Diabetes AND The Eye: Juliana Bentil Deborah Addo

DIABETES
AND
THE EYE
JULIANA BENTIL
DEBORAH ADDO
INTRODUCTION
 The term “diabetes mellitus” describes a metabolic disorder of

multiple etiology characterized by chronic hyperglycemia with
disturbances of carbohydrate, fat and protein metabolism resulting
from defects insulin secretion, insulin action, or both.
 The effects of diabetes mellitus include long term damage,

dysfunction and failure of various organs.
CLASSIFICATION
 There are two main types of diabetes
 Type 1 diabetes : Usually develops in childhood and adolescence;

patients require life long insulin injection for survival.
 Has an abrupt onset, with thirst, increased appetite, excessive urination

and weight loss occurring over a period of several days.
Type 2 diabetes (T2B)
 Usually develops in adulthood and is related to obesity. Lack of physical activity,
and unhealthy diets.
 This is the more common type of diabetes (representing 90% of diabetes cases
worldwide)
 Treatment may involve lifestyle changes and weight loss alone, or oral
medication or even insulin injections.
Another classification
 Insulin-dependent diabetes mellitus (IDDM).

 Know as type 1.
 Develops most frequently between 10 and 20 years of age
 Non-insulin dependent diabetes mellitus (NIDDM).
 Also known as type 2
 develops most frequently between the ages 50 and 70 years.
Lids and conjunctiva
 Prone to infections due to high blood sugar levels
 Recurrent styes and blepharoconjunctivitis
 Loss of tear
Cornea
 Corneal sensitivity is commonly impaired in diabetes. This sensory

deficit may predispose to bacterial corneal ulcers, neurotropic
ulcers and difficulties with contact lenses
 Intrinsic abnormalities of the epithelial basement membrane
complexes, with impaired barrier function leads to:
 Superficial punctate keratitis.
 Poor healing after trauma
Pupils abnormalities
 Rigid pupils – difficulty in mydriasis: The cause is an autonomic

neuropathy, partially denervation both the sphincter and the dilator
muscles.
Iris
 Hydrops of the iris.
 Rubeosis iridis :
 This is due to neovascularization of iris as a consequence of retinal
hypoxia with release of vaso-proliferative substances.
RUBEOSIS IRIDIS
Intraocular Pressure
 Glaucoma :
 is a complication of Rubeosis of the iris.
 diabetes has also been found to be a risk factor of POAG
 A low intraocular pressure is associated with diabetic acidosis.
LENS
With increase in blood glucose, the glucose content of aqueous humor

increases as well and this leads to an increase in glucose content of
the lens. Some of this glucose will be converted to sorbitol whose
accumulation causes the influx of water via osmosis. This leads to an
increase in the size of the lens with changes in refractive power of the
lens.
Lens
HYPERMETROPIC SHIFT
 Decrease in blood sugar level
 Hypoglycemia
 Decrease in osmotic pressure of crystalline lens
 Decrease in refractive index of lens

CATARACT
 Cataract is a major cause of vision impairment in people with

diabetes.
 Patients with diabetes are thought to develop cataract earlier than
those without
 Its thought to be linked to the above pathophysiology
 Control of the diabetes with restoration of normal blood glucose
levels stop progression of the opacity
 Diabetics can develop acute onset cataract known as ‘snow flake
cataract ‘
DIABETES PAPILLOPATHY
 Diabetic papillopathy is an uncommon ocular manifestation of

diabetes mellitus (DM).
 The underlying pathogenesis is unclear but it maybe the result of
small vessel disease.
 Presentation is usually with mild optic nerve dysfunction and slow
progression.
 VA: 6/12 or better in majority of patients
 Non specific unilateral or bilateral mild disc swelling and hyperemia
 It usually resolve spontaneously within several months
NEUROPATHY
 Paralysis of the muscles innervated by the third or sixth nerve.
 Sudden onset of the diplopia and painful muscle paralysis

associated with a homolateral headache.
 Short duration of hyperglycemia in diabetic the paralysis disappears

spontaneously with several weeks.
 Long time of hyperglycemia in diabetic, it persists up to 6 months

PUPILS
 Medical lesion in diabetic usually

spare the pupils, compared with
surgical lesion (eg. aneurysm)
which involve the pupils
 This is because of the
microangiopathy which involves
the vasa nervorum causes
ischemia of the main trunk of
nerve and spares the superficial
pupillary fibers which are supplied
by blood vessels of the pia mater
THEN WHAT IS ; Diabetic
Retinopathy
 Progressive dysfunction of the retinal blood vessels caused by
chronic hyperglycemia. It can be a complication of diabetes type 1
or type 2
 Retinopathy is the most important ocular complication of diabetes

It is the leading cause of blindness in people of working age in
industrialized countries.
Diabetic Retinopathy symptoms
 Diabetic retinopathy is asymptomatic in early stages of the disease

As the disease progresses symptoms may include
1. Blurred vision
2. Floaters
3. Fluctuating vision
4. Distorted vision
5. Dark areas in the vision
6. Impaired colour vision
7. Partial or total loss of vision
RISK FACTORS
 Duration of DM: It is the most important risk factor. Roughly 50% of

patients develop DR after 10years, 70% after 20 years and 90% after
30 years of onset of the disease.
 Sex: Incidence is more in females than in males (4:3)
 Hypertension : usually common in type two diabetics. Good control
is beneficial in diabetics
 Renal disease: known to worsen retinopathy especially when severe
 Pregnancy: worsens diabetic retinopathy
 Obesity, hyperlipidaemia, smoking, aneamia are all risk factors for
disease process.
 Hereditary: It is transmitted as a recessive trait without sex linkage. It
is more on the proliferative retinopathy.
PATHOPHYSIOLOGY OF DIABETIC
RETINOPATHY
 Believed to be a combination of prolonged exposure to
hyperglycemia, biochemical and physiological changes and
vascular endothelial damage
 It affects arterioles, capillaries and venules
 Loss of pericytes from capillary wall is the hallmark of diabetic
retinopathy. This together with thickening of basement membrane,
endothelial cell proliferation thrombus formation leads to increase
permeability from vessels( as a result of separation of tight junctions),
microaneurysms and other manifestations of DR
CLASSIFICATION
 Non-proliferative ( background) :
 Mild
 Moderate
 Severe
 Proliferative :
 Mild – moderate
 Severe
 advanced
Non-proliferative diabetic
retinopathy (NPDR
 Ophthalmoscopic features of NPDR include:
1. Microaneurysms in the macular area (the earliest detectable

lesion).
2. Retinal haemorrhages both deep (dot and blot haemorrhages)
and superficial haemorrhages (flame-shaped).
3. Hard exudates-yellowish-white waxy-looking patches are arranged
in clumps or in circinate pattern. These are commonly seen in the
macular area.
4. Retinal oedema characterized by retinal thickening.
5. Cotton-wool spots (if > 8, there is high risk of developing PDR).
 Venous abnormalities, beading, looping and dilatation. Intraretinal
microvascular abnormalities (IRMA). Dark-blot haemorrhages
representing haemorrhagic retinal infarcts.
 On the basis of severity of the above findings the NPDR has been
further classified as under:
 1. Mild NPDR : At least one microaneurysm or intraretinal
hemorrhage. Hard/soft exudates may or may not be present.
 2. Moderate NPDR :Moderate microaneurysms/intraretinal
hemorrhage
 Early mild IRMA.
 Hard/soft exudates may or may not present
3. Severe NPDR. Any one of the following :
1. Four quadrants of severe microaneurysms/ intraretinal
hemorrhages.
2. Two quadrants of venous beading.
3. One quadrant of IRMA changes.
 4. Very severe NPDR. Any two of the following ;

1. Four quadrants of severe microaneurysms/ intraretinal
hemorrhages.
2. Two quadrants of venous beading.
3. One quadrant of IRMA changes.
MICROANEURYSMS AND
DOT AND BLOT
HEMORRHAGE
INTRA RETINAL
COTTON WOOL SPOTS MICROVASCULAR
ABNORMALITIES
HARD EXUDATES
VENOUS ANORMALIES
VENOUS LOOPS VENOUS BEADING

Proliferative diabetic retinopathy
(PDR)
Proliferative diabetic retinopathy develops in more than 50 percent of
cases after about 25 years of the onset of disease. Therefore, it is more
common in patients with juvenile onset diabetes. The hallmark of PDR is the
occurrence of neovascularisation over the changes of very severe non-
proliferative diabetic retinopathy. It is characterised by proliferation of new
vessels from the capillaries, in the form of neovascularisation at
the optic disc (NVD) and/or elsewhere (NVE) in the fundus, usually along
the course of the major temporal retinal vessels. These new vessels may
proliferate in the plane of retina or spread into the vitreous as vascular
fronds. Later on condensation of connective tissue around the new vessels
results in formation of fibrovascular epiretinal membrane. Vitreous
detachment and vitreous haemorrhage may occur in this stage.
Types. On the basis of high risk characteristics (HRCs) described by
diabetic retinopathy study (DRS) group, the PDR can be further classified
as below
 PDR without HRCs (Early PDR) and 2. PDR with HRCs (Advanced PDR).
 High risk characteristics (HRC) of PDR are as follows :
1. NVD 1/4 to 1/3 of disc area with or without vitreous haemorrhage (VH)
or pre-retinal haemorrhage (PRH)
2. NVD < 1/4 disc area with VH or PRH
3. NVE > 1/2 disc area with VH or PRH
PROLIFERATIVE DR
NVE NVD NVE WITH FIBROSIS

VISUAL LOSS IN DIABETIC
RETINOPATHY
 Caused by :
 Maculopathy; may be due to edema, ischemia or exudative

 Vitreous hemorrhage: may be pre-retinal or intragel
 Retinal detachment: tractional retinal detachment usually caused by
progressive contraction of fibrovascular membranes over areas of
vitreo-retinal attachment
CLINICALLY SIGNIFICANT MACULA
EDEMA
 Clinically significant macular oedema (CSMO) is detected on
clinical examination as defined in the ETDRS :
 Retinal thickening within 500 μm of the centre of the macula.
 Exudates within 500 μm of the centre of the macula, if associated with
retinal thickening; the thickening itself may be outside the 500 μm.
 Retinal thickening one disc area (1500 μm) or larger, any part of which is
within one disc diameter of the centre of the macula .
CSMO
VITREOUS HEMORRHAGE
PRE-RETINAL INTRAGEL
TRACTIONAL RETINAL DETACHMENT
GRADING OF RETINOPATHY
 Grading system currently available in Ghana adopted from the UK

 National screening program currently being worked on
 Grading necessary because it ensure standardization
GRADING
 R – this stands for peripheral retinopathies

 M – represents findings in retina area
 P- represents findings of photocoagulation
Grading
 R 0 – no diabetic retinopathy
 R 1- Background diabetic retinopathy
 R 2 – Pre-proliferative retinopathy
 R 3A – active proliferative retinopathy
 R 3 S – stable proliferative retinopathy
 M0 – no maculopathy ; P0– no photocoagulation

 M1 - maculopathy P1 – Macular of scatter photocoagulation
SIGNS
 R1 ; microaneurysms, dot and blot hemorrhages, exudates, cotton

wool spots and venous loops
 R2 ; venous beading and looping, multiple blot hemorrhages, intr-
retinal microvascular anormalies
 R3A ; NVD,NVE, pre-retinal hemorrhage, vitreous hemorrhage
 R3S ; previously treated R3A, PRP scars, Fibrosed vessels, features of
R1 and R2
 M0 ; No maculopathy- Either no foveal lesions or foveal
miroaneurysms with BCV >6/12
 M1 –diabetic maculopathy ; exudate within 1DD of fovea , group (
½ disc area )of exudate within macula , microaneurysm or
hemorrhage within 1DD of fovea if best corrected VA is equal to or
worse than 6/12
MANAGEMENT
 Medical treatment.
 Observation.
 Laser therapy.
 Anti VEGF.
 Vitrectomy.
MEDICAL TREATMENT
 Patient eduction about condition is very important

 Glucose control :
 controlling diabetes
 maintaining the HbA1C level in the 6-7% range.
 Level of activity :
 maintaining a healthful lifestyle with regular exercise can help reduce the
complication of diabetes and DR.
 Blood pressure control
 Lipid lowering therapy.

FOLLOW UP
Retinal finding Suggested follow-up
Normal Annually
Mild NPDR 1 year
Moderate NPDR 6 months – 1year or refer to

ophthalmologist
Sever NPDR Every 4 months
DME Every 2-4 months
PDR Every 2-3 months

LASER THERAPY
 Aim is to reduce/restore visual loss

 It is employed in proliferative diabetic retinopathy eg in pan-retinal
photocoagulation
 Also employed in diabetic macula edema
Panretinal photocoagulation
PRP
Anti VEGF
 Employed in the use of diabetic macula edema. Usually given intra-

vitreally.
 Bevacizumab Avastin
 Ranibizumab lucentis
 Aflibercept Eylea
VITRECTOMY
 Removes blood
 Removes Traction
 Allows PRP

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DIABETES

 The term “diabetes mellitus” describes a metabolic disorder of

 The effects of diabetes mellitus include long term damage,

 Type 1 diabetes : Usually develops in childhood and adolescence;

 Has an abrupt onset, with thirst, increased appetite, excessive urination

 Insulin-dependent diabetes mellitus (IDDM).

 Prone to infections due to high blood sugar levels

 Recurrent styes and blepharoconjunctivitis

 Corneal sensitivity is commonly impaired in diabetes. This sensory

 Rigid pupils – difficulty in mydriasis: The cause is an autonomic

 Hydrops of the iris.

With increase in blood glucose, the glucose content of aqueous humor

 Decrease in blood sugar level

 Decrease in osmotic pressure of crystalline lens

 Decrease in refractive index of lens

 Cataract is a major cause of vision impairment in people with

 Diabetic papillopathy is an uncommon ocular manifestation of

 Paralysis of the muscles innervated by the third or sixth nerve.

 Sudden onset of the diplopia and painful muscle paralysis

 Short duration of hyperglycemia in diabetic the paralysis disappears

 Long time of hyperglycemia in diabetic, it persists up to 6 months

 Medical lesion in diabetic usually

 Retinopathy is the most important ocular complication of diabetes

 Diabetic retinopathy is asymptomatic in early stages of the disease

 Duration of DM: It is the most important risk factor. Roughly 50% of

1. Microaneurysms in the macular area (the earliest detectable

 4. Very severe NPDR. Any two of the following ;

VENOUS LOOPS VENOUS BEADING

NVE NVD NVE WITH FIBROSIS

 Maculopathy; may be due to edema, ischemia or exudative

 Grading system currently available in Ghana adopted from the UK

 R – this stands for peripheral retinopathies

 M0 – no maculopathy ; P0– no photocoagulation

 R1 ; microaneurysms, dot and blot hemorrhages, exudates, cotton

 Patient eduction about condition is very important

 Blood pressure control

 Lipid lowering therapy.

Retinal finding Suggested follow-up

Mild NPDR 1 year

Moderate NPDR 6 months – 1year or refer to

Sever NPDR Every 4 months

DME Every 2-4 months

PDR Every 2-3 months

 Aim is to reduce/restore visual loss

 Employed in the use of diabetic macula edema. Usually given intra-

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