scott@vtx-cpd.com

Hey Charlotte.

Hope that sounds OK. If your clinics are anything like mine at the moment, I understand why you are a bit behind!

The discussion forum will be live till then, so feel free to keep asking questions.

Scott 🙂

Hello.

Thank you so much. Totally agree, these are challenging cases and the decision making can be difficult. Many will do well with antibiotics, hepatoprotection and supportive care. Much of the decision making will depend on imaging too. If there seems to be disease in the GI tract and pancreas too, I will often be more proactive at taking biopsies. If there is any sign of significant biliary tract obstruction, them may also be more immediate surgical candidates. There is not a definitive answer as how long to wait before GA. Sometimes they are still sick when they go for GA. I am happy to send them for GA if cardiovascular system stable and blood pressure normal.

Regarding the immunophenotyping, it is something that can be done on some FNA tissue and sometimes on blood. It depends very much on the individual lab. I would contact the lab you use and they should have a list of typing and staining they are able to do.

Hope that helps.

Scott 🙂

Regarding the cats with weight loss. The answer might be yes! I definitely will run cobalamin folate and fPL in most of my cases. TLI might depend a bit on signs, but not all cats will display classic signs of diarrhoea. Any case with more chronic signs, I would definitely run all of these.

This may be my favourite question yet!!! Yes, I was just discussing this over on our members discussion forum. Where did you hear this and do you know what the information was based on? I think the following study demonstrates it well:

The full thing is available for free (https://pubmed.ncbi.nlm.nih.gov/28814338/):

Anti-nausea Effects and Pharmacokinetics of Ondansetron, Maropitant and Metoclopramide in a Low-Dose Cisplatin Model of Nausea and Vomiting in the Dog: A Blinded Crossover Study

Abstract
Background: Nausea is a subjective sensation which is difficult to measure in non-verbal species. The aims of this study were to determine the efficacy of three classes of antiemetic drugs in a novel low dose cisplatin model of nausea and vomiting and measure change in potential nausea biomarkers arginine vasopressin (AVP) and cortisol. A four period cross-over blinded study was conducted in eight healthy beagle dogs of both genders. Dogs were administered 18 mg/m2 cisplatin intravenously, followed 45 min later by a 15 min infusion of either placebo (saline) or antiemetic treatment with ondansetron (0.5 mg/kg; 5-HT3 antagonist), maropitant (1 mg/kg; NK1 antagonist) or metoclopramide (0.5 mg/kg; D2 antagonist). The number of vomits and nausea associated behaviours, scored on a visual analogue scale, were recorded every 15 min for 8 h following cisplatin administration. Plasma samples were collected to measure AVP, cortisol and antiemetic drug concentrations.

Conclusions: 5-HT3 receptor antagonist ondansetron demonstrates the greatest anti-emetic and anti-nausea efficacy of the three drugs. AVP and cortisol appear to be selective biomarkers of nausea rather than emesis, providing a means of objectively measuring of nausea in the dog.

The results of the study suggest that both 5-HT3 and NK1 receptors are an integral part of the emetic pathway activated by cisplatin which results in activation of the emetic reflex. The sensation of nausea is produced in cortical forebrain regions, increased activity was recorded in the left amygdala, the ventral putamen and the putative locus coeruleus. Nausiogenic signals travel from the vomiting centre via rostrally projecting pathways to the forebrain and nuclei controlling the physiological response to nausea sensation (e.g. salivating, restlessness). The ability of ondansetron to reduce cisplatin-induced nausea would suggest that 5-HT3 receptors have a role in transmitting nausea stimuli, either from the brainstem, the periphery or both, whereas NK1 receptors are limited to a central emetic triggering mechanism.

I think this demonstrates the exact point you are making!

Scott 🙂

This is a really good point and the number of cases with normal liver enzymes is quite concerning when you look at those percentages.

First thing is always that bigger picture question. Does the rest of the puzzle fit… are there compatible clinical signs? Common clinical signs included lethargy, vomiting, weight loss and decreased appetite. Physical examination abnormalities are not common, but include fever (22%), icterus (34%) and hepatomegaly (21%).

Abnormalities on complete blood counts are detected in less than half of cats with NC and, when present, include leukocytosis (39%), band neutrophils (33%), and anaemia (34%). Cats with moderate to severe cholangitis can have normal serum liver enzyme activities but increases in aspartate transaminase activity (AST) have been noted in 98% of cats. Variable increases in alanine transaminase (ALT) in 50-57%, alkaline phosphatase activities (ALP) in 14-48% and gamma-glutamyl transferase (GGT) have been noted. Many cats with cholangitis have liver enzyme values (ALT, ALP, GGT) within laboratory reference intervals, but about 2/3 are hyperbilirubinemic. Hepatic function parameters were infrequently abnormal (hypoglycaemia 7%, decreased blood urea nitrogen 0%, hypoalbuminemia 13%, and hypocholesterolaemia 6%). Fasting and post-prandial serum bile acid concentrations, using cut offs of 15 micromol/L and 20 micromol/L, respectively, had higher specificity than did enzymatic testing and should be considered if hepatic disease is suspected in cats with normal enzyme activities and bilirubin concentration.

On balance, most cases will have an abnormality that is compatible somewhere along the way. If not, AST and bile acids may play a role in cases where you still have a strong suspicion of NC. I know I have discounted how useful bile acids and AST are before… but they would have a place in this situation.

Hope that helps.

Scott 🙂