Which uroliths are radiopaque

See main articles: ureteric calculi and bladder stones for further discussion of these. By far the most common stone is calcium oxalate, however, the exact distribution of stones depends on the population and associated metabolic abnormalities e. Although some renal stones remain asymptomatic, most will result in pain.

Small stones that arise in the kidney are more likely to pass into the ureter where they may result in renal colic. Strangury is also occasionally present.

Some patients may also present with the complication of obstructive pyelonephritis , and may, therefore, have a septic clinical presentation. The composition of urinary tract stones varies widely depending upon metabolic alterations, geography, and presence of infection, and their size varies from gravel to staghorn calculi.

The more common composition of stones include more detail below :. Most renal calculi contain calcium, usually in the form of calcium oxalate CaC 2 O 4 and often mixed with calcium phosphate CaPO 4 1,6. In most instances, no specific cause can be identified, although most patients have idiopathic hypercalciuria without hypercalcemia.

Brushite is a unique form of calcium phosphate stones that tends to recur quickly if patients are not treated aggressively with stone prevention measures and are resistant to treatment with shock wave lithotripsy.

Interestingly hyperuricosuria is also associated with increased calcium-containing stone formation and is thought to be related to the uric acid crystals acting as a nidus on which calcium oxalate and calcium phosphate can precipitate 6. Rarely the underlying cause is primary oxaluria , a liver enzyme deficiency leading to massive cortical and medullary nephrocalcinosis , and renal failure. Certain medications 14 can predispose to calcium oxalate or calcium phosphate calculi, including:.

Struvite magnesium ammonium phosphate or "triple phosphate" stones are usually seen in the setting of infection with urease-producing bacteria e. Proteus, Klebsiella, Pseudomonas, and Enterobacter , resulting in hydrolysis of urea into ammonium and increase in the urinary pH 6, They can grow very large and form a cast of the renal pelvis and calyces resulting in so-called staghorn calculi.

Uric acid and cystine are also found as minor components. Hyperuricosuria is not always associated with hyperuricemia and is seen in a variety of settings see above , although in most instances uric acid stones occur in patients with no identifiable underlying etiology 6. Uric acid crystals form and remain insoluble at acidic urinary pH below 5. Cystine stones are also formed in acidic urine and are seen in patients with congenital cystinuria. These depend on the stone composition and vary according to modality.

The much greater sensitivity of CT to tissue attenuation means that some stones radiolucent on plain radiography are nonetheless radiopaque on CT. Intravenous urography IVU is a traditional radiographic study of the renal parenchyma, pelvicalyceal system, ureters, and the urinary bladder. It involves the administration of intravenous contrast. This exam has been largely replaced by non-contrast CT. Ultrasound is frequently the first investigation of the urinary tract, and although by no means as sensitive as CT, it is often able to identify calculi.

Small stones and those close to the corticomedullary junction can be difficult to reliably identify. Features include 7 :. Given that one of the commonest sites for a stone to become lodged is the vesicoureteric junction, some centers perform the study in the prone position to establish if the stone is retained within the intravesical component of the ureter or has already passed into the bladder itself.

Dual-energy CT is a technique allowing the composition of the calculus to be determined, by assessing stone attenuation at two different kVp levels. Each CT vendor has its own algorithms for the use of dual-energy CT for assessing stone composition. Dual-energy CT may be useful in detecting stones concealed by the opacification of the collecting system Dual-energy CT has also been shown to predict the success of extracorporeal shock wave lithotripsy Surgical intervention typically involves a retrograde ureteric stent with subsequent laser lithotripsy.

In acutely septic patients who would be unsuitable for an anesthetic or in those who would not be suitable for a retrograde stent, such as those with poor retrograde access or abnormal anatomy, a percutaneous nephrostomy PCN with an antegrade stent followed by laser lithotripsy is preferred. Extracorporeal shock wave lithotripsy ESWL is usually performed in large proximal calculi in patients unsuitable for invasive management.

Percutaneous nephrolithotomy PCNL is usually reserved for large calculi near the pelviureteric junction, especially staghorn calculi, which are unlikely to be removable via retrograde access. Small asymptomatic stones in the kidney can be safely ignored, and if patients maintain good states of hydration, the risk of recurrent symptoms can be dramatically reduced Struvite stones are usually large staghorn calculi and result from infection.

These stones need to be treated surgically and the entire stone removed, including small fragments, as otherwise, these residual fragments act as a reservoir for infection and recurrent stone formation. Uric acid stones usually are the result of low urinary pH, and hydration and elevation of urinary pH to approximately 6 are usually sufficient note rendering the urine too alkali e.

Cystine stones may be difficult to treat and are difficult to shatter with ESWL. Hydration and alkalinisation are usually first-line therapy. The differential of renal calculi is essentially that of abdominal calcifications. On CT there is usually little confusion as not only is CT exquisitely sensitive in detecting stones, but their location can also be precisely noted.

If non-contrast CT is equivocal for the location of the calcification, then a repeat CT with urographic phase contrast is usually able to clarify. Thus the differential diagnosis is predominantly on plain radiograph, and to a lesser degree ultrasound:. Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys.

Updating… Please wait. Unable to process the form. Check for errors and try again. 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. An ECG to record cardiac rhythm and rate and a serum potassium are indicated.

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. In most cases, struvite uroliths form in association with urinary tract infections with urease-producing Staphylococcus or Proteus spp. 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. 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. In dogs with a portosystemic vascular anastomosis, increased urinary ammonium output may partially be due to the increased filtered load of ammonia, because plasma levels of ammonia tend to be increased.

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.

It is important that diets high in purines not be fed to dogs receiving allopurinol because xanthine uroliths may result. 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. They may not be safe for use in dogs with portosystemic vascular shunts.

Such dogs tend to develop hypoalbuminemia, edema, and ascites when fed a low-protein diet. The safety of allopurinol in these dogs has not been established. In addition, alkalinization can predispose to hepatic encephalopathy because of increased GI absorption of dietary protein metabolites.

Stones composed almost entirely of cystine form in dogs that have a renal tubular amino acid reabsorption defect known as cystinuria. Cystine is a relatively insoluble amino acid; therefore, in high concentration it may precipitate and form stones.

Despite excessive urinary loss of cystine in cystinuric dogs, plasma cystine levels remain the same as in healthy dogs; in fact, the only morbidity or mortality associated with the inherited defect of cystine reabsorption is urolith formation.

Identification of cystine crystals by urinalysis indicates the dog is at risk of forming cystine uroliths. For poorly understood reasons, not all cystinuric dogs develop uroliths. However, the absence of uroliths does not preclude their future development, and preventive measures are indicated. Cystinuria is thought to be inherited as a sex-linked trait. However, in Newfoundlands it is transmitted as a simple autosomal recessive trait. Cystinuria has been recognized almost exclusively in male dogs, except in Newfoundlands.

Dogs fed meat-based diets tend to excrete acidic urine, which leads to urine cystine supersaturation. Cystinuria is a lifelong defect of tubular reabsorption and cannot be cured.

Cystine stones tend to recur within 1 yr without management to prevent recurrence, and they often recur despite attempts at prevention. Urinary cystine output should be reduced. Protein-restricted alkalinizing diets have been associated with reducing the size of cystine urocystoliths. Urinary cystine concentration can also be reduced by administering N- 2-mercaptoproprionyl -glycine 2-MPG, tiopronin or penicillamine.

The vomiting may be partially resolved by giving the medication with meals; however, a severe reduction in dosage or complete withdrawal is often necessary.