GLAUCOMA AND CATARACT

MOHD FAUZI BIN M. ZEIN 030.06.312

FACULTY OF MEDICINE TRISAKTI UNIVERSITY Jakarta, January 2010

ABSTRACT Glaucoma and cataract, both lead the cause of blindness in the world and Indonesia.[1] Glaucoma is a disease in which the optic nerve is damaged, leading to progressive, irreversible loss of vision. It is often, but not always, associated with increased pressure of the fluid in the eye.[2] Cataract is a clouding that develops in the crystalline lens of the eye or in its envelope, varying in degree from slight to complete opacity and obstructing the passage of light.[3] There are no direct correlation between glaucoma and cataract, but either glaucoma or cataract can become secondary disease to each other. Keywords: secondary glaucoma, acute glaucoma, complicated cataract, intumescent cataract

INTRODUCTION A) Glaucoma[1,2,4]

Glaucoma is a disease in which the optic nerve is damaged, leading to progressive, irreversible loss of vision. It is often, but not always, associated with increased pressure of the fluid in the eye.

The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. There are many different sub-types of glaucoma but they can all be considered as a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma (above 22 mmHg or 2.9 kPa). One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.

Vaughen classification divides glaucoma into primary (open angle or close angle), congenital, secondary (cause by changes in lens or uvea, trauma, surgery, rubeosis, steroid etc.) and absolute.

Glaucoma has been nicknamed the "sneak thief of sight" because the loss of vision normally occurs gradually over a long period of time and is often only recognized when the disease is quite advanced. Once lost, this damaged visual field can never be recovered. Worldwide, it is the second leading cause of blindness. If the condition is detected early enough it is possible to arrest the development or slow the progression with medical and surgical means.

B) Cataract[3,4] Cataracts are changes in clarity of the natural lens inside the eye that gradually degrade visual quality. The natural lens sits behind the colored part of the eye (iris) in the area of the pupil, and cannot be directly seen with the naked eye unless it becomes extremely cloudy. The lens plays a crucial role in focusing unimpeded light on the retina at the back of the eye. The retina transforms light to a neurologic signal that the brain interprets as vision. Significant cataracts block and distort light passing through the lens, causing visual symptoms and complaints. Cataract development is usually a very gradual process of normal aging but can occasionally occur rapidly. Many people are in fact unaware that they have cataracts because the changes in their vision have been so gradual. Cataracts commonly affect both eyes, but it is not uncommon for cataracts in one eye to advance more rapidly.

Cataract can be classified according to etiology into:-

i) Age-related cataract

Cortical Senile Cataract

Insipience Intumescences Immature senile cataract (IMSC) Mature senile cataract (MSC) Hyper mature senile cataract (HMSC): Morgagnian cataract

Senile Nuclear Cataract

Cataracta brunescens cataracta nigra cataracta rubra

ii) Congenital cataract

Sutural cataract Lamellar cataract Zonular cataract Total cataract

iii) Secondary cataract

Drug-induced cataract (e.g. corticosteroids)

iv) Traumatic cataract

Blunt trauma (capsule usually intact) Penetrating trauma (capsular rupture & leakage of lens materialcalls for an emergency surgery for extraction of lens and leaked material to minimize further damage)

ANATOMY OF THE EYE

HISTOLOGY OF THE LENSE[6]

The lens is a transparent soft biconvex structure composed of crystallins. The adult lens measures about 9 mm in diameter and is 3.5 mm thick. It is completely enveloped by the thickest basement membrane in the body, the capsule (#1 in photomicrograph ), which is 10-20 m thick of hyaline material containing type IV collagen. There is a layer of large cuboidal epithelial cells, (the lens epithelium) beneath the anterior capsule (#2 in photomicrograph). In the center (#3 in photomicrograph) tightly packed cells have lost their nuclei and become packed by special transparent proteins (crystallins) to form so-called lens fibers. New lens cells are added to the margin of the lens throughout life from the lens epithelium, but the cells at the cortex and nucleus (center) of the lens do not undergo turnover or replacement and are therefore the oldest cells in the body of an adult. The lens is avascular and nourished by diffusion from the aqueous and vitreous. The radius of curvature of the anterior surface averages 10 mm, but it is subject to marked changes during accommodation. Because the lens nucleus is formed by increasing density of cortical cells, cortex and nucleus are considered together. Both are made up

exclusively of cells derived from the lens epithelium. The common designation of lens fiber for the cortical cells is a misnomer for the elongated cells of the lens substance. Lens cortical cells are elongated and on cross-section, appear hexagonal in shape. The cortex resembles the cut surface of a honeycomb. In light microscopy, the transition from cortex to nucleus is characterized by less distinct lamellae. The posterior capsule (#5 in the photomicrographs) does not have any epithelium associated with it as the epithelium "migrates" anterior from the len

Photomicrograph of lense

PHYSIOLOGY: Production and drainage of aqueous humor[4,5]

Aqueous humour is secreted into the posterior chamber by the ciliary body, specifically the non-pigmented epithelium of the ciliary body. It flows through the narrow cleft between the front of the lens and the back of the iris, to escape through the pupil into the anterior chamber, and then to drain out of the eye via the trabecular meshwork. From here, it drains into Schlemm's canal by one of two ways: directly, via aqueous vein to the episcleral vein, or indirectly, via

collector channels to the episcleral vein by intrascleral plexus and eventually into the veins of the orbit.

Production

Filtration: As blood flows in the ciliary body's capillaries, it is coarsely filtered by the capillaries' endothelial cells. The resulting plasma is then refiltered by the pigmented and nonpigmented ciliary epithelial cells and is secreted into the posterior chamber before traveling between the lens and iris into the anterior chamber of the eye as aqueous humour.

Diamond-Bossert model: Active transport occurring in the nonpigmented cilary epithelial cells induces small osmotic pressure gradients in between the cells. A higher concentration of solutes in the proximal part of the intercellular space generates a flow of water. The concentration diminishes from the proximal part to the distal part, releasing the liquid into the posterior chamber.

Drainage

Aqueous humour is continually produced by the ciliary processes and this rate of production must be balanced by an equal rate of aqueous humour drainage. Small variations in the production or outflow of aqueous humour will have a large influence on the intraocular pressure.

The drainage route for aqueous humour flow is first through the posterior chamber, then the narrow space between the posterior iris and the anterior lens (contributes to small resistance), through the pupil to enter the anterior chamber. From there, the aqueous humour exits the eye through the trabecular meshwork into Schlemm's canal (a channel at the limbus, i.e., the joining

point of the cornea and sclera, which encircles the cornea) It flows through 25 - 30 collector canals into the episcleral veins. The greatest resistance to aqueous flow is provided by the trabecular meshwork, and this is where most of the aqueous outflow occurs. The internal wall of the canal is very delicate and allows the fluid to filter due to high pressure of the fluid within the eye.

The secondary route is the uveoscleral drainage, and is independent of the intraocular pressure, the aqueous flows through here, but to a lesser extent than through the trabecular meshwork.

The fluid is normally 15 mm (0.6 inch) Hg above atmospheric pressure, so when a syringe in injected the fluid flows easily. If the fluid is leaking, due to collapse and wilting of cornea, the hardness of the normal eye is therefore corroborated. GLAUCOMA AND CATARACT [2-4,7-14] There are no direct relationships between glaucoma and cataract, but the progressivity of those diseases. Cataracts that can cause glaucoma are intumescence cataract, immature cataract (also caused by trauma) and hypermature cataract which are usually occur in older person. There are sudden increased of IOP in intumescence cataract and immature cataract because aqueous humor diffuse from the anterior and posterior chamber of the eye into the lense because of the degeneration process of the lense. Meanwhile, lenses in hypermature cataract which become phacolytic, evidence implicates direct obstruction of outflow pathways by lens protein
released from microscopic defects in the lens capsule that is intact clinically. Glaucoma that can cause cataract is acute glaucoma such as closed angle glaucoma, traumatic glaucoma etc. During acute condition, high IOP compressing the lens, causing ischemic condition to the

cell lining the cortex of the lens. This condition will activate chemical process due to the injury of the cell and later the degenerative process of the lens and deposition of protein in the cortex of the lens. The signs and symptoms patient of glaucoma complicated with cataract and patient of cataract complicated with glaucoma maybe same but differ in the progressivity of the disease. Patient with acute glaucoma will present with sudden severe ocular pain, nausea and vomiting, headache, and blurred,

seeing haloes around lights. Patients may be totally asymptomatic, or they may report incidents of mild pain with slightly blurred vision or seeing haloes around lights. These symptoms resolve spontaneously as the angle reopens. Later when glaucoma reoccur, patient complaint his or her blurred vision does not resolve even there is no glaucoma attack. Meanwhile, glaucoma patient complicated with cataract will come with cataract additional-complains such blurred vision even when there are no glaucoma attacks. Cataract patient comes with glaucoma complication will have the blurred vision first and then as the cataract progress with increased IOP, then there will glaucoma additional-complaint such as ocular pain, headache etc. Aim of the treatment of acute glaucoma attack is to prepare the patient for the surgery which is lowering the increased IOP while the aim of cataract treatment is to remove the cataract. There are many debates in which procedure or treatment is the best for the patient with coincidence glaucoma and cataract. The best management for the treatment of cataract and glaucoma
will likely be the subject of debate for many years to come but it should be remembered that cataract surgery alone can be very helpful, particularly in the setting of angle-closure glaucoma and possibly pseudo-exfoliation. Consideration should be given to the use of mitomycin C(MMC) in combined procedures, especially if a low IOP is desired, and the incision should be positioned to allow for a subsequent trabeculectomy should the bleb fail. There seems to be evidence that separating procedures both in time as well as in location may be preferable. These advantages may be marginal enough that it would be difficult for an individual surgeon to justify altering his or her technique if positive results are

being achieved. Although the care for patients with cataract and glaucoma will always need to be individualized, having evidence-based guidelines can help ophthalmic surgeons optimize the management of these two common and often coexisting conditions.

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