Urinary DISeASES

in Small Animal
Nusdianto Triakoso
Top 3 Health Concerns
MAF (1998)
• Urinary disease the most common
health concerns (Morris Animal Health
Foundation, 1998)
• FLUTD the most common health
concerns (VPI Pet Insurance, 2013)
• FLUTD the second most common
health concerns (Banfield Pet Hospital,
2016; Nationwide Pet Insurance, 2017)
• Canine UTI approximately 14% of dogs
visit to their Veterinarian (Ling, 1984)
Clinical Manifestation
• Hematuria • Renomegali
• Dysuria • Incontinentia urine
• Stranguria • Uremic breath
• Pollakiuria • Oral ulcers
• Poliuria (Polidypsia)
• Oligouria
• Anuria
• Periuria
Fluid Balance
• Ins
• Drink water
• Feed
• Metabolic water

• Outs
• Urine
• Feces
• Respiration
• Sweats
 Indices Dogs Cats
Water intake 60-90 ml/kg/day 45 ml/kg/day
Polydipsia >90 ml/kg/day >45 ml/kg/day
Urine production 20-40 ml/kg/day 10-20 ml/kg/day
Polyuria >45 ml/kg/day >40 ml/kg/day
Oligouria 0.25 ml/kg/h 0.25 ml/kg/h
Anuria <0.08 ml/kg/h <0.08 ml/kg/h
pH urine 5.5-7.5 5.5-7.5
Urine specific gravity 1.020-1.040 1.030-1.045
 • Acute Renal Failure
• Chronic Renal Failure
• Feline Lower Urinary Tracts Diseases
• Feline Urethral Obstruction
• Canine and Feline Urolithiasis
• Feline Idiophatic Cystitis
 Acute
Renal Failure

• Acute Kidney Injury

• Acute uremia is a clinical syndrome characterized by sudden onset of renal
outflow or excretory failure; accumulation of uremic toxins; dysregulation
of fluid, electrolyte, and acid-base balance; and clinical signs of uremia.
• Depending on the underlying cause, acute uremia is potentially reversible
if diagnosed quickly and treated aggressively.
This chapter refers to intrinsic acute kidney injury and ureteral obstruction.
Signs
• Historical Findings
Sudden onset of anorexia, listlessness, depression, vomiting (± blood),
diarrhea (± blood), halitosis, ataxia, seizures, known toxin or drug
exposure, recent medical or surgical conditions, and oliguria/anuria or
polyuria.
• Physical Examination Findings
Normal body condition and hair coat, depression, dehydration (or
iatrogenic overhydration), scleral injection, oral ulceration, glossitis,
necrosis of the tongue, uremic breath, hypothermia, fever, tachypnea,
bradycardia, non-palpable urinary bladder, and asymmetrically
enlarged, painful, firm, kidneys.
CAUSES
• Hemodynamic/Hypoperfusion
Shock, trauma, thromboembolism (e.g., DIC, vasculitis, transfusion reaction), heatstroke,
excessive vasoconstriction (e.g., administration of NSAIDs), adrenal insufficiency, excessive
vasodilation (e.g., ACEI or antihypertensive drugs), prolonged anesthesia, significant
hypertension, heart failure.
• Nephrotoxic
Ethylene glycol, aminoglycoside, amphotericin B, chemotherapeutic agent
(e.g., cisplatin, doxorubicin), thiacetarsamide, NSAIDs, radiographic contrast agents, heavy metals
(e.g., lead, mercury, arsenic, thallium), insect or snake venom, heme pigment, calcium, grape or
raisin ingestion (dogs), and lily ingestion (cats).
• Intrinsic and Systemic Disease
Leptospirosis, Lyme disease, immune-mediated glomerulonephritis and arteritis, pancreatitis,
septicemia, DIC, hepatic failure, heat stroke, transfusion reaction, bacterial endocarditis,
pyelonephritis, cortical necrosis, and lymphoma. Unilateral or bilateral ureteral obstruction (cats)
Pathophysiology
• The kidneys are susceptible to
ischemia and toxicants because
their unique anatomic and
physiologic features
• The kidneys play role in the
biotransformation of many drugs
and toxicants
PATHOPHYSIOLOGY
• AKI may be initiated by ischemia, nephrotoxins, infection, prolonged urine
outflow obstruction and severe non-renal systemic diseases (e.g., pancreatitis,
neoplasia).
• AKI may be divided into four sequential stages: (1) initiation, (2) extension, (3)
maintenance, and (4) recovery. Clinically, transition from one stage to the next
may not be clearly evident, and not all stages need be present in an individual
patient.
• Renal excretory failure is perpetuated by multiple factors including (1) reduced
glomerular surface area and permeability, (2) low renal blood flow, (3)
intratubular obstruction by tubular debris, (4) cellular and interstitial edema, and
(5) “backleak” of filtrate across damaged tubular epithelia. Resolution occurs by
renal regeneration and repair.
• Ureteral obstruction results from ureteroliths, inspissated blood, or inflammatory
debris
DIAGNOSIS
• DIFFERENTIAL DIAGNOSIS
Prerenal azotemia—oliguria, concentrated USG (dogs, ≥ 1.030; cats, ≥ 1.035),
correctable with fluid repletion.
Post-renal azotemia—anuria, dysuria, stranguria, large bladder, urethral
obstruction, uroperitoneum.
CKD—polyuria, polydipsia, history of chronic illness, loss of body condition,
anemia.
Prerenal on CKD—clinical and laboratory features of CKD but partially correctable
with fluid repletion.
Prerenal on AKI—acute onset uremia, partially correctable with fluid repletion.
Hypoadrenocorticism—hyponatremia, hyperkalemia.
Pancreatitis—high serum lipase, cranial abdominal pain, high trypsin-like
immunoreactivity, hyperbilirubinemia, and increase in liver enzyme activity.
Prerenal azotemia vs acute renal failure
Indices Prerenal Azotemia Acute Renal Failure
Urine specific gravity Hypersthenuric Isosthenuric or minimally
concentration
Urine Na <10 to 20 >25 to 40
Urine creatinine to plasma >20:1 <10:1
creatinine ratio
Renal failure index (urineNa/urine <1 >2
to plasma creatinine ratio)
acute vs Chronic Renal Failure
Acute Renal Failure Chronic Renal Failure
History of ischemia or toxicant exposure Histrory renal disease or polyuria-polydipsia
Normal or increased hematocrit Non regenerative anemia
Swollen kidneys Small, irregular kidney
Hyperkalemia Normal or hypokalemia
Metabolic acidosis Normal or mild metabolic acidosis
Abnormal urine sediment Normal urine sediment
Good body flesh Weight loss, hyperparathyroidism (osteodystrophy)
Relatively severe clinical signs for level of renal Relatively mild clinical signs for level of renal
dysfunction dysfunction
DIAGNOSIS
• CBC/BIOCHEMISTRY/URINALYSIS
Normal or high PCV, variable leukocytosis, and lymphopenia.
Progressive (moderate to severe) increases in SUN, creatinine, and phosphorus; variably
high potassium and glucose; and variably low bicarbonate and calcium concentration.
Urine SG ≤ 1.020, mild-to-moderate proteinuria, glucosuria; variable number of cellular,
and/or granular casts, WBCs, RBCs, and tubular epithelial cells; variable bacteriuria and
calcium oxalate crystalluria (sometimes seen in association with ethylene glycol toxicity).
• IMAGING
Survey and contrast radiography—kidneys are normal to large, with bilateral smooth
contours; asymmetric kidneys in cats (“big kidney-little kidney” syndrome) with ureteral
obstruction—small radiodense uroliths in the retroperitoneum.
Percutaneous nephropyleography or contrast CT for ureteral obstruction.
Ultrasonography—severe cortical hyperechogenicity suggests ethylene glycol toxicity.
Moderate cortical hyperechogenicity suggests glomerulonephritis or nephrosis. Pelvic
and/or ureteral dilation or calcific densities suggest outflow obstruction.
Treatment Guidelines
• Discontinue all potentially nephrotoxic drugs
• Start specific antidotal therapy if applicable (alcohol dehydrogenase inhibitors for ethylene glycol; for N-acethylcystein for
acetaminophen)
• Indetify and treat any prerenal or post renal abnormalities
• Start fluid therapy; rehydrate within 6 hours; provide maintenance and continuing loss fluid needs
• Assess volume of urine production
• Correct acid-base and electrolyte abnormalities; rule out hypercalcemic nephropathy
• Provide mild volume expansion while monitoring urine volume; body weight; plasma total solids; hematocrit; and central venous
pressure
• Administer vasodilators and/or diuretics
• Consider peritoneal or pleural dialysis
• Control hyperphosphatemia
• Treat gastroenteritis and gastric hyperacidity
• Provide caloric requirement (70-100 Kcal/kg/day)
MEDICATIONS
• Inadequate Urine Production
Ensure patient is fluid-volume-replete; provide additional isonatric fluid to
achieve 3% volume expansion; failure to induce diuresis indicates severe
parenchymal damage or under-estimation of fluid deficit; if fluid-replete,
administer diuretics.
Hypertonic mannitol (10–20%)—0.25–1 g/kg IV over 15–30 minutes; if effective,
continue as intermittent IV bolus q4–6h; discontinue if ineffective.
Furosemide (alternative or subsequent to mannitol)—2–6 mg/kg IV; if effective,
continue q8h; discontinue if ineffective.
Dopamine—lack of documented efficacy and potential side effects contraindicate
its use except for pressor control. If these treatments fail to induce diuresis
within 4–6 hours, consider dialysis
MEDICATIONS
• Metabolic Disorders, Acid-Base Disorders
Administer bicarbonate if serum bicarbonate ≤ 16 mEq/L; bicarbonate replacement:
mEq = bicarbonate deficit × body weight (kg) × 0.3; give half IV over 30 minutes and
the remainder over 2–4 hours; then reassess.
• Hyperkalemia
Correct dehydration with potassium free (0.9% NaCl) fluids.
Minimize potassium intake
Discontinue medications that promote hyperkalemia (e.g., ACEI, potassium sparing diuretics).
Loop diuretics: furosemide 2–4 mg/kg IV.
Sodium bicarbonate, sufficient to correct existing bicarbonate deficit, if bicarbonate status
unknown, 1–2 mEq/kg IV.
Dextrose ± insulin: 1–2 ml/kg of 50% dextrose (diluted to 25%) IV or regular insulin 0.1–0.2
U/kg IV bolus followed by 1–2 g dextrose/unit insulin
Calcium gluconate: 0.5–1.0 ml/kg of 10% calcium gluconate IV over 10–15 minutes.
Refractory hyperkalemia—dialysis.
MEDICATIONS
• Vomiting
Reduce gastric acid production—famotidine (0.5 mg/kg IM, IV q24h) or
ranitidine (0.5–2 mg/kg IV q8–12h) or omeprazole (0.5–1
mg/kg PO q24h [dogs]).
Mucosal protectant—sucralfate (0.5–1 g PO q6–8h).
Antiemetics—maropitant (1 mg/kg SC q24h); or ondansetron (0.1–0.3 mg/kg
IV q8–12h); or dolasetron (0.5 mg/kg SC, IV q24h) or metoclopramide (0.2–0.5
mg/kg SC, IV, or IM q6–8h; 0.01–0.02 mg/kg/h CRI).
 CHRONIC
RENAL FAILURE
• Chronic Kidney Disease; Chronic Kidney Injury
• Chronic kidney disease has been present for > 3 months. Kidney disease
encompasses functional or structural lesions in one or both kidneys as
detected by blood or urine tests, imaging studies, or kidney biopsy. This
definition includes all cases previously described by the terms renal
insufficiency or renal failure, as well as less advanced forms of kidney
disease.
• Patients are categorized into stages along a continuum of progressive CKD
(IRIS stage of CKD) based on two or more serum creatinine values obtained
over several weeks when the patient is fasted and well hydrated
GENETICS
• Inherited in the following breeds (mode of inheritance, known or
suspected, indicated in parentheses):
• Abyssinian cats (autosomal dominant with incomplete penetrance)
• Persian cats (autosomal dominant)
• Bull terrier (autosomal dominant)
• Cairn terrier (autosomal recessive)
• German shepherd (autosomal dominant)
• Samoyed (X-linked dominant)
• English cocker spaniel (autosomal recessive)
• Renal dysplasia (mode of inherence unresolved): shih tzu, Lhasa apso, golden
retriever, Norwegian elkhound, chow chow, standard poodle, soft-coated Wheaten
terrier, Alaskan malamute, miniature schnauzer, Dutch kooiker, and sporadically in
many other breeds).
PATHOPHYSIOLOGY
• More than approximately 75% reduction in renal function results in
impaired urine-concentrating ability (leading to PU/PD) and retention
of nitrogenous waste products of protein catabolism (leading to
azotemia).
• More advanced CKD results in uremia.
• Decreased erythropoietin and calcitriol production by the kidneys
results in hypoproliferative anemia and renal secondary
hyperparathyroidism, respectively.
PATHOPHYSIOLOGY
• Uremia
• Hyperfiltration
• Functional and Morphological
Change in Remnant Renal Tissue
• External Solute Balance
• Development of Poliuria and
Polidipsia
• Calcium and Phosporus Balance
• Acid Base Balance
• Anemia
• Hemostatic defects
• Gastrointestinal Disturbance
• Cardiovascular complication
• Metabolic complication
SIGNS
• General Comments
Clinical signs are related to the stage of CKD and the presence of
complications such as proteinuria and hypertension.
Cats and dogs with CKD stages 1 and 2 may be asymptomatic; overt
clinical signs typically become apparent in stages 3 and 4.
An animal with stable CKD (particularly stages 3 and 4) may
decompensate, resulting in a uremic crisis.
SIGNS
• Historical Findings
PU/PD (less frequent in cats than dogs); litter box more wet; less color to urine.
Anorexia; Lethargy; Vomiting; Weight loss; Nocturia; Constipation; Diarrhea;
Acute blindness—due to hypertension; Seizures or coma—late.
Cats may have ptyalism and muscle weakness with cervical ventroflexion
(because of hypokalemic myopathy).
• Physical Examination Findings
Small, irregular kidneys, or enlarged kidneys secondary to polycystic kidney
disease or lymphoma.
Dehydration; Cachexia; Lethargy, weakness; Mucous membrane pallor; Oral
ulceration.
Uremic halitosis; Constipation; Hypertensive retinopathy; Renal osteodystrophy
(may manifest as
bone pain, particularly in the skull).
Reduced body temperature
DIAGNOSIS
• Chronic kidney disease (CKD) is diagnosed based on evaluation of all
available clinical and diagnostic information in a stable patient.
Following diagnosis of CKD, the IRIS Board recommends using serum
creatinine or SDMA (ideally both) to stage CKD with substaging based
on assessment of arterial blood pressure and proteinuria.

SDMA, symmetric dymethilarginine. A new renal biomarker

International Renal Interest Society
DIAGNOSIS
• DIFFERENTIAL DIAGNOSIS
See Polyuria and Polydipsia chapter for differential diagnosis.
Azotemia—includes causes of prerenal and post-renal azotemia, acute renal failure, and
hypoadrenocorticism.
Prerenal azotemia—azotemia with urine specific gravity > 1.030 in dogs and > 1.035
in cats; Rapid reduction in azotemia after correcting fluid volume/perfusion issues
indicates prerenal azotemia. Prerenal azotemia is a common finding in vomiting patients
with primary intrarenal azotemia.
Post-renal azotemia—azotemia with obstruction or rupture of the excretory system;
rapid correction of azotemia following elimination of obstruction supports post-renal
azotemia.
Acute renal failure—differentiated by normal to large renal size, cylindruria, lack of
indications of chronicity, (absence of small kidneys, hypoproliferative anemia and renal
osteodystrophy), and a history of recent nephrotoxin exposure or hypotensive episode.
Hypoadrenocorticism—characterized by hyponatremia and hyperkalemia with resting
cortisol value < 1 μg/dl or decreased adrenalresponse to ACTH stimulation.
DIAGNOSIS
• CBC/BIOCHEMISTRY/URINALYSIS
Hypoproliferative anemia (nonregenerative anemia)
High BUN and creatinine
Hyperphosphatemia
Metabolic acidosis (normal or high anion gap)
Hypokalemia or hyperkalemia
Hypercalcemia or hypocalcemia
Urine specific gravity < 1.030 in dogs and < 1.035 in cats
Proteinuria
MEDICATIONS
• Uremic Crisis
Famotidine (0.5–1 mg/kg PO, IM, IV q12–24h) to minimize nausea and vomiting.
Antiemetics (maropitant 1 mg/kg q24h up to 5 days; or ondansetron 0.1–0.2
mg/kg slow IV q12h) to minimize vomiting and impaired appetite due to nausea.
Potassium chloride in IV fluids or potassium gluconate PO (2–6 mEq/cat/day) as
needed to correct hypokalemia.
Sodium bicarbonate to correct metabolic acidosis (IV to raise blood pH > 7.1).
MEDICATIONS
• Compensated CKD
Famotidine (dogs, 0.5–1 mg/kg PO q24h; cats, 5 mg/cat PO q48h) to minimize uremic
gastritis and possible nausea and inappetence.
Anitemetic (maropitant) and potassium gluconate as above.
Intestinal phosphate binders (e.g., aluminum carbonate, 30–100 mg/kg/day PO with
meals) as needed to correct hyperphosphatemia (see Hyperparathyroidism, Renal
Secondary).
Calcitriol (start at 2 ng/kg PO q 24h and monitor effect on PTH and ionized calcium—
avoid inducing hypercalcemia).
Darbepoetin (see Anemia of Chronic Kidney Disease).
Amlodipine (dogs, 0.1–0.6 mg/kg PO q24h; cats, 0.625–1.25 mg/cat PO q24h) or ACE
inhibitors (e.g., enalapril or benazepril,
0.5 mg/kg PO q24h) as needed for hypertension. Amlodipine is more effective than ACE
inhibitors in cats with CKD-induced hypertension. If refractory to monotherapy, consider
combination of amlodipine and ACE inhibitor with frequent monitoring of blood
pressure.
ACE inhibitor (benazepril or enalapril) for proteinuria (start at 0.5 mg/kg PO q24 h; may
increase to 1 mg/kg PO q12h if needed to reduce proteinuria).
Treatment
Patients in uremic crisis—correct fluid and electrolyte deficits with
intravenous fluid therapy (e.g., lactated Ringer’s solution); correct 50–
75% of estimated fluid needs over 4–8 hours to prevent additional
renal injury from ischemia; however, avoid excessive fluid
administration.
Subcutaneous fluid therapy (q24–48h) may benefit patients (especially
cats) with moderate-to-severe CKD. Continue therapy only if clinical
improvement is noted.
Goals and Management CRF
1. Avoid dehydration
GOALS Management
Fresh water available at all times
Parenteral fluid therapy when necessary
2. Control azotemia Dietary protein restriction
3. Control renal secondary hyperparathyroidism Dietary phosphorous restriction
Enteric phosphorous binders
Cimetidine
4. Control systemic hypertension Dietary sodium restriction
B-blockers and vasodilators if necessary
5. Minimize metabolic acidosis Oral sodium bicarbonates
6. Minimized gastric irritation Antiemetics
Cimetidine
7. Avoid stress Treat out-patient basis
Treat infections promptly
Avoid corticosteroids
Avoid adverse drug reactions
 Feline Lower
Urinary Tract
Disease

• Feline Urologic Syndrome

• Feline Idiophatic Lower Urinary Tract Disease
• Feline Idophatic Cystitis
CAUSES
• FLUTD is a multi-factorial disease with no single cause.
• Approximately 50% of cases have no known cause, 20% are caused by little urinary
stones, 20% by urethral plugs (mucus secretions from the urinary tract) and 2-10% by
bacterial infections (cats > 10 years old are more likely to have an infection than younger
cats). Cancerous processes also occasionally occur in cats.
• Factors found to contribute to the development of FLUTD include stress, low water
consumption, being overweight, being male neutered, using litter trays and having a
sedentary indoor lifestyle.
• Without management of these risk factors, FLUTD can be a recurrent disease (please see
below for tips on controlling risk factors). Between 40 and 65% of cats will show signs of
FLUTD again within 1-2 years.
PATHOPHYSIOLOGY
• Initial episodes of idiopathic lower urinary tract diseases usually occur
in the absence of significant numbers of detectable bacteria and
pyuria.
• Prospective diagnostic studies of male and female obstructed and
non-obstructed cats identified bacterial urinary tract infections
in < 3% of young to middle-age adults and approximately 10% of
geriatric adults. The etiopathogenesis of iLUTD is uncertain.
• Purposed mechanisms include dysfunction of the urothelial barrier,
neurogenic cystitis, mast-cell-induced neuroimmune disease, and
systemic psyconeuroendocrine dysfunction..
PATHOPHYSIOLOGY
• Experimental and clinical studies have implicated viruses, especially
caliciviruses, as potential etiologic agents in some cats. Some cats with
lower urinary tract diseases exhibit findings similar to those observed in
humans with interstitial cystitis, a non-malignant neuro-inflammatory
disorder characterized by decreased urine concentrations of
glycosaminoglycans and increased urinary bladder permeability, which is
associated with damage to the glycosaminoglycan layer that covers the
luminal surface of the urinary tract.
These similarities prompted the hypothesis that some lower urinary tract
diseases are analogous to human interstitial cystitis.
• Clinical observations suggest that stress may play a role in precipitating or
exacerbating signs associated with idiopathic cystitis.
SIGNS
• Dysuria
• Stranguria
• Tenesmus
• Hematuria
• Periuria
• Not able to urinate at all
RISKS FACTOR
• Male
• Dry food
• Overweight
• Pedigree cat
• Living with other cats
DIAGNOSIS
IMAGING
• Survey radiography—may exclude radiopaque uroliths or urethral plugs.
• Positive contrast retrograde urethrocystography or antegrade
cystography—may exclude urethral strictures, vesicourachal diverticula,
and neoplasia.
• Double-contrast cystography—may exclude small or radiolucent uroliths,
blood clots, and thickening of the bladder wall due to inflammation or
neoplasia.
• Ultrasonography—may exclude uroliths.
Diagnosis
DIFFERENTIAL DIAGNOSIS
• Metabolic disorders including various types of uroliths and urethral plugs.
• Infectious agents including bacteria, mycoplasma/ureaplasma, fungal agents, and parasites.
• Trauma.
• Neurogenic disorders including reflex dyssynergia, urethral spasm, and hypotonic or atonic
bladder (primary or secondary).
• Iatrogenic disease including reverse flushing solutions, urethral catheters, indwelling urethral
catheters (especially open systems), post-surgical urethral catheters, and urethrostomy
complications.
• Anatomic abnormalities including urachal anomalies and acquired urethral strictures.
• Neoplasia (benign and malignant).
• Clinical signs may be confused with constipation, which can be ruled out by abdominal palpation.
Treatments
• Depending Causes
• Non Obstrutive
• Self limited
• Anti-inflammatory drugs
• Obstructive
• Emergency case
• Catheterization
• Surgical
Treatments
• Catheterization
• Olive-tipped catheter 21G (A)
• Tomcat catheter 3.5 FR (B)
• Slippery Sam (end hole) Tomcat urethral catheter
3.5 FR ©
• Argyle feeding tube 3.5-5 FR (F)
• Red ruber catheter 3.5-5 FR (E)
• IV catheter 20 G, 1.5 inch with stylet remove (D)
• Change feeding (wet foods)
• Increasing water intake
• Correcting obesity
• Encouraging exercise
MEDICATIONS
• Antibiotics or Antimicrobials
• Anti-inflammatory
• Glycosaminoglycan
• Hematostatik
• Furosemide, especially in obstructive case after ascertaining urethral
patency to deplete potassium
 URINARY TRACTS
OBSTRUCTIONS

• Restricted flow of urine from the kidneys through the urinary tract to the external
urethral orifice
• Urethral obstruction is common in male dogs and cats. Urethral obstruction is true
medical emergency. It may occur suddenly or may develop throughout days or weeks.
Initially, the animal may frequently attempt to urinate and produce only a fine stream, a
few drops, or nothing.
• Animals may also exhibit extreme pain manifested by crying out when attempting to
urinate.
• Complete obstruction causes uremia within 36–48 hr, which leads to depression,
anorexia, vomiting, diarrhea, dehydration, coma, and death within ~72 hr. Urethral
obstruction is an emergency condition, and treatment should begin immediately.
Pathophysilogy
• Excess resistance to urine flow through the urinary tract develops
because of lesions affecting the excretory pathway that cause
increased pressure in the urinary space proximal to the obstruction
and may cause abnormal distension of this space with urine.
Ensuing pathophysiologic consequences depend on the site, degree,
and duration of obstruction. Complete obstruction produces a
pathophysiologic state equivalent to oliguric acute renal failure.
• Perforation of the excretory pathway with extravasation of urine is a
functional equivalent.
CAUSES
• Intraluminal Causes
Solid or semisolid structures including uroliths, urethral plugs in cats,
blood clots, and sloughed tissue fragments.
Most common site—the urethra.
Urolithiasis—most common cause in male dogs.
Urethral plugs—most common cause in male cats.
• Miscellaneous Causes
Displacement of the urinary bladder into a perineal hernia.
Neurogenic (see Urinary Retention, Functional)
CAUSES
• Intramural Causes
Neoplasia of the bladder neck or urethra—common cause in dogs.
Pyogranulomatous inflammatory lesions in the urethra—seen occasionally in
dogs.
Fibrosis at a site of prior injury or inflammation can cause stricture or stenosis,
which may impede urine flow or may be a site where intraluminal debris
becomes lodged.
Prostatic disorders in male dogs.
Edema, hemorrhage, or spasm of muscular components can occur at sites of
intraluminal (e.g., urethral) obstruction and contribute to persistent or recurrent
obstruction to urinary flow after removal of the intraluminal material. Tissue
changes might develop because of injury inflicted by the obstructing material, by
the manipulations used to remove the obstructing material, or both.
Ruptures, lacerations, and punctures—usually caused by traumatic incidents
DIAGNOSIS
Abdominal Radiography
Uroliths—often demonstrated by survey radiography; some are difficult
or impossible to see because of their size, composition, or location.
Positive-contrast urethrography is the most sensitive method of
detecting intraluminal and intramural lesions of the urethra; double-
contrast cystography is the most sensitive method of detecting lesions
of the bladder lumen and wall.
Upper urinary tract (i.e., ureter or renal pelvis) obstruction can be
detected by excretory urography if enough renal function is preserved
on the affected side(s) so that radiographic contrast media is excreted
and sufficiently concentrated to be seen proximal to the site of
obstruction.
DIAGNOSIS
Abdominal Ultrasonography
Ultrasonography is highly sensitive in detecting lesions of the bladder
and proximal urethra (including the prostate gland in male dogs) and
upper urinary tract (i.e., ureter or renal pelvis) obstruction. The degree
of sensitivity of ultrasonography is dependent on the experience of the
ultrasonographer.
Diagnosis
• CBC/BIOCHEMISTRY/URINALYSIS
Results of a hemogram are usually normal, but a stress leukogram
may be seen.
Biochemistry analysis reveals azotemia, hyperphosphatemia,
metabolic acidosis, hyperkalemia, and decreased ionized calcium
proportional to the duration of complete obstruction.
Hematuria and proteinuria are common; crystalluria supports a
diagnosis of urolithiasis, and atypical epithelial cells may be seen in
patients with neoplasia.
TREATMENTS
• Complete obstruction is a medical emergency that can be life-threatening; treatment
usually should be started immediately.
• Partial obstruction—not necessarily an emergency, but these patients may be at risk
for developing complete obstruction; may cause irreversible urinary tract damage if not
treated promptly.
• Treat as an inpatient until the patient’s ability to urinate adequately has been restored.
• Surgery is sometimes required.
• Long-term management and prognosis depend on the cause of the obstruction.
• Treatment has three major components: combating the metabolic derangements
associated with post-renal uremia (e.g., dehydration, hypothermia, acidosis,
hyperkalemia, and azotemia); restoring and maintaining a patent pathway for urine
outflow; and implementing specific treatment for the underlying cause of urine
retention.
• Urinary diversion by tube cystostomy is useful in selected cases
Medications
• DRUG(S)
Procedures for relief of obstruction often require, or are facilitated by, giving
sedatives or anesthetics. When substantial systemic derangements exist, start
fluid administration and other supportive measures first. Careful decompression
of the bladder by cystocentesis may be performed before anesthesia and
catheterization. Calculate the dosage of sedative or anesthetic drug using the low
end of the recommended range or give only to effect. Isoflurane is the anesthetic
of choice; however, certainly a variety of other anesthetics or sedatives can give
satisfactory results.
• CONTRAINDICATIONS
Avoid intramuscular ketamine in patients with complete obstruction, because it is
excreted through the kidneys. If the obstruction cannot be eliminated, prolonged
sedation may result.
 Urolithiasis

• The incidence of canine urolithiasis in US 0.4-2.8% and similar incidence in

UK 1.2-2.0%.
• Incidence feline urolithiasis 22% and canine urolithiasis 78% in Canada.
• The large majority of urolith in dogs are found in the bladder or urethra.
• Over past 25 years, several changing trends of feline urolith.
• In 1981, 78% were struvite and 2% calcium oxalate (Minnesota Urolith Center)
• 1994-2001, 33% struvite and 55% calcium oxalate
• 2001-2007, struvite increase to 50%, and calcium oxalate decrease to 41%
Anamnesis
• Nutritional history
• Specific brand(s) of food fed, form (dry, moist, semi-moist or a combination),
• Method of feeding (meal fed, free choice) and whether table food,
supplements or treats are offered.
• Access to other food should also be determined (e.g., other pets in the
household that eat different foods, access to food at other households or in
the outdoor environment).
• Trends in water consumption (i.e., increased, decreased, unchanged)
should also be noted.
Physical Examinations
• The urinary bladder should be palpated carefully to evaluate its size, shape,
surface contours and thickness of the bladder wall. The presence of pain or
masses within the urinary bladder lumen should also be assessed.
• Most feline urocystoliths cannot be detected by abdominal palpation;
however, hearing a “grating” sound during palpation of the urinary bladder
strongly suggests their presence.
• In male cats, the penis and prepuce should be examined for urethral
abnormalities.
• The kidneys should be evaluated for size, shape, surface contour and symmetry.
• If possible, the patient should be observed during urination to evaluate the size
of its urine stream and detect abnormalities such as discolored urine, pollakiuria,
dysuria and stranguria.
Diagnosis
• Initial diagnostic evaluation of all cats with lower urinary tract
• Urinalysis
• Diagnostic imaging (i.e., plain abdominal radiographs, abdominal ultrasound)
• Additional tests
• Urine culture
• Contrast urethrocystography or ultrasonography
Urinalysis
• Results of urinalysis are used to: • pH
• 1) help determine underlying • Urine SG
cause(s) of lower urinary tract
signs, • Sedimen (crystalluria)
• 2) detect conditions that may
predispose to formation of
uroliths or urethral plugs,
• 3) infermineral composition of
uroliths or urethral plugs,
• 4) evaluate response to treatment
or preventive measures
Pathophysiology
• Urolith formation
• Precipitation-crystallization theory
• Matrix nucleation theory
• Crystallization-inhibitor theory
Urolith
RADIOGRAPHIC
Calcium oxalate

Silicate
Calcium phosphate
Struvite

Cystine

Urate
Osborne and Lulich (2014)
Osborne and Lulich (2014)
Osborne and Lulich (2014)
• Renal calculi
• Cats>Dogs
• Tonkinese and Birman cats
• Miniature Schnauzers, Shih Tzus, Lhasa Apsos, Yorkshire Terriers, and female
Pugs. Also at high risk were male Dalmatians and male Basset Hounds
• Small dogs: female>male
• Female dog: struvite , oxalate
• Male dog: urate
Diagnosis
• Imaging
• Radiograph: sensitive for Kidney, Urinary Bladder, Urethra
• Sonograph: sensitive for Urinary Bladder
• Composition urolith can be predicted with fair degree using predictor
parameters (urinalysis, radiographic density, gross physical features of
stoes)
Lulich et al (2016)
 Urethral
Obstruction

• Restricted flow of urine from the kidneys through the urinary tract to the
external urethral orifice
• Urinary obstruction is a life-threatening emergency
• Risk factors
• Urolithiasis, particularly in males
• Feline lower urinary tract disease, particularly in males
• Prostatic disease in male dogs
Pathophysiology
• Excess resistance to urine flow through the urinary tract develops
because of lesions affecting the excretory pathway that cause
increased pressure in the urinary space proximal to the obstruction
and may cause abnormal distension of this space with urine.

• Ensuing pathophysiologic consequences depend on the site, degree,

and duration of obstruction. Complete obstruction produces a
pathophysiologic state equivalent to oliguric acute renal failure.

• Perforation of the excretory pathway with extravasation of urine is a

functional equivalent.
Signs
• Pollakiuria (common) • Dull/depressed mentation
• Stranguria, hematuria • Dehydration
• Periuria • Bradycardia (ie, heart rate 40 breaths
• Reduced velocity or caliber of the per minute)*
urine stream or no urine flow during • Pale mucous membranes and
voiding efforts prolonged capillary refill time
• Signs of uremia that develop when • Weak pulses*
urinary tract obstruction is complete
(or nearly complete): lethargy, dull
attitude, anorexia, and vomiting
• Palpable VU distention, renomegaly
Causes
• Intraluminal Causes
Solid or semisolid structures including
uroliths, urethral plugs in cats, blood clots,
and sloughed tissue fragments.
Most common site—the urethra.
Urolithiasis (male dogs).
Urethral plugs (male cats).
• Intramural Causes
Neoplasia of the bladder neck or
urethra (dogs).
Pyogranulomatous inflammatory lesions in
the urethra (dogs).
Fibrosis at a site of prior injury or
inflammation can cause stricture or stenosis,
which may impede urine flow or may be a site
where intraluminal debris becomes lodged.
Prostatic disorders in male dogs.
Edema, hemorrhage, or spasm of muscular
components can occur at sites of intraluminal
(e.g., urethral) obstruction and contribute to
persistent or recurrent obstruction to urinary
flow after removal of the intraluminal
material. Tissue changes might develop
because of injury inflicted by the obstructing
material, by the manipulations used to
remove the obstructing material, or both.
Ruptures, lacerations, and
punctures—usually caused by traumatic
incidents.
Diagnosis
DIFFERENTIAL DIAGNOSIS IMAGING
• Constipation • Abdominal Radiography
• Hypoadrenocorticism • Plain radiography (uroliths);
• Positive-contrast urethrography
• Ruptured vesica urinaria (intraluminal, intramural urethra);
• Double-contrast cystography (lumen,
lesion bladder);
• Excretory urography (upper urinary tract
(i.e., ureter or renal)

• Abdominal Ultrasonography
bladder and proximal urethra (prostate
gland in male dogs) and upper urinary
tract (i.e., ureter or renal pelvis)
obstruction
 Feline
Idiophatic
Cystitis
• Once all other potential causes have been excluded a diagnosis of FIC
is made.
• Synonyms: Feline Interstitial Cystitis, Steril Cystitis, Feline Idiophatic
Lower Urinary Tract Diseases, Feline Urologic Syndrome