87 | Metabolic bone disease in dogs and cats: 4 quick tips to help you care for these patients

PodcastNursingNutritionRenal Disease
Written By Laura Jones

In this episode, we’re chatting about a disease that - if you’re lucky - you won’t see often, but unfortunately, one that’s on the rise - and that’s metabolic bone disease.

 

There are a few causes of metabolic bone disease, and we’ll focus mainly on the most common one today, which is nutritional secondary hyperparathyroidism. This disease is frustrating, unbelievably sad, and completely preventable - and we play a huge role in caring for patients with it.

We’ll also touch on renal secondary hyperparathyroidism, which many of us will have seen in our CKD patients - so you can advise your clients confidently, and make dietary recommendations that truly meet the patient’s needs.

First things first: What IS metabolic bone disease?!

Metabolic bone disease isn’t a specific diagnosis - it’s an umbrella term for conditions that cause weakened bones due to disruption in calcium and phosphorus metabolism.

In this episode, we’re focusing on secondary hyperparathyroidism, which means the body produces too much parathyroid hormone (PTH) in response to a primary imbalance elsewhere - often in the diet, or in the kidneys.

PTH’s job is to maintain blood calcium levels. When blood calcium levels drop, the parathyroid glands release PTH. This hormone tells the bones to release stored calcium, the kidneys to conserve calcium instead of losing it via the urine, and the intestines to absorb more calcium (in conjunction with vitamin D).

Calcium levels then increase, and PTH release stops - until levels drop again.

Usually, this system works fine and keeps our patients’ calcium balance in check; however, if there are persistent changes in our patients’ calcium or phosphorus levels, we encounter problems.

Patients with persistently low calcium or persistently high phosphate will have continually high PTH levels. This means that more and more calcium is released from bony stores and sent to the bloodstream - and there’s only so long the bones can act as a calcium donor before we start seeing problems with them.

Patients develop weak and brittle bones, pathological fractures, and electrolyte disturbances as a result.

There are two main causes of secondary hyperparathyroidism: nutritional secondary hyperparathyroidism and renal secondary hyperparathyroidism.  

Let’s start with nutritional secondary hyperparathyroidism.

This is something we usually see in young, growing puppies and kittens who are fed an unbalanced or home-prepared diet. These diets are typically high in meat or offal content and often lack sufficient calcium or vitamin D.

Cases of NSHP are on the rise, likely due to an increase in feeding ‘natural’ diets or public disengagement from ‘processed’ food. We see increasing numbers in cats, particularly those fed a raw chicken-only diet.

So why do these patients get NSHP?

The first thing to know is this: calcium and phosphate have a close relationship in the body. They actually have an inverse relationship, meaning that if levels of one increase, levels of the other will decrease in response.

Meat contains a lot of phosphorus, but not much calcium, which can lead to hyperphosphatemia in patients fed a meat-heavy diet. This phosphorus excess lowers blood calcium, which in turn triggers the parathyroid glands to release PTH.

Over time, excessive PTH pulls calcium from the bones, leading to osteopenia - thin, fragile bones that fracture easily. In severe cases, these animals can have pathological fractures, lameness, joint swelling, and even deformities. You might even hear about so-called ‘rubber jaw’ - where the facial bones become so soft that they lose their normal structure.

On top of that, hypocalcaemia is dangerous for our patients, causing weakness, seizures, and muscle twitching; where these signs are seen, emergency supplementation and careful monitoring are indicated. 

What signs do these patients present with?

You’ll usually see a young patient presenting with lameness, stiffness or reluctance to walk; patients are usually incredibly painful and often have fractures which may not be immediately apparent on examination. 

Patients may also have facial bone deformities or swelling, poor growth, poor skin and coat condition, and lethargy. Depending on the severity of their pain and electrolyte abnormalities, they may be recumbent, unable to move, and present with neurological signs.

These patients are incredibly delicate and need extremely careful handling. They come with a high fracture risk, even during normal restraint and handling, due to the severity of their osteopenia. Keep them as calm and comfortable as you possibly can during assessment, and keep restraint to a minimum.

And how do we diagnose these patients?

Diagnosis is usually made via a combination of clinical history and examination findings, alongside radiographs showing generalised osteopenia (+/- fractures).

Bloodwork often shows a normal or low calcium, high phosphate, and increased PTH (if measured). ALP levels can also be elevated from bone turnover, and we may run vitamin D levels in some cases, too. 

Ok, so that’s nutritional secondary hyperparathyroidism… how does CKD fit into things?!

We can also see metabolic bone disease associated with chronic kidney disease (CKD). This is known as renal secondary hyperparathyroidism, or ‘Chronic Kidney Disease: Mineral and Bone Disorder’ aka CKDMBD.

We’ve chatted about CKD in detail here on the podcast, so for all of the lowdown, head back to episode 12. 

But to remind you, as our patients’ kidney function declines:

  • The kidneys cannot properly excrete phosphate

  • Blood phosphate levels increase

  • Increased phosphate levels bind calcium and reduce calcium availability

  • This triggers PTH release

  • The body increases calcium levels by the same mechanisms - freeing it up from bony stores, increasing absorption in the gut, and trying to conserve it in the kidney (bearing in mind these patients have kidney disease!)

In these patients, bone disease is typically more subtle and chronic, but it contributes to pain, lethargy, poor mobility, and occasionally mandibular deformities or fractures.

We’re often so focused on azotaemia or anaemia in CKD patients that we can miss this entirely. But we’re ideally placed to look out for this or question clients about this as nurses and technicians. We’re the ones monitoring and handling these patients in the hospital, checking for subtle changes, and often the ones that clients can mention ‘silly’ things to without fear of judgment. So, look out for signs like reluctance to chew, stiff movement, posture changes, or pain, and alert your team if you notice them.

What about diagnosing renal-secondary hyperparathyroidism?

These patients will undergo many of the same tests as our nutritional-secondary cases, with the addition of renal diagnostics, including blood pressure, urine analysis, and abdominal ultrasound.

Measuring FGF-23 is also recommended in these patients. Fibroblast growth factor 23, or FGF-23, is a newer test used to investigate calcium and phosphate balance in renal patients. It provides an earlier indication of phosphate overload in cats with early-stage CKD, and can be used to guide dietary choices before secondary hyperparathyroidism occurs.

Now that we understand what causes metabolic bone disease and how to diagnose it in our patients, we need to discuss treatment.

And that treatment centres around correcting the underlying imbalances and providing supportive care.

For NSHP, we need to get that patient on an appropriate diet.

This can be challenging, because many patients aren’t used to eating a traditional diet - if a cat has only ever been fed raw meat, for example, getting them to eat a complete and balanced diet can be tricky.

If the client wants to continue feeding a home-formulated or raw diet and they will not switch to an alternative, you’ll need to consult a board-certified nutritionist. They can then work with you (and the client) to ensure the patient’s diet is balanced and meets their specific needs.

Aside from dietary support, we’ll need to provide intensive supportive care.

Many of these patients present with fractures and significant bone pain. Analgesia is a key treatment; usually opioids, with or without additional agents such as ketamine in severe cases.

Fluid therapy is often needed alongside calcium supplementation. Oral calcium and/or vitamin D may be given in mild cases; IV supplementation is used in severely hypocalcaemic patients. IV calcium supplementation can cause arrhythmias, so ECG monitoring is essential throughout administration.

For patients with renal secondary hyperparathyroidism, we focus on restricting their phosphate intake.

This is typically achieved through the administration of a therapeutic renal diet. If a patient will not eat this, dietary phosphate can be ‘trapped’ by phosphate binder medications, preventing that phosphate from being absorbed by the body. However, renal diets come with many other benefits than ‘just’ restricting phosphate, so it’s always better to switch the diet if you can.

Some patients may be started on calcitriol, a vitamin D analogue, to suppress PTH release. And of course, regular monitoring of phosphorus, calcium, and PTH levels is essential alongside renal monitoring.

And then there’s nursing care.

Our role in supporting these patients is vast. From gentle handling and recumbency care to nutritional support and client education, nurses and technicians play a crucial role in recovery. Before I finish up the episode today, I want to leave you with my top 4 tips when managing these patients:

One: Careful handling and support are key.

The severe osteopenia we see with these patients makes fractures a VERY real risk. Minimal and incredibly careful handling is essential. I make these patients a ‘padded cell’ - looking for any opportunities there might be for injury, and then making a plan to minimise those.

Two: Think outside the box with feeding.

We know most NSHP cases won’t eat ‘normal’ food - so getting them to eat a more appropriate diet voluntarily is challenging. A feeding tube may be needed to provide proper nutrition in the short to medium term, while we carefully and gradually transition them to a maintenance diet.

Look at the texture of those maintenance diets, too - try and go for one that is similar in consistency to the previous diet, where possible, whilst still being complete and balanced.

Three: It’s not just about nutrition.

These patients require incredibly careful monitoring and recumbency care, and there are numerous skills we can utilise to support them throughout the process. From ECG and blood pressure monitoring to imaging, vascular access, elimination management, and more, our day-to-day care makes an enormous difference.

Four: Client education is everything.

Most NSHP cases are entirely preventable - if you’ve got a puppy or kitten coming in for clinics and the client mentions they’re home-formulating, ask them how they’re doing that. Gently support them (guiding them, not shaming them) on how they can ensure the diet is balanced. Tools like the ‘Balance It’ checker are great for highlighting nutritional imbalances and are easy and free to use. You don’t need to know all of the ins and outs of nutrition - just the right people to signpost your clients to.


So there you have it, that’s this week’s whistle-stop tour of all things metabolic bone disease, and how we, as vet nurses and technicians, can spot, support, and prevent it.

I hope this episode helped you feel more confident in recognising these signs and understanding the why behind them, and that you feel ready to tackle the next case you see.


Did you enjoy this episode? If so, I’d love to hear what you think. Take a screenshot and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!


References and Further Reading

Laura Jones
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86 | How to ACTUALLY use your skills when caring for dogs with IMPA