Feline lower urinary tract disease (FLUTD)


Contents

  • 1 Introduction
  • 2 Causes
  • 3 Clinical signs
  • 4 Diagnosis
    • 4.1 Calcium Oxalate
    • 4.2 Struvite
    • 4.3 Others
  • 5 Treatment
  • 6 Aftercare
    • 6.1 Medication
    • 6.2 Dietary change
  • 7 References

 

Introduction

The term ‘cystitis’ means an irritation of the urinary bladder. It occurs in both male and female cats and is also known as Feline Lower Urinary Tract Disease (FLUTD). It affects the bladder (not the kidneys), resulting in the production of tiny crystals and bloody urine. The cat often urinates much more frequently than normal, and often passes only a few drops of urine. This can be confused by the cat’s owner with constipation. Many cats will urinate in places other than the litter box due to the urgency of the need to urinate. Blood spots on tile floors, counter tops, sinks, and bathtubs are often the first signs that the cat has a problem.

 

Causes

The exact cause of cystitis is unknown, but certainly many of the usual suspects are incriminated, in order of importance;

  • Idiopathic cystitis (IC) – this is the most common type of FLUTD. Humans with IC appear to suffer from a range of co-morbid conditions, and there is some data to suggest this may be the case in cats. For example, FLUTD has been reported to be a co-morbid condition in cats with separation anxiety syndrome, hypertrophic cardiomyopathy and obesity.
  • Urinary crystals – only about 25% of cats with FLUTD have cystic calculi. Presence of crystals only indicates the potential to form uroliths. Dry foods will aggravate any underlying bladder infection/inflammation. This is because of the higher mineral content (ash) and lower water content of dry foods.
  • Viral – many cats with cystitis have concurrent FHV (herpes virus) infection
  • Cystitis, bacterial – rare in cats.
  • Chronic renal disease with secondary haematuria/cystitis
  • Neoplasia of the urinary tract – usually transitional cell carcinoma. Rare in cats compared with dogs, presumably due to a difference in tryptophan metabolism that results in low urinary concentrations of carcinogenic tryptophan metabolites. The mean age of affected cats is 9 yr, often affecting purebred cats such as Siamese.

The average age of a cat with FLUTD is 4 years. Of all cats with FLUTD:50% will not have a cause which can be determined despite extensive testing

  • 20% will have bladder stones
  • 20% will have a urethral blockage
  • 1-5% will have a true infection
  • 1-5% will have a urinary tract cancer
  • 1-5% will have had trauma to the urinary tract (i.e. have been hit by a car etc.)
  • 1-5% will have a combination of a bladder stone and an infection

Until recently, it was thought that most uroliths in cats were small and resembled sand or were gelatinous plugs that differed from typical uroliths in that they contained a greater amount of organic matrix, giving them a toothpaste-like consistency. Matrix-crystalline plugs are most commonly found within the urethra near the urethral orifice and are primarily responsible for urethral obstruction. Recently, prevalence of urolithiasis with grossly observable stones composed primarily of calcium oxalate has increased in cats. The most common feline uroliths are calcium oxalate, magnesium ammonium phosphate (struvite), and urate.

 

Clinical signs

Haematuria (blood in urine), pollakiuria (frequent urination), and stranguria (painful urination) are the characteristic clinical signs of FLUTD in cats. Urolithiasis is usually suspected based on clinical signs of haematuria, dysuria, or urethral obstruction. Urinalysis, urine culture, radiography, and ultrasonography may be required to differentiate uroliths from urinary tract infection or neoplasia. Radiography, cystoscopy, or ultrasonography are critically important to detect uroliths because only ~10% of feline urocystoliths can be detected by abdominal palpation. Uroliths with a diameter >3 mm are usually radiodense; however, because smaller uroliths are common, double contrast radiography may be required for detection. Radiographic evidence of uroliths is seen in ~20% of cats with haematuria or dysuria. The usual clinical approach to grossly observable urocystoliths is surgical removal or lithotripsy where available, followed by dietary therapy instituted as a preventive measure. For sterile struvite uroliths, medical dissolution is the preferred treatment.

Some cats, especially male cats, can have crystals in the urine which will completely block the urethra (the tube from the bladder to the genitals). In these cases, the bladder cannot empty. Overfilling of the bladder occurs and unless the bladder is catheterised, will burst. These cases are considered emergencies by veterinarians. If the obstruction is not relieved within 48 hours, most cats will die from kidney failure and the retention of toxins that were not removed by the kidneys. Because the urethra is relatively larger in the female cat, the emergency posed by complete obstruction is almost always found in male cats.

 

Diagnosis

1. Combine history including behavioural history, physical examination, laboratory data, radiographs +/- abdominal ultrasonography

2. Complete urinalysis (USG, dipstick, sediment exam, and ideally C+S) should always be performed: haematuria, pyuria, proteinuria is often found. Other finding include crystals, mucoproteinaceous debris, pH imbalance, bacteria, neoplastic cells and inflammatory cells. NB: crystals dissolve in the urine within 4-6 hrs – therefore do in-house sediment exam ASAP to identify crystals

3. Minimum electrolytes and biochemistry blood profile data base required, although TP/PCV, biochemistry and electrolytes/blood gasses may be run. Azotaemia, hyperphosphataemia and acidosis may be noted in more severe cases.

4. Diagnosing this disease can be difficult. Other clinical tests such as X-rays of the bladder can help. Ruling out the presence of bladder stones is very important, which is why many vets will Xray your cat if they are unsure or if the problem recurs.

 

Calcium Oxalate

Calcium oxalate uroliths are the most common feline uroliths and the most common nephrolith, although their underlying cause is unknown. Common management schemes that involve feeding urine-acidifying diets with reduced magnesium, have reduced the incidence of feline struvite urolithiasis. Magnesium has been reported to be an inhibitor of calcium oxalate formation in rats and humans; thus, the reduced magnesium concentration in feline urine may partially explain the increase in calcium oxalate stones in cats.

Medical protocols that promote calcium oxalate dissolution are not known; therefore, surgery and lithotripsy are the primary means for removal (small bladder stones may be eliminated by voiding urohydropulsion). However, some calcium oxalate uroliths, especially those in the kidneys, may not cause clinical signs for months to years. Because of the unavoidable destruction of nephrons during nephrotomy, this procedure is not recommended unless it can be established that the stones are a cause of clinically significant disease. Recurrence remains problematic. A variety of diets has been formulated to restrict the formation of calcium oxalate uroliths and should be considered appropriate for maintenance in cats with nephroliths and following the removal of urocystoliths. Eliminating any associated urinary tract infections, avoiding mineral and vitamin C and D supplementation, and encouraging water consumption are critical1.

 

Struvite

Three distinct types of struvite uroliths are recognized in cats: amorphous urethral plugs with a large quantity of matrix, sterile struvite uroliths (which form perhaps as a result of certain dietary ingredients), and struvite uroliths that form as a sequela of urinary tract infection with urease-producing bacteria. Struvite uroliths induced by infection are less common than sterile struvite uroliths. An additional type of struvite urolith in cats consists of a sterile struvite nidus that predisposes to urinary tract infection with urease-producing bacteria and subsequent formation of infected struvite laminations around the sterile nidus.

Treatment of sterile struvite urolithiasis focuses on reducing the urine pH to ≤6.0 and on reducing the urine magnesium concentration by feeding magnesium-restricted diets. Reducing urine pH and magnesium concentration is best accomplished by feeding a commercially available prescription diet formulated for this purpose. Generally, neither sodium chloride nor urine acidifiers should be given concurrently with these diets because they are already supplemented with sodium chloride and formulated to produce aciduria. In addition, these diets should not be fed to cats that are acidemic, have azotaemia of any cause, or have cardiac dysfunction or hypertension. Urolith size and crystalluria should be monitored every 4 wk by radiographs or ultrasonography and urinalysis, respectively. Struvite crystals should not form if therapy has been effective in producing urine that is undersaturated with magnesium, ammonium, and phosphate. Because small uroliths may not be detected radiographically, the calculolytic diet should be continued for ≥4 wk after radiographic documentation of urolith dissolution. If treatment does not induce complete dissolution of uroliths, it is likely that either the wrong mineral component was identified, the nucleus of the urolith is composed of a different mineral than the outer portion of the urolith, or the owner is not complying with therapeutic recommendations1.

 

Others

Ammonium urate, uric acid, calcium phosphate, and cystine uroliths are less common in cats, but ammonium urate and uric acid account for ~6% of feline uroliths. Although a renal tubular reabsorptive defect and portovascular anomalies have been incriminated as causes in a few cases, the cause of most urate uroliths in cats has not been established. Nonetheless, formation of highly acidic and concentrated urine associated with consumption of diets high in purine precursors (especially liver) appears to be a risk factor.

Medical protocols that consistently promote dissolution of ammonium urate uroliths in cats have not been developed, and surgery remains the most common method of removal. For small stones, voiding urohydropulsion may be effective. Prevention should include feeding a diet low in purine precursors and promoting formation of less acidic urine that is not highly concentrated. Although allopurinol may reduce the formation of urate in cats, studies of the efficacy and potential toxicity of allopurinol in cats are required before meaningful guidelines can be established1.

 

Treatment

In acute medical cases of urethral blockage and bladder overfilling, feline patients should have ECG monitoring before and during anaesthesia for catheterisation. Cardiac disturbances can be seen with K+ above 6.5-7.0 mmol/L; and these may include bradycardia, atrial standstill, spiked T-waves, accelerated idioventricular rhythm, ventricular tachycardia, or fibrillation. Therapy for hyperkalaemia should be instigated.

Relief of obstruction should be attempted without GA in extremely depressed cats. If restraint is required, use low dose diazepam/ketamine (1-2 mg/kg IV) or propofol IV. Otherwise, general anaesthesia is induced (with either propofol, diazepam/ketamine, or alfaxolone) and maintained with isoflurane and oxygen.

Male cats who frequently suffer from cystitis and blockage of the urethra have a high risk of kidney damage and sudden death due to bladder rupture.

In these cases, the cause is usually the presence of large quantities of urinary crystals in the bladder. Surgical intervention usually involves either a cystotomy or perineal urethrostomy. With a perineal urethrostomy, (often called a ‘sex change operation’), the penis is amputated and the urethra exteriorised as a makeshift vagina-like opening, thus preventing any further blockage of urine. Although considered a drastic step, this operation is usually successful and stops further pain and disease in the cat and is recommended in male cats that have had a urethral obstructions three times or more. A cystotomy is much less surgically demanding and has a higher success rate if the cat is prevented form eating dry food in the future. It also has the advantage of being more cost effective in the long term as complications are minimal.

 

Aftercare

 

Medication

Monitor for post-renal azotaemia due to tubular back-pressure causing a reduction in the GFR. Monitor also for post-obstructive diuresis then maintain fluid balance in light of post-obstructive diuresis (normal urine output is 1-2ml/kg/hr). Consider using phenoxybenzamine or prazosin as an alpha-1 antagonist to relax the internal urethral sphincter. Consider starting as soon as the urinary catheter is in place. Acetylpromazine also has alpha-1 antagonist activity, so can be used to sedate and help express bladders if there is some functional obstruction post-catheter removal. The use of pentosan polysulphate to minimise clinical signs is at present debatable.

Routine analgesia is preferred, using NSAIDs (e.g. meloxicam) as a primary choice of drug.

 

Dietary change

The presence of crystals suggests that a diet change is in order, including adding urinary acidifiers such as Acidurin® to help keep the urine acidic and prevent further crystals from forming. It is also important to feed the cat dry food that is low in minerals and which produces and acidic urine (such as Hills C/D diet®) or else avoid dry foods altogether and feed only fresh food or tinned food, which have a higher moisture content. Because cats that get cystitis normally have recurring problems, it is important to keep them on a modified diet, urinary acidifying tablets and reduced stress.

One aspect of long-term management of FLUTD is to promote increased water consumption by the cat. This can be problematic as cats are reluctant drinkers. Increased drinking has been thought to increase the mechanical flushing of the urinary bladder and thus reduce the formation of crystals. One method of stimulating water intake in cats is by increasing the salt content of the food. Canned food are a frequent recommendation as they contain 70-80% water. Several studies have shown that increasing dietary salt (NaCl) can increase water intake and urine volume, and decrease urine specific gravity2. It has been suggested that increased salt intake in cats with existing FLUTD may aggravate underlying kidney disease and elevate blood pressure, but a comprehensive study by Xu et al showed that changes in dietary salt intake had minimal effects on total body hydration status, blood pressure and markers of renal function3. Rather than a risk factor, they also noted that increasing salt in diet had a protective influence against the development of chronic renal disease in cats.

 

References

1. Merck Veterinary Manual http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/130617.htm

2. Kirk, CA et al (2006) Effects of sodium chloride on selected parameters in cats. Vet Ther 7: 333-346

3. Xu, H et al (2009) Effects of dietary sodium chloride on health parameters in mature cats. JFMS 11; 435-441

4.Wallius, BM & Tidholm, AE (2009) Use of pentosan polysulphate in cats with idiopathic, non-obstructive lower urinary tract disease: a double-blind, randomised, placebo-controlled trial. JFMS 11: 409-412


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