Transcript Diabetes mellitus - Moorfields Eye Hospital

Diabetic retinopathy screening
NSF-based training
Diabetes
Tunde Peto
Head of Reading Centre
Diabetes mellitus - pathogenesis,
types, management, complications
Key issues for discussion
• Definition and types of diabetes mellitus
• Current medical and surgical management of diabetes mellitus
• Acute complications of diabetes mellitus: hypo and hyperglycaemia
• Chronic complication of diabetes mellitus: micro- and
macrovascular
Learning outcomes
• Identify types of diabetes and appropriate management strategies
• Identify and able to deal with acute complications especially
hypoglycaemia
• Able to discuss micro- and macrovascular complications
competently
Pathogenesis of diabetic eye
disease
Key issues for discussion
• Discuss details of pathogenesis of diabetic eye disease
• Discuss the importance of good diabetes and blood
pressure control
Learning outcome
• Able to discuss factors associated with the development
and progression of diabetic eye disease
Classification of diabetic eye
disease
Key issues for discussion
• Discuss issues related to diabetes and diabetic retinopathy
• Discuss key features of diabetic retinopathy
• Discuss the grading systems for diabetic retinopathy and develop
an understanding of the severity scale of the diseases
Learning outcome
• Develop knowledge related to classification of diabetic
retinopathy
• Use critical appraisal while discussing the features of grading
systems in use
• Apply the grading system knowledge to teaching slides on
diabetic retinopathy
Introduction
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Definition, symptoms and diagnosis of DM
Epidemiology of DM
Main aims of management of DM
Costs and prevention of DM
Right and responsibilities in DM
Hypoglycaemia
Definition of diabetes mellitus (DM)
• “disease involving a disturbance of
metabolism, the underlying cause of which
is the defective production or action of the
hormone insulin” (WHO Expert Committee,
1985)
• Classification of diabetes mellitus is based
on this definition
Symptoms and diagnosis of DM
• Symptoms
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Thirst
Frequent urination especially at night
Tiredness
Sudden change in weight: weight loss
Genital itching and frequent thrush
Blurred vision
• Diagnosis
– Blood sugar level
– Oral glucose tolerance test
Epidemiology of diabetes
• The DM epidemic is partly the results of the
major public health achievements!
• DM 2000: about 151 million people worldwide
• DM 2010: about 221 million: 46% increase
• The vast majority of the increase will be in the
developing countries
• Rapid increase in type 2 DM, even in children!!
• Type 1 diabetes is the most common chronic
disease in children
Main types of diabetes mellitus
• Impaired glucose tolerance: unknown number of pts
• Results in higher rate of cardiovascular death
• Might develop diabetes mellitus
• Type 1 diabetes mellitus: ~10% of pts
• Usually develops before the age of 40: autoimmune disease
• Dependent on insulin injections
• Type 2 diabetes mellitus: ~ 90% of pts
• Usually develops after the age of 40: metabolic syndrome
• Might require insulin injections
• Gestational diabetes: unknown number of pts
• Develops during pregnancy
• Might develop diabetes afterwards
MIDD
• Mitochondrial tRNS mutation at 3243 (AlaninGuanin)
• Less severe form: MIDD
• Severe form MELAS (mitochondrial myopathy,
encephalopathy, lactacidosis, stroke-syndrome)
• Mutation is found in asymptomatic relatives
• Maternally inherited, so EVERY single offspring
will have the mutant mtlDNS
• Accounts for up to 1-2% of all diabetes!!!!
Clinical signs and symptoms
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Myopathy
Epilepsy
Recurrent stroke, even in childhood
Neuro-sensory deafness (progrediant)
Ataxia
Retinitis pigmentosa-like clinical picture
Diabetes mellitus
Short stature
Myoclonus, neuropathia, n. opticus atrophia
Rarely glomerulosclerosis
Main aims of management of DM
• Improve diabetes control
• Prevent the development of diabetes-related
complications
• Provide better quality of life
Improve diabetes control
• Diet and exercise
• Type 1 diabetes: life depends on insulin
injections
• Type 2 diabetes: add tablets to diet and
exercise regime
– If necessary add insulin injection
• Manage BP and blood lipids appropriately
• Complications depend on blood sugar level
control and control of BP!
Acute and chronic complications
• Acute complications
• Hypoglycaemia and Hyperglycaemia
• Chronic complications
– Microvascular
• Diabetic retinopathy: eye disease
• Diabetic nephropathy: kidney disease, can lead to dyalisis
• Diabetic neuropathy: small nerve disease, “pins and needles”, numbness,
can contribute to amputations
• Autonomic neuropathy: orthostatic hypotension, gastroparesis, impotence,
bladder dysfunction, gustatory sweating
– Macrovascular
• Coronary artery disease, including silent AMI
• Cerebrovascular disease: strokes
• Peripheral vascular disease: amputations
Who is at risk of complications?
• All patients with diabetes are at risk, but:
• People with poor diabetes and blood pressure control
are at even higher risk
• The longer the duration of diabetes the higher the risk,
so age at diagnosis is important factor as well
• There seems to be a genetic component to risk
• Certain ethnic groups, especially migrants are at high
risk
• Smoking can make complications worse
• High risk of retinopathy during pregnancy
Provide better quality of life
• These complications affect the patients’ life
• Also affect ability to cope with the screening
episode, such as unable to come, unable to
transfer to chair, (mobility); unable to
understand commands, etc
• Patients with DM tend to be more depressed
• Employment problems
• Fear of complications
• Ignorance
Costs of DM
• Patients are hospitalised more and for
longer then pts who do not have the disease
• Patients utilise more expensive medical
intervention (eg. dyalisis) and for longer
period
• Need more extensive rehabilitation (stroke,
AMI, amputations, blindness)
Prevention of DM
• Major lifestyle modifications, especially in
pts with impaired glucose tolerance,
gestational diabetes and family history
• Dealing with auto-immune factors in
patients with type 1 diabetes
• Needs more education and intervention
especially in developing countries and
migrant populations
Rights of people with diabetes:UK
• International Diabetes Federation 1994:
– Never use diabetic as an adjunctive
– Exemption: diabetic retinopathy / nephropathy
– But: patient with diabetes and NEVER DIABETIC
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Healthcare free of charge
Choice of GP
Right to see the medical records/ info in NHS
Right to refuse treatment
Make reasonable complaint against NHS
Full or part refund of the cost of treatment
Rights and responsibilities
• Patients should know the members of their
health team and the reasons they are
included
• Patients should receive appropriate
education on their disease
• Patients should take an active part in the
management of their diabetes
Hypoglycaemia
• Medical term for blood sugar levels (BSL) below
4 mmol/L
• Patients normally call it “ a hypo”
• It can happen to anyone!
• Symptoms vary greatly
• It takes time to develop, so usually you have
enough time to react
• Except in hypoglycaemia unawareness
Mechanism of hypoglycaemia
• Insulin works for lowering BSL by making it
available for tissues and storage
• Glucagon works for increasing BSL by making
the liver release some
• Eating food that contains carbohydrates leads to
a rise in BSL
• This stimulates insulin secretion, and BSL is
lowered
• If BSL is low, glucagon stimulates release of
sugar from stores such as liver
Mechanism of hypoglycaemia 2
• In DM this system does not work well
• So, another back-up system comes into play
• ADRENALIN is released and it is
responsible for the warning signs of a hypo
• End-result of a hypo: brain does not get
enough sugar, so it cannot function, the
patient can die
Causes of hypoglycaemia
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Too much insulin / too many tablets
Delayed or missed meals or snacks
Not enough food especially carbohydrate
Unplanned or strenuous exercise
Drinking alcohol without food
No obvious cause
Type 2 diabetes: not on insulin
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Occasionally hypo can happen
More frequent in the elderly
More frequent in active people
More frequent in people taking insulin and
sulphonylureas
• More frequent in people taking Glipizide,
Gliclazide, Chlorpopamide, Gliquidone,
Glimerpiride, Tolbutamide and Repaglinide
Type 2 diabetes: not on insulin: 2
• Some tablets are unlikely to cause a hypo:
Metformin (Glucobay)
• People on Acarbose should always be given
sg like Lucosade as the absorption of sugar
is very slow!
• Some other medications such as antibiotics,
antidepressants modify the action of the
tablets for diabetes
Type 1 diabetes
• Hypo is very common in patients with type 1 DM
• The better the diabetes control the more common the
hypo is
• Requires careful balance between insulin – food exercise
• Hypoglycaemia unawareness is more common
Mild hypo: treat yourself stage
• Signs and symptoms
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Hungry
Trembling and sweating
Irritable, aggressive, unreasonable
Pale, fast pulse, tingling of the limps
Blurring vision
• Treatment
– Immediate: quick carbohydrate: fruit juice,
coke, glucose tablets, sugar, chocolate
– Long acting: sandwich, biscuits, cereal, fruit
Severe hypo: cannot treat yourself
• Signs and symptoms
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Difficulty in concentrating
Confused and vague
Irritable and irrational
Loss of consciousness, fits and coma
• Treatment
– If conscious and can swallow: Hypostop (sugar gel), honey,
treacle or jam inside the mouth and massage gently, once the pt is
better, follow up as per mild hypo
– If unconscious: if you are trained, use Hypostop etc; if not, place
the pt in the recovery position and GET HELP!
– Glucagon or iv glucose should only be given by trained personnel
– When you get help, always specify that the patient has diabetes!
Other hypos
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Hypos at night
Hypos during or following exercise
Hypos following drinking
Hypos while driving
Hypos while pregnant
Screening and hypos
• Patients might be very anxious about
screening and after initial rise in BSL, they
can have a drop
• They might miss a meal while waiting
• They might have had to alter their daily
routine for getting there
• They might bring less food than normal
When to suspect a hypo
• If patient becomes irrational, loud, agitated for
no apparent reason especially if it is mealtime
(morning and afternoon tea, lunch)
• If patient complains about sudden blurring of
the vision and other signs of hypo
• Always check what medication the patient is on
• Always ask if it is mealtime or not or if they
skipped meal to keep their appointment
• Keep sugar/honey or Lucosade at Screening van
• KNOW how to get help!!!!
Diabetes education
• Availability and type of diabetes education
varies a great deal between areas
• Always ask if the patient had diabetes education
or not
• Always ask where the patient received their
diabetes care, opportunities for education will
differ between hospital clinic patients, GP
patients
• Always consider practise nurse, a lot of them are
trained in basic diabetes education
Where to direct the patient to?
• Always have a list of available education
opportunities for your patients
• Consider local guidelines: practice nurses, GPs,
diabetes centre, mobile training units
• Diabetes UK is an excellent source of
information for all patients and they have
excellent leaflets and sessions
• If the patient is registered blind or visually
impaired, ask if they attend the RNIB or local
agencies
Summary
• Two types of diabetes both diagnosed by blood tests
• Vast majority will have type 2 diabetes and will have
multiple disabilities
• The aim of the screening is to help improve diabetes
control, see complication status and help with giving quality
of life
• DM is a costly disease for which there is no prevention and
is difficult to cure
• Both patients and health professionals have right and
responsibilities in DM
• Hypoglycaemia should be prevented and treated
appropriately
Summary
• Screening: 80-90% of pts have type 2 DM
• They will have multiple disabilities, including
difficulty of learning or responding to commands
• They might not see and/or hear you well!
• Do not try to hurry them, they are trying to help
you and please you if you are nice to them.
• Remember, you are only one of many they need to
see because of their diabetes!
• After all, have fun screening, you are doing a
service that gives them better quality of life.
• Diabetic Retinopathy
– 200,000 Type 1, > 1 million Type 2 persons with
diabetes (PWDs), may double by 2012
– Commonest complication of diabetes mellitus
– Commonest cause of blindness in UK between 20 and
55 years of age
Anatomy
Choroid
Macula
Retina
Retinal Pigment Epithelium
fovea
posterior pole
macula
branch retinal vein
(thicker, darker red)
branch retinal artery
(thinner, white line
down middle)
Diagrammatic cross section of normal macula: the lower of the two
capillary circulations is the important one from a clinical standpoint
and the one seen on fluorescein angiography
fovea
foveola
A
GCL
IPL
B
Inner BRB
INL
OPL
ONL
PRC
RPE
Outer BRB
OLM
Pathophysiology
a. Proliferative diabetic retinopathy
Diabetes
VEGF
b. Diabetic maculopathy
Retinal location of diabetic macular oedema due to
breakdown of blood-retinal barrier
GCL
IPL
INL
OPL
ONL
OLM
PRC
RPE Cells
RPE
Management: Relevant clinical
trials
• Diabetic Retinopathy: multicentre trials
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DCCT (Diabetes Control Complications Trial)
UK PDS (UK Prospective Diabetes Study)
DRS (Diabetic Retinopathy Study)
ETDRS (Early Treatment Diabetic Retinopathy
Study)
– DRVS (Diabetic Retinopathy Vitrectomy
Study)
Management: the burden of illness
Diabetic Eye Disease
Retinopathy
Cataract
Maculopathy
(90% blind registrations)
Clinically significant
macular oedema
Macular ischaemia
Medical management
• Glycaemic control
DCCT : IDDM : intensive vs conventional control
50% reduction in onset & progression of diabetic retinopathy
in the intensive control group
% PROG OF RETINOPATHY
60
Conventional
50
Intensive
40
30
20
10
0
1
2
3
4
5
YEARS
6
7
8
9
• UK PDS: Effect of blood pressure control on 2step progression of retinopathy
50
Less tight
More tight
% EVENT RATE
40
30
20
10
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3
6
YEARS
9
12
Management: Laser therapy
Proliferative diabetic retinopathy
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panretinal photocoagulation (PRP)
2 sessions, 1-2 weeks apart, 2000 shots
may need adjunctive sessions
vitreous haemorrhage and tractional retinal
detachment can still occur
– extensive treatment may affect ability to drive
• Good’ treatment: patients do well and blindness
uncommon if treated early enough
• Laser treatment “kills” diseased retina
• Laser treatment reduces VEGF
6 weeks post treatment
3 months post treatment
Incidence of SVL after PRP for high risk characteristic proliferative diabetic retinopathy (DRS)
100
90
80
70
% severe 60
50
visual loss 40
Treated
Untreated
44
30
20
10
0 0
0
26
20
11
2
Years follow up
4
Macular Oedema
– macular laser (ETDRS guidelines)
– stabilises visual acuity, few patients improve
• laser effect due to
– stimulation RPE to ‘pump’ fluid out of the retina
– direct closure of leaking spots
• macular oedema
– ‘not a good treatment’ as macular oedema tends
to recur and may co-exist with macular
ischaemia
leaking microaneurysm
Macula oedema: reduction in incidence of
MVL with focal laser treatment (ETDRS)
50
Treated
Untreated
40
% moderate 30
visual loss 20
10
0
0
1
Years follow up
2
 Driving standards following PRP /
macular laser therapy:
 Binocular Esterman visual field
 120 degree horizontal field
 40 degree vertical field
 no paracentral scotomas
 Visual acuity
 both eyes open 6/9 car number plate at 75 feet
Fail : horizontal < 140degrees
Fail : small paracentral scotoma
Grading of Retinopathy
 Level 1: background: not sight threatening
 haemorrhages and microaneurysms
 Exudates outside of the arcade
haemorrhage
microaneurysm
 Level 1: background: more haemorrhages and MAs
 cotton wool spots: sign of ischaemia, do a search for
venous changes or IRMA, refer if those are found
cotton wool spot
 Level 2: preproliferative: routine referral
 IRMA, venous beading
 Multiple deep haemorrhages
IRMA
Venous beading
IRMA
SP 6B
 Level 3: proliferative: urgent referral
 New vessels on disc or new vessels elsewhere
NVD
NVE
 Level 3: proliferative: urgent referral
 advanced NVD / NVE
 vitreous haemorrhage/pre-retinal haemorrhage
 Tractional retinal detachment
 Fibrovascular proliferation
Vitreous haemorrhage
NVD
Tractional retinal detachment with
fibrovascular proliferation
Rubeosis iridis and
neovascular glaucoma
Maculopathy: +/- REDUCED VA
 hard exudates / haems / microaneurysms in
macula
 Changes within one disc diameter must be
identified
 macular ischaemia:
 loss of blood supply to macular area
 Featureless / white streak vessels
 POOR VA
Referral Patterns
Grading
Level 0
Clinic Referral
Time
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Follow-up
12 months
Level 1
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12 months
Level 1
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6 - 9 months
Level 2
13 weeks
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Level 3
2 weeks
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Level 3
2 weeks
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Maculopathy
13 weeks
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Cataract: most common cause of ungradable
images
Cataract in patients with diabetes
• Changes in blood sugar level can affect vision as
lens swells when blood sugar is high (myopic
change) and releases water and shrinks when
BSL is low (hypermetropic change)
• Lens returns to normal when BSL normal, so
wait for stabilisation in newly diagnosed and
unstable patients before sending them to
optometrist
• Patients with diabetes are 2-4 times more likely
to develop cataract (15 - 20 times more if <40)
What is it?
Cataract (L. cataracta: waterfall) is any
opacity of the crystalline lens, which is
normally almost completely transparent.
The normal function of the lens is to focus light
on the retina.
LENS- nucleus
LENS- capsule
Sclera
Cornea
Iris
Courtesy of Ms
Valerie Saw, MEH,
Cataract Service
Ciliary body
RETINA
Optic
nerve
Choroid
Why does it occur?
Causes of Cataract
1. Ageing
2. Diabetes
3. Trauma
4. Congenital
Nuclear cataract
Cortical cataract
Posterior subcapsular cataract
Blue dot cataract
5. Medications- Steroids, steroid drops
6. Intraocular surgery eg.vitrectomy
7. Other - uveitis, acute glaucoma, atopy
How do I recognise it?
Signs of Cataract
1. Hazy retinal image
2. Slit lamp: nuclear, cortical,
posterior subcapsular lens opacities
3. Red reflex: opacities
4. Myopia, Hyperopia &/or Astigmatism
Symptoms of Cataract
1.Blurry vision, difficulty reading
2. Glare, starburst effects
How do I recognise it?
Types of Cataract
1. Nuclear sclerosis
• Commonly caused by
ageing, diabetes
• Results in myopia
(“second sight of age”)
• Tend to progress
slowly
How do I recognise it?
Types of Cataract
2. Cortical Cataract
• Caused by ageing
• Results in glare and
starburst symptoms
• Can cause
hyperopia
• Can be mixed eg
nuclear + cortical
cataract
How do I recognise it?
Types of Cataract
3. Posterior Subcapsular Cataract
• Associated with
ageing or steroid
medication
• Results in glare and
difficulty reading
• Can be quite
adherent to posterior
lens capsule during
surgery
Congenital posterior polar cataract
How do I recognise it?
Types of Cataract
4. Mature Cataract
• Can be brunescent (brown) or
milky white or Morgagnian
• In some cases urgent surgery
is necessary because the
intumescent lens causes narrow
angle glaucoma (phacomorphic
glaucoma) or intraocular
inflammation and glaucoma
(phacolytic glaucoma)
White cataract
Morgagnian cataract
How do I recognise it?
Types of Cataract
5. Congenital lens opacities
• Visually significant
congenital cataracts are
usually detected at birth, or
shortly afterwards
• Congenital lens opacities in
asymptomatic adults may not
require intervention.
Eg. Blue dot cataract
• Associated metabolic
disorders
Galactosemia
How to deal with cataract in screening?
• Understand local and national guidelines
• If ungradable: <6 weeks referral
• If gradable: refer first to optometrist to correct
with glasses if possible, surgery might not be
needed for years
• Refer for surgery if cataract influences daily
activities or vision is <6/12; or images are
ungradable; when benefits outweigh risks
• Remember: corneal opacity, vitreous haze!
What are the risks of cataract surgery?
• 95% of patients achieve better vision then before
surgery, BUT
• 1% achieves no improvement or deteriorates
after surgery
• 1:1000 chance of retinal detachment
• 1: 1000 chance of infection
• 1: 1000 chance of blindness
• Retinopathy and maculopathy must be treated
before cataract surgery if fundus is visible!
Can the cataract come back?
Posterior capsule opacification (“after-cataract”)
• Thickening of the capsule
behind the intraocular
implant may cause blurry
vision following surgery.
• This is easily treated by
laser in the outpatient clinic
(takes 15-20mins)
• 10% chance per year of
requiring laser surgery, less
with modern implants in the
first 1-2 years.
Summary
• Diabetic retinopathy is a consequence of a multisystem disease.
• Management of DR needs to reflect the chronicity
of the disease.
• Screening is effective, but setting it up is costly
• Grading of retinopathy & maculopathy can be
achieved by non-medically trained graders
• Patient education might be the key factor to
achieve compliance with NSF.