128 | Everything you need to know about calcium (and what ACTUALLY happens when it goes wrong) as a veterinary nurse

PodcastNursingEmergency + Critical CareLabEndocrine
Written By Laura Jones

We're going to spend the next few episodes talking about bloodwork - specifically, the common changes we see, why we see them, and what this all means for us as nurses.

Too often, we look at our results, feel like we're not quite 100% sure what we're really looking at, and then hand them to the vet for them to make the decisions.

And while yes, it is absolutely their job to make those decisions, there's a TON of nursing information we get from those results too - we just need to know how to decipher them.

So that's what we're going to start doing over the next few episodes - and today we're starting with calcium.

We see this go wrong more often than we think - from patients with cancer, kidney disease, endocrine disease, reproductive disorders, toxin ingestion and much more. And that one little mineral can cause significant, and sometimes even life-threatening, changes for our patients.

I know calcium can feel like one of those topics that's all A&P and lots of boring science, and you're probably expecting your eyes to start glazing over by the second sentence - but stick with me, because I promise you, I'm going to keep the theory to what you actually need to know so you can nurse your patients effectively.

This episode, we'll chat about where and how calcium is balanced in the body (and why it goes wrong), the different types of calcium we measure and why, how to take samples that you can actually trust, and then - most importantly - our patients. We'll look at hyper- and hypocalcaemia, what we see, how to nurse these patients, and the skills we need to use in the process.

Where is calcium stored in the body, how is it balanced, and why is all of this important?

In the body, about 99% of our calcium is (unsurprisingly) located in the bone. It's locked up, in the skeleton, as calcium phosphate (aka hydroxyapatite).

So if most of the calcium in our body is in our bony stores, this means that there's only a tiny fraction of calcium circulating in the blood at any one time.

That tiny fraction is really important, though. It does a LOT - it's involved in nerve conduction, muscle contraction - including cardiac muscle - which means it's also a key factor in cardiac function, as well as haemostasis and things like hormone release.

Because we have such a small amount of circulating calcium, and it's responsible for so many vital functions, the body needs to work really hard to maintain it within a very narrow normal range. This also means that even tiny changes in calcium levels can cause significant clinical signs in our patients.

There are 3 main hormones involved in calcium homeostasis.

These are parathyroid hormone, calcitriol, and calcitonin.

The main one of these you've probably heard mentioned is parathyroid hormone, or PTH.

It's made by the chief cells in the parathyroid glands, which sit at the cranial and caudal poles of each thyroid gland.

PTH responds quickly and has a short circulating lifespan, and it works by:

  • Conserving calcium (and encouraging phosphate elimination) in the kidneys

  • Freeing up calcium from bony stores

  • Driving production of calcitriol, or active vitamin D

Speaking of vitamin D, the next hormone we're going to chat about is calcitriol.

Unlike us, our patients - and I want to stress I am talking about cats and dogs here, because I know calcium disorders and metabolism are different in some exotics - can't make enough vitamin D in their skin.

Instead, they rely on getting it from their diet. The liver converts it to calcidiol, and then the kidneys convert calcidiol to calcitriol, the active form.

Calcitriol's main job is increasing calcium absorption from the GI tract, increasing calcium levels.

Lastly, we have calcitonin.

Calcitonin basically opposes PTH. It's made in the thyroid gland, and it slows the normal turnover/breakdown of bone which lowers blood calcium levels.

Compared with PTH and vitamin D, its role in calcium regulation is fairly minor, but it's still worth knowing about.

I also want to briefly mention phosphate - though phosphate is going to get its own episode later in this series.

If you've listened to the recent episodes on kidney disease - episodes 126 and 127 - some of this will be familiar to you, as we've chatted a lot about phosphate, and calcium, as part of it.

Calcium and phosphate are closely linked - they have an inverse relationship, so if one increases, the other decreases.

Parathyroid hormone, when increasing calcium levels, encourages phosphate excretion in the kidneys. And when phosphate levels are high, less vitamin D is activated - meaning less calcitriol, and less calcium absorption in the GI tract.

So if PTH levels increase, calcium goes up and phosphate goes down. And if a patient with renal disease becomes hyperphosphataemic, for example, calcium levels will decrease.

All of this means that really, when examining calcium on our blood results, we want to look at phosphate too - because changes in one can cause changes in the other.

So that's what calcium does, and how it's regulated in the body. But how do we measure it?

The calcium circulating in the blood exists in three forms.

I promise you I am not telling you this because I enjoy getting technical (although I do!) - I am telling you because it means when we check calcium levels, we need to know WHAT we're checking.

About half of the circulating calcium in our bloodstream is 'freely available', or ionised. Ionised calcium is what we call biologically active, meaning it is free to exert its effect on the body, as it isn't bound to anything - so the body senses it and responds to it.

Around 35 to 45% is bound to protein, mostly albumin. This protein-bound calcium isn't doing anything active, because it's not got the availability to. Instead, we can think of bound calcium a bit like a storage and buffering system.

And the remaining 5 to 10% of circulating calcium is complexed. This means it is bound to other ions - such as phosphate, lactate, and bicarbonate.

If you're measuring calcium levels on your biochemistry analyser, what you're actually looking at is total calcium - the ionised, bound AND complexed calcium.

If you're looking at calcium levels on a blood gas analyser, or your machine says iCa or Ca2+, you're measuring the available (ionised) calcium only.

These are not the same thing, and they don't always agree - so generally, ionised calcium is what we want to measure (because it more accurately reflects what's going on in the patient).

As a rough guide, ionised calcium in adult dogs should be around 1.25 to 1.45 mmol/L, and in adult cats around 1.15 to 1.35 mmol/L. Younger patients have slightly higher levels, and there will always be some variation between individual analysers - make sure you're looking at the reference range for your own machine, and you've entered your patient's age correctly when interpreting results.

When is total calcium less accurate?

The classic example is hypoalbuminaemia, for example patients with protein-losing enteropathy, protein-losing nephropathy, or liver failure.

These patients have low albumin levels, and if there's less albumin, there's less protein-bound calcium. This usually means the total calcium reads low - but if we measure the ionised calcium, it's typically normal, meaning the patient isn't truly hypocalcaemic. If we took the total result at face value, they could end up having unnecessary calcium supplementation.

We can also see this balance change in the other direction - for example in chronic kidney disease. Based on total calcium, somewhere between 8 and 19% of dogs with CKD look hypocalcaemic (remember we said as phosphate levels increase, calcium decreases). Based on ionised calcium, though, it's actually somewhere between 36 and 56% - which means a lot of hypocalcaemia could be missed if we're not looking for it in the right place.

Ionised hypocalcaemia is also more common in critically ill patients than you'd ever predict from the total alone, which is one of the reasons we tend to include it in many of our so-called 'minimum database' emergency blood panels.

You may have come across formulas that 'correct' total calcium for albumin, calculating a corrected calcium value. These can be unreliable, so if there is concern for an active calcium abnormality, ionised calcium is the test we want to perform.

Ionised calcium samples can be challenging to take - and as nurses, this is an enormous part of our role when caring for patients with calcium disorders.

The reason for this is that ionised calcium is affected by pH. And the pH of a sample is affected by how we handle it - so sampling technique is really important when submitting or running ionised calcium.

Blood contains carbon dioxide, and if the sample is exposed to air, that CO2 escapes into the atmosphere. CO2 acts as an acid - so if we lose CO2 from the blood, the pH of the sample rises, making it more alkaline.

In a more alkaline sample, more calcium binds to protein in the blood, which means the ionised calcium in the sample drops. But the patient's calcium hasn't changed at all - only the sample has - and we end up with a falsely lower result.

The opposite of this is also true, so if a sample becomes more acidic, calcium comes off the proteins and the ionised calcium reads higher. While this isn't usually as much of a problem during sampling, it can be a problem during storage and handling - especially if you're sending your sample to an external lab, because room temperature storage can increase cell metabolism and acid levels within the sample.

Top tips for ionised calcium sample collection as veterinary nurses and technicians

When drawing blood for ionised calcium:

  • Collect the sample anaerobically wherever you can, avoiding exposure to any room air as far as possible.

  • Get any air bubbles out straight away and cap the syringe, not the needle. Remove the needle and use a closed cap or rubber bung, ensuring there are no air bubbles in the syringe hub.

  • Run it promptly - if you're running samples in house, they should be processed within 15-30 minutes, or chilled if processing will take longer.

  • Fill tubes properly - if you're submitting the sample externally, you need to take enough blood so that all of your tubes - plain tubes AND your spun serum tubes - are free of air bubbles. We also want to avoid serum gel tubes - it needs to be plain serum tubes only. Serum tubes only a quarter or half full give lower ionised calcium than full tubes, because of the air sitting above the sample, so this is really important. You can also purchase microvette tubes that help avoid you needing to take excessive volumes from your patients, too.

Heparin anticoagulants can also lower ionised calcium results, so if you're using a heparin tube or heparinised blood gas syringe to take your sample, ensure you fill it with the correct amount of blood. Otherwise, if you collect less blood than the tube or syringe is designed for, you'll get falsely low results.

A few more things that catch people out when looking at calcium results in cats and dogs

Point-of-care analysers using whole blood tend to read ionised calcium a little lower than serum run on a bench analyser. In dogs, that's roughly 0.05 to 0.26 mmol/L lower, and as calcium levels increase, the disparity between the results increases too. So if you're running multiple samples, always use the same analyser - don't chop and change between in house and external.

Also, some analysers print an ionised calcium 'corrected to pH 7.4' alongside the measured one. This is something I've been asked about before, and several people in the past have said to me that they don't worry about air in their sample tubes because the machine 'corrects' the calcium result. However, the formulas built into many of these machines were developed for people, not veterinary patients, so aren't as accurate.

We'll chat more about calcium disorders in a second, but while we're on the topic of difficult sample handling, I also want to chat briefly about PTH and PTHrP sampling.

PTH - parathyroid hormone - and PTHrP (or parathyroid hormone related protein) are common tests used to investigate hypercalcaemia, and they need incredibly specialised sampling techniques.

When submitting these externally, the usual protocol is this:

  • Collect whole blood into chilled EDTA tubes, ideally using a chilled syringe

  • Centrifuge the samples ASAP, keeping them as chilled as possible

  • Immediately aspirate the plasma, and place into chilled plain tubes

  • Label the samples, freeze them, and then submit to the external laboratory in a frozen transport pack (which the lab will supply).

Unlike ionised calcium sampling, air in the samples isn't an issue - instead, it's keeping the blood cool that is the priority.

For us as veterinary nurses and technicians, collecting and submitting these samples is a really important part of our role - and an important skill for us to use when caring for patients with calcium disorders.

Speaking of calcium disorders, let's talk about what happens when our patients have abnormal calcium levels.

Starting with hypercalcaemia, or elevated calcium...

A classic example of a patient you might see is this:

A mature adult Boxer, presenting with progressive lethargy, inappetence, and marked PUPD. His family initially bring him in because he is urinating so much that they're having to get up in the night, and he's going through multiple bowls of water each day - when he used to go through one.

These signs are typical, and they happen for a variety of reasons.

Hypercalcaemia can affect almost every tissue, particularly the kidneys, nervous system, heart and GI tract - explaining the variety of signs we can see. The severity of these signs depends on a few things, including how high the calcium is, how quickly it rose and how long the hypercalcaemia has persisted.

Patients with hypercalcaemia commonly have:

  • Polyuria and polydipsia - because calcium interferes with antidiuretic hormone, meaning these patients can't concentrate their urine. On urine analysis, we see a low urine specific gravity, often within the isosthenuric range (1.008-1.012).

  • Lethargy, weakness and depression

  • Inappetence, vomiting and constipation

  • Arrhythmias - because calcium interferes with cardiac action potentials, causing a variety of rhythm disturbances.

As we chatted about in the last couple of episodes, the kidneys are a particular worry with hypercalcaemia. This is because hypercalcaemia causes renal vasoconstriction and can lead to mineralisation of kidney tissue. Hypercalcaemia and kidney disease is also challenging as it is a bit 'chicken and egg' - it isn't always obvious which came first. And if phosphate levels are also high, that risk of soft tissue mineralisation increases further.

What conditions cause hypercalcaemia in dogs and cats?

Neoplasia and paraneoplastic hypercalcaemia or hypercalcaemia of malignancy

In dogs, malignancy is the most common cause of persistent hypercalcaemia. Common cancers associated with this include anal sac apocrine gland adenocarcinoma, lymphoma, and multiple myeloma. Many of these tumours produce PTHrP, which mimics PTH. In cats, squamous cell carcinoma is one of the more frequent causes.

For us as veterinary nurses and technicians, this is important to be aware of. If you're seeing a hypercalcaemic patient, careful physical examination, especially including a rectal exam and peripheral lymph node palpation, is an essential step. And while yes, it is usually the vets doing this, we can certainly look for it too.

Primary hyperparathyroidism

Primary hyperparathyroidism is a common cause of hypercalcaemia in dogs - usually due to a parathyroid adenoma. This tumour continues producing PTH, regardless of what the calcium is doing, causing calcium levels to remain increased.

Addison's disease

Around 30% of dogs with Addison's are hypercalcaemic at diagnosis, and in these patients the hypercalcaemia is usually mild. It also tends to normalise once the Addison's is treated.

Chronic kidney disease

We've mentioned CKD quite a bit already here - and we can see normal, low or high calcium levels in chronic kidney disease. Some of these patients are hypercalcaemic, especially if they've had excessive dietary phosphate restriction during the early stages of CKD.

Vitamin D toxicity

An uncommon but important cause of hypercalcaemia is vitamin D toxicity. This includes things like psoriasis creams, certain rodenticides (containing cholecalciferol), ingestion of human vitamin D supplements, and the ingestion of certain plants such as day-blooming jessamine.

Idiopathic hypercalcaemia

Hypercalcaemia can also be idiopathic if no specific identifying cause is located - this is seen more commonly in cats, and many of these patients also have calcium oxalate stones, which can cause or worsen CKD, or cause lower urinary signs.

Lastly, there is one cause which is actually completely normal - and that's age-related change in healthy, young, growing patients.

So how do we treat hypercalcaemia?

The definitive treatment is always going to be managing the underlying cause, so removing the parathyroid tumour, or treating the neoplasia, or the Addison's disease.

But while that's being found, or if definitive treatment is not possible, supportive treatment is also used to bring the calcium down to a more appropriate level and control their clinical signs.

This is achieved with fluid therapy, alongside other medications such as steroids, diuretics, or bisphosphonates, depending on the individual patient.

Fluid therapy in the hypercalcaemic patient

0.9% sodium chloride is the fluid of choice in hypercalcaemia.

There are two reasons we tend to prefer saline - first, Hartmann's contains calcium, and saline doesn't, and second, saline contains more sodium.

If more sodium reaches the kidney tubules, more calcium is excreted in the urine - so using saline helps us bring calcium levels down faster.

And of course, while this is a general consideration, fluid choice and rate should always be tailored to the individual patient, considering their level of dehydration, blood results, and risk of complications like fluid overload.

Diuretics in the management of hypercalcaemia

Once the patient is rehydrated, furosemide might be used in some cases - because it increases calcium loss in the urine.

However, the timing and use of this is really important, because we know hypercalcaemia can cause (or is often associated with) kidney injury/disease - so we don't want to use diuretics in a dehydrated patient, and risk injuring the kidneys further.

From a nursing point of view, the diuresis can be huge. These patients are often losing a lot of fluid, soiling their bed frequently, and hygiene and scalding can be a real challenge - despite our best efforts to walk them frequently.

We need to closely monitor fluid balance, weigh the patients often, ensure they have free access to water, and walk them out really regularly - often as frequently as every 2 hours.

Glucocorticoids in hypercalcaemic dogs and cats

Steroids can lower calcium in several conditions, including lymphoma, vitamin D toxicity and Addison's. But they can make some of these conditions hard to diagnose - especially Addison's disease and neoplasia - so we need to think about WHEN they are used.

If the vet decides they are indicated, they should ideally be withheld until after any required diagnostic samples have been taken - in case they make interpreting them more challenging.

Bisphosphonate medications in the management of hypercalcaemia

These are drugs like pamidronate and zoledronate, and while they're not used often, they are used in severe hypercalcaemia, and neoplasia. These drugs work by reducing the activity of osteoclasts, the cells that break down bone - meaning less calcium is released into the blood.

They don't work immediately - inhibition of bone resorption takes one to two days, but the effects can last for up to 4 weeks.

Patients receiving bisphosphonates need careful nursing:

  • The patient should be rehydrated before a bisphosphonate is given, because the main risk is kidney injury.

  • Pamidronate is given as an IV infusion diluted in 0.9% saline, over at least two hours. Zoledronate is more potent and its infusion is much shorter, around 15 minutes.

  • IVFT with saline is commonly continued before, during and after the infusion to keep the patient well hydrated.

  • Kidney values should be monitored after treatment to look for signs of kidney injury.

We can also see some transient hypocalcaemia after treatment, but this usually is subclinical.

We'll also sometimes use oral bisphosphonates in the ongoing management of things like feline idiopathic hypercalcaemia. In these patients, the tablets can sometimes get stuck in the oesophagus, so it's usually a good idea to tell caregivers to use a little water or food after the dose, just to prevent any complications.

Ok, so that's hypercalcaemia - what about when calcium levels drop too low in our patients?

Hypocalcaemia can have a significant impact on our patients, causing often severe clinical signs.

To understand the signs we see, we need to think about what calcium does, and what happens when there's not enough of it.

Where high calcium reduces excitability and makes nerves and muscles sluggish, low calcium does the opposite - it makes them more excitable.

This means that we see things like:

  • Nervousness/restlessness

  • Behaviour changes

  • Panting

  • Facial rubbing

  • Muscle twitching, especially around the ears and face

  • Muscle cramps

  • Stiff gait

  • Tetany and seizures

  • Hyperthermia (from the increased muscle activity)

  • Tachyarrhythmias, such as ventricular tachycardia

In severe, acute cases, low calcium can reduce cardiac contractility, cause hypotension, and impact respiratory muscle function, causing severe and acute deterioration.

Exercise, excitement and stress can also trigger or worsen the signs - meaning that keeping these patients calm, and quiet (and keeping the environment low-stress and minimally stimulatory) is an important part of nursing these patients.

What causes hypocalcaemia in cats and dogs?

Hypoalbuminaemia (sort of)

This is the most common reason for a low total calcium on a biochemistry profile. As we said earlier, the ionised calcium is usually normal and these patients rarely show signs.

Puerperal tetany, aka eclampsia

We don't tend to see this often, mostly due to the fact that most of our patients aren't bred - but it is a classic example.

Usually it's a small breed dog with a big litter, often around two weeks after whelping, though it can be anywhere from 1-5 weeks. In these patients, the demand for calcium in milk is just bigger than what they can absorb and mobilise within the body.

It's rare in cats, and it can look different. Affected queens may develop it before giving birth, and tend to be depressed, weak and may be hypothermic rather than hyperthermic.

Iatrogenic hypoparathyroidism in hyperthyroid cats

We don't tend to see this as much now as thyroidectomies have fallen out of favour in recent years, but it remains an important cause to be aware of.

The parathyroid glands sit right next to the thyroid, so they can be damaged or removed during surgery for hyperthyroidism - causing hypoparathyroidism.

Hypocalcaemia typically develops in the first 1-3 days post-op, but it has been seen as late as one to two weeks afterwards. How often it happens depends a lot on the surgical technique used, and monitoring calcium levels postoperatively is an important part of nursing these patients.

Post-parathyroidectomy in hyperparathyroid dogs

We also see hypocalcaemia in dogs with primary hyperparathyroidism - after treating them. This is because, while that tumour was overproducing PTH, the parathyroid glands don't need to work - they stop releasing PTH, because they don't want to make more on top of the high levels from the tumour. Once the tumour is removed, it takes time for them to start releasing PTH again, meaning hypocalcaemia can develop quickly post-operatively. We usually begin prophylactic treatment with calcium and calcitriol in these patients, as they can become hypocalcaemic within 24-48 hours otherwise.

Critical patients

Hypocalcaemia is common in a variety of critical illnesses, including things like pancreatitis, SIRS, sepsis, trauma, DKA, and protein-losing enteropathy, as well as ethylene glycol toxicity.

We can also see hypocalcaemia in post-transfusion patients, especially where they've had large volumes of blood products, or there's an inappropriate ratio of blood and anticoagulant. The citrate anticoagulant in blood products can bind to calcium, causing hypocalcaemia.

How do we treat hypocalcaemia, and what do we need to watch out for as veterinary nurses and technicians caring for these patients?

A patient with tetany or seizures from low calcium needs IV calcium, given to effect. This is usually calcium gluconate, given slow IV, diluted, with careful monitoring. Calcium chloride contains much higher levels of calcium, and is highly irritant to tissues if it is given perivascularly - so always double-check what you have in stock, and ensure it is prepared and administered really carefully.

We'll usually begin with a bolus, and then if further treatment is needed, the vet may choose to begin a CRI.

The patient's heart rate and ECG should be monitored really closely during any IV calcium administration, particularly looking for bradycardia, sudden ST segment elevation, or a shortened QT interval on the ECG. If any of these changes are seen, we need to stop or slow the infusion and alert the vet.

We may also not see the patient's clinical signs improve right away - some of them will persist for up to an hour after the hypocalcaemia resolves. Things like nervousness, panting and behaviour changes can still be seen for 30-60 minutes, and hyperthermia can also persist, especially where there has been lots of muscle activity.

And after IV correction - or if IV correction is not deemed necessary - oral treatment is typically started. This typically includes oral calcium, usually calcium carbonate, and calcitriol. These drugs can take anywhere from days to weeks to take effect.

When using calcitriol, excessive dosing can cause hypercalcaemia, so we also need to monitor ionised calcium at regular rechecks.

So those are the things we need to know about calcium - and what happens to our patients when it goes wrong.

To bring this back to our role as nurses and technicians, our priorities when monitoring these patients are:

  • Considering how we assess ionised calcium: Using the same analyser, same sample type and the same collection method each time, so you're comparing like with like.

  • Cardiovascular monitoring: During any IV calcium, and in any patient where arrhythmias are a concern, whether that's due to hypercalcaemia or hypocalcaemia.

  • Hydration, body weight and urine output: Especially in hypercalcaemic patients on fluids and diuretics.

  • The other electrolytes: Because we rarely see calcium change on its own - it can impact potassium, magnesium and phosphate, alongside kidney values.

  • Neuromuscular signs and temperature in the hypocalcaemic patient: Causing twitching, facial rubbing, restlessness, panting, stiffness, and hyperthermia.

  • Post-thyroidectomy or parathyroidectomy complications: Cats in the days, and occasionally weeks, after thyroidectomy, and dogs in the first week after parathyroid surgery.

  • The environment, stress, and excitement: Keeping the kennel and environment quiet and calm, low-stress handling for hypocalcaemic patients.

And then there's caregiver education, which is an enormous part of our role - especially during patient discharge:

  • What signs do they need to look out for? For example twitching, face rubbing, restlessness or stiffness in a pregnant or post-partum patient, or in a post-parathyroidectomy patient (and what to do if these signs are seen).

  • For hypercalcaemic patients, monitoring things like thirst, urination, and activity levels.

  • Medication administration and recheck frequency (and why it's important).

  • And in general, educating caregivers about potential toxins and how to avoid access to them - such as psoriasis creams, vitamin D supplements, antifreeze, and rodenticides.

And of course, for us, sampling is another big part of our role - and while it seems basic, where calcium is concerned, how we do it is incredibly specific and important. Which means it's an essential skill in the management of these patients.

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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127 | Acute kidney injury in dogs and cats: myths, misconceptions, and how we should REALLY nurse these patients in 2026