56 | Help, my patient is losing protein! How to care for patients with protein-losing enteropathy

PodcastGastroenterology
Written By Laura Jones

Today we’re talking all about protein-losing enteropathy - quite possibly the worst chronic GI disease we see.

 

Though these patients are often severely unwell, they need a LOT of intensive nursing care and that means there are lots of skills we can use in the process. But what is PLE, and how does it affect our patients? Let’s take a look.

Protein-losing enteropathy (PLE) is not a specific disease itself, but is a syndrome seen in patients with severe GI disease.

Usually it’s seen in patients that have severe immunosuppressant-responsive enteropathy (as we discussed in episode 55) and lymphangiectasia - abnormal dilation of the lymphatic vessels that run through the intestines.

It can be seen in any patient with severe GI disease, though - including intestinal lymphoma, parvovirus, chronic intussusceptions, and even severe endoparasite infections in very young patients.

As the name suggests, PLE is characterised by protein loss across that diseased intestine.

These patients lose often significant amounts of plasma proteins - albumin and globulin - via their GI tract. The increased permeability in the diseased intestine causes those plasma proteins to ‘leak’ into the intestinal lumen and be lost via the faeces. The result? Our patients develop hypoproteinaemia.

PLE can cause hypoalbuminaemia - low circulating albumin levels - only, or a panhypoproteinaemia - where both albumin and globulin (and therefore total protein, since albumin + globulin = TP) levels are low.

Our plasma proteins are responsible for a whole host of vital functions in the body, including wound healing, immune function, regulating clotting and much much more. One of these functions is maintaining oncotic pressure, aka colloidal oncotic pressure or COP. This is the pressure that the large protein molecules exert inside blood vessels. This pressure ‘holds’ water inside the plasma, maintaining plasma volume and therefore circulating volume and in turn, blood pressure and cardiac output.

Which patients develop PLE?

PLE is primarily a canine disease, though we can see it (albeit rarely) in cats too. Any breed can develop the condition, but several breeds are predisposed, including:

  • Yorkshire Terriers

  • Rottweilers

  • Wheaten Terriers

  • Norwegian Lundehunds

  • German Shepherds

These patients have genetic predispositions for certain chronic enteropathies, for example Lundehunds are predisposed to developing lymphangiectasia, and as we mentioned in episode 55, GSDs and Yorkshire Terriers are predisposed to chronic enteropathies.

Though PLE in cats is rare, we can see it in cats with intestinal lymphoma or severe chronic enteropathy. Cats almost never develop intestinal lymphangiectasia or have intestinal parasite infestations that are severe enough to cause PLE, unlike dogs.

So that’s what PLE is and the patients we see it in. But what signs do we see?

Many of the clinical signs we see in our PLE patients are the same as our other gastrointestinal patients, because PLE is seen on top of existing GI disease.

Unless they’re presenting with acute intussusception or GI obstruction, patients typically have a chronic history of:

  • Diarrhoea

  • Vomiting

  • Melena

  • Haematemesis

  • Weight loss

  • Anorexia

On top of this, we see specific clinical signs associated with protein loss. 

Because PLE causes hypoalbuminaemia and albumin maintains oncotic pressure, when albumin drops, fluid can leak from the plasma into other areas of the body.

This can cause ascites (abdominal effusion), oedema and pleural effusion. And because plasma volume decreases, we may also see cardiovascular changes in severe cases.

These signs are usually only seen when albumin levels severely drop, to levels below 15g/L.

Another important complication of PLE is hypercoagulability. One of the proteins these patients can lose across their diseased GI tract is antithrombin III - a protein responsible for preventing excessive clot formation. 

This, combined with the low albumin levels and active intestinal inflammation, means our patients are at an increased risk of throwing clots. The signs we see depend on where those clots end up; clots affecting the peripheral vessels, cardiac vessels, visceral vessels (vessels supplying organs) and the central nervous system are reported in human PLE patients.

How do we diagnose PLE?

When it comes to diagnosing PLE we really need to diagnose two things - protein loss, and the underlying gastrointestinal disease causing that protein loss. This means that much of our workup is aimed at investigating the patient’s underlying gastrointestinal disease. 

Alongside this, we’ll need to rule out other causes of hypoalbuminaemia - such as protein-losing nephropathy (which if you want a blast from the past, we discussed all the way back in episode 15), and hepatic failure.

Like our other gastrointestinal diseases, we’ll diagnose our patients using a combination of:

  • Biochemistry and haematology

  • +/- Malabsorption testing (vitamin B12, folate)

  • +/- Faecal testing

  • Abdominal ultrasound

  • Gastrointestinal endoscopy with biopsies

Alongside these tests, we’ll need to evaluate coagulation status (ideally using thromboelastography or viscoelastic testing to document hypercoagulability) and perform urine analysis (to look for proteinuria indicating PLN).

Ascites or pleural effusion should be sampled and fluid analysis performed - low-protein fluid (known as transudate) is seen in hypoalbuminaemic patients with body cavity effusions.

A diagnosis of PLE is made in patients with documented underlying gastrointestinal disease and evidence of hypoalbuminaemia +/- panhypoproteinaemia on bloods (not attributed to non-GI disease).

Ok, so that’s our patient diagnosed. But what about treatment?

Because a multitude of GI diseases can cause PLE there is not one single treatment protocol our patients need. Every patient has different needs and treatment is therefore tailored accordingly.

The goal of PLE management is to treat the patient’s underlying GI disease (and therefore prevent further protein loss) whilst providing supportive care and prevent complications associated with PLE (such as a thrombotic event).

Most of the PLE patients we see are dogs with a combination of severe immunosuppressant-responsive enteropathy/IBD and lymphangiectasia, so we’ll focus on those specifically for this episode.

Just like we mentioned last week, severe IBD will require aggressive immunosuppressant therapy. This usually begins with steroids, and an additional agent such as chlorambucil or cyclosporine may be added if the patient does not respond sufficiently on prednisolone alone.

We’ll also administer antithrombotic medications to counteract our patient’s hypercoagulability and minimise the risk of a thrombotic event. Drugs such as clopidogrel (a platelet inhibitor) and rivaroxaban (a clotting factor inhibitor) are commonly used.

We also need to provide aggressive supportive care, including:

  • Fluid therapy to correct dehydration from gastrointestinal losses

  • Analgesia to manage abdominal pain

  • Antiemetics (eg. maropitant, ondansetron) to manage nausea and vomiting and encourage voluntary food intake

  • Appetite stimulants (eg capromorelin) if needed once pain and nausea are under control

  • Prokinetics (eg metoclopramide) if needed to manage low GI motility and ileus

  • Binding agents (kaolin, bentonite clay) to firm faeces

And speaking of that supportive care, let’s talk about nursing these patients.

Nursing the PLE patient can be incredibly intensive. These patients often have significant ongoing diarrhoea +/- vomiting, have marked weight, body and muscle condition loss and need careful nutritional support alongside general nursing care.

There’s a lot to think about when nursing the PLE patient, including fluid balance, nutrition, monitoring, vascular access, skin and coat care, managing eliminations, indwelling device care, sampling and much, much more.

Of these, there are two things I want to draw your attention to specifically - nutrition and elimination management.

Let’s start by looking at nutrition.

Careful nutritional management is essential in the PLE patient. Not only do these patients have an underlying gastrointestinal disease needing specific nutrition, but nutrition is going to be the main way we get our patient’s protein levels back up. So whilst we’re starting treatment and getting the GI tract into a healthier state, we need to be getting that protein back into our patients.

The specific nutritional requirements will depend on the patient’s underlying gastrointestinal disease, but in most cases, we opt for a highly digestible, complete and balanced, low-far or ultra-low-fat hydrolysed diet.

Limiting dietary fat intake decreases intestinal lymph flow and lymphatic vessel distension, thereby minimising protein loss - so opting for a low-fat diet is key.

If our patient has a concurrent chronic enteropathy, we’ll need to select a hydrolysed or novel-protein diet (that is also low in fat) to minimise that antigenic stimulation and inflammation in the GI tract, as we discussed in last week’s episode.

Alongside this, pre- and probiotics, fat-soluable vitamin supplementation and vitamin B12 supplementation are often required.

Most of these patients require an enteral feeding tube - they’ve got such severe disease that we can’t always reliably get sufficient calories into them, and they’re also on many oral medications, so a tube is handy for those, too! If you’re expecting your patient to be anorexic, placing an O tube whilst they’re under anaesthetic for diagnostics is a good idea.

Once your tube is in, start refeeding your patient at an appropriate percentage of their RER, depending on their history and your nutritional assessment.

And then there’s that diarrhoea to deal with.

These patients often have VERY severe diarrhoea. And with that, they’re often very sore, very scalded, and can easily become very dehydrated.

Skin and coat care might sound simple or minor compared to all of the complicated things we’ve discussed this episode - but I’d argue it’s even more important than many of them, since a soiled, scalded back end will be making your patient feel utterly miserable.

Regular bathing, tail dressing, barrier cream application and preventing self-trauma are essential - I chart these patients for back end checks as often as every hour in severe cases. And if they’ve got liquid diarrhoea, a faecal management system is a great way to keep them clean whilst measuring their fluid losses too.

There’s so much we can do to support these patients - and whilst they’re often intensive and challenging to care for, they’re incredibly rewarding, and allow us to use lots of our skills. From feeding tube placement and nutritional planning, to anaesthesia and endoscopy support, to faecal management, fluid therapy and all things in between, nurses really are at the centre of these patient’s care.


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

Laura Jones
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