U5 O1 - Neurological and Ophthalmic Emergencies Flashcards
What is ataxia?
Incoordination of the limbs that can cause swaying,
abnormal carriage of limb(s) etc
What is blepharospasm?
Rapid blinking of the eyelids often in response to ocular pain or irritation.
What is clonus?
Involuntary, regular rhythmic contractions and relaxation of muscles
What is hemiparesis?
Weakness of 2 limbs on the same side.
What is horners syndrome?
Drooping of the eyelid (ptosis), constriction of the pupil
myosis/miosis) and retraction of the eyeball into the socket (enophthalmos
What is Hyphaemia?
Blood in the anterior chamber of the eye
What is Hypopyon?
Pus in the anterior chamber of the eye
What is nystagmus?
Abnormal movement of the eyes in synchrony. There is
usually a slow phase in one direction; and then a fast phase as the eyes flick back to their origin. It may be horizontal, vertical or rotational and it may only occur when the head position is altered (positional nystagmus).
What is Opisthotonus?
Strong contraction of the extensor muscles of the neck and back. This results in arching of the back; and
hyperextension (backward arching) of the head and neck - often with extension of the fore limbs.
What is paralysis?
Loss of motor (muscle) function. Generally used in
reference to a limb but could also be e.g. facial paralysis
What is paresis?
Partial loss of motor (muscle) function. Usually used in
reference to a limb but can also be used in relation to other parts of the body such as the eye
What is proprioception?
The sensory function which allows the animal to be aware of and adopt the normal limb positioning
What is Schiff-Sherrington posture ?
Increased forelimb extensor tone secondary to a serious injury from T3-L3
What is Spasticity?
An increase in the tone/activity of the extensor muscles of limb(s) leading to rigid paralysis: hypertonia
What is a spinal reflex?
Automatic response to a particular stimulus which involves spinal cord nerve pathways. Examples include the patellar reflex, cutaneous trunci reflex and perineal reflex.
What is strabismus?
A squint where both or one eye deviates from the normal position: usually ventrally and medially.
What is syncope?
A collapse/faint
What is tetraparesis?
Partial loss of motor (muscle) function in all 4 limbs.
What is tonus?
Increased extensor tone of muscles
The initial emergency neurological assessment involves assessing what three basic features?
The initial emergency neurological assessment involves assessing three basic features to try and quickly identify the severity and location of the neurological problem. It does not replace a full neurological assessment but can provide valuable
early information to allow emergency treatment to be provided without wasting valuable time. The three features to assess are:
1) Mental status
2) Ambulation
3) Cranial and spinal nerve function
An initial hands- off assessment is important. Visual assessment of level of consciousness and abnormalities is important e.g. nystagmus, miosis, balance issues etc. It is Important to remember that mental status is also affected by cerebral
perfusion so anything that interferes with this could affect the patient’s mental status.
How do you assess the mental status in an initial neurological assessment?
Mental status
This is an assessment of the patient’s level of alertness and can be tested in a number of ways. Hands off observation of the patient is very important - initially a
clinical assessment of the degree of consciousness of the patient should be made i.e. is it alert/awake. This can progress on to an assessment of the response to
external stimuli: such as a loud noise; or light; or the response to touch/noxious stimuli. Response to touch around the head, especially around the nose, medial
canthus of the eye and the ears, is particularly important to assess mental status,
How do you assess the ambulation in an initial neurological assessment?
Ambulation
This is the assessment of the animal’s ability to walk and move normally. If affected, an assessment of the degree of ataxia should be made. If limb function is reduced or impaired, is this localised to one limb, one side, or does it involve all four limbs?
In addition, some postural reactions, including basic proprioception tests, can be performed by knuckling over the paws in turn to see if the patient immediately
replaces the foot to its normal position. Any delay or failure to reposition the foot indicates a loss of sensory and / or motor nerve function to that limb.
Noxious stimuli are useful to test pain pathways and deep nerve function. These are classically performed by applying haemostats across the nail bed of the patient. The response should be vocalisation and / or movement of the head around to the side affected. Lack of response or reduced response suggests reduced function or lack of deep pain sensation which has a poor prognosis. This assessment should not be
performed if a patient has normal limb motor function. Due to the potential to cause pain, deep pain assessment should only be performed on veterinary direction.
How do you assess the mental status in an initial neurological assessment?
Cranial nerves
A full cranial nerve assessment is unlikely to be performed as part of the initial assessment – however an initial brief assessment of cranial nerve abnormalities can be helpful e.g. balance issues might indicate an issue with CN VIII, the vestibulocochlear nerve, or the cerebellum.
The following cranial nerves can be tested to help locate the source of a neurological
problem involving the head and neck:
Cranial nerve II optic nerve
Cranial nerve III oculomotor nerve
Cranial nerve IV trochlear nerve
Cranial nerve VI abducens nerve
Cranial nerve VII facial nerve
Cranial nerve VIII vestibulocochlear nerve
Cranial nerve IX glossopharyngeal nerve
Cranial nerve X vagus nerve
Cranial nerve XII hypoglossal nerve
Cranial nerve II and cranial nerve VII can be tested by assessing the menace response reflex i.e. does the patient blink when an object is moved rapidly towards them? Cranial nerve II travels directly from the back of the globe, through the calvarium and to the vision centre in the forebrain, close to the midbrain. On the
ventral brain there is some crossing over of the left and right optic nerves at the optic chiasma: so part of the left optic nerve crosses over to the right side of the brain and vice versa. The sensory nervous impulses are analysed in the vision centre: resulting in motor nerve impulses being transmitted in cranial nerve VII to the eyelids to cause blinking. An abnormal response can indicate damage or disease of the retina, cranial
nerve II, the vision centre of the forebrain or cranial nerve VII.
What following cranial nerves can be tested to help locate the source of a neurological problem involving the head and neck?
The following cranial nerves can be tested to help locate the source of a neurological problem involving the head and neck:
Cranial nerve II optic nerve
Cranial nerve III oculomotor nerve
Cranial nerve IV trochlear nerve
Cranial nerve VI abducens nerve
Cranial nerve VII facial nerve
Cranial nerve VIII vestibulocochlear nerve
Cranial nerve IX glossopharyngeal nerve
Cranial nerve X vagus nerve
Cranial nerve XII hypoglossal nerve
What is the Cranial nerve II?
Cranial nerve II optic nerve
What is the Cranial nerve III?
Cranial nerve III oculomotor nerve
What is the Cranial nerve IV?
Cranial nerve IV trochlear nerve
What is the Cranial nerve VI?
Cranial nerve VI abducens nerve
What is the Cranial nerve VII?
Cranial nerve VII facial nerve
What is the Cranial nerve VIII?
Cranial nerve VIII vestibulocochlear nerve
What is the Cranial nerve IX?
Cranial nerve IX glossopharyngeal nerve
What is the Cranial nerve X?
Cranial nerve X vagus nerve
What is the Cranial nerve XII?
Cranial nerve XII hypoglossal nerve
How do you test Cranial nerve II and cranial nerve VII?
Cranial nerve II and cranial nerve VII can be tested by assessing the menace response reflex i.e. does the patient blink when an object is moved rapidly towards them? Cranial nerve II travels directly from the back of the globe, through the calvarium and to the vision centre in the forebrain, close to the midbrain. On the
ventral brain there is some crossing over of the left and right optic nerves at the optic chiasma: so part of the left optic nerve crosses over to the right side of the brain and vice versa. The sensory nervous impulses are analysed in the vision centre: resulting in motor nerve impulses being transmitted in cranial nerve VII to the eyelids to cause blinking. An abnormal response can indicate damage or disease of the retina, cranial
nerve II, the vision centre of the forebrain or cranial nerve VII.
How do you test Cranial nerve III?
Cranial nerve III can be assessed by observing the pupil and noting its response to light stimuli: as this nerve is involved in controlling the iris. An initial assessment
should be made of:
Pupil size: normal, abnormally constricted (miosis) or dilated (mydriasis)
Pupils symmetry: asymmetry may suggest a unilateral problem (anisocoria)
Pupil response to light
The pupillary light/motor reflex (PLR/PMR) assesses the function of cranial nerve II, the vison centre and cranial nerve III. If there is damage to this pathway, reduced or
absent pupillary light reflex responses will be evident: i.e. when a bright light is shone into the eye the pupil does not constrict or shows a reduced/sluggish response. Due to the crossing over of fibres of cranial nerves II and III (decussation),there should be a consensual light reflex as well as a direct response: i.e. when light is shone into one eye, the opposite pupil should constrict (consensual response) as well as the
pupil into which the light is shone (direct response). In addition, cranial nerve III (along with cranial nerves IV and VI innervates) innervates the extraocular muscles:
these cause movement of the eyeball/globe in the orbit. Damage to these nerves can interfere with movement or cause a squint: strabismus. As cranial nerve III arises
from the rostral midbrain, damage to this area could affect its function.
What disease simultaneously affects Cranial nerves IV, VI and VIII?
Cranial nerves IV, VI and VIII are often simultaneously affected if a patient has vestibular disease. Loss of function of the trochlear nerve (IV) results in a dorsolateral strabismus; loss of function of the abducens nerve (VI) results in medial strabismus; and loss of the vestibulocochlear nerve (VIII) function results a head tilt, circling, abnormal posture and balance. Vomiting may occur and there may be unilateral loss of hearing: although this is hard to assess. Nystagmus (abnormal horizontal or vertical eye movements) may also be present if cranial VIII is not functioning:
What can damage to cranial nerves IX, X and XII result in?
Damage to cranial nerves IX, X and XII may all result in dysphagia and altered/absent gag reflex (i.e. when something is placed into the back of the patient’s
throat, a gag or swallow reflex should result).
As cranial nerve X (the vagus) has so many functions, damage to it could be associated with various clinical signs e.g. altered heart rate, blood pressure or
phonation.
What are the different spinal reflexes that may be assessed?
Assessment of other nerves Assessment of spinal reflexes may provide information about the spinal cord function and help to localise lesions. There are a large number of spinal reflexes which may be assessed including: Patella reflex Cranial tibial reflex Gastrocnemius reflex Triceps reflex Perineal reflex Withdrawal reflex
What are the many causes of seizures?
There are many causes of seizures: both intra-cranial and extra-cranial e.g. trauma, metabolic disease, toxicity, neoplasia, porto-systemic shunt. The commonest cause of seizures is idiopathic epilepsy
What is a seizure?
Seizures (Fitting)
A seizure is an abnormal event which arises from excessive neuronal activity in the cerebral cortex. It is not a disease process but a sign of an underlying condition.
The pathophysiology of seizures is complex. The condition occurs as a consequence of rapid, uncontrolled firing of nerve cells (neurons) within parts of the brain.
What two types of seizures may an animal present with?
The clinical presentation of an animal having a seizure depends on whether the seizure activity is generalised or partial/localised.
What type of seizures are dogs most likely to demonstrate?
Depending on the underlying cause, dogs are more likely to demonstrate generalised seizure activity:
What type of seizures are cats most likely to demonstrate?
cats more likely to exhibit partial seizure activity
What parts of the brain are involved in generalised seizures and how do generalised seizures affect the patient?
Generalised seizures involve both cerebral hemispheres: the animal is likely to be unconscious with seizure activity affecting both sides of the body. Abnormal neuronal activity on both sides of the brain usually presents as bilaterally symmetrical trunk and limb movements.
Generalised seizures are often associated with tonic/clonic activity
What are partial seizures caused by?
Partial seizures are caused by abnormal neuronal activity that is localised to an area of the forebrain/cerebrum.
What are the two types of partial seizures?
Partial motor:
Psychomotor
What is a partial motor seizure?
Partial seizures are caused by abnormal neuronal activity that is localised to an area
of the forebrain/cerebrum.
These may be:
Partial motor: a partial seizure with signs such as tonus or clonus of one or more limbs or twitching of the face.
What is a partial psychomotor seizure?
Partial seizures are caused by abnormal neuronal activity that is localised to an area
of the forebrain/cerebrum. These may be:
Psychomotor: partial seizures which lead to various behavioural changes such as vocalisation, tail-chasing, aggression etc.
What is status epilepticus?
Status epilepticus is an emergency which requires prompt veterinary attention. Status epilepticus (S.E.) is usually considered to be continuous seizure activity lasting five minutes or longer; or cluster seizures where the patient does not regain consciousness between seizures.
What two categories can the causes of seizures be divided in to ?
Seizures are caused by extra-cranial or intra-cranial causes
What are the possible causes of extracranial seizures?
Extra-cranial causes:
There are many possible causes:
metabolic disorders such as hypoglycaemia or hypocalcaemia
organ disease e.g. cirrhosis of the liver; porto-systemic shunt or kidney failure
toxicity e.g. ethylene glycol
Neurons are very sensitive to toxins (neuro-toxins) and this can cause seizure activity
What are the possible causes of intracranial seizures?
Intracranial causes: There are also many possible causes: trauma infection congenital defects acquired conditions e.g. hydrocephalus neoplasia inflammatory conditions e.g. granulomatous meningo-encephalitis (GME) idiopathic epilepsy which is often inherited
If the seizures are caused by uraemia what other clinical signs may have been seen?
if the seizures are caused by uraemia, secondary to chronic renal failure, the patient may have a history of polyuria and polydipsia, weight loss and vomiting. Clinical findings may include uraemic halitosis
and oral ulceration; dehydration and emaciation
How can idiopathic epilepsy be confirmed?
If the animal has idiopathic epilepsy (this can only be confirmed by ruling out all other potential causes), it is usually young, of a certain breed and was normal prior to the seizure.
What is important at identifying the potential cause of a seizure when carrying out a consultation?
Clinical presentation
As mentioned above, the patient presentation varies depending on the cause of the seizure. The history is very important in attempting to identify an underlying cause: potential access to toxins; recent trauma; previous seizure activity; normal or abnormal before seizures started.
What are the 4 basic stages of a seizure?
There are 4 basic stages to a seizure: 1) the prodromal stage, 2) the aura or pre-ictal stage, 3) the ictal or seizure stage, and 4) the post-ictal stage
Describe the prodromal stage of a seizure?
Depending on the cause, the prodromal stage may precede the actual seizure by hours or days. It may be characterised by a change in mood or behaviour. Humans with epilepsy can experience mood changes, headaches, insomnia or feelings about the impending seizure: ‘seizure alert’ dogs can be trained to recognise impending seizure activity in their owners. Some owners can recognise when their pet is going to have a seizure due to behaviour changes.
Describe the aura stage of a seizure?
The aura stage signals the start of the seizure. Signs are usually localised and can include restlessness, nervousness, whining, trembling, salivation, affection,
wandering, hiding, hysterical running, and apprehension.
Describe the ictal stage of a seizure?
The ictal stage is the actual seizure- if generalised, there is likely to be a sudden increase in muscle tone; loss of consciousness; and stimulation of the autonomic
nervous system, often with hypersalivation, defaecation and urination. The ictus (seizure or fit) is either tonic (rigid) or tonic-clonic (rigidity interspersed with jerking
muscle activity): generally lasting up to 1-3 minutes.
Describe the post-ictal stage of a seizure?
The post-ictal stage may be the only sign of a seizure that the owner sees particularly since many seizures occur at night or early in the morning. For minutes
to days after the seizure, the dog may be confused, disoriented, restless, or unresponsive, or may wander or suffer from transient blindness. At this stage the
animal is conscious but does not behave in their usual manner. They may display signs of exhaustion, altered temperament, polyphagia and/or polydipsia
What telephone advice should be given to an owner who’s pet has been seizuring?
Telephone guidance is often required for these cases. Most animals with idiopathic epilepsy will have seizures which start when resting and stop spontaneously,
especially if external stimuli are controlled e.g. noise, light etc. Telephone advice should be aimed at limiting patient and owner injury- the animal should not be
handled unless its position means it is in danger; if possible, any furniture that may pose a threat should be moved; lights should be dimmed and the time should be noted. It can be helpful to suggest filming their animal’s behaviour.
It is, however, crucial to identify those cases where immediate veterinary attention is
required e.g.
possible status epilepticus
hypoglycaemia
hypocalcaemia
intra or extra-cranial trauma
When is immediate veterinary attention required in a patient that is seizuring?
It is, however, crucial to identify those cases where immediate veterinary attention is required e.g. possible status epilepticus hypoglycaemia hypocalcaemia intra or extra-cranial trauma.
The history is very important e.g. the patient with diabetes mellitus who has had a recent increase in insulin dose requires an emergency source of glucose prior to veterinary attention; the Yorkshire terrier which has recently had puppies need immediate veterinary attention for treatment of hypocalcaemia. If in doubt veterinary guidance should be sought. Appropriate guidance on the safe transport of patients will be required. Secondary complications such as hyperthermia have to be considered.
How do you carry out an initial quick neurological assessment?
Patient Assessment
The patient will need to be assessed on presentation. An initial quick neurological assessment can be made by hands-off observation e.g. conscious, ambulatory,
ataxic, and alert; stuporous; obtunded; unconscious; seizuring etc.
An assessment of respiration and perfusion parameters e.g. pulse rate and quality; mucous membrane colour and CRT should be made. Emergency oxygen should be available.
What sample collection and testing is usually carried out on a patient with seizures and when should sample collection be carried out?
Sample collection and testing
In general, and where possible, blood samples should be obtained prior to treatment.
Any seizuring or unconscious patient should have blood glucose levels assessed immediately to rule out hypoglycaemia or hyperglycaemia. A full haematological and biochemical profile can be helpful in identifying the underlying cause and appropriate
emergency treatment. Ideally this should include blood gas analysis, PCV, blood smear examination and ionised calcium assessment. N.B. cerebral hypoxia can
cause seizures
Samples may additionally be required for toxicology or assessment of serum insulin, thyroid hormones or anticonvulsant levels. Further dynamic testing of liver function e.g. bile acid stimulation test may be required.
It is useful to store and freeze spun down and separated serum, for analysis of anticonvulsant drug levels, should the patient already be on medication for epilepsy.
In addition serum can be used to test for antibodies to viruses such as distemper.
When is medication required in a patient that’s seizuring?
Initial medication
If the seizure is mild and lasts less than a couple of minutes, there may be no need to medicate the animal.
Emergency treatment is required for status epilepticus. There are various definitions of status epilepticus- it is either prolonged seizure activity or two or more seizures without full recovery of consciousness during the inter-ictal period. Any patient that has been seizuring continually, for five minutes or more, needs to be seen as an emergency.
Treatment (although not usually emergency treatment) may also be required for patients that have had two or more seizures within a 24 hour period (known as
cluster seizures). It is important to ascertain whether the patient is currently receiving any medication, including anticonvulsant therapy. Advising owners to bring anticonvulsant medication that has been prescribed to an emergency appointment can be helpful.
What treatment is required for a patient seizuring due to a hypoglycaemic episode?
If the patient is hypoglycaemic on presentation this should be addressed by IV administration of 0.5–1.0 mL/kg of 50% dextrose. As this hyperosmolar solution can cause phlebitis, dextrose can be added to intravenous fluids to make a 2.5% or 5% solution
What are the important considerations when placing an intravenous catheter in a patient that has presented with seizures?
Where possible, intravenous (IV) access, should be obtained initially. For speed of action and to allow titration to effect, most emergency anticonvulsant therapy is administered by the intravenous route- some medications are irritant if injected perivascularly (e.g. diazepam and phenobarbital).
Place a long line that has been flushed.
What emergency drugs are usually administered as an emergency treatment for an animal that is seizuring?
Emergency treatment should be selected by the veterinary surgeon but could include the following options:
Benzodiazepines (diazepam, midazolam)
Phenobarbital, alone or following diazepam/midazolam
Levetiracetam
What are the important considerations when administering benzodiazepines in a seizuring patient?
Benzodiazepines (diazepam, midazolam) are often the first line of treatment in the emergency patient- they can be effective in many patients at a low dose
(Charalambous, 2018). If IV access is not possible, they can be administered by rectal, intramuscular (IM), buccal or sublingual routes – N.B. diazepam should not be injected by the IM route due to the potential for tissue damage.
In addition to IV bolus therapy, diazepam MAY be administered as a CRI (but with extreme caution in cats).
What are the important considerations when administering phenobarbital in a seizuring patient?
Phenobarbital, alone or following diazepam/midazolam, can be administered as a slow IV bolus. This may be repeated as required BUT care should be
taken to leave at least 30 minutes between doses as this drug takes 20-30 minutes to reach full effect. It is also important to ascertain whether the patient is already receiving oral phenobarbitone medication. If so blood should be obtained to assess serum phenobarbitone level and the amount of intravenous phenobarbitone should be calculated with this in mind
What nerve is recognised as having anti-convulsive effects?
Vagal nerve stimulation is also recognised as having anti-convulsive effects
What drugs can be administered if IV access is not possible in a seizuring patient?
If IV access is not possible, diazepam may be administered per rectum at 0.5- 1mg/kg- this can be repeated every ten minutes up to a maximum of three times in a 24-hour period (BSAVA, 2014). The response to this can be quite variable with the response being quite poor in some patients. Recent work has
demonstrated the effectiveness of intranasal administration of midazolam in the emergency management of the seizuring patient. It is also reported to cause less CNS and respiratory depression than diazepam
If seizuring continues despite the administration of initial medication, what is it necessary to do?
If seizuring continues despite the above initial medication it will be necessary to move on to another course of therapy.
1) Propofol may be administered as a series of IV boluses to effect (up to a maximum of 6mg/kg); it is then continued as a lower dose constant rate infusion.
2) Ketamine can be administered as a bolus and continued as a CRI
3) Fosphenytoin can also be used as an IV bolus.
If this is not successful, inhalant anaesthesia with isoflurane can be performed.
What monitoring and post seizure care is required for a patient that has presented with seizures?
Careful patient monitoring is required- this includes ensuring the patient has a patent airway; is breathing adequately; is cardiovascularly stable and is normothermic (the patient may initially be hyperthermic but may then develop hypothermia). The mean arterial blood pressure should be maintained at 80-100 mmHg to ensure adequate cerebral perfusion. It is essential to avoid hypotension - cerebral perfusion (CPP) depends on mean systemic arterial pressure (MAP) and intracranial pressure (ICP) – (CPP = MAP – ICP). Either increased ICP or decreased MAP can decrease cerebral perfusion. If the patient is hypoventilating or has lost its swallow/gag reflex, an endotracheal tube should be placed and ventilation provided. If the patient is breathing well, additional oxygen could be provided via a facemask ( or the means most tolerated). As with traumatic brain injury, the patient should be placed on a board that is raised 15-30 degrees and be turned every 2-4 hours. Appropriate ocular and oral care should be provided e.g. sterile ocular lubricant. Ideally an indwelling urinary catheter should be placed to ensure adequate urine output of 1-2 ml/kg/hr, assess specific gravity and to note urine colour: Myoglobinuria may occur secondary to the muscle damage caused by seizure activity.
Ongoing aseptic management of the intravenous catheter is essential to ensure patency for maintenance of drug and IV fluid administration. Warmed IV fluids should be delivered at the rate indicated by the patient’s hydration and circulation status: both over-infusion and under-infusion must be avoided. 0.9% sodium chloride infusion would not be appropriate for a dog already being medicated with potassium
bromide.
A neurological assessment should be regularly performed and recorded within the medical record: the patient should be monitored carefully for signs of increased intracranial pressure.
Mentation and cranial nerve reflexes should be assessed:
1) PLRs
2) Pupil asymmetry (anisocoria)
3) Pupil size
4) Gag reflex
5) Facial sensation
6) Strabismus
7) Nystagmus
Blood samples should be regularly assessed for glucose, electrolytes, PCV, TP, urea and creatinine levels. Arterial blood gases, SpO2 and blood pressure should be monitored too.
What type of fluids would not be appropriate for a dog already being medicated with potassium bromide?
0.9% sodium chloride infusion would not be appropriate for a dog already being medicated with potassium bromide
What cranial nerve reflexes should be assessed and monitored in a patient post seizure?
Mentation and cranial nerve reflexes should be assessed:
1) PLRs
2) Pupil asymmetry (anisocoria)
3) Pupil size
4) Gag reflex
5) Facial sensation
6) Strabismus
7) Nystagmus
What further investigation (after initial emergency treatment) is required for the diagnosis and treatment of a brain tumour or idiopathic epilepsy?
Further investigation, including MRI/CT, will often be required to reach a diagnosis.
If the patient is diagnosed with a brain tumour or idiopathic epilepsy (IE), ongoing anticonvulsant therapy is likely to be required. For dogs not having cluster seizures, either imepitoin or phenobarbitone is the initial medication of choice for IE.
Depending on response to treatment other medications such as potassium bromide may be added in. Phenobarbitone is used for cats with IE. Serum levels of any anticonvulsant should be regularly checked. A full discussion of IE is beyond the
scope of these course notes.
What might traumatic spinal cord injuries arise due to?
Traumatic spinal cord injuries may arise due to:
1) vertebral trauma
2) intervertebral disc(s) protrusion or prolapse
3) ischaemic myelopathy due to fibro-cartilaginous embolism
What vertebral injuries can occur as a result of trauma?
Vertebral injuries (e.g. fall, RTA) can result in complicated (spinal cord injury) fractures or luxations/subluxations (displacement) of vertebrae.
What breeds do Hansen type I disc extrusions occur relatively frequently in and what is this secondary to?
Hansen type I disc extrusions occur relatively frequently in chondrodystrophic breeds (e.g. Bassett Hound, Dachshund) secondary to chondroid degeneration of the nucleus pulposus in the intervertebral disc
What happens with Hansen type I disc extrusions and how dog usually acquire it?
This, usually inherited tendency, leads to mineralisation and calcification of the affected discs with loss of shock-absorbing ability. The degenerating disc(s) may put gradual pressure on the spinal cord, causing clinical signs but often the extrusion occurs suddenly leading to spinal cord compression. More significantly, dorsal rupture of the annulus fibrosis may occur suddenly resulting the nucleus pulposus and other disc material moving into the spinal canal, causing spinal cord compression and affecting function.
What is Hansen type !! disc protrusion and what is it secondary to?
Hansen type II disc protrusion is secondary to fibroid disc degeneration- a bulging, intact annulus fibrosis or a partially ruptured annulus fibrosis causes spinal cord
compression. In this case, however, the nucleus pulposus remains within the disc. Fibroid disc degeneration can occur in any breed of dog, but is more common in older, large breed dogs. Calcification of the disc is rare and the clinical signs are often more insidious and chronic.
What areas do disc extrusion and protrusion most commonly affect?
Disc extrusion or protrusion is most likely to arise in the cervical, caudal thoracic or
lumbar areas. It is less common between T1 and T11 due to the presence of strong
intercapital ligaments between T2 and T10.
What does the severity of disc extrusion/protrusion depend on?
The severity of the clinical signs depend on:
The force with which the disc extrudes
The degree of damage to the spinal cord caused by the extruded disc material
The extent of the local haemorrhage, inflammatory response and cord
swelling
The degree of spinal cord compression and the progression.
What are Fibrocartilaginous emboli? What clinical signs does it cause? What breeds does it affect most commonly and where does it arise?
Fibrocartilaginous emboli (FCE) are damaged disc fragments (usually from the nucleus pulposus) which can block the local arteries supplying the spinal cord, cutting off the blood supply. The infarction causes a generally painless, nonprogressive ischaemic myelopathy in affected animals. FCE usually occur in younger, medium to large breed dogs ( although all dogs and cats may be affected) with no prior warning They most commonly arise in the lumbar region, interrupting transmission of ascending and descending nerve impulses, thus causing hind limb paresis or paralysis which may be uni or bilateral.
What may be the cause of chronic, non-traumatic spinal cord disease?
Additional, usually more chronic, non-traumatic causes of spinal cord disease
include:
1) Neoplasia
2) Spinal cord or canal haemorrhage (producing a compressive lesion of the spinal cord)
3) Discospondylitis (infection of the vertebrae and disc)
Neoplasms can arise from any structure within the spinal column (or vertebral column) and so can occur at any point.
What is discospondylitis, where does it usually occur and what are the clinical signs?
Discospondylitis (infection of the vertebrae and disc)
Discospondylitis typically occurs around the L7/S1 area and is often associated with haematogenous spread of bacteria, often from urinary tract infections, to the
vertebrae. Affected animals are often systemically unwell with localised pain e.g. pyrexia and anorexia in addition to having neurological clinical signs
How should a patient with a possible or actual spinal injury be moved?
It is very important that any animal with possible or actual spinal cord injury is moved carefully so that no further damage is done. The use of a spinal board and /or stretchers - with rolled towels placed along the animal’s flanks, to prevent rolling and excessive movement, is advised. Lifting of the patient should be performed by two or more people with the aim of minimising movement of the spinal column.
How should you initially manage and assess a patient with a possible or actual spinal cord injury?
It is very important that any animal with possible or actual spinal cord injury is moved carefully so that no further damage is done. The use of a spinal board and /or stretchers - with rolled towels placed along the animal’s flanks, to prevent rolling and excessive movement, is advised. Lifting of the patient should be performed by two or more people with the aim of minimising movement of the spinal column.
The patient should be triaged with airway, breathing and circulation assessed; hypotension, hypovolaemia and hypoxaemia should be managed if necessary. Pain
levels should also be assessed.
Following, initial triage, a detailed history and examination is required which will assist in both localising and gauging the severity of the problem. The assessment of cranial nerve and spinal cord reflex actions can assist in localisation of the lesion;
monitor patient progress.
Clinical signs will depend on the cause and severity of the injury. There may be contusion, laceration, compression, decreased blood supply and vertebral instability.
Vertebral instability can lead to repeated spinal cord trauma. Animals with spinal cord injuries are likely to have normal mentation: although they may be subdued.
Their cranial nerve reflex actions will be unaffected.
How do you localise spinal cord injuries of C1-C5, what signs may be seen?
Spinal segment lesion C1-C5
Depending on the severity of the injury, these cases will have tetraparesis or tetraplegia. Spinal reflexes are likely to be present in all four limbs- they may be
normal or exaggerated
Severe injury could cause paresis or paralysis of the muscles of respiration which could lead to a rapid deterioration in the patient’s condition or sudden death.
How do you localise spinal cord injuries of C6-T2, what signs may be seen?
Spinal segment lesion C6-T2
Depending on the severity of the injury, these cases will have tetraparesis or tetraplegia. Spinal reflexes are likely to be present in the hind limbs where they may
be normal or exaggerated; spinal reflexes will be reduced or absent in the forelimbs.
Breathing may also be affected as the intercostal muscles may be paretic or paralysed: leaving only the diaphragm as the muscle of respiration. Unilateral lesions in the area of T1-T3 often produce an ipsilateral Horner’s syndrome.
How do you localise spinal cord injuries of T3-L3, what signs may be seen?
Spinal segment lesion T3-L3
This is a common site for spinal cord lesions especially from T10-L3. The forelimbs are normal. Depending on the severity of the injury, these cases will have paraparesis or paraplegia. Spinal reflexes are likely to be present in all four limbs they may be normal or exaggerated in the hind limbs.
Schiff-Sherrington posture may be seen in cases of serious of spinal cord injury of this region- there is markedly increased forelimb muscle tone with extensor rigidity: the hind limb reflexes may be normal to decreased.
Whilst this occurs with serious injury it is NOT now considered to be a prognostic indicator for recovery - it indicates the area of spinal cord affected by injury. A better prognostic indicator is presence or absence of deep pain sensation; and the rate at
which this returns.