Urinary tract disorders



Urinary tract disorders


While the incidence of clinically significant disorders of the urinary tract of the horse is less than in many other species, pathological changes are quite frequently recognized at post-mortem examination and it is possible that subclinical urinary tract disease passes largely unnoticed. Foals are markedly more prone to renal disease than adult horses, and this may be associated with the neonatal maladjustment syndrome and septicemic disorders. Normal horse urine has a markedly cloudy appearance, particularly towards the end of the flow, due to the very high calcium carbonate content, and is frequently mucoid or viscid in consistency.


As with some other organ systems, damage to the urinary tract organs may be reflected clinically in a limited number of ways. Thus the clinical appearance of different disorders may be similar and the specific identification of a given problem may be difficult. The general signs of urinary tract disease are associated with variations in the volume of urine produced and abnormalities of micturition including abnormal frequency of urination, or dysuria (difficulty or pain during or after micturition).


Furthermore, the kidney itself has a very large functional reserve and damage may only become clinically obvious when over 70% of the available tissue is non-functional. The implications of this fact for diagnosis and therapy of renal disease are particularly important as the opportunity for therapeutic measures has often been lost before clinical disease is recognized.


Separation of renal disorders into infectious and non-infectious is not always clear-cut as there is frequently an overlap or combination of conditions contributing to renal failure and thus the clinical signs seen.


Diagnosis of urinary tract disorders usually involves obtaining a good history and physical examination coupled with diagnostic imaging and supportive clinical pathology.



Developmental disorders


Congenital or hereditary disorders of the kidneys and ureters are particularly unusual in the horse. Unilateral disorders are likely to be incidental findings at post-mortem examination, whereas bilateral disorders are likely to result in recognizable, if non-specific, clinical signs or the early demise of the foal, possibly even intrauterine death.



Renal agenesis, hypoplasia and dysplasia (Figs. 5.1 & 5.2)


Renal agenesis is the complete absence of renal tissue. It may be unilateral or bilateral. Unilateral is reported more frequently but this simply may be a reflection of the fact that bilateral agenesis is incompatible with life. Other congenital abnormalities such as atresia ani may occur simultaneously. Unilateral disorders are frequently identified incidentally in otherwise healthy horses or may be identified during reproductive examinations or when renal disease is present in the remaining kidney. There is no confirmation of a hereditary basis but this may simply be due to a lack of data and repeat matings of the same sire and dam should be discouraged.




Renal hypoplasia is defined as a kidney 50% smaller than normal or total renal mass decreased by more than one third. If the condition is unilateral there is commonly hypertrophy of the contralateral kidney and normal renal function. As such the hypoplasia may go undiagnosed. Hypoplasia may occur bilaterally, resulting in renal failure, or can occur with renal dysplasia. In many cases the diagnosis is made post-mortem but may be suspected ante-mortem on the basis of ultrasound examinations or computed tomography.


Renal dysplasia is defined as disorganized development of renal tissue. The proposed mechanisms are anomalous differentiation, fetal viral infection, teratogens or intrauterine ureteral obstruction. Renal dysplasia may occur unilaterally and not be associated with renal failure or may occur bilaterally or in association with renal hypoplasia where it leads to chronic renal failure at a young age. This condition may be somewhat more difficult to diagnose ante-mortem as the kidneys may be of normal size and function tests are non-specific for cause.




Renal cysts (Figs. 5.35.6)


Polycystic kidney disease and glomerulocystic disease


Polycystic kidney disease (PKD) is a disorder in which multiple variable-sized cysts are found throughout the cortex and medulla. In PKD cysts may also be found in the bile ducts and pancreas. In comparison glomerulocystic disease consists of microscopic cysts limited to Bowman’s spaces. Both conditions have been described in foals. PKD has been described in a number of adult horses presented for renal failure.









Vascular anomalies


Renal arteriovenous malformations or intrarenal vascular anomalies are rare and may be silent for many years when present. Common clinical signs include hematuria and flank pain.


Anomalies of the vascular supply to the kidneys are also rare and have been associated with hematuria, hemoglobinuria, partial urethral obstruction or hydronephrosis.





Rectourethral and rectovaginal fistulae (Figs. 5.7 & 5.8)


These are rare anomalies that are associated with failure of separation of the urorectal folds. These conditions are frequently associated with atresia ani or other congenital conditions such as agenesis of the coccygeal vertebrae and tail, scoliosis, microphthalmia and severe angular limb deformities.






Ectopic ureter (Fig. 5.9)


In individuals with ectopic ureters, one or both ureteral ostia empties into the bladder or urethra at some point distal to the functional sphincter. In some animals, the aberrant ureters may open into the uterine lumen or vaginal tract.





Patent urachus (Fig. 5.10)


The persistent dribbling of urine from the umbilicus in a neonatal foal should alert the clinician to the possibility of a patent urachus. Foals may be born with the urachus normally closed but then be observed dribbling urine from the external umbilical remnant on the first or second day of postpartum life. This may occur in foals that are constipated or have meconium impaction and strain to defecate; the intra-abdominal pressure created by abdominal press can lead to re-opening of the urachal lumen and the exit of urine via the urachal remnant. Re-opening of the urachus may also occur as a result of infection and is also frequently seen in foals that are largely recumbent for other reasons, e.g. septicemia. Where the urachus fails to close adequately at birth, the patent structure provides a portal for the entry of bacteria, and local abscess, particularly of the umbilical vessels, or even septicemia may result. Ascending infections from the urachus into the bladder (and thence to the ureters and kidneys) and from the umbilical vessels into the general circulation have particularly serious systemic consequences.





Diagnosis and treatment



• The observation of urine dribbling from the umbilical stump of a young foal is the basis for making a diagnosis of patent urachus, although sonographic imaging may be used to confirm the patent status of the structure internally and assess associated structures.


• Currently many practitioners recommend treatment consisting of 5–7 days of antimicrobial support and keeping the foal’s ventral abdomen clean and dry, with twice to four-times-daily dipping of the external umbilical stump with a 1 : 4 chlorhexidine : water or dilute iodophore solution.


• Topical applications of silver nitrate are no longer routinely recommended.


• In cases of foals which are largely recumbent it may be useful to catheterize the bladder, thus removing the physical pressure of bladder distension which may contribute to maintaining a patent urachus.



Uroperitoneum (Figs. 5.115.18)


Uroperitoneum, or urine in the peritoneal cavity, is a common problem of neonatal foals. It is a sign of rupture of some portion of the urinary tract. The urinary bladder is the most common site of rupture, but renal, urachal, ureteral and urethral ruptures or injuries also occur and result in leakage of urine into the peritoneal cavity.









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Figure 5.18 The same foal as Fig. 5.17, 4 days after the placement of the urinary catheter. An area of necrotic skin is apparent; this section was resected and the foal made an uneventful recovery.

Uroperitoneum arising from bladder rupture may occur from disruption of the urinary tract during parturition or as a result of a congenital abnormality. Bladder rupture can also result from septic foci and consequent necrosis and when caused by sepsis may be seen in older foals. Males appear to be affected more frequently but the incidence in the sick or hospitalized is approximately equal between the sexes. Clinical signs of uroperitoneum characteristically develop between 1–3 days after birth, the foal having been normal up to this point. In some cases however the reduced or absent urinary output may have been recognized from an early age. Foals which have septic necrosis of the urachus or bladder may develop signs much later.




Clinical signs



• The earliest sign is usually frequent stranguria and repeated posturing to urinate. Sick foals, especially those that are recumbent, may not show these signs and stranguria is frequently confused with tenesmus.


• Affected foals show progressive abdominal distension and depression with a palpable fluid thrill may be detected across the abdominal cavity.


• The foal may still continue to void urine through the urethra and as such the observation of the passage of urine does not preclude a diagnosis of ruptured bladder.


• As the condition progresses these foals develop hyponatremia, hypochloremia, hyperkalemia and azotemia. Depending on the timing of presentation, the metabolic derangements that develop can result in other signs: hyponatremia can result in neurologic disturbances including convulsions; progressive hyperkalemia results in cardiac dysrhythmias.


• Uroperitoneum may also be caused by disruption of the urethra, urachus or ureters (rarely). In cases of urethral leakage in colts subcutaneous accumulation of urine in the scrotal area is frequently seen. Depending on the site of injury this may occur alone or in combination with uroperitoneum. Uroperitoneum associated with urachal disruption may also be accompanied by subcutaneous leakage of urine in the umbilical area.


• Progressive accumulation of fluid which may be accompanied by persistent straining will force significant amounts of urine down the inguinal canals and result in swelling of the scrotum and prepuce.



Diagnosis



• Transabdominal ultrasound is very useful in examination of foals with suspected uroperitoneum, and quickly reveals anechoic-to-hypoechoic fluid free in the peritoneal cavity, with bowel loops and other viscera floating on and in the fluid. The rent in the bladder, whether congenital or acquired, is nearly always located in the dorsal wall but is generally difficult to visualize.


• A fluid sample may be obtained via abdominocentesis and assayed for creatinine concentration. If the creatinine concentration in the peritoneal fluid is twice or higher than the serum concentration, a diagnosis of uroperitoneum may be rendered. However, it is important to note that serum electrolyte and creatinine concentrations may be normal in the early stages of the disorder and should not be used as a means of ruling out the condition.



Treatment



• In most instances slow drainage of the abdomen is initiated. Removal of urine from the abdomen helps to prevent worsening of the metabolic condition. In cases of severe abdominal distension resulting in respiratory compromise, abdominal drainage is a must.


• Uroperitoneum is a metabolic rather than a surgical emergency and surgery should be delayed to allow for correction of electrolyte abnormalities. Correction of hyperkalemia to a serum concentration <6 Eq/L is the most important consideration prior to general anesthesia. Administration of 1–3 L of 0.9% NaCl/5% glucose solution can be used to treat the hyperkalemia.


• In foals for which surgery is not an option or in foals with urethral or urachal tears, placement of an indwelling urinary catheter in combination with an indwelling peritoneal drain may facilitate sufficient removal of urine to permit healing.


• Placement of a urinary catheter for a couple of days post surgery to maintain an empty bladder is not usually required but should be used in foals where bladder rupture was deemed to be secondary to sepsis with necrosis of the bladder wall. Balloon-tipped Foley catheters with 10–30 ml of sterile saline solution in the balloon to keep it in a dependent position in the bladder lumen work well, but rigorous monitoring and nursing care, including the administration of broad-spectrum antimicrobials, is necessary.




Non-infectious disorders


Bladder rupture (Fig. 5.19)


Bladder rupture has been recognized in adult horses as an accident of parturition or in horses which are repeatedly catheterized, particularly where there is an intercurrent cystitis. More unusually, the bladder may rupture as a result of severe and total urethral obstruction such as might occur with urethral calculi, which is effectively restricted to the male. The speed with which abdominal accumulation of urine occurs depends upon the extent of and reasons for the rupture. Progressive azotemia and hyperkalemia are common sequels to any disruption of the urinary tract within the abdomen. However, it appears that peritonitis is not a common feature, the peritoneum appears to tolerate the presence of urine fairly well, unless there are bacteria present. The possible exception to this is mares that have suffered a ruptured bladder as a result of parturition trauma as in many cases they have also endured bruising or damage to the gastrointestinal tract resulting in translocation of bacteria through the bowel wall.





Polyuria/polydipsia (Fig. 5.20)


Diabetes insipidus


Diabetes insipidus (DI) of central origin arises from failure of the pars distalis of the pituitary gland to produce anti-diuretic hormone (ADH). This occurs secondary to viral encephalitis or to compression of the pituitary gland as part of the Cushing’s disease syndrome.



Nephrogenic diabetes insipidus occurs as a result of failure of tubular response to ADH. In can be inherited as a nephropathy or can occur secondary to bacterial infection, drug therapy, obstruction of the urinary tract or neoplasia.







Psychogenic polydipsia


Psychogenic polydipsia is perhaps the most common cause of polyuria/polydipsia (PU/PD) in young adult horses. It is regarded as a vice associated with boredom in stabled horses. Dietary factors such as a high intake of dry matter or compulsive salt consumption may also contribute. These horses are normally in good body condition with no evidence of renal failure. Horses with a recent onset may concentrate their urine in response to the water deprivation test whereas longer-standing cases may have washout of renal medullary electrolytes resulting in an inability to concentrate urine in response to this test. These horses will have a positive response to the modified water deprivation test although a number of days may be required for normal urinary concentrations to be reached.



Diagnosis and differentiation



• A good history is imperative to determining if the primary problem is polydipsia or polyuria. While they occur together one is usually a physiological response to the other. Therefore a horse for example with psychogenic polydipsia will as a result have polyuria. While similarly, a horse with polyuria due to renal failure will have a physiological polydipsia as a result.


• A good history should also rule in or out behavioral factors, drug administration, concurrent disease that is already being treated or clinical signs consistent with other disorders such as renal failure or Cushing’s.


• In many cases it may be necessary to measure water intake and urine output over a 24-hour period. A complete blood count and serum biochemistry profile should be performed in addition to urinalysis.


• Water deprivation test. If the horse shows no clinical or laboratory features of renal failure, endotoxemia, sepsis or Cushing’s disease then a water deprivation test can be performed to assess the ability of the renal tubules to respond to ADH. The horse is weighed and a urine sample obtained for determination of specific gravity (SG). The horse is then confined without access to water and urine samples collected every 2 hours. The test ends when the urine has a specific gravity (SG) of 1.025 or the horse has lost 5% of its body weight, whichever comes first. If the horse responds by producing urine with a SG >1,025 then he can be diagnosed as a psychogenic water drinker; if he fails to concentrate the urine, then a modified water deprivation test should be performed.


• Modified water deprivation test. Water access is restricted to 40 ml/kg/day for up to 4 days. This will result in concentration of urine in horses with psychogenic polydipsia that have washout of renal medullary electrolytes. The horse should still be weighed daily and the test ended if the horse has lost 10% of its body weight and SG is still <1.025 as these cases may have diabetes insipidus.


• Desmopressin response test. Administration of 20 µg of desmopressin acetate (DDAVP) allows differentiation between central and nephrogenic diabetes insipidus. If the urine concentrates in response to the DDAVP then the diabetes insipidus is central, if not it is nephrogenic.

Feb 27, 2017 | Posted by in EQUINE MEDICINE | Comments Off on Urinary tract disorders
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