Veterinary Internal Medicine Nursing

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31 | The top 5 things you need to know about diabetes insipidus as a vet nurse

Laura Jones

Today, we’re talking all about the other diabetes - diabetes insipidus.

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It might have the same name as ‘traditional’ diabetes, but the two diseases are very different. In this podcast episode, I’ll explain exactly what diabetes insipidus is, what changes it causes to our patients, and how we diagnose, treat, and care for them.

So what IS diabetes insipidus, anyway?

Diabetes insipidus (water diabetes) is an uncommon endocrine disease caused by dysregulation of antidiuretic hormone (ADH). 

If we think back to our renal series and in particular episode 11 (which feels like SO long ago now!), ADH works in the nephrons in the kidney - specifically in the distal tubules - where it reabsorbs large volumes of water from the ultrafiltrate, concentrating the urine. 

When this ADH activity becomes dysregulated, water cannot be effectively reabsorbed from the glomerular filtrate - causing the patient to pass large volumes of dilute urine.

There are two forms of diabetes insipidus - central DI, which affects the pituitary gland, and nephrogenic DI, which affects the kidney.

Let’s start with central DI…

Central diabetes insipidus is caused by reduced secretion of ADH from the posterior pituitary gland. This means the patient doesn’t have enough ADH to reabsorb water in the kidney.

Central or hypophyseal DI develops due to compression and destruction of areas of the pituitary gland itself, either due to cysts, granulomas, traumatic injury or pituitary tumours (which may be endocrinologically active - aka able to secrete hormones - or inactive).

These lesions interrupt the transport of ADH from the hypothalamus, where it is produced, to the pituitary gland, where it is released.

What about nephrogenic DI?

Nephrogenic diabetes insipidus occurs when the kidneys can’t appropriately respond to ADH. In these cases, ADH is produced and released normally from the pituitary gland, but when it reaches the distal tubules in the nephrons, it doesn’t work.

Primary nephrogenic diabetes insipidus is very rare and is a congenital disease. More often, we see secondary nephrogenic DI - due to underlying diseases including:

  • Chronic kidney disease

  • Pyometra

  • Hypokalaemia

  • Hyperadrenocorticism (Cushing’s disease)

  • Hypoadrenocorticism (Addison’s disease)

  • Hepatic failure

  • Hypercalcaemia

  • Certain medications (e.g. tetracycline antibiotics)

What signs do we see in these patients?

Regardless of the mechanism behind the patient’s diabetes insipidus, the main clinical signs are the same - marked polyuria and polydipsia.

As our patients lose the ability to concentrate their urine, they become polyuric, passing large volumes of dilute urine. They then drink massive amounts to compensate for their polyuria.

The urine these patients pass is hypotonic - less concentrated than plasma - and this doesn’t change if the patient is dehydrated. If we were to measure the osmolality (the balance of water and electrolytes in a solution) of the urine, it would be below normal plasma osmolality (300 mOsm/kg), regardless of the patient’s water intake.

If the patient is deprived of water (for example, because the client thinks the patient is drinking too much and limits their intake), they’ll present with marked dehydration, with signs including:

  • Skin tenting

  • Tacky/dry MMs

  • Sunken eyes

  • Acute weight loss

As their dehydration progresses, they can also present with signs of hypovolaemia, with changes to their perfusion parameters - their heart rate, blood pressure, pulse quality, mucous membrane colour and capillary refill time.

So you think your patient has DI. How do you diagnose them?

Diagnosis of diabetes insipidus is based on chronic polyuria, which doesn’t respond to dehydration and isn’t caused by primary renal disease. 

To begin with, we want to perform routine diagnostics to exclude other causes of PUPD, including:

  • Full biochemistry and haematology

  • Complete urine analysis, including chemistry, SG, sediment examination, UPC and culture

  • Abdominal ultrasound

  • Adrenal function testing (e.g. basal cortisol to exclude hypoadrenocorticism)

What about the water deprivation test?

You may have heard of the water deprivation test to diagnose diabetes insipidus. Whilst it can be performed, it usually isn’t - because it’s tough to do accurately and carries a high risk of dangerous dehydration. 

Instead, we tend to measure water intake and urine output (as best we can) in the hospital (if we’re keeping the patient in), ask our clients to keep a water diary, and trial treatment with exogenous ADH, aka desmopressin.

Let’s talk about treating DI.

We treat central diabetes insipidus with a synthetic ADH analogue called desmopressin acetate, aka DDAVP. It’s available as a nasal solution or tablets, and drops of the solution are typically applied to the conjunctival mucosa, or tablets given PO.

The patient usually undergoes a trial period where their response to treatment is assessed as part of their diagnosis before dosage is adjusted as needed.

Trialling ADH response

To trial response to ADH, the client measures the patient’s free-choice water intake over 24 hours for 2-3 days and collects daily urine samples for SG analysis. Synthetic ADH is then administered while the client continues to monitor water intake and collect urine samples.

Water intake and urine SG are compared between the treatment and pre-treatment periods. Dogs with central DI should respond well to treatment, with increased urine SG and decreased water intake noted.

What about treating nephrogenic DI?

DDAVP treats central DI, where the body isn’t able to release sufficient ADH. But what about neprhogenic DI? Our goal is to manage any underlying conditions (e.g., renal or adrenal disease) to improve kidney response to ADH. Unfortunately, there’s not much we can do in patients with primary or congenital nephrogenic DI, and the prognosis is poor, but thankfully, those cases are very rare.

What about nursing a DI patient?

Most patients with DI are relatively stable unless they’re significantly dehydrated on presentation.

Our nursing care mainly aims to monitor fluid balance and treat or prevent dehydration in the hospital.

Hydration and perfusion status should be assessed regularly, including heart rate, pulse quality, MM/CRT, body weight, skin tenting, eye position and MM moistness or dryness. Fluid therapy should be administered at an appropriate rate until these parameters normalise.

Free water should always be available. These patients are polydipsic, and limiting their water intake is absolutely contraindicated. If water is left outside of the kennel, dangerous dehydration can result. Water intake should be measured since this provides us with important diagnostic information, but it should never be limited.

Since these patients are markedly polyuric, regular toileting opportunities should be provided. Dogs often require walking every 1-2 hours with regular bed checks.

Once the patient has been discharged, client advice and support are vital aspects of nursing care. Clients should know never to limit water intake and to ensure large volumes of water are continually available. They should also be taught how to measure water intake at home and advised to keep a water diary, especially in the early stages of treatment.

So there you have it - that’s diabetes insipidus in a nutshell! Though these patients aren’t in the hospital for long, we play an essential role in their monitoring and care - especially when it comes to maintaining fluid balance and providing client advice and support. But we can only do this when we understand DI and how it affects our patients - which you now do after today’s episode!

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

  • Merrill, L. 2012. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell