1 Jan 2011
Fernando Reina
Job TitleFernando Reina DVM, MSc, SA (orthopaedics), MRCVS, looks at the clinical signs and pathology of various canine urinary tract problems
URINARY tract disorders are extremely common in veterinary medicine and might represent a problem for patients and owners, who sometimes are not educated in how to prevent some of the diseases involved.
It has been estimated that about 14 per cent of the worldwide dog population might acquire primary or secondary urinary tract infections, which represents about 10 per cent of canine disorders overall (Lulich and Osbourne, 1997). Despite these figures providing only an indication, it is clear that urinary tract disorders represent a common complaint in practice.
One of the most common complaints reported by pet owners is a change in normal urine functionality, particularly in the quantity, colour and appearance of urine. Sometimes, however, these might be clinically unremarkable and further investigation is needed to reach a final diagnosis.
Urinary tract disorders can be divided into diseases that affect the upper urinary tract (UUTD), including the kidneys and ureters, and those affecting the lower urinary tract (LUTD), from the urinary bladder to the urethra, including the prostate gland in males and the external genitalia in both males and females.
Although some may produce alterations in normal voiding by themselves, two or more diseases commonly act together or as a consequence of the primary one, so different anatomical areas might be simultaneously affected. Untreated infections affecting the lower urinary tract – or those that have not been treated adequately – might result in ascending urinary tract infections, involving the kidneys and ureters.
The range of clinical signs associated with urinary tract disease in dogs includes changes in normal urine colour, difficult or painful urination and straining, increased frequency of voiding and urine incontinence. Identifying and understanding them can provide excellent clues to help in determining whether the upper or lower tract are primarily involved in the clinical pathology.
Haematuria is defined as the presence of blood or red blood cells in the urine. Macroscopic haematuria (changes in normal colour easily identified by observation of red/brown urine discolouration) needs to be distinguished from haemoglobinuria (presence of haemoglobin in urine) and other pigmentary disorders that can alter the normal colour of the urine. Microscopic haematuria is an abnormal finding in urine sediment that is usually related to pathology, although a single transient of mild haematuria could be clinically insignificant and related to strenuous exercise or stressful situations.
Haematuria might be of renal origin, be related to abnormalities of the lower urinary tract, genital tract (including prostate gland in males, and uterus and vagina in females) or secondary to systemic diseases that alter blood cells (Table 1).
Study of the source of the haematuria might provide clues to locate its origin. Urine that remains discoloured after centrifugation is indicative of pigments such as haemoglobin or myoglobin. Presence of blood in urine at the beginning of voiding might have an origin in the bladder neck and/or urethra; or mean that urine has been contaminated with genital discharge (penis and prepuce in males; uterus, vagina and vulva in bitches), where spontaneous bleeding can be identified, not associated with urination. Haematuria at the end of voiding or throughout urination indicates problems with the upper urinary tract (kidneys and ureters) and possibly the urinary bladder.
Clinical signs that cause haematuria must be recognised to determine which system is affected. Increased frequency of urination, pain or discomfort and straining related to the presence of red blood cells is commonly seen in lower urinary tract inflammation. When haematuria is present and no other abnormalities are reported in urinary function, this can indicate upper tract abnormality, although it is usually associated with systemic signs (vomiting, diarrhoea and weight loss).
Cardiovascular and haematological diseases that can cause haematuria are commonly distinguished by the presence of systemic clinical signs, such as weakness, lethargy, inappetence and high temperature.
Based on the full medical history, analysis of the clinical signs that can cause haematuria need to be identified. History of bleeding, coagulopathies, possible access to toxins, previous traumas or fractures, for example, need to be recorded and considered for differential diagnoses. Breed predisposition may be of relevance. The prevalence of transitional cell carcinoma (TCC) in the bladder and/or urethra is higher in Scottish terriers, especially if they have been exposed to herbicides (Glickman L T et al, 2009). Secondly, we need to establish the presence or absence of urinary disorders (dysuria, stranguria) and determine the chronicity of the problem.
Physical examination, including palpation of kidneys and bladder, external genitalia and lymph nodes, must always be accompanied by rectal examination. This allows the clinician to evaluate the pelvic urethra, the prostate gland in males, the trigone (ends of ureters in the urinary bladder) in small dogs and cats, and the pelvic diaphragm.
Some texts mention urine catheterisation as a diagnostic tool to assess the urethral patency and this may be used, depending on the patient and the situation.
Urinalysis is commonly used as a diagnostic tool. Urine obtained by cystocentesis offers better results than voided samples, especially if bacterial culture is needed. Urine should be evaluated within 30 minutes of collection, especially when crystals are suspected, or urine pH might be relevant. Indications about urinalysis interpretation are given in Table 2.
Presence of haematuria accompanied by proteinuria (high amount of protein in urine) might be related to glomerulopathies. Any bleeding in the lower tract will induce proteinuria, but the severity of protein loss in renal diseases can be greater and should be differentiated by examination of the urine sedi ment. When pyuria is also found (presence of active inflammatory cells in urine sediment) it is related to infection or inflammation in the upper or lower urinary tract. It is important to mention that urine specific gravity needs to be determined by refractometer and it can change depending on the hydration status of the patient and the clinical pathology. Presence of white blood cells, red blood cells and crystals will be confirmed by sediment analysis.
Blood analysis, such as complete haematology and chemistry, paying special attention to blood urea and creatinine, are used as a routine screening test.
An electrolyte panel is normally included in the blood work. If excessive blood loss or coagulopathies are suspected, platelet count, clotting times and possibly clotting factors are recommended.
Diagnostic imaging includes plain abdominal radiographs to assess presence of masses, anatomical abnormalities or radio-opaque calculi. If TCC is suspected, thoracic x-rays would confirm pulmonary metastasis (tumour staging). Positive/negative contrast studies, combined or not with intravenous urogram (IVU), can provide a qualitative estimation of the renal perfusion and delineate masses or calculi in the kidneys, ureters or urethra. Abdominal ultrasound is normally combined with collection of samples for cytology and/or biopsy, also for the collection of sterile urine samples for analysis (cystocentesis).
Exploratory surgery might be indicated when diagnostic imaging tools are insufficient to determine the source of the haematuria.
Inflammation in the lower urinary tract might cause increased frequency of voiding (pollakiuria), painful urination (dysuria) and straining (stranguria). Disorders of the upper urinary tract do not tend to cause these clinical signs unless there is a concomitant involvement of the lower tract (for example, ascending urinary tract infections that do not respond to antibiotics).
Among the possible causes, septic and sterile inflammation need to be considered. Primary causes, such as neoplasia or urolithiasis, might be asymptomatic in the first stages and do not cause voiding problems, but they can also predispose to secondary bacterial infection and/or partial urethral obstructions, causing haematuria, dysuria and stranguria. On the other hand, infections with urease-positive bacteria may predispose to struvite urolith formation due to alkalinisation of the urine and increased availability of ammonium ions in the urine, so it is clear how different pathologies might relate to similar clinical signs.
Diagnosis must be based on the clinical history, paying special attention to the presence or absence of systemic signs. Increased water intake, accompanied by increased frequency of urination (polydipsia/polyuria), might indicate renal tubular disease, endocrinopathies, central and nephritic diabetes insipidus, some cardiovascular states and drug therapy, such as corticosteroids or diuretics.
Disorders related to urolith formation include hypercalcaemia, concurrent UTI and hepatic encephalopathy. Information about diet and environment conditions, previous trauma or illness and medication are relevant to determine the source of the pathology. To locate the origin of the pain, determine the frequency and the volume of urine voided. Assess if dysuria is accompanied by haematuria and/or stranguria, if the stream is interrupted or weak, if the animal is choosing unusual areas in which to urinate and if the urine smells different. Determine the duration of the clinical signs and any response to previous treatments.
Physical examination must be performed, taking into account all areas previously mentioned for haematuria. Try to identify distended bladder, masses, stones or thickened bladder walls.
The neurological examination is focused on observation of the bladder contractions, before and after voiding, combined with abdominal and/or rectal palpation and the sphincter muscle tone.
Complete urinalysis includes macroscopic examination, use of urine dipsticks, analysis of sediment and urine culture. The presence or absence of bacteria in the urine sediment might not be relevant. Urine crystals can be identified in healthy patients, but, on the other hand, dogs with uroliths might not have crystals present on the sediment. Samples sent for bacterial culture must be collected by cystocentesis.
Further investigations include blood work, plain and contrast radiographs and abdominal ultrasound.
Proteinuria is described as an abnormally elevated concentration of protein in the urine. It may be related to either renal or non-renal diseases. Proteinuria can also be identified in some physiologic states, such as strenuous exercise (associated or not with haematuria), high body temperature and seizures.
Another way to classify proteinuria is according to its origin. Pre-renal proteinuria is commonly identified in chronic infections and inflammation, some viral diseases, neoplasia and haemolytic disorders (immune-mediated haemolytic anaemia). Elevated concentration of small proteins in blood, as a consequence of pathology, exceeds the capacity of reabsorption by the renal tubules, so the excess of proteins can also be identified in the urine.
Renal proteinuria is usually associated with glomerular disease, defective absorption by the renal tubules or acute/ chronic inflammation of the renal parenchyma (pyelonephritis). Non-renal or post-renal proteinuria is most frequently associated with LUTD, especially when inflammation or bleeding are present. Cystitis, ureter and bladder stones, trauma, acute or recurrent infection, prostatitis or vaginitis can cause proteinuria.
The diagnostic approach should attempt to determine whether proteinuria is persistently present and the amount found. As there are many causes, the diagnostic approach tends to be difficult. To identify the source of the proteinuria, urine dipstick tests can be used. These tend to be more sensitive for albumin, and some false positive results might occur if urine pH is alkaline, urine has been contaminated with ammonium or the strips are left in contact with the urine for too long. False negative results might occur in the presence of globulin and other non-albumin proteins, such as Bence-Jones (found in malignant bone marrow cancer, renal failure, severe osteolysis and anaemia).
Clinical history, paying attention to the presence or absence of systemic signs and physical examination, are as previously described. Dilated or tortuous retinal vessels associated with retinal haemorrhage and retinal detachments during ophthalmic examination can suggest severe hypertension.
Determination of high concentrations of proteins in urine needs to be compared to urine specific gravity. Slightly elevated concentrations can be normal in concentrated urine and clinically relevant proteinuria can be missed in dilute samples. Analysis of urine sediment is always combined with the information obtained by urine dipsticks (Table 3).
Proteinuria associated with haematuria can be identified in upper and lower urinary tract disorders. However, a significantly elevated concentration of proteins in urine is more likely to have an origin in the upper tract. Likewise, glucosuria with normal blood glucose might indicate a renal tubule deficiency that can be associated with urinary loss of electrolytes (not seen in glomerular diseases).
Urine protein: creatinine ratio can be used in combination with a urine sediment examination to distinguish lower urinary tract proteinuria from glomerular diseases. Excretion of creatinine by the kidneys is constant. However, protein loss is dependent on the urine sediment. An active sediment, consisting of numerous white blood cells, red blood cells and urine casts, will give an artificially high UPC. The International Renal Interest Society (IRIS) recommendations include close monitoring of the urine protein ratio as long as the result remains above 0.5 (Table 4). As mentioned previously, analysis of the urine sediment will need to be undertaken.
Elevated concentration of plasma protein and proteinuria might indicate pre-renal origin.
Elevated blood urea and creatinine might suggest glomerular disease. Plain radiographs, abdominal ultrasound, renal cytology and biopsies may be used to confirm a diagnosis.
Urinary incontinence is defined as the involuntary passage or leakage of urine. Diagnosed in puppies, young dogs or geriatric patients, it is a distressing problem for both pets and owners. It affects females more than males and may be associated with UTI or inflammation in the external genitalia. However, anatomical and neurological disorders – congenital or acquired – can cause urinary incontinence.
In juvenile dogs, causes include anatomical disorders (ureteral ectopia, intersexuality, pervious urachus) and neurological dysfunctions (congenital sphincter mechanism incompetence). In adult dogs, urine incontinence is usually secondary to neoplasia, prostatic disease in males, iatrogenic (ureterovaginal fistula), infection/inflammation (detrusor instability), neurological diseases (trauma, spinal lesions) or multifactorial (urethral sphincter mechanism incompetence, [SMI]).
In a normal scenario, urine is stored by the bladder and maintained because of the higher urethral pressure. After neurological stimulation, in which three different mechanisms are involved, increased intravesical pressure and stimulation of the detrusor muscle allows urine elimination. Urethral pressure remains lower compared to that of the bladder. This mechanism is also related to bladder and urethral muscle tone, fleshiness or thickness of the urethral mucosa and the effect of the intraabdominal pressure acting at the bladder and its junction to the urethra. Common causes of urine incontinence are described in Table 5 (Bainbridge and Elliot, 1996).
Breed predisposition may be a factor. Dobermann pinschers, Rottweilers, spaniels and collies are predisposed to urethral SMI, while ectopic ureters may be diagnosed in golden retrievers. Geriatric incontinence is associated with decreased bladder storage capacity or decreased mobility. Endocrinopathies that cause polydipsia and polyuria might exacerbate clinical signs.
Neurological dysfunctions that affect (centrally or peripherally) urinary tract innervations can cause incontinence (brain tumours, cauda equina). Transient urine incontinence might be identified in upper motor neuron lesions or after spinal surgery (reflex dyssenergia). It is identified as a dribbling incontinence when the patient wishes to urinate. It is normally resolved as soon as the inflammation disappears.
Other factors to consider include neutering, body position and obesity, especially if related with urethral SMI. Although the exact abnormality leading to urethral sphincter mechanism incompetence is unknown, a variety of factors are suspected to contribute to urinary incontinence (Holt, Waltham Focus, 1999). Hormonal influence, especially in spayed bitches, and obesity are considered as contributing factors. It is also true that intravesical pressure rises in recumbency, compared to standing.
Diagnosis involves differentiating real incontinence from behavioural disorders, dysuria and/or polyuria. Bladder palpation is useful to establish if it is full and distended, partly or completely emptied. Urine incontinence with a distended bladder might indicate neurological dysfunction or partial obstruction to urinary outflow. Incontinence with a normal-sized or small bladder can be related to bladder hypercontractility or decreased urethral resistance. Besides age, breed and sex, frequency of the incontinence, chronicity of the episodes and description of any changes in urination need to be considered. Likewise, treatments used before and any improvement reported should be considered (urethral SMI usually improves after phenylpropanolamine or oestrogen therapy).
Physical and a complete neurological examination are as previously described. Observation of the patient while voiding must be included routinely.
Further investigations can be used to confirm the diagnosis, as previously described. To determine ureteral peristalsis, presence or masses or obstruction, diagnostic imaging tools can be used, combined with contrast studies. Myelography and electromyography can be used if neurological dysfunction is suspected.
Finally, trial treatment can be used successfully in some cases. Therapy with phenylpropanolamine or exogenous oestrogens has been effectively demonstrated to treat acquired urethral SMI.
Canine urinary tract disorder includes a number of pathologies that can affect the urinary system or organs related to it. The most common clinical signs associated with pathologies of the urinary systems include changes in urine colouration and appearance, painful urination, increased frequency of voiding and involuntary urine leakage. Identification of the clinical signs and determination of the source represents the key to reaching an accurate final diagnosis. This article is intended to provide a simple study of the origin of these abnormalities to identify the systems involved and choose the appropriate diagnostic tools.
Fernando Reina
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