Entropion

Entropion

EntropionEntropion is a disorder of eyelids in which there is inturning of the lid margin due to which the lashes rub against the eye surface.

Cause

There are following causes of entropion:

1. Congenital entropion: This condition is present since birth and is rarely seen. It may be associated with microphtalmos.

2. Cicatricial entropion: It is most commonly seen and usually involves the upper lid. It occurs due to cicatricial contraction of the palpebral conjunctiva, mainly occurs in trachoma, membranous conjunctivitis, chemical burns and stevens johnson syndrome.

3. Senile (involutional) entropion: It is seen in older people and most commonly affects the lower lid. It occurs either due to:

  • Horizontal laxity of the lower lid due to weakening of orbicularis muscle.
  • Vertical lid instability.
  • Over-riding of pretarsal orbicularis.

4. Mechanical entropion: It occurs due to the lack of support provided by the globe to the lids. It commonly occurs in patients of phthisis bulbi, enophthalmos etc.

Symptoms

They occur due to rubbing of the eyelashes against the cornea or conjunctiva. These are:

  • Foreign body sensation
  • Redness of the eye
  • Irritation of the eye and pain
  • Watering from the eyes
  • Decreased vision
  • Photophobia

Signs

Following signs are seen on examination of the patient:

1. Inturning of the lid margin: Lid is found in turned on examination. It is divided into following grades as seen in examination:

  • Grade I entropion: Only the posterior lid border is inrolled.
  • Grade II entropion: Inter-marginal strip is inturned.
  • Grade III entropion: Whole lid margin is inturned including the anterior border.

2. Signs of the underlying causative disease can be seen.

3. Signs of complications like recurrent corneal abrasions, superficial corneal opacities can be seen.

Treatment

1. Congenital entropion resolves with time mostly. Sometimes it requires surgery like plastic reconstruction of the lid crease and correction of the underlying defect.

2. Cicatricial entropion: It is treated by operation which is based on the following principles :

  • Altering the direction of lashes
  • Transplanting the lashes
  • Straightening the distorted tarsus

Surgical techniques are:

  • Anterior lamellar resection: It corrects mild degree of entropion.In this operation, an elliptical strip of skin and orbicualris muscle is resected 3mm away from lid margin.
  • Tarsal wedge resection: It corrects moderate degree of entropion. In this operation, in addition to the elliptical resection of skin and muscle, a wedge of tarsal plate is also removed.
  • Transposition of tarsoconjunctival wedge (modified Ketssey’s operation): It basically involves tarsal fracture and eversion of distal tarsus.
  • Posterior lamellar graft: It corrects severe entropion with upper eyelid retraction. In this operation, the affected conjunctiva and tarsus are replaced by a composite posterior lamellar graft.

3. Senile entropion: Following are the surgical techniques:

  • Transverse everting suture: They offer only temporary cure and are done in old patients generally.
  • Wies operation: Indicated for long term cure. The entropion is corrected by prevention of over riding of pre septal muscle by the horizontal fibrous scar tissue barrier and transferring of the pull of lid retractors to the upper border of tarsus by the everting sutures.
  • Plication of lower lid retractors (Jones operation): Performed in severe cases. Lower lid retractors are exposed by horizontal skin incision at the lower border of the tarsal plate, shortened and the sutures are used to create a barrier to prevent overriding of the pre septal muscle.
  • Quickert procedure: Indicated in patients having associated marked horizontal lid laxity. It consists of a transverse lid split to create barrier for over riding of pre septal muscle, everting sutures to transfer pull of lower lid retractors to upper border of tarsus and horizontal lid shortening to correct the laxity. This procedure basically combines horizontal lid shortening along with weis procedure.

Reference

1. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012).

2. Parsons, Disease of the Eye (Elsevier, 21 Edition).

3. Smolin and Thoft’s The Cornea: Scientific Foundations and Clinical Practice.

Dacryoadenitis

Dacryoadenitis

DacryoadenitisDacryoadenitis is an inflammation of lacrimal gland (tear producing gland) which is situated in supratemporal orbit. The secretions of this gland forms the aqueous layer of the tear film.

Types

Dacryoadenitis is of two types, i.e Acute and Chronic Dacryoadenitis.

Acute dacryoadenitis: It can be caused due to viral infections like mumps, epstein barr virus or bacterial infections like staphylococcus, gonococcus etc. It develops as a primary inflammation of the gland or secondary to any local or systemic infection which can occur in trauma, erysipelas of the face, conjuctivitis and orbital cellulitis.

Chronic dacryoadenitis: It can be caused due to non infectious inflammatory disorders. It is characterised by engorgement and simple hypertrophy of the gland. It may occur either as a sequelae to acute inflammation or in association with chronic inflammations of the conjunctiva and in systemic diseases like tuberculosis, syphilis and sarcoidosis.

Symptoms

In acute dacryoadenitis, symptoms occur early and worsen rapidly. Only one gland is affected in most of the cases. There are following symptoms:

  • Pain and swelling in the outer part of the upper lid with a typical S- shaped curve of its margin.
  • Affected region appears red and warm to touch.
  • There is tenderness and pain increases on touching the affected site.
  • Excess watering and discharge from the affected eye and pain on movement.

In chronic dacryoadenitis, symptoms occur slowly and progresses from days to weeks. Symptoms are:

  • Painless swelling in the upper and outer part of lid associated with ptosis.
  • Eyeball may be displaced down and in.
  • Diplopia may occur in up and out gaze.

Signs

Examination of the eye is done to look for the swelling. In chronic dacryoadenitis, on palpation, a firm lobulated mobile mass may be felt under the upper and outer rim of the orbit.

Further tests are done to confirm the diagnosis:

1. Culture: The discharge coming out from the affected eye is collected and send for culture to look out for the causative organism whether it is bacterial, fungal or viral and treatment is carried out according to that.

2. Lacrimal gland biopsy: It is done in chronic cases. This helps to rule out any malignancy.

3. CT scan: This helps to assess any complications or any lacrimal gland tumour.

Differential diagnosis

  • Orbital cellulitis
  • Preseptal cellulitis
  • Orbital dermoid
  • Chalazion
  • Exophtalmos
  • Hordeolum
  • Ptosis
  • Dry eye syndrome
  • Lacrimal gland syndrome

Treatment

General measures

  • Eyes should be kept clean.
  • Hot compresses on the affected area. It relieves pain and swelling.
  • Gentle massaging over the affected area for few minutes.

Medical measures

Acute Dacryoadenitis

  • If the cause is bacterial, systemic antibiotics like cephalosporins can be used. If fungal, appropriate antifungal agents should be used.
  • Analgesics and anti inflammatory drugs along with hot fomentation.
  • When pus is formed, incision and drainage should be carried out.

Chronic Dacryoadenitis

  • Treat the underlying cause responsible for the disease.
  • In case of long standing swelling, lacrimal gland biopsy is considered.

Reference

1. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012) Chapter: Diseases of the Lacrimal Apparatus p346-347.

2. Parsons, Disease of the Eye (Elsevier, 21 Edition), Chapter: Diseases of the Lacrimal Apparatus p462-463.

3. Smolin and Thoft’s The Cornea: Scientific Foundations and Clinical Practice p700.

Anatomy of Eye

Eyeball ModelThe Almighty has equipped the miraculous human body with the gift of five senses with which we see, touch, feel, hear, smell, taste the things and the world around us. Vision, being one of them, is a very important gift that completes our existence on earth. Without vision and the gift of sight, life would be so much difficult and the function of this gift of life is possible only with the help of two beautiful eyes that we have made with such precision so that we can appreciate the beautiful and not so beautiful around world around us.

Therefore, we came up with this post in which a brief detail about the Anatomy of eye will be discussed which will help us to understand the functions of human eye and its various pathologies more clearly.

The eyeball

The eyeball is of shape of  an oblate spheroid which is kept distended by fluid present inside it, hence, it can be called a cystic structure (cystic means cyst like that is sac containing fluid). An oblate spheroid means a symmetrical ellipse which has a greater equatorial diameter than the vertical diameter and that vertical diameter will divide the equatorial diameter into two equal parts. The equator thus lies between the two poles which are situated on the maximum width of the eyeball. These poles are called the anterior pole and the posterior pole. Anterior means in front and posterior means behind.

Dimensions of an adult eyeball

Eyeball StructuresAntero-posterior diameter: 24 mm

Horizontal diameter: 23.5 mm

Vertical diameter: 23 mm

Circumference: 75 mm

Volume: 6.5 ml

Weight: 7 grams

Coverings of the eyeball

The eyeball has basically three coverings:

Cornea Transparent1. The outer covering: It is formed by the sclera and the cornea. They form the fibrous covering of the eye in order to protect the eye from external environment. Therefore this covering can be also be called an elastic but dense membrane which supports the eyeball. The sclera forms the five-sixth of this fibrous covering and cornea forms the anterior most one-sixth of this fibrous layer. The sclera is also called the white of the eye and is thus opaque. The cornea is a transparent membrane which covers the coloured iris and black pupil. Cornea is an avascular structure that means it does not have its blood supply. The The membrane which covers the white or the sclera of the eye is called conjunctiva, mainly the bulbar conjunctiva. Conjunctiva also covers the back of the eyelid and therefore joins the eyelids to the eyeball hence called conjunctiva that is to join. The conjunctiva which covers the back of the lids is called the palpebral conjunctiva. The junction between the cornea and the conjunctiva is called the limbus.

2. The middle covering: It is formed by the uveal tract that is a triad of iris, ciliary body and the choroid. This middle covering is also known as the vascular covering of the eyeball as it is mainly related to the nutrition of the various structures of the eyeball as it is highly vascular that is supplied by blood vessels. The iris is the part of the eye which has different colours in different individuals, races etc. The reason we call some people black eyed, brown eyed, green eyed, hazel eyed or blue eyed is due to the color of the iris. The iris lies in front( anterior most) amongst the other two parts of the uveal tract and can be compared to a circular disc with hole or an aperture in the centre which is known as the pupil. The pupil is normally black in colour and light enters through it. The pupil decreases in size or increases in size according to the intensity and brightness of the light with the help of contraction and relaxation of muscles of iris.In fact it is the iris which contracts and relaxes the make the hole or the pupil to narrow or widen in size.

The iris has free margin anteriorly and posteriorly is attached to ciliary body. The ciliary body is a triangle like structure with base forwards. It is mainly related to production and flow of aqueous humour (a fluid present in the anterior chamber of the eye). The ciliary body ends at orra serrata from which the innermost covering of the eye-the retina begins.

The ciliary body continues behind as the choroid which is in contact with the sclera from within and is highly vascular. There is a space between the sclera and the cornea which is called the Epichoroidal or the Suprachoroidal space. Choroid is also lined from its inner side (the side towards the inner retina) by a thin membrane or sheath or covering called Bruch’s membrane or the lamina vitrea.

3. The inner layer: The retina forms the innermost layer of the eyeball. This layer is also called the nervous layer of the eyeball as it is richly supplied by nerve fibres and is mainly formed by the different kind of nerve cells, their fibres and their synapses, this layer is thus responsible for vision. The retina is further made up of ten layers which can be seen under the microscope if a histological section is made out of it.

Chambers of the eyeball

Eyeball AnatomyThe eyeball is mainly divided into two segments i.e Anterior and Posterior segment.

1. Anterior segment: It includes all the structures in front of the lens or it is segment anterior to the lens. The lens is placed behind the iris, the ciliary body is lying on both its lateral sides giving out the zonules which hold the lens to its normal position. In front of the lens or anterior to it is the pupil. Therefore, the anterior segment can be divided into further two chambers:

  • Anterior chamber
  • Posterior chamber

a. The anterior chamber: It is the part of the anterior segment up to the iris. Therefore, its boundaries would be:

  • In front-Back of cornea.
  • In back-front of iris and part of ciliary body and part of the lens visible through the pupil.

In normal adults, the depth of the anterior chamber is 2.5mm.

It is slightly shallower in hypermetropes and deeper in myopes.

The anterior chamber contains the aqueous humour. It is approximately 0.25 ml in adults.

The peripheral part of the anterior chamber which is narrowest (that is at the sides of the anterior chamber) forms the ‘angle of the anterior chamber’. It has in front -the junction of the cornea and the sclera and behind-the root of the iris. The angle of the anterior chamber form an important drainage pathway for the aqueous humour and thus is one of the main sites involved in Glaucoma.

b. Posterior chamber: Its boundaries are:

  • In front: The back portion of the iris and some portion of the ciliary body and the pupil.
  • In back: The lens with its zonules.

It contains approximately 0.06 ml of aqueous humour.

2. Posterior segment: It is the segment of the eyeball behind the lens. It is bounded at the back by the choroid and the retina. It contains a gel like material or fluid which fills this space. It is called ‘the vitreous humour’.

Appendages of the eye

Eyeball AnatomyThe eyeball is attached to the various extraocular muscles which help in the movement of the eyeball. The eyeball is placed inside the bony orbit of the skull. It is protected by the eyelids which act as curtains closing and opening that is blinking and attached with help of the conjunctiva. It is also protected by the tears whose production and drainage is via lacrimal apparatus that would be discussed in detail in the separate post. Thus the following structures are the appendages of the eyeball which help it to thrive, support and mainly protect from the external environment:

1. Extraocular muscles

2. Lacrimal apparatus

3. Eyelids and eyebrows

4. Conjunctiva

Clinical anatomy of the eye

External Eyelid Structures

Blood supply of the eye

All the arteries of the eye in man are branches of Ophthalmic artery which is a branch of internal carotid artery.

Venous supply: Most of the blood is drained to the cavernous sinus via the ophthalmic veins.

The superior ophthalmic vein communicates with the angular vein at the root of the nose.

The inferior ophthalmic vein anastomoses with the pterygoid plexus.

Nerve supply

Sensory supply: Optic nerve, ophthalmic division of trigeminal nerve, some of the lacrimal and nasociliary branches.

Motor supply: Oculomotor nerve, trochlear nerve, abducens nerve.

Parasympathetic supply: Edinger Westphal nucleus which synapses with short ciliary nerves in the ciliary ganglion and accompanies the third cranial nerve that is the oculomotor nerve.

Sympathetic supply: T1 fibres which synapse in superior ciliary ganglion.

Reference

1. A.K Khurana, MD “Comprehensive Ophthalmology” (New Age International Publisher, Inc 2012) Page no. 3-4.

2. Parsons, Disease of the Eye (Elsevier, 21 Edition), Page no. 5-16.

Retinitis Pigmentosa

Retinitis Pigmentosa

Retinitis PigmentosaRetinitis pigmentosa is a hereditary disorder in which there is damage to the retina. The patient’s ability to respond to light is affected. In retinitis pigmentosa, the cells in the retina called as rods and cones die. Predominantly rods are more affected than cones. Rods are present mainly in the outer region of the retina and responsible for peripheral and night vision. Therefore this disease causes slow loss of vision, beginning with decreased night vision and loss of side (peripheral) vision.

Cause

It is an inherited disorder and can run in families. It can be caused by a number of genetic defects. It occurs in 1 person per 5000 of the world population. It appears in childhood and progresses slowly. Males are more commonly affected than females.

Inheritance

It may occur as:

1. Sporadic disorder: It is isolated without family history due to mutation of rhodopsin gene.

2. Inherited disorder: It can be autosomal recessive (most common), autosomal dominant or X-linked.

3. Undetermined inheritance

Symptoms

Retinitis Pigmentosa EffectIt creates a “tunnel vision effect”. It causes slow loss of vision with decreased night vision which later on progresses to side vision. Some people may also feel difficulty in identifying colours. The ability to adjust to darkness becomes difficult (night blindness).

Signs

Fundus changes

1. Retinal pigmentary changes: These are perivascular. They are found in equatorial region first and then spread to both the sides.

2. Retinal arterioles: They are narrowed in shape.

3. Optic disc becomes pale. Optic atrophy occurs in late stages.

4. Other associated changes like colloid bodies, choroidal sclerosis, cystoid macular edema etc. are also seen.

Visual field changes

Annular or ring shaped scotoma: It is a typical feature which is due to degenerated equatorial zone of retina. In late stages, scotoma also covers the central vision and the person becomes blind.

Electrophysiological changes

These changes appear early in the disease before the appearance of symptoms and signs.

1. Electroretinogram (ERG): It is subnormal initially and eventually extinguished.

2. Electrooculogram (EOG): It is subnormal with an absence of light peak.

Retinitis pigmentosa can be associated with several ocular conditions like myopia, primary open angle glaucoma, microphthalmos and posterior subcapsular cataract.

It is also associated with several systemic disorders. A number of specific syndromes are:

  • Laurence-Moon-Biedl syndrome
  • Cockayne’s syndrome
  • Refsum’s syndrome
  • Usher’s syndrome
  • Hallgren’s syndrome

There are also some atypical forms of retinitis pigmentosa like:

1. Retinitis pigmentosa sine pigmento: In this there are all the clinical features of RP except the visible pigmentary changes in the fundus.

2.  Sectoral retinitis pigmentosa: In this only one sector of retina is involved.

3. Pericentric retinitis pigmentosa: All the clinical features are same as that of RP except that the pigmentary changes are confined to an area, immediately around the macula.

4. Retinitis punctata albescens: It is characterised by the presence of innumerable discrete white dots scattered over the fundus without pigmentary changes.

Treatment

There is no effective treatment of retinitis pigmentosa till date. However, following measures are taken:

  • Measures to stop progression by vasodilators, placental extracts, transplantation of rectus muscles, vit. A etc.
  • Correct any refractive error by glasses.
  • Systemic acetazolamide.
  • Low vision aids (LVA).
  • Rehabilitation of the patient.
  • Prophylaxis.

Reference

1. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012) Chapter: Diseases of the Retina p260-262.

2. Parsons, Disease of the Eye (Elsevier, 21 Edition), Chapter: Diseases of the Retina p321.

Pinguecula

PingueculaPinguecula is a non malignant degenerative condition of conjunctiva characterized by yellowish white patch on the bulbar conjunctiva near the limbus. It is the most commonly found “bump” on the eye. It can occur at any age, even in young children but more commonly occur in middle-aged or older people.

The word Pinguecula is derived from Latin word “Pinguis” which means fat. It should be differentiated from pterygium which is a wing-shaped fold of conjunctiva encroaching upon the cornea from either side within palpebral fissure. It is also considered as precursor of pterygium.

Cause

It is not known exactly but it has been considered as age change process. It occurs more commonly in persons who are exposed to sunny and windy climate and in persons whose job expose them to UV rays, dust or toxic vapor.

Pathology

There is degeneration of collagen fibers of the substantia propria of conjunctiva leading to thinning of overlying epithelium. It is associated with deposition of amorphous hyaline material in the conjunctiva.

Clinical Features

It is a bilateral condition presenting as yellowish white triangular patch near the limbus. The apex of the triangle lies away from the cornea. It affects the nasal side first and then the temporal side. Mostly, it is an asymptomatic condition but some people can have a feeling of foreign body sensation. The patient may complain of dry eye, itching or scratchy sensation. The conjunctival congestion makes it to appear as a vascular prominence.

Complications

It includes either inflammation of pinguecula itself or intra epithelial abscess formation, and rarely calcification and can also convert into pterygium.

Treatment

Most cases of pinguecula require no medical treatment until it is inflamed. However, if there occurs inflammation, it can be treated by the use of topical steroids. Persons suffering from pinguecula are advised to wear sunglasses to limit exposure to sunlight, wind and dust. It can also be surgically excised.

Reference

1. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012) Chapter: Optics and refraction p105-107.

2. Parsons, Disease of the Eye (Elsevier, 21 Edition), p181-182.

Trachoma or Egyptian ophthalmia

Trachoma or Egyptian blindness was once the most leading cause of preventable blindness in the world. With the advent of antibiotic era and other medical procedures, it has decreased in the past few years but it still continues to be a major threat in the developing countries or wherever there are poor hygienic practices and unsafe water supply.

Many people in fact, still regard it as the major cause of preventable blindness in the world. It is caused by Chlamydia trachomatis. Before going into the medical details of the disease, there is an interesting history that is associated with trachoma and is given below in nutshell.

What is trachoma?

Life Cycle of TrachomaIt is a highly contagious disease which starts as a nonspecific conjunctivitis in its acute form and with the chronic form takes over to lid scarring mostly in turning of the lid margin leading to in turning of the eyelash and thus rubbing on the cornea causing its most dreaded complication which is blindness. It is caused by Chlamydial trachomatis (A, B, Ba, C, D to K serotypes).

History

Trachoma has a very long and an interesting history since it dates back to around 8000 B.C. When first evidence of the blinding disease was found in Australia in Australian skulls that had abnormal structure due to an invasion of some microorganism into the bone but not out of it. Trachoma was the most fitting eye diseases that the scientists said could have caused that picture in those skulls.

Written therapies to cure trachoma were also found in China dating back to 2600 B.C.

It was also present in Ancient Greece and Rome. Few of the plays by Aristophanes also contains some references to Trachoma like in Plutus (one of the plays) where Plutus who is the God of Riches is blinded by Zeus. This is said to be an allusion to the blinding disease that had set its tight claws on Greece.

It was Dioscorides who used the term “trachoma” for the first time in 60 A.D. in his work Materia Medica.

The Hippocratic Corpus also had sections about trachoma dating back to 5th century B.C.

Egyptian OphthalmiaTrachoma is also called Egyptian Ophthalmia because when Napoleon had begun his conquest in Egypt in 1798, the disease infected three thousand of Napoleon’s troops in two and a half months and even blinded many of them. Therefore, it also began to be called Military or Egyptian ophthalmia from then.

Thus these troops spread Trachoma from an endemic Egypt to sporadic Europe and made the problem grave in Europe, the infection now spreading in even European civilians.

Infection also spread to the U.S. through immigrants despite of strict medical screening and checkups.

Halberstaedter and Prowazek discovered trachoma inclusion bodies in 1907.

Mccallen created classification of trachoma into four stages around 1913.

The successful treatment of trachoma occurred for the first time in 1937 with the use of sulphonamides.

While use of Penicillin in treatment of trachoma occurred for the first time in 1940. Use of Streptomycin started in 1943.

Chinese first isolated Chlamydia in a chick embryo in 1954 and so it was called a virus and then it was called a bacteria because it had DNA and RNA both and was susceptible to antibiotics.

In 1996, WHO called to use Azithromycin for the treatment of the disease.

In 1999, there was establishment of Vision 2020, in which one of the goals was to eliminate this blinding disease ‘trachoma’ by the year 2020.

Did you know?

Here are some interesting facts related to trachoma just for the sake of interesting read:

1. For the the treatment of trichiasis (a complication of trachoma in which an eyelash or few eyelashes turn inwards rub on the cornea and lead to blindness), the Ebers papyrus suggested a treatment way back in 1550 B.C. The treatment was to remove the in turned eyelash and apply a mixture of myrrh’s (a lizard) blood, and bat’s blood until healed or a mixture of lizard dung, oxblood ass’ blood, pig blood, hound blood, Goat blood, stibium and malachite.

2. St. Paul, Cicero and Galileo had trachoma.

3. Many governments considered trachoma as a serious threat and thus firm decisions were taken in context to prevent its spread in their own territory through immigrant legislation.

4. Some immigrants used adrenaline topically to mask their trachoma signs and fool the officers. Some immigrants also rubbed sugar cubes on their eyelashes 6 weeks before the immigration to temporarily hide their symptoms.

5. Trachoma also has its mention in Mario Puzo’s ‘The Godfather’, Mark Twain’s ‘Innocents Abroad’, and Bill Bryson’s ‘In A Sunburned Country’.

6. In England, this was one of the procedures to treat trachoma back in the eighteenth century. It was blood letting in which various cuts were made near the eye and blood was let to flow from these cuts until the person fainted.

7. There was something known as the soldiers’ plot to fake ophthalmia to avoid serving in the military.

Prevalence

It is endemic in many parts of the world like the Middle East, Central Asia, India, Pakistan, Bangladesh, Eastern Asia that is China and Japan, The Pacific Islands, North and central Africa, Central and South America. It is estimated to affect around 21.4 million people around the globe with five-sixth of them suffering with active trachoma and one-sixth of them having its complication trichiasis.

Presently it is the second most common cause of preventable blindness after cataracts. The most vulnerable groups are that of women and children with preschool children being most affected 60-90 percent in hyper endemic areas. There is an increased risk of development of blindness and complications in women than in men.

Risk factors or Causes

1. Unhygienic practices like not washing hands often, rubbing eyes with dirty or bare hands frequently and overcrowding.

2. Sharing same towels, clothes.

3. Fomites like door handles (already being touched with infected hands and fingers).

House Fly4. Flies or other vectors which are attracted to eye discharge.

5. Sexual transmission from infected genitals to hands and then from hands to eye.

6. Basically transmission is bye eye to eye or genitals to eye.

5. Coming in contact with eyes of the infected person.

Symptoms

Pure trachoma is mostly symptomless. Symptoms are mainly due to secondary bacterial infection and may be minimal like foreign body sensation in the eyes, mild lacrimation, itching etc. It may also give a picture similar to acute bacterial conjunctivitis when there is severe secondary bacterial infection like mucopurulent discharge, red eye, etc.

The complications or the sequelae may take even 20 years to emerge. In chronic stages there may be intense pain, lacrimation and photophobia when the cornea is involved due to trichiasis.

Signs

  • Conjunctival signs: Signs in the conjunctiva.
  • Corneal signs: Signs in the cornea.

Conjunctival signs include

Congestion and Follicles

a. Congestion or Redness: There is redness of the upper tarsal (palpebral) conjunctiva or say fold of conjunctiva covering the back of the eyelid and can be seen when the eyelid everted. This is mainly due to the response of the body against the invading microorganism in the form of inflammation in this which includes dilatation of the blood vessels of the conjunctiva.

b. Papillary enlargement: There is redness in the tarsal conjunctiva, the reason being the above described that is dilatation of the blood vessels as a protective mechanism in response to the microorganism. But this time the inflammation or the dilatation is extensive and causes jelly like appearance of the tarsal conjunctiva that is more reddish and velvety appearance.

Trachoma Folliclesc. Follicles: Follicles have mostly boiled sagograin like look and are mainly seen on the upper tarsal conjunctiva. They are formed due to collection of the protective cells of the body that is the lymphocytes in response to the microorganism as a part of the inflammation. The centre of the follicle have the protective cells called the mononuclear histiocytes(cells with single nucleus) and leber cells( which are large cells with many nuclei inside a single cells also called giant cells). In the periphery, the follicle is mainly made up of collection of lymphocytes.

If follicles are less than 5mm in diameter than they can be due to follicular conjunctivitis but a follicle with diameter greater than 5 mm is only seen in trachoma. A follicle seen on the bulbar conjunctiva is pathognomonic or a sure shot sign of trachoma.

Conjunctival Scarring Trachomad. There can be Scarring of the conjunctiva.

e. Concretions: They are formed due to collection or mounding up of dead epithelium of the conjunctiva due to invasion and destruction by the Chlamydia. They look like white hard deposits which are usually pinpoint in size.

Corneal signs include

a. Keratitis is the inflammation of the cornea which is usually seen in the upper part and mainly in the superficial layers of the cornea.

b. Herbert follicles: follicles which are present at the junction of conjunctiva and the cornea that is limbus that is at the periphery or margin of the cornea. They are also a part of inflammation and due to collection of lymphocytes.

Pannus infiltration and vascularizationc. Pannus: It means something invading the cornea or something infiltrating the cornea. It is usually associated with entering of blood vessels in the normally avascular cornea which is called vascularization. This infiltration is mainly of the lymphoid cells and it is most commonly seen in the upper part but gradually and slowly it can involve whole of the cornea. The margin of the cornea starts looking cloudy and hazy and unclear due to this infiltration and vessels can be clearly appreciated springing up from outside into the cornea.

Pannus is of two types

  • Progressive
  • Regressive

Progressive pannus: In this the infiltration is ahead of vascularization and the vessels are mainly parallel, vertical and face downwards ahead of which lines a strip of infiltration.

Regressive pannus: In this filtration lags behind the vascularization that is vessels extend a distance beyond the haze of the infiltration.

Such classification is necessary to decide upon the course of the treatment.

PannusThe vessels are usually superficial that is they lie between the bowmanns’s membrane and the epithelium and at that stage the treatment of pannus does not lead to corneal opacity but if the vascularization becomes deep (destroyed the bowmann’s membrane), a permanent corneal opacity may result despite of the treatment.

d. Corneal ulcer: It usually takes place at the edge of the pannus which is advancing already and are generally shallow but may become deep as the time passes by.

Herbert Pitse. Herbert pits: When the herbert follicles explained above heal, they leave scars behind which are called herbert pits. These pits are usually brown in colour and oval in shape.

f. Corneal opacity: A permanent haze or cloudiness can occur in cornea either due to corneal ulceration or due to deep pannus which may affect the vision of the person especially if the opacity is in the region of the pupil by blocking the light entering the pupil.

Complications or sequelae of trachoma:

1. Sequelae in the lids: The most common one being trichiasis, which causes rubbing on the cornea and blindness. Trichiasis is rubbing of the eyelash against the eyeball. It usually takes places because of in turning of the lid margin due to scarring of the palpebral conjunctiva. This in turning of the lid margin is called Entropion, which is another complication. There can be thickening of the lid margin which is called tylosis. There can be drooping eyelid also.

Due to dense infiltration there is a specific type of drooping of the upper eyelid giving the patient a sleepy appearance. It is also called ‘trachomatous ptosis.’

Classification of trachoma:

WHO classification is the most accepted one and that is the FISTO classification:

FISTO classification

Signs of Trachoma by FISTO

There was also MacCallan’s classification:

Diagnosis:

Clinical diagnosis is made by history, specific signs and FISTO classification described above.

Laboratory Diagnosis:

For routine diagnostic use, A simplified form of micro-immunofluorescence test is done using pooled antigens. It does not use the antigens involving individual trachoma inclusion conjunctivitis.

Direct examination of the conjunctival smear with the help of Direct Monoclonal fluorescent antibody microscopy is also a rapid and an inexpensive method.

Conjunctival cytology- Conjunctival smears are taken and stained with Giemsa stain. If the smear shows neutrophils with presence of plasma cells and Leber cells, it is suggestive of trachoma.

Detection of inclusion bodies can also be suggestive of trachoma and is done by staining conjunctival smears with Giemsa,iodine stain or immunofluorescent staining.

ELISA can be done for chlamydial antigens.

Isolation of Chlamydia can be done by yolk sac inoculation method. MacCoy cell culture can also be used and it requires three days.

Treatment:

Treatment is divided into two phases:

  • Treatment of the active phase.
  • Treatment of the sequelae.

1. Treatment of the active phase:

Systemic treatment

Azithromycin remains the first drug of choice presently. It is given as 1g stat (when diagnosed). Tetracycline and Erythromycin have also been tried with success systemically but Tetracycline is not given to children below 8 years, pregnant women or nursing mothers. The schedule is as follows:

  • Oral tetracycline or erythromycin 250 -500mg four times a day for 3-6 weeks.
  • Oral Doxycycline 100mg twice a day for 3-6 weeks
  • Oral Clarithromycin 250-500mg twice a day for 3-6 weeks.

Topical Treatment

Topical treatment with erythromycin and tetracycline is more effective than topical sulfonamides. The treatment is repeated in trachoma control programmes and is called the intermittent treatment that is after the continuous treatment of trachoma for active trachoma for 6 weeks, the intermittent treatment is started by giving the medication for 5 consecutive days of a month for 12 months.

Continuous treatment consists of:

  • Tetracycline 1% eye ointment or erythrocycline 1% eye ointment 4 times a day for 6 weeks or
  • Sulfacetamide 20% eye drops three times a day along with 1% tetracycline ointment at bedtime for 6 weeks.
  • Combined systemic and local therapy is given when the infection is severe.

2. Treatment of trachoma sequelae:

  • Trichiasis: It needs epilation or cryolysis or electrolysis.
  • Entropion is also corrected surgically, it will be dealt as a separate topic too.
  • Dry eye is treated by artificial tears.
  • Pannus requires no treatment as such and usually resolves with regression of the inflammatory activity of the conjunctiva.

Prevention

1. Hygienic living:

  • Proper handwashing.
  • Do not rub eyes frequently.
  • Environmental hygiene, no flies etc.
  • Use separate towels, cloths.
  • Use clean towels and cloths.
  • Use separate handkerchiefs, surma rods or kajal sticks.
  • Proper face washing at regular intervals.
  • Sexual hygiene: No Sexually Transmitted Diseases should be there, if exist, take proper treatment.

2. Any sort of conjunctivitis should be treated properly and at the earliest to prevent transmission.

3. The intermittent therapy described above should be followed in national trachoma control programmes. It is also called WHO Blanket antibiotic therapy.

Safe Strategy4. Various steps were taken by WHO. They started GET 2020 (Global Elimination of Trachoma by 2020) in 1997, under which primary health care activities were initiated and they followed a SAFE strategy.

S: Surgery for the lid.

A: Antibiotic to treat the community pool of infection.

F: Facial cleanliness

E: Environmental changes.

Vision 2020 also included trachoma in its list and runs on the lines of GET 2020 in context of trachoma.

Reference:

1. History of Trachoma by Katherine Schlosser.

2. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012) Chapter: Optics and refraction p59-66.

3. Parsons, Disease of the Eye (Elsevier, 21 Edition), p174-176.

Presbyopia

Presbyopia

PresbyopiaPresbyopia, also known as eyesight of old age, is not just a refractive error, but a condition of physiological insufficiency of accommodation which leads to near loss of vision. It usually begins around the age of 40, when people suffers from blurred vision while reading, sewing or working on computer. It occurs when the natural lens in the eyes loses its flexibility.

Cause

Normally we keep an object or a book at a distance of 25 cm, so that we can read it clearly. This point at 25 cms is called the near point of accommodation, after the age of 40 years, this near point of vision recedes beyond the reading point. This condition of failing near vision due to age related decrease in amplitude of accommodation is called as presbyopia.

It occurs due to:

  • Decrease in the rigidity and flexibility of the lens which results from age related sclerosis.
  • Age related decrease in the power of ciliary muscles.

Causes of premature presbyopia are:

  • Uncorrected hypermetropia.
  • Premature sclerosis of crystalline lens.
  • General debility which leads to pre senile weakness of ciliary muscles.
  • Due to certain drugs and diseases.
  • Chronic simple glaucoma.

Symptoms

  • Difficulty in near vision which mainly starts in the evening and night.
  • Asthenopic symptoms are also complained due to fatigue of ciliary muscles after reading or doing any work.

Diagnosis

Following tests are done to diagnose presbyopia:

  • Examination of retina
  • Muscle integrity test
  • Refraction test
  • Slit lamp examination
  • Visual acuity test: It is done by reading the numbers on the Snellen’s chart.

Treatment

The treatment of presbyopia is the prescription of appropriate convex glasses for near work. A rough idea of the glasses can be made from the age of the patient. About +1DS is required at the age of 40-45 years, +1.5DS at the age of 45-50 years, +2DS at the age of 50-55 years, +2.5DS at the age of 55-60 years. Basic principles for presbyopic correction:

1. Always find refractive error for distance and first correct it.

2. Find out the presbyopic correction needed in each eye separately and add it to the distant correction.

3. Near point should be fixed by taking due consideration for profession of the patient.

4. The weakest convex lens with which an individual can see clearly at the near point should be prescribed since overcorrection can also lead to asthenopic symptoms.

Eyeglasses with bifocal or progressive addition lenses (PALs) are most commonly used for presbyopia.

Surgeries are also done to correct presbyopia. Conductive keratoplasty is done which uses radio waves to create more curvature in the cornea to improve the near vision. LASIK surgery is the new presbyopia correcting surgery nowadays.

Reference

1. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012) Chapter: Optics and refraction p42-43.

2. Image used on this page is taken and copyright to National Eye Institute (www.nei.nih.gov).

Granulomatous Conjunctivitis

Pink Eye or Red Eye 2 (Granulomatous)

Pink eye or red eye has been covered in the pink eye or red eye article, and these terms are basically used to indicate conjunctivitis by the layman and that the definition of conjunctivitis, its causes, general signs, symptoms and treatment have already been dealt in the first post of pink eye or red eye.

This post is the sequelae of the red or the pink eye in which all the granulomatous conditions or long term or chronic pathologies causing the conjunctivitis or the red eye would be discussed.

What are Granulomatous Diseases

Granulomatous conditions or diseases are those in which there is formation of a granuloma.What happens is there are some microorganism or pathogens which are not easily destroyed by the immune system of our body. The cells of the immune system are not able to destroy them even after engulfing some of these pathogens.

So the other stronger cells of the body which are responsible for giving the protection in case of long term infection start to appear at the site of pathogen residual and starts engulfing them although they are also not able to kill them all resulting in collection of the inflammatory cells, giant cells and lymphocytes at the periphery and the necrotic cell structure (which has been destroyed by the microbes or pathogens) in the centre thus forming what is called a granuloma and the conditions in which this granuloma formation takes place are called the granulomatous conditions.

Therefore the granulomatous conditions are mainly caused by the tough microorganisms like the mycobacteria and are usually chronic or say long term infections.

What is Granulomatous Conjunctivitis

Granulomatous ConjunctivitisIn granulomatous conjunctivitis, there is mainly unilateral involvement of the eye that is there is conjunctivitis mainly in one eye with the formation of an inflammatory granuloma which is present or say localised to the route of the entry of the pathogen through the conjunctiva.

Various infectious agents causing conjunctivitis or pink or the red eye are:

  • Chlamydia trachomatis (serovarieties L1, L2, L3)
  • Rochalimaea henselae
  • Mycobacterium tuberculosis
  • Treponema pallidum
  • Francisella tularensis
  • Mycobacterium leprae

[*] If this granulomatous conjunctivitis that is mainly unilateral conjunctivitis with formation of a localised granuloma is also accompanied by lymphadenopathy of the regional or the surrounding areas (swelling of the lymph node), it is called parinaud oculoglandular syndrome.

Conditions causing Granulomatous Conjunctivitis

  • Parinaud oculoglandular syndrome
  • Cat scratch disease
  • Lymphogranuloma venereum
  • Tuberculosis of the conjunctiva
  • Syphilis (conjunctivitis)
  • Tularemia
  • Leprosy

Cat Scratch Disease

Cat Scratch DiseaseThis type of granulomatous conjunctivitis is caused by microorganism Rochalimaea henselae. It is called Cat scratch disease because there is a history of being licked or scratched by a cat 2 weeks or less before the symptoms arise.

Also the infected cat carries the microorganism, which on coming of the cat in contact with humans licking (infected saliva) or scratching inoculates it into the skin or eye (conjunctiva), causing the systemic disease and if the conjunctiva is the entry route then it causes conjunctivitis. It generally causes swelling of the lymph nodes too thus results in parinaud oculoglandular syndrome.

The diagnosis is made on history of cat licking and scratching and can be confirmed by serological tests and Hanger Rose cat scratch skin test.

The disease resolves itself in 4 – 6 weeks, so there is only a need to give supportive treatment. The usual medication is tetracycline or trimethoprim-sulfamethoxazole combination or ciprofloxacin which are given orally for four weeks. Topical eye drops gentamicin can be given for four times a day along with topical eye ointment to be applied four times a day.

Tuberculosis of the conjunctiva

Tuberculosis ConjunctivaMycobacterium tuberculosis is a gram positive, acid fast, rod like organism and because of the mycolic acid present in its cell wall resists staining.It mainly causes systemic disease tuberculosis but it can also cause granulomatous conjunctivitis although its incidence of causing granulomatous conjunctivitis is very rare.

Sometimes if the infection is from structure other than the eye or the conjunctiva, it can present as the only sign or symptom in an individual who has the systemic disease but otherwise does not have any other signs or symptoms.

  • It is seen to be occurring in mainly young people and usually causes ulceration.
  • It can present in many clinical forms in the eye.
  • The ulcers could be multiple.They are mainly present on the palpebral conjunctiva and are small miliary ulcers.
  • It can also present as follicular conjunctivitis that is follicles in the conjunctiva or as gelatinous exudates in the fornix.
  • It can also present as polyp like growth with a stalk or a typical nodule at the limbus.

Infact the ulceration of the conjunctiva should always arise the suspicion of the following pathological conditions:

  • Tuberculosis
  • Foreign body
  • Syphilis

There is usually less pain unless the ulceration is severe and this also causes swelling of the regional nodes and can result in parinauds’s oculoglandular syndrome.

The diagnosis can be made on the basis of conjunctival scrapings or lymph node biopsies which show typical granuloma formation and caseous necrosis on histopathology.

The lesion is usually excised particularly if it is the primary route of entry or can be scraped properly and cauterized by diathermy.

ATT (anti-tubercular treatment) must be given in all the cases.

Syphilis

Syphilis ConjunctivaSyphilis which is caused by the spirochaete Treponema pallidum can also cause granulomatous conjunctivitis in the eye.

Primary chancre stage which is due to invasion of the conjunctiva with the treponema by contact with an oral infected lesion is very rare.

The primary chancre here is less indurated than the usual genital primary chancre. This primary chancre if present in the palpebral conjunctiva can be mistaken for a chalazion.

A chronic ulcer or the gumma stage of the syphilis in the conjunctiva is relatively more common.

There is a formation of the gummation ulcer more commonly in the bulbar conjunctiva than in the palpebral conjunctiva.

Lymph nodes enlargement also take place in this condition and as the others it can also manifest as parinaud oculoglandular syndrome.

Diagnosis is made by taking the scrapings of the lesion and examining it for microorganisms by dark ground microscopy and serological tests.

Treatment is with the topical tetracycline and systemic penicillin.

Tularemia

It is caused by the organism Francisella tularensis and this organism is mainly derived from animals such as squirrels sheep, deer, cattle etc. The vectors of this disease are also there and they can be ticks or deer flies. It enters the human body through abraded skin or mucous membrane of the conjunctiva and also through tick bite. It can present as nodules or ulcers in the tarsal conjunctiva.

It also causes typical parinaud oculoglandular syndrome with manifestations of lymph node enlargement, fever, headache and general weakness. The diagnosis is made by agglutination test.

The treatment is by streptomycin and topical gentamicin drops till the condition resolves.

Lymphogranuloma Venereum

It is a highly infectious venereal disease caused by Chlamydia trachomatis mainly strains L1, L2, L3. The clinical features are typical and start with a vesicle which bursts and leaves behind a grey ulcer. There is also accompanying lymph node enlargement.

Treatment is with antibiotic Azithromycin 1g single dose. Other drugs include doxycycline, erythromycin or ofloxacin.

Parinaud Oculoglandular Syndrome

Parinaud oculoglandular syndrome occurs when there is unilateral conjunctivitis with formation of a localised granuloma is also accompanied by lymphadenopathy of the regional or the surrounding areas (swelling of the lymph node).

Therefore in parinaud oculoglandular syndrome, mainly there is conjunctivitis which is of follicular type and enlargement of preauricular or submandibular lymph nodes of the same or the affected eye.Various diseases which cause this syndrome are:

  • Cat scratch disease
  • Tularemia
  • Tuberculosis
  • Mumps
  • Ssyphilis
  • Lymphogranuloma venereum
  • Infectious mononucleosis
  • Fungal infections
  • Lymphomas
  • Leukaemias
  • Sarcoidosis
  • Patient complains of redness, mucopurulent discharge, and foreign body sensation.

Signs are follicular conjunctivitis, lymphadenopathy, fever, weakness. Fever can be with or without rash.

Treatment includes:

  • Warm compresses locally to the region of enlarged tender lymph nodes
  • Analgesics
  • Anti pyretics
  • Specific therapy for the disease.

Reference

1. Parsons, Diseases of the eye 21st Edition Page no.175-176.

Ocular Hypertension

Ocular HypertensionOcular hypertension also known as glaucoma suspect is said when a patient has an intra ocular pressure constantly more than 21 mm of Hg but there is no optic disc or visual field changes (normal intraocular pressure of eye is between 10 to 21 mm of hg). These cases should be carefully monitored and should be treated as cases of primary open angle glaucoma in the presence of high risk factors.

Ocular hypertension has the following criteria:

  • An intra ocular pressure of more than 21 mm of hg in one or both the eyes on 2 or more occasions.
  • Optic nerve appearing normal.
  • No signs of glaucoma evident on visual field testing.
  • No signs of any ocular disease is present.

Cause

Normally the fluid flows out through a small drain called trabecular meshwork which is a complex network of cells and tissue in an area called as drainage angle. If the aqueous humour does not flow through this trabecular meshwork properly, there is a rise in the fluid pressure, causing ocular hypertension.

Ocular hypertension can also be caused by any injury to the eye, and certain eye diseases. Certain medications like steroids can also cause ocular hypertension.

Risk factors

High risk factors include

  • Significant diurnal variation: there is a difference of more than 8 mm of Hg between the lowest and the highest values of IOP.
  • Significantly positive water drinking provocative test.
  • When associated with splinter haemorrhages over or near the optic disc.
  • IOP constantly more than 28 mm of Hg.
  • Retinal nerve fibre large defects.
  • Parapapillary changes.
  • Central corneal thickness <555 µm.

Other risk factors include

  • Significant asymmetry in the cup size of the two eyes (a difference of more than 0.2).
  • Strong family history of glaucoma.
  • When associated with myopia, diabetes or pigmentary changes in the anterior chamber.

Diagnosis

Following tests are done to diagnose ocular hypertension:

1. Tonometry: This procedure is done to measure the intraocular pressure. It is of two types: indentation and applanation tonometry.

2. Gonioscopy: This procedure is used to examine the draining angle of the eye. This is used to examine what type of glaucoma does the patient have.

3. Visual field test: This test is done by an instrument called perimeter.

4. Ophthalmoscopy: This test is used to examine the optic nerve by an ophthalmoscope.

5. Pachymetry: This test is used to measure the corneal thickness.

Treatment

  • Patients with high risk factors should be treated on the lines of primary open angle glaucoma, which requires therapy to lower IOP. The IOP should be reduced by 20%.
  • Patients with no risk factors should be annually followed by examination of optic disc, perimetry and record of IOP.

Reference

1. Parsons, Disease of the Eye (Elsevier, 21 Edition), Chapter: Diseases of the Optic Nerve p361-362.

2. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012).

3. Ocular Hypertension image used on this page is copyright to Cure Byte (www.trialx.com).

Fuchs Corneal Dystrophy

Fuchs Corneal Dystrophy

Fuchs Corneal DystrophyFuchs Corneal Dystrophy is a degenerative eye disorder which is slowly progressive bilateral condition affecting females more than males, occurring mainly between fifth and seventh decade of life affecting cornea (the transparent front surface).

Cause

Normally in a person the endothelial layer of cornea prevents from accumulation of fluid but in a person suffering from fuchs corneal dystrophy, the endothelial cells start to die and as a result accumulation of fluid occurs which result in oedema, blurring of vision, pain.

Inheritance: It is an autosomal dominant. It means that one gets affected from parent and there are 50% chances of inheriting the gene and 50% chances of having normal gene. Genetic Locus is 13p.

Clinical features

Fuchs Corneal Dystrophy is classified in 4 stages. These stages are:

Fuchs Corneal Dystrophy showing Guttata1. Stage of Corneal Guttata (guttata means mushroom shaped bodies in corneal endothelium):

It is an asymptomatic stage characterized by presence of Hassall-Henle type of excrescences in central part of cornea. With increase of guttae in peripheral part it gives rise to ‘beaten-metal’ appearance.

[*] Hassall-Henle bodies are drop like excrescences in anterior chamber around the corneal periphery arising from Descemet’s membrane.

2. Oedematous Stage: It is characterized by stromal oedema and epithelial dystrophy. There is blurring of vision in this stage.

3. Stage of Bullous Keratopathy: In this stage there is epithelial oedema with formation of bullae which on rupture cause pain, discomfort, irritation and reduced visual acuity.

4. Stage of Scarring: In this stage bullae are replaced by scar tissue which result in opaqueness of cornea. It can be complicated by occurrence of secondary infection or glaucoma.

Diagnosis

The diagnosis of Fuchs Corneal Dystrophy is made by the examination of the cornea using Slit-lamp. This may detect a partial absence of endothelium, corneal edema, bullous changes in the epithelium layer. In addition, pachymetry used to detect the thickness and swelling of the cornea.

Specular Microscopy is used to confirm the diagnosis. It reveals decreased endothelial count, increased average cell diameter with increased variation in cell size.

Treatment

There are no Medication available to cure the Fuchs Corneal Dystrophy. But symptomatic treatment is done using hypertonic saline instillation to draw excess fluid from the cornea, which improves the vision temporarily.

The treatment of choice for Fuchs Corneal Dystrophy is the Penetrating Keratoplasty. But there are high risk of complications  associated with surgery, it is usually assigned when visual acuity of less than 0.1-0.3.

Reference

1. A.K Khurana, MD “Ophthalmology” (New Age International Publisher, Inc 2012).

2. Fuchs Corneal Dystrophy showing Guttata image used on this page is copyright to American Academy of Ophthalmology (www.geteyesmart.org).