21 | How to plan and deliver amazing care to your urolith patients

PodcastRenalUrinary
Written By Laura Jones

Urinary stones are a common cause of lower urinary tract disease in cats and dogs.

 

But before we can start treating them, we need to look at what uroliths we commonly see and what causes them to occur. 

Each type will require different treatment and, therefore, different nursing care… which is exactly what we’re discussing in this episode of the Medical Nursing Podcast.

So what IS a urolith?

Put simply, a urolith is a stone. Urolithiasis is the generalised term used to describe a stone anywhere in the urinary tract; then you’ve got nephroliths, ureteroliths, urocystoliths and urethroliths depending on where in the urinary tract the stone is located - so the kidney, ureter, urinary bladder and urethra, respectively.

Uroltihs form due to the macroscopic aggregation of crystals within the urine. Crystals are precipitated mineral solutes; they can link together and increase in size to form larger crystals and, eventually, stones.

What’s in a urolith?

Uroliths can be formed of various minerals and can contain multiple crystal types in the same stone. 

Each stone consists of a nidus, a body, and a shell. 

The nidus is the area from which the urolith originated, usually directly in the centre of the stone, but not always. It’s the initial cause of the urolith, and treatment is usually aimed at managing the minerals within the nidus.

The body is the major portion of the urolith, comprising the largest bulk of the stone, and the shell is the outermost layer covering the urolith. This layer is the most recently laid-down layer of the urolith and can be different in composition from the body - especially if the patient’s diet, medication, or medical condition has recently changed.

What are the urolith types we see, and when do we see them?

The most common urolith types are calcium oxalate and struvite, though we also see urate stones, cystine stones, and rarely other stones. Each form in urine of different pHs and has different primary causes.

Let’s look at calcium oxalate…

The exact mechanism of calcium oxalate stone formation is unknown. It’s likely due to a combination of genetic, dietary and environmental factors. 

These stones are commonly seen both in cats and dogs. They can develop in any breed, though in dogs, Miniature Schnauzers, Lhasa Apsos, Yorkshire Terriers, Bichon Frises, Shih Tzus and Miniature Poodles may be predisposed. It’s usually seen between 2-10 years of age.

Calcium oxalate stones are commonly reported in older cats (8-12 years) and in male cats. Male domestic short/medium/longhair cats are around 1.4 times more likely to develop calcium oxalate than struvite. Both male and female Persians, Himalayans, Burmese, and Ragdoll cats are at risk in purebred cats. Many cats with CKD also have concurrent calcium oxalate uroliths.

Calcium oxalate stones form in acidic urine (a pH of 5.5 or below) and have a high recurrence rate.

What about struvite?

Struvite is the most common urolith type seen in dogs. Struvite is also known as triple phosphate or magnesium-ammonium phosphate, as it is comprised primarily of those 3 minerals, though sometimes trace amounts of other minerals are also present.

In most cases, struvite stones form in alkaline urine, and in dogs, they commonly form in association with urinary tract infections, Usually, these infections are with urease-producing bacteria.

Urease is an enzyme which converts urea into ammonia and CO2. The CO2 is then metabolised into bicarbonate, and the ammonia combines with magnesium and phosphate to form struvite. Both bicarbonate and ammonia increase urine pH, making the urine more alkaline and decreasing the solubility of struvite crystals.

Bacteria from the patient’s UTI can also become trapped in layers of the stone—and this is worth noting because it means that, as we dissolve the stone in treatment, bacteria can be released back into the bladder to continue that UTI.

In cats, sterile struvite urolith formation is reported in the absence of urinary tract infection. Sometimes, a sterile struvite urolith will form and then act as a nidus for infection, causing a UTI and further struvite formation as a result. The peak incidence of struvite uroliths is in cats between 2-7 years of age, and female cats are at higher risk for struvite urolith formation than males. Cats at an increased risk of a UTI (eg CKD, hyperthyroidism, diabetes) may also be at a higher risk of developing a struvite stone.

Moving on to urate…

Urate uroliths are formed of ammonium urate and can be seen both in dogs and cats. They can occur as a result of abnormal purine metabolism or as a result of excessive ammonia levels within the body.

Urate stones are commonly reported in Dalmations, bulldogs, and black Russian terriers, as these breeds have a congenital defect in urate transport within the body. They are unable to transport uric acid to the liver for update into hepatocytes, causing uric acid to accumulate in the blood instead. This then spills into the urine, where that uric acid can easily become a urate stone.

Patients with hepatic dysfunction also commonly develop urate stones. This is because the liver is responsible for turning ammonia into urea (as we chatted about all the way back in our liver disease series in episodes 4 and 8). When this can’t happen—for example, in a patient with a portosystemic shunt—ammonia builds up in the bloodstream. That high ammonia level spills into the urine, causing ammonium urate crystals to form.

And finally, let’s take a look at cystine

Cystine stones are formed of two molecules of the amino acid cysteine. They are less commonly reported than struvite, calcium oxalate, and urate, but they are still seen, so we must know when they occur and how they are managed.

Cysteine (the amino acid, not the urolith) is low-soluble in urine and typically present in low concentrations. It usually leaves the bloodstream in the glomerulus and is then reabsorbed in the proximal tubule in the kidney. Certain breeds, including Newfoundlands, Labradors, Australian cattle dogs, and miniature pinschers, have genetic mutations affecting this reabsorption, causing increased cysteine levels in the urine. 

Cystine urolithiasis has a strong sex predisposition, with 98% of dogs being male. 

What signs do we see in our urolith patients?

Regardless of the type of urolith your patient has, their clinical signs will be similar. Depending on whether the stone is causing an obstruction, patients can present with dysuria, stranguria, haematuria and pollakiuria; however, none of these signs are specific to urolithiasis and can be seen with any disorder affecting the lower urinary tract.

If an obstruction is present, clinical signs will also depend on where in the urinary tract that obstruction is. Upper urinary tract urolithiasis may cause no clinical signs at all or cause postrenal azotaemia and AKI, as we chatted about in episodes 13 and 18. Lower urinary tract obstructions often cause bladder distension, abdominal pain and paradoxical incontinence alongside systemic signs of postrenal azotaemia and AKI, depending on how long the obstruction has been present (as we chatted about in veterinaryinternalmedicinenursing.com/blog/episode-19).

Depending on the size of the stone and patient, in some cases, they can be palpated on physical examination. Urethroliths can also sometimes be identified via rectal palpation.

How about diagnosis?

Once you suspect your patient has urolithiasis, you’ll need to confirm that diagnosis.

The main differentials for lower urinary tract signs in our patients with stranguria and pollakiuria are urolithiasis, bacterial cystitis, and neoplasia. So we’ll begin investigating this with bloods and urine analysis and follow this up with some imaging.

Biochemistry allows us to identify whether any renal dysfunction is present, assess electrolyte balance, and look at total calcium levels—particularly important in patients with calcium oxalate uroliths. Ideally, we’d measure ionised calcium, which is more accurate in measuring available calcium in the bloodstream. If you’re measuring it in-house, this requires a blood gas analyser. Alternatively, it can be submitted to an external lab for analysis.

We’ll see other biochemical changes in patients with metabolic disease causing urolith formation. For example, a patient with a portosystemic shunt will have changes to their liver function parameters, as we chatted about in episode 8.

Haematology may be normal or show an elevated white blood cell count in the face of marked infection or inflammation within the lower urinary tract.

Urine analysis allows us to identify crystals and evidence of infection and document the urine pH and specific gravity. Ideally, we would analyse urine within an hour of collecting it since sediment changes will occur with sample ageing and due to changes in temperature. Refrigeration can, for example, cause marked struvite crystal formation - making sediment results hard to interpret in urolith patients.

So we’ve got crystals - but have we got stones? Time to take a look…

To identify those uroliths, we’ll need to perform some imaging. This is usually achieved with radiography, though we can also see stones on ultrasound in some cases.

Not every urolith is radiopaque, so we’ll need to use a combination of plain and contrast radiography studies to document their presence definitively.

We’ll need to image the entire urinary tract, including all of the urethra and the kidneys, to look for uroliths in all areas of the urinary tract. We may get an idea of stone size from radiographs - ultrasound tends to overestimate their size by up to 68%, and radiographs can also give us an idea of what type of urolith the patient has (though this is not completely accurate).

Lastly, we can perform urolith analysis to identify the mineral(s) within the stone. This can only be performed once the urolith has been removed, eg following a cystotomy or if you have managed to flush some material out while unblocking a patient. The urolith is submitted dry to a specialist laboratory (such as Minnesota Urolith Center) for analysis, and a report is returned with the exact stone composition. This allows you to tailor treatment accordingly.

And once we’ve diagnosed our patient, how will we treat them?

The first priority is to de-obstruct a blocked patient, regardless of the type of urolith present, as we discussed in episode 19 on managing blocked cats.

The treatment of the urolith itself depends on the type present. Some uroliths are dissolvable with diet, but not all. Some require surgical removal, but not every urolith does. This means we must know the treatment options for each urolith type so we can advise clients accordingly.

Managing calcium oxalate uroliths

Calcium oxalate stones are not amenable to medical dissolution, so they will require surgical removal if they are causing significant clinical signs (or, in the case of ureteral obstruction, a SUB placement to divert the flow of urine around that obstructed ureter, as we chatted about in episode 18). 

Because the recurrence rate for calcium oxalate urolithiasis is high, we need to prevent future recurrence medically. This is achieved by increasing the patient’s water intake to dilute the urine and increase urination, helping to remove crystals from the bladder. On top of this, we want to feed a diet that promotes a target urine pH of 6.5-7. In cats, if their urine pH is consistently below 6.5, alkalinising agents like potassium citrate may be added. This must be done carefully, maintaining a target urine pH of 7-7.5 since over-alkalinisation of the urine can lead to struvite formation.

Speaking of struvite…

Struvite stones can be dissolved medically - so we should ideally not be taking patients with struvite uroliths to theatre! 

Instead, antibiotic therapy to manage any UTI present and a dissolution diet are used. Antibiotic choice should be based on culture and sensitivity results and continue throughout the dissolution period since live bacteria can be shed from the dissolving stone. 

The patient should have regular imaging (abdominal radiographs) and urine analysis performed during dissolution.

Several diets can be used to dissolve struvite uroliths, and the average dissolution time is around 1-3 months.

And what about ammonium urate?

Urate stones can also be dissolved medically in some cases.

Where this is required, dissolution diets for urate stones are typically protein-restricted and contain low-purine protein sources, so they are not suitable for all patients. Growing, pregnant or lactating patients and Dalmatians should not be fed these diets. 

The ideal target pH for urate dissolution is 7 to avoid excessive alkalinisation of the urine and struvite forming as a result.

Allopurinol can be used in patients with urate stone formation. This drug decreases the production of uric acid but can increase xanthine concentrations, increasing the risk of xanthine urolith formation. This drug is not used in patients with things like portosystemic shunts. Instead, their underlying hepatic disease should be managed to minimise ammonia production and enhance ammonia metabolism. 

Alongside this, their uroliths are normally removed surgically at the time of portosystemic shunt surgery.

Lastly, let’s look at cystine

Cystine stones can be dissolved medically and prevented with diet and medical therapy. These uroliths are less likely to form in older patients, so treatment can often be discontinued in later years.

Treatment includes feeding a protein-restricted, alkalinising diet to maintain urine at a target pH of 7-8 and maintain a low USG. Foods high in cystine precursors (an amino acid called methionine), such as dairy, should be avoided.

And how will we nurse these patients?

Our nursing considerations depend on whether our patient is obstructed and whether they’ll be managed medically or surgically, depending on their urolith type.

Firstly - any obstructed patient should receive prompt triage and deobstruction, as we described in episode 19.

If your patient has a ureterolith causing a post-renal AKI, they’ll require emergency management of this, which is usually achieved through placement of a subcutaneous ureteral bypass, aka a SUB - which we chatted about in episode 18.

Surgically-managed patients will typically have a cystotomy, and in most cases, if they only have bladder stones and no urinary obstruction, they’ll be systemically well. 

Anaesthesia is normally routine, and our nursing focus is on assessing and managing pain, monitoring urination, and general nursing care, including monitoring nutrition and hydration, and providing frequent opportunities for urination, since they’ll likely have bladder pain.

Medical management depends on the exact urolith type present but includes increasing water intake, alongside transitioning to a medical dissolution diet if applicable and adding additional medications as needed. 

Most of this will be done as an outpatient, but the veterinary nurse or technician is still vital in client support and education. Areas to discuss include techniques for increasing water intake, how much of the new diet to feed, how to introduce a new diet (especially in cats), monitoring signs at home, and how often the patient should return for repeat appointments to check progress.



So there you have it - that’s an overview of the common (and a few less common!) uroliths we see in practice, why they occur, and how they’re managed. 

Nursing care for these patients varies, from triaging and deobstructing those blocked patients to managing AKI if that obstruction has been there for some time and caused post-renal damage to the ongoing management of that urolith. 

Depending on the type, it’ll either be surgery or dietary adjustments and medications. On top of this, we need to chat to our clients about ongoing care and monitoring at home, and the veterinary nurse or technician is absolutely vital in supporting clients through this process.

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
Previous

22 | The top 4 things you need to know about prostatic disease as a vet nurse
Next

20 | How to manage those stressed-out bladder cats without getting stressed yourself!