6.1.13 Recognises ocular manifestations of systemic disease Flashcards
(33 cards)
What is hypertensive retinopathy?
Ocular manifestation of systemic hypertension
What are the stages of hypertension - BP level values?
- Normal - <120mmHg/80 mmHg
- Prehypertension - 120-139mmHg /80-89mmHg
- Stage 1 hypertension–140-159mmHg/90-99 mmHg
- Stage 2 hypertension- >160mmHg/>100 mmHg
- Stage 3 hypertension- >180mmHg/>110mmHg
What are the features and severe features of hypertensive retinopathy?
Features
* Tortuous Vessels
* Venous compression at A/V crossing
* Focal arteriolar narrowing
* Arteriosclerotic changes
* Nerve fibre haemorrhages (Flame-Shaped)
* Accelerated hypertension: Cotton wool spots, Disc Oedema, Macular star of
exudates
Severe Hypertensive Retinopathy Features
* Swollen Disc
* Macular Star
* Cotton wool spots
* Dilated retinal veins
* Tortuous vessels
Macular oedema
What is the grading of hypertensive retinopathy?
- Grade 1– Mild arteriolar attenuation (narrowing)
- Grade 2
o Focal arteriorlar attenuation
o venous compression at arterio-venous crossings (Nipping)
o exaggerated light reflex (copper wiring) - Grade 3 (>110mmHg DBP)
o Haemorrhages
o Cotton Wool Spots
o Exudates - Grade 4 (>200mmHg/>130mmHg. Malignant Hypertension)
o All of above plus Disc Oedema and Macular Star formation (accumulation
of exudate in NFL)
§ Headaches, Diplopia, Decreased Vision, Scotomas, Photopsia
What are the levels of arteriosclerotic changes that occurs with hypertensive retinopathy?
Grade 1
o Broadening of Arteriolar light reflex
Grade 2
o Deflection of the veins when crossing the arteries (Salus’ sign)
Grade 3
o Copper Wiring of the retinal arterioles
o Banking of veins distal to the crossings (Bonnet’s sign)
o Tapering of veins on either sides of crossings (Gunn’s sign)
o Right angled deflection of veins
Grade 4
o Silver wiring of retinal arterioles
What is the pathogenesis of hypertensive retinopathy?
- Vasoconstriction of Retinal Arterioles (Grade 1)
- Acceleration of atherosclerotic changes in retinal vessels (Grade 2)
- Retinal Vessel alterations impede blood flow, through retinal arterioles and
capillaries – retinal perfusion is reduced as a result - Ischaemia and hypoxia lead to damage of the blood vessel walls
* Blood Retinal barrier is disrupted
* There’s increased vascular permeability - Blood and plasma leak out of blood vessels and into the surrounding retina (G3
and 4)
Differentiate hypertensive and diabetic retinopathy?
- Hypertensive Retinopathy
o few haemorrhages
o rare oedema
o rare exudates
o multiple CWS
o flame shape haemorrhages
o visibly abnormal retinal arteries - Diabetic Retinopathy
o Multiple haemorrhages
o Extensive oedema
o Few CWS
o Dot and Blot Haemorrhages
o Visibly abnormal retinal veins and capillaries
What is the management of hypertensive retinopathy?
o Grade 1/2 - Non-urgent referral – inform GP
o Grade 3 – Urgent Referral
o Grade 4 – Emergency Referral
- if lots of haems may need to go to GP same day
- if mac affected and VA reduced then HES referral
Describe the ocular blood supply?
- Common Carotid Artery
- Internal Carotid Artery
- Ophthalmic Artery
- A. Central Retinal Artery
* Inner Retinal Layers (NFL – INL)
B. Posterior Cillary Arteries
* Outer Retinal Layers (OPL – RPE Via choriocapillaris)
* Optic Nerve
What are the signs of retinal vessel leakage?
- Haemorrhages: Dot/blot, Flame, Microaneurysms
- Oedema
- Hard Exudates
What are the signs of retinal vessel occlusion?
Occlusion causes ischaemia, leading to:
* CWS
* Neovascularisation
What is a CRVO and what are the RFs?
Occlusion of the central retinal vein at the level of the lamina cribosa due to thrombosis.
Risk Factors
* Hypertension
* Hyperlipidaemia
* Diabetes
* Hyper-viscosity of blood
* Smoking
* Contraceptives
* Raised IOP (>30mmHg)
What is the pathogenesis and appearance of CRVO?
- Occlusion of CRV
- Hypoxia
- Leakage
- Capillary Occlusion
- Retinal ischaemia
Appearance
* Tortuous dilated veins in all 4 quadrants of the retina
* Round/Blot and flame haemorrhages
* CWS
* Possible macula and disc oedema
What investigation is required in CRVO/BRVO?
– Investigate underlying cause and blood work up. Assess whether ischaemic or non-ischaemic
Describe non-ischaemic CRVO and sxs and signs?
- Where the outer retinal layers are still perfused as choroidal circulation remains
intact - 30% will progress onto ischaemic
Sx
Sudden onset, unilateral blurred vision (6/36-6/60). Main concern: conversion to
ischaemic
Signs - Tortuous dilated veins in all 4 quadrants of the retina
- Round/Blot and flame haemorrhages - less dark
- Occasional CWS
- Mild Possible macula and disc oedema
- Mild/absent RAPD
Describe ischaemic CRVO and sxs and signs?
Complete retinal ischaemia
Sx
Sudden onset, unilateral, severe vision loss (6/60 - HM). Main concern: development of
neovascularisation.
Signs
* Tortuous dilated veins in all 4 quadrants of the retina
* Extensive Round/Blot and flame haemorrhages - darker
* Multiple CWS
* Macula Oedema and disc oedema
* Marked RAPD
important to detect because neovascularisation may occur and leading to rubeosis iridis and
neovas glaucoma.
What are the complications of BRVO and CRVO?
- Macular Oedema
- NVD (New vessels disc) & NVE (New vessels elsewhere) could possibly cause
vitreous haemorrhage - Rubeosis Iridis
- Neovascular glaucoma (Very High IOP)
What referral, investigations and treatment is required for CRVO/BRVO?
If IOP is normal and signs/sx suggest non-ischaemic:
* Routine to Ophthalmology and GP OR urgent if macula involved
If IOP is elevated and signs and sx suggest ischaemia:
* urgent to GP and Ophthalmology
Investigation – Investigate underlying cause and blood work up. Assess whether
ischaemic or non-ischaemic.
Treatment – Laser PRP for neovascularisation, Intravitreal Anti-VEGF and steroids for
neovascularisation and macula oedema
Describe BRVO and the treatment?
o Appearance depends on which vessels occluded usually in quadrant of retina affected commonly located 1-2
DD from OD however tertiary branches and macular branches can be affected
o Features of haemorrhages and CWS plus exudates
o Occlusion occurs at A/V crossing where arteriole anterior to vein
o Visual prognosis will depend on macular involvement
o Treatment – Investigate and treat systemic cause, Laser PRP for neovascularisation and Intravitreal Anti-VEGF
for oedema and neovascularisation
What is CRAO/BRAO?
Obstruction of artery due to atherosclerosis, a thrombus or embolus (Carotid Embolism)
(usually BRVO If embolus) blocking the artery or inflammation of the artery
What would you expect from H&S of CRAO/BRAO? and what are the sxs?
- Aged 70-80yrs
- Carotid artery occlusive disease
- systemic hypertension
- high cholesterol
- smoking
- diabetes
- history of stroke or TIA
- Amaurosis Fugax attack (sudden blanking of vision lasting a few seconds)
Symptoms – Sudden, painless loss of vision, sometimes preceded by Amaurosis Fugax
attacks
What are the signs of CRAO? and the later developments of CRAO?
- VA – No LP (although LP and HM may be preserved in some parts of vision)
- Marked RAPD
- Central vision may be preserved if the patient has a cilioretinal artery supplying
the macula (<30% of population) - Retinal Signs:
o red foveal ‘cherry red spot’ due to the fovea being the most transparent
part of the retina
o Extensive whitening of Retina due to retinal oedema
o Attenuation of arteries and vein
Later developments of CRAO - Atrophy of inner retinal layers and optic nerve
- Neovascularisation at the disc and iris
- Vessels remain attenuated and cherry red spot reduces over weeks
What are the signs of BRAO?
- Sudden painless altitudinal or sectorial visual field loss
- Central vision may vary accordingly to the involvement of the macula (VA 6/6 –
CF) - Possible RAPD
- Retinal Signs:
o Extensive whitening of Retina due to retinal oedema in one quadrant
o Attenuation of arteries and veins in one quadrant
What is the management of RAOs?
- Massage the globe with px laying down
- Nd-YAG laser of embolus if visible
- Acetazolamide (Carbonic Anhydrase inhibitors): Decreases IOP by decreasing
Aqueous Humour production - Sublingual Isosorbide dinitrate: Causes vasodilation, can help move a clot
- Anti-coagulants (e.g. Warfarin) as risk of stroke/ischaemic heart disease is high.
Management Guidelines - EMERGENCY Referral if caught within <48hrs
- Routine >48hrs due to neovascularisation and need for blood work up to
determine systemic cause.
FV guidance: phone triage line - likely urgent referral
