6.1.13 Recognises ocular manifestations of systemic disease Flashcards

1
Q

What is hypertensive retinopathy?

A

Ocular manifestation of systemic hypertension

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2
Q

What are the stages of hypertension - BP level values?

A
  • 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
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3
Q

What are the features and severe features of hypertensive retinopathy?

A

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

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4
Q

What is the grading of hypertensive retinopathy?

A
  • 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
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5
Q

What are the levels of arteriosclerotic changes that occurs with hypertensive retinopathy?

A

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

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6
Q

What is the pathogenesis of hypertensive retinopathy?

A
  1. Vasoconstriction of Retinal Arterioles (Grade 1)
  2. Acceleration of atherosclerotic changes in retinal vessels (Grade 2)
  3. Retinal Vessel alterations impede blood flow, through retinal arterioles and
    capillaries – retinal perfusion is reduced as a result
  4. Ischaemia and hypoxia lead to damage of the blood vessel walls
    * Blood Retinal barrier is disrupted
    * There’s increased vascular permeability
  5. Blood and plasma leak out of blood vessels and into the surrounding retina (G3
    and 4)
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7
Q

Differentiate hypertensive and diabetic retinopathy?

A
  • 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
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8
Q

What is the management of hypertensive retinopathy?

A

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

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9
Q

Describe the ocular blood supply?

A
  1. Common Carotid Artery
  2. Internal Carotid Artery
  3. Ophthalmic Artery
  4. A. Central Retinal Artery
    * Inner Retinal Layers (NFL – INL)
    B. Posterior Cillary Arteries
    * Outer Retinal Layers (OPL – RPE Via choriocapillaris)
    * Optic Nerve
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10
Q

What are the signs of retinal vessel leakage?

A
  • Haemorrhages: Dot/blot, Flame, Microaneurysms
  • Oedema
  • Hard Exudates
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11
Q

What are the signs of retinal vessel occlusion?

A

Occlusion causes ischaemia, leading to:
* CWS
* Neovascularisation

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12
Q

What is a CRVO and what are the RFs?

A

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)

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13
Q

What is the pathogenesis and appearance of CRVO?

A
  1. Occlusion of CRV
  2. Hypoxia
  3. Leakage
  4. Capillary Occlusion
  5. Retinal ischaemia
    Appearance
    * Tortuous dilated veins in all 4 quadrants of the retina
    * Round/Blot and flame haemorrhages
    * CWS
    * Possible macula and disc oedema
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14
Q

What investigation is required in CRVO/BRVO?

A

– Investigate underlying cause and blood work up. Assess whether ischaemic or non-ischaemic

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15
Q

Describe non-ischaemic CRVO and sxs and signs?

A
  • 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
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16
Q

Describe ischaemic CRVO and sxs and signs?

A

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.

17
Q

What are the complications of BRVO and CRVO?

A
  • Macular Oedema
  • NVD (New vessels disc) & NVE (New vessels elsewhere) could possibly cause
    vitreous haemorrhage
  • Rubeosis Iridis
  • Neovascular glaucoma (Very High IOP)
18
Q

What referral, investigations and treatment is required for CRVO/BRVO?

A

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

19
Q

Describe BRVO and the treatment?

A

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

20
Q

What is CRAO/BRAO?

A

Obstruction of artery due to atherosclerosis, a thrombus or embolus (Carotid Embolism)
(usually BRVO If embolus) blocking the artery or inflammation of the artery

21
Q

What would you expect from H&S of CRAO/BRAO? and what are the sxs?

A
  • 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
22
Q

What are the signs of CRAO? and the later developments of CRAO?

A
  • 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
23
Q

What are the signs of BRAO?

A
  • 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
24
Q

What is the management of RAOs?

A
  • 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
25
Q

Describe TIA - sxs and what to do?

A

Temporary obstruction of blood supply to brain or eye lasting a few seconds to minutes
à high risk of impending stroke
sx:
* Weakness
* Numbness down one side of body
* Vertigo
* Diplopia
* Slurred speech and loss of balance/co-ordination
* Transient vision loss (amaurosis fugax):
o Curtain coming down on vision, can be total or sectorial, resolves
completely (centrally first)
o Most common cause: embolism
o High risk of impending CRAO or vision loss through AION.
Urgent referral to GP and Ophthalmology for MRI and bloods.

26
Q

What is AION?

A

Infarction of the optic nerve head secondary to occlusion of the Posterior Cerebral Arteries (PCAs)

27
Q

What is AAION and what is needed to be done? What can AAION lead to?

A

Due to GCA (an inflammation of medium and large artery walls, e.g: Superficial temporal
artery, Ophthalmic artery, PCA).
Emergency referral for temporal artery biopsy, blood
test for ESR levels, and prompt oral/intravenous steroid administration.
AAION can also lead to:
* CRAO
* 3rd and 4th nerve palsy

28
Q

What are the symptoms of AAION?

A
  • Sudden unilateral vision loss
  • Preceeding amaurosis fugax
  • Possible periocular pain
  • Headache, neck or temple pain
  • Scalp tenderness
  • Jaw claudication
  • Weight loss
  • Fatigue
  • Muscle pain/stiffness
  • Protruding temporal artery – pulseless, tender, doesn’t compress
29
Q

What are the signs of AAION?

A
  • VA <6/60
  • RAPD
  • Swollen optic disc
  • Possible CWS
  • Possible flame haemorrhages
  • Arcuate VF defect
30
Q

What is NAION and what is it due to?

A

Infarction of the optic nerve head due to PCA occlusion as a result of atherosclerosis. No
preceding amaurosis fugax.
Can be due to:
* hypertension
* diabetes
* heart disease
* carotid artery diseaseW

31
Q

What are the signs of NAION and what do you do?

A

Signs:
* Normal – severe reduction in VA
* RAPD
* Dyschromatopsia
* Altitudinal VF defect
* ONH signs:
o Diffuse or sectorial oedema
o Pale or mild hyperaemia
o Possible flame haemorrhages
Emergency referral

32
Q

What is thyroid eye disease and what does it cause?

A

Due to Graves’ disease
* Soft Tissue involvement: Inflammation
* Proptosis
* EOM involvement causing diplopia
* Corneal Involvement
* Sight Loss due to optic nerve involvement

33
Q

What are some autoimmune conditions and what can they cause?

A
  • Ankylosing Spondylitis
  • IBD
  • SLE
  • Arthritis
  • Myasthenia Gravis
  • MS
    Can cause
  • Ant Uveitis
  • Episcleritis
  • Scleritis
  • Dry Eye
  • Optic Neuritis