via grooming.

What clinical signs do we see when a patient is exposed to essential oils?

The signs we see depend on both the type and concentration of the essential oil, as well as the route of exposure. Commonly, patients will preset with:

  • Vomiting

  • Lethargy

  • Hypersalivation

  • Ataxia

  • Anorexia

However, neurological signs, skin irritation, and even hepatic and renal failure can occur depending on the severity of exposure.

Management of these patients includes decontamination as well as supportive care.

Emesis should not be induced due to the risk of aspiration; instead, affected areas on the skin should be washed thoroughly, and supportive care should be administered until signs improve.

This includes intravenous fluid therapy, gastroprotectant mediations, hepatoprotectants such as SAMe or N-acetylcysteine (as we discussed in episode 92), antiseizure medications and oxygen, depending on the patient’s clinical signs.

Like anything in veterinary medicine, prevention is better than cure - so educating caregivers on responsive essential oil use is key.

This is also an area we’re well placed to help with as nurses and technicians. To minimise complications, caregivers should avoid toxic essential oils, use oils diluted and for short periods of time in well-ventilated areas. They should avoid applying any oils directly to their pet, and keep pets out of rooms where diffusers are actively running.

So there you have it - an overview of the common household hazards we see and how they impact our patients, as well as the nursing support these patients need. In most cases, decontamination options are limited and supportive care is the most important consideration - meaning there are lots of opportunities for us to make a difference when caring for these patients.

Did you enjoy this episode? If so, I’d love to hear what you think. Take a screenshot 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
Next

93 | The essential guide to toxicology part four: how to manage rodenticide and pesticide toxicities as a veterinary nurse