Veterinary Internal Medicine Nursing

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52 | Four things every vet nurse needs to know about GI ulcers in dogs and cats

Laura Jones

Today, we’re talking about another common gastrointestinal disease - GI ulceration.

From simple NSAID overdoses to patients with nasty ulcerative chronic GI diseases, we see this disease more often than you might think - and in severe cases these patients can present with marked anaemia from GI blood loss, even requiring transfusions.

Today, we’re exploring what causes GI ulceration, its impact on our patients, and the four things we can do as vet nurses to give them great care.

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So, what is a GI ulcer, and what happens when our patient gets one?

A gastrointestinal ulcer is a sore, eroded area in the lining of the GI tract. They’re usually present in the stomach, but the duodenal mucosa can also be affected. These sores cause bleeding and, in severe cases, can even perforate and cause the gastrointestinal contents to leak into the abdominal cavity.

To understand what causes an ulcer, we must first look at how the GI tract should work.

The gastric mucosa has several defence mechanisms to protect itself from the harsh contents inside the stomach. The mucosal layers are tightly sealed and covered with a thick layer of mucous. This mucous contains lots of bicarbonate, an alkaline substance that helps to neutralise the acidic stomach contents and prevent damage to the underlying cells.

Blood flow to the stomach wall is also increased, so any acid that comes into contact with the mucosal cells is quickly cleared.

Gastric acid contains high levels of hydrogen and chloride and has a pH of 1-2 at its maximum, making it very acidic. Usually, the defence mechanisms of the gastric mucosal barrier and the acidic stomach contents counteract each other, allowing patients to eat, break down and digest food without causing GI damage.

However, many drugs and diseases can impact this normal gastric mucosal barrier - causing ulceration.

When a defect in the GI mucosal barrier occurs, it causes a self-perpetuating cycle of gastrointestinal damage. 

The defect in the mucosal barrier allows stomach acid, bile acids and enzymes to attack the epithelial cells lining the mucosa, causing inflammation and cell death. 

The inflammation this causes can, in turn, cause further acid secretion, and the cycle continues.

Alongside this, the inflammation also decreases blood flow to the affected area—meaning that in addition to the acidic damage, we also have reduced blood and oxygen supply to that tissue, increasing the risk of ischaemic damage and necrosis.

GI ulceration is primarily a canine disease, though we can also see it in cats (usually less commonly, but in true vet nurse style, my cat Mavis has had a few of these secondary to severe IBD and her portosystemic shunt—why is it always vet nurse cats?!).

Ok, that’s what an ulcer is - but what causes them?

The most common causes of GI ulcerations are NSAID administration, neoplasia and hepatic disease, and the mechanisms behind each cause differ quite a bit.

Let’s start with NSAIDs

Non-steroidal anti-inflammatory drugs (aka NSAIDs) can cause direct damage to the GI mucosa and can decrease local prostaglandin production. Though some prostaglandins are involved in inflammation (which is why we use NSAIDs), others are beneficial, particularly those in the GI tract and kidney. When we remove some of those beneficial prostaglandins, we can decrease GI mucosal blood flow and limit the mucosa’s ability to protect itself from that acidic stomach content.

Additionally, recent evidence suggests that these drugs can impair ulcer healing by impacting granulation tissue formation in the ulcer bed and epithelial cell reproduction.

Does this mean that NSAIDs are all unsafe?! No—we know that many patients benefit from them. But it does mean we need to be selective about the prostaglandins we inhibit (which many of our NSAIDs are) and use these drugs carefully—only administering them with food and not to patients with GI signs.

And then there’s neoplasia.

Being a medicine nurse who rarely uses NSAIDs, most of my ulcer patients sadly tend to fall into this category.

Primary GI tumours including:

  • Lymphoma, neoplasia of the GI lymphatic tissue

  • Adenocarcinoma, neoplasia of the GI glandular tissue

  • And leiomyoma and leiomyosarcoma, neoplasia of the smooth muscle tissue in the GI tract

Can all cause ulceration due to their local effects. Some tumours also exhibit paraneoplastic effects on the GI tract, increasing gastric acid secretion. Examples of this include mast cell tumours and gastrinomas, which are tumours of the gastric-acid-secreting cells in the stomach wall.

Neoplasia is the most common cause of GI ulceration in cats, particularly lymphoma and adenocarcinoma.

What about hepatic disease?

Several hepatic diseases, including portosystemic shunts and acute hepatic injuries, are associated with gastroduodenal ulceration in dogs and cats. However, the mechanism behind this is not entirely understood.

Potential causes include increased gastric acid secretion and alterations in gastrointestinal blood flow. In portosystemic shunt patients, for example, venous drainage from the GI tract is reduced since the portal vein (the vessel that carries this blood through the liver for processing) is partially bypassed. When pressure inside this vessel increases, GI bleeding can result.

What about other causes?

Various other causes of gastric ulcers have been described, including:

  • Hypoadrenocorticism (Addison’s disease)

  • GDV,

  • Gastrointestinal foreign bodies,

  • Glucocorticoid administration,

  • Infectious GI diseases (eg. parvovirus),

  • Severe inflammatory bowel disease/chronic enteropathy,

  • Renal disease causing uraemia,

  • Neurological disease.

There is also some evidence that working dog breeds are at an increased risk of developing GI ulceration. However, more studies are needed to confirm this.

So what signs do we see when a patient has a GI ulcer?

The most common sign in dogs and cats with GI ulceration is vomiting. This may or may not contain fresh blood, or digested blood which contains multiple dark flecks, described as a ‘coffee-grounds’ appearance. However, the absence of blood in the patient’s vomit does not exclude an ulcer, and swallowed blood from the nose or nasopharynx may mimick GI haemorrhage - so we need to interpret the patient’s clinical signs with care.

Other signs include:

  • Melena (if significant GI haemorrhage is present),

  • Anorexia,

  • Weight loss,

  • Hypersalivation,

  • Abdominal pain.

If severe haemorrhage is present patients may present with anaemia and acute signs of transfusion-dependence, including tachycardia or bradycardia, bounding or poor pulses, and pale MMs.

And if the ulcer is severe enough to cause perforation, marked abdominal pain, peritonitis and signs of septic shock may be apparent.

We also know that several underlying diseases can cause GI ulceration, including hepatic and renal disease. So, in addition to the signs we’ve already discussed, we may see additional signs consistent with the patient’s underlying disease - such as PUPD and halitosis in a patient with uraemic renal disease.

How do we diagnose these patients?

Let’s start with bloods.

Bloodwork doesn’t tell us specifically that our patient has an ulcer, but it can give us some indication of the underlying cause and tell us how anaemic our patient is from GI bleeding.

Patients with uraemic ulcers will have azotaemia on their biochemistry, and patients with portosystemic shunts, for example, may have high ammonia and a decreased BUN. 

BUN itself can also be increased secondary to GI bleeding, so this can also be an indicator of GI ulceration.

And then there’s imaging

Abdominal radiographs are generally not helpful when diagnosing GI ulcers but can be used to rule out GI obstruction in potential foreign body patients.

Ultrasound can be used to identify intestinal masses and foreign bodies as well as indicate IBD-like changes, and in some cases, ulcers can be visualised with ultrasound.

Endoscopy is required to visualise and definitively diagnose GI ulceration. Ulcers appear as focal areas of erosion in the gastric or duodenal mucosa. They may be actively bleeding, or they may be in various stages of healing.

We can also use that same endoscopy to collect samples and identify any underlying GI disease - however, we need to be very careful with where we sample from. Do not biopsy an ulcer, as you could very easily perforate it. Instead, we tend to sample the safest-looking area near the margin of the ulcer, where the perforation risk is lower.

Just a quick note from me regarding GI sampling here before we move on - be aware that some GI tumours, for example, can’t be diagnosed with endoscopic sampling, so depending on what the vet thinks the most likely diagnosis is, we may need to perform surgery to take full-thickness GI biopsies instead.

Ok, so that’s our patient’s ulcer diagnosed. But how will we treat and care for them?

#1: Cardiovascular stability above all.

We know that GI ulcers bleed, which can be severe in many cases. Patients can easily either present with or become transfusion-dependent as a result of ongoing gastrointestinal bleeding, so keep a close eye on their vital signs and intervene at an early stage if you spot signs of transfusion dependence.

Make sure you’re assessing:

  • Heart rate,

  • Blood pressure,

  • Pulse quality,

  • MM colour,

  • CRT.

Regularly, and if you’re concerned, alert the vet. You’ll likely need to check the PCV, and blood type of your patient and reach for packed red blood cells or whole blood if they’re unstable.

The other common complication of GI ulceration that can destabilise our patient is perforation. If an ulcer perforates, septic peritonitis can quickly result. Sepsis causes vasodilation and distributive shock, impacting all of those parameters we’ve just listed. Be on the lookout for abdominal fluid, increasing abdominal pain, bright red MMs and a rapid CRT in these patients.

#2: Reduce that acid.

The mainstay of ulcer treatment is with antacids. Usually, we use proton pump inhibitors such as omeprazole or pantoprazole. These reduce gastric acid secretion, decrease GI acidity, and reduce acidic mucosal damage.

We don’t tend to use H2-blocker antacids such as famotidine or ranitidine any more (unless you’re my cat who gets diarrhoea on omeprazole… thanks, Mavis) as these are not as effective as PPIs. We also don’t combine these antacid agents since this can decrease their effectiveness.

Another quick note regarding antacids - we don’t want to discontinue their use too suddenly, as we can get rebound hyperacidity - for this reason, we tend to wean patients off of them.

#3: Protect the ulcer.

Another common drug you’ll likely reach for in your ulcer patients is sucralfate, aka antepsin. This cytoprotective drug combines sucrose and aluminium hydroxide, which binds to ulcerated GI mucosa and facilitates healing.

It protects the cells, stimulates mucous and bicarbonate secretion - both components of that protective GI barrier - and reduces cell death.

This drug also inhibits absorption and requires time to sit against that ulcer. For this reason, we need to give this at least 1-2 hours apart from food or other oral medications.

Other drugs, such as misoprostol (cytotec), can also be used in patients with GI ulceration. This is a prostaglandin analogue with both cytoprotective and acid-inhibiting properties.

#4: Care for the whole patient.

Of course, we will stabilise our patients and treat their ulcers, but our care doesn’t stop there - we need to provide supportive care and manage the whole patient, not just their presenting signs.

This includes:

  • Fluid therapy to treat dehydration associated with vomiting and anorexia

  • Antiemetics to manage nausea and vomiting

  • Assisted nutrition where anorexia persists

  • Elimination management and skin and coat care in patients with melena or diarrhoea

  • Analgesia in patients with abdominal pain

And much more.

So there you have it - an overview of gastrointestinal ulcer disease in dogs and cats! We see this more commonly than you might think, and its effects can be severe - with severe anaemia and even septic peritonitis recognised complications of GI ulcers. Careful monitoring alongside medical treatment and supportive care is needed - and thankfully, for us, that’s one of our biggest strengths as vet nurses, as we’re often the eyes and ears on our patients!

I’d love to know a GI ulcer case you’ve seen and how you managed them - drop me a DM on Instagram and let’s chat!

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