Pet Poisoning “Danger in our home”

Ethylene glycol
Ethylene glycol is most commonly encountered in antifreeze, screenwash
or, more rarely, de-icers. Most antifreezes available contain ethylene glycol
or methanol.

Occurrence of poisoning incidence
Since 1992 the VPIS has received a small number of enquiries regarding
ingestion of ethylene glycol by companion animals. Approximately 10% of
these cases involved cats. In these feline cases, all presented with severe
clinical effects and outcomes were fatal in all but 8% of cases.
Ethylene glycol poisoning is more commonly reported in the winter
months.

Diagnosis
Ethylene glycol poisoning may be mistaken for head trauma, encephalitis,
acute gastroenteritis, pancreatitis, ketoacidotic diabetes mellitus and acute
renal failure from other causes. Diagnosis is based on history, clinical signs
and laboratory data. Abdominal palpation may be painful due to renal
oedema. Ethylene glycol poisoning should be suspected in any animal with
the following:
(a) acute onset of signs
(b) raised urea, creatinine and other nitrogenous compounds in the blood
(c) low or fixed urine specific gravity (Grauer and Thrall, 1982).
(azotaemia or uraemia)
Treatment
Therapy for ethylene glycol is principally aimed at blocking the action of alcohol
dehydrogenase to prevent the formation of the toxic metabolites. This is achieved
by administration of the preferred substrate, ethanol, which allows renal excretion
of the unmetabolised parent compound.
4-Methylpyrazole (4-MP, fomepizole). a direct inhibitor of the enzyme alcohol
dehydrogenase, has been suggested as an alternative therapy to ethanol on the
grounds of a lack of adverse effects and slower elimination. Clinical reports suggest
that 4-MP is successful in treating ethylene glycol intoxication in dogs, but it has
been shown to be less effective than ethanol in cats poisoned with ethylene glycol
and is therefore not recommended.
If within 2 hours of ingestion, induce vomiting or perform gastric lavage.
Adsorbents are not useful.
Emetics:
(a) Xylazine Dose: 0.2 mglkg body weight i.v.;
0.5-1 mg/kg body weight i.m.
(b) lpecacuanha Dose: 1-3 mllkg body weight orally
(c) Soda crystal.
Monitor pH and renal function. Correct acidosis with sodium bicarbonate (see
below). Fluids should be given to ensure adequate hydration and a good urine
output. Central venous pressure and renal output should be monitored in cats
with renal dysfunction because of the risk of fluid overload and subsequent pulmonary oedema. Mannitol can be used in a well-hydrated animal to produce an
osmotic diuresis and reduce renal oedema.
Dose: 0.25-0.5 g/kg body weight, i.v. over 5-1 0 minutes.
Peritoneal dialysis is recommended in acidotic cats with oliguria.

In most symptomatic cases reported to the VPIS (London) the animals
show evidence of having bitten through the battery casing and therefore
have local irritant and corrosive effects to the mouth and oesophagus.
Oesophageal impaction may result in irritability, difficulty in swallowing,
salivation, vomiting and, in theory, local burns. Clinical effects from
corrosion or perforation may be delayed.
Batteries which open in the lower gut may cause vomiting, tarry or bloody
stools, and abdominal tenderness.
In the case of mercury batteries, signs of mercury intoxication, initially
severe gastrointestinal upset, may be delayed by several days.

Treatment
Emesis and gastric lavage are not recommended, since these procedures are
unlikely t o evacuate batteries owing t o their density and the risk that they may
lodge in oesophagus. Use of adsorbents is not routinely advocated as they are of
limited benefit and will obscure detection of the batteries and discolour the stools.
The brand and type of battery should be determined where possible. Spare
batteries may be kept at home and may bear an identifying code that poisons
information centres use to identify the type involved.
X-rays should be taken where practicable t o confirm ingestion and t o determine
the position of the battery. The condition of the battery may also be determined
as contents are radiopaque.
If the battery is still in the oesophagus prompt removal is advocated, by endoscopy
where possible.
When batteries are intact and in the stomach o r beyond, laxatives may be given t o
promote transit through the gastrointestinal tract. Ideally, X-rays should be
repeated to monitor the passage of the battery through the gut until passed in the
stools. Surgical removal is indicated when there is no movement of the battery in a
48 hour period, the battery shows evidence of leakage, o r if there is clinical
evidence of significant gastroenteritis o r discolored stools.

Petroleum distillates / White spirit / Kerosene

Paint

Petroleum

They are usually liquid and have characteristic strong odours. Examples are
petrol, paraffin, diesel, solvents for paints (especially gloss paints),
varnishes, glues, glass cleaners, lamp oils, barbecue lighter fluids and
sometimes as a liquid vehicle for pesticides, wood preservatives, and
industrial chemicals.
White spirit is usually a colourless volatile liquid commonly found in the
home as a paintbrush cleaner. Turpentine substitute is white spirit.

Clinical effects
Onset of effects is usually between 1 and 8 hours post-exposure.
Ingestion or oral exposure following grooming after dermal exposure may
cause salivation, severe and protracted vomiting, local irritation and
ulceration of the mouth and throat, abdominal tenderness, diarrhoea,
inappetence and anorexia.
Signs of systemic toxicity include tachycardia, ataxia, tremor, weakness,
excitability and agitation. Convulsions, tachypnoea, hyperaesthesia and
pyrexia are reported for more severe exposures.
Aspiration pneumonia is an occasional complication of ingestion where
coughing or vomiting has occurred. It also occurs following inhalation.
Clinical effects include coughing, fever, dyspnoea, cyanosis and, in severe
cases, CNS depression and pulmonary oedema.
Petroleum distillates are irritant to skin and eyes. Blisters, inflammation and
burns have been reported following dermal exposures and corneal damage
has occurred when such compounds come into contact with eyes.

Treatment
Use of emetics and gastric lavage is contraindicated owing to the risk of aspiration.
Adsorbents are of limited benefit. They reportedly bind aromatic distillates and
longer chain aliphatic hydrocarbons and therefore may help to reduce absorption
of distillate mixtures such as kerosene.
Adsorbents:
(a) Activated charcoal Dose: 2 glkg body weight orally
(b) BCK granulesm Dose: 6-1 8 g orally.
Oral fluids should be encouraged.
Where dermal exposure has occurred, the animal should be thoroughly washed.
Petroleum distillates are not very miscible with water so non-solvent-based
detergents or commercially available hand degreasers, e.g. Swarfega@, may need to
be employed. Where possible the animal should be collared to prevent further
grooming and further ingestion of the distillate.
Contaminated eyes should be irrigated with water or saline, and then stained with
fluorescein and examined for corneal injury.
Treatment thereafter is symptomatic and supportive. Bland diets are recommended
if there is evidence of severe buccal irritation. Care should be taken to
ensure adequate hydration and nutrition. Atropine may be given for excessive
salivation.
An observation period of 12 hours is recommended.
The animal should be assessed for respiratory effects. Aspiration pneumonia
requires conventional therapy, with oxygen supplementation and cage rest. In
severe cases positive end-expiratory pressure ventilation (PEEP) may be
considered, though it should be used with caution as pneumomediastinum and
pneumothorax are potential complications.
The use of antibiotics to prevent secondary lung infections is recommended.