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    Keymaster

    Hello.

    Hope you are well. There is not a definite multiple of normal that would make me withdraw treatment. It depends on a number of factors. I would definitely be taking more notice when the ALT and ALP are getting greater than 3x the reference.

    Hepatotoxicosis from phenobarbital appears to be dependent on cumulative dose, with possible individual modulating factors. Signs typically develop after a year or more of phenobarbital treatment, and the duration of administration is associated with the degree of histologic injury in epileptic dogs. Presentation can range from subclinical increases in serum bile acids to fulminant liver failure. Typical histologic findings in dogs with clinical signs are bridging portal fibrosis, bile duct hyperplasia, and nodular regeneration. Higher phenobarbital dosages or serum drug concentrations have not been correlated with the development of abnormal serum bile acids across epileptic dogs; however, individual dogs with phenobarbital hepatotoxicosis can improve clinically following phenobarbital dosage reduction. For dogs with hepatotoxicosis during chronic phenobarbital treatment, phenobarbital should be discontinued, or the dosage minimized, by adding another anticonvulsant. For example, potassium bromide (KBr) can be substituted at a maintenance dosage of 40-60 mg/kg PO q 24 h, and phenobarbital can then be discontinued with a rapid taper over 1-3 weeks.

    b) It may actually be helpful to include the phenobarbitone levels in your monitoring. Clinically significant hepatotoxicosis can be preempted in most dogs by serial monitoring of serum bile acids, phenobarbital concentrations, and a liver panel, ideally every 6 months. Serum phenobarbital concentrations >40 mcg/mL should be avoided, as this can be a risk factor for hepatotoxicosis. In addition, the presence of hyperbilirubinemia, new hypoalbuminemia, or discordant increases in serum ALT > ALP is clinically significant. This would definitely be a trigger to consider dose reduction/withdrawal. Newly noted sedation on a stable dosage of phenobarbital might also indicate impaired hepatic clearance of the drug, and is an indication for bile acids testing.

    This little table is also useful:

    Phenobarbitone-Monitoring

    Let me know if you have any other questions.

    Scott 🙂

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    Keymaster

    Hello.

    Yes, if there are elevations in liver enzymes and you are pretty sure it is primary liver then ultrasound would be a next good step.

    It is important to remember that the liver may appear sonographically unremarkable even in the presence of severe disease. While an unremarkable ultrasound exam was statistically significantly associated with the absence of histopathologic liver disease (in one study), 63% of these cases had abnormalities on histopathology in a study comparing hepatic ultrasound findings with histopathology. An normal ultrasound would not mean that FNA’s/biopsies would not be carried out.

    While bile acids are quite useful for the diagnosis of PSS in dogs and cats and cirrhosis in dogs (sensitivity of essentially 100%), their value is limited for the screening of most other hepatobiliary diseases (sensitivity 54-74%). Higher pre- than postprandial values may occur secondary to interdigestive gallbladder contraction or due to variations in gastric emptying, intestinal transit, or response to cholecystokinin release. This has no clinical significance, and whichever value is highest is used for interpretation. Falsely elevated postprandial values can occur with lipemia. Falsely decreased postprandial values may result from failure of cholecystokinin release to result in gallbladder contraction if the meal is inadequate in fat or protein content or an insufficient amount is consumed. Severe ileal disease or previous resection of the ileum can decrease bile acid reabsorption, thus decreasing postprandial bile acids. When used as a test of hepatobiliary function, the magnitude of elevation in serum bile acids does not allow differentiation of the category of disease, with the exception that patients with vacuolar hepatopathy rarely have marked elevations (greater than 75-100 mcmol/L).

    I really only find BAS useful in cases where I suspect a vascular abnormality of the liver.

    I hope that helps.

    Scott 🙂

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    Keymaster

    Hello.

    I hope you are well. I am so glad you are enjoying the course. Thank you for the excellent questions!

    The pathogenesis of hyperbilirubinemia in systemic infections and sepsis is multifactorial. The development of jaundice may occur from an aberration in the processing of bilirubin by hepatocytes or from other effects on the liver that lead to the accumulation of bilirubin in the body. Such processes include increased bilirubin load from haemolysis, hepatocellular injury, and cholestasis from the septic state and from various drugs used for the treatment of sepsis. The cytokine profile will change in the body and this will alter the handling of the bilirubin.

    Regarding the increased cortisol levels which will contribute to PUPD, the cortisol levels will be increased because the liver metabolism of the cortisol will be effected/reduced.

    As for the microcytosis! The cause of the microcytic anaemia is not fully understood, although studies suggest a defective iron-transport mechanism, decreased serum iron concentrations, decreased total iron-binding capacity, and increased hepatic iron stores in Kupffer cells. This could suggest iron sequestration. Microcytosis has been reported with or without anaemia in 60-72% of dogs, but only in ≈30% of cats with portosystemic shunts.

    Hope that helps.

    Scott 🙂

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    Keymaster

    Hello.

    I agree, the lack of liver enzyme increase is a bit weird. There may have been an initial increase, but if not lots of ongoing inflammation and infection then the values maybe decreased.

    Regardless of where the needle came from I am surprised that there was not more of a local peritonitis.

    Scott 🙂

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    Keymaster

    Hello.

    Thank you so much for your question.

    Fine-needle aspiration of the liver should be performed with ultrasound guidance and typically using a 22G to 25G needle. Often less blood contamination is obtained with rapid agitation of the needle without a syringe (“sewing machine technique”) compared with aspiration using a syringe. Several aspirates from different sites should be collected in patients with diffuse disease. The collected sample should be sprayed onto glass slides and thin smears should be made.

    I typically use a 1 1/4″ 23g. I would use the same size for dogs and cats.

    Hope that helps.

    Scott 🙂

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    Keymaster

    Really interesting!

    It is really nice that you have a few units in stock. We probably do not see enough cases to justify having it is stock. The Portuguese Blood Bank is amazing. If we order the feline blood before 4pm one day we have it the next!

    What about in an emergency situation when there was not time for the external crossmatch. Based on this paper would you consider using one of the appropriately typed units even if they do not crossmatch?

    Scott 🙂

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    Keymaster

    Was there a peritonitis associated. I presume the penetrating woud was small so not significant leakage?

    Scott x

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    Keymaster

    The cost does seem to be the issue… It is so much easier though.

    Scott x

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    Keymaster

    It is amazing how these sharp objects can migrate through the GI tract wall. I have seen one penetrate the spleen too before.

    The dog had surgery and actually did really well.

    Scott 🙂

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    Keymaster

    I think it is about choosing the right cases. I definitely think they have a place in cases where animals have a diagnosis and are already being appropriately treated. I can understand his concerns as there will be cases where it just becomes a way of making them eat.

    The drug I was talking about above is definitely worth looking in to:

    Entyce

    Scott 🙂

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    Keymaster

    Indeed. I think it is good to have the option.

    Especially in cases that are hospitalised and need more than maropitant. I think it highlights the really good point regarding stopping vomiting and tacking nausea. They are different and need to be tackled differently.

    Scott 🙂

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    Keymaster

    Hey.

    Thanks for this. Interesting comments. Does anyone every administer sorbitol in these cases? I have never given it as a separate thing. Is there an animal safe preparation of sorbitol?

    I have always found activated charcoal difficult to calculate the dose and administer (especially the powder). There is a new suspension that does seem easier to administer:

    Carbomate

    Does anyone have experience of using this?

    Scott x

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    Keymaster

    Intracellular bacteria and neutrophils indeed! Thanks for the comments about the glucose and lactate too!

    The dog has a BBQ skewer through its stomach wall!

    Scott x

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    Keymaster

    I am so pleased she is still with us.

    I definitely think the tylosin would be worth a shot!

    Scott x

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    Keymaster

    How did this case get on? Any improvement?

    Scott x

Viewing 15 posts - 1,531 through 1,545 (of 1,618 total)