Glaucoma Flashcards
Background
A group of eye disorders leading to progressive optic neuropathy.
Partly caused by high IOP.
Types:
- Primary = Open angle (POAG) or closed angle (PCAG)
- Secondary = inflammation, intraocular tumour, developmental abnormalities
- Developmental = primary congenital, etc
Glaucoma can also be classed through age of onset (congenital, infantile, juvenile, or adult), causes primary (no known) or secondary, Rate of onset (acute, subacute, chronic) and by angle (closed or open)
Ocular HTN = >21mmHg consistently or recurrently but no signs of glaucoma
POAG = Chronic open angle G
Basic pathophysiology
PICTURE IN PACK SHOWS IT BEST
POAG (more common)
Main site of damage thought to be optic nerve head. Channel resistance increases IOP. Trabecular meshwork is main route of resistance for outflow. so drainage is restricted.
POAG - affects both eyes
PACG
Closure of the chamber angle = rise in IOP.
Dilator muscle theory - contraction of the dilator muscle results in the peripheral iris obstructing the angle and = rise in IOP; OR
Sphincter muscle theory - the pupil sphincter precipitates angle closure.
ANGLE IS CLOSED NO DRAINAGE
PACG - mainly unilateral
Risk factors
POAG
- Raised IOP
- Age
- Family Hx and genetics
- Ethnicity 2-3X more likely in black than white
- Corticosteroids - Can cause changes in stiffness of trabecular meshwork
- Myopia
- T2DM
- HTN and CVD
PACG
- Age
- Sex
- Ethnicity - more common in asian
- Eye size - short eyes more risk
- Family Hx and genetics
Signs and Symptoms
POAG
IOP>21
- Sus/damaged optic nerve head
- Visual field loss/ Peripheral vison loss
PACG - ACUTE
IOP= 50 -80
- Rapid progressive visual impairment
- Red eyes, blurred vision
- periocular pain
- Congestion of eye
- N+V in severe cases
- Corneal oedema
- Vertical oval pupil and fixed in semi dilated place
- Pupil unreactive to light and accommodation
PACG - CHRONIC
Usually no symptoms happens slowly over time. slowly IOP rises
Diagnosis/ Assessment
Ocular HTN & POAG
Normally checked by optometrist, look for visual issues and raised IOP. Will refer to confirm diagnosis
GP should sus POAG even if only vision loss
PACG
ACUTE:
Sus angle closure if acute painful red eye with risk factors and/or history of =-
- Previous eps of blurred vision headaches, or eye pain with nausea and seeing halos around lights occur typically in evening and relieved by sleep
- A precipitating factor, eg watching TV in a dark room, adopting a semi-prone position (eg, reading), use of adrenergic drug (for example phenylephrine), or an antimuscarinic drug (eg a TCA.)
Refer to signs and symptoms
SUBACUTE:
Similar symptoms to acute but may be less severe and often soon resolve, lying flat and closing eyes, or after sleeping.
CHRONIC:
- Typically asymptotic until severe visual field defects affect vision
- Diagnosis usually made by optometrist
- GP should sus even if no other eye symptoms but vision loss
Treatment
USE preservative free eye drop if they have allergy
AIMS:
Treat IOP, Prevent progression of glaucoma and vision loss.
OCULAR HTN
No risk of vision impairment in lifetime = no treatment - MONITOR
New ocular HTN + IOP=/>24 and risk of visual impairment in life:
1st line - 360° selective laser trabeculoplasty (SLT) Repeat If effect reduced over time. IF fail = REFER to see other treatments
IF they reject SLT/unsuitable:
1st line - Topical generic PGA (latanoprost, tafluprost, travoprost, bimatoprost) - Can be used if waiting for SLT
FAIL = ALT generic PGA THEN topical beta blocker (betaxolol, levobunolol, timolol)
STILL FAIL= non generic PGA, Carbonic anhydrase inhibitor (brinzolamide dorzolamide), Topical sympathomimetic (apraclonidine, brimonidine) OR Topical mitotic (pilocarpine) AS EITHER MONO OR COMBO therapy.
MONO/COMBO therapy with drugs from different class (b blocker PGA etc) also given if IOP not reduced good enough or to prevent vision loss.
POAG
NO treatment IOP<24
IOP=/>24:
1st line - Same as HTN
ALT same EXCEPT NO Mitotic.
Advanced POAG = Glaucoma surgery + Pharmacological (Mitomycin). Topical PGA used until surgery. FAIL/or reject surgery = Combo of topical classes, further surgery, 360 SLT or Cyclodiode laser.
CLOSED angle G:
Acute sus = ADMIT ASAP to specialist. If not possible start emergency treatment =
- Lie flat face up no pillow. If available ; Pilocarpine eye drops - 1 drop 2% blue eyes or 4% brown eyes, acetazolamide 500mg oral (reduce aqueous humour production), analgesia, anti emetic prn.
REFER if intermittent or chronic version sus.
IN Secondary care:
Aims same as POAG
IV Acetazolamide and Topical pilocarpine, beta blockers and steroids - initially
THEN Surgery = iridotomy, phacoemulsification, or iridoplasty
Whittlsea hodgson:
INITIAL PRE OP prep:
- Timolol 0.5% 1 drop q 30 min for 2 doses;
- Pilocarpine 2-4% 1drop q 15 min for the first 1-2 h;
- Apraclonidine 0.5-1% 1 drop q 30 min for 2 doses;
- Acetazolamide 500mg orally initially followed by 250mg q 6 h; and
- An osmotic agent, such as oral glycerol 1 mL/kg diluted with an equal amount cold water, mannitol 1.0 -1.5 mg/kg IV, or isosorbide 100 g (220 mL of a 45% solution).
THEN
DO laser peripheral iridotomy (LPI) - opens another pathway for fluid to pass out the front of eye, breaking the pupillary block. Second eye can be done later.
Treatment children
RARE always managed by specialist.
Primary - surgery 1st line, uses pre or/+ post op as supportive to reduce IOP
Secondary - drug therapy 1st line
Cautions/AE/SE:
Carbonic anhydrase I =
- Metabolic acidosis can occur in children on topical (symptoms poor feed, less weight gain)
- Acetazolamide can = weak diuresis. DONT use long term.
BASIC MOA of treatments
- Reduce aqueous humour formation:
- Beta blockers - good long term. - inhibit the synthesis of cAMP in the ciliary epithelium and = decrease in aqueous secretion
- Carbonic anhydrase i - inhibiting the enzyme carbonic anhydrase in the ciliary body = less bicarbonate ions and their secretions into the posterior chamber = less Na in posterior chamber = less production. - Reduce Aqueous Humour Formation and Increase Its Outflow:
- α2 receptor agonists/ Sympathomimetics - α-mediated vasoconstriction of the ciliary body. - Increase Aqueous Humour Outflow:
- PGA - Exact unknown - possible:
- Increase in extracellular matrix metalloproteinases in ciliary smooth muscle cells
- Remodelling of uveal meshwork
- Increase in blood flow to the optic nerve– possible neuroprotection in the retina. - OTHER AGENTS
Cholinergic/ mitotic (Pilocarpine) - stimulate cholinergic receptors within the eye, = spasming of the ciliary muscle and contraction of the pupil. = trabecular meshwork opens and increases the drainage of aqueous humour. - Surgery
Iridotomy - laser energy to create a small hole in the iris = more drainage.
Laser trabeculoplasty - 120 small burns in trabecular meshwork = increase drainage
laser ciliary ablation - Apply burns
trabeculectomy - Artificial drainage path is made
Phacoemulsification - small probe is put through incision and in lens. The probe emits high-frequency ultrasound waves = break up the cloudy lens into small pieces, which are then suctioned out.
Irdioplasty - open up the drainage angle
Possible COMBOS
Carbonic anhydrase i:
Brinzolamide + Timolol (β blocker) or Brimonidine (PGA)
Dorzolamide + Timolol (β blocker)
PGA:
ANY + Timolol (β blocker) When not good enough alone
Complications of surgery
- Scar tissue (fibrosis) - can close these pathways - mitomycin C and 5-fluorouracil are used to reduce the risk of fibrosis formation
- Ocular inflammation
- Haemorrhage
- Cataract formation
= Low IOP
