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Yr4: Neurology & Special Senses > Ophthalmology: Eye Conditions 4 > Flashcards

Ophthalmology: Eye Conditions 4 Flashcards

1
Q

Remind yourself of what causes:

  • Pupil constriction
  • Pupil dilation
A
  • Pupil constriction: contraction of sphincter pupillae which is under parasympathetic control; parasympathetic travel with CNIII
  • Pupil dilation: contraction of dilator pupillae which is under sympathetic control
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2
Q

State some potential causes of abnormally shaped pupils

A
  • Anterior uveitis (posterior synechiae)
  • Acute angle closure glaucoma (vertical oval due to ischaemic damage to iris muscles)
  • Trauma to sphincter muscles in iris (e.g. due to eye surgery)
  • Rubeosis iridis (neovascularisation can distort shape of iris & pupil- associated with diabetic retinopathy)
  • Coloboma (congenital malformation causing hole in eye)
  • Tadpole pupil (spasm in segment of iris; usually temporary and associated with migraines)
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3
Q

State some causes of mydriasis (dilated pupil)

A
  • Third nerve palsy
  • Holmes-Adie syndrome
  • Raised intracranial pressure
  • Congenital
  • Trauma
  • Stimulants such as cocaine
  • Anticholinergics
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4
Q

State some causes of miosis (constricted pupil)

A
  • Horners syndrome
  • Cluster headaches
  • Argyll-Robertson pupil (in neurosyphilis)
  • Opiates
  • Nicotine
  • Pilocarpine
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5
Q

What three features does a third nerve palsy cause?

A
  • Dilated non-reactive pupil
  • Ptosis (complete)
  • Down & out position of eye (divergent strabismus)
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6
Q

State some causes of third nerve palsy with sparing of the pupil

A

Sparing of pupil suggests microvascular cause (parasympathetic run in periphery):

  • Diabetes
  • Hypertension
  • Ischaemia
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7
Q

State some causes of complete/full third nerve palsy

A

Caused by compression of CNIII (also called a surgical third nerve palsy due to physical compression):

  • Idiopathic
  • Trauma
  • Cavernous sinus thrombosis
  • Posterior communicating artery aneurysm
  • Raised ICP
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8
Q

For Horner’s syndrome, discuss:

  • What it is
  • Features
  • How you can figure out location of lesion based on anhidrosis distribution
A
  • Syndrome caused by damage to sympathetic nerves supplying the face
  • Features: ptosis, miosis & anhidrosis
  • Link between anhidrosis & location:
    • Central lesions: anhidrosis of arm, trunk & face
    • Pre-ganglionic: anhidrosis of face
    • Post-ganglionic: does not cause anhidrosis
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9
Q

Horner’s syndrome can be caused by central lesions, pre-ganglionic lesions and post ganglionic lesions; state some potential causes for each

**HINT: 4S’s (sentral), 4T’s (torso/pre-ganglionic), 4C’s (cervical/post-ganglionic)

A

Central lesions (4 Ss):

  • S – Stroke
  • S – Multiple Sclerosis
  • S – Swelling (tumours)
  • S – Syringomyelia (cyst in the spinal cord)

Pre-ganglionic lesions (4 Ts):

  • T – Tumour (Pancoast’s tumour)
  • T – Trauma
  • T – Thyroidectomy
  • T – Top rib (a cervical rib growing above the first rib above the clavicle)

Post-ganglionic lesion (4 Cs):

  • C – Carotid aneurysm
  • C – Carotid artery dissection
  • C – Cavernous sinus thrombosis
  • C – Cluster headache
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10
Q

What is congenital Horner syndrome associated with?

A

Heterochromia (difference in iris colour)

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11
Q

How can we test for Horner’s syndrome?

A
  • Cocaine eye drops: cocaine prevents noradrenaline re-uptake at neuromuscular junction hence causes a normal eye to dilate; however, in Horner syndrome the nerves are not releasing noradrenalin to start with so blocking re-uptake makes no difference and so there is no pupil reaction
  • Or low concentration adrenaline eye drops: won’t dilate a normal pupil but will dilate a Horner syndrome pupil
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12
Q

What is a Holmes Adie pupil?

What causes a Holmes Adie pupil?

What is Holmes-Adie syndrome?

A
  • Unilateral (80%) dilated pupil that is sluggish to react to light with slow dilation of pupil following constriction (i.e. once it has constricted it remains small for abnormally long time)
  • Damage to post-ganglionic parasympathetic fibres
  • Holmes-Adie pupil in association with absent ankle & knee reflexes
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13
Q

What is an Argyll-Robertson pupil?

What condition is it found in?

*HINT: commonly called ‘prostitutes pupil’

A
  • Constricted pupil, often irregularly shaped, that accommodates but does not react to light
  • Neurosyphilis (also diabetes)

**Called prostitutes pupil as it ‘accommodates but doesn’t react’

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14
Q

For blepharitis, discuss:

  • What it is
  • Presentation
  • Management
A
  • Inflammation of eyelid margins due to either dysfunction of Meibomian glands (posterior blepharitis, more common) or seborrheic dermatitis or staphylococcal infection (anterior blepharitis, less common)
  • Presentation:
    • Gritty sensation
    • Dry eyes
    • Itchy
    • Eyes may be sticky in morning
    • Red eyelid margins
    • Swollen eyelids in Staphylococcal blepharitis
  • Management:
    • Hot compress twice daily
    • Lid hygiene (e.g. clean with cotton bud dipped in cooled boiled water with baby shampoo)
    • Artificial tears (symptomatic relief)
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15
Q

State the two types of hordeolum

A
  • External (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum producing) or glands of Moll (sweat glands).
  • Internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)
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16
Q

For styes, discuss:

  • What they are
  • Presentation
  • Management
A
  • Infection of glands of Zeis (sebaceous glands at base of eyelashes) or glands on Moll (sweat glands at base of eyelashes)
  • Presentation:
    • Tender, red lump along eyelid
    • May contain puss
  • Management:
    • Hot compress
    • Analgesia
    • Topical abx if associated with conjunctivitis or persistent
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17
Q

For chalazions (Meibomian gland cysts), discuss:

  • What they are
  • Presentation
  • Management
A
  • Blockage and subsequent swelling of Meibomian gland (inflammation not infection)
  • Presentation:
    • Eyelid swelling
    • Red eyelid
    • Typically not tender
  • Management
    • Hot compress
    • Analgesia
    • Topical abx if acutely inflamed or associated infection
    • Rarely, surgical drainage
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18
Q

For entropion, discuss:

  • What it is
  • Potential consequences
  • Management
A
  • Eyelid turns inwards (lashes against eyeball)
  • Can result in pain & corneal damage and ulceration
  • Management:
    • Initial: taping eyelid down to prevent inturning & regular lubricating drops (MUST GIVE LUBRICATING DROPS)
    • Definitive: surgery
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19
Q

For ectropion, discuss:

  • What it is
  • Potential consequences
  • Management
A
  • Eyelid turns outwards so that inner aspect of eyelid is exposed
  • Can result in exposure keratopathy as eyeball exposed and not adequately lubricated or protected
  • Management:
    • Mild: lubricating eyedrops if pt feels they would benefit, tape eyelid closed at night
    • More significant: surgery
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20
Q

For trichiasis, discuss:

  • What it is
  • Presentation
  • Management
A
  • Inward growth of eyelashes
  • Result in pain, corneal damage & ulceration
  • Management:
    • Epilation by specialist (removal of eyelashes)
    • Recurrent cases may require further treatments e.g. lasers to prevent eyelashes regrowing
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21
Q

What is pre-septal/periorbital cellulitis?

A

Infection of soft tissues anterior to orbital septum (eyelids, skin & subcutaneous tissue of face)

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22
Q

State some of the most common causative organisms of pre-septal cellulitis

A

Commonly spreads from nearby sites e.g. breaks in skin, sinusitis, URTIs. Most common causative organisms:

  • Staphylococcus aureus
  • Staphylococcus epidermis
  • Streptococcus pneumoniae
  • Anaerobic bacteria
23
Q

Who does pre-septal cellulitis most commonly occur in?

A
  • Children (80% <10yrs)
  • Median age presentation is 21 months
24
Q

Describe symptoms & signs of pre-septal cellulitis

A

Acute onset of….

  • Red, swollen, painful eye
  • Hot to touch around eye
  • Fever
25
Q

How can you differentiate between pre-septal and orbital cellulitis based on symptoms & examination findings (4)? (NOTE: can’t be sure, but may make you think one more than the other)

A

Orbital cellulitis features (that are absent in periorbital cellulitis):

  • Pain on eye movement
  • Reduced eye movements
  • Proptosis
  • Abnormal pupil reactions
  • Vision impairment
26
Q

What investigations would you do if you suspect a pt has pre-septal cellulitis?

A
  • Swabs of any discharge
  • Bloods: FBC, CRP
  • Contrast CT of orbit (can help differentiate periorbital and orbital cellulitis)
27
Q

Discuss the management of pre-septal cellulitis

A
  • All cases should be urgently referred to ophthalmology
  • Antibiotics:
    • PO usually sufficient e.g. co-amoxiclav
    • May give IVE
  • Children require admission to hospital for monitoring whilst having treatment (due to risk of orbital cellulitis)
28
Q

What is the main complication of pre-septal cellulitis that you are worried about?

A

Progressing to orbital cellulitis

29
Q

What is orbital cellulitis?

A

Infection of structures/tissues of the orbit posterior to the orbital septum (includes fat & extra-ocular muscles) BUT DOES NOT INVOLVE THE GLOBE

30
Q

State some of the most common causative organisms of orbital cellulitis

A

Most commonly caused by spread o fan URTI from sinuses. Common causative organisms include:

  • Staphylococcus aureus
  • Staphylococcus epidermis
  • Streptococcus pneumoniae
31
Q

State some risk factors for developing orbital cellulitis

A
  • Childhood
  • Previous sinus infection
  • Lack of Haemophilus influenzae type b (Hib) vaccination
  • Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
  • Ear or facial infection
32
Q

Describe symptoms & signs of orbital cellulitis

A
  • Redness and swelling around the eye
  • Severe ocular pain
  • Visual disturbance
  • Proptosis
  • Ophthalmoplegia/pain with eye movements
  • Eyelid oedema and ptosis
  • Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
33
Q

What investigations would you do if you suspect orbital cellulitis?

A
  • Swabs if discharge
  • Bloods: FBC, CRP, blood cultures
  • Contrast CT of orbit
34
Q

Discuss the management of orbital cellulitis

A
  • Urgent referral to ophthalmologist for admission for IV antibiotics (e.g. Tazocin in adults, co-amoxiclav in children)
  • May require drainage if abscess forms
35
Q

State some potential consequences of orbital cellulitis

A
  • Cavernous sinus thrombosis
  • Loss of vision
  • Intracerebral abscess
  • Meningitis
  • Death (rarely)
36
Q

What is a squint?

Why does a squint need correcting in childhood?

A
  • Misalignment of eyes (also known as strabismus)
  • In childhood, eyes haven’t fully established connections with brain; hence, brain will cope with misalignment by reducing signals from the less dominant eye. Hence they use one eye to see (dominant eye) and ignore the other eye (lazy eye). If this is not treated the lazy eye becomes progressively more disconnected from the brain and problem worsens over time resulting in amblyopia.
37
Q

Define the following:

  • Amblyopia
  • Esotropia
  • Exotropia
  • Hypertropia
  • Hypotropia
A
  • Amblyopia: the affected eye becomes passive and has reduced function compared to the other dominant eye
  • Esotropia: inward positioned squint (affected eye towards the nose)
  • Exotropia: outward positioned squint (affected eye towards the ear)
  • Hypertropia: upward moving affected eye
  • Hypotropia: downward moving affected eye
38
Q

State some potential causes of childhood squint- highlighting most common in otherwise healthy children

A
  • Idiopathic
  • Hydrocephalus
  • Cerebral palsy
  • SOL (e.g. retinoblastoma)
  • Trauma
39
Q

What two tests can you use for childhood squint?

A
  • Hirschberg’s test: shine a pen-torch at the patient from 1 meter away (some sources say 50cm, pass med says 30cm). When they look at it, observe the reflection of the light source on their cornea. The reflection should be central and symmetrical. Deviation from the centre will indicate a squint. Make a note of the affected eye and the direction the eye deviates.
  • Cover test: cover one eye and ask the patient to focus on an object in front of them. Move the cover across to the opposite eye and watch the movement of the previously covered eye. If this eye moves inwards, it had drifted outwards when covered (exotropia) and if it moves outwards it means it had drifted inwards when covered (esotropia).
40
Q

Discuss the management of childhood squints

A

Visual fields are still developing up until 8yrs of age therefore treatment needs to start before 8yrs. Must refer to ophthalmologist:

  • Occlusive patch to cover good eye (to force weaker to develop)
  • Alternative to patch is atropine drops in the good eye (causing vision to be blurred so forcing them to use weaker eye)
41
Q

What is astigmatism?

A
  • The curvature of the cornea is more like that of a rugby ball (as opposed to a football as in a normal eye); this change in curvature changes the path of light and subsequently the image formed at the back of the eye is not as sharply focused.
  • Treat with prescription glasses/contact lens
42
Q

What is optic neuritis?

A

Inflammation of the optic nerve

43
Q

State some potential causes of optic neuritis- highlight most common cause

A
  • Multiple sclerosis
  • Diabetes
  • SLE
  • Sarcoidosis
  • Syphilis
  • Mumps
  • Measles
  • Lyme disease
44
Q

Describe typical presentation of optic neuritis (include symptoms & signs)

A

Unilateral symptoms developing over hours to days:

  • Central scotoma (enlarged blind spot)
  • Decrease in visual acuity
  • Ophthalmoplegia (pain on eye movement)
  • Impaired colour vision
  • RAPD
45
Q

Discuss the management of optic neuritis

A

Urgent referral to ophthalmologist for assessment and treatment with high dose steroids (takes about 4-6 weeks to recover)

46
Q

What is Papilloedema?

What might you see on fundoscopy?

A
  • Optic disc swelling caused by raised ICP; almost always bilateral
  • Fundoscopy findings:
    • Venous engorgement (usually first sign)
    • Blurring of optic disc margin
    • Loss of optic cup
    • Paton’s lines (concentric/radial retinal lines cascading from optic disc)
    • Elevation of optic disc
47
Q

State some potential causes of papilloedema

A
  • space-occupying lesion: neoplastic, vascular
  • malignant hypertension
  • idiopathic intracranial hypertension
  • hydrocephalus
  • hypercapnia
48
Q

What is hyphema?

What is the management of hyphema?

A
  • Blood in anterior chamber of eye
  • Urgent referral to ophthalmologist for assessment & management as there may be raised IOP which can pose a risk to sight
    • Strict bed rest as excessive movement can redisperse blood that had previously settled so high risk cases often admitted
49
Q

If someone has presented with trauma to the eye, you must assess for orbital compartment syndrome (e.g. secondary to retrobulbar haemorrhage) as it is an ophthalmic emergency. State some features of orbital compartment syndrome

What is the management of orbital compartment syndrome?

A

Features:

  • Eye pain
  • Swelling
  • Proptosis
  • “Rock hard” eyeballs
  • RAPD

Management:

  • Urgent lateral canthotomy to decompress orbit (cut lateral canthal ligament to loosen the eyelids and allows the globe to expand out of the orbit and thus relieve pressure on the eye.)
50
Q

What is an orbital blowout fracture?

Where would the pt experience numbness?

A
  • Orbital blowout fractures occur when there is a fracture of one of the walls of orbit but the orbital rim remains intact
  • Features:
    • Numbness in infraorbital nerve region (cheek, upper lip & gum)
    • Diplopia: due to extraocular muscle entrapment (often worse on looking up)
    • Abnormal eye movements (if eye muscle trapped)
    • Redness, swelling etc.. of eye
51
Q

Why may children get double vision following ocular trauma?

A
  • Children can get ‘trapdoor fracture’
  • Extra-ocular muscles can get trapped in the fracture
  • Causing ischaemia of muscle
  • Leading to strabismus and dipoplia

HENCE, they require surgery if muscles trapped.

*****A trapdoor fracture is a fracture of the orbital floor where the inferiorly displaced blowout fracture recoils back to its original position and potentially entraps contents of the orbit. It is seen in children and young adults due to the elasticity of the orbital floor.

52
Q

Which, out of acids and alkalis, cause more severe chemical eye injuries and why?

A

Alkalis

Cause liquefactive necrosis as they react and hence propagate themselves deeper into the eye

Acids cause coagulative necrosis so impede their own process of moving deeper into the eye

53
Q

Discuss the management of chemical eye injuries

A
  • Test pH (if readily available)
  • Irrigate (LOTS)
  • Urgent ophthalmology review
  • Admission may be required for moderate to severe injuries
  • Treatment options:
    • Topical steroids
    • Topical abx
    • Topical cycloplegics
    • Analgesics

Yr4: Neurology & Special Senses (28 decks)

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