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Neurology and special senses (Y4) > 4- Ophthalmology (Adulthood orthoptic conditions) > Flashcards

4- Ophthalmology (Adulthood orthoptic conditions) Flashcards

1
Q

Adult orthoptic conditions

A

Adult orthoptic conditions

  • Nerve palsy
  • Thyroid eye disease
  • MG
  • Orbital blow out fracture
  • SoL/orbital mass
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2
Q

visual testing in adults

A
  • Snellen chart
  • Assessment of near vision (reading text)
  • Colour vision assessment (Ishihara chart)
  • Visual fields
  • Blid spot
  • Pupillary assessment (inspection, direct indirect light)
  • Accommodation reflex
  • Extraocular muscles
  • Fundoscopy
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3
Q

snellen chart

A
  1. Stand the patient at 6 metres from the Snellen chart.
  2. Ask the patient to cover one eye and read the lowest line they are able to.
  3. Record the lowest line the patient was able to read (e.g. 6/6 [metric] which is equivalent to 20/20 [imperial]).
  4. You can have the patient read through a pinhole to see if this improves vision (if vision is improved with a pinhole, it suggests there is a refractive component to the patient’s poor vision).
  5. Repeat the above steps with the other eye.
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4
Q

recording snellen reading

A

If the patient reads the 6/6 line but gets 2 letters incorrect, you would record this as 6/6 (-2).
If the patient gets more than 2 letters wrong, then the previous line should be recorded as their acuity.
When recording the vision it should state whether this vision was unaided (UA), with glasses or with a pinhole (PH).

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5
Q

A, DF, HZP, TXU

A

6/18-1

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6
Q

A, DF, HZP, TXUD, Z

A

6/18+1

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7
Q
A

6/18-2

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8
Q

alternative to snellens

A

LogMar chart

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9
Q

LogMar Chart

A
  • Each line has a score of 0.1
  • Each letter a score of 0.02 (as five letters per line)
  • Advantages over snellon
    o Uniform reduction of letter size
    o Crowding effect on each line
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10
Q

Further steps for patients with poor vision

A

If the patient is unable to read the top line of the Snellen chart at 6 metres (even with pinhole) move through the following steps as necessary:

  1. Reduce the distance to 3 metres from the Snellen chart (the acuity would then be recorded as 3/denominator).
  2. Reduce the distance to 1 metre from the Snellen chart (1/denominator).
  3. Assess if they can count the number of fingers you’re holding up (recorded as “Counting Fingers” or “CF”).
  4. Assess if they can see gross hand movements (recorded as “Hand Movements” or “HM”).
  5. Assess if they can detect light from a pen torch shone into each eye (“Perception of Light”/”PL” or “No Perception of Light”/”NPL”).
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11
Q

visual acuity testing in children

A
  • Keeler preferential looking cards
  • Cardiff acuity cards
    -Kay picutrs
  • LogMArk keeler book
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12
Q

Keeler preferential looking cards

A
  • Examiner objectively observes patients eye to see if looking towards grating
    o 8 weeks -12 months
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13
Q

Cardiff acuity cards

A
  • Examiner objectively observes patients eye to see if looking towards picture
    o 3-18 moths
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14
Q

Kay pictures

A
  • Picture based test – 4 on each line
  • Test at 3m
  • With matching (for shy , second language, non-verbal children)
  • Age 2-4 years old
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15
Q

LogMar Keeler book

A
  • Letter based test
  • 3m
  • With matching (for shy , second language, non-verbal children)
  • Age 4+
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16
Q

types of diploma

A
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17
Q

Ocular motility

A
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18
Q

extra ocular muscles of the eye

A
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19
Q

examination for all oculomotor muscles

A
  • Inspection of resting gaze
  • Eye movement
  • Pupils and pupillary light reflexes
  • Eyelid position (normal or dropping)
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20
Q

way to remember oculomotor muscle innervation

A

Innervation: LR6 SO4 E (everything else) 3

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21
Q

4 rectus muscles

A

All originate from common tendinous ring

Superior rectus
- Action: Elevation (Adduction and medial rotation of eyeball)
- Innervation: Oculomotor nerve (CNIII)

Inferior rectus
- Action: depression (Adduction and lateral rotation of the eye)
- Innervation: Oculomotor (CNIII)

Medial rectus
- Action: Adducts eyeball
- Innervation: Oculomotor (CNIII)

Lateral rectus
- Action: abducts eyeball
- Innervation: Abducens (CNVI)

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22
Q

2 oblique muscles

A

These do not originate from the common tendinous ring. The oblique muscles take ana angular approach to the eyeball.

  • Inferior oblique
    o Action: elevates, abducts and laterally rotates the eyeball
    o Innervation : oculomotor
  • Superior oblique
    o Action: depression, abducts and medially rotates the eyeball
    o Innervation: trochlear nerve (CN IV
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23
Q

Cranial nerve palsy that cause diplopia

A
  • CN III- oculomotor
  • CNIV- trochlear
  • CN VI- abducens
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24
Q

which target muscles does the oculomotor nerve innervate

A

Motor and sympathetic
- Extraocular muscles 4/6
- Levator palpebrae superioris (main eyelid muscle)
- Sphincter pupillae (parasympathetic)

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25
Q

which target muscles does the trochlear nerve innervate

A

Superior oblique muscle – eye movement

26
Q

which target muscles does the abducens nerve innervate

A

lateral rectus- abducting eye movement

27
Q

Two Branches of Oculomotor Nerve

A
  • Superior – LPS, Superior Rectus
  • Inferior – Medial Rectus, Inferior Rectus, Inferior Oblique
28
Q

Aetiologies of oculomotor nerve palsy

A
  • Microvascular – Diabetes and hypertension risk factors (medical)
  • Posterior Communicating Artery (PCA) Aneurysm (surgical)
  • Space occupying lesion
  • Trauma
  • Demyelinating disease
  • Infection
  • GCA
  • Congenital
29
Q

medical or surgical third

A

medical : vascular risk factors e.g. diabetes

Surgical: compression of the 3rd nerve e.g. posterior communicating artery (will be painful)

30
Q

presentation of oculomotor nerve palsy

A
  • Ptosis (complete (LPS) or partial)
  • Eye depressed and abducted (down and out)
  • Pupil may be dilated and unreactive.
  • Diplopia (when ptosis lifted) diagonal (horizontal and vertical).

Pupil Involvement (dilated/unreactive/“blown” pupil) is indicative of compressive aetiology, the nerve is being compressed.

31
Q

pupil involvement in oculomotor palsy

A

lesion of the sympathetic chain supplying the eye

32
Q

investigations of oculomotor nerve palsy

A
  • VA, CT, OM, Pupils
  • General: Blood tests, BP, scan (MRI, CT, MRA), biopsy
33
Q

managements of oculomotor nerve palsy

A
  • Treat underlying aetiology, microvascular likely to recover 6-9 months.
  • Prisms for diplopia.
  • Ptosis prop if only seeing eye.
  • Strabismus surgery if non-recovering to aid ocular alignment and alleviate diplopia.
34
Q

Horners vs Oculomotor

A

Horners is caused by a lesion of the sympathetic chain supplying the eye (pupil constriction)
- Partial ptosis ( Due to denervation of the superior tarsal muscle.)

Oculomotor is caused by a lesion affecting the 3rd nose -> takes out parasympathetic action (pupil dilated)
- Ful ptosis (due to denervation of the elevator palpebrae superioris)

35
Q

Horners causes

A

Lesions are on the same side of the Horners

Think of structures where the sympathetic chain passes
- Pancoast tumour
- Lateral medullary stroke (horners, cereballar, speech and swallow, no motor)
- Carotid artery dissection and aneurysm (if appears with stroke symptoms may be due to embolism causing secondary stroke)

36
Q

horners presentation

A
  • Miosis (constricted pupil),
  • partial ptosis
  • loss of hemifacial sweating (anhidrosis
37
Q

Trochlear nerve palsy (IV)

Background

A
  • Controls only the superior oblique muscle
    o Responsible for depressing and intorting the eye
  • Leaves the brainstem backwards, before curling around and projecting it anteriorly -> increasingly susceptible to damage from head trauma
38
Q

trochlear nerve palsy aetiology

A
  • Head injury (esp back of head)
    o RTC
    o Horse riding
    o Falls from height
  • Microvascular (DM, HTN)
  • MS- demyelinating disease
  • Tumour
  • Aneurysm
  • Congenital – lax SO tendon
39
Q

Congenital 4th nerve weakness

A

– lax SO tendon

40
Q

presentation of trochlear nerve palsy

A

Classic Features:
- Hypertropia (greater at near) slight esodeviation.
- CHP Head tilt to unaffected side, chin depression
- Diplopia vertical (with torsional and horizontal components)
- Torsion

41
Q

presentation of trochlear nerve palsy

A

Classic Features:
- Hypertropia (greater at near) slight esodeviation.
- CHP Head tilt to unaffected side, chin depression
- Diplopia vertical (with torsional and horizontal components)
- Torsion

42
Q

Investigation for trochlear nerve palsy

A
  • Orthoptic: VA, CT, OM, pupils.
  • General: Image if unusual presentation, eg. young patient with no history of head trauma
43
Q

management of trochlear nerve palsy

A

Monitor recovery, Prism, Surgery.

44
Q

Abducens nerve palsy (VI)
Background

A
  • Controls lateral rectus only
    o Responsible for abducting eye
  • Exits pons and runs over petrous temporal ridge – this make sit susceptible to damage due to RICP
45
Q

Aetiology of abducens nerve palsy

A
  • Microvascular – Diabetes and hypertension risk factors
  • Raised intracranial pressure
  • Space occupying lesion
  • Trauma
  • Demyelinating disease
  • Infection (bacterial or viral)
46
Q

presentation of abducens nerve palsy

A
  • Esodeviation (worse in the distance).
  • CHP – Face turn towards affected side.
  • Horizontal diplopia (greater in distance and looking
    towards affected side).
  • Limited abduction.
47
Q

Investigations abducens nerve palsy

A

Orthoptic: VA, CT, OM, pupils, CV, PCT measurements on side gaze
General: BP, bloods, scan (if non-recovering especially), ?LP (bilateral)

48
Q

management of abducens nerve palsy

A

Orthoptic: VA, CT, OM, pupils, CV, PCT measurements on side gaze
General: BP, bloods, scan (if non-recovering especially), ?LP (bilateral)

49
Q

thyroid eye disease (Graves orbitopathy)

A
  • An autoimmune disorder with an active inflammatory phase (lasting months/years) and an inactive fibrotic phase.
  • This affects the extraocular muscles and connective tissues.
  • Usually associated with hyperthyroidism (but may be hypothyroid).
  • Blood test (TSH, free T3, free T4).
50
Q

pathophysiology of thyroid eye disease

A
  • Autoimmune
  • Closely correlating with Graves disease, patients with TED have been found to have elevated antibodies against TSH receptors, which are expressed in orbital fat and connective tissue
  • Causes enlargement and fibrosis of extraocular muscles, which can compress the optic nerve causing blinding
  • Studies have also attribute increased fibroblast activity as well as accumulation of collagen and hyaluronic acid to the enlargement and fibrosis of the extraocular muscles
51
Q

thyroid eye presentation

A

Key Eye Features:
* Proptosis – Finite space in bony orbit, EOM swelling forces globes forwards.
* Optic neuropathy due to stretching and crushing (reduced VA, reduced CV, VF loss, pupil abnormality).
* Upper lid retraction (corneal exposure).
* Increased IOP.
* Strabismus/restricted EOM (diplopia). Commonly the IR is first affected followed by MR.

52
Q

which extra ocular muscle is most commonly first affected by thyroid eye disease

A

inferior rectus

followed by medial rectus

53
Q

Management of thyroid eye disease

A

Systemically: want to obtain a euthyroid status: 1) radiotherapy of thyroid,
2) anti-thyroid medications,
3) thyroidectomy. As hypothyroid post-treatment give synthetic thyroid hormone.

Orbit:
- Stop smoking (to slow progression)
- Steroids may help active inflammatory phase
- Orbital decompression surgery
- Strabismus surgery (in fibrotic phase)
- Lid surgery (in fibrotic phase)

54
Q

SINGLE LARGEST MODIFIABLE RISK FACTOR for thyroid eye disease

A

Smoking

55
Q

Myasthenia gravis

A
  • Autoimmune condition effecting the neuromuscular junction.
  • Causing fatigue and weakness of extraocular muscles, worsening after periods of activity and improving after periods of rest.
  • Ocular Myasthenia Gravis (OMG) often comes before developing Generalised Myasthenia Gravis (GMG).
  • Known as the “Great Mimicker” MG can mimic any nerve palsy or eye movement problem.
56
Q

investigations for ocular myasthenia graves

A
  • AChR antibody
  • ice and rest test for ocular myasthenia gravis
  • edrophonium test
57
Q

management of myasthenia graves

A
  • Orthoptic: to address the symptoms (prism, occlusion)
  • Medical: anticholinesterase agents (pyridostigmine), immunosuppressive drugs (steroids, rituximab, mycophenolate, azathioprine), thymectomy, IV IG (crisis), plasmapheresis (crisis)
58
Q

Blow out fracture

A
  • High speed, high impact injury resulting in a break in the orbital walls, while the orbital rim remains intact.
  • Commonly caused by assault or sporting injury.
  • Most commonly the thin orbital floor breaks as a “crumple zone” to protect the globe.
  • Orbital contents (globe, muscles, fat etc.), drop downwards into the maxillary sinus -> extra ocular muscle can get stuck/restricted
59
Q

which bone is most commonly broken in blow out fracture

A

lamina papyracea of the ethmoid bone

60
Q

Space occupying lesion/orbital mass

A
  • Unilateral Proptosis
  • Ocular and orbital pain

Causes:
* Orbital tumour
* Optic nerve glioma
* Schwannomas
* Sarcomas
* Retrobulbar haemorrhage
* Orbital pseudotumor

61
Q

What could make it appear one eye is proptosed when it is not?

A

Pseudoproptosis.
Enophthalmos, of the other eye, sunken fellow eye.

62
Q

what can cause bilateral abducens nerve palsy

A

raised intracranial pressure

  • Raise ICP -> most commonly involved cranial nerve that arises as- A result of raised intracranial pressure- false localising sign

Neurology and special senses (Y4) (52 decks)

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