49 | How to easily care for patients with megaoesophagus as a vet nurse
Megaoesophagus can be a real headache to manage.
These patients need intensive nursing care, especially if they end up with complications like aspiration pneumonia on top.
But what is megaoesophagus, how does it impact our patients, and how can we give that intensive nursing care? We’ll dive into it all in this episode.
So, what IS megaoesophagus, and how does it affect our patients?
Megaoesophagus is a disease characterised by a loss of motor function in the oesophagus, causing dilation and a lack of peristalsis.
This loss of oesophageal motility can be severe, causing food and fluid to accumulate in the pouch-like dilated oesophagus. This means our patients don’t get sufficient nutrition and end up with often severe regurgitation.
We can see several types of megaoesophagus in our patients, including
Congenital megaoesophagus,
Acquired megaoesophagus,
Idiopathic megaoesophagus.
What is congenital megaoesophagus?
Thankfully, congenital megaoesophagus is less common than acquired megaoesophagus—which is good because it’s an incredibly sad condition, and there is little we can do about it.
It’s seen in young puppies and kittens. These patients are born with megaoesophagus, and clinical signs tend to emerge in most cases around the time of weaning.
We don’t know exactly why it happens, but we suspect that the oesophageal neuromuscular system takes longer to mature in these patients, causing abnormalities in oesophageal tone and motility.
There are certain breeds predisposed to congenital megaoesophagus, including
Wire-haired fox terriers,
Miniature schnauzers
German shepherds
Great Danes
Irish setters
Labrador and Golden retrievers
Siamese cats - though congenital megaoesophagus is very rare in cats compared with dogs.
How does this differ from idiopathic megaoesophagus?
Idiopathic megaoesophagus is also referred to as adult-onset primary megaesophagus. It’s a common form of megaoesophagus, especially in dogs.
It occurs due to a defect in the afferent neural pathway - i.e. the path through which the nerve impulse arrives at the oesophageal muscle. We usually see this disease in older dogs (8+ years old).
And then there’s acquired megaoesophagus…
Acquired or secondary megaoesophagus is caused by several diseases - most of which cause widespread or diffuse neuromuscular disease, affecting many areas within the body.
These diseases include:
Myasthenia gravis, an autoimmune condition where antibodies attach to to receptors in the neuromuscular junction and prevent nerve impulses from reaching the muscle
Polymyopathies, where inflammatory diseases affect the muscle, causing weakness and degeneration
And dysautonomia, a rare disorder of the autonomic nervous system
Patients with chronic oesophageal strictures or partial obstructions can also develop megaoesophagus below the narrowed area.
Other diseases linked to megaoesophagus include hypoadrenocorticism, lupus, hiatal hernias, oesophagitis, thymoma and specific toxicities.
So, what clinical signs do we see in megaoesophagus patients?
Regardless of the cause, we most commonly see regurgitation. With regurgitation, there is always a risk of aspiration and subsequent pneumonia, and if our patient aspirates their regurgitated contents, we’ll often see coughing, dyspnoea, and pyrexia.
These patients also can’t deliver sufficient nutrition to the rest of their GI tract, so we often see weight loss and poor body and muscle conditions.
Inappetence or anorexia may also be seen, associated with the discomfort of oesophageal dilation and regurgitation.
In patients with acquired megaoesophagus, we often see systemic signs - for example, generalised muscle weakness in patients with myasthenia gravis or concurrent respiratory or cardiovascular signs in dysautonomia, as the autonomic nervous system also controls heart rate and breathing.
And how do we diagnose these patients?
Diagnosis is usually made based on a combination of clinical history, physical examination findings and diagnostic imaging, followed by specific testing to identify an underlying cause where one is present.
Let’s start with bloodwork.
We don’t tend to see any particular changes associated with megaoesophagus in our blood results - though we may see a leukocytosis in aspiration cases and elevated CK levels in polymyopathy patients.
We often measure C-reactive protein (aka CRP) in aspiration pneumonia patients as a marker of infection, so this is often added to in-house or external biochemistry panels and repeated during treatment as needed.
Patients with myasthenia gravis require acetylcholine receptor antibody measurement for diagnosis - these antibodies bind to the receptors in the neuromuscular junction, blocking nerve impulses from reaching the muscle.
And what about imaging?
Radiography or fluoroscopy is performed to document the megaoesophagus.
If you’re using plain radiography, a conscious left lateral view of the chest is preferred since it is easier to see the oesophagus in this view. Dilation can be hard to spot without contrast, so barium is often used to highlight the dilated oesophagus.
When doing this, we need to be careful to prevent aspiration - we know that aspiration is a risk in these patients, and feeding them a barium meal and laying them in lateral recumbency will increase this risk further.
If there is a chance your patient could have an oesophageal rupture, barium is contraindicated - instead, iohexol is used, as this is a sterile and water-based contrast medium.
Aside from radiography, fluoroscopy is commonly used to diagnose these patients. Fluoroscopy is essentially a live video x-ray - it’s a dynamic tool where we can watch a patient eat a barium-impregnated meal and record this in real-time, allowing us to determine how much peristalsis is occurring in a patient’s GI tract.
So that’s the diagnosis - but how do we treat these patients?
Well, the treatment options depend on the underlying cause of the patient’s megaoesophagus.
Patients with congenital and idiopathic megaoesophagus have no specific treatment to ‘fix’ their megaoesophagus. Instead, our management aims to provide supportive care and prevent aspiration (or treat it where it’s already present).
Patients with acquired megaoesophagus require supportive care and management of any aspiration pneumonia present and, alongside this, treatment of their underlying disease.
These treatments include pyridostigmine to treat myasthenia gravis, immunosuppressant medications in polymyositis, and dilation of oesophageal strictures or removal of oesophageal foreign bodies.
Managing megaoesophagus supportively
Megaoesophagus patients require adapted feeding - feeding an appropriate consistency diet from a height and holding them up for 15-20 minutes after each meal to aid food movement into the stomach.
In practice, we often do this manually, either holding patients up ourselves or using a chair to support them. There are purpose-made feeding ‘chairs’ called Bailey chairs for megaoesophagus patients, but these are made-to-measure and specific for the size of the affected patient.
If the patient is not eating and a feeding tube is required, we’ll need to place a PEG tube - since we can’t insert a tube directly into that dilated and abnormal oesophagus.
These patients have similar issues with keeping water down. Generally, we avoid having a water bowl in the kennel, offer our patients water, and keep them upright after drinking, just like we do after food. If they have a feeding tube in situ, we may administer water through this or meet their hydration requirements through IV fluids.
Prokinetic agents like metoclopramide or cisapride are commonly administered alongside managing nutrition and hydration.
What about aspiration pneumonia?
Patients with aspiration pneumonia require intensive supportive management with oxygen, nebulisation and mobilisations to loosen and remove respiratory secretions, intravenous fluid therapy and supportive care.
The use of antibiotics in these patients is a controversial topic - generally, it’s recommended only if there are clear signs of infection.
And then there’s long-term treatment…
Megaoesophagus is not a disease that just goes away - these patients need long-term supportive care, regardless of whether they’re at home or in the hospital. As nurses and technicians, we’re closely involved in supporting clients as they continue nursing care at home - educating them on PEG tube use, helping them source postural feeding aids like Bailey chairs, and teaching them how to manage these often challenging patients.
So there you have it - an overview of what megaoesophagus is, the variations we see, and the patients we see it in - alongside how to treat and care for them.
Though most of our management is supportive, providing appropriate nutritional support is vital, as well as managing aspiration and ensuring proper hydration. And even though these patients need intensive care and can be challenging to nurse, they’re ultimately very rewarding, too.
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
Bondy, PJ and Woringer, A.. 2012. Gastrointestinal. In: Merrill, L. ed. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell, pp. 193-261.
Egleston, S. 2018. The forgotten complication: aspiration pneumonia in the canine patient [Online] The Veterinary Nurse. Available from: https://www.theveterinarynurse.com/content/clinical/the-forgotten-complication-aspiration-pneumonia-in-the-canine-patient/
KuKanich, K. 2011. Diagnosis and management of megaoesophagus in dogs [Online] DVM360. Available from: https://www.dvm360.com/view/diagnosis-and-management-megaesophagus-dogs-proceedings#
Rodrigues, NF, et al. 2022. Antimicrobial discontinuation in dogs with acute aspiration pneumonia based on clinical improvement and normalization of C-reactive protein concentration. Journal of Veterinary Internal Medicine, 36 (2), pp. 1082-1088.