scott@vtx-cpd.com

Replying to Hannah Willetts 23/05/2024 - 14:54

Hi Hannah,

In cases where clear clinical signs persist despite initial calcium supplementation, addressing the immediate symptoms takes precedence over concerns regarding mineralization. The risk of inducing hypercalcemia and subsequent mineralization issues is generally lower in these acute scenarios compared to prolonged exposure. In situations where further IV calcium is considered necessary but repeat EPOC (iCa) testing isn’t feasible due to financial constraints, you might consider a cautious approach.

One option could be to administer a lower dose of IV calcium, perhaps titrated to the patient’s response and clinical signs, while closely monitoring for any signs of hypercalcemia. Additionally, supportive treatments such as fluids and monitoring electrolyte levels may be beneficial.

It’s always a balancing act between providing adequate treatment and avoiding potential complications, so individualized patient care and close monitoring are key.

Best regards,

Scott

Replying to Aileen D. 23/05/2024 - 16:03

Hi Aileen,

Welcome to the forum, and thank you for introducing yourself! It’s great to have you here. Respiratory cases can indeed be challenging, but it’s fantastic that you’re looking to improve your knowledge in this area. The course should be a valuable resource for honing your skills in x-ray interpretation and thoracic ultrasonography.

I’ll also be sharing some x-rays in the forum, so feel free to join in the discussions and share your insights. Feel free to ask any questions or share your experiences as you progress through the course. We’re all here to support each other.

Best of luck, and I hope you find the course helpful and rewarding!

Warm regards,

Scott 🙂

Replying to Alison Knight 19/05/2024 - 19:00

Hi Alison,

It’s great to hear from you! Returning to work can be both exciting and challenging, especially when you’re surrounded by enthusiastic new graduates. East Lothian is a nice part of the world.

If there’s anything specific you’re looking to refresh or any particular cases you’d like to discuss, feel free to reach out. Whether it’s brushing up on diagnostic techniques, exploring new treatment options, or managing challenging cases, I’m here to help. It’s always good to exchange knowledge and experiences, and I’m sure your new colleagues can also learn a lot from your experience.

Looking forward to hearing more from you!

Best regards,

Scott

Replying to Jon H. 14/05/2024 - 15:00

Hi Jon,

Welcome to the group! We’re really honoured to have you with us and look forward to learning from your expertise.

Scott 🙂

Replying to Hannah Willetts 04/05/2024 - 17:43

Hello Hannah.

Thank you for your brilliant question. I really hope you are enjoying the course.

In cases of protein-losing nephropathy (PLN), the loss of proteins, including albumin, through the kidneys can contribute to a hypercoagulable state through several mechanisms:

1. Decreased Anticoagulant Proteins: The loss of proteins via the kidneys can include anticoagulant proteins such as antithrombin III and protein C. These proteins normally help regulate the coagulation process by inhibiting clot formation. Their loss can tip the balance towards a pro-coagulant state.

2. Increased Fibrinogen Levels: PLN can lead to increased levels of fibrinogen, a key protein involved in the clotting cascade. Elevated fibrinogen levels can promote clot formation.

3. Altered Platelet Function: PLN can affect platelet function, making them more prone to aggregation and clot formation.

4. Endothelial Dysfunction: Protein loss and associated kidney damage can lead to endothelial dysfunction, which can further promote clot formation.

5. Haemoconcentration: Similar to other conditions causing protein loss, PLN can lead to hemoconcentration, increasing the concentration of clotting factors in the blood.

Overall, the combination of these factors in PLN can contribute to a hypercoagulable state, increasing the risk of thrombosis.

More specifically regarding the albumin part of your question:

Albumin loss can lead to a hypercoagulable state due to several factors. Albumin plays a crucial role in maintaining the balance of oncotic pressure in the blood, which helps prevent fluid from leaking out of the blood vessels into the surrounding tissues. When albumin is lost, there is a decrease in oncotic pressure, leading to increased fluid leakage. This can result in haemoconcentration, where the concentration of cells and proteins in the blood increases, including clotting factors, which can contribute to a hypercoagulable state.

Additionally, albumin is involved in the regulation of fibrinolysis, the process that dissolves clots. A decrease in albumin levels can lead to impaired fibrinolysis, further promoting a pro-coagulant state.

Regarding your second question, there isn’t a specific threshold of albumin loss below which anticoagulants are always indicated. The decision to use anticoagulants would depend on the overall clinical picture, including the presence of other risk factors for thrombosis, such as immobility, underlying diseases, and the specific condition of the patient. In cases where there is significant albumin loss and evidence of a hypercoagulable state, anticoagulants may be considered, but this decision would be made on a case-by-case basis. I would generally consider anticoagulants/antithrombotic when albumin is below 15g/l.

I hope this helps clarify things for you! Let me know if you have any more questions.

Scott 🙂

Replying to Kristin Herstad 03/05/2024 - 14:49

Kristin,

Thank you so much for your brilliant comments and suggestions. It is important to note that no obvious orthopaedic abnormalities were noted, but discomfort reported when palpating the quadriceps muscles suggests a possible muscular issue. The palpable femoral and peripheral pulses indicate normal peripheral circulation.

Given the indoor status of the cat and the absence of typical risk factors for certain diseases, your focus on less common causes such as toxoplasma, cryptococcus, and FIP is appropriate. Running CK and AST for myositis markers, as well as performing radiographs of the chest and ultrasound of the abdomen, are sensible next steps to further investigate potential causes.

Your plan to sample the anterior chamber of the affected eye for cytology and rtPCR for FIP is a brilliant suggestion. However, we were not brave enough to proceed with this step at this time. Similarly, we did not perform serum protein electrophoresis due to increased globulins, but this was also a great suggestion. These tests could provide valuable insights into the underlying cause of the cat’s condition.

Initiating treatment for dehydration and providing nutritional support are crucial steps to stabilize the cat’s condition. Continued monitoring and further diagnostic tests will be essential to confirm a definitive diagnosis and guide appropriate treatment. Great job!

These were the results of the investigations we performed:

Creatine Kinase: Elevated at 1020 U/l (Reference interval 50 – 200 U/l).

Urine protein-to-creatinine ratio (UPCR): Non-proteinuric with a value of 0.1 (Reference ranges: Non-proteinuric: 0.0 – 0.2, Borderline proteinuric: 0.2 – 0.5, Proteinuric: > 0.5).

Urine culture: No growth.

FIV/FeLV ELISA: Both negative.

Blood pressure: Systolic blood pressure of 130 mmHg (measured by Doppler).

Total thyroxine: Total T4 levels within normal range at 30 nmol/L (Reference range: 10 – 60 nmol/l or 2.3 µg/dl Reference range: 0.8 – 4.7 µg/dl).

Coagulation profile: Within normal limits with PT of 12 sec (Reference range: 8.0-15.0 sec), aPTT of 18 sec (Reference range: 9.0-20.0 sec), and D-Dimers of 0.08 mg/L (Reference range: 0-0.56 mg/L).

Toxoplasma serology (Immunofluorescence): IgG positive at 1/512 (Reference range: < 1/32), IgM negative (Reference range: < 1/16). Feline Coronavirus serology: Negative. Thoracic point of care ultrasound (TPOCUS): Presence of free fluid in the pleural space, no B lines evident, left atrium-to-aorta ratio of 1.4. Echocardiography: Unremarkable, no evidence of structural heart disease. Abdominal ultrasound: No free abdominal fluid, unremarkable findings. Thoracic radiography: Identified pleural effusion, unable to evaluate heart and lungs due to the effusion. Thoracic radiography (after thoracocentesis): Revealed a 3cm x 2cm soft tissue mass lesion in the left caudal lung. CT: Thorax, abdomen including hindlimbs: Identified a mass lesion in the left lung lobe, no abdominal abnormalities, and mass lesions in the hind limb musculature. Hindlimb radiography: Showed bilateral soft tissue swelling of the quadriceps muscle. Hindlimb ultrasound: Identified bilateral mass lesions with small fluid pockets in the quadriceps muscle, Doppler examination showed no abnormalities. Pleural fluid analysis: Revealed modified transudate. FNA lung mass: Cytology consistent with epithelial neoplasia with features of malignancy (carcinoma, highly likely) and suppurative inflammation. FNA hind limb masses: Cytology consistent with epithelial neoplasia with features of malignancy (carcinoma, highly likely) and suppurative inflammation. Intraocular pressure: Normal. Thank you again for your brilliant reply! Scott 🙂