scott@vtx-cpd.com
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Replying to Natalie Niven 09/09/2024 - 22:52
Hi Natalie,
Yes, hypophysectomy is the surgical removal of the pituitary gland. It’s a less common treatment option but can be considered in cases of pituitary-dependent hyperadrenocorticism, especially if the owner is looking for a more definitive treatment compared to long-term medical management. By removing the source of excess ACTH production, it eliminates the need for lifelong medication like trilostane.
You’re right, though—there are significant considerations with this surgery. Removing the pituitary gland can lead to deficiencies in other hormones, particularly those regulated by the anterior pituitary, such as thyroid-stimulating hormone (TSH) and growth hormone. Patients would often require lifelong hormone replacement therapy, like levothyroxine and desmopressin, for these other deficiencies. That’s definitely a big downside compared to the relatively simpler trilostane treatment we use in dogs.
The main advantage over trilostane is that surgery offers the possibility of a “cure” for hyperadrenocorticism, which can be appealing in cases where the cat has concurrent issues, like Norman’s diabetes. Stabilizing the Cushing’s syndrome could improve his insulin sensitivity and overall diabetic control, possibly reducing the need for complex insulin management.
Of course, it’s a highly specialized surgery with significant risks and is usually only performed in certain centers with the expertise, which is why it’s less common. But for the right case, it can be a good option to consider. I think the RVC are the only ones doing it in the UK currently… but I might be wrong on that!
Scott 🙂
Hello!
So sorry about the delay in getting back to you, Laura! I have no idea how I missed this. Talking about the overuse of omeprazole is one of my favourite things!
You raise a really good point about omeprazole. While it can be very effective for treating acid-related issues, it’s important to remember that it isn’t without side effects. As you mentioned, omeprazole can potentially worsen nausea, especially in an already nauseous patient. If you’re more focused on mucosal protection rather than significant acid suppression, sucralfate would be a more suitable alternative in many cases.
In this particular scenario—vomiting and diarrhoea post-GA and NSAID use—omeprazole might be justified if you’re concerned about gastric ulceration or significant acid-related disease. However, if there’s no direct evidence of an ulcer (like blood in the vomit), I’d lean towards using sucralfate first. It offers mucosal protection without the potential nausea or long-term effects on gastric pH that omeprazole can cause. Tailoring the treatment to the clinical signs you’re seeing will be key.
Interestingly, I’ve been involved in a forum discussion recently about the use of PPIs like omeprazole, especially in cases of NSAID toxicity. The current VPIS guidelines recommend PPIs for all ibuprofen toxicity cases, but some research suggests that prophylactic use of PPIs can actually be harmful when used alongside NSAIDs. The ACVIM consensus points out that PPIs can alter the small intestinal microbiome, which increases the risk of intestinal injury from NSAIDs. This dysbiosis can lead to serious lesions and anaemia, particularly in the small intestine, which would not have been seen with gastric mucosa injury alone.
Here’s a key excerpt from the ACVIM consensus on gastroprotectant use: ‘’Bacterial overgrowth can have deleterious consequences when PPIs are administered with other drugs that can injure the small intestinal (SI) mucosa. It is common to prescribe PPIs in patients at risk for upper GI injury from nonsteroidal anti-inflammatory drugs (NSAIDs), but PPIs can alter the SI microbiome, increasing the risk of injury to the intestinal epithelium caused by NSAIDs. This effect is acid-independent and unrelated to gastric mucosa injury caused by NSAIDs. Inhibition of intestinal cyclooxygenase 1 and 2 (COX-1, COX-2) enzymes injures the SI mucosa. Enterohepatic recycling of NSAIDs likely plays a role whereby high concentrations of NSAIDs in bile are secreted into the duodenum in close proximity to the major duodenal papilla. Some of the most serious intestinal lesions in dogs caused by NSAIDs occur in this region. Small intestinal injury may be caused by increased numbers of gram-negative facultative anaerobic bacteria that flourish in the SI of patients treated with PPIs. Lesions are characterized by loss of villi, erosions, and multifocal ulcers distributed throughout the small bowel. Anaemia also may occur. Whereas some bacteria play a protective role against intestinal mucosal injury by NSAIDs, the intestinal dysbiosis arising from PPI administration increases the risk of NSAID-induced intestinal injury. Administration of antibiotics or probiotics may mitigate injuries caused by this drug combination, but such studies have not been conducted in dogs or cats.’’
Moreover, prophylaxis for gastroduodenal ulceration isn’t generally recommended in most cases, even for patients on glucocorticoids or NSAIDs. Studies in both cats and dogs suggest that using gastroprotectants in these cases might lead to unwanted consequences unless multiple risk factors for gastrointestinal bleeding are present. Pancreatitis, hepatic disease, and CKD, for example, are not considered risk factors for GI bleeding, and gastroduodenal ulceration or gastric hyperacidity are not commonly found in cats with CKD. Even in cats with acute kidney injury (AKI), gastrointestinal bleeding is thought to be rare. Since these cats already have a high pill burden, gastroprotectants are only recommended when there is a strong suspicion of gastroduodenal ulceration. Also, it’s important to note that gastroprotectants like omeprazole should not be used as antiemetics. A study on CKD cats showed that omeprazole did not reduce vomiting, whereas antiemetics like maropitant did. Chronically vomiting cats should be further evaluated for underlying causes like small bowel disease, especially if weight loss and/or diarrhoea are present.
In light of all this, I’d consider using sucralfate first in your case, especially if there’s no clear evidence of ulceration. Omeprazole could be reserved for cases where there’s clear evidence of a gastric ulcer or if upper GI symptoms persist despite other treatments. Given the risks of microbiome alterations and nausea, omeprazole may not always be the best first choice.
Let me know your thoughts!
Scott 🙂
Replying to Rachel R. 20/09/2024 - 17:11
Hi,
Thanks for your question!
Placing a Libre sensor over the shoulder blades can be a viable option, but you’re right to consider skin thickening, especially in longstanding diabetic patients. While there isn’t specific data on how skin thickening impacts accuracy, it’s something to keep in mind. The biggest issue I’ve seen in some patients is with skin reactions at the sensor site. Thickened or fibrotic skin may affect sensor adhesion or accuracy, but this varies between cases.
Rotating placement sites is a good idea to avoid potential skin issues, so using the thorax or flank can be useful, especially in skinnier cats where depth might pose more challenges. Just be sure to monitor the site for any reaction or sensor dislodgement.
Let me know if you have any other questions!
Best,
Scott
Replying to Sarah W. 18/09/2024 - 14:31
Hey Sarah.
Sorry about the delay with this one.
I will make sure Rodolfo sees this and we will get back to you ASAP.
Hope you have a lovely weekend.
Scott 🙂
Replying to Sarah W. 18/09/2024 - 14:29
I look forward to reading it too!
I wounder if he might share a seek peek before publication!:)
HAHAHAHAHAHAHAH!
Scott 🙂
Replying to Inga K. 15/09/2024 - 19:03
Hi Inga,
I wanted to follow up on our discussion about feline diabetes, especially with regard to velagliflozin. Thank you for the brilliant questions. I recently came across the SENSATION study published in J Am Vet Med Assoc, which offers some exciting insights into its use as a stand-alone therapy for feline diabetes. While insulin has long been the cornerstone of diabetes management, the study suggests that velagliflozin (an SGLT2 inhibitor) is a promising alternative, particularly for insulin-naïve cats. Here are some key points from the study:
Efficacy: Velagliflozin effectively reduced blood glucose and fructosamine levels, with 81% of cats achieving glycemic control by day 180. Clinical signs like polyuria and polydipsia also improved in over 85% of the cats.
Safety: Although ketoacidosis occurred in 7.1% of cats, primarily within the first 14 days, the study found that velagliflozin was generally well-tolerated. However, this does suggest that transitioning from insulin to SGLT2 inhibitors may require more careful monitoring in previously insulin-treated cats.
In addition to that, I came across a J Vet Intern Med study that directly compares velagliflozin to insulin. The findings demonstrated that velagliflozin was noninferior to insulin, with 54% of velagliflozin-treated cats showing treatment success by day 45, compared to 42% in the insulin group. It also had a lower incidence of clinical hypoglycemia (13% vs. 53%), which is an important factor to consider. While velagliflozin had a slightly higher occurrence of ketoacidosis (7% vs. 0% in insulin-treated cats), it still showed excellent glycemic control and quality of life improvements for many cats.
Based on this data, I think we can say that velagliflozin is not necessarily better than insulin, but it does provide a strong alternative, especially when owners find insulin administration challenging. Some of the decision-making will ultimately come down to owner preference. Velagliflozin, as an oral solution, may be more appealing to owners uncomfortable with injections, but it does require careful monitoring, particularly early on, to manage any risks like ketoacidosis.
Regarding Prof. David Church’s advice about administering insulin 1 to 1.5 hours before meals, I don’t disagree with his approach, but I think there are other practical factors to consider. Many owners feed first to distract their cats from the injection, which helps reduce stress for both the cat and the owner. Since cats often eat more ad libitum compared to dogs, the timing of feeding might be less critical. Both strategies can work, as long as there is consistent monitoring to prevent hypoglycemia.
I hope you’re finding the course insightful, and I’d love to hear any feedback you have!
Best regards,
Scott
Replying to Antonia B. 23/09/2024 - 16:42
Hi Antonia, welcome! No worries about being late! How are you finding the course so far? It’s great that you’re getting back into practice after maternity leave—juggling that and continuing to build your confidence is definitely impressive!
Scott 🙂
Hi Hannah,
Interesting question! I hope you are well. To clarify: are you asking about the management of neurological complications in patients with hepatic encephalopathy (HE), or a patient with a previously diagnosed congenital portosystemic shunt (CPSS) who also has idiopathic epilepsy or is seizing for another reason?
If you’re focusing on seizures due to HE, particularly in cases of CPSS, it’s important to note that dogs and cats with CPSS can present with an acute HE crisis, showing severe neurological signs like seizures, lethargy, or coma. In such cases, thorough investigation for precipitating factors—such as dehydration, high-protein meals, gastrointestinal haemorrhage, uraemia, constipation, and sepsis—is crucial. Any concurrent drug therapy should also be reviewed for risks of dehydration, electrolyte imbalances, or hepatotoxicity.
Therapy for acute HE exacerbations involves lactulose enemas after a cleansing warm water enema to reduce ammonia absorption, and antibiotics (e.g., metronidazole, ampicillin, or amoxicillin) to decrease urease-producing bacteria.
Anticonvulsants should be administered in CPSS patients with HE-related seizures, both pre- and post-operatively (POS). Clinicians often start with low-dose midazolam, although the use of benzodiazepines (such as diazepam and midazolam) for HE-related seizures is controversial, as benzodiazepine administration is a known precipitating factor for HE in humans. When managing seizures in patients with HE, levetiracetam is preferred due to its minimal hepatic metabolism and overall safer profile in liver-compromised patients. Phenobarbital, propofol, or potassium bromide can also be considered depending on the case.
In humans, the gamma-aminobutyric-acid (GABA)/benzodiazepine inhibitory neurotransmitter system is implicated in HE pathogenesis. Flumazenil, a GABA receptor antagonist, can improve HE symptoms in humans, especially in cases of benzodiazepine overdose. However, in veterinary cases, flumazenil’s efficacy has been mixed. Studies in dogs with chronic HE, such as those by Meyer et al. (1998) on dogs with Eck fistula, found no significant response to flumazenil, suggesting that endogenous benzodiazepines may not play a major role in the pathogenesis of HE in dogs.
Once stabilized, levetiracetam remains the preferred long-term anti-seizure medication due to its minimal impact on the liver.
Hope this helps answer your questions in more detail, and feel free to clarify any specifics about the case.
Best regards,
Scott
Replying to Steph Sorrell 10/09/2024 - 09:32
Thanks for sharing Steph!
Scott 🙂
Also…
Just FYI. I would be careful with the use of depomedrone longer term as there is a higher incidence of diabetes mellitus becoming a complicating factor.
Scott
Hi,
It seems you’re handling a challenging case of feline chronic gingivostomatitis (FCGS), a complex immune-mediated disease involving chronic oral inflammation. Here’s a detailed breakdown of the current best practices in managing FCGS, along with options beyond full-mouth extraction (FME).
Clinical Management of FCGS
The goal in FCGS is to reduce antigenic stimulation and modulate the abnormal immune response. Nearly all affected cats have moderate to severe periodontitis and tooth resorption, so surgical extraction is often essential to reduce the inflammatory burden.Surgical Extractions:
Full-mouth extractions (FME) or partial mouth extractions (PME) are considered the gold-standard treatment. About 60-80% of cats show significant clinical improvement post-extractions. Even though full-mouth extractions may seem extreme, they have been shown to significantly reduce inflammation, allowing the immune system to focus on any viral contributors, such as feline calicivirus (FCV) or feline leukemia virus (FeLV) .
Periodontitis creates a heavy inflammatory burden, and removing the teeth, particularly those with resorptive lesions or subgingival disease, alleviates part of that burden .
In one large study, up to 28% of cats achieved complete resolution, and an additional 39% showed significant improvement after extractions .
Importantly, the extent of extractions (PME vs. FME) does not seem to significantly affect the success rates . So, if inflammation is limited to the molar and premolar regions, PME might be a valid alternative to FME.
Preoperative Evaluation:A comprehensive workup is crucial, including:
CBC, serum biochemistry, and viral testing (FeLV, FIV, FCV, PFFV).
Viral co-infections like FeLV, FIV, or FCV negatively impact the prognosis, with FeLV-positive cats being 7.5 times more likely to fail surgical management .
Use of the Stomatitis Disease Activity Index (SDAI) to track inflammation and quality of life, which can help gauge treatment response .
Medical Management
For cats that either can’t undergo extractions or for cases refractory to surgery, medical management becomes essential. Here are the options:Glucocorticoids:
Prednisolone and Depo-Medrone are often used to manage inflammation pre- and post-surgery. However, long-term steroid use carries risks, including diabetes mellitus and immunosuppression . You could continue using prednisolone as it has a shorter half-life, making it easier to control side effects compared to long-acting steroids like Depo-Medrone.
Ciclosporin:Ciclosporin has been successful in reducing oral inflammation in many cases, with a study showing 77.8% improvement in cats receiving oral ciclosporin after extractions . It’s worth considering as an alternative to glucocorticoids, especially in long-term management.
Analgesics:Gabapentin or Amantadine are useful for managing neuropathic and chronic pain associated with FCGS. Gabapentin is commonly used for musculoskeletal and neuropathic pain in cats .
Bovine Lactoferrin:Bovine lactoferrin is emerging as a promising adjunct therapy for FCGS. A randomized, double-blind clinical trial evaluated the combination of bovine lactoferrin oral spray (6 mg/cat, q12h) and piroxicam (0.3 mg/kg PO q48h). The study found that 77% of cats showed significant improvement in oral lesions and overall clinical signs over a 12-week period .
Lactoferrin alone has been shown to improve clinical signs and enhance neutrophil phagocytic activity, providing an immune boost for cats with stomatitis, even those with concurrent viral infections like FIV .
Reference: Arzi B, et al. “A randomized, double-blind, placebo-controlled clinical trial of piroxicam and bovine lactoferrin for the treatment of FCGS.” Journal of Feline Medicine and Surgery, 2021 .Recombinant feline interferon-omega (rFeIFN-ω):
This therapy has shown moderate to marked improvement in 55% of treated cats. Subcutaneous administration may be particularly beneficial in cats with FCV .
Mesenchymal Stem Cell Therapy:In refractory cases, stem cell therapy has shown up to 71% improvement or remission in cats with severe stomatitis after extraction therapy .
Surgical Considerations
While surgery is the best long-term solution for most cats with FCGS, a more conservative approach like PME might be acceptable for cases where inflammation is localized.However, if medical management is only offering temporary relief, FME should be considered sooner rather than later. Cats with viral co-infections or severe oral inflammation tend to do worse with medical management alone.
Conclusion
In summary:FME or PME remains the gold standard for FCGS, though adjunct therapies like bovine lactoferrin and ciclosporin may offer additional relief.
Prednisolone can be continued if the cat is responding well, but long-term management should focus on reducing steroid dependence.
Bovine lactoferrin, especially in combination with NSAIDs like piroxicam, could be worth trialing before committing to FME.
Postoperative medical management, including pain control and possibly immunosuppressive or immunomodulatory therapies like rFeIFN-ω or stem cells, is essential for refractory cases.
I hope this provides a clearer picture of your options. If you’d like to discuss further or explore any other treatment pathways, feel free to reach out.Best regards,
Scott
Replying to Emma Henton 09/09/2024 - 13:31
Hi Emma, welcome!
It’s great to hear you’re returning to practice. Are you enjoying the course so far, and how are you finding the transition back into small animal practice after some time away? Would love to hear how it’s going for you!
Scott 🙂
Replying to Laura Jones 20/09/2024 - 09:56
HAHAHAHAHAHA!
This is true!
Scott 🙂
Replying to Kerida Shook 19/09/2024 - 23:17
No problem.
Keep me posted with the case!
Scott 🙂
Replying to Laura Jones 20/09/2024 - 10:00
It is crazy right!
I did not even realise it was a thing! It was obviously a technicians cat!
Scott 🙂
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