scott@vtx-cpd.com

Replying to Laura S. 17/08/2025 - 13:12

Hey Laura!

Lovely to hear from you! Be brave next time! 🙂

The BBQ bristles caught my eye too! the stomach appearance was indeed due to the distribution of the homogeneous fluid/soft tissue opaque material and gas. This changed depending on the view.

I hope you are having a good weekend so far!

Scott 🙂

Replying to Sarah Keir 14/08/2025 - 09:28

Hi Sarah,

I hope you are having a great start to your weekend!

That is a really interesting thought. NAC’s mucolytic effect comes from its ability to cleave disulfide bonds in mucoproteins, reducing the viscosity of secretions, and that is why it is used in respiratory medicine as a nebulised treatment in humans. To date there is no published evidence in veterinary medicine, or in human hepatology (that I can find), to support the use of NAC as a mucolytic in the biliary tract. When we use NAC in hepatobiliary cases, it is primarily for its antioxidant properties and role as a glutathione precursor, not for mucus breakdown. The way it works in the airways is by direct local contact with secretions at high concentration, which is difficult to replicate in the biliary system because systemically administered NAC is unlikely to reach the gallbladder in sufficient local concentration to act as a mucolytic.

For patients with early mucinous hyperplasia, the approaches that currently have the best rationale are monitoring with serial ultrasound, addressing any concurrent endocrinopathies such as hypothyroidism or hyperadrenocorticism, and in some cases using ursodeoxycholic acid to improve bile flow and reduce stasis. Do you agree? What is your approach when you find this sort of thing during your ultrasound scans?

So while in theory NAC’s mucolytic property is attractive, there is no evidence base at present to support its use for preventing or managing mucinous hyperplasia or mucocele development. I would still view NAC as valuable in sick animals that cannot tolerate oral medication, particularly for its hepatoprotective and antioxidant effects, but not as a gallbladder mucolytic. In patients with early mucinous changes I would focus on ursodiol and careful monitoring, and reserve NAC for those that are systemically unwell or unable to take SAMe.

Thanks again for sharing such interesting thoughts!

Scott 🙂

Replying to Aileen D. 20/08/2025 - 16:15

Hello Aileen!

Lovely to see you here! Thanks so much for sharing the article… you know you have made it when you make the Glasgow papers! Very cool case.

I will make sure that Kerry and Neus see this question and we will get back to you ASAP.

Scott 🙂

Replying to Sarah Keir 14/08/2025 - 09:34

Hi Sarah,

Great point! Thankfully that is one complication we are spared in small animal medicine. In people with cirrhosis, portal hypertension leads to development of oesophageal and gastric varices which can rupture and cause catastrophic haematemesis, often fatal even with intervention.

In dogs and cats, while we do certainly see portal hypertension, the sequelae are quite different. Instead of varices, we are more likely to see acquired portosystemic shunts, ascites, or hypertensive gastropathy. The mucosal congestion from portal hypertension can contribute to erosions or low grade bleeding, but the dramatic variceal haemorrhage so characteristic of humans is not a recognised clinical problem in veterinary patients.

Thanks again,

Scott 🙂

Replying to Victoria R. 14/08/2025 - 09:40

Hi Tori,

I’d say I’m the same, I haven’t really noticed a strong pattern either. If anything, I’ve sometimes thought the occasional GI signs might be more about the timing with food rather than the drug itself, since like you, I usually give it alongside a meal. Many of the patients I end up using it in have chronic enteropathy, so they’re already showing GI signs to begin with, which makes it tricky to separate out. I might start paying closer attention to see if there’s any consistent trend.

Scott 🙂