Understanding Glaucoma and Intraocular Pressure

• Glaucoma is a progressive optic nerve disease
• Glaucoma is associated with elevated intraocular pressure
• Glaucoma is characterized by optic disc cupping and visual field loss
• A key risk factor is elevated intraocular pressure (IOP)

Factors Determining Normal IOP

• The rate of aqueous humor production by the ciliary body
• Resistance to aqueous outflow across the trabecular meshwork-Schlemm's canal system
• The level of episcleral venous pressure

Raised Intraocular Pressure

• Intraocular pressure is determined by the balance between aqueous production inside the eye and aqueous drainage out through the trabecular meshwork
• Normal intraocular pressure is 10-21 mm Hg or 16-26 mm

Aqueous Humor Formation

• Aqueous humor formation occurs in two steps
• The first step involves elaboration of a filtrate of plasma from the ciliary body microvasculature into the ciliary body stroma.
• The second step involves the formation of aqueous humor from this filtrate by the ciliary epithelium and its secretion into the posterior chamber.

Aqueous Humor Outflow

• Trabecular outflow accounts for 90%
• Uveoscleral outflow accounts for 10%

The Anterior Chamber Angle

• Features in a Gonioscopic Picture
• Iris
• Ciliary body band
• Scleral spur
• Trabecular meshwork, including uveal, corneoscleral, and juxtacanalicular elements
• Schwalbe's line

Clinical measurement of IOP

• Applanation tonometry – The Goldman applanation tonometer
• Noncontact (air-puff) tonometers
• Electronic applanation
• Pneumotonometry
• Schiotz tonometry
• Digital pressure on the globe

Glaucoma Classification

• Primary, secondary
• Age of the patients: congenital, infantile, juvenile, adult
• The site of obstruction to aqueous outflow: pretrabecular, trabecular, post-trabecular
• Gonioscopic picture: open-angle, close-angle, combined
• IOP and visual field

IOP and VF Degrees

• IOP from 26 till 32mm
• IOP more than 32mm
• Visual Field I degree: some constriction nasal borders of VF
• Visual Field II degree: from 55 ° till 15°
• Visual Field III degree: less than 15° till fixation point
• Visual Field IV degree: there is no visual field
• Open angle O/A Ia glaucoma, or C/A II b gl

Childhood Glaucoma

• Evident at birth or within the first few years of life
• Caused by dysplasia of anterior chamber angle
• Primary congenital
• Infantile glaucoma
• Juvenile gl is recognized later after 3 years of age
• Developmental gl associated with other developmental anomalies

Gonioscopic appearance

• The anterior chamber angle in primary infantile glaucoma, when viewed through a Koeppe diagnostic lens
• The iris is seen to insert anteriorly
• The peripheral iris is hypoplastic and unpigmented and has a scalloped appearance.

Klippel-Trenaunay-Weber Syndrome

• Note the extensive facial telangiectasis that does not respect the vertical midline
• Limb and trunk involvement is characteristic (with profoundly asymmetrical limb growth in severely affected individuals)
• Upper and lower lids are involved, indicating a high likelihood of glaucoma

Clinical Signs

• Epiphora
• Photophobia
• Blepharospasm
• Enlargements of corneal size

Diagnosis

• Diagnosis needs a clinical evaluation
• IOP measurements
• Measurement corneal diameter
• Gonioscopy
• Ophthalmoscopy
• Buphtalmos present – enlargement of the globe

Diode Laser Cyclophotocoagulation

• Trans-scleral application of laser energy to the ciliary body of an eye with Peters' anomaly following numerous glaucoma and corneal transplant procedures.
• Identify the ciliary body by transillumination to better aim the laser on disrupted eyes

Treatment for congenital/infantile Glaucoma

• Goniotomy
• Trabeculotomy

Open Angle Glaucoma Types

• Primary is a chronic, slowly progressive optic neuropathy with optic nerve damage and visual field loss
• Glaucoma suspect
• Normal tension gl
• Secondary

Pathophysiology

• Progressive decrease in the number of retinal ganglion cells
• The optic nerve exits the eye become pinched and die
• Thinning of the neural rim and progressive enlargement of the optic nerve cup
• The loss of nerve fibers causes a permanently decreased visual field

Risk Factors

• Elevated IOP
• Age
• Race
• Family history
• Eye trauma
• Uveitis
• Steroid therapy
• Associated disorders (diabetes, cardio-vascular disease, myopia)

Symptoms

• Patients rarely have symptoms with glaucoma
• After loss of more than 40 percent of the nerve fibers, patients may notice a gradual loss of peripheral vision, or "tunnel vision
• Open-angle glaucoma is usually an incidental finding during an adult eye evaluation performed for other indications

Glaucomatous optic neuropathy

• Generalized enlargement of the cup
• Focal enlargement of the cup
• Loss of nerve fiber layer
• Translucency of the neuroretinal rim
• Development of vessel overpass
• Asymmetry of cupping between the patients eye's
• Peripapillary atrophy

Glaucoma Cupping

• The optic nerve head is deeply cupped
• Atrophy of the optic nerve is determined by comparing the diameter of the optic nerve at its internal surface and posteriorly, where it should double in size
• Loss of axons and myelin cause an increase in size of the subarachnoid space and a proliferation of glial cells, resulting in an increased cellularity of the optic nerve

Glaucomatous optic nerve cupping observation

• the cup in this optic nerve is enlarged to 0.8
• there is typical thinning of the inferior neuroretinal rim, forming a "notch."

Glaucomatous Visual Field Defects

• Generalized depression
• Paracentral scotoma
• Arcuate or Bjerrum scotoma
• Nasal step
• Altidudinal defect
• Temporal wedge

Need for Referral to an Ophthalmologist

• Screening a high-risk patient older than 40 years
• Family history of glaucoma
• Personal history of diabetes or severe myopia
• Repeat screening at undetermined intervals
• Evaluating a patient with findings suggestive of glaucoma
• Elevated pressure on tonometry, if performed
• Suspicious optic disc cupping (cup-to-disc ratio greater than 0.5)
• Optic disc ratio difference between discs of 0.2 or more
• Highly asymmetric cup in one eye
• Apparently abnormal visual fields by confrontation

Medical Treatment

• Intraocular pressure is the only treatable risk factor for open-angle glaucoma

Drugs that Decrease Aqueous Production

• Beta blockers, nonselective: Levobunolol 0.25%, Metipranolol 0.3%, Timolol maleate 0.5% twice a day
• Beta blockers, relatively selective: Betaxolol (Betoptic) 0.25 -0,5% twice a day
• Carbonic anhydrase inhibitors: oral – diacarb 250-500mg, topical Dorzolamide (Trusopt) 2% -twice a day, Brinzolamide (Azopt) 1% - three times a day
• Alpha agonists -Brimonidine tartrate (Alphagan) 0.2% - three times a day, may increase outflow

Drugs that increase aqueous outflow (uveoscleral)

• Prostaglandin analogs: Latanoprost (Xalatan) 0.005%, Travoprost (Travatan) 0.004%- Once a day

Drugs that increase aqueous outflow

• Parasympatho-mimetic - Pilocarpine (Pilocar) 1% Three to four times a day
• Sympathomimetic- Dipivefrin (Propine) 0.1% Twice a day

Combination Medications

• Dorzolamide and timolol maleate (Cosopt) 2%/0.5% Twice a day

Surgical Management

• Laser trabeculoplasty, surgical trabeculectomy (fistulizing procedu-res – trabeculoectomy)
• A full-thickness sclerectomy is indicated when the target intraocular pressure cannot be reached medically

Angle-Closure Glaucoma

• It is defined by the apposition of the peripheral iris to the trabecular meshwork and the resulting reduced drainage of aqueous humor through ACA
• Primary angle-closure glaucoma with relative pupillary block
• Primary angle-closure glaucoma without pupillary block
• Secondary angle- closure glaucoma with pupillary block

Groups most at risk for Angle-closure glaucoma

• People older than 40
• Hypermetropia patients with shallow anterior chambers and shorter axial length eyes face a risk because with increasing age the lens size crowds anterior segment structures
• Women have shallower anterior chambers, live longer, and are therefore at more risk

Gonioscopic view

• Peripheral anterior synechiae
• Pointed, tent-like synechiae are often observed in narrow angles with a relative pupillary block
• Angle-closure glaucoma with pupillary block component: No angle structures are visible in the primary position

Acute Primary Angle Closure results in:

• Sudden blockage of trabecular meshwork by the iris
• Ocular pain, headache, blurred vision, rainbow colored halos around lights, nausea, emesis
• High IOP
• Often irregular pupil
• Corneal edema
• Congested conjunctival blood vessels
• Shallow anterior chamber with aqueous flare
• The optic nerve may be swollen during the attack
• Visual acuity is impaired

Management for Acute Primary Angle Closure

• If it is not possible to get the patient to the hospital immediately, emergency treatment is required to preserve VA
• Give acetazolamide 500 mg intravenously or 250 mg per os twice or hyperosmotic agents such as mannitol or glycerin
• Instill pilocarpine 4% in the eye to constrict the pupil
• Give analgesia and antiemetic if required
• Hot compresses on the legs
• Create a hole in the peripheral iris, either with a laser or surgically, to restore aqueous flow (peripheral iridotomy)
• Treat the other eye similarly as a prophylactic measure

Types of Secondary Glaucoma

• Pigmentary
• Pseudoexfoliation
• Lens-induced glaucoma : phacomorphic, phacolytic, phacotopic
• Postinflamated (uveitis)
• Postoperated
• Neovascular
• Neoplastic (from the tumors)