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Ophthalmology
For medical students
Glucoma
Dr Hossam El Ayashi
M.B B.CH Ain Shams Universty
Dr / Hossam El Ayashi
Episcleral veins
Systemic circulation
3) Functions of the aqueous humour : 1) Supplies ocular tissues specially avascular parts ( the cornea and the lens) with O2 and nutrition and carries the waste products of their metabolism ( it is the lymph of the eye ) 2) Regulate the IOP.
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Dr / Hossam El Ayashi
4) Intraocular pressure ( IOP) : - It ranges from 10-21 mmHg above the atmospheric pressure . -It is higher than the pressure in any other tissue in the body in order to : a) Maintain the regular shape of the globe which is essential to maintain its optical properties against the forces exerted on it by the lid and the extra ocular muscle. b) Regulate the perfusion of the ocular tissues from the capillaries .
2) High IOP
Pathological changes specially in optic nerve (fig 8.3) B) Anatomy of A.C angle : (fig 8.4) It appears triangular in cross section. It formed of 5 structures : 1) Schwalbe s line : Corresponding to the peripheral thick end of Descemet's membrane of cornea. 2) Trabecular meshwork : -Uveal trabecular meshwork ( Large pores ). -Corneoscleral trabecular meshwork ( smaller pores ). -Endothelial trabecular meshwork ( Very small pores ). It is formed of connective tissue occupies the area between the Schwalbe s line and scleral spur. The perforations in each layer alternate with those in the next layer creating some resistance to aqueous drainage . It is translucent but become pigmented in ( dark races , old age , certain types of glaucoma) 3) Scleral spur : It is inward projection of inner surface of the sclera at its most anterior part. It gives attachment to the ciliary muscle posteriorly and the trabecular meshwork anteriorly. It appears as a dens white band or line during gonioscopy. 4) Part of anterior surface of ciliary body : this is the darkest part of the angle. 5) Root of the iris : As it inserts in the anterior surface of the ciliary body. Canal of Schlemm : is a circumfrential venous like channel situated at the corneo-scleral junction on the outer aspect of posterior 2/3 of the trabecular meshwork.
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Dr / Hossam El Ayashi
Glaucoma
1) Definition:
Pathological increase in the I.O.P lead to pathological harmful damage to the ocular structures specially the optic nerve which lead to visual field defect so glaucoma is trait. N.B - Increase IOP +Normal optic nerve+ Normal field=Ocular hypertension. - Normal IOP + Optic nerve damage+ Field defect=Low Tension glaucoma.
2) Classification:
No (1)
Congenital(Infantile) Buphthalmos
Acquired(Adult)
Primary
Secondary Buphthalmos
Primary Glaucoma
Secondary Glucoma
No (2)
According to age
According to Aetiology
According to gonioscopy
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Dr / Hossam El Ayashi
3) Incidence:
a) Age: 80% of cases before the age of 6 months. b) Sex: more common in male . c) Side: bilateral in 75% of the case.
4) C/P: (fig 8.5 a,b) a) Symptoms: -Early: 1) Start with lacrimation. 2) Photophobia. 3 ) Blephrospasm. 4)Sneezing on exposure
To light. Due to irritation of corneal nerve by Corneal edema due to irritation of 5th nucleus which present beside vagus nucleus
With compression on the nerve by edema Pain received by 5th nerve ( Trigeminal) Then to 7th nerve (Facial) Reflex lacrimation Late : 1) Large eye 2) blue sclera 3) poor vision 4) Heazy cornea
b) Signs: i) Cornea: - in horizontal diameter( N=9.5-10.5mm) become 15mm. - in Curvature. - In transparency( hazy cornea) due to presence of Hoab. - May be blue : due to presence of water vacuoles inside the cornea so when rays fall scattered and the most scattered ray is blue because it has short wave length. ii) Sclera: Blue ( due to pigment of the uveal tract)- Stretched-Thinned.
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Dr / Hossam El Ayashi
iii) Anterior Chamber: Deep due to forward bulge of elastic cornea. iv) Pupil: Dilated fixed ( non reactive). Due to optic nerve damage. v) Iris : Flattened, displaced( sub laxated). vi) Tension: Increased. vii) Optic disc ( fundus): Cupping or atrophy. Indicate optic nerve fibers damage. viii) Gonioscopy: Reveals abnormalities in the angle. ix) Refraction: Myopia due to flat and ant. Dislocation of the lens. 5) Diagnosis: ( Tetrad): a) Fundus examination first to be done to exclude Retinoblastoma. b) Gonioscopy to see the angle. ( Under general anesthesia) . c) Measurment of the IOP ( under Ketamine anesthesia). Because it does not decrease IOP while the other anesthesetic agents decrease IOP. d) Measurement of corneal diameter.( under general anesthesia).
6) D.D:
Nasolacrimal duct obstruction
1) lacrimation ( watering of the eye) Ophthalamia Neonatrum (conjunctivitis) -Ve test Buphthalmos
+Ve test
-Ve test
Absent
2) Megalocornea 3) Big Eye Enlargement of cornea Buphthalmos -Increase in corneal diameter. See the Signs -Fundus: normal. -Gonioscopy: normal. -No corneal opacity. blunt trauma or rubella 5) Opacities of cornea 4)Blue sclera -Congenital. See sclera Myopia -Retinoblastoma. -Buphthalmos. -Megalocornea. Buphthalmos
7)Complications of Buphthalmos: 1)Loss of vision due to optic atrophy. 2)Decrease of vision due to Complicated cataract,,Subluxation of lens Bilateral Nystigmus,,Unilateral ambylopia,,Axial myopia. 3)Recurrent glaucoma. 4)Susitability to trauma. 8) Treatment:
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Dr / Hossam El Ayashi
a) In early cases: 1) Corneal diameter is <13mm. 2) IOP <33mmHg. 3) Corneal condition:
Clear
Hazy
1)Goniotomy
1/3 or 1/2 of the angle incised using a special knife to connect the canal of schelem with ant.chamber.
2)Trabeculotomy
-Metal probe is inserted in the canal of schelem -then rotate the probe to cut through the trabeculum and connect the canal to ant.chamber
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Dr / Hossam El Ayashi
Stages of Glaucoma
Prodromal stage Acute congestive stage (fig 8.6 a ) 1) sudden total angle closure. 2) IOP =50mmHg which cause temporary paralysis of sphincter pupillae( ischemia) 3) 50% of cases give a history of previous prodromal attack
Chronic stage
Absolute stage
1)occur as a result of rapid(partial) closure and reopening of the angle. 2)IOP = 45mmHg. 3)Preceded by Precipitating factors. 4) there is closed opening of Vortex veins.
Symptoms 1) Frontal headache. 1) Sever frontal headache. 2) Eye ache. 2) Sever eye ache due to 3) Blurred vision. Stretch of corneal nerves. 4) Transient impaired of 3) Vomiting from sever pain Vision. (reflex vagus stimulation) 5) Colored halos due to 4) Rapid decrease of vision Collected of water in due to corneal edema and Cornea and act as a prism retinal nerve ischemia. analyzing the white light into its compartment wave length. Signs 1) During attack: - Increase IOP. - Corneal edema. 2)Gonioscopy: - narrow angle. - Iris bombi. 3) Provocative tests: its Idea depend on papillary Dilatation. a)Pharmacological test: (mydratic test) -IOP is measured. -weak mydratic added (phenyl ephrine 5%) -Remeasured IOP after Pupil dilated. -Result: if the difference between 2 reading is 8mmHg or more. It indicate increase IOP. - it is diagnostic test b) Physiological test: (Dark room test) Method,result as above.
Resembling POAG
1) eye Lid: edema. 2) Conjunctiva: Ciliary congestion. 2) Cornea: -Bullae 3) Cornea: Hazy. 4) Ant.chamber: shallow. 5) Iris: bombi. 6) Pupil: -semidilated. -irreactive. this due to temporary paralsis of sphincter muscle. -vertically oval. 7) IOP > 50 mmHg. 8) The eye is stony hard on digital assessment of ocular tension. 9) DD: 2ry angle closure glaucoma. there is presence of keratopercipitates.
1) IOP: -High in some. -Hypotonic:IOP<10mmHg due to atrophy of Cilia. body. (Bullous keratopathy) Resembling rupture of bullae lead to POAG Ulcer. Degenerative pannus. due to deposition of ca 3) Ant.chamber: shallow 4) Iris: -atrophic patches Lead to iris shortening -ectropion uvea: due to ischemia of atrophic iris lead to extensive fibrosis 5) Lens: complicated cataract 6) Fundus: optic atrophy Total disc cupping 7) Sclera: staphyloma
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Dr / Hossam El Ayashi
Prodromal stage Treatment 1) During attack: -Pilocarpine 2%(miotic) to get the iris away from The angle. -Pilocarpine 1% Prophylactic is given to other eye. 2) After attack: -Bilateral peripheral Iridectomy -Bilateral laser iridectomy b) Carbonic anhydrase inhibitors: they decrease IOP by aqueous secretion at ciliary body. e.g Acetazolamide 250mg 2 tablets are given initially Then 1 tablet/6h. c) Miotics: start to act only when IOP is lowered so that the temporary sphincter paralysis is relieved. e.g Pilocarpine 2% d) Beta blockers: decrease the aqueous secretion. e.g Timolol Meleate 0.5% eye drops twice/day Acute congestive stage
1) During attack: the patient must be hospitalized -medical preparation for surgery a) Hyper osmotic agents: They are most effective drugs They raise the osmotic pressure of the plasma this lead to draw water out of the eyes. e.g. Mannitol rapid IV drip 1-2gm/Kg.
1) If there is PAS: (peripheral ant. Synechia) -Filtering surgery. 2) If there is no PAS: -Peripheral iridectomy . 3) Prophylactic iridectomy for other eye.
2) After attack: using Gonioscopy a) If there is > 50% of the angle open: - Peripheral irridectomy or Laser irridectomy . b) If there is > 50% of the angle closed: - Filtering surgery( Fistulizing operation) c) Prophylactic Irridectomy to the other eye
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Dr / Hossam El Ayashi
3) Risks:
1) More common in high myopes the incidence is 15%. 2) More common in eyes with retinitis pigmentosa , Fuch s endothelial dystrophy, Diabetes Mellitus, systemic hypertension, Steroids responders. 3) Age: from middle age to old age. 4) Race: black race. 5) Large optic disc cap.
4) Pathogenesis:
- Site of pathology: may be at the endothelium lining Sclemms Canal or its adjoining part of the trabeculum. - The high IOP damage the retinal nerve fibers
Mechanical theory
by direct pressure on the retinal nerve fibers. - Degeneration and atrophy of these fibers result in Characteristic optic cup and visual changes.
Ischemic theory
by compression on the capillaries Interfering perfusion.
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Dr / Hossam El Ayashi
B) Signs: The diagnostic features are: 1) Changes in IOP. 3) Changes in field of vision.
1) Changes in IOP:
-Patients with typical POAG have IOP > 21mmHg. - In eyes with borderline IOP the following tests may be helpful: A) Diurnal variations:- in most normal eyes IOP changes through out the day being usually highest in early morning then decrease gradually by the massaging effect of extraocular muscles. In normal eyes diurnal variation does not exceed 4mmHg. This is due to the effect of corticosteroids in the body ( circadian rhythm of cortisone). - A high diurnal variation is highly suspicious of glaucoma.
B) Difference between the two eyes: if IOP in one eye exceed the other by more than 4mmHg
this is highly suspicious of glaucoma
C) Provocative tests: ( water drinking test) if the patient is asked to drink one liter of water or
large amount of coffee on an empty stomach if there is rise of IOP of 5mmHg or more indicates impaired function of the angle because the normal angle can deal with increased aqueous secretion by increasing aqueous drainage.
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Dr / Hossam El Ayashi
6)The clinically significant field changes are:
7) Management:
A) Medical Treatment: -The initial treatment of POAG is medical for life. - Success of medical treatment means that the IOP is lower to a level which prevents any further deterioration in the appearance of the fundus or in the field of vision. - Regular follow up is an essential step of treatment and should continue for life. - A glaucoma controlled by medical treatment may later on become out of control.. -The members are: ( BBs , Miotics, Adrenaline, Carbonic anhydrase inhibitor). 1) Beta Blockers: ( It is the drug of choice , Expensive) - Mechanism:It decrease IOP by decrease aqueous secretion .( aqueous formation) - Forms: Used in the forms of eye drops.e.g Timolol maleate 0.25 , 0.5% Betaxolol . - Dose: Used once or twice / day.( it is better compliance) - Advantages: 1) Do not alter papillary size. 2) Suitable for all types of glaucoma. - Complication : due to systemic absorption. a) Dry eye so should be taken with artificial tears. b) Decrease in heart rate 3) Bronchospasm. - Contraindication: 1) Heart failure. 2) Heart block. 3) Bronchial spasm. 2) Miotics: ( It is the most effective drug , the Cheapest, the Oldest). - Mechanism of action: ( aqueous formation and aqueous drainage) a) Miosis: -Widening of the angle.( an effect useful only in acute congestive glaucoma) - Strech of the iris increasing its surface and widening the iris crypts available for absorption of aqueous. b) Contraction of ciliary muscle - pulls on the scleral spur widening trabecular meshwork pores. - compress the blood vessels going to ciliary processes decrease aqueous secretion - Side effects: a) The miotics used 4 times / day ( Bad compliance ). b) Miosis : Dimension of vision especially at night and especially in patients with central corneal or lens opacities c) Ciliary muscle contraction : headache and myopic shift. d) May enhance the formation of posterior synechia and anterior cortical cataract.. e) Miotic cysts: Cysts might form at the papillary border.
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Dr / Hossam El Ayashi
3) Adrenaline or epinephrine( 0.5-2%): ( aqueous Drainage ) Mechanism: Lower IOP by increasing aqueous out flow ( adrenergic effect). Dose: twice/day. Forms: Dipivalyl adrenaline: which are free of systemic side effects as headache and arrhythmias. 4) Carbonic anhydrase inhibitors: ( aqueous formation) Forms: -Tablets: Acetazolamide ( Diamox) 250mg. -Drops: 2-3 times/day not produced side effect , not effective as systemic so used with. other anti glaucoma drugs Side effects of tablets. 1) Parathesia( tingling and numbness) most common. 2) GIT upset and abdominal cramps. 3) Renal stones. 4) Impotence. B) Surgery (or Laser trabeculoplasty) : is indicated in cases of : 1) Failure of maximum medical treatment to lower IOP to a level which stops the deterioration 2) Intolerance to medical treatment. 3) Non compliance of the patient. 4) Patients unable to come for regular follow up. Laser trabeculoplasty: Application of scattered laser burns to the trabecular meshwork It reduce the IOP by 8-10 mmHg but transient. Glaucoma surgery: 1)External Fistulizing ( Filtering) operation: The idea: is to create a passage ( fistula) at the limbus for aqueous to pass to subconjunctival space to be absorbed by blood vs of the conjunctiva and episclera. 2) Defunctioning operation: -These procedures are used only in 1) blind eyes ( absolute glaucoma) in which the filtering surgery is dangerous. 2) Cases of neovascular glaucoma. The idea: Reducing IOP by partial destruction of the ciliary body ( cyclo-destructive procedures) and this lead to decrease the aqueous formation . this is achieved either by: a) Freezing the ciliary body: ( cyclo-cryo-thermy): it is most popular form is done. b) Partial destruction of ciliary body by using laser ( cyclo-photo- coagulation) either applied directly or through the sclera.
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Dr / Hossam El Ayashi
Primary angle closure glaucoma (Closed angle glaucoma) (Narrow angle, decompensated , congestive glaucoma)
1) Definition: It is increase of IOP due to sudden closure of the angle (Partial or Complete) by peripheral iris. 2) Characters: Bilateral but one eye precede the other eye. 3) Aetiology:
Predisposing Factors
Precipitating Factors
General
Pupillary dilatation 1) Mydriatics. Emotion 2) Excitiment. 3) Prolong stay in dark ( small eye) in which the lens
Ciliary congestion
Hypermetrope Due to increase in lens thickness pushing the iris and causing the shallowing of ant. chamber and narrowing of the angle
Nervous individuals there is imbalance between sympathetic and parasympathetic tone Lead to unstable vasomotor reaction
4) Iris Forms:
Iris Bombi ( more common) in the eye with narrow angle there is tight apposition of iris to the lens lead to pupillary block result in traps of aqueous in post.chamber so dilatation of pupil lead to relaxation of iris so the trapped aqueous will push the iris root forward lead to angle closure ( do Peripheral iridectomy) Iris Crowdening in which the root of dilated iris is crowded in the angle lead to angle occulosion.
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Dr / Hossam El Ayashi
5) Comparison between 1ry open and closed angle glaucoma: 1ry closed angle glaucoma 1) Incidence 2) age 3) Sex 4) Patient 5) Eye 6) Cause 7) Prodroma 8) Symptoms 9) ttt Less common > 40 yrs old More in female Nervous Hypermetrope Angle closure Present Marked Surgical
1ry open angle glaucoma more common > 50 yrs old Male = Female Any Any Trabecular sclerosis Absent Few Initially Medical then surgical if medical failed
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Dr / Hossam El Ayashi
Red Eye
- It is common problem that is encountered by every physician . - It may signify a mild problem or a serious vision threatening problem that need management.
Conjunctivitis
Keratitis
Uveitis
Improve with blinking due to presence of discharge on ocular surface no pain but - gritty sensation - mild irritation
____
____
_____
_______
2) Pain
present
present
present
______
3) Photophobia
(abnormal sensitivity to the light)
_____
___
______
_____
4) Colored halos
present due to corneal edema present The lids stuck together on walking present present ______
5) Discharge
_____
_____
____
_____
6) Itching 7) Watering
(Excessive tearing)
____
_____
8) Cosmetic disfiguration
_______
present
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Dr / Hossam El Ayashi
Conjunctivitis Keratitis Uveitis
_____
Present
Present
Present
_____
_____ Present
Present ______
Present ___
______ ______
_____ ______
Present ________
_____ ______
6) Pupillary Abnormalities
_____
___
- small due to reflex spasm of iris sphincter -distorted by Post. synechia ____
___
____
______
shallow
____
___ present Purulent : bacterial Serous : viral. Scanty white elastic in allergic conj. -adenoviral conj. -Parinaud oculoglandular syndrome -Upper respiratory tract infection disorder with fever. ( Adenovirus 3 , 7) -Seasonal rhinitis with hay fever ( allergic conj.)
___
___
Elevated
___
____
____
____
___
____
____
____
___
C) Systemic associated
____
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Dr / Hossam El Ayashi
2ry Glaucoma
Definition: It is increase of IOP 2ry to local eye disease. Site of disease: (cornea ant. chamber-iris-lens-intraocular tumors-drugs-trauma-neovascular glaucoma)
The disease of ocular part 1) Cornea a) Infective corneal ulcer ( open angle glaucoma) b) Local adherent + ant. staphyloma which lead to peripheral ant. synechia (PAS) ( Closed angle glaucoma) c) Corneal fitula: after closure lead to PAS ( Closed angle glaucoma) 2) Ant. Chamber normally ant.chamber clear with no presence of any cells or solid particles. Presence of them called(seedling A.C) a) -Hypopyon: Pus in A.C. ( open angle glaucoma). -Hyphema: blood in A.C. ( open angle glaucoma). b) Epithelial cyst: cause pupillary block lead to accumulation of aqueous in post.chamber which elevate the iris lead to closure of angle( closed angle glaucoma) c) Angle recession glaucoma. ( open angle glaucoma) a)Acute iritis: (iridocyclitis) due to presence of hypopyon (open angle glaucoma) b) Chronic iritis: due to seclusiopupillae or occlusiopupillae.(closed angle glaucoma) c) Early rubeosis: Neovessels formed on iris which rupture lead to hge glaucoma.( open angle glaucoma) (fig 8.7) d) Late rubeosis: due to P.A.S (closed angle glaucoma) Management -Atropine.-Antibiotic-Carbonic anhydrase Inhibitor(C.A.I) Keratoplasty + Trabecullectomy
same
-Cryotherapy (freezing) destruction of ciliary body -Trabeculectomy - C.A.I- Atropine- Steroid -Iridectomy + Trabeculectomy - beta blocker + Gonio-photocoagulation
3) Iris
- Cyclocryotherapy
4) Lens
a) Phacomorphic glaucoma: due to pupillary block ttt of lens condition: remove it ( closed angle glaucoma) b) Phacolytic glaucoma: (open angle glaucoma) c) Ant. Dislocation : due to pupillary block (closed angle Gl) because the aqueous will accumulate and elevate the iris against angle (Glaucoma inversus) . d) Post. Dislocation: due to pupillary block by the vitreous ( open angle glaucoma) . e)Sublaxation: due to iritis ( open angle glaucoma) f) Glaucoma capsulature: part of the lens capsule exfoliated which block the angle. (Pseudoexfolation gl) (open angle glaucoma) g) Aphakic glaucoma: it is increased IOP following cataract extraction due to 1) post operative iritis 2) post operative hyphema 3) pupillary block by the vitreous 4) steroid induced glaucoma h) Micro spherophekia and traumatic cataract
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Dr / Hossam El Ayashi
5) Retinal causes:
a) Diabetic Retinopathy and central retinal vessels occlusion. Cause: due to retinal ischemia lead to release of vasogenic factor result in rubeosis iridis or vitreous hge. b) Retinal detachment surgery. Causes: due to 1) Tight scleral buckle. 2) Intraocular injection of gases or silicon oil. 3) Steroid ttt. 6) Intraocular tumors: lead to glaucoma by many ways: a) Direct invasion of the angle in anterior tumours. b) Pushing the iris lens diaphragm forward. c) In loose tumours as in Retinblastoma the malignant cells might rich the ant. Chamber and block the trabecular pores. d) In Rapidly growing tumours might consume most of blood supply creating a state of ischemia (neovascular glaucoma). e) In Rapidly growing tumours there is extensive tumours necrosis lead to toxic iridocyclitis and 2ry glaucoma. f) Acting as a space occupying lesions. g) Pressure on vortex veins lead to vascular engorgement. 7) Drugs: - Steroids: (open angle glaucoma) due to: a) Decrease the aqueous out flow due to deposition of macrophage precipitates in the trabecular meshwork. b) Increase the aqueous formation due to salt and water retention. - Mydriatics: dilate the pupil and push root of iris toward the angle. (closed angle glaucoma). 8) Trauma: which lead to a) Hyphema. b) angle recession glaucoma. 9) Neovascular glaucoma: (fig 8.8) the angle closure is caused by new vessels or hge from ruptured vessels. 10) Miscellaneous : a) Cavernous sinus thrombosis. b) Micro spherophakia. c) Pigmented glaucoma.( occur in young persons with high myopes of dark coloured races) due to deposition of the pigment liberate from the iris in the angle.
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