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1. Basic Ophthalmology Richard Harper Pdf To Excel Online

Glaucoma is a group of eye diseases which result in damage to the and. The most common type is open-angle glaucoma with less common types including closed-angle glaucoma and. Open-angle glaucoma develops slowly over time and there is no pain. May begin to decrease followed by central vision resulting in if not treated. Closed-angle glaucoma can present gradually or suddenly. The sudden presentation may involve severe eye pain, blurred vision, mid-dilated, redness of the eye, and nausea.

Vision loss from glaucoma, once it has occurred, is permanent. Risk factors for glaucoma include increased, a family history of the condition, and. For eye pressures a value of greater than 21 mmHg or 2.8 kPa is often used with higher pressures leading to a greater risk. However, some may have high eye pressure for years and never develop damage.

Conversely, optic nerve damage may occur with normal pressure, known as normal-tension glaucoma. The mechanism of open-angle glaucoma is believed to be slow exit of through the while in closed-angle glaucoma the blocks the trabecular meshwork. Diagnosis is by a dilated. Often the optic nerve shows an abnormal amount of. If treated early it is possible to slow or stop the progression of disease with medication, treatment, or surgery. The goal of these treatments is to decrease eye pressure.

A number of different classes of are available. Laser treatments may be effective in both open-angle and closed-angle glaucoma. A number of types of may be used in people who do not respond sufficiently to other measures.

Treatment of closed-angle glaucoma is a medical emergency. About 6 to 67 million people have glaucoma globally.

The disease affects about 2 million people in the United States. It occurs more commonly among older people. Closed-angle glaucoma is more common in women. Glaucoma has been called the 'silent thief of sight' because the loss of vision usually occurs slowly over a long period of time. Worldwide, glaucoma is the second-leading cause of blindness after. The word 'glaucoma' is from ancient Greek glaukos which means blue, green, or gray. In English, the word was used as early as 1587 but did not become commonly used until after 1850, when the development of the allowed people to see the optic nerve damage.

Photo showing conjunctival vessels dilated at the corneal edge (ciliary flush, circumcorneal flush) and hazy cornea characteristic of acute angle closure glaucoma Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms make screening via regular eye check-ups important. The only signs are gradually progressive, and optic nerve changes (increased on ). About 10% of people with closed angles present with acute angle closure characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (30 ), nausea and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil.

It is also associated with an oval pupil in some cases. Acute angle closure is an emergency. Opaque specks may occur in the lens in glaucoma, known as glaukomflecken. The same view with advanced vision loss from glaucoma Of the several causes for glaucoma, ocular hypertension (increased pressure within the eye) is the most important risk factor in most glaucomas, but in some populations, only 50% of people with primary open-angle glaucoma actually have elevated ocular pressure. Open-angle glaucoma accounts for 90% of glaucoma cases in the United States. Closed-angle glaucoma accounts for less than 10% of glaucoma cases in the United States, but as many as half of glaucoma cases in other nations (particularly East Asian countries).

Dietary No clear evidence indicates vitamin deficiencies cause glaucoma in humans. It follows, then, that oral vitamin supplementation is not a recommended treatment for glaucoma. Increases in those with glaucoma, but does not appear to affect normal individuals. Ethnicity Many people of descent are prone to developing angle closure glaucoma due to shallower anterior chamber depths, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Higher rates of glaucoma have also been reported for populations, compared to white populations, in Canada and Greenland.

Genetics Positive family history is a risk factor for glaucoma. The relative risk of having primary open-angle glaucoma (P.O.A.G.) is increased about two- to four-fold for people who have a sibling with glaucoma. Glaucoma, particularly primary open-angle glaucoma, is associated with in several, including, and, although most cases of glaucoma do not involve these genetic mutations. Normal-tension glaucoma, which comprises one-third of POAG, is also associated with genetic mutations (including and genes). Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally, failure of the normal third-trimester gestational atrophy of the and the is associated with other anomalies.

Angle closure-induced ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies, and has been modelled in mice. Other Other factors can cause glaucoma, known as 'secondary glaucoma', including prolonged use of (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe and (neovascular glaucoma); (angle-recession glaucoma); and inflammation of the middle layer of the pigmented vascular eye structure , known as uveitic glaucoma.

Pathophysiology. Human eye cross-sectional view The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its exact etiology. However, the major risk factor for most glaucomas and the focus of treatment is. Intraocular pressure is a function of production of liquid by the of the eye, and its drainage through the.

Aqueous humor flows from the ciliary processes into the, bounded posteriorly by the and the, and anteriorly by the. It then flows through the of the iris into the, bounded posteriorly by the iris and anteriorly by the. From here, the trabecular meshwork drains aqueous humor via the scleral venous sinus into and general blood circulation.

In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork, due to the degeneration and obstruction of the trabecular meshwork, whose original function is to absorb the aqueous humor. Loss of aqueous humor absorption leads to increased resistance and thus a chronic, painless buildup of pressure in the eye. In close/narrow-angle, the iridocorneal angle is completely closed because of forward displacement of the final roll and root of the iris against the cornea, resulting in the inability of the aqueous fluid to flow from the posterior to the anterior chamber and then out of the trabecular network. This accumulation of aqueous humor causes an acute increase in pressure and pain. The inconsistent relationship of glaucomatous optic neuropathy with increased intraocular pressure has provoked hypotheses and studies on anatomic structure, eye development, nerve compression trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell/axon degeneration, glial support cell, immune system, aging mechanisms of neuron loss, and severing of the nerve fibers at the scleral edge. Diagnosis Screening for glaucoma is usually performed as part of a standard performed by and. Testing for glaucoma should include measurements of the intraocular pressure via, anterior chamber angle examination or, and examination of the optic nerve to look for any visible damage to it, or change in the and also rim appearance and vascular change.

A formal should be performed. The retinal nerve fiber layer can be assessed with imaging techniques such as, and/or (Heidelberg retinal tomogram). Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as Goldmann tonometry should be augmented with to measure the central corneal thickness (CCT). A thicker-than-average cornea can result in a pressure reading higher than the 'true' pressure whereas a thinner-than-average cornea can produce a pressure reading lower than the 'true' pressure. Because pressure measurement error can be caused by more than just CCT (i.e., corneal hydration, elastic properties, etc.), it is impossible to 'adjust' pressure measurements based only on CCT measurements. The can also be used to detect glaucoma with the use of a frequency doubling technology perimeter. Examination for glaucoma also could be assessed with more attention given to sex, race, history of drug use, refraction, inheritance and family history.

Glaucoma tests What test examines How it is accomplished Inner eye pressure The eye is numbed via eye drops. The examiner then uses a tonometer to measure the inner pressure of the eye through pressure applied by a puff of warm air or a tiny tool. (dilated eye examination) Shape and color of the optic nerve The pupil is dilated via the application of eye drops.

Basic Ophthalmology Richard Harper Pdf To Excel Online

Using a small magnification device with a light on the end, the examiner can examine the magnified optic nerve. (visual field test) Complete field of vision The patient looks straight ahead and is asked to indicate when light passes the patient's peripheral field of vision. This allows the examiner to map the patient’s field of vision.

Angle in the eye where the iris meets the cornea Eyedrops are used to numb the eye. A hand-held contact lens with a mirror is placed gently on the eye to allow the examiner to see the angle between the cornea and the iris. Thickness of the cornea The examiner places a pachymeter gently on the front of the eye to measure its thickness. Thickness of the nerve fiber layer Using one of several techniques, the nerve fibers are examined. This section needs additional citations for. Unsourced material may be challenged and removed. (August 2015) Glaucoma is an umbrella term for eye conditions which damage the, and which can lead to a loss of vision.

The main cause of damage to the optic nerve is intraocular pressure (IOP), excessive fluid pressure within the eye, which can be due to various reasons including blockage of drainage ducts, and narrowing or closure of the angle between the iris and cornea. The primary division in categorizing different types of glaucoma is open-angle and closed-angle (or angle-closure) glaucoma. The open angle refers to the angle where the iris meets the cornea being as wide and open as it should be, allowing the fluid from inside the eye to drain, thus relieving the internal pressure. Where this angle is narrowed or closed, pressure can build up, and eventually damage the optic nerve leading to loss of vision.

Primary open-angle glaucoma (also, primary glaucoma, chronic glaucoma) refers to slow clogging of the drainage canals resulting in increased eye pressure which causes progressive optic nerve damage. This manifests as a gradual loss of the visual field, starting with a loss of, but eventually the entire vision will be lost if not treated. This is the most common type of glaucoma, accounting for 90% of cases in the United States, but fewer in Asian countries. Onset is slow and painless, and loss of vision is gradual and irreversible.

Narrow-angle glaucoma (also closed-angle glaucoma) the iris bows forward, narrowing the angle that drains the eye, increasing pressure within the eye. If untreated, it can lead to the medical emergency of angle-closure glaucoma. In angle-closure glaucoma (also closed-angle glaucoma, primary angle-closure glaucoma, acute glaucoma) the iris bows forward and causes physical contact between the iris and trabecular meshwork, which blocks the outflow of aqueous humor from within the eye.

This contact may gradually damage the draining function of the meshwork until it fails to keep pace with aqueous production, and the intraocular pressure rises. The onset of symptoms is sudden and causes pain and other symptoms that are noticeable; it is treated as a medical emergency. Unlike open-angle glaucoma, angle-closure glaucoma is a result of the angle between the iris and cornea closing. This tends to occur in the, who have smaller-than-normal anterior chambers, making physical contact between the iris and trabecular meshwork more likely. Normal-tension glaucoma (also NTG, low-tension glaucoma, normal-pressure glaucoma) is a condition where the optic nerve is damaged although intraocular pressure (IOP) is in the normal range (12-22mm Hg). Individuals with a family history of NTG, those of Japanese ancestry, and those with a history of systemic heart disease are at higher than average risk of developing NTG.

The cause of NTG is unknown. Secondary glaucoma refers to any case in which another disease, trauma, drug or procedure causes increased eye pressure, resulting in optic nerve damage and vision loss, and may be mild or severe.

It can be due to an eye injury, inflammation, a tumor, or advanced cases of cataracts or diabetes. It can also be caused by certain drugs such as steroids. Treatment depends on whether it is open-angle or angle-closure glaucoma. In (also, PEX, exfoliation glaucoma) the pressure is due to the accumulation of microscopic granular protein fibers, which can block normal drainage of the aqueous humor. PEX is prevalent in Scandinavia, primarily in those over 70, and more commonly in women. (also, pigmentary dispersion syndrome) is caused by pigment cells sloughing off from the back of the iris and floating around in the aqueous humor.

Over time, these pigment cells can accumulate in the anterior chamber in such a way that it can begin to clog the trabecular meshwork. It is a rare condition that occurs mostly among Caucasians, mostly males in their mid-20s to 40s, and most are nearsighted. Is a neonate or juvenile abnormality where ocular hypertension is evident at birth or shortly thereafter and is caused by abnormalities in the anterior chamber angle development that blocks the outflow of the aqueous humor. Uveitic Glaucoma is due to uveitis, the swelling and inflammation of the, the middle layer of the eye.

The uvea provides most of the blood supply to the retina. Increased eye pressure in uveitis can result from the inflammation itself or from the steroids used to treat it. Screening The as of 2013 states there is insufficient evidence to recommend for or against screening for glaucoma. Therefore, there is no national screening program in the US. Screening, however, is recommended starting at age 40 by the American Academy of Ophthalmology. There is a glaucoma screening program in the UK. Those at risk are advised to have a at least once a year.

Treatment The modern goals of glaucoma management are to avoid glaucomatous damage and nerve damage, and preserve visual field and total quality of life for patients, with minimal side effects. This requires appropriate diagnostic techniques and follow-up examinations, and judicious selection of treatments for the individual patient. Although intraocular pressure is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment. Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies, including nutritional compounds, some of which may be regarded by clinicians as safe for use now, while others are on trial. Medication. Main article: Intraocular pressure can be lowered with medication, usually eye drops.

Several classes of medications are used to treat glaucoma, with several medications in each class. Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate them or to communicate with the treating physician to improve the drug regimen.

Initially, glaucoma drops may reasonably be started in either one or in both eyes. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid. Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an found half failed to fill their prescriptions the first time, and one-fourth failed to refill their prescriptions a second time. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic medications are also being investigated., such as, and, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow. Topical, such as, and, decrease aqueous humor production by the epithelium of the., such as and, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow. Less-selective, such as, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e.

Further closure of trabecular meshwork, which is responsible for absorption of aqueous humor). , such as, work by contraction of the, opening the and allowing increased outflow of the aqueous humour., an acetylcholinesterase inhibitor, is used in chronic glaucoma., such as, and, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body. Laser Argon laser trabeculoplasty (ALT) may be used to treat open-angle glaucoma, but this is a temporary solution, not a cure. A 50-μm argon laser spot is aimed at the trabecular meshwork to stimulate the opening of the mesh to allow more outflow of aqueous fluid.

Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty uses a thermal argon laser in an laser trabeculoplasty procedure. A newer type of laser trabeculoplasty uses a 'cold' (nonthermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure, selective laser trabeculoplasty (SLT), uses a 532-nm, frequency-doubled, Q-switched, which selectively targets pigment in the trabecular meshwork cells. Studies show SLT is as effective as ALT at lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once. Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma.

During laser iridotomy, laser energy is used to make a small, full-thickness opening in the iris to equalize the pressure between the front and back of the iris, thus correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the trabecular meshwork. In some cases of intermittent or short-term angle closure, this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases, it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular meshwork. Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium. Main article: Both and conventional surgeries are performed to treat glaucoma.

Surgery is the primary therapy for those with glaucoma. Generally, these operations are a temporary solution, as there is not yet a cure for glaucoma. Canaloplasty Canaloplasty is a nonpenetrating procedure using micro technology. To perform a canaloplasty, an incision is made into the eye to gain access to the Schlemm's canal in a similar fashion to a viscocanalostomy. A microcatheter will circumnavigate the canal around the iris, enlarging the main drainage channel and its smaller collector channels through the injection of a sterile, gel-like material called viscoelastic. The catheter is then removed and a suture is placed within the canal and tightened.

By opening the canal, the pressure inside the eye may be relieved, although the reason is unclear, since the canal (of Schlemm) does not have any significant fluid resistance in glaucoma or healthy eyes. Long-term results are not available. Trabeculectomy The most common conventional surgery performed for glaucoma is the. Here, a partial thickness flap is made in the scleral wall of the eye, and a window opening is made under the flap to remove a portion of the trabecular meshwork. The scleral flap is then sutured loosely back in place to allow fluid to flow out of the eye through this opening, resulting in lowered intraocular pressure and the formation of a bleb or fluid bubble on the surface of the eye. Scarring can occur around or over the flap opening, causing it to become less effective or lose effectiveness altogether. Traditionally, chemotherapeutic adjuvants, such as (MMC) or (5-FU), are applied with soaked sponges on the wound bed to prevent filtering blebs from scarring by inhibiting fibroblast proliferation.

Contemporary alternatives to prevent the scarring of the meshwork opening include the sole or combinative implementation of nonchemotherapeutic adjuvants such as the ologen collagen matrix, which has been clinically shown to increase the success rates of surgical treatment. Collagen matrix prevents scarring by randomizing and modulating fibroblast proliferation in addition to mechanically preventing wound contraction and adhesion. Glaucoma drainage implants.

Main article: Professor Anthony Molteno developed the first glaucoma drainage implant, in in 1966. Since then, several types of implants have followed on from the original, the Baerveldt tube shunt, or the valved implants, such as the Ahmed glaucoma valve implant or the ExPress Mini Shunt and the later generation pressure ridge Molteno implants. These are indicated for glaucoma patients not responding to maximal medical therapy, with previous failed guarded filtering surgery (trabeculectomy). The flow tube is inserted into the anterior chamber of the eye, and the plate is implanted underneath the conjunctiva to allow a flow of aqueous fluid out of the eye into a chamber called a. The first-generation Molteno and other nonvalved implants sometimes require the ligation of the tube until the bleb formed is mildly fibrosed and water-tight. This is done to reduce postoperative hypotony—sudden drops in postoperative intraocular pressure.

Valved implants, such as the Ahmed glaucoma valve, attempt to control postoperative hypotony by using a mechanical valve. Ab interno implants, such as the Xen Gel Stent, are transscleral implants by an ab interno procedure to channel aqueous humor into the non-dissected Tenon's space, creating a subconjunctival drainage area similar to a bleb.

The implants are transscleral and different from more other ab interno implants that do not create a transscleral drainage, such as iStent, CyPass, or Hydrus. The ongoing scarring over the conjunctival dissipation segment of the shunt may become too thick for the aqueous humor to filter through. This may require preventive measures using antifibrotic medications, such as or (during the procedure), or other nonantifibrotic medication methods, such as collagen matrix implant, or biodegradable spacer, or later on create a necessity for revision surgery with the sole or combinative use of donor patch grafts or collagen matrix implant.

And for glaucomatous painful blind eye and some cases of glaucoma, cyclocryotherapy for ciliary body ablation could be considered to be performed. Laser-assisted nonpenetrating deep sclerectomy The most common surgical approach currently used for the treatment of glaucoma is, in which the sclera is punctured to alleviate intraocular pressure. Nonpenetrating deep sclerectomy (NPDS) surgery is a similar, but modified, procedure, in which instead of puncturing the scleral bed and trabecular meshwork under a scleral flap, a second deep scleral flap is created, excised, with further procedures of deroofing the Schlemm's canal, upon which, percolation of liquid from the inner eye is achieved and thus alleviating intraocular pressure, without penetrating the eye. NPDS is demonstrated to have significantly fewer side effects than trabeculectomy. However, NPDS is performed manually and requires higher level of skills that may be assisted with instruments.

In order to prevent wound adhesion after deep scleral excision and to maintain good filtering results, NPDS as with other non-penetrating procedures is sometimes performed with a variety of biocompatible spacer or devices, such as the Aquaflow collagen wick, ologen Collagen Matrix, or Xenoplast glaucoma implant. Laser-assisted NPDS is performed with the use of a CO 2 laser system. The laser-based system is self-terminating once the required scleral thickness and adequate drainage of the intraocular fluid have been achieved.

This self-regulation effect is achieved as the CO 2 laser essentially stops ablating as soon as it comes in contact with the intraocular percolated liquid, which occurs as soon as the laser reaches the optimal residual intact layer thickness. Prognosis In open-angle glaucoma, the typical progression from normal vision to complete blindness takes about 25 years to 70 years without treatment, depending on the method of estimation used. The intraocular pressure can also have an effect, with higher pressures reducing the time until blindness.

Epidemiology. Scientists track eye movements in glaucoma patients to check vision impairment while driving Rho kinase inhibitors inhibitors, such as, work by inhibition of the actin cytoskeleton, resulting in the morphological changes in the trabecular meshwork and increased aqueous outflow. More compounds in this class are being investigated in phase 2 and phase 3 trials. Neuroprotective agents A 2013 compared the effect of brimonidine and timolol in slowing the progression of open angle glaucoma in adult participants.

The results showed that participants assigned to brimonidine showed less visual field progression that those assigned to timolol, though the results were not significant, given the heavy and limited evidence. The mean intraocular pressures for both groups were similar. Participants in the brimonidine group had a higher occurrence of side effects caused by medication than participants in the timolol group. Cannabis Studies in the 1970s reported that the use of may lower intraocular pressure. In an effort to determine whether marijuana, or drugs derived from it, might be effective as a glaucoma treatment, the US supported research studies from 1978 to 1984.

These studies demonstrated some derivatives of marijuana lowered intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied to the eye. In 2003, the released a position statement stating that cannabis was not more effective than prescription medications. Furthermore, no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of cannabis use to treat glaucoma compared with the wide variety of pharmaceutical agents now available. In 2012 the American Glaucoma Society published a position paper discrediting the use of cannabis as a legitimate treatment for elevated intraocular pressure, for reasons including short duration of action and side effects that limit many activities of daily living. References.