006 Christmas Hazards for Dogs and Cats

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Likely higher incidence of poisoning around festive period, especially dogs
Three main scenarios:
•    Pet scavenges something poisonous
•    Well intentioned blissfully unaware pet carers offer their pet a poisonous holiday treat or two
•    Kids – or drunk adults! – do not comprehend the risk and give the pet something poisonous

Large number of potential poisons. Here are a few:


Toxic substance is theobromine: methylxanthine-derived alkaloid that occurs naturally in cacao beans and is found in chocolate, cocoa powder and other products produced from these beans.
Chocolate contains a lesser amount of caffeine which is also a methylxanthine
Theobromine concentration varies between types:
Plain (dark) chocolate and cooking chocolate generally contain significantly more than milk chocolate
Theobromine content of white chocolate is considerably lower; theobromine poisoning from white chocolate is rare
Cocoa beans, cocoa powder and cocoa shell mulches contain the highest concentrations of theobromine

Be vigilant as chocolate products may contain other potential hazards, e.g. raisins, currants or sultanas; diabetic chocolate products will most likely contain xylitol

Dose-dependent toxicity
Doses can be found in various online and offline resources

Theobromine stimulates the central nervous system with consequent neurological, muscular, cardiac and/or respiratory effects. Theobromine also causes smooth muscle relaxation, especially of the bronchi, and renal diuresis.

Clinical signs usually develop within 24 hours of ingestion and typically much sooner – within 4 hours. Signs may persist for 48-72 hours in some cases.
Commonly reported clinical signs include vomiting, abdominal discomfort, restlessness, excitability and hyperactivity, ataxia, tachycardia, and tachypnoea or panting. In more severe cases muscle rigidity, muscle tremors, hyperthermia, seizures and dysrhythmias have been reported. Urinary incontinence, polyuria and polydipsia may also occur. Severe seizures and/or cardiovascular compromise are typically reported in fatal cases.

Testing is not indicated in many cases. There are some patients in which doing some form of emergency database, and potentially an ECG, will be appropriate.


Routine GID indicated in appropriate cases. Gastrointestinal absorption is relatively slow in dogs, potentially taking up to 10 hours, so gastric empyting may be appropriate even after a significant delay. Avoid inducing emesis in animals that have contraindications such as significant hyperactivity, other forms of neurological compromise, respiratory issues and so on. Theobromine undergoes enterohepatic circulation so repeated use of charcoal may enhance elimination.
No specific antidote
Therapy is otherwise symptomatic and supportive e.g. intravenous fluid therapy, anti-emetic administration, sedation if excitability is excessive, and routine treatment of seizures. Anti-dysrhythmic therapy may also be indicated in some cases.

Prognosis: generally good with appropriate treatment but may be worse for animals showing marked cardiovascular or neurological signs at presentation.

Vitis vinifera fruits (Grapes, raisins, currants, sultanas)

Nephrotoxicity in dogs; no confirmed cases have been reported in cats thus far but they may be susceptible, unclear.

Same poisoning syndrome may occur following consumption of all types of these fruits including those manufactured organically and regardless of whether the product has been cooked or not. 
Exposure may occur through ingestion of products containing these fruits amongst their ingredients such as some chocolates, Christmas cakes, Christmas puddings, mince pies etc.

Toxin or toxins involved have yet to be identified; mechanism of toxicity is unknown.
Should be considered non-dose dependent or an idiosyncratic type of toxicity. Consider any dog at risk if they consume any of these fruits regardless of how much; not known whether a dog that has previously eaten these fruits and seemingly been fine could the next time they had some go on to develop acute kidney injury. All cases should be treated as soon as possible.

Clinical signs:

Vomiting reported in almost all cases, usually within 24 hours of ingestion. May be related to dietary indiscretion, azotaemia if acute kidney injury has occurred, but a specific effect of these fruits is also suspected given how common vomiting seems to be in these dogs.
Subsequently anorexia, lethargy, diarrhoea and abdominal pain have been reported as has hypersalivation.


Gastric emptying if not already vomiting, then activated charcoal
Hospitalise all cases on intravenous fluid therapy (e.g. 4-6 ml/kg/hour for 48-72 hours): empirical recommendation; not evidence-based but makes theoretical sense
Run baseline blood renal panel and perform urinalysis; repeat 48-72 hours later before discharging the patient. Even if the renal panel remains within normal limits it is worth looking at a urine sediment for casts before discharging the patient because they may suggest that that individual dog has suffered some degree of tubular injury that may prompt a change in the plan.
Standard management for acute kidney injury is indicated in cases in which this occurs


Naturally-occurring sugar alcohol found in low concentrations in various fruits and vegetables; extracted and used extensively commercially.
One main use is as a sweetener in low carbohydrate/low glycaemic index/diabetic products e.g. diabetic Christmas cakes or chocolates
Thought to reduce dental caries formation so increasingly used in various chewing gums, sweets, toothpastes and other oral care products
Also found in some prescription drugs, including veterinary ones as well as some vitamins and nutritional supplements and even canine oral hygiene products!

Xylitol poisoning reported in DOGS; no published reports of feline poisoning

Two phases to toxicity:


Due to dose-dependent increase in pancreatic insulin production that may result in hypoglycaemia +/- hypokalaemia, hypophosphataemia
Usually occurs quickly, certainly within a few hours, but it can be delayed – this will partly depend on the form in which the xylitol was ingested
Rapid gastrointestinal absorption but also some slow-release products; absorption also depends for example on how well the food item was chewed before being swallowed


May cause liver insufficiency or failure
Mechanism(s) unclear
More delayed onset (e.g. 72 hours)
Difficult to predict which dogs will develop liver complications. Not all dogs that develop hypoglycaemia go on to have liver complications; on the flipside a dog may not suffer clinically significant hypoglycaemia but significant hepatotoxicity occurs.

Hepatotoxicity may be dose-dependent but still remains unclear, consider it a non-dose dependent idiosyncratic toxicity at this time. Recommend aggressive treatment for all cases as hepatotoxicity potentially fatal.


Routine gastrointestinal decontamination; tenuous evidence base for activated charcoal but risk-benefit profile positive as is usually the case!
Routine approach to management of hypoglycaemia with parenteral and/or enteral supplementation as indicated
Standard symptomatic and supportive approach to management of hepatotoxicity including appropriate management if coagulopathy develops, possible use of hepatoprotectants, and treatment for hepatic encephalopathy if required. 


Hypoglycaemia alone: generally good with timely and appropriate management. Likely to be worse if repeated bouts of hypoglycaemia occur, especially when associated with central nervous system signs.
Prognosis worse with sustained elevations in liver enzymes; guarded to poor with evidence of hepatic dysfunction; grave for acute hepatic failure.

Dangerous foods potentially more accessible around festive period

Allium species (onions, garlic, leeks, shallots, chives)

These can be harmful even when cooked causing vomiting/diarrhoea but potentially also a non-immune mediated haemolytic anaemia in both dogs and cats. Some of the less obvious sources of exposure include for example sage/onion stuffing, onion gravy.


Some nuts (e.g. peanuts, macademia nuts) may cause vomiting/diarrhoea but potentially also more severe signs affecting the nervous system or muscles.
Potential hazard of chocolate-coated nuts and even chocolate-coated nut and raisin combos!

Mouldy food

May cause neuromuscular signs as a result of tremorgenic mycotoxins; potentially fatal toxidrome that requires aggressive management including intravenous lipid emulsion.



  • All types of lily can cause renal toxicity in cats but not dogs
  • Non-dose dependent idiosyncratic toxicity so all cases should be treated as soon as possible; approach is basically the same as already described for grapes in dogs
  • All parts of the plant can be toxic; also e.g. licking pollen off feet; drinking vase water

Mistletoe: may cause drooling or vomiting but generally not much else in dogs and cats; 

Poinsettia: gets a lot of attention on the internet but usually only causes irritation of the stomach/intestines in cats. Can be more serious but typically isn’t.

If parts of Christmas trees are eaten the ‘needles’ can cause damage and potentially obstruction of the stomach/intestines; rare but be aware!

Potential ‘foreign bodies’: dogs in particular may eat decorations or wrapping paper this may cause drooling, vomiting or diarrhea but in the worst case scenario could cause gastrointestinal obstruction; this is especially the case if a cat tries to eat some tinsel for example and develops a linear foreign body situation.

Weather-related hazards: in countries where Christmas occurs during cold spells, some potential risks include:

Antifreeze (ethylene glycol):

  • Dose-dependent renal toxicity in both dogs and cats
  • All cases should be treated as soon as possible; often by the time patients present the prognosis is grave.

Poisoning from human medications that may be used more during cold periods, e.g.

  • Paracetamol (acetaminophen): cats are much more susceptible
  • Aspirin and other ‘NSAIDs’ (e.g. ibuprofen)
  • Over-the-counter decongestants can be an issue
  • Etc.

May be self-exposure by pet or misguided administration by carer.

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005 Nutritional Management of Acute Pancreatitis

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This episode focuses on the nutritional management of acute pancreatitis in dogs and cats answering questions such as:

  • When should we be providing nutrition to dogs and cats with acute pancreatitis?
  • Should we be using enteral or parenteral nutrition?
  • Should we be using post-pyloric jejunal feeding or is oral or gastric feeding okay?

The episode is largely based around the following clinical practice review article:

Jensen KB, Chan DL. Nutritional management of acute pancreatitis in dogs and cats. J Vet Emerg Crit Care 2014. 24(3):240-250.

As mentioned in the episode, if you would like a FREE copy of some general notes on acute pancreatitis in dogs and cats that cover more than 'just' the nutritional aspects, please click the link box below and follow the instructions:

In the episode I also mention a blog post on syringe feeding which you can find HERE.

One paragraph from the paper that I read out in the episode and promised to include here was as follows:

“The traditional approach to AP centered on the premise that withholding food would reduce pancreatic autodigestion by decreasing pancreatic stimulation and enzyme release. However, the pathogenesis of pancreatitis more likely involves premature intracellular activation of proteolytic enzymes rather than pancreatic stimulation. Avoidance of feeding as a means to decrease pancreatic stimulation may be unwarranted and could lead to malnutrition and impaired gastrointestinal barrier function. Lack of enteral nutrition results in the loss of normal physiologic intestinal motility, is associated with intestinal villus atrophy, and compromises intestinal mucosal blood flow. If sustained, the lack of enteral nutrition could lead to a compromise of local immunoglobulin and biliary salt production with consequent disruption of normal internal bacterial flora and gastrointestinal barrier function. It also has been demonstrated in experimental rodent models and in people with naturally occurring disease that exocrine pancreatic secretion actually decreases during pancreatitis and that the decrease is more pronounced with increasing severity of inflammation. The practice of withholding food for several days from the time of initiation of therapy may prove detrimental as a period of anorexia often precedes the initial clinical presentation to veterinarians in patients with AP. Implementation of nutritional support may be critical for successful management of patients with AP.”

And the list of summary points from the paper is as follows:

  • There is increasing evidence supporting the important role of early EN (ideally within 48 h of diagnosing pancreatitis) in positively impacting outcome in patients with AP.
  • Nutritional support is an integral and key aspect of the successful management of AP.
  • The use of enteral feeding in veterinary medicine is now considered to be safe, effective, and well-tolerated in severe AP.
  • Enteral nutrition is less expensive than parenteral feeding and helps to maintain gastrointestinal mucosal function, and therefore is likely to have a beneficial influence on the disease course.
  • Use of NG, nasoesophageal, jejunal, and oesophagostomy feeding tubes is effective and safe in dogs and cats and should be used unless specific contraindications are identified. There is no evidence at this time to support the superiority of post-pyloric jejunal feeding over oral or gastric feeding.
  • The optimal enteral diet for patients with AP has not been identified, but diets commonly used for convalescing dogs and cats can be used.
  • Avoidance of enteral diets with high fat content does not appear to be necessary in the majority of patients.
  • Despite the growing evidence that EN can be used effectively in the management of patients with AP, there may still be patients that require some form of PN until sufficient EN can be tolerated.
  • And of course we have the usual and completely reasonable conclusion that future veterinary studies investigating feeding routes, dietary composition, and optimal timing of nutritional support in AP are warranted.

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004 Fluid Choice in Tomcat Urethral Obstruction (Blocked Cats)

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Not all blocked cats are hypoperfused on presentation but those that are should be resuscitated with fluid therapy given as boluses to restore perfusion with the approach being tailored to the individual patient. This should be done BEFORE you consider sedating or indeed anaesthetising to attempt catheterisation.

Will I rupture the bladder?

“If I give blocked cats lots of fluid therapy while their bladder is obstructed, won’t I rupture the bladder?"

NO! The risk is very very very small and has to be weighed up against the undoubted benefit of fluid resuscitation in these cases. 

Why won't I rupture the bladder?

For the kidney to make urine it needs to have an adequate blood supply. The blood supply to the kidneys of a blocked cat in shock will be moderately or even severely compromised and this means that the impetus to make urine will be significantly decreased. At the same time as the bladder is obstructed and under high pressure this pressure is transmitted via the ureters to the kidneys; this back pressure on the kidneys will also act to oppose urine production. So on the one hand there is little forward impetus to make urine and on the other hand there is back pressure not to make urine; hence blocked cats in shock are unlikely to be making much urine at all. Obviously as you perform intravenous fluid resuscitation and the blood supply to the kidneys increases you will promote the formation of urine but you will also be going on to deal with the obstruction very soon and so this is not a concern.


Does it matter which fluid we choose for the initial resuscitation phase?

A replacement isotonic crystalloid is used. Typical choice is between Hartmann’s (buffered lactated Ringer’s solution, compound sodium lactate) and  0.9% sodium chloride ('normal' saline).

Blocked cats have:

  • Hyperkalaemia: clinically significant life-threatening hyperkalaemia is not uncommon in the more severe cases
  • Acidaemia due to metabolic acidosis: typically less of a concern but can have significant adverse physiological consequences and can be life-threatening if sufficiently severe

0.9% sodium chloride:

Potassium-free; blocked cats are hyperkalaemic so why would you want to give them more potassium?

But...promotes hyperchloraemic acidosis and can exacerbate existing acidaemia.

Hartmann's solution:

Contains 5 mmol/l potassium - as do Normosol-R and Plasmalyte 148; this is nevertheless lower than clinically significant hyperkalaemia and use will decrease potassium concentration through dilution.

But...solution that promotes alkalosis, alkalinising solution; may help resolve metabolic acidosis.

(Also contains small amount of calcium which is no bad thing given that these cats are often hypocalcaemic.)

Bottom line: choice of fluid between these two types has not thus far been shown to be clinically significant....

Drobatz KJ, Cole SG. The influence of crystalloid type on acid-base and electrolyte status of cats with urethral obstruction. J Vet Emerg Crit Care 2008. 18(4):355-361.

Prospective randomised non-blinded study

Cats that presented to the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania with urethral obstruction between September 2000 and November 2004 were eligible for inclusion.

Inclusion criteria:

  • Baseline blood pH and potassium measured initially
  • At least one subsequent measurement of these parameters within the following 12 hours

Urethral obstruction diagnosed based on compatible clinical signs + large, firm, non-expressible urinary bladder

Exclusion criteria:

  • Owners elected to not pursue treatment and elected euthanasia
  • Baseline blood pH and potassium as well as one subsequent measurement of those variables within 12 hours of admission not obtained

Coin-flip randomisation to receive either Normosol-R or 0.9% sodium chloride.

Blood samples collected before any therapy for analysis of blood pH, bicarbonate, pCO2, base excess, sodium, chloride, potassium, ionised calcium, ionised magnesium, and glucose.
Biochemical analysis of serum urea nitrogen (SUN), serum creatinine, and serum phosphorus performed on some cats.

Further therapy and monitoring at discretion of attending clinician; non-blinded


  • 68 cats: 39 Normosol-R, 29 0.9% sodium chloride
  • Very similar comparable groups including with respect to initial pH and potassium concentrations
  • While there were no statistically significant differences between groups at baseline, cats in the Normosol- R group had a significantly higher blood bicarbonate concentration at 12 hours and significantly higher blood pH at 6 hours and 12 hours.
  • There were no statistically significant differences in blood potassium concentration or the amount of fluid administered between groups at any time.
  • In comparison with the absolute values, the increase in blood pH from baseline was significantly greater in the Normosol-R group than the 0.9% sodium chloride group at 6 hours and 12 hours following admission and this difference also approached significance at 2 hours.
  • Blood potassium levels declined steadily in both groups and no statistically significant differences were found in the rate of decline from baseline between groups.
  • Cats in the 0.9% sodium chloride group had a significantly higher blood sodium concentration at 2 hours and 6 hours, as well as a significantly higher blood chloride concentration at 6 hours and 12 hours. The increase in blood chloride from baseline was significantly higher in the 0.9% sodium chloride group than in the Normosol-R group at 2 hours, 6 hours, and 12 hours.

Use of Normosol-R was associated with a greater increase from baseline in blood pH and bicarbonate values than was the use of 0.9% sodium chloride.

Although Normosol-R contains 5mmol/l of potassium, the absolute value and rate of decline in blood potassium levels were nearly identical between the groups in this study.

Authors say: “While statistically significant, the differences identified between groups in the present study may not have been clinically significant in this patient population. From both prior research and widespread clinical experience, it is clear that both balanced isotonic crystalloid solutions and 0.9% sodium chloride are acceptable fluid choices for the treatment of most cases of urethral obstruction in cats. However, possi-ble implications of the current study pertain to severely affected cats with profound metabolic acidosis. In these cases, any acidifying effect of 0.9% sodium chloride could be deleterious, as severe metabolic acidosis impairs cardiovascular function, compounding the untoward effects of hyperkalemia and hypocalcemia. The use of a balanced isotonic crystalloid would achieve similar results in the treatment of per-fusion abnormalities and hyperkalemia, along with more rapid improvement in acid–base status.”

Study limitations:

  • Not blinded
  • Treatment not standardised across groups
  • No mention of power calculation with respect to sample sizes needed to show significant different between the groups
  • As always...larger sample size if possible!

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003 Intravenous Lipid Emulsion as an Antidote

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002 Antibiotics in Canine Acute Haemorrhagic Diarrhoea

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Referring here to acute bloody watery diarrhoea from typically diffuse small intestinal disorders (e.g. canine idiopathic haemorrhagic gastroenteritis syndrome); not fresh large intestinal haemorrhage or melaena.

Potential indications for antibiotics?

(1) Primary small intestinal bacterial infection with enteropathogenic bacteria:

Relatively rare
Identification in faeces does not mean causative agent

American College of Veterinary Internal Medicine Consensus Statement* (2011):

Marks SL, Rankin SC, Byrne BA, Weese JS. Enteropathogenic Bacteria in Dogs and Cats: Diagnosis, Epidemiology, Treatment, and Control. J Vet Int Med 2011. 25(6):1195-1208.

“The advent of real-time PCR panels for dogs and cats with diarrhea has provided a new paradigm for the rapid and sensitive detection of toxin genes or organisms associated with disease. Interpretation of these panels can be problematic, however, because virtually all of these bacterial organisms have been frequently isolated from the feces of clinically healthy dogs and cats.”

Discusses Clostridium difficile, Clostridium perfringens, salmonella and campylobacter
Take-home message in each case: antibiotics not recommended unless patient is showing signs of systemic illness.

(2) Bacterial or endotoxin translocation:

Intestinal translocation

Literature (experimental animal, human) supports potential occurrence

So there is potential risk and all these patients should receive antibiotics, right?

Well, if some degree of bacterial translocation occurs the systemic immune response should be able to deal with this unless the situation becomes overwhelming.

Risk-benefit analysis:
Potential benefit: may prevent sepsis if appropriate antimicrobial(s) used

  • Promoting antibiotic resistance; some enteric bacteria develop nasty multidrug resistance!
  • Oral administration may harm normal intestinal flora and thereby reduce competitive antagonism
  • Financial costs
  • Potential drug adverse effects; idiosyncratic reactions

My approach:

Dynamic decision to prescribe antibiotics made on individual patient basis
Does the patient have/does the patient develop clinical findings that raise the index of concern for sepsis risk?
Does the patient have a pre-existing reason to be more susceptible to sepsis?

Criteria include:

(1) Hard to stabilise with respect to cardiovascular status and/or hard to keep stable with repeated episodes of hypoperfusion.

(2) Evidence of SIRS criteria with appropriate changes in heart rate, respiratory rate, body temperature and/or white blood cell count; e.g.

  • Persistent tachycardia, pyrexia, tachypnoea
  • Marked degenerate neutrophilic left shift, lots of bands, severe toxicity; inappropriately normal neutrophil count; and especially neutropenia

(3) Hypoglycaemia (or maybe low-normal blood glucose)

(4) Pre-existing immunocompromise (e.g. chemotherapy) or potentially poor immune function (very young animals?)

Vast majority of canine parvovirus cases receive antibiotics.

This is an opinion- and experience-based approach, both mine and that of previous colleagues.

Here is one paper:

Unterer S, Strohmeyer K, et al. Treatment of Aseptic Dogs with Hemorrhagic Gastroenteritis with Amoxicillin/Clavulanic Acid: A Prospective Blinded Study. J Vet Int Med 2011. 25(5):973-979.

Study type: prospective, randomised, placebo-controlled, blinded
Aim: to evaluate the benefit and efficacy of amoxicillin/clavulanic acid in the treatment of dogs with aseptic HGE.

60 dogs diagnosed with HGE
Inclusion criterion: acute onset of bloody diarrhoea (<3 days)
Exclusion criteria:

  • Patients pre-treated with antibiotics
  • Patients with potential signs of sepsis
  • Patients with haemorrhagic diarrhoea because of a disease aetiology unrelated to HGE (e.g. drug adverse effects, gastrointestinal parasites)
  • Detecting bacteria in the faeces that are considered potentially primary enteropathogens (e.g. Salmonella spp. or Campylobacter spp.)

Potential signs of sepsis defined as:

  • Rectal temperature >39.5⁰C (or 103.1F)
  • White blood cell (WBC) count <4 or >25 109/L
  • Band neutrophil count >1.5 109/L)

Describe various other investigations that to allow presumptive diagnosis of idiopathic canine HGE.

Computer-generated randomisation: 30 dogs in treatment group, 30 dogs in placebo group
Treatment group: amoxicillin/clavulanic acid for 7 days
Other treatments standardised and equal for both groups

Treatment efficacy evaluation:

  • Daily assessment of clinical signs by clinician blinded to treatment using “canine HGE activity index”
  • Parameters scored: patient attitude, appetite, vomiting, stool consistency, stool frequency, dehydration
  • Obligatory hospitalisation for 3 days; thereafter scoring based on owner-provided information

Outcomes compared between treatment and placebo groups:

  • Canine HGE activity index (on any individual day and over whole course of disease)
  • Duration of hospitalisation beyond obligatory 3 days
  • Dropout rate
  • Mortality rate


  • Patients in each group similar and considered reliably comparable
  • No statistically significant difference between outcome measures between two groups
  • 6 dogs in placebo group dropped out of study due to concerning signs (e.g. fever, leukopenia, left-shifted neutrophilia) or not improving as expected

Supports approach of withholding antibiotics from aseptic patients; those not considered to be showing signs of systemic compromise.

** Don't forget the importance of client education on the issue of avoiding unnecessary antibiotic use! **

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