Відео

Dear @moa_4777, thank you for your question and kind words. Since insulin (Bag 1) is compatible with salts of calcium, it should be fine to mix it with other replacement solutions, such as those mentioned. However, the data on the stability of insulin in these solutions is minimal, and the majority of literature recommends mixing insulin in NS 0.9%. If you add potassium phosphate to Bag 2, ideally, you don’t want to mix it with salts of calcium or magnesium due to the risk of physical incompatibility. Therefore, using NS 0.9% would be the safest choice. If KCl is the only solution mixed with the replacement fluid in Bag 2, Hartmann’s and Plasmalyte A can be used. That said, there is a lack of studies proving that K-Phos cannot be mixed with Hartmann’s/LRS/Plasmalyte. Until these studies are available, I normally recommend using NS 0.9% if K-Phos is used.

Thank you for your question and I am glad that your cat is doing better! Yes, there is a possibility of FATE development in cats with TMT, especially if there is moderate to severe left atrial enlargement at the time of TMT diagnosis. As TMT resolves, and left atrium gets smaller, the risk of FATE goes down significantly. Also, it is important to remember that FATE may develop in cats without any heart disease or other underlying conditions. This is rare, but may occur in <5-10% of all cats with FATE.

​@@vetemcrit thank you so much for your response. The other thing I was wondering is if she could possibly have paroxysmal Afib as the etiology for the clot she threw (I'm a human EM doc)--in people, we usually do holter monitoring. Is there something similar that could be done for cats to see if they have arrhythmias and need to be on a beta blocker?

Thank you for your question. It is extremely rare and unlikely to see congenital enzymatic defects related to lactic acid regulation in dogs. If you truly believe this is a problem for your dog, first, I would try to rule out more common conditions starting with a thorough physical examination performed by a veterinarian, full bloodwork, and potentially other testing (e.g. x-rays to rule out hip or elbow dysplasia, etc). However, It is possible that this intolerance of higher intensity exercise is completely normal for your dog and could be a behavioral trait as opposed to a true medical condition.

Hi there! Thanks for sharing your case. Using concentrated (40-50%) dextrose transmucosally (i.e. via gums) can indeed be a potential temporary solution to manage hypoglycemia while establishing a venous or intraosseous access. As long as you are applying only 0.1-0.3 ml of dextrose at a time, the risk of aspiration will be minimal since the volume is so low. That said, your number one goal should be to establish a venous access as soon as possible. If peripheral veins are not accessible, using a jugular vein or performing a cut-down will make sense. A regular intravenous catheter can be placed into a jugular vein and then exchanged to a central line (via guide wire) later. You can also learn on how to place intraosseous catheters or needles that may take less than a minute to place (link - ua-cam.com/video/10twNYP1pB0/v-deo.htmlsi=i9mh-Ku-d_IuH9K6). Also, if you need more mentorship, you can join the VETEMCRIT Academy here - academy.vetemcrit.com/courses

​@@vetemcrit Thank you for the answer and the video link. Yeah, I will start with the trial course, then I will go with the next, probably monthly plan. By the way, could we say this bradycardia is caused by hypoglycemia when any other causes of bradycardia are not observed and both of the heart rate and the blood pressure in the cat are normalized after the injection of dextrose?

@@vetvoovlog1243 yes, absolutely bradycardia can be caused by severe hypoglycemia in a cat.

@@vetemcrit Thank you. I knew it, and now I got confident. I will tell this to my coworkers. By the way, I started the free trial. I will watch them little by little.

Hi there! Thanks for sharing your experience!

Thanks for your question! It means that both solutions are going into the same catheter or IV line via the 3 way stopcock or other similar devices.

You're absolutely right. cTnI is an excellent marker for myocardial injury because its increase and duration are proportional to the severity of the damage. In cases of myocarditis, which is the suspected cause of TMT, we often see the highest elevations of cTnI. NT-proBNP, on the other hand, is secreted in response to volume expansion or pressure overload in the heart. While it's a valuable biomarker for diagnosing congestive heart failure, screening for occult disease, and assessing the overall severity of heart disease, it may not be as specific for detecting the myocardial damage caused by myocarditis. Considering that myocarditis is the likely underlying cause of TMT, measuring cTnI levels would provide more relevant information about the extent of myocardial injury, which is the primary pathological process in myocarditis-induced TMT.

@@vetemcrit Thank you so much for your kind response. If I have any questions, I will ask them in the comments.

Thanks for your question. I hope I understood it correctly, but let me know if you meant something else. PPV, or positive pressure ventilation, can significantly impact the pulmonary parenchyma, which is the functional tissue of the lungs responsible for gas exchange. Let me expand on the relationship between PPV and pulmonary parenchymal disease. 1. Barotrauma: PPV delivers air under pressure to the lungs, which can lead to overdistension of the alveoli, causing barotrauma. This may result in complications such as pneumothorax, pneumomediastinum, or subcutaneous emphysema. Barotrauma can further damage the pulmonary parenchyma and worsen pre-existing lung diseases. 2. Volutrauma: In addition to the pressure, the volume of air delivered during PPV can also cause injury to the lung tissue. Excessive tidal volumes can overstretch the alveoli, leading to volutrauma. This can cause inflammation, edema, and structural damage to the pulmonary parenchyma, exacerbating conditions like acute respiratory distress syndrome (ARDS). 3. Atelectrauma: PPV can also lead to cyclic opening and closing of the alveoli, particularly in areas of the lung with poor compliance or atelectasis. This repetitive alveolar collapse and reopening, known as atelectrauma, can cause shear stress and mechanical injury to the pulmonary parenchyma, leading to inflammation and further damage. 4. Ventilator-induced lung injury (VILI): The combination of barotrauma, volutrauma, and atelectrauma can result in VILI, a condition characterized by inflammation, edema, and structural damage to the pulmonary parenchyma. VILI can worsen pre-existing lung diseases and increase the risk of complications such as sepsis and multiple organ dysfunction syndrome (MODS). 5. Ventilation-perfusion mismatch: PPV can alter the normal ventilation-perfusion ratio in the lungs. In some cases, this can lead to overdistension of well-ventilated areas and underinflation of poorly ventilated regions, resulting in ventilation-perfusion mismatch. This can impair gas exchange and exacerbate pre-existing pulmonary parenchymal diseases. To minimize the impact of PPV on pulmonary parenchymal disease, it is essential to use lung-protective ventilation strategies. These include using lower tidal volumes, maintaining appropriate positive end-expiratory pressure (PEEP), and limiting peak inspiratory pressures. Regular monitoring and adjustment of ventilator settings based on the patient's response and underlying lung condition are also crucial in reducing the risk of PPV-associated complications and promoting better outcomes in patients with pulmonary parenchymal disease.

Thanks for sharing!! I hope you are doing well too, Dr.Allen!

Sure! vetemcrit.com/contact/

@@vetemcrit thank you so much, I sent you an email. Looking forward to hearing from you.

This is an excellent question. Calculation of GIR is a more objective, standardized and precise way to quantify the absolute amount of dextrose that a given patient is receiving (in mg/kg/min) as opposed to communicating just rate of administration in ml/hr and percent of dextrose added to the fluids. It makes total sense why it is calculated in human medicine during parenteral nutrition or correction of hypoglycemia in neonates (recommended dose is about 4-8 mg/kg/min). Historically, GIR has not been utilized or studied in veterinary species, therefore it is unclear whether hypoglycemic puppies and kittens will require similar doses. Instead, veterinarians used to "think" about dextrose supplementation in terms of dextrose % and total fluid rate where dextrose has been added (e.g. a 5 kg cat is receiving 5% dextrose added to LRS that is running at 20 ml/hr). I think it will be awesome to do a research project where this information is converted to GIR, and then we could report what range of GIR worked the best to maintain normal blood glucose in veterinary species.

Thank you very much for your answer! So when we give a 5% dextrose CRI to a blocked cat, it does not matter if it is given concurrently to a bolus of fluid, maintenance rate or any other rate? I understand that the quantity of dextrose delivered will be different depending on the rate but this does not matter?

Also, when you add a dextrose CRI to your fluid therapy, do you prefer to add dextrose to the fluid bag or do a buretrol with a given/controlled rate?

In my personal practice, I prefer administering 0.1 unit/kg of regular insulin (IV or IM) in combination with 1 ml/kg of 50% dextrose (given as an IV bolus, diluted 1:4 - 1:6 with LRS or NaCl 0.9% to decrease osmolality and prevent phlebitis) when I manage a blocked cat with moderate to severe hyperkalemia. It will result in an insulin:dextrose ratio of approximately 5 g/unit. This would be followed by the addition of 5% dextrose to the fluid bag the cat is currently receiving (maintenance + rehydration rate). Blood glucose levels would be monitored at intervals of 30-60 minutes for the first 1-2 hours, followed by checks every 2 hours for the next 6-8 hours or sooner if the cat exhibits symptoms of hypoglycemia. If the cat becomes hyperglycemic with this dextrose supplementation rate (i.e. BG>150-200 mg/dl), I will reduce dextrose to 2.5% or may even discontinue it if BG is very high or if serum potassium has normalized (since the goal of dextrose supplementation is to improve hyperkalemia). You can consider using a buretrol if you anticipate changing fluid composition frequently. This way you can prevent wasting an entire fluid bag when you need to change dextrose supplementation from 5% to 2.5%. Alternatively, you can use a syringe pump. In this case, you will draw up 50-60 ml of fluids with dextrose into a syringe at a time.

Thank you very much, this is helpful!

Thank you, Shawn!

I swear that attending your electrolytes course has truly opened up a new chapter for me, I mean seriously. You are an invaluable treasure to me with kindness, patience and knowledge. Thank you.

Thank you, my friend.

Thanks!

The root cause of diabetes mellitus depends on the specific type. In type I, the pathogenic mechanisms responsible for decreased insulin production and secretion are multiple, but usually they are related to destruction of islet cells, secondary to either immune destruction or severe pancreatitis (dogs) or amyloidosis (cats). Cats are more prone to developing type 2 diabetes, which is often associated with obesity and insulin resistance. Certain breeds may have a higher predisposition.

Do you get paid by Nestle (oops, Purina) and Boehringer Ingleheim ? I like a good copy and paste.... Why have you not linked Diabetes and Cancer in animals to the food yet ? It's the same in humans....@@vetemcrit

Certainly, modern diets may contribute to obesity in dogs and cats, worsening insulin resistance.

Question : Can you completely reverse T2DM in humans ? "may contribute" haha...@@vetemcrit

Similar to cats, T2DM may be put into remission in humans. @@adelarsen9776

Wow. There is hope. I wish you and all animals good health and prosperity.@@vetemcrit

Questions : a) What is the root cause of T2DM in dogs and cats ? b) Did dogs and cats have CKD, DKD, T2DM and pancreatitis 100 years ago ?@@vetemcrit

The root cause of diabetes mellitus depends on the specific type. In type I, the pathogenic mechanisms responsible for decreased insulin production and secretion are multiple, but usually they are related to destruction of islet cells, secondary to either immune destruction or severe pancreatitis (dogs) or amyloidosis (cats). Cats are more prone to developing type 2 diabetes, which is often associated with obesity and insulin resistance. Certain breeds may have a higher predisposition.

You can't see it's the carb rich food can you ? Why didn't dogs and cats get diabetes 100 years ago ? I wish you good health and prosperity...@@vetemcrit

Welcome!

​@@vetemcrit my cat won't take the dextrose 50% orally....could I use it as injection shot?

We do 2 units of insulin every 12 hrs

Unfortunately, not for this video.

You can find the example of K Phosphate supplementation here - vetemcrit.com/approach-to-hypokalemia-diagnosis-and-treatment/. NaCl 0.9 is preferred because it doesn’t have calcium in it that may be incompatible with phosphate.

I appreciate your feedback, my friend. I am so glad you are enjoying the "Small Animal Electrolyte and Acid-Base Mastery: Certification Course". This means a lot to me. Anyone who wants to learn more about it - watch this free workshop here - academy.vetemcrit.com/free-workshop-opt-in

An other question is I don’t know how to supply A DKA cat with hypo phosphate concurrent with hypokalemia. I am afraid of KMax. Apart from that, I don’t know if there is any limitations to supply phosphate