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.
How do you localise spinal cord injuries of L4-S3, what signs may be seen?
Spinal segment lesion L4-S3
Depending on the severity of the injury, these cases will have paraparesis or paraplegia. Spinal reflexes will be normal in the forelimbs but absent or reduced in
the hind limbs.
In addition, for the more caudally situated lesions, lack of anal tone and urinary sphincter tone may be apparent, with urinary or faecal incontinence, and an easily expressed, flaccid bladder.
What diagnostic imagine is required for spinal injuries?
Diagnostic Imaging
Advanced diagnostic imaging (MRI/CT) will generally be required for diagnosis and treatment planning. Radiography, if performed with care, can be helpful in the initial assessment of the emergency spinal cord case e.g. survey lateral radiographs may indicate the presence of a vertebral fracture or luxation. It is very important that any further patient movement is minimised if a fracture or luxation is confirmed
What may radiography reveal in a patient with disco-spondylitis? What other signs will be seen?
A patient with disco-spondylitis may have radiographic evidence of lysis of vertebrae in the lumbo-sacral region- the patient may be pyrexic with localised pain and an accompanying urinary tract infection
What are the prognostic indicators that can give an indication of the severity and progression of the spinal cord injury?
Prognostic indicators: The prognosis for full recovery for animals with serious spinal cord injuries is guarded. Initial and ongoing assessment of the voluntary motor deficit, urinary function and presence of deep pain sensation give an indication of the severity and progression of the spinal cord injury.
What grading system can be applied to give an indication of the severity and progression of the spinal cord injury?
The following grading system can be applied (Bush, 2014):
Grade 1 - Pain only. Ambulatory with no other deficits noted.
Grade 2 - Tetra or paraparesis. Ambulatory with loss of proprioceptive function, weakness and ataxia.
Grade 3 - Tetra or paraparesis. Non-ambulatory, but evidence of voluntary movement in the limbs.
Grade 4 - Tetra or paraplegia. Non-ambulatory, with no evidence of voluntary movement in the limbs, deep pain sensation present. +/- Urinary function.
Grade 5 - Paraplegia. As above, with no evidence of deep pain sensation.
How can spinal cord injuries affect the urinary bladder?
Depending on the nature and location of the spinal cord injury, animals may have altered urinary function: there may be reflex urination, urinary incontinence or urinary retention and overflow. Early assessment and appropriate management of urinary function is essential. The bladder of animals with reflex urination and urinary retention and overflow, may be harder to express than normal. Animals with disco-spondylitis may also have a urinary tract infection (UTI): UTI’s can also develop as a complication of spinal cord injury and associated recumbency.
How do you handle, provide initial management and treat spinal cord injuries?
Handling of the patient
It is vital that the patient’s movement is restricted during hospitalisation.
Initial management
Following a full clinical examination +/- diagnostic imaging, a treatment plan will be made. The severity of the injury, poor prognosis or prolonged hospitalisation required may mean that euthanasia is required.
Treatment will be surgical or conservative (medical).
Surgical intervention may be necessary for stabilisation or decompression with fractures, luxations or intervertebral disc disease. Initial medical management usually consists of NSAID and opioid administration
combined with strict cage rest. Benzodiazepines may be used for muscle relaxation. The use of glucocorticoids/steroids is not recommended for spinal cord injuries but may be required for inflammatory conditions.
Animals with disco-spondylitis will require antibiotic therapy based on culture and sensitivity for a period of at least 6-8 weeks.
What neurological function assessment should be carried out on a patient with a spinal injury following ongoing care? How often should this be carried out?
An assessment of neurological function should be made 1-2 x daily. This should include an assessment of the spinal reflexes (including the panniculus reflex),
proprioception and voluntary motor function. Deep pain sensation should be assessed, as appropriate, following consultation with a veterinary surgeon. A
validated pain scoring system should be used to monitor the patient’s progress.
What body systems should be monitored if lesions are high up in the cervical area and why?
As lesions high up in the cervical area, may affect cardiac and respiratory function, it is important to be vigilant in monitoring of respiratory and cardiac function.
How do you manage a recumbent patient’s urinary output?
Any recumbent patient (comatose, stuporous, spinal injury) may require an indwelling urinary catheter with a closed collection system - this requires appropriate
aseptic management. In all recumbent patients, the bladder should be regularly palpated to ensure it is not becoming over-full. The patient should be assessed for
any evidence of urine scald. For more information on urinary catheterisation
What physiotherapy is required in a recumbent patient?
Patient will need to be turned with care every 2-4 hours to prevent decubitus ulceration and hypostatic pneumonia. Appropriate postural, passive and active
physiotherapy, under veterinary direction, will be beneficial at various stages throughout the patient’s recuperation e.g. coupage. Initial passive physiotherapy will encourage blood flow to the limbs helping to maintain muscle tone. Physiotherapy should be avoided where patients are at risk of seizuring and where unstable spinal trauma is present.
It is important to be aware of the challenges and potential complications associated
with nursing neurological patients- these can include depression, hypostatic
pneumonia, decubitus ulcers and urine scald.
How can you manage a recumbent patients faecal output?
Faecal output may need to be managed- diarrhoea, faecal incontinence or constipation may occur. Enemas may be required.
What can be the cause of brain injury or disease?
There are many causes of brain injury and disease. Clinical signs associated with brain disease may develop suddenly in spite of the underlying cause having been present for a longer period e.g. blindness secondary to an expanding brain tumour.
These include
1) Trauma
2) Inflammation (of the brain [encephalitis] or the meninges [meningitis] or both [meningoencephalitis]). This may be sterile or infectious in origin.
3) Congenital defects (e.g. cerebella hypoplasia)
4) Cerebral oedema
5) Vascular infarcts (‘stroke’)
6) Age related degeneration
7) Tumour
8) Epilepsy
What two categories can head trauma be divided into?
Head trauma can be split into primary and secondary injury
How does primary head injury occur and what does it result in?
Primary injury occurs through direct concussive forces e.g. road traffic collision, kick or fall. This results in
haemorrhage and direct neuron damage
How does secondary head injury occur and what does it result in?
Secondary injury occurs in response to, and is a serious complication of, the initial insult. Inflammation with release of inflammatory mediators, including excitatory amino acids, leads to cerebral oedema,
decreased cerebral perfusion and cerebral hypoxia. This leads to brain swelling, increased intracranial pressure and further neuronal damage.
What assessments should be carried out when triaging a patient with head trauma?
As will all emergency patients a brief, rapid history should be obtained with an initial assessment of the three major body systems (cardiovascular, respiratory, and neurological) any immediately life-threatening problems managed accordingly.
Further neurological assessment involves assessing mental status, brainstem reflexes and gait. The Modified Glasgow Coma Score (MGCS) can be used for
objective assessment
What mental alertness would be considered an emergency?
Stupor and coma are considered to be emergencies
Define the term alert?
Alert: aware of surroundings and responsive
Define the term obtunded?
Obtunded: decreased awareness but reacts to stimuli
Define the term stupor?
Stupor: decreased consciousness, difficult to rouse but responsive to strong stimuli
Define the term coma?
Coma: unresponsive to any stimuli
Define the term Opisthotonus?
Opisthotonus: Extreme hyperextended posture with increased extensor tone of the limbs and the neck
Define the term Decerebrate rigidity?
Decerebrate rigidity:
opisthotonus with extensor rigidity of fore and hind limbs.
Animal is comatose; absent PLRs; pinpoint or dilated pupils. Poor prognosis: cerebral lesion
Opisthotonus: Extreme hyperextended posture with increased extensor tone of the limbs and the neck
Define the term Decerebellate rigidity?
Decerebellate rigidity: opisthotonus with extensor rigidity of fore limbs. Animal usually conscious; PLR’s present. Cerebellar lesion.
Opisthotonus: Extreme hyperextended posture with increased extensor tone of the limbs and the neck
What is a cushing reflex?
Cushing’s reflex: this is caused by increased intracranial pressure. Systemic hypertension arises in an attempt to maintain cerebral perfusion: this is accompanied by a reflex bradycardia.
What is a significant alteration in consciousness likely to be associated with?
Significant alteration in consciousness (e.g. coma) is likely to be associated with brainstem disease
What could any sudden alteration in a patients mentation be due to?
Any sudden alteration in a patient’s condition could be due to brain herniation, arising secondary to increased intracranial pressure, and is a very serious complication which should be anticipated in animals presenting with brain injuries
What is Transtentorial herniation of the forebrain? and what can this lead to?
Transtentorial herniation of the forebrain compresses the midbrain, leading to altered consciousness; loss of the pupillary light reflexes; meiosis followed by
mydriasis; decerebrate rigidity and hyperventilation. Prompt recognition of these signs is required if the patient is to have any chance of survival.
What can Herniation through the foramen magnum cause and what is the prognosis?
Herniation through the foramen magnum causes central vestibular signs, coma, altered respiratory rate and pattern and altered heart rate, rhythm and blood
pressure. This is a very serious condition that is unlikely to be reversible.
What are the clinical signs of a traumatic brain injury?
1) Altered mentation
2) Seizuring
3) Nystagmus
4) Miosis/mydriasis
5) Anisocoria
6) Absent PLRs
7) Tetraparesis/plegia; hemiparesis/plegia; decerebrate rigidity; opisthotonus; altered muscle tone
8) Photophobia
What type of diagnostic imaging should a patient with suspected or confirmed traumatic injury ideally have?
Any animal with suspected or confirmed traumatic brain injury, with compatible signs, should ideally have advanced prompt diagnostic imaging (CT/ MRI) to allow
for accurate diagnosis and treatment planning.
What are many of the clinical signs with traumatic brain injury associated with?
Many of the clinical signs described are associated with an increase in intracranial pressure (ICP). Raised ICP is life-threatening (irreversible neuron damage) with brain herniation being a serious consequence - consequently it requires to be recognised promptly
What clinical findings can intracranial pressure provisionally be diagnosed?
Raised ICP can be provisionally diagnosed by patient
assessment, based on several clinical findings, (oedema of the optic disc; pulsating retinal vessels; elevated blood pressure and bradycardia). Noting bradycardia in any patient that has a brain injury/ disease is significant. It is not possible to accurately measure intracranial pressure in veterinary patients but it can be estimated using transcranial Doppler measurements.
What is the normal intracranial pressure in dogs and cats?
Normal ICP in cats and dogs is 5 – 10mmHg
What predominant factor controls blood flow to the brain and what is this dependent on?
When dealing with head trauma patients it is important to maintain an adequate blood supply to the brain. Cerebral perfusion pressure (CPP) is the predominant
factor which controls blood flow to the brain and is dependent on mean arterial pressure (MAP) and intracranial pressure (ICP) as shown in the following equation:
CPP = MAP – ICP
What can an increased blood pressure suggest in a patient with traumatic brain injury?
Normally cerebral blood flow is maintained within narrow limits. However, in a brain trauma patient these control factors are lost and cerebral blood flow becomes directly proportional to systemic blood pressure. Most cases of head trauma present
with increased blood pressure, suggesting corresponding increased intracranial pressure. Associated with increased ICP is bradycardia which is an important clinical parameter to note. This combination of high blood pressure and low heart rate is termed the Cushing’s reflex.
However, there are also cases where hypotension can be present resulting in decreased cerebral perfusion, ischaemia and cerebral oedema.
Regular monitoring, noting any trends, of blood pressure and heart rate is important in the clinical work up of these patients
Why is important to measure blood gas in patient with traumatic brain injury?
Respiration rates may become depressed therefore measurement of blood gases is important in monitoring the patient’s progress.
Why is oxygen therapy often necessary in patients with head trauma?
As with all trauma patients, oxygen therapy is often necessary- ventilation may be reduced due to direct head trauma or damage to nerves supplying the respiratory muscles .The patient must not be stressed by oxygen administration as this may further increase ICP. Methods that may cause sneezing or coughing should be e.g. nasal prongs
How can hyperventilation assist with decreasing intracranial pressure?
Hyperventilation has previously been considered a means of decreasing ICP as the reduced PaCO2, caused by mechanical hyperventilation, results in cerebral vasoconstriction thus aiding reduction of ICP. This, however, will result in cerebral hypoxia which is associated with decreased chance of survival in human patients. Hyperventilation should only be used as a short-term measure if there is imminent risk of brain herniation. Instead the aim should be adequate oxygenation with maintenance of the PaCO2 within the normal range (35-40 mmHg).
How can patient positioning assist with decreasing intracranial pressure?
Another procedure aimed at reducing ICP is patient positioning. Raising the patient’s head by 15-30 degrees above the pelvis, aids venous drainage from the brain, thus reducing ICP. The patient’s neck should not be flexed as this will decrease drainage.
The whole patient should be elevated using a tilting table or a rigid board. The jugular vein should not be used for blood sampling.
Shoud fluid therapy in a patient with intra cranial pressure be restricted to reduce cerebral oedema?
Mean arterial pressure should be maintained between 70 and 110 mmHg - fluid therapy is generally indicated accompanied with blood pressure monitoring. Fluid
therapy should never be restricted for fear of causing cerebral oedema. There is more likelihood of problems arising with cerebral hypoxia (secondary to decreased
perfusion) than with IVFT. It is, however, essential to avoid both over and under perfusion and to monitor the patient carefully to maintain euvolaemia. Isotonic fluids
are generally appropriate for circulatory support- hypotonic fluids are contraindicated as they increase the likelihood of cerebral oedema.
How does hypertonic saline assist in a patient intracranial pressure from a trauma?
Hypertonic saline may be used in the management of both hypovolaemia and ICP.
Hypertonic saline is a concentrated solution of sodium chloride (7.5%) that also draws fluid from the interstitium and intracellular space into the intravascular space.
This results in an abrupt increase in intravascular volume (correcting any hypotension) and reduces the intracranial pressure.
How does mannitol assist in a patient intracranial pressure from a trauma?
Mannitol may also be used in the management of increased ICP. Mannitol is an osmotic diuretic and draws fluid out of oedematous cells within the body, including the brain. Mannitol may be used at 0.5-2g/kg, as a 15-25% solution given over 20-30 minutes - it should only be used in patients that are cardiovascularly stable.
What is the dose of mannitol?
Mannitol may be used at 0.5-2g/kg, as a 15-25% solution given over 20-30 minutes
Are corticosteroids indicated in patients with a traumatic brain injury?
The use of corticosteroids is not recommended in animals with traumatic brain injury
What will analgesia choice in a patient with a traumatic brain injury be affected by?
Opiates are the drug of choice for analgesia- the choice of opiate will be affected by several factors e.g. the potential risk of increased ICP associated with vomiting following morphine administration
What patient parameters should be monitored in a patient with a traumatic brain injury?
It is important that continuous monitoring is provided, noting any trends, to allow rapid instigation of emergency procedures as required.
In addition to monitoring TPR, blood pressure, perfusion parameters, demeanour and pain levels, specific neurological assessment should be performed. Respiratory rate and pattern should be carefully assessed as any alteration in these could be
associated with patient deterioration.
Patient mentation should be assessed as1) Normal (alert)
2) Depressed
3) Obtunded
4) Stuporous
5) Comatose
How can the cranial nerves be assessed and monitored in a patient with a traumatic brain injury?
The patient posture should be assessed noting any abnormal positions e.g. opisthotonus.
The presence of nystagmus, pupillary light reflexes (PLRs), oculo-cephalic reflexes, pupil size and eye position should be noted. Many head trauma patients will have unequal pupil size (anisocoria). Widely dilated pupils that are unresponsive to light (fixed and dilated pupils) are an extremely poor prognostic indicator and suggesting significant brainstem damage. The progression from constricted to dilated pupils can
therefore indicate a worsening of the condition, suggestive of brainstem herniation.
Initially ICP, can stimulate the oculomotor nerve (CNIII) leading to pupillary constriction. With increasing ICP, the brain is displaced caudally. The hind brain and
brain stem are telescoped into the proximal spinal column putting further pressure on the oculomotor nerve and stopping it from working (normally causes miosis).
Consequently, the pupils become dilated and unresponsive. Further herniation of the brain, through the foramen magnum, places further pressure on nerves in the spinal cord leading to limb abnormalities e.g. decerebrate rigidity. As previously discussed,
with decerebrate rigidity, the patient will show opisthotonus, fore and hind limb extensor rigidity and respiratory depression.
How can oxygenation be assessed in a patient with a traumatic brain injury and in which situation would this be especially important?
Oxygenation should be assessed, ideally using blood gases, or by pulse oximetry if blood gas analysis is not possible- especially if the patient is comatose and
mechanical ventilation is required. It is important to also ensure PaCO2 levels are maintained within a range of 35-40mmHg. Hyperventilation due to mechanical ventilation leads to reflex cerebral vasoconstriction which would cause cerebral hypoxia. This situation should be avoided unless the emergency prevention of brain herniation is being attempted.
It is vital to remember that as ICP increases, blood pressure tends to increase and the heart tends to decrease.
What signs are usually seen in patients with meningitis and/or meningoencephalitis?
Patients with meningitis and/or meningoencephalitis may present with neck pain, photophobia and pyrexia, with varying levels of neurological dysfunction. Patients
are commonly depressed and disorientated
What test is used to diagnose meningitis/ meningoencephalitis? What is the contraindication to performing this test?
Cerebro-spinal fluid (CSF) collection and analysis may be indicated in the diagnosis of meningitis/ meningoencephalitis.
There is a significant risk of brain herniation if CSF collection is attempted in patients with increased ICP, therefore this should be recognised and managed prior to CSF sampling
Describe the technique for cerebrospinal fluid collection?
Technique for CSF collection
This is an act of veterinary surgery which cannot be legally delegated to a veterinary
nurse.
The patient will need to be anaesthetised and placed in lateral or sternal recumbency with the muzzle elevated. A ~ 5 cm square area of skin is clipped using the midline, occipital protuberance at the base of the skull and the wings of the atlas as landmarks.
During collection, the head is flexed so that the nose is at right-angles to the neck and parallel to the table top. It is important to ensure the ET tube is not kinked or
obstructed. Monitoring of the heart rate, pulse quality and blood pressure is also important during CSF collection. Because of the risk of hypoventilation due to patient position, oxygenation should be monitored closely. The site for insertion of the spinal needle (1.5 to 3 inch/ 3.8-6.4cm/ 20-22 gauge) is mid-way between the
What is vestibular disease?
Vestibular disease is the name given to any condition which affects the balance centres. There are two main areas which deal with balance- a central brain site (medulla and cerebellum); and the peripheral semi-circular canals and the vestibule of the inner ear. Disease in either area, or the nerve which
transmits impulses from the inner ear to the cerebellum (the vestibulocochlear nerve/cranial nerve VIII), can result in balance disorders.
What are the causes of vestibular disease?
Causes of vestibular disease include
1) Inner/middle ear disease
2) Cerebellar disease
3) Infection (e.g. viral [distemper, FIP], parasitic [Toxoplasma], fungal
[Cryptococcus neoformans])
4) Infarction (‘strokes’)
5) Toxins (e.g. metronidazole toxicity affecting the cerebellum/medulla)
6) Metabolic
7) Neoplasia
8) Idiopathic (unknown cause typical in older dogs and cats) -this is the commonest cause of vestibular disease in dogs.
What are the clinical signs of vestibular disease?
Clinical signs
Vestibular disease is often rapid in onset.
Clinical signs can include
1) Nystagmus
2) Head tilt
3) Rolling
4) Circling
5) Ventral strabismus (may not be noted until head is elevated)
6) Inability to stand
7) Wide-based stance or altered gait: hypermetria or dysmetria.
8) Vomiting and nausea
Inner ear disease may be an extension of middle ear disease- associated clinical signs may be present e.g. Horner’s syndrome and dysfunction of cranial nerve VII
(facial nerve). Horner’s syndrome would be very unlikely to occur in central vestibular disease.
What can horners syndrome arise due to and what are the signs?
Horner’s syndrome arises due to interruption of the sympathetic nervous supply to the eye. Signs of Horner’s syndrome include miosis, enophthalmos, protrusion of the third eyelid and ptosis of the upper eyelid. As a result of facial nerve dysfunction,
the patient may also have keratoconjunctivitis sicca (KCS/ dry eye). If nystagmus is present it tends to be horizontal or rotational with the slow phase towards the side of the head with the lesion. Additionally, the direction of the nystagmus does not
change when the head is tilted.
How do you diagnose vestibular disease and what can aid the differentiation between central from peripheral vestibular disease?
Neurological examination can aid differentiation of central from peripheral vestibular disease, thus helping to establish a cause and prognosis. The prognosis for central vestibular disease is poorer than for peripheral vestibular disease. Establishing a cause of central vestibular disease will need further investigation e.g. MRI With diseases of the inner and middle ear, there may be Horner’s syndrome and damage to the facial nerve.
What is suggestive of vestibular disease affecting the medulla and cerebellum?
With diseases of the medulla and cerebellum there may be other signs suggestive of brain disease such as altered mentation and seizures- often the patient has a widebased stance and sways from side to side. Nystagmus will often change when the head is tilted and can be in any direction. Cranial nerve damage may be present on the same side as the lesion and may affect any cranial nerve from V-XII.
What diagnostic imaging can confirm middle and inner ear disease causing vestibular signs?
With middle and inner ear disease, radiography, CT or MRI of the tympanic bullae may show abnormalities
What type of treatment is required for peripheral and central vestibular disease?
For peripheral vestibular disease the treatment is usually symptomatic and supportive. Treatment for central peripheral disease depends on the cause
What initial medication may be required for patients with vestibular signs?
Initial medication
If seizuring has occurred / is occurring then anti-convulsant therapy may be required (e.g. diazepam or phenobarbital) as discussed previously. The patient should be kept in a quiet environment with dimmed lighting.
Many patients may also be vomiting/feeling nauseous (motion sickness) and so may benefit from the administration of anti-nausea or anti-emetic medications e.g. metoclopramide or maropitant. Middle/ inner ear infections will require appropriate treatment e.g. systemic broad spectrum antibiotics.
Middle ear polyps may require surgery.
What important considerations are there when managing a patient with vestibular signs?
Initial management
Most patients will need strict cage rest, minimal excitement and may need to be kept in a kennel which is padded to reduce trauma.
Care should also be taken to ensure the patient can feed properly. Many cannot position themselves to do this and so may require assisted feeding.
What ongoing medication is usually required for a patient with inner ear disease displaying vestibular signs?
Antibiotics may need to be continued for a period of 4-6 weeks in cases of inner ear disease.
Why are telephone triage of ocular problems difficult?
Telephone triage of ocular problems is very difficult as the eyes have limited responses to insult: a red eye, increased lacrimation and blepharospasm could be
due to conjunctivitis, a penetrating foreign body or anterior uveitis. Ideally all patients should be seen as soon as possible. Rapid recognition of the cause and appropriate management is needed to minimise patient discomfort and prevent irreversible eye damage. If an owner reports that their animal may have a foreign body, they should be advised to come immediately to the veterinary practice and must NOT attempt to remove this themselves. Advice should be given on how to transport the patient so that it does no further harm to itself.
Why should patients with ocular problems be handled carefully and what should part of the triage process include?
Patients should be handled carefully and any procedure which may increase intraocular pressure should be avoided - if the patient is stressed by handling, sedation may be the preferred option. Most ocular emergencies are very painful and there is a risk of the condition worsening due to self-trauma- an Elizabethan Collar should usually be applied. The patient should be in a quiet environment, in dimmed light and will need to be observed continually. As part of the triage assessment, a rapid, visual examination of the eye(s) should be performed, noting any abnormalities, especially those that may require rapid veterinary intervention e.g. prolapse, ruptured globe. First aid measures may be required at this stage.
What does an ophthalmological examination involved and what equipment is needed?
Once the patient’s condition permits it, the veterinary surgeon will require to perform a thorough examination of the eye, including beneath the third eyelid where foreign bodies e.g. grass seeds may be located. Eye examinations are best performed in
dimmed but not entirely dark rooms.
Clinical assessment involves visual examination aided by equipment such as a pen torch, an indirect ophthalmoscope, a direct ophthalmoscope, a tonometer and ultrasound.
Additional equipment that will often be required for ophthalmic examinations includes:
1) Fluorescein pipettes or paper strips
2) Schirmer Tear Test strips
3) Topical local anaesthetic pipettes (proxymetacaine and amethocaine) - these should be stored in the fridge
4) Tropicamide ‘Mydriacyl®’: this is used to dilate the pupil for ocular examinations
Any products in pipettes are intended for single use only, as they contain no preservative. Prolonged or repeated application of local anaesthetic can cause
corneal damage.
What is a corneal ulcer?
A corneal ulcer is present when an area of cornea has lost its outer epithelium and some of the underlying stroma. Corneal ulcers are a result of damage to the
transparent cornea- they are common and can vary significantly in severity. The deeper the ulcer is the more serious it is; especially if it occupies a large area. As the cornea forms part of the outer wall of the eye, damage affects the integrity of the eye- rupture of the globe is a very serious possible complication of corneal
ulceration. Corneal ulcers can be simple or complicated- some heal well and others have delayed healing. During the initial emergency presentation, the healing potential of the ulcer is generally unknown, unless the patient has a history of corneal ulceration. As with all wounds, however, the initial management can have an impact on subsequent healing so it is important to have a good understanding of corneal anatomy and physiology.
What can corneal ulcers occur due to?
Corneal ulcers can occur due to
1) Trauma: abrasion/laceration/surface or foreign bodies
2) Conformation/ inherited tendency e.g. brachycephalic animals
3) Infection e.g. FHV or Chlamydophila in cats; Pseudomonas
4) Decreased tear production keratoconjunctivitis sicca (dry eye)
5) Entropion (inward rolling of the eyelid allowing hairs to rub on the corneal surface)
6) Chemical splashes
Identifying the cause, where possible, ensures appropriate treatment can be
provided
What are some signs of ocular discomfort?
Signs of ocular discomfort could include
1) Blepharospasm
2) Increased lacrimation
3) Enophthalmos
4) Protrusion of the third eyelid
5) Photophobia
6) Reluctance to be handled
What are some signs of a corneal ulcer?
There are numerous pain receptors (nociceptors) within the cornea which are stimulated by corneal injury. Corneal ulceration is a very painful, particularly with
shallow ulcers as there are more nociceptors closer to the surface.
Signs of ocular discomfort could include
1) Blepharospasm
2) Increased lacrimation
3) Enophthalmos
4) Protrusion of the third eyelid
5) Photophobia
6) Reluctance to be handled
Additionally, oedema may be seen around the ulcer as a blue/grey opacity as fluid penetrates the normally dehydrated stroma. In some cases, blood vessels may be seen growing across the, normally avascular, surface of the cornea (corneal neovascularisation). Clinical signs of an associated reflex, anterior uveitis may be
present, in addition, with miosis and pain secondary to ciliary muscle spasm
How can you prevent self trauma in a patient with ocular discomfort?
It is important to prevent the patient doing more damage by self-trauma- an Elizabethan Collar should usually be applied. The patient should be nursed in a quiet environment, in dimmed light and will need to be observed continually.
How do you diagnose a corneal ulcer?
Confirmation of the presence, size, depth of the ulcer and presence of underrun tissue requires administration of fluorescein (new pipette or impregnated paper strip).
An open pipette should not be used as bacteria can grow in fluorescein. Most information about fluorescein uptake by the ulcer can be gained by examination with
a blue light source.
N.B. Descemet’s membrane (the inner endothelial layer of the cornea) does not stain with fluorescein. A non- staining central area in a deep ulcer is a significant finding and veterinary attention should be sought immediately as the eye may be close to rupture.
What initial medication is usually required in a patient with a corneal ulcer?
The medication that may be used will depend on the cause, size and depth of the ulcer.
Analgesia will be required- NSAIDs and/ or opiates. Opiates may be required if there is an accompanying anterior uveitis.
As with all wounds, a moist environment promotes wound healing - artificial tears +/- ocular lubricants will often be used. Other topically applied products, however, may interfere with the healing process due to being foreign material or causing corneal
irritation.
As infection delays healing, topical antibiotic preparations may be indicated.
What medications/products should be avoided in a patient with a corneal ulcer?
Certain products should NOT be used as they are damaging to the cornea or delay healing. Topical corticosteroids should be avoided as they will delay healing; suppress the immune system thus predisposing to bacterial infection; and enhance
collagenase activity which may predispose to the development of a ‘melting ulcer’.
Topical local anaesthetics should not be used for analgesia as they damage the cornea.
How do you treat superficial corneal ulcers?
Superficial ulcers
Most superficial ulcers can be managed symptomatically and should heal within a few days. Occasionally some of these ulcers will not heal due to lifting of the edge of the cornea away from its basement membrane. This can be seen using
fluorescein- the dye can be seen to under-run the edges of the ulcer. In these cases, debridement of the underrun tissue will be required. Additional procedures to stimulate wound healing e.g. grid/ punctate keratotomy may be performed under general anaesthetic to stimulate healing.
Why are deep corneal ulcers serious?
Deep ulcers
These are more serious as there is a greater risk of the globe perforating. Secondary infection is very serious especially with Gram negative bacteria such as
Pseudomonas spp. which produce collagenase enzymes. Collagenase enzymes breakdown the stroma of the cornea, predisposing to melting ulcers which rapidly destroy the cornea increasing the size and the depth of the ulcer
How do you treat deep corneal ulcers?
Deep ulcers
These are more serious as there is a greater risk of the globe perforating. Secondary infection is very serious especially with Gram negative bacteria such as
Pseudomonas spp. which produce collagenase enzymes. Collagenase enzymes breakdown the stroma of the cornea, predisposing to melting ulcers which rapidly destroy the cornea increasing the size and the depth of the ulcer. Appropriate antibiotic therapy will be required in these cases- this should be based on identification of the bacteria, culture and sensitivity (e.g. gentamycin for Pseudomonas).
Anti-collagenases will also be indicated- these help to counteract the collagenase activity as well as promoting corneal repair. Acetylcysteine (5%) is an option but usually autologous (the patient’s own) serum or plasma is used.
In addition to analgesia, a mydriatic e.g. atropine 0.5-1% may be required to overcome iris spasm if anterior uveitis is also present.
How do you get plasma/serum to use in a patient with a deep corneal ulcer?
Blood is obtained from the patient and put into an EDTA, heparin or serum gel tube.
After centrifugation, the serum/plasma is separated and put into a sterile container and refrigerated. It can then be applied very frequently (every 30 minutes to 2 hours) as indicated. The serum/plasma should be handled carefully to prevent microbial
contamination.
Some clinicians use acetyl cysteine in the management of deep/ melting ulcers.
What are the surgical options for a corneal ulcer?
Surgical options may include application of veterinary contact lenses or conjunctival flaps/grafts or, less frequently now, eyelid flap surgical techniques
This is especially likely if a descemetocoele forms
What is A descemetocoele?
A descemetocoele is a sign of impending globe rupture- when the ulcer has eroded through the outer cornea down to the corneal endothelium (Descemet’s membrane), which then protrudes through
the ulcer. As descemet’s membrane does NOT stain with fluorescein, it is very significant to have a very deep ulcer with a central non-staining area especially if a membrane looks to be protruding through the ulcer.
Surgical options may include application of veterinary contact lenses or conjunctival flaps/grafts or, less frequently now, eyelid flap surgical techniques
This is especially likely if a descemetocoele forms
If a descemetocoele is suspected, the veterinary surgeon should be alerted IMMEDIATELY and the animal should not be handled to avoid causing rupture of the globe.
A sudden increase in discomfort and aqueous discharge from the eye of a patient with a deep ulcer could suggest that the eye has ruptured. This requires immediate veterinary attention.
What can chemical burns of the cornea be caused by? What are the potential complications? and what treatment is initially required?
Chemical burns
These can be caused by both acid and alkaline substances - alkali causes more damage to the cornea. Corneal ulceration, sloughing and perforation
are possible complications. Continuous lavage, using warmed sterile saline over 30 minutes, is recommended with the aim of returning the corneal
surface to neutral pH. The pH can be checked using urine dipsticks. Pain management is also essential as is prevention of self-trauma.
What advice could be given to an owner with a pet that has a ocular foreign body? What treatment when arriving in an emergency could be given?
Foreign bodies
These may be periocular, free or embedded. They will cause much discomfort with the patient often trying to rub frantically at the area, potentially causing more harm.
An Elizabethan collar should be applied promptly- the owner could be advised to wrap their pet carefully in a large towel to travel to the surgery.
If the foreign body (FB) is still present but not penetrating, it may be dislodged by flushing with sterile 0.9% saline via a syringe attached to an IV catheter. Some FBs can be securely lodged in or on the cornea- removal should not be attempted until the patient can be safely anaesthetised.
If the foreign body has not penetrated through the full thickness of the cornea, management should be as for a deep corneal ulcer, once removed.
Under GA, leakage of aqueous humour may occur as the FB is removed- this indicates full thickness corneal penetration which requires surgical management as
for a deep corneal ulcer/descemetocoele e.g. conjunctival flap.
Additional analgesia, infection control and management of associate anterior uveitis will be required
What ongoing medication and management should be given a patient with ocular trauma following initial treatment?
Ongoing medication and management
In all cases, ongoing analgesia should be started as ulcers are painful. In addition, an Elizabethan collar is essential to prevent the patient from rubbing the eye which can worsen the condition or precipitate rupture of the globe. Over-zealous restraint can also result in rupture of the globe, where deep ulcers are present, therefore the handling of such patients should be careful.
If the cornea does rupture this may be clearly obvious or may be highlighted by application of fluorescein dye which will form rivulets of stain from the hole (the
Seidel test). Where a conjunctival flap/graft surgery has been performed, regular ongoing assessment of the eye should be performed: wound issues, excessive
discharge or signs of pain should be assessed
What is anterior uveitis?
This is inflammation of the anterior structures of the globe i.e. the iris and ciliary body
Due to iris and ciliary muscle spasm, anterior uveitis is painful and there is usually marked constriction of the pupil.
What can anterior uveitis be caused by?
1) Infection, either local or systemic
2) Trauma ( including ocular surgery)
3) Displaced/ruptured lens/cataract
4) Neoplasia
5) Reflex secondary to e.g. corneal ulceration
6) Immune-mediated
7) Idiopathic (unknown cause).
What are the common causes of anterior uveitis in cats?
It may be a single episode or there may be recurrent episodes, especially in cats.
Infectious causes are common in cats e.g. feline infectious peritonitis (FIP), feline leukaemia virus (FeLV) and feline immunodeficiency virus (FIV) infections.
What are the common causes of anterior uveitis in dogs?
It may be a single episode or there may be recurrent episodes, especially in cats.
In dogs it is generally secondary to other causes e.g. trauma, corneal ulceration or lens luxation.
What are the clinical signs of anterior uveitis?
Clinical signs
These are often inflammatory and pain-related e.g. blepharospasm, increased lacrimation, miosis and episcleral congestion. The iris may appear abnormal in
colour and shape (especially if the uveitis is chronic); there may be corneal oedema, hypopyon or hyphaemia
How do you diagnose anterior uveitis?
This is generally based on the clinical signs especially miosis and pain.
Anterior uveitis may be secondary to other eye problems- it is good practice to assess tear production (Schirmer Tear Test) and exclude corneal ulceration
(fluorescein)
Both tonometry and gonioscopy are useful to rule out glaucoma, another cause of a red painful eye. Glaucoma may arise secondary to anterior uveitis- constriction of the pupil interferes with the flow of aqueous humour, decreasing drainage.
In anterior uveitis, the intra-ocular pressure (IOP) is often less than normal- unless there is secondary glaucoma in which case the IOP will be increased.
Tonometry results may show IOP less than 10 mmHg (normal range 15-25mmHg).
Gonioscopy involves the use of a small diffracting lens placed onto the corneal surface. This allows the clinician to examine the anterior chamber and the drainage angle to try to identify an underlying cause. The eye must be pre-treated with ophthalmic local anaesthetic first.
Finally, anterior uveitis may not be the only clinical sign the patient may be demonstrating, as many of the diseases which lead to anterior uveitis affect the
animal systemically. Careful examination of the rest of the patient may aid diagnosis; combined with haematology, biochemistry, serology, and virology e.g. FIP/FeLV and FIV.
What is the range of intraocular pressure of a patient with anterior uveitis?
In anterior uveitis, the intra-ocular pressure (IOP) is often less than normal- unless there is secondary glaucoma in which case the IOP will be increased.
Tonometry results may show IOP less than 10 mmHg (normal range 15-25mmHg).
What serious complication can occur secondary with anterior uveitis?
A serious complication of anterior uveitis is that secondary to inflammation and inflammatory chemicals, the iris becomes ‘sticky’- this could lead to iris adherence either to the lens behind it (forming posterior synechiae) or to the cornea in front of it
(forming anterior synechiae). The latter is more serious as it can block the drainage angle of the eye and so result in glaucoma.
What initial medication is required for anterior uveitis?
Initial medication
A serious complication of anterior uveitis is that secondary to inflammation and inflammatory chemicals, the iris becomes ‘sticky’- this could lead to iris adherence either to the lens behind it (forming posterior synechiae) or to the cornea in front of it (forming anterior synechiae). The latter is more serious as it can block the drainage angle of the eye and so result in glaucoma. Therefore, the use of a mydriatic (a drug which dilates the pupil) is necessary. Atropine drops are generally used topically 2-3 times daily: to aid pain management by overcoming ciliary spasm; and to maintain dilation of the pupil to prevent glaucoma. If, however, glaucoma is already present atropine is contra-indicated; it should be used with caution in patients with KCS as it will decreased tear production further (Hartley, 2013). Alternatively, tropicamide or adrenaline (1% solution) can be instilled onto the cornea 3 times daily.
If an underlying cause is identified, this should be the focus for treatment. Otherwise, controlling the inflammation and pain is the priority: NSAIDs, analgesics, corticosteroids and immunosuppressants, may all be used in the management depending on the situation. Corticosteroids would be contraindicated if the anterior uveitis was secondary to corneal ulceration.
What ongoing care is required for anterior uveitis?
Where there is an underlying cause such as a viral disease or lens luxation the prognosis is more guarded. Currently the viral conditions are not curable and lens
removal is a specialist operation.
Possible complications of anterior uveitis, as discussed, include pain, adhesions (synechiae) both anterior and posterior, corneal neovascularisation and glaucoma.
Regular assessment for any of these should be included in patient monitoring.
What is uaully the cause of Proptosis/prolapse and rupture of the globe?
Typically this occurs due to trauma such as road traffic accidents- there is also a breed predisposition with brachycephalic breeds being more commonly affected
What is it important to consider when a patient presents with Proptosis/prolapse and rupture of the globe in an emergency?
If the animal has had a traumatic event e.g. RTA, it is important not to be diverted by the prolapsed eye and overlook other potentially life-threatening problems. There may be an associated traumatic brain injury which would be of far greater clinical significance.
Following prolapse there may be irreversible eye or optic nerve damage, meaning that enucleation will be required. PLR and menace reflexes can be tested- lack of response carries a poor prognosis for recovery of vision.
What is the initial management of a patient with Proptosis/prolapse and rupture of the globe in an emergency?
Initial management
The aim of emergency treatment is to protect the eye from any further damage, limit swelling, minimise desiccation, prevent self-trauma and control pain. The prognosis for the eye is improved if it is replaced as soon as possible- so the patient should not be fed and veterinary attention should be sought. The prolapsed/proptosed eye should be kept moist and clean. Debris can be gently washed out of the eye using sterile 0.9% saline- as long as tolerated by the patient.
Handling should be kept to a minimum; and self-trauma prevented by careful application of an Elizabethan collar. Thereafter the eye must be kept moist using an
ocular lubricant e.g. Lacrilube® or K-Y jelly ® to prevent desiccation.
Replacement of the globe in the orbit should NOT be attempted in a conscious patient- the owner should be informed of this. Full assessment and cleaning of the
globe will be required under anaesthesia, once the patient’s general condition is suitably stable. Drugs which may increase IOP e.g. ketamine should be avoided. Pain assessment and analgesia will be required.
How do you prepare a patient for ocular surgery and globe replacement?
Preparation for surgery
For either globe replacement or enucleation careful preparation around the eye should be performed.
Both eyes needs to be protected with sterile ocular lubricant; minimal clipping should be performed to prevent small hair fragments adhering to the globe
The area should be cleaned with sterile 0.9% saline, diluted povidine-iodine (0.2%) or diluted chlorhexidine gluconate (0.05%). Chlorohexidine diacetate should not be used for preoperative ocular preparations due to the high degree of tissue toxicity.
Globe replacement
A lateral canthotomy may be required to replace the globe followed by suturing together of the eyelids for 7-10 days. A small gap between the lids allows topical
medication to be applied to the globe e.g. lubricant and antibiotics.
What post-operative care does a patient with Proptosis/prolapse and rupture of the globe require?
The patient will need to be closely observed for pain, infection and swelling. An Elizabethan collar will be needed to prevent self-trauma.
Careful cleaning of the periocular area is necessary to remove tissue fluids or discharge.
What are the causes of conjunctivitis?
Causes of conjunctivitis include:
1) Infection (particularly Chlamydophila spp. and Herpes virus in cats and
Distemper virus in dogs)
2) Trauma
3) Allergies e.g. atopy
4) Corneal ulceration
5) Contact (chemical) irritants
6) Environmental irritants e.g. wind, grass
7) Foreign bodies
8) Secondary bacterial infection due to keratoconjunctivitis sicca
9) Immune-mediated
What is conjunctivitis?
Conjunctivitis is inflammation of the conjunctiva- the double – layered mucous membrane, epithelial layer that lines the eyelids and attaches at scleral/corneal
junction. Conjunctivitis is not a diagnosis but a sign of some conjunctival trauma/irritation. It may occur alone; or as part of another ocular or systemic problem
What are the clinical signs of conjunctivitis?
Clinical signs
These include conjunctival hyperaemia, blepharospasm, pain, inflammation, increased tear production / ocular discharge and chemosis.
How do you diagnose conjunctivitis?
Diagnosis
Clinical signs may be suggestive of conjunctivitis although the causative agent may not be obvious. Conjunctivitis is not usually very serious but it is important to ensure there is not a more serious associated condition e.g. uveitis, glaucoma, corneal
ulceration. In all cases, a full ophthalmic examination, Schirmer tear test and fluorescein administration will be required for complete assessment e.g. bacteriology
and cytology may be required from conjunctival swabs and smears. In cats, conjunctival swabs may be submitted in appropriate transport medium for
Chlamydophila ssp.; oropharyngeal swabs, also in viral transport medium, may be used for Calicivirus and Herpes virus identification.
What is the initial management and treatment for conjunctivitis?
Initial management
Cleansing and lubrication of the conjunctivae, with sterile 0.9% saline flush and ocular lubricants, will limit further damage and provide protection. Full examination and cleansing, may require sedation/general anaesthesia. An Elizabethan collar should be used in more severe cases to prevent further self-inflicted damage.
Treatment is symptomatic and dependant on the cause e.g. artificial tears and immunosuppressant for KCS; corticosteroids for allergic conjunctivitis.
What is glaucoma?
Glaucoma is a condition that leads to rapid onset retinal degeneration and blindness, as well as being very painful. In cats and dogs this is secondary to increased intraocular pressure (IOP) (Oliver, 2014). Glaucoma is more often recognised in dogs than cats- cats eyes are relatively more resistant to glaucomatous changes.
Increased IOP results from decreased drainage of aqueous humour from the anterior chamber at the drainage angle. Aqueous humour is produced continually at the ciliary body, which supports the lens, and drains at the ciliary cleft, the area created
by the junction of the cornea and iris. Glaucoma is caused by failure of drainage of aqueous humour- resulting in an increase in the volume within the globe. This causes increased intraocular pressure, which can be intensely painful and leads to blindness due to rapid, irreversible damage of the delicate intraocular structures e.g. retina
Glaucoma can be primary or secondary:
What produces aqueous humour and what does it do?
Aqueous humour is produced continually at the ciliary body, which supports the lens, and drains at the ciliary cleft, the area created by the junction of the cornea and iris
What is primary glaucoma due to in dogs?
In dogs, primary glaucoma is due to an inherited, bilateral malformation of the drainage angle at the ciliary cleft- goniodysgenesis. There are two that may occur in primary glaucoma- open angle and closed angle. With both, inadequate drainage of aqueous humour may occur. Whilst the malformation is
congenital, decreased aqueous drainage does not usually start to occur till later in life. Breeds recognised to be affected by primary glaucoma are listed in, and can be assessed under, the BVA, The Kennel Club (KC) and the International Sheep Dog Society (ISDS) eye scheme. malformations
What species does primary glaucoma tend to affect most?
Dogs
What are the two types of malformations in primary glaucoma in dogs?
There are two that may occur in primary glaucoma- open angle and closed angle. With both, inadequate drainage of aqueous humour may occur. Whilst the malformation is congenital, decreased aqueous drainage does not usually start to occur till later in life
What breed of cats are most likely affected by primary glaucoma?
Rarely, primary glaucoma will occur in cat- certain breeds e.g. Burmese and Siamese can be affected
What can be the causes of secondary glaucoma?
Secondary glaucoma arises when another ocular condition leads to blockage of the drainage angle. Secondary causes of glaucoma include:
1) Anterior uveitis
2) Neoplasia
3) Lens luxation
4) Hyphaema
5) Intraocular surgery
6) Pigmentation
What does Glaucoma in cats secondary to anterior uveitis, generally arise due to?
Glaucoma, in cats, secondary to anterior uveitis, generally arises as a result of infection with FIP, FeLV, FIV or toxoplasma. There are other causes of glaucoma in cats
At what intraocular pressure measurement will clinical signs usually be seen?
Clinical signs will usually be seen when the IOP is > 25 mmHg in dogs and > 30 mmHg in cats.
What are the clinical signs of acute glaucoma?
In acute glaucoma, there may not be as many clinical findings as with chronic glaucoma. Usually only one eye is affected with glaucoma initially, even if there is a
bilateral congenital abnormality.
All the signs of a sore, possibly, blind eye are likely to be present- blepharospasm, increased lacrimation and a ‘red eye’. The pupil will usually be fixed and dilated with absent or decreased PLR and menace reflex. The cornea may have a ground-glass/ hazy appearance and there is often marked epi-scleral congestion. The affected eye will sometimes feel more tense/rigid than the unaffected eye, due to increased IOP, although this is not very sensitive means of assessment.
There are various factors, including age, that affect the ability of the eye to be distended. Glaucoma may be acute or chronic depending on the timecourse and underlying cause. If it is slowly progressive, there may be few obvious clinical signs until the condition is advanced. The clinical findings will depend on
how long the condition has been present and whether there is an underlying cause.
Pain is a consistent feature especially in acute cases or end- stage, enlarged, congested eyes.
What are the signs of chronic glaucoma?
There are various factors, including age, that affect the ability of the eye to be distended. Glaucoma may be acute or chronic depending on the timecourse and underlying cause. If it is slowly progressive, there may be few obvious clinical signs until the condition is advanced. The clinical findings will depend on
how long the condition has been present and whether there is an underlying cause.
Pain is a consistent feature especially in acute cases or end-stage, enlarged, congested eyes.
With chronic glaucoma, additional signs may be present due to the gradual stretching of the globe by the increased volume of aqueous humour. There may also
be buphthalmos, protrusion of the third eyelid, linear opacification of the cornea due to endothelial tears (Haab’s striae) and caudal displacement of the lens. There may be central corneal ulceration secondary to poor tear distribution.
Additional findings may be present if the glaucoma is secondary e.g. lens luxation, cataract, intraocular haemorrhage, evidence of neoplasia etc.
An end-stage, chronically glaucomatous eye may have gradually degenerated and be decreased in size- phthisis bulbi.
How do you diagnose Glaucoma?
This is based upon clinical signs and measurement of the intraocular pressure (IOP).
A tonometer is used to measure IOP- different types are available using different physics principles. An applanation/ indentation tonometer- Tono-pen™/Schiotz can be used; or a rebound tonometer- Tonovet™.
With an applanation/ indentation tonometer measurement of intraocular pressure requires the tonometer to be placed onto the corneal surface therefore a topical local anaesthetic needs to be applied to the eyes a few minutes prior to testing. For
Schiotz tonometry, the animal needs to be positioned so that the footplate of the vertically held, tonometer can sit horizontally across the surface of the cornea. The digital tonometer does not require this level of restraint, and is therefore easier to use.
The rebound tonometer does not required the application of local anaesthesia to the
surface of the eye.
It is important to adopt a good technique for recording IOP- the reliability of the readings can be affected by various factors. Correct maintenance and use of the
equipment is important. If the patient struggles or is agitated the readings may be falsely elevated. Occlusion of the jugular vein when restraining will lead to falsely elevated readings.
Normal IOP readings are around 15-25 mmHg although there are various factors that can affect this (e.g. age, time of day) - readings in excess of 35mmHg require
emergency treatment.
As severe, irreversible damage to the retina and optic nerve occurs quickly, acute glaucoma is a true emergency requiring prompt attention.
Gonioscopy can be used to visualise the drainage angle and assess the structures of the anterior chamber. This involves placing a small diffracting lens onto the patient’s cornea, following administration of local anaesthetic.
Ultrasound may be used to image the interior of the eye and show evidence of neoplasia or lens luxation.
What is the aim of emergency treatment in a patient with glaucoma?
In acute cases, the aim of emergency treatment is to decrease IOP, before there are irreversible ocular changes, and manage the pain (Oliver, 2014). Prompt
identification of a potential underlying cause is also important.
In chronic cases, where vision is already likely to be affected, pain management is the priority
What is the management of acute glaucoma?
A rapid decrease in IOP is required, especially if the IOP is > 35 mmHg- this may be achieved by using an osmotic diuretic such as mannitol- although increasingly prostaglandin analogues may be used, as they are very effective, easy to administer and there is less risk of side-effects.
Latanoprost and travatan are prostaglandin analogues that increase the drainage of aqueous humour- they cause profound miosis. These drugs are increasingly used, where available, instead of or, in conjunction, with mannitol for management of acute glaucoma as they are considered to be superior to other treatments. They are contraindicated if there is anterior uveitis or complete lens luxation, although may be used in the management of lens subluxation. Latanaprost
should not be used in cats and there is no current information on the use of travatan in cats.
An intravenous infusion of 1-2 g/Kg of mannitol is administered over a period of 20-30 minutes- an improvement should be seen after one hour. Water should be withheld immediately following administration before being gradually reintroduced.
The dose may be repeated, if the IOP has not decreased to < 30 mmHG, once or twice after 4-8 hours, as long as the patient is not dehydrated and serum electrolytes can be measured.
Extreme care must be taken with mannitol NOT to cause volume overload; fluid and electrolyte abnormalities may arise secondary to treatment.
Side effects from mannitol can include dehydration- it should be used with extreme caution or be avoided in dehydrated, renally or cardiovascularly compromised
patients. Oral glycerol is an alternative if mannitol is not available.
Carbonic anhydrase inhibitors, (brizolamide and dorzolamide) reduce the rate of aqueous humour production thus IOP. They are generally used in dogs and cats in the long–term medical management of glaucoma but can also be used in the acute management stage Miotics e.g. 1-2% pilocarpine drops may be used to decrease IOP by stimulating contraction of the ciliary body (although other preparations are now preferred): pulling the iris away from the drainage angle so encouraging drainage of aqueous humour. Pilocarpine is less likely to be used since the increased use of prostaglandin analogues and carbonic anhydrase inhibitors. It should not be used if a patient has
anterior uveitis or lens luxation and is not recommended in cats.
Pilocarpine is a parasympathomimetic drug- it can cause bradycardia, hypersalivation, vomiting and diarrhoea.
Analgesia is important as glaucoma is intensely painful. The choice of analgesic will depend on the animal’s clinical presentation and severity of the patient’s pain. Dual therapy analgesia (e.g. opioid plus systemic NSAID) may be used (Oliver, 2014).
NSAIDs should be avoided, as ever, if the patient has received corticosteroids, has renal disease/ GI disease or is dehydrated.
In addition it is important to avoid the use of ketamine or any other drug that could increase IOP.
Atropine is also contraindicated due to its pupillary effects.
What is the management of chronic glaucoma?
Chronic management
Carbonic anhydrase inhibitors reduce the rate of aqueous humour production thus IOP- they are generally used in dogs and cats in the long–term medical management of glaucoma. Topical CAIs (brizolamide and dorzolamide) are preferred to oral
preparations (dichlorphenamide) as there is less likelihood of side effects such as vomiting, anorexia and sedation.
Beta-blockers (e.g. timolol maleate) decrease aqueous production and can be used in the management of canine and feline glaucoma. As they cause miosis, they
should not be used in anterior uveitis or lens luxation.
Treatment of the underlying cause is required in patients with secondary glaucoma e.g. uveitis, lens luxation or neoplasia. Surgery may be indicated for some conditions e.g. lens luxation. Enucleation may be required in an end-stage, painful eye. Other surgical options exist for decreasing aqueous production or increasing aqueous drainage. These are not, however, emergency procedures so are not discussed
here.
Ongoing assessments of IOP and pain is required- initially hourly until IOP reduces below 30mmHg and thence once every 3-4 hours until the patient is stabilised.
There are additionally several surgical options although these are not likely to be performed in the emergency setting
Define the following:
Hemiparesis
Clonus
..
Blepharospasm
Syncope
Tonus
Opisthotonus
Tetraparesis
Schiff-Scherrington posture
The correct answer is: Hemiparesis → Weakness in two limbs on one side of the body,
Clonus → Involuntary, regular, rhythmic muscle contractions,
Blepharospasm → Rapid blinking of the eyelids often in response to ocular pain or irritation; or spasm of the muscles making it hard to open the eyelids,
Syncope → A collapse / faint, Tonus → Increased extensor tone of muscles,
Opisthotonus → Strong contraction of the extensor muscles of the neck and back - results in arching of the back and hyperextension (backward arching) of the head and neck - often with extension of the fore limbs., Tetraparesis → Weakness in all four limbs,
Schiff-Scherrington posture → Increased forelimb extensor tone secondary to a serious injury from T3-L3
Which cranial nerve is the vagus?
Select one:
a. IV
b. VII
c. I
d. X
The correct answer is: X
What is a serious clinical finding in a patient at risk of increased intra-cranial pressure?
Select one:
a. Pulse deficit
b. Sinus rhythm
c. Bradycardia
d. Tachycardia
The correct answer is: Bradycardia
An animal with increased intra-cranial pressure should be positioned in
Select one:
a. Ventral recumbancy with the entire body and head raised by 30 degrees
b. Ventral recumbancy with the head raised 30 degrees to the body
c. Dorsal recumbancy with the entire body and head raised by 30 degrees
d. Lateral recumbancy with the head raised 30 degrees to the body
The correct answer is: Ventral recumbancy with the entire body and head raised by 30 degrees
Which terms are used in the assessment of patient mentation?
Select one:
a. Sleepy, dull, obtunded, lethargic and normal
b. Comatose, dull, depressed, timid and normal
c. Sleepy, stuporous, depressed, obtunded and normal
d. Comatose, stuporous, obtunded, depressed and normal
The correct answer is: Comatose, stuporous, obtunded, depressed and normal
Anisocoria means
Select one:
a. Pupils are of different sizes
b. Both pupils are of equal size
c. Both pupils are constricted
d. Both pupils are dilated
The correct answer is: Pupils are of different sizes
Fluoroscein can be used to:
Select one:
a. Dilate the pupil
b. Measure aqueous humour volume
c. Anaesthetise the cornea
d. Demonstrate corneal ulceration
The correct answer is: Demonstrate corneal ulceration
Uveitis is inflammation of the:
Select one:
a. Retina and tapetum lucidum
b. Iris, choroid and ciliary body
c. Cornea and sclera
d. Lens and ciliary body
The correct answer is: Iris, choroid and ciliary body
A tonometer assesses
Select one:
a. Dilation of the pupil
b. The drainage angle
c. Size of the optic disc
d. Intra-ocular pressure
The correct answer is: Intra-ocular pressure
Normal intra-ocular pressure for the dog is:
Select one:
a. 5-15mmHg
b. 35-45mmHg
c. 25-35mmHg
d. 15-25mmHg
The correct answer is: 15-25mmHg
Signs of vestibular disease can be caused by which of the following?
Select one:
a. Disease of the medulla
b. Disease of the cerebellum
c. Disease of the semi-circular canals
d. All of the above
The correct answer is: All of the above
All of the following are signs of Horner’s syndrome, except:
Select one:
a. Ptosis
b. Nystagmus
c. Miosis
d. Enophthalmos
The correct answer is: Nystagmus
Which of the following stages of seizure would most likely be the longest lasting?
Select one:
a. Pre-ictal stage
b. Post-ictal stage
c. Prodromal stage
d. Ictal stage
The correct answer is: Post-ictal stage
The menace response reflex assesses cranial nerves:
Select one:
a. VII and IX
b. IV and II
c. II and VII
d. III and VIII
The correct answer is: II and VII
Of the following, which is the recommended concentration of dextrose to administer to a patient intravenously to avoid phlebitis?
Select one:
a. 10%
b. 25%
c. 50%
d. 2.5%
The correct answer is: 2.5%
The formulae for calculating cerebral perfusion (CP) is:
Select one:
a. Intracranial pressure x Mean arterial pressure
b. Mean arterial pressure – Intracranial pressure
c. Mean arterial pressure ÷ Intracranial pressure
d. Intracranial pressure + Mean arterial pressure
The correct answer is: Mean arterial pressure – Intracranial pressure
Using a spinal cord injury grading system, a non-ambulatory patient with tetra or paraparesis in addition to some voluntary movement, would be graded as a:
Select one:
a. 4
b. 3
c. 5
d. 2
e. 1
The correct answer is: 3
The stage of a seizure best described as a subtle change in mood or behaviour would be called:
Select one:
a. Prodromal stage
b. Pre-ictal stage
c. Ictal stage
d. Post-ictal stage
The correct answer is: Prodromal stage
Breathing difficulties could be present in a patient with a with a spinal cord lesion between:
Select one:
a. T3-T7
b. L3-L7
c. T8-L3
d. C1-T2
The correct answer is: C1-T2
A 6.8 kg dog is placed on a propofol 10mg/ml CRI for status epilepticus. The dose is 3mg/kg/hr for four hours. Calculate the dose required.
The correct answer is: 8.16 ml
