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Opthalmology > Ocular emergencies > Flashcards

Ocular emergencies Flashcards

1
Q

What are some important risk factors for acute angle closure glaucoma?

A

AACG:

  • Progressive headache (usually on side affected)
  • Female (shallower anterior chambers)
  • Blurred vision (cornea becomes oedematous leading to corneal clouding, following increase in intra-ocular pressure)
  • History of vomiting
  • Glasses worn for near vision (hypermetropic patients have smaller eyes and shallower anterior chambers)
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2
Q

What clinical signs are suggestive of a diagnosis of acute angle closure glaucoma?

A
  • Dilated pupil
    Unreactive if light shone through it
  • Red eye
    Due to inflammation, also accompanies pain and loss of vision
  • Blue iris
  • Cloudy cornea
    The cornea becomes oedematous and hazy, this can be picked up using an opthalmoscope at +10
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3
Q

What is the normal intra-ocular pressure?

A

10-20mmHg

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4
Q

What is used to check intra-ocular pressure?

A

Goldmann tonometer

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5
Q

What is the treatment offered for AACG?

A

Peripheral iridotomy

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6
Q

When might we use a peripheral iridotomy phrophylactically?

A

If the patient has already had AACG in one eye, and the other eye is found to have a shallow anterior chamber/raised IOP

The other eye is always treated prophylactically to prevent AACG from affecting it in the future

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7
Q

What follow-up is recommended following resolution of AACG?

A

Follow up the patient in a glaucoma clinic with visual field testing

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8
Q

What should we be mindful of prescribing for a patient with a history of AACG?

A
  • Phenylephrine
  • Tropicamide

Both of the above drugs can increase pupil size, and cause narrowing of the drainage angle

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9
Q

What is a ‘cherry red spot’ seen on fundoscopy suggestive of?

A

Central retinal artery occlusion

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10
Q

What happens in central retinal artery occlusion?

A
  • The retina becomes ischaemic and pale
  • Choroidal circulation remains, and is seen as a cherry red spot
  • The retina is at it’s thinnest over the central macula area (fovea), so this is where choroidal circulation can be seen
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11
Q

If a patient has suspected central retinal artery occlusion, what must be ruled out?

A

Giant cell arteritis

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12
Q

What are risk factors for central retinal artery occlusion?

A
  • Giant cell arteritis
  • Hypercholesterolaemia
  • Hypertension
  • Atherosclerosis

Other risk factors:

  • Diabetes
  • Previous TIA
  • Previous angina
  • Smoking
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13
Q

What should be done for a patient with suspected central retinal artery occlusion?

A
  • Full history (CV) and exam
  • Suspect GCA until proven otherwise
  • Consider high dose prednisolone if GCA
  • Refer urgently to opthamology
  • Early treatment can restore vision
  • This condition is similar to having a stroke - increasing ischaemic time leads to poorer outcomes
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14
Q

What are some risk factors for retinal detachment?

A
  • Trauma
    Causes high velocity vitreous movement, and traction on the retina
  • Myopia
    Larger eyeballs results in a thinner retina at the far periphery, leading to an increase chance of tears/detachments
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15
Q

What are the signs of orbital cellulitis?

A
  • Patient has severe pain and swelling around the eye
  • Vision is reduced
  • Eye movements are painful
  • Fever 39C+
  • Generally unwell
  • Patient cannot move the eye
  • Periocular swelling of the eye
  • Periocular erythema of the eye
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16
Q

Which investigations are essential for orbital cellulitis?

A
  • Orbital scan (MRI or CT)
  • Swab from the conjunctivae
  • Full blood count
  • Blood cultures
17
Q

Which bedside clinical assessments need to be done hourly in orbital cellulitis?

A
  • Blood pressure
  • Visual acuity
  • Pulse
  • Temperature
18
Q

What are the most common causes for orbital cellulitis?

A

Often following an infection of the respiratory tract and sinuses:

  • Haemophilius influenzae
  • Staphyloccocus aureus
  • Streptococcus pneumoniae
  • Betahaemolytic streptococcus

And occasionally:
- Aspergillus
In immunocompromised patients

19
Q

What are the treatments for orbital cellulitis

A
  • Admission
  • Co-amoxiclav oral is first-line
  • If patient is severely unwell consider IV
  • If co-amoxiclav is contraindicated/there is a pencillin allergy, administer clindamycin + metronidazole, either oral or IV
  • If MRSA is suspected/convirmed, IV vancomycin or teicoplanin, OR oral/IV linezolin should be ADDED to one of the above regimes
  • Optic nerve function is monitored ever 4 hours
  • Treatment last for 7 days
  • Surgery may be inficated if there is CT evidence of an orbital collection, or there is no response to abx, or the picture is atypical
20
Q

How does pus in the anterior chamber appear?

A
  • Eye is red and inflamed
  • White ‘fluid’ level in the anterior chamber
  • Called hypopyon and is the accummulation of white blood cells
21
Q

What are some risk factors for infective endopthalmitis?

A
  • Poorly controlled diabetes
  • Painful sudden visual loss
  • Recent ocular surgery
  • Long lines
  • Indwelling tubes/catheters
22
Q

What is the management of infective endophthamlitis?

A
  • Immediate sampling of intraocular fluid (vitreous tap)

- Intravitreal injection of antibiotics

23
Q

What are the signs of infective endophalmitis?

A
  • Sudden painful loss of visual acuity
  • Red eye with hypopyon
  • Pupil does not appear to react to light
  • Poor red reflex
  • No fundal view

Any patient presenting with a red eye, associated with pain and reduced vision should be referred immediately.

24
Q

What is glaucoma?

A
  • Progressive optic neuropathy
  • Changes to the optic nerve head
  • Patterns of visual field loss
  • Leading cause of blindness
  • Either open or closed angle
25
Q

What is AACG?

A
  • Emergency
  • Untreated = permanent optic nerve damage
  • Due to blockage in the iridocorneal angle for the outflow of aqueous humour
  • Leads to increase in IOP and damage to the optic nerve
26
Q

How does aqueous humour flow through the eye?

A
  • Found in anterior and posterior chambers
  • Supplies nutrients to the lens and cornea
  • Produced in ciliary body in the anterior portion of the uveal tract
  • Is secreted into posterior chamber in pars percata
  • Then flows around the lens
  • Fills the anterior chamber
  • Then exits through the trabecular meshwork and the iridocorneal angle
  • Then enters the canal of schlemm
  • Then enters aqueous veins and systemic circulation
27
Q

What are the causes of a blockage of the iridocorneal angle?

A

Closure is usually primary

  • Severe hypetropic
  • Short axial length
  • Thin iris
  • Thick lens
  • Neovascularisation of the cornea (diabetes)
  • Lens (grows with age)
  • Blood clot (less common)
28
Q

What are risk factors for AACG?

A
  • Age
  • Female
  • Family history (first degree)
29
Q

How does AACG present?

A
  • Severe eye pain
  • Occasionally headache
  • Blurred vision
  • Halo around lights when looking (due to corneal oedema, affects refraction)
  • Nausea and vomiting
  • Ciliary flush (red injection around peripheries of cornea)
  • Poorly reactive pupil
  • Eye is hard to touch
  • Hazy cornea
30
Q

What is the management for AACG?

A
  • Refer urgently to opthalmology
  • Slit lamp
  • Tonometry to measure IOP
  • Gonioscopy (looks at iridocorneal angle)
  • Diagnosis can be made with presentation + raised IOP
31
Q

What is the treatment for AACG?

A
  • Immediate referral to opthalmology
  • 1st line treatment is topical eye drops:
    1. Timolol
    2. Apraclonidine
    3. Prednisolone
    4. Pilocarpine
  • IV acetazolamide (carbonic annhydrase inhibitor) or mannitol

THEN
Reduce IOP using peripheral iridotomy

Opthalmology (5 decks)

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