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scott@vtx-cpd.com

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  • scott@vtx-cpd.com
    Keymaster

    What older cat might you be talking about?!?!?!?!

    How long has he been on the Aktivate and the Cobalaplex for? Where did you read about the Cobalaplex… is it helpful because of the B12?

    It could indeed be the Aktivate. Were all bloods completely normal? Has he lost weight recently?

    Scott x

    scott@vtx-cpd.com
    Keymaster

    You are right. It is definitely a thing and quite well recognised now.

    Let me know how the treatment goes.

    I found another useful review:

    https://pubmed.ncbi.nlm.nih.gov/22720812/?from_term=feline+cognative+dysfunction&from_pos=1&from_exact_term=feline+cognitive+dysfunction

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Thanks for this.

    The urine analysis and culture is a useful part of any PUO work up as a urinary tract infection could be a possible focus/trigger for pyrexia.

    What do you think of the initial biochemistry and haematology? Just focus on the first results for now. What about the joint fluid analysis?

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Amazing answer Simon. Could not have said it better myself!

    Let me know if you have any other questions.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Upper Airway Disease

    Nasopharyngeal disease: Infectious (bacterial, fungal, viral), polyps, foreign bodies, neoplasia.
    Layngeal disease: Paralysis, neoplasia, polyps, foreign bodies.

    Lower Airway Disease

    Tracheal: Stenosis / collapse / external compression, foreign bodies, neoplasia.
    Bronchial: Inflammatory airway disease, parasitic bronchitis.
    Pulmonary Disease: Pneumonia / Bronchopneumonia, neoplasia (primary pulmonary carcinoma, lymphoma), pulmonary oedema, haemorrhage, abscess formation, poisoning (paracetamol, paraquat, non-anticoagulant rodenticides).

    • Thoracic Cavity

    Pleural Space Disease: Pneumothorax, pleural effusion (FIP, idiopathic chylothorax, haemothorax, CHF, nephrotic syndrome, lung lobe torsion), thoracic Masses, thymic masses (lymphosarcoma, lymphoma), diaphragmatic hernia, diaphragmatic rupture, pericardioperitoneal hernia.

    • Cardiogenic

    Congenital, cardiomyopathy (primary and secondary).

    • Physiological

    Fear, Pain, Shock, Anaemia, Pyrexic

    What would be your next diagnostic steps and initial treatment?

    scott@vtx-cpd.com
    Keymaster

    On initial presentation the dog was considered 5% dehydrated and painful. Intra venous fluid therapy was administered to correct the fluid deficit over the following 24 hours and analgesia was administered (methadone 0.1mg/kg IV q4 hours). Lactated ringers was started at 5ml/kg/hr for the first 24 hours and then reduced to 2.5ml/kg/hr (maintenance rates).

    Let me know your thoughts from the results I have posted.

    Scott x

    scott@vtx-cpd.com
    Keymaster

    Biochemistry
    Haematology
    Joint-Cytology
    Urine-Analysis
    Joint-Cytology-Image

    I have attached the results you have asked for. We ran some urine as well? Why would that be useful?

    Scott x

    scott@vtx-cpd.com
    Keymaster

    So… based on the clinical presentation my neurology specialist pal made the following comment:

    “Although cerebellum is compatible with some of the current clinical signs, the fact that he also was unresponsive and no proprioception may indicate that the brainstem is also affected. Either way, I agree with you that intracranial seems the most likely. As you said, ischaemic encephalopathy and neoplasia sound like the most likely differential diagnosis… There may be a potato arising/compressing the caudal fossa (brainstem +/- cerebellum)”.

    I will follow up at the clinic and see if I can get more information about the actual case outcome.

    Hope that helps.

    Scott x

    scott@vtx-cpd.com
    Keymaster

    Lameness has many causes, but due to the multiple joint effusions the differentials focused on causes of non-traumatic inflammatory joint disease. Degenerative joint disease was a consideration (but thought less likely due to age), but more likely septic or immune-mediated (erosive and non-erosive) polyarthritis.

    It is always important to distinguish between hyperthermia and pyrexia.

    Increased body temperature may be a result of pyrexia caused by infectious agents (bacteria, protozoa, fungae and parasites), immune-mediated disease, neoplasia, non-septic inflammation, tissue damage, necrosis, pharmacological agents (e.g. colchicine and bleomycin) and idiopathic pyrexia. Causes of hyperthermia; inadequate heat dissipation (heat stroke, hyperpyrexic syndromes), exercise hyperthermia (normal exercise, seizure disorders) and pathologic or pharmacological origin (lesions of the anterior hypothalamus, malignant hyperthermia, hypermetabolic disorders).

    No access to pharmacological agents was reported. Heat stroke, seizure disorders and malignant hyperthermia were excluded as there was no history of exposure to strenuous exercise, history of seizures or administration of halogenated anaesthetics or depolarising agents. Lesions of the hypothalamus and hypermetabolic disorders could not completely ruled out.

    Pyrexia was thought to be more likely as the dog did not seem to attempt to dissipate heat and was most likely to be related to the joint effusions at this stage.

    What initial treatment and investigations would you consider?

    Scott x

    scott@vtx-cpd.com
    Keymaster

    I missed the signalment! Sorry:

    A 2-year-old, neutered female, 12kg, Whippet.

    The primary problems were considered to be the lameness, joint effusion and increased body temperature. The lameness was considered most likely to be secondary to the joint effusion. Additional problems were the muscle atrophy, anorexia, reluctance to exercise, dehydration and were thought to be secondary to the same disease process causing the primary problems.

    Spot on with the problem list, I would always create the problem list and then prioritise them before coming up with my differential list.

    Scott x

    scott@vtx-cpd.com
    Keymaster

    So the basic principals are…

    In peripheral vestibular disease, the nystagmus can be horizontal or rotary and the fast phase is always away from the lesion. In central disease the pathologic nystagmus can be in any plane (including vertical), can change direction with different positions of the head, and the fast phase can be toward the lesion. Therefore, identification of a vertical nystagmus or a nystagmus with the fast phase toward the lesion is an indication of central involvement. However, caution should be exerted when labeling a patient with central disease based on vertical nystagmus alone since it is easy to confound nystagmus with a slight rotary component with vertical nystagmus. One comparative clinical study also suggested that the number of beats of the resting nystagmus was significantly higher in peripheral vs. central disease. A resting nystagmus rate of more than 66 beats per minute was found to be very specific (95%) and sensitive (85%) of peripheral disease.

    I have contacted one of our neurology specialists to get a final call location!

    Scott x

    scott@vtx-cpd.com
    Keymaster

    Also, was the nystagmus evident before sedation? Sorry for all the questions!

    Sx

    scott@vtx-cpd.com
    Keymaster

    Hello.

    Thanks so much again for the question. Could you double check the ACP dose. The only reason I ask is that that would be quite a high dose and may explain the prolonged sedation. Just a thought.

    Scott x

    scott@vtx-cpd.com
    Keymaster

    Thank you so much for your reply!

    I will see if others have thoughts before replying!

    Scott x

    scott@vtx-cpd.com
    Keymaster

    https://imgbb.com/

    You can use this link to upload videos and pictures. Once uploaded paste the like that it generates in another comment.

    Scott x

Viewing 15 posts - 1,966 through 1,980 (of 2,013 total)