Between a rock and a hard place – Urinary tract obstructions in cats


Winter is coming and cats are spending more time indoors. Whether or not this is the reason, we have had a recent spate of a particular type of emergency that we see in cats -> lower urinary tract obstructions.  The blocked cat is your classic all or nothing emergency, like GDVs in dogs.  If it is not fixed urgently, the feline will not survive.  However, it is not necessarily an easy or straightforward complication to deal with. For nomenclature’s sake, we call the condition FLUTD (Feline Lower Urinary Tract Disease) obstructed.

Urinary tract obstruction secondary to FLUTD occurs almost exclusively in male cats.  It is not solely to do with development of crystals and stones in the bladder as sometimes crystals are not identified. Male cats have a longer and more narrow urethra than females, so they do tend to be more prone to blockages.

The exact cause for most cases is not clear -> why do some cats form crystals and others don’t?  Why do some obstruct without crystals being found? The majority of obstructed cats have struvite crystals forming a plug at the tip of the penis, the most narrow point of the anatomy.  Struvite are a particular type of crystal commonly formed in bladders, particularly when the urine pH is abnormal or there are build ups of certain minerals in the urine.  There are thoughts that factors including the cat’s metabolism, stress, genetics, body weight and diet play a role.  Stress does seem to be commonly associated with FLUTD, though is not always easy to identify in cats.  Cats can be very highly strung and very much creatures of habit.  Factors such as small changes in the household environment can play a role (i.e. a new rug or set of cushions even!).  Indoor cats are often overrepresented with urinary tract obstruction.  They may have periods where they do not drink enough to dilute their urine, or may not urinate as often to empty the bladder of the smaller crystals, leading to a build up of crystals resulting in obstruction.

blocked tom

The onset of urinary tract obstructions is not always obvious.  Some cats may show signs of straining to urinate, passing small volumes of bloody urine, occasionally urinating in inappropriate locations.  Others may just become more lethargic and particularly where entirely indoors, may not be noted to urinate for a day or two.  They develop very tense and painful bellies.  Diagnosis is often very quick with palpation of a large, often rock hard bladder in a painful abdomen.  Examining the prepuce may reveal evidence of crystals at the tip of the penis, or sometimes a discoloured (often purple) penis.

It is critical that these patients are attended to as early as possible.  Urine is full of toxic metabolites, on a course for elimination.  If they are unable to be eliminated, they build up in the blood stream leading to a range of complications, the most serious of which involve the heart function.  Untreated, an overload of potassium will eventually cause the heart to stop, and potassium can build to very high levels in urine.  Other signs noted include general malaise, vomiting, dehydration and depression as the problem evolves. Kidney function is also impaired by the pressure building in the bladder backing up to the kidneys, in combination with the dehydration that develops and the resultant cardiovascular compromise.

A quick assessment needs to be followed up by blood tests to evaluate the levels of potassium and kidney enzymes, as well as an ECG to categorize cardiac function.  If the heart function is abnormal and the potassium level very high, medical intervention may be necessary to improve these factors prior to anaesthetising for unblocking the urinary tract.  Once satisfied the patient is stable for an anaesthetic, the unblocking process can proceed, however, some patients won’t be stable until they are unblocked, so tough decisions may need to be made. Unfortunately, some patients will not survive the unblocking process if they are critical enough.

Unstable patients can also be unobstructed under epidural anaesthesia (a particular blockade called a “coccygeal block” can be performed at the tail base).  Relieving the obstruction can be challenging in some patients and potentially traumatising in itself.  In rare cases, an emergency perineal urethrostomy (surgery on the penis) needs to be performed as the only way to relieve the obstruction.

Once the passage is opened, we aim to flush the urethra and bladder with sterile saline to aid removal of as much crystal content as possible.  An indwelling urinary catheter is then placed and maintained for 24-48 hours, usually with a closed collection bag attached to monitor urine production.  Fluid therapy is very important in the post-obstructive phase and the challenge is to balance rehydration of the patient with a potentially greater urine output as the kidneys kick back into action and try to eliminate the accumulated toxins.

Medications, such as muscle relaxants and anti-anxiety drugs, may be utilised after the obstruction is relieved and the patient’s blood work begins to return to normal.  Sometimes very dramatic elevations of kidney enzymes are seen on the blood tests and fortunately, these often improve very quickly once the obstruction is relieved and appropriate fluid therapy is provided.  Antibiotics are rarely needed and should only be used if there is a proven urinary tract infection (UTI).  In general, they ideally should be withheld until the catheter is removed since this can encourage development of UTIs.

The next step is to remove the urinary catheter and monitor the cat until he begins to urinate on his own. This is extremely important, since some cats may obstruct again once the catheter is removed, especially if there are any residual crystals hanging around in the bladder. More often the type of complications I see after catheter removal involve irritation to the urethra caused by the crystals/obstruction, the catheterisation process or a combination of the two. The urethra is quite muscular and when irritated through this process, can spasm after the catheter is removed. This can sometimes lead to a functional obstruction rather than a physical obstruction. Regardless of the issue, if the cat cannot pee, it may need to be recatheterised.

Recurrence is common in these boys, unfortunately. We do send them home with special diets and instructions on environmental enrichment, however, it can occur again despite all best intentions and interventions. When this is the case, surgery can be very successful in reducing the recurrence rate (again may not be 100% successful if a stone lodges high up in the urethra). Amazingly many owners are proud to admit their cat has “had a sex change” – well, it is not really a sex change, but the anatomy of the penis is altered so the tip is more open, and I suppose the “boy bits” do resemble “girl bits” a little more closely. After the surgery, the boys may be more prone to urinary tract infections since one of the primary defence mechanisms has been removed, so cystitis can still occur and urination needs to be monitored.


Urinary tract obstruction is an issue that requires dedication from the feline owners since it can be an expensive outcome with potential for ongoing costs. It certainly highlights the need to closely observe your pets and quickly seek advice if anything seems amiss.



Grapes of wrath…or raisins if you choose

Such sweet, sweet juicy delights can be a dangerous feast for a curious pup.  Grapes and raisins are not something most people would associate with poisons, however, in the wrong belly they can present a serious danger.  Once used as a sweet training tool, today, the grapes should be hidden from your pup instead, lest they are one of the few who react negatively to the fruit.

We have recently had a spate of grape and raisin ingestions seen at the hospital.  Fortunately, all cases were fine and none of our patients developed harmful consequences.  But it got me thinking about the knowledge gap that surrounds commonly accessible household foods and other items that may pose a risk to pets.  I know of many friends and clients whose dogs often eat grapes and do not suffer any ill effects.  However, in the wrong bellies, grapes and raisins have the potential to cause a life threatening acute kidney failure.

How does this happen?  This is what we still do not know, and it is only the past decade or so that grape toxicity has even become a recognised problem.  The actual mechanism of toxicity is not clear and various studies have been performed to try to identify the toxic agent.  Various theories have included a toxin in the skin, in the pulp, or even involving the pesticides used in production.  A more recent study has suggested that one of the sugars may be at fault.  The weird thing is that only a handful of animals will have severe reactions, so it is considered an “idiosyncratic reaction”.  An idiosyncratic reaction is one which occurs rarely and unpredictably, so it may occur in one pet and not another.  There is some thought that a certain amount of grapes need to be eaten but this is not well known either.

At the end of the day, whether or not your dog will react is unpredictable, so the best course of action is to avoid grapes and raisins all together but if exposed, seeking veterinary advice is a must if you wish to avoid potentially losing your friend.

Baskin, one of my recent patients who ate a couple of grapes.  He had intravenous fluids for two days and went well.

Baskin, one of my recent patients who ate a couple of grapes but thanks to committed owners, he recovered uneventfully.

What might happen?  The initial sign that your dog might not be tolerating the grapes may be the development of vomiting within the first couple of hours after exposure, followed by diarrhoea, lethargy and increased thirst over the following 5-6 hours.  Kidney failure can develop during the next 1-3 days and may cause further depression, gastric signs and weakness.  At this point, treatment may not be successful since kidney failure can be rapid and irreversible following acute toxic injury.  It is possible that the earlier signs may not be seen prior to the onset of significant kidney damage so it may not be a good idea to wait, just in case.

Treatment can be commenced from the time of ingestion and ideally your dog should be seen within 2 hours of ingestion so that your vet can make it vomit up the grapes.  After emesis, activated charcoal is given either in food, or by messily syringing into your dog’s mouth.  The charcoal may bind to the toxin, and I say may, because we don’t know what the toxin is so can’t be sure that it will bind to charcoal.  However, this is standard decontamination procedure and is unlikely to lead to any harm.  Gold standard treatment is to admit all animals who eat grapes into hospital to administer intravenous fluids for 48 hours so as to support kidney function.  Kidney enzymes should be examined at the commencement of treatment and followed up over the following 72 hours to ensure they remain normal and ensure the kidneys have not received a significant insult.

So is treatment absolutely necessary?  Essentially deciding to do nothing is potentially putting the pet’s life at risk and the outcome could be dire.  Appropriately treated, animals respond well, so difficulty to know whether they would have reacted or not.  Is it worth the risk?

Summertime fun 3 – Not drowning, waving…


Who doesn’t love a romp on the beach?

I used to enjoy seeing the band of this name back in the 80’s (showing my age) so couldn’t resist the title for my next post on near drowning episodes (hope they don’t mind?).  Oh, the beach is such a wonderful place to spend the summer here in Australia, and who can pass on a cool dip on a hot summer’s day?  Dogs sometimes love the challenge of rushing out through the whitewash to chase a stick or rubber ball (though hopefully after one of my earlier posts, my readers will not be throwing sticks for their dogs!).  But the turbulence can be too much for some of them and while a belly full of water is not a fun way to end the day, lungs full of water is even worse!

Near drowning, or submersion injury, may be seen at the beach or in the backyard.  There have been a few older patients we have seen who have mistakenly stepped off the edge of the pool, not realising exactly where they were. Death from submersion falls into two categories – drowning deaths and near drowning deaths.  The drowned patient is one who succumbs to the event and dies within the first 24 hours.  The patient suffering from near drowning experiences a period of suffocation during the submersion but survives for at least 24 hours or more.  This all sounds a bit depressing so I will insert here that animals can survive near drowning episodes (as can humans), so it is not all bad, but it can be difficult.

The events in near drowning involve the initial submersion and panic with aspiration of a small amount of water which causes the larynx (or voice box) to spasm with a resulting apnoea (discontinuation of breathing for a period).  If the struggling continues, more water may be taken on board, both into the lungs and belly, which may lead to vomiting, aspiration of stomach contents on top of the water, and loss of consciousness.  The most significant effect of near drowning is the disturbed oxygen supply to vital organs which, aside from the lung injury that occurs, leads to secondary organ injury.  This may contribute to death at a later stage as a result of organ failure.  So, near drowning can be a true global disorder.

The take home message at this stage – if your pet survives the initial near drowning insult, it may still die, so try to maintain a positive outlook and let the vets do their job to the best of their abilities.  There could be a long road ahead.

It does not require a lot of water to cause significant impairment of gas exchange in the lungs.  As little as 1-3ml per kg of body weight can interfere with lung function.  I remember a time when we discussed whether it was better to have a salt water vs a fresh water near drowning, but at the end of the day both are very damaging to the lungs.  Fresh water tends to disrupt the surfactant lining the lung.  This is a type of fluid which allows the lung pockets (alveoli) to open and close during ventilation without friction, and so loss of surfactant results in further trauma to the alveoli and collapse (atalectasis), essentially shutting down parts of the lungs.  Salt water tends to draw fluid into the air spaces diluting the surfactant and obstructing the passage of gas exchange through the air pockets.

Other factors which can impact on the severity of lung injury include contaminants in the water.  Chlorine is irritating to lung tissue, and freshwater bodies may be contaminated by bacteria and other organisms.  Salt water/sea water may also contain bacteria and algae, sand and other particulate matter that can irritate and damage the airways.  Pneumonia is, thus, a common consequence of both types of near drowning.


Lateral chest x-ray of a dog after a near drowning episode at the beach. There is some aeration of the top (dorsal) of the chest field but the ventral (lower) field is moderately consolidated


Front on view of the chest of the same patient. The lungs are much “whiter” than they should be as a result of fluid being drawn into the air spaces. This interferes with adequate ventilation and essentially blocks the passage of oxygen across the pulmonary surface.  This patient actually did really well and was discharged two days later.

Aside from lung injury, the resulting hypoxaemia (or, lack of oxygen in the blood) affects normal tissue metabolism and can lead to secondary heart and brain injury.  In fact the most common cause of death in these cases is acute, severe cerebral hypoxia (brain damage due to lack of oxygen).  In some cases, the pressure around the brain can rise as a result of hypoxia, and this requires careful monitoring to detect and control, to help reduce further brain injury.

A lack of oxygen makes the blood more acidic (metabolic acidosis) which can have profound effects on the heart.  Cardiac function is impacted on by direct damage to the heart muscle and the electrical circuitry from hypoxaemia, which will affect the amount of blood the heart is able to pump (cardiac output).  Reduced cardiac output leads to reduced organ perfusion thus promoting a vicious cycle of cardiovascular dysfunction and contributing to death.

Patients who survive the initial episode may be awake and responsive but showing signs of abnormal and rapid breathing, potentially seizures or “syncope” (a sudden loss of consciousness not associated with a seizure), and lethargy with minimal exertion.  They may have cyanotic (purplish/blue) gums and may be coughing.  They may be responsive but in an obtunded or semi-comatose condition.  They should be evaluated by a veterinarian immediately.

At the veterinary hospital, they will be provided with oxygen support and an intravenous catheter will be placed to draw bloods and allow fluids to be provided for support of blood pressure and perfusion (blood flow).  Several parameters will need to be evaluated including general ABC’s if the pet is poorly responsive, body temperature, oxygenation of blood and blood gas analysis, and a neurological assessment.  A chest x-ray will be taken but may not be overly informative initially.  Changes in lung disease can take time to reach their full potential so serial radiographs are most informative.  If severe lung pattern alterations are evident on initial x-rays, the patient may not survive without aggressive respiratory support.

Initial diagnostic tests will likely need to be repeated at points throughout the patient’s stay in hospital (yes, it will be recommended that your pet stays in hospital!).  Things can change dramatically during the first 12-24 hours following a submersion, and often for the worse.  Monitoring of oxygenating ability may indicate that a patient needs support to breathe more effectively.  Some patients will require induction of general anaesthesia for mechanical/assisted ventilation, since this may be the only means of adequately oxygenating the lower airways and aiding gas transportation into the blood stream.  Unfortunately, there is no way of removing fluid from the tiny airways and alveoli of the lungs, so ventilation support is the only means by which some of the collapsed airways can be opened for breathing.  Ventilation may also be required for support of brain injury by ensuring that the body’s carbon dioxide levels do not build up too high if the patient becomes tired of working hard to breathe.

Other therapies may include antibiotics if an infectious pneumonia is proven or suspected, and other medications to help reduce pressure around the brain and support cardiac function, if indicated.  Outcomes in near drowning cases depend on the extent of lung damage (which may not be obvious initially and may progress with time), the neurologic status (severe changes are unlikely to correlate well with survival) and whether the patient requires mechanical ventilation.  The need for ventilation in itself is not a good sign for survival where lung disease is a factor (note that with tick paralysis, the lungs are often healthy, the patient is just tired, so a better outlook can be expected).  If looking for a number that allows us to say what the chances of survival are, a paper written in 2008 by Heffner, et al (JAVMA) suggests a survival rate of 64%.  Not bad but not great either.  Not a great way to end a lovely relaxing day on Australia’s beautiful coastline!

Summertime fun part 2 – sand and sea


The beach can be a great place to walk or run a dog.  Fresh sea air is exhilarating in the summer and many dogs love running in the sand and chasing balls out in the waves.  It’s a great place to be getting some exercise but as pet owners, we need to be on the lookout for potential problems as well.

A romp in the sand can potentially lead to gut problems.  Sand impaction is not a lot of a fun and is occasionally seen in dogs after playing at the beach.  It is not as though most dogs set out to eat half the beach, but picking up balls, sticks or other toys off the sand, digging for interesting smells or other activities can result in a belly full of sand.  Many owners are not even aware that their pet has eaten a significant amount of sand until they see the radiographic evidence.

You can imagine what a cup full of sand looks like in a bowl of water, how heavy it is and how quickly it sinks to the bottom.  As the water is drained out, the sand congeals and runs as a sludge from the edge of the bowl.  In the gut, that is exactly what happens.  The sand compacts and will sit in the intestine, prevent normal gut movement and cause the pet to feel nauseous.

Summer Bummer: Sand Impaction  By Ann Hohenhaus, DVM

The large white loop reveals the hidden sand impacting in the gut

Most dogs with sand impaction present to the vet with vomiting and dehydration.  Without appropriate care, recovery can be very slow and death is a possibility if there is enough sand impacted in the gut for a long enough time.  Intravenous fluid therapy is often vitally important to treat the dehydration and fluid lost from vomiting as well as to hydrate the gut and improve movement of the intestine.  Horses with sand impaction are often given certain types of oils to help loosen the sand and get it moving, however, these mineral oils can have a particularly nasty effect on the airways if they are vomited up.  Horses can’t vomit (truly!) so that is rarely an issue, but aspiration pneumonia from mineral oils in dogs can be devastating.  The alternative is lactulose, a synthetic sugar substance that can help with constipation.  Aspiration pneumonia from vomiting lactulose is still not going to be nice but probably will have a better outcome than mineral oils in the lungs.

It can take days to get the sand moving and out and it can cause a lot of irritation along the way, not to mention the discomfort of actually defecating the material out of a soft fragile anal sphincter!  Ouch!  So lots of fluids, lots of pain relief, and hopefully at the end of it a happy and more comfortable pooch.

The other common issue we see, in terms of what dogs like to ingest at the beach, is salt water ingestion, which can potentially lead to salt toxicity.  The milder forms are not such an issue and I will never forget the day many years ago that I took my young dog to the beach.  She decided salt water was for drinking, and an hour or so later (just to show how rapidly salt water can pass through the gut) she had the nastiest watery diarrhoea I had ever seen.  Picture a hose turned on from her rear end!  She was fine after relieving herself, however, care needs to be observed that there are no ongoing gastrointestinal signs following this type of situation.  Any ongoing vomiting or diarrhoea after the beach needs to be assessed as there may be another underlying cause.  And any signs of depression after a day at the beach should be addressed also.  There may be a toxin involved, or it may be that your dog has drunk enough salt water to cause salt toxicity.

Salt toxicity needs to be treated carefully, particularly if the pet is dehydrated and more importantly if it has been more than 12-24 hours since the inciting event occurred.  Providing too much of the wrong fluid too quickly to rehydrate these patients can cause severe neurological damage which may be permanent.  The mechanism is complicated to explain, but essentially it has to do with a disparity that can develop in the sodium levels between the blood and the brain with a result that the brain tissue can swell inappropriately if too much low sodium fluid is provided too quickly.  The important message from this for the pet owner at home is that if they think their pet is dehydrated from 1-2 days of poor or inappropriate fluid intake careful rehydration is extremely important.

Many dogs love the beach and careful pet ownership extends to keeping a close eye on their behaviour and actions by the seaside.  And don’t think this is the last you’ll hear from beach -> next up, near drowning episodes!

Summertime fun – Beachside delicacies

Spring and summer are busy times in emergency practice, and there have been many distractions keeping me from my blog.  The biggest has been sleepiness – you can only be sleepless for so long before the brain starts to slow down and demand rest.  So that is what I am currently trying to do, catch up on some sleep and enjoy a rest by the seaside.

I started thinking about some of the issues we might face by the seaside.  Of course at this time of the year, there is always the threat of snakes when wandering through bushland on our way to the water’s edge.  Pet emergencies can truly happen anywhere and dogs should always be supervised.  The beach is no less of a threat.

A doggy day out at the beach can easily end in a visit to the emergency room.  Dogs eat sand, drink salt water, try to tackle pounding waves (sometimes nearly drowning in the process), and occasionally they encounter nasty creatures such as the blue-ringed octopus, jelly fish, toxic shellfish and for some reason, the doggy favourite, puffer fish.

Watch out for these beasties on the beach!

Watch out for these beasties on the beach! (Photo: Wikipedia)

Puffer fish (also toad fish and blow fish) are a delight for dogs to try – the stinkier the better!  According to a Western Australian Government Dept of Fisheries fact sheet (…fishing/fact…/fact_sheet_blowfish.pdf‎), they are the second most poisonous vertebrates in the world.  Of course we have them here in Australia!  They are members of the family Tetraodontidae and they carry a poison in their skin and internal organs called tetrodotoxin.  Tetrodotoxin is liberated by bacteria in the fish’s gut, the toxin then being absorbed into the blood and heading toward the liver and skin of the fish.  It is not toxic to the fish themselves, but is a useful defense against predators.  Consequently, for most dogs that just taste the fish, the signs of toxicity may be minimal or non-existent, but for those who eat the whole fish, the result can be fatal.

The toxin is a neurotoxin (affecting the nervous system) and blocks nerve conduction, particularly in the heart and brain.  Signs of toxicity often begin with gastrointestinal signs such as vomiting and/or diarrhoea.  Vomiting can be very helpful and may aid in eliminating the offending agent and providing a diagnosis.  Other signs that may develop include tremors, hind limb weakness/ataxia, breathing difficulties and occasionally seizures.  Without appropriate supportive care, death occurs from respiratory paralysis and cardiac failure.  Neurological signs can take 1-4 hours to develop, so pets should be closely observed if they eat unknown objects from the waterfront.

There is no antidote to tetrodotoxin paralysis but it can be effectively managed with seizure control if indicated, assisted ventilation and cardiovascular support.  The toxin generally wears off over 24 hours following exposure provided appropriate supportive care is instituted.  Most dogs will return to full and normal function as though nothing ever happened.  And so they can run back to the beach, where you may have to watch out for a second problem!

It is one of those unfortunate conditions where an unexpected crisis may result in either death or a hefty veterinary bill.  Another reminder of the benefits of pet insurance.  I will endeavour to write more on summertime ills in the next few weeks, till then, I plan to catch up on some more sleep!

To bleed or not to bleed – Rat bait poisonings

Lots of options for getting even with rats, if that's what you're after.

There are other options to removing rodents if you have pets. I must admit, my cat does a fine job at killing the ones around our house and I’m not talking about the out of doors variety!

Rat bait, or rodenticide, poisonings are a relatively common occurrence in emergency practice.  The majority of cases present after the owner has noticed some baits moved about where their dogs may have access, or occasionally, they notice very green pooh which may indicate what pooch has been eating.  In the past weeks we have seen two clinical cases of rodenticide poisoning in our veterinary hospital, as well as the early non-clinical ones, which made me think, maybe it is time to write a blog about the dangers of rat baits.

Funnily enough, many people think if their dog eats the rat bait, they will get sick very quickly.  I’m not sure what signs they are expecting…vomiting? Diarrhoea? Seizures?  Rodenticides don’t cause any of these signs in the first day or two, and in fact not cause any abnormal signs initially apart, perhaps, from green pooh!  The vomiting, diarrhoea and seizures may develop several days later, but that depends on which organ system is first affected by the poison.

Rat baits cause a slow and probably very horrible death for rats.  They are designed so that the rat will eat the bait and go away to die in their nest, and hopefully the human in charge doesn’t have to see rotting mice bodies lying around their kitchen.  At least that is one way to put it I guess.  When dogs eat the bait (cats are a little smarter but are at risk if they eat the rat before it is killed by the bait) it will similarly take several days before the signs develop.  This can lead to a false sense of security for the pet owner who is expecting their dog to start seizuring or vomiting or show some other sign of poisoning, only to find them flat and pale several days later.

How do they work?  Well, there are a few different generations of rodenticides with the newer ones taking longer to kill and requiring a longer course of treatment.  Warfarin is the earliest type and is still used today.  It is much shorter acting than the newer poisons and only requires a week of therapy to reverse the signs.  The longer acting, newer generation rodenticides require up to 4 weeks of therapy.

Rodenticides act by causing a depletion of vitamin K1 in the liver.  In the healthy animal, vitamin K1 is utilized in the formation of clotting factors and then regenerated in the liver by another mechanism.  It is not a vitamin that is commonly obtained through food, like vitamin C for example.  The rodenticide blocks this recycling step so that there will no longer be any active vitamin K1 for inclusion in the production of clotting factors.  It takes time for all the clotting factors that have been produced to be utilized in the body but once they have passed their “use by date”, the body’s internal homeostatic mechanisms don’t function as well so normal tissue repair cannot occur and animals can bleed to death.

Often the cause of such severe internal bleeding is not obvious, however, without treatment it will not cease and death will occur.  Without fail.  Signs of rodenticide poisoning are not always clear.  In some cases blood loss is not obvious, particularly if the animal has bled into the brain cavity or the spinal cord.  Such bleeds may cause the animal to have seizures or become paralysed, respectively.  In many cases, the bleeding occurs into the abdomen or chest cavities though other sites are occasionally seen.  One of our patients bled into the bladder and was seen to pass urine that looked exactly like blood!

The treatment for rodenticide toxicity is so easy and simple to perform if implemented early, and so there is really no reason why it shouldn’t be sought early when owners are aware of their pet’s access. Treatment involves making the dog vomit if caught within hours of ingestion, possibly followed by administration of activated charcoal to mop up any toxins that may be wandering around the gastrointestinal tract.  Charcoal will not provide any benefit once the clinical signs have developed.

If the ingestion has been caught early, lots of the poison has been vomited up and there is a very strong assumption that the dose eaten may be less than that required to cause clinical poisoning, the dog may not require any treatment.  However, this is ideally a decision for your vet to make.  If the decision to NOT treat is made, it is extremely important that your dog has a blood test 48-72hrs later to determine for certain whether or not treatment is required (one very specific blood test may tell us if there is a problem developing with blood clotting).

Fortunately there is an antidote, vitamin K1 tablets (injection or liquid forms are also available).  That’s right, just a simple, twice daily vitamin tablet!  Yep, this simple vitamin will ensure that your dog, who may have eaten a whole packet of rat bait, will not bleed to death as a result.  Ok, maybe it is not as simple as that, I mean you can’t just go to the pharmacy and buy a multi-vitamin for your dog, and the wrong type of vitamin K won’t do an awful lot of good.  The medication is not cheap, however, much more cost effective and successful than treating with fresh frozen plasma and possibly blood transfusions if the dog reaches the point of severe internal haemorrhage.

It is not worth taking the risk with your pet if you think they may have, or know they have, eaten a rat bait.  Even if you make them vomit at home yourself, it is so important to have a vet check them than to just sit and wait until you see signs of poisoning.  Why gamble with your dog’s life?

Fortunately the two dogs we saw, despite coming into the hospital looking close to death, responded extremely well to therapy and within 24 hours were bright and happy with no further bleeding.  The last point I wish to make is to never assume that because the bait is placed in a position where you think your dog can’t reach it, that your dog won’t reach it.  They are ingenious at accessing the unaccessible, and more so if your rats have shifted the bait from one place to another!

A sticky situation

Who would have thought a fun game of catch could have such a traumatic outcome?  A play in the park with a ball or a stick is usually par for the course for many large active dogs, yet even something as simple as throwing a stick can land in a trip to the emergency room.

 We had a patient in a little while ago, Jasper, an Australian Cattle dog, who simply loves a game of stick chasing with his owners.  At least that was until the night he came in to see us with the end of a stick emerging from his mouth.  Dad had been throwing quite a long narrow stick and Jasper had managed to land end-on on the stick, basically impaling the stick down his throat.  The stick had been longer, but for comfort sake, Jasper had managed to chew the long end off so he could actually close his mouth.  The question was how much more stick was in his mouth/throat, and where had it lodged?  Had it damaged any important structures?

Jasper’s owner was keen to get his boy fixed, so Jasper was anaesthetised to have some x-rays performed to assess the path of the stick prior to carefully removing it.  Sticks and wood are not easily identified on radiographs as they tend to blend in with the surrounding tissues.  So I considered injecting some contrast solution (Iohexol -> a benign sterile agent) around the stick to see if we could see where it was.  The pictures worked well and we could see importantly that it had not penetrated the chest cavity, and did not appear to have caused interference with the oesophagus or trachea.

For those unfamiliar with radiographs of the neck, this may not mean a lot. The normal structures are the vertebral column and the endotracheal tube maintaining gaseous anaesthesia can been seen as the straight lines down the airway. The hazily outlined structure between is the stick!

The stick was carefully removed and we explored the wound with endoscopy.  Unfortunately, Jasper had managed to have this accident with a stick covered in bark, and there were thousands of tiny pieces of bark along the track the stick had made.  There was no way I would be able to remove them all so we attampted to provide a drainage solution.

We see this often with stick injuries where tiny pieces of bark remain in the tissues and cause ongoing problems, developing abscesses intermittently and sometimes requiring repeated investigations.  This material will track around the body via tissue planes and can be exceedingly difficult to locate and remove.  His owner was warned of potential complications with foreign material inside his neck as is commonly seen.

Jasper and the stick we removed from his mouth & neck

Jasper and the stick we removed from his mouth & neck

So not surprisingly, Jasper had a couple of repeated occurrences of draining neck wounds which failed to respond to antibiotics.  He was eventually referred back to our hospital to see our surgeon.  By this point there was a lot of scar tissue and several pockets of pus found.  The surgeons explored these pockets and hoped to remove the source of his infection.  He recovered well and hopefully will be out of trouble now.  These wounds can be very difficult to get on top of at times though and there is still a chance that small amounts of material remain behind.

Interestingly, the Australian Veterinary Association has recently released a report encouraging a ban on throwing sticks for dogs given the number and extent of injuries seen.  A veterinarian from the RSPCA has stated that stick injuries are seen at least once a month at emergency facilities, and I expect our figures would support this.  Many are small wounds to the back of the oral cavity, however they can be far more sinister.  One recent patient seen at the hospital developed severe and critical complications secondarily to a stick injury, and succumbed to those complications despite our best efforts.

Moral of the story, if it is small enough to enter the mouth, and sharp, it is probably too small to play with…  And there is more than one way to impale a dog on a stick, as one of our other vets tells the story of a patient who managed to stop his down hill run on a large branch which went through his chest and abdomen.  He survived fortunately and amazingly!  Maybe a good solid rubber stick is the way to the future of stick play.