ABSTRACT: This article discusses three toxins commonly encountered by dogs in the home environment. Theobromine, which is found in chocolate, can result in vomiting, diarrhoea and seizures. The ingestion of grapes and raisins can result in acute renal failure unless aggressive treatment is instituted. Paracetamol – although largely being displaced by ibuprofen – is licensed for use therapeutically in dogs and can have a significant toxic effect if an overdose is given.

Whilst the dog is man’s best friend, our canine companions can be unwise about what they choose to ingest, and too trusting of what may be offered to them – even by their owners. Boredom arising from a solitary existence, whilst their owners are at work, can sometimes lead dogs to a trip to the veterinary practice for treatment upon their owners’ return, owing to ingestion of unsuitable substances. Most nurses and vets will be all too familiar with the Easter weekend chocolate ingestion case, or a well- meaning owner medicating their lame dog with human drugs for pain relief. Both scenarios are, sadly, relatively common, but their potential for a fatal outcome must not be overlooked.


Although a treat for humans, chocolate can be lethal to dogs.


Theobromine is the naturally occurring stimulant found in cocoa beans. Along with caffeine, theobromine belongs to a class of chemicals called methylxanthines. Dogs metabolise these chemicals more slowly than humans, which leads to their toxic effects.

After ingestion, theobromine is absorbed throughout the gastrointestinal tract, metabolised by the liver and then it stimulates the central nervous system. It inhibits cellular adenosine receptors, resulting in nerve cell hyperactivity causing tremors and seizures. Theobromine metabolism also affects the heart muscle, so hypertension, tachycardia and arrhythmias are often seen at higher toxic doses.

The toxic effect is often unpredictable. The amount of cocoa in the chocolate will determine its toxicity – milk chocolate is not as poisonous as dark or more expensive chocolate, which has a higher cocoa percentage (Figure 1). For instance, 1.3g/kg of baking chocolate will provoke toxic signs, which equates to just 26g being dangerous to a 20kg dog. Toxicity from long-term exposure is also possible; for example, when a small amount is fed regularly (approximately 15g/kg dark chocolate daily), right atrial cardiomyopathy can develop.

Figure 1: Chocolate can vary greatly in its cocoa content, and this has a direct effect on how toxic it can be if ingested by dogs


The treatment for chocolate ingestion is to induce emesis promptly and, following this, to give supportive nursing care. Intravenous fluid therapy and management of clinical signs – including seizure management with benzodiazepines – and continual monitoring are required.

In dogs, the half-life of theobromine is 17.5 hours, so clinical signs can persist for some time in more severe cases.


Owner education about the risks of feeding chocolate to their dog is something of which all nurses should be aware. Some dog owners would admit that they feed their dogs ‘a small amount’ and that they ‘have never come to any harm’. In reality, however, owing to the different types of chocolate available, the dose of toxin given one day which shows no clinical signs could result in a response at a later date from the same amount of a different type of chocolate.


Prognosis is favorable if rapid action is taken and owners are aware of just how dangerous this ‘treat’ can be.

Grapes and raisins

Sometimes given as a ‘healthy’ treat, grapes and raisins have a significant toxic potential in dogs. It is unknown why grape toxicity results in acute renal failure, although it is suspected to be related to metabolic disruption causing nephrotoxic changes.

All parts of the fruit are poisonous to dogs, and toxic doses can be as low as 8g/kg, which equates to a couple of handfuls for a 20kg dog (25g equals four grapes). So any ingestion should be taken seriously.

Clinical signs and laboratory findings

The initial signs are usually vomiting within two hours of ingestion, leading to diarrhoea, lethargy and polydipsia. Within 24 hours to several days, signs of acute renal failure will have ensued, including anorexia, lethargy, depression, abdominal pain and hypervolaemia.

Serum biochemistry will also show elevations in urea and creatinine and hyperphosphataemia at this stage, and urine production will be reduced – this is anuric renal failure.


Diagnosis should be made on known history of exposure, clinical signs and the development of acute renal failure.


As with any poisoning case, prompt treatment is important; and initial decontamination by inducing emesis, followed by giving activated charcoal (1-3g/kg orally), is invaluable in instances when ingestion has taken place within the previous two hours.

Fluid diuresis over the initial 48 hours may help in preventing the onset and development of acute renal failure, and renal biochemistry parameters, in particular, should be regularly checked for up to three days after exposure to monitor deterioration.


Owner education in these cases is paramount, because many dog owners don’t realise quite how dangerous grapes and raisins are to their canine friends, or how unpredictable the reaction may be.


Paracetamol, also known in the US as acetaminophen, is commonly used in people, as it is a widely available over-the-counter drug. It is known for its analgesic and antipyretic properties, and is inexpensive.

Whilst these qualities are occasionally used for therapeutic purposes in dogs at 10 mg/kg orally or intravenously, toxic signs aren’t usually observed unless the dosage exceeds 100 mg/kg. Whether this is the result of the dog’s finding and eating a packet of tablets, or an accidental overdose, treatment requires prompt action.

Paracetamol can also have a cumulative toxic effect if smaller repeated doses are given; for example, if an owner is home- medicating their dog without seeking veterinary advice, this can also lead to hepatotoxic effects.

Pathogenesis of toxicity

The drug itself is metabolised by the liver and the toxic metabolites bind to the lipid components of hepatic cell membranes, causing cell injury and possible cell death to occur. The cells are subjected to oxidative stress and, although the liver is renowned for its regenerative properties, at higher rates of toxic change – s
uch as in the case of paracetamol poisoning – lasting hepatocellular necrosis can occur, resulting in liver failure.

Red blood cell damage also commonly occurs with paracetamol toxicity, as the metabolites act on the cells and result in haemolysis, Heinz body formation and formation of methaemoglobin are evident when red blood cells are damaged and haemoglobin becomes non-functional and unable to transport oxygen. Excess methaemoglobin in the blood alters its colour from red to a chocolate brown’, typically resulting in brown mucous membranes (Figure 2).

Figure 2: Chocolate brown mucous membranes associated with methaemoglobinaemia

Clinical signs

Clinical signs may be expected within the initial 12 hours of exposure; these include lethargy, vomiting and difficulty in breathing caused by methaemoglobinaemia. Following this, within 24 hours, facial swelling (Figure 3) and swelling of the limbs can occur, owing to the hypoproteinaemia following the acute hepatic damage, and seizures and inco ordination can also be expected. As acute liver failure continues to develop, jaundice and abdominal pain will also be evident, with coma and death following in more severe cases.

Figure 3: Facial swelling often associated with paracetamol toxicity


As with most poisonings, unless ingestion is witnessed, diagnosis will be made by evaluating the clinical signs along with the owners history. Blood levels of paracetamol can be analysed, but results may take several days to become available, which is valuable time lost to begin treatment and improve outcome.

It is, however, possible to assess the concentration of methaemoglobin in a patients blood and establishing this will help to develop an accurate treatment plan and to gauge prognosis.


Treatment of paracetamol toxicity can be lengthy and varied owing to the extensive damage it can cause, especially in more severe cases. Induction of emesis within two to three hours of ingestion is important, followed by the oral administration of activated charcoal (l-3g/kg). This binds to remaining toxins in the stomach and can be repeated as required.

Considering the expected hepatic changes, intravenous fluid therapy and regular monitoring of liver biochemistry parameters is also important in these patients. In order to help prevent ongoing damage to the liver, cimetidine should be administered (5-10 mg/kg orally or intravenously) to inhibit oxidative liver damage and aid in reducing further toxin metabolism.

A drug developed for use in humans, acetylcysteine (Parvolex), can also be used in dogs to reduce the extent of liver damage caused by paracetamol overdose, if given within eight hours of ingestion (140 mg/kg intravenously). Acetylcysteine works by deactivating the toxic metabolites and is very effective in preventing lasting hepatocellular damage.

In very severe cases, in which an established methaemoglobinaemia is present, whole blood transfusions may be necessary to restore haemoglobin concentration. Use of intravenous methylene blue (1-2mg/kg) may be indicated artificially to restore the iron concentration in haemoglobin, although it is not often used owing to the further risk of side effects.

Administration of oral ascorbic acid (30mg/kg) can help to convert methaemoglobin back to haemoglobin, although it isn’t always very effective in severe acute cases.

Basic nursing care should not be overlooked and supplemental oxygen is paramount in patients with respiratory distress and reduced oxygen saturation.


With prompt and aggressive treatment, recovery from paracetamol toxicity is possible. However, a number of cases develop permanent liver damage and higher toxic doses predictably result in a more guarded prognosis and can end in death.


To summarise, the poisons discussed are all common household items and it should be possible to prevent dogs ingesting them (Table 1). The key point in discussing these poisons is that owner education is vital to help avoid poisoning in the first place.

No caring dog owner would intentionally harm their pet if they knew the risk involved in giving any of the three agents discussed above, 


Angel Thompson RVN MBVNA

Angel Thompson, RVN, works at Dick White Referrals in Suffolk and has particular interests in internal medicine and oncology.

To cite this article use either

DOI: 10.1111/j.2045-0648.2012.00226.x or Veterinary Nursing Journal Vol 27 pp 380-382

• VOL 27 • October 2012 • Veterinary Nursing Journal