scott@vtx-cpd.com
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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 🙂
Replying to Rosanna Vaughan 30/07/2026 - 15:57
Hi Rosanna,
Thanks very much. I’m glad you found it helpful. I’ve become a real fan of Senvelgo in the right patient.
For CGMs, I still use the FreeStyle Libre 2 a lot. It’s the system I’m most familiar with, it’s the one most of the published veterinary literature has used, and I find it reliable enough for following trends rather than focusing on individual glucose readings. I don’t routinely chase every number, as I think looking at the overall glucose pattern alongside the clinical picture is much more useful.
That said, I have also had several patients start using the FreeStyle Libre 3, and I’ve been really impressed with it. The sensor is noticeably smaller, which seems to make it better tolerated by many cats, and the continuous real-time data are excellent. If owners are comfortable with the technology, I think it’s a really nice evolution of the Libre system.
The LibreLink app works very well for owners, and if they’re happy to share the data through LibreView it makes remote review straightforward. That has probably changed my diabetic monitoring more than anything else over the past few years.
In terms of placement, I generally position the sensor over the lateral thoracic wall, just caudal to the scapula. I clip quite a generous area, degrease the skin thoroughly with alcohol and let it dry completely before application. I then reinforce the adhesive with a little tissue glue around the outer adhesive pad rather than underneath the sensor itself. Finally, I cover the whole thing with a light body suit or recovery shirt for the first week if the cat will tolerate it. Since doing that, I lose very few sensors.
A lot of my clients have also really liked using the commercially available adhesive sensor covers that fit over the Libre sensor. They seem to help keep the sensor in place, particularly in more active cats or those that like to groom excessively, and they’re relatively inexpensive.
One other tip I’ve found useful is to prepare owners that the sensor doesn’t have to last the full 14 days to be worthwhile. Even three to five days of home glucose data is often far more informative than a traditional in-hospital glucose curve, particularly in cats that develop significant stress hyperglycaemia.
I’d be interested to hear how you get on with your first Senvelgo case.
Scott 🙂
Replying to Silvana S. 30/07/2026 - 09:49
No problem!
Ultimately, I am using this drug more and more ‘off label recommendation’ and finding it still works well. It is a very interesting drug!
Scott 🙂
Replying to Silvana S. 30/07/2026 - 10:09
Hello!
This feedback is really helpful. I will absolutely take this in to consideration when we are reviewing the course.
Thank you again for your brilliant contribution.
Scott
Hi Sophie,
That’s a really good question, and I think the answer depends very much on the individual patient and what we think caused the pancreatitis in the first place. I hope you are enjoying the course! Feedback always welcome.
Historically, we recommended prolonged fasting and then lifelong low fat diets for many dogs after pancreatitis. However, our understanding has changed considerably over the last 15 to 20 years. There is now mounting evidence in both human and veterinary medicine that dogs with acute pancreatitis benefit from early enteral nutrition. Enteral nutrition is superior to total parenteral nutrition because it helps maintain intestinal motility, preserves gastrointestinal barrier function, supports a healthy intestinal microbiome, and prevents villous atrophy. Studies in dogs have shown that feeding within 48 hours of hospitalisation is well tolerated, results in an earlier return to voluntary food intake, and reduces gastrointestinal complications. As a result, dogs that are not vomiting should be offered food as soon as possible, while those that remain anorexic should be considered for nutritional support via a feeding tube rather than being left unfed.
The question of what to feed long term is actually much less clear. There is currently very little evidence defining the ideal maintenance diet after recovery from acute pancreatitis. My own approach is that a dog with a single uncomplicated episode of acute pancreatitis that makes a complete clinical recovery does not necessarily need to remain on a low fat diet for life. I will generally keep them on a highly digestible low fat diet for the first one to two weeks after discharge and then reassess. If they continue to do well, have no concurrent disease, no persistent hyperlipidaemia, and this was their first episode, I am often happy to transition them back onto a good quality maintenance diet while advising owners to avoid high fat treats, table scraps, and obvious dietary indiscretions. This is very much in keeping with the current nutritional recommendations, which suggest tailoring long term feeding to the individual patient rather than automatically recommending lifelong fat restriction for every dog.
Where I am much more inclined to recommend long term fat restriction is in dogs with recurrent pancreatitis, chronic pancreatitis, documented hyperlipidaemia, breeds predisposed to lipid disorders such as Miniature Schnauzers, or dogs that clearly developed pancreatitis following a high fat dietary indiscretion. Those patients probably do benefit from remaining on a commercially formulated low fat diet, and I would also recommend avoiding fatty snacks and treats.
It is also worth remembering that pancreatitis is not always caused by dietary fat. Many cases are idiopathic, while others are associated with endocrinopathies, hypertriglyceridaemia, obesity, medications, or concurrent gastrointestinal disease. Because of that, I try not to automatically prescribe lifelong dietary fat restriction for every dog that has had pancreatitis without considering the underlying cause.
For dogs with chronic pancreatitis, my recommendations are different. These patients often do benefit from an ultra low fat diet as part of their long term management, particularly as many also have concurrent chronic inflammatory enteropathy, hepatitis, diabetes mellitus, or hyperlipidaemia. They may also require antiemetics, appetite stimulants, analgesia, and occasionally immunosuppressive therapy if there is suspicion of an immune mediated component and they have failed more conventional management.
So, in summary, I think the key is to individualise the plan. A first episode of acute pancreatitis does not automatically mean lifelong fat restriction. I tend to use a low fat diet during recovery, then reassess based on recurrence, concurrent disease, hyperlipidaemia, and the suspected underlying cause. For recurrent or chronic pancreatitis, I am much more likely to recommend long term dietary fat restriction.
Let me know if you have any other questions.
Scott 🙂
Replying to Rachel C. 15/07/2026 - 16:44
Thanks Rachel, I completely agree. I still think faecal testing has an important role, particularly early in the work-up to exclude parasites and other infectious causes before moving on to more invasive or expensive investigations such as ultrasound or endoscopy. I don’t think this paper suggests we should stop doing faecal testing, but rather that we need to be much more cautious about how we interpret bacterial PCR results. Simply detecting organisms like Clostridium perfringens or E. coli doesn’t necessarily mean they are causing the diarrhoea, and using those results alone to justify antibiotics is probably not appropriate. For me, it’s a useful reminder to interpret faecal PCR in the context of the whole clinical picture, rather than in isolation.
I hope you are well!
Scott 🙂
Hi Rachel,
Thanks for your questions, and I’m glad you enjoyed the lecture.
One of the main things I’m always keen to emphasise is that liver enzymes are not liver function tests. They are markers of hepatocellular injury or cholestasis, but they tell us very little about how well the liver is actually functioning. Equally importantly, liver enzymes can increase because of disease outside the liver. The liver is an incredibly sensitive organ and responds to a huge range of systemic insults, so I always encourage clinicians to interpret liver enzyme elevations within the context of the entire clinical picture rather than assuming they represent primary liver disease.
If I have a patient that is “not quite right”, has mild to moderate liver enzyme elevations, and an essentially unremarkable ultrasound, I don’t routinely jump to liver FNAs or gall bladder aspiration. Unless there is genuine suspicion of a primary hepatobiliary disorder, such as cholangitis or cholangiohepatitis, I don’t think those procedures are necessarily the next logical step.
The first thing I ask myself is whether these are persistent liver enzyme elevations. We certainly see transient increases that resolve completely on repeat testing and never recur. Because of that, if the patient is clinically stable, I don’t think it is unreasonable for the first step simply to repeat the biochemistry in two to four weeks to determine whether the abnormalities persist.
The second thing I commonly do is start a course of Denamarin. I will often add ursodeoxycholic acid, provided there is no evidence of complete biliary obstruction. I’m very comfortable using those medications together. They are generally very safe, and I think they provide sensible supportive therapy while you determine whether the abnormalities are transient or persistent. I would then reassess the liver enzymes after a few weeks.
If the liver enzymes normalise, then you’ve probably avoided unnecessary invasive diagnostics. If they remain persistently elevated, particularly if the ALT is greater than five times the upper reference interval, or the values continue to increase, then I think the conversation changes. At that point, if you’ve excluded obvious extrahepatic causes, the only way to obtain a definitive diagnosis may be liver sampling, whether that is cytology or biopsy depending on the individual case.
I also think it is worth remembering that ultrasound is an excellent tool, but it is not a test of liver function and it is not particularly sensitive for many inflammatory or metabolic hepatopathies. A completely normal appearing liver does not exclude significant microscopic disease, just as a very abnormal looking liver does not necessarily indicate severe dysfunction.
With respect to gall bladder aspiration, I certainly would not perform it routinely. For me, the main indication is suspected bacterial cholangitis or cholecystitis where obtaining bile for culture and cytology is likely to change management. This is particularly relevant in cats because bacterial cholangitis is considerably more common than in dogs.
Other situations where I would consider cholecystocentesis include patients with persistent cholestasis or hyperbilirubinaemia where I am concerned about an ascending biliary infection, dogs or cats with ultrasonographic evidence of abnormal bile such as echogenic debris, thickened gall bladder walls or changes suggestive of cholecystitis, patients with recurrent or poorly responsive hepatobiliary disease despite empirical antibiotics, and cases of pyrexia of unknown origin where the biliary tract remains a potential source of infection. It is also appropriate when you are concerned about antimicrobial resistance and culture results are likely to influence your antibiotic selection.
Conversely, I would generally avoid gall bladder aspiration in patients with a gall bladder mucocele, evidence of gall bladder rupture, significant coagulopathy, severe gall bladder wall necrosis, or where the result is unlikely to alter my management.
So, my approach is usually to ask three questions. Firstly, do I think this is primary liver disease? Secondly, is there evidence of liver dysfunction rather than simply liver injury? Thirdly, will obtaining liver or bile samples genuinely change my treatment plan? If the answer to that last question is no, and the patient is clinically stable, I think it is entirely reasonable to repeat the blood work, provide supportive hepatoprotective therapy with Denamarin and, where appropriate, ursodeoxycholic acid, and reassess before moving on to more invasive diagnostics.
Thanks again for the excellent questions.
Scott 🙂
Replying to Silvana S. 22/07/2026 - 09:55
Hi Silvana,
Thank you for your excellent question. I hope you are doing well.
This is exactly the sort of case where I think we need to step back and think about what is driving the diabetes rather than simply treating the blood glucose.
Hyperthyroidism is one of the recognised causes of insulin resistance, and the new AAHA guidelines list uncontrolled hyperthyroidism as an important concurrent disease that should be identified before selecting an SGLT2 inhibitor. They recommend screening cats over seven years of age for hyperthyroidism and generally favour insulin in cats with significant concurrent disease or where metabolic stability is uncertain.
If the cat is otherwise bright, eating well, well hydrated, has no ketosis, and is genuinely stable, I don’t think there is necessarily an urgent need to stop Senvelgo immediately. However, I would focus aggressively on getting the hyperthyroidism under control and monitor the diabetic response very closely. There is certainly be a possibility that improving the hyperthyroidism will reduce insulin resistance and substantially improve diabetic control.
My concern would be that ongoing weight loss and polyphagia make it difficult to know how much of the clinical picture is due to persistent diabetes versus uncontrolled hyperthyroidism. If those signs persist despite improving thyroid control, or if ketones become a concern, I would have a fairly low threshold for transitioning to insulin.
That said, I don’t think we necessarily need years of direct experience before carefully applying these drugs outside the original label population. It seems to me that they can be extremely valuable in selected cases that are not completely stable or entirely conventional, provided we understand the risks, monitor closely and have informed owners.
Interestingly, a recently published case series explored the use of velagliflozin in non ideal diabetic cats with concurrent diseases. While hyperthyroidism was not included, the authors successfully managed cats with conditions such as chronic kidney disease and hypersomatotropism, in some cases using combination therapy and intensive CGM and ketone monitoring. Their experience suggests that, in carefully selected patients with close monitoring and informed owner consent, there may be scope to use SGLT2 inhibitors outside the original label recommendations.
My own experience has probably reinforced that view. I have used these drugs successfully in several patients that would not have been considered ideal candidates in the original clinical trials. One cat, had IRIS stage 3 chronic kidney disease, significant biliary disease, was receiving corticosteroids and multiple medications for CKD, and still responded remarkably well to treatment. I have also used an SGLT2 inhibitor successfully in a cat with progressive FIP receiving corticosteroids, and in another cat with severe non regenerative immune mediated anaemia that was being treated with cyclosporine and prednisolone. All three of those cases responded very well, despite being far from straightforward.
Obviously these are anecdotal experiences rather than evidence, and I certainly would not advocate indiscriminate off label use. However, they have given me confidence that with careful case selection, very close monitoring, particularly of ketones during the early treatment period, and clear communication with owners, these drugs may have a broader role than we initially thought.
So, in your case, I certainly wouldn’t dismiss Senvelgo simply because the cat has hyperthyroidism. I would be inclined to treat the hyperthyroidism aggressively, monitor the diabetes and ketones closely, and then reassess how the cat is doing clinically over the following few weeks. If the clinical picture improves, I think it is entirely reasonable to continue. If not, then transitioning to insulin would be my next step.
I hope that helps.
Scott 🙂
Case Reports J Feline Med Surg 2026 Feb;28(2):1098612X251414198. doi: 10.1177/1098612X251414198. Epub 2026 Jan 3.
SGLT2 inhibitor therapy in diabetic cats: first clinical experiences with non-ideal candidates
Achilles Vanneste 1, Emma Van Heuckelom 1, Dagmar Vannieuwenhuyse 1, Charlotte De Voogt 1, Sylvie Daminet 1
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PMID: 41482870 PMCID: PMC12929899 DOI: 10.1177/1098612X251414198Replying to Silvana S. 24/07/2026 - 09:33
Hi Silvana,
Thank you so much for your question. I hope you are well.
I’ll make sure Tori sees your question so she can give you her thoughts on the use of coconut oil, baby oil, and products such as Allerderm and Douxo Seb 3 in cases like colour dilution alopecia.
I also really like your suggestion for a future webinar on lumps and bumps in dogs and cats, including some of the newer treatment options. That’s a great idea, and I’ll make sure we add it to our list of topics to consider for future courses. Do you mean an approach to lumps and bumps?
Thanks again for getting in touch, and we’ll get back to you soon.
Scott 🙂
Replying to Lucy Bennett 11/07/2026 - 22:49
Hi Lucy,
Firstly, don’t apologise at all. It is really lovely to hear from you!
Looking at the overall picture, I actually think there are probably two separate questions here. The first is whether this dog has AHDS, and the second is whether there is concurrent gastrointestinal obstruction or another structural disease process.
Clinically, there are certainly lots of features that fit AHDS. The acute onset of haemorrhagic diarrhoea, the haemoconcentration, the dehydration, the rapid progression and the very flat demeanour are all consistent. The falling albumin and total protein are also entirely compatible with acute intestinal protein loss. I wouldn’t call this protein losing enteropathy as a primary diagnosis. Rather, I would describe it as protein loss secondary to severe intestinal disease. Protein losing enteropathy simply tells us that protein is being lost through the gastrointestinal tract. It is a mechanism rather than a disease itself. AHDS absolutely can cause marked enteric protein loss, so in this situation I would say the patient has AHDS with secondary protein loss rather than primary PLE.
You’re also absolutely right about the calcium. Once albumin falls, total calcium commonly falls with it because a significant proportion of calcium is protein bound. Unless the ionised calcium is low or there are compatible clinical signs, I generally don’t become overly concerned by a mildly reduced total calcium in this situation.
The chemistry otherwise doesn’t really raise any major red flags for me. The normal renal parameters despite significant dehydration suggest you caught the patient reasonably early. Liver enzymes are unremarkable. Pancreatic lipase isn’t supportive of pancreatitis, although as always we interpret that alongside the clinical picture rather than in isolation.
The heart rate actually catches my attention more than anything else. A heart rate of around 60 bpm in a flat, dehydrated, painful little Cavapoo is certainly not what I would expect. Coupled with the progressive hypothermia and increasing respiratory rate, I agree with you that I’d be increasingly worried about evolving systemic inflammatory response syndrome. Dogs developing sepsis or severe inflammatory disease don’t always mount the textbook tachycardic response, particularly as they become more decompensated.
As for Addison’s disease, I don’t think you made the wrong decision. It should always sit somewhere on the differential list for acute gastrointestinal disease, but with a normal potassium, no obvious electrolyte pattern to support it and another very plausible diagnosis, I don’t think I would have prioritised a cortisol either. If the case wasn’t progressing as expected, or if the bloodwork became less convincing for AHDS, then absolutely I would revisit it.
The ultrasound is the really interesting part.
Looking at your images, I can completely understand why you were concerned. Those hyperechoic rounded structures with clean distal acoustic shadowing certainly give the impression of luminal foreign material. If I’d been scanning the dog in real time, I suspect I would have been thinking exactly the same thing.
The difficulty is that static images only tell part of the story. What I would really want to know is whether those structures moved independently, whether they maintained their appearance from different imaging planes, whether they remained within the gastric lumen throughout the examination and whether they produced consistent clean acoustic shadowing from every angle. Sometimes compacted ingesta, mineralised material or even gas interfaces can produce surprisingly convincing appearances on still images.
The other thing that stands out is the amount of fluid within the stomach. If the dog genuinely hadn’t eaten since Thursday evening, I would expect the stomach to be relatively empty unless there was ongoing fluid accumulation or delayed gastric emptying. That immediately makes me wonder whether there is gastric outflow dysfunction or ileus.
Could AHDS alone produce that? Absolutely. Severe inflammatory ileus is well recognised in these patients. You can see delayed gastric emptying, fluid filled stomachs and diffusely fluid distended bowel secondary to inflammatory ileus rather than mechanical obstruction.
Equally, however, you cannot confidently distinguish inflammatory ileus from an early mechanical obstruction on a single ultrasound examination if you can’t identify the pylorus and proximal duodenum. That’s exactly why I think referral was the right decision.
I also completely agree with your hesitation about metoclopramide. If I genuinely believed there was a possibility of a mechanical obstruction or gastric outflow obstruction, I would avoid using a prokinetic until I’d excluded that. Once you’re comfortable there isn’t a foreign body, then metoclopramide becomes much more attractive if you think you’re dealing with inflammatory ileus.
One other thing I’d mention is that foreign bodies and AHDS are not mutually exclusive. A foreign body can certainly produce haemorrhagic diarrhoea through severe mucosal injury, and conversely a dog with AHDS may have incidental gastric contents that complicate interpretation. So I don’t think the presence of bloody diarrhoea excludes obstruction at all.
Overall, I actually think your clinical reasoning was excellent. You recognised that the patient wasn’t following the straightforward AHDS script, you identified an imaging finding that made you uncomfortable, you appreciated the uncertainty, and rather than forcing the case into one diagnosis you referred it. That’s exactly what I would hope someone would do.
Please let me know what the referral centre found. I’m genuinely interested to hear how this one turns out.
Scott 🙂
Hello again!
Here is the reply from Jon:
‘ Hi there,
It’s generally quite clearly twisted if there’s an issue. The mesentery holding the spleen can look spiralled and like a tornado. The spleen itself is enlarged and usually darker than normal. It’s also often kind of folded on itself – it can look quite like a rose!
I don’t think I’ve seen one getting accidentally twisted when exteriorising. I’ve seen this once or twice with the intestines though. I suppose it’s not impossible to accidentally untwist one. To expand on that though, it’d have to be a random grab of one but of spleen through a small hole and pulling, and being very lucky to have grabbed the correct end and it unfurling. Most of the time, the twisting up is fairly tight and the whole thing would probably pull as a ball, if that’s sensible makes sense.
It’s an interesting question.
Thanks
Jon’
Replying to Elizabeth C. 21/06/2026 - 09:03
Thank you so much for the feedback!
Really useful for us. I am pleased you are enjoying the course.
Scott 🙂
Replying to Gemma H. 23/06/2026 - 15:41
Thanks Gemma!
I am so glad you are enjoying the course!
Scott 🙂
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