102 | The complete guide to caring for MUO patients as a veterinary nurse (ft Zoe Hatfield, VTS-Neurology)
There’s a lot to think about when it comes to stabilising, treating and nursing cats and dogs with inflammatory CNS disease.
But luckily, we’ve got a guest with us today to guide us through it!
Today I’m delighted to be joined once again by Zoe Hatfield who is bringing us her expertise on nursing neuro patients! Zoe is a neurology RVN and a Veterinary Technician Specialist in neurology, working at Glasgow University’s Small Animal Hospital.
In this episode, Zoe is giving us the lowdown on a surprisingly common neurological condition and one that has a significant impact on our patients - and that’s meningioencephalomyelitis of unknown origin, or MUO.
These patients are often critically unwell and need intensive nursing care, meaning there are lots of ways we can put our skills to good use and advocate for our patients in the process - and that’s exactly what you’ll be able to do confidently after this episode!
So Zoe, perhaps you could start us off by telling us a bit about MUO - what it is, why it happens, and how it impacts our patients.
Meningoencephalomyelitis of unknown origin (MUO) is the term used to describe a group of idiopathic, non-infectious inflammatory diseases that affect the central nervous system (CNS).
The disease causes inflammation to occur in the brain, meninges and/or spinal cord. We don’t know exactly why they happen, but it’s thought to be immune-mediated in origin.
There are three main subtypes; granulomatous meningoencephalomyeitis (GME), necrotizing meningoencephalmyelitis (NME) and necrotizing leukoencephalomyelitis (NLE).
Although these can only be truly distinguished through histopathology, they are collectively referred to as MUO in practice.
MUO is thought to be one of the most common inflammatory diseases affecting the CNS in dogs, with MUO making up approximately 25% of all canine CNS diseases.
Ok, so that’s what MUO is - and while we don’t exactly know why it happens, what do we know about it so far?
While the pathogenesis of MUO is not well understood, it is believed that genetics, immunological and environmental factors (such as an infection) can all act as triggers for the underlying autoimmune inflammatory response.
This autoimmune inflammatory process seen with MUO causes inflammation to the brain and the surrounding meninges (as well as the spinal cord with meningoencephalomyelitis).
Typically, these patients tend to be young to middle-aged small toy/terrier breeds, with females seeming to be more prone than males. Breeds include Maltese, Yorkshire Terriers, Pugs, Chihuahua and French Bulldogs, although any breed, sex or size of dog can be affected.
Moving on to the clinical signs we see in patients with MUO…
The different clinical signs we see, and the severity of those signs, can vary greatly.
As a rough rule, inflammatory conditions tend to be acute onset and progressive, with patients often displaying a multi-focal presentation or neurolocalisation.
Clinical signs are very much dependent on the area or areas affected by the disease, and include:
Vestibular signs
Depression
Altered mentation
Seizures
Facial nerve abnormalities
Blindness
Circling
Gait abnormalities
Neck pain
And many more.
With the variety of vague clinical signs, history and signalment will likely mean that MUO will be one of the diseases on the differential diagnosis list for these patients. MUO carries several similarities to multiple sclerosis in humans, with people displaying visual deficits or spinal cord dysfunction.
This is really interesting and it goes to show the variety of clinical signs - some being quite subtle, and of course others more severe - that we see in these patients. And this is definitely something we’ve mentioned in other episodes in this series, but as veterinary nurses we are ideally placed to spot those subtle signs, as well as look for trends and deterioration, so we can intervene early when things change.
Ok, so that’s the signs these patients present with, but what about stabilising them - how will we manage these often critical neurological patients?
In severe cases patients may require stabilisation, especially if they present with cluster seizures or status epilepticus, or are obtunded or stuporous.
Patients with seizures should be treated to stop the seizure cycle; depending on how long they have been seizuring, these patients could be a risk of oedema and potentially raised intracranial pressure. These patients will require careful, and likely intensive monitoring.
The importance of blood pressure monitoring in critical neurological patients
Blood pressure is critically important in maintaining the careful balance that allows the nervous system to function correctly.
Patients with concerns over raised intracranial pressure should have their blood pressure monitored regularly, since blood pressure changes can ocurr very quickly, alerting us to deterioration and guiding stabilisation as early as possible.
Blood pressure directly affects cerebral perfusion pressure (CPP). CPP is is the pressure required to supply the brain with blood, thereby ensuring it receives enough oxygen and nutrients.
The brain is capable of autoregulating itself, though if it becomes injured it can lose this ability, and therefore needs to rely on mean arterial pressure (MAP) to maintain perfusion.
It is therefore vital that blood pressure is maintained as close to a normal level as possible, to avoid hypotension or hypertension.
Increased intracranial pressure in the critical neurological patient
If we think about the disease, it is likely the patient may have a brain lesion or lesions, and where these are present intracranial pressure will increase. Since altered mentation is a common presenting sign in MUO patients, any patient presenting with altered mentation should naturally be assessed and monitored for raised ICP.
Raised ICP is also known as intracranial hypertension, again demonstrating how vital blood pressure is when assessing and monitoring at-risk individuals.
Knowing the signs of increased ICP is essential since it allows us to intervene promptly before the patient deteriorates further.
Signs such as a sudden change in the level of consciousness, posture or eye size can all indicate a deterioration, depending on the individual patient and their current treatment.
Some medications, for example, may cause neurological depression, and in those cases, changes to mentation, posture or pupil size may be expected.
If a patient has had MRI it may be possible to see the signs of raised ICP, however if the patient is not stable enough for diagnostic imaging, then a presumptive diagnosis may be made in the meantime based on clinical signs and examination findings.
In cases where the patient is rapidly deteriorating, a bolus of hypertonic saline or mannitol should be administered, to decrease intracranial pressure. Since these solutions cause systemic dehydration, a crystalloid should also be administered at an appropriate time.
The pathophysiology of intracranial pressure
If we then take a moment to remember that the skulls volume cannot be changed.
The skull is responsible for protecting the brain, cerebrospinal fluid and blood. These components exist in a physiological equilibrium and disease processes affecting the brain parenchyma can go on to increase the volume of one or more components.
The Monro-Kellie Doctrine (Hypothesis) states that the volume of the brain, blood and cerebrospinal fluid remains constant within the skull.
Any changes to any of these volumes is compensated for to maintain this careful equilibrium. When changes can no longer be compensated for this leads to an increase in ICP.
So you’ve got a big box made of bone, and inside it you’ve got blood, tissue, and CSF. The box isn’t capable of expanding, so if the volumes or one or more of those contents increase, one has to decrease to make space for it. Right? Which is why we use solutions like mannitol or hypertenonic saline, since these will shrink cells by drawing water out, decreasing the volume and therefore decreasing the pressure.
The Cushing’s reflex and how to spot it as a veterinary nurse
And this is where the Cushing’s Reflex comes into play. This reflex is perhaps the best indication of severe increased ICP and imminent brain herniation and requires immediate attention and treatment.
So remember we said the skull is a fixed box, and it can’t expand to make room for that increasing pressure? If we don’t get it down, there’s only one place that content can go - the brainstem will herniate out of the back of the skull, which is fatal, since the cardiovascular and respiratory control centres are in that area.
Cushing reflex is the combination of two classic signs - hypertension and bradycardia, often accompanied by an irregular respiratory pattern. It is marked when you see it - these patients will often have significant hypertension and marked bradycardia.
By the time these signs are apparent, the intracranial hypertension will be so severe the patient cannot control it themselves, meaning they are at risk of impending brain herniation.
These patients must be monitored very closely and aggressively treated (usually with hypertonic saline or mannitol) as soon as possible. As a minimum, their respiratory rate and effort, heart rate and blood pressure should be measured very regularly.
Ok, so we’ve chatted about stabilisation - what about diagnosing these patients?
A diagnosis of MUO is usually based on an assessment of signalment, neurological examination findings, magnetic resonance imaging (MRI) findings, cerebrospinal fluid (CSF) analysis as well as negative infectious disease testing.
We’ll start with bloodwork
Basic biochemistry and haematology should be performed to screen for other systemic illness, and infectious disease testing - particularly toxoplasma and neospora - should be performed, since these infections cause similar clinical signs.
After bloods are performed, imaging and CSF analysis is indicated.
MRI is the preferred imaging modality for viewing the brain and spinal cord, since it identifies areas of ischaemia, haemorrhage and neoplasia as well as signs of increased ICP and herniation. However, it requires a long general anaesthetic compared with CT imaging for example, so patients should be assessed and stabilised before proceeding with imaging.
CSF is an important diagnostic tool. We may not always be able to collect a sample, depending on herniation risk and whether it is physically possible (some patients are just difficult to sample).
CSF analysis will often show the presence of inflammation (though not always) and total protein levels will be elevated. On cytology, a mononuclear or mixed pleocytosis will be present.
For a definitive diagnosis, a brain biopsy is required for pathology review.
However, the procedure requires an incredibly invasive and risky procedure and general anaesthesia, so it is performed very rarely.
The treatment for these conditions are the same, so these are only usually taken if the neurologist is suspecting another cause for the symptoms (such as neosplasia).
After we’ve reached a diagnosis, we need to plan our treatment and nursing care.
Treatment is aimed at suppressing the immune system, in order to reduce the inflammation.
The choice of treatment is very much dependent on the preference of the veterinary surgeon. The main drug of choice is corticosteroids, given at an immunosuppressive dose and reduced gradually if the patient is doing well (this can take a long time, and some patients may require a small dose forever).
Unfortunately, side effects are seen fairly often with steroid use. Common dose-dependent side effects of steroids include increased thirst and hunger (consequently urination and weight gain), lethargy, panting, and an increased risk of infections. As a result, some patients will receive a secondary immunosupressive agent (usually chemotherapy, or another immunosuppressant) to decrease their steroid dose and aid immune support.
Using chemotherapy to support the MUO patient
Chemotherapy is another popular treatment option, with cytosine arabinose or cytarabine being the most popular option. The research available with protocols for MUO is limited so quite often doses, route of administration and treatment duration will vary.
For instance, we will usually administer 100mg/m2 to patients that are stable, but more severely affected patients will receive 200mg/m2. This is given as a CRI, over between 6-8 hours and 24 hours depending on practice protocols.
Depending on the chemotherapy protocol patients will likely have to return often for repeated doses. Again, protocols vary, we tend to do three-week intervals for the first few doses, increase to four-week intervals for another couple of doses then 5, 6 etc. until we get to 8 weeks.
If they do well at eight weeks apart discussion with the owners would be regarding stopping the cytarabine at this point, although they will likely continue prednisolone for longer than this. Owners would also be advised on the possibility of relapse and having to restart treatment if required.
Treating MUO with other immunosuppressive treatments
Of course, no one protocol/treatment option suits all patients.
Some will require medications that can be given at home so there are less trips to the clinic or perhaps even require the addition of another medication to help reduce symptoms further.
This may be due to side effects from the prednisolone or because the patient has been severely affected by the disease. Common additional medications include cyclosporine, azathioprine and mycophenolate mofetil. Lomustine has been reported, but results did not show a significantly longer survival time compared to giving prednisone alone.
Other treatments used in MUO patients
Patients may also be started on a course of clindamycin initially to treat for any potential infectious cause.
Typically clinicians would be suspicious of protozoal infections such as neospora or toxoplasmosis, although tick-borne disease may also be on this list.
Treatment will be stopped once infectious disease titres come back negative, and if a lower prednisolone dose was started (to be on the cautious side) it will likely be increased.
Prognosis in the MUO patient
The prognosis for MUO is highly variable.
A good initial response to treatment may indicate a more favourable prognosis. It is possible for animals to enter full or partial remission from the disease and maintain a good quality of life for many months or years, though patients with poor response to treatment or recurrent relapses have a poorer prognosis.
Ok, so treatment is aimed at immunosuppression and supportive care - but where do we come in as veterinary nurses?
Depending on the severity at the time of presentation these patients may require a more intensive nursing plan to begin with, while other less severe cases may only require basic nursing care - such as chemo barrier care - and be fairly straightforward to nurse.
However, if these patients are going to be receiving cytarabine treatment regularly it is likely they will visit practice fairly often - this gives us as nurses a good chance to get to know our patients and their owners well.
Nursing patients receiving cytotoxic medications
With any chemotherapy treatment it is important to understand the risks to the patient as well as to those around them.
The most commonly used chemotherapy treatment for MUO is typically cytarabine. This can be given subcutaneous or intravenously via a CRI. No matter the chemotherapy drug of choice given or the route care should be taken to follow chemotherapy preparation, administration and nursing protocols.
With these drugs it is worthwhile noting how the drug will be excreted (e.g. cytarabine is excreted through saliva, urine and faeces) and the appropriate care taken. It is also a good idea to familiarise yourself with the possible side-effects so patients can be monitored appropriately.
Nursing non-ambulatory patients
With these patients it is important to think about what they can’t do, so can they turn themselves? Can they reach their food bowls or toilet normally?
Once a list of inabilities has been composed we can cater our nursing plan to address these.
These patients may need regular turning (Q4-6hr) or at least have their hips turned. If they are vestibular they may favour one side over the other and require positioning to help, and rolled up blankets work well for this.
Those patients that are non-ambulatory or vestibular may have difficulties getting to their food bowls to eat or drink, so may require this offered by hand or positioned near to them (if left beside them monitor for nausea to ensure we aren’t making them feel any worse by leaving food next to them that they are unable to remove themselves from).
Exercise will likely require some form of support aid, as well as a harness (to avoid any pressure around the neck).
When it comes to toileting it is important to consider the patient’s current treatment. If they are receiving cytarabine or another chemotherapy drug, it is likely they will pass some of the drug via their urine.
This means if they are non-ambulatory and likely to urinate in their beds (without moving away) or even require bladder expression it will often be easier if an indwelling urinary catheter is placed (although these come with additional risks).
Nursing patients with seizures
It is important to mention, that this will likely be the first time this patient has seizure at home and therefore could make these cases particularly destressing for owners.
This means they will not only have to learn and understand that their pet has MUO, they also have to deal with the reality that this disease is causing their pet to have seizures (that will also require treatment and potentially additional monitoring).
Owners should be helped to understand which medication is for which disease and the importance of timing. They should also be encouraged to keep a seizure diary if relevant.
In hospital these patients should not require much more additional nursing care, they should be on seizure watch and checked regularly so signs of a seizure are not missed.
Remember being hospitalised is an additional stress on the patient’s body, and if they are triggered by stress this could make a seizure more likely.
Supporting caregivers of MUO patients
Promoting general overall health of the patient is vital when we are speaking with these owners.
Patients on corticosteroid treatment will have a tendency to put on weight, add in the likely reduced energy and exercise ability of these patients and the risk of weight gain is further increased. Therefore, it is important that we ensure owners understand the importance of maintaining a healthy weight, especially as their pet will likely demonstrate and increased appetite. Exercise should be encouraged but going by what their pet wants to do as a guide.
Due to the immune-mediated aspect of the disease routine vaccinations are discouraged, and this can be a source of added stress for owners, as nurses we can help put these owners’ minds at ease and help them navigate caring for their pet.
Clients who are handling these immunosuppressive medications in the form of oral medications and their pets’ secretions while on these immunosuppressive medications should be properly guided in safe handling practices, especially those who are immunosuppressed themselves, pregnant or trying to conceive.
In conclusion, MUO patients can be challenging to treat and nurse, particularly if they are critically unwell, develop increased ICP, or are non-ambulatory. They often need extensive follow-up treatment and while this can be tough for them and their families, it provides us with lots of opportunities to get to know our patients well - and make a real difference to their care.
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
Meningoencephalitis of Unknown Origin in Dogs - Veterinary Partner – VIN https://veterinarypartner.vin.com/default.aspx?pid=19239&catId=254099&id=12533305
Beasley, M.J. & Shores, A. 2023, "Perspectives on pharmacologic strategies in the management of meningoencephalomyelitis of unknown origin in dogs", Frontiers in veterinary science, vol. 10, pp. 1167002
Jeffery, N. & Granger, N. 2023, "New insights into the treatment of meningoencephalomyelitis of unknown origin since 2009: A review of 671 cases", Frontiers in veterinary science, vol. 10, pp. 1114798.
Smith, P.M., Stalin, C.E., Shaw, D., Granger, N. & Jeffery, N.D. 2009, "Comparison of Two Regimens for the Treatment of Meningoencephalomyelitis of Unknown Etiology", Journal of veterinary internal medicine, vol. 23, no. 3, pp. 520-526.
Song, J., Yu, D., Lee, H., Hwang, T., Kim, Y.J., An, S. & Jung, D. 2020, "Evaluation of treatment with a combination of mycophenolate mofetil and prednisolone in dogs with meningoencephalomyelitis of unknown etiology: a retrospective study of 86 cases (2009–2017)", BMC veterinary research, vol. 16, no. 1, pp. 192-192
Cornelis, I., Van Ham, L., Gielen, I., De Decker, S. & Bhatti, S.F.M. 2019, "Clinical presentation, diagnostic findings, prognostic factors, treatment and outcome in dogs with meningoencephalomyelitis of unknown origin: A review", The veterinary journal (1997), vol. 244, pp. 37-44.
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.
