Veterinary Internal Medicine Nursing

View Original

33 | Top tips for nursing Addison's disease as a veterinary nurse

Laura Jones

Addison’s, aka hypoadrenocorticism, isn’t called ‘the great pretender’ for nothing.

See this content in the original post

In fact, it’s often missed until the patient presents in an Addisonian crisis. These patients often need intensive nursing care and treatment, especially if they present as an emergency - but to deliver that care, we first need to know what Addison’s is, how it affects our patients, and how we treat it - which is exactly what we’re chatting about in this episode.

So, what IS Addison’s disease?

Well, Addisons or hypoadrenocorticism is an adrenal disorder characterised by a glucocorticoid and/or mineralocorticoid deficiency.

Usually, our adrenal glands release different steroid hormones from different layers of the adrenal cortex. These are:

  • Cortisol, a glucocorticoid is responsible for many functions in the body, from responding to physiological stress to helping to maintain the health and integrity of the GI tract

  • Aldosterone, a mineralocorticoid responsible for maintaining a normal sodium and potassium level in the body and maintaining fluid balance.

In most patients with Addison’s disease, immune-mediated inflammation (adrenalitis) causes loss of functional adrenal tissue. This is the most common form of the disease and is known as primary hypoadrenocorticism.

Other causes include:

  • Granuloma formation destroying the gland

  • Infarction (inadequate blood supply to the gland)

  • Amyloidosis (abnormal protein deposits in the gland)

  • Necrosis

  • Neoplasia

Secondary hypoadrenocorticism is also seen, though less commonly. This is seen due to pituitary gland damage causing a lack of ACTH release:

  • After hypophysectomy (e.g. in acromegaly treatment)

  • Neoplasia of the pituitary gland/hypothalamus

  • Idiopathic causes

Primary hypoadrenocorticism is more commonly seen in Nova Scotia Duck Tolling Retrievers, Portuguese Water Dogs, Standard Poodles, West Highland White Terriers, Great Danes, and Border Collies.

What signs do we see in these patients?

Well, the signs we see depend on how early we diagnose our patient—i.e., whether they’re deficient in just cortisol (known as atypical Addison’s) or both cortisol and aldosterone (typical Addison’s).

Initially, signs are non-specific and waxing and waning, involving multiple body systems - primarily the GI tract. These waxing and waning, non-specific signs earn Addison’s disease its nickname, “the great pretender”. These signs include:

  • Lethargy

  • Weight loss

  • Vomiting

  • Diarrhoea

  • Dehydration

  • PUPD

  • Abdominal pain

Usually, these signs are missed initially, with these patients treated for gastrointestinal disease. They get a little better, then a little worse, and are “ok” but never really great… until they present in an Addisonian crisis.

Classically, patients presenting in an Addisonian crisis are lethargic and dehydrated with hyponatraemia and hyperkalaemia due to the lack of aldosterone needed to maintain normal sodium and potassium levels.

As potassium levels increase, we see cardiovascular changes, including bradycardia and cardiac arrhythmias.

So, once your patient is in, how do you diagnose them?

To diagnose these patients, we’ll use a combination of biochemistry, haematology, endocrine testing, and possibly some diagnostic imaging.

Let’s start by looking at biochemistry

We can see a variety of different changes to the biochemistry results of our addisonian patients, including:

  • Hyperkalaemia

  • Hyponatraemia

  • A decreased Na:K ratio of below 27:1 (even in dogs with a sodium and potassium in the normal range)

  • Azotaemia

  • Hypoglycaemia

  • Hypercalcaemia

  • Hypoalbuminaemia

  • Hyperphosphataemia

What about haematology?

Haematology is often normal - and that’s not always a ‘normal’ finding. A stress leukogram (a combination of neutrophilia, monocytosis, lymphopenia and eosinopenia) is common in patients who are stressed, ill or receiving steroid medications. 

Addisonian patients don’t have the ability to mount this stress response, so do not have a stress leukogram on haematology. This means their normal haematology is often an abnormal finding!

 Sometimes we will also see a mild anaemia in these patients on presentation, too.

And then there’s adrenal testing…

The first test we might perform is a serum basal cortisol measurement. This is a helpful screening test, but is not definitive for Addison’s. These patients will often have a low basal cortisol level of below 55.2mmol/L - but since other things can decrease cortisol levels, we’ll want to confirm a suspicious result with further testing.

And it’s the ACTH stimulation test we use to confirm our patient’s diagnosis. Just like our Cushingoid patients, we’ll collect a baseline serum cortisol sample, inject 5mcg/kg of synthetic ACTH and then repeat a cortisol measurement an hour later.

In an Addisonian patient, results will document reduced adrenal function, with no response to exogenous ACTH. In fact, pre- and post-ACTH cortisol levels below 27.6mmol/L support diagnosis.

If needed, plasma endogenous ACTH levels can be measured to determine whether your patient has primary or secondary hypoadrenocorticism. Low ACTH levels will be seen in patients with secondary hypoadrenocorticism, though this form of the disease is less common.

And then there’s imaging

Imaging is usually reserved for stable patients, after a crisis has been stabilised - since sedation or anaesthesia is risky in patients with Addison’s disease. Abdominal ultrasound may be performed, which typically reveals small adrenal glands bilaterally.

Once you’ve got your patient diagnosed, it’s time to talk treatment.

And the way we treat them will depend on if they’re presenting as a ‘stable’ Addisonian, or in crisis.

Let’s look at crisis patients first

Our goals when it comes to managing an Addisonian crisis are to correct the patient’s hypovolaemia, correct their electrolyte imbalances, and correct any acid-base disturbnces present.

This is achieved with fluid therapy at an appropriate rate (depending on how dehydrated or hypovolaemic your patient is), glucose to correct any hypoglycaemia, and then calcium gluconate, glucose +/- insulin to manage hyperkalaemia.

We want to pull samples for an ACTH stimulation test whilst we’re stabilising our patient, before giving them any steroids. In theory we can give dexamethasone (dexadresson) to our patient without this impacting an ACTH stimulation test, but in reality, it’s better to spend the hour you’re doing the test prioritising fluid therapy, and stabilising glucose and potassium levels - because they’ll be causing the biggest problems to your patient at that moment.

After your ACTH stimulation test is complete and you’ve managed your patient’s arrhythmias and hypovolaemia, it’s time to think about steroids. We’ll need to replace both aldosterone and cortisol, which we often do with a hydrocortisone CRI initially, since this has both glucocorticoid and mineralocorticoid effects.

We’ll then transition our patient either to dexamethasone injections as an interim treatment or straight to prednisolone as a glucocorticoid source, and DOCP (Zycortal) to replace their aldosterone.

What about when your patient is not in crisis?

If you’re diagnosing your patient before they present in crisis, or you’ve stabilised a crisis patient, they’ll need ongoing treatment with prednisolone and DOCP. Pred is usually given at a physiological dose of 0.1-0.22mg/kg per day, with the dose doubled during periods of stress, illness, or hospitalisation.

We monitor prednisolone dose according to the patient’s clinical signs, so collecting an updated clinical history is very important at re-check appointments. Make sure you’re asking your clients about their pet’s thirst, appetite, urination, respiration and activity level - we’re looking for signs of steroid excess, such as PUPD, polyphagia, panting and lethargy.

DOCP replaces fludrocortisone (florinef) as a licensed mineralocorticoid. It’s started at a dose of 1.5mg/kg as a DC injection, given every 25-28 days. The optimal dose and dosing frequency is determined by measuring your patient’s electrolyte levels after treatment; initially these are measured 10 days-post injection, and every 3-4 weeks.

Because DOCP replaces aldosterone and aldosterone is responsible for preventing an Addisonian crisis, clients MUST know that strict dosing is vital. Late injection appointments, missed appointments, or injecting their pet with out-of-date solution can all cause an Addisonian crisis to recur.

So that’s treatment, but how do we nurse these patients?

These patients often present as an emergency requiring intensive nursing care. Prompt triage, careful cardiovascular assessment and monitoring, and fluid resuscitation are important nursing interventions.

After initial stabilisation, monitoring a continuous ECG (looking for evidence of hyperkalaemia, such as bradycardia, atrial standstill and sine waves), non-invasive blood pressure measurement and cardiovasular status is vital.

On top of this, we need to be careful to minimise stress when these patients are in the hospital. They lack the cortisol needed to respond to stress, so preventing additional stress is key.

And then, in addition to general nursing care, we have client education. Addison’s is a disease often diagnosed in young-to-mid adulthood, and is a lifelong condition. These patients require careful management for the rest of their life, especially in times of stress or illness. Clients need to know that regular follow-ups will be needed, careful monitoring at home is indicated, and that they’ll need to adjust medication doses in times of stress or illness, for example.

What about when we anaesthetise these patients?

Anaesthesia is risky in patients with Addison’s, since it places the body under stress, and our patients have a reduced ability to cope with this stress. For that reason, we need to take a few steps to make anaesthetising Addisonian patients as safe as possible.

First, don’t anaesthetise a crisis patient unless it’s an absolutely life-threatening emergency. Thankfully, those times are very rare, and most of the time we’ve got the time to stabilise these patients before thinking about anaesthesia or sedation.

When you’re anaesthetising an Addisonian patient, make sure that their fluid, electrolyte and acid-base status is stable prior to anaesthesia. 

Advise the client to administer their medications as normal prior to their admit. Sometimes, we’ll also administer a dose of dexamethasone in their premedication.

Anaesthetise them as normal, minimising stress in hospital and keeping hospitalisation and GA time as short as possible, and continue the patient’s routine treatment as soon as they’re recovered from GA.

So there you have it - my guide to treating and nursing patients with Addison’s disease! Remember, this disease likes to hide so learning to spot the signs, even when they’re not obvious, is really important. We can easily exclude this disease in our GI patients, for example, by adding a basal cortisol level to their bloods.

When we do see these patients, they’re often in crisis and need rapid triage and stabilisation alongside nursing care.

And this nursing care doesn’t stop when they’re out of crisis - it just looks different. Minimising stress, client education and ongoing monitoring are really important aspects of looking after these patients long term, and they’re also areas that veterinary nurses and technicians are ideally suited to helping with.

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it 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