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a quantum leap in glaucoma detection and monitoring

Intraocular pressure

 

IOP and caring for glaucoma

 

Diagnosing Glaucoma

 

 

 

 

 

 

 

 

Fortuitous or targeted detection of glaucoma usually occurs during a routine checkup when patients over 40 come in to have glasses prescribed for farsightedness.

 

In other cases it is detected in the aftermath of an accident with a car which had suddenly appeared on the side of the patient’s peripheral visual field, this area being the first to be affected by the disease. And finally, it is sometimes uncovered during a check up at the ophthalmologist due to very subtle symptoms such as headaches, eye pain, and visual fatigue.

 

There is no one specific test for diagnosing glaucoma in its early stages. Agencies and/or learned professional societies recommend diagnosing glaucoma by associating the following four examinations[1] :

 

•  Tonometry measures intraocular pressure looking for intraocular hypertonia (above 20 mm of mercury).

•  Examination of the optic nerve or the papilla inside the eye looks for an excavation (assessed by the cup/disk ratio or

   c/d) and/or its alterations.

•  Perimetry evaluates the integrity of the visual field.

•  Gonioscopy measures whether and to what degree the irido-corneal angle is open or closed.

 

According to these diagnostic examinations, glaucoma’s diagnostic criteria are:

 

•  An intraocular pressure > 21 mm Hg for high pressure glaucoma (some authors have even began talking about 18

   mm as the diagnostic threshold).

•  A horizontal or vertical cup/disc ratio > 0.6 or 0.7 or a difference of this ratio between both eyes > 0.2.

•  Optic nerve Papilla alterations such as notches of the neuroretinal ring, diffuse thinning or papillary hemorrhaging.

   Changes in the visual field.

•  An open angle during the gonioscopy for open angle glaucomas and a closed angle (grade 0 to 1) for angle closure

   glaucoma.

 

 

IOP monitoring during treatment

 

 

 

 

 

 

 

 

The primary objective of all types of glaucoma treatment, i.e. medication, laser or surgery, is to reduce intraocular pressure. Their ultimate goal is to preserve visual function and maintain the patient’s quality of life at a reasonable cost.

 

Medical treatment is prescribed for life and should not be stopped. Anti-glaucoma eyedrops lower intraocular pressure through various mechanisms: inhibition of aqueous humor production and/or secretion, increasing its resorption (either by the trabecular meshwork, or via the uveo-scleral pathway) relaxation of the ciliary muscle. The type of anti-glaucoma eyedrops chosen for treatment depends on contra-indications and the adverse effects of each therapeutic class. Precise treatment adjustment and fine tuning can be a complex and long process because it is difficult to measure IOP during an appointment with the ophthalmologist and a single measurement does not always reflect real life pressure.

 

Both clinical follow-up of glaucoma patients and the adaptation of their treatment are still based on a limited amount of information. IOP is the most useful parameter to measure.

 

IOP is currently the only factor with confirmed correlation to glaucoma.

 

Only a 1/3 of the patients continue using the same initial beta adrenergic blocking agent during the first two years following diagnosis. This means treatment needs to be modified several times to control patients’ IOP.

 

However, many factors have an effect on intraocular pressure: the circadian (day/night) cycle, corneal thickness, systolic blood pressure, physical exercise prior to examination, taking drugs, subject’s position during examination, age, tobacco use, cardiac disease…

 

With regular monitoring of IOP throughout the day one can reduce the time spent above a set level and thus control over time the pressure applied on the head of the optic nerve.

 

Repeated IOP measurements are usually necessary to judge whether a treatment is efficient or not2. We would like to highlight the fact that taking a more than 4 point pressure cycle reading over a 24 hour period is a reimbursed medical procedure in France.

 

Thanks to iSonic Medical’s products, this medical procedure, which consists of taking a precise and non-contact measurement of intraocular pressure, will be made easy.

 

A recent study published in the American Journal of Ophthalmology in February 2010 reviews 21,000 cases of people affected by glaucoma and demonstrates that those patients treated by glaucoma eye drops enjoyed a better longevity than those who went untreated.

 

Mortality dropped 74% over a four year period among people treated with either beta blocker eye drops or a prostaglandin analogous or even a combination of a few drugs.

 

[1] Haute Autorité de Santé 2006

[2] P. Denis, G. Berdeaux – Journal français d’ophtalmologie 2004

 

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The Physiology of Intraocular Pressure (IOP)

 

Intraocular pressure is the dynamic result between the production and drainage of the amount of aqueous humor contained in the anterior chamber of the eye. All this is dependent on blood pressure in the ocular globe. The difference between the eye globe’s perfusion pressure and venous pressure must constantly be higher than the IOP to ensure an adequate perfusion of the optical nerve and the retina.

 

And so it is easy to see how intraocular pressure that is too high or blood pressure that is too low – as is the case for some patients during the night – can cause an insufficient flow of blood and oxygen (anoxia or hypoxemia) to the optical nerve and the retina and cause optic nerve damage leading to glaucoma.

 

Aqueous humor is secreted by the ciliary body into an area called the posterior chamber. It then passes through the pupil (between the iris and the lens) to the anterior chamber of the eye which is the region located between the cornea and the iris. It is then absorbed in the irido-corneal angle through a filter called the trabecular meshwork, and then drained into Schlemm’s canal. It flows into the epi-scleral venous plexuses and ends up in the general venous blood circulation.

 

Pathological mechanisms

 

An increase in IOP may have several origins:

 

The most common cause is a reduced elimination caused by an obstruction of the irido-corneal angle. This may be congenital or develop with age due to a sclerosis of the trabecular meshwork. The later case is called chronic open angle glaucoma.

 

As a result of aging the pupil may become blocked by the crystalline lens. It then bulges forward and may cause a blockage of the irido-corneal angle. Aqueous humor subsequently accumulates behind the iris and pushes it forward. In some predisposed patients this results in a total closing of the angle. This is the mechanism of acute glaucoma crises known as angle closure glaucoma. More rarely, a rise in ciliary secretion may be the origin of glaucoma. Acute anterior uveitis typically causes such a rise.

 

Consequences of a rise in IOP

 

The consequences of an increase in IOP essentially occur at the level of optic nerve fibers but also at that of retinal cells. These fibers are the continuation of retinal ganglion cells that will leave the eye at the papilla to form the optic nerve. Ocular hypertension (OHT) will accelerate the damage and degeneration of these fibers. The higher and more prolonged the hypertension, the more quickly the consequences will occur.

 

The impact of OHT also depends on the quality of the patient’s microcirculation, especially if the OHT is chronic. Thus, the following risk factors potentialize the development of glaucoma: genetic (familial), vascular, arteriosclerosis causing illnesses (hypertension, diabetes mellitus, nicotine dependence, hypercholesterolemia) as well as previous eye surgery.

 

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