A Study on the Incidence of Glaucoma in Ocular Trauma

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

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,

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.

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

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

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)

2

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 corneoscleralmeshwork which is attached anteriorly to

3

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

4

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.

5

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

6

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

7

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

8

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)

9

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- _HCO

10

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

11

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

12

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%)

13

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

14

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

15

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

16

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

17

TYPES OF TONOMETRY

Newer tonometers

Trans-palpebral tonometry

Dynamic contour tonometry

Ocular response analyser

18

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

19

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

20

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

21

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

22

 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

23

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.

24

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

25

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

26 • 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

27

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

28

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.

29

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

30

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

31

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

32

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

33

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

34

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,

35

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

36

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

37

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

38

Figure 17. Grading of hyphema

39

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

40

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

41

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

42

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

43

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

44

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

45

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.

46

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

47

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

48

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

49

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

50

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

51

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.

52

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

53

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

54

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

55

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

56

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

57

Types of glaucoma field defects

58

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.

59

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

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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.

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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

62

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

63

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.

64

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

65

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

66

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

67

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}

68

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)_.

69

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

70

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

71

• 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

72

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

73

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

74

TYPE OF INJURY

TYPE OF INJURY NUMBER PERCENTAGE %

BLUNT 103 51.5

PENETRATING 87 43.5

CHEMICAL 8 4

THERMAL 2 1

TOTAL 200 100

Chart 3

In our study, blunt injury is more common than penetrating injury.

0 10 20 30 40 50 60

Blunt Penetrating Chemical Thermal

Type of Injury

75

AGENT CAUSING INJURY

AGENT CAUSING INJURY NUMBER PERCENTAGE %

ACID 2 1

ALKALI 5 2.5

BALL 19 9.5

FIST 16 8

METAL 56 28

OTHERS 7 3.5

STICK 19 9.5

STONE 43 21.5

SHARP INSTRUMENT 11 5.5

WOOD 22 11

TOTAL 200 100

Chart 4

In our study, metal is the most common agent causing injury followed by

stone.

0 5 10 15 20 25 30 acid alkali ball fist metal others stick stone sharp instrument wood

Agent Causing Injury

76

INCIDENCE OF GLAUCOMA

Glaucoma Frequency Percentage % Cum.

Absent 173 86.5 86.5

Present 27 13.5 100

Total 200 100

Chart 5

Over a period of one year of our study, 13.5% of patients developed glaucoma

after ocular trauma.

0 10 20 30 40 50 60 70 80 90

Absent Present

Glaucoma

77

GENDER DISTRIBUTION

Gender Distribution in Glaucoma Frequency Percentage %

Female 8 29.63

Male 19 70.37

Total 27 100

Chart 6

AGE DISTRIBUTION IN TRAUMATIC GLAUCOMA

The mean age of patients with traumatic glaucoma was 41years.

Female, 29.63%

78

LATERALITY

LATERALITY NUMBER PERCENTAGE %

RE 10 37.04

LE 17 62.96

Total 27 100

Chart 7

In our study, left eye was more affected than right eye.

0 10 20 30 40 50 60 70

RE LE