One study, published in the July-August issue of the "Journal of Medicinal Food" found that cranberry juice cocktail prevents bacteria from sticking to the lining of the urinary tract, thereby lowering infection risk. You can also mix these peppers into your favorite cornbread recipe. For sterile struvite uroliths, medical dissolution is the preferred treatment. I had only 3 glasses in 2 days and i was on fire when i urinated. Magnesium has been reported to be an inhibitor of calcium oxalate formation in rats and people; thus, the reduced magnesium concentration in feline urine may partially explain the increase in calcium oxalate stones in cats. Vitamin C has a reputation for being a feel-good nutrient, so it will come as no surprise that this list is full of foods with high levels of it. Walnuts are a great alternative.
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The only clinical sign associated with unilateral urethroliths may be pain, which can be difficult to detect in dogs and cats. If these initial signs of ureteral obstruction do not lead to a diagnosis, unilateral ureteral obstruction may result in hydronephrosis with loss of function of the ipsilateral kidney.
Ureteroliths may also precipitate a uremic crisis in cats with previously compensated chronic renal failure. Because clinical signs of renal dysfunction are generally not apparent until two-thirds or more of total functional renal parenchyma is lost, clinical signs may not be seen except in the following situations: Unilateral ureteroliths may be identified serendipitously during abdominal imaging studies or surgery.
Abdominal palpation can help detect urocystoliths; the bladder wall may be thickened, and a grating sensation may be felt when the bladder is palpated.
Although palpation may reveal a single large urolith or multiple uroliths by their crepitation, it cannot dependably identify all animals with uroliths; urethral calculi may be detected by rectal palpation or located by passing a catheter. Urate, and occasionally cystine, uroliths may be radiolucent, requiring contrast radiography or ultrasonography to confirm their presence. Urinalysis, including identification of crystals on microscopic examination of fresh, warm urine and bacterial culture and sensitivity testing, is a critical part of the evaluation and may help determine the type of urolith present.
Ultrasonography and cystoscopy may also be useful. 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. Urethral obstruction is an emergency condition, and treatment should begin immediately.
If the bladder is intact, it is distended, hard, and painful; care should be used when palpating the bladder to avoid iatrogenic rupture.
If the bladder has ruptured, it cannot be palpated and urine can sometimes, but not always, be obtained from the abdominal cavity by paracentesis.
Animals with spontaneous bladder rupture may appear temporarily improved because the pain associated with bladder distention has been relieved; however, peritonitis and absorption of uremic toxins and potassium occur rapidly and lead to depression, abdominal distention, cardiac arrhythmias, and death. Hyperkalemia and metabolic acidosis are life-threatening complications of urethral obstruction.
Initial emergency care involves immediate relief of obstruction by catheterization and fluid therapy with normal saline. Occasionally, an obstruction at the external urethral orifice can be dislodged by gentle massage.
Sometimes, when a portion of the urethra is dilated with fluid under pressure and then suddenly released, urethral calculi can be flushed out. The urolith nearly always can be flushed back into the bladder by using the largest catheter that can be easily passed to the calculus, occluding the distal end of the urethral lumen around the catheter, and infusing a sterile mixture of equal parts of isotonic saline solution and an aqueous lubricant.
If the urethrolith cannot be flushed back into the bladder, a urethrotomy should be performed to remove the obstructing stone s. Depending on the clinical circumstances, the urethrotomy site may be sutured or a permanent urethrostomy created. Calculi flushed back into the bladder should be removed by cystotomy to prevent recurrence, although in some cases they can be dissolved.
The stone should be sent for quantitative analysis, with the animal managed medically to prevent stone recurrence based on the results.
The most common canine uroliths are magnesium ammonium phosphate, calcium oxalate, or urate; less common uroliths include cystine, silica, calcium phosphate, and xanthine. While general management includes surgical removal and medical management, the appropriate treatment protocol depends on the location of the urolith and its chemical composition, as well as on patient-specific factors.
Nephrolithiasis is generally not associated with an increase in the rate of progression of kidney injury; thus, it is recommended that animals with nephrolithiasis be managed without surgery in most cases. The most common urinary stones in dogs are composed of struvite. Although they are frequent in cats, sterile struvite uroliths rarely form in dogs. They have been detected in a family of English Cocker Spaniels, suggesting a genetic predisposition. Medical management involves dissolution and prevention of stone formation.
For dissolution, urine should be extremely undersaturated for struvite; for prevention, the degree of struvite saturation should be sufficiently low to make crystallization unlikely. The choice between surgery, lithotripsy, and medical treatment may not be easy.
If stone dissolution is prolonged or fails, it may be more costly than surgical treatment. Surgical removal of uroliths is often incomplete, with small, hidden uroliths often inadvertently left in the urinary tract serving as a nidus for recurrence. Before beginning stone dissolution by medical therapy, a physical examination, CBC, serum chemistry profile, urinalysis, urine culture and sensitivity, abdominal radiographs to document stone size, and blood pressure measurement if possible should be performed.
Contraindications to stone dissolution include heart failure, edema, ascites, pleural effusion, hypertension, hepatic failure, renal failure, and hypoalbuminemia. However, chronic kidney disease is not always a contraindication for dissolution of struvite nephroliths. While the use of urinary acidification to reduce urine pH to Urease-producing urinary tract infections must be treated. The choice of antibacterial should be based on sensitivity testing when possible.
Most Staphylococcus and Proteus infections are sensitive to levels of amoxicillin or ampicillin achieved in the urine of healthy dogs. A urease inhibitor can be given but is not usually necessary. Concurrent treatment with a urease inhibitor such as acetohydroxamic acid enhances the rate of struvite stone dissolution, particularly when antibiotic resistance precludes effective antibacterial sterilization of the urine.
A reasonably safe dose of acetohydroxamic acid appears to be A reversible, mild hemolytic anemia has been seen in dogs given higher dosages. The stone dissolution protocol should be discontinued if severe adverse effects develop, although a mild degree of hypoalbuminemia is to be expected and can be tolerated. With good compliance, the following results can be anticipated: When surgery is performed to remove multiple small struvite calculi, removing all stone material is often difficult.
In such cases, a 4-wk dissolution protocol starting at the time of suture removal aids in preventing recurrence due to residual crystalline material. Once the urinary tract is free of stones, prevention strategies are much more likely to be successful. The key to prevention of recurrence in animals with a struvite stone associated with infection is to achieve and maintain sterile urine.
Routine testing of urine pH by the owner is important. If fresh urine is alkaline, a urinalysis and culture should be done, with the dog treated appropriately if an infection is present.
Once stone dissolution is completed, a prevention program can be considered. The aim is to prevent urinary tract infections with urease-producing microbes. The concentration of major struvite solutes in urine should also be reduced. A commercially available diet may be fed to lower urinary phosphate and magnesium and to maintain an acidic urine. Urease-producing infections should be eliminated, after which owners should regularly check the pH of the first voided urine in the morning after an overnight fast; in most dogs on a normal diet, the urine will be acidic.
Checking urine pH weekly is sufficient. Calcium oxalate uroliths have been increasing in frequency in dogs. Most affected dogs are 2—10 yr old. Hypercalciuria leading to calcium oxalate stone formation can result from increased renal clearance of calcium due to excessive intestinal absorption of calcium absorptive hypercalciuria , impaired renal conservation of calcium renal leak hypercalciuria , or excessive skeletal mobilization of calcium resorptive hypercalciuria.
Absorptive hypercalciuria is characterized by increased urine calcium excretion, normal serum calcium concentration, and normal or low serum parathormone concentration. Because absorptive hypercalciuria depends on dietary calcium, the amount of calcium excreted in the urine during fasting is normal or significantly reduced when compared with nonfasting levels. Renal leak hypercalciuria has been recognized in dogs less frequently than absorptive hypercalciuria.
In dogs, renal leak hypercalciuria is characterized by normal serum calcium concentration, increased urine calcium excretion, and increased serum parathormone concentration.
During fasting, these dogs do not show a decline in urinary calcium loss. The underlying cause of renal leak hypercalciuria in dogs is not known. Resorptive hypercalciuria is characterized by excessive filtration and excretion of calcium in urine as a result of hypercalcemia. Hypercalcemic disorders have been associated only infrequently with calcium oxalate uroliths in dogs. Routine laboratory determinations should include serum calcium, phosphate, total CO 2 , and chloride to eliminate the possibility of hyperparathyroidism and renal tubular acidosis.
Dissolution of calcium oxalate stones by medical means has not currently been established. Treatment requires surgical removal or lithotripsy followed by preventive strategies.
Recurrence is a major problem with calcium oxalate uroliths. Effectiveness of therapy should be reevaluated at 1- to 4-mo intervals by urinalysis. Chlorothiazide diuretics may also be of value. Ammonium urate stones are most common in Dalmatians and in dogs with congenital portosystemic vascular shunts. The formation of ammonium urate calculi depends on the urine concentrations of urate and ammonium and on other poorly understood factors.
Dalmatians do not convert most of their metabolic urate to allantoin and thus excrete the bulk of nucleic acid metabolites as relatively insoluble urate.
The biologic mechanism responsible for decreased hepatic conversion of urate to allantoin lies not in reduced uricase activity but in reduced hepatic transport of urate; the rate of urate hepatic transport is approximately three times faster in breeds other than Dalmatians.
Dalmatians fed a diet high in animal protein excrete a net acid load in the urine, and urinary ammonium output is subsequently increased. The combined high concentration of ammonium and urate in urine increases the risk of formation of ammonium urate stones. The excretion of acidic metabolites of an animal protein diet is believed to be important in this process, because urinary ammonium excretion is enhanced and ammonium urate is insoluble.
Urate output has been reported to be the same in Dalmatians that form stones and in those that do not, although in some studies the methods used to determine urine uric acid concentrations were unreliable. Urinary urate output should be reduced. This can be accomplished by feeding a low-purine, low-protein commercial diet.
However, the effectiveness of allopurinol in reducing urinary urate output is variable, and urinary urate levels should be measured although this may be difficult. Allopurinol must be used cautiously in dogs with hepatic disease or primary renal failure, because it is metabolized to its active form in the liver and is excreted via the kidneys.
Urine volume should be increased to reduce the concentration of all dissolved solutes in urine. This can be achieved by feeding canned diets restricted in protein. By reducing formation of urea, renal medullary urea concentration declines, interfering with the countercurrent system of urine concentration.
Salt should not be given to animals with hypertension but otherwise poses little risk in normotensive dogs without chronic kidney disease, proteinuria, or hypoalbuminemia. Prevention strategies aim to reduce the concentration of ammonium and urate in urine to levels unlikely to induce flocculation. A low-protein, low-purine diet should be fed to reduce urinary urate output.
Alkalinization should be used as needed to ensure alkalinuria. Ideally, allopurinol is not needed as a supplement to dietary management; however, if urate crystals persist, a low-maintenance dose of allopurinol is appropriate.
These dissolution and prevention strategies were developed for use in Dalmatians in which hepatic conversion of urate to allantoin is reduced but the liver is otherwise normal.
Nuts, seeds and oily fish, such as salmon, provide healthy alternatives to saturated fat-rich foods, such as high-fat meats and dairy products. The oil fish contains may be particularly helpful if you have high triglyceride levels because it helps your gallbladder empty more efficiently.
Snack on moderate amounts of mixed nuts or seeds instead of chips or pretzels, and choose baked or poached fish over fatty meats. Feeding your sweet tooth occasionally with a sugary dessert probably won't cause major harm, but an overall sugary diet increases your risk for gallstones and gallbladder disease.
The "Indian Journal of Community Medicine" study showed a significant link between high refined sugar intake and gallbladder conditions. Limit your intake of particularly sugary items, such as soft drinks, pancake syrup, frosting and candy. More often, choose naturally sweet, nutritious fare, such as baked sweet potatoes dusted with cinnamon, unsweetened applesauce or fruit smoothies.
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