Urethral Obstruction

In this episode, Dr. Lottie talks all about urethral obstruction, why it occurs and how we should go about managing the condition

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Timeline:
00:00 Intro
00:43 Case
01:54 Aetiology & Pathogenesis
06:55 Clinical Signs
07:45 Diagnosis
10:48 Treatment
16:38 Prevention
18:34 Key Points
20:29 Outro

Recommended Reading

• 2025 iCatCare consensus guidelines on the diagnosis and management of lower urinary tract diseases in cats – gives a great overview of the causes, diagnosis and how to manage the condition

References

• Taylor, S. et al. (2025) ‘2025 iCatCare consensus guidelines on the diagnosis and management of lower urinary tract diseases in cats’, Journal of Feline Medicine and Surgery, 27(2), p. 1098612X241309176. Available at: https://doi.org/10.1177/1098612X241309176.
• Cooper, E.S. (2015) ‘Controversies in the management of feline urethral obstruction’, Journal of Veterinary Emergency and Critical Care, 25(1), pp. 130–137. Available at: https://doi.org/10.1111/vec.12278.
• Hanson, K.R. et al. (2021) ‘Effect of prazosin on feline recurrent urethral obstruction’, Journal of Feline Medicine and Surgery, 23(12), pp. 1176–1182. Available at: https://doi.org/10.1177/1098612X211001283.
• Segev, G. et al. (2011) ‘Urethral obstruction in cats: Predisposing factors, clinical, clinicopathological characteristics and prognosis’, Journal of Feline Medicine and Surgery, 13(2), pp. 101–108. Available at: https://doi.org/10.1016/j.jfms.2010.10.006.

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Creators and Guests

Host

Dr. Lottie Wilkinson

Creator and host of the Current Vet podcast

What is Current Vet?

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Intro

Hello, hello and welcome back to Current Vet if you're new here. This is the podcast that makes Veterinary Medicine simple. I'm your host, Dr. Lottie, and as part of our cat month, we are going to talk about feline urethral obstruction. Also referred to in practice as being a blocked cat. Although urethral obstruction is of course not only seen in cats, it is extremely common and most often seen in cats.

So we're gonna throw it in with this month with our cat episodes. We also had a couple of requests to hear this topic, so thank you to you guys for requesting it. Let's start with our case.

Case

It's early evening in your emergency clinic and a 4-year-old male neutered, domestic short hair wasabi is brought in by his owner.

She tells you that he's been in and outta the litre all day, straining repeatedly, vocalizing and producing little to no urine. He's been hiding more than usual and hasn't eaten since this morning. On physical exam, wasabi is quiet but responsive. When you palpate his abdomen, his bladder feels large, firm and painful.

He tenses and turns and hisses. When you touch it, you check his vitals. His heart rate is 140 beats per minute, which you flag as being low for a stress cat in an emergency environment. You suspect that there's urethral obstruction and possibly hyperemic, bradycardia secondary to that obstruction.

So you explain to the owner that Wasabi needs treatment right away, but how does this urinary problem have such a huge effect on the heart rate?

Aetiology & Pathogenesis

Urinary obstruction refers to a partial or complete blockage of urine outflow anywhere along the urinary tract. In practice, when we talk about obstruction, we are usually referring to urethral obstruction where urine can't pass through the urethra, so from the bladder through the urethra to be expelled.

Just note that the ureter. Is the tube that connects the kidneys to the bladder, and we are not talking about that. We're talking about from the bladder to the outside world. Urethra obstruction is most common in male cats. It is a true emergency and it is often fatal if left untreated.

However, it is really important to remember that this is not just a feline disease. We do also see urethral obstruction in dogs, often secondary to urolithiasis or prostatic disease, urethral strictures, or a neoplasia, and we also see it in male sheep and goats where obstruction frequently occurs at the urethral process at the end of the penis, which is also called the verma form Appendage.

Males of any species are more commonly affected by urethral obstruction than females. And this is because the male urethra is longer and thinner than the female urethra, so blockages are more common along a narrower tube, and there is a longer length of urethra along which a blockage can occur.

The best way to think about the causes of urethral obstruction is to divide them anatomically. So we have intraluminal causes, intramural causes, and extra luminal causes. These intraluminal causes are causes within the urethral lumen itself. So for example, we could have a urethral plug.

This is particularly common in cats. These are gonna be mixtures of mucus inflammatory debris and crystals. We can then have uroliths, so for example, with struvite or calcium oxalate stones, blood clots can occur and these are associated more with trauma or inflammation. Or we can just have some crystalline sediment causing a blockage in the tube.

We then have our intramural causes, and these involve the urethral wall. So some examples include urethral spasm, which is especially common in cats with feline lower urinary tract disease. We can have inflammation and edema in the urethra, wool neoplasia, or fibrosis or strictures, which often occur after trauma surgery or repeated catheterization.

Our extra luminal causes are ones that compress the urethra from outside. So examples include prostatic disease, which often occurs in intact male dogs, pelvic trauma. And masses within the pelvis or in the perineum. So obstruction can result from many different causes, but now let's connect that obstruction to the systemic effects that we see.

So when the urethra is obstructed, urine cannot leave the bladder, the bladder pressure rises. And as urine accumulates in the bladder and up into the ureters, that pressure is transmitted back up the urinary tract to the kidneys. As a result, this means that glomerular filtration rates through the kidneys decreases a postrenal.

Azotemia develops because their problem is occurring after the kidneys, so it's postrenal. And then that causes an accumulation of potassium and nitrogenous waste products in the bloodstream because they're not being adequately filtered out and excreted by the kidneys. Potassium is normally excreted in urine, and when urine flow stops or is obstructed , potassium is not being excreted, and levels can rise rapidly.

High potassium reduces the resting membrane potential in cardiac myocytes. This means that electrical conduction through the heart slows down, which is why we see bradycardia, conduction delays and arrhythmias. And this explains why wasabi has a low heart rate despite stress. At the same time, metabolic acidosis can develop calcium shifts, further destabilize the cardiac conduction and severe bladder distension risks damage occurring to the detrusor muscle or possibly even bladder rupture if it's severe.

Clinical Signs

Clinical signs that we're gonna see if a cat is obstructed or any animal is obstructed, are gonna be frequent attempts to urinate, but only producing very small amounts of urine or no urine at all, straining or vocalization. And particularly in cats, we see them hiding away from other people. We can also see lethargy or in appt.

On clinical exam, our biggest red flags are going to be a large firm and painful bladder depression or tonation, and especially that bradycardia in a stressed patient. Any male cat that is straining a not producing urine, should be considered obstructed until proven otherwise.

Diagnosis

So what are we gonna do for diagnostics? Because urethral obstruction can become life-threatening very quickly. This is not a diagnosis that you want to delay or overcomplicate. The goal of diagnostics in an obstructed patient is not to immediately find the cause, but it's to Assess how unstable the patient is, and identify any immediately life-threatening consequences of the obstruction.

So our immediate priorities are gonna be a thorough clinical exam with particular attention to the bladder size, pain, hydration, and perfusion parameters. So checking things like capillary refill time, mucus membrane color and moisture. We're then gonna check an ECG trace if it's available, especially in patients with a low or inappropriately normal heart rate.

Point of care. Blood tests can also be used to assess metabolic stability. So seeing things like hyperkalemia or a metabolic acidosis, low blood pH, those sorts of things. In an emergency setting, a minimum database or big four is often sufficient in an initial assessment.

So this is gonna include a PCV. Total solids or total protein, blood glucose and blood urea nitrogen. These results give you a rapid insight into hydration, status, tissue perfusion, if the patient is anemic or amic, or if there's something like a protein losing enteropathy or nephro. So if we take our obstructed patient, common abnormalities that we are gonna find on these initial investigations are gonna be ECG changes consistent with hyperkalemia.

So things like a shortened or absent P wave wide QRS complexes and tall, narrow peaked T waves. We'll also see Azotemia due to that increase in urea and creatinine levels and metabolic acidosis because of that reduced renal excretion of hydrogen ions. And once the patient has been stabilized, further diagnostics become more useful.

At that stage, we can then do hematology and biochemistry. Urinalysis and imaging can help. This can help to see if we have lys or crystalline material. We can assess the bladder and urethral integrity with ultrasound, and it helps to guide long-term management and prevent recurrence by identifying the underlying cause of obstruction. But it's really important to note that these further investigation should never delay stabilization treatment of hyperkalemia or decompression of the bladder in a patient with suspected obstruction.

These are things to look at once we have stabilized the cap.

Treatment

So let's go through how we're going to treat these cases.

Step one, as we said, is going to be stabilization. Before we attempt catheterization, we must stabilize the patient. So this is gonna include placing an IV, providing analgesia, so opioids like methadone or buprenorphine starting. IV crystal fluids to restore profusion and promote dilution of those high potassium levels.

There is some debate about whether we should only use crystal fluids that don't contain any potassium, so, for example, using 0.9% NACL over normosol R and normosol R contains potassium chloride. But the current evidence is that the tiny amount of potassium in these balanced electrolyte solutions doesn't have enough of an effect on the patient. So crystal fluid choice is kind of much of a muchness. It doesn't really matter in these cases.

If our potassium levels are significantly elevated, we can also administer calcium gluconate to stabilize the myocardium insulin with dextrose, which is going to shift the potassium intracellularly.

Or we can give sodium bicarbonate to try and shift that potassium intracellularly because it's gonna be exchanged for hydrogen ions. Remember though that calcium gluconate does not directly reduce potassium levels. It just helps to stabilize and counteract the potassium in order to protect the heart.

Step two of treatment is going to be at bladder decompression. Once stabilized, a cystocentesis can be performed. To relieve bladder pressure, improve patient comfort, and make catheterization easier and safer. It's not going to resolve the obstruction or remove the cause, but it buys you time. It is worth noting though that this procedure is considered controversial by some clinicians due to the risk of bladder rupture or urine leakage into the peritoneum.

But evidence actually shows that this risk is low when the procedure is performed properly. Step three of treatment is going to be urethral catheterization.

Catheter placement should be performed under heavy sedation or general anesthesia to make sure that the patient is calm still. And the urethral muscles are relaxed, and this all works to enable easier catheterization. Strict asepsis is also really important. A couple of things to remember when catheterizing are never forced, the catheter use gentle flushing while advancing the catheter to help ease it in.

And select an appropriate catheterized. Once the catheter has been confirmed to be placed in the bladder place, a closed urinary collection system on the catheter to make sure that the bladder environment is remaining sterile. Once urine float has been restored, we need to make sure that we're monitoring for post obstructive diuresis, and this is when once an obstruction has been relieved, there is an increase in urine production or polyuria.

If it goes unnoticed, it can lead to dehydration, but just monitoring for this occurrence and being aware of it and adjusting the IV fluid rate accordingly is sufficient. Also make sure to recheck electrolyte levels, especially potassium really regularly to ensure that levels have normalized.

Step four of treatment is going to be. Aftercare. So after around 48 hours, the indwelling catheter should be removed. The time to remove a catheter is really a balance between the catheter, maintaining urethral patency and ensuring urine can flow well. First is the fact that the catheter being in the urethra causes irritation and inflammation.

So after removal, medical management typically includes prazoxin or . Phenoxybenzamine, which helps to reduce urethral tone and minimize the risk of re obstruction and also ongoing analgesia with opioids. Of course, NSAIDs are gonna be contraindicated throughout this whole process, because of the risk of renal injury, especially in dehydrated patients.

A final step of treatment is going to be surgical management if required. So surgery is considered when there is re obstruction or chronic re obstruction when catheterization completely fails and you can't get bladder access, or if there are structural diseases like strictures or urethral tears.

Our option is gonna be peritoneal urothrostomy, and that is the go-to surgery. And this is when a new opening is made in the urethra, in the peroneal region between the anus and scrotum.

In small ruminants, if they have the urethral process that has been obstructed, just removing that urethral process and leaving the penis intact and the rest of the, the urethra intact, can resolve the condition completely. So surgery can be lifesaving. But it's going to require lifelong management and a lot of owner input and dedication to patient care

Prevention

once the acute obstruction has been resolved. We then need to think about how we're gonna prevent obstruction from happening again. And this is especially important in cats because recurrence rates are high and many cases are part of a broader picture of feline lower urinary tract disease, rather than being a single, isolated event.

Our prevention protocol needs to bring together multiple different strategies and be tailored to the individual patient. Urinary diets can help by reducing the formation of lys, promoting dilute urine formation, and in some cases, they can help dissolve certain types of lys by making the urine more acidic or alkaline, depending on , the urolith type present.

Encouraging more water intake is really important too, so this can be through feeding wet food, providing multiple water sources, providing water in a water fountain, and that can actually really help cats increase their intake and separating food and water bowls if needed. Environmental and behavioral factors also play a really significant role, especially in cats with stress related conditions.

So key considerations are gonna be reducing household stresses, ensuring adequate literature numbers, and that they are clean, providing environmental enrichments and making sure that they have predictable routines. Owner education is a critical part of prevention, and we should be advising them to monitor for changes in literature, habits, straining, vocalization, reduced urine output, or behavior changes such as hiding or inappetence.

Key Points

So to pull everything together, let's go through the key points that you have to know about urethral obstruction. Urethral obstruction is a true emergency, and although we most often see it in male cats, it's a condition that can affect multiple species and has various different causes. What actually makes these cases life threatening is the fact that when you can't flow, the glomerular filtration rate drops, waste products and potassium levels build up in the blood, and metabolic acidosis develops.

That rise in potassium destabilizes, the cardiomyocyte electrical threshold, which leads to those classic bradycardia and ECG changes. The main clinical finding of urethral obstruction is straining to urinate, but producing little or no urine. Diagnosis and practice is largely clinical. A good history, careful bladder palpation an ECG assessment and your big four minimum database tell you what you need to know early on.

More detailed diagnostics like UR analysis and imaging are important, but they come later once the patient is stable. For treatment, we should first stabilize the patient address electrolyte abnormalities. Then we can decompress the bladder if needed, relieve the obstruction, whether that's via catheterization or via surgery.
And finally, prevention is gonna include addressing the diet, water intake stress. And the home environment alongside clear owner education. So early signs of obstruction are recognized before complete obstruction develops again.

Outro

And that is urethral obstruction. Thank you so much for listening to this episode.

If you found it helpful, follow, subscribe. Like the podcast, wherever you listen to your podcasts, and share it with someone who is heading onto their emergency rotations or needs to go over this topic again. For our daily quiz questions and more vet content, you can find us on Instagram and TikTok at Veterinary Vista, and if there's a topic that you wanna hear explained next, just let us know.

Come back next week to continue our cat topic series with Feline Leukemia Virus or FELV. See you next time.