अधिमन्थ की तुलना Glaucoma से की जा सकती है।
Glaucoma is a group of conditions that have a characteristic optic neuropathy associated with visual field defects and elevated intraocular pressure.
Pathophysiology of glaucoma revolves around the aqueous humour circulation.
Aqueous humour – It is derived from the plasma with-in the capillary network of the ciliary The rate of aqueous formation and its drainage are in a state of dynamic equilibrium and thus maintains normal intra ocular pressure (IOP) which ranges between 12 and 20 mm Hg.
The normal outflow is by two routes:
1. Conventional route (Trabecular outflow):
About 80% of the outflow is through this route. The aqueous humour flows to the posterior chamber.
It then flows into anterior chamber via pupil and through the canal of schlemm drains to the episcleral veins.
2. Unconventional route (Uveoscleral outflow):
About 20% of outflow is by this route.
This is the second accessory exit through the ciliary body into the suprachoroidal space and is drained by venous circulation of the ciliary body, choroid and sclera.
Angle of Anterior Chamber-
It plays an important role in the process of aqueous drainage, from anterior to posterior, it is formed of the following structures:
- Schwalbe’s line (Prominent end of Descemet’s membrane of cornea)
- Trabecular meshwork.
- Scleral spur
- Anterior most part of the ciliary body
- Root of iris.
Clinically the various angle structures can be visualised by gonioscopic examination.
- Developmental glaucoma
(a) Congenital glaucoma (Buphthalmos) :- manifests at birth or during the first year of life.
(b) Infantile glaucoma :- occurs within first few years of life.
- Juvenile glaucoma :- occurs between 3 and 16 years of age.
- Primary open-angle glaucoma (POAG) :-
- Primary angle-closure glaucoma (PACG) :-
- Secondary glaucoma
Primary open-angle glaucoma (POAG)
It is a chronic, slowly progressive optic neuropathy associated with elevated I.O.P. and visual field defects.
It is more common than primary angle closure glaucoma.
The intraocular pressure increases dues crease in the aqueous outflow across the trabecular meshwork due to trabecular sclerosis and cells.
Risk factors of POAG include IOP, age, race, family history of glaucoma, myopia, diabers hypertension.
The disease is insidious (spreading gradually without being noticed) and usually asymptomatic and patients have non specific complain such as headache, eyeache of mild intensity and frequent changes in presbyopic correction.
Initially pupil is briskly reacting to light but later becomes sluggish.
The diagnosis depends on
- Raised IOP
- Cupping of optic disk
- Visual field defects
An intraocular pressure of more than 21 mm of Hg on more than one occasion and there could also be an asymmetry of an intraocular pressure of more than 5mm Hg in the two eyes.
The optic disc changes include :
- Vertically oval cup due to selective loss of neural rim tissue in the inferior and superior poles.
The tissue between the cup and disk margin is known as neuroretinal rim.
Normally it has orange color. The rim is widest in the inferior disk regions followed by the superior, the nasal and the temporal disk region (ISNT rule)
- Splinter haemorrhage may be seen on or near the disk in approximately one third of the glaucomatous patients.
- Asymmetry of the cups.
Asymmetry of cup/disk ratio greater than 0.2 between the two eyes is generally seen in nearly 70% of patients with POAG.
- Large cup i.e. 0.6 or more. The normal size is 0.3 to 0.4
- Pallor areas on the disc.
- Pulsation of the retinal arterioles may be seen at the disc margin.
- Nasal shifting of retinal vessels which have the appearance of being broken off at the margin (Bayonetting sign)
- Dark room test : The patient is placed in completely dark room for half an hour. If there is rise in I.O.P. more than 8 mm of Hg test is positive.
- Mydriatic Test : The patients eye is dilated with weak mydriatic. If the tension rises more than 8 mm of Hg, the test is positive.
Primary closed Angle Glaucoma (PACG)
This is a condition in which the intra ocular pressure is raised as a result of obstruction to the outflow of the aqueous humour by closure of a narrower angle of the anterior chamber.
- It is common in 5th-6th decade.
- Women are more prone than males
- Usually bilateral.
- Usually the hypermetropic eye with shallow anterior chamber
- More common in anxious persons with unstable vasomotor system.
The clinical course is divided into following stages:
- Prodromal stage
- Stage of constant instability
- Acute congestive stage
- Chronic closed angle glaucoma
- Absolute glaucoma.
- There are occasional attacks of raised intraocular pressure with blurring of vision.
- Coloured haloes due to corneal oedema.
- Mild headache
- The eye remains white i.e. without congestion even though there may be transient sudden rise in I.O.P. upto 40-50 mm Hg.
Stage of constant instability
- The attacks of raised I.O.P. are more frequent and occur with regularity.
- Exaggeration of normal diurnal variation of intra ocular tension so that the intraocular pressure is raised in the late afternoon.
Acute congestive stage
- Profound diminution of vision
- Intense ciliary congestion
- Intense pain which radiates along the branches of the 5th nerve.
- Rainbow colored haloes around the light.
- Lacrimation, photophobia
- Pupil is semidilated.
- Optic disc is oedematous and hyperaemic.
Chronic closed angle glaucoma
This stage can develop either after acute angle closure or when the angle closes gradually IOP, rises slowly.
A gradual asymptomatic angle closure is known as creeping angle closure.
Clinical picture of chronic angle closure glaucoma resembles that of POAG.
It presents a few symptoms : moderate rise of IOP, opticneuropathy and characteristic visual field defects.
Stage of absolute glaucoma
- The eye becomes painful and blind.
- The anterior ciliary veins are dilated.
- The anterior chamber is very shallow
- The cornea is oedematous and may develop epithelial bullae (bullous keratopathy).
- The iris may show atrophic patches.
- The pupil is dilated and does not react to light and accommodation.
- The optic nerve head is deeply cupped.
- IOP is very high and eyeball is stony hard.
The treatment of glaucoma depends on the nature and severity of each case.
In general it cannot be cured but it can be controlled.
Eye drops, pills, laser procedures and surgical operations are used to prevent further damage.
Types of eye drops
1. Prostaglandin analogue : These increase the flow of aqueous humour out of the eye which reduces the pressure within the eye.
Side effects include –
- Eye pain and irritation
- Sensitivity to light
- Iris pigmentation
- Conjunctival hyperaemia
Some types of prostaglandin analogues include:
Beta-Blockers- They reduce intra ocular pressure by slowing down the production of aqueous humour in the eye.
They are used once or twice a day and can cause side effects such as:
- Burning sensation
- Itchy eye
- Dry eyes
However, they should no be used in patients with bronchial asthma and cardiovascular problems.
Some type of beta-blockers includes –
Timolol maleate- It is a non selective beta-blocker used in 0.25 or 0.5% concentration and administered twice daily.
Levobunolol- It is a nonselective beta-blocker available in 0.25-0.5% concentration.
Betaxolol– It is a selective beta blocker which blocks mainly the b1 -receptor.
Carbonic anhydrase inhibitors- They reduce the amount of aqueous humour produced in eye which reduces intraocular pressure.
These drops are used two of three times a day and may cause :
- A bitter taste in mouth
- Dry mouth
- Eye irritation
Carbonic anhydrase inhibitor may be administered systemically or topically.
Systemic Carbonic anhydrase inhibitors include :
Dichlorphenamide – (Daranide)
Dorzolamide hydrochloride (2%) – lt is administered 3 times daily
Brinzolamide (1%) is used 2-3 times daily.
They are of great use to treat acute forms of glaucoma.
They act by drawing the water out of the eye and reduce the IOP. These medications must be used cautiously as they have significant side effects such as nausea, fluid accumulation in the heart or lungs (Congestive heart failure and pulmonary edema).
Their use is prohibited in patients with uncontrolled diabetes, heart, kidney or liver problems.
The commonly used hypcrosmotic agents are glycerol, mannitol and isosorbide.