Dissertation on
“INCIDENCE OF GLAUCOMA IN OCULAR TRAUMA”
Submitted in partial fulfilment of requirements of M. S. OPHTHALMOLOGY
BRANCH III Of
REGIONAL INSTITUTE OF OPHTHALMOLOGY MADRAS MEDICAL COLLEGE
CHENNAI – 600 003
THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY CHENNAI-600 003
MAY - 2019
CERTIFICATE
This is to certify that this dissertation entitled “INCIDENCE OF GLAUCOMA IN OCULAR TRAUMA” is a bonafide record of the research work done by Dr. A. RANI PRIYADHARSINI, Post graduate in Regional Institute of Ophthalmology, Madras Medical College and Research Institute, Government General Hospital,Chennai-03, in partial fulfillment of the regulations laid down by The Tamil Nadu Dr.M.G.R. Medical University for the award of M.S. Ophthalmology Branch III, under my guidance and supervision during the academic years 2016-2019.
Prof. Dr. M. R. CHITRA, M.S., Chief, Glaucoma services ,
Regional Institute of Ophthalmology
Madras Medical College & Research Institute, Govt. General Hospital,
Chennai – 600 008
Prof. Dr. M.ANANDA BABU, M.S. D.O., Director and Superintendent,
Regional Institute of Ophthalmology
Madras Medical College & Research Institute, Govt. General Hospital,
Chennai – 600 008
Dr. R. JAYANTHI, M.D., FRCP (Glasg), Dean,
Madras Medical College,
Government General Hospital & Research Institute, Chennai-600003
ACKNOWLEDGEMENT
I would like to thank Prof. Dr. JAYANTHI., M.D.,FRCP (Glasg), Dean, Madras Medical College and Research Institute for giving me permission to conduct the study in this Institution.
With due respect and gratitude, I thank Prof.Dr.ANANDA BABU, M.S., D.O., Director and superintendent, Regional Institute of Ophthalmology and Govt.
Ophthalmic Hospital, Chennai for permitting me to conduct this study.
Prof.Dr.M.R.CHITRA M.S., Unit Chief, Glaucoma services, and my guide for assigning me this topic for study and guiding me throughout my Post graduate course. I wish to express my sincere thanks for the valuable help, encouragement and guidance at various stages of the study.
My sincere thanks to my Assisstant Professors Dr.R.SARAVANAN, M.S., Dr.T.VIMALA M.S., Dr.C.USHA M.S., D.O., for their timely help and guidance in conducting this study.
I wish to express my sincere thanks to my family, friends and all my colleagues who helped me in bringing out this study.
Last but not the least, my heartful gratitude and sincere thanks to all my patients without whom this endeavor would not have been possible.
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation entitled, “INCIDENCE OF GLAUCOMA IN OCULAR TRAUMA” is a bonafide and genuine research work conducted by me under the guidance of Prof. Dr. M. R. CHITRA, M.S., Head of Department of glaucoma services, Regional institute of ophthalmology &
Government Ophthalmic Hospital. Chennai - 600008.
Dr. A. RANI PRIYADHARSINI
Place: Chennai Date
CONTENTS
S.NO TITLE PAGE
NUMBER PART – I
1. INTRODUCTION 1
2. ANATOMY OF ANGLE STRUTURES AND
GONIOSCOPY 2
3. AQUEOUS HUMOR DYNAMICS 8
4. TONOMETRY 16
5. OPTIC NERVE HEAD ANATOMY AND FUNDUS
CHANGES IN GLAUCOMA 24
6. AETIOPATHOGENESIS OF TRAUMATIC GLAUCOMA 29
7. INVESTIGATIONS IN TRAUMATIC GLAUCOMA 51
8. REVIEW OF LITERATURE 65
PART II
9. AIM AND OBJECTIVES 69
10. MATERIALS AND METHODS 70
11. RESULTS 72
12. DISCUSSION 83
13. CONCLUSION 86
PART III
14. BIBLIOGRAPHY 87
15. PROFORMA 89
16 PATIENT INFORMATION FORM 91
17. PATIENT CONSENT FORM 93
18. KEY TO MASTER CHART 94
19. MASTER CHART 98
20. ETHICAL COMMITTEE APPROVAL 107
21. ANTI-PLAGIARISM CERTIFICATE 108
PART 1
1
INTRODUCTION
DEFINITION OF GLAUCOMA
Glaucoma is a chronic, progressive optic neuropathy which leads to characteristics optic nerve head changes with corresponding visual field defect in which raised intraocular pressure, is the only modifiable risk factor.
CLASSIFICATION OF GLAUCOMA Classification based on aetiology A] Primary
B] Secondary
Classification based on mechanism of aqueous outflow obstruction through anterior chamber angle
A] Angle closure glaucoma
a. Anterior (Pulling mechanism)
1. Contracture of membranes in anterior chamber angle 2. Contracture of inflammatory precipitates
b. Posterior (Pushing mechanism) 1. with pupillary block
2. without pupillary block B] Open angle glaucoma
a. Pretrabecular (membrane overgrowth)
b. Trabecular (occlusion of intertrabecular spaces) c. Post- trabecular
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C] Developmental glaucoma a. High insertion of iris
b. Incomplete development of trabecular meshwork c. Iridocorneal adhesion
ANATOMY OF ANGLE STRUCTURES:
Angle structure from posterior to anterior – Ciliary body
Scleral spur
Trabecular meshwork Schwalbe’s line
Ciliary body – anterior part of ciliary body which lies between the iris root and scleral spur
Scleral spur- scleral spur is the posterior lip of scleral sulcus. Anteriorly, it is attached to the corneoscleral meshwork and posteriorly to the longitudinal fibres of ciliary body. It prevents the collapse of schlemm’s canal.
Trabecular meshwork- it is formed by three portions.
Innermost portion is uveal meshwork, which bridges the iris root and ciliary body. It has many irregular openings.
Middle one is the corneoscleral meshwork which is attached anteriorly to the scleral spur and extends to scleral sulcus. It has an elliptical opening.
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Outermost part is the juxtacanalicular meshwork which is lined by endothelium. It forms a narrow channel between the corneoscleral meshwork and schlemm’s canal.
Schwalbe’s line- it is termination of descement’s membrane.
GONIOSCOPY
It is the procedure to visualise the anterior chamber angle. It is used for both therapeutic and diagnostic procedures.
Principles of gonioscopy
• Anterior chamber angle cannot be visualised directly through the intact cornea because light rays from angle structures undergoes total internal reflection.
• Critical angle – when the light rays travel from higher medium to lower refractive index (such as from cornea to air), it will be reflected between the two unless the angle of incidence is less than the critical angle depending on their refractive index difference.Normal critical angle is 46º for the tearfilm-air interface.
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Figure 1.
A: Light ray is refracted when angle of incidence (i) at interface of two media with different indices of refraction (n and n) is less than the critical angle.
B: Angle of refraction (r) is 90 degrees when i equals the critical angle.
C: Light is reflected when i exceeds the critical angle.
D: Light from the anterior chamber angle exceeds the critical angle at the cornea- air interface and is reflected back into the eye.
E and F: Contact lenses have an index of retraction (n) similar to that of the cornea, allowing light to enter the lens and then be refracted (goniolens) or reflected (gonioprism) beyond the contact lens-air interface.
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GONIOSCOPIC FINDING OF ANGLE STRUCTURE
Figure 2. Angle of Anterior Chamber
Ciliary body (CBB) – It is grey or dark brown in colour. It is wider in myopes and narrow in hypermetropes.
Scleral spur (SS) - It is a prominent white line located immediately posterior to the trabeculum. It may be obscured by iris process, iris bombe, peripheral anterior synechiae.
Trabecular meshwork (TM) –it extends from schwalbe’s line to scleral spur.
It looks faint tan to dark brown. The pigmentation increases with age. Anterior part of trabecular meshwork is non-functional. The posterior pigmented part is functional and is the primary site for aqueous outflow.
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Schwalbe’s line- A fine ridge anterior to trabecular meshwork which is identified by a small build up of pigments. Corneal wedge is useful to identify the inconspicuous schwalbe’s line. It helps to differentiate wide open with non pigmented trabecular meshwork (eg; young patients) and angle closer.
Indentation Gonioscopy – It helps to differentiate appositional vs synechiael angle closure.
GRADING OF ANGLES
Shaffers and Modified Shaffers grading
Grade Angle
width Configuration Chances of closure
Structures visible on Gonioscopy
0 O degree Closed Closed No angle structures visible
I 10 degree Very narrow High Schwalbe’s line only
II 20 degree Moderately
narrow Possible From schwalbe’s line to trabecular meshwork
III 20-
35degree Open angle Nil
From schwalbe’s line to scleral spur
IV 35-45
degree Wide open Nil From schwalbe’s line to ciliary body
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Limitation of Gonioscopy
Cannot be performed in painful inflamed eye Hyphema
Compromised cornea
Lacerated or perforated globe
Gonioscopy can be done 6 to 8 weeks after traumatic hyphema.
LIMBAL CHAMBER DEPTH IS ESTIMATED BY MODIFIED VAN HERICK GRADING
On slit lamp examination, the brightest, narrowest, vertical beam of light is focused at the temporal limbus with the illumination column at 60º from the axis of microscope. Under maximum magnification, the beam should be kept at the most peripheral point of temporal limbus.
Closed
angle Absent peripheral anterior chamber
Slit angle Anterior chamber depth extremely shallow Grade 1 Anterior chamber depth < ¼ corneal thickness
Grade 2 Anterior chamber depth more than ¼ corneal thickness Grade 3 Anterior chamber depth ¼ to ½ corneal thickness Grade 4 Anterior chamber depth equal to corneal thickness
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Figure 3. a) Van Herick grade 1 b) Van Herick grade 4
AQUEOUS HUMOR FORMATION
Aqueous humor is secreted by non pigmented epithelial cells of ciliary process in to posterior chamber, it reaches the anterior chamber via pupil. Aqueous humor drained through the trabecular meshwork (conventional pathway) and uveoscleral flow (unconventional pathway)
MECHANISM OF AQUEOUS HUMOR FORMATION 1. Ultrafiltration (under hydrostatic pressure)
2. Active secretion (against electrochemical process) 3. Diffusion (along concentration gradient)
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Figure 4. Aqueous Humor Formation
Ciliary processes are the site of aqueous humor formation. Aqueous humor derived from plasma within the capillary network of ciliary processes. Presently it agreed that diffusion, ultrafiltration and secretion play arole in aqueous production at different levels. Major factors are active secretion (70%), ultrafiltration (20%) and osmosis accounts for 10%.
Plasma secreted into the ciliary process stroma from the ciliary capillaries due to ultrafiltration and diffusion.
Then it transports into the pigment epithelial cells from stroma by active transport. Following mechanism are mainly involved in this process:
1. Na+K+2Cl- symport 2. Na+H+ antiport 3. Cl- HCO3- antiport
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Then it transports into nonpigmented epithelial cells with low resistance from pigmented epithelial cell.
Then it transports to posterior chamber by active transport.
VARIOUS SECRETORY PROCESSES
• Sodium
Na-K ATPase Na –K-2Cl symport
Na-H antiport, Cl-HCO3 antiport
• Bicarbonate
Maintain pH and proper function of Na-K ATPase.
• Potassium
Transport by active secretion and diffusion
• Chloride
Affected by pH and Na+ ion concentration Rate limiting step in Aqueous flow
• Water
Transport through aquaporin channel
• O2 and glucose pass the BAB by simple and facilitated diffusion.
• Ascorbic acid
Na dependent L-ascorbic acid transporter
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AQUEOUS HUMOR
It maintains structural integrity of the eyeball and intraocular pressure It provides clear medium for optical property
It provides nutrition, delivers oxygen and eliminates metabolic waste It delivers antioxidant like ascorbate and provides local immunity PHYSIOLOGICAL CHARACTER
pH - 7.2,
Refractive index – 1.36
Osmotic pressure higher than blood Specific gravity slightly more than water
Total volume – 0.31ml, anterior chamber- 0.25ml, posterior chamber – 0.05ml Rate of formation – 2 to 2.5microlitre (1% of AC volume/ min)
COMPOSITION
Inorganic ions- increase chloride content, decrease bicarbonate than plasma Organic ions- lactate, ascorbic acid (30 fold higher than plasma), hyaluronic acid, hydrogen peroxide.
Carbohydrate, glutathione and urea Less protein
Growth modulatory factors, oxygen and carbon dioxide.
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BLOOD AQUEOUS BARRIER
Adjacent non pigmented epithelial cells connected by tight junctions in apical portion of the cells, forms a blood aqueous barrier.
It maintain the chemical composition between the plasma and aqueous
Figure 5. Blood aqueous barrier
AQUEOUS HUMOR DRAINAGE
Conventional or Trabecular pathway (80 -90%) Unconventional or Uveoscleral pathway (10-20%)
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Trabecular pathway
Uveal meshwork Corneoscleral meshwork
Juxta canalicular trabecular meshwork Trabecular meshwork
Trabecular meshwork
Schlemm’s canal
Aqueous vein of ascher
Episcleral vein conjunctival vein
Anterior scleral artery and angular and palpebral vein Superior ophthalmic vein
Facial vein and superior ophthalmic vein
Cavernous sinus
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Mechanism of aqueous humor transport to schlemm’s canal:
Leaky pores in endothelial cells Microfilaments contracture Vacuolation theory
Aqueous outflow pump
Figure 6. Aqueous outflow system UVEOSCLERAL OUTFLOW
Pressure independent (10 to 20%)
0.3micro litre /min and independent of IOP Ciliary body
Suprachoroidal space Ciliary body venous circulation Choroid
Sclera
Vortex vein/ Orbital tissue
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Figure 7. Uveoscleral Outflow
Factors affecting blood aqueous barrier
Trauma to the iris (contusion, iridodialysis, sphincter tear) Mechanical trauma to the lens
Chemical injury like acid, alkali, formaldehyde Inflammatory mediators
Trigeminal nerve stimulation Factors affecting aqueous formation
Diurnal variation- 1.5 to 4.5 micro litre /min. aqueous humor production increase in morning 8 AM to noon. Decrease in midnight to early morning 6AM.
Age Sleep
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Inflammation
Breakdown of blood brain barrier Blood flow to ciliary body
Factors affecting aqueous outflow Age
Myopia
Diabetes mellitus Steroid
Inflammation (inflammatory cells clogged the trabecular meshwork) Trauma (breakdown of blood aqueous barrier, hyphema, late closure of cyclodialysis cleft) and Drugs
TONOMETRY
IDEAL TONOMETER
• Should give accurate and reasonable IOP measurement
• Convenient to use
• Simple to calibrate
• Free of maintenance problems
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TYPES OF TONOMETRY
Newer tonometers
Trans-palpebral tonometry Dynamic contour tonometry Ocular response analyser
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Digital tonometry / Palpation method:
It is an indirect method of measuring the IOP.
Intraocular pressure (IOP) is estimated by response of eye to pressure applied by finger.
PROCEDURE: Ask the patient looks down and place the Index finger of both hands over the closed eyelids. One finger is kept stationary which feels the fluctuation produced by the indentation of globe by the other finger.
GOLDMANN APPLANATION TONOMETRY
It is the Gold standard method for measurement of intraocular pressure.
It is a type of variable force applanation tonometer.
It determines the force necessary to applanate an area of cornea of 3.06 mm in diameter.
Principle:
Modified Imbert ficks law
It states that the pressure inside an ideal dry, thin walled sphere equals the force necessary to flatten its surface divided by the area of flattening.
P= F/A
At 3.06 mm of corneal diameter, the resistance to flattening is counterbalanced by the capillary attraction of the tear film meniscus for the tonometer head.
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Figure 8. Goldmann Applanation Tonometry Procedure
Patient is asked not to drink large quantity of fluids for two hours before doing the test
Explain the procedure to the patient. The patient is instructed to relax, maintain the position, holds the eye wide open.
Then, one drop of topical anesthesia is placed in each eye, commonly used is 0.5% proparacaine. Moistened fluorescein strip is placed in the lower fornix to stain the eye.
Contact lens should be removed before fluorescein staining because it stains the contact lens.
Before using the tonometer tip, we have to clean it with sterilizing solution and allow to dry.
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The tension knob is set at one grams. If the knob set as 0, the prism head will vibrate when it touches the eye and produce corneal abrasion.
The 0 mark of the prism is set at white line on the prism holder. Then illuminate the prism head with cobalt blue filter opened maximally.
The angle between the illumination column and the microscope axis should be 60º.
The microscope is advanced towards the patient with the examiner observing from the side until the limbal zone has a bluish hue. The prism should not touch the lids or lashes.
When viewed monocularly two fluorescent semicircles are seen through the biprism. The fluorescein rings undergo rhythmic movement in response to cardiac cycle.
Adjust the tension knob until the inner edges of the two semicircle touch each other at the midpoint of their pulsations.
Contraindication:
Active eye infection Recurrent corneal erosion
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POTENTIAL ERRORS:
Falsely low IOP
Too little fluorescein
Thin cornea
Corneal edema
With the rule astigmatism
Prolonged contact
Repeated tonometry
Falsely high IOP
too much fluorescein
thick cornea
steep cornea
against the rule astigmatism 1mm Hg per 3D
wider meniscus
Widening the lid fissure excessively
Elevating the eyes more than 15°
Normal intraocular pressure -11 to 21mmHg.
IMPACT-REBOUND TONOMETER (ICARE)
It is an updated version of an indentation tonometer.
It consists of pair of coils coaxial with probe shaft, a solenoid coil and sensing coil.
PROCEDURE
A light weight sterile probe is propelled forward into the cornea by a solenoid and sensing coil monitors the movement.
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The time taken for the probe to return to its resting position and the
characteristics of the rebound motion are indicates IOP and biomechanical properties of the cornea.
Time taken
longer in eyes with lower IOP and
faster in eyes with higher IOP.
Figure 9. I care ADVANTAGES
Icare can be used without anesthetizing the eye because the probe is extremely light and its contact with the cornea is very short .
Used in situations when patients are unable to be seated or measured at the slit lamp.
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DISADVANTAGES
Tend to read slightly higher than the Goldmann.
Accuracy falls off in scarred corneas.
Mackay marg tonometer
Principle - constant area and variable force, applanation contact tonometer.
It is used for the measurement of IOP in eyes with edematous, scarred or irregular cornea.
It is also accurate when used over therapeutic or soft contact lens Tonopen :
Principle- same principle of mackay marg tonometer Its portable and battery operated.
The probe tip is protected by disposable latex which reduces infection transmission.
The device displays the average of 10 independent reading.
Figure 10. Tonopen
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OPTIC NERVE HEAD ANATOMY
The normal optic nerve consist of 1.2 million axons which originate from the the cell bodies of the ganglion cells of the retina. The distal part of the optic nerve is optic nerve head. Nerve fibres arise from the ganglion cell layer which travel in the superficial retinal nerve fibre layer. Then they make 90º turn and remain at the outer edge of optic nerve head which is called as neuro- retinal rim. The axons from the central region occupies the superficial layer of retina. The neuroretinal rim is reddish orange in colour because it consist of capillaries, glial cells and astrocytes.
The axons exit the globe through the lamina cribrosa. Optic cup is the centre of optic nerve head which is pale due to visibility of lamina cribrosa and connective tissues.
DIVISIONS OF OPTIC NERVE HEAD
Surface nerve fibre layer- it is formed by the axons of ganglion cells which is supplied by the retinal arteries and intraocular branches of central retinal artery.
Prelaminar region- it is composed of axons, astrocytes and astroglial tissue which are more than surface nerve fibre layer. This region receives blood supply from the direct branches of posterior ciliary arteries.
Lamina cribrosa- it consists of series of fenestrated collagen plates, through which axons of nerve fibre layer pass to the retrolaminar region. Larger pores and less connective tissue support are present in inferior and superior areas. It receives blood supply from the short posterior ciliary arteries and pial plexus.
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The retrolaminar region- Myelinated axons start from this region. It receives blood supply from posterior ciliary arteries and small branches from central retinal artery and pial plexus.
OPTIC NERVE HEAD EVALUATION
There are various methods to measure optic nerve head clinically:
Direct ophthalmoscope- The Welch-Allyn 5º spot light diameter is 1.5 which is used to measure the optic disc size.
Slit-lamp biomicroscopy- On slit-lamp examination with hand held high power convex lens like volks 60D (magnification 1×), 78D (×1.1), 90D(×1.3), optic nerve head can be measured. These measurements are not influenced by distance of the lens or by refractory errors up to 8D of ametropia but influenced by axial length.
FUNDUS CHANGES IN GLAUCOMA
Normal optic disc is vertically oval, 1.5 mm in diameter. Neuro retinal rim lies between disc margin and cup. Normally it is pink in color. It follows ISNT rule.
That implies, inferior neuro retinal rim is the broadest, followed by superior, nasal and temporal neuro retinal rim. As glaucoma advances, neuro retinal rim will be thinned out and lost.
CUP DISC RATIO
• It is expressed as diameter of the cup as a fraction of diameter of optic disc.
Vertical cup disc ratio is more important than horizontal cup disc ratio, because pores are larger in superior and inferior poles and also less glial support to superior and inferior pole areas.
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• Cup disc ratio of > 0.3 or
• Asymmetry of cup disc ratio >0.2 between two eyes are considered significant.
• Disc size is also important while measuring cup disc ratio
Figure 11. Neuro Retinal Rim Thickness
Figure 12. This picture shows Nasalization of vessels and Laminar dot sign
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Laminar dot sign – it is due to loss of neural tissues, leading to exposure of underlying laminar pores.
BARING OF CIRCUMLINEAR VESSEL
As the neuroretinal rim recedes, normal circumlinear vessel which outlines the cup will be bared from cup margin.
BAYONETTING OF VESSELS- Double angulation of the vessels
Due to loss or absent of neuroretinal rim, the vessels pass through the overhanging edges of the cup and take sharp angulation at the cup margin.
Figure 13. This picture depicts Cup disc ratio 0.9, circumferential Neuroretinal rim thining and bayonetting of vessels
RETINAL NERVE FIBRE LAYER
Retinal nerve fibre layer will be seen as striations in light reflex. On red free filter retinal nerve fibre layer defects can be visualized as darker areas of slit or wedge shaped defects.
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PERIPAPILLARY PIGMENTATION There are 2 zones, alpha and beta zones.
- Beta zone lies between outer alpha and optic disc margin. It occurs due to atrophy of retinal pigment epithelial layer, reduction in photoreceptors and choroidal degeneration. Changes in Zone beta is significant in glaucoma. It produces absolute scotoma.
- Zone alpha is the outer zone, which lies external to beta zone. It occurs due to retinal pigment epithelial changes.
Figure 14. Retinal nerve fibre layer defect
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TRAUMATIC GLAUCOMA
Traumatic eye injury is one of the most common causes of unilateral blindness worldwide. Glaucoma is a common and often devastating consequence of ocular trauma.
Traumatic glaucoma can be present as secondary open angle or secondary closed angle glaucoma. Transient or prolonged elevation of intraocular pressure in early or late phase after trauma which damage the trabecular meshwork and other structures predisposing traumatized eye to the development of glaucomatous optic nerve head changes.
Traumatic glaucoma can occur in following condition 1. Blunt injury
2. Penetrating injury 3. Chemical injury 4. Thermal injury 5. Radiation exposure 6. Electric shock
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MECHANISM OF GLAUCOMA FOLLOWING OCULAR TRAUMA GLAUCOMA FOLLOWING BLUNT INJURY
a. Early onset
1. Trauma to trabecular meshwork 2. Inflammation
3. Hyphema
4. Traumatic lens subluxation with pupillary block 5. Traumatic lens swelling with pupillary block 6. vitreous filling the anterior chamber
7. Schwartz matsuo syndrome (fluctuation in intraocular pressure associated with retinal detachment accompanied by tears of nonpigmentary epithelium of the ciliary body.)
b. delayed onset
1. Angle recession 2. Ghost cell glaucoma 3. Hemolytic glaucoma
4. Peripheral anterior synechiae
5. Posterior synechiae with pupillary block 6. Neovascular glaucoma
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Figure 15. Iridodialysis
GLAUCOMA FOLLOWING PENETRATING INJURY
a. Flat anterior chamber with formation of peripheral anterior synechiae b. Inflammation
c. Ghost cell glaucoma d. Hyphema
e. Lens subluxation with pupillary block f. Traumatic lens swelling
g. Lens particle glaucoma h. Epithelial downgrowth i. Fibrous ingrowth
j. Retained intraocular foreign body
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Figure 16. Postop central corneal tear suture with subconjuctival hemorrhage
CHEMICAL INJURY
TYPES OF CHEMICAL INJURY Alkaline agents
It will penetrate the ocular tissues deeply and may lead to glaucoma. Dicrotic pressure rise is noted - immediate pressure rise followed by normal pressure for sometimes and again rise in intraocular pressure.
Acidic chemicals
It causes coagulation of tissue protein which limits the penetration.
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Mechanism of raised intraocular pressure following chemical injury
1. Early phase ( minutes to hour) due to scleral shrinkage and prostaglandin release
2. Intermediate phase due to inflammation, acute swelling of lens and posterior synechiae
3. Late phase ( weeks to months) due to trabecular scarring and formation of posterior synechiae
Management
Early phase- Antiglaucoma drugs like Beta-adrenergic antagonist, Alpha2 adrenergic agonist, carbonic anhydrous inhibitors and hyperosmotics.
Intermediate phase-
Topical corticosteroids use with caution, because of the risk of stromal lysis.
Oral corticosteroids - to reduce inflammation.
Cycloplegic/ Mydriatics- to alleviate pain, prevent synechiae formation.
Late phase
Filtering surgery
Glaucoma shunt device Cyclodestructive procedures
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THERMAL INJURY
Rarely cause raised intraocular pressure
Mechanism of raised intraocular pressure is due to orbital congestion and massive periorbital swelling
Treatment- lateral canthotomy RADIATION DAMAGE
Raised intraocular pressure is due to neovascular glaucoma or intraocular hemorrhage. It has a poor prognosis.
ELECTRICAL SHOCK
Raised intraocular pressure due to venous dilatation, contracture of extraocular muscle and pigment dispersion.
CAUSES OF OPEN ANGLE GLAUCOMA IN OCULAR TRAUMA Early – Inflammation, Hyphema and Lens particle glaucoma.
Late – Angle recession glaucoma, Ghost cell glaucoma, Hemolytic glaucoma, and Retained intraocular foreign body (e.g: Hemosiderosis glaucoma)
CAUSES OF CLOSED ANGLE GLAUCOMA IN OCULAR TRAUMA Early causes
1. Flat anterior chamber leading to peripheral synechiae, 2. Anterior subluxation of lens with pupillary block, 3. Anterior dislocated lens with pupillary block, 4. Traumatic lens swelling.
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Late causes
1. posterior synechiae with pupillary block, 2. Peripheral anterior synechiae,
3. Epithelial ingrowth
4. Late closure of ciliary cleft 5. Fibrous downgrowth
TRAUMATIC IRITIS
Traumatic iritis produces both open angle and closed angle glaucoma. In acute inflammation IOP is low, due to ciliary shock and reduced aqueous production.
Distruption of blood aqueous barrier causes release of protein and inflammatory cells in anterior chamber which results in increased viscosity of aqueous humor.
Trabecular meshwork is obstructed by inflammatory cells and debris Scarring and dysfunction of outflow channels (trabecular meshwork) Forward displacement of iris- lens diaphragm by uveal effusion Neovascularization in the angle
Posterior synechiae with pupillary block Peripheral anterior synechiae
Liberation of prostaglandins and substance-P
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CLINICAL FEATURES
Pain, redness, photophobia, defective vision Corneal edema, circumcorneal congestion Anterior chamber – flare, cells
TREATMENT
Topical Cycloplegics - to reduce ciliary spasm, prevent the formation of synechiae, break the formed synechiae, reduce release of inflammatory cells, open the corneal lamellae to increase drug penetration
Topical corticosteroids (used with caution because of possibility of steroid induced glaucoma)
Filtering surgery with adjuvant antimetabolite therapy
Glaucoma drainage device such as Molteno, Baerveldt, and Ahmed implants.
HYPHEMA DEFINITION
Blood in the anterior chamber of the eye is called hyphema. It results from iris or ciliary body tear leading to bleeding from anterior ciliary and iris stromal vessels. Hyphema occurs in both blunt and penetrating injury.
Sickle cell patients are more prone for rebleed and glaucomatous changes even with moderate rise in intraocular pressure.
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PATHOGENESIS
In penetrating injury, hyphema develop by direct injury to the iris, ciliary body, trabecular meshwork and their blood vessels.
In blunt trauma, due to compressive force on eyeball, it causes stretching of the limbal tissue, scleral expansion, peripheral displacement of aqueous, increase the pressure in the angle which injure the angle structures (tear in the anterior face of ciliary body), iris (iridodialysis, sphincter tear, iridoschisis), lens and posterior segment.
MECHANISM
Obstruction of trabecular meshwork by blood cells and fibrin
Secondary fibrosis and descemetization of angle leads to late rise in intraocular pressure which is very rare.
GRADING OF HYPHEMA
Grading by volume of anterior chamber filled with blood after layering of the red blood cells.
Grade I Less than one third of anterior chamber
Grade II One third to one half of the anterior
chamber
Grade III One half to nearly total
Grade IV Total( eight ball)
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Figure 17. Grading of hyphema
Figure 18. Total hyphema
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MANAGEMENT
Conservative management
Monitor daily for 3 to 5 days to look for rebleed and measurement of intraocular pressure.
Bed rest in semi upright posture, limitation of activity to prevent rebleed.
Discontinue use of anticoagulant medications if any.
Antifibrinolytic agents such as Aminocaproic acid or tranexamic acid Usually total resorption occur within 5 to 7days.
Patient with raised intraocular pressure Medical management-
Topical Cycloplegics- to alleviate pain by relieving ciliary spasm, prevent posterior synechiae formation.
Topical steroids and oral steroids- inhibition of fibrinolysis and stabilization of blood ocular barrier.
Antiglaucoma medications- beta blockers, alpha2 adrenergic agonist, carbonic anhydrase
Inhibitors (should not be used in sickle cell patients). In cases of intraocular pressure more than 30mmHg, intravenous mannitol 200ml IV every 12hours should be given.
Surgical management-
Anterior chamber irrigation and aspiration Indications:
To prevent corneal staining Total hyphema more than 4 days
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Failure in the control of intraocular pressure elevation medically One proposed guidelines for intervention are IOP of 60mmHg for 2days IOP of 50mmHg for 5days IOP of 35mmHg for 7days.
If IOP higher than 30mmHg for more than 24hours in sickle cell patients, surgical intervention should be considered.
• Intracameral injection of tissue plasminogen activator COMPLICATIONS
Corneal blood staining Rebleeding
Pupillary block
Peripheral anterior synechiae, posterior synechiae
Amblyopia (early intervention is needed in pediatric hyphema) ANGLE RECESSION GLAUCOMA
It is a type of secondary open angle glaucoma.
Angle recession refers to a tear between the circular and longitudinal fibres of the ciliary body.
Presents with an elevated intraocular pressure up to years after blunt trauma.
This condition may be underdiagnosed because onset is often delayed and because of history of injury may be distant or forgotten.
Clinically, patients with angle recession glaucoma are usually detected during a routine eye examination later in life.
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CLINICAL FEATURES
Anterior chamber- deep or irregular
Signs of previous injuries like iridodialysis, iris sphincter tear, rosette shaped cataract, trabecular meshwork pigmentation.
Gonioscopy – angle recession (irregular widening of ciliary body band) seen
Chances of developing glaucoma in angle recession:
Angle recession <180 degrees- glaucoma is unusual Angle recession >180 degrees - 4 to 9%
Angle Recession >270 degrees- higher risk of chronic glaucoma
Figure 19. Angle recession
Irregularly widened ciliary body band
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PATHOGENESIS
Blunt injury to the globe
Sudden indentation of cornea
Anteroposterior compression
Equatorial expansion
Hydrodynamic effect which displaces aqueous laterally
Shearing force applied to the angle structure shearing of anastomosing branch of
Anterior ciliary arteries Tear between the longitudinal and
Circular muscle of ciliary body HYPHEMA
ANGLE RECESSION
Trabecular dysfunction CHRONIC Elevated IOP
GLAUCOMATOUS OPTIC ATROPHY
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Figure 20. Blunt Injury
TREATMENT
Antiglaucoma medications - Beta blockers, Alpha adrenergic agonists, carbonic anhydrase inhibitors, prostaglandin analogues.
If medical therapy fails, surgical management is advisable.
Surgical procedures
Trabeculectomy with antimetabolites Glaucoma drainage devices
Laser therapies- Nd: YAG laser trabeculopuncture Argon laser trabeculoplasty
Cyclodestructive procedures in cases of eyes with poor visual potency.
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GHOST CELL GLAUCOMA
It occurs in intraocular haemorrhages especially in vitreous hemorrhage.
It is a type of secondary open angle glaucoma in which degenerated red blood cells (ghost cells) in the vitreous cavity enter the anterior chamber through the disrupted anterior hyaloid face and obstruct the aqueous outflow facility.
Following trauma, surgery or retinal disease, blood enters the vitreous cavity. Fresh erythrocytes in the vitreous cavity transformed into ghost cells which are khaki coloured, spherical and less pliable. So it cannot pass readily through the trabecular meshwork and accumulate there leading to temporary obstruction of aqueous outflow.
Clinical features
Pain, corneal edema, pseudohypopyon which is rarely associated with a layer of fresh red blood cells ( candy stripe sign) khaki coloured cells in anterior chamber, corneal endothelium and angle of anterior chamber.
DIAGNOSIS
Ghost cell glaucoma is confirmed by anterior chamber paracentesis, aspirated fluid is tested under phase contrast microscopy or millipore filter and staining with hematoxylin eosin. TREATMENT
Medical management- Antiglaucoma drugs Surgical management- Anterior chamber wash Vitrectomy.
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HEMOLYTIC GLAUCOMA
In this type, RBC laden macrophages accumulate in the trabecular meshwork and obstruct the aqueous outflow temporarily.
Treatment: Antiglaucoma medications. If tension is not controlled with medications, Filtering surgery and Cyclodestructive procedures can be done.
HEMOSIDEROTIC GLAUCOMA
It occurs due to intraocular hemorrhage. Hemoglobin which is released by the degenerative red blood cells is engulfed by the trabecular endothelium. It obstructs the aqueous outflow pathway.
LENS INDUCED GLAUCOMA LENS SWELLING
Blunt or penetrating injury may alter the lens fibres, lens capsule. It results in hydration of lens which leads to lens swelling. Swollen lens causes the forward displacement of the lens iris diaphragm which reduces the iridocorneal angle.
It causes angle closure glaucoma secondary to pupillary block.
Definitive treatment is cataract extraction.
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LENS DISLOCATION OR SUBLUXATION
Blunt trauma
Rupture of portion of zonules
Subluxation of lens dislocation of lens
posterior anterior
Aqueous flow obstruction from vitreous blocks the angle pupillary block posterior chamber to anterior chamber
ANGLE CLOSURE GLAUCOMA forward displacement of lens-iris diaphragm
reduce iridocorneal angle Angle closure glaucoma
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Treatment
Lens removal with anterior vitrectomy for anterior dislocation of lens Pars plana vitrectomy with lens removal for posterior dislocation of lens
Figure 21. Anterior dislocated lens LENS PARTICLE GLAUCOMA
Rupture of lens capsule resulting in liberation of lens material which obstruct the trabecular meshwork and increase the intraocular pressure. It occurs most commonly in penetrating injury,rarely in blunt trauma.
Management
Medical – Topical cycloplegics, steroids, Antiglaucoma drugs Surgical - Lens removal is mainstay of treatment.
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RETAINED INTRAOCULAR FOREIGN BODY
If the retained intraocular foreign body is Organic, it produces inflammation. Iron produces siderosis and copper produces chalcosis.
Early IOP rise is due to inflammatory reaction caused by foreign body.
Siderosis – Excess iron from retained foreign body cause tissue damage which leads to iris heterochromia, rust like deposits in the corneal endothelium, anterior lens surface and in trabecular meshwork. In the trabecular meshwork, iron deposits produce sclerosis and loss of intertrabecular space. It cause outflow obstruction which leads to rise in intraocular pressure and optic nerve head changes.
Chalcosis- Copper is also toxic. It produces more retinal damage than glaucomatous changes.
PERIPHERAL ANTERIOR SYNECHIAE
Peripheral anterior synechiae form due to apposition of peripheral iris against the trabecular meshwork as a result of pupillary block or posterior pushing mechanism.
Pupillary block occurs in uveitis when the pupil is secluded by 360º posterior synechiae or by occluding pupillary membrane. If the pupillary block is not corrected immediately, iris bombe and peripheral anterior synechiae will develop. Other causes of pupillary block include anterior subluxated lens and traumatic lens swelling.
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In the presence of inflammatory cells, membrane forms between the iris and the trabecular meshwork and the membrane contracts and form peripheral anterior synechiae.
Ocular injury results in inflammation, blood in anterior chamber, flat anterior chamber which leads to iridocorneal apposition and pupillary block. Penetrating injury commonly results in peripheral anterior synechiae
Figure 22. Peripheral anterior synechiae
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DIFFERENCE BETWEEN PERIPHERAL ANTERIOR SYNECHIAE AND IRIS PROCESS IN GONIOSCOPY
PERIPHERAL ANTERIOR
SYNECHIAE IRIS PROCESS
Broad, irregular Fine, lacy
Extend upto schwalbe’s line
Extend upto inferior portion of trabecular meshwork
Bridge the underlying structures, Interference in seeing the angle structures
Follow the concavity of recess No interference to see the structure
In indentation gonioscopy- PAS drag
the iris vessels with them Do not affect movement of the iris
LATE CLOSURE OF A CYCLODIALYSIS CLEFT
Ciliary body is separated from scleral spur due to trauma. It results in temporary or permanent hypotony. Late closure of cyclodialysis cleft reduces the trabecular meshwork permeability which affects aqueous outflow leading to increase in intraocular pressure. Cyclodialysis cleft usually involves less than 90degree of the angle. Treatment is with Antiglaucoma drugs.
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Figure 23. Cyclodialysis Cleft INVESTIGATION MODALITIES
PERIMETRY Types of perimetry Static perimetry-
A stimulus is presented at a known location for a known duration with varying luminance to find local threshold.
Kinetic perimetry-
A stimulus of known luminance is placed in an unseen area (outside the border of hill of vision) and move towards seeing area to find the local threshold.
Generally performed centripetally. The hill of vision is found by approaching it horizontally.
Cyclodialysis cleft
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AUTOMATED PERIMETRY
• Humphrey
• Octopus
PROGRAM HUMPHREY
• 30-2
• 24-2
• 10-2
OCTOPUS
• G1
• G2
• M2
TESTING STRATEGIES Octopus
Normal
Dynamic
TOP (Tendency oriented perimetry)
Humphrey
SITA (Swedish Interactive Oriented Perimetry)
SITA fast
Full threshold
RELIABILITY INDICES
• False positives/ positive catch trial
False positive response represents the tendency of the patient to press the trigger not in response to seeing a stimulus but at random, either as a response to audible cue or due to the expectation of stimulus.
Trigger happy patients can also respond to stimuli in blind spot leading to high fixation losses.
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Abnormal high sensitivity white scotoma
• False negatives/negative catch trial
Failure of the patient to respond to stimuli, which are suprathreshold to the sensitivity already measured at that point or adjacent point due to patient inattention or fatigue or high threshold.
High false negatives can also be a result of disease rather than inattentiveness of the patient.
High false negatives cloverleaf pattern.
• Fixation loss
Patient response to stimuli at the location of the blind spot (Heiji krakau). Pseudo fixation losses are due to headtilt or anatomical variations.
Perimetry is unreliable if fixation loss is more than or equal to 20%
• Gaze tracking
Monitoring the eye movement of the patient during visual field testing.
In Humphrey, it is represented as a graphical diagram at the bottom of visual field printout.
Factors affecting Automated Perimetry
• Background luminance
• Stimulant size
• Fixation control
• Refractive errors
• Cataracts and other media opacities
• Miosis
• Fatigue
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INTERPRETATION OF RESULTS
Figure 24.Octopus Perimetry Validity of the test
• False positive response: >33% unreliable
• False negative response : >33% unreliable
• Short term fluctuation: Normal =1-3dB
• Fixation loss: >20% unreliable
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Glaucoma Hemifield test
• 5zones in the upper field are compared to mirror images of those in the lower field.
If value in the two zones differ to an extent that found in - <0.5% of the normal population (highly sensitive) - <1% of normal population (outside normal limit) - <3% of the normal population (borderline)
- <5% of the normal population (can be a normal plot) ANDERSON CRITERIA
i. A cluster of 3 or more non edge points in a location typical of glaucoma all of which are depressed on the pattern derived plots at p<5% ; and one of which is at p<1% level on 2 consecutive fields.
ii. A CPSD or PSD (in SITA) that occurs in less than 5% of normal fields on 2 consecutive fields
iii. A GHT outside normal limits on 2 consecutive fields.
GLOBAL INDICES IN OCTOPUS
• Mean sensitivity – represents the arithmetic mean of the threshold
determined at all the points in that field. It is represented in dB.
• Mean defect – is the arithmetic mean of the difference between the values measured in the examination and that of the age matched normal. It is the
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measure of generalized depression rather than a focal change. Normal value is -2 to +2 dB
• Loss variance – represents the local non uniformity of the visual field loss.
It reflects focal alterations rather than an overall depression of the field. Loss variance more than 6decibel is significant.
• Short term fluctuation – is obtained by testing the thresholds twice at the same locations and is used to determine the corrected loss variance. It represents the intra-test variability.
• Corrected loss variance – represents the non uniformity of the field independent of the short term fluctuations
INDICES IN HUMPHREY FIELD ANALYZER (HFA)
• Visual field index : It is a measure of patient’s overall visual field function
expressed as a percentage, the normal age-adjusted value being 100%
• Mean deviation (MD): (mean defect in octopus) It gives an indication of the
overall sensitivity of the field.
• Pattern standard deviation (PSD) : It is a measure of focal loss or variability within the field taking into account any generalized depression in the hill of vision. An increased PSD is therefore a more specific indicator of glaucomatous damage than mean deviation.
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Types of glaucoma field defects
Figure 25.Field Defects
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ARTEFACTS
• Obstruction
i. Rim artefacts ii. Ptosis
iii. Media opacities iv. Angioscotoma
• Miosis
• Refraction artefacts
High power plus and minus lenses B SCAN
It is a non-invasive technique.
It is useful in conditions where fundus examination is not possible because of hazy media.
Figure 26. B Scan
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Uses in ocular trauma
• Media opacities like hyphema, corneal opacity and Intumescent cataract
• To find out Intraocular foreign body
• Measure Angle anatomy- angle recession
• Subluxated and dislocated lens – dislocated lens looks like round or globular structure in the vitreous.
• Posterior capsule status
• Vitreous hemorrhage- small white echoes with low amplitude spikes.
• Posterior vitreous detachment- undulated membrane in the retinochoroidal layer that moves with movement of the eye. On A-scan it appears as a tall spike, but not as tall as the spike of the retinal detachment.
• Retinal detachment- detachment of retina from the chorio-scleral layer with 100% amplitude tall spikes. It is attached however, to the optic nerve and the ora serrata. B-scan is used to findout the extent of retinal detachment, mobility of the detached retina, configuration and proliferative vitreoretinal changes.
• Peripheral retinal tear- larger tear easily detectable by breached and rolled out tissue. Small tears need meticulous examination.
• Uveal effusion- effusions are notable for their anterior angle and extension to the ora serrata.
• Choroidal detachment- smooth, dome shaped, thick membranous structure that does not insert to the optic nerve.
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• Endophthalmitis- generally opacities are noted and membrane formation in severe cases. Associated findings are choroidal thickening, choroidal detachment, retinal detachment and intraocular foreignbody.
• Intraocular foreignbody
ULTRASOUND BIOMICROSCOPY
UBM is used to identify fine structural details and thus makes it extremely helpful in understanding conditions where structural alteration in the tissues contribute to the pathogenesis. It is extensively used in glaucoma followed by anterior intraocular and surface tumors.
Role of UBM in traumatic glaucoma:
It is a non-invasive procedure
High frequency and less penetration of tissues.
Useful in diagnosis and management of ocular trauma when view is limited by media opacities and abnormal anterior segment anatomy.
Uses in ocular trauma
• To find out intraocular foreign body,
• Angle recession – widening of the anterior chamber angle
• Uveal effusion
• Cyclodialysis cleft- disruption of interface in between the sclera and ciliary body leading to direct communication between the anterior chamber and suprachoroidal space.
• Zonular dehiscence
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• Iris hemorrhagic cyst
• Subluxated or Dislocated lens
• Peripheral anterior synechiae
Figure 27. Angle Recession
DISADVANTAGES
This procedure can be performed in Supine position only.
It requires a plastic or silicone eyecup to hold a coupling medium, hence it is difficult to perform in uncooperative patients, children, recently operated and ocular trauma individuals.
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OPTICAL COHERENCE TOMOGRAPHY
OCT has become a routine part of the management of macular and other retinal diseases. The same machine can be used for the assessment of glaucoma and has been widely used for this purpose.
• Peripapillary retinal nerve fibre layer (RNFL)
This involves the acquisition of a circular scan of the retina around the optic nerve head
• Optic nerve head
Radial cross sectional scans permit an objective and repeatable assessment of disc morphology, with reasonable discriminatory value.
• Ganglion cell complex analysis
It involves measurement of retinal thickness at the macula in an attempt to detect early stage glaucomatous damage. Using older time domain OCT, it was found to be regarded as inferior to assessment of other parameters such as peripapillary RNFL assessment; with newer OCT technology interest in GCC analysis has been renewed and it is regarded as comparable and supplementary
• Progression analysis software has been introduced on several machines, providing a computed assessment of the extent of damage over time presented in graphical form
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ANTERIOR SEGMENT OPTICAL COHERENCE TOMOGRAPHY
• It is used to study the normal anatomy and physiology of iris and anterior chamber angle structures.
• Screening of angle closure.
• Plateau iris
• Malignant glaucoma
• Efficacy of laser peripheral iridotomy
• Patency of Glaucoma drainage device.
Figure 28. Anterior Chamber Angle Measurements
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Figure 29. Angle recession with choroidal hemorrhage
Advantages
It is a noncontact method therefore do not cause indentation of the angle by placement of the scleral cup on the eye.
It is a more physiological examination as patient is imaged sitting upright.
Shorter imaging time and rapid image acquisition.
It is very safe to scan eyes with filtering blebs, uncooperative patients, children and recently operated cases
Disadvantages
Unable to image structures posterior to iris as the optical beam cannot penetrate the iris pigment adequately.
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REVIEW OF LITERATURE
Ajite KO, et al.
This study was conducted to findout the frequency, clinical types and treatment modalities of traumatic glaucoma (7)
Totally 365 ocular trauma patients were taken for analysis. All of them were subjected for complete ophthalmic evaluation like Visual acuity, Slit lamp examination, Intraocular pressure measurement, Optic disc stereoscopic evaluation by 78D, Gonioscopy and Perimetry. They excluded patients who were already under treatment of glaucoma.
Among them 31 patients (8.5%) were diagnosed as traumatic glaucoma. The range of age was 10 to 79 years (median 45 years± 3 years). Males were more likely to be affected than females about 2:1 ratio. The clinical type of secondary open angle glaucoma (54.8%) was higher than the secondary angle closure glaucoma (45.2%).
61% patients had very low vision (moderate to severe visual impairment). Peripheral anterior synechiae (29%), adherent leucoma (16.1%), hyphema (16.1%) were common clinical findings in this study(7).
Osman, et al.
This study evaluated the incidence and risk factors of glaucoma after open globe injury.
They selected 775 patients who underwent repair of open globe injury over a period of 15years were retrospectively reviewed from medical records. They were followed up over a period of 12± 6.5months(8).
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Their analysis revealed that age more than 18 was critical for traumatic glaucoma. Incidence of post-traumatic glaucoma was 5.3%. Risk factors of glaucoma were Zone II injury (p=0.027), penetrating injury (p=0.0008%), lens injury (p=0.011), vitreous hemorrhage (p=0.002%) and presence of intraocular foreign body (p<0.0001)(8)
Turalba et al.
In this study, they evaluated predictors and outcomes of increased IOP after open globe injury. This retrospective, case control study reviewed the records of 658 patients with open globe injury over a period of Febraury 1999 to January 2007(19).
This study concluded that 17% patients developed increased IOP after trauma. Risk factors for increased IOP were increasing age p<0.001, hyphema (0.025), lens injury (p<0.0001%) and zone II injury (p=0.0254)(19). Early diagnosis and timely intervention had improved the visual acuity and normalization of IOP over time.
Girkin, et al.
This study analysed the association between baseline structural and functional ocular characteristics and risk of developing posttraumatic glaucoma after penetrating injury.
3,627 patients of penetrating injury were taken for analysis. This study concluded that risk of developing glaucoma was 2.67%. Risk factors included advancing age, lens injury, poor visual acuity and intraocular inflammation(17).
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Girkin, et al.
This study was designed to evaluate risk factors for glaucoma in blunt trauma.
Total of 6021 patients who experienced blunt ocular trauma were taken for analysis. They were followed over the period of 6 months(18).
This study concluded that 6months incidence of developing glaucoma in blunt ocular trauma was 3.39%(18). They determined several independent predictive factors like poor initial visual acuity ( worse than 20/200), advancing age, lens injury, angle recession, and hyphema.
Wang WQ, et al.
This study determined the classification and management of early secondary glaucoma associated with ocular trauma(21).
They classified secondary glaucoma associated with trauma by their clinical findings: hemorrhagic type, chamber angle injury type, lens related type, synechiae and proliferation type(21). They concluded that early secondary glaucoma associated with trauma was complex.
Bai et al.
In this study, they classified the glaucoma into three stages according to the time interval between trauma and development of glaucoma like early, intermediate, late stages. In early stage (1 – 4weeks), there were 33 cases due to inflammation, 36 cases due to hyphema and 22 cases were lens induced. In intermediate stage (1- 6months, 3 cases due to pupillary block and 2 cases due to phacoanaphylaxis)(9). In advanced stage(>6months), 6 cases due to angle recession, 1 case due to siderosis.
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Stanic, et al.
This study presented the frequency, clinical forms and therapeutic results of traumatic glaucoma in 511 patients(10). They submitted all injured eyes to visual acuity examination, Gonioscopy, slit lamp examination, fundus examination, intraocular pressure measurement and perimetry.
They concluded that traumatic glaucoma was found in 6.6%. It was more frequent in contusion injuries than perforation injuries. The patients with traumatic glaucoma were 9 -86 years of age (mean 60.2.). Males were more affected than females. One third of the patients were blind and one half had visual acuity below 0.1(10).
PART 2
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AIM
• To study the incidence of glaucoma in ocular trauma in tertiary care centre.
OBJECTIVES
• To study the incidence of different types of glaucoma in ocular trauma
• To analyse the etiopathogenesis in case of glaucoma due to ocular trauma
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METHODOLOGY
200 Patients with Ocular trauma reporting to the glaucoma clinic Regional Institute Of Ophthalmology for one year duration from 01. 05. 2017 to 01. 05.2018, Government Ophthalmic Hospital will be registered, consent obtained and evaluated.
INCLUSION CRITERIA
• Patients with Blunt injury/ Penetrating injury/ Chemical injury/
Thermal injury.
EXCLUSION CRITERIA Patients with
• Pre-existing open angle glaucoma/ angle closure glaucoma
• Pre-existing ocular diseases such as those with anterior segment infections and inflammation.
METHODS
In our study of 200patients with ocular trauma,detailed history was recorded.
They were subjected for the following examination
• Visual acuity by Snellen’s chart,
• Anterior segment evaluation with Slit lamp examination,
• Fundus examination by direct ophthalmoscopy and slit lamp biomicroscopy using 90D, Indirect ophthalmoscopy,
• IOP measurement by Goldmann applanation tonometer / Rebound tonometer/ Tonopen,
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• Gonioscopy,
• Automated perimetry,
• B scan, Ultrasound Biomicroscopy, X-ray orbit if needed.
FOLLOW UP
All the patients were followed up weekly for the first two weeks, biweekly for a month and then monthly for 12months. Patients were asked to visit hospital as early as possible whenever they have any complaints.
STATISTICAL ANALYSIS PLAN
Data collected were entered in Excel Spread sheet and analyzed using STATA statistical software package release 11. We used the two-sided independent- samples t test to compare means across dichotomous variables (i.e. men versus.
women); the one way ANOVA test to comparison of means across multilevel variables. Simple calculations like Percentages, Propotions and mean values were derived. A type I error of 0.05 was considered in all analysis.
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RESULTS
ANALYSIS OF 200 CASES
In our study of 200cases with age group from 4 -81years, the mean age of ocular trauma is 35.76 years.
GENDER DISTRIBUTION
GENDER NUMBER PERCENTAGE
Female 39 19.5
Male 161 80.5
Total 200 100
Chart 1
Males (80.5%) were more affected than females (19.5%).
19.5
80.5
Gender Distribution
Female Male
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MODE OF INJURY
MODE OF INJURY NUMBER PERCENTAGE %
AGRICULTURE 19 9.5
ASSAULT 25 12.5
DOMESTIC 40 20
FIRE CRACKER 12 6
INDUSTRIAL 49 24.5
RTA 26 13
SCHOOL 8 4
SPORTS 21 10.5
TOTAL 200 100
Chart 2
In our study, the most common mode of injury is industrial (24.5%) followed by domestic injury (20%).
0 5 10 15 20 25
Agriculture Assault Domestic Fire Cracker Industrial RTA School Sports
