scott@vtx-cpd.com

Replying to Sarah Keir 14/08/2025 - 09:37

Thanks Sarah, totally agree, DCM is a real consideration at this stage and something we’ll need to keep on the radar going forward, I must admit I often forget this sort of thing!. Look forward to your thoughts on the liver side when you’re back.

Best,

Scott 🙂

Replying to Victoria R. 14/08/2025 - 10:09

Hi Tori,

That’s really interesting, thanks for sharing. I must admit I don’t use antihistamines in many of my own patients. I’m working in Canada now, and they love Benadryl here! I do tend to reach for antihistamines more often in cases of lymphocytic–plasmacytic rhinitis, usually alongside an NSAID. That said, I’m not sure how effective I actually find them, and I often end up reaching for steroids instead.

Scott 🙂

Replying to Elizabeth Murch 14/08/2025 - 13:46

Radiography report:

Abdomen

Serosal detail: Within normal limits for both peritoneal and retroperitoneal spaces.

Foreign material: Multiple, thin, linear metallic opacities within the peritoneal cavity and possibly in the small intestinal lumen (Figure 1, arrowheads) – likely incidental barbecue brush bristles.

Stomach: Moderately to markedly distended with homogeneous fluid/soft tissue opaque material and gas (Figure 1, ovals). Gas redistributes normally between views. The pylorus appears empty in the left lateral view (Figure 1, arrow).

Small intestine: Descending duodenum and several other loops are overdistended with homogeneous fluid/soft tissue opaque material and scant gas, with a stacked appearance (Figure 1, #). Other loops are empty (**Figure 1, ***).

Colon: Mildly distended with formed soft tissue opaque fecal material and gas. Cecum not identified.

Other abdominal structures: Liver, spleen, visible renal margins, urinary bladder, and musculoskeletal structures are within normal limits.

Thorax

Pulmonary pattern: Alveolar patterns are present in the ventral right middle lung lobe, caudal subsegment of the left cranial lung lobe, and caudoventral aspect of the right cranial lung lobe (Figure 2, ovals).

Other thoracic structures: Trachea normal in diameter and position, cardiac silhouette, pulmonary vessels, and caudal vena cava are small. No pleural abnormalities. Musculoskeletal structures within normal limits.

Conclusions

Abdomen: Two populations of small intestine most consistent with a mechanical ileus. Metallic peritoneal/intestinal foreign bodies (barbecue brush bristles) likely incidental.

Thorax: Aspiration pneumonia in the right cranial, right middle, and left cranial lung lobes.

Additional Comments

Findings are most consistent with a small intestinal obstruction, which likely explains the clinical signs. Cause is not identified, but given chronicity, possibilities include:

Intestinal mass

Chronic, non-mineral foreign body

Intussusception

Abdominal ultrasound is recommended to determine the cause.

Replying to Julia Biernat 12/08/2025 - 15:19

No problem!

Let me know if you have any other questions.

Scott 🙂

Replying to valerie dromey 04/08/2025 - 22:46

It was an interesting case…

Sad outcome with this one however.

Have a great eek.

Scott 🙂

Replying to Iulia M. 07/08/2025 - 17:27

Hi Lulia,

Chlorphenamine can certainly be effective, but its shorter duration of action and higher sedation potential can be limiting. Cetirizine generally allows once-daily dosing, causes less sedation, and has some evidence in dogs, mainly small pharmacokinetic and clinical studies—suggesting it may help control allergic symptoms, particularly in atopic dermatitis. Direct head-to-head comparisons in veterinary patients are lacking, so choice is still based largely on individual response and tolerability. In my experience, cetirizine is worth trialling if chlorphenamine gives only partial control or causes unwanted sedation.

Hope you have a great week.

Scott 🙂

Replying to Julia Biernat 11/08/2025 - 09:45

Hi Julia,

Thank you so much for joining the course and thank you for your question!

I think this is an area where the use of PPIs in liver disease is often a bit over-generalised.

In most stable chronic hepatopathies, I don’t use PPIs routinely. My main indications would be when I have reasonable clinical suspicion or confirmation of an upper GI bleed — for example, haematemesis, melaena, or gastric/duodenal erosions or ulceration seen on endoscopy — and I think the bleed is likely due to a combination of portal hypertension–related mucosal congestion, secondary erosive gastritis, or concurrent drug effects (e.g., corticosteroids, NSAIDs). I might also consider a PPI if there’s marked hyperacidity suspected in a case with concurrent GI disease or after a known ulcerogenic insult.

If I have a patient with evidence of bleeding but significantly prolonged clotting times, then yes, I’d generally want to correct the coagulopathy before performing any invasive diagnostics and ideally before starting acid suppression. This is particularly relevant if you think the bleed is related to mucosal friability secondary to hypocoagulability rather than an acid-mediated ulcer. In those cases, fresh frozen plasma (FFP) is my first step, as it provides both clotting factors and, in some cases, volume support for hypoalbuminaemic patients.

In terms of how often I see GI bleeding purely due to clotting factor abnormalities, I’d say it’s uncommon as the sole cause in liver disease. When it does occur, it’s usually in the context of advanced decompensation, either severe synthetic failure with markedly prolonged PT/aPTT or DIC. In those situations, GI bleeding is often part of a broader haemorrhagic tendency affecting multiple sites (e.g., petechiation, ecchymoses, haematuria). I do occasionally see bleeding in patients with severe thrombocytopaenia — whether from DIC, immune-mediated mechanisms, or bone marrow suppression — but in my experience, portal hypertensive gastropathy or erosive gastritis from systemic illness are more frequent contributors in liver patients.

For additional context, the ACVIM consensus on acid suppressant use notes that although hepatic disease has been associated with gastroduodenal ulceration (GUE) in dogs, evidence that it is a direct cause is scarce, and the prevalence of upper GI bleeding in dogs and cats with hepatic disease has not been established. The pathogenesis is uncertain. In humans, altered mucosal blood flow from portal hypertension (hypertensive gastropathy) is the most common cause for GI bleeding, while in dogs, decreased hepatic degradation of gastrin with subsequent hyperacidity has been proposed — though experimental data do not support hypergastrinemia as a major factor. Experimental bile duct ligation can produce ulceration in dogs. In people, gastric acid suppression generally does not reduce bleeding from portal hypertensive gastropathy because these patients already tend to have hypochlorhydria, although PPIs may indirectly help by raising gastric pH enough to stabilise clots. There is one retrospective canine study in which implementation of lifelong PPI therapy around the time of intrahepatic shunt closure was associated with a lower rate of death from GI haemorrhage, but the underlying mechanism was unclear and may not have been related to the hepatic dysfunction itself.

Overall, the consensus opinion is that there is weak evidence to support prophylactic acid suppression in dogs and cats with hepatic disease in the absence of clinical or endoscopic evidence of GI bleeding. My own approach mirrors this, I reserve PPIs for patients with documented or strongly suspected ulceration or erosive gastritis, rather than using them as blanket prophylaxis in all liver cases.

I hope you have a wonderful week!

Scott 🙂