Hi melissa this is a mixed
Hi melissa this is a mixed bag of likely interstitial cystitis (of who knows what etiology) mucous debris, likely mural vasciulitis and ulceration, and sand.

We are doing a study on this right now and a portion of these cases have LP infiltrates as the inflammatory cell population. Occasionally you get bladder lsa as well on bx. But if documented LP inflammation they respond to pred.. (unpublished results but you can search cystitis in the sonopath search and come up with a case or 2)….i.e inflammatory bladder disease (IBD:)) But I would not use pred until you have histopath to justify it for long term management during flare-ups. I would do a cystotomy with sand analysis and UB wall culture and histopath and ask for predominant cell type and refine tx from there. This is a young cat so will be dealing with this for some time so I would encourage the scalpel here.

Remo anything new on
Remo anything new on potential infectious agents playing a role here?

Here is a similar case
Here is a similar case without the sand.

and this case in the pathology search is similar though no histopath… there are others in processing that have histopath as well.

06_00082 Sally W Interstitial cystitis

Thanks Eric. Does
Thanks Eric. Does LP=lymphoplasmacytic? What are the hyperechoic foci that the arrows in the above are pointing at? Fibrosis? Adherent debris? Trapped gas?

LP= lymphoplasmacytic yes.
LP= lymphoplasmacytic yes. Non shadowing echogenic debris is usually adhered mucous and debris, occasionally ulceration and fibrosis.

Again, thanks. I am looking
Again, thanks. I am looking forward to seeing your study when it come out.

Apologies for the delay in
Apologies for the delay in replying.

Here is a short synopsis on the proposed pathophysiology of feline interstitial cystitis (FIC):

The pathophysiology of FIC is not fully understood and may involve complex interactions between a number of body systems as a variety of abnormalities have been found in the bladders, nervous system, and hypothalamic-pituitary-adrenal axis of cats with FIC. Thus it is important that this syndrome is not just considered a “bladder disease” amenable to simple diet or drug therapies.

In both IC and FIC smaller amounts of total urinary glycosaminoglycan (GAG) and a specific GAG (GP-51) are secreted. GAG and GP-51 contribute to the surface mucus covering the urothelium that is believed to inhibit bacterial adherence and urothelial injury from the constituents of the urine. A defective GAG layer or damaged urothelium could permit hydrogen, calcium, potassium ions, or other constituents of urine to come into contact with sensory neurons innervating the urothelium. These ions can stimulate local release of neurotransmitters and result in neurogenic bladder inflammation. Sensory neurons reach the bladder via the pelvic and hypogastric nerves, and the central processes of these nerves synapse in the dorsal horn of the sacral and lumbar spinal cord, respectively. These neurons include unmyelinated nociceptive fibres, commonly referred to as C fibres.

Increased sensory nerve fibre density is found in the bladder of patients with IC. These fibres contain a variety of neuropeptides, which suggests a role for neurogenic inflammation in the pathophysiology of IC. In both IC and FIC, Substance P containing fibres are increased in the submucosa of bladders. Mammalian bladders usually express either the NK1 (high affinity) or the NK2 (low affinity) Substance P receptor, or both. In normal cat bladders, the NK2 receptor is identified, whereas NK1 receptors are at or below the threshold of detectability. In contrast, inflamed bladders have higher concentrations of NK1 Substance P-binding sites and are associated with inflammatory events in urinary bladders of cats.

Abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis have been observed in cats with FIC as they show decreased serum cortisol response to ACTH as well as lower adrenal gland size and volume. Therefore it appears that although the sympatho-neural system is fully activated in FIC the HPA axis is not. The significance of this finding is however, not known.

Although feline calici virus, bovine herpes virus, and feline syncytia-forming virus have been implicated as a cause of FIC, the actual role that they play remains unknown.

Thanks, Remo. What are your
Thanks, Remo. What are your thoughts on using maropitant to treat FIC?

Macropitant targets NK-1
Macropitant targets NK-1 receptors and inhibits binding of substance P, which occurs in the chemoreceptor trigger zone and emetic center. In theory it could work in FIC but cannot find anything about it. May be worth a try, however, difficult to judge efficacy as FIC typically waxes and wanes, dispute any therapy.

Thanks Remo for the in depth
Thanks Remo for the in depth explanation….along this pathway do you see any parallels with Triad disease and other organs that could be related? I see FIC waxing and waning in triad cats all the time but don’t know if there is a link…. i.e. they will often have chronic panc liver and IBD looking GI with/without clinical signs for those organs but they are having FIC issues that caused the call for sonogram. Then again triad cats will have pancreatic issues one day, renal issues another, Gi another and liver another so could there be a “Pentad” disease going on here?? Especially if I can prove the histopath on this bladder population of LP infiltrates. Consipiracy theory I know but I can’t ignore all these “Triad,” “Quadrad,” “Pentad” cases that come across the probe every day so maybe there is a common denominator out there. Tough to even find a normal cat sonographically these days.

Here is an example of a case
Here is an example of a case that Denise Bruno RDMS scanned in NYC and I read out for her. The first 2 images are presurgical with typical interstitial bladder wall thickening, and an echogenic ulcer or embedded mucous in the apex.

& another image different
& another image different angle same cat at the time of presenting clinical signs, hematuria, dysuria, inappropriate elimination and so forth.

Surgical resection of the
Surgical resection of the apical UB wall revealed ….

So 3 weeks days post sx the
So 3 weeks days post sx the cat was still a bit symptomatic and this is what the bladder looked like 3 1/2 weeks post sx.

But at a different angle
But at a different angle there was still an apical thickening which could have been Sx healing and suture. At 3 1/2 weeks post surgery the clinical signs diminished significantly by removal of the pathological tissue but the cat was still having some signs similar to those prior to sx.

So in order to manage the
So in order to manage the clinical signs we put this cat on prednisolone (antiinflammatory dose don’t have exact dose but could find out) based on the LP infiltrates and the patient has been asymptomatic ever since and has been weaned off pred and I believe we put this cat on a hypoallergenic diet as if its had “IBD” just to reduce antigenicity…but in this case I called it “Inflammatory Bladder Disease.” 🙂 I haven’t heard on follow-up but this is a good client that went to sx and post and so I think if there were more issues we would have heard but will check with Denise. I will search for a later bladder image as I don’t recall if we got a follow -up or not. I think the owner was just happy to not have the urinary issues.

Fun stuff but I don’t advocate pred without histopath in these because I have seen them perforate as well and surely if there is sand involved and someone does hydropulsion without scanning the bladder first…. I have seen bladder rupture from this as well. usually these cats are from 3-8 years old..any older I get worried about bacterial cystitis and bladder lymphoma.

Was just informed that the
Was just informed that the cat is asymptomatic on urinary SO diet