Blepharitis is inflammation of the eyelids, which typically occurs at the lid edge or “margin” at the root of the eyelashes. Specifically, blepharitis affects meibomian glands, which secrete an oily substance which prevents evaporation of the tear film.
Blepharitis causes irritation and burning which can continue on for months and years if left untreated. It can also lead to crusting of the margins of the eyelids and can cause small cysts to be formed on the eye itself.
While blepharitis is reasonably common and a nuisance to sufferers, it can occasionally affect vision.
Blepharitis is not caused by infection but is an immune reaction to the toxins produced by bacteria living on the surface of the eye.
Blepharitis can also be associated with Rosacea, which is a common condition in which the glands on the face, cheeks and the nose are inflamed – as well as on the eyelids.
Patients with Blepharitis are often been treated for dry eye with no effect. Theses lack of results are due to the fact that the primary problem – gland inflammation – remains untreated.
Most people find relief by using artificial tears ointment and lid hygiene.
Often the control of dry eye requires the control of blepharitis (inflammation of the glands of the eyelid.) This is achieved though daily lid hygiene, steroid drops, ointments and Doxycycline ointments. There are other forms of treatment in severe cases which you can discuss with your Doctor.
There is no cure for Blepharitis however it can be managed successfully with treatment which consists of keeping the eyelid margins clean.
To assist you in removing the crustations from the lid margin we recommend that you soak a clean washcloth in warm water and then place the cloth on the lid surface with your eyelids closed for 5-10 minutes. When symptoms are severe preform this 2-4 times a day.
Steroid creams can also be prescribed by a Doctor but these are only for short term use as they can create cataracts or glaucoma.
An antibiotic called “doxycycline” also slowly reduces the inflammation in the eyelid glands but always read the product sheet carefully before using any medication.
To assist in the reduction of inflammation it may be of benefit to increase the intake of Omega 3 fatty acids like flaxseed oil supplements or garlic.
A cataract occurs when the natural, crystalline lens inside the eye becomes cloudy, affecting vision. Cataract usually occurs from the age of 60 upwards, although it can occur in younger adults and rarely even in children and babies.
Most cataracts are a result of the natural ageing of the eye. From age 40 onwards, metabolic changes start occurring in the crystalline lens that cause it to take on water and become less flexible. The first signs of this are difficulty focusing on near objects – called presbyopia. Presbyopia occurs in everyone after a certain age and is corrected with glasses.
Eventually, these lens changes progress to the point where cloudy opacities develop in the lens which at first can cause difficulty with glare and driving at night, but eventually cause blurring and alteration of colour perception. This can only be improved through surgery.
Laser Cataract Surgery: Laser Cataract Surgery was available at Newcastle Eye Hospital, but this procedure was discontinued due to lack of evidence of benefits for our patients. Read about our internationally recognised research into Laser Cataract Surgery here.
During cataract surgery, a fine ultrasound probe (less than 2mm in diameter) is inserted through a tiny opening in the cornea, and the cloudy lens is literally sucked out, leaving its’ supporting bag (or lens capsule) behind. A prosthetic lens is then inserted into the lens capsule to restore vision.
Cataract surgery takes 5-10 minutes using local anaesthetic. You can ask for light sedation if required.
Most people are thrilled with the results from cataract surgery. For most patients, vision improvement is experienced immediately or within the first day. Other patient’s vision will clear within the month, occasionally this may take longer. You will still need glasses to achieve best quality vision including reading.
Sometimes diseases of the macula hinder results. These conditions evade detection prior to your surgery due to the cataract obstructing the doctor’s ability to view your retina. Your doctor will perform OCT scans to gauge whether the macula will affect your vision after surgery.
After surgery you will have a shield over your eye. Your eye will feel irritated, you may have double vision or a slight discharge (this is treatable with lubrication drops). Your eye shouldn’t ach or throb.
Instructions will be given to you on how to care for your eye and you will be supplied with a month’s duration of drops. The doctor will see you one day after your operation and again over the next month.
Laser surgery may be required over the following months and years after as the membrane behind the lens can become cloudy (read about Posterior Capsule Opacity)
Complications post-surgery are rare. 2% of people require more intensive post operative care and less than 1% need further surgery to fix surgery complications.
For the vast majority of patients, the benefits of cataract surgery can be experienced almost immediately and improve both independence and quality of life.
Laser Cataract Surgery: Laser Cataract Surgery was available at Newcastle Eye Hospital, but this procedure was discontinued due to lack of evidence of benefits for our patients. Read about our internationally recognised research into Laser Cataract Surgery here.
Diabetes can effect your eyes, so regular eye checks are essential. Early treatment means effective results. Late treatment of diabetic eye disease means reduced vision.
Without a healthy retina the eye is not much use. Diabetes is a threat to the retina, as the small blood vessels supplying blood to the retina can become leaky. This condition is called retinopathy.
When tiny blood vessels in the retina leak fluid, fat or blood that seeps from the vessels can blur vision. Fluid sitting in the retina for prolonged periods of time causes damage to the retina and the macula. These small blood vessels can become blocked therefore the retina doesn’t get enough blood flow to function well. The body then produces more blood vessels to attempt to restore blood supply to the retina. This is known as diabetic retinopathy.
These new blood vessels are leaky and fragile causing major bleeds within the eye and resulting in loss of vision. These blood vessels also creates scar tissue in the eye which eventually contracts causing the retina to detach from the back of the eye. This is called a retinal detachment and will require surgery.
Developing diabetic retinopathy is dependent on how long you have had diabetes and how well you managed your diabetes over that time.
50 % of young insulin dependent (Type I) diabetics after 10 years develop diabetic retinopathy. This increases to 90% after 30 years and about 30 % will go on to develop proliferative retinopathy after 15 years.
For maturity onset (Type II) diabetes 80% of sufferers will go on to develop retinopathy after 15 years. As many as fifteen percent develop proliferative diabetic retinopathy. The most important thing that you can do for your eyes is to control your diabetes well.
Regular eye checks – early treatment equals best results.
During these regular eye checks your doctor may require you to have a fluorescein angiogram. A dye is injected into a vein in your arm which allows photographs to be taken of the blood vessels in the retina. This assists the Doctor in accurate diagnosis and treatment.
“Water logging” of the macula (macular oedema) is treated in the clinic with gentle laser therapy to the retina. If swelling is excessive Avastin can be injected into the eye to help dry the macular followed by laser treatment. These treatments may need to be repeated and are not meant to improve vision but to prevent future complications.
With proper and prompt treatment of retinopathy there is a high chance the effects of retinopathy can be prevented or minimised.
Dry eye is a condition that occurs when your eyes either produce too few tears or they lack the ingredients that lubricate and protect the surface of the eye.
Dry eye patients have abnormal tear composition. This occurs because the glands that make up the tears are inflamed, and fail to maintain the oily layer that prevents tears evaporating.
Occasionally patients do not produce enough tears so the eye over compensates by producing an excess of tears. Dry eye also often co-exists along with blepharitis.
Tears are Important: They are the eye’s first natural defence mechanism. They coat, protect and nourish the eye. Tears are the first lens of the eye and any abnormalities with tears produces blurry vision.
Dry eye is caused by an autoimmune inflammation of the lacrimal glands. By the age of 40 you have half of the tear production that you had as a ten year old child. Women after menopause are often affected with dry eye.
Currently there is no cure for dry eyes. It is a chronic condition and it must be treated constantly.
Treatments for Dry Eye include:
As we increase in age the jelly (vitreous) at the back of the eye shrinks and begins to separate into strands and water. These strands are called floaters. They appear as fine dark shapes, lines or as cobwebs that move around your vision.
During this process, in some cases, the back surface of the jelly within your eye can pull away from the retina. This is a posterior vitreous detachment (PVD). This can cause the retina to tear and peel off the back of the eye wall – this is a retinal detachment.
Sometimes the jelly leaves behind some cells on the retina, and these cells can grow a sheet called an epiretinal membrane. This can greatly reduce/distort vision.
In order to remove the epiretinal membrane a doctor will perform a vitrectomy to remove and replace the jelly. A local anaesthetic is used and you will need to lie flat for an hour to allow the Doctor access to the macula (the central part of the retina).
The macula is the part of the retina that gives the finest central vision. The macula is extremely delicate. During surgery the macula will be stressed and blood vessels will be damaged so not all patients with epiretinal membrane will be offered the surgery. If symptoms are mild it is reasonable to monitor the eye, however with moderate to severe symptoms this procedure is successful in removing the membrane and reducing or removing the distortion.
The inside of the eye is filled with a gel substance which helps maintain its shape, known as the vitreous humour. The vitreous attaches onto the surface of the retina through millions of fine fibres.
As we age, the vitreous loses water and begins to shrink, slowly pulling away from the retina. Sometimes the fibres break, allowing the vitreous to detach and shrink from the retina. The pulling away of the vitreous from the retina is called “Posterior Vitreous Detachment”. As this occurs, the tugging on the retina can generate random nerve signals which the brain interprets as flashes of light. These flashes of light can be quite distracting although quite harmless.
Once flashes subside, small floaters can often be left behind which will be noticed in certain light conditions
In most cases, vitreous detachment is not sight threatening and requires no treatment. However, if the detachment leads to retinal tears or to a retinal detachment, intervention is required as these can lead to a permanent loss of vision.
Most commonly, you will experience a sudden increase of small floaters. Floaters appear as dark cobwebs or stringy specks that float about in your vision. There may also be flashes of light in you peripheral or side vision.
Aging – people over the age of 50 and especially those over the age of 80 are more at risk.
Myopia – people who are short- sighted have an increased risk of vitreous detachment.
Surgery for floaters consists of a vitrectomy (removal of vitreous gel). This surgery is almost always preformed using anaesthetic eye drops, sedation and local anaesthetic.
A microscope with a small light will be used throughout the procedure while a surgical instrument/probe is placed within the eye to remove the vitreous containing the floaters, then replacing it with gas. The gas interferes with vision for a few weeks after which the full benefit of surgery can be experienced.
While this surgery is straightforward, a common complication is acceleration of cataract formation which will often require surgery within 6-12 months following vitrectomy.
Fluorescein angiography is a photographic test of the retina, the film at the back of the eye. The water soluble dye is injected into a vein in your arm, travelling to the eye.
An advanced camera called a Heidelberg HRA system uses low power laser light to take photographs of the retina while dye passes through the blood vessels. This provides vital information about your retina and nearby tissue.
This form of imaging is used to diagnose certain eye conditions and determine treatment. It also assists with monitoring conditions such as diabetic retinopathy, and to diagnose wet macular degeneration and other retinal vascular diseases.
After a fluorescein angiogram your skin will turn a yellow colour for several hours. The dye will filter out through your urine as a dark yellow/orange for 24 hours. Your vision may be temporarily blurred, therefore driving following this procedure is discouraged.
Fluorescein angiography has been performed extensively. The chances of adverse effects are low due to the use of highly advanced equipment meaning lower doses of fluorescein dye. The Heidelberg HRA camera used at Hunter Eye Surgeons requires even lower doses than standard fluorescein angiography, and so risks are also lower.
Glaucoma is diagnosed when there is damage to the optic nerve at the back of the eye. The retina thins as Glaucoma progresses. This gives the optic nerve a characteristic appearance in severe cases.
Intra-ocular pressure (or IOP) is the pressure within the eye. When the IOP rises above 21 this is above the normal range. Raised pressure is one risk factor of glaucoma. High IOP means patients are more likely to develop glaucoma damage to the optic nerve.
Risk factors for glaucoma include family history, age, elevated blood pressure, steroid use, migraines, cold hands, diabetes or an eye injury. Patients with glaucoma have no symptoms as unfortunately glaucoma attacks side vision initially. The brain compensates well for this, meaning that symptoms often go un-noticed for quite some time. Successful prevention and treatment of glaucoma is dependent on effective monitoring.
The most accurate way to monitor glaucoma is by measuring the optic nerve using Optical Coherence Tomography, or OCT. As glaucoma progresses the nerve fibre layers in the optic nerve thin. This leads to a large central cup forming in the centre of the nerve.
An OCT scan monitors the thickness of the nerve fibre layer. The results that are collected over time allow accurate comparisons. An OCT also allows any changes to the Optic Nerve to be detected early.
Our technicians also measure peripheral vision (side vision) using a visual field test. This also allows us to monitor the progression of the disease.
When IOP is elevated, this is called ocular hypertension. Elevated IOP does not always result in glaucoma, however in these cases close monitoring is required. When there is damage to the Optic Nerve we diagnose glaucoma and then commence the necessary treatment. This treatment will continue for a lifetime.
Not all cases of glaucoma are related to high IOP. Some patients have normal IOP when tested but may experience spikes during the night or have other factors causing glaucoma. The only way to treat glaucoma IOP is with drops, laser or surgery. Most patients are treated successfully with drops.
Each person has a “safe level” of IOP which is determined by regular monitoring of IOP, optic nerve scans and visual fields. We compare tests to gauge the progression of the disease and then treat accordingly. IOP varies throughout the day so the results only give us a snap shot into what is happening during the day. Examinations such as visual fields are repeated every 6-12 months and disc analysis is repeated every 1-2 years. Once treatment has commenced or changed you will need to have frequent reviews to determine whether the IOP is responding to treatment.
The retina is the layer at the back of the eye which captures light like the film of a camera. The macula is the central part of the retina as is the fovea the central part of the macula. These are responsible for fine-detailed vision, such as reading, recognising faces and driving.
Macular Degeneration is damage of the macula causing central vision loss which, if left untreated, can result in legal blindness.
AMD (or Age-Related Macular Degeneration) is primarily an age related disease.
In the early stages of macular degeneration, the waste removal function of the retinal pigment layer breaks down, leading to accumulation of waste deposits called “drusen”. As more and more drusen appear over time, this leads to a diagnosis of macular degeneration.
There are two types of AMD.
“Dry” macular degeneration develops slowly over a period of time as drusen increase in size and clump together. Patches of the retina die off, therefore effecting central vision.
There is no cure for dry AMD, so preventative measures are encouraged (more about AMD prevention).
In wet macular degeneration, the accumulation of drusen causes the choroid (the blood vessel layer beneath the retina) to grow new blood vessels, in an effort to supply oxygen to the macula above. These vessels are frail and weak which causes them to leak, leading to deterioration of vision. The macula and the photoreceptors are affected which, in turn, diminishes central vision.
Wet AMD is treatable however at this stage dry AMD is not.
Vision loss due to wet macular degeneration can be halted and in some cases partly reversed, with monthly injections of drugs called anti-VEGFs.
Treatment can only commence once diagnosis has been confirmed with the aid of a fluorescein angiogram and had an OCT scan of the macula indicating the location of the AMD.
The price of these drugs is very high, however the cost is subsidised by the Government, with a small co-payment required to be paid at the time of treatment.
What to include in your diet:
Things to exclude:
Things to do:
The eye is divided into two sections by the iris and the lens. The back section of the eye is filled with a jelly substance called the vitreous. The vitreous presses up against the back wall of the eye (retina).
As we age the jelly (vitreous) shrinks and separates into strands and water. These strands are called floaters. They appear as fine dark shapes, lines or cobwebs, and move around your vision.
As a result of this shrinking process, the back surface of the vitreous can pull away from the retina. This is called a posterior vitreous detachment or a PVD. In rare cases, the retina can be torn from the back wall of the eye when a PVD occurs- this is a retinal detachment.
Occasionally the shrinking vitreous jelly can pull a hole in the macula which is part of the retina. This greatly reduces vision as the macula is responsible for the finest vision possible, central vision.
If this occurs, swift treatment is required in order to save vision.
To close the hole in the macula our surgeons perform a vitrectomy – which is an operation to remove the vitreous from the eye. This is operation is performed using local anaesthetic. You will need to lie flat for an hour making the macula more accessible.
During the procedure a membrane is peeled off the macula using extremely fine forceps. This can place stress on the macula and can cause some damage. If you have cataracts they may need to be removed to obtain a clear view of the macula. The surgeon will replace the cataract with a new lens at the conclusion of surgery.
After surgery you may be asked to posture face down to cause the gas that has been placed within your eye to push up against the back wall of the eye closing the macular hole. In most cases however maintaining an eye position “below the horizon” is all that is required.
This surgery is successful in 85-90 % of patients. If the surgery is unsuccessful it can be repeated with a 70 % success rate. Most patients are pleased with the results however vision rarely improves to normal levels, in some instances vision may worsen.
During cataract surgery a new lens is placed within the capsular bag behind the iris. The rear wall of this bag is a thin membrane called the posterior capsule.
With time the posterior capsule can become cloudy causing blurry vision, glare and haze. This opacity is called a Posterior Capsule Opacification (PCO).
PCO is treatable and can be cleared using a YAG laser. This procedure takes just a few minutes, is painless, does not require a hospital admission or anaesthetic and the membrane almost never grows back again.
A pterygium is associated with excessive exposure to ultra-violet light (sunlight), and therefore is very common in Australia amongst the surfing population.
The symptoms one can experience range from persistent redness, inflammation, dry and itchy eyes to a foreign body sensation within the eye. They can also be cosmetically toublesome to the sufferer.
The first line of defence against pterygium growth is to protect the eyes from ultraviolet light. This should stabilise the pterygium’s growth across the cornea. In many cases this is the only form of intervention that is required. However, due to the irritation that pterygiums can create, eye drops and eye ointments would also be recommended.
Pterygiums are benign growths that require surgery if they are threatening to distort vision by growing extensively across the cornea and the pupil. The surgery to remove pterygiums is performed under a local anaesthetic and it is recommended thatthe surgery is carried out before it interferes with vision.
Your local Optometrist can monitor the growth of your ptygrium and refer you to Hunter Eye Surgeons for an assessment and possible surgical removal if it is deemed necessary.
In 2008, Newcastle Eye Hospital adopted a new technique for pterygium surgery. Instead of sutures, we use Tisseel glue. We also developed instrumentation here in Newcastle, which shortened the surgery and reduced the discomfort for patients.
A Pterygium is a wing like triangular membrane that grows over and erodes the cornea of the eye. It usually begins from the nasal side of the eye.
The cornea is the clear window at the front of the eye. It is the first lens of the eye, and needs a perfect round shape for clear vision. As a pterygium grows, it erodes the surface of the cornea like an open-cut mine.
The eye is divided into two parts. The back section of the eye is filled with jelly called the vitreous. This presses against the retina, the wall of the eye. The central part of the retina is called the Macula. It is responsible for central vision.
During ageing, the vitreous pulls away from the retina – called a posterior vitreous detachment (PVD). In 3% of people PVDs cause a hole in the retina with bleeding or floaters needing immediate treatment. The retina can also peel off the back of the eye. This is called a retinal detachment, and causes the retina to shrivel within the eye.
If the macula stays attached, vision often stays near normal. If the macula detaches (a macula-off detachment) it requires urgent surgery to save sight. Vision reduces quickly in these cases and the time to surgery is critical to a good result.
Retinal detachments are repaired with an operation called a vitrectomy. The vitreous is removed, the retina is flattened, the hole is sealed. The vitreous is replaced with gas pushing the back of the eye upwards. There are alternatives to gas with varying results. Some detachments require heavy liquid or a silicone band to be attached to the outside of the eye.
Retinal detachment surgery is performed at Newcastle Eye Hospital with local anaesthetic and sedation.
The retina is lies against the wall of the eye and captures images sending them to the brain. The macula is central within the retina and is responsible for central vision.
The optic nerve has one vein supplying the retina with blood and oxygen. The branches of this vein cross over multiple times. They can become blocked at these crossover points causing the blood supply to slow or stop causing the macula to swell and vision to reduce.
RVO has no cure. Treatment can be provided to improve blood flow, reduce retinal/macular swelling and the growth of new blood vessels. Some patient’s vision improves due to the decrease of macular swelling. Commonly macular scarring occurs so we prefer to treat RVO from diagnosis.
The first priority of treatment is to prevent total loss of the eye. Damage is assessed using a fluorescein dye test and OCT imaging. The entire retina can be lasered to prevent new blood vessels growing.
Treatments are balanced against the degree of blockage and the severity of vision loss.
The body compensates for the lack of blood supply by growing more blood vessels haphazardly presenting the eye with new problems, retinal detachment, bleeding, glaucoma and total blindness.
Diabetes can effect your eyes, so regular eye checks are essential. Early treatment means effective results. Late treatment of diabetic eye disease means reduced vision.
Without a healthy retina the eye is not much use. Diabetes is a threat to the retina, as the small blood vessels supplying blood to the retina can become leaky. This condition is called retinopathy.
When tiny blood vessels in the retina leak fluid, fat or blood that seeps from the vessels can blur vision. Fluid sitting in the retina for prolonged periods of time causes damage to the retina and the macula. These small blood vessels can become blocked therefore the retina doesn’t get enough blood flow to function well. The body then produces more blood vessels to attempt to restore blood supply to the retina. This is known as diabetic retinopathy.
These new blood vessels are leaky and fragile causing major bleeds within the eye and resulting in loss of vision. These blood vessels also creates scar tissue in the eye which eventually contracts causing the retina to detach from the back of the eye. This is called a retinal detachment and will require surgery.
Developing diabetic retinopathy is dependent on how long you have had diabetes and how well you managed your diabetes over that time.
50 % of young insulin dependent (Type I) diabetics after 10 years develop diabetic retinopathy. This increases to 90% after 30 years and about 30 % will go on to develop proliferative retinopathy after 15 years.
For maturity onset (Type II) diabetes 80% of sufferers will go on to develop retinopathy after 15 years. As many as fifteen percent develop proliferative diabetic retinopathy. The most important thing that you can do for your eyes is to control your diabetes well.
Regular eye checks – early treatment equals best results.
During these regular eye checks your doctor may require you to have a fluorescein angiogram. A dye is injected into a vein in your arm which allows photographs to be taken of the blood vessels in the retina. This assists the Doctor in accurate diagnosis and treatment.
“Water logging” of the macula (macular oedema) is treated in the clinic with gentle laser therapy to the retina. If swelling is excessive Avastin can be injected into the eye to help dry the macular followed by laser treatment. These treatments may need to be repeated and are not meant to improve vision but to prevent future complications.
With proper and prompt treatment of retinopathy there is a high chance the effects of retinopathy can be prevented or minimised.
During cataract surgery a new lens is placed within the capsular bag behind the iris. The rear wall of this bag is a thin membrane called the posterior capsule.
With time the posterior capsule can become cloudy causing blurry vision, glare and haze. This opacity is called a Posterior Capsule Opacification (PCO).
PCO is treatable and can be cleared using a YAG laser. This procedure takes just a few minutes, is painless, does not require a hospital admission or anaesthetic and the membrane almost never grows back again.