Glucoma

The simplest of

Ophthalmology For medical students

GlucomaGlucomaGlucomaGlucoma

Dr Hossam El AyashiDr Hossam El AyashiDr Hossam El AyashiDr Hossam El Ayashi M.B M.B M.B M.B –––– B.CH Ain Shams UniverstyB.CH Ain Shams UniverstyB.CH Ain Shams UniverstyB.CH Ain Shams Universty

Dok Ayman KhalilDok Ayman KhalilDok Ayman KhalilDok Ayman Khalil 5555thththth Year Ain Shams UniverstyYear Ain Shams UniverstyYear Ain Shams UniverstyYear Ain Shams Universty

2012012012011111----2020202011112222

Dr / Hossam El Ayashi Dok Ayman Khalil

The Simplest of Ophthalmology | Page 2

A) Physiology : -The pressure inside the eye depend on the volume of its contents . -All the ocular contents are almost static from the volume point of view as: Lens , Retina , Vitreous body , Uveal tract except the aqueous humour which is a dynamic state it is always produced and drained to maintain a normal level of IOP. 1) Aqueous production : (fig 8.1) It is produced by the ciliary processes by filteration and ultra filteration from the blood vessels of ciliary processes. Its production need alpha , beta receptors and carbonic anhydrase enzyme. It starts in the posterior chamber then circulates through the pupil and then fills the anterior chamber. 2) Aqueous drainage : it is filtered through:(fig 8.2) a)Angle of anterior chamber b)Uveoscleral pathway (80% of aqueous) (20% of aqueous) Trabecular meshwork Absorbed by vessels of the uveal tract ( present in the angle of anterior chamber) or through ciliary body Enter the canal of Schlemm Supra choroidal space Collector channels and aqueous veins blood vessels of sclera Outer surface of the sclera 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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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 . 1) Low IOP ( Hypotony ) 2) High IOP Tissue edema Impair tissue perfusion ( optic disc edema) ( Ischemia) 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.



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)

No (2) According to age According to Aetiology According to gonioscopy

Congenital(Infantile) Buphthalmos

Acquired(Adult)

Primary Primary Buphthalmos Secondar Secondary Buphthalmos

Primary Glaucoma Secondary

Glucoma

Narrow angle (Angle closure) congestive glaucoma

Open angle Chronic simple Non congestive glaucoma

Glaucoma of Adult

Congenital Glaucoma (Buphthalmos)

Primary Glaucoma

Secondary Glaucoma

Open angle Glaucoma

Angle Closure Glaucoma



A)Congenital Glaucoma (Buphthalmos)

1)Definition: Increase I.O.P due to Congenital Anomaly closing the angle.( most of cases ) 2)Aetiology: A) Primary Buphthalmos: ( most of cases ) occurring at birth or 1-3 yrs after birth 1) Abnormal presence of mesodermal membrane called (Barkan's membrane) which obstruct Trabecular meshwork.( it is the most common cause). 2) Failure of complete separation between iris and cornea. 3) Forward insertion of the Ciliary muscle and iris root instead of scleral spure. 4) Absence of canal of schlemm. B) Secondary Buphthalmos: = any cause of 2ry glaucoma in adult + the following 1)Microphthalmos. 2)Sturge Weber syndrome( with haemangioma). 3)Marfan's syndrome. 4)Retinoblastoma. 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 due to irritation Corneal edema 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.



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: 1) lacrimation ( watering of the eye) Nasolacrimal duct Ophthalamia Buphthalmos obstruction Neonatrum (conjunctivitis) 1)Regurge +Ve test -Ve test -Ve test Test: 2) Signs a) Lid edema. Absent b) Injection of eye. c) Discharge. 2) Megalocornea 3) Big Eye 4)Blue sclera Enlargement of cornea Buphthalmos -Congenital. See sclera -Increase in corneal diameter. See the Signs Myopia -Fundus: normal. -Retinoblastoma. -Gonioscopy: normal. -Buphthalmos. -No corneal opacity. -Megalocornea. blunt trauma 5) Opacities of cornea Buphthalmos or rubella - opaque cornea( vertical) - Horizontal,, - not in lower 1/2 - in lower 1/2 -not branched - branched 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:



a) In early cases: 1) Corneal diameter is <13mm. 2) IOP <33mmHg. 3) Corneal condition: Clear Hazy 1)Goniotomy 2)Trabeculotomy 1/3 or 1/2 of the angle incised -Metal probe is inserted in the using a special knife to connect canal of schelem the canal of schelem with ant.chamber. -then rotate the probe to cut through the trabeculum and connect the canal to ant.chamber b) In Late cases: 1) Corneal diameter is >13mm. 2) Fail goniotomy or trabeculotomy 3) Filtering ( External Fistulizing Trabeculotomy) operation e.g Sub-scleral trabeculotomy in Children there is a greater tendency to closure of the fistula due excessive conjunctival scarring . this controlled by the local use of antimetabolites(5 fu,,mitomycin) at the time of the surgery 4) Shunt Tube( Glaucoma device) Used only in cases of failure of repeated trabeculectomies



Stages of Glaucoma Prodromal stage Acute congestive stage Chronic stage Absolute stage (fig 8.6 a ) 1)occur as a result of 1) sudden total angle closure. Most of cases rapid(partial) closure and 2) IOP =50mmHg which follow acute 1) It is complete reopening of the angle. cause temporary paralysis of phase or irreversible 2)IOP = 45mmHg. sphincter pupillae( ischemia) prodromal 2) It is the 3)Preceded by 3) 50% of cases give a history stage end of any Precipitating factors. of previous prodromal attack uncontrolled 4) there is closed opening of glaucoma. Vortex veins. Symptoms 1) Frontal headache. 1) Sever frontal headache. Resembling Painful blind eye 2) Eye ache. 2) Sever eye ache due to POAG 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: 1) eye Lid: edema. 1) IOP: -High in some. - Increase IOP. 2) Conjunctiva: Ciliary -Hypotonic:IOP<10mmHg - Corneal edema. congestion. due to atrophy of Cilia. body. 2) Cornea: -Bullae 2)Gonioscopy: 3) Cornea: Hazy. (Bullous keratopathy) - narrow angle. 4) Ant.chamber: shallow. Resembling rupture of bullae lead to - Iris bombi. 5) Iris: bombi. POAG Ulcer. 3) Provocative tests: its 6) Pupil: -semidilated. –Degenerative pannus. Idea depend on papillary -irreactive. due to deposition of ca Dilatation. this due to temporary paralsis 3) Ant.chamber: shallow a)Pharmacological test: of sphincter muscle. 4) Iris: -atrophic patches (mydratic test) -vertically oval. Lead to iris shortening -IOP is measured. 7) IOP > 50 mmHg. -ectropion uvea: due to -weak mydratic added 8) The eye is stony hard on ischemia of atrophic iris (phenyl ephrine 5%) digital assessment of ocular lead to extensive fibrosis -Remeasured IOP after tension. 5) Lens: complicated Pupil dilated. 9) DD: 2ry angle closure cataract -Result: if the difference glaucoma. there is presence 6) Fundus: optic atrophy between 2 reading is of keratopercipitates. Total disc cupping 8mmHg or more. It 7) Sclera: staphyloma indicate increase IOP. - it is diagnostic test b) Physiological test: (Dark room test) Method,result as above.



Prodromal stage Acute congestive stage Chronic stage Absolute Glaucoma Treatment 1) During attack: 1) During attack: 1) If there is PAS: 1) Enucleation. (peripheral ant. 2) Defunctiong -Pilocarpine 2%(miotic) the patient must be Synechia) operation to get the iris away from hospitalized -Filtering surgery. The angle. -medical preparation for 3) Peripheral -Pilocarpine 1% surgery 2) If there is no PAS: irridectomy Prophylactic is given to a) Hyper osmotic agents: for other eye. other eye. They are most effective drugs -Peripheral iridectomy . They raise the osmotic 2) After attack: pressure of the plasma this 3) Prophylactic -Bilateral peripheral lead to draw water out of the iridectomy for other eye. Iridectomy eyes. e.g. -Bilateral laser Mannitol rapid IV drip iridectomy 1-2gm/Kg. 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 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



Primary Open Angle Glucoma ( Chronic simple, Compensated, glaucoma simplex)

(POAG)

1)Definition: It is a primary glaucoma resulting from decrease in outflow of aqueous through the trabecular Meshwork although the angle is open and looks normal result in increase of IOP lead to damage of optic nerve which result in visual field defect. 2)Incidence: - It is the commonest type of glaucoma – the incidence is 2% of general population. - It is usually bilateral and asymmetrical. - No sex predilection. M=F. 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 Sclemm’s Canal or its adjoining part of the trabeculum. - The high IOP damage the retinal nerve fibers Mechanical theory Ischemic theory by direct pressure on the retinal by compression on the capillaries nerve fibers. Interfering perfusion. - Degeneration and atrophy of these fibers result in Characteristic optic cup and visual changes. 5) Clinical Picture: A) Symptoms: 1) It is Symptom less because of the following: Sensory nerves are adapted to the slowly rising IOP so there is no pain or headache. 2) Field defects are usually of negative type( not felt by the patient) ,the visual acuity remains normal till very late stages when the macular fibers are affected. 3) In many cases the disease discovered when one eye is lost. 4) It is common discovered accidentally in patients attending ophthalmic clinics for other reasons e.g Changing glasses. 4) Some cases suffered from: -Delayed dark adaptation from lowered retinal sensitivity caused by ischemia. -Pathological presbyopia: due to weakness of Ciliary muscle and usually progresses faster than the physiological one. -Decreased sensitivity to the light: Patient notices that he need stronger illumination to see around satisfactorily. -Headache and blurring of vision.



B) Signs: The diagnostic features are: 1) Changes in IOP. 2) Changes in Optic disc. 3) Changes in field of vision. 4) Open angle.

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.

2) Changes in optic disc and fundus: - by examination of nerve fiber layer of the retina using red-free illumination there is defects can be seen and detected even before visible changes in optic disc appear -The normal cup/disc ratio (C/D ratio) varies from 0.0 to 0.3 and depends on the volume of nerve fibers in relation to the size of the scleral foramen. In glaucoma due to atrophy of the fibers, cupping of the nerve occurs in the form of increase in C/D ratio accompanied by deepening of the cup. The cup become large its shape vertical or oval. -Detected by Binocular ophthalmoscopy: - Pallor of the disc . -Nasal shifting of central retinal vessels. - Kinking and undermined retinal blood vessels. - Mechanism:- Mechanical theory: increase IOP lead to backward displacement of lamina cribrosa. - Vascular theory: sclerosis of disc blood vs lead to optic nerve fiber atrophy.

3) Changes in the field of vision: - Damage to nerve fiber layer of retina in glaucoma tend to involve bundles of fibers resulting in corresponding defects in visual field - The arcuate fibers coming from the temporal retina above and below the papillo macular bundle are the most susceptible to damage by glaucoma. -while the macular fibers are usually the last to suffer. - Field defects in glaucoma start as relative defects and then become absolute in advanced cases. - Normally Scotomata ( blind spot) are usually of the negative( objective) type. Evaluation of field changes is done by:

1) Static perimeters: (e.g Octopus) which evaluate the sensitivity numerically in each point of the field examined.

2) Kinetic perimeter: (e.g Goldmann perimeter or Bjerrum screen) Used in glaucoma or neurological lesions. Used only in glaucoma. Detect the central or peripheral changes Detect the central changes. Used for follow up. Used for early detection . Prognostic Diagnostic.



6)The clinically significant field changes are:

-Central field changes are: (detected by Bjerrum screen).(fig. 8.6b) a) Baring of blind spot : mean that it become enlarged. It may occur in early the disease but not Specific for the glaucoma. b) Isolated paracentral scotoma: detected in early glaucoma. c) Siedle scotoma: enlargement of paracentral scotoma and fused together with blind spot. d) Arcute scotoma: which arches from blind spot above and not beyond the horizontal meridian. e) Double arcute ( Annular scotoma + Ronne step).: due to fusion of double arcute scotoma may be open nasaly to peripheral field.( peripheral breakthrough).

-Peripheral field changes are: ( detected by Gold man perimeter). 1) The field defects enlarged peripherally and centrally that may end in a Temporal island or Tubular field . 2) Both fields above are disappear end by complete blindess.

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.



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-photocoagulation) either applied directly or through the sclera.



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 Local General Pupillary dilatation Ciliary congestion Narrow angle as in 1) Mydriatics. Emotion 2) Excitiment. 3) Prolong stay in dark Old age > 35 yrs Hypermetrope Due to increase ( small eye) in lens thickness in which the lens pushing the iris and causing the shallowing of ant. chamber and narrowing of the angle Sex Age Nervous individuals F > M > 35 Yrs there is imbalance between 4:1 sympathetic and parasympathetic tone Lead to unstable vasomotor reaction Ciliary body congestion With pushing iris forward ( Iris bombe) 4) Iris Forms: Iris Bombi ( more common) Iris Crowdening in the eye with narrow angle there is tight apposition in which the root of dilated iris of iris to the lens lead to pupillary block result in is crowded in the angle lead to traps of aqueous in post.chamber so dilatation of pupil angle occulosion. lead to relaxation of iris so the trapped aqueous will push the iris root forward lead to angle closure ( do Peripheral iridectomy)



5) Comparison between 1ry open and closed angle glaucoma: 1ry closed angle glaucoma 1ry open angle glaucoma 1) Incidence Less common more common 2) age > 40 yrs old > 50 yrs old 3) Sex More in female Male = Female 4) Patient Nervous Any 5) Eye Hypermetrope Any 6) Cause Angle closure Trabecular sclerosis 7) Prodroma Present Absent 8) Symptoms Marked Few 9) ttt Surgical Initially Medical then surgical if medical failed



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 Angle closure Sub conj. glaucoma hemorrhage A) Symptoms Improve with blinking due to ____ ____ _____ _______ 1) Blurred presence of vision discharge on ocular surface 2) Pain no pain but - gritty sensation present present present ______ - mild irritation 3) Photophobia Iritis alone or (abnormal sensitiv- _____ ___ 2ry to corneal ______ _____ ity to the light) Inflammation 4) Colored halos present due to corneal edema 5) Discharge present The lids stuck _____ _____ ____ _____ together on walking 6) Itching present _____ _____ ____ _____ 7) Watering present present present present (Excessive tearing) 8) Cosmetic ______ _____ _______ _______ present disfiguration



Conjunctivitis Keratitis Uveitis Angle closure Sub conjunctival glaucoma hemorrhage B) Signs 1) decrease _____ Present Present Present _____ visual acuity 2)Ciliary injection _____ Present Present Present 3) Conjunctival Present ______ ___ _____ ______ Congestion 4) Corneal haze ______ ______ _____ Present _____ 5)Corneal epithet ______ present by ______ ________ ______ - lial disruption fluorescein test 6) Pupillary - small due to -oval with Abnormalities _____ ___ reflex spasm wider vertical ___ of iris diameter sphincter -distorted by -sluggish in Post. reaction synechia 7) Ant.Chamber ____ ______ ____ shallow ____ depth 8) IOP ___ ___ ___ Elevated ___ 9) Discharge present Purulent : bacterial Serous : viral. Scanty white elastic ____ ____ ____ ___ in allergic conj. 10) LNs -adenoviral conj. Enlargement -Parinaud oculoglandular ____ ____ ____ ___ syndrome C) Systemic -Upper respiratory associated tract infection disorder with fever. -D.M ( Adenovirus 3 , 7) ____ -Hypertension. -Blood disease -Seasonal rhinitis with hay fever ( allergic conj.)



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 Management 1) a) Infective corneal ulcer ( open angle glaucoma) -Atropine.-Antibiotic-Carbonic Cornea anhydrase Inhibitor(C.A.I) b) Local adherent + ant. staphyloma which lead to Keratoplasty + Trabecullectomy peripheral ant. synechia (PAS) ( Closed angle glaucoma) c) Corneal fitula: after closure lead to PAS same ( Closed angle glaucoma) 2) Ant. normally ant.chamber clear with no presence of any cells Chamber or solid particles. Presence of them called(seedling A.C) a) -Hypopyon: Pus in A.C. ( open angle glaucoma). 1) C.A.I 2)Paracentisis 3)Semi setting -Hyphema: blood in A.C. ( open angle glaucoma). b) Epithelial cyst: cause pupillary block lead to accumulation of aqueous in post.chamber which elevate -Cryotherapy (freezing) destruction of the iris lead to closure of angle( closed angle glaucoma) ciliary body c) Angle recession glaucoma. ( open angle glaucoma) -Trabeculectomy 3) Iris a)Acute iritis: (iridocyclitis) due to presence - C.A.I- Atropine- Steroid of hypopyon (open angle glaucoma) b) Chronic iritis: due to seclusiopupillae or -Iridectomy + Trabeculectomy occlusiopupillae.(closed angle glaucoma) c) Early rubeosis: Neovessels formed on iris which - beta blocker + Gonio-photocoagulation rupture lead to hge glaucoma.( open angle glaucoma) (fig 8.7) d) Late rubeosis: due to P.A.S (closed angle glaucoma) - 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



5) Retinal causes: ttt: Enucleation 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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Glucoma