What are the features of glaucoma?
increased intraocular pressure in the eye causing optic nerve damage (Glaucomatous cupping of the optic disc) due to the impaired drainage of aqueous humour from the anterior chamber of the eye. This results in visual field loss that starts peripherally and progresses centrally. 30-40
Early Glaucoma is completely asymptomatic, however there are often changes in the peripheral (superior due to inferior nasal field nerve fiber loss) visual fields that are undetected by the patient. 30-40% nerve fibres can be lost before demonstrable visual defect, 90% before becoming symptomatic because of compensation by other eye/brain. Early changes in the optic disc= OVAL CUP (due to infarction of the nerve fibres causing expansion of the cup)
Intermediate Glaucoma enlarged cup but a return to a normal shape. Arcuate scotoma is the pattern of vision loss associated.
Advanced stage glaucoma cup=disc and ring scotoma pattern of vision loss (aka tunnel vision).
What are the causes of optic disc swelling. Describe their pathophysiology.
Papilloedema (bilateral) due to raised ICP e.g. due to tumour, haemorrhage,
optic neuritis (MS)
arteritic anterior ischaemic optic neuropathy
non-arteritic anterior ischemic optic neuropathy
malignant HT
What are the stages of Diabetic Retinopathy? Describe the features seen on Opthalmoscopy.
- Background/ Non-Proliferative: Early changes are observed but pt asymptomatic. Microaneuyrsms (focal dilatation of capillaries), haemorrhages (red): dot, blot, flame shaped, hard exudates (yellow-white) (distinct edges- leaked lipoproteins), cotton wool spots (greyish) due to focal areas of infarction of axons in the retina (indistinct edges), intraretinal microvascular abnormalities (IRMA).
Common after 8-10y of DM but may be mild-severe.
NO NEW VESSELS
In severe Non-proliferative, dark haemorrhages, beading/ loops of veins, and other IRMA. Will progress to Proliferative within 12/12. - Proliferative: Neovascularization (abnormal new blood vessels due to release of angiogenic growth factors) is the hallmark of this stage. Either NVD (of the disc) or NVE ( elsewhere except for disc). Pattern of these vessels- like seaweed/ ink in water (irreg branching). High risk of bleeds with due to the fragility of these endothelial buds that rupture easily causing pre-retinal/ vitreous haemorrhage. More common T1DM.
Late features: retinal fibrosis, traction retinal detachment, iris neovascularization – neovascular glaucoma due to growth of vessels in the angle.
What is the pathophysiology of Diabetic retinopathy?
- Hyperglycaemia which leads to altered Hb and resulting hypoxia of the retina (highly metabolically active neurones)
- Hypoxia results in changes in the blood vessels (capillaries, arterioles, venules) and cytoskeleton, “ultrastructural changes” such as:
- thickened Basement Memb of arterioles
- decreased mitochondria
- increased stickiness of platelets
- more rigid RBC - These changes in particular to the BM and the RBC lead to the formation of micro emboli occluding the microvasculature leading to further hypoxia and ischaemia.
- In the venous system, intramuscular pericytes die by apoptosis in clusters leading to sectional dilatation- saccular/ out-touching stagnating venous flow leading to leakage of the contents, retinal oedema and contributing to hypoxia. Macrophages engulf leaked plasma proteins forming hard exudates in the retina.
- Retina tries to respond to the hypoxia by opening parallel pre-existing channels of blood flow to divert past occlusions but these shunt vessels (IRMA) are not sufficient to provide relief therefore ultrastructural changes persist.
- Prolonged ischaemia results in the release of angiogenesis factors e.g. VEGF causing the retinal vascular bed to sprout abnormal vessels particularly veins.
- Diabetic Maculopathy can accompany background or proliferative retinopathy.
What are the RF for cataracts? How is cataracts treated?
- Ageing
- Trauma: blunt, sharp, XR, radiotherapy, chemical injuries, UV light
- DM
- Malnutrition
- F more than M
- Systemic steroids
- smoking
Extracapsular surgery using phacoemulsification + aspiration of the lens with maintenance of the posterior capsule to support implanted lens. Dexamethasone + gentamicin/ cefuroxime is used post-surgery to reduce risk of Refractory uveitis.
What is the ddx for acute red eye?
- Haemorrhage
2. Congestion on surface of eye which is generalised: ciliary/ conjunctival, or localised.
What are the two types of haemorrhage that may cause red eye?
- Subconjunctival: where posterior border of blood patch is visible. More common older patients, those on aspirin/ warfarin, foreign body, sometimes trauma. May shift in location due to gravity.
- Retrobulbar: this is blood accumulating behind the eye ball. The posterior border of the blood patch is not visible.
Signs: raised pressure (behind eye can compress Optic n), proptosis (like exophthalmos), reduced eye movement, dilated pupil (indicates optic n compromise). These last two signs indicate an emergency.
Common cause: iatrogenic, trauma, head injury/ fracture floor of orbit, bleeding disorders.
CAN CAUSE SUDDEN IRREVERSIBLE BLINDNESS
V homogenous red sclera but NOT congestion- no blood vessels visible, as though sclera has been dyed red. Even when patient moves the affected eye, no posterior border will be visible.
What are the generalised congestive causes of red eye?
Conjunctivitis: viral, bacterial, allergic Keratitis (cornea) Acute Glaucoma Iridocyclitis Uveitis (iris, ciliary body, choroid)
What are the localised congestive causes of red eye?
episcleritis (autoimmune). tender. common SLE, RA. No effect on site. Anti-inflamms either steroidal/ non-steroidal.
Scleritis- severe pain, localised pain.
phylctenular conjunctivitis
How do you differentiate circumcorneal and conjunctival congestion?
circumcorneal/ ciliary: dusky red, blood flow from limbus to fornix, vessels do not blanch with topical vasoconstrictors/ move with conjunctiva.
conjunctival: bright red (bc involves superficial vessels), blood flows from fornix to limbus (periphery to cornea), vessels blanch (go white!) with topical vasoconstrictors (phenylephrine) and move with the conjunctiva, more marked in the fornices (i.e. where conjunctiva reflect onto lids) and the periphery of the bulbar conjunctiva (i.e. where conjunctiva is covering sclera).
What are the features of Horner’s Syndrome? What is it caused by?
- Partial ptosis (disruption to muller’s/tarsal muscle which only lifts eyelid slightly whereas main lifter is levator palpebrae superioris which is supplied by CNIII)
- Anhydrosis
- Meiosis due to unopposed action sphincter papillae (ANAISOCORIA)
- Apparent enopthalmos
- If longstanding/ congenital heterochromia of irises
It is due to disruption of the sympathetic output to the eye and face. This disruption can be anywhere along the path of the output from the hypothalamus, along the spinal cord, through the cervical sympathetic chain, the sup cervical ganglion the path along the common carotid (ECA for sweat glands) and ICA and then via the different individual nerves to the eyelid and pupil.
Describe the types of Glaucoma?
Open angle 1° and 2°
Narrow angle 1° and 2°
Normal tension Glaucoma
OPEN 1°: idiopathic and most common type due to reduced drainage through trabecular meshwork. usually bilateral and slowly progressing (years).
Rarely seen before age 40.
OPEN 2°: caused by clogging of the trabecular meshwork. Pigment Dispersion syndrome- pigment cells of iris are shed when iris touches lens clogging meshwork. Pseudoexfoliation fibrous deposition from lens etc that occludes trabecular meshwork. Other causes: inflammatory (uveitis), neovascular (DM/ central retinal vein occlusion) retinal ischaemic causes release of vasoproliferative factors resulting in new vessels occluding the angle and therefore blocking outflow.
NARROW 1°: “wrong size” eye (small) long-sighted hypermetropic.
NARROW 2°: lens growth causes the lens to abut the iris.
What is raised intraocular pressure called? and how is it identified?
Ocular HT (provided no damage to the 0ptic nerve evident) Above 21 mmHg (provided cornea is of average thickness).
What normal process causes narrowing of the Angle of the anterior chamber?
Continued lens growth through life can sometimes causes the narrowing of the angle due to the pushing of the lens onto the iris.
What are the RF for Open Angle Glaucoma?
Increased Intra Ocular P Fhx African American Myopic DM
What is the pathophysiology of Open Angle Glaucoma?
Raised intraocular pressure due to increased resistance of drainage channels which leads to compression of the microcirculation of the disc leading to indirect ischaemia (some vascular factors may also play a part in the pathogenesis). The nerve fibres to be affected first are usually those found at the position of 12 and 6 in the rim of the cup which are thought to be watershed areas leading to the early stage of glaucoma: Oval Cup due to disc “excavation”.
What are the pathonomic features of Glaucoma?
- Oval cup due to infarction of retina nerve fibres causing extension of the cup (disc excavation) in an irregular pattern.
- Arcuate Scotoma the peripheral vision loss associated with Glaucoma (maintained central vision) due to the death of nerve fibres at the 12 and 6 position in the optic disc that correspond with the temporal fibres that arc towards the optic disc leading to either sup/ inf visual field loss due to inf/sup retinal damage. But visual acuity is unaffected.
How is glaucoma diagnosed?
cup:disc ratio (normal is 0.4-0.5) IOP measurement (expect >21mmHg) resistance to the Goldmann tonometer machine depression on the surface of the eye. visual field analysis (Arcuate scotoma will be seen first i.e. peripheral vision loss)- Humphrey visual field analyser (scattered around two intersecting lines) visual acuity (unaffected)
What are the medical treatment options for Glaucoma?
- Prostaglandin Analogues (Latanaprost)
- Beta Blockers (1 and 2 are commonly combined) (Timolol)
- Carbonic Anhydrase (can be combined with 2.)
- Alpha agonists
- Pilocarpine
What are the general treatment options for Open Angle Glaucoma?
- Medical treatment
- Surgical: Trabeculectomy= create a flap in sclera i.e. controlled fistula to allow for some drainage of Aq onto conjunctiva and absorption of this Aq by the conjunctival blood vessels. not always successful and last resort bc at risk of infection of “bleb”. may fail and stop draining due to scar tissue formation.
- Argon laser trabeculoplasty: to ablate the ciliary body reduce the production of Aqueous and also activates Phages to clearer meshwork increasing drainage.
What are prostaglandin analogues used in the treatment of? How do they work and what are their SE?
Glaucoma, first line tx. e.g Latanoprost (-prost is common ending) because most effective
cause low grade inflammation increasing uveoscleral outflow of aq humour increasing drainage. SE: Red eyes (conjunctival congestion) initially, increased melanin deposition in iris (makes pigment darker), increase in length of eye lashes, pigmentation around eyes (black circles).
CI: pregnancy, uveitis, cystoid macular oedema.
What is the second line medical treatment option for glaucoma? How does it work? What are the SE/ CI?
Beta blockers
these are almost as effective as PG Analogues.
Work by reducing Aq production by ciliary body.
e.g. Timolol
CI: Asthma, COPD, HF, heart block, myasthenia gravis, dépression
When are carbonic anhydrase inhibitors used? How do they work?
used in acute angle closure glaucoma IV
or in open angle glaucoma oral/ drops.
They work by inhibiting the catalysing action of Carbonic Anhydrase of Bicarb to CO2 and H2O which is an imp step to the prod of Aqueous humour thereby decreasing production. (end in zolamide) e.g. Dorzolamide. SE: burning sensation in eyes on instillation, bitter taste and topical allergy, acidosis (usually -oral).
What is pilocarpine? When is it used? What are the SE?
Cholinergic. It is used in acute angle closure glaucoma to cause pupillary constriction releasing the iris tissue from blocking the angle structures by attaching to the lens. It also stimulates the muscles around the angle of anterior chamber to contract increasing drainage of aq. No longer used in Chronic glaucoma bc of effect on pupils and the associated reduced visual acuity.
SE: Eye ache, dim vision.
