Felis ISSN 2398-2950

Idiopathic cystitis

Synonym(s): Feline Idiopathic Cystitis [FIC], Idiopathic Feline Lower Urinary Tract Disease [iFLUTD], Feline Interstitial Cystitis is a subgroup of Feline Idiopathic Cystitis, Feline Idiopathic Cystitis used to be considered as a subgroup of Feline Urological Syndrome [FUS]

Contributor(s): Danielle Gunn-Moore, Martha Cannon, Ellie Mardell

Introduction

  • The majority (~55-69%) of cases of idiopathic feline lower urinary tract disease (iFLUTD) Feline lower urinary tract disease (FLUTD) are thought to be due to Feline Idiopathic Cystitis (FIC).
  • FIC is thought to have a similar pathophysiology to interstitial cystitis in humans.
    Print off the owner factsheetCystitis (bladder inflammation) Cystitis (bladder inflammation) to give to your client.

Pathogenesis

Predisposing factors

General

  • FIC is seen most frequently in cats which:
    • Are over weight.
    • Take little exercise.
    • Use an indoor litter-box.
    • Have restricted access outside.
    • Eat a dry diet.
  • Affected cats often live in multi-animal households with at least one other animal with which they are in conflict.
  • An altered response to stress is believed to be involved in the pathogenesis of FIC.
  • Genetics is also believed to play a role (reflected by the increased incidence of FIC in Persian cats).
  • Certain, as yet undefined, virus infections may also be involved.

Pathophysiology

  • Urethral obstruction leads to acute renal failure with post-renal uremia and hyperkalemia. The former can be associated with reduced rates of drug clearance. The latter may be associated with brady-dysrhythmia and cardiac failure.
  • The effects of the hyperkalemia can be countered by giving i.v. calcium, or the hyperkalemia can be corrected using intravenous fluids, i.v. glucose (and, if required, insulin).
  • The systemic uremia is often self-correcting following rehydration and continued i.v. fluid support to adequately compensate for post-obstructional diuresis.
  • Research over the last 30 years has failed to find a consistent cause for the inflammation in FIC. Various hypotheses are available. Possibly the most inclusive one suggests that FIC may result from alterations in the nervous system of the cats and their inability to cope with environmental stress; cats with FIC tend to have smaller adrenal glands and a blunted response to stress, and produce higher levels of catecholamines than counterparts not suffering from FIC. This results in alterations in the interaction between the neuronal supply to and from the bladder, and is exacerbated by noxious compounds within the urine. This may then be further exacerbated by altered interactions with the protective glycosaminoglycan (GAG) layer that lines the bladder Neurogenic inflammation in FIC flowchart.
  • This theory is termed the 'neurogenic inflammation theory of FIC'. In more detail, it suggests that stimulation of the C-fibers (via central or local triggers) can cause the release of neuropeptides (e.g. substance P and others), which can in turn result in pain, vasodilatation of the intramural blood vessels, increased vascular and bladder-wall permeability, edema of the submucosa, smooth muscle contraction, and mast cell de-granulation. Mast cell de-granulation results in the release of a variety of inflammatory mediators (including histamine, heparin, serotonin, cytokines, and prostaglandins) which can further exacerbate the effects of the C-fibers. Stimulation of C-fibers and the resulting neurogenic inflammation can therefore explain many of the changes recorded in FIC. The nerve endings can be stimulated in response to central triggers (such as "stress"), or via compounds within the urine (eg acid pH Urinalysis: pH, potassium, magnesium, and calcium ions). This in turn may result in further recruitment of C-fibers, and intensification of disease.
  • The exact role of the thin layer of GAG-rich mucus which covers the bladder epithelium is still unclear. It is known that it helps to prevent microbes and crystals from sticking to the bladder lining. In addition, it has been shown that some cats with FIC have altered urine concentrations of GAG and increased urinary bladder permeability. This increased permeability may allow noxious substances within the urine to pass through the urothelium and cause inflammation.
  • While it appears that neurogenic inflammation may play an important role in the development of the clinical signs of FIC, it is unclear whether or not it is as a primary factor, or a secondary event, perhaps triggered by an, as yet, unidentified infectious agent.
  • It has been suggested that FIC may have similarities to Interstitial Cystitis, which is an idiopathic, non-malignant, bladder disease of humans.
  • It can be very difficult to fully differentiate between the pathogenesis of FIC and other causes of FLUTD. This is because different causes of FLUTD may occur individually, or in various interacting combinations Urinary clinical presentations flowchart. For example, the formation of urethral plugs may result from concurrent, but not necessarily related, disorders, eg the simultaneous occurrence of urinary tract inflammation (FIC) and crystalluria*. While obstruction most typically results from the formation of urethral plugs, it may also be caused by the passage of small uroliths, or from pain or inflammation-induced urethral spasm. Although inflammation without crystalluria can result in obstruction with colloid matrix, it more typically causes hematuria and dysuria. Crystalluria is usually clinically silent, but if severe and persistent, it may predispose to the development of uroliths, and these, in turn can lead to urethral obstruction, and bladder inflammation, and/or, crystals can become embedded in urethral plugs and contribute to urethral obstruction.
    Normal cats, when fed a significant percent of their food as a dry diet, will produce concentrated urine. It is important to remember that it is normal for crystals to form in concentrated cat urine, especially when it has been allowed to cool down from body temperature. Finding anything other than large numbers and/or clusters of crystals in a freshly collected and still warm urine sample is unlikely to be of clinical significance.

Timecourse

  • Obstructive cases of FIC require immediate medical and/or surgical intervention.
  • Most cases of non-obstructive FIC are self-limiting; usually resolving within 5-10 days.
  • Most affected cats have episodes of clinical signs, which recur with variable frequency, but generally tend to decrease in frequency and severity over time.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Wallius B M, Tidholm A E (2009) Use of pentosan polysulphate in cats with idiopathic, non obstructive lower urinary tract disease, a double-blind, randomised, placebo-controlled trial. J Feline Med Surg 11 (6), 409-412 PubMed.
  • Buffington C A, Westropp J L, Chew D J et al (2006) Clinical evaluation of mulitmodal environmental modification (MEMO) in the management of cats with idiopathic cystitis. J Feline Med Surg (4), 261-268 PubMed.
  • Westropp J L, Kass P H, Buffington C A (2006) Evaluation of the effects of stress in cats with idiopathic cystitis. AVJR 67 (4), 731-736 PubMed.
  • Cameron M E, Casey R A, Bradshaw J W et al (2004) A study of environmental and behavioural factors that may be associated with feline idiopathic cystitis. JSAP 45 (3), 144-147 PubMed.
  • Gunn-Moore D A & Cameron M E (2004) A pilot study using synthetic feline facial pheromone for the management of feline idiopathic cystitis. J Feline Med Surg (3), 133-138 PubMed.
  • Gunn-Moore D A & Shenoy C M (2004) Oral glucosamine and the management of feline idiopathic cystitis. J Feline Med Surg (4), 219-225 PubMed.
  • Gunn-Moore D A (2003) Feline Lower Urinary Tract Disease. JFMS (2), 133-138 PubMed.
  • Kraijer M, Fink-Gremmels J & Nickel R F (2003) The short-term clinical efficiency of amitriptyline in the management of idiopathic feline lower urinary tract disease: a controlled clinical study. JFMS (3), 191-196 PubMed.
  • Kruger J M, Conway T S, Kaneene J B et al (2003) Randomized controlled trial of the efficacy of short-term amitriptyline administration for treatment of acute, nonobstructive, idiopathic lower urinary tract disease in cats. JAVMA 222 (6), 749-58 PubMed.
  • Lekcharoensuk C, Osborne C & Lulich J (2001) Epidemiological study of risk factors for lower urinary tract diseases in catsJAVMA 218 (9), 1429-1435 PubMed.
  • Sturgess CP, Hesford A, Owen H et al (2001) An investigation into the effects of storage on the diagnosis of crystalluria in cats. JFMS (2), 81-85 PubMed.
  • Buffington C A, Chew D J & Woodworth B E (1999) Feline interstitial cystitis. JAVMA 215 (5), 682-687 PubMed.
  • Markwell P J, Buffington C A, Chew D J et al (1999) Clinical evaluation of commercially available urinary acidification diets in the management of idiopathic cystitis in cats. JAVMA 214 (3), 361-365 PubMed.
  • Chew D J, Buffington C A, Kendall M S et al (1998) Amiytiptyline treatment for severe recurrent idiopathic cystitis in cats. JAVMA 213 (9), 1282-1286 PubMed.
  • Straeter-Knowlen I M, Marks S L, Rishniw M et al (1995) Urethral pressure response to smooth and skeletal muscle relaxants in anesthetized, adult male cats with naturally acquired urethral obstruction. Am J Vet Res 56 (7), 919-923 PubMed.
  • Buffington C A, Chew D J & DiBartola S P (1994) Lower urinary tract disease in cats: Is diet still a cause? JAVMA 205 (11), 1524-1527 PubMed.
  • Straeter-Knowlen I M, Marks S L, Speth R C et al (1994) Effect of succinylcholine, diazepam, and dantrolene on the urethral pressure profile of anesthetized, healthy, sexually intact male cats. Am J Vet Res 55 (12), 1739-1744 PubMed.
  • Osborne C A, Kruger J P, Lulich J P et al (1992) Feline matrix-crystalline urethral plugs: A unifying hypothesis of causes. JSAP 33 (4), 172-177 VetMedResource.
  • Kruger J M, Osborne C A, Goyal S M et al (1991) Clinical evaluation of cats with lower urinary tract disease. JAVMA 199 (2), 211-216 PubMed.

Other sources of information

  • Buffington C A (2011) Idiopathic cystitis in domestic cats - beyond the lower urinary tract. JVIM 25 (4), 784-796 PubMed.
  • Westropp J L & Buffington C A (2006) Etiopathogenesis of Feline Idiopathic Cystitis. In:Consultations in Feline Medicine 5. Ed August J R, Elsevier, pp 435-438.
  • Gunn-Moore D A (2002) Investigation of feline lower urinary tract disease (FLUTD). UK Vet(1), 49-58.
  • Gunn-Moore D A (2001) Pathophysiology of feline lower urinary tract disease (FLUTD). UK Vet(5), 20-26.
  • Gunn-Moore D A (2001) Treatment of feline lower urinary tract disease (FLUTD). UK Vet(5), 27-32.
  • Gunn-Moore D A (2000) Feline Lower Urinary Tract DiseaseIn Practice 22 (9), 534-542.
  • Davies M (1998) Urinary System. In: Manual of Small Animal Clinical Pathology. Eds Davidson M, Else R, Lumsden J. BSAVA, Cheltenham, p 287-336.
  • Kalkstein T S, Kruger J M & Osborne C A (1999) Feline Idiopathic Lower Urinary Tract Disease. Part I. Clinical ManifestationsComp Cont Ed Pract Vet21 (1): 15-26.
  • Kalkstein T S, Kruger J M & Osborne C A (1999) Feline Idiopathic Lower Urinary Tract Disease. Part II. Potential CausesComp Cont Ed Pract Vet21 (2): 148-154.
  • Kalkstein T S, Kruger J M & Osborne C A (1999) Feline Idiopathic Lower Urinary Tract Disease. Part III. DiagnosisComp Cont Ed Pract Vet21 (5): 387-448.
  • Kalkstein T S, Kruger J M & Osborne C A (1999) Feline Idiopathic Lower Urinary Tract Disease. Part IV. Therapeutic Options .Comp Cont Ed Pract Vet21 (6): 497-509.
  • Buffington C A T, Chew D J & DiBartola S P (1996) Interstitial cystitis in catsVet Clin North Am26 (2): 317-326.


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