scott@vtx-cpd.com
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Hey Inga.
I thing the possibilities are endless with this drug!
“Tranexamic acid (TXA) is an antifibrinolytic agent that exerts its effects by reversibly binding to the lysine sites on plasminogen molecules and inhibiting plasmin. TXA is widely used in human medicine and decreases mortality, reduces blood loss after trauma or surgery, and lowers transfusion requirements in trauma patients with bleeding. TXA has been shown to decrease mortality over placebo in trauma patients, It is also noted to have good safety parameters upon administration and is recommended for use in human trauma patients with bleeding.
In veterinary medicine, TXA has been used to reduce blood loss by slowing fibrinolysis in various diseases causing clinical bleeding such as hemoperitoneum, haemothorax, thrombocytopenia, anticoagulant rodenticide intoxication, peri-operative bleeding, epistaxis, and feline interstitial cystitis-associated bleeding. It has a wide safety margin and is rarely associated with hypersensitivity reactions. In humans, common side effects of TXA are mild symptoms including nausea, flushing, vomiting, allergic skin reactions and headache, although anaphylactic shock is rarely reported. In dogs, the main reported side effect is vomiting”.
I think there is a lot more to come!
Scott 🙂
Hello!
Hope you are well. Great question. I do find these cases really frustrating to manage medically! I would go for as low fat a diet as possible. Hills ID low fat would probably be a good starting point. Would the owners consider surgical managemnt/pleural port?
Scott 🙂
Hello.
Are you thinking about specific. Neither of these infectious diseases will cause a specific hepatopathy. E canis has been reported, but not commonly:
There is one report of an adult German Shepherd presenting with clinical signs and biochemical abnormalities consistent with acute hepatitis where the eventual diagnosis was Ehrlichia canis infection; following identification of E. canis using cytologic, immunohistochemical, and polymerase chain reaction (PCR) testing, the dog was treated successfully with supportive care and doxycycline.
With both infections, particularly Babesia, there are lots of reasons that liver exzymes would be increased. Hypoxia, anaemia and systemic inflammation.
Hope that helps.
Scott 🙂
Thanks for this.
Following on from what Sara has said… was the thinking that this dog was having seizures due to the liver disease? What other meds was this dog on? You are right, there is very little evidence to support exactly what drugs to use in cases that have seizures due to severe liver disase/hepatic encephalopathy. I think it would be fine in these cases to escualte yo the 60mg/kg dose for short term control. The following drugs can be cnsidered:
1. Avoid benzodiazepines
2. Phenobarbital (4 mg/kg IV q 3-6 h for 4 doses)
3. Potassium Bromide: Loading: 400-600 mg/kg/day divided over 1-5 days PO with food; can be given per rectum if needed. Maintenance: 20-30 mg/kg PO q 24 h. Sodium bromide can be used if an IV form is necessary.
4. Propofol 1-3.5 mg/kg IV bolus, followed by CRI of 0.01-0.25 mg/kg/min.
5. Keppra 20 mg/kg (up to 60 mg/kg) PO or IV q 8 h (there is no evidence-based medicine to support this).Hope that helps.
Scott x
Hey everyone.
I love the M&M suggestion, but understand the challenges of doing these when you are a locum.
I was having a really interesting conversation with Lou Northway the other day (Lou the vet nurse for thouse of you on Instagram). She was saying that one of the biggest barriers to peple doing M&M’s is that is seems like a very formal process with a presentation etc. M&M rounds could actually be a 10 minute informal chat over a cup of tea. We should feel comfortable to chat about what we can do better.
I passionately belive that every member of the team is equal! We can all learn from each other.
Sara, do you find you are able to M&M’s at Vets Now?
Scott x
Thanks so much for this.
Really helpful. The images are great!
Scott 🙂
Thanks so much!
I will try and cover these final points in the liver session tonight.
Scott 🙂
Hey.
Shar-Pei dogs can experience short (12- to 48-hour) recurrent bouts of fever, accompanied by inflammation of joints (especially the hocks, i.e., swollen hock syndrome). This disorder also is known as familial Shar-Pei fever (FSF). Episodes typically are more frequent during the first years of life and become less frequent with age. Nonsteroidal anti-inflammatory drug (NSAID) administration seems helpful during episodes. The major constituent of the thickened skin of Shar-Peis is hyaluronic acid (HA), and HA is overexpressed in Shar-Peis compared with other canine breeds. The extent of hyaluronanosis varies among individual Shar-Peis, although almost all are affected. The administration of corticosteroids decreases cutaneous mucinosis in Shar-Peis, perhaps by decreasing expression of hyaluronan synthase. The role that excessive HA in Shar-Peis plays in FSF needs to be investigated further. Shar-Pei dogs affected with FSF are at risk of developing reactive systemic AA amyloidosis and subsequent kidney or liver failure. Treatment of FSF-affected Shar-Peis with colchicine (0.025-0.03 mg/kg [maximum per dose: 0.6 mg] PO q 12 h) has been recommended. The benefit of long-term colchicine, corticosteroid, or other immunosuppressant administration, however, remains to be published.
Scott 🙂
I think that is a great approach Simon!
It really is all about communication… and respect. We all have to listen to each other and realise that we all have so much to learn from each other. I would be greatful to be told a better way to do it!
You are right about the reversal first if HR super low.
While I am on… massive congratulations to Gail on her place on the Masters in anaesthesia at Edinburgh University!
Scott 🙂
Indeed! You would have to rely on all of these parameters. You could run a BAST, but I would not rely on that alone. It would have to be part of the bigger picture.
Scott 🙂
Hello again.
Hepatotoxicosis from phenobarbital appears to be dependent on cumulative dose. 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. Patients are likley to improve when the phenobarbital is withdrawn.
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. 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 > AP is clinically significant. 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.
Overall, it matters less about the AP, treatment decisions would be made on the parameters above.
Hope that helps.
Scott 🙂
Hello.
Thanks for the great question. About 1-2% of hyperthyroid cats that are given the antithyroid drug methimazole develop clinical evidence of hepatopathy with jaundice, typically in the first month of treatment. These changes are distinct from “innocent” increases in ALT and ALP seen with untreated hyperthyroidism. Hepatopathies can present with a predominantly hepatocellular or cholestatic pattern, with or without hyperbilirubinemia. These reactions usually are reversible with drug discontinuation, but can be fatal if not detected promptly. The increases in ALT and ALP tend to be higher with the methoimazole toxicity. Often, if hyperthyroidism is well treated, the innocent pre-treatment increases will normalise. The drug reaction will often occur with jaundice which would also help to distinguish. I would stop treatment if you suspected an adverse reaction.
Cats treated with methimazole should be screened for increases in ALT and AP if clinical signs of lethargy or anorexia are noted. If cats develop adverse clinical signs, idiosyncratic toxicosis (hepatopathy, blood dyscrasias, or facial excoriation) should be ruled out with a physical exam, CBC, and biochemical panel. The presence of these idiosyncratic adverse events warrants discontinuation of methimazole, given the risk of progression to more severe manifestations.49 The transdermal route does not appear to be beneficial in preventing idiosyncratic methimazole toxicosis, including hepatotoxicosis. Given the role of glutathione depletion in methimazole hepatotoxicosis in experimental models, the efficacy of glutathione precursors needs to be evaluated in the management of this adverse drug reaction.
You would have to find an alternative treatment in this situation. These severe adverse reactions seen with methimazole therapy are not reported with carbimazole, but they can still happen. It makes little sense that adverse reaction profiles would be very different between the two drugs because carbimazole is metabolized to methimazole in order to exert its therapeutic effect.
Hope that helps.
Scott 🙂
Hello.
Thank you so much for the question. I generally will monitor while the patient is on steroids. There is little need to monitor specifically for a steroid hepatoapthy when the steroids have been discontinued or when the patient is on a much lower tapered dose. The intensity of monitoring will also depend on the condition that the steroids are treating. Overall, while on higher doses of steroids I would be running biochemistry (to include at least ALT) as a minimum every 4-6 weeks. Normally all changes (blood and liver) are reversible.
There a a few reasons I think that is important. Steroid hepatopathy traditionally has been considered benign in dogs. However, the reported association between glycogen-like hepatopathy and hepatic remodeling and carcinoma in Scottish Terrier dogs, and between hyperadrenocorticism and gallbladder mucocele, suggests that all canine vacuolar hepatopathies should be taken more seriously, particularly when they are chronic and severe. The most effective treatment for steroid hepatopathy is to remove the source of exogenous or endogenous glucocorticoids. Where this is not possible, antioxidants are indicated. S-adenosylmethionine given to dogs with steroid-induced hepatopathy has increased total hepatic glutathione and had a beneficial effect on the oxidized : total glutathione ratio in hepatocytes, but had no effect on the histological appearance of vacuoles.
As you mention, PUPD will be part of the clinical signs anyways. Any sign of the patient becoming more systemically unwell (V+/D+, lethargy, anorexia) would warrent repeat blood work. In these cases liver function parameters would have to be evaluated. It would be unusual for a steroid hepatoapthy to progress to severe liver failure.
Hope that helps.
Scott 🙂
Hello again.
This is the reply from my specialist anaesthesia pal!
“Hi Scott. I’ve tried to get hold of the Dechra data as to where this dose came from, and evidence of efficacy to have obtained the licence for Pardale, but with no success. The UK vet advisors were keen to help (they don’t know either) but access was blocked by their central R&D team. I personally tend to dose at the lower doses you mention, although I know some anaesthetists are happy to go with the higher dose for the first few days then drop to 10mg/kg if staying on it longer term. Not sure any evidence behind this either though!”
Overall, I would stick to the 10-15mg/kg dose, but use of Pardale with the higher doses should also be fine.
Scott 🙂
Hello.
Hope you are well. This is not a drug I really use. I would normally use the 10-15 mg/kg dose.
I have contacted a specialist anaesthesia friend to get a bit more information for you about this higher dose.
Will get back to you ASAP!
Scott 🙂
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