COMMON EYE PROBLEMS IN ELDERLY PEOPLE
Human eye compared with a Camera
•Eye lidswith the Lens cap.•Pupilwith the Shutter of the camera.
•Corneaand the Crystalline lenswith the lens of the camera.[The lens system of the eye and Camera focus and project an upside down image on the Photo sensitive layer.]
•Retinawith the film of camera.
Common changes in your vision as you age are
•Reduced sensitivity to light:you might notice that you need brighter lighting near your favourite reading chair.•Decreased visual acuity:Colours appear dim and glare , when light shines directly at you .This might cause you to avoid night driving.
* Difficulty in reading small print. The lens in your eye becomes less elastic and loses its ability to focus. A condition called Presbyopia. You might require reading glasses to read smaller print.
•Dryness of your eyesmight increase with age.Increase of lid laxity,harmonal changes cause tear instability.
Common eye problems faced by elderly people
BLINDING CAUSES
•Cataract[reversible]
•Glaucoma
•Diabetic Retinopathy
•Age Related Macular Degeneration[ARMD]
•Glaucoma
•Diabetic Retinopathy
•Age Related Macular Degeneration[ARMD]
NON BLINDING CAUSES
•Lid Problems like Meibobinitis,Chalazion,Ectropion,Entropion,Ptosis.
•Dry eye syndrome [itching,dryness,grittyness,watering,eye strain]
•Dry eye syndrome [itching,dryness,grittyness,watering,eye strain]
What is CATARACT?
•It causes reversible Blindness.
•Is a clouding that develops in the Crystalline Lensof the eye.
•Affects both the sexes and all the ages but common in the Elderly people
•Common in Diabetics.
•Trauma.
•Secondary eye diseases like uveitis
•The Crystalline lens appears opaque when light is thrown on the eye.
•Is a clouding that develops in the Crystalline Lensof the eye.
•Affects both the sexes and all the ages but common in the Elderly people
•Common in Diabetics.
•Trauma.
•Secondary eye diseases like uveitis
•The Crystalline lens appears opaque when light is thrown on the eye.
Symptoms of Cataract
•Blurring of the Vision.
•Night glare
•Double /poly vision.
•Frequent change of glasses.
•Improvement of Near vision (index Myopia).
•Fading of colours.(yellowing of the lens blocks blue light.)
•Night glare
•Double /poly vision.
•Frequent change of glasses.
•Improvement of Near vision (index Myopia).
•Fading of colours.(yellowing of the lens blocks blue light.)
Treatment for Cataract
•No medical Treatment, only Surgical.•Not an emergency,can take time,plan well.
•Good control of Bloodsugars in Diabetics.
•To stopantiplatelet agents before surgery.
(Asprin,Clopitab,etc).
•A-scanto know the axial length of eye ball.
•Keratometryto know the power of eyeball.
•IOL power calculation is done with advanced formulae.
Surgeries for cataract.
•. ICCE[intracapsular cataract extraction].•ECCE with IOL implantation[Extracapsular cataract extraction]with sutures.
•SICS with Posterior chamber IOL [small incision cataract surgery]without sutures.
•Phaco Emulsification with Foldable IOL implantation[key hole,no stitch,no pad,no prick]is todays modern surgery.
Cataract Surgery with IOL implantation
Small Incision Cataract Surgery
•Day care surgery.
•SuturelessMicroscopic surgery.
•Require anaesthetic injection.
•Manuallydone.
•Incision of 6.5mm.
•Rigid PMMA IOL placed in the eye.
•Less Expensive
•SuturelessMicroscopic surgery.
•Require anaesthetic injection.
•Manuallydone.
•Incision of 6.5mm.
•Rigid PMMA IOL placed in the eye.
•Less Expensive
Phaco emulsification
•Day care surgery.
•No Prick,No suture,No pad,Keyhole surgery[2.5mm]
•The Cataract is emulsified in the eye and sucked out.
•Involves a probe vibrating with ultrasound frequency-emulsifying lens.
•Placement of a FoldableIOL(Acrylic,Hydrophobic lenses) in the eye.
•No Prick,No suture,No pad,Keyhole surgery[2.5mm]
•The Cataract is emulsified in the eye and sucked out.
•Involves a probe vibrating with ultrasound frequency-emulsifying lens.
•Placement of a FoldableIOL(Acrylic,Hydrophobic lenses) in the eye.
What is Glaucoma?
•It refers to a group of diseases that effect optic nerve[carry visual impulses from retina to brain] associated with elevatedIntra Ocular Pressure (IOP).
•Blindness prevalence for all types of Glaucoma was estimated at more than 8million people.(responsible for 15% of blindness in the population.)
What happens in Glaucoma?
•Prolonged Increase in IOP damages the back part of the eye[the optic nerve head]leading to cupping of the disc and visual field damage.
•Blindness prevalence for all types of Glaucoma was estimated at more than 8million people.(responsible for 15% of blindness in the population.)
What happens in Glaucoma?
•Prolonged Increase in IOP damages the back part of the eye[the optic nerve head]leading to cupping of the disc and visual field damage.
What is IOP?
•Intraocular pressure is the pressure with in the eye.
•It is determined by the Aqueous humour secreted with in the eye.
•It circulates from the posterior chamber to the anterior chamber.
•Normal range of IOP :10 –22mmHg.
•Excess pressure cause damageto the Optic nerve head.
•The balance between production & drainage of the Aqueous determines IOP.
•It is determined by the Aqueous humour secreted with in the eye.
•It circulates from the posterior chamber to the anterior chamber.
•Normal range of IOP :10 –22mmHg.
•Excess pressure cause damageto the Optic nerve head.
•The balance between production & drainage of the Aqueous determines IOP.
Who are at the risk of developing Glaucoma?
•Advanced age:the prevalence of Glaucoma increases with age after 40yrs.
•The risk raises by 3 –8 times by age of 70
•Women has a higher risk in getting Glaucoma.
•Positive Family History of Glaucoma increases the risk 3-6 times.
•Blacks have higher risk than whites.
•Diabetics
•Myopia
•Drugs—Corticosteriods,antidepressants.
•The risk raises by 3 –8 times by age of 70
•Women has a higher risk in getting Glaucoma.
•Positive Family History of Glaucoma increases the risk 3-6 times.
•Blacks have higher risk than whites.
•Diabetics
•Myopia
•Drugs—Corticosteriods,antidepressants.
Types of Glaucoma
•Primary Open angledGlaucoma.
•Primary Closed angleGlaucoma.
•Secondary Glaucomas.
•Traumatic
•Pigmentary Glaucoma.
•Primary Closed angleGlaucoma.
•Secondary Glaucomas.
•Traumatic
•Pigmentary Glaucoma.
Symptoms of Glaucoma
•No symptoms initially-insideous in onset.
•Visual field loss could be late symptom.
•Severe eye pain,Headache,Nausea,Vometing with colored Haloes could be an acute attack.
•Coloured Haloesin the early mornings
•Decreased Visual acuity-late stage.
•Visual field loss could be late symptom.
•Severe eye pain,Headache,Nausea,Vometing with colored Haloes could be an acute attack.
•Coloured Haloesin the early mornings
•Decreased Visual acuity-late stage.
Investigations In Glaucoma
•Visual acuityand pupillary examination.
•Measuring Intra Ocular Pressure by Gold man Applanation tonometry.
•Gonioscopy:applying a contact lens with mirrors on the eye to know the angles.Normal angles should be 45`
•Fundoscopy:for clinical evaluation of the optic nerve head.
•Visual Field Examination:Humphrey automated perimeter. [para central scotomas,arcuate scotomas,nasalstepping,temporal wedge.]
•General Population:
Age40-64:should get checked once every one to two years.
After Age 65:every one year.
In order to preserve vision in glaucoma, early detection and thus disease control.
1.Medical treatment:eye drops that reduce IOP by lowering the secretion or increasing the drainage of aqueous fluid.
2.Laser: to create an alternate drainage channel with in the eye.
3.Surgery:Trabeculectomy,Shunt devices are available.
GLAUCOMA CAN ONLY BE PREVENTED BY EARLY DIAGNOSIS,EFFECTIVE TREATMENT AND COMPLIANCE WITH TREATMENT.
•If left untreated,it may lead to blindness.
•If checked promptly,blindness is mostly Preventable.
•It occurs in patients of bothInsulin dependent and NonInsulin Dependent Diabetes mellitus.
•Hypertention
•Smoking
•Anaemia
•Hyper lipidemias
•Effects both the sexes equally.
•Proliferationof fragile blood vessels perpendicularly in to the Vitreous body in response to the hypoxia.
•Bleedingof the fragile bloodvessels cause gross blurring of the vision.
•The process of repeated bleeding and healing stimulates fibrous tissue to proliferate.This fibrous tissue cause tractionon the retinal surface leading to Retinaldetachment.(total loss of vision.)
•Dot & Blot Heamorrhages
•Macular edema.
•Heamorrhages with Hard exudates.
•In Proliferative stage new vessels proliferate in to the vitreous body & bleed.
•2.Fundus Flouroscein Angiographycaptured by a Fundus camera.
-Aim is to reduce the oxygen demand of the retina hence decrease vascular proliferation.
Intraocular injections:-
Anti VeGF (avastin)is given to reduce the macular edema & Vascular proliferation.
Surgical:-
Vitrectomy removing the traction elements and giving Endolaser to the damaged retina.
•Patients with DR needs to be examined every 3-6 monthsdepending on the requirement.
•It is an eye disease with its onset usually after age of 60 yrs.
•It does not have any Blood vessels.
[ Injury to the macula can impair the ability to see straight ahead clearly.Making it difficult to read,drive and perform daily activities that require central vision.]
•Light sesitive cells of macula slowly get degenerated.
•Usually effects unequally in both eyes.
•Central vision is reduced.
•Usually rapid in onset.
•Abnormal vessels grow under the macula causing fluid accumilation.
•Straight lines appear wavy.
•Distortion of the vision.
•Visual loss is rapidin wet type of AMD.
•Patient requires extra light for reading and near work.
•Some patients might notice a blind spot centrally.
•Smoking.
•Obesity.
•Racial—Whites are at more risk than blacks.
•Immediate family membersare at increased risk of getting AMD.
•Women have a little higher risk than men in getting AMD.
1. Visual acuity
2.Fundusexamination
3.Amsler Grid:
The pattern appears as a checker board.
Look with one eye for any wavy patternor any missingportions of the lines.
2.Photo Dynamic Therapy.
3.Inta ocular injections[Anti VeGF].
None of these treatments is a cure for wet AMD.The disease and loss of vision may progress despite treatment.
4.Medical treatment:[For Intermediate and Advanced AMD]
Taking of specific high dose of Antioxidants and Zinc reduces the riskof advanced AMD and its visual loss.
[vit c 500mg,vit E 400IU,15mg Betacarotene,80mg Zinc]
•Weight control
•Control of Blood pressure.
•Regular Exercise.
•Non Smoking
•Measuring Intra Ocular Pressure by Gold man Applanation tonometry.
•Gonioscopy:applying a contact lens with mirrors on the eye to know the angles.Normal angles should be 45`
•Fundoscopy:for clinical evaluation of the optic nerve head.
•Visual Field Examination:Humphrey automated perimeter. [para central scotomas,arcuate scotomas,nasalstepping,temporal wedge.]
How often should some one get checked for Glaucoma
•In high risk people:during the age 30-39 one or two times.•General Population:
Age40-64:should get checked once every one to two years.
After Age 65:every one year.
In order to preserve vision in glaucoma, early detection and thus disease control.
What is Treatment for Glaucoma?
Though it doesn’t get reversed,can be controlled.1.Medical treatment:eye drops that reduce IOP by lowering the secretion or increasing the drainage of aqueous fluid.
2.Laser: to create an alternate drainage channel with in the eye.
3.Surgery:Trabeculectomy,Shunt devices are available.
GLAUCOMA CAN ONLY BE PREVENTED BY EARLY DIAGNOSIS,EFFECTIVE TREATMENT AND COMPLIANCE WITH TREATMENT.
What is Diabetic Retinopathy?
•A common longterm complication of Diabetes affecting the blood vessels of Retina [eye].•If left untreated,it may lead to blindness.
•If checked promptly,blindness is mostly Preventable.
•It occurs in patients of bothInsulin dependent and NonInsulin Dependent Diabetes mellitus.
Risk factors effecting the Progression of the disease.
•Patients with longterm Uncontrolled blood sugars.•Hypertention
•Smoking
•Anaemia
•Hyper lipidemias
•Effects both the sexes equally.
What happens in DR?
•Narrowingof the lumen of the Blood vessels of retina—Hypoxia (reduced oxygen supply)—Leaky walls of the blood vessels-Edema of the retina.•Proliferationof fragile blood vessels perpendicularly in to the Vitreous body in response to the hypoxia.
•Bleedingof the fragile bloodvessels cause gross blurring of the vision.
•The process of repeated bleeding and healing stimulates fibrous tissue to proliferate.This fibrous tissue cause tractionon the retinal surface leading to Retinaldetachment.(total loss of vision.)
Types of Diabetic RetinopathyNonproliferative Proliferative DR
•Micro aneurisms.•Dot & Blot Heamorrhages
•Macular edema.
•Heamorrhages with Hard exudates.
•In Proliferative stage new vessels proliferate in to the vitreous body & bleed.
How to Diagnose?
•1.Fundus examinationby Direct ophthalmoscopy,Indirect ophthalmoscopy,Slitlamp biomicroscopy with use of special lenses.•2.Fundus Flouroscein Angiographycaptured by a Fundus camera.
Treatment of Diabetic Retinopathy
Lasers:-nature of laser treatment depends on the stage of the disease. -Depending on the stage of the disease single or multiple sittings should be given.-Aim is to reduce the oxygen demand of the retina hence decrease vascular proliferation.
Intraocular injections:-
Anti VeGF (avastin)is given to reduce the macular edema & Vascular proliferation.
Surgical:-
Vitrectomy removing the traction elements and giving Endolaser to the damaged retina.
Follow up in patients with Diabetes.
•Screening of all the diabetic people irrespective of age and sex every year.•Patients with DR needs to be examined every 3-6 monthsdepending on the requirement.
Age related Macular Degeneration [AMD]
•AMD is a disease associated with aging, that gradually destroys sharp and central vision.•It is an eye disease with its onset usually after age of 60 yrs.
Which part of the eye is effected in AMD?
•Macula is the most sensitive region of the retina responsible for Central,Sharp & day vision.•It does not have any Blood vessels.
[ Injury to the macula can impair the ability to see straight ahead clearly.Making it difficult to read,drive and perform daily activities that require central vision.]
TYPES OF AMD
Dry AMD
•More common type.•Light sesitive cells of macula slowly get degenerated.
•Usually effects unequally in both eyes.
•Central vision is reduced.
Wet AMD
•Less common type•Usually rapid in onset.
•Abnormal vessels grow under the macula causing fluid accumilation.
Types of AMD
DRY AMD
WET AMD
What are the symptoms ?
•There is no pain.•Straight lines appear wavy.
•Distortion of the vision.
•Visual loss is rapidin wet type of AMD.
•Patient requires extra light for reading and near work.
•Some patients might notice a blind spot centrally.
Vision in AMD
Who is at risk for AMD?
•Greatest risk factor is Age(>60yrs).The risk increases to nearly 30% by the age 70yrs.•Smoking.
•Obesity.
•Racial—Whites are at more risk than blacks.
•Immediate family membersare at increased risk of getting AMD.
•Women have a little higher risk than men in getting AMD.
How is AMD diagnosed?
•By an Ophthalmologist looking for1. Visual acuity
2.Fundusexamination
3.Amsler Grid:
The pattern appears as a checker board.
Look with one eye for any wavy patternor any missingportions of the lines.
How is AMD treated?
1.LASERS2.Photo Dynamic Therapy.
3.Inta ocular injections[Anti VeGF].
None of these treatments is a cure for wet AMD.The disease and loss of vision may progress despite treatment.
4.Medical treatment:[For Intermediate and Advanced AMD]
Taking of specific high dose of Antioxidants and Zinc reduces the riskof advanced AMD and its visual loss.
[vit c 500mg,vit E 400IU,15mg Betacarotene,80mg Zinc]
PREVENTION OF A M D
•Eating healthy food rich in Greens.•Weight control
•Control of Blood pressure.
•Regular Exercise.
•Non Smoking
DONATE EYES AFTER DEATH AND LIVE TWICE
THANK YOU
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