Veterinary Internal Medicine Nursing

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38 | How to give great care to your insulinoma patients as a vet nurse

An insulinoma is a malignant tumour of the endocrine pancreas, causing sudden insulin release.

We might not see these cases as often as our other endocrine diseases, but that doesn’t mean they don’t need careful nursing - in fact, spotting the signs of this disease and performing careful diagnostics is really important.

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So, what is an insulinoma?

An insulinoma is a malignant tumour of the pancreatic islets that affects the beta cells, which are responsible for producing and releasing insulin.

Pancreatic tumours are either exocrine or endocrine in origin. Exocrine pancreatic tumours include acinar or ductal carcinomas, and since they don’t involve the endocrine tissue, we won’t see changes like hypoglycaemia, for example, in those cases.

Endocrine tumours, on the other hand, involve the cells inside the islets of Langerhans, such as the beta cells.

Insulinomas are capable of suddenly releasing insulin, causing sudden and often profound hypoglycaemia.

Which patients get insulinomas?

Dogs of any breed, age, and sex can be affected, but insulinomas are more commonly seen in large breeds. In humans, females are overrepresented, but dogs have no sex predilection. Insulinomas are possible in cats, but they are very, very rare.

Lastly, whilst humans tend to get benign insulinomas (adenomas), this isn’t the case in animals. All insulinomas are considered malignant, with most spreading to organs such as the liver, the omentum and the lymph nodes by diagnosis.

What signs do we see in these patients?

To understand why we see the clinical signs we do in our patients, we first need to examine how glucose homeostasis works in the body.

Let’s talk glucose

When carbohydrates, fats and proteins are ingested, they provide energy for cellular metabolism for around 4-8 hours. After this time, the liver provides this energy for cellular processes since the liver is a significant site of glucose storage and release in the body.

The liver stores glucose as glycogen. When additional glucose is needed, these stores can be tapped into through glycogenolysis.

Once the glycogen stores are depleted, other substances, such as amino acids and fatty acids, provide glucose for energy through gluconeogenesis.

Usually, when a patient eats, their glucose exceeds the normal range, and the pancreatic beta cells release insulin. This allows glucose to be used as energy and stored as glycogen. The body detects the dropping glucose level and shuts off insulin secretion before hypoglycaemia occurs.

And what happens when our patients become hypoglycaemic?

Hypoglycaemia is a particularly dangerous condition for the body since the central nervous system needs glucose to function. The brain is actually the body’s largest user of glucose, requiring around 50% of the body’s glucose to function.

The body, therefore, has several in-built ‘protection mechanisms’ to prevent sustained hypoglycaemia:

  • Insulin secretion stops

  • Glucagon secretion increases

  • Catecholamine (e.g. adrenaline, noradrenaline) secretion increases

  • ACTH secretion increases

  • Cortisol secretion increases

  • Growth hormone secretion increases

These counter-regulatory hormones are released rapidly in response to hypoglycaemia, restoring an adequate supply of glucose to the brain. Glucagon and catecholamines increase first, followed by cortisol and growth hormone.

Within minutes of release, glucagon rapidly increases glucose breakdown from stored glycogen in the liver. Catecholamines like adrenaline stimulate glucose breakdown from the liver’s glycogen stores and stop skeletal muscle cells from using glucose.

So, what signs do we see if our patient is hypersecreting insulin from the tumour cells and experiencing periods of hypoglycaemia?

Well, the signs are usually episodic. Shortly after that spike in insulin release, the body detects hypoglycaemia and releases all those counter-regulatory hormones.

This means our patients usually experience short periods of acute neurological signs, which spontaneously resolve. Common presenting signs include:

  • Seizures

  • Weakness

  • Collapse

  • Ataxia

Patients may also be clinically normal on presentation because their blood glucose is often within normal limits when they arrive.

You suspect your patient has insulinoma - but how will you diagnose them?

Our diagnostic approach to these cases involves routine bloodwork, measuring insulin levels, and performing diagnostic imaging.

Let’s start with bloods

On biochemistry, the only consistent abnormality is hypoglycaemia, and due to the effects of those counter-regulatory hormones, we may not even see that if the patient isn’t actively showing clinical signs on presentation.

We need to measure serum insulin levels, but we must do this when our patient shows clinical signs. If you take the sample when they don’t have hypoglycaemia, you could get a false normal insulin result.

We need a paired glucose and insulin sample when our patient is showing clinical signs to diagnose the condition—documenting a combination of hypoglycaemia with increased insulin levels.

We also need to rule out other medical conditions that can cause hypoglycaemia, such as:

  • Addison’s disease

  • PSS/Hepatic failure

  • Sepsis

  • Xylitol toxicity

  • Small/toy breeds, young puppies

When sampling these patients, it’s also essential to separate and process the blood very quickly (or use a fluoride oxalate tube for your glucose measurement). This is important because RBCs will continue to consume glucose in vitro, causing a falsely low result.

And what about imaging?

Insulinomas are usually tiny nodules in the pancreas (<3cm), making them hard to spot without advanced imaging. Radiographs, for example, are generally not helpful, except for chest X-Rays later in the patient’s disease, where pulmonary metastases are more likely.

Ultrasound is preferred, but due to the small lesion size, a ‘normal’ ultrasound can still be seen.

For this reason, CT is the preferred imaging modality. It’s more sensitive at detecting the primary lesion and any metastases.

Top tips for diagnosing your insulinoma patients

Firstly, don’t give any IV glucose before pulling the patient’s blood samples—it will prevent you from getting a diagnosis on your bloods. If the history fits, grab the blood first and then pop in the glucose—you can very quickly and easily grab your samples via the patient’s IV catheter without it significantly delaying stabilisation.

Lastly, cage rest can also reduce or resolve hypoglycaemia, as patients who are resting will use less glucose compared with their normal daily activities and exercise.

So that’s your diagnosis. How will we treat and nurse this patient?

Well, the way we manage our insulinoma patients will depend on whether they require emergency stabilisation of acute or prolonged hypoglycaemia or whether they’re having surgery.

Let’s look at our hypoglycaemic emergency patients first

When treating these patients, our goals are to prevent acute hypoglycaemia, collect a diagnosis, minimise the patient’s clinical signs, and establish how rapidly the patient needs surgery.

Stabilisation involves giving IV glucose supplementation—usually via a CRI at a 2.5-5% concentration. Ideally, we’d want to avoid giving frequent boluses as this can cause spikes in glucose and, in turn, stimulate insulin release.

In severe cases where hypoglycaemia persists despite a dextrose CRI, a glucagon infusion can be given. 

And then there’s surgery…

The goal of surgery is to debulk the pancreatic tumour whilst minimising postoperative complications like pancreatitis. This is achieved by a partial pancreatectomy.

Surgery is generally not curative (in most cases) but does improve response to chronic medication and prolong survival times.

When preparing these patients for surgery, it’s important to continue glucose supplementation during the pre-anaesthetic fasting period and throughout the GA—measuring blood glucose regularly and keeping it above 2.2mmol/L (40mg/dL) throughout.

I’d consider placing a central venous catheter or sampling line (assuming the clinician agrees with this) under that anaesthetic to facilitate regular blood sampling - and in the case of a central line, allow concentrated glucose solutions to be administered.

Another alternative is to place a continuous glucose monitor, but these have a lag time and are less useful in patients with rapidly fluctuating glucose levels.

Postoperative complications are common in partial pancreatectomy patients and include things like pancreatitis, diabetes mellitus and sustained hypoglycaemia. These should be managed accordingly (in the case of diabetes mellitus, after sufficient time with consistent hyperglycaemia to ensure it is a permanent change).

What about chronic medical management?

Many dogs will do well without surgery for months or years. In these cases, patients require medications such as prednisolone (an insulin antagonist) or, very rarely, diazoxide or somatostatin. 

Alongside medication, clients should feed their dog frequently (3-6 times per day) to maintain a constant source of calories and avoid insulin peaks.

What about long-term nursing care?

Much of our long-term role is to provide client education and support. Our clients will often see their pet’s neurological signs at home, which can be distressing, so managing expectations and providing education on at-home first aid (where needed) is essential.

In most cases, the condition is lifelong, as surgery is generally not a permanent fix but does make long-term medical management easier. Without surgery, our patient’s signs will persist—however, these are usually manageable for months to years.

So there you have it—a guide to treating and nursing insulinomas in your dogs! This disease can be hard to spot if the patient isn’t hypoglycaemic at the time of presentation, but by being aware of the signs, knowing when the right time to take samples is, and knowing what care these patients need, we can make sure they get the best possible nursing care.

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

References and Further Reading