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Opthalmology

The document provides a comprehensive overview of key concepts in ophthalmology, including refractive errors like myopia, hyperopia, and astigmatism, along with their causes and corrective measures. It covers cataracts, their types, management, and surgical options, as well as corneal diseases and their treatments. Additionally, it discusses the anatomy and physiology of the lens and cornea, along with diagnostic techniques and complications associated with various conditions.
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0% found this document useful (0 votes)
142 views49 pages

Opthalmology

The document provides a comprehensive overview of key concepts in ophthalmology, including refractive errors like myopia, hyperopia, and astigmatism, along with their causes and corrective measures. It covers cataracts, their types, management, and surgical options, as well as corneal diseases and their treatments. Additionally, it discusses the anatomy and physiology of the lens and cornea, along with diagnostic techniques and complications associated with various conditions.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF or read online on Scribd
OPHTHALMOLOGY QUICK REVISION NOTES OPTICS + Total Power- 58 - 60D + 2/3rd is by Air-Cornea interface: most important refractive surface: 45D EMMETROPLA - Absence of refractive error AMETROPLA - Presence of refractive error BDO: 91 Qo) 1, Myopia + Short sightedness without the use of glasses. + Eyeball is longer in size + Concave lenses , mirus lenses (Diverging lenses) 2. Hyperopia + Long sightedness + Eyeball is smaller in size + Convex lenses, Plus lenses 3. Astigmatism + Refractive error whichis different indifferent direction . + Cylindrical lenses Refractive errors can be caused by + Axial - Change in eyeball size + Curvature - Curvature of the cornea is different, Corrected by refractive surgery + Index - Change in the refractive index of the lens , Age related Nuclear Cataract > Myopic shift. DOC in May! + Positional ~ Change in the position of the lens ‘Anteriorly / Posteriorly MYOPIA + High Myopia ~ Refractive error is > 6 D + Pathological Myopia ~ Changes in the retina of the eye. Different pathological changes: +The Myopic Fundus + Temporal myopic crescent ~ seen at the optic disc on the temporal side + Thinning of retina + Macular degeneration - Foster fuch spots (Hyperpigmentation / Hemorrhage). + Tessellated Fundus- Tigroid fundus, Underlying choroidal vessels are visible, ing & + Patients are predisposed to Retinal Detachment in High myopia -> Peripheral Retinal degeneration: Lattice degeneration + Stophyloma~ (Bulging of the outer coat of eye) MCC of Posterior staphyloma - High Myopia ® + Pseudo Popillitis Types of Hypermetropia : 75 Ophthalmology Equatorial choroiditis Staphyloma - seen after recurrent Anterior Staphyloma - seen after corneal ulcer perforation where there is pseudo cornea formation. iliary Staphyloma - At the ciliary body, outbulging of the outer coat Intercalary Staphyloma - At the root of Tris. HYPERMETROPIA ype + Able to see far object without accommodation + Not able to see near object + Asthenopia + Eyeball size is smaller + Predisposed to Angle closure Glaucoma? + Silk shot retina | TOTAL HYPERMETROPIA | Latent hypermetropia Manifest hy ypermetropia Tone of ciliary muscles | Facultative hypermetropia Absolute hypermetropia foconeedatve oor | DOC in MayKing & Cerebellum Quick Revision Notes ASTIGMATISM Type of Astigmatism: ‘There are two types of astigmatism 1, Regular astigmatism 2 Primary Axes; Steepest 2. Irregular astigmatism - seen in corneal Scar or & Flattest seen in keratoconus, Ne ZI No Regular Astigmatism Astigmatism RETINOSCOPY + Differentiate b/w the types of refractive error. + Reflected light from the retina appears like a streak of light. Movement of reflected light at the retina with respect to Retinoscopy fig Anan telnet aed 9 etrwzoe projects eon tina he eye urge DOC in MayKing & “motor tn 1. Against / Opposite movement ~ Myopia »-1 D 2. With / same movement - Myopia < -1 D or Emmetropia = 0 or Hypermetropia = + value 3. No movement = Myopia = -1D 7 Ophthalmology letoscoic ace rest Ey is spherical err Astron (tatoos spo ‘chem ‘rat menos) Refractive error = Retinoscopy value - 1/distance - Cycloplegic used + For atropine- 1 + Cyclopentolate- 0.75 + Homatropine- 0.5 + Tropicamide- 0.25 Mydeiasis ycloplegia brug % Maximal Hours | Recovery Maximal Hours | Recovery Deys Anteopine 10 30-40 7-10 doys 13 72 Homatrapine 10 40-60 1-3 days 05-1 13 Cyclopentolete 05-1 30-60 1 days 05-1 1 Tropicamide 05-1 20-40 3-6 hours we a4 Phenylephrine 05-1 20-60 3-6 hours None None APHAKIA + Traumatic extrusion of lens “Aphoki erly means absence of crstaling PEER ACTIVE CORRECTION + From an ophthalmological point of view, aphakia is the absence of lens in the pupillary area, Causes of aphakia: + Congenital aphakia + Surgical aphakia- removal of lens as in cataract extraction + MC- Surgical aphakia : Findirgs- Tridodonesis , Deep Anterior chamber , Jet black Pupil . #10- +11 correction , Jack in the Box phenomena , Rovsing Ring Scotoma + Aphakia due to absorption of lens- sometimes seen in children after trauma OPTIONS + Cornea based surgeries - ~ LASIK - Excimer laser used- 198rm, ArF used? - SMILE surgery- femtolaser used, argon glass laser + Lens based surgeries - phakic TOL Criteria for choosing Candidate: ~ Pt> 18 age ~ Stable refractive error ~ No coexisting diseases DOC in MayKing & 7 Cerebellum Quick Revision Notes LENS EMBRYOLOGY AND ANATOMY OF LENS le ae de ~ 2 ~ + Eye~Neuroectoderm - 3rd Wk of gestation + Lens - Surface ectoderm + Biconvex structure. + 15-17 Dof total eye + Copsule » Cortex > Nucleus + Oldest fibres are in the centre of the lens + Anterior surface : has Epithelium + Posterior surface - devoid of ary epithelium + Equatorial region ~ new lens fibres are being formed + Pre equatorial region - Thickest Lens capsules Physiology of Lens: + avascular structure + Nutrition supplied by Aqueous + Metabolism is mostly anaerabic CATARACT - Opacification of lens and/or capsule CONGENITAL AND DEVELOPMENTAL CATARACT = presents since birth + MC Cataract®: Blue Dot cataract / Cataracta Punctata Cerulea = Stationary ~ Visually non significant + MC Visually significant cataract ~ Lamellar / Zorular cataract® = A zone of opacity in the fetal nucleus ~ Spoke like opacities called Riders ~ Seen in Hypercalcaemia , Vit D deficiency + Cataracta centralis pulverulenta In Embryonic nucleus Powdery opacities present ~ Visually insignificant Stationary + Total / Membranous Cataract : Congenital Rubella Triad: C = Cataract (eye has Salt & Pepper Retinopathy, Congenital Glaucoma) seen in H- Heart diseases D = Deafness (SNHL) Surgery for Congerital Cataract: Lens Aspiration with Primary Post Capsulorrhexis + Partial Anterior Vitrectomy + PCIOLs ACQUIRED CATARACT + Cortical Cataract + Nuclear Cataract Cortical Cataract 1, Immature Senile Cataract MC Type of Senile Cataract ~ Cuneiform Cortical Cateract . Hyper mature Cortical Cataract Complications: 1, Phacomorphic Glaucoma? + Anterior chamber shallow + Narrowing of angle DOC in MayKing & + Angle closure glaucoma 2, Phacolytie Glaucoma + Cortex has undergone lysis + Leads to Hypersensitivity reaction Hyper mature Nuclear Cataract Complications: + Spontaneous Subluxation / dislocation of lens ROSETTE CATARACT + Seen in Blunt Trauma + Flower shaped cataract either in the anterior or posterior chamber + Vossius Ring - Iris pigment deposition on the anterior capsule COMPLICATED CATARACT? Occurs as Complication of Intra ocular Disease Tumour I~ Inflammatory disease 6 - Glaucoma E- Endophthalmitis R- Retinal diseases eg, Retinitis Pigmentosa , Retinal Ophthalmology Detachment, High Myopia Features + Posterior Subscapular location of cataract + Bread crump appearance? + Polychromatic Lustre? + Axial Spread SNOW FLAKE/ SNOW STORM CATARACT + Seen in pt. With Diabetic Mellitus (sorbitol pathway) SUNFLOWER CATARACT? + Wilson disease / Cu Metabolism + KF Ring / KAYSER-FLETSHER rings - Golden brown discolouration at the Descemet membrane, MANAGEMENT OF CATARACT: Surgical Types of Anaesthesia - 1, General Anaesthesia Children / Mentally unstable J adults DOC in MayKing & Cerebellum Quick Revision Notes, 2. Local anaesthesia: + Retrobulbar block + Facial nerve block Peribulbar block Subtenon’s block Topical anesthesia ~ Proparacaine eye drops Types of Surgeries + ECCE ( Incision 10 - 12mm): sutures + + SICS (Incision 6 -8 mm ): suture +/- Phacoemulsification surgery (incision- 3mm) MICS Micro incision cataract surgery (incision- 2mm) + FLACS - Femtosecond laser assisted cataract surgery. Laser used for- ~ Incision ~ Capsulorrhexis ~ Primary Fragmentation of Nucleus ~ Astigmatism Neutralising incision INTRAOCULAR LENS + Non-foldable: PMMA + Foldable: Acrylic ~ Morofocal Lenses - Single focus ~ Multifocal Lenses - Multiple rings, Glare & Halos EDOF - Extended depth of focus COMPLICATIONS OF CATARACT SURGERY: Expulsive choroidal Haemorrhage + Endophthalmitis (J vision, ? pain, 7 redness)? ‘Tit Intravitreal Antibiotics, Vitrectomy ‘Most imp. step in prevention - Perioperative Povidone Iodine + Posterior complication) T/t: NAYAG laser (anterior capsulotomy) (1064 rim) capsular Opacification (MC * Spontaneous subluxation / dislocation of lers. + MC 2. Marfaris Syndrome - Up & out + Weil-Marchesani syndrome + Ehler Danlos + Homocystinuria- down and in Vossius ring? + = Deposition of pigment in the anterior capsule seen after blunt trauma, CORNEA j toe =, ae | ---— = | = eee |} DOC in MayKing & 1. Epithelium- stratified squamous non keratinised epithelium, 5-6 layer thick Bowman's Membrane- does rot regenerate Stroma Duc's layer- strongest layer Descemet’s Membrane Endothelium - does not regenerate INVESTIGATIONS IN CORNEA + Pachymetry : assessment of the thickness of ‘the cornea + Keratometry : assessment of the curvature of the cornea + Topography : assessment of the corneal ‘thickness, shape & surface. + Keratoscopy : assessment of the corneal shape + Corneal Aesthesiometry : assessment of the corneal sensations + Sodium Fluorescent dye: to stain the corneal ulcers / defect + Rose Bengal stain : to stain Dead cells s + Sodium Fluorescene dye = Orange colour dye ~ Cobalt blue light used Ophthalmology Defect appears green DISEASES OF CORNEA BACTERIAL ULCERS Pain, photophobia, watery eyes Hypopyon : sterile, has Inflammatory cells v Pus in anterior chamber MC Contact lens induced ulcer - Pseudomonas? Hypopyon corneal ulcer / Ulcus serpens - Pneumococcus® Topical antibiotics - cone, Tobramycin / Cefazolin / Gentamicin ‘Adjuvant therapy ~ Atropine (For pain relief) FUNGAL ULCER Filamentous furgi DOC- Natamyein Dry looking ulcer Cheesy necrotic base Satellite lesions? Hypopyon ~ Non sterile H/O injury with animal tailor leaf Signs >> symptoms Non filamentous furgi : DOC - Amphotericin B VIRAL ULCER HSV - Corneal lesions, Dendritic lesions —> forms a geographic ulcer -> Stroma necrotic ulcers -> Disciform keratitis Loss of corneal sensation HZV ~ Corneal lesion: Punctate keratitis» pseudodendritic ulcer, Uveitis, Retinitis, Oculomotor involvement. T/t- steroids given under antiviral cover. Hutchinsor's Rule -If Lesion on the tip of rose +, 7 risk of corneal ulcer because both are supplied by same Nasociliary branch Dendritic Ulcer - Fluorescence stain® DOC in MayKing & Cerebellum Quick Revision Notes ACANTHAMOEBA ULCER + Weak interlinkage in the corneal stroma + Myopic Shifts : Irregular myopic astigmatism + Retinoscopy: Scissor reflex / Yawning reflex + TOP Applanation :Pulsating mires + S/L: Vogt's Striae - vertical striae, stress lines which disappear on counter pressure on cornea, + Munson's Sign - Notching of lower lid on looking down, + Fleischer Ring: iron deposition on epithelium + Rx: C3R- Corneal collagen cross linking with Riboflavin + For Flattening - INTACS are used + Neurotrophic ulcer + Pain out of proportion + Pseudo dendrites + Ring uleer® + cultured on Non rutrient agar enriched with [Link] ° DEGENERATIONS- DYSTROPHIES + Stained by Calcoflour white + Arcus Serilis (MC correal degeneration ) + Lactophenol blue + Degenerations - acquired + DOC-PHMB (Poly Hexa Methylene Biguanide), + Dystrophy - Hereditary Chlorhexidine Q, Recurrent corneal erosion is a feature of: + H/O contact lens users using home made contact lens saline, tap water , swimming with ‘A. Keratoglobus conic lene 8. Keratoconus CORNEAL ECTASIA C. Glaucoma Keratoconus® D. Corneal dystrophy + Bulging of cornea + Epithelial dystrophy: Mop dot dystrophy / Finger print dystrophy DOC in MayKing & Stromal Dystrophy (MC dystrophy) + Macular ‘Mucopolysaccharidosis present ~ Aleain Blue stain + Granular dystrophy ~ Hyaline deposits ~ Masson Trichrome stain + Lattice dystrophy ~ Amyloid deposits ~ Congo red stain (Marilyn Monroe always gets her man in L A city) CORNEAL TRANSPLANT "@ @©® Ophthalmology + Full thickness transplant + Cadaveric donor 1, Lamellar Keratoplasty: Partial thickness + Deep Anterior Lamellar Keratoplasty (DALK) + Descemet's Stripping Automated Endothelial Keratoplasty (DSAEK) CONJUNCTIVA 27 Fomiceal Bulbar areal Conjunctiva Marginal Conjunctiva \3— Fomiceat Conjunctiva Papillae consist of hyperplastic conjunctival tissue full of inflammatory cells, normally seen in the palpebral conjunctiva, Associated with bacterial and allergic conjunctivities Follicles consist of hyperplastic lymphoid tissue & appear as elevated lesions encircled by blood vessels. Typically seen in reaction to topical agents, adenoviral & chlamydial disease DOC in MayKing & Cerebellum Quick Revision Notes CONJUNCTIVITIS - inflammation of conjunctiva 1. Bacterial Conjunctivitis Adenoviral Conjunctivitis Viral Conjunctivit ‘Membranous conjunctivitis- by C. diphtheria (bleeds on peeling) Pseudomembranous Conjunctivitis (does not bleed on peeling) ~ Stophs ~ Strep ~ H. influenza ~ Neisseria gonorrhoea ‘Angular conjunctivitis? ~ Moraxella axenfeld, on inner canthus of eye Picorra virus Adeno virus Coxsackie virus Echo virus Pharyngoconjunctival Fever (PCF) Follicular conjunctivitis Epidemic keratoconjunctivitis (EKC) ~-Mild, transient disease| —No care sought ~~ Serotypes 3, 7 ~~ Follicular conjiitis + fevet|- +HA + Pharyngitis ~~ Looks like the flu Chlamydial Conjunctivitis + Trachoma + Caused by Chlamydia trachomatis A, B, C2 + D~Kcauses Inclusion conjunctivitis, swimming pool conjunctivitis. ~~ serotypes 8, 19, 37 May be preceded by URTI = + 2nd eye involved in 3-7 days DOC in MayKing & WHO 2.5 Follicles on upper palpebral conjunctiva is Pathognomic Scarring ~ Arlt line Pannus Herbert's follicle Herbert's Pits ‘Surgery for trichiasis, Antibiotics Facial cleanliness Environment Hygiene = DOC- Azithromycin 1g single dose stat ~ spread through fomites ~ Imp. cause of preventable blindness NEONATAL CONJUNCTIVITIS - Ophthalmia Neonatorum Causes: Chemical : 1% silver Nitrate solution used to prevent gonococcal conjunctivitis Bacterial - gonococcal Viral: HSV-2 Chlamydial (most common) boc Ophthalmology VERNAL KERATOCONJUNCTIVITIS + Spring Catarrh / VKC + Occurs in summer + Hypersensitivity reaction + Giant papillae on upper tarsal conjunctiva (Paving stone appearance) + Moxwell lyon sign + Pseudogerontoxon + Shield Corneal ulcer + Rx: Steroids, Mast cell stabilizers (Sodium cromoglycate) PHLYCTENULAR CONJUNCTIVITIS + Type IV hypersensitivity reaction + TB Antigens + Staphylococcus antigen + Rx: Steroids DEGENERATIVE CONDITIONS + Pinguecula - remains stationary / localized, doesrit encroach cornea + Pterygium - forms a wing shaped fold, encroaches over the cornea, elastotic degeneration, has + 3parts-Head, Neck, Body, T/t: Surgical Excision (conjunctival autograft), mitomycin C, 5-FU MayKing & 85 Cerebellum Quick Revision Notes XEROPHTHALMIA -d/t Vit A deficiency + XN- Night blindness + XF- fundal changes + XIA = Conjunctival Xerosis + XIB ~ Bitot’s spots + X2~ Corneal Xerosis + X3A- Keratomalacia «1/3rd + X38 Keratomalacia > 1/3rd XS ~ Corneal Scarring Rx: Vit A supplements + Child > ye ,> 8 kgs : 2 lakh ZU Orally - 0,1, 14 days + Child <1yr, «8 kgs: 1 lakh IU Orally /IM vit A DOC in May NEURO-OPHTHALMOLOGY Papilledema Pathophysiology of Papilledema (Hayreh's theory): + Disturbance in axoplasinic Flow causes stasis and swelling of axors + Increased intracranial pressure is transmitted ‘along the subarachnoid space with optic nerve sheath, + Increased ICT leads to increases optic nerve tissue pressure which alters pressure gradient H —choris ‘Shoe! Fostehor cary artnos High CSF Pressure (Paoiiedera) Axoplasmic Stass Fat Tortuous Veins AG Normal ntraoeslar Pressure (18:20 mm Ha) exams) Etiology: + Tumours + Hemorrhage + Aneurysms + Infections + Orbital Causes + Intracranial Causes ing © ‘Systemic conditions ‘Ocular causes - Retrograde axoplasmic flow ~ Trauma - Marked Ocular hypotony = CRVO - Hemorrhages ~ AION = Chronic Uveitis - Phthisis Clinical Features: Transient obscuration of vision- amaurosis Fugax® Normal Colour vision Normal Pupillary reaction Visual Fields- Enlargement of physiological blind spot? Features of Raised ICP Focal neurological deficits with changes in level of consciousness Signs: Normal Pupillary reaction Fundus Picture ~ Obscuration of Disc Margin- Nasal margins cre ist Sign ~ Hyperemia of Dise ~ Elevated Disc (champagne cork appearance/ cork screw appearance) ~ Swelling of surrounding retina producing concentric retinal folds- Paton's lines ~ Dilated tortuous retinal veins = Loss of Venous pulsations ~ Splinter hemorrhages in peripapillary region Visual Fields - Normal 87 Ophthalmology BENIGN INTRACRANIAL HYPERTENSION ‘Also krown as Idiopathic intracranial hypertension/ Pseudotumour cerebri Tt isa diagnosis of exclusion CT scan normal CSF composition normal + CSF pressure Commonly seen in fat, fertile female > 40 yrs old Drugs causing BIH? F-00Ps A-Vitamin A Toxicity, Amiodarone Lithium S- Long term Steroids or too rapid taper E T-Tetracycline, Doxycycline Treatment: Weight Loss ‘Medical Rx. ~ €.A Inhibitors- acetazolamide ~ Diuretics- Furosemide Surgical Rx ~ Serial Lumbar Punctures ~ Shunt Placement- (L-P Shunt/ V-P Shunt) DOC in MayKing & Cerebellum Quick Revision Notes OPTIC NEURITIS Popilitis Retrobulbar Neuritis Neuroretinitis 2 Optic Nerve Head affected Optic Nerve offected behind the | Optic Nerve affected along with eyeball Retira (maculer ares) * Hyperemio ord edema of the Optic |+ Optic Nerve appears normel, |» Macular Star-° exudates that nerve head + Typically described as ‘neither | form araurd the macula get May be associated with per-popillary | the patient sees anything ror the | arranged in starlike manner hemorrhages doctor sees anything” > Mest frequent type nodults [+ Least common type Most common type in Children + Frequently associated with + Mostly associated with Viral Demyelinating disease- Multiple | diseases Sclerosis + Rorely d/t demyelination Etiology: Optic Neuritis + Tdiopethie + Demyelinating Disorder - Multiple sclerosis Symptoms: + Sudden profound U/L vision loss ® + Dull Boring Pain in eye worsened with ocular movements (on Upgaze) + Impaired dark adaptation * Colour vision defect + Movement phosphenes & sound induced phosphenes + Uhthof Phenomenon - worsening of symptoms when there is raise in body temperature Pulfrich Phenomenon - impaired depth perception (swinging pendulum test) + Decreased Visual Acuity © + Decreased Color Vision (red desaturation) + Decreased contrast/brightness sense + RAPD/ Marcus Gunn Pupil boc Disc Edema ‘Any Scotoma on Amsler Grid- most common is Central scotoma VEP shows reduced amplitude and delayed trarsmission time ‘Treatment High-dose intravenous steroids are the treatment of choice for acute ON® = Lgm IV steroid x 3 days ~ followed by 1 mg /Kg / day Oral steroids x 11 days Oral steroids alone in conventional doses are contraindicated, ical trials CHAMPS and CHAMPIONS TOMS Benefit Precise. CHAMPS - Controlled High-Risk AVONEX Multiple Sclerosis Prevention Study (Interferon beta 1a) MayKing & + CHAMPIONS STUDY- compared those who had been receiving drug from start of CHAMPS versus those who switched after receiving placebo + ETOMS- Early Treatment of Multiple Sclerosis ‘Study-Interferon beta 1a + BENEFIT- Betaseron (Interferon beta 1b) in Newly Emerging Multiple Sclerosis For Initial ‘Treatment Study + Precise Study - early Glatiramer Acetate treatment in delaying Presenting with a Clinically Tsolated Syndrome RELATIVE AFFERENT PUPILLARY DEFECT: Marcus Gunn Pupil? + Afferent loop of the pupillary light reflex is impaired (loss of sensory information) + Lesion- Optic nerve. + Main association: Optic neuritis due to multiple sclerosis + Swinging Flashlight test for diagnosis + Dilation of the affected pupil in response to light Ophthalmology HOLMES ADIE'S PUPIL + Regular and mildly dilated pupil (4-6mm): + Light-near dissociation: + Usually Unilateral: + Slow pupillary dilation in response to dark: + Slow redilation when re exposed to light: + Normal response to mydriatics + Pupil constricts with 0.125% pilocarpine (cholinergic super sensitivity) + Lesion- ciliary ganglion oe 6 fo oe ARGYLL ROBERTSON PUPIL + Miotic, irregular pupils + Usually Bilateral + Pupils dilate very poorly with mydriaties + Caused by lesion in the pretectal area + Most commonly seen in tertiary neurosyphilis, DOC in MayKing & Cerebellum Quick Revision Notes WERNICKE'S HEMIANOPIC PUPIL + Optic tract lesion® + LIGHT REFLEX ABSENT on stimulating- ~ Affected side - temporal half of retina ~ Opposite side - nasal half of retina HORNER’S SYNDROME? + LIGHT REFLEX PRESENT on stimulating- + Defect in the sympathetic Pathway ~ Affected side - nasal half of retina = Opposite side - temporal half of retina ee a Accommodation Reflex Present ARP Pupillary Reflex Absent HUTCHINSON'S PUPIL + Ptosis 1. Pupil on the side of Injury constricts + Miosis + Due to irritation of 3rd CN. + Anhidrosis + Pupil on other side-Normal + Apparent Enophthalmos 2, Pupil on the Injured side becomes DILATED + Dilatation lag + Due to paralysis of 3rd CN. + Heterochromia Tridis + Pupil on other side Constricts 3. Papils of Both sides are DILATED : No reaction to light ‘Masle Primary Secondary Teetary | Medal ects Adduction Loteral rectus Abduction Inferior rectus Depression Exeyloterton Adetion Siperior rectus Etotion Treyeotorsion adduction Terr ebique Excyelotorson Elevation Abduction Superior oblique Treyelotorsion Depression Abdvction boc Lata 6th C.N. PALSY Presentation: Double vision Esotropia in the primary position Limitation of abduction on the side of the lesion Normal adduction ‘A compensatory face turn is towards the side of the paralysed muscle in urilateral palsy. Most common single EOM pelsy Causes: 1, Ischaemia 2, Tumor (acoustic neuroma, meningioma) 3. Trouna 4, Elevated Intracranial pressure boc Ophthalmology Congenital 6th N. palsies almost never occur in isolation, Leukemia & brainstem glioma are. important considerations in children 3rd C.N. PALSY Cculomotor nerve Entirely motor in function Supplies ~ All the Extraocular muscles except superior oblique and lateral rectus ~ Levator palpebrae superioris ~ Intra ocular muscles- Sphincter pupillae and ciliary muscle Presentation: Prosis ‘Abduction of globe-DOWN & OUT? Intortion of the globe which increases on ‘attempted down gaze Limitation of adduction Limitation of elevation Limitation of depression Dilated pupil with defective accommodation Causes Idiopathic - about 25% Vascular-Hypertersion & Diabetes (commonly pupil sparing) ‘Areurysm-posterior communicating artery at its junction with internal carotid artery Trauma- subdural haematoma with uncal herni- ction MayKing & 31 2 Cerebellum Quick Revision Notes 4th C.N. PALSY- TROCHLEAR NERVE + Asymptomatic + Diplopia vertical + Head tilt position opposite to the side of the lesion? + Hypertropia on the affected side. + Limitation of depression, most marked in adduction + Extorsion, greatest in abduction. + Bilateral involvement should always be excluded, particularly following head trauma. + Park's three-step test:2 ~ Step one- In the primary position. In a fourth nerve palsy, the involved eye is higher Step two- The eyes are examined in right and left gaze to determine where ‘the hypertropia is greater. In superior oblique weakness the deviation is worse on opposite gaze — WOO6. ~ Step three- The Bielschowsky head till test (BHT) boc ane ou =] [eneereeae] Causes of 4th CN palsy 1. Idiopathic + Most are congenital ‘+ Symptoms may appear late in adult life + Old photograph will help (AHP) 2. Trauma + Frequently cause bilateral 4" nerve palsy 3. Microvascular 4, Aneurysms & Tumor INTERNUCLEAR OPHTHALMOPLEGIA MayKing & + Lesion at the Medial Longitudinal Fasciculus Mu connection b/w 6th & 3rd CN + Impaired Adduction of ‘ipsilateral eye with Nystogmus of the abducting eye + One and half syndrome- I/L MLF + PPRF Lesion + Eight and half syrdrome- T/L MLF + PPRF + 7th rerve Lesion col Ophthalmology MBINED C.N. PALSY Orbital Apex Syndrome Cavernous Sirus Thrombosis Superior Orbital Fissure Syndrome Tolosa Hunt Syndrome Orbital Tumours Fungal Infection in uncontrolled DM. ‘Mucormycosis, Aspergillosis apart ote (Kite poster Lowertank ott caer ay cca) Visual Field Defects Laine) (6) Meroe en as O @ ©) Btongranonacpa © Oo D, G, & H) Contralateral chon coat, — K) Contralateral io Prey RETINA RETINAL VASCULAR DISORDER Prevalence IDD 40%, NIDD 20% ‘Microangiopathy - reduction in the number of pericytes causing distension of capillary walls, break down of the blood- retinal barrier - leakage The consequence of retinal nor-perfusion is retinal ischaemia hypoxia, Hypoxia- causes A-V_— shunts and neovascularization. Nonproliferative DR: DOC in MayKing & 93 Cerebellum Quick Revision Notes, Intraretinal HE , hard exudates , oedema Micro aneurysm? Dot & Blot haemorrhage ~ Cotton wool spots + Proliferative DR ~ Neovascularisation® ~ T/t- laser photocoagulation = Complication - Hge, tractional retinal detachment Nonproliferative DI Proliferative DR Proliferative DR Fluorescein Angiography Retinal Photocoagulation HYPERTENSIVE RETINOPATHY + Prolonged hypertension + Fundus picture = Vasoconstriction - arteriolar narrowing (AV2 1:3) Leakage - abnormal vascular permeability ~ hemorrhages, exudates, retinal oedema Arteriolosclerosis - thickening of the vessel wall - changes at AV crossings- Salus sign, Gunn sign, Bonnet sigh CENTRAL RETINAL ARTERY OCCLUSION + Cherry red spot + Causes: Embolism- 1. From the heart 2. Carotid artery fibrinoplatelet, caleific) 3, Vaso-obliteration- atherosclerosis, periarteritis - associated with systemic vascular, haematological disorders disease (cholesterol, Presentation + Acute loss of vision + Retinal ischemia time- 90 min. DOC in MayKing & re a ger Signs + Retina white, foveo appears red + arterioles and verules- arrow + Central, branch Treatment: Ocular massage, TOPL Causes of Cherry Red spot: (GEE STING) + Berlin's cedema + Sialosis + Tay Sach’s disease + Ischaemia (CRAO) + Niemann Pick + Gangliosidosis type T CENTRAL RETINAL VEIN OCCLUSION + Splashed tomato fundus + Predisposing factors 1. Systemic age, systemic _ hypertension, diabetes (veins compressed by the thicked artery), blood hyperviseosity 2, Ocular - TEP, hypermetropia, congenital abrormal. * Central, branch 95 Ophthalmology + Presentation -Moderate loss of visual acuity * Signs: © Tortuosity and dilatation of retinal © Hemorrhages © Cotton-wool spots Optic dise oedema + Complication - CME neovascularization Types: + Ischaemic type: 90 day Glaucoma/100 day Glaucoma / Neovascular Glaucoma + Non Ischaemic : better prognosis INFECTION The Most Important Causes of Retinal Vasculitis + Idiopathic + Behcet's disease + Multiple sclerosis + Lupus erythematosus + Wegener's granulomatosis + Polyarteritis nodosa + Horton's arteritis + Sarcoidosis DOC in MayKing & Cerebellum Quick Revision Notes + Tuberculosis + Borreliosis (Lyme disease) Listeriosis + Brucellasis + Syphilis + Viruses Eales Disease + MCC Vitreous haemorrhage in young males with no h/o hypertension no h/o trauma + Aetiology ; TB / Idiopathic ACQUIRED MACULER DISORDERS ‘Age- Related Macular Degeneration ARMI ‘Types- 1. Atrophic- (non- exudative) - slowly progressive, 90% 2. Exudative -wet form -detachment of RPE, choroidal neovascularization Human retina es seen through an apthalmoscope, Atrophic, Dry, Non exudative AMD boc + The most common type, 90% + Slowly progressive atrophy of the RPE and photoreceptors? + Presentation - gradual mild- to maderata impairment of vision over several month or years. + Drusens deposited? + Deposition of abnormal material in Bruch membrane® + Risk factor: UV rays / Smoking / lack of Anti oxidation Atrophic AMD Early - drusen Late - geographic atrophy Exudative AMD + Exudative detachment of the RPE + Choroidal neovascularization grow from the choriocopillaries through defects in Bruch membrane into the sub- RPE space. Choroidal Neovacularization MayKing & 7 Ophthalmology Disciform Scar ‘about 1-15 um, which is 10 to 100 times better ‘than ultrasound or MRT + Anatomic layers within the retina can be differentiated and retinal thickness can be measured. CYSTOID MACULAR EDEMA Cystoid Macular Oedema oo Pseudophakic Non- Pseudophakic 4 Diabetic Retinopathy J Retina Vein Occlusions J Choroidal Neovascular ‘Membrane Amsler Grid Fundus Fluorescein Angiography: + The Amsler grid is used to detect small irregularities in the central 20 degrees of the field of vision + Is.a quick and simple test that patients are asked to use to monitor changes in their vision ocT + Typical petaloid pattern in the central macula secondary to dye leckage from perifoveal capillaries + The dye accumulates in the cystic spaces in ‘the outer plexiform layer + Optical Coherence Tomography (OCT) is a new I Coherence T imaging technique that provides high resolution OP tHCA! Coherence Tomography and cross-sectional images of the eye : Shows central cysts, loss of foveal depression + Analogous to ultrasound, but instead of using of acoustic waves (as in ultrasound), it uses light to achieve micrometer axial resolution. + The axial resolution of OCT in retinal tissue is ‘and macular thickening Test of choice for diagnosis and follow up of patients with CME DOC in MayKing & Cerebellum Quick Revision Notes Management Medical Treatment Rx: Steroids Long standing - Intravitreal steroids Intravitreal Anti VEGF CENTRAL SEROUS RETINOPATHY Tdiopethic, self-limited disease of young or middle-aged adult Usually unilateral, localized detachment of the sensory retina, Presentation ~ Sudden blurred vision in one eye, associated with metamorphopsia ~FAG-breakdown of the blood- retinal barrier which allows the passage of fluorescein into subretinal space, Prognosis ~ 80% spontaneous resolution normal vision within 1-6 month = 20% resolve within 12 month Prolonged detachment or recurrent attacks-permanent ~ Impairment of visual function ocr + OCT can detect detachments that remained undetected in FA, + It can also detect subretinal deposits like fibrin and subretinal precipitates 4, Sub sensory fluid accumulation in CSC b, Detected shallow SRD along with PED HEREDITARY FUNDUS DYSTROPHY Retinitis Pigmentosa + Triad : Vascular attenuation + Bony spicules pigment + Optic Atrophy ( waxy)? + MC: Sporadic type + MC: AR (out of inherited) + AD: best prognosis + XLR: Worst prognosis + Group of hereditary disorders - progressive loss of photoreceptors + Diffuse, usually bilateral, symmetrical + Cones, rods- predominant + Presentation-defective dark adaptation (right blindness-nyctalopia) DOC in MayKing & MYOPIC RETINOPATHY + Degenerative myopia + Progressive elongation of the globe is followed by degenerative changes in the retina and choroid + Signs ~ Islands of chorioretinal atrophy = Atrophy around the optic disc Macule-brecks in bruch ——memb,, Neovascularization haemorrhage ~ Posterior staphyloma, peripheral degereration RETINAL DETACHMENT + Separation of the sensory retina from the Pigment epithelium + Rhegmatogenous- retinal break + Non-rhegmatagerous Tractional Exudative Ophthalmology Rhegmatogenous Retinal Detachment : + Ttoccurs in patients with History of previous trauma to the eye ~ Myopia ~ Peripheral retiral degenerations like lattice degereration + Presentsas flashes and floaters, curtain falling in front of the eye. Peripheral Retinal Degenerations Benign Predisposing Cystoid degeneration Lattice Degeneration Equatorial Drusens ‘rail Track small holes Reticular Pigmentary Degeneration Traction Retinal Detachment 100 Cerebellum Quick Revision Notes Exudative Retinal Detachment Definition: The retina is pulled into the vitreous cavity by transvitreal traction Etiology: Diabetic PvR, old penetrating injuries Clinicial features: The detached retina is smooth, immobile, and concave toward the pupil. No breaks are usually found on ophthalmoscopy. Management: Vitrectomy, with release of vitreous tractions is required retinopathy, Definition: The result of collection of fluid beneath an intact sensory retina Etiology: Choroidial neoplasm (e.g. melanoma), chorioretinal inflammatory diseases, malignant hypertension (as in toxcemia of regnancy),hemorrhage from a sub retinal rneo- vascular membrane (as in AMD), systemic vascular and inflammatory diseases. Clinical features: Smooth, transparent retinal elevation, no retinal breaks nor pigment clumps or red blood cells in the vitreous are identified ‘Management: Treat the underlying condition of possible Management Each procedure requires location of the tear and treating the retina around its edges by cryotherapy or laser in order to create firm adhesions between the sensory retina and the RPE layer and preventing detachment, Pneumatic retinopexy is best done for superior breaks ‘The gas bubble will expand and being lighter ‘than the ocular fluids, will migrate upward to ‘tamporade superior breaks Positioning-if the break is in the posterior pole (close to the macula), the patient should remain face down, If the break was in the right temporal retina, he should face on his left side. Positioning should be applied for the first 2 weeks. Scleral Buckle: Silicone explant-over the sclera 360 degrees- in order to indent the sclera and make it apposed to the underlying detached retina Pneumatic Retinopexy: -Intra-ocular injection of gas (air or expandable gos) in order to tamporade the retinal detachment and break while the choroidal adhesions form Vitrectomy with silicone oil PPV (pars plana vitrectomy) PPV was first introduced in 1972. 20-gauge 3 port PPV became the gold standard Surgical Indications: Pars plana vitrectomy is commonly recommended for the following conditions: = Macular hole. ‘Macular pucker Vitreomacular traction Refractory macular edema ~ Vitreous haemorrhage DOC in MayKing & Tractional retinal detachment Rhegmatogenous retinal detachment ~ Dislocated intraocular lens ~ Refractory wveitis ~ Retained lens material ~ Intraocular foreign bodies - Floaters X ANATOMICAL CLASSIFICATION- (US6) INTERNATIONAL Uveitis Study Group Anatomical: + Anterior uveitis + Intermediate uveitis + Posterior uveitis + Pan uveitis ANTERIOR UVEITIS ‘Symptoms: + Pain + Photophobia + Redness + Lacrimation + Blurring of vision Signs boc 101 Ophthalmology Keratin precipitates - aggregates on the ‘endothelium: Pathognomonic of uveitis Cells: indicate Active uveitis Flare: because of leaked proteins Post Synechiae formation Pupil : Miotic Festooned Pupil INTERMEDIATE UVEITIS Intermediate uvei inflammation of the ciliary body (cyclitis, pars planatis). L = ZZ * Redness Loss of vision Floaters Snow balls & snow banks Anterior vitreous Snowballs ‘Snow Banking 102, Cerebellum Quick Revision Notes POSTERIOR UVEITIS Signs: + Vitreous + Furdus lesions Choroiditis Retinitis Old inactive lesion ~ Vasculitis + Poin + Redness + Loss of vision PAN- UVEITIS Inflammation of the entire uveal tract. TREATMENT: Aims + Relief pain & inflammation + Prevent ocular structural damage + Prevent visual loss & retinal or optic damage Include: + Cycloplegia: Long acting cycloplegic agents (Atropine, cyclopentolate, homatropine Jused torrelief pain & photophobia by mydriasis + Corticosteroids A. Local delivery of corticosteroids: + Topical corticosteroids + Periocular injections- in form of sub tenon injections + Intravitreal injections and inserts B. Systemic oral steroids (oral and intravenous) + Immunosuppressants + Biologics + Adjuvant therapy: ~ Cycloplegic = Newer nonsteroidal anti-inflammatory agents ~ Anti-vascular endothelial growth factor (onti-VEGF) therapy: bevacizumab, ranibizumab UVEITIS AND SYSTEMIC DISEASE Cause of anterior uveitis: HLA positive or seronegative group: ‘A-Ankylosing spondylitis, B-Reiter's syndrome. C-IBD" Inflamatory bowel disease’. D-Psoriatic arthritis. ANKYLOSING SPONDYLITIS + Young adults + Male are affected more with Arthritis + Axial skeleton intervertebral joints + 90% positive HLA-B27 + Acute, Recurrent, non-granulomatous Anterior Uveitis sacroiliac joint and JUVENILE CHRONIC ARTHRITIS 1, Pauciarticular (<5) 2, Polyarticular (> 5 ) DOC in MayKing & 3. Systemic + Bilateral, Chronic, non-granulomatous Ant. Uveitis, painless. + Commoner in female patients, the young, + Pauciarticular disease <5 joints. Complications: + Glaucoma (20%) + Cataract (40%) + Band Keratopathy (40%) FUCHS HETOROCHROMIC IRIDOCYCLITIS + Small stellate pan-corneal keratic precipitates + Star shaped KPs + Absence of posterior synechiae + Catareet Posner - Schlossman Syndrome + Recurrent attacks of unilateral, acute mild anterior uveitis with raised LOP + Rare, young adults + TOT few hours to several days + a/w HLA Bw54 + Intervals between attack vary + Presentation-mild discomfort, haloes + Signs- corneal epithelial edema, few aqueous cells, Fine preciprtates + T/t -topical steroids, antiglaucomatics Ophthalmology Pan Uveitis: Vogt Koyanagi Harada (VKH) \V- Visual symptoms ; serous retinal detachment -Kutaneous symptom H- Head + Multi-systemic auto-immune disorder affect pigmented cells in the body. + Involves CNS, eyes, and skin + Neurological and auditory manifestations + Headache, Tinnitus + Integumentary findings, not preceding onset of central nervous system or ocular disease, such as alopecia, poliosis and vitiligo Toxoplasmosis + MCC Congenital U/L Blindness + Headlight in fog appearance + Punched out lesions + Treatment: Antiprotozoal drugs- Clindamycin, Sulphonamides, Steroids Sarcoidosis + Eye lid + conjunctivitis , episcleritis, scleritis, and sometime keratoconjuctivitis sicca + Anterior uveitis + Vitreous: diffuse vitritis, snowball opacities. + Fundus changes: periphlebitis (candle-wax dripping), retinal granuloma, small and large choroidal granuloma, optic nerve lesions, BEHCET'S DISEASE Ocular Features: + Bilateral, chronic with exacerbation and remission, non- granulomatous pan-uveitis DOC in MayKing & 103 Cerebellum Quick Revision Notes, + Tridocyclitis - associated with transient hypopyon + Vitritis + Retinitis + Vasculitis: venous occlusion, neovascularization, Sympathetic Ophthalmitis + Bilateral granulomatous panuveitis trauma ( penetrating trauma ) + Onset :5 days to 66 years after trauma + Retina- Dalen fuch nodules present after + Removal of injured eye after onset does not help + Treatment: Aggressive _immunosuppressive therapy GLAUCOMA 10P> 24mm Ho ow sion TYplcaais changes Tyla el changes Triad Of Abnormalities in: Die, Field And Intra~ Ocular Pressure (IOP) For The Diagnosis Of Glaucoma ‘Aqueous Formation: + Diffusion + Ultrafiltration + Secretion Drainage + Trabecular mesh work + Uveoscleral outflow Raised TOP > 21 mm Hg : Glaucoma Top Measurement + Schiotz indentation tonometer + Applanation Tonometry - gold standard? + Perkins handheld Tonometry + Tonopen Tonometer DOC in MayKing & Ophthalmology + Isopter contraction + Scotoma in Bjerrum's area + Seidel's Scotoma + Arcuate scotoma + Double arcuate scotoma + Ronne nasal step + Tunnel vision Dise Signs + C:D ratio + Deep cup + Laminar dot sign + Asymmetry of C:0 of 0.2 between two eyes Vascular signs + Bayoneting sign + Nasal shifting of vessels Peripapillary signs + Flame shaped haemorrhage + Loss of nerve fibre layer VISUAL FIELD CHANGES GONIOSCOPY + Perimetry: Humphrey visual perimeter To differentiate b/w Angle open type & Angle closure type Direct Gonioscopy DOC in MayKing & 106 Cerebellum Quick Revision Notes, Some features of this technique are: + Patients must lie on their back + Gives adirect view of the anterior chamber angle * Good magnification + Easy orientation for the observer + Possible simultaneous comparison of both eyes Indirect Gonioscopy Some features of this technique are: + Patient must be at the slit lamp + Indirect view of the anterior chamber angle + Faster than direct gonioscopy during routine ophthalmological exam + Tt can be used to see the fundus (using the central part of the lens) at the slit lamp + Inability tocompare the twoeyessimultaneously CONGENITAL GLAUCOMA / BUPHTHALMOS Pathology: Hazy cornea - d/t Trabeculodysgenesis (Trabecular meshwork not formed) The Classical Triad of Signs/Symptoms + Epiphora/lacrimation + Photosensitivity + Blepharospasm Cornea + Cloudiness secondary to edema + Haob’s Striae® + Horizontal Diameter »11.5 mm GLAUCOMA IN ADULTS Primary open angle glaucoma (POAG) - Raised IOP (21 mm of Ha) associated with definite glaucomatous optic disc cupping and visual field changes. Ocular hypertension or glaucoma suspect - IOP constantly more than 21 mm of Hg but no optic disc or visual field changes Normal tension glaucoma (NT6) or low-tension glaucoma (LT6) - glaucomatous disc cupping with or without visual field changes associated with TOP constantly below 2imm of Hg ‘Angle Closure (narrow angle, acute congestive) Glaucoma + Emergency situation occurring in person with narrow Tridocorneal angle and shallow anterior chamber. + TOP raised after it is being precipitated by mydriasis + TOP rise rapidly to very high levels (40-60 mm Hg) + Marked congestion headache of eyes and severe + Failure to lower TOP-» loss of sight DOC in MayKing & + Definite treatment ~ surgery Closed angle glaucoma Normat angle Angle closure Trabecular meshwork iis — Sclora Collecting venule + Be adrenergic blockers: Timolol , Betaxolol and Levobunolol + adrenergic agonists: Dipivefrine, Apracloni- dine and Brimonidine + PG analogues: Latanoprost, Travoprost, Bi- ‘matoprost, Tafluprost + Carbonic anhydrase int Brinzolamide, Dorzolamide itors: Acetazolamide + Mioties: Pilocorpine and Physostigmine + Rho Kinase Inhibitors : Netarsudil and Ripasudil B - adrenergic blocker in glaucoma - MOA: + Topical p -adrenergic blockers have been ist line of drugs ~ now P6 F2a + Lower TOP by reducing aqueous formation, + Advantages over mioties - produce less ocular side effects, lipophilic and weak anesthetic (Corneal hypoesthesia and damage) + Contrast to miotics ~ no effects on pupil size tone of ciliary muscle and outflow facility + Ocular S/E : Ocular side effects: mild and ‘Ophthalmology infrequent ~ Stinging, redness, dryness ~ Corneal hypoesthesia ~ Blepharoconjunctivitis + Systemic adverse effects: Major limitation of use ~ Nasolacrimal duct obstruction ~ Life threatening bronchospasm - COPD and asthma ~ Bradycardia, heart block and CHF - ADR + Will be not effective ino patient on systemic + Non selective ones are contraindicated in newborns, + Effect has long term escape. + Inner canthus pressure - applied for 5 min a - adrenergic agonists-MOA + al constrict ciliary BVs - reduced aqueous secretion + a2 in ciliary epithelium reduce aqueous secretion + Secondary role in enhancing drainage of ‘aqueous mainly through wveescleral outflow and also trabecular outflow + {OP by 1 aqueous production (at +22), Tuveoscleral outflow, 7 trabecular outflow (62), + Dipivefrine (0.1%): Prodrug of adrenaline “adr + Apraclonidine (0.5-1%}: Clonidine congener + Brimonidine (0.2%) : Newer clonidine congener, more selective to a2 1. Brimonidine is contraindicated in infants: & children aged up to 5 years, 2. Lesser effect during sleep 3, The most common antiglaucoma drug to couse allergic reaction, 4. Cautious use in patients on Mono Amine Oxidase Inhibitors or Tricyclic Antidepressants, Prostaglandin analogues Low concentration of PGF 2 a analogues | TOP by: + Increase uveoscleral outflow ( ciliary tissue permeability and vascular permeability)? DOC in MayKing & 107 108 Cerebellum Quick Revision Notes, + Trabecular outflow less marked. + TOP in normal pressure glaucoma also + Topically TOT 425- 35%, well sustained + Ocular irritation ard pain + Good efficacy, once daily application and absence of systemic complications - first choice in open angle glaucoma + Other ADRs: iris pigmentation, thickening and darkening of eye lashes etc. 1, Not effective in angle closure glaucoma and corgenital glaucoma 2, Paradoxical rise in IOP if used more than once daily 3. Prostaglandin Associated Orbitopathy may occur with long term use (reversible). + Latanoprest(0,005% eye drop) + Travoprest (0.004%) + Bimatoprost(0,03% or 0.01%) + Tafluprost (0.015%) Carbonic anhydrase inhibitors- MOA + Carbonic anhydrase present within ciliary epithelial cells generates HCO3 ion secreted into og. Humour + Inhibition of carbonic anhydrase - Limits generation of bicarbonate ion-> reduction of aqueous humour. Acetazolamide: + Orally or /v + Used to supplement ocular hypotensive drugs for short term indication like angle closure, before & after surgery/laser therapy. + Long term use when IOP not controlled by topical drugs. + Side effects: Systemic s/e - paresthesia, anorexia, hypokalemia, acidosis, malaise, depression (on long term use) Dorzolamide: 2% eyedrop topical Brinzolamide 1. Should be avoided inpatients with compromised or failing corneal endothelium 2. Systemic CATs should be used with care in patient on diuretics to avoid hypokalemia, 3. Cautious use in older patients, diabetics and cko. 4, Contraindicated in patients with kidney stones ‘nd sulphate allergy Miotics + 1n1970s- were standard antiglaucoma drugs. + Last option because of several drawbacks myopia, diminution of vision, headache Pilocarpine: + Causes miosis by contraction of iris sphincter muscle -rremoves pupillary block and reverses obliteration of iridocorneal angle. + Contraction of ciliary muscle -»pulls on scleral spur ard improves trabecular patency. + Max of 10-20% IOP reduction - 0.5% to 4% solution TREATMENT OF ANGLE CLOSURE GLAUCOMA + Hypertonic mannitol (20%) 15-2g/kg or Glycerol (10%) ~ IV infusion -decongest eye by osmotic action = Glycerin 50% - retention enema + Acetazolamide (0.59) IV followed by oral 8D started concurrently + Miotic: If above reduced the IOP - topical Pilocarpine 1-4% every 10 mins initially & then cat longer intervals + Topical B blocker: Timolol 0.5% 12 hourly in addition + Latanoprost (0.005%) / Apraclonidine (1%) may also be added. + Chronic rarrow angle: miotic/other drugs for longer period STRABISMUS + Strabismus: misaligrment of the visual axes + Orthophoria: perfect alignment of the visual DOC in MayKing & Ophthalmology ‘axes. Most individuals have heterophoria with effort, + Heterophoria (latent squint) tendency of the + Heterotropia: (manifest squint) which is eyes to deviate. Ocular alignment maintained present at all times squint hee Apparent Latent squint = (eterophoray Mani Comitah squint alternating | Convergent Divergent Convergent Divergent HETEROTROPIA + Non accommodative esotropia- it includes congenital or infantile esotropia and acquired Manifest Squint era + Dissociation of the eyes wherein the deviation inall the direction of gaze NEAR TRIAD=accommodatioon+convergence: miosis] * Types The left eye is turned inward-note that the light ~ Comitant/ non paralytic squint reflection in the eyes is rot symmetric ~ Tncomitant / paralytic squint Comitant squint + It isa type of squint characterized by normal extraocular movements and constant degree of ‘squint inall the direction of gaze + Types ~ Esotropia(convergent squint) ~ Exotropia (divergent squi Exotropia (divergent squint) Essential/congenital ET Clinical features: + Presents at 6 months of birth ~ Hypertropia or hypotropia (Vertical squint) 1, Esotropia + Convergent strabismus with eye deviated rasally + Family history common + Accommodative esotropia- is due to the * Characteristic of ET increased convergence associated with ee accommodation reflex DOC in MayKing & 10 Cerebellum Quick Revision Notes ~ Large angle (> 30 prism D) ~ Angle at distance = near + Normal refractive error (therefore not accommodative ET) + Alternating fixation in primary position but cross fixation in side-gaze + Need to exclude VI CN palsy (cover one eye, elicit Dolls reflex) + Latent nystagmus and asymmetrical OKN response may be present 2. Exotropia + Divergent strabismus with eye deviated outward temporally is called exotropia + Tteanbe infantile exotropia, primary exotropia, and secondary exotropia The right eye is turned outward-again, not the light reflection in the eyes is not symmetrical 3. Hypertropia + This characterized by vertical misalignment of eyes with upward deviation of the squinting eye + The common causes are. ~ Trochlear nerve palsy ~ Thyroid eye disease. ~ Brown's syndrome The right eye is turned upward- light reflection not symmetrical 4 4. Hypotropi + Tt is characterized by vertical misaligrment of the eyes with downward deviation of the squinting eye The right eye is turned downward: light reflection in eyes is not symmetric Incomitant squint + It is characterized by limited or restricted extraocular movements and varying degree of squint in different directions of gaze types + Paralytic and restrictive squint 1. Paralytic squint + Tt is characterized by limited extraocular movements in the direction of action of the paralyzed muscle and varying degree of squint indifferent directions of gaze ci: + Diplopia, + Vertigo, + Nausea, and vomiting + False projection of the object + Limitation of the ocular movements in the direction of action of the paralyzes muscles + Compensatory head posture to neutralize the diplopia Clinical Types + Oculomotor nerve palsy + Trochlear nerve palsy + Abducent nerve palsy + Total ophthalmoplegia + Interruclear ophthalmoplegia DOC in MayKing & Ophthalmology 2. Restrictive Squint “What is the pathogenesis?" Pontine. + It is characterized by restriction of the Gysgerasia with 3rd CN ‘extraocular movements with small deviation in the primary position of gaze innervating both MR and LR Etiology: DIAGNOSIS OF SQUINT * Usually caused by the fibrosis of the + Assessment of visual acuity and refractive extraocular muscle or by restriction of the exer movement of the extraocular muscle + Corneal reflex test + The common clinical syndromes associated restrictive squint includes, + Cover test + Brown's syndrome. + Prism bar cover test + Strabismus fixus + Maddox rod test + Duane's retraction syndrome + Maddox wing test Duane's Retraction Syndrome + Assessment of binocular vision + The main clinical feature is retraction of the globe on attempted adduction TREAT AEN OF SGQUINT Tec cist! ttn tye + Optical correction of the underlying refractive error Glossifieation + Orthoptic exercises Type 1 + Surgical correction of the affected muscle - on (resection of recession of the muscle) ~ Limitation in abduction eye reel ~ Can present as an ET ~ The stronger eye is patched to force ‘the brain to interpret images from the Type 2 strabismic eye. 15% ~ Eye patches will not change the angle of the Limitation in adduction ‘strabismus. ~ Gon present as an XT Typically, eye patching is used only if amblyopia is present. Type 3 ~ 25% ~ Limitation in both adduction and abduction Usually orthophoric Clinical features: + Females more common + Left eye in 60%, bilateral in 20% + Retraction of globe on adduction (sine qua non) ~ Co-contraction of MR and LR ‘Associated with narrowing of palpebral fissure DOC in MayKing & Mm m2 Cerebellum Quick Revision Notes PRINCIPLES OF STRABISMUS SURGERY : Weakening procedures . + Recession + Margirel myotemy + Posterior Fixation suture Strengthening procedures + Resection + Tucking + Advancement Recession Surgery Resection Surgery . Frontal bone Zygomatic bone Maxillary bone Ethmoid bone. ‘Sphenoid bone Lacrimal bone Palatine bone Dimensions- Alignments of Orbit Alignment of the orbits medial walls are saan parallel bf 5 lateral walls are peas perpendicular a C7 cn soo eyeballs make an angle of 22.5 with the orbital axes. ‘Medial Walls are parallel Lateral Walls are perpendicular Walls of Orbit For esotropia + Recession of MR & resection of LR of squinting eye + Recession of medial rectus of both the eyes For exotropia + Recession of LR and resection of MR of squinting eye + Recession of lateral rectus of both the eyes The ORBIT : Anatomy of Orbit Quadrangular truncated pyramidal in shape. ‘Seven bones make up the bony orbit: boc May bony orbit has four walls ‘Medial wall Lateral wall Roof Floor Clinical Application : Medial Orbital Wall ing ©

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