What type of visual loss occurs from damage to the optic nerve?
- Damage to Optic Nerve → complete loss of vision in one eye (Anopia)
- Damage to Optic Chiasm (ie. by pituitary tumours) → bitemporal hemianopia
- Upper Quadrant Defect = pituitary tumour
- Lower Quadrant Defect = craniopharyngioma - Damage to Optic Tract → homonymous hemianopia (of opposite side - ie. right optic tract damage ⇒ left homonymous hemianopia)
- Occipital lesion= contralateral homonymous hemianopia & Macular Sparing (central vision remains intact) (PCA infarct) - Damage to optic radiation (key white matter structures that cross the temporal lobe.) → Homonymous Quadrantopia
- A lesion in the temporal lobe would cause contralateral homonymous superior (upper) quadrantanopia
- A lesion in the parietal lobe would cause contralateral homonymous inferior (lower) quadrantanopia
(to remember this: PITS ⇒ parietal-inferior and temporal-superior )
- Occur on opposite side
- Stroke affecting specific pathways in the optic radiation, trauma, craniopharyngioma
What is glaucoma?
Glaucoma refers to a group of conditions with heterogeneous causes that results in damage to the optic nerve head and loss of visual field. It is usually associated with an increase in intraocular pressure (IOP) above the normal value (intra-ocular pressure > 21 mm Hg)
Describe the epidemiology of glaucoma
Prevalence:
- 1% in over 40 yrs
- 10% in over 80 yrs
- Affects males and females equally
- 3rd most common cause of blindness worldwide
What are the different types of glaucoma?
In open angle glaucoma, despite the normal clinical appearance, the aqueous outflow is restricted, and in closed angle glaucoma tissue physically obstructs the angle.
a) PRIMARY:
1. Acute closed-angle glaucoma (ACAG)= “someone’s iris suddenly block the drainage angle in their eye- pressure builds up rapidly”
- Ophthalmic emergency
- hypermetropia (long-sightedness), age and small eyeballs is a risk factor
- Chronic closed-angle glaucoma:
- develops slowly as the iris blocks the eye’s drainage angle
- no symptoms at first, so they don’t know they have it until the damage is severe or unless they have an attack of acute angle closure - Primary open-angle glaucoma (POAG) - MOST COMMON (iris is clear of meshwork and uveoscleral drainage canals are clear)
- occurs when the drainage channels are open, but do not drain fluid properly (still get raised intraocular pressure)- resistance to outflow
- no other underlying disease
b) SECONDARY:
- caused by an underlying eye condition, such as inflammation of the eye (uveitis)
c) CONGENITAL
- Buphthalmos (enlargement of the eye balls)
- the child is either born with ocular enlargement or enlargement of eyes is noticed within one month of life
- It is believed that the IOP is raised in the intrauterine life itself
What are the causes of glaucoma?
- Primary:
- Increasing age
- Genetics: first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease - Those with a positive family history of glaucoma should be screened annually from aged 40 year - Secondary:
- Trauma
- Uveitis
- Steroids
- Rubeosis iridis (formation of new blood vessels on the surface of the iris, associated with diabetic retinopathy)
Describe the pathophysiology behind glaucomas
- Ocular hypertension leads to compression and stretching of the retinal nerve fibres
- This leads to scotomas (partial loss of vision) and visual field defects
- Ocular hypertension is due to reduced outflow of aqueous humour caused by:
- ACAG: Obstruction to the outflow (caused by narrowing of the iridocorneal angle and, hence, narrowing of the canal of Schlemm leading to a rapid and severe rise in IOP)
- POAG: Resistance to the outflow through the trabecular meshwork
(Blockage of trabecular meshwork by blood or inflammatory cells)
What are the presenting symptoms of ACAG?
- Painful red eye
- Nausea and vomiting
- Impaired vision
- Haloes seen around lights
What are the presenting symptoms of POAG?
- Usually ASYMPTOMATIC
- Peripheral visual field loss - Arcuate visual field defects: ‘tunnel vision’
- Optic disc cupping – a cup:disc ratio of >0.7 suggests cupping
What are the presenting symptoms of congenital glaucoma?
- Buphthalmos
- Watering
- Cloudy cornea
What signs of ACAG can be found on physical examination?
- Red eye
- Hazy cornea
- Loss of red reflex
- Fixed and dilated pupil
- Eye is tender and rock hard on palpation
- Cupping of optic disc
- Visual field defect
- Moderated raised intra-ocular pressure
What signs of POAG can be found on physical examination?
- Usually NO signs
- Optic disc may be cupped
- Increased IOP
- Visual field defect
What is the difference between open and closed angle glaucoma?
O:
- progressive visual loss
- initially asymptomatic
- Mild nonspecific symptoms
C:
- sudden onset
- severely painful
- N&V, cloudy cornea, headache, dilated pupil
What investigations are used to diagnose/ monitor glaucoma?
- Goldmann-type Applanation Tonometry
- Standard method of measuring intra-ocular pressure
- Normal IOP = 15 mm Hg - Fundoscopy
- Detects pathologically cupped optic disc - Gonioscopy
- Assess iridocorneal angle (differentiate between closed and open angle) - Slit lamp examination
- To assess optic nerve and fundus for a baseline - Pachymetry
- Using ultrasound or optical scanning to measure central corneal thickness (CCT)
- CCT < 590 mm = higher risk of glaucoma - Automated perimetry (Visual Field Testing)
- Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy - Screening programme for chronic glaucoma
How is acute closed angle glaucoma managed?
- Medical Emergency - admit immediately for specialist ophthalmology assessment
- if not immediately possible: Topical pilocarpine- constricts the pupil and increases trabecular outflow - Reduce intraocular pressure:
- IV acetazolamide (carbonic anhydrase inhibitor)
- Topical eyedrops (prostaglandin analogues [bind to EP and FP receptors in the ciliary muscle, resulting in ciliary muscle relaxation and increased aqueous humor outflow.] & beta blockers e.g. timolol)
- IV mannitol occasionally required - Prevent further development/progression:
- Laser iridotomy (creates hole in iris for aqueous humour to drain) - it is performed bilaterally, even in the “healthy” eye as the other eye is at risk
- Iridoplasty (moulds the iris away from the anterior chamber angle)
How is primary open angle glaucoma managed?
- Eye drops
- first line: prostaglandin analogue (PGA) eyedrop:
*Latanoprost (Side effects include excessive eyelash growth and brown pigmentation of the iris)
- second line:
*beta-blocker (Contraindicated in patients with asthma and heart block)
carbonic anhydrase inhibitor (Side effects include sulphonamide-like reactions)
(both reduce aqueous production)
OR give sympathomimetic eyedrop
- if more advanced: surgery (trabeculectomy- removing part of the eye’s trabecular meshwork) or laser (trabeculoplasty) treatment can be tried
- Reassessment
- important to exclude progression and visual field loss
- needs to be done more frequently if: IOP uncontrolled, the patient is high risk, or there is progression
What are the risk factors of acute- closed angle glaucoma?
- Hyperopia (long-sightedness) and short axial length of the eyeball
- Age – the lens grows with age and can push the iris forwards into the angle
- Ethnicity – Asian or Inuit populations
- Pupillary dilatation – either iatrogenically (eg. topical mydriatics or systemic alpha-adrenergic agonists) or owing to the patient being in a dimly lit environment (eg. watching television in a dark room)
*Atropine: it is an anti-cholinergic agent that causes mydriasis
