scott@vtx-cpd.com
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Hi,
Thanks for the question. This makes complete sense, and I can see exactly what you are trying to achieve with making the CRIs much more straightforward and practical for everyone to use.
Let me speak to our anaesthesia team and get their thoughts on the best way to structure the dilutions and template, and I will get back to you!
Scott 🙂
Replying to Alison H. 24/09/2026 - 23:01
Yes, Alison, I think that is exactly how I would interpret it too. I don’t think the catheter itself is what is resolving the azotaemia once the obstruction has been relieved. The interesting bit for me was really the association, the more azotaemic cats tended to have their catheters left in for longer and stayed in hospital longer, rather than evidence that keeping the catheter in longer caused the azotaemia to resolve.
As you say, once you have relieved the obstruction, renal perfusion/GFR should recover and the post-renal component of the azotaemia should start improving. The catheter is then buying you reliable urine drainage while the urethral inflammation and spasm settle, as well as allowing us to monitor urine output, particularly when there is significant post-obstructive diuresis.
I suspect there is quite a bit of clinician decision-making wrapped up in the association they found. If I have a cat that arrives markedly azotaemic, hyperkalaemic and unwell, I am much more likely to continue IV fluids, monitor urine output and electrolytes closely, and be cautious about removing the catheter too early. So yes, longer catheterisation may partly be a consequence of those cats simply being sicker and needing longer hospitalisation rather than the catheter being necessary to correct the azotaemia itself.
That is actually one of the reasons I liked the paper, but I wouldn’t interpret it as saying we should leave a urinary catheter in until the creatinine has normalised.
I hope you are enjoying the course!
Scott 🙂
Replying to Laura S. 27/09/2026 - 14:31
No problem!
Thank you again for all of the great questions!
Scott 🙂
Hi Raquel,
Great question. Yes, I have used both Spec fPL and the newer Catalyst Pancreatic Lipase assay, and I think the quantitative in-house test is a useful development. I would be quite happy using the Catalyst PL in the way you describe, alongside the history, clinical findings and ultrasound—rather than routinely sending every sample to the reference laboratory for Spec fPL.
One important distinction is that the Catalyst pancreatic lipase test isn’t the same thing as a conventional serum lipase activity assay. IDEXX designed it specifically to measure pancreatic lipase and to align clinically with their Spec fPL/Spec cPL assays. In their validation data, the feline Catalyst PL showed 87.5% overall categorical agreement with Spec fPL, with good analytical precision. So if you already have the Catalyst in practice, getting a quantitative result in less than 10 minutes is genuinely useful and, as you say, may also be considerably cheaper than sending Spec fPL away.
The change in the feline cut-off is also interesting, but there is a bit of history behind it. The older literature commonly used ≥5.4 µg/L as the Spec fPL threshold for pancreatitis. One clinical study using that threshold reported sensitivity of 79.4% and specificity of 79.7% when cats considered definitely/probably pancreatitis were compared with those considered probably/definitely not pancreatitis.
IDEXX subsequently changed its interpretation following a re-evaluation of the Spec fPL assay. That analytical validation established an upper reference limit of 4.4 µg/L in healthy cats and calculated 8.8 µg/L as a diagnostic decision threshold designed to give approximately 99% specificity against the healthy population. IDEXX therefore now essentially divides results into three groups: ≤4.4 µg/L = pancreatitis unlikely/within the reference range; 4.5–8.7/8.8 µg/L = equivocal, pancreatitis possible; and around ≥8.8/8.9 µg/L = consistent with pancreatitis, depending on whether you are looking at the Catalyst or reference-laboratory reporting convention.
I actually prefer thinking about the test that way rather than treating pancreatic lipase as a binary positive/negative result.
The important caveat is that increasing the diagnostic threshold doesn’t somehow make pancreatic lipase a definitive test for pancreatitis. What it primarily does is make a markedly increased result more specific. There is inevitably a trade-off between sensitivity and specificity as we move the cut-off. A cat with a PL of 5 or 6 doesn’t suddenly cease to have pancreatitis because it falls below 8.8; it means that the biochemical evidence alone is insufficiently specific for us to confidently attribute the clinical signs to pancreatitis.
That is particularly important in cats because pancreatic abnormalities can coexist with gastrointestinal, hepatobiliary and other disease. IDEXX themselves make this point in their current diagnostic algorithm: if another disease is identified, pancreatic involvement may be concurrent rather than necessarily being the primary cause of the clinical presentation.
So I approach these results roughly as follows. If I have a cat with convincing clinical signs, compatible ultrasonographic pancreatic changes and a PL ≥8.8, I am considerably more confident that pancreatitis is genuinely part of the clinical problem. If the result is 4.5–8.7, I regard it as supporting information but certainly wouldn’t diagnose pancreatitis from that result alone. I look particularly carefully at the ultrasound, clinical presentation and concurrent disease. If it is ≤4.4, clinically important pancreatitis becomes less likely, but I still wouldn’t allow one laboratory result to completely overrule a very convincing clinical picture.
That is also why I like what you are already doing by combining pancreatic lipase with ultrasound and the clinical presentation. Neither test is perfect. Ultrasound is operator-dependent and pancreatic changes are not synonymous with clinically significant pancreatitis, while pancreatic lipase gives us biochemical evidence of pancreatic injury but doesn’t tell us whether the pancreas explains everything that is happening to that particular cat. Even studies comparing pancreatic lipase with histopathology have demonstrated the limitations of trying to make pancreatitis a simple positive/negative diagnosis.
The other reason I prefer the quantitative Catalyst test to the SNAP when it is readily available is simply that I get much more information from a number. The SNAP fPL was deliberately developed primarily as a screening/rule-out test and prioritises sensitivity; IDEXX did not change the SNAP when they revised the quantitative Spec fPL reference intervals. A value of 3, 6 and 15 µg/L gives me substantially more clinical information than simply knowing whether a SNAP is normal or abnormal. It is also much more useful if I subsequently want to look at the direction of travel in a patient.
Would I still send a Spec fPL to the external laboratory? Occasionally, yes. If I had an unusual or difficult case where the Catalyst result didn’t make sense in the context of everything else, or I particularly wanted laboratory confirmation, I might. But I don’t think every elevated Catalyst PL needs to be followed by Spec fPL. That rather defeats the purpose of having a validated quantitative patient-side assay, particularly given the good agreement between the two methods. I would spend the money on the rest of the diagnostic investigation where appropriate.
One small technical point worth remembering is that Catalyst PL and Spec fPL don’t report identical units—Catalyst PL is reported in U/L whereas Spec fPL is µg/L—so although the feline numerical decision limits were deliberately aligned, I wouldn’t describe the assays as analytically interchangeable measurements of exactly the same thing. They are different assays intended to give clinically concordant interpretation.
So overall, yes, I think the in-house quantitative PL is a useful test and I am very comfortable using it. I actually prefer the newer three-zone interpretation to the old idea that anything above 5.4 automatically means pancreatitis. It forces us to retain an equivocal zone and gives greater weight to markedly increased results, while still making us interpret the number in the context of the cat in front of us.
And I think your current approach—history + clinical signs + quantitative pancreatic lipase + good-quality ultrasound—is exactly the sensible way to use it. I would never diagnose or exclude feline pancreatitis from any one of those pieces of information in isolation.
Hope that helps!
Scott 🙂
Replying to Hannah B. 16/09/2026 - 11:15
Hi Hannah,
Lovely to hear from you!
Yes, this is one of the areas where things have changed since I originally recorded the course. Eluracat (capromorelin) has only become available here in Canada within the last few weeks, so my own experience with the feline formulation is still relatively limited. Entyce is also capromorelin, but it is the canine formulation, whereas Eluracat is the product specifically developed and licensed for cats. Eluracat has been available in the UK for longer than we have had access to it in Canada.
Your question about whether I would use Eluracat or mirtazapine first line is a really good one, because I don’t think we currently have evidence that allows us to say that one should routinely come before the other. I looked into this again because of your question, and importantly, I cannot find a published head-to-head clinical trial directly comparing capromorelin with mirtazapine in cats. Both have evidence supporting their use, but they have essentially been studied separately against placebo or control groups. So, at the moment, I don’t think we can legitimately say that Eluracat is a better appetite stimulant than mirtazapine, or vice versa.
They are also pharmacologically quite different drugs. Capromorelin is a ghrelin-receptor agonist. Ghrelin is involved in the physiological regulation of hunger, food intake and energy balance, so capromorelin stimulates appetite through that pathway. This makes it particularly interesting in cats with chronic disease where reduced appetite, loss of body weight and loss of muscle mass are becoming persistent problems rather than simply a cat that needs encouragement to eat for a couple of days.
There is good clinical evidence that this translates into meaningful weight gain. The pivotal feline study looked at cats with chronic kidney disease and unintended weight loss. Cats receiving capromorelin at 2 mg/kg orally once daily gained an average of approximately 5.2% of their body weight over 55 days, whereas the placebo-treated cats lost approximately 1.6%. The estimated difference between the groups was around 0.25 kg. That is quite impressive in a cat and is one of the reasons I think capromorelin is a useful addition to what we have available.
Mirtazapine works very differently. Its appetite-stimulating effect is related principally to antagonism of central serotonergic and adrenergic receptors, and we have considerably more clinical experience with it in cats. There are controlled studies demonstrating improved appetite and weight gain, including in cats with CKD. We also have the advantage of the transdermal preparation, Mirataz, which can be extremely useful in the cat that is difficult to medicate orally.
Another difference that matters to me clinically is nausea. Mirtazapine has anti-nausea/antiemetic effects as well as stimulating appetite. Therefore, if I have a cat that approaches food, sniffs it and walks away, lip-licks, salivates, seems interested but then won’t eat, or otherwise makes me suspicious that nausea is contributing to the inappetence, I may have an additional reason to choose mirtazapine. Depending on the severity, I may of course use a more conventional antiemetic such as maropitant or ondansetron as well.
Conversely, if I have a cat with a chronic disease that is reasonably well controlled but simply isn’t consuming enough calories and is progressively losing weight, capromorelin is very attractive. In that situation I am specifically trying to influence appetite and food intake over a sustained period, and its mechanism and the weight-gain data fit that objective very nicely. The recent feline CKD guidance essentially reflects this distinction: both drugs have a place, with mirtazapine having appetite-stimulating and anti-nausea effects and capromorelin targeting the ghrelin pathway involved in appetite regulation.
There are practical considerations as well. Some cats dislike oral medications intensely, in which case transdermal mirtazapine can be enormously helpful. Other cats tolerate a liquid medication perfectly well. Individual adverse effects matter too. With mirtazapine we can see behavioural changes, vocalisation, agitation, increased activity and occasionally tremors or other serotonergic effects, particularly if doses are excessive or dosing intervals are inappropriate. Capromorelin has its own potential adverse effects, including gastrointestinal signs such as vomiting and hypersalivation, and transient reductions in heart rate and blood pressure have been reported. Hyperglycaemia is another consideration with capromorelin, so I would be more cautious about reaching for it in a diabetic cat or one where glucose regulation is already a concern.
So, at the moment, my practical approach would be that I haven’t replaced mirtazapine with Eluracat. I still use mirtazapine frequently, and I probably have a lower threshold for it when nausea is part of the picture or when I want relatively short-term appetite support. Eluracat gives us another very useful option, and I am particularly interested in it for cats with chronic disease and persistent inadequate food intake or progressive weight loss where longer-term appetite and weight support is the objective.
For the moment, though, I would choose between them according to the individual cat rather than regarding one as first line and the other as second line. There simply isn’t a direct mirtazapine-versus-capromorelin study demonstrating superiority of one over the other, which is an important limitation when we are making these decisions.
Hope that helps, and it is a really useful question because this is definitely an area where our options have changed since I recorded the lecture.
Scott 🙂
Replying to Hannah B. 16/09/2026 - 12:40
Hi Hannah,
Yes, neutropenia is one of the findings that would push me much more towards antibiotics in a dog with AHDS, but I wouldn’t use the presence of haemorrhagic diarrhoea itself as the indication. That distinction is probably the most useful thing to agree on as a practice. A dog can have spectacular amounts of bloody diarrhoea and still not have an indication for antibiotics.
For me, the question is whether I am worried about sepsis or clinically important bacterial translocation, rather than how dramatic the diarrhoea looks. I would be much more inclined to use antibiotics if there is neutropenia, particularly significant or progressive neutropenia, or systemic features that concern me for sepsis: persistent pyrexia or hypothermia, cardiovascular instability/hypotension despite appropriate fluid resuscitation, marked lethargy or obtundation, worsening perfusion, hypoglycaemia, or other evidence of organ dysfunction. I would also have a lower threshold in an immunocompromised patient.
So, as a practical hospital rule, I think you can simplify it to: AHDS + otherwise stable patient = supportive care, not routine antibiotics. AHDS + evidence of sepsis/systemic compromise or significant neutropenia = antibiotics are reasonable. I wouldn’t use leukocytosis on its own as an indication.
The other important point is that hospitalisation itself isn’t an indication. Quite a few AHDS dogs need admission because of the severity of their fluid losses, vomiting and dehydration, but once their circulating volume is restored they are bright, cardiovascularly stable and improve remarkably quickly. I don’t routinely give those dogs antibiotics even though the diarrhoea may still look horrendous.
And yes, keep fighting the metronidazole battle! Giving metronidazole routinely for uncomplicated acute diarrhoea is increasingly difficult to justify, particularly given its effects on the intestinal microbiome. Interestingly, the newer CIE literature makes the same broader antimicrobial-stewardship point: antimicrobial treatment can produce substantial and long-lasting dysbiosis, and the recommendation is to reserve antibiotics for situations where there is a genuine indication rather than using them routinely for gastrointestinal disease.
On your fibre question, no, I don’t restrict fibre to chronic large-bowel diarrhoea. That’s where we traditionally think about it, and it can be extremely useful in chronic colitis, but I also use soluble fibre in selected acute diarrhoea cases. Psyllium is usually my first choice because it is cheap, readily available and easy to adjust.
I tend to start fairly conservatively rather than use a rigid mg/kg dose—something like ¼–½ teaspoon twice daily in a small dog, around 1 teaspoon twice daily in a medium dog and 1–2 teaspoons twice daily in a large dog, mixed into food, then adjust according to stool response. The exact amount isn’t particularly sacred; different psyllium products vary and there is quite a bit of individual variation in response. Owners can simply buy plain, unflavoured psyllium husk rather than needing a veterinary product. I just make sure it doesn’t contain sweeteners or other additives.
For acute large-bowel diarrhoea, I think it is very reasonable to use fibre early, especially when there is urgency, mucus, frequent small-volume stools or fresh blood. For chronic disease I’ll often continue it longer term if the dog clearly responds. There is actually reasonable evidence for fibre-responsive chronic large-bowel disease: the recent ACVIM CIE consensus describes good responses to highly digestible diets supplemented with psyllium, as well as an RCT showing improvement with a fibre-containing therapeutic diet.
Hope that gives you something practical to take back to the rest of the team!
Scott 🙂
Replying to Hannah B. 16/09/2026 - 13:05
Hi Hannah,
Great question. The main reason I used Vivomixx alongside Cobalaplex in that case was that I was trying to achieve two slightly different things. Cobalaplex was primarily there for the cobalamin support, whereas Vivomixx is the De Simone multi-strain probiotic formulation, which has probably the best specific evidence among probiotics in dogs with chronic inflammatory enteropathy. The recent ACVIM consensus reflects this quite nicely. Overall, the evidence for probiotics in CIE is fairly modest, but the De Simone formulation is specifically mentioned as something that can be considered, particularly in dogs that have not responded completely to dietary treatment.
That does not mean I think Protexin Enterogenic, FortiFlora or Pro-Kolin Advanced are inappropriate. I use these sorts of products too. I tend to think of probiotics as very product-specific rather than assuming that evidence for one probiotic can automatically be extrapolated to another. Studies using different strains and combinations have produced quite variable results, and several controlled studies have found no additional clinical benefit when a probiotic or synbiotic was added to an elimination diet.
So, I certainly wouldn’t suggest replacing FortiFlora as your routine probiotic simply because of this example. Likewise, Pro-Kolin Advanced remains a very useful product when I want the additional symptomatic benefits of a paste formulation, including the adsorbent component. My choice changes depending on what I am trying to achieve.
For a dog with significant or persistent CIE where I specifically want to trial microbiome modulation, I tend to reach for Vivomixx because there is evidence relating to that particular formulation. In one study, dogs receiving it achieved clinical remission, albeit more slowly than dogs receiving prednisone/metronidazole, and there was evidence of a more tolerogenic mucosal immune response. That is quite different from saying it is a universally “better probiotic.”
The bigger message from the newer evidence is probably that we shouldn’t place too much emphasis on probiotics at the expense of diet. Dietary intervention remains the first-line treatment for CIE, and the consensus now recommends considering multiple properly conducted therapeutic diet trials because some dogs don’t respond until the second or third diet.
Hope that helps explain my thinking!
Scott
Hi Silvana,
I did a bit more digging into this as it really interested me. It looks as though GingiPro is available through Bova in the UK as well as Australia, although there are some important considerations around its use.
The combination contains EIDD-1931, doxycycline and meloxicam, which raises a few questions for me. Ideally, before considering something like this, I think I would want to be confident that concurrent periodontal disease had been properly assessed and treated, including dental radiographs and extraction of diseased teeth where appropriate. I would also want confirmation of FCV by PCR rather than using an antiviral empirically, and obviously the individual cat needs to be an appropriate candidate for an NSAID.
There are also some wider stewardship questions around whether doxycycline is necessary in every case and around antiviral use in cats without confirmed calicivirus. EIDD-1931 itself is interesting, but potential adverse effects and owner exposure/handling need consideration, particularly as there are teratogenicity concerns. Applying a medication directly to the gingiva of a cat with a very painful mouth may not always be particularly straightforward either!
The other limitation at the moment seems to be the evidence base. There are apparently good anecdotal results, but the optimal duration of treatment has not yet been properly studied or published. Molnupiravir/EIDD-related antiviral treatment on its own has also been investigated in FCV-positive cats with encouraging results, so I suspect this is an area we are going to hear considerably more about.
So, potentially very interesting, and I can certainly see a role for this type of antiviral treatment in carefully selected FCV-positive cats, but I think I would currently be a little cautious about the one-size-fits-all combination product approach until we have more published data.
Thanks for bringing it up — I genuinely hadn’t come across it before!
Scott
Replying to Silvana S. 26/08/2026 - 09:20
Thanks Silvana! I am in exactly the same place. I haven’t had the opportunity to use lorazepam for this yet either, but the results are interesting enough that I would definitely consider it in an appropriate case, alongside all the usual multimodal management of course.
It will be interesting to see whether the findings hold up in larger studies and, in the meantime, to hear what experiences people have as they start using it clinically.
Scott 🙂
Hi Silvana,
Super interesting, thanks for sharing. I haven’t used GingiPro myself and haven’t come across it clinically here in Canada. I’ll reach out to Sam Taylor and see if she has any experience with it or knows more about its availability.
I’ll let you know what I hear back.
Scott ::
Replying to Raquel M. 24/08/2026 - 12:41
Thanks Raquel.
I hope all is well with you! You are absolutely right, lorazepam is only one small part of managing these cats, and identifying an underlying cause where possible, analgesia, diet, weight management and particularly addressing environmental stress are probably much more important than simply reaching for another drug.
Great to hear your outpatient UO case did so well too. Sometimes we have to work with what is realistically possible for the owner, particularly when the alternative is euthanasia.
I think I am in a similar place with lorazepam. The results are interesting enough that I would certainly consider it, particularly in selected cats, but I would like to see the findings reproduced in a larger study before it becomes routine for every first-time UO.
The CE event sounds very timely! I would be really interested to hear what the criticalist thinks about lorazepam and whether they have started incorporating it into their own UO protocols.
Scott 🙂
Replying to Silvana S. 16/08/2026 - 16:59
Hi Silvana, thanks – that’s a really good question. I tend to use once-daily prednisolone as well where the clinical situation allows, and I think this study gives us a little more reason to favour that approach, particularly when PU/PD is becoming troublesome.
The morning dosing question is interesting because you will quite often see the recommendation that glucocorticoids should be given in the morning in dogs, with the rationale that this more closely matches endogenous cortisol production and might therefore be less disruptive to the hypothalamic-pituitary-adrenal axis. Some veterinary prednisolone product information specifically recommends morning administration in dogs for this reason. The difficulty is that the evidence for a strong circadian cortisol rhythm in dogs is actually much less convincing than it is in people. The ACVIM consensus literature notes that dogs do not demonstrate a clearly established circadian pattern of cortisol secretion, so I don’t think we have strong evidence that giving prednisolone at, for example, 8 am rather than 6 pm produces a meaningful clinical benefit.
For hypoadrenocorticism specifically, I generally recommend giving the replacement prednisolone once daily in the morning. Partly that is physiologically intuitive and partly it creates a simple, consistent routine for the owner, but I wouldn’t be concerned if an individual dog was receiving it consistently at another time of day and was clinically doing very well. Current AAHA guidance focuses much more on giving an appropriately low physiological daily dose and adjusting it according to clinical signs and steroid adverse effects than it does on a particular time of day. Many stable Addisonian dogs actually require less than 0.1 mg/kg/day of prednisone/prednisolone, with up to 0.25 mg/kg/day generally being sufficient for stable long-term management.
So my short answer would be: morning is my preference, particularly for Addisonian dogs, but I don’t think we currently have good evidence that morning administration is clinically superior to evening administration in an otherwise stable dog. Consistency, using the lowest effective replacement dose, monitoring the individual dog’s clinical response, and remembering to increase glucocorticoid supplementation appropriately during periods of stress are probably much more important.
Great question.
Scott 🙂
Replying to Laura S. 04/08/2026 - 15:11
Hi Laura,
That is a really good question, and yes, I absolutely think cholecystocentesis is something that can be performed at GP level provided you are comfortable identifying the gall bladder ultrasonographically and can maintain good visualisation of the needle throughout the procedure. In many ways, I think it can be an incredibly useful and relatively accessible diagnostic procedure, particularly in exactly the situation you describe where referral, liver biopsy, or more advanced investigations are financially unrealistic for the owner.
I would probably say, however, that I would want someone to be reasonably confident with ultrasound guided FNAs before making cholecystocentesis their next procedure. The gall bladder is obviously a less forgiving target than the liver, so being able to confidently visualise your needle and needle tip is really important. If your confidence with liver FNAs is growing, though, I certainly do not think cholecystocentesis should be regarded as something that can only be performed in a referral hospital.
Cholecystocentesis can be completed using a percutaneous transhepatic ultrasound-guided approach, by laparoscopic assistance, or during exploratory abdominal surgery. If completed under ultrasonographic surveillance, a transhepatic approach allows adjacent liver tissue to provide a tamponade effect, limiting bile leakage. Whatever approach is used for cholecystocentesis, it is prudent to empty the gallbladder of most bile to limit postcentesis leakage. Samples of collected bile are used for cytologic evaluation and culture of aerobic and anaerobic bacteria and fungi. It is important to empty the gallbladder to collect bile with particulate debris or sediment in gravitationally dependent regions, as this material typically contains bacterial biofilm that will disclose organisms detected by cytologic evaluation and culture.
In terms of technique, I generally prefer a transhepatic approach where possible. In other words, I pass the needle through a small amount of liver parenchyma before entering the gall bladder rather than puncturing the exposed gall bladder wall directly. The idea is that the surrounding hepatic tissue provides some tamponade to the needle tract and potentially reduces the risk of bile leakage afterwards. I would use a relatively small gauge needle, typically around 22 to 25 gauge depending on the patient and the viscosity of the bile, attached to a syringe. A butterfly needle can certainly be used if that is what you are most comfortable controlling, although personally I think the most important consideration is not whether it is a butterfly or a standard needle but whether you can see and control the needle tip throughout the procedure.
There are obviously situations where I would be much more cautious. If the gall bladder wall looks compromised or discontinuous, there is pericholecystic fluid, there is concern about impending rupture, or I suspect a gall bladder mucocele with significant wall compromise, I would not regard that as a straightforward diagnostic cholecystocentesis. Equally, if there is significant coagulopathy or the gall bladder is extremely small and difficult to access safely, the risk benefit calculation changes.
I do think bile sampling can be extremely valuable when you suspect bacterial cholangitis or cholecystitis. One of its major advantages is that bile culture can provide information that bloodwork, ultrasound and even liver cytology cannot. If I am considering several weeks of antimicrobial therapy for suspected bacterial biliary disease, I would much rather have aerobic and anaerobic culture and susceptibility results to guide me, particularly because antimicrobial resistance amongst biliary isolates is certainly something we encounter.
Regarding performing cholecystocentesis at the same time as a liver biopsy, yes, I think that can be very sensible when the clinical picture supports it. If I am investigating suspected cholangitis or cholangiohepatitis and I am already obtaining hepatic tissue, then obtaining bile for cytology and culture at the same time can give you complementary information. The liver biopsy tells you what is happening within the hepatic tissue and biliary structures, while the bile sample can help determine whether bacteria are present and, importantly, what they are susceptible to. I suspect that is the context in which Penny was recommending it.
Complications of cholecystocentesis may include intraperitoneal bile leakage (decreased by using a transhepatic approach), haemorrhage, haemobilia, bacteraemia, and a biliary-cardiac reflex (vasovagal reaction). The latter adverse reaction is mediated by the vagal nerve, is more common in cats, and may result in ventilatory arrest, severe bradycardia, and death.
The point about gall bladder rupture is interesting because I would distinguish between an accidental needle related bile leak and a gall bladder that is already severely diseased and genuinely at risk of spontaneous rupture. I would not assume that every gall bladder that leaks following cholecystocentesis was inevitably going to rupture anyway, and equally I would not regard accidental rupture as universally fatal. The prognosis is going to depend enormously on the underlying gall bladder pathology, the degree and duration of bile contamination, whether infection is present, and how quickly the problem is recognised and treated.
If I genuinely suspected that the gall bladder had ruptured during the procedure, that would become a surgical emergency rather than something I would try to manage medically. I would involve a surgeon immediately. Management would generally involve exploratory laparotomy, assessment of the gall bladder and biliary tract, copious abdominal lavage, and addressing the source of leakage. Depending on what the gall bladder actually looks like, that may mean cholecystectomy rather than simply suturing the puncture site. I would also provide appropriate analgesia and supportive care, and if septic bile peritonitis were suspected, institute appropriate antimicrobial therapy while obtaining samples for culture wherever possible.
I therefore would not want the potential complication to put you off performing cholecystocentesis altogether. It is about patient selection and technique. In an appropriately selected patient with an intact gall bladder wall, a good transhepatic window and continuous ultrasound guidance, I think it is a very reasonable procedure for a GP with developing ultrasound skills to work towards. Perhaps the ideal first few cases would be performed alongside somebody with more ultrasound experience if that opportunity exists, simply because having someone beside you to confirm the approach and needle position can make that initial transition much less intimidating.
And importantly, in the situation you describe where an owner cannot afford referral or liver biopsy, a carefully selected cholecystocentesis may provide genuinely useful diagnostic information rather than simply being viewed as a lesser alternative to referral.
I hope that helps!
Scott
Replying to Lesley M. 09/08/2026 - 17:01
Really interesting thought, Lesley, and not completely off the wall at all! We already use the same principle with intraoperative autotransfusion.
And in principle, yes, some of the blood left within the abdomen will be reabsorbed over time, so there is potentially a degree of natural “autotransfusion” occurring. The difficulty is that this process is relatively slow and unpredictable, and therefore wouldn’t give us the immediate restoration of circulating red cell mass that we would want following significant haemorrhage. There are also potential downsides to deliberately leaving a large volume of blood behind, including peritoneal inflammation and discomfort, and potentially infection depending on the surgical situation.
Where your idea becomes really interesting is autotransfusion itself. Rather than discarding that blood, could we collect and reinfuse it during surgery, particularly when donor blood is limited? That can certainly be useful in appropriate cases, although suspected malignancy has traditionally made people cautious because of the theoretical concern about returning tumour cells to the circulation. Interestingly, none of the dogs in this particular study received autotransfusion, so unfortunately the paper doesn’t help us answer that question.
So yes, physiologically some of that abdominal blood will ultimately be reabsorbed, but I’m not sure there would be an advantage to deliberately leaving it there after surgery versus actively collecting and reinfusing it when autotransfusion is considered appropriate.
Definitely not an off-the-wall thought though!
Scott 🙂
Replying to Lesley M. 09/08/2026 - 17:04
Hi Lesley, this is the company we use here in North America: https://animalbiome.vet/pages/vet_fmt_capsules
I’m not sure whether they currently ship to the UK, but definitely worth having a look! I’d be interested to know if you find a UK supplier too.
Scott 🙂
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