#vulnera-sanentura

[vulnera-sanentura]

Cat Facts: Why’s this Cat Vomiting?

Like most of my posts, this is coming more from a veterinary student/pre-vet education perspective, but hopefully some owners that follow me can get some useful info from this!

Unsurprising to most vet students, there’s about as many reasons for vomiting as there are diagnoses in general. We’re going to attempt to narrow that down a bit, break them into categories which makes it more useful for diagnostics and relevant differentials.

First off, you have to differentiate vomiting from regurgitation.

Vomiting: nausea (drooling, lip licking, swallowing, depression/restlessness), abdominal muscle contraction, contains bile/digested blood/digested food

Regurgitation: no nausea, no abdominal contractions or bile, presence of undigested food in a tubular shape.

Once you’re sure it’s actually vomiting, you’ll need to differentiate it into acute or chronic, as well as emergency/non-emergency. Acute will be in the last few days or day of presentation, often multiple times in the same day, and will often present as more “sick” than the chronic vomiter.

In chronic cases, the vomiting is usually more than 2 times a month and has been going on for months to years. Chronic vomiters can be “apparently healthy” and the vomiting only brought up at a wellness check or prompted by the vet/nurses and the owner didn’t think to bring it up because “cats just vomit, and they seem fine other than that.” History can help a lot! If there’s an acute case, and the cat has access to toxic substances, a habit or likelihood of eating foreign objects (hair ties, string, q-tips, etc), or has had a recent change in diet, that could lead you immediately to the most likely cause and the most appropriate next steps. Acute vomiting generally has fewer causes or at least more obvious causes, and next steps generally include abdominal radiographs or triage/supportive care if indicated. Physical exam can locate a linear foreign body that’s anchored to the underside of the tongue.

So, what if that doesn’t help? That’s when you start your baseline diagnostics! CBC/Chem/UA can rule in or rule out a lot of potential causes for vomiting:

Diabetes: hyperglycemia, glucosuria, ketonuria, low USG

Liver disease: hyperbilirubinemia, decreased BUN, increased liver enzymes, bilirubinuria

Renal disease: increased BUN/creatinine, low USG

Hyperthyroidism: increased T4, increased liver enzymes (ALP, ALT), mild increase in PCV, low USG

Electrolyte/acid-base derangements: Na, K, Cl, Ca, pH, bicarb, tCO2

Eosinophilia: parasites, IBD, hypereosinophilic syndrome, mast cell tumors

Neutrophilia: gastroenteritis, neoplasia

Neutropenia: salmonellosis, retroviruses

Hemoconcentration: dehydration

Anemia: chronic disease, GI blood loss

Fecal may also show parasites, and FeLV/FIV positive snap test might be supportive of vomiting from a FeLV/FIV related illness

Secondary diagnostics beyond bloodwork and urinalysis would be the next step after that. Radiographs may show abnormalities in organ size/architecture (small kidneys, enlarged liver), foreign bodies, GI obstruction, or masses.

Ultrasound is the diagnostic of choice for **chronic vomiting and normal bloodwork**. It can reveal thickening of the stomach/small intestines, wall layer changes, and/or enlarged lymph nodes. It can also show or allow better examination of abdominal masses, or the presence of free fluid.

fPLI may be indicated if pancreatitis is suspected, but may be normal in chronic pancreatitis cases. Heartworm testing if the cat lives in an endemic area, after other causes have been ruled out.

Intestinal biopsy and histopathology is recommended in cases of chronic vomiting with GI thickening seen on ultrasound. This will differentiate between IBD and lymphoma, which cannot be done without the histopath! Though presumptive and empirical treatment may be considered in cases of financial concern. IBD is often in younger cats and lymphoma in older, however that’s simply a generalization and not a hard and fast rule. IBD and lymphoma are the two most common causes of chronic vomiting in cats. Exploratory surgery and full thickness biopsies is preferred over endoscopic biopsy, as you can retrieve intestinal samples from more than just the duodenum, the samples will be higher quality for your pathologist, and you can determine the staging of the lymphoma (if that’s the cause).

What should I tell owners to keep a look out for? 2x a month or more vomiting, INCLUDING HAIRBALLS, is abnormal and justifies an ultrasound study. Cats should in theory be able to process hair since they evolved to groom their fur (a bit more leeway is given to long-haired cats since that’s a genetic mutation we’ve selected for), and vomiting hairballs regularly is suggestive of hypomotility of the GI tract.

The only exception to this is eating grass and vomiting, as grass is irritating to the stomach and can cause vomiting, but is more or less harmless on its own.

Due to this being a very wide topic I didn’t go much into specifics, but I can if you all are interested in any specific parts of this!

[vulnera-sanentura]

I wish people knew more about how much time and effort goes into patient care at a teaching hospital. When you ask to put your dog on a ventilator for the night because you need more time to make a decision, for something both of us know is 100% not fixable, they don't just get magically whisked away to ventilator wards. 4 vet students will get called in to forgo most if not all of their sleep to make sure your dog remains alive and nonpainful, because icu doesn't have the manpower to give up their students to this one job.

Most special circumstances are like that. And though the doctors know that this is a bad situation for both the students and the animal, they'll still offer it for your peace of mind. And will never elaborate on the circumstances for that same reason.

I'm not saying this to dissuade people from attempting last-ditch lifesaving measures on their animals. Just.. be appreciative. There's no "night" surgeon, neurosurgeon, internal medicine doctor, anesthesiologist, or radiologist. More times than not the doctors and students are sacrificing food, sleep, and occasionally sanity for your animals.

What is one unfortunately unintuitive fact about pet health that you wish people could understand better? As a vet I'm sure you talk about the obvious stuff pretty often--call your vet if you have a health concern, yes Fido does need to take his medicine for the entire length of the prescription, etc. But what's one thing that isn't immediately obvious, but is nonetheless really important for the average pet owner to know about?

vet-and-wild here.

I wish people would understand that medicine isn’t magic. You don’t know how many times people ask if I can just “give him a shot” to make their animal better. Sometimes the treatment is that simple, and that’s great! But if we offer a certain approach with various diagnostics, you can be pretty sure the answer is no. And also, even if we do everything right, sometimes we can’t save animals. I wish we could, I really do. But people seem to have this idea in their head that once they get their pets to us, the work is done.

Another thing is I wish people would understand is how important preventative care is, especially for exotics. So many of our patients only come in for vaccines (cats, dogs, ferrets, pet pigs) or when they’re sick. Especially exotics. Yes you will have to pay a yearly or bi-yearly exam fee but if we can catch problems earlier (AKA the point of preventative med) you will save money in the long run and your animal will likely live longer. Dogs we at least tend to see yearly because we have to write a prescription for heartworm meds (which requires a current exam) but other animals we may only see when they’re legitimately on their death bed.

I wrote a little blerb about preventative care for exotics here.

gettingvetted here.

I wish people would realize that it is literally illegal to prescribe medication of any kind without having seen the patient in the past year. I’m not trying to get your money - I literally can’t give you any medications if you don’t bring the pet in for an exam.

I wish people would not give whatever drug they have laying around at home before coming to see me. I’ve had people giving Bactrim (trimethoprim/sulfa) for their dog’s urinary tract infection, eye drops that they were given by their own doctor for weeping eyes, and Aleve for pain relief. So in those instances, I can’t perform an accurate urine culture to treat the UTI, the dog’s autoimmune dry-eye went for longer without treatment so it got an ulcer, and the dog on Aleve died in the owner’s arms from liver toxicity. A call to the vet is free, so don’t make any treatment decisions without one!

Sueanoi here.

please don’t ever give any human medication to your animal without a vet prescribing it. 

i absolutely feel very bad when i end up having to treat for acetaminophen toxicity instead of treating whatever made a cat sick.

Ferox here.

An animal does not have to be screaming to still be in pain, especially for chronic pain that has been there a while. You don’t see elderly people with arthritis screaming with every step as they wander around the supermarket getting their shop done, they just bare it and get on with it. Same with our pets, if the pain has been there for a while they’re not going to scream about it.Still hurts.

[gettingvetted]

I really like your blog and ones similar to it. I was curious t there’s any other good ones related to biology, ecology, vet stuff, etc?

Sure. (these are in no particular order, just the order that I followed them) I follow a ton of other great blogs but I tried to keep the list to those that regularly post about the topics you mentioned. So the farming blogs and petcare blogs I follow didn’t get included. I can add those in if you’re interested.

@sciencenewsforstudents@nurseconnect@askavettech@vetricular-techycardia@champawattigress@randomlostgirl@pharmdup@foodscienceyo@zoologicallyobsessed@wildlifeaid@hopefulveterinarian@vetnurseventure@sciencesideanswers@science-side-of@coffeeanimalsandscrubs@thebabydogtor@veterinaryshitposting@veterinarynurse@thenearlyvetstudent@vetschooliscool@thestudentvet@vetstudentnl@scandinavian-vet@thoughtsfromavetreceptionist@aboutsixplums@vetvetvet@allthingsveterinary@drmannimal@fractiousrvt@vetloading@stuff-from-vetblr@scottishvn@vveterinary@thegamervet@vetschoolvinegar@asillysillyname@wildliferehabstudent@clinics-and-kettlebells@vetstudentlive@lizziedoesvetschool@llcoolswick@vetsetgo@thelifeofavettech@zookeeperrick@loveofvetnursing@avoidingclaws-mostly@neaq@vulnera-sanentura@noaasanctuaries@vet-student@talesfromtreatment@montereybayaquarium@strangebiology@journey-to-dvm@booprenorphine@drownedwednesday@followthebluebell@vetdownunder@missnoodliness@why-animals-do-the-thing@shityouhearatvetschool@youfoundyourvet@vetnursetails@mylifeasadvmstudent@dxvetstudent@thatvetmedchick@vetintraining@love-vetsurgeon-acvs@vet-and-wild@inseltierdoktor@sarahseesarahdew@sueanoi-the-vet@criticalcaredvm@futurevetmedicalfacts@datvetlife@justvetschoolthings@thehappyvet@destinationveterinarian@cullenwebbanimaleyedoctors@itsavetlifeforme@alaskanvetstudent@just-like-a-real-doctor@ausvetstudent@vet-in-progress@ivetyouamilliondollars@pivotal-moment@verylittleveterinarian@awomanofletters@cowsandpickles@wineingveterinarian@getyourveton@astressedvetstudent@drferox@vetstudent-tears@savetstudent@vetisinmyfuture@allvet@ashleygoestovetschool@soontobedvm@anaspiringvet@mylifeasavetstudent@iheartvmt@totesmahgoatess@theexoticvet@veterinaryrambles@why-i-am-a-veterinarian@fortheloveofcows@veterinarianinprogress@veterinaryhumor@vetmedirl@equinevetadventures

This is not an exhaustive list - I think that does exist somewhere. But it’s a great start!

[vulnera-sanentura]

Hello! I kinda dropped off the face of Tumblr but...

I graduated! I'm a doctor!!!

Can't believe I'm finally done with school, forever 🥰

[vulnera-sanentura]

Science is always changing

There's been a lot of uproar and concern about pet food diets, especially grain free and DCM in dogs after the FDA study citing a link between the two.

The truth is, science is messy. We're always learning new things. Which is great, that's how we get from the 4 humors and bleeding people to what we call medicine today.

As of June 2020, a literature review was published investigating the link between DCM and grain free diets. The ultimate conclusion? More research is necessary, but it may ultimately be genetically linked.

And that's frustrating. We want to know more to serve our patients as best as possible. We want definitive answers. But a lot of time, there isn't one easy answer, and easy fix. Will I recommend grain free diets now after this study? Probably still no. Retrospective studies have their own issues, and the best study on this link would be a long term, prospective study on these diets.

As scientists, we need to keep learning more, and not hold on too tightly to any previous ideas in the case they're disproven in the past. And as vets, we need to be advocates for our patients, using the most scientifically proven medical recommendations.

I wish science and medicine were more black and white, but more often than not it's complicated shades of grey.

[vulnera-sanentura]

Started my pathology advanced rotation on Monday. Now get to: sleep in, go home at a normal time, no on call shifts, and don’t have to come back later after I’ve already left.

Wild shit.

@lizziedoesvetpath you’ve got the right idea XD

[vulnera-sanentura]

Cat Facts: Diabetes and DKA

Diabetes can often get a bit overwhelming in physiology and info, so here’s the short and sweet of it:

Affects 1:200 cats (similar rate for dogs)

Caused by an insulin deficiency (effectively)

Clinical signs include - polyuria, polydipsia, and polyphagia (eat, drink, and urinate a lot, abbreviated as PU/PD/PP), and weight loss

Treatment is - insulin, special diet, +/- weight loss

DKA is - metabolic derangements secondary to insulin deficiency. VERY serious, often VERY sick kitties

So breaking that down, let’s start with the physiology: Specific cells, called beta-cells, in the pancreas create insulin. Insulin is anabolic (think anabolic steroids that bodybuilders use), decreases blood glucose, and facilitates tissue uptake of glucose while inhibiting breakdown of tissues.

In diabetes, cats have what’s called a “relative” insulin deficiency (whereas dogs have a “true” insulin deficiency). Which means they’re producing insulin, but due to a combination of beta-cell dysfunction and insulin resistance in the body tissues, there isn’t enough to do the job of what a normal, healthy body would need. This also means it’s often later in life when symptoms show up, and there’s a potential for them to go into remission and no longer have to be treated for diabetes.

Who gets diabetes? The typical diabetic feline patient is an older, neutered male. Weirdly, Burmese are also predisposed but only in Australia is there a correlation. Because this is a relative insulin deficiency and not a “born with it” disease in cats, there’s also risk factors, which increase the likelihood of developing diabetes due to increasing insulin resistance:

Obesity

Pancreatitis (beta-cells are in the pancreas!)

Steroids (either due to medications or steroid hormones created by the cat)

Progesterone

Infection (UTI, periodontitis)

Stress

Why did I highlight infection? It’s important to remember because if your patient is on a high dose of insulin but not responding, it may be due to an infection! Check for a UTI, clean their teeth if they need it, it could help enormously in management.

How do you diagnose it? Clinical history helps: cat often comes in with the owner complaining that they’re peeing so much they’re flooding the litterbox, and eating a ton but they’re still losing weight. If you read my other posts, you’ll recognize this sounds a bit like hyperthyroidism too, but it narrows down the differentials!

Diabetes in dogs is easy to diagnose. Check a blood glucose, it’s sky high out of reference range? Well, you’ve got diabetes! The problem in cats, however, is they can get stress hyperglycemia. This means coming into the vet for a visit can jump up their glucose out of reference range and initially make it seem like diabetes. The good news is you can often differentiate it by how high the glucose is above normal. Stress hyperglycemia is often <250mg/dL, and cats with diabetes will present much higher than that on initial visit, generally >350. Diabetic cats will always have glucose in their urine, while it’s less likely (though not impossible) for a stressed cat to have glucosuria.

And treatment? Insulin! The goal of diabetic management is the reduction of clinical signs, and improving quality of life of both the cat and the owner. Remission is possible, and a bonus, not a true goal as it’s not achievable in all patients.

You can also pair this with a diet of increased protein and decreased carbs (Hill’s DM is a common choice). NO RAW MEAT. Diabetes leads to immunosuppression and they’re much more likely to contract an infection from raw diets.

Vets should ask owners to monitor clinical signs at home (drinking more or less than normal, eating more or less, gaining or losing weight), and the dose at recheck should be adjusted based on those clinical signs.

So, onto DKA. DKA, or diabetic ketoacidosis, is a serious metabolic disorder caused by insulin deficiency or resistance, leading to excess liver production of ketoacids and progressively worsening metabolic acidosis, hyperosmolality, serum electrolyte derangements, and systemic signs of illness.

That’s... a lot of big words and I’m not a vet. Come again? DKA is when diabetes has been so uncontrolled or thrown out of whack that it leads to an acidification of the bloodstream, and due to that low pH, starts a snowball effect of changing other physiologic mechanisms like the electrolytes in the blood. These cats come in often very sick, potentially only able to lay on their side, almost comatose.

How do you diagnose this one? DKA is diagnosed by high blood glucose, glucose in the urine, as well as ketones in the urine. They generally have a history of diabetes, though some are undiagnosed at presentation.

Additionally, bloodwork will show a metabolic acidosis, and maybe hyponatremia, hypokalemia, hypochloremia (all the low e-lytes!), pre-renal azotemia (high BUN), increased liver enzymes, and hypercholesterolemia.

This is serious, what do I do?! DKA can be scary, especially when you know the ~30% mortality rate. For treatment goals, you want to:

Provide adequate insulin to maintain BG between 100-300 

Restore fluid and electrolyte losses

Correct the metabolic acidosis

Identify and treat concurrent illness

Provide dextrose and food as need to avoid hypoglycemia

Avoid overly aggressive therapy!! Correct the problems slowly over 24-48 hours

I won’t go too much into the ICU workup since that can get long and complicated, lots of math, but essentially you’ll start fluids, add some potassium if indicated, start them on insulin, and monitor them. While stabilization of the critical patient is most important, it’s also important to know that DKA doesn’t occur in a vaccuum. Pancreatitis, cholangiohepatitis, hyperthyroidism, or a number of other diseases may be underlying that pushed them from a regulated diabetic patient into DKA. Look for the cause!

That was long but I hope you all enjoy it :)

[vulnera-sanentura]

Holy fuck, I'm gonna be a doctor in 2 months

[veterinaryshitposting]

my dude @vulnera-sanentura you have been Summoned to explain just exactly what the fuck you meant by that

[vulnera-sanentura]

Room full of 4th year students:

Classmate: ... is a bone an organ?

The entire rest of the room: I.... don’t know

Don’t think you’re ever too far along in your studying to ask some dumb questions XD

[vulnera-sanentura]

Next in the Cat Series: Hyperthyroidism!

One of my favorite cat diseases, because unlike other chronic health issues, it’s not only easy to diagnose, but curable too! (phew, not all of them are just supportive care)

Who gets it? The typical hyperthyroid cat is older (mean age of 13 years), with females being predisposed and with no breed predilection beyond “mixed breed.” It can be diagnosed in cats from 4 to 22 years old, though it’s very uncommon to see it in cats younger than 8 years.

What’s it look like? These cats are usually thin or losing weight, despite a ravenous appetite (polyphagic). They can also be PU/PD (polyuric/polyphagic, ei, they drink and pee waaay more than is normal). They can become more active, literally putting the hyper in hyperthyroid, or more aggressive than they used to be. Other signs that aren’t very specific to hyperthyroidism are vomiting and diarrhea.

So what is it? Hyperthyroidism is a condition where a tumor in the thyroid gland, located in the neck on each side of the trachea, causes excess production of thyroid hormones, especially notable is T4. Thyroid hormone is responsible for a variety of metabolic functions, and this increase in metabolism is what causes many of the presenting signs: hyperactivity, weight loss despite appetite, aggression.

How do you diagnose it? The most definitive diagnosis of hyperthyroidism is through checking blood concentrations of T4. It’s increased? Congrats, you’ve diagnosed hyperthyroidism! Though a lot of feline specialty practices have it always on the normal blood chemistry, it may be an add-on at other general practices, and that’s when it may get a bit trickier to diagnose originally.

The history should help clue you in a lot, but on physical exam you’ll also potentially see:

Thin/decreased weight from last visit

Dehydration

A palpable “thyroid slip” - the thyroid gets large enough you can feel it when you run your fingers along the side of the trachea. Not all hyperthyroid cats have it, and it can be hard to get used to finding the slip

Poor hair coat

Cardiac abnormalities: tachycardia (>220 bpm), murmur, arrhythmias, a gallop rhythm

Hypertension, which can cause ocular or neurologic issues

Besides increased T4 on bloodwork, you may also see an increased ALT and/or ALP, sometimes insanely high while all the other liver enzyme values are normal. A fifth will also have azotemia (increased BUN), either due to dehydration or concurrent renal disease.

And since they’re older cats, there may be other chronic illnesses like CKD, diabetes, or GI disease.

You said this one’s not just treatable, but curable?? Yes! The treatment of choice is radioactive iodine therapy. Iodine is taken up by the thyroids to create thyroid hormone, so once the radioactive iodine is injected it’s selectively picked up by the thyroid. And since the tumor cells are working overtime, the radioactive iodine (I-131) is picked up by the tumor cells, killing them, and leaving the currently-dormant normal thyroid cells intact.

Pros:

It works rapidly (improvement within 2 weeks, back to full normal in 3 months)

Very effective, with an over 90% cure rate

No pills in angry old cats

Permanent, one time correction

Cons:

Expensive, usually costing over $1000 (~1400)

Requires special facilities, so it’s not available everywhere

Using radioactive materials, so requires containment of your cat at the hospital from anywhere from 2 days to 2 weeks, and usually the shorter time periods require special at home distancing from your cat

May need retreatment if it’s a thyroid carcinoma (2% of cases), so more $$$

What if I can’t afford that? Any other options? Yep, there’s methimazole, which come in a pill form or a transdermal cream. It works by blocking thyroid hormone synthesis, so while it doesn’t cure hyperthyroidism, it will lower T4 levels and mitigate clinical signs.

Pros:

Not as expensive up front, though can cost more over the course of the disease

No hospitalization

Available anywhere cats are seen

Cons:

Pilling angry cats sucks, some don’t like the cream either

Twice daily, nonpermanent medication

Manages, doesn’t treat the disease. The thyroid tumor can grow, requiring more medication, or transform into a carcinoma instead of a benign tumor

Side effects! - GI upset, neutropenia/thrombocytopenia, GI upset (pill), and the worst: facial excoriation, where the cats’ faces are so itchy they scratch off their skin. Reversible with discontinuation.

There’s also surgical removal of the thyroids, which has fallen out of favor, and Hill’s Y/D hyperthyroidism food, which is iodine restricted and not highly recommended by endocrinologists.

I’ve heard hyperthyroid treatment causes renal disease, is that true? No, but it often unmasks kidney disease. These two diseases, hyperthyroidism and CKD, have a very common demographic in older cats. Hyperthyroidism can increase the filtration rate of the kidneys, which makes the bloodwork levels, BUN and creatinine, that we use to diagnose CKD, decrease. Once the hyperthyroidism is cured, the filtration rate decreases, and those values jump up.

If the kidneys already look bad before treatment, the vet may want to do a “methimazole trial” before committing to radioiodine. This will allow the T4 to drop and uncover the true extent of renal disease, and since methimazole isn’t permanent it can be discontinued if the renal disease is too bad.

Most feline specialists still recommend treating the hyperthyroidism even if there is severe underlying kidney disease, but this can help us prepare for what to expect after radioiodine.

What’s the prognosis, almost-doc? Well, it depends. These cats are already fairly old, so part of the shorter lifespan can be due to other concurrent old age changes/diseases. If properly managed, the median survival time is 2-4 years, though if cured with iodine at 10 years old they could truly live into their 20s. I heard of a cat treated with radioiodine in their 20s and is now in their 30s!

[vulnera-sanentura]

Because for some reason what I want to do after a 4 hour practice exam is look at more vet stuff, here’s: Hypertrophic Cardiomypathy!

Hypertrophic cardiomyopathy, or HCM is the most common cardiac disease of cats. It’s characterized by an enlargement of the heart, specifically of the walls of the left ventricle. This is a hypertrophic enlargement, so the walls get thicker, and consequently the volume that the ventricle can hold gets smaller. It’s the same increase in muscle mass you see in weight lifters, except you don’t want to see that in the heart, it decreases appropriate cardiac function.

Who gets this disease? The poster child for HCM is a 6 year old, male cat. Due to them being the most common breed of cats, the majority (89.1%) of HCM cases are domestic shorthair cats. This is followed by Persians (6.5%), domestic longhairs (2.2%), and then the classic case is a Maine Coon (2.2%) because they have an autosomal dominant gene running through their breed that predisposes them to HCM. Not all Maine Coons have the gene, and not all that have the gene will develop HCM, but it increases their risk of developing it earlier, and with higher chance of acute death (especially with two genes).

75% of cases are male cats (I don’t believe it’s known why), and though the mean age is 6 years old it has been detected in cats from 8 months to 16 years.

What are the clinical signs? It varies, a lot. Many have NO signs at diagnosis! It can be an incidental finding, a murmur, arrhythmia, or gallop rhythm (actually sounds like a gallop) leading to a further workup and echocardiogram (ultrasound of the heart, aka an echo).

Some are only diagnosed after very severe clinical signs, like dyspnea (difficulty breathing) due to pulmonary edema (fluid in the lungs), pleural effusion (fluid in the space around the lungs), or a thromboembolism - where a blood clot forms and travels from the heart to a different place in the body. Often the place an embolism lodges in cats is at the very base of the aorta, and the cat becomes acutely unable to use their hindlimbs and is extremely painful. In these cases, after triage and supportive care, and echo may be done as a further diagnostic and find the HCM.

Most cats with HCM have a murmur to some degree, but there’s about 10% of cats with HCM that don’t, called “silent HCM.”

40% have a gallop rhythm

25% have some other arrhythmia

You keep talking about “echos,” what are they and how do you use them? Echocardiograms are ultrasounds of the heart, which can be used to detect abnormal structure or function of the heart.

In cat’s with HCM, you’ll see thickening of the left ventricular walls, especially the free wall, and potential increased fractional shortening. Fractional shortening is the percent change from when the heart is at “rest” and when it contracts - diastole to systole. Normal hearts will have 30-50% fractional shortening, but HCM hearts, due to their limited volume, contract down more to compensate, having a FS even into the 90%s.

Left atrial enlargement, in this case dilation not hypertrophy, is also seen in HCM, and the severity of the enlargement is often correlated to the prognosis with HCM. When the atrium is enlarged, it becomes a place for blood to stagnate and form clots, which is when thromboembolisms can form.

You can also see systolic anterior motion (SAM) of the mitral valve in 2/3 of cases, which is where the mitral valve flips up into the left ventricular outflow tract. It can be the cause of sudden hypotension in surgeries of HCM cats, and may be the reason for the murmur in some cases.

This sounds like a radiologist thing... shouldn’t I just leave the echos to them? Nope! Well, if it’s a legal echocardiogram, such as in the case of a breeding animal, maybe suggest a radiologist. But general practitioners can do echos too! I knew next to nothing about ultrasound or echos going into my externship, and now I’m confident I could diagnose HCM, some even from just a passing glance without the measurements, if they’re severe enough. Don’t believe me? He’s a video that can help you learn how to do echos yourself! Other diagnostic things: ECG: left atrial enlargement can show up as widened P waves and left ventricular enlargement can cause an increase in QRS amplitude, though this won’t lead to a definitive diagnosis. There may also be secondary arrhythmias, sinus tachycardia, and intraventricular blocks

Radiographs: since the muscles of the heart are hypertrophied not dilated, the heart isn’t always enlarged on rads. But it may look “taller” as an indication of enlargement, see the left atrial enlargement, or signs of congestive heart failure (CHF), such as pulmonary edema/pleural effusion

So... how do you treat it? Well, it almost all cases, it’s not treatable, just managed. The only cases of reversible HCM are in hyperthyroid patients (I’ll get to that topic eventually), where once you cure they hyperthyroidism, the heart returns to normal.

In most cases though, you ‘treat’ them by reducing their stress. Removing pleural fluid buildup, oxygen therapy, and furosemide if the HCM has sent them into CHF.

There’s a few secondary therapeutics:

Diltiazem: may increase cardiac relaxation and control arrhythmias

Atenolol: ventricular arrhythmia control and potentially help with outflow obstruction from SAM of the mitral valve THIS ONE SLOWS HEART RATE THOUGH, DON’T USE IN CHF PATIENTS

Enalapril: can help reduce left ventricular hypertrophy (cardiac remodeling)

Clopidogrel: anti-thrombus formation

What’s the prognosis? If there’s not clinical signs at diagnosis, the median survival time is about 5 years. If they present in congestive heart failure, the median survival time is only 3 months, however with advances in therapeutics the MST may be actually higher. They’re also likely to have CHF again if they have in the past.

Hope this helps you learn something! I think I’ll cover hyperthyroid next, which [SPOILERS] has a much better prognosis than CHF and HCM.

[lizziedoesvetpath]

@vulnera-sanentura yeah my school did a similar thing because we weren't associated with a commercial lab, so as with your school offering free or discounted necropsies was the main way we got anything for students to learn off of. Where I am now (as I say above) we have a state lab joint with the uni so there are plenty of "real" cases coming through, meaning submitters do pay.

Unsurprisingly, the money side of things is complicated!

Re: the post that was shared about necropsies. While I understand they’re an important tool, why are owners asked to pay for it? On the two separate occasions I’ve been asked by vets (at a teaching hospital) for permission to do a necropsy, I was also asked to foot the bill. I’d already spent thousands ($8-10k) trying to save those dogs’ lives, and was facing a $250-350 cremation bill for each one. Why ask for even more of my money so the vet students could learn more via necropsy?

Hi there! Thanks for the question, I think it’s a good one to clear up for people because I can totally understand why it’s come up for you. I also think it’s part of why vets find it so hard to ask clients to do this.

We’ll start with why necropsies cost money. I’m not being condescending, i just think it’s important when answering these questions to have a discussion about where the bill actually comes from. A necropsy (with histology) where I work costs $60 - $300 USD, depending on the type of animal, its size, and whether you’re sending it from in state or not. That money covers the necessary materials - keeping knives sharp, scalpels, formalin (fixative), jars, scalpel blades, cleaning up afterwards, slides, stains and so on. It also covers the time of at least one pathologist and a handful of technicians. Technicians may help perform the necropsy (a job that may be filled by a veterinary student at a teaching hospital) but mostly they process the tissues collected to be put onto slides. The pathologist who is doing/overseeing the necropsy, reading all the histology slides, and writing up the reports is an expensive person to hire, because we’re so highly trained. To become a veterinary pathologist you need to go to veterinary school (5-8 years depending on where you live and upwards of $100K debt), then you need to do another minimum 3 years training to become board certified and/or get a PhD. Again, depending on the animal submitted and what’s wrong with it, a necropsy takes around 20mins - 1hr. Reading the slides takes about 30mins, and writing the report can take up another 30mins. So in that $300 bill you are getting around 2hrs professional pathologist time, maybe an hour of technician time, and all those supplies. Plus a commercial lab needs to turn a bit of a profit to stay afloat, and many vet school pathology departments are joint with a commercial lab (for example - where I work the pathologists are jointly employed as teachers for the university and as diagnosticians for the state lab, which is on campus so that this symbiotic relationship can work. The necropsy is run by the lab, not the school).

So that’s where your money is going. Onto your question - why is it your money we’re asking for?

The main reason is usually that if you, the client, is getting something out of this process, you need to be paying for it. So even if vet students are learning from the case, if we are sending out a report to you, we are providing you with a service. And like anything else in this world, that comes with a fee. At some schools people have the option to donate the body of their animal for teaching - that would mean that the students would get to perform the necropsy and learn from it, but the client won’t get anything back. Usually this means that a student will do the necropsy, teaching budget will cover those supplies and pay the teaching pathologist for holding what is essentially a class, and then it likely won’t go any further. A full report may not be written up, histology won’t necessarily be done, and that way a school can cut costs while still obtaining learning opportunities for their students. But, as is kind of discussed in the post you came here from, there aren’t many clients comfortable with having the body of their animal cut up and not getting any answers back. Which is understandable. Unfortunately schools only have so much teaching budget to throw around, and often pathology is not the first department to get that money. So we ask clients to come to the table.

I think where vet schools often fall down in this arena is that they use learning as an example of a positive outcome for this process, and that can make it sound like the necropsy is only being done for the students to learn from. And that’s not an invaluable thing! But as I say above, a service is being provided to you. The knowledge and the information you get from a necropsy report is actually really valuable and it takes a lot of skills and expertise to reach those conclusions. It’s the same as paying for a consult when you take a live animal to the vet, or paying a lawyer for advice on a contract. We talk about how much it can educate a student, the clinician who saw the case, and pathology trainees like myself, because those things provide comfort to a client who is uncertain about what a necropsy can achieve, but you are still getting something out of it. And often going through a vet school will get you a discount where teaching budget kicks in as compared to a private commercial lab.

I don’t know if I’ve done a great job of clearing that up, but I hope it helps a little bit. Please do feel free to ask more questions about how veterinary pathology works, I feel like so many people really don’t know what we do and why, so I’m happy to chat about these things!

[vulnera-sanentura]

Cats, Chronic Kidney Disease, and More Food Controversy

Let’s start from the beginning: what is chronic kidney disease?

Chronic kidney disease (CKD) is a progressive disease of lost renal function. It’s a very common cause of death in cat’s over 14 years old. Kittens are born with 100% function of their kidneys, but as they age, function slowly decreases leading to clinical signs. This can be distinguished from acute kidney injury (AKI) by multiple factors, but the main difference is that CKD is an almost inevitable consequence of age, while AKI can happen at any age, and usually has an inciting factor like trauma or a bad infection.

Renal disease is classified into 4 stages, IRIS stages, based on bloodwork levels of 3 waste products: SDMA, BUN, and creatinine.

Stage 1 & 2: often no clinical signs, very early to early renal disease

Stage 3: can see polyuria and polydipsia (increased thirst and urination), decreased appetite, weight loss, and lethargy as creatinine rises in the blood

Stage 4: usually very sick! Poor to absent appetite, rapid weight loss, very lethargic and anti-social, and often extremely dehydrated

Protein requirements of cats

Cats are obligate carnivores, unlike dogs which are facultative carnivores, and this is reflected in their protein requirements! Cats generally require approximately 34% protein or more on a dry matter basis (I’ll touch on dry matter vs crude protein that at the end) to maintain lean muscle mass, or they begin to metabolize it for energy (LaFlamme & Hannah, 2013; Salauq, 2016).

As cats age, they need more protein in their diet! As cats age (greater than 12 years old), the absorptive abilities of their digestive system wane so they need an almost overload of protein to help their gut absorb enough: at lowest 40% protein and up to 50% protein. Due to the decreased absorption they also have an increased fat requirement (>20%), especially omega fatty acids, and supplemental B vitamins, especially B12 are recommended (Sparkes, 2011; LaFlamme & Gunn-Moore, 2014).

So what’s the controversy?

In renal disease, the kidneys are less able to filter out waste products the body makes, leading them to overload the body and make the animal sick. Many of these waste products, including BUN and creatinine, are created from the breakdown of proteins: either in muscle or in food. (Fun fact: intensely muscled horses may have high creatinine just due to the immense amount of muscle they have, while conversely very skinny, atrophied animals will have lower). Protein also contains high levels of phosphorus, which can be detrimental to cats with kidney disease.

The main thought behind the low-protein renal diets is to not overload the animal’s kidneys with excess protein and make them sicker.

However, Dr Gary Norsworthy, one of the leading feline specialists, recommends a high protein diet to all cats but those in the latest stages of CKD. Why?

Hyperthyroidism, diabetes, and GI disease, 3 of the most common diseases in senior cats, can all lead to muscle wasting

Starting cats out with a restricted protein diet that may have these diseases in hopes of preventing/stalling CKD would likely only cause even further atrophy, especially since senior cats already have decreased protein absorption.

The important clinical goals of managing early (IRIS 1 & 2) CKD are:

Maintain hydration! Kidneys love water, and keeping kitties hydrated can prevent or slow degradation of the kidneys. - water fountains, wet food, Purina Hydracare, IV/sub-Q fluids 

Maintain normal phosphorus levels. Hyperphosphatemia directly correlates to an increased mortality in both human and feline patients with CKD - low phosphate diets, phosphate binders

Control other risk factors, like hypertension and hypokalemia

Very high blood pressures can further damage the kidneys (like “spraying a fire hose on a delicate filter”)

If you control these factors, high protein should not be an issue for cats with early CKD

Norsworthy is generally against traditional renal diets in cats, which often have 23-27% protein, below the threshold of muscle wasting in cats! (As a note: Hill’s K/D has only slightly lower protein in it than their standard adult food: 30% in K/D, 34% in K/D early care, and 36% in adult. Purina NF is still following a more restricted protein diet at 26%, but their NF early care is 34%)

Restricted protein will lower BUN and creatinine, which may be giving clinicians a false sense of security that the renal disease has been controlled (also lowers phosphorus, but that can usually be controlled without lowering protein)

Another fun fact: cats on high protein diets (Like Dr Elsey’s which has 59% protein) will often have an above-threshold BUN, but is not an indicator of renal function! Just their diet.

There’s also little evidence to support protein restriction in cats! Many studies on low protein are extrapolated out of other species, and cats aren’t small dogs, or small humans. They need their own studies!

In advanced kidney disease (IRIS 3 & 4), the greatest challenge to maintaining quality of life in these cats is food intake. Remember, the increased severity of kidney disease often leads to loss of appetite and subsequent weight loss, and these poor cats end up wasting away to skin and bones. Increased weight loss and muscle atrophy correlates to a shorter lifespan in senior cats (Sherk, “Skinny Old Cats”). However, cats prefer eating high protein diets over low protein! So to keep their weight and muscle from decreasing, a higher protein, increased palatability diet is recommended.

What about in severe renal disease cases?

Norsworthy recommends in IRIS 4 cats with uremia (high BUN) and hyperphosphatemia that cannot be controlled by other means, only then should protein be restricted, and only to 30-38% protein, and only if the cat will eat enough to meet caloric needs. 

**Dry matter vs crude protein: Important when feeding wet food, as crude protein is in relation to everything in the food including the water, so wet foods may look insanely low in protein when in fact they’re just high in water! There’s math to figure it out, but I think this is long enough as is

[vulnera-sanentura]

Passed NAVLE!!!

What a way to start my morning.

[vulnera-sanentura]

Ok, some kitty cat topics I've thought might be interesting (feel free to add your own):

-Feline GI issues: aka why the heck is my cat vomiting so much??

-Hyperthyroidism: the excitable, skinny senior cat

-HCM: kitties with the biggest hearts

-Enrichment for your little beast

Whatcha think should be next?