Obstructive urolithiasis, an active stone disease in ruminants is the retention of urine subsequent to lodgment of calculi anywhere in the urinary conduct from up to urethral orifice. The condition can cause significant economic losses due to urethral obstruction; rupture of the urethra or bladder or death from the build up of toxic substances that are usually removed through the urine. It is an important disease of feeder animals but is also seen in mature breeding animals. Urolithiasis is seen most often during winter in steers and wethers on full feed, or on range during severe weather conditions with limited water intake, especially when the water has a high mineral content. Urolithiasis has no specific geographic distribution, and the different urolith types reflect the mineral distribution of the feed.The number of affected animals is usually low but can be as high as 10% annually in exceptional circumstances. The condition occurs more frequently in feedlot situations. Many surgical approaches and techniques for the diagnosis and the treatment of the disease have been described with their relative merits and demerits in the literature.
Urolithiasis affects both sexes, but urinary blockade is a major problem only in males. Steers are most commonly affected by the obstructive form of the disease because of the anatomical confirmation of their urinary tract (Larson, 1996). Urethral obstruction has been extensively reported in ruminant species (Smith, 1989) and is a common problem encountered in male sheep, goat and cattle (Van saun, 2007). The calculi are mostly found in urinary bladder (Sharma, 1977), but can also occur in renal pelvis & urethra (Divers et.al, 1989). The calculi dislodged from bladder may get trapped in narrow male urethra (Sharma, 1977); Sigmoid flexure (Singh and Singh, 1990) or at preputial opening. Urinary obstruction may also occur due to cystitis (Stone and Barsanti, 1992) or due to prostate disease.
An overall incidence of 5.04 percent in animals has been reported in India (Amarpal et.al, 2004). The species wise incidence has been reported as: goats 49.83 percent, cattle 32.87 percent, dogs 14.53 percent, horses 1.38 percent, sheep 1.04 percent and cats 0,34 percent ((Amarpal et.al, 2004). From Kashmir valley an overall incidence of 12 percent in cases of obstructive urolithiasis in cattle calves has been reported (Muhee, 2006). Makhdoomi et al 2008 documented incidence of urolithiasis as high as13.4%, in Anantnag, 12.6%, Budgam 11.9%, Pulwama 6.9%, and Srinagar 10.5% in male cow calves
The etiology is complex and multifactorial. Although urolithiasis is known to have numerous predisposing etiology factors (Coe et.al., 1989), but exact mechanism of stone formation and growth is not fully known. Urinary calculi formation usually results from a combination of various physiological, nutritional and management factors. It may occur due to excessive or imbalanced intake of minerals (Radostitis et.al 2000) in feedlots while fattening cattle receive rations high in cereal grain and oil meals. These feedstuffs have high levels of phosphorous and magnesium but relatively low level of calcium and potassium predispose to disease condition (Payne 1989, Radostitis et.al 2000). A calcium phosphorous imbalance results in high urinary phosphate excretion which is an important factor in the genesis of phosphate calculi (Radostitis et.al 2000). Numerous additional factors have been incriminated as contributing causes of the development of phosphate calculi with resultant obstructive urolithiasis in cattle. These include heavy concentrate-low roughage diets, limited intake or deprived of water, dehydration, urine alkalinity, mineralized artesian water, alkaline water supplies, excess of sodium bicarbonate in diet, vitamin imbalance e.g hypovitaminosis and hypervitaminosis and high protein rations (Larson, 1966; Radostitis et.al 2000). Less frequently uroliths composed of silica, carbonates or oxalates (Larson, 1996). Livestock grazing in pastures containing large quantities of oxalates, estrogen or silica are prone to develop these types of calculi (Radostitis et.al. 2000). Urolithiasis in castrated beef cattle has been reported to be associated with diethylstilbestrol implants (Clotide et.al 1980). Geographical and seasonal influences play an important role for range herds in semi-arid areas (Wallace, 2005).
Despite the sophisticated surgical techniques and various supportive treatments prognosis of urolithiasis in bovine still remains In an attempt towards in-depth understanding of the phenomenon, investigation into pathophysiological changes from onset of the urolithiasis workers have developed varieties of experimental models of urolithiasis (Gera and Nigam 1980), they could not fetch much about the aspect other than damages restricted to lower urinary conducts. Studies on urodynamics during obstructive uropathy revealed damage to bladder wall, ureters, kidneys and urine peritonitis. (Marudwar and Sahu, 1982.). There is an increased severe intracystic, and intra urethral pressure developing in pace with duration of obstruction upto 64 to72hours of obstruction which declines after re-establishing the free urine flow/ or the seepage of urine from bladder (Makhdoomi and Marudwar 1992). The increased retrograde pressure built up in the ureter leads to failure of vesico-ureteral reflux and with resultant mild, moderate to degree of nephropathy depending upon duration of obstruction. During their experimental in vitro and vivo studies on cystogram, reported the seepage fluid from the bladder wall consequent to retrograde introduction of normal saline into the bladder. Under clinical situations this retrograde pressure nephropathy seems to set at 48 hours of post-obstructive period and thereafter. But whether it could be evidenced before 48 hours of urethral obstruction can not be ascertained. obstruction of urine flow wheather located in renal pelvis ureter, urinary bladder or urethra causes back pressure induced by the obstructing urine flow impaired the mechanisim of tubular reabsorption and tubular secretion, significantly reduced glomerular filteration rate and renal blood flow, thus Post renal obstructive uropathy and uraemia developes either due to obstruction to urine flow or destruction of renal parenchyma or both. Blood et.al (1979) reported that because of retrograde pressure consequent to obstruction of urethra, renal pelvis gets enlarged at the cost of renal parenchyma and the exclusion of the blood flow due to increased pressure inside the inexpansible renal capsule which leads to a disuse atrophy.
Due to continuous formation of urine and its accumulation in the bladder subsequent to urethral obstruction the bladder gets distended. The increasing pressure and distended stretching of bladder wall resulted in inflammation, pressure ischaemia, devitalization, thinning, trabeculae formation, herniation of mucosa through the musculature of the urinary bladder leading to seepage or voiding of whole of the stagnated urine into the the peritoneal cavity (Dukes 1955, Gera and Nigam 1980) resulting in uroperitoneum and peritonitis .In Bovine urolithiasis very little is documented about uropathy. The data regarding it is available mostly in dogs or human beings. There occurs a secondary damage to kidney caused by a retrograde intracystic pressure in complete urinary obstructed cases resulting in the uraemia. (Makhdoomi and Marudwar 1992).
The clinical signs associated with urolithiasis depend upon the degree of obstruction to free flow of urine. Severity of surrounding tissue reactions (Dart 1997). The major clinical signs reported during the onset of urolithiasis include anorexia, suspended rumination and decreased water intake. Animals suffering from partial obstruction dribble blood tinged urine after prolonged, painful attempts of urination (Radostitis et.al 2000).As the disease progress the symptoms depicted are abdominal bilateral distention, tenesmus, colic, and weight shifting, and grinding of teeth, urethral pulsation(Radostitis et.al 2000)and tendency of rectal prolapsed. There is severe damage to the bladder and urethral mucosa by uroliths which leads to haematuria (Gangwar et.al 1990), oligouria and dysuria (Clark et.al 1999).In terminal stages, the temperature start decreasing, due to retention of metabolic wastes and their reabsorption results in toxaemia (Blood et.al 1983) and (Reddy et.al 1995). Urinary tract infections are the known risk in the spontaneously occurring urolithiasis in cat, dogs, rabbit and guinea pigs (Linsenmeyer and Ottenweller, 2003). Complete urethral obstruction results in death due to uraemia (Lorette et.al 2003).
The available literature regarding Haematobiochemical alterations during the phase of urolithiasis reveal that the changes are dynamic. There is haemoconcentration and neutrophilia (Rajathi et.al 2006). Haemoconcentration occurs due to dehydration as a result of fluid leakage across peritoneum. The increase in PCV, TLC and TEC was also reported (Gangwar et.al 1990; Reddy, 1992). An increase in nuetrophil count and leuckocytosis is due to stress (Socket et.al 1986; Berkow, 1998).Blood urea nitrogen(BUN) has been used as an index of uraemia because of its dependability and simplicity in assessment(Blood et.al 1983).there is rising trend of BUN (Kulkarni et.al; 1985, Socket et.al 1986, Makhdoomi and Marudwar 1992) during urolithiasis from the normal values in bovine which stand estimated so for by different owkers as 19.71mg% in bullocks,(Gera and Nigam 1980)in calves 7.27mg% (Saha et.al 1981) in yearling bulls 3.8mole/liter (Donecker and Bellamy 1982).During the phase of obstruction Bun levels are much higher ranging from 136.0-420 mg% (Rajamni and Ganapathy 1965). There has been a progressive report in BUN levels at the rate of 53 mg% per day in an induced obstruction in Bullocks, owever BUN above 200 mg% are reported to be detrimental for the surgical treatment. As the disease progresses there is increase in the levels and creatinine (Socket et.al 1986; Makhdoomi and Marudwar 1992). Decrease in plasma glucose levels (Gangwar, 1990) There is severe hypoprotinemia (Bush, 2002), elevated alkaline phosphate. Possible tissue hypoxia following retained urine with breakdown of high energy phosphate compounds cause hyperphosphataemia and it appears to be more reliable index (Brobst et.al 1978). Hyperkalemia is also due to obstructive nephropathy, poor renal perfusion, uroperitoneum, metabolic acidosis and hemolysis (Brobst et.al 1978 and Bani et.al 2007). The cardiotoxic effects of hyperkalemia may be excerbated by concurrent hyponatremia or hypocalcemia (Lewis and Morris 1984). Hypochloraemia is due to sequestration of chloride in the digestive tract (Brobst et.al 1978), retention of chloride in the gut to compensate for large increase in potassium ions, decrease intake of chloride following anorexia (Socket et.al 1986), diffusion of chloride to peritoneal cavity (Donecker and Bellamyl, 1982; Socket et.al 1986). And total body water expansion relative to total body chloride. Thus, in urolithiasis there is derangement of acid-base balance and electrolyte. Majority of the animals develop alkalosis but metabolic acidosis have also been recorded (Tyagi and Singh 1999). Uraemia due to Urolithiasis is a threat to survival of animals.As the animal start taking normal feed and water after initiation of treatment, PCV, Hb, TEC shows slight fall probably due to rehydration.
Diagnosis is based on history, clinical signs, and physical examination. However radiology & ultrasonography may be required to differentiate patients with uroliths from urinary tract infections, granulomatous urethritis, prostatic disease and neoplasia (Straub et.al 2012). Making a diagnosis involves integrating findings from the signalment, history, physical examination, clinical signs, time course of the disease and urinary tract imaging (Roger et.al 2005). The modality of imaging chosen may include a combination of plain abdominal radiographs, ultrasonography of the urinary bladder and urethra (Nicolle, 1994). Location of calculi can be determined by radiography (Busk and Ackermann, 1986). Radiography helps in differentiating between different types of uroliths as their radio densities provide a clue to the stone type (Klausner and Osborn, 1986). Multiple stone in urethra and urinary bladder can also be recorded by radiography (Saini et.al 2000). Sonography a non-invasive method for diagnosis of urolithiasis, localization urethral calculi and rupture of urethra or the urinary bladder (Braun, 1993). It is safer for both patient and the operator as it does not involve the use of ionizing radiation (Cartee et.al 1980). The volume, size and shape of the urinary bladder can be detected by cystosonography (Kundu and Ghosh 2006), besides changes in the wall thickness, intraluminal defects and seat of calculi lodgement can be detected (Makhdoomi and sheikh 2008). Abdominal sonography is useful to evaluate the bladder (Janene and henry 1995) but is unrewarding for evaluation of the entire length of the urethra. It can detect small calculi, radiolucent calculi and bladder mass like polyps neoplasia (Roger et.al 2005), stones of 1 to 2mm of diameter that can not be seen on X-ray, structures of varying size 1.50 to 2.7 cm floating in anechoic fluid (urine) in the urinary bladder with strong distal acoustic shadow can be detected (Singh et.al 2005). Scanning of bladder revels rounded to unevenly hyperechoic shadows with multiple spread tiny hyperechoic patterns (Makhdoomi and Shiekh 2008).
Various treatment modalities, both medical and surgical for the management of urolithiasis have been developed in almost all the species (Dubey et.al 2006). In ruminants, obstructive urolithiasis can be successfully treated if recognized early in the clinical course (Radostitis et.al 2005). In mild cases, the animals can be treated by using tranquilizers and antispasmodics (Gasthuys et.al 1993), litholytic drugs like cystone (Joshi et.al 1988). Diuresis should not be used before the removal of calculi and afterwards their administration is generally not required (Tyagi and Singh 1999)Since there is hyperkalemia, hyponatremia and hypocalcaemia, therefore stabilization of such metabolic derangements often involves administration of intravenous fluids for several hours, with repeated assessment of hydration, acid-base balance and serum electrolyte concentrations. Such treatments occasionally involve concerns about exacerbation of bladder distention in animals with an intact bladder. The animals that shows raised levels of BUN and creatinine can be effectively treated by peritoneal dialysis (Makhdoomi and Marudwar, 1992 and Pawde et.al 1992).
The treatment of obstructive urolithiasis is primarily surgical (Larson 1996; Van Metre et.al 1996; Khan et.al 2011). Recurrent urolithiasis, calculi at multiple sites, badly damaged urethra, atonic bladder or severe cystitis leads to failure of surgical repair in obstructive urolthiasis (Dubey et.al 2006). Urethrotomy, either post scrotal or post-ischial at the site of calculi lodgement is widely recommended and practiced to relieve the obstruction (Fischer and Vanchon 1992). However, postoperative leakage of urine from the site of obstruction leads to necrosis of urethra and subcutaneous tissues. Further, postoperative urethral constriction and recurrent urolithiasis are potential factors that results in the unfavorable outcome after urethrotomy, (Dubey et.al 2006). Other surgical methods include penile catheterization,cytotomy (Gera and Nigam 1980); bladder fistulation, intra pelvic cystic catheterization and peile amputation (Jenning, 1984)pesently, tube cystotomy is in voyage. The technique of tube cystotomy is a method of fixation of tube in the urinary bladder for the free passage of urine, followed by chemical dissolution of calculi which shows excellent results.
Cystotomy tubes provide a practical method for the urinary diversion when more radical surgical procedures are not feasible (Hajashi and Hardie 2003). Cystotomy tubes bypass urinary outflow obstructions or as an alternative to the urethral catheterization .Several different types of tubes are available, including Foleys catheters, Mushroom tip catheters and percutaneous catheters; more recently low profile gastrostomy tubes have been adapted for the use in cystotomy tubes (Kalim et.al 2011). Cystotomy tubes should remain in place for at least 14 days before removal to ensure adequate adhesions between the bladder and the body wall to reduce the possibility of urine leakage or peritonitis (Hajashi and Hardie 2003). Tube cystotomy is not free from complications and some complications involved are urine leakage, wound infection or dehiscence problems with the tube itself such as irritation at the stoma site, obstruction or accidental dislodgment and problems related to ascending infection due to the presence of the tube (Smith et.al 1995; Stevenson et.al 2001; Notle et.al 2002)
Critical preventive measures such as providing calcium to phosphorous ratio of 2:1 in the complete ration, increasing the salt levels to 4 percent of the diet in order to stimulate water consumption and to increase urine volume and maintenance of adequate and abundant water supplies should be highly considered .Struvite crystals can be prevented by the dietary modification to induce urine acidification (Van Saun 2007). The ration should be modified, which includes elimination of alfa-alfa feeding, reduction or elimination of grain feeding, a change to grass hay as primary forage, encouragement of grazing and ammonium chloride supplementation. These modifications are intended to reduce the urinary load of calculogenic minerals, especially calcium and phosphorous through elimination of alfa-alfa and grain feeding respectively. Besides potentially altering the mineral content of the diet, free access to grazing may increase the daily amount of water intake, which may in turn dilute urine, thus limiting calculogenesis. Changing from legume to grass hay and feeding ammonium chloride may move the dietary balance of strong cations and anions towards greater concentration of strong anions. Those areas where sheep exclusively are fed on paddy grasses in winters due to non availability of pastures, fortification of the dry paddy grass need to be undertaken to reduce the oxalate content of the grass. Provision of clean water in multiple sites and intentional salting moistened grass hay, induction of diuresis and maintenance of dilute urine would help a long way keeping urolithiasis in check
By means of physicochemical methods one can determine the type of urolithiasis which is important for the clinical guideline and prevention of recurrence. Urolithiasis occurs especially in cattle receiving rations high in cereal grains, oil meals or grazed in pastures containing large quantities of oxalate, estrogen of silican. In the prophylaxis and metaphylaxis of urolithiasis the essential role of food consumption is recognized. Nowadays the urolithiasis represents about 1-2% of all diseases and about 12-40% among kidney diseases. Dilution of calculogenic ions in the urine is of primary importance in prevention of urolithiasis in ruminants. The incidence of obstructive urolithiasis, is mostly found in winter under temperate conditions, pointing towards the inadequate water intake as another predisposing factor for the development of disease. Obstructive urolithiasis, in ruminants especially in cattle, can therefore be prevented if precautionary measures like balanced feeding and encouraging the animals to take adequate amounts of water in order to induce diuresis, by addition of sodium chloride to their feed especially during the chilly winter season. The dietetic recommendations are: an increased daily liquid intake, a correct and balanced diet (i.e. animal and vegetal foods), three meals daily with the avoidance of a too rich dinner. If there is known the type of lithiasis in order to prevent a recurrence the diet must include food with minimum lithiasis risk.
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