99 | The complete guide to caring for patients with myasthenia gravis as a veterinary nurse (ft Zoe Hatfield, RVN, VTS-Neurology)
Today we’re talking about Myasthenia gravis - and I am super excited because I’m joined by a special guest!
One of my main goals with the podcast this year is to bring in new educators and other VTS guests to help me educate and inspire nurses in lots of different areas - and we’re starting things off with a neurology series!
I’m delighted to introduce Zoe Hatfield, a RVN and VTS in Neurology. We actually sat our VTS exams together back in 2019, though our paths didn’t end up crossing properly until much later. Zoe is a RVN at Glasgow University Small Animal Hospital and also provides CPD on a wide range of neurology topics. You can find out more about her in the show notes.
Over the next few weeks, Zoe will be taking us through some of the most common neurological diseases we see, giving us the need-to-know information to manage these patients confidently, and an insight into how we can use our skills to care for these patients as nurses and technicians.
The first disease we’ll be chatting about is one of the most common diseases we see - and one I often see in medicine as well - and that’s Myasthenia gravis.
What is Myasthenia gravis, and what happens when our patient gets it?
Myasthenia gravis is one of the most common neuromuscular diseases, it most typically causes patients to develop episodes of muscle weakness, or exercise-induced weakness.
Weakness occurs due to a disorder at the level of the neuromuscular junction.
So our neuromuscular junction is the point at which our nerve impulses are transferred to the muscles (so the muscles can work). This innervation of the muscles requires a neurotransmitter, acetylcholine, to allow our neurons and muscle fibres to communicate.
In MG, there is either a lack of functional acetylcholine receptors, or malfunction at the neuromuscular junction which interferes with or impairs acetylcholine transmission.
This in turn causes the nerve impulses to the muscles to not be communicated fully, leading to the weakness we commonly see in these patients.
The disease can be congenital or acquired, and both dogs and cats can be affected, although the disease is rarer in cats.
Acquired MG is usually immune-mediated or seen secondary to a cranial mediastinal mass, usually a thymoma. In acquired MG, antibodies bind to acetylcholine receptors at the neuromuscular junction, blocking acetylcholine transmission.
There are three forms of acquired MG: focal (affecting the oroesophageal muscles), generalised (affecting the appendicular muscles as well as the oeosphagus) an fulminant (an acute, severe form of generalised MG).
Congenital MG is seen less commonly. These patients are born with fewer acetylcholine receptors, meaning less availability for acetylcholine transmission.
Treatment of acquired MG is aimed at putting a patient into remission but is not a cure.
What signs do we see in the Myasthenia gravis patient?
On presentation the neurological examination can be normal, although if the history is suggestive of MG repeated testing of the palpebral reflex may result in it tiring.
Exercising these patients usually results in the gait becoming stiff with short choppy steps, before the patient weakens to the point that they are unable to ambulate (they usually adopt a hunched position or sternal recumbency).
After a period of rest patients should be able to ambulate again, until they ultimately tire once more.
So I feel like MG is one of those diseases where there is quite a bit of crossover between medicine and neurology, because whilst it’s a primarily neurological disease, many of these patients present to us with things like megaoesophagus or aspiration pneumonia initially, and it’s after further investigation that we end up diagnosing MG and getting neuro involved.
It’s interesting, because many of the clinical signs that I see in these patients are different, likely because those inital subtle signs or periods of weakness have perhaps been missed. Many of the patients I see with MG have things like regurgitation and respiratory signs if aspiration is present, where the neuromuscular changes have impacted the muscle in the GI tract.
Usually it’s only after this we start doing things like exercising the patient and neurological examination we see those more subtle signs. So I guess that looking for those subtle changes in your at-risk patients, for example, is a key area for nurses and technicians to get involved in!
Ok, so that’s what Myasthenia gravis is, and the signs we see. But if they’re mild and hard to spot, how will we diagnose them?
We approach diagnosis in 3 main ways: via blood testing, in-house testing and diagnosting imaging.
Let’s start by looking at blood testing.
The gold standard diagnostic test in these patients is serology testing for autoantibodies to ACh receptors.
This needs to be carried out before the patient has received any corticosteroid treatment, to prevent any false-negative results (although it is still possible for these to come back negative on rare occasions if the antibodies level is not high enough at time of testing).
That test can take quite a while for results to come back (depending on where you submit your sample), so we often also perform an in-house acetylcholinesterase test.
An in-house acetylcholinesterase test can be carried out to make the diagnosis more or less likely while awaiting the antibody test results (Bongers et. al. 2020).
Often referred to as the ‘Tensilon Test’ as patients were administered edrophonium chloride (aka Tensilon), however this is no longer commercially available.
Alternatively, neostigmine can also be used. This is a short-acting anticholinesterase agent which should allow for more ACh molecules to become available and interact with the remaining functional ACh receptors.
After 15-20 minutes approximately there should be a marked increase in their exercise tolerance shown by the patient if the test is positive. A negative response to this test does not rule out MG entirely, it will however be less likely.
It really is quite amazing when I see our neuro team do this, because these patients go from being weak and sometimes even unable to really move, to suddently running around completely normally. But because the effects of the drug are short-lived, they will wear off quite quickly and return to their ‘normal’ weak state (until we start treatment, of course).
And then there’s imaging.
Chest radiographs should be performed to assess if there is the presence of megaoesophagus or a mediastinal thymoma. MG patients have a high incidence of megaoesophagus and should routinely be tested for it. There has also been a documented link to MG with the presence of a mediastinal thymoma in acquired cases.
From my point of view, this is probably the diagnostic I’m involved in the most, since most of the cases I see have megaoesophagus.
A couple of points regarding your chest X-rays if you’re specifically looking for MO: first, do them conscious if at all possible, since firstly the regurgitation risk is high so we’d ideally avoid sedation for aspiration reasons. Also, sedation or anaesthesia actually causes oesophageal dilation, so if your X-ray suggests MO, it can be hard to determine whether that really is the case.
Also, if you can, take a left lateral radiograph: the oesophagus lies to the left, so we tend to get a better view from this recumbency. And if you’re worried about aspiration and need to look at the lungs too, that’s when you’d ideally want inflated orthogonal views (ie two laterals and a DV).
Ok, so your patient has been diagnosed. What next? How do we treat and nurse them?!
Once the patient has been diagnosed treatment involves administering patients with anticholinesterase therapy orally (pyridostigmine bromide 0.5mg - 3mg/kg 2-3 times daily PO).
The dose should be started off at the lower end of the dose range and gradually increased until the desired effect has been achieved. If the patient is not able to take oral meds, they can be started off with an IV dose.
Patients need to be carefully monitored for any cholinergic responses occurring, by giving a lower dose to start off with this should hopefully be avoided. Signs of cholinergic response include hypersalivation, vomiting, diarrhoea and bradycardia.
Some patients may also require immunomodulatory therapy as well such as azathioprine, cyclosporine, or prednisolone. Generally, these are only used if the anticholinesterase therapy is not showing successful results.
In patients where there is a mediastinal thymoma present, complete surgical removal may result in clinical signs fully resolving, however if resection is not complete the tumour may regrow, and symptoms worsen.
Therapeutic plasma exchange is a viable treatment option in many human studies but the use in veterinary medicine is limited at the moment. Mainly due to a lack of equipment available and trained staff.
I think the point about TPE is really interesting, because we’re starting to see it used more and more in the management of so many immune-mediated diseases, like IMHA for example - I never realised it could also be used in MG, but that makes so much sense! So I guess the idea is that with the plasmapharesis we’re removing those autoantibodies, freeing up the receptors at neuromuscular junction to receive acetylcholine normally?
Really interesting - I think we’ll see so much more evidence on just how beneficial TPE is over the next few years!
Whilst not a ‘true’ treatment for MG we also know many of these patients have regurgitation and potentially aspiration - and where that is present, we’ll need to treat that too. Whilst we can’t do much about the regurgitation (aside from treating the MG), any respiratory complications need to be treated with intensive monitoring, oxygen therapy and supportive care - just like we would any other pneumonia patient.
And then there’s where we come in - the nursing care patients with Myasthenia gravis need.
Patients with MG often require a fair amount of nursing care, the main aim of nursing these patients is to try and prevent them developing any co-morbidities while hospitalised. Nutritional and hydration status are very important with these patients.
Due to the weakness these patients suffer they are likely to require support to be walked and may need to be trollied outside to prevent them tiring before reaching the toileting area.
As severe cases may affect respiration, respiratory rate and effort should be monitored regularly, and an SpO2 taken if concerned.
Patients with megaoesophagus may require additional support to eat (typically feeding soft food in small meatballs from a height) and will require being held upright for 15-20mins to avoid regurgitation and aspiration.
The use of devices such as a Bailey Chair © may help owners manage these cases better at home and prevent further complications from occurring.
If this still results in regurgitation a feeding tube may be required, although these carry their own set of risks.
Absolutely, and I feel like nutrition is one of the most important (and sometimes easy to overlook) areas of care for these patients. I wonder sometimes if people think I’m being pedantic when I’m being really over-the-top about meatball size, how these patients are fed, how water is offered, how long they’re held up for and even things like how their walks are scheduled around their meals. But in reality it’s so important - because the risk of things like aspiration is so high.
When there is the presence of megaoesophagus in these patients there is an increased risk of aspiration pneumonia occurring therefore they require careful monitoring of their respiratory rate, effort and any signs of a cough developing.
Patients that develop aspiration pneumonia carry a poorer prognosis. A more intensive nursing care plan is required, this often involves oxygen therapy, coupage and nebulisation.
Patients that are severely affected may also be recumbent so will require additional care such as turning and physiotherapy, as well as bladder and bowel management.
So a LOT for us to be thinking about with these patients, then - but the nursing care is what really makes the difference in hospital whilst that treatment takes effect, showing just how vital our role is in managing this disease!
So there you have it - an overview of Myasthenia gravis, the impact it has on our patients, and our crucial role in their management.
Myasthenia gravis cases require a high standard of nursing care to try and prevent patients developing any co-morbidities. Treatment will likely be started before serology for autoantibodies to ACh receptors results come back; therefore, other in-house tests are used to help make the diagnosis more likely while awaiting confirmation.
Ensuring patients with megaoesophagus do not develop aspiration pneumonia is one of the main aims of nursing care while the patient is in the hospital, but caregivers should be educated on this risk and shown how to care for their pet at home to try and reduce this risk.
Patients with aspiration pneumonia and megaoesophagus carry a grave prognosis, and require more intensive treatment and supportive care to maximise their outcomes - and as veterinary nurses and technicians, our role in this cannot be overlooked.
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
Bongers, J., Gutierrez‐Quintana, R. & Stalin, C.E. 2021, "External ophthalmoparesis as part of generalised myasthenia gravis in a dog: are there more similarities to the human counterpart than originally thought?", Veterinary record case reports, vol. 9, no. 2, pp. n/a
Downey Koos, L. 2024, “Acquired myasthenia gravis in companion animals”, Today’s Veterinary Practice, available from: https://todaysveterinarypractice.com/neurology/acquired-myasthenia-gravis-in-companion-animals/
Foy, D.S., Trepanier, L.A. & Shelton, G.D. 2011, "Cholinergic crisis after neostigmine administration in a dog with acquired focal myasthenia gravis", Journal of veterinary emergency and critical care (San Antonio, Tex. : 2000), vol. 21, no. 5, pp. 547-551.
Haskey, E. 2020, "Nursing the recumbent patient", In practice (London 1979), vol. 42, no. 5, pp. 268-278.
Khorzad, R., Whelan, M., Sisson, A. & Shelton, G.D. 2011, "Myasthenia gravis in dogs with an emphasis on treatment and critical care management", Journal of veterinary emergency and critical care (San Antonio, Tex.: 2000), vol. 21, no. 3, pp. 193-208.
Platt, S.R. & Olby, N.J. 2014, BSAVA manual of canine and feline neurology, Fourth edn, British Small Animal Veterinary Association, Gloucester, [England].
Mignan, T., Targett, M. & Lowrie, M. 2020, "Classification of myasthenia gravis and congenital myasthenic syndromes in dogs and cats", Journal of veterinary internal medicine, vol. 34, no. 5, pp. 1707-1717
Mignan, T. & Lowrie, M. 2019, "Feline myasthenia gravis: a review", Companion animal (London, England), vol. 24, no. 3, pp. 156-161
Vitalo, A., Buckley, G. & Londoño, L. 2021, "Therapeutic plasma exchange as adjunct therapy in 3 dogs with myasthenia gravis and myasthenia‐like syndrome", Journal of veterinary emergency and critical care (San Antonio, Tex. : 2000), vol. 31, no. 1, pp. 106-111.
Vercesi, I. 2021, "Myasthenia gravis in the canine patient", Veterinary Nursing Journal, vol. 36, no. 10, pp. 298-301.
About Zoe Hatfield, RVN, VTS(IM-Neurology)
Zoe qualified as a registered veterinary nurse in 2012. After spending her first year as a RVN working in first opinion practice, she moved to referral joining the University of Glasgow Small Animal Hospital nursing team in 2013.
Since joining the nursing team, Zoe has developed her passion for neurology and in 2019 gained the VTS certificate in Neurology.
Working within the vet school she enjoys using her extensive experience in neurology to teach and educate students and newer members of staff.
She also presents CPD on a wide variety of neurological topics, including at BSAVA Alba, ExcelCPD, VetTrust, AIMVT and BVA Live.
Watch Zoe’s excelCPD webinar series here.
