118 | Just a bit of HGE? Here's what you REALLY need to know about acute haemorrhagic diarrhoea syndrome as a vet nurse

Acute haemorrhagic diarrhoea syndrome, or AHDS, is one of those conditions that arrives as a proper emergency - a really flat dog with severe GI signs, passing basically frank blood. And the care these patients need from us as veteinary nurses and technicians, especially in the early stages of their disease, makes a HUGE difference. 

It's also a condition where the evidence has really changed how we approach it. When I was in practice in earlier years, I just thought HGE wasn’t really that big of a deal - except for maybe the smell. These patients seemed to ‘mostly’ be stable. They had fluids, antibiotics, and supportive care, and went home a few days later, in most cases. But as I spent more time working in referral and emergency settings, I saw just how bad they could be - and just how much how we treat them (and nurse them) has evolved.

In recent years, we’ve changed the condition’s name, we’ve changed our understanding of what causes it, and we’ve changed how we treat it - especially when it comes to things like antibiotics.

And this means the way we approach these patients as veterinary nurses needs to change, too.

In this episode of the podcast, that’s exactly what we’ll be doing. We’re going to look at what AHDS is, what causes it, and how we can use more of our skills when supporting these patients.

Let's get started.

So, what actually is canine acute haemorrhagic diarrhoea syndrome, and how does it affect our patients?

AHDS is defined as a sudden onset of severe, bloody, watery diarrhoea. It’s accompanied by significant fluid losses, as fluid shifts into the intestinal lumen, and it’s often preceded by vomiting - so this may be the initial sign the caregiver notices.

The fluid losses we see with AHDS are often more significant than they might initially seem, and this is really important for us to understand as nurses and technicians.

Because these patients are not necessarily ones with marked outward fluid losses. They certainly can be, but many of the large fluid volumes these patients are losing are internal, meaning we can’t see or measure it. Often, these patients will shift fluid into the intestine - so they can be significantly dehydrated and even hypovolaemic, despite not passing significant volumes of diarrhoea.

These fluid shifts can happen rapidly - in fact, I had an AHDS patient not so long ago who went from looking relatively stable to showing signs of hypovolaemia over just a few hours. I was called back to wards to check on them, and found that they were increasingly lethargic, with tachycardia and bounding pulses - when the check I had done just a few hours before was normal. 

The bloody diarrhoea is what we all tend to notice more, because it looks outwardly quite scary and dramatic - but the fluid INSIDE the gut is often causing a bigger problem for the patient.

Why did we stop calling it HGE?

For years, this condition was called haemorrhagic gastroenteritis or HGE. And you'll still hear it called that all the time, even though that name is a little misleading.

The problem with that name is the G - ‘gastro’. We used to believe that this was a disease of the stomach and intestine, which, when we think about the presenting signs of vomiting and diarrhoea we often see in these patients, makes sense. 

But the stomach actually isn’t the problem. In fact, one study showed that dogs with AHDS have a completely normal stomach on endoscopy and biopsies, even in dogs who were actively vomiting blood. However, when they looked in the intestines, there was severe, necrotising, coagulative damage through the small intestine and - worst of all - the colon.

So AHDS far better describes what’s really happening inside our patient’s GI tract, and while you might think I’m being pedantic about terminology (especially given I’ve just spent the last few episodes doing this) this change does matter.

Because if I say ‘gastroenteritis’ the treatment that immediately jumps to mind is probably different. Maybe you think of antacids or gastroprotectants for example - and in reality these can actually make things worse, for example by impacting the microbiome as we discussed in episode 117.

So that’s what AHDS is (and what it isn’t) - but what causes it?

For a long time we thought AHDS was idiopathic - we didn’t know what the underlying cause was. But now, we’ve got more evidence, and with this a better idea of the pathogens involved.

AHDS is thought to be caused by a bacterial toxin - called NetF. It originates from a strain of Clostridium perfringens (type A). If you listened to episode 117 on the microbiome, you'll already know that C. perfringens is a completely normal resident of the gut - it lives quite happily in loads of healthy dogs, causing no trouble at all. In AHDS, though, certain strains overgrow - and these particular strains carry the gene for a pore-forming toxin called NetF.

'Pore-forming' pretty much does exactly what it sounds like - the toxin causes pores to form in the enterocytes - the cells lining the intestine. The holes in the enteral cell membranes mean these cells can’t hold themselves together normally, causing water to rush in, and the cell to burst.

This happens across the intestines, so you get significant amounts of intestinal lining basically dying off. And that intestinal necrosis, along with the huge shifting of fluid into the gut, is what causes the marked haemorrhagic diarrhoea we see in these patients.

What’s really interesting, though, is that the NetF toxin actually clears itself very quickly. Within about seven days of the dog presenting, it drops below the level our PCR tests can even detect - and that happens whether or not we treat it. 

And this is important to remember, because if the toxin causing the disease is self-limiting and clears regardless of treatment, antibiotics are not going to be indicated in the majority of these patients.

Another interesting point, and one I think we actually get wrong quite often, is that AHDS is not contagious. So technically we don’t need to isolate/barrier these patients - but to begin with, we can’t be sure that AHDS is the true cause for the patient’s signs. So until things like parvo, giardia and other infectious causes have been ruled out, barrier nursing will be indicated. Sometimes these patients will end up neutropenic, so at increased risk of infection, and if this is the case, they’ll need to be barrier nursed for their own protection - it all depends on the individual patient.

OK, so that’s what AHDS is, and what causes it. But which patients get it, and what signs do they present with?

We typically see AHDS in young to middle-aged, small or toy breeds - though one study found that Labradors were actually the most common breed presenting with AHDS, so we do see this in larger breeds too.

Interestingly, AHDS seems to be more prevalent in the winter, with suggestions that cold weather is associated with the disease. And diet changes or scavenging does not seem to be associated with it, which goes against what many of us thought for a long time.

Patients typically present with an initial history of vomiting, followed by profuse, watery, bloody diarrhoea, often described as having a ‘pberry jam’ type appearance.

Alongside this, patients will be lethargic, have varying appetite changes, and significant fluid balance disruption, even in the absence of external fluid losses.

As I touched on before, the fluid changes can happen so quickly in these patients than the external signs of dehyration - the prolonged skin tent, or dry MMs - haven’t had chance to keep up. So rather than focusing solely on the ‘traditional’ signs of dehydration, perfusion is the thing we need to prioritise here.

Checking things like heart rate, pulse quality, mucous membrane colour and CRT, alongside things like mentation and blood pressure, is really important. Look for tachycardia and bounding pulses, as these indicate compensatory hypovolaemia and are often an early change we’ll see in these patients.

Interestingly, these patients are also not typically pyrexic. Their temperature is typically normal or slightly low - so if the patient is pyrexic, this should raise concerns for things like sepsis.

How is AHDS diagnosed, and how do we fit into this as veterinary nurses?

AHDS is a diagnosis of exclusion. We need to rule out things that mimic it, while assessing the patient’s overall health and using things like blood results to guide treatment and stabilisation.

Common diagnostics include PCV and total solids, venous blood gas analysis, routine biochemistry and haematology, and potentially GI imaging, eg via ultrasound.

We often see a relative increase in PCV in these patients, since lots of fluid moves from the intravascular space and into the gut. This increased PCV sits in the face of a normal or even low (often low) total solids, because protein leaks through the diseased gut wall.

So while in a traditionally dehydrated patient we’d expect a high PCV and TS, we don’t see that with AHDS.

We’ll also use our diagnostics to exclude parvo, parasites, Addison’s disease, GI foreign bodies, and other causes of diarrhoea, before the vet arrives at a diagnosis of AHDS and begins to think about treatment.

How do we treat and nurse patients with acute haemorrhagic diarrhoea syndrome?

These patients require often intensive treatment and supportive care, but usually for short periods. If we catch AHDS early and treat it properly, most dogs recover within 24-72 hours, with low mortality rates of <10% with appropriate hospitalisation and treatment.

And the most important treatment is fluid therapy.

These patients need intensive fluid support with a balanced crystalloid solution such as Hartmann’s. We need to resuscitate hypovolaemia first, then rehydrate the patient, considering maintenance and ongoing losses too.

And (yes I know I’ve said this a lot) - those ongoing losses may not be as obvious as they initially seem, as most of the loss is happening inside the patient, rather than externally. So yes, we need to quantify things like diarrhoea production, but also, this is a great argument for things like serial POCUS, looking at intestinal content. And this is an area we’re ideally placed to monitor as RVNs. Alongside this, weighing these patients regularly is really important, because acute weight changes are typically associated with fluid balance rather than things like nutritional status.

Alongside fluid therapy, we need to consider electrolyte supplementation. Hypokalaemia, for example, is common and electrolytes will need to be regularly monitored and supplemented as needed.

Hypoproteinaemia is also common in these patients, and where this is the case, we can see further shifts in fluid balance - for example oedema, and third-spacing of fluid into body cavities.

What else do we need to consider?

Alongside fluid therapy, supportive care is a huge part of treatment. These patients may need antiemetics, anti-nausea medication, analgesia, etc as needed, with careful monitoring of things like pain and nausea levels.

Perhaps more importantly than what we do use is what we do NOT use. Antacids like omeprazole, and antibiotics, should not routinely be used in patients with AHDS. They don’t have significant benefit, and we know they cause significant disruption to the microbiome - which, in the case of antibiotics, can persist long past the diarrhoea.

Multiple studies (which I’ve included in the references within the show notes, if you want to read them) have investigated the use of antibiotics in AHDS patients, without significant benefit. 

Interestingly, in most cases, the liver will actually mop up translocated bacteria, so even if bacterial translocation is suspected across the diseased gut, antibiotics may not be needed.

That being said, if a patient is not improving on supportive treatment and fluid therapy, or there’s evidence of sepsis or systemic infection, antibiotic use is indicated. So patients who have a band neutrophilia, neutropenia, immunocompromise, or who is not responding to appropriate first-line treatment.

And then there’s nutrition.

Just like most other GI diseases, early enteral nutriton is a vital consideration for AHDS - and one we’re ideally suited to manage as nurses and technicians.

We want to get food in to that gut, as early as possible, using a highly digestible diet. By feeding the gut, we can actually help that lining heal, support the GI barrier, and feed the microbiome.

If the patient won’t eat sufficient volumes volunarily, a NG tube is a great option for these patients - assuming their vomiting is appropriately controlled.

Alongside this, regular tempting to eat, calculating and quantifying caloric intake, and regular reassessment of nutritional status, is a vital part of our role as RVNs.

What happens to these patients long-term?

Interestingly, we know that AHDS has a far bigger impact on our patients than ‘just’ their period of hospitalisation.

We usually think that AHDS is a scary few days of intensive care, and then a quick recovery (or hopefully a quick recovery). And that’s what it looks like - the dog goes home, and their signs improve.

But actually, we now know that many of these patients will go on to develop chronic GI signs in later life.

Studies have shown that around 30% of patients will have recurrent GI signs, compared to 14% of matched control dogs - so these patients actually have twice the risk for chronic enteropathy in the future.

The theory behind why this happens is that the gut barrier damage during the acute period of disease allows things like food proteins to cross the GI tract, where they’re exposed to the immune system. This is thought to impact the dog's tolerance to their own food - the immune system becomes sensitised, and you can end up with a chronic, food-responsive enteropathy in the future. And the dysbiosis we see in AHDS almost certainly feeds into it as well, because we know that lasting changes to the microbiome can occur.

For me, this is another reason why it’s so important to use antibiotics appropriately in these patients - because they can cause further changes to the microbiome, often for significantly long periods, which may increase the risk of further disease in the future.

So how can we use more of our skills to support AHDS patients as veterinary nurses?

AHDS is a disease that asks a lot of us as veterinary nurses and technicians. These patients might be with us for only a few days (hopefully!) but when they are, they need intensive nursing care and monitoring - and with this, there are lots of ways we can use our skills.

From triage and stabilisation, to initial diagnostics, careful monitoring, nutritional planning and support, and antimicrobial stewardship, our knowledge and skills make a real difference in the care of these patients.

And this care persists after hospitalisation. We need to talk to our caregivers about things like at-home nutrition, monitoring, and when to come back and see us - and we can continue this support remotely in the days following discharge.

So let’s recap what we’ve learned about AHDS, and our role in caring for these patients.

AHDS is far more than ‘just’ HGE - it’s an acute-onset condition causing severe changes to the intestine, but leaving the stomach mostly unharmed.

It’s characterised by severe intestinal wall necrosis, due to an overgrowth of Clostridium perfringens type A, and more specifically its NetF toxin.

Regardless of treatment, that toxin clears within about a week - explaining why we see an intensive, but short, duration of disease - and why we avoid antibiotics routinely.

Fluid balance is everything in these patients, even in the absence of outward losses. These patients can dump fluid into their intestines and go from stable to hypovolaemic in a matter of hours, and it’s careful nursing monitoring and intervention that allows us to spot this and correct it quickly.

Alongside this, we need to prioritise early enteral nutrition, restoring nutrition and healing back to the intestinal lining, and provide supportive care.

And, as always, we're ideally placed to help with every bit of this as veterinary nurses and technicians - from initial triage, all the way to discharge and beyond.

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

• Busch, K. and Unterer, S. (2022). Update on acute haemorrhagic diarrhoea syndrome in dogs. Advances in Small Animal Care, 3(1), 133-143. https://doi.org/10.1016/j.yasa.2022.06.003

• Cavanah, A. (2018). Acute haemorrhagic diarrhoea syndrome: the bloody truth [Online] Clinician’s Brief. Available from: https://assets.ctfassets.net/4dmg3l1sxd6g/52qgaWRxjiwoZtx6mBKBBU/aa689fdc55b3325852b3ba14d23ef415/CO_AcuteHemorrhagicDiarrheaSyndrome.pdf

• Collier, A. and Carnevale, J. (2025). Acute haemorrhagic diarrhoea syndrome in dogs [Online] MSD Veterinary Manual. Available from: https://www.msdvetmanual.com/digestive-system/diseases-of-the-large-intestine-in-small-animals/acute-hemorrhagic-diarrhea-syndrome-in-dogs

• Dupont, N., Jessen, L. R., Moberg, F., Zyskind, N., Lorentzen, C., & Bjørnvad, C. R. (2021). A retrospective study of 237 dogs hospitalized with suspected acute hemorrhagic diarrhea syndrome: Disease severity, treatment, and outcome. Journal of veterinary internal medicine, 35(2), 867–877. https://doi.org/10.1111/jvim.16084

• Reisinger, A., Stübing, H., Suchodolski, J. S., Pilla, R., Unterer, S., & Busch, K. (2024). Comparing treatment effects on dogs with acute hemorrhagic diarrhea syndrome: fecal microbiota transplantation, symptomatic therapy, or antibiotic treatment. Journal of the American Veterinary Medical Association, 262(12), 1657-1665. https://doi.org/10.2460/javma.24.03.0153

• Skotnitzki, E., Suchodolski, J. S., Busch, K., Werner, M., Zablotski, Y., Ballhausen, B. D., Neuerer, F., & Unterer, S. (2022). Frequency of signs of chronic gastrointestinal disease in dogs after an episode of acute hemorrhagic diarrhea. Journal of veterinary internal medicine, 36(1), 59–65. https://doi.org/10.1111/jvim.16312 

• Unterer, S., & Busch, K. (2021). Acute Hemorrhagic Diarrhea Syndrome in Dogs. The Veterinary clinics of North America. Small animal practice, 51(1), 79–92. https://doi.org/10.1016/j.cvsm.2020.09.007 

• Unterer, S., Busch, K., Leipig, M., Hermanns, W., Wolf, G., Straubinger, R. K., Mueller, R. S., & Hartmann, K. (2014). Endoscopically visualized lesions, histologic findings, and bacterial invasion in the gastrointestinal mucosa of dogs with acute hemorrhagic diarrhea syndrome. Journal of veterinary internal medicine, 28(1), 52–58. https://doi.org/10.1111/jvim.12236

• Unterer, S., Strohmeyer, K., Kruse, B. D., Sauter-Louis, C., & Hartmann, K. (2011). Treatment of aseptic dogs with hemorrhagic gastroenteritis with amoxicillin/clavulanic acid: a prospective blinded study. Journal of veterinary internal medicine, 25(5), 973–979. https://doi.org/10.1111/j.1939-1676.2011.00765.x