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Eye disease > Diabetic eye disease: management of DR, diabetic cataracts and other complications > Flashcards

Diabetic eye disease: management of DR, diabetic cataracts and other complications Flashcards

1
Q

at stated by the NICE guidelines, when will you manage someone with an annual review by the optometrist/screening service

A

R1

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2
Q

at stated by the NICE guidelines, from which 4 findings will you refer a DR patient to Hes to be seen soon within 4 weeks

A

R2 (pre-proliferative changes)
Unexplained retinal findings
M1 (referable maculopathy)
Unexplained drop in VA

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3
Q

at stated by the NICE guidelines, from which finding will you refer a DR patient to Hes to be seen urgently within 1 week

A

New vessels formation

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4
Q

at stated by the NICE guidelines, from which 4 findings will you refer a DR patient to Hes to be seen as an emergency

A

Sudden loss of vision
Evidence of retinal detachment
Pre-retinal/ vitreous haemorrhage
Rubeosis iridis

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5
Q

how will you manage a P1 patient

A

Post treatment: annual review

Refer to HES: if not recorded before

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6
Q

what does the CoO guidelines state you should ask you DM patient

A

You should ask the patient if they are being screened in an NHS diabetic eye screening programme. If they are - when did they last have screening

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7
Q

what does the CoO guidelines state about if DM patients are under an NHS DESP

A

recall should be the same as for
patients who do not have diabetes, and you do not necessarily need to dilate (unless theres signs or symptoms that indicates thats advisable)

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8
Q

what does the CoO guidelines state about if a patient does not attend the local NHS DESP, the 4 things that you should do

A
  • offer them a dilated retinal examination
  • encourage them to attend an NHS DESP
  • tell them if you believe their screening is overdue
  • this is the case even if you provide a dilated fundus photography service
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9
Q

what does the CoO guidelines state about what you should report with all DM patients

A

You should report all relevant findings to whoever is responsible for the overall care and clinical management of the patient’s condition (often to the GP)

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10
Q

what should you do in addition to referring a DR patient for their ophthalmological condition and why

A

they should be referred to their GP for systemic condition

to be diagnosed / treated (as DM will cause damage to other organs as well as the eyes)

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11
Q

which 4 modifiable risk factors of DR can be managed

A
  • blood sugar levels
  • lipid levels
  • blood pressure
  • smoking (not a clearly defined risk factor)
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12
Q

how is blood sugar levels a modifiable risk factor for DR and how can it be managed

A

Level of control: Type I and Type II DM show increased risk
progression of DR with poor glycaemic control

‘Legacy effect’ whereby good glycaemic control in past protects
against future DR progression.

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13
Q

how can lipid levels be controlled as a modifiable risk factor for DR and against what features of DR in particular

A

Reducing lipid levels can reduce risk of progression

esp macular oedema and exudation

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14
Q

what did the Early Treatment of Diabetic Retinopathy Study

(EDTRS) find about the use of focal laser therapy

A

focal last therapy used for clinically significant macular oedema reduced the risk of moderate vision loss

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15
Q

what did the Early Treatment of Diabetic Retinopathy Study

(EDTRS) find about the use of scatter laser treatment

A

scatter laser treatment should be considered for eyes with severe non-proliferative/early proliferative DR, especially if its Type 2

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16
Q

what did the Early Treatment of Diabetic Retinopathy Study

(EDTRS) state when all eyes should be treated with argon laser photocoagulation treatment

A

All eyes with severe proliferative DR should be treated

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17
Q

what are the 3 classifications set out by the Early Treatment of Diabetic Retinopathy Study (EDTRS) that a DR patient needs to meet any one of, to be classified as having significant macula oedema and will be responsive to laser treatment

A

Retinal thickening at or within 500um of the centre of the macula

Hard exudates at or within 500μm of the centre of the macula, if associated with thickening of the adjacent retina

Retinal thickening of one disc area or larger any part of which is
within one disc diameter of the centre of the macula

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18
Q

what are the 2 types of laser treatment that ca be used to treat clinically significant macula oedema

A

focal laser photocoagulation: for specific blood vessels

laser grid photocoagulation: for diffuse leakage by capillaries

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19
Q

which type of laser treatment is used to treat clinically significant macula oedema if specific blood vessels are leaking and how does this laser treat it

A

focal laser photocoagulation

for focal diabetic macular oedema

it seals the leaking blood vessels in the small area of the retina

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20
Q

which type of laser treatment is used to treat clinically significant macula oedema if theres diffuse leakage from capillaries in the macula and how does this laser treat it

A

laser grid photocoagulation

for diffuse diabetic macular oedema

it places numerous coagulations around the fovea in attempt to restore the blood-retinal barrier

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21
Q

what is laser photocoagulation for clinically significant macula oedema not do and what is it proven to do instead

A

it does not always improve visual acuity

but it prevents additional deterioration of vision

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22
Q

what will be seen in a DR fundus of someone who has been treated with focal laser scars for clinically significant macula oedema

A

laser burn scars

there will still be some exudates and dot blot haemorrhages but main thing is oedema is resolved

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23
Q

what is used in grid laser photocoagulation for treating diffuse clinically significant macula oedema to minimise damage

A

low energy laser burns

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24
Q

what other therapy in addition to laser photocoagulation is used to treat clinically significant macula degeneration

A

anti-VEGF therapy

25
Q

what does VEGF do

and what causes it to up regulate

A

increases the permeability of capillaries in the macula, which increases macular oedema

VEGF is up regulated in DR in response to hypoxia

26
Q

name the 2 anti-VEGF therapies that are used to treat clinically significant macula oedema

A

Ranibizumab (lucentis)

Bevacizumab (avastin)

27
Q

what type of anti-VEGF is Ranibizumab (lucentis)

A

a monoclonal antibody fragment, which binds to and inactivates all isoforms of VEGF-A

28
Q

what is used as a cheaper anti-VEGF alternative to Ranibizumab (lucentis) and why is it not the main anti-VEGF for clinically significant macula oedema

A

Bevacizumab (avastin)

not licensed for use in the eye, but is cheaper, so widely used globally
but rarely prescribed the the NHS

29
Q

what does the NICE guidelines feb 2013 state about anti-VEGF therapy

A

“You should be able to have
Ranibizumab [Lucentis] if the central retina…is above a
certain thickness (400 microns or more) when treatment is
started.”

30
Q

what is the outcome other than getting rid of the macula oedema of anti-VEGF treatment

A

some vision loss will recover

31
Q

list the 3 compared therapies for clinically significant macula oedema and when/why each one may be used

A

Laser therapy for macular oedema:

  • stabilises but often fails to improve VA
  • Laser scar expansion causes areas of scotoma

Ranibizumab therapy:

  • Superiority over laser treatment for CSMO in trials
  • May be used in combination with laser therapy (so doesn’t have to be one or the other)

Intravitreal Steroid therapy:
- May be used for resistant cases
- Use limited by side effects of raised IOP and cataract
formation

32
Q

what may the use of intravtireal steroid therapy be limited by in treating clinically significant macula oedema

A

its side effects of raised IOP and cataract formation

33
Q

what is the concern of pre-proliferative R2 DR

what will be your management for a px with R2 DR

A

ischaemic retina = at risk of new vessel growth

refer to ophthalmologist and for GP to check bloods, HbA1c, blood pressure, lipids

ophthalmologist will review at intervals dependent on severity of symptoms

may consider prophylactic laser photocoagulation (especially if compliance is poor or retinopathy is progressing

34
Q

how will the ophthalmologist review at patient who has been referred for pre-proliferative R2 DR

A

ophthalmologist will review at intervals dependent on severity of symptoms

may consider prophylactic laser photocoagulation (especially if compliance is poor or retinopathy is progressing

35
Q

what is your management for a px with proliferative R3 DR

and what is the ophthalmological management

A

refer to ophthalmologist

these people definitely require treatment

Ophthalmological management:

  • Pan retinal photocoagulation (PRP) recommended for
    patients with active proliferative DR
  • Intravitreal anti-VEGF injections may be used to help stabilise retinopathy
  • Vitrectomy considered in patients with vitreous haemorrhage, especially:
    – Non clearing vitreous haemorrhage,
    – Vitreous haemorrhage associated with retinal detachment (esp if it involves the macula) or ghost cell glaucoma

Also used in patients with tractional retinal detachment,
especially involving macula

36
Q

describe the mechanism of how pan retinal photocoagulation works in treating the new blood vessels growth in proliferative DR

A
  • Laser burns applied to peripheral retina
  • Light energy is absorbed by melanin in RPE and choroid, that converts to heat, which denatures proteins and causes necrosis (death of small patch of retina)
  • ~1500 burns (0.5mm diameter) reduces outer retinal o2 consumption by ~20%
  • Reduced outer retinal oxygen consumption means oxygen from
    the choroid can reach the inner retina
  • By producing o2 to the inner retina, there is reduced hypoxia which means reduced VEGF production which means reduced neovascularisation
  • May also work by killing ischaemic retina, so reducing
    VEGF production
37
Q

what is the aim of pan retinal photocoagulation in treating proliferative R3 DR
what was the outcome of it’s results

A

aims to stabilise (not improve) vision

in the diabetic retinopathy study, PRP for high risk PDR = it halved the risk of severe visual loss

38
Q

list 4 disadvantages to pan retinal photocoagulation used to to proliferative DR R3

and what may be used as an alternative to laser photocoagulation

A
  • Causes collateral damage to retinal tissue
  • Can cause macular oedema (decrease in VA), colour vision
    defects, generalised field restriction, difficulty adjusting to
    changes in light levels
  • Can be painful
  • Repeated laser treatment may be needed
  • cryotherapy may be used as an alternative - by freezing patches of the retina (it is still killing off the retina, so reduces o2 demand)
39
Q

what is the appearance of the of the fund from the laser burns caused by pan retinal photocoagulation

A

grey/white appearance due to disruption of neurosensory retina

strong white patches indicates full thickness burns and visibility of sclera

older laser scars are pigmented

40
Q

list 5 other structures/diseases of the eye that can be affected by diabetes

A
  • optic nerve disease: non-arteritic anterior ischamic optic neuropathy
  • glaucoma
  • ocular motility disorders
  • crystalline lens: true and age related cataracts
  • cornea
41
Q

what is non-arteritic anterior ischamic optic neuropathy

what symptoms does it produce

what signs are seen

which types of eyes are most commonly affected

how is it treated

A

Acute vascular condition of ONH

Rapid, painless, loss of vision, often on wakening. VA usually better than 6/60. Stays
stable over time

Disc oedema and peripapillary flame shaped haemorrhages. Disc pallor develops over time

Most likely to occur in small optic disc with small optic cup (‘disc at risk’)

No treatments with proven efficacy - but still ant to refer this px on for an ophthalmic assessment

DM is also, rarely, associated with diabetic papillopathy (disc oedema, mild visual loss)

42
Q

as well as non-arteritic anterior ischamic optic neuropathy being a optic nerve disease associated with DM, name another optic nerve disease than can be associated

A

rare condition, associated with diabetic papillopathy (disc oedema, mild visual loss)

43
Q

how is glaucoma associated with diabetes and which 4 types are these
what is contradictive about these findings

A

increased risk of glaucoma in patients with DM

- neovascular glaucoma
(caused by rubeosis iridis)
- Open angle glaucoma (not
conclusive association)
- Narrow / closed angle
glaucoma
- Secondary glaucoma

But, reduced risk proliferative
DR and macular oedema in
patients with higher IOP! so this may be a protective effect

44
Q

how will you as an optom manage neovascular glaucoma

how is it treated ophthalmological

A

ocular emergency referral

treated with panretinal photocoagulation (to reduce hypoxia) + medical treatments e.g. atropine to reduce congestion, steroids to reduce inflammation of vessels

45
Q

how is DM associated with ocular motility
what is it responsible for
what is the outcome like

A

associated with 3rd, 4th and 6th cranial nerve palsy
a diabetic 3rd nerve palsy often spares the pupils

responsible for 25-30% of cases of acute extra ocular muscle palsy in patients ages over 45 years

often recover within 3 months, but may recur

so by doing OM test, will be able to diagnose the CN palsy

46
Q

how is DM associated with cataracts

A

DM px has an increased risk at an earlier age

increased risk if: poor blood sugar control, increased duration of DM

47
Q

how does DM cause the cataract

A

glucose is reduced to sorbitol which accumulates in the lens causing osmotic stress i.e. water drawn into lens causing the lens to swell

osmotic stress can cause cataract (lens fibres swell and rupture)

diabetic lenses also show increased levels of free radicals (oxidative stress), and reduced antioxidant activity (precipitates the early onset of the age related cataracts)

48
Q

what visual symptoms can DM cataract cause

A

this can cause a transient hypermetropic or myopic shift and reduced amplitude of accomodation – px may report
blurred vision

49
Q

what is a true diabetic cataract called
what are the signs
what causes this cataract

A

Snowflake cataract

rare
usually bilateral
rapid onset
only type of cataract seen in diabetic patients

related to very high serum glucose levels in the young type 1 diabetic px
so these px need to be referred to have their blood sugar control evaluated

multiple white anterior and posterior sub capsular and cortical opacities seen

50
Q

what types of cataract are the most common age related diabetic cataract

when may it appear in comparison to a non diabetic px

A

usually posterior sub capsular or cortical and less commonly nuclear

may appear ~10 years earlier than in non-diabetic px

51
Q

name 3 ways of how is diabetes associated with the cornea

what do all of these corneal changes end up doing

what things do you need consider certain things before doing due to the px being diabetic

A

associated with:

  • reduced corneal sensitivity due to corneal neuropathy
  • aqueous tear deficiency causing dry eye syndrome
  • corneal endothelial dysfunction

all of these changes leave the cornea prone to trauma and infection

it is important to consider when fitting a px with CLs or discussing refractive surgery
as they may need an more intense programme of a/c appointment and more rigorous checks of corneal health before prescribing the CLs

52
Q

name another corneal condition apart from the 3 main ones which is associated with DM and what 3 things happen in this condition

A

diabetic epitheliopathy

  • recurrent erosions
  • corneal abrasions
  • persistent epithelial defects
53
Q

what are the 3 main assessments you will want to carry out on a px with DM in practice

A

history and symptoms
functionals assessments
structural assessments

54
Q

what 3 functional assessments do you want to carry out on a px with DM

A

visual acuity
contrast sensitivity
colour vision

55
Q

what 2 structural assessments do you want to carry out on a px with DM and name the methods that can be used for each

A

retinal vasculature
- flourescein angiography (in hospital)

fundus evaluation

  • binocular indirect ophthalmoscopy
  • fundus photography
  • OCT
56
Q

what are the symptoms associated with someone with DR:
pre-proliferative

M1

R3 proliferative

A

pre-proliferative:
vision generally unaffected, unless macula is involved M1

M1:
macular oedema associated with reduced va

R3 proliferative - can be associated with significant symptoms:
- haemorrhage: sudden loss of vision, dark floaters

  • tractional retinal detachment: flashing lights, sudden loss of vision, curtain/shadow/veil across vision
57
Q

explain how a lack of symptoms doesn’t mean a px doesn’t have proliferative R3 DR

A

because if the new vessels haven’t yet haemorrhaged and they’re away from the macula, they may be asymptomatic

58
Q

list all the potential symptoms associated with DM from:
neovascular glaucoma

AION

retinal vein and artery occlusions

fluctuating blood sugar

cataract

nerve palsy

A

Neovascular glaucoma:
due to iris and angle neovascularisation, usually accompanied by R3 retinal changes
- haloes in vision
- hazy vision
- extreme pain
- redness
(similar as closed angle glaucoma, treated as a ocular emergency)

AION:
- rapid painless loss of vision

Retinal vein and artery occlusions:
- rapid painless loss of vision

Fluctuating blood sugar:
- fluctuating rx = blurred vision

Cataract:
- gradual worsening of vision and contrast sensitivity

Nerve palsy:
- diplopia

59
Q

how is OCT used in the management of diabetic maculopathy

A

to measure thickness of macula and observe oedema

can assess pre-post treatment change

Eye disease (22 decks)

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