Glaucoma

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  • Glaucoma
    • IOP is the most common risk for development of glaucoma.
    • ocular hypertension’ is used for cases having constantly raised IOP without any associated glaucomatous damage.
    • normal or low tension glaucoma (NTG/LTG) is suggested for the typical cupping of the disc and/or visual field defects associated with a normal or low IOP.
  • Classification
    • Congenital and developmental glaucomas
      • Primary congenital glaucoma (without associated anomalies).
      • Developmental glaucoma (with associated anomalies).
    • Primary adult glaucomas
      • Primary open angle glaucomas (POAG)
      • Primary angle closure glaucoma (PACG)
      • Primary mixed mechanism glaucoma
    • Secondary glaucomas
  • Pathogenesis of glaucomatous ocular damage
    • all glaucomas are characterized by a progressive optic neuropathy
    • results from the death of retinal ganglion cells (RGCs)
    • Retinal ganglion cell death is  associated with loss of retinal nerve fibres.
  • Etiological factors
    • Raised intraocular pressure (Mechanical theory).
      • causes mechanical stretch on the lamina cribrosa
      • leads to axonal deformation and ischaemia by altering capillary blood flow
      • neurotrophins (growth factors) are not able to reach the retinal ganglion cell bodies in sufficient amount needed for their survival.
    • Pressure independent factors (Vascular insufficiency theory).
      • Failure of autoregulatory mechanism of blood flow.
        • NTG is vasospastic disorders (migranous headache and Raynaud’s phenomenon).
      • Systemic hypotension
        • nocturnal dips in patients with night time administration of antihypertensive drugs cause low vascular perfusion of optic nerve head resulting in NTG.
    • Secondary insults (Excitotoxicity theory)
      • glutamate (excitatory toxin), oxygen free radicals, or nitric oxide which are released when RGCs undergo death due to primary insults
  • Primary developmental/congenital glaucoma
    • abnormally high IOP which results due to developmental anomaly of the angle of the anterior chamber, not associated with any other ocular or systemic anomaly.
    • True congenital glaucoma
      • labelled when IOP is raised during intrauterine life
      • child is born with ocular enlargement.
    • Infantile glaucoma
      • labelled when the disease manifests prior to the child’s third birthday.
      • It occurs in about 50 percent of cases.(most common type )
      • eyeball enlarges and so the term‘buphthalmos’ (bull-like eyes) is used.
      • results due to retention of aqueous humour – it is called ‘hydrophthalmos
    • Juvenile glaucoma
      • develop pressure rise between 3-16 years of life.
  • Prevalence and genetic pattern
    • over 65 percent of the patients are boys.
    • disease is bilateral in 75 percent cases
  • Pathogenesis
    • Trabeculodysgenesis
      • Maldevelopment of trabeculum including the iridotrabecular junction
      • responsible for impaired aqueous outflow resulting in raised IOP.
      • Flat iris insertionis more common than the concave iris insertion.
  • Clinical features
    • Photophobia, blepharospasm, lacrimation and eye rubbing often occur together (MCQ)
    • Corneal signs
      • Corneal oedema.
        • It is frequently the first sign which arouses suspicion.
      • Corneal enlargement.
        • Normal infant cornea measures 10.5 mm.
        • A diameter of more than 13 mm confirms enlargement. (MCQ)
        • Prognosis is usually poor in infants with corneal diameter of more than 16 mm.
      • Tears and breaks in Descemet’s membrane (Haab’s striae). (MCQ)
        • Tears are usually peripheral and concentric with the limbus.
    • Sclera becomes thin and appears blue due to underlying uveal tissue.
    • Anterior chamber becomes deep.
    • Iris may show iridodonesis and atrophic patches in late stage.
    • Lens becomes flat due to stretching of zonules and may even subluxate. (MCQ)
    • Optic disc may show variable cupping and atrophy especially after third year.
    • IOP is raised which is neither marked nor acute.
    • Axial myopia may occur because of increase in axial length which may give rise to anisometropic amblyopia.
  • Differential diagnosis
    • Raised IOP in infantsmay also be associated with retinoblastoma, retinopathy of prematurity, persistent primary hyperplastic vitreous, traumatic glaucoma and secondary congenital glaucoma seen in rubella, aniridia and Sturge-Weber syndrome.
  • Treatment
    • Treatment of congenital glaucoma is primarily surgical.
    • IOP must be lowered by use of hyperosmotic agents, acetazolamide and beta- blockers till surgery is taken up.
    • Miotics are of no use in such cases.
  • Surgical procedures for congenital glaucoma
    • Goniotomy
    • Trabeculotomy. (MCQ)
      • This is useful when corneal clouding prevents visualization of the angle or in cases where goniotomy has failed.
      • The main difficulty in this operation is localization of the Schlemm’s canal.
    • Combined trabeculotomy and trabeculectomy is now-a-days the preferred surgery with better results. (MCQ)
  • Developmental glaucomas with associated anomalies
    • Glaucoma associated with iridocorneal dysgenesis.
      • posterior embryotoxon characterised by a prominent Schwalbe’s ring (Axenfeld anomaly)
      • Rieger anomaly
      • Peter’s anomaly
    • Glaucoma associated with ectopia lentis syndromes
      • Marfan’ s syndrome,
      • Weil-Marchesani syndrome
      • homocystinuria.
    • Glaucoma associated with phakomatosis
      • Sturge-Weber syndrome ( 50% cases)
      • Von Recklinghausen’s neurofibromatosis (25% cases).
    • Lowe’ s syndrome – oculo-cerebro-renal syndrome
  • Primary open angle glaucoma
    • also known as chronic simple glaucoma of adult onset
    • typically characterised by slowly progressive raised intraocular pressure (>21 mmHg)
    • It forms about one- third cases of all glaucomas.
  • Etiopathogenesis
    • Predisposing and risk factors.
      • POAG has a polygenic inheritance
      • POAG is more commonly seen in elderly between 5th and 7th decades.
      • develops earlier and is more severe in black people than in white.
      • Myopesare more predisposed than the normal (MCQ)
      • Diabeticshave a higher prevalence of POAG (MCQ)
      • Cigarette smokingis also thought to increase its risk.
      • Systemic hypertension does not rise IOP
      • prevalence of POAG is more in hypertensives than the normotensives.
      • Thyrotoxicosis is not a risk factor for POAG (MCQ)
      • prevalence of POAG is more in patients suffering from Graves’ ophthalmic disease
    • Corticosteroid responsiveness.
      • six weeks topical steroid therapy cause  significant rise of IOP.
  • CLINICAL FEATURES
    • Symptoms
      • The disease is insidious
      • usually asymptomatic, until it has caused a significant loss of visual field
        • Therefore, periodic eye examination is required after middle age.
      • Patients may experience mild headache and eyeache.
      • Rarely, patient may notice a defect in the visual field.
      • Reading and close work often present increasing difficulties
        • accommodative failure due to constant pressure on the ciliary muscle and its nerve supply.
        • patients usually complain of frequent changes in presbyopic glasses (MCQ)
      • Patients develop delayed dark adaptation
    • Signs
      • Anterior segment signs
        • slit-lamp biomicroscopy may reveal normal anterior segment
        • In late stages pupil reflex becomes sluggish and cornea may show slight haze.
      • Intraocular pressure changes.
        • In the initial stages
          • the IOP may not be raised permanently
          • but there is an exaggeration of the normal diurnal variation.
        • Diurnal variation test
          • repeated observations of IOP (every 3-4 hour), for 24 hours is required during this stage).
          • Patterns of diurnal variations of IOP
            • morning rise seen in 20% cases of POAG
            • afternoon rise seen in 25% cases of POAG;
            • biphasic variation seen in 55% cases of POAG.
          • In most patients IOP falls during the evening, contrary to what happens in closed angle glaucoma
          • A variation in IOP of over 5 mm Hg (Schiotz) is suspicious and over 8 mm of Hg is diagnostic of glaucoma. (MCQ)
        • In later stages, IOP is permanently raised above 21 mm of Hg and ranges between 30 and 45 mm of Hg. (MCQ)
    • Optic disc changes
      • provide an important clue for suspecting POAG
      • These are typically progressive, asymmetric
      • present a variety of characteristic clinical patterns.
      • It is essential to record the appearance of the nerve head
      • Record subtle glaucomatous changes over the course of follow-up evaluation.
      • Confocal scanning laser topography (CSLT) i.e., Heidelberg retinal tomograph (HRT) is an accurate and sensitive method for this purpose.
      • advanced imaging techniques
        • optical coherence tomography (OCT)
        • scanning laser polarimetry i.e., Nerve fibre analyser (NFA).
      • Early glaucomatous changes
        • Vertically oval cup (MCQ)
          • due to selective loss of neural rim tissue in the inferior and superior poles.
        • Asymmetry of the cups
          • A difference of more than 0.2 between two eyes is significant.
        • Large cup
          • 0.6 or more (normal cup size is 0.3 to 0.4)
          • occur due to concentric expansion.
        • Splinter haemorrhages present on or near the optic disc margin.
        • Pallor areas on the disc.
        • Atrophy of retinal nerve fibre layer (MCQ)
          • may be seen with red free light.
      • Advanced glaucomatous changes in the optic disc
        • Marked cupping (cup size 0.7 to 0.9) (MCQ)
          • Excavation may even reach the disc margin
          • the sides are steep and not shelving (unlike deep physiological cup).
        • Thinning of neuroretinal rim
          • seen as a crescentric shadow adjacent to the disc margin.
        • Nasal shifting of retinal vessels
          • Bayonetting sign (MCQ)
            • have the appearance of being broken off at the margin
            • When the edges overhang, the course of the vessels as they climb the sides of the cup is hidden.
        • Pulsations of the retinal arterioles
          • seen at the disc margin
          • a pathognomic sign of glaucoma (MCQ)
          • occur when IOP is very high.
        • Lamellar dot sign (MCQ)
          • pores in the lamina cribrosa are slit-shaped and are visible up to the margin of the disc.
  • Glaucomatous optic atrophy.
    • optic nerve head appears white and deeply excavated
    • Cavernous optic atrophy
          • ischaemic atrophy of the nerve fibres without corresponding increase of supporting glial tissue.
          • As a result, large caverns or lacunae are formed
  • Visual field defects.
        • Distribution of retinal nerve fibres
          • Fibres from nasal half of the retina
            • come directly to the optic disc
            • as superior and inferior radiating fibres (srf and irf).
          • Those from the macular area
            • come horizontally as papillomacular bundle (pmb).
          • Fibres from the temporal retina
            • arch above and below the macula and papillomacular bundle
            • arch as superior and inferior arcuate fibres with a horizontal raphe in between (saf and iaf).
        • Arrangement of nerve fibres within optic nerve head
          • fibres from the peripheral part of the retina
            • lie deep in the retina
            • occupy the most peripheral (superficial) part of the optic disc.
          • fibres originating closer to the nerve head
            • lie superficially in the retina
            • occupy a more central (deep) portion of the disc.
        • Arcuate nerve fibres Versus Macular fibres (MCQ)
          • Arcuate nerve fibres occupy the superior and inferior temporal portions of optic nerve head
            • most sensitive to glaucomatous damage (MCQ)
            • account for the early loss in the corresponding regions of the visual field.
          • Macular fibres
            • most resistant to the glaucomatous damage
            • explain the retention of the central vision till end
  • Progression of field defects.
  • Visual field defects in glaucoma are initially observed in Bjerrum’s area (MCQ)
    • Bjerrum’s area isan arcuate area extending above and below the blind spot to between 10o and 20o of fixation point
  • Sequence of changes in natural history of the progressive glaucomatous field loss
    • Isopter contraction (MCQ)
          • mild generalised constriction of central as well as peripheral field
          • It is the earliest visual field defect occurring in glaucoma.
          • it is of limited diagnostic value, as it may also occur in many other conditions.
    • Baring of blind spot (MCQ)
          • exclusion of the blind spot from the central field
          • occur due to inward curve of the outer boundary of 30° central field
          • an early glaucomatous change
          • very non-specific and thus of limited diagnostic value.
    • Small wing-shaped paracentral scotoma
          • It is the earliest clinically significant field defect.
          • It may appear either below or above the blind spot in Bjerrum’s area.
    • Seidel’s scotoma. (MCQ)
          • With the passage of time paracental scotoma joins the blind spot to form a sickle shaped scotoma known as Seidel’s scotoma
    • Arcuate or Bjerrum’s scotoma. (MCQ)
          • It is formed at a later stage
          • Formed by the extension of Seidel’s scotoma in an area either above or below the fixation point to reach the horizontal line
          • Damage to the adjacent fibres causes a peripheral breakthrough.
    • Ring or double arcuate scotoma.
          • It develops when the two arcuate scotomas join together
    • Roenne’s central nasal step. (MCQ)
          • It is created when the two arcuate scotomas run in different arcs and meet to form a sharp right-angled defect at the horizontal meridian
        • The peripheral nasal step of Roenne’s
          • results from unequal contraction of the peripheral isopter.
    • Advanced glaucomatous field defects.
          • eventually only a small island of central vision (tubular vision) and an accompanying temporal island are left.
          • The temporal island of the visionis more resistant and is lost in the end leaving the patient with no light perception.
  • POAG may sometimes be associated with
      • high myopia
      • Fuchs’ endothelial dystrophy
      • retinitis pigmentosa
      • central retinal vein occlusion
      • primary retinal detachment.
  • INVESTIGATIONS
    • Tonometry.
      • Applanation tonometry should be preferred over Schiotz tonometry
      • Diurnal variation test is especially useful in detection of early cases
    • Gonioscopy.
      • It reveals a wide open angle of anterior chamber.
      • Its primary importance in POAG is to rule out other forms of glaucoma.(MCQ)
    • Documentation of optic disc changes is of utmost importance
    • Slit-lamp examination of anterior segment to rule out causes of secondary open angle glaucoma.
    • Perimetry to detect the visual field defects.
    • Nerve fibre layer analyzer (NFLA)
      • helps in detecting the glaucomatous damage to the retinal nerve fibres before the appearance of actual visual field changes and/or optic disc changes.
    • Provocative testsare required in border-line cases.
      • water drinking test – test commonly performed
        • A rise of 8 mm of Hg or more is said to be diagnostic of POAG.
      • combined water drinking and tonography(MCQ)
      • bulbar pressure test
      • prescoline test
      • caffeine test.
  • DIAGNOSIS
    • 3 diagnostic entities
      • Primary open angle glaucoma (POAG).
        • raised IOP (>21 mm of Hg) is associated with definite glaucomatous optic disc cupping and visual field changes.
      • Ocular hypertension or glaucoma suspect.
        • when a patient has an IOP constantly more than 21 mm of Hg but no optic disc or visual field changes
      • Normal tension glaucoma (NTG) or low tension glaucoma (LTG)
        • when typical glaucomatous disc cupping with or without visual field changes is associated with an intraocular pressure constantly below 21 mm of Hg

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  • MANAGEMENT
    • perform a good baseline examination with which future progress can be compared. visual acuity
      • slit-lamp examination of anterior segment
      • tonometry (preferably with applanation tonometer)
      • optic disc evaluation (preferably with fundus photography)
      • gonioscopy
      • visual field charting.
  • Medical therapy
    • The initial therapy of POAG is still medical, with surgery as the last resort.(MCQ)
    • Basic principles of medical therapy of POAG
      • Identification of target pressure.
      • progression is uncommon if IOP is maintained at less than 16 to 18 mm of Hg in patients having mild to maderate damage.
      • Lower target pressures (12-14 mmHg) are required in patients with severe damage.
    • Treatment regimes.
      • Single drug therapy
        • Topical beta-blockers
          • first drug of choice for medical therapy of POAG in poor and average income patients.
          • Lower IOP by reducing the aqueous secretion due to their effect on beta – receptors in the ciliary processes.
        • Timolol maleate  
          • should not be used in patients having associated bronchial asthma and/or heart blocks.(MCQ)
        • Betaxolol
          • a selective beta-1 blocker
          • it is preferred as initial therapy in patients with cardiopulmonary problems.
        • Levobunolol
          • Its action lasts the longest (MCQ)
          • more reliable for once a day use than timolol.
        • Carteolol
          • It affect lipid profile the least.
          • Therefore, it is the best choice in patients with POAG having associated hyperlipidemias or atherosclerotic cardiovascular disease.
        • Pilocarpine
          • contracts longitudinal muscle of ciliary body and opens spaces in trabecular meshwork
          • it mechanically increases aqueous outflow.
          • It is sheet anchor in the medical management of POAG for a long time.(MCQ) presently it is not being preferred as the first drug of choice or even as second choice.
          • presently pilocarpine is being considered only as an adjunctive therapy
          • in younger patients it causes problems due to
            • spasm of accommodation
            • miosis.
          • Most, but not all, older patients tolerate pilocarpine very well
            • axial lenticular opacities when present precludes its use in many such patients.
        • Latanoprost (MCQ)
          • It is a prostaglandin
          • decreases the IOP by increasing the uveo-scleral outflow of aqueous.
          • considered the drug of first choice for the treatment of POAG
          • it is expensive to buy
          • it is a very good adjunctive drug to beta-blockers, dorzolamide and even pilocarpine when additional therapy is indicated.
        • Dorzolamide
          • topical carbonic anhydrase inhibitor
          • lowers IOP by decreasing aqueous secretion.
          • It has replaced pilocarpine as the second line of drug and even as an adjunct drug.
        • Adrenergic drugs
          • Epinephrine hydrochloride and dipivefrine hydrochloride  (MCQ)
          • lower the IOP by increasing aqueous outflow by stimulating beta recepters in the aqueous outflow system.
          • These are characterized by a high allergic reaction rate.
          • long-term use is a risk factor for failure of filtration glaucoma surgery.
          • epinephrine compounds are no longer being used as first line or second line drug.
        • Brimonidine  (MCQ)
          • It is a selective alpha-2-adrenergic agonist
          • lowers IOP by decreasing aqueous production.
          • increased allergic reactions and tachyphylaxis rates
      • Combination topical therapy
        • a combination of two drugs
          • one drug which decreases aqueous production
            • timolol
            • other betablocker,
            • brimonidine
            • dorzolamide
          • other drug which increase aqueous outflow
            • latanoprost
            • brimonidine
            • pilocarpine
  • Argon or diode laser trabeculoplasty (ALT or DLT)
    • considered in patients where IOP is uncontrolled despite maximal tolerated medical therapy.
    • shown to lower IOP by
      • 8-10 mm of Hg in patients on medical therapy
      • 12-16 mm in patients who are not receiving medical treatment.
    • Complications.
      • transient acute rise of IOP
        • can be prevented by pretreatment with pilocarpine and/or acetazolamide
      • inflammation
        • can be lessened by use of topical steroids for 3-4 days.
      • Haemorrhage
      • Uveitis
      • peripheral anterior synechiae
        • reduced accommodation
  • Surgical therapy
    • Eyes with advanced disease  having very high IOP, advanced cupping and advanced field loss should be treated with filtration surgery as primary line of management.
    • Trabeculectomy
      • most frequently performed filtration surgery now-a-days.
      • successfully controls the IOP (below 21 mm of Hg)
  • Ocular hypertension or glaucoma suspect
    • when a patient has an IOP constantly more than 21 mm of Hg but no optic disc or visual field changes.
    • should be treated as cases of POAG in the presence of high risk factors
    • High risk factors
      • Significant diurnal variation
        • difference of more than 8 mm of Hg between the lowest and the highest values of IOP.
      • Significantly positive water drinking provocative test.
      • When associated with splinter haemorrhages over or near the optic disc.
      • IOP constantly more than 28 mm of Hg.
      • Retinal nerve fibre large defects.
      • Parapapillary changes.
      • Central corneal thickness < 555 μm.
      • Significant asymmetry in the cup size of the two eyes, i.e., a difference of more than 0.2.
      • Strong family history of glaucoma.
      • When associated with high myopia, diabetes or pigmentary changes in the anterior chamber.
  • Normal tension glaucoma
    • when typical glaucomatous disc changes with or without visual field defects are associated with an intraocular pressure (IOP) constantly below 21 mm of Hg. Characterstically the angle of anterior chamber is open on gonioscopy
    • there is no secondary cause for glaucomatous disc changes.
    • result from chronic low vascular perfusion, which makes the optic nerve head susceptible to normal IOP.
    • Associations of NTG
      • Raynauld phenomenon i.e., peripheral vascular spasm on cooling,
      • Migraine
      • Nocturnal systemic hypotension
      • Overtreated systemic hypertension.
      • Reduced blood flow velocity in the ophthalmic artery (as revealed on transcranial Doppler ultrasonography).
    • Treatment
      • Betaxolol may be considered the drug of choice because in addition to lowering IOP it also increases optic nerve blood flow.
      • Other beta blockers and adrenergic drugs (such as dipiverafrine) should better be avoided
        • these cause nocturnal systemic hypotension
        • likely to affect adversely the optic nerve perfusion
      • Drugs with neuroprotective effect like brimonidine may be preferred.
      • Prostaglandin analogues, e.g., latanoprost tend to have a greater ocular hypotensive effect in eyes with normal IOP.
      • Trabeculectomy may be considered when progressive field loss occurs despite IOP in lower teens.
      • Systemic calcium channel blockers (e.g., nifedipine)
      • Monitoring of systemic blood pressure should be done for 24 hours.
        • If nocturnal dip is detected, it may be necessary to avoid night dose of anti-hypertensive medication.
      • Primary angle-closure glaucoma (PACG) UCOMA
  • Predisposing risk factors.
    • Anatomical factors
      • Hypermetropic eyes with shallow anterior chamber.(MCQ)
      • Eyes in which iris-lens diaphragm is placed anteriorly.
      • Eyes with narrow angle of anterior chamber, which may be due to:
        • small eyeball
        • relatively large size of the lens and smaller diameter of the cornea
        • bigger size of the ciliary body.
      • Plateau iris configuration.
    • General factors i
      • PACG is comparatively more common in 5th decade of life.
      • Females are more prone to get PACG than males (male to female ratio is 1:4)
      • It is more common in nervous individuals with unstable vasomotor system.
      • Peak incidence is reported in rainy season.
      • Family history.
      • It is more common in South-East Asians, Chinese and Eskimos but uncommon in Blacks.
      • In Asians it presents in the 5th to 6th decade and accounts for 50% of primary adult glaucomas in this ethnic group.
  • Precipitating factors (MCQ)
    • Dim illumination,
    • Emotional stress,
    • Use of mydriatic drugs like atropine, cyclopentolate, tropicamide and phenylephrine.
  • Mechanism of rise in IOP – Sequence of events
    • First of all there occurs mid dilatation of the pupil which increases the amount of apposition between iris and anteriorly placed lens with a considerable pressure resulting in relative pupil block
    • Consequently the aqueous collects in the posterior chamber and pushes the peripheral flaccid iris anteriorly (Iris bombe)
    • results in appositional angle closuredue to iridocorneal contact
    • Eventually there occurs rise in IOP which is transient to begin with.
    • But slowly the appositional angle closure is converted into synechial angle closure (due to formation of peripheral anterior synechiae)
      • an attack of rise in IOP  lasts long.
  • CLINICAL PRESENTATION
    • In clinical practice following clinical presentations are seen:
      • Latent primary angle-closure glaucoma (primary angle-closure glaucoma suspect).
      • Subacute (intermittent) primary angle-closure glaucoma.
      • Acute primary angle-closure glaucoma.
      • Postcongestive angle-closure glaucoma,
      • Chronic primary angle-closure glaucoma, and
      • Absolute glaucoma
  • Latent primary angle-closure glaucoma
    • eyes have shallow anterior chamber associated with an occludable angle.
      • Clinical features
        • Symptoms are absent in this stage.
        • Signs.
          • Eclipse sign.
            • Indicates decreased axial anterior chamber depth
            • can be elicited by shining a penlight across the anterior chamber from the temporal side and noting a shadow on the nasal side
          • Slit-lamp biomicroscopic signs include:
            • Decreased axial anterior chamber depth,
            • Convex shaped iris lens diaphragm
            • Close proximity of the iris to cornea in the periphery.
          • Gonioscopic examination shows
            • very narrow angle – Shaffer grade I
            • pigmented trabecular meshwork is not visible without indentation or manipulation in at least three of the four quadrants
          • Van Herick slit-lamp grading of the angle
            • peripheral anterior chamber depth (PACD) is compared to the adjacent corneal thickness (CT)
            • Grade 4 (Wide open angle): PACD = 3/4 to 1 CT  
            • Grade 3 (Mild narrow angle): PACD = 1⁄4 to 1⁄2 CT
            • Grade 2 (Moderate narrow angle): PACD = 1⁄4 CT
            • Grade 1 ( Extremely narrow angle): PACD <1⁄4CT
            • Grade 0 (closed angle): PACD = Nil
      • Diagnosis
        • Prone-darkroom test
        • Best and physiologic
        • An increase in IOP of more than 8 mm Hg is considered diagnostic of PACG.
        • Mydriatic provocative test
          • not physiological
          • drugs  used to produce a mid-dilated pupil
            • a weak mydriatic (e.g., 0.5% tropicamide)
            • simultaneously a mydriatic and miotic (10% phenylephrine and 2% pilocarpine)
          • A pressure rise of more than 8 mm Hg is considered positive.
        • Inferences from provocative tests
          • A positive provocative test indicates that angle is capable of spontaneous closure.
          • A negative provocative test in the presence of a narrow angle of anterior chamber does not rule out a possibility of spontaneous closure.
      • Treatment
        • Prophylactic laser iridotomy should be performed in both eyes of all the patients diagnosed as latent angle-closure glaucoma.
        • If untreated, the risk of acute pressure rise during the next 5 years is about 50%.
  • Subacute or intermittent primary angle-closure glaucoma
    • an attack of transient rise of IOP (40-50 mmHg) which may last for few minutes to 1-2 hours.
    • Such an attack in a patient with occludable angle is usually precipitated by :
      • Physiological mydriasis
        • while reading in dim illumination
        • watching television or cinema in a darkened room
        • during anxiety (sympathetic overactivity)
      • Physiological shallowing of anterior chamber
        • after lying in prone position.
  • Clinical features
    • The episode of subacute PACG
      • unilateral transient blurring of vision
      • coloured halos around light (MCQ)
      • headache
      • browache and eyeache on the affected side.
    • Self-termination of the attack occurs possibly due to physiological miosis induced by bright light, sleep or otherwise.
    • Usually during examination the eye is white and not congested.
  • Differential diagnosis of coloured halos in PACG.
    • Coloured halos in PACG
      • occur due to
        • accumulation of fluid in the corneal epithelium
        • alteration in the refractive condition of the corneal lamellae.
      • Patient typically gives history of seeing colours distributed as in the spectrum of rainbow (red being outside and violet innermost) while watching on a lighted bulb or the moon.
    • Coloured halos in acute purulent conjunctivitis
      • the halos can be eliminated by irrigating the discharge.
    • Fincham’s test (MCQ)
      • halos of glaucoma and immature cataract can be differentiated
      • a stenopaeic slit is passed across the pupil
      • During this test glaucomatous halo remains intact
      • a halo due to cataract is broken up into segments
  • Acute primary angle-closure glaucoma
    • occurs due to a sudden total angle closure leading to severe rise in IOP
    • It usually does not terminate of its own
    • This is sight threatening emergency.
  • Clinical features
    • Pain.
      • sudden onset of very severe pain in the eye
      • radiates along the branches of 5th nerve.
    • Nausea, vomiting and prostrations are frequently associated with pain.
    • Rapidly progressive impairment of vision, redness, photophobia and lacrimation develop in all cases.
    • Past history. in 5 percent patients
    • Lids may be oedematous,
    • Conjunctiva is chemosed, and congested
      • Both conjunctival and ciliary vessels are congested
    • Corneabecomes oedematous and insensitive,
    • Anterior chamber is very shallow.
      • Aqueous flare or cells may be seen in anterior chamber
    • Angle of anterior chamber is completely closed as seen on gonioscopy (shaffer grade 0),
    • Iris may be discoloured,
    • Pupil
      • semidilated, vertically oval and fixed. It
      • is non-reactive to both light and accommodation, (MCQ)
    • IOP is markedly elevated, usually between 40 and 70 mm of Hg,
    • Optic disc is oedematous and hyperaemic,
    • Fellow eye shows shallow anterior chamber and a narrow angle (latent angle closure glaucoma).
  • Management
    • It is essentially surgical
    • Medical therapy
      • Systemic hyperosmotic agent intravenous mannitol
      • Acetazolamide (a carbonic anhydrase inhibitor) (MCQ)
      • Analgesics and anti-emetics as required.
      • Pilocarpine eyedrops
        • should be started after the IOP is bit lowered by hyperosomtic agents.
        • At higher pressure iris sphincter is ischaemic and unresponsive to pilocarpine.
      • Beta blocker eyedrops like timolol maleate or betaxolol
      • Corticosteroid eyedrops
    • Surgical treatment
      • Peripheral iridotomy.
        • Indications
          • peripheral anterior synechiae are formed in less than 50 percent of the angle of anterior chamber
          • as prophylaxis in the other eye.
          • Peripheral iridotomy re-establishes communication between posterior and anterior chamber
          • it bypasses the pupillary block and thus helps in control of PACG
      • Laser iridotomy
        • a non-invasive procedure
        • good alternative to surgical iridectomy. (MCQ)
      • Filtration surgery.
        • Indications
          • IOP is not controlled with the best medical therapy following an attack of acute congestive glaucoma
          • when peripheral anterior synechiae are formed in more than 50 percent of the angle of the anterior chamber.
    • Clear lens extraction by phacoemulsification with intraocular lens implantation
    • Prophylactic treatment in the normal fellow eye
      • Prophylactic laser iridotomy (preferably) or surgical peripheral iridectomy should be performed on the fellow asymptomatic eye. (MCQ)
  • Postcongestive angle-closure glaucoma
    • refers to the clinical status of the eye after an attack of acute PACG with or without treatment.
    • Ciliary body shut down
    • temporary cessation of aqueous humour secretion
    • occurs due to ischaemic damage to the ciliary epithelium after an attack of acute PACG.
    • IOP is low and pain is markedly reduced.
    • Subsequent recovery of ciliary function may lead to chronic elevation of IOP with cupping and visual field defects.
    • Vogt’s triad (MCQ)
      • seen in patients with
        • any type of postcongesive glaucoma
        • treated cases of acute congestive glaucoma.
      • It is characterized by:
        • Glaucomflecken (anterior subcapsular lenticular opacity)
        • Patches of iris atrophy
        • Slightly dilated non-reacting pupil (due to sphincter atrophy)
  • Chronic primary angle-closure glaucoma
    • Gonioscopy
      • gonioscopic findings provide the only differentiating feature between POAG and chronic PACG.
      • reveals a variable degree of angle closure.
      • Permanent peripheral anterior synechiae do not usually develop until late.
    • Treatment
      • Laser iridotomyalone or along with medical therapy should be tried first.
      • Trabeculectomy (filtration surgery) is needed when the above treatment fails to control IOP.
      • Prophylactic laser iridotomyin fellow eye must also be performed.
  • Absolute primary angle-closure glaucoma
    • Painful blind eye. (MCQ)
    • Perilimbal reddish blue zone
      • a slight ciliary flush around the cornea due to dilated anterior ciliary veins.
    • Caput medusae
      • a few prominent and enlarged vessels are seen in long standing cases.
    • Cornea in early cases is clear but insensitive.
      • Slowely it becomes hazy
      • develops epithelial bullae (bullous keratopathy) or filaments (filamentary keratitis).
    • Anterior chamber is very shallow.
    • Iris becomes atrophic.
    • Pupil becomes fixed and dilated and gives a greenish hue.
    • Optic disc shows glaucomatous optic atrophy.  
    • Intraocular pressure is high
    • eyeball becomes stony hard.
    • Management of absolute glaucoma
      • Retrobulbar alcohol injection
        • It destroys the ciliary ganglion.
      • Destruction of secretory ciliary epithelium to lower the IOP
        • carried out by
          • cyclo cryotherapy
          • cyclodiathermy
          • cyclophotocoagulation.
      • Enucleation of eyeball. (MCQ)
        • It may be considered when pain is not relieved by conservative methods.
    • Complications.
      • Corneal ulceration.
      • Staphyloma formation.
        • sclera becomes very thin and atrophic
        • sclera ultimately bulges out either in the
          • ciliary region (ciliary staphyloma) (MCQ)
          • equatorial region (equatorial staphyloma).
      • Atrophic bulbi.
        • Ultimately the ciliary body degenerates
        • IOP falls and the eyeball shrinks.(MCQ)
  • LENS-INDUCED (PHACOGENIC) GLAUCOMAS
    • Phacomorphic glaucoma
          • acute secondary angle-closure glaucoma
          • caused by :
            • Intumescent lens main cause of phacomorphic glaucoma.
              • swollen cataractous lens due to
                • rapid maturation of cataract
                • following traumatic rupture of capsule
            • Anterior subluxation
            • dislocation of the lens and spherophakia (congenital small spherical lens)
          • Cataract extractionwith implantation of PCIOL
            • main treatment of phacomorphic glaucoma
            • should be performed once the eye becomes quite
        • Phacolytic glaucoma (Lens protein glaucoma)
          • a type of secondary open angle glaucoma
          • trabecular meshwork is clogged by the lens proteins and macrophages which have phagocytosed the lens proteins.
          • Leakage of the lens proteins occurs through an intact capsule in the hypermature (Morgagnian) cataractous lens.(MCQ)
          • Management.
            • extraction of the hypermature cataractous lens with PCIOL implantation.
        • Lens particle glaucoma
          • a type of secondary open angle glaucoma
          • trabecular meshwork is blocked by the lens particles floating in the aqueous humour.
          • occur due to lens particles left after
            • extracapsular cataract extraction (MCQ)
            • following traumatic rupture of the lens.
          • Management
            • medical therapy to lower IOP
            • irrigation-aspiration of the lens particles from the anterior chamber.
        • Glaucoma associated with phacogenic uveitis
          • IOP is raised due to inflammatory reaction of the uveal tissue excited by the lens matter.
          • trabecular meshwork is clogged by both inflammatory cells and the lens particles.
          • Management
            • medical therapy to lower IOP
            • treatment of iridocyclitis with steroids and cycloplegics
            • Irrigation-aspiration of the lens matter from anterior chamber
        • GLAUCOMAS-IN-APHAKIA/PSEUDOPHAKIA
          • It includes following conditions:
            • Raised IOP with deep anterior chamber in early postoperative period:
              • It may be due to hyphaema, inflammation, retained cortical matter or vitreous filling the anterior chamber.
            • Secondary angle-closure glaucoma due to flat anterior chamber.
              • It may occur following long- standing wound leak.
            • Secondary angle-closure glaucoma due to pupil block.
              • It may occur following formation of annular synechiae or vitreous herniation.
            • Undiagnosed pre-existing primary open-angle glaucoma may be associated with aphakia/ pseudophakia.
            • Steroid-induced glaucoma.
              • develop in patients operated for cataract due to postoperative treatment with steroids.
            • Epithelial ingrowth
              • may cause an intractable glaucoma in late postoperative period by invading the trabeculum and the anterior segment structures.
            • Aphakic/pseudophakic malignant glaucoma (MCQ)
        • STEROID-INDUCED GLAUCOMA (MCQ)
          • a type of secondary open-angle glaucoma
          • develops following topical, and sometimes systemic steroid therapy.
        • PERIPHERAL IRIDECTOMY
          • Indications
            • Treatment of all stages of primary angle-closure glaucoma.(MCQ)
            • Prophylaxis in the fellow eye.
          • Laser iridotomy should always be perferred over surgical iridectomy.
        • Trabeculectomy
          • Trabeculectomyis the most frequently performed partial thickness filtering surgery till date.
          • Indications
            • Primary angle-closure glaucoma with peripheral anterior synechial involving more than half of the angle.
            • Primary open-angle glaucoma not controlled with medical treatment.
            • Congenital and developmental glaucomas where trabeculotomy and goniotomy fail.
            • Secondary glaucomas where medical therapy is not effective.
          • Mechanism
            • A new channel (fistula) is created around the margin of scleral flap, through which aqueous flows from anterior chamber into the subconjunctival space.
            • If the tissue is dissected posterior to the scleral spur, a cyclodialysis may be produced leading to increased uveoscleral outflow.
  • CYCLO-DESTRUCTIVE PROCEDURES
        • Cyclo-destructive procedures lower IOP by destroying part of the secretory ciliary epithelium thereby reducing aqueous secretion.
        • Indications. These procedure are used mainly in absolute glaucomas.
        • Cyclo-destructive procedures in current use are:
        • Cyclocryotherapy (most frequent),
        • Nd: Yag laser cyclodestruction, and
        • Diode laser cyclophotocoagulation.

Introduction To Glaucoma

Glaucoma

Development of Glaucoma Animation, Open Angle vs Angle Closure Glaucoma

Glaucoma: The Silent Blinding Disease

Cure for Glaucoma

What Is Glaucoma?

Glaucoma Surgery