scott@vtx-cpd.com
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Replying to Talia C. 12/01/2025 - 17:28
Dear Talia,
Happy New Year to you as well, and thank you for the update! It’s excellent to see that the desmopressin trial has provided some meaningful data, even though the challenges of snow and multiple dogs have made it tricky to fully assess water intake.
From the data you’ve shared, there does appear to be a significant improvement in USG during the day compared to pre-treatment values. Before desmopressin, her afternoon and evening USG values were consistently dilute (1.006 and 1.005), whereas now, these readings are markedly higher (e.g., 1.029, 1.027, 1.030). This suggests that the desmopressin is having an effect and supports a diagnosis of central diabetes insipidus (CDI), particularly given the consistent improvement in her ability to concentrate urine.
The similarity in her morning USG before (1.028) and during treatment (1.033) may be due to the fact that her baseline morning USG was already reasonably concentrated, which can occasionally happen in partial CDI cases. It’s also worth noting that psychogenic polydipsia (PD) would be less likely to show such a clear improvement in daytime USG following desmopressin administration. If it were primary PD, the effect on urine concentration would typically be minimal, as plasma osmolality in these cases already suppresses ADH production.
While there is still some overlap in the presentation of partial CDI and primary PD, the overall improvement during the day, combined with the owner’s observation of reduced water intake, strongly points toward CDI as the most likely diagnosis.
I would recommend continuing desmopressin treatment and monitoring her long-term response. If possible, getting a few more morning USG readings once the snow clears may help confirm whether this improvement remains consistent across all times of the day.
How are you enjoying the lectures?
Best regards,
Scott 🙂
Replying to shimin cheong 04/01/2025 - 05:57
Shimin,
Thank you so much for your thoughts and questions—it’s great to hear your perspective, and you’ve brought up some excellent points to consider!
Siichba’s Case Details
He’s a domestic shorthair kitten with no known genetic predisposition. His adoption history is limited, but there haven’t been any obvious breed-related concerns.
He’s in a single-cat household, entirely indoors, and while his environment seems low-stress overall, stress as a contributing factor is still something we’re mindful of. Adding environmental enrichment and ensuring hydration (wet food with added water, fresh water sources) has been part of the plan.Congenital Concerns
You’re absolutely right that congenital anomalies, such as ectopic ureters, could predispose him to recurrent infections or stone formation. While the initial ultrasound and imaging didn’t highlight any obvious structural abnormalities apart from the calculi, further investigation could be warranted if he develops recurrent infections or persistent haematuria despite resolution of the current stones.
Your example of the kitten with portal vein agenesis and a bladder stone is fascinating—thank you for sharing! Congenital liver disease does seem less likely in Siichba.
Current Approach
At the moment, Siichba is doing reasonably well, though he’s had intermittent setbacks, including lethargy and reduced appetite, which we’re managing supportively. His urine is bacteria-free, and we’re closely monitoring for any signs of blockage, especially given the risk associated with ureteral stones.
We do have the option of lithotripsy here, though I haven’t considered it yet for this case. It could certainly be an option in the future if his condition changes or the stones become problematic.
Regarding prazosin, it’s an interesting topic with quite a bit of debate about its effectiveness in managing lower urinary tract disease. I haven’t used it for Siichba yet, but I suppose it could be considered if there were signs of more acute obstruction.
Thank you again for sharing your insights and questions—it’s such an interesting case, and I appreciate the discussion. Let me know if you have any further thoughts or ideas!
Interestingly, I had my first case of ectopic ureters in a cat this week! It is the first one I have diagnosed in a cat!
All the best,
Scott 🙂
Replying to Rosanna Vaughan 25/01/2025 - 11:30
No problem!
Keep us posted!
Scott 🙂
Hi Sarah! 😊
Great questions, pancreatitis in Miniature Schnauzers can definitely be a tricky topic!
1. Predisposition to Pancreatitis in Miniature Schnauzers:
Miniature Schnauzers do have a known predisposition to pancreatitis, primarily related to their increased incidence of idiopathic hypertriglyceridemia. Elevated triglyceride levels can directly contribute to pancreatic injury through lipotoxicity and the formation of toxic byproducts during lipid metabolism, which damage pancreatic tissue and initiate inflammation.That said, it is worth noting that Miniature Schnauzers may also have an independent predisposition to pancreatitis unrelated to hypertriglyceridemia. Genetic studies have not conclusively linked specific mutations (e.g., SPINK1 variants) to pancreatitis in Schnauzers, but their breed-specific metabolic and pancreatic characteristics likely play a role. Additionally, dietary factors, obesity, and concurrent conditions like hypothyroidism or diabetes mellitus can exacerbate their risk.
2. CRP in Chronic Pancreatitis:
C-reactive protein (CRP) is a well-established marker for systemic inflammation and is typically elevated in acute pancreatitis (AP), correlating with disease severity. However, its role in chronic pancreatitis (CP) is less clear. Chronic pancreatitis often involves low-grade, ongoing inflammation and fibrosis, which might not provoke as significant a CRP response as acute inflammation.That said, CRP could still be mildly elevated in cases of active or acute-on-chronic pancreatitis episodes, where there is a surge in inflammation. Studies have shown a correlation between CRP levels and clinical disease activity, so it can be a useful adjunct marker to assess disease progression or flare-ups, particularly when paired with cPLI and imaging findings.
It sounds like you’re managing a complex case. If hypertriglyceridemia is a factor, managing lipid levels (e.g., through diet or omega-3 supplementation) might help reduce pancreatic stress. Let me know if you’d like to discuss further!
Cheers,
Scott 🙂
Replying to Rosanna Vaughan 24/01/2025 - 13:01
No problem!
Let me know if you try it!
Scott 🙂
Hi Rosanna,
Sorry to hear about your wee cat! Sending lots of healing thoughts. The team at Langford will take great care of you. I have tried to pull together information from the resources I have. There is not a huge amount of information out there! Chronic lymphocytic leukaemia (CLL) in cats is indeed rare and poorly understood, but I’ve gathered extensive information to help address your questions and provide context about this condition.
Understanding Feline CLL
CLL is a hematologic neoplasm characterized by the proliferation of small, mature lymphocytes in the peripheral blood, bone marrow, and sometimes other organs. In cats, it is most commonly a T-cell neoplasm, specifically CD4+ T-helper cells.
Key Characteristics:
Signalment: CLL affects middle-aged to older cats, with a median age of 12.5 years (range: 5–20 years) (Campbell et al., 2013). This aligns with your cat’s age. Males are slightly more affected, with a male-to-female ratio of approximately 2:1 (Workman & Vernau, 2003). Domestic shorthair and longhair breeds are most commonly diagnosed, though CLL can occur in purebred cats like Bengals or British Shorthairs.
Presentation: 50% of cases are diagnosed incidentally during routine bloodwork (Campbell et al., 2013). The most common clinical sign is chronic weight loss, reported in 44% of cases. Other signs include lethargy, reduced appetite, vomiting, diarrhea, or unremarkable physical examination findings (Campbell et al., 2013; Workman & Vernau, 2003). Cats are often asymptomatic early in the disease.
Diagnostic Findings: Peripheral lymphocytosis is a hallmark of CLL. In most cases, lymphocyte counts exceed 9,000 cells/μL, with a median of 34,200 cells/μL (range: 9,561–325,477 cells/μL) (Campbell et al., 2013). Bone marrow lymphocyte infiltration (>15–20% of total nucleated cells) is common but not universal. Cytopenias, such as anemia (50%) or thrombocytopenia (11%), are observed in some cases (Workman & Vernau, 2003; Campbell et al., 2013). Biochemical abnormalities are generally mild and non-specific, with occasional hyperglobulinemia or elevated ALT levels. Infectious disease testing (e.g., FeLV, FIV, tick-borne diseases) is typically negative.
Immunophenotyping and Classification
Immunophenotyping and clonality testing (e.g., flow cytometry and PARR) are essential for confirming CLL. Studies show that most feline CLL cases are T-cell in origin (94%), with the majority being CD3+/CD4+/CD8− T-helper cells (Campbell et al., 2013). Rarely, B-cell CLL is diagnosed (6%), characterized by CD21+ malignant lymphocytes (Workman & Vernau, 2003). The use of these techniques ensures accurate diagnosis and helps distinguish CLL from other lymphoproliferative disorders, such as lymphoma or reactive lymphocytosis.
Treatment Recommendations
Treatment decisions are based on clinical signs, lymphocyte counts, and disease progression. In asymptomatic cats or those with mild disease, treatment may not be immediately necessary (Campbell et al., 2013; Workman & Vernau, 2003). Chemotherapy is recommended for cats with significant clinical signs, progressive lymphocytosis (typically >60,000 cells/μL), cytopenias, or organ involvement (e.g., hepatosplenomegaly or lymphadenopathy). The mainstay of treatment is chlorambucil (0.2 mg/kg or 2 mg per cat every other day) and prednisolone (1 mg/kg daily). These medications are generally well-tolerated and effective in inducing remission. For refractory or advanced cases, protocols incorporating vincristine, cyclophosphamide, or other chemotherapeutics (e.g., L-CHOP) may be considered.
Prognosis and Outcomes
CLL is considered an indolent disease in cats, with median survival times of 14.4 months (range: 0.9–25.3 months) reported in one study (Campbell et al., 2013). The overall remission rate for treated cats is 88%, with a median remission duration of 15.7 months. Second remissions are possible, with durations of up to 18.1 months. Treatment-related side effects are uncommon but may include gastrointestinal upset or mild cytopenias (Campbell et al., 2013; Workman & Vernau, 2003). Cats with T-cell CLL typically have a good quality of life during treatment. B-cell CLL is so rare in cats that prognostic differences between the two phenotypes are not well-characterized.
To Address Your Specific Questions:
Life Expectancy: Based on available studies, median survival is approximately 14–17 months for treated cats (Campbell et al., 2013). Many cats achieve complete or partial remission with treatment, and survival can extend beyond two years in some cases. Since your cat is asymptomatic, this may positively influence his prognosis.
Chemotherapy Necessity: Chemotherapy is not always required in asymptomatic cats with stable disease (Workman & Vernau, 2003). A “watchful waiting” approach, with regular monitoring of bloodwork and clinical signs, is often appropriate. Treatment is reserved for cases with clinical progression, high lymphocyte counts, or cytopenias.
Bone Marrow Biopsy: While bone marrow examination is valuable for staging and diagnosis, it is not always necessary if clonality and immunophenotyping have already confirmed CLL (Campbell et al., 2013). Langford’s team can help determine if further invasive diagnostics are warranted.
Comparisons to Human Medicine
In humans, CLL is primarily a B-cell malignancy, characterized by the overexpression of anti-apoptotic proteins (e.g., Bcl-2) and an indolent course (Workman & Vernau, 2003). While feline CLL shares some similarities, the predominance of T-cell neoplasms in cats suggests differing pathophysiology. Unlike human medicine, advanced diagnostic tools like cytogenetics and molecular markers (e.g., ZAP-70) are not widely available for cats.
Summary
Feline CLL is a manageable disease, often allowing for good quality of life. With early diagnosis and appropriate treatment, many cats respond well to therapy. Chlorambucil and prednisolone remain the mainstays of treatment, and remission rates are encouraging. Your proactive approach and Langford’s expertise will ensure the best possible outcome for your cat.
If you’d like further literature summaries or clarification, I’m happy to help. Wishing you and your cat all the best as you navigate this journey!
Key References:
Campbell MW, Hess PR, Williams LE. Chronic lymphocytic leukaemia in the cat: 18 cases (2000–2010). Vet Comp Oncol. 2013 Dec;11(4):256-64. doi: 10.1111/j.1476-5829.2011.00315.x.
Workman HC, Vernau W. Chronic lymphocytic leukemia in dogs and cats: the veterinary perspective. Vet Clin Small Anim. 2003;33(6):1379-1399.Please keep me updated. Best regards,
Scott 🙂
Replying to Stephanie B. 24/01/2025 - 17:27
Hello Stephanie!
It is lovely to hear from you. I am so glad you are enjoying the course!
Let me make sure Ingrid sees this and we will get back to you ASAP!
Speak soon.
Scott 🙂
Replying to Raquel M. 17/01/2025 - 17:54
Hi Raquel,
You’re very welcome! I’m so glad the advice has been helpful, and I appreciate you keeping me updated. Regarding your question about Hill’s I/D Digestive Care, you’re absolutely correct—it is labelled for growth and could be a good alternative if it’s easier to source than Purina HA. Both diets are formulated for GI support and growth, so either would be suitable for Lloyd, depending on availability and owner preference. If Hill’s I/D Digestive Care is more readily stocked on the island, it could simplify things for the owner while still providing the nutritional and therapeutic benefits he needs.
I’d be happy to help draft a protocol and provide materials for your clinic to address acute uncomplicated diarrhea. This can include a clear step-by-step process, evidence summaries, and recommended product options like probiotics and dietary interventions. I’ll prepare something comprehensive that you can present to your colleagues to encourage this positive change. Let me know if there’s anything specific you’d like included, and I’ll make sure it’s tailored to your clinic’s needs.
Thanks again for your thoughtful questions and for keeping me informed about Lloyd’s progress.
Kind regards,
Scott 🙂
This is so interesting!
Have you ever seen this in a dog or a cat?
Scott 🙂
This is so interesting!
I never thought we would be discussing a Chinchilla, but very excited we are!
Thanks for sharing.
Scott 🙂
Hello everyone!
I wanted to let you know about exciting live online events we have planned for 2025:
A whole day of interactive CPD from the comfort of your own home!
Scott 🙂
Replying to Rosanna Vaughan 20/01/2025 - 13:17
Let us know how you get on!
Scott 🙂
Replying to Laura S. 19/01/2025 - 19:49
Hahaha!
Made me think… how many of the things we do now were due to being told off at some point!
Scott 🙂
Hey Rosanna.
Definitely not my are of expertise! I have reached out to some surgeon pals to comment too!
Thanks again for the great question!
Scott 🙂
Replying to Samantha T. 23/12/2024 - 11:03
Hey pal!
We identified stone formation affecting the ureters, bladder, and potentially the urethra, with a partial obstruction causing hydronephrosis in the left kidney. Based on his age, the most likely stone types were struvite or calcium oxalate. The presence of E. coli in his urine suggested the stones might be infection-induced struvites, but without definitive analysis, we worked with probabilities.
To manage the infection, we transitioned from Clavaseptin to a fluoroquinolone to improve penetration into the urinary tract and stones. This choice was guided by culture results and proved effective. For dietary management, we started with a struvite dissolution diet (feline c/d) for two weeks before transitioning to feline i/d to ensure nutritional adequacy for a growing kitten while supporting urinary health. Monitoring urine pH was a key part of this approach, and no alkalinization was required during this stage.
The elevated ionized calcium presented an additional challenge. I opted to incorporate 1 gram of soaked chia seeds daily into Siichba’s diet as a low-risk intervention to help manage calcium levels and reduce the likelihood of calcium precipitation. It felt like a safe approach, but I’d love to hear your thoughts on whether this was the right move for such a young patient.
Supportive care was central to Siichba’s recovery. We provided pain management with buprenorphine and used Prazosin to relax the ureters and encourage potential stone passage. IV fluids were administered to maintain hydration and dilute the urine, reducing the risk of further stone aggregation. Regular monitoring with serial ultrasounds and bloodwork helped us track his progress, which showed no worsening of the obstruction. Thankfully, his kidney function remained stable, and over time, his symptoms, including haematuria, resolved. Imaging also indicated improvement in the bladder and ureteral findings.
This case highlighted the importance of a multifaceted approach, balancing stone dissolution, infection control, and supportive care while being mindful of the patient’s age and growth needs. It was rewarding to see him respond well to the treatment plan, but I’m curious to know how you might have approached a similar case. Do you have any concerns about using chia seeds or this type of dietary management in younger patients? Any insights would be greatly appreciated!
Over time, the urine pH was trending on the acidic side, so I have introduced potassium citrate.
Would love to hear your thoughts!
Scott 😊
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