scott@vtx-cpd.com

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 🙂

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

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

Replying to Kerida Shook 19/09/2024 - 23:17

No problem.

Keep me posted with the case!

Scott 🙂