Dr. Samarth Mishra

introductionCharacterized by-

o Raised IOP

o Open angles

o A/w underlying disorder leading toalteration in aq. humor dynamics

o A/w OD & VF changes

classification

SOAG

Pre-trabecular

TrabecularPost-

trabecular

pretrabecular Aq. Flow obstructed by a membrane covering TM

Consists of –

6. Fibrovascular memb.--neovascular glaucoma

7. Descement like memb.—IEC, trauma

8. Epithelial downgrowth

9. Fibrous downgrowth

10. Inflammatory memb– Fuch,s cyclitis

Neovascular glaucomaNeovacular tissue arbourise in the angle

Form a fibrovascular memb.

Blocks TM

SOAG

Stages of neovascular glaucoma. (A)Pre-glaucoma stage with new vessels appearing at pupillary margin

and in angle.(B) Open-angle glaucoma stage with new vessels spreading and

fibrovascular tissue covering angle.(C) Heavy neovascularization and extensive peripheral anterior

synechiae.(D) Regression stage with angle sealed and vessels less visible.

Treatment options of neovascular glaucoma• Atropine and steroids to decrease inflammation• Beta-bockers•intravitreal VEGF inhibitor injection

Panretinal photocoagulation- in early cases

Artificial filtering devices- in very advanced cases

Cyclodestructive procedures- to relieve pain

Retrobulbar alcohol injection to relieve pain

Topical

(A)Membrane forms in one area of angle.(B) Additional areas of angle are involved, and contraction of

membrane displaces pupil.

Trabecular causesCLOGGING

Erythrocytes: haeme, ghost cell

Macrophages: phacolytic, hemolytic, melanolytic

Neoplastic: melanoma, NF, naevus of Ota, JXG

Pigment: PDS, Uveitis, melanoma

Proteins: PXF, uveitis, lens particle

Mucopolysaccharides: vitreous, viscoelastic

Gas & oil: C3F8, SF6, Air, silicone oil

Retinal photoreceptors : Swartz’s syn

TM ALTERATION

Edema/ inflammation

Chemical burn

Blunt trauma, angle recession

Fe IOFB, siderosis of TM

Steroid induced

Pigmentary glaucoma B/L condition due to pigment dispersion in AC

Risk factors is young adolescent male, whites, high myopic, AD located at 7q35-36

Pathogenesis is rubbing of pig. Epi. Of iris against zonules -> liberation of pig -> deposited in angle by convection current in aq.

Signs are:- cornea – krukenberg’s spindle

AC – deep, homogeneous fine hyperpig. over post. Trabeculum

Iris – radial, spoke like, mid peripheral transillumination defect, concave iris

Lens – Scheie’s line/Zentmayer’s ring

Zonules - pigmentation

Contd… Management ->

1) medical—beta blockers, adrenaline, dipivefin, CA inhibitor, miotic

2) Laser – ALT, PI, Peri. Iridoplasty

3) Surg - trabeculectomy

Exfoliation glaucoma TM clogging up by PXF material &/or pig. From iris

Risk factors are –fem, in Scandinavia, mutation in LOXL1 gene at 15q22 locus

Patho ---grey-white fibrillary extracellular material composed of protein core surrounded by GAGs produced by abnormal BM of ageing epi. Cells of TM, equatorial lens capsule & CB.

Signs –cornea -> dandruff like deposi, in endo.

AC -> Sampolesi’s line

iris -> absence of pupi. Ruff, moth-eaten trans illumination defect

lens -> cataract, exfo. Deposi. As central disk with peri. Band & a clear zone in middle

Pseudoexfoliation glaucoma

Pseudoexfoliative material Iris sphincter atrophy Gonioscopy

Central disc with peripheral band

Trabecular hyperpigmentation- may extend anteriorly(Sampaolesi line)

On retroillumination

Contd.. T/T ---

1) Medical - beta blockers, epinephrine, miotics

2) Laser – ALT

3) Surg – trabeculectomy

4) Trabecular aspiration

Lens induced glaucoma1) PHACOLYTIC:-

. Due to protein leakage from mat./hypermat. cat

. mechanism is –a) high molecular wt. soluble protein directly block

b)macrophages engulf the proteins & block

. c/f – seen in elderly with h/o poor vision for mons

- acute onset of uniocular pain, redness & watering

- grossly decres. Vision & raised IOP

- signs of uveitis

-hypermat/ morgagnian cat

- AC shows heavy flare a/w hyper refringent crystals which are ca++ oxalate / cholesterol crystals

. t/t – medical (hyperosmotic, CA inhi.,topical b-blockers & steroids

- surg ( ECCE with PCIOL)

Phacolytic glaucoma

Pathogenesis Signs

• Deep anterior chamber• Control IOP medically

• Remove cataract • Floating white particles

Treatment

Calcium oxalate crystal in the lens of a patient with glaucoma associated with hypermature cataract. (Hematoxylin and eosin stain.)

Phacolytic glaucoma with bloated macrophages and lens material obstructing the trabecularmeshwork.

Contd…2) LENS PARTICLE:-. k/a phacotoxic uveitis

. Mechanism is – due to trauma/ surg.retained lens material

disruption of lens capsule

lens material liberation raised IOP

inflammatory response

raised IOP

. c/f – features of uveitis, rai IOP, chunky white particles in AC, hypopyon

. Diag. by paracentesis

. t/t – medical as phacolytic

- surg. ( removal of lens material)

Contd…3)PHACOANAPHYLAXIS :-

. occur when patients become sensitized to their own lens protein k/a endophthalmitis anaphylactica

. typically develops after penetrating trauma or extracapsular cataract extraction

. granulomatous inflammation of the lens with polymorphonuclear leukocytes, lymphocytes, epithelioid

cells, and giantcells.

. t/t is surg. Removal of residual lens material

Glaucoma after trauma1) CHEMICAL :-

. Alkali>acid

. caused by scleral shrinkage and release of active substances, including prostaglandins

. IOP measured more accurately with the pneumatic or MacKay-Marg tonometers

.managed by – medical ( topical and systemic medications)

2) ELECTRIC :-

. pressure rise to venous dilation, contraction of the extraocular muscles, and pigment dispersion

. No therapy due to transient rise of IOP

Contd…3) RADIATION :-

. Mechanism are neovascularization/ ghost-cell glaucoma associated with radiation retinopathy and vitreous hemorrhage.

4) PENETRATING :-

. Due to retained organic material / FB / severe inflammation / TM damage

5) CONTUSION :-

. can cause hyphema, iridocyclitis, iris sphincter tears, iridodialysis, cyclodialysis, lens subluxation, retinal tear or dialysis, retinal detachment, vitreous hemorrhage, choroidal rupture, and glaucoma.

Contd…

Glaucoma a/w intraocular haemorrhage

1) GHOST CELL:-

.mecha. - retinal disease/ trauma/surgery /snake poisoning

vitreous haem.

degenerated RBC’s travel thr. Disruped ant hyaloid face

obstructs TM

. Diag. by paracentesis & cyto. Exam. which shows HEINZ bodies i.e. RBCs in the vitreous degenerate to tan-colored spheres (ghost cells), which appear empty except for clumps of denatured hemoglobin

. t/t is AC wash / pars plana vitrectomy to remove remaining ghost cells

Contd…2) HEMOLYTIC :-

. Due to macrophages laden with pigments, RBC’s & debris

3) HEMOSIDEROSIS :-

. Due to iron liberted from Hb causing siderosis of TM

4) HYPHEMA :-

. Due to blood & blood products

. Total hyphema changing color from red to black (black-ball or eightball hyphema)

. t/t – topical anti glaucoma

- surgical removal of hyphema

Glaucoma a/w uveitis. Mechanism are-

(1) increased viscosity of aqueous humor;

(2) obstruction of the trabecular meshwork by inflammatory cells and debris

(3) swelling and dysfunction of the trabecularmeshwork;

(4) liberation of active substances such as prostaglandins;

(5)scarring of the outflow channels;

(6) development of a cuticular endothelial membrane over the angle;

(7) neovascularization;

(8) elevation of episcleral venous pressure;

Contd…Causes are:-

1) FUCH’S HETEROCHROMIC IRIDOCYCLITIS

. Mild form of anterior uveitis associated with cataract and glaucoma.

.c/f – mild uveitis, fine filaments on the endothelium between the keratic precipitates, a patchy loss of the iris pigment epithelium, hypochromia, grey-white nodules on the anterior iris, a few opacities in the anterior vitreous, and chorioretinal scars

. Gonioscopy reveals fine vessels that bridge the angle

Contd…2) GLAUCOMATOCYCLITIC CRISIS:-

. k/a POSNER – SCHLOSSMAN SYNDROME

. young to middle-aged adults and consists of recurrent episodes of mild anterior uveitis and marked elevations of IOP

. mild ciliary flush, a dilated or sluggishly reactive pupil, corneal epithelial edema, IOP in the range of 40–60 mmHg, decreased outflow facility, open angles, faint flare, and 1–20 fine

keratic precipitates

Contd…3) JRA:-

. most common in young girls with iridocyclitis and monoarticular or pauciarticular involvement

. Due to inflammation of the trabecular meshwork

4) HERPES :-

. Due to trabeculitis , inflamm. Of TM

. Commonly in disciform & necrotising sromal type

5) SYPHILIS:-

. Due to acute interstitial keratitis

Contd…6) SARCOIDOSIS:-

. swelling and dysfunction of the trabecular meshwork, obstruction of the trabecular meshwork by inflammatory cells and debris

7) PRECIPITATES IN THE TM

Diag. by lab. & imaging technique

t/t- medical ( topical, sys. & periocular steroids, cycloplegics, NSAIDS, immunomodulators, anti glaucoma)

- surg (ALT, filtering procedure, tube shunts, cycloablative, Nd:YAG laser cyclophotocoag.)

Glaucoma a/w intraocular tumors

Mechanisms are:-

(1) direct extension of the tumor into the trabecularmeshwork

(2) seeding of tumor cells into the outflow channels

(3) pigment dispersion

(4) inflammation

(5) Hemorrhage,inducing hemolytic glaucoma, and suprachoroidal hemorrhage

(6) neovascularization of the angle

(7) obstruction of the trabecular meshwork by macrophages containing melanin released by a necrotic tumor (melanomalytic glaucoma)

Contd… Tumors causing rai. IOP:-

1) Iris- neavus, melanocytoma, malignentmelanoma, metastatic

2) CB- medullocytoma, melanocytoma, malignentmelanoma

3) Choroid- malignent melanoma, metastatic

4) ON- melanocytoma, metastatic

5) Retina – retinoblastoma

6) Metastatic CA

7) Others- leukemia, lymphoma, multiple myeloma, juvenile xanthogranuloma

Contd… Diag. by- gonio., indirect & direct ophthalmoscope, USG,

MRI, FNAC, Aq. Aspiration, excisional biopsy

t/t –medical (anti glaucoma with surg./radiation/ chemo/a combination)

- surg—

. smaller tumor ( observation till growth)

. Iridectomy / iridocyclectomy for smaller tumor

. Ant. Tumor ( argon laser trabeculopexy)

. Post. Tumor ( local resection/ photocoagulation/ episceralradiopaque therapy / enucleation/exenteration)

Corticosteroid glaucoma Seen in steroid responders who use topical, creams, oientment

on eyelids, systemic, periocular, inhaled steroids

Steroid responders are those who showed rai. IOP to topical steroids in 4-6 wks as compared to general population

3 groups- low (manifest with no change in IOP)

intermediate ( mod. Elevation of IOP to 22-30)

high ( marked rise to >30)

Patho.:- stabilize lysosomal memb. Prevents polymerization of GAG GAG accumulation in TM

t/t :- dicontinuation of drug

- anti glaucoma medication

- trabeculectomy / seton implantation in uncontrolled

Glaucoma after cataract surgery Mechanism are:-

1. Inflammation with the release of active substances, including prostaglandins and the formation of secondary aqueous humor.

2. A watertight wound closure with multiple fine sutures limiting the ‘safety valve’ leak of aqueous humor.

3. Deformation of the limbal area, reducing trabecular outflow.

4. Obstruction of the trabecular meshwork by pigment, blood,lens particles, inflammatory cells, and viscoelastic substances.

Contd…A. Early onset (within first postoperative week) 1. Pre-existing chronic open-angle glaucoma 2. alpha- Chymotrypsin-induced glaucoma 3. Hyphema/debris 4. Viscoelastic material 5. Idiopathic pressure elevationB. Intermediate onset (after first postoperative week) 1. Pre-existing chronic open-angle glaucoma 2. Vitreous in the anterior chamber 3. Hyphema 4. Inflammation 5. Lens particle glaucoma 6. Corticosteroid-induced glaucoma 7. Ghost-cell glaucomaC. Late onset (more than 2 months postoperatively) 1. Pre-existing chronic open-angle glaucoma 2. Ghost-cell glaucoma 3. Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser capsulotomy 4. Vitreous in the anterior chamber 5. Late-occurring hemorrhage 6. Chronic inflammation

1.alpha-Chymotrypsin Glaucoma

used widely to facilitate intracapsular cataract extraction.

mechanism for alpha-chymotrypsin glaucoma

is that zonular fragments obstruct the outflow channels

t/t by using a lesser concentration of the drug (1:10 000 instead of 1:5000) in a lower volume(0.25–0.5 ml instead of 2 ml)

anterior chamber should be irrigated before lens extraction to remove zonular fragments

Scanning electron micrograph of the zonular fragmentsobstructing the trabecular meshwork after alpha-chymotrypsin administration

2. Glaucoma From ViscoelasticSubstances

Sodium hyaluronate blocks TM

tiny ruby-like globs of hemorrhage on the iris surface or suspended in the anterior chamber

3. Glaucoma with Pigment Dispersion from Intraocular Lenses

Mechanism:-

Decentered, tilted, excessively mobile, too small, or reversed in position

excess friction between the optic or haptic and the iris pigment epithelium

Pigment particles block TM

c/f :- geographical loss of iris pigment

4. Uveitis-Glaucoma-HyphemaSyndrome Seen in iris supported ACIOL / PCIOL

c/f:- rai.IOP, iridocyclitis & recurrent hyphema for wks to mons after surg.

Due to excessive chafing of the iris by the pseudophakics because the lenses are too mobile

5.Glaucoma After nD: yag LaserPosterior Capsulotomy

occurs within 2–4 hours of the laser treatment and then abates spontaneously over the next 24 hours

usually associated with particulate debris clogging the trabecular meshwork

Pretreatment with apraclonidine 1% 1 hour prior to surgery and one drop 1 hour after surgery has been shown to decrease the number and severity of postoperative pressure spikes

6. Glaucoma from Vitreous in the Anterior Chamber

Common in aphakic eyes

after a spontaneous rupture of the hyaloid face or after an extensive posterior vitreous detachment.

Retinal detachment and glaucoma Due to vitreous loss

Schwartz Syndrome- RD + Rai. IOP + decrea. Outflow + open angles + cells & flare in AC

Mechanism:- a)angle recession,inflammation, pigment granules released by the retinal pigment epithelium, and glycosaminoglycans synthesized by the photoreceptors blocks TM

- b) photoreceptor outer segments migrate through the retinal hole and obstruct the trabecular meshwork

Glaucoma after vitrectomyPre-existing glaucoma Angle recession Ghost cell Primary open-angle glaucoma Pigmentary glaucomaAssociated with intraocular hemorrhage Hyphema Ghost cell Hemolytic HemosiderosisRelated to lens material Phacolytic Lens particle PhacoanaphylacticNeovascularInflammatoryCorticosteroid inducedIntraocular gas or liquid Air Viscoelastic substances Perfluorocarbons Silicone

Post- trabecular causes TM is normal but aq. Flow is impaired due to elevated

episcleral venous pressure For every 1mm rise in EVP-> 0-8 mm rise in IOP Causes are :-I. Obstruction of venous drainageA. Episcleral-1. Chemical burns 2. RadiationB. Orbital -1. Retrobulbar tumors 2. Thyroid eye disease

3. Pseudotumor 4. PhlebitisC. Cavernous sinus thrombosisD. Jugular vein obstructionE. Superior vena cava obstructionF. Pulmonary venous obstructionII. Arteriovenous fistulasA. OrbitalB. Intracranial-1. Carotid-cavernous fistula 2. Dural fistula

3. Venous varix 4. Sturge-Weber syndromeIII. Idiopathic

Superior Vena Cava Obstructions

Mainly due to tumors, aortic aneurysms, mediastinal masses, hilar adenopathy, and intrathoracic goiter

produces edema and cyanosis of the face and neck (pumpkinhead appearance) as well as dilated vessels in the head, neck, chest, and upper extremities

ocular findings include exophthalmos, papilledema, and prominent blood vessels in the conjunctiva, episclera, and retina

IOP is elevated mainly in supine position

Arteriovenous Fistulas Carotid-cavernous fistulas-

- It provide a free communication between the internal carotid artery and the surrounding cavernous sinus in high blood flow and high mean pressure in the shunt

- reversal of blood flow in the vessels leads to congestion of the orbital veins and soft tissues

- c/f--- pulsating exophthalmos, chemosis, lid edema, vascular engorgement, and restriction of ocular motility

Carotid-cavernous fistula.

Contd… Sturge-Weber Syndrome

- k/a enchephalotrigeminal angiomatosis

- Congenital, sporadic oculocutaneous disorder

- Glaucoma is seen in 30% of pt’s having ipsilateral facial hemangiomata during first 2yrs of life

- Patho isolated trabeculogenesis

-> raised episcleral venous pressure

- t/tmedical (topical PG’s)

goniotomy

combined trabeculotomy & trabeculectomy

THE END