NBE CME programme for DNB consultants - National Board Of ...

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NBE CME programme for DNB consultants/ 90 D. Look for Retinal Breaks/ RD Configuration / Traction Bands / Retinal degenerations /Previous RD Surgery bands / Drawing of color coded retinal diagram; Any otherDiscussion- Confirmation of Retinal diagram; Lincoff Role; location of retinal break; Management/ Whether to treat or not / ; Surgical procedure; V R SurgeryMacular LesionsPoints - Micropsia / Macropsia / Metamorphopsia; Smoking; Examine both eyes; Amsler Chart AskFor; 90 D/ 78D / Goldman 3 mirror mandatory MASTER SLIT LAMP BIOMICROSCOPY; Note thesize of Lesion in Disc Diameters; Note other Fundus findings; Whether fresh lesion / old lesion;You may be asked which further investigations you would like to do;Angle Closure GlaucomaHistory- Age ( 40 – 50 yrs); Sex (Female Predisposition); C/o episodes of redness, visual blurring,colored halos formation, mild severe pain, nausea/vomiting; H/o precipitating or relieving factors,if any reading in dim illumination, watching movie in cinema hall, psychological factors, and anxiouspersonality; Timing of attacks; evening or morning (Attacks of ACG occur in evenings/times of dimligh); Frequency & duration of episodes; Spontaneous resolution of such attacks or not; H/o use ofhypermetropic glasses; Differential diagnosis of other causes of colored halos in history; Familyhistory.Clinical Examination-Latent angle closure glaucoma/prod oval stage Pt is a symptomatic; Shallowanterior chamber; Convex lens iris diaphragm; Gonioscopy show occludable angles in at leastthree of four quadrants; Sub acute angle closure glaucomaSigns & symptoms similar to acuteACG, but mild and papillary reactions are present; Resolution is spontaneous. Acute angle closureglaucoma Redness & marked pain in eye, colored halos; Visual acuity – severe diminution ofvisual acuity (may be reduced to light perception or hand motions); Marked ciliary congestion;Pupillary reactions – fixed & mid-dilated pupil; IOP measurement – marked & acute rise of IOP;Examination of cornea – corneal edema; Examination of AC – shallow anterior chamber; Gonioscopy– closed angles on gonioscopy; Fundas optic disc edema in acute stage; Examination of felloweye – the fellow eye shows narrow, occludabel angles or other forms of ACG; Signs of past attacksof ACG patchy iris atrophy (mainly around sphincter area, pigment on the posterior surface ofcornea (Krukenberg spindle), lens glaucomflecken (Vogt’s triad), wide areas of synedchial orappositional closure. Chronk angle closure Progressive diminution of vision; Few symptoms; Mildciliary congestion; Increased IOP; Glaucomatous cupping of optic disc; Gonioscopy showappositional or synechial closure; Fellow eye show similar gonioscopic pictures or narrow angles;Absolute glancoma Painful blind eye; Fixed dilated pupil; Corneal edema; Iris atrophy; Markedlyraised IOP; May be associated with leticular changes or neovascularisation of iris; Advancedglaucomatous cupping.Investigation- Refraction usually hypermetropic. Gonioscopy the following must be observedGrading of angle; Level of iris insertion, both true and apparent; Shape of peripheral iris – convex,concave, flat; Degree of trabecular pigmentation; Areas of iridotrabecular apposition or synechiae;Dynamic indentation gonioscpy to differentiate between appositional or syechial closure; Slit lampgrading of peripheral anterior chamber depth – Van Herick method; Ultrasound biomicroscopy ofthe anterior segment – visualization of iris, iris root, corneoscleral junction, ciliary body andlens.Provocative tests Dark room test; Prone test; Dark room-prone test; (Ensure patient does not go tosleep during above tests); Mydiratic test (homatropine 2%); Combined mydriatic miotic test (Oneeye to be done at a time for the fear of precipitation of attack of ACG).Differential Diagnosis- It mainly requires to differentiate other causes of acute of IOP. Phacolyticglaucoma open angles, mature lens, cells & flare in AC; Phacomorphic glaucoma intumescentcataractous lens with widely dilated pupil; inflammatory glaucoma cells, flare, KPs, open angles;Ghost cell glaucoma H/O vitreous hemorrhage, open angles, khaki cored cells in AC; Neovascularglaucoma closed angles, dilated pupil with ectropin uveae, NVI; Differentiate other causes of104
NBE CME programme for DNB consultantscolored haloes early cataract, mucopurulent conjunctivitis; Differentiate other causes of red eyeacute conjunctivitis, acute uveitis.Non- Surgical Management Acute angle closure The aim is to break the attack; Lower IOP; Safeguardthe fellow eye by appropriate treatment- Intravenous hyperosmotic agent (mannitol 20%), oralacetazolamide and glycerol 50% (consider side effects and contraindications of these when using);Intensive topical pilocarpine 2%. Topical corticosteroid are given to reduce inflammation; Dependingupon IOP control & corneal clarity, laser iridectomy is done; Prophylactic iridectomy in the felloweye; Peripheral argon laser iridoplasty may help breaking an attack; Sub acute ACG Laserirideectomy; Chronic ACG Laser iridectomy with medical treatment / filtering surgery.Argon laser trabeculoplasty Indications- Plateau iris configuration; Acute attack of ACG. ; Discusslimitations of Argon Laser Trabeculoplasty;Surgical treatment- Surgical iridectomy when peripheral anterior synechiae are present in lessthan 50% of angle or when IOP can be controlled by use of miotics only.Trabeculectomy & its modification- when peripheral anterior synechiae are present more than 50%of angle / when miotics fail to control IOP; Goniosynechiolysis.Treatment of absolute glaucoma- (when painful eye) Cyclocrytherapy or cydophotocoagulation;Retrobulbar injection of alcohol; Enucleation as last resort.Always remember to manage fellow eye.Pseudoexfoliation (Pex)History-Usually Asymptomatic; Loss of vision If the disease is very far advanced when diagnosed,the patient may be aware of the loss of vision; Many patients with PEX also develop cataracts andmay present with loss of vision on that basis.Clinical examination- Deposition of whitish exfoliative material. There is deposition of whitish flakelike material on the anterior lens capsule that looks as though it is arising from the surface of thelens; typically there is a disc shaped opacity centrally, a mid-peripheral clear zone and additionalmaterial deposited on the peripheral portion of the lens; the clear zone corresponds to the area ofthe lens in contact with the papillary margin of the iris; additional deposits of this whitish materialmay be seen on the papillary margin, anterior iris stroma, corneal endothelium and the trabecularmeshwork. Pigment Dispersion Some degree of pigment dispersion in the anterior segment isusually seen with corneal endothelial pigment pigment dotting of the anterior iris stroma, and quitecommonly heavy pigment in the trabecular meshwork more marked inferiorly than superiorly; thereis a pigment line seen anterior to the schwalbe’s line on gonioscopy (Sampaolesi’s line). IrisTrans-Illumination Atrophy and trans-illumination defects of the peripupillary iris are often seen.Elevated intra-ocular pressure (IOP) Usually signinficantly elevated and often markedly asymmetriceven without overt signs of glaucoma; often very labile in exfoliative glaucoma; about 20% of patientswith newly diagnosed PEX have glaucoma or elevated IOP; about 50% of patients with PEX willultimately develop exfoliative glaucoms. Shallow Anterior Chamber The anterior chamber isshallower, and the angle is more narrow than average in many patients with exfoliation; howeverangle closure glaucoma is unusual. Optic Disc Cupping Indistinguishable from other forms ofopen-angle glaucoma. Visual Field Loss As with other forms of open-angle glaucoma.Investigations - Diagnosis is based on slit lamp examination; examination under mydriasis ismandatory.Differential diagnosis - Few things are easily confused with PEX - Pigmentary Glaucoma Thepigmentation is diffuse darker “mascara” type and bilateral. The iris trans-illumination defects areelongated radial spokes in the iris periphery contrary to peripupillary location in PEX. Synechiae,Fibrin or Cyclitic Membrane May involve the anterior lens capsule as debris but may lack thehomogenous granular appearance and characteristics flakes of PEX. True Exfoliation (CapsularDelamination) Trauma, exposure to intense heat (e.g., glass blowers) or severe uveitis can causea thin membrane to peel off the anterior less capsule. This usually presents as diaphanous105
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