gradually damage the function of the meshwork until it fails to keep pace with aqueous production, and the pressure rises. in over half of all cases, prolonged contact between iris and tm causes the formation of synechiae (effectively "scars"). these cause permanent obstruction of aqueous outflow. in some cases, pressure may rapidly build up in the eye, causing pain and redness (symptomatic, or so-called "acute" angle closure). in this situation, the vision may become blurred, and halos may be seen around bright lights. accompanying symptoms may include a headache and vomiting. diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, and pain. however, the majority of cases are asymptomatic. prior to the very severe loss of vision, these cases can only be identified by examination, generally by an eye care professional. once any symptoms have been controlled, the first line (and often definitive) treatment is laser iridotomy. this may be performed using either nd:yag or argon lasers, or in some cases by conventional incisional surgery. the goal of treatment is to reverse and prevent contact between the iris and trabecular meshwork. in early to moderately advanced cases, iridotomy is successful in opening the angle in around 75% of cases. in the other 25%, laser iridoplasty, medication (pilocarpine) or incisional surgery may be required. primary open-angle glaucoma is when optic nerve damage results in a progressive loss of the visual field. this is associated with increased pressure in the eye. not all people with primary open-angle glaucoma have eye pressure that is elevated beyond normal, but decreasing the eye pressure further has been shown to stop progression even in these cases. the increased pressure is caused by trabecular meshwork blockage. because the microscopic passageways are blocked, the pressure builds up in the eye and causes imperceptible very gradual vision loss. peripheral vision is affected first, but eventually the entire vision will be lost if not treated. diagnosis is made by looking for cupping of the optic nerve. prostaglandin agonists work by opening uveoscleral passageways. beta-blockers, such as timolol, work by decreasing aqueous formation. carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing the formation of aqueous humor. parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production (via inhibition of ac) and increase drainage. developmental glaucoma developmental glaucoma (q15.0) primary congenital glaucoma infantile glaucoma glaucoma associated with hereditary or familial diseases secondary glaucoma secondary glaucoma (h40.3-h40.6) inflammatory glaucoma uveitis of all types fuchs heterochromic iridocyclitis phacogenic glaucoma angle-closure glaucoma with mature cataract phacoanaphylactic glaucoma secondary to rupture of lens capsule phacolytic glaucoma due to phacotoxic meshwork blockage subluxation of lens glaucoma secondary to intraocular hemorrhage hyphema hemolytic glaucoma, also known as erythroclastic glaucoma traumatic glaucoma angle recession glaucoma: traumatic recession on anterior chamber angle postsurgical glaucoma aphakic pupillary block ciliary block glaucoma neovascular glaucoma (see below for more details) drug-induced glaucoma corticosteroid induced glaucoma alpha-chymotrypsin glaucoma. postoperative ocular hypertension from use of alpha chymotrypsin. glaucoma of miscellaneous origin associated with intraocular tumors associated with retinal detachments secondary to severe chemical burns of the eye associated with essential iris atrophy toxic glaucoma neovascular glaucoma, an uncommon type of glaucoma, is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (pdr) or central retinal vein occlusion (crvo). it may also be triggered by other conditions that result in ischemia of the retina or ciliary body. individuals with poor blood flow to the eye are highly at risk for this condition. neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. people with such condition begin to rapidly lose their eyesight. sometimes, the disease appears very rapidly, especially after cataract surgery procedures. a new treatment for this disease, as first reported by kahook and colleagues, involves the use of a novel group of medications known as anti-vegf agents. these injectable medications can lead to a dramatic decrease in new vessel formation and, if injected early enough in the disease process, may lead to normalization of intraocular pressure. currently, there are no high-quality controlled trials demonstrating a beneficial effect of anti-vegf treatments in lowering iop in people with neovascular glaucoma. toxic glaucoma is open-angle glaucoma with an unexplained significant rise of intraocular pressure following unknown pathogenesis. intraocular pressure can sometimes reach 80 mmhg (11 kpa). it characteristically manifests as ciliary body inflammation and massive trabecular oedema that sometimes extends to schlemm's canal. this condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior chamber and a lack of aqueous misdirection. also, the corneal appearance is not as hazy. a reduction in visual acuity can occur followed neuroretinal breakdown. associated factors include inflammation, drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. gede pardianto (2005) reported on four patients who had toxic glaucoma. one of them underwent phacoemulsification with small particle nucleus drops. some cases can be resolved with some medication, vitrectomy procedures or trabeculectomy. valving procedures can give some relief, but further research is required. absolute glaucoma absolute glaucoma (h44.5) is the end stage of all types of glaucoma. the eye has no vision, absence of pupillary light reflex and pupillary response, and has a stony appearance. severe pain is present in the eye. the treatment of absolute glaucoma is a destructive procedure like cyclocryoapplication, cyclophotocoagulation, or injection of 99% alcohol. types glaucoma is an umbrella term for eye conditions that damage the optic nerve and that 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 caused by factors such as blockage of drainage ducts and narrowing or closure of the angle between the iris and cornea. glaucoma is primarily categorized as either open-angle or closed-angle (or angle-closure). in open-angle glaucoma, the iris meets the cornea normally, allowing the fluid from inside the eye to drain, thus relieving the internal pressure. when this angle is narrowed or closed, pressure increases over time, causing damage to the optic nerve and leading to blindness. primary open-angle glaucoma (also called primary or chronic glaucoma) involves the slow clogging of 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 peripheral vision, but eventually all vision will be lost if the condition is not treated. this is the most common type of glaucoma, accounting for 90% of cases in the united states, but is less prevalent in asian countries. onset is slow and painless, and loss of vision is gradual and irreversible. with narrow-angle glaucoma (also called 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. with angle-closure glaucoma (also called closed-angle, primary angle-closure or 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 noticeable symptoms, and the condition is treated as a medical emergency. unlike open-angle glaucoma, angle-closure glaucoma is a result of the closing of the angle between the iris and cornea. this tends to occur in the farsighted, who have smaller anterior chambers, making physical contact between the iris and trabecular meshwork more likely. a variety of tests may be performed to detect those at risk of angle-closure glaucoma. normal-tension glaucoma (ntg, also called low-tension or normal-pressure glaucoma) is a condition in which the optic nerve is damaged although intraocular pressure (iop) is in the normal range (12 to 22 mmhg (1.6 to 2.9 kpa)). individuals with a family history of ntg, those of japanese ancestry, those with a history of systemic heart disease and those with flammer syndrome are at an elevated 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, which may be mild or severe. this may be the result of 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 the condition is identified as open-angle or angle-closure glaucoma. with pseudoexfoliation glaucoma (also known as pex or exfoliation glaucoma) the pressure results from 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. pigmentary glaucoma (also known as 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 and begin to clog the trabecular meshwork. it is a rare condition that occurs mostly among white males in their mid-20s to 40s, most of whom are nearsighted. primary juvenile glaucoma is a neonate or juvenile abnormality in which 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 caused by uveitis, the swelling and inflammation of the uvea, the middle layer of the eye. the uvea provides most of the blood supply to the retina. increased eye pressure can result from the inflammation itself or from the steroids used to treat it. visual field defects in glaucoma