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Ocular and dermatologic manifestations of disease > Eye assessment > Flashcards

Eye assessment Flashcards

1
Q

What ophtho tests need to be done?

A

Initial observation of the animal’s behaviour from a distance
 Vision testing: obstacle course
 Hands-off assessment of head position, adnexae, orbit, globe, facial/pupillary symmetry under normal ambiant light
 Testing of ocular reflexes
 Schirmer tear test
 Detailed examination of adnexae and globes in a darkened room
 Specific ocular testing: swabbing, fluorescein, tonometry

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2
Q

What reflexes should be tested

A
  • OCULO-PALPEBRAL REFLEX
  • DAZZLE REFLEX
  • PUPILLARY LIGHT REFLEXES
  • CORNEAL REFLEX
  • OCULAR MOVEMENT
  • VESTIBULO-OCULAR REFLEX
  • MENACE
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3
Q

Outline the menace test

A

Acquired protective response at +/- 12 weeks old
 Response: blink, globe retraction, head withdrawal
 Affected by stress, distraction
 Avoid wind currents
 Tests retina, optic nerve (afferent), optique radiation,
visual cortex, cerebrocortical connections and facial nerve

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4
Q

Outline the oculopalprebral reflex

A

 Touching the medial canthus and lateral canthus
 Palpebral reflex – end stage of many reflexes, perform early to avoid false negative results
 Upper and lower eyelids must touch each other
 Reduction or prevention of lid closure:
- Neurological disease (eg: facial paralysis, oculomotor
neuropathy) vs
- Physical abnormalities (eg: buphthalmos/exopthalmos
of the globe, lagophthalmos common in brachycephalic
breeds)

Afferent - cranial nerve V
Efferent Cranial nerve VII

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5
Q

Outline the dazzle reflex

A

A subcortical response to bright light
 Positive response: rapid, partial ipsilateral eyelid closure
 Contralateral lid closure possible

Afferent: Retina, CN II, supraoptic nuclei of the hypothalamus (?), rostral colliculus,
 Efferent: CN VII (orbicularis oculi)
 Abnormal: stress, non-cortical blindness, pathology in
mesencephalon, CN VII
 Normal with cortical blindness

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6
Q

Outline fundic reflections

A

Fundic reflex = light reflected by the tapetal layer
through the pupil facilitates interpretation of pupil size
and symmetry
 Assessed by retroillumination: shine a bright focal light at arm’s length distance

Breeds without tapetum (e.g. husky) will be red

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7
Q

Outline the PLR

A

 Subcortical reflex
 Afferent: retina, optic nerve, optic chiasm, optic tract, to EW oculomotor nucleus, pretectal zone in midbrain,
 Efferent: parasympathetic fibres of oculomotor nerve,
short ciliary nerves to iris constrictor muscle
 Decussation at optic chiasm
Dog – 75%
Cat – 65%
Don’t expect full constriction of the consensual
Positive is not an indicator of vision as very little retinal function is needed

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8
Q

Outline the innervation of the oculomotor muscles

A

III - Superior and inferior rectus (top and bottom), medial rectus, (ventrolateral strabismus)
VI - lateral rectus and retractor bulbi
(medial strabismus & absent globe retraction)
Trochlear n. (IV)  dorsal oblique muscle
(rotational strabismus)

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9
Q

Outline the corneal reflex

A

 Tested by touching the cornea with a cotton tip or wisp of cotton wool
 Response = retraction of the globe and lid + eyelid closure
 Afferent: ophthalmic branch of trigeminal n.
 Efferent: Facial n. - orbicularis oculi m.
Abducens n. - retractor bulbi m.

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10
Q

Outline the vestibulo ocular reflex

A

 Indirectly assesses CN III, IV, VI (extraocular muscles), CN VIII & medial longitudinal fasciculus that coordinate movement
 Input via vestibulocochlear nerve (CN VIII) via bony
and membranous labyrinth and receptor organ.
 Efferent response mediated by oculomotor (CN III),
trochlear (CN IV) and abducens (CN VI) nerves.

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11
Q

What are the signs of Horner’s?

Loss of sympathetic innervation to the eye

A
  • Eyelid ptosis
  • Third eyelid protrusion
  • Enopthalmos
  • Miosis
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12
Q

Where may the lesion be with Horner’s?

A
  • Cervical spinal cord
  • Thoracic T1-T3 spinal cord
  • Brachial plexus
  • Midbrain, middle ear, eye
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13
Q

Outline first order neurons

A

The cell bodies of the first order neurons are located in the hypothalamus and rostral midbrain. The axons pass caudally through the brainstem and in the lateral part of the cervical spinal cord (tectotegmental spinal tract) to reach the first three thoracic spinal cord segments (T1-3). Here, the first order neurons synapse on the cell bodies of the second order neurons (preganglionic neurons) located in the intermediolateral grey column of the spinal cord.

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14
Q

Outline second order neurons

A

exit the spinal canal through the intervertebral foramina together with the ventral nerve root arising from the first three thoracic spinal cord segments (T1-3). The axons of the second order neurons leave the spinal nerve as the ramus communicans and join the thoracic sympathetic trunk
he thoracic sympathetic trunk courses inside the thorax ventrolateral to the vertebral bodies and runs cranially along the neck, associated with the vagus nerve forming the vagosympathetic trunk within the carotid sheath. The axons of the second order neurons travel rostrally to the cranial cervical ganglion, which is located ventromedially to the tympanic bulla.

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15
Q

Outline third order neurons (post ganglionic)

A

From the cranial cervical ganglion, the postganglionic neurons project through the ventral part of the tympanic bulla and enter the cranial cavity through the tympano-occipital fissure together with the carotid artery and glossopharyngeal nerve (CN IX).

Within the cranial cavity the axons travel rostrally adjacent to the middle cranial fossa. The postganglionic fibres then exit the cranial cavity through the orbital fissure with the ophthalmic branch of the trigeminal nerve to innervate the smooth muscle of the eyelids (including third eyelid), orbit and iris dilator muscles. The sympathetic innervation also supplies the smooth muscles of the blood vessels to the head

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16
Q

Outline the phenylephrine test

A

Apply to the eye, time how long it takes to get dilation of the pupil
< 20 mins - 3rd order
20-40 mins - 2nd order
>40 or doesn’t dilate - 3rd order

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17
Q

What is the most common cause of Horner’s

A

Idiopathic (greater than 50%)

Golden retrievers predisposed

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18
Q

How do you decide if to investigate Horners?

A

Phenyephrine test
If post ganglionic, most will resolve within 7 weeks
If Pre - do imaging, ideally CT or MRI

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19
Q

What suggests eye pain?

A

Blepharospasm = excessive eyelid blinking
 Discharge = excessive tear production
 Photophobia = ocular pain due to exposure to bright
light

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20
Q

What types of eye discharge are there?

A

• Serous: (viral infection, superficial corneal ulcer)
• Mucous: white-grey thick secretion (Allergic conjunctivitis/ chronic ocular irritation/ conjunctival
parasites)
• Purulent: yellow-green thick secretion (dry eye/ bacterial or fungal infection)

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21
Q

Compare serous discharge and epiphora

A

Epiphora - decreased drainage

DC - increased production

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22
Q

What types of globe size changes are there?

A

• Microphtalmia : abnormally small globe; may be congenital or acquired (phthisis bulbi = atrophy)
• Globe enlargement
- megalocornea
- buphthalmos (uncontrolled chronic glaucoma/ intraocular tumour)
- Not the same as exophthalmos!

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23
Q

What changes in globe position are there?

A

• Exophthalmos
- Abnormal forward globe protrusion
- Retropulsion used to assess retrobulbar space
- Trauma, retrobulbar mass, extraocular myositis or physiologic in brachycephalic breeds
• Enophthalmos
- Normal globe size, sunk in orbital cavity
- Acute ocular pain, Horner’s syndrome, senile atrophy of retrobulbar fat

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24
Q

Outline the STT

A
  • Dogs: > 15 mm/minute
  • 10-15 mm/min: suspect low tear production and
    recheck at a later stage
  • < 10 mm/min = diagnostic for keratoconjunctivitis
    sicca
  • Cats: normal >7 - 12 mm/minute
  • Dehydrated/ debilitated/ recently anaesthetised
    animals often have low tear production & require
    artificial tears

Dogs tend to have higher readings in the am, cats lower in the am

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25
Q

What do you check during eyelid examination?

A
  • Periocular discharge
  • Dermatitis/ blepharitis
  • Palpebral fissure size, shape
  • Eyelid position, movement
  • Disorders of cilia or periocular hair
  • Disorder of meibomian glands
26
Q

Outline examination of the nasolacrimal system

A
  • Ocular discharge
  • Tear staining
  • Negative Jones test
  • Occlusion, narrowing, absence of conjunctival puncta
  • Disorders of cilia or periocular hair
  • Canicular foreign body
  • Dacryocystitis
27
Q

Compare conjunctival and episcleral hyperaemia

A

Conjunctival:

  • Fine, tortuous vessels, branch frequently
  • Pink, red
  • Mobile
Episcleral:
- Larger, straighter vessels, branch
occasionally
- Dive throught the sclera just before limbus
- Dark red
- Fixed
28
Q

What do you assess with the pupil

A

Altered pupil shape (dyscoria)/ position (correctopia)
Synecchiae, iris atrophy, iris hypoplasia, iris coloboma,
chronic uveitis
Altered pupil size: Miosis: uveitis, Horner’s, drugs, CNS disease
Mydriasis: glaucoma, retinal/optic nerve disease, CNIII
paralysis, drugs, lens luxation, CNS disease
Altered pupil colour Cataract, vitreal haemorrhage, retinal detachment.

29
Q

What do you assess with the iris

A

Multiple apertures in iris - Iris coloboma, persistent pupillary membranes, iris atrophy, iris hypoplasia, polycoria
Iridal masses - Iris cyst, neoplasia, abscess or granuloma
Altered iris texture - Atrophy/hypoplasia, loss of crypts, “velvety” with melanosis or neoplasia, irregularly thickened (lymphoma) or nodular (lymphoplasmacytic, leishmania..)
Altered iris colour - Heterochromia iridis, rubeosis iridis, melanocytic neoplasia, icterus, haemorrhage, oedema, abscess…
Iridodenesis (fluttering of iris) Surgical aphakia or lens dislocation

30
Q

What occurs in synechia?

A

where the iris adheres to either the cornea (i.e. anterior synechia) or lens (i.e. posterior synechia)

31
Q

What is iris bombe?

A

apposition of the iris to the lens or anterior vitreous, preventing aqueous from flowing from the posterior to the anterior chamber. The pressure in the posterior chamber rises, resulting in anterior bowing of the peripheral iris

32
Q

What is an aphakic crescent?

A

As subluxation progresses to luxation, the lens usually sinks ventrally due to gravity, and the dorsal edge becomes visible in the pupil. The dorsal area of the pupil where the lens is missing is called the aphakic crescent.

33
Q

What makes up the fundus?

A 
Vitreous
 Neurosensory retina
 Retinal pigment epithelium
 Choroid
 Sclera
34
Q

How does the fundus appear in the dog?

A

Tapetal fundus
 Variation in tapetal colour common, often clearly
demarcated zones of varying tapetal colour (blue /green/ yellow/ orange)
 Tapetum may be absent normally
 Fine granular appearance
 Tapetal-nontapetal junction irregular

Non-tapetal fundus
 Most often deep brown in colour
 Homogenous to slightly mottled appearance
 Varying degrees of pigment dilution
 Choroidal vessels visible normally in colour diluted animals due to lack of pigment in RPE

35
Q

What general things do you want to assess in the fundus?

A 
RETINA
 Changes in colour
 Altered tapetal reflectivity
 Difficulty focusing on all of the
Assess Localization, Colour, Clarity, Size, Shape, 
 Changes in vascular appearance
OPTIC NERVE HEAD
 Increased size or prominence
 Decreased size or prominence
 Vascular changes
36
Q

Outline tapetal reflectivity changes

A

 Increased reflectivity of the tapetum = thinning of the neurosensory retina (more chronic change)
Associated with retinal degeneration
 Decreased reflectivity of the tapetum = indicates retinal detachment, choroidal effusion, inflammatory exudates or neoplasia

37
Q

Why may you get an altered pigmentation of the fundus?

A

Proliferation, migration and aggregation of RPE cells and/or choroidal melanocytes = non-specific response to insults such as inflammation, injury and degenerative processes.
 Proliferation of melanocytes due to neoplasia

38
Q

Outline how retinal detachment may appear

A

 Neurosensory retina only firmly attached at optic disc & anteriorly, at ora ciliaris retinae
 Retinal detachment  separation of the neurosensory
retina from the RPE
 Detachment/exudate = focal gray areas within the
tapetal fundus (local reduction in tapetal reflectivity) or
non-tapetal fundus (appear paler than surrounding area)
 Extensive retinal detachments appear as gray sheets
and folds

39
Q

What is a normal IIOP

A

10-20

Should be no more than 20% difference/ 5mmHg difference between eyes

40
Q

What sort of staining does a SCEDD produce?

A

Has a halo of bright stain uptake

41
Q

How do you assess the fundus?

A

dilate the pupil, one drop of topical 1 per cent tropicamide will cause mydriasis within 20 minutes, and lasts six to eight hours in the dog

42
Q

What does vitreal haemorrhage look like?

A

‘keel‐boat’ appearance

43
Q

What is collie eye anomaly?

A

congenital syndrome and bilateral condition, comprising defects of the posterior ocular structures as a result of abnormal mesenchymal differentiation. Ophthalmoscopic signs can include:
Choroidal hypoplasia, the hallmark lesion, which is seen as a pale patch with abnormal choroidal vessels lateral to the optic disc. The extent may vary between the two eyes.

Colobomas of the optic disc or peripapillary area; in the disc these appear as grey or pink indentations and the retinal vessels can be seen to dip into them.

Secondary complications, which include retinal detachments or haemorrhage.

44
Q

Who and when should be tested for collie eye anomaly

A

Breeds affected include the rough and smooth collie, the border collie, the Shetland sheepdog, and the Lancashire heeler. In the UK, the prevalence among the Shetland sheepdog and rough and smooth collies is relatively high. The lesions are best seen at five to seven weeks of age. After this age, mild cases can be masked by the development of the tapetum and pigment in the retinal pigment epithelium (RPE), a phenomenon known as ‘go‐normal’. The ‘go‐normal’ rate has been estimated to be as high as 53 per cent in Shetland sheepdogs and 63 per cent in rough and smooth collies
Is an autosomal recessive condition

45
Q

What does progressive retinal atrophy look like?

A

Initially retinal thinning indicated by a slight hyperreflectivity and mild vascular attenuation, this progresses to a more widespread and generalised tapetal hyperreflectivity with pigment clumping in the nontapetal fundus and severe vascular attenuation (Fig 23), and finally to an ‘end‐stage retina’ with total tapetal hyperreflectivity, complete absence of retinal vasculature, and a pale atrophic optic disc.

46
Q

What can retinal dysplasia be caused by?

A

viral infection, vitamin A deficiency, x-irradiation, certain drugs and intrauterine trauma, most cases are inherited

47
Q

What is uveodermatologic syndrome?

A

uveitis, chorioretinitis, skin depigmentation (vitiligo) and loss of hair pigment
Mainly in akitas
Dogs present with a severe anterior and/or posterior granulomatous uveitis, which frequently leads to intractable glaucoma necessitating enucleation. The principal ophthalmoscopic lesions are serous retinal detachments. It appears to be an autoimmune disease directed at melanocytes, but because of the breed incidence, genetic factors may be involved.

48
Q

What is Sudden acquired retinal degeneration syndrome (SARDs)

A

an acute bilateral blinding condition for which there is currently no treatment
PLRs may be retained in the early stages. Typically, the affected dog is middle-aged, overweight, small breed, female and neutered. Before blindness develops, many dogs will show cushingoid signs, such as polyphagia, polydipsia, weight gain and alterations in serum biochemistry (eg, raised serum alkaline phosphatase, aminotransferase, cholesterol or bilirubin), however, most dogs do not test positively for hyperadrenocorticism.
Fundic examination is completely normal in the early stages, but a few months after the initial presentation, signs of retinal degeneration, and ultimately an end-stage retina, indistinguishable from that caused by PRA, will show upon examination.

49
Q

What can cause chorioretinits

A

infectious, neoplastic, traumatic, immune-mediated or idiopathic.

50
Q

How does chorioretinitis appear?

A

The appearance of lesions may hint at the aetiology. Inflammatory lesions can be uni- or bilateral and are usually irregular in shape. In contrast to inherited retinopathies, the two eyes are rarely bilaterally symmetrical. The ophthalmoscopic appearance is very different depending on whether the inflammation is acute or inactive

51
Q

What can cause retinal detachment?

A

Congenital retinal detachments – are associated with CEA and total retinal detachment (TRD) in affected breeds.
Rhegmatogenous – a tear or hole in the neuroretina allows fluid from the vitreous to enter and pull it away from the RPE. Such detachments may be primary (eg, the giant retinal tears seen in the shih tzu), or secondary, as a result of trauma, glaucoma, lens surgery, laser retinopexy or other posterior segment surgery
Non-rhegmatogenous
Exudative – resulting from fluid or cell accumulation in the space between the photoreceptors and the RPE. Causes include systemic hypertension, chorioretinitis and neoplasia.
Traction – resulting from a band of tissue that develops in the vitreous and pulls the retina away from the RPE. This often occurs following intraocular haemorrhage or inflammation. Potential causes are trauma and intraocular surgery.
Steroid responsive – an exudative type of retinal detachment, principally a diagnosis of exclusion, occurring mostly in German shepherd dogs and their crosses (Andrew and others 1997). Retinal reattachment can occur following treatment with systemic steroids.

52
Q

Outline hyperviscosity syndromes

A

associated with IgG, IgA or IgM macroglobulinaemia and results from increased serum viscosity. The underlying cause may be neoplastic (eg, lymphoma, plasmacytoma, or multiple myeloma), or infectious (eg, ehrlichiosis). Ophthalmoscopic signs include dilated, tortuous retinal vessels with ‘sausaging’, retinal haemorrhages, and bullous retinal detachments

53
Q

Outline hyperlipidaemia in the eye

A

Primary hyperlipidaemia has been described in several breeds including the briard, rough collie, Shetland sheepdog and miniature schnauzer. It can also occur secondarily to systemic diseases (eg, hypothyroidism, diabetes mellitus, hyperadrenocorticism and pancreatitis). Elevations of triglycerides may result in visible lipaemia, detectable in the fundus as pale pink retinal vessels (lipaemia retinalis), and most obvious in the nontapetal fundus

54
Q

what can occur in the diabetic eye?

A

retinal haemorrhages and microaneurysms (1 in 5)

Cataracts

55
Q

What primary tumours can occur in the fundus

A

Choroidal melanoma – a darkly pigmented, clearly demarcated, raised mass lesion underlying the retina and tapetum – is often found adjacent to the optic disc. Generally benign, these can occasionally extend into the optic nerve and retrobulbar tissue. Retinal detachment and haemorrhages can occur.
Other primary tumours reported include: astrocytoma teratoid medulloepithelioma and tumours similar to human retinoblastoma

56
Q

What secondary tumours can occur in the fundus?

A

Lymphoma is the most common secondary tumour and affected dogs may present with anterior and/or posterior ocular signs. Ophthalmoscopic lesions include chorioretinitis, retinal haemorrhages, changes in tapetal colour and papilloedema. Lymphoma with ocular involvement tends to equate to a shorter survival time. Secondary tumours may also extend into the posterior segment from the anterior eye, optic nerve or extraocular tissue, or metastasise from a distant site (eg, adenocarcinomas, sarcomas, malignant melanoma or pheochromocytoma)

57
Q

How can GME present in the fundus

A

Granulomatous meningoencephalitis (GME) is an idiopathic inflammatory disease of the central nervous system (CNS), which can affect the posterior eye and uvea. Characterised by perivascular cuffing of CNS vessels by inflammatory cells, the condition produces clinical signs of multifocal CNS disease, typically in young small-breed dogs. When the eyes are affected, ocular signs may develop before CNS abnormalities, usually bilateral blindness. Ophthalmoscopically, signs of optic neuritis and peripapillary oedema may be seen. Choroidal involvement may lead to retinal detachments

58
Q

What are colobomas?

A

Colobomas are congenital malformations of the ONH and peripapillary retina. Described as ‘typical’ when they occur at the six o’clock position, they are related to incomplete closure of the optic fissure during embryonic development. They are seen in collie breeds as part of CEA, but are a separate entity in other breeds

59
Q

What is papilloedema

A

passive, non-inflammatory disc swelling associated with increased intracranial pressure. It is almost always bilateral and is often not associated with visual deficits, apart from late in the course of the primary disease. In the dog, it is principally associated with brain tumours

60
Q

What is optic neuritis

A

Optic neuritis can have a neoplastic, immune-mediated, idiopathic or infectious cause. It can be uni- or bilateral, and both the optic papilla and retrobulbar optic nerve can be involved. Affected dogs present with sudden-onset blindness and fixed dilated pupils. Ophthalmoscopically, the optic disc appears swollen, hyperaemic and oedematous with blurring of its margins and loss of the physiological cup. Blood vessels on the surface are raised and prominent. Haemorrhages and peripapillary retinal oedema may be seen. In the retrobulbar form there are no ophthalmoscopic signs

61
Q

Outline optic nerve tumours

A

Dogs with optic nerve tumours present with exophthalmos and sometimes papilloedema and optic neuritis, which can be visualised ophthalmoscopically. Primary neoplasms include teratoid medulloepithelioma, gliomas and meningioma, but extension of squamous cell carcinomas, nasal and orbital tumours into the optic nerve may occur.

Ocular and dermatologic manifestations of disease (8 decks)

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