Frequently asked questions


Below we provide you with information about the most common eye conditions.

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Myopia is derived from the term “muopia” which, in Greek, means to close the eyes. It manifests itself as blurred distance vision, hence the popular term “short or near-sightedness.” Clear distance vision is usually restored with minus power (concave) spectacle or contact lenses or corneal modification procedures in which corneal refractive power is decreased.

Myopia is the refractive anomaly of the eye in which the conjugate focus of the retina is at some finite point in front of the eye when the eye is not accommodating. It can also be described as the refractive condition in which parallel light rays from an object at optical infinity are focused by the eye in front or short of the retina, in a relaxed state of accommodation.

Signs and symptoms

The most common symptom associated with uncorrected myopia is blurred distance vision. In simple myopia and degenerative myopia, the distance blur is constant. In nocturnal myopia, distance vision is blurred only in dim illumination or in dark conditions.

Children with simple myopia are often unaware that they have reduced distance vision until they discover that other children see better than they can. For example, many school children first notice that they cannot read the chalkboard as well as their classmates. For others who never report a problem, poor distance vision is first detected during vision screening or comprehensive eye and vision examination. The primary sign of myopia is reduced unaided distance visual acuity, which can be corrected to standard or near-standard levels with the appropriate minus power optical correction.

Detection and Prevention

Myopia or short-sightedness

Reduced unaided distance visual acuity is a possible indication of myopia, particularly when unaided near visual acuity is normal or better than unaided distance acuity. Myopia can be detected by visual acuity testing, retinoscopy, autorefraction, or photorefraction during vision screening or clinical examination.

There is no universally accepted method of preventing myopia. However, some clinicians identify nearpoint vision stress as a possible contributor to the development of simple myopia. When presented with signs of nearpoint vision stress, such as distance blur, poor accommodative facility, and refraction at about plano (zero lens strength is required for clear distance vision), some clinicians recommend regimens such as the following:

  • Plus power lenses in single-vision or bifocal form for reading and near work
  • Vision therapy or orthoptics to eliminate deficiencies in accommodation and vergence function

Further research into the risk factors relating to incipient myopia is needed to clarify and support these clinical interventions.



Minus (concave) lenses

The goals for management of the patient with myopia are clear, comfortable, efficient binocular vision and good ocular health. The primary symptom in patients with low and moderate myopia is lack of clear vision at distance, which can be restored by optical correction. Treatment directed to slowing the progression of myopia is referred to as “myopia control”. Effective myopia control results in less severe myopia and less vitreous chamber elongation than would otherwise have occurred.

Optical correction in the form of spectacles or contact lenses provides clear distance vision. Whether spectacles or contact lenses are preferable in a given case depends upon numerous factors, including patient age, motivation for wearing contact lenses, compliance with contact lens care procedures, corneal physiology, and financial considerations. It is the optometrist’s responsibility to advise and counsel the patient regarding the optical correction options available and to guide the patient in the selection of the appropriate spectacles and/or contact lenses.

Hyperopia, also termed hypermetropia or farsightedness, is a refractive error in which parallel rays of light entering the eye reach a focal point behind the plane of the retina, while accommodation is maintained in a state of relaxation.

Hyperopia is a common refractive error in children and adults. Its effect varies greatly, depending upon the magnitude of hyperopia, the age of the individual, the status of the accommodative and convergence system, and the demands placed on the visual system.

Signs and symptoms

Young persons with hyperopia generally have sufficient accommodative reserve to maintain clear vision without any asthenopia or eyestrain. However, both younger and older hyperopic patients, even those with mild hyperopia, may be symptomatic as a result of inadequate accommodative reserves for their levels of hyperopia. When the level of hyperopia is too great or the accommodative reserves are insufficient, due to age or fatigue, blurred vision and asthenopia develop. Presbyopia brings an increase in absolute hyperopia, causing blur, especially at near.

The presence and severity of these symptoms varies widely. Some young patients with hyperopia, including those with moderate and high hyperopia, may be relatively free of signs and symptoms.

Individuals with uncorrected hyperopia may experience, especially when the amount varies between the two eyes:

  • Blurred vision
  • Asthenopia
  • Accommodative dysfunction
  • Binocular dysfunction
  • Amblyopia
  • Strabismus

Detection and Prevention

Hyperopia or far-sightedness

A positive family history of hyperopia, amblyopia, or strabismus increases the likelihood that a young patient with suspected eye or vision problems actually has a similar problem.106 The effect of hyperopia on visual acuity depends upon the magnitude of the hyperopia and the patient’s age, visual demands, and accommodative amplitude available to overcome the hyperopia. Young patients with low to moderate facultative hyperopia generally have normal visual acuity, but when visual demands are high, they may experience blurred vision and asthenopia. Visual acuity testing of patients with high hyperopia, even when the patients are young, is likely to reveal measurable deficits, especially under significant visual demand.

The patient who has never been optically corrected for a high degree of hyperopia, with or without astigmatism, is at risk for isoametropic amblyopia. Older patients with hyperopia invariably experience reduced vision, especially at near. Pre-presbyopic and early presbyopic patients with hyperopia manifest deficits of near vision before distance visual acuity is adversely affected. In patients with absolute hyperopia, the reduction in visual acuity at both distance and near occurs.



Plus (convex) lenses

Significant hyperopia, if uncorrected, can produce visual discomfort, blurred vision, amblyopia, and binocular dysfunction, including strabismus, and contribute to learning problems. Treatment should be initiated both to remediate symptoms and to reduce the future risk of vision problems resulting from the hyperopia.

The primary modality for treating significant hyperopia is correction with spectacles. Plus-power spherical or spherocylindrical lenses are prescribed to shift the focus of light from behind the eye to a point on the retina.
Accommodation plays an important role in determining the prescription. Some patients with hyperopia do not initially tolerate the full correction indicated by the refraction, and many patients with latent hyperopia do not tolerate the full correction of hyperopia indicated under cycloplegic refraction. <br
To determine the final spectacle lens prescription, the optometrist carefully considers the patient’s vision needs. The lenses prescribed may be either single vision or multifocal.

Newer high-index lens materials and aspheric lens designs have reduced the thickness and weight of high plus-power lenses required with hyperopia, thus increasing their wearability and patient acceptance. Spectacles, especially those with lenses of polycarbonate material, provide protection against trauma to the eye and orbital area.</br

The cornea of the normal eye generally has a uniform curvature, resulting in equal refracting power over its entire surface. Most astigmatic corneas are are healthy, yet in some astigmatic individuals the cornea is irregular , resulting in irregular astigmatism. When the curvature is greater in one meridian (plane) of the eye compared to the other meridian, much like a rugby ball, a “splif” focus results.
Light rays refracted by this cornea are not brought to a single point of focus and the retinal image from objects both distant and near are blurred or distorted and may appear broadened or elongated.

Signs and symptoms


Distortion or blurring of images at all distances is one of the most common astigmatism symptoms. This may happen vertically, horizontally, or diagonally. There can be indistinctness of objects, circles become elongated into ovals and a point of light begins to tail off.

Symptoms of eye strain such as headaches, photophobia and fatigue are also among the most common astigmatism symptoms, including the reading of small print during near work.

Although astigmatism may be asymptomatic, higher degrees of astigmatism may cause symptoms such as:

  • squinting
  • eye discomfort
  • blurred vision
  • headaches
  • distortion in the visual field
  • monocular diplopia
  • glare sensitivity
  • reduced night vision

Some research has pointed to the link between astigmatism and higher prevalence of migraine headaches.


The various modes of non surgical treatment of astigmatism include, spectacles, contact lenses and treatment of the cause. A cylindrical spectacle lens is the simplest and safest means of correcting the refractive error resulting from astigmatism. However as most astigmatic individuals are also either hyperopic or myopic, they require correction in more than one meridian. To provide the correction they need, a lens formed from the combination of cylinder and sphere is generally required, called a sphero-cylindrical lens.

Irregular astigmatism occurs when when the principal meridians of the cornea, as a whole, are not perpendicular to one another. Although all eyes have a small amount of irregular astigmatism, this term is clinically used only for grossly irregular corneas such as those occurring with keratoconus or corneal scars. Cylindrical spectacle lenses can do little to improve vision in these cases, and so for best optical correction, rigid contact lenses are more commonly needed.

Custom designed soft Toric contact lenses or soft disposable lenses often provide another means to correct astigmatic refractive errors. These contact lenses offer good centration when properly fitted, a flexible wear schedule and improved comfort compared to hard lens designs. Regardless of the design chosen, adequate contact lens movement is essential for comfortable wear and maintenance of corneal integrity.
Presbyopia is a loss of accommodative abilities, mostly commonly resulting in reduced near vision in the early stages and is usually, but not always an age-related visual impairment. The gradual decrease in accommodation can have a significant impact on visual clarity and the quality of life. Though not incapacitating if corrected, presbyopia without optical correction results in an inability to perform once effortless near tasks at a customary working distance without experiencing visual symptoms.
Presbyopia has been described as “an irreversible optical failure, an unexplained evolutionary blunder that comes as a psychologic shock.” As the amplitude of accommodation diminishes, the range of clear vision may become inadequate for the commonly performed tasks. The impact of this process varies from one person to another and those who are involved in more frequent or more demanding near vision tasks are likely to have greater difficulty. Because the need to read and work at near and intermediate distances is important in all industrialized societies, presbyopia has both clinical and social significance.

Signs and symptoms

The onset of presbyopia is gradual, although blurred near vision signals the onset of presbyopia, the symptoms reach significance only when the patient’s accommodative amplitude becomes inadequate for his or her visual needs. Difficulty in performing vocational or avocational activities largely determines when the symptoms of impairment are manifest.
Blurred vision and the inability to see fine detail at the customary near working distance are the hallmarks of presbyopia, yet other symptoms include:

  • Focusing delays
  • Ocular discomfort
  • Headaches
  • Asthenopia
  • Squinting
  • Fatigue or drowsiness
  • Increased working distance
  • A need for brighter light for reading
  • Diplopia


The evaluation and management of presbyopia are important because significant functional deficits can occur when the condition is left untreated. Furthermore, the onset of presbyopia frequently motivates the individual to seek eye care, presenting the optometrist the opportunity to check for the presence of other disorders, some of which might threaten sight or life. This opportunity underscores the public health benefit of comprehensive optometric care for patients with presbyopia.
As primary eye care providers, optometrists have the expertise to examine, diagnose, treat, and manage a wide variety of eye and vision problems.

For patients requiring other health care services related to systemic conditions detected in the course of their eye examination, the optometrist becomes the point of entry into the broader health care system. Under corrected or uncorrected presbyopia can cause significant visual disability and have a negative impact on the patient’s quality of life. Gaining an understanding of the patient’s specific vocational and avocational visual requirements helps the optometrist recommend the treatment most appropriate for enhancing visual performance.

A variety of options are available for optical correction of presbyopia, dependent on ocular health, patient’s specific vocational and avocational needs, the following spectacle treatment methods for presbyopia include:

  • Single vision lenses
  • Anti-fatigue lenses
  • Bifocal lenses
  • Multifocal lenses
  • Near progressive lenses
  • Occupational lenses

All types of corrections for presbyopia represent some visual compromise, compared with normal accommodative ability. Ultimately, the success of treatment depends on the lens power, the optical correction, the specific visual tasks, characteristics of the individual patient, and the appropriate patient education given by the practitioner.

Optical correction with contact lenses (both rigid and soft lens designs) can be used for contact lens correction of presbyopia and include the following:

  • Monovision contact lenses
  • Bifocal/ Multifocal contact lenses
  • Enhanced monovision lenses
  • Combination of contact and spectacle lens

Many contact lens wearers gain some advantage by combining the use of spectacles with their contact lenses. One common example is the patient who uses contact lenses for distance viewing and adds glasses over the contact lenses for reading. A second example is the patient who has critical near vision tasks for most of the day and chooses to wear contact lenses for near, adding glasses for distance tasks. A third example is the monovision contact lens wearer who sometimes wears glasses to improve binocular vision for the performance of specific tasks. Some contact lens wearers use spectacles to correct residual astigmatism when performing more critical visual tasks.

Emmetropia (from Greek emmetros, “well-proportioned” or “fitting”, + -opia) describes the state of vision where a faraway object at infinity is in sharp focus with the crystalline lens in a neutral or relaxed state.

Emmetropia does not require visual correction (most commonly spectacles and contact lenses) should not be confused with ametropia, which results in blurred uncorrected vision.

Emmetropia is a state in which the eye is relaxed and focused on an object more than 6 meters or 20 feet away. The light rays coming from that object are essentially parallel, and the rays are focused on the retina without effort. Accommodation of the lens does not occur in emmetropia. In emmetropia, the lens is about 3.6 mm thick at the center; in accommodation, it thickens to about 4.5 mm. A relatively thin lens and relatively dilated pupil are also associated. The lens usually stiffens with age, causing less ability to focus thus requiring optical intervention to restore focus and clear vision.

If the gaze shifts to something closer, light rays from the source are too divergent to be focused without effort. In other words, the eye is automatically focused on things in the distance unless a conscious effort is made to focus elsewhere.
For a wild animal or human prehistorical ancestors, this arrangement would be adaptive because it allows for alertness to predators or prey at a distance.


The development of an eye towards emmetropia is known as emmetropization. This process is guided by visual input, and the mechanisms that coordinate this process are not fully understood. It is assumed that emmetropization occurs via an active mechanism by which defocus drives growth of the eye and that genetic factors and emmetropization both influence the growth of the eye’s axis.

Newborns begin hypermetropic and then undergo a myopic shift to become emmetropic.


Ametropia is the collective name for any deviation in the relaxed focus of the eye from the normal state in which distant objects form sharp and clear images on the retina. If you are not emmetropic, then you have a refractive error and referred to as ametropic.

Examples of refractive error are the following:

  • Myopia or short-sightedness
  • Hyperopia or far-sightedness
  • Astigmatism
  • Presbyopia

All of which requires optical intervention, most commonly spectacles and contact lenses to restore clear vision.

There has been some research on causal factors involved in the development of ametropia. In particular, statistics show that prolonged near work correlates with the development of myopia, but it is still unclear whether there is a causal relation.Furthermore, outdoor activity has been found to have a protective effect on myopia development in children.









A pterygium (pronounced “te-ridge-e-um”) is an elevated wedge -shaped growth on the conjunctiva or mucous membrane that covers the white part of your eye. It usually originates from the inside corner of the eye, but less commonly from the outside corner. The word Pterygium is from the Greek word “pterygos” meaning “wing”, Typically that of a butterfly. The Ptyrigium resembles a butterfly wing in both shape and appearance. These growths are non-cancerous, but they do contain blood vessels and can form scar tissue that can permanently disfigure the eye. Exposure to ultraviolet light has been identified as the main culprit regarding the growth of a pterygium. Wind, dust, and exposure to ultraviolet light will cause the pterygium to become inflamed, dry, and very itchy. These growths need to be surgically removed by an eye specialist before they invade the cornea and affect vision. Ptyrigia that occur on the surface of the eye are commonly mistaken as cataracts which is actually inside the eye. Recurrence of the pterygium is minimised by wearing good quality sunglasses with a 100% UV filter.

Signs and Symptoms

A pterygium starts as redness and thickening in the corner of the eye – usually the corner closest to the nose. The growth can extend across the surface of the eye towards the iris (the coloured part of the eye). Often a person may notice the formation of a pterygium but may not experience any other symptoms.

Typical Signs of a pterygium are:

  1. Wedge-shaped, translucent membrane with apex extending onto cornea.
  2. White to pink in color, depending on vascularity.
  3. Vascular straightening in the direction of the advancing head of the pterygium.
  4. Stocker line: iron line on cornea at leading edge of pterygium.
  5. Regular or irregular astigmatism
  6. Degenerative changes.

Symptoms may vary, but the most common are

  1. Eye redness and inflammation.
  2. A gritty feeling in the eye.
  3. A feeling that there is a foreign object in the eye.
  4. Dryness of the eye due to reduced tear production.
  5. Blurring of vision if the corneal surface is altered or “warped”.
  6. Obscuring of vision if growth encroaches across the pupil.

Causes and Risks

The cause is unclear. It appears to be partly related to long term exposure to UV light and dust. Genetic factors also appear to be involved. It is a benign growth. Other conditions that can look similar include a pinguecula, tumor, or Terrien’s marginal corneal degeneration.

Risk Factors typically include:

  1. Ultraviolet exposure (single most significant risk factor).
  2. Exposure to irritants (dust, sand, wind).
  3. Inflammation.
  4. Dry ocular surface.
  5. A pterygium can lead to severe scarring on your cornea, but this is rare.
  6. Scarring on the cornea needs to be treated because it can cause vision loss.


The pterygium itself is normally harmless and treatment is purely to relieve symptoms when they occur. A pterygium often causes a dry eye problem, and most symptoms tend to be relieved by an artificial tear drop.

If the lesion causes persistent discomfort or interferes with vision, it can be surgically removed during an outpatient procedure. The operation can be performed under local anaesthesia (awake) or general anaesthesia (asleep). The choice is based on anticipated length of surgery, the size of the pterygium, the surgeon’s advice and the patient’s own preferences.

Surgical intervention is considered if:

  1. Your symptoms are not adequately relieved by the eye drops.
  2. Your symptoms recur frequently.
  3. There is pus in the eye or the eyelids stick together on waking in the morning.
  4. The pterygium covers part of the iris and grows onto the cornea and towards the pupil.
  5. You have any deterioration of vision.
  6. You would like the pterygium to be removed for cosmetic reasons.

The type of surgery most commonly used today uses a graft from the patient’s own conjunctiva (surface eye tissue) or preserved amniotic membrane (the thin tissue forming the sac in which a foetus grows) to fill the empty space created by the removal of the pterygium. In this procedure, the pterygium is removed and the conjunctiva or amniotic membrane is glued or stitched onto the affected area.

Prevention, and specifically post operatively, wearing sunglasses and a hat if in an area with strong sunlight is essential. Following surgery, a pterygium may recur in around half of cases.

A pinguecula can be described as a small elevated mass on the white of the eye. It is usually slightly yellow in colour. The main culprit for the formation of a pinguecula is ultraviolet exposure, and this is further aggravated by wind and dust. When one has a history of a dry eye, this can further add to the development of a pinguecula. They are often confused with a ptyrigium, but they differ in that they don’t invade the cornea, they are slightly raised, and their development and growth is a lot slower than that of a ptyrigium. They do however have the same symptoms as a ptyrigium being itchy and burning when they occasionally become inflamed.

Symptoms and inflamed flare-ups can be minimised by wearing good quality sunglasses with a 100% UV filter. Regular use of dry eye drops can further offer relief, especially if they have become inflamed. Surgical removal is only indicated in extreme cases.

Signs and Symptoms

A pinguecula can make your eye feel irritated or dry. It can also make you feel like you have something in your eye. Or you might have a gritty feeling as though you had sand or other rough particles in your eye. The affected eye might also itch or become red and inflamed. These symptoms caused by pingueculae can be mild or severe. Your eyecare practitioner should be able to diagnose this condition based on the pinguecula’s appearance and location.

A pinguecula is yellowish in colour and typically has a roundish or oval shape. It’s a small raised patch that grows close to your cornea. Your cornea is the transparent layer that lies over your pupil and iris. Pingueculae are more common on the side of your cornea closer to your nose, but they can also grow next to your cornea on the other side. Some pingueculae can grow larger, but this occurs at a very slow rate and is rare.

In most people, pingueculae don’t cause many symptoms. But when they do, those symptoms usually stem from a disruption of the tear film which may not spread evenly across the surface of the eye around it, causing dryness. This can cause dry eye symptoms, such as a burning sensation, stinging, itching, blurred vision and foreign body sensation. Another symptom of pingueculae is the appearance of extra blood vessels in the conjunctiva that covers the sclera, causing red eyes. In some cases, pingueculae can become swollen and inflamed. This is called pingueculitis.

Causes and Risks

A pinguecula forms when the tissue in your conjunctiva changes and creates a small bump. Some of these bumps contain protein, fat, and calcium, while others contain protein and either fat or calcium.

Ultraviolet radiation from the sun is the primary cause of the development of pingueculae, but frequent exposure to dust and wind also appear to be risk factors. Dry eye disease also may be a contributing factor and can promote the growth of pingueculae.

To decrease the risk of pinguecula, it’s important to wear sunglasses outdoors even on overcast and cloudy days, because the sun’s UV rays penetrate cloud cover. Sunglasses are as important in winter as they are in summer, even though the sun is lower in the sky in winter. For the best protection, choose sunglasses with a wraparound frame design, which block more sunlight than regular frames.


You usually don’t need any type of treatment for a pinguecula unless it causes discomfort. If your eye does hurt, your eyecare practitioner can give you eye ointment or eye drops to relieve redness and irritation.

You can talk to your eyecare practitioner about having the pinguecula surgically removed if its appearance bothers you. In some cases, a pinguecula might need to be removed. Surgery is only considered when it causes extreme discomfort when wearing contact lenses, or is constantly and severely inflamed even after you apply eye drops or ointments.

Pingueculae are known to grow back after surgery in some cases. Your doctor might give you medication or use surface radiation to help prevent this.

Finally, although a pinguecula is non-cancerous, you should report any changes in size, shape or color of any bump on your eyeball to your eye care practitioner.

Corneal Neovascularization can be defined as the excessive growth of blood vessels that occurs at the level of the cornea. The main cause of the problem is represented by the oxygen deprivation. In healthy individuals, the cornea is transparent and it lacks vascularization. Both ocular insults and ocular hypoxia are responsible for the appearance of corneal vascularization.

The condition is often encountered in those who wear contact lenses. Risk factors for the appearance of corneal neovascularization include high myopia, the dry eye syndrome and different conditions with ocular involvement (compromised immune system, Sjögren’s syndrome or acne rosacea). Hydrogel contact lenses present the highest risk for corneal neovascularization.

If the progression of vessels persists, reduced wearing time is the first course of action, and careful monitoring of the progression by your eyecare professional is essential. In some cases, rigid gas permeable (hard lenses) are an option to slow down the progression. If, in extreme cases, the progression is not contained, one may have to refrain from wearing contact lenses altogether.

This condition is not life-threatening but it can lead to loss of vision in more severe cases. The vision can be threatened by the direct invasion of the blood vessels at the level of the cornea or because of secondary changes, such as the haemorrhage or scarring.

It can be stopped or slowed down by decreasing contact lens wear. But if it is very significant, the only treatment is corneal transplant surgery.

Signs and Symptoms

During a routine eye exam, the following changes can be identified

  1. Limbal hyperemia (Redness around the cornea) – earliest sign of corneal neovascularization.
  2. Superficial vessels identified at the level of the cornea (single or multiple).
  3. In the situation that the deep stromal vessels are responsible for the corneal neovascularization, these are identified at the level of the cornea (sometimes accompanied by nerve fibres).
  4. Active engorged vessels and lipid exudate.
  5. Light sensitivity.
  6. Decreased vision or blurring when wearing contact lenses.
  7. Intolerance to contact lens after wearing them for a short time.
  8. Corneal edema and leakage.
  9. Lipid deposition – yellow-white opacities (surround the stromal vessels).

Causes and Risks

These are the most common causes that lead to corneal neovascularization

  1. Wearing contact lenses.
  2. Viral infection (Common – herpes simplex).
  3. Corneal ulcers.
  4. Infectious keratitis.
  5. Immunological conditions.
  6. Corneal trauma.
  7. Alkali injury.

Risk factors that can increase the risk for corneal neovascularization are

  1. poor compliance.
  2. inadequate hygiene of the contact lenses.
  3. poor follow-up care.

The invasion of the cornea by the deep stromal vessels presents the biggest risks, with the optical transparency being lost due to a series of changes. Among the most important changes, there are the hemorrhage and scarring that can occur at the level of the cornea. The deposits of lipids can also affect the optical transparency, complicating the already existent corneal neovascularization.


Left untreated, the corneal neovascularization can progress and have a negative impact on the eyesight. Those who wear contact lenses should visit their eye care practitioner on an annual basis, for a routine eye exam.


A study performed on lab rats has demonstrated that both triamcinolone and doxycycline can be used to reduce the neovascularization process at the level of the cornea (topical instillation). Other studies recommend using angiotensin II receptor blocker drug telmisartan as a prophylactic measure (prevention of corneal neovascularization). The topical application of bevacizumab (anti-VEGF) has also been recommended as a treatment for corneal neovascularization.

Other treatment measures include

  1. Discontinuing the current contact lenses and replacing them with better ones (higher oxygen permeability).
  2. Refitting the current contact lenses.
  3. Permanent discontinuation of the contact lenses in patients diagnosed with severe forms of corneal neovascularization (reducing the risk of losing one’s eyesight).
  4. Treatment of the underlying cause or of the associated conditions (acne rosacea, dry eye syndrome, blepharitis, viral or bacterial infections – particularly those with staphylococcus).
  5. Topical corticosteroids for active neovascularization.
  6. Superficial keratectomy is recommended in combination with topical and subconjunctival bevacizumab.
  7. Corneal transplantation for patients who present with central corneal scarring, however they present a high risk for rejection in severe cases of corneal neovascularization.
  8. Photodynamic therapy.
  9. Argon laser obliteration performed at the level of the vessel lumen.
  10. Hyperbaric oxygen treatment, but with limited success.
  11. Amniotic membrane transplantation for the regeneration of the ocular surface.

Allergic conjunctivitis is an inflammation of the thin clear membrane that covers the white of the eye, and the inside layer of the eyelids. It is to an allergic reaction to a substance, most commonly grasses, dust, feathers, pollen from flowers or trees, mould, animal hair or fur, and many household detergents, and in some cases fabric softeners and perfumes or deodorants (especially the aerosol types).

The Symptoms of allergic conjunctivitis might include severe hayfever, redness, itching, and excessive tearing. Swollen Lids, burning eyes, and sensitivity to bright light are also common symptoms. Treatment is mainly avoidance of the causative substance, and treatment with antihistamines, in either tablets taken orally or eyedrops, or in severe cases both. Treatments are safe and usually effective. This condition is most common during spring, but some individuals report the symptoms all year round.

Allergic conjunctivitis is quite common. It’s your body’s reaction to substances it considers potentially harmful.

Signs and Symptoms

Allergic conjunctivitis comes in two main types:

Acute allergic conjunctivitis This is a short-term condition that is more common during allergy season. Your eyelids suddenly swell, itch, and burn. You may also have a watery nose.

Chronic allergic conjunctivitis A less common condition called chronic allergic conjunctivitis can occur year-round. It is a milder response to allergens like food, dust, and animal dander. Common symptoms come and go but include burning and itching of the eyes and light sensitivity.

What are the symptoms of allergic conjunctivitis?

  1. Both eyes are usually affected and symptoms tend to develop quickly.
  2. The eyes are usually itchy and gritty.
  3. The skin on the inside of the eyelids looks red and sore.
  4. The whites of the eyes look red or pink.
  5. A burning feeling may occur, although the eyes are not usually painful.
  6. The eyelids tend to swell.
  7. The eyes water more than usual; however, they do not become too gluey or sticky.
  8. Vision is not affected.
  9. In severe cases the conjunctiva under the upper eyelids may swell and look lumpy.

Causes and Risks

You experience allergic conjunctivitis when your body tries to defend itself against a perceived threat. It does this in reaction to things that trigger the release of histamine. Your body produces this potent chemical to fight off foreign invaders. Some of the substances that cause this reaction are:

What causes allergic conjunctivitis?

  1. household dust
  2. pollen from trees and grass
  3. mold spores
  4. animal dander
  5. chemical scents such as household detergents or perfume

Some people may also experience allergic conjunctivitis in reaction to certain medications or substances dropped into the eyes, such as contact lens solution or medicated eye drops.

Who is at risk for allergic conjunctivitis?

  1. People who have allergies are more likely to develop allergic conjunctivitis. According to the Asthma and Allergy Foundation of America, allergies affect 30 percent of adults and 40 percent of children, and often run in families.
  2. Allergies affect people of all ages, though they are more common in children and young adults. If you have allergies and live in locations with high pollen counts, you are more susceptible to allergic conjunctivitis.



Home care

Treating allergic conjunctivitis at home involves a combination of prevention strategies and activities to ease your symptoms. To minimize your exposure to allergens:

  1. close windows when the pollen count is high
  2. keep your home dust-free
  3. use an indoor air purifier
  4. avoid exposure to harsh chemicals, dyes, and perfumes

To ease your symptoms, avoid rubbing your eyes. Applying a cool compress to your eyes can also help reduce inflammation and itching.


In more troublesome cases, home care may not be adequate. You will need to see a doctor who might recommend the following options:

  1. an oral or over-the-counter antihistamine to reduce or block histamine release
  2. anti-inflammatory or anti-inflammation eye drops
  3. eye drops to shrink congested blood vessels
  4. steroid eye drops

The Meibomian glands are composed of acinar cells connected to a central duct, which opens onto the mucocutaneous junction at the lid margin. Lipids slowly emerge from this orifice throughout the day and night, but the pressure of Riolan’s muscle contracting with the blink causes the most considerable release. The lower lid houses about 20 to 25 glands while the longer, upper lid accommodates 30 to 40, each about 1 mm wide and 3 to 12 mm long.

Meibomitis is typically an Inflammation of the small glands that produce this oily component of the tearlayer that keeps the eye moist and lubricated when we blink, or for the rotation of the eyeball while looking in different directions. Typical Symptoms are red eye, excessive watering blurry vision, dry eye, and swollen lids. Blepharitis and meibomitis usually occur together, and then the symptoms are more severe. Treatment is typically nightly warm compress, Lid scrubs and ointment. Drops to relieve symptoms, and where necessary antibiotic tablets or eyedrops are also often indicated. This condition is also referred to as meibomian gland dysfunction

Signs and Symptoms

People with Meibomitis (known also as Posterior Blepharitis) complain of chronic sandy-gritty eye irritation. But in these people, the irritation is worse upon awakening because the inflammation is in the eyelids. During sleep, tear production decreases, eye closure brings the inflamed lids right up against the eye, and the released inflammatory mediators act on the cornea all night, creating a symptom peak upon eye opening. When these people awake, tear flow increases, the lids pull away from the cornea, and their symptoms improve as the day goes on.

Eventually the chronic meibomian gland inflammation leads to meibomian gland dysfunction. When that happens, these patients develop a second peak in symptoms from dryness toward the end of the day. Finally, when the meibomian gland inflammation and secondary healing obliterate the meibomian glands, the morning symptoms resolve and patients are left with symptoms from dryness alone, with sandy-gritty irritation that gets worse as the day goes on.

Symptoms may vary, but the most common are

  1. Red eye
  2. Red eyelid margins
  3. Watery eye
  4. Dry eye
  5. Itching
  6. Burning eye
  7. Blurry vision
  8. Foreign Body Sensation
  9. Light sensitivity (especially in the morning hours)

Causes and Risks

When a patient is affected by an inflammation the produced oil is less in quantity and worse in quality as a result quicker tear evaporation. In addition, these oils become stagnant and bacteria, usually staph bacteria, colonize inside the meibomian glands. Moreover, these bacteria produce toxins that cause the lids to become red and inflamed. The symptoms are different for each patient but most of the times are similar to common blepharitis.

The most common causes of Meibomianitis are

  1. Allergies
  2. Hormonal changes associated with adolescence
  3. Skin conditions, such as rosacea, acne or scalp dandruff
  4. Eyelash mites or lice
  5. Medications that increase bacteria on the eyelids, including isotretinoin for acne
  6. Some contact lens solutions
  7. Eye make-up
  8. Poor eye hygiene
  9. Poor nutrition
  10. Compromised immunity



The most successful treatments of Meibomianitis consists of

  1. Warm therapy first thing in the morning by applying a clean, hot towel, or facecloth for 10 minutes on the eyelids. This warming of the eyelids will help the oil in the glands to flow more easily.
  2. Massaging your eyelids will also help oil to flow more easily. The efficiency of this treatment is increased if applied after warm therapy.
  3. Lid Hygiene is essential for patients who have been diagnosed with meibomitis. Many cleaning solutions exist for the eyelid margins and eyelashes. The best way to clean your eyes is by using a specialized eyelid cleanser as recommended by your eyecare practitioner. Close your eyes, clean and massage the skin over the eye area every morning for 30 seconds.
  4. Oral antibiotics can be prescribed, to not to kill the bacteria but to increase the quality of the oil. Antibiotic treatment might last several months. Only your doctor can prescribe antibiotics.
  5. Recent research proved that omega 3 acids diet help meibomian oil to restore its quality and stabilize inflammation. Alternatively, for high efficiency and quick result, there is the option to buy omega-3 supplements.
  6. Topical Steroids can be used in severe cases to reduce the inflammation and protect the eye from damage.
  7. Vitamin C and A

It affects people of all ages. Although uncomfortable, blepharitis is not contagious and generally does not cause any permanent damage to eyesight. Blepharitis can’t usually be cured, but the symptoms can be controlled with good eyelid hygiene. Blepharitis is a long-term (chronic) condition.

Blepharitis can be classified according to anatomic location: anterior blepharitis affects the eyelid skin, base of the eyelashes and the eyelash follicles, and posterior blepharitis affects the meibomian glands and gland orifices. Blepharitis has traditionally been clinically subcategorized as staphylococcal, seborrheic, meibomian gland dysfunction (MGD), or a combination thereof. Staphylococcal and seborrheic blepharitis involve mainly the anterior eyelid and can each be referred to as anterior blepharitis.

There is considerable overlap of symptoms of all types of blepharitis. Blepharitis frequently leads to associated ocular surface inflammation, including conjunctivitis, functional tear deficiency, and keratitis. Blepharitis may also exacerbate symptoms of coexisting ocular surface disease, including allergy and aqueous tear deficiency. The chronic nature of blepharitis, the uncertain etiology, and the frequent coexistence of ocular surface disease make blepharitis difficult to manage. In cases where a bacterial infection is the cause, medications may be prescribed along with eyelid hygiene. Nutritional supplements such as Omega 3, and flaxseed oil are also recommended.

Signs and Symptoms


Symptoms can include:

  1. itchy, sore and red eyelids that stick together
  2. crusty or greasy eyelashes
  3. a burning, gritty sensation in your eyes
  4. increased sensitivity to light (photophobia)
  5. swollen eyelid margins
  6. finding contact lenses uncomfortable to wear
  7. abnormal eyelash growth or loss of eyelashes in severe cases
  8. In most cases both eyes are affected, but one eye can be more affected than the other. The symptoms tend to be worse in the morning.

Staphylococcal blepharitis is characterized by scaling, crusting, and erythema of the eyelid margin with collarette formation at the base of the cilia. Chronic inflammation may be punctuated by acute exacerbations that lead to the development of ulcerative blepharitis. Loss of eyelashes and corneal involvement, including punctate epithelial erosions, marginal infiltrates, and neovascularization, may occur

Causes and Risks

There are three main types of blepharitis:

  1. anterior blepharitis – where the inflammation affects the skin around the base of your eyelashes
  2. posterior blepharitis – where the inflammation affects your Meibomian glands, found along the eyelid margins behind the base of the eyelashes
  3. mixed blepharitis – a combination of both anterior and posterior blepharitis

Anterior blepharitis can be caused by either a reaction to Staphylococcus bacteria – these usually live harmlessly on the skin of many people, but for unknown reasons they can cause the eyelids to become inflamed, or seborrhoeic dermatitis – a skin condition that causes skin to become oily or flaky and sometimes irritate the eyelids, causing the Meibomian glands to block

Posterior blepharitis is caused by a problem with the Meibomian glands, where the glands get blocked by either debris, skin flakes or inflammation. Sometimes blockages in the Meibomian glands are associated with a skin condition called rosacea. If too much oily substance is being produced, this may be caused by seborrhoeic dermatitis.

Mixed blepharitis, which is the most common, is caused by a combination of both anterior and posterior blepharitis.

Blepharitis isn’t contagious.


Blepharitis is usually a long-term condition. Most people experience repeated episodes, separated by periods without symptoms. It can’t usually be cured, but a daily eyelid-cleaning routine can help control the symptoms and prevent permanent scarring of the eyelid margins.

There are three main steps to eyelid hygiene that should be performed once or twice a day:

  1. using a warm compress – to make the oil produced by the glands around your eyes more runny
  2. gently massaging your eyelids – to push the oils out of the glands
  3. cleaning your eyelids – to wipe away any excess oil and remove any crusts, bacteria, dust or grime that might have built up

More severe cases may require antibiotics that are either applied to the eye or eyelid directly, or taken as tablets.

For posterior blepharitis, long-term oral tetracycline, minocycline, or doxycycline is more effective than topical antibiotics, especially for patients with rosacea. As little as one pill twice a week can maintain a relatively good therapeutic dose in these patients for long periods.

“Giant papillary” refers to large bumps that form under your eyelid. GPC is an eye irritation, not an infection.

This is condition that often occurs with the over-wearing of contact lenses, and, or an allergic reaction to the lenses themselves, or a reaction to a particular brand of lens cleaner or storage solution. It can also result from an allergic reaction to some types of makeup or skin products. Other common causes are a reaction to the pillow that one sleeps on, or even the laundry washing soap or fabric softener you are using. It is essentially an allergic reaction of the delicate soft tissue on the insides of the eyelids. The clue that GPC is evident might not be obvious to the wearer, but a regular visit and examination by your eyecare professional will detect the early onset of GPC.

Many variables can affect the onset and severity of the presenting signs and symptoms. Nonionic, high-water-content soft contact lenses tend to produce less severe signs and symptoms than ionic, low-water-content soft contact lenses. Enzymatic treatment appears to lessen the severity of signs and symptoms. The association of an allergy appears to play a role in the onset of the severity of the signs and symptoms but does not appear to affect the final ability of the individual to wear contact lenses.

A subtle hint for the wearer that there might be early onset of GPC is that your contact lenses seem to move a lot in your eye, and “sticking” to your upper eyelid. To isolate the offending substance or circumstance can be tedious, but one can start by switching to daily disposable lenses where available. Careful monitoring of the progression by your eyecare professional is essential. In some cases, rigid gas permeable (hard lenses) are an option to slow down the progression. If, in extreme cases, the progression is not contained, one may have to refrain from wearing contact lenses for a long period of time, or altogether.

Signs and Symptoms

Signs and symptoms of GPC include

  1. Itching and redness of the eye(s), burning sensation.
  2. Eye pain and inflammation of the eyelid; with gritty feeling of sand-like particle inside the eye.
  3. Regular discharge of watery mucus from the eyes, blurred vision.
  4. Contact lens users may often find their lens uncomfortable, slipping out of position (as they blink), sticking to the inside of the eyelid, or requiring frequent cleaning.

Giant papillary conjunctivitis is a common complication of contact lens wear. It has also been called contact lens–induced papillary conjunctivitis (CLPC). Prior to the popularization of hydrogel (soft) contact lenses over the past 4 decades, such reactions were primarily seen as immunoglobulin E (IgE)–mediated ocular allergies. Giant papillary conjunctivitis symptoms and signs, such as papillary changes in the tarsal conjunctiva, have been associated with the use of all types of contact lenses (eg, rigid, hydrogel, silicone hydrogel, piggyback, scleral, prosthetic).

Similar reactions have been noted with ocular prostheses, extruding scleral buckles, exposed ocular sutures, and even elevated corneal scars. The initially small papillae eventually coalesce with expanding internal collections of inflammatory cells. When the lesions reach a diameter of more than 0.3 mm, often approaching or exceeding 1 mm, the condition is referred to as giant papillary conjunctivitis.

Causes and Risks

Giant Papillary Conjunctivitis is essentially an allergic inflammatory response caused by the constant friction between the conjunctiva and other physical device/implant/suture present in the eye against which it rubs, as the eyes blink regularly or close, for a prolonged period. This is described as a kind of mechanical micro-trauma

Some typical causes also include:

  1. A chronic use of contact lens (of any type) is the most frequent causal factor for GPC.
  2. Sometimes the material of the contact lens (or the chemical it is stored in), or certain deposits that form over the contact lens, cause the build-up of certain proteins in the eye. Such situations may also bring about some changes in the soft tissue of the eye, which triggers an allergic reaction.
  3. When the allergen comes into contact with the conjunctiva and mucus membranes lining the eyes, the body releases histamine (an organic chemical) triggering the allergy symptoms. This may be due to an extremely sensitive body immune system.
  4. The presence of other diseases or disorders (like asthma, eczema, hay fever) may initiate Giant Papillary Conjunctivitis.
  5. Lack of proper cleaning of contact lenses, using worn-out lenses, lens with rough edges, wearing lenses while sleeping, using unapproved (or stale) solutions to store lenses, are all factors that encourage the formation of papillae.

All contact lens wearers are potential GPC patients, but you are at greater risk of getting this condition if you:

  1. Wear reusable soft contact lens.
  2. Wear contact lens for prolonged periods.
  3. Sleep in contact lens (even if they are approved for night wear).
  4. Don’t clean your contact lens properly.
  5. Use old contact lens solutions.
  6. Have asthma.
  7. Have chronic allergies or hay fever.
  8. Have a family history of allergies.

It is important to note that having a risk factor does not mean that one will get the condition. A risk factor increases ones chances of getting a condition compared to an individual without the risk factors.

Because of the high prevalence of giant papillary conjunctivitis in contact lens wearers, every patient who wears contact lenses should be considered as a potential patient with giant papillary conjunctivitis. GPC is however, not contagious.


Management measures for Giant Papillary Conjunctivitis include controlling factors responsible for an allergic trigger, treating the symptoms, and moderating the body immune response system.

They are as follows:

  1. GPC is primarily managed by avoiding contact lens wear for several weeks, or as required (and using spectacles instead).
  2. Correction of other factors such as implants or exposed sutures, are considered; if they are the causative factors of GPC.
  3. Application of cold compress can help reduce discomfort.
  4. If necessary, medications such as oral antihistamines and mast cell stabilizers (a non-steroid drug), may be used depending on the type of symptoms.
  5. Other drugs to provide relief from symptoms are corticosteroids (prescribed in severe cases only),
  6. lubricating or anti-inflammatory eye-drops, and ointments.
  7. Immunotherapy (allergy shots) is used to desensitize the body and prevent it from overreacting to such external triggers. This method is usually considered, in case of a severe allergic attack that does not respond well to treatment, or when other medical disorders are also present.
  8. Proper choice and care of contact lenses (including ensuring proper hygiene), frequent changing of the lens set (using daily or weekly disposable lenses), are steps that can help prevent recurrence of the condition.

Anterior & corneal pathology





This condition is also known as Keratoconjunctivitis Sicca, but more commonly referred to as Dry Eye Disease (DED). The tear layer is made up of three layers; a lipid, aqueous and mucin layer; which becomes deficient in one or more of the layers. Systemic conditions, medications and environmental factors, like PCs and aircons often result in DED. The most common treatment of DED is the instillation of tear supplements combined with the implementation of a good lid cleaning regimen. The constant dry eye leads to micro erosions occurring on the corneal surface, and these micro breaks are an easy route into the cornea for various organisms leading to constant infections, and in some cases, severe conditions requiring urgent intervention.

Signs and Symptoms

Sometimes, dry eyes create too many tears. This confusing condition is called reflex tearing. It happens because the lack of moisture irritates your eye. It sends a distress signal through your nervous system for more lubrication. Your body sends a flood of tears to try to make up for the dryness. It’s a lot like what happens when you get sand in your eye and it runs. But these tears are mostly water, so they don’t act like normal tears. They can wash debris away, but they can’t coat your eye’s surface.

Dry eye symptoms may include any of the following:

  1. stinging or burning of the eye.
  2. a sandy or gritty feeling as if something is in the eye.
  3. episodes of excess tears following very dry eye periods.
  4. a stringy discharge from the eye.
  5. pain and redness of the eye.
  6. episodes of blurred vision.
  7. heavy eyelids.
  8. inability to cry when emotionally stressed.
  9. uncomfortable contact lenses.
  10. decreased tolerance of reading, working on the computer, or any activity that requires sustained visual attention.
  11. eye fatigue.

Causes and Risks

Typical common causes of chronic Dry Eye mostly include:

  1. Side effects of some medications, including antihistamines, nasal decongestants, tranquilizers, certain blood pressure medicines, Parkinson’s medications, birth control pills and anti-depressants.
  2. Skin disease on or around the eyelids.
  3. Meibomian gland dysfunction.
  4. In women during pregnancy.
  5. Women who are on hormone replacement therapy.
  6. Women taking only estrogen are 70 percent more likely to experience dry eye, whereas those taking estrogen and progesterone have a 30 percent increased risk of developing dry eye.
  7. After Lasik refractive surgery.
  8. Chemical and thermal burns.
  9. Chronic allergies.
  10. Infrequent blinking, associated with long hours working on computer or video screens.
  11. Both excessive and insufficient dosages of vitamins can contribute to dry eye.
  12. Homeopathic remedies may have an adverse impact on a dry eye condition.
  13. Loss of sensation in the cornea from long-term contact lens wear.
  14. Immune system disorders such as Sjögren’s syndrome, lupus, and rheumatoid arthritis.
  15. Chronic inflammation of the conjunctiva, or the lacrimal gland.
  16. If the surface area of the eye is increased, as in thyroid disease when the eye protrudes forward or after cosmetic surgery.
  17. Exposure keratitis (eyelids do not close completely during sleep).

Several risk factors for the development of Dry Eye Disease have been identified repeatedly in epidemiological studies, such as increasing age and female sex (particularly postmenopausal women). In clinical experience, menopausal and postmenopausal women both tend to have dry eye symptoms; this can be attributed to the significant decrease of tear production around the sixth decade of life in women. Hormonal studies suggest that sex hormones influence ocular surface conditions through their effects on tear secretions, meibomian gland function, and conjunctival goblet cell density. A study pointed out that women who were taking oral contraceptives had significantly higher goblet cell density than those who were not taking oral contraceptives. This was particularly true for women who used estrogen alone.


Artificial tear drops and ointments are the most common treatment. Many types of drops are available. No one product works for everyone, so you might have to try a few to figure out the one that’s right for you. If you have chronic dry eye, you need to use the drops even when your eyes feel fine, or they won’t stay wet enough. If your eyes dry out while you sleep, you can use a thick product, like an ointment, at night.

If artificial tears do not adequately address these inflammatory changes, your doctor may recommend steroid eye drops to better manage the underlying inflammation associated with dry eyes. Steroid eye drops are generally used short-term to quickly manage symptoms. They are typically used in conjunction with artificial tears.

Punctal plugs are also an option. Small, sterile devices are inserted into one or both of the small openings (puncta) that are located in the inner corner of the upper and lower eyelids. After these openings have been plugged, tears can no longer drain away from the eye through these ducts. In this way the tear film stays intact longer on the surface of the eye.

A very significant percentage of dry eye cases are caused by inadequate oil (meibum) being secreted from meibomian glands located along the margin of the eyelids. Gently massaging the eyelids can aid the release of the oily component of the tear layer. An alternative (and potentially more comfortable) way to help open clogged meibomian glands to treat dry eyes is to simply apply warm compresses to the closed eyelids to soften the hardened meibum.

Studies have found that supplements containing omega-3 fatty acids can decrease dry eye symptoms. Good sources of omega-3s include cold-water fish such as salmon, sardines, herring and cod. For a vegetarian source of omega-3s, flaxseed oil can help to relieve dry eye.

In extreme cases, surgical cautery is a procedure to permanently seal the ducts of the lacrimal drainage system

If you have mild dry eye symptoms be sure to:

  1. Blink more frequently.
  2. Take frequent breaks during computer use.
  3. Remove eye makeup thoroughly.
  4. Clean your eyelids.
  5. Wear quality sunglasses.

This condition is characterized by a progressive thinning of the cornea which is the clear layer over the Iris. The thinning causes the cornea to “bulge out”, which “distorts” the vision. As the light entering the eye is not passing through a smooth regular surface, but rather through a warped distorted cornea, the effect is like looking through a piece of distorted glass. A common misconception that providing stronger spectacle lenses will correct this condition, but due to the irregular corneal surface, and the resulting distortions, the only way to offer a better optical solution is by providing an artificial smoother front surface to the cornea. In the early stages, this can often be achieved with soft contact lenses, but as the condition progresses, satisfactory vision can only be achieved with hard contact lenses, or Scleral contact lenses. Collagen Cross-linking is a procedure that is offered to patients diagnosed with Keratoconus. This treatment strengthens the cornea, and can slow the progression of Keratoconus. Keratoconus develops very slowly, and in most cases, if this condition progresses, and the patient is no longer able to achieve good vision with contact lenses, surgical intervention by means of corneal buckling, or a transplant is the only option.

Signs and Symptoms

The classic symptom of keratoconus is the perception of multiple “ghost” images, known as monocular polyopia. This effect is most clearly seen with a high contrast field, such as a point of light on a dark background. Instead of seeing just one point, a person with keratoconus sees many images of the point, spread out in a chaotic pattern.

As the cornea becomes more irregular in shape, it causes progressive near-sightedness and irregular astigmatism to develop, creating additional problems with distorted and blurred vision. Glare and light sensitivity also may occur. The effect can worsen in low light conditions, as the dark-adapted pupil dilates to expose more of the irregular surface of the cornea. Often, keratoconic patients experience changes in their spectacle prescription every time they visit their eye care practitioner.

At early stages, the symptoms of keratoconus may be no different from those of any other refractive defect of the eye. As the disease progresses, vision deteriorates, sometimes rapidly. Visual acuity becomes impaired at all distances. Some individuals have vision in one eye that is markedly worse than that in the other. The disease is often bilateral, though asymmetrical. There is normally little or no sensation of pain. It may cause luminous objects to appear as cylindrical pipes with the same intensity at all points.

Other Symptoms include:

  1. Increased light sensitivity.
  2. Difficultly driving at night.
  3. A halo around lights and ghosting (especially at night).
  4. Eye strain.
  5. Eye irritation, excessive eye rubbing.

Causes and Risks

The exact cause of keratoconus is unknown. There are many theories based on research and its association with other conditions such as allergies and genetic causes however, no one theory explains it all and it may be caused by a combination of things.

One scientific view is that keratoconus is developmental (i.e., genetic) in origin because in some cases there does appear to be a familial association. Some studies show that keratoconus corneas lack important anchoring fibrils that structurally stabilize the anterior cornea. This increased flexibility allows that cornea to “bulge forward” into a cone-shaped appearance.

Many who have keratoconus report vigorous eye rubbing and also have allergies (which cause eye itching and irritation, leading to eye rubbing), however the link to allergic disease also remains unclear. A higher percent of keratoconic patients have atopic disease than the general population. Disorders such as hay fever, eczema, asthma, and food allergies are all considered atopic diseases.

Some studies indicate an abnormal processing of the superoxide radicals in the keratoconus cornea and an involvement of oxidative stress in the pathogenesis of this disease. Keratoconus corneas lack the ability to self-repair routine damage easily repaired by normal corneas. Like any tissues in the body, the cornea creates harmful byproducts of cell metabolism called free radicals. Normal corneas, like any other body tissue, have a defence system in place to neutralize these free radicals so they don’t damage the collagen, (the structural part of the cornea), weakening it and causing the cornea to thin and bulge. The keratoconus corneas do not possess the ability to eliminate the free radicals so they stay in the tissue and can cause structural damage.


In the mildest form of keratoconus, spectacles or soft contact lenses may help. But as the disease progresses and the cornea thins and becomes increasingly more irregular in shape, glasses and regular soft contact lens designs no longer provide adequate vision correction.

Treatments for progressive keratoconus include:

  1. Corneal cross-linking. This procedure, also called corneal collagen cross-linking or CXL, strengthens corneal tissue to halt bulging of the eye’s surface in keratoconus. (CXL).
  2. Custom soft contact lenses can be purpose made and fitted during the early stages of this condition.
  3. Gas permeable contact lenses are the preferred treatment when soft lenses can no longer control the progression of Keratoconus. Their rigid lens material enables GP lenses to vault over the cornea, replacing its irregular shape with a smooth, uniform refracting surface to improve vision.
  4. “Piggybacking” contact lenses are an option if there are complications with fitting rigid GP lenses, specifically from a comfort point of view.
  5. Hybrid contact lenses, are hard in the centre and encompassed by a soft skirt. Hybrid lens technology has improved, giving people an option that combines the comfort of a soft lens with the visual acuity of an RGP lens.
  6. Scleral and semi-scleral lenses are sometimes prescribed for cases of advanced or very irregular keratoconus. These lenses cover a greater proportion of the surface of the eye and hence can offer improved stability. Easier handling can find favor with people with reduced dexterity, such as the elderly..
  7. Intacs are tiny plastic inserts are placed just under the eye’s surface in the periphery of the cornea and help re-shape the cornea for clearer vision. These are sometimes used when keratoconus patients no longer can obtain functional vision with contact lenses or eyeglasses.
  8. Corneal transplant is the only option when the condition progresses to a point where contact lenses or other therapies no longer provide acceptable vision.

The lens in the eye must be clear in order to receive a sharply focussed image. If the lens is cloudy or opaque due to the gradual formation of a cataract, the image becomes progressively blurry and visual performance is affected. Patients with early cataracts often have difficulty in appreciating colours, changes in contrast, reading, driving, recognizing faces, and glare from bright lights. These symptoms may be improved with new spectacle lenses, better lighting, anti-reflective coatings and UV protective sunglasses. If your eye care professional finds a cataract, you may not need cataract surgery for several years. You might in fact never need cataract surgery. By having your vision tested regularly, you and your eye care professional can monitor the progression and discuss the options available to you, and help you make an informed decision regarding surgical removal of the cataract by an Ophthalmologist. A typical clue for you that the cataract might be progressing, is the feeling that your spectacles are always dirty, and you find yourself constantly cleaning your spectacles. Cataract removal is never an emergency. Delaying cataract surgery will not cause long-term damage to your eye.

Signs and Symptoms

A cataract starts out small and at first has little effect on your vision. You may notice that your vision is blurred a little, like looking through a cloudy piece of glass or viewing an impressionist painting. You may notice when you drive at night that the oncoming headlights cause more glare than before. Colours may not appear as bright as they once did.

The most common symptoms of a cataract are:

  1. Cloudy or blurry vision.
  2. Colours seem faded.
  3. Glare. Headlights, lamps, or sunlight may appear too bright. A halo may appear around lights.
  4. Poor night vision.
  5. Double vision or multiple images in one eye.
  6. Frequent prescription changes in your eyeglasses or contact lenses.
  7. Vision that’s cloudy, blurry, foggy, or filmy.
  8. Nearsightedness (in older people).
  9. Problems with glare during the day.
  10. Trouble with spectacles or contact lenses not working well.

These symptoms also can be a sign of other eye problems. If you have any of these symptoms, check with your eye care professional, to be sure that the cause of the symptoms is only that of early cataract formation.

By simply changing your spectacles at this time will improve your vision, however in the future it might become necessary to refer you to an ophthalmologist to have the cataracts surgically removed.

Causes and Risks

The lens inside the eye works much like a camera lens, focusing light onto the retina for clear vision. It also adjusts the eye’s focus, letting us see things clearly both up close and far away. The lens is mostly made of water and protein. The protein is arranged in a precise way that keeps the lens clear and lets light pass through it, but as we age, some of the protein may clump together and start to cloud a small area of the lens. This is a cataract, and over time, it may grow larger and cloud more of the lens, making it harder to see.

No one knows for sure why the eye’s lens changes as we age, forming cataracts. But researchers worldwide have identified factors that may cause cataracts or are associated with cataract development.

Besides advancing age, cataract risk factors include:

  1. Ultraviolet radiation from sunlight and other sources
  2. Diabetes
  3. Hypertension
  4. Obesity
  5. Smoking
  6. Prolonged use of corticosteroid medications
  7. Statin medicines used to reduce cholesterol
  8. Previous eye injury or inflammation
  9. Previous eye surgery
  10. Hormone replacement therapy
  11. Significant alcohol consumption
  12. High myopia
  13. Family history


When symptoms begin to appear, you may be able to improve your vision for a while using, new spectacles, stronger bifocals, extra magnification, appropriate lighting or other visual aids. Your eyecare practitioner is obliged to advise you if they notice that you have of early cataracts. This is often long before they start to affect you. It is common for your practitioner to detect and diagnose cataracts that only need surgical intervention 4 to 6 yrs later.

Many people consider poor vision an inevitable fact of aging, but early cataracts can affect you in your daily life. What to do about the cataracts depends largely on the particular patients’ needs. For example, if one spends a lot of time driving at night, particularly on unfamiliar roads, the need for surgical intervention will be a lot sooner than for a retired person who takes walks, reads the newspaper, and watches TV in the evenings.

One is always able to delay cataract surgery. It is never an emergency, and you are not damaging your eye by delaying the surgery. The cataracts will however continue to progress very slowly over a period of time. It is recommended to visit your eyecare practitioner annually so they are able to assess and measure the progression of the cataracts and advise you accordingly.

One need only think about surgery when your cataracts have progressed enough to seriously impair your vision and affect your daily life. It’s important to understand that it is the patient who must make the decision to undergo cataract surgery. It is your eyecare practitioner’s responsibility to educate patients and give them the knowledge they need to make an independent and well-informed decision regarding cataract treatment.

A cataract is a clouding that develops in the crystalline lens of the eye varying in degree from a slight to a complete opacity which limits, or obstructs the passage of light to the back of the eye. We have determined that stronger spectacle lenses will not improve your vision. A typical clue for you that the cataract is progressing, is the feeling that your spectacles are always dirty, and you find yourself constantly cleaning your spectacles.

A visit to an Ophthalmologist is recommended to determine if cataract surgery is indicated. If this is the case, and, you and the Surgeon choose the option to remove the cataracts then after the surgery, the eye prescription will need to settle, which usually takes 4 to 6 weeks after your last operation. During this time our office will lend you a pair of reading glasses so that you are at least able to get by during the settling process, where after we will schedule an appointment to do a complete eye examination and provide you with a new balanced prescription to take advantage of the new clear lenses that have been inserted into your eyes to give you the best far and near vision possible.

You need to be aware that off the shelf reading glasses are often not balanced and can leave you squinting, and with avoidable reading fatigue and eyestrain. Should you have any further queries please contact our offices.

Signs and Symptoms


A cataract starts out small and at first has little effect on your vision. You may notice that your vision is blurred a little, like looking through a cloudy piece of glass or viewing an impressionist painting. You will notice that when you drive at night, the oncoming headlights cause more glare than before. Colours do not appear as bright as they once did.

The most common symptoms of a cataract are:

  1. Cloudy or blurry vision.
  2. Colours seem faded.
  3. Glare. Headlights, lamps, or sunlight may appear too bright. A halo may appear around lights.
  4. Poor night vision.
  5. Double vision or multiple images in one eye.
  6. Frequent prescription changes in your eyeglasses or contact lenses.
  7. Vision that’s cloudy, blurry, foggy, or filmy.
  8. Nearsightedness (in older people).
  9. Problems with glare during the day.
  10. Trouble with spectacles or contact lenses not working well.

These symptoms also can be a sign of other eye problems. If you have any of these symptoms, check with your eye care professional, to be sure that the cause of the symptoms is only that of the cataract formation.

Causes and Risks

The lens inside the eye works much like a camera lens, focusing light onto the retina for clear vision. It also adjusts the eye’s focus, letting us see things clearly both up close and far away. The lens is mostly made of water and protein. The protein is arranged in a precise way that keeps the lens clear and lets light pass through it, but as we age, some of the protein may clump together and start to cloud a small area of the lens. This is a cataract, and over time, it will grow larger and cloud more of the lens, making it harder to see.

No one knows for sure why the eye’s lens changes as we age, forming cataracts. But researchers worldwide have identified factors that may cause cataracts or are associated with cataract development.

Besides advancing age, cataract risk factors include:

  1. Ultraviolet radiation from sunlight and other sources
  2. Diabetes
  3. Hypertension
  4. Obesity
  5. Smoking
  6. Prolonged use of corticosteroid medications
  7. Statin medicines used to reduce cholesterol
  8. Previous eye injury or inflammation
  9. Previous eye surgery
  10. Hormone replacement therapy
  11. Significant alcohol consumption
  12. High myopia
  13. Family history


If an individual has blurred vision that makes it difficult to read print or read signs while driving, or has disabling glare while driving at night. A typical complaint regarding the development of cataracts is having difficulty engaging in hobbies such as knitting, crocheting, or card games. If this is the case, it is now the time to consider cataract surgery. In short, if an individual has a cataract and resultant blurred vision that makes it difficult to do anything he or she wants and needs to do, it is time to consider cataract surgery.

If there are cataracts in both eyes that require surgery, the surgeries are usually performed several weeks apart. Cataract surgery on both eyes at the same time is not recommended because there is a possibility of complications affecting both eyes; the most worrisome is infection.

During surgery, the surgeon will remove your clouded lens and in most cases replace it with a clear, plastic intraocular lens (IOL). Cataract surgery is the most frequently performed surgery in the United States, with more than 3 million Americans undergoing cataract surgery each year. Nine out of 10 people who have cataract surgery regain very good vision, somewhere between 20/20 and 20/40.

It’s important to understand that it is the patient who must make the decision to undergo cataract surgery. It is the doctor’s responsibility to educate patients and give them the knowledge they need to make an independent and well-informed decision regarding cataract treatment. Simply buying a strong pair of reading glasses from a retail outlet is not going to alleviate the problem.







Macular degeneration (MD) is an eye disorder that occurs when the tissue in the macula deteriorates. The health of the macula determines our ability to read, recognize faces, drive, watch television, use a computer, and perform any other visual task that requires us to see fine detail. This loss of detail only occurs in the central area of our visual field, and for this reason, it does not cause total blindness.

There are 2 types of macular degeneration:

  1. Dry Macular degeneration which is very slowly progressing.
  2. Wet Macular degeneration which progresses over a very short period of time.

The dry form is more common than the wet form, with about 85 to 90 percent of AMD patients diagnosed with dry AMD which progresses very slowly over a period of many years. Severity ranges from a total loss of central vision, whilst for some, it may only cause slight distortions. The wet form which causes a sudden loss of vision over a short time usually leads to more serious vision loss.

Your eyecare practitioner can advise you and show you how to detect and monitor the progression of MD. If you have been diagnosed with Macular Degeneration, it is strongly advised that you have your eyes checked at least once a year to monitor for any changes so that your practitioner can intervene, advise, and refer if necessary.

Signs and Symptoms

Age-related macular degeneration usually produces a slow, painless loss of vision. In rare cases, however, vision loss can be sudden. Early signs of vision loss from AMD include shadowy areas in your central vision or unusually fuzzy or distorted vision. There are 2 types of Macular degeneration.

Dry macular degeneration (non-neovascular).

Dry AMD is an early stage of the disease and may result from the aging and thinning of macular tissues, depositing of pigment in the macula or a combination of the two processes. This condition is diagnosed when yellowish spots known as drusen begin to accumulate in and around the macula. It is believed these spots are deposits or debris from deteriorating tissue.Gradual central vision loss may occur with dry macular degeneration but usually is not nearly as severe as wet AMD symptoms.

Wet macular degeneration (neovascular).

In about 10 percent of cases, dry AMD progresses to the more advanced and damaging form of the eye disease. With wet macular degeneration, new blood vessels grow beneath the retina and leak blood and fluid. This leakage causes permanent damage to light-sensitive retinal cells, which die off and create blind spots in central vision. Choroidal neovascularization (CNV), the underlying process causing wet AMD and abnormal blood vessel growth, is the body’s misguided way of attempting to create a new network of blood vessels to supply more nutrients and oxygen to the eye’s retina. Instead, the process creates scarring, leading to sometimes severe central vision loss.

This Grid Pattern is used to map
the progression of Macular Degeneration

Typical Visual symptoms include:

  1. Distorted vision, in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at things like miniblinds in their home or telephone poles while driving. There may also be central shadows or missing areas of vision.
  2. Slow recovery of visual function after exposure to bright light (photostress test).
  3. Visual acuity drastically decreasing (two levels or more), e.g.: 20/20 to 20/80.
  4. Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss (often caused by leakage and bleeding of abnormal blood vessels).
  5. Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones.
  6. A loss in contrast sensitivity.

Macular degeneration by itself will not lead to total blindness. For that matter, only a very small number of people with visual impairment are totally blind. In almost all cases, some vision remains, mainly peripheral.

Causes and Risks

Though macular degeneration is associated with aging, research suggests there also is a genetic component to the disease. Duke University and other researchers have noted a strong association between development of AMD and presence of a variant of a gene known as complement factor H (CFH). This gene deficiency is associated with almost half of all potentially blinding cases of macular degeneration.

Research has shown that oxygen-deprived cells in the retina produce a type of protein called vascular endothelial growth factor (VEGF), which triggers the growth of new blood vessels in the retina.

Common risk factors for developing macular degeneration include:

    1. Aging. Significant vision loss accompanying more advanced forms of AMD increases from fewer than 1 percent among people in their 60s to more than 15 percent among people in their 90s, according to the Canadian Medical Association Journal (February 2004).
    2. Obesity and inactivity. Overweight patients with macular degeneration had more than double the risk of developing advanced forms of macular degeneration compared with people of normal body weight, according to one study reported in Archives of Ophthalmology (June 2003). In the same study, those who performed vigorous activity at least three times weekly reduced their risk of developing advanced AMD, compared with inactive patients.
    3. Heredity. As stated above, recent studies have found that specific variants of different genes are present in most people who have macular degeneration. Studies of fraternal and identical twins may also demonstrate that heredity is a factor in who develops AMD and how severe it becomes.
    4. High blood pressure (hypertension). Investigative Ophthalmology and Vision Science reported the results of a European study demonstrating that high blood pressure may be associated with development of macular degeneration (September 2003).
    5. Smoking. Smoking is a major AMD risk factor and was found in one British study to be directly associated with about 25 percent of AMD cases causing severe vision loss. The British Journal of Ophthalmology in early 2006 also reported study findings showing that people living with a smoker double their risk of developing AMD.
    6. Drug side effects. Some cases of macular degeneration can be induced from side effects of toxic drugs such as Aralen (chloroquine, an anti-malarial drug) or phenothiazine. Phenothiazine is a class of anti-psychotic drugs, including brand names of Thorazine (chlorpromazine, which also is used to treat nausea, vomiting and persistent hiccups), Mellaril (thioridazine), Prolixin (fluphenazine), Trilafon (perphenazine) and Stelazine (trifluoperazine).

The American Academy of Ophthalmology notes that findings regarding AMD and risk factors have been contradictory, depending on the study. The only risk factors consistently found in studies to be associated with the eye disease are aging and smoking.


There is as yet no outright cure for age-related macular degeneration, but some treatments may delay its progression or even improve vision. This treatment depends on whether the disease is in its early-stage, dry form or in the more advanced, wet form that can lead to serious vision loss. No FDA-approved treatments exist yet for dry macular degeneration, although nutritional intervention may help prevent its progression to the wet form.

Many organizations and independent researchers are conducting studies to determine if dietary modifications can reduce a person’s risk of macular degeneration and vision loss associated with the condition. And some of these studies are revealing positive associations between good nutrition and reduced risk of AMD.

Some studies have suggested a diet that includes plenty of salmon and other coldwater fish, which contain high amounts of omega-3 fatty acids, may help prevent AMD or reduce the risk of its progression. Other studies have shown that supplements containing lutein and zeaxanthin increase the density of pigments in the macula that are associated with protecting the eyes from AMD.

For wet AMD, treatments aimed at stopping abnormal blood vessel growth include FDA-approved drugs called Lucentis, Eylea, Macugen and Visudyne used with Photodynamic Therapy or PDT. Lucentis has been shown to improve vision in a significant number of people with macular degeneration.

Your eye doctor may ask you to check your vision regularly with the Amsler grid described above. Viewing the Amsler grid separately with each eye helps you monitor your vision loss. The Amsler grid is a very sensitive test and it may reveal central vision problems before your eye doctor sees AMD-related damage to the macula in a routine eye exam. For those who have vision loss from macular degeneration, many low vision devices are available to help with mobility and specific visual tasks.

Hypertensive Retinopathy (HR) is a result of damage to the back of the eye, due to increased blood pressure, more commonly referred to as hypertension. Systemic hypertension may be undiagnosed, and an eye exam can often yield the first signs of this systemic disease. Typical signs of HR include narrowing of the small arteries and arterioles and haemorrhages which eventually lead to a noticeable loss of vision.

The Keith-Wagener-Barker Hypertensive Retinopathy Classification is the clinically accepted method of grading the progression of this condition.

There are 4 stages.

  1. Mild retinal vascular changes (generalized arteriolar narrowing).
  2. Moderate to severe retinal vascular changes (arteriovenous crossing changes).
  3. Stage 1 and 2 findings, plus cotton-wool spots, retinal haemorrhages and exudates.
  4. Stage 3 findings, plus associated optic nerve head swelling and macular star formation.

HR is one of the leading causes of preventable blindness in the world and visits to your eye care practitioner is essential to detect and monitor changes associated with this condition.

Signs and Symptoms

The signs and symptoms of Hypertensive Retinopathy can be similar to the signs of diabetic retinopathy. The two conditions can be differentiated and properly diagnosed with a thorough workup of the individual. The main symptom of Hypertensive Retinopathy is altered vision.

When your eyecare practitioner examines the eye, the following signs may be noted:

  1. Tortuosity of the retinal blood vessels (twisted blood vessels).
  2. Focal narrowing of the retinal blood vessels (arteries and veins start to cross).
  3. Haemorrhaging (bleeding) in the retina.
  4. Cotton wool spots: Yellowish areas of the retina that have decreased oxygen from lack of blood flow.
  5. Exudates (lipids, or fats, that have leaked from the blood vessels): This usually occurs in a star configuration around the macula, which can indicate swelling of the macula and cause vision loss.
  6. Retinal edema (swelling of the retina in other areas), which can lead to retinal detachment and vision loss.
  7. Papilledema (swelling of the optic nerves); a condition that requires immediate hospitalization.
  8. Most people with hypertensive retinopathy do not have symptoms until late in the disease.

The most widely accepted classification is the Keith-Wagener-Baker system, which categorizes four stages of HTR

Stage 1.

    Mild generalized arteriole sclerosis with increased arteriole light reflex, secondary to thickening within the blood vessel wall. This presentation typically signifies a chronic hypertensive change. These changes can and do occur in the normal elderly population.

Stage 2.

    Moderate to severe retinal vascular changes are synonymous with decrease in lumen size and hyalinized arterial walls, which may lead to arteriovenous nicking, a pathognomonic feature of HTR (figure 1). At the arteriovenous crossing, the artery typically lies over the vein, sharing the same outer sheath. With increased arteriole sclerosis, the vein becomes susceptible to compression, which hinders normal blood flow.

Stage 3.

    In this stage, acute elevation in blood pressure causes a breakdown of the blood-retina barrier. Contributing signs include retinal edema, cotton-wool spots, exudates and hemorrhage. These microvascular changes are often difficult to distinguish from diabetic retinopathy. Unlike diabetic retinopathy, HTR usually exhibits a drier retina associated with more cotton-wool spots and less exudates and/or hemorrhages. Also, the predominant retinal hemorrhages associated with HTR are flame-shaped hemorrhages rather than dot-and-blot hemorrhages.

Stage 4.

    The most advanced stage of HTR is known as malignant hypertension. Malignant hypertension is accelerated high blood pressure that consists of a systolic pressure higher than 200mm Hg and a diastolic pressure higher than 140mm Hg. This serious increase in blood pressure is often associated with morbidity and/or mortality secondary to stroke, myocardial infarction, and renal and heart failure. Patients often present with complaints of decreased vision, headaches, diplopia, scotomas and/or photopsis. This stage is characterized by the signs of stage 3 HTR plus optic nerve head swelling and macular edema (macular star).

Most patients with hypertensive retinopathy have no symptoms, but patients who have acute malignant hypertension often complain of eye pain, headaches, or reduced visual acuity.

Chronic arteriosclerotic changes from hypertension will not cause any symptoms alone. However, the complications of arteriosclerotic hypertensive changes will cause patients to present with the typical symptoms of vascular occlusions or macro-aneurysms.

Causes and Risks

Hypertensive Retinopathy is caused by an increased blood pressure (BP) in the blood vessels within the retina. The higher the blood pressure and the longer it has been high, the more severe the damage is likely to be. You have a higher risk of damage and vision loss when you have diabetes, high cholesterol level, or you smoke. Rarely, blood pressure readings suddenly become very high. However, when they do, it can cause severe changes in the eye.

This increased or high BP damages the small retinal blood vessels in a variety of ways.

  1. Blood vessels change shape.
  2. They are more prone to leaking blood consisting of fats and fluids.
  3. Swelling of the macula and optic nerve
  4. Swelling in other areas of the retina can cause a retinal detachment
  5. Damage to the nerves in the eye due to poor blood flow
  6. Blockage of the blood supply in the arteries to the retina
  7. Blockage of the veins that carry blood away from the retina

The risk factors for developing Hypertensive Retinopathy include:

  1. Longstanding increased blood pressure (chronic hypertension).
  2. high salt diet.
  3. Obesity.
  4. tobacco use.
  5. Alcohol.
  6. Family history.
  7. Stress.
  8. Ethnic background.
  9. The duration of elevated blood pressure.
  10. The amount that the blood pressure is elevation above normal.
  11. Systemic blood pressure of 140/110 mmHg (minimum) for advanced stages
  12. Systemic blood pressure of 180/120 mmHg (minimum) for malignant stage (stage 4)
  13. Severe haemorrhaging and/or swelling of the optic nerve

It is important to note that having a risk factor does not mean that one will get the condition. A risk factor increases one’s chances of getting a condition compared to an individual without the risk factors. Some risk factors are more important than others. Also, not having a risk factor does not mean that an individual will not get the condition. It is always important to discuss the effect of risk factors with your healthcare provider.


Currently, treatment for patients with stage 1, 2 or 3 HTR includes close observation, management of high blood pressure and regular dilated fundus exams. Malignant HTN, however, is a clinical emergency that warrants immediate referral for proper anti-hypertensive treatment. The reported three-year survival rate in patients with malignant hypertension is 6%, vs. 70% for those with stage 1 HTR. Fortunately, fewer than 1% of HTR cases are associated with malignant hypertension, primarily because it does not typically occur in treated hypertensive patients.

If the condition is diagnosed during stage 1 or 2, the progress to stages 3 and 4 Hypertensive Retinopathy can easily be prevented by:

  1. Managing the systemic blood pressure with any wide-range of treatment options available for hypertension.
  2. Administering injections to the eye to control swelling and preserve vision (in the case of macular edema).
  3. Repair/reattachment of the retina via surgery; in case of retinal detachment.

Diabetes mellitus (DM) is a major medical problem throughout the world. Diabetes causes an array of long-term systemic complications that have considerable impact on the patient as well as society, as the disease typically affects individuals in their most productive years. An increasing prevalence of diabetes is occurring throughout the world. In addition, this increase appears to be greater in developing countries. The etiology of this increase involves changes in diet, with higher fat intake, sedentary lifestyle changes, and decreased physical activity.

Diabetes is one of the top causes of blindness in the world occurring in both type I & type II diabetes. The blood vessels on the retina become brittle, and fracture, causing small blood leakages that obscure the light from reaching the delicate light sensing cells. This blood is usually absorbed, but scar tissue forms, which is permanent, which also blocks the light from reaching the sensing cells. If you have diabetes, initially you may not notice any changes to your vision. However, in time, diabetic retinopathy can cause mild to severe vision loss in one or both eyes. As a diabetic, it is vital to control and maintain one’s sugar count at a level suggested by your doctor.

The exact mechanism by which diabetes causes retinopathy remains unclear, but several theories have been postulated to explain the typical course and history of the disease. In the initial stages of diabetic retinopathy, patients are generally asymptomatic, but in more advanced stages of the disease patients may experience symptoms that include floaters, distortion, and/or blurred vision. Microaneurysms are the earliest clinical sign of diabetic retinopathy.

Regular eye examinations by an eye-care professional are essential to map out, and best monitor the progression of diabetic retinopathy.

Signs and Symptoms

There are two main stages of diabetic eye disease.

NPDR (non-proliferative diabetic retinopathy) is the early stage of diabetic eye disease. Many people with diabetes have it. With NPDR, tiny blood vessels leak, making the retina swell. When the macula swells, it is called DME (diabetic macular edema). This is the most common reason why people with diabetes lose their vision.

PDR (ProliferativeDiabetic retinopathy) often has no early warning signs. PDR leads to macular edema, which can cause rapid vision loss, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day.

Diabetic Retinopathy can be divided into 4 stages:

  1. Mild nonproliferative retinopathy. Small areas of balloon-like swelling in the retina’s tiny blood vessels, called microaneurysms, occur at this earliest stage of the disease.
  2. Moderate nonproliferative retinopathy. Blood vessels that nourish the retina may swell and distort. They may also lose their ability to transport blood. Both conditions cause characteristic changes to the appearance of the retina and may contribute to DME.
  3. Severe nonproliferative retinopathy. Many more blood vessels are blocked, depriving blood supply to areas of the retina. These areas secrete growth factors that signal the retina to grow new blood vessels.
  4. PDR (proliferative diabetic Retinopathy) This is the 4th stage stage of diabetic eye disease. It happens when the retina starts growing new blood vessels. This is called neovascularization. These fragile new vessels often bleed into the vitreous. If they only bleed a little, you might see a few dark floaters. If they bleed a lot, it might block all vision.

PDR is very serious, and can steal both your central and peripheral (side) vision. The first time this bleeding occurs, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots floating in a person’s visual field, though the spots often go away after few hours. These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs the vision. In extreme cases, a person may only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep.

Causes and Risks

Chronically high blood sugar from diabetes is associated with damage to the tiny blood vessels in the retina, leading to diabetic retinopathy. In its most advanced stage, new abnormal blood vessels proliferate (increase in number) on the surface of the retina, which can lead to scarring and cell loss in the retina.

All people with diabetes mellitus are at risk – those with Type I diabetes and those with Type II diabetes. The longer a person has diabetes, the higher their risk of developing some ocular problem. Between 40 and 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy. After 20 years of diabetes, nearly all patients with Type I diabetes and >60% of patients with Type II diabetes have some degree of damage.

During pregnancy, diabetic retinopathy may also be a problem for women with diabetes. It is recommended that all pregnant women with diabetes have dilated eye examinations each trimester to evaluate their vision.

Risk factors for diabetic retinopathy include:

  1. People with type 1 or type 2 diabetes are at risk for developing diabetic retinopathy. The longer a person has diabetes, the more likely he or she is to develop diabetic retinopathy, particularly if the diabetes is poorly controlled.
  2. Hispanics and Africans are at greater risk for developing diabetic retinopathy.
  3. Individuals with other medical conditions, such as high blood pressure and high cholesterol, are at greater risk.
  4. Pregnant women face a higher risk for developing diabetes and diabetic retinopathy. If a woman develops gestational diabetes, she has a higher risk of developing diabetes as she ages.
  5. Protein in Urine is an indicator of higher risk of developing DR.
  6. Diabetics should, however, be aware that a rapid increase in blood glucose levels can lead to a worsening of retinopathy.


There is no cure for diabetic retinopathy. But laser treatment (photocoagulation) is usually very effective at preventing vision loss if it is done before the retina has been severely damaged. It involves directing a high-focused beam of light energy to create a coagulative response in the target tissue. Panretinal photocoagulation (PRP) is used in the treatment of PDR. It involves applying laser burns over the entire retina, sparing the central macular area.

Cryotherapy is administered when laser photocoagulation in PDR is precluded in the presence of an opaque media, such as in cases of cataracts or vitreous hemorrhage, cryotherapy may be applied instead.

Surgical removal of the vitreous gel (vitrectomy) may also help improve vision if the retina has not been severely damaged. The Diabetes Control and Complications Trial found that intensive glucose control in patients with type 1 diabetes (previously called insulin-dependent diabetes mellitus [IDDM]) decreased the incidence and progression of diabetic retinopathy.

According to The Diabetes Control and Complications Trial controlling diabetes and maintaining the HbA1c level in the 6-7% range can substantially reduce the progression of diabetic retinopathy. One of the most important aspects in the management of diabetic retinopathy is patient education. Inform patients that they play an integral role in their own eye care. Regular checkups by an eyecare practitioner is essential to monitor the progression of DR.

Primary Open Angle Glaucoma (POAG) is a disease whereby the optic nerve at the back of the eye is damaged due to an intolerance of the pressure inside the eye. Glaucoma can only be detected by an eye care professional. There are no noticeable symptoms for the patient during the early stages of the disease when it is critical to start treatment that will limit or avoid blindness. Typical treatment involves the daily instillation of eye drops.

The pressure in the eye slowly rises and the cornea adapts without swelling. If the cornea were to swell, which is usually a signal that something is wrong, symptoms would be present. But as this is not the case, this disease often goes undetected. It is painless, and the patient often does not realize that he or she is slowly losing vision until the later stages of the disease.

Glaucoma is really about the problems which occur as a result of increased IOP. The average IOP in a normal population is 14-16 millimeters of mercury (mmHg). In a normal population pressures up to 20 mmHg may be within normal range. A pressure of 22 is considered to be suspicious and possibly abnormal. However, not all patients with elevated IOP develop glaucoma-related eye damage. What causes one person to develop damage while another does not is a topic of active research.

This increased pressure destroys the optic nerve cells. Once a sufficient number of nerve cells are destroyed, blind spots begin to form in the field of vision. These blind spots usually develop first in the peripheral field of vision, the outer sides of the field of vision. In the later stages, the central vision is affected. Once visual loss occurs, it is irreversible.

6 monthly visits to an eyecare practitioner to check the pressures in your eyes is recommended, and an annual visual field analysis is the essential to do a comparative analysis of the progression of the disease. progression can be controlled and reduced to a minimum with intervention.

POAG is a chronic disease. It may be hereditary. There is no cure for it at present, but the disease can be slowed or arrested by treatment. Since there are no symptoms, many patients find it difficult to understand why lifelong treatment with expensive drugs is necessary, especially when these drugs are often bothersome to take and have a variety of side effects.

Signs and Symptoms

Most people who have open-angle glaucoma feel fine and do not notice a change in their vision at first because the initial loss of vision is of side or peripheral vision, and the visual acuity or sharpness of vision is maintained until late in the disease. There are typically no early warning signs or painful symptoms. It develops slowly and sometimes without noticeable sight loss for many years.

By the time a patient is aware of vision loss, the disease is usually quite advanced. Without proper treatment, glaucoma can lead to blindness. The good news is that with regular eye exams, early detection, and treatment, you can preserve your vision.

Significant attention should be given to the following in the patient’s clinical history:

  1. Past ocular history.
  2. Previous ocular surgery, including photocoagulation or refractive procedures.
  3. Ocular/head trauma.
  4. Past medical history.
  5. Current medications.
  6. Risk factors for glaucomatous optic neuropathy.

Because open-angle glaucoma has few warning signs or symptoms before damage has occurred, it is important to see a doctor for regular eye examinations. If glaucoma is detected during an eye exam, your eye doctor can prescribe a preventative treatment to help protect your vision.

You are at increased risk for glaucoma if your parents or siblings have the disease, if you are African American or Latino, and possibly if you are diabetic or have cardiovascular disease. The risk of glaucoma also increases with age.

Causes and Risks

It is important to have your eyes examined regularly. Your eyes should be tested:

  1. before age 40, every two to four years.
  2. from age 40 to age 54, every one to three years.
  3. from age 55 to 64, every one to two years.
  4. after age 65, every six to 12 months.

Everyone is at risk for glaucoma. However, certain groups are at higher risk:

  1. After cataracts, glaucoma is the leading cause of blindness among Africans.
  2. People Over 60 are more likely to get glaucoma.
  3. Family history increases risk of glaucoma four to nine times.
  4. Steroid Users have a 40% increase in the incidence POAG.
  5. Injury to the eye can cause secondary open-angle glaucoma. Sometimes years later.
  6. Blunt injuries that “bruise” the eye can lead to traumatic glaucoma.
  7. The most common cause is sports-related injuries such as baseball or boxing.
  8. High myopia (nearsightedness).
  9. Hypertension.
  10. Central corneal thickness less than 0.5 mm.


The only proven treatment for POAG is lowering IOP. There is now substantial evidence from randomized trials that lowering IOP reduces the risk of progression of POAG. IOP may be lowered by medical therapy (topical and systemic), laser therapy and surgical procedures. There is no strong evidence supporting which of medical, laser or surgical therapy should be given initially. For example, the CIGTS (Collaborative Initial Glaucoma Treatment Study) showed no significant difference in outcome between patients randomized to either medical therapy or trabeculectomy. Commonly, patients are started on medical therapy with possible adjunctive laser therapy, and only if these measures fail is surgery considered.

Topical therapy includes:

  1. Alpha-agonists (apraclonidine, brimonidine)
  2. Beta-blockers (timolol, betaxolol, carteolol, levobunolol,etc.)
  3. Carbonic anhydrase inhibitors (brinzolamide, dorzolamide)
  4. Miotics (pilocarpine,etc.)
  5. Prostaglandins (latanoprost, bimatoprost, travoprost, etc.)

The most efficacious class of drops is the prostaglandin analogues. They are also the most convenient drops with once nightly dosage. Side effects are mainly local and include hyperemia, lengthening of lashes, darkening of iris color and peri-ocular skin pigmentation. These are reversible on stopping the medication.

The best locally tolerated drops are the beta-blockers, with very few patients experiencing ocular discomfort or redness. However, non-selective beta blockers are contraindicated in patients with respiratory diseases and some cardiac conditions.

Typical first line therapies are prostaglandin analogues and beta-blockers. Prostaglandin analogues are more efficacious and have less systemic side effects. Beta-blockers may be preferred in younger patients’ due to less local side effects, or in unilateral glaucoma to avoid cosmetically undesirable asymmetrical side-effects (such as lash growth).

This is an acute condition. Fluid is continually produced inside the front part of the eye, and drains out of the normal eye. This fluid, called aqueous humor, is unrelated to the tears, which are only on the outside of the eye. High pressure inside the occurs when there is an imbalance in the production and drainage of fluid in the eye. If the channels within the eye that normally drain the fluid from inside the eye are blocked, the pressure within the eye will rise suddenly. In this case, more fluid is continually being produced but cannot be drained because of the blocked drainage channels. This results in too much fluid inside the front chamber of the eye, thus raising the intraocular pressure. This usually occurs when it is dark. Acute angle-closure glaucoma occurs suddenly.

Typical symptoms include:

  1. Eye pain.
  2. Headaches.
  3. Rainbow halos around lights.
  4. Dilated pupils.
  5. Vision loss.
  6. Red eyes.
  7. Excessive tearing.
  8. Nausea and vomiting.

Farsighted individuals are at a slightly higher risk of developing closed angle glaucoma because they typically have a flatter cornea which narrows the area where the fluid is drained.

These signs may last for hours or until the eye pressure is reduced. With each narrow-angle glaucoma attack, part of your peripheral vision may also be lost. Acute angle-closure glaucoma is a medical emergency. If the high eye pressure is not reduced within hours, it can cause permanent vision loss. Anyone who experiences these symptoms should contact their optometrist, or ophthalmologist immediately.

Your ophthalmologist might choose to do a procedure known as a Trabeculectomy, where they remove a small piece of the iris (usually at the top which is typically covered by the upper eyelid). This procedure can prevent the blockage from reoccurring.

Signs and Symptoms

If you have the acute form of the condition, you will likely experience a sudden onset. You won’t be able to ignore them.

Typical symptoms include:

  1. Eye pain.
  2. Severe headaches.
  3. Rainbow halos around lights.
  4. Dilated pupils.
  5. Very blurry or Hazy vision.
  6. Pupils of different sizes.
  7. Red eyes.
  8. Excessive tearing.
  9. Nausea and vomiting.

Causes and Risks

With angle-closure glaucoma, the iris is not as wide and open as it should be. The outer edge of the iris bunches up over the drainage canals, when the pupil enlarges too much or too quickly. This can happen when entering a dark room.

Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG (acute Angle Closure Glaucoma). These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens, and a shorter axial eye length. Recent studies have suggested that increased iris thickness and cross-sectional area are associated with increased risk. Of the many predisposing anatomical variations, a narrow angle has the most devastating consequences.

In the traditional model of AACG, the eye’s natural response of dilation to environmental or chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the iris is called pupillary block. Furthermore, pupillary block describes a state in which the forward-most surface of the lens is anterior to the plane of the iris insertion into the ciliary body. As a result, aqueous flow from the posterior chamber to the anterior chamber is obstructed or altogether blocked. When pupillary block occurs in conjunction with the iris, the increasing pressure in the posterior chamber causes the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris bombé further closes the already narrow angle and compromises aqueous drainage, thus increasing IOP.

Your risk for closed-angle glaucoma is greater if you:

  1. are older than 40 years of age, especially if you are between 60 and 70 years old.
  2. are farsighted.
  3. are female.
  4. have a brother, sister, or parent with the disease.
  5. are of Southeast Asian or Alaska Native origin.


Treatment of angle-closure glaucoma usually involves drugs, and or either laser or conventional surgery to remove a small portion of the bunched-up outer edge of the iris. Surgery helps unblock the drainage canals so that the extra fluid can drain. If you have angle-closure glaucoma in one eye, doctors may go ahead and treat the other eye as a safety measure.

Typical drugs that are used to treat AACG are:

  1. Acetazolamide, which reduces the fluid in your eye.
  2. Beta blockers, which lower the amount of fluid your eye produces.
  3. Steroids, which reduce inflammation.
  4. Painkillers (as a comfort measure).
  5. Drugs to treat nausea and vomiting.
  6. Pilocarpine, which opens the angle between your iris and cornea.
Once the pressure in your eye has decreased, you will need further treatment to prevent the pressure from rising again.

There are two surgeries used to address closed-angle glaucoma:

  1. Peripheral Iridotomy. This is a laser treatment that creates two tiny drainage holes in your iris. It is used to treat both acute and chronic closed-angle glaucoma.
  2. Surgical Iridectomy. In this less-common treatment, a surgeon makes a small triangular opening in your iris.

In general, surgery for angle-closure glaucoma is successful and long lasting. Regular checkups are still important though, because a chronic form of glaucoma could still occur.

These are usually small particles or protein strands in the jelly inside your eye. They are harmless, and are usually only an irritation. As they move around inside your eye, the strands cast shadows on the retina on the back of your eye, and these are then perceived as small particles or strands, or wispy threads. They always move, and appear to “jump” out of the way when you try to look at them. They are more obvious if you are looking at a light surface, like the blue sky, or a white piece of paper. As we get older (50 to 70 yrs), the jelly substance inside our eyes becomes more fluid like, and floater activity gradually increases.

Eye floaters can be clumpy or stringy; light or dark. They are caused by clumps or specks of undissolved vitreous gel material floating in the dissolved gel-like fluid (vitreous) inside the eye.


They might annoy you, but they shouldn’t interfere with your sight. You can learn to live with floaters and ignore them. You may notice them less as time passes. Only rarely do they get bad enough to require treatment.

Signs and Symptoms

Floaters earn their name by moving around in your eye. They tend to dart away when you try to focus on them.

They come in many different shapes:

  1. Black or gray dots
  2. Squiggly lines
  3. Threadlike strands, which can be knobby and almost see-through
  4. Cobwebs
  5. Rings

The shrinking vitreous can tug on the retina and pull away from it. This event, called a posterior vitreous detachment, or PVD is common, and usually doesn’t threaten vision. In about one in six people, a posterior vitreous detachment causes the retina to tear.

Fluid from inside the eye can then seep through the tear and separate the retina from the tissues that nourish it. This separation called retinal detachment, is an ocular emergency, and can lead to permanent vision loss.

Light flashes known as photopsias can occur when your retina receives non-visual (mechanical) stimulation, which can happen when it is being tugged, torn or detached. These light flashes may appear as lightning bolts, flickering lights or random sparks.

Key warning signs include:

  1. A sudden new onset of floaters and flashes of light, usually only in one eye.
  2. A shower of floaters and spots, especially if they are accompanied by flashes of light.
  3. Gradual shading of vision from one side (like a curtain being drawn).
  4. Rapid decline in sharp, central vision.

The sudden appearance of these symptoms could mean that the vitreous is pulling away from your retina, or it could mean that the retina itself is becoming dislodged from the back of the eye’s inner lining, which contains blood, nutrients and oxygen vital to healthy function.

Noticing a few floaters from time to time is not a cause for concern. However, if you see any of the above signs, you should seek medical attention immediately from an eye care professional.

Sadly, retinal tears and detachments are completely painless, and people tend to ignore them till it is too late to recover much functional vision. Do not ignore these symptoms. Seek attention immediately.

Causes and Risks

Floaters occur when the vitreous, a gel-like substance that fills about 80 percent of the eye and helps it maintain a round shape, slowly shrinks.

As the vitreous shrinks, it becomes somewhat stringy, and the strands can cast tiny shadows on the retina. These are floaters.

In most cases, floaters are part of the natural aging process and simply an annoyance. They can be distracting at first, but eventually tend to “settle” at the bottom of the eye, becoming less bothersome. They usually settle below the line of sight and do not go away completely.


For people who have floaters that are simply annoying, no treatment is recommended.

On rare occasions, floaters can be so dense and numerous that they significantly affect vision. In these cases, a vitrectomy which is a surgical procedure that removes floaters from the vitreous, may be needed. This procedure removes the vitreous gel, along with its floating debris, from the eye. The vitreous is replaced with a salt solution. Because the vitreous is mostly water, you will not notice any change between the salt solution and the original vitreous.

This procedure does however carry significant risks to sight because of possible complications.

Complications can include:

  1. Retinal detachment.
  2. Bleeding.
  3. Retinal tears.
  4. Cataracts.

Most eye surgeons are reluctant to recommend this surgery unless the floaters seriously interfere with vision.

If a tear is detected early, treatment can prevent the retina from detaching. Tears can be treated several ways. Pinpoints of laser light can be used to fuse the retina to the back wall of the eye. Extreme cold, a procedure called cryopexy, does much the same thing.

Cold and laser light can also be paired with the injection of a gas bubble into the eye (pneumatic retinopexy) to repair a detached retina. Two operations, scleral buckling and vitrectomy, can also be used to reattach the retina.

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