Glaukoma Neovaskuler

Glaukoma Neovaskuler

Batasan :
Merupakan glaucoma sekunder yang disebabkan adanya neovaskularisasi permukaan iris, sudut dan jarring trabekula.

Patofisiologi :
Neovaskularisasi pada iris (rubeosis iridis) merupakan suatu respon terhadap adanya hipoksia dan iskemia retina akibat berbagai penyakit, baik pada mata maupun di luar mata yang paling sering adalah retinopati diabetic. Neovaskularisasi iris pada awalnya terjadi pada tepi pupil sebagai percabangan kecil, selanjutnya tumbuh dan membentuk membrane fibrovaskuler pada permukaan iris secara radial sampai ke sudut, meluas dari akar iris melewati ciliary body dan sclera spur mencapai jaring trabekula sehingga menghambat pembuangan akuos dengan akibat Intra Ocular Presure meningkat dan keadaan sudut masih terbuka.
Suatu saat membrane fibrovaskuler ini konstraksi menarik iris perifer sehingga terjadi sinekia anterior perifer (PAS) sehingga sudut bilik mata depan tertutup dan tekanan intra okuler meningkat sangat tinggi sehingga timbul reaksi radang intra okuler.

Gejala Klinis :

Pada Stadium sudut terbuka :
- mata tidak merah, tidak nyeri
- visus kabur ( oleh karena keadaan pada retina )
- neovaskularisasi pada iris
- IOP meningkat
- Sudut bilik mata depan terbuka

Pada stadium sudut tertutup :
- Mata tiba-tiba sangat nyeri, merah dan berair
- Visus sangat kabur
- Kornea suram
- Neovaskularisasi pada iris
- IOP sangat tinggi
- Sudut bilik mata depan tertutup

Diagnosis / Cara pemeriksaan
Glaukoma neovaskular sudut terbuka : anamnesis mata nyeri, tidak merah tapi kabur, visus menurun
Dengan lampu celah biomikroskop : tampak neovaskularisasi pada iris dari tepi pupil sampai perifer
Tonometri : IOP > 21 mmHg
Gonioskopi : sudut bilik mata depan terbuka, neovaskularisasi

Glaukoma neovaskular sudut tertutup: anamnesis mata tiba-tiba sangat nyeri, merah, keluar air mata, sangat kabur dan visus sangat menurun bahkan sampai nol.
Dengan lampu celah biomikroskop : Hiperemia perilimbal (silier), kornea suram, di BMD tampak flare moderat dan kadang hifema, tampak neovaskularisasi luas pada seluruh permukaan iris dari tepi pupil sampai perifer
Tonometri : IOP sangat tinggi > 40 mmHg
Gonioskopi : biasanya sangat sulit karena kornea sangat suram, sudut bilik mata depan tertutup, neovaskularisasi.

Differential Diagnosis :

Primary Angle Closure Glaucoma

Primary Angle Closure Glaucoma

Batasan :
Kelainan mata yang terjadi karena Intra Ocular Pressure (IOP) meningkat secara cepat sebagai akibat dari tertutupnya sudut bilik mata depan secara total dan mendadak akibat blok pupil karena kondisi primer mata dengan segmen anterior yang kecil.

Patofisiologi :
Mata dengan segmen anterior yang kecil dan sumbu aksial yang pendek dengan bilik mata depan yang dangkal, dengan meningkatnya usia, lensa membesar sehingga kondisi irido-lentikular meningkat dan bila tiba-tiba mengalami kondisi yang menyebabkan pupil mid-dilatasi, terjadi aposisi iris-lensa yang maksimal, blok pupil, kontak iris dengan trabecular meshwork, sudut bilik mata depan tertutup, aquos terbendung, intra ocular pressure meningkat dengan cepat.

Gejala klinis :
Keluhan dan gambaran klinis timbul sebagai akibat dari peningkatan IOP yang mendadak dan sangat tinggi.
Keluhan : nyeri periokuler, penglihatan sangat menurun dan melihat warna sekitar sumber cahaya (halo), mual dan muntah.
Gambaran klinis : Hiperemia limbal dan konjungtiva, edema kornea, bilik mata depan dangkal disertai flare and cells, IOP sangat tinggi, Papil saraf optic hyperemia, sudut BMD tertutup.

Diagnosis :
Hiperemia limbal dan konjungtiva, edema kornea, BMD dangkal dengan flare dan cell, iris bomban tanpa adanya rubeosis iridis, pupil dilatasi bulat lonjong vertical reflex negative, lensa posisi normal tidak didapatkan katarak, IOP sangat tinggi, sudut BMD tertutup.

Diagnosis Banding :
1. Glaukoma sudut tertutup sekunder karena kelainan lensa :
- Glaukoma Fakomorfik ( lensa yang membesar )
- Glaukoma Ektopia lentis anterior
2. Glaukoma sudut tertutup sekunder karena blok pupil akibat inflamasi intra ocular.
3. Glaukoma sudut tertutup sekunder karena rubeosis iridis ( glaucoma neovaskuler)
4. Glaukoma maligna

Penatalaksanaan :
a. Segera turunkan IOP
1. Hiperosmotik : Glycerin 1,5 gr/kg.BB. 50% larutan dapat dicampur dengan sari jeruk, bila sangat mual dapat diganti dengan Manitol 1 – 1,5 gr/kg.BB , 20% larutan intravena ( dalam infuse 3-5 cc/menit = 60-100 tetes/menit
( hati-hati pada orang tua, penderita penyakit jantung, ginjal dan hati )
2. Acetazolamide 500 mg intravena bila IOP sangat tinggi atau 500 mg oral dilanjutkan 250 mg sehari 4 kali. ( hati-hati pada : penderita batu ginjal, obstruksi paru menahun dan gangguan fungsi hati)
b. Menekan Reaksi radang : steroid topical, prednisolone 1% atau dexamethasone 0,1% sehari 4 kali
c. Penderita dalam posisi “supine” untuk memudahkan lensa bergerak ke posterior mengikuti dehidrasi vitreous akibat hiperosmotik agar sudut dapat terbuka.
d. Sesudah ± 1 jam, periksa IOP dan BMD
1. Pada umumnya IOP sudah mulai turun dan bila sudah < 40 mmHg, beri pilocarpine 2% dan setelah ½ jam bila IOP tetap turun dan sudut mulai terbuka beri pilocarpine 1% sehari 4 kali
Pilocarpine tidak perlu diberi secara “intensive”, bila kondisi mata sudah mulai tenang terutama bila kornea sudah jernih, dilakukan laser iridotomi (laser peripheral iridotomi = laser PI) atau Bedah iridektomi perifer (bedah IP)
2. Bila IOP tetap tinggi dan sudut tetap tertutup, harus dipikirkan kemungkinan glaucoma sudut tertutup karena kelainan lensa jangan diberi pilocarpine, akan menambah lensa bergerka ke depan, kemudian timbul blok pupil. Siapkan untuk dilakukan Argon Laser Peripheral Iridoplasty (ALPI) yang mnegkerutkan iris perifer sehingga sudut terbuka. IOP turun kondisi mata menjadi tenang (2-3 hari) untuk selanjutnya dilakukan laser PI.
e. Pasca Laser PI atau bedah IP
Gonikoskopi :
1. Sudut terbuka; pilocarpine diteruskan sampai tampak jelaslubang IP, Timolol dan prednisolone atau dexamethasone diteruskan sampai kondisi mata tenang (bebas dari inflamasi)
2. Sudut tetap tertutup; dengan Glaukoma plateau iris, Glaukoma ektopia lentis anterior, Glaukoma maligna.
f. Untuk mata Jiran ( fellow eye)
Sementara Pilocarpine 1% sehari 4 kali sampai saat terbaik untuk dilakukan laser atau bedah IP.
Pilocarpine pada mata jiran dalam jangka waktu lama tidak dianjurkan.

Glaucoma

Glaucoma
Glaucoma is a disease that affects the optic nerve and involves loss of retinal ganglion cells in a characteristic pattern. There are many different sub-types of glaucoma but they can all be considered as a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma (above 22 mmHg or 2.9 kPa). One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.
Glaucoma can be divided roughly into two main categories, "open angle" and "closed angle" glaucoma. Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open angle, chronic glaucoma tends to progress more slowly and the Glaucoma has been nicknamed the "sneak thief of sight" because the loss of vision normally occurs gradually over a long period of time and is often only recognized when the disease is quite advanced. Once lost, this damaged visual field can never be recovered. Worldwide, it is the second leading cause of blindness.[1] Glaucoma affects 1 in 200 people aged fifty and younger, and 1 in 10 over the age of eighty. If the condition is detected early enough it is possible to arrest the development or slow the progression with medical and surgical means.
Signs and symptoms
There are rarely any symptoms in the early stages of the disease so regular eye checks by qualified professionals are important. Ophthalmologists and optometrists will diagnose glaucoma on the basis of intraocular pressure, visual field tests and optic nerve head appearance.
Patients will sometimes notice patchy loss of peripheral vision or reduced clarity of colours and these people may benefit from a review by an eye specialist.
Symptoms of angle closure glaucoma can include pain in or around the eye ball, headache, nausea / vomiting and visual disturbances e.g halos around lights. In some cases there are no symptoms.
Pathophysiology
The major risk factor for most glaucomas and focus of treatment is increased intraocular pressure. Intraocular pressure is a function of production of liquid aqueous humor by the ciliary processes of the eye and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here the trabecular meshwork drains aqueous humor via Schlemm's canal into scleral plexuses and general blood circulation.[2] In open angle glaucoma there is reduced flow through the trabecular meshwork;[3] in angle closure glaucoma, the iris is pushed forward against the trabecular meshwork, blocking fluid from escaping.
The inconsistent relationship of glaucomatous optic neuropathy with ocular hypertension 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, and aging mechanisms of neuron loss.[4][5][6][7][8][9][10][11][12][13][14]
The major types of glaucoma are discussed below.
Causes
This article may require cleanup to meet Wikipedia's quality standards. Please improve this article if you can. (April 2008)



A normal range of vision. Courtesy NIH National Eye Institute


The same view with advanced vision loss from glaucoma.
Ocular hypertension (increased pressure within the eye) is the largest risk factor in most glaucomas, but in some populations only 50% of patients with primary open angle glaucoma actually have elevated ocular pressure.[15]
Those of African descent are three times more likely to develop primary open angle glaucoma. People who are older, have thinner corneal thickness, and myopia also are at higher risk for primary open angle glaucoma. People with a family history of glaucoma have about a six percent chance of developing glaucoma.
Many East Asian groups are prone to developing angle closure glaucoma due to their shallower anterior chamber depth, with the majority of cases of glaucoma in this population consisting of some form of angle closure.[16] Inuit also have a twenty to forty times higher risk than Caucasians of developing primary angle closure glaucoma. Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallower anterior chambers.
Other factors can cause glaucoma, known as "secondary glaucomas," including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle recession glaucoma); and uveitis (uveitic glaucoma).
Primary open angle glaucoma (POAG) has been found to be associated with mutations in genes at several loci [17]. Normal tension glaucoma, which comprises one third of POAG, is associated with genetic mutations.[18]
There is increasing evidence that ocular blood flow is involved in the pathogenesis of glaucoma. Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.
A number of studies also suggest a possible correlation between hypertension and the development of glaucoma. In normal tension glaucoma, nocturnal hypotension may play a significant role.
There is no clear evidence that vitamin deficiencies cause glaucoma in humans. It follows then that oral vitamin supplementation is probably not useful in glaucoma treatment.[19]
Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally, failure of the normal third trimester gestational atrophy of the hyaloid canal and the tunica vasculosa lentis is associated with other anomalies. Angle closure induced ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies.[20][21][22] and modelled in mice [23].
Those at risk for glaucoma are advised to have a dilated eye examination at least once a year.[24]
Diagnosis
Screening for glaucoma is usually performed as part of a standard eye examination performed by ophthalmologists and optometrists. Testing for glaucoma should include measurements of the intraocular pressure via tonometry, changes in size or shape of the eye, anterior chamber angle examination or gonioscopy, and examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc ratio and also rim appearance and vascular change. A formal visual field test should be performed. The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence tomography (OCT), scanning laser polarimetry (GDx), and/or scanning laser ophthalmoscopy also known as Heidelberg Retina Tomography (HRT3).[25][26] Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as Goldmann tonometry should be augmented with pachymetry to measure 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 Frequency Doubling Illusion can also be used to detect glaucoma with the use of a Frequency Doubling Technology (FDT) perimeter.[27] Examination for glaucoma also could be assessed with more attention given to sex, race, history of drugs use, refraction, inheritance and family history.[25]
Management
The modern goals of glaucoma management are to avoid glaucomatous damage, preserve visual field and total quality of life for patients with minimal side effects.[28][29] 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
Intraocular pressure can be lowered with medication, usually eye drops. There are several different classes of medications to treat glaucoma with several different 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 these, 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.[30]
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 HMO found that half failed to fill their prescription the first time and one in four failed to refill their prescriptions a second time.[31] 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.[19][32][33][34]
Commonly used medications
• Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow
• Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan), and betaxolol decrease aqueous humor production by the ciliary body.
• Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism, decreasing aqueous production and increasing trabecular outflow.
• Less-selective sympathomimetics like epinephrine and dipivefrin (Propine) increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action.
• Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous humour. Ecothiopate is used in chronic glaucoma.
• Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.
• Physostigmine is also used to treat glaucoma and delayed gastric emptying.
Surgery


Conventional surgery to treat glaucoma makes a new opening in the meshwork. This new opening helps fluid to leave the eye and lowers intraocular pressure.
Main article: Glaucoma surgery
Both laser and conventional surgeries are performed to treat glaucoma.
Surgery is the primary therapy for those with congenital glaucoma.[35]
Generally, these operations are a temporary solution, as there is not yet a cure for glaucoma.
Canaloplasty
Canaloplasty is a nonpenetrating procedure utilizing microcatheter technology. To perform a canaloplasty, an incision is made into the eye to gain access to 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.[36][37]
Laser surgery
Laser trabeculoplasty may be used to treat open angle glaucoma. It is a temporary solution, not a cure. A 50 μm argon laser spot is aimed at the trabecular meshwork to stimulate opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty utilizes a thermal argon laser. The procedure is called Argon Laser Trabeculoplasty or ALT. A newer type of laser trabeculoplasty exists that uses a "cold" (non-thermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure which uses a 532 nm frequency-doubled, Q-switched Nd:YAG laser which selectively targets melanin pigment in the trabecular meshwork cells, called Selective Laser Trabeculoplasty or SLT. Studies show that 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 or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make a small full-thickness opening in the iris. This opening equalizes the pressure between the front and back of the iris 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.[25]
Trabeculectomy
The most common conventional surgery performed for glaucoma is the trabeculectomy. Here, a partial thickness flap is made in the scleral wall of the eye, and a window opening made under the flap to remove a portion of the trabecular meshwork. The scleral flap is then sutured loosely back in place. This allows 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. One person can have multiple surgical procedures of the same or different types.
Glaucoma drainage implants
There are also several different glaucoma drainage implants. These include the original Molteno implant (1966), 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 flow of aqueous fluid out of the eye into a chamber called a bleb.
• The first-generation Molteno and other non-valved implants sometimes require the ligation of the tube until the bleb formed is mildly fibrosed and water-tight[38] This is done to reduce postoperative hypotony—sudden drops in postoperative intraocular pressure (IOP).
• Valved implants such as the Ahmed glaucoma valve attempt to control postoperative hypotony by using a mechanical valve.
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 anti-fibrotic medication like 5-fluorouracil (5-FU) or mitomycin-C (during the procedure), or additional surgery. And for Glaucomatous painful Blind Eye and some cases of Glaucoma, Cyclocryotherapy for ciliary body ablation could be considered to be performed.[25]
Veterinary implant
TR BioSurgical has commercialized a new implant specifically for veterinary medicine, called TR-ClarifEYE. The implant consists of a new biomaterial, the STAR BioMaterial, which consists of silicone with a very precise homogenous pore size, a property which reduces fibrosis and improves tissue integration. The implant contains no valves and is placed completely within the eye without sutures. To date, it has demonstrated long term success (> 1yr) in a pilot study in medically refractory dogs with advanced glaucoma [39]
Laser assisted non penetrating deep sclerectomy
The most common surgical approach currently used for the treatment of glaucoma, is trabeculectomy, in which the sclera is punctured to alleviate inner eye pressure (IOP). Non-penetrating deep sclerectomy (NPDS) surgery is a similar but modified procedure, in which instead of puncturing the scleral wall, a patch of the sclera is skimmed to a level, upon which, percolation of liquid from the inner eye is achieved and thus alleviating IOP, without penetrating the eye. NPDS is demonstrated to cause a significantly less side effects than trabeculectomy.[citation needed] However, NPDS is performed manually and requires great skill to achieve a lengthy learning curve.[citation needed]
Laser assisted NPDS is the performance of NPDS with the use of a CO2 laser system. The laser-based system is self-terminating once the required scleral thickness and adequate drainage of the intra ocular fluid have been achieved. This self-regulation effect is achieved as the CO2 laser essentially stops ablating as soon as it comes in contact with the intra-ocular percolated liquid, which occurs as soon as the laser reaches the optimal residual intact layer thickness.
Epidemiology


Disability-adjusted life year for glaucoma per 100,000 inhabitants in 2002.[40]
no data less than 25 25-50 50-75 75-100 100-125 125-150 150-175 175-200 200-225 225-250 250-350 more than 350
Research
• Advanced Glaucoma Intervention Study (AGIS) - large American National Eye Institute (NEI) sponsored study designed "to assess the long-range outcomes of sequences of interventions involving trabeculectomy and argon laser trabeculoplasty in eyes that have failed initial medical treatment for glaucoma." It recommends different treatments based on race.
• Early Manifest Glaucoma Trial (EMGT) -Another NEI study found that immediately treating people who have early stage glaucoma can delay progression of the disease.
• Ocular Hypertension Treatment Study (OHTS) -NEI study findings: "...Topical ocular hypotensive medication was effective in delaying or preventing onset of Primary Open Angle Glaucoma (POAG) in individuals with elevated Intraocular Pressure (IOP). Although this does not imply that all patients with borderline or elevated IOP should receive medication, clinicians should consider initiating treatment for individuals with ocular hypertension who are at moderate or high risk for developing POAG."
• Blue Mountains Eye Study "The Blue Mountains Eye Study was the first large population-based assessment of visual impairment and common eye diseases of a representative older Australian community sample." Risk factors for glaucoma and other eye disease were determined.
Compounds in research
Natural compounds
Natural compounds of research interest in glaucoma prevention or treatment include: fish oil and omega 3 fatty acids, bilberries, vitamin E, cannabinoids, carnitine, coenzyme Q10, curcurmin, Salvia miltiorrhiza, dark chocolate, erythropoietin, folic acid, Ginkgo biloba, Ginseng, L-glutathione, grape seed extract, green tea, magnesium, melatonin, methylcobalamin, N-acetyl-L cysteine, pycnogenols, resveratrol, quercetin and salt.[32][33][34] Magnesium, ginkgo, salt and fludrocortisone, are already used by some physicians.
Cannabis
Studies in the 1970s showed that marijuana, when smoked, effectively lowers intraocular pressure. [41] In an effort to determine whether marijuana, or drugs derived from marijuana, might be effective as a glaucoma treatment, the US National Eye Institute supported research studies from 1978 to 1984. These studies demonstrated that some derivatives of marijuana lowered intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied to the eye. Many of these studies demonstrated that marijuana — or any of its components — could safely and effectively lower intraocular pressure more than a variety of drugs then on the market.
In 2003 the American Academy of Ophthalmology released a position statement which said that "studies demonstrated that some derivatives of marijuana did result in lowering of IOP when administered orally, intravenously, or by smoking, but not when topically applied to the eye. The duration of the pressure-lowering effect is reported to be in the range of 3 to 4 hours".[41][42]
However, the position paper qualified that by stating that marijuana was not more effective than prescription medications, stating that "no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of marijuana use to treat glaucoma compared with the wide variety of pharmaceutical agents now available."
The first patient in the United States federal government's Compassionate Investigational New Drug program, Robert Randall, was afflicted with glaucoma and had successfully fought charges of marijuana cultivation because it was deemed a medical necessity (U.S. v. Randall) in 1976.[43]
5-HT2A agonists
Peripherally selective 5-HT2A agonists such as the indazole derivative AL-34662 are currently under development and show significant promise in the treatment of glaucoma.[44][45]
Classification of glaucoma
Glaucoma has been classified into specific types:[46]
Primary glaucoma and its variants (H40.1-H40.2)
• Primary glaucoma
• Primary angle-closure glaucoma, also known as primary closed-angle glaucoma, narrow-angle glaucoma, pupil-block glaucoma, acute congestive glaucoma
• Acute angle-closure glaucoma
• Chronic angle-closure glaucoma
• Intermittent angle-closure glaucoma
• Superimposed on chronic open-angle closure glaucoma ("combined mechanism" - uncommon)
• Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple glaucoma, glaucoma simplex
• High-tension glaucoma
• Low-tension glaucoma
• Variants of primary glaucoma
• Pigmentary glaucoma
• Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare
Primary angle-closure glaucoma - This is caused by contact between the iris and trabecular meshwork, which in turn obstructs outflow of the aqueous humor from the eye. This contact between iris and trabecular meshwork (TM) may 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 headache and vomiting. Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, pain. However, the majority of cases are asymptomatic. Prior to 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 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 - Optic nerve damage resulting in progressive visual field loss[47]. 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 blockage which is where the aqueous humor in the eye drains out. Because the microscopic passage ways 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. Prostoglandin 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 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 (Q15.0)
• Developmental glaucoma
• Primary congenital glaucoma
• Infantile glaucoma
• Glaucoma associated with hereditary of familial diseases
Secondary glaucoma (H40.3-H40.6)
• Secondary glaucoma
• 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 is an uncommon type of glaucoma that is difficult or nearly impossible to treat. This condition 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. Patients with such condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, specially after cataract surgery procedure. A new treatment for this disease, as first reported by Kahook and colleagues, involves 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.
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) reports on four patients who had toxic glaucoma. One of them underwent phaecoemulsification 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.[48]
1. ^ Health Guide: A New Understanding of Glaucoma, New York Times, July 15, 2009
2. ^ a b Ritch R (June 2007). "Natural compounds: evidence for a protective role in eye disease". Can J Ophthalmol. 42 (3): 425–38. doi:10.3129/I07-044. PMID 17508040.
3. ^ a b Tsai JC, Song BJ, Wu L, Forbes M (September 2007). "Erythropoietin: a candidate neuroprotective agent in the treatment of glaucoma". J Glaucoma 16 (6): 567–71. doi:10.1097/IJG.0b013e318156a556. PMID 17873720.
4. ^ a b Mozaffarieh M, Flammer J (November 2007). "Is there more to glaucoma treatment than lowering IOP?". Surv Ophthalmol 52 (Suppl 2): S174–9. doi:10.1016/j.survophthal.2007.08.013. PMID 17998043.
5. ^ Online 'Mendelian Inheritance in Man' (OMIM) Glaucoma, Congenital: GLC3 Buphthalmos -231300
6. ^ Shingleton B, Tetz M, Korber N (March 2008). "Circumferential viscodilation and tensioning of Schlemm canal (canaloplasty) with temporal clear corneal phacoemulsification cataract surgery for open-angle glaucoma and visually significant cataract: one-year results". J Cataract Refract Surg 34 (3): 433–40. doi:10.1016/j.jcrs.2007.11.029. PMID 18299068. http://www.jcrsjournal.org/article/S0886-3350(08)00004-7/abstract.
7. ^ Lewis RA, von Wolff K, Tetz M, et al. (July 2007). " Pediatric Glaucoma and Cataract Family Association

Neovascular Glaucoma

Glaucoma, Neovascular
Background
Neovascular glaucoma (NVG) is classified as a secondary glaucoma. First documented in 1871, historically, it has been referred to as hemorrhagic glaucoma, thrombotic glaucoma, congestive glaucoma, rubeotic glaucoma, and diabetic hemorrhagic glaucoma. Numerous secondary ocular and systemic diseases that share one common element, retinal ischemia/hypoxia and subsequent release of an angiogenesis factor, cause NVG. This angiogenesis factor causes new blood vessel growth from preexisting vascular structure. Depending on the progression of NVG, it can cause glaucoma either through secondary open-angle or secondary closed-angle mechanisms. This is accomplished through the growth of a fibrovascular membrane over the trabecular meshwork in the anterior chamber angle, resulting in obstruction of the meshwork and/or associated peripheral anterior synechiae.
NVG is a potentially devastating glaucoma, where delayed diagnosis or poor management can result in complete loss of vision or, quite possibly, loss of the globe itself. Early diagnosis of the disease, followed by immediate and aggressive treatment, is imperative. In managing NVG, it is essential to treat both the elevated intraocular pressure (IOP) and the underlying cause of the disease.
Pathophysiology
Retinal ischemia is the most common and important mechanism in most, if not all, cases that result in the anterior segment changes causing NVG. Various predisposing conditions cause retinal hypoxia and, consequently, production of an angiogenesis factor.
Several angiogenesis factors have been identified as potential agents causing ocular neovascularization. Recent studies suggest that vascular endothelial growth factor (VEGF) might play a central role in angiogenesis.
Once released, the angiogenic factor(s) diffuses into the aqueous and the anterior segment and interacts with vascular structures in areas where the greatest aqueous-tissue contact occurs. The resultant growth of new vessels at the pupillary border and iris surface (neovascularization of the iris [NVI]) and over the iris angle (neovascularization of the angle [NVA]) ultimately leads to formation of fibrovascular membranes. The fibrovascular membranes, which may be invisible on gonioscopy, accompany NVA and progressively obstruct the trabecular meshwork. This causes secondary open-angle glaucoma.
As the disease process continues, the fibrovascular membranes along the NVA tend to mature and contract, thereby tenting the iris toward the trabecular meshwork and resulting in peripheral anterior synechiae and progressive synechial angle closure. Elevated IOP is a direct result of this secondary angle-closure glaucoma.
Frequency
United States
Incidence of NVG is rare.
Mortality/Morbidity
Treatment of NVG is difficult. Maintaining visual acuity in patients with NVG also is difficult.
Age
NVG is more prevalent in elderly patients.
Clinical
History
A careful and detailed ocular and systemic history is imperative in diagnosing both NVG and the underlying problem causing it.
Physical
A complete ocular examination of both eyes, particularly of the posterior segment, will almost certainly provide the etiology of neovascularization. Of the 3 most common causes of NVG, ocular ischemic syndrome presents as a diagnostic dilemma and, thus, deserves special mention.
The typical clinical presentation of NVG is the same regardless of the underlying cause. The typical clinical presentation can be divided into the following 2 stages: the early stage and the advanced stage. These stages generally follow each other in progression, and the early stage is subdivided further into rubeosis iridis and secondary open-angle glaucoma.
• Early stage (rubeosis iridis)
o Normal IOP
o Presence of tiny, neovascular, dilated capillary tufts at pupillary margin
o High magnification on slit lamp (to view earliest finding in NVG)
o NVI (irregular, nonradial vessels usually not in the iris stroma)
o NVA (can occur with or without NVI)
o Careful gonioscopy in all eyes at high risk for NVG even without pupillary and iris involvement
o Poorly reactive pupil
o Ectropion uvea
• Early stage (secondary open-angle glaucoma)
o Elevated IOP
o NVI continuous with NVA
o Proliferation of neovascular tissue over the angle
o Fibrovascular membranes (develop circumferentially across the angle, blocking the trabecular meshwork)
• Advanced stage: In this stage, secondary angle-closure glaucoma is characterized by some or all of the following:
o Acute severe pain, headache, nausea, and/or vomiting
o Photophobia
o Reduced visual acuity (counting fingers to hand motion)
o Elevated IOP (¡Ý60 mm Hg)
o Conjunctival injection
o Corneal edema
o Plus/minus hyphema
o Aqueous flare
o Synechial angle closure
o Severe rubeosis
o Distorted, fixed, mid-dilated pupil and ectropion uveae
o Retinal neovascularization and/or hemorrhage
o Optic nerve cupping (possibly)
• Ocular ischemic syndrome
o Ocular ischemic syndrome occurs in the presence of more than 90% of patients with carotid artery stenosis, but it can occur as a result of aortic arch disease (eg, syphilis, Takayasu arteritis, dissecting aneurysm), in which case the presentation may be bilateral.
o Symptoms include a dull periocular/periorbital pain that can be secondary to the ischemia and/or NVG.
o Signs include the following:
 Vision can vary from 20/20 to no light perception.
 Midperipheral intraretinal hemorrhage (in contrast to diabetic retinopathy and CRVO where the hemorrhage is mostly situated in the posterior pole)
 IOP can be elevated secondary to NVG, decreased secondary to ciliary body hypoperfusion, or normal as a result of both processes.
 Other signs include corneal decompensation, iritis, iris atrophy, cataract, and spontaneous pulsations of the central retinal artery.
 Intravenous fluorescein angiogram will demonstrate prolonged choroidal filling and increased arteriovenous transit time.
Causes
• Relatively frequent causes of NVG include the following:
o Central retinal vein occlusion (CRVO)
o Proliferative diabetic retinopathy
o Carotid artery occlusive disease (CAOD)
• Less frequent causes of NVG include the following:
o Branch retinal vein occlusion
o Central retinal artery occlusion (CRAO)
o Intraocular tumor
o Chronic retinal detachment
o Secondary to intraocular lens (uveitis-glaucoma-hyphema [UGH] syndrome)
o Chronic or severe ocular inflammation
o Endophthalmitis
o Sickle cell retinopathy
o Retinopathy of prematurity
o Radiation retinopathy
o Eales disease
o Coats disease
o Carotid-cavernous fistula
o Ocular ischemic syndrome/carotid insufficiency
o Takayasu disease
o Giant cell arteritis
o Anterior segment ischemia (ie, previous extraocular muscle surgery)
o Trauma

Differential Diagnoses
Glaucoma, Angle Closure, Acute
Other Problems to Be Considered
Inflammatory glaucoma
Fuchs heterochromic iridocyclitis
Workup
Imaging Studies
• Intravenous fluorescein angiogram and electroretinography (ERG) to assess retinal ischemia
• B-scan ultrasound
Treatment
Medical Care
• General principles for treating patients with NVG include the following:
o Identifying the underlying etiology is fundamental in the management of NVG.
o CRVO, diabetic retinopathy, CAOD, and CRAO require systemic workup and appropriate intervention to prevent further complications.
o The management of NVG is approached through the following 4 stages that reflect the progression of the disease: prophylactic treatment, early-stage treatment, advanced-stage treatment, and end-stage treatment.
• Prophylactic treatment
o Most patients are either at high risk for developing NVI/NVG or have early NVI with normal IOP. Prevention of NVG is the single most important aspect in its management.
o Reducing the amount of viable retina is known to inhibit and even to reverse new vessel proliferation in the anterior segment. The mainstay in prevention is retinal ablation achieved via panretinal photocoagulation (PRP) or cryophototherapy because of media opacities (ie, corneal edema, cataract, vitreous hemorrhage) or other patient factors. Other treatment options in this stage include goniophotocoagulation.
o PRP can be delivered in the following 3 ways: slit lamp delivery system, indirect laser, or endolaser at time of vitrectomy.
o The amount of PRP required varies. The Diabetic Retinopathy Study (DRS) guidelines recommend 1200-1500 burns, with a spot size of 500 µm to be applied to the peripheral retina. Many retina specialists recommend 1500-2000 burns, with a spot size of 500-800 µm, using a wide-angle fundus contact lens (eg, Rodenstock). The types of laser include argon, krypton (better with media opacities and retinal hemorrhages), and diode (same utility as krypton laser).
o To begin, a 360° peritomy is performed with isolation of the 4 recti muscles. A 2.5-mm retinal cryoprobe is used to create cryoapplication burns just anterior to the equator. Three spots are placed between each rectus muscle. Two additional rows of application are performed posterior to the first so that the third row is just outside the major vascular arcades. In total, 32 cryoapplications are performed under direct visualization. The probe tip remains in contact with the sclera until 70° has been maintained for 5-10 seconds. This procedure causes considerable inflammation, and complications (eg, tractional and exudative retinal detachment, vitreous hemorrhage) can occur.
o Goniophotocoagulation, another laser therapy, is performed directly to NVI before the development of NVG. Its role in management of NVG is unclear, and it has not proven to be beneficial in preventing synechial closure of angle or advanced NVG.
o All patients should undergo fluorescein angiography to delineate nonischemic CRVO from ischemic CRVO. Virtually no patients with nonischemic CRVO develop NVG. Overall incidence of NVG is 40% for an ischemic CRVO. NVI and NVG can appear from 2 weeks to 2 years. More than 80% of patients with NVI/NVG present within the first 6 months. Fifteen percent of patients with nonischemic CRVO can convert to ischemic CRVO within 8 months. The strongest predictors of NVI/NVG following CRVO include extensive retinal capillary nonperfusion of intravenous fluorescein angiography (IVFA), extensive retinal hemorrhages, short duration of occlusion, and male sex. In the Central Retinal Vein Occlusion Study, PRP was indicated for IVFA confirmed ischemic CRVO if development of 2 clock hours of NVI occurred or any NVA was present. No benefit occurred when prophylactic PRP was performed prior to the development of NVI or NVA when frequent follow-up care was provided.
o Prophylactic PRP still is recommended by many retinal specialists before the development of NVI or NVA, especially in case of the following: clear extensive capillary nonperfusion, extensive systemic vascular disease, patient who is monocular, and/or noncompliance or poor follow-up results. Preoperative care is fundamental for all types of cataract surgery, capsulotomy, and vitreous surgery.
o For patients with diabetic retinopathy, ensure frequent follow-up care and tight glycemic control. If proliferative diabetic retinopathy exists, then complete PRP is recommended as treatment.
• Early-stage treatment: This stage is characterized by the development of a fibrovascular membrane across some or all of the angle, obstructing the trabecular meshwork, and an increase in IOP.
o With secondary open-angle glaucoma, treatment is identical to prophylactic treatment and includes PRP (filler PRP if already performed initially), panretinal cryotherapy, and medical therapy.
o The most important medical therapy for this stage includes topical atropine 1% to decrease ocular congestion and topical steroids (eg, Pred Forte, Inflamase Forte) to decrease inflammation. Standard antiglaucoma medications to treat secondary open-angle glaucoma are recommended. Other agents include topical beta-blockers (eg, Betagan, Timoptic), topical brimonidine (eg, Alphagan), topical carbonic anhydrase inhibitor (eg, Trusopt, Azopt), and oral carbonic anhydrase inhibitor (eg, Diamox). Topical pilocarpine is contraindicated because it may increase inflammation. The role of topical latanoprost (eg, Xalatan) is unclear in the treatment of early NVG.
o The successful use of photodynamic therapy with verteporfin directed at the iris and the angle to obliterate neovascularization and to reduce IOP has been reported.
• Advanced-stage treatment: This stage is characterized by synechial closure of the angle and secondary angle-closure glaucoma.
o PRP is still the initial and most important treatment, both to prevent further NVI/NVA and angle closure and to prepare the eye for surgical intervention (see Surgical Care). Surgical intervention is indicated in eyes with potential for useful vision.
o Medical therapy is indicated, with topical atropine and steroids being the most important agents. Antiglaucoma medications, topical beta-blockers, and carbonic anhydrase inhibitors also are recommended. The role of topical brimonidine and latanoprost in advanced disease is unclear. Topical pilocarpine and echothiophate iodide are contraindicated (may cause increased inflammation and hyperemia). Oral glycerol and intravenous mannitol are recommended only if IOP is elevated symptomatically.
• End-stage treatment: This stage is characterized by complete angle closure by peripheral anterior synechiae with no remaining useful vision.
o The primary goal of treatment in this stage is pain control. Medical therapy includes topical atropine 1% and steroids. If corneal decompensation occurs, use a bandage contact lens. Cyclodestructive procedures are performed if medical therapy fails to provide symptomatic relief. With cyclocryotherapy, the IOP-lowering effect is achieved by destroying secretory ciliary epithelium and/or reducing blood flow to the ciliary body. It is indicated as a last resort only if relief of pain is the main goal. In a large series, 34% of eyes achieved IOP of less than 25 mm Hg; however, 34% of eyes became phthisical and 57% of eyes lost all light perception. Other complications include sympathetic ophthalmia and anterior segment ischemia.
o With Nd:YAG laser transscleral cyclophotocoagulation, 2 approaches, contact and noncontact, are used. In the contact approach, one study reported a 40% decrease in IOP to less than 19 mm Hg in eyes with NVG. In the noncontact approach, out of 27 eyes with NVG, only 15% achieved satisfactory IOP control.
o The results of diode laser transscleral cyclophotocoagulation are similar to Nd:YAG cyclophotocoagulation.
o Direct laser cyclophotocoagulation is performed under direct observation using the argon laser. Two approaches, transpupil or with endoscopy, are used. Its role in NVG management is secondary. Success in controlling IOP is limited (may have less inflammation and pain versus cyclocryotherapy).
o Retrobulbar alcohol injection is indicated after all medical and surgical options have been explored and the patient does not want an enucleation. Complications include external ophthalmoplegia and blepharoptosis. Enucleation is indicated only if intractable pain is not relieved by any other treatment modality.
Surgical Care
Surgical care is indicated in patients with remaining useful vision. Preoperative care is fundamental to the postoperative success of any surgical intervention.
• With surgical care, ensure that adequate PRP is completed to reduce vasoproliferative stimulus. Atropine and steroids are indicated to decrease inflammation, and antiglaucoma medication is indicated to decrease IOP. Wait approximately 3-4 weeks to allow the eye to quiet down.
• Surgical modalities include trabeculectomy with or without an antifibrotic agent and valve implant surgery.
o Trabeculectomy with the antifibrotic agents mitomycin-C and 5-fluorouracil (5-FU) is one modality. Trabeculectomy in NVG has a significant failure rate. Using standard trabeculectomy (without antifibrosis), an IOP of less than 25 mm Hg on one medication or less has been reported to occur in 67-100% of patients in 3 studies. Using injections of 5-FU subconjunctivally in the postoperative period, the surgical success has been reported to be 68% over 3 years. Inject 0.1 mL of 5 mg/mL 5-FU subconjunctivally either superiorly above the bleb or inferiorly (just above the lower fornix). Mitomycin-C used intraoperatively has been shown to be more effective than 5-FU in routine trabeculectomies. No significant follow-up studies exist on the use of mitomycin-C with trabeculectomy in NVG.
o Valve implant surgery is another modality and is indicated when trabeculectomy fails or extensive conjunctival scarring exists, thereby preventing a standard filtering procedure. Molteno, Krupin, and Ahmed valve implants commonly are used. One large series using the Krupin valve reported 79% of eyes with NVG had a 67% success rate in controlling IOP (<24 mm Hg) with mean follow-up of 23 months. Long-term results are mixed. Using the Molteno implant, 60 eyes with NVG achieved a satisfactory IOP (<21 mm Hg) and maintenance of visual acuity over 5 years of only 10.3%. If combined with the need for vitrectomy, consideration of pars plana tube-shunt insertion may reduce anterior segment complications.
o Complications include postoperative hypotony with associated complications, blockage of internal fistula, blockage of external filtration site (fibrosis of the filtering bleb), and corneal endothelial loss.
Medication
The most important medications include a regimen of topical steroids and atropine. Antiglaucoma medications include both topical and oral agents.
Cycloplegic drugs
Paralyze ciliary muscle, preventing ciliary muscle spasm; provide pain relief; and decrease ocular congestion.

Atropine sulfate 1% (Isopto, Atropair, Atropisol)
Acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to acetylcholine, causing mydriasis and cycloplegia.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt to affected eye bid/qid
Pediatric
Administer as in adults
• Dosing
• Interactions
• Contraindications
• Precautions
Coadministration with other anticholinergics have additive effects; pharmacologic effects of atenolol and digoxin may increase with atropine; antipsychotic effects of phenothiazines may decrease with this medication; tricyclic antidepressants with anticholinergic activity may increase effects of atropine
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity; asthma; obstructive uropathy; paralytic ileus; toxic megacolon; myasthenia gravis
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in patients with Down syndrome and/or children with brain damage to prevent hyperreactive response; caution in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, hypertension, peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization
Steroidal anti-inflammatory
Decreases ocular inflammation.

Prednisolone acetate 1% (Pred Forte)
Treats acute inflammations following eye surgery or other types of insults to eye. Decreases inflammation and corneal neovascularization. Suppresses migration of polymorphonuclear leukocytes and reverses increased capillary permeability. In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt to affected eye qid; taper dosage to clinical severity and response
Pediatric
Administer as in adults
• Dosing
• Interactions
• Contraindications
• Precautions
None reported
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity; ocular fungal infections; ocular viral infections; ocular tuberculosis
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in hypertension; known to cause cataract formation with chronic use; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate); concurrent contact lens wear may increase risk of infection; may delay healing if corneal abrasion is present
Alpha2-adrenergic agonists
Decrease IOP by reducing aqueous humor production.

Brimonidine tartrate 0.5% (Alphagan)
Selective alpha2-receptor that reduces aqueous humor formation.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt to affected eye bid
Pediatric
Not established
• Dosing
• Interactions
• Contraindications
• Precautions
Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants, such as barbiturates, opiates, and sedatives, may potentiate effects of brimonidine
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity; MAOIs
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack, and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy
Carbonic anhydrase inhibitors
By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic anhydrase in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.

Dorzolamide hydrochloride 2.0% (Trusopt)
Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt to affected eye bid/tid
Pediatric
Not established
• Dosing
• Interactions
• Contraindications
• Precautions
Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral carbonic anhydrase inhibitors
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy)

Acetazolamide (Diamox, Diamox Sequels)
Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
250 mg PO qid; 500 mg PO bid; one 500 mg PO dose, followed by 250 mg PO qid
Pediatric
8-30 mg/kg/d or 300-900 mg/m2/d PO divided q8h
Alternatively, 20-40 mg/kg/d PO divided q6h; not to exceed 1 g/d
• Dosing
• Interactions
• Contraindications
• Precautions
Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine; may affect elimination rates of certain drugs cleared by renal elimination; may result in anorexia, tachypnea, lethargy, coma, and death if taken concomitantly with high-dose aspirin
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity; hypokalemia; depressed renal or hepatic function; hyperchloremic acidosis; long-term use in chronic noncongestive angle-closure glaucoma
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some patients with diabetes
Prostaglandins
Used to reduce IOP in patients who are intolerant or resistant to other IOP-lowering medications. They are contraindicated in glaucomas in which inflammation is a prominent ocular finding.

Bimatoprost (Lumigan)
Prostaglandin analog that selectively mimics effects of naturally occurring substances, prostamides. Exact mechanism of action unknown but believed to reduce IOP by increasing outflow of aqueous humor through trabecular meshwork and uveoscleral routes.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt of 0.03% solution in affected eye(s) hs; not to exceed 1 dose/d
Pediatric
Not established
• Dosing
• Interactions
• Contraindications
• Precautions
None reported
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
High incidence of hyperemia; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; bacterial keratitis may occur; caution in uveitis or macular edema; do not instill if wearing contact lenses

Travoprost ophthalmic solution (Travatan)
Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but believed to reduce IOP by increasing uveoscleral outflow.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt in affected eye(s) hs; not to exceed 1 dose/d
Pediatric
Not established
• Dosing
• Interactions
• Contraindications
• Precautions
None reported
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity; pregnancy
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Commonly causes ocular hyperemia; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; bacterial keratitis may occur; caution in uveitis or macular edema; do not instill if wearing contact lenses

Unoprostone ophthalmic solution (Rescula)
Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but believed to reduce IOP by increasing uveoscleral outflow and facilitating conventional outflow through the trabecular meshwork
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt in affected eye(s) bid
Pediatric
Not established
• Dosing
• Interactions
• Contraindications
• Precautions
None reported
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Well tolerated ocularly; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; may cause bacterial keratitis; caution in uveitis or macular edema; do not instill if wearing contact lenses
Beta-adrenergic blockers
The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous humor production.

Levobunolol (AKBeta, Betagan)
Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt to affected eye bid
Pediatric
Not established
• Dosing
• Interactions
• Contraindications
• Precautions
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons

Timolol maleate 0.5% (Timoptic, Timoptic XE, Blocadren)
May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1 gtt of 0.25% or 0.5% in affected eye(s) bid; if IOP is maintained at satisfactory levels, change dosage to 1 gtt in affected eye(s) qd
If clinical response not adequate, change dosage to 1 gtt of 0.5% solution in affected eye(s) bid; if IOP is still not at satisfactory level, consider concomitant therapy
Pediatric
Administer as in adults
• Dosing
• Interactions
• Contraindications
• Precautions
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
• Dosing
• Interactions
• Contraindications
• Precautions
Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock
• Dosing
• Interactions
• Contraindications
• Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, and mental changes (especially in elderly patients)
Follow-up
Further Outpatient Care
• Ophthalmologists should provide long-term follow-up care for patients with NVG, closely monitoring for any worsening in the patient's condition.
• Intensity of follow-up care is related to the conditions predisposing the patient to the development of NVG (ie, CRVO, diabetic retinopathy).
Complications
• Complications include uncontrolled glaucoma, hyphema, and loss of vision.
Prognosis
• Generally, NVG carries a very guarded prognosis. Prognosis is highly dependent on the following 2 factors: prevention and treatment of NVG early in its course and the underlying disease process.
Patient Education
• Patients with NVG must be educated about the disease process and its poor prognosis.
• For excellent patient education resources visit eMedicine's Glaucoma Center and Diabetes Center. Also, see eMedicine's patient education articles Glaucoma Overview, Glaucoma FAQs, Understanding Glaucoma Medications, and Diabetic Eye Disease.
Miscellaneous
Medicolegal Pitfalls
• Early detection of NVG and patient education about its poor prognosis are essential.

malignant Glaucoma

Glaucoma, Malignant
Background
In 1869, von Graefe first used the term malignant glaucoma to describe an entity characterized by elevated intraocular pressure (IOP) with a shallow or flat anterior chamber in the presence of a patent peripheral iridectomy. In its classic form, malignant glaucoma is rare but one of the most serious complications of glaucoma filtration surgery in patients with narrow-angle or angle-closure glaucoma.
The term malignant glaucoma refers to a sustained ongoing process that is difficult to treat and characteristically progresses to blindness. It is sometimes unresponsive and occasionally worsened with conventional management.
Many different terms, including ciliovitreal block and aqueous misdirection syndrome, have been proposed based on diverse unproven pathophysiological and anatomical mechanisms. In the international literature, a common term used to describe a flat anterior chamber is "athalamia." However, it seems appropriate to continue using well-established nomenclature.
Pathophysiology
A blockage of the normal aqueous flow at the level of the ciliary body, lens, and anterior vitreous face is believed to cause malignant glaucoma. Posterior misdirection of aqueous humor into the vitreous cavity occurs producing a continuous expansion of the vitreous cavity and increased posterior segment pressure. This accumulation of aqueous fluid in the vitreous cavity causes anterior displacement of the lens-iris diaphragm in phakic and pseudophakic eyes or forward displacement of the anterior hyaloid in aphakic patients. The resulting shallow or flat chamber is believed to exacerbate the condition because of the decreased access of aqueous to the trabecular meshwork. The IOP is often markedly increased but may be normal.
Epstein et al proposed that forward displacement of the vitreous into apposition with the posterior ciliary body caused a decrease in available hyaloid surface, increasing the resistance to flow from the vitreous body.2 Small hyperopic eyes are at higher risk for malignant glaucoma.
Malignant glaucoma has been described following: cataract surgery with or without intraocular implant (aphakic or pseudophakic malignant glaucoma), implantation of a large posterior chamber intraocular lens, cessation of topical cycloplegic therapy, induction of miotic therapy, laser iridotomy, laser capsulotomy, Nd:YAG cyclophotocoagulation, laser sclerotomy, Molteno implantation, Baerveldt glaucoma drainage device implantation, viscoelastic use, intravitreal injection of triamcinolone acetonide, Aspergillus flavus intraocular infection, and acute hydrops in Down syndrome. Malignant glaucoma has also been described spontaneously in an eye with no antecedent of surgery or miotics. A pseudomalignant glaucoma syndrome has been reported after pars plana vitrectomy.
Frequency
United States
Malignant glaucoma has been reported to occur in 0.6-4% of eyes following filtration surgery for angle-closure glaucoma. Trope et al reported that 71% of 14 patients with malignant glaucoma had chronic angle-closure glaucoma.3 Malignant glaucoma also can be a rare complication of extracapsular cataract extraction with posterior chamber intraocular lens implantation.
International
In Germany, Duy and Wollensak reported 2 cases of ciliary block in 9000 patients following cataract extraction.4 However, both patients had previous filtration procedures with temporary shallowing of the anterior chamber postoperatively.
Mortality/Morbidity
Malignant glaucoma remains a difficult clinical problem that results in irreversible blindness if not promptly treated. The surgeon should be aware preoperatively of eyes at risk and observe them closely postoperatively. Early recognition is the most important step to prevent irreversible vision loss.
Age
Trope et al reported that the average age of patients with malignant glaucoma was 70 years.3
Clinical
History
Typically, patients with narrow-angle or acute or chronic angle-closure glaucoma, who recently underwent filtration surgery, present shortly after surgery; however, it can develop months later or even in the absence of surgery.
• Patients may present with pain and discomfort, increasing redness, blurring, or decreased visual acuity.
• Pain may be severe enough to cause nausea and induce vomiting, similar to an attack of acute angle-closure glaucoma.
• Precipitating factors are suture lysis, initiation of miotic therapy, or discontinuation of cycloplegics.
• Shallowing of the anterior chamber due to wound leak must be ruled out by performing a Seidel test during slit lamp examination.
Physical
• In malignant glaucoma, slit lamp examination reveals anterior displacement of the lens-iris diaphragm in phakic patients and the anterior hyaloid face in aphakic patients, shallowing of the central and peripheral anterior chamber, and elevated intraocular pressure with a patent iridectomy present.
• Optically clear spaces can be observed within the vitreous cavity and have been interpreted as pockets of fluid.
• With the Goldman lens, a completely closed angle can be observed. Choroidal detachments or suprachoroidal hemorrhage should be ruled out using the goniolens mirrors and indirect ophthalmoscopy. The retina should be evaluated for vascular occlusions, and the vitreous should be evaluated for possible hemorrhages. B-mode ultrasound can be extremely useful if direct visualization is not possible.
• Malignant glaucoma is not caused by pupillary block where laser iridotomy can relieve the flow obstruction. In malignant glaucoma, a patent iridectomy must be demonstrated. If not, a new laser iridotomy must be performed.
• Ultrasound biomicroscopy has demonstrated anterior rotation of the ciliary body with apposition to the ciliary process in contact with the lens equator and anterior displacement of the ciliary body and lens, causing iridocorneal touch and appositional angle closure in these patients.
Causes
The exact mechanism that leads to malignant glaucoma is not clearly understood. Movement of aqueous humor from the posterior chamber into the vitreous instead of draining to the anterior chamber may be the cause.
• Malignant glaucoma may occur within hours to days or years after surgery. Most commonly, it is seen after trabeculectomy or surgical iridectomy. This condition may be noted after the cessation of cycloplegic drops or the initiation of miotic therapy after surgery for angle-closure glaucoma.
• The fellow eye is predisposed strongly to develop malignant glaucoma.
• In 1954, Shaffer proposed that misdirection of aqueous humor into the vitreous body or around it was the pathogenic mechanism.5
• In 1972, Levene suggested that malignant glaucoma results from forward movement of the lens with direct closure of the angle intensified by surgery, and it represents a more severe form of angle-closure glaucoma.6 The tone of the ciliary body muscle and the tension of the zonules could explain the anterior movement of the lens.
• Epstein et al hypothesized that a sustained expansion in total vitreous volume moves available peripheral anterior hyaloid into apposition with the posterior ciliary body increasing the resistance for anterior fluid transfer and causing forward displacement of the lens-iris diaphragm and shallowing of the anterior chamber.2
• In 1980, Quigley incorporated data from Fatt into this theory and proposed that dehydrated and compressed vitreous with a decreased fluid conductivity establishes a vicious circle of elevated pressure and anterior chamber shallowing.7,8

Differential Diagnoses
Choroidal Detachment

Pupillary Block, Aphakic

Pupillary Block, Pseudophakic
Other Problems to Be Considered
Suprachoroidal hemorrhage
Overfiltration
Wound leak
Occult annular ciliary body detachment
Workup
Imaging Studies
• A-mode ultrasound is used to measure axial length.
• B-mode ultrasound can discover occult choroidal effusions or hemorrhages or vitreous hemorrhage.
• Ultrasound biomicroscopy (UBM) is used to obtain cross-sectional images of the anterior segment, cornea, iris, lens, and ciliary body at 50 µm resolution with a tissue penetration of 5 mm.
Procedures
• Bleb or wound leaks should be identified and treated first.
• Because of its simplicity, a new laser iridotomy should be performed if suspicion of pupillary block exists.

Treatments for Malignant glaucoma
The list of treatments mentioned in various sources for Malignant glaucoma includes the following list. Always seek professional medical advice about any treatment or change in treatment plans.
• Cycloplegic agents
• Topical phenylephrine
• Topical beta-blockers
• Alpha-adrenergic agonists
• Topical and oral carbonic anhydrase inhibitors
• Osmotic agents
• Argon or Yag laser
• Pars plana vitrectomy

Prognosis for Malignant glaucoma
Prognosis for Malignant glaucoma: The prognosis depends on the length and the severity of the attack. In patients with relatively healthy optic nerves, the prognosis can be good if the attack is abated and intraocular pressure is controlled.

Malignant Glaucoma

Malignant Glaucoma

Background

In 1869, von Graefe first used the term malignant glaucoma to describe an entity characterized by elevated intraocular pressure (IOP) with a shallow or flat anterior chamber in the presence of a patent peripheral iridectomy. In its classic form, malignant glaucoma is rare but one of the most serious complications of glaucoma filtration surgery in patients with narrow-angle or angle-closure glaucoma.

The term malignant glaucoma refers to a sustained ongoing process that is difficult to treat and characteristically progresses to blindness. It is sometimes unresponsive and occasionally worsened with conventional management.

Many different terms, including ciliovitreal block and aqueous misdirection syndrome, have been proposed based on diverse unproven pathophysiological and anatomical mechanisms. In the international literature, a common term used to describe a flat anterior chamber is "athalamia." However, it seems appropriate to continue using well-established nomenclature.

Pathophysiology

A blockage of the normal aqueous flow at the level of the ciliary body, lens, and anterior vitreous face is believed to cause malignant glaucoma. Posterior misdirection of aqueous humor into the vitreous cavity occurs producing a continuous expansion of the vitreous cavity and increased posterior segment pressure. This accumulation of aqueous fluid in the vitreous cavity causes anterior displacement of the lens-iris diaphragm in phakic and pseudophakic eyes or forward displacement of the anterior hyaloid in aphakic patients. The resulting shallow or flat chamber is believed to exacerbate the condition because of the decreased access of aqueous to the trabecular meshwork. The IOP is often markedly increased but may be normal.

Epstein et al proposed that forward displacement of the vitreous into apposition with the posterior ciliary body caused a decrease in available hyaloid surface, increasing the resistance to flow from the vitreous body. Small hyperopic eyes are at higher risk for malignant glaucoma.

Malignant glaucoma has been described following: cataract surgery with or without intraocular implant (aphakic or pseudophakic malignant glaucoma), implantation of a large posterior chamber intraocular lens, cessation of topical cycloplegic therapy, induction of miotic therapy, laser iridotomy, laser capsulotomy, Nd:YAG cyclophotocoagulation, laser sclerotomy, Molteno implantation, Baerveldt glaucoma drainage device implantation, viscoelastic use, intravitreal injection of triamcinolone acetonide, Aspergillus flavus intraocular infection, and acute hydrops in Down syndrome. Malignant glaucoma has also been described spontaneously in an eye with no antecedent of surgery or miotics. A pseudomalignant glaucoma syndrome has been reported after pars plana vitrectomy.

Frequency

United States

Malignant glaucoma has been reported to occur in 0.6-4% of eyes following filtration surgery for angle-closure glaucoma. Trope et al reported that 71% of 14 patients with malignant glaucoma had chronic angle-closure glaucoma. Malignant glaucoma also can be a rare complication of extracapsular cataract extraction with posterior chamber intraocular lens implantation.

International

In Germany, Duy and Wollensak reported 2 cases of ciliary block in 9000 patients following cataract extraction. However, both patients had previous filtration procedures with temporary shallowing of the anterior chamber postoperatively.

Mortality/Morbidity

Malignant glaucoma remains a difficult clinical problem that results in irreversible blindness if not promptly treated. The surgeon should be aware preoperatively of eyes at risk and observe them closely postoperatively. Early recognition is the most important step to prevent irreversible vision loss.

Age

Trope et al reported that the average age of patients with malignant glaucoma was 70 years.

Clinical

History

Typically, patients with narrow-angle or acute or chronic angle-closure glaucoma, who recently underwent filtration surgery, present shortly after surgery; however, it can develop months later or even in the absence of surgery.

• Patients may present with pain and discomfort, increasing redness, blurring, or decreased visual acuity.
• Pain may be severe enough to cause nausea and induce vomiting, similar to an attack of acute angle-closure glaucoma.
• Precipitating factors are suture lysis, initiation of miotic therapy, or discontinuation of cycloplegics.
• Shallowing of the anterior chamber due to wound leak must be ruled out by performing a Seidel test during slit lamp examination.

Physical

• In malignant glaucoma, slit lamp examination reveals anterior displacement of the lens-iris diaphragm in phakic patients and the anterior hyaloid face in aphakic patients, shallowing of the central and peripheral anterior chamber, and elevated intraocular pressure with a patent iridectomy present.
• Optically clear spaces can be observed within the vitreous cavity and have been interpreted as pockets of fluid.
• With the Goldman lens, a completely closed angle can be observed. Choroidal detachments or suprachoroidal hemorrhage should be ruled out using the goniolens mirrors and indirect ophthalmoscopy. The retina should be evaluated for vascular occlusions, and the vitreous should be evaluated for possible hemorrhages. B-mode ultrasound can be extremely useful if direct visualization is not possible.
• Malignant glaucoma is not caused by pupillary block where laser iridotomy can relieve the flow obstruction. In malignant glaucoma, a patent iridectomy must be demonstrated. If not, a new laser iridotomy must be performed.
• Ultrasound biomicroscopy has demonstrated anterior rotation of the ciliary body with apposition to the ciliary process in contact with the lens equator and anterior displacement of the ciliary body and lens, causing iridocorneal touch and appositional angle closure in these patients.

Causes

The exact mechanism that leads to malignant glaucoma is not clearly understood. Movement of aqueous humor from the posterior chamber into the vitreous instead of draining to the anterior chamber may be the cause.

• Malignant glaucoma may occur within hours to days or years after surgery. Most commonly, it is seen after trabeculectomy or surgical iridectomy. This condition may be noted after the cessation of cycloplegic drops or the initiation of miotic therapy after surgery for angle-closure glaucoma.
• The fellow eye is predisposed strongly to develop malignant glaucoma.
• In 1954, Shaffer proposed that misdirection of aqueous humor into the vitreous body or around it was the pathogenic mechanism.
• In 1972, Levene suggested that malignant glaucoma results from forward movement of the lens with direct closure of the angle intensified by surgery, and it represents a more severe form of angle-closure glaucoma. The tone of the ciliary body muscle and the tension of the zonules could explain the anterior movement of the lens.
• Epstein et al hypothesized that a sustained expansion in total vitreous volume moves available peripheral anterior hyaloid into apposition with the posterior ciliary body increasing the resistance for anterior fluid transfer and causing forward displacement of the lens-iris diaphragm and shallowing of the anterior chamber.
• In 1980, Quigley incorporated data from Fatt into this theory and proposed that dehydrated and compressed vitreous with a decreased fluid conductivity establishes a vicious circle of elevated pressure and anterior chamber shallowing.

Differential Diagnoses

Choroidal Detachment

Pupillary Block, Aphakic

Pupillary Block, Pseudophakic

Other Problems to Be Considered

Suprachoroidal hemorrhage

Overfiltration

Wound leak

Occult annular ciliary body detachment

Workup

Imaging Studies

• A-mode ultrasound is used to measure axial length.
• B-mode ultrasound can discover occult choroidal effusions or hemorrhages or vitreous hemorrhage.
• Ultrasound biomicroscopy (UBM) is used to obtain cross-sectional images of the anterior segment, cornea, iris, lens, and ciliary body at 50 µm resolution with a tissue penetration of 5 mm.

Procedures

• Bleb or wound leaks should be identified and treated first.
• Because of its simplicity, a new laser iridotomy should be performed if suspicion of pupillary block exists.

Treatments for Malignant glaucoma

The list of treatments mentioned in various sources for Malignant glaucoma includes the following list. Always seek professional medical advice about any treatment or change in treatment plans.

• Cycloplegic agents
• Topical phenylephrine
• Topical beta-blockers
• Alpha-adrenergic agonists
• Topical and oral carbonic anhydrase inhibitors
• Osmotic agents
• Argon or Yag laser
• Pars plana vitrectomy

Prognosis for Malignant glaucoma

Prognosis for Malignant glaucoma: The prognosis depends on the length and the severity of the attack. In patients with relatively healthy optic nerves, the prognosis can be good if the attack is abated and intraocular pressure is controlled.