Ophthalmology SC010: Chronic Visual Loss Flashcards
Approach to chronic visual loss
- History taking
- HPI
—> Onset (usually insidious for chronic visual loss)
—> Duration
—> ***Symptoms (VA, distortion, visual field defect)
- PMH
—> ***Systemic diseases (DM, HT —> retinopathy)
—> Previous surgery
—> Trauma - Family history
—> Glaucoma, Cataract
- PE
- ***Slit lamp
—> Anterior segment: Conjunctiva, Sclera, Cornea, Iris, Aqueous
—> Posterior segment: Retina, Disc, Macula, Vessels
- ***Dilated fundus exam with fundoscopy
- Diagnosis
- Investigations
- Severity
- Disease monitoring
Common ocular disease spectrum
Systematic: Front —> Back:
1. Cornea / Anterior segment
- ***Cataract
—> Senile (degenerative)
—> Congenital (chromosomal abnormality / congenital infection)
—> Traumatic (traumatic cataract)
—> Drug-related (steroid: posterior subcapsular cataract)
- Optic nerve
- ***Glaucoma - Retina / Posterior segment
- **DM retinopathy (DR)
- **DM macular edema (DME)
- ***Age-related macular degeneration (AMD)
- Epiretinal membrane (ERM)
Cataract
Risk factors:
1. Age
2. ***DM
3. UV light
4. Steroid
Types:
1. ***Nuclear sclerotic cataract
- degeneration of core of lens
- lens initially yellow —> orange —> brown
- increased myopia
- ***Cortical cataract
- affect cortex (layer outside nucleus)
- white, spokes-like changes cataract -
**Posterior subcapsular cataract
- **steroid
BUT all can co-exist (∵ all due to degeneration)
Types of cataract determine:
1. Predict difficulty in cataract surgery
- Prognosis
- NS type go harder over time (cannot perform phacoemulsification, ∵ not enough US energy)
- PSC affect vision most + progress fastest (consider early surgery, also PSC surgery more difficult, more complication e.g posterior capsular rupture) - Underlying cause
- e.g. PSC caused by steroid
Senile cataract
Symptoms:
1. Gradual BOV
2. **Glare (esp. cortical cataract type)
3. **Diplopia (monocular instead of binocular (usually ∵ CN deficit e.g. CN3/6 palsy))
4. ***↑ Myopia (∵ ↑ in refractive power of lens esp. in nuclear sclerosis) (might say 老花 improved)
etc.
Treatment:
Cataract extraction + Intraocular lens implantation
1. ***Phacoemulsification (use US energy)
- ***Extracapsular cataract extraction (ECCE)
- if US energy requirement is too high —> might damage corneal endothelium —> consider ECCE
- if zonular fibres loose already —> consider ECCE - Intracapsular cataract extraction (ICCE) (seldom performed now)
- if lens already subluxed
3C’s to describe fundoscopy
- Colour of Neuroretinal rim (i.e. area of disc excluding cup)
- Pink
- Pale (Optic neuropathy) - Contour
- Clear
- Blur (Optic disc swelling) - Cup-disc ratio
Glaucoma (Chronic glaucoma)
A form of **Optic neuropathy
- characteristic **VF loss
- in context of chronic visual loss —> refers to **Chronic glaucoma i.e. **POAG, **CACG
- usually associated with **↑ IOP
- exceptions:
—> **normal tension glaucoma (IOP <21)
—> **ocular hypertension (↑ IOP but no signs of optic neuropathy)
***Classification:
1. Chronicity
- Acute (pain, redness, BOV) / Chronic (insidious onset, may not experience vision change until late stage)
- Etiology
- Primary (without cause) / Secondary (e.g. neovascularisation, uveitis, trauma) - IOP
- High / Normal - Angle status
- Open / Closed
—> determined by ***gonioscopy
—> change treatment options
Examples:
1. POAG
2. CACG
3. NTG
4. Secondary open angle glaucoma
5. Secondary angle closure glaucoma
***Symptoms and Signs of (Chronic) Glaucoma
Symptoms:
- None until late stage (usually) —> picked up incidentally
- **Constriction of VF (Peripheral VF affected first —> **ISNT rule (Inferior —> Superior —> Nasal —> Temporal))
- Bumping into objects on side
- ***Dull eye pain (not a usual symptom, ∵ IOP only range from 20-30 vs Acute glaucoma: 60-70 (intense pain))
Signs:
Glaucomatous disc changes
1. Colour: **Pale disc / neuroretinal rim (only in late stage, early stage: still **pink disc, must consider other causes of optic neuropathy if cup-disc ratio is still borderline but disc already pale)
2. Contour: No change (∵ no disc swelling in glaucoma)
3. Cup-disc ratio: **>0.7 (normal: 0.3-0.5)
4. Notching of disc rim (*ISNT rule)
5. Peripapillary atrophy (Temporal crescent)
(vs APAC / AACG:
Symptoms:
1. **Severe ocular pain, **acute onset (∵ sudden buildup of IOP: >45), may radiate other areas (e.g. periocular area, forehead)
2. Frontal headache
3. **BOV (cornea become hazy if prolonged ↑ IOP)
4. **Halos around lights
5. N+V
Signs:
1. **Fixed mid-dilated pupil (∵ high IOP —> ciliary muscle becomes ischemic —> can no longer constrict the pupil)
2. **Corneal haze / edema
3. **Shallow anterior chamber (on slit lamp exam)
4. Conjunctival injection (Ciliary flush)
5. **Very high intraocular pressure (>45 mmHg))
***Diagnosis of (Chronic) Glaucoma
Gold standard:
1. **Disc morphology
- must see disc changes —> **specific to glaucoma —> further do tests to rule out physiological cup (born with high cup-disc ratio)
- increase cup-disc ratio (narrowing of neuroretinal rim: composed of axons of ganglion cells) (SpC Revision)
-
IOP measurement (Goldmann Applanation Tonometer)
- non-specific -
**VF assessment
- **Humphrey (automated) vs Goldman (manual, for poor vision / uncooperative patient)
- non-specific -
**Optical coherence tomography (OCT) / Nerve fibre analyser
- assess whether there is thinning of **retinal nerve fibre layer (RNFL)
- non-specific
If only 1 but 2-4 indefinite —> ***Glaucoma suspect —> FU patients in a few months for progression
(5. Gonioscopy: to confirm angle)
***Treatment of (Chronic) Glaucoma
- Medication
- Topical anti-glaucoma drops
- Oral IOP lowering agents (**Acetazolamide)
- IV IOP lowering agents (Acetazolamide, **Mannitol) —> usually for acute glaucoma (rapid IOP lowering), ensure good RFT - Surgery
1st line:
- Laser: **Selective laser trabeculoplasty (SLT) (for open angle)
- **Trabeculectomy (open small hole in sclera): Penetrating vs Non-penetrating
- Minimally invasive glaucoma surgery
2nd line:
- ***Glaucoma implant: Valved (ensure outflow not too rapid to develop hypotony) vs Non-valved implant
Last line:
- ***Cyclo-destructive procedures +/- endoscopic guidance (if visual prognosis too poor, cyclo = ciliary body —> stop aqueous production from ciliary body)
***DM Retinopathy (DR)
DM can cause:
1. **DM Retinopathy (DR)
2. **DM Macular Edema (DME)
—> both can induce gradual visual loss
—> both can ***co-exist
Clinical presentation:
1. **Gradual BOV with DM history
2. Milder form of DR may NOT cause any symptoms —> require annual screening in DM patients
3. **Vitreous haemorrhage (in proliferative DR —> sudden visual loss)
Signs:
1. **Intraretinal haemorrhage
- usually visually insignificant (for **Dot & Blot haemorrhage)
- Dot & blot haemorrhage: small areas of haemorrhage ∵ confined by retinal tissue
-
**Hard exudates
- ∵ breakdown of blood-retinal barrier —> exudation into retina —> **Retinal edema
- lipoproteins following partial / complete resorption of retinal edema - ***Cotton wool spots (aka soft exudates)
- focal areas of ischaemic infarcts - ***Venous beading
- increasing ischaemia -
**Intraretinal microvascular abnormalities (IRMA)
- anastomosis between retinal artery and vein (dilation of capillary network?)
- **pre-neovascularisation retinal vascular abnormalities —> Preretinal haemorrhage
- do **NOT leak contrast on FFA
- vs Neurovascularisation (*network-like) (IRMA: much smaller) —> will leak contrast
Important risk factors for DR:
1. Longer duration of DM
2. Poor DM control
3. Comorbidities (e.g. renal impairment, HT), smoking
Pathophysiology:
1. **Retinal microangiopathy
—> Breakdown of blood-retinal barrier
—> **Macular edema (although other areas of retina can also develop edema)
-
**Retinal ischaemia
—> Elaboration of vasoproliferative substances (e.g. VEGF)
—> Preretinal **neovascularisation
Classification of DR
Based on **Early Treatment Diabetic Retinopathy Study (ETDRS)
1. Non-proliferative DR (NPDR)
- mild / moderate / severe
- severe:
—> >20 **intraretinal haemorrhages in each 4 quadrants
—> definite venous beading in >=2 quadrants
—> prominent **IRMA in >=1 quadrants (*see IRMA —> severe)
- Proliferative DR (PDR)
- presence of **Neovascularisation (on disc / other areas apart from retina e.g. iris)
—> **Preretinal haemorrhage (much larger area than dot and blot haemorrhage e.g. “boat haemorrhage”, overlying the retinal vessels)
—> Vitreous haemorrhage
—> Tractional retinal detachment
—> Glaucoma
- low / moderate / high-risk / advanced
- advanced:
—> **Tractional retinal detachment (∵ fibrous proliferation + regression of proliferated vessels, but if macula not involved —> may not have symptoms)
—> **Rubeosis iridis (Neovascularisation of Iris) —> **Neovascular glaucoma
—> Fundus partially obscured (∵ **Vitreous haemorrhage) - DME
- ***Clinically significant macular edema (CSME) - Ischaemic maculopathy
- also important clinically but no treatment available
Diagnosis of DR
- Clinical exam
- Dilated pupil for fundoscopy - ***Fundus fluorescein angiography (FFA)
- serve as treatment guideline
- look at areas of ischaemia (hypofluorescence area), leaking of contrast from vessels (indicative of neovascularisation) - Optical coherence tomography (OCT)
- serve as treatment guideline
Diabetic Macular Edema (DME) / Clinically significant macular edema (CSME)
Clinically significant: Area of macular edema is close to fovea (i.e. centre of macula)
Definition (X details):
1. Retinal thickening at / within 500um of centre of macula
2. Hard exudates at / within 500um of centre, if associated with thickening of adjacent retina
3. An area of thickening > 1 disc area, if located within 1 disc diameter of centre
Ischaemic maculopathy
- No treatment
- Cannot be seen on PE / Fundoscopy —> Need fundus fluorescein angiogram
- ***Enlarged foveal avascular zone on fundus angiogram
- Poor prognosis
***Treatment of Diabetic retinopathy (DR)
(From CFB L32:
Mild / Moderate NPDR
- ***Glycaemic control (diet, medication)
Severe NPDR / PDR
- ***Panretinal laser photocoagulation (PRP)
—> killing of retinal tissue to prevent progression + preserve macula
—> impair peripheral vision + night vision
Clinically significant macula edema (CSME)
- Intravitreal **anti-VEGF (Ranibizumab / Aflibercept)
- Intravitreal **steroid (Triamcinolone / Ozurdex)
- ***Focal / grid laser if no macula ischaemia —> obliterate leaking microaneurysm + stimulate retinal pigmented epithelium to absorb more water in cystic space)
PDR:
1. ***Laser Panretinal Photocoagulation (PRP)
- 1st line treatment
- can perform >1000 shots per eye every time
- usually need >=5000 shots per eye
- take ~1 month to act, permanent effect
- MOA: sacrifice peripheral retina
—> limited oxygen / nutrients can be supplied to more useful area for vision
—> SE: decreased peripheral vision + poor night vision + lose some accommodation
- ***Anti-VEGF injection
- fast action (act within 2-3 days) but limited duration of action (effect go away within 1 month —> re-inject)
- if do not have good view of fundus (e.g. dense cataract, vitreous haemorrhage) for PRP
- SE of systemic Anti-VEGF: MI, stroke
CSME:
1. ***Focal / Grid macula laser
- much milder laser energy compared to PRP (no laser marks afterwards)
- avoid >=350um diameter from centre of fovea (i.e. Foveola) —> avoid scar formation —> Scotoma —> if macula involved: Anti-VEGF / Intravitreal steroid
- obliterate aneurysms to stop leakage
- ***Anti-VEGF injection
- can resolve macular edema without causing any scar
- invasive —> risk of retinal break / detachment, haemorrhage, endophthalmitis - ***Intravitreal steroid
- can resolve macular edema without causing any scar
- invasive —> risk of retinal break / detachment, haemorrhage, endophthalmitis
- can cause ↑ IOP + cataract —> not good in patients with pre-existing glaucoma
Surgery:
- Vitrectomy + Endolaser PRP for non-resolving VH, Tractional RD
