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Visual Perception Deficit: Cataract and Glaucoma

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Liceo de Cagayn university – graduate studies | Visual Perception Deficits | Cataract & Glaucoma | Submitted by: | Nadine Angelica C. Gadia – Casiño, RN | March 18, 2012Submitted to:Ms. Delia V. Realista, RN, MANProfessor |

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I. Intoduction
Cataract
Cataracts are common and significant cause of visual defects all over the world. A cataract is an opacification or clouding of the lens of the eye. Cataracts develop because of the alteration of transport of nutrients and metabolism in the lens. This interferes with light transmission to the retina therefore affecting the ability to perceive images clearly. All cells of the lens formed in the lifetime is retained therefore prevalence of cataracts increase rapidly with aging.
WHO estimates that cataracts account for 48% of reversible blindness worldwide, which translates to about 18 million people. Cataracts affect slightly more women than men. The Beaver Dam Eye Study in the US found that 23.5% of women and 14.3% of men had a visually significant cataract by the age of 65 years. Although cataracts can be surgically removed, in many countries surgical services are inadequate, and cataract remains the leading cause of blindness.
Age is the greatest risk factor in the occurrence of cataracts. Cataract, though with unclear links, may be acquired through heredity and genetics (e.g., Wilson's disease, galactosaemia, myotonic dystrophy). Early formation of cataracts is associated with the following risk factors: * Environmental and lifestyle factors such as long term exposure to glares (e.g. welding) and sunlight, smoking and heavy alcohol consumption * Diabetes mellitus particularly in patients with poor control of blood glucose. * Long-term use of corticosteroids
With the clouding of the lens light rays scatter as they pass through thus decreasing visual acuity. There are complaints of glare and impaired color discrimination, particularly in the blue to purple range which explains poor night vision.
Glaucoma
Glaucoma is a condition characterized by optic neuropathy with gradual loss of peripheral vision and increased intraocular pressure. It often goes unnoticed until late in the disease. There are several types of glaucoma, however, the two most common are primary open angle glaucoma, having a slow and insidious onset, and angle closure glaucoma, which is less common and tends to be more acute. Globally, 60.5 million had glaucoma in 2010. Given the aging of the world's population, this number may increase to almost 80 million by 2020. The number of persons estimated to be blind as a result of primary glaucoma is 4.5 million, accounting for slightly more than twelve per cent of all global blindness. The incidence of primary open angle glaucoma rises with age and its progression is more frequent in people of African origin. Often called as chronic simple glaucoma, it accounts for approximately 90% of individual cases. Angle closure glaucoma, on the other hand is less common, accounting to 5% to 10% of all cases as of 2005. Angle closure glaucoma is the common form of glaucoma in people of Asian origin. Commonly, the classification of glaucoma is based on the angle formed at the point where the iris meets the cornea in the anterior chamber.
In open angle glaucoma, the anterior chamber angle between the iris and the cornea is normal; however the flow of aquaeous humor out of the canal of schlemm and trabecular meshwork is obstructed. The mechanism of blockage is unclear. A rise in increased intra-ocular pressure results, characterised by retinal ganglion cell damage, then peripheral vision loss in early disease and central vision loss in late disease. This typically affects both eyes although pressures and progression may not be symmetric.
On the other hand, in angle closure glaucoma, there is narrowing of the anterior chamber angle either from corneal flattening or iris bulging. When the lens thickens in accommodation or when the iris thickens in pupil dilation the angle can close completely. This abruptly increases intraocular pressure damaging the neurons of the retina and the optic nerve leading to rapid and permanent loss of vision if not treated promptly.

II. Anatomy and Physiology The wall of the eye is formed of 3 layers, the fibrous layer – the sclera, the vascular layer – Uvea and the innermost layer – the retina.
The sclera is the thick, white, outermost, fibrous layer. It protects the intraocular contents and maintains the shape of the eyeball. It becomes transparent at the central anterior region to form the cornea. The epithelium, Bowman’s membrane, stroma, Descemet’s membrane and epithelium are the 5 layers that make up this transparent and avascular dome-shaped structure. The epithelial cells are capable of rapid replication and are completely replaced in 7 days. There are 2 structures important in the drainage of the aquaeous humor which is vital in maintaining normal intraocular pressure. This is the Canal of Schlemm and the trabecular meshwork. Found within the sclerocorneal junction of the eye and draining the aqueous humor from the anterior chamber into the veins draining the eyeball is the Canal of Schlemm. The trabecular meshwork separates the angle of the anterior chamber from the canal of Schlemm and contains the spaces of Fontana through which aqueous humor normally drains from the anterior chamber into the canal of Schlemm.
The Uvea is the layer rich in blood vessels. It consists of the iris, the ciliary bodies, and the choroid. The iris is the pigmented collection of fibers surrounding the pupil. The iris has a pigmented layer, dilator muscle and sphincter muscle. The pigmented layer gives color to the eyes, the dilator muscles controlled by sympathetic nervous system dilates in response to dark environment and the sphincter muscle controlled by the parasympathetic nervous system constricts in bright environment. The iris controls the pupils to regulate the light entering the eye. The ciliary body controls accommodation and produces aquaeous humor. The epithelium of the ciliary processes has two layers: an inner, non-pigmented layer in contact with the aqueous humor in the posterior chamber, and an external, pigmented layer in contact with the ciliary process stroma. The external layer is connected to the zonular fibers attached to the cilliary muscle and the lens and controls accommodation – the ability to focus for near vision and refocus in distance vision. When one changes focus from far to near, the ciliary muscle quickly contracts, causing the crystalline lens to accommodate (become thicker) and the object at a near distance to become clear. Then, when looking back again at a far distance, the ciliary muscle immediately relaxes, causing the crystalline lens to revert to a thin shape and one’s far-distance vision to become clear again. The lens controlled by the cilliary bodies and held in place by the zonular fibers is avascular and has no nerve or pain fibers. The lens cellular structure is very susceptible to the degenerative effects of aging because all the cells formed throughout life are retained by it. The choroid is the layer that lies between the retina and the sclera which contains blood vessels that nourish the retina.
The crystalline lens is important in the management of cataracts because it is the main appendage affected by it. The lens has 4 layers, from the surface to the center: capsule, subcapsular epithelium, cortex, and nucleus. The capsule is a smooth, transparent basement membrane that completely surrounds the lens. The capsule is elastic and is composed of collagen. It is very elastic and so causes the lens to assume a more globular shape, a shape it must assume for the eye to focus at a near distance. This is where this is where the zonule fibres insert into. The lens capsule is generated by the cells of the subcapsular epithelium. The cells of the subcapsular epithelium are mitotically active. As they divide, cells gradually move towards the equator of the lens where they transform into lens fibres. The lens fibers form the bulk of the lens. Lens fibres are nucleated in the soft, outer cortex of the lens. As new lens fibres are added to the periphery of the cortex, lens fibres located deeper in the cortex lose their nuclei and become part of the somewhat harder nucleus of the lens. The middle of each fiber lies on the equator. Moving outwards from the central, oldest layer, the lens is split into an embryonic nucleus, the fetal nucleus, the adult nucleus, and the outer cortex. New lens fibers, generated from the lens epithelium, are added to the outer cortex. Learning the structure of the lens allows us to understand the different surgical approaches in cataract extraction. Secretion of aqueous humor and regulation of its outflow are physiologically important processes for maintaining IOP in the normal range. Thus, understanding the complex mechanisms that regulate aqueous humor circulation is essential for management of glaucoma. The two main structures related to aqueous humor dynamics are the ciliary body and the trabecular meshwork. Three mechanisms are involved in aqueous humor formation: diffusion, ultrafiltration and active secretion. Active secretion is the major contributor to aqueous humor formation. The aqueous humor flow in humans follows a circadian rhythm, being higher in the morning than at night. The aqueous humor leaves the eye by passive flow via two pathways - the trabecular meshwork and the uveoscleral pathway (canal of schlemm). Aqueous humour provides nutrients for the avascular lens and corneal endothelium. It is produced by the ciliary body in the posterior chamber, circulates around the lens, through the pupil, and throughout the anterior chamber. Eighty percent of the outflow is through the trabecular meshwork and into the episcleral venous system; the remaining 20% drains out of the uveoscleral pathway via the interstitial spaces between the iris root and ciliary muscle. Aquaeous humor is not only important in maintaining normal intraocular pressure but it is also important in nourishing the avascular corneas and lens.
The retina is the innermost surface of the eye which contains rods and cones, the photoceptors that convert light energy to nerve impulses. Rods, densest at the periphery, are responsible for periphery and dim light vision. Cones, densest in the center of the retina, are color and detail receptors. The retina’s landmarks are the optic disk, the retinal vessels and the macula. The optic disc is the point of entrance of the optic nerve into the retina. It is pink with a sharp oval or circular margin. In the disc is as centrall cupping from which retinal vessels emanate from it. The retinal vessels arise from the optic disc and line the vitreous chamber. These vessels branch out to supply blood to its neighbouring parts. The macula is seen as the slightly oval-shaped, blood vessel-free reddish spot (the fovea) which is at the center of the area responsible for central vision. The rest of the retina is for peripheral vision. There are two sources of blood supply to the retina: the central retinal artery and the choroidal blood vessels. The choroid receives the greatest blood flow (65-85%) and is vital for the maintenance of the outer retina (particularly the photoreceptors) and the remaining 20-30% flows to the retina through the central retinal artery from the optic nerve head to nourish the inner retinal layers. The arterial intraretinal branches then supply three layers of capillary networks
1) the radial peripapillary capillaries (RPCs) - most superficial lying in the inner part of the nerve fiber layer
2) inner layer - lie in the ganglion cell layers under and parallel to the RPCs
3) outer layer - run from inner plexiform layer to the outer plexiform layer thought the inner nuclear layer
The choroidal arteries arise from long and short posterior ciliary arteries and branches of Zinn’s circle (around the optic disc). Each of the posterior ciliary arteries break up into fan-shaped lobules of capillaries that supply localized regions of the choroid. The macular areas of the choroidal vessels are not specialized like the retinal blood supply is. The arteries pierce the sclera around the optic nerve and fan out to form the three vascular layers in the choroid: outer (most scleral), medial and inner (nearest Bruchs membrane of the pigment epithelium) layers of blood vessels. The corresponding venous lobules drain into the venules and veins that run anterior towards the equator of the eyeball to enter the vortex veins. One or two vortex veins drain each of the 4 quadrants of the eyeball. The vortex veins penetrate the sclera and merge into the ophthalmic vein.
The human retina is a delicate organization of neurons, glia and nourishing blood vessels. In some eye diseases, the retina becomes damaged or compromised, and degenerative changes set in that eventually lead to serious damage to the nerve cells that carry the vital messages about the visual image to the brain.
The arterial supply to the optic nerve is derived from the short ciliary arteries. Immediately behind the lamina cribrosa vessels derived from the Circle of Zinn (supplied by the short ciliary arteries) enter the optic nerve. The orbital portion of the optic nerve derives its blood supply from the pial circulation and perhaps also to some extent from the ophthalmic artery and its branches, including the central retinal artery. That portion of the optic nerve lying in the optic canal derives its arterial blood supply from the ophthalmic artery, whilst the intra-cranial part of the optic nerve is supplied centripetally through the pial vessels. Venous drainage from the ocular and orbital portions of the optic nerve is chiefly into the central retinal vein.

III. Disease Process CATARACT | Predisposing Factors | Precipitating Factors | * Age (>60 y.o.) - Changes in lens proteins increase with age and reduce transparency. Increased age allows more time for formation of cortical (outer) layers of the lens that reduces the ability of the lens to accommodate. * Congenital influences - Lamellar or zonular cataracts are the most commonly seen form of congenital cataracts. These are usually bi-lateral and symmetrical.Cataracts may be due to transient toxic influences during lens development, or may be inherited in an autosomal-dominant pattern. * Metabolic or hereditary conditions - These include galactosaemia, Wilson's disease, Marfan's syndrome, and myotonic dystrophy. They may be associated with particular types of cataract (e.g., Christmas tree cataract in people with myotonic dystrophy; sunflower cataract in people with Wilson's disease). Strength of association varies depending on each condition. | * Smoking - Oxidative stress has been linked to changes in crystalline lens proteins leading to the formation of cataract. * Long-term UV exposure - Experimental evidence has shown that the lens is susceptible to UV damage. It has been found that changes in lens proteins, caused by ageing or mutation, can lead to beta-crystallin protein aggregation when exposed to UV radiation. * Eye trauma - Cataracts may be associated with blunt or penetrating injury to the globe. * Long-term ocular corticosteroid use * Diabetes Mellitus * Higher glucose levels lead to retention of glucose in the lens and its conversion to sorbitol. * The vacuoles and clefts seen in diabetic cataracts can cause either the spoke-like cortical cataract or opacities just under the anterior or posterior capsule. * These cataracts often progress very rapidly, especially in young people with poorly controlled diabetes. The most likely reason for this sudden change has been shown to be osmotic stress as a result of sorbitol accumulation. |

Diagnostic tests for Cataract | Test | Normal Values/Results | Alterations | Opthalmoscopy * should be performed following pupillary dilation. | Red reflex clearly visible | Dark shadow on opthalmoscope | Glare vision test * Vision is checked using the best-corrected spectacle prescription and a formal eye chart. * Glare stress is induced using the brightness acuity tester, a hand-held instrument with an illuminated field pierced with a viewing aperture. This instrument allows the examiner to measure the patient's visual acuity under glare conditions that the patient might experience in the real world. | Accommodation to glare stress | significant cataract: reduced visual acuity under the conditions of glare stress | Slit lamp examination * lens is physically examined using the slit-lamp bio-microscope. | Clear lens | Visible lens clouding |

Glaucoma | Predisposing Factors | Precipitating Factors | * Age >50 years * Incidence increases with age. * Risk is 0.02% at 45 years and 10% at 85 years. * The mechanism is unknown. * Family History of glaucoma * Affected first-order family members have a 1 in 10 chance of disease. * Race * Black people are five times more likely to develop disease than white people (open-angle glaucoma). * Inuit and Asian ethnicity have highest rates of angle-closure glaucoma * Gender * Women are 2 to 4 times more likely to have ACG than men. | * Myopia * May be increased risk in myopic patients who have a refractive error of greater than -6 dioptres. * Risk for open-angle glaucoma * Hyperopia * The anterior chamber depth and volume are smaller in hyperopic eyes (farsighted). * Risk for angle-closure glaucoma * Medications * Use of medications that induce angle narrowing. Anticholinergic topical pupil dilators (e.g., cyclopentolate or atropine) or systemic medication (e.g., sulfonamides, topiramate, phenothiazines). |

Diagnostic tests for Glaucoma | Test | Normal Values/Results | Alterations | Tonometry * Measurement of IOP * Goldmann tonometry >Most common, accurate, and most expensive method.> A topical anaesthetic is placed on the patient's eye while the patient is sitting at the slit lamp. A small, sterile cone makes contact with the cornea, and the clinician looks through the lamp for an image of two aligned crescents before determining the reading on the dial.> underestimates pressures in patients with thin corneas and overestimates them in patients with thick corneas- Tono-Pen >A portable device also used with a topical anaesthetic and a sterile cover. It is repeatedly placed on the cornea and beeps when producing a digital readout. If a slit lamp is unavailable or the patient is young and/or unco-operative, this method is particularly useful. | Normal intraocular Pressure = 10-21 mmHg | Chronic open-angle glaucoma: >21mmHgNormal tension glaucoma: IOP = <21 mmHg but with optic nerve damage and visual field defectsAcute Closed Angle Glaucoma: IOP >21 mmHg | Opthalmoscopy * visualisation of optic disc and retina quality | Reflections from the retina at the superior and inferior poles of the optic disc are bright in healthy eyesThe normal cup to disc ratio (the diameter of the cup divided by the diameter of the whole nerve head or disc) is about 1/3 or 0.3. | Optic disc marked pallor and disc cuppingDull reflection of retinaVisible optic nerve damage | Gonioscopy * assess filtration angle of anterior chamber * view of the anatomical angle formed between the eye's cornea and iris | No visible obstruction in anterior chamber filtration angleThere are four structures in the anterior chamber that are of particular interest to view in a gonioscopy exam: Schwalbe’s line, trabecular meshwork, scleral spur, and ciliary body. These have a brown or gray and white color and are arranged in 360 degree bands in the iridocorneal angle. | primary open-angle glaucomagonioscopy = four anterior chamber structures are visible tonometry = intraocular pressure is elevatedopthalmoscopy = with optic nerve damage, optic disc cuppingprimary angle-closure glaucoma. gonioscopy = one or more of the four anterior chamber structures is not visibletonometry = intraocular pressure is elevatedopthalmoscopy = optic nerve damage, optic disk cupping | Perimetry * evaluates field of vision | No scotoma findingsNormal average extentUpward – 65 degreesDownward – 75 degreesInward – 60 degreesOutward – 95 degrees | Scotomas present. Peripheral visual field loss | Pachymetry * a simple, painless test to measure the thickness of your cornea * A probe is gently placed on the front of the cornea to measure its thickness. * Helps diagnosis, because corneal thickness has the potential to influence eye pressure readings. | | Thick corneas = overestimated IOPThin corneas = underestimated IOP |

IV. Medical - Surgical Management
Cataract
Surgical removal is the only treatment. Surgery is only indicated when the cataract has developed to a point that vision and activity are already affected. But it can also be removed when it causes secondary conditions such as glaucoma or uveitis.
Restoration of visual function through a safe and minimally invasive procedure is the surgical goal in cataract removal. When the client presents with bilateral cataracts surgery is performed on one eye at a time. The delay gives time for the patient to recover and the surgeon to evaluate any complications. The surgeon may decide to perform the second procedure differently based on his evaluation.

Surical Management for Cataract: 1. Intracapsular Cataract Extraction – Removal of entire lens and surrounding capsule 2. Extracapsular Cataract Extraction – Removal or anterior capsule, nucleus and cortex 3. Phacoemulsification – An extracapsular surgery using an ultrasonic device that liquefies nucleus and cortex that are suctioned out through a tube. 4. Femtosecond Laser Assisted Cataract Surgery

Perioperative Plan for Cataract Sugery | Pre-operative Phase | Objective for treatment: | a) correction of visual impairmentb) maintenance of quality of lifec) prevention of progression | Physical Examination: | Dilated fundoscopy/OpthalmoscopyVisual acuity testing Slit lamp examination,Tonometry | Diagnostic Procedures: | Visual acuity = 20/40 or better further evaluation contrast glare sensitivity may be done to detect potential problems in night time vision | Prognostic Factors: | Assess socio-demographic characteristicsa) ageb) sexc) social stratad) educatione) raceAssess medical history:a) diabetesb) hematologic disordersc) rheumatoid disordersd) alcohol abusee) ocular trauma and concomitant ocular symptomsf)myopiag) steroid use | Indications for surgery: | a) patient’s preference and needsb) functional disability as measured by Snellens’ visual acuity test and modified VF-14c) cataracts with concomitant ocular problems | Patient Orientation: | a) benefitsb) possible side effects and complications c) costs of available alternative surgical and anesthesia procedures | Pre-operative Preparations: | * Surgeon’s assessment of IOL power to be inserted * Admission on out-patient basis * Withhold anti-coagulant therapy unless otherwise indicated to reduce risk of retrobulbar hemorrhage * Among healthy adult patients scheduled for cataract surgery under local or topical anesthesia, no routine preoperative medical testing is necessary. * For patients who are symptomatic and are at high risk of developing cardiopulmonary complications, pre-operative work-up may be done. * Administration of preoperative medications (e.g. mild sedative, antibiotics) as ordered * Instillation of dilating drops every 10 minutes for four doses at least 1 hour before surgery * Obtain consent for surgery | Operative Phase | Surgical Procedure: | * phacoemulsification or manual phacofragmentation * extracapsular cataract extraction (ECCE) * Laser Cataract Removal | Anesthetic Plan: | * Local anesthesia – Retrobulbar block * Topical anesthesia - avoids the risks and pain associate with needle injections and provides a much quicker return of vision * General Anesthesia - may be used when any of the following conditions exist: a) extremely anxious patient who is unable to cooperate with the surgical teamb) known allergy to local anestheticsc) presence of medical disorders that are best managed under general anesthesia (e.g. severe back pain, postural problems) | Extracapsular cataract extraction with posterior chamber intraocular lens (ECCE-PCIOL) | * Check validity of consent and ensure pre-op files complete and valid * Position safely in operating table in supine * Hook to monitors * Aseptic skin preparation * Proper site draping * Implement surgical safety checklist * Before induction of anesthesia. Sign-in: * Correct identity? * Correct site (left or right eye)? * Correct procedure? * Valid consent? * Functioning pulse oximeter? * Anesthesia safety check? * Known allergy? * Local anesthesia induction via retrobulbar block * Before incision.Time-in: * Surgical team confirm roles * Surgical team confirm patient, procedure, site * Surgeon review critical and unexpected steps, operative time and blood loss * Anesthesia team review patient concerns * Nursing team ensures sterility, proper functioning of equipment and confirms initial count of sponges, instruments and sharps. * Antibiotic prophylaxis in the last 60minutes? * Essential imaging displayed? * Sterile eyelid retractor positioned in place * Use of microscope to make small incision at the edge of the cornea * Capsulorhexis is made manually * Lens separated from the surrounding capsular bag and chopped into pieces with the ultrasonic power of the phacoemulsification instrument. *Complications could be induced during this step (e.g. rupturing the posterior of the capsular bag and causing traumatic injury to the delicate zonular fibers that hold the capsular bag in place) * Manual extraction of lens via emulsification or ultrasound and vibrations to break lens (phacoemulsification) * Posterior capsule left to support lens implant and to protect retina * Debris suctioned out * Intraocular lens implanted (either unifocal or multifocal) * Silicone * Acrylic * poly(methylmethacrylate) (PMMA) (no statistically significant differences in rates of irregular astigmatism post-operatively) * Intermittently irrigate eye with PNSS * Before operation ends.Time-out: * Name of procedure recorded? * Confirmed complete count of sponges, instruments and sharps * Surgeon, anesthesist, and nurse mention key concerns for recovery and management * Corneal flap sutured or left as is * Apply eye patch * Transport to recovery room | Femtosecond Laser Assisted Cataract Surgery | * Check validity of consent and ensure pre-op files complete and valid * Position safely in operating table in supine * Hook to monitors * Aseptic skin preparation * Proper site draping * Implement surgical safety checklist * Before induction of anesthesia. Sign-in: * Correct identity? * Correct site (left or right eye)? * Correct procedure? * Valid consent? * Functioning pulse oximeter? * Anesthesia safety check? * Known allergy? * Powerful topical anesthesia * Before incision.Time-in: * Surgical team confirm roles * Surgical team confirm patient, procedure, site * Surgeon review critical and unexpected steps, operative time and blood loss * Anesthesia team review patient concerns * Nursing team ensures sterility, proper functioning of equipment and confirms initial count of sponges, instruments and sharps. * Antibiotic prophylaxis in the last 60minutes? * Essential imaging displayed? * Sterile eyelid retractor positioned in place * Femtosecond laser is used to make an opening incision, an opening in the lens (capsulorhexis). *"perfect" incisions in terms of size and architecture, which is important in order to have the incision seal properly without the use of stitches and to prevent infection. * Femtosecond laser liquefy the cataractous lens. * Use phacoemulsification instrument to remove the liquefied cataract at a much lower power and in less time or vacuum it using a simple aspiration instrument with no ultrasonic power at all. *uses lesser ultrasonic energy compared to traditional ECCE surgeries. This preserves integrity of the posterior capsular bag and prevents traumatic injury to the delicate zonular fibers * Soft foldable IOLs implanted (either unifocal or multifocal) * Silicone * Acrylic * poly(methylmethacrylate) (PMMA) * Eye seals itself, typically without sutures. It remains tightly closed by the pressure within the eye. *Provides a faster and much more comfortable recovery period * Before operation ends.Time-out: * Name of procedure recorded? * Confirmed complete count of sponges, instruments and sharps * Surgeon, anesthesist, and nurse mention key concerns for recovery and management | Post-operative Phase | ECCE-PCIOL | * Postoperative medications are given as ordered (topical antibiotics, steroids or NSAIDs are recommended.) * Close follow-up with refractive evaluation of the patient is recommended until best corrected vision achieved. * Provide safe environment for patient ambulation (clear pathways from unnecessary furniture and do not rearrange) * During 1st week postoperatively, instruct to avoid shutting eyelids tightly, sneezing, coughing, bending over, lifting (nothing over 25 pounds) or straining. Teach to wear protective glasses * Instruct to avoid swimming or hot tubs for 2 weeks * Explain and demonstrate procedure for administering eye drops * Explain mild bruising around orbital area may be expected from trauma due to local anesthesia * Explain and watch out for signs of complications. Report immediately if there is pain, unbearable discomfort, corneal edema. | Femtosecond Laser Assisted Cataract Surgery | * Released soon after the procedure to go home and relax. * No eye patch needed * Vision improvement almost immediately. * Complete visual recovery varies from patient to patient, but most patients return to their everyday activities within a day or two. * If you have cataracts in both eyes, the second procedure will most likely be scheduled within a week or two. * Serious complications are extremely rare but because it is a form of surgery, there are some potential risks involved. * Report for pain or discomfort immediately | Possible complications after cataract surgery in general: | Complication | Description | Timeframe | Likelihood | supra-choroidal or intra-ocular haemorrhage | Fluctuations in eye pressure or trauma to the intra-ocular structures during surgery can cause bleeding. In some cases, surgery needs to be aborted and can be finished at another time. An expulsive choroidal haemorrhage is the most dire intraoperative complication in cataract surgery. This results from rupture or fracture of a choroidal artery and leads to massive bleeding into the supra-choroidal space. The increased pressure in the supra-choroidal space lifts the retina, and can result in the vitreous and retina being expelled from the eye through the cataract incision leading to blindness. | Short term | Low | corneal oedema | The cornea is kept relatively dehydrated through the pumping action of the corneal endothelial cells. These cells, which line the cornea, are very delicate and non-replicating. Depending on the density of the cataract, significant ultrasonic power may be necessary to fracture the nucleus, causing collateral damage to the corneal endothelial cells and resulting in postoperative oedema.Unless there are pre-existing problems with the corneal endothelium, such as Fuchs's dystrophy, most oedema resolves with time. | Short term | Low | elevated intra-ocular pressure | If the viscoelastic gels used to maintain spaces during cataract surgery are left in the eye following surgery, they can occasionally cause a blockage of the trabecular meshwork.These materials are cleared from the anterior chamber in about 24 hours, and pressure elevations resulting from these materials will generally resolve without sequelae. The use of topical glaucoma medications or the release of a small amount of aqueous fluid from one of the surgical incisions (done in the clinic) can help control the pressure in the short term. | Short term | Low | blindness | If cataracts are not removed and allowed to progress, they can cause functional blindness. Removal commonly restores vision to the pre-cataract level, barring other posterior disease processes. | Long term | Low | infection (endophthalmitis) | The rate of infection (endophthalmitis) after cataract surgery is about 0.07% to 0.12%. The most common organism responsible has been found to be coagulase-negative Staphylococcus. The source for infective organisms is thought to be the normal lid flora, although outbreaks of endophthalmitis due to contaminated solutions and instruments used in surgery have been reported. Postoperative checks at 1 day and 1 week help identify signs of infection. Topical and/or intra-vitreal antibiotics or surgery, depending on the severity of the infection, is the necessary treatment. | Variable | Low | cystoid macular oedema | Even an uneventful surgery can cause some disturbance of the vitreous and cause inflammation in the eye leading to cystic spaces developing in the fovea of the retina. This is more commonly seen in people with diabetes mellitus. Treatment with topical corticosteroids and NSAIDs, or injection of corticosteroids around or into the eye, generally results in resolution of this postoperative problem. | Variable | Low | posterior capsular tear and vitreous loss | Cataract surgery can be complicated by a tear in the posterior surface of the bag that holds the lens in place in about <1% to 4% of cases. This lens capsule is about 5 micrometres in thickness and can become torn during surgery. If a tear occurs, the vitreous humour usually sequestered in the posterior chamber of the eye can come forwards and/or increase the chance of endophthalmitis postoperatively. Traction on the vitreous can increase the risk of macular oedema and/or retinal tears or detachment after cataract surgery. | Variable | Low | retinal detachment | Traction on the vitreous can increase the risk of retinal tears or detachment after cataract surgery. This may require further surgery to repair the detachment. | Variable | Low |

Glaucoma
Glaucoma treatment is a lifelong therapy. It cannot be cured. The main goal treatment is prevention of optic nerve damage. Treatment focuses on pharmacologic therapy, laser procedures, surgery or a combination of these approaches. Although treatment cannot reverse present optic nerve damage, further damage may be controlled. Managing intraocular pressure to ensure it is within a range unlikely to aggravate present condition.
Pharmacologic Therapy for Glaucoma: The primary pharmacologic agents used to treat glaucoma are topical cholinergics, adrenergics, beta-adrenergic blocking agents, prostaglandin analogs and carbonic anhydrase inhibitors.

Pharmacologic Agents | Therapeutic Effects | Adverse Effects | Nursing Responsibility | Cholinergics(e.g. Pilocarpine, Carbachol) | * Increase AH outflow by miosis * Open TM | * Periorbital pain * Blurred vision * Dificulty seeing in the dark * Systemic effects such as, bradycardia, bronchoconstriction | * Remind of dim light precaution * Teach punctual occlusion to prevent systemic effects | *Not commonly used for the treatment of open angle glaucoma and ocular hypertension mainly because of poor tolerance of side effects of these drugs. The use of miotics is almost exclusively confined to the treatment of narrow angle or angle closure glaucoma and some secondary glaucomas. | Adrenergics (e.g. Alphagan, epinephrine) | * Decrease AH production * Increase AH absorption | * Systemic effects, such as Tachycardia, palpitations, elevated BP, anxiety * Bronchodilation * Eye redness burning | * Assess for risk for AACG, hypertension, cardiac dysrythmias, coronary heart disease * Stress to patient to report changes in visual acuity or eye pain (indication of AACG) * Teach occlusion to prevent systemic effects | Beta-Adrenergic Blockers (e.g. Timolol, Betaxolol) | * Decrease AH production * No effect on pupil size | * Systemic effects such as, bradycardia, bronchoconstriction, hypotension | * Asssess for asthmas, COPD, heart blocks and heart failure * Contraindicated for COPD, 2o or 3o heart blocks, cardiac failure | Carbonic Anhydrase Inhibitor (e.g. Acetazolamide, Dorzolamide | * Decrease AH production | * Anaphylactic reaction to sulphonamide * Electrolyte loss, gastrointestinal upset, weight loss, lethargy, impotence | * Asses for allergy to sulfa drugs and presence of severe renal or hepatic disease * Monitor for drug interactions * Assess daily weight, strict input and output monitoring, serum electrolyte monitoring, and vital signs taking for patients taking oral and parenteral medications. | Prostaglandin Analogs (e.g. Latanoprost, Bimatoprost) | * Increase AH outflow * Advantage: single daily dose | * Permanent darkening of iris * Increased eyebrow and eyelash growth * Conjunctival redness | * Assess and note eye color, presence of inflammation and exudates * Instruct to follow orders, use once daily at bedtime |

Surgical Management for Glaucoma:
Open-Angle Glaucoma 1. Laser Trabeculoplasty – Aimed through a gonioscope to create multiple laser burns spaced evenly around the trabecular meshwork. As the scars heal they cause tension, stretching and opening of the meshwork. This is noninvasive and the treatment of choice a. argon laser trabeculoplasty (ALT) - an outpatient procedure. A contact lens is placed on the eye to focus an aiming beam onto the trabecular meshwork (TM) and half of the TM is treated (180 degrees) at one sitting. ALT is thought to work by activating cells called trabeculocytes and thus improving TM function. It may take up to six weeks for treatment to have the full effect and after this, if further IOP lowering is needed, the second 180 degrees of the TM is treated. Re-treatments in the same area can cause scarring of the TM and raised IOP b. selective laser trabeculoplasty (SLT) - similar to ALT but uses a different laser with a discharge of a very short duration. The spot size of the laser beam is much larger than that used for ALT so accurate identification of the TM is not as critical and the procedure is technically simpler. The mechanism of action is thought to be the same as ALT but re-treatments are said to be less likely to cause raised IOP because there is less photocoagulative damage to adjacent tissue 2. Trabeculectomy – type of filtration surgery in which a permanent fistula is created to drain aquaeous humor. 3. Ciliary body ablation (cycloablation) - permanent destruction of the ciliary body, it is usually the.last line of treatment 4. Insertion of filtering device – Insertion of microtechnology to regulate the drainage and outflow of aquaeous humor

Perioperative Plan for Chronic Primary Open Angle Glaucoma | Pre-operative Phase (Chronic Open Angle Glaucoma) | Objective for treatment: | Control IOP and prevent further damage to optic nerve. | Recommended diagnostic tests: | For patients suspected of having COAG or who have OHT: * IOP measurement using Goldmann applanation tonometry (slit lamp mounted) * central corneal thickness (CCT) measurement * peripheral anterior chamber configuration and depth assessments using gonioscopy * visual field measurement using standard automated perimetry (central thresholding test) * optic nerve assessment, with dilatation, using stereoscopic slit lamp biomicroscopy with * fundus examination | History Taking: | Ensure that all of the following are made available at each clinical episode to all healthcare professionals involved in a person's care: * records of all previous tests and images relevant to COAG and OHT assessment * records of past medical history which could affect drug choice * current systemic and topical medication * glaucoma medication record * drug allergies and intolerances | Monitoring of patients with Chronic Open Angle Glaucoma and Ocular Hypertension:* Benefits of regular monitoring: * a low risk of ever developing visual impairment within their lifetime * an acceptable IOP | Clinical Assessment | Monitoring Interval in months | | IOP at target | Risk of conversion to COAG | Action | IOP Monitoring | IOP, Optic Nerve, Visual field | | YES | Low | No change in tx plan | n/a | 12 – 24 months | | YES | High | No change in tx plan | n/a | 6 – 12 months | | NO | Low | Review IOP and change tx plan | 1 – 4 months | 6-12 months | | NO | High | Review IOP and change tx plan | 1 – 4 months | 4- 6 months | Recommendations on treatment for patients with COAG | * Check that there are no relevant comorbidities or potential drug interactions before offering medication. * Offer people newly diagnosed with early or moderate COAG and at risk of significant visual loss in their lifetime treatment with a prostaglandin analogue. * Offer people with advanced COAG surgery with pharmacological augmentation * Informed consent should be obtained and documented * Offer people who present with advanced COAG and who are listed for surgery interim treatment with a prostaglandin analogue. * Encourage people using the prescribed pharmacological treatment to continue with the same treatment unless: * IOP cannot be reduced sufficiently to prevent the risk of progression to sight loss * there is progression of optic nerve head damage * there is progression of visual field defect * they are intolerant to the drug | Pre-operative Preparations: | * Admission on out-patient basis * Withhold anti-coagulant therapy unless otherwise indicated to reduce risk of retrobulbar hemorrhage * Administration of preoperative medications (e.g. mild sedative, antibiotics) as ordered | Preoperative Considerations for Trabeculectomy* Trabeculectomy is a commonly performed glaucoma surgical procedure when medications fail to adequately control the IOP. | * Performed only in COAG * Necessary to have intact, non-scarred conjunctiva. * Trabeculectomy can be difficult to perform in an eye that has had previous ocular surgeries with scarred tissue. | Preoperative Considerations and instructions for Glaucoma Drainage Device Implant | * Drainage implant surgery is used in patients who may have failed other filtering surgeries and need a lower IOP. * Useful in patients at higher risk of failure from trabeculectomy, due to previous scarring or inflammation of conjunctival tissue. * Patients with neovascular glaucoma, uveitis (inflammatory) glaucoma, and conjunctival scarring from previous ocular surgeries are are candidates for GDD surgery | Ciliary body ablation (cycloablation) Considerations | * last line of treatment for uncontrolled glaucoma * When trabeculectomy or glaucoma drainage tube (seton) has failed to control glaucoma * | Operative Phase | Surgical Management Options: | * Trabeculectomy * Trabeculotomy ab interno * Trabecular stent bypass microsurgery * Laser Therapy * Glaucoma Drainage Devices * Ciliary body ablation (cycloablation) | Sign in to time- in | * Check validity of consent and ensure pre-op files complete and valid * Position safely (Supine or sitting) * Hook to monitors * Aseptic skin preparation * Proper site draping * Implement surgical safety checklist * Before induction of anesthesia. Sign-in: * Correct identity? * Correct site (left or right eye)? * Correct procedure? * Valid consent? * Functioning pulse oximeter? * Anesthesia safety check? * Known allergy? * Local anesthesia induction * Before incision.Time-in: * Surgical team confirm roles * Surgical team confirm patient, procedure, site * Surgeon review critical and unexpected steps, operative time and blood loss * Anesthesia team review patient concerns * Nursing team ensures sterility, proper functioning of equipment and confirms initial count of sponges, instruments and sharps. * Antibiotic prophylaxis in the last 60minutes? * Essential imaging displayed? * Sterile eyelid retractor positioned in place | Trabeculectomy | | * Goal: Create a small hole in the anterior chamber of the eye to allow drainage of the aqueous fluid toward the outside. * Local anesthesia : Retrobulbar block * Incision through the conjunctiva. * Creates a partial-thickness sclera flap (or trapdoor) on the sclera (eye wall). * Underneath the scleral flap, a surgeon cuts a small hole into the anterior chamber, which allows the drainage of aqueous fluid through the scleral flap and into the sub-conjunctival space. * An iridectomy (hole in the iris) is performed at this point to allow the scleral opening to stay open without being blocked by the iris tissue. * The scleral flap is then tied down with stitches that are loose enough to allow continuous drainage of the aqueous fluid. * Overlying conjunctival tissue is closed with stitches to allow formation of a bleb or an elevation of conjunctival tissue formed by the aqueous fluid, which is being filtered out of the scleral flap (trapdoor) underneath. * The filtering bleb is usually located in the superior aspect of the eye and covered by the upper lid. * The aqueous fluid from the filtering bleb is then slowly absorbed by the conjunctival and episcleral (on the surface of the sclera) blood vessels and drain into the orbital venous system. | Trabeculotomy ab interno | * removing a portion of the trabecular meshwork to improve drainage of aqueous humour. It avoids the creation of a subconjunctival bleb associated with traditional trabeculectomy | * scleral incision is made and a viscoelastic is inserted into the anterior chamber * Electrical ablation (aided by a goniolens) is used to remove a strip(s) of the trabecular meshwork. * The eye is then irrigated and the viscoelastic aspirated from the anterior chamber. * The incision is sutured. | Trabecular stent bypass microsurgery | * reduce IOP by creating a bypass channel between the anterior chamber and Schlemm's canal to improve drainage of aqueous humour | * This procedure is often combined with phacoemulsification and intraocular lens insertion for the concomitant treatment of cataracts * small corneal incision is made and viscoelastic is inserted into the anterior chamber * Under gonioscopic guidance and using a special applicator, an L-shaped stent is slid through the trabecular meshwork and into Schlemm's canal. * The position of the stent is verified * viscoelastic is removed * applicator withdrawn * More than one stent may be inserted during the same procedure. | Laser Therapy | Argon Laser Therapy (ALT)OrSelective Laser Trabeculoplasty (SLT)* utilizes a neodynium:YAG laser. | * A topical glaucoma eye drop (e.g. brimonidine) is given 15 minutes prior to the procedure to prevent a post-laser IOP elevation. * Gonioscopic contact lens is placed on the surface of the cornea *allows visualization of the drainage angle. * (for ALT) The laser spots are then delivered to the trabecular meshwork. Either 180º or 360º of the angle is treated per treatment session. *Each area of the angle is treated only once to avoid scar formation in the angle. * (for SLT) . Either 180º or 360º of the angle is treated. Can be repeated. *Laser targets only the pigmented cells in the trabecular meshwork while sparing the non-pigmented cells from thermal damage | Glaucoma Drainage Devices | The GDDs are tubes are attached to a plate, and allow aqueous fluid to drain from the inside to outside of the eye. | * Goal: Allow aqueous fluid to leave the eye so that IOP will be lowered and halt the progression of glaucomatous visual loss * Local anesthesia. Either a periocular injection of anesthetic is given, and/or topical medications to provide adequate pain control. * The conjunctiva in the designated quadrant of the eye is opened so that the eye muscles may be identified. * Both the tube and plate are covered by donor tissue and by patient’s own conjunctiva. * A GDD can be with or without a valve. * With valve (Ahmed and Krupin) - made so that a set pressure is required before the tube opens and begins to drain aqueous fluid. They are usually implanted in cases where an immediate lowering of IOP is desired. * Without a valve (Baerveldt and Molteno) - have no resistance to outflow of aqueous fluid, which may result in too low of an IOP (hypotony) initially. Severe or prolonged hypotony may lead to decreased vision or hemorrhage. To avoid these complications, the non-valved tube is often tied off with a dissolvable suture. The suture dissolves in approximately 6 weeks. Scar tissue develops over the tube plate which causes the required resistance to outflow that is necessary to avoid hypotony. Patients with non-valved GDDs are forewarned that the vision may suddenly become blurry with floaters about 6 weeks after surgery when the tube opens. The symptoms typically resolve over time. * The plate of the tube is placed between or underneath the eye muscles of the eye. * It is fastened to the underlying sclera with permanent sutures. * The tube is then cut to appropriate length and inserted into the anterior chamber. * A small piece of donor tissue (sclera, cornea, pericardium, or dura) is then placed over the tube so that it does not erode through the overlying conjunctiva. * The conjunctiva is placed back into place over the plate to cover the tube. * In non-valved tube, a dissolvable suture may be used to tie off the tube. | Ciliary body ablation (cycloablation) | | * Goal: Destroy AH producing cillary bodies * Anesthesia: Loacal anesthesia – Retrobulbar block * Portable diode laser is used to perform Cyclo PhotoCoagulation (CPC) * Laser Targets cilliary processes * Opertion may be repeated as needed | Time-Out | * Before operation ends.Time-out: * Name of procedure recorded? * Confirmed complete count of sponges, instruments and sharps * Surgeon, anesthesist, and nurse mention key concerns for recovery and management * Corneal flap sutured or left as is * Apply eye patch * Transport to recovery room | Post-operative Phase | Post-operative Instructions | * Postoperative medications are given as ordered (topical antibiotics, steroids or NSAIDs are recommended.) * Close follow-up with regular monitoring * IOP measurement using Goldmann applanation tonometry (slit lamp mounted) * central corneal thickness (CCT) measurement * peripheral anterior chamber configuration and depth assessments using gonioscopy * visual field measurement using standard automated perimetry (central thresholding test) * optic nerve assessment, with dilatation, using stereoscopic slit lamp biomicroscopy with * fundus examination * Provide safe environment for patient ambulation (clear pathways from unnecessary furniture and do not rearrange) * During 1st week postoperatively, instruct to avoid shutting eyelids tightly, sneezing, coughing, bending over, lifting (nothing over 25 pounds) or straining. Teach to wear protective glasses * Instruct to avoid swimming or hot tubs for 2 weeks * Explain and demonstrate procedure for administering eye drops * Explain mild bruising around orbital area may be expected from trauma due to local anesthesia * Explain and watch out for signs of complications. Report immediately if there is pain, unbearable discomfort, corneal edema. * Stress on importance of strict medication compliance to preserve visual integrity. Noncompliance will result to irreversible vision loss. | Laser Therapy Postoperative Considerations | * After the laser procedure, another glaucoma eye drop is administered to prevent post-operative IOP spike. * The IOP is measured 1 hour after the procedure to ensure that it is stable. * Patients are advised to continue the glaucoma medications that they were using prior to the laser treatment. * Short course of topical steroids is given to reduce post-operative inflammation. * Patients return for follow-up examination in 4-6 weeks to determine if the ALT treatment decreased the IOP. * If IOP is still uncontrolled, additional surgical intervention may be necessary. | Trabeculoplasty Considerations | * Recovery period is between 6-8 weeks * Post-operative follow-up is particularly important because the success of the surgery depends on the rate and extent of conjunctival healing process. * Follows the patient closely, usually on a weekly (sometime more frequent) basis initially. * During follow-up visits, adjustments can be made to reduce the IOP if is too high. This can be done by cutting (or pulling) stitches from the scleral flap with a laser to allow additional filtration (laser suturelysis). * Occasionally, the surgeon may elect to needle the bleb post-operatively if there is excessive conjunctival scarring process. A small gauge needle is used to break up the scar tissue to allow more filtration of the aqueous fluid, and usually performed in a minor procedure room under topical anesthesia. * If the IOP is too low, the surgeon may reduce the amount of anti-inflammatory (or steroid) medications to allow additional healing process. In short, there are many adjustments that may be done postoperatively to maximize the chance of surgical success. * Emphasis on proper postoperative follow-up under the direction of the treating surgeon. | GDD Considerations | * Patients who receive a valved implant are asked to discontinue their glaucoma medications after surgery, since the tube is expected to lower IOP immediately. * Glaucoma medications may be re-instituted based upon the level of IOP. * Non-valved implants do not work until approximately 6 weeks after surgery when the suture dissolves, patients are often asked to continue their glaucoma medications until this occurs. Once the tube opens and the IOP decreases, medications are discontinued as tolerated. * In both types of implants, patients are treated with topical steroids and antibiotics post-operatively. Occasionally pupil-dilating drops (cycloplegics) are used to keep the eye comfortable and to keep the anterior chamber well-formed. * Patients are asked to avoid heavy lifting, bending their head down below the waist, and getting dirty water in the eye. A shield is often used at night for eye protection initially. * Postoperative visits are important since medication adjustments will be made after the IOP is checked. * Important not to dwell too much on the IOP in the early postoperative period since it can fluctuate significantly. It is not uncommon to have significant fluctuation in IOP during the first several weeks after glaucoma surgery. | Ciliary body ablation (cycloablation) Postoperative Considerations | * The recovery period is usually 4-6 weeks * . The follow up visits are not as intensive as the filtering surgery * Post-operatively, the eye is treated with tapering regimen of anti-inflammatory steroids. * Potential complications associated with CPC * Decrease in vision post-operatively. *Reserved for patients who already have reduced vision from either glaucoma or other causes pre-operatively. * Associated with increased inflammation, bleeding, and hypotony (low IOP usually below 5 mmHg). Hypotony is a particularly feared complication of CPC because it is often difficult to raise the IOP after a permanent destruction of the ciliary body | Postoperative Complications for PCOAG Surgery: | Laser Therapy (ALT or SLT) | * Post-laser IOP spike – most common laser therapy complication * Pressure elevation is often transient * typically causes no long-term complication. * Occurs from the inflammation that ensues after laser energy is delivered to the trabecular meshwork. * Treated with additional glaucoma medications as needed. * Anterior segment inflammation (iritis) - is another complication * Post-laser topical steroids are given to control inflammation. Topical steroids are used for several days to a week after treatment. | Trabeculectomy | * Failure to adequately lower the IOP - The most common short-term complication of trabeculectomy surgery * Due to the excessive scarring of the conjunctival tissue with decreased filtration of the aqueous fluid out of the eye. * Hypotony - extremely low IOP * Due to the excessive filtering of the aqueous fluid or leaking wound. * Low IOP (typically below 5 mmHg) can cause: * blurry vision * shallowing of the anterior chamber * cataract formation * greater risk of intraocular fluid accumulation (choroidal effusion) or intraocular bleeding (suprachoroidal hemorrhage). * Suprachoroidal hemorrhage - A particularly feared complication after trabeculectomy * Often associated with pain, elevated IOP, and permanent decrease in vision. * Requires additional surgery to drain the blood.(long-term complications) * trabeculectomy bleb around the eye * If there is a leak from the bleb, the IOP may become too low. * The bleb leak can increase the risk of infection. * Post-trabeculectomy Infection - Serious condition because of the surgical hole in the sclera may allow a direct access to micro-organism * Intraocular infection can seriously compromise the vision and even integrity of the eye itself. * Eye such as pain, decreased vision, redness, and purulent discharge, should be reported and examined promptly. * This may occur even years after the surgery. * Post-trabeculectomy patients are encouraged to always wear goggles during swimming and are discouraged from wearing contact lenses in order to decrease the possibility of a bleb infection (called blebitis or bleb-associated endophthalmitis). | GDD Insertion | * Vision loss from bleeding, infection, retinal detachment, swelling of the cornea or retina, hastening of cataract formation, or too low an eye pressure (hypotony). * Additional glaucoma medications or surgery may be needed if the IOP remains higher than desired. * Implant may migrate or become exposed by eroding through the conjunctival tissue. * Ptosis after surgery * Double vision (diplopia) These complications can be treated medically or surgically. If they occur, additional medication or surgery may be needed. | CPC | * associated with increased inflammation, bleeding * Hypotony is a particularly feared complication of CPC because it is often difficult to raise the IOP after a permanent destruction of the ciliary body.. |

Closed-Angle Glaucoma 1. Gonioplasty – The healing and scarring of microscopic lesions created at the periphery of the iris. This draws the iris away from the cornea widening the anterior chamber angle. 2. Laser Iridotomy – Noninvasive procedure using a laser to create multiple perforations in the iris of the eye to aid in the outflow of AH to the trabecular meshwork and canal of Schlem. Iridectomy removes a segment of the iris to achieve the same effect. Perioperative Plan for Acute Angle Closure Glaucoma | Preoperative Phase | Objective for treatment: | Lower the IOP as soon as possible and to prevent further attacks | Recommended diagnostic tests and signs of AACG: | * Goldmann applanation tonometry (slit lamp mounted)= Reveal rapid elevation in IOP * fundus examination/ Opthalmoscopy = haziness of the cornea, and a mid-dilated pupil * Gonioscopy = Forward bowing of iris * Anterior chamber angle less than 45O * Redness of conjunctiva * Pain * Halos around lights | First line of Treatment | * Administration of IOP lowering medications * Ensure stability of IOP before opting for surgery * carbonic anhydrase inhibitors and/or topical beta-blocker and/or topical alpha-2 agonistCarbonic anhydrase inhibitors decrease aqueous humour formation and are used commonly as first-line therapy in combination with beta-blockers and alpha-2 agonists. Topical dorzolamide and brinzolamide are preferred over systemic acetazolamide and methazolamide. Topical beta-blockers lower intra-ocular pressure (IOP) through suppression of aqueous humour production. Beta-blockers reduce IOP by around 20% to 30% within 1 hour of instillation. Topical alpha-2 adrenergic agonists lower IOP through suppression of aqueous humour production. Alpha-agonists reduce IOP by around 26% within 2 hours post-dose. | Adjunct Treatment | 1. If ACG is be secondary to pupillary block or plateau iris syndrome and IOP is <40 mmHgUse topical ophthalmic cholinergic agonists as adjunct treatment. * Cause pupil constriction with thinning of the iris and its pulling away from the inner eye wall and trabecular meshwork * Instillation frequency and concentration of pilocarpine is determined by response. * Heavily pigmented iris may require higher strengths * Acute attack 1% to 2% is the preferred solution. * Stronger miotics may increase the pupillary block. They cause shallowing of the anterior chamber and narrowing of the angle in eyes with angle closure secondary to lens-induced mechanism or aqueous misdirection. They are therefore contraindicated in these cases.Patients may be maintained on pilocarpine as long as IOP is controlled and no deterioration in visual fields occurs. 2. If there is failure of initial medical treatment or IOP is greater than 50 mmHg,Use hyperosmotic agents (1st: Glycerol, 2nd: Mannitol) * Used to control acute episodes of elevated IOP. * Transient effects *Rarely administered longer than a few hours | Before any attacks occur (prevention for both eyes) | * Critically narrow drainage angles must be recognized prior to an attack of acute angle closure. * When detected, critically narrow drainage angles need treatment with a laser peripheral iridotomy to prevent attacks of acute angle closure glaucoma. Laser peripheral iridotomy is performed in one eye at a time, within a few weeks of each other. | After an attack (prevention in the other eye) | * Attack of acute angle closure glaucoma in one eye, it is treated emergently. * In many cases, the fellow eye also has a critically narrow drainage angle and is at high risk for acute angle closure as well. * A laser peripheral iridotomy should be performed to prevent acute angle closure in the fellow eye as soon as the eye with acute angle closure becomes stable after treatment. | Preoperative preparation for Laser Peripheral Iridotomy | * Resolve acute attack before proceeding to surgery * Ensure IOP stability before performing surgery * Glaucoma medication is given to prevent any post-laser IOP elevation. * Pilocarpine given. Constrict pupil so that the hole can be placed peripherally * If cornea too swollen and hazy (which precludes a good view of the iris) Administer glaucoma medications, both topical and oral, to decrease the IOP. This can reduce corneal swelling and increase the clarity of the cornea. * Glycerin is another agent which acts to draw fluid from the cornea and temporarily improve the corneal clarity. | Preoperative Preparation for Laser Iridoplasty | Indication for Laser Iridotomy: * If plateau iris configuration present. Plateau iris is caused by a forward rotation of the ciliary body, which causes narrowing of the drainage angle peripherally. | Operative Phase | Laser Peripheral IridotomyLPI is done to create a bypass channel for aqueous to flow from behind the iris to the front of the iris, and subsequently, into the drainage angle | * The procedure typically lasts 10-15 minutes. * Once the view is adequate, the laser procedure can be performed. * LPI is done under topical anesthesia. * Special iridotomy contact lens is placed on the cornea. * The laser is then performed through the contact lens. Different lasers are utilized for this procedure including the Argon and YAG laser. Sometimes a combination of the two lasers is used to create the LPI * The Argon laser typically requires pigment for the uptake of the laser energy and therefore, is better for darker colored (i.e., brown) eyes * The YAG laser disrupts the tissue and is better suited for lighter colored (i.e., blue) eyes * A hole is made in the peripheral part of the iris, typically under the upper eyelid * After the procedure, another glaucoma medication is given. | Laser Iridoplasty or gonioplasty | * Iridoplasty is similar to the other laser procedures with regard to intra- and post-operative care. * Topical anesthesia is used as well as a glaucoma medication (e.g. brimonidine) to prevent post-laser IOP elevation. * A contact lens is used to visualize the peripheral iris and its contraction with Argon laser energy * Argon laser to shrink the peripheral iris. Pulls iris away from the trabecular meshwork and improves the aqueous outflow. | Postoperative Phase | * An IOP check is performed 1 hour after the laser treatment. * Topical steroids are given for several days and then tapered or discontinued. This helps alleviate any inflammation from the laser. * The inflammatory cell and pigments released during iridotomy may cause decreased vision after the laser, but this typically subsides in 3-4 days. * After LPI relieves the pupillary block, a narrow angle will usually deepen when observed through a goniolens. | Postoperative Complications of AACG | Complication | Description | Timeframe | Likelihood | retinal vein occlusion | This complication may be prevented by prompt reduction of intra-ocular pressure (IOP). Once it occurs there is no specific immediate treatment. | short term | Medium | loss of vision | Prevented by prompt IOP management | short term | Medium | fellow eye attack | * The fellow eye is at high risk of developing acute angle closure, Other eye usually shares the anatomical predisposition for increased pupillary block, * An untreated fellow eye has a 40% to 80% risk of developing an acute attack. * Contraralateral eye treated prophylactically with laser peripheral iridotomy if the chamber angle is found to be anatomically narrow | variable | High | permanent decrease in visual acuity | * Primary angle-closure glaucoma (PACG) patients present with higher IOP and more advanced visual field loss * PACG is a more IOP-dependent disease * After successful treatment of acute primary angle closure, there is some evidence that retinal nerve fibre layer thickness significantly decreases within 16 weeks after the attack. * Adequate and prompt treatment with lowering of IOP will reduce the risk for permanent injury to the retinal ganglion cells and axons. | variable | Medium | repeat episode of acute ACG | * If the mechanism of angle closure was not eliminated, an acute episode can recur. * In this case the clinician should look for the specific mechanism of angle closure, and treat it accordingly. * Verify if the peripheral iridotomy is patent. | Variable | Low |

V. Nursing Management Assessment | Nursing Diagnosis | Goals | Implementation | Evaluation | (Cataract) * Cloudy lens * (+)Blurry vision * Complaints of glare * Complaints of decreased visual acuity * Complaints of poor night vision(Primary Open Angle Glaucoma) * ( - ) Peripheral vision * Disc cupping on opthalmoscopy * IOP >21mmHg(Acute Angle closure glaucoma) * Halos around light * Hazy cornea * Red conjunctiva * Rapid increase in IOP | Disturbed Sensory (Visual) Perception related to clouding of lens secondary to cataractDisturbed Sensory (Visual) Perception related to optic nerve damage secondary to glaucoma | Enforce optimum functioning despite of visual compromise.Provide safe environment Prevent further damage and aggravation of present condition | 1. Adress patient by name, identify self with each interaction, orient to time, place, person and situation, state purpose of visit before any interaction*Lack of visual cues increases the importance of verbal cues to keep oriented 2. Orient to the environment. Explain the location of personal things, call light, personal items and furniture in the room. *Orientation to environment keeps patient comfortable and safe. They become more capable of self-care in a known environment. Easy access encourages to use these items and enhance ability for self care 3. Provide items that can compensate for diminished vision (e.g. Reading materials in large print, Audio books, Gadgets, tactile stimulants) 4. Assist with meals by: * Describing position of food on tray according to clock system * Placing utensils in accessible position * Remove lids from containers*Assistance during eating is important to maintain nutritional status. Be aware of nonverbal cues, the client might be embarrassed upon requesting and claim not to be hungry. 5. Assist with mobility and ambulation as needed * Allow the patient to hold your arm or elbow walk slightly ahead as a guide * Describe surroundings. Warn in advance of potential hazards. Use correct clear directions. 6. If unilateral vision loss is present and recent, provide instruction related to change of depth and perception (e.g. be careful in going down the stairs) 7. Emphasize on proper medication compliance and proper administration*Especially in glaucoma, medication therapy is lifelong to prevent further vision loss 8. Emphasize importance of regular follow-up of condition particularly in patients with cataract. *Regular check up and monitoring is needed to see efficacy of therapeutic regimen or deterioration of condition | * Prevention of further vision loss * Proper management of IOP at optimum range * No observed aggravation of optic nerve damage * Self-care is maintained * No mobility associated injuries reported because of vision loss * Optimum functioning |

Assessment | Nursing Diagnosis | Goals | Implementation | Evaluation | * Poor eye contact * Verbalization of fears * Quivering in voice * Tachycardia * Irritability * Restlessness | Anxiety related to fear of vision loss and inability to carry out roles | Alleviate anxietiesEstablish coping strategies | 1. Use therapeutic communication to encourage verbalization of feelings*Verbalizing helps externalize the anxiety and allows fears to be addressed 2. Discuss perception of eye condition and its effects on lifestyle and roles*Discussion provides opportunity to correct misconceptions and introduce alternative activities and assistive devices for clients 3. Identify coping strategies that have been useful in the past to increase the client’s sense of control | More relaxed nonverbal cues evidenced by normal breathing, warm hands, establishment or eye contactVerbalization of coping strategies and positive outlook in condition |

Assessment | Nursing Diagnosis | Goals | Implementation | Evaluation | (Primary Open Angle Glaucoma) * ( - ) Peripheral vision * Disc cupping on opthalmoscopy * IOP >21mmHg * Mismanaged IOP * Further deterioration of vision(Acute Angle closure glaucoma) * Halos around light * Hazy cornea * Red conjunctiva * High IOP = >21 mmHg * No signs of improvement in condition | Non compliance to medication regimen related to lack of financial resources and social support | Identify social systems to support therapeutic Regimen | 1. Provide information on available support systems from the government, sight foundations and the like 2. Emphasize compliance to medication regimen important to prevent further vision loss 3. Collaborate with social services to provide support to keep up with medication regimen | Identification of support systemPrevention of further damage |

VI. Health Education 5. Emphasize on regular monitoring and strict adherence to medication regimen to maintain optimum vision. 6. Emphasize to attend to scheduled appointments for follow ups and teach signs and symptoms of complications for direct referral 7. Teach proper instillation and administration of eye medications i. Shake milky suspensions ii. Wash hands before instilling medications iii. Ensure adequate lighting iv. Assume comfortable position v. Hold lower lid down without pressing the eyeball vi. Instill eyedrops first before eye ointments vii. Keep eye lids lightly closed and apply gentle pressure to the inner canthus for 1-2 minutes to prevent systemic effects viii. Using a clean tissue gently pat skin to absorb extra eyedrops ix. Wait 5 minutes before applying on next eye. 8. Improve diet. Include food rich in Vitamin A and antioxidants. 9. Prevent injury. Keep environment safe for patient with evident visual loss. Do not rearrange furniture and keep obstructions and hazards out pathways (e.g. loose rugs, stools, corner tables). 10. Advise eye protection from UVB. Discuss lifestyle changes for smokers. Inform about link between heavy smoking and development of eye problems. Smoking can precipitate to prompt cataract development and it can damage fine retinal vessels. 11. Inform family members of hereditary disposition of cataract and glaucoma. Eye exam should be every 1 to 2 years. While people above 40 without genetic factors should receive eye exam every 2 to 4 years

Bibliography:
Internet sources: http://www.benthamscience.com/open/toophtj/articles/V004/52TOOPHTJ.pdf http://www.who.int/blindness/causes/priority/en/index7.html http://www.ahaf.org/glaucoma/about/understanding/flow-of-aqeous-humor.html http://www.ahaf.org/glaucoma/about/understanding/facts.html http://www.ahaf.org/glaucoma/about/understanding/anatomy-of-the-eye.html http://bestpractice.bmj.com/best-practice/monograph/372/highlights.html http://bestpractice.bmj.com/best-practice/monograph/373/highlights.html http://bestpractice.bmj.com/best-practice/monograph/499/highlights.html http://webvision.med.utah.edu/book/part-i-foundations/simple-anatomy-of-the-retina/ http://www.mastereyeassociates.com/eye-diseases-treatments/glaucoma-surgery---istent/ http://www.revophth.com/content/d/glaucoma/c/22742/ http://www2.cfpc.ca/cfp/2005/Sep/vol51-sep-cme-3.asp http://www.lab.anhb.uwa.edu.au/mb140/corepages/eye/eye.htm http://books.google.com.ph/books?id=Cphm_fxwvl8C&pg=PA129&lpg=PA129&dq=episcleral+vein+anatomy&source=bl&ots=obSZn1faQy&sig=41co5k8htpvU57ulNcDxC-A5ExI&hl=en&sa=X&ei=kFJhT_KhJK2tiQeJ5J3HBw&ved=0CDkQ6AEwAw#v=onepage&q=episcleral%20vein%20anatomy&f=false http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712693/ Books:
Smeltzer et.al, Brunner and Suddarth’s Textbook of Medical-Surgical Nursing, 11th edition, Lippincott & Wilkins, 2008
Sarrosa et.al, Funda-tips Comprehensive guide to holistice fundamentals of nursing review, 2010

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