Sunday, July 24, 2011

Notes from July 2011 St. Louis AVMA Conference-Idiopathic Cystitis

These are papers from the July 2011 St. Louis AVMA conference.  I’ve edited them to delete some of the vet only jargon and for space considerations.  If you see (…) that means that information has been deleted due to these considerations.  The ones listed here include HCM, and other heart related papers, treatments, papers on x-rays and echos, thrombosis, kidney disease, idiopathic cystitis, pain management, anesthesia and cardiac disease, supplements and other hazards for pets, and some other basic information I hope is helpful.

Feline Idiopathic Cystitis

Larry G. Adams, DVM, PhD, Diplomate ACVIM (SAIM)

Purdue University School of Veterinary Medicine

Feline idiopathic cystitis, formerly called  idiopathic feline lower urinary tract disease, is

defined as a disease of undetermined etiology characterized by hematuria, dysuria, pollakiuria

and possible urethral plug formation.  This condition overlaps with 2 clinical syndromes of

dysuria/pollakiuria syndrome and urinary obstruction. The syndrome of dysuria/pollakiuria in

cats is often associated with hematuria and was initially referred to as the "feline urologic

syndrome" or "FUS".  Idiopathic cystitis is one of several differential diagnoses for

dysuria/pollakiuria in cats.  Unfortunately many veterinarians assume all cats with

dysuria/pollakiuria or urinary obstruction should all receive the same stereotyped  treatment

without  first obtaining a diagnosis. This leads to frustration when cases don’t resolve with


Differential diagnoses for lower urinary tract diseases in young adult cats from most

common to least common include idiopathic cystitis (with or without urethral plug formation),

urolithiasis, iatrogenic disorders (urethral tears, urethral stricture), bacterial UTI, neoplasia

(lymphoma, transitional cell carcinoma), fungal UTI, prostate disease, and idiopathic detrusor

instability.  The role of urachal diverticula in lower urinary tract disease in cats is controversial.

While cats with diverticula may have persistent clinical signs that have been suggested  to be

caused by the diverticula, diverticula may spontaneously regress with resolution of lower

urinary tract disease suggesting the diverticula are a result of the disease rather than a cause

of the disease.  

The causes of lower urinary tract disease in geriatric cats are different than

young adult cats.  In one study of geriatric cats, the causes from most common to least

common were UTI (46%), urolithiasis with UTI (17%), urolithiasis without UTI (10%), urethral

plugs (7%), traumatic injury (7%), idiopathic cystitis (5%), and neoplasia (3%).  The higher

incidence of UTI in geriatric  cats versus only 1-2% incidence of UTI in young adult cats with

lower urinary tract disease is due to underlying diseases that predispose geriatric cats to UTI

such as chronic kidney disease, diabetes mellitus, and hyperthyroidism.

Diagnosis of idiopathic cystitis is based on ruling out other known causes of lower urinary

tract disease; it is an exclusion diagnosis.  The minimum work-up should consist of a

urinalysis, urine culture, and abdominal radiographs, although these do not rule-out all possible

causes of lower urinary tract disease. Cases that persist beyond 5 to 7 days may require

additional work-up, such as ultrasound or contrast radiographs to rule out radiolucent uroliths

and neoplasia, and urine cultures for unusual organisms (mycoplasma and ureaplasma).

Cystoscopy may be used to confirm the diagnosis of idiopathic cystitis

Idiopathic cystitis

There are two clinical forms of idiopathic cystitis: non-obstructive and obstructive.  In the

Non-obstructive form, male or female cats present with a history of hematuria, dysuria, and

pollakiuria.  There tends  to be episodic clinical signs with acute onset. Understanding  the natural

course of the disease is critical to accurately interpret any proposed  treatment effects.

Idiopathic cystitis usually resolves spontaneously within 5 to 7 days regardless of treatment,

thus any therapy may appear effective. Recurrence is common but unpredictable; cats can be

normal  for days to years between episodes. The obstructive form occurs in male cats due to

occlusion of the urethra by urethral "plugs".  Urethral plugs are not uroliths; rather uroliths are a

differential diagnosis for cause of urethral obstruction.  Urethral plugs differ from  uroliths in that

they lack organized  internal structure. They are semi-solid plugs composed of matrix and

crystals (usually struvite) and often have the consistency of thick toothpaste. The matrix

consists of varying quantities of proteins and cellular debris (RBC, WBC, epithelial cells).

Crystalluria probably does play a role in the genesis of urethral obstruction due to urethral

plugs.  The crystals act to solidify the plug resulting in obstruction.  While most urethral plugs

contain struvite crystals entrapped within the matrix plug,  some urethral plugs may contain

calcium  oxalate or urate crystals or some plugs lack any crystalline component.  Indirect

evidence suggests that dietary therapy designed to prevent struvite crystalluria reduces the

incidence of recurrent urinary obstruction. 

 If obstruction is due to true uroliths, the cause  is urolithiasis, not idiopathic cystitis.  

Massive crystalluria can lead to the formation of multiple small uroliths, which are like "sand" and can cause obstruction.  This illustrates a continuum between urethral plugs and  urolithiasis.

Urethral obstruction may occur abruptly without prior

clinical signs or may be preceded by dysuria/pollakiuria. Urethral matrix plugs may begin to

form in female cats and non-obstructed male cats, but they pass out the urethra without

becoming lodged. Increased crystalline component of urethral plugs may solidify the plug

causing obstruction.  Urethral obstruction is life-threatening.  Urethral obstruction tends to recur

with subsequent episodes of idiopathic cystitis…Cats with idiopathic cystitis have decreased size and function

of their adrenal glands.  The specific cause and effect link between the adrenal abnormalities and FIC in

these cats is not known, but this may provide insight into the pathogenesis of this disorder.

This also correlates to observations that cats with idiopathic cystitis tend  to have recurrences

during periods of environmental “stress”.  Cats with idiopathic cystitis have increased

catecholamine levels and  increased bladder permeability during periods of stress.

Treatment of Idiopathic Cystitis

There is no proven effective therapy for treatment of idiopathic cystitis.  The disease

usually resolves spontaneously within 5-7 days in non-obstructed cats.  Antibiotics are only

indicated for documented  UTI or prophylaxis following indwelling urethral catheterization.

Management of urinary obstruction is similar to urinary obstruction of other causes.  Although

several treatments have been suggested for idiopathic cystitis, none have been proven more

effective than placebo. Antibiotics are not effective in treatment of idiopathic cystitis.

Methylene blue (a urinary antiseptic) and phenazopyridine (a urinary analgesic) are

contraindicated in cats because they cause Heinz body hemolytic anemia  and

methemoglobinemia. Corticosteroids have been suggested to reduce inflammation in

idiopathic cystitis, but a double-blind clinical trial showed no improvement with steroids

compared to placebo.   Prednisone also did not reduce inflammation in an experimental model

of idiopathic cystitis and predisposed the cats to UTI and pyelonephritis. Steroids increase

catabolism, which can worsen postrenal uremia from obstruction.  Intravesical DMSO also was

not beneficial, and it may predispose the cat to UTI and pyelonephritis.  Intravesical PGE1

was also not effective in an experimental model of interstitial cystitis.  Propantheline is an

antispasmodic that may reduce the severity and frequency of "urge" incontinence in cats with

non-obstructed idiopathic cystitis. However, this is symptomatic only and does not affect the

rate of recovery. Although there is no research data to support narcotics, some clinicians

recommend narcotic analgesia to reduce clinical signs during acute episodes of idiopathic

cystitis. Oral butorphanol (0.5-1 mg/kg PO q6-8h) or sublingual (buccal) buprenorphine (0.01-

0.03 mg/kg q 6-8 h) may be used to alleviate pain.

Prevention of Idiopathic Cystitis

There is also no proven preventative therapy for idiopathic cystitis. Uncontrolled clinical

trials suggest that dietary therapy designed to prevent crystalluria, such as a canned dietary

therapy, may reduce the incidence of recurrent FIC episodes and urethral obstruction .

Other medical therapies have been recommended to reduce struvite crystalluria in cats with

idiopathic cystitis which have not been proven effective including distilled water for drinking

water, salt supplementation, semi-moist cat foods or adding water to the diet, etc. Of these

measures, adding water to the diet and/or feeding canned diets is the main treatment that

appears to reduce recurrence of idiopathic cystitis.

A non-controlled open label clinical trial suggested that amitriptyline (5-10 mg per cat q24h)

may be effective for prevention of recurrence of idiopathic cystitis; however clinical response is

often minimal.  Perineal urethrostomy (PU) has been advocated for prevention of recurrent

urethral obstruction.  Perineal urethrostomy may reduce the incidence of obstruction; however,

it does not address the underlying disease process.  Perineal urethrostomy can also

predispose to ascending UTI, which can lead to infection-induced struvite urolithiasis, along

with potential complications including urethral stricture.  Although GAG replacement

therapy (e.g., glucosamine, pentosan polysulfate) has been recommended for treatment of

idiopathic cystitis, one study did not demonstrate any benefit of glucosamine over placebo  treated

cats.  In this study, most cats were fed more canned  food during  the study and both

glucosamine-treated and placebo-treated cats improved to a similar degree.   In a multicenter

clinical trial of GAG therapy, pentosan polysulfate (Elmiron) had a small beneficial effect on

cystoscopic scores in cats with idiopathic cystitis, but there was no difference in clinical signs

compared to placebo…a placebo-controlled study of pheromone therapy also failed to demonstrate

any benefit.  A suggested  that environmental enrichment along with other behavioral modifications …significant improvement of the clinical signs of feline lower urinary tract disease and warrants further

study.  Environmental enrichment normalized many of the catecholamine levels and

increased bladder permeability in cats with idiopathic cystitis.

Urinary Obstruction

Complete lower urinary tract obstruction causes death due to acid-base and electrolyte

abnormalities associated with postrenal uremia. Damage from urinary obstruction is

accelerated if UTI is also present. Urinary obstruction in a patient with UTI may result in sepsis

(urosepsis). Urethral obstruction may cause excessive bladder distension resulting in detrusor

atony or weakness, which disrupts tight junctions between muscle cells. This is common in

cats obstructed by urethral plugs, and usually resolves over several days if the bladder is kept


Severe hyperkalemia is the usual cause of death from urethral obstruction. An ECG will

reveal tall T waves, prolonged P-R, QRS, and Q-T intervals, bradycardia, and ventricular

asystole. Severe metabolic acidosis also occurs due to lack of excretion of metabolic acids.

Hypothermia and dehydration are also common with severe postrenal uremia. Urinary

obstruction causes increased tubular pressure, which impairs glomerular filtration, renal blood

flow, and tubular function. Tubular function is often impaired for several days after the relief of

obstruction. Post-obstructive diuresis may result in massive polyuria for several days. The

mechanism of post-obstructive diureses may be tubular dysfunction, solute diuresis, volume

expansion, or humoral factors such as atrial natruretic factor.

Treatment of Urinary Obstruction

Patient Stabilization: The goals in treating urethral obstruction are to re-establish urine

flow via low pressure excretory pathway, treat metabolic consequences of obstruction,

treat/prevent UTI, and preserve renal function. In the treatment of complete urethral

obstruction, the bladder should be decompressed by careful cystocentesis with samples saved

for urinalysis and culture. This relieves intravesical pressure and allows the kidneys resume

urine production, and relieves intravesical pressure, which makes relieve of obstruction easier.

Intravenous fluid therapy is needed to correct the azotemia, hyperkalemia, acidosis, and

dehydration…Intravenous bicarbonate was previously recommended to correct the acidosis and to decrease

serum potassium levels; however this will also decrease serum ionized calcium

concentrations, which are commonly decreased with obstruction. A more effective means to

correct hyperkalemia by transcelluar shifts is intravenous glucose and insulin therapy.

Intravenous calcium gluconate may be necessary to treat the ionized hypocalcemia and to

counteract the cardiac affects of hyperkalemia in patients at risk for dying from cardiac

arrhythmias. Hypothermic animals should be placed on a warm water blanket until the

temperature is normal.

Relief of urethral obstruction: Urethroliths should NOT be pushed back to the urinary

bladder using a rigid urinary catheter. Urethroliths should be retropulsed back into bladder for

medical dissolution or surgical removal. Urethral plugs should be dislodged manually or

flushed back into bladder…If necessary, an indwelling urinary catheter

should be maintained connected to a closed collection system.  Indwelling urethral catheters

predispose to UTI, and may promote urethral inflammation, edema, and potentially, urethral

stricture formation.  Indications for an indwelling urethral catheter in cats are: inability to

produce adequate size and force of urine stream by bladder compression following urethral

flushing, repeated episodes of obstruction occurring over a period of hours, severely azotemia

cats with severe electrolyte abnormalities, and cats with large amounts of urine sediment

and/or blood clots in the urine. After urethral catheter removal, cats should be monitored

closely for recurrent obstruction for 24-48 hours.

Alternate protocol for male cats without catheterization: The pathogenesis of urethral

obstruction in cats with idiopathic cystitis includes not just the intraluminal plug, but also

includes urethral spasm and mucosal edema in response to the intraluminal plug. A recent

report indicates that some cats can be managed without urethral catheterization by a

combination of repeated cystocentesis and medications to relieve pain and urethral spasm.30

Increased sympathetic tone and pain may both contribute to increased urethral contraction and

perpetuation of the urethral obstruction. This protocol was used as alternative to euthanasia

for clients who could not afford traditional treatment with urethral catheterization.30 Cats should

be evaluated with abdominal radiographs to rule out radiopaque uroliths before pursuing this

approach. The cats were sedated with 0.25 mg of acepromazine given IM and 0.075 mg

buprenorphine given IM or PO. The bladder was decompressed by cystocentesis q 8 h until

the cats were able to urinate on their own. The cats were housed in quiet, darkened ward away

from traffic and dogs in an attempt to reduce stress and catecholamine release. .

Acepromazine (2.5 mg PO) and buprenorphine (0.075 mg PO) were repeated q 8 h. If the cat

had not urinated by 24 hours, medetomidine (0.1 mg IM q 24 h) on day 2 and 3. In this report,

11 of 15 cats were able to urinate on their own 35 + 22 hours after treatment was started (9/11

within 48 hours).30 Recurrence rates were seemingly lower than cats treated by urethral

catheterization. The cats that failed the protocol developed uroabdomen (3) or hemoabdomen

(1) as a result of repeated cystocentesis and excessive urine production. The uroabdomen

was likely from bladder over distention following cystocentesis and was not from ruptured

bladder in any of the cats. The cats that failed had higher baseline creatinine and thus likely

had intense post-obstructive dieresis. Therefore the protocol might be more successful with

more frequent cystocentesis, but this has not been evaluated.


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