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Feline Lower Urinary Tract Disease
Feline Lower Urinary Tract Disease
Feline Lower Urinary Tract Disease
PATHOPHYSIOLOGY
Feline Lower Urinary Tract Disease (FLUTD), or formerly Feline Urologic Syndrome (FUS), is typically seen in 1-
7 year old indoor and overweight male cats. More recently, it has been associated with a stressful event or
environment leading to changes in the patients urogenital tract, not to mention inflammatory signaling and
gastrointestinal status. Though there is no single leading cause, contributing factors have been attributed to a
longer and tapering urethra compared to females, formation of distal plug from inflammatory components
(mucus, protein, cells), uroliths, crystalluria, infectious vs sterile cystitis, and increased sympathetic tone to
the proximal urethra. Despite these, the majority are identified as idiopathic and given the name Feline
Idiopathic Cystitis (FIC).
On presentation, FLUTD is typically associated with immediate palpation of a distended bladder, however,
this can vary in size. Patients with cystitis typically have a completely empty bladder. Palpation of a medium
sized, but turgid bladder in such a patient is a likely indicator of urethral obstruction and treatment is
indicated. When in doubt a focussed urogenital ultrasound scan can be useful.
The first treatment priority is assessment and stabilisation of the patients cardiovascular status. Bradycardia
(HR< 160) is a critical finding and immediate treatment of hyperkalaemia is required. The magnitude of
hyperkalaemia was previously thought to correlate with the severity of clinical signs, but this has recently
been disproven. Multiple pathological processes contribute to poor cardiac output and sudden death in
FLUTD patients, so the current recommendation is to treat aggressively when there are signs of bradycardia
and ECG abnormalities rather than tailoring treatment to the magnitude of hyperkalaemia.
The effects of bradycardia are considered 2-fold, a reduction in cardiac output and reduced organ perfusion,
and its compensatory increase in sympathetic drive and vascular tone, resulting in improved pressure but
reduced blood volume, both of which reduce GFR further.
The reduction in GFR consequently leads to a direct reduction in renal tubular flow and other electrolyte
abnormalities. Once relieved, normal kidney function typically resumes, though post-obstructive diuresis
(POD) can occur (polyuria). This latter process is not well understood, though is possibly related to osmotic
diuresis from elevated urea, high tubular sodium and water retention, and the inability for ADH to have an
Regardless of the cause and ease of unblocking the urethra, the recommendation is to leave the urinary
catheter in place for at least 24hrs. This allows time for reduction of inflammatory effects on the bladder wall,
reduction in effects of sympathetic drive, monitor effects of possible POD, reduce crystalluria, and allow a
change in urinary characteristics from a possible infection. It is well-known struvite crystals form in alkaline
and high Magnesium (Mg) environments, and a high suspicion for an infectious cystitis should be considered
as urease-producing bacteria cleave urea to ammonia causing an increase in pH.
TREATMENT
INITIAL MANAGEMENT
UNSTABLE Patient (hyperkalaemia vomiting, obtunded, HR <160)
• Place IV Catheter
• Analgesia – care with contributing to worsening demeanour/respiratory drive (C1)
o Methadone 0.2-0.3mg/kg IM, or
o Buprenorphine 0.01-0.02mg/kg IM or IV
• Treat Shock by administering 10-15ml/kg boluses of crystalloid fluid until improvement in
cardiovascvular status (max 60ml/kg- usually 10-30ml/kg required)
• Treat Hyperkalaemia – monitor with ECG during treatment
o Calcium Gluconate 10%: 1ml/kg over 10 minutes (C1)
(max effect in 3-5mins)
o Glucose: given at 0.5g/kg (1ml/kg 50% glucose diluted 1 in 4) (C1)
(max effect in 30mins)
o +/- Insulin: 0.25-0.5 IU/kg IV or IM (C2)
(max effect in 30mins)
*NB: glucose MUST have been given first
*NB: 2.5% Glucose MUST be added to IV fluid (50ml of 50% added to 1L crystalloid)
o +/- NaHCO3: 1ml/kg (only if absolutely necessary), pH <7.2 and HCO3 <12 (C2).
Bicarbonate should be administered slowly >30min
• Relieve urethral obstruction and place indwelling urinary catheter under appropriate sedation
*Avoid isoflurane due to vasodilating effects on an already CV compromised patient (C1)
o Fentanyl 3-5ug/kg IV (0.3-0.5ml/5kg Cat, assuming 50ug/mL) +
Midazolam 0.2mg/kg IV (0.2ml/5kg Cat, assuming 5mg/mL) - same syringe (PREFERRED)
o Ketamine 2-4mg/kg IV (0.1-0.2ml/5kg Cat, assuming 100mg/kg) +
Diazepam 0.3mg/kg IV (0.3ml/5kg Cat, assuming 5mg/ml) – same syringe
(Only if NO Cardiac concerns)
o +/- Alfaxan PRN (1-2mg IV boluses as required)
o provide flow-by oxygen during procedure due to mild hypoventilation
o have intubation equipment at the ready
o no anaesthetic if moribund on presentation. In this situation, stabilising cardiovascular
status and enabling bladder decompression should be the first priority, and placing an
indwelling catheter performed without anaesthetic (local infiltration of prepuce) or delayed
until the patient is stable. Bladder decompression can be achieved without sedation by
Guidelines: Class 1 (C1) – Definitely perform (good evidence)
Class 2 (C2) – Consider performing (some evidence)
Class 3 (C3) – Do not perform (unsound evidence and/or deleterious)
AES – Protocols\Excellence Program\FLUTD Page 2 of 6
unblocking with a 22g IV catheter, or by cystocentesis.
MEDICATIONS TO BE DISPENSED
• Analgesia
o Buprenorphine 0.01-0.02mg/kg IV or SL q8-12hrs (C1)
• Muscle relaxants: started 24-36hrs after urinary catheter is placed only
REFERENCES
1. Drobatz, K., Costello, M. (2010). Feline Emergency and Critical Care Medicine Pp281-288
2. Roger A. Hostutler,
Dennis J. Chew, Stephen P. DiBartola. (2005). Recent Concepts in Feline Lower
Urinary Tract Disease. Vet Clin Small Animal 35: 147–170
3. Silverstein, D., Hopper, K. (2009). Small Animal Critical Care Medicine. Saunders Elsevier. PP 638
4. Buffington, C.A.T. (2011). Idiopathic Cystitis in Domestic cats – Beyond the Lower Urinary Tract. JVIM 25:
784-796
5. Hetrick, P.F. & Davidow, E.B. (2013). Initial treatment factors associated with feline urethral obstruction
recurrence rate: 192 cases (2004-2010). JAVMA 243(8): 1140-1146
6. Segev, G. et al. (2011). Urethral obstruction in cats: predisposing factors, clinical and clinicopathological
characteristics and prognosis. JFMS 13: 101-108
7. Huggonard, M. et al. (2013). Occurrence of bacteriuria in 18 catheterised cats with obstructive lower
urinary tract disease: a pilot study. JFMS 15(10): 843-848
8. Cannon, A. Evaluation of trends in urolith composition in cats: 5230 cats (1984-2004). JFMS 231(4): 570-
576
9. Buffington CA, Westropp JL, Chew DJ, et al. (2006). Clinical evaluation of multimodal environmental
modification (MEMO) in the management of cats with idiopathic cystitis. Journal of Feline Medicine and
Surgery 8 (4): 261-268
10. Griffith CA, Steigerwald ES, Buffington CA. (2000). Effects of a synthetic facial pheromone on behavior of
cats. J Am Vet Med Assoc 217: 1154-1156.
11. www.vin.com. (2007-2013). Veterinary Information Network